Approach to the trauma patient – ABCDE of trauma care

Approach to the trauma patient – ABCDE of trauma care


Jane Doe, 22-year-old female, was in a major car crash and is approaching the trauma bay via an ambulance. You are aware that the patient’s condition is critical, so you do a quick run-through in your head about the approach that you will have to care for them once they arrive to your emergency department. What should your approach to a trauma patient be?

The ABCDE of Trauma Care

The Airway, Breathing, Circulation, Disability, Exposure (ABCDE) approach is a clinically proven approach to any critically ill patient that needs emergent care and treatment. It has been proven to improve patient outcomes, optimize team performance and save time when patients are in life-threatening conditions [1]. This approach is applicable to all patients (both adults and children), regardless of their underlying condition. However, the ABCDE approach is not applicable to patients who are in cardiac arrest, in which case the cardiopulmonary resuscitation guidelines should be used [2].

With the ABCDE approach, initial assessment and treatment are performed simultaneously. Once the entire survey is completed, reassessment should be conducted until the patient is stable enough for the care team to be able to move on to the secondary survey and look for a definitive diagnosis.

A - Airway

First, the care team should assess if the patient’s airway is patent. If the patient responds to the team in a normal voice, then that is a good sign that the airway is intact. It is important to note that airway obstruction can be complete or partial, and can be caused by upper airway obstruction or reduced level of consciousness.

Signs of complete airway obstruction are lack of respiration despite great effort. Signs of partial airway obstruction include:
– Changes in the patient’s voice
– Snoring or gurgling
– Stridor (noisy breathing)
– Increased breathing effort

Assess the patient’s airway by looking for rocking chest wall motion and any signs of maxillofacial trauma or laryngeal injury. Perform the head-tilt and chin-lift maneuver to open the airway (note that caution should be conducted in patients with C-spine injury). If there is anything that is noticeably obstructing the airway, suction or remove it. If possible, remove foreign bodies that are causing airway obstruction. Provide high-flow oxygen to the critically ill patient and perform definitive airway if needed [1].

B – Breathing

Generally, airway and breathing are examined simultaneously. Determine if breathing is intact by assessing the respiratory rate, inspecting the chest wall movement for symmetry, depth, and respiratory pattern. Additionally, assess for tracheal deviation and use of respiratory muscles. Percuss the chest for dullness or resonance, auscultate for breath sounds and apply a pulse oximeter [1].

Injuries that impact breathing should be immediately recognized, and life-threatening injuries should be addressed and managed [3]. For example, tension pneumothorax must be promptly relieved by needle thoracocentesis, bronchospasms should be managed with inhalation and assisted ventilation should be considered if breathing continues to be insufficient [1].

C – Circulation

Conditions that threaten the patient’s circulation and can be fatal include shock, hypertensive crises, vascular emergencies such as aortic dissection and aortic aneurisms. These conditions should be immediately identified and managed [1].

Circulation can be assessed by looking at the general appearance of the patient, including signs of cyanosis, pallor, flushing and diaphoresis. Assess for any obvious signs of hemorrhage, blood loss and level of consciousness. Additionally, capillary refill time and pulse rate should be assessed. Auscultate the chest for heart sounds, and blood pressure measurement and electrocardiography should be performed as soon as possible [1].

Additionally, assess for signs of hypovolemia and shock. If these are identified, obtain an intravenous access and infuse saline to restore circulating volume [1]. If there are life-threatening conditions that are compromising the patient’s circulation, promptly identify and treat them as needed. For example, tension pneumothorax should be immediately treated with needle decompression and cardiac tamponade can be relived with pericardiocentesis.

D - Disability

The main disability in the primary survey to be assessed for is the brain. Abnormal neurological status can be caused by primary brain injury or systemic conditions that effect brain perfusion, such as shock, hypoxia, intoxication etc. Assess the level of consciousness by using the Glasgow Coma Scale [4], look for pupillary response and limb movement.

The best way to prevent injury to the brain is to maintain adequate airway, breathing and circulation. Glucose levels can be assessed at bedside for decreased level of consciousness due to low blood glucose levels, and corrected with oral or infused glucose [1].

