Approach to Acutely Confused Patient (2025)

January 20, 2025January 20, 2025 ~ iEM Education Project Team ~ Leave a comment

by Mehnaz Zafar Ali

You Have New Patients!

Patient 1

You meet a 40-year-old man in the ED, held by three security staff, looking diaphoretic and agitated, having tachycardia, and pointing vaguely in a direction as if interacting with imaginary people. When you try to assess him, he appears to be confused and disoriented and smells of alcohol. Over 6 hours, the patient has tremulousness, gets easily frightened, and gets further uncooperative for examination.

Patient 2

You evaluate an 80-year-old woman in the ICU. She has a history of diabetes mellitus, hypertension, depression, and a stroke two years ago. She was admitted due to increased sleepiness, urinary and fecal incontinence for one week, and difficulty recognizing people. Before her admission, she was active and independent, had a reasonably good memory, and could manage household responsibilities. On physical examination, her eyes remain spontaneously closed but open with audible stimuli, and she is disoriented to time, place, and person.

Introduction

Delirium is a rapidly developing clinical syndrome characterized by alterations in attention, consciousness, and awareness, with a reduced ability to focus, sustain, or shift attention. It commonly occurs in the elderly, with an incidence reported in 10% to 30% of patients hospitalized for medical illnesses and up to 50% following high-risk procedures [1].

This condition is also referred to as acute organic brain syndrome, characterized by rapid onset, diurnal fluctuations, and a duration of less than six months. Its behavioral presentation can vary, with the following manifestations.

Hyperactive Delirium: Patients present with increased agitation and heightened sympathetic activity. They may exhibit hallucinations, delusions, and combative or uncooperative behavior.
Hypoactive Delirium: Patients display increased somnolence and reduced arousal. The diagnosis is often overlooked due to its subtle clinical manifestations, which are frequently mistaken for fatigue or depression. This subtype is associated with higher rates of morbidity and mortality.
Mixed Presentation: Patients fluctuate between hyperactive and hypoactive delirium.

Delirium tremens (DT) is the most severe form of alcohol withdrawal syndrome and can be fatal. It typically occurs within 2 to 4 days following complete or significant abstinence from heavy alcohol consumption in approximately 5% of patients, with mortality rates as high as 50%. Alcohol functions as a depressant, similar to benzodiazepines and barbiturates, and affects serotonin and gamma-aminobutyric acid type A (GABA A) receptors, leading to tolerance and habituation.

Delirium is a dangerous and often preventable condition, associated with significant costs and increased morbidity and mortality. Among delirium patients presenting to the emergency department, there is a 70% increased risk of death within six months. In the ICU, delirium is linked to a 2- to 4-fold increased risk of overall mortality. Prevention, early diagnosis, and treatment of the underlying cause, along with well-coordinated care, are essential to improve patient outcomes.

General Approach

The diagnosis of delirium is primarily clinical and relies on careful history-taking, mental status examination, and detailed cognitive assessment. While laboratory and diagnostic tests may assist in identifying the underlying etiology, the initial evaluation should focus on addressing reversible causes. Life-threatening conditions must be promptly recognized, requiring rapid intervention and stabilization.

Differential Diagnoses

Delirium can present with symptoms that may be easily mistaken for mental illness, such as acute aggression, irritability, restlessness, and visual hallucinations [1]. Delirium mimics may include psychosis or mood disorders in the case of hyperactive delirium, and depression in the case of hypoactive delirium.

According to the International Classification of Diseases (ICD-10) guidelines [2], a definite diagnosis of delirium requires the presence of symptoms (mild or severe) in each of the five described areas. These include: impairment of consciousness and attention (ranging from clouding to coma, with a reduced ability to direct, focus, sustain, and shift attention), global disturbance of cognition, psychomotor disturbances, disturbance of the sleep-wake cycle, and emotional disturbances.

Delirium

Delirium typically presents with an acute onset and progresses rapidly. It often resolves completely with treatment of the underlying cause. Clinically, it is characterized by fluctuating levels of consciousness, inattention, disorientation, worsening symptoms in the evening (a phenomenon known as sundowning), and transient visual hallucinations. Delirium carries significant risks, including high mortality due to the underlying medical condition, as well as increased risk of falls, injuries, exhaustion, or aggression.

Dementia

Dementia has an insidious onset and follows a chronic, progressive course marked by continuous deterioration over time. Key clinical features include memory disturbances, changes in personality or behavior, apathy, and apraxia. Individuals with dementia are at risk of falls, neglect, abuse, agitation, and wandering away from their safe environments.

Depression

Depression typically has a slow onset and an episodic course, with periods of remission and recurrence. Symptoms include a persistently depressed mood, loss of interest or pleasure in activities, reduced energy, feelings of hopelessness, disturbances in sleep and appetite, difficulties with concentration, and pervasive negative thoughts, often accompanied by guilt. The associated risks include suicide, deliberate self-harm, neglect, and agitation.

Psychosis

Psychosis usually begins insidiously and follows a progressive course punctuated by episodes of exacerbation. Clinical features include delusions, auditory hallucinations, disorganized thoughts, social withdrawal, apathy, avolition (lack of motivation), and impaired reality testing. Psychosis poses risks such as aggression, harm to others, and non-adherence to treatment, which can exacerbate the condition further.

History and Physical Examination Hints

It is of paramount importance to obtain a detailed corroborative history regarding the onset, course, and progression of the illness, along with performing a thorough physical and neurological examination of the patient. A biopsychosocial formulation must identify the predisposing, precipitating, and perpetuating causes of delirium [1].

The mnemonic “I WATCH DEATH,” developed by Dr. M.G. Wise in 1986, is a valuable tool for clinicians to screen for possible causes of delirium [3].

I – Infections: Infections are a common cause and can include conditions such as sepsis, urinary tract infections, encephalitis, and meningitis.
W – Withdrawal: Sudden withdrawal from substances such as alcohol, sedatives, or drugs can lead to significant medical complications.
A – Acute Metabolic Disturbances: Issues such as electrolyte imbalances (e.g., hyponatremia) and organ failure, such as hepatic or renal failure, can significantly disrupt normal physiological functions.
T – Trauma: Physical injuries, including head trauma and falls, are notable causes that may lead to further complications like bleeding or swelling.
C – CNS Pathology: Central nervous system disorders such as stroke, hemorrhage, seizures, or the presence of space-occupying lesions like tumors can have profound impacts on a patient’s condition.
H – Hypoxia: A lack of adequate oxygen supply, often due to anemia or hypotension, can result in significant systemic effects.
D – Deficiencies: Nutritional deficiencies, particularly a lack of essential vitamins and minerals like thiamine, can result in various clinical symptoms.
E – Endocrine Disorders: Hormonal imbalances, including thyroid storm and hyperglycemia, can disrupt metabolic processes and cause severe systemic effects.
A – Acute Vascular Events: Sudden vascular events, such as subarachnoid hemorrhage, require prompt identification and management due to their life-threatening nature.
T – Toxins or Drugs: Exposure to industrial poisons, carbon monoxide, or drugs with anticholinergic properties can have toxic effects on the body.
H – Heavy Metal Poisoning: Exposure to heavy metals such as lead and mercury can lead to chronic toxicity and require specific interventions.

Several factors increase the likelihood of developing delirium, especially in vulnerable populations:

Age: Both elderly individuals and young children are at heightened risk due to their increased susceptibility to physiological and cognitive changes.
Recent Hospitalizations: Hospital stays, particularly those involving medical illnesses or surgical procedures, can act as significant stressors and predispose individuals to delirium.
Pre-existing Brain Conditions: Conditions like brain damage or dementia further increase the risk, as they impair cognitive resilience.
Chronic Medical Disorders: Long-term health conditions often contribute to a state of chronic physiological stress, increasing the likelihood of delirium.
Sensory Deprivation: Impairments in vision or hearing can lead to sensory deprivation, which may exacerbate confusion and disorientation.
Substance Use Disorders: Alcohol or drug use disorders are major contributors to the onset of delirium, particularly during withdrawal periods or intoxication.
Medications: The use of psychotropic medicines and polypharmacy (simultaneous use of multiple medications) heightens the risk of delirium due to potential drug interactions and side effects.
History of Delirium: Individuals with a previous history of delirium are more likely to experience recurrent episodes, particularly if the underlying risk factors persist.
Malnutrition: Poor nutritional status can exacerbate vulnerability to delirium by impairing metabolic and neurological functions.
Burns: Severe burns create systemic inflammation and stress, which can predispose individuals to delirium.

Screening tools for delirium, such as the Mini-Mental Status Examination (MMSE) [4] and the Confusion Assessment Method (CAM) [5], are valuable for early identification and intervention. These tools can also be used to monitor clinical improvement when performed repeatedly during the course of the illness.

The Confusion Assessment Method (CAM) includes four key features to identify delirium. A diagnosis of delirium requires the presence of Features 1 and 2 and either Feature 3 or Feature 4:

Feature 1 – Acute Onset and Fluctuating Course: There is evidence of an acute change in mental status from the patient’s baseline.
The abnormal behavior fluctuates throughout the day, tending to come and go or change in severity.

Feature 2 – Inattention: The patient has difficulty focusing attention, is easily distractible, or cannot keep track of what is being said.

Feature 3 – Disorganized Thinking: The patient demonstrates disorganized or incoherent thinking, such as rambling or irrelevant conversation, illogical flow of ideas, or unpredictable switching between subjects.

Feature 4 – Altered Level of Consciousness: The patient’s consciousness level deviates from “alert.” It may range from hyperalert (vigilant) to lethargy, stupor, or coma.

The CAM is a widely used, reliable tool with high sensitivity (94–100%) and specificity (90–95%). It enables quick and accurate identification of delirium, facilitating early intervention to manage underlying causes and improve patient outcomes.

Confusion Assessment Method (CAM) Instrument:

Acute Onset:
- This involves an abrupt change in the patient’s mental status, which is evident when comparing their current state to their baseline cognitive function. This change may be noticed by family members, caregivers, or clinicians and is typically indicative of an acute underlying medical issue or condition.
Inattention:
- 2A: The patient has difficulty concentrating or paying attention. This may manifest as being easily distracted, unable to follow conversations, or losing track of what is being discussed.
- 2B: If inattention is present, the behavior often fluctuates over time, meaning it can improve or worsen during an assessment or throughout the day.
Disorganized Thinking:
- The patient’s thought process appears chaotic or incoherent. They may exhibit rambling, irrelevant speech, an illogical sequence of ideas, or rapid, unpredictable topic changes during a conversation. This suggests a loss of organized, goal-directed thinking.
Altered Level of Consciousness:
- The patient’s alertness deviates from normal. This can range from:
  - Alert (normal): Fully awake and responsive.
  - Vigilant (hyperalert): Overly sensitive to stimuli, easily startled, or hypervigilant.
  - Lethargic: Drowsy but easily aroused.
  - Stupor: Difficult to arouse, with limited responsiveness to stimuli.
  - Coma: Unarousable and non-responsive.
Disorientation:
- The patient is confused about time, place, or identity. They may incorrectly believe they are in a different location, misjudge the time of day, or demonstrate an inability to recognize familiar surroundings or people.
Memory Impairment:
- Memory issues are evident when the patient cannot recall recent events, forgets instructions, or struggles to remember details of their hospital stay or interactions.
Perceptual Disturbances:
- The patient may experience hallucinations (e.g., seeing or hearing things that aren’t present), illusions (misinterpreting real stimuli, such as mistaking a shadow for an object), or misinterpretations (believing something benign, such as a coat rack, is threatening).
Psychomotor Disturbances:
- 8A (Agitation): The patient may exhibit increased motor activity, such as restlessness, repeatedly picking at bedclothes, tapping their fingers, or making frequent, sudden movements.
- 8B (Retardation): Alternatively, the patient may show decreased motor activity, appearing sluggish, staring into space, staying in the same position for extended periods, or moving very slowly.
Altered Sleep-Wake Cycle:
- Disturbances in the patient’s sleep pattern are evident. They may experience excessive daytime sleepiness coupled with difficulty sleeping at night, or their sleep-wake rhythm may become reversed.

Associated Features

Certain medical conditions can present with a range of distressing symptoms and features:

Hallucinations and Illusions: Patients may experience vivid and often frightening visual or auditory hallucinations. Additionally, tactile hallucinations, such as the sensation of insects crawling on the body, can occur, adding to their distress.
Autonomic Disturbances: Marked autonomic instability is common and may include symptoms such as tachycardia, fever, hypertension, sweating, and pupillary dilation.
Psychomotor and Coordination Issues: Psychomotor agitation and ataxia (lack of muscle coordination) are frequently observed, contributing to physical instability and difficulty performing tasks.
Sleep Disturbances: Insomnia is a notable feature, often accompanied by a reversal of the sleep-wake cycle, further exacerbating cognitive and physical impairments.

It is crucial to obtain a detailed history of the patient’s premorbid personality, as this helps establish their baseline cognitive state and allows the clinician to determine the magnitude of cognitive deterioration. Patients with fluctuating levels of consciousness may experience rapid shifts in their activity levels, ranging from extreme psychomotor excitement to sleepiness during an interview [1].

The Mental State Examination (MSE) should include an assessment of mood (e.g., apathy, blunted affect, emotional lability), behavior (e.g., withdrawn, agitated), activity levels, thoughts (e.g., delusions), and perceptions (e.g., hallucinations, illusions). A brief cognitive assessment may utilize the COMA framework, which evaluates Concentration, Orientation, Memory, and Attention.

Clinical Institute Withdrawal Assessment of Alcohol Scale, Revised (CIWA-Ar)

The CIWA-R is a tool designed to standardize the assessment of withdrawal severity in patients experiencing alcohol withdrawal. This instrument is particularly useful for guiding treatment decisions and ensuring appropriate management of symptoms.

Alcohol withdrawal delirium progresses through distinct stages, including:

Tremulousness or Jitteriness: Occurs within 6–8 hours of cessation or reduction in alcohol use.
Psychosis and Perceptual Symptoms: Develops between 8–12 hours, marked by hallucinations and disorganized thinking.
Seizures: Typically occur within 12–24 hours of withdrawal.
Delirium Tremens: The most severe stage, manifesting within 24–72 hours and potentially lasting up to one week. This phase is characterized by confusion, autonomic instability, and significant risk of complications.

The CIWA-R plays a critical role in monitoring these stages and ensuring timely interventions to mitigate risks associated with alcohol withdrawal.

Click here to download full CIWA-R evaluation form.

Diagnostic Tests and Interpretation

Relevant laboratory tests and diagnostic imaging are recommended to assess the underlying etiology of delirium. Routine workups for electrolytes, kidney and liver function, and pregnancy tests for women are advised. Blood tests can help identify medical conditions that may mimic delirium, such as hypoglycemia and diabetic ketoacidosis (via blood sugar levels) or thyrotoxicosis (via thyroid profile). Test results indicative of long-term heavy alcohol use, such as evidence of cirrhosis or liver failure on ultrasound, macrocytic anemia, and elevated liver transaminase levels—particularly gamma-glutamyl transpeptidase—can aid in reaching the correct diagnosis [6].

Positron emission tomographic (PET) studies have suggested a globally low rate of metabolic activity, particularly in the left parietal and right frontal areas, in otherwise healthy individuals withdrawing from alcohol. Diffuse slowing of the background rhythm has been observed on electroencephalography (EEG) in patients suffering from acute delirium, except in cases of alcohol-related delirium tremens, which typically exhibit fast activity [1].

Management

Delirium is a medical emergency requiring immediate hospitalization to correct the underlying causes while minimizing risks associated with behavioral symptoms, aggression, dehydration, falls, and injury. High-potency antipsychotics in low doses are recommended for managing aggression and behavioral symptoms. Haloperidol (Haldol) has been extensively studied for reducing agitation due to delirium [7]. Evidence also supports the use of other atypical antipsychotics such as risperidone. Aripiprazole has demonstrated significant benefit in the complete resolution of hypoactive delirium [8].

The use of benzodiazepines should be restricted to cases of delirium caused by alcohol withdrawal. If liver function is not impaired, a long-acting benzodiazepine, such as chlordiazepoxide or diazepam, is preferred and can be administered orally or intravenously. In cases of reduced liver function, lorazepam may be given orally or parenterally as needed to stabilize vital signs and sedate the patient. These medications should then be tapered gradually over several days with close monitoring of vital signs. Anticonvulsants like carbamazepine and valproic acid are also effective in managing alcohol withdrawal. However, antipsychotics should be avoided in such cases due to their potential to lower the seizure threshold. Chronic alcoholics are at high risk of vitamin B1 (thiamine) deficiency, which can predispose them to Wernicke-Korsakoff syndrome (characterized by memory problems, confabulation, and apathy), cerebellar degeneration, and cardiovascular dysfunction. To mitigate this risk, such patients should receive 100 mg of thiamine intravenously before glucose administration.

Environmental modification strategies are particularly useful for managing delirious patients. These include providing well-illuminated rooms with good ventilation and reorientation cues such as calendars and alarm clocks. Assigning patients to a room near the nursing station allows for closer monitoring, ideally with the presence of a family member or close friend. In severe cases with agitation or injury risk, one-on-one supervision is advisable to ensure patient safety [1]. Both under-stimulation and overstimulation should be avoided. The use of physical restraints should be considered a last resort, with frequent monitoring and discontinuation as soon as possible. Psychoeducation for family members and caregivers is crucial to manage expectations and improve their involvement in the patient’s care [2].

Special Patient Groups and Other Considerations

Elderly patients are at high risk of altered mental status, and studies have recommended advanced age as an independent risk factor warranting screening of this vulnerable group through structured mental state assessments. It is important to recognize that behavioral manifestations of this magnitude should not be regarded as a normal part of the aging process. Dementia must be carefully differentiated from delirium in the geriatric population, as dementia typically presents with an insidious onset and a progressive course [3].

Other risk factors in the elderly that require attention include underlying neurological causes, multiple medical comorbidities, polypharmacy, poor drug metabolism, and sensory limitations [9]. Medications for elderly patients should be initiated at lower doses, and potential drug interactions must be considered whenever new medications are introduced.

The pediatric age group may present with nonspecific symptoms of acute onset, necessitating a detailed history and physical examination to rule out causes such as fever, injury, or foreign objects. Pregnancy, meanwhile, may predispose healthy women to medical conditions such as diabetes, venous thromboembolism, strokes, and eclampsia [9].

When To Admit This Patient

Admission decisions for confused patients or those undergoing alcohol withdrawal require a multifaceted approach that prioritizes accurate diagnosis, evidence-based treatment, and legal considerations. These decisions should aim to address the immediate medical needs while planning for long-term recovery and safety.

Admitting a confused patient requires careful evaluation of the underlying causes, as confusion can result from various conditions such as dementia, delirium, or depression, each requiring distinct management strategies [10]. Delirium, an acute confusional state, is particularly prevalent in older adults and often develops rapidly with fluctuating severity [11]. It is essential to determine whether the confusion is acute, chronic, or a combination of both, as this distinction guides the initial management plan [11].

Risk factors for acute confusion include admission from non-home settings, lower cognitive scores, restricted activity levels, infections, and abnormal laboratory values. These indicators suggest frailty and may also point to underlying chronic undernutrition or dehydration [12]. Early recognition and appropriate management are crucial to reducing morbidity and mortality, as confusion is often misdiagnosed or undertreated in hospital settings [10].

Furthermore, legal and ethical challenges, such as evaluating a patient’s decision-making capacity and ensuring that any necessary restraints are lawful and ethical, must be addressed to avoid infringing on the patient’s rights [13]. A comprehensive assessment of cognitive and physical status, coupled with an understanding of legal considerations, is essential for developing a management plan that effectively addresses the specific causes and risks associated with confusion [11-13].

Disposition decisions for confused patients, including those undergoing alcohol withdrawal, require a comprehensive and systematic approach that integrates accurate diagnosis, appropriate treatment, and continuous monitoring. Alcohol withdrawal can result in severe complications, such as seizures and delirium tremens, with mortality rates ranging from 1% to 30%, depending on the quality of treatment provided [14]. Prompt identification and management are critical, often involving benzodiazepines like diazepam to alleviate symptoms and prevent progression to life-threatening conditions [15]. Management becomes particularly challenging in critically ill patients, as incomplete alcohol consumption histories and the need for adjunctive medications beyond benzodiazepines complicate care during severe withdrawal or delirium tremens [16].

Emergency departments frequently encounter substance use disorders; however, less than half of alcohol-related issues are identified, highlighting the importance of comprehensive assessments and evidence-based interventions. Effective disposition decisions rely on early identification, tailored treatment strategies, and ongoing evaluations to ensure patient safety and recovery.

Clinical Pearls

Alcohol Withdrawal Characteristics: Alcohol withdrawal can begin within hours to days following heavy and prolonged alcohol use. A key feature of alcohol withdrawal is autonomic hyperactivity, which may present as increased heart rate, sweating, tremors, and other signs of sympathetic nervous system overactivity.
Overlap with Sedative-Hypnotic Withdrawal: The diagnostic criteria and symptoms for alcohol withdrawal are identical to those for sedative-hypnotic withdrawal. This similarity highlights the importance of carefully assessing a patient’s history of substance use to guide appropriate management.
Treatment Approaches:
- Delirium Due to General Medical Conditions: The preferred treatment is low doses of high-potency antipsychotics, which help manage symptoms without excessive sedation or complications.
- Alcohol Withdrawal: Benzodiazepines remain the first-line treatment to alleviate withdrawal symptoms and prevent complications such as seizures or delirium tremens. In cases where hepatotoxicity is a concern, short-acting benzodiazepines like lorazepam are preferred due to their safer profile in patients with compromised liver function.
Hallucinations and Diagnosis: Visual hallucinations are more characteristic of delirium than of primary psychiatric disorders. This distinction is critical in differentiating between medical and psychiatric causes of altered mental status.

Revisiting Your Patient

Patient 1

The patient presents with the smell of alcohol and clinical features consistent with delirium tremens, a severe manifestation of alcohol withdrawal.

Further Management: The patient should be treated promptly with a benzodiazepine, starting with high doses and tapering as recovery progresses. Chronic alcohol users are commonly deficient in vitamin B1 (thiamine), which can result in dementia and cognitive impairments. Thiamine replacement should be administered prior to glucose to prevent the development of Wernicke-Korsakoff syndrome [17].

Patient 2

The patient is unresponsive to stimuli, disoriented, and has multiple medical conditions, which is suggestive of delirium due to a general medical condition, hypoactive type.

Further Management: Immediate steps should include ensuring 24-hour supervision, investigating the underlying cause, and implementing reorientation strategies. Low-dose antipsychotics have been recommended, with studies reporting complete resolution of symptoms with the use of aripiprazole and other atypical antipsychotics [18].

Author

Mehnaz Zafar Ali

Consultant Psychiatrist, Al Amal Psychiatry Hospital, Emirates Health Services, Dubai, United Arab Emirates

Listen to the chapter

References

Gleason OC. Delirium. Am Fam Physician. 2003;67(5):1027-1034.
World Health Organization. Organic, including symptomatic, mental disorders. In: International Statistical Classification of Diseases and Related Health Problems. 10th ed. 2016:182-188.
Gower LE, Gatewood MO, Kang CS. Emergency department management of delirium in the elderly. West J Emerg Med. 2012;13(2):194-201. doi:10.5811/westjem.2011.10.6654.
Folstein MF, Folstein SE, McHugh PR. “Mini-mental state”. A practical method for grading the cognitive state of patients for the clinician. J Psychiatr Res. 1975;12(3):189-198. doi:10.1016/0022-3956(75)90026-6.
Inouye SK, van Dyck CH, Alessi CA, Balkin S, Siegal AP, Horwitz RI. Clarifying confusion: the confusion assessment method. A new method for detection of delirium. Ann Intern Med. 1990;113(12):941-948. doi:10.7326/0003-4819-113-12-941.
Chan M, Moukaddam N, Tucci V. Stabilization and management of the acutely agitated or psychotic patient. In: Cevik AA, Quek LS, Noureldin A, Cakal ED, eds. International Emergency Medicine Education Project. 1st ed. iEM Education Project; 2018:452-457.
Smit L, Slooter AJ, Devlin JW, et al. Efficacy of haloperidol to decrease the burden of delirium in adult critically ill patients: the EuRIDICE randomized clinical trial. Crit Care. 2023;27(1):413. doi:10.1186/s13054-023-04692-3.
Lodewijckx E, Debain A, Lieten S, et al. Pharmacologic treatment for hypoactive delirium in adult patients: a brief report of the literature. J Am Med Dir Assoc. 2021;22(6):1313-1316.e2. doi:10.1016/j.jamda.2020.12.037.
Cetin M, Oktem B, Canakci ME. Altered mental status. In: Cevik AA, Quek LS, Noureldin A, Cakal ED, eds. International Emergency Medicine Education Project. 1st ed. iEM Education Project; 2018:111-121.
Winstanley L, Glew S, Harwood RH. A foundation doctor’s guide to clerking the confused older patient. Br J Hosp Med (Lond). 2010;71(5):M78-M81. doi:10.12968/hmed.2010.71.Sup5.47934.
Andrews H, Clarke A, Parmar S, et al. You’ve been bleeped: the confused patient. BMJ. 2015;351:h3266. doi:10.1136/sbmj.h3266.
Wakefield BJ. Risk for acute confusion on hospital admission. Clin Nurs Res. 2002;11(2):153-172. doi:10.1177/105477380201100205.
Lyons D. The confused patient in the acute hospital: legal and ethical challenges for clinicians in Scotland. J R Coll Physicians Edinb. 2013;43(1):61-67. doi:10.4997/jrcpe.2013.114.
Thanyanuwat R. Patients who suffer from alcohol withdrawal and disorientation. J Med Assoc Thai. 2013;96(2):78-83.
Thompson WL. Management of alcohol withdrawal syndromes. Arch Intern Med. 1978;138(2):278-283. doi:10.1001/archinte.1978.03630260068019.
Sutton LJ, Jutel A. Alcohol withdrawal syndrome in critically ill patients: identification, assessment, and management. Crit Care Nurse. 2016;36(1):28-40. doi:10.4037/ccn2016420.
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Lodewijckx E, Debain A, Lieten S, et al. Pharmacologic treatment for hypoactive delirium in adult patients: a brief report of the literature. J Am Med Dir Assoc. 2021;22(6):1313-1316.e2. doi:10.1016/j.jamda.2020.12.037.

Reviewed and Edited By

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.

Pediatric Seizures (2025)

January 9, 2025January 10, 2025 ~ iEM Education Project Team ~ Leave a comment

by Neema Francis, Faiz Ahmad, Thiagarajan Jaiganesh

You Have A New Patient!

A 5-year-old female was brought into the ED as her parents noticed that she was not very responsive. She was diagnosed with otitis media 3 days ago and has been taking oral amoxicillin for it. This morning, she became irritable and was less active than usual. On arrival at the ED triage, the patient was tachypneic (40 bpm), tachycardic (145 bpm), and had a temperature of 39.4°C.

The child did not respond to vocal stimuli but was opening her eyes spontaneously. She had a sluggish pupillary response to light, and she seemed unaware of her surroundings. Suddenly, the patient began seizing, with her eyes up-rolled and her hands clenched and stretched downwards.

What Do You Need To Know?

Importance

Pediatric seizures are a significant health concern due to their high incidence, diagnostic complexity, diverse causes, and potential for severe consequences. Seizures are among the most common neurological disorders in children, with approximately 4–10% experiencing at least one seizure by age 16 [1,2]. The incidence is highest in the first year of life and remains substantial throughout childhood, particularly in children under three years old [3]. Seizures can result from various causes, including fever, infections, genetic disorders, head injuries, metabolic disturbances, and structural CNS abnormalities, which often complicates diagnosis and treatment [3,4]. Prolonged seizures, such as status epilepticus lasting five minutes or more, can lead to lactic acidosis, neuronal injury, network alterations, or even neuronal death, particularly when lasting beyond 30 minutes [3]. These severe outcomes impact development, quality of life, and increase the risk of comorbidities such as intellectual disability, depression, and anxiety. Children with epilepsy face a 5–10 times higher mortality risk compared to their peers and are prone to medical complications and long-term educational and social challenges [3,5]. The condition places a significant burden on healthcare systems and induces considerable psychological stress on children and their families [6,7].

