Meningitis (2024)

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by J. Austin Lee

Authors
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You have a new patient!

A 21-year-old male presented to a clinic. He is a refugee and has been here with a high-grade fever and a severe headache for the past three days. The patient had been working as a laborer in construction sites in the area for the past six months. At triage, his vital signs are as follows: temperature of 39.1°C (102.5°F), blood pressure of 110/70 mmHg, heart rate of 110 beats per minute, and respiratory rate of 22 breaths per minute.

Further examination reveals that the patient is quite photophobic. You note that he prefers to sit still, and when you examine him further, you feel that his neck is quite uncomfortable when flexed, and there is discomfort with flexed hips and passive knee extension. The patient was accompanied by a co-worker who reported that this morning, the patient was vomiting and had been confused. The patient had no history of recent travel or vaccination.

What do you need to know?

Importance

Meningitis is an important infectious disease with severe consequences if not promptly recognized and treated. Meningitis is caused by inflammation of the meninges, the membranes covering the brain and spinal cord. It can be caused by a bacterial, viral, fungal, or parasitic infection. Moreover, meningitis can be triggered by physical injury, autoimmune disorders, cancer, or certain drugs that can cause meningitis. Generally, when discussing meningitis, we are primarily concerned with infectious etiologies. In addition to the high mortality associated with meningitis, survivors may suffer from long-term sequelae, such as hearing loss, cognitive impairment, and neurologic deficits [1]. Infants, children, and immunocompromised patients are at a higher risk of developing meningitis, and outbreaks can occur in crowded living conditions, with classic examples including crowded urban areas (including slums), university dormitories, and military barracks [2]. Prompt recognition and treatment with appropriate antibiotics or antivirals are critical for improving outcomes in patients with meningitis [3].

Epidemiology

Meningitis is a significant global health problem, particularly in low- and middle-income countries. According to the World Health Organization (WHO), there are an estimated 1.2 million cases of bacterial meningitis each year, resulting in 250,000 deaths [4]. According to the Global Burden of Disease study, meningitis is responsible for an estimated 21.9 million disability-adjusted life years (DALYs) globally [5]. The burden of meningitis is particularly high in sub-Saharan Africa, where large-scale epidemics of meningococcal meningitis occur. In these regions, outbreaks are often associated with overcrowding, malnutrition, and poor sanitation, and can cause high rates of mortality and long-term disability. While vaccination has helped to reduce the burden of meningitis in many parts of the world, there is still a need for continued surveillance and control measures, particularly in high-risk populations.

Pathophysiology

Bacteria (and viruses and chemicals) can cross the blood-brain barrier to infect or inflame the meninges by spreading from the bloodstream. Pathogens can also spread from contiguous infection (from a source such as the sinuses or middle ear), trauma, neurosurgery, or indwelling medical devices [6]. Nasopharyngeal colonization from infected droplets of respiratory secretions or distant localized infection (lungs, urine) with subsequent bloodstream invasion are other sources of infection [6].

Once the pathogen reaches the meninges, it triggers an immune response, releasing pro-inflammatory cytokines, which attract immune cells to the site of infection. This immune response leads to the characteristic symptoms of meningitis, including fever, headache, neck stiffness, and altered mental status. In severe cases, the inflammation can lead to increased intracranial pressure, cerebral edema, and brain herniation, which is life-threatening and frequently fatal [6].

Bacterial meningitis poses an emergent risk to the neurological system; progression can result in rapid fatality. Furthermore, bacterial meningitis has the potential to cause long-term complications, including hearing and vision impairment, memory and concentration issues, epilepsy, coordination and balance difficulties, learning challenges, and behavioral disorders [6]. In community-acquired meningitis, S. pneumoniae has become the most common pathogen since routine immunization of infants against H. influenzae type B [7]. It’s important to note that the most common causes of meningitis can vary depending on the patient’s age, geography, and immune status [8]. Table 1 summarizes most common pathogens of meningitis.

Table 1: Common Infectious Causes of Meningitis [7-14].

Pathogen

Common Etiologies

Bacteria

Neisseria meningitidis, Streptococcus pneumoniae, Haemophilus influenzae, Listeria monocytogenes

Viruses

Enteroviruses (e.g. Coxsackie virus, Echovirus), Herpes simplex virus, Varicella-zoster virus, Mumps virus

Fungi

Cryptococcus neoformans, Histoplasma capsulatum, Coccidioides immitis

Parasites

Naegleria fowleri, Acanthamoeba species

Medical History

Key features in the medical history of meningitis include the onset and duration of symptoms, recent travel or exposure to infectious agents, immunization status, underlying medical conditions, and medication use. It is important to obtain a detailed history of present illness, including the timing and progression of symptoms such as fever, headache, neck stiffness, altered mental status, and rash. Patients may also report symptoms such as nausea, vomiting, photophobia, and seizures. Recent travel or exposure to individuals with known or suspected meningitis can help identify potential infectious agents. Immunization status, particularly regarding vaccines against meningococcal and pneumococcal infections, is also important to determine. Patients with chronic medical conditions or who are taking immunosuppressive medications may be at increased risk for certain pathogens or complications.

Physical Examination

The physical exam findings in a patient with meningitis include vital signs, general appearance, and specific neurological findings. Vital signs such as fever, tachycardia, and hypotension are common. Patients may appear acutely ill, with a lethargic or altered mental status. They may exhibit signs of meningeal irritation, such as photophobia, neck stiffness, and a positive Kernig or Brudzinski sign. Kernig’s sign is the inability to straighten the leg when the hip is flexed to 90 degrees; Brudzinski’s sign is positive when forced flexion of the neck elicits a reflex flexion of the hips [6]. Both Kernig and Brudzinski have reported low sensitivity (5%) but high specificity (95%) [6]. Neurological findings such as altered level of consciousness, focal neurologic deficits, and seizures may also occur or be present. Skin findings such as a petechial or purpuric rash may present in meningococcal meningitis patients. In infants, bulging fontanelles and poor feeding are concerning. Jolt accentuation testing can provide additional value: the patient horizontally rotates the head at two to three rotations per second [15]. The worsening of an existing headache indicates a positive result, though the sensitivity of jolt accentuation for diagnosing meningitis varies widely, with estimates ranging from 40-96% [15].

Table 2: Common signs/symptoms of meningitis, with sensitivity [8-10]

Sign / Symptom

Sensitivity

Neck stiffness

30-100

Headache

70-100

Photophobia

50-90

Nausea/vomiting

50-90

Altered mental status

50-80

Jolt accentuation

40-90

Fever

70-80

Seizures

10-30

Focal neurological deficits

<10

Alternative & Differential Diagnoses

  • Encephalitis: inflammation and swelling of the brain parenchyma; encephalitis tends to cause more neurological symptoms such as confusion, seizures, and changes in behavior or personality.
  • Chemical meningitis (e.g., due to contrast agents, medications, or illicit drugs): The patient should have a history of exposure to a triggering agent, such as a medication or contrast dye.
  • Carcinomatous meningitis (e.g., metastatic cancer cells in cerebrospinal fluid); history or imaging with evidence of metastatic disease.
  • Aseptic meningitis (e.g., due to autoimmune disorders, sarcoidosis, or drug reactions) symptoms are usually milder. They may include fever, headache, and neck stiffness, often including other symptoms such as rash or joint pain.
  • Cerebral vasculitis is inflammation and damage to the blood vessels that supply the brain. It may have a more insidious onset and a chronic or recurrent course.
  • Traumatic meningitis (e.g., due to head injury or neurosurgical procedures)
  • Brain abscess or subdural empyema; likely to include more focal neurological symptoms/deficits such as weakness or paralysis, seizures, or speech and vision problems.
  • Subarachnoid bleeding is commonly associated with sudden, severe headaches, nausea, vomiting, and, at times, syncope.
  • Tetanus is commonly associated with other symptoms such as jaw stiffness, diffuse muscle rigidity/spasm, difficulty swallowing, and respiratory distress.
  • Malaria, particularly cerebral malaria, is typically found in areas with high transmission rates of malaria, and cerebral malaria typically has a more gradual onset. It can progress over several days to weeks.

Acing Diagnostic Testing

Acute diagnostic testing is crucial in managing meningitis as it allows for early detection and appropriate treatment. The accepted gold standard for diagnosing meningitis is cerebrospinal fluid (CSF) analysis, obtained through a lumbar puncture [6,16]. CSF analysis includes cell count, protein and glucose levels, culture, and gram stain [16]. Elevated CSF white blood cell count and protein levels are common findings in meningitis, while glucose levels are often decreased. CSF culture and gram stain are essential to identify the causative organism, guide antimicrobial therapy, and can be used to monitor response to treatment.

In addition to CSF analysis, imaging studies such as computed tomography (CT) or magnetic resonance imaging (MRI) may also be obtained to evaluate for complications of meningitis, such as hydrocephalus, cerebral edema, or abscess formation. However, these imaging studies are typically not used for the initial diagnosis of meningitis. CT is a strong consideration to be performed before lumbar puncture (LP) to exclude increased intracranial pressure (ICP) or mass lesion when CT is available and a patient has any of these criteria: immunocompromised state, history of CNS disease, new-onset seizure, papilledema, severe decreased consciousness (GCS<12) or focal neurologic deficit [6].

Blood cultures may also be obtained to help identify the causative organism and determine appropriate antimicrobial therapy. In particular, meningococcemia can rapidly lead to shock and multiorgan failure. Other laboratory tests, such as complete blood count (CBC), chemistry panel, and coagulation studies, are also routinely obtained to evaluate potential complications or comorbidities.

Rapid diagnostic tests, such as polymerase chain reaction (PCR) or antigen tests, may also be available in some settings. These tests can help quickly identify some causes of meningitis, such as bacterial or viral meningitis. They can provide near real-time speciation of the causative organism and help tailor appropriate treatment.

Table 3: CSF Testing Characteristics [9-11, 17-19]

Test

Normal Results

Bacterial Meningitis Results

Viral Meningitis Results

Fungal Meningitis Results

Appearance

Clear, colorless

Cloudy or turbid

Clear to slightly cloudy

Cloudy or turbid

WBC count

<5 cells/microliter

Elevated

Elevated, often lymphocytic

Elevated, often lymphocytic

Glucose

40-70 mg/dL

Decreased

Normal or slightly decreased

Decreased

Protein

15-45 mg/dL

Elevated

Normal to slightly elevated

Elevated

Gram stain

No organisms

Gram-positive or gram-negative organisms

Negative for bacteria, positive for virus

Negative for bacteria and virus

Culture

Negative

Positive for bacterial growth

Negative for bacteria, positive for virus

Positive for fungal growth

Risk Stratification

Several features in the history, physical examination, and testing can indicate a worse outcome in a patient with meningitis. Some of these include advanced age, altered mental status, presence of seizures, hypotension, tachycardia, high cerebrospinal fluid (CSF) protein and low glucose levels, high white blood cell count in CSF, and delayed initiation of appropriate antimicrobial therapy.
Various risk stratification tools have been developed for meningitis, such as the Glasgow Meningococcal Septicemia Prognostic Score (GMSPS), which is used to predict mortality in meningococcal disease. This tool includes variables such as age, Glasgow Coma Scale score, presence of meningismus, and presence of shock. This tool is most helpful in identifying the most sick cases, which are likely to be evident based on the clinical history and exam. Although this score exists, it is not routinely used in clinical practice. Another tool is the Bacterial Meningitis Score (BMS), which helps clinicians differentiate bacterial from aseptic meningitis based on the presence of certain clinical and laboratory features. The BMS includes age, cerebrospinal fluid protein level, cerebrospinal fluid neutrophil count, and peripheral blood absolute neutrophil count.

Management

In patients with whom you have concerns about meningitis, stabilization of an unstable patient is the priority. Assess the airway and breathing, including monitoring the respiratory rate and saturation levels. Administer supplemental oxygen if necessary. Evaluate circulation by checking the pulse, capillary refill time, and blood pressure. Provide fluids or administer medications as required. Next, the neurological function can be evaluated using tools like the Glasgow Coma Scale or AVPU (Alert, Verbal, Painful, Unresponsive) scale. Additionally, glucose levels and the presence of focal neurological signs, seizures, and papilledema should be assessed.

Empiric antibiotics should be started as soon as possible, even before the results of CSF culture and sensitivity are available, in order to reduce the risk of mortality and morbidity. In addition, supportive measures such as fluid and electrolyte management, seizure prophylaxis, and management of increased intracranial pressure are essential in managing meningitis. Patients with severe disease or complications may require ICU admission. Close follow-up with repeat CSF analysis and neuroimaging may be necessary to monitor response to treatment and identify potential complications.

Empiric treatment for bacterial meningitis typically involves using third-generation cephalosporins, such as ceftriaxone or cefotaxime, with or without vancomycin to cover for potential penicillin-resistant strains of Streptococcus pneumoniae. In infants under 1 month of age and patients over 50 years, ampicillin is often added to cover for Listeria monocytogenes [2]. Dexamethasone, a corticosteroid, is also given prior to or at the time of antibiotic initiation in adults and children with suspected or confirmed bacterial meningitis to reduce the risk of neurologic sequelae. The administration of corticosteroids has been shown to significantly reduce hearing loss and neurological complications in patients with meningitis.

However, using corticosteroids has not significantly impacted overall mortality rates [20]. The management of viral meningitis is mainly supportive. Antiviral treatment may be considered for specific viral pathogens, such as acyclovir for herpes simplex virus (HSV) or ganciclovir for cytomegalovirus (CMV). However, empiric antiviral treatment is not recommended in most cases of viral meningitis. The use of corticosteroids, such as dexamethasone, is controversial in viral meningitis and is not generally recommended [20].
Pre-exposure prophylaxis, though intrapartum prophylaxis of group B streptococcus in pregnant women, has significantly reduced the risk of early-onset group B strep meningitis [21]. Post-exposure prophylaxis is also an important consideration in contacts of patients diagnosed with meningitis; close contacts are defined as individuals who have had prolonged close contact with the index case, such as household contacts, healthcare workers, or individuals who shared a room or had direct contact with respiratory or oral secretions. Antibiotic prophylaxis is typically recommended within 24-48 hours of identification of the index case and may include rifampin, ciprofloxacin, or ceftriaxone, depending on the age and health status of the contact. In addition to antibiotics, vaccination with the meningococcal conjugate vaccine may be recommended for close contacts, particularly those at increased risk.

The recommended antibiotic prophylaxis is usually a single dose of intramuscular ceftriaxone (250 mg for adults and children weighing > 45 kg and 125 mg for children weighing < 45 kg). Alternatively, oral antibiotics such as rifampin, ciprofloxacin, or azithromycin can be used as alternatives. For exposure to Streptococcus pneumoniae, oral amoxicillin is recommended for prophylaxis, and for exposure to Haemophilus influenzae type b (Hib), rifampin or ceftriaxone is recommended.

Special Patient Groups

Elderly individuals, particularly those over 65, may present with atypical meningitis characterized by lethargy, minimal signs of meningismus, and the absence of fever. Conversely, younger individuals such as neonates, infants, and children often present with symptoms such as poor feeding, irritability, fever, and in babies, a shrill cry, decreased appetite, rash, and vomiting. In young children, the presentation of meningitis can mimic flu-like symptoms, including cough or respiratory distress, and it is not uncommon for them to have a history of respiratory tract infection. Seizures are also more frequently observed in this age group with meningitis. When evaluating a febrile child who appears unwell, it is crucial to consider bacterial meningitis as a potential diagnosis until ruled out. It is worth noting that blood and cerebrospinal fluid results may appear normal, especially in extremely young or old age groups.

When To Admit This Patient

Patients with suspected meningitis should be admitted to the hospital from the emergency department, as this is a potentially life-threatening condition that requires urgent evaluation and treatment. Admission should be considered for patients with a high likelihood of meningitis based on clinical presentation and laboratory findings. Patients with severe symptoms such as altered mental status, seizures, or signs of sepsis are particularly high-risk and should be admitted promptly. Patients with risk factors such as immunocompromised status, recent head trauma, or history of neurosurgical procedures should also be admitted.

Patients with meningitis who present with severe symptoms or complications such as altered mental status, seizures, respiratory distress, or signs of sepsis should be considered for admission to the intensive care unit (ICU). In addition, patients with bacterial meningitis or other severe forms of meningitis, such as fungal or tuberculous meningitis, and those immunocompromised should also be admitted to the ICU for close monitoring and aggressive treatment. Patients with a high risk of developing cerebral edema or increased intracranial pressure, such as those with hydrocephalus or brain abscess, may also require ICU admission. Close monitoring of vital signs, neurologic status, and laboratory parameters, such as blood glucose and electrolytes, is likely best done in an ICU.

Revisiting Your Patient

Let’s go back to the clinical presentation of your 21-year-old male refugee. He has fever, tachycardia, vomiting and confusion, and meningitis was suspected. You performed a lumbar puncture, and the cerebrospinal fluid analysis showed a white cell count of 1500 cells/µL with predominant neutrophils, protein level of 150 mg/dL, and glucose level of 30 mg/dL. The patient was started on treatment with intravenous ceftriaxone and vancomycin and admitted to the hospital. The patient was diagnosed with bacterial meningitis and was continued on intravenous antibiotics for a total of 14 days.

The patient responded well to the treatment and was discharged after completing the course of antibiotics. Appropriate public health notification was made, and the patient was scheduled for post-discharge follow-up care and vaccination.

Author

Picture of J. Austin Lee, MD MPH DTMH

J. Austin Lee, MD MPH DTMH

Austin Lee, MD MPH DTMH, is a practicing emergency medicine doctor in the United States. He currently works with Indiana University Health, across several hospital sites. Dr. Lee obtained an MPH at the George Washington University before going to medical school at Indiana University. He completed his emergency medicine residency at the University of Virginia, and then worked at Brown University where he was a part of the Global Emergency Medicine fellowship. Austin has worked on a number of international emergency medicine projects, and is actively engaged in supporting the development of emergency medicine in Kenya.

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References

  1. Tunkel AR, Scheld WM. Acute meningitis. In: Jameson JL, Fauci AS, Kasper DL, Hauser SL, Longo DL, Loscalzo J, eds. Harrison’s Principles of Internal Medicine. 20th ed. Vol 1. New York, NY: McGraw-Hill Education; 2019:894-900.
  2. Mandell GL, Bennett JE, Dolin R. Principles and Practice of Infectious Diseases. 8th ed. Vol 2. Philadelphia, PA: Elsevier; 2015:1116-1132.
  3. Longo DL, Kasper DL. Bacterial meningitis. In: Longo DL, ed. Harrison’s Infectious Diseases. 3rd ed. New York, NY: McGraw-Hill Education; 2018:360-373.
  4. World Health Organization. Defeating meningitis by 2030. Accessed May 25, 2023. https://www.who.int/initiatives/defeating-meningitis-by-2030.
  5. GBD 2016 Meningitis Collaborators. Global, regional, and national burden of meningitis, 1990-2016: a systematic analysis for the Global Burden of Disease Study 2016. Lancet Neurol. 2018 Dec;17(12):1061-1082.
  6. Parežnik A. Meningitis. October 12, 2018. Accessed May 25, 2023. https://iem-student.org/meningitis/.
  7. McGill F, Heyderman RS, Panagiotou S, Tunkel AR, Solomon T, Connor MD. Acute bacterial meningitis in adults. The Lancet. 2016;388(10063):3036-3047.
  8. Lu CH, Chang WN, Chang HW, et al. Adult bacterial meningitis in southern Taiwan: epidemiological trend and prognostic factors. J Neurol Sci. 2005;22(2):133-139.
  9. van de Beek D, de Gans J, Spanjaard L, et al. Clinical features and prognostic factors in adults with bacterial meningitis. N Engl J Med. 2004;351(18):1849-1859.
  10. Tunkel AR, Hartman BJ, Kaplan SL, et al. Practice guidelines for the management of bacterial meningitis. Clin Infect Dis. 2004;39(9):1267-1284.
  11. van de Beek D, de Gans J, Tunkel AR, et al. Community-acquired bacterial meningitis in adults. N Engl J Med. 2006;354(1):44-53.
  12. McGill F, Griffiths MJ, Solomon T. Viral meningitis: current issues in diagnosis and treatment. Curr Opin Infect Dis. 2017 Apr;30(2):248-256.
  13. Góralska K, Blaszkowska J, Dzikowiec M. Neuroinfections caused by fungi. Infection. 2018 Aug;46(4):443-459.
  14. Pana A, Vijayan V, Anilkumar AC. Amebic Meningoencephalitis. 2023 Jan 21. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan
  15. Iguchi M, Noguchi Y, Yamamoto S, Tanaka Y, Tsujimoto H. Diagnostic test accuracy of jolt accentuation for headache in acute meningitis in the emergency setting. Cochrane Database Syst Rev. 2020 Jun 11;6(6):CD012824.
  16. Roberts JR, Custalow CB, Thomsen TW. Roberts and Hedges’ Clinical Procedures in Emergency Medicine and Acute Care. Elsevier; 2018.
  17. Kumar R, Bose M, Singh SN, et al. Clinicoradiological and neurophysiological correlation in Japanese encephalitis. Ann Trop Paediatr. 1994;14(4):311-318.
  18. González-Duarte A, Cárdenas G, Torres-Narbona M, et al. Cerebrospinal fluid lactic acidosis in aspergillosis meningitis. Arch Neurol. 2007;64(9):1362-1364.
  19. Brouwer MC, Tunkel AR, van de Beek D. Epidemiology, diagnosis, and antimicrobial treatment of acute bacterial meningitis. Clin Microbiol Rev. 2010;23(3):467-492.
  20. van de Beek, D., de Gans, J., McIntyre, P., Prasad, K., & Weisfelt, M. (2004). Corticosteroids for acute bacterial meningitis. The Cochrane Database of Systematic Reviews, (1), CD004405.
  21. Thigpen MC, Whitney CG, Messonnier NE, Zell ER, Lynfield R, Hadler JL, et al. Bacterial meningitis in the United States, 1998-2007. N Engl J Med. 2011;364(21):2016-2025.

Reviewed and Edited By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Delirium and Dementia (2024)

~ iEM Education Project Team ~ Leave a comment

by Lo Lucian Simeon, Ngai Oona Wing Yan, & Lo Yat Hei

Authors
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You have a new patient!

Adam is a 76-year-old man who is brought to the emergency room by his family members, complaining of a lack of responsiveness and general lethargy. According to his family, Adam has been having increasing memory problems in the past year and has gotten lost while walking around his neighborhood multiple times. His personality has changed and becomes agitated easily. He is also becoming less attentive to personal hygiene, wearing dirty clothes for several days, and having several episodes of urinary incontinence. Today, his family members noted that he had fallen asleep multiple times and showed no interest in his food. He did not respond when addressed by name. At the time of presentation, he is conscious, but appears lethargic and uncooperative. He cannot tell where he is and does not seem to recognize his family members. His past medical history includes hypertension and hypercholesterolemia. He is taking amlodipine and simvastatin.

Vitals show a heart rate of 108 beats per minute, blood pressure 154/84 mmHg, temperature 36.7℃, respiratory rate 20 breaths per minute, and an oxygen saturation of 98% on room air. His Glasgow coma score is E4V4M6.

What do you need to know?

Importance

Dementia and delirium are two medical conditions that significantly impact the health and well-being of older adults and their families. In this case, Adam’s symptoms suggest that he may be experiencing one or both of these conditions, and it is important to understand their relevance in clinical practice.

Dementia is defined as an acquired global decline in cognitive function, affecting one’s memory, language, learning, and behavior without impairment of consciousness. Dementia is associated with a gradual, progressive decline. It is a leading cause of disability and dependence among older adults, with advancing age being one of the most significant risk factors [1]. With the global population aging, the number of individuals living with dementia is expected to rise significantly. The World Health Organisation estimates that 47 million people worldwide live with dementia, and this number is expected to triple by 2025 [2].

Delirium, conversely, is a clinical syndrome characterized by an acute state of confusion, inattention, and cognitive impairment. It can occur in people of any age, but is particularly common among the older population and hospitalized patients [1]. Delirium can wax and wane over time, unlike dementia, which is more progressive and persistent.

Dementia and delirium pose a tremendous burden not only on patients and caregivers, but also on our healthcare system and society. Therefore, understanding the significance of dementia and delirium is crucial in clinical practice. Identifying and managing these conditions early improves clinical outcomes and optimizes quality of life.

Epidemiology & Pathophysiology

Dementia is a condition that is more commonly seen in older individuals, with the incidence increasing from the age of 65.  An exception is frontotemporal dementia, a rare type of dementia that is usually diagnosed from the age of 40 to 60. The most prevalent type of dementia is Alzheimer’s disease, which accounts for 60-80% of all cases. Other neurodegenerative dementias, such as vascular dementia, dementia due to Lewy bodies, Parkinson’s disease, and frontotemporal dementia, account for the remaining cases [3].

The underlying pathophysiology of dementia varies depending on the type and subtype, with most types involving damage to neurons and their connections in the brain. Abnormal protein accumulation is a common feature for many types of dementia, including amyloid and tau in Alzheimer’s disease, Lewy bodies with alpha-synuclein protein in Lewy body disease, and mutations causing the deposition of TDP-43 and tau proteins in frontotemporal dementia. Other factors, such as ischemic injury, HIV infection, and alcohol consumption, can also lead to cytotoxic processes in the brain and contribute to the development of dementia [4].

On the other hand, the epidemiology of delirium is more complex as it varies depending on age and underlying medical conditions. Although delirium is more prevalent in older individuals, with rates increasing after the age of 70, it is also common in younger patients suffering from chronic illnesses such as cardiovascular and renal comorbidities, dementia, or psychiatric illnesses [5].

The pathophysiology of delirium can result from various physiological and structural lesions in the brain. While its mechanisms are not fully understood, delirium can be caused by neurotransmitter imbalances, brain lesions involving the ascending reticular activating system, as well as disrupted blood-brain barrier function that causes the leakage of neurotoxic agents into the brain. Patients with impaired cholinergic transmission, such as those with Alzheimer’s disease, are particularly susceptible to delirium caused by medication use. Additionally, delirium can result from alcohol abuse, drug withdrawal, mental illnesses, psychosocial stress, and sleep deprivation [6].

Epidemiological and pathophysiological data on dementia and delirium allow physicians to identify individuals at risk and intervene appropriately. Since the development of dementia and delirium are multifactorial and the pathophysiology is variable among patients, evaluating and treating delirium and dementia is based on clinical gestalt and the presumed underlying cause.

Medical History

Dementia and delirium are two diagnoses that must be considered in elderly patients presenting with cognitive change to the emergency department. Differentiation between the two conditions is based on features noted in the history and physical examination. Table 1 lists symptoms that can help differentiate between the two conditions.

Delirium typically presents with sudden onset of impaired awareness, confusion, clouding of consciousness, and disturbances of perception (e.g., illusions or hallucinations). Delirium should be suspected when there is an acute deterioration in behavior, cognition, and daily functioning [7]. Delirious patients usually have short-term memory issues and may be disoriented by time and place. Abnormalities of cognition and behavior can fluctuate over brief periods. The level of awareness may range from hypervigilant and agitated to blunt and unreactive. The patient’s speech may be incoherent, nonsensical, or tense. The patient usually has no discernible focal neurological defect [8].

Dementia has various presentations according to the specific types, but symptoms often overlap. Alzheimer’s dementia, the most common type, presents with a history of a chronic, steady decline in cognitive ability, especially memory. It is often associated with difficulties in social relationships, activities of daily living, and work. During the early stages of dementia, clinical presentations can be quite subtle, and patients may try to hide their cognitive impairments [9].

Patients who present to the emergency department with symptoms of dementia are most likely in the later stages of disease progression. Acute presentation of dementia is possible in vascular dementia, and this subtype may present with symptoms of focal neurological deficit. Patients who are demented typically do not present with any impairment of consciousness. However, acute episodes of delirium can be superimposed on patients who have dementia.  For example, Lewy body dementia can present with fluctuating levels of consciousness. Diagnosing uncommon variants poses a challenge to emergency physicians and is often done only after referral to a neurologist [10].

Obtaining a thorough history is essential in diagnosing delirium and dementia. Unfortunately, delirious or demented patients are often disoriented and cognitively impaired, resulting in the inability to provide accurate information about their condition. A detailed history should be obtained from family, caregivers, and healthcare staff (nurses, healthcare assistants, and other allied health professionals).

Important features to note during history are the onset of symptoms, factors that worsen or improve symptoms, drug or alcohol use, pre-existing endocrine or psychiatric disorders, exposure to toxins or traumatic injury, social history, and previous similar episodes of confusion or altered mental status. Drug history is particularly important as the use of drugs that impair cognition (e.g., analgesics, anticholinergics, psychotropic medications, and sedatives) may explain the presenting symptoms. 

Determining the onset of symptoms, in particular, for patients with dementia, can be difficult due to the gradual nature of the disease. Questions like, “When did you first notice the memory loss?” and “How has the memory loss progressed since then?” can give a general idea on the patient’s current condition. The patient’s social history, especially work, educational history, and ability to conduct activities of daily living, can help establish a baseline for the patient.

Table 1: Key symptoms to look for to differentiate between delirium and dementia during history taking [11]

 

Delirium

Dementia

Onset

Acute

 Insidious/chronic

Course

 

 Fluctuating

Progressive

Duration

 Days to weeks

 Months to years

Consciousness

 

 Altered

Clear

Alertness

 Impaired

Normal, except for in severe cases of dementia

Behaviour & Speech

 

Agitated/withdrawn/ depressed/combination of symptoms

Intact early on

Typical presentations of dementia of various type

Dementia manifests in various forms, each with distinct characteristic presentations. Alzheimer’s dementia typically involves memory loss, mood instability, apathy, and may include depressive or paranoid features. Additionally, patients may experience apraxia, anosognosia, sensory inattention, and progressive personality and intellectual deterioration. Vascular dementia, on the other hand, often has an abrupt onset with a stepwise deterioration and a fluctuating course. It is marked by slowed thinking, difficulties in organization, preserved personality and insight, and may include focal neurological deficits. Dementia with Lewy bodies is characterized by Parkinsonism, cognitive and alertness fluctuations, as well as visual hallucinations, delusions, and autonomic dysregulation. Frontotemporal dementia commonly occurs at a younger age, typically between 40 and 60 years, and is associated with early personality changes, disinhibition, and overactivity.

Physical Examination

The physical exam of the dementia and delirium patient starts with taking vital signs, assessing the airway, breathing, circulation, and performing a focused neurological exam.  Calculating the Glasgow Coma Score (GCS) and checking blood glucose should be checked on all patients with behavioral or cognitive changes.

Table 2 lists the key signs of differentiating delirium and dementia. Key features such as acute onset, fluctuations in awareness, orientation, and consciousness, cognitive decline, and potential sensory disruptions can help distinguish delirium from dementia. This includes declining memory function, language ability, and judgment. When in doubt, the general rule of thumb is to assume the patient is having an episode of delirium and try to rule out the common causes. This rule can be applied even for patients with known psychiatric illnesses like depression and dementia, as they are also susceptible to delirium superimposed on their existing condition.

Table 2: Key signs to look for to differentiate between delirium and dementia during physical exam [11]

 

Delirium

Dementia

Conscious level

Abnormal

 Normal

Psychomotor changes

Increased/decreased

Often normal

Reversibility of symptoms

Reversible usually

 Irreversible

On neurological examination, look for signs of stroke, parkinsonism, gait abnormalities, and abnormal eye movements. Dementia caused by Alzheimer’s disease generally has no sensory or motor deficits. Whereas for delirium, it is essential to identify any co-existing neurological disorders that may cause a presentation of delirium. Special tests for gait, daily living, and cognitive function assessment should be done to assess the severity of the patient’s condition. A thorough physical examination of other systems should also be conducted to look for signs of encephalopathy and drug and alcohol abuse.

Use the physical exam to help identify any exacerbations of an underlying medical illness (e.g., signs of diabetic ketoacidosis in a diabetic patient) and to evaluate for signs that may reveal an underlying cause.  For example, a high fever, low blood pressure, rapid or slow heart rate, difficulty breathing, severe pain, or malaise may indicate delirium caused by an infection, sepsis, or shock that requires immediate medical attention. Severe thirst, nausea, and vomiting may indicate dehydration or electrolyte disturbances that should be promptly treated. Signs of unresponsiveness, difficulty breathing, or seizures may indicate intracranial bleeding or alcohol or drug intoxication. Since these conditions can cause delirium and have symptoms that overlap with dementia, it is important to prioritize and appropriately manage these urgent and life-threatening cases [12].

Alternative Diagnoses

Table 3 shows alternative diagnoses to consider when evaluating for dementia and delirium. In patients presenting with altered cognitive levels, life-threatening causes that need to be ruled out ​​include hypoglycemia, electrolyte abnormalities such as hyponatremia and hyperkalemia, dehydration, stroke, intoxication/overdose, encephalopathy, cerebral infection, sepsis, and shock.

Psychiatric disorders such as psychosis, schizophrenia, and depression are among the list of differential diagnoses that could present with similar symptoms. Frequently, in patients with delirium, they do not have any previous history of psychiatric illness. In delirium, hallucinations and illusions are acute or subacute and fluctuate over time. In addition, the patient has impaired memory, orientation, and judgment, as well as clouding of consciousness. Elderly patients with a depressed mood, hopelessness, and suicidal ideation may be suffering from “pseudodementia” (false dementia). When the symptoms of depression are treated, the dementia-like condition usually resolves itself [13].

Investigations, such as bloodwork, toxicology screening, biochemical tests, and imaging can help determine a delirium patient’s underlying cause and identify an alternative diagnosis.  Investigations to consider are listed below under “Acing diagnostic testing.”

Table 3: Alternative diagnoses of altered cognitive level [14]

Central nervous system: brain abscess, cerebral neoplasm, encephalitis, intracranial haemorrhage, meningitis, normal pressure hydrocephalus, variant Creutzfeldt-Jakob Disease and bovine spongiform encephalopathy

Electrolyte: hyper/hypocalcemia, hyperkalemia, hyper/hyponatremia

Dehydration

Environmental: heat stroke, snake bite

Infective: sepsis, rabies, malaria

Metabolic: diabetic ketoacidosis, hyperosmolar hyperglycemic nonketotic coma, hypoglycemia, hypothyroidism, uremia, hepatic encephalopathy

Nutrition deficiency: folate, thiamine (Wernicke encephalopathy), vitamin B12,

Poisoning: amphetamine, anticholinergic, antidepressant, cocaine, hallucinogen, lithium, tricyclic antidepressant, valproate, withdrawal

Psychiatric: depression, psychosis

Transient global amnesia

Acing Diagnostic Testing

Initial Investigations

  • Complete Blood Count with Differential: This test is critical for assessing overall health and detecting a variety of conditions, such as infections, anemia, and blood disorders. The differential component provides a breakdown of different types of white blood cells, which can help to identify specific types of infections (e.g., bacterial or viral) and help diagnose other hematological disorders like leukemias or other abnormalities in blood cell production.

  • Electrolyte Panel: The electrolyte panel is essential for assessing the balance of minerals in the body, such as sodium, potassium, calcium, and chloride. Disturbances in these levels can indicate a variety of issues. For instance, hyponatremia (low sodium) can be a sign of dehydration or kidney dysfunction, while hyperkalemia (high potassium) could indicate kidney failure or metabolic acidosis. These imbalances can have significant effects on muscle function, nerve transmission, and overall cellular processes.

  • Liver Function Test: Liver function tests are crucial in diagnosing liver diseases such as hepatitis, cirrhosis, and alcoholic liver disease, as well as conditions like hepatic encephalopathy. These tests measure the levels of enzymes, proteins, and substances like bilirubin, which indicate how well the liver is working. Abnormal results may suggest liver damage, bile duct obstruction, or liver dysfunction that can lead to brain symptoms, especially in severe cases of hepatic encephalopathy.

  • Renal Function Test: This test evaluates how well the kidneys are filtering waste from the blood. It includes measurements like serum creatinine and blood urea nitrogen (BUN), which are key indicators of kidney function. Elevated levels may suggest renal failure, and abnormalities in these values can also help diagnose uremia, a condition where kidney dysfunction leads to the accumulation of waste products in the blood, potentially affecting multiple organ systems.

  • Blood Sugar: Blood sugar levels are measured to rule out conditions like hypoglycemia (low blood sugar) and hyperglycemia (high blood sugar). In patients with diabetes, particularly in cases of diabetic ketoacidosis (DKA) or hyperosmolar hyperglycemic nonketotic syndrome (HHNS), these levels can be critically elevated and require immediate treatment. Monitoring blood sugar is essential for managing and preventing complications related to these conditions.

  • Urine Dipstick: The urine dipstick test is a quick and convenient method for identifying potential urinary tract infections (UTIs), which are a common cause of sepsis in elderly patients. It can detect substances like white blood cells, nitrites, and protein in the urine, all of which suggest infection or inflammation. Early detection of UTIs is crucial, as they can quickly progress to sepsis if untreated.

  • Chest X-ray: A chest X-ray is an important imaging tool for identifying lung consolidation, a hallmark of chest infections such as pneumonia. Pneumonia is another common cause of sepsis, particularly in elderly patients with weakened immune systems. The X-ray can also help detect other lung-related issues like fluid accumulation, pulmonary edema, or lung tumors that could complicate the clinical picture.

  • CT Scan of the Brain: A CT scan of the brain is used to identify structural abnormalities, including the presence of tumors, stroke, or brain hemorrhages. It is also used to detect cerebral atrophy (shrinkage of brain tissue) and ventricular enlargement, which can be indicative of conditions like dementia. This imaging modality is important in diagnosing neurological disorders and guiding further management for patients with cognitive or neurological impairments.

Further Investigations If A Differential Is Suspected

  • Urine and Blood Toxicology: This test is performed to detect the presence of drugs, alcohol, or other toxic substances in the body. Toxicology screens can identify intentional or unintentional overdoses, exposure to toxic substances, and drug or alcohol misuse. In cases of altered mental status or cognitive impairment, toxicology testing helps to rule out substance-induced confusion or delirium, which can mimic other medical or psychiatric conditions.

  • Thyroid Function Test: Thyroid hormones play a significant role in regulating metabolism and overall brain function. Abnormal thyroid function, whether hypothyroidism (underactive thyroid) or hyperthyroidism (overactive thyroid), can lead to symptoms of cognitive impairment, mood changes, and lethargy. A thyroid function test measures levels of thyroid hormones (such as TSH, T3, and T4) to determine if an imbalance is contributing to the patient’s cognitive or neurological symptoms, which can be reversible with appropriate treatment.

  • Vitamin B12 and Folate Levels: Both Vitamin B12 and folate are essential for nerve function and the production of red blood cells. A deficiency in either of these vitamins can lead to cognitive impairment, memory loss, and other neurological symptoms. Vitamin B12 deficiency, in particular, is known to cause a condition called subacute combined degeneration of the spinal cord and brain, which can lead to irreversible damage if left untreated. Checking these levels helps to rule out nutritional deficiencies as a potentially treatable cause of cognitive decline.

  • Bacteriology and Viral Detection: Infection-related causes of cognitive impairment or altered mental status may be identified through bacteriology and virology testing. This typically involves blood and urine microscopy, as well as culture tests to detect bacterial, viral, or other pathogenic organisms. Infections, especially in elderly or immunocompromised patients, can lead to sepsis or encephalitis, which can significantly impact cognitive function. Identifying and treating an underlying infection can prevent further deterioration and improve cognitive outcomes.

Risk Stratification

Cognitive assessment tools help identify and grade abnormal cognitive performances. They can also be integrated into the emergency medicine physical exam to screen patients for mild cognitive impairment or dementia.

Instead of an extended mental status examination or formal neuropsychological testing, more focused screening tools are more relevant and feasible for use in the emergency department [15]. Examples of screening tools validated for use in the emergency department include the abbreviated mental test score (AMTS) and its abbreviated four-item version (AMT4), the mini-mental state examination (MMSE), and the Montreal Cognitive Assessment (MoCA). They assess a broad range of cognitive domains, including memory, language, and orientation. These tests are designed to be administered in 15 minutes or less and have pre-determined cut-off scores to help distinguish patients with normal cognitive function and those with impaired cognitive function [16].

These screening tools are intended to help screen individuals who may require more extensive neurological assessments. They should only be used as a reference and must be integrated with history and physical examination findings for a holistic approach. Multiple factors, such as altered mood, disorientation, and education level, can affect the accuracy of these screening tools.

Table 4: Abbreviated mental test score four-item version (AMT4)

Ask the patient to state each of the following. A score less than 4 should prompt further cognitive screening.

Age

Correct (+1) / Incorrect (0)

Date of birth

Correct (+1) / Incorrect (0)

Place

Correct (+1) / Incorrect (0)

Year

Correct (+1) / Incorrect (0)

Management

The ABCDE approach is used for the initial management of patients with cognitive changes, behavioral changes, and alterations in consciousness, which may be present in delirium or dementia.

The acute management of dementia and delirium is variable and depends on the patient’s underlying medical conditions and presenting symptoms. The main goal of managing dementia and delirium in the emergency department is to identify and treat any life-threatening underlying causes. Based on the patient’s signs and symptoms, a thorough history, physical exam, and pertinent investigations should be ordered. Patient and staff safety should also be prioritized, as these patients may be aggressive and combative.

Obtaining investigations to evaluate for the underlying cause may be hindered by the patient’s aggressive and combative state. If this is the case, the first attempt is to calm the patient and de-escalate the situation verbally.  If unsuccessful, chemical sedation should be considered for the safety of the patient and the healthcare staff. Examples of chemical sedation used in an emergency department setting include benzodiazepines, antipsychotics, and dexmedetomidine [17,18]. Close monitoring is necessary after the patient is sedated. Sedatives should be used only when necessary, as they have the potential to worsen delirium and disorientation.

Physical restraints and environmental seclusion are other adjunctive treatments for agitated delirium or dementia patients. However, their use should be weighed with the psychological and physical risks they may cause (e.g., emotional distress, skin and soft tissue injuries, orthopedic injuries, rhabdomyolysis, etc.). Alternative methods of managing agitation should always be attempted prior to physical restraint, such as explaining your desire to care for the patient, orienting the confused patient to his or her surroundings, using verbal de-escalation techniques, providing psychosocial support, and relocating to a calm and quiet environment, if possible [19].

Special Patient Groups

Most patients presenting with delirium and/or dementia are elderly patients. Younger patients (<60 years) presenting with delirium or patients who have rapidly progressing dementia may require extensive evaluation to discover the underlying cause. Further investigations could include lumbar puncture, electroencephalography, advanced neuroimaging, neuropsychological, and genetic testing [20]. Regardless of age, the most common causes of early-onset dementia are still Alzheimer’s disease, vascular dementia, and frontotemporal dementia [21].

When To Admit This Patient

Admission of dementia and delirious patients depends on various factors, including the severity of symptoms, comorbidities, and safety concerns. Patients who present with acute changes in their mental status, such as sudden confusion or agitation, should be further assessed for any underlying medical conditions and often require hospitalization. Delirious patients, particularly those with severe symptoms or who are at risk of harming themselves and others, should also be admitted until stabilized. Ultimately, the decision to admit dementia and delirious patients in an emergency department setting should be based on a comprehensive evaluation of the patient’s medical history, current symptoms, and risk factors.

The patient who is coming to the emergency department for a chronic presentation of Alzheimer’s dementia could be discharged if life-threatening conditions have been ruled out and home safety is not a concern. They should be referred to an outpatient primary care doctor or a geriatrician for follow-up and prescription medications to manage behavioral symptoms. Be sure to educate the patient’s family members on the diagnosis and to monitor for any new or worsening symptoms that may require urgent medical attention. Advise the family on managing certain scenarios, prioritizing the patient’s basic daily needs, addressing any medical concerns, and maintaining patient and family safety. Refer the patient to a geriatric community support program, if available.

Revisiting Your Patient

Adam’s initial vital signs are stable, and you have decided to continue his management in the consultation room. His history of cognitive and behavioral change over the past year is consistent with dementia. However, his acute presentation of impaired consciousness level and disorientation raises your suspicion of concurrent delirium from an underlying medical condition. Collateral history from the family indicates that Adam lives with his wife, who is 85 years old and limited in her ability to assist Adam with his daily needs. Focused drug and alcohol history is unrevealing.

Further neurological exams do not identify any focal neurological signs or gait disturbance. Physical examinations of the cardiovascular, respiratory, and abdomen are unremarkable. Blood glucose is within the normal range. Due to his disorientation, his Glasgow coma score is 14 (E4/V4/M6).

You consider using AMT4 to screen for cognitive impairment. He can recall his age and date of birth and tell where he is, but he fails to tell us the current year. You establish that he has delirium with impaired alertness and likely an underlying cognitive impairment.

You decide to conduct further investigation to look for potential underlying causes, especially those which may prompt immediate treatment. You arrange blood tests, including complete blood count, electrolytes, liver, and renal function tests, in consideration of potential sepsis, electrolyte disturbance, and acute organ failure. You arrange a CT brain to rule out any acute cerebral hemorrhage and space-occupying lesion. Chest X-ray and ECG are performed, as well. As you order these investigations, you consider that the patient may become agitated and uncooperative during these tests, so you review options for chemical sedation should they be needed.

You discuss openly with Adam and his family on his diagnosis of delirium and likely dementia. Your preliminary investigations show a urinary tract infection; one dose of intravenous antibiotics has been ordered. You suggest admitting Adam for monitoring and investigations due to safety concerns and his inability to care for himself due to his recent rapid decline.  You discuss the importance of appropriate follow-up care and geriatric resources specializing in dementia. The patient is admitted to the general medical floor for further testing and monitoring.

Authors

Picture of Lo Lucian Simeon

Lo Lucian Simeon

Lucian Lo is a medical student at The Chinese University of Hong Kong. An avid enthusiast of emergency medicine and humanitarian work, he hopes to one day combine his two great passions as a front-line healthcare professional in conflict and disaster zones. He is a certified Advanced Medical Life Support Provider and Youth Mental Health First Aid Provider. In addition, he has led and organized multiple medical service projects in Hong Kong, Nepal, and Thailand. In regard to emergency medicine, his interests include trauma care, intensive care medicine, and pre-hospital emergency medicine.

