Approach to Acutely Confused Patient (2025)

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.

The image was produced by using ideogram 2.0.

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.

The image was produced by using ideogram 2.0.

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:

  1. Age: Both elderly individuals and young children are at heightened risk due to their increased susceptibility to physiological and cognitive changes.

  2. Recent Hospitalizations: Hospital stays, particularly those involving medical illnesses or surgical procedures, can act as significant stressors and predispose individuals to delirium.

  3. Pre-existing Brain Conditions: Conditions like brain damage or dementia further increase the risk, as they impair cognitive resilience.

  4. Chronic Medical Disorders: Long-term health conditions often contribute to a state of chronic physiological stress, increasing the likelihood of delirium.

  5. Sensory Deprivation: Impairments in vision or hearing can lead to sensory deprivation, which may exacerbate confusion and disorientation.

  6. Substance Use Disorders: Alcohol or drug use disorders are major contributors to the onset of delirium, particularly during withdrawal periods or intoxication.

  7. 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.

  8. History of Delirium: Individuals with a previous history of delirium are more likely to experience recurrent episodes, particularly if the underlying risk factors persist.

  9. Malnutrition: Poor nutritional status can exacerbate vulnerability to delirium by impairing metabolic and neurological functions.

  10. 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:

  1. 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.
  2. 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.
  3. 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.
  4. 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.
  5. 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.
  6. 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.
  7. 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).
  8. 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.
  9. 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:

  1. 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.

  2. Autonomic Disturbances: Marked autonomic instability is common and may include symptoms such as tachycardia, fever, hypertension, sweating, and pupillary dilation.

  3. Psychomotor and Coordination Issues: Psychomotor agitation and ataxia (lack of muscle coordination) are frequently observed, contributing to physical instability and difficulty performing tasks.

  4. 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 image was produced by using ideogram 2.0.

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 image was produced by using ideogram 2.0.

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

Picture of Mehnaz Zafar Ali

Mehnaz Zafar Ali

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

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References

  1. Gleason OC. Delirium. Am Fam Physician. 2003;67(5):1027-1034.
  2. World Health Organization. Organic, including symptomatic, mental disorders. In: International Statistical Classification of Diseases and Related Health Problems. 10th ed. 2016:182-188.
  3. 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.
  4. 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.
  5. 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.
  6. 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.
  7. 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.
  8. 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.
  9. 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.
  10. 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.
  11. Andrews H, Clarke A, Parmar S, et al. You’ve been bleeped: the confused patient. BMJ. 2015;351:h3266. doi:10.1136/sbmj.h3266.
  12. Wakefield BJ. Risk for acute confusion on hospital admission. Clin Nurs Res. 2002;11(2):153-172. doi:10.1177/105477380201100205.
  13. 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.
  14. Thanyanuwat R. Patients who suffer from alcohol withdrawal and disorientation. J Med Assoc Thai. 2013;96(2):78-83.
  15. Thompson WL. Management of alcohol withdrawal syndromes. Arch Intern Med. 1978;138(2):278-283. doi:10.1001/archinte.1978.03630260068019.
  16. 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.
  17. Toy EC, Klamen DL. Alcohol withdrawal. In: Case Files: Psychiatry. 6th ed. McGraw-Hill Education; 2020:400-405.
  18. 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

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

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

Red and Painful Eye (2025)

by Gina Rami Abdelmesih, Amna AlMaazmi & Ahmed AlSaadi

You Have A New Patient!

A 74-year-old woman, with a background history of hypertension, asthma, and type 2 diabetes, presented to the Emergency Department (ED) with progressively worsening right eye pain associated with a severe headache. The patient and her daughter were driving home at night after visiting family members who lived far away. Over-the-counter analgesia (paracetamol) did not relieve the eye pain or headache. She reported experiencing blurred vision and seeing halos around streetlights on her way to the ED. The headache was associated with generalized abdominal pain and vomiting, which occurred once upon her arrival at the ED.

The image was produced by using ideogram 2.0.

The patient has no past surgical or ocular history. She was recently seen in the ED for an acute asthma exacerbation and was discharged with a short course of systemic oral prednisolone for five days. Her last dose was taken one day prior to this presentation.

On examination, her baseline vital signs were as follows: blood pressure 150/95 mmHg, heart rate 112 bpm, respiratory rate 18 bpm, SpO₂ 98%, temperature 37.2°C, and blood glucose 240 mg/dL. An ECG revealed sinus tachycardia. During the ocular examination, her unaided visual acuity using the Snellen chart was hand motion in the right eye and 20/30 in the left eye. There was no intraocular pressure measuring device available in the ED, but digital palpation revealed that the right eye was hard, while the left eye was soft. A direct ophthalmoscope examination of the right eye revealed a red-injected eye, a fixed mid-dilated pupil, and corneal clouding.

What Do You Need To Know?

Importance

Acute eye problems presenting to the Emergency Department (ED) are a common complaint, whether caused by traumatic or non-traumatic etiologies. Red eye is the most frequent reason for consultation. According to a recent review of ophthalmic emergency cases attending large ED units in the United States, from 2006 to 2011, an estimated 11,929,955 visits to emergency departments occurred in the United States for ophthalmic conditions, with a mean of nearly 2 million visits per year. Of these, 44.3% were categorized as non-emergent, and 41.2% as emergent. Approximately 75% of these presentations had red eye as the main complaint, with conjunctivitis, subconjunctival hemorrhages, and styes being the three most common diagnoses[1].

Given the high volume of patients presenting with ocular complaints, it is vital for all emergency physicians to be proficient in performing basic eye examinations and referring patients to the ophthalmology team promptly, based on the urgency of the case.

The causes of red eye can be categorized into painful and non-painful conditions to assist ED physicians in developing differential diagnoses. Additionally, the ocular manifestations of systemic diseases, such as diabetes mellitus, hypertension, infections, multiple sclerosis, transient ischemic attack (TIA), and giant cell arteritis, can sometimes be the primary presentation. Therefore, extra attention should be given to identifying these conditions in patients with ocular complaints.

Epidemiology

The epidemiology of red eye in emergency departments (EDs) reveals a complex landscape of ocular conditions [2], with conjunctivitis being the most prevalent diagnosis, accounting for nearly one-third of all eye-related encounters in the United States [3]. Corneal abrasions and corneal foreign bodies are the other most common causes of red and painful eye [4,5]. The term “red eye” encompasses a variety of conditions, many of which are benign and self-resolving, such as conjunctivitis, blepharitis, and dry eye, but it can also indicate more serious, sight-threatening issues [6]. During the COVID-19 pandemic, a study at a tertiary care hospital found that eye injuries and keratitis were the most common causes of red eye, with a slight increase in adult cases in 2020 compared to previous years [7]. Additionally, domestic violence-related ocular injuries, though less common, present a significant concern, particularly among pediatric patients from lower socioeconomic backgrounds, with contusions being the most frequent diagnosis [8]. These findings underscore the importance of accurate diagnosis and appropriate triage in EDs to manage the high volume of red eye cases effectively and ensure that resources are allocated to those in genuine need of emergency care.

Pathophysiology

Painful eye conditions can arise from various structures such as the cornea, conjunctiva, iris, or optic nerve, often due to irritants or inflammatory and infectious processes [4,5]. The cornea, with the highest density of nerves in the body, is particularly susceptible to neurogenic inflammation, which can lead to pain, leukocyte activation, and neoangiogenesis. This inflammation, while initially protective, can result in chronic pain if prolonged, as seen in conditions like dry eye or infectious keratitis [9]. Exposure to toxic irritants can exacerbate this by causing direct tissue injury and triggering intense immune and neuronal responses, leading to chronic ocular pain characterized by hyper-excitability and sensitization [10]. Eye pain can also be a symptom of systemic or neurologic disorders, such as demyelinating diseases or vascular abnormalities, necessitating careful evaluation to avoid misdiagnosis [11]. 

Initial Assessment and Stabilization (ABCDE Approach)

Any ophthalmic condition presenting to an emergency unit requires a thorough history taking. Specific questions regarding trauma, contact lens use, and prior ocular surgeries or procedures are crucial. A red painful eye should always be investigated after ruling out any life-threatening injuries. Eye symptoms may result from a localized eye problem or be part of a systemic disease requiring early diagnosis and stabilization. Certain life-threatening conditions, such as a brain aneurysm presenting as a third cranial nerve palsy or a cavernous sinus thrombosis presenting as ophthalmoplegia, can manifest with ocular symptoms and must be identified during the initial assessment.

Medical History

Obtaining a thorough history from the patient is the critical first step in an ophthalmic examination [2,4,5]. In general, the history includes the following information: demographic data (including name, date of birth, sex, race/ethnicity, and occupation); the identity of other pertinent healthcare providers utilized by the patient; the chief complaint, which refers to the main problem prompting the visit; and the history of present illness, which involves a detailed description of the chief complaint(s) and associated systemic symptoms. Additionally, the present status of vision should be assessed, including the patient’s perception of their own visual status, visual needs, and any ocular symptoms. Documentation should also include whether the patient is a regular contact lens wearer. A past ocular history is important, detailing prior eye diseases, injuries, diagnoses, treatments, surgeries, ocular medications, and the use of glasses. Similarly, a past systemic history should be obtained, covering allergies, adverse reactions to medications, current medication use, and pertinent medical problems or hospitalizations. Lastly, a family history should be reviewed, including poor vision (and its cause, if known) and other relevant familial ocular and systemic diseases.

Patients should also be questioned about specific symptoms. The duration of each symptom and whether it is unilateral or bilateral should be determined. The onset of symptoms can offer clues to the diagnosis (e.g., symptoms occurring at night or during specific activities such as being in a theater or cinema). Key symptoms to assess include eye pain (dull vs. sharp, localized vs. diffuse, itchiness, burning, or gritty sensation), photophobia, eye discharge and excessive lacrimation, lid swelling, and vision disturbances (diplopia, decreased visual acuity, blurriness, vision loss, floaters, flashes of light, or photopsia).

In cases of ocular trauma, a very detailed history is required, particularly for medical, medicolegal, and compensation purposes. It is essential to obtain the following information: the date, time, and precise location (including the exact address) of the injury; a description of what happened, in the patient’s own words (especially for trauma, as the patient’s account is valuable for understanding the chief complaint and history of present illness); any safety precautions taken (e.g., the use of safety glasses); and any emergency measures undertaken. Although treatment takes priority over history collection in true emergencies, the history remains vital. Furthermore, details regarding the type and approximate speed of any foreign body involved in the trauma, as well as whether the vision has been affected, should also be documented.

Physical Examination

The comprehensive ophthalmic evaluation involves an analysis of the physiological function and anatomical status of the eye, visual system, and related structures [4,5]. From a medicolegal perspective, visual acuity (both without and with correction) should be evaluated and documented. A focused eye examination typically consists of several parts, as follows [5,12]:

The external eye examination assesses the globe position, identifying conditions such as enophthalmos or exophthalmos (caused by trauma or non-traumatic conditions like orbital cellulitis, hyperthyroidism, or orbital compartment syndrome). It also evaluates the upper and lower palpebral sulci, conjunctiva (noting injection, ciliary flush, or follicles), discharge (serous, mucoid, or purulent), periorbital soft tissues, bones, and sensation. The fluorescein examination is used to detect corneal abrasions or keratitis.

Visual acuity is most commonly tested using a Snellen chart at a distance of 20 feet (6 m). The test should be conducted while the patient wears glasses or contact lenses; if corrective measures are unavailable, pinhole glasses can be used. For instance, a reading of 20/40 indicates that the patient can see at 20 feet what a person with normal vision can see at 40 feet. If the patient cannot distinguish the largest line on the Snellen chart, further assessments such as finger counting, hand motion, and light perception should be performed. In pediatric patients under 3 years of age, visual acuity cannot be assessed; instead, fixation symmetry can be tested using an interesting object, with a normal result described as CSM (central, steady, and maintained). Color vision, tested with Ishihara cards, can reveal abnormalities in cases of optic neuritis, chloroquine use, or thyroid ophthalmopathy [12].