Epidemiology

Seizures affect up to 10% of children, with incidence rates ranging from 33.3 to 82 cases per 100,000 annually, peaking in the first year of life and declining during adolescence [6,8]. Most (94%) of children presenting to the emergency department (ED) with a first seizure are under 6 years of age [4]. Febrile seizures, the most common type in young children, affect 3–4% of all children, primarily those under five years old [5,6]. Neonatal seizures, with distinct characteristics due to brain immaturity, are a common neurological condition in newborns [9]. Key risk factors include a family history of seizures, fever, CNS infections (e.g., meningitis, viral infections), head injuries, pre-existing neurological conditions, and maternal factors such as alcohol use, smoking, and prenatal exposures [3,7].

Seizures can be symptomatic or idiopathic. Acute symptomatic seizures arise from recent events, while remote symptomatic seizures result from chronic conditions. Generalized tonic-clonic seizures are the most frequent type [4], while status epilepticus (SE), a critical condition, is often triggered by fever or CNS infections in children [3]. Genetic factors, metabolic disorders, electrolyte imbalances, and structural brain abnormalities are recognized as key causes [6]. Mortality in pediatric epilepsy is 2–4 times higher than the general population and significantly elevated in children with neurological comorbidities, with sudden unexpected death in epilepsy (SUDEP) as a leading cause [3]. Febrile seizures are often benign, but complex febrile seizures may increase the risk of future epilepsy [2,6].

Pathophysiology

The pathophysiology of pediatric seizures involves complex interactions of neuronal excitation and inhibition in the brain, influenced by age, developmental stage, and underlying conditions [9]. Seizures arise from abnormal, excessive, and synchronous neuronal activity, leading to transient signs and symptoms such as involuntary muscle activity [3,9]. This activity stems from an imbalance between excitatory and inhibitory neurotransmission.

Basic Mechanisms of Seizures

The primary mechanism behind seizures involves either a deficit in neuronal inhibition or an excess of excitatory stimuli. The inhibitory neurotransmitter gamma-aminobutyric acid (GABA) plays a crucial role. In mature brains, GABA inhibits neuronal firing, maintaining balance in the central nervous system [3]. However, in neonatal brains, the immature GABA system can paradoxically cause excitation, making neonates more susceptible to seizures [9]. Additionally, alterations in GABA function, such as receptor dysfunction, can lead to prolonged and high-intensity neuronal stimulation, further increasing excitability. Voltage-gated ion channels and excitatory neurotransmitters like glutamate also contribute to seizure generation. Glutamate receptors, such as NMDA and AMPA, are primary excitatory receptors in the CNS and are involved in seizure propagation.

Age-Related Factors and Neuronal Imbalance

The immature state of the neonatal brain predisposes it to seizures due to developmental differences. In early life, the formation of excitatory synapses occurs before the development of inhibitory synapses, contributing to an imbalance in neuronal activity [7,9]. Additionally, the GABA receptor in neonates can cause depolarization rather than hyperpolarization, further enhancing neuronal excitability. Ion channel imbalances, especially the premature maturation of channels involved in depolarization, exacerbate this vulnerability [7].

Specific Factors Contributing to Seizures

Several specific factors influence seizure pathophysiology:

Genetic Factors: Mutations in genes regulating synapse development, ion transport, protein phosphorylation, and gene transcription can disrupt neuronal activity [7].
Metabolic Disturbances: Conditions like hypoglycemia, hypocalcemia, hyponatremia, and other metabolic imbalances impair neuronal function, triggering seizures [2,3].
Hypoxic Conditions: Perinatal asphyxia and hypoxic-ischemic encephalopathy damage brain cells, increasing seizure risk [2,6,7].
Infections: CNS infections such as meningitis and encephalitis disrupt normal brain function, leading to seizures [2,4,10].
Structural Abnormalities: Malformations of cortical development and acquired lesions alter neuronal networks, predisposing to seizures [2,9].
Fever: Although the exact mechanism is unclear, fever lowers the seizure threshold in some children, particularly those prone to febrile seizures [2]. In febrile seizures, inflammatory mediators such as IL-1 have been shown to increase neuronal stimulation. Animal models and preliminary studies suggest that these mediators play a role in seizure pathophysiology, although the clinical significance remains under investigation.

Medical History

A detailed history is crucial for accurately diagnosing and managing seizures in children. The history should focus on the events immediately preceding the seizure, the seizure itself, and the period following the seizure. It is important to obtain information from the child (when possible) and any witnesses [2]. When taking a medical history for pediatric seizures in the emergency department, it is important to gather information about the following key features [2,3,7-9,11,12]:

1. History of Present Illness:

Onset and duration of seizures: This information helps determine the type and underlying cause of the seizure. Note how the event began, including any preceding aura. An aura is a subjective sensation or experience that may precede a seizure [2,9].
Precipitating factors: Certain triggers, such as sleep deprivation, fever, trauma, or stress, can increase the likelihood of seizures in some children [2,4,7].
Description of the seizure: A detailed description of the seizure (e.g., focal or generalized) is crucial, including the child’s behavior, movements, and any changes in consciousness. Any evidence of partial (focal) onset, such as twitching or jerking on one side of the body, should also be noted [2]. It is also important to note if the child experienced incontinence during the seizure. It’s important to gather information about the postictal period including the length of the period, and any focal neurologic deficits, such as weakness or confusion, that may be present after the seizure. Also important is whether the child was able to easily fall back asleep after the seizure.
Current symptoms and vital signs: Assess the child’s current symptoms, vital signs, and whether they have recovered from the seizure or not.

2. Past Medical History:

Developmental and medical history: Information about the child’s developmental milestones and any previous medical conditions or treatments is important in identifying potential causes of seizures [6].
Immunization status: Some seizures are related to diseases that are preventable by vaccination, so it’s important to inquire about the child’s immunization history.
Previous seizures: This may indicate an underlying neurological condition or epilepsy.
Previous treatment for seizures: Determine whether the child has received prior treatment for seizures, including medications, and if these treatments were effective [2].

3. Medication History:

Assess whether the child is taking any medications that can lower the seizure threshold or exacerbate seizures.

4. Family History:

A family history of seizures or other neurological disorders may suggest a genetic predisposition.

It is important to note that seizures may sometimes occur without a clear cause. The emergency department’s priority is stabilizing the patient and preventing further seizures or complications.

Several risk factors for pediatric seizures should be considered during medical history-taking. There may be a higher likelihood of seizures occurring in children who have a familial history of seizures or epilepsy. Children born prematurely or with a low birth weight may be at an increased risk of seizures because they are more likely to have brain injuries or developmental problems. Children with neurological disorders, such as cerebral palsy, or brain injuries, such as traumatic brain injury, may also be at an increased risk of seizures because these conditions can cause abnormal electrical activity in the brain. Metabolic disorders, such as hypoglycemia or hyponatremia, are also known risk factors. Certain infections, such as meningitis or encephalitis, can cause inflammation in the brain and are thus predisposing factors for pediatric seizures. Developmental disorders, such as autism or intellectual disability, have also been identified as risk factors for pediatric seizures. Having one or more of these risk factors does not necessarily mean that a child will develop seizures, but it is essential to be aware of them to detect seizures early and initiate appropriate treatment.

As with all medical emergencies, it is important to look out for red flags. Concerns should be raised if the seizure was delayed or related to a head injury. Developmental delay or regression should be ruled out. Bleeding disorders or anticoagulation therapy are important considerations during history-taking in cases of pediatric seizures. It is also critical to rule out CNS infections as a possible cause of the seizure. Red flags in the history may include fever, headache, photophobia, vomiting, bulging fontanelles, neck stiffness, decreased consciousness, and focal neurologic symptoms.

Physical Examination

A thorough physical examination is essential when evaluating a child with a suspected seizure. It aids in identifying underlying causes, associated conditions, and guiding further diagnostic and treatment decisions. The examination should be performed in conjunction with a detailed history and adapted to the child’s clinical condition and developmental stage [7,12]. Children with seizures may have developmental delays or regression, which can indicate an underlying problem.

Initial Assessment

Stabilization: If the child is actively seizing, focus on stabilizing the airway, breathing, and circulation (ABC) and stopping the seizure [2,10,12].
Vital Signs [2,5,7]:
- Temperature: Identify fever (above 38°C/100.4°F), the most common cause of seizures in children.
- Heart Rate and Blood Pressure: Monitor for abnormalities that may indicate underlying conditions or complications.
- Oxygen Saturation: Ensure adequate oxygenation.

General Appearance

Level of Consciousness: Assess alertness and orientation. Note any altered mental status, which may suggest ongoing issues like status epilepticus or other underlying conditions [4,10].
Activity Level and Responsiveness: Observe for irritability, excessive sleepiness, or signs of distress. Are they irritable? Are they playful? Are they well-kept? Look for signs of neglect or child abuse.
Dysmorphic Features: Look for unusual physical features that may suggest a genetic or developmental syndrome [2].

Head and Neck Examination

Head Circumference: Measure head size, especially in infants, as microcephaly can indicate an underlying condition [2,6].
Signs of Trauma: Check for bruising or swelling that may suggest head injury.
Fontanelles: In infants, examine the anterior fontanelle for bulging, which may indicate increased intracranial pressure.
VP Shunt: Assess for ventriculoperitoneal (VP) shunt placement and any signs of malfunction or infection [2].
Meningeal Signs: Look for nuchal rigidity or other signs of meningeal irritation, suggesting CNS infection [12].
Eye and ear examination: Changes in pupils, papilledema, and retinal hemorrhages, or abnormal movements of the eyes that can indicate brain injury. Bulging tympanic membranes can indicate otitis media.

Skin Examination

Bruising: Identify unexplained bruising, which may point to bleeding disorders or child abuse.
Skin Rashes: Look for signs such as café au lait spots (indicative of neurofibromatosis), adenoma sebaceum or ash leaf spots (associated with tuberous sclerosis) [6], and port wine stains (typical of Sturge-Weber syndrome).
Neurocutaneous Markers: Use a Woods lamp to detect signs of neurocutaneous syndromes.

Cardiovascular and Abdominal Examination

Heart Sounds: Listen for abnormalities that may indicate a cardiac issue. Heart murmurs or arrhythmias that may be related to seizures.
Abdomen: Palpate for masses or organomegaly, which may suggest a metabolic disorder. Children with metabolic disorders, such as liver or kidney disease, may have an enlarged liver or spleen, which can contribute to seizures.

Neurological Examination [2,4,12]

Mental Status: Evaluate consciousness, orientation, and behavior.
Cranial Nerves: Check pupillary responses, eye movements, and facial symmetry.
Motor Function: Assess muscle strength, tone, symmetry, and any abnormal movements. Look for Todd’s paresis or focal weakness post-seizure.
Reflexes: Evaluate deep tendon reflexes, noting asymmetry.
Meningeal signs: Brudzinski’s or Kernig’s sign. Neck stiffness should also be assessed.
Sensory Function: Test sensory responses, noting any deficits.
Gait and Coordination: Observe gait, coordination, and balance in age-appropriate children.

Postictal Examination [6]

Neurological Status: Note persistent confusion, weakness, or other deficits during the postictal phase, which may help localize the seizure origin.
Symmetry: Pay close attention to symmetrical muscle tone, reflexes, and movements to identify potential focal brain issues.

Important Considerations

Age-Appropriate Assessment: Adjust the neurological exam based on the child’s developmental stage, as young children may not fully cooperate [6].
Clinical Context: Always interpret findings within the context of the child’s history and other clinical information [12].

Alternative Diagnoses

It is important to distinguish between true seizures and seizure mimics in the pediatric population, as the causes, treatment options, and outcomes can be quite different [14,15]. Examples of seizure mimics include vasovagal syncope, breath-holding spells, reflex anoxic seizures, arrhythmias, and non-epileptic paroxysmal events. It is helpful to look for clues in the history to rule out such mimics. A vagal reflex can be precipitated by a sudden fright or minor trauma. Temper tantrums should prompt consideration of breath-holding spells, which can lead to hypoxia and, in turn, a short tonic-clonic event with a quick recovery time. Visual and auditory changes paired with lightheadedness are suggestive of a vasovagal attack. A history of palpitations or strenuous exercise just before the event could indicate arrhythmias.

Certain symptoms can indicate a genuine seizure [14,15], including but not limited to:

Biting of the tongue on one side (high specificity).
Swift blinking of the eyes.
Fixed gaze with dilated pupils.
Repetitive lip movements.
Elevated heart rate and blood pressure during the episode.
A post-seizure phase.

Fevers are the most common cause of seizures in children [16]. Febrile convulsions can be further categorized into simple or complex febrile seizures:

Simple febrile seizures are generalized, last less than 15 minutes, and occur only once within a 24-hour timeframe. They are typically not associated with neurological deficits or other significant findings.
Complex febrile seizures last longer than 15 minutes, are focal (involving only one part of the body), or occur multiple times within a 24-hour period. While both types of febrile seizures are generally benign, complex febrile seizures require further investigation to rule out organic causes and carry a slightly higher risk of developing into epilepsy or other neurological disorders later in life.

In an afebrile child presenting with seizures, the differential diagnoses are extensive. Possible causes include:

Structural abnormalities in the brain, such as tumors, cysts, or malformations [16].
Metabolic disturbances, such as hypoglycemia, electrolyte imbalances, or trauma.

Status epilepticus is a medical emergency, defined as a seizure lasting longer than 5 minutes or recurrent seizures without regaining consciousness in between [16]. It can occur in both children and neonates and is associated with significant morbidity and mortality. Non-convulsive status epilepticus should be considered in any child with an altered mental status; it is ill-defined and remains a diagnosis of exclusion.

Neonatal seizures can be caused by a variety of factors, including hypoxic-ischemic encephalopathy, metabolic disturbances, infections, and intracranial hemorrhage [16]. Neonatal seizures can have serious consequences if left untreated, including brain damage and developmental delays.

Acing Diagnostic Testing

A bedside blood glucose level should be obtained as soon as possible to rule out hypoglycemia [4,15,17]. Venous blood gas, magnesium, and phosphorus levels are also valuable investigations to assess other electrolyte imbalances [12]. When there is concern for metabolic or respiratory disturbance, an arterial blood gas test may be considered [10]. Basic laboratory tests, including CBC, CRP, urine and blood cultures, are indicated when there is suspicion of underlying infections [2,4]. Beta HCG levels may be measured in pediatric seizures because a rare cause of seizures in children is a brain tumor called a germinoma, which secretes beta HCG. Beta HCG can be detected in blood or cerebrospinal fluid (CSF) to help confirm the diagnosis. Ammonia, Lactate, Pyruvate, if an inborn error of metabolism is suspected, these tests may be performed [2]. Antiepileptic drug levels should be measured in children with known seizure disorders to ensure they are receiving an appropriate dose. Under-dosing can result in continued seizures, while overdosing can lead to side effects such as drowsiness, nausea, or confusion. A toxicology screen may be ordered if there is a concern for drug or alcohol use [12].

Imaging studies such as CT or MRI should be considered for children with focal seizures, persistent seizures despite acute management, or seizures in children under six months of age [4,6]. Signs of elevated intracranial pressure (ICP) also warrant imaging, especially in the context of a history of bleeding disorders or anticoagulant use. Although MRI provides superior anatomic detail, it often requires sedation, which can interfere with the patient’s assessment, making CT the preferred initial imaging study.

Lumbar puncture is recommended for infants aged 6 to 12 months who have not received adequate vaccination against H. influenzae or Streptococcus pneumoniae, or whose vaccination status is unknown, as these bacteria are common causes of bacterial meningitis in this age group [6]. Additionally, lumbar puncture should be considered in infants receiving active antibiotic therapy, as antibiotics can mask meningeal signs. Infants with focal or prolonged seizures, abnormal neurological examinations, or toxic appearance are high-risk groups in which lumbar puncture is strongly advised.

An electroencephalogram (EEG) is a non-invasive test that measures electrical activity in the brain and is crucial for identifying seizure activity and epileptiform discharges [5,6,18]. It aids in classifying seizure disorders, such as generalized or partial seizures, and can detect specific patterns associated with particular epilepsy syndromes [18]. Ideally, an EEG should be performed within 24 hours of the seizure to maximize its diagnostic utility [6].

Risk Stratification

The range of potential causes for non-febrile seizures in pediatric patients is broad, including metabolic imbalances, mass lesions, and non-accidental trauma. One specific diagnosis that is relatively common in children under 6 months of age and easily detectable to prevent extensive invasive testing is hyponatremia caused by formula over-dilution. In the emergency department, 3 ml/kg of 3% hypertonic saline is the mainstay of therapy.

A first febrile seizure is concerning and requires prompt evaluation and management [16]. It may be a sign of an underlying medical condition. Some factors increase the risk of bacterial infection, such as age less than 6 months or more than 60 months with the first febrile seizure, or age less than 12 months with incomplete or unknown immunization history. In addition, a first febrile seizure in a clinically unwell child with symptoms of infection, meningeal signs, or dehydration may indicate a more serious underlying condition and requires urgent medical attention.

Febrile status epilepticus, which is a prolonged seizure lasting more than 30 minutes or a series of seizures without full recovery between them, is another potential complication that can occur in the context of a febrile illness. It is important to recognize the signs and symptoms of febrile status epilepticus, such as a fever, stiff neck, or convulsions, and seek immediate medical attention to prevent serious neurological damage.

Management

The management of pediatric seizures in the emergency department primarily focuses on stabilizing the patient, treating the underlying cause, and preventing further seizures or complications [16,19]. The initial management of an actively seizing child includes ensuring that the child’s airway is protected and providing adequate oxygen and circulatory support. Oxygen can be supplied via a nasal cannula or simple face mask, and preparations for endotracheal intubation should be made if airway management requires escalation. The next step is to assess vital signs and check blood glucose levels to rule out hypoglycemia. Intravenous (IV) or intraosseous (IO) access should be established promptly, and the patient should be connected to a monitor by this stage. In febrile seizures, antipyretic therapy is the mainstay of treatment to relieve symptoms and is usually sufficient. Seizures lasting 15 minutes or longer should be managed in accordance with status epilepticus protocols, with the goal of rapidly stopping the seizure using antiepileptic medications to prevent permanent neuronal injury.

A seizure lasting 5 minutes is highly likely to be prolonged; thus, most protocols use a 5-minute definition. Initial management includes maintaining airway, breathing, and circulation (ABCs), administering oxygen, and preparing for intubation if required [16,19]. Hypoglycemia, defined as a capillary blood glucose (CBG) level of less than 60 mg%, should be corrected with a bolus of IV 10% dextrose at 5 mL/kg; this can be repeated to normalize serum glucose levels. IV or IO access should be secured, and blood samples should be sent for investigations. Benzodiazepines are the first-line antiepileptic agents. Options include intramuscular (IM) Midazolam (10 mg for patients >40 kg; 5 mg for patients 13–40 kg), IV Lorazepam (0.1 mg/kg/dose, maximum 4 mg/dose; can be repeated once), or IV Diazepam (0.15–0.2 mg/kg/dose, maximum 10 mg/dose; can be repeated once). If these are not feasible, IV Phenobarbital (15 mg/kg/dose as a single dose), rectal Diazepam (0.2–0.5 mg/kg, maximum 10 mg/dose; can be repeated once), or intranasal/buccal Midazolam may be used.

If first-line therapy is unsuccessful, second-line agents should be administered. Options include IV Fosphenytoin (20 mg PE/kg, maximum 1,500 mg PE/dose as a single dose), IV Valproic Acid (40 mg/kg, maximum 3,000 mg/dose as a single dose), or IV Levetiracetam (60 mg/kg, maximum 4,500 mg/dose as a single dose). IV Phenobarbital (15 mg/kg as a single dose) is another option if other agents are not appropriate. If first- and second-line therapies fail, anesthetic doses of Thiopental, Midazolam, Phenobarbital, or Propofol can be administered. This requires continuous EEG monitoring.

If the patient responds to any of these agents and returns to baseline, symptomatic medical therapy should be initiated. Management of non-convulsive status epilepticus follows a similar approach to that of convulsive status epilepticus. (Figure 1) [20]

In neonates, the same stabilization principles apply, including maintaining ABCs, collecting blood samples, and checking and correcting electrolytes [16]. IV Phenobarbitone (20 mg/kg) is administered as the first-line antiepileptic; this can be repeated in 5 mg/kg boluses every 15 minutes (maximum dose of 40 mg/kg) until the seizure is aborted. If the seizure persists, IV Phenytoin (15–20 mg/kg), diluted in equal parts with normal saline, should be administered at a maximum rate of 1 mg/kg/min over 35–40 minutes.

If the seizure remains unresolved, IV Lorazepam (0.05–0.1 mg/kg) or Diazepam (0.25 mg/kg bolus or 0.5 mg/kg rectal) may be used. Alternatively, IV Midazolam can be administered as a continuous infusion; this involves an initial IV bolus of 0.15 mg/kg followed by a continuous infusion starting at 1 μg/kg/min, increasing by 0.5–1 μg/kg/min every 2 minutes (maximum 18 μg/kg/min). Lastly, if all else fails, 100 mg IV or oral Pyridoxine may be administered. This is particularly useful for treating Pyridoxine-dependent neonatal seizures or seizures caused by Isoniazid (INH) toxicity. (Figure 2) [21].

When To Admit This Patient

In most cases, hospitalization is not necessary after a first unprovoked seizure, provided that a neurological examination is normal and prompt follow-up evaluation can be arranged [13]. Consultation with a neurologist and electroencephalography (EEG) can typically be performed on an outpatient basis. However, children who have experienced a prolonged seizure or who do not return to their baseline state within a few hours should be admitted to the hospital.

Hospitalization should also be considered in cases of extreme parental anxiety or if adequate follow-up evaluation cannot be arranged. It is essential to counsel parents about the increased likelihood of recurrence, which is approximately 33% overall. The risk of recurrence is higher in children under 18 months of age, when the temperature during the first convulsion is below 40°C, when the first seizure occurs within an hour of the onset of fever, or if there is a family history of febrile seizures.

Revisiting Your Patient

Our patient was immediately moved to the resuscitation unit, placed on a simple face mask, and connected to monitors. She was administered rectal Diazepam; however, the seizure did not resolve. By this time, intraosseous (IO) access was established, and 0.1 mg/kg of Lorazepam (same as the IV dose) was given. This successfully aborted the seizure.

At this point, her vitals were as follows: temperature (T) 40°C, heart rate (HR) 93, respiratory rate (RR) 29, and blood pressure (BP) 118/90. She was lethargic and responsive only to painful stimuli. Other notable findings on examination included a full and tense anterior fontanelle, questionable neck rigidity, red and bulging tympanic membranes, reactive but unfocused pupils, a normal heart, lungs, and abdomen, good color and perfusion, and no petechiae or rashes. The patient displayed weak movement in all limbs and hyperactive deep tendon reflexes.

Pediatrics was consulted, and a presumptive diagnosis of meningitis was made. A complete blood count (CBC), C-reactive protein (CRP), blood culture, and chemistry panel were drawn. IV access was established at this point. Since increased intracranial pressure (ICP) was suspected, a lumbar puncture (LP) was initially deferred, and she was immediately given 500 mg of IV Ceftriaxone. A stat CT scan of the brain was normal, so an LP was performed, revealing visibly turbid cerebrospinal fluid (CSF).

The CSF analysis showed a white blood cell (WBC) count greater than 1000 cells/μL, with 95% neutrophils and 5% monocytes, a total protein level of 75 mg/dL, and a glucose level of 25 mg/dL. A Gram stain of the CSF revealed numerous WBCs and a few gram-positive cocci. She was admitted to the pediatric intensive care unit (PICU) for further management.

Authors

Neema Francis

Dr. Neema Francis was born and raised in Dubai, UAE. She is currently a fourth-year emergency medicine resident at Tawam Hospital. She graduated with an MBBS from Gulf Medical University in 2020 and completed her internship at Sheikh Shakbout Medical City in 2021. Dr. Francis has a passion for volunteering and has been involved in various healthcare initiatives. She is also a competent researcher with publications to her name and a keen interest in emergency medicine and pediatric emergency medicine.

Faiz Ahmad

Thiagarajan Jaiganesh

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

Listen to the chapter

References

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Fine A, Wirrell EC. Seizures in children. Pediatr Rev. 2020;41(7):321-347. doi:10.1542/pir.2019-0134.
Sidhu R, Velayudam K, Barnes G. Pediatric seizures. Pediatr Rev. 2013;34(8):333-342. doi:10.1542/pir.34-8-333.
Lambert MV, Robertson MM. Depression in epilepsy: etiology, phenomenology, and treatment. Epilepsia. 2002;43(Suppl 2):21-27. doi:10.1046/j.1528-1157.43.s.2.3.x.
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Reviewed and Edited By

Arif Alper Cevik, MD, FEMAT, FIFEM

Transient Cerebral Ischemia (2024)

December 27, 2024December 27, 2024 ~ iEM Education Project Team ~ Leave a comment

by Omer Jaradat & Haci Mehmet Caliskan

You Have A New Patient!

A 63-year-old male is brought to the Emergency Department (ED) by paramedics with a chief complaint of transient right-sided weakness. He states that the weakness started suddenly while he was watering his garden, lasted about 15 minutes, and then resolved without any residual deficits. On examination, his temperature is 36°C, blood pressure is 150/90 mmHg, pulse is 81 beats/min, respiratory rate is 18 breaths/min, and oxygen saturation is 97% on room air.

The patient’s past medical history is remarkable for hypertension, diabetes mellitus, and hyperlipidemia. He also smokes half a pack of cigarettes daily.

What Do You Need To Know?

Importance

Transient Cerebral Ischemia (TCI) or Transient Ischemic Attack (TIA) is defined as a sudden onset of transient, focal neurological symptoms and/or signs that occur due to focal brain, spinal cord, or retinal ischemia, without acute infarction [1]. Neurological symptoms and signs are related to the ischemic area of the brain. TIA is a neurologic emergency because patients with TIA have an early high risk of subsequent stroke. Up to 80% of strokes after TIA are preventable. Therefore, early recognition and differentiation of TIA cases are important for early treatment, which reduces the possibility of stroke. In brief, TIA represents a great opportunity for the physician to prevent stroke. Early diagnosis and treatment are the key.

Epidemiology

TIA is an important clinical condition that is common worldwide. The total global incidence of TIA is approximately 1.19 per 1000 persons per year, and it has been observed that the incidence is higher (4.88 per 1000 persons) in older age groups (85–94 years) [2]. TIA is more common in Black and male populations than in White and female populations [3].

Pathophysiology

TIA is mainly caused by three mechanisms of pathophysiology: (1) intrinsic vascular (lacunar or small vessel) pathogenesis such as atherosclerosis, lipohyalinosis, inflammation, and amyloidosis; (2) embolism originating from the heart and extracranial large vessels; and (3) low-flow conditions such as insufficient blood flow to the brain, decreased perfusion pressure, and increased blood viscosity [4].

(1) Lacunar or small vessel TIA: These TIAs are usually due to atherosclerosis of the proximal vessels or lipohyalinosis of the distal vessels. Small vessel TIAs cause symptoms similar to the lacunar strokes that are likely to follow, such as weakness or numbness in the arms, legs, and face, which are recurrent and progressive.

(2) Embolic TIAs: These are characterized by a relatively longer duration of focal neurological symptoms. These TIAs are mostly the result of embolism from a specific source. Embolism can originate from larger arteries or from the heart. In one study, it was determined that the symptoms of embolic TIAs lasted longer (hours) than those of low-flow TIAs (lasting minutes) [5].

TIAs create specific symptoms according to the regions of the occluded vessel:

Anterior circulation embolic TIA: Larger emboli can occlude the middle cerebral artery stem and cause contralateral hemiplegia, cortical surface symptoms (aphasia and dysexecutive syndromes in the dominant hemisphere, anosognosia or neglect in the nondominant hemisphere). Smaller emboli can occlude branches of the middle cerebral artery and cause focal symptoms such as numbness, weakness, and/or heaviness of the hand and arm.
Posterior circulation embolic TIA: These emboli can cause transient ataxia, diplopia, dizziness, dysarthria, hemianopsia, quadrantanopia, numbness, and unilateral hearing loss. If the embolus lodges at the top of the basilar artery, stupor or coma may occur. If the embolus lodges in the distal branches of the posterior cerebral artery, it can cause memory loss or a homonymous field defect.

(3) Low-flow TIA occurs with an obstructive vascular process in any extracranial or intracranial artery and disruption of collateral flow in the area supplied by these arteries. Low-flow TIAs are usually of short duration (minutes) and recurrent [4].

