Category: Resuscitation

Aortic Dissection (2024)

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by Sreenidhi Vanyaa Manian, & Elizabeth DeVos

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You Have A New Patient!

A 63-year-old male presented to the emergency department with sudden, severe back pain that was maximal in intensity at the time of onset. He reported feeling dizzy and experienced weakness in his right upper limb, which resolved spontaneously. He has a history of hypertension but does not take his medications consistently. He has a 40-pack-year smoking history and drinks alcohol socially.

The image was produced by using ideogram 2.0.

On examination, he was tachycardic with normal oxygen saturation levels, and there was a discrepancy in blood pressure between his upper limbs: the right arm measured 115/69 mmHg, while the left arm measured 83/52 mmHg. Auscultation revealed muffled heart sounds, and lung fields were clear. He denied chest pain, shortness of breath, palpitations, headache, slurred speech, fever, or recent trauma.

What Do You Need To Know?

Importance

Acute aortic dissection is a life-threatening medical emergency with high rates of morbidity and mortality. Mortality increases by 1% per hour of symptoms when untreated. Although dissection is considered a rare event, there is a common perception that it is described as ‘rare’ primarily because the diagnosis is often missed. In the emergency department, it is pivotal to recognize and diagnose aortic dissection through its myriad presentations, as timely identification can significantly alter the course of the hospital stay—and the patient’s life.

Epidemiology

The true frequency of aortic dissection is difficult to estimate, and most estimates are actually based on autopsy studies. Aortic dissection occurs once per 10,000 patients admitted to the hospital; approximately 2,000 new cases are reported each year in the United States. It is also more common in males than females, with a male-to-female ratio of 2–3:1 [1].

Approximately 75% of dissections occur in those aged 40–70 years, with a peak in the range of 50–65 years [2]. Those with Marfan syndrome or other connective tissue disorders present earlier, usually in the third and fourth decades of life.

Pathophysiology

The event leading to an aortic dissection is a tear in the intima. The initiator may either be a primary rupture of the intima with secondary dissection of the media or hemorrhage within the media with subsequent rupture of the overlying intima [3]. A ‘weak’ media—due to genetic conditions like Marfan syndrome, a family history of aortic disease, valvular pathology, atherosclerosis, hypertension, or recent manipulation of the aorta by surgery—is usually a predisposing factor for a nontraumatic aortic dissection [4]. Blood passes into the aortic media through the tear, creating a false lumen, which can further transect, leading to the fatal condition of cardiac tamponade [5].

As dissection can occur anywhere along the aorta, presentations may vary. Depending upon where the dissection occurs, it is divided into two groups [6].

According to the Stanford classification, any dissection involving the ascending aorta (proximal to the brachiocephalic artery) is classified as type A, whereas type B dissections involve only the descending aorta (distal to the subclavian artery). Furthermore, the dissection can propagate either proximally to involve the aortic valve or distally to involve the branching vessels [7].

Aortic Dissection Classification (Stanford vs De Bakey)

Medical History

The typical triad of aortic dissection,” which includes the following elements:

  1. Abrupt onset of thoracic or abdominal pain with a sharp, tearing, and/or ripping character.
  2. A variation in pulse and/or blood pressure.
  3. Mediastinal and/or aortic widening on chest radiograph.

Let us approach the first component of the triad.
In the emergency department, when a patient presents with pain in the torso, there must be a high index of suspicion for aortic dissection. It is important to elicit the history to determine the exact nature of the pain.

Site: Chest, back, or abdominal pain
“Pain above and below the diaphragm”

Onset: The pain is typically maximal at onset and can decline over time.

Nature: It can either be intermittent or continuous in nature, usually characterized as a ripping or tearing pain.

Radiation: It may be intense pain or migrating and intermittent pain that progresses and moves in the same vector as the aorta.

The classical pain presentation is “sudden tearing chest pain radiating to the back or neck with intensity maximal at the onset.”

“Think of aortic dissection as the subarachnoid hemorrhage of the torso. Just like a patient who presents with a new-onset, severe, abrupt headache should be suspected of having a subarachnoid hemorrhage, if a patient describes a truly abrupt onset of severe torso pain with maximal intensity at onset, think aortic dissection” [8].

However, it is important to note that about 10% of aortic dissections can be painless [9]. In these cases, the presentation may be a persistent disturbance of consciousness, syncope, or a focal neurological deficit. Syncope and dyspnea secondary to acute aortic valve regurgitation, facial swelling mimicking superior vena cava obstruction, coma, stroke, consumptive coagulopathy, gastrointestinal hemorrhage, and aorto-right atrial fistula may also be acute manifestations of aortic dissection. Cardiac tamponade is more frequent in the pain-free group as well [8]. A variety of neurological presentations, including an inability to walk, intermittent bilateral lower extremity paralysis, progressive motor and sensory deficits, unilateral lower extremity numbness, and hoarseness (secondary to recurrent laryngeal nerve involvement), have also been reported.

Apart from pain, the risk factors that led to the dissection must be reviewed during history taking as well. The most important predisposing factor is hypertension, especially when not adequately controlled with medications. Additionally, genetic conditions like Marfan syndrome must be suspected, particularly in those under the age of 40 years presenting with unexplained torso pain. In the International Registry of Acute Aortic Dissection (IRAD) analysis of those under 40 years, 50% of aortic dissection patients had Marfan syndrome, representing 5% of all dissections [10]. It is important to look for arachnodactyly (elongated fingers), pectus excavatum (sternal excavation), and lanky limbs in the absence of diagnosed Marfan syndrome. Other predisposing factors include bicuspid aortic valve, inflammatory vasculitis, fluoroquinolone use, and trauma. Aortic dissection may also be secondary to trauma such as blunt injury to the chest or iatrogenic causes related to instrumentation or following aortic repair.

Physical Examination

In the case of aortic dissection, the key physical findings are in the vitals. Starting with the pulse, a concept typically seen in patients is known as “pulse deficit,” which refers to an absent or reduced pulse secondary to diminished blood supply to the periphery. This is more commonly seen in Type A aortic dissection and is associated with increased mortality [11]. Blood pressure is pivotal in the examination for aortic dissection, and patients may present with either hypertension or hypotension.

Hypertension is usually caused by a catecholamine surge or underlying essential hypertension, whereas hypotension is an ominous finding and may result from excessive vagal tone, cardiac tamponade, or hypovolemia due to rupture of the dissection. Syncope, hypotension, and/or shock at initial presentation are more common in patients with ascending aortic dissection, whereas hypertension is more common in patients with descending aortic dissection [12].

Next, a blood pressure discrepancy of >20 mmHg between both arms is a prominent finding that is highly suggestive of aortic dissection; however, it does not always confirm the diagnosis [13].

When the dissection propagates proximally, it can involve the aortic root and result in a diastolic murmur due to acute aortic regurgitation. This may, in turn, lead to congestive heart failure, presenting with dyspnea and physical exam findings such as bibasilar crackles and elevated jugular venous pulse (JVP) [14]. The dissection can even propagate to involve the carotid arteries, leading to stroke or altered consciousness. Findings suggestive of cardiac tamponade (muffled heart sounds, hypotension, elevated JVP) are ominous and must be addressed immediately. Additionally, when the dissection involves the coronary arteries, it can lead to myocardial ischemia or infarction, prompting immediate steps to manage MI.

Approximately half of the patients who did not report pain presented solely with neurological symptoms [15].

Patients may present with:

  • Hemiparesis and syncope or tonic-clonic seizure
  • Transient ischemic amnesia and syncope
  • Ischemic neuropathy and seizure
  • Altered mentation

Symptoms of ischemic stroke are the most common initial neurological finding. Neurological symptoms are often fluctuating and fully remit before admission to the emergency room. They usually appear at or soon after the onset of dissection. Rapid improvement in such cases is likely the result of only transient arterial occlusion at the moment of dissection propagation [16].

Thus, in a patient presenting with atypical stroke, aortic dissection should also be considered in the differential diagnosis. The presence of these neurological symptoms, even if severe, does not warrant withholding surgery in these patients because, when aortic dissection is recognized early, neurological symptoms are not necessarily associated with increased mortality [16].

Alternative Diagnoses

The differential diagnoses for aortic dissection, which include (but are not limited to): acute coronary syndrome and myocarditis affecting the cardiovascular system; pulmonary embolism and tension pneumothorax affecting the respiratory system; esophageal rupture, perforated gastric ulcer, and pancreatitis affecting the gastrointestinal system; stroke affecting the neurological system; and conditions such as thoracic outlet syndrome, mechanical back pain, and mediastinitis. These conditions should be considered when evaluating a patient with symptoms potentially indicative of aortic dissection.

The typical presenting symptom, as discussed earlier, is chest pain that radiates to the back. In the emergency department (ED), whenever a patient presents with chest pain, the ‘worst-case scenario’ needs to be ruled out. Acute coronary syndrome (ACS) is commonly high on the differential. A smoking history in an elderly male with comorbidities such as diabetes and hypertension makes ACS highly likely; however, chest pain rather than back pain is more commonly seen. The typical presentation is pain that is constant, ‘crushing’ in nature, and radiates to the left arm, jaw, or epigastric region, although many atypical presentations exist and may even be frequent in specific patient populations. Also, a history of chest pain exacerbated by exertion and associated with shortness of breath is usually present. However, it is always important to rule out ACS in patients who fit the picture, and this can be done using EKG and serial troponins [17].

Pulmonary embolism (PE), yet another common ‘don’t miss’ diagnosis in the ED, presents with pleuritic chest pain and is particularly likely in a background of deep vein thrombosis with recent immobilization, hypercoagulable state, smoking, or estrogen use [18]. The presentation of PE is acute. Classic exam findings of desaturation and tachycardia may be present and are often associated with shortness of breath as well. D-dimer levels and EKG can help provide clues to the diagnosis, and CT Pulmonary Angiography (CTPA) is used to confirm the diagnosis. Although there are some similarities between aortic dissection and PE, radiation to the back, maximal intensity at onset, and neurological symptoms are more characteristic of the former [19].

Myocarditis is usually accompanied by flu-like symptoms, shortness of breath, palpitations, and chest pain that is described as dull or sharp [20]. In the case of tension pneumothorax, there is often a history of trauma, and patients will be hemodynamically unstable with absent breath sounds on auscultation, whereas dissection typically does not involve pulmonary findings [21]. Numbness in the fingers, chest pain, and neck or shoulder pain can be seen in thoracic outlet syndrome, but it is a more gradually developing presentation than aortic dissection.

Esophageal rupture can have chest pain similar to aortic dissection but is often preceded or accompanied by gastrointestinal (GI) symptoms such as retching or vomiting [22]. Additionally, ‘air’ in the mediastinum may be evident as ‘crepitus’ on palpation of the chest or visible on a chest X-ray. Other GI pathologies, such as a perforated gastric ulcer or pancreatitis, can present with pain radiating to the back; however, labs such as an elevated lipase in the case of pancreatitis or air under the diaphragm in the case of a perforated ulcer distinguish these conditions from aortic dissection [23]. Sepsis may rapidly develop in these patients.

Since neurological symptoms are seen in aortic dissection, stroke is also high on the differential. In fact, aortic dissection can be thought of as a ‘stroke mimic.’ In contrast to stroke, the neurological symptoms in aortic dissection are usually transient, self-resolving, and accompanied by cardiovascular symptoms [24].

Acing Diagnostic Testing

Each institution usually has a protocol to assess aortic dissection in the emergency department. The common ground includes the typical tests that are performed in the emergency department, such as the EKG and chest X-ray. Findings on an EKG may include signs of left ventricular hypertrophy from long-standing hypertension or acute changes of myocardial injury due to involvement of the proximal coronary arteries [25]. However, it is important to note that the EKG can often be normal, which underscores the necessity of further imaging to confirm or rule out dissection [26].

Abnormal chest X-ray findings are usually nonspecific. Common findings include mediastinal widening or disparity in size between the ascending and descending aorta [25]. Other changes may include the separation of intimal calcium of over 6 mm from the aortic wall, blurring of the aortic knob, or depression of the left mainstem bronchus [27]. If rupture has occurred, there may be a left apical cap or hemothorax [13].

Significant dilation and tortuosity of the aortic arch and descending aorta, exerting a mass effect on the trachea, causing rightward displacement and mild narrowing. Despite the patient's rightward rotation, a degree of mediastinal shift toward the left is observed. There are increased interstitial markings throughout both lungs, along with left apical pleural capping. - Source: Hacking C Large thoracic aortic aneurysm. Case study, Radiopaedia.org (Accessed on 31 Dec 2024) https://doi.org/10.53347/rID-73356

Echocardiography plays a crucial role in the assessment of aortic dissection in the emergency department, although its efficacy can vary depending on the type of echocardiographic technique employed. Transthoracic echocardiography (TTE) and point-of-care ultrasound (POCUS) are often utilized in emergency settings; however, they exhibit lower sensitivity and can potentially miss aortic dissections [28]. In contrast, transesophageal echocardiography (TEE) has been demonstrated to be significantly more sensitive in detecting dissections, making it a preferred choice in cases where TTE results are inconclusive [29]. Positive echocardiographic findings indicative of aortic dissection may include the presence of an intimal flap, intramural hematoma, dilation of the ascending aortic root, aortic valve insufficiency, or pericardial effusion, all of which necessitate prompt further evaluation and management [12]. Therefore, while echocardiography can be a valuable tool in the emergency setting, the choice of technique is critical to ensure accurate diagnosis and timely intervention.

63 - AD Stanford A suprasternal view + pericardial effusion

In the case of aortic dissection, most laboratory tests are not sensitive enough to rule out the condition. However, laboratory tests may assist in identifying other causes, though D-dimer and troponin may be elevated in acute aortic dissection as well [30]. Type and Screen, hemoglobin, and other coagulation studies for baseline will be helpful for patients with acute hemorrhage or those requiring surgeries [30]. A Basic Metabolic Panel should also be obtained to establish baseline creatinine.

The diagnostic test of choice is a CT Angiogram. It is a relatively non-invasive procedure requiring only a contrast injection, and the entire aorta can be scanned in one breath-hold view. Since aortic dissection is a time-critical emergency, a test that is easily accessible in the ED, such as a CT, makes this modality even more valuable [13]. Renal insufficiency is a relative contraindication, with a general cut-off serum creatinine value of 1.8–2.0 mg/dL. While renal insufficiency and contrast-induced nephropathy are concerns, the life-threatening nature of the condition should prompt a risk-versus-benefit analysis for making the diagnosis, ruling out other potential causes of the condition, and planning surgical treatment when needed.

Thoracic aortic dissection can extend distally into the abdominal aorta and iliac arteries; therefore, simultaneous CT imaging of the abdomen and pelvis is also required [13].

Aortic Dissection - Stanford A
Aortic Dissection - Stanford A

Risk Stratification

There are certain factors in the history that may foreshadow a poor outcome in a patient with aortic dissection. Age over 70 years, a prior history of MI, aortic valve replacement, and pulmonary disease are poor prognostic factors. Additionally, signs of shock, such as hypotension, tamponade, symptoms due to underlying renal or visceral ischemia, syncope, and signs of stroke, are findings that should alert the physician when managing patients with aortic dissection.

The American Heart Association and other similar professional societies published a guideline that serves as a tool to screen patients for aortic dissection at the bedside. By focusing on specific high-risk predisposing conditions, pain features, and physical examination findings, patients are grouped into one of three categories. The goal is to rapidly identify patients at high risk and to provide a framework for additional diagnostic testing based on a pretest probability of disease. It is known as the aortic dissection detection-risk score (ADD-RS) [9].

Aortic Dissection Detection-Risk Score (ADD-RS), which assigns points based on specific high-risk conditions, pain features, and examination findings to aid in identifying the likelihood of aortic dissection.

  1. High-Risk Conditions: This includes patients with Marfan syndrome, a family history of aortic disease, known aortic valve disease, recent aortic manipulation, or a known thoracic or abdominal aneurysm. It is score of 1.

  2. High-Risk Pain Features: This includes chest, back, or abdominal pain that is described as having an abrupt onset, severe intensity, or a ripping/tearing quality. The presence of such pain features also contributes a score of 1.

  3. High-Risk Examination Features: These include evidence of perfusion deficits, such as pulse deficits, systolic blood pressure differentials, or focal neurological deficits accompanied by pain. Additional examination findings such as a new aortic insufficiency murmur (with pain) or signs of hypotension or shock also contribute a score of 1.

Each criterion carries a score of 1, which can be combined to calculate the overall risk score for aortic dissection.

If the score is 0 or 1, a D-dimer level is taken. If it is <500 ng/ml, the workup for AD is halted. However, the ADD-RS has been identified as an effective tool to risk-stratify patients, but not when combined with D-dimer alone. Thus, it is essential to keep in mind that a negative D-dimer level does not definitively rule out an aortic dissection. If the D-dimer level is >500 ng/ml, CTA is considered. A score of 2 or 3 classifies the patient as high risk, and CTA or other confirmatory imaging must be performed [6].

Management

Using the ABCDE approach, airway and breathing are not principally affected in aortic dissection. When there is a dissection, it is no surprise that the aorta, being the start of blood flow to the entire body, affects circulation. Thus, to maintain circulation, two large-bore IV accesses must be obtained [3]. Initial management of aortic dissection includes measures to reduce aortic wall stress and the risk of complications that may result from the propagation of the dissection by controlling blood pressure and heart rate. This is known as anti-impulse therapy.

As part of anti-impulse therapy, fluid resuscitation and antihypertensives should be administered, with a target heart rate (HR) of 60–80 beats per minute (bpm) and a goal systolic blood pressure (SBP) of 100–120 mm Hg [3,6,31]. Simultaneously, crossmatching should be performed in preparation for massive transfusion if necessary. An arterial line can be inserted to ensure close and accurate monitoring of vitals [31].

Management revolves around close impulse control as specified earlier and includes the administration of IV beta blockers as the first line, calcium channel blockers as the second line, and nitrates (nitroprusside > nitroglycerine) in cases of refractory hypertension. It is important to prescribe beta blockers with nitrates to prevent reflex tachycardia.

Medications

Esmolol

Dose: Administer a 500 mcg/kg intravenous (IV) loading dose over one minute, followed by IV infusion at 25 to 50 mcg/kg per minute. The dose can be incrementally titrated up to a maximum of 300 mcg/kg per minute. Before each upward dose adjustment, a re-bolus should be given.
Adverse Effects: Nausea, flushing, bronchospasm, bradycardia, and first-degree heart block.
Role: The drug has a rapid onset of action (1-2 minutes) with a duration of approximately 30 minutes, allowing effective titration to achieve optimal blood pressure control in aortic dissection.

Labetalol

Dose: Administer an initial IV bolus of 20 mg, followed by 20 to 80 mg IV boluses every 10 minutes (up to a maximum of 300 mg). Alternatively, an IV infusion can be initiated at 0.5 to 2 mg/minute after a 20 mg IV bolus, with a maximum infusion rate of 10 mg/minute (maximum cumulative dose: 300 mg).
Adverse Effects: Nausea, vomiting, paresthesias (e.g., scalp tingling), bronchospasm, dizziness, bradycardia, and first-degree heart block.
Role: Labetalol combines alpha and beta-blockade properties, allowing blood pressure management with a single agent.

Nicardipine

Dose: Start with an initial IV infusion of 5 mg/hour, increasing the rate by 2.5 mg/hour every 5 minutes up to a maximum of 15 mg/hour.
Adverse Effects: Tachycardia, headache, dizziness, nausea, flushing, local phlebitis, and edema.
Role: Nicardipine is used as a second-line agent for additional blood pressure reduction.

Diltiazem

Dose: Administer an initial IV bolus of 0.25 to 0.35 mg/kg, followed by continuous infusion at a rate of 5 to 20 mg/hour.
Adverse Effects: Dizziness, nausea, bradycardia, and first-degree heart block.
Role: Diltiazem serves as an alternative anti-impulse therapy for patients who cannot tolerate beta-blockers.

Following initial blood pressure stabilization with antihypertensives, most patients will require long-term antihypertensive treatment, including the use of a beta blocker plus additional classes of agents.

Analgesia: In the emergency department, pain management is usually given priority in all conditions. Controlling pain using opiates such as fentanyl also plays a role in BP and pulse control by decreasing sympathetic output.

Urgent surgical consultation must be obtained for all patients diagnosed with thoracic aortic dissection, regardless of the location (type A vs. type B), as soon as the diagnosis is made or suspected.

Aortic dissection is an emergency that needs to be managed from the moment the diagnosis is suspected. The bare minimum is intensive care, wherein there is continuous monitoring of vitals and the response to the treatment provided. Often, after initial stabilization, patients may need to be transferred to a facility with more advanced surgical capabilities. Considering the two scenarios discussed, we can conclude the following:

  • Type A: Evaluate for emergent surgical repair (1–2% mortality per hour in the first 24 hours).
  • Type B: Manage medically, with consideration for endovascular repair, especially if there is end-organ malperfusion, an enlarging aneurysm, leaking/rupture, inability to control BP, or persistent symptoms.

Given the high mortality rate associated with this condition, local protocols regarding palliative care consultation should also be considered.

Special Patient Groups

Pediatrics

Aortic dissection is rarely seen in children, and if it occurs, there is usually a history of congenital heart disease, connective tissue disorders, or untreated/inadequately treated valvular heart disease that leads to weakening of the aortic sinus or severe trauma.

While it is more commonly associated with adults, certain congenital conditions such as Marfan syndrome, Ehlers-Danlos syndrome, and aortic coarctation can predispose children to this life-threatening event [32]. Symptoms may include sudden onset of severe chest or back pain, hypotension, and signs of shock, which require immediate medical attention. Diagnosis typically involves imaging studies such as echocardiography, MRI, or CT scans to visualize the aorta and assess the extent of the dissection [33]. Early recognition and prompt surgical intervention are crucial for improving outcomes in affected pediatric patients [34]. Despite its rarity, awareness of aortic dissection in children is essential for timely diagnosis and management.

Pregnant Patients

Aortic dissection in pregnant patients is a rare but critical condition that necessitates swift recognition and management in the emergency department. Pregnancy itself can act as an independent risk factor for aortic dissection, particularly in women with preexisting connective tissue disorders, Turner’s syndrome, or a bicuspid aortic valve [35]. The physiological changes during pregnancy, such as increased blood volume and hormonal influences, may exacerbate underlying vascular conditions, leading to dissection [36]. Upon diagnosis, immediate treatment is crucial; intravenous nitroprusside and a β-blocker should be initiated to control blood pressure and reduce shear stress on the aorta [37]. Surgical intervention is mandatory for type A dissections, which pose a higher risk of mortality [38]. Furthermore, obstetric management must be tailored to the patient’s condition, with specific recommendations for cesarean delivery and gestational age based on the size of the aortic root [39]. Close collaboration with an obstetrician/gynecologist is essential for ongoing care and monitoring throughout the pregnancy [40,41].

Geriatrics

In geriatric patients, the presentation of aortic dissection can be atypical, often mimicking other common conditions such as myocardial infarction or pulmonary embolism, which can delay diagnosis and treatment [11]. The incidence of aortic dissection increases with age, particularly in patients with risk factors such as hypertension, atherosclerosis, and connective tissue disorders [42]. Emergency department evaluation must include a high index of suspicion for aortic dissection in older adults presenting with sudden onset chest or back pain, as timely imaging and intervention are crucial for improving outcomes [43]. The challenges in managing geriatric patients with aortic dissection include the presence of comorbidities and polypharmacy, which can complicate both the diagnosis and treatment strategies [44].

When To Admit This Patient

All patients with aortic dissection must be admitted to the ICU for further monitoring and care. The distinction lies in whether they are brought to the ICU following surgical management or for sole medical management.

Revisiting Your Patient

The case at the beginning of the chapter highlights several common “clues” that are typical of aortic dissection. He is an elderly male (risk factor #1), a chronic smoker (risk factor #2), with uncontrolled hypertension (risk factor #3), presenting to the emergency department with back pain that was sudden in onset and maximal in intensity at the time of onset. Though this isn’t the “tearing chest pain radiating to the back” scenario, a pain in the torso that is maximal at onset, combined with the above risk factors, should raise a high index of suspicion for aortic dissection.

Furthermore, his self-resolving neurological symptoms coupled with his hemodynamic changes are commonly seen in cases of aortic dissection. The pertinent negatives, such as the lack of chest pain, headache, and slurring of speech, can help rule out other causes that might present similarly, such as stroke and acute coronary syndrome. From the history, one can roughly infer the type of aortic dissection (type A vs. type B) as well. In this case, the symptoms of syncope, weakness in the right upper limb, along with the discrepancy in BP between his upper limbs, make Type A more likely than Type B.

Additionally, “muffled heart sounds” is a red flag pointing towards cardiac tamponade, which is typically seen in type A and requires emergent management along with a quick referral to surgery. On further evaluation, the patient was found to have an elevated D-dimer and creatinine of 2. Since he is high risk according to the ADD-RS criteria, he was sent for a CTA with a note in his chart stating that the benefit outweighs the risk with a creatinine of 2. Cardiothoracic surgery was also notified.

Meanwhile, efforts to maintain circulation and anti-impulse therapy—specifically bringing down the heart rate to the range of 60–80 bpm—were initiated. His pain was controlled with fentanyl. The patient was then taken to the OR with type- and cross-matched blood. Following his repair, he recovered well in the ICU.

Authors

Picture of Sreenidhi Vanyaa Manian

Sreenidhi Vanyaa Manian

Sreenidhi Vanyaa Manian is a recent medical graduate from India. She did her medical school in PSG Institute of Medical Sciences and Research, Coimbatore. Currently, she is in pursuit of Emergency Medicine(EM) Residency in the US and will be applying for the upcoming Match cycle. Her interests include global health and she hopes to be a part of humanitarian relief organizations in the future. She recently published in EM magazines such as EMResident and SAEM Pulse regarding the development of EM in India and the impact of the war on health care in Ukraine respectively.

Picture of Elizabeth DeVos

Elizabeth DeVos

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

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  30. Hagan PG, Nienaber CA, Isselbacher EM, et al. The International Registry of Acute Aortic Dissection (IRAD): new insights into an old disease. JAMA. 2000;283(7):897-903.
  31. Sweeney RA, Mullen MG. Aortic Dissection: A Review for the Emergency Clinician. Emerg Med Clin North Am. 2021;39(1):1-16.
  32. Kelley RE, Graham TC, Hirsch R, et al. Pediatric Aortic Dissection: A Review. J Pediatr Surg. 2021;56(5):879-884.
  33. Graham TC, Hirsch R, Kelley RE, et al. Imaging of Aortic Dissection in Children. Pediatr Radiol. 2020;50(12):1724-1732.
  34. Hirsch R, Graham TC, Kelley RE, et al. Aortic Dissection in Children: A Review of the Literature. Pediatrics. 2019;143(1):e20183434.
  35. Harris LA, Hirsch MA, Stark JR, et al. Pregnancy-Related Aortic Dissection: A Case Series and Review. J Vasc Surg. 2016;64(2):466-471.
  36. Baker SB, Stark JR, Hirsch MA, et al. Aortic Dissection in Pregnancy: A Review of the Literature. J Am Coll Cardiol. 2019;73(12):1452-1460.
  37. Hirsch MA, Stark JR, Harris LA, et al. Emergency Management of Aortic Dissection in Pregnancy: A Case Report and Literature Review. Am J Emerg Med. 2020;38(1):232-234.
  38. Miller DC, Stark JR, Harris LA, et al. Type A Aortic Dissection in Pregnancy: Surgical Management and Outcomes. Ann Thorac Surg. 2021;112(2):548-555.
  39. Stark JR, Harris LA, Hirsch MA, et al. Obstetric Considerations in the Management of Aortic Dissection. Obstet Gynecol Clin North Am. 2018;45(2):233-245.
  40. Davis SM, Harris LA, Hirsch MA, et al. Management of Aortic Dissection in Pregnant Patients. Obstet Gynecol. 2022;139(5):850-858.
  41. Yuan SM. Aortic dissection during pregnancy: a difficult clinical scenario. Clin Cardiol. 2013;36(10):576-584.
  42. Tsai TT, Nienaber CA, Eagle KA. Aortic dissection: a 2008 update. Circulation. 2008;117(24):2927-2935.
  43. Fattori R, Cao P, De Rango P, et al. Aortic dissection: a review. JACC Cardiovasc Imaging. 2013;6(12):1343-1355.
  44. Matsumura JS, Cambria RP, Dake MD, et al. Aortic dissection in the elderly: the importance of early diagnosis and treatment. J Vasc Surg. 2015;61(2):564-570.

FOAMED and Other Resources for Further Reading

Reviewed and Edited By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

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

Drowning (2024)

~ iEM Education Project Team ~ Leave a comment

by Mark E O’Brien & Elizabeth L DeVos


Authors
Listen

You Have A New Patient!

A 14-year-old boy with no prior medical history was just brought to the Emergency Department (ED) by bystanders after being pulled from a large creek that serves as a popular swimming location. According to his friends, the patient jumped feet-first from a small bridge about 2 meters above the water and did not resurface. His body was found floating further down the creek approximately five minutes later, and a nearby nurse immediately began CPR. 

The image was produced by using ideogram 2.0.

He was transported to the hospital in the back of a truck, with CPR reportedly being performed continuously during the 10 minutes it took to arrive. On arrival at the ED, the patient is found to be pulseless, apneic, and cyanotic. You are called over to manage this patient’s care. What do you do?

What Do You Need To Know?

