Fever in Children (2024)

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by Camilo E. Gutierrez

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Disclaimer: The guidelines for evaluating febrile infants in this publication are based on current U.S. practices and epidemiology. These may not apply to other regions, particularly low- and middle-income countries, where vaccination rates, healthcare access, and local factors may differ. Local guidelines should be consulted in those settings.

You have new patients!

You are working in an emergency department, and during your shift, you see a number of different patients.

Bed 1

In bed 1, a parent brings a full-term 2-month-old male infant who has been complaining of fever at home for 1 day. The child has been drinking well, has normal urine output, and has no associated symptoms.

Prenatal care was normal, infant was born by normal vaginal delivery with no complications and went home with mom after a couple of days. Of note, the mother had a fever during delivery and received antibiotics—no sick contacts at home.

The male infant is vigorous and appears well during your examination. Currently afebrile with normal vital signs.

Bed 2

In bed 2, you find a well-appearing 2-month-old female infant with complaint of fever at home. This child has had fever for 1 day. She also has a runny nose and a couple of episodes of vomiting after feeding. The family is visiting from out of town and has no way to contact their pediatrician.

Prenatal care was normal, infant was born by normal vaginal delivery with no complications and went home with mom after a couple of days—no sick contacts at home.

The female infant is vigorous and well-appearing during your examination. Currently afebrile with normal vital signs.

Bed 3

In bed 3, you have a 3-year-old fully vaccinated boy who has had fever of up to 38.5°C every day for the last week. Aside from the fever, there were no significant respiratory symptoms, vomiting, or diarrhea. He has been able to drink well, although not eating his usual amount.

Vital signs are remarkable for fever of 39°C, mild tachycardia to 120 bpm, and respiratory rate of 32 rpm. On exam, he has mildly injected conjunctiva, cervical adenopathy, and some peeling of his fingers.

How will you approach each of these patients?

Introduction

Fever is a common childhood complaint frequently encountered in emergency medicine [1]. It is a symptom of an underlying illness or infection and occurs when the body’s temperature rises above its normal range [2]. In children, a fever is generally defined as a temperature of 38°C (100.4°F) or higher in infants under 3 months and 38.5°C (101°F) in older toddlers and children [3].

Many causes of fever in children include viral or bacterial infections, autoimmune disorders, allergies, and reactions to medication. In some cases, the cause of the fever may be difficult to determine [2].

In emergency medicine, the primary concern with fever in children is identifying the underlying cause and treating it appropriately. This may involve a thorough physical examination, blood tests, imaging studies, or other diagnostic tests to help identify the cause of the fever.

In addition to treating the underlying cause of the fever, several measures can be taken to help manage the symptoms of fever in children. These may include administering acetaminophen or ibuprofen to help lower the child’s temperature, ensure adequate hydration, and closely monitor the child’s temperature and other vital signs  [4].

It is important to seek medical attention promptly if your child has a fever accompanied by other symptoms such as difficulty breathing, severe headache, rash, or lethargy. With prompt diagnosis and treatment, most cases of fever in children can be successfully evaluated and managed in the emergency department.

Temperature should ideally be measured rectally in infants [5]. In older toddlers and children, oral or axillary measurements are acceptable, understanding there is an approximate 0.5°C difference between the latter and rectal temperatures [6]. Also, rectal or oral measurements might be contraindicated in patients with immunodeficiency or neutropenia.

The pathophysiology of fever is associated with the liberation of cellular mediators such as interleukins, tumor necrosis factor, and interferon and their impact on prostaglandins at the hypothalamic level, raising the endogenous thermostat [7]. Fever is thought to be a benign and useful mechanism to stimulate the immune system, although it does increase metabolic demands, which can affect homeostasis at various levels [8].

This chapter will review the evaluation of febrile children in the emergency department.

What do you need to know?

Fever in infants

The American Academy of Pediatrics (AAP) recently updated its guidelines [9] for evaluating and managing fever in infants, providing evidence-based recommendations for healthcare providers.

According to the new guidelines, any infant younger than 60 days of age with a fever (rectal temperature of 38°C or higher) should be evaluated promptly. Fever in this age group can be a sign of a serious bacterial infection or invasive infection that requires urgent medical attention. The evaluation should include a complete physical examination, blood tests, urine tests, and possibly a lumbar puncture.

The guidelines also emphasize the importance of assessing the infant’s overall clinical appearance, including their hydration status, activity level, and interaction with caregivers. Any infant who appears ill, dehydrated, or has other concerning symptoms should be evaluated and managed as an inpatient.

Overall, the AAP guidelines aim to provide a systematic approach to evaluating and managing fever in infants, focusing on early recognition and treatment of serious bacterial infections while minimizing unnecessary diagnostic testing and hospitalization. It is important for healthcare providers and parents to be aware of these guidelines and to seek prompt medical attention if an infant develops a fever.

Prenatal risk factors should be assessed and include prematurity, prenatal care, maternal infections such as Group B Streptococcus and herpes, prolonged rupture of membranes, birth by C-section of normal vaginal delivery, maternal fever, and need for peripartum antimicrobial administration. Postnatal factors may include admission to the neonatal intensive care unit, the presence of respiratory support, central or peripheral lines, exposure to sick contacts, or the use of antibiotics as a newborn. Social determinants of health, such as access to healthcare, education, adequate environment, economic stability, and social and community support, play a key role in the decision-making process considering the disposition of the febrile infant once assessed in the emergency department.

Clinical prediction rules have been developed and validated, and guidelines have been adapted to include their use. Currently, the Step-by-step and the PECARN prediction rules offer a high sensitivity (96.7% and 92%, respectively) for the detection of SBI/IBI in infants and, more importantly, a very high negative predictive value (>99%) by which if all the high-risk lab criteria, including inflammatory markers, are negative, the presence of IBI/SBI is extremely unlikely [10] [11].

Infants < 21 days of age

The risk of serious bacterial infection (SBI), which includes bacteremia, urinary tract infection, and meningitis in infants younger than 21 days of age, is very high, and clinical examination parameters are not sensitive or specific enough to determine which infants are not at risk of sepsis. Patients at this age with a fever > 38°C, hypothermia, bradycardia, or apnea have a high risk of sepsis and septic shock. Infants under 21 days of age require thorough evaluation, including complete blood cell counts (CBC), blood culture, catheterized urine sample for microscopic urinalysis and urine culture, and a spinal puncture (LP) for evaluation and culture of cerebrospinal fluid. In addition, these patients should receive parenteral antibiotics such as Ampicillin, Gentamycin, and/or Cefotaxime as per local guidelines. For patients of this age, it is important always to consider the possibility of herpes simplex virus (HSV) infection, and parenteral acyclovir should be considered pending results of HSV nucleic amplification tests (HSV DNA PCR) or viral culture studies [12]. These patients should be admitted to an inpatient level of care for close monitoring and pending results of blood, urine, and CSF cultures.

Infants 22-28 days

It is important to understand that any current guidelines for evaluating febrile infants apply to well-appearing children. Suppose there is any concern or clinical finding regarding an ill-appearing infant. In that case, a thorough examination and laboratory testing, including blood, urine, CSF cultures, broad-spectrum antibiotics, and admission to a hospital service, are indicated [13].

Infants in this age range are still considered at high risk for serious invasive infections, especially if there are any risk factors, as described above. Current guidelines still strongly recommend considering full evaluation of the patients 22 to 28 days old, strongly consider antibiotic management pending culture results, and possible admission to a hospital.

However, in select infants of this age range, a more conservative approach has been suggested: obtaining catheterized urine samples, a complete blood count, urine and blood cultures, and introducing inflammatory markers. Currently studied and available inflammatory markers include c-reactive protein (CRP), Procalcitonin, and absolute neutrophil count (ANC). These tests’ recommended cut-offs are CRP > 20 mg/L, Procalcitonin > 0.5 ng/ml, and ANC > 4000/µL or <1000/µL, respectively.

If a well-appearing infant has normal urinalysis, normal WBC, and negative inflammatory markers, one possibility would be admission to a hospital service with or without obtaining a lumbar puncture. However, this opens the opportunity to admit without giving antimicrobial agents and observing pending culture results [14]. However, if any of the screening labs or inflammatory markers are elevated, antibiotics and admission are necessary. Still, the possibility of HSV infection should be considered at this age.

Infants 29-60 days

For this age group, for well-appearing infants with a temperature >38°C, the recommendation is to obtain urine and blood, including cultures and inflammatory markers [15]. At this age, obtaining a lumbar puncture is no longer mandatory for a well-appearing child with otherwise normal laboratory evaluation and negative inflammatory markers. If inflammatory markers are elevated in the absence of a positive urinalysis, a lumbar puncture is indicated to rule out meningitis. If the urinalysis is positive and inflammatory markers are below the threshold, there is no clear indication to perform a spinal tap, and the infant can be treated for a urinary tract infection potentially with oral antimicrobials and can be considered a candidate to be discharged home with close follow up within 24 hours. Suppose all the screening labs and inflammatory markers are within normal limits. In that case, there is no indication for antibiotic treatment, and the patient can be observed at home with close follow-up in 24 hours [16]. Recent literature suggests that well-appearing infants with an uncomplicated urinary tract infection (UTI) have a very low risk of bacteremia and an even lower risk of meningitis.

In order to discharge an infant home, the clinician must ensure that the parents understand the degree of risk, the importance of prompt follow-up within 24 hours, the capacity and ability to return to medical care, and the understanding to return immediately if there is any deterioration in the infant’s status. If not all of these criteria can be fulfilled, and there are social, language, or intellectual barriers to healthcare, the patient should be admitted to the hospital for observation.

In infants older than 30 days of age, antimicrobial regimens can include ceftriaxone for the treatment of bacteremia and/or urinary tract infections, with the consideration of ceftazidime or vancomycin for the treatment of bacterial meningitis. Oral regimens of first or second-generation cephalosporins can be considered for uncomplicated urinary tract infections. Always consider the local flora, antibiograms, and susceptibility to antibiotics before prescribing antimicrobial courses.

Also, it’s important to remember that if there is any concern, a full septic workup should be obtained, and broad-spectrum antibiotics should be used pending the culture results.

Infants older than 2 months of age

Vaccination has significantly reduced the incidence of bacterial infections in children, including serial bacterial infections. For example, the Haemophilus influenzae type b (Hib) vaccine has been highly effective in reducing the incidence of invasive Hib disease, which can cause meningitis, pneumonia, and other serious infections in young children. The introduction of the pneumococcal conjugate vaccine (PCV) has also led to a significant reduction in the incidence of invasive pneumococcal disease, including pneumonia and meningitis. E. coli has become the most common pathogen responsible for IBI in infants, bacteremia, and meningitis.

Furthermore, vaccination can indirectly reduce the incidence of serial bacterial infections by reducing the overall burden of bacterial infections in the community. When fewer people are infected with a particular bacterium, there is less opportunity for that bacteria to be transmitted from person to person, known as herd immunity, reducing the risk of serial infections for the general population.

Vaccination has significantly reduced the incidence of bacterial infections in children, including serial infections. Vaccination is a safe and effective way to protect children from serious bacterial infections and is an important part of routine healthcare for children.

For the evaluation of well-appearing, febrile infants older than 2 months of age, the main recommendation is always to consider the possibility of a urinary tract infection (UTI). The incidence of bacteremia and meningitis in areas with adequate vaccination coverage has decreased to approximately 1% risk of bacteremia and <0.5% risk of bacterial meningitis. However, the risk of UTI remains at 10-20% risk.

In general, the risk of UTI is similar in females and males up to 6 months of age. However, it drops for circumcised males after 6 months. The prevalence of UTI remains high in females up to 24 months of age.

As discussed above, if there is any concern about a high fever or a child who is not well-appearing, a more aggressive evaluation should be undertaken, and appropriate antimicrobial therapy should be considered.

The need to obtain a lumbar puncture (LP) in a well-appearing infant in this age group is of less debate currently as the incidence of bacterial meningitis is so rare, especially with a reassuring examination and low-risk screening labs.

After 2 months of age, it is important to consider the prevalence of viral infections. Common viral infections such as Respiratory Syncytial Virus (RSV), Influenza Virus, Rhinovirus, Enterovirus, Metapneumovirus, and Coronavirus, including SARS-COVID-2 virus, are prevalent in infants, and studies reveal that the presence of these viral infections is related to less possibility of serious invasive bacterial etiology perhaps with the exception of UTI’s. The incidence of UTIs in children with associated RSV infection is still high and warrants evaluation. However, it is important always to be vigilant of the possibility of HSV disease, a thorough maternal history, exposure, and physical examination is important, as well as considering obtaining blood, skin, mucosal, and CSF samples to send for culture or nucleic acid amplification and consider starting antiviral therapy presumptively due to the severity of these infections in infants, specially central nervous system or disseminated disease, which carry high morbidity and mortality.

Recent antimicrobial use also needs to be considered in infants within this age group. If any oral antimicrobials have been administered within 72 hours, the clinician should consider the possibility of partially treated infection or masking of signs and symptoms of bacterial infection. In this scenario, obtaining urine and blood cultures should be strongly considered.

There is poor evidence regarding the extent of evaluation in recently immunized infants. Recent immunizations are generally considered vaccinations administered in the previous 24 to 48 hours. In general, for a well-appearing infant older than 2 months, with a normal physical examination after a recent immunization less than 24 hours prior to the evaluation, the general consensus is not necessarily to obtain any testing but to direct the patient for a follow-up evaluation in the next 24 hours to ensure fever is not further present within 48 hours after vaccinations. However, the clinician should consider the possibility of catheterized urine evaluation within 48 hours of immunization due to the prevalence of UTI.

Invasive Bacterial Infections (IBI)

IBI is used to discuss the evidence of localized bacterial infections in infants and toddlers. A thorough physical examination should provide a clue of the presence of any of these disease processes. The term usually includes acute otitis media, cutaneous cellulitis or omphalitis around the umbilicus in infants, bacterial arthritis, skin abscess, and mastitis. Occult causes of IBI are less evident by physical examination and require a high index of suspicion, and the likely need for laboratory or imaging evaluation includes bacterial pneumonia, osteomyelitis, epidural abscess, brain abscess, or meningitis. Ill-appearing infants with focal infections do require a thorough evaluation, including cultures of abscess drainage, fluid aspirates, and skin or mucosal discharge [17].

Hyperpyrexia

The literature describes a linear correlation between high fever and serious bacterial infection. Hyperpyrexia is defined as rectal temperature ≥40°C (104°F) and is uncommon among febrile infants but is highly associated with invasive bacterial infection. If an infant presents with hyperpyrexia, blood cultures should be obtained and treated with broad-spectrum antimicrobials pending the blood culture results.

Fever of unknown origin / Fever without a source

Fever of unknown origin (FUO) is generally defined as a temperature >38.3°C (101°F), at least once daily, that lasts for at least 8 days and for which the cause cannot be identified after an initial workup. FUO can be challenging to diagnose, especially in children, as it can be caused by a variety of infectious, inflammatory, and neoplastic diseases, usually in this order of prevalence. Fever without a source (FWS) is generally defined as fever for less than 1 week without adequate explanation after a thorough history and physical examination.

The evaluation of FUO in children typically involves a comprehensive history and physical examination, as well as laboratory tests, imaging studies, and sometimes more invasive procedures [18]. It is important to understand the local distribution of infectious agents and the regional or ethnic presentation of specific inflammatory or rheumatologic conditions. Still, there is a small minority of patients in whom, after thorough evaluations, no cause is identified.

The following is a general approach to the evaluation of FUO in children:

History and physical examination: A thorough history and physical examination are critical in identifying any clues that may help narrow down the potential causes of the fever. Important details to gather include the child’s age, travel history, recent infections, medication use, and exposure to animals or sick contacts. Concerning fever, it is important to verify its height, duration, pattern, if it is documented or subjective, and any other associated symptoms surrounding febrile spikes. Associated complaints or symptoms can be useful in helping establish a correlation. Respiratory symptoms, gastrointestinal complaints, bone and muscle aches, and skin rashes may suggest specific etiologies that may present with prolonged fevers. Travel and exposure are key questions that can help narrow the possibility of etiologic agents. Contact with sick individuals, pets, farms, and other animals can point to specific infectious etiologies. It is easy to find lists of common infectious diseases by geographic location.

Vital signs should be documented, and discrepancies should be analyzed. For example, fever and bradycardia might suggest a few specific conditions (tick-borne or mosquito-related illnesses, legionella, Leptospira). Weight loss might suggest systemic diseases or malignancy.

The physical examination should include a detailed examination of all organ systems. Detailed skin evaluation might suggest dermatologic manifestations, as skin rashes can be associated with specific infectious or rheumatologic diseases. Examination of mucosal surfaces, including conjunctiva, mouth, and genitalia, might provide clues to systemic, rheumatologic, infectious, or inflammatory diseases. Lung and cardiovascular exam might reveal evidence of effusions or endocarditis. Attention to typical and atypical lymphadenopathy, organomegaly, or bone or muscle tenderness that might suggest infiltrative disease, inflammatory or infectious process. The genitourinary examination should be considered to exclude sexually transmitted diseases, pelvic masses, and inflammatory or malignant etiologies. Finally, a detailed neurological assessment might suggest subtle neuro deficits that might point to neuropathies, spinal pathology, medication, or toxic overdoses.

The physical exam should be repeated frequently in children, as it often evolves and changes according to disease progression.

Often, the initial assessment will be performed by a primary care clinician in an outpatient setting unless the child has become ill, has rapidly progressing symptoms or deterioration, or initial common studies have been performed and need for more complex testing needs to be performed.

Laboratory tests: A complete blood count with differential cell count, blood cultures, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), liver and renal function tests, and urinalysis should be obtained as part of the initial workup. Depending on the clinical presentation and suspected etiology, additional tests such as serologic studies, viral cultures, and molecular diagnostic tests may be indicated. Leukocytosis, cytopenia, anemia, thrombocytosis or thrombocytopenia, and atypical cell lines such as atypical leukocytes, bandemia, eosinophilia, can all point to various infectious etiologies, and might suggest viral, fungal, parasitic, rickettsial, and chronic disease or malignancy. Inflammatory markers are non-specific but can help the clinician trend the progression of a disease process.

Secondary-tier testing may involve ANAs, cryoglobulins, immunoglobulins, ferritin, and targeted rheumatologic and immunologic tests to help identify a more specific etiology. Additionally, tumor markers and specialized viral and infectious testing—such as DNA and RNA viral profiles, serologies for viral, bacterial, or rickettsial infections, and RPR or VDRL for presumed syphilis—can be utilized. Stool studies can reveal infectious etiologies, and calprotectin or occult blood can suggest inflammatory pathology.

Imaging studies: Chest X-ray, abdominal ultrasound, and/or computed tomography (CT) scans may be necessary to evaluate for pulmonary, abdominal, or pelvic pathology. Plain films can help evaluate bony malignancy or infections, soft tissue calcifications, and bone density. Magnetic resonance imaging (MRI) or positron emission tomography (PET) scans may be helpful in identifying occult infections or tumors. A conscious balance between radiation, costs, risks and benefits should guide imaging studies. A discussion with radiology experts might help direct the imaging study of choice and the need for contrast material.

Invasive procedures: Depending on the clinical presentation and initial workup, invasive procedures such as bone marrow biopsy, lymph node biopsy, or liver biopsy may be necessary to establish a diagnosis.

It is important to note that the evaluation of FUO in children should be individualized based on the patient’s clinical presentation and suspected etiology. A multidisciplinary approach involving infectious disease specialists, hematologists/oncologists, and rheumatologists may be necessary to establish a diagnosis and guide management.

Revisiting Your Patient

In bed 1, the 2-month male infant with fever at home for 1 day with history of maternal fever during delivery underwent a full septic workup due to the risk factors, received a dose of ceftriaxone and was admitted to the hospital for observation for 24 hours, until urine, blood, and CSF cultures were negative.

In bed 2, your 2-month-old female infant with fever at home only underwent a catheterized urine sample that was unremarkable. Because the mom had no good follow-up with a primary care provider, the infant was admitted to the hospital for 24 hours with no antibiotics until the urine culture was negative for 24 hours.

In bed 3, you have a 3-year-old fully vaccinated child who has had fever of up to 38.5◦C every day for the last week—examination with fever, conjunctivitis, and skin peeling.

This child underwent laboratory workups, including inflammatory markers, blood counts, chemistry, and liver function tests. He was admitted to the hospital for consultation with Cardiology and infectious Diseases to consider further evaluation for Kawasaki disease.

Author

Picture of Camilo E. Gutierrez

Camilo E. Gutierrez

Dr. Gutiérrez is an Associate Professor of Pediatrics and Emergency Medicine at George Washington University School of Medicine and Health Sciences, practicing Pediatric Emergency Medicine at Children’s National Hospital in Washington, DC. He is a renowned Pediatric Emergency Physician with extensive experience in clinical care, education, and global health. He leads international initiatives to improve pediatric emergency systems, having served in leadership roles for various global organizations. With over 90 international lectures, 30 publications, and a focus on pediatric trauma, critical care, and ultrasound, he is a key advisor in developing acute care systems worldwide.

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References

  1. Courtney, L., Franklin., Bernie, Carter., David, Taylor-Robinson., E., Carrol. “P09 Understanding the reasons behind paediatric attendances to emergency departments for febrile illness in the UK: A qualitative study.” JECH (2023). doi: 10.1136/jech-2023-.
  2. Jayashree M, Parameswaran N, Nallasamy K, et al. Approach to fever in children. Indian J Med Microbiol. 2024;50:100650. doi:10.1016/j.ijmmb.2024.100650
  3. Rajesh, Kasbekar., Aftab, Naz., Lorenzo, Marcos., Yingjie, Liu., Kristine, Hendrickson., James, C, Gorsich., Matt, Baun. “Threshold for defining fever varies with age, especially in children: A multi-site diagnostic accuracy study..” (2021).:2705-2721.
  4. “The management of fever in children.” Minerva pediatrics, 74 (2022). doi: 10.23736/s2724-5276.22.06680-0.
  5. Luis, Ángel, Bolio, Molina., Gabriela, Toledo, Verónico. “1. New Technique to Verify Permeability and Anorectal Malformations, and Take Rectal Temperature in Neonates And Infants.” (2023). doi: 10.33425/2689-1085.1057.
  6. Mohammed, Baba, Abdulkadir., W, B, Johnson. “6. A comparative study of rectal tympanic and axillary thermometry in febrile children under 5 years of age in Nigeria.” Paediatrics and International Child Health (2013). doi: 10.1179/2046905513Y.00.
  7. Soszyński D. Mechanizmy powstania i znaczenie goraczki [The pathogenesis and the adaptive value of fever]. Postepy Hig Med Dosw. 2003;57(5):531-554.
  8. Norbert, J., Roberts., Juan, C., Sarria. “4. Recognizing the Roles of Fever in Host Survival and in Medical Intervention in Infectious Diseases..” The American Journal of the Medical Sciences, (2024). doi: 10.1016/j.amjms.2024.05.013.
  9. https://www.aap.org/
  10. Tahir, Hameed., Sereen, AlMadani., Walaa, Shahin., Husam, Ardah., Walaa, A, Almaghrabi., Mohammed, Alhabdan., Ahmed, Mohammed, Alfaidi., Asma, Abuthamerah., Mamdouh, Al‐Ahmadi., Majed, Almalki., Mona, Al-Dabbagh. “1. Application of the Pecarn Prediction Rule for Febrile Infants up to 90 Days of Age: A Multi- Center Study. doi: 10.21203/rs.3.rs-4761730/v1.
  11. Natalia, Sutiman., Zi, Xean, Khoo., Gene, Yong-Kwang, Ong., Rupini, Piragasam., Shu-Ling, Chong. “2. Validation and comparison of the PECARN rule, Step-by-Step approach and Lab-score for predicting serious and invasive bacterial infections in young febril. e infants..” Annals Academy of Medicine Singapore (2022). doi: 10.47102/annals-acadmedsg.2022193.
  12. Stacy, Lund., Tine, Brink, Henriksen., Anja, Poulsen., Kia, Hee, Schultz, Dungu., Emma, Louise, Malchau, Carlsen., Bo, Mølholm, Hansen., Lise, Aunsholt., Ulrikka, Nygaard. “1. [Herpes simplex virus infection in newborns]..” Ugeskrift for Læger, 2022.
  13. Pantell RH, Roberts KB, Adams WG, et al. Evaluation and Management of Well-Appearing Febrile Infants 8 to 60 Days Old [published correction appears in Pediatrics. 2021 Nov;148(5):e2021054063. doi: 10.1542/peds.2021-054063]. Pediatrics. 2021;148(2):e2021052228. doi:10.1542/peds.2021-052228
  14. Rajendra, Prasad, Anne., Sourabh, Dutta., Haribalakrishna, Balasubramanian., Ashutosh, N., Aggarwal., Neelima, Chadha., Praveen, Kumar. “2. Meta-analysis of Cerebrospinal Fluid Cell Count and Biochemistry to Diagnose Meningitis in Infants Aged < 90 Days.”. American Journal of Perinatology. (2024), doi: 10.1055/a-2095-6729.
  15. Jamie, M., Pinto., Vaidehi, Patel., Anna, Petrova. “Role of viral pathogen(s) detection in hospital-based management of 29-90-day-old infants with unexplained fever..” MINERVA Pediatrica. (2023). doi: 10.23736/S2724-5276.23.07207-5.
  16. Rachel, G., Greenberg., Tamara, I., Herrera. “4. When to Perform Lumbar Puncture in Infants at Risk for Meningitis in the Neonatal Intensive Care Unit.” (2019). doi: 10.1016/B978-0-323-54391-0.00008-4.
  17. Dana, M., Foradori., Michelle, A., Lopez., Matthew, Hall., Andrea, T., Cruz., Jessica, L., Markham., Jeffrey, D., Colvin., Jennifer, A., Nead., Mary, Ann, Queen., Jean, L., Raphael., Sowdhamini, S., Wallace. “2. Invasive Bacterial Infections in Infants Yo. unger Than 60 Days With Skin and Soft Tissue Infections. Pediatric Emergency Care, doi: 10.1097/PEC.0000000000001584.
  18. Sandra, Trapani., Adele, Fiordelisi., Mariangela, Stinco., Massimo, Resti. “1. Update on Fever of Unknown Origin in Children: Focus on Etiologies and Clinical Approach.” Children (Basel), (2023). doi: 10.3390/children11010020.