Picture of Ngai Oona Wing Yan

Ngai Oona Wing Yan

Oona Ngai is a medical student at The Chinese University of Hong Kong with a passion for emergency medicine and humanitarian work. She has organized and participated in various volunteer services for vulnerable communities in Hong Kong, including the homeless, refugees, and domestic helpers. Oona is also a St. John’s certified Advanced Medical Life Support Provider and aspires to better equip herself with the necessary skills and knowledge to provide effective medical care in emergency situations. In addition, she has published a life story book on rare diseases to raise awareness and advocate for those in need.

Picture of Lo Yat Hei

Lo Yat Hei

Dr. Lo Yat Hei is an emergency physician who is trained and grew up in Hong Kong. He now serves at the Accident and Emergency Department of Prince of Wales Hospital and teaches at the Accident and Emergency Medicine Academic Unit of the Chinese University of Hong Kong. When not practicing medicine, he enjoys gardening, ceramics and playing mahjong.

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References

  1. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5). American Psychiatric Association; 2013.
  2. World Health Organization. “Dementia.” Fact Sheet, https://www.who.int/news-room/fact-sheets/detail/dementia.
  3. Ljubenkov PA, Geschwind MD. Dementia. Semin Neurol. 2016;36(4):397-404. doi:10.1055/s-0036-1585096
  4. Plum F. The pathophysiology of dementia. Gerontology. 1986;32 Suppl 1:67-72. doi:10.1159/000212832
  5. Wilson JE, Mart MF, Cunningham C, et al. Delirium [published correction appears in Nat Rev Dis Primers. 2020 Dec 1;6(1):94]. Nat Rev Dis Primers. 2020;6(1):90. Published 2020 Nov 12. doi:10.1038/s41572-020-00223-4
  6. Maclullich AM, Ferguson KJ, Miller T, de Rooij SE, Cunningham C. Unravelling the pathophysiology of delirium: a focus on the role of aberrant stress responses. J Psychosom Res. 2008;65(3):229-238. doi:10.1016/j.jpsychores.2008.05.019
  7. Fong TG, Tulebaev SR, Inouye SK. Delirium in elderly adults: diagnosis, prevention and treatment. Nat Rev Neurol. 2009;5(4):210-220. doi:10.1038/nrneurol.2009.24
  8. Avelino-Silva TJ, Campora F, Curiati JAE, Jacob-Filho W. Prognostic effects of delirium motor subtypes in hospitalized older adults: A prospective cohort study. PloS one. 2018;13(1):e0191092. doi:10.1371/journal.pone.0191092
  9. Emmady PD, Schoo C, Tadi P. “Major Neurocognitive Disorder (Dementia).” In: StatPearls. StatPearls Publishing; 2023. Available from: https://www.ncbi.nlm.nih.gov/books/NBK557444/
  10. Morandi A, Davis D, Bellelli G, et al. The Diagnosis of Delirium Superimposed on Dementia: An Emerging Challenge.  J Am Med Dir Assoc. 2017;18(1):12–18. doi:10.1016/j.jamda.2016.07.014
  11. Han JH, Suyama J. Delirium and Dementia. Clin Geriatr Med. 2018;34(3):327-354. doi:10.1016/j.cger.2018.05.001
  12. Han JH, Wilson A, Ely EW. Delirium in the older emergency department patient: a quiet epidemic. Emerg Med Clin North Am. 2010;28(3):611-631. doi:10.1016/j.emc.2010.03.005
  13. Brodaty H, Connors MH. Pseudodementia, pseudo-pseudodementia, and pseudodepression. Alzheimers Dement. 2020;12(1):e12027. doi:10.1002/dad2.12027
  14. Ross GW, Bowen JD. The diagnosis and differential diagnosis of dementia. Med Clin North Am. 2002;86(3):455-476. doi:10.1016/s0025-7125(02)00009-3
  15. Carpenter CR, Banerjee J, Keyes D, et al. Accuracy of Dementia Screening Instruments in Emergency Medicine: A Diagnostic Meta-analysis. Acad Emerg Med. 2019;26(2):226-245. doi:10.1111/acem.13573
  16. Nasreddine ZS, Phillips NA, Bédirian V, et al. The Montreal Cognitive Assessment, MoCA: a brief screening tool for mild cognitive impairment. J Am Geriatr Soc. 2005;53(4):695–699. doi:10.1111/j.1532-5415.2005.53221.x
  17. Barr J, Fraser GL, Puntillo K, et al. Clinical practice guidelines for the management of pain, agitation, and delirium in adult patients in the intensive care unit. Critical Care Medicine. 2013;41(1):263-306. doi: 10.1097/CCM.0b013e3182783b72
  18. Hall JE, Uhrich TD, Barney JA, Arain SR, Ebert TJ. Sedative, amnestic, and analgesic properties of small-dose dexmedetomidine infusions. Anesth Analg. 2000;90(3):699-705. doi: 10.1097/00000539-200003000-00033
  19. Lightfoot CB, Breden C, Moczygemba LR. Delirium: diagnosis, prevention and management. Am J Health Syst Pharm. 2017;74(18):1365-1375. doi: 10.2146/ajhp160950
  20. Lempert T, Schmidt D, Rosemeyer J. Psychogenic nonepileptic seizures: a guide. J Neurol Neurosurg Psychiatry. 2006;77(2):297-303. doi:10.1136/jnnp.2005.082149.
  21. Rossor MN, Fox NC, Mummery CJ, Schott JM, Warren JD. The diagnosis of young-onset dementia. Lancet Neurol. 2010;9(8):793–806. doi:10.1016/S1474-4422(10)70159-9

Reviewed and Edited By

Picture of Joseph Ciano, DO, MPH, MS

Joseph Ciano, DO, MPH, MS

Dr. Ciano is a board-certified attending emergency medicine physician from New York, USA. He works in the Department of Emergency Medicine and Global Health at the Hospital of the University of Pennsylvania. Dr. Ciano’s global work focuses on capacity building and medical education and training in low-middle income countries. He is thrilled to collaborate with the iEM Education Project in creating free educational content for medical trainees and physicians.

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

The ABCDE Approach to Undifferentiated Critically Ill and Injured Patient (2024)

~ iEM Education Project Team ~ Leave a comment

by Roxanne R. Maria, Hamid A. Chatha

Authors
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You have a new patient!

A 40-year-old male, a truck driver, is involved in a head-on collision with another vehicle. He has been brought in by ambulance. According to the paramedics, the vehicles were traveling at approximately 85 km/hr, and the patient was restrained by a seatbelt. On arrival at the Emergency Department (ED), the patient is agitated and mildly disoriented. He is tachypneic with a respiratory rate of 30/min, maintaining an O2 saturation of 95% on 12 L/min oxygen via a non-rebreather mask, heart rate of 128 beats/min, blood pressure of 90/52 mmHg, and temperature of 36.1°C. The patient also received 1 L of 0.9% normal saline and 1 unit of O-negative packed red cells in the ambulance. Despite this, his respiratory rate, heart rate, and level of disorientation have worsened.

Emergency Department

In the ED, patients present with a variety of clinical presentations, including both life-threatening and non-life-threatening. Some may have been seen and referred by a clinician before arrival or brought to the department after pre-hospital assessment and care by the emergency medical services (EMS) [1]. Health emergencies affect all age groups and include conditions like acute coronary syndrome, strokes, acute complications of pregnancy, or any chronic illness. Emergency health care providers should respond to these clinically ‘undifferentiated’ patients with symptoms for which the diagnosis may not be known [2].  The root cause of most life-threatening conditions in the ED may be medical or surgical, infection or trauma [2].

In the Emergency Department (ED), there are several potentially life-threatening presentations that demand immediate stabilization. These include trauma, which can result from various forms of accidents or injuries, and shortness of breath, which might indicate critical respiratory distress. An altered mental state also requires prompt attention, as it may signal underlying neurological or systemic issues. Shock, often evidenced by dangerously low blood pressure. Chest pain or discomfort, which could be indicative of a cardiac event, are other urgent concerns. Additionally, cases of poisoning, ingestion of harmful substances, or exposure to toxic materials also necessitate rapid intervention to prevent further harm. Each of these presentations is a medical priority, highlighting the importance of timely and effective response in the ED to ensure patient safety and stability.

These symptoms maybe the only picture that the patients present with, and may constitute the early stage of a critical illness requiring rapid, appropriate intervention and resuscitation, even when the patient seems to appear relatively well [2].

Emergency conditions often require immediate intervention long before a definitive diagnosis is made to stabilize the critically ill patient [3]. Thus, this chapter intends to briefly introduce a basic systematic approach to identifying and managing acute, potentially life-threatening conditions in these patients. This approach will enable all frontline providers, including students, nurses, pre-hospital technicians, and physicians, to manage these patients even in the setting of limited resources [2].

A complete assessment and management of each of the presentations mentioned above is beyond the scope of this chapter. However, the initial approach remains the same, regardless of the patient population or setting [4].

History of the ABCDE approach

The ABC mnemonic’s origins may be traced back to the 1950s. The first two letters of the mnemonic, A and B, resulted from Dr Safar’s description of airway protection techniques and administration of rescue breaths. Kouwenhoven and colleagues later added the letter C to their description of closed-chest cardiac massage [3].

Styner is credited with further developing the Airway, Breathing, Circulation, Disability, and Exposure (ABCDE) approach. After a local aircraft disaster in 1976, Styner and his family were taken to a local healthcare facility, where he saw an insufficiency in the emergency treatment offered. He then founded the Advanced Trauma Life Support course, emphasizing a methodical approach to treating severely injured patients.

The ABCDE approach is universally accepted and utilized by emergency medicine clinicians, technicians, critical care specialists, and traumatologists [3]. Thus, this approach is recommended by international guidelines for suspected serious illness or underlying injury, irrespective of the diagnosis [5]. It is also the first step in post-resuscitation care after the patient achieves return of spontaneous circulation (ROSC) from a cardiac arrest [3]. This systematic approach also aims to improve coordination among the team members and saves time to make critical decisions [3].

The ABCDE approach

Since time is of the essence, the ABCDE method is a systematic approach that can be easily and quickly practiced in the ED. This is incorporated into what is known as ‘Initial patient assessment,’ one of the most crucial steps in evaluation [6]. At each step of this approach, life-threatening problems must be addressed before proceeding to the next assessment step. After the initial assessment, patients must be reassessed regularly to evaluate the treatment response. Anticipate and call for extra help early [7]. Appropriate role allocation and good communication are important for effective team working [7]. Once the patient is stabilized, a secondary survey should be conducted, which includes a thorough history, physical examination, and diagnostic testing [8]. Finally, the tertiary survey is done within 24 hours of presentation to identify any other missed injuries in trauma. Once it is recognized that the patient’s needs exceed the facility’s capabilities, the transfer process must be initiated to an appropriately specialized care center accordingly [8].

Ensure Safe Environment

Before initiating the ABCDE approach, it is essential to ensure both personal safety and a secure environment. This preparation includes addressing any potential risks, such as unexpected or violent behavior, environmental hazards, and the risk of exposure to communicable diseases. Health professionals should consider using appropriate personal protective equipment (PPE) suited to the situation, which may include gloves, gowns, masks, goggles, and thorough hand washing. These precautions are vital to protect both the healthcare provider and the patient, ensuring a safe environment for medical intervention [4].

Initiate First Response

The Resuscitation Council UK (RCUK) (2015) recommends performing a range of initial activities before proceeding with the ABCDE approach [4].

Examine the patient in general (skin color, posture, sensorium, etc.) to determine whether they seem critically ill [4].

After introducing yourself, an initial assessment can be completed in the first 10-15 seconds by asking patients their names and about their active complaints. If they respond normally, it means the airway is patent and brain perfusion is expected [9]. Check for breathing and pulse if the patient appears unconscious or has collapsed. If there is no pulse, call for help and immediately start cardiopulmonary resuscitation (CPR), adhering to local guidelines [9].

Detailed ABCDE Evaluation

Primary Survey

Patients are assessed and prioritized according to their presentations and vital signs. In primary survey, critically ill patients are managed efficiently along with resuscitation. The approach represents the sequence of steps as described below [10]:

A – Airway (with C spine control in Trauma patients)

B – Breathing and Ventilation

C – Circulation (With Hemorrhage control in active bleeding)

D – Disability

E – Exposure / Environment control

A – Airway

Airway obstruction is critical! Gain expert help immediately. If not treated, it can lead to hypoxia, causing damage to the brain, kidneys, and heart, resulting in cardiac arrest and death [4].

Airway management remains the cornerstone of resuscitation and is a specialized skill for the emergency clinician [9].

Assessment of airway patency is the first step. Can the patient talk? If yes, then the airway is patent and not in immediate danger. If not, look for the signs of airway compromise: Noisy breathing, inability to speak, presence of added sounds, stridor or wheezing, choking or gagging, cyanosis, and use of accessory muscles.

The next step is to open the mouth and look for anything obstructing the airway, such as secretions, blood, a foreign body, or mandibular/tracheal/laryngeal fractures [10].

While examining and managing the airway, great care must be taken to restrict excessive movement of the cervical spine and assume the existence of a spinal injury in cases of trauma [11].

Several critical factors can compromise a patient’s airway and must be addressed promptly in emergency settings. A depressed level of consciousness, which may result from conditions such as opioid overdose, head injury, or stroke, can impair airway protection and lead to significant risk [10]. Additionally, an inhaled foreign body, or the presence of blood, vomit, or other secretions, can obstruct the airway and necessitate immediate intervention. Fractures of the facial bones or mandible further complicate airway management due to potential structural damage. Soft tissue swelling, whether caused by anaphylaxis (angioedema) or severe infections like quinsy or necrotizing fasciitis, also seriously threatens the airway. These conditions highlight the importance of vigilant monitoring and rapid response to maintain airway patency and prevent complications.

angioedema - DermNet New Zeeland, CC BY NC ND 3.0
uvula edema - WikiMedia Commons - CC-BY-SA-3.0

Intervention: Several basic maneuvers can help maintain a clear airway. Suctioning should be performed if there are any secretions or blood present. Additionally, using the head-tilt, chin-lift, and jaw-thrust maneuvers can aid in keeping the airway open. For patients with a low Glasgow Coma Scale (GCS) score, placing an oropharyngeal or nasopharyngeal airway can be beneficial in maintaining airway patency. It’s also important to inspect the airway for any obvious obstructions; if a visible object is within reach, it may be removed carefully using a finger sweep or suction. It is crucial to remember that assistance from an anesthetist may be required in some cases. 

Head-Tilt, Chin-Lift maneuver

In trauma patients, to protect the C-spine, perform a jaw-thrust rather than a head-tilt chin-lift maneuver and immobilize the C-spine with a cervical collar [9].

A definitive airway, such as endotracheal intubation, may be necessary in patients with airway obstruction, GCS ≤ 8, severe shock or cardiac arrest, and at risk of inhalation injuries [8].

If intubation has failed or is contraindicated, a definitive airway must be established surgically [11].

B – Breathing and Ventilation

Effective ventilation relies on the proper functioning of the lungs, chest wall, and diaphragm, along with a patent airway and sufficient gas exchange to optimize oxygenation [10]. To assess breathing and ventilation, clinicians should evaluate oxygen saturation, monitor the respiratory rate for any signs of abnormality—such as rapid breathing (tachypnea), slow breathing (bradypnea), or shallow breathing (Kussmaul breathing)—and observe for increased work of breathing, such as accessory muscle use, chest retractions, or nasal flaring. Other critical assessments include checking for neck vein distention, examining the position of the trachea, chest expansion, and any injuries or tenderness, as well as auscultating for bilateral air entry and any additional sounds. Chest percussion should be performed to identify dullness, which may indicate hemothorax or effusion, or hyperresonance, suggestive of pneumothorax. Certain pathologies, like tension pneumothorax, massive hemothorax, open pneumothorax, and tracheal or bronchial injuries, can rapidly disrupt ventilation. Other conditions, including simple pneumothorax, pleural effusion, simple hemothorax, rib fractures, flail chest, and pulmonary contusion, may compromise ventilation to a lesser degree [10].

Interventions:

  • Oxygen – Ensure all patients are adequately oxygenated, with supplemental oxygen delivered to all severely injured trauma patients [11]. Place them on well-fitted oxygen reservoir masks with a flow rate > 10 L/min, which can then be titrated as needed to maintain adequate saturations. Other means of oxygen delivery (nasal catheter, nasal cannula, non-rebreather) can also be used.
  • Bag mask valve ventilation with oxygen – should be given to unconscious patients with abnormal breathing patterns (slow or shallow respiration).
  • Other interventions include salbutamol nebulizers, epinephrine, steroids, needle decompression, chest tube insertion, and the use of noninvasive ventilation and pressure support in different clinical scenarios.

C – Circulation (With Hemorrhage control in active bleeding)

Major circulatory compromise in critically ill patients can result from either blood volume loss or reduced cardiac output. In trauma cases, hypotension is assumed to be due to blood loss until proven otherwise. To assess the hemodynamic status, several key evaluations should be performed. These include checking the level of consciousness, as an altered state may indicate impaired cerebral perfusion, and assessing skin perfusion for signs like pallor, cyanosis, mottling, or flushing. Vital signs such as heart rate and blood pressure should be monitored for abnormalities like tachycardia, bradycardia, hypotension, or hypertension. Auscultation can reveal muffled heart sounds, which may suggest cardiac tamponade or pneumothorax, as well as murmurs or a pericardial friction rub that could indicate pericarditis. Checking the extremities for capillary refill and skin temperature is also essential. Additionally, palpation of the abdomen for tenderness or a pulsatile mass may reveal an abdominal aortic aneurysm, while peripheral edema, such as pedal edema, might indicate heart failure.

Interventions:

  • Two large-bore IV cannulations must be placed. If this attempt fails, intraosseous access is necessary. Hemorrhagic shock—A definitive control of bleeding along with replacement of intravascular volume is essential. Initial resuscitation should start with warm crystalloids, and blood products should be used. Massive Transfusion Protocol (MTP) should be activated according to local guidelines. In hemorrhagic shock, vasopressors and reversal of anticoagulation (if required) can be considered.
  • Hemorrhage control: External hemorrhage can be controlled by direct manual pressure over the site of the wound or tourniquet application.
  • In the case of pelvic or femur fractures, placement of pelvic binders or extremity splints may help to stabilize, although definitive management may be surgical or interventional radiological procedures.
  • Obstructive shock – Immediate pericardiocentesis for cardiac tamponade, chest tube insertion for tension pneumothorax, and thrombolysis for massive pulmonary embolism.
  • Distributive shock – intramuscular epinephrine for anaphylactic shock, empiric antibiotics for sepsis, and hydrocortisone for adrenal crisis.
  • Appropriate antihypertensives in hypertensive emergency.

D – Disability

Evaluate neurological status either with AVPU (Alert, Verbal, Pain and Unresponsive) [5] or GCS (Glasgow Coma Scale).

Evaluate for agitation, head and neck trauma, focal neurological signs (seizure, hemiplegia, etc), lateralizing signs, meningeal signs, signs of raised intracranial pressure, and pupillary examination (size and symmetry). Identify any classic toxidromes (sympathomimetic, cholinergic, anticholinergic, opioid, serotonergic, and sedative-hypnotic toxidromes). 

Choose the best response of patient
EYE OPENING
4: Spontaneously
3: To verbal command
2: To pain
1: No response
BEST VERBAL RESPONSE
5: Oriented and converses
4: Disoriented and converses
3: Inappropriate words; cries
2: Incomprehensible sounds
1: No response
BEST MOTOR RESPONSE
6: Obeys command
5: Localizes pain
4: Flexion withdrawal
3: Flexion abnormal (decorticate)
2: Extension (decerebrate)
1: No response
Glasgow Coma Score (GCS) (Modified from Teasdale, G., & Jennett, B. (1974). Assessment of coma and impaired consciousness: a practical scale. The Lancet, 304(7872), 81-84.) - Please read this article to get more insight regarding GCS.

The Glasgow Coma Scale (GCS) is a critical tool for assessing the level of consciousness in critically ill patients, providing a score based on eye, verbal, and motor responses. A GCS score ranges from 3 to 15, with lower scores indicating more severe impairment. Scores of 13-15 generally indicate mild impairment, 9-12 suggest moderate impairment, and scores of 8 or below (comatose patient) represent severe impairment and a high risk of poor outcomes. In critically ill patients, a declining GCS score can signal worsening neurological status, potentially due to factors like traumatic brain injury, hypoxia, or systemic deterioration, and often warrants immediate intervention to address underlying causes.

E – Exposure and Environmental control

It is necessary to expose the patient appropriately whilst maintaining dignity and body temperature.

Look at the skin for any signs of trauma (burns, stab wounds, gunshot wounds, etc.), rashes, infected wounds, ulcers, needle track marks, medication patches, implantable devices, tubes, catheters, and stomas; measure core body temperature, and perform logroll (trauma).

Do not forget to check frequently concealed and overlooked areas such as the genital, inguinal, perineal, axilla, back and under dressings [8].

Interventions:

  • Use specialized personal protective equipment (PPE), remove all possible triggers such as wet or contaminated clothing, and maintain core body temperature.
  • Minimize hypothermia (external rewarming, warm IV fluids) and hyperthermia (surface cooling, cold IV fluids, antipyretics for fever).

Adjuncts to primary survey

1. Electrocardiography (ECG)
2. Pulse oximetry
3. Carbon dioxide (CO2) monitoring
4. Arterial blood gas (ABG) analysis
5. Urinary catheterization (to assess for hematuria and urine output)
6. Gastric catheterization (for decompression)
7. Blood lactate level measurement
8. Chest and pelvis X-rays
9. Extended focused assessment with sonography for trauma (eFAST)

These adjuncts help provide a comprehensive evaluation of the patient’s condition [10].

Secondary Survey

After the initial primary survey and stabilization, proceed to the secondary survey. This includes a detailed history (SAMPLE)and a head-to-toe examination, including reassessment of vital signs, as there is a potential for missing an injury or other findings in an unresponsive patient [10].

The SAMPLE mnemonic is a structured approach for gathering essential patient history in emergency settings. It stands for Signs and Symptoms, Allergies, Medications, Past Medical History, Last Oral Intake, and Events leading to the illness or injury [5].

  • “Signs and Symptoms” involves asking the patient, family, or other witnesses about any observable signs or reported symptoms.
    “Allergies” are crucial to identify to prevent harm and may help recognize conditions like anaphylaxis.
  • “Medications” requires a comprehensive list of all current and recent medications, including any changes in dosage.
  • “Past Medical History” provides insights into underlying health conditions that may influence the current illness.
  • “Last Oral Intake” is important for assessing risks of aspiration or complications if the patient requires sedation or surgery.
  • Finally, understanding the “Events” surrounding the illness or injury aids in determining its cause and severity.

Together, these components guide healthcare providers in developing a more accurate and effective treatment plan.

In the secondary survey, a thorough approach is taken to ensure comprehensive care for the patient. This includes performing relevant and appropriate diagnostic tests based on the clinical assessment to confirm diagnoses and guide further treatment. Critical, targeted treatments should be initiated promptly, along with adequate supportive care to stabilize the patient’s condition. If necessary, specialized consults are obtained to address specific medical needs. Additionally, the healthcare team must assess the need for escalation of care or consider an interfacility transfer if the patient requires more specialized resources or advanced care options [8]. This structured approach ensures that all aspects of the patient’s condition are managed effectively. 

Adjuncts to secondary survey

Additional x-rays for the spine and extremities, CT scans of the head, chest, abdomen, and spine, urography and angiography with contrast, transesophageal ultrasound, bronchoscopy, and other diagnostics [10].

If the patient starts to deteriorate, immediately go back to the ABCDE approach and reassess!

Special Patient Groups

In recent ATLS updates, the ABCDE approach has been modified to the xABCDEF approach, where “x” stands for eXsanguinating eXternal hemorrhage control and “F” stands for further factors such as special groups (pediatric, Geriatric, and Pregnancy).  While the xABCDEF approach is universal and applies to all patient groups, specific anatomic and physiological differences in different populations should be considered while evaluating and treating life-threatening conditions. Some special population groups are discussed here:

Pediatrics [10]

Children have smaller body mass but higher body surface area than their body mass and proportionately larger heads than adults. These characteristics cause children to have increased energy transfer, hypothermia, and blunt brain trauma.

A useful adjunct is the Broselow® Pediatric Emergency Tape, which helps to rapidly identify weight-based medication doses, fluid volumes, and equipment sizes.

The ABCDE approach in children should proceed in the same manner as in adults, bearing in mind the anatomical differences.

Airway – Various anatomical features in children, such as large tissues of the oropharynx (tongue, tonsils), funnel-shaped larynx, more cephalad and anteriorly placed larynx and vocal cords, and shorter length of the trachea, make assessment and management of the airway difficult. Additionally, in smaller children, there is disproportionality in size between the cranium and the midface, making the large occiput in passive flexion of the cervical spine, resulting in the posterior pharynx being displaced anteriorly. The neutral alignment of the spine can be achieved by placing a 1-inch pad below the entire torso of the infant or toddler.

The most preferred technique for orotracheal intubation is under direct vision, along with restriction of the cervical spine, to achieve a definitive airway.

Infants are more prone to bradycardia due to laryngeal stimulation during intubation than older children and adults. Hence, when drug-assisted intubation is required, the administration of atropine sulfate pretreatment must be considered. Atropine also helps to dry out oral secretions, further enhancing the view of landmarks for intubation.

When the airway cannot be maintained by bag-mask ventilation or orotracheal intubation, a rescue airway with either a laryngeal mask airway (LMA), an intubating LMA, or a needle cricothyroidotomy is required.

Red flag signs in children include stridor, excessive drooling, airway swelling, and the child’s unwillingness to move the neck. Examine the airway carefully for any foreign bodies, burns, or obstruction.

Breathing and ventilation – Children’s respiratory rates decrease with age. The normal tidal volumes in infants and children vary from 4-6 ml/kg to 6-8 ml/kg while assisting in ventilation. Care must be taken to limit pressure-related barotrauma during ventilation. It is recommended that children weighing less than 30 kg use a pediatric bag valve mask.

Injuries such as pneumothorax, hemothorax, and hemopneumothorax should be treated by pleural decompression, for tension pneumothorax, and needle decompression in the 2nd intercostal space (over the top of the third rib) at the midclavicular line. The site for chest tube insertion remains the same as in adults.

The most common cause of pediatric cardiac arrest is hypoxia, and the most common acid-base abnormality encountered is respiratory acidosis due to hypoventilation.

Circulation – Important factors in assessing and managing circulation and shock are looking for signs of circulatory compromise, ascertaining the patient’s weight and circulatory volume, gaining timely peripheral venous access, delivering an appropriate volume of fluids with or without blood replacement, evaluating the adequacy of resuscitation, and aiming for thermoregulation.

Children have increased physiological reserves. A 30% decrease in the circulating blood volume may be required for a fall in the systolic blood pressure. Hence, it is important to look for other subtle signs of blood loss, such as progressive weakening of peripheral pulses, narrow pulse pressure to less than 20 mm Hg, skin mottling (in infants and young children), cool extremities, and decreased level of consciousness.

The preferred route is peripheral venous access, but if this is unsuccessful after two attempts, intraosseous access should be obtained.

Fluid resuscitation must be commenced at 20 ml/kg boluses of isotonic crystalloids. If the patient has ongoing bleeding, packed red blood cells may be initiated at 10 ml/kg as soon as possible. Given that children have increased metabolic rates, thinner skin, and lack of substantial subcutaneous tissue, they are prone to develop hypothermia quickly, which may impede a child’s response to treatment, increase coagulation times, and affect the central nervous system (CNS) function. Therefore, overhead lamps, thermal blankets, as well as administration of warm IV fluids, blood products, and inhaled gases may be required during the initial phase of evaluation and resuscitation.

Disability – Hypoglycemia is a very common cause of altered mental state in children, and children can present with altered mental state or seizures. Check for blood glucose in children; if low, administer glucose (IV D10 or D25).

Geriatric [10]

In cases of trauma in geriatric patients, physiological events that may have led to it (e.g., cardiac dysrhythmias) must be considered. A detailed review of long-term medical conditions and medications, along with their effect on vital signs, is necessary. Risk factors for falls include physical impairments, long-term medication use, dementia, and visual, cognitive, or neurological impairments.

Elderly patients are more prone to sustaining burn injuries due to decreased reaction times, hearing and visual impairment, and inability to escape the burning structure. Burn injury remains the cause of significant mortality.

Airway – Due to loss of protective airway reflexes, airway management in the elderly can be challenging and requires a timely decision to establish a life-saving definitive airway. Opening of the mouth and cervical spine maneuvering may be challenging with arthritic changes. Loose dentures should be removed, while well-fitted dentures should be better left inside. Some patients may be edentulous, making intubation easier, but bag-mask ventilation is difficult.

While performing rapid sequence intubation, it is recommended to lower the doses of barbiturates, benzodiazepine, and other sedatives to 20% to 40% to avoid the risk of cardiovascular depression.

Breathing – Elderly patients have decreased compliance of the lungs and the chest wall, which leads to increased breathing work, placing them at a higher risk for respiratory failure. Aging also results in suppressed heart rate during hypoxia, and respiratory failure may present alongside.

Circulation – These patients may have increasing systemic vascular resistance in response to hypovolemia, given that they may have a fixed heart rate and cardiac output. Also, an acceptable blood pressure reading may truly indicate a hypotensive state, as most elderly patients have preexisting hypertension.

A systolic blood pressure of 110 mm Hg is used as a threshold for identifying hypotension in adults over 65.

Several variables, namely base deficit, serum lactate, shock index, and tissue-specific lab markers, can be used to assess for hypoperfusion. Consider early use of advanced monitoring of fluid status, such as central venous pressure (CVP), echocardiography, and bedside ultrasonography, to guide resuscitation.

Disability – Traumatic brain injury is one of the significant complications among the elderly. The dura becomes more adherent to the skull with age, which increases the risk of epidural hematoma. Moreover, these patients are commonly prescribed anticoagulant and antiplatelet medications, which puts these individuals at a higher risk of developing intracranial hemorrhage. Therefore, a very low threshold is indicated for further CT scan imaging in ruling out acute intracranial and spinal pathologies.

Exposure – Increased risk of hypothermia due to loss of subcutaneous fat, nutritional deficiencies, chronic medical illnesses, and therapies. Complications of immobility, such as pressure injuries and delirium, may develop.

Rapid evaluation and relieving from spine boards and cervical collars will help to reduce these injuries.

Pregnant [10]

Evaluation and management of pregnant individuals can be challenging due to the physiological and anatomical changes that affect nearly every organ system in the body. Therefore, knowledge of the physiological and anatomical changes during pregnancy regarding the mother and the fetus is important to provide the best and most appropriate resuscitation and care for both.  

The best initial treatment for the fetus is by providing optimal resuscitation of the mother.

Female patients in the reproductive age who present to the ED must be considered pregnant until proven by a definitive pregnancy test or ultrasound exam.

A specialized obstetrician and surgeon should be consulted early in the assessment of pregnant trauma patients; if not available, early transfer to an appropriate facility should be sought.

The uterus is an intrapelvic organ until the 12th week of gestation, around 34 to 36 weeks when it rises to the level of the costal margin. This makes the uterus and its contents more susceptible to blunt abdominal trauma, whereas the bowel remains somewhat preserved. Nevertheless, penetrating upper abdominal trauma in the late gestational period can cause complex intestinal injury due to displacement.

Amniotic fluid embolism and disseminated intravascular coagulation are significant complications of trauma in pregnancy. In the vertex presentation, the fetal head lies in the pelvis, and any fracture of the pelvis can result in fetal skull fracture or intracranial injury.

A sudden decrease in maternal intravascular volume can lead to a profound increase in uterine vascular resistance, thus reducing fetal oxygenation regardless of normal maternal vital signs.

The volume of plasma increases throughout pregnancy and peaks by 34 weeks of gestation. Physiological anemia of pregnancy occurs when there is an increase in red blood cell (RBC) volume, leading to decreased hematocrit levels. In normal, healthy pregnant individuals, blood loss of 1200 to 1500 ml can occur without showing any signs or symptoms of hypovolemia. Nonetheless, this compromise may be seen as fetal distress, indicated by an abnormal fetal heart rate on monitoring.

Leukocytosis is expected during pregnancy, peaking up to 25,000/mm3 during labor. Serum fibrinogen and other clotting factors may be mildly increased, with shorter prothrombin and partial thromboplastin times. However, bleeding and clotting times remain the same.

During late pregnancy, in a supine position, vena cava compression can cause a decrease in cardiac output by 30 % due to lesser venous return from the lower extremities.

In the third trimester of pregnancy, heart rate increases up to 10-15 beats/min than the baseline while assessing for tachycardia in response to hypovolemia. Hypertension, along with proteinuria, indicates the need to manage preeclampsia. Be mindful of eclampsia as a complication during late pregnancy, as its presentation can be similar to a head injury (seizures with hypertension, hyperreflexia, proteinuria, and peripheral edema)

An increase in the tidal volume causes increases in the minute ventilation and hypocapnia (PaCO2 of 30 mm Hg), which is common in the later gestational period. Therefore,

Maintaining adequate arterial oxygenation during resuscitation as oxygen consumption increases during pregnancy is also important.

By the seventh month of gestation, the symphysis pubis widens to about 4 to 8 mm, and sacroiliac joint spaces increase. These alterations must be kept in mind while evaluating pelvic X-ray films during trauma. Additionally, the pelvic vessels that surround the gravid uterus can become engorged, leading to large retroperitoneal hemorrhage after blunt trauma with pelvic fractures.

Every pregnant patient who has sustained major trauma must be admitted with appropriate obstetric and trauma facilities.

Pregnant individuals may present to the ED with non-obstetric causes such as intentional (intimate partner violence, suicide attempt) and unintentional trauma (MVC, fall), and obstetric causes such as ectopic pregnancy, vaginal bleed, contractions, abdominal pain, decreased fetal movement, etc.

“To optimize outcomes for the mother and fetus, assessment and resuscitation of the mother is performed first and then the fetus, before proceeding for secondary survey of the mother.”

Primary Survey - Mother

Airway – Ensure the patient has a patent and maintainable airway with adequate ventilation. In cases where intubation is necessary, maintain appropriate PaCO2 levels according to the patient’s gestational age.  Due to the superior displacement of abdominal organs and delayed gastric emptying, there is an increased risk of aspiration during intubation.

Breathing – These patients may have an increased rate of respiration due to pressure effects or hormonal changes. Pulse oximetry and arterial gas must be monitored as adjuncts. It must be remembered that normal maternal bicarbonate levels will be low to compensate for the respiratory alkalosis.

Circulation – Attempt to manually reposition the uterus towards the left side to relieve the pressure on the inferior vena cava and improve the venous return.

Since pregnant individuals have increased intravascular volumes, they can lose a large amount of blood before the onset of tachycardia, hypotension, or other signs of hypovolemia. Therefore, it is essential to remember that the fetus and the placenta are deprived of perfusion, leading to fetal distress while the maternal conditions appear stable.

Administer crystalloid IV fluids and type-specific blood. Vasopressors must be used only as a last resort to raise maternal blood pressure, as these agents can further cause a reduction of the uterine blood flow, leading to fetal hypoxia.

Primary Survey - Fetus

Leading causes of fetal demise include maternal shock and death, followed by placental abruption.

Assess for signs of abruptio placentae (vaginal bleeding, uterine tenderness, frequent uterine contractions, uterine tetany, and irritability). Another rare injury is the uterine rupture (abdominal tenderness, rigidity, guarding or rebound tenderness, abnormal fetal lie, etc.) accompanying hypovolemia and shock.

By 10 weeks of gestation, fetal heart tones can be assessed by Doppler ultrasound, and beyond 20-24 weeks of gestation, continuous fetal monitoring with a tocodynamometer must be performed. At least 6 hours of continuous monitoring in patients with no risk factors for fetal death is recommended, and 24 hours of monitoring in patients with a high risk of fetal death.

Secondary Survey

Perform the secondary survey for non-pregnant individuals, as mentioned.

An obstetrician should ideally examine the perineum, including the pelvis. The presence of amniotic fluid in the vagina, PH greater than 4.5, indicates chorioamniotic membrane rupture.

All pregnant patients with vaginal bleeding, uterine irritability, abdominal tenderness and pain, signs and symptoms of shock, fetal distress, and leakage of amniotic fluid should be admitted for further care.

All pregnant trauma patients with Rh-negative blood group must receive Rh immunoglobulin therapy unless the injury is remote from the uterus within 72 hours of injury.

Obese Patients [10]

In the setting of trauma, procedures such as intubation can be challenging and dangerous due to their anatomy. Diagnostic investigations such as E-FAST, DPL, and CT scans may also be challenging. Moreover, most of these patients have underlying cardiopulmonary diseases, which hinders their ability to compensate for the stress and injury.

Athletes [10]

Owing to their prime conditioning, they may not exhibit early signs such as tachycardia or tachypnea in shock cases. Additionally, they usually have low systolic and diastolic blood pressure.

Revisiting Your Patient

Let’s get back to the patient we discussed earlier and start assessing him:

Airway – The patient maintains his airway but finds breathing hard. Intervention: Apply 15L Oxygen via a nonrebreather mask.

Breathing—A strap mark contusion is seen with multiple bruises. His chest expansion is asymmetrical, with reduced breath sounds on the right side of his chest. There is a dull percussion note on the right lower half of his chest. He maintains oxygen saturation. Intervention: Prepare for chest tube insertion on the right side.

Circulation – Heart sounds are muffled with marked engorgement of the external jugular veins in the neck, a good pulse still palpable in his left radial, but cold clammy extremities. His pulse is 128/min, and his blood pressure is 92/50 mm Hg. Bedside ultrasound FAST (Focused Assessment Sonography in Trauma) shows a pericardial tamponade. Intervention: IV access was gained with two large-bore IV cannulas, blood was drawn for labs, the massive transfusion protocol for blood products was activated, a Foley catheter was inserted to monitor urinary output, and the surgery team was on board to plan for emergent pericardiocentesis.

Disability – Patient’s GCS remains 15, unremarkable pupillary examination and POC glucose is 7 mmol/dl.

Exposure – you notice the strap mark on his chest secondary to his seatbelt restraint, and the multiple bruises. The remaining evaluation is unremarkable, with no head, spine, abdomen, or limb injury.

Adjunct investigations – A portable chest x-ray shows increased cardiac shadow and multiple bilateral rib fractures. There is opacification in the right lung [12]. 

Discussion

This patient sustained a blunt trauma leading to pericardial tamponade and right-sided hemothorax, leading to hypovolemic shock. The most common cause of shock in a trauma patient is hypovolemic shock due to hemorrhage. However, other types of shock like cardiogenic shock (due to myocardial dysfunction), neurogenic shock (due to sympathetic dysfunction), or obstructive shock (due to tension pneumothorax, obstruction of great vessels) can occur.

Early signs of shock include tachycardia, which is the body’s attempt to preserve cardiac output and cool peripheries, and reduced capillary refill time caused by peripheral vasoconstriction. This is caused by the release of catecholamine and vasoactive hormone, which leads to increased diastolic blood pressure and reduced pulse pressure. For this reason, measuring pulse pressure rather than systolic blood pressure allows earlier detection of hypovolaemic shock, as the body can lose up to 30% of its blood volume before a drop in systolic blood pressure is appreciated.

Initiate fluid resuscitation in these patients and do not wait for them to develop hypotension.
The main aim is to maintain organ perfusion and tissue oxygenation. In children, start with crystalloid fluid boluses of 20 ml/kg, and in adults, an initial 1 L can be given. In patients who have sustained a major blood loss, consider initiating the Massive Transfusion Protocol (MTP) for blood products as soon as possible.

A few current trauma guidelines have recommended ‘permissive hypotension’ or ‘balanced resuscitation,’ where the principle is to stabilize any blood clots that may have been formed, and aggressive blood pressure resuscitation may disrupt this ‘first formed clot’ and may contribute to further hemorrhage.

To evaluate response to fluid resuscitation, assess the level of consciousness, improvement in tachycardia, skin temperature, capillary refill, and urine output (>0.5 ml/kg/hour in adults).
Besides administering packed red blood cells, do not forget to transfuse platelets, fresh frozen plasma, or cryoprecipitate, as large blood loss can develop coagulopathy in 30% of these injured patients. Tranexamic acid (TXA), an antifibrinolytic, can be utilized in addition as a 1 g bolus over 10 minutes followed by 1 g over 8 hours within 3 hours of trauma without an increased risk of thromboembolic events [11].

This systematic approach focuses on identifying and treating this hemorrhagic shock case. Bedside adjuncts such as FAST examination and portable chest X-ray can provide valuable clues to the cause of shock. A trauma CT scan is only performed once the patient is stable enough to go to the scan room.

This patient’s vital signs improve slightly but remain unstable, and blood is kept draining into the chest drain. The patient is taken to the operation theatre for an emergency thoracotomy [12].

Authors

Picture of Roxanne R. Maria

Roxanne R. Maria

Picture of Hamid A. Chatha

Hamid A. Chatha

Listen to the chapter

References

  1. Initial Assessment of Emergency Department patients, The Royal College of Emergency Medicine, Feb 2017
  2. World Health Organization. BASIC EMERGENCY CARE : Approach to the Acutely Ill and Injured.World Health Organization; 2018.
  3. Thim T. Initial assessment and treatment with the airway, breathing, circulation, disability, exposure (ABCDE) approach. International Journal of General Medicine. 2012;5(5):117-121. doi:https://doi.org/10.2147/IJGM.S28478
  4. Peate I, Brent D. Using the ABCDE Approach for All Critically Unwell Patients. British Journal of Healthcare Assistants. 2021;15(2):84-89. doi:https://doi.org/10.12968/bjha.2021.15.2.84
  5. Schoeber NHC, Linders M, Binkhorst M, et al. Healthcare professionals’ knowledge of the systematic ABCDE approach: a cross-sectional study. BMC Emergency Medicine. 2022;22(1). doi:https://doi.org/10.1186/s12873-022-00753-y
  6. Learning Objectives. https://www.moh.gov.bt/wp-content/uploads/moh-files/2017/10/Chapter-2-Emergency-Patient-Assessment.pdf
  7. Resuscitation Council UK. The ABCDE Approach. Resuscitation Council UK. Published 2021. https://www.resus.org.uk/library/abcde-approach#:~:text=Use%20the%20Airway%2C%20Breathing%2C%20Circulation
  8. Management of trauma patients – Knowledge @ AMBOSS. http://www.amboss.com. https://www.amboss.com/us/knowledge/Management_of_trauma_patients/
  9. Oxford Medical Education. ABCDE assessment. Oxford Medical Education. Published 2016. https://oxfordmedicaleducation.com/emergency-medicine/abcde-assessment/
  10. HENRY SM. ATLS Advanced Trauma Life Support 10th Edition Student Course Manual, 10e. 10th ed. AMERICAN COLLEGE OFSURGEO; 2018.
  11. Walls RM, Hockberger RS, Gausche-Hill M, Erickson TB, Wilcox SR. Rosen’s Emergency Medicine : Concepts and Clinical Practice. Elsevier; 2.
  12. Eamon Shamil, Ravi P, Mistry D. 100 Cases in Emergency Medicine and Critical Care. CRC Press; 2018.

Reviewed By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Maxillofacial Trauma (2024)

~ iEM Education Project Team ~ Leave a comment

by Maitha Ahmad Kazim & David O. Alao

Authors
Listen

You have a new patient!

A 48-year-old man was brought to the ED by ambulance shortly after sustaining blunt trauma to the face. The patient was off-loading his quad bike from a truck when it accidentally flipped over and fell directly on his face. He could not recall the incident.

Upon arrival, his vitals were BP: 144/85 mmHg, HR: 104 bpm, T: 36.8°C, RR: 23 bpm, and SPO2: 99% on room air. He was awake on the AVPU score. On examination, the patient was bleeding profusely from his nostrils, breathing from his mouth, and having diffuse facial swelling. You are concerned about the extent of the injuries sustained, and you assemble a team to manage the patient.

Importance

The significance of proficiently managing maxillofacial trauma in the fast-paced emergency medicine setting cannot be overstated. Not only do these traumas cause direct physical harm, but they also impact the patient’s appearance and their ability to perform vital functions like breathing, speaking, and chewing. Given the complex and sensitive nature of the maxillofacial region, emergency physicians must comprehensively understand how to manage such injuries effectively. Proficiency in diagnosing and managing maxillofacial trauma ensures timely and appropriate treatment and prevents potential complications and long-term sequelae. 

Epidemiology

Maxillofacial injuries are a prevalent global health concern. There were an estimated 7.5 million new facial fractures globally in 2017, with 1.8 million individuals living with a disability from a facial fracture [1]. Undoubtedly, the incidence and prevalence vary significantly from one country to another. Singaram et al. reported that the prevalence varied between countries from 17% to 69% [2]. In many regions, inadequate infrastructure, limited access to healthcare, and poor safety regulations contribute to a higher incidence of maxillofacial injuries.

Pathophysiology

Road traffic accidents, interpersonal violence, industrial accidents, and sports-related incidents are the most common etiologies of maxillofacial injuries globally. However, the predominant causes differ in developed and developing countries. Assault is the most common mechanism of injury in developed countries, while motor vehicle accident (MVA) is the most common mechanism in developing countries [3].

Low or high-impact forces can cause maxillofacial injuries. The force needed to cause damage differs from one bone to another. For instance, the zygoma and nasal bones can be damaged by low-impact forces. In contrast, the frontal bone, supraorbital rim, maxilla, and mandible are damaged by high-impact forces [4].

Furthermore, the etiology of maxillofacial trauma can predict the type of facial injuries and fractures sustained. For example, MVAs have been associated with higher instances of mandibular fractures. That is mainly due to its position compared to the rest of the facial bones and its relatively thin structure [5].

