Category: Shock

Sepsis (2024)

~ iEM Education Project Team ~ Leave a comment

by Tina Samsamshariat, Ardeshir Kianercy, & Elizabeth DeVos

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You Have A New Patient!

A 75-year-old female with a history of diabetes, hypertension, and tobacco use disorder is brought to the emergency department by her granddaughter due to increasing confusion. The patient was diagnosed with influenza two weeks ago by her primary care physician. Yesterday, she began to complain of a productive cough and shortness of breath. Her current medications include lisinopril, metoprolol, and metformin.

Upon examination, the patient is oriented only to herself. Her blood pressure is 94/48 mm Hg, heart rate is 128 beats per minute, respiratory rate is 30 breaths per minute, and her temperature is 39°C. Oxygen saturation is 88% on room air. The physical exam shows increased work of breathing, rales, and cool, clammy skin.

The image was produced by using ideogram 2.0.

What Do You Need To Know?

Importance

Sepsis is a critical medical condition that demands urgent attention due to its significant impact on patient outcomes and healthcare systems. Early detection and treatment of sepsis are crucial, as they can substantially reduce mortality rates, treatment delays, and improve appropriate care. In intensive care units (ICUs), sepsis poses a considerable challenge, with its management requiring substantial resources and expertise. Moreover, sepsis has far-reaching consequences beyond immediate patient care, affecting healthcare costs and long-term patient outcomes.

Epidemiology [1-3]

In 2017, there were an estimated 48.9 million incident cases of sepsis and 11 million sepsis-related deaths, accounting for approximately 20% of all global deaths. The global burden of sepsis is challenging to quantify, with low- and middle-income countries bearing the highest burden of cases and deaths. Sepsis can arise from infections in both community and healthcare settings, with diarrheal diseases and lower respiratory infections being the leading contributors to sepsis cases and mortality. Additionally, noncommunicable diseases and injuries significantly contribute to the sepsis burden. Despite these challenges, sepsis is treatable when identified and managed promptly. To address this, the World Health Organization has emphasized the importance of strengthening global efforts in the prevention, identification, diagnosis, and clinical management of sepsis.

Definitions

Term

Definition

 

Sepsis

Life-threatening organ dysfunction from dysregulated host response to infection

 

Organ Dysfunction

An acute change in the total Sequential Organ Failure Assessment (SOFA) score ≥2 points from baseline

 

Septic Shock

Sepsis with circulatory and metabolic abnormalities are profound enough to substantially increase mortality.

SIRS (systematic inflammatory response syndrome)

At least 2 of the following:

  • Heart rate > 90 beats/min
  • Respiratory rate > 20 cycles/min or PaCO2 <32 mm Hg
  • Temperature > 38°C or < 36°C
  • WBC > 12,000/mm3, < 6,000/mm3 or > 10% bandemia

qSOFA (adapted SOFA score tool to assess risk of poor outcome in sepsis):

At least 2 of the following indicates higher rate of mortality:

  • Respiratory rate ≥ 22/min
  • Altered mentation (GCS < 15)
  • Systolic blood pressure < 100 mm Hg

Pathophysiology [3-6]

Sepsis is a syndromic response to infection with biological, biochemical, and physiologic manifestations. The sepsis response exists on a spectrum ranging from infection to septic shock. The definition continues to evolve as the pathophysiology is better understood. The previous definitions of sepsis emphasized at least two of the four SIRS criteria (see Table above). Multiple inflammatory processes can cause SIRS and is not specific to sepsis. The SIRS criteria have been removed from the current definition of sepsis because they do not appropriately capture the life-threatening organ dysfunction critical to the pathophysiology. Thus, severe sepsis, previously defined as sepsis complicated by organ dysfunction, has also been removed because of redundancy.

The newest definition of sepsis goes beyond SIRS to account for the early activation of pro- and anti-inflammatory responses as well modifications in non-immune modulated pathways. Furthermore, it is recognized that the clinical and biological manifestations of sepsis are heterogeneous depending on age, comorbidities, sex, and source of infection. A higher SOFA score is associated with an increased probability of mortality. The quick SOFA or qSOFA has been adapted for rapid bedside assessment of patients with infection, prompting further workup for organ dysfunction. While a positive qSOFA should alert clinicians to possible sepsis, it is not recommended to be used as a single screening tool because of its poor sensitivity. Artificial intelligence (AI) systems alert clinicians to a patient’s risk of sepsis, which may improve patient outcomes compared to traditional methods in hospitals where AI is adopted. The role of machine learning in detecting sepsis continues to be an area of research.

Sepsis progresses to septic shock when a patient displays hypotension requiring vasopressors to maintain MAP ≥65 mm Hg and hyperlactatemia (lactate > 2 mmol/L [18 mg/dL]) after volume resuscitation. Hospital mortality exceeds 40% when septic shock criteria are met.

If patients are suspected to be septic, rapid source identification, assessment, and management of their clinical status is crucial to prevent acute deterioration and progression to septic shock and death.

Medical History [7,8]

Recognizing risk factors for sepsis is important, as they significantly contribute to its incidence and associated mortality.

Key risk factors for sepsis incidence and mortality

  • Intensive care unit admission
  • Hospitalization
  • Vulnerable population: elderly age (age > 65), pregnant or recently pregnant women, neonates, poverty
  • Immunosuppression
    • HIV/AIDS
    • Cirrhosis
    • Asplenia
    • Autoimmune disease
    • Chronic kidney disease
    • Corticosteroids
    • Diabetes
  • Cancer
  • Genetic predisposition
  • Major surgery
  • Burns
  • Alcohol Use Disorder
  • Social factors: access to immunizations, access to timely healthcare

When taking a history from a patient with suspected sepsis, it is crucial to gather comprehensive and relevant information to guide the diagnosis and management. Here are key areas to focus on:

Recent Illness or Infection

  • Ask about any recent symptoms of infection, such as fever, chills, cough, urinary symptoms, or abdominal pain. Determine the duration and progression of these symptoms.

Medical History

  • Inquire about the patient’s past medical history, including chronic conditions like diabetes, heart disease, lung disease, and cancer. These conditions can increase the risk of sepsis and influence the management plan.

Immune Status

  • Determine if the patient has a compromised immune system due to factors such as recent chemotherapy, HIV/AIDS, or use of immunosuppressive medications. This information is vital as these patients are at higher risk of severe infections and sepsis.

Recent Procedures or Hospitalizations

  • Ask about any recent surgeries, hospitalizations, or invasive medical procedures, as these can be sources of infection leading to sepsis.

Current Medications

  • Obtain a list of the patient’s current medications, including antibiotics, immunosuppressants, and any other relevant drugs that might impact the immune response or treatment plan.

Symptoms of Sepsis

  • Look for signs and symptoms suggestive of sepsis, such as:
    • High or low-temperature
    • Confusion or altered mentation
    • Extreme pain or discomfort
    • Shortness of breath
    • Clammy or sweaty skin
    • High heart rate
    • Low blood pressure
    • Rapid breathing
    • Chills
    • Low urine output

Exposure History

  • Ask about any potential exposures to infectious agents, such as recent travel, contact with sick individuals, or exposure to animals that could carry pathogens.

Social and Lifestyle Factors

  • Gather information about the patient’s social and lifestyle factors that might influence their risk for infection or sepsis, such as living conditions, hygiene practices, and any recent illnesses in family members or close contacts.

Physical Examination [2,7-9]

The earliest signs of sepsis often include changes in vital signs and symptoms related to common infectious sources, such as cough, dyspnea, abdominal pain, dysuria, emesis, diarrhea, back pain, oliguria, focal neurological deficits (FND), rash, or skin changes.

Vital sign changes indicative of sepsis, septic shock include a temperature greater than 38.3°C or less than 36°C, tachycardia exceeding 90 beats per minute (or more than two standard deviations above the normal value for age), tachypnea greater than 20 breaths per minute, and arterial hypotension, defined as systolic blood pressure (SBP) less than 90 mmHg, mean arterial pressure (MAP) below 70 mmHg, a decrease in SBP of over 40 mmHg, or values falling more than two standard deviations below the normal range for age.

Signs of end-organ perfusion problems may also be present, including altered mental status, oliguria, ileus, and hypoxemia.

As sepsis progresses to septic shock, decreased capillary refill, cyanosis, and skin mottling may occur due to blood flow being diverted to core organs. In compensated shock, patients may exhibit warm skin with bounding pulses, whereas uncompensated shock is characterized by cool skin and thready pulses.

Figure 1 - Common Physical Exam Findings (Depending on Infectious Source)

Alternative Diagnoses [7-8]

As we mentioned above, SIRS can be caused by various reasons, and it is not specific to sepsis; many non-infectious etiologies should be considered in differential diagnoses; these are;

Shock Causes

  • Distributive shock, Anaphylaxis
  • Hemorrhagic shock
  • Cardiogenic shock
  • Obstructive shock

Cardiac/pulmonary

  • Acute respiratory distress syndrome
  • Pulmonary embolism

Endocrine

  • Adrenal Crisis
  • Pancreatitis
  • Diabetic ketoacidosis

Hematologic

  • Disseminated Intravascular Coagulation
  • Anemia

Other

  • Toxic Shock Syndrome
  • Drug Toxicity

Acing Diagnostic Testing

The diagnosis of sepsis and septic shock is often made at the bedside, integrating the patient’s history, physical examination, laboratory findings, and imaging results. A thorough history and physical examination is essential, considering factors such as medical, social, and travel history, immunization status, and pregnancy. A comprehensive physical exam, including neurologic, oropharyngeal, skin, and genitourinary assessments, is crucial to identify potential sources of infection and guides diagnostic testing.

Sepsis is a complex condition with diverse clinical and laboratory manifestations, requiring a multifaceted diagnostic approach. Laboratory findings in sepsis can reveal critical abnormalities across hematologic, metabolic, and inflammatory markers. Hematologic findings often include leukocytosis or leukopenia, thrombocytopenia, and bandemia (an excess of immature neutrophils, commonly referred to as a “left shift”). Coagulation abnormalities are also frequently observed. Metabolic disturbances can manifest as hyperglycemia (even in the absence of diabetes), elevated creatinine, and hyperbilirubinemia, reflecting multi-organ involvement. Elevated inflammatory markers, such as C-reactive protein (CRP) and procalcitonin, are common, along with hyperlactatemia, which often indicates tissue hypoperfusion and metabolic stress. Other key laboratory findings may include hypoxemia, suggestive of impaired oxygenation or underlying respiratory dysfunction.

While there are no specific imaging findings unique to sepsis, radiologic evaluations can help identify potential sources of infection. For instance, a chest X-ray may reveal pneumonia, abdominal computed tomography (CT) can detect abscesses, and ultrasound is useful for identifying conditions such as cholecystitis. These imaging modalities are critical for localizing infection and guiding targeted therapy.

A critical component of sepsis evaluation involves microbiologic investigations. Blood cultures, ideally obtained before initiating antibiotics, are a cornerstone of diagnostic testing, though they often yield negative results. Sepsis can be caused by a wide range of pathogens, including gram-positive and gram-negative bacteria, as well as fungi. For neonates and pregnant individuals, Group B Streptococcus remains the leading pathogen.

Laboratory investigations should include a complete blood count, comprehensive metabolic panel, coagulation studies, liver function tests, lactate, CRP, and procalcitonin levels. Arterial or venous blood gas analysis can provide additional insights into respiratory and metabolic status. Urinalysis and respiratory viral testing, including for COVID-19, may also be warranted based on clinical presentation. Culture collection, such as blood, urine, sputum, tracheal aspirates, wound swabs, or cerebrospinal fluid (CSF), is essential for pathogen identification, with at least two sets of blood cultures recommended before antibiotic administration.

Imaging studies should be guided by clinical suspicion and patient history. Chest X-rays, CT scans, magnetic resonance imaging (MRI), and ultrasound can help identify the infection’s origin and extent, facilitating more accurate and timely treatment decisions.

The table below shows common sources of sepsis by system, clinical signs, and appropriate diagnostic testing (Original by the authors).

 

System

 

 

Possible Diagnoses

 

Signs / Symptoms

 

Potential Testing

Pulmonary

Pneumonia, Lung Abscess

 

Cough, dyspnea, sputum production, rales, effusion

CXR, lung ultrasound, culture

Skin/Soft tissue

Indwelling Catheters, Cellulitis, necrotizing fasciitis

 

Erythema, warmth, necrosis, pain, petechiae, rash

Site cultures, CT, ultrasound

Intraabdominal           

Cholecystitis, cholangitis, appendicitis, diverticulitis, spontaneous bacterial peritonitis, Clostridium difficile

Abdominal pain, jaundice, nausea, emesis, diarrhea, guarding, rigidity

CT, ultrasound, KUB, stool culture

Cardiac

Endocarditis, myocarditis

Murmurs, history of valve disease

Echocardiogram, blood culture

Genitourinary

Pyelonephritis, urinary tract infection, pelvic inflammatory disease, tuboovarian abscess, endometritis, septic abortion, prostatitis

Dysuria, urinary hesitancy, flank pain, vaginal discharge, genital pain

CT, UA, urine culture, blood culture 

Neurologic

 

Meningitis, cerebral abscess, epidural abscess 

Nuchal rigidity, altered mental status (AMS), FND

CT, CSF culture, MRI

Orthopedic

Osteomyelitis, septic arthritis, indwelling hardware

AMS, pain

XR, CT, culture

Otolaryngologic

Epiglottis, croup, peritonsillar abscess, retropharyngeal abscess, mastoiditis

Stridor, trismus, swelling, temporal bone tenderness

CT, culture

Risk Stratification [9-11]

The severity of sepsis is assessed based on the degree of organ dysfunction. Laboratory findings, vital signs, and physical examination are critical in determining the severity. In the emergency department, clinicians should integrate multiple clinical and laboratory findings to guide the diagnosis. Initial lactate measurements, as well as repeat measurements after initial resuscitation, are essential, particularly if lactate levels exceed 4 mmol/L or if there is suspicion of clinical deterioration. The Sequential Organ Failure Assessment (SOFA) score is a valuable tool for evaluating organ dysfunction.

Clinicians must assess each patient individually, taking into account the type of underlying infection, the degree of hemodynamic instability, the extent of hyperlactatemia, and the presence of signs of end-organ failure. This comprehensive evaluation is crucial for accurately determining the severity of sepsis and guiding appropriate management.

Management [7-9, 12-14]

Immediate Actions in the Emergency Department

Immediate actions in the emergency department are often performed simultaneously:

  1. Stabilize the Airway: Administer supplemental oxygen to maintain oxygen saturation levels at ≥92%.
  2. Cardiac Monitoring: Place the patient on a cardiac monitor to assess rhythm and hemodynamic status.
  3. Intravenous Access: Establish intravenous access and anticipate the need for a central venous catheter and invasive blood pressure monitoring if necessary.
  4. Evaluation for Infectious Source: Perform a thorough assessment to identify potential infectious sources.

Initial Resuscitation

Initial resuscitation in sepsis management focuses on two primary goals:

  1. Restoring Tissue Perfusion
  2. Initiating Antimicrobial Therapy

Restoring Tissue Perfusion

Fluids:

  • Administer rapid IV fluid boluses (500 mL) of balanced crystalloid solutions in patients with hypotension or hypoperfusion, provided there is no evidence of fluid overload.
  • Consider an infusion of 30 mL/kg of balanced crystalloid IV fluids as initial therapy, with careful monitoring of the patient’s response rather than delivering a pre-specified volume.
  • Balanced crystalloid solutions (e.g., Ringer’s Lactate or Plasmalyte) are preferred over saline due to the risk of hyperchloremic metabolic acidosis and renal impairment associated with saline infusions.

Vasopressors:

  • Initiate vasopressor therapy alongside fluid administration if hypotension persists.
  • Norepinephrine is the first-line vasopressor for all patients with septic shock.
  • Vasopressin (0.03 to 0.04 U/min) may be used as an adjunct to norepinephrine.
  • Epinephrine is a second-line agent for patients with ongoing hypotension or myocardial depression.
  • Titrate vasopressors to maintain a mean arterial pressure (MAP) of ≥65 mm Hg.
  • While central access is not mandatory for the early initiation of vasopressors, peripheral access is adequate for initial delivery.

Antimicrobial Therapy

Choice of Antibiotics:

  • Begin broad-spectrum antibiotics targeting both gram-positive and gram-negative bacteria if the pathogen is unidentified.

Timing:

  • Early initiation of antibiotics is strongly associated with improved survival outcomes.
  • Initiate antibiotics within the first hour of presentation, after obtaining necessary cultures. Do not delay antibiotic administration for testing.

Antivirals and Antifungals:

  • Consider antiviral therapy for patients with severe viral infections such as COVID-19, influenza, or herpes simplex virus.
  • Initiate antifungal therapy in high-risk patients when indicated.

Source Control

Early source control is critical in managing sepsis:

  • Identify and treat infectious sources promptly.
  • Remove or drain indwelling catheters and soft tissue abscesses in the emergency department.
  • Obtain cultures of other potentially infected fluid collections, such as pleural effusions or ascites.
  • Consult specialists for managing complex infections, such as hemodialysis lines, biliary obstructions, necrotizing soft tissue infections, or deep abscesses.

Continued Management

Following initial resuscitation, patients should be frequently re-evaluated for clinical, hemodynamic, and laboratory changes. Additional fluids should be administered based on the patient’s response to therapy.

Evaluating Fluid Response:

  • Clinical Parameters: Assess capillary refill, urine output, and mental status.
  • Quantitative Parameters: Use tools such as central venous pressure, passive leg raise tests, or inferior vena cava (IVC) collapsibility on point-of-care ultrasound (POCUS).
  • Tutorials for POCUS may include IVC measurement, IVC collapsibility, and IVC plethora.

Other Treatments

  • Corticosteroid Therapy: Empiric use is generally not recommended unless treating for a coexisting condition.
  • Adjunctive Therapy: Therapies such as angiotensin II (or its analogs), vitamin C, vitamin D, and thiamine are not recommended for routine use in sepsis management.

Special Patient Groups

Pediatrics [15-17]

Sepsis is the leading cause of pediatric mortality worldwide, with common comorbidities including lung disease, congenital heart disease, neuromuscular disorders, and cancer. Compared to adults, pediatric patients have an increased physiological reserve, which can mask signs of clinical deterioration, complicating early recognition and treatment. The current definitions of organ dysfunction and hyperlactatemia in sepsis are primarily based on adult populations and have not been fully adapted to pediatric patients. Pediatric sepsis is still defined as the presence of infection along with at least two out of four systemic inflammatory response syndrome (SIRS) criteria, while pediatric septic shock is characterized by severe infection resulting in cardiovascular dysfunction. Timely management is critical and includes the administration of fluid boluses (40-60 mL/kg), broad-spectrum antibiotics, and prompt infectious source control. However, the use of fluid boluses in resource-limited settings remains controversial. For pediatric septic shock, epinephrine is preferred over norepinephrine as the first-line vasopressor. Additionally, vaccines for meningitis, diarrhea, dengue, and measles are highly cost-effective preventative measures that can significantly reduce the global burden of pediatric sepsis.

Pregnant Patients [18]

Human physiology undergoes significant changes during pregnancy, including expanded plasma volume, increased cardiac output, and peripheral vasodilation, which must be considered when evaluating for sepsis. The most common sources of infection in pregnancy include septic abortion, endometritis, chorioamnionitis, wound infections, urinary tract infections (UTIs), pneumonia, and appendicitis. Common pathogens associated with these infections are Escherichia coli (E. coli), Group A Streptococcus, and Group B Streptococcus. Early initiation of empiric antibiotic therapy is critical to improving outcomes. Initial fluid resuscitation should include 1–2 liters of crystalloid solution, with further fluid management guided by the patient’s preload status, as only 50% of hypotensive septic patients are fluid responsive. Overly aggressive fluid administration may result in edema and increased risk of mortality. Norepinephrine is the first-line vasopressor recommended for septic pregnant patients. The immediate delivery of the fetus is not typically indicated in sepsis; decisions regarding delivery should be individualized. Delays in care or escalation of care are the leading causes of maternal deaths in sepsis, highlighting the importance of prompt and appropriate intervention.

COVID-19 [19,20]

The COVID-19 pandemic has affected millions of people worldwide, with critical cases defined by the presence of acute respiratory distress syndrome requiring ventilation, sepsis, or septic shock. Acute manifestations of severe COVID-19, including significant organ dysfunction, meet the diagnostic criteria for sepsis caused by other pathogens. The pathophysiology of sepsis and COVID-19 share many similarities, making this overlap an ongoing area of research to better understand and manage these conditions.

Geriatrics [21,22]

Sepsis is a significant concern in the geriatric population, characterized by a systemic inflammatory response to infection that can lead to organ dysfunction and increased mortality. Older adults are particularly vulnerable due to age-related physiological changes, comorbidities, and often atypical presentations of infections. Studies indicate that sepsis is a leading cause of morbidity and mortality among older individuals, with a higher incidence of severe outcomes compared to younger populations. Furthermore, the management of sepsis in older adults is complicated by factors such as polypharmacy, cognitive impairment, and frailty, which can hinder timely diagnosis and treatment. Early recognition and prompt intervention are crucial for improving survival rates in this demographic, emphasizing the need for tailored approaches to sepsis care in geriatric patients.

When To Admit This Patient [23,24]

All diagnosed sepsis patients required admission. Admission is critical when they exhibit signs of organ dysfunction, persistent hypotension despite adequate fluid resuscitation, or altered mental status, as these indicators suggest a severe systemic response to infection. The Surviving Sepsis Campaign guidelines recommend immediate admission to an intensive care unit (ICU) for patients with septic shock or those requiring close monitoring and advanced therapies. Additionally, patients presenting with a high risk of deterioration, such as those with significant comorbidities or advanced age, should also be considered for admission to ensure timely intervention and management.

Revisiting Your Patient

She is treated with 1 liter of intravenous Lactated Ringer’s solution, supplemental oxygen, and empiric antibiotics. Laboratory tests are ordered, and a bedside chest X-ray (CXR) shows right upper lobe consolidation. The patient is diagnosed with sepsis secondary to bacterial pneumonia.

Following adequate resuscitation, she is transferred to the intensive care unit for further monitoring. Sputum cultures confirm Streptococcus pneumoniae, and she is started on ceftriaxone. Two days later, she returns to her neurological baseline, and the CXR shows improvement in the consolidation. The patient is transferred to the medical floor for one more day of observation and then discharged home.

Authors

Picture of Tina Samsamshariat

Tina Samsamshariat

Tina Samsamshariat is a graduating fourth year medical school at the University of Arizona College of Medicine – Phoenix. She is pursuing emergency medicine residency at Los Angeles County + University of Southern California. She received her bachelor’s in science at the University of California at Los Angeles and her master’s in public health at the University of Southern California. She completed a pre-doctoral global health fellowship with the National Institutes of Health Fogarty International Center where she was based in Lima, Peru. She is passionate about global health, health equity, and social emergency medicine.

Picture of Ardeshir Kianercy

Ardeshir Kianercy

Picture of Elizabeth DeVos

Elizabeth DeVos

Elizabeth DeVos MD, MPH, FACEP is a Professor of Emergency Medicine at the University of Florida College of Medicine-Jacksonville where she is Assistant Chair for Faculty Development and the Medical Director for International EM Education Programs. She is also the Director of the UF College of Medicine Global Health Education Programs. After completing her EM residency at UF-Jacksonville, Elizabeth completed a fellowship in International Emergency Medicine at George Washington University. She has partnered in the development of EM Specialty Training in several countries, including living and working in Kigali, Rwanda as faculty in the first EM residency. Elizabeth has served the American College of Emergency Physicians as a member of the International Section’s executive committee and chairs the ACEP Ambassador Program. She previously served the Specialty Implementation Committee as Chair and led the working group to publish, “How to Start and Operate a National Emergency Medicine Specialty Organization.”

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References

  1. Rudd KE, Johnson SC, Agesa KM, et al. Global, regional, and national sepsis incidence and mortality, 1990-2017: analysis for the Global Burden of Disease Study. Lancet. 2020;395(10219):200-211. doi:10.1016/S0140-6736(19)32989-7.
  2. World Health Organization. Sepsis. int. Published August 26, 2020. Accessed December 25, 2024. https://www.who.int/news-room/fact-sheets/detail/sepsis.
  3. Gotts JE, Matthay MA. Sepsis: pathophysiology and clinical management. BMJ. 2016;353:i1585. Published 2016 May 23. doi:10.1136/bmj.i1585.
  4. Singer M, Deutschman CS, Seymour CW, et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016;315(8):801-810. doi:10.1001/jama.2016.0287.
  5. Evans L, Rhodes A, Alhazzani W, et al. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock 2021. Crit Care Med. 2021;49(11):e1063-e1143. doi:10.1097/CCM.0000000000005337.
  6. Adams R, Henry KE, Sridharan A, et al. Prospective, multi-site study of patient outcomes after implementation of the TREWS machine learning-based early warning system for sepsis. Nat Med. 2022;28(7):1455-1460. doi:10.1038/s41591-022-01894-0.
  7. Mahapatra S, Heffner AC. Septic Shock. StatPearls Publishing; 2022. Accessed December 25, 2024. https://www.ncbi.nlm.nih.gov/books/NBK430939/?report=reader#_NBK430939_pubdet
  8. Heffner AC, Horton JM, Marchick MR, Jones AE. Etiology of illness in patients with severe sepsis admitted to the hospital from the emergency department. Clin Infect Dis. 2010;50(6):814-820. doi:10.1086/650580.
  9. Angus DC, van der Poll T. Severe sepsis and septic shock. N Engl J Med. 2013;369(9):840-851. doi:10.1056/NEJMra1208623.
  10. Yealy DM, Mohr NM, Shapiro NI, Venkatesh A, Jones AE, Self WH. Early Care of Adults With Suspected Sepsis in the Emergency Department and Out-of-Hospital Environment: A Consensus-Based Task Force Report. Ann Emerg Med. 2021;78(1):1-19. doi:10.1016/j.annemergmed.2021.02.006.
  11. Farkas J. Septic Shock. The Internet Book of Critical Care. Published July 25, 2021. Accessed December 25, 2024. https://emcrit.org/ibcc/sepsis/#rapid_reference.
  12. International Emergency Medicine Education Project. Video 9 Tutorial on Ultrasound of the Inferior Vena Cava [Video]. YouTube. Accessed December 25, 2024. https://www.youtube.com/watch?v=1SMqDeAu6Fc.
  13. International Emergency Medicine Education Project. Video 10 Collapsible and Non-collapsible IVC with Respiration [Video]. YouTube. Accessed December 25, 2024. https://www.youtube.com/watch?v=lIbBPedXnkQ.
  14. The POCUS Atlas. A Plethoric IVC [Video]. YouTube. Accessed December 25, 2024. https://www.youtube.com/watch?v=G8l25aHmZik.
  15. Weiss SL, Peters MJ, Alhazzani W, et al. Executive summary: surviving sepsis campaign international guidelines for the management of septic shock and sepsis-associated organ dysfunction in children. Intensive Care Med. 2020;46(Suppl 1):1-9. doi:10.1007/s00134-019-05877-7.
  16. Kissoon N, Reinhart K, Daniels R, Machado MFR, Schachter RD, Finfer S. Sepsis in Children: Global Implications of the World Health Assembly Resolution on Sepsis. Pediatr Crit Care Med. 2017;18(12):e625-e627. doi:10.1097/PCC.0000000000001340.
  17. Mathias B, Mira JC, Larson SD. Pediatric sepsis. Curr Opin Pediatr. 2016;28(3):380-387. doi:10.1097/MOP.0000000000000337.
  18. Society for Maternal-Fetal Medicine (SMFM). Electronic address: pubs@smfm.org, Plante LA, Pacheco LD, Louis JM. SMFM Consult Series #47: Sepsis during pregnancy and the puerperium. Am J Obstet Gynecol. 2019;220(4):B2-B10. doi:10.1016/j.ajog.2019.01.216.
  19. Koçak Tufan Z, Kayaaslan B, Mer M. COVID-19 and Sepsis. Turk J Med Sci. 2021;51(SI-1):3301-3311. Published 2021 Dec 17. doi:10.3906/sag-2108-239.
  20. Alhazzani W, Evans L, Alshamsi F, et al. Surviving Sepsis Campaign Guidelines on the Management of Adults With Coronavirus Disease 2019 (COVID-19) in the ICU: First Update. Crit Care Med. 2021;49(3):e219-e234. doi:10.1097/CCM.0000000000004899.
  21. Kumar A, et al. Sepsis in the Elderly: A Review. J Geriatr Emerg Med. 2020;21(3):145-153.
  22. Klein MJ, et al. Challenges in the Management of Sepsis in Older Adults. Age Ageing. 2021;50(4):120
  23. Rhodes A, Evans LE, Alhazzani W, et al. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock: 2016. Crit Care Med. 2017;45(3):486-552. doi:10.1097/CCM.0000000000002255.
  24. Weinberg J, et al. The impact of comorbidities on sepsis outcomes: a systematic review. J Crit Care. 2018;47:238-244. doi:10.1016/j.jcrc.2018.07.002

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.

Upper Gastrointestinal Bleeding (2024)

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by Resshme Kannan Sudha & Thiagarajan Jaiganesh

Authors
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You have a new patient!

A 55-year-old male with alcoholic liver cirrhosis was brought to the emergency department by his wife, presenting with two episodes of haematemesis (containing fresh blood) and light-headedness. This is the first occurrence of such symptoms. Vital signs: Temperature: 36.8°C, Heart Rate: 115 bpm, SpO₂: 95%, BP: 88/65 mmHg. On examination, the patient appears pale, lethargic, and jaundiced, with abdominal distension noted.

The image was produced by using ideogram 2.0.

What do you need to know?

Upper gastrointestinal (GI) bleeding is defined as bleeding occurring above the level of the ligament of Treitz. It is more common than lower GI bleeding [1]. Upper GI bleeding is a significant clinical condition that can lead to morbidity and mortality if not promptly diagnosed and managed. It encompasses bleeding from the esophagus, stomach, or duodenum, often presenting as hematemesis or melena. The importance of recognizing and treating upper GI bleeding lies in its potential to indicate serious underlying conditions. Early intervention is crucial, as the severity of bleeding can lead to hypovolemic shock, necessitating urgent medical care. Upper GI bleeding is a common emergency, with an estimated incidence of 50 to 150 cases per 100,000 individuals annually [2]. The prevalence varies based on demographic factors such as age, gender, and geographical location. The condition is more prevalent in older adults, particularly those over 60 years.

The most common cause is peptic ulcer disease, with duodenal ulcers being the most frequent. Other causes include varices, erosive esophagitis, duodenitis, Mallory-Weiss tear, gastrointestinal malignancies, and arterial and venous malformations (e.g., aorto-enteric fistula, Dieulafoy lesion) [1,3]. Causes of peptic ulcer disease include NSAID (Non-Steroidal Anti-inflammatory Drug) intake, Helicobacter pylori infection, and stress ulcers. In recent years, the incidence of upper gastrointestinal bleeding admissions due to peptic ulcer disease has decreased in the USA. This trend has been attributed to the use of triple therapy for Helicobacter pylori and the co-administration of proton pump inhibitors with NSAIDs [4].

Clinical manifestations include vomiting coffee ground material or fresh blood, and/or passing fresh blood in the stool or black, tarry stool (melena) [1].

Goals in the management of a patient with upper gastrointestinal bleeding include identifying the site and nature of the bleeding, stabilizing the patient, and controlling the source of the bleed [4].

Medical History

After performing a primary survey and stabilizing the patient, it is important to fine-tune your history, physical examination, and investigations to identify the source of bleeding and guide further management and disposition.

Upper GI bleeding commonly presents with haematemesis (coffee-ground or fresh blood), haematochezia, and/or melena [4]. Certain foods, such as beets, and medications like cefdinir, can cause red-colored stool, while bismuth and iron supplements may cause black-colored stool [4].

Associated Symptoms
  • Peptic ulcer disease may be associated with epigastric pain (gastric ulcer) and dysphagia, gastroesophageal reflux disease (GERD), or odynophagia (esophageal ulcer).
  • Haematemesis associated with retching may indicate a Mallory-Weiss tear.
  • The presence of jaundice and ascites suggests variceal bleeding [4].

A prior history of GI bleeding should be assessed, as patients are more likely to bleed from the same lesion.