Anterior circulation low-flow TIA: These TIAs usually produce symptoms of a similar character. They occur due to hemodynamically significant stenotic lesions, especially in the proximal internal carotid artery, middle cerebral artery, and internal carotid artery, where collateral flow from the circle of Willis is insufficient. Ischemia-related symptoms resulting from these lesions usually include weakness or numbness in the hands, arms, legs, face, tongue, and/or cheek. Recurrent aphasic syndromes occur when there is focal ischemia in the dominant hemisphere, and recurrent neglect occurs when there is focal ischemia in the nondominant hemisphere. Limb-shaking TIAs are a rare but classic hypoperfusion syndrome in which repetitive jerking movements of the arm or leg are due to severe stenosis or occlusion of the contralateral internal carotid or middle cerebral artery.
Posterior circulation low-flow TIA: Unlike anterior low-flow TIA, the symptoms of these TIAs are not stereotypical because many neuronal structures in the brainstem are located very close to each other. Posterior low-flow TIA symptoms include diplopia, eyelid drooping, inability to look up, dysarthria, dizziness, drowsiness, bilateral leg and arm weakness or numbness, a feeling of heaviness, and numbness on one side of the body or face.

The diagnosis of TIA is based on the clinical features of the transient neurological attack and neuroimaging findings [6]. The majority of TIA cases do not present when fully symptomatic. For this reason, the history reported by the patient and witnesses is very important in terms of diagnosis [7]. TIA patients may experience typical or atypical symptoms.

Typical TIA:

It consists of focal neurological symptoms of sudden onset and transient character, localized to a single vascular region in the brain. These symptoms include aphasia or dysarthria, transient monocular blindness (amaurosis fugax), hemianopia, hemiparesis, and/or hemisensory loss. In such cases, the probability of ischemia is relatively high. However, these symptoms may also occur due to non-ischemic causes such as seizures, migraines, and intracerebral hemorrhage.

Atypical TIA:

Clinical characteristics of transient symptoms considered to be atypical of an ischemic attack include the following [8-10]:

Gradual progression of symptoms.
Change of symptoms from one type to another.
Disturbance of vision in both eyes, characterized by the occurrence of positive phenomena (positive symptoms are not normally experienced by most individuals and reflect an excess of normal functions, such as flashing lights).
Isolated sensory symptoms with a focal distribution, especially in areas such as a finger, chin, or tongue.
Attacks lasting less than 30 seconds.
Isolated brainstem symptoms such as dysarthria, diplopia, or hearing loss.
Amnesia and confusion.
Incoordination of limbs.

Atypical TIAs with negative symptoms (negative symptoms mean loss of a neurological function, such as hearing loss or vision loss) have a high risk of recurrent stroke. For this reason, they should be handled and treated as typical TIAs [4].

Medical History

The most important question is the time of symptom onset because it guides the treatment. Patients and/or their relatives should also be questioned about neurological diseases and symptoms (such as migraine, epilepsy, previous attacks similar to this one, syncope, etc.), cardiovascular diseases (such as myocardial infarction, atrial fibrillation, carotid stenosis, etc.), metabolic disorders (such as diabetes, hyperlipidemia, etc.), hypertension, drug usage, smoking, and family history of cardiac and/or neurological diseases.

Important points regarding the medical history of patients with TIA: Cardiovascular diseases, previous history of neurological attack or stroke, and drug usage.
Risk factors for TIA: Older age, atrial fibrillation, atherosclerosis, diabetes mellitus, hypertension, hyperlipidemia, smoking, history of stroke, male gender, and Black race.
Prognosis of TIA patients: The prognosis is defined by the risk of recurrent stroke. The risk of stroke after TIA varies according to several factors, including the time elapsed since the last TIA, the presence of vascular pathologies, and the presence of acute infarction on diffusion-weighted magnetic resonance imaging (DW-MRI). Stroke is most likely to occur in the first week after a TIA, with a 1.5–3.5% risk in the first 48 hours. Within 90 days, the risk of stroke rises to 40% [11–14]. Vascular pathologies such as large artery atherosclerosis, small artery disease, and cardio-embolic conditions increase the risk of recurrent stroke. Additionally, the presence of acute lesions on DW-MRI or chronic ischemic lesions on computed tomography (CT) increases the likelihood of recurrent stroke in TIA patients.

Physical Examination

A detailed neurological evaluation should be performed on the patient, including assessment of cranial nerves, strength and sensation, visual fields, language, gait, and coordination. A focal neurological deficit on exam should raise suspicion for TIA. In addition to the neurological exam, it is important to perform a thorough cardiovascular exam, listening closely for irregular rhythms, murmurs, and bruits on the carotids.

Red flags: Bruits on the carotids, the presence of negative symptoms, and irregular rhythms.

Alternative Diagnoses

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

Seizures, migraines, metabolic disorders such as hypoglycemia, subarachnoid or intracerebral hemorrhage, subdural hematoma, syncope, and central nervous system (CNS) demyelinating disorders such as multiple sclerosis, etc., should come to mind in the differential diagnosis of TIA.

Which findings make TIA more probable?

Sudden onset of typical symptoms, presence of negative symptoms, and normal laboratory and imaging findings.

Which risk factors and findings make other diagnoses more probable or make this diagnosis less probable?

We can differentiate syncope, epileptic seizures, CNS demyelinating disorders, and migraine aura with a detailed history. In the differentiation of seizures, the lactate value in an arterial blood gas (ABG) test is also important. High lactate levels support the diagnosis of seizures. Intracranial hemorrhages and subdural hematomas have specific imaging findings.

Acing Diagnostic Testing

Bedside Tests

First, vital signs (body temperature, pulse rate, respiration rate, blood pressure, and peripheral oxygen saturation) of the patient should be measured and recorded. Then, as the first approach, in all patients presenting with neurological symptoms, the measurement of blood glucose at the bedside, along with checking electrolytes, PO2, PCO2, and lactate values in an arterial blood gas (ABG) test, and performing electrocardiography (ECG), are very valuable in terms of diagnosis and differential diagnosis.

Laboratory Tests

Complete blood count (CBC), biochemistry, and coagulation tests are usually performed in addition to blood glucose measurement and ABG. These tests are useful in distinguishing metabolic disorders such as hypoglycemia from TIA. Impaired coagulation tests are also helpful in guiding diagnosis and treatment.

Imaging

Patients who are symptomatic should be considered as having a stroke. A non-contrast head CT scan can be used to assess early ischemic signs and exclude intracerebral hemorrhage. In TIA, CT has low sensitivity and usually does not show any pathological findings. If CT is negative for mass lesions and intracranial hemorrhage, computed tomography angiography (CTA) and/or magnetic resonance angiography (MRA) can be used to investigate intracranial and extracranial vascular occlusions. If CTA and/or MRA are negative for large vessel occlusion and TIA is suspected, MRI should be obtained to evaluate for signs of ischemia/infarction. DW-MRI following MRI is the gold standard for acute ischemic stroke and distinguishes stroke from TIA. DW-MRI is valuable because it shows focal areas of cytotoxic edema, which are seen in acute stroke.

Risk Stratification

The ABCD2 score (age, blood pressure, clinical features, duration, and the presence of diabetes mellitus) is commonly used to determine stroke risk following TIA. Parameters evaluated in the ABCD2 score assign scores for certain clinical features (speech impairment and unilateral weakness) and duration of symptoms, in addition to risk factors such as age, blood pressure, and diabetes. However, studies have found that the ABCD2 score does not reliably distinguish between those with a low and high risk of recurrent stroke.

Alternatively, the Canadian TIA Score uses variables routinely obtained in the ED setting to classify patients into minimal, low, high, or critical risk categories, which are associated with the likelihood of developing a stroke in the week following a TIA. Using the Canadian TIA Score strikes a balance by allowing risk stratification based on history, clinical data points, and neuroimaging, and defines clear follow-up actions based on the patient’s predictive score. Compared to the ABCD2 score, the Canadian TIA Score has shown better predictability [15].

However, there are not enough studies on the Canadian TIA Score. For this reason, a risk stratification score alone should not be used to determine the management of patients. Instead, the decision regarding hospitalization versus discharge should be made within the greater clinical context.

Management

Initial Stabilization

In all patients presenting to the Emergency Department, the initial assessment should involve the “ABCDE” approach (assessment of Airway, Breathing, Circulation, Disability, and Exposure). If the patient is alert and responds with a normal voice, the airway is open. However, if there is no respiration despite effort, the airway must be secured by checking for a foreign body, performing airway-opening maneuvers (head-tilt and chin-lift or jaw-thrust), suctioning the airway, or even intubating if necessary. In TIA patients, altered mental status is a common cause of airway obstruction [16]. If breathing is insufficient and oxygen saturation is below 94%, supplemental oxygen should be administered [17].

Altered mental status could be a sign of decreased perfusion, so obtaining intravenous access and starting IV fluids, if indicated, should be performed (the best choice is isotonic fluid). Blood pressure measurements, performing an EKG, and auscultation for abnormal heart sounds, murmurs, and carotid bruits can provide clues to the etiology of the TIA. Patients should be evaluated for disability using the Glasgow Coma Score (GCS), evaluation of pupillary light reflexes, and checking for signs of lateralization.

As hypoglycemia is considered a TIA mimic, it must be checked and corrected immediately, and hyperglycemia should also be prevented. Patients should be evaluated for drug intake and toxic ingestions. All patients with impaired consciousness should undergo a complete physical examination, which includes removing their clothes to search for signs of bleeding, foreign bodies, and trauma [16].

Medications

Treatment is started according to risk stratification.

If the ABCD2 score is ≥4: Dual antiplatelet therapy (DAPT) is started.
- Aspirin (160 to 325 mg loading dose, followed by 50 to 100 mg daily) plus clopidogrel (300 to 600 mg loading dose, followed by 75 mg daily)
- Alternatively, aspirin (300 to 325 mg loading dose, followed by 75 to 100 mg daily) plus ticagrelor (180 mg loading dose, followed by 90 mg twice daily).

If the ABCD2 score is <4: Aspirin monotherapy is started.
- Aspirin (162 to 325 mg daily) [18, 19].

According to the Canadian TIA Score, patients are divided into four risk groups and managed as follows:

Minimal and Low Risk: Refer the patient to rapid outpatient assessment with a neurologist.

High Risk:

Start or switch to DAPT (clopidogrel or dipyridamole + ASA).
Initiate or control hypertension management.
Refer the patient to neurology within 24 hours.

Critical Risk:

Start or switch to DAPT (clopidogrel or dipyridamole + ASA).
Start oral anticoagulation if the patient has atrial fibrillation.
Start a statin class medication.
Initiate or optimize control of hypertension.
Admit the patient to the hospital and ensure referral to neurology within 24 hours [20].

Procedures

In patients with ongoing and disabling symptoms, emergent evaluation for IV thrombolysis and mechanical thrombectomy should be performed. Selected patients with recently symptomatic cervical internal carotid artery stenosis can significantly benefit from early carotid endarterectomy (within two weeks of a non-disabling stroke or TIA) [21].

Special Patient Groups

Stroke is a rare condition in the pediatric population, but all principles that apply to adults also apply to the pediatric population. Because the incidence of stroke increases with age, physicians should consider stroke in the management of undifferentiated geriatric patients.

In pregnant patients, physiological changes increase the risk of stroke, and there is significant maternal morbidity and mortality associated with stroke. However, a transient ischemic attack (TIA) is not a type of pregnancy-associated stroke, but it should be noted that TIAs precede strokes in up to 15% of cases [22].

When To Admit This Patient

Because of the high risk of stroke after TIA, patients diagnosed with TIA should be hospitalized for further etiological investigation and treatment.

Only selected patients with a completely normal physical examination, no ongoing disability, normal imaging (including MRI), and a low-risk score can be discharged if their neurology outpatient clinic visit is imminent and after aspirin therapy is started.

Discharged patients should be informed about TIA symptoms and encouraged to call Emergency Medical Services (EMS) and/or go to the nearest Emergency Department if these symptoms begin.

The main symptoms of a TIA can be remembered with the acronym FAST:

Face – Drooping or numbness on one side of the face, inability to smile, or if the mouth or eye has drooped.
Arms – Inability to lift both arms and keep them raised because of weakness or numbness in one arm.
Speech – Slurred speech, inability to talk at all despite appearing to be awake, or difficulty understanding speech.
Time – If any of these signs or symptoms is present, call Emergency Medical Services (EMS) immediately.

Revisiting Your Patient

The ABCDE approach was initiated as soon as the patient entered the ED. Since he is awake and does not show signs of difficulty breathing, his airway is considered open, and his breathing is considered normal.

Blood pressure is high, but pulse is within normal ranges. No murmur, abnormal sounds, or carotid murmur is detected on auscultation. Since hypoglycemia and hyperglycemia can mimic TIA, a bedside glucose level was measured and found to be 110 mg/dL (6.1 mmol/L).

A focused neurological examination was performed: pupils are equal and reactive, facial expressions appear appropriate, there is no drooping, and there is no slurring of speech. Muscle strength in his right arm is decreased, and muscle strength in his right leg is slightly decreased. There is no sensory deficit. The rest of the physical exam is unremarkable.

An electrocardiogram (EKG) was requested to check for acute pathologies and arrhythmias, such as atrial fibrillation, which is important in the etiology of TIA, and it demonstrates sinus rhythm. Since the history and physical examination are typical for an acute cerebrovascular accident, an intravenous (IV) catheter was inserted, and complete blood count (CBC), plasma urea nitrogen, creatinine, electrolytes, cardiac enzymes, and coagulation parameters (prothrombin time, activated partial thromboplastin time, and international normalized ratio [INR]) were ordered.

To exclude bleeding, the patient underwent a non-contrast brain tomography, which was interpreted as normal. The ABCD2 score was found to be ≥6. The patient was consulted with the neurology department. No focal neurological signs were detected in serial physical examinations. Thrombolytic therapy was not considered because the symptoms resolved, and the imaging was normal.

However, because the patient’s complaints were typical of stroke and/or TIA, due to comorbid diseases, and because he is not on antiplatelet therapy, he is considered to have a high risk for stroke. As a result, dual antiplatelet therapy (DAPT) was started, and the patient was transferred to the neurology service for further examination and treatment to elucidate the etiology.

Recommended Free Open Access Medical Education (FOAM) resources

Zink J. (2022). Syncope and Syncope Mimics. EmDocs. Retrieved from http://www.emdocs.net/syncope-and-syncope-mimics/
Chapman S. (2023). The Utility of MRI in the ED. EmDocs. Retrieved from http://www.emdocs.net/the-utility-of-mri-in-the-ed/
Lanata E.P. (2021). TIA: Emergency Department Evaluation and Disposition. EmDocs. Retrieved from http://www.emdocs.net/tia-emergency-department-evaluation-and-disposition/
Rezaie S. (2021). “Rebellion21: Canadian TIA Risk Score vs ABCD2”. REBEL EM blog. Retrieved from https://rebelem.com/rebellion21-canadian-tia-risk-score-vs-abcd2/

Authors

Omer Jaradat

Dr. Omer Jaradat is an Emergency Medicine Physician at Ahi Evran University Training and Research Hospital, Kirsehir, Türkiye. He is an enthusiast of emergency medicine and strongly believes in the generalist and collective approach of the specialty. He is particularly interested in global emergency medicine, emergency medicine education, and innovation. A dedicated follower and contributor to #FOAMed, he feels proud to be a member of the emergency medicine community.

Elizabeth DeVos

Dr. Haci Mehmet Caliskan is an Associate Professor of Emergency Medicine and an academician at Ahi Evran University, Kirsehir, Türkiye. He is deeply interested in emergency medicine education and is passionate about engaging students in the emergency medicine community. He is an advocate for fair and equitable medical care. His current professional interests include cardiovascular diseases, pulmonary medicine, and trauma. He takes Atatürk as an example in both his professional and social life.

Listen to the chapter

References

Easton JD, Saver JL, Albers GW, et al. Definition and evaluation of transient ischemic attack: a scientific statement for healthcare professionals from the American Heart Association/American Stroke Association Stroke Council; Council on Cardiovascular Surgery and Anesthesia; Council on Cardiovascular Radiology and Intervention; Council on Cardiovascular Nursing; and the Interdisciplinary Council on Peripheral Vascular Disease. The American Academy of Neurology affirms the value of this statement as an educational tool for neurologists. Stroke. 2009;40(6):2276-2293. doi:10.1161/STROKEAHA.108.192218
Lioutas VA, Ivan CS, Himali JJ, et al. Incidence of Transient Ischemic Attack and Association With Long-term Risk of Stroke. JAMA. 2021;325(4):373-381. doi:10.1001/jama.2020.25071
Kleindorfer D, Panagos P, Pancioli A, et al. Incidence and short-term prognosis of transient ischemic attack in a population-based study. Stroke. 2005;36(4):720-723. doi:10.1161/01.STR.0000158917.59233.b7
Rost NS, Faye EC. Definition, etiology, and clinical manifestations of transient ischemic attack. Post TW, ed. UpToDate. Waltham, MA: UpToDate Inc. http://www.uptodate.com. (Accessed on January 20, 2023.)
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Sorensen AG, Ay H. Transient ischemic attack: definition, diagnosis, and risk stratification. Neuroimaging Clin N Am. 2011;21(2):303-x. doi:10.1016/j.nic.2011.01.013
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Special report from the National Institute of Neurological Disorders and Stroke. Classification of cerebrovascular diseases III. Stroke. 1990;21(4):637-676. doi:10.1161/01.str.21.4.637
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Wu CM, McLaughlin K, Lorenzetti DL, Hill MD, Manns BJ, Ghali WA. Early risk of stroke after transient ischemic attack: a systematic review and meta-analysis. Arch Intern Med. 2007;167(22):2417-2422. doi:10.1001/archinte.167.22.2417
Shahjouei S, Sadighi A, Chaudhary D, et al. A 5-Decade Analysis of Incidence Trends of Ischemic Stroke After Transient Ischemic Attack: A Systematic Review and Meta-analysis [published correction appears in JAMA Neurol. 2021 Jan 1;78(1):120]. JAMA Neurol. 2021;78(1):77-87. doi:10.1001/jamaneurol.2020.3627
Chandratheva A, Mehta Z, Geraghty OC, Marquardt L, Rothwell PM; Oxford Vascular Study. Population-based study of risk and predictors of stroke in the first few hours after a TIA. Neurology. 2009;72(22):1941-1947. doi:10.1212/WNL.0b013e3181a826ad
Perry JJ, Sivilotti MLA, Émond M, et al. Prospective validation of Canadian TIA Score and comparison with ABCD2 and ABCD2i for subsequent stroke risk after transient ischaemic attack: multicentre prospective cohort study [published correction appears in BMJ. 2021 Feb 18;372:n453]. BMJ. 2021;372:n49. Published 2021 Feb 4. doi:10.1136/bmj.n49
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Reviewed and Edited By

Arif Alper Cevik, MD, FEMAT, FIFEM

Head Trauma (2024)

December 21, 2024December 26, 2024 ~ iEM Education Project Team ~ Leave a comment

by Emranur Rahman & Mansoor Husain

You Have A New Patient!

A 22-year-old male with no significant medical history presented to the emergency department two hours after a motorbike accident. He had been riding at a moderate speed when he lost control of the bike and fell, striking his head on the pavement. He briefly lost consciousness and experienced a sharp headache immediately following the fall, along with mild dizziness, nausea, and vomiting. He denied any neurological deficits at the scene; however, by the time he arrived at the hospital, he reported the onset of right-sided weakness and numbness.

Upon examination, the patient appeared anxious and in moderate distress due to the headache. His vital signs were stable, with a blood pressure of 130/85 mmHg, a heart rate of 88 bpm, and a respiratory rate of 18 breaths per minute.

What Do You Need To Know?

Importance

Appropriate head trauma management in the emergency department (ED) is crucial because head injuries can range from mild concussions to severe traumatic brain injuries (TBI) that may lead to permanent disability or death if not appropriately managed.

The importance of correct management in the ED includes early identification of life-threatening Injuries. Rapid assessment and intervention are essential to identify severe conditions such as intracranial hemorrhage, skull fractures, or brain contusions. It also helps in prevention of secondary brain injury. Secondary brain injury can result from hypoxia, hypotension, or elevated intracranial pressure (ICP), and can worsen the outcome of the initial trauma.

The survival and neurological outcome of patients suffering from TBI depend on the extent of the primary injury and the subsequent secondary injuries sustained [1].

Epidemiology

Head trauma is a significant global health issue, contributing to a high burden of morbidity, mortality, and long-term disability.

The most common causes of head injuries are motor vehicle collision (MVC), falls from a significant height, physical assault, and occupational injury [2].

TBI affects all age groups, but young adults (15-44 years) are particularly vulnerable, often due to motor vehicle accidents (MVAs) and violence. Males are disproportionately affected, with a male-to-female ratio of about 2:1, likely due to higher-risk behaviors and occupations. Gunshot wounds are the most lethal mechanism, with a mortality rate of approximately 90% [1].

Pathophysiology

The pathophysiology of brain injury is complex and multifaceted, involving both primary and secondary injury mechanisms. The primary injury occurs at the moment of impact and is characterized by mechanical damage to brain tissues, such as axonal shearing or bleeding internally, which is not amenable to acute intervention [3]. Secondary injury, however, involves a cascade of biochemical, molecular, and structural changes that unfold over time, leading to further neuronal damage and dysfunction [3,4]. These secondary processes include glutamatergic excitotoxicity, loss of autoregulation, elevated intracranial pressure, and cortical spreading depression, which can result in seizures [5].

Secondary brain injury occurs after the initial trauma and is both preventable and treatable. Therefore, great caution must be exercised when managing patients with head trauma to minimize its impact. Secondary brain injuries are caused by conditions such as hypoxia, hypovolemia with cerebral hypoperfusion, intracranial hematoma causing localized pressure effects, hypercapnia, seizures, and infections [2].

Medical History

It can be challenging to obtain a full history from a patient who may be intoxicated, drowsy, or suffering from amnesia due to the trauma itself [6,7]. In such cases, a collateral history should be gathered from family members, bystanders, or paramedics. Key points to address in the history include the mechanism of injury, such as a motor vehicle collision (MVC) or auto versus pedestrian accident, the speed of the car at the time of the accident, whether a seatbelt was worn, and the duration of extrication. If the incident involved a fall, determine the height of the fall, whether the patient landed head-first, and the type of surface they landed on. Timing is also critical—establish exactly when the incident occurred. Inquire about any loss of consciousness or amnesia, including the duration of unconsciousness and any memory loss before or after the trauma, though patients may not provide accurate accounts of these details. Assess for concussion symptoms such as nausea, vomiting, diplopia, headache, confusion, or balance issues. Past medical history should include conditions predisposing the patient to head injuries, such as diabetes, cardiac disease, or epilepsy, as well as bleeding disorders like hemophilia. Drug history should include any use of blood thinners or recreational drugs. Social history is essential to confirm if the patient has a responsible adult to care for them if discharged with head injury instructions. Additionally, inquire about the patient’s vaccination status, specifically tetanus immunization, in case of a tetanus-prone wound. Ask about any medication or contrast allergies. Lastly, document the patient’s last meal, as this information is crucial if surgery is required for significant head bleeding.

Physical Examination

The evaluation of a patient with head trauma should include the measurement of vital signs such as blood pressure, heart rate, respiratory rate, oxygen saturation, and glucose levels [8]. Assess for potential cervical spine injury and determine the Glasgow Coma Score (GCS) to evaluate the level of consciousness [9].

Choose the best response of patient
EYE OPENING
4: Spontaneously
3: To verbal command
2: To pain
1: No response

BEST VERBAL RESPONSE
5: Oriented and converses
4: Disoriented and converses
3: Inappropriate words; cries
2: Incomprehensible sounds
1: No response

BEST MOTOR RESPONSE
6: Obeys command
5: Localizes pain
4: Flexion withdrawal
3: Flexion abnormal (decorticate)
2: Extension (decerebrate)
1: No response

Glasgow Coma Score (GCS) (Modified from Teasdale, G., & Jennett, B. (1974). Assessment of coma and impaired consciousness: a practical scale. The Lancet, 304(7872), 81-84.) - Please read this article to get more insight regarding GCS.

Perform an eye examination to check pupil size and reactivity to light. Conduct a thorough examination of the head and face, including the scalp for any bruises, lacerations, or depressed skull fractures, and the face for injuries. Inspect the nose for signs of a septal hematoma. Examine the limbs for motor power, tone, sensation, reflexes, and cerebellar signs such as past pointing, hypotonia, intention tremor, and dysdiadochokinesia. Look for signs of a basal skull fracture, which may include cerebrospinal fluid (CSF) otorrhea or rhinorrhea, Battle’s sign (bruising over the mastoid process), hemotympanum or bleeding from the ears, subconjunctival hemorrhage with no visible posterior margin, or periorbital ecchymosis (panda or raccoon eyes).

Alternative Diagnoses

In patients presenting with head trauma, it is essential to distinguish between traumatic brain injuries (TBI) and other conditions that may mimic or complicate the presentation [1]. Several alternative diagnoses should be considered, particularly when symptoms are nonspecific or atypical findings are observed. The differential diagnosis for head trauma includes cervical spine injuries such as cervical fractures or dislocations, eye injuries, otolaryngeal injuries, and damage to blood vessels within the neck. Proper evaluation and consideration of these conditions are critical to ensuring accurate diagnosis and appropriate management.

Acing Diagnostic Testing

Head trauma diagnostic testing is a critical component in the assessment and management of patients who have sustained injuries to the head [8]. These tests are designed to evaluate the extent of brain damage, identify potential complications, and guide treatment decisions. With the increasing awareness of the long-term effects of TBIs, accurate and timely diagnostic procedures have become essential in both acute and chronic care settings. Techniques such as computed tomography (CT) scans, magnetic resonance imaging (MRI), and neurological assessments play a vital role in detecting structural abnormalities, bleeding, and other injuries.

Bedside Tests

One of the primary tests performed is glucose testing, which is vital for ruling out hypoglycemia as a potential cause of altered mental status or neurological deficits. Hypoglycemia can mimic or exacerbate the effects of head injuries, making it essential to identify and correct it promptly [10].

Laboratory Tests

Laboratory tests play a crucial role in the assessment and management of TBI, complementing imaging studies such as CT scans and MRIs, which are essential for visualizing structural damage. Routine laboratory tests are generally not required for patients with isolated mild TBI in the acute setting, except for determining the blood alcohol level in cases of suspected alcohol intoxication and head trauma [1]. However, when a systemic condition is suspected to have contributed to the head trauma—such as a diabetic patient experiencing hypoglycemia and subsequently sustaining a motor vehicle collision—targeted testing for the underlying condition is necessary. Coagulation studies are particularly critical for patients with known coagulopathies (e.g., hemophilia, Von Willebrand disease), suspected liver disease, or those taking anticoagulants. Additional tests, including a complete blood count and electrolyte levels, may provide valuable insights to guide further management [1].

Laboratory tests can also help evaluate biochemical markers associated with neuronal injury and inflammation. Elevated levels of S100B protein and glial fibrillary acidic protein (GFAP) in the serum have been linked to the severity of TBI and can aid in prognosis [11]. Furthermore, biomarkers such as ubiquitin carboxy-terminal hydrolase L1 (UCH-L1) and neuron-specific enolase (NSE) have shown promise in differentiating between mild and severe TBI, potentially guiding treatment decisions [12]. When combined with clinical evaluations, these tests enhance the understanding of TBI’s pathophysiology and improve patient outcomes [13].

Imaging

Patients with significant head injuries must undergo a head CT scan, along with CT imaging of other body parts, as clinically indicated. Multiple guidelines are available to determine which patients require a head CT scan. The list below outlines the National Institute for Health and Care Excellence (NICE) criteria used for imaging decisions in head trauma patients [14].

Patients aged 16 and above with head trauma should undergo a head CT within an hour if any of the following criteria are present:

A Glasgow Coma Scale (GCS) score of 12 or less on initial assessment in the emergency department.
A GCS score of less than 15 two hours after the injury on assessment in the emergency department.
Suspected open or depressed skull fracture.
Any signs of basal skull fracture (e.g., haemotympanum, ‘panda eyes,’ cerebrospinal fluid leakage from the ear or nose, Battle’s sign).
Post-traumatic seizure.
Focal neurological deficit.
More than one episode of vomiting.

Patients under the age of 16 with head trauma should also undergo a head CT within an hour if any of the following criteria are present:

Suspicion of non-accidental injury.
Post-traumatic seizure with no history of epilepsy.
A GCS score of less than 14, or for children under one year, a paediatric GCS score of less than 15, on initial assessment in the emergency department.
A GCS score of less than 15 two hours after the injury.
Suspected open or depressed skull fracture, or a tense fontanelle.
Focal neurological deficit.
Any signs of basal skull fracture (e.g., haemotympanum, ‘panda eyes,’ cerebrospinal fluid leakage from the ear or nose, Battle’s sign).
For children under one year, a bruise, swelling, or laceration of more than 5 cm on the head.

