Approach to Acutely Confused Patient (2025)

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

by Mehnaz Zafar Ali

You Have New Patients!

Patient 1

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

Patient 2

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

Introduction

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

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

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

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

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

General Approach

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

Differential Diagnoses

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

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

Delirium

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

Dementia

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

Depression

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

Psychosis

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

History and Physical Examination Hints

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

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

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

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

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

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

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

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

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

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

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

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

Confusion Assessment Method (CAM) Instrument:

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

Associated Features

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

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

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

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

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

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

Alcohol withdrawal delirium progresses through distinct stages, including:

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

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

Click here to download full CIWA-R evaluation form.

Diagnostic Tests and Interpretation

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

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

Management

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

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

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

Special Patient Groups and Other Considerations

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

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

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

When To Admit This Patient

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

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

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

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

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

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

Clinical Pearls

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

Revisiting Your Patient

Patient 1

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

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

Patient 2

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

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

Author

Mehnaz Zafar Ali

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

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References

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Gower LE, Gatewood MO, Kang CS. Emergency department management of delirium in the elderly. West J Emerg Med. 2012;13(2):194-201. doi:10.5811/westjem.2011.10.6654.
Folstein MF, Folstein SE, McHugh PR. “Mini-mental state”. A practical method for grading the cognitive state of patients for the clinician. J Psychiatr Res. 1975;12(3):189-198. doi:10.1016/0022-3956(75)90026-6.
Inouye SK, van Dyck CH, Alessi CA, Balkin S, Siegal AP, Horwitz RI. Clarifying confusion: the confusion assessment method. A new method for detection of delirium. Ann Intern Med. 1990;113(12):941-948. doi:10.7326/0003-4819-113-12-941.
Chan M, Moukaddam N, Tucci V. Stabilization and management of the acutely agitated or psychotic patient. In: Cevik AA, Quek LS, Noureldin A, Cakal ED, eds. International Emergency Medicine Education Project. 1st ed. iEM Education Project; 2018:452-457.
Smit L, Slooter AJ, Devlin JW, et al. Efficacy of haloperidol to decrease the burden of delirium in adult critically ill patients: the EuRIDICE randomized clinical trial. Crit Care. 2023;27(1):413. doi:10.1186/s13054-023-04692-3.
Lodewijckx E, Debain A, Lieten S, et al. Pharmacologic treatment for hypoactive delirium in adult patients: a brief report of the literature. J Am Med Dir Assoc. 2021;22(6):1313-1316.e2. doi:10.1016/j.jamda.2020.12.037.
Cetin M, Oktem B, Canakci ME. Altered mental status. In: Cevik AA, Quek LS, Noureldin A, Cakal ED, eds. International Emergency Medicine Education Project. 1st ed. iEM Education Project; 2018:111-121.
Winstanley L, Glew S, Harwood RH. A foundation doctor’s guide to clerking the confused older patient. Br J Hosp Med (Lond). 2010;71(5):M78-M81. doi:10.12968/hmed.2010.71.Sup5.47934.
Andrews H, Clarke A, Parmar S, et al. You’ve been bleeped: the confused patient. BMJ. 2015;351:h3266. doi:10.1136/sbmj.h3266.
Wakefield BJ. Risk for acute confusion on hospital admission. Clin Nurs Res. 2002;11(2):153-172. doi:10.1177/105477380201100205.
Lyons D. The confused patient in the acute hospital: legal and ethical challenges for clinicians in Scotland. J R Coll Physicians Edinb. 2013;43(1):61-67. doi:10.4997/jrcpe.2013.114.
Thanyanuwat R. Patients who suffer from alcohol withdrawal and disorientation. J Med Assoc Thai. 2013;96(2):78-83.
Thompson WL. Management of alcohol withdrawal syndromes. Arch Intern Med. 1978;138(2):278-283. doi:10.1001/archinte.1978.03630260068019.
Sutton LJ, Jutel A. Alcohol withdrawal syndrome in critically ill patients: identification, assessment, and management. Crit Care Nurse. 2016;36(1):28-40. doi:10.4037/ccn2016420.
Toy EC, Klamen DL. Alcohol withdrawal. In: Case Files: Psychiatry. 6th ed. McGraw-Hill Education; 2020:400-405.
Lodewijckx E, Debain A, Lieten S, et al. Pharmacologic treatment for hypoactive delirium in adult patients: a brief report of the literature. J Am Med Dir Assoc. 2021;22(6):1313-1316.e2. doi:10.1016/j.jamda.2020.12.037.

Reviewed and Edited By

Arif Alper Cevik, MD, FEMAT, FIFEM

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

Approach to Suicidal Patient (2025)

January 12, 2025January 20, 2025 ~ iEM Education Project Team ~ Leave a comment

by Faisal A. Nawaz

You Have A New Patient!

A 19-year-old male was brought to the emergency room (ER) by his family with the assistance of an ambulance. The patient was discovered unconscious in his car, surrounded by leftover pills of an unknown medication. Upon arrival at the ER, he was assessed by the medical team and found to have regained consciousness, with a Glasgow Coma Scale (GCS) score of 12 and stable vital signs.

Introduction

Suicide is one of the top ten causes of death worldwide, with increasing rates of occurrence and mortality observed across various countries and patient populations in recent years [1]. It is the second most common cause of death among individuals aged 10-14 and 20-34 years [1]. Suicide is defined as “an act with a fatal outcome, that is deliberately initiated and performed by the person in knowledge or expectation of its fatal outcome.”

Durkheim classifies suicide into four types: egoistic suicide, altruistic suicide, anomic suicide, and fatalistic suicide [2]. The act of suicide can be completed using various methods, with risks influenced by factors such as gender, age, family history of suicide, comorbid mental and physical disorders, and social and psychological stressors (e.g., poor financial stability, unemployment, divorce, isolation).

It is well established that females have higher rates of suicide attempts, while males have higher rates of completed suicide. The most common method of suicide among men is hanging, whereas women most often use drug overdose as a method of suicide [3,4].

Notable psychiatric risk factors predisposing individuals to suicide include depressive disorders, alcohol dependence or abuse, schizophrenic disorders, and personality disorders. Medical risk factors include chronic physical illnesses and epilepsy. Despite advancements in suicide prevention, the most significant risk factor remains a past history of suicide attempts or deliberate self-harm [5].

General Approach

When approaching a patient with suicidal thoughts or behaviors, it is essential to provide empathetic and patient-centered care to ensure their safety and well-being. Key steps include implementing safety precautions, such as placing the patient in a private, secure environment without access to dangerous objects and ensuring continuous observation or restraints when necessary [6]. A focused medical assessment should be conducted, emphasizing the evaluation of cognitive and emotional status, drug ingestion, or other medical conditions that may influence the patient’s mental state. This targeted approach is preferable to routine “medical clearance,” as it avoids the misconception that standard diagnostic testing is always required [6,7].

In cases of an active suicidal attempt, immediate stabilization is paramount, with a focus on addressing any abnormalities in airway, breathing, or circulation. Initial interventions include checking vital signs, obtaining a rapid blood glucose level, initiating cardiac monitoring and pulse oximetry, and establishing IV access. Oxygen administration and IV fluids may also be warranted depending on the patient’s condition [7]. Physical signs such as pupillary changes (indicating drug intoxication), altered consciousness (assessed by the Glasgow Coma Scale), respiratory distress or depression, and self-harm injuries should be carefully evaluated [2]. Comprehensive vital assessments, laboratory investigations (e.g., electrolytes, liver and renal function tests), and ECGs may provide further insight into the patient’s medical condition and guide interventions.

The cornerstone of management is a comprehensive suicide risk assessment, which involves evaluating the patient’s personal and psychiatric history, current mental state, and specific suicidal thoughts or behaviors. This assessment should explore the presence of a suicide plan, prior attempts, mental illness, substance abuse, and agitation. For low-risk patients, management by the emergency department provider and discharge home may be appropriate. However, most patients require a thorough risk evaluation, which can be aided by tools like the Suicide Assessment Five-step Evaluation and Triage (SAFE-T) if mental health specialists are unavailable [6]. Establishing rapport with the patient through a sympathetic yet direct approach is crucial for obtaining reliable information, including details about suicidal ideation, and collateral sources such as family or friends can provide additional context [6].

Once medically stabilized, a mental status examination is necessary to evaluate the patient’s affect, attention, orientation, memory, and behavior, with particular attention to changes in cognition and alertness [7]. If the patient is deemed to pose a high risk of harm to themselves or others, inpatient admission is often warranted to provide intensive monitoring and care. Conversely, if the patient demonstrates insight, judgment, and stability, outpatient follow-up with close monitoring may suffice. Obtaining collateral history from family or other reliable sources is a critical component of the psychiatric evaluation, providing context for the patient’s condition and ensuring a comprehensive risk assessment. It is essential to remember that asking about suicidal thoughts does not incite suicidal behavior, and most suicidal crises are transient, underscoring the importance of timely and appropriate intervention [6].

Physical Examination

A thorough physical examination is an essential component of evaluating patients with psychiatric complaints and should be conducted with the same diligence as in patients presenting with medical conditions. Along with the patient’s history and mental status examination (MSE), the physical exam helps to distinguish between functional (psychiatric) and organic (medical) causes of the symptoms. A complete and systematic approach ensures that critical diagnoses are not missed, as studies have highlighted that incomplete evaluations often result in missed medical conditions and potentially dangerous outcomes [7].

Key Aspects of the Physical Examination

The general appearance of the patient should be carefully observed for signs of anxiety, distress, or other physical manifestations of their condition. For example, in one case study, the patient appeared anxious, which provided an important clue to their mental and physical state [7].

Vital signs are a critical starting point. These include heart rate, blood pressure, respiratory rate, oxygen saturation, and temperature. Abnormalities in vital signs should be promptly evaluated and managed. However, studies indicate that vital signs are not consistently documented, with complete sets recorded in only 52% of cases. This underscores the importance of thorough documentation during assessments [7].

The cardiovascular examination involves assessing the pulse for rate and regularity. For instance, in a referenced case, the patient presented with an irregular pulse, which necessitated further evaluation with an electrocardiogram (EKG) to assess for potential arrhythmias [7].

In the respiratory system, clinicians should observe the patient for signs of tachypnea or respiratory distress and auscultate the lungs for abnormal sounds like crackles. In the same case study, the patient exhibited tachypnea and crackles at the lung bases, prompting the need for a chest x-ray to investigate potential causes such as pneumonia or heart failure [7].

The extremities should be examined for signs of edema or dryness, as these can provide clues about systemic or localized medical conditions. Similarly, the abdomen should be assessed for tenderness and abnormalities, ensuring it is soft and non-tender [7].

The neurological examination plays a pivotal role in identifying focal deficits, meningeal signs, or changes in alertness, cognition, and behavior. Basic neurological assessments can provide insight into potential underlying causes of psychiatric complaints, such as an organic brain disorder [7].

Skin and hair changes should also be noted, as they may indicate systemic illnesses. Additionally, other physical complaints such as cough, fever, heat intolerance, headache, neck pain, or stiffness should be carefully documented and investigated [7].

Integrating Findings with Further Testing

The findings from the physical exam, combined with the history and MSE, should guide laboratory investigations and imaging studies. For example, abnormal vital signs may warrant blood tests or imaging such as chest x-rays or EKGs. Missed diagnoses often stem from inadequate physical evaluations, reinforcing the need for comprehensive assessments to ensure patient safety and optimal outcomes.

Risk Assessment

Through History

During the history-taking component of the assessment, the most critical indicator of high suicide risk is a direct statement indicating intent for suicide. Research shows that many patients verbalize their suicidal intent to close contacts prior to an attempt and may have also visited their general practitioner or psychiatrist before the suicide attempt. History-taking should incorporate questions addressing potential risk factors for suicide, such as:

Previous history of suicide attempts
Marked hopelessness
Social isolation
Depressive disorder
Alcohol dependence
Current death wishes
Current suicidal intent
Auditory hallucinations of a commanding or derogatory nature

The SAD PERSONS mnemonic is a helpful tool in assessing suicidality in patients by highlighting common risk factors that can be identified during history-taking [8].

Risk Factor	Description
Sex	Male gender has an increased risk of suicide
Age	Age <19 or >45 years
Depression	Including bipolar depression
Previous Attempt	Previous suicide attempt
Excess Alcohol	Alcohol or substance use
Rational Thinking Loss	Poor judgment in different situations
Social Support	Lacks social support
Organized Plan	Use of death notes or wills
No Partner	Unmarried, divorced
Sickness or Stress	Chronic illnesses or stressful life events

The SAD PERSONS scale, widely used for assessing suicide risk, categorizes individuals into three risk levels based on cumulative scores: low risk (0–4 points), moderate risk (5–6 points), and high risk (7–10 points). Despite its popularity, the scale has faced significant criticism regarding its clinical utility. A key concern is its low sensitivity. Another major critique is its oversimplification of complex individual risk factors. The scale’s binary scoring system may overlook the nuanced aspects of a patient’s mental health, potentially leading to inadequate risk assessment.

Given these limitations, clinicians are encouraged to consider alternative or supplementary assessment instruments:

Columbia-Suicide Severity Rating Scale (C-SSRS): This tool evaluates the severity of suicidal ideation and behavior, offering a more nuanced risk assessment.
Beck Scale for Suicide Ideation (BSI): A widely used instrument that assesses the intensity of an individual’s suicidal intentions.
Suicide Behaviors Questionnaire-Revised (SBQ-R): A self-report measure that evaluates various dimensions of suicidality, including ideation, attempts, and future risk.

Continuous assessment during initial presentations, inpatient or outpatient encounters, and post-discharge follow-ups is essential to ensure the long-term safety of patients at risk for suicide. It is noteworthy that the first two weeks of inpatient stay and the first week post-discharge are high-risk periods for suicidal attempts among individuals with mental illness [9]. The presence of a strong social support system can significantly enhance care and reduce risk after discharge.

It is also important to assess abnormal personality traits that may increase suicide risk. Borderline personality disorder and traits such as anxiety, impulsivity, aggression, or obsessive tendencies are associated with elevated suicide risk [10].

In cases of active or past suicide attempts, history-taking should focus on the method and intent of the attempt, preparations made beforehand, the presence of a death note, and any overt communication regarding the act. These factors strongly suggest increased suicidal intent. The intent of suicide may also help differentiate between “deliberate self-harm” (also known as parasuicide) and an unsuccessful suicide attempt.

Deliberate self-harm is described as an “episode of intentional self-harm that did not lead to death and may or may not have been motivated by a desire to die.” Reasons for deliberate self-harm include the need to escape unbearable stressors, seek relief, or, in some cases, as a call for help. It is important to note that deliberate self-harm significantly increases the risk of suicide in the future [11].

In this case, the use of drug overdose as a suicide attempt is a relatively common presentation. The type and quantity of medication or drug used during the attempt are critical in determining appropriate antidotes for overdose reversal, as well as in understanding potential physical complications to organ systems caused by drug toxicity.

Helpful Interview Questions [12] for Assessing Suicide Risk:

Suicidal Ideation: With increased stress, have you had any thoughts of hurting or killing yourself?
Suicidal Intent: How likely are you to try to kill yourself today or in the near future?
Suicidal Plan: Do you have a plan for how you would like to kill yourself or end your life?

Protective Factors:

Assessing protective factors is crucial to determining suicide risk. For example:

Is there anything or anyone that stops you from attempting suicide?

Mental Status Examination

A Mental Status Examination (MSE) is a critical component of evaluating patients with psychiatric complaints. It systematically assesses seven key areas: affect, attention, language, orientation, memory, visual-spatial ability, and conceptualization [7]. The MSE provides insights into changes in alertness, cognition, and behavior, helping clinicians differentiate between conditions such as delirium, dementia, and psychiatric illnesses, which have distinct management strategies and prognoses. Delirium, for example, is associated with decreased survival when encountered in emergency settings [7]. Alternatives to the traditional MSE, like the Quick Confusion Scale, offer a structured and easily interpretable tool for assessing mental status [7].

The MSE should be conducted in an organized and focused manner, aiming to identify whether a patient’s complaints stem from functional or organic etiologies. It is crucial to note sudden changes in behavior, mood, or thought in patients, as these may indicate underlying medical conditions. Additionally, a thorough evaluation should include an assessment of substance use, medication adherence, and medical comorbidities, alongside a careful review of physical findings such as trauma, fever, or abnormal vitals [7]. These components play a pivotal role in identifying patients whose altered mental status might otherwise be misattributed to psychiatric causes. In a review of psychiatric ward admissions, it was found that many patients with medical diagnoses had not received appropriate medical screenings, underscoring the importance of thorough medical evaluations [7].

The MSE also holds particular significance in assessing suicide risk, as it offers a snapshot of the patient’s current mental state, which may fluctuate over time. This makes it a valuable tool for monitoring recovery and ensuring the patient’s safety. The appearance of suicidal patients can vary widely, from restlessness and agitation during heightened suicidality to expressions of guilt or disappointment after a failed suicide attempt. In some cases, outward signs of suicidal risk may be absent, emphasizing the need for a thorough evaluation of the patient’s mood, current suicidal ideations, intent, and plan. Homicidal ideations may also occasionally accompany suicidal thoughts, reflecting a patient’s belief that their actions might “relieve” loved ones from perceived burdens.

Evaluating a patient’s insight into suicidal behaviors, recognition of the need for treatment, and judgment in managing future crises provides valuable guidance for clinical decision-making during risk assessment. The MSE serves as both a diagnostic and monitoring tool, helping clinicians evaluate and address the complex interplay of medical, psychological, and social factors that influence mental health.

Differential Diagnoses

When evaluating patients with psychiatric complaints, it is essential to adopt a systematic approach that encompasses a broad range of differential diagnoses, addressing both psychiatric and medical conditions. Medical conditions such as sepsis, diabetic ketoacidosis, pneumonia, pulmonary embolism, meningitis, encephalitis, hyperthyroidism/thyroid storm, intoxication, withdrawal syndromes, overdose, and trauma can mimic or exacerbate psychiatric symptoms. These conditions may also include infectious, pulmonary, thyroid, diabetic, hematopoietic, hepatic, or CNS disorders and require prompt recognition to avoid misdiagnosis [7].

Psychiatric conditions, including schizophrenia, bipolar disorder, psychosis, mood disorders, anxiety disorders, delirium, and dementia, often present with overlapping features. Differentiating between functional (psychiatric) and organic (medical) causes is particularly important in patients with sudden changes in behavior, mood, or cognition or in those with a deteriorating chronic disorder [7]. Additional considerations, such as substance abuse, alcohol withdrawal, medication effects, or salicylate ingestion, can further complicate the clinical presentation. In particular, intoxicated patients may struggle to provide a reliable history, adding complexity to the diagnostic process [7].