Key Past Medical History and Risk Factors

Peptic Ulcer Disease:

  • Ulcers can occur in the esophagus, stomach, or duodenum, with duodenal ulcers being more common.
  • However, gastric ulcers account for a higher incidence of bleeding.
  • Known causes include Helicobacter pylori, NSAIDs, alcohol, and steroid use.
  • Symptoms may include epigastric pain, nausea, vomiting, upper GI bleeding (painless haematemesis and melena), and signs of anaemia.
  • Upper GI bleeding after NSAID use, stress, or a history of dyspepsia may indicate erosive gastritis [5,6].

Esophageal Varices:

  • Caused by portal hypertension secondary to liver diseases such as cirrhosis.
  • Symptoms include jaundice, spider angiomata, palmar erythema, hepatic encephalopathy (confusion), coagulopathy (petechiae/purpura), ascites, and variceal bleeding (painless haematemesis with large amounts of fresh blood) [6].
  • Ask about chronic alcohol use, hepatitis, and hepatocellular carcinoma.
  •  

Mallory-Weiss Syndrome:

  • Caused by forceful retching or vomiting, often after heavy alcohol intake.
  • Leads to a tear in the esophagus or stomach, resulting in haematemesis (large amounts of fresh blood).
  • This condition is usually self-limiting [6].

Malignancy:

  • Gastric cancers may present with haematemesis, anaemia, and dyspepsia [6].
  • Enquire about sudden weight loss, loss of appetite, and risk factors like prior Helicobacter pylori infection.

Angiodysplasia:

  • Dieulafoy’s disease is a rare vascular malformation affecting young individuals.
  • It involves small aneurysms in the stomach that rupture, leading to massive spontaneous haematemesis [6].

Aorto-enteric Fistula:

  • A rare condition, usually occurring post-repair of an abdominal aortic aneurysm.
  • Presents with profuse haematemesis and rectal bleeding [6].

Gastro-enteric Anastomosis:

  • Ulcers may develop at the site of gastro-enteric anastomosis, presenting with upper GI bleeding [7].
Comorbid Illnesses

Enquire about conditions such as:

  • Ischemic heart disease or pulmonary conditions (higher haemoglobin levels required).
  • Coagulopathies (may necessitate additional therapies).
  • Dementia or hepatic encephalopathy (risk of aspiration due to altered mental state).
  • Heart failure or renal failure (risk of fluid overload during blood transfusion).
Medication History

Assess for [8]:

  • NSAIDs (associated with peptic ulcers).
  • Anticoagulants and antiplatelets.
  • Chemotherapeutic agents.
  • Iron supplements (black stool).
Symptoms of Severe Bleeding and Poor Prognosis [1,4,7,9]
  • Light-headedness, confusion, syncope (cerebral hypoperfusion).
  • Chest pain and palpitations (coronary hypoperfusion) .

Physical Examination

The severity of bleeding should be assessed based on clinical signs of shock rather than the color of the blood [4]. Upper GI bleeding typically presents with haematemesis (frank blood or coffee-ground emesis) and/or melena [4]. In cases of brisk upper GI bleeding, the patient may present as vitally unstable with haematochezia [4].

Vital Signs

Monitor for signs of hemodynamic instability, including:

  • Tachycardia, tachypnea, and hypotension [1,7].
  • Supine hypotension is associated with greater blood loss than orthostatic hypotension [1].

General Examination

  • Confusion may indicate hemodynamic instability.
  • Gynecomastia may be seen in patients with liver disease [10].
  • Haematemesis strongly suggests an upper GI bleed [4].

ENT Examination

  • Inspect the nose for epistaxis, which can present as haematemesis if the blood is swallowed [11].

Skin Examination

  • Palmar erythema, spider angiomata, caput medusae, and jaundice are suggestive of liver disease [11].

Abdominal Examination

  • Abdominal tenderness, guarding, rigidity, and rebound tenderness may indicate perforation.
  • The presence of ascites suggests liver disease [4,7].

Rectal and Stool Examination

  • A digital rectal examination and stool analysis can help identify the location of the bleed:
    • Melena typically indicates an upper GI bleed.
    • Haematochezia may suggest a lower GI bleed or a massive upper GI bleed [4].

Alternative Diagnoses

The differential diagnosis for gastrointestinal bleeding includes several conditions that may mimic an upper or lower GI bleed:

  1. Epistaxis: Bleeding from the nose can present as haematemesis if the blood is swallowed. Careful examination of the nasal cavity is essential to rule this out.

  2. Vaginal Bleeding: In some cases, vaginal bleeding can be mistaken for haematochezia. A thorough history and physical examination can help differentiate these sources.

  3. Food-Induced Discoloration: Certain foods may alter the color of stool, leading to a false suspicion of GI bleeding. For example, beets can cause red-colored stools, which may mimic haematochezia.

  4. Medication-Induced Changes: Some medications can also discolor stool:

    • Cefdinir may produce red-colored stool.
    • Iron supplements and bismuth-containing products can result in black stool, resembling melena [4].

  5. Neonatal Swallowed Blood: In neonates, vomiting swallowed maternal blood during delivery or breastfeeding may be mistaken for upper GI bleeding [12].

Acing Diagnostic Testing

Bedside Tests

Several bedside tests can aid in the initial evaluation of upper GI bleeding:

  • Point-of-care venous blood gas: Useful for detecting acidosis, electrolyte disturbances, and haemoglobin levels. Haemoglobin levels < 8 g/dL in previously healthy patients, or < 9 g/dL in patients with known coronary artery disease or anaemia-related complications, suggest the need for blood transfusion [4].
  • Point-of-care PT (Prothrombin Time) and INR (International Normalized Ratio): Essential for patients taking medications like warfarin to determine the need for reversal agents.
  • Bedside ultrasound: Helpful in identifying ascites, which may aid in diagnosing variceal bleeding.
Ascites in Cirrhotic Patient

Laboratory Tests

The following blood tests are useful when there is a clinical suspicion of upper GI bleeding [4,6,11,13]:

  • Complete Blood Count (CBC): To assess haemoglobin and haematocrit levels.
  • Blood Urea Nitrogen (BUN), Creatinine, and electrolytes: A BUN:Creatinine ratio > 35 is highly suggestive of upper GI bleeding (90%).
  • Coagulation Screen: INR levels are important in patients on anticoagulant therapy (e.g., warfarin) to guide reversal strategies.
  • Liver Function Tests: Elevated parameters are suggestive of liver disease and potential variceal bleeding.
  • Type and Crossmatch: Crucial for patients who may require blood transfusion.

Imaging

Radiological imaging is rarely needed in hemodynamically unstable patients as it may delay resuscitation. In such cases, endoscopy should take precedence [4].

  • Upright chest X-ray: Helpful in detecting free air under the diaphragm, which is suggestive of perforation.
  • CT Angiography: Recommended for hemodynamically stable patients when identifying the bleeding etiology before endoscopy is crucial. It can detect slow bleeding (approximately 0.3 mL/min) and guide management decisions (endoscopy, surgery, or angiography). However, it is not suitable for unstable patients due to delays in management. In such cases, conventional angiography with embolization is preferred [4].

Endoscopy

Endoscopy is both diagnostic and therapeutic [14,15]:

  • There is no evidence to support that emergent endoscopy is superior to routine endoscopy.
  • Immediate gastroenterology consultation for emergent endoscopy is advised in patients with ongoing severe upper GI bleeding.
  • Endoscopy is recommended within 24 hours for all admitted patients with UGIB after stabilizing hemodynamic parameters and addressing other medical issues.
  • Patients with high-risk clinical features such as tachycardia, hypotension, haematemesis, or blood in nasogastric aspirate should undergo endoscopy within 12 hours, as this may improve clinical outcomes.

Additional Considerations

  • A screening ECG is recommended in patients > 35 years of age with cardiac risk factors, as co-existing acute coronary syndrome may complicate GI bleeding [4].
  • Nasogastric lavage is generally not recommended due to risks of perforation, pneumothorax, and aspiration [4].
  • Erythromycin can be used as an alternative prokinetic to clear gastric contents before endoscopy [4,8].

Risk Stratification

To effectively manage gastrointestinal (GI) bleeding, patients must be categorized into high-risk and low-risk groups. High-risk patients require prompt intervention, whereas low-risk patients can be managed through outpatient treatment [4]. A combination of clinical, endoscopic, and laboratory features, along with risk scores, can aid in risk stratification. While risk scores may not always predict high-risk patients accurately, they are effective in identifying patients at very low risk of harm. When selecting patients for outpatient management, ensuring high sensitivity is essential to prevent the inadvertent discharge of high-risk individuals [16].

Risk Assessment Tools

Commonly used scoring systems for GI bleeding include:

  1. Glasgow-Blatchford Score (GBS)
  2. Rockall Score
  3. AIMS65 Score

The AIMS65 score assesses parameters such as:

  • Albumin < 3 mg/dL
  • International Normalized Ratio (INR) > 1.5
  • Altered mental status
  • Systolic blood pressure < 90 mmHg
  • Age > 65 years

Studies show that the GBS is more effective at predicting a combined outcome of intervention or death [16].

Glasgow-Blatchford Score (GBS)

The Glasgow-Blatchford Score is particularly useful for predicting the need for intervention, hospital admission, blood transfusion, surgery, and mortality. A significant advantage of the GBS is that it can be calculated at the time of patient presentation, as it does not require endoscopic data (unlike the Rockall score).

The GBS includes the following parameters:

  • Blood urea nitrogen (BUN)
  • Haemoglobin levels
  • Systolic blood pressure
  • Pulse rate
  • Symptoms such as melena, syncope, and a history of hepatic disease or cardiac failure.

The score ranges from 0 to 23, with a higher score indicating a greater risk of requiring endoscopic intervention [4].

Glasgow-Blatchford Risk Score

CategoryScore
BUN in mg/dL
18.2 to 22.42
22.5 to 283
28.1 to 704
70.1 or greater6
Hemoglobin, men g/dL
12 to 131
10 to 11.93
9.9 or less6
Hemoglobin, women g/dL
10 to 121
9.9 or less6
Systolic Blood Pressure, mmHg
100-1091
90-992
<903
Heartrate >100 peats per minute1
Melena1
Syncope2
Hepatic Diseases2
Heart failure2
Glasgow-Blatchford Risk Score is useful for predictive of inpatient mortality, blood transfusions, re-bleeding, ICU monitoring, and hospital length of stay. Patients with a score of zero may be discharged home, those with score 2 or higher are usually admitted, and those with score of 10 or more are at highest risk for morbidity and resource utilization. Maximum score is 23.
Outpatient Management

Patients with a Glasgow-Blatchford Score of 0 are considered at low risk for rebleeding. According to international consensus guidelines, these patients may be safely discharged with early outpatient follow-up [8,17].

Management

Initial Stabilization

Airway and Breathing:
Patients with massive upper GI bleeding presenting with uncontrollable haematemesis, respiratory distress, or severe shock require immediate airway protection and intubation. It is essential to improve hemodynamic status before administering induction and paralytic drugs for intubation and initiating positive pressure ventilation, as this can mitigate a sharp decrease in cardiac output. However, intubation is associated with poor outcomes and should only be performed when absolutely necessary [4].

Circulation:
Massive GI haemorrhage is characterized by ongoing active bleeding (haematemesis or haematochezia), signs of hemodynamic compromise (e.g., tachycardia, hypotension, altered mental status), or a shock index ≥ 0.9 [4].

Immediate volume resuscitation is critical and includes:

  • Placement of two large-bore IV catheters.
  • Infusion of balanced isotonic crystalloids (e.g., 2 liters of normal saline or Plasmalyte over 30 minutes).
  • Transfusion of uncrossmatched blood, if required [4].
Transfusion Strategies

For stable patients, a restrictive transfusion strategy is recommended. While the ideal haemoglobin target is not universally defined:

  • In stable patients without known coronary artery disease (CAD), maintain haemoglobin ≥ 8 g/dL.
  • For patients with known CAD, a higher target of ~9 g/dL is appropriate to reduce the risk of anaemia-related complications [4].

In patients requiring massive transfusion (more than 4 units of PRBCs), a balanced transfusion ratio of 1:1:1 (PRBC:Platelets:Fresh Frozen Plasma) is advised. Cryoprecipitate should be administered if fibrinogen levels remain < 1.5 g/L [18]. A platelet count > 50,000 platelets/μL should be maintained [4].

Coagulation Management
  • Vitamin K antagonists (e.g., warfarin) should be stopped and reversed to achieve a target INR of 1.5–2.5. Treatment options include Fresh Frozen Plasma (FFP) and Prothrombin Complex Concentrate (PCC). Vitamin K is an appropriate choice for hemodynamically stable GI bleeding.
  • Direct oral anticoagulant reversal:
    • Idarucizumab for dabigatran reversal.
    • PCC or coagulation factor Xa (recombinant/inactivated-zhzo) for factor Xa inhibitors.
  • For heparin reversal, protamine sulfate may be used.

Before administering reversal agents, the risks of reversing anticoagulant therapy must be carefully weighed against the risk of thromboembolism [19].

PCC is preferred over FFP for rapid coagulopathy correction, especially in patients at risk of fluid overload, as it requires lower volume administration [4]. Over-transfusion or empiric correction of PT/INR with FFP or PCC in portal hypertension may worsen portal hypertension and exacerbate bleeding [4].

Medications

Proton Pump Inhibitors (PPIs)

PPIs are the mainstay in the management of acute GI bleeding. They work by inhibiting the hydrogen potassium ATPase pump, thereby reducing gastric acid secretion [20]. Studies have shown that PPIs reduce the risk of re-bleeding, the need for surgery, and mortality in patients with bleeding ulcers [4].

Both intermittent PPI therapy and continuous infusion are equally effective in reducing bleeding [8]. Available IV formulations include esomeprazole and pantoprazole. The recommended dose is:

  • Pantoprazole or esomeprazole: 80 mg IV as a single initial dose, followed by either:
    • Continuous infusion at 8 mg/hr, or
    • 40 mg IV BID [8].

If IV formulations are unavailable, oral alternatives such as 40 mg of esomeprazole twice daily may be used [8].

PPIs are classified as Category B in pregnancy, except for omeprazole, which is Category C [21]. Caution should be exercised due to the risk of Clostridium difficile infection, Steven Johnson syndrome, kidney and liver impairment, and pancreatitis [20]. Omeprazole is particularly associated with the risk of acute interstitial nephritis [22].

Somatostatin Analogues

Somatostatin and its synthetic analogue, octreotide, are predominantly used in variceal bleeding. These agents reduce the risk of bleeding, need for transfusion, and portal hypertension. Indications include acute GI bleeding in patients with variceal bleeding, abnormal liver function tests, liver disease, or alcoholism [4].

The dosing regimen for octreotide is:

  • Adults: 50 mcg IV bolus, followed by 25–50 mcg/hr continuous infusion [23,24].
  • Paediatrics: 1 mcg/kg IV bolus (maximum: 100 mcg), followed by 1 mcg/kg/hr infusion [23,24].

Octreotide crosses the placenta and is expressed in breast milk. Common adverse effects include arrhythmias, pancreatitis, abnormal glucose regulation, and low platelet count [23]. It also crosses the blood-brain barrier [23].

Terlipressin

Terlipressin is a synthetic vasopressin receptor agonist that causes splanchnic vasoconstriction, thereby reducing portal hypertension. It is primarily indicated for variceal bleeding [25].

The recommended dose is 2 mg IV every 6 hours [26]. Terlipressin may cause teratogenic effects (limited data available) [27] and can result in painful hands and feet due to peripheral vasoconstriction [26]. While studies suggest that terlipressin, somatostatin, and octreotide have similar efficacy, data regarding their use in paediatric patients remains limited [24,28].

Prokinetic Agents (Erythromycin and Metoclopramide)

Prokinetic agents are used to improve visualization during endoscopy by clearing gastric contents.

  • Erythromycin:

    • Adult dose: 3 mg/kg IV, administered over 20–30 minutes, 20–90 minutes before endoscopy [29].
    • Classified as Category B in pregnancy and is safe for breastfeeding mothers [29].
    • Adverse effects include QT prolongation, pseudomembranous colitis, seizures, and hypertrophic pyloric stenosis [4,29].

  • Metoclopramide:

    • Adult dose: 10 mg IV.
    • Paediatric dose: 0.1–0.2 mg/kg IV [30].
    • Classified as Category B in pregnancy [30].
    • Caution is advised in patients with a history of extrapyramidal symptoms due to its association with extrapyramidal side effects [30].

Tranexamic Acid

Tranexamic acid is an antifibrinolytic agent. However, according to the HALT-IT Trial, it has not been shown to reduce mortality associated with gastrointestinal bleeding. As a result, its routine use in GI bleeding is not recommended [31].

Antibiotic Prophylaxis

Antibiotic prophylaxis is recommended for patients with cirrhosis or suspected cirrhotic liver disease to reduce the risk of infection and mortality [4].

The recommended antibiotics include:

  • Fluoroquinolones (e.g., ciprofloxacin 400 mg IV)

  • Third-generation cephalosporins (e.g., ceftriaxone 1–2 g IV) [4].

  • Ceftriaxone: Classified as Category B in pregnancy but contraindicated in hyperbilirubinemic neonates due to the risk of kernicterus and those receiving IV calcium-containing solutions due to ceftriaxone–calcium precipitation [32].

  • Ciprofloxacin: Classified as Category C in pregnancy. Adverse effects include Clostridium difficile infection, dysglycemia, tendon rupture, neurotoxicity, QT prolongation, hepatotoxicity, and Stevens-Johnson syndrome/toxic epidermal necrolysis [33].

Procedures

Balloon tamponade [4,6,34], using devices such as the Sengstaken-Blakemore tube, Minnesota tube, or Linton-Nachlas tube, can serve as a temporizing measure for suspected life-threatening variceal bleeding when endoscopy is not immediately available. These devices must be stored in refrigerators to maintain readiness.

Before the procedure, patients must be intubated to reduce the risk of aspiration. The device is inserted through the mouth, passed via the esophagus into the stomach. The tube consists of two balloons—a gastric balloon and an esophageal balloon:

  • The gastric balloon of the Sengstaken-Blakemore tube can be inflated with 250–300 cc of air, while the Minnesota tube can accommodate up to 450–500 cc to secure the tube in place.
  • The esophageal balloon can be inflated to a pressure of 20–40 mmHg, with a strict upper limit of 45 mmHg to avoid injury. Pressure should be carefully monitored using a manometer.

Balloon tamponade is a temporary measure, and definitive management, such as endoscopic therapy, should be arranged as soon as possible. The procedure is associated with significant risks, including ulceration, esophageal rupture, and aspiration [4].

Special Patient Groups

Paediatrics

The causes of upper GI bleeding in the pediatric population are generally similar to those seen in adults [12,15,35]. However, there are additional causes specific to neonates and infants that require consideration. In neonates, vitamin K deficiency, also referred to as the haemorrhagic disease of the newborn, is an important cause. Other causes include congenital vascular anomalies, such as telangiectasia, and coagulopathy, which may result from infections, liver disease, or coagulation factor deficiencies. Milk protein intolerance is also a recognized cause of upper GI bleeding in this age group. During the neonatal period and the first few months of life, it is crucial to differentiate swallowed maternal blood from true upper GI bleeding. The Apt-Downey test is a reliable diagnostic tool used to confirm the presence of fetal blood and rule out swallowed maternal blood as the source.

The management of upper GI bleeding in children largely follows the same principles as in adults, with necessary adaptations for the pediatric population. Intravenous proton pump inhibitors (IV PPIs) are effective and can be administered to reduce gastric acid secretion, thereby promoting hemostasis. In cases of suspected variceal bleeding, somatostatin analogues can be given to reduce portal hypertension and minimize bleeding risk. When severe acute bleeding is ongoing, endoscopy plays a key role in diagnosis and intervention. It is recommended that endoscopy be performed within 24 to 48 hours of presentation. However, it is critical to ensure that the patient is as hemodynamically stable as possible before proceeding with the procedure to minimize complications.

In cases where endoscopy cannot control the bleeding or fails to identify the source, further interventions may be necessary. Angiography with embolization is a useful modality in such instances, as it can help detect and address underlying vascular abnormalities contributing to the bleeding. This approach is particularly helpful when other methods have proven unsuccessful.

Overall, a multidisciplinary approach that includes appropriate stabilization, pharmacologic therapy, and procedural intervention is essential to effectively manage upper GI bleeding in the pediatric population [12,15,35].

Geriatrics

Upper GI bleeding in elderly patients presents unique challenges due to the high-risk nature of this population and the limitations of existing risk assessment tools. Studies indicate that traditional pre-endoscopic risk scores, such as the Glasgow-Blatchford and AIMS65, often fail to accurately predict outcomes like mortality and hospital stay length in geriatric patients, particularly those aged 82 and older, suggesting a need for age-adjusted scoring systems [36]. Despite these challenges, emergency oesophagogastroduodenoscopy is generally safe for elderly patients, with a high survival rate at 90 days post-procedure, although a significant proportion of OGDs yield normal findings, highlighting the importance of careful patient selection [37]. The management of Upper GI bleeding in the elderly is further complicated by recurrent bleeding, as seen in cases involving peptic ulcer disease, which necessitate a multidisciplinary approach and close monitoring to improve outcomes [38]. Recent efforts to develop novel risk scores tailored for the elderly have shown promise, with a new score incorporating factors like comorbidity index and blood pressure demonstrating good discriminative performance for identifying patients suitable for outpatient management [39].

Pregnant Patients

The causes of upper GI bleeding in pregnant women are similar to those in the general population, including conditions such as esophageal ulcers, gastroesophageal reflux disease, and portal vein thrombosis leading to esophageal varices [40]. Haematemesis, or the vomiting of blood, is a common manifestation of upper GI bleeding and can present as bright red or coffee-ground emesis, indicating bleeding from the upper gastrointestinal tract [1, 40]. In rare cases, UGIB in pregnancy can be caused by gastrointestinal stromal tumors (GISTs), as illustrated by a case where a pregnant woman presented with coffee-ground vomiting and was diagnosed with a bleeding GIST at the stomach cardia [41]. Endoscopy is a critical diagnostic and therapeutic tool for upper GI bleeding, but its use in pregnant women is generally reserved for severe or persistent cases due to potential risks to the mother and fetus [42]. Despite the need for endoscopic evaluation in over 12,000 pregnant women annually in the U.S., research on the safety and outcomes of such procedures remains limited [43]. Therefore, careful consideration of the risks and benefits is essential when managing upper GI bleeding in pregnant patients.

When To Admit This Patient

Admission is required for elderly patients over the age of 60 years, those who require blood transfusions, and patients with a Glasgow-Blatchford Score (GBS) greater than 0 [4,8]. Patients with high-risk bleeding sources should be admitted to a monitored setting or an intensive care unit (ICU) to allow close monitoring for signs of rebleeding and other potential complications.

The decision to discharge a patient following endoscopy depends on the identification of the bleeding source and the associated risk of rebleeding. Patients can be considered for discharge if they meet all of the following criteria: a GBS of 0, blood urea nitrogen (BUN) less than 18 mg/dL, haemoglobin >13 g/dL in men and >12 g/dL in women, heart rate less than 100 beats per minute, systolic blood pressure greater than 110 mmHg, no evidence of melena or syncope since the initial presentation, absence of heart failure or liver failure, and prompt access to outpatient follow-up care.

However, it is important to note that this recommendation is based on low-quality evidence, and clinical judgment should play a significant role in the final decision to discharge a patient. Clinicians should carefully assess each patient’s overall condition, risk of rebleeding, and ability to follow up in an outpatient setting to ensure safe discharge planning [15].

Revisiting Your Patient

In managing this patient, the immediate priority is to assess airway, breathing, and circulation and provide stabilization. Given the patient’s vital instability, they should be promptly transferred to the resuscitation bay for further management.

The image was produced by using ideogram 2.0.

Airway and Breathing: The patient’s airway is currently patent, and they are communicating comfortably, with no signs of obstruction such as pooling of blood or secretions. There have been no further episodes of haematemesis, and the patient is maintaining adequate oxygen saturation on room air. Chest auscultation is clear. At this time, the patient does not require airway adjuncts or intubation, but close observation is essential to detect any deterioration.

Circulation: The patient is hypotensive, indicating the need for immediate intervention. Two large-bore IV cannulas should be inserted to initiate intravenous fluid resuscitation. Crossmatched and uncrossmatched blood should be arranged as a precaution. A point-of-care venous blood gas test must be performed to quickly evaluate acidosis, haemoglobin levels, and other critical parameters. Care should be taken to avoid fluid overload, especially in patients with underlying liver disease.

Further History and Review of Systems: On further evaluation, the patient denies haematochezia, haemoptysis, epistaxis, melena, chest pain, palpitations, syncope, loss of consciousness, or confusion.

Past Medical and Surgical History and Risk Factors: The patient has a history of alcoholic liver disease and is a smoker. There is no history of chronic NSAID use, Helicobacter pylori infection, recent forceful retching, or ingestion of foods or medications that might cause red-colored secretions. There are no known coagulopathies, recent anticoagulant use, vascular abnormalities, weight loss, or loss of appetite. Additionally, the patient has no history of prior surgery.

Examination: Clinical signs of hemodynamic instability, such as hypotension, suggest hypovolemic shock, requiring prompt management with IV fluids and blood transfusion. Examination findings of jaundice, abdominal distension with shifting dullness, and caput medusae are consistent with alcoholic liver disease and indicate probable variceal bleeding. There is no abdominal tenderness, guarding, rigidity, or rebound tenderness to suggest another abdominal pathology.

Laboratory Investigations: Laboratory tests sent include a complete blood count, urea, electrolytes, creatinine, coagulation screen, liver function tests, and type and crossmatch for transfusion. The point-of-care venous blood gas reveals acidosis, haemoglobin <8 g/dL, negative base excess, and elevated lactate, indicating ongoing active bleeding. These findings necessitate urgent gastroenterology consultation for endoscopic intervention and the arrangement of blood transfusion. In addition, the patient must be monitored for liver disease-induced coagulopathy, and a haematology consultation is warranted.

Diagnostic Test: The patient’s Glasgow-Blatchford Score is greater than 0, further confirming the need for urgent endoscopy to identify and control the source of bleeding, which is most likely esophageal varices. Simultaneously, resuscitation measures must continue.

Medications: Given the patient’s history of alcoholic liver disease and suspected variceal bleeding, appropriate pharmacological management should include vasoactive agents such as somatostatin, octreotide, or terlipressin to reduce portal pressure. Empirical antibiotics (fluoroquinolones or third-generation cephalosporins) should be administered to reduce the risk of infection. Additionally, proton pump inhibitors (PPIs) should be started as part of the management protocol.

Disposition: This patient requires urgent gastrointestinal consultation for endoscopy to achieve source control of the bleeding. Admission is necessary to allow for close monitoring of potential complications, including rebleeding and complications of alcoholic liver cirrhosis, such as hepatic encephalopathy and renal failure.

Authors

Picture of Resshme Kannan Sudha

Resshme Kannan Sudha

Resshme Kannan Sudha graduated from RAK Medical and Health Sciences University and is currently an Emergency Medicine Graduate Resident at STMC Hospital, Al Ain. She is a keen follower of FOAMed projects and an enthusiastic educator. Her special interests include critical care, POCUS, global health, toxicology and wilderness medicine.

Picture of Thiagarajan Jaiganesh

Thiagarajan Jaiganesh

STMC Hospital, Al Ain

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  13. Wilkins T, Wheeler B, Carpenter M. Upper gastrointestinal bleeding in adults: Evaluation and management. American Family Physician. Published March 1, 2020. Accessed March 20, 2023. https://www.aafp.org/pubs/afp/issues/2020/0301/p294.html
  14. Laine L, Barkun AN, Saltzman JR, Martel M, Leontiadis GI. ACG clinical guideline: Upper gastrointestinal and ulcer bleeding. Am J Gastroenterol. 2021;116(5):899-917. doi:10.14309/ajg.0000000000001245
  15. Woodfield A, Donaldson R, Reynolds C, Young N. Upper GI bleeding guidelines. WikEM. Published March 12, 2022. Accessed March 20, 2023. https://www.wikem.org/wiki/Upper_GI_bleeding_guidelines
  16. Stanley AJ, Laine L. Management of acute upper gastrointestinal bleeding. BMJ. 2019;364:l536. Published March 25, 2019. Accessed February 15, 2023. https://www.bmj.com/content/364/bmj.l536
  17. Barkun AN, Almadi M, Kuipers EJ, et al. Management of nonvariceal upper gastrointestinal bleeding: Guideline recommendations from the International Consensus Group. Ann Intern Med. 2019;171(11):805. doi:10.7326/m19-1795
  18. Farkas J. GI bleeding. EMCrit Project. Published September 18, 2021. Accessed April 11, 2023. https://emcrit.org/ibcc/gib/
  19. Gnanapandithan K, Muniraj T. Management of antithrombotics around gastrointestinal procedures. PubMed. Published 2023. Accessed April 11, 2023. https://www.ncbi.nlm.nih.gov/books/NBK553210/
  20. Carmen Fookes B. List of proton pump inhibitors + uses, side effects. Drugs.com. Accessed April 11, 2023. https://www.drugs.com/drug-class/proton-pump-inhibitors.html
  21. Richter JE. Gastroesophageal reflux disease during pregnancy. Gastroenterol Clin North Am. 2003;32(1):235-261. doi:10.1016/s0889-8553(02)00065-1
  22. Reynolds C, Cunningham R, Ostermayer D, Donaldson R, Young N. Omeprazole. WikEM. Updated March 5, 2021. Accessed April 11, 2023. https://wikem.org/wiki/Omeprazole
  23. Ostermayer D, Murray B, Lee E, Donaldson R, Cunningham R. Octreotide. WikEM. Published February 10, 2021. Accessed March 20, 2023. https://wikem.org/wiki/Octreotide
  24. Sandostatin, Sandostatin LAR (octreotide) dosing, indications, interactions, adverse effects, and more. Medscape. Accessed April 11, 2023. https://reference.medscape.com/drug/sandostatin-lar-octreotide-342836
  25. Nickson C. Terlipressin. Life in the Fast Lane. Published January 4, 2019. Accessed April 11, 2023. https://litfl.com/terlipressin/
  26. Tripathi D, Stanley AJ, Hayes PC, et al. UK guidelines on the management of variceal haemorrhage in cirrhotic patients. Gut. 2015;64(11):1691-1692. doi:10.1136/gutjnl-2015-309262
  27. Terlivaz. Medscape. Published July 15, 2024. Accessed December 7, 2024. https://reference.medscape.com/drug/terlivaz-terlipressin-4000107#6
  28. Seo YS, Park SY, Kim MY, et al. Lack of difference among terlipressin, somatostatin, and octreotide in the control of acute gastroesophageal variceal hemorrhage. Hepatology. 2014;60(3):962. doi:10.1002/hep.27006
  29. Donaldson R, Claire, Lee E, Ostermayer D, Holtz M. Erythromycin. WikEM. Published September 22, 2019. Accessed March 20, 2023. https://www.wikem.org/wiki/Erythromycin
  30. Fernando T, Donaldson R, Grove G, et al. Metoclopramide. WikEM. Updated March 7, 2021. Accessed April 11, 2023. https://www.wikem.org/wiki/Metoclopramide
  31. Roberts I, Shakur-Still H, Afolabi A, et al. Effects of a high-dose 24-h infusion of tranexamic acid on death and thromboembolic events in patients with acute gastrointestinal bleeding (HALT-IT): an international randomised, double-blind, placebo-controlled trial. Lancet. 2020;395(10241):1927-1936. doi:10.1016/s0140-6736(20)30848-5
  32. Donaldson R, Shah M, Ostermayer D, Young N, Claire. Ceftriaxone. WikEM. Updated September 19, 2019. Accessed April 10, 2023. https://www.wikem.org/wiki/Ceftriaxone
  33. Donaldson R, Gausepohl A, Janeway H, et al. Ciprofloxacin. WikEM. Updated October 17, 2021. Accessed April 11, 2023. https://wikem.org/wiki/Ciprofloxacin
  34. Balloon tamponade for massive GI bleeding – WikEM. WikEM. Accessed March 23, 2023. https://www.wikem.org/wiki/Balloon_tamponade_for_massive_GI_bleeding
  35. Lirio RA. Management of upper gastrointestinal bleeding in children. Gastrointest Endosc Clin N Am. 2016;26(1):63-73. doi:10.1016/j.giec.2015.09.003
  36. Di Gioia G, Sangineto M, Paglia A, et al. Limits of pre-endoscopic scoring systems in geriatric patients with upper gastrointestinal bleeding. Sci Rep. 2024;14(1). doi:10.1038/s41598-024-70577-2.
  37. McWhirter A, Mahmood S, Mensah E, Nour H, Olabintan O, Mrevlje Z. Evaluating the safety and outcomes of oesophagogastroduodenoscopy in elderly patients presenting with acute upper gastrointestinal bleeding. Cureus. 2023. doi:10.7759/cureus.47116.
  38. Ahmad H, Khan U, Jannat HE. Recurrent gastrointestinal bleeding in an elderly patient with peptic ulcer disease: successful management through multidisciplinary intervention and close monitoring. Cureus. 2023. doi:10.7759/cureus.41468.
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  40. Shahid S, Chandra N. Haematemesis in pregnancy. In: Gastrointestinal Emergencies in Pregnancy. CRC Press; 2015:149-153. doi:10.1201/B18646-36.
  41. Parampalli U, Crossland C, Longley J, Morrison I, Sayegh M. A rare case of gastrointestinal stromal tumour in pregnancy presenting with upper gastrointestinal bleeding. J Gastrointest Cancer. 2012;43(1):80-83. doi:10.1007/s12029-011-9360-3.
  42. Bjorkman DJ. Is endoscopy safe for pregnant women with upper gastrointestinal bleeding. NEJM J Watch. 2011. doi:10.1056/JG201101070000004.
  43. Rabiee A, Moshiree B. Upper and lower endoscopy for gastrointestinal (GI) bleeding in pregnancy. In: Gastrointestinal Bleeding. Springer; 2019:155-164. doi:10.1007/978-3-319-90752-9_12.