E – Exposure

The exposure portion of the ABCDE approach involves assessment of the whole-body to avoid any signs of missing injuries. During this part of the management, undress the patient fully and examine the back for any signs of C-spine precautions. Additionally, check for clues for any signs of underlying conditions, such as:

  • Signs of trauma (i.e. burns, gunshot wounds, stab wounds)
  • Rashes
  • Causes of sepsis (i.e. infected wounds, gangrene)
  • Toxins and drugs (i.e. needle track marks, chemicals, patches)
  • Other wounds such as bite marks, insect bites, embedded ticks
  • Iatrogenic causes (i.e. catheters, tubes, implants, surgical sites and scars)

Concluding Remarks

The ABCDE approach to the critically ill patient is a strong and proven clinical tool for initial assessment and treatment of patients in medical emergencies. Widespread knowledge of this skill is critical for healthcare workers and any team providing emergent care to trauma patients. 

*Note that this is a general approach to the trauma patient. Always consult your care team for adequate management of trauma patients and resort to reliable resources for more information on the ABCDE approach. 

References and Further Reading

  1. Thim, T., Krarup, N. H. V., Grove, E. L., Rohde, C. V., & Løfgren, B. (2012). Initial assessment and treatment with the Airway, Breathing, Circulation, Disability, Exposure (ABCDE) approach. International journal of general medicine5, 117.
  2. Koster, R. W., Baubin, M. A., Bossaert, L. L., Caballero, A., Cassan, P., Castrén, M., … & Sandroni, C. (2010). European Resuscitation Council Guidelines for Resuscitation 2010 Section 2. Adult basic life support and use of automated external defibrillators. Resuscitation81(10), 1277-1292.
  3. Subcommittee, A. T. L. S., & International ATLS Working Group. (2013). Advanced trauma life support (ATLS®): the ninth edition. The journal of trauma and acute care surgery74(5), 1363-1366.
  4. Sternbach, G. L. (2000). The Glasgow coma scale. The Journal of emergency medicine19(1), 67-71.
Cite this article as: Maryam Bagherzadeh, Canada, "Approach to the trauma patient – ABCDE of trauma care," in International Emergency Medicine Education Project, January 19, 2022,, date accessed: December 11, 2023

Focused Assessment with Sonography in Trauma (FAST): An Overview

Traumatic injuries are one of the leading causes of death, and intraperitoneal bleeds occur in approximately 12% of blunt traumas [1]. A quick assessment of trauma and detection of intraperitoneal fluid is increasingly essential in trauma patients’ assessment. The implementation of point-of-care ultrasound (POCUS) has had a significant impact on patient management, especially in a trauma setting. POCUS is easy to use at the bedside, non-invasive and inexpensive.

The Focused Assessment with Sonography in Trauma (FAST) is an ultrasound protocol used to assess hemoperitoneum and hemopericardium [2]. The FAST protocol is sensitive and specific for detecting intraperitoneal free fluid. According to previous studies, sensitivity ranges from 75-100%, and specificity ranges from 88-100% [3]. The FAST exam is rapid and can be completed in less than 5 minutes. It also has multiple advantages, including decreased time to interventions like surgery and length of stay at the hospital [4]. The Extended FAST (eFAST) protocol, which involves examinations of each hemithorax for hemothorax and pneumothoraces, has recently been introduced by several institutions [2].

Regions Examined

The FAST exam assesses the pericardium and multiple potential spaces within the peritoneal cavity for free fluid. The patient is often assessed in the supine position.

The right flank or right upper quadrant (RUQ) view assesses the hepatorenal recess (also known as Morrison’s pouch), as well as the right paracolic gutter, the hepato-diaphragmatic area, and the caudal edge of the left liver lobe [2]. The pericardial view, also known as the subcostal or the subxiphoid, is usually assessed next. The liver is commonly used as a sonographic window of the heart to evaluate pericardium. Ultrasound can detect little pericardial fluid with sensitivity and specificity approaching 100% [5]. The pericardial view also helps to differentiate between pleural and pericardial effusions and visualize right ventricular collapse during diastole [2]. Next, the left upper quadrant (LUQ) is used to visualize the splenorenal recess, the subphrenic space and the left paracolic gutter. If the eFAST protocol is being conducted, the RUQ and LUQ views are also used to examine the left and right hemithorax. Lastly, the pelvic or the suprapubic view is used to assess for free fluid in the rectovesical pouch in males and rectouterine and vesicouterine pouches in women [2]. The bladder acts as a sonographic window for this view.