Reviewed and Edited By

Picture of Jonathan Liow

Jonathan Liow

Jonathan conducts healthcare research in the Emergency Department at Tan Tock Seng Hospital. A graduate of the University at Buffalo with a BA in Psychology and Communication, he initially worked on breast cancer research studies at GIS A*STAR. His research interests focus on integrating AI into healthcare and adopting a multifaceted approach to patient care. In his free time, Jonathan enjoys photography, astronomy, and exploring nature as he seeks to understand our place in the universe. He is also passionate about sports, particularly badminton and football.

Picture of James Kwan

James Kwan

James Kwan is the Vice Chair of the Finance Committee for IFEM and a Senior Consultant in the Department of Emergency Medicine at Tan Tock Seng Hospital in Singapore. He holds academic appointments at the Lee Kong Chian School of Medicine, Nanyang Technological University, and the Yong Loo Lin School of Medicine, National University of Singapore. Before relocating to Singapore in 2016, James served as the Academic Head of Emergency Medicine and Lead in Assessment at Western Sydney University's School of Medicine in Australia. Passionate about medical education, he has spearheaded curriculum development for undergraduate and postgraduate programs at both national and international levels. His educational interests focus on assessment and entrustable professional activities, while his clinical expertise includes disaster medicine and trauma management.

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
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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.

Listen to the chapter

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.

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Asthma (2024)

~ iEM Education Project Team ~ Leave a comment

by Mohamed Elamin Salama & Ahmed Norain 

Authors
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You have a new patient!

A 40-year-old female with a known case of asthma presents to the emergency department (ED) with complaints of cough, difficulty breathing, chest tightness, and audible wheezing. She has had fever and flu symptoms for three days, which she believes she caught from a colleague at work. She has taken her prescribed home medications with no relief. Her symptoms got worse over the last 2 hours. Her vitals were BP 140/90 mmHg, HR 122 bpm, RR 42 bpm, and SpO2 92% on room air. The physical exam revealed the use of accessory muscles for respiration, expiratory wheezing, and decreased breath sounds with expiratory rhonchi bilaterally. 

a-photo-of-a-40-year-old-female-(image produced by using ideogram2.0)

Nebulized short-acting beta2-agonists (SABA) and systemic corticosteroids were ordered. Peak expiratory flow (PEF) measurements before and after treatment were 125 and 360, respectively. Auscultation after initial treatment revealed much-improved airflow. The patient was discharged following clinical improvement, with a prescription of oral corticosteroids in addition to her current medications.

What do you need to know?

Importance

Asthma is characterized by recurrent symptoms of reversible airway obstruction that range in severity, including bronchial hypersensitivity, hyperresponsiveness, bronchospasm, inflammation, and bronchial hypersensitivity [1,2]. While the exact causes of asthma, a complex chronic disease of the airways, are still not fully understood, researchers continue to study the condition. The high cost of managing and treating asthma is a barrier to effective asthma management. Lack of access, non-compliance with asthma treatment, and excessive reliance on emergency rooms significantly impact asthma morbidity and mortality [1].

Epidemiology

The prevalence of asthma is higher in children than in adults, in women than in men, and in Puerto Ricans and African Americans than in whites or other Hispanics. Adults aged 65 and older have been reported to have the highest death rates, while children 0 to 4 years old have the lowest rates. Asthma deaths were 1.3 times more common in women than in men. The mortality rate from asthma was 2.5–3 times higher among African Americans than among whites [1].

Pathophysiology

Asthma can be divided into allergic and non-allergic based on the presence or absence of immunoglobulin E (IgE) antibodies to common environmental antigens (pollen, dander, mites) and microbiologic antigens (bacteria, viruses). The presence of airway T-helper cells, which release cytokines like interleukin [IL]-4, IL-5, and IL-13 to promote basophil, eosinophil, mast cell, and leukocyte migration to the airways and increase IgE production, is a characteristic of all types of asthma. The outcome is an exacerbation of the inflammatory response in the airways and, over time, irreversible remodeling of the airways. Clinical manifestations of these intricate cellular interactions include bronchospasm, mucus production, airway edema, and airflow restriction [1].

Medical History

Initial history inquiries should include potential triggers, symptom onset, and severity, particularly compared to prior exacerbations. Physicians should also identify comorbidities, particularly those that might be worsened by systemic corticosteroids, like diabetes, peptic ulcer disease, hypertension, and psychosis. All current asthma medications and the times and dosages taken recently should be highlighted. Moreover, any potential asthma aggravators, such as aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs), beta-blockers (including topical agents used for glaucoma), and angiotensin-converting enzyme inhibitors, should also be noted. The use of beta-blockers, both cardioselective and nonselective, increases emergency room visits and hospitalizations. There is a variance in dyspnoea perception among asthmatics with the same degree of airway narrowing. Patients with poor perceptions of their dyspnoea are more likely to require emergency room visits and hospital stays and experience near-fatal and fatal asthma attacks [1].

Physical Examination

Asthma is characterized by classical symptoms such as cough, shortness of breath, and wheezing. Additional clinical features often observed in asthma patients include tachypnea, tachycardia, chest tightness, and cyanosis. In more severe cases, patients may present with the use of accessory muscles for breathing, a “silent chest” (indicative of minimal airflow), altered level of consciousness, or even collapse, highlighting the potential severity of this respiratory condition.

The physical examination findings and some bedside test results for asthma patients vary depending on the severity of the acute asthma attack [3].

For moderate asthma, patients may exhibit increasing symptoms with a peak expiratory flow (PEF) of 50–75% of the predicted value, but they show no physical signs of acute severe asthma.

In acute severe asthma, physical examination may reveal a PEF of 33–50% of the predicted value, a respiratory rate ≥25 breaths per minute, a heart rate ≥110 beats per minute, and an inability to complete sentences in one breath due to shortness of breath.

For life-threatening asthma, physical findings can include altered consciousness, exhaustion, cyanosis (bluish discoloration of the skin), a silent chest (indicative of critically reduced airflow), arrhythmias, and hypotension. Measurements include a PEF of less than 33% of the predicted value, oxygen saturation (SpO₂) below 92%, and normal arterial partial pressure of carbon dioxide (PaCO₂) between 4.6–6.0 kPa, despite the severity of the attack.

In the case of near-fatal asthma, the physical exam may demonstrate poor respiratory effort, and the condition is characterized by elevated PaCO₂ levels or the need for mechanical ventilation with raised inflation pressures, reflecting a critically severe respiratory compromise.

These findings collectively aid in categorizing the severity of asthma attacks and guiding appropriate management.

Alternative Diagnoses

When treating acutely breathless patients, it is imperative to consider aetiologies other than asthma. The differential diagnoses include pneumonia, COPD exacerbation, upper airway obstruction, foreign body aspiration, pulmonary embolism, congestive heart failure, allergic anaphylactic reaction, and gastroesophageal reflux disease. Any of these diagnoses can present concurrently with asthma [1,3].

Acing Diagnostic Testing

In the evaluation and management of acute asthma exacerbations, several diagnostic tools can aid in assessing the severity of the condition and guiding treatment decisions:

Peak Expiratory Flow Rate (PEFR)

Peak Expiratory Flow Rate (PEFR) should be measured in all asthma patients presenting with acute exacerbations as it provides an objective assessment of airway obstruction severity. If a patient is unable to perform the PEFR test, this inability is a critical indicator of severe airway obstruction and necessitates urgent management. PEFR is most valuable when compared to the patient’s previous personal best measurement, as it reflects their baseline respiratory function. In cases where the personal best measurement is unavailable, the predicted PEFR percentage, calculated based on the patient’s age, sex, and height, serves as a practical alternative to estimate the severity of the airway obstruction. Regular monitoring of PEFR can assist in early detection of exacerbations and guide treatment adjustments.

Pulse Oximetry

This non-invasive method is crucial for determining the effectiveness of oxygen supplementation, especially in children or other patients unable to perform PEFR. The target SpO₂ is 94%-98%, with levels below 90% signaling the need for more aggressive therapy.

Capnography

Capnography is valuable for monitoring hypercapnia and respiratory failure in asthma patients. Waveform capnography provides continuous monitoring, showing changes in airway diameter and improvements during acute asthma management.

Blood Gas Analysis

Routine arterial blood gas (ABG) analysis is not typically indicated in acute asthma exacerbations. However, ABG testing should be considered when SpO₂ is below 92% or when PEFR is less than 50% of the patient’s personal best or predicted value, to identify hypercapnia and guide critical care.

Other blood testing

Routine blood testing is not recommended for acute asthma exacerbations. However, in older patients with cardiovascular comorbidities, B-type natriuretic peptide (BNP) levels may be useful to detect unrecognized congestive heart failure.

A chest radiograph (CXR)

Although not routinely required, a chest X-ray may be warranted in cases of suspected complications such as pneumonia, pneumothorax, pneumomediastinum, subcutaneous emphysema, or congestive heart failure.

Electrocardiogram (ECG)

ECG is helpful for assessing patients with chest pain or cardiovascular disease, where the asthma exacerbation may act as a physiologic stressor. In severe asthma, ECG may show a reversible right ventricular strain pattern. Continuous cardiac monitoring is advised for patients with severe hypoxemia.

Point of care ultrasound (POCUS)

Increasingly used in emergency settings, POCUS aids in diagnosing complications like pneumothorax and heart failure in patients with acute dyspnea, offering rapid, bedside insights [4].

Risk Stratification

There are several risk stratification tools for asthma, particularly for the pediatric population. MDCalc offers various tools to evaluate asthma severity and predict future exacerbations. One such tool is the PEFR (Peak Expiratory Flow Rate) estimator, which provides expected PEFR values based on the patient’s age, height, and ethnicity. Additionally, this tool allows clinicians to input the patient’s measured PEFR and offers management suggestions tailored to the patient’s condition. These tools, among others, can assist physicians in managing asthma patients more effectively.

However, in time-sensitive situations, there may not be enough time to use such tools, requiring immediate recognition of risk factors for death from asthma [1,5], which include:

  • History of sudden severe exacerbations
  • Prior intubation for asthma
  • Prior asthma admission to an intensive care unit (ICU)
  • Two or more hospitalizations for asthma in the past year
  • Three or more emergency department (ED) care visits for asthma in the past year
  • Hospitalization or an ED care visit for asthma within the past month
  • Use of more than two MDI short-acting beta-2 agonist canisters per month
  • Current use of or recent withdrawal from systemic corticosteroids
  • Difficulty perceiving severity of airflow obstruction.
  • Comorbidities such as cardiovascular diseases or other systemic problems
  • Serious psychiatric disease or psychosocial problems
  • Illicit drug use, especially inhaled cocaine, and heroin

Management

Effective management of acute asthma exacerbations involves a combination of pharmacological and non-pharmacological interventions tailored to the severity of the patient’s condition. Below is a detailed explanation of these management strategies:

Oxygen Therapy

Oxygen supplementation should be provided to all hypoxemic patients to maintain oxygen saturation (SpO₂) within the target range of 94%-98%. Adequate oxygenation is critical for preventing further respiratory compromise.

Beta-2 Agonist Bronchodilators

Short-acting beta-2 agonists, such as albuterol, are first-line agents for treating acute asthma attacks and should be initiated promptly. Albuterol can be administered via nebulization at a dose of 2.5–5 mg or with a metered-dose inhaler (MDI) delivering 6–12 puffs. The use of an MDI with a spacer provides comparable benefits to nebulization in both adults and children in emergency settings [6]. For patients who cannot use inhaled therapy effectively, intravenous (IV) or subcutaneous beta-2 agonists may be considered, although evidence supporting their use in ventilated or critically ill patients remains limited.

Anticholinergic Agents

Anticholinergic medications, such as ipratropium, are less potent than beta-2 agonists and have a slower onset of action, so they should not be used alone for acute attacks. However, combining a short-acting beta-agonist (SABA) with ipratropium is particularly beneficial in moderate to severe exacerbations, reducing hospitalizations and improving peak expiratory flow rates (PEFR). The initial adult dose of ipratropium is 250–500 mcg.

Corticosteroids

Corticosteroids are essential in the early management of acute asthma exacerbations. Both oral and intravenous (IV) corticosteroids are equally effective, with no additional benefit from adding inhaled corticosteroids to systemic therapy. The recommended oral dose is 50 mg of prednisone, while IV therapy typically involves 125 mg/day of methylprednisolone in one or two divided doses.

Magnesium

Magnesium sulfate is a bronchodilator that relaxes bronchial smooth muscles, making it particularly useful in severe asthma attacks. It is recommended for adults with PEFR <25% of the predicted value, adults and children with persistent hypoxia after initial treatment, and children with PEFR <60% after one hour of care. Magnesium has been shown to reduce hospital admission rates in these patients.

Epinephrine

For asthma patients with concurrent angioedema or anaphylaxis, epinephrine should be administered intramuscularly at a dose of 0.3 mg. This is an adjunct to standard asthma therapies.

Heliox (Helium-Oxygen Therapy)

Heliox reduces airway resistance and enhances the bronchodilatory effects of albuterol [7]. It also reduces respiratory muscle workload and improves ventilation by facilitating carbon dioxide diffusion. Heliox may be considered in severe airflow obstruction (PEFR <30% predicted), rapid onset of symptoms within 24 hours, a history of labile asthma or prior intubation, or in cases where mechanical ventilation is inadequate.

Ketamine

Ketamine, an IV dissociative agent with bronchodilatory properties, is a valuable adjunctive therapy in refractory status asthmaticus when standard treatments are insufficient [8].

High-Flow Nasal Cannula (HFNC)

HFNC delivers high concentrations of oxygen, reduces work of breathing, and provides continuous positive airway pressure. While its role in adults with asthma is not well-defined, small studies suggest it may alleviate respiratory distress in children.

Non-Invasive Ventilation (NIV)

NIV may benefit select patients with severe and resistant asthma. However, it is not a substitute for endotracheal intubation and mechanical ventilation when these are indicated.

Intubation and Mechanical Ventilation

Approximately 2% of all asthma exacerbations, and 10%-30% of cases requiring ICU admission, necessitate intubation. Indications for intubation include altered consciousness, coma, respiratory or cardiac arrest, paradoxical breathing patterns, refractory hypoxemia, and failure of NIV.

Extracorporeal Membrane Oxygenation (ECMO)

In patients with asthma refractory to conventional ventilator management, ECMO may be considered as a last resort to provide oxygenation and ventilation support.

These therapeutic approaches, used in a stepwise manner based on severity, help optimize outcomes for patients experiencing acute asthma exacerbations. Early intervention, combined with evidence-based management, remains critical in preventing complications and reducing mortality.

Special Patient Groups

Pediatrics

For pediatric patients, the recommended initial dose of albuterol is 0.15 mg/kg/dose (0.03 mL/kg/dose), with a maximum dose of 5 mg via nebulization. Alternatively, administering 4–12 puffs of a short-acting beta-agonist (SABA) via a metered-dose inhaler (MDI) with a spacer provides equivalent bronchodilation compared to nebulized therapy. The initial dose of ipratropium bromide depends on the child’s weight: 250 micrograms for children weighing less than 20 kg and 500 micrograms for those over 20 kg.

In terms of corticosteroids, dexamethasone is an effective alternative to prednisone for managing acute asthma in the emergency department, offering comparable efficacy with fewer doses, less vomiting, and improved compliance. For moderately to severely ill children, continuous nebulized albuterol, corticosteroids, magnesium sulfate, and parenteral SABAs form the cornerstone of management.

Admission to the Pediatric Intensive Care Unit (PICU) is indicated for children with continued severe respiratory distress, altered mental status, or the need for advanced interventions such as intravenous SABAs, non-invasive ventilation (e.g., BiPAP), or mechanical ventilation.

Geriatrics

In elderly patients, asthma symptoms may go unreported as they may attribute their shortness of breath to aging, obesity, or comorbid cardiovascular conditions. It is essential for physicians to inquire about all home medications, including eye drops, and carefully consider potential drug interactions to avoid complications.

Pregnancy and Breastfeeding

Asthma exacerbations during pregnancy should be treated in the same manner as in nonpregnant patients. There are no contraindications to using any asthma medication in breastfeeding patients, making treatment decisions more straightforward and ensuring both maternal and infant safety.

When To Admit This Patient

Relapse rates among asthmatic patients discharged from the emergency department (ED) vary significantly, ranging from 11% within 3 days to 45% at 8 weeks.

The Emergency Department Disposition Decision-Making Guidelines assist in determining the appropriate care site for asthmatic patients based on their peak expiratory flow (PEF) percentages and response to treatment [1]. Below are the key details for each category:

Good Response

  • PEF (% predicted/personal best): Approximately 60% or higher.
  • Disposition Site: Patients with a good response are typically discharged home. Hospitalization is not necessary.

Incomplete Response

  • PEF (% predicted/personal best): Between 40% and 60%.
  • Disposition Site: The decision to send patients home or hospitalize them depends on the presence of risk factors outlined in Box 1. A careful evaluation is required to decide the appropriate course of action.

Poor Response

  • PEF (% predicted/personal best): Less than 40%.
  • Disposition Site: Patients in this category are not discharged home and require continued therapy in the emergency department. Hospitalization is necessary if the facility is available and appropriate.

Additional Factors Increasing the Likelihood of Admission

  • Female sex, older age, and non-white race.
  • Use of more than 8 beta-agonist puffs in the past 24 hours.
  • Severity of exacerbation, such as the need for rapid medical intervention upon arrival, respiratory rate >22, oxygen saturation <95%, and final PEF <50% predicted.
  • Past history of intubations or asthma-related hospital admissions.
  • Previous use of oral corticosteroids (OCS).
    These guidelines ensure that patients receive care tailored to the severity of their asthma exacerbation and associated risk factors.

The risk factors for death from asthma can be categorized into asthma history and other factors [1]:

Asthma History:

  • A history of near-fatal asthma that required intubation and mechanical ventilation.
  • Hospitalization or emergency department (ED) visits for asthma in the past year.
  • Current or recent use of oral corticosteroids, which is a marker of event severity.
  • Not currently using inhaled corticosteroids.
  • Overuse of short-acting beta-agonists (SABAs), particularly using more than one canister per month.
  • Poor adherence to asthma medications or a lack of adherence to a written asthma action plan.

Other Factors:

  • Presence of psychosocial problems.
  • Psychiatric diseases.
  • Food allergies in individuals with asthma.

Revisiting Your Patient

The patient in the case presentation is a 40-year-old female with known asthma. She presented with asthma exacerbation due to upper respiratory tract infection with sick contact at work. In the history, asking for any other potential triggers of an acute exacerbation, including potential allergen, onset of symptoms, and severity, is useful. Physical examination should focus on signs that help categorize the disease’s severity and guide a management plan. Like any other emergency, initial evaluation and management should highlight the “ABCDs” assessment (Airway, Breathing, Circulation, and Disability), along with imitation of the appropriate and time-sensitive diagnostic and therapeutic interventions (in our case, initiation of SABA and systemic steroids).
Additionally, Peak Expiratory Flow Rate (PEFR) should be performed for all asthmatics presenting with acute exacerbation who can perform the test. Patients who are unable to perform the test should be considered to have severe airway obstruction. If the patient is fit for discharge, prescription medications and appropriate follow-up appointments should be initiated, with strict return precautions to the emergency department as needed.

Authors

Picture of Mohamed Elamin Salama

Mohamed Elamin Salama

Dr. Salama is currently a Specialty Registrar in Emergency Medicine at the Thames Valley Deanery, Oxford School of Emergency Medicine. He completed his emergency medicine training at Zayed Military Hospital and has obtained both the Arab and Emirati Board certifications in Emergency Medicine. Dr. Salama is dedicated to advancing his clinical practice and actively sharing the most current developments in medical knowledge. His professional interests encompass trauma, resuscitation, sports medicine, and the promotion of public health initiatives.

Picture of Ahmed Norain

Ahmed Norain

Emergency Department, Zayed Military Hospital, Abu Dhabi

Listen to the chapter

References

  1. Walls RM, Hockberger RS, Gausche-Hill M, Erickson TB, Wilcox SR. Rosen’s Emergency Medicine: Concepts and Clinical Practice, 10th edition. Elsevier; 2023.
  2. Gary T Kitching, Jason B Lee. Asthma in Adults. RCEMLearning. Accessed March 8, 2023. https://www.rcemlearning.co.uk/reference/asthma-in-adults/#1568193285479-ef3b01a0-b2ab
  3. Global Initiative for Asthma. GLOBAL STRATEGY for ASTHMA MANAGEMENT and PREVENTION Updated 2022.; 2022. https://ginasthma.org/wp-content/uploads/2022/07/GINA-Main-Report-2022-FINAL-22-07-01-WMS.pdf
  4. Zanobetti M, Scorpiniti M, Gigli C, et al. Point-of-Care Ultrasonography for Evaluation of Acute Dyspnea in the ED. Chest. 2017;151(6):1295-1301. doi:10.1016/j.chest.2017.02.003
  5. D’Amato G, Vitale C, Molino A, et al. Asthma-related deaths. Multidiscip Respir Med. 2016;11:37. Published 2016 Oct 12. doi:10.1186/s40248-016-0073-0
  6. Krylov V, Greuel J. Are bronchodilator nebulizers superior to MDIs for the treatment of acute asthma exacerbations? Evidence-Based Practice. 2018;21(6):3. doi:https://doi.org/10.1097/01.EBP.0000545148.85715.aa
  7. Kress JP, Noth I, Gehlbach BK, et al. The utility of albuterol nebulized with heliox during acute asthma exacerbations. Am J Respir Crit Care Med. 2002;165(9):1317-1321. doi:10.1164/rccm.9907035
  8. Ueoka m, antonette subia g, lai hipp c, tawata w, chung-esaki h. Ketamine infusion for refractory status asthmaticus: a case series. Chest. 2021;160(4):a5. doi:https://doi.org/10.1016/j.chest.2021.07.062

Additional 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, 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 asthma content on iem-student.org

Clinical Decision Rules (2024)

~ iEM Education Project Team ~ Leave a comment

by Stacey Chamberlain

Authors
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Definitions and Overview

Clinical Decision Rules (CDRs), also known as Decision “Instruments” or “Aids,” are evidence-based tools to assist the practitioner in decision-making for common complaints. In the Emergency Department (ED) setting, these decision aids are often used to help identify patients who might be at higher risk for serious conditions such as pulmonary embolism (PE) or intracranial hemorrhage (ICH), or they are used to prevent overuse of unnecessary testing, which is how many of the orthopedic rules are applied. 

CDRs, despite being called “Rules,” are not meant to replace critical thinking from experienced practitioners. In fact, many CDRs have been directly compared against clinician gestalt or clinical practice, and they are not always better [1,2]. Additionally, some rules incorporate clinician gestalt, whereas the rule cannot even be applied unless the pre-test probability (based on the physician’s judgment of the likelihood of the disease) is below a pre-determined threshold [3]. Also, for a CDR to be useful to a practitioner, it must be practical. If a CDR is developed that has too many complicated variables, it is unlikely to be applied in a busy clinical environment  [4].