Medical History

Maxillofacial injuries often occur in association with other injuries and, thus, can be missed initially. Obtaining a systemic and thorough history can aid the diagnosis. At the initial presentation, the mnemonic “AMPLE” (Allergies, Medications currently used, Past illness/Pregnancy, Last meal, Events/Environment related to the injury) can be used to assess the patient’s pre-injury health status. Then, the following should be probed:

  • What was the mechanism of injury?
    Understanding the cause of the injury (e.g., fall, vehicle collision, assault) provides insights into potential injuries and the extent of trauma. Different mechanisms (blunt vs. penetrating, low vs. high-impact) influence the pattern and severity of injuries and aid in anticipating associated injuries.

    • Environment related to the injury
      Environmental context (e.g., construction site, sports field) can highlight additional risk factors or clues about the nature and potential complications of the injury. It may also help assess the likelihood of secondary injuries or infections.

    • Blunt vs. penetrative
      The type of trauma affects the damage pattern. Blunt trauma may result in fractures or soft tissue injuries, while penetrating trauma may involve more focal injury with a higher risk of infection and internal damage.

    • Low vs. high-impact force
      High-impact injuries are more likely to cause fractures and significant soft tissue damage. Knowing the force helps anticipate the severity and depth of injuries.

    • Direction of force
      The direction can indicate which structures might be compromised (e.g., anterior force could affect the nose, mandible, and dental structures, while lateral force may impact the zygomatic arch or TMJ).

  • Was there a loss of consciousness or an altered level of consciousness?
    Altered consciousness or loss of consciousness may indicate a head injury or neurological involvement, which necessitates further investigation and monitoring for brain injury.

  • Are there any visual disturbances?
    Vision changes can signal orbital fractures or injuries to the optic nerve, potentially affecting ocular function or indicating damage to the orbit and nearby structures.

  • Is there any change in hearing? Is the patient experiencing tinnitus or vertigo? Did they notice any discharge from the ears (clear or bloody)?
    Hearing changes, tinnitus, vertigo, or ear discharge suggest possible basilar skull fractures or damage to the auditory system, which are essential to identify to avoid long-term complications.

  • Any trouble breathing through the nose? Did they notice any discharge (clear or bloody)?
    Difficulty breathing through the nose or nasal discharge may indicate nasal fractures, airway obstruction, or cerebrospinal fluid (CSF) leakage if clear, which is critical to address in traumatic injuries.

  • Any pain while talking? Do the teeth come together normally?
    Pain when speaking or abnormal occlusion may signal fractures in the mandible, maxilla, or TMJ dislocation, impacting facial symmetry, function, and long-term outcomes.

  • Is there difficulty opening or closing the mouth? Is there any pain when biting down the teeth?
    Difficulty or pain in mouth movement often suggests mandibular fractures or TMJ injury. Restricted movement can help identify specific injury locations and aid in planning management.

  • Numbness or tingling sensation in any area of the face?
    Sensory changes suggest possible nerve damage, often related to fractures affecting the infraorbital, mental, or other facial nerves. This information helps predict potential complications and guides treatment planning.

Consider the following symptoms when obtaining a history from maxillofacial trauma patients:

  • Orbital floor fractures commonly present with symptoms such as tingling or numbness around the nose, upper lip, and maxillary gums due to infraorbital nerve damage, along with difficulty looking upward or laterally, double vision (diplopia), and pain during eye movement.
  • Nasal fractures are characterized by swelling, pain, and nosebleeds (epistaxis).
  • Nasoethmoidal fractures can cause cerebrospinal fluid (CSF) rhinorrhea, epistaxis, and tearing (epiphora) due to nasolacrimal duct obstruction.
  • Zygomaticomaxillary complex (ZMC) fractures may lead to numbness around the nose and upper lip, issues with eye movement, double vision, and difficulty opening the mouth (trismus).
  • Maxillary fractures often result in CSF rhinorrhea or epistaxis and may cause mobility in the upper teeth and gingiva.
  • Alveolar fractures are typically associated with gingival bleeding.
  • Mandibular fractures can present as painful jaw movements and tingling or numbness affecting half of the lower lip, chin, teeth, and gingiva.

Red Flags in History

Due to the complex nature of the maxillofacial region, one should be vigilant for red flags when taking history from the patients. Its proximity to the brain and central nervous system makes injuries to these very likely. Thus, identifying them early on can prevent irreversible sequelae and medicolegal implications. Red flags include memory loss, fluctuations in the level of consciousness, nausea/vomiting, and headache that does not improve with analgesia [6].

Neurological involvement can further be assessed by asking about the presence of diplopia or a change in visual acuity. Vision loss usually occurs immediately, but in 10%, symptoms are delayed [7]. Another red flag that is associated with high morbidity and mortality is cervical cord syndrome. Maxillofacial injuries associated with falls are often associated with cervical spinal injury. The patient may complain initially about neck pain or a loss of motor/sensory function in the arms [8].

Physical Examination

Maxillofacial trauma is commonly associated with polytrauma [9]. Thus, it often gets missed in examinations. Physical examination should be done systematically to ensure that all injuries are noted. Like all trauma cases, life-threatening injuries should be addressed first, and the ATLS protocol should be applied accordingly. After that, a physical examination of maxillofacial trauma would involve several key steps. Hard and soft tissue injuries (hematoma, laceration, foreign body, swelling, missing tissue, bleeding, or clear discharge) should be noted upon general inspection of the head and face. Symmetry and alignment of the face should also be noted, bearing in mind that asymmetry may be hidden by edema [10]. Facial elongation and flattening can be seen in midface fractures. Increased intercanthal distance, also known as telecanthus, indicates a nasoethmoidal injury.

Palpation of the whole face should follow, going from top to bottom to avoid missing any injury. Identify step-offs, crepitus, instability or excessive mobility, and malocclusion. Le Fort fractures, complex midface fractures, can be identified during physical examination. 

Next, a complete ocular examination should be done. Assess visual acuity, visual field, pupillary reflex, anterior chamber, and extraocular movements. An ophthalmologic consultation is recommended if any abnormalities are present [10]. The nose and septum should be inspected for any hematoma, bulging mass, or CSF leakage and palpated for any signs of fracture. The oral cavity should be inspected for palatal ecchymoses, lacerations, malocclusion, or missing teeth. Manipulate each tooth individually for movement or pain. Palpate the entire mandible for step-offs or injury. Motor and sensory functions of the face should be evaluated. A thorough cranial nerve examination will help identify sensorimotor injuries. 

Le Fort Classification

Le Fort I Fracture: A Le Fort I fracture, often referred to as a “floating palate,” is a horizontal maxillary fracture that separates the teeth from the upper face. The fracture line passes through the alveolar ridge, lateral nose, and the inferior wall of the maxillary sinus. Patients with this fracture often present with a swollen upper lip, open bite malocclusion, and ecchymosis of the hard palate. When the forehead is stabilized, the maxilla may also have noticeable mobility (including the hard palate and teeth).

Le Fort II Fracture: Known as a “floating maxilla,” the Le Fort II fracture builds upon the characteristics of Le Fort I but extends to involve the bony nasal skeleton, giving it a pyramidal shape. This fracture often leads to a widening of the intercanthal space, bilateral raccoon eyes, epistaxis, and open bite malocclusion. Physical examination may reveal mobility of the maxilla and nose, ecchymosis of the hard palate, and cerebrospinal fluid (CSF) rhinorrhea. Patients may also experience sensory deficits in the infraorbital region extending to the upper lip.

Le Fort III Fracture: Referred to as a “floating face” or “craniofacial disjunction,” the Le Fort III fracture involves a separation of the midfacial skeleton from the base of the skull. The fracture line extends from the frontozygomatic suture across the orbit and through the base of the nose and ethmoid region, running parallel with the skull base. Physical signs include bilateral raccoon eyes, ecchymosis of the hard palate, and a dish-face deformity characterized by elongation and flattening of the face. Additional signs may include enophthalmos (sunken eyes), Battle’s sign (ecchymosis over the mastoid bone), CSF rhinorrhea or otorrhea, and hemotympanum.

Red Flags in Examination

Look for “red flags” during physical examination. These red flags include cervical spine injuries, loss of teeth, Battle’s sign/Raccoon eyes with CSF rhinorrhea, and Le Fort fractures. Facial bones should not be manipulated until cervical spine injuries, which are present in 2.2% of cases, have been ruled out [11]. The oral cavity should be carefully examined for loss of teeth, as it may be aspirated during the injury. For missing teeth, a chest X-ray should be done to rule out or confirm aspiration.

Moreover, facial fractures can extend to the cranium [4]. Depending on the mechanism of injury, the patient may suffer from a concomitant base of the skull fracture, which may present with Battle’s sign and Raccoon eyes as well as CSF rhinorrhea in some cases [11]. LeFort fractures are complex fractures of the midface and are further classified into LeFort I, II, and III. These fractures are considered a red flag as they may cause airway obstruction and life-threatening bleeding [12].

Alternative Diagnoses

Given that the cause is usually known, doctors must identify the injuries sustained and the extent of injuries sustained. While blunt trauma to the face is an apparent cause of maxillofacial injuries, concomitant and alternative diagnoses should not be missed. Patients with maxillofacial trauma can present with a wide range of symptoms that are similar to those from intracranial and cervical spinal injuries.

Acing Diagnostic Testing

The diagnosis of maxillofacial injuries is not based on a single diagnostic test. It is a correlation between history, physical examination, and imaging studies. Given that the etiologies of the injury vary, the differentials are vast, and the clinical presentation differs from one patient to another. Thus, bedside testing and laboratory studies should be tailored to each patient’s clinical presentation and existing symptoms.

Bedside Testing

ECG monitoring is essential for all trauma patients. Dysrhythmias, atrial fibrillation, and ST segment changes can be seen in blunt cardiac injury. Point-of-care (POCT) glucose testing quickly assesses the patient’s glucose level. Hypoglycemia can cause confusion and an altered mental status, which are common findings in patients with maxillofacial trauma. Point-of-care blood gas testing may be beneficial in case of excessive bleeding or airway compromise. In case of tissue hypoperfusion and shock, metabolic acidosis and elevated lactate levels may be noted. Oxygen saturation and carbon dioxide should be monitored in case of midface fractures and suspected airway compromise. A POCT pregnancy test should be done in women of childbearing age, as almost all maxillofacial trauma patients require imaging for diagnosis.

Laboratory Testing

A complete blood count (CBC), particularly hemoglobin and hematocrit, is indicated when the patient is bleeding profusely. LeFort II and III have been associated with an increased risk of life-threatening hemorrhage compared to other facial fractures [12]. Therefore, blood typing and crossmatching are crucial if the patient needs a blood transfusion. A coagulation panel is done to rule out trauma-induced coagulopathy, a preventable factor for progressive brain injury and massive bleeding [13].

A CSF analysis is warranted when there are secretions from the nose or ear. Beta-2 transferrin testing is the current preferred test to confirm the presence of a CSF leak [14]. Other less used methods include beta-trace protein, double-ring sign, and glucose oxidase test. A blood ethanol test and urine toxicology screen can be considered in agitated patients or those with altered levels of consciousness.

Imaging Studies

CT scans are the “gold standard” diagnostic modality for evaluating maxillofacial trauma [15]. Using narrow-cut CT scans without contrast provides detailed cross-sectional images of the facial structures, thus allowing for a comprehensive evaluation of complex fractures. In addition to identifying facial fractures, it can detect head and cervical spinal injuries, air and fluid in the intracranial space and sinuses, periorbital injury, soft tissue injury, and embedded foreign bodies. A non-contrast head CT helps identify intracranial bleeding and distinguish between the types of bleeds if present. This is recommended, especially when the patient experiences loss of consciousness for several minutes. Because maxillofacial trauma is highly associated with cervical spine injury, the physician must have a high index of suspicion for cervical spine fractures. The NEXUS criteria is used to guide imaging in these situations. 

Plain radiographs of the head are used when CT scans are not available. They may be used to screen for fractures and provide some insight into displaced fragments, but they have low sensitivity for detecting and establishing the extent of the injuries. A chest x-ray should be done when a missing tooth is noted on physical examination, as the patient may have aspirated it.

Ultrasound is a helpful bedside diagnostic tool in any trauma patient, and it has been shown to be an accurate diagnostic method when evaluating orbital trauma [16]. It is used when an isolated orbital injury is suspected or a CT scan is not readily available. It can pick up muscle entrapment, soft-tissue herniation, and orbital emphysema.

Risk Stratification

Several risk stratification tools have been developed for maxillofacial trauma. However, these are commonly used in clinical research to assess injury severity and determine the appropriate course of action. Although no specific tool was developed for use in an emergency department, other nonspecific tools like the Glasgow Coma Scale (GCS) and NEXUS criteria come in handy. The GCS score is used to rapidly assess the patient’s level of consciousness, guiding immediate interventions. The NEXUS criteria is used to clear patients from cervical injury clinically without imaging. 

The diagnosis of maxillofacial trauma is based on a combination of clinical assessment and diagnostic imaging. A thorough evaluation of both helps predict the risk. Some common clinical factors that may contribute to poorer outcomes include severe and complex fractures, extensive soft tissue injury, high-energy trauma, open fractures, ocular injuries, and pediatric and geriatric age groups [17,18].

Management

Initial Stabilization

Treating patients with maxillofacial trauma aims to restore function and optimize appearance. However, the primary focus upon presentation is to stabilize the patient. Initial management begins with a primary survey, which constitutes the “ABCDE” approach to identify life-threatening conditions and treat them promptly. 

Airway

Airway patency is a serious concern in maxillofacial trauma, and the nature of the injury often complicates airway management. Airway compromise may be complete, partial, or progressive [9]. Early signs of airway compromise include tachypnea, inability to speak in complete sentences, and abnormal noisy breathing. Agitation and abnormal behavior may indicate hypercapnia.

If the patient has obstruction from soft tissue, perform a jaw thrust maneuver. Cervical spine injury should be presumed in all maxillofacial injury patients until proven otherwise. Therefore, avoid mobilizing the neck until it is cleared. Inspect the oral cavity for any bleeding or secretions and suction accordingly. Consider manual removal with a finger sweep or forceps if a foreign body or debris is identified. Control patients with nasopharynx or oropharynx bleeding with nasal packing or compression with gauze [19].

The need for airway protection increases with severe maxillofacial fractures, expanding neck hematoma, stridor, profuse bleeding or continuous vomiting, and unconsciousness [9]. A nasopharyngeal airway is indicated in a conscious patient without a midface trauma. If the patient was unconscious or had a midface injury, an oropharyngeal airway may help temporarily. However, a definitive airway must be secured in patients who cannot maintain airway integrity. Definitive airway control is done by an endotracheal intubation (nasal or oral). Nasal endotracheal intubation is contraindicated in a base of skull fracture. Given the area’s delicacy and complexity of the injuries sustained, fiberoptic intubation by a skilled physician may provide immediate confirmation of tracheal placement and avoid further complications [10]. If the previous methods cannot be accomplished, a surgical airway (cricothyroidotomy or tracheostomy) should be considered. 

Breathing

The patient’s breathing, ventilation, and oxygenation should be assessed. Check the alignment of the trachea and listen to the patient’s chest bilateral for air entry and added sounds. Deviated trachea and decreased air entry upon auscultation increase the likelihood of tension pneumothorax, and a needle decompression should be performed. Look for soft tissue abnormalities and subcutaneous emphysema.

The patient should be connected to a pulse oximeter to monitor adequate hemoglobin oxygen saturation. If the patient is hypoxic, they should receive oxygen supplementation. Non-invasive ventilation should precede invasive ventilation methods. However, in severe injuries, mask ventilation may be difficult due to the disrupted anatomy of the face [20].

Like all trauma patients, a “full stomach” should be presumed in patients with maxillofacial trauma as digestion stops during trauma. In addition, blood is often swallowed and accumulates in the stomach. Regurgitation and aspiration are a big risk in such patients, and evacuation of stomach content is recommended [20]. A nasogastric tube is contraindicated in a skull base fracture. An orogastric tube is recommended instead to prevent intracranial passage [21].

Circulation

Maxillofacial trauma can cause profuse bleeding that can lead to shock. Monitor blood pressure and heart rate, auscultate, and check capillary refill and hand warmth. Tachycardia precedes low blood pressure in shock. Establish bilateral IV access with two large bore cannulas and draw blood for type and crossmatch. Fluid therapy with crystalloids should be initiated. Identify the source of hemorrhage. If external or intraoral bleeding occurs, apply direct pressure, pack, and suture. Carefully examine the tongue, as persistent bleeding can obscure the airway. In the case of epistaxis, anteroposterior packing will control the bleeding in most cases [10]. Additionally, topical tranexamic acid can be used in anterior epistaxis. In cases of LeFort fractures, intermaxillary fixation might be required when packing fails to stop the bleeding [10]. If the previously mentioned measures fail, consult IR, ENT, or surgery for more advanced interventions like arterial embolization and fracture reduction [22].

Disability

The patient’s mental status and neurologic function should be assessed initially. Glucose is measured at this point if not done upon arrival. The Glasgow Coma Scale helps assess the patient’s level of consciousness. Note any change in the mental status. A brief neurological exam is recommended. 

Exposure

Expose the patient fully while keeping them warm. Look for bruises, bite marks, lacerations, and other injuries, as the etiology of maxillofacial trauma is broad and often presents as polytrauma. Decontamination might be required depending on the nature of the trauma.

Medications

Isotonic crystalloid fluids and blood products are common treatments in trauma patients. Adequate pain management should be provided with NSAIDs, opioids, or local anesthesia. There are no guidelines on the use of prophylactic antibiotics in maxillofacial trauma. Nonetheless, there are specific scenarios where prophylactic antibiotics administration is recommended. Depending on the type of injury sustained, additional medications might be required. Refer to Table to explore the additional medications used in the setting of maxillofacial trauma:

Drug name (Generic)

Potential Use

Dose

Frequency

Cautions / Comments

Acetaminophen

mild-moderate pain (can be given with NSAIDs, with or without Opioids)

325-1,000 mg PO

 

Max Dose: 4 g daily

q4-6h

  • Ask for allergies
  • Ask for if/when they took Acetaminophen at home

Ibuprofen

mild-moderate pain (can be given with Acetaminophen)

600 mg PO

 

Max Dose: 3,200 mg daily

q6h

  • Can cause GI upset and increase risk of GI bleed
  • Renal insufficiency

Hydromorphone

Moderate – severe pain

0.5-4 mg IV/IM/SC

 

Max Dose: n/a

q4-6h

  • Risk of respiratory depression
  • Risk of addiction and abuse

Morphine sulfate

Moderate – severe pain

2.5-10 mg IV/IM/SC

 

Max Dose: n/a

q2-6h

  • Risk of respiratory depression
  • Risk of addiction and abuse
  • Hypotension

Metoclopramide

Nausea and vomiting (to prevent risk of aspiration)

1 to 2 mg/kg/dose IV

 

Max Dose: n/a

Every 2 hours for the first two doses, then every 3 hours for the subsequent doses.

  • Extrapyramidal side effects
  • If acute dystonic reactions occur, 50 mg of diphenhydramine may be injected IM.

Ondansetron

Nausea and vomiting (to prevent risk of aspiration)

0.15 mg/kg IV (not to exceed 16 mg)

 

Max Dose: n/a

q8hr PRN

  • Increased risk of QT prolongation, which increases the risk of cardiac arrhythmia and cardiac arrest.

Amoxicillin-clavulanic acid

Nasal packing (ppx for epistaxis – TSS)

 

Facial fractures communicating with open wounds of the skin

 

Mandibular fractures that extend into the oral cavity

2g PO (extended-release tablets)

 

Max Dose: n/a

q12h (7 days)

  • Ask for allergies
  • Ask if they have taken any antibiotic recently.
  • Hives and skin rash

Procedures

Epistaxis: Epistaxis is a common issue in maxillofacial trauma due to damage to the nasal structures and blood vessels. Managing epistaxis is crucial to prevent blood loss and ensure the airway remains clear. For anterior epistaxis, anterior nasal packing can effectively apply pressure to stop the bleeding. If the bleeding source is posterior, posterior nasal packing using a balloon catheter or Foley’s catheter may be necessary. These techniques help control bleeding and stabilize the patient, especially in cases where blood loss might obstruct the airway or lead to hemodynamic instability.

Inability to Protect Airway: In cases of severe maxillofacial trauma, there may be a risk of airway compromise due to swelling, bleeding, or physical obstruction from broken facial structures. If a patient cannot protect their airway, endotracheal intubation is required to secure it and maintain ventilation. Intubation provides a definitive airway, bypassing obstructions and ensuring adequate oxygenation, which is critical in trauma patients to prevent hypoxia and support life-sustaining measures.

Failed Intubation: Occasionally, intubation may be unsuccessful, particularly in patients with extensive facial injuries or anatomical challenges. In such cases, a cricothyroidotomy is performed. This emergency surgical procedure creates an opening in the cricothyroid membrane, providing an alternative airway route directly into the trachea. Cricothyroidotomy is a life-saving measure when intubation fails, ensuring oxygen can still be delivered to the lungs when other methods are ineffective.

Tension Pneumothorax: Maxillofacial trauma can sometimes be associated with thoracic injuries, leading to complications like tension pneumothorax, where air is trapped in the pleural cavity and compresses the lungs and heart, causing a life-threatening situation. Needle decompression is the first step in relieving the pressure by inserting a needle into the pleural space to allow trapped air to escape. This is followed by a tube thoracostomy (chest tube placement) to maintain the release of air and prevent the recurrence of tension pneumothorax. This procedure is essential to restore normal lung function and stabilize the patient’s respiratory status.

Special Patient Groups

Pediatrics

Pediatric patients’ anatomical and developmental differences should be considered when evaluating them for maxillofacial trauma. An infant’s frontal bone dents, while a child’s frontal bone experiences a depressed fracture under a force that causes facial fractures in adults [4]. Smaller force loads are needed to damage the facial bones than adults [4]. Given pediatric patients’ underdeveloped facial skeletons and sinuses, growth dysplasia is a common outcome of suboptimal treatment. Standard facial radiographs often miss fractures; a CT scan is more reliable in this age group [23]. Assess for orbital fracture thoroughly, as children’s orbital floor is pliable, increasing the risk of entrapment and rectus muscle ischemia [6].

Geriatrics

The impaired physiologic response and frailty of geriatric patients make their treatment more challenging. Although they are subject to the same mechanism of maxillofacial trauma as the other age groups, their response to the injuries differ. They are at a high risk of intracranial hemorrhage, but their basal vital signs often do not reflect signs of hemorrhage or hypoperfusion, making diagnosing shock difficult. Comorbidities and polypharmacy in this age group further mask the normal shock response. In addition, the likelihood of associated injuries in this group is high [24]. Elderly patients were reported to have more frequent cerebral concussions and internal organ injuries [25]. Nonetheless, a GCS of <15 has also been associated with higher mortality rates, especially in those older than 70 years [25]. Putting all of this into perspective when assessing elderly patients, a lower threshold for extensive investigations and referral is necessary.

When to admit this patient

Definitive repair of facial fractures is not a surgical emergency, and patients can be discharged home with a close follow-up in the clinic in most cases. An awake patient with good home care and isolated stable injuries (i.e., mandibular or nasal fracture) may be discharged home. However, admission should be considered in a number of situations. These include severe complex facial fractures, open fractures, the presence of comorbidities, and cases of associated injuries that need close monitoring. Admission is made to the intensive care unit or a surgical ward with a high level of monitoring.

Revisiting Your Patient

A 48-year-old male was brought to the ED by ambulance shortly after sustaining blunt trauma to the face. The patient was loading his quad bike off a truck when it accidentally flipped over and fell directly on his face and upper body. He could not recall what happened thereafter.
Upon arrival, his vitals were BP: 144/85 mmHg, HR: 104 bpm, T: 36.8°C, RR: 23 bpm, and SPO2: 99% on room air. He was awake on the AVPU score. On examination, the patient was bleeding profusely from his nose, breathing from his mouth, and having diffuse facial swelling. You are concerned about the extent of injuries sustained and have assembled your team to manage the patient adequately.

History was taken from his brother, who witnessed the incident. The brother confirmed that the patient had no LOC, dizziness, or vomiting but reported that the patient kept complaining of neck pain. He is known to have L5-S1 disc prolapse, does not take any medication, and has no known allergies.

You worry that the patient might suffer from airway compromise and quickly begin your primary survey. You hear gurgling noises and check the patient’s mouth to find it filled with blood. You suction and look for sources of bleeding in the mouth but find none. The airway becomes patent. You notice that EMS has placed a C-spine collar on the patient already. His lungs are clear bilaterally, and you insert an orogastric tube to suction his stomach contents. He is bleeding profusely from his nostrils, so you pack his nose anteriorly. This does not stop the bleeding, and the patient is spitting out blood. You then apply topical tranexamic acid and more packs, and the bleeding stops. His pulses are present, extremities are warm, and capillary refill time is less than 2 seconds. His GCS is 15/15, and his pupils are reactive to light. Upon exposing him, you notice lacerations on his lips and ears but no other injuries on the rest of his body.

Two large bore IV lines are inserted peripherally, blood is drawn for laboratory investigations, and intravenous normal saline is administered immediately. A 12-lead ECG demonstrated sinus tachycardia. You perform a bedside E-FAST to rule out pneumothorax/hemothorax, pericardial fluid, and peritoneal fluid. You ask for urgent CT scans, including a CT Head and Neck without contrast and a Maxillofacial CT. The CT scan report confirms no C-spine fractures, skull fractures, or brain injury. However, it identifies a Le Fort 1 fracture and fracture involving the right orbital wall. You safely remove the c-spine collar. You consult the Oral and Maxillofacial surgeon and the Ophthalmologist, and both agree to see the patient. You give the patient morphine to alleviate his pain.

You performed a secondary survey to ensure the patient was not deteriorating and to identify any additional injuries. The patient remained stable, and he was admitted to the surgical floor.

Figure: Fracture of the lateral wall left maxilla (long arrow) and a tripod fracture of the right zygoma (short arrows).

Author

Picture of Maitha Ahmad Kazim

Maitha Ahmad Kazim

Dr. Maitha Ahmad Kazim is an Emergency Medicine Resident at Dubai Health, recognized for her dedication in patient care and medical research. She earned her Doctor of Medicine degree from the United Arab Emirates University, where she graduated with distinction. Dr. Kazim is known for her commitment to advancing emergency care, demonstrated by her active engagement in research, mentorship, and medical education.

Picture of David O. Alao

David O. Alao

David is a senior consultant in emergency medicine and associate professor of medicine College of Medicine and Health Sciences, United Arab Emirates University, Al Ain, UAE
He graduated from the University of Ibadan, Nigeria. After initial training in general surgery in Leeds and Newcastle Upon-Tyne, United Kingdom, he had higher specialist training in emergency medicine in the South West of England.
He was a consultant in emergency medicine for 15 years at the University Hospitals Plymouth, United Kingdom where he was a Clinical Tutor, Academic Tutor and, Assistant professor at Plymouth University Peninsular School of Medicine and Dentistry (PUPSMD) UK.
David is a fellow of the Royal College of Surgeons of Edinburgh and the Royal College of Emergency Medicine UK.
His interests are undergraduate and postgraduate medical education, skills training and transfer, trauma systems development and resuscitation science. He has published over 30 papers in peer-reviewed journal.

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  24. Shumate R, Portnof J, Amundson M, Dierks E, Batdorf R, Hardigan P. Recommendations for Care of Geriatric Maxillofacial Trauma Patients Following a Retrospective 10-Year Multicenter Review. J Oral Maxillofac Surg. 2018;76(9):1931-1936. doi:10.1016/j.joms.2017.10.019
  25. Kokko LL, Puolakkainen T, Suominen A, Snäll J, Thorén H. Are the Elderly With Maxillofacial Injuries at Increased Risk of Associated Injuries?. J Oral Maxillofac Surg. 2022;80(8):1354-1360. doi:10.1016/j.joms.2022.04.018

Reviewed By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Fundamentals of ACLS (2024)

~ iEM Education Project Team ~ Leave a comment

by Mohammad Anzal Rehman

Authors
Listen

You have a new patient!

A 56-year-old man presents to the Emergency Department with complaints of chest pain and dizziness that began an hour ago. Upon assessment by the triage nurse, his vital signs are as follows: his heart rate is 107 beats per minute, and his respiratory rate is 22 breaths per minute. His blood pressure is  96/70 mmHg, and his oxygen saturation is at 90% on room air. His temperature is 36.8°C.

You are the student on shift when this patient arrives, and immediately, your mind begins to jump across differential diagnoses for this patient. As you rush toward the patient’s room to join your senior, you prepare to list out all the potential causes of chest pain proudly. This must be a Myocardial Infarction, or maybe even an Aortic Dissection. Perhaps it is that rare Boerhaave syndrome you read about last night!

You finally catch up to the Emergency Physician, but before you can open your mouth to wax lyrical about esophageal ruptures, the Doctor states “Let’s begin by evaluating the ABCs.”

Initial Assessment

Emergency Medicine is one of the few specialties in medicine where patient evaluation begins in the same way for every patient, regardless of the probable diagnosis. Most clinicians are wired to jump straight to the ‘mystery-solving’ component of clinical presentation, with many undergraduate curriculums based around disease recognition. Emergency Medicine, however, places an emphasis on systematic assessment of the patient, starting with ‘The Primary Survey’.

The Primary Survey – ABCDE Approach

The Primary Survey aims to identify life-threatening conditions rapidly and systematically in critically ill patients, with appropriate stabilizing interventions performed when an abnormality is recognized. Besides streamlining the process in a high-stakes and often chaotic environment, the alphabetical order is designed first to address the most severe causes of mortality [1].

The Primary Survey aims to identify life-threatening conditions rapidly and systematically in critically ill patients, with appropriate stabilizing interventions performed when an abnormality is recognized. Besides streamlining the process in a high-stakes and often chaotic environment, the alphabetical order is designed first to address the most severe causes of mortality [1].

Airway

A patient’s airway connects air, and therefore oxygen, from outside the body to the lungs. Airway management is a term used to evaluate and optimize the passage of oxygen in the upper airway, which may be impaired when there is a blockage or narrowing of this pathway. The most common cause of upper airway obstruction is the tongue, which may ‘close’ the oropharynx posteriorly in patients who are comatose or in cardiopulmonary arrest, for example.

Assessment of the airway typically starts by evaluating any external features that may impact the passage of air through the naso- and oro-pharynx, such as facial or neck trauma, fractures, deformities, and any masses or swelling that may disrupt the airway tract. Allergies, especially anaphylaxis, and significant burns may cause edema of the laryngeal airway and produce obstruction. Excessive secretions may also congest the oropharynx and produce airway obstruction.

A patent or ‘normal’ airway allows a responsive patient to speak in full sentences without difficulty, implying a non-obstructed air passage down the oropharynx and through the vocal cords.

Clinical signs of obstruction may include stridor, gurgling, drooling, choking, gagging, or apnea. A physician may also identify an impending airway obstruction where loss of gag reflex, intractable vomiting, or worsening laryngeal edema may inevitably compromise the passage of air to the lungs and produce a failure to oxygenate or ventilate, prompting a decision to secure the tract through intubation.

Management

In the responsive patient, allow for the patient to be seated or lying in their most comfortable position as you assess the patency of the airway.

‘Opening’ the airway involves positioning the patient’s head in the ‘sniffing position’. In this position, a slight extension of the head with flexion of the neck, keeping the external auditory meatus in line with or above the sternal notch, is used to optimally align the pharyngeal and laryngeal airway segments, preventing obstruction posteriorly by the tongue (Figure 1). This is useful in patients who are unresponsive and cannot consciously protect their airway.

Figure 1 – Use of ‘sniffing position’ to open the airway

Two maneuvers are helpful in opening an unresponsive or sedated patient’s airway, optimizing air entry to the lungs:

1. Head tilt chin lift (Figure 2A) – Using fingertips under the chin, lift the mandible anteriorly while simultaneously tilting the head back using the other hand. Do not use this if cervical spine injury is suspected!

Figure 2A – Head-tilt chin lift

2. Jaw thrust (Figure 2B) – With thenar eminences of both hands anchored over both maxillary regions of the patient’s face, use your fingers at both angles of the mandible to lift it anteriorly. This maneuver is preferable in cases of suspected cervical spine injury as it does not cause hyperextension of the neck.

In unresponsive patients with excessive secretions, use of a rigid suction device can clear fluid and particulate matter such as vomitus.

Intubation may be performed if airway assessment deems it necessary to protect or secure the airway tract in a definitive way. If intubation is required, it should be performed as early as possible to prevent the evolution of a difficult airway, which would lower the chances of a successful intubation. It may also be useful to establish the risk of an inherently difficult airway using the L-E-M-O-N airway assessment method as below:

Look externally – facial trauma, large incisors and/or tongue, hairy beard, or moustache

Evaluate the 3-3-2 rule – where optimal distance between incisors on mouth opening should be 3 finger breadths. Similarly, 3 finger breadths (patient’s fingers) should span the distance from chin to hyoid bone, while the distance from hyoid to thyroid should measure 2 finger breadths.

Mallampati score – grades the view of an open mouth, with class 3 or more predicting a difficult intubation

Obesity/obstruction – Epiglottitis or a tonsillar abscess can inhibit easy passage of an endotracheal tube.

Neck mobility – if limited, positioning is difficult and causes suboptimal views during intubation.

iEM-infographic-pearls-airway - Assessing Airway Difficulty
assessing airway difficulty

Cervical spine immobilization

When the patient arrives in the Emergency Department (ED) following a significant physical trauma, such as head injury or motor vehicle collision, it is crucial to consider the integrity of the cervical spine. If injury is present in this region, further manipulation or movement of the neck may lead to spinal cord damage. Therefore, evaluation and management of airway for these patients should go hand in hand with cervical spine immobilization.

If no specialized equipment is available, or until one is prepared for use, attempts to limit neck movement can be done using manual in-line stabilization, where the provider’s forearms or hands may be positioned at the sides of the patient’s head to prevent indirect movements that could exacerbate underlying injury (see Figure 3).

Cervical spine immobilization is then performed using a rigid cervical collar. It may be augmented with head blocks on lateral sides to limit movement further as the patient is evaluated for injury (see Figure 4). The thoracolumbar region of the spine is immobilized using a spinal backboard, which keeps the patient in a supine position with minimal external force on the spine. Frequently utilized in Emergency Medical Services (EMS) during extrication and transport, all efforts should be made to transition the patient off the spinal board in the ED as it is quite uncomfortable, with prolonged use associated with pressure ulcers and pain.

Breathing

The lungs perform the vital function of delivering oxygen from the airway to the alveoli through ventilation. Perfusion at the alveoli allows for gas exchange; therefore, effective ventilation and perfusion both play a key role in the availability and utilization of oxygen by the human body. Evaluation of the Breathing component assesses factors that would indicate a compromise in ventilation.

The chest inspection should look for respiratory rate, use of accessory muscles, position of trachea (midline versus deviated), symmetry of chest rise, and/or any visible trauma to the thorax. Auscultation evaluates breath sounds for any bilateral inequal air entry or presence of crackles, crepitus, or wheeze. Percussion, though sometimes useful, is often difficult to perform adequately in a resuscitation environment.

Let’s compare the findings in normal lungs, pleural effusion, and pneumothorax based on chest rise, trachea position, percussion, and auscultation.

Normal Lungs: Chest rise is symmetrical with the trachea in the midline position. Percussion reveals a resonant sound. Auscultation presents vesicular breath sounds peripherally and bronchovesicular sounds over the sternum, with no added sounds.

Pleural Effusion: Chest rise remains symmetrical, and the trachea is midline. Percussion is dull over the area of effusion, and auscultation shows decreased breath sounds in the region of the effusion.

Pneumothorax: Chest rise is unequal, and the trachea may be deviated in cases of tension pneumothorax. Percussion reveals a hyper-resonant sound in the area of the pneumothorax, and auscultation shows decreased breath sounds over the pneumothorax region.

Measuring oxygen saturation using pulse oximetry (spO2) provides a percentage of oxygen in circulating blood, with normal levels typically at 95% or above. However, in patients with chronic lung disease, baseline oxygen saturation levels may decrease and can be as low as 88% in many cases. For patients experiencing shortness of breath and showing signs of hypoxia, pulse oximetry readings below 94% suggest that supplemental oxygen may be necessary. This can be administered through various oxygen delivery systems, as outlined in Figure 5 and described below.

Figure 5 – Common equipment used in airway management 1- Nasal cannula, 2- Simple face mask, 3- Nebulizer,* 4- Non-rebreather mask, 5- Venturi mask valves, 6- Rigid suction tip, 7- Bag-valve mask device, 8- Oropharyngeal airway (OPA), 9- Nasopharyngeal airway (NPA), 10- Direct Laryngoscope, 11- Endotracheal tube with stylet, 12- Colorimetric end-tidal CO2 detector, 13- Bougie, 14- Laryngeal Mask Airway (LMA) *NOT an oxygen delivery device, used to administer inhaled medication such as bronchodilators and steroids CO2: Carbon dioxide

General concepts—We typically breathe in room air, which contains 21% oxygen. Each Liter per minute of supplemental oxygen provides an additional 4% inspired oxygen (FiO2) to the patient.

Nasal cannula – Administered through patient nostrils, can provide a maximum flow rate of 4-6 Liters per minute of oxygen, which equals roughly 37 – 45% FiO2

Simple face mask – Applied over the patient’s nose and mouth, can provide a maximum flow rate of 6-10 Liters per minute of oxygen, which equals roughly 40 – 60% FiO2

Venturi mask – Typically used in COPD, where over-oxygenation is avoided. Different colors deliver various flow rates to limit oxygen delivery to the required amount only; Blue (2-4L/min, FiO224%), White (4-6L/min, FiO2 28%), Yellow (8-10L/min, FiO235%), Red (10-12 L/min, FiO2 40%), Green (12-15 L/min, FiO260%)

Non-rebreather mask – Utilizes an attached bag with a reservoir of oxygenated air along with one-way valves on the mask to prevent rebreathing of expired air, optimizing oxygenation. It can provide a maximum flow rate of 15 Liters per minute of oxygen, which equals roughly 85 – 90% FiO2.

Non-invasive ventilation (CPAP/BiPAP) is a tight-fitting mask device that uses high positive pressure to keep the airway open and enhance oxygenation. It is particularly useful in conditions such as COPD exacerbation, acute pulmonary edema/heart failure, and sleep apnea.

Bag-valve mask device: A self–inflating bag attached to a reservoir delivers maximal, high-flow 100% oxygen. This method of manual ventilation is used in rescue breathing and oxygen delivery in nonresponsive or cardiopulmonary arrest patients.

Circulation

The circulation component of the Primary Survey evaluates the adequacy of perfusion by the cardiovascular system. The patient’s general appearance is assessed for signs of pallor, mottling, diaphoresis, or cyanosis, which indicate inadequate or deteriorating perfusion status. Pulses are checked centrally (e.g. carotid pulse, especially if patient with impaired breathing) and peripherally (e.g. radial) alongside hemodynamic assessment, including blood pressure and heart rate checks. Information from this segment also provides valuable insight into potential signs of shock. Extremities are palpated in order to determine any delays in capillary refill time (more than 2 seconds signifies inadequate perfusion, e.g. hypovolemia), peripheral edema in lower extremities (signs of heart failure), and skin temperature (cool or warm to touch).

In cases of trauma, systematic evaluation of circulation also seeks to ascertain areas of potential blood loss or collection, with interventions for any long-bone deformities and/or bleeding from open wounds performed as they are discovered.
Intravenous (IV) line insertion is also performed as part of the management of circulation, as any required fluid or blood products can then be administered through a large-bore IV line (16 gauge or higher). If IV insertion is difficult on multiple attempts, when volume resuscitation is urgently required, Intraosseous (IO) access should be sought to prevent delay in any needed treatment. Insertion of a peripheral venous line often occurs concomitant to blood extraction for any urgent laboratory investigations and/or point-of-care testing. Some common examples of tests performed on critically ill patients include venous blood gas, complete blood count, type and crossmatch, troponin, urea, electrolytes, and creatinine.

Finally, circulation assessment requires an evaluation of cardiac rhythm. Basic auscultation may reveal the rate and regularity of rhythm along with murmurs. However, a critically ill patient will also benefit from the immediate attachment of cardiac pads to the bare chest and connection to a cardiac monitoring device, which provides the physician with the patient’s current cardiac rhythm.

A normal sinus rhythm (Figure 6) consists of a P wave (atrial depolarization), followed by a QRS wave (ventricular depolarization – normally less than 120 ms), with a subsequent T wave (ventricular repolarization). P-R intervals typically have a duration of 120 – 200 ms. A regular rhythm, with a consistent P wave preceding QRS complexes, with a normal heart rate (between 60 – 100 beats per minute (bpm)) is required to consider a rhythm to be normal sinus on the cardiac monitor.

Figure 6 – Normal sinus rhythm

The American Heart Association’s (AHA) Advanced Cardiac Life Support (ACLS) course and guidelines outline a series of internationally recognized cardiac rhythms and their general management when encountered [2]. Some of the most important rhythms, along with the AHA bradycardia and tachycardia algorithms, are summarized below:

Figure 7.1 - Sinus bradycardia (HR < 50 bpm)

Several different conditions, including abnormal heart conduction, damage to the myocardium, metabolic disturbances, or hypoxia, can cause bradycardia. A lower heart rate can result in decreased perfusion to end-organs, such as the brain, with resultant signs and symptoms such as dizziness, confusion, shortness of breath or chest pains. Management (Figure 7.2) aims to treat the underlying cause and increase the heart rate (atropine, dopamine/epinephrine and/or cardiac pacing) if needed to restore the heart’s ability to perfuse organs adequately.

Figure 7.2 – American Heart Association’s Bradycardia Algorithm

Tachycardia (Figure 8.1) is a heart rate of more than 100 bpm that may present as several types of waveforms on the cardiac monitor. Supraventricular tachycardia (SVT) originates in the upper chambers of the heart. The rapid heart rate prevents adequate filling of the heart between contractions, causing signs and symptoms such as dizziness, palpitations, or chest pain.

Figure 8.1 - Supraventricular Tachycardia (SVT)

Management (Figure 8.2) typically involves Valsalva maneuvers, medication (e.g. adenosine), and/or synchronized cardioversion as needed to revert the rhythm back to baseline.

Figure 8.2 – American Heart Association’s Tachycardia Algorithm

SVT produces a narrow-complex tachycardia (QRS segments < 120 ms). In comparison, monomorphic Ventricular Tachycardia (Figure 8.3) originates in the lower chambers of the heart and produces a wide-complex (QRS segments > 120 ms) tachycardia on the cardiac monitor. Similarly, this rhythm may cause dizziness, shortness of breath, or chest pain and is managed with medication or synchronized cardioversion.

Figure 8.3 - Ventricular Tachycardia

ACLS algorithms often divide patients based on “stable” and “unstable” categories. This grouping aims to ascertain which individuals have a pathology severe enough to impair cardiac output to the point of causing serious inadequacies in end-organ perfusion. This ‘instability’ is manifested by altered mental status, ischemic chest pain, drastically low hemodynamic parameters (e.g. systolic BP < 90 mmHg), signs of shock, and signs of acute decompensated heart failure.

Disability

This segment evaluates the level of consciousness and responsiveness of the patient. Level of consciousness may be assessed generally using the AVPU scale (below);

Alert: fully alert patient
Verbal: some form of verbal response is present, though not necessarily coherent.
Pain: response to painful stimulus
Unresponsive: no evidence of motor, verbal or eye-opening response to pain

or more explicitly, using the Glasgow Coma Scale (GCS)

Choose the best response of patient
EYE OPENING
4: Spontaneously
3: To verbal command
2: To pain
1: No response
BEST VERBAL RESPONSE
5: Oriented and converses
4: Disoriented and converses
3: Inappropriate words; cries
2: Incomprehensible sounds
1: No response
BEST MOTOR RESPONSE
6: Obeys command
5: Localizes pain
4: Flexion withdrawal
3: Flexion abnormal (decorticate)
2: Extension (decerebrate)
1: No response
Glasgow Coma Score (GCS) (Modified from Teasdale, G., & Jennett, B. (1974). Assessment of coma and impaired consciousness: a practical scale. The Lancet, 304(7872), 81-84.) - Please read this article to get more insight regarding GCS.

Exposure

Complete exposure of the patient may be necessary to completely evaluate for any external signs of infection, injury, and rash. This is especially useful in trauma, where log-rolling of the patient is included to ensure the back and spine are also included in a complete assessment for any traumatic injuries. As you expose the patient, obtain consent, be mindful of their dignity, and uncover each segment of the body sequentially, covering it back to prevent any hypothermia for the patient. A core temperature reading also completes vital sign measurements for the patient.

Practical implementation of the Primary Survey

The “cursory” primary survey

It may seem surprising to consider that virtually every patient who enters the Emergency Department, despite the severity of the illness, undergoes some form of a Primary Survey by the treating physician. However, the practicality of this becomes quite obvious when you consider a simple question frequently asked at the beginning of a patient encounter:

“How are you?”

An adequate response of “I am all right” or “Well, I have had this pain in my stomach…” seems fairly standard, but it addresses most of the components detailed in the previous section. A patient who can form words without difficulty or added sounds generally has an intact or patent Airway. Their ability to form words depends on air that has been sufficiently ventilated and moving through the vocal cords, hence the Breathing is adequate. An appropriate response to the question allows us to assume that Circulation adequately perfuses the brain to allow comprehension and formulation of new words oriented to the circumstances of the encounter, hence providing insight into Circulation and, to a degree, Disability.

