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.
Toy EC, Klamen DL. Alcohol withdrawal. In: Case Files: Psychiatry. 6th ed. McGraw-Hill Education; 2020:400-405.
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.

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

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

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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References

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

Reviewed and Edited By

Arif Alper Cevik, MD, FEMAT, FIFEM

Autism in the Emergency Department

July 19, 2021June 19, 2021 ~ Ibrahim Sarbay, Turkey ~ Leave a comment

An Emergency Department (ED) is undoubtedly one of the most complex and chaotic places on earth where every individual can visit, regardless of age, gender, socioeconomic status, and existing conditions. Patients with autism may also visit EDs with any medical complaints. So, as Emergency Medicine physicians, what can we do to provide them the best health care possible? Of course, there is no limit to what we can individually do to help them, but it may be a good start to think about our EDs’ conditions and find the ways to improve them to serve ALL patients best.

About Autism

The Word “Autism” is derived from Greek autos (“self”) and -ισμός (-ismós) (“-ism”) and was used for the first time by psychiatrist Eugen Bleuler in 1908. He used it to describe a schizophrenic patient who had withdrawn into his own world. Until the 1970s, many scientists confused autism with mental retardation and psychosis and blamed the parents for their lack of parental skills. “A morbid self-admiration and withdrawal within the self” was the definition of Autism in this time period. In the 1970s Autism correctly described at last as “conditions characterized by challenges with social skills, repetitive behaviors, speech, and nonverbal communication” and autism and schizophrenia were recognized as completely different conditions. Treatment modalities in autism have undergone a dramatic shift with the help of this level of awareness – from pain and punishment to behavioral therapies.

In 2013, the American Psychiatric Association merged four distinct autism diagnoses (autistic disorder, childhood disintegrative disorder, pervasive developmental disorder-not otherwise specified (PDD-NOS), and Asperger syndrome) into one diagnosis: Autism spectrum disorder (ASD). (1)

Society’s Perspective

The fact that individuals with autism experience various difficulties in communication may cause them and their relatives to be “labeled” and encounter many problems throughout their lives, from education to transportation, from neighborhood relations to social life. It has been shown in various studies that families of individuals with autism are exposed to high levels of stress.

The general view and attitude of society are included in a wide spectrum of negative behaviors such as pitying, excluding, avoiding, and harming the individual with autism.

Why It’s Important to Be Cautious?

The average number of ED visits is nearly 30 percent higher for children with ASD, and their experience is generally far from good. In a comprehensive literature review, it was found that young patients (aged 0-17 years) with ASD were up to 30 times more likely to present to the ED, were likely to have repeat visits, and more likely to be admitted to the hospital. (2)

Caregivers of children with ASD are more likely to report “difficulty utilizing services, lack of shared decision making and care coordination, and adverse family impact”. (3)

Because of language and learning problems, children with ASD may have difficulty understanding hospital procedures and medical tests, which can increase their already high-stress levels. In addition, ED personnel often do not have enough knowledge about the special needs of patients with ASD. (4)

Early mortality is markedly increased in ASD due to a multitude of medical conditions. This is particularly important in ASD as it may indicate insufficient awareness of comorbid diseases, misdiagnosis, and mistreatment in the health system, in addition to the increased susceptibility to various diseases.

In a population-based cohort study, it was shown that the risk of death due to all diseases examined increased compared to the normal population. (5) In another study, all major psychiatric disorders, immune system disorders, nearly all medical conditions (including epilepsy, obesity, dyslipidemia, hypertension, and diabetes), suicide attempt and rarer conditions such as stroke and Parkinson’s was found to be significantly more common among adults with autism. (6)

These results indicate that physicians working in all medical specialties should have a better level of knowledge about ASD.

Remember These Words: See – Hear – Feel – Speak

There are many recommendations in various sources regarding the clinical approach to patients with ASD in the ED (7-10). In this article, I will be content with introducing a highly memorable 4-step system, which was developed by Samet and Luterman in order to facilitate patient-centered encounters with pediatric patients with ASD: (11)

Before examining a patient with ASD presenting to your ED, immediately think of these words: See – Hear – Feel – Speak.

Step 1: See – Remove non-essential visual stimuli. Dim the lights if possible, or try to place the patient in a dimmer room in the ED. Eliminate flickering lights like old fluorescents and avoid fluorescent lighting altogether if possible. Move active flashing lights or monitors out of the patient’s direct visual field.