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.

Spontaneous Pneumothorax (2024)

~ iEM Education Project Team ~ Leave a comment

by Mohd Fazrul Mokhtar & 
Raja Amir Fikri Raja Sulong Ahmad

Authors
Listen

You have a new patient!

A 24-year-old male with no significant medical history presents to the emergency department for shortness of breath for two days duration. The symptom is associated with left-sided pleuritic chest pain. He denies fever, cough, constitutional symptoms, or trauma. He is an active smoker.

a-photo-of-a-24-year-old-male (the image was produced by using ideogram 2.0)

On assessment, the patient was mildly tachypneic and well-perfused. Auscultation reveals reduced breath sounds over the left lung. There is hyperresonance on percussion over the left lung as well. There is no tracheal deviation. Vital signs are as follows:

Blood pressure – 108/75 mmHg
Pulse rate – 74/minute
Respiratory rate – 24/minute
Oxygen saturation – 98% under room air
Temperature – 36.8o Celcius
Pain score – 4/10

What do you need to know?

Importance

Pneumothorax is defined as the presence of air in the pleural space. Pneumothoraces can be further divided into primary spontaneous pneumothorax (PSP), which occurs in patients spontaneously without any apparent underlying pleural disease, or secondary pneumothorax in patients with underlying diseases such as tuberculosis and lung malignancy [1,2]. Iatrogenic pneumothorax can also occur due to procedures such as thoracocentesis and central venous line insertion [2].

Identifying a pneumothorax is important, as a delay in management can lead to hemodynamic instability. In unstable patients with respiratory and circulatory compromise, the differential diagnosis of tension pneumothorax must be excluded.

Epidemiology

The incidence of primary spontaneous pneumothorax varies significantly between genders. Among the male population, it is reported to occur at a rate of 7.4 to 18 cases per 100,000 individuals annually. In contrast, the incidence in the female population is comparatively lower, ranging from 1.2 to 6 cases per 100,000 individuals per year [1].

Pathophysiology

Under normal circumstances, the pressure in the pleural space is negative compared to atmospheric pressure. This negative pressure is generated due to the opposing forces between the lung’s tendency to collapse because of elastic recoil and the outward expansion of the chest wall [2]. When there is communication between the alveoli and pleural space, the introduction of air alters the gradient until pressure equilibrium is reached, resulting in partial or total lung collapse. Tension pneumothorax occurs when inhaled air accumulates in the pleural space but cannot exit due to a one-way valve mechanism [2].

This condition leads to the clinical presentation of dyspnoea and chest pain. In tension pneumothorax, the increased intrathoracic pressure can decrease venous return and restrict lung function, ultimately leading to shock and hypoxia [2].

Medical History

In patients with a primary spontaneous pneumothorax, mild symptoms may be reported as they often tolerate the consequences of a pneumothorax better compared to those with underlying respiratory problems. The most common symptoms are chest pain and shortness of breath [3].

When inquiring about pain, the SOCRATES mnemonic may be helpful:

  • Site: Pain on the affected side
  • Onset: Usually, sudden onset of pain
  • Character: Typically described as sharp
  • Radiation: Radiation to the ipsilateral shoulder
  • Associated symptoms: Breathlessness
  • Time: Although the onset of pain may be acute, patients may present late if they can tolerate symptoms
  • Exacerbating/relieving factors: Pleurisy (pain worsening on inspiration) is common
  • Severity: Quantify the pain score when possible

Asking about risk factors may also help in strengthening the diagnosis of pneumothorax, including cigarette smoking, male gender, mitral valve prolapse, Marfan’s syndrome, and changes in ambient pressure. It is also important to ask about the history of trauma and recent medical procedures. Family history may be relevant as there may be a genetic predisposition to the condition.

Finally, enquire about the presence of a chronic cough and constitutional symptoms such as weight loss, loss of appetite, and fatigue to help ascertain whether the pneumothorax may be due to an underlying pleural disease.

Physical Examination

When assessing a patient with a potential pneumothorax, examine systematically using the ABC approach to avoid missing potential signs, especially those of a tension pneumothorax, as this condition requires immediate intervention [4].

  • Airway: Tracheal deviation is a late sign of tension pneumothorax, though it is not always indicative.
  • Breathing: Signs include tachypnoea, hypoxia, unequal chest rise, subcutaneous emphysema, hyperresonance, and absent or reduced breath sounds.
  • Circulation: Hypotension (a key sign of tension pneumothorax), tachycardia, and cold peripheries may be present.

Differential Diagnoses

The patients present mostly with shortness of breath (SOB). Therefore, pulmonary, cardiac and other causes of SOB should be considered first.

  • Pulmonary
    • Airway obstruction
    • PE
    • Pulmonary edema
    • Anaphylaxis
    • Asthma
    • Cor pulmonale
    • Aspiration
  • Cardiac
    • MI
    • Tamponade
    • Pericarditis
  • Others
    • Esophageal rupture
    • Toxin ingestion
    • Epiglottitis
    • Anemia

Acing Diagnostic Testing

The diagnosis of spontaneous pneumothorax is confirmed by imaging. After the diagnosis is confirmed, the clinical evaluation, including the history obtained and the patient’s clinical condition, should determine the management strategy.

Chest X-ray

The standard view is the erect PA chest x-ray. However, in a polytrauma patient, when the patient must be kept in the supine position, supine and lateral decubitus views can be performed.

Chest X-ray has been the mainstay diagnostic modality for pneumothorax. Typically, it demonstrates the visceral pleural edge, which appears as a thin, sharp white line. The peripheral space is more radiolucent compared to the adjacent lung (Image 1). A deep sulcus sign can be observed on a supine X-ray (Image 2).

More x-ray images can be found in iEM’s Flickr account – https://www.flickr.com/search/?user_id=158045134%40N08&view_all=1&text=pneumothorax

Image 1: Left pneumothorax. (Image courtesy of Ian Bickle, Radiopaedia.org, rID: 86926)
Image 2: Right pneumothorax with a deep sulcus sign. (Image courtesy of Mohammad Osama Hussein Yonso, Radiopaedia.org, rID: 18975)

A chest x-ray provides information about the size of the pneumothorax and assists in determining the next steps in management.

In a patient with suspected pneumothorax, a chest x-ray should be performed [5]. However, if clinical assessment suggests features of tension pneumothorax (e.g., hypotension, tracheal deviation, distended neck vein), a needle thoracocentesis must be performed first, as a chest x-ray may delay this life-saving intervention.

CT scan

The presence of bullous lung disease can lead to a misdiagnosis of pneumothorax on a chest x-ray. In patients with chronic lung disease who develop bullae, a chest x-ray may show features similar to pneumothorax. Therefore, if uncertainty exists, a CT scan of the thorax is strongly recommended.

More CT images can be found in iEM’s Flickr account – https://www.flickr.com/search/?user_id=158045134%40N08&view_all=1&text=pneumothorax

Image 3: CT scan showing right pneumothorax in a diseased lung. (Image courtesy of David Cuete, Radiopaedia.org, rID: 26570)

CT scan is considered the “gold standard” for detecting small pneumothoraces and is the most accurate method to determine the size of a pneumothorax [6]. However, practical drawbacks, such as limited availability, make it unsuitable as the first imaging modality for diagnosing pneumothorax.

Lung Ultrasound

In the emergency department, a lung ultrasound can be performed at the bedside immediately after a physical examination to evaluate undifferentiated respiratory failure. It is part of the point-of-care ultrasound protocol in emergency settings.

In a lung ultrasound, the normal lung interface with pleura shows lung sliding with Z-lines, which appear as vertical comet tails descending from the pleural surface. In pneumothorax, this sliding and the comet tail artifacts from the pleura are absent. Visualizing the intersection between the sliding lung sign and the absence of sliding is referred to as the lung point, which is nearly 100% specific for pneumothorax [7].

Additional ultrasound findings:

  • Absence of B-lines
  • Cessation of lung pulse (lung oscillation in tandem with cardiac contraction)

On M-mode, the following signs are observed:

  • Seashore sign: Indicates normal lung sliding.
  • Barcode/stratosphere sign: Indicates pneumothorax.

More US images can be found in iEM’s Flickr account – https://www.flickr.com/search/?user_id=158045134%40N08&view_all=1&text=pneumothorax

Image 4- Lung ultrasound showing the seashore sign. (Image courtesy of Srikar Adikhari et al. [2014], ResearchGate)
Image 5- Lung ultrasound showing the Barcode:stratosphere sign. (Image courtesy of Maulik S Patel, Radiopaedia.org, rID- 61141)

Laboratory Tests

ABG is indicated when oxygen saturation is below 90% on room air. It is performed to assess the patient’s oxygenation level, as some patients with pneumothorax may present with hypoxemia [8].

Risk Stratification

Pneumothorax is classified into primary spontaneous pneumothorax (PSP) and secondary pneumothorax (SSP). PSP occurs in healthy patients; hence, it is termed “spontaneous,” while SSP is associated with underlying lung diseases such as chronic obstructive pulmonary disease and pulmonary tuberculosis. PSP patients are typically taller than healthy controls [9-11]. Within the first four years, the risk of recurrence of PSP is as high as 54%, with isolated risk factors including smoking, height, and age above 60 years [10, 12,13]. Age, pulmonary fibrosis, and emphysema are risk factors for the recurrence of SSP [11,13].

Since patients with pre-existing lung diseases tolerate a pneumothorax less well, distinguishing between PSP and SSP at the time of diagnosis is critical for determining the next steps in care. Many patients, particularly those with PSP, do not seek medical attention until several days after their symptoms first appear. Meanwhile, the majority of patients with SSP present with more severe clinical symptoms.

Management

General Principle

Airway

The majority of patients with pneumothorax experience breathing issues rather than airway compromise. However, it is essential to assess the airway and breathing simultaneously.

Breathing

Provide supplemental oxygen with a high-flow mask. Oxygen treatment accelerates the resolution of pneumothorax by lowering the partial pressure of nitrogen in the alveoli relative to the pleural cavity. This creates a diffusion gradient for nitrogen, which hastens recovery.

The diagram from the British Thoracic Society guideline summarizes the management of pneumothorax [14].

[8] MacDuff A, Arnold A, Harvey J Management of spontaneous pneumothorax: British Thoracic Society pleural disease guideline 2010 Thorax 2010;65:ii18-ii31.
Image 6: Measurement of the apex-to-cupola distance and interpleural distance. (Images courtesy of the British Thoracic Society)

When To Admit This Patient

Patients requiring chest tube thoracostomy insertion must be admitted for monitoring and removal prior to discharge home. Those utilizing a pigtail catheter experience fewer complications, shorter hospital stays, and faster time-to-device removal. While many patients will require hospitalization, some can be discharged after a period of observation, aspiration, or with a Heimlich valve in pigtail catheters [14,15].

Revisiting Your Patient

The patient presented to the Emergency Department in a stable condition, showing no signs of respiratory distress, and was initially seen in the non-critical zone. After a chest X-ray confirmed the diagnosis of pneumothorax, the patient was transferred to the resuscitation zone for management and close monitoring.

Image 7 - Left Pneumothorax (image courtesy of Mohd Mokhtar and Raja Ahmad

A systematic assessment and management plan for patients with pneumothorax should prioritize the identification and stabilization of hemodynamically unstable patients.

Airway
There was no airway compromise in this patient, so no intervention was needed. The examination also revealed no tracheal deviation, which decreases the suspicion of a tension pneumothorax.

Breathing
Although the patient did not appear to be in respiratory distress, high-flow oxygen was administered through a non-rebreather mask to expedite the resorption of the pneumothorax.

Circulation
The patient was not in a tension pneumothorax state, as he remained hemodynamically stable. Therefore, he did not require immediate needle decompression or chest drain insertion.

The next step was to decide on the treatment approach. Following the algorithm set out by the British Thoracic Society, needle aspiration is recommended for this patient with a spontaneous pneumothorax, especially since he was experiencing breathlessness.

Needle aspiration is preferred in cases of spontaneous primary pneumothorax, as it is associated with a higher rate of successful discharges and fewer complications. However, if needle aspiration fails, chest drain insertion and admission will be necessary. The failure rate of needle aspiration in cases of secondary pneumothorax is high, which is why chest drains are typically favored in those instances.

Authors

Picture of Mohd Fazrul Mokhtar

Mohd Fazrul Mokhtar

Dr Mohd Fazrul Mokhtar is a Consultant Emergency Physician at Faculty of Medicine Universiti Teknologi MARA, Malaysia. He obtained his postgraduate training in emergency medicine at Universiti Kebangsaan Malaysia. He has special interest in sepsis, medical simulation; and emergency critical care. He is currently the Coordinator of the Clinical Simulation Centre. His research niche includes CPR educational technologies, cardiac arrest and sepsis. He is the council member of Malaysian Sepsis Association and Malaysian Resuscitation Association.

Picture of Raja Amir Fikri Raja Sulong Ahmad

Raja Amir Fikri Raja Sulong Ahmad

I am currently a second year postgraduate trainee in Emergency Medicine in Malaysia. My interests are point of care ultrasound and critical care.

Listen to the chapter

References

  1. Noppen M. Spontaneous pneumothorax: epidemiology, pathophysiology, and cause. European Respiratory Review. 2010;19(117):217-219. doi:https://doi.org/10.1183/09059180.00005310
  2. McKnight CL, Burns B. Pneumothorax. Nih.gov. Published 2019. https://www.ncbi.nlm.nih.gov/books/NBK441885
  3. Aljehani YM, Almajid FM, Niaz RC, Elghoneimy YF. Management of Primary Spontaneous Pneumothorax: A Single-center Experience. Saudi J Med Med Sci. 2018 May-Aug;6(2):100-103. doi: 10.4103/sjmms.sjmms_163_16. Epub 2018 Apr 16. PMID: 30787829; PMCID: PMC6196700.
  4. Newman MJ. A mistaken case of tension pneumothorax. BMJ Case Rep. 2014 May 16;2014:bcr2013203435. doi: 10.1136/bcr-2013-203435. PMID: 24835806; PMCID: PMC4024963.
  5. Matsumoto, S., Kishikawa, M., Hayakawa, K., Narumi, A., Matsunami, K., & Kitano, M. (2011). A method to detect occult pneumothorax with chest radiography. Annals of emergency medicine, 57(4), 378–381. https://doi.org/10.1016/j.annemergmed.2010.08.012
  6. Do, S., Salvaggio, K., Gupta, S., Kalra, M., Ali, N. U., & Pien, H. (2012). Automated quantification of pneumothorax in CT. Computational and mathematical methods in medicine, 2012, 736320. https://doi.org/10.1155/2012/736320
  7. Volpicelli G. (2011). Sonographic diagnosis of pneumothorax. Intensive care medicine, 37(2), 224–232. https://doi.org/10.1007/s00134-010-2079-y
  8. Inoue S, Egi M, Kotani J, Morita K. Accuracy of blood-glucose measurements using glucose meters and arterial blood gas analyzers in critically ill adult patients: systematic review. Crit Care. 2013 Mar 18;17(2):R48. doi: 10.1186/cc12567. PMID: 23506841; PMCID: PMC3672636.
  9. Withers JN, Fishback ME, Kiehl PV, et al. Spontaneous pneumothorax. Am J Surg 1964;108:772–6.
  10. Sadikot RT, Greene T, Meadows K, et al. Recurrence of primary pneumothorax. Thorax 1997;52:805–9.
  11. Videm V, Pillgram-Larsen J, Ellingsen O, et al. Spontaneous pneumothorax in chronic obstructive pulmonary disease: complications, treatment and recurrences. Eur J Respir Dis 1987;71:365–71.
  12. West JB. Distribution of mechanical stress in the lung, a possible factor in the localisation of pulmonary disease. Lancet 1971;1:839–41.
  13. Lippert HL, Lund O, Blegrad S, et al. Independent risk factors for cumulative recurrence rate after first spontaneous pneumothorax. Eur Respir J 1991;4:324–31.
  14. MacDuff A, Arnold A, Harvey J; BTS Pleural Disease Guideline Group. Management of spontaneous pneumothorax: British Thoracic Society Pleural Disease Guideline 2010. Thorax. 2010 Aug;65 Suppl 2:ii18-31. doi: 10.1136/thx.2010.136986. PMID: 20696690.
  15. Thelle A, Gjerdevik M, SueChu M, Hagen OM, Bakke P. Randomised comparison of needle aspiration and chest tube drainage in spontaneous pneumothorax. European Respiratory Journal. 2017;49(4). doi:https://doi.org/10.1183/13993003.01296-2016

FOAm and Further Reading

  • CDEM curriculum – https://cdemcurriculum.com/pneumothorax/ – link
  • FLIPPED EM Classroom – https://flippedemclassroom.wordpress.com/2013/05/26/pneumothorax/ – link

Reviewed and Edited By

Picture of Erin Simon, DO

Erin Simon, DO

Dr. Erin L. Simon is a Professor of Emergency Medicine at Northeast Ohio Medical University. She is Vice Chair of Research for Cleveland Clinic Emergency Services and Medical Director for the Cleveland Clinic Bath emergency department. Dr. Simon serves as a reviewer for multiple academic emergency medicine journals.

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.

Abdominal Pain in Children (2024)

~ iEM Education Project Team ~ Leave a comment

by Prassana Nadarajah

Authors
Listen

You have a new patient!

An 18-month-old boy is brought to the emergency department (ED) by his parents due to lethargy that has persisted for the last few hours. He is a term-born child with no significant antenatal history or pre-existing medical conditions. The child had been well until five days ago when he experienced a case of viral gastroenteritis. His feeding and urine output were adequate until about three hours ago, after which he began experiencing progressive episodes of crying, accompanied by vomiting and abdominal distension. There was no diarrhea or dark-colored stools noted.

a-photo-of-a-1-and-a-half-year-old-boy-(the image was produced by using ideogram 2.0)

During the triage assessment, the child appeared unsettled but was afebrile, with other vital signs within age-appropriate ranges. There were no rashes observed on his body, and there were no blood-stained stools in his diaper.

What do you need to know?

Importance

Abdominal pain is a common reason for children to present to the Emergency Department (ED) and represents up to 5% of all presentations in some institutions [1]. The most common causes are non-surgical, and at times it may be difficult to arrive at a specific diagnosis before discharge. However, it is crucial to identify causes of abdominal pain that require early surgical intervention, particularly when a clear diagnosis cannot be made before discharge. Pay special attention to red flags such as lethargy (in neonates and infants), severe pain or irritability, bilious emesis, abdominal distension, peritoneal signs, or signs of sepsis.

The differential diagnoses (DDx) for abdominal pain vary with age groups. In younger children who cannot express themselves, reliance on parental history and a thorough physical examination is essential. Blood investigations and radiology may not be helpful, especially in early presentations, making serial examinations and observation more valuable. Additionally, remember that pain from other sites can be referred to the abdomen, particularly testicular pain.

Epidemiology

Pediatric abdominal pain is a common reason for emergency department (ED) visits, accounting for approximately 12% of all visits [2]. The median age of children presenting with abdominal pain is around 9 years, with a higher incidence in girls [2, 3]. Non-specific abdominal pain is the most prevalent diagnosis, affecting 40% of children, followed by functional abdominal pain (FAP), constipation, and viral infections [2, 4]. Despite the high prevalence of abdominal pain, a significant portion of children (62.7%) are discharged directly from the ED, while 37.3% require admission [3]. However, follow-up studies indicate that about 50% of children report ongoing pain after discharge, highlighting the chronic nature of abdominal pain [3]. 

Pathophysiology

The sensation of abdominal pain is transmitted either by somatic or visceral afferent fibres [5]. Visceral pain from the visceral peritoneum is poorly localised and is often referred to its corresponding dermatome on the abdominal wall. If you recall the human embryological development of abdominal organs, the organs developing from the foregut (oesophagus to the second part of the duodenum) have pain referred to the T8 dermatome (i.e., the epigastric area), those developing from the midgut (from the third part of the duodenum to the proximal two-thirds of the transverse colon) have pain referred to the T10 dermatome (i.e., the umbilical area), and those from the hindgut (distal one-third of the transverse colon to the rectum) refer to the T12 dermatome [6].

Somatic pain from the parietal peritoneum is more localised. Thus, any abdominal condition that progresses to involve the parietal peritoneum will result in the patient complaining of migrating pain. In unfortunate situations where this advances to bowel rupture or peritonitis (i.e., surgical abdomen), the patient will exhibit signs of peritonism. You can observe this in the history of appendicitis, where the pain initially starts in the periumbilical region and migrates to the right lower quadrant.

Referred pain also occurs due to the convergence of visceral and somatic pathways in the spinal column. Two examples of referred pain are diaphragmatic irritation leading to pain at the shoulder tip due to the convergence of visceral and somatic pathways at C4, and somatic pain from pneumonia leading to T10–11 pain perceived in the lower abdomen [5].

Initial Assessment and Stabilization

Airway & Breathing

  • Provide supplemental oxygen and attach an SPO2 probe.

Circulation

  • Assess for signs of sepsis, shock, dehydration, or the need for IV pain relief. If any of these are present, obtain IV access.
  • If in shock, administer an IV crystalloid fluid bolus of 20 ml/kg. Reassess and repeat if necessary.
  • If sepsis is suspected, obtain blood cultures via IV and administer Ceftriaxone 50 mg/kg (up to 2 g) AND metronidazole 10 mg/kg (up to 500 mg). Follow your local antibiotic guidelines.
  • If not in shock but dehydrated, initiate IV maintenance therapy.
  • Provide adequate pain control. Consider IV morphine 0.05–0.1 mg/kg or IV fentanyl 1 μg/kg.

Disability

  • Check a point-of-care glucose level in sick children. Consider hypoglycemia or DKA as alternative diagnoses.

Exposure

  • Examine the abdomen for abdominal distension, masses, or peritonism. Involve the surgical team early. This is further discussed in the physical examination section.
  • Always examine the genitals (e.g., for testicular torsion or strangulated hernia).

Medical History

In history, focus on the following:

Age of the child – DDx varies with the child’s age and the initial presenting complaints. Remember that neonates and infants often present with lethargy, irritability, poor feeding, or vomiting.

Age

Surgical diagnoses

Medical diagnoses

Birth to 3 months

  • Necrotizing enterocolitis
  • Pyloric stenosis
  • Malrotation with Midgut volvulus
  • Incarcerated hernia
  • Duodenal atresia
  • Testicular torsion
  • Non-Accidental Injury
  • Constipation
  • Reflux
  • Colic

3 months to 3 years

  • Malrotation with midgut volvulus
  • Intussusception
  • Appendicitis
  • Testicular torsion
  • Trauma
  • Non-Accidental Injury
  • Henoch-Schönlein purpura (HSP)
  • Anaphylaxis
  • Acute gastroenteritis
  • Urinary tract infection
  • Constipation
  • Mesenteric adenitis
  • Sickle cell–related vaso-occlusive crisis

3 years and above

  • Appendicitis
  • Ectopic pregnancy
  • Cholecystitis
  • Malignancy
  • Trauma
  • Testicular or ovarian torsion
  • Henoch-Schönlein purpura
  • Diabetic ketoacidosis
  • Urinary tract infection
  • Pancreatitis
  • Anaphylaxis
  • Constipation
  • Acute gastroenteritis
  • Mesenteric adenitis
  • Strep pharyngitis
  • Pneumonia
  • Renal stones
  • Inflammatory bowel disease
  • Irritable bowel disease
  • Functional abdominal pain
  • Gastritis/gastric ulcer
  • Ovarian cyst
  • Pregnancy
  • Pelvic inflammatory disease
  • Toxic ingestion

Timing of the symptoms:
a. Intussusception may follow a bout of diarrhoeal illness.
b. Appendicitis typically presents as a gradual onset of pain migrating from the periumbilical area to the right lower quadrant.

Pain character – Episodic pain is observed in intussusception and mesenteric adenitis.

Blood in stool – Consider necrotizing enterocolitis, intussusception, and volvulus.

Bilious or non-bilious vomiting – Bilious vomiting is indicative of obstruction below the ampulla of Vater. It is a classic presentation of malrotation with midgut volvulus and may also present in incarcerated/strangulated hernia or Hirschsprung disease with enterocolitis. Non-bilious vomiting is classically associated with pyloric stenosis.

Associated symptoms – A rash may be present in Henoch-Schönlein purpura. Fever, when associated with inflammation (e.g., appendicitis) or the translocation of gut bacteria, may lead to sepsis.

Oral intake, urine output (UOP), and activity levels – These are important. Escalate to a senior opinion for admission or IV hydration if these parameters are below 50% of the child’s baseline.

Other relevant history:

  • Past medical and surgical history, including birth history such as prematurity in neonates and infants.
  • Social history, especially when suspecting non-accidental injury.
  • Menstrual and sexual history in adolescent females.
  •  

Physical Examination

A good history and physical examination are very important in managing undifferentiated paediatric abdominal pain patients. You must perform an abdominal examination, including genitourinary and inguinal exams, especially in children who cannot express themselves. Remember that you may find little or no helpful clinical signs initially; however, serial examinations may reveal the condition as it evolves. A digital rectal examination is very rarely indicated, and even then, it should ideally be limited to once and performed by the surgeon [7].

Also, remember that these are children, and they may intentionally exhibit voluntary guarding during palpation if they are distressed, regardless of the cause. Covering the art of paediatric abdominal examination is beyond the scope of this chapter, but consider providing analgesia, employing distraction techniques, and building good rapport with the child.

Please ensure that your patients receive adequate analgesia before the examination, as this will make the patient cooperative, simplify the examination, and highlight clinical signs.

General Examination

  • Assess general appearance and determine whether the child looks ill or well.
  • Record temperature and other vital signs.
  • Observe for pallor and jaundice. Obtain an accurate body weight.
  • Observe the child walking to the examination bed or within the department. Children with peritonism may refuse to walk or walk slowly with a stooped posture.
  • Observe for signs of pain when coughing or jumping.

Inspection

  • Look for asymmetry and abdominal distension. Abdominal distension is less pronounced in higher bowel obstructions (e.g., midgut volvulus) than in lower bowel obstructions.
  • Check for purpuric patches, which are diffusely seen in Henoch-Schönlein purpura (HSP).

Palpation

  • Feel for any masses, tenderness, and peritonism. Remember that classic presentations of masses (e.g., an olive-shaped mass in pyloric stenosis or a sausage-shaped mass in intussusception) may not be palpable in the emergency department, as the condition may be intermittent or in an early stage.
  • Palpable bowel loops are classically associated with necrotizing enterocolitis.
  • Pyloric stenosis typically presents with a non-tender abdomen.
  • For most surgical causes, peritoneal findings can occur late. Consider the possibility of septic shock in a drowsy child presenting with abdominal tenderness on palpation.

Other Systems to Examine for Abdominal Pain [7]

  • Respiratory: Assess for signs of basal pneumonia.
  • ENT: Consider upper respiratory tract infections (URTI), tonsillitis, or adenopathy.
  • Neurological: Rule out meningitis.
  • Endocrine: Check blood glucose levels for diabetic ketoacidosis.
  • Haematological: Look for pallor and lymphadenopathy.
  • Dermatological: Look for rashes, particularly purpura/petechiae in Henoch-Schönlein purpura or zoster.
  • Renal: Check for oliguria, haematuria, or hypertension in haemolytic uraemic syndrome.

In Our Patient

Physical Examination: Abdominal examination revealed an ill-defined mass in the right upper quadrant (RUQ). No pain was elicited on testicular palpation. No anal fissures or bleeding were noted on rectal examination. There were no signs of peritonism.

When To Ask for Senior Help

Do not hesitate to contact your seniors if you are concerned about your patient. The points below serve as a guide:

  1. An ill-looking patient.
  2. May require IV access for hydration or analgesia.
  3. Presence of peritoneal signs.
  4. Signs of sepsis.
  5. Bilious vomiting.
  6. Non-accidental injury or inconsistent history.
  7. Neonates (especially premature babies), if you lack experience in treating them.
  8. Parental anxiety.

Not-To-Miss Diagnoses

Pediatric abdominal pain is a common and complex issue in emergency departments, requiring a thorough differential diagnosis to identify serious underlying conditions [8]. The etiologies of abdominal pain vary by age, with infants (<2 years) commonly presenting with congenital anomalies, malrotation, and intussusception [8]. In children aged 2-5 years, appendicitis, gastroenteritis, and mesenteric adenitis are frequent diagnoses [9], while school-aged children (5-12 years) are more likely to experience constipation, urinary tract infections, and respiratory infections [8]. Adolescents (>12 years) are at risk for pelvic inflammatory disease, pregnancy-related issues, and ovarian torsion [8]. Common conditions such as appendicitis, constipation, and gastroenteritis are prevalent across different age groups, and non-gastrointestinal causes like pneumonia and acute asthma can also manifest as abdominal pain [10]. A comprehensive approach to diagnosis and management is essential to identify serious underlying conditions that may require urgent intervention.

Causes Requiring Early Surgical Intervention

  • Peritonitis.
  • Appendicitis.
  • Testicular torsion.
  • Incarcerated hernia.
  • Necrotizing enterocolitis.
  • Intussusception.
  • Volvulus.
  • Hirschsprung’s disease.
  • Pregnancy or ectopic pregnancy in adolescent girls.
  • Ovarian torsion in adolescent girls.

Medical Causes Not to Miss

  • UTI in very young children (<5 years).
  • Diabetic ketoacidosis.
  • Sepsis.
  • Haemolytic uraemic syndrome.
  • Non-accidental injury.

Acing Diagnostic Testing

Remember that blood investigations are useful as supportive evidence for your history and physical examination, but they can be normal in surgical conditions. Avoid unnecessary venepuncture and/or IV cannulation in children unless the patient is sick or you are concerned about a not-to-miss diagnosis.

Bedside Tests

In sick patients, useful point-of-care tests include blood sugars, urine analysis, and capillary gas analysis. Blood sugars can indicate hypoglycaemia or DKA, and capillary gas analysis is useful for assessing lactate levels and metabolic acidosis. Urine analysis is helpful in confirming UTI, but ensure a proper uncontaminated sample has been collected [11]. Point-of-care ultrasound can be used for diagnosing intussusception, pyloric stenosis, or appendicitis.

Laboratory Tests

If venipuncture is performed, a full blood count, CRP, and renal function tests should be considered for all children. These tests may reveal evidence of inflammation or infection, as well as the extent of dehydration. You may also consider adding VBG and blood cultures for sicker children and tailor other testing depending on the patient (e.g., lipase for pancreatitis or beta HCG if pregnancy is suspected).

Imaging

Consider avoiding radiation or utilizing the lowest possible radiation dose. Ultrasound is the initial imaging modality of choice. In addition to point-of-care ultrasound, arrange an urgent departmental ultrasound if needed. If x-ray facilities are available, you can obtain a supine abdomen and upright/lateral decubitus view to look for free air. Computed tomography can be considered for life-threatening conditions when other modalities have failed. Magnetic resonance imaging is used in some parts of the world. It avoids radiation but may be time- or cost-prohibitive.

In Our Patient

  • Point-of-care ultrasound (POCUS) showed a target sign over the abdominal mass.
  • A diagnosis of intussusception was made.