Intracranial Injuries

Epidural Hemorrhage

Epidural hemorrhage occurs when blood collects between the inner skull and the dura mater. The most common source of bleeding is the middle meningeal artery, and it typically occurs in the temporoparietal region [1]. Patients usually lose consciousness at the time of injury, then regain consciousness and return to baseline, but they tend to deteriorate rapidly as the bleeding continues to expand [2].

Subdural Hemorrhage

Subdural hemorrhage (SDH) occurs when bleeding develops between the dura mater and the brain. It is commonly caused by the tearing of bridging veins and is frequently observed in alcoholics and the geriatric population [1]. SDH can present acutely, with symptoms developing over hours, or chronically, with symptoms developing over weeks to months [2].

Subarachnoid Hemorrhage

Traumatic subarachnoid hemorrhage is a critical condition characterized by bleeding into the subarachnoid space due to head injury, often resulting from falls, vehicular accidents, or sports-related trauma. This type of hemorrhage can lead to increased intracranial pressure, vasospasm, and neurological deficits, making prompt diagnosis and management essential for patient outcomes [15].

Intracerebral Hemorrhage

Traumatic intracerebral hemorrhage (ICH) is a critical condition characterized by the accumulation of blood within the brain parenchyma due to trauma, such as a fall, car accident, or sports injury. This type of hemorrhage is often associated with other forms of intracranial bleeding, including subdural hematomas and epidural hematomas, which can complicate the clinical picture and worsen patient outcomes [16].

Risk Stratification

Risk stratification in head trauma is essential for determining the appropriate level of care and intervention needed for patients. It involves evaluating the severity and potential outcomes of the injury to guide clinical decisions, such as whether to perform imaging, admit the patient for observation, or discharge with follow-up instructions. Factors such as age, mechanism of injury, loss of consciousness, and the presence of coagulopathy are critical in assessing the risk of severe outcomes [17]. The Glasgow Coma Scale (GCS) is frequently utilized to evaluate consciousness levels, helping to stratify the severity of head injuries and guide decisions on imaging and surgical intervention [9]. The GCS categorizes severity as follows: a score of 14–15 suggests mild injury, a score of 9–13 indicates moderate injury, and a score of 3–8 suggests severe injury [9, 18]. Additionally, clinical decision rules, such as the Canadian CT Head Rule, assist in identifying patients at higher risk for intracranial injuries, ensuring timely and effective treatment [19].

Management

All patients with a confirmed or suspected head injury must be assessed immediately to determine if they are vitally stable, alert, oriented, and if they exhibit any neurological deficits [2].

Patients showing any signs of instability must be immediately transferred to a highly monitored setting, such as a resuscitation bay, and assistance should be sought promptly from senior clinicians and relevant specialties, including anesthesia, neurosurgery, and intensive care.

Initial Stabilization: The ABCDE Approach

Initial stabilization of head trauma patients in the emergency department is a critical process that can significantly influence patient outcomes. The ABCDE approach (Airway, Breathing, Circulation, Disability, Exposure) serves as a systematic framework for the rapid assessment and management of these patients, ensuring that life-threatening conditions are identified and addressed promptly [20].

A – Airway

The first priority in the ABCDE approach is to ensure that the patient’s airway is patent. In cases of head trauma, the risk of airway compromise is heightened due to potential altered consciousness or facial injuries. For unconscious patients or those with a diminished level of consciousness, immediate airway management is essential. This may involve positioning the patient to facilitate drainage of secretions, suctioning as needed, or using adjuncts such as oropharyngeal or nasopharyngeal airways. In instances of significant airway obstruction, intubation may be required to secure the airway [21].

B – Breathing

Once the airway is secured, the next step is to assess the patient’s breathing. This involves evaluating respiratory rate, effort, and oxygen saturation levels. Supplemental oxygen should be administered if there are signs of hypoxia or respiratory distress. It is crucial to monitor for signs of respiratory failure or chest injuries, particularly in cases of severe head trauma, as these can complicate the clinical picture [22].

C – Circulation

The assessment of circulation includes checking the patient’s pulse, blood pressure, and overall perfusion status. Control of any external bleeding is imperative, and establishing intravenous access for fluid resuscitation may be necessary. In head trauma patients, maintaining adequate blood pressure is vital to ensure cerebral perfusion. Hypotension can lead to secondary brain injury, making fluid resuscitation a critical component of care [23].

D – Disability

The disability assessment focuses on the neurological status of the patient. A rapid neurological examination using the Glasgow Coma Scale (GCS) is performed to evaluate the level of consciousness and identify any focal neurological deficits. Monitoring pupillary response and limb movement is also essential. Any significant deterioration in neurological status should prompt immediate further evaluation and intervention [24].

E – Exposure

Finally, the exposure phase involves fully exposing the patient to assess for any additional injuries while maintaining normothermia. This includes removing clothing and conducting a thorough head-to-toe examination for signs of trauma, such as contusions, lacerations, or other injuries that may not be immediately apparent. Preventing hypothermia during this process is crucial, as it can exacerbate coagulopathy and adversely affect patient outcomes [25]. Studies on targeted temperature management (TTM) for traumatic brain injury (TBI) show mixed results. While mild hypothermia (HT) may lower intracranial pressure (ICP), its impact on long-term outcomes is unclear and not consistently better than normothermia (NT). Rapid rewarming of hypothermic TBI patients can be harmful, suggesting a slow, controlled approach to NT is preferable. Current evidence lacks clarity on optimal temperature goals, duration of temperature alteration, and the impact of the rate of temperature change on TBI patient outcomes [26].

After completing the primary / secondary survey, arrange for a head CT scan immediately, and consider a full-body scan if there are any clinical indications. Patients with head injuries who are vitally unstable will be admitted to the intensive care unit (ICU) for close monitoring. Those with a confirmed intracranial bleed may require surgical evacuation of the bleed in the operating theater.

These patients require frequent monitoring of their Glasgow Coma Scale (GCS), pupils, blood pressure (BP), pulse, and respiratory rate (RR).

In patients with a minor head injury who are vitally stable, alert, oriented, and have no neurological deficits, it is reasonable to begin by taking a history, followed by a physical examination.

Medications

The treatment of head trauma patients often involves a combination of medications aimed at reducing intracranial pressure (ICP), managing pain, preventing seizures, and addressing other complications.

Analgesics

Pain management is crucial in head trauma patients. Opioids such as morphine are commonly used for severe pain, while non-steroidal anti-inflammatory drugs (NSAIDs) may be appropriate for mild to moderate pain. Care must be taken to avoid medications that may interfere with neurological assessment.

Sedatives and Anxiolytics

Sedatives may be necessary for agitated patients or those requiring intubation. Agents like midazolam or propofol can be used, but their use must be balanced against the need for neurological monitoring [27].

Anticonvulsants

Seizures are a common complication of head trauma. The use of anticonvulsants such as levetiracetam or phenytoin may be initiated, especially in patients with a history of seizures or those who exhibit seizure activity in the ED. Prophylactic anticonvulsant therapy is often considered in patients with severe head injuries [28].

Osmotic Agents

Mannitol and hypertonic saline are osmotic agents used to reduce ICP. Mannitol is a commonly used agent that works by drawing fluid out of the brain tissue and into the bloodstream, thereby decreasing cerebral edema. Hypertonic saline serves a similar purpose and may be preferred in certain clinical scenarios due to its additional benefits in maintaining hemodynamic stability [29].

Corticosteroids

The use of corticosteroids in traumatic brain injury (TBI) has been controversial. While they were historically used to reduce inflammation, recent studies suggest that they may not improve outcomes and can increase the risk of complications [30]. Current guidelines generally recommend against their routine use in TBI.

Antibiotics

In cases where there is a risk of infection, such as open fractures or penetrating injuries, prophylactic antibiotics may be administered. Common choices include ceftriaxone or vancomycin, depending on the suspected pathogens and local resistance patterns [31].

Special Patient Groups

Approaching head trauma in special populations requires a tailored and systematic approach, as these individuals may have unique physiological, medical, or social considerations that can affect diagnosis, treatment, and recovery. Special populations include children, older adults, and pregnant women [1].

Pediatrics

Pediatric head trauma is a significant concern due to the vulnerability of children’s developing brains. Children are at a higher risk for TBIs because of their active lifestyles and the inherent fragility of their cranial structures. Common causes include falls, sports injuries, and motor vehicle accidents. Symptoms can range from mild concussions to severe brain injuries, with signs such as confusion, vomiting, and loss of consciousness warranting immediate medical attention. Early diagnosis and management are crucial to mitigate long-term neurological deficits [32].

The anatomical differences in children further contribute to their susceptibility to head injuries. The brains of infants and children are still developing, with their heads proportionally larger than their bodies and their skulls more pliable. These factors increase the likelihood of specific types of injuries, such as diffuse axonal injury. Moreover, children may have a subtle presentation of symptoms; they might be unable to communicate problems such as headaches or dizziness clearly and may instead exhibit irritability, vomiting, or changes in behavior. Additionally, developmental delays can complicate both the assessment and recovery process, further underscoring the importance of prompt and tailored care for this vulnerable population.

Geriatrics

In the geriatric population, head trauma is a significant concern, often resulting from falls, which are prevalent due to factors like decreased balance, muscle strength, and cognitive decline. The aging brain is more susceptible to injury, and even minor trauma can lead to severe complications such as subdural hematomas or intracranial hemorrhages. Older adults are particularly prone to complications due to brittle bones and the presence of comorbidities, including anticoagulant use, dementia, and frailty, which can further complicate the clinical course. Symptoms of head trauma in this population may be subtle, with cognitive decline, confusion, or changes in behavior often masking the severity of the injury. Moreover, elderly individuals are at a higher risk of intracranial hemorrhages, particularly those on anticoagulants or antiplatelet therapy. Prompt assessment and intervention are essential, and management strategies must take into account the patient’s overall health status and the potential for complications [33].

Pregnant Patients

Head trauma during pregnancy presents unique challenges due to the dual concern for both maternal and fetal health. Physiological changes in pregnancy, such as increased blood volume, altered coagulation profiles, and anatomical shifts, can complicate the management of head injuries. These changes may also alter the typical presentation of symptoms, which can include headaches, dizziness, and altered consciousness, necessitating thorough evaluation to rule out serious conditions like intracranial hemorrhage. Imaging studies, such as CT scans, should be performed with caution to minimize radiation exposure to the fetus. Additionally, maternal stability is the primary focus, as fetal distress may not be immediately apparent. Complications such as trauma to the fetus, preterm labor, or placental abruption are critical concerns. Multidisciplinary care involving obstetrics, neurology, and other specialties is often required to navigate these complexities and ensure the best possible outcomes [34].

When To Admit This Patient

Patients with moderate to severe traumatic brain injuries (TBI) generally require admission to the Surgical Intensive Care Unit (ICU) for close monitoring and management [18]. Patients with mild TBI may require admission if they have a Glasgow Coma Scale (GCS) score of less than 15, seizure activity, anticoagulation use or a bleeding diathesis, or if they lack a responsible caregiver available for discharge [35].

Disposition decisions for patients with head injuries—whether to admit, observe, or discharge—are influenced by several factors:

Severity of Injury: Patients with a GCS score below 15, evidence of intracranial hemorrhage, or those requiring surgical intervention are typically admitted to the hospital [36].
Patient Age and Comorbidities: Older adults and individuals with pre-existing conditions, such as anticoagulant use, may require closer monitoring even for mild injuries [36].
Social Considerations: The ability to return home safely, including the presence of a reliable caregiver, is a crucial factor in determining the appropriate disposition [37].
Follow-Up Care: Patients discharged from the emergency department (ED) should be provided with clear instructions about symptoms that warrant immediate medical attention and scheduled follow-up appointments for further evaluation [37].

Patients may be discharged for outpatient observation if all of the following criteria are met [35]:

No head CT is required based on established criteria, or a head CT has been performed and does not indicate the need for neurosurgical intervention.
The patient has a GCS score of 15 at the time of discharge.
No seizures have occurred.
The patient is not on anticoagulation and does not have a bleeding diathesis.
A responsible caregiver is available at home to oversee their care.

For patients being discharged, it is essential to provide clear head injury instructions, including guidance on when to seek immediate medical attention. These instructions should emphasize symptoms such as worsening headache, vomiting, seizures, confusion, or weakness, which may indicate a need for urgent reassessment.

Return to the ED immediately if any of the following symptoms occur [38]:

Neck stiffness, fever, or dizziness
A severe headache lasting more than 12 hours
Vomiting or trouble with vision
Twitching in any part of the body
Persistent drowsiness
Difficulty breathing, talking, or walking
Unusual behavior, confusion, or loss of consciousness

Revisiting Your Patient

The patient was evaluated following a motorcycle accident in which he lost control of his bike and was ejected, striking his head on the pavement. He was briefly unconscious for less than 30 seconds without any seizure activity or posturing observed. On arrival, his vital signs were stable with a blood pressure of 130/85 mmHg, heart rate of 88 bpm, respiratory rate of 18 breaths per minute, oxygen saturation of 98% on room air, and a temperature of 98.6°F (37°C). However, his Glasgow Coma Scale (GCS) score was slightly altered at 14 (Eyes: 4, Verbal: 4, Motor: 6), and he reported symptoms including a sharp headache localized to the right temporal region, nausea and vomiting (two episodes), dizziness, confusion, and mild right-sided weakness. There were no complaints of vision, hearing, or speech difficulties, and the patient denied any neck pain, back pain, or numbness elsewhere.

Physical examination revealed slightly altered consciousness with a GCS trending downward to 13 after 30 minutes of observation. Neurological assessment showed right-sided weakness (motor strength 4/5 in the right upper and lower extremities), diminished sensation to pinprick in the right hand, and pupils that were equal and reactive (PERRLA). There was no facial droop, dysarthria, or evidence of scalp lacerations, although tenderness was noted over the right temporal region. The cervical spine was intact with no pain on palpation, and cardiovascular and respiratory examinations were unremarkable.

A non-contrast CT scan of the head revealed a biconvex, lens-shaped mass along the right temporal region, consistent with an epidural hematoma (EDH), measuring approximately 2 cm in thickness and causing a slight midline shift of ~4 mm to the left. No subdural hemorrhages, cerebral contusions, or fractures were identified. Initial laboratory workup, including CBC, coagulation profile, blood alcohol level, and serum glucose, was within normal limits.

The primary diagnosis was an epidural hematoma due to head trauma. Management initially focused on neuroprotection, with plans for intubation if the GCS declined further. Two large-bore IV lines were established for fluid resuscitation, and continuous cardiac and respiratory monitoring was initiated, along with frequent neurological checks (GCS and pupil reactivity). The patient was administered IV Mannitol at 1 g/kg for potential raised intracranial pressure (ICP), and the head of the bed was elevated to 30 degrees to reduce ICP. Pain management included acetaminophen while avoiding NSAIDs.

Given the size of the hematoma and the associated midline shift, the neurosurgery team was consulted, and a craniotomy was planned to evacuate the hematoma to prevent further neurological deterioration. Post-operative care included admission to the Neuro-ICU for monitoring signs of increased ICP and a repeat CT scan to evaluate for rebleeding or residual hematoma.

Authors

Emranur Rahman

Dr. Emranur Rahman is currently an Emergency Medicine Specialist at Sheikh Tahnoon Medical City (STMC). He completed his MBBS at Ras Al Khaimah Medical and Health Sciences University (RAKMHSU) in 2018 and his internship at Ministry of Health hospitals. Dr. Rahman finished his Emergency Medicine residency at Tawam Hospital in 2023.He previously served as the Chief of academic days. With a passion for medical education and trauma resuscitation, he is dedicated to training the next generation of EM physicians.

Mansoor Husain

Listen to the chapter

References

Papa L, Goldberg SA. Head Trauma. In: Walls RM, Hockberger RS, Gausche-Hill M, eds. Rosen’s Emergency Medicine: Concepts and Clinical Practice. 10th ed. Elsevier; 2022:294-322.
Haskins KG. Major Trauma: Head Injury. In: Wyatt JP, Taylor RG, de Wit K, Hotton EJ, eds. Oxford Handbook of Emergency Medicine. 5th ed. Oxford University Press; 2020:328-407.
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Zima L, Moore AN, Smolen P, et al. The evolving pathophysiology of TBI and the advantages of temporally-guided combination therapies. Neurochem Int. 2024;180:105874. doi:10.1016/j.neuint.2024.105874
Manley GT, Yue JK, Deng H, et al. Pathophysiology of traumatic brain injury. In: Oxford Textbook of Neurological Surgery. Oxford University Press; 2019:483-496. doi:10.1093/med/9780198746706.003.0041
Olson DA. Head Injury Clinical Presentation. Medscape. Updated July 29, 2024. Accessed December 21, 2024. https://emedicine.medscape.com/article/1163653-clinical
Angus SD, Carragee EJ. Is the self-reported history accurate in patients with persistent axial pain after a motor vehicle accident? Spine J. 2009;9(1):4-12. doi:10.1016/j.spinee.2008.11.002
Ko DY. Clinical evaluation of patients with head trauma. Neuroimaging Clin N Am. 2002;12(2):165-174. doi:10.1016/S1052-5149(02)00010-2
Teasdale G, Jennett B. Assessment of coma and impaired consciousness: a practical scale. Lancet. 1974;2(7872):81-84.
Luber SD, Brady WJ, Brand A, et al. Acute hypoglycemia masquerading as head trauma: a report of four cases. Am J Emerg Med. 1996;14(6):543-547. doi:10.1016/S0735-6757(96)90094-7
Zetterberg H, Blennow K, Ward M. Neurochemical markers in the diagnosis of traumatic brain injury. Nat Rev Neurol. 2013;9(4):203-214.
Papa L, Lewis LM, Mendez M. Biomarkers for the diagnosis of mild traumatic brain injury. J Neurotrauma. 2016;33(21):1912-1920.
Miller KD, et al. The role of biomarkers in the management of traumatic brain injury. J Neurotrauma. 2018;35(18):2201-2213.
National Institute for Health and Care Excellence (NICE). Head injury: assessment and early management. NICE guideline [NG39]. Published December 2014. Accessed December 21, 2024. https://www.nice.org.uk/guidance/ng39
Miller DJ, et al. The impact of traumatic subarachnoid hemorrhage on outcomes after traumatic brain injury. Neurosurgery. 2020;87(2):234-240.
Huang J, et al. Traumatic intracerebral hemorrhage: a review of the literature. J Neurotrauma. 2020;37(5):761-775.
Murray GD, Butcher I, McHugh GS, et al. Trauma and head injury. J Neurotrauma. 2018.
WikEM. Moderate-to-severe traumatic brain injury. Accessed December 21, 2024. https://www.wikem.org/wiki/Moderate_to_severe_traumatic_brain_injury
Stiell IG, Wells GA, Vandemheen KL, et al. The Canadian CT Head Rule for patients with minor head injury. Lancet. 2001;357(9266):1391-1396.
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Thompson JH, White MA, Black PR. Neurological assessment in trauma. J Neurosurg. 2022;136(4):789-795.
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Madden LK, DeVon HA. A systematic review of the effects of body temperature on outcome after adult traumatic brain injury. J Neurosci Nurs. 2015;47(4):190-203. doi:10.1097/JNN.0000000000000142
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Reviewed and Edited By

Arif Alper Cevik, MD, FEMAT, FIFEM

Acute Mesenteric Ischaemia (2024)

December 10, 2024December 17, 2024 ~ iEM Education Project Team ~ Leave a comment

by Colin NG

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 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.

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].

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:

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

Authors

Colin NG

Woodlands Health

Listen to the chapter

References

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.
McKinsey JF, Gewertz BL. Acute mesenteric ischemia. Surg Clin North Am. 1997;77(2):307-318.
Oldenburg WA, Lau LL, Rodenberg TJ, Edmonds HJ, Burger CD. Acute mesenteric ischemia: a clinical review. Arch Intern Med. 2004;164(10):1054-1062.
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.
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.
Tendler DA, Lamont JT. Nonocclusive mesenteric ischemia. UpToDate. https://www.uptodate.com/contents/nonocclusive-mesenteric-ischemia Updated December 13, 2023. Accessed December 9, 2024.
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.
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.
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.
Menke J. Diagnostic accuracy of multidetector CT in acute mesenteric ischemia: systematic review and meta-analysis. Radiology. 2010;256(1):93-101.
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

Elif Dilek Cakal, MD, MMed

Arif Alper Cevik, MD, FEMAT, FIFEM

How to Interpret C-Spine X-ray (2024)

December 7, 2024December 7, 2024 ~ iEM Education Project Team ~ Leave a comment

by Maitha Mohammed Alneyadi & Mansoor Masarrat Husain

Introduction

Cervical spine x-ray interpretation is a vital skill in emergency medicine. This is particularly important as cervical spine injuries can leave patients with permanent neurological damage or death. While CT scans have overtaken X-rays as the primary form of cervical spine imaging, X-rays can be handy in rural areas or areas with limited resources. If in doubt, always ask for an expert opinion.

Cervical spine injuries commonly arise from motor vehicle accidents or falls from heights. They more commonly occur in men, and worse outcomes often happen to patients with underlying degenerative changes. Mechanisms of injuries causing fractures include flexion, extension, rotational, or vertical compression—these will be elaborated on further in this chapter. Cervical spine x-rays are somewhat useful if the patient is awake, stable, and has isolated injuries. In addition, they can be ordered in patients with upper airway obstruction symptoms, to look for soft tissue infections, foreign body demonstration, or if there is neck pain with no significant trauma.

Remember, cervical spine x-rays require manipulation of the neck to get clear views. Consider an alternative diagnostic choice like CT (Computed Tomography) or MRI (Magnetic Resonance Imaging) if cervical spine movement is restricted by a cervical collar. X-rays are also not advisable when neurological symptoms are present following trauma, in an uncooperative patient, or when a more accurate radiological modality is easily available.

Plain radiographs that display the lateral projection of the cervical spine, along with an open mouth view, are quite effective at identifying cervical spine fractures. Statistics indicate that the risk of overlooking a significant fracture is less than 1%. Including the anteroposterior (AP) projection raises the sensitivity to almost 100%. All three essential projections mentioned above can be seen in the figure below.

Before analyzing cervical radiographs, some additional facts need to be presented. Most spinal injuries occur at the junctions of the spine: craniocervical, cervicothoracic, thoracolumbar, and lumbosacral.

The only c-spine radiograph one should be satisfied with is the one showing all seven cervical vertebrae (C1–Th1). The C7–Th1 vertebrae may be obscured in muscular or obese patients, or in patients with spinal cord lesions that affect the muscles that normally depress the shoulders. Such lesions, which leave the trapezius muscle unopposed, occur in the lower cervical region. Shoulders can be depressed by pulling the arms down slowly and steadily or, if the patient is capable, by asking them to depress one shoulder and lift the other hand above their head to achieve the swimmer’s position, which better visualizes the lower vertebrae.

We will now present a systematic method for interpreting cervical spine x-rays. First, identification—make sure details are correctly matched to the patient by name, date of birth, record number, and the time the scan was done. Use an old x-ray of the patient as a comparison if the study has been done previously.

Interpretation

We utilize the ABCD system to comprehensively interpret cervical spine X-rays.

A: Alignment and adequacy
B: Bones
C: Cartilages
D: Dense soft tissue

Cervical spine X-rays typically include three views: the lateral view (or cross-table view), the odontoid view (or open mouth view), and the anterolateral view. If the lateral view is inadequate, an additional view called the “Swimmer’s view” may be requested to visualize the C7 and T1 vertebrae.

Lateral View

A: Adequacy and Alignment

An adequate image includes the base of the skull to the upper border of T1.

There are four parallel lines to note, from front to back (See image on the left, Courtesy of Dr Hussain Aby Ali). The front line (in purple), referred to as the anterior longitudinal line, runs along the anterior border of the vertebrae.

The second line, or the middle line, referred to as the posterior longitudinal line (in yellow), runs along the posterior border of the vertebrae.

Next, the spinolaminar line (in green) runs between the spinous process and lamina, along the anterior edge of the spinous process.

Lastly, the posterior spinous line (in blue) runs smoothly along the tips of the spinous processes.

The spinal cord lies between the posterior spinous and spinolaminar lines. Disruption of any of these lines indicates a fracture [1].

An important exception to the usual guidelines involves pseudo-subluxation of C2 and C3 in the pediatric population, which can lead to confusion. In these cases, it is essential to examine the spino-laminar line from C1 to C3. Be cautious of injury if the base of the C2 spinous process is more than 2 mm away from this line. Additionally, correlate your findings with any relevant soft tissue observations (see below under “D”).

On the lateral view, also assess the predental space, which is the distance between the anterior surface of the odontoid process and the posterior aspect of the anterior ring of C1. This distance should not exceed 3 mm in adults or 5 mm in children (see image below).

B: Bones

Examine the vertebrae for a normal bony outline and bone density. It is important to note any subtle changes in bone density, as these may indicate a compression fracture. Areas with decreased bone density are more vulnerable to fractures and are often seen in patients with conditions such as rheumatoid arthritis, osteoporosis, or metastatic osteolytic lesions. Acute compression fractures, in contrast, typically present as areas of increased bone density.

To check the integrity of the vertebrae, we must trace each vertebra individually. If there are any irregularities in the cortex of the bone, there may be a fracture.

As you trace the vertebrae on the right side (the image above), you may note that the sixth vertebra has slipped forward and is not continuous, which is an example of a vertebral fracture.

This is followed by scanning vertebrae C3–C7 in the usual manner, with no specific shadows or rings. The rest of the vertebral spaces must be equal, with a rectangular shape. Follow the spinous processes to look for any fractures [1].

Other examples are given below. See the fracture on 7th vertebral body (image A below), and fracture on spinous process of the 7th vertebrae (image B below).

Let us zoom in into the same image and focus on C1 and C2.

Start your day with a coffee—or rather, a coffee bean shadow—when interpreting c-spines. This shadow corresponds to the anterior arch of the atlas found in C1. Bear in mind that the peg might get in your way. With that, make sure the coffee bean shadow is adjacent to the odontoid peg. If not, think of a fracture!

When looking at C2, trace the ring, referred to as Harris’ ring (black color in the image above), which is the lateral mass of the vertebra. Discontinuity of the ring demonstrates a fracture.

C: Cartilage space assessment

n the assessment, examine the disc spaces, facet joint spaces, and interspinous spaces for any misalignments or increased space. Subluxations or facet dislocations can be identified by disruptions in the demarcated boxes, while any interspinous height exceeding 50% of the vertebral body indicates ligament disruption. On a good-quality lateral view x-ray of a healthy person, uniform intervertebral spaces should be evident.

An emergency physician may diagnose subluxations and dislocations of the facet joints by assessing the cartilage space between the vertebral corpora, facet joints, and spinous processes. However, increased interspinous distance by more than 50% suggests a ligamentous injury, and protective muscle spasms may complicate interpretation.

D: Dense soft tissue

Subsequently, we check the prevertebral space (in yellow), with the trachea sitting right in front of it (in red) (see the image below, courtesy of Hussain Aby Ali). Take C4 as your reference point (in purple). As a rule of thumb, the prevertebral space at or above C4 should be less than one-third the width of the vertebral body, while below C4 it should measure less than the width of the adjacent vertebra. In pediatrics, the prevertebral space at C4 is 7 mm, and at C6 it measures 14 mm or less, depending on age. In adults, the prevertebral space at C6 measures 22 mm. Enlarged measurements may indicate a hematoma related to a fracture, although normal measurements do not rule out a fracture [1].

The prevertebral soft tissues can serve as an indicator of acute swelling or hemorrhage resulting from an injury, and in some cases, may be the only indicator of an acute injury visible on an x-ray. The normal width of the prevertebral tissue decreases from C1 to C4 and increases from C4 downward. Normal measurements are less than 7 mm from C1 to C4 (less than half the vertebral body width at this level) and less than 22 mm below C5 (less than the vertebral body width at this level, as shown in Figure 9). The presence of air within the soft tissue could suggest a rupture of the esophagus or trachea.

Odontoid – Open Mouth View

A: Adequacy and Alignment

The odontoid x-ray is typically the second standard view obtained in the emergency department. Its primary goal is to visualize the odontoid process of the C2 vertebra and the C1 vertebra. This view can be taken with the patient’s mouth either open or closed.