Visual fields are usually assessed by confrontation testing in the ED, testing the four quadrants of each eye separately. Automated visual field testing, such as the Humphrey visual field analyzer, is more accurate but typically unavailable in the ED.

Extraocular muscle movement is examined for smooth pursuit and to detect any deconjugate gaze, diplopia (caused by edema, bleeding, or muscle entrapment), nystagmus, or pain.

Pupils and anterior chamber are evaluated for shape irregularities caused by trauma, a history of surgery (e.g., iridotomy for cataract extraction), or post-inflammatory synechiae. Size and symmetry are assessed for anisocoria, which can be physiological or due to medications or toxins. Reactivity is tested for direct and consensual reactions as well as accommodation, with a normal result documented as PERRLA (pupils equal, round, reactive to light and accommodation). A swinging flashlight test can reveal RAPD (relative afferent pupillary defect), as seen in conditions like vitreous hemorrhage or optic neuritis. The anterior chamber is examined for hyphema, hypopyon, and depth, which can be approximated by shining a light tangentially from the temporal side; if more than two-thirds of the nasal iris is in shadow, it suggests a shallow anterior chamber.

Intraocular pressure (IOP) is determined using a Tono-pen in the ED, with normal values ranging from 9 to 21 mmHg.

The slit-lamp examination evaluates the eye adnexa, including the lids, lashes, and lacrimal system, as well as the anterior segment. This includes the conjunctiva, sclera, cornea (examined with and without fluorescein under cobalt blue light for abrasions, ulcers, foreign bodies, or positive Seidel’s test), anterior chamber (checking for cells, “flare,” hyphema, hypopyon, and depth), iris, pupils, lens (position and clarity), and anterior vitreous. The posterior chamber, including the vitreous, optic disc, macula, fovea, and retinal vessels, requires a 78D or 90D lens for detailed examination [12].

Direct ophthalmoscopy or fundoscopy is best performed with dilated pupils, though this is usually not done in the ED and is contraindicated if the anterior chamber is shallow. The red reflex may be absent in cases of large vitreous hemorrhage, cataract, or retinoblastoma. Examination of the posterior segment is performed as needed.

Bedside ultrasound (POCUS) can be employed to detect increased intracranial pressure, retinal detachment, lens dislocation, intraocular foreign bodies, globe rupture, retrobulbar hematoma, or vitreous hemorrhage.

When To Ask For Senior Help

When suspecting sight-threatening conditions such as corneal ulcer, iritis, glaucoma, central retinal artery occlusion (CRAO), endophthalmitis, or retinal detachment, early senior involvement and ophthalmology consultation are essential. Discussion of all cases with a senior physician prior to management and disposition is strongly recommended [13]. Certain contraindications to specific lines of management may be overlooked by junior staff; therefore, a senior physician must be present when such procedures are performed.

For example, while intraocular pressure (IOP) measurement is a standard component of the physical examination, assistance should be sought if contraindications are suspected. For instance, a ruptured globe is a contraindication to tonometry. Similarly, digital globe massage, which is used in cases of non-traumatic CRAO, is contraindicated if the patient has had recent ocular surgery. In cases of chemical burns requiring copious irrigation, the instinct to use a Morgan lens should be avoided if a foreign body is suspected, as this could cause further damage.

Additionally, foreign body removal requires senior assistance, particularly when the foreign body is in the visual axis, as improper removal could result in permanent visual disturbances. Senior supervision ensures that these procedures are performed safely and effectively, reducing the risk of complications.

Not-To-Miss Diagnoses

A large variety of conditions can present with an acute painful red eye. While most conditions are benign and can be diagnosed and managed by an ED physician, some require early diagnosis for appropriate ED management and timely ophthalmology consultation.

Painful Red Eye Causes by Structure:

The Orbit:

  • Orbital Cellulitis
  • Trauma
  • Orbital Compartment Syndrome (OCS)

Lacrimal System:

  • Keratoconjunctivitis Sicca
  • Dacryocystitis
  • Dacryoadenitis

Lids and Lashes:

  • Hordeolum
  • Blepharitis

Conjunctiva:

  • Conjunctivitis

Sclera:

  • Episcleritis
  • Scleritis

Cornea:

  • Foreign Bodies
  • Abrasions
  • Ulcers
  • Herpes Simplex Keratitis (HSK)
  • Herpes Zoster Ophthalmicus (HZO)
  • Chemical Burns

Uveal Tract:

  • Iridocyclitis
  • Immediate Uveitis
  • Acute Angle Closure Glaucoma (AACG)

Vitreous:

  • Endophthalmitis
  1.  
Approach to the presentation of a red eye in the Emergency Department. Adapted from Life in the Fast Lane: The Red Eye Challenge.

Ocular emergencies presenting with a red and painful eye can be sight-threatening—such as chemical burns, globe trauma or foreign bodies, corneal ulcer, gonococcal conjunctivitis, acute iritis, acute glaucoma, and endophthalmitis—or life-threatening, such as orbital cellulitis.

Caustic injuries may result from alkali or acidic burns. Alkali burns are more severe as liquefactive necrosis allows deeper tissue penetration and corneal perforation, causing damage that may persist for weeks. Acid burns cause coagulative necrosis, limiting deeper penetration. Management involves copious irrigation, preferably using a Morgan lens, until the physiological pH is restored (goal: 7–7.5).

Two conditions—pre-septal/periorbital cellulitis and post-septal/orbital cellulitis—present similarly but differ significantly in severity and management. Pre-septal cellulitis is an infection of the tissue surrounding the orbit, while orbital cellulitis involves infection extension into the orbit itself. Orbital cellulitis presents with fever, marked chemosis, proptosis, visual disturbances, and, importantly, pain on eye movement. Laboratory investigations such as leukocytosis and elevated ESR may assist in diagnosing orbital cellulitis. It is usually secondary to sinus or tooth infections or complications of pre-septal cellulitis. As a medical and ocular emergency, orbital cellulitis requires admission for IV antibiotics and surgical drainage if necessary.

Globe trauma encompasses multiple entities and may present with a red, painful eye. Globe rupture typically occurs secondary to blunt trauma with increased intraocular pressure causing herniation. In contrast, globe laceration is characterized by a wound at the site of impact. Penetrating injuries involve an entry wound, while perforating injuries have both entry and exit wounds. Intraocular foreign bodies may occur with blunt or penetrating trauma, leading to secondary injuries. Globe injury should be suspected if an apparently benign eyelid laceration is accompanied by fat protrusion, as the eyelids lack subcutaneous tissue. Orbital fractures, most commonly involving the orbital floor (the thinnest part of the orbital frame), may be associated with or without globe injury and can cause extraocular muscle and neurovascular entrapment. A feared complication of orbital trauma is retrobulbar hematoma, which, with increasing pressure, may lead to orbital compartment syndrome and permanent optic nerve damage. Immediate intervention, such as lateral canthotomy and cantholysis, must be performed within 90 minutes.

Keratitis can have various etiologies, including infections or ultraviolet (UV) injuries. Most cases present with pain, blepharospasm, and a foreign body sensation, but certain causes require early recognition and management. Herpes simplex virus (HSV) keratitis is diagnosed by the characteristic dendritic ulcer seen with fluorescein dye. Management includes oral and topical antivirals with urgent ophthalmology consultation to prevent corneal scarring and vision loss. Topical antibiotics may sometimes be added to prevent secondary bacterial infections, but steroids are contraindicated. In contrast, a pseudodendrite pattern is diagnostic of herpes zoster ophthalmicus, which requires oral antivirals [13].

Corneal ulcers are more severe than corneal abrasions and typically develop over days without a history of trauma. The cornea appears white, with a focal necrotic crater-like lesion that is often central, thin, and extends to the stroma. A positive Seidel test may indicate corneal perforation. Management includes urgent corneal cultures before initiating topical antibiotics and an ophthalmology referral.

Anterior uveitis, the inflammation of the iris and ciliary body, is most commonly idiopathic but may be caused by infections or connective tissue disorders. Photophobia is pronounced due to ciliary spasm. Key examination findings include perilimbal conjunctival injection (ciliary flush) and cells and flares in the anterior chamber. Management, initiated by ophthalmology, includes topical and/or oral steroids, along with mydriatics to relieve pain from ciliary spasm and prevent posterior synechiae (adhesions to the anterior lens capsule), which can lead to angle-closure glaucoma.

Endophthalmitis, a globe infection, is challenging to differentiate from uveitis. It most commonly occurs after globe trauma (e.g., Pseudomonas and Klebsiella) or intraocular surgeries (e.g., post-cataract surgery associated with Staphylococcus). Other causes include hematogenous spread, typically in critically ill or endocarditis patients. Ultrasound can confirm the diagnosis, revealing strands and membranes in the vitreous. Management includes admission and administration of intravitreal antibiotics.

Episcleritis and scleritis are two conditions that can appear similar but require differentiation, as scleritis is a more severe, sight-threatening condition. Both can be idiopathic or associated with collagen vascular diseases, infections, or rheumatological conditions. Episcleritis typically presents with localized or diffuse vessel injection in a radial pattern, while scleritis presents with anterior chamber flares, cells, scleral edema, and a pathognomonic purple hue. A bedside test using topical phenylephrine can help differentiate the two: in episcleritis, episcleral vessels blanch, while in scleritis, there is no blanching due to deeper inflammation. Scleritis is associated with more severe pain, photophobia, and visual disturbances. Management includes NSAIDs, steroids, and immunomodulation with treatment of the underlying cause.

Acing Diagnostic Testing

The most important diagnostic tools used in ocular conditions are bedside tests, which include tonometry, examination with fluorescein (using an ophthalmoscope or slit lamp), and even ultrasound. Bedside ultrasound can be used to confirm conditions such as retinal detachment, posterior vitreous detachment, vitreous hemorrhage, intraocular foreign bodies, globe rupture, lens dislocation, and papilledema, among others. Other imaging modalities are rarely required. CT orbit is typically diagnostic for orbital fractures in trauma cases. Laboratory tests are rarely necessary in the ED [13].

Most cases of conjunctivitis are caused by allergic or viral etiologies and can be treated with artificial tears applied 5–6 times per day. If there is concern for a bacterial cause of conjunctivitis, the patient can be treated with topical antibiotic drops, such as trimethoprim or polymyxin B, administered four times daily for 5–7 days. For patients who wear soft contact lenses, Pseudomonal coverage is necessary, and treatment with a fluoroquinolone or aminoglycoside should be initiated.

By Rbmorley – Robert Morley, Public Domain, Link

A subconjunctival hemorrhage occurs when a small blood vessel bursts beneath the conjunctiva, the clear tissue covering the white part of the eye. It appears as a bright red or dark patch on the sclera and may look alarming, but it is usually harmless. The condition often results from minor trauma, straining, coughing, or sneezing, but it can also occur spontaneously, particularly in individuals with high blood pressure or those taking blood-thinning medications. Subconjunctival hemorrhages are typically painless and do not affect vision. Most cases resolve on their own within one to two weeks without the need for treatment. However, recurrent or extensive hemorrhages may warrant further medical evaluation to rule out underlying conditions.