Risk Factors and Diagnostic Approach

Certain groups are at an increased risk of medical causes for psychiatric symptoms, including the elderly, individuals with substance abuse histories, those without prior psychiatric diagnoses, and patients with new or pre-existing medical complaints. A comprehensive history, physical examination, and mental status examination (MSE) are critical for identifying the underlying etiology of psychiatric complaints. Gathering collateral information from family or caregivers helps ensure the accuracy of the history, as missed medical diagnoses have been shown to result from insufficient history-taking or physical examination [6,7].

Diagnostic testing should be tailored to the patient’s presentation. Common evaluations include laboratory studies (e.g., CBC, metabolic panel, thyroid function tests, alcohol level, urine drug screen, acetaminophen and salicylate levels), imaging studies (e.g., chest x-ray, CT scan of the brain), cardiac assessments (e.g., ECG, troponin, BNP), and infectious workups (e.g., urinalysis, urine culture, blood cultures, lumbar puncture). These tools help distinguish between psychiatric and medical conditions and guide appropriate management [7].

Differential Diagnoses for Suicide Attempts

When addressing a suicide attempt, specific psychiatric diagnoses must be considered, including Major Depressive Disorder, Bipolar Disorder, Psychotic Disorders, Substance-Induced Mood or Psychotic Disorders, and Cluster B Personality Disorders. Each condition requires a tailored treatment approach based on the underlying diagnosis [1].

For Major Depressive Disorder, first-line treatment often involves antidepressants, while Bipolar Disorder may require antipsychotics or a combination of antipsychotics with mood stabilizers. Psychotic Disorders are typically managed with antipsychotics, whereas substance-induced mood or psychotic disorders may necessitate antidepressants, mood stabilizers, or antipsychotics, depending on the clinical presentation. Cluster B Personality Disorders benefit from a detailed personality assessment and psychotherapy approaches such as Cognitive Behavioral Therapy (CBT) or Dialectical Behavior Therapy (DBT) [1].

Management

Emergency Treatment and Interventions

Effective emergency treatment for patients presenting with psychiatric or medical emergencies involves a combination of medical stabilization and supportive interventions. Medical stabilization is the first priority and focuses on addressing any identified medical issues. This may include administering supplemental oxygen, managing acute conditions such as hyperthyroidism or thyroid storm, and providing appropriate medications or therapies based on the patient’s needs [7].

For patients who are medically stable and being discharged, brief interventions are essential to ensure safety and continuity of care. These interventions often include patient education, personalized safety planning, and counseling to reduce access to lethal means [6]. Safety plans should identify warning signs, coping strategies, and emergency contacts, tailored to the individual’s circumstances. Lethal means counseling involves discussing strategies for the safe storage of firearms and toxic medications to mitigate risk [6].

Rapid referral for outpatient follow-up care is a critical component of post-discharge planning. Efforts should be made to arrange follow-up appointments within 24 hours and no later than 7 days. Providing patients with specific appointments and addressing potential barriers to follow-up care, such as transportation or availability, ensures better adherence to treatment plans [6].

Another important intervention includes caring contacts after discharge, such as brief communications via telephone calls, text messages, emails, or mail [6]. These contacts serve to maintain connection with the patient, encourage treatment adherence, and demonstrate ongoing support during their recovery process. By combining these strategies, emergency treatment not only addresses immediate medical needs but also promotes long-term safety and mental health stability.

When To Admit This Patient

The disposition of patients presenting with psychiatric crises, particularly those at risk for suicide, should be guided by their assessed level of risk and the availability of supportive resources [6]. Psychiatric hospitalization is appropriate for patients in acute crisis with moderate to high suicide risk. When feasible, voluntary admission is preferred to foster patient cooperation and engagement in treatment. For patients assessed to have a low risk of imminent suicide, outpatient management may be appropriate if they have a stable living environment, supportive relationships, and restricted access to lethal means [6]. Additionally, all patients should be provided with the National Suicide Prevention Hotline, if available, as an immediate resource for crisis support and suicide prevention, ensuring they have access to help when needed. This tailored approach to disposition ensures both immediate safety and continuity of care.

Additional ED Considerations

Proper management of patients presenting with psychiatric crises requires attention to several important considerations. Thorough documentation is essential to ensure a clear record of the patient’s history, physical examination, mental status evaluation, risk assessment, and any interventions or treatments administered [7]. Comprehensive documentation not only supports continuity of care but also provides a medico-legal record of the clinical reasoning and decisions made during the encounter.

Emergency departments (EDs) should have a written policy outlining the care of suicidal patients. Such policies help clarify care pathways, standardize procedures, and support provider actions, ensuring consistent and effective care delivery for this vulnerable population [6].

Collaboration with mental health professionals, including psychiatrists, psychologists, and social workers, is critical for delivering comprehensive care [6]. This interdisciplinary approach allows for a more holistic understanding of the patient’s needs and facilitates the development of individualized treatment plans that address both immediate and long-term concerns.

Further Management Considerations

Inpatient Management

If inpatient admission is required, the patient should be assessed for any underlying diagnoses that may have contributed to the suicide attempt. Medications tailored to the underlying diagnosis should be prescribed, with the patient under close observation during their stay. Inpatient staff must ensure the safety of the environment by removing sharp objects or any potential items that could be used for self-harm. Psychotherapy sessions may be initiated during this time. Upon discharge, safety netting is crucial to ensure the patient is aware of early warning signs and available support systems to help manage future crises.

Outpatient Management

For outpatient treatment, the patient must maintain regular follow-up appointments to monitor symptoms and assess ongoing suicide risk. Appropriate medications and psychotherapy sessions should be provided as needed. Depending on the treatment regimen, regular follow-up laboratory tests may be required to monitor for potential side effects. Psychotherapy sessions should also continue during this period.

Community Management

Community management involves collaboration with social services to support the patient in transitioning back to professional and personal life activities after discharge. Family support and adherence to the treatment plan are vital to maintaining the patient’s stability and preventing future crises.

Clinical Pearls

Discharge Medications:

For patients with a history of suicide attempts or an increased risk of future suicide, medications should be prescribed cautiously upon discharge. It is important to avoid providing large quantities of medications, as these may be misused in potential future suicide attempts.

Anti-Suicide Medications:

Certain medications have been shown to effectively reduce the risk of suicide:

Lithium: Proven to be effective in the management of mood disorders.
Clozapine: Demonstrated efficacy in reducing suicide risk in patients with schizophrenia [13].

Revisiting Your Patient

The findings in our case suggest that the patient is currently medically stable but requires close observation for any potential changes. Further psychiatric evaluation is essential to assess underlying mental health issues and suicide risk factors. A definitive diagnosis cannot be established at this stage and will depend on the outcomes of additional assessments.

Author

Faisal A. Nawaz

Dr. Faisal Nawaz is a Psychiatry Resident Doctor at Al Amal Psychiatric Hospital in Dubai. Dr. Nawaz’s research expertise extends across health, global health, digital health, and medical education with over 60 peer-reviewed publications in the field. Beyond his clinical pursuits, Dr. Nawaz serves as the Co-founder of the Global Remote Research Scholars Program.

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References

Harrison PJ, Cowen P, Burns T, Fazel M. Shorter Oxford Textbook of Psychiatry. 7th ed. Oxford University Press; 2018.
Durkheim E. Suicide: A Study in Sociology. Translated by JA Spaulding and G Simpson. Free Press; 1951.
Shenava M, Hitching R, Dunn LB. Suicide in the Geriatric Population: Risk Factors, Identification, and Management. In: Bhattacharya R, Agarwal V, Chaturvedi SK, eds. Clinical Geriatric Psychopharmacology. Springer; 2019:153-167. doi:10.1007/978-3-030-10401-6_8.
Centers for Disease Control and Prevention. Multiple Cause of Death, 2018-2020, Single Race Request. Accessed January 10, 2025. https://wonder.cdc.gov/mcd-icd10-expanded.html.
Kirkcaldy BD, Siefen RG, Urkin J, Merrick J. Risk factors for suicidal behavior in adolescents. Minerva Pediatr. 2006;58(5):443-450.
Betz ME, Boudreaux ED. Managing Suicidal Patients in the Emergency Department. Ann Emerg Med. 2016;67(2):276-282. doi:10.1016/j.annemergmed.2015.09.001.
Siever K, Tucci V. Medical Clearance – Suicidal Thought/Ideation. International Emergency Medicine Education Project. Accessed January 10, 2025. https://iem-student.org/medical-clearance-suicidal-thought-ideation/.
Patterson WM, Dohn HH, Bird J, Patterson GA. Evaluation of suicidal patients: The SAD PERSONS scale. Psychosomatics. 1983;24(4):343-349. doi:10.1016/S0033-3182(83)73213-5.
Bickley H, Hunt IM, Windfuhr K, Shaw J, Appleby L, Kapur N. Suicide Within Two Weeks of Discharge From Psychiatric Inpatient Care: A Case-Control Study. Psychiatr Serv. 2013;64(7):653-659. doi:10.1176/appi.ps.201200026.
Paris J. Suicidality in Borderline Personality Disorder. Medicina (Kaunas). 2019;55(6):223. doi:10.3390/medicina55060223.
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Reviewed and Edited By

Arif Alper Cevik, MD, FEMAT, FIFEM

Approach To Acutely Agitated Patient (2025)

January 10, 2025January 12, 2025 ~ iEM Education Project Team ~ Leave a comment

by Mazin A Mukhtar

You Have A New Patient!

A 35-year-old male was brought to the emergency department by police due to violent behavior, including damaging vehicles and threatening individuals in a public area. On initial assessment, he was highly agitated, hostile, and uncooperative, exhibiting signs of psychomotor agitation characterized by verbal outbursts, exaggerated hand gestures, and shouting phrases such as “Leave me!”

He demonstrated persecutory delusions, expressing a belief that law enforcement and medical personnel were conspiring to harm him by damaging his brain, which necessitated his transport to the hospital.

Despite stable vital signs, his aggressive and uncooperative behavior made a complete physical examination impractical. Efforts at verbal de-escalation and pharmacologic intervention with rapid tranquilization were ineffective. Given the severity of his agitation and the potential risk to himself and others, physical restraints were applied to ensure safety. Following stabilization, the patient was initiated on an oral antipsychotic regimen, which resulted in a gradual return to baseline functioning within three weeks.

Introduction

Psychosis is one of the most common presentations in hospital emergencies and can sometimes pose significant challenges for physicians. The main challenges in managing psychosis include the uncooperativeness of patients during the acute phase and the unavailability of collateral resources, particularly when the patient is brought in from the street [1]. Physicians must remain vigilant to avoid overlooking organic disorders that present with behavioral disturbances. Approximately three out of 100 people will experience at least one episode of psychosis during their lifetimes.

During psychosis, patients’ thoughts and perceptions are distorted, leading to difficulty in distinguishing what is real from what is unreal, which can result in violent behavior.

The symptoms of psychosis can be categorized into two dimensions [2]:

Positive symptoms: These involve the acquisition of new symptoms, including delusions, hallucinations, disorganized speech, and disorganized behavior.
Negative symptoms: These involve the loss of abilities or functions, such as alogia, avolition, flattening of affect (reduced facial expression), self-neglect, or social withdrawal.

Psychosis can occur in various psychiatric disorders, such as schizophrenia spectrum disorders, bipolar disorder, and major depressive disorder. It can also manifest as a result of substance use or other medical conditions [3].

General Approach and History Taking

Always ensure the safety of yourself and your staff. Be mindful of both verbal and nonverbal communication. Listen actively to your patient and demonstrate genuine interest in their story. Use open-ended questions to encourage the patient to express what’s on their mind. Maintain a neutral stance and avoid showing approval or disapproval unless absolutely necessary. Be honest and sincere to build a trusting relationship.

Remember, when there is a risk to the patient or others, confidentiality may need to be overridden. Ensure that you gather the highest-quality information to inform your decisions. Perform a thorough physical examination and order the necessary investigations. Always consider potential organic causes of psychiatric manifestations.

Document your assessment and decisions clearly and comprehensively. Do not hesitate to act immediately if the situation demands urgent intervention [4].

Evaluating an acutely agitated patient presents unique challenges, as obtaining a thorough history is often difficult [5,6]. Despite these limitations, gathering as much information as possible is critical, and collateral information from family, emergency personnel, or police can be invaluable. Key elements to obtain include the patient’s past medical and psychiatric history, including any current or past psychotropic medications and known allergies. A detailed review of home medications and social history—such as alcohol use, substance abuse, living situation, and caregiving arrangements—can provide important context. Recent health changes, such as headaches, which might suggest an intracranial process, or dysuria in elderly patients, which could indicate urosepsis, should also be explored. Establishing the patient’s baseline mental status is vital to differentiate acute changes from pre-existing conditions. While history is often a cornerstone of diagnosis, in cases of acute agitation, a thorough physical examination becomes even more essential due to the frequent limitations of the patient’s ability to provide accurate information.

Differential Diagnoses

When evaluating a patient presenting with acute agitation or psychosis, it is essential to consider a broad differential diagnosis encompassing both organic (medical) and inorganic (psychiatric) causes. Organic causes are often rooted in medical conditions such as hypercalcemia, hypercapnia, hypoxia, and infections like encephalitis, meningitis, or sepsis. Substance-related causes, including the use of alcohol, hallucinogens, steroids, stimulants, or synthetic marijuana, must also be considered. Other organic disorders, such as delirium, hypoglycemia, stroke, carbon dioxide poisoning, neurosyphilis, Wilson’s disease, AIDS, vitamin B12 deficiency, and drug overdose, should be ruled out early in the evaluation. Drug-related problems, including intoxication, withdrawal, or complications like Wernicke’s encephalopathy, also warrant investigation [5,6].

In contrast, inorganic causes are primarily psychiatric and include schizophrenia spectrum disorders, bipolar disorder, posttraumatic stress disorder (PTSD), psychotic depression, and mood disorders with psychotic features, such as major depressive disorder or bipolar affective disorder. Other psychiatric considerations include malingering, factitious disorders, personality disorders (e.g., schizoid, schizotypal, or borderline personality disorders), and autistic spectrum disorders [5,6].

Differentiating between organic and inorganic causes is critical, particularly in cases of acute, undifferentiated agitation where limited history and physical examination findings may complicate the assessment. Organic causes often present with abnormal vital signs, disorientation, fluctuating symptoms, or signs of trauma, indicating an underlying medical condition. In contrast, inorganic causes typically lack these features, suggesting a primary psychiatric etiology. A thorough evaluation of symptoms and key clinical features is essential to guide diagnosis and management effectively [5,6].

Physical Examination

In cases of acute agitation, a thorough physical examination is critical due to the typically limited history and review of systems. The examination should include a comprehensive neurologic evaluation and a head-to-toe inspection for signs of trauma or injury. Although a full neurologic examination may not always be feasible during the initial assessment, it should be completed as soon as possible and before final disposition [6].

The first priority in the physical examination is to assess and ensure the patient’s airway, breathing, and circulation (ABCs) are intact. This process begins with a focus on safety, as the patient may pose an immediate threat to themselves or medical staff. Factors such as the patient’s age, psychiatric history, suspected or known substance abuse, and the severity of their agitation should be considered when determining the need for intervention, including medication. The patient should be placed on monitors, and a complete set of vital signs, including temperature, should be obtained [6].

The primary survey of the patient can be guided by the mnemonic “ABCDE” [6]. A stands for airway, assessing its patency to ensure there are no obstructions. B involves evaluating respiratory effort and adequacy. C focuses on circulation, ensuring adequate perfusion and ruling out hypotension or arrhythmias. D addresses disability by assessing the patient’s level of consciousness and screening for reversible causes of altered mental status, such as hypoglycemia, hypoxemia, or abnormal pupil responses. Finally, E involves exposing the patient fully by changing them into a hospital gown to facilitate a rapid visual assessment for trauma or concealed items such as weapons.

A full neurologic examination should be performed as soon as possible to evaluate for underlying neurologic conditions contributing to the agitation [6]. Additionally, a head-to-toe inspection is essential to identify any signs of trauma or physical injury that may explain the presentation [6]. In cases of acute undifferentiated agitation, the examination findings can help differentiate between organic and inorganic causes. Organic causes are often associated with abnormal vital signs, disorientation, fluctuating symptoms, or signs of trauma. In contrast, inorganic causes, such as primary psychiatric conditions, typically lack these features. A systematic and detailed physical examination is crucial for identifying the underlying cause and guiding appropriate management.

A thorough physical examination is also important, as individuals with psychiatric disorders have a mortality rate 2-4 times higher than that of the general population. Deviations in vital signs may signal infections, while abnormalities in pupil size (constriction or dilation) can indicate substance use or withdrawal. Signs such as optic neuritis, neuropathy, and muscle weakness should prompt consideration of multiple sclerosis. A bull’s-eye rash suggests Lyme disease, while a malar rash may indicate systemic lupus erythematosus (SLE).

Dermatitis, particularly on exposed skin, may point to pellagra (vitamin B3 deficiency), and choreiform movements raise suspicion for Huntington’s disease. Findings such as a pill-rolling tremor and bradykinesia are characteristic of Parkinson’s disease, whereas tremor, dysarthria, and gait disturbances may suggest Wilson’s disease. Cognitive assessments revealing memory impairment and disorientation are consistent with dementia, while deficits in attention and orientation often indicate delirium [7].

Diagnostic Testing

The investigation of psychosis should be guided by findings from the physical examination, ensuring that potential underlying medical causes of behavioral disturbances are identified and addressed. A series of common tests are routinely performed to evaluate possible contributing factors.

Hematology screening is conducted to rule out anemia, which can impact mental and physical health. Urea and creatinine levels are measured to assess for uremia, a condition associated with kidney dysfunction that may present with altered mental status. Similarly, glucose levels are checked to exclude hypoglycemia or hyperglycemia, both of which can lead to behavioral disturbances or psychosis.

Urine screening plays a pivotal role in identifying substance abuse, a common and reversible cause of psychotic symptoms [8]. Additionally, urine analysis is performed to detect urinary tract infections or alterations in pH, which could indicate tampering, such as dilution with water, in cases of drug screening.

Inflammatory and autoimmune causes are considered through tests like ESR (erythrocyte sedimentation rate), which helps identify systemic inflammatory processes, and antinuclear antibodies (ANA), used to rule out autoimmune diseases that may present with neuropsychiatric symptoms. Screening for infectious diseases is crucial, particularly for conditions like HIV, hepatitis B and C, and neurosyphilis, which are known to affect the central nervous system and contribute to psychosis.

For suspected metabolic or genetic causes, ceruloplasmin levels may be assessed to rule out Wilson’s disease, a rare disorder that can lead to neuropsychiatric symptoms. CT scans are considered in specific circumstances, such as cases of late-onset psychosis, to identify structural brain abnormalities or other intracranial pathologies [9].

These investigations provide a systematic approach to diagnosing psychosis by addressing potential medical, infectious, metabolic, and autoimmune causes, ensuring comprehensive and accurate patient evaluation.