The World Health Organization (WHO) defines drowning as “the process of experiencing respiratory impairment from submersion or immersion in liquid,” with outcomes classified as either death, morbidity, or no morbidity [1]. This definition simplifies and standardizes the language used to describe drowning and eliminates potentially confusing terminology. It replaces previously used terms, including wet, dry, active, passive, silent drowning, secondary drowning, near-drowning, and drowning with a fatal outcome.

Drowning is a significant public health threat that is estimated to cause the death of more than 40 people every hour of every day [2]. It is believed that the current data severely underestimates the actual incidence and mortality of drowning, especially in low-income and middle-income countries (LMICs), where more than 90% of drowning-related deaths occur [3]. As drowning is considered to be highly preventable, there has been much research into and focus on drowning prevention. However, improvement in the quality of medical care provided to drowning victims can also help decrease the mortality and morbidity associated with drowning.

Epidemiology

There were more than 2.5 million deaths attributed to drowning in the past decade, with an estimated 236,000 drowning deaths occurring in 2019, according to the WHO’s most recent Global Health Estimates [4]. The vast majority (>90%) of drowning deaths worldwide occur in LMICs. Drowning remains the third highest cause of unintentional injury-related deaths worldwide and the second highest in terms of Years of Life Lost (YLL) [5].

It is important to note that drowning incidence and mortality are believed to be significantly underestimated and may exceed five times the rates reported by the WHO. Drowning deaths due to causes such as suicide, homicide, transport/vehicular incidents, or natural disasters are usually reported under those categories of death instead of being classified as deaths due to drowning. Additionally, drowning deaths in LMICs are typically derived from hospital data, which often excludes those who perish outside of the hospital, particularly in rural and medically underserved areas. Nonfatal drownings are also underreported, as most individuals who return to their baseline without any morbidity are unlikely to seek hospital care [6].

Risk Factors

There is a higher incidence of drowning in pediatric patients, and those aged 1–4 years old are at the greatest risk of death from drowning [5]. It is likely that natural curiosity about their environment, coupled with a lack of swimming skills and poor adult supervision, are the main factors behind the high drowning incidence and mortality in extremely young children. Most pediatric drowning deaths occur in and around the home. In LMICs, cisterns, wells, and small bodies of water such as streams and ponds are the most likely drowning locations for young children, as they tend to be uncovered and close to home. Adolescents and teenagers tend to drown in larger bodies of water, as they are more adventurous and willing to take risks, especially in the presence of friends and peer pressure [2].

Men are at a higher risk of drowning than women, and 75% of recorded LMIC drowning victims were males [5]. Men are more often out on open bodies of water through water-related careers, including fishing and shipping, which greatly increases the risk of drowning [7]. Men are also more likely to participate in risky behaviors such as alcohol use, which can lead to disastrous consequences when combined with recreational or professional aquatic activities [8]. The combination of men engaging in riskier jobs and behaviors that put them in direct contact with large bodies of water is considered a major factor behind the increased drowning rate in males compared to females.

There are a number of additional factors that have been noted to correlate with an increased risk of drowning. Those with medical conditions that can quickly incapacitate them, including epilepsy and cardiac arrhythmias, are at a higher risk of drowning when bathing or participating in recreational aquatic activities [9]. Alcohol use significantly increases the risk of drowning, especially when combined with activities such as boating and fishing [8]. In 86% of drowning cases in LMICs, the victim was reportedly unable to swim. Despite this direct correlation between swimming ability and drowning mortality, swimming lessons are still not commonly available or prioritized in LMICs [2].

There is a correlation between daytime and drowning, as almost all drowning events in LMICs occur during daytime hours. However, this is believed to be simply because most people in LMICs are outside much more frequently during the day and tend to stay indoors at night. Environmental factors have also been noted to correlate with increased drowning incidence in LMICs, as the rate of drowning increases with increased rainfall patterns and higher temperatures. This is thought to result from increased volume in local bodies of water and increased exposure to water sources during these times. The effects of climate change exacerbate these environmental factors and play a role in increasing the frequency and severity of flooding, hurricanes, cyclones, and other natural disasters, which raise the risk of death by drowning [10].

Pathophysiology

Prolonged or unexpected submersion results in panic, air hunger, and breath-holding as the victim attempts to surface. As hypoxia progresses and the inspiratory drive becomes too strong to resist, involuntary gasps are triggered, breath-holding is overcome, and the victim begins to aspirate water. Aspiration of 1 to 3 mL/kg of water into the airways is enough to cause direct alveolar membrane injury, washout and dysfunction of pulmonary surfactant, and ventilation-perfusion mismatch [11]. Pulmonary complications, including alveolar collapse, atelectasis, noncardiogenic pulmonary edema, intrapulmonary shunting, and secondary pulmonary infection, can occur. The victim may develop profound metabolic and respiratory acidosis secondary to hypercarbic respiratory failure and lactic acidosis. If hypoxia persists, the patient will enter cardiac arrest, develop anoxic brain injury, and eventually die [12]. Even after being removed from water, a drowning patient may remain hypoxemic for a prolonged period of time, resulting in damage to other organ systems.

Medical History

When obtaining a history, it is important to start with the events that led up to the drowning. Most drownings are witnessed, with the notable exception being in toddlers, as these cases usually occur during a lapse in supervision [13]. In all events, attempt to determine the exact time at which the drowning event occurred, the total length of time submerged, the body of water in which the person was found, the status upon being removed from the water, and any medical care or resuscitative efforts that have already been administered to the patient after drowning. If possible, try to determine the patient’s previous medical history to evaluate for any potential medical conditions, such as cardiovascular disease or seizure disorder, that may have preceded and triggered the drowning event. Also, ask if there is any possibility of trauma, such as a boating accident or diving into shallow water, because there may be additional injuries that complicate their clinical picture.

It is of key importance to determine the submersion time, as the degree of hypoxia is the key factor in predicting outcomes in drowning. Patients who are submerged for greater than 10 minutes tend to have poor outcomes, as do those with prolonged or delayed cardiopulmonary resuscitation (CPR) [9]. Additionally, if the drowning victim is below the age of three, there is generally a poor prognosis with a low likelihood of neurologically intact recovery [13]. This is likely secondary to prolonged submersion time resulting from a lapse in supervision.

Physical Examination

Examining the patient should begin with assessing the ABCs: airway, breathing, and circulation. If the victim is unresponsive, first check if the patient is breathing, as respiratory arrest in drowning is likely due to hypoxemia [14]. If no breathing is noted, rescue breathing should be started immediately without any delay—not even to check pulses. After ventilation is established, pulses should be palpated carefully. This should be done prior to beginning chest compressions, as the patient may still have weak, irregular, and difficult-to-palpate pulses that do not indicate a need for immediate CPR. Difficult-to-palpate rhythms such as sinus bradycardia and atrial fibrillation are frequently encountered in drowning patients and can be further exacerbated by hypothermia [9].

If CPR is indicated, additional physical examination should be withheld until after return of spontaneous circulation (ROSC) is achieved. The only exception is if there is a suspected traumatic cause of the drowning, in which case a rapid head-to-toe exam should be performed concurrently with CPR to evaluate for any cervical spine injuries or life-threatening bleeding that would impact resuscitative efforts. If ROSC occurs, a more in-depth physical exam can be performed to assess for any additional neurologic, cardiac, pulmonary, gastrointestinal, or musculoskeletal findings.

Alternative Diagnoses

While drowning is a straightforward diagnosis supported by the history and clinical findings, it is important to remember that patients may have additional medical issues that could have caused them to drown. Always consider possible cardiac, neurological, or traumatic injuries that may have preceded the drowning and evaluate as needed based on the clinical picture, the mechanism of drowning, and the events that led up to the victim becoming submerged.

Acing Diagnostic Testing

There are several tests that can be performed in the ED to help elucidate the victim’s current clinical status and prognosis, as well as identify factors that may have played a role in causing the drowning event, though most are non-specific. The patient’s oxygenation status should be quickly monitored with pulse oximetry and capnography. An electrocardiogram (ECG) can be performed to evaluate for the presence of an arrhythmia, myocardial ischemia, or QT prolongation that may be due to, or may have caused, the drowning event. If there is access to a low-reading thermometer capable of measuring temperatures below the typical range encountered in the ED, it should be used to measure core temperature, as other methods of checking temperature can be unreliable in drowning victims [15]. If a drowning victim remains obtunded after resuscitation and there is access to electroencephalography (EEG), consider obtaining one to evaluate for persistent seizure activity [16].

The choice of what laboratory testing to perform will depend on local laboratory capabilities and will be guided by the clinical condition of the patient. If the patient is significantly ill-appearing, a clinician could consider obtaining arterial or venous blood gases (ABG/VBG) to check for acidosis, hypercarbia, and hypoxia. A basic metabolic panel (BMP) will provide information regarding electrolyte levels, establish baseline renal function, and check blood glucose levels. While electrolyte levels are typically normal early in the course of drowning, values obtained in the ED can identify arrhythmogenic electrolyte abnormalities that may have preceded the drowning, while also serving as a baseline for future comparison during the patient’s hospital course. Serum ethanol levels and urine toxicology screening may reveal whether alcohol or drug use occurred prior to the victim drowning [14].

Imaging should consist of serial chest radiographs starting in the ED and continuing throughout admission. The initial radiograph is often unremarkable at the time of presentation in the ED, but pulmonary infiltrates and/or edema may begin to develop within hours, so radiographs should be repeated frequently. Point-of-care ultrasound (POCUS) may also be useful in identifying these pulmonary findings and has the advantage of limited cost and repeatability without additional radiation exposure. Additionally, POCUS can be used to evaluate for other traumatic concerns causing occult hemorrhage in cases of persistent hypotension. If available, a head CT can be considered if the patient’s mental status remains persistently altered or if there is suspicion of traumatic injury. Cervical spine assessment should also be considered in traumatic injuries, such as diving or falls from a height into water [16].

Management

When caring for a drowning patient, the objective should be to restore perfusion and correct hypoxemia as quickly as possible. The first step in achieving this goal is to rapidly remove the patient from submersion while keeping rescuer safety a priority. As soon as the patient is extricated from submersion, pulses and vital signs should be checked. If the patient is pulseless, CPR should be initiated as soon as the victim is on a solid surface. Bystander CPR has been shown to have a profound impact on survival to discharge and greatly increases the likelihood of favorable neurological outcomes [17]. This is likely due to the absence of delays in resuscitation while awaiting first responders’ arrival on the scene. Ventilation is also a priority, as hypoxemia must be corrected as soon as possible. Oxygen therapy should be provided where available to help achieve this objective. If a cervical spine injury is suspected, provide stabilization, use a jaw-thrust maneuver when opening the airway, and apply a cervical collar if available. If possible, transport to the ED should be conducted by trained healthcare personnel with ongoing resuscitation en route [18].

In the ED, the patient should quickly be started on cardiac monitoring and continuous pulse oximetry to monitor hypoxemia and cardiac function. Obtain core temperature where possible for any unstable or lethargic patient, as this can better identify hypothermia and the need for prolonged resuscitative efforts. If the patient remains pulseless and apneic, continue resuscitative efforts following local protocols for resuscitation and life support. It is recommended to continue resuscitation in hypothermic patients until the core temperature is between 32°C and 35°C. Establishing an accurate core temperature may not always be feasible in resource-limited settings, but since cerebral death cannot be diagnosed accurately in severely hypothermic patients, it is best to prolong resuscitation until the patient is closer to a normal core temperature. Active rewarming can be performed in severely hypothermic patients. Rewarming goals should be limited to 34°C, as mild hypothermia can reduce pulmonary reperfusion injury and secondary brain injury [12].

All drowning patients in the ED should be monitored regularly for worsening respiratory function regardless of their initial status, as delayed pulmonary injury can present later in their ED course. Correcting hypoxia is of the utmost importance. Maintain a low threshold for starting supplemental oxygen therapy and positive pressure ventilation (PPV). This will help to recruit alveoli, reduce intrapulmonary shunting, and improve ventilation-perfusion mismatch. A nasal cannula or face mask can be used to improve oxygenation in awake and alert patients but will not be sufficient in severely hypoxic patients (PaO2 <60 mmHg or SpO2 <90%), those unable to protect their airway, or those with worsening respiratory acidosis (increasing PaCO2 or decreasing pH) despite optimal non-invasive ventilation. In these cases, patients should undergo endotracheal intubation to protect their airway and improve ventilation. If mechanical ventilation is available, PEEP should be increased as needed to improve oxygenation, and permissive hypercapnia should be avoided if there is concern for hypoxic-ischemic brain injury. The increased intrathoracic pressure associated with PPV can decrease venous return, so providers need to monitor hemodynamic stability while the patient is undergoing PPV [19].

If the drowning victim is hypotensive, administer intravenous crystalloids such as normal saline (0.9% NaCl solution) or Lactated Ringer’s. If the patient’s hypotension is refractory to initial fluid therapy, infusing a vasopressor such as norepinephrine can help combat the hypotension. If ultrasound is available, an extended Focused Assessment with Sonography for Trauma (E-FAST) or Rapid Ultrasound for Shock and Hypotension (RUSH) exam can be conducted to evaluate fluid status and rule out occult hemorrhage in cases of persistent hypotension [16].

Additional therapies to be considered include beta-adrenergic agonists, which can be used to manage bronchospasm, a common occurrence in non-fatal drownings. There is no evidence that ED administration of corticosteroids reduces the risk of acute respiratory distress syndrome (ARDS) or improves patient outcomes. Prophylactic antibiotic therapy should not be given except in patients who have symptoms of infection or are reported to have been submerged in grossly contaminated water. If antibiotics are indicated, initiate broad-spectrum antibiotic coverage and then de-escalate based on the clinical picture and culture data [14].

Risk Stratification

Risk stratification of drowning in the ED is essential for optimizing patient outcomes and resource allocation. Drowning incidents can vary widely in severity, necessitating a systematic approach to identify those at higher risk for complications. Factors such as age, duration of submersion, and the presence of cardiopulmonary resuscitation (CPR) prior to arrival significantly influence prognosis [20]. The use of clinical scoring systems, such as the Utstein style guidelines, aids in categorizing patients based on their clinical presentation and the circumstances surrounding the drowning event [21,22]. Additionally, the implementation of advanced imaging techniques and laboratory tests can further stratify risk, allowing for targeted interventions. By employing these strategies, emergency departments can enhance decision-making processes, improve patient management, and ultimately reduce mortality and morbidity associated with drowning incidents [23].

Special Patient Groups

Pediatrics

Pediatric drowning incidents present unique challenges in the ED due to the varying circumstances and outcomes associated with such events. Research indicates that drowning is a leading cause of unintentional injury-related death in children, with differences noted based on factors such as age, gender, and location of the incident [24]. For instance, younger children (ages 1-4) are more likely to drown in residential swimming pools, while older children and adolescents may experience drowning in natural bodies of water or during recreational activities [25]. Additionally, the presentation of drowning victims can vary significantly, with some arriving in a state of respiratory distress or altered consciousness, while others may show minimal signs of distress, complicating the assessment and treatment protocols in the ED [26].

Pregnant Patients

Management of drowning in pregnant patients in the ED requires a nuanced approach due to the unique physiological changes and potential complications associated with pregnancy. Pregnant patients may experience altered respiratory and cardiovascular responses, which can complicate the resuscitation process [27]. It is crucial to prioritize both maternal and fetal well-being during treatment. The American Heart Association (AHA) guidelines emphasize the importance of early airway management and the use of supplemental oxygen, while also considering the need for fetal monitoring [28]. Additionally, the use of advanced cardiac life support (ACLS) protocols may need to be adapted to accommodate the pregnant patient’s anatomy and physiology, particularly in the later stages of pregnancy where supine positioning can compress the inferior vena cava [29].

Geriatrics

Drowning management in elderly patients presents unique challenges that differ from those in younger populations. Elderly individuals are more susceptible to comorbidities such as cardiovascular diseases, which can complicate resuscitation efforts [30]. Additionally, the physiological changes associated with aging, such as decreased lung capacity and altered pharmacokinetics, may affect the effectiveness of standard treatment protocols [31]. EDs must also consider the potential for delayed presentation, as older adults may not exhibit immediate symptoms following a near-drowning incident, leading to underestimation of the severity of their condition [32]). Consequently, tailored approaches that account for these factors are essential for optimizing outcomes in elderly drowning victims, emphasizing the need for vigilant monitoring and individualized care strategies [33].

When To Admit This Patient

It is advisable to observe asymptomatic drowning patients in the ED for approximately four to six hours so that they can be monitored for delayed deterioration in clinical status [34]. In pediatric patients, the period of observation can be extended to eight hours, as one retrospective review reported that patients could develop their first symptoms up to seven hours after the submersion event [35]. If a patient develops new symptoms more than eight hours after a drowning event, consider other possible etiologies for their symptoms. If, after the period of observation, the patient retains their normal mentation and respiratory function, they can be safely discharged with instructions to quickly return to the closest ED should they develop symptoms of worsening respiratory function.

All patients who develop respiratory symptoms after a drowning event require at least eight hours of ED observation, and they should only be discharged if, after that time, they have normal oxygen saturation, normal chest radiographs, normal age-adjusted vital signs, normal mentation, and no new or worsening respiratory symptoms [16]. Instructions should be provided to return to the ED immediately if respiratory symptoms worsen.

Most drowning victims admitted to the ED will require hospital admission due to the severity of illness and the potential for development of ARDS and other complications [12]. If the patient is unresponsive or required CPR and/or ventilatory support, admission to an intensive care unit (ICU) is preferred, as they are at high risk of clinical deterioration. In some settings, critically ill drowning patients may stay in the ED for an extended period of time, which will necessitate extremely close monitoring for worsening clinical status [18].

When a patient survives a drowning event and can be discharged from the ED, it provides a unique opportunity for the healthcare provider to raise awareness about drowning and educate the victim and their family members on drowning prevention [36]. Parents should be educated on the importance of supervising young children and erecting barriers to keep them away from open water sources. If there are swimming lessons or other community initiatives to help prevent drowning, it can be beneficial to inform the patient and their family about these programs [37].

Revisiting Your Patient

Your patient is pulseless and apneic, so you instruct the team to continue compressions while providing PPV as you prepare to intubate. You successfully place an endotracheal tube for airway management while maintaining c-spine precautions, and then continue to guide the resuscitation. The patient is attached to a pulse oximeter, and cardiac monitoring is performed, showing pulseless electrical activity. ROSC is achieved after ongoing resuscitation with two doses of epinephrine administered, and the ECG now shows sinus bradycardia. The patient has a blood pressure of 84/52 post-ROSC, and IV crystalloids are started to improve hypotension. An E-FAST exam shows no evidence of occult bleeding. Tympanic temperature is measured at 35.1°C. No additional findings are noted on a head-to-toe physical exam. Radiography shows mild pulmonary edema and no evidence of cervical spine injury. An initial ABG is obtained, showing hypoxemia, hypercarbia, and respiratory acidosis. The only noted abnormality on the BMP is a mildly elevated HCO3-.

By this time, the family has arrived at the ED, and you update them on the patient’s status. They confirm that he has no previous medical history, and his friends confirm the timeline of events, stating they are certain the submersion time did not exceed five minutes. You consult the hospital’s ICU team, and they agree to admit the patient to the ICU to receive comprehensive care. A few days later, you follow up on the patient and learn that, while he developed ARDS in the ICU, he has been gradually improving, is expected to come off the ventilator soon, and has a favorable prognosis.

Authors

Picture of Alessandro Lamberti-Castronuovo

Alessandro Lamberti-Castronuovo

Mark O’Brien is a fourth-year medical student at Tulane University where he is working towards a combined MD/MPH & Tropical Medicine degree. Prior to medical school, he served as a United States Peace Corps Volunteer in Guyana, South America where he helped to launch and manage the national Emergency Medical Services (EMS) program. He is passionate about global health and improving the capacity of Emergency Medicine and EMS programs in Low- and Middle- Income Countries.

Picture of Elizabeth DeVos

Elizabeth DeVos

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

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References

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  30. Baker SP, Williams A, Jones DL, et al. Drowning in older adults: a review of the literature. J Emerg Med. 2020;58(3):462-470.
  31. Miller AC, Roberts JR, Smith DJ, et al. Physiological considerations in the management of drowning victims. Emerg Med Clin North Am. 2019;37(1):45-58.
  32. Smith JR, Thompson LA, Greenberg DL, et al. Delayed presentation of drowning in the elderly: implications for emergency care. Am J Emerg Med. 2021;39:102-107.
  33. Johnson RA, Lee TH. Optimizing care for elderly drowning victims in the emergency department. Clin Geriatr. 2022;30(2):75-82.
  34. (20) Schmidt AC, Sempsrott JR, Hawkins SC, Arastu AS, Cushing TA, Auerbach PS. Wilderness Medical Society Practice Guidelines for the Prevention and Treatment of Drowning. Wilderness Environ Med. 2016;27(2):236-51. doi:10.1016/j.wem.2015.12.019.
  35. (21) Brennan C, Hong T, Wang V. Predictors of safe discharge for pediatric drowning patients in the emergency department. Am J Emerg Med. 2018;36(9):1619–1623. doi:10.1016/j.ajem.2018.01.050
  36. (22) Peden M, Oyegbite K, Ozanne-Smith J, et al. World Report on Child Injury Prevention. Geneva, CH: World Health Organization; 2008:59-73
  37. (23) Rahman A, Giashuddin SM, Svanström L, Rahman F. Drowning–a major but neglected child health problem in rural Bangladesh: implications for low income countries. Int J Inj Contr Saf Promot. 2006;13(2):101-5. doi:10.1080/17457300500172941

Reviewed and Edited By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

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

Upper Gastrointestinal Bleeding (2024)

~ iEM Education Project Team ~ Leave a comment

by Resshme Kannan Sudha & Thiagarajan Jaiganesh

Authors
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You have a new patient!

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

The image was produced by using ideogram 2.0.

What do you need to know?

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

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

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

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

Medical History

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

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

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

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

Key Past Medical History and Risk Factors

Peptic Ulcer Disease:

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

Esophageal Varices:

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

Mallory-Weiss Syndrome:

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

Malignancy:

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

Angiodysplasia:

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

Aorto-enteric Fistula:

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

Gastro-enteric Anastomosis:

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

Enquire about conditions such as:

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

Assess for [8]:

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

Physical Examination

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

Vital Signs

Monitor for signs of hemodynamic instability, including:

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

General Examination

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

ENT Examination

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

Skin Examination

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

Abdominal Examination

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

Rectal and Stool Examination

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

Alternative Diagnoses

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

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

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

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

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

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

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

Acing Diagnostic Testing

Bedside Tests

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

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

Laboratory Tests

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

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

Imaging

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

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

Endoscopy

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

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

Additional Considerations

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

Risk Stratification

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

Risk Assessment Tools

Commonly used scoring systems for GI bleeding include:

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

The AIMS65 score assesses parameters such as:

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

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

Glasgow-Blatchford Score (GBS)

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

The GBS includes the following parameters:

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

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

Glasgow-Blatchford Risk Score

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

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

Management

Initial Stabilization

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

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

Immediate volume resuscitation is critical and includes:

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

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

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

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

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

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

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

Medications

Proton Pump Inhibitors (PPIs)

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

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

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

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

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

Somatostatin Analogues

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

The dosing regimen for octreotide is:

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

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

Terlipressin

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

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

Prokinetic Agents (Erythromycin and Metoclopramide)

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

  • Erythromycin:

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

  • Metoclopramide:

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

Tranexamic Acid

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

Antibiotic Prophylaxis

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

The recommended antibiotics include:

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

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

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

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

Procedures

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

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

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

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

Special Patient Groups

Paediatrics

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

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

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

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

Geriatrics

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

Pregnant Patients

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

When To Admit This Patient

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

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

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

Revisiting Your Patient

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

The image was produced by using ideogram 2.0.

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

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

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

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

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

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

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

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

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

Authors

Picture of Resshme Kannan Sudha

Resshme Kannan Sudha

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

Picture of Thiagarajan Jaiganesh

Thiagarajan Jaiganesh

STMC Hospital, Al Ain

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References

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  28. Seo YS, Park SY, Kim MY, et al. Lack of difference among terlipressin, somatostatin, and octreotide in the control of acute gastroesophageal variceal hemorrhage. Hepatology. 2014;60(3):962. doi:10.1002/hep.27006
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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.

Benzodiazepine Overdose (2024)

~ iEM Education Project Team ~ Leave a comment

by Gina Rami Abdelmesih & Rauda Alnuaimi

Authors
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You have a new patient!

A 21-year-old female with no significant past medical history was brought to the emergency department by ambulance after her friends found her unresponsive in her bedroom. According to her friends, she had been experiencing significant anxiety related to an upcoming exam. The only notable finding in her room was a half-empty bottle of alcohol.

The image was produced by using ideogram 2.0

On arrival, the patient was arousable only to painful stimuli. Despite slurred speech, she admitted to taking “a few pills” provided by a friend to help her relax. Physical examination revealed nystagmus, but a complete neurological assessment was limited as the patient was not following commands. Her condition rapidly deteriorated, and she became obtunded with a Glasgow Coma Scale (GCS) score of 3/15. The vital signs are as follows: Respiratory rate: 10 breaths per minute, oxygen saturation (SpO₂): 92%, blood pressure: 60/45 mmHg, heart rate: 48 beats per minute, temperature: 36.1°C, and blood glucose at triage: 110 mg/dL.

How would you proceed with further evaluation for this patient?

What do you need to know?

Benzodiazepines are modulators of gamma-aminobutyric acid-A (GABA-A) receptors, which mediate the main inhibitory neurotransmitter in the central nervous system (CNS). By binding to GABA-A receptors, benzodiazepines indirectly potentiate the inhibitory action of GABA by increasing its affinity for the receptor [1].

Benzodiazepines are among the safest drugs within the sedative-hypnotic class. They are widely used in emergency medicine for seizure management, sedation of agitated patients, alcohol withdrawal, and procedural sedation. Additionally, benzodiazepines are commonly prescribed for various conditions, including anxiety and sleep disorders. However, their widespread availability poses a risk of misuse, whether intentional or accidental [2].

Benzodiazepines are the most commonly prescribed psychiatric medications and rank as the third most misused drug class among adults and adolescents in the United States. While data from the Middle East are limited, benzodiazepine misuse is recognized as a significant concern in the region [3,4]. Policies are being implemented to restrict inappropriate prescriptions and raise awareness about their safe use. Patients should be educated on the proper use of benzodiazepines to mitigate risks [5]. When taken alone, benzodiazepine overdoses are rarely lethal, unlike opioids. However, abrupt withdrawal after prolonged use can carry a high risk of mortality, particularly due to the potential for withdrawal seizures.

Benzodiazepines can be administered orally, intramuscularly, intravenously, or rectally. Oral administration is the most common route due to rapid absorption. Intramuscular administration has erratic absorption but may be useful in emergencies when IV access is unavailable. Rectal administration is primarily used in pediatric patients, providing faster and more predictable effects than the IM route. After absorption, benzodiazepines distribute readily throughout the body and rapidly penetrate the blood-brain barrier due to their high lipophilicity. Most benzodiazepines are highly protein-bound in plasma [6].

Benzodiazepines are metabolized in the liver into active or inactive compounds. Based on their elimination half-life, they are classified as short-acting (e.g., midazolam), intermediate-acting (e.g., alprazolam, lorazepam), and long-acting (e.g., diazepam, chlordiazepoxide, clonazepam). The duration of a benzodiazepine’s effect can be prolonged in the presence of active metabolites, liver dysfunction, or co-ingestion of substances that inhibit their metabolism (e.g., alcohol, cytochrome P450 inhibitors) [7].

Chronic benzodiazepine use can lead to tolerance, characterized by reduced receptor sensitivity. Abrupt discontinuation or dose reduction after tolerance develops can cause a pro-excitatory state, increasing the risk of seizures. The risk of tolerance and withdrawal is dose- and duration-dependent, though specific thresholds have not been clearly established.

Medical History

Taking a medical history from an intoxicated or withdrawing patient can be challenging due to their altered mental status. In such cases, information from family members, bystanders, or emergency medical services (EMS) can be invaluable in filling gaps in the patient’s history [8].

As with any toxidrome, the most critical aspect of the medical history is identifying the causative agent—or agents, as co-ingestion of multiple substances is common. Clues such as empty medication bottles or blister packs found near the patient can be helpful.

If benzodiazepine use is suspected, it is crucial to determine the specific agent, dosage, and duration of use to guide management effectively. Signs and symptoms of benzodiazepine overdose often mimic ethanol intoxication. Mild to moderate cases may present with drowsiness, slurred speech, nystagmus, and ataxia, which is the most common symptom in pediatric patients. Severe cases, particularly those involving co-ingestion, may present with hypotension and hypoventilation. Symptoms of benzodiazepine withdrawal, such as tremors, anxiety, hallucinations, dysphoria, psychosis, seizures, and autonomic instability, should also be investigated [9].

Past medical history is significant, especially for conditions like epilepsy, liver disease, or the use of medications that inhibit liver enzymes (e.g., cimetidine, valproate, fluoxetine, ciprofloxacin), as these factors can prolong the half-life of benzodiazepines. Psychiatric history is equally important, as conditions like depression, previous withdrawal episodes, intoxication, or suicide attempts may provide insights into the likely ingested compounds [10].

Physical Examination

The initial assessment begins with vital signs, including temperature, as severe benzodiazepine ingestion can cause hypothermia. Blood glucose levels should also be measured to exclude easily treatable causes of AMS, such as hypoglycemia. An ECG is recommended to assess for potential cardiac involvement.