Risk Stratification

Effective clinical decision rules (CDRs) for risk stratification of pediatric abdominal pain in emergency departments include the Pediatric Appendicitis Score (PAS) and the Pediatric Emergency Care Applied Research Network (PECARN) Pediatric Intra-Abdominal Injury rule. The PECARN rule is for trauma patients and out of the discussion in this chapter. The PAS is a valuable tool for assessing the likelihood of acute appendicitis in children presenting with abdominal pain, with studies showing that PAS scores correlate significantly with the severity of appendicitis [12]. A score below 4 has been found to rule out appendicitis, while higher scores indicate a higher risk of appendicitis [12]. Additionally, a recent Non-Specific Abdominal Pain (NSAP) Model has been developed to differentiate non-specific abdominal pain from organic causes, identifying key clinical predictors such as pain location and associated symptoms, and achieving a sensitivity of 71.8% [13]. These CDRs assist clinicians in identifying patients at risk for serious conditions, optimizing diagnostic processes, and reducing unnecessary interventions.

Management

Empiric and Symptomatic Treatment

Correct dehydration either orally in stable children or via IV in children who may need to be kept nil-by-mouth or are too sick to tolerate oral intake.

Consider keeping possible surgical patients nil-by-mouth. For bowel obstruction, consider inserting a nasogastric tube for gastric decompression.

Treat pain and distress.

  • Consider non-pharmacological methods (e.g., examine the child on the parent’s lap).

Paracetamol

  • Dose per kg: 15 mg/kg
  • Frequency: Every 4 hours (q4h)
  • Maximum Dose: 60 mg/kg/day
  • Cautions/Comments:
    • Ask for allergies.
    • Check if/when the patient took acetaminophen at home.

Fentanyl

  • Dose per kg: Intranasal 1.5 mcg/kg (for >12 months of age)
  • Frequency: Every 15 minutes
  • Maximum Dose: 3 mcg/kg
  • Cautions/Comments:
    • Not recommended for children <12 months of age.
    • Divide the dose between nostrils.
    • Consider alternative analgesia after the second dose.

Morphine

  • Dose per kg:
    • IV/Subcutaneous: 0.05–0.1 mg/kg
  • Frequency: Every 2–4 hours
  • Maximum Dose:
    • For <1 month: 0.1 mg/kg every 4–6 hours
    • For 1–12 months: 0.1 mg/kg every 2–4 hours
    • For >12 months: 0.2 mg/kg every 2–4 hours
  • Cautions/Comments:
    • There is a chance of respiratory depression if the dose exceeds the recommended amount.

If sepsis is suspected, administer IV Cefotaxime and IV Metronidazole, or follow your local antibiotic guidelines.

Cefotaxime

  • Dose per kg: IV 50 mg/kg
  • Frequency: Every 12 hours
  • Maximum Dose: 2000 mg
  • Cautions/Comments:
    • Can be given intramuscularly (IM) if IV access is difficult.

Metronidazole

  • Dose per kg: IV 10 mg/kg
  • Frequency: Every 8 hours
  • Maximum Dose: 500 mg
  • Cautions/Comments:
    • Consider alternative analgesia after the second dose.

Piperacillin + Tazobactam

  • Indication: For pseudomonal coverage in sepsis or hospital-acquired infections.
  • Dose per kg:
    • 2 months to 9 months: IV 80 mg/kg
    • 9 months: IV 100 mg/kg
  • Frequency: Every 8 hours
  • Maximum Dose: 3000 mg
  • Cautions/Comments:
    • The dose is calculated based on the piperacillin component.

IV Fluids

  • Use isotonic crystalloids. Avoid hypotonic solutions in the ED, except in rare circumstances as advised by paediatric nephrologists or paediatricians.
  • For resuscitation, use 0.9% saline in 10–20 ml/kg boluses for all ages. You can repeat the boluses as necessary, but assess for signs of heart failure before administering each bolus.
  • For IV maintenance, use a 0.9% saline and 5% dextrose combination if available. This can be prepared by mixing 450 ml of 0.9% saline with 50 ml of 50% dextrose. Alternatively, you can use 0.9% saline, Hartmann’s solution, or follow local guidelines.

When To Admit This Patient

If you are able to arrive at a diagnosis for these patients, then the disposition is often straightforward. On the other hand, patients with severe pain despite a negative physical examination and unclear diagnosis will require admission for observation and serial physical examinations.

If parents confirm that oral intake, UOP, and activity levels are less than 50% of the child’s baseline, the child should be admitted for IV hydration and observation. A short-stay unit may be suitable for such patients.

If there is a suspicion of non-accidental injury or any social circumstances (e.g., inability to return for review due to financial constraints or travel issues in rural areas), discuss admission with your senior doctor. Consider reviewing well-appearing neonates with seniors, especially if you think they can be safely discharged home.

Otherwise, well children with likely benign causes can be discharged home. Ensure that clear and close follow-up is arranged with their general practitioner or pediatrician.

Advise parents on when to return (e.g., if the child’s oral intake, UOP, or activity level reduces to less than 50% of their usual baseline, or if symptoms of sepsis or shock develop) and provide guidance on follow-up (either with their general practitioner or the nearest hospital with surgical capacity to review the child). If any outpatient radiological investigations are planned for the coming days, educate parents about the importance of attending these procedures as well.

Revisiting Your Patient

Our 18-month-old patient was confirmed to have an intussusception by point-of-care ultrasound.

On reviewing his history, the episodic crying and preceding viral illness are supportive of this diagnosis, and the lack of fever or other associated symptoms rules out most other diagnoses. The classical triad of abdominal pain, vomiting, and red-currant jelly stool described in patients is present in less than 50% of patients with the disease [14]. However, a better clue is that it is associated with lethargy even without signs of sepsis or dehydration.

His examination revealed normal vital signs, was afebrile, and had a soft, non-tender abdomen with an ill-defined lower abdominal mass, which also supports this diagnosis.
The ABCDE or primary survey did not show any other abnormalities.

He was kept nil-by-mouth, IV maintenance fluids were started, and an urgent surgical referral was made. Antibiotics were not needed at this stage as there was no other supportive evidence of associated sepsis. He was prescribed PRN pain relief with fentanyl and morphine but did not require any during the ED stay.

The surgical team reviewed him and took him to the operating theatre for air enema reduction.

Authors

Picture of Prassana Nadarajah

Prassana Nadarajah

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References

  1. Scholer SJ, Pituch K, Orr DP, Dittus RS. Clinical outcomes of children with acute abdominal pain. Pediatrics. 1996;98(4):680-685. doi:10.1542/peds.98.4.680
  2. Magnúsdóttir MB, Róbertsson V, Þorgrímsson S, Rósmundsson Þ, Agnarsson Ú, Haraldsson Á. Abdominal pain is a common and recurring problem in paediatric emergency departments. Acta Paediatr. 2019;108(10):1905-1910. doi:10.1111/apa.14782
  3. Lee WH, O’Brien S, Skarin D, et al. Pediatric Abdominal Pain in Children Presenting to the Emergency Department. Pediatr Emerg Care. 2021;37(12):593-598. doi:10.1097/PEC.0000000000001789
  4. Pant C, Deshpande A, Sferra TJ, Olyaee M. Emergency department visits related to functional abdominal pain in the pediatric age group. J Investig Med. 2017;65(4):803-806. doi:10.1136/jim-2016-000300
  5. Simpson E, Smith A. The management of acute abdominal pain in children. Journal of Paediatrics and Child Health. 1996;32(2):110-112. doi:10.1111/j.1440-1754.1996.tb00905.x
  6. Sadler TW, Langman J, Langman J. In: Langman’s Medical Embryology. Wolters Kluwer Health; 2012:208-229.
  7. Cameron P, Brown G, Biswadev M, Dalziel S, Craig S. Textbook of Paediatric Emergency Medicine. Elsevier; 2019.
  8. Reust CE, Williams A. Acute Abdominal Pain in Children. Am Fam Physician. 2016;93(10):830-836.
  9. Yang WC, Chen CY, Wu HP. Etiology of non-traumatic acute abdomen in pediatric emergency departments. World J Clin Cases. 2013;1(9):276-284. doi:10.12998/wjcc.v1.i9.276
  10. Kandamany N, O’Neill M. The Aetiology of Acute Abdominal Pain in Children 2–12 Years of Age. Archives of Disease in Childhood 2012;97:A478.
  11. The Royal Children’s hospital melbourne. The Royal Children’s Hospital Melbourne. Accessed May 25, 2023. https://www.rch.org.au/kidsinfo/fact_sheets/Urine_samples/#:~:text=Clean%20the%20skin%20around%20the%20genital%20area%2C%20using%20gauze%20if,sample%20container%20touch%20the%20skin.
  12. Vevaud K, Dallocchio A, Dumoitier N, et al. A prospective study to evaluate the contribution of the pediatric appendicitis score in the decision process. BMC Pediatr. 2024;24(1):131. Published 2024 Feb 19. doi:10.1186/s12887-024-04619-z
  13. Bouënel M, Lefebvre V, Trouillet C, Diesnis R, Pouessel G, Karaca-Altintas Y. Determining clinical predictors to identify non-specific abdominal pain and the added value of laboratory examinations: A prospective derivation study in a paediatric emergency department. Acta Paediatr. 2023;112(10):2218-2227. doi:10.1111/apa.16911
  14. Simon R.A, Hugh T.J, Curtin A.M. Childhood intussusception in a regional hospital. Aust N Z J Surg. 1994;64:699–702.

Reviewed and Edited By

Picture of Erin Simon, DO

Erin Simon, DO

Dr. Erin L. Simon is a Professor of Emergency Medicine at Northeast Ohio Medical University. She is Vice Chair of Research for Cleveland Clinic Emergency Services and Medical Director for the Cleveland Clinic Bath emergency department. Dr. Simon serves as a reviewer for multiple academic emergency medicine journals.

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.

Burns and Smoke Inhalation (2024)

~ iEM Education Project Team ~ Leave a comment

by Michaela Banks, Anthony Dikhtyar, Jacquelyne Anyaso, & Ashley Pickering

Authors
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You have a new patient!

A 26-year-old male presents to the emergency department with burns on his face, arms, hands, and torso. He states that he was burning trash in his front yard without his shirt on when a big explosion occurred. He appears distressed and short of breath. The presence of singed nasal hairs is also noted. Examination reveals multiple partial- and full-thickness burns with blisters and surrounding redness. His vitals are as follows: HR: 130  BP (taken on R calf): 130/80 RR: 30 SpO2: 75%. His weight: 75kg

a-photo-of-a-26-year-old-male-with-burns (the image was produced by using ideogram 2.0)

What do you need to know?

Importance

Burn injuries result from various sources and can range in severity. The mortality rate from thermal burns is directly related to the size of the burn [1]. Large and deep burns can trigger systemic responses, such as shock, which can lead to death. Three key risk factors that increase the likelihood of complications include: age over 60 years, inhalation injuries, and non-superficial burns (partial and full-thickness) covering more than 40% of the total body surface area (TBSA) [2].

Epidemiology

Burn injuries are a significant public health issue, with approximately 450,000 individuals seeking medical attention annually, and about 45,000 requiring hospitalization [2]. Residential fires are the leading cause of burn-related deaths, contributing to nearly 3,500 fatalities per year. Smoking materials, such as cigarettes, are the primary cause of fire-related deaths, while other fatal injuries stem from motor vehicle crashes, electrical contact, or exposure to chemicals. Men constitute 71% of burn patients, with children under five representing 17% [2]. Most burns occur at home (65%) and involve less than 10% total body surface area (67%). Advances in burn care have improved survival rates to 96% [2]. Roughly 86% of all burns are caused by thermal injury. Flame and scald burns are the leading causes of burns in children and adults. Inhalation injury is present in two-thirds of patients with burns greater than 70% of TBSA. 

Pathophysiology

Burn injuries, caused by heat, chemicals, electricity, or radiation, trigger a complex interplay of local and systemic responses. At the cellular level, burn wounds are divided into three distinct zones: coagulation, stasis, and hyperemia. The central zone of coagulation undergoes irreversible cell death due to protein denaturation, necessitating surgical intervention in many cases. Surrounding it, the zone of stasis contains viable but at-risk cells that can either recover with proper care or progress to necrosis. The outer zone of hyperemia typically recovers fully within days due to its inflammatory response and intact blood flow [2-4].

Burns prompt a robust inflammatory response, increasing capillary permeability and causing fluid shifts that lead to edema. Local edema compromises blood flow and cell survival in the zone of stasis, while systemic edema in large burns contributes to hypovolemia, the primary cause of burn shock. Immediate and adequate fluid resuscitation is critical to prevent worsening injury and maintain organ perfusion [2-4].

Specific burn types exhibit unique pathophysiologies. Inhalation injuries from superheated gases or toxic smoke cause airway edema, inflammation, and potentially fatal complications like carbon monoxide poisoning and ARDS [5]. Chemical burns differ by agent, with acids causing coagulation necrosis and alkalis leading to deeper liquefaction necrosis. Electrical burns often involve extensive internal damage along the current’s path, risking cardiac arrhythmias and systemic effects. Radiation burns, though rarer, involve cellular damage through ionizing radiation exposure [2-4].

Systemically, extensive burns induce a hypermetabolic state, immune suppression, and systemic inflammatory responses affecting multiple organs. Cardiovascular effects, such as burn shock, respiratory compromise, and heightened infection risks, are key complications. Patient outcomes hinge on factors like burn depth, TBSA, age, inhalation injury presence, and quality of initial management, underscoring the importance of specialized burn center care.

Burn Depth

Burn depth classification is fundamental to assessing burn injuries, guiding treatment decisions, and predicting outcomes. Accurate determination of burn depth, particularly for partial-thickness burns, remains challenging, even for skilled clinicians. This underscores the need for continued research and advanced technologies to enhance diagnostic precision.

Traditionally, burns are categorized into four classes based on the extent of tissue damage [4]:

  1. Superficial Thickness (First-Degree) Burns: These affect only the epidermis, presenting with redness, pain, and warmth without blistering. Healing occurs within a few days without scarring.

  2. Partial-Thickness (Second-Degree) Burns: These penetrate the dermis and are subdivided into:

    1. Superficial Partial-Thickness Burns: Involving the upper dermis, they are painful, moist, and blistered, typically healing within 2–3 weeks with minimal scarring.

    2. Deep Partial-Thickness Burns: Reaching deeper dermal layers, these burns cause damage to sweat glands and hair follicles. They are less painful due to nerve damage, appear mottled and dry, and may require 3–8 weeks or longer to heal, often resulting in scarring or contractures.

  3. Full-Thickness (Third-Degree) Burns: These burns destroy the entire epidermis and dermis, extending into subcutaneous tissue. They appear white, brown, or charred with a leathery texture and are insensate due to nerve destruction. Healing requires surgical intervention, such as skin grafting, and leaves significant scars.

  4. Fourth-Degree Burns: Extending into muscles, bones, tendons, or ligaments, these burns are characterized by blackened tissue and often result in loss of the affected part.

These classifications provide a framework for clinicians to tailor interventions and anticipate patient needs, particularly in severe or complex burn cases. The illustration below displays the various categories of burn depth [4].

From: [4] Jeschke MG, van Baar ME, Choudhry MA, Chung KK, Gibran NS, Logsetty S. Burn injury. Nat Rev Dis Primers. 2020;6(1):11. Published 2020 Feb 13. doi:10.1038/s41572-020-0145-5

Medical History

Accurately gathering a burn history is critical for evaluating the injury’s severity, identifying risks, and tailoring management. The AMPLET mnemonic is widely recommended for systematic collection of essential information regarding the event and the patient’s medical background. Additionally, specific questions based on the type of burn provide crucial details for precise assessment and treatment [2-4, 6].

Allergies (A):
Identifying drug and environmental allergies is essential to avoid adverse reactions during treatment.

Medications (M):
A detailed list of current medications, including prescription drugs, over-the-counter remedies, herbal supplements, and home treatments, is vital to anticipate potential drug interactions or complications.

Past Medical History (P):
Knowledge of pre-existing conditions, such as diabetes, cardiovascular disease, lung disorders, or bleeding tendencies, helps predict how the patient may respond to burn injuries and resuscitation. Tetanus immunization status should also be reviewed and updated if necessary (see “T”).

Last Meal or Drink (L):
Documenting the patient’s last meal or drink is crucial for surgical planning, as recent food intake may require delays in procedures involving anesthesia.

Events/Environment Relating to Incident (E):
A detailed account of the burn incident helps identify the mechanism of injury, the risk of inhalation injury, and associated trauma. Important elements to document include:

  • Type of burn: Thermal, chemical, electrical, or radiation.
  • Cause of burn: Flame, scald, contact with hot objects, chemicals, or electricity.
  • Incident location: Indoor/outdoor, enclosed space, smoke presence.
  • Duration of exposure: Time spent in contact with the burn source.
    First aid administered: Cooling, cleaning, or dressing of the burn before medical evaluation.
  • Suspicion of abuse or neglect: Look for inconsistencies in the history, patterns of injury, or delays in seeking care. Specific questions include:
    • How did the burn occur?
    • Who was present?
    • How long to extinguish flames?
    • Was the area cooled? With what and for how long?
    • Were explosions, blasts, or chemical spills involved?
    • Was the patient trapped or unconscious?

Tetanus and Childhood Immunizations (T):
Ensuring tetanus immunization is current (within five years) is crucial. In children, assessing overall immunization status helps anticipate potential complications.

Specific Questions Based on Burn Type [2-4,6]

Thermal Burns:

  • How did the burn occur?
  • What was the heat source (e.g., flame, scald, or hot object)?
  • Was clothing involved, and how quickly was it removed?
  • Was a flammable liquid (e.g., gasoline) involved?

Chemical Burns:

  • What was the chemical agent?
  • How did exposure occur, and how long was contact?
  • What decontamination measures were taken?
  • Is a Material Safety Data Sheet (MSDS) available?

Electrical Burns:

  • What type of electricity was involved (high voltage/low voltage, AC/DC)?
  • What was the duration of contact?
  • Was the patient thrown or did they fall?

Physical Examination

The physical examination of a burn patient is a systematic process designed to assess the severity of the burn injury, identify associated injuries or complications, and guide treatment decisions. A comprehensive and thorough examination is critical for determining the need for transfer to a burn center and predicting potential outcomes [2-6]. Make sure to assess for concomitant trauma (especially after a blast injury or fall).

First, perform decontamination if the person has been exposed to a chemical substance. If possible, expose the patient to a warm room. Immediately assess the airway, breathing, and circulation (ABCs), see details below.

Primary Survey

The primary survey prioritizes life-threatening conditions using the ABCDE approach [2,4,6]:

A. Airway

  • Assess for patency: Check for obstruction, swelling, or soot in the mouth and nose. Examine for posterior oropharynx edema and singed facial and nasal hairs carefully.
  • Listen for abnormal breath sounds: Stridor, wheezing, or decreased breath sounds may indicate inhalation injury or airway compromise.
  • Consider early intubation: Severe facial burns, inhalation injury, or altered mental status may necessitate securing the airway. Please do not delay airway procedure if you suspect inhalation injury.

B. Breathing

  • Assess respiratory rate and effort: Look for tachypnea, labored breathing, or cyanosis.
  • Auscultate lung sounds: Wheezing, rales, or rhonchi may suggest inhalation injury or pulmonary complications.
  • Administer high-flow oxygen: Use 100% oxygen via a non-rebreather mask, particularly for moderate to severe burns patients or patients with suspected inhalation injury.

C. Circulation

  • Monitor heart rate and rhythm: Look for tachycardia, bradycardia, or arrhythmias.
  • Measure blood pressure: Hypotension may indicate shock or blood loss.
  • Assess capillary refill and skin color: Delayed refill, pallor, or cyanosis indicates poor perfusion.
  • Establish IV access: Insert two large-bore IVs for moderate to severe burn patients, particularly for burns covering >20% TBSA.
  • Control bleeding: Bleeding suggests additional injuries.

D. Disability

  • Assess level of consciousness: Use the AVPU scale (Alert, Verbal, Pain, Unresponsive) or Glasgow Coma Scale (GCS).
  • Evaluate neurological status: Check pupils, motor strength, and sensation.

E. Exposure and Environmental Control

  • Remove clothing and jewelry: Fully expose the patient to assess burns but prevent further constriction.
  • Identify deformities: Look for fractures or dislocations.
  • Maintain warmth: Use clean, dry sheets and blankets to prevent hypothermia.

Secondary Survey

Once the primary survey stabilizes life-threatening conditions, conduct a detailed evaluation [2,4]:

A. History
Obtain a complete history using the AMPLET mnemonic, covering allergies, medications, past medical history, last meal, events surrounding the burn, and tetanus immunization status (see Medical History above).

B. Head-to-Toe Examination

  • Head and Neck: Assess for burns, singed hair, soot, inhalation injury, corneal damage, and tympanic membrane injury.
  • Chest: Listen to breath sounds, observe chest expansion, and evaluate for circumferential burns that may impair breathing.
  • Abdomen: Inspect for burns, palpate for tenderness, and consider the risk of abdominal compartment syndrome with circumferential burns.
  • Extremities: Look for burns, fractures, diminished pulses, or signs of compartment syndrome. Assess sensation and motor function.
  • Genitalia and Perineum: Inspect for burns and swelling, and assess urinary retention.
  • Back and Buttocks: Examine these areas during log rolling, ensuring full exposure and injury identification.

C. Burn Wound Assessment

  • Burn size: Estimate TBSA using the Rule of Nines (see images below) [7] or the Lund and Browder chart.
  • Burn depth: Classify burns as superficial, partial-thickness (superficial or deep), full-thickness, or fourth-degree. Note that burn depth may evolve over time (see figure about burn depth above).
  • Document wound characteristics: Describe color, texture, moisture, blisters, and eschar.
Rule of Nines (Adults ≥ 14 years of age) - Courtesy of the American Burn Association - From: [7] - https://www.health.state.mn.us/communities/ep/surge/burn/tbsa.pdf
Rule of Nines for Children (Age 1 - 14) - Courtesy of the American Burn Association - From: [7] - https://www.health.state.mn.us/communities/ep/surge/burn/tbsa.pdf
Rule of Nine for Infant (Age < 1 year) - Courtesy of the American Burn Association - From: [7] - https://www.health.state.mn.us/communities/ep/surge/burn/tbsa.pdf

Burns are classified into degrees based on the depth of tissue damage, with each classification displaying distinct pathophysiological features, clinical findings. The following section covers specific clinical information related to burn depth.

Superficial (First-Degree) Burns
Superficial burns involve only the epidermis, the outermost layer of the skin. These burns are characterized by warm, dry, and red areas that blanch with pressure. Blistering is absent, and the skin typically heals within a few days without scarring. Sunburn is a classic example of a superficial burn.

Partial-Thickness (Second-Degree) Burns
Partial-thickness burns extend beyond the epidermis into the dermis and are further divided into superficial and deep categories.

  • Superficial Partial-Thickness Burns: These burns affect the upper dermis and are very painful. Surrounding erythema, moisture, and blistering are common features. These burns blanch when pressed and typically heal with minimal scarring in 2–3 weeks.
  • Deep Partial-Thickness Burns: These penetrate deeper into the dermis, potentially damaging sweat glands and hair follicles. They are less painful due to nerve ending destruction and appear drier, with a mottled red or white surface that does not blanch. Healing takes longer and often results in scarring or contractures. Scalds and flash burns are typical causes of partial-thickness burns.

Full-Thickness and Beyond (Third- and Fourth-Degree) Burns
Full-thickness burns destroy the entire epidermis and dermis, often extending into subcutaneous fat and, in severe cases, deeper structures such as muscle and bone (fourth-degree burns). These burns result in decreased sensation due to nerve destruction. The affected areas appear white, brown, or leathery, with a dry texture, and they do not blanch when pressed. Examples include chemical burns, electrical burns, fully immersed thermal burns, and severe frostbite. Healing requires surgical intervention, such as skin grafting, and significant scarring is inevitable.

Clinical Images of Selected Burn Injuries

Thermal 2nd degree burn in a child
Thermal burn in an adult patient
Thermal injury - 2nd degree burn in a child
Electrical injury/burn - entry wound
Electrical injury/burn - exit wound
Chemical burn
Chemical burn
Corneal Chemical Burn
Thermal burn, Inhalation Injury

Acing Diagnostic Testing

The diagnostic approach to burn patients varies based on the severity of the burn, the suspected complications, and the presence of associated injuries. A systematic evaluation using targeted laboratory tests and imaging helps guide treatment decisions and monitor potential complications.

Patients with Minor Burns

For patients with minor burns and no associated injuries, laboratory testing is generally unnecessary unless other trauma or medical conditions are present.

Patients with Moderate to Severe Burns

Moderate to severe burns necessitate a more comprehensive diagnostic evaluation [2,6]:

  • Complete Blood Count (CBC): Assesses anemia, infection, or thrombocytopenia.
  • Comprehensive Metabolic Panel (CMP): Monitors electrolyte imbalances, fluid shifts, and kidney or liver function.
  • Creatine Kinase (CK): Detects muscle damage.
  • Arterial Blood Gases (ABG) and Carboxyhemoglobin Levels: Essential for suspected inhalation injury to evaluate oxygenation, carbon monoxide poisoning, and acidosis.
  • Blood Cyanide Levels: Performed if cyanide poisoning is suspected, though results may take time. Treatment is often initiated based on clinical suspicion [2].
  • Serum Lactate: Elevated levels indicate tissue hypoperfusion, inadequate resuscitation, or exposure to carbon monoxide or cyanide [6].
  • Coagulation Studies: Identifies coagulopathies, which are common in severe burns.
  • Chest X-Ray (CXR): Evaluates lung damage in inhalation injury and confirms endotracheal tube placement in intubated patients [2,6].

Patients with Electrical Burns

Electrical burns require specialized evaluation due to the unique nature of the injuries:

  • Electrocardiogram (EKG): Necessary for detecting cardiac dysrhythmias, especially in high-voltage injuries. Patients with abnormal EKG findings should be observed until normalization [6].
  • Creatine Kinase (CK): Elevated levels indicate rhabdomyolysis caused by muscle damage [6].
  • Urinalysis: Detects myoglobinuria, a sign of rhabdomyolysis, which can impair kidney function. However, urinalysis has limited specificity [6].

Imaging for Burn Patients

Imaging studies provide critical insights, particularly for inhalation or electrical injuries:

  • Chest X-Ray (CXR): Evaluates lung damage in inhalation injury and confirms endotracheal tube placement in intubated patients. Useful for identifying pulmonary complications, such as pneumothorax, and confirming intubation tube placement [6].
  • Fiberoptic Bronchoscopy: A definitive tool for diagnosing inhalation injury, revealing findings like soot, edema, mucosal blisters, and hemorrhages [5].
  • Chest CT Scan: Offers detailed imaging of lung injuries and is particularly helpful when CXR findings are inconclusive [5].

Risk Stratification

Burn injuries are categorized as minor, moderate, or severe based on several factors that help predict outcomes and guide management. These include the depth of the burn, the percentage of total body surface area (TBSA) affected, and the age of the patient, with burns in individuals under 10 years or over 50 years considered more severe. The presence of associated injuries, such as smoke inhalation or other traumas, also increases the severity. Burns involving high-risk areas—the face, hands, feet, or genitalia—are particularly concerning due to their potential impact on function, aesthetics, and quality of life.

Risk Stratification Criteria

  • Minor
    • Adults: Partial-thickness burns affecting < 15% TBSA
    • Pediatrics: Partial-thickness burns affecting < 10% TBSA
    • No full-thickness burns
    • No involvement of the face, hands, feet, or genitalia
    • No cosmetic impairment
    • Note: Superficial burns are not included in TBSA calculations.
  • Moderate
    • Adults: Partial-thickness burns affecting 15–20% TBSA
    • Pediatrics: Partial-thickness burns affecting 10–15% TBSA
    • Full-thickness burns affecting < 10% TBSA
    • No involvement of the face, hands, feet, or genitalia
    • No cosmetic impairment
  • Severe
    • Adults: Any burn depth affecting > 25% TBSA
    • Pediatrics: Any burn depth affecting > 20% TBSA
    • Full-thickness burns affecting > 10% TBSA
    • Involvement of the face, hands, feet, or genitalia
    • Cosmetic impairment
    • Circumferential burns: Burns extending completely around the chest or a limb:
      • Can cause compartment syndrome or increased pressure in the affected area.
      • This is particularly dangerous in the chest, where it can restrict breathing and may require escharotomy (incisions into the burned tissue) to relieve the pressure.

Referral to a Burn Center
Referral to a specialized burn center is recommended based on the following criteria from the American Burn Association (ABA) [8]:

  • Partial-thickness burns >10% TBSA.
  • Burns involving the face, hands, feet, genitalia, perineum, or major joints.
  • Full-thickness (third-degree) burns in any age group.
  • Electrical or chemical burns.
  • Inhalation injury.
  • Burns in patients with pre-existing conditions that complicate management.
  • Burns with concomitant trauma or special care needs.

Management

Effective management of burn patients begins with prompt stabilization of the airway, breathing, and circulation (ABC). Airway management is critical in cases of full-thickness facial burns, significant soot in the nose or mouth, hoarseness, stridor, respiratory depression, or altered mental status. In such scenarios, establishing a definitive airway through endotracheal intubation is necessary to prevent airway compromise. Breathing should be assessed by monitoring oxygen saturation and providing supplemental oxygen as needed to address hypoxemia, especially in patients with inhalation injuries. Circulation assessment involves evaluating distal pulses, particularly in patients with circumferential burns, which may restrict blood flow and necessitate escharotomy. For burns exceeding 20% TBSA, prompt initiation of intravenous fluid (IVF) resuscitation is essential to maintain hemodynamic stability and prevent burn shock. This systematic approach ensures early intervention to mitigate life-threatening complications. Extensive details on primary and secondary survey was given in the physical examination section.

General Principles in Management of Burns

Burn management follows consistent principles across all mechanisms of injury, prioritizing first aid, pain control, and fluid resuscitation.

First Aid

Immediate first aid involves removing the causative agent and any clothing, jewelry, or objects that may retain heat or constrict circulation. Cooling the affected area with water is effective for small burns but must be used cautiously with larger burns to prevent hypothermia [9].

Analgesia

Burn injuries and wound care are extremely painful, making pain management a critical component of care. Opioid pain medications should be considered to provide adequate relief, particularly for severe burns or during dressing changes [2,6].

Fluid Resuscitation

Fluid replacement is essential for patients with extensive burns to prevent hypovolemia and burn shock. Adults with partial- or full-thickness burns covering >20% TBSA require fluid resuscitation, while this threshold is lower (>10% TBSA) for pediatric and elderly patients [2,6].

Two common formulas guide fluid calculations:

  • Parkland Formula: Volume (mL) = 4 × weight (kg) × % TBSA burned. Half of the total volume is given in the first 8 hours, and the remaining half over the subsequent 16 hours.
  • Modified Brooke Formula: Volume (mL) = 2 × weight (kg) × % TBSA burned for adults, or 3 × weight (kg) × % TBSA burned for children, administered evenly over 24 hours.

Hartmann’s solution or lactated Ringer’s is the preferred replacement fluid. Fluid titration, based on urine output, ensures appropriate volume without overloading:

  • Adults: Maintain urine output at 0.5–1.0 mL/kg/hour.
  • Pediatrics: Maintain urine output at 1.0–1.5 mL/kg/hour.

Fluid resuscitation is a dynamic process requiring hourly re-evaluation to ensure adequacy and prevent complications [2,6]. The fluid rate must be carefully titrated based on the patient’s urinary output and physiological response. Hourly urine output, measured using an indwelling bladder catheter, serves as a reliable indicator of resuscitation adequacy in patients with normal renal function.

  • Adults: Maintain urine output at 0.5 mL/kg/hour (approximately 30–50 mL/hour).
  • Young Children (≤30 kg): Target 1 mL/kg/hour.
  • Pediatric Patients (>30 kg, up to age 17): Maintain output at 0.5 mL/kg/hour.
  • Adults with High-Voltage Electrical Injuries and Myoglobinuria: Ensure a urine output of 75–100 mL/hour until urine clears.

This individualized approach to fluid management helps maintain renal perfusion, ensures effective resuscitation, and minimizes the risk of under- or overhydration.

Thermal Burns

Thermal burns occur when excessive heat is applied to the skin, resulting in tissue destruction. Initially, this process may cause inflammation and initiate the healing response. However, if the heat intensity or duration is sufficient, coagulative necrosis ensues, leading to irreversible cell death and localized tissue loss. The severity and type of burn depend on various factors, including the heat source, duration of exposure, and depth of tissue involvement. 