Step 2: Hear- Remove excessive auditory stimuli before interacting. Turn off any unnecessary alarms or beeps from devices in the room, mute the TV, and move the patient to the least noisy room in the ED, if possible.

Step 3: Feel- Ask both the patient and care providers if they have any textures, which they find calming or agitating. Patients with ASD may have specific tactile stimuli they find soothing or aggravating.

Step 4: Speak – Say aloud in simple language to the patient everything you are doing before and as you are doing it. Ideally, speak directly in front of the patient’s plain view, because they may have difficulty with localizing the sounds.

Conclusion

It is possible to provide better healthcare to individuals with ASD through better training of health workers and structural changes to the EDs.

In this long journey to perfection, the first step could be increasing our awareness.

Because they deserve the best.

References

Autism Speaks, What Is Autism?, Accessed June 4, 2021, https://www.autismspeaks.org/what-autism
Lytle S, Hunt A, Moratschek S, Hall-Mennes M, Sajatovic M. Youth With Autism Spectrum Disorder in the Emergency Department. J Clin Psychiatry. Published online June 27, 2018. doi:10.4088/jcp.17r11506
IBCCES . Autism and the Emergency Department (ED): Why it’s Important. IBCCES. Published June 5, 2020. Accessed April 4, 2021. https://ibcces.org/blog/2020/06/05/autism-and-the-emergency-department-ed-why-its-important/
When a Psychiatric Crisis Hits: Children with Autism in the Emergency Room. SPARK. Accessed April 4, 2021. https://sparkforautism.org/discover_article/when-a-psychiatric-crisis-hits-children-with-autism-in-the-emergency-room/
Hirvikoski T, Mittendorfer-Rutz E, Boman M, Larsson H, Lichtenstein P, Bölte S. Premature mortality in autism spectrum disorder. Br J Psychiatry. Published online March 2016:232-238. doi:10.1192/bjp.bp.114.160192
Croen LA, Zerbo O, Qian Y, et al. The health status of adults on the autism spectrum. Autism. Published online April 24, 2015:814-823. doi:10.1177/1362361315577517
Taylor K, Cadman E, Burkitt S, Langseth A. G338(P) Improving the emergency department experience for children with autism, and their families. In: Association of Paediatric Emergency Medicine. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health; 2018. doi:10.1136/archdischild-2018-rcpch.328
Kirsch SF, Meryash DL, González-Arévalo B. Determinants of Parent Satisfaction with Emergency or Urgent Care When the Patient Has Autism. J Dev Behav Pediatr. Published online June 2018:365-375. doi:10.1097/dbp.0000000000000573
Giarelli E, Nocera R, Turchi R, Hardie TL, Pagano R, Yuan C. Sensory Stimuli as Obstacles to Emergency Care for Children With Autism Spectrum Disorder. Advanced Emergency Nursing Journal. Published online April 2014:145-163. doi:10.1097/tme.0000000000000013
Nicholas DB, Muskat B, Zwaigenbaum L, et al. Patient- and Family-Centered Care in the Emergency Department for Children With Autism. Pediatrics. Published online April 2020:S93-S98. doi:10.1542/peds.2019-1895l
Samet D, Luterman S. See-Hear-Feel-Speak. Pediatric Emergency Care. Published online February 2019:157-159. doi:10.1097/pec.0000000000001734

[cite]

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

Sharing is caring

Like this:

You have a new patient!

What do you need to know?

Importance

Epidemiology

Pathophysiology

Medical History

Physical Examination

Alternative Diagnoses

Acing Diagnostic Testing

Bedside Tests

Laboratory Tests

Imaging

Risk Stratification

Management

Initial Stabilization

Antibiotic Administration

Ceftriaxone

Metronidazole

Special Patient Groups

When To Admit This Patient

Revisiting Your Patient

Authors

Colin NG

Listen to the chapter

References

FOAM and Further Reading

Reviewed and Edited By

Elif Dilek Cakal, MD, MMed

Arif Alper Cevik, MD, FEMAT, FIFEM

Sharing is caring

Like this:

You have a new patient!

What do you need to know?

Importance

Epidemiology

Pathophysiology

Medical History

Risk Factors for ICH

Physical Examination

Alternative Diagnoses

Acing Diagnostic Testing

Bedside Tests

Laboratory Tests

Electrocardiogram (ECG)

Toxicology Screening

Imaging

Risk Stratification

ICH score

FUNC score

Management

Triage