Another caveat to the application of CDRs is that they must be applied appropriately.  CDRs evolve through a process of derivation to validation to impact analysis of the tool. After the tool is derived (level 4 evidence), the tool is validated in a limited patient setting (level 3 evidence), then a broader validation setting (level 2 evidence), and finally, the impact of the tool is assessed (level 1 evidence) [5]. These levels are important to caution the novice learner against applying every CDR which has been derived and published automatically into their clinical practice. The tool must be validated in a patient population with similar characteristics to the practitioner’s patient population. For example, the tool may not perform the same (have the same sensitivity and specificity) if the prevalence of disease is different between the study and actual patient populations. Also, the practitioner must be familiar with a particular tool’s inclusion and exclusion criteria. If not, the tool could be misused. For example, if the tool was derived and validated for a patient population over the age of 18, it should not be inappropriately applied in a pediatric setting.

The practitioner must also understand the purpose of the CDR and whether it is a one-way or two-way rule. As noted by Green, for example, the Ottawa Ankle Rules are intended to be a two-way rule; if the patient meets the criteria, you do an X-ray; if they don’t meet the criteria, you do not do an X-ray [6]. There are two paths you can take after you apply your CDR. Alternatively, the pulmonary embolism rule-out criteria (PERC) demonstrate a one-way rule. This tool was developed to identify a subset of patients at very low risk for PE so that no further testing is needed. If the patient is “PERC positive,” this should not imply that further testing for PE, such as a D-dimer or CT angiogram of the chest, should be done. Whether or not additional testing should be done remains up to the practitioner and depends on many variables, including whether an alternate diagnosis is much more likely. PERC was designed to help “rule out” the diagnosis of PE, not “rule in.” This rule only guides you down one path: potentially, to do no testing; it makes no judgment as to what you should do if the patient is “PERC positive.”

In addition to CDRs, many risk stratification tools or scales have been used for serious conditions such as pulmonary embolism (PE) and acute coronary syndrome (ACS). Others have more recently been developed for use in the ED setting for common conditions such as congestive heart failure (CHF), chronic obstructive pulmonary disease (COPD), and transient ischemic attack (TIA) to identify patients at higher risk for acute severe complications [7]. From a practical perspective, the ED physician will often use these risk stratification devices to help determine which patients require admission. However, these tools are less prescriptive in that they are not rules that suggest what a practitioner should or should not do, but rather, they help the physician more objectively look at the risk for an individual patient. Then the practitioner must decide what level of risk they are comfortable with in regards to inpatient or outpatient management, which may greatly depend on the resources available in those environments. Most of the risk stratification tools encompass multiple variables with more complicated scoring systems; as they are not easily memorized, most of these would typically be used by ED physicians with real-time access to a computer or smartphone with appropriate apps.

Given the many pitfalls noted above of CDRs, the goals of using evidence-based medicine to reduce practice variability, maximize cost-effective use of resources, and help identify and diagnose high-risk conditions are important.  It is equally important that the ED physician critically appraise these tools and selectively apply them in appropriate ways [8]. The remainder of this chapter will use case scenarios to review the most commonly used CDRs in the ED setting.

The useful FOAM reference MDCalc.com provides a summary of the most common tools that are being used with easy-to-use online calculators and additional information on inclusion and exclusion criteria, evidence basis for the tools, as well as pearls and pitfalls for each tool.

Orthopedic CDRs

Ottawa Knee, Ankle and Foot Rules

Case 1

A 28-year-old man presents to the ED with left ankle pain after twisting his ankle while playing basketball.  He is able to bear weight and notes pain and swelling to the lateral aspect of the ankle (he points to just below the lateral malleolus).  He denies weakness, numbness, or tingling and has no other injuries.  On exam, he is neurovascularly intact.  Edema and tenderness are noted slightly anterior and inferior to the lateral malleolus.  There is no point tenderness to the distal posterior malleoli bilaterally.

Should you obtain an X-ray to check for a fracture?

Ankle sprain - Image was created by ideogram 2.0

Ottawa Ankle Rule

Pain in the malleolar zone and any one of the following:

  • Bone tenderness along the distal 6 cm of the posterior edge or tip of the tibia (medial malleolus), OR
  • Bone tenderness along the distal 6 cm of the posterior edge or tip of the fibula (lateral malleolus), OR
  • An inability to bear weight immediately and in the emergency department for four steps.
Tenderness over posterior tibial malleolus (image generated by using virtual human body and Canva)
Tenderness on posterior or tip of the lateral malleolus (image generated by using virtual human body app and Canva).

Ottawa Foot Rule

Pain in the midfoot zone and any one of the following:

  • Bone tenderness at the base of the fifth metatarsal, OR
  • Bone tenderness at the navicular bone, OR
  • An inability to bear weight immediately and in the emergency department for four steps.
Tenderness at the base of the fifth metatarsal OR navicular bone (image generated by using virtual human body app and Canva).

Ottawa Knee Rule

Knee injury with any of the following:

  • Age 55 years or older
  • Tenderness at the head of the fibula
  • Isolated tenderness of the patella
  • Inability to flex to 90°
  • Inability to bear weight both immediately and in the emergency department (4 steps)
Tenderness at the patellar OR head of the fibula (image generated by using virtual human body app and Canva).

The Ottawa knee, ankle, and foot rules are some of the longest-standing and most widely accepted CDRs. These rules help practitioners identify patients with an extremely low risk of fracture such that X-rays do not need to be done, thus limiting the risks and costs of unnecessary testing. The sensitivity of these rules has been found to be 98.5-100% [9-11]. In impact study of the Ottawa knee rule, application of the rule decreased the use of knee radiography without patient dissatisfaction or missed fractures and was associated with reduced waiting times and costs. These rules have also been validated in pediatric populations with similar sensitivities (98.5-100%) [12-14].

Case 1 Discussion

Base on the Ottawa ankle rule, an X-ray is unnecessary. The patient can be treated supportively for an ankle sprain. When it comes to treating an ankle sprain, supportive care is typically the most effective approach. This involves several key strategies aimed at reducing pain and promoting healing. First and foremost, it’s important to follow the R.I.C.E. method:  

  1. Rest: Avoid putting weight on the injured ankle to prevent further damage. This might mean using crutches or a brace, especially in the initial days after the injury.
  2. Ice: Applying ice packs to the ankle for 15-20 minutes every couple of hours can help reduce swelling and numb the pain. It’s crucial to wrap the ice pack in a cloth to protect the skin.
  3. Compression: Using an elastic bandage or compression wrap around the ankle can help minimize swelling and provide support. It’s essential not to wrap it too tightly, as this could impede circulation.
  4. Elevation: Keeping the ankle raised above the level of the heart can also help reduce swelling and improve blood flow to the area, speeding up the healing process.

In addition to the R.I.C.E. method, over-the-counter pain relievers like ibuprofen or acetaminophen can be used to manage pain and inflammation. Gradually reintroducing movement and gentle stretching exercises can aid in restoring strength and flexibility, but this should be done cautiously and ideally under the guidance of a healthcare professional. Physical therapy may also be beneficial in some cases, especially if the sprain was severe or if there are concerns about stability in the ankle after healing. A physical therapist can provide tailored exercises and techniques to regain strength and prevent future injuries. Overall, the goal of supportive treatment for an ankle sprain is to promote recovery while alleviating pain, allowing the patient to return to their normal activities as safely and quickly as possible.

Trauma CDRs

Canadian Cervical Spine and NEXUS Rules

Case 2

A 57-year-old man fell from a height of 12 feet while on a ladder. He did not pass out; he reports losing his footing. He fell onto a grassy area, hitting his head, and complains of neck pain. He did not lose consciousness and denies headache, blurry vision, vomiting, weakness, numbness or tingling in any extremities. He denies other injuries. He was able to get up and ambulate after the fall and came in by private vehicle. He has not had previous spine surgery and does not have known vertebral disease. On exam, he is neurologically intact with a GCS of 15, does not appear intoxicated, and has moderate midline cervical spine tenderness.

Should you obtain imaging to rule out a cervical spine fracture?

a-photo-of-a-57-year-old-male-who-fell-from-a-ladder (image generated by ideogram2.0)

Canadian C-spine Rule

  • Age ≥ 65
  • Extremity paresthesias
  • Dangerous mechanism (fall from ≥ 3ft / 5 stairs, axial load injury, high-speed MVC/rollover/ejection, bicycle collision, motorized recreational vehicle)

NEXUS Criteria for C-spine Imaging

  • Focal neurologic deficit
  • Midline spinal tenderness
  • Altered level of consciousness
  • Intoxication
  • Distracting injury

Case 2 Discussion

Applying either criteria to this case would require C-spine imaging, as by CCR, the patient would meet the criteria for dangerous mechanism, and by NEXUS, the patient has midline tenderness to palpation.

Canadian CT Head Rule and NEXUS Head CT Instrument

Case 3

A 36-year-old woman slipped on ice and fell and hit her head. She reports loss of consciousness for a minute after the event, witnessed by a bystander. She denies having headaches. She denies weakness, numbness, or tingling in her extremities and no changes in vision or speech. She has not vomited. She remembers the event except for the transient loss of consciousness. She doesn’t use any blood thinners or have any known coagulopathy. On physical exam, she has a GCS of 15, no palpable skull fracture or scalp hematoma, no signs of a basilar skull fracture, normal mentation, and no neurologic deficits.

Should you obtain a CT head for this patient to rule out a clinically significant brain injury?

a-photo2-of-a-36-year-old-woman-who-slipped-on-ice-(image generated by ideogram2.0)

Canadian CT Head Rule

High Risk Criteria (rules out need for neurosurgical intervention)

  • GCS < 15 at two hours post-injury
  • Suspected open or depressed skull fracture
  • Any sign of basilar skull fracture (hemotypanum, Raccoon eyes, Battle’s sign, CSF oto or rhinorrhea)

Medium Risk Criteria (rules out clinically important brain injury)

  • Retrograde amnesia to event  ≥ 30 minutes
  • Dangerous mechanism (pedestrian struck by motor vehicle, ejection from motor vehicle, fall from > 3 feet or > 5 stairs)

NEXUS Head CT Instrument

  • Evidence of significant skull fracture
  • Scalp hematoma
  • Neurologic deficit
  • Altered level of alertness
  • Abnormal behavior
  • Coagulopathy
  • Persistent vomiting
  • Age ≥65 years

The Canadian CT Head Rule (CCHR) only applies to patients with an initial GCS of 13-15, witnessed loss of consciousness (LOC), amnesia to the head injury event, or confusion [18]. The study was only for patients > 16 years of age. Patients were excluded from the study if they had “minor head injuries” that didn’t even meet these criteria. Patients were also excluded if they had signs or symptoms of moderate or severe head injury, including GCS < 13, post-traumatic seizure, focal neurologic deficits, or coagulopathy. The CCHR was designed to identify clinically important injuries and injuries requiring neurosurgical intervention. A potential limitation of its use could be if one works in a practice environment where the standard of care is to identify all intracranial injuries versus only those that require acute intervention.

The NEXUS Head CT Instrument was developed and validated more recently to address some of the limitations of rules, including the CCHR, where the inclusion and exclusion criteria may preclude its application in over one-third of blunt head injury cases, as well as other rules that focused only on pediatric populations such as PECARN [19-22]. The NEXUS Instrument is a one-way decision instrument for patients of all ages to identify low-risk patients who do not require CT imaging. The developers of the tool acknowledge that although its sensitivity is 100%, it is no better than the equal 100% sensitivity of clinical judgment [23]. Therefore, the benefit of its use is limited to “ruling out” significant intracranial injuries and reducing unnecessary testing. The developers also highlight that the use of CT imaging provides little information on concussions and post-concussive syndromes and that negative imaging does not preclude concussive injuries that can result in long-term brain injury and impairment.

Case 3 Discussion

By applying both rules to the above case, the patient does not require imaging despite her transient loss of consciousness after the injury.

PECARN Pediatric Head Trauma Algorithm

Case 4

A 20-month-old female was going up some wooden stairs, slipped and fell down four stairs, and hit the back of her head on the wooden landing at the bottom of the stairs. She did not lose consciousness and cried immediately. According to her parents, she was consolable after a few minutes and acted normally. She has not vomited. On exam, she is well-appearing, alert, and has a normal neurologic exam. She is noted to have a left parietal hematoma measuring approximately 4×4 cm.

Should you obtain CT imaging of this child to rule out clinically significant head injury?

a-photo-of-a-20-month-old-female-child-(image generated by ideogram2.0)

PECARN Pediatric Head Trauma Algorithm

Age < 2
  • GCS < 15, palpable skull fracture, or signs of altered mental status
  • Occipital, parietal or temporal scalp hematoma; History of LOC≥5 sec; Not acting normally per parent or Severe Mechanism of Injury?
Age ≥ 2
  • GCS < 15, palpable skull fracture, or signs of altered mental status
  • History of LOC or history of vomiting or Severe headache or Severe Mechanism of Injury?

The PECARN (Pediatric Emergency Care Applied Research Network) Pediatric Head Trauma Algorithm was developed as a CDR to minimize unnecessary radiation exposure to young children. The estimated risk of lethal malignancy from a single head CT in a 1-year-old is 1 in 1000-1500 and decreases to 1 in 5000 in a 10-year-old [24]. Due to these risks, in addition to costs, length of stay and potential risks of procedural sedation, this CDR is widely employed given the frequency of pediatric head trauma ED visits. This CDR uses a prediction tree to assess risk, and unlike some other risk stratification tools, the PECARN group provides recommendations based on their definitions of acceptable risk levels. In the less than 2-year-old group, the rule was found to be 100% sensitive, with sensitivities ranging from 96.8%-100% sensitive in the greater than 2-year-old group [25,26].

This algorithm does have some complexity and ambiguity. It requires the practitioner to know what were considered signs of altered mental status and what were considered severe mechanisms of injury. In addition, certain paths of the decision tree lead to intermediate risk zones. In these cases, the recommendation is “observation versus CT,” allowing the ED physician to base their decision to image or not on numerous contributory factors, including physician experience, multiple versus isolated findings, and parental preference, among others.

Other pediatric head trauma CDRs have been derived and validated; however, in comparison trials, PECARN performed better than the other CDRs [1]. Of note, in this study, physician practice (without using a specific CDR) performed as well as PECARN with only slightly lower specificity.

Case 4 Discussion

The patient falls into an intermediate risk zone of clinically important brain injury. However, a sub-analysis of patients less than two years old with isolated scalp hematomas suggests that patients were at higher risk if they were < 3 months of age, had non-frontal scalp hematomas, large scalp hematomas (> 3cm), and had severe mechanism of injury [27]. Given the large hematoma in the case study patient and a severe mechanism of injury (a fall of > 3 feet in the under 2 yo age group), one should consider imaging due to these two additional higher risk factors.

PECARN Abdominal Trauma

  • Evidence of abdominal wall trauma/seatbelt sign or GCS < 14 with blunt abdominal trauma (if no, go to next point) – 5.4% risk of needing intra-abdominal injury intervention
  • Abdominal tenderness (if no, go to next point) – 1.4 % risk of intra-abdominal injury intervention
  • Thoracic wall trauma, complaints of abdominal pain, decreased breath sounds, vomiting – 0.7% risk of intra-abdominal injury intervention

The PECARN group has also developed a CDR, which was externally validated for pediatric blunt abdominal trauma [28,29]. This CDR uses a seven-point decision rule. If the patient does not have any of these findings, the patient would be considered “very low risk,” with a 0.1% risk of intra-abdominal injury intervention required. A study compared the PECARN CDR versus clinical suspicion and found that the CDR had significantly higher sensitivity (97.0% vs. 82.8% but lower specificity (42.5% vs. 78.7%) [30]. However, abdominal CTs were done in 33% of patients with clinical suspicion < 1%, meaning that even though clinical suspicion had higher specificity, this often did not translate into clinical practice. A recent external validation study supported the use of the CDR in decreasing CT use in pediatric patients at very low risk for clinically important intra-abdominal injuries [29].

NEXUS Chest Decision Instrument for Blunt Chest Trauma

NEXUS Chest was derived and validated for blunt chest trauma patients to identify very low-risk patients that do not require imaging [31,32].  It was developed only to rule out injury, not ruling it in. In other words, finding one or more NEXUS Chest criteria does not mean you must image that patient. The CDR creators suggest using NEXUS Chest only in patients for whom imaging was planned, then apply NEXUS Chest to determine whether one can safely forego imaging.

Pulmonary CDRs

Case 5

A 19-year-old female presents with sharp right flank pain and shortness of breath, which started suddenly the day before arrival. The pain is worse with deep inspiration but not related to exertion and not relieved with ibuprofen. She denies anterior chest pain, cough, and fever. She denies leg pain or swelling and recent travel, immobilization, trauma, or surgery. She has no anterior abdominal pain, no dysuria or hematuria, and no personal or family history of gallstones, kidney stones, or blood clots. She’s never had this pain before, has no significant past medical history, and her only medication is birth control pills. On exam, her vital signs are within normal range; she has normal cardiac and pulmonary exams, no costo-vertebral angle tenderness, no chest wall or abdominal tenderness, and no leg swelling.

Do you need to do any studies to evaluate this patient for a pulmonary embolism?

a-photo-of-a-19-year-old-female-patient-(image generated by ideogram2.0)

Pulmonary Embolism Rule-Out Criteria (PERC)

  • Age ≥ 50
  • Heart rate ≥ 100
  • O2 sat on room air < 95%
  • Prior history of venous thromboembolism
  • Trauma or surgery within 4 weeks
  • Hemoptysis
  • Exogenous estrogen
  • Unilateral leg swelling

The PERC CDR was originally derived and validated in 2004 and with a subsequent multi-study center validation in 2008 [33,34]. In the larger validation study, the rule was only applied in those patients with a pre-test probability of < 15%, therefore incorporating clinical gestalt before using the rule. As mentioned above, PERC is a one-way rule that tries to identify patients with low risk for pulmonary embolism (PE) so as not to require any testing. It does not imply that testing should be done for patients who do not meet criteria, and it is not meant for risk stratification, as opposed to the Wells and Geneva scores.

Case 5 Discussion

To apply the PERC CDR to the case, the ED physician pre-supposes a pre-test probability of < 15%. If the ED physician has a higher pre-test probability than that, the physician should not use the PERC CDR. If the ED physician in this case did indeed have a pre-test probability of < 15%, the case study patient would fail the rule-out due to her use of oral contraceptives. In that case, the ED physician would need to determine if he/she would do further testing, which could include a D-dimer, CT chest with contrast, ventilation/perfusion scan, or lower extremity Doppler studies to evaluate for deep vein thromboses (DVTs). The PERC CDR gives no guidance in this case.

Wells and Revised Geneva Score for Pulmonary Embolism (PE)

Wells’ Criteria for Pulmonary Embolism

Point Value

Clinical signs and symptoms of DVT

+3

PE is #1 diagnosis, or equally likely

+3

Heart rate > 100

+1.5

Immobilization at least 3 days, or Surgery in the Previous 4 weeks

+1.5

Previous, objectively diagnosed PE or DVT

+1.5

Hemoptysis

+1

Malignancy w/ Treatment within 6 mo, or palliative

+1

Geneva Score (Revised) for Pulmonary Embolism

Point Value

Risk factors

Age > 65

+1

 

Previous DVT or PE

+3

 

Surgery (under general anesthesia) or lower limb fracture in past 1 month

+2

 

Active malignant condition

+2

Symptoms

Unilateral lower limb pain

+3

 

Hemoptysis

+2

Signs

Heart rate < 75

0

 

Heart rate 75 – 94

+3

 

Heart rate ≥ 95

+5

 

Pain on lower limb deep venous palpation and unilateral edema

+4

The Wells’ Criteria for PE is a risk stratification score with different point values assigned to different criterion. Its purpose is to identify patients with a lower PE risk to avoid unnecessary testing and the associated risks and costs [35]. The criteria have been validated in the ED setting [36]. The initial study used a three-tier model to classify patients as low, medium, or high risk. Subsequent studies have been done to apply a simplified version of the Wells’ Criteria and also to use the Wells’ Criteria along with D-dimer testing in a dichotomous manner (two-tier model) where a score of 4 or less (“PE Unlikely” group) combined with a negative D-dimer would achieve sufficiently low probability of PE so as not to pursue further work-up [37-39].  This two-tier model is supported by the American College of Physicians (ACEP) Clinical Guidelines [40]. A two-tier model using a cut-off of less than 6 for low-risk was also studied in pregnant patients with a negative predictive value of 100% [41].  

The original Geneva score included chest radiography and an ABG, whereas the revised score (rGeneva) uses only clinical criteria [42]. A patient with an rGeneva score of 0-3 is considered low risk with a < 10% prevalence of PE.  A score of 4-10 identifies intermediate-risk patients, and a score of 11+ is high risk (>60% prevalence or PE).

The Wells and rGeneva scores have been compared and found to have overall similar accuracy [43-45]. These PE risk stratification tools are meant to be applied to patients with concern for PE as a diagnosis. If PE is not under consideration, the tools should not be applied. Practically speaking, for many ED physicians, these tools are used to help risk stratify patients to identify those who are very low-risk such that no testing should be done, low to intermediate risk such that D-dimer testing would be a useful diagnostic tool, or high risk such that even if a D-dimer were negative, the post-test probability would remain high enough that further testing should be pursued. One recent study found that physician gestalt performed better than the Wells or rGeneva scores [45]. However, guidelines from the Clinical Practice Committee of the American College of Physicians (ACP) were published in 2015 that outline best practice advice including advocating that clinicians should use validated CDRs to estimate pre-test probability in patients in whom acute PE is being considered [46].

YEARS Algorithm for Pulmonary Embolism

The YEARS Algorithm was derived in 2017 and subsequently validated in studies in 2018 and 2021 [47-49]. It consists of the three most predictive criteria of the Well’s Score for PE and incorporates variable D-dimer thresholds, depending on the number of criteria fulfilled. It has the benefit of reducing the use of CT Pulmonary Angiogram by more broadly utilizing the results of D-dimer testing for selected patients. Additionally, a pregnancy-adapted algorithm was developed in 2019, which may be useful for clinicians struggling with the challenge of excluding PE in this sub-group, which has both a higher risk of PE and of radiation exposure to the fetus of performing the “gold standard” test which is considered a CT angiogram [50]. A recent study found that using the YEARS algorithm in combination with an age-adjusted D-dimer strategy was non-inferior to conventional diagnostic strategies and decreased chest imaging by 14% [51].

Pneumonia Severity Index (PSI) Score

The PSI Score estimates mortality for adult patients with community-acquired pneumonia (CAP). It is recommended as a Clinical Practice Guideline by the American Thoracic Society and Infectious Disease Society to use the PSI, in addition to clinical judgment, to determine the need for hospitalization in patients with CAP [52]. Although it has more variables than the CURB-65 Score, it was found to identify larger proportions of patients as low risk and found to have better discriminative power in predicting mortality. It includes variables such as age and sex as well as vital signs, co-morbidities, lab values, and imaging findings, which may limit its use in some resource-limited settings.

Ottawa COPD Risk Scale

The Ottawa COPD Risk Scale predicts 30-day mortality or serious adverse events in ED patients with COPD [53]. It was developed and validated to assist with disposition decisions to avoid admitting low-risk patients suitable for discharge and to avoid discharging high-risk patients [54]. It incorporates elements of the patient’s medical history and exam in the ED as well as testing, including an EKG, chest X-ray, hemoglobin, urea, and CO2.

Cardiac CDRs

Case 6

A 50-year-old male presents to the ED complaining of chest pain for two days. His pain is substernal and non-radiating. He described it as a tightness and is not related to exertion. He has no associated shortness of breath, nausea, or diaphoresis. No cough or fever. He’s never had this pain before. He has a history of hypertension but no other cardiac risk factors. His exam in the ED is normal, and his EKG and initial troponin are normal.

Does this patient require additional cardiac workup in the ED or admission to the hospital for further workup? Can this patient be safely discharged for outpatient follow-up?

a-photo-of-a-50-year-old-male-patient-(image generated by ideogram2.0)

HEART Score for Cardiac Events

HEART Score

 

Points

History

Highly suspicious

+2

 

Moderately suspicious

+1

 

Slightly suspicious

0

EKG

Significant ST depression

+2

 

Non specific repolarization disturbance

+1

 

Normal

  0

Age

≥ 65

+2

 

45-65

+1

 

≤ 45

0

Risk Factors (include: hypercholesterolemia, hypertension, diabetes mellitus, cigarette smoking, positive family history, obesity)

≥ 3 risk factors or history of atherosclerotic disease

+2

 

1-2 risk factors

+1

 

No risk factors known

0

Troponin

≥ 3× normal limit

+2

 

1-3× normal limit

+1

 

≤ normal limit

0

The HEART Score is used to risk stratify chest pain patients in the ED to identify those at risk for major adverse cardiac events (MACE) within six weeks [55]. In the HEART Score, patients with a low risk (score between 0 and 3) indicate a less than 2% risk of major adverse cardiovascular events (MACE) within six weeks. The HEART Score differs from the Thrombolysis in Myocardial Infarction (TIMI) and Global Registry of Acute Coronary Events (GRACE) scores as those scores measure the risk of death for patients with diagnosed acute coronary syndromes (ACS) rather than identifying patients who have cardiac-related chest pain in the first place [56,57]. Additionally, even with low TIMI scores for those diagnosed with ACS in the ED, there is still a 4.7% risk of a bad outcome [56]. This may be of little utility to the ED physician, who finds this risk level unacceptable.