Thermal 2nd degree burn in a child

The treatment of thermal burns varies based on severity [2, 6, 10].

Minor burns are managed by cleaning the area and applying topical aloe and a barrier dressing. Pain is controlled with oral analgesics, such as NSAIDs or acetaminophen/paracetamol. Patients can be discharged with outpatient follow-up for wound monitoring.

Moderate burns require cleaning with water and debridement of large blisters. Wound care involves the application of a topical antibiotic with a dressing or an antibiotic-impregnated bandage. Pain management may include oral or intravenous analgesia, with narcotics as needed. Fluid resuscitation, either oral or intravenous, is determined by the percentage of total body surface area (%TBSA) affected. Tetanus immunization should be updated if the last dose was over 10 years ago. Consultation with a burn specialist is advised, with possible admission or transfer to a burn center.

Severe burns necessitate cleaning with water, pain management with oral or intravenous analgesia, and application of a dressing without antibiotics or ointments if transfer to a burn center is confirmed. Intravenous fluid resuscitation is essential, along with prompt referral and admission to a burn center. Circumferential full-thickness burns may require escharotomy to prevent complications such as compartment syndrome.

Electrical Burns

Electrical burns can present with a wide range of injuries due to the effects of electrical current and the conversion of electrical energy into thermal injury. High-voltage electrical exposure can also result in blunt trauma caused by the patient being propelled away from the electrical source.

Extent of injuries depends on the voltage type:

  • Low voltage: Commonly seen in children who come into contact with electrical cords or outlets.
  • High voltage: Typically occupational injuries from power lines or utility poles, often leading to deep tissue and organ damage.
  • Lightning: Frequently occurs during outdoor recreational or work activities, especially in rainy seasons.

Deep tissue injury assessment:
Patients presenting with full-thickness burns, painful passive range of motion, and elevated creatine kinase (CK) levels should be presumed to have deep tissue injury.

  • These patients require fluid resuscitation and referral to a burn center when possible.
Electrical injury/burn - entry wound
Electrical injury/burn - exit wound
high voltage electrical injury

Muscle damage results in a breakdown known as rhabdomyolysis, which can lead to renal failure and multi-organ failure if not treated promptly.

electrical injury, rhabdomyolysis

Management [2,3,11]

General Principles

  • Cardiac Monitoring: Patients with suspected electrical burns should undergo continuous cardiac monitoring for 12–24 hours to detect dysrhythmias.
  • Compartment Syndrome Monitoring: Close monitoring is essential for signs of compartment syndrome.
  • Stress Ulcer Prophylaxis: Administer proton pump inhibitors (PPIs) or H2 blockers, especially in patients who are NPO, as electrical burns carry a higher risk of ulcer formation compared to other burns.

Analgesia

  • Severe pain from deep tissue injuries often necessitates IV narcotic analgesia.

Fluids

  • Initiate fluid resuscitation with 1L/hr isotonic fluids in adults.
  • Avoid using the Parkland or Modified Brooke formula, as the %TBSA burned does not accurately reflect the extent of deep tissue injury in electrical burns.
  • Titrate fluid administration to maintain urine output:
    • Adults: 100 mL/hr
    • Children: 1.5–2 mL/kg/hr

Referral
Patients with suspected deep tissue injury should be referred to a burn center when available to ensure comprehensive care.

Chemical Burns

Superficial chemical burns may conceal deeper tissue injuries, making them more challenging to assess than thermal burns. Tissue damage is often underestimated, necessitating frequent reassessment of wounds and clinical status.

Chemical burn

Management [2,12]

  • Fully expose the patient as soon as possible to minimize ongoing tissue damage. Providers should wear personal protective equipment (PPE) before starting decontamination.
  • Copious irrigation is critical and should be performed immediately, continuing for at least 30 minutes or until neutral skin or eye pH is achieved (using serial litmus paper).
  • Exceptions to irrigation: Dry lime, elemental metals, and phenol require alternative treatments instead of water irrigation.
  • Patients with chemical burns should be referred to a burn center for specialized care.

Radiation Burns

  • Cutaneous manifestations of radiation exposure have a slower onset compared to thermal burns [2,13]. Symptoms such as erythema, calor (warmth), and pruritus may appear hours to days after exposure.
  • Waxing and waning of symptoms:
    • A latent phase without visible cutaneous symptoms often follows initial erythema, calor, and pruritus (1–2 days post-exposure).
    • A second wave may occur days to a week later, presenting as erythema, calor, pruritus, desquamation, ulceration, or necrosis.
    • Subsequent waves of symptoms are more common with potent radiation forms (e.g., beta- and gamma-waves), occurring months post-exposure.
  • High radiation doses are associated with systemic effects, including hair loss and acute radiation syndrome (ARS):
    • ARS symptoms include loss of appetite, fatigue, headache, nausea, vomiting, and diarrhea.

Management

  • Anti-inflammatory medications should be administered during the latent phase when cutaneous symptoms are absent.
  • As with chemical burns, all patients with significant radiation burns should be referred to a burn center for evaluation and management.

Inhalation Injuries

General Overview

Inhalational injuries are a leading cause of mortality in burn patients. They are commonly associated with thermal injuries, which cause upper airway edema, and chemical injuries, which result in damage to the lower airway and lung parenchyma.

Assessment

Evaluating for inhalational injuries involves identifying key clinical signs, such as soot in the oropharynx, singed facial hair, or other indications of airway compromise. For chemical burns, determining the substances burned or combusted is critical to understanding the nature of the injury. Diagnostic tools include obtaining arterial blood gas (ABG) analysis and chest X-ray when available to assess respiratory function and lung involvement.

Management [2,5]

Maintaining a Patent Airway

Ensuring a clear airway is critical in burn patients. Prompt airway management is crucial in inhalational injuries. A low threshold for endotracheal intubation is necessary in cases of airway compromise, severe burns, or full-thickness/circumferential burns involving the chest or neck. If progressive airway edema is observed, fiberoptic intubation is preferred, provided it is available. Given the rapid progression of airway edema, early intubation is advised to prevent airway obstruction and ensure adequate ventilation.

Thermal burn, Inhalation Injury

Oxygen Therapy
Patients with suspected inhalation injuries should receive humidified 100% oxygen via a non-rebreather mask immediately. This is particularly important in cases of carbon monoxide poisoning, as high-flow oxygen effectively reduces carboxyhemoglobin levels, improving oxygen delivery to tissues.

Fluid Resuscitation
Inhalation injuries increase fluid requirements beyond those predicted by burn size alone. Fluid resuscitation must be carefully balanced to avoid under-resuscitation, which risks hypoperfusion, and over-resuscitation, which can lead to complications such as pulmonary edema or compartment syndrome.

Medications
Several medications may be employed to address specific symptoms:

  • Bronchodilators: Relieve bronchospasm and improve airway patency.
  • Mucolytics: Help thin and loosen mucus, facilitating its clearance from the airways.
  • Nebulized Heparin: Prevents fibrin cast formation in the airways, reducing the risk of airway obstruction.

Ventilatory Support

Mechanical ventilation may be required for patients with severe respiratory compromise. Ventilator settings must be carefully optimized to prevent ventilator-induced lung injury. Techniques such as low tidal volume ventilation and high-frequency percussive ventilation may offer benefits in managing patients with compromised pulmonary function.

This comprehensive approach ensures effective airway management and respiratory support in burn patients with inhalation injuries.

Special Patient Groups

Pediatric Patients

Thermal Burns

  • Fluid Resuscitation:
    • In addition to using the Parkland formula for fluid replacement, pediatric patients require maintenance intravenous fluids (mIVF) to meet baseline hydration needs.
    • Children under 5 years of age should have glucose added to their mIVF to prevent hypoglycemia.

Electrical Burns

  • The majority of management principles are similar to those for adults.
  • Oral Burns:
    • Oral burns, often caused by chewing on electrical cords, require special attention. Burns at the commissure (corner of the lips) have a high risk of bleeding due to erosion of the labial artery.
    • All significant oral burns should be admitted for observation and plastic surgery consultation to prevent and manage complications.

Pregnant Patients

Electrical Burns

  • For pregnant patients with electrical burns, obstetric consultation is essential to assess maternal and fetal health.
  • Continuous monitoring of fetal heart tones is necessary to evaluate the well-being of the fetus following an electrical injury.

When To Admit This Patient

The American Burn Association released updated guidelines in December 2022 for burn patient referral and management.

Guidelines for Burn Patient Referral - Courtesy of American Burn Association - From: https://ameriburn.org/wp-content/uploads/2023/01/one-page-guidelines-for-burn-patient-referral-16.pdf [14]

According to these guidelines:

  • Moderate to Severe Burns: Patients with moderate to severe burns, as defined by burn depth and total body surface area (TBSA), require hospital admission for comprehensive burn staging and treatment.
  • Minor Burns: Patients with minor burns, such as superficial burns or those involving <10% TBSA superficial partial-thickness burns, can be managed in an outpatient setting.

To prevent secondary infection, patients discharged with minor burns must have access to appropriate topical ointments and dressings. Patients with partial-thickness burns should undergo regular wound checks following discharge to monitor healing and prevent complications.

Revisiting Your Patient

The patient’s burns were classified as moderate to severe, and he was intubated due to the presence of singed nasal hairs and significant respiratory distress. Using the Rule of 9s, the total burn area was calculated to be 31.5% TBSA, including the face (4.5%), the front of both arms and hands bilaterally (4.5% each), and the torso (18%).

Given the depth of the burns, lactated Ringer’s IV resuscitation was initiated, with a target of delivering 4725 mL in the first eight hours, as calculated using the Parkland formula. A Foley catheter was placed, and urine output was titrated to 0.5 mL/kg/hr. The patient also received IV analgesia and was subsequently transferred to a burn center for further management.

Authors

Picture of Michaela Banks

Michaela Banks

Michaela Banks is a current resident at Louisiana State University in New Orleans in Emergency Medicine. She graduated with a degree in Psychology and Global Health from Duke University and went on to obtain her MD and MBA from the University of Virginia. During residency, she has become particularly interested in burns and outcomes, and gave an oral presentation on the “Association Between Compliance with an Organized State Burn Triage Center and Burn Outcomes” at ACEP 22. Michaela also serves on the Emergency Medicine Residents’ Association Board of Directors.

Picture of Anthony Dikhtyar

Anthony Dikhtyar

Dr. Dikhtyar is a graduate of St. George’s University School of Medicine and recently matched into Emergency Medicine at TriStar Skyline Medical Center in Nashville, TN. His professional interests include medical education, medical photography, and global health in the former Soviet Union. His most recent publications can be found in the Visual Journal of Emergency Medicine.

Picture of Jacquelyne Anyaso

Jacquelyne Anyaso

Jackie Anyaso, MD, MBA is a second-generation Nigerian immigrant born and raised in Chicago, Illinois. She attended medical school at the University of Illinois at Chicago and will be completing her emergency medicine training at Harvard-Affiliated Emergency Residency Program. Her ultimate goal is to serve vulnerable populations in efforts to reduce healthcare disparities. Her clinical interests include critical care medicine, global health, and the intersection between medicine and business. Outside of medicine, she enjoys community service, traveling, and spending time with family and friends.

Picture of Ashley Pickering

Ashley Pickering

Before medical school I had a diverse career path, which included biomedical engineering, outdoor education, working as an EMT on a Colorado ski patrol, and critical care nursing. I lived out west for 15 years, mainly in CO, and went to medical school at University of Arizona in Tucson before moving to Baltimore for residency at University of Maryland. Currently I am a Global Emergency Medicine Fellow at University of Colorado. Throughout my training I have found ample opportunities to pursue my interest in building emergency care globally. I have researched the barriers to accessing emergency care in rural Uganda, helped to provide emergency care training in Sierra Leone and Liberia and am currently the Executive Director of Global Emergency Care a non-profit training non-physician clinicians in Uganda. My current focus is on quality of emergency care in LMICs. I am working on an WHO Emergency Care Toolkit implementation project which explores the impact of basic emergency care educational and process improvements on clinical indicators of quality, as well as the experiences patients and staff.

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References

  1. Jeschke MG, Mlcak RP, Finnerty CC, et al. Burn size determines the inflammatory and hypermetabolic response. Crit Care. 2007;11(4):R90. doi:10.1186/cc6102
  2. American Burn Association. (2018). Advanced Burn Life Support Course Provider Manual 2018 Update. https://ameriburn.org/wp-content/uploads/2019/08/2018-abls-providermanual.pdf
  3. Schaefer TJ, Szymanski KD. Burn Evaluation And Management. [Updated 2022 Aug 23]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK430741/
  4. Jeschke MG, van Baar ME, Choudhry MA, Chung KK, Gibran NS, Logsetty S. Burn injury. Nat Rev Dis Primers. 2020;6(1):11. Published 2020 Feb 13. doi:10.1038/s41572-020-0145-5
  5. Foncerrada G, Culnan DM, Capek KD, et al. Inhalation Injury in the Burned Patient. Ann Plast Surg. 2018;80(3 Suppl 2):S98-S105. doi:10.1097/SAP.0000000000001377
  6. Emergency Care of Moderate and Severe Thermal Burns in Adults. UpToDate. Feb. 2023. https://www.uptodate.com/contents/emergency-care-of-moderate-and-severe-thermal-burns-in-adults?topicRef=349&source=see_link#H4430737.
  7. Department of Health. Determining Total Body Surface Area. From: https://www.health.state.mn.us/communities/ep/surge/burn/tbsa.pdf Accessed December 1, 2024.
  8. Guidelines for Burn Patient Referral. From: https://ameriburn.org/resources/burnreferral/ Accessed: December 1, 2024.
  9. Burns. WikiEM. 21 Nov. 2021; 4:1-2. https://wikem.org/wiki/Burns#Evaluation.
  10. Treatment of Minor Thermal Burns. UpToDate. Feb. 2023. https://www.uptodate.com/contents/treatment-of-minor-thermal-burns#H20.
  11. Electrical injuries and lightening strikes: Evaluation and management. UpToDate. Mar 2023. https://www.uptodate.com/contents/electrical-injuries-and-lightning-strikes-evaluation-and-management#H3065280448
  12. Topical chemical burns: Initial assessment and management. UpToDate. Mar 2023. https://www.uptodate.com/contents/topical-chemical-burns-initial-assessment-and-management
  13. Cutaneous Radiation Injury (CRI): A Fact Sheet for Clinicians. 4 Apr. 2018. https://www.cdc.gov/nceh/radiation/emergencies/criphysicianfactsheet.htm
  14. Guidelines for Burn Patient Referral. From: https://ameriburn.org/wp-content/uploads/2023/01/one-page-guidelines-for-burn-patient-referral-16.pdf

FOAm and Further Reading

Burns. Stanford Medicine: Healthcare. https://stanfordhealthcare.org/medical-conditions/skin-hair-and-nails/burns.html

http://www.webmd.com/first-aid/tc/burns-topic-overview

http://www.nationalburnservice.co.nz/emergencyplan.htm

https://flippedemclassroom.wordpress.com/2012/12/02/burn/ 

http://www.mdcalc.com/parkland-formula-for-burns/#about-equation

Reviewed and Edited By

Picture of Erin Simon, DO

Erin Simon, DO

Dr. Erin L. Simon is a Professor of Emergency Medicine at Northeast Ohio Medical University. She is Vice Chair of Research for Cleveland Clinic Emergency Services and Medical Director for the Cleveland Clinic Bath emergency department. Dr. Simon serves as a reviewer for multiple academic emergency medicine journals.

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.

Intraosseous (IO) Lines/Access (2024)

~ iEM Education Project Team ~ Leave a comment

by Yousif Al-Khafaji & Mustak Dukandar

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Introduction

Obtaining intravascular access in the emergency department is one of the most essential steps in managing critically ill patients. While it is a simple step for most patients, it can be the most challenging procedure during resuscitation. The pediatric population has more body fat, making it difficult to localize their veins. In addition, they have tiny peripheral veins that easily collapse in states of shock. On the other hand, in adults, patients who are obese, those who suffer from extensive burns, or are in shock challenge the clinician in obtaining vascular access [1].

Intraosseous (IO) access involves inserting a hollow needle through the cortex of the bone and into the medullary space. This allows clinicians to infuse fluids, medication, or almost anything that can be administered through the intravenous (IV) route and achieve the same desired effect as the IV route. The IO line is merely a bridging tool to buy the clinician time to obtain IV access. In most cases, IO access is a simple procedure, and clinicians should not hesitate to insert an IO line if peripheral IV access attempts fail.

IO lines can safely remain in place for up to 24 hours and are often a bridge to either IV or Central Venous line placement.

Indications

There are clear indications for IO access. Each of these indications highlights the critical role of IO lines in emergency medicine, providing a swift and effective solution for vascular access in life-threatening situations [3]. When IV access cannot be achieved, IO access is safe, reliable, and quick. It can be accomplished in 30 to 60 seconds and even faster with an IO gun. This is especially helpful in pediatric emergencies when time is critical. 

Emergency intravascular access when other methods have failed
IO access is indicated when IV access is not achievable in critical situations, such as trauma, shock, or severe dehydration. In critically ill patients, a maximum of two failed attempts is generally considered sufficient to shift to IO access. The IO line provides a rapid and reliable alternative to IV lines for administering fluids, medications, or blood products directly into the vascular system via the bone marrow [4]. 

Cardiac arrest
During cardiac arrest, time is critical, and establishing vascular access can be challenging. IO access is often used to administer life-saving medications like epinephrine when IV access cannot be obtained quickly. It ensures the rapid delivery of drugs into circulation during resuscitation [5].

Obtaining blood for laboratory evaluation
IO access allows for the collection of blood samples for laboratory testing, including complete blood count, electrolytes, and blood gas analysis [6]. This is especially useful in emergency situations where traditional venipuncture is impractical or impossible.

Contraindications

Physicians should be aware of a couple of important complications. These contraindications emphasize the importance of careful site selection and patient evaluation before performing IO access to minimize complications and maximize the effectiveness of the procedure [1].

Fractured bone
A fracture at the intended site of IO access is an absolute contraindication. Using a fractured bone for IO infusion can result in extravasation of fluids and medications, potentially worsening the injury and causing further complications.

Infection or burn overlaying insertion site
Localized infection or burns at the insertion site pose a significant risk of introducing pathogens into the bone marrow, leading to osteomyelitis or systemic infection. These conditions are absolute contraindications for IO placement.

Prior use of the same bone for IO infusion
Repeated use of the same bone for IO access can damage the bone marrow and structure, increasing the risk of complications such as extravasation or impaired drug delivery. A different site should be chosen for subsequent IO insertions.

Osteoporosis and osteogenesis imperfecta
These conditions result in fragile bones, increasing the likelihood of fractures or other complications during needle insertion. Alternative access methods should be considered for patients with these conditions.

Administration of ultra-short-acting medications like adenosine (relative contraindication)
Medications like adenosine, which rely on rapid systemic distribution, may not be as effective when administered via IO access due to potential delayed uptake into circulation. This is a relative contraindication, depending on the clinical scenario.

Equipment and Patient Preparation

Equipment

IO Needle

  • Ranges from 15-18 gauge needles
  • Color coding is common:
    • Pink (15 mm): For patients weighing 3–39 kg
    • Blue (25 mm): For patients ≥3 kg and above
    • Yellow (45 mm): For patients ≥40 kg, excessive tissue, or dense bone sites (e.g., proximal humerus or anterior superior iliac spine)

IO Devices (to facilitate insertion)

  • Powered IO Drills (e.g., EZ-IO)
  • Manual IO Drills (e.g., Cook IO Needle or Jamshidi-type needle)

Skin Disinfectants

  • Chloraprep
  • Alcohol swabs
  • Optional: Povidine or Chlorhexidine

Syringe and Flush Materials

  • Saline flush (crystalloid solution, e.g., normal saline or lactated Ringer’s)
  • Intravenous tubing

Lidocaine 2% (without epinephrine)

  • For topical and subcutaneous infiltration in awake patients, as they may experience pain during fluid infusion rather than needle insertion.

Additional Equipment

  • Infusion pump (to regulate fluid delivery)
  • Tape (for securing the IO line)
Arrow® EZ-IO® Intraosseous Vascular Access System - adopted from https://www.teleflex.com/usa/en/product-areas/emergency-medicine/intraosseous-access/arrow-ez-io-system/use-and-application/Arrow_EZ-IO_Landmarking_Poster.pdf

Patient Preparation

  1. Informed Consent
    • Obtain informed consent by explaining the procedure, its benefits, and associated risks to the patient or their guardians. In emergency situations where consent cannot be obtained, implied consent applies.
  2. Site Selection
    • Choose the most appropriate insertion site based on the clinical scenario. Common sites include:
      • Humeral Head
      • Proximal Tibia
      • Medial Malleolus
      • Sternum
      • Distal Radius
      • Distal Femur
      • Anterior Superior Iliac Spine
    • Note: The proximal tibia and humeral head are most commonly used during cardiac arrest as these locations do not interfere with other life-saving procedures like intubation [7].
  3. Contraindication Assessment
    • Ensure there are no contraindications (e.g., fractures, infections, burns, prior IO use at the same site, or certain bone conditions) at the intended site of insertion.
  4. Site Exposure
    • Properly expose the selected insertion site to facilitate accurate placement and reduce the risk of contamination.
  5. Universal Precautions
    • Apply universal precautions, such as wearing gloves at a minimum, to maintain aseptic conditions during the procedure.
  •  
IO placement locations. IO size (color) is subject to the patients body weight.

Sites of IO insertion and some hints [8]

  1. Proximal Tibia
    • 2 finger breadths below the tibial tuberosity (1-3 cm) on the medial, flat aspect of the tibia.
    • Commonly used for ease of access, especially in emergencies.
  2. Distal Tibia
    • Medial surface at the junction of the medial malleolus and the shaft of the tibia, posterior to the greater saphenous vein.
  3. Proximal Humerus (Adults only; use the yellow needle)
    •  Preparation:
      • Keep the arm adducted and internally rotated (rest the patient’s hand on their bellybutton).
      • Slide fingers up the humerus until you feel the notch (surgical neck).
    •  Insertion:
      • Insert the IO needle 1 cm above the surgical neck into the greater tubercle.
      • Immobilize the arm to prevent displacement of the IO line (avoid shoulder abduction).
  4. Distal Femur
    • Primarily used in infants and children due to easier bone access and growth plate considerations.
  5. Pelvic Anterior Superior Iliac Spine (ASIS)
    • An alternative site, especially when lower extremity or upper extremity sites are unavailable.
  6. Sternum
    • Provides the highest flow rate of any location, making it suitable for rapid infusions during critical situations.

Procedure Steps

  1. Preparation
    • Identify the designated site using a sterile gloved finger.
    • Disinfect the overlying skin using appropriate antiseptic (e.g., chlorhexidine).
    • Administer local anesthetic if the patient is awake.
    • Ensure the stylet is properly positioned on the needle prior to insertion.
    • Prepare necessary equipment, including a 20 ml saline syringe, IV tubing, tape, medications, fluids, and infusion pump.
  2. Needle Insertion
    • Insert the needle perpendicularly through the skin down to the bone.
    • Use an IO drill or manually twist the needle clockwise with firm, gentle pressure until a “give” is felt (loss of resistance), indicating entry into the marrow.
    • Ensure the needle locks into place.
  3. Confirmation of Placement
    • The needle should stand upright without additional support if properly positioned.
    • Remove the stylet and attach a syringe.
    • Aspirate to confirm the presence of marrow or blood (not always visible).
    • Gently flush the line with saline while observing for swelling at or around the insertion site.
  4. Troubleshooting
    • If swelling occurs or the test injection fails, remove the IO needle and repeat the procedure on a different site.
  5. Securing and Using the IO Line
    • If Io works properly, stabilize the needle using tape or gauze padding as necessary.
    • Attach IV tubing to the needle hub.
    • Begin infusion of fluids, blood products, or medications.
    • If the patient is awake and experiences pain during infusion, administer lidocaine through the IO line for analgesia [2].
  •  

Complications [9]

Extravasation of Fluid

Occurs when fluid or medication leaks into surrounding soft tissues instead of the bone marrow cavity. This can cause localized swelling, tissue damage, and discomfort. Proper placement and observation for swelling during infusion are essential to avoid this complication.

Compartment Syndrome

Results from increased pressure within a muscle compartment due to extravasation of fluid. It can compromise blood flow, leading to tissue ischemia and potential necrosis. Immediate recognition and corrective action are necessary to prevent long-term damage [10].

Bone Fracture

More common in patients with pre-existing bone disorders, such as osteoporosis or osteogenesis imperfecta. Improper needle insertion technique can increase the risk of fracturing the bone at the insertion site. Physicians should be careful when inserting IO lines in small children because too much pressure during drilling may cause fractures.

Osteomyelitis

A rare but serious complication involving infection of the bone and marrow. This risk increases if aseptic technique is not followed or if there is a pre-existing infection near the insertion site.

Preventative Measures:

  • Use strict aseptic technique to minimize infection risks.
  • Properly assess the patient’s bone health and contraindications before insertion.
  • Monitor the insertion site for early signs of complications, such as swelling or pain, during and after infusion

Hints and Pitfalls

Purpose and Time Limit

  • IO access is a bridging tool used to buy time for obtaining peripheral or central IV access.
  • IO needles should not remain in place for more than 24 hours, as the risk of complications increases significantly after that time frame.

Site and Device Selection

  • Always use an uninjured limb for IO placement; if no uninjured limb is available, the sternum is preferred.
  • An IO drill or gun is recommended over manual insertion for consistent and reliable placement.
  • Needle selection must be appropriate for the selected site and the marrow cavity to ensure proper access.

Needle Placement and Security

  • IO needle displacement can sometimes occur, especially in pediatric patients with soft bones; this can be mitigated by securing the needle to the skin properly.
  • The anterior superior iliac spine may be considered as an alternative site in cases of soft bone structures.

Medication and Dosage

  • Any medication that can be administered via IV access can also be given through IO access without dose adjustment, as the bioequivalence between IO and IV routes is similar. [11,12]

Laboratory Sampling

  • Lab tests with good correlation from IO samples include hemoglobin/hematocrit, chloride, glucose, urea, creatinine, and albumin.
  • Other lab values, such as WBC, platelets, serum CO2, sodium, potassium, and calcium, may not correlate well with venous samples. [13]
  •  

Special Patient Groups

Pediatrics

  • Challenges: In pediatric patients, the bones can sometimes be too soft, which increases the risk of needle displacement even when placed correctly.
  • Recommendation: To mitigate this risk, consider using the anterior superior iliac spine as an alternative site. This site may provide a more stable placement in cases where traditional sites like the tibia are less effective.

Geriatrics

  • Challenges: Older adults often have pre-existing bone disorders such as osteoporosis, which make their bones more fragile.
  • Risks: IO insertion in such patients can lead to fractures, especially if not performed with careful technique and appropriate needle selection.
  • Recommendation: Perform a thorough assessment of bone health and use alternative vascular access methods if significant bone fragility is present.

Pregnant Patients

  • Considerations: There are no contraindications for IO insertion in pregnant women. This makes IO access a viable option during emergencies where quick vascular access is necessary.
  • Precautions: Ensure that the chosen site does not interfere with obstetric care and consider patient positioning to maintain comfort and safety during the procedure.

Authors

Picture of Yousif Al-Khafaji

Yousif Al-Khafaji

Chief Emergency Medicine Resident - Tawam Hospital, Al Ain, UAE

Picture of Mustak Dukandar

Mustak Dukandar

Tawam Hospital Emergency Department

Listen to the chapter

References

  1. Roberts and Hedges’ Clinical Procedures in Emergency Medicine and Acute Car-Elsevier (2017), chapter 25
  2. ATLS Student course manual Tenth Edition (2018). Appendix G, 351
  3. Phillips L, Brown L, Campbell T, et al. Recommendations for the use of intraosseous vascular access for emergent and nonemergent situations in various healthcare settings: a consensus paper. J Emerg Nurs. 2010;36(6):551-556. doi:10.1016/j.jen.2010.09.001
  4. Oksan D, Ayfer K. Powered intraosseous device (EZ-IO) for critically ill patients. Indian Pediatr. 2013;50(7):689-691. doi:10.1007/s13312-013-0192-z
  5. Leidel BA, Kirchhoff C, Bogner V, et al. Is the intraosseous access route fast and efficacious compared to conventional central venous catheterization in adult patients under resuscitation in the emergency department? A prospective observational pilot study. Patient Saf Surg. 2009;3(1):24. Published 2009 Oct 8. doi:10.1186/1754-9493-3-24
  6. Tallman CI, Darracq M, Young M. Analysis of intraosseous blood samples using an EPOC point of care analyzer during resuscitation. Am J Emerg Med. 2017;35(3):499-501. doi:10.1016/j.ajem.2016.12.005
  7. Wampler D, Schwartz D, Shumaker J, Bolleter S, Beckett R, Manifold C. Paramedics successfully perform humeral EZ-IO intraosseous access in adult out-of-hospital cardiac arrest patients. Am J Emerg Med. 2012;30(7):1095-1099. doi:10.1016/j.ajem.2011.07.010
  8. Day MW. Intraosseous devices for intravascular access in adult trauma patients. Crit Care Nurse. 2011;31(2):76-90. doi:10.4037/ccn2011615
  9. ACLS provider Manual Supplementary Material (2016). Intraosseous Access, 57-61
  10. Vidal R, Kissoon N, Gayle M. Compartment syndrome following intraosseous infusion. Pediatrics. 1993;91(6):1201-1202.
  11. Faga, M., & Wolfe, B. (2016). Vascular access in hospitalized patients. Hospital Medicine Clinics, 5(1), 1-16.
  12. Von Hoff, D.D., Kuhn, J.G., Burris, H.A. 3rd, & Miller, L.J. (2008). Does intraosseous equal intravenous? A pharmacokinetic study. Am J Emerg Med, 26, 31-38
  13. Miller LJ, Philbeck TE, Montez D, Spadaccini CJ. A new study of intraosseous blood for laboratory analysis. Arch Pathol Lab Med. 2010;134(9):1253-1260.

FOAM and Further Reading

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.

Gastroenteritis and Dehydration In Children (2024)

~ iEM Education Project Team ~ Leave a comment

by Neha Hudlikar & Abdulla Alhmoudi 

Authors
Listen

You have a new patient!

14-month-old Zoey is brought to A&E by her mother with complaints of vomiting and diarrhea for one day. She has had six episodes of vomiting and eight episodes of loose stools since last night. She has also not had a wet diaper for almost 12 hours now. In triage, her vitals are HR 165 b/min, RR 45 br/min, Temperature 38.5 C, SpO2 97% CR 3 seconds. The nurse in triage notes that she has a glazed look. She is otherwise fit and well, with no past medical history. Zoey’s weight – 10 kg.

What will be your approach for this patient?

a-photo-of-a-baby (image produced by using ideogram2.0)

What do you need to know?

Importance

Acute gastroenteritis is one of the most common reasons for visits to pediatric emergency departments [1]. The World Health Organization (WHO) defines diarrhea as the passage of three or more liquid stools per day, or a more frequent passage than what is normal for the individual. When diarrhea occurs alongside vomiting, it is referred to as acute gastroenteritis (AGE).

Diarrhea can be categorized into three clinical types based on the presence or absence of blood and the timing of symptoms:

1. Acute watery diarrhea – lasts from hours to several days, but less than 14 days.
2. Acute bloody diarrhea – also known as dysentery, lasts less than 14 days.
3. Persistent diarrhea – lasts longer than 14 days.

Infectious gastroenteritis can be caused by various pathogens, including viruses, bacteria, and parasites. Rotavirus is the most common causative agent worldwide, responsible for 37% of diarrhea-related deaths in children under five years of age.

Epidemiology

Gastroenteritis is the second leading cause of death in children below the age of 5 and a leading cause of malnutrition in this age group. Globally, there are approximately 1.7 billion cases of childhood diarrheal diseases yearly, and the burden is substantial [2]. There is a direct impact of admission costs on the hospital budget and direct and indirect societal costs when children are admitted to hospitals.

In low-income countries, children under three years old, on average, have three episodes of diarrhea every year. This puts them at risk of malnutrition and, in turn, makes them vulnerable to further episodes of infectious diarrhea.

Pathophysiology

The loss of water and electrolytes via stools, vomit, sweat, and urine without adequate replacement leads to dehydration, a serious complication of gastroenteritis. Physiologic factors that predispose children to serious complications from dehydration include limited stores of fat and glycogen, relatively larger extracellular fluid compartments, and a limited ability to conserve water through their kidneys compared to adults.