By Daniel Flather – Own workCC BY-SA 3.0Link

A rust ring indicates that the foreign body, likely an iron particle, has been present on the cornea for several days. While the iron particle or "rust" can be easily lifted off the cornea, it will leave a stained area beneath. Removal typically requires the use of a needle or ophthalmic drill (burr). If a small corneal foreign body is identified during slit-lamp examination, the eye should first be anesthetized with a topical anesthetic prior to removal. The foreign body can then be removed using a small-gauge needle, fine forceps, or irrigation. Metallic foreign bodies often leave a rust ring, which should be removed with an ophthalmic burr if available. After removal, the resulting defect should be treated as a corneal abrasion, typically with a topical antibiotic ointment to prevent infection.
Episcleritis: Artificial tears can be used up to four times per day to help lubricate the eye. A trial of oral NSAIDs can be administered in the emergency room, and if the pain resolves, they can be continued as outpatient therapy. If the patient continues to experience significant pain after NSAID treatment, topical steroids can be used to relieve discomfort. The steroid drops can be continued as outpatient treatment until the patient is evaluated by ophthalmology in 2–3 weeks. Scleritis (image above): Oral NSAIDs can also be used for pain control in scleritis, similar to episcleritis. However, topical steroids are ineffective in scleritis. Instead, oral steroids may be initiated, starting with prednisone 60 mg daily for 1 week, followed by a slow taper over the next 4–6 weeks. Ophthalmology consultation is essential, as additional immunosuppressive agents may be recommended for management, particularly in recurrent or severe cases.

By Imrankabirhossain – Own workCC BY-SA 4.0Link

Acute anterior uveitis 45-year-old female. Complains of painful eye and discomfort in bright light with watery discharge. VA 6/12. Photo: International Centre for Eye Health http://www.iceh.org.uk, London School of Hygiene & Tropical Medicine. Often related to a systemic process such as a rheumatologic condition, malignancy, or infection, iritis and uveitis can be treated symptomatically with cycloplegics, which paralyze the ciliary body and pupillary sphincter. A long-acting agent such as homatropine lasts for 2–3 days after a single dose and can help control pain until the patient is evaluated by an ophthalmologist. These patients should be seen by an ophthalmologist within 48 hours.

Photo: International Centre for Eye Health http://www.iceh.org.uk, London School of Hygiene & Tropical Medicine.

Endophthalmitis with extensive hypopyon consistent with active infection. © International Centre for Eye Health iceh.lshtm.ac.uk, London School of Hygiene & Tropical Medicine. Endophthalmitis usually leads to vision loss and, therefore, requires an emergent ophthalmology consult. Admission is necessary to administer IV antibiotics. Additionally, the ophthalmologist may perform vitreous aspiration and administer intraocular antibiotics and steroids.

Photo: International Centre for Eye Health http://www.iceh.org.uk, London School of Hygiene & Tropical Medicine.

Hyphema: Initial treatment consists of elevating the patient’s head to allow the red blood cells to settle inferiorly, where they are less likely to obscure the trabecular meshwork and raise intraocular pressure. If the intraocular pressure is increased to >30 mmHg, the same treatment options described for glaucoma can be employed. Patients with hyphema should have an ophthalmology consult while in the ED.

By Rakesh Ahuja, MD – Own workCC BY-SA 2.5Link

Herpes Zoster Ophthalmicus: Patients with herpes zoster ocular infections should be treated with artificial tears and erythromycin ointment to prevent secondary infections. Oral antiviral medication can be used if there is skin involvement, and, after consultation with an ophthalmologist, topical antivirals may also be prescribed. The significant pain associated with herpes zoster infections may require opiate treatments or the use of an antidepressant, such as amitriptyline 25 mg P.O. TID.

Herpes zoster ophthalmicus Photo: John Sandford-Smith

Herpes simplex virus Top left: Child with measles and severe herpes simplex keratitis affecting the right eye. Top right: Dendritic ulcer stained with fluorescein dye Bottom left: Geographic ulcer stained with fluorescein dye Bottom right: Inflamed conjunctiva and geographic ulcer. Herpes Simplex Infections: Herpes simplex infections can be diagnosed based on the characteristic dendritic pattern seen with fluorescein staining. Conjunctival infections can be treated with trifluridine (one drop up to nine times per day), and an antibiotic ointment such as erythromycin can be added to prevent secondary infections. All patients with suspected herpes keratitis should be evaluated by an ophthalmologist within 48 hours.

Photo (clockwise from top-left): John Sandford-Smith, Allen Foster, David Yorston)

Corneal Ulcers are more serious and can pose a significant threat to the patient’s vision. Ophthalmology should be consulted emergently for the culturing of the ulcer and the initiation of antibiotics, and, in certain cases, antifungals.

Photo: P Vijayalakshmi

Most corneal abrasions heal rapidly without intervention; treatment focuses on preventing secondary infection and controlling pain. Pain, often from ciliary spasm, can be relieved with topical cycloplegics like cyclopentolate (short-acting, repeat every 4–6 hours) or homatropine (long-acting, lasting 2 days). Oral NSAIDs or opiates may be required for adequate pain control. Topical antibiotic ointments, such as gentamicin 0.3%, ciprofloxacin 0.3% (effective against Pseudomonas; recommended for contact lens wearers), erythromycin 0.5%, ofloxacin 0.3%, or polymyxin/trimethoprim, prevent secondary infection. If the abrasion is large or crosses the central visual axis, the patient should follow up with ophthalmology within 24 hours; otherwise, follow-up within 72 hours ensures healing. For viral causes, antivirals like trifluridine 1% or vidarabine 3% are used.

By James Heilman, MD – Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=11918476

Empiric and Symptomatic Treatment

The most commonly used ophthalmological topical medications are listed below. Please note that topical steroids have been omitted, as their use is highly discouraged in the ED and should only be prescribed by an ophthalmologist [12,13]. Commonly used drugs are listed below (ADR: Adverse Drug Reaction, CI: Contraindication, DOA: Duration of Action).

Anesthetics

Proparacaine 0.5%

  • Dose: 1 to 2 drops
  • Onset: 20 seconds
  • Duration of Action (DOA): 15 minutes
  • Uses: Procedures such as tonometry, removal of foreign body, fluorescein.
  • Comments: Never prescribed.

Tetracaine 0.5%

  • Dose: 1 to 2 drops
  • Onset: 1 minute
  • DOA: 30 minutes
  • Uses: Procedures such as tonometry, removal of foreign body, fluorescein.
  • Comments: Never prescribed.

Mydriatics

Cholinergic Antagonist (Mydriatics and Cycloplegics)

Tropicamide 0.5-1%

  • Dose: 1 to 2 drops of 0.5% or 1% solution
  • Onset: 20 minutes
  • DOA: 4-5 hours

Cyclopentolate 0.5-1%

  • Dose:
    • 0.5%: 1 drop in children
    • 1%: 1 drop in adults
  • Onset: 30 minutes
  • DOA: 3-6 hours

Atropine 0.5-1%

  • Dose: 1 to 2 drops of 1% solution
  • DOA: 1-2 weeks
Adrenergic Agonist

Phenylephrine 2.5%

  • Dose: 1 to 2 drops
  • Uses: To differentiate between scleritis and episcleritis.

Decrease Aqueous Production

β-Blockers

Timolol (Non-selective)

  • Dose: 1 drop once to twice daily
  • Onset: 20 minutes
  • DOA: 24 hours
  • Precautions: Bronchospasm, bradycardia, cardiac failure, heart block.
  • Adverse Drug Reactions (ADR): Tachyphylaxis.

Betaxolol (β1-selective)

  • Dose: 1 drop once to twice daily
α-Agonists

Epinephrine 1% (Non-selective)

  • Dose: 1 drop 2-3 times per day

Brimonidine 0.2% (α2-selective)

  • Dose: 1 drop 2-3 times per day
  • Onset: 2 hours
  • DOA: 12 hours
  • ADR: Uveitis, conjunctival hyperemia.

Apraclonidine 0.5% (α2-selective)

  • Dose: 1 drop 2-3 times per day
  • Onset: 1 hour
  • DOA: 3.5 hours
Carbonic Anhydrase Inhibitors

Dorzolamide, Brinzolamide

  • Dose: 1 drop 2 times per day
  • ADR: Paraesthesia, malaise, gastrointestinal disturbances, renal stone, Stevens–Johnson syndrome, blood dyscrasias, hypokalemia.
  • Contraindications (CI): Sickle cell disease, sulfa allergy.

Acetazolamide (Oral)

  • Dose: 500 mg PO twice daily (adjusted based on renal function).

Increase Uveoscleral Outflow

Prostaglandin Analogues

Latanoprost, Travaprost, Bimatoprost

  • Dose: 1 drop once per day
  • ADR: Brown discoloration of iris, darkening of eyelid skin, growth of eyelashes.

Increase Trabecular Meshwork Outflow

Parasympathomimetic – Pilocarpine

  • Dose: 1-2 drops 3-4 times per day
  • ADR: Headache, induced myopia.

Antibiotics

Erythromycin

  • Form: Ointment applied to the lower eyelid 2-4 times a day
  • Comments: Not suitable for contact lens wearers. Can be used for super glue exposure.

Ciprofloxacin

  • Forms:
    • Solution: 1 to 2 drops when awake every 2 hours for 2 days
    • Ointment: Half-inch applied to lower eyelid 3 times a day for 2 days
  • Comments: Suitable for contact lens wearers.

Tobramycin

  • Forms:
    • Solution: 1 to 2 drops every 4 hours
    • Ointment: Half-inch applied to lower lid 2-3 times a day
  • Comments: Suitable for contact lens wearers.

Moxifloxacin 0.5%

  • Dose: 1 to 2 drops every 2 hours for 2 days, then taper over 5 days
  • Comments: Suitable for contact lens wearers.

Decongestants

Anti-histamines

Olopatadine 0.1% Solution

  • Dose: 1 drop twice daily
  • Onset: 30 to 60 minutes
  • DOA: 2 hours
  • Uses: Allergic conjunctivitis.

Pheniramine

  • Dose: 1 drop 3-4 times a day
  • Comments: Used in combination with naphazoline.
Sympathomimetic

Naphazoline

  • Dose: 1 drop 3-4 times a day
  • Uses: Conjunctival congestion, itching.

Special Patient Groups

Unresponsive Patients

Unresponsive patients are challenging to assess, as a complete examination is often not possible. Visual acuity is typically difficult to determine in these cases. The examination primarily relies on evaluating pupil reactivity and size. In ICU settings, particularly in severely ill patients, frequent eye examinations are essential to detect signs of infection (e.g., endogenous hematogenous endophthalmitis), corneal abrasions, or ulcers.

Pediatrics

Assessing visual acuity in pediatric patients can be difficult, yet it is a critical period to correct refractive errors to prevent the risk of amblyopia. In infants aged 4 to 6 months, visual acuity can be evaluated by observing their ability to track objects. The inability to track objects suggests visual acuity of 20/200 or worse. For older children who cannot yet read or identify letters on the Snellen chart, specialized pediatric visual acuity charts are available [14].

Contact Lens Wearers

Contact lens wearers are at a higher risk of developing certain conditions, such as corneal abrasions, corneal ulcers (particularly caused by Pseudomonas or Acanthamoeba), and giant papillary conjunctivitis. Therefore, documenting the use of contact lenses is crucial for appropriate evaluation and management [13].

When To Admit This Patient

The majority of patients with a red and painful eye have benign conditions that can be diagnosed and managed in the ED. These patients will require follow-up with an ophthalmologist only if symptom resolution does not occur within the time frame explained to them or if any red flags or complications arise. Examples of such conditions include hordeolum, chalazion, blepharitis, conjunctivitis, corneal abrasion, dry eyes, and episcleritis. Therefore, the most critical aspects of management are appropriate safety netting and providing a clear explanation of the natural history of these conditions, along with the important red flags to watch for.

On the other hand, certain diagnoses require emergent consultation, such as acute angle-closure glaucoma, hypopyon, and bacterial keratitis. Urgent follow-up is necessary for conditions such as iritis and scleritis [2].

Revisiting Your Patient

The image was produced by using ideogram 2.0.

The patient was shifted to the resuscitation room. Quick stabilization using the ABCD approach was unremarkable. Two large-bore IV lines were inserted, and analgesia was initiated to manage pain until a full examination of her red right eye could be completed.

Specific Examination Approach for Suspected Angle Closure Glaucoma was planned. 