Synchrony in the Emergency Department

Although systematic assessment during the Primary Survey is laid out in order, it is also important to note that an Emergency Department consists of teams of healthcare professionals who often have the personnel and resources to simultaneously perform tasks to efficiently address all components of the Primary assessment, without delay between segments.
In practice, an example of how synchrony works would involve a patient who, on initial, immediate assessment, is deemed to be in significant distress and/or critically ill. The patient is immediately moved into the ED to a resuscitation area, where team members expose the chest, attach cardiac pads to connect the patient to a cardiac monitor, obtain a fresh set of vital signs, including spO2monitoring, with IV cannula insertion, blood extraction for testing as needed. At the same time, a primary survey is conducted simultaneously by another physician who moves through Airway, Breathing, Circulation, Disability and Exposure. In more advanced systems, a member may be dedicated to each component of the Primary Survey.

Adjuncts

A number of resources are accessible to the Emergency Physician that may aid in diagnosing and investigating the critically ill patient. Utilizing these alongside the initial Primary Survey provides valuable, relevant information that can further guide clinical decision-making and diagnosis during evaluation.

  1. Electrocardiogram – A 12-lead electrocardiogram provides a complete picture of the heart’s electrical activity in various vectors and segments, allowing for a more accurate evaluation for rhythm disturbances, such as in acute myocardial infarction, hyperkalemia, bundle branch blocks, and torsade de pointes. This often ties into the Circulation assessment and allows for a more comprehensive look into the heart’s electrophysiology.
  2. Portable X-rays – Particularly in trauma, urgent chest and pelvic X-ray films can often be obtained without having to transfer the patient to Radiology, hence providing more information on suspected lung pathologies (e.g. pneumothorax, effusion/hemothorax) and pelvic abnormalities (e.g. fracture, displacement).
  3. Urinary/ gastric catheters – Urinary catheters are useful to evaluate fluid status and monitor output for the patient undergoing volume resuscitation. When relevant, gastric tube insertion can assist in gastrointestinal decompression, if needed, as well as minimize the risk of aspiration in certain patients.
  4. Point-of-Care Ultrasonography (PoCUS) – A rapidly evolving and increasingly prevalent modality in the ED is the ultrasound.[3] Various probes, at different frequencies, utilize ultrasound waves to provide the physician with real-time visualization of the body’s internal structures. These images are fast and often very reliable in determining major findings that can guide decision-making in critically ill patients (e.g. presence of post-traumatic intra-abdominal free fluid, pneumothorax, cardiac tamponade). Figure outlines some examples of information that can be extracted using PoCUS.

 

HI-MAP in Shock

Reassessment

Each intervention performed in the Primary Survey should ideally be accompanied by a reassessment of vital signs and patient clinical status and a restarted Primary Survey beginning from Airway. Identifying any improvements, deteriorations, or non-responses that will be pivotal in guiding the initiation or discontinuation of further intervention as per the clinical case is crucial.

Focused History and Secondary Survey

If the patient is appropriately evaluated and stabilized following the Primary Survey, the treating physician may proceed with a focused history and secondary survey appropriate to the clinical circumstances. One example of a focused history incorporates the mnemonic SAMPLE to organize pertinent information as follows:

S – Signs/symptoms of presenting complaint

A – Allergies to any food or drugs

M – Medications (current, recent changes)

P – Pertinent past medical history

L – Last oral intake

E – Events leading to the illness or injury

A secondary survey in the Emergency Department is a more comprehensive physical examination performed systematically in a head-to-toe fashion to investigate any clinically relevant findings. In case of trauma, this also involves careful inspection for any missed injuries, deformities, or signs of underlying blood collection.

As the secondary survey is performed, relevant investigations and/or imaging may be ordered to augment the evaluation of the present clinical condition (e.g. Computerized Tomography (CT) of the brain after signs of basal skull fracture noted on inspection of the face and head). Information gathered from the survey and results of any ordered investigations, coupled with the clinical condition and/or response to therapy in the ED, if any, is used to determine patient disposition at the end of the ED encounter.

Revisiting Your Patient

You assist the Emergency Physician in performing a Primary Survey. The airway is patent, with the patient phonating in full sentences and breathing with mild tachypnea but no added sounds on auscultation. You initiate supplemental oxygen through a non-rebreather mask, with an increase in spO2 to 99%. You reassess and proceed through Airway, Breathing, and Circulation. As you discuss initiating IV fluids with your senior, the patient complains of worsening chest pain, palpitations, and dizziness.You attach the patient to the cardiac monitor and notice the rhythm below:

Cardiac pads have already been attached to the patient. Noting the presence of ischemic chest pain, you correctly identify the patient as having an unstable, narrow-complex tachycardia, most likely an SVT and prepare for synchronized cardioversion. Conscious sedation is conducted after explaining the procedure and obtaining consent from the patient. 50 joules of biphasic energy is then administered for synchronized electrical cardioversion. The rhythm changes on the monitor to the reading below:

You observe an organized rhythm but note that the patient is now unresponsive, with eyes closed and no palpable carotid pulse.

Basic Life Support

Cardiopulmonary arrest occurs when the heart suddenly stops functioning, resulting in lack of blood flow to vital organs in the body, such as the lungs and brain. Therefore, signs of arrest are manifested as a lack of breathing (apnea), lack of pulse and unresponsiveness. The most common cause of cardiac arrest is coronary artery disease.[4] Respiratory arrest refers to a cessation of lung activity, but with a present, palpable pulse and functioning heart.
The International Liaison Committee on Resuscitation (ILCOR) and the American Heart Association (AHA) are some of the key figures who have developed international guidelines on the recognition and management of cardiac arrest patients.[5] Basic Life Support (BLS) and Advanced Cardiac Life Support (ACLS) courses were established to optimize the workflow and, therefore, patient outcomes in Cardiopulmonary Resuscitation (CPR).

CPR forms the cornerstone of BLS to effectively maintain the victim’s circulatory and ventilatory function until circulation either spontaneously returns or is hopefully restored through intervention. The general concepts within BLS are outlined below:

1. A person who has a witnessed collapse, lack of response or who is suspected of being unresponsive due to cardiac arrest should be approached for further assessment and management. However, it is important for the rescuer to first determine whether the scene is safe around the patient before attempting any intervention. An example of this would be a victim drowned in water, who should be removed from the body of water onto a dry surface prior to attempting life-saving chest compressions or defibrillation.

Figure 9 - Witness
Figure 10 - Check for responsiveness

2. Check for responsiveness. Firmly tapping both shoulders with the palms of your hands and a clear, verbal prompt, such as “Hey, are you okay?” should be incorporated to ensure that the victim is, indeed, unresponsive to an otherwise arousable stimulus.

3. You have determined that the patient is unresponsive. If you are alone, shout loudly and clearly for help and assistance. If no help is nearby, call Emergency Medical Services using your mobile phone.

Figure 11 - Call for help
Figure 12 - Open airway, palpate carotid artery, observe the chest

4. Open the patient’s airway (tilt chin upward into sniffing position). Palpate the carotid pulse by placing two fingers (index and middle finger) just lateral to the trachea on the side closest to you while simultaneously observing the chest for any spontaneous chest rise (breathing). The pulse check should take a minimum of five (5) seconds but no more than 10 seconds to avoid delay in life-saving intervention.

5. When help is available, the chain of survival begins by activating the Emergency Response System. In addition to activating the Emergency Response, ask the person who has responded to your call for help getting an Automated External Defibrillator (AED) device. An example of instruction to a bystander (out of hospital) would be to ‘call an ambulance and get an AED!’. Inside a hospital, if another healthcare provider has come to aid, you may ask them to ‘activate the Emergency Response System/’Code Blue’ and get the crash cart/AED.’

6. Begin high-quality chest compressions. Hands are placed with fingers interlaced to exert pressure using the heel of one hand at the center of the chest, over the lower half of the breastbone (sternum), in line with the nipples (in men), with shoulders directly over your hands and arms straight at a perpendicular angle to the victim’s chest. High-quality chest compression is one of the few variables which have been evidenced to improve patient survival in cardiac arrest.

Figure 13 - Chest compression

Keep the following features in mind to maintain high-quality chest compressions:

  • More than 80% of the time in resuscitation or more should be spent on compressions (Chest compression fraction of > 80%)
  • The frequency of compressions should follow a rate of 100–120 compressions per minute.
  • Compression depth in adults is at least 2 inches. In infants and children, depth should be at least one-third of the anterior-posterior diameter of the chest.
  • After each compression, the hands should be withdrawn to allow adequate chest recoil and fill the heart between compressions.
  • Minimize interruptions in chest compression
  • Avoid hyperventilation (see next point).
Figure 14 - Bag-Valve-Mask Ventilation. Two-Hand technique

7. Compressions should follow the ratio 30:2, that is, 30 compressions followed by 2 rescue breaths delivered by a mouth barrier device (pocket mask) in the sniffing position or a Bag-valve mask (BVM) device if another rescuer is present to manage the airway in hospital. The BVM’s mask should be held with a tight seal using the E-C technique over the bridge of the nose and covering the mouth. 

Breaths should be over 1 second, with enough air pushed in to observe a chest rise and no hyperventilation or excessive bagging of the BVM to avoid gastric insufflation. Two attempts at rescue breaths are performed, minimizing time to under 10 seconds and resuming chest compressions immediately after. If a definitive airway (e.g. endotracheal tube) is in place, resume compressions without pause at a rate of 100-120 compressions per minute while breaths are delivered once every 6 seconds.

8. Once an AED or cardiac monitor/defibrillator is available, place the pads on the victim’s bare chest (dry the skin if wet) in either an anterior-lateral or anterior-posterior position.When in doubt, follow the machine’s prompts and the instructions on the pads themselves to guide placement.

Figure 15 - Correct placement of transcutaneous pacing pads.jpg

9. Follow the prompts on the AED. Stop compressions when the device analyzes rhythm and stay clear of the patient (not touching any part of the patient’s body). During an in-hospital resuscitation, as per ACLS workflow, stay clear, as the team leader should analyze the initial rhythm to ascertain the presence of a shockable or non-shockable rhythm. Either way, the device or team leader should prompt whether a shock is advised. Continue compressions as the device charges, but ensure that all rescuers are clear of the patient when the shock is delivered using the AED/defibrillator device.

Figure 16 - Shock delivery.

A victim who is unresponsive but has a palpable pulse has respiratory arrest, which is managed using rescue breathing only. Breaths are delivered once every 6 seconds without chest compressions while transport to a higher level of care and/or management of any underlying cause for the condition is initiated.

Advanced Cardiac Life Support

The Advanced Cardiac Life Support algorithms were designed to deliver a higher level of resuscitative care where providers with increased training and improved resources are available. This type of augmented management is customary to the Emergency Department, where a Rapid Response Team or Code Blue team would respond when activated and initiate a more team-based approach to cardiopulmonary resuscitation.

Instead of an AED, in-hospital settings have a cardiac monitor/defibrillator, usually mounted atop a crash cart consisting of a CPR back-board (to support chest compressions by providing a firm surface to use under the patient’s chest), drawers with medication used during cardiac arrest, and various equipment for airway management and IV/IO access. Once brought to the bedside, the cardiac pads are similarly placed on the patient’s chest while BLS maneuvers (chest compressions and rescue breaths) continue. Once placed, however, compressions should be paused to assess the cardiac monitor’s cardiac rhythm. The type of rhythm should be identified as ‘shockable’ or ‘non-shockable’ (Figure 17s).

Figure 17.1 - NON-SHOCKABLE - Asystol
Figure 17.2 - NON-SHOCKABLE - Pulseless electrical activity – organized rhythm in the absence of palpable pulse
Figure 17.3 - SHOCKABLE - Pulseless Ventricular Tachycardia
Figure 17.4 - SHOCKABLE - Ventricular fibrillation

“Shockable” rhythms (pulseless Ventricular Tachycardia and Ventricular Fibrillation) are a product of aberrant electrical conduction of the heart. Rapid, early correction of this rhythm is the most important step in returning the body to its normal circulatory function. Early defibrillation is one of the few variables that has been evidenced to improve patient survival in cardiac arrest, the other notable one being high-quality chest compressions.[6]

Defibrillation involves using an asynchronous 200J of biphasic (360J if monophasic) energy, delivering an electric current through the cardiac pads attached to the patient’s chest to revert the heart to a rhythm that can sustain spontaneous circulation. Chest compressions should be ongoing while charging, but all persons should stay clear of the patient when shock is being delivered, and this is frequently verified with verbal feedback (‘Clear!’) before pressing the defibrillator button to deliver the shock. Immediately after the shock, chest compressions should resume to minimize interruptions between compressions.

Two minutes of chest compressions and rescue breaths make up each cycle of CPR, at the end of which a rhythm check should be performed for any changes and/or presence of pulse. Figure 18 outlines the ACLS algorithm used to manage shockable and non-shockable rhythms in cardiac arrest. Early shock in shockable rhythms is followed by a cycle of CPR, a second shock if still with a shockable rhythm, after which 1mg of IV epinephrine is given, with subsequent doses every 3 to 5 minutes. During the third cycle of CPR, after 3 shocks have been delivered for a persistent shockable rhythm, a bolus of IV Amiodarone 300mg is typically administered, with a dose of 150mg in a subsequent CPR cycle if still with a shockable rhythm.

“Non-shockable” rhythms (pulseless electrical activity (PEA) and asystole) are not typically a product of disorganized electrical activity in the heart. Instead, an underlying cause has resulted in cardiac arrest for these patients. While the majority of cardiac arrest is caused by coronary artery disease, the consideration of reversible causes by use of the H’s (hypovolemia, hypoxia, hyper-/hypokalemia, hydrogen ions (acidosis), and hypothermia) and T’s (thrombosis/embolism, toxins, tension pneumothorax, and cardiac tamponade) may help recognize and manage other possible etiologies in patients.

The management of non-shockable rhythms focuses on consistent, high-quality CPR, with regular pulse checks every 2 minutes, addressing reversible causes, and administering IV epinephrine 1mg every 3 to 5 minutes.
A palpable pulse with measurable blood pressure signals the Return of Spontaneous Circulation (ROSC).

Figure 18 - ACLS Adult Cardiac Arrest Algorithm

Resuscitation Team Dynamics

The Emergency Department is equipped with the resources and personnel to provide care beyond basic life support. Resuscitation is optimized when multiple providers work together to effectively perform tasks toward management of the patient, thereby multiplying the chances of a successful outcome for the patient. A high-performance team typically consists of members allocated to the following roles and responsibilities:

  • Airway – Opens and maintains the airway. Manages suctioning, oxygenation, and ventilation (Bag-valve mask) and assesses the need for a definitive airway if needed.
  • Medication – Inserts and maintains IV/IO access. Manages medication administration and fluids.
  • Monitor/defibrillator – Ensures attached cardiac pads and AED/cardiac monitor/defibrillator device are working appropriately to display the patient’s cardiac rhythm in clear view of the team leader. Administers shocks using the devices as needed. May alternate with the compressor every 5 cycles or 2 minutes to prevent compression fatigue
  • Compressor – Performance of high-quality chest compressions as part of CPR for the cardiac arrest patient. Focuses on quality and consistency of compressions. You may switch to another standby compressor or monitor/defibrillator every 5 cycles or 2 minutes if compressions are affected by fatigue.
  • Recorder – Documents the timing of medication, intervention (shocks, compression), and communicates these to the Team Leader, with prompts to enable timely dosing of frequent medication (e.g., ensuring epinephrine every 3 to 5 minutes is administered as per the verbalized order)
  • Team leader – A defined leader who coordinates the team’s efforts and organizes them into roles and responsibilities that are clear, well-understood, and within their individual limitations. Provides explicit instructions and direction to the resuscitation effort, focused on patient care and optimized performance from all team members. Promotes understanding and motivates members, identifying any potential deficit or depreciation of quality during resuscitation and facilitating improvement in performance as needed.

All team members are encouraged to conduct themselves with mutual respect and practice closed-loop communication, where each message or order is received with verbal confirmation of understanding, then execution of the order, centralizing all information back to the team leader. Figure 19 provides an example of the possible placement of each member during resuscitation that may optimize their workflow through the resuscitation attempt. Ideally, the team leader remains at the foot of the bed, in clear view of all members, with involvement limited to coordination of the team’s efforts and minimal direct execution of tasks.

Figure 19 - An example of optimized team placement during resuscitation

Post Arrest Care

If the patient is found to have Return of Spontaneous Circulation (ROSC), post-cardiac arrest care should be initiated to enhance the preservation of brain tissue and heart function. This involves a sequential assessment and optimization of Airway, Breathing, and Circulation in the initial stabilization phase. A definitive airway may be placed so ventilation is more appropriately controlled, with parameters set to optimize oxygen administered with ventilatory function. Figure 20 outlines the ACLS algorithm and parameters often used to help guide post-cardiac arrest care. Circulation incorporates fluids, vasopressors, and/or blood products to achieve an adequate systolic blood pressure above 90 mmHg, with Mean Arterial Pressure of at least 65 mmHg typically indicating perfusion within stable parameters.

It is imperative to obtain a 12-lead ECG early to ascertain the presence of an ST-elevation myocardial infarction (STEMI), which will require expedited transfer of the patient to a Cath Lab for definitive reperfusion therapy. The patient’s responsiveness should be reassessed, and the determination for additional investigation should be performed in conjunction with other critical care management as needed.

Of note, unresponsive patients may benefit from Targeted Temperature Management (TTM), which involves the maintenance of core body temperature at a target of 32 – 36 ℃ for 24 hours, or preferably normothermia at 36 °C to 37.5 °C with an emphasis on prevention of hyperthermia, in order to protect and optimize brain recovery post-arrest.[7]

Almost all cardiac arrest survivors will require a period of intensive care observation and management. If no immediate intervention is needed (e.g., reperfusion therapy), patients inside a hospital will need to be transitioned to an Intensive Care Unit (ICU) for further care.

Figure 20 – Post-Cardiac Arrest Care

What do you need to know?

  • Emergency Medicine, especially in critical care, emphasizes a systematic approach to the unwell patient.
  • The Primary Survey is designed to recognize and address life-threatening conditions effectively and timely.
  • The Primary Survey components are Airway (& and C-spine in trauma), Breathing, Circulation, Disability, and Exposure.
  • If an intervention is performed at any level of the survey, you must reassess the patient by commencing the Primary Survey again, starting with Airway.
  • Reassess and review your patient for changes frequently.
  • Many of the actions performed in the initial assessment of the critically ill patient may occur simultaneously when more team members are present in an Emergency Department. Do not let the chaos of the scene distract you from completing each step of the assessment.
  • The AHA has well-established guidelines for assessing and managing patients through the Primary Survey. Use the algorithms and the patient’s status as ‘stable’ or ‘unstable’ to guide the management of recognized pathologies, especially in Circulation.
  • The ED is home to a variety of adjuncts, including portable X-rays, ECG, and point-of-care ultrasound, which can provide the physician with rapid, readily accessible information to guide management.
  • Remember the SAMPLE mnemonic for a focused history in the critically ill patient.
  • An unresponsive patient should be immediately recognized, and Emergency Response Systems should be activated.
  • Performance of Basic and Advanced cardiac life support focuses on preserving blood circulation transiently to maintain the perfusion of organs, such as the brain, until the cause of the condition is reversed or managed.
  • The majority of cardiac arrest is caused due to coronary artery disease.
  • The two most important predictors of patient survival in cardiac arrest are high-quality CPR and early defibrillation (for a shockable rhythm)
  • An effective resuscitation in the ED often relies on the concerted efforts of multiple team members, led by a team leader who coordinates tasks in an organized, effective way to improve patient survival and outcomes.

Author

Picture of Mohammad Anzal Rehman

Mohammad Anzal Rehman

EM Residency Graduate from Zayed Military Hospital in Abu Dhabi, UAE. Founder/President of the Emirates Collaboration of Residents in Emergency Medicine (ECREM). Editor-in-Chief for the Emirates Society of Emergency Medicine (ESEM) Monthly Newsletter. I have a vested interest in sharing updated knowledge and developing teaching tools. As a healthcare professional, I continually strive to incorporate the newest clinical research into practice and am an active advocate for the use of Point of Care Ultrasonography (POCUS) in the ED.

Listen to the chapter

References

  1. Reynolds T. Basic Emergency Care: Approach to the Acutely Ill and Injured. World Health Organization; 2018.
  2. 2020 Advanced Cardiac Life Support (ACLS) Provider Manual. American Heart Association; 2021.
  3. Hashim A, Tahir MJ, Ullah I, Asghar MS, Siddiqi H, Yousaf Z. The utility of point of care ultrasonography (POCUS). Ann Med Surg (Lond). 2021;71:102982. Published 2021 Nov 2. doi:10.1016/j.amsu.2021.102982
  4. Cardiac Arrest Registry to Enhance Survival (CARES) 2022 Annual Report; 2022, https://mycares.net/
  5. Wyckoff MH, Singletary EM, Soar J, et al. 2021 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations: Summary From the Basic Life Support; Advanced Life Support; Neonatal Life Support; Education, Implementation, and Teams; First Aid Task Forces; and the COVID-19 Working Group. Resuscitation. 2021;169:229-311. doi:10.1016/j.resuscitation.2021.10.040
  6. Soar J, Böttiger BW, Carli P, et al. European Resuscitation Council Guidelines 2021: Adult advanced life support [published correction appears in Resuscitation. 2021 Oct;167:105-106]. Resuscitation. 2021;161:115-151. doi:10.1016/j.resuscitation.2021.02.010
  7. Lüsebrink E, Binzenhöfer L, Kellnar A, et al. Targeted Temperature Management in Postresuscitation Care After Incorporating Results of the TTM2 Trial. J Am Heart Assoc. 2022;11(21):e026539. doi:10.1161/JAHA.122.026539

Acknowledgements

  • Marina Margiotta – Illustrator
  • Paddy Kilian – Emergency Physician – Mediclinic City Hospital, Dubai, Director of Academic Affairs – Mohammed Bin Rashid University Of Medicine and Health Sciences
  • Rasha Buhumaid – Consultant Emergency Physician – Mediclinic Parkview Hospital, Dubai, Assistant Professor of Emergency Medicine – Mohammed Bin Rashid University Of Medicine and Health Sciences, President of the Emirates Society of Emergency Medicine (ESEM)
  • Amog Prakash – Medical Student – Mohammed Bin Rashid University Of Medicine and Health Sciences
  • Fatima Al Hammadi- Medical Student – Mohammed Bin Rashid University Of Medicine and Health Sciences

Reviewed By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

COVID-19 (2024)

~ iEM Education Project Team ~ Leave a comment

by Pei Shan Hoe, Andrew Mariotti, Prem Menon, Alexandra Digenakis

Authors
Listen

You have a new patient!

A 64-year-old male, Mr Fox, with a history of type II diabetes mellitus, hypertension, congestive heart failure, and cerebrovascular accident with chronic left-sided weakness, presented to the emergency room from a nursing home due to fever, cough, and difficulty in breathing. Per EMS, the patient’s nursing home has had an outbreak of COVID-19 infections. Mr Fox is unvaccinated against COVID-19 and has not been tested for COVID-19 before arrival. The onset of symptoms was 2 days ago, and his symptoms have progressively worsened. At the nursing home, the patient was in acute distress and was tachycardic (130 bpm), tachypneic (30 rpm), and hypoxic (82% on room air). Oxygen saturation improved to 89% on placement of a nonrebreather mask by EMS. He was borderline hypotensive (90/50 mmHg) but improved to 100/60 mmHg after 500cc of IV normal saline. On arrival, the patient appears diaphoretic and tachypneic with O2 saturation of 90% on 15L of O2 via a nonrebreather mask. Mr. Fox is alert but confused and unable to answer questions. He is febrile to 102.3F (39.1oC), remains tachycardic (132 bpm), and his blood pressure is stable at 103/67 mmHg, with delayed capillary refill (2 to 3 seconds). Mr Fox is coughing throughout the examination and has diffuse rales on auscultation of his lungs but has no obvious pitting oedema or JVD.

What do you need to know?

Importance

The COVID-19 pandemic threw the world into a tumultuous few years of fear, death, and isolation as many countries tightened borders and restricted activities. As of March 2023, there have been over 761 million confirmed cases of COVID-19 globally – including almost 7 million deaths – since the virus was first discovered in late 2019, as reported by the World Health Organisation (WHO) [1]. Healthcare institutions bore the brunt of the pandemic’s wrath as wave after wave of case surges drained resources and manpower, overwhelming hospitals and exposing healthcare workers to increased risks. Emergency departments became the frontlines of this battle against a new virus, unprecedented in its worldwide scale and extent of physical and economic disruption. This chapter lays out key information in the assessment and management of the COVID-19 infection, which are important as the virus continues to plague humankind and mutations surface.

Epidemiology

The COVID-19 virus belongs to a family of coronaviruses, which are known to produce respiratory diseases in humans. There have been three major coronavirus outbreaks in recent times, beginning with the severe acute respiratory syndrome coronavirus (SARS) in 2002, followed by the Middle East respiratory syndrome coronavirus (MERS) in 2012, and now the COVID-19 pandemic in 2019 [2].

Reports of COVID-19 cases first emerged from Wuhan, China, at the end of 2019; the virus spread rapidly to other countries worldwide, with cases reported in all continents. On March 11, 2020, WHO declared COVID-19 as a pandemic [3].

Person-to-person spread is the main mode of COVID-19 transmission. The mean or median incubation period ranges from 5 to 6 days. The duration for which a patient with COVID-19 remains infective is unclear. Viral load in the oropharyngeal secretions is highest during the early symptomatic stage of the disease. The patient can continue to shed the virus even after symptom resolution [4,5].

Pathophysiology

The virus is transmitted via respiratory droplets and aerosols from person to person. Once inside the body, the virus binds to host receptors and enters host cells through endocytosis or membrane fusion. After membrane fusion, the virus enters the lungs’ alveolar epithelial cells, and the viral contents are released. The virus undergoes replication within the host’s cells [5].

Medical History

What are the key features that should be interrogated in medical history?

Common symptoms: fever, cough and fatigue.

Other reported symptoms, typically milder and less common, are loss of taste or smell, conjunctivitis, headache, muscle aches and pains, nasal congestion, runny nose, sore throat, diarrhoea, nausea or vomiting, and different types of skin rashes.

Ask also about symptoms of pulmonary embolism, as COVID-19 can be a risk factor. These include sudden and sharp chest pain, dyspnea that worsens on exertion, and coughing that may produce bloody mucus.

There are also some people who become infected but remain asymptomatic and well [6,7,8].

What are the risk factors related to the specific disease in focus that should be picked up in medical history?

Check for any COVID-19 contact, and if the patient is vaccinated against COVID-19 Unvaccinated patients with positive contact are at higher risk of developing infection though vaccinated patients can contract COVID-19 despite vaccination.

What are the red flags that indicate a worse outcome in a patient with this specific disease?

Red flag symptoms that patients should monitor for include difficulty breathing or shortness of breath, confusion, loss of appetite, persistent pain or pressure in the chest [6,8].         

Physical Examination

What are the key features that should be checked during a physical examination?

Check the patient’s following systems:

  • Head, ear, nose and throat
  • Cardiovascular system
  • Respiratory system
  • Gastrointestinal system
  • Skin

What are the findings related to the specific disease in focus that should be picked up during physical examination?

Look out for signs such as [6-10]:

  • Abnormal breath sounds in lungs suggestive of pneumonia, which is the most frequent serious manifestation of infection
  • Abdominal tenderness
  • Conjunctivitis
  • Skin changes, such as maculopapular/morbilliform, urticarial, and vesicular eruptions, transient livedo reticularis, reddish-purple nodules on the distal digits similar in appearance to pernio (chilblains), also known as “COVID toes”
  • Leg swelling, erythema or tenderness on examination

What are the red flags that indicate a worse outcome in a patient with this specific disease?

Red flag signs include [6-10]:

  • Signs of venous thromboembolism, such as deep vein thrombosis — erythema, tenderness and swelling of the lower limbs
  • Arrhythmias
  • EncephalopathyRespiratory distress

Alternative Diagnoses

What other diseases can present with similar clinical features/conditions?

Differential diagnoses of COVID-19 include [11]:

  • Community acquired pneumonia, and other forms of pneumonia (e.g. aspiration pneumonia, pneumocystis jirovecii pneumonia)
  • Influenza
  • Middle East respiratory syndrome (MERS)
  • Avian influenza virus infection
  • Pulmonary tuberculosis

Which risk factors make COVID-19 more probable than alternative differentials?

Risk factors for COVID-19 include:

  • Close contact with COVID-19 patients
  • Lack of COVID-19 vaccinations

Acing Diagnostic Testing

Diagnosing COVID-19 infections may involve the use of multiple modes of testing and evaluation. In this section, we will discuss the role that bedside tests, lab studies, and imaging play in diagnosing and treating COVID-19.

Bedside Tests

Testing for COVID-19 that can be done at the bedside falls into one of two categories: antigen testing or nucleic acid amplification testing (NAAT), sometimes known as PCR testing due to the use of polymerase chain reaction (PCR) methods to amplify the DNA samples in question. Both have a place in testing for COVID but indications for use and the subsequent results should be approached thoughtfully.

Antigen Testing

With antigen testing, a nasal or oropharyngeal swab – or even a blood sample – is used to collect mucosal secretions and saliva from the patient with a suspected COVID infection. The sample is placed in a lateral flow assay that contains antibodies to COVID antigen with a detector molecule attached. If the sample contains COVID antigen, the antibodies will bind and read as a positive test. Rapid testing can yield results in under a half-hour with 99.4% specificity and 68.4% sensitivity, is conducive for self and at-home administration, and has been an effective method for increasing access to testing [12]. Due to its high specificity, rapid testing is reliable when positive, however, one of the major drawbacks is its low sensitivity. It is important to understand that patients who test negative for COVID via an antigen test cannot be reliably ruled out for the disease until it has been verified with NAAT testing.

NAAT Testing

This form of testing – while still utilizing swabbed samples of mucosal secretions and saliva as in antigen testing – relies on a different method of disease verification using PCR and COVID specific RNA primers to amplify any viral DNA present in the sample. Results yield similar levels of specificity (98.9 – 99.2%) but have a markedly higher sensitivity of 83.2 – 84.8% making this a much more reliable testing option [13]. The major drawback to this method of testing is that it cannot be administered at home and must be done where there is a lab present that has a technician with the knowledge to perform the testing using the PCR machine.

Laboratory Tests

If both antigen and NAAT testing returns negative – or if NAAT results are pending after a negative antigen test – clinicians will often opt to send for a respiratory viral panel to determine if there is an underlying primary or comorbid infection. A respiratory viral panel uses PCR to test for a standard slate of viruses that usually includes influenza, respiratory syncytial virus (RSV), adenovirus, parainfluenza virus, adenovirus, rhinovirus, enterovirus, and human metapneumovirus.

While no specific set of labs is directly indicative of a COVID-19 infection, a specific constellation of lab findings has been found to be suggestive of potential COVID infection when pretest probability is high. These lab findings include lymphopenia, transaminitis – specifically elevations in AST – and an elevated c-reactive protein [14]. While not diagnostic, this constellation of laboratory results can lend support to a future diagnosis and help guide early treatment.

Imaging

Neither Magnetic Resonance Imaging (MRI), Computed Tomography (CT), nor X-ray can provide a conclusive diagnosis of COVID-19. Ground glass opacities seen on CT are a typical finding in COVID-19 infection and have been proven effective at differentiating COVID-19 and non-COVID-19 viral illnesses in certain retrospective analyses [15]. Despite this, the presence of ground glass opacities alone does not provide definitive diagnosis and would only be indicated for diagnostic purposes if COVID pre-test probability was already high due to known community presence or recent exposures [16].

Figure 1: ground glass opacities on chest CT[16]

Imaging becomes far more important when diagnosing two major sequelae of COVID-19: pneumonia and acute respiratory distress syndrome (ARDS). The prolonged, severe pulmonary inflammation of COVID-19 causes damage to capillaries and leakage of fluid into the alveoli leading to ARDS. This should be suspected in those who develop acute onset shortness of breath, hypoxemia, and/or rattling breath sounds. A chest x-ray showing a classic “white out” appearance can greatly aid in diagnosis of ARDS.

Figure 2: A chest x-ray showing classic ARDS findings[17]

Similarly, opportunistic bacterial infections can take root in damaged lung tissue secondary to COVID infection, leading to bacterial pneumonia. This should be a major consideration in patients who rapidly develop shortness of breath or pleuritic chest pain. A chest x-ray showing lung field consolidations can greatly aid in the diagnosis of pneumonia.

Figure 3: A chest x-ray showing classic consolidated findings of pneumonia[18].

Risk Stratification

When stratifying the potential risk of severity of COVID-19, the two major considerations are age and the number and type of comorbidities. Global data evaluating age in relation to COVID mortality during the early stages of the pandemic demonstrated a less than a 1.1% mortality rate in those younger than 50 years but an overall mortality rate of 12.1% among those greater than 80 years old, with each subsequent decade in between demonstrating increased mortality rates from the prior decade [19].

Furthermore, the presence of comorbid conditions increased morbidity and mortality compared to the general population, with cardiovascular disease and diabetes respectively acting as significant predictors for future intensive care requirements and lower survival rates [20]. Though individual comorbidities present a lesser risk than age alone, patients with multiple comorbidities are at greater risk of mortality than those who present with one comorbid condition. Studies have shown 10 or greater comorbidities result in a 3.8-fold increase in RR as compared to those with 1 comorbidity [21].

Risk Stratification Tools

Many tools exist to stratify patients into risk categories based on covid infection based on the setting and presentation of the patient. The notable tools with a description of their intended use are described below.

  • 4C Mortality Score – This tool was developed by the International Severe Acute Respiratory and emerging Infection Consortium (ISARIC) to predict in-hospital mortality of COVID based on age, oxygenation, renal function, and other statistical measures.
  • ACEP ED COVID-19 Management Tool – Developed by emergency physicians from around the world, this tool walks the clinician through the steps of managing a patient with COVID in an emergent setting from severity classification to treatment.
  • Pediatric COVID Risk Assessment Tool – Physicians at the University of California San Francisco created this tool to assess the risk of children with asymptomatic infection.

Management

Management options in unstable patients begin with determining the severity of disease. Mild disease presents with symptoms characteristic of upper respiratory infections such as fever, cough, malaise, and rhinorrhea. Acute, life-threatening airway, breathing and circulation concerns are absent in mild disease.

In moderate to severe disease, one of the initial signs is dyspnea. Severe disease specifically is defined by hypoxemia (oxygen saturation at or below 94% on room air) which may or may not require supplemental oxygen or even intubation. In the case of severe disease initial stabilization is followed by medical management and even certain procedures. These are described below.

Initial Stabilization

The steps to initial stabilization for severe COVID-19 infection are described below in terms of the ABCs of emergency medicine.

  • Airway – The patient should be evaluated for the ability to protect and maintain the airway. Signs that a patient may require or soon require intubation include worsening hypoxia despite maximized oxygen supplementation, increased work of breathing, and signs of distress.
  • Breathing & Circulation—Assuming patients can maintain their airway but their oxygen saturation is still below 94% on room air, they will require supplemental oxygen. Low-flow supplemental oxygen with the nasal cannula at 1-2 liters/minute can be used initially, but high-flow supplementation via non-rebreather and even non-invasive ventilation, such as a high-flow nasal cannula or BiPap, should be considered depending on patient needs.

Once the patient is stabilized per their needed oxygen and ventilation requirements, pharmaceutical and bedside management can begin with the goal of ultimately weaning the patient from their oxygen requirements.

Medical Management

The ensuing table outlines the major pharmaceutical agents used in the treatment of COVID-19. They are described based on class, indication, contraindications and adverse effects, and dosing.

Drug

Class

Indication

Contraindications (CI) &

Adverse Effects (AE)

Dosing

Nirmatrelvir/

Ritonavir (Paxlovid)

Anti-viral

Mild to moderate COVID-19 infection for patients at risk for increased severity

CI: <12 years old or eGFR <30ml/min as well as many medications interactions

AE: dysgeusia, diarrhea, hypertension, and myalgia

eGFR > 60ml/min: 300/100mg twice daily for 5 days

 

eGFR 30-60ml/min: 150/100mg twice daily for 5 days

Dexamethasone

Glucocorticoid

Severe disease in patients requiring oxygen or ventilatory support

AE: Hyperglycemia, increased secondary infection risk

6mg/day for up to 10 days

Baricitinib

JAK Inhibitor

Severe disease in patients requiring high-flow oxygen supplementation but not intubation.

CI: Already on IL-6 inhibitors, lymphopenia, neutropenia, CKD

Max 4mg/day oral

Tocilizumab

IL-6 Inhibitor

Markedly elevated inflammatory markers (D-dimer, CRP, etc.)

CI: must already be taking dexamethasone

AE: secondary infection risk

Single dose at 8mg/kg IV

Anakinra

IL-1 Inhibitor

Severe disease in patients who are at high risk of progressing to ventilatory support

AE: anaphylaxis, stomach pain, headache, nausea

100mg/day for 10 days, subcutaneous

Remdesivir

Antiviral

Severe disease in patients who are not intubated or in need of ventilatory support. Benefits uncertain in non-severe cases.

CI: under 12 years of age

AE: nausea, vomiting, fever, hyperglycemia, transaminitis

Loading dose: 200mg IV

Maintenance Dose: 100mg/day IV for up to 10 days

Monoclonal Antibodies

Antibody Based Therapy

No longer indicated due to decreased benefit from increased circulating variants

N/A

N/A

Convalescent Plasma

Antibody Based Therapy

Patients with impaired humoral immunity who have severe disease

AE: serum sickness, anaphylaxis

1 unit of high titer convalescent plasma

Ivermectin

Anthelmintic

Patients with latent Strongyloides infection undergoing glucocorticoid therapy for COVID

CI: no studies to prove efficacy against COVID-19 itself as a primary therapeutic

AE: GI upset, neurological disturbances

200ug/kg for 1-2 days

Procedures

There are few COVID specific procedures though intubation and mechanical ventilation are common requirements in severe cases. Some patients will even progress in severity to a point that extracorporeal membrane oxygenation (ECMO) will be required.

Patients who develop ARDS, independent of COVID, may benefit from proning – a technique by which the patient is rolled onto their abdomen to increase ventilation/perfusion matching of the lungs [22].  It should be noted that any procedure which must be done that involves aerosolization (bronchoscopy, intubation and extubation, suctioning, etc.) should be done under extreme caution and only after all who are present have the appropriate personal protective equipment, as these procedures increase the risk of spreading the virus to non-infected individuals. 

Complications: Long COVID

The United States Department of Health defines Long COVID as “signs, symptoms, and conditions that continue or develop after initial COVID-19 or SARS-CoV-2 infection.” These are typically present four weeks or more after the initial phase of infection and may be multisystemic [23]. Some patients may have a “relapsing-remitting pattern and progression or worsening over time, with the possibility of severe and life-threatening events even months or years after infection.”

Those who are at higher risk of developing Long COVID include patients with more severe COVID-19 illness, or with underlying health conditions, without the COVID-19 vaccine, or who experienced multisystem inflammatory syndrome (MIS) during or after COVID-19 illness.

Special Patient Groups

This chapter has already touched on the severity of this disease from the standpoint of age and comorbidities; however, this section seeks to expand on that topic by presenting special considerations for other demographics who may be infected with COVID-19.

Pediatric Populations

Pediatric populations generally have far fewer severe outcomes and are more likely to present asymptomatically when infected with COVID-19 [24]. However, it is important to be aware of a rare but potentially life-threatening complication known as multi-system inflammatory syndrome in children (MIS-C). If a patient develops MIS-C, signs and symptoms begin to present within 2-6 weeks of infection and include ongoing fever accompanied by any of the following: stomach pain, bloodshot eyes, diarrhea, lightheadedness, rash, and vomiting. If the child’s condition continues to worsen and they develop difficulties breathing, medical attention should be sought immediately. Physicians can provide supportive care as well as treatment of the underlying infection or co-occurring infections. With timely and appropriate care, MIS-C rarely leads to death or long-term complications [24].

Geriatric Populations

Geriatric populations are those defined as over the age of 65 years and represent an extremely high-risk category even in the absence of comorbidities. Because of this, geriatric patients who contract COVID-19 infections should be watched closely and receive antiviral treatments – such as Paxlovid – as soon as possible to stem the progression of disease. Other considerations for geriatric populations that may not be immediately apparent are concerns with access. Elderly patients often require assistance walking, driving, or navigating to clinic appointments due to a higher prevalence of comorbid conditions (dementia, osteoporosis, wasting, etc.) and making care more accessible to these populations is the first step in ensuring they can get the treatment they need. This position is notably called out by the World Health Organization in their considerations for caring for elderly with COVID-19.

Pregnant Populations

Individuals who are pregnant are at increased risk of complications from COVID-19 for themselves and their child. One of the best ways to help these patients is to provide timely vaccination to either prevent or reduce the severity of initial infection. Despite controversy, a myriad of clinical trials has proven that mRNA vaccines for COVID-19 are safe and without adverse outcomes for either the mother or baby during pregnancy [25]. If a mother and her unborn child do contract COVID-19 and require hospitalization, these patients should be taken care of in facilities that have the capability to monitor the status of the fetus and uterine contractions to ensure the health and safety of mom and baby. 

When To Admit This Patient

Admission criteria for COVID-19 is very specific to the individual patient and institution practices and guidelines. In general, however, admission should be considered for patients presenting with severe COVID-19 infection. This includes but is not limited to patients that are in respiratory distress, patients requiring oxygen therapy to maintain oxygen saturations >90%, or patients unable to tolerate food, fluid, or meds by mouth. Abnormal lab work can also warrant hospital admission including patients with significant electrolyte abnormalities, kidney injury, ischemic changes on EKG or elevation in cardiac markers. Persistent vital sign abnormalities could also warrant admission, including COVID-19 patients that are persistently tachycardic even after IV fluid resuscitation and fever reduction. Age can also contribute to the threshold for admission. For example, a patient over 65 with COVID-19 infection and pneumonia on X-ray could warrant admission.

Patients that are presenting with mild COVID-19 disease, have access to follow-up, have normal vital signs and with no significant abnormalities on lab and imaging studies may be safely discharged with primary care follow-up.

It is important to provide patients with COVID-19 strict return precautions should their symptoms worsen. Particularly, these patients should be told to return if they experience any worsening shortness of breath, difficulty in breathing or abnormal home oxygen saturation readings. Patients should be warned that they may lose their sense of taste and/or smell and this is a common symptom of the disease. If patients are unable to tolerate food and/or fluid, they should be instructed to return back to the emergency department. Any new altered mental status, confusion, chest pain, focal weakness or seizures should also prompt patients to return immediately to the emergency department.

Revisiting Your Patient

Let’s return to Mr. Fox, who presented to the emergency department in respiratory distress from his nursing home. The providers have high clinical suspicion for COVID-19 infection given his exposure to COVID-19 at the nursing home, and are concerned considering his risk factors for severe disease. He is placed on contact and droplet precautions and COVID-19 tests are collected. Given his severe presentation there is concern for sepsis, a lactic acid level and blood cultures to be obtained. He is started on high-flow nasal cannula oxygenation to improve his oxygen saturation, and IV fluid resuscitation is initiated to improve his hemodynamic status. He is given acetaminophen for his fever. A chest x-ray is obtained, which demonstrates bilateral patchy infiltrates. Per discussion with Mr. Fox’s nursing home, he has not been hospitalized recently or been on any antibiotic treatment. He receives cefepime and vancomycin to treat possible hospital-acquired pneumonia given he is a nursing home resident – please refer to your institution’s antibiotics guidelines – while awaiting his COVID-19 test results. Given the high concern for COVID-19 infection and Mr. Fox’s severe hypoxia, he is also started on Dexamethasone, as this has been shown to improve mortality in patients with severe COVID-19 infections.

Despite these interventions, Mr. Fox continues to have increased work of breathing and is becoming fatigued. An arterial blood gas is obtained, which demonstrates worsening respiratory acidosis. Mr. Fox is confirmed to be full code by the nursing home, and thus the decision is made to proceed with intubation. He is placed on a ventilator and started on lung-protective ventilation settings. His COVID-19 test comes back positive. He remains persistently tachycardic despite appropriate IV fluid resuscitation and correction of his fever. His providers are concerned that he may have developed a pulmonary embolism in the setting of possible hypercoagulability associated with his COVID-19 infection. A CT scan of his chest with contrast is obtained, which demonstrates multiple right-sided pulmonary emboli without evidence of right heart strain. Mr. Fox is started on a heparin drip. He is admitted to the medical intensive care unit with the diagnoses of acute hypoxic respiratory failure secondary to COVID-19 infection and right-sided pulmonary emboli.

Authors

Picture of Pei Shan Hoe

Pei Shan Hoe

Medical Officer, Ministry of Health Holdings, Singapore.

Pei Shan Hoe is a former journalist-turned junior doctor currently working at Singapore General Hospital. She studied comparative literature as an undergrad at New York University, obtained a Masters in investigative journalism from Columbia University, and then an MD from Duke-NUS Medical School. She is an ACEP/EMRA Global EM Student Leadership Program mentee (‘22-23) and co-author of published articles related to Covid-19 and ED design. Her interests lie in global health, acute care, medical education, healthcare systems and services research. She is certified for overseas disaster deployment under Singapore Red Cross and has also participated in peacetime medical missions.

Picture of Andrew Mariotti

Andrew Mariotti

Resident Physician, University of Colorado Department of Anesthesiology

Andrew Mariotti, M.H.A, has been caring for patients since 2015 as both an emergency medical technician and administrator. In 2020, Mr. Mariotti worked as an administrative fellow under the executive board of the University of Colorado Hospital where he directly aided the coordination of the hospital’s emergency response to the COVID-19 pandemic in Denver and Aurora, Colorado. He is currently a medical student at the University of Colorado, where he serves as Vice President of the student body and his research in quality improvement has led to abstract publications with the Society of Hospital Medicine and American Society of Anesthesiologists.