While there are no complications related to the FAST exam itself, the use of ultrasound does have some limitations, one of which is the requirement for at least 150-200 cc of intraperitoneal fluid for an ultrasound to be able to detect. This can lead to false negatives when free fluid is in fact present [6]. False positives in the FAST exam may also occur and can be due to the presence of ascites, pre-existing pleural or pericardial effusions unrelated to the trauma, ruptured ovarian cysts or ruptured ectopic pregnancies [2]. Healthcare workers should be aware that POCUS and the FAST protocol have limitations dependent on the provider’s experience and the patient’s body habitus.   

Further Reading and Free Online Course


  1. Poletti, P. A., Mirvis, S. E., Shanmuganathan, K., Takada, T., Killeen, K. L., Perlmutter, D., Hahn, J., & Mermillod, B. (2004). Blunt abdominal trauma patients: can organ injury be excluded without performing computed tomography?. The Journal of Trauma57(5), 1072–1081.
  2. Bloom, B. A., & Gibbons, R. C. (2020). Focused Assessment with Sonography for Trauma.
  3. Brenchley, J., Walker, A., Sloan, J. P., Hassan, T. B., & Venables, H. (2006). Evaluation of focussed assessment with sonography in trauma (FAST) by UK emergency physicians. Emergency Medicine Journal23(6), 446–448.
  4. Melniker, L. A., Leibner, E., McKenney, M. G., Lopez, P., Briggs, W. M., & Mancuso, C. A. (2006). Randomized controlled clinical trial of point-of-care, limited ultrasonography for trauma in the emergency department: the first sonography outcomes assessment program trial. Annals of Emergency Medicine48(3), 227–235.
  5. Mandavia, D. P., Hoffner, R. J., Mahaney, K., & Henderson, S. O. (2001). Bedside echocardiography by emergency physicians. Annals of emergency medicine38(4), 377–382.
  6. Von Kuenssberg Jehle, D., Stiller, G., & Wagner, D. (2003). Sensitivity in detecting free intraperitoneal fluid with the pelvic views of the FAST exam. The American journal of emergency medicine21(6), 476–478.
Cite this article as: Maryam Bagherzadeh, Canada, "Focused Assessment with Sonography in Trauma (FAST): An Overview," in International Emergency Medicine Education Project, September 20, 2021,, date accessed: December 11, 2023

Approach to Jaundice in the Emergency Department

A 50-year-old male presents to the emergency department (ED) with nausea and vomiting, diminished appetite, and recent changes in his skin color, which he describes as turning “yellow.” This seemed to have worsened over the past few weeks, after which he began to worry and presented to the ED.

The patient’s vital signs are normal. His physical exam is positive for icteric sclerae, jaundice in the face and chest, and hepatomegaly. He is not tender to palpation on the abdomen. The rest of his exam is otherwise normal.


Jaundice is not a diagnosis, but a clinical manifestation of an underlying problem, specifically elevated serum bilirubin. Patients with Jaundice present with yellow discoloration of the skin, mucous membranes, and sclera. They can present to the ED with Jaundice in isolation or along with other symptoms. It is the Emergency Physician’s task to evaluate the patient, find the underlying cause, order the appropriate investigation and decide whether the patient requires admission to the hospital and consultation with other physicians.

Normal physiology of bilirubin metabolism

Bilirubin is the end product of heme metabolism. This occurs in three phases: pre-hepatic, hepatic, and post-hepatic phases. Approximately 75-80% of bilirubin comes from the catabolism of red blood cells. Initially, this bilirubin is unconjugated, which is insoluble in water and soluble in fat. Therefore, unconjugated bilirubin can easily cross the blood-brain barrier and the placenta [1].

Unconjugated bilirubin is actively transported to the liver by albumin and is conjugated by the enzyme glucuronosyltransferase. Subsequently, conjugated bilirubin is either stored in bile in the gallbladder or excreted through the biliary tract, where it eventually reaches the intestines and is excreted from the body [1,2].

Pathophysiology and differential diagnosis

The classic definition of jaundice is a serum bilirubin level greater than 2.5 to 3 mg per dL (42.8 to 51.3 µmol per L), with a clinical presentation of yellow skin and sclera [1]. As described in the above section, bilirubin metabolism occurs in three phases, and dysfunction of any of these steps can lead to jaundice.