Management

The management of psychosis, particularly in acute cases, requires a holistic approach grounded in the biopsychosocial model, addressing biological, social, and psychological factors to ensure comprehensive care. The primary goals are to recognize the issue early, intervene before behavior escalates, stabilize life-threatening conditions, and ensure the safety of both the individual and others [6]. A systematic approach combining non-pharmacological and pharmacological interventions is critical for achieving these objectives while addressing the underlying causes of agitation or psychosis [10].

A thorough risk assessment is an essential first step for patients presenting with acute psychosis or agitation in the emergency department. Tools such as the unstructured interview, HCR-20, and DASSA scales can help determine the appropriate level of observation and the patient’s disposition [11]. When verbal de-escalation or medication fails to control aggression, physical or mechanical restraints may be necessary. Before applying restraints, the physician should clearly explain the rationale to the patient, and staff should remain nearby to provide reassurance, alleviate fear, and release the patient as soon as they are calm. This integrated approach ensures patient safety while promoting stabilization and recovery.

The first step in managing an acutely agitated or psychotic patient is to assess and ensure that the patient’s airway, breathing, and circulation (ABCs) are intact. If the patient poses an immediate threat to themselves or medical staff, factors such as age, psychiatric history, substance use, and severity of agitation should guide the intervention. Patients should be placed on monitors, and a complete set of vital signs, including temperature, should be obtained. A primary survey using the ABCDE mnemonic is critical (details are given in the physical examination section):

A: Assess airway patency.
B: Evaluate respiratory effort and adequacy.
C: Ensure adequate circulation, ruling out hypotension or arrhythmias.
D: Assess consciousness, check pupils, and measure blood glucose.
E: Fully expose the patient to identify signs of trauma or concealed weapons.

The management of psychosis is best approached through a biopsychosocial model, which addresses biological, social, and psychological factors across three stages: immediate, intermediate, and long-term management. This structured approach combines non-pharmacological and pharmacological strategies, creating a comprehensive framework to ensure patient safety, stabilization, and recovery while preventing future episodes [6].

Biological management focuses on medication to address the symptoms of psychosis. In the immediate phase, oral antipsychotics should be offered, with injectable options used if the patient refuses. Pharmacological interventions typically involve the use of antipsychotics and benzodiazepines [6], administered intramuscularly or intravenously for rapid tranquilization. Haloperidol, an antipsychotic, is effective for patients with a known history or high suspicion of psychosis [6]. Lorazepam, a benzodiazepine, is preferred for undifferentiated agitation or psychosis due to its anxiolytic properties and efficacy in cases of substance-related psychosis, such as PCP intoxication or alcohol withdrawal [6]. During the intermediate phase, medication dosages should be adjusted, and side effects closely monitored. In the long-term phase, maintaining a stable medication regimen helps prevent relapse and ensures sustained symptom control.

Social management emphasizes the importance of stabilizing the patient’s environment and facilitating reintegration. Immediate interventions may include hospital admission to relieve family burdens and ensure patient safety. In the intermediate phase, a social study can identify stressors contributing to the psychosis, while long-term support focuses on helping the patient return to work or prior activities to promote social reintegration.

Psychological management addresses both the patient’s and family’s understanding and adaptation to the condition. In the immediate phase, family education provides insight into the condition and support mechanisms. Non-pharmacological strategies are essential for creating a safe and calming environment [6]. These include environmental modifications such as screening for weapons, minimizing noise, and dimming lights to reduce sensory overstimulation. De-escalation techniques, such as establishing rapport, addressing basic needs (e.g., safety, hunger, and comfort), and maintaining a calm, respectful demeanor, can effectively reduce agitation [6]. Acknowledging the patient’s feelings, respecting personal space, and avoiding confrontational behavior further enhance the effectiveness of these strategies. When non-pharmacological approaches fail, mechanical restraints or seclusion may be used as a last resort, though these measures carry risks and should be applied cautiously. During the intermediate phase, psychometric tools like the Positive and Negative Syndrome Scale (PANSS) can assess symptom severity and progression. The long-term phase emphasizes ongoing psychological support to prevent relapse, enhance insight, and promote well-being.

Medications

The pharmacological management of agitated patients involves the use of various drug categories, each tailored to the severity of agitation and underlying clinical conditions. Below is an overview of the commonly used pharmacological agents, their dosages, onset times, and important considerations [1].

First-Generation Antipsychotics

Haloperidol (Haldol)
Haloperidol is commonly used for agitation across mild, moderate, and severe cases. The dosage varies depending on the severity: 2.5 mg orally for mild cases, 5 mg orally for moderate agitation, and 5 mg intramuscularly for severe agitation. The time of onset is approximately 30 minutes for all routes. However, haloperidol carries a high risk of extrapyramidal symptoms (EPS). Co-administration with agents such as benztropine, diphenhydramine, lorazepam, or promethazine can help reduce this risk. Care should be taken to avoid combining three of these medications simultaneously. Intravenous use is associated with an increased risk of QTc prolongation, and the medication may lower the seizure threshold. The maximum daily dose is 30 mg, and repeat dosing is allowed every 0.5–4 hours as needed.
Droperidol (Inapsine)
Droperidol is primarily used in severe agitation, with a dose of 5 mg administered intramuscularly or intravenously. The onset of action is faster than haloperidol, typically around 15 minutes. It shares a similar risk profile for EPS and QTc prolongation. Combining droperidol with midazolam (5 mg) is recommended to optimize efficacy. The maximum daily dose ranges between 10–20 mg.

Second-Generation Antipsychotics

Olanzapine (Zyprexa)
Olanzapine is effective for agitation and can be administered as 5 mg orally disintegrating tablets (ODT) for mild cases, 5–10 mg ODT for moderate cases, and 10 mg intramuscularly for severe agitation. The onset of action is approximately 15–60 minutes depending on the route of administration. Concomitant use with benzodiazepines should be avoided within one hour. The maximum daily dose is 20 mg.
Risperidone (Risperdal)
Risperidone is used at 1 mg ODT for mild agitation and 2 mg ODT for moderate agitation, with an onset time of approximately 60 minutes. It is particularly effective for undifferentiated or substance-related agitation but should not be used in cases of CNS depressant intoxication. Risperidone carries the highest risk of EPS among second-generation antipsychotics and may cause orthostatic hypotension. Repeat dosing is allowed every 4–6 hours, but caution is advised for doses exceeding 10 mg per day.
Ziprasidone (Geodon)
Ziprasidone is typically reserved for severe agitation, with doses of 10–20 mg intramuscularly and an onset time of 15–30 minutes. It has a high risk of QTc prolongation, exceeding even that of haloperidol, making it unsuitable for patients with cardiac disease or pre-existing QTc prolongation. The medication requires reconstitution before administration, and the maximum daily dose is 40 mg.

Benzodiazepines

Lorazepam (Ativan)
Lorazepam is a versatile benzodiazepine used for mild agitation (2 mg orally), moderate agitation (5 mg intramuscularly or 2.5 mg intravenously), and severe agitation (10 mg intramuscularly or 5 mg intravenously). The onset of action is 20–30 minutes for oral administration and faster for intramuscular or intravenous routes. While effective for undifferentiated agitation, caution is required in patients with CNS depression (e.g., ethanol intoxication).
Midazolam (Versed)
Midazolam, administered as 5 mg intramuscularly or intravenously, has a faster onset time of 5–15 minutes depending on the route. It is often used in combination with haloperidol or droperidol for severe agitation. Care must be taken due to its sedative effects.

Dissociative Anesthetic

Ketamine (Ketalar)
Ketamine is a dissociative anesthetic used for severely agitated patients, such as those experiencing excited delirium. Doses range from 1–2 mg/kg intravenously or up to 5 mg/kg intramuscularly, with an onset time of 1–2 minutes (IV) or 3 minutes (IM). Ketamine can cause emergence reactions, bronchorrhea, and, rarely, laryngospasm, and may increase the need for intubation. It is known to elevate heart rate, cardiac output, and blood pressure, making it suitable for patients requiring rapid sedation.

When To Admit This Patient

Disposition decisions for acutely agitated or psychotic patients should be guided by the underlying cause of the agitation, once the patient has been stabilized [6]. For cases involving organic causes, such as sepsis, acute intracranial hemorrhage, or severe metabolic disturbances, hospitalization is necessary until the underlying condition is adequately treated and stabilized. Patients with substance-induced psychosis may be eligible for discharge if they are no longer clinically intoxicated and have returned to their baseline mental status. However, if a thorough medical evaluation reveals no medical cause for the agitation or psychosis, the patient should undergo a psychiatric assessment [6]. Psychiatric admission is typically indicated for patients with acute psychosis due to an underlying psychiatric disorder if they pose a high risk of harm to themselves or others. Additionally, admission is strongly recommended for first episodes of psychosis attributed to psychiatric causes to ensure appropriate evaluation and management [6].

Clinical Pearls

Patients with a brief psychotic disorder experience psychotic symptoms that last at least one day but not more than one month, with gradual recovery. If symptoms persist beyond one month but less than six months, the condition is termed schizophreniform disorder. If symptoms extend beyond six months, it is classified as schizophrenia [12].
Children and elderly patients should generally be dosed at the lower end of the dosing spectrum to account for their increased sensitivity to medications.
Neuroleptic malignant syndrome can develop at any time during treatment. Physicians should remain vigilant for clinical symptoms, which include hyperthermia, muscle rigidity, altered mental status, and autonomic dysregulation.

Revisiting Your Patient

This patient presented with prominent symptoms of grossly disorganized behavior, auditory hallucinations, and paranoid delusions, followed by a rapid return to baseline mental state, consistent with a diagnosis of Brief Psychotic Disorder (BPD) [12]. This diagnosis includes two specifiers: with marked stressors or without marked stressors, previously classified under the term Brief Reactive Psychosis.

When a patient is admitted with an unclear duration of psychotic symptoms, they are often initially diagnosed with Unspecified Psychotic Disorder. However, if symptoms resolve within one month, the diagnosis is revised to Brief Psychotic Disorder. Antipsychotic treatment has been shown to reduce the duration of symptoms in BPD, facilitating quicker recovery. If symptoms persist beyond one month, the diagnosis transitions to Schizophreniform Disorder; persistence beyond six months supports a diagnosis of Schizophrenia.

Positive symptoms, such as hallucinations and delusions, are generally associated with a better prognosis than negative symptoms due to their typically acute onset and favorable response to treatment. It is critical to exclude organic etiologies, medication side effects, or substance-induced psychosis through a comprehensive physical examination and targeted investigations based on clinical findings. In this case, all relevant investigations were unremarkable, supporting a primary psychotic diagnosis.

Author

Mazin A Mukhtar

Dr. Mazin Mukhtar is a psychiatrist with over 15 years of experience, currently practicing at Amal Hospital in Dubai. Before moving to Dubai, Dr. Mukhtar served as an Assistant Professor of Psychiatry at the University of Bahri, where he was appointed as Head of the Department in 2015. In addition to his qualifications in psychiatry, Dr. Mukhtar has a strong interest in leadership and holds a Professional Diploma in Clinical Leadership from the Royal College of Surgeons of Ireland. He also possesses a Clinical Diploma in Cognitive Behavioural Therapy (CBT) from Notting Hill College.

Listen to the chapter

References

Roppolo LP, Morris DW, Khan F, et al. Improving the management of acutely agitated patients in the emergency department through implementation of Project BETA (Best Practices in the Evaluation and Treatment of Agitation). J Am Coll Emerg Physicians Open. 2020;1(5):898-907. doi:10.1002/emp2.12138.
Psych Central. What Are the Symptoms of Psychosis? Updated May 28, 2021. Accessed January 10, 2025. https://psychcentral.com/lib/symptoms-of-psychosis#signs-and-symptoms.
National Institute of Mental Health. Understanding Psychosis. Updated 2023. Accessed January 10, 2025. https://www.nimh.nih.gov/health/publications/understanding-psychosis.
Harrison PJ, Cowen P, Burns T, Fazel M. Shorter Oxford Textbook of Psychiatry. 7th ed. Oxford University Press; 2018.
Sadock BJ, Sadock VA, Ruiz P. Kaplan & Sadock’s Synopsis of Psychiatry: Behavioral Sciences/Clinical Psychiatry. 11th ed. Wolters Kluwer; 2015.
Chan M, Moukaddam N, Tucci V. Stabilization and Management of the Acutely Agitated or Psychotic Patient. International Emergency Medicine Education Project. Accessed January 10, 2025. https://iem-student.org/stabilization-and-management-of-the-acutely-agitated-or-psychotic-patient/.
Vyas CM, Petriceks AH, Paudel S, Donovan AL, Stern TA. Acute Psychosis. Prim Care Companion CNS Disord. 2023;25(2). doi:10.4088/pcc.22f03338.
Reidy L, Junquera P, Van Dijck K, Steele BW, Nemeroff CB. Underestimation of substance abuse in psychiatric patients by conventional hospital screening. J Psychiatr Res. 2014;59:206-212. doi:10.1016/j.jpsychires.2014.08.020.
Khandanpour N, Hoggard N, Connolly DJA. The role of MRI and CT of the brain in first episodes of psychosis. Clin Radiol. 2013;68(3):245-250. doi:10.1016/j.crad.2012.07.010.
Schleifer JJ. Management of acute agitation in psychosis: an evidence-based approach in the USA. Adv Psychiatr Treat. 2011;17(2):91-100. doi:10.1192/apt.bp.109.007310.
Frick PJ, Barry CT, Kamphaus RW. Structured Diagnostic Interviews. In: Clinical Assessment of Child and Adolescent Personality and Behavior. 3rd ed. Springer; 2010:253-270. doi:10.1007/978-1-4419-0641-0_11.
American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders (DSM-5). 5th ed. American Psychiatric Publishing; 2013.

Reviewed and Edited By

Arif Alper Cevik, MD, FEMAT, FIFEM

Pediatric Seizures (2025)

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

by Neema Francis, Faiz Ahmad, Thiagarajan Jaiganesh

You Have A New Patient!

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

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

What Do You Need To Know?

Importance

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

Epidemiology

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

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

Pathophysiology

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

Basic Mechanisms of Seizures

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

Age-Related Factors and Neuronal Imbalance

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

Specific Factors Contributing to Seizures

Several specific factors influence seizure pathophysiology:

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

Medical History

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

1. History of Present Illness:

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

2. Past Medical History:

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

3. Medication History:

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

4. Family History:

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

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

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

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

Physical Examination

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

Initial Assessment

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

General Appearance

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

Head and Neck Examination

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

Skin Examination

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

Cardiovascular and Abdominal Examination

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

Neurological Examination [2,4,12]

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

Postictal Examination [6]

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

Important Considerations

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

Alternative Diagnoses

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

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

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

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

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

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

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

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

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

Acing Diagnostic Testing

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

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

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

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

Risk Stratification

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

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

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

Management

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

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

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

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

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

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

When To Admit This Patient

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

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

Revisiting Your Patient

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

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

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

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

Authors

Neema Francis

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

Faiz Ahmad

Thiagarajan Jaiganesh

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

Listen to the chapter

References

Glauser T, Ben-Menachem E, Bourgeois B, et al. Updated ILAE evidence review of antiepileptic drug efficacy and effectiveness as initial monotherapy for epileptic seizures and syndromes. Epilepsia. 2013;54(3):551-563. doi:10.1111/epi.12074.
Friedman MJ, Sharieff GQ. Seizures in children. Pediatr Clin North Am. 2006;53(2):257-277. doi:10.1016/j.pcl.2005.09.010.
Kazemi H, Rahmati M, Soltani Z, Kazemi A. Association of epilepsy and migraine headache. J Clin Med. 2019;8(1):39. doi:10.3390/jcm8010039.
Chen CY, Chang YJ, Wu HP. New-onset seizures in pediatric emergency. Pediatr Neonatol. 2010;51(2):103-111. doi:10.1016/S1875-9572(10)60019-8.
El-Radhi AS. Management of seizures in children. Br J Nurs. 2015;24(3):152-155. doi:10.12968/bjon.2015.24.3.152.
Fine A, Wirrell EC. Seizures in children. Pediatr Rev. 2020;41(7):321-347. doi:10.1542/pir.2019-0134.
Sidhu R, Velayudam K, Barnes G. Pediatric seizures. Pediatr Rev. 2013;34(8):333-342. doi:10.1542/pir.34-8-333.
Lambert MV, Robertson MM. Depression in epilepsy: etiology, phenomenology, and treatment. Epilepsia. 2002;43(Suppl 2):21-27. doi:10.1046/j.1528-1157.43.s.2.3.x.
Krawiec C, Muzio MR. Neonatal Seizure. In: StatPearls. Treasure Island (FL): StatPearls Publishing; January 2, 2023.
Lawton B, Deuble N. Seizures in the paediatric emergency department. J Paediatr Child Health. 2016;52(2):147-150. doi:10.1111/jpc.12979.
Wirrell EC, Grossardt BR, Wong-Kisiel LC, Nickels KC. Incidence and classification of new-onset epilepsy and epilepsy syndromes in children in Olmsted County, Minnesota from 1980 to 2004: A population-based study. Epilepsy Res. 2011;95(1-2):110-118. doi:10.1016/j.eplepsyres.2011.03.017.
Adams SM, Knowles PD. Evaluation of a first seizure. Am Fam Physician. 2007;75(9):1342-1347.
Helman A. Emergency management of pediatric seizures. Emergency Medicine Cases. December 1, 2015. Accessed January 17, 2023. https://emergencymedicinecases.com/emergency-management-of-pediatric-seizures/
Mayo Clinic. Seizures – Symptoms and causes. Mayo Clinic. February 24, 2021. Accessed January 17, 2023. https://www.mayoclinic.org/diseases-conditions/seizure/symptoms-causes/syc-20365711
Wilfong A. Seizures and epilepsy in children: clinical and laboratory diagnosis. In: UpToDate. February 12, 2022. Accessed January 17, 2023. https://www.uptodate.com/contents/seizures-and-epilepsy-in-children-clinical-and-laboratory-diagnosis
Richhariya D. Signs and Symptoms in Clinical Practice. Jaypee Brothers Medical Publishers; 2020:152-161.
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Reviewed and Edited By

Arif Alper Cevik, MD, FEMAT, FIFEM

Tetanus (2025)

January 7, 2025January 12, 2025 ~ iEM Education Project Team ~ Leave a comment

by Grace Bunemann, Alex Gallaer, Jerry Oommen & Ashley Pickering

You Have A New Patient!

An 11-year-old female was brought in by ambulance after being attacked by her neighbor’s American Pitbull dog approximately 1 hour prior to arrival. She had attempted to pet the dog and sustained multiple bite wounds to her face and hands. She is crying loudly and is accompanied by her mother and father, who report that she previously had “German Measles” but has no other known medical conditions, though her medical care has been inconsistent.

Her temperature is 37.0°C, pulse is 133/min, and blood pressure is 98/62 mmHg. On examination, she has a dirty, macerated, oozing wound on the left side of her face and multiple deep wounds on her hands and distal arms, all contaminated with soil.

What Do You Need To Know?