Case 6 Discussion

This patient’s HEART Score is 3 if the physician considers the history “moderately suspicious.” The patient is at low risk for a major cardiac event in the next six weeks so that the ED physician could consider outpatient follow-up. Again, the risk stratification scores are not prescriptive, however. The clinician must make decisions based on his/her judgment, available resources, and comfort with certain levels of risk.

Emergency Department Assessment of Chest Pain Score (EDACS)

Similar to the HEART Score, the EDACS is used to further risk stratify patients with chest pain or other anginal symptoms requiring evaluation for possible acute coronary syndrome who may be potentially low risk and appropriate for early discharge from the emergency department [58]. It should only be applied in patients without ongoing chest pain. The score was 99-100% sensitive in the original derivation paper, and some studies showed it to be more sensitive than the HEART score and better at identifying more low-risk patients [59,60]. That said, a more recent meta-analysis reported a pooled sensitivity of only 96.1%, which may not be considered adequately sensitive by some providers or in some practice environments [61].

Ottawa Heart Failure Risk Score

The Ottawa Heart Failure Risk Scale (OHFRS) was derived in 2013 and validated in 2017 in Canada [62, 63]. It identifies ED patients with heart failure (HF) at high risk for serious adverse events, including death, MI, and the need for ICU/intubation. It is to be used for ED patients presenting with HF exacerbation who have responded to treatment in the ED to help clinicians determine whether admission might be warranted versus discharge for low-risk patients. The study authors looked at the performance of the CDR both with and without a Quantitative NT-proBNP diagnostic test. They found the CDR was valuable even without the availability of this test, which might improve its usefulness in different resource settings. That said, regional practice patterns should be considered when applying this score, such as differences overall in heart failure admission rates.

Atrial Fibrillation – the CHA2DS2-VASc and HAS-BLED Scores

The main clinical decision instruments regarding atrial fibrillation (afib) relate to whether or not to anticoagulate a patient in afib, weighing the risk of stroke without anticoagulation versus the risk of a major bleeding event. The CHA2DS2-VASc Score was developed in an era where Non-Vitamin K Antagonist Oral Anticoagulants (NOACs) are available in higher-resource settings, in addition to traditional warfarin, and in light of more recent evidence regarding the lack of efficacy and safety of aspirin for stroke prevention in afib [64,65]. The score is simple to use with variables of age, sex, and the patient’s medical history. The European Society of Cardiology guidelines recommend using the score to identify truly low-risk patients (0 for males or 1 for females) who do not need anticoagulation therapy [66]. The American Heart Association and American College of Cardiology guidelines also endorse using the CHA2DS2-VASc score as the stroke risk assessment tool of choice [67].

In addition to considering the risk of stroke in patients with afib, however, one also has to consider the risk of bleeding due to taking anticoagulants. Unfortunately, many risk factors for the former are also risk factors for the latter. The score that performs best for identifying the risk of bleeding is the HAS-BLED score [68-70]. The HAS-BLED authors note that while it does not identify absolute cut-offs for when not to use anticoagulants, it does help identify some risk factors that could be avoided or reversed, for example, by controlling hypertension or avoiding alcohol use or other medications that may predispose to bleeding. The decision of whether or not to anticoagulated a patient in afib is complex, but these CDRs provide some objective assessment of risk to inform decision-making and educate patients, and include them in shared-decision making.

Abdominal CDRs

Gastrointestinal Bleeding

Case 7

A 30-year-old male presents to the ED with nausea, vomiting, and epigastric discomfort for one day. He vomited multiple times, initially non-bloody, then developed some blood in the vomit during the last two episodes, which he quantified as a teaspoon in each. He denies melena or hematochezia. He has no diarrhea, fever, or syncope. He denies a history of liver or heart problems. On exam, he has normal vital signs with an initial blood pressure of 128/78 mmHg in the ED, and his abdomen is non-tender. His hemoglobin is 13.5, and his BUN is 5.

Does this patient need admission for further monitoring or evaluation of his upper GI bleed?

The image was produced by using ideogram 2.0.

Glasgow-Blatchford Bleeding Score (GBS)

  • Hemoglobin < 13 for men or < 12 for women
  • BUN > 6.5
  • Initial systolic blood pressure < 110
  • Heart rate ≥ 100
  • Melena present
  • Recent syncope
  • Hepatic disease history
  • Cardiac failure

The Glasgow-Blatchford Bleeding Score (GBS) uses clinical information and some diagnostic testing to risk stratify upper GI bleeding patients[71,72]. It should not be used for lower GI bleeding patients or patients in whom the source of GI bleeding is unclear. A score of 0 is considered low risk. Any score higher than 0 is considered high risk for needing a medical intervention of transfusion, endoscopy, or surgery; therefore, any of the above criteria would be considered high risk. The tool assigns different point values to different gradations of the variables present to a possible highest possible score of 29. The GBS has performed better than other CDRs in predicting patients likely to need hospital-based intervention or are at risk for mortality [73].

Case 7 Discussion

The patient does not meet any of the GBS criteria and would be considered low-risk. Based on this risk stratification, the patient does not demonstrate any signs of lower GI bleeding and could likely be safely discharged home.

Oakland Score for Safe Discharge After Lower GI Bleed

Similar to the GBS Score, the Oakland Score helps identify low-risk patients with lower GI bleeding who are candidates for outpatient management. It is simple to use in most settings and includes age, sex, history, physical exam findings in the ED, and hemoglobin level [74,75].

Appendicitis - Alvarado Score and Pediatric Appendicitis Risk Calculator (pARC)

The Alvarado Score was developed to predict the likelihood of acute appendicitis in patients with abdominal pain [76]. It utilizes a combination of signs, symptoms, and a WBC count with differential to create a risk score. The score is best utilized to avoid unnecessary CT imaging in very low-risk patients or even potentially in very high-risk patients, particularly in low-resource settings where CT is not commonly available [77]. In a study comparing the Alvarado Score with another CDR for pediatric appendicitis, the Pediatric Appendicitis Score, the gestalt of a pediatric surgeon was found to be higher than either scoring system; however, the Alvarado Score may be useful in emergency settings without experienced clinicians [78].

The pARC was also developed specifically for pediatric patients aged 5-18 to identify risk for acute appendicitis [79]. It may be used to help determine the need for advanced imaging and identify low-risk patients who could be observed or discharged from the ED with follow-up or return precautions. The Alvarado Score relies on signs, symptoms, and the availability of WBC and neutrophil counts. In its validation study, it performed better than the Pediatric Appendicitis Score [80].

STONE Score for Uncomplicated Ureteral Stone

The STONE Score was developed to identify patients with a high likelihood of uncomplicated ureterolithiasis who could be managed empirically, minimizing the use of CT or possibly using a low radiation CT protocol [81-83]. It has simple demographic and symptom-based variables with the addition of a urine dipstick; it is, therefore, easy to apply across resource settings. A high STONE Score can decrease the likelihood of an alternative diagnosis to < 2%, potentially limiting unnecessary costs and radiation exposure associated with CT imaging. Ultrasound demonstrating hydronephrosis, in addition to the score, can further increase the likelihood of a stone [84]. Given the increased availability and use of point-of-care ultrasound (POCUS) in emergency settings, using the STONE score in combination with ultrasound is a prudent approach to avoid CT use. A caveat to the STONE score is that it should not be used in ill-appearing patients or those with signs or symptoms suggestive of a possible complicated ureterolithiasis, for example, if there is evidence of a concomitant infection.

Neurologic CDRs

Case 8

A 24-year-old woman presents with a headache that began three hours before arrival at the ED. The patient was at rest when the headache started. The headache was not described as a “thunderclap,” but it did reach maximum severity within the first 30 minutes. The headache is generalized and rated 10/10. She denies head trauma, weakness, numbness, and tingling in her extremities. She denies visual changes, changes in speech, and neck pain. She has not taken anything for the headache. She does not have a family history of cerebral aneurysms or polycystic kidney disease. She had a normal neurologic exam and normal neck flexion during the physical exam.

Should you do a head CT and/or a lumbar puncture to evaluate for a sub-arachnoid hemorrhage in this patient?

a-photo-of-a-24-year-old-woman-sitting-on-an-ed-(mage generated by ideogram2.0)

Ottawa SAH Rule

Investigate if ≥1 high-risk variable is present:

  • Age ≥ 40
  • Neck pain or stiffness
  • Witnessed loss of consciousness
  • Onset during exertion
  • Thunderclap headache (instantly peaking pain)
  • Limited neck flexion on exam

A CDR to determine the risk for subarachnoid hemorrhage (SAH) was derived and externally validated in a single study [85,86]. The purpose of the CDR was to identify individuals at high risk for SAH. This included those experiencing acute non-traumatic headaches that reached maximal intensity within one hour and had normal neurological examinations. Notably, the rule consists of several criteria for inclusion and exclusion, which the emergency department physician must understand. Additionally, it was derived only for patients aged 16 years and older. The study authors note that the CDR is to identify patients with SAH; it is not an acute headache rule. In the validation study, of over 5000 ED visits with acute headaches, only 9% of those met the inclusion criteria [86]. Additionally, clinical gestalt plays a significant role as the authors recommend not applying the CDR to individuals who are at ultra-high risk with a pre-test probability of SAH greater than 50%.

The Ottawa SAH Rule was 100% sensitive but did not reduce testing compared to current practice [85]. The authors state that the rule’s value would be standardizing physician practice and avoiding the relatively high rate of missed sub-arachnoid hemorrhages.

Case 8 Discussion

By applying the Ottawa SAH Rule, this patient is low risk and does not require further investigation for a SAH.

Canadian Transient Ischemic Attack (TIA) Score

The Canadian TIA Score was developed to identify patients at high risk for stroke in the next seven days after a TIA [87,88]. It is calculated based on clinical findings and ED testing, including an EKG, CT, platelet count, and glucose. The validation study also looked at the outcome of carotid endarterectomy or carotid artery stenting within seven days and found that the Canadian TIA Score outperformed the ABCD2 risk stratification tool. It is unclear yet how the application of the tool will impact ED practice, which will likely depend on many factors, including inpatient versus outpatient access to resources. The validation study authors suggest, “The optimal management pathway at the local or regional level can be determined on the basis of the expected risk at a given risk category (for example, same day computed tomography with routine follow-up for patients at low risk, computed tomography angiography and rapid follow-up for those at medium risk, and neurology consultation in the emergency department for those at high risk) [88].”

Other CDRs

San Francisco Syncope Rule

The San Francisco Syncope Rule uses five factors to identify patients who are at high risk of serious outcomes at seven days, including a history of congestive heart failure, hematocrit < 30%, abnormal EKG, shortness of breath, and systolic BP < 90mmHg at triage. In its initial derivation and validation studies, it was found to have 92% and 98% sensitivity, respectively [89, 90]. Its use is controversial, however, due to inconsistent validation studies where it has not performed as well [91,92]. A systematic review of the literature from 2011 suggested that “the probability of a serious outcome given a negative score with the San Francisco Syncope Rule was 5% or lower, and the probability was 2% or lower when the rule was applied only to patients for whom no cause of syncope was identified after initial evaluation in the emergency department [93].” Although there is no consensus on using this tool to safely discharge patients with syncope home if they do not meet these criteria, patients with criteria would be considered a higher risk, possibly warranting observation, admission, and/or further diagnostic studies.

Centor Score for Streptococcal Pharyngitis

The Centor Score is a risk stratification tool that looks at clinical criteria that suggest a greater likelihood of strep pharyngitis, which may prompt the ED physician to prescribe antibiotics [94]. It was initially designed for use in adults. However, a modified score has been validated for use in children > 2 years of age and adults that includes age criteria, as strep pharyngitis is a more common condition in children [95,96]. With a score of 4 or more points, the probability of strep is greater than 50%, and some would advocate for empiric antibiotics in this group to reduce suppurative (peritonsillar abscess, cervical lymphadenitis, and mastoiditis) and non-suppurative (e.g., acute rheumatic fever) complications of strep pharyngitis and shorten the duration of clinical symptoms and as well as to reduce transmission [97]. Rapid antigen detection tests have been found to have a sensitivity of between 70 and 90% and a specificity of ≥95% [97]. Some authors recommend rapid antigen detection testing (RADT) only for children with high clinical scores or if the results of the standard throat culture will not be available for more than 48 hours [97,98]. Studies have found that tonsillar exudates conferred the highest odds of strep infection [96,99].

Conclusion

Clinical Decision Rules (CDRs) or Instruments are increasingly being used to assist ED clinicians in navigating complex decision-making regarding diagnostic testing, clinical care, and disposition determination of emergency patients. These tools have the potential to supplement clinician gestalt, maximize the use of limited and expensive resources (e.g., inpatient beds, CTs), and minimize the use of possibly unnecessary costly or dangerous testing or treatments (e.g., CTs, anticoagulants).

While CDRs are a valuable adjunct to the emergency clinician, ED providers must carefully apply these based on validation cohorts representative of the clinician’s patient population and carefully consider the inclusion and exclusion criteria in the studies. CDRs should not supplant physician critical decision-making based on individualized patient-centered factors and circumstances including resources available, ability to establish outpatient follow-up, and shared-decision making with informed patients. CDRs may be particularly valuable for less experienced clinicians who are learning to identify patient characteristics, symptoms, physical exam findings, risk factors and testing that will help them diagnose and manage complex emergency patients in variable practice environments.

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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Additional Online Resources

  • Emergency Medicine Cases podcast: Clinical Decision Rules and Risk Scales. This hour-long podcast discusses the overall use of CDRs and Risk Scales and how they are developed and used, with a discussion with Dr. Ian Stiell, the “father of clinical decision rules” from Ottawa, Canada. http://emergencymedicinecases.com/episode-56-stiell-sessions-clinical-decision-rules-risk-scales/
  • Agile MD app.  You can download the AgileMD app for free and then download the EM Cases Summaries for free.  Within EM Cases Summaries is a link to the “Ottawa CDRs and Risk Scales.” This includes shortcut to the Ottawa Ankle and Knee Rules, the Canadian C-spine and CT Head Rules, and the Ottawa COPD, Heart Failure, and TIA Risk Scores.
  • EmDOCS.net is a FOAMed initiative with a series of posts on Clinical Decision Rules.
  • There are numerous EM blogs and podcasts that provide education for EM trainees and physicians.  Many are listed here: https://www.emra.org/about-emra/publications/recommended-blogs-and-podcasts/. The podcast EMCrit and EM:RAP in particular have episodes on Clinical Decision Rules.

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.

Cardiac Monitoring (2024)

~ iEM Education Project Team ~ Leave a comment

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.

Listen to the chapter

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.

Heat Illnesses (2024)

~ iEM Education Project Team ~ Leave a comment

by Patrick Joseph G. Tiglao, Rhodney P. Canada, & Emmanuel Luis S. Mangahas

Authors
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You have a new patient!

A 24-year-old man was brought to your Emergency Department by his football coach. His coach informed you that he started “behaving strangely” and responding inappropriately to questions a few hours ago during a practice session on the football field. His initial vital signs are BP 80/50 mmHg, HR 115 bpm, RR 24 bpm, T 41.5oC, and SpO2 98%. His GCS is 13 (E3V4M6).

What do you need to know?

Climate change is widely considered the greatest threat to human health globally in the coming decades [1]. According to the assessment of the Intergovernmental Panel on Climate Change (IPCC), the next decades might witness global warming above 1.5 °C, exceeding the goals of the Paris Agreement [2]. Concomitantly, heat-related mortality has developed as a growing public health concern. Populations with pre-existing chronic diseases are more sensitive to climate change, warranting closer attention and more effective interventions to manage heat-related health risks [3]. Therefore, a comprehensive medical understanding of heat-related illnesses is required as the world faces climate change [1].

Heat-related illnesses include a spectrum of diseases, ranging from mild and self-limiting conditions such as heat edema, heat cramps, and heat stress to the life-threatening condition known as heat stroke. These conditions occur when the body’s thermoregulatory mechanisms fail to keep body temperature within normal limits in a hot and humid environment [4].

The emergency physician needs to have a high index of suspicion for heat stroke because these patients can mistakenly be diagnosed with other conditions that may present similar to heat stroke.  Some examples are sepsis, intracranial bleeding, stroke, thyroid storm, anticholinergic toxicity, or other conditions where patients may have high fevers or altered mental status, similar to heat stroke. The most critical initial intervention in heat stroke is rapid cooling to <39°C. A misdiagnosis can result in a delay in rapid cooling.  Failing to implement this intervention results in higher mortality [5].

According to the World Health Organization, more than 166,000 people died due to extreme temperatures between 1997 and 2017.  This includes 70,000 deaths in the 3-month European heatwave of 2003 and 53,000 deaths in the 44-day Russian heatwave of 2010 [5]. A 2003 prospective study from France reported a 28-day and 2-year mortality rate of 58% and 71%, respectively, for patients diagnosed with heat stroke [6].

Body temperature is controlled by the hypothalamus. The body gains heat from metabolism and the environment, and this heat must be dissipated to maintain core body temperature between 36°C and 38°C (96.8°F and 100.4°F). Thermoregulation relies on four primary mechanisms: dilatation of blood vessels, particularly in the skin, increased sweat production and subsequent evaporation, decreased heat production, and behavioral heat control. Vasodilation contributes to the orthostatic pooling of interstitial fluid in the lower extremities, as seen in heat edema. When these processes are overwhelmed, core temperature will rise and may result in heat stress [4].

Cellular injury can begin when the core body temperature exceeds 39oC, especially if the elevation in temperature is sustained [7]. As the body temperature rises to 40°C, an acute phase response is elicited from heat-stressed cells.  This involves the release of cytokines and heat shock proteins, materials that can cause damage to organ systems and result in heat stroke [4,8]. The incremental damage to cells and organ systems as body temperature rises above 39oC exemplifies the importance of rapid cooling in a patient with hyperthermia.

Heat stroke due to high external temperature and humidity without much contribution from physical exertion is termed classical heat stroke (CHS).  Heat stroke is due to increased heat generation from strenuous physical activity, usually under extreme heat conditions and in a poorly acclimatized and conditioned body, and is termed exertional heat stroke (EHS). For example, classical heat stroke may be seen in elderly individuals sitting in poorly cooled and ventilated homes during the summer; exertional heat stroke may be seen in athletes exercising hours in the sun during a prolonged sporting event or race. Another heat-related illness that may be encountered in the athlete patient is heat cramps. These cramps occur from relative deficiencies in electrolytes such as sodium, potassium, and magnesium brought about by replenishing lost fluids with hypotonic drinking solutions after vigorous physical activity. This leads to painful involuntary contractions of skeletal muscles, most commonly the calves [4].

The exercising body has thermoregulatory mechanisms it utilizes when exposed to prolonged heat. During exercise, blood vessels dilate to release heat, the heart rate increases, and stroke volume decreases. Sweat production and evaporation from the skin surface also assist in cooling the body during exercise. These mechanisms may be diminished in patients with underlying cardiovascular disease (e.g., congestive heart failure) or those taking certain medications (e.g., beta-blockers or anticholinergic medications). These patient groups are at increased risk of heat-related illnesses during exercise [9].

Medical History

Ask patients with heat edema about exposure to hot and humid environments. The presence of other symptoms, such as dyspnea, easy fatigability, orthopnea, paroxysmal nocturnal dyspnea, and oliguria, are red flags that may point to alternative causes of the edema, such as congestive heart failure or kidney failure [4].

For patients with heat cramps, verify recent participation in strenuous activities, such as sports events and practices, military exercise, or procession-like activities. Ask if the patient took fluid during exertional activities and, if so, what type of fluid was consumed. Drinking hypotonic solutions, such as plain water, puts patients at risk for relative deficiencies in electrolytes and subsequent heat cramps. Ask about vomiting, diarrhea, and medications, like diuretics or antihypertensives, which can also put the patient at risk for electrolyte disturbances [4].

Heat stress is a diagnosis of exclusion because patients usually come in febrile with non-specific symptoms such as nausea, headache, weakness, and dizziness [4]. Again, patients with a recent history of exposure to hot and humid environments are at increased risk of heat stress. Still, the emergency physician should be aware of other more dangerous conditions, such as sepsis, CNS infection, endocrine dysfunction, myocardial infarction, and drug overdose. Ask for recent history of dyspnea, cough, dysuria, and headache, which may point to infectious diseases such as pneumonia, urinary tract infection, and CNS infection.

To diagnose heat stroke, the patient must have both Central Nervous System (CNS) impairment and a core temperature greater than 40°C. The spectrum of neurological abnormalities ranges from mild confusion to coma with a GCS of 3. Situational awareness is a vital skill for emergency physicians, as one should be aware of days with high ambient temperatures and high humidity that can increase the risk of CHS. Usage of medications that impair sweating, like anticholinergic medications, is another risk factor for developing heat illnesses. Generally speaking, CHS is uncommon in geographical areas where the average temperature throughout the year is high, as communities living there will develop behavioral tactics to avoid the heat. Intense exercise, military training, sports competitions, or prolonged labor, on the other hand, puts patients at risk for EHS. Patients not trained in hot environments may not be physiologically acclimatized, increasing their risk for EHS [4].

Physical Examination

Whenever heat illnesses are considered in the differential diagnosis of a given patient, measuring a core body temperature (e.g., rectal temperature) is the most important physical assessment. Using the physical exam to evaluate for other causes of elevated body temperature is important.  Physical signs of infection (e.g., cellulitis, abscess, drainage from wounds, asymmetric breath sounds), intoxication (e.g., dilated pupils), and endocrine dysfunction (e.g. goiter) should be assessed.

Obtaining an accurate and continuous core body temperature is a crucial part of the physical examination. Core temperature should be assessed and monitored using rectal, bladder, or esophageal probes. Peripheral temperature measurements, like oral, axillary, or temporal temperatures, are unreliable and may not reflect actual core temperatures. A common pitfall in measuring rectal temperature is not inserting the probe to a sufficient depth, rendering readings inaccurate, mainly if ice packs have been applied to the groin area for cooling. Rectal probes, in general, have to be inserted 15 cm inside the rectum to mitigate the effects mentioned above, but manufacturers may recommend different depths.  Note that unlike heat stroke and heat stress, heat edema, and heat cramps will not have an increased core temperature [4]. Tachycardia and hypotension may be seen on examination as a response to thermoregulatory peripheral vasodilation. This phenomenon contributes to other heat illnesses, such as heat edema and heat syncope.

After vital signs, a head-to-toe physical exam should be conducted with special care in conducting a thorough neurological examination. A hallmark finding of heat stroke, other than a core temperature above 40°C, is an abnormal neurological exam. CNS effects might range from mild confusion to deep coma. Ataxia and slurred speech may also be seen. CNS effects help distinguish heat stress from heat stroke, as only heat stroke will have CNS changes [4].

Assess for neurologic signs such as nuchal rigidity, lateralizing spasticity, and pathologic reflexes (e.g. extensor toe reflex) to determine the possibility of a central neurologic etiology. Seizures, in general, are common in heat stroke and might be confused with shivering during cooling.  Both seizures and shivering should be treated for neural protection and prevention of heat generation, respectively.  Benzodiazepines are appropriate for treating both conditions.

Alternative Diagnoses

Minor heat illnesses, like heat cramps and heat edema, can be diagnosed clinically based on the history. Alternative diagnoses for heat edema include congestive heart failure, renal failure, and chronic hepatic disease. The presence of exertional dyspnea, orthopnea, or paroxysmal nocturnal dyspnea would suggest congestive heart failure. Progressively decreasing urine output and generalized edema would suggest renal failure. A jaundiced patient with progressively enlarging abdomen would indicate a chronic hepatic disease. Alternative diagnoses for heat cramps are infectious conditions and electrolyte derangements. Many viral syndromes, like influenza, COVID-19, or Dengue, can be associated with myalgias.  Other conditions, like Leptospirosis, can also present with lower extremity myalgia and calf tenderness. However, the absence of decreasing urine output, fever, and jaundice would make this diagnosis unlikely.

Heat stroke, with its cardinal features of hyperpyrexia and altered sensorium, has numerous alternative diagnoses.  Some important diagnoses to consider are sepsis, CNS infections, thyroid storm, sympathomimetic or anticholinergic toxidromes, serotonin syndrome, alcohol withdrawal, stroke, or status epilepticus. Investigate accordingly for a focus of infection for these patients. Thyroid storm patients may also present with atrial fibrillation, diarrhea, and a trigger (e.g., missed thyroid medications, infection, or surgery). The presence of signs and symptoms such as sudden-onset lateralizing weakness, slurring of speech, headache, nuchal rigidity, and recurrent seizures despite adequate cooling may suggest central neurologic etiology for the patient’s condition. It may require a more tailored neurologic work-up.  Reported illicit substance or alcohol use, or lack thereof, would support intoxication or withdrawal. Epilepsy history, missed doses of antiepileptic medications, or active seizure activity during the exam would support status epilepticus as a diagnosis.