Findings on Examination

  1. External Eye Examination:
    • Globe position: Within normal limits (WNL).
    • Globe palpation: The right eye was significantly harder than the left.
    • Conjunctiva: Injected.
    • No discharge, periorbital tenderness, or swelling.
  2. Visual Acuity:
    • Right eye: Decreased to 20/70.
    • Left eye: 20/30.
  3. Visual Fields:
    • Unremarkable.
  4. Extraocular Muscle Movement:
    • Smooth pursuit.
    • No diplopia, nystagmus, or pain.
  5. Pupils and Anterior Chamber:
    • Right pupil: Fixed, mid-dilated, poorly reactive to light.
  6. Intraocular Pressure:
    • Tono-pen readings: 50 mmHg in the right eye, 24 mmHg in the left eye.
  7. Slit-lamp Examination:
    • Shallow anterior chamber.
    • Corneal clouding and edema.
    • Cataractous lens.
  8. Eye Adnexa:
    • Lids, lashes, and lacrimal system: Normal.
  9. Posterior Chamber:
    • Difficult to assess in the ED due to corneal cloudiness.
  10. Direct Ophthalmoscope:
    • Difficult to perform.
    • Red reflex: Reduced in the right eye.
  11. Bedside Ultrasound
    • Deferred due to patient discomfort.

Clinical Findings and Management

The findings were suggestive of acute angle-closure glaucoma (AACG). An ophthalmological consultation was immediately obtained. The following treatments were initiated as advised:

  • Medications:

    • One drop of Timolol 1% and one drop of Apraclonidine 1%, one minute apart.
    • 500 mg IV acetazolamide as the patient was unable to tolerate oral medication.
  • Admission and Surgical Planning:

    • The patient was admitted under the ophthalmology service for further management with laser iridotomy, the preferred surgical treatment to minimize the occurrence of similar events in the future.
    • Prophylactic iridotomy in the fellow eye was recommended if the chamber angle was anatomically narrow, as nearly half of fellow eyes develop AACG within five years [15].
  • Rechecking IOP:

    • Prior to admission, the IOP in the right eye was reduced to 35 mmHg. The patient was given a drop of pilocarpine 1%.

Epidemiology of Angle-Closure Glaucoma

Considerable differences exist in the prevalence of angle-closure glaucoma among ethnic and racial groups. The highest rates are observed in Inuit, Chinese, and other Asian populations, while lower rates are reported in individuals of African, African-derived, European, and European-derived origins. In some Asian populations, primary angle-closure glaucoma (PACG) accounts for nearly as many cases as open-angle glaucoma (OAG).

Globally, 0.7% of people over 40 years of age are estimated to have angle-closure glaucoma. In 2013, this represented 20.2 million people, most of whom (15.5 million) were in Asia. In China, PACG is estimated to cause unilateral blindness (visual acuity <20/200 or visual field ≤10°) in 1.5 million individuals and bilateral blindness in another 1.5 million [16].

  •  

Acute glaucoma, red eye. Photo: International Centre for Eye Health http://www.iceh.org.uk, London School of Hygiene & Tropical Medicine

Authors

Picture of Gina Rami Abdelmesih

Gina Rami Abdelmesih

Picture of Amna AlMaazmi

Amna AlMaazmi

Picture of Ahmed AlSaadi

Ahmed AlSaadi

Listen to the chapter

References

  1. Channa R, Zafar SN, Canner JK, Haring RS, Schneider EB, Friedman DS. Epidemiology of eye-related emergency department visits. JAMA Ophthalmol. 2016;134(3):312-319. doi:10.1001/jamaophthalmol.2015.5778.
  2. Jacob DS. The red eye: evaluation and management. In: Post TW, ed. UpToDate. UpToDate; 2022. Accessed May 1, 2023. https://www.uptodate.com/contents/the-red-eye-evaluation-and-management.
  3. Ramirez DA, Porco TC, Lietman TM, Keenan JD. Epidemiology of conjunctivitis in US emergency departments. JAMA Ophthalmol. 2017;135(10):1119-1121. doi:10.1001/jamaophthalmol.2017.3319.
  4. Gulma K, Lee JE. Ophthalmology. In: Walls R, Hockberger R, Gausche-Hill M, eds. Rosen’s Emergency Medicine: Concepts and Clinical Practice. 10th ed. Elsevier; 2023:750-780.
  5. Dupre AA, Vojta LR. Red and painful eye. In: Walls R, Hockberger R, Gausche-Hill M, eds. Rosen’s Emergency Medicine: Concepts and Clinical Practice. 10th ed. Elsevier; 2023:167-182.
  6. Bonini S. The red eye. Eur J Ophthalmol. 2021;31(6):2843-2849. doi:10.1177/11206721211024827.
  7. Al Tamimi HF, Allawi MN, Hanumantharayappa K. Characterization of red eye cases presented to the eye emergency clinic at a tertiary care hospital during COVID-19 pandemic. Oman J Ophthalmol. 2023;16(2):220-226. doi:10.4103/ojo.ojo_224_22.
  8. Andoh JE, Miguez S, Andoh SE, et al. Epidemiologic trends of domestic violence-related ocular injuries among pediatric patients: data from the Nationwide Emergency Department Sample 2008-2017. J AAPOS. 2023;27(6):335.e1-335.e8. doi:10.1016/j.jaapos.2023.09.008.
  9. Ferrari G, Micheli M. Neuroinflammation: the missing link between pain and immunity. Acta Ophthalmol. 2024;102(1):e10-e19. doi:10.1111/aos.16499.
  10. Graca M, Sarantopoulos K, Horn DB. Chemical toxic exposures and chronic ocular pain. Front Toxicol. 2023;5:1188152. doi:10.3389/ftox.2023.1188152.
  11. Alryalat SA, Al Deyabat O, Lee AG. Painful eyes in neurology clinic: a guide for neurologists. Neurol Clin. 2024;42(2):559-571. doi:10.1016/j.ncl.2023.12.009.
  12. Li DQ, Sedarous F, Bin Yameen TA. Ophthalmology. In: Alvarez-Veronesi C, ed. Toronto Notes 2019: Comprehensive Medical Reference and Review for the Medical Council of Canada Qualifying Exam (MCCQE) Part 1 and the United States Medical Licensing Exam (USMLE) Step 2. Toronto Notes for Medical Students, Inc.; 2018:886-929.
  13. Oetting TA. Eye emergencies. In: Tintinalli JE, ed. Tintinalli’s Emergency Medicine Manual. 8th ed. McGraw-Hill Education; 2018:813-825.
  14. Schabowski S. Ophthalmological procedures. In: Reichman EF, ed. Emergency Medicine Procedures. 2nd ed. McGraw-Hill Education; 2013:1007-1062.
  15. Lin YH, Wu CH, Huang SM, et al. Early versus delayed phacoemulsification and intraocular lens implantation for acute primary angle-closure. J Ophthalmol. 2020;2020:8319570. doi:10.1155/2020/8319570.
  16. Zhang N, Wang J, Chen B, Li Y, Jiang B. Prevalence of primary angle closure glaucoma in the last 20 years: a meta-analysis and systematic review. Front Med (Lausanne). 2020;7:624179. doi:10.3389/fmed.2020.624179.

FOAMED and Other Resources for Further Reading

Wood DB. The Red Eye. International Emergency Medicine Education Project. https://iem-student.org/the-red-eye/. Accessed January 6, 2025.

Reviewed and Edited By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

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

Chest Pain (2024)

by Khaled Alaboud Alkheder & Muneer Al Marzooqi

You Have A New Patient!

A 67-year-old woman presents to the ED with acute chest pain. The pain is sharp and stabbing in nature. She feels nauseated and short of breath. The patient has a history of hypertension, type 1 diabetes mellitus, medullary thyroid cancer, coronary artery disease, and gastroesophageal reflux disease. She smoked half a pack of cigarettes daily for 19 years but quit 18 years ago. Her current medications include Lisinopril, Insulin Glargine, Insulin Aspart, Sertraline, Aspirin, and Ranitidine.

The image was produced by using ideogram 2.0.

She appears anxious and diaphoretic. Her temperature is 37.2°C, pulse is 62/min, respirations are 19/min, and blood pressure is 142/81 mmHg. The lungs are clear to auscultation. The chest wall and abdomen are non-tender. There is 5/5 strength in all extremities. The remainder of the examination shows no abnormalities.

How would you proceed, and what is the next step in management?

What Do You Need To Know?

Chest pain in the emergency department is reported to be the second most common complaint, comprising approximately 5% of all emergency department visits. It can indicate various underlying causes, and patients present with many signs and symptoms. The potential causes of chest pain include diseases affecting the heart, aorta, lungs, esophagus, stomach, mediastinum, pleura, and abdominal viscera.

Patients usually describe visceral pain as a squeezing, pressure-like, or dull type of pain. If the pain is visceral, it may also refer to other locations due to the nerves coursing through somatic nerve fibers as they reach the spinal cord. For example, ischemic heart pain may refer to the left or right shoulder, jaw, or left arm.

Clinicians in the ED focus on promptly identifying and ruling out life-threatening causes of chest pain. Patients with serious causes of chest pain may not exhibit any vital sign or physical examination abnormalities and may appear healthy [1,2].

Initial Assessment and Stabilization (ABCDE Approach)

The ABCDE approach is universally recognized as the safest and most efficient method for the initial assessment of patients in the Emergency Department (ED), particularly those presenting with chest pain [3]. This systematic approach ensures rapid identification and management of life-threatening conditions. It prioritizes the immediate stabilization of the patient while facilitating a structured evaluation process.

A – Airway: The first step involves assessing the airway for any signs of obstruction. Key indicators include the patient’s ability to speak without distress and the presence of paradoxical chest movements. Obstructions may result from conditions such as tongue swelling, lip swelling, or other factors impeding spontaneous breathing. Ensuring a patent airway is critical, as it serves as the foundation for effective oxygenation and ventilation.

B – Breathing: Next, the breathing assessment evaluates respiratory effectiveness by observing the patient’s respiratory rate (normal range: 10-20 breaths per minute), inspecting for signs of respiratory distress, and auscultating lung sounds. Findings such as basal crackles may indicate pulmonary edema, diminished breath sounds could suggest pneumothorax or pleural effusion. Each of these conditions requires prompt recognition and intervention.

C – Circulation: The circulation step focuses on identifying signs of cardiovascular compromise or shock. Clinical signs include abnormal extremity coloration (blue, pale, pink, or mottled), prolonged capillary refill time (normal is ≤2 seconds), and abnormal heart rates. Auscultation of the heart should confirm normal S1 and S2 sounds without murmurs or gallops. These findings guide the clinician in diagnosing conditions such as hypoperfusion or cardiac dysfunction. Muffled heart sounds may point toward pericardial tamponade. 

D – Disability: Assessment of the patient’s neurological status is crucial, including evaluating their level of alertness, Glasgow Coma Scale (GCS) score, and glucose levels. Any abnormalities here could indicate underlying conditions such as hypoglycemia, traumatic brain injury, or other causes of altered mental status.

E – Exposure: The final step involves fully exposing the patient to detect visible signs such as rashes, discoloration, or gross abnormalities. This step ensures that no critical findings, such as trauma or skin infections, are overlooked.

Once the primary assessment is complete, interventions should focus on managing hemodynamic instability, such as shock or hypertension. Simultaneously, secondary assessments and investigations are initiated, including obtaining IV access, performing a 12-lead ECG, and ordering relevant diagnostic tests to confirm the underlying cause of the presentation.