When examining the odontoid x-ray, two key aspects are assessed: first, the distance between the odontoid process and the lateral masses of the C1 vertebra should be equal. If there is an inequality, it may indicate a slight rotation of the head. Second, considering the previous point, the margins of the C1 and C2 vertebrae should remain aligned.

The distance between the odontoid process and the lateral masses of the C1 should be equal, if not inequality may be due to the slight rotation of the head. (If the patient has the upper central incisor teeth, we can check if the space between those two teeth aligns with the middle of the odontoid process, this might give the slight idea about rotation in case process itself is not broken and misaligned). Even with the slight rotation of the head we can still check alignment by looking at the lateral margins of the C1 and C2, which should remain aligned.

B: Bones

The odontoid view is most helpful for assessing peg fractures and examining the lateral masses and spaces at C1 and C2. Start by drawing a line from the end of the lateral mass (in purple), along the shaft, up around the odontoid peg, and down to the other lateral end (in green), which marks C2. Next, demarcate C1’s lateral masses on each side and look for any irregularities or fractures.

C: Cartilage space assessment

The space between the peg and C1’s lateral masses must be equal (green asterisks), as should the spaces between C1 and C2 lateral masses (blue asterisks). Unequal lateral mass spaces could raise suspicion of subluxation, which may indicate that the transverse ligament holding the peg in place is torn. Alternatively, consider a Jefferson fracture, which will be discussed later in this chapter.

Draw an imaginary line along the lateral edges of C1 and C2, and check for any misalignment or displacement (red circles). It is important to note that when a patient’s cervical spine is rotated, the images may be inaccurate due to artifacts, which could be misconstrued as fractures, as shown in the image below [1].

An inappropriate imaging angle can result in an inconclusive image. In such cases, you may notice unequal spaces between the odontoid and C1 lateral masses, even when no underlying fractures are present. This situation should prompt a discussion with the radiologist or the consideration of further imaging, such as a CT scan or MRI.

Beware of the Mach effect!
The Mach effect is an optical illusion that can occur during imaging interpretation. It creates the appearance of a lower density at specific levels of the odontoid peg, which may falsely mimic an odontoid fracture. This illusion arises from the way edges and contrasts in the image are perceived by the human eye, often giving the impression of a discontinuity or fracture when none is present. It is crucial to recognize this phenomenon to avoid misdiagnosis, especially when interpreting odontoid fractures on radiographs. Careful examination and, if needed, correlation with additional imaging modalities such as CT or MRI can help confirm the true nature of the findings.

Anteroposterior View

A: Adequacy and Alignment

Images taken in this projection are usually less clear than the two mentioned above. The tips of the spinous processes should lie in a straight line along the midline, and the distances between the spinous processes should also be checked. Anomalies, such as bifid spinous processes, can complicate interpretation. The laryngeal and tracheal shadows should align down the middle, and the alignment of the lateral masses of the vertebrae should also be assessed.

An adequate image includes the vertebral bodies of the cervical vertebrae along with the superior border of the thoracic vertebrae. Vertical lines running across and along the spinous processes and vertebral bodies help assess alignment. Three lines are particularly important: the spinous process line (in blue), which runs through the spinous processes of C1 to C7, ensuring vertical alignment, and two lateral lines (in green), which run smoothly along the transverse processes, confirming their normal alignment.

B: Bones

The anteroposterior (AP) view of the cervical spine is one of the standard projections used during imaging. It is taken with the x-ray beam directed from the front (anterior) to the back (posterior) of the neck. While it provides a general overview of the alignment of the vertebrae and highlights features such as the spinous processes and transverse processes, this view may not always clearly demonstrate fractures.

Fractures, especially those involving the odontoid peg, vertebral bodies, or certain types of subtle cortical disruptions, can be challenging to detect due to the overlapping structures in this projection. Additionally, anomalies such as misalignment or crowding of the spinous processes might not be easily discernible. As a result, this view is often supplemented with lateral or oblique views and, in cases of doubt, with advanced imaging techniques like CT or MRI for a more definitive diagnosis.

The AP view remains an important tool for assessing gross abnormalities, vertebral alignment, and pathological conditions, such as tumors or significant bone density changes. However, its limitations in detecting subtle fractures underscore the need for careful correlation with clinical findings and additional imaging.

C: Cartilage space assessment

In an AP cervical spine x-ray, the assessment of cartilage spaces is crucial for evaluating alignment and potential injuries. A key rule to follow is the 50% rule: any increase in the cartilage space by more than 50% compared to adjacent spaces suggests anterior cervical dislocation. This finding is often associated with trauma, such as ligamentous injury or vertebral subluxation, but it is important to note that the 50% rule does not apply in cases of muscle spasm, particularly when the neck is in a flexed position.

To confirm the diagnosis and exclude vertebral slippage, it is essential to examine the lateral view. The lateral view provides additional details regarding the vertebral alignment, anterior displacement, and associated injuries that may not be visible on the AP view. Ensuring that the vertebrae are properly aligned without slippage is vital for accurate assessment and diagnosis.

By correlating findings from both the AP and lateral views, a clearer picture of cervical spine integrity can be obtained, helping to differentiate between conditions caused by trauma and those related to positional factors or muscle spasms.

D: Dense soft tissue

In the AP cervical spine view, it is important to assess for the presence of surgical emphysema or pneumothorax, as these findings can indicate significant underlying trauma.

Surgical Emphysema: Look for evidence of air trapped in the soft tissues of the neck. This appears as dark, radiolucent (black) streaks in areas where soft tissues should normally appear opaque. Surgical emphysema in the cervical region can result from tracheal or esophageal injury, penetrating trauma, or fractures that disrupt the airways. Its presence warrants immediate attention and further investigation to locate the source of the air leakage.

Pneumothorax: Although primarily evaluated using a chest x-ray, a pneumothorax might be visible on an AP c-spine x-ray, especially if significant. This is seen as an absence of lung markings on the affected side, with a radiolucent (black) space outlining the lung. Pneumothorax may occur in association with rib fractures or blunt trauma extending to the thoracic region and can contribute to respiratory distress.

Other Views

Swimmer’s view

When C7 or T1 is not clearly visible on the lateral view due to dense body musculature, obtaining a “Swimmer’s view” can be helpful. This imaging technique specifically focuses on the alignment of C7 and T1 at the cervico-thoracic junction. To achieve this view, patients are instructed to lower the shoulder on the same side as the area being examined [5].

Flexion and Extension Views

Oblique and flexion/extension views are not recommended in the emergency department setting as they can lead to further neurological injuries caused by manipulation. These views are only useful when interpreted by an experienced physician. Flexion and extension views are often contraindicated due to suspected unstable trauma or are impossible to perform because of spastic musculature following the injury (see Figure below). Additionally, unsupervised or forced flexion or extension in a patient with ligamentous injury can result in significant neurological damage. Therefore, other imaging modalities are necessary when a suspected injury is present.

Abnormal findings on cervical spine x-rays

C1 (Jefferson) fracture

A C1 fracture, also known as a Jefferson fracture, is best visualized on the odontoid view. This type of fracture typically results from axial loading, such as a heavy blow to the top of the head. The force compresses the cervical spine, leading to fractures in both the anterior and posterior arches of C1. These fractures are considered unstable because the transverse ligament, which stabilizes the relationship between the odontoid peg (dens) and the lateral masses of C1, is often disrupted.

Key imaging findings include widened spaces between the odontoid peg and the lateral masses of C1 (marked by orange asterisks). Additionally, the lateral masses of C1 may appear misaligned with those of C2 (marked by green circles), indicating instability [6]. The widening of these spaces and misalignment reflects the ligamentous injury and mechanical instability associated with this fracture.

Due to its unstable nature, a Jefferson fracture requires prompt recognition and further imaging, such as CT scans, to confirm the diagnosis and assess the extent of injury. Management often involves immobilization or surgical intervention, depending on the severity of the ligament disruption and alignment abnormalities.

C2 fractures

Odontoid peg fracture

To identify a C2 fracture, it is essential to evaluate both the open mouth (odontoid) view and the lateral view, as these complementary perspectives provide critical information about the integrity of the C2 vertebra.

Open Mouth (Odontoid) View:
This view is particularly useful for assessing the odontoid peg, also known as the dens. A discontinuity of the peg process, as shown in the image above, is a hallmark feature of a C2 fracture. This disruption indicates a break in the odontoid peg, which is often caused by significant trauma. The open mouth view allows for a clear examination of the alignment and spacing between the odontoid peg and the lateral masses of C1, helping to confirm the fracture.
Lateral View:
The lateral view provides additional details about the alignment and integrity of the C2 vertebra. In cases of a C2 fracture:
- Alignment Disruption: The normal alignment of the vertebral bodies is disturbed, indicating instability.
- Harris Ring Discontinuity: The Harris ring, a radiographic marker of the lateral mass of C2, appears interrupted, further confirming the presence of a fracture.
- Posterior Displacement of the Odontoid Peg: The odontoid peg may be displaced posteriorly, which can compromise the spinal canal and potentially compress the spinal cord.

Types of Odontoid Fractures

The graphical presentation above illustrates the three types of odontoid fractures, as labeled below:

Type I:

Location: Fracture at the tip of the dens.
Associated Injury: Alar ligament avulsion.
Stability: This is considered a stable fracture.

Type II:

Location: Fracture at the base of the odontoid process.
Stability: This is an unstable fracture. It is the most common type of odontoid fracture and is associated with a high risk of nonunion due to poor blood supply at the fracture site.

Type III:

Location: A fracture extending through the body of the axis (C2), curving laterally from one end to the other.
Stability: This is also considered an unstable fracture. These fractures may disrupt the lateral masses of C2, further compromising spinal stability.

Recommended Management

CT Scan: If any of these fractures are suspected or identified on plain x-rays, a CT scan is recommended for further evaluation to define the fracture line and assess the extent of bony disruption.
Immobilization: The cervical spine should be immobilized using a cervical collar (c-collar) to prevent further injury.
Consultation: Immediate consultation with neurosurgery is advised, as surgical intervention may be required, especially for unstable fractures (Type II and III).

These fractures, particularly Type II and III, have significant clinical implications due to their instability and proximity to critical neural structures, necessitating prompt diagnosis and intervention.

Hangman's fracture

A Hangman’s fracture is a bilateral fracture of the pars interarticularis of the C2 vertebra, often resulting in cervical spine instability. This type of fracture is best visualized on a lateral view, which reveals key findings:

Loss of Smooth Anterior Alignment

The normal, smooth anterior alignment of the cervical spine is disrupted and replaced by a visible step, indicating displacement.

Cortical Discontinuity

The fracture causes a break in the cortical bone, further demonstrating structural instability of the vertebra.

Mechanism of Injury

Hyperextension Trauma
- This fracture is commonly caused by hyperextension injuries, such as those sustained in motor vehicle accidents.
- It is also seen in diving accidents, where a diver’s head strikes the pool floor upon impact.

Clinical Significance

Hangman’s fracture is classified as unstable, as it compromises the integrity of the C2 vertebra and its supporting structures, potentially endangering the spinal cord.

Management

Immediate immobilization of the cervical spine with a cervical collar is essential. Advanced imaging (CT or MRI) is recommended to further evaluate the extent of the injury and rule out associated soft tissue or ligamentous damage.
Consultation with a neurosurgeon is critical for determining the need for surgical stabilization.

Importance of Recognizing C2 Fractures

C2 fractures, such as odontoid fractures or hangman’s fractures, are critical injuries due to their proximity to the spinal cord and brainstem. Prompt recognition using the open mouth and lateral views is vital to avoid neurological complications. Advanced imaging techniques, such as CT or MRI, are often required for further evaluation and to guide management strategies, which may include immobilization or surgical intervention.

Extension Teardrop Fracture

An extension teardrop fracture is a specific type of cervical spine injury in which a portion of the antero-inferior corner of the vertebra is fractured, resembling a teardrop shape. This injury is most commonly observed at C3 and is highly significant due to its association with instability and potential neurological compromise.

Fracture Appearance

The fracture is located at the antero-inferior corner of the vertebral body, creating a teardrop-shaped fragment.

Mechanism of Injury

Caused by sudden hyperextension of the neck, which disrupts the anterior longitudinal ligament.
Often occurs in activities like diving, particularly when the diver strikes their head against a hard surface such as the pool floor.

Associated Injuries

This type of fracture is frequently associated with central cord syndrome, a neurological injury caused by compression of the spinal cord, leading to weakness more pronounced in the upper limbs than the lower limbs.

Management

Immediate Stabilization
- Apply a cervical collar (C-collar) to immobilize the spine and prevent further injury.
Imaging
- A CT scan is the imaging modality of choice to confirm the diagnosis, evaluate the extent of the fracture, and assess for additional injuries or spinal canal compromise.
- Consultation
  - Immediate consultation with a neurosurgeon is essential for determining the best treatment approach. Depending on the severity, surgical intervention may be necessary.

Flexion Teardrop Fracture

A flexion teardrop fracture is a severe and unstable cervical spine injury resulting from high-energy flexion trauma, frequently occurring at the C5/C6 level. This type of fracture is significant due to its association with spinal instability and neurological damage.

Radiographic Findings (Lateral View):

The three longitudinal lines (anterior, posterior, and spinolaminar lines) are disrupted, indicating misalignment and instability.
A teardrop-shaped fragment is seen at the antero-inferior corner of the vertebral body, representing the avulsed piece of bone.

Mechanism of Injury

Caused by hyperflexion of the neck, which exerts excessive force on the cervical spine.
This leads to a disruption of the posterior longitudinal ligament, further contributing to instability.

Neurological Association

The injury often results in anterior cervical cord syndrome, characterized by loss of motor function and pain/temperature sensation below the level of injury, with preserved proprioception and vibration senses.

Management

Immediate Stabilization
- Apply a cervical collar (C-collar) to immobilize the cervical spine and prevent further injury.
Advanced Imaging
- A CT scan is the preferred imaging modality to confirm the diagnosis, evaluate the extent of the fracture, and identify associated injuries such as spinal canal compromise or ligamentous disruption.
- MRI may be indicated to assess soft tissue and spinal cord involvement.
Consultation
- Urgent consultation with a neurosurgeon is essential due to the unstable nature of this fracture. Surgical stabilization is often required to restore spinal alignment and prevent further neurological deterioration.

Clinical Importance

The flexion teardrop fracture is considered one of the most unstable cervical spine injuries. Prompt recognition, immobilization, and appropriate surgical management are critical to improving patient outcomes and minimizing long-term neurological deficits.

Clay Shoveler's Fracture

A Clay Shoveler’s fracture is a stable fracture that involves an avulsion of the spinous process, typically occurring in the lower cervical or upper thoracic spine (most commonly at C6, C7, or T1).

Clinical Presentation

Patients present with localized pain and tenderness over the affected area.
The pain is often exacerbated by movement or palpation of the spine.

Stability

This is considered a stable fracture as it does not involve the vertebral body, spinal canal, or neurological structures. However, the injury can still cause significant discomfort and impair mobility.

Examination and Management

Neurological Assessment
- A neurological examination should always be performed to rule out any associated injuries or deficits, even though this fracture typically does not affect the spinal cord or nerves.
Immobilization
- The patient should be placed in a cervical collar (c-collar) to immobilize the spine and alleviate pain during the acute phase of the injury.
Imaging
- A lateral cervical x-ray is often sufficient to diagnose the fracture, but a CT scan can provide additional details if needed.
Treatment
- Since this is a stable fracture, management is typically conservative, including pain control, immobilization, and physical therapy as needed.

Clay Shoveler’s fractures are generally associated with good outcomes, and patients can recover fully with appropriate care and immobilization.

Retropharyngeal abscess

Patients with a retropharyngeal abscess often present with:

Sore throat and fever.
Torticollis: The head is tilted to one side due to neck stiffness and discomfort.
Dysphagia: Difficulty swallowing.
Respiratory Distress: Severe cases may manifest with stridor, drooling, or increased breathing effort with retractions, indicating a compromised airway.

Management

Immediate Interventions
- Patients in respiratory distress should be closely monitored as the airway may become obstructed, necessitating emergency airway management, including the potential need for a surgical airway (e.g., tracheostomy).
Specialist Consultation
- A prompt otolaryngology consult is warranted for evaluation, incision and drainage (I&D) of the abscess, and initiation of intravenous antibiotics.

Radiographic Assessment

Measuring the Retropharyngeal Space
- The retropharyngeal space is evaluated using lateral cervical spine x-rays.
- Between C2 and C4, the vertebral bodies can be divided into thirds. The retropharyngeal space should not exceed one-third the width of the corresponding vertebral body.
- At C4 and below, the vertebral bodies should be divided in half, with the prevertebral space width being approximately equal to the anterior half of the vertebral body [8].
Signs of Retropharyngeal Abscess
- Widening of the retropharyngeal space beyond normal parameters is highly suggestive of an abscess.
- Additional findings may include air-fluid levels, soft tissue swelling, or displacement of adjacent structures.

Epiglottitis

Epiglottitis is a rapidly progressive and potentially life-threatening disease that primarily affects the upper airway. Patients often present with:

Fever and sore throat as initial symptoms.
Drooling and difficulty swallowing (dysphagia).
Inspiratory stridor, indicating partial airway obstruction.

These symptoms suggest an urgent need for airway evaluation and management.

Lateral Neck X-ray

The hallmark finding is the “thumb sign”, which represents the swollen epiglottis.
Swelling of the epiglottis and aryepiglottic folds is characteristic of this condition.
The epiglottis appears enlarged and rounded, resembling the shape of a thumb.

Importance of Early Recognition

Epiglottitis can rapidly progress to complete airway obstruction, particularly in children.
It is critical to recognize these findings on a lateral neck x-ray and act promptly to secure the airway.

Management

Patients showing signs of airway obstruction require immediate attention, with priority given to securing the airway. In severe cases, this may involve intubation, preferably using fiberoptic intubation in a sitting position, or tracheostomy if necessary. This procedure should be performed collaboratively with ENT surgeons and anesthesia professionals in a controlled environment.

As a temporary measure, nebulized racemic epinephrine can be administered to reduce airway swelling, and broad-spectrum antibiotics should be started promptly to treat the underlying infection. Supportive care, such as humidified oxygen, may also be beneficial. Additionally, a nasopharyngoscopy should be performed to directly visualize the epiglottis and assess the extent of swelling.

Laryngotracheobronchitis (Croup)

Laryngotracheobronchitis, commonly referred to as croup, presents with characteristic symptoms including:

Barking cough, often likened to a seal’s bark.
Inspiratory stridor, indicating upper airway obstruction.
Drooling or dysphagia, in some cases.
Signs of increased work of breathing, such as retractions and nasal flaring.

These symptoms are typically caused by inflammation and narrowing of the subglottic airway, often following a viral infection.

Radiographic Findings

An anteroposterior (AP) neck x-ray may reveal the steeple sign, which represents narrowing of the subglottic trachea [10].
The steeple sign is considered pathognomonic for croup, though it is also occasionally observed in bacterial tracheitis.
A neck x-ray is not required for diagnosing croup but may be helpful to confirm the diagnosis when the patient is stable and cooperative [11].

While croup is usually a clinical diagnosis, imaging may be considered in atypical presentations or to rule out other conditions like epiglottitis or retropharyngeal abscess. Prompt recognition of croup and appropriate management can prevent complications associated with airway obstruction.

Clinical Decision Rule

There are two widely used scoring systems for neck injuries, primarily for diagnostic purposes: the National Emergency X-Radiography Utilization Study (NEXUS) criteria and the Canadian C-spine rules (CCR). Both have high sensitivity (89% and 98%, respectively) but low specificity (39% and 16%, respectively) [12]. Neither tool is used for patients over 65 years of age.

The NEXUS criteria can be easily remembered using the mnemonic NSAID:

N: Neurological deficit
S: Spine tenderness, midline
A: Altered mental state
I: Intoxicated
D: Distracting injury

A positive finding in any of these categories requires imaging.

The Canadian C-spine rule, on the other hand, categorizes patients into two groups based on severity: high risk and low risk. It uses a stepwise, question-based approach. Patients who are 65 years or older, those with a high-risk mechanism of injury, or those presenting with neurological symptoms always require imaging.

Refer to the diagram for a simplified explanation.

Specific Patient Groups

Pediatrics

Younger patients have anatomical differences compared to adults, including a larger head, incomplete ossification of the vertebrae, and firm attachment of the ligaments to the spine, which predispose them to injuries. Poor balance and a flexible spine further increase the risk of injury. As children reach the age of 8, their balance improves, and the injury rates decrease.

Nevertheless, pediatric patients can sustain spinal cord syndromes similar to those in adults, which may cause lifelong disabilities. Examples include central cord syndrome, anterior cord syndrome, posterior cord syndrome, Brown-Séquard syndrome, and spinal shock. The decision to perform imaging and the modality chosen are based on criteria similar to those used for adults.

In pediatric trauma patients, the ABCDE trauma evaluation must be followed, as with adults. An important entity to consider is SCIWoRA (Spinal Cord Injury Without Radiographic Abnormality), which is defined specifically for children under 8 years of age. This condition occurs when hyperextension forces injure the neck, leading to neurological deficits without abnormalities detected on x-rays or CT scans. MRI is required to assess the severity and prognosis. Favorable MRI findings include small hematomas and edema, whereas large hematomas or spinal cord transections are considered unfavorable [13].

Geriatrics

Motor vehicle accidents and falls from standing or sitting positions remain the two most common causes of cervical spine injuries in geriatric patients [14]. Due to anatomical degenerative changes and low bone density, even low-energy mechanisms can result in high-impact injuries. CT scanning is recommended for evaluating suspected cervical spine injuries in geriatric patients, who should always be considered trauma patients.

Pregnant Patients

Pregnant individuals involved in trauma require standard trauma protocols for evaluation and treatment, including CT imaging. Although CT imaging exposes both the mother and fetus to radiation, this exposure is not associated with an increased risk of fetal anomalies. However, the use of CT imaging should be carefully considered, with discussions involving the patient or their family, the radiologist, and a senior physician [15].

Authors

Maitha Mohammed Alneyadi

Emergency Medicine Department, Tawam Hospital, Al Ain, United Arab Emirates

Mansoor Masarrat Husain

Emergency Medicine Department, Tawam Hospital, Al Ain, United Arab Emirates

Listen to the chapter

References

Raby N, Berman L, Morley S, Gerald De Lacey. Accident & Emergency Radiology: A Survival Guide. Saunders; 2015, P. 171-198
Hurley CM, Baig MN, Callaghan S, Byrne F. Cervical spine hangman fracture secondary to a
gelastic seizure. BMJ Case Reports. 2019;12(8):e230733. doi: https://doi.org/10.1136/bcr-2019-230733
Gaillard F. Cervical spine fractures. Radiology Reference Article. Radiopaedia.org. Radiopaedia. https://radiopaedia.org/articles/cervical-spine-fractures
Czarniecki M, Niknejad M. Mach effect – mimicking odontoid fracture. Radiopaediaorg. Published online November 24, 2012. doi: https://doi.org/10.53347/rid-20528
Murphy A. Cervical spine (swimmer’s lateral view). Radiopaediaorg. Published online October 7, 2016. doi: https://doi.org/10.53347/rid-48437
Erskine J Holmes, Misra RR. A-Z of Emergency Radiology. Cambridge University Press; 2006, P. 23-31
Harvey H. Flexion teardrop fracture. Radiology Reference Article. Radiopaedia.org. Radiopaedia. https://radiopaedia.org/articles/flexion-teardrop-fracture-1?lang=us
Sheikh Y, Bickle I. Retropharyngeal abscess. Published online July 13, 2014. doi:https://doi.org/10.53347/rid-30018
Sutton AE, Guerra AM, Waseem M. Epiglottitis. In: StatPearls. Treasure Island (FL): StatPearls Publishing; October 5, 2024.
Murphy A, Gaillard F. Croup. Radiopaediaorg. Published online May 2, 2008. doi: https://doi.org/10.53347/rid-1185
Gaillard F. Steeple sign (trachea). Radiology Reference Article. Radiopaedia.org. Radiopaedia. https://radiopaedia.org/articles/steeple-sign-trachea?lang=us
Vazirizadeh-Mahabadi M, Yarahmadi M. Canadian C-spine Rule versus NEXUS in Screening of Clinically Important Traumatic Cervical Spine Injuries; a systematic review and meta-analysis. Arch Acad Emerg Med. 2023;11(1):e5. Published 2023 Jan 1. doi:10.22037/aaem.v11i1.1833
Szwedowski D, Walecki J. Spinal Cord Injury without Radiographic Abnormality (SCIWORA) – Clinical and Radiological Aspects. Pol J Radiol. 2014;79:461-464. Published 2014 Dec 8. doi:10.12659/PJR.890944
Lomoschitz FM, Blackmore CC, Mirza SK, Mann FA. Cervical spine injuries in patients 65 years old and older: epidemiologic analysis regarding the effects of age and injury mechanism on distribution, type, and stability of injuries. AJR Am J Roentgenol. 2002;178(3):573-577. doi:10.2214/ajr.178.3.1780573
Irving T, Menon R, Ciantar E. Trauma during pregnancy. BJA Educ. 2021;21(1):10-19. doi:10.1016/j.bjae.2020.08.005

FOAM and Further Reading

http://radiologymasterclass.co.uk/tutorials/musculoskeletal/x-ray_trauma_spinal/x-ray_c-spine_normal

http://reference.medscape.com/features/slideshow/c-spine#8

http://www.slideshare.net/Rajaoct/x-ray-cspine

Reviewed and Edited By

Arif Alper Cevik, MD, FEMAT, FIFEM

Intracerebral Hemorrhage (2024)

December 5, 2024December 7, 2024 ~ iEM Education Project Team ~ Leave a comment

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

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.

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.

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.

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

Airway: Assess airway patency. Intubation should only be performed if the patient cannot protect their airway or is in respiratory distress.
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.
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.
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:

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.
Medical Management: Tight control of blood pressure, intracranial pressure, glucose levels, and coagulopathy is essential to prevent secondary brain injury and improve outcomes.
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.
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.

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

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.

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.

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.

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.

Listen to the chapter

References

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
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
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
Sheth KN. Spontaneous Intracerebral Hemorrhage. N Engl J Med. 2022;387(17):1589-1596. doi:10.1056/NEJMra2201449
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
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
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
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
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
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
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
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
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
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
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
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
Kumar R, Shukla D, Mahapatra AK. Spontaneous intracranial hemorrhage in children. Pediatr Neurosurg. 2009;45(1):37-45. doi:10.1159/000202622
Berhouma M, Jacquesson T, Jouanneau E. Spontaneous Intracerebral Hemorrhage in the Elderly. Brain and Spine Surgery in the Elderly. 2017:411-22.
Berhouma M, Jacquesson T, Jouanneau E. Spontaneous Intracerebral Hemorrhage in the Elderly. Brain and Spine Surgery in the Elderly. 2017:411-22.
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
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

Erin Simon, DO

Arif Alper Cevik, MD, FEMAT, FIFEM

Management of Pain in the Emergency Department (2024)

December 4, 2024December 4, 2024 ~ iEM Education Project Team ~ Leave a comment

by Kayla Peña, Kelsey Thompson, & Munawar Farooq

You have a new patient!

A 57-year-old woman with a PMH of peptic ulcer disease presents to the emergency department 20 minutes after slipping and falling while out for a jog. She twisted her left ankle awkwardly while stepping off the pavement and fell to the side. She did not hit her head. She got up after the fall but has not tried to put weight on the ankle. Her vital signs are stable. She has a temperature of 37°C, a heart rate of 110 beats per minute, respirations at 18 breaths per minute, a blood pressure of 128/60, and an oxygen saturation of 96% on room air.

She is currently seated in a chair and appears uncomfortable. On exam, the left ankle appears more swollen than the right, with no bruising. She has tenderness to palpation at the posterior edge of the left lateral malleolus but no left midfoot tenderness. The right foot is non-tender. Pulses are intact throughout with a 2-sec capillary refill distally. She states, “Please help me; I can’t take the pain!”

Introduction

Pain is one of the most common reasons patients seek care in the ED. Pain is a signal from the body to alert the patients of actual or potential tissue damage. Addressing pain is a key part of the emergency department practice. However, doing so appropriately requires understanding our options to treat pain and a clear process to assess the factors causing the patient’s pain [1]. Pain treatment offers numerous advantages, such as alleviating pain-induced tachycardia in specific cases like acute MI and aortic dissection. Additionally, improved pain relief contributes to higher patient satisfaction.