Acing Diagnostic Testing

Heat stroke and other heat illnesses are diagnoses made clinically.  However, diagnostic testing can help rule out alternative diagnoses and evaluate for concurrent organ dysfunction and metabolic derangements.

Immediately test point-of-care glucose because hypoglycemia is a common and easily reversible cause of altered sensorium. Hypoglycemia also sometimes accompanies exertional heat stroke since glucose reserves may become depleted from physical activity. Blood work-ups can include a complete blood count to evaluate for infection, creatinine to rule out acute kidney injury, and metabolic profile to assess for electrolyte imbalance. Hypernatremia may be present in severe dehydration. Hyponatremia and hypercalcemia may be present in patients who are dehydrated with hypotonic solutions after extreme physical activity. Hyperkalemia may be associated with acute kidney injury.

Blood gas analysis may help differentiate classical and exertional heat stroke. Classical heat stroke usually presents with respiratory alkalosis from hyperventilation as a compensatory mechanism to extreme heat. In contrast, exertional heat stroke may present with lactic acidosis from repeated muscular contractions from physical exertion [4]. Moreover, elevation of liver enzymes is very common in both EHS and CHS, mainly due to direct thermal injury and hypoxia from splanchnic vascular redistribution. Hepatic damage is almost always mild and reversible despite rare reports of fulminant hepatic failure from heat stroke [4,10].

Concerns for a central neurologic etiology for the patient’s encephalopathy can be assessed with CT brain imaging and CSF analysis.  These studies should be especially considered if focal neurologic deficits, slurring of speech, nuchal rigidity, or meningeal signs persist despite lowering the core temperature.

Risk Stratification

Minor heat illnesses are generally self-limited and have good outcomes. Heat stroke, on the other hand, is a life-threatening emergency. Mortality rate is correlated with the maximum core temperature and time to initiate cooling methods [4]. A study in 2018 also showed that the presence of disseminated intravascular coagulation is an independent prognostic factor for hospital mortality in patients with heat stroke [11]. Patients suffering from multiple organ injuries due to thermal injury also have poorer prognosis, so it is imperative to closely monitor renal, hepatic, and cardiovascular status of heat stroke patients [10,12].

Management

A core temperature above 40°C should prompt the clinician to consider heat stroke and initiate rapid cooling. 

Heat stroke is a time-sensitive condition where cooling takes precedence over everything else, including confirmation of the diagnosis. Every patient should be approached with the ABCDE assessment to ensure that all critical decisions are made promptly. Heat stroke is not an exception to this role, as the disturbance in consciousness could result in significant airway complications. A complete airway assessment should be immediately performed when the patient arrives in the emergency department while cooling measures are being set up. Many heat stroke patients may have a depressed level of consciousness, but the decision to intubate is ultimately clinical and based on local resources. Airway protection is paramount and should take priority over any other diagnostic or therapeutic procedures. Peripheral blood pooling is a component of heat stroke pathology, so hypotension is common in these patients. Intravenous fluid administration should be judicious, as blood pressure usually picks up as the core temperature drops. Aliquots of 250cc of crystalloids should be used when fluids are needed, and repeated dosing should take place after volume status assessments.

In heat stroke, external cooling methods are the main pillar of therapy. Antipyretics, such as Paracetamol, have no proven benefit in such cases. The fastest way to cool patients is through conduction, the direct transfer of heat between molecules. Full body water immersion can do this, and although this is theoretically the best cooling method, it is clinically challenging. Immersion of the patient in water poses a risk of aspiration and renders the patient’s accessibility quite difficult. Alternatively, ice packs can be placed on the patient’s neck, axilla, and groin areas. Convection, heat loss due to gas movement around the body, combined with evaporation, can achieve a cooling speed similar to full-body immersion. This combination can be achieved by spraying the patient with lukewarm water followed by fanning with warm air. Mist fans are very convenient and have the added benefit of their ability to fan multiple patients at once.

Figure 1- monitor showing the current vitals while the patient is cooled.
Figure 2. The row of beds with mist fans in a sunstroke unit. A cooling unit can be seen at the far right.
Figure 3. Fiberglass grooved beds with waterproof mattresses in a sunstroke unit.

One complication of these cooling maneuvers is shivering. Shivering needs to be controlled as it increases internal heat generation. This can be overcome by administering benzodiazepines. It should be noted that high ambient temperature and high humidity make convection and evaporation less effective. For this reason, if these patients are encountered in the prehospital setting, the first priority is to remove them from the hot and humid environment [4,7].

Internal cooling procedures, such as cold IV fluids and internal cold fluid lavages, do not have high quality to support their safety and efficacy in heat stroke patients [4]. Internal cooling with cardiopulmonary bypass can be considered in severe cases that do not respond to typical cooling methods. However, it is costly, resource-intensive, and unavailable in many contexts [4]. Rapid and aggressive external cooling with evaporative cooling, cold water immersion, and ice packs should be prioritized as the initial preferred cooling methods. Invasive measures, like thoracic, bladder, rectal, or peritoneal lavage, should only be used when other measures fail.

Special Patient Groups

Patients at extremes of age are at increased risk for heat-related illnesses and should be carefully considered for these conditions when presenting with fever [4].

Pediatrics

Classical heat stroke can occur in pediatric patients, but these patients are also at risk of another type of heat stroke known as confinement hyperpyrexia. This happens when a child is left inside a vehicle with poor ventilation during extreme heat. Pediatric patients are especially susceptible to heat stroke because they still lack adequate thermoregulatory mechanisms and the instinctive capacity to replace their fluid losses [4]. Child abuse should be considered, and necessary actions should be taken to protect the child from abuse or maltreatment.

Pregnant Patients

Pregnant individuals are particularly vulnerable to heat-related illnesses due to physiological changes that increase metabolic and cardiovascular demands. Conditions such as heat cramps, heat exhaustion, and heat stroke can arise from prolonged heat exposure, posing risks to both maternal and fetal health, including preterm birth and low birth weight. Management involves moving the patient to a cooler environment, ensuring hydration with non-caffeinated drinks or intravenous fluids if needed, applying cooling measures like wet cloths and fans, and monitoring vital signs closely. Preventive measures are crucial and include staying hydrated, wearing lightweight clothing, avoiding outdoor activities during peak heat, and utilizing air-conditioned spaces. Recognizing early symptoms, such as excessive sweating, dizziness, or confusion, and seeking immediate medical care when necessary are critical to preventing complications.

Geriatrics

Geriatric patients may have comorbidities or take daily medications that impair thermoregulation or mobility, making them prone to heat-related illnesses. This population has a higher heat stroke mortality rate and is more likely to experience complications of heat stroke [4]. Advocating for closer community ties, monitoring by family or peers, and improved socioeconomic support may help elderly patients evade health-related illnesses.

Mass Gatherings

Preparing for a mass gathering event should involve mitigation measures for a possible mass casualty incident of heat stroke and heat exhaustion patients, especially during hot or humid summer months. Public education should be employed to seek shade, drink enough fluids, and use umbrellas. Preparations should also include installing mist pipes, vent fans, and nearby cooling stops.

When to admit this patient

Patients with minor heat illness (e.g., heat edema, cramps, and stress) can generally be discharged home. They should be advised to refrain from strenuous activities during extreme heat conditions, drink plenty of fluids, and wear light and loose-fitting clothing. Those who suffer from heat cramps should be advised to avoid hypotonic solutions for fluid replacement to prevent relative electrolyte deficiencies [4].

Consider admission for patients with minor heat illness but have comorbidities, such as congestive heart failure and renal failure, and those with severe electrolyte abnormalities. Patients suffering from heat stroke must be admitted after resuscitation and rapid cooling in the emergency department.  Heat stroke patients need admission to adequately monitor core temperature and possible occurrence of late complications, such as renal failure, hepatic injury, and electrolyte abnormalities. Patients who are intubated or unstable hemodynamically require ICU admission for closer monitoring [4].

Revisiting Your Patient

You immediately assess the patient’s ABCDEs as part of the primary survey. You assess the patient’s airway for the presence of stridor and pooling of oral secretions. The airway is normal. The patient is able to speak in sentences, albeit confused. He is tachypneic but has normal work of breathing and clear breath sounds. Again, you note that the patient is hypotensive at BP 80/50, tachycardic at HR 115, and hyperthermia at 41.5oC. You start infusing 500 mL of normal saline intravenously as a bolus. The patient was confused but did not exhibit lateralizing weakness, slurring of speech, or nuchal rigidity. Point-of-care glucose was done to rule out hypoglycemia, which revealed 146 mg/dL. You did not elicit any history of trauma, and you did not note any obvious abrasions, lacerations, or bleeding. After the IV bolus, reassessment was as follows: BP 90/60, HR 110, RR 24, T 41.5oC, SpO2 98%, and GCS 13 (E3V4M6)

On further history taking, you elicit that the patient has no allergies, no daily medications, no known comorbidities, and last ate 3 hours ago. You learn the patient was at football team practice for 2 hours at noon today when they noted that the patient had decreased verbal responses, responded inappropriately, and was extremely warm to touch. There was no vomiting, headache, lateralizing weakness, or trauma noted during the incident. There was no history of cough, dyspnea, and fever in the preceding days. The coach said the patient had only joined the football team 4 days prior. You insert a rectal thermometer and note a temperature of 42.0oC. With this information, you suspected that the patient may be suffering from an exertional heat stroke and decided that the goal was to decrease the core temperature to less than 39oC as soon as possible. You immediately remove the patient’s clothing while still maintaining modesty. You direct a vent fan to the patient by incorporating water sprays and placing ice packs on the patient’s neck, axillary, and groin areas.

After 30 minutes of cooling, you observe shivering. To decrease the internal heat production that shivering may cause, you administer diazepam 2.5 mg IV, and the shivering subsides. A cardiac monitor with pulse oximetry is connected, and blood samples are drawn to evaluate for organ dysfunction and possible sepsis. After reaching a rectal temperature of 39°C, you direct your team to dry cover the patient with a light bed sheet. Upon subsequent examination, the patient was conscious, alert, and oriented. Vitals are BP 110/60, HR 105, RR 22, T 38.5oC O2Sat 96% on room air. Laboratories are remarkable for metabolic acidosis and elevated liver enzymes. Complete blood count is unremarkable. You admit the patient to a general medical ward for further monitoring and management.

Authors

Picture of Patrick Joseph G. Tiglao

Patrick Joseph G. Tiglao

Dr. Patrick Joseph G. Tiglao, FPCEM is a practicing Emergency Medicine Physician at the University of the Philippines - Philippine General Hospital. He is also affiliated with DOH regional hospitals in the other parts of the Philippines namely, Corazon Locsin Montelibano Memorial Regional Hospital in Bacolod City, Negros Occidental and Eastern Visayas Medical Center in Tacloban City, Leyte Province.

Picture of Rhodney P. Canada

Rhodney P. Canada

Dr. Rhodney P. Canada graduated, being the top of his class, Doctor of Medicine from the University of St. La Salle – Bacolod in 2018. He spent a year of post-graduate internship at the University of the Philippines Manila – Philippine General Hospital from 2018-2019. Currently, he is a senior 4th year and Chief Resident of the Department of Emergency Medicine in Corazon Locsin Montelibano Memorial Regional Hospital, Bacolod City, Negros Occidental, Philippines.

Picture of Emmanuel Luis S. Mangahas

Emmanuel Luis S. Mangahas

Philippine General Hospital

Acknowledgement

The authors would like to express their utmost gratitude to Dr. Abdulaziz Al Mulaik, the author of this chapter in the previous edition.

Listen to the chapter

References

  1. Zhou L, He C, Kim H, et al. The burden of heat-related stroke mortality under climate change scenarios in 22 East Asian cities. Environ Int. 2022; 170
  2. Tollefson J. Top climate scientists are sceptical that nations will rein in global warming. Nature. 2021; 599(7883):22-24.
  3. Yang J, Zhou M, Ren Z, et al. Projecting heat-related excess mortality under climate change scenarios in China. Nat Commun. 2021; 12 (1039)
  4. LoVecchio F. Heat Emergencies. In Tintinalli J, ed. Emergency Medicine A Comprehensive Study. 9th ed. USA: McGraw Hill; 2020: 1345-1350
  5. Heat and Health. World Health Organization. https://www.who.int/news-room/fact-sheets/detail/climate-change-heat-and-health. Published June 2018. Accessed April 2023.
  6. Argaud L, Ferry T, Le QH, et al. Short- and long-term outcomes of heatstroke following the 2003 heat wave in Lyon, France. Arch Intern Med. 2007;167(20):2177-2183
  7. Beltran G. Heat-related Illneses. In Cone D, ed. Emergency Medical Services Clinical Practice and Systems Oversight. 3rd ed. New Jersey, USA: John Wiley & Sons; 2021: 403-409
  8. Benedetto W. Heat Stroke. In Parsons P, Wiener-Kronish J, ed.Critical Care Secrets. 5th ed. Mosby; 2013: 541-544
  9. Hifumi T, Kondo Y, Shimizu K, Yasufumi M: Heat stroke. J Intens Care. 2018: 6(30)
  10. Grogan H, Hopkins PM. Heat stroke: implications for critical care and anaesthesia. BJA. 2002: 88(5):700–707
  11. Hifumi T, Kondo Y, Shimazaki J, et al. Prognostic significance of disseminated intravascular coagulation in patients with heat stroke in a nationwide registry. J Crit Care. 2018;44:306-311
  12. Liu S, Xing L, Wang J, et al. The Relationship Between 24-Hour Indicators and Mortality in Patients with Exertional Heat Stroke. Endocr Metab Immune Disord Drug Targets. 2022;22(2):241-246

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Reviewed and Edited By

Picture of Joseph Ciano, DO, MPH, MS

Joseph Ciano, DO, MPH, MS

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

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

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

Headache (2024)

~ iEM Education Project Team ~ Leave a comment

by Shailaja Sampangi Ramaiah

Authors
Listen

You have a new patient!

A 60-year-old male is brought to the Emergency Room by a family who gives a history of sudden onset severe headache with vomiting and right-sided weakness. The symptoms began one hour ago. He is a known diabetic on Metformin and has been hypertensive on Losartan for the past 20 years. The patient has poor compliance with his home medications. The family denies any history of trauma, seizures, or antiplatelet or anticoagulation drug intake.

On examination, the patient is unresponsive with HR -98/min, BP: 210/120 mmHg, RR: 16/min, oxygen saturation: 80% room air, and temperature: afebrile.  The GCS is 5 (E1V1M3), and the patient has right-sided weakness 0/5, absent deep tendon reflexes, glucose is 198mg/dl, and pupils are bilaterally midsized, equal, and reactive to light.

What do you need to know?

Headache is a common complaint in the Emergency Room (ER). It constitutes 1 – 4 % of all ER visits [1]. The true global prevalence of headache is unknown because the pathophysiology and causes of headache are broad. Headache disorders collectively constitute the seventh highest cause of years lived with disability (YLDS) [2].

Headaches are classified as primary headache disorders (when pain is the disease) and secondary headache disorders (when headache is a symptom of another disease). Primary headache disorders include migraine, tension headache, and cluster headache. Secondary headache disorders are listed below in Table 1.

Table 1 – Secondary headache disorders

Pathology

Examples

Headache attributed to head or neck trauma

Post-traumatic headache

Concussion

Headache attributed to cervical or cranial vascular disorders

Subarachnoid hemorrhage

Intraparenchymal hemorrhage

Subdural or epidural hematoma

Cavernous/venous sinus thrombosis

Arteriovenous malformation

Temporal arteritis

Carotid/vertebral artery dissection

CNS infections

Meningitis

Encephalitis

Cerebral abscess

Intracranial non vascular space occupying lesions

Tumors

Parasitic or inflammatory lesions

Headache attributed to substance or withdrawal

Nitrates and nitrites

Mono amine oxidase inhibitors

Alcohol withdrawal

Abuse of analgesics

Headache or facial pain due to head, ears, eyes, nose, or throat disorders

Glaucoma

Sinusitis

Optic neuritis

Iritis

Headache attributed to altered homeostasis

Fasting headache

High altitude cerebral edema

Hypoxia

Hypercarbia

Hypothyroidism

Obstructive sleep apnea

Miscellaneous causes

Preeclampsia

Post dural puncture headache

Most patients presenting to the ER with headache have a primary headache disorder, with migraine being the most common [3]. However, it is vital to evaluate for headache signs and symptoms that point towards secondary causes.  The SNNOOP 10 list in Table 2 reviews important red flag signs and symptoms to consider in a patient with headache [4].  

Table 2 – Red flag signs and symptoms of headache (SNNOOP 10 list)

Sign or symptom

Related secondary headache cause

Systemic symptoms including fever

Headache attributed to infection or nonvascular intracranial disorders, like carcinoid or pheochromocytoma

Neoplasm in history

Neoplasms of the brain, metastasis

Neurologic deficit or dysfunction (including decreased consciousness)

Headaches attributed to vascular, nonvascular intracranial disorders; brain abscess and other infections

Onset of headache is sudden or abrupt

Subarachnoid hemorrhage and other headaches attributed to cranial or cervical vascular disorders

Older age (after 50 years)

Giant cell arteritis and other headache attributed to cranial or cervical vascular disorders; neoplasms and other nonvascular intracranial disorders

Pattern change or recent onset of headache

Neoplasms, headaches attributed to vascular, nonvascular intracranial disorders

Positional headache

Intracranial hypertension or hypotension

Precipitated by sneezing, coughing, or exercise

Posterior fossa malformations; Chiari malformation

Papilledema

Neoplasms and other nonvascular intracranial disorders; intracranial hypertension

Progressive headache and atypical presentations

Neoplasms and other nonvascular intracranial disorders

Pregnancy or postpartum

Headaches attributed to cranial or cervical vascular disorders; post dural puncture headache; hypertension-related disorders (e.g., preeclampsia); cerebral sinus thrombosis; hypothyroidism; anemia; diabetes

Painful eye with autonomic features

Pathology in posterior fossa, pituitary region, or cavernous sinus; Tolosa-Hunt syndrome; ophthalmic causes

Posttraumatic onset of headache

Acute and chronic posttraumatic headache; subdural hematoma and other headache attributed to vascular disorders

Pathology of the immune system such as HIV

Opportunistic infections

Painkiller overuse or new drug at onset of headache

Medication overuse headache; drug incompatibility

Primary Headache Disorders

Migraine

Migraines are one of the most common primary headache disorders.  Migraines affect females more than males and are more common in the third and fourth decade of life. The clinical presentation includes unilateral or bilateral pulsating pains with moderate to severe intensity.  Migraines may have associated auras, photophobia, phonophobia, blurred vision, lightheadedness, vertigo, nausea, and vomiting. Most patients seek dark, quiet rooms. The triggers for migraines include sleep deprivation, hunger, hormonal changes during menstruation, and certain medications (e.g., nitrates and oral contraceptive pills) [5].

Cluster Headache

Cluster headaches occur suddenly, last 15 minutes to 3 hours in duration, and tend to occur repeatedly during a defined time interval.  This type of headache is more common in men than women. Precipitating factors include ingestion of alcohol, stress, and climate change. The headache begins as unilateral sharp stabbing pain in the eye, exclusively in the trigeminal territory, accompanied by ipsilateral autonomic symptoms such as ptosis, miosis, forehead, and facial swelling [5].

Tension Headache

Tension headaches, like migraines, are a common cause of primary headaches and affect women more than men. Tension headaches may last from minutes to days. Physical examination reveals tender areas on the scalp and neck. Patients complain of a tight, band-like discomfort around the head that is non pulsating and dull in nature. The headache does not worsen with physical activity. Anxiety and depression may coexist with chronic tension type headaches [6].

Secondary Headache Disorders

There are various secondary causes of headaches, ranging from benign to severe. This section will focus on a small list of etiologies relevant to the emergency medicine practitioner.

Subarachnoid Hemorrhage (SAH)

SAH is a life-threatening cause of headache that should be considered in all ER patients with headache. Accumulation of blood in the subarachnoid space activates meningeal nociceptors, causing headache and meningismus. Causes for non-traumatic SAH include ruptured saccular aneurysms, arteriovenous malformations, cavernous angiomas, and coagulopathy. The risk of brain aneurysmal rupture increases with age, hypertension, smoking, excessive alcohol consumption, and use of sympathomimetic drugs [7].

Patients with SAH historically present with a severe, acute onset headache that is maximal intensity at onset (thunderclap headache). The onset of headache may be spontaneous or after physical exertion. Associated signs and symptoms are nausea, vomiting, neck stiffness, photophobia, seizures, depressed consciousness, and focal neurological abnormalities. Retinal hemorrhage may be present on fundoscopic examination. SAH patient prognosis can be predicted with the Hunt and Hess classification system [7], as shown in Table 3.

Table 3 – Hunt and Hess classification of cerebral aneurysms and subarachnoid hemorrhage

Grade

Condition

0

Unruptured aneurysm

1

Asymptomatic or minimal headache and slight nuchal rigidity

2

Moderate or severe headache, nuchal rigidity, no neurological deficit other than cranial nerve palsy

3

Drowsiness, confusion or mild focal deficit

4

Stupor, moderate to severe hemiparesis

5

Deep coma, decerebrate posturing, moribund appearance

  • Grades 1 or 2 – good prognosis
  • Grade 3 – moderate prognosis
  • Grades 4 or 5 – poor prognosis

Intracranial Neoplasms

Headache is a common presenting symptom of patients with a brain tumor, but the symptoms are variable.  Symptoms depend on the site of tumor, traction on meninges or large vessels, increase in intracranial pressure, or hydrocephalus.  Other than headache, patients may have sleep disturbances, nausea and vomiting, seizures, focal neurologic deficits, alterations in consciousness, personality disorders, and cognitive difficulties [8].

Meningitis

Acute bacterial meningitis may present with headache, fever, nuchal rigidity, nausea, vomiting, photophobia, new skin rash, seizures, focal neurologic deficits, or alterations in consciousness. The most common pathogens causing bacterial meningitis in adults are Streptococcus pneumoniae and Neisseria meningitidis. Bacterial meningeal invasion occurs when bacteria colonize host mucosal epithelium, invade and survive within the bloodstream, cross the blood-brain barrier, and multiply within the CSF. Once inflammation is initiated, a series of injuries occur to the endothelium of the blood-brain barrier that result in vasogenic brain edema, loss of cerebrovascular autoregulation, and increased intracranial pressure. This results in localized areas of brain ischemia, cytotoxic injury, and neuronal death [9].

Giant Cell Arteritis (GCA, or Temporal arteritis)

GCA is an inflammatory vasculopathy affecting mainly the extracranial branches of the carotid artery (temporal and occipital). The common features of giant cell arteritis are advanced age, female gender, headache, visual symptoms, jaw claudication, temporal artery tenderness, and systemic symptoms (e.g., fever, weight loss, fatigue).  One of the most serious complications of GCA is blindness, but a range of visual symptoms and signs may occur, such as diplopia, visual field deficits, amaurosis fugax, or an afferent pupillary defect. Typical GCA headaches are worse in the morning than later in the day and can be constant or intermittent. Other complications include transient ischemic attacks, peripheral neuropathies, and stroke. Palpation of the temporal artery may reveal absent pulses, erythema, and nodular swellings [10].

Carotid and Vertebral Artery Dissection

The classic symptoms of carotid artery dissection include:

  • Unilateral headache or neck pain.
  • Ipsilateral partial Horner’s syndrome.
  • Blindness (dissection into retinal artery).
  • Contralateral motor deficits.

Vertebral artery dissection may also present with severe unilateral headache or neck pain.  Dissection along the vertebral artery may result in brainstem or cerebellar ischemia, causing vertigo, vomiting, diplopia, ataxia, tinnitus, unilateral facial weakness, alterations in consciousness, or cranial nerve deficits.

Both carotid and vertebral artery dissection should be considered in a patient presenting with headache or neck pain with a history of recent head or neck trauma, sudden neck movement, neck torsion, coughing, chiropractic manipulation, minor falls, weight lifting, basketball, volleyball, or a motor vehicle collision [11].

Cerebral Vein Thrombosis (CVT)

Patients with this diagnosis often have a headache lasting days to weeks, along with other signs and symptoms, like seizures, focal neurologic deficits, orbital pain, proptosis, chemosis, and papilledema. Symptoms are due to raised intracranial pressure from occlusion of the cerebral venous system, causing ischemia, infarction, or hemorrhage.

Major risk factors for CVT include pregnancy, post-partum state, malignancy, head trauma, recent surgery, parameningeal infections, oral contraceptives, history of vasculitis, inflammatory bowel disease, and connective tissue disease [12].

Initial Assessment and Stabilization (ABCDE approach)

When a patient presents with headache to the ER, it is vital to follow the ABCDE sequence of initial assessment.  