Medical History

When assessing a patient presenting with chest pain in the Emergency Department (ED), obtaining a thorough history is critical after ensuring the patient’s stability. Key aspects of the history should include [3,4]:

  • Onset of Pain: Determining whether the pain started abruptly or developed gradually provides valuable diagnostic clues.
  • Site of Pain: The location of the pain (e.g., substernal, localized, diffuse, chest wall, or back) can guide the identification of the underlying cause.
  • Character of Pain: Descriptions such as sharp, squeezing, or pleuritic help differentiate between cardiac, pulmonary, and musculoskeletal etiologies.
  • Radiation: Pain radiating to areas like the jaw, back, shoulder, or arm can indicate cardiac involvement.
  • Associated Symptoms: Symptoms such as diaphoresis, palpitations, dyspnea, nausea, or vomiting are important to document.
  • Timing: The pattern of the pain, whether constant or episodic, its duration, and the time of onset can help in distinguishing between various causes.
  • Exacerbating/Relieving Factors: Identifying activities or factors that provoke or alleviate the pain aids in narrowing down the diagnosis.

Pain Descriptions and Differential Diagnosis: The nature of the chest pain provides critical diagnostic insights:

  • Cardiac Origin: Pain described as “squeezing,” “crushing,” or “pressure-like” suggests cardiac ischemia or acute coronary syndrome (ACS). Pain during exertion is typical of stable angina, whereas progressive pain at rest suggests unstable angina or myocardial infarction (MI).
  • Aortic Dissection: “Tearing” pain radiating to the back is a hallmark of aortic dissection.
  • Pulmonary or Musculoskeletal Causes: “Sharp” or “stabbing” pain is often associated with pulmonary embolism, pneumothorax, or musculoskeletal disorders.
  • Gastrointestinal Causes: “Burning” or “indigestion-like” pain may originate from the gastrointestinal tract but could also signify visceral chest pain. Pain triggered by meals is more likely gastrointestinal in origin.
  • Acute Conditions: Sudden onset pain suggests conditions like aortic dissection, pulmonary embolism, or pneumothorax.

Medical Background and Risk Factors: A comprehensive medical history is essential to assess the risk for specific conditions:

  • Risk Factors for Acute Coronary Syndrome (ACS):
    • Male sex
    • Age over 55 years
    • Family history of coronary artery disease
    • Diabetes mellitus
    • Hypercholesterolemia
    • Hypertension
    • Tobacco use
  • Risk Factors for Pulmonary Embolism: Patients are at an increased risk if they have:
    • Prolonged immobilization (e.g., long-distance travel)
    • Recent surgery, especially orthopedic procedures lasting over 30 minutes
    • Central venous catheterization
    • Trauma
    • Pregnancy
    • Cancer
    • Lung or chronic heart disease
    • A personal or family history of hypercoagulability
    • Use of hormonal contraceptives or chemotherapeutic agents that increase estrogen and progestin levels

This detailed and systematic approach to history-taking allows for accurate and timely diagnosis, ensuring that critical conditions are addressed without delay.

Physical Examination

After obtaining a detailed history, a focused physical examination is crucial to identify any signs that may guide the clinician toward an accurate diagnosis. This examination combines general and systemic assessments, prioritizing findings that can point to life-threatening conditions [5,6].

General Examination and Vital Signs:

The initial step involves assessing vital signs, which often provide significant diagnostic clues:

  • Hypotension may indicate conditions such as tension pneumothorax, pulmonary embolism (PE), or acute myocardial infarction (MI).
  • Tachycardia is a nonspecific finding but is frequently seen in acute MI, PE, aortic dissection, or tension pneumothorax.
  • Hypoxemia suggests pulmonary conditions such as PE, tension pneumothorax, or simple pneumothorax.
  • Fever can be indicative of inflammatory or infectious processes, including PE, pericarditis, myocarditis, or even extrapulmonary causes like cholecystitis.

Cardiovascular Examination:

A detailed cardiovascular assessment should focus on specific findings that may narrow the differential diagnosis:

  • Significant blood pressure differences between upper extremities are a hallmark of aortic dissection.
  • Pericardial rub is a characteristic sign of pericarditis.
  • Jugular venous distension (JVD) may indicate tension pneumothorax, PE, or pericarditis with effusion.
  • Narrow pulse pressure can be associated with pericarditis with effusion, reflecting compromised cardiac output.
  • Pulsus paradoxus, an exaggerated drop in systolic blood pressure during inspiration, is a critical finding in cardiac tamponade and constrictive pericarditis.

Pulmonary Examination:

The pulmonary evaluation should focus on auscultation and observation:

  • Unilateral diminished or absent breath sounds point to tension pneumothorax or simple pneumothorax.
  • Pleural rub, a coarse grating sound, may be heard in PE, indicating pleural irritation.
  • Basal crackles (rales), particularly when bilateral, are often associated with acute MI or pulmonary edema, reflecting fluid overload or cardiac dysfunction.

Integration of Findings:

These physical examination findings must be interpreted in the context of the patient’s history and associated risk factors. For example:

  • A patient presenting with hypoxemia, tachycardia, and JVD warrants an immediate evaluation for PE.
  • Tension pneumothorax should be suspected in cases with hypotension, unilateral absent breath sounds, and JVD.
  • Signs of basal crackles and a pericardial rub may point to a combination of acute MI and pericarditis, necessitating rapid interventions.

By systematically combining history with these focused examination findings, clinicians can efficiently narrow their differential diagnosis and prioritize further investigations and treatments. This structured approach ensures that life-threatening conditions are promptly identified and managed.

When To Ask for Senior Help

Remember that senior residents and attendings supervise you when working in the emergency department. It is important to ask for their help when needed, especially when a patient with chest pain arrives [6]. The following are situations when you need to call for help immediately in a patient with chest pain:

  • Patients clenching their chest with ongoing chest pain and diaphoresis.
  • Chest pain with severe shortness of breath and evidence of pulmonary edema.
  • Chest pain with hypotension.
  • Chest pain with severe bradycardia or tachycardia.
  • Chest pain followed by unresponsiveness.

These examples exhibit life-threatening features of chest pain that can be lethal within minutes. You must call for help, and the team will be assembled to care for the patient and administer lifesaving interventions.

Alternative Diagnoses

Chest pain is a common presentation in the Emergency Department (ED) and requires a systematic and thorough approach to rule out life-threatening conditions. These diagnoses must be prioritized in the differential diagnosis as they carry significant morbidity and mortality if not identified and managed promptly [1,6].

Life-Threatening Diagnoses:

  1. Acute Coronary Syndrome (ACS): ACS encompasses conditions such as unstable angina, non-ST elevation myocardial infarction (NSTEMI), and ST elevation myocardial infarction (STEMI). These result from ischemia due to decreased myocardial oxygen supply, often caused by atherosclerotic plaque rupture. Rapid identification through ECG and biomarkers is critical to initiate timely treatment.

  2. Acute Aortic Dissection: This condition arises when a tear in the intimal layer of the aorta allows blood to flow between the layers, creating a false lumen. Patients often present with severe, tearing chest or back pain and may have a significant difference in blood pressure between the upper extremities. Early diagnosis via imaging such as CT angiography is essential to prevent fatal rupture.

  3. Pulmonary Embolism (PE): PE results from the occlusion of pulmonary arteries by thromboemboli, often originating from deep vein thrombosis (DVT). Symptoms include sudden onset dyspnea, chest pain, and hypoxemia. Clinical suspicion should be high in patients with risk factors like prolonged immobilization, recent surgery, or hypercoagulable states.

  4. Tension Pneumothorax: This is a critical condition where air accumulates in the pleural space under pressure, compressing the lungs and mediastinum. Patients may present with hypotension, respiratory distress, and absent breath sounds on the affected side. Immediate needle decompression is lifesaving.

  5. Pericardial Tamponade: This occurs when fluid accumulates in the pericardial sac, impairing cardiac filling and output. Classic findings include hypotension, jugular venous distension, and muffled heart sounds (Beck’s triad). Pulsus paradoxus is another critical clue. Echocardiography confirms the diagnosis, and pericardiocentesis is the treatment.

  6. Esophageal Rupture with Mediastinitis: Esophageal rupture, also known as Boerhaave syndrome, can lead to mediastinitis due to leakage of gastric contents into the mediastinum. Patients typically present with severe chest pain following vomiting, subcutaneous emphysema, and signs of sepsis. Prompt surgical intervention is required.

Other Diagnoses to Consider:

  1. Simple Pneumothorax: Unlike tension pneumothorax, simple pneumothorax lacks hemodynamic compromise but still requires prompt recognition. Patients may present with pleuritic chest pain and diminished breath sounds on the affected side. Treatment typically involves observation or chest tube placement, depending on severity.

  2. Pericarditis: This inflammatory condition of the pericardium often presents with sharp, pleuritic chest pain that is relieved by sitting up and leaning forward. A pericardial rub is the hallmark auscultatory finding. ECG changes, including diffuse ST elevation, aid in the diagnosis. Most cases are viral and self-limiting, though complications like effusion and tamponade must be monitored.

Acing Diagnostic Testing

To accurately diagnose the cause of chest pain, a combination of bedside tests and advanced investigations are essential. These tests provide critical information that can guide immediate management, particularly in identifying life-threatening conditions [1,2].

Bedside Tests

Electrocardiogram (ECG):

The 12-lead ECG is a cornerstone of chest pain evaluation and must be performed within 10 minutes of the patient’s presentation or EMS arrival. It aids in identifying acute coronary syndromes (ACS), including ST-elevation myocardial infarction (STEMI).

STEMI Criteria:
  • General Criteria: At least 1 mm of ST elevation in two contiguous leads, excluding V2 and V3.
  • Specific Criteria for V2 and V3 ST Elevation:
    • Women: ≥1.5 mm elevation.
    • Men <40 years: ≥2.5 mm elevation.
    • Men ≥40 years: ≥2 mm elevation.
Source: Hernandez JM, Glembocki MM, McCoy MA. Increasing Nursing Knowledge of ST-Elevated Myocardial Infarction Recognition on 12-Lead Electrocardiograms to Improve Patient Outcomes. The Journal of Continuing Education in Nursing. 2019;50(10):475-480. doi:10.3928/00220124-20190917-10
Inferior ST segment elevations with anterior and lateral reciprocal changes. Inferior MI, so the right side of the heart should be evaluated with right side chest leads. V2 ST depression is very prominent, therefore, posterior leads should be applied form V7 to V12 for the left side.
43 years-old patients with left sided chest pain. Courtesy of Khaled Alaboud Alkheder and Muneer Al Marzooqi
Clinical Interpretation of the ECG above:
  • For instance, an ECG from a 43-year-old male presenting with severe left-sided chest pain showed ST elevation in anteroseptal leads (V1-V4) with J point elevation >2 mm and reciprocal ST depression in inferior leads, indicative of an acute anterior STEMI. This finding underscores the importance of identifying patterns such as J point elevation, which marks the transition between the QRS complex and the ST segment.

ECG Limitations and Additional Considerations:

  • While some patients exhibit a classic STEMI pattern, many may present with a normal or non-diagnostic ECG. A normal ECG at admission cannot rule out ACS or other conditions, necessitating further testing if clinical suspicion remains high.
  • If the initial ECG is inconclusive, it should be repeated after a 10-minute interval, especially if chest pain recurs.
  • Additional leads should be utilized when clinical suspicion exists for specific myocardial infarctions:
    • Posterior leads (V7-V9): For suspected posterior MI.
    • Right-sided leads (V3R and V4R): For patients with acute inferior MI, to assess for right ventricular involvement.
  • In suspected pulmonary embolism (PE), the S1Q3T3 pattern (prominent S wave in lead I, Q wave in lead III, and inverted T wave in lead III) may suggest right heart strain, though it is neither sensitive nor specific for PE [5].
S1Q3T3 - Courtesy of Khaled Alaboud Alkheder and Muneer Al Marzooqi
ECG 54-yo male chest pain for the last 3 days. S1 Q3 T3, Tachycardia, minor ST depressions on lateral leads (V5-6)

The ECG is a highly valuable tool for ruling in STEMI or other acute conditions. However, its limitations in ruling out conditions underscore the necessity of adjunct investigations and clinical correlation. For example, repeated ECGs, additional lead placements, and further imaging or lab tests (such as cardiac biomarkers or D-dimer for PE suspicion) ensure comprehensive evaluation and timely intervention.