Importance

Tetanus is an acute but often fatal disease caused by an exotoxin produced by the bacterium Clostridium tetani. It remains an important public health concern worldwide, particularly in areas with low immunization rates against tetanus [1]. Tetanus infection is characterized by generalized rigidity and convulsive spasms of skeletal muscles [2]. Muscle stiffness typically begins in the head and neck region before becoming generalized.

The CDC reports that in the US, tetanus has been fatal in approximately 11% of reported cases in recent years, while global fatality rates are closer to 50% [2]. In 2019, according to the Global Burden of Disease database, there were nearly 74,000 new worldwide cases of tetanus, corresponding to an incidence rate of 0.95 [3,4]. That same year, there were just under 35,000 deaths attributed to tetanus [3,4]. Since 1990, the global death rate from tetanus has decreased by an astounding 87% [3,4]. This decline is credited to widespread vaccination, improved wound care, and the use of postexposure immunoglobulin.

Epidemiology

A tetanus infection is caused by Clostridium tetani. C. tetani is an anaerobic, spore-forming bacterium that gains access through broken human skin and causes toxin-mediated infection. The spores are found everywhere in the environment, particularly in soil, ash, intestinal tracts/feces of animals and humans, and on the surfaces of skin and rusty tools like nails, needles, or barbed wire[1]. While present worldwide, it is more common in warm, damp climates with rich soil. The organism is sensitive to heat and cannot survive in the presence of oxygen. The spores, in contrast, are extremely resistant to heat and the usual antiseptics [2].

Anyone can get tetanus, but like many diseases, it has a predilection for specific groups. There is an increased risk of tetanus in newborns, pregnant persons with insufficient immunization, intravenous drug users, the elderly, and those lacking primary immunization. Typically, tetanus infections are categorized into the following four categories: generalized (full-body symptoms), localized (symptoms in one area, e.g., leg), cephalic (cranial nerve involvement), and neonatal (history of home birth, soil on umbilical stump, unsterilized instruments) [5].

Pathophysiology

Tetanus is a serious disease caused by the bacterium Clostridium tetani, which produces toxins that disrupt the nervous system, resulting in muscle spasms and rigidity. The pathophysiology of tetanus involves several key stages [6-9]. The process begins when C. tetani spores, which are commonly found in the environment, enter the body through wounds or injuries. These entry points may include minor or unnoticed injuries, burns, surgical sites, intravenous drug use, or unsanitary practices such as umbilical cord cutting in newborns. Once inside the body, the spores encounter anaerobic conditions, often in devitalized tissue, which allow them to germinate into bacteria [7].

The bacteria produce two main toxins: tetanospasmin and tetanolysin [7,8]. Tetanospasmin, a potent neurotoxin, is the primary agent responsible for the clinical features of tetanus. Tetanolysin, a hemolysin, has no clear role in the disease’s pathology. Tetanospasmin enters the lymphatic and circulatory systems, eventually binding irreversibly to receptors at the neuromuscular junctions of the peripheral nervous system. The toxin is then transported retrogradely along nerve axons to the central nervous system (CNS), where it exerts its effects on inhibitory interneurons in the spinal cord and brainstem.

Within the CNS, tetanospasmin blocks the release of inhibitory neurotransmitters such as gamma-aminobutyric acid (GABA) and glycine, disrupting the balance between excitatory and inhibitory signals [5,7,8]. This blockade leads to unregulated muscle activity, characterized by the hallmark symptoms of tetanus: severe muscle spasms and rigidity. The uninhibited release of excitatory neurotransmitters results in continuous muscle contractions, which can be painful and are often triggered by minimal external stimuli like noise, light, or touch. In severe cases, these spasms can cause fractures, tendon ruptures, or respiratory failure [6,8].

Tetanus also affects the autonomic nervous system, leading to symptoms such as fluctuating blood pressure, rapid heart rate, and excessive sweating [6,8]. This autonomic dysfunction results from the toxin’s disinhibitory effects on the sympathetic nervous system. Additionally, the uninhibited release of catecholamines by the adrenal glands contributes to hypersympathetic activity. The effects of the neurotoxin are seen until a new axon terminal is produced which takes 4-6 weeks [2]. The cumulative effects of these pathophysiological processes make tetanus a potentially life-threatening condition that requires prompt recognition and treatment.

Medical History

Tetanus infection should be suspected in any patient presenting for wound management. However, tetanus has an average incubation period of 14 days, though it can range between 3–21 days after exposure. As a result, symptoms of infection are unlikely to be present at the time of initial presentation for an injury. Symptoms of an acute infection may include jaw cramping or the inability to open the mouth, muscle spasms (often in the back, abdomen, and extremities), and sudden painful muscle spasms, which can be triggered by sudden noises. Additional symptoms include trouble swallowing, seizures, headache, fever and sweating, and changes in blood pressure or a rapid heart rate [1].

When assessing a patient for potential tetanus infection, gathering detailed information about their history is essential. Several aspects of the patient’s history can provide crucial insights into the likelihood and severity of tetanus.

Immunization History

Understanding the patient’s vaccination status is critical in evaluating tetanus risk. Key details include the number of vaccine doses received and the timing of the most recent dose. Tetanus commonly occurs in individuals who are unvaccinated, under-vaccinated, or whose immunity has diminished over time. A history of incomplete or absent immunization is a frequent factor in tetanus cases, emphasizing the importance of vaccination in preventing this disease [7,8].

Questions: What is your immunization history against tetanus? Did you receive your childhood vaccinations? When was the last time you received an immunization other than those for flu or COVID? Have you seen a doctor recently for a cut or injury and received an immunization?

Important: Most cases occur in patients who are unimmunized or partially immunized.

Wound and Injury History

A thorough wound history is essential in identifying potential entry points for Clostridium tetani spores [6]. Recent injuries, even seemingly minor ones, should be noted, as traumatic wounds are the primary source of infection in most cases [8]. However, tetanus can sometimes develop without any obvious wounds or identifiable source of infection.

Question: How, what, and when did this injury occur?

In 70% of patients, a history of injury is present.
Most common points of entry include puncture wounds, abrasions, and lacerations.
Rare points of entry include chronic wounds, dental procedures, foreign bodies, and corneal abrasions.

Question: Was the object/item clean or dirty?

Ask about exposure to soil, ash, intestinal tracts/feces of animals and humans, or rusty tools such as nails, needles, and barbed wire.

Question: Has this happened before?

Explore any history of previous tetanus exposure or symptoms.

Wound Characteristics

The type and nature of the wound can provide additional clues. Punctures, lacerations, burns, surgical wounds, or injuries involving intravenous drug use are particularly susceptible to tetanus [8]. Unsanitary practices, such as home deliveries with contaminated tools for umbilical cord cutting, can also introduce the bacterium [8]. Wounds that are heavily contaminated, caused by blunt trauma, or involve animal or human bites carry a higher risk of infection. High-risk wounds include those older than 6 hours, deeper than 1 cm, contaminated, infected, and ischemic.

Incubation Period

The time between the injury and the onset of symptoms (the incubation period) is a key diagnostic factor [7]. A shorter incubation period, typically less than 48 hours, is associated with more severe disease [8]. While the incubation period can range from 1 to 60 days, most cases develop within 7 to 14 days, with an average of 7–10 days [1].

Early Symptoms

Tetanus often begins with subtle symptoms that progress over time. Common early signs include trismus (lockjaw), facial and neck muscle rigidity, and difficulty swallowing (dysphagia) [6,7]. Patients may report a sore throat or localized rigidity around the site of the infection. These early symptoms are often indicative of localized tetanus, where muscle stiffness is confined to a specific area [6].

Symptom Progression

In cases of generalized tetanus, the symptoms typically spread from the face and neck to the rest of the body [7]. Generalized painful muscle spasms and reflex spasms triggered by stimuli such as noise or touch are hallmark signs [8].

Risk Factors

Specific risk factors may increase the likelihood of tetanus. These include intravenous drug use, diabetes, recent surgical procedures, or unsanitary childbirth practices [6]. Neonatal tetanus, often resulting from unclean umbilical cord cutting, underscores the importance of the mother’s immunization status and sterile delivery practices [8]. Note that patients with an impaired immune system or a history of poor healing are at increased risk.

Additional Symptoms

Other reported symptoms may include fever, sweating, high blood pressure, rapid heart rate episodes, drooling, involuntary urination or defecation, and severe back arching spasms (opisthotonus) [1,6]. These manifestations often reflect the systemic effects of the tetanus toxin and its impact on the nervous system.

Special Populations

Special populations require targeted questions to better assess risk:

Intravenous drug users:
- Do you share needles?
- Where are your injection sites?
- Is there a history of injecting in the neck region?
Newborns:
- What is the mother’s immunization history? Did she receive a Tdap booster during this pregnancy?
- Was the baby born at home or in a hospital?
- Was soil applied to the umbilical stump?
- What instruments were used, if any (applies to both home and hospital births)?
- Has the neonate received any immunizations?

Finally, it is important to note that not all patients will present with an obvious injury. Approximately 3–5% of patients may have cryptogenic tetanus, where no identifiable entry point can be determined [5,6].

Physical Examination

The physical examination findings in tetanus are pivotal for diagnosis, which is primarily clinical and based on the presence of characteristic signs and symptoms. These features guide timely diagnosis and intervention, as delays in treatment can result in life-threatening complications. Findings vary depending on the type and severity of the infection, but certain hallmark features are common across all forms of tetanus.

General Physical Findings

Tetanus is primarily characterized by muscle rigidity and spasms, which often begin in the jaw and neck before progressing to other parts of the body [2]. A classic early finding is trismus (lockjaw), where patients cannot open their mouths due to masseter muscle spasms [6]. Another distinctive feature is risus sardonicus, a rigid, scornful smile caused by sustained contraction of the facial muscles [6]. Neck stiffness and dysphagia (difficulty swallowing) are other early symptoms caused by pharyngeal and neck muscle spasms [2].

Patients may also exhibit reflex spasms, which are generalized muscle contractions triggered by minimal external stimuli such as noise, light, or touch [6]. Signs of autonomic dysfunction include labile blood pressure, cardiac arrhythmias, and excessive sweating. Fever may be present in some cases, although patients are often afebrile. Importantly, patients with tetanus typically maintain an intact sensorium, remaining conscious and alert unless other brain dysfunction is present [7].

Findings in Generalized Tetanus

In generalized tetanus, muscle spasms follow a descending pattern, starting with the face (trismus and risus sardonicus) and progressing to the neck, back, and extremities [2]. A characteristic posture known as opisthotonus may develop, where the back and legs hyperextend while the arms flex, resembling decorticate posturing [6]. These spasms are often intense and may come in waves. Abdominal rigidity is another common feature, with patients exhibiting tenderness and guarding, sometimes mimicking an acute abdomen [2,7].

Findings in Localized Tetanus

Localized tetanus is marked by persistent muscle contractions confined to the area of the injury [2,6]. Patients may experience localized pain and spasms near the wound [6]. While typically less severe than generalized tetanus, localized tetanus can progress to more widespread symptoms in some cases.

Findings in Cephalic Tetanus

Cephalic tetanus involves dysfunction of the cranial nerves, most commonly the facial nerve. Physical exam findings include cranial nerve palsies, such as deviation of the eyes, eyelid retraction, and facial paralysis. Other associated symptoms include neck stiffness, dysphagia, and a deviated gaze [7].

Findings in Neonatal Tetanus

Neonatal tetanus often presents with poor feeding and difficulty sucking or breastfeeding [6]. Affected infants develop generalized rigidity and spasms, including opisthotonus, along with severe spastic contractions triggered by touch [8]. Additional findings include irritability and excessive crying [1,8].

Specific Diagnostic Tests and Other Findings

The spatula test is a clinical test with high sensitivity and specificity for tetanus [7]. Normally, touching the posterior pharyngeal wall with a spatula induces a gag reflex. In tetanus, it causes a reflex spasm of the masseter muscles, leading to the patient biting down instead of gagging.

Other findings include respiratory distress caused by spasms of respiratory muscles, including the diaphragm and larynx [1,2,8]. Severe muscle contractions can lead to complications such as joint dislocations, long bone fractures, and difficulty breathing [7]. Population studies reveal that lower extremity injuries are the most common antecedent to tetanus, followed by upper extremity and head or trunk injuries.

Alternative Diagnoses

Diagnosis of generalized tetanus is based entirely on the patient’s history and physical examination. Though the majority of cases will involve a preceding injury, making the presentation quite unique, there are aspects of the presentation that may mimic other conditions, which are important to rule out.

The initial presentation could include cranial nerve palsies, particularly in cephalic tetanus. For this reason, it is important to rule out critical conditions, including strokes, neoplasms, infections, or aneurysms. To accurately rule out other diagnoses, it is essential to familiarize yourself with the risk factors and presentations of each condition. Risk factors for stroke include uncontrolled hypertension, diabetes, and hyperlipidemia. Symptomatology may also include headache and localized extremity weakness. Strokes such as venous sinus thrombosis may occur in individuals who are pregnant, have hypercoagulable blood disorders, or use hormones. Neoplasms may present with a more insidious onset and a constellation of symptoms depending on the tumor’s location [6,7], such as headaches, seizures, fatigue, vision changes, gait abnormalities, nausea, and vomiting, in addition to cranial nerve palsy.

Infections will typically have an obvious source near the affected nerve. Parotitis may affect the facial nerve, and otitis media may involve the trigeminal nerve [6,7]. Peritonsillar abscess can cause trismus and neck stiffness, and must be differentiated from tetanus. Meningitis can also lead to cranial nerve palsies but will likely present with preceding neck rigidity, altered mental status, and systemic symptoms concerning for sepsis. Lyme disease may also cause facial nerve palsy and classically follows a tick bite, often occurring after hiking in the Northeastern United States. Botulism is severe neurological condition caused by a toxin produced by Clostridium botulinum. It presents with flaccid paralysis, dysphagia, and cranial nerve palsies, but does not involve muscle spasms or hypertonia [8].

Muscle spasms and rigidity described in tetanus may also present similarly to other conditions, such as dystonic reactions or neuroleptic malignant syndrome [7,8]. However, these conditions are closely linked to the use of antipsychotic medications and could likely be ruled out after a thorough review of the patient’s medication list [7]. Administration of medications such as diphenhydramine or benztropine would reverse the symptoms in a dystonic reaction but not in tetanus. Strychnine poisoning, a chemical sometimes used in pesticides, is also associated with ingestion and presents with symptoms of hyperreflexia, clonus, and muscle rigidity [6,7]. Critical to this diagnosis is the patient’s history before presentation, as well as the rapid onset of symptoms, typically within 10–20 minutes. Serotonin Syndrome can cause muscle rigidity, and should be considered in the differential diagnosis of tetanus [7]. Low calcium levels can cause muscle spasms, but the autonomic features of tetanus, such as fluctuating blood pressure and heart rate, are usually absent [8].

In addition to contractions and cranial nerve palsies, tetanus may present with systemic symptoms related to autonomic overactivity. These include diaphoresis, tachycardia, cardiac arrhythmias, labile hypertension, and fever. These symptoms might overlap with those seen in sympathomimetic or cholinergic toxicities; however, these toxicities are usually closely tied to the patient’s medications or a reported history of ingestion.

Acing Diagnostic Testing

The diagnosis of tetanus is primarily clinical, relying heavily on the patient’s history and physical examination. There is no single diagnostic test that can definitively confirm or rule out tetanus. However, diagnostic tests may be useful to exclude other potential etiologies that mimic tetanus symptoms.

Bedside Tests

Point-of-Care Glucose: Hypoglycemia can mimic certain neurological symptoms, such as cranial nerve palsies, and should be assessed promptly.
Spatula Test: This bedside test involves touching the posterior oropharynx with a tongue blade [7].
- Normal Response: In normal circumstances, this action elicits a gag reflex, and the patient will try to expel the spatula.
- Positive Test (Tetanus): If tetanus is present, the patient will develop a reflex spasm of the masseter muscles and will bite down on the spatula instead of gagging. A positive response, where the patient bites down rather than gagging, is 94% sensitive and 100% specific for tetanus [6].
Electrocardiogram (ECG): If the patient presents with tachycardia, an ECG can help evaluate for arrhythmias and identify other possible underlying causes.

Laboratory Tests

Blood Counts and Blood Chemistry: These tests are typically unremarkable in tetanus, meaning they do not show specific changes that help in diagnosing the condition [6]. They can be useful in excluding other causes of a patient’s symptoms.
Calcium: Hypocalcemia may cause muscle spasms and cramping, and it is important to rule this out.
Creatine Kinase (CK): Prolonged muscle spasms and rigidity in tetanus can result in muscle damage, potentially leading to rhabdomyolysis, making CK levels crucial to monitor.
Creatinine: Kidney function should be evaluated, particularly if rhabdomyolysis is suspected, as it can lead to acute kidney injury.
Drug Screen: This may help rule out the ingestion of sympathomimetics, such as cocaine, which can cause symptoms similar to tetanus.
Wound cultures: Wound cultures can occasionally isolate Clostridium tetani, but they are not a reliable diagnostic tool for tetanus. Cultures are positive in only about 30% of confirmed tetanus cases, and the organism can sometimes be isolated from wounds of individuals who do not exhibit any symptoms of tetanus. Additionally, the challenges in culturing C. tetani and the possibility of isolating non-toxigenic strains further limit the diagnostic utility of this method [2,7,8].
The antitoxin assay measures serum levels of tetanus antitoxin. While not widely available, a serum antitoxin level of 0.01 IU/mL or higher is typically considered protective and reduces the likelihood of tetanus. However, this test is not consistently reliable and is not commonly utilized for diagnostic purposes.

Imaging

CT of the Head: A head CT scan can help exclude intracranial pathologies, such as stroke or mass lesions, that may mimic tetanus symptoms, especially in cases involving cranial nerve palsies.
CT of the Abdomen: In cases of localized tetanus affecting the abdomen, a CT scan might be necessary, as the presentation can resemble an acute abdomen.

Risk Stratification

The severity of a tetanus infection is multifactorial. Factors such as age, immunity, location of injury, depth of injury, and ultimately the quantity of tetanus toxin contribute to the development of generalized tetanus. A longer interval between symptom onset and the appearance of spasms has been linked to milder features. Ultimately, risk stratification after the onset is difficult to accurately assess, as all forms of tetanus may develop into generalized tetanus. Therefore, prevention via immunization and subsequent boosters for high-risk wounds is crucial.

Management

In severe cases of tetanus, critical patients should be managed systematically using the ABCDE approach [5]. This approach ensures comprehensive assessment and treatment of the patient’s condition.

Airway and Breathing

Early intubation and mechanical ventilation should be strongly considered to manage airway compromise caused by trismus, laryngospasm, and neck and chest wall rigidity, which can impair airway access and create ventilation challenges [5]. The use of succinylcholine and other depolarizing paralytic agents should be avoided due to the risk of hyperkalemia.

Circulation

For patients exhibiting systemic illness, standard sepsis treatment should be initiated, including the administration of intravenous fluids, blood cultures, and broad-spectrum antibiotics [5].