  • Airway: look for airway patency.  Assess if the patient is talking normally or if there are signs of airway obstruction or aspiration. Patients with SAH, intraparenchymal bleed, CVT, or recent seizure may have airway compromise due to poor GCS.  These patients may require interventions, such as manual opening of the airway with a head-tilt-chin lift or jaw thrust maneuver, insertion of an oropharyngeal or nasopharyngeal airway, or suctioning of secretions or vomitus from the airway.  Patients with GCS under 8 should be considered for supraglottic airway insertion or endotracheal intubation.  
  • Breathing: look for tachypnea or bradypnea, changes to oxygen saturation, and abnormal breath sounds. Intracranial bleeds or mass lesions may influence the central respiratory center, causing decreased, abnormal, or absent respirations [7]. Administer supplemental oxygen for hypoxia.  Consider oxygen via face mask, positive pressure bag valve mask ventilation, or intubation, based on respiratory effort, GCS, and concern for aspiration.  
  • Circulation: check the heart rate, blood pressure, peripheral and central pulses, and capillary refill time. Severe hypertension with headache and altered mentation should raise concern for intracranial bleeding [7]. Headache with severe hypertension in a pregnant patient should raise concern for pre-eclampsia or eclampsia. Fever with headache should raise concern for infectious conditions, like meningitis or encephalitis.  Intravenous antihypertensive medications should be initiated during this step if needed.  Monitor for bradycardia, hypertension, and abnormal breathing, which can indicate impending brain herniation from elevated intracranial pressure.
  • Disability: check pupillary size and reactivity, calculate a Glasgow coma score, and check a glucose level.  Perform a focused neurological examination with assessment of the cranial nerves, sensory and motor function, and cerebellar signs. Patients with complex migraine headaches may exhibit photophobia, diplopia, paresthesias, dysarthria, tinnitus, or vertigo. Patients with stroke, intraparenchymal bleeding, subarachnoid hemorrhage, CVT, carotid or vertebral artery dissection, intracranial space-occupying lesions, and encephalitis may present with focal neurological deficits and varying levels of GCS [7,8].
  • Exposure: Fully undress your patient and perform a head-to-toe examination. Any signs of head trauma, including headache, should raise suspicion for intracranial bleeding. Petechiae and purpura on the skin may point towards infective pathologies, like septicemia or meningococcal meningitis [13].

Medical History

A detailed history in a patient with headaches can provide clues to the cause. Ask your patient about the time of symptom onset, pain location, headache characteristics, and associated symptoms. Ask about past medical history, surgical history, relevant family history, and drug or alcohol use.

  • Time of onset: sudden onset symptoms may be seen in subarachnoid hemorrhage, ischemic or hemorrhagic strokes, or carotid artery dissection. Gradual onset of symptoms is more common in migraine, cluster headache, tension headache, headaches due to infective pathology, and CVT [5,6].
  • Site of headache: Most migraine and cluster headaches present with unilateral pain with cluster headache involving branches of the trigeminal nerve (around orbit). Tension headaches present more often as bilateral head pain.  Sinus headaches have pain behind the maxillary and frontal sinuses [5,6].
  • Characteristics and associated symptoms: Migraines are associated with auras, photophobia, phonophobia, blurred vision, lightheadedness, nausea, or vomiting [5]. Cluster headaches may have ipsilateral autonomic symptoms, such as ptosis, miosis, eye tearing, or facial swelling [5]. Tension headaches may present with tender areas on the scalp and neck [6]. Ask about associated symptoms for secondary headaches, like fever and neck stiffness (meningitis), vision changes (acute glaucoma, giant cell arteritis), new seizures, vomiting, or focal motor or sensory changes (space-occupying lesion, intracranial bleeding, CVT, etc.) [8-10,12].
  • Risk factors:
    • Intraparenchymal Bleeding: hypertension, smoking, alcohol abuse, anticoagulation medication usage, recent head trauma [3,7].
    • Subarachnoid Bleeding: hypertension, smoking, cocaine use, family history of brain aneurysms in close relatives, polycystic kidney disease, Marfan syndrome, Ehlers-Danlos syndrome [7].
    • Carotid Artery Dissection: recent neck trauma, recent neck torsion during sporting activities or medical treatments (e.g., chiropractic maneuvers) [11]
    • Cerebral Venous Thrombosis: pregnancy, recently postpartum, oral contraceptive use, hypercoagulable conditions (thrombophilias, antithrombin III, protein C and S deficiency, factor V Leiden mutation, antiphospholipid syndrome, malignancy), recent surgery [12].
    • Post Dural Puncture Headache: recent lumbar puncture

Physical Examination

Patients presenting with headache should undergo a thorough head-to-toe physical exam after the ABCDE assessment.  Special care should be taken in examining the head, ears, eyes, neck, and throat, as well as in performing a focused neurological exam.  The neurological exam should include calculating a Glasgow coma score, cranial nerve testing, assessment of motor and sensory deficits in the extremities, and assessment of gait and coordination. A full set of vitals, including a temperature and glucose level, should be taken.

When To Ask Your Senior for Help

If you are immediately concerned about a life-threatening condition, or if the patient needs any interventions during the ABCDE assessment, you should notify a supervising doctor.

Patient details that should trigger you to alert your senior:

  • Inability to talk or
  • Altered breathing pattern or use of accessory muscles of respiration
  • Severe hypertension, hypotension, or hypoxia
  • Asymmetric pupillary sizes 
  • Severe headache with acute onset
  • Signs of meningeal irritation or raised intracranial pressure

Not-To-Miss Diagnoses

Headaches have many causes. As an emergency medicine provider, it is important not to miss certain diagnoses that have a high rate of morbidity or mortality. Some diagnoses to always consider in the patient with headache are intraparenchymal bleeding, subarachnoid bleeding, giant cell arteritis, acute glaucoma, meningitis, encephalitis, cerebral vein thrombosis, carotid and vertebral artery dissection, brain malignancy, and pre-eclampsia.

Acing Diagnostic Testing

The investigations you order for your headache patient will depend on your history, physical exam, and top conditions on your differential diagnosis list.

Some investigations to consider in headache patients:

  • Glucose testing should be ordered in any patient with headache plus altered mental status, focal neurologic deficits, or seizures.
  • Urine pregnancy testing should be ordered for any female of child-bearing age presenting with headache.
  • ECG abnormalities in the form of arrhythmias and non-specific ST-T wave changes can be seen in patients with intracranial bleeding or space-occupying lesions
  • Complete blood count can help support infective etiologies if leukocytosis is present.
  • Serum chemistry is used to evaluate for any electrolyte abnormalities in patients with new seizures or vomiting.
  • ESR or CRP is considered if you are concerned about Giant cell arteritis [10]
  • HIV testing is considered based on the history and physical exam if there are clinical signs of immunocompromise
  • CT or MRI imaging is often unnecessary in a patient with a primary headache.  It should be ordered based on patient history and physical exam, particularly with concerns for SAH, intracranial bleeding, or a space-occupying lesion should have non-contrast CT brain imaging [7,8]. Patients with concerns for carotid or vertebral artery dissection should have a CT angiogram of the neck and head [11]. Patients with concerns for cerebral venous thrombosis should have an MR venogram or CT venogram [12].

Examples of CT images of patients with conditions that may present with headache are below.

Figure 1a
Figure 1b

Figure 1a (left) and Figure 1b (right): Subarachnoid bleed on CT brain without contrast.  Acute bleeding is demonstrated as a bright white (radio-opaque) substance.  The distribution of blood seen in Figure 1a is sometimes termed the “starfish of death.”

Figure 2 - Acute epidural bleed on CT brain without contrast. Note the biconvex shape that is characteristic of epidural hemorrhages.
Figure 3 - Acute subdural bleed on CT brain without contrast. Note the sickle shape that is characteristic of subdural hemorrhages.
Figure 4 - Acute intra-parenchymal bleed on CT brain without contrast. A white arrow identifies the bleed on the left-hand image. Note the midline shift on the right-hand image.
Figure 5 - Large brain mass. CT brain without contrast, sagittal cut.

Empiric and Symptomatic Treatment

Medications for symptom control should be considered for any patient with headache and other associated symptoms. Table 4 below lists some common medications to consider for migraine headaches.

Table 4- Medications for migraine headaches

Drug

Dose

Comments

Acetaminophen

500 – 1000 mg PO every 6hrs

Safe in pregnancy

Ibuprofen

600 -800 mg PO every 6hrs

Can cause GI upset

Avoid in pregnancy

Caution in patients with renal insufficiency

Ketorolac

15-30 mg IV or IM every 6hrs

Same as ibuprofen

Metoclopramide

10 mg IV or IM every 6hrs

Administer slowly to avoid extrapyramidal symptoms

Diphenhydramine

25-50 mg IV or IM every 6hrs

May cause drowsiness

Dihydroergotamine

1 mg IV or IM

Maximum 3mg/24hours

Contraindicated in pregnancy, uncontrolled HTN, or coronary artery disease 

Sumatriptan

6 mg SC injection x 1

(max 12mg SC/24hrs)

Same as Dihydroergotamine

Basic analgesics, like acetaminophen or NSAIDs, are first-line treatments for tension headaches [6]. High-flow oxygen therapy via a non-rebreather mask at 12-15 liters/min is the first-line treatment for cluster headaches [5].

Patients with signs and symptoms of elevated intracranial pressure (e.g., asymmetric pupil size, depressed GCS, vomiting, etc.), brain edema on CT imaging, or impending herniation on CT imaging should receive IV mannitol, IV 3% NaCl, or IV steroids, in consultation with a neurosurgical specialist [8]. High-dose IV steroids are also used in patients with giant cell arteritis [10].

There is no role for routine prophylactic antiepileptic medications in patients with headache and most types of intracranial bleeding.  However, antiepileptics, like Levetiracetam, are generally well tolerated and are sometimes recommended by neurosurgical specialists for seizure prevention.  For most patients with headache and seizure, IV benzodiazepines should be first-line for seizure treatment.  One exception is eclampsia, where IV magnesium is the preferred therapy.

Anticoagulation, such as IV unfractionated heparin, should be administered in patients with cerebral venous thrombosis and for extracranial carotid or vertebral artery dissection [11]. Patients presenting with headache and signs of ischemic stroke may be candidates for thrombolysis with IV Alteplase or Tenecteplase, depending on local resources and the time since symptom onset. IV antibiotics should be administered empirically for patients with headache with suspected meningitis or encephalitis [3,9].

Procedures

Lumbar Puncture [14]

  • Indications for the procedure: CSF collection with a lumbar puncture can help to evaluate for a CNS infection, such as meningitis. This procedure can also assist in assessing for subarachnoid hemorrhage. CT head is highly sensitive in detecting SAH in the first 6 hours after headache onset, but the sensitivity diminishes beyond hour 6.  A lumbar puncture can be considered in a patient with deep clinical concern for SAH and a negative CT scan with symptoms over 6 hours [7].
  • Contraindications: Raised intracranial pressure (e.g., brain mass or intracranial bleeding with midline shift on CT), coagulopathy, or trauma or infection at the site of needle insertion
  • Complications: Bleeding, infection, post-dural puncture headache, pain during the procedure

Before the procedure:

  1. Explain the procedure, obtain consent, and gather materials (Figure 6) to maintain aseptic precautions.
  2. Place the patient in the lateral decubitus or seated position.
  3. Identify the highest points of iliac crests bilaterally.

The equipment needed for a lumbar puncture procedure includes a sterile lumbar puncture tray, which typically contains a spinal needle with stylet (commonly 20G–22G), local anesthetic (e.g., lidocaine), antiseptic solution (e.g., povidone-iodine or chlorhexidine), sterile gloves, drapes, and gauze. Additionally, a manometer with tubing is required for measuring cerebrospinal fluid (CSF) pressure, along with collection tubes for CSF sampling. Optional items may include a face mask, eye protection, and an assistant for patient positioning and monitoring.

Figure 6 – Equipment for a Lumbar Puncture

To identify the L4 interspace for a lumbar puncture (Figure 7), start by positioning the patient appropriately—either sitting and leaning forward or lying in the lateral decubitus position with knees drawn to the chest and the back flexed to maximize exposure of the vertebral spaces. Palpate the iliac crests on both sides, noting their highest points. Draw an imaginary line connecting these points, known as the intercristal or Tuffier’s line, which usually crosses the spinous process of the L4 vertebra. The L4-L5 interspace is located just below this line. Confirm the space by palpating the spinous processes to ensure accurate identification before proceeding.

Figure 7 – Landmark of L4 Space

This level corresponds to L4-L5 intervertebral space where the spinal needle should be inserted.  Instruct the patient to arch their spine posteriorly to open the interspinous spaces. Clean and drape the area. Administer local anesthesia to the planned site of the procedure. Prepare four marked containers to collect the CSF.  Using aseptic technique, advance the spinal needle at the L4-L5 interspace until a popping sensation is felt and CSF drips from the spinal needle. Measure CSF opening pressure by connecting a manometer as soon as fluid appears and note the reading. Collect about 1 mL of CSF in all 4 marked containers in a consecutive fashion (Figure 8). Once sufficient CSF is collected, place the stylet back in the needle, remove the spinal needle, and cover the site with gauze or a Band-Aid.  Send the CSF to the laboratory for analysis, re-evaluate your patient, and provide advice regarding puncture headache [14].

Figure 8 – Collection of CSF in serial numbered containers (tubes)

The chart below describes how CSF is interpreted by the clinician once it is analyzed by the laboratory.

Table 5 – CSF interpretation [15]

 

Normal

Bacterial Meningitis

Viral Meningitis

Subarachnoid Hemorrhage

Opening pressure (mmHg)

7-18

>30

Normal

Increased

Appearance

Clear, colorless

Turbid

Clear

Xanthochromia present

Protein (mg/dl)

23-38

Increased

Normal to decreased

Increased

Glucose

2/3rd of serum glucose

Decreased

Normal

Normal

Gram stain

Negative

Positive

Negative

Negative

WBC count

<5 cells

Predominantly neutrophils

Predominantly lymphocytes

May be increased due to bleeding

Special Patient Groups

Pregnant Patients

Pregnant patients with headache are at increased risk for some diagnoses more than nonpregnant women due to pregnancy being a hypercoagulable state. Pregnant patients with headaches are unable to receive all the same medications as nonpregnant patients. Headache medications that are safe in pregnancy are paracetamol, metoclopramide, diphenhydramine, magnesium, and opioids for severe pain. Drugs to avoid during pregnancy include ergotamine, NSAIDS, valproate, lithium, and topiramate [16]. Specific causes of headache to consider in pregnancy are pre-eclampsia, eclampsia, cerebral venous thrombosis, and stroke. Treatment of headache should primarily focus on the cause [16].

Children

Headache is a common cause of ED visits in the pediatric population [17]. The causes of headaches in the pediatric population range from more benign primary headache etiologies to more secondary severe etiologies. CT imaging should be limited to cases where more serious signs and symptoms are present, such as change in behavior, confusion, unexplained vomiting, unexplained high fevers, head trauma, or focal neurologic deficits [17]. Medications for pediatric headaches are weight-based in their dosing. The standard pediatric dose for ibuprofen is 10 mg per kilogram (mg/kg) of body weight per dose. This dosage can be administered every 6 to 8 hours as needed, with a maximum of three doses in a 24-hour period. It’s important not to exceed a total daily dose of 40 mg/kg or 1,200 mg, whichever is less. For acetaminophen, the recommended pediatric dose ranges from 10 to 15 mg/kg per dose. This can be given every 4 to 6 hours as needed, with a maximum of five doses in 24 hours. The total daily dose should not exceed 75 mg/kg or 3,000 mg, whichever is less.

Elderly

Elderly patients experiencing headaches may have additional health conditions that raise the risk of serious underlying causes, such as a history of hypertension, cancer, previous brain surgeries, stroke, or the use of anticoagulant medications. When evaluating and treating these patients, it’s important to tailor your approach based on the suspected diagnosis. However, it is advisable to have a lower threshold for ordering diagnostic tests in elderly patients with unexplained headaches.

When To Admit

Primary headache disorders, like migraine, cluster headache and tension headaches, do not require admission and should be treated symptomatically in the ER.  Upon discharge, these patients should be advised to have adequate sleep, stay hydrated, consume regular meals, and avoid any headache triggers. Patients with a headache secondary to a dangerous etiology, such as meningitis or intracranial bleeding, should be admitted for further treatment and monitoring. Patients with red flag signs or symptoms of a dangerous etiology should also be admitted for further management, even without a confirmed diagnosis.

Revisiting Our Patient

You return to your 60-year-old male patient with sudden onset headache and right-sided weakness.  You note his severe hypertension, hypoxemia, right-sided motor deficits, and low GCS.

You follow your ABCDE approach to be sure not to miss any critical steps in management.

  • Airway: This patient has a depressed mental status and no gag reflex. You notice some secretions in his airway and prepare for intubation.
  • Breathing: His lungs are bilaterally clear and equal. After his airway is suctioned, you apply supplemental oxygen via a non-rebreather mask.

After the patient is intubated, you continue your assessment.

  • Circulation: The patient continues to be hypertensive to 210/120 mmHg after intubation. You administer IV labetalol 10mg and begin a fentanyl infusion for sedation.
  • Disability: The glucose is 198mg/dL. Your initial brief exam demonstrated right-sided motor deficits and normal mid-sized pupils.
  • Exposure: There are no physical signs of trauma or rashes on the exam

Once the patient is stabilized, he receives a CT head without contrast, showing an acute subarachnoid bleed.  Basic pre-operative laboratory tests are drawn and you contact the neurosurgeon on call.  The neurosurgery team recommends strict blood pressure control and admission to the ICU for operative management.  You explain the diagnosis and plan of care to the patient’s family with understanding and agreement.

Author

Picture of Shailaja Sampangi Ramaiah

Shailaja Sampangi Ramaiah

Dr. Shailaja Sampangi Ramaiah is a Professor and Head of Emergency Medicine at Father Muller Medical College, Mangalore, India. With advanced qualifications in anesthesia and medical education, she is a FAIMER fellow and ACME-certified educator. Dr. Shailaja leads initiatives in simulation training and clinical quality improvement and is a life member of several prestigious medical associations. She is passionate about advancing emergency care education.

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References

  1. Locker T, Mason S, Rigby A. Headache management–are we doing enough? An observational study of patients presenting with headache to the emergency department. Emerg Med J. 2004;21(3):327-332. doi:10.1136/emj.2003.012351
  2. GBD 2015 Disease and Injury Incidence and Prevalence Collaborators. Global, regional, and national incidence, prevalence, and years lived with disability for 310 diseases and injuries, 1990-2015: a systematic analysis for the Global Burden of Disease Study 2015 [published correction appears in Lancet. 2017 Jan 7;389(10064):e1]. Lancet. 2016;388(10053):1545-1602. doi:10.1016/S0140-6736(16)31678-6
  3. Thomas K, Benjamin W.F, Rosen’s emergency medicine: concepts and clinical practice: St. Louis, Mosby; 2002. Chapter 93, Headache disorders; p.1265-77.
  4. Do TP, Remmers A, Schytz HW, et al. Red and orange flags for secondary headaches in clinical practice: SNNOOP10 list. Neurology. 2019;92(3):134-144. doi:10.1212/WNL.0000000000006697
  5. Leone, Massimo and Paola Di Fiore (2014), “Migraine and Cluster Headache.”
  6. Millea, Paul J. and Jonathan J. Brodie (2002), “Tension-Type Headache,” American Family Physician.
  7. Vivancos J, Gilo F, Frutos R, et al. Clinical management guidelines for subarachnoid haemorrhage. Diagnosis and treatment. Neurologia. 2014;29(6):353-370. doi:10.1016/j.nrl.2012.07.009
  8. Alentorn, Agusti, Khê Hoang-Xuan, and Tom Mikkelsen (2016), “Presenting signs and symptoms in brain tumors.”
  9. Siddiqui, Emaduddin (2012), “Neurologic Complications of Bacterial Meningitis.”
  10. Smith, Jonathan H. and Jerry W. Swanson (2014), “Giant Cell Arteritis,” Headache.
  11. Sheikh, Huma U. (2016), “Headache in Intracranial and Cervical Artery Dissections,” Current Pain and Headache Reports.
  12. Mehta, Amit, Julius Danesh, and Deena E. Kuruvilla (2019), “Cerebral Venous Thrombosis Headache,” Current Pain and Headache Reports.
  13. Bollero, Daniele, Maurizio Stella, Ezio Nicola Gangemi, L. Spaziante, J. Nuzzo, G. Sigaudo, and F. Enrichens (2010), “Purpura fulminans in meningococcal septicaemia in an adult: a case report,” Annals of burns and fire disasters.
  14. Niemantsverdriet, Ellis, Hanne Struyfs, Flora H. Duits, Charlotte E. Teunissen, and Sebastiaan Engelborghs (2015), “Techniques, Contraindications, and Complications of CSF Collection Procedures.”
  15. Gomez-Beldarrain, Marian and Juan Carlos Garcia-Monco (2014), “Lumbar Puncture and CSF Analysis and Interpretation.”
  16. Negro A, Delaruelle Z, Ivanova TA, et al. Headache and pregnancy: a systematic review. J Headache Pain. 2017;18(1):106. Published 2017 Oct 19. doi:10.1186/s10194-017-0816-0
  17. Raucci U, Della Vecchia N, Ossella C, et al. Management of Childhood Headache in the Emergency Department. Review of the Literature. Front Neurol. 2019;10:886. Published 2019 Aug 23. doi:10.3389/fneur.2019.00886
  18. Reinisch, Veronika M., Christoph J. Schankin, J. Felbinger, P. Sostak, and Andreas Straube (2008), “Headache in the elderly,” Schmerz.

Reviewed and Edited By

Picture of Joseph Ciano, DO, MPH, MS

Joseph Ciano, DO, MPH, MS

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

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

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

Mechanical Ventilation (2024)

~ iEM Education Project Team ~ Leave a comment

by Elham Pishbin, Hamidreza Reihani

Authors
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You have a new patient!

A 70-year-old male with a history of severe chronic obstructive pulmonary disease (COPD) presents to the emergency department (ED) with complaint of progressive dyspnea and productive cough. Vital signs are as follows: PR=108/min, RR=46/min, BP=130/90 mm Hg, T=37.8°C (axillary), SpO2=76% (with 5 L/min O2with nasal cannula). He is awake but confused. You request a blood gas test and initiate standard medical treatment for COPD exacerbation (Nebulized short-acting beta-agonists, antibiotics, and systemic glucocorticoids). You are concerned about the patient’s respiratory status and prepare for the possibility that he may need additional respiratory support in the emergency department.

Introduction

Mechanical ventilation (MV) is often essential to successfully managing critically ill patients. Patients may require MV because of respiratory failure, airway protection, or as part of the management of their illness to support their respiratory function and to reduce the work of breathing. Emergency physicians should have a solid understanding of mechanical ventilation and its indications, modes, and troubleshooting. Here, we provide a simplified guide to managing MV in the emergency department (ED) setting.

Physics of MV

MV involves pumping air with a positive pressure into the patient’s lungs and allowing the patient to exhale the air spontaneously.  The aim is to deliver oxygen to the lungs, keep the distal airways open for oxygen exchange, and allow carbon dioxide release upon exhalation. The ventilator uses pressurized air to overcome the resistance of ventilator tubing, the endotracheal tube (ETT), and airways. When the resistance to airflow increases or lung compliance decreases (lung compliance is inversely related to the elastic recoil of the lungs), higher pressure is required to inflate the lung [1, 2]. Common causes of high resistance are obstruction of the ETT by tube biting or a mucus plug, airway secretions, and bronchospasm. Common causes of poor compliance are pneumothorax, alveolar oedema, right main stem intubation, and air trapping [2].

Exhalation occurs passively due to pressure differences between the alveoli (higher pressure) and the ventilator (lower pressure). Notably, ventilators can administer a positive end-expiratory pressure (PEEP) to decrease this pressure gradient, thereby preventing the lungs from excessive collapse [2].

Control Variables and Ventilator Modes

The control variables on a ventilator determine how to pump the air (the air volume, the time over which the air is delivered, the frequency of delivering the air over a minute, and the speed at which the air travels). The alarms and monitors show whether the controls we set are appropriate and how the lungs respond [3]. 
After a patient is intubated and connected to a ventilator, the ventilator mode and settings should be established.  First, specify volume-controlled ventilation (VC) or pressure-controlled ventilation (PC) [1].

VC ventilation

VC ventilation is the most familiar and the most commonly used of MV modes in the ED [4].