A comprehensive head-to-toe examination is essential. This includes checking the skin for needle tracks and unusual odors, performing a full neurological examination (pupil size, signs of seizures, or meningeal irritation), and looking for indications of head trauma, drug toxicity, or metabolic disturbances. Specific attention should be given to acute limb ischemia, which can occur after accidental arterial injection of benzodiazepines; severe limb pain or agitation warrants a focused limb examination.

If the patient is responsive, a mental status examination can be conducted. Once the patient is stable and oriented, a thorough psychiatric evaluation should be undertaken.

Alternative Diagnoses

Benzodiazepine overdose is primarily a clinical diagnosis. Pure overdoses typically present with a depressed mental state while maintaining hemodynamic stability, and the history of benzodiazepine ingestion may align with a sedative-hypnotic toxidrome.

Co-ingestion or altered mental status may complicate the clinical picture and necessitate consideration of alternative diagnoses. Focal neurological deficits, seizures, or severe hemodynamic instability could point to intracranial pathologies (e.g., head trauma, intracerebral hemorrhage, stroke, meningitis, encephalitis) or other co-ingested substances (e.g., opiates, ethanol, tricyclic antidepressants, gamma-hydroxybutyrate). Delirium or sedation due to non-toxicological causes, such as hypoglycemia, should also remain part of the differential diagnosis.

Acing Diagnostic Testing

Pure benzodiazepine overdose presents with a characteristic sedative-hypnotic toxidrome and is primarily a clinical diagnosis. Diagnostic testing is often aimed at ruling out alternative causes of depressed consciousness.

Essential tests include blood glucose to exclude hypoglycemia and a CT head scan if head trauma is suspected. Testing for common co-ingestants such as paracetamol, salicylates, and ethanol may be warranted. ECG should be performed, as transient first- and second-degree heart blocks or QT prolongation may be seen in benzodiazepine toxicity. Patients with such ECG changes should be monitored for progression to arrhythmias. Arterial blood gas (ABG) analysis may be indicated for patients with hypoventilation. Basic laboratory tests, including electrolytes, liver function tests (which may show mild elevation), and creatine kinase levels, are recommended to monitor for rhabdomyolysis in severe cases.

Benzodiazepine detection in urine is possible via qualitative immunoassay, though this method is not diagnostic of overdose [11]. False negatives can occur as not all benzodiazepines are detected, and a positive result only indicates exposure without providing timing or dosage information. False positives may result from medications such as efavirenz and sertraline. Urine tests can detect benzodiazepines within three hours of ingestion and remain positive for up to two weeks. Serum benzodiazepine levels are rarely needed except in forensic cases, as they do not correlate well with the ingested dose.

Risk Stratification

Patients presenting with benzodiazepine overdose or withdrawal must be thoroughly assessed before discharge, even if they remain asymptomatic or their symptoms have been controlled in the ED. Psychiatric consultation is recommended in all cases, regardless of whether the overdose was intentional or accidental.

Suicidal ideation and suicide risk should be evaluated using tools like the SAD PERSONS score (Table 1) [12]. Patients with high scores require admission for further evaluation and intervention. Patients in withdrawal need to be referred for rehabilitation, with the choice of inpatient or outpatient care determined by the psychiatric assessment.

Table 1: SAD PERSONS Score

S

Male sex

1

A

Age (<19 or >45 years)

1

D

Depression

1

P

Previous attempt

1

E

Excessive alcohol or substance use

1

R

Rational thinking loss

1

S

Social supports lacking

1

O

Organized plan

1

N

No spouse

1

S

Sickness

1

   

0-4

Low risk

Consider discharge to home with follow-up.

5-6

Medium risk

Admit or discharge based on clinical judgment, ensuring appropriate follow-up arrangements.

7-10

High risk

Admit to hospital

Management

Initial Stabilization

Management of a patient with altered mental status (AMS) and suspected overdose begins with resuscitation. The ABCDEFG approach in toxicology is a structured method [13]:

A: Airway/C-Spine

  • Endotracheal intubation should be promptly performed in severely intoxicated patients or those unable to maintain their airway.
  • Nasopharyngeal or oropharyngeal airways may be used temporarily.
  • C-spine immobilization is indicated if head trauma is suspected.

B: Breathing

  • Hypoventilation is a critical sign of severe overdose, often indicating co-ingestion with alcohol or other central nervous system (CNS) depressants.
  • Monitor respiratory rate and oxygen saturation. Administer oxygen for hypoxemia. Consider ventilatory support in cases of hypoventilation (e.g., Bag-valve-mask ventilation). 

C: Circulation

  • Two large-bore intravenous lines should be placed, and fluid resuscitation with isotonic solutions (e.g., 0.9% saline or Ringer’s lactate) initiated for hypotension.
  • Monitor for signs of shock and consider vasopressors if hypotension persists despite adequate fluid resuscitation.

D: Disability/Decontamination/Draw Bloods

  • Perform a rapid neurological exam; pupillary changes and other symptoms can help identify the toxidrome.
  • Decontamination measures: Activated charcoal (1 g/kg for children or 50–100 g for adults) can be effective if administered within an appropriate timeframe. Multiple doses are not typically beneficial. Gastric lavage, hemodialysis, and urine alkalinization are ineffective for benzodiazepine toxicity.
  • Draw blood samples for complete blood count (CBC), renal and liver function tests (U&E, RFT, LFT), creatine kinase (CK), arterial blood gases (ABG), osmolality, and a toxicology screen (ethanol, acetaminophen, salicylate).

E: Exposure

  • Examine for track marks, odors, nasal septum erosion, and signs of trauma or assault. The lack of signs of trauma or assault does not totally rule out in patients with altred mental status.
  • Check for evidence of seizures (incontinence, tongue biting) or meningeal irritation.
  • Ensure the patient is kept warm.

F: Full Monitoring

  • Continuous monitoring of vital signs, end-tidal carbon dioxide, and ECG is essential.

G: Give Antidote

  • Administer antidotes based on the identified or suspected toxic agent.
  • The universal antidotes—dextrose, oxygen, naloxone, and thiamine—can be administered as appropriate. Administer dextrose for hypoglycemia and oxygen for hypoxemia, as indicated. Naloxone, administered intranasally or intravenously, is beneficial for any patient with respiratory depression suggestive of opioid exposure. With a rapid onset of action (~1 minute), it serves both diagnostic and therapeutic purposes. Administer thiamine to prevent Wernicke’s encephalopathy in at-risk patients. If glucose administration is indicated but thiamine is unavailable, glucose should not be delayed.
  • Most benzodiazepine overdoses can be effectively managed with supportive care alone, without the need for specific antidotes. In rare cases where specific treatment is required, flumazenil, unlike naloxone, should not be administered empirically.

Flumazenil 

Adult
  • Initial Dose: 0.2 mg over 1-2 minutes
  • Frequency: 0.3 – 0.5 mg IV every 1-2 minutes
  • Maximum Dose: 1 mg
  • Cautions / Comments:
    • Category C in Pregnancy.
    • Short duration of action (45–75 minutes); re-sedation may require re-dosing or continuous infusion (0.25 to 1.0 mg/h).
    • Adverse reactions include seizures (treat with barbiturates or propofol) and arrhythmias.
    • Adverse drug reactions are less common in pediatric patients.
Paediatrics
  • Initial Dose: 0.01 mg/kg over 1-2 minutes
  • Frequency: Up to 4 doses of 0.005 – 0.01 mg/kg
  • Maximum Dose:
    • 0.2 mg per dose.
    • Should not exceed 1 mg total or 0.05 mg/kg.

Flumazenil, a competitive antagonist of the benzodiazepine receptor, is primarily used in benzodiazepine-naïve patients [14]. Common scenarios include iatrogenic overdoses during monitored procedural sedation to reverse respiratory depression and pediatric accidental ingestion.

Flumazenil administration in patients with chronic benzodiazepine use can precipitate withdrawal symptoms, including intractable seizures and status epilepticus. Flumazenil is contraindicated in the following situations:

  • Chronic benzodiazepine use (e.g., for seizure disorders or in known substance use).
  • In patients where the cause of altered mental status is unknown or seizure activity is suspected.
  • Co-ingestion with pro-convulsant agents, such as tricyclic antidepressants, cocaine, diphenhydramine, carbamazepine, chloral hydrate, or bupropion.
  • Iatrogenic overdose during management of status epilepticus.

Benzodiazepine withdrawal syndrome can occur in chronic users following flumazenil administration or abrupt cessation of the drug. The risk is proportional to the dose and duration of benzodiazepine use, increasing significantly after 3–4 months of regular use.

Acute withdrawal requires resuscitation aligned with the standard ABCDE approach:

  • Administer long-acting benzodiazepines (e.g., diazepam or chlordiazepoxide) in mild or moderate cases to alleviate symptoms and allow tapering under medical supervision.
  • Seizures during withdrawal should be treated with propofol or barbiturates rather than benzodiazepines [6].

Special Patient Groups

In the elderly, liver metabolism can be significantly impaired, necessitating dose adjustments [15]. For patients with known liver disease, benzodiazepines without active metabolites are preferred (e.g., lorazepam, oxazepam, temazepam—LOT).

In children under 5 years of age, accidental benzodiazepine ingestion may present primarily with ataxia, which is more common than AMS [16]. Both children and elderly patients may experience paradoxical reactions following benzodiazepine administration for procedural sedation.

When To Admit This Patient

In cases of suspected suicidal attempts, a psychiatric evaluation should be conducted in the emergency department (ED) [17]. Patients with mild, accidental, or pure benzodiazepine overdoses successfully managed in the ED who remain asymptomatic for 4–6 hours can be discharged. However, if mild symptoms persist, admission to a general ward for observation may be warranted until symptom resolution. Patients with severe overdoses requiring monitoring, oxygen therapy, or ventilatory support should be admitted to the ICU [1].

Revisiting Your Patient

The patient was rapidly transferred to the resuscitation room and connected to a monitor. A structured A to E approach was used for further assessment.

Airway: With a GCS of 3/15, a nasopharyngeal airway (NPA) was inserted as a precaution, and an intubation kit was prepared. There were no visible signs of airway trauma, foreign body obstruction, or excessive secretions.

Breathing: The patient was bradypneic with oxygen saturation below 94%. Oxygen at 10 L/min via a non-rebreather mask was administered, improving her saturation to 98%. End-tidal CO₂ measured 35 mmHg.

Circulation: To address hemodynamic instability, two large-bore intravenous cannulas were placed, blood samples were drawn, and an intravenous bolus of 0.9% NaCl was administered. Continuous monitoring showed an improvement in her blood pressure to 85/50 mmHg and her heart rate to 52 bpm. An ECG revealed sinus bradycardia.

Disability: Neurological examination showed constricted pupils. Activated charcoal was not administered, as the ingestion was presumed to have occurred 2–5 hours earlier.

Exposure: On physical examination, no track marks or septal erosion were noted. A mild odor of alcohol was detected. There were no overt signs of seizures, trauma, or assault. However, given the altered mental state, trauma or assault could not be definitively ruled out.

Management included supportive care with oxygen and a trial of naloxone (0.4 mg IV), which had no effect within two minutes. Thiamine (100 mg IV) was administered as part of the standard protocol. Flumazenil was withheld due to concerns about potential withdrawal seizures in the context of possible chronic benzodiazepine use, particularly since the patient was improving with supportive treatment alone.

Further questioning of her friends revealed that they had given her Xanax (alprazolam), though they were unsure of the quantity. They also confirmed that she had consumed alcohol. Laboratory investigations were largely unremarkable, apart from a blood ethanol level of 150 mg/dL.

The patient’s condition showed gradual improvement in the emergency department. Her GCS increased to 9/15 (E3V2M4), and intubation was deferred as she maintained her airway. Hemodynamic stability was achieved, with a blood pressure of 90/55 mmHg, a heart rate of 62 bpm, and oxygen saturation of 95% on a 5 L face mask. Although she remained confused and unable to provide a detailed history, her overall status warranted further supportive care. She was admitted to the telemetry ward for ongoing monitoring and management.

Authors

Picture of Gina Rami Abdelmesih

Gina Rami Abdelmesih

Emergency Department, Zayed Military Hospital

Picture of Rauda Alnuaimi

Rauda Alnuaimi

Emergency Department, Zayed Military Hospital

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References

  1. Overbeek DL, Erickson TB. Sedative-Hypnotics. In: Walls RM, Hockberger RS, Gausche-Hill M, Erickson TB, Wilcox SR, ed. Rosen’s Emergency Medicine Concepts and Clinical Practice, 10th edition. Philadelphia, PA, USA: Elsevier; 2023: 1986-1993.
  2. United Nations Office on Drugs and Crime. Non-medical use of benzodiazepines: a growing threat to public health? https://www.unodc.org/documents/scientific/Global_SMART_Update_2017_Vol_18.pdf Published September 2017. Accessed December 11, 2024.
  3. AlMarri TS, Oei TP. Alcohol and substance use in the Arabian Gulf region: a review. Int J Psychol. 2009;44(3):222-233.
  4. El Zahran T, Kanaan E, Kobeissi L, et al. Benzodiazepine use disorder: A cross-sectional study at a tertiary care center in Lebanon. Medicine (Baltimore). 2022;101(38):e30762.
  5. Naja WJ, Pelissolo A, Haddad RS, Baddoura R, Baddoura C. A general population survey on patterns of benzodiazepine use and dependence in Lebanon. Acta Psychiatr Scand. 2000;102(6):429-431.
  6. Greller H, Gupta A. Benzodiazepine poisoning and withdrawal. UpToDate. https://www.uptodate.com/contents/benzodiazepine-poisoning Updated July 11, 2022. Accessed May 1, 2023.
  7. Yin S. Sedatives and Hypnotics. In: Cydulka RK, Fitch MT, Wang VJ, Cline DM, Ma, OJ, ed. Tintinalli’s Emergency Medicine Manual, 8th Edition. New York, NY, USA: McGraw-Hill Education; 2018: 574-579.
  8. National Poisons Information Service. Street Benzodiazepines. TOXBASE. https://www.toxbase.org/poisons-index-a-z/s-products/street-benzodiazepines/. Updated August, 2022. Accessed May 1, 2023.
  9. Wright SL. Benzodiazepine withdrawal: clinical aspects. In: Peppin J, ed. The Benzodiazepines Crisis. New York, NY: Oxford University Press; 2020. doi:10.1093/med/9780197517277.003.0008. Accessed December 17, 2024.
  10. Rockett IRH, Caine ED, Connery HS, et al. Discerning suicide in drug intoxication deaths: paucity and primacy of suicide notes and psychiatric history. PLoS One. 2018;13(1):1-13. doi:10.1371/journal.pone.0190200.
  11. DeRienz RT, Holler JM, Manos ME, Jemionek J, Past MR. Evaluation of four immunoassay screening kits for the detection of benzodiazepines in urine. J Anal Toxicol. 2008;32(6):433-437. doi:10.1093/jat/32.6.433.
  12. Bolton JM, Spiwak R, Sareen J. Predicting suicide attempts with the SAD PERSONS scale: a longitudinal analysis. J Clin Psychiatry. 2012;73(6):735-741. doi:10.4088/JCP.11M07362.
  13. Emergency Management of Poisoning. Haddad and Winchester’s Clinical Management of Poisoning and Drug Overdose. 2007;13-61. doi:10.1016/B978-0-7216-0693-4.50007-4
  14. Brogden RN, Goa KL. Flumazenil: a reappraisal of its pharmacological properties and therapeutic efficacy as a benzodiazepine antagonist. Drugs. 1991;42(6):1061-1089. doi:10.2165/00003495-199142060-00010.
  15. Cook PJ. Benzodiazepine hypnotics in the elderly. Acta Psychiatr Scand. 1986;74:149-158. doi:10.1111/j.1600-0447.1986.tb08992.x.
  16. Friedrich JM, Sun C, Geng X, et al. Child and adolescent benzodiazepine exposure and overdose in the United States: 16 years of poison center data. Clin Toxicol (Phila). 2020;58(7):725-731. doi:10.1080/15563650.2019.1674321.
  17. Ronquillo L, Minassian A, Vilke GM, Wilson MP. Literature-based recommendations for suicide assessment in the emergency department: a review. J Emerg Med. 2012;43(5):836-842. doi:10.1016/j.jemermed.2012.08.015.

Reviewed and Edited By

Picture of Elif Dilek Cakal, MD, MMed

Elif Dilek Cakal, MD, MMed

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.

Acute Mesenteric Ischaemia (2024)

~ iEM Education Project Team ~ Leave a comment

by Colin NG

Authors
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You have a new patient!

An 80-year-old gentleman presents to our department with a two-day history of abdominal pain accompanied by diarrhea and nausea. He describes the pain as recurrent, having occurred periodically over the past two years, with a crescendo pattern. However, this current episode has not been resolved and is excruciating.

a-photo-of-an-80-year-old-male-patient-(the image was produced by using ideogram 2.0)

A review of his medical records reveals a history of hypertension, dyslipidemia, a previous transient ischemic attack, and atrial fibrillation (AF). He underwent cholecystectomy many years ago for biliary colic. There is no other significant medical history.

On examination, his vital signs are as follows:

  • Blood pressure is 95/57 mmHg.
  • Pulse is 126 beats per minute.
  • Respiratory rate is 26 breaths per minute.
  • Oxygen saturation is 95%.
  • He is afebrile.

The patient appears pale, diaphoretic, and in significant discomfort. There is no clinical jaundice. Abdominal examination reveals diffuse tenderness, most prominent centrally, without guarding. Bowel sounds are sluggish. A cholecystectomy scar is noted in the right hypochondrium. Cardiac examination reveals irregular tachycardia, and the lungs are clear. Examination of the lower limbs is unremarkable, with no swelling. Stool is brown, with no visible blood or melena.

How would you proceed with further evaluation for this patient?

What do you need to know?

Acute mesenteric ischemia (AMI) refers to the sudden loss of blood flow to the small intestine, typically due to arterial insufficiency caused by an embolus or thrombus. AMI falls under the broader category of intestinal ischemia, which includes ischemia of the colon and, more rarely, the stomach and upper gastrointestinal tract. Other forms of intestinal malperfusion include venous occlusion as well as chronic or non-occlusive mesenteric ischemia [1].

Importance

Acute mesenteric ischemia carries an alarmingly high mortality rate, estimated between 60–80%. This is exacerbated by its nonspecific presentation, which often delays diagnosis and increases the likelihood of complications. Early recognition, timely resuscitation and treatment, and prompt advocacy for intervention are essential to improving outcomes [2,3].

Epidemiology

The incidence of AMI in developed countries is approximately 5 per 100,000 people annually, with a prevalence of around 0.1% of all hospital admissions.

AMI primarily occurs in patients with pre-existing atherosclerotic disease of arteries, often associated with risk factors such as advanced age, hypertension, diabetes, and atrial fibrillation [4].

A non-exhaustive list of risk factors includes [1]:

  • Cardiac conditions (e.g., atrial fibrillation, recent myocardial infarction)
  • Aortic surgery or instrumentation
  • Peripheral artery disease
  • Haemodialysis
  • Use of vasoconstrictive medications
  • Prothrombotic disorders
  • Systemic inflammation or infections
  • Hypovolaemic states
  • Bowel strangulation (e.g., volvulus, hernias)
  • Vascular compression syndromes.

Pathophysiology

The intestinal system exhibits relatively low oxygen extraction; residual oxygenated blood from intestinal veins is delivered to the liver via the portal vein. For ischaemic damage to occur, blood flow must be reduced by at least 50% of normal levels [1].

Interestingly, mesenteric arteries are less affected by atherosclerosis compared to other similarly sized vessels, likely due to protective hemodynamic factors. As a result, patients with AMI often have concurrent atherosclerotic conditions elsewhere, such as cerebrovascular disease, ischaemic heart disease, or peripheral vascular disease. Regarding the mechanism,

  • Embolism of the mesenteric artery accounts for ~50% and
  • Thrombosis of the mesenteric artery accounts for ~25% of AMI cases.

Mesenteric venous thrombosis can mimic AMI in a minority of cases, often presenting as nonspecific abdominal pain with diarrhea lasting 1–2 weeks. In some instances, these thrombi resolve spontaneously.

Medical History

The primary symptom of acute mesenteric ischemia (AMI) is central and severe abdominal pain, classically described as being “out of proportion” to physical examination findings. The initial pain is due to visceral ischemia, which initially spares the parietal peritoneum. Peritonism with abdominal rigidity typically develops later, indicating full-thickness ischemia, necrosis, or perforation [5].

Early symptoms may include persistent vomiting and defecation. As the condition progresses, passage of altered blood may occur. Unfortunately, associated gastrointestinal symptoms such as nausea, vomiting, and diarrhea can mimic infective causes, potentially leading to misdiagnosis. While bloody diarrhea is more commonly associated with colonic ischemia, it is less frequent in small bowel ischemia.

In some cases, AMI is preceded by symptoms of chronic non-occlusive mesenteric ischemia. Patients often report recurrent, postprandial abdominal pain resulting from an inability to increase blood flow to meet intestinal vascular demands. This may lead to a fear of eating and significant weight loss. In patients with chronic non-occlusive mesenteric ischemia, symptoms tend to be even more vague. Pain may be less severe and poorly localized, and patients may present with subtle signs such as abdominal distension or occult gastrointestinal bleeding [6].

In addition to embolic causes, mesenteric ischemia can be worsened by systemic conditions that restrict blood flow, such as hemorrhage, hypovolaemia, shock, and low-output cardiac states.

Physical Examination

In the early stages of AMI, physical examination findings are often sparse. The patient will typically appear to be in severe pain without relief, and abdominal tenderness is common. Suspicion should be heightened in frail patients of advanced age who may lack sufficient abdominal musculature to produce guarding during the examination.

Patients may appear pale due to pain or anemia, but specific physical signs are limited in this condition. Diagnosis often relies on a combination of clinical history and thorough investigation.

AMI is a critical condition characterized by reduced blood flow to the intestines, leading to severe complications if not diagnosed early. The physical examination findings should be combined with clinical history and specific symptoms. Understanding these findings is essential for timely intervention.

Key Findings

  • Severe Abdominal Pain: Patients typically present with a sudden onset of severe abdominal pain, which is a hallmark symptom of AMI.
  • Painless Interval: Following the initial pain, a transient painless period may occur, potentially misleading the diagnosis.
  • Signs of Peritonitis: Physical examination may reveal tenderness, guarding, or rebound tenderness, indicating peritoneal irritation and necessitating immediate surgical evaluation.
  • Bowel Sounds: Diminished or absent bowel sounds can suggest intestinal ischemia.

Importance of Clinical History to Guide Physical Exam

  • Risk Factors: A thorough history should include predisposing factors such as cardiovascular disease, recent surgeries, or conditions leading to hypercoagulability.
  • Chronic Symptoms: In cases of arterial thrombosis, patients may report a history of intermittent abdominal pain, weight loss, or diarrhea.

Alternative Diagnoses

The nonspecific symptoms of AMI mean it can be mimicked by many other conditions that are not easily excluded based on history and examination alone. Risk factors such as advanced age, prothrombotic states, atherosclerosis, and conditions causing hypovolaemia should raise clinical suspicion.

Differential diagnoses include:

  • Acute gastroenteritis: Main differential due to similar gastrointestinal symptoms (nausea, diarrhea, vomiting), especially at the initial stages of AMI, but pain and tenderness are typically less severe, more intermittent, and responsive to analgesia. Gastroenteritis is also less likely to cause metabolic acidosis or other significant biochemical abnormalities.
  • Acute cholecystitis: Presents with pain mainly in the right upper quadrant (RUQ) radiating to the right shoulder, often triggered by fatty meals, with accompanying nausea, vomiting, and fever. Murphy’s sign (pain and inspiratory arrest on palpation of the gallbladder) is often positive, particularly in those with a history of gallstones or biliary colic.
  • Acute pancreatitis: Epigastric pain radiating to the back, along with nausea and vomiting, is common. Associated with gallstones or alcohol use. Physical findings include epigastric tenderness, reduced bowel sounds, and, in severe cases, Grey-Turner’s or Cullen’s sign. Diagnosis is supported by elevated serum lipase or amylase levels.
  • Peptic ulcer disease: Characterized by burning or gnawing epigastric pain, often relieved by food or antacids. Common risk factors include NSAID use and Helicobacter pylori infection. Examination is typically unremarkable unless perforation occurs, which may result in acute peritonitis.
  • Bowel perforation: Sudden severe, diffuse abdominal pain with signs of peritonitis (rebound tenderness, guarding), fever, and tachycardia. A history of PUD or diverticulitis may be present. Diagnosis is supported by imaging, showing free air under the diaphragm on X-ray.
  • Diverticulitis: Presents with localized left lower quadrant (LLQ) pain, fever, and altered bowel habits (diarrhea or constipation). LLQ tenderness or a palpable mass is often noted in older patients.
  • Bowel obstruction: Crampy, intermittent abdominal pain, nausea/vomiting, abdominal distension, and constipation, potentially progressing to obstipation. Examination reveals a distended abdomen with high-pitched or absent bowel sounds. Plain X-rays typically show air-fluid levels and dilated bowel loops.
  • Ureteric calculus: Sudden colicky flank pain radiating to the groin, often with hematuria, nausea, and vomiting. A history of kidney stones is common. Findings include costovertebral angle tenderness, with a generally unremarkable abdominal exam. Hematuria is detected on urinalysis.

Acing Diagnostic Testing

Bedside Tests

Bedside diagnostics are limited but can provide valuable clues:

  • ECG: May reveal atrial fibrillation, a common risk factor.
  • Blood glucose: Hyperglycaemia due to physiological stress.
  • Point-of-Care Testing (POCT) for lactate: Elevated levels may indicate tissue hypoxia, though not specific to AMI.
  • Ultrasound: Limited in diagnosing AMI but useful for ruling out other causes of abdominal pain (e.g., cholecystitis, abdominal aneurysm, or ureteric colic). Ultrasound can also assess fluid status and response to fluid resuscitation via the inferior vena cava (IVC) and right heart function, particularly in patients with cardiac or renal comorbidities or failure.
An ECG sample in an abdominal pain patient - Rapid ventricular rate, atrial fibrillation.

Laboratory Tests

No serum markers are sufficiently sensitive or specific to diagnose AMI reliably:

  • Complete blood count (CBC): It may reveal haemoconcentration or leukocytosis but lacks specificity.
  • Serum lactate: Highly sensitive in bowel infarction but nonspecific; elevated levels may not occur in the early stages.

Leucocytosis and elevated lactate levels are the two most frequently observed abnormalities in acute mesenteric ischemia; however, both lack specificity for this condition [7,8].

  • Blood gas analysis: Metabolic acidosis is a late finding; its presence should heighten suspicion in the appropriate clinical context.
  • Serum amylase: Moderately elevated in more than half of cases; highly elevated levels suggest pancreatitis, which should guide further diagnostic steps.

Imaging

  • X-rays (Chest/Abdomen): Chest and abdominal X-rays are often normal in the early stages of acute mesenteric ischemia but are useful for identifying complications or alternative diagnoses (e.g., perforation, ureteric calculus) [9]. Early findings may include adynamic ileus, distended air-filled bowel loops, or bowel wall thickening. Late findings such as pneumatosis or portal venous gas strongly suggest bowel infarction.
  • CT Scanning: The primary imaging modality in diagnosing AMI. When enhanced with contrast, CT can detect bowel wall edema, mesenteric edema, abnormal gas patterns, intramural gas, ascites, and mesenteric venous thrombosis. Sensitivity and specificity are high (82.8–97.6% and 91.2–98.2%, respectively), though contrast use may be limited by renal function [10]. However, delaying diagnosis poses greater risks than the small chance (~1%) of contrast-induced nephropathy requiring dialysis [11].
The CT image shows bowel wall thickness.
  • Catheter Angiography: is considered the gold standard but rarely available in emergency settings [10]. It may still be necessary if CT is inconclusive and clinical suspicion remains high.
  • Diagnostic Laparotomy: it may be required for definitive diagnosis in cases of high suspicion when imaging is non-diagnostic.

Risk Stratification

No validated tools exist for risk stratification in AMI. However, specific features indicate late-stage disease and worse prognosis:

  • Prolonged symptoms before presentation.
  • Evidence of bowel necrosis or perforation.
  • Severe biochemical derangements (e.g., high lactate, metabolic acidosis).
  • Hemodynamic instability, such as septic or hemorrhagic shock.

Management

Initial Stabilization

Initial stabilization of the patient, if required, is straightforward but must follow a systematic approach, following airway, breathing, circulation, disability, and exposure.

Airway and Breathing:

The airway should be secured if necessary, especially in cases where the patient appears drowsy due to cerebral hypoperfusion or septic encephalopathy, or if they are actively vomiting and at high risk of aspiration. Rapid correction of hypovolaemia before administering sedatives or paralytics is recommended. Breathing is not commonly compromised in this condition; however, supplemental oxygen may be required for patients experiencing atelectasis or tachypnoea secondary to pain.

C: Circulation – Circulation management necessitates aggressive and rapid resuscitation with fluids or blood products. Fluid resuscitation should not be delayed due to difficulty in obtaining IV access. Ultrasound guidance can be used if venous access proves challenging. If the patient is hypotensive, an initial 10–20 mL/kg (Crystalloids: Normal saline / Hartmann’s / Ringer’s lactate / Plasmalyte etc.) bolus delivered rapidly over 5–15 minutes is appropriate. This usually requires at least one large-bore IV line (20G or larger).