Antimicrobial therapy options include:

Metronidazole 500 mg intravenously every 6 to 8 hours (first-line therapy).
Penicillin G 2 to 4 million units intravenously every 4 to 6 hours (second-line therapy).
Doxycycline 100 mg intravenously every 12 hours.

To neutralize unbound tetanus toxin, the following measures are recommended:

Human Tetanus Immune Globulin (HTIG) 500 units intramuscularly [9]:
- Administer a portion of the dose at a different site from the tetanus toxoid vaccine.
- Inject part of the dose directly around the wound.
- This dosage is the same for adults and pediatric patients.
If HTIG is unavailable, intravenous immune globulin should be used.

In cases of autonomic dysfunction, pharmacological interventions include:

Labetalol (0.25 to 1 mg/minute) to block adrenergic responses through dual alpha- and beta-blockade. Note that beta-selective blockers should be avoided due to increased associated mortality [5].
Magnesium sulfate:
- Loading dose: 40 mg/kg over 30 minutes.
- Continuous infusion: 2 g/hour for patients >45 kg or 1.5 g/hour for patients ≤45 kg.
- This is considered first-line or adjuvant therapy to reduce muscle spasms,

and toxicity monitoring should include checking for hyporeflexia.

Morphine (0.5 to 1 mg/kg/hour) can be used as a continuous infusion for managing autonomic dysfunction and sedation.

Disability: Control of Muscle Spasms

Effective spasm control is essential to prevent complications such as rhabdomyolysis, fractures, and apnea [5]. Recommended treatments include:

Benzodiazepines:
- Diazepam: 10–40 mg intravenously every 1 to 4 hours as needed.
- Midazolam: Continuous infusion at 5–15 mg/hour.
If benzodiazepines fail, neuromuscular blockade may be necessary. This requires endotracheal intubation and the use of:
- Vecuronium: Initial bolus dose of 0.08 to 0.1 mg/kg, followed by continuous infusion at 0.8 to 1.7 µg/kg/minute.
- Rocuronium: Initial bolus dose of 0.6 to 1 mg/kg, followed by continuous infusion at 8 to 12 µg/kg/minute.
- Consider intravenous propofol or intrathecal baclofen for refractory spasms.

Exposure: Identifying and Managing the Source

A thorough skin examination is necessary to identify potential sites of inoculation, including acute skin breaks and chronic wounds. Proper wound care includes cleaning and debridement to remove the source of infection.

To minimize muscle spasms triggered by sensory stimuli, patients should be admitted to the ICU with precautions such as:

Reducing exposure to loud noises, bright lights, and sudden movements.
Avoiding other forms of sensory stimulation.

In cases where a tetanus infection is possible, but no clinical signs or symptoms are present, the patient should undergo thorough wound irrigation and debridement. In addition, the patient’s immunization record should be reviewed. If it is unclear whether the patient has ever received their initial series of tetanus shots (part of the WHO-recommended childhood immunization series), proceed with a primary series of 3 tetanus shots and boosters every 10 years. If the patient presents with high-risk wounds and their last booster was received more than 5 years prior, provide a booster.

Patients who are unimmunized, incompletely immunized, or for whom immunization history is unclear should also receive Human Tetanus Immunoglobulin (HTIG). HTIG neutralizes the tetanus toxin and provides passive immunization for 3–4 weeks while the tetanus immunization series begins to provide immunity [9]. People with severe immunodeficiency or HIV infection presenting with high-risk wounds should also receive tetanus immune globulin, regardless of vaccination history [2].

This medication is administered by intramuscular injection. A dose of 250 IU (250 IU/ml, 1 ml) is given for wounds sustained within 24 hours, or 500 IU (250 IU/ml, 2 ml) for wounds older than 24 hours [9]. HTIG is also given for the treatment of tetanus once symptoms arise, to bind any circulating tetanus toxoid not bound to neurons and prevent further binding [2]. The treatment dose is 500 IU as a single dose, to be injected into 2 different sites, for all ages, from neonates through adults [10].

Medications

Human Tetanus Immunoglobulin (HTIG)

Dosage and Administration

For wound prophylaxis, the recommended dosage of Human Tetanus Immunoglobulin (HTIG) is based on the time elapsed since the injury [9]:

Within 24 hours: 250 IU (250 IU/mL, 1 mL).
After 24 hours: 500 IU (250 IU/mL, 2 mL).

HTIG is administered as a single dose via intramuscular (IM) injection. It should not be given intravenously to avoid complications.

Use During Pregnancy and Breastfeeding

HTIG is considered safe in pregnancy and breastfeeding and is categorized as Category C for all trimesters [10]. A small number of case reports suggest that IgG and IgM antibodies may transfer into colostrum and breast milk [10].

Cautions and Considerations

Allergic Reactions: Although rare, allergic reactions may occur. HTIG should not be administered to patients with a known allergy to the immunoglobulin.
Injection Technique: Proper technique is critical to avoid complications:
- Ensure the injection does not enter a blood vessel, as this can lead to shock. To confirm, aspirate prior to administering the dose.
General Precautions: Monitor the patient for any signs of an adverse reaction following administration.

Special Patient Groups

Pediatrics

Primary immunization is key in this group. Passive immunization from a fully vaccinated mother provides protection before infant vaccines are begun. Additionally, living environments free from high-risk exposures (e.g., rusty nails, fences) is important. Dtap is used for children ≤7 years old, while Tdap or Td is recommended for children >7 years old and adolescents [2].

Pregnant Patients

All pregnant women should receive a tetanus booster during every pregnancy, regardless of prior vaccination history, with Tdap vaccination recommended between 27–36 weeks of gestation [2,6]. This protects the newborn from pertussis, tetanus, and diphtheria by transferring maternal antibodies for passive immunity. If the childhood immunization series was completed but the last booster was over 10 years ago, a single booster dose is recommended. For unvaccinated or incompletely vaccinated individuals, at least two doses of a tetanus toxoid-containing vaccine (one of which must be Tdap) should be administered during pregnancy, with the series completed postpartum [2]. Preventive strategies to reduce neonatal tetanus risk include clean delivery practices and proper umbilical cord care, as unsanitary home deliveries or contaminated tools are common causes of neonatal infections [1,8]. For wound management, Tdap is indicated if more than five years have elapsed since the last dose, and TIG is recommended for tetanus-prone wounds in inadequately vaccinated women. Vaccination during pregnancy is safe, with no evidence of adverse outcomes, and plays a critical role in global efforts to eradicate maternal and neonatal tetanus.

Geriatrics

Tetanus in geriatric populations presents unique challenges due to waning immunity, comorbidities, and increased disease severity [6]. Older adults face a higher incidence of tetanus, with mortality rates significantly greater than in younger populations. For example, in the U.S., individuals aged 65 years or older have an incidence rate of 0.23 cases per 1 million, compared to 0.08 cases per 1 million in those under 65, and they account for the majority of tetanus deaths [6]. Waning immunity is a major factor, with only 28% of adults over 70 years immune. Clinical presentations often include trismus, rigidity, and spasms, but geriatric patients are at greater risk for complications such as respiratory failure, cardiac arrhythmias, and aspiration pneumonia, leading to poor prognosis [2]. Individuals in this group need to receive booster doses every 10 years and should have living environments free from high-risk exposures [2,6]. Intensive care management, supportive care, and public health education are crucial to improving outcomes [5,8].

When To Admit This Patient

Tetanus carries a significant burden of morbidity and mortality for patients who experience an infection. Accordingly, it is appropriate to maintain a low threshold to admit any patient in whom you suspect an acute tetanus infection.

In individuals presenting with signs or symptoms of tetanus infection, or in individuals deemed to be at high risk of developing tetanus who did not receive prophylactic vaccination or immunoglobulins after initial exposure, admission to the Intensive Care Unit (ICU) or a similarly capable unit with ventilator support is recommended. For hospitals without an ICU, it is recommended to pursue transfer to a facility with higher-level care whenever possible.

In individuals presenting immediately following exposure to tetanus toxins, risk stratification should be performed as outlined earlier, with vaccination status playing a significant role in determining intervention. Asymptomatic patients who are exposed to tetanus toxins but are adequately vaccinated or receive immunization with or without tetanus IVIG in the emergency department may be safely discharged. For discharged patients, extensive teaching about the signs and symptoms of tetanus infection should be provided, along with strict instructions to return immediately to the Emergency Department if any symptoms develop.

Revisiting Your Patient

A thorough physical exam reveals a 4 cm, linear wound on the left cheek that is oozing dark blood and contains soil. There is no disruption of the underlying buccal mucosa. Additionally, there are multiple deep, penetrating wounds to the bilateral hands and distal forearms that also contain dirt and soil but are currently hemostatic. No evidence of other injuries is observed. Visual acuity is intact in both eyes. A neurologic exam, including cranial nerves, is diffusely within normal limits. The patient is neurovascularly intact in all extremities, with no signs of cyanotic tissue. The wounds are copiously irrigated and cleansed while further information is gathered.

The patient’s parents report that she has received inconsistent medical care since birth because “she has been healthy.” They also state that they do not believe she has received standard childhood vaccinations. X-rays of the bilateral wrists and forearms do not demonstrate foreign bodies or bony injuries.

This patient is hemodynamically stable with hemostatic wounds. Based on the findings from the history and physical exam, you decide that this patient should receive tetanus immunization as well as tetanus immunoglobulin therapy. Red flags in this patient’s case include the history of inconsistent medical care, previous infection with “German Measles” (Rubella), which children are routinely vaccinated against in many countries, and the presence of deep, contaminated wounds.

Moreover, due to this child’s lack of vaccination history, it is recommended that she receive a full 3-dose primary tetanus vaccination series. Wound care should also be initiated, and sutures are likely indicated for this patient.

Authors

Grace Bunemann

Grace Bunemann, DO is an emergency medicine resident at Rush University Medical Center in Chicago, Illinois. She currently serves on the Emergency Medicine Residents’ Association Board of Directors as Director of Leadership Development. She also assists with the EMRA Global Emergency Medicine Student Leadership Program. She plans to pursue a global emergency medicine fellowship after finishing residency with a focus in equitable health systems and medical education.

Alex Gallaer

Alex Gallaer, MD is an Emergency Medicine resident in the Global Health track at the University of Utah. He is a facilitator for EMRA’s Global Emergency Medicine Leadership Program and has interests in equitable medical care, establishment of global health infrastructure, prehospital/disaster medicine, and medical education.

Jerry Oommen

Jerry Oommen, DO is a global emergency medicine fellow at The George Washington University and a fellow co-director of ACEP's Global Emergency Medicine Student Leadership Program. Primary areas of global health interest include medical education and capacity building.

Ashley Pickering

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

Listen to the chapter

References

World Health Organization. Tetanus. https://www.who.int/news-room/fact-sheets/detail/tetanus. Published July 12, 2024. Accessed April 5, 2023.
Centers for Disease Control and Prevention. Chapter 21: Tetanus. In: Epidemiology and Prevention of Vaccine-Preventable Diseases. Updated April 25, 2024. Accessed January 7, 2025. https://www.cdc.gov/pinkbook/hcp/table-of-contents/chapter-21-tetanus.html
Behrens H, Ochmann S, Dadonaite B, Roser M. Tetanus. Our World in Data. Published March 2019. Updated January 2024. Accessed January 7, 2025. https://ourworldindata.org/tetanus
Li J, Liu Z, Yu C, et al. Global epidemiology and burden of tetanus from 1990 to 2019: A systematic analysis for the Global Burden of Disease Study 2019. Int J Infect Dis. 2023;132:118-126. doi:10.1016/j.ijid.2023.04.402
Jain Rupal, Felipe Naillid. EM:RAP. Tetanus. In: CorePendium. Accessed January 7, 2025. https://www.emrap.org/corependium/chapter/recGn75URBGNVcZTD/Tetanus
Yabes JM Jr. Tetanus. Medscape. Updated December 15, 2024. Accessed January 7, 2025. https://emedicine.medscape.com/article/229594-overview
Bae C, Bourget D. Tetanus. [Updated 2023 May 31]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK459217/
George EK, De Jesus O, Tobin EH, et al. Tetanus (Clostridium tetani Infection) [Updated 2024 Feb 26]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK482484/
Médecins Sans Frontières. Human Tetanus Immunoglobulin (HTIG). In: MSF Medical Guidelines. Accessed January 7, 2025. https://medicalguidelines.msf.org/en/viewport/EssDr/english/human-tetanus-immunoglobulin-htig-16688425.html
Physician’s Desk Reference: Tetanus Immune Globulin Human. HyperTET S/D (tetanus immune globulin (human)) dose, indications, adverse effects, interactions… from PDR.net. https://www.pdr.net/drug-summary/HyperTET-S-D-tetanus-immune-globulin–human–2085.1437. Accessed April 5, 2023.

Reviewed and Edited By

Arif Alper Cevik, MD, FEMAT, FIFEM

Red and Painful Eye (2025)

January 6, 2025January 7, 2025 ~ iEM Education Project Team ~ Leave a comment

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 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

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 work, CC BY-SA 3.0, Link

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.

By Community Eye Health

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 work, CC BY-SA 4.0, Link

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.

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

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)

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 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

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.
Visual Acuity:
- Right eye: Decreased to 20/70.
- Left eye: 20/30.
Visual Fields:
- Unremarkable.
Extraocular Muscle Movement:
- Smooth pursuit.
- No diplopia, nystagmus, or pain.
Pupils and Anterior Chamber:
- Right pupil: Fixed, mid-dilated, poorly reactive to light.
Intraocular Pressure:
- Tono-pen readings: 50 mmHg in the right eye, 24 mmHg in the left eye.
Slit-lamp Examination:
- Shallow anterior chamber.
- Corneal clouding and edema.
- Cataractous lens.
Eye Adnexa:
- Lids, lashes, and lacrimal system: Normal.
Posterior Chamber:
- Difficult to assess in the ED due to corneal cloudiness.
Direct Ophthalmoscope:
- Difficult to perform.
- Red reflex: Reduced in the right eye.
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

Gina Rami Abdelmesih

Amna AlMaazmi

Ahmed AlSaadi

Listen to the chapter

References

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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.
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.
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.
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.
Bonini S. The red eye. Eur J Ophthalmol. 2021;31(6):2843-2849. doi:10.1177/11206721211024827.
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.
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.
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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.
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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

Arif Alper Cevik, MD, FEMAT, FIFEM

Approach To Undifferentiated Patients (2025)

January 6, 2025January 6, 2025 ~ iEM Education Project Team ~ Leave a comment

by Ibrahim Sarbay

Introduction

Emergency medicine differs significantly from other healthcare settings where patients are treated. Anyone can present to the Emergency Department (ED) at any time, on any day. Many patients may believe that the ED is capable of diagnosing and treating all their medical problems, as they are often unaware of the broader healthcare system’s structure and the specific purpose of EDs. Additionally, some patients may view the ED as a shortcut to quickly access medical care without the need for appointments. However, EDs worldwide are often overcrowded. As a result, Emergency Medicine (EM) physicians must evaluate patients as quickly as possible and proceed to the next patient waiting for care.

Furthermore, ED resources are limited. It is often not feasible to perform all the laboratory tests and imaging studies necessary for a definitive diagnosis within the ED setting.

Patients who present to the ED often believe they require urgent medical attention, and they are typically unfamiliar with the emergency physician treating them. This creates three critical challenges:

The patient is often anxious about their health condition and seeks quick, clear answers.
The physician must establish a relationship of trust with the patient in a very short time and under suboptimal conditions.
The physician may find it challenging to identify subtle changes in the patient’s condition at first glance, as they lack a baseline understanding of the patient’s “normal” appearance or state.

These challenges may initially seem daunting. However, as Dan Sandberg famously remarked, “Emergency Medicine is the most interesting 15 minutes of every other specialty.” Emergency physicians thrive on overcoming these obstacles by employing powerful and innovative approaches.

In this section, we will explore how Emergency Medicine specialists approach complex and undifferentiated patients in the ED, taking a journey through the thought processes and strategies of Emergency Medicine.

Triage

We mentioned above that EDs are unique. It is not possible to predict how many patients will present to the ED at any given time or how many resources will be required for their diagnosis and treatment. Triage is used both to evaluate the urgency of patients and to prioritize them accordingly, as well as to organize and evaluate EDs.

Patients admitted to the ED are first evaluated by a healthcare professional trained in triage, provided their clinical condition allows. The patient’s chief complaint and symptoms, vital signs, allergies, medications, past medical/surgical history, last food and drink, and a brief history of present illness are recorded. Afterward, the triage professional determines the patient’s triage level according to the triage system used in their ED.

There are various triage systems that are widely accepted worldwide. One of the most commonly used 5-level triage systems is the Emergency Severity Index (ESI) [1]. ESI classifies patients according to the severity of their complaints and the estimated number of resources needed, with level 1 being the most urgent and level 5 being the least urgent, as follows [2]:

ESI Level 1 (Immediate) – Patients with life-threatening conditions requiring immediate medical intervention.
ESI Level 2 (Emergent) – Patients with high-risk situations or severe distress, necessitating rapid attention.
ESI Level 3 (Urgent) – Patients with multiple or complex problems requiring multiple resources but able to tolerate a short wait.
ESI Level 4 (Semi-Urgent) – Patients with less complex issues, needing one resource and able to wait longer for care.
ESI Level 5 (Non-Urgent) – Patients with minor complaints, requiring minimal resources and able to wait without significant risk.

After the patient’s triage level is determined, he/she is directed to the appropriate area in the ED. The emergency physician begins the evaluation of the undifferentiated patient by reviewing the triage notes in the patient’s file.

For many patients, the triage notes provide sufficient information to formulate a probable diagnosis, enabling a focused examination without requiring a detailed clinical evaluation or further investigations. For example, if the triage notes indicate a patient is complaining of pain in their third finger after being hit by a ball while playing basketball, the physical examination can be focused on their hand.

However, patients presenting to the ED are often more complex, and the triage notes are frequently insufficient for making an immediate diagnosis. For these patients, a systematic approach is employed, starting with the Primary Survey, to identify the proper diagnosis and performing life saving actions.

Primary Survey

After quickly reviewing the triage notes, we proceed with the Primary Survey. In this stage, we aim to rapidly identify and address any life-threatening conditions using the ABCDE assessment. Each letter of ABCDE represents a distinct step of the evaluation: Airway, Breathing, Circulation, Disability, Exposure. At each step, we ensure there are no issues in the focused area of the patient. If any problems are identified, they must be managed before proceeding to the next step.

If the patient is conscious and alert, we may directly ask, “How are you?” If the patient’s eyes are closed or he/she appears unresponsive, we may touch his/her shoulder and ask, “Are you okay?” If the patient responds normally, it indicates that the airway is patent, breathing is adequate, and brain perfusion is sufficient. However, if the patient can only speak in short sentences, this may be a sign of respiratory distress. If the patient is completely unresponsive, this is a clear indication that he/she is in a critical condition.