Pre-hepatic causes

Unconjugated hyperbilirubinemia or elevated levels of unconjugated bilirubin before it reaches the liver can lead to jaundice. This can occur due to excessive heme metabolism from increased red blood cell breakdown (hemolysis) and the saturation of enzymes that conjugate it. A few underlying etiology for this include hemolytic anemia, sickle cell anemia, spherocytosis, glucose-6-PD deficiency, hemolytic uraemic syndrome, and transfusion reaction [1,3].

Hepatic causes

Any process that impacts liver functioning can lead to jaundice. Some of the hepatic causes of jaundice in adults include viral hepatitis, chronic alcohol consumption, autoimmune diseases such as primary biliary cirrhosis, genetic disorders such as Gilbert syndrome, hereditary metabolic defects such as Dubin-Johnson syndrome, and some drugs that can lead to drug-induced liver disease such as acetaminophen, oral contraceptives, estrogenic and anabolic steroids [4-6].

Post-hepatic causes

Any process that instigates post-hepatic obstruction can lead to jaundice due to elevated levels of conjugated bilirubin. Some of these include cholelithiasis leading to obstruction of the biliary duct system, biliary tract tumors, biliary duct strictures, and jaundice secondary to pancreatitis [1, 7].

History and physical examination

A good history and physical examination of patients presenting with jaundice to the ED is key in their diagnosis.

On history, the patient should be asked about alcohol and drug use, recent travel, sexual contact with a person with known or suspected hepatitis, recent tattoos or body piercings, and previous biliary surgery. A focused review of systems should also be conducted. For example, a history of fever and viral symptoms can point towards viral hepatitis, while the presence of constitutional symptoms such as weight loss and night sweat may point towards a malignancy [8].

The physical examination should comprise vital signs and a complete abdominal examination, assessing for right upper quadrant tenderness, ascites, hepatomegaly, splenomegaly, and ascites [9]. Additionally, the physical examination should focus on evaluating encephalopathy by looking for asterixis and changes in mental status and underlying liver disease by assessing for bruising, spider angiomas, gynecomastia, and palmar erythema [1, 8-9]. Lastly, it is important to remember that the presence of painless jaundice and an abdominal mass may point towards obstruction from a malignancy.


Laboratory assessment

First line serum testing should include a complete blood count (CBC) to check for hemolysis, bilirubin level with fractionation, aminotransferases (AST and ALT) to assess for hepatocellular injury (although these may be normal in chronic liver disease), alkaline phosphatase, prothrombin time and/or international normalized ratio, albumin, and protein to assess for liver synthetic function. If these tests come back normal, further tests may be needed to identify the underlying cause of the patient’s jaundice, such as hepatitis serology, autoimmune markers, and investigation for acetaminophen levels [1,8].


The majority of diagnostic imaging will be done outside of the ED. However, emergency physicians can conduct initial ultrasound screening to assess for bile duct dilation, biliary obstruction, and the presence of cholelithiasis. A CT scan can also be ordered to assess for intraparenchymal liver and pancreas disease [1,8]. Outside of the ED, investigation with Endoscopic Retrograde Cholangio-Pancreatography (ERCP), Magnetic Resonance Cholangio-Pancreatography (MRCP), and a liver biopsy may be warranted.


In the ED, emergency physicians are often involved in the initial investigation of a patient with jaundice in ruling out life-threatening conditions and to decide whether a patient should be discharged or admitted for further management. For example, physicians should first assess medical emergencies that can present with jaundice, such as ascending cholangitis, acute hepatic failure, and massive hemolysis. Timely diagnosis, resuscitation, treatment initiation, and emergent consultation of these conditions are critical in the ED. Additionally, patients with elevated AST/ALT levels should be admitted if there are any signs of sepsis, coagulopathy, altered mental status, and intractable pain and vomiting. The presence of hepatocellular injury, coagulopathy, and altered mental status may point towards fulminant liver failure and may require acute fluid resuscitation and hemodynamic monitoring in an acute care setting [10]. Otherwise, depending on the underlying cause of a patient’s jaundice, surgical, gastroenterological or interventional radiological consultation may be required in an outpatient setting.