Picture of Prem Menon

Prem Menon

Global Emergency Medicine Fellow, Brigham and Women’s Hospital

Prem Menon is a chief resident at Emory University’s Emergency Medicine residency program in Atlanta, Georgia. Prem began his training during the height of the COVID-19 pandemic and has managed many critically ill COVID-19 patients. His interests within Emergency Medicine include Refugee, Immigrant and Asylee health and Global Emergency Medicine. During his residency training he worked to improve emergency care globally, specifically in the country of Liberia. He is originally from Austin, Texas and obtained his medical degree at the University of Texas Health San Antonio – Long School of Medicine. He will be starting fellowship in Global Emergency Medicine at Brigham and Women’s Hospital/Harvard in the Fall of 2023.

Picture of Alexandra Digenakis

Alexandra Digenakis

Clinical Assistant Professor, East Carolina University Emergency Medicine

Alexandra Digenakis, D.O., completed her undergraduate degree at Penn State University. She completed her medical school training at the Philadelphia College of Osteopathic Medicine in 2019. She completed her emergency medicine residency at the University of North Carolina in 2022. She is currently a clinical assistant professor of emergency medicine at East Carolina University. She has a strong interest in providing education, opportunities and exposure to global health to medical students and resident physicians. She has participated in the EMRA/ACEP Global Emergency Medicine Student Leadership Program as a medical student mentee, resident co-director, faculty advisor and faculty co-director.

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References

  1. WHO coronavirus (COVID-19) dashboard. World Health Organization. https://covid19.who.int/. Accessed April 13, 2023.
  2. COVID-19: Epidemiology, virology, and prevention. UpToDate. https://www.uptodate.com/contents/covid-19-epidemiology-virology-and-prevention. Accessed April 13, 2023.
  3. Dhar Chowdhury S, Oommen AM. Epidemiology of COVID-19. Journal of Digestive Endoscopy. 2020;11(1):3-7. doi:10.1055/s-0040-1712187
  4. Coronavirus disease (covid-19) faqs. United Nations. https://www.un.org/en/coronavirus/covid-19-faqs. Accessed April 13, 2023.
  5. Parasher A. COVID-19: Current understanding of its Pathophysiology, Clinical presentation and Treatment. Postgraduate Medical Journal. 2021;97(1147):312-320. doi: 1136/postgradmedj-2020-138577
  6. COVID-19: Clinical features. UpToDate. https://www.uptodate.com/contents/covid-19-clinical-features. Accessed April 14, 2023.
  7. COVID-19: Cutaneous features and issues related to dermatologic care. UpToDate. https://www.uptodate.com/contents/covid-19-cutaneous-manifestations-and-issues-related-to-dermatologic-care. Accessed April 14, 2023.
  8. Coronavirus disease 2019 (covid-19). Centers for Disease Control and Prevention. https://www.cdc.gov/coronavirus/2019-ncov/index.html. Accessed April 14, 2023.
  9. Clinical care information for covid-19. Centers for Disease Control and Prevention. https://www.cdc.gov/coronavirus/2019-ncov/hcp/clinical-care.html. Accessed April 14, 2023.
  10. Clinical care quick reference for covid-19. Centers for Disease Control and Prevention. https://www.cdc.gov/coronavirus/2019-ncov/hcp/clinical-care-quick-reference.html. Accessed April 14, 2023.
  11. Coronavirus disease 2019 (covid-19). Coronavirus disease 2019 (COVID-19) – Differentials. BMJ Best Practice US. https://bestpractice.bmj.com/topics/en-us/3000168/differentials. Accessed April 14, 2023.
  12. Jegerlehner, S., Suter-Riniker, F., Jent, P., Bittel, P., & Nagler, M. (2021). Diagnostic accuracy of a SARS-COV-2 rapid antigen test in real-life clinical settings. International Journal of Infectious Diseases, 109, 118–122. https://doi.org/10.1016/j.ijid.2021.07.010
  13. Butler-Laporte, G., Lawandi, A., Schiller, I., Yao, M., Dendukuri, N., McDonald, E. G., & Lee, T. C. (2021). Comparison of saliva and nasopharyngeal swab nucleic acid amplification testing for detection of SARS-COV-2. JAMA Internal Medicine, 181(3), 353. https://doi.org/10.1001/jamainternmed.2020.8876
  14. Brinati, D., Campagner, A., Ferrari, D., Locatelli, M., Banfi, G., & Cabitza, F. (2020). Detection of covid-19 infection from routine blood exams with Machine Learning: A feasibility study. Journal of Medical Systems, 44(8). https://doi.org/10.1007/s10916-020-01597-4
  15. Elmokadem, A. H., Bayoumi, D., Abo-Hedibah, S. A., & El-Morsy, A. (2021). Diagnostic performance of chest CT in differentiating COVID-19 from other causes of ground-glass opacities. Egyptian Journal of Radiology and Nuclear Medicine, 52(1). https://doi.org/10.1186/s43055-020-00398-6
  16. Parekh, M., Donuru, A., Balasubramanya, R., & Kapur, S. (2020). Review of the chest CT differential diagnosis of ground-glass opacities in the covid era. Radiology, 297(3). https://doi.org/10.1148/radiol.2020202504
  17. Zompatori, M., Ciccarese, F., & Fasano, L. (2014). Overview of current lung imaging in acute respiratory distress syndrome. European Respiratory Review, 23(134), 519–530. https://doi.org/10.1183/09059180.00001314
  18. De Vega Sanchez, B., Disdier Vicente, C., & Lopez Pedreira, M. R. (2017). An asymptomatic man with pathological chest radiography. Breathe, 13(4). https://doi.org/10.1183/20734735.008717
  19. Bonanad, C., García-Blas, S., Tarazona-Santabalbina, F., Sanchis, J., Bertomeu-González, V., Fácila, L., Ariza, A., Núñez, J., & Cordero, A. (2020). The effect of age on mortality in patients with COVID-19: A meta-analysis with 611,583 subjects. Journal of the American Medical Directors Association, 21(7), 915–918. https://doi.org/10.1016/j.jamda.2020.05.045
  20. Khedr, E. M., Daef, E., Mohamed-Hussein, A., Mostafa, E. F., Zein, M., Hassany, S. M., Galal, H., Hassan, S. A., Galal, I., Zarzour, A. A., Hassan, H. M., Amin, M. T., Hashem, M. K., Osama, K., & Gamea, A. (2022). Comorbidities and outcomes among patients hospitalized with covid-19 in Upper Egypt. The Egyptian Journal of Neurology, Psychiatry and Neurosurgery, 58(1). https://doi.org/10.1186/s41983-022-00530-5
  21. Kompaniyets L, Pennington AF, Goodman AB, et al. Underlying Medical Conditions and Severe Illness Among 540,667 Adults Hospitalized With COVID-19, March 2020-March 2021. Prev Chronic Dis. Jul 1 2021;18:E66. doi:10.5888/pcd18.210123
  22. Hadaya, J., & Benharash, P. (2020). Prone positioning for acute respiratory distress syndrome (ARDS). JAMA, 324(13), 1361. https://doi.org/10.1001/jama.2020.14901
  23. Long Covid or post-covid conditions. Centers for Disease Control and Prevention. https://www.cdc.gov/coronavirus/2019-ncov/long-term-effects/index.html. Accessed April 14, 2023.
  24. Acevedo L, Pineres-Olave BE, Nino-Serna LF, et al. Mortality and clinical characteristics of multisystem inflammatory syndrome in children (MIS-C) associated with covid-19 in critically ill patients: an observational multicenter study (MISCO study). BMC Pediatr. Nov 18 2021;21(1):516. doi:10.1186/s12887-021-02974-9
  25. Ciapponi, A., Berrueta, M., P.K. Parker, E., Bardach, A., Mazzoni, A., Anderson, S. A., Argento, F. J., Ballivian, J., Bok, K., Comandé, D., Goucher, E., Kampmann, B., Munoz, F. M., Rodriguez Cairoli, F., Santa María, V., Stergachis, A. S., Voss, G., Xiong, X., Zamora, N., … Buekens, P. M. (2023). Safety of covid-19 vaccines during pregnancy: A systematic review and meta-analysis. Vaccine, 41(25), 3688–3700. https://doi.org/10.1016/j.vaccine.2023.03.038

Reviewed By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Chest Trauma (2024)

CHEST TRAUMA
~ iEM Education Project Team ~ Leave a comment

by Ivan Low & Jeremy Wee Choon Peng

Authors
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You have a new patient!

A fifty-year-old male patient is brought into the resuscitation room following a motor vehicle accident. The patient is a motorcyclist who was hit on his left side by a lorry moving at 40mph (64.4 kph). He was flung 3 metres, and his helmet remained intact, while the motorcycle was badly damaged. Vital signs are as follows: T 36.5, BP 168/98, HR 112, RR 32, and SpO2 95% on 10L facemask. A cervical collar has been applied by paramedics on scene. On arrival, the patient appears to be in respiratory distress, using his accessory muscles of respiration.

What do you need to know?

Chest trauma occurs in approximately one-third [1] of trauma patients and causes up to 25% mortality [2] in a multiply injured patient. More than 80% of thoracic injuries were blunt [1] rather than penetrating, and 70% of blunt injuries were a result of road traffic accidents [2,3,4], with drivers and front-seat passengers being placed at highest risk [2].

Thoracic injuries can lead to clinical deterioration and death by impairing a patient’s ‘ABCs.
Airway obstruction can directly result from distortion of tracheobronchial anatomy. Breathing can be affected in two broad ways: 1) Ventilation-perfusion (V/Q) mismatch: Hypoventilation can result from mechanical chest wall or diaphragmatic disruptions, or abnormal collections of air or fluid in the pleural space limiting lung expansion. Hypoperfusion can be caused by vascular disruptions or thrombosis in a damaged lung. 2) Gas exchange abnormalities: Gas exchange can be impaired by direct damage to the alveolocapillary membrane, or dilution of the surfactant layer with blood or interstitial fluid causing alveolar collapse. Circulation can be compromised due to: hemorrhagic shock from vascular or parenchymal injuries, cardiogenic shock from cardiac injury, and obstructive shock from high intrathoracic or intrapericardial pressures (see Table 1). 
 
Table 1: Pathophysiology and patterns of injury in chest trauma

Pathophysiology

Example of injuries (non-exhaustive)

Airway

Tracheobronchial injury

Breathing

(a) V/Q mismatch

 

 

 

(b) Gas exchange abnormalities

 

Sternal or rib fractures +/– flail chest

Pneumothorax +/– hemothorax

Diaphragmatic injury

Pulmonary vascular injury or thrombosis

Pulmonary contusion or laceration

Circulation

(a) Hemorrhagic shock

(b) Cardiogenic shock

(c) Obstructive shock

 

Great vessel (e.g. aortic) disruption

Cardiac contusion or laceration

Tension pneumothorax

Cardiac tamponade

 

Medical History

The mnemonic “AMPLE” highlights several critical aspects of a patient’s history that should be gathered from all trauma patients: Allergies, Medications currently used, Past illnesses and pregnancy, Last meal, and Events related to the injury [5]. Alert patients can often provide details about the mechanism of their injury and the level of force or impact experienced. They may also report symptoms such as pain in the chest, back, or abdomen, dyspnoea, noisy breathing, hemoptysis, hematemesis, syncope or pre-syncope. Eyewitness accounts from passers-by and paramedics may be helpful in supplementing an overall picture of the scene, particularly if the patient is unable to provide a history at this point in time. The ATMIST template, which includes age, time, mechanism, injuries, signs and symptoms, and treatment, is an effective tool for guiding handovers from prehospital teams [6].

Physical Examination

A comprehensive physical examination is crucial to detect major thoracic injuries early to facilitate timely intervention. The patient’s vital signs often help identify patients who are decompensating or at higher risk of deterioration. These include abnormalities such as tachycardia, bradycardia, tachypnea, bradypnea, hypotension, and hypoxemia.

Inspection

On inspection, assess the patient for:

(a) Airway obstruction, respiratory distress, or decompensation:

  • Stridor
  • Use of accessory muscles
  • Asterixis, drowsiness, or obtundation

(b) Chest wall injuries:

  • Steering wheel or seatbelt imprints
  • Chest wall contusions, deformities, or wounds
  • Asymmetric and paradoxical chest wall movements
  • For penetrating injuries, always check for exit wounds, and assume involvement of adjacent body cavities e.g. abdomen

(c) Peripheral signs of shock or major thoracic injury:

  • Cold and clammy peripheries (most types of shock)
  • Jugular venous distension (tension pneumothorax or cardiac tamponade)

Palpation

On palpation, assess the patient for:

(a) Pneumothorax, hemothorax, or lung collapse:

  • Tracheal deviation
  • Subcutaneous emphysema

(b) Rib fractures and associated complications:

  • Bony tenderness
  • Step deformities
  • Flail segments

(c) Pulses:

  • Irregular heart rhythm (arrhythmia from cardiac injury)
  • Pulse delay or differential (aortic dissection)

Percussion

On percussion, assess the patient for:

(a) Hyperresonance: pneumothorax

(b) Dullness: hemothorax, lung collapse

Auscultation

On auscultation, assess the patient for:

(a) Stridor or wheeze: airway obstruction

(b) Reduced breath sounds: pneumothorax or hemothorax

(c) Muffled heart sounds or pericardial rub: pericardial effusion

As patients with thoracic injuries often present with concomitant abdominal and shoulder injuries, complete your examination with a thorough evaluation of the abdomen and shoulder girdles (including the clavicle and scapula).

Alternative diagnoses

The important injuries to assess all patients with chest trauma are summarised in literature as the ‘Deadly Dozen’, as listed in Table 2 [7]. The first six (‘Lethal Six’) are immediately life-threatening and ought to be detected during the primary survey, while the next six (‘Hidden Six’) may not be immediately apparent but are potentially life-threatening and should be picked up during the secondary survey.

Table 2: ‘Deadly Dozen’ in Thoracic Trauma

‘Lethal Six’

‘Hidden Six’

1. Airway obstruction

1. Thoracic aortic disruption

2. Tension pneumothorax

2. Tracheobronchial disruption

3. Cardiac tamponade

3. Myocardial contusion

4. Open pneumothorax

4. Traumatic diaphragmatic tear

5. Massive hemothorax

5. Esophageal disruption

6. Flail chest

6. Pulmonary contusion

Diagnostic testing

Apart from the ‘Lethal Six’ pathologies, early diagnostic testing can aid in the detection of life-threatening pathologies, including but not limited to the ‘Hidden Six’. A combination of point-of-care tests (POCT), chest imaging, and laboratory tests can help physicians make critical decisions in the assessment of a patient with chest trauma.

POCT

  • Arterial or venous blood gas (ABG/VBG):
    • When to do it: Signs and symptoms of respiratory distress or decompensation, or when there is a clinical suspicion of shock.
    • Findings to look for: A low PaO2:FiO2 (P/F) ratio indicates degree of respiratory failure; an elevated PaCO2level suggests hypoventilation and respiratory decompensation; an elevated serum lactate level indicates poor end-organ perfusion and shock.
  • Electrocardiogram (ECG)
    • When to do it: Mechanism suggests major chest trauma, signs and symptoms of chest wall injury, or features of active ongoing cardiac disease [8].
    • Findings to look for: Arrhythmias and ischemic changes may suggest cardiac injury; small or alternating QRS complexes may indicate pericardial effusion.
  • Point-of-care ultrasonography (POCUS):
    • When to do it: Mechanism suggests major polytrauma or chest trauma, hemodynamic instability[9,10]
    • Findings to look for: Reduced cardiac contractility or wall rupture, pericardial effusion, absence of lung sliding or presence of lung point, sternal or rib fractures [11]
    • Pitfalls: Due to poor sensitivity and operator dependence, normal findings do not exclude cardiac, pulmonary, aortic, or musculoskeletal injury [9,10]; serial assessments are recommended to improve sensitivity.

Imaging

Table 3: NEXUS Chest Radiography Rule [12]

This applies to patients 15 years or older who sustained blunt trauma within the last 24 hours. No thoracic imaging is required if none of the following criteria are met:

  • Age >60 years
  • Rapid deceleration mechanism (fall from >20ft, MVC >40mph)
  • Chest pain
  • Intoxication
  • Altered mental status
  • Distracting painful injury
  • Tenderness to chest wall palpation
  • Computer tomography of thorax or aortogram (CT Thorax / Aortogram):
    • When to do it: Mechanism suggests major polytrauma or chest trauma [9,10]; suspicion of thoracic injury based on clinical findings or CXR / POCUS; unable to exclude significant thoracic injury by NEXUS Chest CT Decision Instrument (Table 4) [14].
    • Findings to look for: Cardiac, pulmonary, aortic, or musculoskeletal injuries.
    • Pitfalls: Risk-benefit ratio needs to be assessed and possibly discussed with the patient and/or their next-of-kin in patients at risk of contrast-induced nephropathy or who are pregnant.

Table 4: NEXUS Chest CT Decision Instrument [14]

This applies to patients with stable vital signs, 15 years or older. No chest CT is required if none of the following criteria are met:

  • Chest wall, sternum, thoracic spine, or scapular tenderness
  • Abnormal chest X-ray (e.g. clavicle fracture or widened mediastinum)
  • Distracting injury
  • Rapid deceleration mechanism (fall from >20ft, MVC >40mph)

Laboratory tests

  • Cardiac enzymes:
    • When to do it: Hemodynamic instability, ECG abnormalities
    • Pitfalls: Prognostic yield remains unclear

Risk stratification

The two useful clinical tools in the emergency department are the NEXUS rules above, which both have 99% sensitivity in excluding significant thoracic injuries in the absence of all criteria, and hence may guide the judicious use of chest imaging.

There are several risk stratification tools developed to predict poorer outcomes (e.g. mortality, pneumonia, acute respiratory distress syndrome) in patients with chest trauma, including the Thoracic Trauma Severity Score (TTSS) [15,16], Chest Trauma Score (CTS)[17,18], and Rib Fracture Score (RFS)[19]. However, none are routinely used in the emergency department setting given that they do not affect clinical management in the ED and typically require advanced imaging as part of the risk stratification process.

Management

Patients with chest trauma are managed according to Advanced Trauma Life Support (ATLS) [20] principles in order to detect and address ‘ABCDE’ issues in a timely fashion.

(a) Airway

  • Establish definitive airway (intubation, front-of-neck access) if partial or complete airway obstruction is identified.

(b) Breathing

  • Administer 100% O2 if hypoxemic.
  • Apply one-way seal to open chest wounds.
  • Intubate for mechanical ventilation if there is respiratory failure (oxygenation, ventilation).
  • Finger and tube thoracostomy if there is suspicion of pneumothorax or hemothorax.

(c) Circulation

  • Administer IV crystalloids if there are signs of shock and end-organ hypoperfusion.
  • Transfuse blood products and consider activating the massive transfusion protocol if suspecting hemorrhagic shock.
  • Consider pericardiocentesis if in cardiac tamponade and no surgeon is readily available.
  • If the patient goes into traumatic circulatory arrest, there may be a role for emergency department thoracotomy (EDT), unless (1) there were no signs of life on scene, (2) the injuries are unsurvivable, or (3) prolonged downtime exceeding 15 minutes.

(d) Disability

  • Consider early intubation if the patient is drowsy (which could be a result of shock, hypercarbia, hypoxemia, or concomitant head injury).
  • Check for concomitant thoracic spine injury.

(e) Environment / Exposure

  • Assess for injuries across the chest, back, and adjacent areas such as the shoulder girdles and abdomen.
  • Keep the patient warm.

Urgent surgical consultation is often warranted in all cases of penetrating chest trauma and if there is suspicion of any of the ‘Deadly Dozen’ pathologies.

Medications

  • Analgesia is crucial for relieving pain and preventing atelectasis, but when using opioids, careful dosing is necessary to avoid hypoventilation.
  • Tranexamic acid stabilises blood clots and reduces mortality in patients with significant ongoing bleeding presenting within 3 hours of injury [21].
  • Prophylactic antibiotics and the tetanus vaccine are used to prevent infection, particularly in patients with penetrating chest trauma, significant hollow viscus injuries, or those undergoing invasive procedures. The use of these medications should follow institutional guidelines.

Special patient groups

  • Paediatric patients: Children have more compliant chest walls and hence may sustain significant intrathoracic injuries without obvious chest wall abnormalities. In addition, multiple chest wall injuries or a mechanism of injury that is incompatible with the child’s developmental milestones should raise suspicion for non-accidental injury. A careful evaluation and a high index of suspicion are required in this patient group.
  • Geriatric patients: Older adults, due to reduced pulmonary reserves, are at an increased risk of developing respiratory complications. This patient group should be counselled on the increased risks of atelectasis, pneumonia, and acute respiratory distress syndrome. Adequate analgesia and incentive spirometry may help to reduce the risk of these complications.

When to admit the patient

  • All patients with penetrating chest trauma or blunt trauma with suspicion of significant intrathoracic injury should be admitted for evaluation and monitoring.
  • Patients who remain symptomatic despite a normal initial evaluation can be observed for 8 hours, with serial physical examinations or chest radiographs scheduled.
  • Most other patients can be safely discharged with appropriate advice (to return to the ED if developing pain, dyspnoea, fever, haemoptysis, or hematemesis, which may suggest missed injuries or complications such as chest infection).

Revisiting your patient

The patient is managed according to ATLS [20] principles.

Airway: There is no stridor or obvious facial injury. The cervical spine has been immobilised.

Breathing: He is tachypnoeic and hypoxaemic. The trachea is deviated to the right. There is a left chest wall deformity with bruising, asymmetric chest wall movements, and left-sided paradoxical movements. There is no obvious penetrating injury. Crepitus and step deformities are palpated on the left chest wall. Breath sounds are reduced on the left. Tension pneumothorax and flail chest are suspected. POCUS demonstrates absent lung sliding on the left. An arterial blood gas demonstrates hypoventilation with a PaCO2 of 42 mm Hg despite the patient’s tachypnoea (PaCO2 is expected to be low). Left finger thoracostomy is performed, with a gush of air noted upon entry into the pleural cavity, and a large-bore chest tube is inserted. Intubation with manual in-line stabilisation is performed in view of impending type 2 respiratory failure.

Circulation: The patient is tachycardic and has borderline low blood pressure. His peripheries are cold and clammy. Pulses are regular and there is no pulse delay or differential. An initial FAST scan is negative for free fluid in the abdomen or pericardial sac. Heart sounds are normal. Two large-bore intravenous cannulas are inserted for crystalloid administration.

The rest of the primary survey and adjuncts: The rest of the primary survey is normal. A plain chest radiograph confirms the presence of a left pneumothorax with subcutaneous emphysema and multiple left-sided rib fractures constituting a flail segment (see example videos below). There is no obvious hemothorax, widened mediastinum, or raised hemidiaphragm. Analgesia, prophylactic antibiotics, and the tetanus vaccine are administered.

Disposition: The patient is admitted to the surgical intensive care unit and planned for further advanced imaging and operative interventions by the surgical team.

Authors

Picture of Ivan Low

Ivan Low

Ivan Low is a Resident in Emergency Medicine in Singapore's public healthcare system. He graduated from the National University of Singapore (NUS) in 2018, and is currently working as a military doctor in the Republic of Singapore Navy. He is a Designated Workplace Doctor (Compressed Air Works) and is trained in Diving and Hyperbaric Medicine. He is actively involved in medical education, particularly in the Singapore Medical Association. He has been awarded the NUS Junior Doctor Teaching Award several times in recognition of his work.

Picture of Jeremy Wee Choon Peng

Jeremy Wee Choon Peng

Dr Jeremy Wee serves as a Senior Consultant at the Department of Emergency Medicine at the Singapore General Hospital. Besides being actively involved in the care of patients at the Emergency Department, Dr Wee has a special interest in Trauma care as well as Medical Education. This led to his completion of the Masters of Science in Health Professions Education and the Masters in Trauma Sciences. He is currently the Program Director of the Singhealth Emergency Medicine Residency Program and is actively involved in undergraduate education as an Adjunct Assistant Professor Duke-NUS Graduate Medical School, Clinical Senior Lecturer with Yong Loo Lin School of Medicine.

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References

  1. Lundin A, Akram SK, Berg L, Göransson KE, Enocson A. Thoracic injuries in trauma patients: Epidemiology and its influence on mortality.Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine. 2022;30(1). doi:10.1186/s13049-022-01058-6.
  2. Milisavljevic S, Spasic M, Arsenijevic M. Thoracic trauma. Current Concepts in General Thoracic Surgery. 2012. doi:10.5772/54139.
  3. Chrysou K, Halat G, Hoksch B, Schmid RA, Kocher GJ. Lessons from a large trauma center: Impact of blunt chest trauma in polytrauma patients—still a relevant problem? Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine. 2017;25(1). doi:10.1186/s13049-017-0384-y.
  4. Eghbalzadeh K, Sabashnikov A, Zeriouh M, et al. Blunt chest trauma: A clinical chameleon. Heart. 2017;104(9):719-724. doi:10.1136/heartjnl-2017-312111.
  5. Initial Assessment and Management. In: Advanced Trauma Life Support: Student Course Manual. Chicago, IL: American College of Surgeons; 2018:2-21. 
  6. Loseby J, Hudson A, Lyon R. Clinical handover of the trauma and medical patient: A structured approach. Journal of Paramedic Practice. 2013;5(10):563-567. doi:10.12968/jpar.2013.5.10.563. 
  7. Yamamoto L, Schroeder C, Morley D, Beliveau C. Thoracic trauma. Critical Care Nursing Quarterly. 2005;28(1):22-40. doi:10.1097/00002727-200501000-00004. 
  8. Sybrandy KC. Diagnosing cardiac contusion: Old Wisdom and new insights. Heart. 2003;89(5):485-489. doi:10.1136/heart.89.5.485.
  9. American College of Radiology. Major blunt trauma. ACR Appropriateness Criteria Major Blunt Trauma. https://acsearch.acr.org/docs/3102405/Narrative/. Accessed April 1, 2023. 
  10. American College of Radiology. Blunt chest trauma – suspected cardiac injury. ACR Appropriateness Criteria Blunt Chest Trauma. https://acsearch.acr.org/docs/3082590/Narrative/. Accessed April 1, 2023. 
  11. Chan KK, Joo DA, McRae AD, et al. Chest ultrasonography versus supine chest radiography for diagnosis of pneumothorax in trauma patients in the emergency department. Cochrane Database of Systematic Reviews. 2018. doi:10.1002/14651858.cd013031. 
  12. Rodriguez RM, Hendey GW, Mower W, et al. Derivation of a decision instrument for selective chest radiography in blunt trauma. Journal of Trauma: Injury, Infection & Critical Care. 2011;71(3):549-553. doi:10.1097/ta.0b013e3181f2ac9d. 
  13. Ahmadzadeh K, Abbasi M, Yousefifard M, Safari S. Value of NEXUS chest rules in assessment of traumatic chest injuries; a systematic review and a meta-analysis. The American Journal of Emergency Medicine. 2023;65:53-58. doi:10.1016/j.ajem.2022.12.038. 
  14. Rodriguez RM, Langdorf MI, Nishijima D, et al. Derivation and validation of two decision instruments for selective chest CT in blunt trauma: A multicenter prospective observational study (NEXUS Chest CT). PLOS Medicine. 2015;12(10). doi:10.1371/journal.pmed.1001883. 
  15. Subhani SS, Muzaffar MS, Khan MI. Comparison of outcome between low and high thoracic trauma severity score in blunt trauma chest patients. Journal of Ayub Medical College Abbottabad. 2014;26(4):474-7. PMID: 25672168.
  16. Daurat A, Millet I, Roustan J-P, et al. Thoracic trauma severity score on admission allows to determine the risk of delayed ARDS in trauma patients with pulmonary contusion. Injury. 2016;47(1):147-153. doi:10.1016/j.injury.2015.08.031. 
  17. Chen J, Jeremitsky E, Philp F, Fry W, Smith RS. A chest trauma scoring system to predict outcomes. Surgery. 2014;156(4):988-994. doi:10.1016/j.surg.2014.06.045. 
  18. Fokin A, Wycech J, Crawford M, Puente I. Quantification of rib fractures by different scoring systems. Journal of Surgical Research. 2018;229:1-8. doi:10.1016/j.jss.2018.03.025. 
  19. Seok J, Cho HM, Kim HH, et al. Chest trauma scoring systems for predicting respiratory complications in isolated rib fracture. Journal of Surgical Research. 2019;244:84-90. doi:10.1016/j.jss.2019.06.009. 
  20. Galvagno SM, Jr., Nahmias JT, Young DA. Advanced Trauma Life Support((R)) Update 2019: Management and Applications for Adults and Special Populations. Anesthesiol Clin. 2019;37(1):13-32.
  21. Roberts I, Shakur H, Coats T, et al. The crash-2 trial: A randomised controlled trial and economic evaluation of the effects of tranexamic acid on death, Vascular occlusive events and transfusion requirement in bleeding trauma patients. Health Technol Assess. 2013;17(10). doi:10.3310/hta17100. 
  1.  

Reviewed By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Bradyarrhythmias (2024)

Bradyarrhythmias
~ iEM Education Project Team ~ Leave a comment

by Hassan M. Alshaqaq & Danya Khoujah

Authors
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You have a new patient!

An 80-year-old male patient was brought to the emergency department (ED) by ambulance from a long-term care facility with a chief complaint of altered mental state for 2 hours. On arrival, his vitals were as follows: heart rate= 42 beats/min, blood pressure (BP)=70/50 mmHg, SpO2=95% on room air, respiratory rate=23 breaths/min, temperature=37.6°C, glucocheck= 215 mg/dL. The patient was pale, diaphoretic, alert, and disoriented. Pupils were equal and reactive to light. No neurological deficits or lateralizing signs were identified. The patient has a history of diabetes mellitus, hypertension, and ischemic heart disease. There is no history of drug ingestion or recent symptoms of infection. The patient was given 1 liter of intravenous (IV) normal saline during transport. A 12-lead electrocardiogram (ECG) was obtained (Figure 1). What are your initial assessment steps? What are the ECG features? What is the most likely diagnosis? How will you stabilize this patient?

Figure 1. Courtesy of Dr. Ahmad Alsaif. Digitized using PMcardio app. 
Figure 1. Courtesy of Dr. Ahmad Alsaif. Digitized using PMcardio app. 

Importance and Epidemiology

Bradyarrhythmias are defined as rhythms with a ventricular rate lower than 60 beats/min in adults and lower than the age-appropriate rate in pediatrics. Bradycardia may cause symptoms at a rate of <50 beats/min, which is the functional definition that most guidelines use [1]. Bradyarrhythmias are categorized into bradycardias and atrioventricular (AV) blocks [2].

Bradycardias are characterized by a slow rate of both atria and ventricles and include sinus bradycardia, junctional rhythm, idioventricular rhythm, and hyperkalemia-related sinoventricular rhythm. Bradyarrhythmias due to AV blocks are characterized by ventricular beats slower than the atria and include second- and third-degree AV blocks. Uncommonly, atrial fibrillation or flutter may present with a slow ventricular rate secondary to either significant conduction disturbance or excessive nodal-blocking medications.

Patients with bradyarrhythmias can be either stable or unstable. Patients with hemodynamically unstable bradycardia are at a high risk of cardiovascular collapse [3]. On the other hand, stable asymptomatic bradycardia could be physiological in athletes and well-conditioned individuals [4,5].

Compromising bradycardia has an incidence of 6 per 10,000 patients presenting to the ED for any reason; 20% of those require temporary pacing and 50% require a permanent pacemaker [6]. One percent of admission to the intensive care units (ICUs) from the ED are patients with compromising bradycardia, and 10% of syncope can be attributed to bradycardia [6,7]. Due to the significant potential for instability in bradycardic patients [3], emergency clinicians play a critical role in their initial stabilization, identification of underlying etiology, and treatment.

Pathophysiology

Normal cardiac electrophysiology starts with an impulse generated in the sinoatrial (SA) node, traveling into the atria via interatrial conduction pathways leading to atrial contraction, which appears as a P wave on the ECG. The impulse is then conducted down to the AV node, then from the AV node into the bundle of His and bundle branches, and finally into the Purkinje system leading to a ventricular contraction. The AV conduction appears as the PR interval, whereas the ventricular depolarization appears as the QRS complex (Figure 2). Several electrolytes, such as potassium and calcium, play a crucial role in initiating and regulating the cardiac action potential.

Figure 2. Cardiac conduction system. Used with permission from OpenStax licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0). Access for free at https://openstax.org/books/anatomy-and-physiology/pages/1-introduction
Figure 2. Cardiac conduction system. Used with permission from OpenStax licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0). Access for free at https://openstax.org/books/anatomy-and-physiology/pages/1-introduction

There is an anatomical variance in the blood supply of the SA and AV nodes. The blood supply of the SA node arises from the right coronary artery in 63% and the left circumflex artery in 37% of the population [8]. The AV node is supplied by a branch of the right coronary artery in 90% and the left circumflex artery in 10% [8]. This is most relevant in acute myocardial infarction (MI), as different may arise from ischemia of the conduction system [9]. MI may also lead to ischemia through a vagal-mediated response.

Cardiac output is dependent on the heart rate and stroke volume. Initially, the reduced heart rate increases the diastolic filling leading to an augmentation in the stroke volume. This compensatory mechanism is eventually overwhelmed, leading to decreased cardiac output, hypoperfusion and potentially cardiogenic shock [2,10].

Blood pressure equals the cardiac output multiplied by the systemic vascular resistance. In patients with reduced cardiac output, endogenous sympathetic reflex leads to vasoconstriction and increased systemic vascular resistance. Therefore, patients could have hypoperfusion despite normal-appearing blood pressure.

The underlying cause of bradyarrhythmias could be either conditions affecting the automaticity of cardiac cells (i.e., their ability to generate impulses) or the conduction of impulses within the cardiac conduction system [11,12]. be intrinsic (due to an innate dysfunction of the heart) or extrinsic (Table 1). A practical mnemonic is DIE, which stands for Drugs, Ischemia, and Electrolytes. Half of the patients with compromising bradycardia have a treatable underlying etiology [6].

Table 1. Causes of bradyarrhythmias [7]

Intrinsic:

  • Myocardial ischemia/infarction
  • Cardiomyopathy
  • Congenital heart disease
  • Degenerative fibrosis (with aging)
  • Traumatic (e.g., Denervation post cardiac surgery, cardiac ablation)
  • Infectious/inflammatory (e.g., myocarditis, endocarditis, Lyme disease, syphilis, sarcoidosis, lupus)
  • Sepsis
  • Infiltrative disorders (amyloidosis, hemochromatosis)

Extrinsic:

  • Autonomic-mediated (e.g., athletes, carotid sinus hypersensitivity, situational)
  • Electrolyte disturbances (e.g., hyperkalemia, hypokalemia, hypocalcemia)
  • Hypothermia
  • Endocrinopathy (e.g., hypothyroidism)
  • Raised intracranial pressure
  • Medication overdose (e.g., β-Blockers, calcium channel blockers, digoxin, clonidine, opioids)
  • Toxicologic exposure (e.g., organophosphate)

Types of Bradycardia

Sinus Bradycardia

Sinus bradycardia is characterized by ECG findings of a P wave preceding each QRS, a fixed P-P interval equal to the R-R interval, and a ventricular rate lower than 60 beats/min (Figure. 3). Sinus bradycardia can be found in healthy individuals, particularly athletes with high resting vagal tone.

Figure 3. Sinus bradycardia. ECG shows sinus and regular rhythm, normal PR interval, and a rate of 46 beats/min. Courtesy of Dr. Ahmad Alsaif. ECG digitized using PMcardio app.
Figure 3. Sinus bradycardia. ECG shows sinus and regular rhythm, normal PR interval, and a rate of 46 beats/min. Courtesy of Dr Hassan Alshaqaq and Dr Danya Khoujah.

It could also be secondary to pathological conditions, such as acute MI (Figure 4) [9]. Patients with sinus bradycardia are usually asymptomatic and do not require any specific treatment. However, profound bradycardia causing hypoperfusion requires emergent treatment of the underlying cause. Atropine may be used, as well as cardiac pacing.

Figure 4. Sinus bradycardia with inferior STEMI. ECG shows sinus and regular rhythm, normal PR interval, and a rate of 58 beats/min combined with ST-segment elevation in the inferior leads (Leads III and aVF), hyperacute T waves in leads III and aVF with relative loss of R wave height, early Q-wave formation in leads II, III and aVF, and reciprocal ST depression and T wave inversion in leads I and aVL. Courtesy of Dr. Ahmad Alsaif. ECG digitized using PMcardio app.
Figure 4. Sinus bradycardia with inferior STEMI. ECG shows sinus and regular rhythm, normal PR interval, and a rate of 58 beats/min combined with ST-segment elevation in the inferior leads (Leads III and aVF), hyperacute T waves in leads III and aVF with relative loss of R wave height, early Q-wave formation in leads II, III and aVF, and reciprocal ST depression and T wave inversion in leads I and aVL. Courtesy of Dr. Hassan Alshaqaq and Dr. Danya Khoujah.

Junctional Rhythm

When the SA node fails to discharge or the discharge of the SA node fails to reach the AV node, the AV node generates “junctional escape beats” at a ventricular rate ranging between 40 and 60 beats/min (Figure. 5). These QRS complexes on the ECG are not usually preceded by P waves. However, in some cases, the junctional beats conduct in retrograde into the atria, producing a P wave before or after the QRS. If present before the QRS complex, the PR interval will be abnormally short (<120 msec).

Figure 5. Junctional rhythm. ECG shows an absence of sinus P waves, regular and narrow QRS complexes, and a ventricular rate of 54 beats/min. Also, there is evidence of 2 premature ventricular contractions (PVCs). Courtesy of Dr. Ahmad Alsaif. ECG digitized using PMcardio app.
Figure 5. Junctional rhythm. ECG shows an absence of sinus P waves, regular and narrow QRS complexes, and a ventricular rate of 54 beats/min. Also, there is evidence of 2 premature ventricular contractions (PVCs). Courtesy of Dr. Ahmad Alsaif. ECG digitized using PMcardio app.

Sustained junctional escape rhythm may be caused by inferior MI with right ventricle (RV) extension (Figure 6) [9], posterior MI, myocarditis, hypokalemia, and digitalis toxicity. Infrequent junctional escape beats do not require treatment. Treating the underlying etiology is the mainstay of treatment in symptomatic patients and atropine can be used as a bridge until then. Atropine enhances SA node discharge rate and AV nodal conduction, therefore suppressing slower pacemakers. In case of hemodynamic compromise, cardiac pacing might be necessary [9].

Figure 6. Junctional rhythm with inferior STEMI with posterior extension. ECG shows an absence of sinus P waves, regular and narrow QRS complexes, and ventricular rate of 43 beats/min combined with ST-segment elevation in the inferior leads (Leads II, III, and aVF), ST elevation in lead III > II, early Q-wave formation in lead III, horizontal ST segment depression and upright T waves in leads V2-V3 (posterior MI), and reciprocal ST depression in leads V4-V6, lead I, and aVL. Courtesy of Dr. Anas Halim. Digitized using PMcardio app.
Figure 6. Junctional rhythm with inferior STEMI with posterior extension. ECG shows an absence of sinus P waves, regular and narrow QRS complexes, and ventricular rate of 43 beats/min combined with ST-segment elevation in the inferior leads (Leads II, III, and aVF), ST elevation in lead III > II, early Q-wave formation in lead III, horizontal ST segment depression and upright T waves in leads V2-V3 (posterior MI), and reciprocal ST depression in leads V4-V6, lead I, and aVL. Courtesy of Dr. Anas Halim.

Idioventricular Rhythm

In idioventricular rhythm, beats originate from the ventricles with wide (>120 ms) and regular QRS complexes and a rate of 30-50 beats/min. In idioventricular rhythms, ECG shows no P waves (Figure 7). It is usually non-sustained; present for a short duration only. The significance of idioventricular rhythm is that it is most commonly seen in the setting of an ST-segment elevation MI (STEMI) [13].

Figure 7. Idioventricular rhythm. ECG shows regular and wide QRS complexes (>120 ms), absence of P wave, and ventricular rate of 49 beats/min. Courtesy of Dr. Anas Halim. ECG digitized using PMcardio app.
Figure 7. Idioventricular rhythm. ECG shows regular and wide QRS complexes (>120 ms), absence of P wave, and ventricular rate of 49 beats/min. Courtesy of Dr. Hassan Alshaqaq and Dr. Danya Khoujah.

Atropine may be utilized in symptomatic patients but is usually unsuccessful. If the rhythm persists and is compromising, cardiac pacing may be attempted. Antiarrhythmic agents are best avoided as these could lead to asystole by suppressing the rescue functioning pacemaker [9,14,15].

Table 2 compares ECG features of bradycardic rhythms.

Sinus bradycardia

Junctional rhythm

Idioventricular rhythm

 
  • Sinus P waves present.
  • PR interval 120-200 msec (normal).
  • Rate < 60 beats/min.
  • Absence of normal sinus P waves (may be retrograde).
  • Ventricular rate 40-60 beats/min.
  • Narrow QRS complexes.
  • Absence of P waves.
  • Ventricular rate 30-50 beats/min.
  • Regular and wide QRS complexes.
 
 
 
 

Sinus Node Dysfunction

Sinus node dysfunction is caused by the failure of the sinus node to generate or conduct appropriate cardiac potentials. It can be associated with various supraventricular rhythms, including tachycardia and bradycardia, as well as prolonged pauses (>3 secs). It is most often due to age-dependent fibrosis of the nodal tissue [16,17] or post-cardiac transplantation [18], and might also be seen in patients with myocardial ischemia [19,20], myocarditis [19], and cardiomyopathy [7, 21, 22]. On ECG, it is characterized by episodes of bradycardia and/or sinus arrest with episodes of supraventricular tachycardia (Figure 8).

Figure 8. Sinus node dysfunction. ECG shows tachycardia interspersed with long sinus pauses (absence of any electrical activity). Courtesy of Dr. Anas Halim. ECG digitized using PMcardio app.
Figure 8. Sinus node dysfunction. ECG shows tachycardia interspersed with long sinus pauses (absence of any electrical activity). Courtesy of Dr. Hassan Alshaqaq and Dr. Danya Khoujah.

First-Degree AV Block

First-degree AV block (more accurately described as AV delay) is characterized by delayed AV conduction of all atrial impulses to the ventricles at the level of the atria, AV node, or His-Purkinje system. There is no blocked atrial conduction. Therefore, the ECG reveals a 1:1 atrioventricular conduction (P wave for each QRS complex) and prolonged PR interval (>200 milliseconds) (Figure 9).

Figure 9. First-degree AV block. ECG shows sinus rhythm, 1:1 atrioventricular conduction, with a fixed prolonged PR interval (PR interval = 203 ms). Courtesy of Dr. Anas Halim. ECG digitized using PMcardio app.
Figure 9. First-degree AV block. ECG shows sinus rhythm, 1:1 atrioventricular conduction, with a fixed prolonged PR interval (PR interval = 203 ms). Courtesy of Dr. Hassan Alshaqaq and Dr. Danya Khoujah.

Table 3 illustrates a comparison between ECG features of the AV block types.

 

Type of Block

 

First-degree AV block

Second-degree AV block Mobitz type I

Second-degree AV block Mobitz type II

Third-degree AV block

PQRS

 

Sinus rhythm (P wave for each QRS complex)

 

Nonconducted atrial impulse (P wave not followed by QRS complex)

Cycle repeats after a dropped beat (atrial impulse is completely blocked)

Nonconducted atrial impulse (P wave not followed by QRS complex)

PR interval remains constant after the non-conducted atrial impulse

No association between P waves and QRS complexes (complete dissociation)

Atrial rate higher than ventricular rate

 

PR interval

PR interval >200 msec

Progressively prolonged PR interval

Fixed prolonged PR interval

PR interval remains constant after the non-conducted atrial impulse

Variable PR interval

QRS

Narrow

Regular

Narrow

Narrow

Wide

Regular

First-degree AV block could be found as a normal variant or may be secondary to increased vagal tone, medication toxicity, inferior MI (Figure 10) [9], or myocarditis [15]. Those with a new-onset first-degree AV block in the setting of ACS may be at a higher risk of progression to complete heart block [9,15]. Patients with first-degree AV block usually do not require specific treatment,1 especially if asymptomatic. Symptomatic patients should have their management focused on the underlying cause. Agents with AV nodal blocking effect (Table 4) should be avoided as they would worsen the conduction delay [23].

Figure 10. First-degree AV block with inferolateral STEMI. ECG shows sinus rhythm, 1:1 atrioventricular conduction, with a fixed prolonged PR interval (PR interval = 205 ms) combined with ST-segment elevation in the inferior leads (Leads II, III, and aVF) and lateral leads (V5-V6), ST depression in V1-V2 is suggestive of associated posterior infarction, and reciprocal ST depression in leads I and aVL. Courtesy of Dr. Anas Halim. ECG digitized using PMcardio app.
Figure 10. First-degree AV block with inferolateral STEMI. ECG shows sinus rhythm, 1:1 atrioventricular conduction, with a fixed prolonged PR interval (PR interval = 205 ms) combined with ST-segment elevation in the inferior leads (Leads II, III, and aVF) and lateral leads (V5-V6), ST depression in V1-V2 is suggestive of associated posterior infarction, and reciprocal ST depression in leads I and aVL. Courtesy of Dr. Hassan Alshaqaq and Dr. Danya Khoujah.

Table 4. List of agents with AV nodal blocking/slowing activity [24].

Agents with potent AV nodal blocking activity:

  • Beta-blockers (e.g., Esmolol, Metoprolol)
  • Calcium channel blockers (e.g., Diltiazem, Verapamil)
  • Digoxin
  • Adenosine
  • Sotalol

Other cardiovascular agents with AV nodal blocking/slowing activity:

  • Amiodarone
  • Procainamide
  • Quinidine
  • Lidocaine
  • Flecainide
  • Propafenone
  • Disopyramide
  • Dronedarone

Second-Degree AV Block

Second-degree AV block is characterized by intermittent conduction failure, where one or more atrial impulses are not conducted; some conduction is still present. The atrial rate (P waves) is <100 bpm. The ECG shows P waves that are not followed by a ventricular contraction (QRS complex). It is classified into two types based on the pathophysiology and ECG features.