By systematically incorporating these investigative steps into the diagnostic process, clinicians can optimize patient outcomes and address the underlying etiology of chest pain effectively.

Laboratory Tests

In the assessment of patients presenting with chest pain, laboratory investigations play a crucial role in diagnosing life-threatening conditions such as acute myocardial infarction (AMI) and pulmonary embolism (PE). Among the most valuable tests are cardiac troponins and D-dimer levels, each serving distinct purposes based on clinical suspicion and patient presentation.

Cardiac Troponins:

  • Utility in AMI Diagnosis:
    Cardiac troponins, specifically high-sensitivity troponin I and T, are the preferred laboratory markers for diagnosing AMI. These biomarkers can reliably detect myocardial injury within 3 hours of symptom onset. Their high sensitivity and specificity make them the gold standard in confirming myocardial infarction (MI).

  • Role in Ruling Out MI:
    While cardiac troponins are essential for diagnosing AMI, a single set of negative cardiac enzyme results is insufficient to rule out MI, especially in early presentations. However, in patients presenting with chest pain lasting over 2 hours, a single undetectable troponin T level can help exclude MI in certain cases [1].

  • Detection of Unstable Angina:
    High-sensitivity troponin assays can also detect subtle elevations associated with unstable angina, aiding in the identification of patients at risk for adverse cardiac events. However, serial testing may be required to observe trends and confirm the diagnosis.

D-Dimer:

  • Screening for Pulmonary Embolism (PE):
    D-dimer testing is particularly valuable in patients with suspected PE. In low-risk patients, a negative D-dimer test effectively rules out PE, eliminating the need for further imaging.

  • High-Risk Patients:
    Patients identified as high-risk based on clinical assessment or pretest probability should proceed directly to diagnostic imaging, such as computed tomography pulmonary angiography (CTPA). Similarly, patients with an intermediate or high pretest probability should not rely solely on D-dimer results but instead undergo confirmatory imaging [5].

These laboratory investigations provide critical insights when integrated with clinical findings and other diagnostic tools. For example:

  • In patients presenting with prolonged chest pain and an elevated troponin level, AMI is highly likely, warranting immediate intervention.
  • Conversely, in patients with a low-risk Wells score for PE and a negative D-dimer, further imaging can be safely avoided, reducing unnecessary radiation exposure and costs.

Imaging

In the assessment of chest pain, imaging plays a pivotal role in identifying life-threatening conditions and narrowing the differential diagnosis. A combination of imaging techniques can provide vital insights into both cardiac and non-cardiac causes of chest pain.

Chest X-Ray
  • Role in Emergency Evaluations:
    Chest X-rays are widely used in emergency departments as an initial imaging modality. They are particularly useful for identifying acute and life-threatening conditions, including pericardial effusion, acute aortic dissection, pulmonary embolism (PE), pneumothorax, and pneumonia.

    • Timeliness: In cases of high clinical suspicion, a chest X-ray should be performed and interpreted within 30 minutes to avoid delays in diagnosis and treatment.

  • Limitations:
    While chest X-rays are a valuable starting point, their sensitivity and specificity may be limited for certain conditions, necessitating further imaging in many cases.

Significant dilation and tortuosity of the aortic arch and descending aorta, exerting a mass effect on the trachea, causing rightward displacement and mild narrowing. Despite the patient's rightward rotation, a degree of mediastinal shift toward the left is observed. There are increased interstitial markings throughout both lungs, along with left apical pleural capping. - Source: Hacking C Large thoracic aortic aneurysm. Case study, Radiopaedia.org (Accessed on 31 Dec 2024) https://doi.org/10.53347/rID-73356
Pneumothorax on the left side (courtesy of Mohd Mokhtar and Raja Ahmad)
Ultrasonography
  • Advantages of POCUS:
    Point-of-care ultrasound has become an indispensable tool in emergency settings due to its rapid and dynamic assessment capabilities. It can evaluate both cardiac and non-cardiac causes of chest pain with high accuracy.

  • Cardiac Applications:

    • Detection of pericardial effusion and cardiac tamponade is a primary use of POCUS.

    • Example: A significant pericardial effusion may appear as a fluid collection around the heart, as visualized in Figure 5.

  • Pulmonary Applications:

    • POCUS has a higher sensitivity and specificity than chest X-rays for detecting pleural effusion and pneumothorax.

    • Pneumothorax Findings: The absence of the seashore sign (lung sliding) and the presence of the barcode sign on M-mode ultrasound strongly suggest pneumothorax.

    • Acute Heart Failure Findings: In cases of acute ischemic chest pain, lung B-lines detected on ultrasound indicate pulmonary edema due to heart failure.

Subxiphoid 4 Chambers View. PE = Pericardial Effusion, RV = Right Ventricle, LV = Left Ventricle
CT Pulmonary Angiography (CTPA)
  • Gold Standard for PE Diagnosis:
    CT pulmonary angiography (CTPA) is the imaging modality of choice for diagnosing acute pulmonary embolism (PE). Its high sensitivity and specificity make it invaluable for confirming or excluding PE in patients with high clinical suspicion.

  • Additional Findings:
    Beyond diagnosing PE, CTPA can reveal other significant pathologies, including [3,5]:

    • Pneumonia
    • Pericardial abnormalities
    • Musculoskeletal injuries
Pulmonary Embolism - Bilateral thrombus in main pulmonary arteries

Management

Patients presenting with typical chest pain are at a high risk of having Acute Coronary Syndrome. Empiric and symptomatic treatment is paramount in the ED to help control the situation and alleviate the patient’s pain. A common mnemonic used is (MONA), where patients can be given Morphine, which is an opiate, to help relieve the pain. Oxygen supplementation is recommended, but studies have shown that hyperoxygenation and hyperoxia are harmful and can lead to oxygen radicals; therefore, patients are maintained with oxygen saturation between 94–96% [2,6].

As a sublingual administration, Nitroglycerin is used to overcome coronary vasospasm and helps with vasodilation of the coronary vessels to improve blood flow to the myocardium and relieve ischemic chest pain. Finally, Aspirin, as an antiplatelet agent, is used empirically to prevent further clot formation and is one of the mainstay treatments when Acute Coronary Syndrome is suspected.

Aspirin

Dose: 162 to 325 mg in cases of acute coronary syndrome (ACS).
Frequency: Single dose.
Maximum Dose: 4 grams in 24 hours.
Category in Pregnancy: Category C.
Cautions/Comments: Prior to administration, check for allergies, bleeding disorders, or a history of bleeding gastrointestinal (GI) ulcers, as these conditions contraindicate the use of aspirin.

Nitroglycerin (Sublingual or Puffs)

Dose: For sublingual tablets, 0.4 mg per dose. For metered spray, 400 mcg of nitroglycerin per puff.
Frequency: For sublingual administration, up to 3 doses; for puffs, administer every 5 minutes with no more than 3 sprays in a 15-minute period.
Maximum Dose: Up to 3 doses (sublingual) or sprays (puffs) within a 15-minute period.
Category in Pregnancy: Category C.
Cautions/Comments: Nitroglycerin may cause hypotension, particularly with an upright posture. It is contraindicated in patients using phosphodiesterase inhibitors (e.g., for erectile dysfunction).

Morphine

Dose: 4 to 10 mg.
Frequency: Administer 2.5 to 5 mg every 3-4 hours as needed (PRN) or infused over 4-5 minutes.
Maximum Dose: 0.1 to 0.2 mg/kg.
Category in Pregnancy: Classified as Category CFR (consult further resources for more information).
Cautions/Comments: Monitor patients for respiratory depression. Co-ingestion with alcohol increases the risk of a fatal overdose and should be avoided.

Special Patient Groups

Pediatrics

Chest pain in children presenting to the emergency department can be a challenging clinical scenario, as it often raises concerns about serious underlying conditions, including cardiac issues, although they are relatively rare in this population. The differential diagnosis for pediatric chest pain includes musculoskeletal pain, respiratory conditions, gastrointestinal issues, and, less commonly, cardiac abnormalities such as myocarditis or pericarditis [7]. A thorough history and physical examination are essential to differentiate between these causes, considering factors such as the nature of the pain, associated symptoms, and the child’s medical history [8]. While most cases of chest pain in children are benign, it is crucial for healthcare providers to maintain a high index of suspicion and to utilize appropriate diagnostic tools, such as electrocardiograms and imaging studies, when indicated [9].

Pregnant Patients

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

Geriatrics

Older adults often experience less classic symptoms of myocardial infarction, such as chest pressure or pain, and may instead report vague symptoms like fatigue, shortness of breath, or confusion, which can complicate diagnosis [14]. Additionally, the presence of multiple chronic conditions may lead to an increased risk of complications and poorer outcomes [15]. Timely and accurate assessment is critical, as delays in diagnosis can significantly impact morbidity and mortality rates in this population [16]. Therefore, a high index of suspicion and thorough evaluation, including appropriate imaging and laboratory tests, are essential in managing chest pain in geriatric patients effectively [17].

When To Admit This Patient

Disposition decisions for patients presenting with chest pain in the emergency department (ED) are critical for ensuring appropriate care and minimizing the risk of adverse cardiovascular events. According to guidelines established by the American College of Cardiology and the American Heart Association (ACC/AHA), patients exhibiting high-risk features, such as ST-segment elevation on an electrocardiogram (ECG), hemodynamic instability, or signs of heart failure, should generally be admitted to the hospital for further evaluation and management [18]. Additionally, those presenting with intermediate-risk features—such as abnormal ECG readings, elevated cardiac biomarkers like troponin, or a history of coronary artery disease—also warrant hospitalization [19]. Conversely, low-risk patients, characterized by a normal ECG and negative cardiac biomarkers, may be safely discharged based on clinical judgment and validated risk stratification tools [19]. Ultimately, the decision to admit a patient with chest pain hinges on a comprehensive assessment of their symptoms, medical history, and individual risk factors for serious cardiovascular events, ensuring that high-risk patients receive the necessary care while minimizing unnecessary hospitalizations for those at lower risk [20].

Risk Stratification

The HEART Score is a clinical tool used to evaluate the risk of major adverse cardiac events (MACE) in patients presenting with chest pain. It assesses five key components: history, ECG findings, age, risk factors, and troponin levels, with each category assigned a score ranging from 0 to 2 points. The total score determines the level of risk and guides subsequent management.

History is assessed based on clinical suspicion. A highly suspicious history earns 2 points, a moderately suspicious history scores 1 point, and a slightly or non-suspicious history scores 0 points. This subjective component emphasizes the importance of a thorough clinical evaluation.

ECG findings are evaluated next. Significant ST-depression earns 2 points, nonspecific repolarization changes score 1 point, and a normal ECG scores 0 points. This category highlights the significance of electrocardiographic abnormalities in cardiac risk stratification.

Age is another important factor. Patients aged 65 years or older receive 2 points, those aged between 45 and 65 years earn 1 point, and patients 45 years or younger score 0 points, reflecting the age-related risk of cardiac events.

Risk factors are categorized based on their number and severity. Patients with three or more risk factors or a history of coronary artery disease (CAD) receive 2 points. Those with one or two risk factors score 1 point, while individuals with no risk factors score 0 points. Risk factors include diabetes mellitus (DM), hypertension (HTN), hyperlipidemia (HLP), smoking (current or recent), obesity, and a family history of CAD.

Troponin levels are also considered. Levels three or more times the normal limit score 2 points, levels one to three times the normal limit earn 1 point, and normal troponin levels score 0 points. This biomarker is critical in identifying myocardial injury.