References and Further Reading

  1. Roche, S. P., & Kobos, R. (2004). Jaundice in the adult patient. American family physician69(2), 299-304.
  2. Wolfson, A. B., Hendey, G. W., Ling, L. J., Rosen, C. L., Schaider, J. J., & Sharieff, G. Q. (2012). Harwood-Nuss’ clinical practice of emergency medicine. Lippincott Williams & Wilkins.
  3. Sackey K. (1999). Hemolytic anemia: part 1. Pediatr Rev, 20,152-8.
  4. Pasha, T. M., & Lindor, K. D. (1996). Diagnosis and therapy of cholestatic liver disease. Medical Clinics of North America80(5), 995-1019.
  5. Schramm, C., Kanzler, S., Zum Büschenfelde, K. H. M., Galle, P. R., & Lohse, A. W. (2001). Autoimmune hepatitis in the elderly. The American journal of gastroenterology96(5), 1587-1591.
  6. Lewis, J. H. (2000). Drug-induced liver disease. Medical Clinics84(5), 1275-1311.
  7. Custis, K., Brown, C., & El Younis, C. M. (2000). Common biliary tract disorders. Clinics in Family Practice2(1), 141-154.
  8. Fargo, M. V., Grogan, S. P., & Saguil, A. (2017). Evaluation of jaundice in adults. American family physician95(3), 164-168.
  9. Winger, J., & Michelfelder, A. (2011). Diagnostic approach to the patient with jaundice. Primary Care: Clinics in Office Practice38(3), 469-482.
  10. Vaquero, J., & Blei, A. T. (2003). Etiology and management of fulminant hepatic failure. Current gastroenterology reports5(1), 39-47.
Cite this article as: Maryam Bagherzadeh, Canada, "Approach to Jaundice in the Emergency Department," in International Emergency Medicine Education Project, May 17, 2021,, date accessed: December 11, 2023

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Saturday Night Palsy: A Case Discussion

Saturday Night Palsy

Case Presentation

In his mid-twenties, a patient presents to the emergency department with a profound drop in their wrist and some paresthesia to the dorsal of his hand. He is otherwise fit and healthy. When taking the history, he gives the classic story of having a few too many drinks the night before and falling sleep on a chair in an uncomfortable position, with his arm draped over the edge of the chair. When he woke up the next day, he felt a dull pain in their upper arm and could not extend his wrist. The patient attempted to neglect the problem and tried to do some exercises to alleviate the pain. However, two hours later, his arm remained quite flaccid to extension. The patient began to worry and presented to the emergency department.

Saturday Night Palsy

Saturday night palsy refers to a compressive neuropathy of the radial nerve that occurs due to prolonged and direct pressure to the upper medial arm by an object or a surface [1]. The radial nerve originates from the brachial plexus, carrying fibres from the C5-T1 ventral nerve roots. It innervates the medial and lateral heads of the triceps brachii muscle, as well as all twelve muscles in the posterior osteofascial compartments of the forearm. It provides motor innervation to the dorsal arm muscles and extrinsic extensors of the wrist and hand, as well as sensory innervation to most of the back of the hand (except the back of the 5th digit and adjacent half of 4th digit) [2].

Saturday night palsy is also known as the “honeymoon palsy”, which describes an event where an individual falls to sleep on their partner’s arm, compressing the person’s radial nerve for an extended period. Other terms for Saturday night palsy include “lover’s palsy”,” park bench palsy” and “crutch palsy”. Essentially, Saturday night palsy can be caused by any unnatural positioning or use of equipment that compresses the radial nerve, which is where the terms have originated from [1,3].

History and Physical Examination

As described in the case above, patients often report symptoms following excessive alcohol consumption and sleeping in an unnatural position. Otherwise, they may report other mechanisms in which their inner arm may have been compressed. Sometimes, symptoms do not present until several days after the nerve compression, making the diagnosis of this presentation difficult. Patients can also report other symptoms such as weakness, numbness, tingling and pain in the arm [1].

On physical exam, patients present with a characteristic wrist drop and inability to extend the wrist and fingers to the metacarpophalangeal joints’ level. Patients may also present with loss of triceps reflex, and sensory deficits involving the back of the hand [1,4].