Second-Degree Mobitz Type I AV Block

Mobitz type I (also known as Wenckebach’s block) is characterized by a progressive prolongation of the AV conduction with a nonconducted atrial impulse. The ECG shows progressive prolongation of the PR interval until an atrial impulse is blocked (not followed by a QRS complex) (Figure 11). These cyclic features lead to a grouped beating in a rhythm strip.  Mobitz Type I could be identified in healthy individuals and might also be seen in patients with acute or chronic heart disease such as inferior MI [9], medication toxicity, myocarditis, or in patients after cardiac surgery. In most cases, specific treatment is not required unless hypoperfusion is present, in which case atropine is the first-line therapy [9].

Figure 11. Second-degree Mobitz type I AV Block. ECG shows progressive prolongation of PR interval with a subsequent nonconducted P wave, then the cycle repeats after the dropped beat. Courtesy of Dr. Harry Patterson, FACEM. Used with permission from Life in the Fast Lane licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License (CC BY-NC-SA 4.0). Source: https://litfl.com/. ECG digitized using PMcardio app.
Figure 11. Second-degree Mobitz type I AV Block. ECG shows progressive prolongation of PR interval with a subsequent nonconducted P wave, then the cycle repeats after the dropped beat. Courtesy of Dr. Harry Patterson, FACEM. Used with permission from Life in the Fast Lane licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License (CC BY-NC-SA 4.0). Source: https://litfl.com/.
Second-Degree Mobitz Type II AV Block

Mobitz type II block is characterized by a fixed AV conduction delay followed by a nonconducted atrial beat. ECG shows a fixed prolonged PR interval, each P wave is followed by a QRS complex until a nonconducted P wave is noted without a QRS complex (Figure 12). If 2 or more P waves are not conducted, it is called a high-grade AV block (Figure 13). Mobitz type II block represents electrical intranodal conducting system structural damage. In acute MI (most commonly anterior), it could progress into a complete heart block [9].

Figure 12. Second-degree Mobitz II AV block. The rhythm strip shows non-conducted P waves (arrows), with constant PR interval, constant P-P interval, and the RR interval surrounding the dropped beat is multiple the preceding RR interval. Used with permission from Life in the Fast Lane licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License (CC BY-NC-SA 4.0). Source: https://litfl.com/
Figure 12. Second-degree Mobitz II AV block. The rhythm strip shows non-conducted P waves (arrows), with constant PR interval, constant P-P interval, and the RR interval surrounding the dropped beat is multiple the preceding RR interval. Used with permission from Life in the Fast Lane licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License (CC BY-NC-SA 4.0). Source: https://litfl.com/
Figure 13. Second-degree “high-grade” AV block. ECG shows a 4:1 conduction ratio, atrial rate is approximately 140 beats/min, and ventricular rate is approximately 35 beats/min. Used with permission from Life in the Fast Lane licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License (CC BY-NC-SA 4.0). Source: https://litfl.com/
Figure 13. Second-degree “high-grade” AV block. ECG shows a 4:1 conduction ratio, atrial rate is approximately 140 beats/min, and ventricular rate is approximately 35 beats/min. Used with permission from Life in the Fast Lane licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License (CC BY-NC-SA 4.0). Source: https://litfl.com/

These patients should be placed on transcutaneous pacing pads in anticipation of clinical deterioration. Although atropine is usually ineffective, it may be utilized during preparation for pacing as it is not harmful. Patients with second-degree Mobitz type II AV block and features of hypoperfusion require emergent cardiac pacing. Eventually, these patients require transvenous cardiac pacing, especially those with underlying acute MI [9].

Third-Degree AV Block

Third-degree (complete) heart block is characterized by the lack of any AV conduction between atria and ventricles, leading to AV dissociation. Atrial impulses are not conducted at all, and an escape pacemaker arises to pace the ventricles with a rate of 40-60 beats/min or lower for the intranodal level. The ECG features no association between the P waves and QRS complexes, an atrial rate higher than the ventricular rate, and wide QRS complexes (Figure 14).

Figure 14. Third-degree AV block. ECG shows complete dissociation between P waves and QRS complexes, wide QRS complexes (QRS duration=154 ms), atrial rate of ~100 beats/min, Ventricular rate of ~30 beats/min, and the rhythm is maintained by a junctional escape rhythm. Courtesy of Dr. Ahmad Alsaif. Digitized using PMcardio app.
Figure 14. Third-degree AV block. ECG shows complete dissociation between P waves and QRS complexes, wide QRS complexes (QRS duration=154 ms), atrial rate of ~100 beats/min, Ventricular rate of ~30 beats/min, and the rhythm is maintained by a junctional escape rhythm. Courtesy of Dr. Ahmad Alsaif. Digitized using PMcardio app.

Depending on the block’s location, it may be termed “nodal” (such as in inferior MI) or “infranodal” (such as in anterior MI) [9]. Patients with third-degree AV block are usually unstable due to the inadequate cardiac output generated by the ventricular escape pacemaker. Atropine might work in cases of nodal blockade; however, it is unlikely to be effective in infranodal blockade. If the response to atropine is inadequate, transcutaneous cardiac pacing should be started. In those patients, consider beta-adrenergic medications (epinephrine or dopamine). Eventually, transvenous pacing is necessary in the majority of cases.

Atrial Fibrillation With a Slow Ventricular Response

Patients with atrial fibrillation may present with a slow ventricular response in the setting of an overdose of nodal-blocking medications (e.g., beta-blockers, calcium channel antagonists, digoxin) or significant conduction disease [25]. A very low ventricular rate may lead to hemodynamic compromise [26]. The hallmark ECG feature in these patients is an irregularly irregular ventricular rhythm without discernible P waves, either chaotic or flat isoelectric baseline (Figure 15). Patients with an irreversible cause of slow ventricular response (such as those with intrinsic conduction system disease) may require a permanent pacemaker [27].

Figure 15. Atrial fibrillation with a slow ventricular response. ECG shows irregular rhythm with no evidence of organized atrial activity, fine fibrillatory waves, with a ventricular rate of 60 beats/min. Courtesy of Dr. Ahmad Alsaif. ECG digitized using PMcardio app.
Figure 15. Atrial fibrillation with a slow ventricular response. ECG shows irregular rhythm with no evidence of organized atrial activity, fine fibrillatory waves, with a ventricular rate of 60 beats/min. Courtesy of Dr. Hassan Alshaqaq and Dr. Danya Khoujah.

Hyperkalemia-induced Bradycardia

Patients with hyperkalemia demonstrate several features on the ECG, including peaked T waves, PR prolongation, QRS widening, and sine-wave morphology [28]. Junctional rhythm is the most common bradycardic rhythm in patients with severe hyperkalemia [29], and patients may show other types of bradydysrhythmias [29]. Obtaining a serum potassium level is critical in any bradydysrhythmia, even without other ECG changes suggestive of hyperkalemia [29].

BRASH Syndrome

BRASH syndrome (Bradycardia, Renal failure, AV blockade, Shock, and Hyperkalemia) is caused by a synergistic effect of hyperkalemia and AV-blocking medications that produce dramatic bradycardia [30]. The marked bradycardia leads to poor renal perfusion, exacerbating hyperkalemia and leading to a vicious cycle, with resulting hemodynamic instability and multiorgan failure [30]. Precipitating factors identified include nephrotoxins, potassium-sparing diuretics, angiotensin-converting enzyme inhibitors, angiotensin-receptor blockers, and digitalis [30].

Medical History

After stabilizing the patient, a comprehensive medical history often helps identify the underlying etiology. In patients unable to provide history (e.g., altered mentation), collateral history from family, emergency medical service (EMS) personnel, or nursing facility staff can be helpful.

Determining the stability of patients starts with their medical history. Symptoms of end-organ hypoperfusion, such as ischemic chest pain, dyspnea, altered mental state, and syncope,  may indicate hemodynamic instability [3,6]. Lack of symptoms, or only mild symptoms such as palpitations, lightheadedness, nausea, generalized fatigability, or mild anxiety [31], may indicate hemodynamic stability. It is essential to determine whether the presenting symptoms in patients with bradycardia are secondary to the bradycardia itself or whether the presence of bradycardia is coincidental.

Analyzing the characteristics of presenting symptoms is vital, including onset, progression (gradual vs. abrupt), duration, precipitating factors, preceding events, and any associated symptoms. Specific precipitating events include emotional distress, positional changes, urination, defecation, cough, prolonged standing, shaving, and head-turning [7]. Additionally, ask about symptoms of ACS, infectious diseases, and hypothyroidism.

A past medical history of rhythm disturbance, ischemic heart disease, structural heart disease, pacemaker placement, or coronary artery bypass graft (CABG) is relevant. Patients post transcatheter aortic valve replacement are at high risk for conduction system abnormalities [7]. A history of renal failure increases the risk of hyperkalemia.

Reviewing the medication list, as well as herbal substances and recreational drugs, including timing, doses, recent changes in patterns, compliance, and the possibility of overdose, is essential.

Travel history to areas endemic for infectious diseases, such as Chagas or Lyme, is relevant. Sexual history, specifically for history of or risk factor for syphilis, is relevant. Occupational history and chemical exposures (e.g., organophosphate) may offer clues for a toxicologic etiology.

Physical Examination

Physical examination of patients with rhythm disturbance primarily focuses on clues of end-organ hypoperfusion and underlying etiology. Assess the level of consciousness, and confirm adequate perfusion by examining the capillary refill, peripheral pulses, and temperature of extremities; cool extremities and delayed capillary refill (>3 sec) indicate hypoperfusion.

The cardiovascular examination includes palpating the radial pulse to determine the rate and rhythm, auscultating the heart sounds for the presence of murmurs, as well as looking for signs of heart failure (jugular venous distention, rales, edema of the extremities). Chest wall inspection for a midline sternotomy scar adds important information regarding the medical history. Palpating the skin overlying an implanted pacemaker may uncover lead abnormalities [32].

Look for signs of underlying pathology, including toxidromes (e.g., cholinergic, opioid-like), an arteriovenous fistula or dialysis catheter (indicates renal failure), head trauma, and signs of hypothyroidism. Core temperature measurement is vital in patients suspected to have hypothermia. In patients with head trauma, look for Cushing’s triad (hypertension, bradycardia, and irregular respirations). Table 5 illustrates a constellation of signs and symptoms indicating a possible underlying cause.

Table 5. Signs and symptoms suggestive of the underlying cause of bradycardia.

Possible underlying etiology

History

Physical examination

Myocardial infarction

  • Chest pain
  • Dyspnea
  • Anginal equivalent symptoms
  • Hypotension
  • Rales
  • New murmur

Myopericarditis

  • Fever
  • Dyspnea
  • Pleuritic chest pain
  • Recent respiratory or gastrointestinal infection
  • Malaise
  • Myalgias
  • Pericardial friction rub

Hyperkalemia

  • History of renal failure / dialysis
  • Arteriovenous fistula or dialysis catheter

Pacemaker malfunction

  • History of implanted cardiac device
  • History of cardiac conduction abnormality
  • Pacemaker identification card
  • Obvious device or lead abnormalities by palpation of the overlying skin

Increased ICP

  • History of head trauma
  • Headache
  • Vomiting
  • Decreased level of consciousness
  • Signs of basilar fracture
  • Depressed skull fracture
  • Focal neurologic deficit
  • Decreased level of consciousness

Beta blocker toxicity

  • Confusion
  • History of seizure
  • History of drug ingestion
  • History of underlying cardiac disease
  • Presence of cardioactive agents at home
  • Empty medication bottles
  • Depressed mental state
  • Hypoglycemia
  • Bronchospasm
  • Hypotension
  • Shock

Calcium channel blocker toxicity

  • History of drug ingestion
  • History of underlying cardiac disease
  • Presence of cardioactive agents at home
  • Empty medication bottles
  • Hyperglycemia
  • Hypotension
  • Shock

Digoxin toxicity

  • GI symptoms (abdominal pain, nausea, vomiting, anorexia)
  • Fatigue
  • Visual disturbance
  • Lethargy
  • Confusion
  • History of drug ingestion
  • History of underlying cardiac disease
  • Presence of cardioactive agents at home
  • Empty medication bottles
  • Altered mental status
  • Seizures
  • Hypotension
  • Shock

Local anesthetics toxicity

  • Perioral numbness
  • Visual disturbance
  • Confusion
  • Dizziness
  • Seizure
  • History of regional or topical anesthesia procedure
  • Altered mental status (ranging from agitation to unresponsiveness)
  • Weakness
  • Slurred speech

Clonidine overdose

  • History of drug ingestion
  • Miosis
  • Respiratory depression

Hypothyroidism

  • History of thyroid disease
  • Cold intolerance
  • Weight gain
  • Fatigability
  • Hypothermia
  • Constipation
  • Skin and hair changes
  • Thyroidectomy scar
  • Goiter
  • Pretibial myxedema
  • Coarse skin
  • Muscle hypertrophy
  • Hypothermia
  • Delayed relaxation phase of reflexes

Acing Diagnostic Testing

A 12-lead ECG is diagnostic for bradyarrhythmia. A single lead, most commonly lead II, is often adequate to make the diagnosis. ECG reading requires noting the rate, regularity, P waves, P-R interval, the relation between P waves and QRS complexes, and QRS width.

Furthermore, ECG may identify the underlying cause, such as acute ischemic changes (e.g., hyperacute T waves, ST-segment elevation/depression, T waves inversions, Q-waves), hyperkalemic changes (e.g., peaked T waves, P wave flattening, PR prolongation, wide QRS), cerebral T-waves (i.e., deep, symmetric, inverted T waves) in elevated intracranial pressure (ICP), downsloping ST depression in digoxin toxicity, and Osborn wave (i.e., positive deflection at the J point) in severe hypothermia (<32˚C). In patients with a malfunctioning implanted pacemaker, the ECG may show pacing spikes not followed by a QRS complex (electrical non-capture).

Given the intermittent nature of some bradyarrhythmia, a normal ECG does not exclude the diagnosis, especially in asymptomatic patients. Moreover, bradyarrhythmia may evolve; therefore, serial ECGs are advisable [2]. 

Point-of-care ultrasound (POCUS) helps in the assessment of volume status (inferior vena cava [IVC] assessment) and pulmonary edema (B-lines: vertical comet tail artifact).

Laboratory work-up to uncover the underlying etiology should be tailored to the clinical assessment. It may include the following:

  • Cardiac biomarkers (e.g., troponin) for identifying acute MI.
  • Electrolytes profile for identifying electrolyte abnormalities (particularly potassium and calcium).
  • Creatinine and blood urea nitrogen (BUN) can help diagnose acute and chronic renal failure.
  • Brain natriuretic peptide (BNP) elevation may indicate fluid overload and heart failure in the appropriate context.
  • Infectious work-up: 3 sets of peripheral cultures for infective endocarditis, serologic testing for syphilis, Lyme serology for Lyme disease, and thick and thin blood smear for Chagas disease.
  • Thyroid function test (TSH and free T4) for suspected hypothyroidism or myxedema coma.
  • Drug levels such as digoxin.

As for imaging, a chest X-ray may show evidence of pulmonary edema in patients with heart failure. In patients with pacemakers, it can identify lead fracture and migration.

Transthoracic echocardiography is essential in evaluating patients with newly identified Mobitz type II or third-degree AV block for cardiac wall motion abnormalities (indicative of an MI), valvular abnormalities, and structural heart disease. However, in patients with asymptomatic bradycardia or first-degree AV block, routine echocardiography is usually not indicated [7].

In patients with signs of a head injury and suspected increased ICP, obtain a head computed tomography (CT) scan.

Risk Stratification

Stability of Patient

Determining the hemodynamic stability of patients with bradyarrhythmia critical to management. Unstable patients require immediate treatment. Instability indicators include hypotension (defined as systolic BP [SBP] of <90 mm Hg), signs of shock (cold and moist skin, pale skin, delayed capillary refill time), ischemic chest pain, altered mental state, and dyspnea secondary to pulmonary edema (Table 6). Patients’ condition may change during treatment or ED stay, necessitating frequent reassessment to recognize impending clinical deterioration.

Table 6. Indicators of instability in patients with bradydysrhythmias

  1. Hypotension (SBP <90 mm Hg)
  2. Signs of shock
  3. Altered mental status
  4. Ischemic chest pain
  5. Dyspnea secondary to pulmonary edema

Symptomatic versus Asymptomatic

The presence of symptoms guides management. Generally, asymptomatic patients do not require treatment and may need monitoring only. In symptomatic patients, it is important to determine whether symptoms are caused by bradycardia or if the bradycardia is incidental to the actual cause of the presenting complaint.

Management

Pre-hospital care considerations

Stabilization might be started by EMS personnel, such as administration of atropine, epinephrine/dopamine infusion, and transcutaneous cardiac pacing [11,33-37], depending on their capabilities and local protocols. Transportation to a PCI-capable center is optimal for patients suspected to have an underlying ischemic pathology.

Initial Stabilization

Initial stabilization must start with a rapid assessment of the circulation, airway, and breathing “the CABs”), as well as the vital signs and signs of instability (Table 6). Patients with symptomatic bradyarrhythmia require a monitored bed with flat positioning [7]. Perform fingerstick glucose, establish two large-bore IVs, attach the patient to a continuous cardiac rhythm monitor, obtain a 12-lead ECG, and prepare for drug and electrical therapy simultaneously. If IV access cannot be obtained, attempt intraosseous (IO) access or a central line. Patients with significant symptomatic bradyarrhythmia, those with advanced heart block, and those predicted to deteriorate should be placed on pacer pads, irrespective of stability.

Although electrical cardiac pacing is immediately indicated in unstable patients, medical management may be more immediately available, making it reasonable to administer both while simultaneously identifying and treating the underlying cause [1,11]. However, atropine administration should never delay the initiation of transcutaneous pacing in unstable patients.1

A resuscitation cart, transvenous pacer kit, and airway equipment should be available at the bedside in anticipation of deterioration of critically ill patients with bradyarrhythmia. Oxygen is indicated to target SpO2 ≥94%. In select patients with hypotension (SBP < 90 mmHg), crystalloid fluids may improve blood pressure; caution must be taken in patients with decompensated heart failure. Hypotension refractory to fluid resuscitation may require inotropic and/or vasopressor support (e.g., epinephrine).

For unstable Mobitz Type II or third-degree AV block, initiate transcutaneous pacing, as well as atropine, if immediately available.  If ineffective, administer epinephrine 2-10 µg/min IV infusion. Although atropine is considered the first line of medical therapy, epinephrine may be preferred in critically unstable patients [38,39], and may be administered short-term through a peripheral IV access [40].

In patients with a wide QRS complex, atropine is unlikely to be effective due to a block at the distal conduction system; therefore, proceed immediately to epinephrine and transcutaneous pacing [1,41].

Patients with symptomatic bradycardia, or second- or third-degree AV block should be placed on continuous ECG monitoring (Class I recommendation) [42].

Figure 16 illustrates emergency approach and management of acute bradyarrhythmia in the ED.

Figure 16. Emergency management approach of patients with bradydysrhythmia. *Atropine should not be given to patients after heart transplantation. Abbreviations: BP, blood pressure; ECG, electrocardiogram; HR, heart rate; ICP, intracranial pressure; IV, intravenous; kg, kilogram; mA, milliampere; mg, milligram; mcg, microgram; MI, myocardial infarction; PCI, percutaneous coronary intervention; RR, respiratory rate; SpO2, oxygen saturation.
Figure 16. Emergency management approach of patients with bradydyarrhythmia. *Atropine should not be given to patients after heart transplantation. Abbreviations: BP, blood pressure; ECG, electrocardiogram; HR, heart rate; ICP, intracranial pressure; IV, intravenous; kg, kilogram; mA, milliampere; mg, milligram; mcg, microgram; MI, myocardial infarction; PCI, percutaneous coronary intervention; RR, respiratory rate; SpO2, oxygen saturation. Courtesy of Dr. Hassan Alshaqaq and Dr. Danya Khoujah.

Treatment Considerations

The anatomical location causing the bradycardia may predict the management and outcomes of bradyarrhythmia. Narrow QRS complex bradycardia indicates dysfunction at the level of the SA or AV node, usually requires minimal intervention, and is rarely life-threatening. On the other hand, wide QRS complex bradycardia indicates dysfunction at the level of distal His-Purkinje, usually requires aggressive management, is unlikely to respond to atropine, may require electrical pacing, and is associated with an elevated mortality rate [3].

Medications

Atropine

Atropine is the first-line treatment to increase the heart rate in patients with symptomatic bradycardia [1,2]. Atropine is an antimuscarinic medication with direct vagolytic activity, increasing the SA node’s automaticity and potentiating the AV node’s conduction. Atropine is most effective in sinus bradycardia and junctional rhythm. It is usually not useful in infranodal blocks presenting with wide QRS bradyarrhythmia. Atropine should be used cautiously in the setting of ACS due to the potential risk of exacerbating ischemia and infarct size from the resulting tachycardia [43-48]. Additionally, atropine should not be used in patients who have undergone heart transplants due to the lack of vagal innervation, as atropine may cause paradoxical AV block and asystole [1,7,49,50]. The dose of atropine is 0.5-1 mg IV every 3-5 min until resolution or maximum dose is reached (3 mg) [1,7].

Epinephrine

Epinephrine is an alternative medical therapy for bradyarrhythmia, and is the preferred adjunct medical management to electrical therapy in unstable patients, particularly those with Mobitz Type II and third-degree AV block [7]. Epinephrine acts on β1- and β2-receptors, working on the entire myocardium to increase the heart rate (inotropic and chronotropic effects), as well as enhancing the AV nodal conduction [51-52]. The dose of epinephrine is 2-10 mcg/min IV infusion, titrated to desired heart rate [7].

In peri-arrest bradycardia, some experts recommend a temporizing bolus dose of 20-50 mcg of epinephrine as an IV push, followed by infusion and electrical pacing [38,39,53,54], despite the lack of supporting data [53,54].

Dopamine

Dopamine may be used in bradyarrhythmia refractory to atropine (Class IIb) [7]. It acts on dopaminergic α1-, β1-, and β2-receptors. Higher doses (>10 mcg/kg/min) have a vasoconstrictive effect, while lower doses (1-2 mcg/kg/min) have a selective inotropic effect on the heart rate [1]. The dose of dopamine is 2 to 20 mcg/kg/min IV infusion titrated by 5 mcg/kg/min every 2 minutes to the desired heart rate [7,33], monitoring peripheral perfusion to avoid profound vasoconstriction [7].

Dobutamine

Dobutamine is a β-agonist agent with a weak α-adrenergic activity that may be used in symptomatic bradycardia; its predominant effect is inotropic via stimulation of β1-receptors [55]. Dobutamine can lead to vasodilation (via β2-receptors) and hypotension, thus, it should not be used in hypotensive patients. It can be used in cases of bradycardia resistant to standard therapy with normal or elevated blood pressure [7,38]. Dobutamine is administered as a 2-20 µg/kg/min IV infusion, titrated to desired heart rate.

Isoproterenol

Isoproterenol infusion is indicated in post-heart transplant patients with unstable bradycardia [7]. It can also be used in refractory bradyarrhythmia and AV blocks not responding to epinephrine [38]. It is a non-selective β-agonist stimulating β1– and β2-receptors, speeding up the SA and AV nodes and enhancing cardiac contractility (chronotropic and inotropic) [56]. It does not have any vasopressor effects.  Isoproterenol is given as a 2-10 mcg/min IV infusion, titrated to effect, or can be administered as an IV bolus of 1-2 mcg [1]. Isoproterenol is contraindicated in patients with angina/active ischemia due to concerns about increasing myocardial oxygen demand (β1 effect) and decreasing coronary perfusion (β2 effect), as well as in digoxin toxicity [7,57-60].

Aminophylline and Theophylline

Aminophylline and theophylline are methylxanthines, which exert positive chronotropic effects on the myocardium, likely by inhibiting the suppression effect of the adenosine on the SA node [7]. Both are reasonable to use if clinically indicated in symptomatic post-cardiac transplant patients [7,61-63] and sinus node dysfunction secondary to spinal cord injury, based on a limited case series [7,64-67].

In addition, aminophylline (250 mg IV bolus) has been used in treating second- and third-degree AV block associated with acute inferior MI, despite the limited direct evidence [7,68-70]. Aminophylline is administered with a dose of 6 mg/kg over 20-30 minutes, followed by an infusion of 0.3-0.5 mg/kg/hour [7]. Theophylline is administered as a bolus dose of 300 mg IV, followed by an oral dose of 5–10 mg/kg/day titrated to effect [7]. Although recommended by the guidelines, evidence for the use of methylxanthines is limited [7].

Table 7. Present bradyarrhythmia medications’ mechanism of action, dosing, pharmacokinetics, contraindications, and adverse events. 

Table created by authors

Electrical Cardiac Pacing

Electrical cardiac pacing is a procedure that aims to stimulate effective cardiac depolarization. Cardiac pacing is the mainstay management of acutely symptomatic patients with bradyarrhythmia, particularly unstable bradyarrhythmia or stable symptomatic bradyarrhythmia refractory to medical therapy, including type II second-degree and third-degree AV blocks [7]. It is of little value in toxin-induced bradyarrhythmia [32]. Cardiac pacing is performed using either a transcutaneous or transvenous approach. Transcutaneous cardiac pacing is a temporary bridging treatment until transvenous pacing or resolution of symptoms [7,32,38,39]. Transvenous pacing is also temporary until the resolution of the underlying cause or placement of a permanent pacemaker [7]. 

In crashing bradycardia, transcutaneous pacing should be started immediately. It is minimally invasive, instituted rapidly, and effectively treats hemodynamically unstable bradydysrhythmia [32]. The pacing pads are placed on the patient’s chest using one of two positions, an anterolateral or anteroposterior (Figure 17); positioning placement is selected based on the patient’s habitus and clinician’s preference [32]. Sedation and analgesia should be initiated as soon as possible utilizing hemodynamically stable agents such as low-dose fentanyl and/or ketamine, keeping in mind that most patients requiring electrical pacing are hemodynamically unstable.

Figure 17. Correct placement of transcutaneous pacing pads. A, anterolateral position; the anterior adhesive pad is placed inferior to the right clavicle, and the lateral adhesive pad is placed on the left fifth intercostal space at the anterior axillary line. B, anteroposterior position; the anterior adhesive pad is placed on the sternum, and the posterior adhesive pad is placed on the left infrascapular area. “Illustration by Malak Alraygi / re-designed Arif Alper Cevik”
Figure 17. Correct placement of transcutaneous pacing pads. A, anterolateral position; the anterior adhesive pad is placed inferior to the right clavicle, and the lateral adhesive pad is placed on the left fifth intercostal space at the anterior axillary line. B, anteroposterior position; the anterior adhesive pad is placed on the sternum, and the posterior adhesive pad is placed on the left infrascapular area. “Illustration by Malak Alraygi / re-designed by Arif Alper Cevik”

Adjust the pacing setting targeting a rate of 80-100 beats/min (start at 80 mA and reduce to the lowest energy) [2,39]. If the pacing is successful, the ECG will show electrical capture, which are pacing spikes followed by wide QRS complexes. Mechanical capture is demonstrated by a palpable pulse corresponding to each paced QRS complex on the cardiac monitor, preferably the femoral pulse to avoid the muscular contractions triggered by the pacer near the carotid artery, which may be confused with a pulse [32]. POCUS may be used to confirm myocardial contractions corresponding to each pacing spike and in confirming femoral pulse. In cases of cardiac arrest during transcutaneous pacing, chest compressions can be safely performed over the pacing pads [32].

Transvenous pacing has a high success rate (>95%) and is preserved for unstable bradyarrhythmias refractory to medications and transcutaneous pacing [6]. Transvenous pacing is contraindicated in patients with severe hypothermia [32]. Transvenous pacing is performed by introducing a transvenous pacing catheter into the right ventricle through a central venous catheterization (either right internal jugular or left subclavian central line). Pacemaker wire may be advanced into the endocardial wall of the right ventricle either blindly, or under the guidance of ECG or ultrasound (four-chamber view) [32]. Observe the cardiac monitor during the advancement of the wire [32]. Capture is confirmed by pacer spikes followed by QRS and ST-segment elevation, which indicates proper positioning [32]. Set the pacer generator on full-demand mode, with an output of 5 mA and a rate of 80 beats/min or at least 10 beats/min faster than the underlying ventricular rhythm [32]. Afterward, confirm electrical and mechanical capture. Continuous electrocardiographic monitoring is recommended for all patients on pacing (both transcutaneous and transvenous) until pacing is discontinued (class I) [42].

Patients with structural or electrophysiological conduction abnormalities often require definitive management with permanent pacemaker implantation. Class I recommendations have been issued for the implantation of permanent pacemakers in patients with acquired Mobitz type II AV block, high-grade AV block, and third-degree AV block not caused by reversible or physiologic causes, irrelevant of the presence of symptoms, due to the high risk of decompensation [7]. The decision to place a permanent pacemaker in patients with symptomatic sinus node dysfunction, persistent and symptomatic sinus bradycardia, and atrial fibrillation with symptomatic bradycardia in the absence of nodal blocking medications is dependent on the presence of symptoms and its correlation with the block itself [7].

Treatment of underlying etiology

Ischemia-related bradycardia

Patients with symptomatic bradyarrhythmia secondary to acute MI require stabilization and immediate reperfusion therapy, either PCI or thrombolysis, depending on feasibility.

Toxicity-related bradycardia

Patients with toxic or metabolic causes of bradycardia respond poorly to atropine and electrical pacing, and those patients require immediate treatment of the underlying cause, by eliminating the offending agent, utilizing supportive care, and administering an agent-specific antidote, if available [7]. Consulting toxicology and/or the local poison center early is paramount. Table 8 presents specific treatment strategies for toxicities related to bradycardia. In cardiac arrest secondary to an overdose, extracorporeal membrane oxygenation (ECMO) might be indicated to maintain perfusion until the underlying agent level is reduced or eliminated [6].

Table 8. Management of toxicologic causes of bradycardia.

Toxicity

Treatment

Beta-blocker toxicity

  • High-dose insulin 1 unit/kg IV bolus, followed by an infusion of 0.5 units/kg/h co-administered with dextrose 7,24,111
  • Glucagon 3-10 mg IV bolus over 3-5 min, followed by an IV infusion of 1-5 mg/h 7,96
  • Intravenous lipid emulsion112

Calcium channel blockers toxicity

  • 10% Calcium chloride 1-2 g IV bolus every 10-20 min or an infusion of 0.2-0.4 mL/kg/h7,113]
  • 10% calcium gluconate 3-6 g IV every 10-20 min or an infusion at 0.6-1.2 mL/kg/h7
  • High-dose insulin 1 unit/kg bolus, followed by an infusion of 0.5 units/kg/h co-administered with dextrose7,24,113
  • Glucagon 3-10 mg IV bolus over 3-5 min, followed by an IV infusion of 1-5 mg/h7,96
  • Intravenous lipid emulsion113

Digoxin toxicity

  • Digoxin-specific antibody fragments (dosage is dependent on amount of ingestion or serum level and whether acute or chronic toxicity)7. It is indicated in unstable bradydysrhythmias or K+ >5.0.

Organophosphate poisoning

  • Decontamination.
  • Atropine 1-3 mg IV every 5 min (0.01-0.04 mg/kg IV in children) with doubling the dose each time, followed by IV maintenance of 0.4-4 mg/hr.
  • Pralidoxime 1-2 g IM (20-40 mg/kg in children) with normal saline infused over 5-10 min followed by IV infusion of 500 mg/h (5-10 mg/kg/h in children).

Local anesthetic systemic toxicity

  • Intravenous lipid emulsion, initial bolus of 100 mL IV over 2–3 min, followed by an infusion of 200–250 mL IV over 15–20 min (for those <70 kg, the bolus dose is 1.5 mL/kg IV over 2–3 min, followed by 0.25 mL/kg/min IV infusion)114,115

Opioids toxicity

  • Naloxone 0.4-2 mg IV/IM/SC bolus repeated every 3 min (pediatrics: 0.1 mg/kg IV/IO/ET75).

Abbreviations: ET, endotracheal; ; g, gram; h, hour; IM, intramuscular; IO, intraosseous;  IV, intravenous; kg, kilogram; mg, milligram; min, minutes; mL, milliliter; mcg, microgram; SC, subcutaneous.

Hyperkalemia-related bradycardia treatment
Hyperkalemia may lead to profound bradycardia and mimic AV blocks [116]. Treatment should include the administration of 2 g calcium gluconate IV or 1 g calcium chloride IV to stabilize the cardiac membrane, in addition to treatments that shift the potassium across the cellular membrane and enhance its elimination.
BRASH syndrome treatment

Treating patients with BRASH syndrome involves a simultaneous approach that targets all associated conditions. The treatment strategy includes usual care of bradycardia (medications [such as epinephrine infusion] and/or pacing), hyperkalemia therapy (IV calcium, IV insulin and dextrose, and/or emergent dialysis), and fluid resuscitation [30]. In addition, it may include further advanced therapies in refractory cases or patients with AV-nodal blocking medication toxicity (e.g., lipid emulsion, glucagon, high-dose insulin, and digoxin-specific antibody) [30].

Hypothermia-related bradycardia treatment

In hypothermia, the first management line is rewarming, even before pacing. Due to the arrhythmogenic effect of hypothermia, pacing severely hypothermic patients has not been recommended due to concerns of precipitating ventricular fibrillation [23, 117]; however, case reports of successful pacing have been reported [118]. ECMO might be considered for severe hypothermia (<32 °C) and cardiac instability [119,120].

Myxedema coma-related bradycardia treatment

Patients with bradycardia secondary to myxedema coma require emergent thyroid hormone replacement (Levothyroxine [T4] 200-400 mcg IV, lower dose in geriatric patients) [121,122]. Adjunctive therapy includes hydrocortisone (100 mg IV), correction of hypoglycemia and electrolyte abnormalities (such as hyponatremia) and supportive care [121,122]. Moreover, identify and treat triggers causing decompensated hypothyroidism (e.g., infection, medications, MI, heart failure, and GI bleeding) [121]. 

Elevated ICP-related bradycardia treatment
For patients with bradycardia secondary to head trauma and increased ICP, treatment should be directed to lower the ICP, such as head elevation, hyperventilation, and mannitol or hypertonic saline.

Special Patient Groups

Considerations of bradycardia in pediatrics

The initial assessment of children is unique. The Pediatric Assessment Triangle is a rapid assessment tool to identify patients with respiratory or circulatory compromise who require immediate stabilization, and stands for appearance, breathing, and circulatory status [123, 124]. This is followed by a primary assessment using the ABCDE approach, similar to adults.

Clinically significant bradycardia in pediatric patients is defined as a heart rate less than the age-appropriate rate with impaired systemic perfusion [125]. The heart rate definition of pediatrics differs based on age, and in infants, an asleep heart rate has a different cut-off than an awake heart rate [126].

In pediatrics, always consider bradycardia as secondary to a reversible cause until proven otherwise. Bradycardia in the pediatric age group is usually associated with hypoxia (the most common cause), hypotension, acidosis, hypothermia, and medications, whereas primarily cardiac causes are rare [74,126].

Bradyarrhythmia in pediatrics is commonly a pre-arrest rhythm125; therefore, an early aggressive approach in children with bradycardia with poor perfusion has been recommended [127]. Immediate evaluation of adequate oxygenation and ventilation is necessary. In patients with a persistent heart rate of <60 and poor perfusion despite adequate oxygenation and ventilation, start chest compressions and follow the pediatric advanced life support (PALS) bradycardia algorithm [74,127], even if there is a detectable pulse.

Considerations for bradycardia in geriatrics

Older adults have a relatively high incidence of symptomatic bradycardia (6%), admission rate for symptomatic bradycardia (39%), rate of unstable bradycardia (16%), and mortality (5%) [128]. In older adults, ischemia tends to present atypically; thus, clinicians should have a high index of suspicion for an underlying ischemic cause. Moreover, polypharmacy is more common in older adults, thereby increasing the risk of drug-induced bradycardia and drug interactions.

Considerations of bradycardia in pregnancy

In critically ill pregnant patients, no medication should be withheld due to concerns of fetal teratogenicity [129,130]. Atropine crosses the placenta and risks and benefits of its use in stable patients should carefully weighed [131]. In unstable patients, atropine or epinephrine may be administered [132]. Epinephrine is preferred over dopamine in pregnancy [133].

Pregnant patients with symptomatic bradycardia necessitating atropine or vasoactive agents (e.g., epinephrine or dopamine) or those with advanced heart block require a multidisciplinary team, including obstetricians and neonatologists for maternal–fetal intensive monitoring [129], which may require transfer.

Bradycardia in patients with a heart transplant

Resting heart rate in heart transplant recipients ranges from 80-110 beats/min [134,135]. Therefore, bradycardia in these patients is defined as a heart rate persistently <70-80 beats/min [7,18,136]. Post-transplant bradycardia could be attributed to several mechanisms, including sympathetic denervation, SA ischemic injury, graft ischemia, and drug-induced [137-139].

Atropine is contraindicated due to the potential risk of paradoxical AV block and asystole [7,49]. Medications used to increase the heart rate include isoproterenol, aminophylline, and theophylline [7,61,140]. Target heart rate for temporary pacing, if indicated, is over 90 beats/min [140].

Following stabilization, those patients may require transport to an advanced heart transplant center for monitoring. It is recommended (Class I) to treat sinus node dysfunction medically in the postoperative period (1-6 weeks) and observe for resolution before attempting pacemaker implantation [21], which is eventually required in 7-24% of patients [136,141,144].

Disposition

All patients with symptomatic bradyarrhythmias require cardiology consultation [23]. Patients presenting with unstable or symptomatic bradyarrhythmias, particularly Mobitz type II or third-degree heart block, require admission to a cardiac ICU for monitoring.  Patients with secondary bradycardia often require admission for definitive treatment of the underlying etiology, either to the ICU or an intermediate care unit (i.e., stepdown). On the other hand, asymptomatic patients with benign ECG features and a normal ED work-up may be followed by cardiology on an outpatient basis; ambulatory electrocardiography monitoring and/or electrophysiology studies may be considered.

Revisiting your patient

The patient was rushed into a monitored bed. IV lines were established. The patient was placed on pacer pads. Atropine 1 mg IV was given with no response. ECG confirmed evidence of third-degree heart block (complete dissociation between P waves and QRS complexes, wide QRS complexes [QRS=154 ms], atrial rate of ~100 beats/min, Ventricular rate of ~30 beats/min, rhythm is maintained by a junctional escape rhythm). Epinephrine and transcutaneous pacing were initiated. Electrical capture was demonstrated on the ECG. The pacing rate was 85 beats/min.

The patient returned to his baseline mental state. Capillary refill improved, extremities became warm, the peripheral pulse became strong, and lactate clearance was appropriate.  Central line access was obtained to transition the patient into transvenous pacing. Cardiac biomarkers resulted, revealing a significantly elevated troponin level at seven times the upper limit of normal. The patient was diagnosed with non-ST elevation occlusive MI. Cardiology was consulted, and they admitted the patient to the cardiac ICU. The patient was taken to the cardiac catheterization laboratory for PCI the following day.

Authors

Picture of Hassan M. Alshaqaq, MBBS

Hassan M. Alshaqaq, MBBS

Hassan Alshaqaq is an Emergency Medicine PGY1 Resident at King Saud University Medical City. He is passionate about EM, research, medical education, resuscitation, and critical care. His research work has appeared in various medical journals and has been awarded by EM and critical care societies. He has been involved with several medical societies in different leadership and educational roles. He is interested in developing clinical practice guidelines and has contributed to the Saudi Critical Care Society guidelines. He is the student club president of the Saudi Society of EM. He is an enthusiast in contributing to EM education, particularly FOAMed.

Picture of Danya Khoujah, MBBS, MEHP

Danya Khoujah, MBBS, MEHP

Dr. Danya Khoujah is an American board-certified Emergency Physician with a keen interest in medical education. She completed her emergency medicine residency and faculty development fellowship at the University of Maryland in Baltimore and a Master of Education in Health Professions from Johns Hopkins University. She has developed over 120 lectures, 75 podcasts, and 50 publications on various emergency medicine and medical education topics that have been well received. She is most passionate about simplifying the science to allow healthcare practitioners to better care for their patients, whether seasoned physicians, resident physicians-in-training, medical students, or allied health professionals.

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Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Disaster Medicine Triage (2024)

Disaster Medicine Triage
~ iEM Education Project Team ~ Leave a comment

by Parker Maddox, Hassan Khuram & Scott Goldstein

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A Brief Introduction to Disaster Medicine

Disaster Medicine is a medical discipline that centers around events significant enough that, without external aid, emergency departments (ED) would not be able to adequately provide care to those affected [1]. For example, a multi-vehicle car accident may result in multiple casualties, but would not be considered a disaster if the responding medical infrastructure was able to handle the influx of patients. Many entities including the United Nations International Strategy for Disaster Reduction (UNISDR) and the World Health Organization (WHO) have amended their definitions of the term “disaster” to specify occurrences that exceed a community’s ability to cope with the effects of said disaster [2,3]. Incidents that have satisfied this requirement include natural disasters and more modern occurrences such as water contamination, human conflict, chemical spills, radiation, power outages resulting in infrastructure collapse, etc. [1]. The field of disaster medicine operates with the goal of aiding with these disaster-level events and all of the associated medical, logistical, and ethical issues that come along with them [4].

This is accomplished through a joint effort by many disciplines within healthcare including emergency medicine (EM), Emergency Medical Services, pediatrics, public health, social work, and many more [5]. However, emergency medicine providers’ experience in high acuity, large patient volume settings set them up to take a leadership role in disaster medicine. The emergency department is also typically the first point of contact between patients and health care providers in a disaster setting providing emergency medicine physicians an advantage in these responses [6]. In addition to their traditional responsibilities of stabilization and disposition of disaster patients, EM physicians are typically delegated the responsibilities of coordinating disaster response as chief medical officer, interfacing with government and community relief efforts, and directing disaster triage efforts [6].  

Disaster Triage

When a disaster occurs, hospital systems experience what is known as a critical care surge. This is defined as “any increase in the number of critically ill or injured patients beyond the baseline rate a hospital or critical care unit usually experiences.” [7]. These surges are classified based on the size of the critical patient increase with disasters typically causing large surges or megasurges. Megasurges are caused by grand scale, unexpected disaster events (tsunamis, earthquakes, terrorist attacks, etc.) and can require greater than 200% of the resource capacity a hospital has to care for patients [7]. This dramatic scarcity of resources in the face of overwhelming casualties results in an inevitable need to ration resources.
 

According to the World Health Organization, “triage” is the rapid examination and sorting of patients into groups according to their medical needs and the availability of resources [8]. In this setting of mass casualties and resource scarcity, disaster triage protocols are governed by the utilitarian concept of doing the greatest good for the greatest number[9]. As opposed to routine triage seen in the ED, this requires a shift of focus from the outcomes of single patients to outcomes on a population level [7].

However, despite the common misconception, disaster triage is not simply making the decision of whether to treat a patient or not. Disaster triage is more complex with most decisions centering around what level of treatment a patient should receive [7]. Rarely is it decided or even proposed that a patient should receive no treatment at all [7]. The consensus within disaster medicine is that disaster triage should optimize patient care and resource allocation by considering the incremental improvement in survival that a treatment would provide a patient in their current condition[10]. In order to make these decisions, the foundation of disaster triage lies in the use of triage tools and protocols to systematically assess patient conditions and prognoses following these devastating events. With proper triage and resultant treatment, it has been shown that trauma patients can experience at least a 25% reduction in mortality [11]. In disaster settings where hundreds to thousands of lives hang in the balance, 25% is not an insignificant number.

Measures of Success: Undertriage and Overtriage

Prior to discussing the wide array of triage methods used in disasters, it is pertinent to describe the terms used describe and assess them. Triage efficacy is typically judged by its validity, or how accurate the acuity assigned during triage, by tool or clinical assessment, is to the actual acuity of the patient. In order to measure this validity, we rely on rates of undertriage and overtriage observed during real world scenarios (Table 1) [12].

Concept

Definition

Impact

Sensitivity & Specificity

Acceptable Rate

Undertriage

Patient condition is classified as a lower acuity than it actually is.

Patients are under prioritized, under treated, and providers may miss savable lives.

Low sensitivity

Low (<5-10% of patients)

Overtriage

Patient condition is classified as a higher acuity than it actually is.

Patients are overtreated leading to disorganization, misallocation of scarce resources, and wasting time that could be used to save other patients.

Low specificity

Variable depending on context (25-35% and others 50-60%)

Table 1:  Definitions, major impacts, relationships to sensitivity and specificity, and acceptable rates of overtriage and undertriage [11, 12, 13, 15, 17].

Undertriage

Undertriage is when a patient’s condition or injury is under classified in terms of acuity, and the patient is under prioritized or under treated as a result. This results in situations where critically ill patients could have benefited from a justifiable use of resources to further evaluate and treat their injuries [13, 14]. An example of this could be a severely injured patient that was transferred to a non-trauma center, or a patient that could have survived with prioritized evacuation and admission to the ICU or OR. However, it is worth noting that moderately injured patients are the most often undertriaged since severe acuity patients are more easily recognized [11]. Nonetheless, these are essentially missed opportunities to save patients and, statistically, this would represent a low sensitivity of the triage process. Therefore, there is a low tolerance for undertriage with most entities recommending an acceptable undertriage level of less than 5-10% of patients [15].

Overtriage

Overtriage is defined as the inaccurate classification of a patient as high priority or acuity when their injuries are actually non-urgent [11].  A classic example of overtriage would be when a stable, non-critical patient is unnecessarily expedited ahead of sicker patients for a surgery they do not acutely require. According to Foley and Reisner, another form of overtriage is when patients with little to no chance of surviving receive aggressive medical treatment, inappropriately allocating scarce resources [13]. Compared to undertriage, overtriage represents a poor specificity and complicates triage by creating disorganization that misallocates time and resources [14,16]. In the setting of a disaster, overtriage can be just as dangerous as undertriage as this misallocation can take away scarce resources and time that could be used to save other patients. The acceptable level of overtriage is more debated, with some sources recommending 25-35% [15] and others 50-60% of patients [13].