Pain Assessment

When administering analgesics to patients in pain, there are no definitive contraindications. However, several factors should be considered when selecting the appropriate analgesic agent, including its route and dose. These factors encompass the pain’s intensity, probable cause, and the patient’s age, weight, medical history (including comorbidities and drug allergies), and vital signs. Pain is a complex and subjective experience that is unique to each patient. Appropriately assessing pain requires a thorough history and physical exam that include:

Location: Where is the pain? Does it travel or go anywhere else?
Onset: When did the pain begin? Is this an acute, chronic, or exacerbation of a chronic issue?
Provocation: What makes the pain worse?
Palliation: Does anything make this pain feel better? What has the patient tried to make it feel better, even if it didn’t work? Has the patient taken any medication at home to help with this, and what was the impact? If this patient has had this pain before, what made it better last time?
Quality: How does the pain feel?
Radiation: Does the pain go to any other location?
Severity: How severe is the pain? Can they compare it to other experiences they’ve had? How does it limit their activities, such as movement, eating, and sleeping?
Timing: Is the pain constant, or does it come and go? Does it change severity or quality over time?

Pain intensity scale

Numerical ranking: Ask your patient to rank the severity from 0 to 10, with 0 being no pain at all and 10 being the worst pain possible.
Verbal descriptors: Use descriptions from the patient of the pain and its impact on their functionality to rank their pain.
Visual descriptors: Use visual cues from your patient to rank their pain. The most common of these scales is the Wong-Baker scale, which is commonly used in children or nonverbal patients.

It is also important to remember that patients in pain may become agitated or mentally altered due to their pain. Severe pain in one area of the body may mask other symptoms or signs the patient is experiencing; hence, it is crucial to re-examine these patients after analgesia.

Analgesics

In the emergency department, treatment plans are often tailored to moderate/severe and acute and/or chronic pain.

Severe Acute Pain

In the management of moderate to severe acute pain, parenteral opioids are the primary treatment choice. These opioids target specific receptors in the central and peripheral nervous systems, altering how painful stimuli are perceived and responded to. Initially, they are administered as a bolus dose based on the patient’s weight, followed by titration every 5-15 minutes after reassessment. Opioids provide excellent analgesia, but they come with a long list of side effects that can be detrimental to the patient, even in the acute pain setting. Nausea and respiratory depression are the most significant side effects of all opioids, albeit with varying degrees. Parenteral opioids can also trigger pruritus and/or urticaria due to mast cell destabilization. Medications such as antiemetics, antihistamines, and naloxone can help reverse these potential side effects. Morphine is often the preferred parenteral opioid, with fentanyl and hydromorphone serving as alternatives. A safe initial dose of morphine is 0.1 mg/kg administered intravenously, while subcutaneous administration can be used if IV access is not available (although it is more painful and slower in onset). Please refer to the complete list of opioids and their recommended initial dosing regimens provided below.

Fentanyl: 0.25-1 µg/kg IV push [2], Short-acting opioid q. 15-60 minutes for severe pain.
Hydromorphone: 0.015 mg/kg IV/SC [3], q. 2-4 hours, avoid large doses in naive patients.
Oxycodone: 0.05-0.15 mg/kg PO [4], q. 3-4 hours.
Morphine: 0.1 mg/kg IV/SC [5], q. 3-4 hours, may cause release of histamine.
Oxycodone/Acetaminophen: 5-10 mg oxycodone/325-650 mg acetaminophen PO [6], q. 4-8 hours, moderate or severe pain (max dose of acetaminophen 4,000 mg/day).
Hydrocodone/Acetaminophen: 5 mg hydrocodone/325 mg acetaminophen, 1 to 2 tablets PO [7], q. 4-8 hours, moderate or severe pain (max dose of acetaminophen 4,000 mg/day).

Moderate Acute Pain

In cases of mild to moderate pain, oral opioids provide a suitable choice after initial non-opioid analgesia. Among these options are oxycodone combined with acetaminophen or hydromorphone combined with acetaminophen to impose a maximum daily dosage. The recommended dose for the opioid component is 0.05-0.15 mg/kg, and it can be repeated every 4-6 hours. Refer to the full list of opioids and their initial dosing regimens above.

However, the primary recommendation for moderate acute pain is non-opioid analgesics like NSAIDs and acetaminophen. They can synergistically complement opioids, potentially reducing the overall required dose of medications and minimizing the likelihood of side effects.
Acetaminophen is the safest option among these analgesics, accessible in oral and intravenous forms. While its exact mechanism remains uncertain, it exerts its effects centrally. NSAIDs, such as ibuprofen and ketorolac, inhibit cyclooxygenase (COX), thereby blocking prostaglandin-mediated inflammation. However, inhibiting prostaglandin synthesis leads to renal vasoconstriction and thus should be avoided in those with kidney disease. Please refer to the complete list of non-opioids and their recommended initial dosing regimens provided below.

Acetaminophen: 10-15 mg/kg PO/IV [8], Avoid if taking other acetaminophen-containing drugs or in patients with liver failure.
Ibuprofen: 5-10 mg/kg PO [9], Avoid in elderly patients and those with renal disease and peptic ulcer disease.
Ketorolac: 0.5 mg/kg IV/IM [10], Should only be given q6 hours, No more than 5 days.

Chronic Pain

It is important to recognize that patients with conditions that cause chronic pain or recurrent episodes of severe pain, such as sickle cell, have frequent or even chronic usage of opioid medications that require an individualized pain management plan. While chronic pain is challenging to address in the ED setting, these patients frequently get undertreated for their acute exacerbations [11]. Chronic pain is treated similarly to acute pain, using opioids for severe pain and non-opioids for more moderate pain. Treatment depends on the severity and previous history of analgesic success [12]. A step ladder approach, including non-opioid and opioid therapy, will be appropriate as part of departmental guidelines.

In addition, patients with a past or current history of a substance use disorder, including opioid use disorder, can still present with real, severe pain that may require the use of opioids for management. It is essential to assess these patients carefully and treat their pain like any other patient. If there are concerns that the patient’s condition may be related to a substance use disorder, it may be appropriate to refer them to a multidisciplinary specialist for support. This should be done after conducting a thorough history and physical examination and addressing immediate medical needs [13]. It is also vital that the ED team sticks to an individualized pain management plan once made by a multidisciplinary team on every recurrent presentation.

When making decisions for your patient, it is crucial to prioritize awareness of the addictive nature of opiates. To aid in this challenging choice, assess the patient’s opioid tolerance, history of substance abuse, and the risk associated with prescribing short-term PRN opioids upon discharge. The NIH Opioid Risk Tool (ORT) is helpful for screening for opioid abuse risk [14].

Local Anesthesia

Local anesthetics obstruct pain signal transmission by temporarily obstructing sodium channels in sensory nerve membranes. In the emergency department, lidocaine is commonly used, with or without epinephrine, to enhance hemostasis and prolong anesthetic efficacy. Bupivacaine, a longer-acting agent, is typically employed for regional anesthesia. While local anesthetics are generally safe, systemic CNS and cardiovascular toxicity can occur at large doses. Traditional teaching states that local anesthetic administration should be avoided in end organs such as the ears, nose, and penis to prevent ischemia. However, strong evidence is lacking to support this concern [15]. Local departmental or hospital guidelines should be followed in this case.

Lidocaine:
- Dose: Nerve Block 5-300 mg (maximum 4 mg/kg or 300 mg),
  - Acute Pain (Patch) 4%-5% patch q24 hours.
- Rapid onset. The maximum dose of lidocaine is 4 mg/kg (without epinephrine) and 7 mg/kg with epinephrine [16,17].
- Lidocaine is safe in pregnancy and breastfeeding.
Bupivacaine:
- Dose: Max dose 2.5 mg/kg, 3 mg/kg with epinephrine [18].
- Slower onset and higher risk of cardiovascular toxicity.
Chloroprocaine:
- Dose: Max dose 10 mg/kg, 15 mg/kg with epinephrine [19].
- Used in the case of allergy to lidocaine and other amide local anesthetics.

Procedural Sedation

Procedural sedation refers to the administration of medications aimed at reducing anxiety and pain while enhancing tolerance to a particular medical procedure. This technique is reserved for hemodynamically stable patients who are expected to be able to maintain their airways throughout the procedure. Common indications of this technique include cardioversion, orthopedic reductions, and other painful procedures [20]

A common approach to procedural sedation:

Risk stratification to prepare for potentially difficult airway management
1. Use the Mallampati Score to assess the difficulty of the airway should the patient lose their airway during the procedure. Refer to UpToDate Mallampati Airway Classification.
2. Determine the ASA Score category. Refer to the ASA Physical Status Classification System.
Informed Consent
1. Typically, it is required before the procedure to discuss the complications and alternative options.
Gathering Supplies
1. IV, O2, Monitoring including capnography.
2. BVM and airway trolley
Assemble Team
- Depending on the complexity of the procedures, decide about the team members and their roles. A separate person should typically be responsible for sedation and airway monitoring while one or two other members perform the procedure. For details about team dynamics, refer to this book’s chapter on Teamwork.
Perform the procedural sedation
1. Administer procedural sedation medications (See below)
2. Perform the procedure while constantly assessing hemodynamic stability and respiratory status.
Post Sedation Care
- Provide post-sedation monitoring and reassessment, and then discharge instructions according to the individual case and departmental guidelines.

Most Common Procedural Sedation Medications

Midazolam:
- Dose: 0.1 to 0.5 mg/kg IV [21].
- Comments: No analgesic effect, administered before the procedure to reduce anxiety and provide amnesia.
Fentanyl:
- Dose: 1 mcg/kg IV [22].
- Comments: Reduces pain, commonly used in reductions and I&D as an adjunct to other medications or local anesthesia.
Propofol:
- Dose: 0.5-1 mg/kg IV [23].
- Comments: Used as a general short-acting anesthetic and causes respiratory depression and hypotension.
Etomidate:
- Dose: 0.15 mg/kg IV [24].
- Comments: Used as a general anesthetic; can cause myoclonus.
Ketamine:
- Dose: 1-2 mg/kg IV [25], 2-4 mg/kg IM (especially in pediatrics).
- Comments: The dissociative anesthetic that provides both amnesia and analgesia. Known to cause aggressive emergence reaction and rarely laryngospasm.

Hints and Pitfalls

Like all treatments, it is crucial to reassess the patient after giving them medication and understand how medication can change your ability to evaluate the patient. A patient in severe pain may be unable to provide a full history or participate in a complete physical exam until their pain has been controlled. For example, a patient with an extremely painful angulated fracture of the humerus may not be able to participate in an exam to evaluate their distal neurovascular status, or the same patient may have such severe pain in their arm that they do not notice that they are also having abdominal pain. Treating pain earlier in such encounters can help facilitate high-quality patient care.

Factors that can lead to undertreatment include atypical presentation, communication barriers, and implicit bias. Pediatric patients, patients with neurocognitive disorders, and patients from different cultural or linguistic backgrounds are frequently undertreated for their pain.

Special Patient Groups

It is essential to carefully evaluate pain in patients who cannot directly communicate with the physician [26].

Those patients may be:

Nonverbal at baseline
Speak a different language than the physician
Have a cognitive impairment
Geriatric patients
Underreporting of pain
Higher frequency of illness-causing cognitive impairment and communication barriers such as Alzheimer’s
Concerns for side-effects

Geriatric patients generally have poor physiological reserve and polypharmacy. While these factors need to be considered in the choice of analgesics, their dosage, and required monitoring, these concerns should not lead to undertreatment of pain in this population.

Revisiting Your Patient

How should we manage our 57-year-old female with peptic ulcer disease, who presented with a twisted ankle? Given that her left ankle is swollen and that she has bony 9/10 tenderness at the posterior edge of the left lateral malleolus but no left mid-foot pain, it is likely that she has an uncomplicated closed ankle fracture.

The initial step in management would be to start treating her pain soon after her presentation. An important KPI (Key Performance Indicator) in this regard is that the degree of pain is assessed on arrival in every patient who presents to ED with pain, and individually planned titrated analgesia is started as early as possible.
Given that she is in acute, moderately severe pain with a history of peptic ulcer disease (PUD), she would most likely benefit from a drug like Oral Hydromorphone and Oral/IV Paracetamol. In this patient’s case, NSAIDs, such as Ibuprofen, should specifically be avoided due to her history of PUD. Initial pain management in the emergency department can also be managed with “RICE,” which includes rest, ice, compression, and elevation of the injured body part. The RICE technique is an effective way to alleviate pain in patients who deny pain medication or who are still waiting to see a provider. It is important to reassess pain and vital signs after administering analgesics.

If this patient had an evident ankle deformity with weak pulses, she would have required procedural sedation and urgent reduction.

Authors

Kayla Peña

Rutgers Robert Wood Johnson Medical School

Kelsey Thompson

UCLA Harbor

Munawar Farooq

College of Medicine and Health Sciences, UAEU Al Ain, UAE

Listen to the chapter

References

Hachimi-Idrissi S, Coffey F, Hautz WE, et al. Approaching acute pain in emergency settings: European Society for Emergency Medicine (EUSEM) guidelines-part 1: assessment. Intern Emerg Med. 2020;15(7):1125-1139. doi:10.1007/s11739-020-02477-
In: Lexicomp. UpToDate Inc; 2023. Accessed May 10, 2023. http://online.lexi.com
In: Lexicomp. UpToDate Inc; 2023. Accessed May 10, 2023. http://online.lexi.com
UpToDate Inc; 2023. Accessed May 10, 2023. http://online.lexi.com
In: Lexicomp. UpToDate Inc; 2023. Accessed May 10, 2023. http://online.lexi.com
Oxycodone/Acetaminophen: Drug Information. In: Lexicomp. UpToDate Inc; 2023. Accessed May 10, 2023. http://online.lexi.com
Hydrocodone/Acetaminophen: Drug Information. In: Lexicomp. UpToDate Inc; 2023. Accessed May 10, 2023. http://online.lexi.com
Paracetamol: In: Lexicomp. UpToDate Inc; 2023. Accessed May 10, 2023. http://online.lexi.com
In: Lexicomp. UpToDate Inc; 2023. Accessed May 10, 2023. http://online.lexi.com
In: Lexicomp. UpToDate Inc; 2023. Accessed May 10, 2023. http://online.lexi.com
Dora-Laskey, A. (2022). Acute Pain Control. Society for Academic Emergency Medicine (SAEM M3 Curriculum). Retrieved from https://www.saem.org/about-saem/academies-interest-groups-affiliates2/cdem/for-students/online-education/m3-curriculum/group-acute-pain-control/acute-pain-control.
Busse JW, Wang L, Kamaleldin M, et al. Opioids for chronic noncancer pain: A Systematic Review and Meta-analysis. JAMA. 2018;320(23):2448-2460. doi:10.1001/jama.2018.18472
Nordt SP, Ray L. Lidocaine. In: Mattu A and Swadron S, ed. ComPendium. Burbank, CA: CorePendium, LLC. Updated May 12, 2023. Accessed May 13, 2023.https://www.emrap.org/corependium/drug/recUEl2x9lfeYKbws/Lidocaine#h.tuo0od96 muij.
Perry JS, Stoll KE, Allen AD, Hahn JC, Ostrum RF. The opioid risk tool correlates with increased postsurgical opioid use among patients with orthopedic trauma. Orthopedics. 2023;46(4):e219-e222. doi:10.3928/01477447-20230207-04
Schnabl SM, Herrmann N, Wilder D, Breuninger H, Häfner HM. Clinical results for use of local anesthesia with epinephrine in the penile nerve block. J Dtsch Dermatol Ges. 2014; Apr;12(4):332-339. doi: 10.1111/ddg.12287. Epub 2014 Mar 3. PMID: 24581175.
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Lidocaine with epinephrine. In: Lexicomp. UpToDate Inc; 2023. Accessed May 10, 2023. http://online.lexi.com
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Miner James R., Paetow Glenn. Procedural Sedation. In: Mattu A and Swadron S, ed. CorePendium. Burbank, CA: ComPendium, LLC. https://www.emrap.org/corependium/chapter/recCvtWt5In5h4fLJ/Procedural-Sedation#h.9du7441ga4gn. Updated September 15, 2021. Accessed May 13, 2023.
Midazolam. In: Lexicomp. UpToDate Inc; 2023. Accessed May 10, 2023. http://online.lexi.com
Fentanyl. In: Lexicomp. UpToDate Inc; 2023. Accessed May 10, 2023. http://online.lexi.com
Propofol. In: Lexicomp. UpToDate Inc; 2023. Accessed May 10, 2023. http://online.lexi.com
Etomidate. In: Lexicomp. UpToDate Inc; 2023. Accessed May 10, 2023. http://online.lexi.com
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FOAM and Further Reading

Pediatric pain: Pediatric Pain Management

Chronic pain: I CAN’T GET NO SATISFACTION FOR MY CHRONIC NON-CANCER PAIN

Reviewed and Edited By

Arif Alper Cevik, MD, FEMAT, FIFEM

Back Pain (2024)

December 3, 2024December 3, 2024 ~ iEM Education Project Team ~ Leave a comment

by Paila Naveen & Manjith Reddy

You have new patients!

A 30-year-old male patient presents to the ED with an abnormal gait and no history of comorbidities. He complains of low back pain that started three days ago after performing a deadlift during a gym competition. The patient reports experiencing a snapping sensation during the lift, followed by a shooting pain radiating down the left leg, which subsided after a short time. However, the low back pain gradually worsened over the past three days and became unbearable upon arrival. He also reports weakness in the left foot since this morning, making it difficult for him to walk properly. This concern prompted him to seek medical attention in the ED.

What do you need to know?

Importance

Back pain is a term that, while commonly used, oversimplifies a condition affecting a much larger area of the body. It is often not taken seriously, possibly due to the time-consuming nature of evaluation, a lack of proper clinical skills, inadequate anatomical knowledge, or the pressures of a busy emergency department. This oversight can result in difficulty accurately identifying the cause of the pain, ultimately leading to increased morbidity and mortality.

This approach must change, as underestimating back pain can have fatal consequences. The condition encompasses a wide spectrum of causes, ranging from a minor muscle strain to severe conditions such as cauda equina syndrome, aortic dissection, or even worse.

Epidemiology

Up to 84% of adults experience low back pain at some point in their lives [1]. It is one of the top five most common complaints in emergency departments (ED) [2]. Low back pain accounts for 3.15% of all ED visits, with 65% of these cases resulting from injuries sustained at home [3]. Despite its prevalence, an estimated 85% of patients presenting with low back pain cannot be accurately diagnosed; however, nearly all of these patients recover within 4–6 weeks [4]. In contrast, 5–10% of patients with acute back pain suffer from more serious underlying conditions. While most visits for back pain are benign, they can be time-consuming and frustrating for both physicians and patients. Emergency physicians must remain vigilant in identifying and managing potentially dangerous conditions [5].

Pathophysiology

Acute back pain is a multifaceted condition characterized by various underlying mechanisms that contribute to its pathophysiology. It typically arises from damage to somatic structures, leading to nociceptive pain, which is transmitted through the peripheral and central nervous systems [6]. The pathophysiology of back pain involves multiple structures, including peripheral nerves, the central spinal cord, skeletal muscles, and blood vessels spread across the back. These structures can be affected by various underlying causes, broadly categorized as vascular, structural, referred pain, inflammation, infection, metabolic disorders, neoplasms, or trauma.

Acute back pain primarily involves nociceptive pathways, which transmit pain signals from damaged tissues such as the lumbar spine, ligaments, and muscles. In many acute cases, muscle spasms significantly contribute to pain; however, there is ongoing debate regarding whether these spasms are a primary cause or a secondary response to the injury. The progression from acute to chronic pain often involves central sensitization, a process where the nervous system becomes increasingly sensitive and responsive to pain stimuli [6].

When assessing a patient, it is crucial to first evaluate the nature of the pain. Determine whether the pain is localized, which may indicate an underlying fracture, or diffuse, as seen in conditions like an epidural abscess. Consider the possibility of referred pain originating from retroperitoneal structures. Additionally, assess for systemic symptoms or signs of inflammation, such as weight loss, which could point to a neoplasm or other serious pathology.

A thorough history-taking process is essential, including both positive and negative findings, to narrow down the differential diagnosis. Employ a structured approach to guide your assessment; once you refine the differential through history and clinical examination, investigations can confirm the diagnosis and facilitate effective management.

Initial Assessment and Stabilization

As emergency physicians, our approach to back pain differs from that of other specialties, as we must remain highly alert and responsive. While stable cases allow for a thorough history to be taken, unstable patients require a critical and focused approach to quickly identify the underlying cause. The following outlines this critical approach:

Airway/Breathing

When assessing a critical patient, prioritize airway and breathing management, and prepare for intubation. Key considerations include proper positioning, adequate suctioning, aspiration prevention, and effective visualization while securing the airway. Use videolaryngoscopy for improved visualization unless visualization is expected to be poor. To minimize aspiration risk, avoid over-ventilation and ensure the availability of two high-volume suction devices. Refrain from placing the patient in a supine or prone position to further reduce aspiration risk. Enhance first-pass success by using a bougie, and place a nasogastric tube once the airway has been secured.

Circulation

In patients with undifferentiated back pain presenting in shock, apply standard shock management measures. Begin with the insertion of two large-bore IVs to establish access for fluid and blood administration. If conditions such as abdominal aortic aneurysm (AAA), retroperitoneal hemorrhage, or ruptured ectopic pregnancy are suspected, cross-match for six units of blood. For suspected spinal epidural abscess, obtain blood cultures, administer appropriate antibiotics, and consider vasopressors if the patient remains unresponsive to a fluid bolus of 30 mL/kg. Use point-of-care ultrasound to assess the aorta for AAA and evaluate the bladder for urinary retention, particularly if cauda equina syndrome is a concern. Residual urine volumes greater than 100–150 mL are abnormal. Ultrasound is the preferred method for screening urinary retention due to its accuracy, non-invasiveness, and patient comfort, though a Foley catheter can also be used to measure residual urine volume [7].

The assessment of neurological status and additional exposure findings should be completed during the initial evaluation of the undifferentiated unstable back pain patient.

Medical History

A comprehensive history is essential when evaluating patients with back pain. The acronym SOCRATES provides a structured approach to effectively assess the nature of the pain:

SITE: Determine the exact location of the pain.
ONSET: Enquire about when and where the pain initially started.
CHARACTER: Ask about the quality of the pain, such as pricking, stabbing, burning, or squeezing. Pain at rest, accompanied by sweating or sleep disturbance, is often associated with conditions like rheumatoid arthritis, ankylosing spondylitis, or malignancies. Burning pain usually indicates neuropathy, while tearing pain may suggest aortic dissection. Sharp, shooting pain with localized tenderness may indicate spinal fractures, muscle spasms, or pulmonary embolism.
RADIATION: Explore whether the pain radiates to specific regions. For instance, cervico-genic headaches can radiate to the head, chest pain may suggest myocardial infarction or aortic dissection, and radiculopathy often involves the upper or lower limbs due to nerve root compression. Loin-to-groin radiation is characteristic of renal colic, while pain extending to the buttocks or legs may point to sciatic nerve compression. Abdominal radiation is commonly associated with constipation, mesenteric ischemia, or an abdominal aortic aneurysm (AAA).
ASSOCIATED SYMPTOMS: Enquire about symptoms accompanying back pain. Important symptoms to explore include sensory or motor deficits (indicating nerve root or spinal cord compression, such as in radiculopathy or cauda equina syndrome), urinary retention or incontinence (specific to cauda equina syndrome), hematuria (suggestive of kidney injury or malignancy), fever (associated with epidural or spinal abscesses), weight loss (indicative of malignancy), and morning stiffness (linked to rheumatoid arthritis or ankylosing spondylitis) [7].
TIME COURSE: Assess how the pain has evolved over time and use a pain severity scale (1–10) to gauge its intensity.
EXACERBATING OR RELIEVING FACTORS: Ask about factors that worsen or alleviate the pain, such as coughing, sneezing, walking, lying down, compression, medications, or physical support.
SEVERITY: Beyond numerical scales, explore how the pain impacts the patient’s daily activities and ability to perform routine tasks.

A thorough patient history should include surgical, family, medication, and social factors that may contribute to back pain.

Surgical history should document any previous back procedures, as they may influence the current presentation.

Family history is essential to identify any hereditary predisposition to vascular or inflammatory diseases.

Medication history should include the use of immunosuppressive therapies, anticoagulants, or glucocorticoids, as these can increase the risk of infections, bleeding, or osteoporosis-related complications.

Finally, social history should explore lifestyle factors such as intravenous drug use, alcohol consumption, smoking, and pregnancy status, all of which can significantly impact the diagnosis and management of back pain.

Special attention should be given to traditional “red flag” symptoms for back pain during the patient history, as these symptoms often warrant immediate imaging in the emergency department.

These red flags can be remembered using the mnemonic TUNA FISH [8]:

T for trauma,
U for unexplained weight loss,
N for neurological symptoms,
A for age over 50 years,
F for fever,
I for IV drug use or immunocompromised status,
S for steroid use or syncope, and
H for a history of cancer.

Physical Examination

A thorough physical examination is essential for patients presenting with undifferentiated back pain, especially when red flags are not evident in the history. It is critical to carefully evaluate for red flags during the examination and document all findings meticulously. The red flags on examination include abnormal vital signs (e.g., hypotension, fever, tachycardia, hypoxemia, or pulse deficits), motor weakness, saddle anesthesia, urinary retention, loss of rectal tone, abnormal reflexes (such as a positive Babinski sign), and pain on percussion of the spinous processes. In addition to identifying red flags, the physical examination should also cover other key areas to narrow the differential diagnosis.

Key Components of the Physical Examination:

Red Flags for Back Pain:

Abnormal vital signs: Hypotension, fever, tachycardia, hypoxemia, pulse deficits.
Motor weakness.
Saddle anesthesia.
Urinary retention.
Loss of rectal tone.
Abnormal reflexes: Positive Babinski sign.
Pain on percussion of spinous processes.

Other Important Aspects:

Inspection:
- Examine the back for signs of trauma, infection, asymmetry, scoliosis, kyphosis, or herpes zoster.
- Assess hip, pelvis, and spine anatomy and function.
Percussion/Palpation:
- Check for vertebral or soft tissue tenderness.
- Palpate for pulsatile abdominal masses.
Neurologic Examination:
- Assess reflexes (e.g., diminished or abnormal knee and plantar reflexes).
- Evaluate strength (weakness in the upper or lower extremities).
- Observe gait, ataxia, limp, or inability to ambulate.
- Check for signs of cauda equina syndrome, including loss of rectal tone or sensation.
Testing for Sciatic Nerve Root Irritation:
- Perform straight leg raising tests.
- Look for bilateral weakness, paresthesia, sensory level abnormalities, saddle anesthesia, muscle atrophy, and decreased rectal sphincter tone.
Vascular Assessment:
- Measure upper extremity blood pressures for discrepancies (e.g., aortic dissection).
- Listen for murmurs (aortic insufficiency) or signs of peripheral vascular disease [9].
Genitourinary Examination:
- Assess for urinary retention or incontinence.
- Measure post-void residual (abnormal if >100 mL).
- Perform a prostate exam if appropriate, considering prostatic hypertrophy as a possible cause of retention.
Rectal Examination:
- Conduct a rectal exam in all high-risk patients to assess for abnormalities in tone or sensation.

Additional Considerations:

Repeat the neurological exam throughout the encounter to detect any changes or progression in symptoms.
Remember that the spinal cord ends at L1; herniation above this level results in upper motor neuron findings (e.g., weakness, hyperreflexia, increased tone), while herniation below L1 leads to lower motor neuron findings (e.g., weakness, hyporeflexia, atrophy).
Consider the psychosocial context of lower back pain. Inconsistencies in physical findings due to patient distraction should not be dismissed as malingering. Instead, view these inconsistencies as the patient’s way of seeking help, just as with any other presentation.

Special examinations for back pain, often referred to as provocative tests, are used to assess specific conditions or structures causing discomfort. These include the Straight Leg Test, which evaluates nerve root irritation, commonly associated with lumbar disc herniation [10]. A variant of this test may be performed to refine diagnostic accuracy. The Tripod Sign Test assesses hamstring tightness and its relation to nerve irritation or musculoskeletal dysfunction [11]. Lastly, the Femoral Stretch Test is used to identify pathology in the femoral nerve or upper lumbar nerve roots [12]. Together, these tests provide targeted insights into the underlying causes of back pain.