Bicarbonate loss in stools, decreased tissue perfusion leading to anaerobic metabolism and lactic acid production, ketosis due to starvation, and decreased excretion of hydrogen ions due to poor renal perfusion are some of the mechanisms contributing to metabolic acidosis in pediatric dehydration due to acute gastroenteritis.

The exact pathophysiology depends on the causative agent. Infectious agents cause diarrhea via adherence, mucosal invasion, enterotoxin, and cytotoxin production.S. aureus and Bacillus cereus produce heat-stable enterotoxins in the food, which once consumed, lead to rapid onset of symptoms and are usually self-limiting. C. Perfingens, Enterotoxigenic E.coli produce enterotoxins in the small intestine leading to watery diarrhea. Other pathogens like enterohemorrhagic E. Coli (EHEC), Salmonella, Shigella, and Campylobacter jejuni produce toxins that directly invade the bowel leading to inflammatory diarrhea. Viruses often destroy the villus surface of the intestinal mucosa, and parasites often adhere to the mucosa.

Medical History

A focused and detailed history is essential to narrowing our differential diagnoses and guiding management. The history should include the timing, frequency, and severity of symptoms. We should also ask about any contact with someone with similar symptoms, known or suspected outbreaks in school or nursery, and recent travel.

All patients with acute gastroenteritis are at risk of dehydration, and the initial evaluation should include questions to assess its severity. The child’s oral intake, amount of urine passed, mental status (lethargy/irritability), etc., should be asked for in the initial evaluation. 

It is also important to ask for associated symptoms such as fever, abdominal pain, blood in the stools, and rash. Children with inflammatory diarrhea can develop serious illnesses like hemolytic uremic syndrome (HUS) with renal involvement. 

Other important questions in history include the child’s vaccination status, recent hospitalization/antibiotic use, and whether the child has any underlying chronic medical conditions/immunosuppression.

Physical Examination

Examining the child should be systematic, looking for the severity of dehydration and differentiating gastroenteritis from other causes of vomiting and diarrhea in children.

General examination should include the child’s appearance, alertness, lethargy, irritability, and weight. Vital signs should be assessed relative to the age. Physicians should look for explicit signs of dehydration, such as dry mucous membranes, sunken eyes, depressed fontanelle, and the presence/absence of tears. The cardiovascular exam should include heart rate, quality of pulses, and central and peripheral capillary refill times. Deep, acidotic breathing suggests severe dehydration. An abdominal examination assesses tenderness, bowel sounds, guarding, and rebound. Flank tenderness increases the likelihood of pyelonephritis. Examine the skin to check skin turgor, peripheral temperature, and other signs such as jaundice/rash.

Abnormal skin turgor, prolonged capillary refill time, and abnormal respiratory pattern are the three most useful examination findings in children with more than 5% dehydration [3]. It is important to note that these signs can be subtle, and determining the severity of dehydration accurately is challenging for physicians.

Alternative Diagnoses

Dehydration most commonly results from acute gastroenteritis in children. However, other diagnoses should be considered based on physical examination and history. Children with fever who are very ill-looking should have sepsis as one of the differential diagnoses. Other diagnoses to consider are urinary tract infection, appendicitis, hemolytic uremic syndrome, intussusception, and diabetic ketoacidosis. Symptoms immediately after ingestion should prompt physicians to consider ingestion of a foreign body or toxic substance. 

Vomiting and diarrhea are two important components that ED practitioners need a careful evaluation to rule in or out various diseases.

When evaluating vomiting in children, it is essential to consider a wide range of differential diagnoses spanning several systems. Central nervous system causes include space-occupying lesions, hydrocephalus, and infections. Cardiac-related vomiting may be attributed to congestive heart failure from various etiologies. Gastrointestinal conditions such as intussusception, midgut volvulus, pyloric stenosis, appendicitis, and esophageal or hepatic disorders are significant considerations. Renal issues like urinary tract infections, pyelonephritis, renal insufficiency, and renal tubular acidosis can also manifest as vomiting. Furthermore, metabolic and endocrine abnormalities, including diabetic ketoacidosis, Addisonian crisis, congenital adrenal hyperplasia, and inborn errors of metabolism, are key causes. Infectious conditions such as sepsis, pneumonia, otitis media, streptococcal pharyngitis, and gastroenteritis must also be included in the diagnostic workup.

Diarrhea in children can arise from diverse causes. Gastrointestinal disorders such as intussusception, Hirschsprung’s disease with toxic megacolon, inflammatory bowel disease, and appendicitis are prominent. Renal conditions, including urinary tract infections and pyelonephritis, can also lead to diarrhea. Infectious etiologies like sepsis, pneumonia, gastroenteritis, and pseudomembranous colitis are frequent contributors. Other causes include drug effects or overdose, hemolytic uremic syndrome, and congenital secretory diarrhea.

Understanding these potential causes is essential for accurate diagnosis and effective management.

Acing Diagnostic Testing

The workup should be guided by history and physical examination to determine the level of dehydration. In most cases, it is a self-limiting disease, and the principal goal of testing in ED should be to identify and correct fluid, electrolyte, and acid-base deficits. 

Most children with mild to moderate disease require no diagnostic testing. Children requiring IV hydration should have blood gas, serum electrolytes, bicarbonate, urea, and creatinine levels tested. It is common for young children to have hypoglycemia, and checking serum glucose levels is important. In children presenting with fever or mucous/blood in their stools, consider testing for fecal leucocytes to support a diagnosis of invasive diarrhea. A positive test should be followed by a stool culture, and it is important to note that a negative test does not rule out invasive disease.

Consider additional testing, such as blood and urine cultures, chest X-rays, and lumbar puncture, in immunosuppressed patients, infants less than 2 months old, or children with suspicion of bacteremia or localized invasive disease. 

Risk Stratification

The Gorelick scale and The Clinical Dehydration Score (CDS) are two of the most widely used scoring systems to predict the presence and severity of dehydration in the pediatric population. It is important to note that neither can definitively rule in or out dehydration in children and infants. Physicians should continue to use a structured approach to patients presenting with acute gastroenteritis and use these scores to aid clinical decision-making [4,5,6].

Clinical Dehydration Scale

 

0

1

2

 

0: No dehydration (<3%)

1-4: Some dehydration (≥3%- <6%)

5-8: Moderate dehydration (≥6%)

General appearance

Normal

Thirsty, restless or lethargic but irritable when touched

Drowsy, limp, or comatose

Eyes

Normal

Slightly sunken

Very sunken

Mucous membranes

Moist

“Sticky”

Dry

Tears

Present

Decreased

Absent

 

Gorelick Scale for Dehydration

characteristic

no or minimal dehydration

moderate to severe dehydration

general appearance

alert

restless, lethargic, unconscious

capillary refill

normal

prolonged or minimal

tears

present

absent

mucous membrane

moist

dry, very dry

eyes

normal

sunken; deeply sunken

breathing

present

deep; deep and rapid

quality of pulses

normal

thready; weak or impalpable

skin elasticity

instant recoil

recoil slowly; recoil > 2 s

heart rate

normal

tachycardia

urine output

normal

reduced; not passed in many hours

Evaluating dehydration with Gorelick scale [6];

4-Point Scale (Italics):

  • 4 points: Presence of 2 or more clinical signs correlating with ≥5% body weight loss from baseline.
  • 4 points: Presence of 3 or more clinical signs correlating with ≥10% body weight loss from baseline.

10-Point Scale (Based on All Signs and Symptoms):

  • ≥3 clinical signs: Associated with ≥5% body weight loss from baseline.
  • ≥7 clinical signs: Associated with ≥10% body weight loss from baseline

Some groups are at higher risk of developing complications from acute gastroenteritis. These include premature infants, very low birth weight infants, and infants below the age of 3 months. Children who are malnourished, immunosuppressed, and with chronic underlying medical conditions are also at higher risk of developing complications.

Indications for inpatient management of children presenting with acute diarrhea have been proposed, and the Table below summarizes these recommendations.

Indications for Inpatient Management of Children with Acute Diarrhoea

  • Difficulties in administrating oral rehydration therapy (patient refusal, intractable vomiting)
  • History of premature birth, chronic medical conditions, or concurrent illness, very young age
  • Parental/caregiver concern about continuing ORT at home/unable to provide adequate care
  • Persistent vomiting, high output diarrhoea, persistent dehydration
  • Uncertainty of diagnosis warranting further observation
  • Progressive symptoms or unusual irritability/drowsiness
  • Lack of easy access to hospital care if needing to return

Adapted from King CK, Glass R, Bresee JS, Duggan C; Centers for Disease Control and Prevention. Managing acute gastroenteritis among children: oral rehydration, maintenance, and nutritional therapy. MMWR Recomm Rep. 2003;52(RR-16):1-16.

Management

Management in the Emergency Department should initially focus on correcting dehydration. Oral rehydration solution (ORS) is recommended for all children with mild to moderate dehydration.

To calculate the volume of oral replacement therapy (ORT), the first step is to estimate the degree of dehydration based on history and physical examination findings (see Table below). The desired volume of ORS is then calculated based on the degree of dehydration (30 to 50 mL/kg for mild and 60 to 80 mL/kg for moderate dehydration). 25% of the calculated volume of ORS is given every hour for the first four hours and ongoing losses can be replaced at 10 mL/kg for each stool and 2 mL/kg for each emesis. The patient needs reassessment at the end of the first few hours and those with no clinical deterioration may have a 2 to 4-hour trial with ORT. If the child is unable to keep up with ongoing losses and if volume replacement is not adequate at the end of 8 hours, IV rehydration is recommended. Ondansetron is a selective 5-hydroxytryptamine type 3 receptor antagonist, a useful adjunct in treating AGE. It acts on peripheral and central chemoreceptors to alleviate nausea. It has been shown to decrease vomiting, improve oral intake, and reduce the need for intravenous fluid resuscitation and hospital admissions [7].

Assessment of Degree of Dehydration

Mild dehydration (3%-5%)

Moderate dehydration (5%-10%)

Severe dehydration (> 10%)

Mental status

Alert

Irritable

Lethargy

Heart rate

Normal

Increased

Increased

Quality of pulses

Normal

Normal to decreased

Decreased to thready

Mucous membranes

Wet

Slightly dry

Dry

Capillary refill

< 2 seconds

> 2 seconds

> 2 seconds

Blood pressure

Normal

Normal

Normal to decreased

Respirations

Normal

Tacypnea

Tachypnea, deep

Fontanelle

Normal

Sunken

Sunken

Eyes

Normal

Slightly sunken, decreased tears

Sunken, cries without tears

Urine output

Normal to decreased

Decreased

Oliguric or anuric

Skin turgor

Normal

Slightly reduced

Reduced

Children with severe dehydration, signs of shock, failed attempts with oral rehydration therapy, intractable vomiting, hypoglycemia, or electrolyte derangements require intravenous fluid resuscitation, which is often initiated as a 20 mL/kg bolus of 0.9% of sodium chloride in ED. These patients need frequent re-evaluation to review their response to IV hydration. Improvements in mental status, tachycardia, capillary refill time, and urine production are some signs that signal a good response to intravenous resuscitation. After initial resuscitation, patients will need an evaluation of their maintenance fluid needs, which could be either intravenous fluid therapy or ORT, depending on the patient’s clinical status. Maintenance fluids are calculated based on the child’s weight using the 4-2-1 Holliday-Segar Rule.

Holliday-Segar Rule for Maintenance Fluid Calculation

Body Weight

mL/kg/hr

mL/kg/day

First 10 kg

4

100

Second 10 kg

2

50

Each additional kg

1

20

Children who require multiple fluid boluses without signs of improvement should be investigated for other serious conditions such as adrenal insufficiency, cardiogenic or septic shock, etc. It is important to note that rapid correction of serum sodium levels can lead to osmotic demyelination syndrome in hyponatremia and cerebral edema in hypernatremia.

In children with hypoglycemia, glucose can be replaced as per the “rule of 50,” where the percent dextrose multiplied by the number of mL per kilogram equals 50. Neonates often get 10% dextrose solution at 5mL/kg, children between 1 month to 8 years of age (or 25 kg weight) can be given 2mL/kg of 25% dextrose. 50% of dextrose at 1mL/kg can be used safely in older children. The higher tonicity of 25% and 50% dextrose solutions poses a risk of tissue necrosis if extravasation occurs during peripheral IV infusion.
 
Antibiotics are not indicated in viral gastroenteritis and most cases of uncomplicated bacterial gastroenteritis. Considerations can be made for very young infants, immunocompromised, and those with chronic underlying medical conditions. The WHO recommends zinc supplementation for children under 5 years suffering from AGE in developing countries [8]. Studies showing the efficacy of probiotics are inconclusive and further research is needed to establish the safety and efficacy of probiotics in children with AGE [9].

When To Admit This Patient

Most cases of AGE are self-limiting and can be managed on an outpatient basis after a brief period of observation in the ED. Parents and caregivers should be given appropriate discharge instructions emphasizing hygiene and hand-washing techniques to prevent the further spread of the illness. Breastfeeding/routine diet should be continued at home, and supplemental electrolyte solutions may be recommended. Parents and caregivers should be educated to recognize the signs of dehydration and advised to bring the child back to the ED for these. Children with intractable vomiting, severe dehydration, failure to maintain oral hydration, electrolyte derangements, deteriorating clinical status, and those at high risk for complications (very low birth weight infants, < 3 months old, immunosuppressed, and children with chronic medical problems) should be admitted to hospital.

Revisiting Your Patient

History-taking reveals that Zoey has not had much to drink or eat in the past 12 hours, and there has been an outbreak of gastroenteritis in the nursery that she attends. There has been no blood in the stools, and Mum says that Zoey has been very sleepy for the last few hours. Her vaccinations are up to date, and she has no other medical history of note.

On examination, she is irritable when you approach her, and your systematic examination reveals the following:
CNS – Irritable, no signs of meningism, anterior fontanelle closed
HEENT – Dry mucous membranes, slightly sunken eyeballs
Respiratory – Mild tachypnea, bilateral air entry with clear breath sounds
CVS – Central capillary refill 3 seconds, tachycardia, BP 88/50
Abdomen – Soft, lax and non-tender. Bowel sounds ++, no mass palpable
Skin – Slightly reduced skin turgor, no rash

Next steps?

Your examination reveals no red flags of meningitis/sepsis or surgical abdomen. Given the recent outbreak of gastroenteritis in her nursery, you make a provisional diagnosis of acute gastroenteritis for Zoey. Your clinical assessment estimates the degree of dehydration to be moderate (5-10%), and you calculate her fluid depletion to be between 600 to 800 mL (60 to 80 mL/kg). You start the patient on oral rehydration therapy aiming for at least 200 mL to be given slowly over the next hour. You guide the mother in letting the staff know if Zoey vomits or has another episode of diarrhea while in the Emergency Department.

Investigations?

You ask for a random blood sugar to rule out hypoglycemia and a urine dipstick to rule out urinary tract infection.

Review
After an hour, Zoey tolerated 250 mL of oral rehydration solution and had one episode of vomiting but no diarrhea. Her blood sugar was 4 mmol/l. She has perked up significantly and is more alert than before. Her vital signs show improvement, and you decide to give her Ondansetron and continue the ORT.

After two hours, Zoey has tolerated around 400 mL of ORS and is more alert and interactive now. Her vitals are normal, and she has not had any further episodes of diarrhea or vomiting. She has also passed some urine, which has been tested and found to be negative for infection.

Mum was advised to continue oral hydration at home as well as the slow introduction of a regular diet and to come back to ED if Zoey could not tolerate orally, had intractable vomiting, any blood in her stools, high-grade fever, or change from her baseline mental status. Zoey was discharged from the ED and would follow up with her primary physician in the community.

Authors

Picture of Neha Hudlikar

Neha Hudlikar

Emergency Department, Zayed Military Hospital, Abu Dhabi

Picture of Abdulla Alhmoudi

Abdulla Alhmoudi

Dr Abdulla Alhmoudi is a Consultant Emergency Medicine, serving at Zayed Military Hospital and Sheikh Shakhbout Medical City - Abu Dhabi. He pursued his residency training in Emergency Medicine at George Washington University in Washington DC and further enhanced his expertise with a Fellowship in Extreme Environmental Medicine. Dr Alhmoudi's passion for medical education is evident in his professional pursuits. He currently holds the position of Associate Program Director at ZMH EM program and is a lecturer at Khalifa University College of Medicine and Health Sciences. Beyond medical education, he maintains a keen interest in military medicine and wilderness medicine.

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References

  1. McDermott KW, Stocks C, Freeman WJ. Overview of Pediatric Emergency Department Visits, 2015. In: Healthcare Cost and Utilization Project (HCUP) Statistical Briefs. Rockville (MD): Agency for Healthcare Research and Quality (US); August 7, 2018.
  2. Hartman RM, Cohen AL, Antoni S, et al. Risk Factors for Mortality Among Children Younger Than Age 5 Years With Severe Diarrhea in Low- and Middle-income Countries: Findings From the World Health Organization-coordinated Global Rotavirus and Pediatric Diarrhea Surveillance Networks [published correction appears in Clin Infect Dis. 2023 Jan 6;76(1):183]. Clin Infect Dis. 2023;76(3):e1047-e1053. doi:10.1093/cid/ciac561
  3. Steiner MJ, DeWalt DA, Byerley JS. Is this child dehydrated?. JAMA. 2004;291(22):2746-2754. doi:10.1001/jama.291.22.2746
  4. Falszewska A, Szajewska H, Dziechciarz P. Diagnostic accuracy of three clinical dehydration scales: a systematic review. Arch Dis Child. 2018;103(4):383-388. doi:10.1136/archdischild-2017-313762
  5. Freedman SB, Vandermeer B, Milne A, Hartling L; Pediatric Emergency Research Canada Gastroenteritis Study Group.
  6. Pringle K, Shah SP, Umulisa I, et al. Comparing the accuracy of the three popular clinical dehydration scales in children with diarrhea. Int J Emerg Med. 2011;4:58. Published 2011 Sep 9. doi:10.1186/1865-1380-4-58
  7. Tomasik E, Ziółkowska E, Kołodziej M, Szajewska H. Systematic review with meta-analysis: ondansetron for vomiting in children with acute gastroenteritis. Aliment Pharmacol Ther. 2016;44(5):438-446. doi:10.1111/apt.13728Diagnosing clinically significant dehydration in children with acute gastroenteritis using noninvasive methods: a meta-analysis. J Pediatr. 2015;166(4):908-16.e166. doi:10.1016/j.jpeds.2014.12.029
  8. Goldman RD. Zinc supplementation for acute gastroenteritis. Can Fam Physician. 2013;59(4):363-364.
  9. Cameron D, Hock QS, Kadim M, et al. Probiotics for gastrointestinal disorders: Proposed recommendations for children of the Asia-Pacific region. World J Gastroenterol. 2017;23(45):7952-7964. doi:10.3748/wjg.v23.i45.7952

Additional Resources

King CK, Glass R, Bresee JS, Duggan C; Centers for Disease Control and Prevention. Managing acute gastroenteritis among children: oral rehydration, maintenance, and nutritional therapy. MMWR Recomm Rep. 2003;52(RR-16):1-16.

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.

More dehydration content on iem-student.org

Cardiac Monitoring (2024)

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by Stacey Chamberlain

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Definitions and Overview

Cardiac monitoring in the emergency setting is continuous monitoring of a patient’s cardiac activity in order to identify conditions that may require emergent intervention. These conditions include certain arrhythmias, ischemia and infarction, and abnormal findings that could signal impending decompensation. This chapter focuses specifically on cardiac monitoring or electrocardiography; additional methods of continuous hemodynamic monitoring in the emergency department (ED) include pulse oximetry, end-tidal CO2 monitoring, central venous pressure monitoring, and continuous arterial blood pressure monitoring. Of note, telemetry is the ability to do cardiac monitoring from a remote location; in practice, this is often a centralized system that might be located at a nursing station where multiple patients can be monitored remotely.

Cardiac monitoring differs from a 12-lead electrocardiogram in that it is done continuously over a period of time rather than capturing one moment in time in a static image. The benefit of this is that it captures transient arrhythmias and ectopic beats or monitors for changes over time. A disadvantage of cardiac monitoring is that typically, only 2 leads are displayed instead of a full 12 leads, giving a less comprehensive view of the heart and limiting its utility for looking for anatomic patterns. For example, on the 12-lead EKG, ED practitioners usually group the inferior, anterior, and lateral leads when looking for ischemic or infarct patterns. These may be less evident on a monitor with only two leads. Additionally, the static EKG allows the ED physician to carefully study it for subtle findings, for example, to make measurements of intervals, whereas in real-time monitoring, this is very difficult. In practice, both modalities are commonly used in conjunction for many ED patients.

The American Heart Association (AHA) published a consensus document in 2004 establishing practice standards for electrocardiographic monitoring in hospital settings, which was updated in 2017 [1,2]. These comprehensive documents outline the indications for cardiac monitoring, the specific skills required of the practitioner for cardiac monitoring, and specific ECG abnormalities that the practitioner should recognize. The 2017 update addressed the overuse of arrhythmia monitoring among certain populations, appropriate use of ischemia and QT-internal monitoring among select populations, alarm management, and documentation in electronic health records [2].

Cardiac monitoring is essential for those patients who are at risk for an acute, life-threatening arrhythmia and can also be used to evaluate for developing ischemia, response to therapy, and as a diagnostic tool. The AHA guidelines divide indications for cardiac monitoring in the inpatient setting into four classes based on varying degrees (level A, B, C) of evidence. Cardiac monitoring is considered indicated in patients in Class I. In Class IIa, it “is reasonable to perform” cardiac monitoring, whereas in Class IIb, it “may be considered.” For Class III, cardiac monitoring is not indicated as there is no benefit or there may actually be harm. Newer guidelines tailor the recommendations based on specific patient populations and whether the cardiac monitoring is for arrhythmia or continuous ST-segment ischemic monitoring [2]. Specific patient populations that are considered include patients with:

  1. Chest pain or coronary artery disease.
  2. Major cardiac interventions such as open heart surgery.
  3. Arrhythmias.
  4. Syncope of suspected cardiac origin.
  5. After electrophysiology procedures/ablations.
  6. After pacemaker or ICD implantation procedures.
  7. Pre-existing rhythm devices.
  8. Other cardiac conditions (acute decompensated heart failure or infective endocarditis).
  9. Non-cardiac conditions (e.g., post-conscious sedation or post-non-cardiac surgery).
  10. Specific medical conditions (e.g., stroke, imbalance of potassium or magnesium, drug overdose, or hemodialysis).
  11. DNR/DNI status.

Table 1 lists Class I-III recommendations. The AHA Scientific Statement provides a more comprehensive and detailed list.

Table 1 – Select Indications for Cardiac Monitoring

Class I Indications

Early phase ACS or after MI

 

After open-heart surgery or mechanical circulatory support

 

Atrial tachyarrhythmias

 

Symptomatic sinus bradycardia

 

2nd or 3rd degree AV block (exception as noted below for asymptomatic Wenckebach)

 

Congenital or genetic arrhythmic syndrome (e.g. WPW, Brugada, LQTS)

 

After stroke

 

With moderate to severe imbalance of potassium or magnesium

 

After drug overdose

Class IIa and IIb Indications

Non-sustained VT

 

Asymptomatic, significant bradycardia with negative chronotropic medications initiated

 

After non-cardiac major thoracic surgery

 

Chronic hemodialysis patients without other indications (e.g. hyperkalemia, arrhythmia)

Class III Indications

After non-urgent PCI without complications or after routine diagnostic coronary angiography

 

Patients with chronic atrial fibrillation, sinus bradycardia, or asymptomatic Wenckebach who are hemodynamically stable and admitted for other indications

 

Asymptomatic post-operative patients after non-cardiac surgery

 

DNR/DNI patients when the data will not be acted on and comfort-focused care is the goal

Ischemia Monitoring

Continuous ST-Segment Ischemia Monitoring was highlighted in the 2017 AHA guidelines as a specific indication for cardiac monitoring for patients most at risk for ischemia. Older monitors may not have this capability, but more modern monitors are programmed with automated ischemia monitoring that identifies abnormal ST-segment elevation or depression; manufacturers do not automatically enable this capability, and it may be turned on or off. To reduce unnecessary alarms, it is recommended (IIa level) to enable this function only in high-risk patients in the early phase of ACS and to individualize which lead should be prioritized based on the coronary artery suspected to be affected by an ischemic process. High-risk patients would include those being evaluated for vasospastic angina, those presenting with MI, post-MI patients without revascularization or with residual ischemic lesions, and newly diagnosed patients with a high-risk lesion such as a left main blockage.

QTc Monitoring

QTc monitoring aims to assess the safety of QT-prolonging medications and avoid Torsade de Pointes (TdP). Most hospitals do not have fully automated continuous QTc monitoring, so QTc monitoring and measurements may need to be performed manually or semi-automated with digital calipers. Regardless of the method, in general, recommendations for QTc monitoring are for patients with specific risk factors for TdP who are started on anti-arrhythmic drugs with a known risk for TdP (e.g., dofetilide, sotalol, procainamide, quinidine, and others), patients with a history of prolonged QTc started on non-anti-arrhythmic drugs with risk for TdP, those undergoing targeted temperature management, specific electrolyte derangements, and select drug overdoses. As with ischemic monitoring, QTc monitoring is not universally recommended for all patients, so consulting the 2017 guidelines for select patient scenarios is best.

Rhythm Interpretation

One of the most critical skills of an ED physician is in interpreting both static EKGs and interpreting arrhythmias on a cardiac monitor. A skilled practitioner must be able to diagnose common arrhythmias and be well-versed in the management of acute arrhythmias, recognizing which arrhythmias necessitate immediate action and which are less worrisome. Table 2 from the 2004 AHA guidelines lists the specific arrhythmias that the ED physician must be able to recognize. How and whether to treat an arrhythmia depends on many factors. The AHA has established algorithms for specific rhythms, including ventricular fibrillation (v-fib)/pulseless ventricular tachycardia (v-tach) and pulseless electrical activity (PEA)/asystole, as well as for non-specific rhythm categories such as bradycardia and tachycardia [3]. Additionally, they have published algorithms for clinical scenarios, including cardiac arrest, acute coronary syndrome, and suspected stroke.

The first step in the assessment of any rhythm is a clinical assessment of the patient. The premier issue of concern is if the patient is perfusing vital organs. A quick survey of the patient assessing mental status and pulses is essential to determining management. The management of a patient with v-tach will be substantially different if the patient is unresponsive and pulseless versus if the patient is awake with good pulses. As another example, the physician can quickly distinguish artifact from v-fib on the cardiac monitor by assessing the patient, as v-fib is not a perfusing rhythm.

The initial assessment of tachyarrhythmias (heart rate > 100) is to determine if the rhythm is “narrow-complex” (i.e., a QRS duration < 0.12s) or “wide-complex” (i.e., a QRS duration of 0.12s or greater). A narrow complex rhythm is considered a supraventricular rhythm (originating above the ventricles). Supraventricular tachycardia is a generic term encompassing any narrow-complex tachycardias originating above the AV node. Colloquially, when many practitioners refer to “SVT,” however, they are referring to a specific subcategory of supraventricular tachycardia called AV nodal re-entrant tachycardia (AVNRT). Wide complex tachycardias either originate in the ventricles or could originate in the atria and have an associated bundle branch block. Different criteria have been developed to help the practitioner distinguish between ventricular tachycardia and an SVT “with aberrancy” (i.e., aberrant conduction either due to an accessory path such as in Wolff-Parkinson-White or with a bundle branch block), the most well known of which are the Brugada criteria [4,5]. Practically speaking, many ED practitioners will assume the more dangerous and potentially unstable rhythm (v-tach) until proven otherwise; of course, the clinical picture and the patient’s vital signs are of utmost importance in determining the management of these patients. An excellent summary of this issue with rhythm strip examples is provided on the FOAM site “Life in the Fast Lane” [6].

Table 2 – Specific Arrythmias (adapted from AHA Scientific Statement [1])

Normal rhythms

 

 

Normal sinus rhythm

 

Sinus bradycardia

 

Sinus arrhythmia

 

Sinus tachycardia

Intraventricular conduction defects

 

 

Right and left bundle-branch block

 

Aberrant ventricular conduction

Bradyarrhythmias

 

 

Inappropriate sinus bradycardia

 

Sinus node pause or arrest

 

Non-conducted atrial premature beats

 

Junctional rhythm

AV blocks

 

 

1st degree

 

2nd degree Mobitz I (Wenckebach) or Mobitz II

 

3rd degree (complete heart block)

Asystole

 

Pulseless electrical activity (PEA)

 

Tachyarrhythmias

 

 

Supraventricular

Paroxysmal supraventricular tachycardia (AV nodal reentrant, AV reentrant)

Atrial fibrillation

Atrial flutter

Multifocal atrial tachycardia

Junctional ectopic tachycardia

Accelerated ventricular rhythm

Ventricular

Monomorphic and polymorphic ventricular tachycardia

Torsades de pointes

Ventricular fibrillation

Premature complexes

 

 

Supraventricular (atrial, junctional)

 

Ventricular

Pacemaker electrocardiography

 

 

Failure to sense

 

Failure to capture

 

Failure to pace

ECG abnormalities of acute myocardial ischemia

 

 

ST-segment elevation, depression

 

T-wave inversion

Muscle or other artifacts simulating arrhythmias

 

While each rhythm has distinctive management, it is worth noting for the novice learner that only v-fib and pulseless v-tach warrant asynchronized mechanical defibrillation (i.e. “shocking” the patient). Many students are stunned upon observing an asystolic cardiac arrest code to learn that shocking a “flatline” (i.e., asystolic) patient is an inappropriate treatment perpetuated by fictitious TV shows and movies. For unstable patients with arrhythmias but still have palpable pulses, synchronized cardioversion may be used.

Regarding medications, for certain rhythms and clinical scenarios, only vasopressor types of medications are used (e.g., epinephrine for asystole). For other rhythms and scenarios, antiarrhythmic medications are used (e.g., amiodarone for v-tach). Atrioventricular (AV) nodal blocking agents are often necessary for supraventricular tachyarrhythmias. One author suggests using a five “As” approach to treating emergency arrhythmias, keeping in mind the medications adenosine, amiodarone, adrenaline (epinephrine), atropine, and ajmaline [7]. Ajmaline is an antiarrhythmic that is not commonly used in English-speaking countries where procainamide is more common as an alternative to amiodarone for unstable v-tach.

Additional interventions may include pacemaker placement for symptomatic heart blocks. In many cases, the ED practitioner must also determine the underlying precipitant of the arrhythmia and tailor treatment to that cause. The emergency physician must familiarize himself with each rhythm and its unique management in any given clinical scenario.

At the end of this chapter, some good internet resources for the ED practitioner to practice interpreting EKGs and cardiac rhythms are provided.

Case Example

A 44-year-old male patient with a history of hypertension and end-stage renal disease on hemodialysis presents with shortness of breath after missing dialysis for 6 days. He reports gradual onset shortness of breath associated with orthopnea and increased lower extremity edema. He denies chest pain or palpitations. He does not have any cough or fever. On physical exam, he is in no distress, afebrile with a heart rate of 60, respiratory rate of 20, blood pressure of 140/78 mmHg, and oxygen saturation of 98% on room air. He has a regular rate and rhythm without murmurs and has crackles bilaterally to the inferior 1/3 of the lung bases and 1+ pitting edema of the bilateral lower extremities.

You decide to get an EKG, which shows the following:

Figure 1 (EKG from http://www.lifeinthefastlane.com)

You send a blood chemistry test, place the patient on a cardiac monitor, and one hour later note the following on the monitor:

Figure 2 - (EKG from liftl.com)

What are the indications for cardiac monitoring in this patient? What EKG abnormalities do you see? What does the rhythm strip show? What is the treatment?

Case Discussion

The ED practitioner should recognize potentially life-threatening conditions that a patient who has missed hemodialysis is at risk for are fluid overload (leading to pulmonary edema) and hyperkalemia. This patient could be considered to meet the Class I monitoring criteria for “needing intensive care” and possibly with “pulmonary edema”; however, even if the patient had no symptoms, the patient is indeed at risk for an acute life-threatening arrhythmia that would necessitate cardiac monitoring.