The reason for less stringency surrounding acceptable overtriage rates is due to the influence the two rates have on each other. Overtriage and undertriage do not exist independently of one another and demonstrate an inverse relationship [13]. As overtriage rates increase and patients are treated more liberally, undertriage rates decrease as less savable patients are missed. Therefore, when faced with the decision of overallocating resources or missing a potential savable life, most entities recommend maintaining a higher allowance for overtriage in order to reduce undertriage. Previously, it was reported that 50% of overtriage was required to reduce the rate of undertriage to 0% [17], but more recently that recommendation has been decreased to 25-35% [15] due to the detrimental effects higher overtriage can have on triage efforts with minimal decrease in undertriage rates [11, 18].

However, when applying these rules to real life disaster triage, it is important to also factor in the environment and working conditions of the disaster. The amount of acceptable overtriage and undertriage in a mass casualty event should change depending on resources and casualties present [13]. For example, in a scenario where casualties are few and resources are plenty, the risks of raising the overtriage rate are outweighed by the benefit of possibly reducing undertriage as there would be little chance of running out of resources or time. On the other hand, in a grand scale disaster where resources are extremely limited, a lower overtriage rate would be acceptable, despite the possible increase in undertriage, due to the higher likelihood of running out of resources and time. Therefore, it is imperative in disaster triage to always perform an initial survey of the amount of casualties and resources available in order to form an educated plan to maximize the greatest benefit for the greatest number of people [19].

Primary, Secondary, and Tertiary Triage

In comparison to traditional triage in an ED, disaster victims are triaged multiple times throughout their medical course beginning at the site of the incident and continuing through possible admission to the ICU or OR. These multiple points of reevaluation account for the evolving nature of disasters over time in terms of resource availability, treatment delays, and injury progression or resolution [20]. Triage in the setting of mass casualties can be broken down into three different types: primary, secondary, and tertiary triage (Table 2). These different classifications differ based on the triage timing, location, and what level of care is being addressed [19, 21, 22].

Primary Triage

Primary triage occurs at first contact with patients after a disaster [22]. This can occur at the scene of the disaster, or any other setting outside of the hospital including an area away from the incident [19]. The goal of primary triage is to establish the priority of injured patients for on-site treatment and evacuation to the nearest available hospital [21]. This can also include decisions such as routing patients to trauma versus non-trauma centers or performing life saving measures in the field [7, 19]. Primary triage is regarded as the most critical stage in the disaster triage process with the greatest potential to save lives and influence population outcomes [21, 23]. As a result, many different tools and methods for primary triage have been developed and primary triage will be the major focus of this chapter [14]. The tools and specifics of primary triage will be discussed in more detail in the Triage Tools section.

Secondary Triage

Secondary triage is the second evaluation of patients’ condition and overall acuity. This occurs upon patient arrival to the hospital and commonly takes place in the emergency department [21]. However, the level of care being addressed in secondary triage changes depending on the context of the disaster and the resulting bottlenecks in ED patient care. If it is a mass casualty event involving patients with highly acute complaints such as trauma, then secondary triage will focus on prioritizing patients for initial stabilizing measures in the ED [7]. Alternatively, if the disaster takes a less acute and more extended course, such as the Coronavirus Disease 2019 pandemic, then secondary triage will focus on determining disposition of patients from the ED after the initial stabilization has been performed. The disposition prioritization can include what patients are admitted to the hospital, transferred to more specialized areas within the ED, or discharged home [19, 21]. Secondary triage is especially vital when evacuation from the site of a disaster is prolonged resulting in a large influx of deteriorating patients arriving to the hospital [22].

Tertiary Triage

Tertiary triage is the third evaluation of patients involved in a disaster taking place after initial stabilization or hospital admission. This also occurs within the hospital, but does not need to be in the ED [19]. Tertiary triage is when questions of definitive care are addressed and prioritized such as ICU admission, surgery, and other procedures including those performed by interventional radiology [21]. This final form of triage is typically performed by a physician with critical care training or a surgeon [22]. This is also a chance to reassess continued medical management of severe patients in the setting of dwindling resources such as continuing life support measures or additional treatment after poor prognostic laparoscopic findings [19]. In disasters with fewer critical patients with life threatening injuries, tertiary triage is less utilized [7].

Triage

Timing

Location

Level of Care (LOC)

Primary Triage

First patient contact

At the scene of the disaster

Determines the priority order for treatment in the field and emergency transport. Can also prioritize patients to be transported to trauma vs. non-trauma centers.

Secondary Triage

Second evaluation upon entry into the hospital

In the emergency department

Determines priority order for resuscitation in the ED and disposition after stabilization

Tertiary Triage

After initial treatment and stabilization in the ED

Anywhere in the hospital, not restricted to the ED

Determines the priority order for definitive care including ICU admission, surgery, or transfer to a higher-level facility,

Table 2: Definitions, timing, location, and level of care being decided on for the three levels of triage: primary, secondary, and tertiary [19, 21, 22].

How to Triage: Primary Triage Classification & Tools

Classification

How to properly perform primary triage in the field of a disaster has been a highly contentious area of research since before the establishment of disaster medicine [14]. In non-disaster level traumas, most medical providers in North America minimize their pre-hospital evaluation and treatment in favor of more expedient transportation to the hospital[24]. This is known as “scoop and run” and restricts pre-hospital treatment to Basic Life Support (BLS) with minimal classification of patient acuity. “Scoop and run” has been proven to have significant benefits in terms of trauma outcomes[24, 25], but more rigid triage systems are typically utilized in disasters to expedite patient prioritization, minimize uncertainty, and maximize effective use of resources to do the “greatest good for the greatest number” [26].

Globally, differing disaster triage tools and systems are implemented without any clear consensus in the literature on their efficacy [21]. However, one commonality among the majority of these systems is the four-level classification schema they use to group and prioritize disaster victims [26, 27]. First proposed by the World Medical Association (WMA), this system categorizes disaster victims into four different groups based on their acuity and how urgently they require medical intervention (Table 3) [26]. The literature labels these groups in various manners including by triage tag color (red, yellow, green, black), urgency of required treatment (emergency/immediate, delayed, minimal, expectant), or their priority level (P1, P2, P3, P4) [13, 21, 26, 28].

The immediate/emergency group consists of patients who are in critical condition, but can still be saved with immediate treatment within, at most, the next few hours. A red triage tag is commonly used to label this group [28].

The delayed patients are those who are not experiencing an imminent threat to their life, but urgent, definitive medical care will be required at some point. These patients are often labeled with a yellow triage tag [26].

The minimal group are sometimes referred to as the “walking well” or “walking wounded” and have the least severe injuries [27, 29]. These nicknames stem from the fact that most patients in the minimal group can walk following the incident. Various triage tools will even use the ability to ambulate in their algorithms since multiple studies have shown that walking following a disaster is a strong indicator of a relatively low risk patient with a good prognosis [22, 30]. These patients are labeled with a green triage tag and often require only minimal treatment that can be delayed until the rest of the patient categories have been treated.

The final category, deemed expectant, is marked with a black triage tag, and is made up of patients that are either dead or critically ill to the point that efforts to save them are deemed futile. This classification is typically made in situations where the patient’s condition is beyond treatment or when the complex treatment required to save the patient would be putting other patients at risk by misallocating already limited time and resources [21, 26]. It is important to acknowledge that this can be an especially difficult classification for providers to make. The WMA has addressed this by releasing a statement expressing that “It is unethical for a physician to persist, at all costs, at maintaining the life of a patient beyond hope, thereby wasting to no avail scarce resources needed elsewhere.[31]” However, as disasters are fluid and ever-evolving, it is the responsibility of a triage to repeatedly reassess the situation including reviewing the priority designations previously assigned to patients [28].

Table 3 Priority number, color, name, and description for the four commonly used triage tags [21, 26, 28, 30].

Table 3: Priority number, color, name, and description for the four commonly used triage tags [21, 26, 28, 30].

Tools

Despite a consensus on what priority groupings are used to sort patients during a disaster, how to place patients in each grouping is still highly divisive. The literature has been unable to provide any significant evidence for or against specific triage strategies resulting in a wide array of disaster triage systems used internationally [14, 21, 22]. In the 1980’s, formal triage scoring systems were developed for primary triage that categorized patients based on objective measures. The most used scoring systems are the Revised Trauma Score (RTS) and Champion’s Trauma Score (CTS), both of which utilize a patient’s Glasgow Coma Scale (GCS), systolic blood pressure, and respiratory rate to calculate a total score that sorts patients into the appropriate priority groupings [32]. However, triage scoring systems have been shown to not be as efficacious in the pre-hospital setting since objective measures of vital signs do not always correlate with clinical condition. As a result, triage scores have demonstrated poor sensitivity in the field and there have been instances where normal vital signs masked critical illness in disaster patients resulting in undertriage [13, 32]. Additionally, vital signs taken at the scene of a disaster are not always reliable due to various confounding variables and can create provider uncertainty in the field [32]. Therefore, triage scoring systems have fallen out of favor in disaster triage and this chapter will focus on the use of multi-tier triage algorithms.

Formalized triage algorithms are a set of rigid, pre-determined decision trees that quickly guide providers through the initial assessment of disaster victims in the field [14]. Triage algorithms base their decision making more in components of clinical presentation such as ability to ambulate and breathe rather than objective measures. These algorithms tend to be more suitable for mass casualty disasters as they minimize the time spent making active decisions and are easy to learn in a restricted amount of time [13]. The disadvantage of these algorithms is their lack of flexibility. As discussed previously in the Measures of Success: Undertriage and Overtriage section, it is important to be able to tailor your protocol, and subsequently your over and undertriage rates, depending on the number of casualties and the availability of resources. However, the rigid procedure of these algorithms does not allow for modifications of treatment criteria when time and resources are more plentiful [13]. Many algorithms have been developed with slightly different applications based on patient demographics, mechanism of the disaster, geography, etc. [14]. Due to the sheer number of triage algorithms currently available, this chapter will focus on the most used primary triage tools in disaster medicine: the Simple Triage and Rapid Treatment (START) and Sort, Assess, Lifesaving interventions, Treatment/Transport (SALT) algorithms.

The Simple Triage and Rapid Treatment (START) triage algorithm was originally developed as a result of joint efforts between a California Fire department, Marine department, and medical providers in 1983 [33].  This was one of the first triage systems developed outside of the military and, following its conception, the Domestic Preparedness Program of the Department of Defense made it standard practice in disaster events [28]. It is now the most prolific mass casualty triage system used in the United States [27].

The START triage algorithm was designed as an expedient triage system that would be easily teachable to emergency providers with minimal training [26]. The objective of the system is the be able to evaluate patients older than eight years old within 30-60 seconds and triage them into one of the four priority groupings discussed previously: immediate/emergency (red), delayed (yellow), minimal (green), expectant (black) [14, 27]. This is accomplished through strict criteria looking at patient ambulation, respiratory rate, radial pulse, mental status, and capillary refill, though many versions of START no longer assess capillary refill due to variabilities from the environment [13, 22, 33].

As depicted in Figure 5, the initial step of START is to prompt patients to walk [27]. If a patient can walk following a disaster, this has been shown to be an indicator of low risk and good prognosis [22, 30]. Therefore, patients who can walk are immediately classified as minimal, green, or priority 1. Following this initial step, the remaining non-minimal patients are evaluated based on their respiration, perfusion, and finally mental status. Examples of methods used to assess mental status during START triage include asking patients to perform simple command such as opening and closing their eyes or squeezing a hand [34]. A Yellow tag or delayed status is assigned to all patients that were not originally deemed minimal, but meet the respiratory, perfusion, and mental status criteria set by START. An easy mnemonic to remember the parameters looked at by START is “RPM:30-2-can do”, with RPM standing for Respiration,Perfusion, Mental status. The second portion “30-2-can do” are the associated cut off values for each category: > 30 respirations per minute, presence of radial pulse or capillary refill <2 seconds, and can follow simple commands [26, 27].

Figure 1 START Algorithm to triage patients based on severity

Figure 1: START Algorithm to triage patients based on severity [22, 28].

Though there is little research analyzing the overall efficacy of START, the triage system has demonstrated higher overtriage rates in more critically ill patients during a disaster [28]. In a study by Kahn et. al, START was shown to have an overall accuracy of 44.6% in assigning the correct acuity level for patients. Upon further analysis, START was shown to perform well when identifying patients in the minimal category, with the walk test demonstrating accurate prognostic predictions [35].  However, the triage system experienced higher levels of overtriage (53.38%) in the two more critical patient categories with a significant number of patients inappropriately being placed in the immediate/emergency classification when they belonged in the delayed category [35].

The Sort, Assess, Lifesaving interventions, Treatment/Transport (SALT) algorithm was designed to unify the many existing triage algorithms. Due to a significant lack of research surrounding the efficacy of these triage tools, the Center for Disease Control and Prevention (CDC) assembled a committee in 2008 to combine the most effective features of the current mass triage algorithms into a national standard [22, 28]. This resulted in a new triage algorithm that is very similar to START, but with some key differences. SALT performs a more comprehensive triage of patients of all ages by performing multiple stages of sorting and prioritization with opportunities for reassessment [27]. Additionally, SALT prioritizes life-saving interventions by incorporating them into the triage algorithm leaving less room for hesitancy and uncertainty [13]. The protocol and unique features of SALT can be further elucidated by breaking down what SALT stands for.

            Sort refers to the first step, unique to the SALT protocol, which entails an initial sorting of patients into three groups, prior to formal evaluation, to determine what order patients should be clinically assessed. This pre-sorting is based on their ability to ambulate and perform simple commands (Figure 2) [36]. If patients are able to ambulate, then they are placed in the “Walk” or “Able to walk” group. These patients will be assessed last due to the low risk associated with the ability to ambulate [22, 30]. Patients who are unable to walk, but are able perform purposeful movements such as waving will be placed in the “Wave” or “Able to make purposeful movements category” and assessed second. Finally, patients who have obvious life-threatening injuries or remain still despite prompts to walk or wave are placed in the “Still” or “Severely injured” category. These patients will be clinically evaluated first [27].

Figure 2. Step 1 of SALT algorithm to prioritize who to clinically assess first

Figure 2: Step 1 of SALT algorithm to prioritize who to clinically assess first [22, 27, 28].

The Assess and Lifesaving interventions steps come next and are performed almost simultaneously. Assessrepresents the clinical evaluations that are performed after the three priority groupings have been established during the Sort step. This step is looking for any life-threatening injuries that require immediate stabilization [14]. As threats to life are found during this evaluation, the Lifesaving interventions step calls for immediate medical intervention during triage to stabilize these patients. These interventions typically include opening the airway, hemorrhage control, needle thoracostomy for pneumothoraxes, and antidote auto-injection for poisoning [14, 22].

The last phase of SALT, Treatment/Transport, requires an additional evaluation of patients following lifesaving interventions in order to place patients in the same four priority classifications for evacuation and definitive treatment utilized in START (Figure 3). This step affords the triage an opportunity to reassess patients following life-saving interventions and factor in their response [14]. This reassessment involves many of the same parameters looked at in START including breathing, mental status, and peripheral pulse. However, it also includes a step to consider the patient’s condition in the setting of the resources available [22]. Similar to START, once the patients have been sorted and tagged, they are transported and treated according to their priority group.

Figure 2 Step 2 of SALT algorithm [31, 36, 37].

Figure 3: Step 2 of SALT algorithm [31, 36, 37].

SALT has taken over as one of the major triage algorithms used in disasters and is endorsed by numerous entities including the American College of Surgeons Committee on Trauma, American Trauma Society, National Association of EMS Physicians, National Disaster Life Support Education Consortium, American College of Emergency Physicians, and more [36]. Studies have already begun to show that SALT provides more accurate triaging when compared to START and other triage systems [37, 38]. On the other hand, some studies have observed high levels of overtriage in SALT, similar to those seen in START, and even instances of high undertriage [28, 37, 38]. However, it is important to keep in mind that no clear conclusions can be drawn regarding SALT’s efficacy until more research is performed.

Summary

Disaster Medicine Triage focuses on managing medical care during events that overwhelm local emergency departments, necessitating additional aid. Definitions of “disaster” have evolved to describe situations beyond a community’s coping capability, encompassing natural and man-made incidents like water contamination and power outages. Emergency Medicine, among other healthcare disciplines, plays a crucial role, particularly in disaster response coordination and triage, aiming to do the best possible care for the greatest number. Triage, a core component, involves sorting patients based on their medical needs versus resource availability. With mass casualties, effective use of resources becomes inevitable, underpinning the need for efficient triage to optimize care and resource allocation, emphasizing the utilitarian principle of maximizing survival on a population level.

Authors

Picture of Parker MADDOX BA, MS

Parker MADDOX BA, MS

Parker Maddox is a fourth-year medical student at Sidney Kimmel Medical College at Thomas Jefferson University in Philadelphia. He graduated from the University of Virginia with a double major in Biology and Chemistry and went on to obtain a master’s degree in Biophysics and Physiology at Georgetown University. Since arriving to medical school, Parker has developed a passion for Emergency Medicine and has performed research on a wide range of topics including early sepsis recognition, pandemic viruses including Coronavirus 2019 and Monkeypox, ischemic stroke, Bell’s palsy, and international ECMO critical care protocol. This work has yielded multiple publications and a presentation at the Society for Academic Emergency Medicine (SAEM) 2022 Conference.

Picture of Hassan KHURAM BS, MS

Hassan KHURAM BS, MS

Hassan Khuram is a 4th year medical student at Drexel University College of Medicine, with a background in psychology, biotechnology, and business of healthcare. He graduated Magna Cum Laude with a Bachelor of Science in Psychology from Virginia Commonwealth University and a Master of Science in Biotechnology from Georgetown University. He is passionate about neurocritical care, medical education, and bioethics. He has an extensive background in research, having conducted studies on various subjects, including substance misuse, Parkinson's disease, mindfulness meditation and more. He has published articles on neurological emergencies and ethical issues in neurological care.

Picture of Scott GOLDSTEIN, DO, FACEP, FAEMS, FAAEM, EMT-PHP

Scott GOLDSTEIN, DO, FACEP, FAEMS, FAAEM, EMT-PHP

Dr. Scott Goldstein started his medical career at New York College of Osteopathic Medicine in New York where he received his Doctorate of Osteopathy and continued his training at Einstein Healthcare Network in the field of  Emergency Medicine, Philadelphia. Dr. Goldstein is dual-boarded through the American Board of Emergency Medicine in Emergency Medicine and Emergency Medicine Services (EMS). He currently works at a Level 1 academic trauma center, Temple University Hospital, in Philadelphia where he is the Chief of EMS and Disaster Medicine. He has continued to be an active member of the education community and EMS community where he holds the title of Fellow of American College of Emergency Medicine through ACEP, Fellow of the Academy of Emergency Medical Services through NAEMSP and Fellow of the American Academy of Emergency Medicine through AAEM.  His current academic title is one of Clinical Associate Professor of Emergency Medicine at Lewis Katz School of Medicine at Temple University. 

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References

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  20. Jenkins JL, McCarthy ML, Sauer LM, et al. Mass-Casualty Triage: Time for an Evidence-Based Approach. Prehosp Disaster med. 2008;23(1):3-8. doi:10.1017/S1049023X00005471
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  25. Haas B, Nathens AB. Pro/con debate: Is the scoop and run approach the best approach to trauma services organization? Critical Care. 2008;12(5):224. doi:10.1186/cc6980
  26. Iserson KV, Moskop JC. Triage in Medicine, Part I: Concept, History, and Types. Annals of Emergency Medicine. 2007;49(3):275-281. doi:10.1016/j.annemergmed.2006.05.019
  27. Clarkson L, Williams M. EMS Mass Casualty Triage. In: StatPearls. StatPearls Publishing; 2023. Accessed April 15, 2023. http://www.ncbi.nlm.nih.gov/books/NBK459369/
  28. Lee CH. Disaster and Mass Casualty Triage. AMA Journal of Ethics. 2010;12(6):466-470. doi:10.1001/virtualmentor.2010.12.6.cprl1-1006
  29. Foley E, Reisner A. Triage. Ciottone’s Disaster Medicine. Published online January 1, 2016:337-343. doi:10.1016/B978-0-323-28665-7.00054-6
  30. Meredith W, Rutledge R, Hansen AR, et al. Field Triage of Trauma Patients Based upon the Ability to Follow Commands: A Study in 29,573 Injured Patients. Journal of Trauma and Acute Care Surgery. 1995;38(1):129.
  31. WMA – The World Medical Association-WMA Statement on Medical Ethics in the Event of Disasters. Accessed April 15, 2023. https://www.wma.net/policies-post/wma-statement-on-medical-ethics-in-the-event-of-disasters/
  32. Gabbe BJ, Cameron PA, Finch CF. Is the Revised Trauma Score Still Useful? ANZ Journal of Surgery. 2003;73(11):944-948. doi:10.1046/j.1445-1433.2003.02833.x
  33. START Adult Triage Algorithm – CHEMM. Accessed April 16, 2023. https://chemm.hhs.gov/startadult.htm
  34. Disaster Preparedness Section – Los Angeles Fire Department Manual. Accessed April 16, 2023. https://www.cert-la.com/downloads/education/english/start.pdf
  35. Kahn CA, Schultz CH, Miller KT, Anderson CL. Does START triage work? An outcomes assessment after a disaster. Ann Emerg Med. 2009;54(3):424-430, 430.e1. doi:10.1016/j.annemergmed.2008.12.035
  36. SALT Mass Casualty Triage: Concept Endorsed by the American College of Emergency Physicians, American College of Surgeons Committee on Trauma, American Trauma Society, National Association of EMS Physicians, National Disaster Life Support Education Consortium, and State and Territorial Injury Prevention Directors Association. Disaster med public health prep. 2008;2(4):245-246. doi:10.1097/DMP.0b013e31818d191e
  37. Hartman EN, Daines B, Seto C, et al. Sort, Assess, Life-Saving Intervention, Triage With Drone Assistance in Mass Casualty Simulation: Analysis of Educational Efficacy. Cureus. 2020;12(9). doi:10.7759/cureus.10572
  38. McKee CH, Heffernan RW, Willenbring BD, et al. Comparing the Accuracy of Mass Casualty Triage Systems When Used in an Adult Population. Prehospital Emergency Care. 2020;24(4):515-524. doi:10.1080/10903127.2019.1641579

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Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Being a team member/leader and team dynamics in ED (2024)

~ iEM Education Project Team ~ Leave a comment

by Munawar Farooq & Bret Nicks

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Introduction

Emergency care worldwide has organizational and regional nuance, mainly due to differences in healthcare systems, infrastructure, resources, and history. However, the team’s value proposition remains critical for success in all emergency departments. Over the past several decades, it has become evident that teams and teamwork can positively impact many aspects of the care environment and the engagement of those serving there. When we consider the myriad challenges impeding quality decision-making in the emergency department (ED), such as a lack of time, evolving information, chaotic environment, limited resources, and constant interruptions, amongst others, having a dedicated team can make a significant difference. 

While the concept of a team is not new, our understanding of the value proposition of a team and the attributes of effective teams continues to evolve. For many of us in medicine, working in a group is expected. However, there are distinct differences between working in a group and being part of a team. What differentiates a team from a group is the commitment to a common purpose, shared desired outcomes, collaborative and complementary approach, value team over self, and shared accountability. A team’s foundation develops from those that collaborate around a shared goal. However, successful Emergency Medicine (EM) teams require a broader understanding of the essential attributes, processes, and expectations needed for a highly variable, chaotic, intellectually challenging environment dedicated to exceptional patient care. For these reasons and many others, EM epitomizes the ideal of team sports in healthcare.

Psychology of Team

Team dynamics are the learned, unconscious psychological forces influencing a team’s behavior and performance. Organizational culture and departmental culture significantly affect team dynamics. Further influencing factors include the nature of the work, the work environment, work relationships within and across teams within the department, the level of perceived support, and the work effort itself.[1] Recognizing the challenging environment of acute and emergency medicine, awareness of and creating an integrated and positive team dynamic is essential. High-functioning teams demonstrate better clinical outcomes, increased team retention, increased wellness, higher resiliency, and better comparative financials.

High Performing Team Characteristics

Characteristics of successful teams and team members have been studied extensively in various professions ranging historically from the aviation industry to more modern companies like Google. [2] The aviation industry mandates that the flight and cabin crew work together as a team using standard operating procedures (SOPs) and formal training to facilitate teamwork and communication. They recognize that cognitive and psychological stressors can lead to human errors that can occur in high-stakes environments. 

Looking at a very different workplace, researchers at Google asked what makes a (Google) team effective. While they anticipated finding the mix of those on the team to be the most influential on the team’s success, they found that the way team members interacted with each other mattered more than the composite of the team [1]. While competency requirements exist in EM and other clinically-based teams, much of Google’s findings apply. They identified five characteristics that promoted effective teams: psychological safety, dependability, structure, clarity, meaning, and impact (Figure 1).

Figure 1: Characteristics of Highly Functioning Teams.

Adopted from Rozovsky J. The five keys to a successful Google team. 2015. URL:
https://rework.withgoogle.com/blog/five-keys-to-a-successful-google-team/

Although EM is not Google, recognize that the foundation of all highly effective teams remains the same: trust. In the 5 Dysfunctions of a Team, Lencioni states that you cannot have a successful team without trust. Further, with a lack of trust, team members fear engagement in healthy conflict, essential to reaching better decisions and team member commitment. Only committed team members can hold each other accountable so that the team remains focused on collective goals (Figure 2).

Figure 2: Lencioni, Patrick. The five dysfunctions of a team. London: Wiley, 2002

Figure 2:  Lencioni, Patrick. The five dysfunctions of a team. London: Wiley, 2002

In emergency medicine (and perhaps medicine in general), metrics and outcomes are commonly the focus of many teams. While quality, safety, and administrative outcomes are essential, one should recognize that top performance of these outcomes flows from teams built on trust, embracing conflict, commitment to a common goal, and shared accountability. When these are in place, quality metrics follow. Addressing team dysfunctions takes work. It requires a desire for positive change, courage, and creating team alignment.

Further, emergency medicine teams are dynamic interdisciplinary teams working in a constantly changing environment with highly fluid teams of junior and senior emergency physicians, nurses, other specialists, students, residents, and other medical assistants. With so many variable team inputs, solidifying the departmental culture and creating the expectation for and practice of highly functional teams helps ensure that any patient receives safe and efficient healthcare, meeting high-quality standards without fail regardless of date, time, and acuity of presentation.

Literature on high-performing teams across multiple professions supports these and additional common characteristics.  Dr Tim Baker, in his book ‘Winning Teams’ presents eight characteristics of Winning Teams, as shown in Figure 3.

Figure 3: Adopted with permission Winning Teams, Dr. Tim Baker.

Figure 3: Adopted with permission Winning Teams, Dr. Tim Baker. Used with copyright permission from DBOS. 8 Key Characteristics of a High-Performing Team | by DBOS AU | Medium

Fulfilling this model, our emergency room teams are diverse but flexible. We adopt safe and effective working procedures like cognitive aids and structured communication tools. We aspire to achieve a shared goal of efficient and safe patient care. We create teams that build trust and mutual respect through transparent communication and clear leadership. We accomplish this by continuously learning and practicing together the necessary clinical skills and critical human factors.

Team development and its success are predicated on a supportive culture that recognizes a just cause.  For high-performing organizations, that culture is well-established across all departments and levels. Regardless, organizational culture is simply what you see when you watch and experience the service provided. It comprises a complex pattern of values, expectations, ideas, attitudes, and behaviors around a shared goal.

Effective Emergency Team Leadership

One key challenging but rewarding role of the emergency physician is to orchestrate and lead diverse teams in a relatively stressful and unpredictable environment. While this may represent one of the major attractions of the emergency physician, it can be daunting for some. For a junior physician, it is essential to identify good leadership attributes early and apply them continuously, as it benefits the team and a leader’s clinical navigation during resuscitation. Something can be learned from every member of an interprofessional resuscitation team.  Observing how they serve as role models and clinical leaders in any situation and how they interact with colleagues, patients, and families provides a basis for personal growth and reflection.

Advanced life support simulation studies identified better outcome metrics (higher quality cardiopulmonary resuscitation with better technical performance, shorter pre-shock pauses, with lower total hands-off ratio, and shorter time to first shock) with teams having leaders with more experience and refined leadership attributes. [3] Although variability exists with healthcare leader experience, having a high-performing team enhances team dynamics and outcomes.  Regardless, effective team leaders must embrace and demonstrate the following leadership elements:

  • Understand the team value proposition and roles of its members
  • Manage well in challenging and changing situations
  • Effectively communicate
  • Embrace mutual accountability and responsibility
  • Set specific goals while persevering to achieve them
  • Balance individual tasks and promote teamwork
  • Build solid connections and relationships
  • Demonstrate adaptive learning from their experiences.

It is important to note that most of these attributes are not related to knowledge and skills commonly taught in medical schools but rather experientially or intentionally developed emotional intelligence skills. Developing and deploying these elements can positively influence everyday tasks performed by emergency physicians, such as:

  1. Organize the team and resources to maximize performance
  2. Articulate clear goals with delegation of tasks
  3. Make decisions through the collective input of members
  4. Empower team members to speak up and challenge the leader when appropriate, using group norms to guide behavior
  5. Actively promote and facilitate good team processes
  6. Skillfully prevent and resolve any conflict

Although historically called soft skills or abstract skills, data would suggest that these critical leadership skills are as necessary as clinical competencies. Effective leaders not only work on their clinical and content competence but also on emotional intelligence, communication skills, and performance under pressure.

The Team Player

What makes a team player exceptional? When you think about your current team(s), are they made up of ideal team players?  If not, what are you doing about it?

While exceptional team leaders can navigate the professional nuances of their team members, the team’s success is often limited by the leader’s capacity and by the attributes of those team members.  High-performing teams are far more multiplicative rather than the simple sum of individual member performances.  How we identify future team members or invest time and effort into developing current team members impacts not only outcomes but also influences the quality and capacity of the team.

Often, we hire team members based on their clinical competencies, educational accomplishments, and career success.  However, moving beyond competence to team and organizational cultural alignment is essential as we look more closely at developing high-performing teams.  Leaders must identify and employ people with three traits that all good team players share: humility, hunger, and smart people (interpersonal intelligence). In his book, “The Ideal Team Player,” Lencioni recommends considering aligning the essential virtues of a team player into three characteristics:

  • Humble (not arrogant or ego-centric; team-focused)
  • Hungry (great work ethic; never settling for the minimum)
  • Smart (skilled in emotional intelligence and people skills)

The ideal team player must have all three characteristics to be a trusted and proficient team member. Assessing teams requires self-reflection regarding these three traits, a conscious desire, and a focused effort to improve. Awareness and growth in this area catalyze individual and team success. When only one or two of these attributes are present, team leaders must consider the value proposition of developing these team members or identifying other opportunities that might be better for that team member.

Key Principles of Teamwork

In addition to discussing the psychology of teams, attributes of high-performing teams, effective team leadership, and ideal team players, further studies have looked at systematic approaches to creating a culture of teamwork within healthcare.  TeamSTEPPS, an educational program about teamwork, highlights the fundamental principles of an effective team structure, clear communication process, transforming leadership, situational awareness, and mutual support. [2]

Leaders use Delegation, Pre-Brief and Debrief, and Group Huddles in effective teams to clarify team goals, roles, and expectations. Both team leaders and members maintain situational awareness, cross-monitor each other, and provide constructive feedback. Everyone uses structured communication tools like SBAR (Situation, Background, Assessment, Recommendation), Checking Back, Advocacy, and Gradual Assertiveness to communicate clearly and deliver the safest and best possible care.

Practical Tips to Improve Teamwork

Understanding the attributes of high-performing teams, team leaders, and team members considering the challenges of emergency medicine is foundational to change.  However, identifying practical applications that begin to create change and further support culture is essential. [5] Below are some typical applications that have been suggested in the literature and through clinical experience:

  • Department awareness: Before you start working in a new department, visit, observe, identify the culture, and ask yourself how you can be a catalyst.
  • Bring your clinical competence and communicate medical decision-making with your team.
  • Developing empathy in daily challenges requires intentionally understanding another’s perspective, avoiding early judgment, recognizing inherent emotions, and responding genuinely to that emotion. (Brene Brown)
  • Understand and set role expectations while understanding how your personal attributes influence how you perceive your role.
  • Huddle first, then get started. Know your team – names and roles. Set expectations for team goals and find opportunities to engage and communicate in person with colleagues throughout the shift.
  • Consider the patient and their family an essential and valuable team member. The ‘nothing about me without me’ principle applies to everyone, including the patients and staff.
  • Lend a helping hand. Look for such opportunities and do not wait for the request.
  • Self-reflection increases continuous learning and improvement. Make it a regular practice regardless of the outcome or situation.
  • In any resuscitation or other emergency team management situation, follow the principles of clear roles, closed-loop communication, task focus, situational awareness, and the courage to speak up if required for patient or staff safety.
  • Listen actively by paying attention to non-verbal clues and perspectives while being aware of your own. Listen to understand – do not listen to respond.
  • Avoid negatively inferred language that feigns responsibility and creates blame or division. This rapidly erodes teamwork and a supportive culture.
  • Handoffs matter. Align your approach and expectations, as this directly impacts patient and team outcomes.
  • Offer compliments and appreciation genuinely and frequently. Recognize a job well done with gratitude. It reinforces positive effort and builds team rapport.
  • Build relationships outside the work environment when feasible. Know your colleagues through their interests, values, goals, achievements, and challenges.
  • Advocate for patient safety. Learn how to challenge a team member or leader if there is any concern for patient safety. Use a structured tool like “CUS” (Figure 4) or simply state, “I have a concern.”
  • Never think you are alone. Help is always available. Working in the emergency department is not easy – recognize it. If you need assistance, clinically or personally, ask.
Figure 4: CUS, graded assertiveness tool

Figure 4: CUS, graded assertiveness tool. Source: TeamSTEPPS. https://www.ahrq.gov/teamstepps/instructor/essentials/pocketguide.html

Case Scenario Application of Team Dynamics

Let us apply all the above learning to a resuscitation scenario and understand how a resuscitation team works. You are part of a resuscitation team when EMS encodes that they are bringing a 10-year-old boy whose scooter was hit by a car. The suspected injuries include a head injury and a possible right thigh injury. The trauma resuscitation team manages the patient very well through the following teamwork processes:

Pre-arrival

  • Assigned roles. The assigned team leader knows the team members’ strengths, limitations, and expectations. Every member acknowledges their assigned role and any concerns or needs they may have. Doing so before the patient’s arrival helps mitigate positional limitations during the resuscitation. Any members outside this team are also informed as required according to local resources, e.g.  Radiographer, Pediatric Surgeons, Orthopedics, etc.
  • Environment and equipment are prepared with enough space to work around. Airway and resuscitation equipment, confirmed at the beginning of the shift, is assessed based on any specified checklists and procedures.

Post Arrival

  • On arrival of EMS, handover is taken using pre-defined handover tools or processes with prehospital teams. The noise and distractions are kept to a minimum to optimize patient care information handoff and prompt transfer.
  • The team leader directs care with the team – and, when possible, stands at the foot of the bed to maintain situational awareness and monitor the team’s performance.
  • Team members perform assigned roles while maintaining situational awareness, monitoring the patient and teammates, and reporting back.
  • Clear and respectful closed-loop communication. Team leaders direct requests to every member using their names, and team members acknowledge the understanding of the task by repeating back and then announcing the completion of the task.
  • The team leader frequently shares ongoing medical decision-making with the team throughout the resuscitation by describing the situation and plan. For example, after completion of the primary survey, the team leader announces, “It appears that the child has an isolated head injury. Let us aim to intubate this patient and transport him to a CT scan within the next 15 minutes”. This provides directional clarity and offers an opportunity for feedback.
  • Teams use cognitive aids like checklists to prevent any medical errors. In contrast, the team leader maintains an open, respectful, and empowering environment where every member can challenge and raise patient safety concerns. Team members use graded assertiveness tools like ‘CUS’ to raise their concerns.
  • A culture of vulnerability and trustworthiness is maintained when team leaders or team members express when they are unsure of something and freely ask for help or a second opinion. Before any significant high-risk decision, the team leader shares the medical decision-making rationale and plan with the team.
  • Updating or briefing new members from other teams by the team leader or a designated member allows for clarity of ongoing care and consultative expectations. Recognize the emergency department is your home, but that may not be true for others.
  • After resuscitation, a hot debrief is performed with the team to express objective gratitude, provide compliments, discuss what went well, and identify areas for improvement. Critical issues should be addressed in a more formal debrief, especially if future application is intended.

As mentioned throughout this chapter, the benefits of developing a high-performing team in the emergency department are myriad.  It will improve departmental morale and greatly influence the quality of care provided, create mission alignment, foster resiliency, and attract exceptional team members.  Table 1 presents additional benefits of effective teamwork [6].

Organizational benefits

Team benefits

 

Patient benefits

Benefits to team members

Reduced time and costs of hospitalization

Improved coordination of care

 

Enhanced satisfaction with care

Enhanced job satisfaction

Reduction in unexpected admissions

Efficient use of healthcare services

 

Acceptance of treatment

Greater role clarity

Services are better accessible to patients.

Enhanced communication and professional diversity

 

Improved health outcomes and quality of care, reduced medical errors

Enhanced well-being

Table 1: The benefits of effective teamwork

Summary

Successful teamwork is challenging but worthwhile. Trust represents the foundation of all successful teams. They also embrace a shared common purpose and a dedication to quality in an environment where team members work together, communicate effectively, anticipate and meet each other’s demands, and inspire confidence, resulting in coordinated collective action. For many, the phrase, ‘teamwork can make the dream work,’ resonates with them. It is an uphill climb. It starts with trust. It requires courage. And it requires effort. If the dream is high-quality patient care in a safe and respectful department, start with your team.

Authors

Picture of Munawar FAROOQ

Munawar FAROOQ

Dr. Munawar Farooq, with qualifications including MBBS, FCPS (Pak), MRCS (UK), FACEM (Australia), and a Pg. Dip. in Medical Toxicology from Cardiff University, UK, is currently an Assistant Professor of Emergency Medicine at CMHS, UAEU. His prior roles include Consultant in Emergency Medicine in Canberra, Australia, and Doha, Qatar, Clinical Lecturer at Australian National University (ANU) in Canberra, ACT Australia, and Honorary Senior Lecturer in MSc Resuscitation at Queen Mary University London, UK. His special interests are in resuscitation medicine, toxicology, trauma, and medical education. His research focuses on detecting deteriorating patients, early warning scores, oxygen delivery device requirements in COVID outbreak, on-floor low fidelity simulations, and Leadership Training. In medical education, he is particularly interested in teaching leadership skills, Emotional Intelligence, and Human factors.

Picture of Bret NICKS

Bret NICKS

Bret Nicks, MD, MHA is an emergency physician that embraces the breadth of our specialty. He is a Professor and Executive Vice Chair of Emergency Medicine at Wake Forest University School of Medicine. He is the past president of the North Carolina College of Emergency Medicine. He served as the Chief Medical Officer of the award-winning Wake Forest Baptist Davie Medical Center. Dr. Nicks served as the founding Associate Dean for the Wake Forest Office of Global Health. He has lived, practiced, and led in many resource austere locations globally, although calls the academic tertiary care emergency department his home. He is passionate about, consults and lectures on the interface of clinical quality, leadership and team culture – and is dedicated to developing EM leaders for the future of our specialty and the transformation of healthcare. He loves anything outdoors, enjoys blogging on various life and leadership topics; http://www.bretnicksmd.com/blog, and recently published his first book.

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Please replace “iEM Education Project Team” below with the author(s) surname and initials.

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References

  1. Rice MM. Strategies for clinical team building: the importance of teams in medicine. Emergency Department Leadership and Management: Best Principles and Practice. 2014 Nov 27:47
  2. Rozovsky, Julia. “The five keys to a successful Google team. 2015.” URL: https://rework. withgoogle. com/blog/five-keys-to-a-successful-google-team (2015).
  3. Yeung JH, Ong GJ, Davies RP, Gao F, Perkins GD. Factors affecting team leadership skills and their relationship with quality of cardiopulmonary resuscitation. Crit Care Med. 2012;40(9):2617-2621. doi: 10.1097/CCM.0b013e3182591fda
  4. Clapper TC, Kong M. TeamSTEPPS®: The patient safety tool that needs to be implemented. Clinical Simulation Nursing. 2012;8(8):367-373
  5. Vazquez CE. Successful work cultures: recommendations for leaders in healthcare. Leadersh Health Serv (Bradf Engl). 2019;32(2):296-308. doi:10.1108/LHS-08-2018-0038
  6. Babiker A, El Husseini M, Al Nemri A, et al. Health care professional development: Working as a team to improve patient care. Sudan J Paediatr. 2014;14(2):9-16. 

Free online resources for further self-learning

  1. CanadiEM Frontline Primer, Emergency Department Culture 101. https://canadiem.org/canadiem-frontline-primer-emergency-department-culture-101/
  2. Rozovsky J. The five keys to a successful Google team. 2015. URL: https://rework.withgoogle.com/blog/five-keys-to-a-successful-google-team/
  3. Lencioni P. The 5 Dysfunctions of a Team. Teamwork 5 Dysfunctions | The Table Group
  4. Pocket Guide: TeamSTEPPS https://www.ahrq.gov/teamstepps/instructor/essentials/pocketguide.html
  5. Podcast; Dr. Randy Sorge with Dr. Ryan Stanton, Teamwork makes the dream work – Team Dynamics in the ED. https://music.amazon.com/podcasts/816785e7-0c23-47c0-96f4-38017c4b11ba/episodes/6a12c8fd-71f1-4b64-8274-ea72e4189fe3/acep-frontline—emergency-medicine-teamwork-makes-the-dream-work—team-dynamics-in-the-ed

Reviewed By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Discharge Communications (2023)

Discharge Communications
~ iEM Education Project Team ~ Leave a comment

by Dominique Gelmann, Bret Nicks

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Introduction

The process of emergency department (ED) discharge provides critical information for patients regarding the next steps of their care. Discharge instructions are often required by hospital accreditation and governmental organizations for quality or monitoring metrics. However, studies show that many patients do not fully understand or recall the instructions they receive [1,2]. In addition to patient-specific factors contributing to lack of comprehension and care compliance, the myriad situational challenges inherent to every emergency department as well as individual clinician skills and knowledge of best discharge practices further impact patient experience, understanding, and subsequent outcomes.

In many instances, the discharge process is often limited to a brief exchange of documents, prescriptions, and verbal description of the diagnosis, frequently leaving patients with uncertainty about their care plan. Understanding discharge instructions can be very challenging for a variety of reasons. Physical or emotional discomfort can impact receptiveness to and comprehension of imparted information, for example. Patients or family members eager to leave may be less interested in the instructions; conversely those presented with a devastating diagnosis may be less able to process specific details.

Moreover, a significant number of patients have low literacy and/or health literacy levels. In addition, the busy ED setting may distract the patient’s attention from such instructions. Understanding the challenges surrounding discharge communications in the ED from the patient’s perspective and having a clear approach and purpose is essential. Much more critical than an afterthought, discharge is the first step of a patient’s care transition and greatly impacts quality outcomes, litigation, experience, and team morale [3,4]. 

Understanding the Challenges

Emergency physicians face unique challenges while ensuring high-quality care due to distractions and time limitations that are common throughout ED settings. In most cases, emergency physicians have little or no previous knowledge of their patients and are unlikely to partake in the follow-up process, making effective communication paramount when patients are discharged from the ED.  Providing clear and consistent communication throughout the entire patient care encounter, including the discharge process, is an important aspect of quality and patient-centered emergency medical care.

Unfortunately, many patients are discharged from the ED with an incomplete understanding of the information needed to safely care for themselves at home or when to promptly return to the ED [1, 5-6]. Patients have particular difficulty comprehending post-ED care instructions regarding medications, home care, and follow-up expectations.  And while all patients discharged from the emergency department should be provided instructions for ongoing management of their medical condition, studies demonstrate that patient recall and understanding of diagnosis, treatment, and follow-up plan are generally quite poor [1,2,5-9].  This raises significant concerns for care plan adherence and medical outcomes, which studies show are poorer in cases of low health literacy.  Given current trends toward value-based care and the fact that nearly half of the lawsuits in emergency medicine revolve around discharge instructions and plans, ongoing improvements in the discharge communication process is essential [3,4].

While some of this relates heavily to the ability of the provider to establish a trusting and positive patient-provider relationship within the ED constraints, several additional strategies can be used to enhance the recall of instructions, improve compliance, and minimize litigation.

Discharge Essentials

Effective discharge communication provides an opportunity for the emergency department team to summarize a patient’s visit, teach them how to safely care for themselves at home, and provide specifics regarding the next steps in their care process. It also gives ED physicians a chance to address any remaining questions or concerns, often augmenting patient and family understanding while improving care plan retention.  Although patient education at discharge typically begins with initial assessments and conversations with patients and family, other factors can also influence the success or failure of how information is transmitted at discharge.

Common interventions promoting an effective ED discharge process include using a standardized approach to relaying content, providing various modes of information delivery and tailoring them to the individual patient, confirmation of comprehension, post-discharge care follow-up planning, review of vital signs, and a patient-centered closure (Table 1) [8,9].