Saturday night palsy is mainly a clinical diagnosis and does not require further investigative measures. However, some tools may help evaluate differential diagnoses and prognosis of the presenting condition. Electromyography and nerve conduction studies may localize the lesion and help differentiate between other neuropathies such as the brachial plexus or peripheral neuropathies. Ultrasound is a low-cost and low-risk method that can help visualize the nerve and identify areas of damage. MRI can assist in visualizing the finer details that may not be noticeable on ultrasound, as well as other presenting problems such as soft-tissue masses. The X-ray can guide in assessing for fractures and dislocations that may be causing the nerve compressions [1,5]. While none of these measures is necessary for diagnosing Saturday night palsy, it may be worthwhile to consider them for individual patients that require further investigations and where other diagnoses are being considered.


Treatment of Saturday night palsy is mainly through physical therapy, involving a dynamic splint that holds the arm in extension and allows for full passive range of motion during use. This can be complemented with the help of supportive care, including analgesics such as non-steroidal anti-inflammatory drugs (NSAIDs), resting the arm, corticosteroids use, and steroid injections [2]. To prevent re-injury of the nerve, it is important to counsel the patient on not repeating the same mechanism that caused the initial neural compression. Patients should also be counseled on the importance of physical therapy and following up in case of delayed recovery, which may necessitate other considerations such as surgical interventions [1,2].

References and Further Reading

  1. Ansari FH, Juergens AL. Saturday Night Palsy. [Updated 2020 May 13]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from:
  2. Bumbasirevic, M., Palibrk, T., Lesic, A., & Atkinson, H. D. (2016). Radial nerve palsy. EFORT open reviews1(8), 286-294.
  3. Latef, T. J., Bilal, M., Vetter, M., Iwanaga, J., Oskouian, R. J., & Tubbs, R. S. (2018). Injury of the radial nerve in the arm: A review. Cureus10(2).
  4. DeCastro A, Keefe P. Wrist Drop. [Updated 2020 Jul 21]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from:
  5. Agarwal, A., Chandra, A., Jaipal, U., & Saini, N. (2018). A panorama of radial nerve pathologies-an imaging diagnosis: a step ahead. Insights into imaging9(6), 1021-1034.
Cite this article as: Maryam Bagherzadeh, Canada, "Saturday Night Palsy: A Case Discussion," in International Emergency Medicine Education Project, March 1, 2021,, date accessed: December 11, 2023

Recent Blog Posts by Maryam Bagherzadeh

Hypertrophic Cardiomyopathies

Hypertrophic Cardiomyopathies

Hypertrophic cardiomyopathy is an inherited cardiovascular disease [1]. The condition can lead to sudden death in young adults and other problems such as heart failure, arrhythmias and stroke. It is prevalent in the world, with cases reported in over 50 countries and in people of all sexes, ethnicities and races. In diverse regions including the USA, Europe and East Africa, the prevalence of hypertrophic cardiomyopathy is 1 in 500 in the general population [2]. While considered a common and possibly fatal disease, most affected individuals remain undiagnosed in their lifetime and do not experience symptoms or reduced life expectancy [1].

Hypertrophic cardiomyopathy is passed on by an autosomal dominant fashion through mutations in more than 12 genes that encode for thick and thin myofilament proteins. However, sporadic cases caused by de-novo mutations in the predisposing genes can also occur [3]. Genetic testing for the identification of causative mutations can be conducted via DNA sequencing; however, pathogenic mutations are identified in roughly fewer than 50% of clinically affected patients [1].

Clinical Presentation, Signs and Symptoms

Clinical diagnosis of hypertrophic cardiomyopathy entails a hypertrophied but non-dilated left ventricle without evidence of any other disorders, such as cardiac or systemic diseases that may cause cardiomyocyte hypertrophy [4]. Often, patients with hypertrophic cardiomyopathy do not have any symptoms, and diagnosis is made either incidentally or through familial genetic screening. However, symptomatic patients may experience chest pain with exertion and varying rates of dyspnoea on a daily basis. Chest pain may also present at rest and can be caused by large meals. Some patients can also experience syncope [5]. Dyspnoea, chest pain and syncope are common symptoms that we faced in the emergency department. Although there are more common and deadly presentations with those symptoms, hypertrophic cardiomyopathy should always be in our differential diagnoses, particularly in cases with additional findings explained below.

Clinical Exam and Investigations

Clinical examination of patients with hypertrophic cardiomyopathy often reveals little information. In patients with dynamic left ventricular outflow tract obstruction, a systolic murmur may be heard with auscultation at the left sternal edge, radiating to the aortic and mitral areas [5]. However, if hypertrophic cardiomyopathy is suspected, either due to familial screening, the presence of a murmur or an abnormal 12-lead electrocardiogram (ECG), its diagnosis needs to be confirmed with either echocardiography and/or cardiovascular MRI [1].