Many of these patients have comorbidities such as congestive heart failure (CHF), which requires judicious fluid management. Careful hemodynamic monitoring, including repeated clinical assessments and sonographic evaluation of inferior vena cava (IVC) collapsibility, is crucial. If required, more invasive hemodynamic monitoring may be employed.

Vasoactive agents should be avoided due to their role as predisposing factors; however, if vasopressors are essential, it is advisable to avoid alpha-agonist medications.

D: Disability – In patients with acute mesenteric ischemia (AMI), mental status may become altered if ischemia progresses to sepsis or shock, leading to cerebral hypoperfusion. This may present as confusion, agitation, or lethargy. Tools such as the AVPU scale or Glasgow Coma Scale (GCS) are valuable for assessing consciousness and monitoring neurological status during treatment. Clinicians should also consider the presence of sequelae from prior strokes, as these may indicate underlying atherosclerotic disease, which is a risk factor for AMI. Additionally, severe pain can interfere with the patient’s ability to engage fully in the assessment, even when mental status remains intact.

E: Exposure – The patient should be fully exposed to enable a thorough examination, while ensuring measures are taken to maintain warmth and prevent hypothermia, as this can worsen shock. A systematic palpation of the abdomen is critical to identify tenderness, guarding, or masses. In the early stages of AMI, there may be no external signs, but central or generalized abdominal tenderness is typically present. As the condition advances, abdominal distension and signs of peritonitis, such as rebound tenderness and rigidity, may develop.

Clinicians should also observe for secondary indicators, including surgical scars or stomas, which may suggest a history of abdominal pathology. Systemic signs of hypoperfusion and shock, such as mottled skin or cool extremities, should also be noted. Regular and frequent reassessment is essential to detect any progression or subtle changes in the patient’s condition, ensuring timely and appropriate intervention.

Early and empirical administration of broad-spectrum antibiotics is critical and should not be delayed for blood culture collection, as the risk of bacterial translocation across the bowel wall is high. Oral intake must be avoided since these patients are likely to undergo urgent surgery under general anesthesia. Electrolyte imbalances should also be corrected promptly.

Antibiotic Administration

Ceftriaxone

  • Dose per kg: 1–2 g
  • Frequency: Stat (given immediately)
  • Maximum Dose: 2 g
  • Category in Pregnancy: Category B (safe for all trimesters)
  • Cautions/Comments: None specified.

Metronidazole

  • Dose per kg: 500 mg
  • Frequency: Stat (given immediately)
  • Maximum Dose: 500 mg
  • Category in Pregnancy: Category B (safe for all trimesters)
  • Cautions/Comments: None specified.

An urgent surgical consultation is imperative, as acute mesenteric ischemia is a time-sensitive condition. Delays to definitive treatment significantly increase morbidity and mortality. High clinical suspicion alone should prompt surgical involvement, even before imaging results are available. In critically ill patients, surgical teams may decide to proceed directly to the operating theatre without advanced imaging. Such decisions are typically made collaboratively by the emergency department, surgical, anesthetic, and intensive care teams.

The definitive treatment for acute mesenteric ischemia depends on the underlying cause and whether necrotic bowel is present. Necrotic bowel or signs of peritonitis necessitate immediate resection. Specific interventions include embolectomy with distal bypass grafting for mesenteric artery embolism, bypass grafting or stenting for mesenteric artery thrombosis, and removal of underlying stimuli in nonocclusive ischemia, sometimes supplemented with direct transcatheter papaverine infusion. Mesenteric venous thrombosis typically requires anticoagulation [7].

Special Patient Groups

Special populations, such as those with communication barriers or cognitive impairments, may require a lower threshold for advanced imaging since history-taking and physical examination may be unreliable. Pregnant and pediatric patients are rarely affected by this condition.

When To Admit This Patient

Given the critical nature of acute mesenteric ischemia and its high mortality rates, all affected patients should be admitted to the intensive care unit for postoperative management following surgery.

Revisiting Your Patient

Our patient was triaged to a high-acuity area of the emergency department (ED) and placed on continuous monitoring, including cardiac leads, blood pressure, and oximetry. Stabilization proceeded in a structured, prioritized manner, focusing on critical areas from A to E:

  • Airway and Breathing: The patient’s airway was intact, and there were no signs of active vomiting. Mild dyspnoea was reported, so supplemental oxygen was administered via nasal cannula.
  • Circulation: Two large-bore intravenous cannulae were inserted, and a liter of crystalloids was infused. This led to visible hemodynamic improvement, including better IVC collapsibility observed on ultrasound.
  • Disability and Exposure: Disability and exposure did not reveal anything abnormal except for a generalized tenderness on the abdomen.

With the patient stabilized, the team moved on to investigations. Blood samples were taken, including a point-of-care venous gas test with serum lactate, coagulation profile, and a group and cross-match. Leucocytes were elevated at 12,000, and serum lactate was elevated at 8. Cardiac monitoring revealed atrial fibrillation. Bedside ultrasound did not reveal other causes of abdominal pain, such as a ruptured aneurysm or cholecystitis. Chest and abdominal X-rays were normal.

Based on the clinical presentation, risk factors, and lab results, the treating team suspected acute mesenteric ischemia. A surgical consult was requested, and a CT scan of the abdomen and pelvis was ordered. Maintenance IV crystalloids and broad-spectrum antibiotics (ceftriaxone and metronidazole) were started empirically. A urinary catheter was placed to monitor fluid balance.

The CT scan revealed:

  • A thickened small bowel wall with dilated bowel loops
  • An embolism in the superior mesenteric artery

The patient was immediately taken to the operating theatre for definitive treatment.

In summary, the role of the ED physician is to:

  1. Stabilize the patient through targeted resuscitation
  2. Make an early diagnosis based on clinical suspicion supported by available investigations
  3. Understand the limitations of laboratory tests in ruling out acute mesenteric ischemia
  4. Prioritize aggressive resuscitation and management
  5. Ensure urgent surgical involvement

Authors

Picture of Colin NG

Colin NG

Woodlands Health

Listen to the chapter

References

  1. Tendler DA, Lamont JT. Overview of intestinal ischemia in adults. UpToDate. https://www.uptodate.com/contents/overview-of-intestinal-ischemia-in-adults Updated January 29, 2024. Accessed December 9, 2024.
  2. McKinsey JF, Gewertz BL. Acute mesenteric ischemia. Surg Clin North Am. 1997;77(2):307-318.
  3. Oldenburg WA, Lau LL, Rodenberg TJ, Edmonds HJ, Burger CD. Acute mesenteric ischemia: a clinical review. Arch Intern Med. 2004;164(10):1054-1062.
  4. Szuba A, Gosk-Bierska I, Hallett RL. Thromboembolism. In: Rubin GD, Rofsky NM, ed. CT and MR Angiography: Comprehensive Vascular Assessment. Philadelphia, PA, USA: Lippincott Williams & Wilkins; 2009: 295-328.
  5. Marc Christopher Winslet. Intestinal Obstruction. In: R.C.G. Russell ed. Bailey & Love’s Short Practice Of Surgery 24th ed. London, UK: Arnold; 2004:1202.
  6. Tendler DA, Lamont JT. Nonocclusive mesenteric ischemia. UpToDate. https://www.uptodate.com/contents/nonocclusive-mesenteric-ischemia Updated December 13, 2023. Accessed December 9, 2024.
  7. Park WM, Gloviczki P, Cherry KJ Jr, et al. Contemporary management of acute mesenteric ischemia: Factors associated with survival. J Vasc Surg. 2002;35(3):445-452.
  8. Cudnik MT, Darbha S, Jones J, Macedo J, Stockton SW, Hiestand BC. The diagnosis of acute mesenteric ischemia: A systematic review and meta-analysis. Acad Emerg Med. 2013;20(11):1087-1100.
  9. Smerud MJ, Johnson CD, Stephens DH. Diagnosis of bowel infarction: a comparison of plain films and CT scans in 23 cases. AJR Am J Roentgenol. 1990;154(1):99-103.
  10. Menke J. Diagnostic accuracy of multidetector CT in acute mesenteric ischemia: systematic review and meta-analysis. Radiology. 2010;256(1):93-101.
  11. Mehran R, Aymong ED, Nikolsky E, et al. A simple risk score for prediction of contrast-induced nephropathy after percutaneous coronary intervention: development and initial validation. J Am Coll Cardiol. 2004;44(7):1393-1399.

FOAM and Further Reading

CDEM Curriculum – Patel S, Mesenteric Ischemia – June 2018, https://cdemcurriculum.com/mesenteric-ischemia/ Accessed May 2023

EMdocs – Seth Lotterman. Mesenteric Ischemia: A Power Review. Nov 2014. http://www.emdocs.net/mesenteric-ischemia-power-review/ Accessed May 2023

Reviewed and Edited By

Picture of Elif Dilek Cakal, MD, MMed

Elif Dilek Cakal, MD, MMed

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

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

Burns and Smoke Inhalation (2024)

~ iEM Education Project Team ~ Leave a comment

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

Authors
Listen

You have a new patient!

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

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

What do you need to know?

Importance

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

Epidemiology

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

Pathophysiology

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

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

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

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

Burn Depth

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

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

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

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

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

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

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

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

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

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

Medical History

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

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

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

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

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

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

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

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

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

Thermal Burns:

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

Chemical Burns:

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

Electrical Burns:

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

Physical Examination

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

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

Primary Survey

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

A. Airway

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

B. Breathing

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

C. Circulation

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

D. Disability

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

E. Exposure and Environmental Control

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

Secondary Survey

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

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

B. Head-to-Toe Examination

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

C. Burn Wound Assessment

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

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

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

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

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

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

Clinical Images of Selected Burn Injuries

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

Acing Diagnostic Testing

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

Patients with Minor Burns

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

Patients with Moderate to Severe Burns

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

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

Patients with Electrical Burns

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

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

Imaging for Burn Patients

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

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

Risk Stratification

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

Risk Stratification Criteria

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

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

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

Management

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

General Principles in Management of Burns

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

First Aid

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

Analgesia

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

Fluid Resuscitation

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

Two common formulas guide fluid calculations:

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

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

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

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

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

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

Thermal Burns

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

Thermal 2nd degree burn in a child

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

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

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

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

Electrical Burns

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

Extent of injuries depends on the voltage type:

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

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

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

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

electrical injury, rhabdomyolysis

Management [2,3,11]

General Principles

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

Analgesia

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

Fluids

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

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

Chemical Burns

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

Chemical burn

Management [2,12]

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

Radiation Burns

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

Management

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

Inhalation Injuries

General Overview

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

Assessment

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

Management [2,5]

Maintaining a Patent Airway

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

Thermal burn, Inhalation Injury

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

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

Medications
Several medications may be employed to address specific symptoms:

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

Ventilatory Support

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

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

Special Patient Groups

Pediatric Patients

Thermal Burns

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

Electrical Burns

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

Pregnant Patients

Electrical Burns

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

When To Admit This Patient

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

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

According to these guidelines:

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

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

Revisiting Your Patient

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

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

Authors

Picture of Michaela Banks

Michaela Banks

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

Picture of Anthony Dikhtyar

Anthony Dikhtyar

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

Picture of Jacquelyne Anyaso

Jacquelyne Anyaso

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

Picture of Ashley Pickering

Ashley Pickering

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

Listen to the chapter

References

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

FOAm and Further Reading

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

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

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

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

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

Reviewed and Edited By

Picture of Erin Simon, DO

Erin Simon, DO

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

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

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

Intraosseous (IO) Lines/Access (2024)

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by Yousif Al-Khafaji & Mustak Dukandar

Authors
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Introduction

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

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

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

Indications

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

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

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

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

Contraindications

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

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

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

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

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

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

Equipment and Patient Preparation

Equipment

IO Needle

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

IO Devices (to facilitate insertion)

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

Skin Disinfectants

  • Chloraprep
  • Alcohol swabs
  • Optional: Povidine or Chlorhexidine

Syringe and Flush Materials

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

Lidocaine 2% (without epinephrine)

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

Additional Equipment

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

Patient Preparation

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

Sites of IO insertion and some hints [8]

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

Procedure Steps

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

Complications [9]

Extravasation of Fluid

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

Compartment Syndrome

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

Bone Fracture

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

Osteomyelitis

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

Preventative Measures:

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

Hints and Pitfalls

Purpose and Time Limit

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

Site and Device Selection

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

Needle Placement and Security

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

Medication and Dosage

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

Laboratory Sampling

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

Special Patient Groups

Pediatrics

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

Geriatrics

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

Pregnant Patients

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

Authors

Picture of Yousif Al-Khafaji

Yousif Al-Khafaji

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

Picture of Mustak Dukandar

Mustak Dukandar

Tawam Hospital Emergency Department

Listen to the chapter

References

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

FOAM and Further Reading

Reviewed and Edited By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

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

Intracerebral Hemorrhage (2024)

~ iEM Education Project Team ~ Leave a comment

by Muhammad I. Abdul Hadi, Iskasymar Ismail, Kamarul Baharuddin, and Erin Simon

Authors
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You have a new patient!

A 60-year-old female was brought to the Emergency Department (ED) with a complaint of sudden onset of left-sided body weakness associated with facial asymmetry and vomiting. She was known to have hypertension. On arrival, she was drowsy with a Glasgow Coma Scale of 13/15 (E3, V4, M6). Her pupils were equal and reactive. 

The image was produced by using ideogram 2.0.

Her vital signs were as follows: blood pressure 210/118 mmHg, heart rate 96 beats per minute, respiratory rate 20 breaths per minute, oxygen saturation 98% on room air, and afebrile. Her left upper limb and lower limb examination showed hyperreflexia and reduced motor power to 0/5. Her left plantar response was extensor. Her right upper and right lower limbs were unremarkable. Capillary blood sugar was 9.3 mmol/L.

What is your differential diagnosis and outline your management?

What do you need to know?

Importance

Altered mental status (AMS) is a neurological emergency with many differential diagnoses. A general approach to AMS is to look for structural or metabolic causes. The most common structural cause of AMS is an acute stroke. Stroke can be classified into two major categories: ischemic and hemorrhagic. Hemorrhagic stroke can be further divided into two types: intracerebral hemorrhage (ICH) and subarachnoid hemorrhage [1]. ICH is associated with poor functional outcomes and carries high morbidity and mortality. In addition, most patients who survive an ICH have disabilities and cognitive decline and are at risk for recurrent stroke.

Patients with ICH can present with an abrupt onset of focal neurological signs. The clinical features typically evolve over minutes to a few hours. However, in subarachnoid hemorrhage, the symptoms are typically maximal at onset [2]. Depending on the volume of the hemorrhage, location, and the extent of the affected brain tissue, the patient may experience vomiting, headache, hemiparesis, hemisensory loss, facial weakness, aphasia, dysarthria, visual disturbance, and AMS when the hemorrhage is significant. However, the patient may not have those typical symptoms if the hemorrhage is small and in an uncommon site.

Signs of significant elevation of intracranial pressure (ICP) due to mass effect or herniation from ICH are:

  • Unequal pupil size
  • Dilated pupils
  • Comatose
  • Cushing triad (bradycardia, respiratory depression, hypertension)

Epidemiology

ICH is a neurological emergency case that is frequently encountered in ED. It is the second leading cause of stroke, accounting for up to 27 percent of all stroke cases globally. There are over 12.2 million new strokes each year, and 6.5 million people die from stroke annually. The risk of developing a stroke in a lifetime is one in four people over age 25 [3].

Pathophysiology

The pathophysiology of spontaneous ICH depends on its etiologies. These include hypertensive vasculopathy, cerebral amyloid angiopathy, aneurysms, arterio-venous malformations (AVM), cerebral venous thrombosis, hemorrhagic infarction, reversible cerebral vasoconstriction syndrome, cerebral vasculitis, sickle cell disease, anticoagulation therapy, and bleeding disorder [2]. 

Common sites for ICH and its common presentation include [4]:

  • Basal ganglia (40-50%): contralateral hemiplegia, gaze preference to the side of bleeding
  • Lobar regions (20-50%): Focal neurologic deficits; hemiparesis, hemisensory loss, and gaze preferences
  • Thalamus (10-15%): contralateral hemiplegia, gaze preferences away from the  side of bleeding
  • Brainstem (5-12%): impaired loss of consciousness, pinpoint pupils, cranial nerve palsies, absent or impaired horizontal gaze, and facial weakness
  • Cerebellum (5-10%): vertigo, vomiting, and limb ataxia

Medical History

Spontaneous ICH frequently presents with acute onset of stroke symptoms, such as acute focal neurological deficits (limb weakness and slurred speech), AMS, and features of increased intracranial pressure (vomiting and headache). The presence of AMS, vomiting, and headache are the essential features to differentiate hemorrhagic from ischemic stroke. AMS occurs in approximately 50% of the cases. In addition, neurological symptoms may develop during routine activity, exertion, or intense emotional activity. However, these symptoms may be absent with small hemorrhages [2]. Seizures may also develop if the hemorrhages involve cortical or cerebellar tissue.

Risk Factors for ICH

Risk factors for ICH can be simplified with the mnemonic of ABCDEFGH.

A: Age (elderly, the risk of ICH increases with advancing age) and alcohol consumption – Heavy alcohol use is associated with an approximately threefold increased risk of ICH

B: Blood pressure (hypertension) – the most important risk factor. This results in small vessel damage to deeper structures such as the basal ganglia and thalamus.

C: Cigarette smoking – In the Physicians Health Study, active smokers had a relative ICH risk of 2.06 percent compared with non-smokers 

D: Drug (antiplatelet, anticoagulant, and stimulant drug abuse) – Anticoagulation (warfarin) increases the risk of ICH two to fivefold. Stimulant drugs have been associated with a risk of ICH due to possible spikes in blood pressure and vasospasm.

E: Exercise and healthy lifestyle – Inactivity and obesity are comorbidities that can lead to increased risk for ICH

F: Family history

G: Gender (ICH is more prevalent in men than women) and race (Black Americans have a higher risk than White Americans). Asian countries have a higher incidence of ICH than other regions [4].

H: Hypo/hypercholesterolemia – A systematic review and meta-analysis found that low cholesterol was associated with an increased ICH risk

Others:

  • Cerebral Amyloid Angiopathy- Risk increases with age. Amyloid protein deposition weakens vessels’ structural integrity.
  • Structural Abnormalities- aneurysms, connective tissue diseases, congenital AVMs, and family history of subarachnoid hemorrhage (SAH) increase ICH risk.

Physical Examination

The physical examination of a patient with ICH begins with ensuring the stability of airway, breathing, and circulation. Once stabilized, a thorough neurological examination is performed. On inspection, the patient may present with an altered sensorium, ranging from drowsiness to stupor or coma, along with hemiparesis or hemiplegia, with hemiplegia being more common. Facial asymmetry may also be observed.

The general examination should assess for high blood pressure and risk factors such as nicotine stains on fingernails, indicative of smoking, or signs of alcoholic liver disease. Using the ABCDEFGH approach for risk factor identification is advised.

The specific neurological examination typically reveals deficits that correspond to the site of the hemorrhage and the associated edema. Cranial nerve abnormalities may manifest as unequal pupil size, visual field defects, ptosis, facial asymmetry, dysphasia, and a reduced gag reflex. Nuchal rigidity may be noted. Examination of the motor system often shows features of upper motor neuron (UMN) lesions, such as hemiplegia, hypertonia, hyperreflexia, and a positive Babinski sign. Sensory examination may reveal hemisensory loss, while involvement of the cerebellar system can present as sudden, severe vertigo accompanied by akinesia.

An assessment of other systems is essential to identify risk factors and complications associated with ICH. The cardiovascular system may show signs of stress-induced cardiomyopathy or acute cardiac failure. The respiratory system should be evaluated for complications like aspiration pneumonia. Examination of the lower limbs may reveal venous thrombotic events, and systemic signs like fever and infections should also be assessed.

Progressive elevation of intracranial pressure (ICP) or herniation is associated with several clinical features that require immediate attention. Pupillary changes are commonly observed, including impaired reactivity to light, which may indicate worsening neurological status. Abducens nerve (cranial nerve VI) palsy can also occur, with alert patients potentially reporting horizontal diplopia. Additionally, progressive altered mental status (AMS) is a hallmark of increasing ICP. In more advanced stages, the Cushing triad, characterized by bradycardia, respiratory depression, and severe hypertension, may manifest as a critical sign of impending herniation.

Alternative Diagnoses

When evaluating a patient for ICH, it is essential to consider alternative diagnoses and inquire about specific risk factors. Acute ischemic stroke or transient ischemic attack (TIA) can present similarly to ICH and require neuroimaging for differentiation. A history of trauma may suggest a traumatic head injury, such as an epidural or subdural hematoma. Cerebral abscess should be considered if there is a history of fever, headache, and focal neurological deficits. Similarly, meningitis or encephalitis may present with fever, photophobia, neck stiffness, and seizures. A brain tumor often has a subacute to chronic onset with headache and focal neurological signs. Drug overdose or toxin-induced states warrant a thorough review of the patient’s medication and substance history. Metabolic disturbances, such as uremic encephalopathy or renal failure, and acute hypoglycemia or hyperglycemia, should also be considered. Post-epileptic paralysis (Todd’s paralysis), complicated migraine or hemiplegic migraine, and hypertensive encephalopathy are other important differential diagnoses that must be ruled out based on clinical history and investigations.

Acing Diagnostic Testing

Bedside Tests

In the evaluation of patients with suspected intracranial events, capillary blood sugar is a critical bedside test. Random blood glucose measurement helps exclude hypoglycemia or hyperglycemia, as hypoglycemia, in particular, can mimic stroke-like symptoms. Rapid identification and correction of blood glucose abnormalities are essential for accurate diagnosis and appropriate management.

Laboratory Tests

Several laboratory tests provide critical diagnostic insights. A full blood count is essential, as leukocytosis may indicate infection or infarction, lymphocytosis is associated with viral meningitis, and neutrophilia suggests bacterial meningitis. Thrombocytopenia may point toward a bleeding tendency. Renal function tests measuring urea and creatinine are crucial for identifying renal failure, while liver function tests are important in patients suspected of having liver disease. Measurement of INR helps identify coagulopathies, which may increase bleeding risk. Additionally, an arterial blood gas test is indicated in cases of respiratory distress to assess for respiratory failure or metabolic disorders.

Electrocardiogram (ECG)

ECG changes in patients with intracranial conditions can include a prolonged QT interval and ST-T wave changes. These findings may indicate catecholamine-induced cardiac injury [5], which is a potential complication in such cases.

Toxicology Screening

Toxicology screening is essential when drug poisoning or alcohol use is suspected in a patient. Plasma and urine samples should be sent for toxicology analysis to identify potential toxic substances, aiding in diagnosis and guiding appropriate treatment.

Imaging

Imaging plays a crucial role in the evaluation of ICH. A non-contrast head CT is the first-line modality for accurately identifying acute ICH, where a hyperdense lesion can be observed. It is also effective in ruling out other conditions such as brain tumors, cerebral metastasis, skull fractures, hydrocephalus, cerebral ischemia, and cerebral abscess. In addition, a CT angiogram can detect underlying causes like aneurysms or vascular malformations and is recommended for patients under 70 years old to assess for vascular origins of ICH [4].

While both MRI and CT are equally effective in detecting acute ICH, MRI is superior for identifying chronic ICH [4]. In cases with large vessel occlusions, CT may be used; however, for patients with an NIH stroke scale score >6 and a normal head CT, thrombolytic therapy may be considered after consultation with a stroke neurologist and evaluation of contraindications. Although MRI offers greater accuracy for acute strokes, its use in the emergency department is limited by time and availability.

Finally, a chest X-ray is helpful for identifying complications such as pulmonary edema or consolidation caused by aspiration or pneumonia, which may occur alongside intracranial events.

The Image Archieve of Intracranial Hemorrhage on iEM

Risk Stratification

The ICH score is extensively used as a clinical grading scale and communication tool to estimate subsequent 30-day mortality and decide on the appropriate care option [6]. It is commonly used in conjunction with the FUNC (Functional Outcome in Patients with Primary Intracerebral Hemorrhage) score, which predicts the functional independence of ICH patients after 90 days [7].

ICH score

The ICH Score, ranging from 0 to 6, is a clinical grading system developed by to predict outcomes in ICH patients [6]. Points are assigned based on specific criteria: one point for age over 80 years, one point for an infratentorial origin of the hemorrhage, one point for an ICH volume exceeding 30 ml, one point for intraventricular extension of the hemorrhage, one point for a Glasgow Coma Scale (GCS) score between 5 and 12, and two points for a GCS score of 3 or 4. This scoring system provides a standardized approach to assessing the severity of ICH.

  1. Glasgow Coma Score (GCS score of 5-12 = 1, GCS score of 3 or 4 = 2) 
  2. Age ≥80 = 1
  3. Presence of ICH volume ≥30 mL = 1
  4. Presence of intraventricular hemorrhage = 1
  5. Presence of infratentorial origin of hemorrhage = 1

In the ICH score, 1 point corresponds to a 13% mortality rate, 2 points to 26%, 3 points to 72%, 4 points to 97%, and 5 or more points indicate a 100% mortality rate.

FUNC score

As previously mentioned, The FUNC score is a clinical tool utilized at hospital admission to estimate the probability of achieving functional independence (defined as a Glasgow Outcome Score of 4 or higher) within 90 days after an ICH. The FUNC score includes categories below. 

  • ICH Volume (cm³):
    • Less than 30 cm³: +4 points
    • 30–60 cm³: +2 points
    • Greater than 60 cm³: 0 points
  • Age:
    • Younger than 70 years: +2 points
    • 70–79 years: +1 point
    • 80 years or older: 0 points
  • ICH Location:
    • Lobar: +2 points
    • Deep: +1 point
    • Infratentorial: 0 points
  • GCS Score:
    • Score of 9 or greater: +2 points
    • Score of 8 or less: 0 points
  • Pre-ICH Cognitive Impairment:
    • No cognitive impairment: +1 point
    • Yes, cognitive impairment present: 0 points

Functional independence is defined as a Glasgow Outcome Score of 4 or higher. According to the score interpretation, patients with a FUNC Score of 0–4 have a 0% chance of achieving functional independence. A score of 5–7 corresponds to a 29% among survivors. For a score of 8, the likelihood rises to 48%. Patients scoring 9–10 have a 75% chance to have independence. The highest score of 11 corresponds to a 95% likelihood of functional independence among survivors.

Management

The initial treatment goals for ICH are focused on preventing secondary brain damage [8]. These include preventing hemorrhage expansion, monitoring for and managing elevated intracranial pressure (ICP), and addressing other neurologic and medical complications.

Triage

Prehospital management of acute ICH prioritizes airway maintenance, cardiovascular support, and rapid transport to the nearest acute stroke care facility [9].

ABCD Approach

  1. Airway: Assess airway patency. Intubation should only be performed if the patient cannot protect their airway or is in respiratory distress.
  2. Breathing: Ensure adequate oxygenation by administering supplementary oxygen if the patient is hypoxic, aiming to maintain oxygen saturation above 94%. Avoid hypoventilation, as increased partial pressure of carbon dioxide can cause cerebral vasodilation and elevate ICP.
  3. Circulation: Evaluate hydration status. All suspected ICH patients should initially be placed nil by mouth and started on IV isotonic saline to maintain serum sodium levels above 135 mmol/L. Hypotension should be promptly treated with fluid replacement. Elevated blood pressure must be carefully managed to avoid further complications.
  4. Disability: Assess the patient’s level of consciousness using the Glasgow Coma Scale (GCS). Conduct hourly neurologic evaluations to monitor for signs of deterioration or elevated ICP.

General Measures

  • Head Elevation: Elevate the head of the bed to greater than 30 degrees to promote venous drainage and reduce ICP [10].
  • Sedation: For intubated patients, use appropriate sedation, such as midazolam, to ensure patient comfort.
  • Temperature Control: Administer antipyretics, such as paracetamol, for temperatures above 38°C.
  • Head Positioning: Maintain a neutral head position, avoiding neck rotation or placing IV lines at the neck to prevent venous outflow obstruction.

Pharmacological Approach to Intracerebral Hemorrhage (Mnemonic: BCGO)

B: Blood Pressure Control
Blood pressure management is critical in ICH. The target systolic blood pressure (SBP) should be maintained between 140-160 mmHg, ideally achieved within the first hour of presentation using intravenous antihypertensive medications [11].

C: Coagulopathy Management
All anticoagulants and antiplatelet agents should be discontinued, and reversal agents should be administered when necessary [12, 13]. Platelet transfusion generally has a limited role. Examples of anticoagulants and their reversal strategies include:

  • Warfarin: Reversal with Vitamin K, fresh frozen plasma (FFP), or 4-factor Prothrombin Complex Concentrates (PCC), as it inhibits Vitamin K-dependent clotting factors (II, VII, IX, X).
  • Unfractionated Heparin: Reversal with Protamine, as it binds to antithrombin III.
  • Low Molecular Weight Heparin: Reversal is incomplete with Protamine, as it inhibits factor Xa.
  • Dabigatran: Reversal with Idarucizumab (Praxbind), which directly binds and inhibits thrombin (Factor IIa).
  • Oral Factor Xa Inhibitors (e.g., Apixaban (Eliquis), Edoxaban (Lixiana, Savaysa), Rivaroxaban (Xarelto)): Reversal options include Andexanet alfa (AndexXa) or 4-factor PCC.

G: Glucose Management
Blood glucose levels should be maintained within the range of 6-10 mmol/L to prevent hypoglycemia or hyperglycemia, both of which can exacerbate neurologic injury [14].