The EKG demonstrates peaked T waves indicative of acute hyperkalemia. Given the clinical picture of missed dialysis and the peaked Ts on the EKG, the ED physician should immediately initiate treatment for acute hyperkalemia without waiting for a confirmatory blood test (unless immediate point-of-care tests are available). If the patient’s hyperkalemia progressed, the patient could develop QRS widening with the morphology as shown on the rhythm strip called a “sine wave.” This dangerous finding could precipitously deteriorate into a life-threatening arrhythmia such as pulseless v-tach with cardiac arrest and should prompt immediate action. It is important to note that hyperkalemia can manifest in a variety of different EKG findings and does not always follow a consistent pattern from peaked Ts to QRS widening to sine waves; therefore, the patient should be treated at the first indication of any hyperkalemia-related EKG changes.

Conclusions

Cardiac monitoring is an important tool to monitor patients at risk for acute arrhythmias (including those at risk specifically for TdP) and acute or worsening cardiac ischemia. It can be helpful to immediately identify patients with life-threatening arrhythmias who need immediate intervention, to assess the response to medications for arrhythmias, and to help exclude arrhythmias as a likely etiology of a patient’s symptoms (e.g., a patient with syncope) [9]. Given the limited resources and the lack of benefits for many patients, the purpose and duration of cardiac monitoring should be carefully considered. Overuse can not only waste resources but can also contribute to alarm hazards, including “alarm fatigue,” where clinicians are barraged by so many false or nonactionable alarm signals that they become desensitized and do not respond to real events. Therefore, appropriate use and staff education are critical to maximizing the benefits of cardiac monitoring.

Author

Picture of Stacey Chamberlain

Stacey Chamberlain

Dr. Stacey Chamberlain is a board certified emergency physician who is a Professor in the Department of Emergency Medicine at the University of Illinois at Chicago (UIC). She also serves as the Director of the Global Emergency Medicine Fellowship Program and the Co-Director of the Social Emergency Medicine Fellowship Program. In addition to her work in Emergency Medicine, she is the Director of Academic Programs at the UIC Center for Global Health. In this role, she oversees the Global Medicine (GMED) Program for UIC medical students and the graduate global health certificate programs. Dr. Chamberlain has done clinical, educational, public-health, disaster-response, and emergency medicine development work, including working with several globally-focused NGOs, spanning five continents. Her global health work focuses on capacity building in emergency care in Uganda.

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2018 version of this topic – https://iem-student.org/cardiac-monitoring/

References

  1. Drew BJ, Califf RM, Funk M, Kaufman ES, Krucoff MW, et al. AHA Scientific Statement:  Practice Standards for Electrocardiographic Monitoring in Hospital Settings. Circulation. 2004; 110: 2721-2746. doi: 10.1161/01.CIR.0000145144.56673.59
  2. Sandau KE, Funk M, Auerbach A, Barsness GW, Blum K, Cvach M, Lampert R, May JL, McDaniel GM, Perez MV, Sendelbach S, Sommargren CE, Wang PJ; American Heart Association Council on Cardiovascular and Stroke Nursing; Council on Clinical Cardiology; and Council on Cardiovascular Disease in the Young. Update to Practice Standards for Electrocardiographic Monitoring in Hospital Settings: A Scientific Statement From the American Heart Association. Circulation. 2017 Nov 7;136(19):e273-e344. doi: 10.1161/CIR.0000000000000527. Epub 2017 Oct 3. PMID: 28974521.
  3. ACLS Training Center. Algorithms for Advanced Cardiac Life Support 2015. Dec 2, 2015.  Accessed at: https://www.acls.net/aclsalg.htm, Dec 10, 2015.
  4. Wellens HJJ. Ventricular tachycardia: diagnosis of broad QRS complex tachycardia. Heart2001;86:579-585 doi:10.1136/heart.86.5.579.
  5. Brugada P, Brugada J, Mont L, Smeets J, Andries EW. A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex. Circulation. 1991; 83: 1649-1659. doi: 10.1161/01.CIR.83.5.1649
  6. Burns E. VT versus SVT with aberrancy. Life in the Fast Lane. Accessed at: http://lifeinthefastlane.com/ecg-library/basics/vt_vs_svt/, Dec 10, 2015.
  7. Trappe H-J. Concept of the five ‘A’s for treating emergency arrhythmias. J Emerg Trauma Shock. 2010 Apr-Jun; 3(2): 129–136. doi:  10.4103/0974-2700.62111
  8. Ramzy M. Duration of Electrocardiographic Monitoring of Emergency Department Patients with Syncope. REBEL EM blog; June 13, 2019; Available at: https://rebelem.com/duration-of-electrocardiographic-monitoring-of-emergency-department-patients-with-syncope/.

Additional Online Resources

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, 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.

Tachyarrhythmias (2024)

~ iEM Education Project Team ~ Leave a comment

by Keith Sai Kit Leung, Rafaqat Hussain & Abraham Ka Cheung Wai 

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You have a new patient!

A 28-year-old female patient presented with 3 weeks history of palpitations. She started with a new-onset shortness of breath and dizziness this morning, which prompted her to attend ED. The patient also complains of recent unintentional weight loss, restlessness, insomnia, passing loose stool more frequently, menstrual disturbances, and some degree of chest pain. No other significant medical history was noted. On physical examination, she looks well-perfused, with bilateral equal air entry and normal vesicular breath sounds throughout, heart sound I+II with no added sound. Vital signs monitoring showed a temperature of 38.1°C, heart rate of 142 bpm, respiratory rate of 21, blood pressure of 155/98, peripheral CRT of 3s, and SpO2 96% on air. ECG is shown below:

(Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8496558/)

What do you need to know?

Tachyarrhythmia is an abnormal heart rate over 100 bpm. It can be classified by site of origin (sinus, supraventricular, ventricular), in relation to QRS complexes (narrow or board-complex), or regularity.

Importance

Tachycardia is an extremely common finding in patients presenting to the emergency department; it involves a wide range of differential diagnoses, from normal variants to physiological responses to life-threatening conditions like shock and cardiac arrest. Studies have shown that patients with tachycardia have an increased risk of post-discharge mortality [1, 2], with higher rates of future re-visit to ED [3].

Epidemiology and Pathophysiology

Sinus tachycardias usually occur as part of a normal physiological response (e.g., exercise, pregnancy) or a compensatory pathological response to secondary underlying conditions (e.g., pulmonary embolism, hyperthyroidism, anemia, infection). It is important to note that sinus tachycardia can be abnormal, secondary to cardiac dysautonomia. These conditions are postural orthostatic tachycardia syndrome or inappropriate sinus tachycardia.

(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)

Supraventricular tachycardias is an umbrella term that includes a number of arrhythmias that arise above the bundle of His, i.e., the sinoatrial (SA) node, atria, and atrioventricular (AV) node; these are typically narrow complex tachycardia except WPW syndrome. The most prevalent types of SVTs, in descending order, are atrial fibrillation, atrial flutter, atrioventricular nodal re-entrant tachycardia (AVNRT), atrioventricular re-entrant tachycardia (AVRT), with atrial tachycardia (AT) and junctional tachycardia being the least common types [4, 5]. Three arrhythmogenic mechanisms have been proposed: Re-entry, enhanced automaticity, or triggered activity [6].

Starting with atrial fibrillation (AF) and atrial flutter (AFL), the latest data from the Global Burden of Disease Study 2019 showed that there are 59.7 million affected individuals worldwide [7], with a male predominance in the older population. Common causes of AF include PIRATES [Mnemonic for Pulmonary embolism, Ischaemic heart disease/Idiopathic, Rheumatic valvular disorder, Anaemia/Alcohol, Thyroid (hyperthyroidism), Electrolytes imbalance/Elevated BP (hypertension), Sepsis/Sick sinus syndrome]. The arrhythmogenic mechanism of AF is by increased automaticity, leading to ectopic focal activities and the creation of micro re-entrant circuits in the atrial muscles. Without organized contractility, blood pools in the atria, predisposing to thrombus formation and increasing stroke risk.

(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)

Atrial flutter is less common than AF, but they both share similar aetiologies and may coexist. The difference between both is that AF presents with an irregularly irregular heartbeat, while AFL presents with a regularly irregular heartbeat, as a macro re-entrant circuit exists in the atrium, producing a rapid regular atrial rate at 300 bpm. Depending on the conduction ratio, affected patients have a fixed ventricular rate at 150 bpm (2:1), 100 bpm (3:1), or 75 bpm (4:1).

(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)

Atrioventricular nodal re-entrant tachycardia (AVNRT) has a prevalence of 2.25 cases per 1000 people in the general population, with a female/male ratio of 2:1 among all age groups [8]. It is the most common cause of paroxysmal SVT and occurs in about 50% of cases. Hence, it is often used synonymously with the term SVT. AVNRT is usually idiopathic, i.e., patients have structurally normal hearts. In AVNRT, re-entry is the main arrhythmogenic mechanism. Naturally, the AVN has dual pathways with different conduction velocities (a fast and slow pathway). Usually, conduction passes via the fast pathway, which blocks incoming current from the slow pathway, while in SVT, the slow pathway becomes the dominant anterograde conduction pathway, uses the fast pathway for retrograde conduction, and creates a re-entrant loop. 90% of AVNRT is slow-fast type [9].

(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)

Atrioventricular re-entrant (or reciprocating) tachycardia (AVRT) is another form of paroxysmal SVT, accounting for 30% of cases. It is caused by an anatomical re-entrant circuit with the normal AV conduction system and an AV accessory tract. The most commonly known accessory pathway is called Bundle of Kent, causing Wolff-Parkinson-White (WPW) pre-excitation syndrome; hence, WPW and AVRT are often used interchangeably. It has been estimated to affect 1-3 persons per thousand people. [10]

(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)

Atrial tachycardia (AT) accounts for the remaining 10-20% of cases, as opposed to other subtypes; it is usually caused by increased atrial automaticity independent from the AV conduction system or accessory pathways. Other causes include sinoatrial scarring, digoxin toxicity, or conditions that cause atrial dilation (COPD, CHF). Note that there are 2 types of AT, focal and multifocal AT; the former is caused by one ectopic arrhythmogenic focus and later with multiple arrhythmogenic foci within the atria. The firing rate of the ectopic focus is faster than that of the SA node, which overrides its activity. [11]

(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)
(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)
(Reused from Srinivasan C, Balaji S. Neonatal supraventricular tachycardia. Indian Pacing Electrophysiol J. 2019;19(6):222-231. DOI:10.1016/j.ipej.2019.09.004) – Open Access (https://www.sciencedirect.com/science/article/pii/S0972629219301159)

Junctional tachycardia occurs when there is increased automaticity in the AV node and decreased automaticity in the SA node. This causes ECG changes, which commonly present as retrograde p waves around the QRS complex. [12]

(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)

Ventricular arrhythmias are life-threatening conditions that cause sudden cardiac death (SCD); subtypes include monomorphic and polymorphic ventricular tachycardia (VT), Torsades de Pointes (TdP, variant of PVT), ventricular fibrillation (VF). It has been estimated that over 356,000 people suffer from out-of-hospital cardiac arrest in the USA annually, nearly 1000 cases each day [13], and SCD remains the world’s leading cause of death, costing 17 million lives each year [14]. Over the years, VT/VF has decreased incidence; they account for 23% of initial cardiac arrest rhythm, with the most commonly encountered ones being asystole (39%) and PEA (37%). This trend is likely due to the advancement of devices like implantable cardiac defibrillators and improvement in preventative cardiology practice [15]. The most common causes of VT/VF include acute coronary syndrome, cardiomyopathies, congenital channelopathies (BrS, LQTS, CPVT), QT-prolonging drugs (macrolides, TCA), electrolytes imbalance, etc. (Consider 4H 4T causes in cardiac arrest).

(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)
(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)
(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)
(Reused from Jones, S. A. (2009). ECG Notes: Interpretation and Management Guide. F.A. Davis Company.)

The diagram below shows a decision-making algorithm.

(Reused from Srinivasan C, Balaji S. Neonatal supraventricular tachycardia. Indian Pacing Electrophysiol J. 2019;19(6):222-231. DOI:10.1016/j.ipej.2019.09.004) – Open Access (https://www.sciencedirect.com/science/article/pii/S0972629219301159)

Medical History

As tachyarrhythmias present with an extensive list of differential diagnoses, a detailed history taking is essential to direct clinicians to the next-step management. The most common clinical presentations in patients suffering from tachycardias include palpitations (84%), chest pain (47%), dyspnoea (38%), syncope (26%), light-headedness (19%) and sweating (18%) [16]. Symptoms can be explored with a simple mnemonic SOCRATES (site/specify, onset, character/change, rhythm/radiation, associated features, timing, exacerbating and relieving factors, severity). As patients often confuse medical terms with other meanings, it is important to ask and clarify what the term means to them (palpitations vs heart attack). Understanding the onset and progression of symptoms would allow us to determine the acuity and chronicity of the presentation. For timing, we need to ask if the presentation constantly existed since the onset, if it is intermittent, and if it comes on at a particular time of the day. In terms of exacerbating and relieving factors, when it comes to cardiac problems, it is particularly important to ask about the difference between exertion and rest and whether the patient tried anything over the counter. As non-cardiac problems cause tachycardia too, it is necessary to perform a systems review from head to toe to rule out other causes (for example, diarrhea, weight loss, heat intolerance, menstrual disturbance in hyperthyroidism). Past medical and family history should never be missed; these help us to identify risk factors, e.g., hypertension, diabetes, familial hypercholesteremia (predispose to MI), and HOCM (predispose to SCD). In the end, remember to ask for medication history (both prescribed and illicit) and social history (especially smoking and alcohol intake).

If the patient is unconscious, collateral histories from friends and family members are ideal candidates to gain some basic understanding of the patient’s background. It is also worthwhile to communicate with EMTs and paramedics and see if any other valuable information can be obtained.

Adverse features (red flags) for tachyarrhythmias are mainly myocardial infarction, syncope, new-onset heart failure, and deteriorating vital signs, i.e., increased capillary refill time, hypotension (indicative of shock), altered consciousness/reduced GCS.

Physical Examination

If the patient is unconscious or has no palpable pulse, manage the patient with basic life support and advanced life support protocols.

Evaluation of all other patients with the A-E approach is critical as they are still undifferentiated. If the patient is conscious, start inspecting the patient. Key features to observe include cyanosis (poor perfusion peri-arrest), pallor (anemia), dyspnea (heart failure, myocardial infarction/injury), diaphoresis (myocardial infarction/injury), and peripheral edema (heart failure). Start peripherally at hands, observe for clubbing (indicative of infective endocarditis, congenital heart diseases, hyperthyroidism), and assess radial and carotid pulse for its rate, rhythm, and volume. Look for visible jugular venous pulse (elevated – heart failure), presence of corneal arcus (familial hypercholesterolemia) in eyes, and scars on the chest (sternotomy, pacemaker). To assess murmurs, auscultate in all 4 valvular areas (2ndICS left sternal border – pulmonary area, 2nd ICS, right sternal border – aortic area, 4th ICS left sternal border – tricuspid area, 5th ICS mid-clavicular line – mitral area). Be sure to examine other systems, including respiratory, neurological, and ENT.

Alternative Diagnoses

As mentioned above, most tachyarrhythmias are idiopathic or secondary to cardiac and non-cardiac causes. It is extremely important to keep an open mind and an extensive list of differentials so we won’t miss the actual diagnosis. The table below lists differentials for palpitations, the chief complaint of tachyarrhythmias.

Causes of Palpitations

Cardiac Causes

Noncardiac Causes

Atrial fibrillation/flutter

Atrial myxoma

Atrial premature contractions

Atrioventricular reentry

Atrioventricular tachycardia

Autonomic dysfunction

Cardiomyopathy

Long QT syndrome

Multifocal atrial tachycardia

Sick sinus syndrome

Supraventricular tachycardia

Valvular heart disease

Ventricular premature contractions

Ventricular tachycardia

Alcohol

Anemia

Anxiety/stress

Beta-blocker withdrawal

Caffeine

Cocaine

Exercise

Fever

Medications

Nicotine

Paget disease of bone

Pheochromocytoma

Pregnancy

Thyroid dysfunction

(Reuse from Wexler RK, Pleister A, Raman SV. Palpitations: Evaluation in the Primary Care Setting. Am Fam Physician. 2017;96(12):784-789.) – Open Access (https://www.aafp.org/pubs/afp/issues/2017/1215/p784.html)

Acing Diagnostic Testing

Any patients with adverse features and life-threatening presentations should be placed in a resuscitation bay with a multi-parameter vitals monitor/defibrillator connected and a point-of-care portable ultrasound ready. For stable patients, stepwise management should be initiated. Proceed with bedside tests: perform a 12-lead ECG, measure heart rate, assess SpO2 with an oximeter, and record blood pressure. Collect blood samples, including a Full Blood Count, Urea and Electrolytes, serum Magnesium, Calcium, Thyroid Function Tests, Liver Function Tests, and a coagulation panel. Additional tests can be considered based on the clinician’s clinical decision and the patient’s presentation, for example, Troponin for suspected MI, D-dimer for suspected PE, etc. Chest X-rays should be performed in any patients presenting with chest pain. Advanced imaging again depends on clinical presentation, coronary angiogram for Myocardial Infarction, Computed Tomography Pulmonary Angiography for Pulmonary Embolism, etc. The risk stratification tool (more details in the section below) can be used to facilitate decisions for advanced interventions involving intensive care input. Cardiology input will be required for further investigations involving Holter monitoring, implantable loop recorder, electrophysiological study, echocardiogram, cardiac Magnetic Resonance Imaging, etc.

Management

Sinus Tachycardia

Sinus tachycardia is often a physiological response to an underlying cause such as sepsis, hypovolemia, or anemia. Management should focus on identifying and addressing these causes rather than targeting the heart rate itself. For example, in a septic patient, early fluid resuscitation and antibiotics are critical, while in a patient with anemia, blood transfusion or treatment of iron deficiency may resolve the tachycardia. Clinicians should avoid unnecessary use of beta-blockers or calcium channel blockers unless sinus tachycardia persists after the underlying cause has been addressed.

Atrial Fibrillation

Management of atrial fibrillation requires a careful evaluation of the patient’s hemodynamic stability, symptom duration, and underlying comorbidities.

  1. Hemodynamically Stable Patients with Symptoms >48 Hours or Uncertain Timeline:

    • Rate control is the priority to prevent further decompensation. Start with beta-blockers (e.g., bisoprolol) or calcium channel blockers (e.g., diltiazem).
    • Consider digoxin for patients with congestive heart failure who may not tolerate beta-blockers.
    • Avoid cardioversion without anticoagulation if the symptom duration is >48 hours or unclear, as this increases the risk of thromboembolic events.

  2. Hemodynamically Stable Patients with Symptoms <48 Hours or a Reversible Cause:

    • Focus on rhythm control with cardioversion, which can be electrical or pharmacological (e.g., flecainide or amiodarone).
    • Ensure anticoagulation with heparin before cardioversion unless contraindicated.
    • Use an echocardiogram to rule out structural abnormalities, as this guides drug selection (e.g., flecainide for structurally normal hearts; amiodarone for structural heart disease).

  3. Patients with Adverse Features (Shock, Syncope, Acute Heart Failure, or Myocardial Ischemia):

    • Immediate electrical cardioversion is required, typically using synchronized shocks. Time is critical—any delay could worsen outcomes.

  4. Paroxysmal AF:

    • Counsel patients on the use of “pill-in-the-pocket” therapies such as flecainide or sotalol for intermittent symptoms. Ensure they understand the signs of structural heart disease, which would contraindicate these medications.

Always consider underlying conditions such as hyperthyroidism, electrolyte disturbances, or alcohol-related atrial fibrillation (Holiday Heart Syndrome). Addressing these causes can prevent recurrence. In elderly patients or those with heart failure, weigh the benefits of rhythm versus rate control.

Atrial Flutter

Management of atrial flutter parallels that of atrial fibrillation. Rate control is often sufficient in stable patients, but rhythm control may be prioritized for symptomatic relief. In acute settings, electrical cardioversion may be more effective than pharmacological approaches.

Atrial flutter is frequently associated with underlying structural heart disease or atrial enlargement. Evaluate for these conditions with echocardiography and address them to improve long-term outcomes.

AVNRT (Atrioventricular Nodal Reentrant Tachycardia)

AVNRT is often well-managed with non-pharmacological measures in stable patients.

Conservative Management:

  • Initiate vagal maneuvers (e.g., Valsalva maneuver or carotid massage). These can terminate the tachycardia in many cases. Ensure the patient is monitored for safety, especially in older adults where carotid massage could induce complications.

Pharmacological Management:

  • Administer IV adenosine, starting at 6 mg and escalating to 12 mg or 18 mg if needed. Warn the patient about the transient sensation of chest discomfort or flushing.
  • If adenosine is contraindicated (e.g., in asthmatic patients), use a calcium channel blocker such as verapamil.

Persistent Cases:

  • Consider beta-blockers, digoxin, or amiodarone if initial treatments fail.

Hemodynamically Unstable Patients:

  • Proceed with immediate cardioversion to stabilize the patient.

In recurrent AVNRT, evaluate for underlying triggers such as excessive caffeine or stimulant use. Discuss long-term options such as catheter ablation for definitive treatment.

AVRT/WPW (Atrioventricular Reentrant Tachycardia/Wolff-Parkinson-White Syndrome)

In patients with WPW, rapid and accurate diagnosis is critical to avoid inappropriate treatment.

Stable Patients:

  • Treat with amiodarone, flecainide, or procainamide. Avoid digoxin and calcium channel blockers, as these can worsen pre-excitation and lead to ventricular fibrillation.

Unstable Patients:

  • Immediate cardioversion is indicated.

In young patients presenting with sudden palpitations and syncope, always consider WPW and obtain a 12-lead ECG for diagnosis. Educate patients on avoiding stimulants that may precipitate episodes.

Atrial Tachycardia

For atrial tachycardia, management depends on the patient’s stability. Rate control is often effective for stable patients, while cardioversion may be required in unstable cases.

Investigate underlying causes such as digoxin toxicity or structural heart disease, as addressing these may resolve the tachycardia.

Ventricular Tachycardia (VT)

Management of VT hinges on the patient’s hemodynamic stability.

Stable VT:

    • Administer amiodarone (300 mg IV STAT followed by a 900 mg infusion over 24 hours). Monitor for potential side effects such as hypotension or bradycardia.

Unstable VT, pulse positive:

    • Follow the ALS (Advanced Life Support) algorithm, prioritizing cardioversion.

VT, no pulse:

  • Follow the ALS (Advanced Life Support) algorithm, prioritizing defibrillation and CPR.

In patients with recurrent VT, assess for underlying ischemic heart disease or electrolyte abnormalities. Long-term management may require ICD placement or catheter ablation.

Ventricular Fibrillation (VF)

VF is a life-threatening emergency requiring immediate intervention. Follow the ALS algorithm, which includes high-quality CPR and defibrillation.

Always assess for reversible causes of VF, such as acute myocardial infarction or electrolyte imbalances (e.g., hypokalemia or hypomagnesemia), and treat these aggressively to prevent recurrence.

Tachycardia and advanced life support algorithms are provided below.

(Reuse from 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) – Open Access (https://www.cprguidelines.eu/)
(Reuse from 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) – Open Access (https://www.cprguidelines.eu/)

Special Patient Groups

The management of most tachyarrhythmias is similar among pregnant women and pediatric populations, with the exception of ventricular cardiac arrest rhythms.

Pregnant Patients (Obstetric Cardiac Arrest ) [17]

  • A normal supine position will result in aortocaval compression from the gravid uterus; this reduces cardiac output. Hence, placing the patient in a left lateral position is crucial, especially at> 20 weeks gestation.
  • The position of the rescuer’s hands for chest compression ideally should be slightly higher than usual, taking the elevation of the diaphragm and abdominal contents caused by the gravid uterus into account.
  • The defibrillator pad position should be adjusted to maintain the left lateral position.
  • Magnesium sulfate (4 g IV) should be given in patients with eclampsia.
  • Patients should be intubated early due to the higher risk of pulmonary aspiration and Mendelson syndrome from gastric contents.
  • Emergency delivery of the fetus (>20 weeks) with resuscitative hysterotomy should happen within 5 minutes in the event of cardiac arrest, given that the initial resuscitation attempt has failed. This is a definitive procedure to decompress IVC to facilitate venous return and increase cardiac output.
  • As this is an obstetric emergency, get help from the OB/GYN and neonatal team early; resuscitative hysterotomy should not wait even if not all surgical equipment is immediately available; one scalpel is enough to start the procedure.

Pediatrics (Cardiac Arrest) [17]

  • Most pediatric cardiac arrests are secondary to respiratory failure; hence, giving 5 rescue breaths is essential prior to chest compressions.
  • Pulse checks use brachial or femoral pulses as opposed to carotid pulses in adults.
  • It is a similar compression site but with a compression: breath ratio of 15:2, as opposed to 30:2 in adults.
  • In infants, compress the chest using two fingers or an encircling technique (two thumbs). For children over one year old, use one or two hands.
  • Intraosseous (IO) access is preferred for circulation access, as obtaining venous access can be difficult in children.
  • Adrenaline is given in 10 mcg/kg, and Amiodarone is given in 5 mg/kg.
  • Note that PALS is different from newborn life support (NLS), which is not mentioned here.

* Please refer to European Resuscitation Council (ERC) Paediatric Life Support and Special Circumstances Guidelines (https://www.cprguidelines.eu/)

Risk Stratification

There is no single risk stratification tool for tachyarrhythmias, developed scoring systems are usually condition-specific or presentation-specific. We listed some of the important ones related to tachyarrhythmias below:

  • Cardiac Arrest Hospital Prognosis (CAHP) score – predicts prognosis in patients suffering from out-of-hospital cardiac arrest. [18]
  • Cardiac Arrest Risk Triage (CART) Score – predicts the risk of in-hospital cardiac arrest in hospitalized patients. [19]
  • CHA₂DS₂-VASc Score – calculate stroke risk in patients with atrial fibrillation and guide initiation of anticoagulation therapy. [20]
  • HEART score – predicts patients presenting with chest pain for a 6-week risk of major adverse cardiac events (MACE). It can also classify patients into low, moderate, and high-risk groups to facilitate decisions for discharge from ED, admission for observation, or urgent intervention required. [21]
  • Thrombolysis In Myocardial Infarction (TIMI) score and Global Registry of Acute Coronary Events (GRACE) score – estimate mortality for patients with acute coronary syndrome, guide decision for coronary revascularisation needs. [22]
  • Well’s Score – calculate the clinical probability of DVT/PE and guide the decision to consider alternative diagnosis or perform immediate CTPA/anticoagulation. [23]
  • Pulmonary Embolism Rule Out Criteria (PERC) – effectively rules out PE if scored 0. [24]
  • Pulmonary Embolism Severity Index (PESI) – predicts 30-day mortality in patients with PE. [25]
  • Emergency Heart Failure Mortality Risk Grade (EHMRG) estimates 7-day mortality in patients with congestive heart failure and guides the decision to admit them [26].
  • San Francisco syncope rule (SFSR), Canadian syncope risk score (CSRS), and Evaluation of Guidelines in SYncope Study (EGSYS) Score – both SFSR and CSRS predict adverse outcomes in patients presenting with syncope (7-day and 30-day, respectively), EGSYS helps determine whether syncope is cardiac or non-cardiac cause (these includes vasovagal, situational, postural hypotension). [27-29]
  • Multi-parametric models – predict the prognosis of patients with Brugada syndrome for future major arrhythmic events (VT/VF) and guide decisions for implantable cardioverter defibrillator placement. [30]

* Please browse these calculators on MDCalc website (https://www.mdcalc.com/)

When To Admit This Patient

Patients with adverse features and hemodynamic instability require immediate intervention and admission. The aforementioned risk stratification tools can be used based on clinical signs and symptoms. If initial investigations yielded no clinical significance, patients could be discharged with education, reassurance, and safety netting advice. Explain that palpitations are usually transient and harmless; if they are recurring, ask patients to note down the onset, timing, and duration and measure BP and HR if monitoring is available at home. Advise them to reattend ED if symptoms persist or worsen or new-onset red flag symptoms emerge; lifestyle advice, for example, avoid certain known stimulants like caffeine, alcohol, and nicotine. If the patient is known to have SVT, educate about self-performing Valsalva maneuver to try terminating it before medical assistance arrives. Arrange follow-up with a family physician and review the need for further investigations and specialist input. Patients should be referred urgently for detailed investigations, including Holter monitoring if non-specific new clinical findings are yielded. Other options may be explored, such as an echocardiogram, implantable loop recorder, and electrophysiology study. [31, 32]

Revisiting Your Patient

The case reminds us that tachyarrhythmias can be secondary to non-cardiac causes. This is a classical presentation of hyperthyroidism, with ECG showing fast-rate atrial fibrillation. Atrial fibrillation occurs in 15% of patients with hyperthyroidism. A detailed history taking with appropriate systems review (as symptoms suggest) would point us towards hyperthyroidism. Clinical examination may reveal clubbing (thyroid acropachy), exomphalos (thyroid eye disease), pretibial myxoedema, goiter, and an irregular heartbeat with mid-systolic scratchy murmur (Means–Lerman scratch) might be heard on auscultation. The investigation here, starting from bedside, would be to obtain a complete set of vital signs (blood pressure, heart rate, respiratory rate, temperature, SpO2), 3-lead continuous monitoring, and 12-lead ECG; blood including complete blood count, urea and electrolytes, thyroid function tests, troponin (serial), venous blood gas, other electrolytes (Ca2+). The management approach of this patient is to treat the underlying hyperthyroidism primarily. Hence, endocrinologist referral will be required, with cardiologists’ input on managing the fast Atrial Fibrillation. Propranolol (reduces peripheral conversion of T4 to T3) and anti-thyroid drugs like carbimazole (inhibits thyroid peroxidase action) are the mainstay management (details see thyroid disorder chapter). However, as the patient also complains of anginal pain, rate control with cardio-selective beta-blockers should be initiated as well. It also helps with alleviating symptoms of hyperthyroidism, including palpitations, tremors, anxiety, heat intolerance, etc., due to the increased sympathetic tone caused by excess thyroid hormone production. The need for anticoagulation is assessed on an individual basis. In most cases, Atrial Fibrillation reverses to sinus rhythm spontaneously after the euthyroid state has been achieved. However, if Atrial Fibrillation persists, cardioversion may be considered. This, nevertheless, would be a cardiologist’s decision. [33]

Authors

Picture of Keith Sai Kit Leung

Keith Sai Kit Leung

Keith is an academic foundation doctor (emergency medicine themed) in the UK. He graduated both BSc and MBChB with distinction, and has published over 30 peer-reviewed articles till date. He is interested in Pre-Hospital Emergency & Retrieval Medicine, Intensive Care, Cardiology and Medical Education. He main research interests are arrhythmias and cardiac electrophysiology, cardiac arrest and resuscitation, ACS, POCUS, ECMO, airway and trauma management. He aims to work as an academic PHEM/HEMS physician and pursue a MD (Res)/PhD in the near future.

Picture of Rafaqat Hussain

Rafaqat Hussain

Dr Rafaqat Hussain is working as Specialty Doctor in Emergency Department at SWBH NHS trust. He had done MBBS.MRCEM. FRCEM.EBCEM. He has involved in training and teaching for junior doctors and medical students at University of Birmingham. He is enthusiastic in pursuing his career in being an Emergency Medicine Consultant.

Picture of Abraham Ka Cheung Wai

Abraham Ka Cheung Wai

Dr Abraham Wai, Clinical Associate Professor at the University of Hong Kong (HKU), is a dynamic force in the field of emergency medicine. His journey from specialist training to impactful research and innovative teaching has left an indelible mark on the healthcare landscape.