Natural History and Clinical Course of Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathies can present at any age from infancy to adulthood. Many patients with this cardiovascular disease are expected to have a normal life expectancy without any major complications or even therapeutic interventions [6]. However, complications may occur in some patients and can include a range of events. Sudden death may occur in patients who are mildly symptomatic or even asymptomatic. Progressive heart failure with possible obstructive outflow obstruction and normal systolic function can occur, which may slowly lead to systolic dysfunction [4]. Cardiac arrhythmias may also develop – most commonly atrial fibrillation. This can lead to symptoms of heart failure and embolic stroke in 20% of the patients [7].

Sudden Death

Sudden death is the most unpredictable and devastating consequence of hypertrophic cardiomyopathy and is the most common cause of sudden death in young patients (under the age of 30) and young athletes [1,4,8]. However, the risk of sudden death falls gradually with older age. Although sudden death from mild physical activity or even inactivity can occur, death due to vigorous exertion amongst this patient population is more common [1]. Sudden death from hypertrophic cardiomyopathy usually occurs due to ventricular fibrillation and tachycardia. Risk stratification of high-risk patients for sudden death is important and can lead to the prevention of sudden death using various approaches, such as an implantable defibrillator [1,9]. Additionally, young professional athletes should be screened to detect silent signs of cardiovascular disorders that may lead to sudden death. Unfortunately, if young athletes are found to have hypertrophic cardiomyopathy, implementation of a cardiovert-defibrillator is not sufficient to grant athletes to return to competing. Athletes are often advised to stop participating in competitive sports, unless it is of low intensity such as golf [8].

Heart Failure

Symptoms of heart failure associated with preserved left-ventricular systolic function most often occur in middle-aged patients but can occur at any age [13]. Functional limitations can occur at differing rates but are often gradual and involve day to day variability. Women with hypertrophic cardiomyopathy have been shown to experience more severe symptoms of heart failure later in life compared to male patients. Frequently, these symptoms experienced in women have been associated with left-ventricular outflow-tract obstruction [14]. Some causes of heart failure in hypertrophic cardiomyopathy patients include left-ventricular outflow-tract obstruction, atrial fibrillation and diastolic dysfunction [1,4]. Treatment strategies include drugs and surgical myectomy or alcohol septal ablation for relief of symptoms of heart failure and outflow obstruction, and pharmacological strategies to treat atrial fibrillation and prevent stroke (such as blood thinners).

Hypertrophic Cardiomyopathy Management in the ED

Patients with hypertrophic cardiomyopathy exacerbation may present to the ED with a range of symptoms including syncope, chest pain, dyspnea, cardiac arrhythmia and worst of all, sudden cardiac death [10]. Diagnosis of hypertrophic cardiomyopathy patients presenting with these symptoms to the ED may be difficult as most of these patients are not aware of their underlying cardiovascular disease. Therefore, ED staff should keep this differential in mind and should be aware of certain diagnostic tools and approaches for acute management of hypertrophic cardiomyopathy.

Primarily, ED staff should conduct a complete history of the patients, including family history of relatives with early cardiovascular disorders or sudden death at a young age. Physical examination of the patient may be inconclusive, as patients usually don’t present with any specific cardiovascular symptoms, unless their disease has progressed to having left-ventricular outflow obstruction tract. An electrocardiogram (EKG) should be conducted, as most patients with hypertrophic cardiomyopathy will have abnormal EKGs. Specifically, their EKGs will show signs of left ventricular hypertrophy through large amplitude QRS, and deep, narrow Q waves particularly in the lateral leads if the patient has septal hypertrophy [11]. Physical examination should be coupled with EKG to rule out other cardiac problems.

Adopted from - Ed Burns. Hypertrophic Cardiomyopathy (HCM).