Airway:

In the airway step, we aim to ensure that the patient’s airway is open and unobstructed. We check if the patient’s voice is clear and if breathing sounds are normal. We evaluate for signs of airway obstruction, such as facial trauma, swelling, hoarseness, or stridor. Conditions such as the presence of a foreign body in the mouth or excessive secretions may block the airway. In such cases, the patient may require aspiration of oral secretions.

If the patient’s airway is blocked by a foreign body, we encourage coughing. If he/she is unable to cough, we deliver back blows and perform abdominal thrusts (Heimlich Maneuver). If the patient becomes unresponsive, we proceed with cardiopulmonary resuscitation.

If there is a suspicion that the patency of the airway is at risk, we secure the airway with intubation or, if intubation is not possible, surgical airway techniques. If the patient’s oxygen saturation is low, we provide supplemental oxygen therapy.

For trauma patients, we assess for possible cervical spine injuries at this step and provide neck stabilization if necessary.

Breathing:

We evaluate whether the patient is breathing abnormally by checking the respiratory rate (12–20/min), observing chest wall movements, and performing chest percussion. We auscultate the lungs and monitor oxygen saturation levels (97–100%) using pulse oximetry.

A shift in the trachea’s position to one side at the suprasternal notch may indicate a mediastinal shift, which can occur with conditions like tension pneumothorax. If a tension pneumothorax is diagnosed, we perform decompression.

Chest expansion should be symmetrical; unequal expansion may occur with conditions such as pneumonia or thoracic trauma. Absent breath sounds may indicate airway obstruction, hyperinflation, pneumothorax, pleural effusion, or obesity. Additional respiratory sounds, such as wheezes, crackles, or stridor, may provide diagnostic clues [3].

Circulation:

We assess circulation by evaluating the patient’s pulse, blood pressure, and peripheral perfusion. If the patient has a radial pulse, it usually indicates that the blood pressure is within normal limits. If a radial pulse cannot be palpated, we check the carotid pulse.

Is the pulse irregular or weak? We palpate the pulse rate (60–100 bpm), assess skin color and sweating, auscultate the heart, and initiate cardiac monitoring. Capillary refill time, typically less than 2 seconds, can provide insight into peripheral perfusion, although external factors like cold environments or poor lighting may affect this assessment.

We also check for external bleeding, managing it with direct pressure and other necessary interventions. Low blood pressure combined with an increased pulse rate may indicate shock, requiring immediate fluid resuscitation via large-bore IV lines.

Disability:

We evaluate the patient’s neurological status by assessing level of consciousness, orientation, cooperation, facial symmetry, pupillary reflexes, and motor function.

The AVPU method is a quick tool for assessing consciousness:

A: Alert
V: Responds to verbal stimuli
P: Responds to pain stimuli
U: Unresponsive

Alternatively, the Glasgow Coma Scale (GCS) provides a more detailed neurological evaluation. Impaired consciousness is not always caused by neurological problems; conditions such as hypoglycemia, hypotension, hypercarbia, or carbon monoxide poisoning can also present with neurological symptoms. These can be excluded by evaluating pulse oximetry, finger-stick blood glucose, and arterial blood gas analysis.

Exposure:

We fully expose the patient to inspect the entire body for trauma, bleeding, rashes, needle marks, medication patches, or other abnormalities [4]. If the patient is a trauma victim, we ensure cervical spine immobilization during this step.

Completion of the Primary Survey:

Once the Primary Survey is completed, we address all identified life-threatening conditions. Patients deemed unstable by the emergency physician should always have vascular access, cardiac monitoring, and required blood tests performed. If necessary, oxygen therapy should be initiated. These interventions must be performed simultaneously, as time is critical in managing critically ill patients.

Differential Diagnosis

There may be thousands of diseases and clinical conditions that lead a patient to visit the ED. However, Emergency Medicine aims to distinguish potentially life-threatening conditions (life- or limb-threatening conditions) among these causes. We review vital signs, patient notes, and the results of the Primary Survey to formulate possible differential diagnoses.

Medical decision-making is a skill that can be developed over time through a combination of professional experience and accurate clinical information. Unfortunately, as humans, we are prone to cognitive biases [5]. However, understanding which cognitive biases exist and recognizing the most common mistakes in each clinical situation will undoubtedly enhance our success in clinical decision-making processes.

Secondary Survey

After treating our patient’s immediate life-threatening conditions and ensuring they are stable, the next step is the Secondary Survey. In this step, we take a focused history and perform a physical examination.

SAMPLE is an abbreviation commonly used in medical history-taking. By asking just six basic but very important questions, we can gain insight into the key aspects of the patient’s history: Symptoms, Allergies, Medications, Past Medical History, Last Oral Intake, and Events leading up to the illness or injury [6].

The SOCRATES acronym is a useful tool for further evaluating each of the patient’s current symptoms. Not every step may be suitable for every symptom; we focus on the steps that are appropriate for the symptom we aim to elaborate on. These steps are: the location of the complaint, its onset, character, radiation, associated symptoms, how it changes over time, exacerbating or relieving factors, and its severity. We ask the patient to rate the severity of the symptom (e.g., pain) on a scale of 1 to 10. This information is especially helpful for assessing changes in symptom severity following treatment (e.g., changes in the severity of pain).

The clinical condition of the patient also determines the extent of the physical examination we perform. For a patient presenting with a clear minor clinical diagnosis (e.g., foot sprain), an additional core physical examination may be sufficient. In contrast, for a critically ill patient (e.g., impaired consciousness), a comprehensive systematic physical examination is essential [7].

In the next step, we conclude by selecting diagnostic tests to support our differential diagnoses.

Clinical Decision Rules and Diagnostic Tests

At this stage of managing an undifferentiated patient, we should have a short list of probable diagnoses. Now is the time to reach the final diagnosis with the help of additional information. Focusing on the key points in signs & symptoms and physical examination, while differentiating each possible diagnosis, may help us achieve this goal.

Differential diagnoses for every major symptom are well-defined in the literature, and algorithms and clinical decision rules are widely available [8] (e.g., HEART Score or Ottawa C-spine Rules). Clinical Decision Rules are “evidence-based tools to assist the practitioner in decision-making for common complaints” [9]. While these rules are scientifically supported, they all have pearls and pitfalls. It is important to remember that they are not meant to replace critical thinking, and clinical decisions should not be made solely based on them.

There are many diagnostic tests that we can order in the ED. However, it is crucial to remember that we should never order a test simply because we can. When ordering a test, we must always consider its indications and (if any) contraindications, the way the test result will guide us, and its limitations. Therefore, a deep understanding of pre-test probabilities and test characteristics is essential for every clinician.

Decisions

The timeframe between the onset of symptoms in patients and their visits to the ED is not standardized. Sometimes, patients arrive at the ED within minutes (e.g., trauma). However, the patient may not show any signs of the disease at that exact moment, which may lead us to miss the real diagnosis. Therefore, it is vital to observe and re-evaluate patients multiple times over a period of time. This allows us to monitor the course of the illness, assess the effects of treatment, and ensure the accuracy of our initial diagnosis.

There are three possible decisions for an ED patient: hospital admission, transfer, or discharge. While each illness diagnosed in the ED has different admission and discharge statistics available in the literature, factors such as the capabilities of our facility, severity of the disease, comorbidities, and social support status influence the decision for each patient. As the sayings go: “Treat the patient, not just the disease” (Hominem non morbum cura) and “Treat the patient, not just the lab results.”

Sometimes, the need for admission will be clear to both you and the consultant. At other times, you may be certain that the patient requires admission, but the consultant may disagree. Similarly, some patients may accept your decision for admission, while others may not. In every scenario, it is essential to stay on the patient’s side and ensure that the chaotic moments in the ED or your own fatigue do not deprive the patient of the medical care he/she deserves.

To draw an analogy, consider construction sites: safety nets are installed to catch falling workers and reduce the likelihood of injury or mortality. If we think of the ED as a construction site, patients who are incorrectly discharged are akin to individuals falling from heights without a safety net. Telling patients, “You have no problems, you are just fine” without providing further guidance during discharge could result in missed opportunities for correction. Should the patient’s condition worsen, they might not return to a health facility, relying on the false assurance that they were told they had no issues.

This is why discharge recommendations are critically important—a concept known as “safety netting.” For example, let’s assume we are discharging a patient who presented with abdominal pain, and all investigation results are within normal limits. By explaining the red flags of abdominal pain and advising the patient to return to the ED immediately if symptoms worsen, we increase the likelihood that they will seek care again if needed, giving us a second chance. The difference between saying “You don’t have anything wrong” and “There are no signs of an emergency for now, but…” is as significant as the difference between installing a safety net at a construction site and not installing one.

Never say, “It won’t happen to me/my patient” out of false optimism. Remember, “Whatever can happen, will happen,” and as healthcare providers, we must always remain skeptical and prepared for any eventuality.

After all, a life is at stake.

Author

Ibrahim Sarbay

Ibrahim Sarbay is an Emergency Medicine Specialist living in İstanbul, Turkey. He graduated from KOU School of Medicine in 2011 and has a Master's Degree in Health Care Administration. He is particularly interested in managing Emergency Departments, working on decision support systems & diagnostic algorithms, and improving patient care in underrepresented patient groups. Writing online since 2002, Sarbay has published more than 1,000 posts mostly about science, life tips, self-improvement, and values. He co-founded Opereyşın, one of Turkey's most notable community blogs, in 2005. He was selected as a Top Writer of Medium Turkey in 2016. He won the Young Talents Award at TATKON 2019 Congress. His dissertation was one of the very first dissertations about COVID-19 published in Turkey. Currently, he writes for a favorite Turkish FOAMed blog, acilci.net, and iEM Education Project. He also shares his journey of learning through social media and likes researching, web programming, and making infographics.

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References

Kuriyama A, Urushidani S, Nakayama T. Five-level emergency triage systems: variation in assessment of validity. Emerg Med J. 2017;34(10):703-710. doi:10.1136/emermed-2016-206295.
Gilboy N, Tanabe P, Travers D, Rosenau A, Eitel D. Emergency Severity Index, Version 4: Implementation Handbook. Rockville, MD: Agency for Healthcare Research and Quality; 2005.
Sarkar M, Madabhavi I, Niranjan N, Dogra M. Auscultation of the respiratory system. Ann Thorac Med. 2015;10(3):158-168. doi:10.4103/1817-1737.160831.
Thim T, Krarup NH, Grove EL, Rohde CV, Løfgren B. Initial assessment and treatment with the Airway, Breathing, Circulation, Disability, Exposure (ABCDE) approach. Int J Gen Med. 2012;5:117-121. doi:10.2147/IJGM.S28478.
Morgenstern J. Decision Making in Emergency Medicine: We can’t escape bias. First10EM. March 7, 2022. doi:10.51684/FIRS.125798.
The Art of Questioning – Part 1. REAL First Aid. Accessed January 1, 2025. https://www.realfirstaid.co.uk/sample
Rodriguez RM, Phelps MA. An evaluation of the core physical exam in patients with minor peripheral chief complaints. Emerg Med J. 2007;24(12):820-822. doi:10.1136/emj.2007.050336.
Cowley LE, Farewell DM, Maguire S, Kemp AM. Methodological standards for the development and evaluation of clinical prediction rules: a review of the literature. Diagn Progn Res. 2019;3:16. doi:10.1186/s41512-019-0060-y.
Chamberlain S. Clinical Decision Rules. International Emergency Medicine Education Project. Accessed January 1, 2025. https://iem-student.org/clinical-decision-rules/

Reviewed and Edited By

Arif Alper Cevik, MD, FEMAT, FIFEM

Ultrasound-Guided Vascular Access (2025)

January 5, 2025January 5, 2025 ~ iEM Education Project Team ~ Leave a comment

by Zackary Funk & Petra Duran-Gehring

Introduction

Ultrasound (US) guidance has become an increasingly common technique for vascular access in the Emergency Department (ED), with applications for both central and peripheral lines [1-4]. Initially adopted for central venous catheter (CVC) insertion, particularly in the internal jugular vein, US improved placement success rates, decreased complication rates, and shortened insertion times. As US technology and training advanced, its use expanded to peripheral intravenous line (PIV) placement, where studies have demonstrated increased success rates, reduced complications, and less pain, especially for patients with difficult access [1-4]. Difficult IV access, occurring in 10% to 30% of ED patients—particularly those with morbid obesity, IV drug use, hypovolemia, or chronic illness—can delay cannulation due to multiple failed attempts [5]. Ultrasound-guided PIV placement can mitigate these challenges, with one study reporting an 85% reduction in the need for CVCs in non-critical patients through the implementation of a US-guided PIV catheter program [6]. The overall benefits of US-guided vascular access include improved success rates, fewer complications, decreased pain, reduced time to cannulation, fewer attempts required, and improved patient satisfaction [1-4]. While it may add some complexity compared to landmark or “blind” approaches, the ability to directly visualize target vessels makes US-guided vascular access a highly effective and patient-centered technique.

Indications

Intravenous (IV) access is often critically important for many aspects of patient care in the ED [1-3]. These include:

US-Guided Peripheral IV Access:

Patients who have had three or more blind attempts without successful cannulation.
Patients with a history of difficult IV access.
- Always evaluate the patient using traditional visual inspection and palpation before preparing for US-guided peripheral IV access. Factors that contributed to difficult IV access during previous encounters, such as hypovolemia, may not be present during subsequent visits.
Patients who have previously required central line placement solely for IV access.
- As mentioned above, when the clinical situation permits, patients with a history of requiring US-guided vascular access should be evaluated for landmark-based IV sites and/or US-guided peripheral IV sites before proceeding to the more invasive procedure of central venous access.

US-Guided Central Venous Access:
Whenever possible, it is highly recommended to use ultrasound guidance for invasive vascular access procedures, such as central venous cannulation, due to its demonstrated ability to decrease the occurrence of severe complications and increase success rates. The primary indication for ultrasound guidance in central venous access is the need for central venous access itself. Below is a list of specific indications for central venous access [1-4]:

Inability to obtain peripheral IV access required for critical interventions or investigations.
Long-term administration of vasoactive substances (e.g., norepinephrine/epinephrine infusions).
Administration of high-concentration or potentially caustic medications (e.g., hypertonic saline, concentrated or large volumes of potassium chloride).
High-pressure or large-volume infusions, such as massive transfusions in trauma patients with hemorrhagic shock.
Emergent dialysis or plasmapheresis access in patients without established arteriovenous fistulas or other dialysis-capable access.
Transvenous pacemaker placement.

Contraindications

Although there are many benefits of US-guided venous access, some contraindications and considerations should be kept in mind [3,4,7]:

Presence of cellulitis, burns, massive edema, or injuries at or proximal to the proposed insertion sites.
Other injuries, diseases, or anatomical distortions of the affected limb/site that may lead to complications during or after access (e.g., compartment syndrome, extravasation, bleeding from neoplasms, etc.).
Risk of compromised vascular flow distal to the site.
Coagulopathy (considered a relative contraindication).
A capacitated patient declines to undergo the procedure after demonstrating an understanding of the risks and benefits as explained by the care team.

Equipment and Patient Preparation

While the materials and equipment required for peripheral IV access are very similar to those needed for central vascular access, we have separated them into two lists to highlight some key differences. Regardless of the procedure, adherence to hand hygiene practices and the universal use of personal protective equipment are absolutely essential for every procedure.

Equipment for Peripheral IV Access

Ultrasound machine equipped with a high-frequency linear probe.
Examination gloves.
Skin disinfectant (e.g., alcohol swabs, chlorhexidine swabs, povidone-iodine, etc.).
Occlusive ultrasound probe cover.
Sterile ultrasound gel.
Elastic tourniquet.
IV catheter.
IV securement device and dressing.
IV extension tubing and IV port.
Normal saline flush.
Sharps disposal device/container.
Stool or chair (recommended).

Equipment for Central Venous Access

Ultrasound machine with a high-frequency linear probe.
Sterile gloves.
Eye protection.
Central Venous Catheter Kit (if available), which often includes:
- Sterile gown.
- Face mask.
- Bouffant or scrub cap.
- Skin disinfectant swabs (e.g., chlorhexidine, povidone-iodine, etc.).
- Vial of local anesthetic, needle, and syringe.
- 18-gauge introducer needle and syringe.
- #11-blade scalpel.
- Gauze.
- Guidewire.
- Dilator(s).
- Central venous catheter.
- Sterile saline flush syringes.
- Needle driver.
- Suture.
- Dressing.
- Sharps disposal hub.
Sterile occlusive ultrasound probe cover sheath.
Sterile ultrasound gel.
IV ports.

Patient Preparation

Proper patient preparation is essential to ensure the accuracy of line placement and minimize patient discomfort or complications.

Introduction and Identification
Begin by introducing yourself to the patient and confirming their full name.

Patient History and Consent
Inquire about any allergies, phobias, or a history of fainting during previous IV line procedures. Clearly explain the purpose, benefits, and potential risks of the procedure in simple terms. Once the patient or their next of kin fully understands the information, obtain verbal consent. Note that written consent is not required in emergency situations unless mandated by institutional policy.

Alleviating Anxiety
Address any patient concerns and provide reassurance to help alleviate fear or anxiety. Ensuring the patient is calm can significantly improve their experience and the procedure’s success.

Procedure Steps

Here, we will describe the procedural steps for both ultrasound-guided peripheral intravenous access and ultrasound-guided central vascular access. For each procedure, ensure that the ultrasound machine and probes are in good working order and that there is sufficient power or a reliable power source to successfully and safely complete the procedure. Ultrasound probes should be disinfected before and after each use to protect both patients and providers from exposure to bloodborne and other pathogens, even when sterile probe covers are used. For an overview of the procedural steps for ultrasound-guided peripheral IV access, please review the accompanying video.

Image Acquisition in Vascular Access Procedures

Optimizing the image of the target vessel is critical for procedural safety and success in ultrasound-guided vascular access. This section will describe the general principles and equipment needed to obtain and optimize target visualization.

The high-frequency linear ultrasound probe is most commonly used for vascular access procedures as it provides high-resolution images of superficial structures in the body (Figure 2). Although this resolution comes at the cost of limited penetration into deeper tissues, this limitation is rarely an issue due to specific factors influencing the appropriate depth of target vessels for cannulation, as discussed below.

The next step is to ensure proper left-right probe orientation. This is accomplished prior to image acquisition by aligning the probe indicator on the ultrasound screen with the probe indicator on the linear probe itself. According to standard convention, the probe indicator on the device screen will appear as a dot, arrow, manufacturer logo, or other marking on the upper left side of the screen (Figure 3a).

The image nearest the probe indicator on the screen corresponds to the signal emitted from the probe transducer head closest to the physical probe indicator, typically a raised marking or similar feature. A simple technique to confirm orientation involves applying a small amount of ultrasound gel to one side of the probe face, touching this area with a gloved finger, and observing where the movement appears on the screen (Video 1). Once the two markers are aligned, rightward movement on the screen will correspond to movement away from the probe indicator in physical space.