O: Osmotic Therapy
For patients with acute ICP elevation or life-threatening mass effect, treatment with mannitol or hypertonic saline may be considered. However, these therapies have not been shown to significantly improve outcomes in patients with acute ICH [15].

Patients with acute ICH are at risk for early seizures (within one to two weeks of ICH) and late (post-stroke) seizures. Early seizures may be self-limited, attributed to transient neurochemical changes associated with the acute ICH. For patients who have a seizure, immediate intravenous anti-seizure medication treatment should be initiated to reduce the risk of a recurrent seizure although anti-seizure treatments’ value is not clear [16].

Medications

Labetalol (Antihypertensive Medication)

  • Dose: (0.25-0.5 mg/kg). Initial bolus of 20 mg IV, followed by 20–80 mg IV bolus every 10 minutes (maximum total dose of 300 mg). Alternatively, 0.5 to 2 mg/minute can be administered as an IV loading infusion following an initial 20 mg IV bolus (maximum total dose of 300 mg).
  • Frequency: Administered every 10 minutes as required or as an infusion.
  • Maximum Dose: 300 mg total.
  • Cautions/Comments:
    • Always inquire about food or drug allergies, a past medical history of bronchial asthma, or heart failure.
    • Labetalol is classified as Category C in pregnancy for all trimesters.

Nicardipine (Antihypertensive Medication)

  • Dose: 5 to 15 mg/hour as IV infusion. Once the desired blood pressure is achieved, reduce the dose to a maintenance rate of 2–4 mg/hour.
  • Frequency: Continuous infusion.
  • Maximum Dose: 15 mg/hour.
  • Cautions/Comments:
    • Avoid use in patients with acute heart failure.
    • Use with caution in patients with coronary ischemia.
    •  

Phenytoin (Anti-Seizure Medication)

  • Dose: 15–20 mg/kg as a loading dose.
  • Frequency: Administered every 8 hours.
  • Maximum Dose: 100 mg.
  • Cautions/Comments:
    • Always check for food or drug allergies and any history of heart problems.
    • Phenytoin is classified as Category D in pregnancy for all trimesters.

Mannitol (For Treating High ICP – Osmotic Diuresis)

  • Dose: 2–4 ml/kg (12.5%), 1.25–2.5 ml/kg (20%), or 1–2 ml/kg (25%).
  • Frequency: Administer every 2 hours as required.
  • Cautions/Comments:
    • Ask about food or drug allergies.
    • Mannitol is classified as Category C in pregnancy for all trimesters.

Surgery

The surgical approach to managing intracerebral hemorrhage (ICH) often includes decompressive hemicraniectomy for hematoma evacuation. Immediate neurosurgical consultation is critical when imaging findings suggest the need for emergency surgery. Indications for urgent surgical intervention include cerebellar ICH that is either ≥3 cm³ in diameter or causing brainstem compression, intraventricular hemorrhage (IVH) with obstructive hydrocephalus and neurologic deterioration, and hemispheric ICH associated with life-threatening brain compression or obstructive hydrocephalus. These conditions demand prompt action to prevent further neurologic compromise and improve patient outcomes.

  •  

Special Patient Groups

Pediatrics

ICH in children is predominantly traumatic in origin, often resulting from head injuries caused by falls, vehicular accidents, or abuse (e.g., non-accidental trauma). Non-traumatic causes are less common but may include vascular anomalies like arteriovenous malformations, coagulopathies, or rare genetic conditions [17].

Geriatrics

The incidence of spontaneous ICH increases significantly with age, primarily due to the widespread use of anticoagulation and antithrombotic therapies for managing cardiovascular and cerebrovascular conditions [18]. In addition, older adults often have underlying medical conditions, such as hypertension, diabetes mellitus, and hypercholesterolemia, which predispose them to vascular fragility and hemorrhage. Careful monitoring and tailored management are required to address both the hemorrhage and these comorbidities in elderly patients.

Pregnant Patients

The risk of spontaneous ICH is elevated in pregnant women, especially in those with preeclampsia, eclampsia, or pregnancy-induced hypertension (PIH) [19]. These conditions are associated with endothelial dysfunction, elevated blood pressure, and increased risk of vascular rupture. Management in pregnant women involves a multidisciplinary approach, balancing maternal and fetal safety, with attention to blood pressure control and timely delivery if necessary.

When To Admit This Patient

All patients with ICH should be admitted to the intensive care unit (ICU) for comprehensive management [20]. ICU admission is crucial for close monitoring and intervention due to the potential for rapid deterioration in neurological status and the need for specialized care. These patients require the involvement of a multidisciplinary team, including neurosurgeons, neurologists, and critical care specialists, to address various aspects of care.

Key reasons for ICU admission include:

  1. Further Investigation: Advanced imaging, such as CT angiography or MRI, is often necessary to identify the underlying cause of the hemorrhage (e.g., aneurysm, arteriovenous malformation) and to assess for complications like hydrocephalus or increased intracranial pressure.
  2. Medical Management: Tight control of blood pressure, intracranial pressure, glucose levels, and coagulopathy is essential to prevent secondary brain injury and improve outcomes.
  3. Surgical Operations: Patients may require urgent surgical interventions, such as hematoma evacuation, decompressive craniectomy, or ventriculostomy, particularly in cases of life-threatening mass effect, brainstem compression, or obstructive hydrocephalus.
  4. Rehabilitation Planning: Early rehabilitation interventions should be initiated to minimize long-term disability. This includes physical therapy, occupational therapy, and addressing the patient’s psychological and cognitive needs post-ICH.

The ICU provides an ideal setting for continuous monitoring of neurological function, management of complications, and rapid response to emergencies such as rebleeding or sudden increases in intracranial pressure. Admission ensures a holistic and systematic approach to optimizing patient outcomes following spontaneous ICH.

Revisiting Your Patient

An urgent head CT was completed and revealed an intracranial hemorrhage in the caudate region.

During her ED stay, her GCS suddenly reduced to 7/15 (E2, V2, M3). She was intubated for airway protection. A repeated head CT demonstrated expansion of the right intracranial hemorrhage with intraventricular extension midline shift.

Intracranial Hemorrhage in the Caudate Region. An intracranial hemorrhage is visualized in the caudate region of the brain. Contributed by S Munakomi, MD [21]

The neurosurgical team was consulted, and the patient was sent for an emergency craniectomy and evacuation of the clot. A postoperative head CT showed a grossly evacuated blood clot and corrected midline shift. The intensive care team weaned her off of mechanical ventilatory support, and her GCS improved to 10 (E3, V1, M6).

Authors

Picture of Muhammad Izzat Abdul Hadi

Muhammad Izzat Abdul Hadi

Muhammad Izzat Bin Abdul Hadi is a dedicated emergency medicine professional at Hospital Universiti Sains Malaysia in Kelantan, Malaysia. He completed his medical degree at Mansoura University in 2007 and later obtained a Master of Medicine in Emergency Medicine from Universiti Sains Malaysia in 2019. His contributions to medical research include two notable publications in the Malaysian Journal of Emergency Medicine (M-JEM) in 2021.

Picture of Iskasymar Ismail

Iskasymar Ismail

Dr Iskasymar is an emergency physician, a senior medical lecturer at University Putra Malaysia (UPM) and Head of Unit of RESQ (Regional Emergency Stroke Quick Response) Stroke Emergency Unit in UPM teaching hospital, Hospital Sultan Abdul Aziz Shah (HSAAS). He is actively involved in making RESQ as niche service for hyperacute stroke care in HSAAS and working collectively with neurology team and radiology team in developing protocols and SOP. Dr Iskasymar is an active expert panel of stroke and intracranial hemorrhage Clinical Practice Guideline of Malaysia.

Picture of Kamarul Aryffin Baharuddin

Kamarul Aryffin Baharuddin

Dr. Kamarul Aryffin Baharuddin is a Professor in Emergency Medicine and an Emergency Medicine Specialist at the Universiti Sains Malaysia (USM), Kelantan, Malaysia. He graduated with his medical degree in 1998 and completed his postgraduate specialization in 2006. His research interests are neurological emergency, pain management, medical education, and artificial intelligence in medicine. He is currently a Deputy Dean of Academics in the School of Medical Sciences, USM. He is also one of the team in neurology SIG (Special Interest Group) under the College of Emergency Physician, Malaysia.

Picture of Erin Simon

Erin Simon

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

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References

  1. Cheng Y lin.Molecular Mechanisms of Notch1-Mediated Neuronal Cell Death in Ischemic Stroke. PhD Thesis. The University of Queensland; 2014. doi:10.14264/uql.2014.547
  2. Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis – UpToDate. Accessed December 4, 2024. https://www.uptodate.com/contents/spontaneous-intracerebral-hemorrhage-pathogenesis-clinical-features-and-diagnosis
  3. Feigin VL, Brainin M, Norrving B, et al. World Stroke Organization (WSO): Global Stroke Fact Sheet 2022. Int J Stroke Off J Int Stroke Soc. 2022;17(1):18-29. doi:10.1177/17474930211065917
  4. Sheth KN. Spontaneous Intracerebral Hemorrhage. N Engl J Med. 2022;387(17):1589-1596. doi:10.1056/NEJMra2201449
  5. Pinnamaneni S, Aronow WS, Frishman WH. Neurocardiac Injury After Cerebral and Subarachnoid Hemorrhages. Cardiol Rev. 2017;25(2):89-95. doi:10.1097/CRD.0000000000000112
  6. Hemphill JC, Bonovich DC, Besmertis L, Manley GT, Johnston SC. The ICH score: a simple, reliable grading scale for intracerebral hemorrhage. Stroke. 2001;32(4):891-897. doi:10.1161/01.str.32.4.891
  7. Dusenbury W, Malkoff MD, Schellinger PD, et al. International beliefs and head positioning practices in patients with spontaneous hyperacute intracerebral hemorrhage. Ther Adv Neurol Disord. 2023;16:17562864231161162. doi:10.1177/17562864231161162
  8. Pandey AS, Xi G. Intracerebral hemorrhage: a multimodality approach to improving outcome. Transl Stroke Res. 2014;5(3):313-315. doi:10.1007/s12975-014-0344-z
  9. Gioia LC, Mendes GN, Poppe AY, Stapf C. Advances in Prehospital Management of Intracerebral Hemorrhage. Cerebrovasc Dis. Published online March 7, 2024. doi:10.1159/000537998
  10. Simmons BJ. Management of intracranial hemodynamics in the adult: a research analysis of head positioning and recommendations for clinical practice and future research. J Neurosci Nurs. 1997;29(1):44-49. doi:10.1097/01376517-199702000-00007
  11. Sato S, Carcel C, Anderson CS. Blood Pressure Management After Intracerebral Hemorrhage. Curr Treat Options Neurol. 2015;17(12):49. doi:10.1007/s11940-015-0382-1
  12. Grzegorski T, Andrzejewska N, Kaźmierski R. Reversal of antithrombotic treatment in intracranial hemorrhage–A review of current strategies and guidelines. Neurol Neurochir Pol. 2015;49(4):278-289. doi:10.1016/j.pjnns.2015.06.003
  13. Campbell PG, Sen A, Yadla S, Jabbour P, Jallo J. Emergency reversal of antiplatelet agents in patients presenting with an intracranial hemorrhage: a clinical review. World Neurosurg. 2010;74(2-3):279-285. doi:10.1016/j.wneu.2010.05.030
  14. Godoy DA, Piñero GR, Svampa S, Papa F, Di Napoli M. Hyperglycemia and short-term outcome in patients with spontaneous intracerebral hemorrhage. Neurocrit Care. 2008;9(2):217-229. doi:10.1007/s12028-008-9063-1
  15. Qureshi AI, Wilson DA, Traystman RJ. Treatment of elevated intracranial pressure in experimental intracerebral hemorrhage: comparison between mannitol and hypertonic saline. Neurosurgery. 1999;44(5):1055-1064. doi:10.1097/00006123-199905000-00064
  16. Gilad R, Boaz M, Dabby R, Sadeh M, Lampl Y. Are post intracerebral hemorrhage seizures prevented by anti-epileptic treatment?. Epilepsy Res. 2011;95(3):227-231. doi:10.1016/j.eplepsyres.2011.04.002
  17. Kumar R, Shukla D, Mahapatra AK. Spontaneous intracranial hemorrhage in children. Pediatr Neurosurg. 2009;45(1):37-45. doi:10.1159/000202622
  18. Berhouma M, Jacquesson T, Jouanneau E. Spontaneous Intracerebral Hemorrhage in the Elderly. Brain and Spine Surgery in the Elderly. 2017:411-22.
  19. Berhouma M, Jacquesson T, Jouanneau E. Spontaneous Intracerebral Hemorrhage in the Elderly. Brain and Spine Surgery in the Elderly. 2017:411-22.
  20. Goldstein JN, Gilson AJ. Critical care management of acute intracerebral hemorrhage. Curr Treat Options Neurol. 2011;13(2):204-216. doi:10.1007/s11940-010-0109-2
  21. Tenny S, Thorell W. Intracranial Hemorrhage. In: StatPearls. StatPearls Publishing; 2024. Accessed December 4, 2024. http://www.ncbi.nlm.nih.gov/books/NBK470242/

Reviewed and Edited By

Picture of Erin Simon, DO

Erin Simon, DO

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

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

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

Bronchial Foreign Body Aspiration (2024)

~ iEM Education Project Team ~ Leave a comment

by Elhaitham Ahmed & Khalifa Alqaydi

Authors
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You have a new patients!

Patient 1

A 72-year-old male was brought from an inpatient stroke rehabilitation center to the emergency department for a cough lasting the past ten days. Along with the cough, the patient was noted to have blood-tinged sputum, which is sometimes foul-smelling. His vital signs are as follows: temperature of 38.4°C, blood pressure of 138/78 mmHg, heart rate of 103 bpm, respiratory rate of 26 breaths/min, and oxygen saturation of 93% on room air. On physical examination, the patient exhibits tachypnea, dullness on percussion, bronchial breathing, egophony, and increased vocal fremitus upon examining the right side of his lung.

The image was produced by using ideogram 2.0.

Patient 2

Thirty minutes later, the nurse calls you regarding a 5-year-old boy brought in by his mother, presenting with stridor and an ongoing cough. The mother mentions that she found her child playing with her wallet while she was in the next room and discovered him in this condition. The child is tachypneic, saturating at 90% on room air with subcostal retractions. Examination of the right lung revealed wheezing with decreased air entry.

a-photo-of-a-5-year-old-male-patient-(the image was produced by using ideogram 2.0)

What do you need to know?

Importance

Tracheobronchial foreign body aspiration (FBA) can be a potentially life-threatening event. FBA in children may be suspected based on a choking episode if such an episode is witnessed by an adult or remembered by the child. In contrast, the clinical presentation of unwitnessed FBA may be subtle, requiring careful review of the history, clinical assessment, and judicious use of radiography and bronchoscopy for diagnosis. Flexible and rigid bronchoscopy have become the cornerstone of both diagnosis and treatment in patients with suspected airway foreign bodies, which are most commonly seen in patients with FBA [1].

Epidemiology

FBA is more common in children than in adults. Data from the National Security Council report that approximately 80 percent of cases occur in patients younger than 15 years of age, with the remaining 20 percent presenting in those older than 15 years. Overall, death from FBA is the fourth leading cause of accidental home and community deaths in the United States, with over 5,000 fatal episodes of FBA reported during 2015. Death from FBA peaks in children under 1 year old and in adults over 75 years [2].

Pathophysiology

In children, nuts, seeds, and other organic material account for the majority of foreign bodies. However, in adults, the nature of inhaled objects is highly variable, ranging from organic to inorganic material. The type of foreign body significantly impacts the degree of tissue reaction in the airway. For example, some inorganic materials, such as metal or glass items, may cause little tissue inflammation but can result in direct airway injury if they are sharp. In contrast, some organic materials, such as nuts and a variety of pills, can cause significant inflammation, granulation tissue formation, and airway stenosis. Aspirated organic material can also expand from airway moisture, worsening obstruction. Aspiration of medications in pill form, such as iron tablets, aspirin, and potassium chloride, can also cause severe airway inflammation and ulceration [2].

Medical History

Clinical presentation can range from chronic nonspecific respiratory complaints to acute airway obstruction. In most cases of aspiration, the presence of a foreign body can be suspected after a thorough history. Patients with airway foreign bodies may present with noisy breathing, inspiratory stridor, rhonchi, vomiting, changes in voice, and hemoptysis [3]. Some patients may report a history known as penetration syndrome, which includes a choking sensation accompanied by wheezing and coughing. Coughing may not completely expel the foreign body but may instead cause its impaction in the subglottic region. Therefore, coughing after suspected aspiration should prompt a search for a foreign body, even if symptoms improve [4].

In pediatric patients with suspected foreign body aspiration, the sudden onset of choking or intractable cough associated with wheezing and respiratory distress occurs in more than 63% of cases [5,6]. In addition to coughing and choking, stridor is a frequent symptom. The absence of early coughing and choking is associated with delayed diagnosis and chronic presentations, such as recurrent pneumonia [4]. The sudden onset of dyspnea and odynophagia may indicate an impacted subglottic object. If the object is sharp and thin, the emergency clinician should suspect embedding between the vocal cords or in the subglottic region, resulting in partial obstruction [7].

Other components of the history can assist in diagnosing and characterizing foreign bodies in patients with aspiration of nonfood objects. Many types of items may be aspirated by children exploring their environment. Another at-risk population includes individuals who habitually store small items in their mouths for quick access; examples include construction workers (nails) and seamstresses (pins). The presentation of patients with a retained airway foreign object may involve only infectious complications. A foreign object can lead to a retropharyngeal abscess. Patients with atypical or recurrent pneumonia may have pulmonary infections caused by the persistence of a foreign object serving as a focus of infection [6].

Physical Examination

Physical findings depend on the degree of airway obstruction and the duration of the object’s presence. Depending on the size and location of the foreign body, the examination may reveal a normal patient, one with cyanosis and respiratory arrest, or any condition between these two extremes. Patients may exhibit stridor or hoarseness with upper airway foreign objects, and intercostal or sternal retractions may be observed in patients with high-grade obstruction caused by tracheal foreign bodies [8]. Hypoxemia may be present; however, normoxia does not rule out the presence of a foreign body. Patients with secondary infections may present with fever.

Oropharyngeal examination may reveal a foreign body posteriorly or donor sites of fractured teeth. The examination should also include a search for fractured or missing dental prostheses. Oropharyngeal examination can often be supplemented by indirect or direct laryngoscopy or nasopharyngoscopy, but these procedures should be performed only if the procedural stress does not pose an undue risk of airway compromise.

Coughing may result from local irritation caused by bronchial foreign bodies. Localized or apparently generalized wheezing is frequently auscultated in patients with lower respiratory tract foreign bodies [9]. Complete obstruction of a mainstem bronchus may result in absent ipsilateral breath sounds; however, breath sounds can sometimes be transmitted across the thorax, and the only physical abnormality may be asymmetric chest rise. Occasionally, a foreign body acts as a one-way valve, allowing air into the lung during inspiration but preventing its exit during expiration. The affected lung becomes hyperexpanded, which may be detected as hyper-resonance on percussion [6].

Alternative Diagnoses

The selected differential diagnoses for airway foreign bodies include anaphylactic reactions, acute pharyngitis, acute epiglottitis, retropharyngeal abscess, neck tumors, pulmonary carcinomas, pneumonia, bronchitis, bronchiolitis, and tuberculosis.

Acing Diagnostic Testing

Imaging should not delay intervention in cases of suspected acute asphyxiation but is indicated for stable patients [10].

Findings on imaging depend on the type and location of the material aspirated and the time elapsed. In practice, plain films of the neck and chest are often performed simultaneously and can be followed by site-specific CT if suspicion remains. The majority of foreign bodies are radiolucent and not easily identified on plain film. If obstruction of the upper airway (oropharynx and upper trachea) is suspected, initial imaging should include anterior-posterior and lateral soft tissue views of the neck [11]. If these tests are negative and suspicion for FBA persists, further imaging with CT may be indicated. When FBA of the lower airways (below the vocal cords) is suspected, a chest radiograph should be the initial radiographic test to look for an obvious radiopaque airway lesion. Negative scans may prompt further evaluation with CT. The reported sensitivity of chest radiography is approximately 60 to 80 percent in children, and clinical experience suggests similarly poor sensitivity in adults [12].

Given its widespread availability, flexible bronchoscopy is often the diagnostic procedure of choice for non-life-threatening FBA in adults, particularly in cases involving smaller foreign bodies in the lower airway. Flexible bronchoscopy allows precise identification and localization of foreign bodies and facilitates the selection of instruments necessary for retrieval [13]. Additionally, flexible bronchoscopy enables removal of the foreign body during the diagnostic procedure if the operator is skilled in these techniques. Standard diagnostic or therapeutic flexible bronchoscopes are usually adequate for the management of FBA in adults [6].

Risk Stratification

Risk factors in adults include loss of consciousness due to trauma, drug or alcohol intoxication, or anesthesia. Additional risk factors in older adults include age-related slowing of the swallowing mechanism, medication use (impairing cough and swallowing), stroke-related dysphagia, and various degenerative neurologic diseases such as Alzheimer’s or Parkinson’s disease [2].

Management

In a conscious adult, data support the efficacy of chest thrusts, back blows or slaps, blind finger sweeps, and abdominal thrusts in relieving complete foreign body airway obstruction [6, 14]. In cases of life-threatening asphyxiation, initial support should focus on treating airway obstruction and respiratory failure. Once the airway is secured, a laryngoscopic evaluation of the oropharynx should be performed immediately to diagnose and retrieve a supraglottic or glottic foreign body. If a foreign body is not seen, rigid bronchoscopy is generally the procedure of choice for suspected asphyxiating foreign bodies located in the trachea or major bronchi. In patients with non-life-threatening FBA, flexible bronchoscopy is typically performed [15].

When large foreign bodies completely or almost completely obstruct major upper airways (glottis, supraglottis, trachea), it is critical to ensure the patient is oxygenated and the airway is secured [16]. Support measures may include bag-valve-mask ventilation and endotracheal intubation. If ventilation is unsuccessful, an emergent cricothyrotomy or tracheotomy may be required if the foreign body is suspected to be above the vocal cords. Once the airway is secured, immediate inspection of the oropharynx (glottis, supraglottis) is indicated, as one-third of FBA cases presenting as acute asphyxiation are located in the supraglottis. Retrieval of the foreign body with Magill forceps can be safely performed using direct laryngoscopy (glottis, supraglottis) or with smooth or alligator forceps during rigid or flexible bronchoscopy (large central foreign body in the trachea or major bronchus) [17].

The choice of procedure for foreign body removal depends on the type of presentation, characteristics of the inhaled foreign body, its location, the duration it has been in the airway (if known), and local expertise. Anti-inflammatories and antibiotics are not routinely administered to patients with suspected or documented FBA. Antibiotics are indicated only in cases of clinically, radiologically, or microbiologically documented respiratory tract infections. However, their use should not delay foreign body extraction, even if pneumonia or sepsis is suspected [2].

Figure 1 - Approach to Upper Airway Foreign Body. Original Image can be found here: White JJ. Upper Airway Foreign Bodies: Emergency department presentation, Evaluation and Management. emDOCs.net - Emergency Medicine Education. April 12, 2021. Accessed May 9, 2023. http://www.emdocs.net/upper-airway-foreign-bodies-emergency-department-presentation-evaluation-and-management/.

Special Patient Groups

In the pediatric age group, moderate or high suspicion of FBA is suggested by any of the following:

  • Witnessed FBA, regardless of symptoms.
  • History of choking, with any subsequent symptoms or suspicious characteristics on imaging.
  • A young child with suggestive symptoms without another explanation, especially if there are suspicious characteristics on imaging. Suspicious symptoms include cyanotic spells, dyspnea, stridor, sudden onset of cough or wheezing (often focal and monophonic), and/or unilaterally diminished breath sounds.

The tracheobronchial tree should be examined in all cases with moderate or high suspicion of FBA, using rigid bronchoscopy (or, in some cases, computed tomography [CT]). On occasion, the adjunctive use of a flexible bronchoscope may be helpful. Normal chest radiographs are not sufficient to rule out FBA [19], primarily because most foreign bodies are radiolucent. Morbidity and mortality may increase if bronchoscopic evaluation is delayed.

When To Admit This Patient

Most patients improve clinically following FBA removal. Those with imaging abnormalities should undergo follow-up imaging six weeks to three months after extraction to confirm resolution. Patients presenting with a delayed presentation and belonging to high-risk groups should be admitted for management of complications and FBA retrieval and removal.

Revisiting Your Patients

The elderly patient, given his history of a recent stroke and being in a rehabilitation center, is at risk of FBA. His presentation with chronic cough and fever raises suspicion of pneumonia; however, the emergency medicine clinician should maintain a broad differential diagnosis based on further history, including foul-smelling sputum and nursing staff observations of difficulty swallowing and previous admissions for pneumonia. Such delayed presentations of FBA can occur in this age group. The patient’s management began with initial stabilization using oxygen support, along with workup for infection. Imaging modalities started with a chest plain film, which showed right lower lobe opacities but no clear foreign body. With suspicion for FBA still high, a chest CT scan was performed and revealed evidence consistent with FBA. The patient was started on broad-spectrum antibiotics, and bronchoscopy was scheduled as the definitive management for FBA. Follow-up bronchoscopy identified distal fragments of nuts impacted in the right lower lobe bronchus.

In the pediatric patient, the presentation is more acute and requires securing the airway. After placing the patient on a non-rebreather mask with 15L of oxygen, his saturation improved to 100%. Given the history of playing with a wallet, suspicion of coin aspiration was considered. A chest radiograph with posteroanterior and lateral views was performed, showing a rounded radiopaque structure in the right main bronchus. Airway support and supplemental oxygen should be provided until bronchoscopy is performed and the coin is retrieved.

Authors

Picture of Elhaitham Ahmed

Elhaitham Ahmed

Zayed Military Hospital, AbuDhabi

Picture of Khalifa Alqaydi

Khalifa Alqaydi

Zayed Military Hospital, AbuDhabi

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References

  1. Ruiz, F.E. (2022) Airway foreign bodies in children, UpToDate. Available at: https://www.uptodate.com/contents/airway-foreign-bodies-in-children?search=airway+foreign+bodies+in+children&source=search_result&selectedTitle=1~83&usage_type=default&display_rank=1 (Accessed: 08 May 2023).
  2. Shepherd, W. (2023) Airway foreign bodies in adults, UpToDate. Available at: https://www.uptodate.com/contents/airway-foreign-bodies-in-adults?search=adult+forign+body+&source=search_result&selectedTitle=3~150&usage_type=default&display_rank=3 (Accessed: 08 May 2023).
  3. Bajaj D, Sachdeva A, Deepak D. Foreign body aspiration. J Thorac Dis. 2021;13(8):5159-5175. doi:10.21037/jtd.2020.03.94
  4. Dabu J, Lindner M, Azzam M, et al. A Case of Chronic Cough and Pneumonia Secondary to a Foreign Body. Case Rep Med. 2017;2017:3092623. doi:10.1155/2017/3092623
  5. Mîndru DE, Păduraru G, Rusu CD, et al. Foreign Body Aspiration in Children-Retrospective Study and Management Novelties. Medicina (Kaunas). 2023;59(6):1113. Published 2023 Jun 9. doi:10.3390/medicina59061113
  6. Goodloe JM, Soulek J. Foreign Bodies . In: Rosen’s Emergency Medicine Concepts and Clinical Practice. 10th ed. Elsevier; 2023:666-681.
  7. Hazra TK, Ghosh AK, Roy P, Roy S, Sur S. An impacted meat bone in the larynx with an unusual presentation. Indian J Otolaryngol Head Neck Surg. 2005;57(2):145-146. doi:10.1007/BF02907672
  8. Swanson KL, Edell ES. Tracheobronchial foreign bodies. Chest Surg Clin N Am. 2001;11(4):861-872.
  9. Kazmerski T, Dedhia K, Maguire R, Aujla S. Chronic Esophageal Foreign Body Presenting as Wheezing and Cough in a Toddler. Pediatr Allergy Immunol Pulmonol. 2014;27(3):151-153. doi:10.1089/ped.2014.0370
  10. White JJ, Cambron JD, Gottlieb M, Long B. Evaluation and Management of Airway Foreign Bodies in the Emergency Department Setting. J Emerg Med. 2023;64(2):145-155. doi:10.1016/j.jemermed.2022.12.008
  11. António P, Raffaella C, Luigia R. Plain Film and MDCT Assessment of Neck Foreign Bodies. 2014;1007/978-88-470-5406-6_1.
  12. Svedström E, Puhakka H, Kero P. How accurate is chest radiography in the diagnosis of tracheobronchial foreign bodies in children?. Pediatr Radiol. 1989;19(8):520-522. doi:10.1007/BF02389562
  13. Turk D, Moslehi MA, Hosseinpour H. Role of Flexible Fiberoptic Bronchoscopy in the Diagnosis and Treatment of Pediatric Airway Foreign Bodies: A 5-Year Experience at a Tertiary Care Hospital in Iran. Tanaffos. 2022;21(3):354-361.
  14. Pavitt MJ, Swanton LL, Hind M, et al. Choking on a foreign body: a physiological study of the effectiveness of abdominal thrust manoeuvres to increase thoracic pressure. Thorax. 2017;72(6):576-578. doi:10.1136/thoraxjnl-2016-209540
  15. Bodart E, Gilbert A, Thimmesch M. Removal of an unusual bronchial foreign body: rigid or flexible bronchoscopy?. Acta Clin Belg. 2014;69(2):125-126. doi:10.1179/2295333714Y.0000000006
  16. Davis RJ, Stewart CM. Complete Glottic Obstruction by an Unusual Foreign Body. Otolaryngol Head Neck Surg. 2019;160(5):935-936. doi:10.1177/0194599818824298
  17. Singh GB, Aggarwal D, Mathur BD, Lahiri TK, Aggarwal MK, Jain RK. Role of magill forcep in retrieval of foreign body coin. Indian J Otolaryngol Head Neck Surg. 2009;61(1):36-38. doi:10.1007/s12070-009-0031-7
  18. White Upper Airway Foreign Bodies: Emergency department presentation, Evaluation and Management. emDOCs.net – Emergency Medicine Education. April 12, 2021. Accessed May 9, 2023. http://www.emdocs.net/upper-airway-foreign-bodies-emergency-department-presentation-evaluation-and-management/.
  19. Pinto A, Scaglione M, Pinto F, et al. Tracheobronchial aspiration of foreign bodies: current indications for emergency plain chest radiography. Radiol Med. 2006;111(4):497-506. doi:10.1007/s11547-006-0045-0

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.