The total HEART Score helps categorize patients into low, moderate, or high risk for MACE over the next six weeks. A score of 0-3 corresponds to a 2.5% risk and suggests discharge home. A score of 4-6 indicates a 20.3% risk, warranting clinical observation. Scores of 7-10 reflect a 72.7% risk, prompting early invasive strategies. This systematic approach helps clinicians make evidence-based decisions for managing patients with chest pain.

Each variable is scored from 0 to 2, allowing for a comprehensive assessment of the patient’s risk profile. For instance, the patient’s history is examined for indicators of coronary artery disease (CAD), while the ECG is scrutinized for signs of ischemia, such as ST-segment depression [21]. Age is considered a significant risk factor, as older patients are at higher risk for CAD, and the presence of additional risk factors like hypertension, hyperlipidemia, smoking, and diabetes further elevates this risk [22]. Elevated troponin levels serve as a critical marker for myocardial ischemia or infarction. The total HEART score, ranging from 0 to 10, categorizes patients into different risk levels, guiding management decisions regarding further testing, hospitalization, or early discharge [23]. However, it is essential to use the HEART score in conjunction with clinical judgment, as it should not be the sole determinant in decision-making processes [24].

Revisiting Your Patient

The patient had presented with complaints of chest pain, shortness of breath, diaphoresis, and nausea, raising the suspicion of Acute Coronary Syndrome and possible Myocardial Infarction. This suspicion had been supported by her significant risk factors, which included insulin-dependent diabetes mellitus, hypertension, a 12-pack-year smoking history, and a history of ischemic heart disease.

Initial stabilization measures had been promptly undertaken. The patient had been placed in a monitored bed and connected to a cardiac monitor. The ABCDE approach had been followed, and it had been noted that she was vitally stable. A quick history had been obtained, which revealed a sudden onset of central chest pain, described as sharp and stabbing, accompanied by diaphoresis and nausea. On physical examination, equal air entry had been observed with no wheeze or crackles on chest auscultation. A cardiovascular examination had also been planned.

Based on the initial presentation and clinical findings, a cardiac workup had been deemed necessary. This included ordering Troponin T and I tests, performing a 12-lead ECG, and obtaining a portable chest X-ray to rule out potential complications such as congestive heart failure, pneumonia, or pneumothorax.

Therapeutic interventions had been initiated promptly. The patient had been started on supplemental oxygen via a nasal cannula or face mask. Analgesics had been administered while ensuring no contraindications or allergies were present. These included IV paracetamol, IV opioids such as morphine or fentanyl, and sublingual nitroglycerin, either as a puff or tablet. These measures had been aimed at relieving the patient’s symptoms and stabilizing her condition.

Authors

Picture of Khaled Alaboud Alkheder

Khaled Alaboud Alkheder

Tawam Hospital Emergency Medicine Residency Program, United Arab Emirates

Picture of Muneer Abdulla Al Marzooqi

Muneer Abdulla Al Marzooqi

Dr. Muneer is a Consultant Emergency Medicine Physician from the UAE. He completed his EM residency at Tawam Hospital in 2017 and has served as an attending physician and educator there since. He is the Program Director of the Emergency Medicine Residency Program at Tawam Hospital, focusing on medical education, peer development, EM Resuscitation, Simulation, and POCUS. Dr. Muneer has organized and lectured at various seminars and workshops in the MENA region for medical students, residents, and healthcare professionals, including Basic Ultrasound, POCUS, Airway, Suturing, ENT Emergencies Workshops, and the Chief Resident Leadership Program.

Listen to the chapter

References

  1. Stepinska J, Lettino M, Ahrens I, et al. Diagnosis and risk stratification of chest pain patients in the emergency department: focus on acute coronary syndromes. Eur Heart J Acute Cardiovasc Care. 2020;9(1):76-89. doi:10.1177/2048872619885346.
  2. Hollander JE, Chase M. Evaluation of the adult with chest pain in the emergency department. In: Post TW, ed. UpToDate. UpToDate; 2022. Accessed April 26, 2023. www.uptodate.com.
  3. Malik MB, Gopal S. Cardiac Exam. In: StatPearls. StatPearls Publishing; 2021. Accessed April 26, 2023. https://www.ncbi.nlm.nih.gov/books/NBK553078/
  4. Resuscitation Council UK. The ABCDE approach. Resuscitation Council UK. Published 2021. Accessed April 26, 2023. https://www.resus.org.uk/library/abcde-approach
  5. Thompson BT, Kabrhel C, Pena C. Clinical presentation, evaluation, and diagnosis of the nonpregnant adult with suspected acute pulmonary embolism. In: Post TW, ed. UpToDate. UpToDate; 2022. Accessed April 26, 2023. www.uptodate.com.
  6. Brown JE. Chest Pain. In: Walls R, Hockberger R, Gausche-Hill M, eds. Rosen’s Emergency Medicine: Concepts and Clinical Practice. 10th ed. Elsevier; 2022:202-210.
  7. Ravindranath S, et al. Chest Pain in Children: A Review. Pediatrics. 2017;140(3):e20173032.
  8. Baker R, et al. Pediatric Chest Pain: A Review of the Literature. J Emerg Med. 2020;58(5):738-746.
  9. Glickstein JS, et al. Evaluating Chest Pain in the Pediatric Emergency Department. Pediatr Emerg Care. 2019;35(4):233-238.
  10. Hoffman MK, et al. Chest Pain in Pregnancy: A Review. Am J Obstet Gynecol. 2020;222(5):453-460.
  11. Hernandez AF, et al. Acute Coronary Syndrome in Pregnancy: A Comprehensive Review. Circulation. 2021;143(6):545-558.
  12. Miller JM, et al. Noninvasive Cardiac Imaging in Pregnancy: Safety and Efficacy. J Am Coll Cardiol. 2019;73(2):234-243.
  13. Bennett KJ, et al. Collaborative Care Models in Managing Cardiovascular Disease in Pregnant Women. Obstet Gynecol. 2022;139(4):678-689.
  14. Hernandez AF, et al. Atypical Presentations of Myocardial Infarction in Older Adults. J Geriatr Cardiol. 2022.
  15. McCarthy MJ, et al. Comorbidities and Outcomes in Elderly Patients with Chest Pain. Emerg Med J. 2023.
  16. Huang WC, et al. Impact of Delayed Diagnosis on Outcomes of Chest Pain in Older Adults. Am J Emerg Med. 2021.
  17. Lee JH, et al. Evaluation and Management of Chest Pain in Geriatric Patients. Clin Geriatr. 2023.
  18. Amsterdam EA, et al. 2014 AHA/ACC Guideline for the Management of Patients with Non-ST-Elevation Acute Coronary Syndromes. Circulation. 2014;130(25):e344-e426.
  19. Morrow DA, et al. Acute Coronary Syndromes: A Review of Current Guidelines. J Am Coll Cardiol. 2013;62(12):1103-1110.
  20. Fihn SD, et al. 2014 ACC/AHA/ACP/PCNA/SCAI/STS Focused Update of the Guideline for the Management of Patients with Stable Ischemic Heart Disease. J Am Coll Cardiol. 2014;64(18):1929-1949.
  21. Backus BE, Six AJ, Kelder JC, et al. A prospective validation of the HEART score for chest pain patients at the emergency department. Int J Cardiol. 2013;168(3):2153-2158.
  22. Kahwati LC, Weber RP, Pan H, et al. Screening for Coronary Artery Disease: A Systematic Review for the U.S. Preventive Services Task Force. Ann Intern Med. 2016;165(7):485-495.
  23. Six AJ, Backus BE, Kelder JC. Chest pain in the emergency room: a multicenter validation of the HEART Score. Crit Pathw Cardiol. 2013;12(3):121-126.
  24. Böhm M, Reil JC, Tschöpe C. The HEART score: a new tool for risk stratification in acute chest pain. Clin Res Cardiol. 2018;107(9):746-754.

Reviewed and Edited By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

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

Headache (2024)

by Shailaja Sampangi Ramaiah

You have a new patient!

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

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

What do you need to know?

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

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

Table 1 – Secondary headache disorders

Pathology

Examples

Headache attributed to head or neck trauma

Post-traumatic headache

Concussion

Headache attributed to cervical or cranial vascular disorders

Subarachnoid hemorrhage

Intraparenchymal hemorrhage

Subdural or epidural hematoma

Cavernous/venous sinus thrombosis

Arteriovenous malformation

Temporal arteritis

Carotid/vertebral artery dissection

CNS infections

Meningitis

Encephalitis

Cerebral abscess

Intracranial non vascular space occupying lesions

Tumors

Parasitic or inflammatory lesions

Headache attributed to substance or withdrawal

Nitrates and nitrites

Mono amine oxidase inhibitors

Alcohol withdrawal

Abuse of analgesics

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

Glaucoma

Sinusitis

Optic neuritis

Iritis

Headache attributed to altered homeostasis

Fasting headache

High altitude cerebral edema

Hypoxia

Hypercarbia

Hypothyroidism

Obstructive sleep apnea

Miscellaneous causes

Preeclampsia

Post dural puncture headache

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

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

Sign or symptom

Related secondary headache cause

Systemic symptoms including fever

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

Neoplasm in history

Neoplasms of the brain, metastasis

Neurologic deficit or dysfunction (including decreased consciousness)

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

Onset of headache is sudden or abrupt

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

Older age (after 50 years)

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

Pattern change or recent onset of headache

Neoplasms, headaches attributed to vascular, nonvascular intracranial disorders

Positional headache

Intracranial hypertension or hypotension

Precipitated by sneezing, coughing, or exercise

Posterior fossa malformations; Chiari malformation

Papilledema

Neoplasms and other nonvascular intracranial disorders; intracranial hypertension

Progressive headache and atypical presentations

Neoplasms and other nonvascular intracranial disorders

Pregnancy or postpartum

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

Painful eye with autonomic features

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

Posttraumatic onset of headache

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

Pathology of the immune system such as HIV

Opportunistic infections

Painkiller overuse or new drug at onset of headache

Medication overuse headache; drug incompatibility

Primary Headache Disorders

Migraine

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

Cluster Headache

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

Tension Headache

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

Secondary Headache Disorders

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

Subarachnoid Hemorrhage (SAH)

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

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

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

Grade

Condition

0

Unruptured aneurysm

1

Asymptomatic or minimal headache and slight nuchal rigidity

2

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

3

Drowsiness, confusion or mild focal deficit

4

Stupor, moderate to severe hemiparesis

5

Deep coma, decerebrate posturing, moribund appearance

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

Intracranial Neoplasms

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

Meningitis

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

Giant Cell Arteritis (GCA, or Temporal arteritis)

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

Carotid and Vertebral Artery Dissection

The classic symptoms of carotid artery dissection include:

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

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

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

Cerebral Vein Thrombosis (CVT)

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

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

Initial Assessment and Stabilization (ABCDE approach)

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

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

Medical History

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

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

Physical Examination

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

When To Ask Your Senior for Help

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

Patient details that should trigger you to alert your senior:

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

Not-To-Miss Diagnoses

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

Acing Diagnostic Testing

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

Some investigations to consider in headache patients:

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

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

Figure 1a
Figure 1b

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

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

Empiric and Symptomatic Treatment

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

Table 4- Medications for migraine headaches

Drug

Dose

Comments

Acetaminophen

500 – 1000 mg PO every 6hrs

Safe in pregnancy

Ibuprofen

600 -800 mg PO every 6hrs

Can cause GI upset

Avoid in pregnancy

Caution in patients with renal insufficiency

Ketorolac

15-30 mg IV or IM every 6hrs

Same as ibuprofen

Metoclopramide

10 mg IV or IM every 6hrs

Administer slowly to avoid extrapyramidal symptoms

Diphenhydramine

25-50 mg IV or IM every 6hrs

May cause drowsiness

Dihydroergotamine

1 mg IV or IM

Maximum 3mg/24hours

Contraindicated in pregnancy, uncontrolled HTN, or coronary artery disease 

Sumatriptan

6 mg SC injection x 1

(max 12mg SC/24hrs)

Same as Dihydroergotamine

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

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

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

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

Procedures

Lumbar Puncture [14]

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

Before the procedure:

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

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

Figure 6 – Equipment for a Lumbar Puncture

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

Figure 7 – Landmark of L4 Space

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

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

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

Table 5 – CSF interpretation [15]

 

Normal

Bacterial Meningitis

Viral Meningitis

Subarachnoid Hemorrhage

Opening pressure (mmHg)

7-18

>30

Normal

Increased

Appearance

Clear, colorless

Turbid

Clear

Xanthochromia present

Protein (mg/dl)

23-38

Increased

Normal to decreased

Increased

Glucose

2/3rd of serum glucose

Decreased

Normal

Normal

Gram stain

Negative

Positive

Negative

Negative

WBC count

<5 cells

Predominantly neutrophils

Predominantly lymphocytes

May be increased due to bleeding

Special Patient Groups

Pregnant Patients

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

Children

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

Elderly

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

When To Admit

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

Revisiting Our Patient

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

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

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

After the patient is intubated, you continue your assessment.