Once orientation is established, perform a survey scan of the site. After applying an elastic tourniquet (if peripheral IV access is being attempted), position the probe perpendicular to the long axis of the extremity or the anticipated course of the target vessel (Figure 4).

This generates a “transverse,” “short-axis,” or “cross-sectional” image of the vessel. If the screen appears too dark to delineate structures, increase the gain setting to brighten the image. Conversely, if the screen is too bright, decrease the gain setting. Vessels should appear as circular structures with a dark or “anechoic” center, indicating blood within the lumen that allows the ultrasound beam to pass through easily (Figure 5).

Several critical aspects of the target vessel must be assessed during imaging to ensure suitability for cannulation, including vessel type (venous vs. arterial), diameter, depth, patency, and proximity to other structures.

Vessel Assessment: Begin by verifying that the target is a vein. Veins have thinner walls compared to arteries and are compressible. Gentle pressure applied to the vein should cause the walls to collapse inward and meet, confirming its venous nature. Compression also ensures there is no intraluminal obstruction, such as a venous clot (Video 2).

Video 2 – applying pressure to the vessels

Next, assess the vessel’s depth using the depth markers displayed on the ultrasound screen, which typically indicate depth in centimeters. For example, a vessel aligned with the second hash mark from the top of the screen would be located at a depth of 2 cm from the skin surface (Figure 6).

Once the depth is measured, determine the vessel diameter, which is essential for selecting the appropriate catheter size for peripheral IV access. Finally, rotate the transducer 90 degrees to visualize the vessel in its long axis, ensuring that the target location is not near a branch point or valve.

Catheter Selection: In peripheral IV access, depth and diameter measurements determine the appropriate catheter size. Peripheral IV catheters vary in diameter (gauge), with smaller gauge numbers indicating larger catheter diameters (e.g., 16G is larger than 22G). A vessel diameter greater than 4 mm (0.4 cm) can accommodate an 18G or smaller catheter without occlusion.

Catheters also come in various lengths, which affect their stability and suitability for deeper vessels. The depth of the target vessel determines the required catheter length, as longer catheters provide greater stability within the vein [2,3].

The needle length required to reach the target vessel can be approximated using the Pythagorean theorem:

a² + b² = c²,

where c represents the needle track (hypotenuse. figure 8), a is the vessel depth, and b is the distance from the probe to the needle insertion point. For example, for a vessel 1.2 cm deep with a needle insertion point 1.2 cm distal to the probe, the calculation would be:

1.2² + 1.2² = c²,

resulting in c = 1.69 cm. A simpler method is to multiply the vessel depth by 1.4 (e.g., 1.2 cm × 1.4 = 1.68 cm). To ensure catheter stability within the vein, use the following formula to estimate the necessary catheter length:

Catheter Length = (Vein Depth × 1.4) × 3

This formula accounts for 1/3 of the catheter length reaching the vessel and 2/3 residing within the vein lumen. For example, a 6 cm catheter should not be used for vessels deeper than 1.6 cm.

For peripheral venous access, the following characteristics define an appropriate target vessel for US-guided peripheral IV access:

Easily compressible with light pressure applied using the ultrasound probe.
Follows a straight path as it travels proximally.
Lacks valves that would impede the passage of the cannula or flow after insertion.
Diameter greater than 0.4 cm.
Close to the skin surface, at a depth of less than 1.6 cm.

For central venous access, the same general principles apply. Regarding vessel diameter and depth, large-diameter vessels that are as superficial as possible are optimal. However, given the nature of these vessels in adult patients and the equipment used for central venous access, the exact parameters regarding diameter and depth mentioned for peripheral vein characteristics do not rigidly apply. Large-diameter vessels such as the internal jugular veins, subclavian veins, and femoral veins are preferred, and access should ideally be attempted at the point where the vessel is located as superficially as possible [4].

Regardless of whether peripheral or central IV access is utilized, the procedure under ultrasound guidance involves dynamically guiding the needle tip to prevent complications. Dynamic cannulation can be performed using either a transverse, out-of-plane approach or a longitudinal, in-plane approach. The transverse view, also known as the out-of-plane approach, is the most commonly used and involves visualizing the needle as a hyperechoic (bright) dot on the ultrasound screen. In contrast, the in-plane approach allows direct visualization of the entire needle length in a long-axis plane but is more challenging for novices, as the needle must remain within the ultrasound beam.

As the metallic needle within the catheter is hyperechoic, it appears as a white dot in the transverse plane and a long hyperechoic line in the longitudinal plane (Figure 9).

In the transverse plane, it is critical to track the needle tip as it pierces the ultrasound beam, as the appearance of the needle looks the same regardless of its position along the beam. This tracking is achieved by alternating movements of the transducer and the needle. By “leading” with the transducer, then advancing the needle, the tip can be visualized first. Once the needle is seen, advancement should pause, and the transducer should slide slightly proximal up the vein where the needle is no longer visible, after which the needle can be advanced again (Figure 10). This alternating movement allows visualization of the tip as it progresses through the soft tissue and can be repeated until the vein is cannulated (Video 3).

Figure 10a - Walking down the vein: This sequence illustrates the process of "walking down the vein" as observed on an ultrasound. From left to right: the needle initially appears, then disappears, and later re-emerges deeper within the soft tissue before vanishing again. This phenomenon occurs due to the probe moving away, and when the needle reappears, it simply aligns with the ultrasound beam. Note that in real-time, the needle’s positional changes are more gradual than shown here; the figure above is a simplified representation of the concept (refer to the accompanying video for details). [The image was provided by authors].

Video 3 – Walking down the vein

Once the needle is visualized within the vein, the transducer can be rotated to ensure that the needle tip is within the vein lumen and has not pierced the back wall of the vessel. This visualization also allows for redirection of the needle before catheter insertion, ensuring smooth placement when the catheter is advanced off the needle (Video 4). For central venous catheters, a guidewire is inserted after confirming the needle’s position within the vein lumen.

Video 4 – provided by authors

After successfully inserting the IV line, blood return should be verified, and the catheter should be secured in place. As a final confirmation, flush the line. For peripheral IVs, place the ultrasound transducer proximally from the IV site, flush the line, and observe for turbulence or a “glitter artifact” caused by fluid rushing through the vein (Video 5).

Video 5 – provided by authors

This step confirms successful IV cannulation and can also assist in troubleshooting. If the “glitter” does not appear within the vein, the IV catheter is outside the vessel and unusable. For central lines, this confirmation can be performed by visualizing the “glitter” artifact in the right ventricle using the subxiphoid plane within three seconds of flushing the distal port of the line (Video 6).

Video 6 – Glitter Artifact [the video was provided by authors]

Step by Step Guide for US-Guided Peripheral IV Access [3,8]

Verify the identity of the patient who is to undergo IV access and explain the procedure to the patient/healthcare surrogate (when possible).
Position the ultrasound machine on the same side of the patient as the operator.
Don examination gloves.
Clean the ultrasound probe with institution-approved disinfectant.
Remove gloves and replace with clean gloves.
Position stool/chair and adjust the ultrasound machine for the best screen viewing when obtaining access.
Apply an elastic tourniquet proximal to the site to be screened for potential access sites.
Apply ultrasound gel to the target area and orient the probe perpendicularly to the patient’s extremity to obtain a transverse/short-axis view of the target vessels.
Orient the probe indicator to match the orientation displayed on the ultrasound screen, with both conventionally indicating the patient’s right side (Figure 3a).
Assess potential veins for appropriate depth, diameter, and patency.
Veins should:
- Be greater than or equal to 0.4 cm in diameter for an 18G catheter.
- Be less than 1.6 cm in depth for a 6 cm length catheter.
- Be easily compressible without evidence of clots, valves, or other obstructions to blood flow.
Clean off ultrasound gel and release the tourniquet.
Clean the selected site with skin disinfectant and allow it to air dry per manufacturer instructions.
Set up supplies (prepare IV catheter, securement device, port, flush, and dressing).
Cover the ultrasound probe with an occlusive cover.
Avoid touching the head of the probe or the portion of the cover that will contact the patient’s skin.
Reapply the tourniquet and ensure the patient’s arm remains in the appropriate position.
Apply sterile ultrasound gel to the site.
Do not touch the site with gloves or allow uncleaned materials/surfaces to come into contact with the site.
If the site is potentially contaminated, remove the gel and clean the site again before attempting vascular access.
Position the probe and locate the target vein again.
At approximately a 45-degree angle, puncture the skin underneath the ultrasound probe head, observing on ultrasound for the needle tip in the subcutaneous tissue.
Once the needle tip has been visualized, slide the probe proximally away from the needle tip.
Once the needle tip is no longer visualized on ultrasound, carefully advance the needle in 1-2 mm increments until the needle tip returns into view on ultrasound.
Repeat this alternating probe-needle advance until the needle has been advanced into the target vessel (Video 3).
Decrease the angle of the needle as needed to continue advancing the needle in the alternating probe-needle manner within the vessel, keeping the needle tip in the center of the vessel lumen.
Once the needle has been advanced several millimeters into the target vessel, anchor the hand holding the needle to ensure it does not advance further and lay down the ultrasound probe.
Keeping the needle still, advance the catheter over the needle into the vessel.
Once the catheter has been advanced, keep the catheter in place with the hand which advanced the catheter and use the other hand to carefully remove the needle.
Ensure the safety needle capping mechanism on the needle has activated (if automatic upon needle removal from catheter) or activate the safety needle capping mechanism (if not designed to engage automatically) and dispose of the needle into a designated sharps container.
Attach extension tubing and port to the catheter hub (some catheters come with the extension tubing and hub pre-attached).
Clean any remaining ultrasound gel or blood from the access site and secure the catheter with an occlusive dressing.
Attach a saline flush to the hub.
If any air remains in the catheter extension tubing (if applicable), be sure to aspirate any air prior to attempting to flush the line.
Retrieve the ultrasound probe and place it along the vessel proximal on the extremity to the catheter.
After confirming the absence of air in the catheter and extension tubing, flush several cc’s of crystalloid solution through the catheter.
If the catheter is in the correct position and functioning correctly, a “glitter” artifact effect should be visualized within several seconds of pushing the fluid through the catheter (Video 6).
Dispose of supplies in appropriate containers and clean the ultrasound probe with disinfectant wipes.
Remove gloves and wash hands.
Document the access site in the patient’s chart, including site location, catheter gauge, time placed, and operator placing the line.
Ensure you and your team frequently assess the site and extremity for evidence of extravasation, hematoma formation, or other complications.

Step by Step Guide for US-Guided Central Venous Access [4,9]

Verify the identity of the patient who is to undergo IV access and explain the procedure to the patient/healthcare surrogate (when possible).
Position the ultrasound machine on the opposite side of the patient as the operator in the operator’s line of sight.
Don examination gloves.
Clean the ultrasound probe with institution-approved disinfectant.
Remove gloves and replace with clean gloves.
Apply ultrasound gel to the target area and orient the probe perpendicularly to the patient’s extremity to obtain a transverse/short-axis view of the target vessels.
Orient the probe indicator to match the orientation displayed on the ultrasound screen, with both conventionally indicating the patient’s right side (Figure 3a).
Assess potential veins for appropriate depth, diameter, and patency:
Veins should:
- Be greater than or equal to 0.4 cm in diameter for an 18G catheter.
- Be less than 1.6 cm in depth for a 6 cm length catheter.
- Be easily compressible without evidence of clots, valves, or other obstructions to blood flow.
Clean off ultrasound gel.
Clean the selected site with skin disinfectant and allow it to air dry per manufacturer instructions.
Open the central venous catheter kit (or, if unavailable, establish a sterile field upon which to place sterile equipment).
Don eye protection, face mask, and bouffant/scrub cap.
Don a sterile gown and gloves.
Drape the patient in a sterile fashion.
Place the dominant hand within a sterile ultrasound probe cover (if rubber bands to secure the sheath to the probe are included, consider applying rubber bands around the thumb of the dominant hand before placing the hand within the sheath).
Apply sterile gel to the inside of the sheath, which will contact the ultrasound probe head.
Have an assistant pass the linear probe and grab the probe head with the dominant hand surrounded by the ultrasound probe sheath.
Carefully extend the sheath around the probe. Once able, ask an assistant to grab the open end of the probe sheath and pull it toward them along the probe’s wire until it is well away from the sterile field. The assistant can gently release the probe wire now covered in the sheath, being careful not to let the contaminated end of the probe cover touch the sterile field.
Apply the rubber bands (if applicable) to the head of the probe and smooth any air bubbles or irregularities which may have formed along the transducer surface while inserting the probe.
Draw up several cc’s of local anesthetic into a syringe.
Apply sterile ultrasound gel to the target site and confirm there has been no change in positioning of the target vessel during setup.
Inject the local anesthetic into the skin and along the track of the needle to the target vessel, being sure to aspirate before each injection.
It is recommended that the injection of the local anesthetic be performed under active ultrasound guidance to minimize the chance of accidental injection into the vessel and to confirm the anesthetic is applied along the intended tract of the needle.
Ensure that air bubbles have been removed from the local anesthetic solution prior to injection, as these air bubbles will distort visualization of the target vessel area due to scattering of the ultrasound beam as it comes into contact with air.
While the local anesthetic takes effect, flush the lumens of the catheter with saline to prevent the introduction of air into the patient’s vasculature and test that the guidewire feeds smoothly and is free of kinks or defects.
With the introducer needle at an approximately 45-degree angle, puncture the skin underneath the ultrasound probe head, observing on ultrasound for the needle tip in the subcutaneous tissue.
Once the needle tip has been visualized, slide the probe proximally away from the needle tip.
Once the needle tip is no longer visualized on ultrasound, carefully advance the needle in 1-2 mm increments until the needle tip returns into view on ultrasound (Figure 8).
Repeat this alternating probe-needle advance until the needle has been advanced into the target vessel, pulling back on the needle plunger to aspirate blood upon entry into the vessel.
Decrease the angle of the needle as needed to continue advancing the needle in the alternating probe-needle manner within the vessel, keeping the needle tip in the center of the vessel lumen.
Once the needle has been advanced several millimeters into the target vessel, anchor the hand holding the needle to ensure it does not advance further and lay down the ultrasound probe.
Keeping the needle still, lay down the ultrasound probe, remove the syringe from the needle, and retrieve the guidewire.
Advance the guidewire through the introducer needle approximately 20 cm, ensuring that it passes freely without resistance. If resistance is encountered, stop advancing immediately and assess the situation.
Keeping one hand on the guidewire at all times, withdraw the introducer needle over the guidewire and place it in a sharps disposal device or bin.
Confirm that the guidewire is in the target vessel using ultrasound to visualize the guidewire in the vessel in long-axis (Figure 9).
Place gauze nearby the guidewire insertion site for use in the upcoming step.
Place the dilator over the guidewire and advance it toward the skin, stopping several centimeters above the skin.
Using the scalpel, make a small linear incision with the blade directed away from the guidewire and the patient. Consider placing gauze over the site after the incision to minimize bleeding.
Using the dominant hand, insert the dilator to the approximate depth of the vessel visualized on ultrasound, using the other hand to hold the guidewire.
It is recommended to use a twisting motion while advancing the dilator with the hand gripping the dilator just above the patient’s skin.
Ensure that the guidewire remains stationary during dilatory insertion.
Remove the dilator over the guidewire and thread the central venous catheter over the guidewire.
Advance the catheter into the vessel over the guidewire while keeping one hand on the guidewire at all times.
The guidewire should emerge from the distal port of the catheter (typically marked with a brown hub and located in the center of the available ports).
Once the catheter has been placed at the appropriate depth into the target vessel, aspirate blood using a syringe from all ports to ensure patency.
Flush all ports with saline to minimize the chance of clotting.
Use the needle driver and suture to secure the line in place.
Clean the site once more and apply an institution-approved antimicrobial dressing.
If the line was placed in an internal jugular or subclavian vein site, obtain a post-procedural chest radiograph to confirm appropriate placement and assess for complications (e.g., pneumothorax).

Complications

Ultrasound-guided venous access, while generally safer than traditional landmark techniques, still carries potential complications, both for peripheral and central line placement.

Complications of US-Guided Peripheral IV Access [1-3,8]

Infiltration/Extravasation: This is a common complication where IV fluid or medication leaks into the surrounding tissue instead of flowing into the vein. It is a leading cause of catheter failure and may occur more frequently with deep brachial veins compared to other antecubital veins. Using a longer catheter can help minimize the risk of infiltration.

Catheter Dislodgement: Catheter dislodgement occurs when the catheter moves out of the vein, leading to loss of venous access and potential extravasation. This complication is more common with deep veins compared to superficial veins. To reduce the risk, it is essential to ensure that a sufficient length of the catheter is properly positioned within the vessel.

Thrombophlebitis: Thrombophlebitis refers to the inflammation of the vein, which may occur during or after IV placement.

Infection: Although studies have shown no increased infection rates with ultrasound guidance compared to traditional methods, the risk of infection remains. Using sterile gel and adhering to proper cleaning techniques can significantly reduce this risk.

Damage to Adjacent Structures: There is a risk of damaging nearby structures, such as arteries and nerves, during peripheral IV placement. This risk is heightened when using deep veins, which are often located closer to these critical structures.

Posterior Vessel Wall Puncture: The short-axis technique, commonly used during ultrasound-guided IV access, has been associated with a higher risk of puncturing the posterior (back) wall of the vessel.

Hematoma: Bleeding and hematoma formation can occur as a result of vein trauma during catheter placement.

Premature Catheter Failure (PCF): Premature catheter failure occurs when the catheter fails within 24 hours of placement. Studies suggest that PCF rates are higher in ultrasound-guided cannulations compared to traditional methods. Common causes include infiltration, dislodgement, and thrombophlebitis.

Complications of Ultrasound-Guided Central Venous Catheter (CVC) Access [4,9,10]

Arterial Puncture/Cannulation: Accidental puncture or cannulation of an artery, such as the carotid artery during internal jugular vein access, is a serious complication. This risk can be mitigated by using real-time ultrasound guidance and ensuring careful visualization of surrounding structures.

Hematoma: Bleeding and hematoma formation are potential complications during central venous catheter placement, especially if there is accidental puncture of surrounding tissues.

Pneumothorax: A collapsed lung (pneumothorax) is a known complication, particularly during subclavian vein access. Ensuring proper technique and real-time imaging can help reduce this risk.

Hemothorax: Bleeding into the pleural space (hemothorax) may occur during central venous access, especially if there is inadvertent damage to vascular structures near the pleural cavity.

Infection: Catheter-related bloodstream infections are a significant risk associated with central lines. Adherence to strict aseptic technique, including the use of sterile drapes, gloves, and probe covers, is essential to minimize this risk.

Thrombosis: Deep vein thrombosis and catheter-related bloodstream infections can occur as a result of CVC placement. Proper placement, routine monitoring, and prompt intervention are critical in reducing this risk.

Nerve Injury: There is a risk of nerve damage, such as brachial plexus injury, during internal jugular vein catheterization. Careful visualization of anatomical landmarks using ultrasound is critical to avoid this complication.