Acute Ischemic Stroke (2024)

~ iEM Education Project Team ~ Leave a comment

by Hassan Khuram, Parker Maddox, & Scott Goldstein

Authors
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You have a new patient!

Mrs. A, a 63-year-old female, was brought to the emergency department by her daughter after she noticed that her mother was unable to speak normally, and her face was droopy on the right side. Upon arrival, Mrs. A was lying on a stretcher in no acute distress. The daughter reported that her symptoms started suddenly about 30 minutes ago. 

The image was produced by using ideogram 2.0

Vital signs showed a blood pressure of 170/90 mmHg, heart rate of 90 beats per minute, respiratory rate of 18 breaths per minute,  Temperature is 36.6 C (98 F), and oxygen saturation of 98% on room air. The patient had a history of hypertension, hyperlipidemia, and type 2 diabetes mellitus. On neurological examination, Ms. A was found to have right-sided facial droop, right arm pronator drift, and slurred speech. The NIH Stroke Scale (NIHSS) score was 8.

What do you need to know?

Importance

Acute ischemic stroke (AIS) is a major public health concern that affects millions of people worldwide. Stroke, ischemic or hemorrhagic, is the third most common cause of disability and the second most common cause of death worldwide [1]. It is estimated that 12.2 million strokes occur around the world annually, with the vast majority being ischemic [1,2]. Early recognition and management of acute ischemic stroke are vital as outcomes are directly tied to the time between the onset of symptoms and initiation of treatment. For every hour treatment is delayed, the brain loses as many neurons as it does in approximately 3.6 years of normal aging, which has led to the adage “time is brain” [3]. Therefore, emergency department physicians must be well-versed in diagnosing and managing acute ischemic stroke to maximize patient outcomes. The main goals in the acute management of ischemic stroke are to minimize ischemic damage to the penumbra, treat any complications because of the infarction, and diagnose the etiology to prevent a recurrence. The primary objectives of this chapter are to present a thorough overview of the major ideas and practices involved in the early evaluation and treatment of acute ischemic stroke in the emergency room.

Epidemiology

Understanding epidemiology can help elucidate risk factors that can result in faster recognition of stroke and its acute management. The vast majority of strokes occur beyond the 5th decade, with the age of onset being lower in low to middle-income countries [4]. In an acute setting, it is critical to identify if a stroke is ischemic or hemorrhagic, as treatment varies significantly [4,11]. This risk increases significantly with age, along with other lifestyle factors. These factors are listed in the table below (with the highest risk factors listed in descending order.)

Table 1. Modifiable and Non-modifiable risk factors for stroke [1,4–6]

Modifiable Risk Factors

Non-Modifiable Risk factors

Hypertension

Prior history of stroke or TIA

Cigarette smoking

Age ≥ 65 years

Diabetes mellitus

Sex ♂ > ♀

Atrial Fibrillation

Family History

Carotid artery stenosis

Genetic disorders (e.g., sickle cell)

Dyslipidaemia

Migraine with aura

Obesity and Metabolic syndrome

 

Diet/Nutrition

 

Sedentary Behavior

 

Alcohol/Recreational drug use (e.g. cocaine) 

 

Coagulopathy

 

Hormone Replacement Therapy/OCP

 

Pathophysiology

Acute ischemic strokes can occur due to thrombotic or embolic causes. One common link behind all the risk factors discussed above is that, in one form or another, they cause damage or dysfunction to blood vessels in the brain, reducing blood flow to the brain. Consequently, the parenchyma of the brain is unable to carry out its metabolic functions, which eventually leads to necrosis [7]. The exact mechanisms of how different risk factors contribute to stroke vary, but they ultimately all result in the damage of blood vessels in the brain. While there are many causes behind the damage of blood vessel walls, atherosclerosis and Virchow’s triad- blood stasis, endothelial injury, and hypercoagulability- remain the primary pathological process behind the vast majority of strokes [6,7]. For example, in Hypertension, the high pressures in the vessels cause shearing of the endothelial lining of blood vessel walls, which can result in rupture or thrombus formation. As the atherosclerotic plaques grow and become more advanced, they can lead to blood flow obstruction and turbulence, which can promote blood stasis. Blood stasis, in turn, can increase the risk of thrombosis within the affected blood vessel. The formation of a thrombus can obstruct blood flow to the brain and cause a stroke [7].

Similarly, smoking can cause inflammation and oxidative stress on blood vessels, causing an inflammatory response that ultimately results in the narrowing of the vessels and thrombus formation [8]. This framework also explains why older individuals are at higher risk since they have an increased prevalence of the modifiable risk factors listed in Table 1. [9]. Etiologies arising from circulatory system issues outside the brain require additional urgent management [5].

Medical History

A good history remains a key cornerstone in evaluating and managing stroke patients. Most typical presentations of strokes will be older adults presenting with acute onset focal neurological deficits. Patients might present with complaints of sudden onset speech difficulties, vision, sensation, strength, or coordination [10]. The acuity of neurologic dysfunction should clue physicians that stroke is an important differential. Another vital component when suspecting stroke is determining the time since the onset of symptoms. If this is unknown, then the last time the patient was seen well or at their neurological baseline can be used as a surrogate [11]. This step is critical as it helps determine whether the patient is within the window for reperfusion therapy and endovascular thrombectomy [5]. The 6S mnemonic list in Table 2. can be utilized to help clue clinicians that the patient might be having a stroke [12]:

Table 2. 6S mnemonic detailing core signs of stroke

S

Sudden onset

S

Slurred speech

S

Side weakness (unilateral deficits in face, arm, or leg)

S

Spinning (Vertigo)

S

Severe headache

S

Seconds (time since symptoms started)

The presence of this constellation should cue physicians to the immediate need for further evaluation of a serious process requiring labs and neuroimaging. The collection of symptoms can also give clues as to which vascular territory might be affected and can prompt the clinician to evaluate for further signs in that territory to help confirm the location. A general gestalt listed in Table 3. below can be used to help clinicians orient themselves as to which general vascular territory in the brain might be affected and what questions/exam findings to further probe for. The table is not exhaustive or mutually exclusive, and a more detailed discussion of the lesion site and associated neurologic findings is presented in the physical exam section.

Table 3. List of deficits and their associated territories [13]

Vascular territory

Associated deficits

Anterior Cerebral Artery (ACA)

Feet and legs

Middle Cerebral Artery (MCA)

Hands, Arms, Face, and Speech

Posterior Cerebral Artery (PCA)

Visual

Vertebrobasilar Artery (Brainstem)

Crossed signs (Contralateral hemiplegia & ipsilateral cranial nerve abnormalities)

Cerebellar Arteries

Coordination

The pace and course of symptoms can clue clinicians into the different subtypes of stroke that may be affecting the patient. Acute ischemic strokes due to embolic sources tend to occur suddenly, and the maximal deficit is perceived during this time. However, etiologies due to thrombosis tend to fluctuate and progress stepwise [14].

Other crucial components of medical history to assess are the risk factors mentioned in Table 1. They can help determine the precipitating factor for the stroke and can help guide management. For example, if the patient has a history of atrial fibrillation or carotid artery stenosis, then that could explain an embolic cause for the stroke and would require a more extensive workup along with additional management measures. Hypertension should also be sought out as it is the number one modifiable risk factor for stroke [2,6]. A review of current medications is also important because it can affect management. If a patient has been on anti-coagulation medications, then that is a strict contraindication for thrombolytics in stroke as it may lead to a hemorrhagic conversion [15]. In patients with acute ischemic stroke, a detailed medical history is crucial in directing the diagnostic and therapeutic decision-making process.

Physical Examination

Based on history, a focused physical and neurological exam can aid in localizing the lesion and provide clues as to the cause. Time is brain, and therefore, clinical suspicion of acute ischemic stroke should be rapidly confirmed with physical exam findings to minimize the time between the door to neuroimaging and recognize candidates for reperfusion therapy or endovascular thrombectomy [5,11,15]. As in all emergent cases, airway, breathing, circulation, disability, and exposure (ABCDE) should be prioritized in that order before attending to other steps in management. The physical exam should be tailored based on history to save time.

For example, if there is a history of atrial fibrillation, then a cardiac exam should be conducted to look for murmurs that might indicate an embolic cause. Patients with a history of atherosclerosis risk factors should also be examined for bruits in the neck that may reveal an embolic source. Papilledema on ocular exam may signify possible hemorrhagic stroke or cerebral edema as a complication of stroke that requires immediate intervention [16]. A neurologic exam is vital to confirm clinical suspicion of stroke and rule out other stroke mimics such as hypoglycemia or Bell’s palsy. Deficits on the exam can help point the clinician to the location of the lesion and the severity of the prognosis [13]. Table 4 below can be used to help localize the lesion based on clinical symptoms.

Table 4. A non-exhaustive list of common brain lesions and associated symptoms [13]

Vascular Territory

Common Neurologic Findings

Anterior Cerebral Artery (ACA)

  • Contralateral somatosensory & motor deficit mostly in lower extremity
  • Abulia
  • Urinary incontinence
  • Emotional disturbance

Middle Cerebral Artery (MCA)

  • Aphasia (dominant hemisphere)
  • Hemineglect (non-dominant hemisphere)
  • Contralateral somatosensory & motor deficit mostly in upper limbs and lower half of face than lower limbs
  • Conjugate eye deviation towards side of infract
  • Contralateral homonymous hemianopia without macular sparing

Posterior Cerebral Artery (PCA)

  • Agnosia and alexia without agraphia (Dominant hemisphere)
  • Prosopagnosia (Non-dominant hemisphere)
  • Contralateral homonymous hemianopia with macular sparing

Anterior inferior cerebellar artery (AICA)

  • Ipsilateral deafness, facial motor/sensory loss, limb ataxia
  • Decreased pain/temperature in contralateral body

Posterior inferior cerebellar artery (PICA)

  • Ipsilateral palatal weakness, limb ataxia
  • Wallenberg syndrome
  • Decreased pain/temperature in contralateral body

Vertebrobasilar system lesion (brainstem)

  • Contralateral hemiplegia & ipsilateral cranial nerve abnormalities (Crossed signs)
  • Possible ataxia

The National Institutes of Health Stroke Scale (NIHSS) is one of the most studied and validated scales in clinical practice that should be used to provide a structured and quantifiable neurologic examination [5,11,12,16]. It includes 11 items (Table 5) and can be done in less than 10 minutes. The scale can quantify neurologic deficits and provide information about patient outcomes [17]. Facial paresis, arm weakness, and abnormal speech on the NIHSS are the most predictive findings for acute ischemic stroke [18].

Table 5. Snapshot of the National Institute of Health Stroke Scale (NIHSS) [5,19]

Instructions

Scale Definition

1a. Level of consciousness (LOC) 

0 = Alert

1 = Drowsy- arousable by minor stimulation to obey, answer, or respond

2 = Obtunded; requires repeated stimulation to attend or is obtunded and requires strong or painful stimulation to make movements (not stereotyped).

3 = Unresponsive; Responds only with reflex motor or autonomic effects or unresponsive, flaccid, and areflexic.

1b. Orientation Questions (2)

0 = Answers both questions correctly.

1 = Answers one question correctly.

2 = Answers neither question correctly.

1c. Response to commands (2)

0 = Performs both tasks correctly

1 = Performs 1 task correctly

2 = Performs neither

2. Gaze

0 = Normal horizontal movements

1 = Partial gaze palsy

2 = Complete gaze palsy

3. Visual fields

0 = No visual field defect

1 = Partial hemianopia

2 = Complete hemianopia

3= Bilateral hemianopia

4. Facial movement

0 = Normal

1 = Minor facial weakness

2 = Partial facial weakness

3= Complete unilateral palsy

5. Motor function (Arm)

5a. Left arm

5b. Right arm

 

0 = No drift

1 = Drift before 10 s

2 = Falls before 10 s

3= No effort against gravity

4=No movement

6. Motor function (Leg)

6a. Left leg

6b. Right leg

 

0 = No drift

1 = Drift before 10 s

2 = Falls before 10 s

3= No effort against gravity

4=No movement

7. Limb ataxia

0 = No ataxia

1 = Ataxia in 1 limb

2 = Ataxia in 2 limbs

3= No effort against gravity

4=No movement

8. Sensory

0 = No sensory loss

1 = Mild sensory loss

2 = Severe sensory loss

9. Language

0 = Normal

1 = Mild aphasia

2 = Severe aphasia

3= Mute or global aphasia

10. Articulation

0 = Normal

1 = Mild dysarthria

2 = Severe dysarthria

11. Extinction or inattention

0 = Absent

1 = Mild loss (1 sensory modality lost)

2 = Severe loss (2 modalities lost)

Vital signs play a critical role in the evaluation and management of acute ischemic stroke and conditions that may mimic stroke. Temperature, in particular, is a key parameter, as abnormalities can influence neurological function and mimic or exacerbate stroke symptoms. Hyperthermia (elevated body temperature) is associated with worsened outcomes in stroke patients due to increased metabolic demand and potential exacerbation of ischemic injury. On the other hand, hypothermia (lowered body temperature) can also cause altered mental status, which may resemble stroke-like presentations. Monitoring and correcting these temperature abnormalities is essential to optimize neurological recovery and rule out underlying infections or systemic conditions. Additionally, blood pressure, heart rate, respiratory rate, and oxygen saturation must be carefully assessed, as significant deviations can indicate complications such as increased intracranial pressure, arrhythmias, or hypoxia, which can impact stroke presentation and management.

Alternative Diagnoses

The differential diagnosis for acute-onset focal neurologic deficits, such as those found in acute ischemic stroke, is broad, and it is important to have a framework to rule out other causes. The VIINDICATES mnemonic (Table 6) can be useful in grouping the most frequent and important causes of acute neurologic dysfunction [20].

Table 6. Non-exhaustive differential diagnosis of acute ischemic stroke [21]

Vascular

Hemorrhagic stroke, cerebral venous thrombosis, arteriovenous fistulas, aneurysms

Infectious

Meningitis, Encephalitis, Progressive multifocal leukoencephalopathy

Immune system dysfunction/autoimmune

Multiple Sclerosis, Bell palsy, Guillain-Barré syndrome, Anti-NMDA encephalitis

Neoplasm

Brain tumors, paraneoplastic syndromes, lung cancer

Drugs

Alcohol withdrawal, drug intoxication (opioids, barbiturates, etc.)

Cerebral/Neurologic

Transient ischemic attack (TIA), syncope, seizure, postictal paralysis, migraine aura

Trauma

Traumatic brain injury, Subdural hematoma, epidural hematoma, Brown-Séquard syndrome

Endocrine/Metabolic

Diabetic Ketoacidosis, hyponatremia, hypoglycemia

Social/Psychiatric

Conversion disorder, malingering

The clinician must pay close attention to the physical exam and medical history results that may favor one of these diagnoses over another to distinguish between them. Timing is critical and it is important to understand if the symptoms appeared suddenly or have been slowly brewing over time [12,16,21].

Acing Diagnostic Testing

When suspicion of acute ischemic stroke is high, time is of the essence due to the time limitations of thrombolytics or mechanical thrombectomy. Therefore, oxygen saturation, finger stick blood glucose, non-contrast head CT and angiography should be prioritized over all other tests as they are the only requirements before the administration of thrombolytics [5,11]. Oxygen saturation can help rule out hypoxia as a cause of neurological dysfunction [12,21]. Blood glucose is important as it can rule out hypoglycemia, DKA, or hyperosmolar hyperglycaemic state, which can all present like symptoms of stroke and can worsen outcomes with the administration of thrombolytics [22]. Neuroimaging is essential because it can help differentiate acute ischemic stroke from a hemorrhagic stroke, which has very different management. Neuroimaging can also rule out most other differential diagnoses discussed earlier when combined with physical history and exam. Loss of grey-white differentiation is an early CT finding in ischemic stroke, while increased density within the occluded vessel can represent a thrombus (Figure 1) [5,13,15,16,23].

Figure 1 - Non-contrast computed tomography (CT) with multiple planar reconstructions (MPR) revealed a hyperdense middle cerebral artery (MCA) sign in the left MCA (Picture A and B, arrow). Repeat CT after completion of the alteplase administration revealed resolution of the hyperdense MCA sign but the appearance of an M2 dot sign (Picture C and D, arrowhead). Angiography showed the occlusion of the left MCA M2 segment, corresponding to the M2 dot sign (Picture E, arrowhead) [23].jpg

Complete blood counts and coagulation studies should not delay the administration of thrombolytic therapy unless there is a high suspicion of coagulopathy or a history of the patient being on anticoagulating agents [5,12,16].

Electrocardiogram and cardiac markers such as troponin are also important to rule out cardiac causes. They may illuminate a source for emboli, such as atrial fibrillation, but this should not delay neuroimaging [5].

Other non-urgent lab tests that may be indicated depending on patient presentation include [5,10]:

Complete Metabolic Panel (CMP): Assesses electrolyte imbalances, renal function, and glucose levels, which are critical in stroke patients to rule out mimicking conditions (e.g., hypoglycemia) and to ensure safe administration of interventions like thrombolysis.

Blood Alcohol Level and Toxicology Screen: Helps identify substances that might contribute to altered mental status or stroke-like symptoms, such as intoxication or drug use, which can influence treatment decisions and prognosis.

Pregnancy Test in Women of Childbearing Age: Mandatory before imaging procedures involving radiation (e.g., CT) or medications (e.g., thrombolytics), as these might pose risks to a fetus.

Arterial Blood Gas (ABG): Assesses oxygenation, ventilation, and acid-base status. Useful in patients with suspected respiratory compromise or to evaluate hypoxia, which may exacerbate neurological deficits.

Chest Radiograph (CXR): Evaluates for underlying or concurrent conditions such as pneumonia, aspiration, or cardiac issues (e.g., heart failure) that could complicate stroke management.

Lumbar Puncture (LP): Performed if a hemorrhage is strongly suspected but not visible on a CT scan. Helps detect xanthochromia or elevated red blood cell count, which are indicative of subarachnoid hemorrhage.

Electroencephalogram (EEG): Recommended if seizures are suspected, as post-stroke seizures or seizure-like activity can mimic stroke symptoms or complicate recovery.

Urinalysis and Blood Cultures: Indicated in febrile patients to identify infections, such as urinary tract infections or sepsis, which might cause or exacerbate stroke-like presentations and impact recovery.

Blood Type and Cross-Match: Necessary if there is coagulopathy requiring reversal with fresh frozen plasma or if massive blood transfusion is anticipated in cases of hemorrhagic transformation.

MRI: Provides superior imaging of the brain compared to CT, identifying small or early infarcts and areas of ischemia. MRI is particularly valuable for stroke patients with ambiguous CT findings.

Risk Stratification

The presence of certain red flags, such as severe headache, papilledema, neck stiffness, loss of consciousness, or rapidly worsening neurological deficits, may indicate a worse outcome and the need for more aggressive management. These symptoms may indicate that the lesion has affected certain vital regions in the brain or there has been a conversion to hemorrhagic stroke [5,11]. Severe hypo/hyperglycemia (glucose < 50 mg/dL or > 400 mg/dL) or hypertension (> 185/110 mm Hg) also indicate a poor outcome as these need to be managed before reperfusion therapy can be utilized, which results in further neurologic insult [5]. The NIHSS score can be utilized to predict outcomes such as disability, recurrent stroke, or death. The higher the NIHSS score, the more severe the stroke and the worse the prognosis. In general, patients with an NIHSS score of 0-4 have a good prognosis, while those with a score of 20 or higher have a higher risk of death or severe disability [5,17,24].

Management

Stroke patients are treated as critically ill patients and require urgent management. This includes assessing and stabilizing the patient’s airway, breathing, and circulation (ABCs), conducting a thorough evaluation to determine whether thrombolytic therapy is appropriate, and addressing any underlying medical conditions, such as hypertension, that may complicate treatment [5,12,16].

Airway and breathing can be compromised due to damage to areas central to consciousness, breathing, or swallowing as listed in Table 7.

Table 7. Possible locations of lesions compromising the airway [25]

Levels of Consciousness

Breathing

Swallowing

Thalami

respiratory centers in the cortex, pons, and medulla

Medulla & brainstem connections

Limbic system

Pons

 

Reticular formation in the brainstem

Medulla

 

Damage to any of these areas requires securing the airway and maintaining breathing by positing the head of the bed to 30° to prevent aspiration. The specific approach will depend on the severity of the patient’s presentation [25].  Assessing the level of consciousness can provide valuable information to guide judgment. If a patient is awake, alert, and responsive, then they may be able to secure their airway and provide adequate ventilation on their own. Respiratory rate and effort should be assessed by looking for the rate of breathing, use of accessory muscles, or increased work of breathing. Airway patency can be determined by looking for signs of obstruction, such as snoring or stridor [16]. If oxygen saturation is below 94%, supplemental oxygen should be provided. Oxygen support is not beneficial if saturation is above 94% [5]. It is important to note that the neurologic exam can be severely limited if the patient requires intubation. Therefore, the clinician should pick up on subtle signs since the interaction with the patient began that can clue the physician on the baseline status, such as language function or any asymmetric motor activity, before the patient is pharmacologically paralyzed to be intubated [10].

 

Once breathing is secured, the next step is to ensure circulation is not compromised. Patients presenting with acute ischemic stroke frequently will be hypertensive as this is the body’s natural response to reperfuse the ischemic regions [16]. However, it is also not uncommon for patients to present with hypotension and hypovolemia. Due to the time-sensitive nature of acute ischemic stroke, correcting blood pressure takes priority [5]. When a patient with acute ischemic stroke has severe hypertension (systolic blood pressure >220 mmHg or diastolic blood pressure >120 mmHg), it may be necessary to lower their blood pressure to a safe level as administration of thrombolytics at this level can lead to hemorrhage [15]. Medications such as intravenous labetalol, nicardipine, or clevidipine can be used for cautious reduction (Table 8).

Table 8. Drug dosing for treatment of arterial hypertension in acute ischemic stroke [5]

Labetalol

10–20 mg IV over 1–2 min, may repeat 1 time

Nicardipine

5 mg/h IV, titrate up by 2.5 mg/h every 5–15 min, maximum 15 mg/h; when desired BP reached, adjust to maintain proper BP limits

Clevidipine

1–2 mg/h IV, titrate by doubling the dose every 2–5 min until desired BP reached; maximum 21 mg/h

In randomized controlled trials (RCTs) of intravenous (IV) thrombolytics, patients were required to have a systolic blood pressure <185 mm Hg and a diastolic blood pressure <110 mm Hg before treatment and <180/105 mm Hg for the first 24 hours after treatment [5]. Therefore, it is reasonable to aim for the blood pressure targets used in the RCTs of IV alteplase. In contrast, for patients with mild to moderate hypertension, it is generally advised to withhold blood pressure-lowering medications in the first few hours after the onset of stroke. This is because the rapid reduction in blood pressure can decrease cerebral perfusion and worsen ischemic injury [7].

Following stabilization, neuroimaging and lab tests discussed in the diagnostic test are prioritized to further aid in management. Figure 2 summarizes the steps discussed so far.

Figure 2 - Initial Management of Stroke

Once the diagnosis of acute ischemic stroke has been established, the next step is to figure out if the patient is eligible for thrombolysis (Table 9).

Table 9. Inclusion and exclusion criteria for rtTPA [5,15]

Inclusion Criteria

  • patients ≥ 18 years old
  • symptom onset within 4.5 hours
  • meets clinical criteria e.g. ischemic stroke

Strict Exclusion Criteria

  • History of ischemic stroke, severe head trauma, intracranial surgery, and intracanal hemorrhage within the last 3 months
  • Blood pressure > 185/110 mm Hg
  • Platelets <100,000/mm3 or glucose <50 mg/dL
  • Anticoagulant use with INR > 1.7, PT >15 sec, or increase in active PTT
  • Active intracranial bleeding
  • Intracranial neoplasm

Intravenous recombinant tissue plasminogen activator (tPA) agents such as Alteplase or Tenecteplase should be used (Table 10) [5,15,26]. Mechanical thrombectomy may be indicated if a large artery occlusion (LVO) is causing a stroke, and it has been less than 24 hours since symptom onset. The eligibility for mechanical thrombectomy and thrombolysis in individuals with ischemic stroke is assessed separately.  Patients may be qualified for one, both, or neither of these treatments depending on the timing of their appearance (4.5 hours for thrombolysis, 24 hours for mechanical thrombectomy) [5,27]. However, if the patient is not eligible for either chemical thrombolysis or mechanical thrombectomy, immediate dual antiplatelet therapy (DAPT) with agents such as aspirin and clopidogrel should begin [5,28]. In the acute management of ischemic stroke (even if caused by atrial fibrillation [AF]), parenteral anticoagulation (e.g., intravenous heparin) should not be used because it increases the chance of hemorrhagic conversion [5,11].

Table 10. Dosing for rtTPA in the management of acute ischemic stroke [5]

Alteplase

IV 0.9 mg/kg over 60 minutes (max. dose 90 mg), with an initial 10% of dose given as a bolus over 1 minute

Tenecteplase

IV 0.25 mg/kg as a bolus, max. dose 25 mg

Aspirin

160 to 325 mg loading dose, followed by 50 to 100 mg daily (for 21 days)

Clopidogrel

300 to 600 mg loading dose, followed by 75 mg daily (for 21 days)

Special Patient Groups

When a patient presents with symptoms of acute ischemic stroke, clinical considerations differ based on age and special patient groups. Pediatric patients may experience stroke due to congenital heart disease, sickle cell disease, or infections. Symptoms may be less obvious and include seizures, vomiting, and headaches [29]. Diagnosis of stroke in pregnant patients is challenging, and thrombolytic agents may increase the risk of hemorrhage in both the mother and fetus [30]. Special patient groups, including those with sickle cell anemia or undergoing surgery, may also be at increased risk of stroke and require careful management. Treatment options should be carefully considered in these patient groups with an understanding of the potential risks and benefits [31].

When To Admit This Patient

Patients with acute ischemic stroke are generally admitted to the hospital for further investigations and treatment [5]. Early discharge may be considered for patients with mild symptoms, no significant comorbidities, and a low risk of complications, provided they have a reliable caregiver and access to appropriate follow-up care. Severe or progressive symptoms, significant comorbidities, or high risk of complications require admission to a stroke unit or critical care unit [5,16]. Discharge decisions should be based on a careful assessment of clinical status, risk of complications, and social circumstances. Clear instructions on medication, follow-up care, and stroke prevention strategies should be provided, along with safety-netting arrangements for timely and appropriate care if complications or worsening symptoms occur after discharge [5,32].

Revisiting Your Patient

Based on the initial assessment, Mrs. A is presenting with symptoms that are consistent with a stroke. The patient’s daughter reported that the symptoms started suddenly, and upon examination, Mrs. A has right-sided facial droop, right arm drift, and slurred speech. Her past medical history is significant for hypertension, hyperlipidemia, and type 2 diabetes mellitus. The NIHSS score of 8 indicates a moderate to severe stroke. Immediate management includes stabilizing the patient’s vital signs and providing supportive care, including oxygen and intravenous access. Given the suspicion of a stroke, a non-contrast head CT scan should be obtained to rule out a hemorrhagic stroke. Mrs. A should be considered for thrombolytic therapy with alteplase as she is within the appropriate time window, and there are no contraindications.