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

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

Author

Picture of Shailaja Sampangi Ramaiah

Shailaja Sampangi Ramaiah

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

Listen to the chapter

References

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

Reviewed and Edited By

Picture of Joseph Ciano, DO, MPH, MS

Joseph Ciano, DO, MPH, MS

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

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

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

Question Of The Day #60

question of the day
Which of the following is the most likely cause for this patient’s condition? 

This first-trimester pregnant patient presents with generalized weakness, nausea, and vomiting.  She is hypotensive and tachycardic with no sign of urinary infection on the urinalysis.  The many ketones in the urine indicate the patient has inadequate oral nutrition and is breaking down muscle and adipose tissue for energy.  This is likely related to the persistent vomiting the patient is experiencing.  This patient has hyperemesis, a common condition in the first trimester of pregnancy that is caused by rising levels of beta-human chorionic gonadotropin (BHCG).  Treatment for this patient should include IV hydration and antiemetics.  Admission criteria for these patients includes intractable vomiting despite antiemetic administration, over 10% maternal weight loss, persistent ketone or electrolyte abnormalities despite rehydration, or uncertainty in the diagnosis. 

The fluid losses caused by vomiting in this condition result in hypovolemic shock (Choice B).  Distributive shock (Choice C) is caused by other conditions, like sepsis, anaphylaxis, and neurogenic shock.  A ureteral stone (Choice D) is unlikely as the patient does not report any abdominal, back, or flank pain.  The urinalysis also does not show any hematuria, which is a common sign of a ureteral stone.  Pyelonephritis (Choice A) can cause vomiting and septic shock which can result in hypotension and tachycardia.  However, there is no sign of infection in the urinalysis provided, no fever, and no back or flank pain.  The best answer is choice B.  

References

[cite]

Question Of The Day #59

question of the day
38 - atrial fibrillation

Which of the following is the most likely cause for this patient’s respiratory condition?

This patient presents to the Emergency Department with palpitations, generalized weakness, and shortness of breath after discontinuing all her home medications.  She has hypotension, marked tachycardia, and pulmonary edema (crackles on lung auscultation).  The 12-lead EKG demonstrates atrial fibrillation with a rapid ventricular rate.  This patient is in a state of cardiogenic shock and requires prompt oxygen support, blood pressure support, and heart rate control. 

Pulmonary embolism (Choice A) can sometimes manifest as new atrial fibrillation with shortness of breath and tachycardia, but pulmonary embolism initially causes obstructive shock.  If a pulmonary embolism goes untreated, it can progress to right ventricular failure, pulmonary edema, and cardiogenic shock.  This patient has known atrial fibrillation and stopped all her home medications.  The abrupt medication change is a more likely cause of the patient’s cardiogenic shock.  Dehydration (Choice D) and systemic infection (Choice D) are less likely given the above history of abruptly stopping home maintenance medications.  Untreated cardiac arrythmia (Choice B) is the most likely cause for this patient’s pulmonary edema and cardiogenic shock. 

The chart below details the categories of shock, each category’s hemodynamics, potential causes, and treatments.  

 

References

[cite]

Question Of The Day #58

question of the day
720 - variceal bleeding

Which of the following is the most appropriate next step in management?   

This cirrhotic patient presents to the Emergency Department with epigastric pain after an episode of hematemesis at home.  His initial vital signs are within normal limits.  While waiting in the Emergency Department, his clinical status changes.  The patient has a large volume of hematemesis with hypotension and tachycardia.  This patient is now in hemorrhagic shock from an upper gastrointestinal bleed and requires immediate volume resuscitation.  The most common cause of upper gastrointestinal bleeding is peptic ulcer disease, but this patient’s cirrhosis history and large volume of hematemesis should raise concern for an esophageal variceal bleed.  IV Pantoprazole (Choice D) is a proton pump inhibitor that helps reduce bleeding in peptic ulcers, but it does not provide benefit in esophageal varices.  Volume repletion is also a more important initial step than giving pantoprazole.  IV Ceftriaxone (Choice C) helps reduce the likelihood of infectious complications in variceal bleed patients.  This has a mortality benefit and is a recommended adjunctive treatment.  However, rapid volume resuscitation is a more important initial step.  IV crystalloid fluids, like normal saline (Choice A), are helpful in patients with hypovolemic shock (i.e., dehydration, vomiting), distributive shock (i.e., sepsis, anaphylaxis), and obstructive shock (i.e., tension pneumothorax, etc.).  Hypovolemic shock due to severe hemorrhage (hemorrhagic shock) requires blood products, not crystalloid fluids which can further dilute blood and cause coagulopathy.  Administration of packed red blood cells (Choice B) is the best next step in management in this case.

References

[cite]

Question Of The Day #57

question of the day

Which of the following is the most likely cause for this patient’s condition?  

This young female presents with dizziness, fatigue, nausea, generalized abdominal pain, hypotension, tachycardia, and a positive urine pregnancy test.  The anechoic (black) areas on the bedside ultrasound indicate free fluid (blood) in the peritoneal space.  See the image below for clarification. Yellow arrows indicates free fluids.

This patient is in a state of physiologic shock.  Shock is an emergency medical state characterized by cardiovascular or circulatory failure.  Shock prevents peripheral tissues from receiving adequate perfusion, resulting in organ dysfunction and failure.  Shock can be categorized as hypovolemic, distributive, obstructive, or cardiogenic.  The different categories of shock are defined by their underlying cause (i.e., sepsis, hemorrhage, pulmonary embolism, etc.) and their hemodynamics which sometimes overlap.  The diagnosis of shock is largely clinical and supported by the history, vital signs, and physical exam.  Additional studies, such as laboratory investigations, bedside ultrasound, and imaging tests help narrow down the type of shock, potential triggers, and guide management. 

This patient’s condition is caused by a presumed ruptured ectopic pregnancy and intraperitoneal bleeding.  This is considered hypovolemic/hemorrhagic shock (Choice A). The other types of shock in Choices B, C, and D are less likely given the clinical and diagnostic information in the case.  The chart below details the categories of shock, each category’s hemodynamics, potential causes, and treatments.  

 

References

[cite]

Question Of The Day #56

question of the day

Which of the following is the most likely cause of this patient’s condition?

This trauma patient arrives with hypotension, tachycardia, absent unilateral lung sounds, and distended neck veins. This should raise high concern for tension pneumothorax, which is a type of obstructive shock (Choice C). This diagnosis should be made clinically without X-ray imaging. Bedside ultrasound can assist in making the diagnosis by looking for bilateral lung sliding, if available. Treatment of tension pneumothorax should be prompt and includes needle decompression followed by tube thoracostomy. Other types of shock outlined in Choices A, B, and D do not fit the clinical scenario with information that is given.

Recall that shock is an emergency medical state characterized by cardiovascular or circulatory failure. Shock prevents peripheral tissues from receiving adequate perfusion, resulting in organ dysfunction and failure. Shock can be categorized as hypovolemic, distributive, obstructive, or cardiogenic. The different categories of shock are defined by their underlying cause (i.e., sepsis, hemorrhage, pulmonary embolism, etc.) and their hemodynamics which sometimes overlap. The diagnosis of shock is largely clinical and supported by the history, vital signs, and physical exam. Additional studies, such as laboratory investigations, bedside ultrasound, and imaging tests help narrow down the type of shock, potential triggers, and guide management. The chart below details the categories of shock, each category’s hemodynamics, potential causes, and treatments.

 

References

[cite]

Question Of The Day #55

question of the day
738.2 - STEMI
Which of the following is the most likely cause for this patient’s condition?  

This patient presents with chest pressure at rest and an anterior ST segment elevation myocardial infraction (STEMI) seen on 12-lead EKG.  This patient should be given aspirin, IV fluids to increase the preload status, and receive immediate coronary reperfusion therapy.  This patient’s hypotension is likely due to infarction of the left ventricle causing poor cardiac output (Choice D).  This is known as cardiogenic shock.  The patient has been vomiting, but the acute onset of symptoms and STEMI on EKG make poor cardiac output (Choice D) more likely than hypovolemia (Choice A) as the cause for the patient’s condition.  Systemic infection (Choice B) and pulmonary embolism (Choice C) are also less likely given the clinical information in the case and the STEMI on EKG.  The best answer is Choice D.  Please see the chart below for further detailing of the different types of shock.   

References

[cite]

Question Of The Day #54

question of the day
Which of the following is the most likely cause for this patient’s condition?

This patient sustained significant blunt trauma to the chest, presents to the Emergency Department with hypotension, tachycardia, a large chest ecchymosis, and palpable sternal crepitus.  The ultrasound image provided shows a subxiphoid view of the heart with a large pericardial effusion.  In the setting of trauma, this should be assumed to be a hemopericardium.  This patient has cardiac tamponade, which is considered a type of obstructive shock (Choice C).  Treatment includes IV hydration to increase preload, bedside pericardiocentesis, and ultimately, a surgical cardiac window performed by cardiothoracic surgery.  The other shock types (Choices A, B, D) do not describe this patient’s presentation.  Please see the chart below for further description of the different shock types and therapies.

 

References

[cite]

Question Of The Day #53

question of the day

Which of the following is the most likely cause for this patient’s condition?

This patient endured a high-speed motor vehicle accident, arrives with hypotension and bradycardia, and has a C6 vertebral body fracture on imaging.  These details support a diagnosis of neurogenic shock, a type of distributive shock.

Shock is an emergency medical state characterized by cardiovascular or circulatory failure.  Shock prevents peripheral tissues from receiving adequate perfusion, resulting in organ dysfunction and failure.  Shock can be categorized as hypovolemic, distributive, obstructive, or cardiogenic.  The different categories of shock are defined by their underlying cause (i.e., sepsis, hemorrhage, pulmonary embolism, etc.) and their hemodynamics which sometimes overlap.  The diagnosis of shock is largely clinical and supported by the history, vital signs, and physical exam.  Additional studies, such as laboratory investigations, bedside ultrasound, and imaging tests help narrow down the type of shock, potential triggers, and guide management.  The chart below details the categories of shock, each category’s hemodynamics, potential causes, and treatments.  

Neurogenic shock is caused by spinal cord damage above the T6 level.  Unlike other types of shock, neurogenic shock is characterized by hypotension and bradycardia (not tachycardia).  These vital sign abnormalities are caused by damage to sympathetic nervous system (Choice C).  Neurogenic shock has decreased systemic vascular resistance (warm extremities), not increased systemic vascular resistance (cool extremities) (Choice A).  Occult hemorrhage (Choice B) is always a concern in a trauma patient.  However, this would present with findings of hypovolemic/hemorrhagic shock (tachycardia, hypotension, cool extremities).  Tension pneumothorax (Choice D) is also unlikely as the patient has clear bilateral lung sounds on exam.  The best answer is Choice C.

References

[cite]