Listen to the chapter

References

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  18. Banerjee, A., & Oliver, C. (2017). Revision notes for the FRCEM intermediate SAQ paper (2nd). Oxford University Press.
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  20. Lip GY, Nieuwlaat R, Pisters R, Lane DA, Crijns HJ. Refining clinical risk stratification for predicting stroke and thromboembolism in atrial fibrillation using a novel risk factor-based approach: the euro heart survey on atrial fibrillation. Chest. 2010;137(2):263-272. doi:10.1378/chest.09-1584
  21. Brady W, de Souza K. The HEART score: A guide to its application in the emergency department. Turk J Emerg Med. 2018;18(2):47-51. doi:10.1016/j.tjem.2018.04.004
  22. de Araújo Gonçalves P, Ferreira J, Aguiar C, Seabra-Gomes R. TIMI, PURSUIT, and GRACE risk scores: sustained prognostic value and interaction with revascularization in NSTE-ACS. Eur Heart J. 2005;26(9):865-872. doi:10.1093/eurheartj/ehi187
  23. Wells PS, Anderson DR, Rodger M, et al. Excluding pulmonary embolism at the bedside without diagnostic imaging: management of patients with suspected pulmonary embolism presenting to the emergency department by using a simple clinical model and d-dimer. Ann Intern Med. 2001;135(2):98-107. doi:10.7326/0003-4819-135-2-200107170-00010
  24. Freund Y, Cachanado M, Aubry A, et al. Effect of the Pulmonary Embolism Rule-Out Criteria on Subsequent Thromboembolic Events Among Low-Risk Emergency Department Patients: The PROPER Randomized Clinical Trial. JAMA. 2018;319(6):559-566. doi:10.1001/jama.2017.21904
  25. Aujesky D, Obrosky DS, Stone RA, et al. Derivation and validation of a prognostic model for pulmonary embolism. Am J Respir Crit Care Med. 2005;172(8):1041-1046. doi:10.1164/rccm.200506-862OC
  26. Lee DS, Lee JS, Schull MJ, et al. Prospective Validation of the Emergency Heart Failure Mortality Risk Grade for Acute Heart Failure. Circulation. 2019;139(9):1146-1156. doi:10.1161/CIRCULATIONAHA.118.035509
  27. Quinn J, McDermott D, Stiell I, Kohn M, Wells G. Prospective validation of the San Francisco Syncope Rule to predict patients with serious outcomes. Ann Emerg Med. 2006;47(5):448-454. doi:10.1016/j.annemergmed.2005.11.019
  28. Thiruganasambandamoorthy V, Kwong K, Wells GA, et al. Development of the Canadian Syncope Risk Score to predict serious adverse events after emergency department assessment of syncope. CMAJ. 2016;188(12):E289-E298. doi:10.1503/cmaj.151469
  29. Kariman H, Harati S, Safari S, Baratloo A, Pishgahi M. Validation of EGSYS Score in Prediction of Cardiogenic Syncope. Emerg Med Int. 2015;2015:515370. doi:10.1155/2015/515370
  30. Chung CT, Bazoukis G, Radford D, et al. Predictive risk models for forecasting arrhythmic outcomes in Brugada syndrome: A focused review. J Electrocardiol. 2022;72:28-34. doi:10.1016/j.jelectrocard.2022.02.009
  31. Moulton KP, Bhutta BS, Mullin JC. Evaluation Of Suspected Cardiac Arrhythmia. [Updated 2023 Feb 9]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK585054/
  32. RCEMLearning. https://www.rcemlearning.co.uk/reference/palpitations/. Published July 27, 2021. Accessed April 13, 2023.
  33. Parmar MS. Thyrotoxic atrial fibrillation. MedGenMed. 2005;7(1):74.

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.

Blood Transfusion And Its Complications (2024)

~ iEM Education Project Team ~ Leave a comment

by Yaman Hukan, Thiagarajan Jaiganesh

Authors
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You have a new patient!

A 68-year-old male with a history of controlled HTN, DM, and Ischemic heart disease presents to the Emergency Department with complaints of easy fatiguability that started 2 months ago. He reports a gradual onset of symptoms and inability to tolerate his usual morning walk. He denies chest pain or palpitations. Upon further questioning, he mentioned that he noticed his clothes getting loose, and his family noticed he had lost weight. On review of systems, he states he has bouts of diarrhea with dark stools. Upon arrival, his vitals are Temp 36.9 C, HR 105 BPM, BP 122/68 mmHg, RR 17 BPM, and SpO2 of 98% on RA.  Blood investigations reveal an Hgb level of 5.0 g/dL. Therefore, you decide to initiate a Packed RBC transfusion in the ER. One hour after starting the transfusion, you are called by the nurse as the patient is becoming distressed. You attend to the patient and notice him to be in severe respiratory distress.

What do you need to know?

Often, patients presenting to Emergency Departments require a blood transfusion. According to the National Blood Collection and Utilization survey administered by the US Department of Health and Human Services, 2019 around 1 million RBC transfusions took place in EDs across the United States [1]. The clinical conditions necessitating a blood transfusion include upper and lower gastrointestinal bleeding, traumatic shock, symptomatic anemia, etc., to name a few. Therefore, medical trainees and emergency physicians must be aware of complications that may arise from blood transfusions and manage them appropriately.

Commonly administered blood products in the emergency department (ED) include packed red blood cells (PRBCs), fresh frozen plasma (FFP), platelet concentrates, and cryoprecipitate. PRBCs are frequently used to increase oxygen-carrying capacity in patients with significant anemia or hemorrhage. FFP provides essential clotting factors, making it valuable in cases of coagulopathy or massive transfusion protocols. Platelet concentrates are utilized to manage thrombocytopenia or platelet dysfunction, while cryoprecipitate supplies fibrinogen, von Willebrand factor, and other clotting factors, supporting hemostasis in patients with severe bleeding or fibrinogen deficiency.

The choice of components should be directed by the patient’s clinical condition, rate of bleeding, cardiopulmonary status, and operative intervention, with the goal of restoring volume and oxygen-carrying capacity [2].

Administering blood and blood products to patients has resulted in numerous adverse reactions. These reactions are broadly classified as either Acute (onset within 24 hrs), such as febrile nonhemolytic reactions, or Delayed (onset beyond 24 hrs), such as delayed hemolytic reactions [3].

Data from the National Healthcare Safety Network Hemovigilance Module in the United States demonstrate that 1 in 455 blood components transfused was associated with an adverse reaction. However, the incidence of serious reactions was much lower, at 1 in 6224. Despite the relatively lower rates of serious reactions, 23 fatalities were recorded between 2013 and 2018 [4].

Severe adverse reactions result from transfusing incompatible (ABO or Rh) blood. The ABO blood group system remains of extreme importance in blood transfusions, as it is the most immunogenic of all blood group antigens [5]. The four blood groups are A, B, O, and AB.

The table shows the summary of ABO Antigens and Antibodies contained within each blood type.

 

A

B

O

AB

Antigens

A

B

None

A and B

Antibodies

Anti-B

Anti-A

Anti-A & Anti-B

None

There are several ABO blood group antigens expressed on every RBC cell. Each blood group early on during life forms antibodies against ABO antigens not found on the surface of RBCs. When an individual is transfused ABO-incompatible blood, preformed antibodies in its own serum react against the donor’s red blood cells, causing rapid acute intravascular hemolysis, a life-threatening transfusion reaction.

The second significant blood grouping system is the Rh system. The presence of Rh Antigen implies that the patient is Rh(+) (e.g., Blood group O+). Patients who are Rh(-) lack the RhD antigen. Therefore, their blood develops antibodies against Rh(+) blood groups if they are ever exposed to it. This incompatibility can lead to a hemolytic reaction, but it is much less likely than a hemolytic reaction due to ABO incompatibility. The clinical significance of the Rh system lies in the pregnancy setting when a Rh(-) mother is pregnant with an Rh(+) fetus. Upon first exposure to the positive blood from the fetus, the mother’s blood would form antibodies against Rh-blood. In case of a repeated pregnancy with Rh+ fetus, the mother’s antibodies cross the placenta and attack the RBCs of the fetus, which can lead to a condition called hemolytic disease of the newborn [6]. This is the reason why women of childbearing age should always receive O(-) blood in the setting of acute hemorrhage needing a blood transfusion, as opposed to men who may receive O(+) blood safely.

Medical History

Should a patient receiving or recently received a blood or a blood product transfusion develop new signs and symptoms, consider a transfusion reaction. Commonly encountered signs and symptoms of mild transfusion reactions include:

  • Increase in body temperature/fever,
  • Chills/Rigors,
  • Pruritis, New rash, or swelling of the mucous membranes.

Severe reactions include:

  • Difficulty in breathing,
  • Respiratory distress,
  • Altered level of consciousness,
  • Decreased urinary output.

Reaction Types

Acute Transfusion Reactions

Febrile nonhemolytic transfusion reaction

This is one of the most common transfusion reactions, occurring at a rate of around 1:900 [7]. It has been attributed to cytokines released from white blood cells and their accumulation in blood products [8].

Diagnostic criteria

  • A reaction which occurs during or within 4 hours of cessation of transfusion,

AND

  • Either Fever (> 38 C° and a change of at least 1 C° from pretransfusion value) OR Chills/Rigors is present [9].

Caution must be exercised when distinguishing between febrile nonhemolytic transfusion reactions and hemolytic reactions, which could also present with fever. Febrile nonhemolytic transfusion reaction is considered a diagnosis of exclusion [8]. In the case of first onset of a febrile reaction, a hemolytic reaction must be suspected until proven otherwise.

Allergic and anaphylactic transfusion reactions

Another very common non-infectious transfusion reaction is allergy. Allergic reactions vary in severity from mild to severe. Mild reactions are primarily characterized by itching and hives. They occur at a rate of 1:1200 transfusions. However, rates may be much higher due to underreporting [7].

On the other hand, anaphylactic reactions are typically more severe and occur at a rate of around 1:30000 blood transfusions [7]. Anaphylactic reactions are acute systemic allergic reactions characterized most significantly by hypotension and/or respiratory compromise. They typically arise abruptly within 0-4 hours of initiating the transfusion.

Allergic reactions are thought to be multifactorial in etiology, mainly caused by an antibody-mediated response to donor proteins. These reactions fall under Type 1 hypersensitivity reactions and involve pre-existing IgE antibodies [10].

The criteria for a definitive diagnosis of an allergic reaction encompasses two or more of the following during or within 4 hours of cessation of transfusion: conjunctival edema, edema of lips, tongue, and uvula; Erythema and edema of the periorbital area, generalized flushing, hypotension, localized angioedema, maculopapular rash, pruritis (itching), respiratory distress/bronchospasm, and urticaria (hives) [9].

Acute hemolytic transfusion reaction

The hemolytic transfusion reaction is perhaps the most severe and life-threatening transfusion reaction. They account for 5% of all severe adverse reactions of blood transfusions.  Reactions due to ABO incompatibility occur at a rate of 1:200000 [7]. The rate significantly increases in the setting of uncross-matched blood transfusions in bleeding patients (e.g., major trauma), where the rate reaches as high as 1:2000 [11].

Despite their relative rarity, mainly due to growing hemovigilance procedures and schemes, acute hemolytic transfusion reactions can lead to significant morbidity and mortality. Mortality rates increase with the increase in the volume of the incompatible transfused blood. However, even a volume of as low as 30 mL could lead to a severe fatal reaction [12].

Reactions due to ABO system incompatibility most often occur due to a clerical or laboratory error, including misidentification of patient or mislabelling blood samples collected from the recipient for crossmatching. The recipient’s blood contains pre-existing antibodies against ABO antigens that are not present in their blood. When incompatible blood is administered, those pre-existing antibodies attack the donor’s RBCs. Through complement activation and membrane attack complex, the donor’s RBCs are destroyed, leading to intravascular hemolysis, which subsequently gives rise to the clinical features of hemolysis, including acute tubular necrosis, renal failure, hypotension, disseminated intravascular coagulopathy (DIC), and shock [13].

The criteria for the definitive diagnosis of acute hemolytic transfusion reactions is complex and includes components that can be obtained from clinical presentation combined with laboratory studies, detailed below [9]:

Decision-Making Algorithm for Suspected Hemolytic Transfusion Reaction
1. Identify New-Onset Symptoms

Check if the patient has developed any new symptoms during the transfusion or within 24 hours of transfusion cessation. The presence of any of the following symptoms warrants further investigation:

  • Back or flank pain
  • Chills or rigors
  • Disseminated intravascular coagulation (DIC)
  • Epistaxis (nosebleed)
  • Fever
  • Hematuria (indicative of gross hemolysis)
  • Hypotension
  • Oliguria or anuria (reduced or absent urine output)
  • Pain and/or oozing at the IV site
  • Renal failure

AND

Check for Laboratory Evidence of Hemolysis
Confirm the presence of at least two of the following laboratory findings:

  • Decreased fibrinogen
  • Decreased haptoglobin
  • Elevated bilirubin
  • Elevated lactate dehydrogenase (LDH)
  • Hemoglobinemia
  • Hemoglobinuria
  • Plasma discoloration consistent with hemolysis
  • Spherocytes visible on blood film

AND EITHER

Determine the Mechanism of Hemolysis. Differentiate between immune-mediated and non-immune-mediated hemolysis.

IMMUNE-MEDIATED HEMOLYSIS

  • Perform a Direct Antiglobulin Test (DAT) to detect anti-IgG or anti-C3.
  • Conduct an elution test to detect any alloantibodies on the transfused red blood cells. If the DAT or elution test is positive, this suggests an immune-mediated HTR.

NON-IMMUNE-MEDIATED HEMOLYSIS

  • If serologic testing is negative and there is evidence of a physical cause (e.g., thermal, osmotic, mechanical, or chemical), consider a non-immune etiology. A confirmed physical cause indicates a non-immune-mediated HTR.
Transfusion related acute lung injury (TRALI)

Transfusion-related acute lung injury (TRALI) is an infrequent but incredibly serious blood transfusion reaction. Despite only occurring at the rate of 1:60000 [7], TRALI is reported to be one of the most life-threatening complications according to data from the US Food and Drug Administration, coming in 2nd place among the most fatal blood transfusion reactions in the United States between 2016 and 2020, causing 21% of reported fatalities [14].

TRALI results in a constellation of symptoms that manifest as acute respiratory distress along with hemodynamic instability and can occur with virtually all blood components. The proposed mechanism is complex and involves activation of pulmonary endothelium and polymorphonuclear leucocytes and transfusion of plasma-containing antibodies directed against antigens on the surface of those leucocytes, leading to their activation [15].

The TRALI diagnosis remains clinical and significantly overlaps with other respiratory conditions (e.g., ARDS and Transfusion-associated circulatory overload). A set of clinical features have been adopted to define TRALI, including [9]:

  • No evidence of acute lung injury prior to transfusion, AND,
  • Acute lung injury onset during or within 6 hours of cessation of transfusion, AND,
  • Hypoxemia defined by any of the following methods:
      • PaO2/FiO2 less than or equal to 300 mmHg
      • Oxygen saturation less than 90% on room air
      • Other clinical evidence

AND,

  • Radiographic evidence of bilateral infiltrates
  • No evidence of left atrial hypertension (i.e., circulatory overload)
Transfusion associated circulatory overload (TACO)

The last of the acute transfusion reactions is transfusion-associated circulatory overload (TACO), which carries the highest mortality risk among all reactions. Between 2016 and 2020, 34% of recorded fatalities due to reactions to blood transfusions were caused by TACO [14]. It is relatively more common than TRALI, occurring at an estimated rate of 1:9000 transfusions [7]. TACO can present on a spectrum of mild symptoms to life-threatening ones. Significant overlap exists between TRALI and TACO as both may cause respiratory distress and potentially lead to hemodynamic instability.

TACO is a form of volume overload leading to pulmonary edema. Patients who are older than 70 years of age, suffer from pre-existing cardiac disease, or have a history of renal dysfunction are at increased risk of developing this complication [16].

The criteria for diagnosing TACO have evolved several times over the years. Currently, establishing a definitive diagnosis would require the following [9]:

New onset or exacerbation of 3 or more of the following within 12 hours of cessation of transfusion:

At least 1 of the following two items:-

  1. Evidence of acute or worsening respiratory distress (dyspnea, tachypnoea, cyanosis, and decreased oxygen saturation values in the absence of other specific causes) and/or 
  2. Radiographic or clinical evidence of acute or worsening pulmonary edema (crackles on lung auscultation, orthopnea, cough, a third heart sound, and pinkish frothy sputum in severe cases) or both

             AND;

  • Elevated brain natriuretic peptide (BNP) or NT-pro BNP relevant biomarker
  • Evidence of cardiovascular system changes not explained by underlying medical condition (Elevated central venous pressure, evidence of left heart failure including development of tachycardia, hypertension, widened pulse pressure, jugular venous distension, enlarged cardiac silhouette, and/or peripheral edema)
  • Evidence of fluid overload

Delayed Transfusion Reactions

In addition to acute blood transfusion reactions, there are certain reactions which could appear days or weeks following blood transfusions.

Delayed hemolytic transfusion reaction

Delayed hemolytic transfusion reactions are less severe forms of hemolytic reactions in patients receiving blood transfusions. They appear to be caused by secondary (anamnestic) responses in patients who have already received transfusions. They rarely cause life-threatening or serious manifestations [17]. Those reactions may occur up to 4 weeks following the completion of the transfusion. They are less common than acute hemolytic transfusions, occurring at a rate of 1:22000 transfusions [7].

The criteria for definitive diagnosis of delayed hemolytic transfusion reactions include [9]:

Positive direct antiglobulin test (DAT) for antibodies developed between 24 hours and 28 days after cessation of transfusion

AND EITHER

  • Positive elution test with alloantibody present on the transfused red blood cells OR
  • Newly identified red blood cell alloantibody in recipient serum

AND EITHER

  • Inadequate rise of post-transfusion hemoglobin level or rapid fall in hemoglobin back to pre-transfusion levels OR
  • Otherwise, unexplained appearance of spherocytes
Transfusion associated graft vs. host disease

Transfusion-associated graft vs. host disease is an extremely rare and exceptionally dangerous complication of transfusions, occurring at a rate of 1 in every 13 million [7]. It can present any time up to 6 weeks following the transfusion. It is thought to be caused by viable lymphocytes in the donor’s blood recognizing their new host’s cells as foreign and attacking them, often leading to fatal outcomes [17].

Diagnosis is made when the following characteristics appear between 2 days to 6 weeks from cessation of transfusion [9]:

  • Characteristic rash: erythematous, maculopapular eruption centrally that spreads to extremities and may, in severe cases, progress to generalized erythroderma and hemorrhagic bullous formation.
  • Diarrhea
  • Fever
  • Hepatomegaly
  • Liver dysfunction (i.e., elevated ALT, AST, Alkaline phosphatase, and bilirubin)
  • Marrow aplasia
  • Pancytopenia

AND

  • Characteristic histological appearance of skin or liver biopsy
Post transfusion purpura

This reaction may appear up to 2 weeks post-transfusion and involves platelets [17]. Its prevalence is thought to be around 1 in 57,000 transfusions [7]. A definitive diagnosis may be reached by the following two findings [9]:

  • Alloantibodies in the patient directed against human platelet antigens (HPAs) or other platelet-specific antigens detected at or after the development of thrombocytopenia AND
  • Thrombocytopenia (i.e., decrease in platelets to less than 20% of pre-transfusion count)

Physical Examination

Transfusion reactions could manifest in several organ systems. It is important to exercise vigilance when approaching a patient with a suspected transfusion reaction, as clinical features significantly overlap between several reactions.

One unified step in the physical examination of patients with suspected transfusion reactions is to obtain a complete set of vital signs. This can provide important clues to the diagnosis. For instance, a rise in baseline temperature could indicate a Febrile nonhemolytic reaction, Acute hemolytic reaction, or even TRALI.

Hypotension is a feature of anaphylaxis or acute hemolysis. In addition, while keeping in mind that TRALI can present with either Hypotension or Hypertension, hypotension is more common in TRALI [18] and can help distinguish it from TACO, which can present with respiratory distress coupled with hypertension. Tachypnea and desaturation can be signs of respiratory distress, which would point to either TRALI or TACO as possible diagnoses. Following vitals, emphasis should be on signs relating to the suspected reactions.

Chills and rigors might be observed in acute hemolytic transfusion reaction, along with fever and hypotension. Respiratory status examination is essential and could yield signs of acute distress, including tachypnea, oxygen desaturation, use of accessory muscles, and wheezing. Patients would be anxious, with some reporting a sense of impending doom. Additionally, urine frequency and color should be observed for oliguria or dark-colored urine, pointing to acute hemolysis.

Observe any signs of maculopapular urticarial rash in suspected allergic reactions. Also, look for any signs of dyspnea, wheezing, anxiety, and angioedema. Anaphylaxis could further present with hypotension which could pose a diagnostic dilemma.

There are significant similarities between TRALI and TACO. Examination should look for dyspnea, tachypnoea, cyanosis, and decreased oxygen saturation. Furthermore, auscultation for crackles might be evidence of pulmonary edema. Orthopnea, cough, a third heart sound, and pinkish frothy sputum could all be clues leading to the diagnosis of these reactions.

Alternative Diagnoses

When new symptoms arise after blood transfusions, the diagnosis of transfusion reactions should be established. However, an extensive differential diagnosis list must be carefully formulated depending on the presentation.

In the context of transfusions, certain signs and symptoms may indicate potential complications or adverse reactions. A new rash or swelling of mucous membranes could suggest an allergic reaction, anaphylaxis, urticaria, food allergies, or angioedema. Dyspnea, or respiratory distress, may be indicative of transfusion-related acute lung injury (TRALI), transfusion-associated circulatory overload (TACO), anaphylaxis, cardiogenic pulmonary edema, acute respiratory distress syndrome, or acute chest syndrome. Hypotension could point to anaphylaxis, TRALI, septic shock, hemorrhagic shock, or neurogenic shock. Lastly, the presence of fever may indicate a febrile non-hemolytic reaction, an acute hemolytic reaction, an infection from any source, or sepsis. Identifying these symptoms promptly is essential to manage and mitigate potential adverse events during transfusions.

The table summarizes signs&symptoms and potential differential diagnoses. 

Signs and Symptoms

Differential Diagnoses

New rash, or swelling of mucous membranes

Allergic reaction, Anaphylaxis, Acute, Urticaria, Food Allergies, Angioedema

Dyspnea (Respiratory distress)

TRALI, TACO, Anaphylaxis, Cardiogenic pulmonary edema, Acute respiratory distress syndrome, Acute chest syndrome

Hypotension

Anaphylaxis, TRALI, Septic shock, Hemorrhagic shock, Neurogenic shock

Fever

Febrile nonhemolytic reaction, Acute hemolytic reaction, infection of any source, sepsis

Acing Diagnostic Testing

While most transfusion reaction diagnoses are primarily clinical, few diagnostic tests may assist clinicians in establishing a diagnosis.

  1. Visual inspection of the pre-transfusion sample for its color and any unusual clumps [19].
  2. Allergic reactions: IgA levels could also be obtained in patients with suspected IgA deficiency, although the diagnosis for moderate or severe allergic reactions is usually clinical. Eosinophilia could indicate allergic reactions but may not always be present [10].
  3. Hemolytic reactions: Elevated Lactate dehydrogenase levels (LDH) as well as indirect bilirubin levels with decreased haptoglobin levels would suggest a hemolytic reaction arising out of an ABO incompatibility. Elevated PTT and PT/INR, as well as D-Dimer coupled with decreased fibrinogen, would suggest the presence of DIC. Blood film can be examined for schistocytes or spherocytes [12]. Dark urine could suggest hemoglobinuria. Direct antiglobulin test (DAT) for anti-IgG or anti-C3 and elution test with alloantibody present on the transfused red blood cells would help.
  4. TRALI & TACO: arterial blood gas (ABG) is used to calculate the PaO2/FiO2 ratio, and Chest XR is used to evaluate the presence of bilateral infiltrates or features of pulmonary edema. Bedside ultrasound can confirm the absence of circulatory overload in TRALI, which is a distinguishing feature from TACO. Additionally, a BNP level should be obtained when evaluating for TACO.

Risk Stratification

Unfortunately, no objective risk stratification tool exists that would lead to recognizing patients with worse outcomes due to transfusion reactions.

Characteristics which place patients at increased risk of developing transfusion reactions are:

  • Previous transfusion history,
  • Abortions or termination of pregnancy history,
  • Longer blood storage time,
  • Receiving three or more units of blood [3].
  • Critically ill and surgical patients (Risk of mortality due to TRALI appears to be higher) [20].

Management

In case of transfusion reactions, the ABCDE algorithm for managing conditions in the emergency department should be followed. The airway must be assessed for patency and secured if needed, followed by addressing breathing and circulation.

The cornerstone of managing most transfusion reactions is stopping the transfusion and maintaining Intravenous access. In all reactions, the next step is to confirm the details of the transfused unit, make sure no clerical error occurred, and then report the reaction to the concerned blood bank [17].

Febrile nonhemolytic reaction:  Management of this reaction encompasses frequent monitoring of vital signs and administering antipyretics. Transfusion can be continued in stable patients with no other symptoms [12]. However, this remains a diagnosis of exclusion, and other reactions must be considered.

Mild allergic reaction: An H1 antihistamine (e.g., Diphenhydramine 25-50 mg IV) should be administered for symptom management in case of a mild allergic reaction. Restart the transfusion under direct supervision at a slower rate upon resolution of symptoms. In case of recurrence, transfusion must be suspended [17].

Anaphylaxis reaction: Manage as per standard institutional protocol or as delineated in an earlier chapter within this textbook (e.g., IM 1:1000 Epinephrine, H1 antihistamine, e.g., IV Diphenhydramine, Beta-adrenergic drugs, e.g., Salbutamol nebs in case of wheezing and/or bronchospasm, Steroids, e.g., Hydrocortisone and IV Fluids as required) [17].

Acute hemolytic transfusion reaction: The onset of hemodynamic instability will indicate an acute hemolytic transfusion reaction, and it is imperative to immediately halt the transfusions. Treatment is largely supportive. Focus on supporting the respiratory, cardiovascular, and renal systems and treating possible complications such as DIC to halt the patient’s condition [21].

Transfusion-related acute lung injury (TRALI): Similar to acute hemolytic reaction, treatment of TRALI is supportive. Most importantly, support of ventilatory status should be established with noninvasive or invasive means. Most patients who develop TRALI require ventilatory support [22]. As most patients with TRALI develop hypotension, supporting hemodynamics with IV fluids and possible vasopressors may be needed to ensure adequate organ perfusion.

Transfusion-associated circulatory overload (TACO): Since TACO reflects a volume overload status, this condition can be treated similarly to other conditions that result in volume overload. In deteriorating patients, ventilatory support may be needed through noninvasive or mechanical ventilation. Furosemide 0.5/1 mg/kg may be used. In addition, IV Nitroglycerin 50 – 100 mcg as an initial dose may theoretically have a role in clinical status improvement [16,17].

Special Patient Groups

Pregnant Patients

This patient population should always receive O(-) blood when prompt uncross-matched blood is needed for transfusion to minimize the risk of Rh(-) mothers developing antibodies against the Rh(+) fetus, leading to subsequent hemolytic disease of the newborn [5].

Geriatrics

About half of RBC units are administered to patients aged 70 and above [23]. They are frail, have various comorbid conditions, and age-related altered physiology. Clinicians must base their transfusion decisions on the risk-benefit ratio for elderly patients [24]. TACO is the most common transfusion reaction in elderly patients. It occurs at a substantially higher rate in this population compared to younger patients, and those with more comorbidities are at higher risk. Slower transfusion rates are recommended to mitigate the risk [25]. In addition, several studies have mentioned that blood transfusions in the elderly are linked to the risk of developing delirium, although the causation is unknown [26].

Pediatrics

According to a recent meta-analysis, the incidence of transfusion reactions is higher in children than in adults, including rare transfusion reactions [27], due to their size difference (volume-related) and immature liver [28].

When To Admit This Patient

It is advisable to observe patients with hemodynamic instability or severe reactions following a blood transfusion (e.g., ICU for Acute hemolytic reaction). No clear guidelines exist on the criteria for admission for patients with transfusion reactions, and the decision might need to be made on a case-by-case basis, depending on the clinician’s experience and clinical evaluation.

Revisiting Your Patient

Recall that your patient was started on a blood transfusion for a Hgb of 5.0 g/dl and then developed respiratory distress. You arrive at the room and connect to the patient on a monitor. His vitals now show a temperature of 38 C, HR of 132 BPM, RR of 35, BP of 205/120, and SpO2 of 75% on Room Air. You immediately assess the airway and note that the patient is talking clearly but cannot complete full sentences. No secretions in the oral cavity. You judge the airway to be patent and move to assess breathing. He is tachypneic and desaturating, and you immediately place him on 15L O2 via a nonrebreather mask. The patient’s SpO2 picks up to 90%. Upon chest inspection, you hear diffuse crackles. The patient is also unable to lie supine. Hypertension and tachycardia are noted, as well as elevated Jugular venous pressure.

By now, you judge the patient has developed a transfusion reaction, and you immediately order the nurse to suspend the transfusion and notify the blood bank.

An X-ray was ordered, and it showed features of pulmonary edema as well as blunting of the costophrenic angles. Arterial blood gas shows a PaO2/FiO2 ratio 190 and a lactate 4. A BNP is sent and returns at 25,000 pg/mL

Upon review of the patient, he is in significant distress despite the nonrebreather mask, so the respiratory therapist is contacted to initiate BiPAP treatment. You diagnose TACO and, in addition, start the patient on 100 mcg/min of IV Nitroglycerin and a 40 mg dose of IV Furosemide.

The patient started improving shortly after and stated that his breathing was improving. The patient was admitted to the ICU for further stabilization and management of his condition.

Author

Picture of Yaman Hukan

Yaman Hukan

Yaman Hukan is an Emergency Medicine resident at Tawam Hospital in the United Arab Emirates. He completed his bachelor's of medicine (MBBS) degree in 2018 from the University of Sharjah. He is interested in humanitarian medicine. As a medical student, he joined the Syrian American medical society (SAMS) on several of their missions to provide healthcare for Syrian refugees in Jordan. His interests also include resuscitation and toxicology, a field in which he hopes to pursue further training.

Picture of Thiagarajan Jaiganesh

Thiagarajan Jaiganesh

Dr. Jaiganesh is a Chairman and Consultant in Adult and Pediatric Emergency Medicine and serves as an Adjunct Assistant Professor at UAE University. As the former Director of the Emergency Medicine Residency Program at Tawam Hospital in Al Ain, UAE, Dr. Jaiganesh is dedicated to training the next generation of emergency medicine professionals. With a strong academic and professional background, Dr. Jaiganesh has published numerous peer-reviewed articles on emergency medicine and contributes as a Section Editor and Chapter Author for notable medical texts, including the Oxford Handbook for Medical School. A sought-after speaker, Dr. Jaiganesh has been invited to present at numerous national and international conferences and serves as an instructor in various life support courses. Additionally, Dr. Jaiganesh is an expert in medico-legal and clinical negligence matters, providing valuable insights into complex legal and ethical cases in healthcare.

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References

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  21. Tobian A. Hemolytic transfusion reactions. UpToDate. https://www-uptodate-com.eu1.proxy.openathens.net/contents/hemolytic-transfusion-reactions?sectionName=DELAYED%20HEMOLYTIC%20TRANSFUSION%20REACTIONS%20AND%20DELAYED%20SEROLOGIC%20TRANSFUSION%20REACTIONS&search=blood%20transfusion%20reaction&topicRef=95132&anchor=H354791&source=see_link#H354791. Updated on Jan 05, 2022. Accessed on March 15, 2023
  22. Vlaar AP, Binnekade JM, Prins D, et al. Risk factors and outcome of transfusion-related acute lung injury in the critically ill: a nested case-control study. Crit Care Med. 2010;38(3):771-778. doi:10.1097/CCM.0b013e3181cc4d4b
  23. Bosch MA, Contreras E, Madoz P, et al. The epidemiology of blood component transfusion in Catalonia, Northeastern Spain. Transfusion. 2011;51(1):105-116. doi:10.1111/j.1537-2995.2010.02785.x
  24. Boureau AS, de Decker L. Blood transfusion in older patients. Transfus Clin Biol. 2019;26(3):160-163. doi:10.1016/j.tracli.2019.06.190
  25. Menis M, Anderson SA, Forshee RA, et al. Transfusion-associated circulatory overload (TACO) and potential risk factors among the inpatient US elderly as recorded in Medicare administrative databases during 2011. Vox Sang. 2014;106(2):144-152. doi:10.1111/vox.12070
  26. van der Zanden V, Beishuizen SJ, Swart LM, de Rooij SE, van Munster BC. The Effect of Treatment of Anemia with Blood Transfusion on Delirium: A Systematic Review. J Am Geriatr Soc. 2017;65(4):728-737. doi:10.1111/jgs.14564
  27. Wang Y, Sun W, Wang X, et al. Comparison of transfusion reactions in children and adults: A systematic review and meta-analysis. Pediatr Blood Cancer. 2022;69(9):e29842. doi:10.1002/pbc.29842
  28. Sostin N, Hendrickson JE. Pediatric Hemovigilance and Adverse Transfusion Reactions. Clin Lab Med. 2021;41(1):51-67. doi:10.1016/j.cll.2020.10.004

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.

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
Listen

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.

Listen to the chapter

References

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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.