The key parameters which should be set on the ventilator include [2]:

  1. Tidal volume (Vt): the amount of air pumped into the patient in each breath (measured in milliliters)
  2. Respiratory rate (RR)
  3. Fraction of inspired oxygen (FiO2)
  4. Positive end-expiratory pressure (PEEP): the baseline airway pressure at the end of expiratory. PEEP stents open the distal airways for gas exchange.
  5. Flow rate*: the speed at which Vt is pumped through the circuit (measured in liters per minute)
  6. Inspiratory time (Ti) *: the time (in seconds) over which the ventilator pumps the Vt

(*These parameters are often automatically set, but this depends on the ventilator)

In VC ventilation, pressure cannot be set as it depends on airway resistance and lung compliance. Increased airway resistance or worsened lung compliance will increase pressures in the airways, increasing the risk of barotrauma. Barotrauma due to elevated pressures is one disadvantage to VC. The advantage of VC ventilation is that the VT is guaranteed, and minute ventilation is stable.

PC ventilation

PC ventilation applies constant inspiratory pressure throughout inspiration, whether the ventilator or the patient triggers the breath [2]. In PC ventilation, the Vt cannot be set directly, so the operator sets the inspiratory pressure instead of Vt. Flow rate and Vt are dependent variables in PC ventilation. This is a disadvantage of PC ventilation since increased resistance or decreased compliance will lead to smaller Vt delivery, diminished ventilation, and carbon dioxide retention. Other key parameters, like Vt, PEEP, RR, and FiO2, are the same as VC ventilation. The advantage of PC ventilation is that airway and pulmonary pressures are set at the inspiratory pressures, preventing barotrauma. In addition, the patients can regulate their inspiratory flow rate and increase it according to their inspiratory efforts. This improves patient-ventilator synchrony [2].

A ventilator mode is a specific setting on the ventilator that determines how the ventilator assists the patient by giving a breath. It also defines the amount of respiratory support that the ventilator provides for the patient [5].

It is important to note that each ventilator mode has advantages and disadvantages.  There is no perfect ventilation mode that fits all patients. The best mode is the mode with which you and your team are most familiar [2].

Two primary ventilator modes that are most commonly used in the ED are Assist/Control Ventilation (ACV) Mode and Synchronous Intermittent Mandatory Ventilation (SIMV) Mode [4].

Assist/Control ventilation (ACV)

This mode is designed to offer full respiratory support for patients with minimal or no spontaneous breathing by delivering a preset number of mandatory breaths. However, if the patient tries to breathe, the ventilator will also assist that breath [5]. The patient will always receive at least the preset number of breaths (regardless of his/her respiratory effort). In this regard, ACV is the most appropriate initial mode in ED patients who are initially paralyzed and sedated [1].

ACV can be set as either volume-control or pressure-control. In VC/ACV, we set these parameters: Vt, flow rate, basal respiratory rate, and sensitivity to the patient’s respiratory effort (trigger). We can adjust the sensitivity control to make it easier or harder for the patient to trigger an assisted breath from the ventilator.
In PC/ACV, instead of Vt, we set the Ti.  In this mode, Vt is dependent on the patient’s lung compliance and airway pressure. The advantage is avoiding barotrauma, but the disadvantage is that a specific preset Vt cannot be guaranteed [4].

To ensure ventilator synchronization, a breath initiated by the patient takes precedence over a preset breath. If the ventilator is programmed to deliver 12 breaths per minute, it will provide a breath every five seconds in the absence of spontaneous breathing. However, if the patient makes a spontaneous effort, the ventilator will provide an extra breath and reset the timer for another five seconds. The main challenge is that patient-initiated breaths are not proportional to his effort. When the patient makes an inspiratory effort, the ventilator provides a full Vt, which can lead to hyperventilation and poor patient-ventilator synchronization. Adequate sedation is necessary to prevent spontaneous breathing efforts when a patient is ventilated in the ACV mode. [1].

Synchronous Intermittent Mandatory Ventilation (SIMV)

This mode offers intermittent ventilatory support to patients by delivering mandatory breaths and supporting spontaneous breaths. Mandatory breaths are delivered at a preset rate. The ventilator delivers at least a preset number of mandatory breaths to the patient, similar to ACV. Patients with no respiratory effort, will receive the preset number of breaths. Patients with spontaneous breathing at a lower rate than the ventilator preset rate will receive the preset number of breaths with full Vt. In these two scenarios, SIMV is very similar to ACV. However, if a patient has spontaneous breathing at a rate higher than the preset respiratory rate, additional respiratory effort beyond the preset rate will only be partially supported proportional to the patient’s respiratory effort. This makes SIMV an appropriate mode for less sedated patients with some degree of spontaneous breathing [1].

Pressure Support Ventilation (PSV)

In this mode, the ventilator assists the patient’s spontaneous breaths during the inspiratory phase of breathing. It is often used to help the patient overcome the airway resistance caused by the endotracheal tube and the ventilator circuit. The patient should be alert or on light sedation and able to follow commands. When the patient triggers a breath, the ventilator supports it by adding pressure to facilitate breathing. The operator sets the FiO2, PEEP, and inspiratory pressure on the ventilator based on how much support the patient needs to receive. In PSV, RR, Ti, and flow rate are determined by the patient. The higher the pressure support, the easier it will be for the patient to take a breath. The ventilator supports inspiration until the inspiratory flow falls below a preset measure [2,6].

When choosing PSV, it is also necessary to set an appropriate backup mode (for example, SIMV) and ventilator alarms [6].

Typical initial ventilator settings: Although required settings depend on whether PC or VC ventilation is selected, the principles are similar in both modes [1]. Typical initial ventilator settings include the following: [1,2,4]

  1. Tidal volume (Vt): a Vt of 6 to 8 mL/kg of estimated ideal body weight (IBW) is appropriate for most patients. The inspiratory pressure should be set in PC ventilation to achieve these Vt targets. Ongoing patient assessment is necessary to avoid excessive Vt. Regardless of VC or PC, initial pressure targets should not exceed 30 cm H2O.
  2. Respiratory rate: a rate of 12 to 18 breaths per minute would be reasonable for most patients and provide adequate ventilation. In special situations, such as patients with severe metabolic acidosis, the respiratory rate should be increased to match pre-intubation minute ventilation.
  3. FiO2: initially should be set at 100%, then lowered to target a SpO2 of 92% – 96% (PaO2 of 60 to 100 mmHg)
  4. PEEP: is routinely set initially at 5 cm H2O, but it can be set at 4 to 20 cm H2O
  5. I/E time ratio: The ratio of inspiratory time to expiratory time. It is commonly set as a ratio of 1:2. In some modes, it is automatically set based on other parameters. In some other modes, it needs to be set by the operator.
  6. Flow rate: is typically set at 60 L/min. (Vt will be delivered at the speed of 60 L/min). Increasing the flow rate will deliver the set Vt faster, reducing the inspiratory time. (It is found in VC modes)
  7. The trigger is a preset change in pressure or flow detected by the ventilator as the patient tries to initiate a breath, and the ventilator supports that breath. It should be set at a level that enables the patient to trigger the ventilator without great effort. For most patients, pressure sensitivity trigger from -0.5 to -2 cm H2O is effective and safe. The 1–3 L/min threshold is appropriate for the flow trigger setting.

When choosing a ventilator mode and parameters, it is essential to ensure adequate ventilation, but it is also important to ensure that the pressure in the ventilator circuit (including the lung) is appropriate [1]. Some important pressures are:

  • Peak inspiratory pressure (PIP) is the maximum pressure during inspiration. It is a dynamic pressure measured during the inspiration, so it incorporates airflow and reflects the resistance to airflow. It is also reflective of dynamic compliance of the entire respiratory system. Decreasing compliance or increasing resistance to airflow will increase PIP. It can never be lower than P. plat [4].
  • Plateau pressure (P. plat) is a static pressure that can be measured at the end of inspiration with a short breath-hold (Figure 1). The goal is to be less than 30 cm H2O. Decreasing the compliance will increase P. plat. Decreasing the Vt will decrease P. plat [4]
Figure.1: Airway pressure-time curve demonstrating PEEP, PIP, Pplat (Provided by the authors)
  • Positive End-Expiratory Pressure (PEEP) is the airway pressure at the end of expiration. It helps to keep the smaller airways and the alveoli open, prevents atelectasis, and improves oxygenation. Increased levels of PEEP may lead to lung injury. Additionally, high PEEP can depress cardiac output and lead to hemodynamic compromise [1,4]. When talking about PEEP, most authors mean extrinsic PEEP (PEEPe). In this chapter, when we use PEEP, we refer to PEEPe.
  • Intrinsic PEEP or auto-PEEP (PEEPi) results from air trapping in the airways. It occurs due to increased expiratory resistance (e.g., bronchospasm, kinked ETT), impaired elastic recoil (e.g., emphysema), and increased minute ventilation (inadequate expiratory time). PEEPi can lead to hemodynamic instability similar to high levels of PEEP [2,4].

Noninvasive ventilation (NIV)

NIV provides continuous positive pressure throughout the breathing cycle via a tight-fitting mask (nasal, oro-nasal, or full-face mask, as shown in Figure 2) rather than an endotracheal tube [7].

Figure.2: NIV masks: A, B: Oro-nasal mask, C: Nasal mask, D: Full face mask (provided by authors)

No mandatory breath is given by the ventilator so the patient must have spontaneous breathing. The ventilator provides a preset level of pressure when the patient initiates a breath, but inspiratory flow and Ti are completely patient-dependent [4,7]NIPPV can be delivered as continuous positive airway pressure (CPAP) or bi-level positive airway pressure (BiPAP).

CPAP provides constant positive pressure throughout the entire respiratory cycle. Its main effect is applying positive pressure at the end of expiration and exerts a minimal effect on inspiration [4,7].

BiPAP supplies a positive airway pressure during inspiration (IPAP) and a lower positive airway pressure during expiration (EPAP) [4].

IPAP provides pressure support and decreases the patient’s work of breathing. Increasing the IPAP will improve tidal volume and minute ventilation, thereby helping to eliminate CO2 from the alveoli.

EPAP acts similar to PEEP and improves alveolar recruitment and oxygenation by maintaining positive pressure at the end of expiration. EPAP prevents the lung from being fully deflated at the end of expiration, aiding in oxygen exchange across the alveolar-capillary membrane. Therefore, when you need to improve oxygenation, you should increase the EPAP.

The difference between the IPAP and EPAP is called delta pressure. The delta pressure is the same as pressure support in invasive ventilation. When the difference between the IPAP and EPAP is larger, the patient is able to have a larger tidal volume. Therefore, when you need to increase the clearance of CO2, you need to increase the delta pressure. [1,7].

Contraindications to NIV are patients who are uncooperative, hemodynamically unstable, lack protective airway reflexes, lack good respiratory effort, or have maxillofacial trauma. [7,8]

Initial NIV Settings

Initial settings depend on the amount of support that the patient requires, patient comfort, and patient cooperation.

BiPAP usually is initiated at 10 cm H2O for IPAP and 5 cm H2O for EPAP. Based on the patient’s clinical response, these parameters can be titrated later by 1 to 2 cm H2O at a time. However, the maximum pressure for IPAP should not exceed 20 cm H2O because this may lead to barotrauma [8,9].

Typical initiated settings for CPAP are 5 to 15 cm H2O [4,7].

Ventilator Troubleshooting

Patient-ventilator dys-synchrony refers to patients who develop respiratory distress after undergoing mechanical ventilation [10]. Emergency physicians must be familiar with patient-ventilator interactions so that life-threatening complications of mechanical ventilation can be promptly identified and managed [11]. In Figure 3, we present a systematic approach to detect life-threatening conditions in patients who suddenly deteriorate and become hemodynamically unstable (profound hypotension or cardiac arrest) under mechanical ventilation [1, 10].

Figure-3: Evaluation of respiratory distress in hemodynamically unstable mechanically ventilated patients (Provided by authors)

Revisiting Your Patient

After 30 minutes, you reevaluate your patient. The patient remains in respiratory distress with SpO2 of 79%, despite nebulized beta-agonists, steroids, antibiotics, and the use of 7 L/min O2 via face mask. The patient’s blood gas reveals a pH of 7.22, PCO2 of 80 mm Hg, and PaO2 of 55 mmHg. You decide to put him on NIV using an oro-nasal mask. You choose BiPAP mode and set IPAP=12 cm H2O, EPAP=7 cm H20, and FIO2= 90%.  After 5 minutes, the patient becomes agitated on the NIV mask, even with verbal direction and support. The pulse oximeter remains low at a SpO2 of 85%.

What would be the next appropriate step in the management of this patient?

You recognize your patient has not sufficiently improved despite maximal medical therapies. You decide to prepare for intubation and mechanical ventilation. The patient is fully sedated, paralyzed, and intubated using RSI (rapid sequence intubation). You prepare to choose a ventilation mode and set the parameters on your ventilator.

Which mode of ventilation and control parameters are most ideal for your patient?

The patient is sedated and paralyzed during RSI, so the VC/ACV mode is the best choice. Your senior says, “The best mode is the mode most familiar to you.”  No data suggest the advantage of PC over VC (or vice versa) in patients with COPD. You review your goals in MV of your COPD patient: improve oxygenation and ventilation, minimize PEEPi, and prevent barotrauma. 

You set the ventilator as:

  • Mode: ACV (VC/ACV)
  • FiO2= 100%
  • Vt= 500 cc
  • Respiratory rate= 14
  • PEEP= 5cm H2O
  • I/E: 1/4

You base your tidal volume on the patient’s 170 cm height and weight of 90 kg. You set the I/E ratio at 1:4 to optimize a longer expiratory time and titrate the FiO2 until the SpO2 falls between 88% to 92% [12]. A chest X-ray confirms the tip of the endotracheal tube is located above the carina.  The patient is admitted to the medical ICU for further management and treatment.

Authors

Picture of Elham Pishbin

Elham Pishbin

Elham Pishbin is a full-time associate professor of emergency medicine (EM) with 16 years of experience as a faculty member of the department of EM at Imam Reza Hospital, affiliated with Mashhad University of Medical Sciences, Mashhad, Iran. She is a member of the Iranian national board of EM and contributed to establishing the first EM residency program at Mashhad University of Medical Sciences in 2008, the fifth EM residency program in Iran, and a significant milestone in the development of EM in the country.

Picture of Hamidreza Reihani

Hamidreza Reihani

Dr. Hamidreza Reihani, a professor of emergency medicine at Mashhad University of Medical Sciences in Iran, is also a member of the national board of emergency medicine. He holds fellowships in medical education, research, and clinical informatics. With 15 years of experience in emergency medicine, he has made significant contributions, including founding an academic Emergency Department (ED) at his university and educating over 100 specialists in the field. Dr. Reihani has also been actively involved in interdisciplinary and undergraduate education, research (with more than 60 published articles), peer review, and editorial roles for two academic journals. His expertise and dedication are reflected in his contributions to both the previous and current editions of this book.

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References

  1. Seigel T.A, Johnson N.J. Mechanical ventilation and noninvasive ventilatory support. In: Walls R.M, ed. Rosen’s emergency medicine: concepts and clinical practice. 10th ed. Philadelphia PA: Elsevier; 2023:24-33
  2. Ward J, Noel C. Basic Modes of Mechanical Ventilation. Emerg. Med. Clin. N. Am. 2022;40(3):473-88
  3. Gomersall C, Joynt G, Cheng C, et al. Basic Assessment and Support in Intensive Care. Hong Kong: Chinese University of Hong Kong; 2013:37-54.
  4. Santanilla J.I. Mechanical Ventilation. In Roberts J.R, Hedges J.R, eds. Roberts and Hedges’ clinical procedures in emergency medicine and Acute Care. 7th ed. Philadelphia PA: Elsevier; 2018:152-172.
  5. Hickey S, Giwa A. Mechanical ventilation. StatPearls. 2023 Jan 26.
  6. Abramovitz A, Sung S. Pressure Support Ventilation. StatPearls. 2022. Sep 18.
  7. Gill HS, Marcolini EG. Noninvasive mechanical ventilation. Emerg. Med. Clin. N. Am. 2022;40(3):603-13.
  8. Carlson J.N, Wang H.E. Noninvasive Airway Management. In: Tintinalli J.E, ed. Tintinalli’s emergency medicine: a comprehensive study guide, 9th ed. McGraw Hill Education; 2020: 178-183.
  9. Baker DJ, Baker DJ. Basic Principles of Mechanical Ventilation. Artificial Ventilation: A Basic Clinical Guide. 2020:113-37.
  10. Keith RL, Pierson DJ. Complications of mechanical ventilation: a bedside approach. Clinics in chest medicine. 1996 Sep 1;17(3):439-51.
  11. Gilstrap D, MacIntyre N. Patient–ventilator interactions. Implications for clinical management. American journal of respiratory and critical care medicine. 2013 Nov 1;188(9):1058-68.
  12. Atchinson P.R, Roginski M.A. Chronic obstructive pulmonary disease. In: Walls R.M, ed. Rosen’s emergency medicine: concepts and clinical practice. 10th ed. Philadelphia PA: Elsevier; 2023:806-815

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Picture of Joseph Ciano, DO, MPH, MS

Joseph Ciano, DO, MPH, MS

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

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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.

Tachyarrhythmias (2024)

~ iEM Education Project Team ~ Leave a comment

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

Authors
Listen

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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  8. Orejarena LA, Vidaillet H Jr, DeStefano F, et al. Paroxysmal supraventricular tachycardia in the general population. J Am Coll Cardiol. 1998;31(1):150-157. doi:10.1016/s0735-1097(97)00422-1
  9. George SA, Faye NR, Murillo-Berlioz A, Lee KB, Trachiotis GD, Efimov IR. At the Atrioventricular Crossroads: Dual Pathway Electrophysiology in the Atrioventricular Node and its Underlying Heterogeneities. Arrhythm Electrophysiol Rev. 2017;6(4):179-185. doi:10.15420/aer.2017.30.1
  10. Chhabra L, Goyal A, Benham MD. Wolff Parkinson White Syndrome. [Updated 2023 Jan 28]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK554437/
  11. Liwanag M, Willoughby C. Atrial Tachycardia. [Updated 2022 Jun 27]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK542235/
  12. Hafeez Y, Grossman SA. Junctional Rhythm. [Updated 2023 Feb 5]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK507715/
  13. Srinivasan NT, Schilling RJ. Sudden Cardiac Death and Arrhythmias. Arrhythm Electrophysiol Rev. 2018;7(2):111-117. doi:10.15420/aer.2018:15:2
  14. Tsao CW, Aday AW, Almarzooq ZI, et al. Heart Disease and Stroke Statistics-2022 Update: A Report From the American Heart Association [published correction appears in Circulation. 2022 Sep 6;146(10):e141]. Circulation. 2022;145(8):e153-e639. doi:10.1161/CIR.0000000000001052
  15. Keller SP, Halperin HR. Cardiac arrest: the changing incidence of ventricular fibrillation. Curr Treat Options Cardiovasc Med. 2015;17(7):392. doi:10.1007/s11936-015-0392-z
  16. Yetkin E, Ozturk S, Cuglan B, Turhan H. Clinical presentation of paroxysmal supraventricular tachycardia: evaluation of usual and unusual symptoms. Cardiovasc Endocrinol Metab. 2020;9(4):153-158. doi:10.1097/XCE.0000000000000208
  17. Maupain C, Bougouin W, Lamhaut L, et al. The CAHP (Cardiac Arrest Hospital Prognosis) score: a tool for risk stratification after out-of-hospital cardiac arrest. Eur Heart J. 2016;37(42):3222-3228. doi:10.1093/eurheartj/ehv556
  18. Banerjee, A., & Oliver, C. (2017). Revision notes for the FRCEM intermediate SAQ paper (2nd). Oxford University Press.
  19. Churpek MM, Yuen TC, Park SY, Meltzer DO, Hall JB, Edelson DP. Derivation of a cardiac arrest prediction model using ward vital signs. Crit Care Med. 2012;40(7):2102-2108. doi:10.1097/CCM.0b013e318250aa5a
  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.
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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
Listen

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

  1. Mowla SJ, Sapiano MRP, Jones JM, Berger JJ, Basavaraju SV. Supplemental findings of the 2019 National Blood Collection and Utilization Survey. Transfusion. 2021;61 Suppl 2(Suppl 2):S11-S35. doi:10.1111/trf.16606
  2. Kumar TA, Geet A. Blood transfusion therapy and related complication. In: Richhariya D, ed. Textbook of Emergency Medicine including intensive care and trauma. New Delhi: Jaypee brothers medical publishers; 2022: 990
  3. Gelaw Y, Woldu B, Melku M. Proportion of Acute Transfusion Reaction and Associated Factors Among Adult Transfused Patients at Felege Hiwot Compressive Referral Hospital, Bahir Dar, Northwest Ethiopia: A Cross-Sectional Study. J Blood Med. 2020;11:227-236. Published 2020 Jun 30. doi:10.2147/JBM.S250653
  4. Kracalik I, Mowla S, Basavaraju SV, Sapiano MRP. Transfusion-related adverse reactions: Data from the National Healthcare Safety Network Hemovigilance Module – United States, 2013-2018. Transfusion. 2021;61(5):1424-1434. doi:10.1111/trf.16362
  5. Dean L. The ABO Blood Group. In: internet, ed. Blood Groups and Cell Antigens. Bethesda MD: National Center for Biotechnology Information (US); 2005: 25-31
  6. Dean L. The ABO Blood Group. In: internet, ed. Blood Groups and Cell Antigens. Bethesda MD: National Center for Biotechnology Information (US); 2005: 39-44
  7. Goel R, Tobian AAR, Shaz BH. Noninfectious transfusion-associated adverse events and their mitigation strategies. Blood. 2019;133(17):1831-1839. doi:10.1182/blood-2018-10-833988
  8. Shmookler AD, Flanagan MB. Educational Case: Febrile Nonhemolytic Transfusion Reaction. Acad Pathol. 2020;7:2374289520934097. Published 2020 Jul 14. doi:10.1177/2374289520934097
  9. Division of healthcare quality promotion. National healthcare safety network biovigilance component hemovigilance module surveillance protocol. Atlanta, GA: Center of disease control and prevention; February 2023: 9-22
  10. Tobian A. Immunologic transfusion reactions. UpToDate. https://www-uptodate-com.eu1.proxy.openathens.net/contents/immunologic-transfusion-reactions?search=anaphylaxis%20transfusion&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1 . Updated on Sep 06, 2022. Accessed on March 15, 2023.
  11. Fiorellino J, Elahie AL, Warkentin TE. Acute haemolysis, DIC and renal failure after transfusion of uncross-matched blood during trauma resuscitation: illustrative case and literature review. Transfus Med. 2018;28(4):319-325. doi:10.1111/tme.12513
  12. San Miguel C. & Kaide C. Blood and Blood Components. In: Walls R., ed. Rosen’s Emergency Medicine: Concepts and Clinical Practice. Philadelphia, PA: Elsevier; 2023: 1452-1561
  13. Panch SR, Montemayor-Garcia C, Klein HG. Hemolytic Transfusion Reactions. N Engl J Med. 2019;381(2):150-162. doi:10.1056/NEJMra1802338
  14. Center for Biologics Evaluation and Research. Fatalities reported to FDA following blood collection and transfusion. United States: Food and drug administration; 2020: 4-5
  15. Otrock ZK, Liu C, Grossman BJ. Transfusion-related acute lung injury risk mitigation: an update. Vox Sang. 2017;112(8):694-703. doi:10.1111/vox.12573
  16. van den Akker TA, Grimes ZM, Friedman MT. Transfusion-Associated Circulatory Overload and Transfusion-Related Acute Lung Injury [published correction appears in Am J Clin Pathol. 2022 Nov 3;158(5):665]. Am J Clin Pathol. 2021;156(4):529-539. doi:10.1093/ajcp/aqaa279
  17. Delaney M, Wendel S, Bercovitz RS, et al. Transfusion reactions: prevention, diagnosis, and treatment. Lancet. 2016;388(10061):2825-2836. doi:10.1016/S0140-6736(15)01313-6
  18. Vlaar AP, Juffermans NP. Transfusion-related acute lung injury: a clinical review. Lancet. 2013;382(9896):984-994. doi:10.1016/S0140-6736(12)62197-7
  19. Al-Riyami AZ, Al-Hashmi S, Al-Arimi Z, et al. Recognition, Investigation and Management of Acute Transfusion Reactions: Consensus guidelines for Oman. Sultan Qaboos Univ Med J. 2014;14(3):e306-e318.
  20. Gajic O, Rana R, Winters JL, et al. Transfusion-related acute lung injury in the critically ill: prospective nested case-control study. Am J Respir Crit Care Med. 2007;176(9):886-891. doi:10.1164/rccm.200702-271OC
  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.

Hyperkalemia (2024)

~ iEM Education Project Team ~ Leave a comment

by Chelsea N. Allen

Authors
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You have a new patient!

A 58-year-old female is brought into the emergency department (ED) by her family for dizziness and fatigue that started today. She has a history of hypertension for which she takes a calcium channel blocker and end-stage renal disease (ESRD) and has been on dialysis for the last four years. She did miss her dialysis session today due to her symptoms, with her last session four days ago.