Deep narrow Q waves in chest leads are typical ECG finding of the hypertrophic cardiomyopathy patients. For more ECG information please visit –

In managing hypertrophic cardiomyopathy patients, following the ACLS algorithm if the patient is hemodynamically unstable is first priority. Otherwise, the goal of acute treatment of hypertrophic cardiomyopathy is to restore normal sinus rhythm or control the ventricular rate. Appropriate vasopressors should be given if patients are experiencing volume fluctuations due to diarrhea or other consequences of their disease. If patients present with a new onset of atrial fibrillation, approach of rate versus rhythm control and thromboembolism risk management should be considered [10]. If acute pharmacological treatment of hypertrophic cardiomyopathy patients is required, caution should be taken considering the state of their disease. For example, caution must be exercised when giving diuretics to patients with severe heart failure, as reduction in left ventricular preload can exacerbate obstruction and lead to hypotension [12]. The same considerations must be applied to any other treatment and guidelines should be followed closely. In conclusion, quick identification of the patient’s underlying cardiovascular problem and acute pharmacological management in the ED is critical to help the patient until a specialist can see them.

References and Further Reading

  1. Maron, B. J., & Maron, M. S. (2013). Hypertrophic cardiomyopathy. The Lancet381(9862), 242-255.
  2. Maron, B. J., Gardin, J. M., Flack, J. M., Gidding, S. S., Kurosaki, T. T., & Bild, D. E. (1995). Prevalence of hypertrophic cardiomyopathy in a general population of young adults: echocardiographic analysis of 4111 subjects in the CARDIA study. Circulation92(4), 785-789.
  3. Alcalai, R., Seidman, J. G., & Seidman, C. E. (2008). Genetic basis of hypertrophic cardiomyopathy: from bench to the clinics. Journal of cardiovascular electrophysiology19(1), 104-110.
  4. Maron, B. J. (2002). Hypertrophic cardiomyopathy: a systematic review. Jama287(10), 1308-1320.
  5. Elliott, P., & McKenna, W. J. (2004). Hypertrophic cardiomyopathy. The Lancet363(9424), 1881-1891.
  6. Maron, B. J., Casey, S. A., Hauser, R. G., & Aeppli, D. M. (2003). Clinical course of hypertrophiccardiomyopathy with survival to advanced age. Journal of the American College of Cardiology42(5), 882-888.
  7. Olivotto, I., Cecchi, F., Casey, S. A., Dolara, A., Traverse, J. H., & Maron, B. J. (2001). Impact of atrial fibrillation on the clinical course of hypertrophic cardiomyopathy. Circulation104(21), 2517-2524.
  8. Maron, B. J. (2003). Sudden death in young athletes.New England Journal of Medicine349(11), 1064-1075.
  9. Maron, B. J., Shen, W. K., Link, M. S., Epstein, A. E., Almquist, A. K., Daubert, J. P., … & Estes, N. M. (2000). Efficacy of implantable cardioverter–defibrillators for the prevention of sudden death in patients with hypertrophic cardiomyopathy.New England Journal of Medicine342(6), 365-373.
  10. Gardner, M., Nair, V., Hu, D., & Derry, S. (2018). The evaluation and management of decompensated hypertrophic cardiomyopathy in the emergency department.The American journal of emergency medicine36(12), 2286-2288.
  11. Kelly, B. S., Mattu, A., & Brady, W. J. (2007). Hypertrophic cardiomyopathy: electrocardiographic manifestations and other important considerations for the emergency physician.The American journal of emergency medicine25(1), 72-79.
  12. Efthimiadis, G. K., Pagourelias, E., Zegkos, T., Parcharidou, D., Panagiotidis, T., Arvanitaki, A., … & Karvounis, H. (2016). An overview of pharmacotherapy in hypertrophic cardiomyopathy: current speculations and clinical perspectives.Reviews in Cardiovascular Medicine17(3-4), 115-123.
  13. Melacini, P., Basso, C., Angelini, A., Calore, C., Bobbo, F., Tokajuk, B., … & Thiene, G. (2010). Clinicopathological profiles of progressive heart failure in hypertrophic cardiomyopathy.European heart journal31(17), 2111-2123.
  14. Olivotto, I., Maron, M. S., Adabag, A. S., Casey, S. A., Vargiu, D., Link, M. S., … & Maron, B. J. (2005). Gender-related differences in the clinical presentation and outcome of hypertrophic cardiomyopathy.Journal of the American College of Cardiology46(3), 480-487.


Cite this article as: Maryam Bagherzadeh, Canada, "Hypertrophic Cardiomyopathies," in International Emergency Medicine Education Project, December 9, 2020,, date accessed: December 11, 2023