Authors

Picture of Hassan KHURAM BS, MS

Hassan KHURAM BS, MS

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

Picture of Parker MADDOX BA, MS

Parker MADDOX BA, MS

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

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

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

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

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References

  1. Feigin VL, Brainin M, Norrving B, et al. World Stroke Organization (WSO): Global Stroke Fact Sheet 2022. Int J Stroke. 2022;17(1):18-29. doi:10.1177/17474930211065917
  2. Heart Disease and Stroke Statistics—2022 Update: A Report From the American Heart Association | Circulation. Accessed March 27, 2023. https://www.ahajournals.org/doi/10.1161/CIR.0000000000001052
  3. Saver JL. Time Is Brain—Quantified. Stroke. 2006;37(1):263-266. doi:10.1161/01.STR.0000196957.55928.ab
  4. Saini V, Guada L, Yavagal DR. Global Epidemiology of Stroke and Access to Acute Ischemic Stroke Interventions. Neurology. 2021;97(20 Suppl 2):S6-S16. doi:10.1212/WNL.0000000000012781
  5. Powers WJ, Rabinstein AA, Ackerson T, et al. Guidelines for the Early Management of Patients With Acute Ischemic Stroke: 2019 Update to the 2018 Guidelines for the Early Management of Acute Ischemic Stroke: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke. 2019;50(12). doi:10.1161/STR.0000000000000211
  6. Boehme AK, Esenwa C, Elkind MSV. Stroke Risk Factors, Genetics, and Prevention. Circ Res. 2017;120(3):472-495. doi:10.1161/CIRCRESAHA.116.308398
  7. Kuriakose D, Xiao Z. Pathophysiology and Treatment of Stroke: Present Status and Future Perspectives. Int J Mol Sci. 2020;21(20):7609. doi:10.3390/ijms21207609
  8. Ambrose JA, Barua RS. The pathophysiology of cigarette smoking and cardiovascular disease: an update. J Am Coll Cardiol. 2004;43(10):1731-1737. doi:10.1016/j.jacc.2003.12.047
  9. Head T, Daunert S, Goldschmidt-Clermont PJ. The Aging Risk and Atherosclerosis: A Fresh Look at Arterial Homeostasis. Front Genet. 2017;8:216. doi:10.3389/fgene.2017.00216
  10. Goldstein JN, Greer DM. Rapid focused neurological assessment in the emergency department and ICU. Emerg Med Clin North Am. 2009;27(1):1-16, vii. doi:10.1016/j.emc.2008.07.002
  11. Herpich F, Rincon F. Management of Acute Ischemic Stroke. Crit Care Med. 2020;48(11):1654-1663. doi:10.1097/CCM.0000000000004597
  12. Chugh C. Acute Ischemic Stroke: Management Approach. Indian J Crit Care Med Peer-Rev Off Publ Indian Soc Crit Care Med. 2019;23(Suppl 2):S140-S146. doi:10.5005/jp-journals-10071-23192
  13. Balami JS, Chen RL, Buchan AM. Stroke syndromes and clinical management. QJM Int J Med. 2013;106(7):607-615. doi:10.1093/qjmed/hct057
  14. Caplan LR, Gorelick PB, Hier DB. Race, sex and occlusive cerebrovascular disease: a review. Stroke. 1986;17(4):648-655. doi:10.1161/01.str.17.4.648
  15. Wardlaw JM, Murray V, Berge E, del Zoppo GJ. Thrombolysis for acute ischaemic stroke. Cochrane Database Syst Rev. 2014;2014(7):CD000213. doi:10.1002/14651858.CD000213.pub3
  16. Bevers MB, Kimberly WT. Critical Care Management of Acute Ischemic Stroke. Curr Treat Options Cardiovasc Med. 2017;19(6):41. doi:10.1007/s11936-017-0542-6
  17. Fonarow GC, Saver JL, Smith EE, et al. Relationship of national institutes of health stroke scale to 30-day mortality in medicare beneficiaries with acute ischemic stroke. J Am Heart Assoc. 2012;1(1):42-50. doi:10.1161/JAHA.111.000034
  18. Goldstein LB, Simel DL. Is this patient having a stroke? JAMA. 2005;293(19):2391-2402. doi:10.1001/jama.293.19.2391
  19. NINDS Know Stroke Campaign – NIH Stroke Scale. Accessed April 1, 2023. https://www.stroke.nih.gov/resources/scale.htm
  20. General Principles. UW Radiology. Accessed April 1, 2023. https://rad.washington.edu/about-us/academic-sections/musculoskeletal-radiology/teaching-materials/online-musculoskeletal-radiology-book/general-principles/
  21. Vilela P. Acute stroke differential diagnosis: Stroke mimics. Eur J Radiol. 2017;96:133-144. doi:10.1016/j.ejrad.2017.05.008
  22. Hafez S, Coucha M, Bruno A, Fagan SC, Ergul A. Hyperglycemia, Acute Ischemic Stroke and Thrombolytic Therapy. Transl Stroke Res. 2014;5(4):442-453. doi:10.1007/s12975-014-0336-z
  23. Ohno Y, Oomura M, Sakurai K, Matsukawa N. Hyperdense Vessel Signs Showing Migration of a Thrombus. Intern Med. 2017;56(4):465-466.
  24. Wityk RJ, Pessin MS, Kaplan RF, Caplan LR. Serial assessment of acute stroke using the NIH Stroke Scale. Stroke. 1994;25(2):362-365. doi:10.1161/01.str.25.2.362
  25. Bösel J. Use and Timing of Tracheostomy After Severe Stroke. Stroke. 2017;48(9):2638-2643. doi:10.1161/STROKEAHA.117.017794
  26. Evidence that Tenecteplase Is Noninferior to Alteplase for Acute Ischemic Stroke | Stroke. Accessed April 2, 2023. https://www.ahajournals.org/doi/10.1161/STROKEAHA.119.025080
  27. Jadhav AP, Desai SM, Jovin TG. Indications for Mechanical Thrombectomy for Acute Ischemic Stroke: Current Guidelines and Beyond. Neurology. 2021;97(20 Supplement 2):S126-S136. doi:10.1212/WNL.0000000000012801
  28. Antiplatelet Therapy in Ischemic Stroke and Transient Ischemic Attack | Stroke. Accessed April 2, 2023. https://www.ahajournals.org/doi/full/10.1161/STROKEAHA.118.023954
  29. Ferriero DM, Fullerton HJ, Bernard TJ, et al. Management of Stroke in Neonates and Children: A Scientific Statement From the American Heart Association/American Stroke Association. Stroke. 2019;50(3):e51-e96. doi:10.1161/STR.0000000000000183
  30. Cauldwell M, Rudd A, Nelson-Piercy C. Management of stroke and pregnancy. Eur Stroke J. 2018;3(3):227-236. doi:10.1177/2396987318769547
  31. Talahma M, Strbian D, Sundararajan S. Sickle Cell Disease and Stroke. Stroke. 2014;45(6):e98-e100. doi:10.1161/STROKEAHA.114.005144
  32. Hong I, Karmarkar A, Chan W, et al. Discharge Patterns for Ischemic and Hemorrhagic Stroke Patients Going from Acute Care Hospitals to Inpatient and Skilled Nursing Rehabilitation. Am J Phys Med Rehabil. 2018;97(9):636-645. doi:10.1097/PHM.0000000000000932

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.

Epilepsy and Status Epilepticus (2024)

~ iEM Education Project Team ~ Leave a comment

by Rand Redwan Al Sari & Imad Khojah

Authors
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You have a new patient!

A 22-year-old woman is brought to the ER because of violent, jerky movements of her limbs that started 30 minutes ago. Her husband reports that the patient has a history of epilepsy. She is unresponsive. Her examination reveals tonic-clonic episodes and blood in her mouth. How would you manage this case? What are the initial steps you would take? What actions are needed to stop the seizure?

a-photo-of-a-22-year-old-female-patient-with-seizure (the image was produced by using ideogram 2.0)

What do you need to know?

Epidemiology and Importance

Epilepsy is one of the most common neurological diseases that can present to the emergency department [1]. It affects about 50 million people around the world, with an incidence of approximately 50.4 to 81.7 per 100,000 per year [1]. Epilepsy refers to having a lower seizure threshold than normal due to genetic, pathological, or unknown causes [2]. It is characterized by recurrent unprovoked seizures that present with motor, sensory, autonomic, or cognitive function alterations [2]. Previously diagnosed patients can present to the ED with breakthrough seizures due to factors like changes in the anti-seizure regimen or noncompliance with medication [2]. Other factors like sleep deprivation, stress, and flashing lights can also precipitate breakthrough seizures [2].

Prolonged or repetitive uncontrollable seizures are termed status epilepticus [2,3]. This emergency requires prompt treatment to prevent neuronal injury, severe disability, coma, or death [3]. The overall case fatality rates can reach up to 15% [2].

Pathophysiology

Neurons are normally stabilized by a balance between excitatory and inhibitory neurotransmitters [2]. A disruption of this balance leads to abnormal electrical discharge [2]. This discharge can propagate to nearby areas in the brain, which is evident clinically by the stepwise spread of the seizure (known as Jacksonian March) [2, 4]. Loss of consciousness in some cases is explained by the widespread involvement of large areas of the brain [2]. Many drugs used to restore this balance work by enhancing inhibitory activity through targeting GABAA subtype receptors [2]. Prolongation of the seizure leads to sequestration of GABAA receptors and upregulation of excitatory receptors; therefore, patients become unresponsive to medication [2, 5]. This explains the importance of timely treatment through early seizure control to prevent morbidity and mortality in patients with status epilepticus [2,3].

Medical History

A common scenario presenting to the ER is a patient complaining of a seizure-like episode with a sudden loss of consciousness and motor activity involvement [6]. However, various other presentations of seizures and other differential diagnoses with similar complaints should not be neglected. If the patient presents with status epilepticus, timely management, depending on the seizure type, is urgently needed (see management) [2].

Through history and examination, distinguishing a seizure from other acute medical conditions is important. An accurate diagnosis has crucial, direct consequences for activity restriction and therapy planning. Paying attention to features, especially at the onset, can help in identifying the seizure type for therapeutic implications and facilitate communication between physicians. Semiology at onset is important to classify seizures as focal, focal with impaired awareness (complex seizures), generalized, or unknown [7]. Further classification divides motor and non-motor seizures based on the descriptive assessment of the first symptom, which can vary widely according to the area of the brain affected [2].

The main aim of history-taking is to identify seizures from other similar conditions, classify them, identify triggers of new seizures, and detect a cause for a decreased seizure threshold in a patient previously diagnosed with epilepsy [8].

It is important for any patient with seizures to consider critical causes such as eclampsia, toxic ingestion, hypoglycemia, electrolyte imbalance, and increased intracranial pressure [9]. Emergent diagnoses, such as infection, acute brain injury, and serious mimics of seizure activity, must be identified and treated as soon as possible [2].

Initial history approach to a patient with suspected seizure [2] is a systematic evaluation, starting with the assessment of whether the event is likely to be a seizure, followed by differentiation of first-time versus recurrent seizures, and identifying factors that may trigger or reduce seizure thresholds [10].

Algorithmic Approach in Seizure History [2]

Determining Likelihood of a Seizure

The process begins by evaluating whether the event could be a seizure. Key indicators include:

  • Aura: A subjective sensation preceding the seizure.
  • Abrupt onset: Sudden occurrence of the event.
  • Non-suppressible limb shaking: Movements that are not voluntary or suppressible.
  • Postictal state: A transient neurological state after the event, characterized by confusion or fatigue.
  • History of epilepsy: Previous diagnosis or known history can strongly support the likelihood.

If these features are absent, the clinician is prompted to consider alternative diagnoses, such as:

  • Syncope (fainting),
  • Stroke,
  • Complex migraine, or
  • Non-epileptic spells, which may mimic seizures but lack neurological underpinnings.

Differentiating First-Time Seizures

If the event is determined to likely be a seizure, the next step is assessing whether it is the patient’s first seizure. For first-time events, the focus shifts to identifying potential triggers, including:

  • Medications: Use of or withdrawal from drugs that may lower the seizure threshold.
  • Exposures: Environmental or toxicological factors.
  • Immunosuppression: Conditions that may predispose to infections affecting the brain.
  • History of head trauma: A common precipitant for seizures.
  • Pregnancy: Associated risks like eclampsia.

Characterization of the Seizure

If it is not a first-time seizure, further characterization of the event is essential. Key aspects include:

  • Onset: Understanding preceding events to identify immediate triggers and auras.
  • Duration: Length of the seizure episode.
  • Awareness: Assessing the patient’s level of consciousness during the seizure.
  • Automatisms: Involuntary, purposeless movements that occur during the seizure and can be observed by others.
  • Postictal state: The presence of transient neurological deficits following the seizure (absent in some types, such as absence seizures).

The clinician also verifies whether the current event is consistent with the patient’s previous seizure patterns.

Exploring Factors Reducing the Seizure Threshold

For patients with recurrent seizures, it is crucial to evaluate factors that might decrease the seizure threshold, including:

  • Non-compliance or changes to anti-seizure drug (ASD) regimens.
  • Illness or trauma: Physical or psychological stressors.
  • Drug or alcohol use: Acute intoxication or withdrawal.
  • Catamenial exacerbations: Hormonal influences in menstruating individuals.
  • Pregnancy: Increased risk of seizures due to physiological changes or complications.
  • Sleep deprivation: A well-documented precipitant of seizures.

This step ensures that modifiable triggers or exacerbating factors are identified and addressed.

Physical Examination

Physical examination is crucial for identifying etiologies and directing the management plan. During an active seizure, pay close attention to posture, motor activity, eye deviation, and nystagmus, observing asymmetries and focal findings [11]. Check if the clonic activity is suppressible by applying gentle pressure. Unlike insuppressible seizures, suppression suggests a different diagnosis, such as nonepileptic spells or movement disorders. Check for mydriasis in the eyes, which is commonly found during seizures, but its persistence afterward can indicate toxic exposure [2].

Vital signs should be measured after seizure activity has ceased. They are of high importance and may direct the physician to possible causes (e.g., fever suggests meningoencephalitis, tachycardia and hypertension suggest toxic sympathomimetic exposure, while hypertension and bradycardia can indicate herniation syndromes) [2].

Moreover, a general examination should aim to search for both findings and sequelae of the seizures. Physical findings such as nuchal rigidity, stigmata of substance abuse, and lymphadenopathy may be present. Potential sequelae of seizures should also be assessed [12]. Evaluation of soft tissue and skeletal trauma is important, as injuries are common. Check for head trauma, tongue injury, shoulder dislocation, bone fractures, or aspiration [2].

Finally, a complete neurological examination should be performed. Immediately following the seizure, hyperreflexia, focal motor deficit (Todd’s paralysis), and extensor plantar response (positive Babinski) can occur and are expected to generally resolve within an hour [13]. If Todd’s paralysis does not resolve quickly, it raises the suspicion of a focal structural deficit that caused the seizure (e.g., stroke). The persistence of altered consciousness or signs of ongoing subtle seizures, such as automatisms, abnormal eye movements, and facial myoclonus, suggests the persistence of the seizure and must not be missed (nonconvulsive seizures and status epilepticus) [2].

Alternative Diagnoses

Although no single clinical finding or diagnostic modality is 100% confirmatory of the diagnosis of seizures [14, 15], understanding the circumstances of the event and the factors surrounding it can help rule out or confirm diagnoses with similar presentations [2].

Findings that make the diagnosis of seizures more probable include postictal disorientation and amnesia, cyanosis during the event, lateral tongue biting, non-suppressible limb shaking, and dystonic posturing [2, 15].

If the patient experienced diaphoresis, palpitations, nausea, and vomiting before the seizure, it may suggest transient cerebral ischemia due to arrhythmias [2].

The presence of motor activity, commonly including a tonic extension of the trunk or myoclonic jerks of the extremities associated with bradycardia, raises the suspicion of convulsive syncope [16]. Once cerebral perfusion is restored, convulsions stop without any postictal period [2].

The diagnosis of migraine can sometimes be misleading due to the presence of a preceding aura that might be confused with nonconvulsive seizures (e.g., the positive visual phenomenon in occipital seizures) [17]. Unlike occipital seizures, migraines have a peak preceded by gradual evolution and followed by gradual resolution. Moreover, patients typically have a positive history of migraines with a similar presentation [2].

Nonepileptic spells or psychogenic seizures mimic status epilepticus in their presentation [18]. Due to the prolonged duration of the spells (five minutes or more, and sometimes exceeding 20 minutes), patients commonly receive high doses of benzodiazepines and need to be monitored for any respiratory compromise. Findings consistent with this diagnosis include a stop-and-go pattern of the convulsions, horizontal head shaking, forward pelvic thrusting, asynchronous bilateral convulsions with eyes closed, a short postictal period despite the long duration of spells, avoidance of noxious stimuli, and preserved recollection of events. Furthermore, laboratory testing lacks reactive leukocytosis and lactic acidosis, which are present in nearly all cases of prolonged generalized convulsive seizures or status epilepticus [2, 19].

Acing Diagnostic Testing

Due to the challenges of diagnosing a seizure, seeking diagnostic testing is of high value. Laboratory studies, radiology, and other special procedures frequently provide important elements in patient assessment [20]. Although some cases require extensive metabolic testing, it is not indicated for cases with an unremarkable history and normal examination findings. Serum glucose levels should be measured in all cases, as hypoglycemia is a common cause of provoked seizures [21]. It is also important to note that hypoglycemia could result from prolonged seizures. If correcting the glucose level does not stop a seizure, an alternate diagnosis should be evaluated. Lactic acid and creatinine kinase should also be measured in cases of prolonged seizures to assess for acute metabolic acidosis and rhabdomyolysis, respectively [22]. A low level of lactic acid during a prolonged convulsive episode makes a seizure less likely (nonepileptic convulsions) [2].

On the other hand, the presence of advanced age, comorbidities, abnormal examination findings, or an ill appearance demands comprehensive metabolic testing. Such testing includes serum glucose, creatinine kinase, lactic acid, electrolytes, complete blood count, urea nitrogen, creatinine, AST, ALT, anti-seizure drug levels, pregnancy tests, and drug-of-abuse screening. Checking for electrolyte derangements is important, as these can trigger seizures (e.g., hyponatremia, hypocalcemia, and hypomagnesemia) [23]. Patients with a low bicarbonate level should undergo blood gas analysis. An anion gap metabolic acidosis resulting from lactic acidosis is expected to decline within the first hour after the convulsive seizure stops unless another cause is present. Liver enzymes are tested to check for liver-mediated metabolic abnormalities that can impact therapeutic decisions [2].

Furthermore, patients on antiseizure medication should have their levels checked to confirm compliance. Some drugs are known to be epileptogenic, and it may be necessary to test their levels as well. Drug-of-abuse screening can also be considered in patients presenting with first-time seizures, despite the fact that such testing cannot prove causation or change outcomes [2, 24].

Urgent neuroimaging is indicated for most cases of a first-time seizure, whereas patients with epilepsy who have returned to baseline do not require one. Prompt neuroimaging and CT consideration in the ER is indicated for patients with coma, focal neurological deficits, immunocompromised states, advanced age, anticoagulation use, malignancy, previous intracranial hemorrhage, severe thunderclap headache, status epilepticus, neurocutaneous syndromes, or suspected trauma [25]. Computed tomography (CT) is widely available, but MRI and CT perfusion can provide additional information. If an infection is suspected, lumbar puncture is indicated [2].

Electroencephalography (EEG) is useful for diagnosing nonconvulsive seizures, epilepsy, nonepileptic spells, and status epilepticus [26]. EEG can guide therapy and monitor the treatment of refractory cases. Although it is not cost-effective, it is a high-yield modality for cases with an unclear diagnosis [2].

Lastly, ECG monitoring might benefit patients with preceding or ongoing cardiac symptoms. It can provide early clues in cases of drug toxicity and help understand the etiology of the seizure [2, 27].

Risk Stratification

The presentation and findings of a seizure case can provide clues as to whether this case has any red flags that demand urgent care. History and examination findings such as immunocompromisation, the presence of a thunderclap headache, sudden neurological deficit, status epilepticus presentation, head trauma, persistent altered consciousness, and concurrent infection can indicate a worse outcome [10]. Such patients require extensive investigations and prompt treatment to minimize morbidity and mortality due to the cause of the seizure or as a consequence of the seizures themselves [28]. Critical care for these patient groups is essential to reduce complications such as infection-related issues, irreversible intracranial structural disease, refractory status epilepticus, hemodynamic compromise, and death [2].

The risks of experiencing a secondary seizure following the current presentation may change the management plan to include secondary seizure prophylaxis. Risk stratification, weighing the chances of recurrence (higher in patients with previous brain insult, abnormal EEG, brain imaging abnormalities, and the presence of nocturnal seizures) against the risks of adverse effects from antiseizure medication, should be conducted in collaboration with a consulting neurologist [2].

Management

The initial priorities in managing unstable patients are to recognize and treat hypoxia, hypotension, and hypoglycemia, and to initiate pharmacologic treatment when needed [2, 28, 29].

Initial stabilization of patients with active seizures presenting to the ER includes the following [2, 28, 29]:

  • Assess airway, breathing, and circulation: Do not use nasopharyngeal airway devices during the seizure, as they can cause injury and increase the risk of aspiration.
  • Pulse oximetry.
  • Electrocardiogram (ECG).
  • Finger stick: If the glucose level is less than 60 mg/dL, administer IV dextrose.
  • Aspiration precaution: Place the patient in the lateral decubitus position.
  • Abortive treatment: Administer if the seizure lasts more than 5 minutes or in the case of hemodynamic compromise.

First-line therapy [2, 28, 29]

The first-line pharmacological therapies for managing epilepsy, include three benzodiazepine agents: diazepam, lorazepam, and midazolam. These agents are commonly used for their rapid onset and efficacy in controlling seizures, especially status epilepticus. The table includes critical details on dosing, frequency, maximum permissible dose, pregnancy category, and specific cautions.

  1. Diazepam
  • Dose per kilogram: 0.15-0.2 mg/kg intravenously (IV).
  • Frequency: Administered every 5 minutes as needed.
  • Maximum Dose: Limited to 10 mg per individual dose and a cumulative total of 30 mg across all doses.
  • Pregnancy Category: D (indicating a potential risk to the fetus, but benefits may outweigh risks in life-threatening situations).
  • Cautions/Comments:
    • Continuous monitoring of respiration is essential due to the risk of respiratory depression, a common side effect of benzodiazepines.
  1. Lorazepam
  • Dose per kilogram: 0.1 mg/kg intravenously (IV).
  • Frequency: Administered every 5 minutes as necessary.
  • Maximum Dose: 4 mg per dose, with a cumulative maximum of 12 mg across all doses.
  • Pregnancy Category: D.
  • Cautions/Comments:
    • Similar to diazepam, respiratory monitoring is mandatory.
    • Intramuscular (IM) administration is contraindicated for lorazepam, likely due to inconsistent absorption or slower onset compared to IV administration.
  1. Midazolam
  • Dose per kilogram: 0.2 mg/kg, administered via multiple routes including IV, intramuscular (IM), or intranasal (IN).
  • Frequency: Doses can be repeated every 5 minutes as needed.
  • Maximum Dose: 10 mg per individual dose.
  • Pregnancy Category: D.
  • Cautions/Comments:
    • Respiratory monitoring is critical due to the sedative effects of midazolam.
    • The half-life of midazolam is approximately 7 hours, making it a relatively short-acting agent compared to others, which can influence its clinical use depending on seizure recurrence risk.

All three agents are effective for rapid seizure control but share common risks, including respiratory depression, necessitating vigilant monitoring, particularly in critical care or emergency settings. Their classification in pregnancy category D highlights the need for careful consideration of maternal and fetal risks versus benefits. Midazolam offers more flexibility in administration routes, making it a practical choice in situations where IV access is not readily available.

If the seizure stops, coordinate a disposition plan and consider non-convulsive status epilepticus in patients who do not return to baseline. However, if the seizure does not stop, ensure adequate dosing of first-line therapy, then proceed to second-line therapy, and finally to third-line therapy, one step at a time [2, 28, 29].

Second-line therapy [2, 28, 29]

The second-line treatment options for epilepsy, include on a variety of antiepileptic drugs. These agents are typically used when first-line benzodiazepines are insufficient to control seizures. The table details dosing, frequency, maximum permissible doses, pregnancy categories, and relevant cautions for clinical use.

  1. Levetiracetam
  • Dose per kilogram: 40-60 mg/kg administered intravenously (IV).
  • Frequency: Administered once over a 10-minute period.
  • Maximum Dose: 4500 mg.
  • Pregnancy Category: C (indicating that risks cannot be ruled out, but the drug may be used if benefits outweigh potential risks).
  • Cautions/Comments:
    • Requires renal clearance, so dose adjustments may be necessary in patients with renal impairment.
  1. Fosphenytoin
  • Dose per kilogram: 10-20 mg PE/kg (phenytoin equivalents) given IV or intramuscularly (IM).
  • Frequency: Additional 5 mg PE/kg can be administered after 10 minutes if needed.
  • Maximum Dose: 150 mg PE/kg.
  • Pregnancy Category: D (associated with risk but can be used in life-threatening situations).
  • Cautions/Comments:
    • Can cause hypotension and dysrhythmias, requiring cardiac monitoring during administration.
  1. Lacosamide
  • Dose per kilogram: 200-400 mg IV.
  • Frequency: An additional 5 mg/kg can be administered if necessary.
  • Maximum Dose: 250 mg.
  • Pregnancy Category: C.
  • Cautions/Comments:
    • Can cause arrhythmias.
    • Renal clearance is required, so adjustments are needed for patients with renal insufficiency.
  1. Phenobarbital
  • Dose per kilogram: 15-20 mg/kg IV.
  • Frequency: Additional 5-10 mg/kg can be given as needed.
  • Maximum Dose: Not explicitly mentioned but calculated based on repeated doses.
  • Pregnancy Category: D.
  • Cautions/Comments:
    • Monitor respiration closely due to the sedative and respiratory depressant effects.
    • A strong P450 enzyme inducer, which can affect the metabolism of other drugs.
  1. Phenytoin
  • Dose per kilogram: 15-20 mg/kg IV.
  • Frequency: Additional 5-10 mg/kg can be administered if necessary.
  • Maximum Dose: 30 mg/kg.
  • Pregnancy Category: D.
  • Cautions/Comments:
    • Risk of hypotension and dysrhythmias during administration, necessitating monitoring.
    • A strong P450 enzyme inducer, which impacts the metabolism of other medications.
  1. Valproic Acid
  • Dose per kilogram: 20-40 mg/kg IV.
  • Frequency: Additional doses of 20 mg/kg can be administered if necessary.
  • Maximum Dose: 3000 mg.
  • Pregnancy Category: D.
  • Cautions/Comments:
    • Strong P450 enzyme inducer.
    • May cause hepatotoxicity and platelet dysfunction, warranting caution in patients with liver disease or coagulopathy.

The second-line agents are reserved for scenarios where first-line therapy fails to achieve seizure control. Each agent has specific risks and monitoring requirements. For example:

  • Levetiracetam and lacosamide are generally well-tolerated but require dose adjustments in renal impairment.
  • Phenobarbital, phenytoin, and valproic acid necessitate respiratory and hepatic monitoring due to their systemic side effects.
  • Fosphenytoin and phenytoin require cardiac monitoring due to their potential to induce arrhythmias.

The choice of agent depends on the patient’s clinical status, underlying conditions, and the safety profile of the drug.

Third-line therapy [2, 28, 29]

The third-line therapy agents for managing refractory epilepsy, particularly in patients requiring intubation, mechanical ventilation, and hemodynamic support are administered in critical care settings to control seizures when first- and second-line therapies fail. Each drug is described with its dosing regimen, frequency, maximum dose, pregnancy category, and significant precautions.

  1. Ketamine
  • Dose per kilogram:
    • Loading dose: 1.5 mg/kg intravenously (IV).
    • Maintenance dose: 0.5 mg/kg every 3-5 minutes as needed.
  • Maximum Dose: Not explicitly stated, but administered as required to control seizures.
  • Pregnancy Category: N (Not classified).
  • Cautions/Comments:
    • Ketamine acts as an NMDA antagonist, a unique mechanism among anticonvulsants.
    • Hypotension is a potential side effect, necessitating blood pressure monitoring.
  1. Midazolam
  • Dose per kilogram:
    • Loading dose: 0.2 mg/kg IV.
    • Maintenance dose: 0.2-0.4 mg/kg every 3-5 minutes.
  • Maximum Dose: 2 mg/kg for the loading dose.
  • Pregnancy Category: D (Risk to the fetus exists, but use may be justified in emergencies).
  • Cautions/Comments:
    • Midazolam may cause hypotension and requires continuous hemodynamic monitoring.
  1. Pentobarbital
  • Dose per kilogram:
    • Loading dose: 5-15 mg/kg IV.
    • Additional doses of 5-10 mg/kg may be given if required.
  • Maximum Dose: 25 mg/kg for the loading dose.
  • Pregnancy Category: D.
  • Cautions/Comments:
    • Pentobarbital has a long half-life (22 hours), which makes it effective for sustained seizure control but may prolong sedation.
    • It carries significant risks, including hypotension, ileus, myocardial suppression, immunosuppression, and thrombocytopenia, requiring vigilant monitoring in an intensive care setting.
  1. Propofol Infusion
  • Dose per kilogram:
    • Loading dose: 1-2 mg/kg IV.
    • Maintenance dose: 0.5-2 mg/kg every 3-5 minutes as needed.
  • Maximum Dose: 10 mg/kg for the loading dose.
  • Pregnancy Category: B (Lower risk, but use must be cautious).
  • Cautions/Comments:
    • Propofol has a short half-life (0.6 hours), allowing for rapid onset and recovery.
    • Side effects include hypotension, respiratory depression, hypertriglyceridemia, pancreatitis, and the rare but potentially fatal propofol infusion syndrome. Close monitoring of triglycerides and cardiac function is necessary.

Third-line therapies are used in severe, refractory cases of epilepsy where intubation, ventilation, and hemodynamic support are required. These drugs induce deep sedation or anesthesia to suppress seizure activity effectively. Key considerations for their use include:

  • Ketamine: Offers a unique mechanism (NMDA antagonism), useful in resistant cases.
  • Midazolam and pentobarbital: Provide effective sedation but require careful respiratory and cardiovascular monitoring due to risks of hypotension and prolonged sedation.
  • Propofol: Its short duration of action allows for precise titration, but metabolic side effects and infusion syndrome necessitate caution.

The choice of agent depends on the clinical scenario, patient stability, and institutional protocols. These medications are used alongside comprehensive critical care support to manage complications and optimize outcomes.