Table 1: Interventions in the ED Discharge Process

Domain

Intervention

Content

Standardize approach

Delivery

Verbal instructions (language and culture appropriate)

 

Written instructions (mindful of lower literacy levels)

 

Basic Instructions (including return precautions)

 

Media, visual cues, or adjuncts

Comprehension

Confirm comprehension (teach-back method)

Implementation

Resource connections (Rx, appointment, durable medical supplies, follow-up)

 

Medication review

Content refers to the education provided to our patients related to their ED testing, procedures, and treatment, as well as further education on diagnosis, expected course of illness, post-ED treatment and follow-up plan, and medication reconciliation. Instructions should specifically highlight time-sensitive next steps in care plans, including when and how to schedule follow-up appointments with whom and why. Further, emergency physicians should assist in arranging critical follow up prior to discharge as able.  Precautions regarding when to return to the ED versus waiting for any follow-up appointments should additionally be provided, as well as instructions for how to care for oneself until follow-up. These basic tenants of discharge, often described as the ‘rules of the road’ (Table 2), may serve as a basic framework for the discharge process.

Table 2: Rules of the Road for Successful Discharge

  1. Have the right diagnosis
  2. Time & Action Specific Instructions
    • What to do
    • When to do it
  3. Provider Specific
    • Who to contact
    • Why and When
    • Printed Information
    • Verbally explained
    • Verbally confirmed

In addition to the content itself, the importance of the quality and approach of its delivery cannot be overstated. The ED provider and care team members must consider the wide range in literacy, health literacy, cultural backgrounds, and access to outpatient resources when delivering the ongoing care instructions [6,7]. In many instances, EDs attempt to improve patient and family understanding of discharge instructions through standardization and simplification of written and verbal instructions. Due to literacy variability, current literature recommends instructions are written at a late elementary educational level [10]. Verbal discussions in conjunction with written instructions have been shown to be superior to written instructions alone [11]. For patients with a primary language differing from that of the clinician, use of interpreter services, when available, has been shown to improve quality of discharge communication and clinical understanding [12]. Other approaches that may benefit patient outcomes include providing supplemental written information and using visual and multimedia adjuncts to support understanding [8,9].

Essential to any successful approach is the comprehension of the patient regarding all of the information provided. After all, if the content and delivery are exceptional but the comprehension is poor, this should be seen as a discharge failure as it decreases care compliance and outcome quality.  To address this specific aspect of the discharge process, instituting a read-back or teach-back method is recommended. This method involves asking the patient to repeat back their understanding of the information imparted, which allows the physician to identify any remaining gaps in understanding and provide additional instruction as needed.

The implementation of discharge care processes frequently falls short due to unidentified social and medical factors that prevent the plan from being carried out.  Social factors could include homelessness, low income, uninsured/underinsured status, lack of transportation, or lack of primary care.  Medical factors could include concurrent psychiatric illness, substance abuse, cognitive impairment, inability to care for self, or young/advancing age. Understanding these circumstances will help identify patients at high risk for discharge complications and trigger additional resource considerations for these patients.

The discharge process provides an opportunity to ensure the patient’s condition is well understood, that no additional medical red flags need to be addressed, and that the care plan and follow-up are well understood. In an online video, Dr. Oller provides another process to engage the ‘moment of safety‘ related to discharge and outlines 5 essential steps (Table 3) for any ED discharge [13].

Table 3: ED Discharge: Moment of Safety
  1. Has the medical provider discussed the findings, diagnosis and plan of care (including medications and follow-up plan)?
  2. Confirm the discharge instructions and prescriptions match the patient identifiers
  3. Review all prescriptions and clarify any changes
  4. Review current vital signs
  5. Provide closure

Barriers to Successful Discharge

The barriers to successful discharge are myriad.  Some are intrinsic to the ED work environment and nature of emergency department patient arrival and flow.  Others relate to the challenging or often unidentified social and medical factors that prevent the plan from being completely carried out.  In a recent American College of Emergency Physician Quality Improvement and Patient Safety section meeting, Dr. Pham shared a conceptual framework for understanding the barriers to success and improving the discharge process (Figure 1) [14].

Figure 1: Barriers to Successful ED Discharge

While this framework may not be uniformly representative of all EDs, it addresses many of the operational failures that occur outside of the ED and outlines opportunities for hospitals and health systems to align for improved patient care outcomes.  And while screenings for high-risk discharges in EDs occur, the additional resources needed to ensure appropriate social work or case management care coordination are often limited.

Post-discharge follow-up processes for patients at risk for failing discharge instructions exist in some systems. This may include flagging a patient’s chart for a social work follow-up to assess and assist with the patient’s ability to obtain necessary medications, make and attend follow-up appointments, or address other concerns identified by the provider. Some physician groups routinely call patients the next day to see how the patient is doing and ensure understanding of their discharge instructions and care plan [7,8].

Types of Discharge Information Packets

Discharge instructions vary widely by practice location and resources available. However, there remain 3 primary means of providing discharge information and instruction: a basic care instruction note, a preformatted illness specific instruction sheet, and a templated software-based discharge product [8].

Commonly used, an instruction note is simply a set of instructions handwritten or typed on plain paper, without the assistance of computer programs. In settings with limited resources, this may be the only means of providing essential care information for the patient, their family, and the provider with whom they may follow-up. While uniquely tailored, they may lack substantial content for care, take time to prepare, and be limited by literacy and handwriting.

Information sheets are pre-printed education and instruction documents that describe care information related to one specific illness. They can be developed for the most common medical illnesses for each institution and have essential information regarding plans of care.  Information sheets are immediately available, inexpensive, reproducible, and can be designed to include simple language and or pictorial education.   They are not patient specific, may not provide adequate instruction in difficult or complicated cases, and require computer, printer, and copying capacity.

For settings with an integrated EHR, software products that create discharge packets (including discharge diagnoses, medications, medical care instructions and information regarding the illness, outlined care course after leaving the ED, and essential contact information for those next steps) are available.  These are highly resource dependent and therefore may not be routinely available.

Each form of written discharge materials offers its own unique benefits and drawbacks. Regardless of type utilized, physicians should exercise the basic principles outlined above in ensuring appropriate readability and quality of information provided. While specific details are helpful and important, distilling instructions into a short, high-yield sheet has been shown to be more effective than providing a large stack of superfluous [information] that patients may not entirely review [15].

Leave Against Medical Advice and Elopement

In certain circumstances, patients may request to leave prior to completion of their medical evaluation and treatment. In this situation, it is essential for the last health care professional caring for the patient to clearly document why the patient left and attest that the patient had the mental capacity to make such a decision at that time. While some electronic documentation systems have templates in place to assist with this documentation, Table 4 provides basic information for against medical advice (AMA) discharge documentation that can be used to create a uniform template [3,4,16,17].

Table 4: Documentation for Patients Leaving Against Medical Advice

Component

Description

Capacity

Establish a patient’s decision-making capacity, and clarify aspects of care which may affect capacity (i.e. patient is now clinically sober, etc.)

Risks

Specific condition-associated risks that were discussed (missed diagnosis, potential harms from untreated disease process, etc.)

Verify comprehension

Patient’s understanding of the risks

Patient’s decision

Include the patient’s decision, and any alternative plans (i.e. patient refused admission, but agreed to follow up with the primary physician tomorrow)

Signatures

Patient’s and provider’s signatures

An attempt should be made to provide the patient with appropriate discharge instructions, even in the event that a complete diagnosis may not yet be determined.  Include advice for the patient to follow up with their own physician, strict return precautions, and concerning symptoms that should prompt the patient to seek further care. In addition, it should be made clear that leaving against medical advice does not prevent the patient from returning to the emergency department for further evaluation if their symptoms worsen or if they change their mind about receiving care.  Despite a common notion to the contrary, AMA discharge does not automatically provide the emergency physician with immunity from potential medical liability [16,17]. In the event that a patient lacks decision-making capacity to adequately understand the rationale and consequences of leaving AMA and their condition places them at risk for imminent harm, involuntary hospitalization is warranted and often legally required depending on the location of practice.  In unclear circumstances and if available, a psychiatrist can assist in determining capacity, especially in the case of patients with mental health conditions.

Elopement is a similar process in which patients disappear during the care process. While it is difficult to provide discharge paperwork for these patients, documenting the actions taken to find the patient is essential (e.g. searching the ED, having security check the surrounding areas).  In addition, clinicians should attempt to reach the patient by phone to discuss their elopement and any additional care issues or concerns. Documentation of these attempts or any additional conversation is critical in mitigating legal risks [3,4].

Conclusion

Discharge instructions are a very important part of the emergency department care process and record.  It is essential to ensure each patient has a complete understanding of their instructions in order to promote care compliance and improve transitions in care. Verbal instructions remain more effective than written instructions, but both are needed and a multimodal approach to relaying information is preferable to a single modality. Be explicit, keep it simple, and have the patients repeat back instructions to ensure understanding. These simple steps will improve patient outcomes and compliance, and help clinicians avoid medical and legal pitfalls.

Authors

Picture of Dominique GELMANN

Dominique GELMANN

Dominique Gelmann is an Emergency Medicine resident at Wake Forest University. Her interests include patient-physician communication and health literacy. During medical school she completed a one-year research and leadership fellowship investigating health literacy as a social determinant of health, and helped author an institutional white paper with actionable strategies for improving health literacy education. She has given several lectures on the topic to various audiences, and developed a curriculum on health literacy and best-practice patient-provider communication principles for a free student-run health clinic. She looks forward to continuing strengthening her passion for this work throughout her career.

Picture of Bret NICKS

Bret NICKS

Bret Nicks, MD, MHA is an emergency physician that embraces the breadth of our specialty. He is a Professor and Executive Vice Chair of Emergency Medicine at Wake Forest University School of Medicine. He is the past president of the North Carolina College of Emergency Medicine. He served as the Chief Medical Officer of the award-winning Wake Forest Baptist Davie Medical Center. Dr. Nicks served as the founding Associate Dean for the Wake Forest Office of Global Health. He has lived, practiced, and led in many resource austere locations globally, although calls the academic tertiary care emergency department his home. He is passionate about, consults and lectures on the interface of clinical quality, leadership and team culture – and is dedicated to developing EM leaders for the future of our specialty and the transformation of healthcare. He loves anything outdoors, enjoys blogging on various life and leadership topics; http://www.bretnicksmd.com/blog, and recently published his first book.

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Cite This Article

Please replace “iEM Education Project Team” below with the author(s) surname and initials.

[cite]

2018 version of this topic – https://iem-student.org/discharge-communications/

References

  1. Clarke C, Friedman SM, Shi K, et al. Emergency department discharge instructions comprehension and compliance study. CJEM 2005 Jan;7(1):5-11.
  2. Clark PA, Drain M, Gesell SB, et al. Patient perceptions of quality in discharge instruction. Patient Educ Couns. 2005 Oct;59(1):56-68.
  3. Henry GL, Gupta G. (2013). Medical-Legal Issues in Emergency Medicine. In Adams (Ed.), Emergency Medicine Clinical Essentials, 2nd Ed; 1759-65. Philadelphia, PA: Elsevier.
  4. Siff JE. (2011). Legal Issues in Emergency Medicine. In Tintinalli’s (Ed.), Emergency Medicine, 7th Ed; 2021-31. McGraw-Hill.
  5. Crane JA. Patient comprehension of doctor-patient communication on discharge from the emergency department. J Emerg Med 1997;15:1–7
  6. Engel KG, Buckley BA, Forth VE, et al. Patient Understanding of Emergency Department Discharge Instructions: Where Are Knowledge Deficits Greatest? Acad Emerg Med 2012; 19(9):1035-1044.
  7. Sameuls-Kalow ME, et al. Unmet Needs at the Time of Emergency Department Discharge. Acad Emerg Med. 2015 Dec 18.
  8. Taylor DM, Cameron PA. Discharge instructions for emergency department patients: what should we provide? J Acad Emerg Med. 2000; 17:86-90.
  9. Zeng-Treitler Q, Kim H, Hunder M. Improving Patient Comprehension and Recall of Discharge Instructions by Supplementing Free Texts with Pictographs. AMIA Annu Sympo Proc 2008:849-853.
  10. Choudhry AJ, Baghdadi YM, et al. Readability of discharge summaries: with what level of information are we dismissing our patients? Am J Surg. 2016 Mar; 211(3): 631–636. PMID: 26794665.
  11. Al-Harthy N, Sudersanadas KM, Wagie AE, et al. Efficacy of patient discharge instructions: A pointer toward caregiver friendly communication methods from pediatric emergency personnel. J Family Community Med. 2016 Sep-Dec; 23(3): 155–160. PMID: 27625582.
  12. Gutman CK, Cousins L, Gritton J, et al. Professional interpreter use and discharge communication in the pediatric emergency department. Acad Pediatr. 2018;18(8):935–943. PMID: 30048713.
  13. Oller C. Discharge Moment of Safety. Available at: https://www.youtube.com/watch?v=xuLjBWkfomE Accessed January 30, 2016.
  14. Pham JC, Ijagbemi M. Improving the ED Discharge Process. ACEP. Available at: http://www.acep.org/content.aspx?id=90940 Accessed January 15, 2016.
  15. DeSai C, Janowiak K, Secheli B, et al. Empowering patients: simplifying discharge instructions. BMJ Open Qual. 2021 Sep; 10(3).
  16. Levy F, Mareiniss DP, Lacovelli C. The Importance of a Proper Against-Medical-Advice (AMA) Discharge. How Signing Out AMA May Create Significant Liability Protection for Providers.  J Emerg Med. 2012;43(3):516-520.
  17. Devitt PJ, Devitt AC, Dewan M. An examination of whether discharging patients against medical advice protects physicians from malpractice charges. Psychiatr Serv. 2000;51:899-902.

Reviewed By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, vice-chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Shock (2023)

Shock
~ iEM Education Project Team ~ Leave a comment

by Joseph Ciano

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You have a new patient!

A 55-year-old male enters your Emergency Department with sudden onset of shortness of breath with chest pain. He states his symptoms began several hours ago, and he is now feeling generally weak and dizzy. Vital signs on initial assessment are: 125 beats/min, 86/40 mmHg, 24 breaths/min, 37.5°C, and 93% SpO2 on room air. You are concerned by the patient’s vital signs and begin to organize your medical team for treatment of the patient.

What do you need to know?

Importance

Shock is a true emergency. Shock has a wide array of clinical causes (e.g., sepsis, hemorrhage, pulmonary embolism), categories, and different hemodynamic physiologies. The mortality rate of untreated shock is high, but it varies depending on the specific cause and type of shock. For example, the mortality rate of septic shock is 26% and is almost 50% for cardiogenic shock [1]. This means that rapid identification and treatment of shock matters in order to improve outcomes.

Epidemiology

Because shock has many different causes and no single accepted test for diagnosis, it is difficult to measure its prevalence accurately. The different causes of shock may also vary across different country contexts. A systematic review defining shock as a systolic blood pressure under 90 mmHg estimated 0.4-1.3% of patients arrive at the Emergency Department in shock [2]. Other studies have shown variable rates among the different shock categories, but the obstructive shock is typically the least common type of shock [3,4].

Pathophysiology

Shock is a state of circulatory collapse where the body is unable to adequately perfuse tissues to meet the body’s metabolic demands. Shock is characterized by global hypoperfusion and hypoxia. The four major categories of shock are hypovolemic, distributive, cardiogenic, and obstructive shock. Each category of shock has differences in hemodynamics, causes, and treatments. If left untreated, shock will lead to multiorgan system dysfunction and failure.  Shock is often associated with hypotension (systolic blood pressure under 90 mmHg), but shock can occur with a “normal blood pressure”. For example, a systolic blood pressure of 100-120 mmHg in conjunction with other signs and symptoms could be considered a relative hypotensive state and indicate shock in a chronically hypertensive patient. The chart below summarizes the different types of shock.

Type of shock

Hemodynamics

Potential causes

Potential treatments

Hypovolemic

↓preload

↑SVR

↓CO

Dehydration, vomiting/diarrhea, burns, hemorrhage (GI bleed, traumatic wound, etc.)

IV fluids

Blood products (if due to hemorrhage)

Distributive

↓preload

↓SVR

↓/↑CO

Sepsis, anaphylaxis, adrenal insufficiency, neurogenic shock

IV fluids +/- antibiotics and vasopressors.

Treat underlying cause.

Epinephrine (anaphylaxis)

Norepinephrine (sepsis or neurogenic)

Phenylephrine (neurogenic)

Cardiogenic

↑preload

↑SVR

↓CO

Heart failure, tachy/bradyarrythmias, myocardial infarction, valve failure, myocarditis, cardiomyopathy,

beta-blocker overdose

Dobutamine or Epinephrine

Treat underlying cause

Obstructive

↓preload

↑SVR

↓CO

Tension pneumothorax, cardiac tamponade, pulmonary embolism

IV fluids

Treat underlying cause.

Tension Pneumothorax–

Needle decompression then tube thoracostomy

Cardiac tamponade-Pericardiocentesis then pericardial window

Pulmonary embolism-Anticoagulation, consider thrombolytics or surgical embolectomy

(CO= Cardiac Output; SVR= Systemic Vascular Resistance)

Medical History

Key questions to ask on history-taking

Since shock has a multitude of causes, the patient’s history helps us identify shock and guides us in determining the underlying cause. Certain nonspecific presenting symptoms, such as generalized weakness, syncope, or altered mental status, can be seen in all types of shock as these symptoms indicate hypoperfusion. History-taking should be symptom based and also include review of the past medical history, past surgical history, medications, allergies, and drug or alcohol use. The mnemonic “OPQRST” (Onset of symptoms, Provoking/Palliating factors, Quality, Radiation, Severity, Timing) can be used to assist in gathering symptom-based information from the patient.

Being able to narrow down the potential causes will help decide which laboratory and imaging investigations to order and what initial treatments are indicated. Suggestions for key questions to ask are illustrated in the table below. 

Type of shock

Presenting symptoms that may indicate shock

Key questions to ask based on cause of shock

Hypovolemic

Weakness

Syncope

Altered mental status

Vomiting/diarrhea

Hematemesis

Hematochezia/Melena

Burn injury

Trauma/fall

Dehydration

  • Last PO intake? Diuretic usage? Recent travel?

 

Vomiting/diarrhea

  • How many times? Presence of blood? Recent travel? Fevers?

 

Hemorrhage (GI bleed, traumatic wound, etc.)

  • How much blood loss? Any anticoagulant use?

 

Distributive

Weakness

Syncope

Altered mental status

Fever, chills

Cough

Difficulty breathing

Dysuria

Lip/tongue swelling

Rash

Sepsis

  • Fevers, cough, dyspnea, dysuria, skin changes, headaches, neck stiffness, chest or abdominal pain?

 

Anaphylaxis

  • Known inciting factor or allergies? Angioedema?

 

Adrenal insufficiency

  • Steroid use? Medication changes? TB history?

 

Neurogenic shock

  • Spinal trauma? Focal weakness/numbness?

 

Cardiogenic

Weakness

Syncope

Altered mental status

Chest pain

Back or shoulder pain

Palpitations

Difficulty breathing Orthopnea

Peripheral edema

Heart failure, Cardiomyopathy, Valve failure

  • Medication changes? Chest pain? Body edema or dyspnea?

 

Tachy/bradyarrythmias

  • Syncope? Palpitations/heart fluttering?

 

Myocardial infarction

  • Chest or back pain? Diaphoresis?

 

Obstructive

Weakness

Syncope

Altered mental status

Difficulty breathing

Chest pain

Penetrating chest trauma

Unilateral leg pain/edema

Tension pneumothorax

  • Chest trauma?

 

Cardiac tamponade

  • Chest trauma? History of renal disease, HIV, or cancer history?

 

Pulmonary embolism

  • Sudden onset dyspnea or chest pain? Leg pain or swelling? Use of hormones? Recent travel, hospitalizations, or surgeries? Cancer history?

 

Identifying “red flags”

Shock can sometimes be subtle without marked hypotension or tachycardia, so it is important to be vigilant for red flags detected on history-taking to aid in early identification.  Some red flags include altered mental status or confusion, syncope, or chest pain. These symptoms may indicate hypoperfusion of the brain or heart and can point towards shock. Belonging to a special patient group, such as an elderly or neonatal patient, an immunosuppressed patient, or a pregnant patient, may be associated with a more atypical presentation of shock or less favorable patient outcomes.  

Physical Examination

Key physical exam features

Shock is a state of global hypoperfusion, so many physical exam features will reflect this (e.g., delirium, comatose state, tachypnea, etc.). However, shock exists along a continuum of severity and is impacted by patient age, medications, comorbidities, the cause of shock, and other factors. Hypotension and tachycardia are often regarded as key findings of shock, but these vital sign changes may not be present on initial examination depending on where the patient is in the timeline of their shock, as well as other factors described above. For this reason, it is important to look at the combination of the patient’s physical exam findings, rather than a single finding to assist in the diagnosis of shock [1]. Refer to the chart below for physical exam findings seen in shock.

shock - physical exam findings chart

Identifying “red flags”

Similar to patient history-taking, it is important to identify “red flags” during physical examination to aid in the early identification and treatment of shock. Some red flags on physical examination include hypotension with a MAP below 65mmHg, severe bradycardia, low urine output, delirium or altered mental status, and angioedema of lips or tongue [5]. A MAP below 65mmHg indicates severe hypoperfusion that requires prompt aggressive intravenous fluid or vasopressor administration. Bradycardia below 45bpm in shock may indicate poor cardiac output and a lack of physiologic ability to increase cardiac output properly in a shock state. Low urine output and altered mental status are signs of renal and cerebral hypoperfusion, respectively. Angioedema can occur in anaphylactic shock and can pose an acute airway emergency.

Alternative Diagnoses

Shock can have a variety of causes and clinical presentations that can range from the subtle to the severe. Determining the patient’s type of shock and specific diagnosis responsible for the shock state is dependent on details from the patient history, physical exam, and diagnostic testing (discussed more in next section). See the chart below for a list of differential diagnoses for the different categories of shock. Use this table in conjunction with the tables provided in the previous sections to assist in differentiating shock types and causes.

Shock Type

Differential diagnosis 5,6

Hypovolemic

  • GI losses (gastroenteritis, colitis, fistulas)
  • Skin burns
  • Renal losses (excess diuretic use, diabetes insipidus)
  • Hemorrhage (e.g., GI bleed, traumatic wound, aortic aneurysmal rupture, ruptured ectopic pregnancy, coagulopathy, etc.)

Distributive

  • Sepsis
  • Anaphylaxis
  • Adrenal insufficiency (primary vs secondary causes)
  • Thiamine deficiency (beriberi)
  • Pancreatitis
  • Thyroid storm
  • Toxins (salicylates, cyanide, carbon monoxide)
  • Neurogenic shock (trauma, spinal anesthesia)

Cardiogenic

  • Tachyarrhythmia or bradyarrhythmia
  • Left ventricular failure/Cardiomyopathy
    • Ischemic (myocardial infarction)
    • Nonischemic (postpartum, Takotsubo, myocarditis, myocardial contusion,
  • Ca channel/beta-blocker overdose, autoimmune)
  • Valve dysfunction
    • Endocarditis, post MI papillary muscle rupture, prosthetic valve problem
  • LV outflow obstruction
    • Hypertrophic obstructive cardiomyopathy (HOCM), aortic stenosis
  • Device malfunction (ECMO, Ventricular assist device)

Obstructive

  • Tension pneumothorax
  • Cardiac tamponade
  • Pulmonary embolism
  • Auto PEEP (“breath stacking”) in obstructive lung disease patient

Acing Diagnostic Testing

There is no single diagnostic test to rule in or rule out shock. The diagnosis of shock is based on a constellation of diagnostic test results in combination with the history and physical exam of the patient. Whenever possible, diagnostic testing should be based on the presumed cause of shock (e.g., CT pulmonary angiogram for pulmonary embolism, EKG for myocardial infarction, etc.). The table below summarizes different bedside tests, laboratory tests, and imaging tests to consider ordering in patients with shock.  Rational and use behind these tests is discussed in more detail in sections that follow the table.

Bedside tests

Laboratory tests

Imaging tests

  • EKG
  • Point of care testing, if available (pregnancy, glucose, arterial or venous blood gas testing)

 

  • Serum lactate
  • CBC with differential
  • Serum chemistry (BUN, creatinine, electrolytes)
  • Hepatic function panel
  • Coagulation studies
  • Type and screen
  • Venous or arterial blood gas testing
  • Cultures (blood, urine, wound)
  • Pregnancy test
  • Urinalysis
  • Cortisol level
  • Chest X-ray
  • CT of chest/abdomen/pelvis as supported by history + physical
  • Ultrasound (lung, heart, abdomen)

 

Bedside Tests

The EKG is a basic screening test helpful in all shock patients to assess for cardiac dysrhythmias, myocardial infarction, or EKG interval disturbances from medication overdoses. The EKG is clearly valuable in potential cardiogenic shock patients, but it is also helpful in obstructive shock (e.g., low voltage QRS in cardiac tamponade, EKG changes in pulmonary embolism).

Point of care pregnancy testing can help rule out a ruptured ectopic pregnancy.  Glucose testing screens for hypoglycemia which can be seen in septic shock, GI losses with decreased oral intake, and adrenal insufficiency. Point of care blood gas testing can aid in the assessment of the patient’s acid-base and blood gas status which can assist in immediate therapeutic decisions at the bedside. 

Laboratory Tests

Lactate is a common test ordered and trended in shock.  Lactate is a nonspecific marker for poor perfusion and anaerobic metabolism. An elevated lactate >2mmol/L can occur in all types of shock as it indicates poor perfusion, but it does not necessarily mean the patient has a diagnosis of shock. Increasing lactate levels have been associated with increased mortality in many shock types [1].

CBC and type and screen testing are helpful in hemorrhagic shock to measure hemoglobin and prepare for the need for blood product transfusion. The CBC can assess the white blood count which can be helpful in septic shock, especially when trended overtime. Serum chemistry, a hepatic function panel, and coagulation studies screen for signs of end-organ damage (e.g., acute kidney injury, transaminitis (“shock liver”), coagulopathy, etc.).

Blood gas testing is valuable as a screening test in any type of shock to evaluate acid-base and blood gas balance. Urinalysis testing and cultures, blood cultures, and wound cultures do not change management in the emergency department, but they are helpful in identifying sources of infection in septic shock which can be utilized to make antibiotic therapy more targeted as part of the patient’s larger plan of care. Cortisol testing can be beneficial in making the diagnosis of adrenal insufficiency.

Imaging Tests

The chest X-ray is another basic screening test that can be performed as a portable test in the unstable shock patient.  The chest X-ray screens for pneumonia (septic shock), cardiomegaly (cardiogenic and obstructive shock), tension pneumothorax (diagnosis should be made clinically prior to X-ray), pulmonary edema (cardiogenic shock), hemothorax (hemorrhagic shock), amongst other relevant findings.

CT imaging can be used to identify the source of infection or bleeding in septic and hemorrhagic shock, respectively.  However, it should be used after reviewing the risks and benefits in an unstable shock patient.  For example, CT imaging may involve the patient travelling to a less monitored setting outside of the emergency department with less resources and tools for resuscitation.  Contrast-induced nephropathy is another risk to consider when ordering CT imaging with IV contrast in shock patients who likely have hypo-perfused kidneys.  Conversely, CT imaging can lead to a definitive diagnosis (e.g., acute appendicitis, retroperitoneal bleed, ruptured spleen, etc.) that can direct management [1].

Ultrasound is an incredibly valuable bedside diagnostic modality in shock.  Ultrasound can be used to determine the patient’s type of shock through a physiologic assessment of the heart, lungs, and abdomen.  Specific diagnostic information that can be gathered by ultrasound includes the cardiac ejection fraction, presence of a large pericardial effusion with right ventricular compression (cardiac tamponade),  right ventricular dilation (may indicate pulmonary embolism), Inferior vena cava (IVC) dilation or collapse, presence of abdominal free fluid in trauma (hemoperitoneum), abdominal aortic aneurysm presence, absence of bilateral lung sliding (pneumothorax), pulmonary edema (cardiogenic shock if diffuse, infectious if localized), and pleural effusions (infectious or hemothorax depending on the historical context). Organized ultrasound protocols exist that aim to assess these body systems in an algorithmic manner.  One example is the RUSH protocol (Rapid Ultrasound for Shock and Hypotension) [1,5]. This protocol can be executed using the curvilinear (abdominal) or phase-array (cardiac) probe.  Operator competency is needed to obtain meaningful diagnostic data from bedside ultrasound, but with practice and education, proficiency can be achieved.  See the images below for a visual representation of the RUSH protocol and a summary of ultrasound findings in the different types of shock [5,7].

Ultrasound findings in shock

Risk Stratification

Since shock has many potential causes and clinical presentations, there is no single risk stratification tool that is broadly applicable to all types of shock.  There are some tools available to assist in early diagnosis of sepsis by identifying risk factors, like the SIRS criteria (Systemic inflammatory response syndrome criteria) and qSOFA score (Quick sequential organ failure assessment score) [8]. These scores are not specific and can be “positive” in conditions other than sepsis, like diabetic ketoacidosis or severe anxiety.  The shock index measurement is another tool that takes into account heart rate and systolic blood pressure to identify occult shock, especially in trauma or acute hemorrhage. A shock index above 0.5-0.7 may point towards occult shock in the presence of normal vital signs [9].   

Shock is ultimately a clinical diagnosis, so clinical assessment of the patient with the history, physical exam, and diagnostic test results are often used in combination with the clinical picture to predict risk.  Clinical factors that may be associated with poorer outcomes are high serum lactate levels not responsive to fluid resuscitation, severe acidosis, low MAP, elderly and neonatal patient populations, and immunosuppressed patients [1,5,8]. 

Management

Initial management in unstable patients

Management of the shock patient starts with the primary survey, or the “ABCs” (Airway, Breathing, Circulation).  The primary survey is an algorithmic approach used for ill patients to help organize patient assessment, identify life-threatening conditions quickly, and treat time sensitive conditions. 

Airway (“A”)

Establishing a definitive airway may be needed to prevent aspiration or as the precursor to mechanical ventilation for respiratory failure.  Listen for any gurgling sounds or poor effort in phonation that may indicate a risk for aspiration.  Since shock is a state of hypoperfusion, many patients may have poor cerebral perfusion, somnolence, and require an invasive airway.  Positive pressure ventilation and many pre-intubation sedation medications can cause hypotension, so strongly consider initiating volume resuscitation or vasopressors to improve hemodynamics prior to performing intubation [1]. 

Assess for any obvious external swelling of the face, lips, or tongue, which may occur in anaphylaxic shock.  Although this angioedema should improve with prompt epinephrine administration, airway management is sometimes needed.  Look for tracheal deviation which can occur in tension pneumothorax.  Be sure to consider cervical spinal fracture and provide a rigid cervical collar for spinal immobilization in the presence of trauma.

Breathing (“B”)

Assistance in respiration is sometimes needed in the shock patient due a primary pulmonary cause of shock (e.g., septic shock due to pneumonia), respiratory compensation for lactic acidosis, or respiratory changes due to toxic overdoses causing shock (e.g., distributive shock from salicylate overdose).  Noninvasive positive pressure ventilation, such as BIPAP or CPAP, or invasive mechanical ventilation with intubation may be required to manage work of breathing and respiratory failure.

Circulation (“C”)

Shock is a state of systemic hypoperfusion, so a key part of treatment often involves some type of volume resuscitation.  Most commonly this involves administration of crystalloid fluids (e.g., normal saline, lactated ringers solution) or blood products.  If the specific type or cause of shock is unclear after assessment of the patient, start with administration of small volume boluses of fluids with frequent reassessments.  A 250-500mL crystalloid fluid bolus is a reasonable initial intervention in the undifferentiated shock patient.  Fluid should be administered rapidly over 5-20minutes to a total of 20-30mL/kg, depending on the cause of shock [1]. Balanced isotonic crystalloid fluids, like lactated ringers solution, may provide a small mortality benefit over normal saline, especially if large volumes of fluid administration are expected [1]. Large volume administration of normal saline can also cause hyperchloremic metabolic acidosis.   For this reason, if lactated ringers solution is readily available and a cost-effective alternative to normal saline, it may be a worthwhile alternative.  Blood products, rather than crystalloid fluids, should be prioritized if hemorrhagic shock is the assumed cause of shock.

Although volume resuscitation is a crucial component of treatment, caution should be taken in aggressive fluid administration in the presence of cardiogenic shock as this may lead to pulmonary edema.  If the patient remains hypotensive after fluid administration with a MAP below 65mmHg, vasopressors should be initiated [1,5].

Medications

Intravenous crystalloid fluids and blood products are common treatments in shock, but depending on the cause of shock, additional medications may be needed.  Some examples are broad spectrum antibiotics in septic shock, steroids in adrenal insufficiency, or thrombolytics in massive pulmonary embolism with obstructive shock.  See the charts below for a list of adjunctive medications along with their doses and uses.   

Common antibiotics used in shock

Drug name

(Generic)

Potential use

Dose

Frequency

Maximum Dose

Cautions / Comments

Piperacillin-Tazobactam

Intra-abdominal, genitourinary, skin/soft tissue, pneumonia infections, febrile neutropenia

3.375-4.5g

(IV)

Q6 hours

4.5gm IV

Common first line broad spectrum antibiotic in septic shock

Cefepime

Intra-abdominal, genitourinary, skin/soft tissue, meningitis, pneumonia infections, febrile neutropenia

1-2g

(IV)

Q8-12 hours

2gm IV

Common first line broad spectrum antibiotic in septic shock.

 

Similar uses as piperacillin-tazobactam

Vancomycin

Severe bacterial infections, especially MRSA, pneumonia, endocarditis, systemic anthrax, meningitis

15-20 mg/kg/

dose (IV)

Q8-12 hours

3gm IV

Common first line broad spectrum antibiotic in septic shock used in combination with cefepime or piperacillin-tazobactam

Ceftriaxone

Meningitis, pneumonia, UTI, endocarditis, typhoid fever, gonococcal infections, pelvic inflammatory disease

1-2g (IV)

Q24 hours

2gm IV

First line medication for bacterial meningitis in adults, also commonly used for UTIs and community-acquired pneumonia

Ciprofloxacin

UTI, intra-abdominal infections, prostatitis, pneumonia, bone/joint infections, typhoid fever, salmonella/shigella infections

200-400mg

(IV)

Q8-12 hours

400mg IV (1000mg PO)

Can prolong QT interval and increase risk for tendon rupture

Metronidazole

Anaerobic coverage for intra-abdominal infections, Pelvic inflammatory disease, C. difficile

500mg (IV)

Q8-12 hours

500mg IV

(500mg PO)

Causes disulfiram-like reaction with alcohol (avoid alcohol with this medication)

Azithromycin

Community-acquired pneumonia, chlamydial infections, COPD exacerbation, MAC treatment, pertussis

500mg then 250mg

(IV)

Q24 hours

500mg IV (1000mg PO)

Can prolong QT interval

Often given IV with ceftriaxone for community acquired pneumonia patients

Common vasopressors used in shock

Drug name

(Generic)

Potential use

Dose

Frequency

Maximum Dose

Cautions / Comments

Norepinephrine (Noradrenaline)

First line vasopressor for most types of shock, especially if loss of vascular tone is primary problem

0.02-1 mcg/kg/min

(IV)

Titrate as needed to maintain MAP >65

See dose

May cause tachyarrhythmia

Epinephrine (Adrenaline)

First line for anaphylactic shock

0.05-2 mcg/kg/min (IV)

0.3-0.5mg (SubQ or IM)

Titrate as needed to maintain MAP >65

See dose

In anaphylaxis, start with 0.3mg subQ/IM dose. This can be repeated every 10min as needed versus starting a continuous infusion.

May cause tachyarrhythmia

Dobutamine

Frequently used in cardiogenic shock due to heavy beta-adrenergic receptor preference

2-20

 mcg/kg/min (IV)

Titrate as needed to maintain MAP >65

See dose

May cause tachyarrhythmia

Phenylephrine

Pure alpha-adrenergic receptor agonist used as a 2nd or 3rd line vasopressor in shock

10-200 mcg/min (IV)

Titrate as needed to maintain MAP >65

See dose

May cause reflex bradycardia and headache

Consider use when tachydysrhythmias are present

Vasopressin

Often used as a 2nd or 3rd line vasopressor after norepinephrine or epinephrine

0.01-0.04 units/min (IV)

Titrate as needed to maintain MAP >65

See dose

Primarily causes vasoconstriction, similar to phenylephrine

Common additional adjunctive medications used in shock

Drug name

(Generic)

Potential use

Dose

Frequency

Maximum Dose

Cautions / Comments

Acetaminophen

Fever or pain

325-1000mg PO or IV

Q4-6 hours

4gm daily

Be careful with dosing this common medication to avoid overdose

Ibuprofen

Fever or pain

200-800mg PO

Q4-6 hours

3200mg daily

Can cause GI upset and increase risk for peptic ulcer disease

Morphine

Moderate-severe Pain

2.5-10mg (IV)

Q2-6 hours

n/a

Risk of respiratory depression, addiction and abuse, hypotension

 

Use naloxone for reversal

Hydrocortisone

Adrenal crisis, vasopressor-refractory hypotension in shock

100-300mg (IV)

Q6-8 hours

1200mg daily for septic shock adjunct

Start at 100mg IV for adrenal insufficiency

 

Taper dose over 5-7 days for septic shock adjunctive treatment

Dexamethasone

Adrenal crisis, vasopressor-refractory hypotension in shock

0.03- 0.15 mg/kg/

day

Q6-12 hours

0.15mg/kg

daily for adrenal insufficiency

Alternative to hydrocortisone

Alteplase

Massive PE with obstructive shock

100mg (IV)

Single dose over 2 hours

100mg

Bleeding is main side effect

Procedures

Some patients in shock may need emergent procedures as part of their treatment plan.  The chart below summarizes relevant procedures that may be encountered in the care of the shock patient.

Indication or Problem

Procedure

Tension pneumothorax

Needle thoracostomy (Followed by tube thoracostomy)

Cardiac tamponade

Pericardiocentesis (Followed by pericardiotomy)

Persistent hypotension despite intravenous fluids with need for prolonged vasopressor administration

Inability to establish IV access in hemodynamically unstable patient

 

Central venous line placement (Triple lumen catheter)

 

 

Inability to establish IV access in hemodynamically unstable patient

 

Intraosseous line placement (or central venous line)

Respiratory failure or inability to protect airway

Endotracheal tube placement (Intubation)

Empyema, hemothorax, or after needle decompression of tension pneumothorax

Tube thoracostomy (Chest tube placement)

Patient reassessment

Reassessment is an important part of management.  The primary survey (“ABCs”) is conducted on initial evaluation of the patient to guide management, but it can be repeated after therapies have started as clinical changes can occur. Fluid administration too rapidly in a patient with cardiac or renal comorbidities may result in pulmonary edema, requiring fluid administration to be halted.  Patients may develop worsening mental status or hypoxemia overtime due to respiratory muscle fatigue, requiring supplemental oxygen or more aggressive airway management.  Complications can develop after procedures, such pneumothorax after internal jugular central venous line placement or re-expansion pulmonary edema after chest tube placement.  These changes in clinical course are only identified if the patient is reassessed after treatment is initiated. 

Bedside ultrasound can also assist in patient reassessment.  A RUSH exam can be repeated or used as a framework to guide sonographic reassessments.  Some examples of pertinent findings on reassessment include pulmonary B-lines after IV fluid administration (alveolar fluid present), the absence of lung sliding (may indicate pneumothorax), or changes in the IVC size after IV fluid administration (a flat IVC may indicate fluid responsiveness) [5,7].  

Special Patient Groups

Pediatrics

Pediatric patients in shock are often well compensated physiologically and may not have hypotension on initial presentation.  For this reason, unexplained tachycardia in the pediatric patient should always raise concern for possible occult or early shock [10]. Hypovolemic shock is the most common type of shock in the pediatric patient population, while obstructive shock is the least common type of shock.  Volume status in infants can be assessed through evaluation of the fontanelles (flat or sunken), the presence or absence of tears, and changes in urine output estimated by the number of wet diapers per day (e.g., less than baseline or baseline) [10]. Similar to adults, shock should be managed aggressively with volume resuscitation with the exception of cardiogenic shock where fluids should be used judiciously and vasopressors used early (e.g., epinephrine).  Septic shock is the most common type of distributive shock in pediatric patients, and volume resuscitation should be aggressive with up to three 20mL/kg fluid boluses given (60mL/kg total) [10]. This should be contrasted with the recommendation of a 20-30mL/kg fluid bolus in adults for most types of shock [1].

Geriatrics

The diagnosis and treatment of shock in geriatric patients may be more challenging due to unique factors associated with this population.  Unlike pediatric patients, elderly patients often do not have a robust physiologic reserve to compensate in a shock state.  Elderly patients often have more comorbidities and take more medications than adults and children which may blunt the tachycardia response or lead to an atypical clinical presentation [11,12]. For example, beta blockers and calcium channel blockers may prevent a tachycardic response in a hypoperfusion state.  Blood pressure may also be “normal” in elderly patients in shock who are chronically hypertensive [11]. For example, blunt trauma patients over 65 years-old with systolic blood pressures below 110mmHg and heart rates above 90 beats/min have an association with an increase in mortality [12]. Elderly patients with sepsis are also less likely to have a fever or leukocytosis than younger adult patients [13]. Do not rely only on vital signs or abnormal investigations to diagnose shock in the elderly patient.

Management of shock in the elderly patient should involve more gentle volume resuscitation with small fluid boluses (e.g., 250-500mL) and frequent reassessments for response or a change in clinical status (e.g., pulmonary edema).  Have a low threshold to start blood products in elderly hemorrhagic shock patients to avoid excess crystalloid fluid administration and volume overload [12]. Consider drug-drug interactions and the impact of baseline comorbidities (e.g., chronic renal insufficiency) when prescribing antibiotics or other therapies for the elderly patient in shock [13].     

Pregnant patients

Pregnant patients have physiologic and hormonal changes that make certain causes of shock more likely than others.  Some common causes of shock to consider in the pregnant patient include pulmonary embolism, hyperemesis gravidarum, peripartum or postpartum hemorrhage, pyelonephritis, and peripartum cardiomyopathy amongst other causes.  

Other pregnancy-related factors include a higher circulating plasma and blood volume in pregnancy, hypercoagulability due to hormonal changes, and risk of vena caval compression by the growing uterus [14]. Volume resuscitation in pregnancy should accommodate for the pregnant patient’s increase in blood and plasma volume. It is recommended that a 50% additional volume of fluids be given to the pregnant patient in shock to account for this [14]. Standard vasopressors administered in shock, like norepinephrine (noradrenaline), dopamine, and vasopressin, may decrease uterine blood flow from vasoconstriction but have limited data on use in pregnancy.  However, these medications are typically given in pregnant shock patients as the benefit of restoring normal maternal perfusion and hemodynamics outweighs any potential risk to the fetus [14]. Treatment of the pregnant shock patient should also incorporate positioning the patient in the left lateral decubitus position.  This avoids compression of the inferior vena cava by the gravid uterus which could reduce cardiac preload [14].

Other patient groups

Other patient groups that may have more nonspecific or atypical findings in shock are immunosuppressed patients, such as those on chemotherapy for malignancies, post-splenectomy patients, post-transplant patients on immunomodulators, or patients on chronic steroid therapy [5,8]. Diagnosing shock in these special patient groups starts with identifying risk factors and keeping occult shock on the differential diagnosis list.  These patient groups should, similar to typical adult patients, receive aggressive and early volume resuscitation, vasopressors when needed, and adjunctive therapies as appropriate (e.g., broad spectrum antibiotics for septic shock). 

When to admit shock patients

All patients with a diagnosis of shock should be admitted due to the high morbidity and mortality associated with shock [1]. Many patients may need to go to a hospital ward with a high level of monitoring, such as an intensive care unit, due to risk of hemodynamic decompensation [1].  Although some causes of shock are “reversible”, such as tube thoracostomy for tension pneumothorax, these patients should be admitted for further monitoring and treatment due to high risk for poor outcomes.

Revisiting your patient

A 55-year-old male enters your Emergency Department with sudden onset of shortness of breath with chest pain. He states his symptoms began several hours ago, and he is now feeling generally weak and dizzy. Vital signs on initial assessment are: 125 beats/min, 86/40 mmHg, 24 breaths/min, 37.5°C, and 93% SpO2 on room air. You are concerned by the patient’s vital signs and begin to organize your medical team for treatment of the patient.

You identify that your patient is hypotensive, tachycardic, tachypneic, and appears to be in a shock state. You quickly perform a primary survey and note that the airway is patent, lungs are clear bilaterally, and distal extremities are cool with bounding pulses. Two large bore peripheral IV lines are placed, comprehensive laboratory investigations are drawn and sent, supplemental oxygen is applied, and 2 liters of normal saline are administered rapidly. 

A 12-lead EKG demonstrates sinus tachycardia without acute ischemic abnormalities. A bedside ultrasound exam shows diffuse pulmonary A lines (no alveolar fluid) with good lung sliding bilaterally, no pericardial effusion, and a dilated inferior vena cava.  The right ventricle appears dilated and hypokinetic. You diagnose the patient with obstructive shock, likely due to massive pulmonary embolism. You rule out tension pneumothorax and cardiac tamponade as alternative diagnoses with your physical exam and bedside ultrasound findings.  Thrombolytics are promptly administered. The patient’s vital signs slowly stabilize, and he is admitted to the medical intensive care unit for continued monitoring and care.

Author

Picture of Joseph CIANO

Joseph CIANO

Dr Ciano is an Emergency Medicine Physician from New York, USA. He completed his Emergency Medicine Residency in Brooklyn, NY and a Fellowship in Global Emergency Medicine in the Northwell-LIJ Health System. He is interested in building the educational infrastructure of EM in countries where Emergency Medicine is not yet recognized as a field and in countries that are in the early stages of this process. He has partnered with international NGOs in Emergency Medicine educational projects and works as a visiting Emergency Medicine faculty member in West Bengal, India. He is excited to collaborate with the other authors of the iEM Education Project to contribute to the world of FOAM-ed.

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2018 version of this topic – https://iem-student.org/shock/

References

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Acknowledgement

The patient image was created with the assistance of DALL·E 2 by iEM editorial team.

Reviewed By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, vice-chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.