At triage, her vital signs are as follows: BP 170/90 mmHg, HR 30/min, RR of 18/min, temperature 37.1 degrees Celsius, SpO2 of 98% on room air. She appears fatigued but is able to answer questions appropriately and has no obvious focal neurologic deficits.

Triage EKG is below

What do you need to know?

Hyperkalemia is one of the most important electrolyte abnormalities you will encounter in the emergency department (ED), given the potential for cardiac arrest in these patients. It refers to when the serum potassium (K) is greater than 5.5mEq/L. In all patients suspected of hyperkalemia, it is essential to place them on a cardiac monitor, obtain IV access, and perform an EKG due to the significant role potassium plays in the cardiac cycle. These patients may have non-specific symptoms, such as weakness and fatigue, and thus can make it hard to discern the diagnosis up front. Patients with a high pretest probability, such as those who miss dialysis or have had prior episodes of hyperkalemia, are usually treated for hyperkalemia before lab results are available due to the potential life-threatening nature of the condition. Potassium is stored in the body’s cells. It can be excreted during cellular damage, such as in rhabdomyolysis, or during certain physiologic states to balance the body’s pH when the serum becomes acidotic (e.g., DKA) [1,2].  Potassium is then excreted from the body by the kidneys/urinary system, so in patients whose kidney function has declined, such as ESRD, or in patients with an obstruction (bladder stone, enlarged prostate), potassium must be excreted through dialysis or by removal.

Medical History

Patients with hyperkalemia often present with non-specific symptoms, such as fatigue, muscle weakness, and cramps, which can often lead to a delay in the diagnosis and can be detrimental, even fatal to the patient. Elevations of potassium in a patient’s serum can be caused when there is a disruption in the storage or excretion mechanisms in the body and can cause cardiac arrhythmias, such as premature beats (PVCs), irregular beats (atrial fibrillation) or cardiac arrest (ventricular fibrillation) due to the role of potassium in regulating the cardiac membrane potential [1-5]. Since an underlying elevation in potassium can cause these non-specific symptoms, it is imperative to do a thorough history, keying in on a history of kidney issues, dialysis appointments, and urinary symptoms.

Physical Examination

The most crucial physical exam components in patients with hyperkalemia are the cardiac and skin exam, especially in patients who may not be able to give you much information, as a thorough skin exam can elicit an AV fistula/graft or tunnel catheter, which would clue you into the patient being on dialysis. If the patient does not have a history of ESRD on dialysis, the cardiac exam could be another clue, elucidating irregular rhythms or bradycardia and prompting you to get further evaluation with an EKG.

Alternative & Differential Diagnoses

Given that hyperkalemia can cause a myriad of non-specific symptoms, patients can sometimes have a long list of differential diagnoses. Outside of the cardiac complications, hyperkalemia can cause muscle cramping, fatigue, or feeling weak. Unless you have a high index of suspicion, these symptoms can be attributed to muscle strains or viral illnesses, which in patients who are otherwise healthy or have a good history of these may be more likely than hyperkalemia [5].

Acing Diagnostic Testing

One of the most important tests for patients suspected of having hyperkalemia is the EKG, given how quickly this bedside test can be performed and the wealth of information that can be obtained, especially regarding electrolytes [4,5]. The classic EKG finding in patients with hyperkalemia is peaked T waves. However, hyperkalemia can mimic many EKG changes, and other findings suggest hyperkalemia are a widened QRS, flattened P waves, and heart blocks [3,4,5]. The EKG may follow a step-wise pattern of peaked T waves, followed by progressively lengthening QRS. However, generally, they do not always follow this pattern, so it is important to have a high index of suspicion when you see these changes. The next step is usually laboratory testing with a basic metabolic panel to confirm hyperkalemia. It can also indicate the patient’s electrolyte levels, provide insight into their acid-base balance, and suggest other potential diagnoses. You may also get other testing depending on the cause of the hyperkalemia, such as CT or US imaging, if urinary tract obstruction is the suspected cause. However, in general, imaging is not needed to make the diagnosis.

Risk Stratification

Most of the patients with hyperkalemia are going to be chronic kidney disease or dialysis patients, which are inherently at higher risk given their underlying disease process as well as the fact that the kidneys process and excrete potassium in the body. Specifically, anuric patients within this group are going to be at higher risk for complications, given that the only way to excrete potassium is through dialysis, putting them at risk for the potentially fatal complications of hyperkalemia [1,2].

Management

As always, following the ABCs of emergent patient management is crucial in deciding how quickly you need to intervene, especially in hyperkalemic patients, where cardiac arrest is a high possibility. Once you have assessed that your patient has a patent airway by speaking to them, their breathing by listening for bilateral breath sounds, and their circulation by ensuring they have a pulse, the next critical step in managing hyperkalemia is the reduction of potassium within the body and serum. This is achieved in two ways: shifting and elimination [2,3,4,5]. One medication we use in hyperkalemia where we have EKG changes attributed to elevations in potassium is Calcium (gluconate or chloride) which the sole purpose of this medication is stabilization of the cardiac membrane to prevent further deterioration into unstable rhythms and is usually given first in the line of medications [2]. Its onset is rapid (15-30 min) with a duration of 30-60 min. Monitor closely as it does not lower potassium but rather protects the heart. Calcium chloride is more concentrated than calcium gluconate, so it requires a central line due to the risk of tissue damage.

Shifting medications will be Insulin and Albuterol, given that these medications work in the cAMP pathway on the cell membranes, causing extracellular potassium to shift intracellularly, thereby transiently decreasing serum potassium. Dextrose is usually given with insulin to prevent the drop in glucose associated with insulin use, and it does not shift/eliminate potassium, but it is still vital. If your patient is able to make urine, giving a dose of Furosemide (or another potassium-depleting diuretic) is useful to help start the process of potassium elimination, as these medications will pull extracellular potassium into the waste product (urine). If your patient is unable to make urine, giving Sodium zirconium cyclosilicate, a potassium binder in your gastrointestinal tract, to help eliminate potassium is another way to help deplete body potassium. If severe enough (e.g., arrhythmias/cardiac arrests, ESRD patients), most patients will need to undergo hemodialysis for definitive treatment/removal of potassium. Listed below are the medications mentioned above, as well as the recommended doses and frequency.

Table: Medications frequently used in hyperkalemia treatment [5,6]

Drug generic Name

Dose

Effect

Duration

Pregnancy

Cautions / Comments

Calcium gluconate

1-3gm IV

15-30min

30-60min

C, only if clearly needed

 

Calcium chloride

1gm IV

15-30min

30-60min

C, only if clearly needed

Concentrated Calcium, needs central line

Albuterol

15-20mg nebulized

30min

2hrs

C

 

Insulin/Dextrose

10u Regular insulin IV; 25-50gm of 50% dextrose IV

30min-45min

3-6hrs

B (insulin); C (dextrose)

Usually given together, but can be omitted if Glucose >300

Furosemide

40-80mg IV

15-20min

2hrs

C

 

Sodium zirconium cyclosilicate

10mg TID PO

Can take up to 48hrs

 

Not Assigned

Usually not first line in the ED

Special Patient Groups

Given its life-threatening nature, hyperkalemia is generally treated the same way in all patient populations, including children and pregnant patients [5]. The above medications are all for adults, but they do have weight-based dosing for pediatric patients that is easily accessible on Broselow tapes found in the Emergency Department. Additional considerations for each group as follows;

Pediatrics

Hyperkalemia in children is often linked to kidney insufficiency, acidosis, and certain genetic conditions affecting potassium balance [7]. Pediatric hyperkalemia treatment includes insulin-glucose therapy, calcium gluconate, and sometimes sodium bicarbonate for acidosis [7]. Dosing is weight-based; careful monitoring is essential to prevent hypoglycemia following insulin administration [7].

Geriatrics

Older adults are prone to hyperkalemia due to decreased renal function and polypharmacy, especially with medications like ACE inhibitors and potassium-sparing diuretics [8]. Geriatric patients require slower dose titration and close monitoring of cardiac function. Reducing or discontinuing potassium-elevating medications may be prioritized before more invasive treatments. Assessing patient’s medication profile carefully to minimize potential interactions and electrolyte disturbances is important.

Pregnant Patients

Hyperkalemia is rare in pregnancy but may occur due to conditions like preeclampsia or excessive potassium supplementation. Treatment is similar to that of the general population but focuses on the safety of both the mother and fetus. Agents like insulin-glucose therapy are used with caution, and glucose and potassium levels are monitored closely to avoid fetal complications.

Caution!

The drugs listed in the table do have specific considerations for pediatric, geriatric, and pregnant patients, as follows:

  1. Calcium Gluconate and Calcium Chloride:
    • Pregnant Patients: Generally considered safe for use when needed (Pregnancy Category C), but only administered if benefits outweigh the risks due to limited data on safety in pregnancy.
    • Pediatrics: Dosing is usually adjusted based on weight, and administration must be done with caution due to the risk of tissue necrosis with calcium chloride if extravasation occurs.
  2. Albuterol:
    • Pregnant Patients: Classified as Category C. Used in asthma or bronchospasm, but risks must be considered, as inhaled bronchodilators are typically preferred.
    • Pediatrics and Geriatrics: Pediatric dosing is weight-based, while elderly patients may require lower doses due to sensitivity to stimulants.
  3. Insulin/Dextrose:
    • Pregnancy: Insulin is preferred for managing blood glucose in pregnant women with diabetes, categorized as B for insulin, while dextrose is safe when needed.
    • Pediatrics: Used in hyperkalemia or diabetic ketoacidosis with dose adjustments based on age and weight.
  4. Furosemide:
    • Geriatrics: Lower doses are generally recommended due to increased risk of dehydration and electrolyte imbalance.
    • Pregnancy: Considered Category C, used only if necessary as it may affect fetal renal development.
  5. Sodium Zirconium Cyclosilicate:
    • Limited data on its use in pediatric and pregnant populations, and generally not a first-line treatment in the emergency department for these groups.

Infographic

Hyperkalemia

When To Admit This Patient

There are very few instances where hyperkalemic patients will be discharged from the ED, given the potential life-threatening arrhythmias. However, ESRD patients who receive dialysis, are back to their baseline and have to follow up/able to make it to their scheduled dialysis sessions will most likely be able to be discharged if a cause for their hyperkalemia is something simple, such as missed dialysis appointments. Ensure clear, specific follow-up arrangements to minimize recurrence risk. Confirm with her dialysis provider for her next sessions. Most other patients will be admitted for monitoring to ensure their potassium levels are normalizing and to identify a cause.

Revisiting Your Patient

As you recall, we had a 58-year-old female with dizziness/fatigue who had missed her dialysis session and was found to be bradycardic and hyperkalemic on her initial workup. She was initially treated with calcium gluconate with improvement in her EKG as well as her symptoms and was able to receive dialysis in the ED. After a brief period of observation after her dialysis sessions and repeat BMP showing normalization of her potassium, she was discharged home with her family to continue her outpatient dialysis schedule.

Author

Picture of Chelsea N. Allen, DO

Chelsea N. Allen, DO

Originally from Adel, GA, USA, graduated college with a degree in biology from Columbus State University in Columbus, GA, USA. Then attended medical school at the Edward Via College of Osteopathic Medicine in Auburn, AL before completing her emergency Medicine residency at the University of Florida, Jacksonville, in Jacksonville, FL, USA. She is currently the Assistant Program Director for the Emergency Medicine program at UF-Jacksonville as well.

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References

  1. Harris AN, Grimm PR, Lee HW, et al. Mechanism of Hyperkalemia-Induced Metabolic Acidosis. Journal of the American Society of Nephrology. 2018;29(5):1411-1425. doi:https://doi.org/10.1681/ASN.2017111163
  2. Mount D. Potassium balance in acid-base disorders. Accessed: November 14, 2024. https://www.uptodate.com/contents/potassium-balance-in-acid-base-disorders.
  3. Lindner G, Burdmann EA, Clase CM, et al. Acute hyperkalemia in the emergency department: a summary from a Kidney Disease: Improving Global Outcomes conference. Eur J Emerg Med. 2020;27(5):329-337. doi:10.1097/MEJ.0000000000000691
  4. Helman, A, Baimel, M, Etchells, E. Emergency Management of Hyperkalemia. Emergency Medicine Cases. September, 2016. Accessed November 14, 2024. https://emergencymedicinecases.com/alcohol-withdrawal-delirium-tremens/
  5. Wachira BW. Fluids, Electrolytes, and Acid-Base Disorders. In: Cydulka RK, Fitch MT, Joing SA, Wang VJ, Cline DM, Ma O. eds. Tintinalli’s Emergency Medicine Manual, 8e. McGraw-Hill Education; 2017. Accessed November 14, 2024. https://accessemergencymedicine-mhmedical-com.uaeu.idm.oclc.org/content.aspx?bookid=2158&sectionid=162269029
  6. Rafique Z, Peacock F, Armstead T, et al. Hyperkalemia management in the emergency department: An expert panel consensus. J Am Coll Emerg Physicians Open. 2021;2(5):e12572. Published 2021 Oct 1. doi:10.1002/emp2.12572
  7. Lederer Hyperkalemia. Accessed: November 14, 2024. https://emedicine.medscape.com/article/240903-overview?form=fpf
  8. Ortiz A, Galán CDA, Carlos Fernández-García J, et al. Consensus document on the management of hyperkalemia. Nefrologia (Engl Ed). 2023;43(6):765-782. doi:10.1016/j.nefroe.2023.12.002

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.

More hyperkalemia content on iem-student.org

Testicular Torsion (2024)

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by Vlad Panaitescu, Elizabeth Zorovich, Vincent Gonzalez

Authors
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You have a new patient!

You are on a busy overnight shift at the local emergency department when you pick up the chart of an 18-year-old male with abdominal pain and vomiting. You walk into the room and see a young male sitting in bed and appearing in moderate distress. His mother accompanies him. He states that he woke up from sleep with severe lower abdominal pain. He reports associated nausea and two episodes of non-bloody, non-bilious vomiting.

Vital signs are as follows: Blood Pressure 140/65 mmHg, Heart Rate 110 bpm, Respiratory Rate 20 bpm, Oxygen Saturation 100% in room air, and Temperature 98.7 (37.0 Celcius) oral.

The patient appears guarded as if he is holding back information. 

You politely ask his mother to step out of the room so that you can examine the patient. With his mother gone, he states the pain is actually in his testicle. It woke him up from sleep and caused him to vomit. The pain is described as severe and began acutely two hours ago. 

What do you need to know?

Importance

Testicular torsion is a urological emergency necessitating emergent intervention. Time is testicle! This can-not-miss diagnosis needs to be made quickly, as salvage rates are directly related to detorsion time. Testicular ischemia can develop as early as 4-8 hours after the onset of testicular torsion [1]. Early recognition of testicular torsion has been associated with an increase in the rates of testicular salvage and the prevention of complications, such as testicular infarction and infertility [2].

Epidemiology

Testicular torsion can occur at any age but occurs more often after birth or between 12-18.  The peak incidence of testicular torsion is at age 13-14 years. The incidence of torsion in males below the age of 25 is approximately 1 in 4000 [2].

Pathophysiology

Testicular torsion occurs when the testicle rotates around its spermatic cord, leading to impaired testicular blood supply, tissue ischemia, and pain [3]. Torsion results from abnormal fixation of the testis to the tunica vaginalis, an anatomical layer outside the testis that forms a sac. Torsion may occur spontaneously, after episodes of minor trauma, during periods of testicular growth (e.g., puberty), or during sleep when unilateral cremasteric muscle contraction results in twisting of the testis. Inadequate fixation of the tunica vaginalis to the posterior scrotal wall, known as the bell-clapper deformity, also places the testis at increased risk of torsion [4].

Initial Assessment and Stabilization (ABCDE approach)

Obtaining a detailed history is critical to developing your differential diagnoses. When concerned about testicular torsion, ask about the pain’s location and time of onset. Associated symptoms are also important, as nausea or emesis often accompanies this diagnosis. Ask about fevers, trauma, rashes, dysuria, hematuria, diarrhea, or blood stools, as these additional symptoms may make other diagnoses more likely.

Key features in the history that may heighten the index of suspicion include young patient age, sudden onset of symptoms, and severe unilateral testicular pain lasting less than 24 hours. However, testicular pain lasting over 24 hours does not necessarily rule out the presence of a testicular torsion [1].

Risk factors to ask about are the presence of an undescended testicle or a bell-clapper deformity. Testicular salvage rates are directly correlated to detorsion time, so gathering a focused history is important.  The testicular salvage rate is 90-100% with symptoms <6 hours and 0-10% when torsion is >24 hours [1].

Medical History

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

Physical Examination

A thorough abdominal and genitourinary exam needs to be completed on a patient with suspected testicular torsion.  Have a chaperone in the examination room, and consider asking the parent(s) to leave the room in the adolescent-age child.  The exam focuses on the scrotum and testicles, but evaluating for inguinal hernias ab, abdominal tenderness, or distension is important. A skin and penile exam should also be performed, taking time to evaluate for skin changes or any evidence of infection.

Exam findings in testicular torsion may include scrotal swelling or erythema, testicular tenderness, an elevated or “high riding” testicle (Brunzel sign), horizontal lie of the testicle, and dimpling of the scrotal skin (Ger’s sign).  Testicular pain is generally not relieved with elevation of the affected testicle (Prehn’s sign).  Evaluating an absent cremasteric reflex on the affected testicle is also highly sensitive for testicular torsion [2].

Pain from testicular torsion can be constant or intermittent since a torsion/detorsion phenomenon can occur. In intermittent testicular torsion, it is important to maintain a high clinical suspicion based on symptoms, risk factors, and demographics [2].

When to Ask for Senior Help

If you are not confident about your exam findings or approach to the patient, you should ask for assistance.  If suspicion of testicular torsion is high, inform your senior resident or supervising doctor to confirm that your patient assessment and plan are appropriate.

Not-to-Miss Diagnoses

Testicular torsion is a time-sensitive diagnosis to consider for any male patient with testicular pain, unexplained abdominal or flank pain, low back pain, or vomiting. There are other diagnoses that have overlapping signs and symptoms with testicular torsion.  See below for these alternative diagnoses to consider.  

Other diagnoses include:

  • Scrotal wall cellulitis
  • Scrotal hematoma
  • Scrotal abscess
  • Epididymitis
  • Orchitis
  • Fournier gangrene
  • Hematocele, hydrocele, spermatocele, pyocele, or varicocele
  • Incarcerated or strangulated inguinal hernia
  • Lymphadenitis
  • Tinea cruris
  • Testicular rupture
  • Testicular tumor or malignancy
  • Torsion of testicular appendage
  • Appendicitis
  • Bowel obstruction
  • Sexually transmitted infection
  • Urinary tract infection or pyelonephritis

Acing Diagnostic Testing

The diagnosis of testicular torsion is based on the patient’s symptoms and physical exam.  Investigation can be ordered if the diagnosis is unclear or alternative diagnoses are strongly considered.  However, a urology specialist should be consulted based on clinical suspicion of torsion.  Consultation for definitive management should not be delayed for investigations.

The TWIST score is a proposed score for assessing testicular torsion in children [5].

Patients receive:

  • 2 points for testicular swelling
  • 2 points for a hard testicle
  • 1 point for an absent cremasteric reflex
  • 1 point for nausea or vomiting
  • 1 point for a high-riding testicle

A TWIST score greater than 5 was found to have a positive predictive value of 100% (suggesting a stat urological consult). A score less than 2 was found to have a negative predictive value of 100% (suggesting clinical clearance). Scores between 2-5 require ultrasound for further assessment [5].

Investigations to consider based on the patient’s history and physical exam are below:

  • Testicular ultrasound.  Consider ultrasound in equivocal cases (TWIST Score 2-5) [5].
  • A positive exam will show unilateral absence of blood flow, an enlarged testicle, and asymmetric testicular echotexture on sonogram [6].
  • Pre-operative labs, such as blood count, chemistry, and coagulation studies
  • Urinalysis
  • Testing for sexually transmitted infections
  • CT imaging of the abdomen and pelvis to evaluate for alternative diagnoses (e.g., appendicitis)  
Scrotal/Testicular Ultrasound

Ultrasound is the preferred method. In patients with testicular torsion, the ultrasound shows a hypoechoic and enlarged testis. Reduced blood flow and parenchymal heterogeneity are other signs of testicular torsion.

The testicular ultrasound shows bilateral normal blood supply in the Doppler investigation.
The testicular ultrasound shows no blood supply in the right testicle.

Management

Empiric and Symptomatic Treatment

Patients with concern for testicular torsion may need analgesia and antiemetic medications for symptom control. Some recommendations are below.

Analgesics:

  • Acetaminophen (peds), 15mg/kg PO, q4-6h, Max 4000mg/day, caution with allergies or if they have already taken
  • Ibuprofen (peds), 10mg/kg PO, q6h, Max 2000mg/day, caution with allergies or if they have already taken
  • Morphine, 0.1mg/kg IV, initial dose than 0.05mg/kg q30min until desired analgesia, caution with allergies or depressed mental status
  • Fentanyl, 1mcg/kg IV, initial dose than 0.5mg/kg q15min until desired analgesia, caution with allergies or depressed mental status

Antiemetics:

  • Ondansetron, 0.1mg/kg IV; give 2mg in patients <20kg and 4mg in patients >20 kg

Procedures

If there is a high index of suspicion for testicular torsion, a urologic specialist should be promptly consulted for definitive surgical intervention.  If urology is unavailable, or a prolonged time to surgical treatment is anticipated, manual de-torsion can be attempted in the emergency department [1].

Manual de-torsion [1]

  • Temporizing measure if a urologist is not immediately available
  • De-torsion in the emergency department does not replace formal intraoperative de-torsion and surgical fixation of the testis (orchiopexy) 
  • First, provide intravenous analgesia or administer a spermatic cord anesthetic block.
  • Second, grasp the affected testicle and rotate it from medially to laterally (“open the book”). Rotate the testicle at least 360 degrees or until pain is improved.
  • Consider repeating rotation in the medial to lateral direction 2-3 more times or until pain is decreased.
  • If pain worsens after rotation or if rotation is not successful, attempt to rotate the testicle in the opposite direction.

When To Admit This Patient

Patients with high clinical concern for testicular torsion should be evaluated promptly by a urologist. If no urologist or surgical specialist is immediately available, these patients should be transferred to another facility for urologic evaluation. Testicular torsion patients should be admitted for surgical detorsion and orchiopexy by urology [1].

If the clinical diagnosis of torsion is unclear (e.g., TWIST score 2-5), further testing with testicular ultrasonography can aid in disposition planning [5].

Revisiting Your Patient

You carefully perform a genitourinary exam with the patient’s mother outside of the examination room.  You note an elevated, firm, swollen, erythematous left testicle with an absent cremasteric reflex on the left side.

You immediately call your senior for help. You calculate a TWIST score of 6, raising testicular torsion high on your differential diagnoses list, and urology is consulted for suspected testicular torsion. While you await urology, you give the patient 0.1mg/kg IV morphine and attempt manual detorsion in the emergency department. Pain does improve slightly by the time urology arrives. Despite the high TWIST score, they perform a quick bedside ultrasound that shows diminished flow to the left testicle. They informed you that they would take the patient to the operating room for detorsion and orchiopexy. The patient is admitted to the urology service and leaves the emergency department for the operating room. 

Authors

Picture of Vlad Panaitescu

Vlad Panaitescu

Picture of Elizabeth Zorovich

Elizabeth Zorovich

Picture of Vincent Gonzalez

Vincent Gonzalez

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References

  1. Sharp VJ, Kieran K, Arlen AM. Testicular torsion: diagnosis, evaluation, and management. Am Fam Physician. 2013;88(12):835–840. 
  2. Laher A, Ragavan S, Mehta P, Adam A. Testicular Torsion in the Emergency Room: A Review of Detection and Management Strategies. Open Access Emerg Med. 2020;12:237-246. Published 2020 Oct 12. doi:10.2147/OAEM.S236767
  3. Fujita N, Tambo M, Okegawa T, Higashihara E, Nutahara K. Distinguishing testicular torsion from torsion of the appendix testis by clinical features and signs in patients with acute scrotum. Res Reports Urol. 2017;9:169–174. doi: 10.2147/RRU.S140361
  4. Davis JE. Male Genital Problems. In: Tintinalli JE, Stapczynski J, Ma O, Yealy DM, Meckler GD, Cline DM. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e. McGraw Hill; 2016. 
  5. Barbosa JA, et al. Development of initial validation of a scoring system to diagnose testicular torsion in children. The Journal of Urology. 2013; 189:1853-8.
  6. University of Arkansas for Medical Sciences, Department of Radiology. Testicular Torsion. https://medicine.uams.edu/radiology/kb/testicular-torsion/ . Published on 8 October 2022. Accessed on 12 November 2024.

Reviewed and Edited By

Picture of Joseph Ciano, DO, MPH, MS

Joseph Ciano, DO, MPH, MS

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

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

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