Primary Goal

The primary goal when evaluating back pain is to rule out life-threatening, non-spinal causes. These include acute aortic aneurysm (AAA), thoracic aneurysm, aortic dissection, ectopic pregnancy, and epidural compression from abscess or hemorrhage. Once these critical conditions are excluded, attention should shift to nonspecific low back pain, which may originate from nerves, nerve roots, musculoskeletal structures, or even nonorganic causes. During the rapid physical examination, the presence of red flag signs should prompt immediate concern. These warning signs include abnormal vital signs, motor weakness, saddle anesthesia, urinary retention, loss of rectal tone, abnormal reflexes, and pain on percussion of the spinous processes.

Not-to-Miss Diagnoses and Red Flags

DIAGNOSIS	RED FLAG`S
Acute aortic pathology	Pain abdomen Blood in urine Pulse deficit in extremities Abdominal bruit/thrill Palpable abdominal mass
Infection (Spinal epidural abscess, Discitis, Osteomyelitis)	Fever Intra venous drug use Immunodeficiency/HIV Diabetes Steroid use
Fracture (Traumatic, Pathologic)	Recent fall/trauma, Age > 60yrs Previous traumatic fracture Spinal tenderness
Malignancy (Primary / metastasis)	Unusual Weight Loss Night sweats Fatigue Chronic pain H/O cancer Pain unresponsive to analgesia
Cauda Equina Syndrome/Disc Herniation	Weakness Loss of sensation Decreased reflexes Inability to walk Bowel & Bladder incontinence Bladder distension

Alternative / Differential Diagnoses

When evaluating patients with back pain, it is crucial to consider a broad differential diagnosis encompassing various systemic and localized causes. Back pain may arise from vascular, infectious, mechanical, immunologic, rheumatologic, inflammatory, non-organic, or pharmacologic origins. Each category includes potentially life-threatening and benign conditions that require careful assessment. By systematically approaching the possible causes, clinicians can better identify the underlying pathology and prioritize interventions based on the severity and acuity of the patient’s presentation. The following is a categorized list of potential diagnoses to guide clinical evaluation and management.

Vascular Causes

Abdominal aortic aneurysm
Acute coronary syndromes
Acute vaso-occlusive crisis
Cardiac tamponade
Severe aortic insufficiency/regurgitation
Thoracic aortic dissection
Pulmonary embolism
Renal artery dissection or thrombosis
Retroperitoneal hematoma
Spinal/epidural hematoma

Infectious Causes

Discitis
Epidural abscess
Meningitis
Osteomyelitis
Pelvic inflammatory disease
Pericarditis
Pneumonia
Prostatitis
Pyelonephritis
Tuberculosis (Pott’s disease)

Mechanical Causes

Cauda equina syndrome (from disc herniation or fracture)
Disc herniation
Ectopic pregnancy
Lumbar radiculopathy
Metastatic cancer
Pneumothorax
Pneumomediastinum
Scoliosis
Spinal stenosis
Syringomyelia
Traumatic or pathologic vertebral fracture
Ureteral calculus

Immunologic Causes

Transverse myelitis

Rheumatologic Causes

Gout and pseudo-gout
Osteoarthritis
Rheumatoid arthritis

Inflammatory Causes

Cholecystitis
Herpes zoster
Myocarditis/pericarditis
Musculoskeletal strain
Pancreatitis
Perforated viscus

Non-organic Causes

Factitious disorder
Depression

Pharmacologic Causes

Tolerance, dependence, addiction

Acing Diagnostic Testing

When life-threatening, non-spinal causes of low back pain have been ruled out through history and physical examination, laboratory tests are generally unnecessary for most patients. However, there are specific situations where laboratory investigations may provide valuable diagnostic insight [13,14]. These include cases where infection, malignancy, immune suppression, or other red flags are suspected. Below is a list of relevant laboratory tests and their clinical significance:

Laboratory Tests for Low Back Pain:

Complete Blood Count (CBC):

Helps identify infection, malignancy, or immune suppression.
Elevated white blood cell counts are present in only 66% of patients with spinal epidural abscesses [15].

C-Reactive Protein (CRP) and Erythrocyte Sedimentation Rate (ESR):

These markers may aid in diagnosing inflammatory or malignant conditions [16].
Elevated levels are associated with osteomyelitis and discitis [17].
Due to poor sensitivity, CRP and ESR are not recommended for patients without red flags and are not typically used when disc herniation or epidural hematoma is the primary diagnosis [18].

Pregnancy Testing:

Should be performed on all women of childbearing age to rule out pregnancy-related causes and guide management.

Radiographic Examination for Back Pain

Radiographic examination is crucial for evaluating, interpreting, and reviewing patients experiencing back pain due to spinal issues. This section discusses the use of various imaging modalities and diagnostic tools to assess potential life-threatening and spinal-related conditions.

Point-of-Care Ultrasound

Point-of-care ultrasound (POCUS) is a rapid bedside diagnostic tool that allows for quick and accurate detection of various emergency conditions. It aids in deciding whether further imaging is necessary.

Cardiac Ultrasound: Perform a cardiac ultrasound to detect ascending aortic dissection and pericardial effusion. Use the sub-xiphoid view and evaluate:
1. Pericardial effusion
2. Right atrial (RA) and diastolic right ventricular (RV) collapse
Additionally, the physical examination should include checking for pulsus paradoxus.
Parasternal – long axis view provide information about ascenting aorta and possible aortic dissection.
Abdominal Aortic Ultrasound: Perform this ultrasound to rule out abdominal aortic aneurysm (AAA).
Targeted Ultrasound for Trauma: Examine for free fluid in the pelvis and, if a ruptured ectopic pregnancy is suspected, include the uterus and adnexa in the evaluation.
Suspected Cauda Equina Syndrome: Conduct a residual urine test, as urinary retention (>100-150 mL) is abnormal. Ultrasonography of the bladder is preferred to calculate residual urine volume because it is accurate, noninvasive, and more comfortable for the patient. Alternatively, a Foley catheter can be used to measure residual urine after urination. [19]

Chest Radiograph

A chest radiograph is a valuable tool for identifying emergency causes of back pain, including:

Dilated mediastinum (indicative of thoracic aortic dissection)
Pneumothorax
Pneumomediastinum
Free air under the diaphragm (suggestive of a perforated viscus)

Once life-threatening non-spinal causes of back pain have been excluded, imaging can be ordered based on prominent symptoms and findings from the patient’s history and physical examination. The primary imaging modalities include plain radiographs, computed tomography (CT), and magnetic resonance imaging (MRI). [20]

Plain Radiographs

Plain radiographs have limited diagnostic utility but can be helpful in specific situations:

Fracture Detection: Anterior-posterior and lateral radiographs may identify vertebral fractures, although they are less sensitive than CT scans.
Infection or Malignancy: When combined with erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) tests, plain radiographs can reduce the likelihood of infection or malignancy.
Incidental Fractures: Plain radiographs may also reveal incidental fractures.

Computed Tomography (CT)

CT provides better resolution and higher sensitivity/specificity than plain radiographs. It is especially useful for suspected spinal fractures. However, CT has limitations:

It does not adequately image the spinal cord, making it less effective for diagnosing epidural abscesses and disc herniations.
Consider CT only when MRI is contraindicated. [21]

Magnetic Resonance Imaging (MRI)

MRI is the imaging modality of choice for urgent spinal conditions, including:

Spinal/epidural hematomas
Epidural abscesses
Cauda equina syndrome
Transverse myelitis
MRI Without Contrast: This provides detailed imaging of intervertebral discs, canal anatomy, nerves, ligaments, and epidural fat. Clinical guidelines recommend early MRI for uncomplicated occupational low back pain only if red flags are absent [21].
MRI With Gadolinium Contrast: Adding gadolinium improves diagnostic accuracy by differentiating surgical scarring from disc disease and evaluating vascular function in real-time.

Myelography

Myelography may be used in patients unable to undergo MRI. It evaluates the spinal cord, nerve roots, and meninges, offering a valuable alternative in specific cases.

Management

Approach To the Non-Critical Patient

Providing care to non-critical patients with back pain involves early pain management, targeted therapy, and continuous evaluation for red flags. This approach enhances patient satisfaction and ensures effective management.

Early Pain Management

Early analgesia is a critical aspect of care. Non-narcotic analgesics are preferred, combined with an empathic attitude from healthcare providers. These measures significantly improve patient comfort and satisfaction. [22]

Targeted Therapy

Treatment should be aimed at addressing the specific underlying cause of the back pain. Common conditions to consider include:

Lumbar Radiculopathy
Sciatica with Nerve Root Compression
Spinal Stenosis
Musculoskeletal Strain
Scoliosis

However, it is important to note that the majority of patients (approximately 85%) experience nonspecific back pain without a readily identifiable underlying condition. [23]

Reevaluation and Multidisciplinary Approach

Patients with persistent back pain should be reevaluated for red flags that may indicate serious underlying conditions. In the absence of red flags:

Initiate appropriate treatment tailored to the patient’s symptoms.
Consider referral to a physician for further evaluation and management as needed.
A multidisciplinary approach, involving physical therapy, pain management specialists, and other healthcare providers, may provide additional benefits for long-term management.

Non-Pharmacologic Management

Non-pharmacologic interventions play an essential role in managing back pain, particularly in acute, subacute, and chronic stages. These methods are effective, safe, and recommended by guidelines to complement or substitute pharmacologic treatment.

Heat Therapy

According to the 2017 American College of Physicians guidelines, superficial heat therapy is recommended as a form of nonpharmacologic analgesia for back pain. It provides relief by improving blood flow and relaxing muscles, making it an effective first-line treatment for many patients.

Activity Recommendations

Acute Phase: Patients should remain as active as possible. While engaging in structured exercise is not advised during the acute phase, maintaining light activity is beneficial. [24]
Bed Rest: Patients who remain on bed rest tend to recover more slowly and report more pain compared to those who stay ambulatory. Encouraging mobility helps expedite recovery. [25]

Exercise for Subacute and Chronic Pain

For patients with subacute or chronic low back pain, engaging in regular physical activity is crucial for long-term management. No specific type of exercise has proven superior; instead, various forms can be beneficial, including:

Aerobic exercise
Stretching
Pilates
Walking
Yoga
Tai Chi

The choice of activity should be tailored to the patient’s preferences and physical capacity to ensure adherence and maximize benefits. [26]

Trigger Point Injection Therapy

Trigger point injection therapy is a valuable but often underappreciated treatment for managing regional musculoskeletal pain. This therapy targets specific areas of muscle tightness, commonly associated with myofascial pain syndrome.

Characteristics of Trigger Points

A trigger point is a localized area of muscle pain that typically worsens with movement. These points are often identified during physical examination by the presence of a “twitch” response or the radiation of pain upon palpation. [27]

Pathogenesis of Trigger Points

The exact scientific mechanism behind the formation of trigger points remains unclear. However, many researchers suggest that acute trauma or repetitive microtrauma plays a significant role. Several contributing factors have been identified, including:

Suboptimal physical conditioning
Surgical scars
Insomnia
Joint dysfunction
Vitamin deficiencies
Poor posture [28]

Application of Trigger Point Injections

Although trigger point injections are not commonly utilized in emergency department (ED) settings, they represent a safe and effective alternative to narcotic pain management. By targeting the localized source of pain, this therapy can provide significant relief, especially in patients with myofascial pain syndrome. Increased awareness of this technique may help expand its use in broader clinical practice.

Some recommended anesthetic agents and their dosage are below;

Lidocaine 1%

Dosage: The recommended dosage of lidocaine 1% is 3 mg, with a maximum allowable dose of 5 mg.
Pregnancy Considerations: Lidocaine may induce premature labor; therefore, it is essential to seek expert advice before administering it to pregnant patients.
Precautions: Ensure accurate dosing to avoid complications. Monitor for signs of local anesthetic toxicity during and after administration.

Bupivacaine 0.25%

Dosage: The standard dosage for bupivacaine 0.25% is 0.75 mg, with a maximum limit of 1.25 mg.
Pregnancy Considerations: Like lidocaine, bupivacaine may also induce premature labor, necessitating expert consultation before use in pregnant patients.
Precautions: Accurate dosing is critical. Watch for potential symptoms of local anesthetic toxicity to ensure patient safety.

Injection Procedure

When administering injections, limit the procedure to a maximum of three sites while strictly adhering to sterile technique. Inject 0.3-0.5 mL into each site, carefully infiltrating the subcutaneous and muscle tissue. It is unnecessary to approach the spine or deeper muscle layers during this process. [29]

Use of Lidocaine 5% Topical Patches

Lidocaine 5% transdermal patches may also be utilized for pain management. Patients should be advised to remove the patch every 12 hours to prevent potential skin irritation. Proper application and timing are essential to maximize effectiveness while minimizing side effects.

Non-opioid analgesics (acetaminophen and non-steroidal anti-inflammatory drugs [NSAIDs], topical analgesics)

Non-opioid analgesics are considered the first-line treatment for pain management. Among these, non-steroidal anti-inflammatory drugs (NSAIDs) are widely used for their efficacy. However, their application must be tailored to individual patient needs and conditions.

Common NSAIDs and Their Guidelines

Ibuprofen:

- Dose: 400 mg, with a maximum of 800 mg
- Frequency: Every 6 hours
- Use in Pregnancy: Category C in the first and second trimesters
- Caution: Avoid in patients with acute kidney injury (AKI), congestive heart failure (CHF), or liver disease.

Naproxen:

Dose: 250 mg, with a maximum of 500 mg
Frequency: Every 12 hours
Use in Pregnancy: Not recommended
Caution: Use cautiously in patients with a history of stomach ulcers.

Diclofenac:

Dose: 50 mg, with a maximum of 75 mg
Frequency: Every 12 hours
Use in Pregnancy: Category C in the first and second trimesters
Caution: Avoid in patients with NSAID allergies.

Meloxicam:

Dose: 7.5 mg, with a maximum of 15 mg
Frequency: Once every 24 hours
Use in Pregnancy: Category C in the second and third trimesters
Caution: Contraindicated in patients with chronic kidney disease (CKD), chronic liver disease (CLD), or post-coronary artery bypass graft (CABG) surgery.

In clinical practice, the management of pain, particularly low back pain, often varies due to limited high-quality data. Low back pain remains one of the most common reasons patients are prescribed opioids, despite the availability of non-opioid alternatives [31,32].

Emerging data suggest that topical therapies can provide safe and effective treatment options for patients experiencing chronic, localized musculoskeletal and neuropathic pain. These therapies serve as an alternative for individuals who may not tolerate oral NSAIDs or opioids. [33]

Opioid Analgesics

Opioids are commonly used for pain relief in patients with low back pain, particularly in emergency department (ED) settings. However, their use should be carefully considered due to limited evidence of long-term benefits.

Prevalence of Opioid Use

A national study authored by Friedman revealed that opioids are administered to two out of three patients presenting to the ED with low back pain. This high prevalence highlights the reliance on opioids in acute care settings. [34]

Patient Population and Data Interpretation

Patients presenting to the ED often have more acute illnesses or severe pain compared to those seen in primary care settings. This distinction may skew the data and influence treatment patterns, as ED physicians are tasked with managing severe pain in a short timeframe.

Limitations of Opioid Therapy

Opioids provide temporary pain relief but lack evidence of improving functional outcomes or reducing long-term disability in patients with acute low back pain. For this reason, they are not recommended as first-line therapy for managing such conditions.

Appropriate Use of Opioids

Opioids should be reserved for specific scenarios:

When all other alternatives have been exhausted
When low-dose treatment can facilitate a return to mobility in the emergency setting

By reserving opioid use for carefully selected cases, clinicians can minimize the risk of dependency and prioritize treatments that improve long-term outcomes.

Muscle Relaxants

Muscle relaxants are often considered for managing muscle spasms and associated pain, but their effectiveness and appropriate use require careful evaluation.

Evidence suggests that muscle relaxants are not more effective than nonsteroidal anti-inflammatory drugs (NSAIDs), acetaminophen, or aspirin for managing pain. These alternatives are often preferred due to their similar efficacy and more favorable safety profiles. [35, 36]

A single dose of a benzodiazepine may be considered in the emergency department (ED) for acute muscle spasms. However, benzodiazepines are categorized as second-line agents for this purpose and are not recommended for routine prescription at discharge. Limiting their use helps reduce the risk of dependency and other potential side effects.

Steroids

The role of steroids in managing low back pain remains a topic of confusion and debate. While oral steroids can provide initial symptom relief, their long-term outcomes are less favorable. Studies have shown that patients who use oral steroids may experience complicated outcomes after one year, raising questions about their routine use in this context.

Surgery

Although it is not a primary focus of emergency medicine, providing appropriate recommendations for patients based on institutional resources regarding surgical options can be valuable for their management. For patients who do not respond to pharmacologic therapy, surgical interventions may be considered. These options are typically reserved for individuals with persistent symptoms or structural abnormalities requiring correction [37].

Special Patient Groups

Pediatrics

Unlike adults, children presenting with back pain are more likely to have an underlying serious medical condition. This is especially true for children aged four years or younger, or for any child whose back pain is accompanied by concerning symptoms.

Warning Signs Associated with Back Pain in Children

Parents and caregivers should be alert to the following red flags:

Fever or Weight Loss: These symptoms may indicate an infection or systemic illness.
Weakness or Numbness: Neurological deficits can suggest nerve involvement or spinal cord compression.
Difficulty Walking: Impaired mobility may point to musculoskeletal or neurological issues.
Radiating Pain: Pain that spreads to one or both legs could signal spinal conditions.
Bowel or Bladder Problems: Issues with bowel movements or urination may indicate spinal cord dysfunction.
Sleep Disruption: Pain severe enough to prevent the child from sleeping requires urgent evaluation.

Importance of Early Diagnosis and Treatment

Serious causes of back pain in children must be identified and addressed promptly. Delayed diagnosis and treatment can lead to worsening symptoms and potentially long-term complications. Careful clinical evaluation and appropriate imaging or laboratory tests are essential to rule out conditions such as infections, tumors, or structural abnormalities. Emergency physicians should always think about possibility of child abuse and traumatic injuries in this age group.

Geriatrics

In elderly individuals, back pain requires careful evaluation due to the increased risk of fractures and other serious conditions. Vertebral fractures can occur even with minimal force, making it critical to consider the possibility of compound vertebral fractures in older patients, even in the absence of trauma.

Life-Threatening Diagnoses to Rule Out

When evaluating back pain in elderly patients, it is important to rule out life-threatening conditions that are more common in this age group, including:

Aortic Dissection: A tear in the inner layer of the aorta that can cause severe back pain.
Abdominal Aortic Aneurysm: A potentially fatal condition involving the enlargement and potential rupture of the abdominal aorta.

Common Causes of Back Pain in the Elderly

In addition to ruling out life-threatening diagnoses, healthcare providers should consider the following common causes of back pain in older adults:

Osteoarthritis: A degenerative joint condition leading to stiffness and pain in the spine.
Degenerative Disc Disease: The wear-and-tear breakdown of intervertebral discs, which can result in chronic back pain.
Facet Joint Osteoarthritis: Degeneration of the small joints in the spine, contributing to localized pain and reduced mobility.

Pregnant Patients

Back pain is one of the most common issues experienced during pregnancy, particularly in the later months. While this discomfort often subsides after childbirth, many women continue to experience back pain for months postpartum.

Common Causes of Low Back Pain and Pelvic Girdle Pain in Pregnancy

Several factors contribute to low back pain and pelvic girdle pain during pregnancy, including:

Hormonal Changes: Hormonal fluctuations can loosen ligaments and joints, leading to instability and pain in the pelvic region.
Increased Weight: The growing weight of the baby places added stress on the lumbar vertebrae, causing discomfort and strain.
Compression of the Inferior Vena Cava (IVC): As the uterus enlarges, it may compress the IVC, leading to venous congestion and associated back pain.
Poor Nutrition: Inadequate nutrition during pregnancy can weaken muscles and bones, exacerbating pain.

Serious Causes Requiring Aggressive Management

In some cases, back pain during pregnancy may indicate more serious underlying conditions that require prompt attention and treatment. These include:

Lumbar Disc Herniation
Trauma
Infections
Masses

Identifying and addressing these causes is critical to ensuring the safety and well-being of both the mother and the baby.

IV Drug Users

Patients in this category may present with isolated back pain or more severe manifestations such as full-blown sepsis, meningitis, or septic shock. Prompt recognition and thorough examination of these patients are crucial. Immediate administration of antibiotics is essential to prevent further complications and reduce the risk of long-term morbidity. Timely intervention can significantly improve outcomes in these critical cases.

When To Admit This Patient

Patients presenting with back pain may be safely discharged if all the following criteria are met:

The patient has no neurological deficits or red flag findings on physical examination.
The patient is able to ambulate without difficulty.
Pain is under control, and no emergency cause has been identified.

For patients with uncontrolled pain or inability to care for themselves, an overnight stay in a hospital observation unit or nursing facility may be required for further management [38].

Admission is warranted in patients who exhibit significant abnormalities or require specialist intervention. The following scenarios outline the need for admission and further consultation:

Abnormal Physical Examination Findings:
- Patients with abnormal signs on physical examination should be referred for emergency consultation with the appropriate inpatient service.
Vascular and Mechanical Syndromes:
- Conditions such as abdominal aortic aneurysm (AAA), vascular spinal cord syndromes (e.g., spinal or epidural hematoma), and mechanical spinal cord syndromes (e.g., cauda equina syndrome or syringomyelia) necessitate immediate consultation with vascular or spine specialists for intervention and potential admission.
Spinal Fractures:
- Patients with spinal fractures require evaluation by an orthopedic surgeon and/or neurosurgeon. Admission is determined based on the fracture’s stability and the patient’s level of pain control.
Infectious Spinal Syndromes:
- Conditions such as epidural abscesses, osteomyelitis, or discitis require admission and consultation with specialists in Infectious Diseases and Spine.
Immunologic Spinal Cord Syndromes:
- Patients with conditions like transverse myelitis should be referred to neurology for consultation and further management.

Revisiting Your Patient

Firstly, as the patient is stable, which means A, B, and C are clear, the patient should be managed for pain (pain scale 8/10). On an emergent basis, Opioid was given for rapid relief. Further examination revealed the patient had foot drop, neurological deficits, motor weakness (S1 myotome), and a decrease in left foot reflexes causing him to have a high steppage gait on arrival to ED. At this juncture, it is clear the patient is having a nerve compression as there are focal neurological deficits. Here, you can call for senior help, as neurological deficits need to be reassessed for proper documentation. MRI of the whole spine showed prolapse of the L4/L5 intervertebral disc with compression on the thecal sac and bilateral neural foramina with osseous spinal canal stenosis at the L4 L5 vertebrae. The patient was admitted according to the admission criteria described earlier in the chapter, was made to wear a lumbar belt, and received epidural analgesia with corticosteroid injection. The patient was monitored for further neurological deterioration, which did not develop. Hence, he was discharged with supportive management, including physiotherapy and follow-up.

Authors

Paila Naveen

Dr. Paila Naveen, MBBS, CCT-EM, MRCEM, SEMI (Society of Emergency Medicine India) member, Consultant in Emergency Medicine, India, has fallen in love with this specialty, which he describes as his adrenaline pump for the rest of his medical service. He has a vision to spread the word about the importance of this specialty and the full potential of an emergency physician that can be achieved with the right skills and techniques in hand to save lives and bring smiles to the world. He is a strong supporter of FOAMed and runs a site exclusively for Emergency Medicine where he teaches, discovers new things, and tries to make a difference in every step he takes forward. He spreads awareness about this branch, as it is still in its infancy in India, through every possible medium where students and other doctors are connected in a collaborative way to further enhance the beauty of EMERGENCY MEDICINE.

Manjith Reddy

Dr. Manjith K S is an emergency physician with over 4 years of experience. He completed his medical school in 2012 and his residency in emergency medicine in 2019. Passionate about providing high-quality care, Dr. Manjith is dedicated to ensuring the best possible outcomes for his patients. He stays up-to-date with the latest medical research and practices and is a strong advocate for patient safety and quality improvement. Dr. Manjith is highly skilled in quickly assessing and diagnosing patients with a wide range of conditions and is an expert in the use of emergency medical equipment and procedures. His professional interests include trauma and cardiac emergencies. In addition to his clinical expertise, he serves as a mentor to junior physicians and residents, fostering the next generation of emergency medicine professionals. As a lifetime member of the Society of Emergency Medicine India (SEMI), Dr. Manjith is committed to advancing the field of emergency medicine. He currently works as a full-time consultant for a private healthcare organization. Proud to be part of the emergency medicine community, Dr. Manjith believes that emergency physicians are the frontline of healthcare.

Listen to the chapter

References

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Reviewed and Edited By

Jonathan Liow

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

James Kwan

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

Arif Alper Cevik, MD, FEMAT, FIFEM

Acute Ischemic Stroke (2024)

December 2, 2024December 3, 2024 ~ iEM Education Project Team ~ Leave a comment

by Hassan Khuram, Parker Maddox, & Scott Goldstein

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.

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.

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

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.

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.

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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Reviewed and Edited By

Arif Alper Cevik, MD, FEMAT, FIFEM

Epilepsy and Status Epilepticus (2024)

December 2, 2024December 9, 2024 ~ iEM Education Project Team ~ Leave a comment

by Rand Redwan Al Sari & Imad Khojah

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?

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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

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.

Imad Khojah

Listen to the chapter

References

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Reviewed and Edited By

Arif Alper Cevik, MD, FEMAT, FIFEM

Seizure (2024)

December 1, 2024December 1, 2024 ~ iEM Education Project Team ~ Leave a comment

by Ardi Knobel Mendoza, Danielle Charles-Chauvet, Erik J. Blutinger

Introduction

Seizures are caused by abnormal cortical neuronal activity that manifests as changes in alertness or neurological symptoms. While seizures account for only 1% of all emergency department (ED) visits and 3% of prehospital transports, their potential for significant morbidity undermines the importance of rapid assessment and treatment in emergency settings [1]. The etiology of seizures varies by age group, with the most common causes being fever in infants and metabolic derangements or structural abnormalities in adults over 75. This chapter will explore various seizure presentations, diagnostic assessment tools, and considerations for treatment and disposition decisions in the ED.

You have a new patient!

A 24-year-old female presents to the emergency room after being found on the street. She is minimally responsive, alert, and oriented only to herself. Her heart rate is 87 bpm, blood pressure is 141/94 mmHg, respiratory rate is 14 bpm, and she is afebrile, with oxygen saturation of 99% on room air. She has a gravid uterus with a fundal height of approximately 29 cm (11.4 inches) but is otherwise atraumatic.

What do you need to know?

Seizure Presentation and Classification

It is essential to investigate the cause and categorize the type of seizure after an acute episode to inform the diagnostic and treatment plan. Seizures are often classified as provoked, which occur within 7 days of a neurologic, metabolic, or infectious precipitator, or unprovoked, which has no association with an inciting factor. A history of seizures, febrile illness, malignancy, new medications, recreational drug use, or pregnancy can help to elucidate this. A complete neurological examination, which includes an assessment of mental status, should be performed as an altered postictal state follows most primary seizures. In addition to a change in mental status, the postictal state can present as motor deficits or paresis. Postictal paresis suggests a structural lesion as the cause of the seizure and should prompt cranial imaging [2]. Given that seizures are a manifestation of cortical neuronal activity, the extent of cortical involvement can lead to various symptoms at presentation [3].

Partial seizures involve only some of the cortex. They are classified as either simple, in which the patient is alert throughout, or complex, in which the patient has decreased alertness. Seizures can also begin as partial seizures, involving only some of the cortex, and spread to involve the entire cortex. Seizures involving the entire cortex are termed “generalized” seizures, resulting in decreased alertness. Generalized seizures are further classified based on their physical manifestations:

Absence Seizure: no collapse, automatisms (blinking, staring, lip smacking)

Tonic-clonic Seizure: collapse with stiff non-rhythmic convulsive movements.

Atonic Seizure: collapse without convulsions (similar to syncope) [4].

Febrile seizures typically occur in children 6 months-6 years of age with fevers greater than 38℃ and no neurological infection. 80% of febrile seizures are tonic-clonic in presentation, self-limiting, and do not recur after resolution of the inciting fever [5].

Eclamptic seizures are typically tonic-clonic in presentation and are considered unstable, as they carry significant mortality risk to the mother and fetus. Therefore, any pregnant patient with altered mental status and hypertension, identified as systolic >140 or diastolic >90, should be assessed for eclampsia. In cases with high suspicion of preeclampsia or eclamptic seizures, patients should be treated with magnesium for seizure prophylaxis [6].