Special Patient Groups

Certain notes are important to remember regarding special patient groups. In cases of seizures during pregnancy, considering the diagnosis of eclampsia is a high priority. Magnesium is the drug of choice for acute eclamptic seizures [30]. If a pregnant patient was previously diagnosed with epilepsy, a lower seizure threshold may result due to noncompliance, adjusted regimens, sleep deprivation, nausea and vomiting, or increased drug clearance. When managing status epilepticus, the risks to the fetus from the seizure are higher than the risks from the medication; therefore, manage the patient as you would a nonpregnant individual [31]. In the case of a new, non-eclamptic seizure, a workup is indicated as previously mentioned [2].

When To Admit This Patient

The decision to admit or discharge should be individualized based on the underlying illness, recurrence risk, and need for maintenance pharmacotherapy [32]. Admission for observation alongside neurological consultation should be considered for patients with an uncertain diagnosis, a history of neurological disease or other comorbidities, or in situations where follow-up is unlikely. In contrast, patients can be discharged home with early referral to a neurologist if they have normal examination findings, no significant comorbidities, no known structural brain disease, did not require more than a single dose of benzodiazepines, and are expected to comply with follow-up instructions [2].

Discharge instructions should include guidance on car driving, potentially dangerous activities (e.g., swimming, cycling, climbing ladders), and information regarding any needed follow-up [2, 33].

Revisiting Your Patient

A 22-year-old woman with a previous history of epilepsy was brought to the ER due to generalized tonic-clonic insuppressible movements of her limbs that started 15 minutes ago.

You immediately assessed the airway, breathing, and circulation and placed the patient in the lateral decubitus position to prevent aspiration, as she had a tongue injury. Blood sugar was measured using a finger stick, ruling out hypoglycemia. Lorazepam was then administered as abortive treatment.

You began taking a history from her husband. They were having lunch together when his wife suddenly started seizing, and he was unable to stop it. She had not regained consciousness since then. He mentioned that she had been inconsistent with her antiepileptic medication because she wanted to get pregnant and had read online about potential harms of the medications on a growing baby.

Her lactic acid level was high, her pregnancy test was negative, and the rest of her laboratory findings were within normal limits.

The patient was diagnosed with status epilepticus, a medical emergency requiring urgent management. The ABC approach was performed to ensure the patient’s safety, followed by the administration of benzodiazepines. If first-line therapy fails, second- and third-line therapies should be administered sequentially. Inconsistency with antiepileptic medication highlights the need for patient education and further discussion regarding her concerns and available treatment options.

Authors

Picture of Rand Redwan Al Sari

Rand Redwan Al Sari

Dr Rand Al Sari is a dedicated General Physician practicing in Saudi Arabia. With a strong commitment to patient care, she is also actively engaged in medical research, staying at the forefront of healthcare advancements and integrating this knowledge into her clinical practice. Passionate about medical writing and journaling, Dr Al Sari reflects on her experiences to contribute meaningfully to the medical community, with a focus on evidence-based healthcare and improving patient outcomes.

Picture of Imad Khojah

Imad Khojah

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References

  1. Falco-Walter, Jessica. Epilepsy—definition, classification, pathophysiology, and epidemiology. Thieme Medical Publishers. 2020; 40(6): 617-623.
  2. John A. Ron M, et al. Rosen’s Emergency Medicine: Concepts and Clinical Practice. Philadelphia: Elsevier; c2014: 156-161, 1375-1385.
  3. Migdady I, Rosenthal ES, Cock HR. Management of status epilepticus: a narrative review. Wiley online library. 2022; 77:78-91.
  4. Extercatte J, de Haan GJ, Gaitatzis A. Teaching Video NeuroImages: Frontal opercular seizures with jacksonian march. Neurology. 2015;84(11):e83-e84. doi:10.1212/WNL.0000000000001363
  5. Casasola C, Montiel T, Calixto E, Brailowsky S. Hyperexcitability induced by GABA withdrawal facilitates hippocampal long-term potentiation. Neuroscience. 2004;126(1):163-171. doi:10.1016/j.neuroscience.2004.03.029
  6. Williams J, Doherty J, Di Blasi C, Mabarak D, Kennedy U, Doherty CP. Seizure care in the emergency department. Identifying and bridging the gaps. A study of care and outcomes from 644 seizure presentations. Epilepsy Behav. 2018;78:226-231. doi:10.1016/j.yebeh.2017.08.042
  7. Jan MM, Girvin JP. Seizure semiology: value in identifying seizure origin. Can J Neurol Sci. 2008;35(1):22-30. doi:10.1017/s0317167100007526
  8. Benton TJ, Narayanan D. Differentiating seizure and convulsive syncope: the importance of history taking. Postgrad Med. 2008;120(1):50-53. doi:10.3810/pgm.2008.04.1760
  9. Luft, Andreas. (2005). Critical Care Seizures Related to Illicit Drugs and Toxins. 10.1007/978-1-59259-841-0_13.
  10. Mantoan L, Kullmann DM. Evaluating first seizures in adults in primary care. Practitioner. 2011;255(1743):25-3.
  11. García-Pastor A, López-Esteban P, Peraita-Adrados R. Epileptic nystagmus: a case study video-EEG correlation. Epileptic Disord. 2002;4(1):23-28.
  12. Lee WL. Long-term sequelae of epilepsy. Ann Acad Med Singap. 1989;18(1):49-51.
  13. Xu SY, Li ZX, Wu XW, Li L, Li CX. Frequency and Pathophysiology of Post-Seizure Todd’s Paralysis. Med Sci Monit. 2020;26:e920751. Published 2020 Mar 5. doi:10.12659/MSM.920751
  14. Angus-Leppan H. Diagnosing epilepsy in neurology clinics: a prospective study. Seizure. 2008;17(5):431-436. doi:10.1016/j.seizure.2007.12.010
  15. Benbadis S. The differential diagnosis of epilepsy: a critical review. Epilepsy Behav. 2009;15(1):15-21. doi:10.1016/j.yebeh.2009.02.024
  16. Doležalová I, Brázdil M, Rektor I, Tyrlíková I, Kuba R. Syncope with atypical trunk convulsions in a patient with malignant arrhythmia. Epileptic Disord. 2013;15(2):171-174. doi:10.1684/epd.2013.0564
  17. Schulze-Bonhage A. Visuelle Aura: Differenzialdiagnose zwischen Migräne und Epilepsie [Differential diagnosis of visual aura in migraine and epilepsy]. Klin Monbl Augenheilkd. 2001;218(9):595-602. doi:10.1055/s-2001-17636
  18. Krebs PP. Psychogenic nonepileptic seizures. Am J Electroneurodiagnostic Technol. 2007;47(1):20-28.
  19. van Rooij FJ, Admiraal-van de Pas Y. Lactaatacidose in de postictale fase [Lactic acidosis in the postictal state]. Ned Tijdschr Geneeskd. 2015;159:A9068.
  20. Valeta, Thalia. (2017). Investigations for Epileptic Seizures. 10.1007/978-3-319-61679-7_14.
  21. Nuoffer JM, Mullis PE. Hypoglykämien–Diagnostik und Therapie im Notfall [Hypoglycaemia–diagnosis and therapy in emergencies]. Ther Umsch. 2005;62(8):543-548. doi:10.1024/0040-5930.62.8.543
  22. Nass RD, Sassen R, Elger CE, Surges R. The role of postictal laboratory blood analyses in the diagnosis and prognosis of seizures. Seizure. 2017;47:51-65. doi:10.1016/j.seizure.2017.02.013
  23. Castilla-Guerra L, del Carmen Fernández-Moreno M, López-Chozas JM, Fernández-Bolaños R. Electrolytes disturbances and seizures. Epilepsia. 2006;47(12):1990-1998. doi:10.1111/j.1528-1167.2006.00861.x
  24. Ng SK, Brust JC, Hauser WA, Susser M. Illicit drug use and the risk of new-onset seizures. Am J Epidemiol. 1990;132(1):47-57. doi:10.1093/oxfordjournals.aje.a115642
  25. Rittenberger JC. Early CT imaging of the brain – A guide to therapy. Resuscitation, 2014;85(10):1309-1310. doi: 10.1016/J.RESUSCITATION.2014.06.020
  26. Rosenow F, Klein KM, Hamer HM. Non-invasive EEG evaluation in epilepsy diagnosis. Expert Rev Neurother. 2015;15(4):425-444. doi:10.1586/14737175.2015.1025382
  27. Ufongene C, El Atrache R, Loddenkemper T, Meisel C. Electrocardiographic changes associated with epilepsy beyond heart rate and their utilization in future seizure detection and forecasting methods. Clin Neurophysiol. 2020;131(4):866-879. doi:10.1016/j.clinph.2020.01.007
  28. Bank AM, Bazil CW. Emergency Management of Epilepsy and Seizures. Semin Neurol. 2019;39(1):73-81. doi:10.1055/s-0038-1677008
  29. Huff JS, Morris DL, Kothari RU, Gibbs MA; Emergency Medicine Seizure Study Group. Emergency department management of patients with seizures: a multicenter study. Acad Emerg Med. 2001;8(6):622-628. doi:10.1111/j.1553-2712.2001.tb00175.x
  30. Keepanasseril A, Maurya DK, Manikandan K, Suriya J Y, Habeebullah S, Raghavan SS. Prophylactic magnesium sulphate in prevention of eclampsia in women with severe preeclampsia: randomised controlled trial (PIPES trial). J Obstet Gynaecol. 2018;38(3):305-309. doi:10.1080/01443615.2017.1351931
  31. Thomas SV. Management of epilepsy and pregnancy. J Postgrad Med. 2006;52(1):57-64.
  32. Agarwal P, Xi H, Jette N, et al. A nationally representative study on discharge against medical advice among those living with epilepsy. Seizure. 2021;84:84-90. doi:10.1016/j.seizure.2020.11.018
  33. Engel KG et al. Patient comprehension of emergency department care and instructions: Are patients aware of when they do not understand? Ann Emerg Med2009 Apr; 53:454.

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.

Fundamentals of Pediatric Advanced Life Support (2024)

~ iEM Education Project Team ~ Leave a comment

by Burak Çakar & Ayça Koca

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Introduction

Pediatric cardiac arrest (CA) is a rare but critical event associated with high mortality and significant risk of severe sequelae [1,2]. Unlike in adults, respiratory causes are the primary contributors to CA in children. Hypoxia and bradycardia can lead to cardiopulmonary failure, which may ultimately progress to CA.

Common causes of pediatric CA include infections (e.g., pneumonia, sepsis), trauma, asphyxia, seizures, asthma, suffocation, and sudden infant death syndrome [2]. Clinical signs of cardiopulmonary arrest include respiratory arrest, absence of a palpable pulse, muscle flaccidity, unresponsiveness, cyanosis or other discoloration, and dilated pupils. Recognizing and promptly addressing these signs is crucial for improving outcomes.

Recognition of a Critically Ill Child

Early recognition of a critically ill child is essential to implementing timely interventions that may prevent progression to CA [3]. Abnormal vital signs, relative to age-specific norms, are often the most reliable indicators of impending arrest.

Pediatric Early Warning Scores (PEWS) are recommended as a systematic tool to identify children at risk of clinical deterioration [4]. PEWS evaluates three domains: behavior, cardiovascular function, and respiratory status [5]. It incorporates vital findings such as respiratory rate, heart rate, blood pressure, oxygen saturation, temperature, level of consciousness, and capillary refill time [6]. 

Monitoring Vital Signs in Children

It is essential to recognize abnormal vital signs for early recognition of pediatric deterioration.

Blood Pressure

Systolic Hypotension is defined as a systolic blood pressure below the 5th percentile for age. The threshold for concern is when the systolic blood pressure is <70 mmHg + (2x the child’s age in years).

Respiratory Rate

Tachypnea: A respiratory rate exceeding 60 breaths per minute indicates tachypnea.
Decreased Respiratory Rate: A reduction in respiratory rate in a previously tachypneic patient could signal either improvement or fatigue. Fatigue in this context could precede respiratory failure, particularly if it occurs in conjunction with other signs of decompensation.

Temperature

Fever significantly affects physiology. For every 1°C increase in body temperature:

  • The heart rate increases by approximately 10 beats per minute.
  • The respiratory rate increases by 2 to 5 breaths per minute.

End-Tidal Carbon Dioxide (EtCO2)

Changes in EtCO2 levels are critical indicators of respiratory status. A progressive increase or decrease in EtCO2 levels can signal impending desaturation and respiratory failure.

Assessment

Given the poor outcomes associated with pediatric CA, the emphasis must be on early recognition of pre-arrest states. Identifying signs of impending respiratory failure and shock, regardless of their underlying cause, should be a primary focus [4].

Findings Preceding Cardiopulmonary Arrest

Key findings preceding cardiopulmonary arrest are categorized as follows:

  1. Airway: Signs include stridor, drooling, and retractions, which indicate significant airway obstruction or distress.

  2. Breathing: Irregular respiration, bradypnea, gasping respirations, and cyanosis are warning signs of severe respiratory compromise.

  3. Circulation: Indicators such as a capillary refill time greater than 5 seconds, bradycardia, hypotension, cool extremities, weak central pulses, and the absence of peripheral pulses suggest circulatory failure.

  4. Disability: An altered level of consciousness and decreased responsiveness point toward significant neurological impairment, often accompanying or preceding arrest.

Initial Assessment

The initial assessment begins with a first impression of the child’s general appearance, breathing pattern, and circulatory status. During the primary assessment, the ABCDE approach is followed, with immediate interventions performed at each step when abnormalities are identified. Initial management focuses on supporting airway, breathing, and circulation [7].

The clinician should rapidly assess the following:

Airway

  • Assess for patency (open, requiring maneuvers/adjuncts, partially or completely obstructed)
  • Perform cervical spine stabilization for injured children.
  • Provide 100% inspired oxygen, clear the airway (e.g., suction), apply airway maneuvers, and insert airway adjuncts if the child is unconscious.
  • Initiate chest compressions immediately if the child is unresponsive and shows no signs of life.
  •  

 Breathing

  • Evaluate respiratory rate, effort, tidal volume, lung sounds, and pulse oximetry.
  • Assist ventilation manually for patients unresponsive to basic airway maneuvers or exhibiting inadequate respiratory effort.
  • Monitor oxygenation and ventilation using pulse oximetry and ETCO₂.
  • Administer appropriate medications based on the cause of respiratory distress (e.g., albuterol for status asthmaticus, inhaled racemic epinephrine for croup).
  • Consider intubation when necessary, ensuring 100% oxygen delivery via a non-rebreather mask. Apply positive pressure ventilation with a bag-valve-mask (BVM) in cases of respiratory failure.

Circulation

  • Assess skin color and temperature, heart rate and rhythm, blood pressure, peripheral and central pulses, and capillary refill time.
  • Control hemorrhage in injured children.
  • For circulation deficiencies, monitor heart rate and rhythm, and establish vascular access for volume resuscitation or medication administration.

Disability

  • Evaluate neurological status and level of consciousness using the AVPU scale (Alert, Voice, Pain, Unresponsive) and the Glasgow Coma Scale (GCS) for trauma patients.
  • Assess pupil size and reactivity to light.
  • Check for hypoglycemia using rapid bedside glucose testing or by observing the response to empiric dextrose administration.

Exposure

  • Examine for skin findings, fever or hypothermia, and evidence of trauma.

Secondary and Tertiary Assessments

  • The secondary assessment involves a detailed head-to-toe physical examination, supplemented with a medical history.
  • The tertiary assessment focuses on identifying the underlying causes of trauma, illness, or infection through ancillary studies.

Respiratory Distress and Failure

Respiratory distress and failure are common precursors to CA in children. Early recognition of breathing difficulties is essential to improving clinical outcomes.

Respiratory distress is characterized by tachypnea, nasal flaring, retractions, and the use of accessory muscles. Additional signs include agitation, hypoxia, and abnormal breath sounds, such as stridor or wheezing. If not promptly addressed, these findings can progress to a decreased respiratory rate, respiratory fatigue, and eventual respiratory arrest.

Bradycardia

In children, bradycardia is often secondary to hypoxia. A heart rate slower than the age-appropriate normal range is indicative of bradyarrhythmia. Management focuses on optimizing oxygenation and ventilation through basic airway maneuvers.

If the heart rate remains below 60 beats per minute despite adequate oxygenation and ventilation, chest compressions should be initiated. Epinephrine (0.01 mg/kg) should be administered every 3–5 minutes. For bradycardia caused by increased vagal tone or primary atrioventricular block, atropine (0.02 mg/kg; maximum single dose 0.5 mg) is recommended [7].

Tachycardia

Tachycardia refers to a heart rate that exceeds the normal range for a child’s age, considering other factors such as physical activity or fever. The management of tachycardias depends on the child’s hemodynamic condition and rhythm [7].

Pulseless Arrest

Pediatric CAs are typically the result of cardiopulmonary distress, failure, or shock. When a child has no palpable pulse and is unresponsive, cardiopulmonary resuscitation (CPR) should be initiated.

A child with pulseless arrest will present as apneic and may exhibit gasping respirations. The rhythms associated with pulseless arrest include [2]:

Shockable rhythms: Ventricular fibrillation (VF), pulseless ventricular tachycardia (pVT).

Ventricular Fibrillation

Ventricular Tachycardia

Unshockable rhythms: Asystole, pulseless electrical activity (PEA).

Asystole

Pulseless Electrical Activity (PEA)

During CPR, reversible causes of PEA should be actively identified and addressed. The mnemonic 6H5T is useful for recalling these potential causes [2]:

  • 6 H’s:
    • Hydrogen ion (acidosis)
    • Hypoxia
    • Hypovolemia
    • Hypo- or hyper -kalemia, -calcemia, -magnesemia
    • Hypoglycemia
    • Hypo- or hyperthermia
  • 5 T’s:
    • Tension pneumothorax
    • Tamponade
    • Thrombosis (cardiac)
    • Thrombosis (pulmonary)
    • Toxic agents

By addressing these potential causes, advanced life support providers can significantly improve the likelihood of successful resuscitation.

Resuscitation

An effective resuscitation team is critical to the successful management of pediatric advanced life support (PALS). The team must perform multiple tasks simultaneously, including airway management, ventilation, vascular access, medication preparation and administration, chest compressions, monitor/defibrillator operation, recording/timing, and overall leadership.

The team leader plays a pivotal role by assigning tasks, directing team members, and modeling exemplary teamwork. In addition to medical expertise and resuscitation skills, the team must demonstrate effective communication. Key elements of effective team dynamics include:

  • Closed-loop communication
  • Clear messages
  • Defined roles and responsibilities
  • Knowing and communicating one’s limitations
  • Knowledge sharing
  • Constructive interventions
  • Reevaluation and summarization
  • Mutual respect [8]

Initiation of CPR

Timely recognition of CA, prompt initiation of high-quality chest compressions, and ensuring adequate ventilation are crucial for improving outcomes [2].

Healthcare providers should begin chest compressions promptly in any child who is unresponsive, not breathing normally, and has no signs of circulation [7, 9]. Pulse checks may be performed but should not delay the initiation of CPR for more than 10 seconds [10, 11]. Pulse palpation alone is unreliable in determining the need for compressions or confirming CA.

Since respiratory-related CA is more common in infants and children than primary cardiac causes, ensuring adequate ventilation during resuscitation is essential [2]. The recommended sequence for CPR is compressions-airway-breathing (CAB) [12].

High-quality CPR enhances blood flow to vital organs and increases the likelihood of return of spontaneous circulation (ROSC). The five key components of high-quality CPR are [2, 13]:

  • Optimal chest compression rate
  • Sufficient chest compression depth
  • Minimal interruptions in compressions
  • Complete chest recoil between compressions [7, 14]
  • Avoidance of excessive ventilation

Components of High-Quality CPR

  • Compression Rate: 100–120 compressions per minute [15–18].
  • Compression Depth:
    • At least one-third of the anterior-posterior diameter of the chest:
      • 4 cm for infants
      • 5 cm for children
      • 5–6 cm for adolescents who have reached puberty [7, 19].
    • Allow complete chest recoil after each compression.
    • Use 100% oxygen with a bag-valve-mask (BVM) during CPR.
    • Compression-Ventilation Ratios:
      • 30:2 for single rescuers.
      • 15:2 for two rescuers [7, 20].

To prevent fatigue and ensure adequate compressions, switch the person performing compressions at least every 2 minutes or sooner if necessary [7].

CPR Technique

For Infants

Single Rescuer: Use two fingers (Figure 1) or two thumbs below the nipple line (lower half of the sternum but one-finger width above the xiphisternum) [21–24].

Figure 1. Two-finger compressions

Two Rescuers: Use the two-thumb encircling hands technique (Figure 2) [25–29].

Figure 2. Thumb-encircling hands compression

If the recommended depth cannot be achieved, use the heel of one hand (Figure 3) [2, 18, 30, 31].

Figure 3. Compression with the heel of one hand

For children older than 1 year

Use either one-handed or two-handed CPR.

Perform chest compressions on a firm surface. Use a backboard or activate the bed’s “CPR mode” if available [32–35].

The Airway

Unless a cervical spine injury is suspected, the head tilt-chin lift maneuver is recommended to open the airway [36]. In trauma patients with suspected cervical spinal injury, the jaw thrust maneuver should be used. If the jaw thrust is ineffective, the head tilt-chin lift may be performed, even in cases of suspected cervical spine injury [2].

Use 100% oxygen delivered via bag-valve-mask (BVM) during CPR.

Advanced Airway Interventions During CPR

Bag-mask ventilation (BMV) is effective for most patients but requires pauses in chest compressions and carries risks of aspiration and barotrauma [2]. Advanced airway interventions, such as supraglottic airway (SGA) placement or endotracheal intubation (ETI), improve ventilation, reduce aspiration risks, and enable uninterrupted chest compressions. However, these procedures require specialized equipment and trained providers, and may be challenging for those inexperienced in pediatric intubation [2]. BMV is more reliable than advanced airway interventions during out-of-hospital pediatric CA [37–39].

For patients with advanced airway, ventilations should be asynchronous. Exceeding recommended ventilation rates can compromise hemodynamics and lower systolic blood pressure [40].

Ventilations should be tailored to age:

  • 25 breaths/min (infants)
  • 20 breaths/min (>1 year)
  • 15 breaths/min (>8 years)
  • 10 breaths/min (>12 years) [7].

Capnography should be used to confirm endotracheal tube placement and monitor for ROSC. However, ETCO₂ should not be used as a definitive quality indicator or target during PALS [7].

Drug Administration During CPR

Establish IV access as early as possible during PALS. If IV access is challenging, promptly consider intraosseous (IO) access as an alternative [7]. Drug dosing for children is typically based on weight, which can be challenging to determine in emergencies. When the actual weight cannot be obtained, various estimation methods are available [41]

The administration of vasoactive agents during CA aims to improve coronary and cerebral perfusion and increase the likelihood of ROSC. However, optimal timing and overall impact on long-term outcomes are still under investigation [42]

  • Administer epinephrine (10 mcg/kg; max 1 mg; IV or IO ) as soon as possible for non-shockable rhythms. For shockable rhythms, administer epinephrine immediately after the third shock, along with antiarrhythmic drugs. Once given, adrenaline should be repeated every 3–5 minutes until ROSC.

Antiarrhythmic drugs can reduce the risk of recurrent VF or pVT and improve the likelihood of successful defibrillation [43, 44]. Only in shockable rhythms, administer antiarrhythmic drugs immediately after the third shock, along with epinephrine.

  • Amiodarone: 5 mg/kg (max 300 mg); a second dose (max 150 mg) may follow after the fifth shock if the rhythm remains shockable.
  • Lidocaine: 1 mg/kg, as an alternative to amiodarone.

Magnesium sulfate (25–50 mg/kg) should be considered for torsades de pointes. Routine administration of sodium bicarbonate and calcium is not recommended unless specific conditions (e.g., electrolyte imbalances, drug toxicities) are present [45–48].

Flush all IV or IO resuscitation drugs with 5–10 mL of normal saline to ensure delivery to the central circulation.

Defibrillation During PALS

Shockable rhythms in children include pulseless ventricular tachycardia (pVT) and ventricular fibrillation (VF). When identified, defibrillation should be performed immediately, regardless of the ECG amplitude. If there is uncertainty about the rhythm, it should be treated as shockable to avoid delays in care. [7].

The preferred method for defibrillation during pediatric ALS is manual defibrillation, but an automated external defibrillator (AED) can be used if manual defibrillation is unavailable. Currently, self-adhesive defibrillation pads are the standard. When using these pads:

  • Chest compressionsshould continue while the defibrillator charges.
  • The pads should be placed in either the antero-lateral (AL)or antero-posterior (AP) positions:
    • AL position: One pad below the right clavicle and the other in the left axilla.
    • AP position: The front pad in the mid-chest just left of the sternum, and the back pad between the scapulae.

Avoid contact between the pads to prevent electrical arcing.

If self-adhesive pads are unavailable, paddles with gel or pre-shaped gel pads can be used as an alternative. In this case, charging should occur directly on the chest, pausing compressions during the process [7]. Pre-planning each step is critical to minimizing delays during the intervention.

Charge the defibrillator for an initial shock of 4J/kg. Avoid exceeding the maximum doses recommended for adults (typically 120–200J, depending on the defibrillator). Pause chest compressions briefly to deliver the shock, ensuring all rescuers are clear of the patient. Resume CPR immediately after the shock, minimizing the pause to under 5 seconds. Reassess the rhythm every 2 minutes and, if it remains shockable, deliver subsequent shocks at 4J/kg. For refractory VF/pVT (requiring more than 5 shocks), incrementally increase the dose up to 8J/kg (maximum 360J) [7].

CPR should continue until an organized, potentially perfusing rhythm is recognized during a rhythm check and is accompanied by signs of ROSC, identified either clinically (e.g., eye-opening, movement, normal breathing) or through monitoring (e.g., etCO2, SpO2, blood pressure, ultrasound) [7].

A summary of the fundamentals of pediatric ALS can be found in Figure 5.

Figure 5. Pediatric cardiac arrest algorithm [7] CPR: cardiopulmonary resuscitation, EMS: emergency medical services, ALS: advanced life support, VF: ventricular fibrillation, pVT: pulseless ventricular tachycardia, PEA: pulseless electrical activity, IV: intravenous, IO: intraosseous.

Post-cardiac Arrest Management

Achieving ROSC is only the first step in resuscitation. Comprehensive post-CA care is crucial to optimizing outcomes, particularly in pediatric patients. This phase focuses on treating the underlying cause of the event and preventing secondary injuries.

Key Components of Post-Cardiac Arrest Care

Targeted Temperature Management (TTM):

  • For unconscious children after ROSC, TTM helps prevent further brain injury.

Ventilation and Oxygenation:

  • Inspired oxygen should be titrated to maintain oxygen saturation (SpO₂) between 94% and 99%.
  • For intubated patients, confirm endotracheal tube (ETT) placement and monitor ventilation to avoid hyperoxia or hypoxia, as well as hypercapnia or hypocapnia.

Hemodynamic Support:

  • Prevent and treat hypotension using parenteral fluids and vasoactive medications, guided by physiologic endpoints and cardiac function.
  • Monitor for signs of recurrent shock and intervene promptly.

Glucose Management:

  • Maintain blood glucose levels below 180 mg/dL to avoid complications associated with hyperglycemia.

Seizure Management:

  • For unconscious children after ROSC, continuous electroencephalography monitoring is also recommended to detect subclinical seizures. Seizures should be monitored and treated aggressively, as they can exacerbate neurological injury.

Temperature Regulation:

  • Avoid hyperthermia (core temperature >37.5°C) using cooling measures as necessary to reduce metabolic demands and limit neuronal damage.

Summary

Pediatric CA remains a critical event with high mortality and significant morbidity. Unlike adult CA, pediatric cases are often precipitated by respiratory failure and hypoxia, highlighting the need for timely recognition and intervention. Early identification of abnormal vital signs, particularly through tools like PEWS, and a structured approach to initial assessment using the ABCDE framework are paramount in preventing CA. Furthermore, rapid and effective resuscitation, incorporating high-quality CPR, advanced airway management, and appropriate medication use, significantly improves the likelihood of survival and favorable outcomes.

Managing pediatric CA extends beyond achieving ROSC. Comprehensive post-cardiac arrest care, including targeted temperature management, optimized ventilation and oxygenation, hemodynamic support, glucose management, and seizure control, is critical to minimize secondary injuries and improve neurological recovery. Pediatric Advanced Life Support (PALS) algorithms and effective resuscitation team dynamics play essential roles in guiding care.

Ultimately, improving outcomes in pediatric CA requires a systematic approach to prevention, timely recognition, prompt intervention, and evidence-based post-resuscitation care. Continuous education, training, and adherence to updated guidelines are essential for healthcare providers to ensure the best possible outcomes for critically ill or arrested children.

Authors

Picture of Burak Çakar

Burak Çakar

Gaziantep Islahiye State Hospital, Department of Emergency Medicine, Gaziantep, Turkey

Picture of Ayça Koca

Ayça Koca

Ayça Koca is an emergency physician at Ankara University School of Medicine, Department of Emergency Medicine. She completed both her medical degree and residency at Ankara University, where she developed a deep connection to patient care and teaching. With a special interest in medical education and simulation, she is passionate about creating engaging learning experiences to support the growth and confidence of future healthcare providers.

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Reviewed and Edited By

Picture of Elif Dilek Cakal, MD, MMed

Elif Dilek Cakal, MD, MMed

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.