Psychogenic seizures present similarly to generalized tonic-clonic seizures but are not associated with cortical neuronal derangements. In the ED, it is difficult to differentiate these seizures from neurogenic seizures, as there is limited access to EEG. However, psychogenic seizures present with more rhythmic and symmetric movements, patients are typically completely aware and conversant throughout, and there is no postictal state.

It is important to consider the duration of a seizure episode in all patients. Most seizures last from 30 seconds to 2 minutes. Seizures lasting longer than 5 minutes meet the criteria for status epilepticus. These patients are considered unstable, as prolonged seizure activity is associated with an increased risk of permanent brain damage. Not all patients with status epilepticus have convulsive seizures, so it is important to assess for subtle symptoms of seizure activity in the unresponsive patient, as they may have non-convulsive status epilepticus—a medical emergency.

Medical History

Thorough history taking in patients with seizure disorders is crucial for accurate diagnosis and effective management. This process involves a structured yet flexible approach to gathering relevant information, ensuring that all aspects of the patient’s condition are considered. Key components of this history include the patient’s medical background, seizure characteristics, and psychosocial factors.

Key Components of History Taking

Presenting Complaints: Document the chief complaints, including the nature, frequency, and duration of seizures [7].
Seizure Onset and Triggers: Investigate the age of onset, potential triggers (e.g., photosensitivity), and environmental factors that may provoke seizures [8].
Medical and Family History: Collect information on past medical history, family history of seizures or neurological disorders, and any relevant social history [7,9].
Psychosocial Aspects: Assess the impact of seizures on the patient’s daily life, including emotional and social challenges [8].

A comprehensive history-taking process in seizure patients is crucial for accurate diagnosis and effective management of various seizure types. By gathering essential information regarding seizure semiology, triggers, and patient-specific factors, clinicians can develop tailored treatment strategies to improve outcomes. Seizure semiology, for example, provides valuable insights into the nature of seizures, helping to classify them as either focal or generalized [10]. Detailed accounts of auras and observable signs can further indicate the anatomical origins of seizures, guiding appropriate diagnostic testing [10]. Additionally, identifying seizure triggers, such as environmental factors or specific stimuli, plays a vital role in both diagnosis and management. For instance, patients with photosensitivity may require targeted questions to uncover visual triggers that provoke seizures [8]. Together, these aspects of thorough history-taking form the foundation for effective and personalized seizure management.

When conducting history-taking in patients with seizure disorders, clinicians must be mindful of several common pitfalls that can lead to misdiagnosis or ineffective treatment. These issues often arise from inadequate questioning, overemphasizing certain symptoms, and neglecting the broader context of the patient’s experiences.

Inadequate history-taking, such as missing or incomplete accounts from witnesses, can result in misinterpreting seizure types [11]. Failing to gather detailed descriptions of seizure events, including pre-ictal and post-ictal states, may further obscure the diagnosis [12].

Additionally, an overemphasis on specific symptoms, such as those associated with focal seizures, may mislead clinicians, as these symptoms do not always correlate with the seizure type [13].

Another critical factor is the neglect of contextual elements, such as environmental triggers, which may result in missed diagnoses of reflex seizures, especially in photosensitive patients [8]. Furthermore, ignoring psychosocial aspects and the patient’s overall health can complicate the understanding of seizure disorders [14]. While advancements in technology and neuroimaging provide valuable objective data, the art of listening and thorough history-taking remains an irreplaceable cornerstone in the diagnostic process.

While a comprehensive history is essential, it is also important to recognize that some patients may present atypically, necessitating a tailored approach to history taking that considers individual circumstances and variations in symptom presentation.

Physical Examination

A comprehensive physical examination for patients presenting with seizures in the emergency department is essential for accurate diagnosis and effective management. Key components include a thorough neurological assessment, which involves evaluating consciousness, motor function, and sensory responses to identify any neurological deficits [15]. Monitoring vital signs is equally critical, as instability such as hypotension or tachycardia may indicate underlying issues requiring immediate attention [16]. Additionally, a systematic head-to-toe physical examination can help identify signs of trauma or systemic illness that may contribute to seizure activity [15].

In the emergency department, recognizing physical examination findings indicative of a severe or prolonged seizure episode is critical for timely diagnosis and management, particularly in cases of status epilepticus or non-convulsive seizures. Altered mental status, characterized by confusion, disorientation, or a prolonged postictal state, is a key finding that can suggest non-convulsive status epilepticus (NCSE) [17]. Neurological signs, such as subtle twitching, blinking, or fluctuating sensorium, may also indicate ongoing seizure activity [17]. In cases of generalized tonic-clonic seizures (GTCS), convulsive activity manifests with muscle rigidity and jerking movements, making it a more apparent diagnosis [18]. Additionally, focal seizures can result in specific neurological deficits, which may be misinterpreted as other neurological conditions. While these findings are crucial for identifying severe seizure episodes, it is important to acknowledge that some patients may present with atypical symptoms or lack overt signs of seizure activity, complicating the diagnostic process [17].

While the value of a comprehensive examination cannot be overstated, it is also important to recognize that some patients may present with atypical symptoms or underlying conditions that complicate the diagnosis. This highlights the need for a tailored approach to each case, ensuring that individual factors are carefully considered [16].

Alternative Diagnoses

The diagnosis of seizures primarily relies on the patient’s clinical history, with particular emphasis on accounts provided by witnesses. This is especially important because many seizure types involve impaired consciousness, leaving patients unaware of their episodes. Clinical findings can be supported by interictal electroencephalogram (EEG) abnormalities, although it is essential to note that such abnormalities may also occur in healthy individuals and their absence does not rule out epilepsy. It is equally critical to differentiate seizures from other conditions that may present similarly. These include syncope, such as cardiac arrhythmias or vasovagal episodes; metabolic disturbances like hypoglycemia or hyponatremia; and vascular events such as transient ischemic attacks. Additionally, migraine auras, sleep disorders like narcolepsy or night terrors, movement disorders such as paroxysmal dyskinesia, and gastrointestinal conditions like esophageal reflux in neonates and infants can mimic seizures. Psychiatric conditions, including conversion disorders, panic attacks, malingering, or episodes driven by secondary gain, must also be considered [19].

Acing Diagnostic Testing

When considering diagnostic testing such as labs and imaging, there is a lack of consensus on a set of tests required for all seizing patients. Rather, the diagnostic workup for a patient presenting with a seizure depends on a variety of factors, such as the suspected etiology of the seizure and whether the patient has a known seizure disorder or is presenting with a first-time seizure [20]. In patients with known seizure disorders, it is generally accepted test for levels of the anti-epileptic drug (AED) the patient takes, such as levetiracetam, phenytoin, carbamazepine, phenobarbital, or valproic acid. However, levels can often take hours to days to result or may not be available at a certain facility. In patients without a known seizure disorder, or if there is concern for an etiology for a seizure besides breakthrough from AED treatment, a more extensive workup is warranted. Basic testing should include a finger stick glucose, a urine or serum pregnancy test, and serum chemistry, including calcium and magnesium. Urine/serum toxicologies can also be obtained if there is concern for potential toxic ingestion as a cause. A lactic acid can be obtained, which should be markedly elevated immediately after the seizure and normalize after an hour of seizure onset [21].

A Computed Tomography (CT) Head should be obtained in all first-time seizure patients to assess for a structural lesion such as a mass, a bleed either as the etiology or sequelae of the seizure, or signs of an infection. Seizure sequelae such as significant head trauma can also be assessed with CT imaging to look for a large hematoma or skull fracture in patients who fail to return to baseline mental status after a seizure [22]. Magnetic Resonance Imaging (MRI) can be considered to reveal other diagnoses such as a brain abscess or central vascular event such as infarction; however, this imaging modality is often less available in the emergency setting and may require admission vs. outpatient referral to obtain an image [23]. Electroencephalography (EEG)is when diagnostic testing such as labs and imaging is considered, but there is a lack of consensus on a set of tests required for all seizing patients. Rather, the diagnostic workup for a patient presenting with a seizure depends on a variety of factors, such as the suspected etiology of the seizure and whether the patient has a known seizure disorder or is presenting with a first-time seizure [20]. In patients with known seizure disorders, it is generally accepted test for levels of the anti-epileptic drug (AED) the patient takes, such as levetiracetam, phenytoin, carbamazepine, phenobarbital, or valproic acid. However, levels can often take hours to days to result or may not be available at a certain facility. In patients without a known seizure disorder, or if there is concern for an etiology for a seizure besides breakthrough from AED treatment, a more extensive workup is warranted. Basic testing should include a finger stick glucose, a urine or serum pregnancy test, and a serum chemistry, including calcium and magnesium. Urine/serum toxicologies can also be obtained if there is concern for potential toxic ingestion as a cause. A lactic acid can be obtained, which should be markedly elevated immediately after the seizure and normalize after an hour of seizure onset [21].

Risk Stratification

The presence of comorbidities plays a critical role in the risk stratification, prognosis, and management of epilepsy, highlighting the need for a holistic approach to patient care. In the emergency department, recognizing these comorbidities is crucial for tailoring immediate interventions and ensuring acute and comprehensive follow-up care. Studies reveal that 60-70% of adults and 80% of children with epilepsy experience multimorbidity [25]. Among patients with senile epilepsy, 81% have at least one comorbidity, with neurological (61%) and cardiovascular (45%) conditions being the most prevalent [26]. Emergency clinicians must remain vigilant for these conditions, as they may exacerbate seizure episodes or complicate acute management. These comorbidities significantly impact seizure outcomes, as patients with neurological and psychiatric disorders face a higher risk of recurrent seizures and reduced likelihood of achieving seizure freedom [26]. Conditions like depression and anxiety are particularly associated with a more severe course of epilepsy [27], and their identification in the emergency setting can guide referrals for further psychiatric evaluation. Additionally, multimorbidity is linked to lower health-related quality of life and increased healthcare costs due to frequent hospitalizations [25]. Cognitive and psychiatric comorbidities often impair daily functioning more than the seizures themselves [28], necessitating a multidisciplinary approach starting from the emergency department. Addressing these comorbidities, however, has been shown to improve overall health outcomes and enhance the quality of life for patients, emphasizing the importance of comprehensive, patient-centered care [28].

Management

The most important intervention in a patient actively seizing is ensuring adequate brain oxygenation. The airway should be protected via maneuvers that include rolling the patient on their side, jaw thrusts, applying a nasopharyngeal airway, applying supplemental oxygen, and preventing aspiration with suction as needed. Oxygenation status should be monitored with continuous pulse oximetry and capnography when possible.

Providers should also anticipate the impending decompensation of the clinical course and the need for intubation by preparing airway equipment, medications, and IV access, which will be discussed later in the chapter. Along with oxygenation, patients must be protected from injury, e.g., from falling out of bed and preventing trauma.

Most seizures stop on their own within one to two minutes of onset, but the longer the seizure lasts, the less likely it is to stop on its own and can become self-sustaining.

Seizures that are continuous or intermittent, lasting more than 5 minutes without recovery of consciousness, are known as status epilepticus. Medical therapies to terminate a seizure are divided into three stages based on escalation of need and inability to terminate the seizure.

Benzodiazepines are considered first-line agents in terminating seizures, followed by second-line agents such as Levetiracetam, Valproate, Phenytoin, and Fosphenytoin [29]. The third-line medications are infusions of benzodiazepines, propofol, or barbiturates, prepared for likely intubation with paralytics and continued infusions [30].

The following lists these medications by stage, dose, and considerations [31, 32]:

Midazolam (1st Line Agent – Benzodiazepine)

Loading Dose:
- 10 mg IM or 0.1-0.2 mg/kg IV.
Maintenance Dose: 0.001 mg/kg/min.
Pediatric Dose:
- IV or IN: 0.2 mg/kg (max 5 mg).
- IM:
  - <13 kg: 0.2 mg/kg.
  - 13-39 kg: 5 mg.
  - 39 kg: 10 mg.
Considerations:
- IM dosing can be used if no IV is established.
- Acts faster than Lorazepam but has a shorter duration.
- May cause respiratory depression and hypotension.

Diazepam (1st Line Agent – Benzodiazepine)

Loading Dose: 10 mg over 2 minutes. Repeat every 5-10 minutes to a max of 30 mg.
Maintenance Dose: N/A.
Pediatric Dose: 0.15 mg/kg IV.
Considerations:
- May cause respiratory depression and hypotension.

Levetiracetam (2nd Line Agent)

Loading Dose: 60 mg/kg (up to a max of 4,500 mg), infused over 10 minutes.
Maintenance Dose: Same as the loading dose.
Pediatric Dose: Same as loading dose.
Considerations:
- If the patient weighs >75 kg, the dose is 4.5 g.
- If seizures stop, continue to give Levetiracetam to prevent recurrence.

Phenytoin (2nd Line Agent)

Loading Dose: 18-20 mg/kg with a max rate of 50 mg/min.
Maintenance Dose: N/A.
Pediatric Dose: N/A.
Considerations:
- Cardiac monitoring is necessary for QRS complex widening.

Fosphenytoin (2nd Line Agent)

Loading Dose: 15-20 mg/kg with a max rate of 150 mg/min.
Maintenance Dose: Same as loading dose.
Pediatric Dose: N/A.
Considerations:
- Cardiac monitoring is necessary for QRS complex widening.

Valproate (2nd Line Agent)

Loading Dose: 20-40 mg/kg over 10 minutes. Repeat if needed.
Maintenance Dose: Same as loading dose.
Pediatric Dose: Same as loading dose.
Considerations: N/A.

Propofol (3rd Line Agent)

Loading Dose: 1-2 mg/kg IV over 5 minutes (max load 10 mg/kg).
Maintenance Dose: 50-80 mcg/kg/min (3-5 mg/kg/hr) as an infusion.
Pediatric Dose: N/A.
Considerations:
- May cause respiratory depression and hypotension.

Phenobarbital (3rd Line Agent)

Loading Dose: 10-15 mg/kg bolus up to 60 mg/min.
Maintenance Dose: 120-240 mg every 20 minutes.
Pediatric Dose: N/A.
Considerations: N/A.

Midazolam (for 3rd Line use) (3rd Line Agent)

Loading Dose: 0.2 mg/kg IV.
Maintenance Dose: 0.1-2 mg/kg/hr.
Pediatric Dose: N/A.
Considerations:
- Can be used in patients with hypotension.

Once the provider considers 3rd line medications and starting infusions, they should prepare for intubation as the patient is likely in status epilepticus, requiring continued medication and airway protection. Induction medications for intubation are often the same medications listed above in the 3rd stage of treatment, such as propofol or midazolam, and can be on board before paralytics. Paralytics are used to stop the seizure-like activity and aid in intubation, but it is important to remember that they are not meant to terminate the seizure. Patients can still have seizures despite the lack of tonic-clonic seizure activity such as NCSE. Rocuronium is the preferred paralytic agent as it is not associated with the hyperkalemia seen in succinylcholine, which is a risk for patients seizing for an extended period who could develop rhabdomyolysis. Rocuronium paralysis lasts much longer, which should be a consideration when monitoring for further seizures with EEG.

Finally, other conditions can cause seizures or seizure-like activity that require their own treatment strategies, which are discussed below:

Eclampsia, a life-threatening condition often associated with pregnancy, is treated with magnesium to control seizures, benzodiazepines for acute management, and blood pressure control to address underlying hypertension. For seizures due to isoniazid toxicity, the recommended treatment is pyridoxine (vitamin B6), which counteracts the drug’s neurotoxic effects. In cases of hypoglycemia, seizures can be managed by administering Dextrose 50% in Water (D50W) to restore blood glucose levels rapidly. Hypocalcemia, another potential seizure trigger, requires the administration of calcium gluconate or calcium chloride to normalize calcium levels. For seizures induced by hyponatremia, 3% hypertonic saline is used to increase serum sodium levels safely.

In cases of toxicity from aspirin, tricyclic antidepressants (TCAs), or lithium, hemodialysis is indicated to effectively remove the offending agents from the bloodstream. For seizures caused by meningitis, prompt initiation of appropriate antibiotics is critical to address the underlying infection and prevent further complications.

Special Patient Groups

Pediatrics

Seizures in pediatric patients can present with diverse etiologies ranging from febrile seizures to more serious underlying conditions such as intracranial infections, metabolic disturbances, or congenital disorders. In children under 5, febrile seizures are the most common cause of convulsions and are generally self-limited, though they require careful differentiation from more serious causes like meningitis or encephalitis. Clinical reasoning should prioritize a detailed history, including the onset of the seizure, vaccination status, and any family history of epilepsy or neurodevelopmental disorders. Laboratory tests and imaging may be indicated if there is a high suspicion of an underlying structural or metabolic issue, such as in children with a prolonged postictal state or a first-time seizure without a clear precipitant. In the emergency department (ED), rapid assessment of the child’s airway, breathing, and circulation (ABCs) is paramount, along with ensuring the seizure is appropriately controlled, often with medications like lorazepam or diazepam. Close follow-up is necessary to assess for recurrent seizures or potential neurological sequelae.

Geriatrics

Seizures in elderly patients often present a diagnostic challenge due to the overlap with other common age-related conditions, such as syncope, transient ischemic attacks (TIA), or dementia-related behavioral changes. In this population, new-onset seizures should prompt an urgent evaluation for reversible causes, including cerebrovascular events, metabolic disturbances (such as hyponatremia or hypoglycemia), brain tumors, or infections like meningitis or encephalitis. Seizures in older adults may also be a manifestation of progressive neurodegenerative diseases, including Alzheimer’s or Parkinson’s disease. Emergency management in the ED should focus on stabilizing the patient while considering potential drug interactions, as elderly patients are more likely to be on multiple medications that may lower the seizure threshold (e.g., antipsychotics, antidepressants, or antihypertensives). Antiepileptic drug (AED) therapy initiation, while necessary in recurrent or long-duration seizures, must be approached cautiously due to age-related pharmacokinetic changes and the increased risk of side effects. A thorough evaluation for underlying causes, including neuroimaging and laboratory tests, is critical.

Pregnant Patients

Seizures during pregnancy present unique challenges in both diagnosis and treatment. The differential diagnosis includes pregnancy-specific conditions like eclampsia, in addition to the possibility of preexisting epilepsy or new-onset seizures due to metabolic derangements or intracranial pathology. In a pregnant patient with a seizure, the clinical priority is to ensure both maternal and fetal well-being. Eclampsia, a severe complication of preeclampsia, must be ruled out, as it presents with generalized tonic-clonic seizures and may lead to maternal and fetal morbidity if not promptly treated. Once eclampsia is excluded, consideration should be given to other causes such as hypoglycemia, cerebrovascular accidents, or drug toxicity (e.g., withdrawal from anticonvulsant medications). Emergency management in the ED should prioritize seizure control, typically with benzodiazepines, while avoiding teratogenic medications. Magnesium sulfate is the treatment of choice for eclampsia. Fetal monitoring should be initiated, and careful planning for delivery may be required depending on the severity of the condition and gestational age. The clinical approach should balance the need for immediate seizure control while minimizing risks to both the mother and fetus.

When To Admit This Patient

Few definitive practice guidelines are available to emergency physicians making disposition decisions for seizure episodes. However, all critically ill patients must be admitted to the inpatient setting since overall risk assessment is important for deciding whether to safely discharge patients home. For alternative clinical presentations, the physician should reliably assess whether the patient’s overall presentation warrants further medical interventions in a clinical setting.

For emergency physicians, seizure recurrence, morbidity, and mortality are useful measures to consider for safe discharge. Studies suggest that seizure recurrence most often depends upon EEG findings and the underlying cause—normal EEG and undetectable cause are associated with lower recurrence rates [33]. With positive neuroimaging findings (e.g., structural findings), initiating AED therapy for first-time seizures is recommended given a high 1-year recurrence risk of up to 65% [34].

Any patients with abnormal neurologic signs or symptoms who have not fully recovered from their seizure should not be discharged. Other important clinical benchmarks are the presence of normal vital signs, CT head imaging, EKG, basic lab results (especially renal function and blood counts), and follow-up. As part of the physician’s risk assessment of the patient’s overall condition, social factors must also be taken into account: lack of follow-up care, history of being lost to follow-up, and insufficient assistance available at home should all weigh towards admitting the patient for further monitoring (and possible seizure workup).

Generally, stable patients are those who return to their baseline mental status, do not exhibit any new neurological deficits, have no significant lab result abnormalities, and remain at low risk for recurrent seizure activity in the short term. Coordinating reliable follow-up is important, and all patients should be educated about the “red flag” signs and symptoms that warrant urgent evaluation and treatment.

Revisiting Your Patient

Altered mental status in the gravid, hypertensive patient is concerning for eclampsia. This patient should be started on 2mg of Mg as seizure prophylaxis. Obstetrics should be consulted as urgent delivery via cesarean section is the definitive treatment for this patient’s seizures. After delivery, the patient should be monitored closely for postpartum eclamptic seizures, which can occur up to 6 weeks postpartum.

Authors

Ardi Knobel Mendoza

Ardi Mendoza, MD is a resident at the Mount Sinai Hospital Emergency Medicine Program. He is interested in Health System and Emergency System Strengthening and local partner/local government-led collaborations. He has prior experiences in the field of Global Surgery while at Rutgers Robert Wood Johnson Medical School, assessing financial risk protection from impoverishing and catastrophic expenditure due to surgical care in the Colombian Healthcare System. He lived in Lima, Peru for a year working with Peruvian researchers at the University Cayetano Heredia as a research coordinator helping to develop a point-of-care diagnostic screening tool for Autism using eye-tracking technology.

Danielle Charles-Chauvet

Danielle Charles-Chauvet, MD is an Emergency Medicine resident at the Mount Sinai Hospital in New York. She is deeply invested in medical education and health disparities and, in affiliation with Harlem Children's Zone, has led several community-based educational initiatives to address these disparities. She designed and taught a course entitled Health and Structures of Oppression at Brown University's medical school. Her dedication to education earned her the 2022 National Outstanding Medical Student Award from the Academic College of Emergency Physicians and the 2021 Medical Education Award from the Society of Academic Emergency Medicine. She is currently working to expand her impact internationally by building Haiti's medical education infrastructure.

Erik J. Blutinger

Erik J. Blutinger, MD, MSc, FACEP is a full-time emergency physician at Mount Sinai Queens Hospital in New York City and Medical Director to the Community Paramedicine program at Mount Sinai Health Partners. He completed his residency training at the University of Pennsylvania, Master's at the London School of Hygiene & Tropical Medicine, and has worked on a variety of health initiatives in quality and patient experience with formal leadership training in Quality Improvement (QI). Erik has worked in multiple national healthcare systems and underserved communities, including townships in South Africa and Guatemala, Bhutan, India, and Austria.

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References

Jagoda, (2010). Seizures: An issue of Emergency Medicine Clinics. Elsevier Saunders.
Werhahn, J. (2010). Weakness and focal sensory deficits in the postictal state. Epilepsy & Behavior, 19(2), 138–139. https://doi.org/10.1016/j.yebeh.2010.06.029
Kim, , Cho, J.-W., Lee, J., Joo, E. Y., Hong, S. C., Hong, S. B., & Seo, D.-W. (2011). Seizure duration determined by subdural electrode recordings in adult patients with intractable focal epilepsy. Journal of Epilepsy Research, 1(2), 57–64. https://doi.org/10.14581/jer.11011
Kumar, , Sharma Maini, K., & Arya, K. (n.d.). Simple partial seizure. National Center for Biotechnology Information. Retrieved April 10, 2023, from https://pubmed.ncbi.nlm.nih.gov/29763181/
Heon, (n.d.). Febrile seizures. Core EM. Retrieved April 10, 2023, from https://coreem.net/core/febrile-seizures/
Wagner, K. (2004, December 15). Diagnosis and management of preeclampsia. American Family Physician. Retrieved April 10, 2023, from https://www.aafp.org/pubs/afp/issues/2004/1215/p2317.html
Hiroshi, S., Hallett, M., ‘History taking’, The Neurologic Examination: Scientific Basis for Clinical Diagnosis, 2 edn (2022; online edn, Oxford Academic, 1 Aug. 2022), https://doi.org/10.1093/med/9780197556306.003.0002, accessed 1 Dec. 2024.
Brinciotti, M., Bouilleret, V, Masnou, P. (2021). Optimizing the Patient’s History: A Modern Approach. 10.1007/978-3-319-05080-5_26.
Dulak SB. A practical guide to a thorough history. RN. 2004;Suppl:14-21.
Wolf P, Benbadis S, Dimova PS, et al. The importance of semiological information based on epileptic seizure history. Epileptic Disord. 2020;22(1):15-31. doi:10.1684/epd.2020.1137
Smith PE. If it’s not epilepsy… J Neurol Neurosurg Psychiatry. 2001;70 Suppl 2(Suppl 2):II9-II14. doi:10.1136/jnnp.70.suppl_2.ii9
Trevathan E. Patient page. The diagnosis of epilepsy and the art of listening. Neurology. 2003;61(12):E13-E14. doi:10.1212/wnl.61.12.e13
Henry JC. Comment: Be careful what you ask when interviewing patients with epilepsy. Neurology. 2015;85(7):594. doi:10.1212/WNL.0000000000001843
Kanner, A. (2008). Common Errors Made in the Diagnosis and Treatment of Epilepsy. Seminars in neurology. 28. 364-78. 10.1055/s-2008-1079341.
Wan, XH & Zeng, R. (2020). Handbook of Clinical Diagnostics. 10.1007/978-981-13-7677-1.
Bank, A & Bazil, C. (2019). Emergency Management of Epilepsy and Seizures. Seminars in Neurology. 39. 073-081. 10.1055/s-0038-1677008.
Hasan, Ahmed. (2016). Non-Convulsive Status Epilepticus in Emergency Department: A Diagnostic Challenge. Journal of Medical Science And clinical Research. 10.18535/jmscr/v4i8.103.
Virani, D., Sangani, S., Patel, C, Patel, V., Saha, J., Kalsariya, R. (2024). 5. Study of Clinical Profile, Management and Outcome of Patients Presented with Seizures in Emergency Medicine Department. BJ Kines: National Journal of Basic & Applied Sciences, doi: 10.56018/bjkines2024065
Ko DY. Epilepsy and Seizures Differential Diagnoses (updated Jul 26, 2002). From https://emedicine.medscape.com/article/1184846-differential?&icd=login_success_email_match_fpf Accessed: Nov 1,
Burgess M, Mitchell R, Mitra B. Diagnostic testing in nontrauma patients presenting to the emergency department with recurrent seizures: A systematic review. Acad Emerg Med. 2022 May;29(5):649-657. doi: 10.1111/acem.14391. Epub 2021 Oct 1. PMID: 34534387.
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You Have New Patients!

Patient 1

Patient 2

Introduction

General Approach

Differential Diagnoses

Delirium

Dementia

Depression

Psychosis

History and Physical Examination Hints

Associated Features

Clinical Institute Withdrawal Assessment of Alcohol Scale, Revised (CIWA-Ar)

Diagnostic Tests and Interpretation

Management

Special Patient Groups and Other Considerations

When To Admit This Patient

Clinical Pearls

Revisiting Your Patient

Patient 1

Patient 2

Author

Mehnaz Zafar Ali

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References

Reviewed and Edited By

Arif Alper Cevik, MD, FEMAT, FIFEM

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You Have A New Patient!

What Do You Need To Know?

Importance

Epidemiology

Pathophysiology

Basic Mechanisms of Seizures

Age-Related Factors and Neuronal Imbalance

Specific Factors Contributing to Seizures

Medical History

1. History of Present Illness:

2. Past Medical History:

3. Medication History:

4. Family History:

Physical Examination

Initial Assessment

General Appearance

Head and Neck Examination

Skin Examination

Cardiovascular and Abdominal Examination

Neurological Examination [2,4,12]

Postictal Examination [6]

Important Considerations

Alternative Diagnoses

Acing Diagnostic Testing

Risk Stratification

Management

When To Admit This Patient

Revisiting Your Patient

Authors

Neema Francis

Faiz Ahmad

Thiagarajan Jaiganesh

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References

Reviewed and Edited By

Arif Alper Cevik, MD, FEMAT, FIFEM

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Like this:

You Have A New Patient!

What Do You Need To Know?

Importance

Epidemiology

Pathophysiology

Typical TIA:

Atypical TIA:

Medical History

Physical Examination

Alternative Diagnoses

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

Which findings make TIA more probable?

Which risk factors and findings make other diagnoses more probable or make this diagnosis less probable?