Catheter Malposition: The catheter may be unintentionally placed in an incorrect location, leading to functional and clinical complications. Real-time imaging during and after placement can ensure proper positioning of the catheter.

Air embolism: It is a rare but serious complication associated with both peripheral and central vein catheterization, which can cause significant neurological deficits and seizures if not promptly diagnosed and treated. The pathophysiology involves air entering the venous system due to a pressure gradient between the atmosphere and the veins, which can occur during catheter insertion, maintenance, or removal. The risk of air embolism is heightened by improper patient positioning. In cases of massive air embolism, immediate interventions such as resuscitation, positioning the patient in the left lateral decubitus and Trendelenburg position, and using hyperbaric oxygen therapy or extracorporeal membrane oxygenation can be life-saving.

Hints and Pitfalls

Universal safety precautions are critical for every procedure. This includes the consistent use of personal protective equipment (PPE) and cleaning all equipment before and after use. These practices are essential to protect both the operator and the patient from harm, including the risk of infections or cross-contamination.

Preparation is paramount to ensuring procedural success and minimizing complications. Proper assessment of the target vessel, including its depth, diameter, and patency, along with setting up the necessary equipment in advance, significantly increases the chances of success during cannulation. Needle tip visualization is also crucial throughout the procedure to prevent iatrogenic injuries caused by inadvertently advancing the needle tip into non-target structures near the vessel.

If a cannulation attempt fails or if the intravenous (IV) line fails due to infiltration, subsequent attempts should ideally be made at a different site to avoid cumulative damage to the same area. If a new site cannot be used, attempts should occur proximal to the initial site.

Strategies to Reduce Complications [1-3, 7-10]

Adequate training is a cornerstone of safe and successful ultrasound-guided venous access. Providers must be proficient in real-time ultrasound guidance techniques, which allow precise needle advancement and proper placement. Additionally, sterile technique is essential during all stages of the procedure, including the use of sterile gel and probe covers to minimize infection risk.

Choosing the appropriate vein for cannulation is another key strategy to reduce complications. This decision should be based on careful vein selection, including evaluating its accessibility and suitability for the intended catheter size. Proper catheter length and size selection are equally important, with tools like the Pythagorean theorem aiding in determining the optimal catheter length for stable placement within the vessel.

Visualization of the needle tip during insertion is vital to avoid injury to surrounding structures. The long-axis approach can provide continuous visualization of the needle tip, ensuring accurate placement within the vessel lumen. After catheter placement, ultrasound can confirm the catheter’s position and patency, reducing the risk of complications such as malposition or infiltration.

Post-procedural monitoring is just as important as the procedure itself. Regular assessment of the insertion site is necessary to detect early signs of infection, thrombophlebitis, or other complications, allowing for timely intervention if needed.

Special Patient Groups

Pediatrics

US-guided venous access in pediatric patients has been shown to significantly enhance the success rates and reduce complications associated with vascular access procedures. A retrospective analysis of 1028 US-guided central vascular access procedures in children demonstrated a high success rate of 97.2%, with the left brachiocephalic vein showing a higher success rate than the right [11]. The integration of ultrasound guidance in pediatric venous access procedures is associated with improved outcomes, emphasizing its role as a preferred method in clinical practice.

Geriatrics

US-guided venous access in geriatric patients has been shown to be a highly effective and safe method for catheter placement. The use of ultrasound guidance significantly reduces failure (success rate of 96.36%) and complication rates (7.27%) [12]. US-guided peripherally inserted central catheter insertion in elderly patients also reported high success rate, with minimal complications [13]. The use of ultrasound guidance for internal jugular vein catheterization further supports its efficacy in reducing failure and complication rates for central venous port placement [14]. Overall, the integration of ultrasound guidance in venous access procedures for geriatric patients enhances safety, reliability, and patient outcomes, making it a valuable tool in the management of this vulnerable population [12-14].

Pregnant patients

US-guided venous access provides significant benefits for pregnant patients, particularly by reducing complications and improving procedural success. Real-time ultrasonographic imaging enables clear visualization of target vessels, which is especially critical in cases of challenging anatomy during pregnancy [15]. This approach aligns with the growing adoption of point-of-care ultrasound (POCUS) to enhance success rates in both peripheral and central venous catheterization. By improving patient safety and minimizing complications, ultrasound guidance has become an essential tool for optimizing venous access procedures and ensuring safer care for pregnant patients [16].

Authors

Zackary Funk

Petra Duran-Gehring

Petra Duran-Gehring M.D., graduated from medical school at LSU Health Sciences Center in New Orleans, and completed her residency in emergency medicine at the University of Florida College of Medicine – Jacksonville. She achieved certification through the American Registry of Diagnostic Medical Sonographers and founded the emergency ultrasound program for the department of emergency Medicine at UFCOMJ. She is a nationally recognized leader in emergency ultrasound education and research, including serving as co-director of the ACEP Ultrasound Management Course, and director for the SEMPA Ultrasound Course. She has lectured throughout the country, and has received numerous teaching awards. When not teaching ultrasound, she loves spending time with her husband and three young sons.

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References

Duran-Gehring P. Ultrasound-Guided IV Access. The Essential Emergency Ultrasound Course; 2019. Accessed August 5, 2023.
Duran-Gehring P, Bryant L, Reynolds JA, Aldridge P, Kalynych CJ, Guirgis FW. Ultrasound-Guided Peripheral Intravenous Catheter Training Results in Physician-Level Success for Emergency Department Technicians. J Ultrasound Med. 2016;35(11):2343-2352. doi:10.7863/ultra.15.11059
Gottlieb M, Sundaram T, Holladay D, Nakitende D. Ultrasound-Guided Peripheral Intravenous Line Placement: A Narrative Review of Evidence-based Best Practices. West J Emerg Med. 2017;18(6):1047-1054. doi:10.5811/westjem.2017.7.34610
Leung J, Duffy M, Finckh A. Real-time ultrasonographically-guided internal jugular vein catheterization in the emergency department increases success rates and reduces complications: a randomized, prospective study. Ann Emerg Med. 2006;48(5):540-547. doi:10.1016/j.annemergmed.2006.01.011
Jacobson AF, Winslow EH. Variables influencing intravenous catheter insertion difficulty and failure: an analysis of 339 intravenous catheter insertions. Heart Lung. 2005;34(5):345-359. doi:10.1016/j.hrtlng.2005.04.002
Au AK, Rotte MJ, Grzybowski RJ, Ku BS, Fields JM. Decrease in central venous catheter placement due to use of ultrasound guidance for peripheral intravenous catheters. Am J Emerg Med. 2012;30(9):1950-1954. doi:10.1016/j.ajem.2012.04.016
Shokoohi H, Armstrong P, Tansek R. Emergency department ultrasound probe infection control: challenges and solutions. Open Access Emerg Med. 2015;7:1-9. Published 2015 Jan 5. doi:10.2147/OAEM.S50360
Blanco P. Ultrasound-guided peripheral venous cannulation in critically ill patients: a practical guideline. Ultrasound J. 2019;11(1):27. Published 2019 Oct 17. doi:10.1186/s13089-019-0144-5
Saugel B, Scheeren TWL, Teboul JL. Ultrasound-guided central venous catheter placement: a structured review and recommendations for clinical practice. Crit Care. 2017;21(1):225. Published 2017 Aug 28. doi:10.1186/s13054-017-1814-y
Parienti JJ, Mongardon N, Mégarbane B, et al. Intravascular Complications of Central Venous Catheterization by Insertion Site. N Engl J Med. 2015;373(13):1220-1229. doi:10.1056/NEJMoa1500964
D’Alessandro P, Siffredi JI, Redondo Pertuz E, et al. Retrospective analysis of 1028 ultrasound-guided central vascular access in neonates and children. J Vasc Access. Published online September 26, 2024. Doi:10.1177/11297298241278385
Sun X, Zhang Y, Yang C, et al. Ultrasound-guided totally implantable venous access device through the right innominate vein in older patients is safe and reliable. Geriatr Gerontol Int. 2019;19(3):218-221. doi:10.1111/ggi.13611
Nakano Y, Kondo T, Murohara T, Yamauchi K. Option of Using Peripherally Inserted Central Catheters in Elderly Patients With Dementia: An Observational Study. Gerontol Geriatr Med. 2020;6:2333721420906922. Published 2020 Feb 18. doi:10.1177/2333721420906922
Canfora A, Mauriello C, Ferronetti A, et al. Efficacy and safety of ultrasound-guided placement of central venous port systems via the right internal jugular vein in elderly oncologic patients: our single-center experience and protocol. Aging Clin Exp Res. 2017;29(Suppl 1):127-130. doi:10.1007/s40520-016-0680-9

Reviewed and Edited By

Arif Alper Cevik, MD, FEMAT, FIFEM

Arterial Blood Gas Sampling (2025)

January 4, 2025January 4, 2025 ~ iEM Education Project Team ~ Leave a comment

by Gan Kiat Kee & Arif Alper Cevik

Introduction

Arterial blood gas (ABG) sampling is a critical procedure performed in the emergency department (ED) that involves obtaining blood from a peripheral artery to assess a patient’s respiratory and metabolic status. This technique is essential for diagnosing and managing various acute conditions, particularly in critically ill patients. The common sites for ABG sampling include the radial, brachial, femoral, and dorsalis pedis arteries. The radial artery is often preferred due to its accessibility and the presence of collateral circulation, which minimizes the risk of complications [1]. ABG sampling can be performed via a single percutaneous needle puncture or through an indwelling catheter for repeated measurements, which is particularly useful in ongoing monitoring of patients with unstable conditions [2].

The analysis of ABG provides vital information regarding the patient’s acid-base balance and respiratory function. Key parameters measured include the partial pressures of oxygen (PaO2) and carbon dioxide (PaCO2), pH, and bicarbonate (HCO3) levels. These measurements are crucial for evaluating the efficacy of gas exchange in the lungs and the metabolic status of the patient [3]. For instance, a low pH coupled with elevated PaCO2 may indicate respiratory acidosis, while a low HCO3 may suggest metabolic acidosis. Additionally, advanced blood gas analyzers can provide further insights by measuring total hemoglobin (tHb), oxyhemoglobin saturation (HbO2), and dysfunctional hemoglobins such as methemoglobin (MetHb) and carboxyhemoglobin (COHb), which are particularly relevant in cases of carbon monoxide poisoning or other hemoglobinopathies [3].

The ability to interpret ABG results is an essential skill for healthcare professionals, particularly in emergency settings where rapid decision-making is crucial. Medical trainees are encouraged to gain proficiency in ABG sampling and interpretation under supervision, as these skills are fundamental to the effective management of patients experiencing respiratory distress, shock, or metabolic derangements [1].

Indications

ABG sampling is primarily indicated for evaluating the adequacy of oxygenation and ventilation in patients. By measuring the partial pressures of oxygen (PaO2) and carbon dioxide (PaCO2), healthcare providers can assess respiratory function and the effectiveness of gas exchange in the lungs. For instance, a low PaO2 may indicate hypoxemia, necessitating immediate intervention, while elevated PaCO2 can signify respiratory failure or impaired ventilation [4]. This immediate assessment is crucial in emergencies such as acute respiratory distress or exacerbations of chronic obstructive pulmonary disease (COPD), where timely identification of respiratory compromise can significantly influence patient outcomes [5].

In addition to evaluating oxygenation and ventilation, ABG sampling is essential for identifying and monitoring acid-base disturbances. The measurement of pH, PaCO2, and bicarbonate (HCO3) levels provides critical information regarding the patient’s metabolic and respiratory status. For example, an acidic pH coupled with elevated PaCO2 may suggest respiratory acidosis, commonly seen in conditions such as acute asthma attacks or severe pneumonia [6]. Conversely, metabolic acidosis may be indicated by a low pH with normal or low PaCO2 levels, often observed in patients with diabetic ketoacidosis or renal failure. Monitoring these parameters can guide therapeutic decisions and help clinicians tailor interventions to restore acid-base balance effectively [6].

Furthermore, ABG sampling plays a significant role in detecting and quantifying abnormal hemoglobin levels, such as methemoglobin (MetHb) and carboxyhemoglobin (COHb). These conditions can arise from exposure to certain chemicals or gases, and their identification is critical in emergency settings. For instance, elevated COHb levels indicate carbon monoxide poisoning, which requires immediate treatment [7]. The ability to quickly diagnose such abnormalities through ABG sampling can be life-saving, particularly in cases of suspected toxic exposure.

Lastly, ABG sampling is invaluable in assessing the response to therapeutic interventions, particularly in hypoxic patients receiving oxygen therapy. By comparing pre- and post-intervention ABG values, clinicians can evaluate the effectiveness of treatments and make necessary adjustments to optimize patient care. In situations where venous sampling is not feasible due to the patient’s condition or the urgency of the situation, ABG sampling serves as a critical alternative for obtaining essential blood gas information [4].

Contraindications

Certain contraindications must be considered to ensure patient safety and the accuracy of results. One primary contraindication is the presence of a known deficiency in collateral circulation, which can be assessed using the modified Allen’s test. An abnormal result indicates insufficient blood flow to the hand, increasing the risk of ischemia if an artery is punctured [8-10]. Therefore, performing an ABG in such cases could lead to serious complications, including limb ischemia or necrosis.

In addition to collateral circulation issues, the presence of local infections at the puncture site is another significant contraindication. An infected site can introduce pathogens into the bloodstream, leading to systemic infections or further complications for the patient [11]. Moreover, anatomical abnormalities such as full-thickness burns, arteriovenous fistulas, stents, or vascular grafts at the puncture site can complicate the procedure and increase the risk of complications. These malformations may alter normal blood flow patterns or make it difficult to locate the artery accurately, which can lead to unsuccessful attempts or injury to surrounding structures [8-10].

Severe peripheral vascular disease, including conditions like Buerger’s disease or limb ischemia, also serves as a contraindication for ABG sampling. In patients with these conditions, blood flow to the extremities is already compromised, and the additional trauma of arterial puncture could exacerbate ischemic symptoms [12]. Lastly, patients suffering from active Raynaud syndrome should be excluded from ABG sampling, as the procedure could trigger or worsen their vasospastic episodes, leading to further complications [13].

Some conditions may pose relative contraindications [8-10] to this procedure. Patients with Raynaud disease may experience exacerbated symptoms during and after the puncture, potentially resulting in complications such as ischemia or necrosis at the site of the arterial puncture [14]. Furthermore, even in the absence of spasm, individuals with a history of Raynaud disease may have altered peripheral vascular function, increasing the likelihood of complications during ABG sampling.

Another important relative contraindication is the presence of poor peripheral perfusion, which can severely affect the ability to obtain an adequate blood sample. In patients with compromised perfusion, such as those in shock or with peripheral vascular disease, the risk of inadequate sampling and subsequent complications at the puncture site is elevated. Poor perfusion can lead to difficulties in locating the artery, increasing the risk of multiple punctures and subsequent tissue trauma [15]. Thus, clinicians must assess the patient’s peripheral circulation before proceeding with ABG sampling to avoid unnecessary complications.

Additionally, patients with supratherapeutic anticoagulation or those receiving thrombolytic agents, such as streptokinase or tissue plasminogen activator, represent another group with relative contraindications for ABG sampling [16]. The risk of bleeding complications in these patients is significantly heightened due to their altered coagulation status. Similarly, individuals with existing coagulopathy should be approached with caution, as the likelihood of significant bleeding increases, which could lead to hematoma formation or other vascular complications. In these cases, the clinical necessity of obtaining an ABG sample must be carefully weighed against the potential risks involved, and alternative methods of assessment should be considered if appropriate.

Equipment and Patient Preparation

Equipment

The equipment used in ABG sampling includes the following [16]:

Gloves: Non-sterile gloves may be used, but it is essential to avoid touching the puncture site after the area has been cleaned.
Syringe for Sampling: A standard syringe with a 25-gauge needle and a 3-mL capacity is preferred. Using a higher-capacity syringe may reduce maneuverability, while smaller needles may increase the risk of traumatic hemolysis, potentially affecting the accuracy of hemoglobin and potassium measurements. A 23-gauge needle may also be used.
Lithium Heparin: Aspirate 1-2 mL of lithium heparin (1000 U/mL) into the syringe through the needle and then expel it. Leave the plunger depressed to allow arterial blood flow to fill the syringe.
Pre-Heparinized ABG Syringe (Alternative): Many ABG kits include a prefilled heparinized syringe with features like a protective needle sleeve and a syringe cap. Some syringe models have vented plungers that enable presetting a specific blood volume; for these, the plunger is positioned midway in the syringe before the puncture and not pulled back during the procedure. Expel the prefilled heparin before repositioning the vented plunger at the 2-mL mark.
Antiseptic Skin Solution: Commonly used solutions include chlorhexidine, povidone-iodine, or 70% isopropyl alcohol.
Needle and Syringe for Local Anesthesia (Optional): A 25-gauge needle with a syringe and 1% lidocaine hydrochloride without epinephrine may be used for local anesthesia if needed.
Sterile Gauze and Adhesive Bandage: Sterile gauze (2 × 2 inches or 5 × 5 cm) is used to cover the puncture site, secured with an adhesive bandage after sample collection.
Syringe Cap: Usually included in ABG kits to seal the syringe after sampling.
Sharps Container: A container specifically designed for the safe disposal of needles and other sharp objects.
Ice Bag: A bag with crushed ice to transport the sample to the laboratory if point-of-care analysis is unavailable.
Non-Sterile Apron: Optional protective clothing to maintain hygiene during the procedure.
Rolled Towel: Used to position the hand optimally for the procedure.

Site Selection

Arterial blood gas sampling requires selecting an appropriate site for puncture based on accessibility, patient tolerance, and anatomical considerations. Below are the common sites used for ABG sampling [17]:

Radial Artery
The radial artery is the preferred site for ABG sampling due to its superficial location, good collateral blood supply, and better patient tolerance. It is located medial to the radial styloid process and lateral to the flexor carpi radialis tendon, approximately 2-3 cm proximal to the ventral surface of the wrist crease. The artery can be palpated between the styloid process of the radius and the flexor carpi radialis tendon with the wrist extended.

Brachial Artery
The brachial artery is harder to access due to its deeper location compared to the radial artery. It is best identified in the antecubital fossa, medial to the biceps tendon, with the shoulder abducted, elbow extended, and the forearm supinated with the palm facing upward. The needle is typically inserted at a 30° angle just above the elbow crease. Higher up, the artery can also be palpated in the groove between the biceps and triceps tendons. The basilic vein and brachial nerve are located in close proximity to this artery.

Femoral Artery
The femoral artery is ideal in cases where the radial and brachial arteries are inaccessible. It is located in the midline between the symphysis pubis and the anterior superior iliac crest, approximately 2-4 cm distal to the inguinal ligament. The artery can be palpated just below the midpoint of the inguinal ligament with the lower limb extended and the patient in a supine position. Needle insertion is performed just below the inguinal ligament at a 90° angle. The femoral artery lies medial to the femoral nerve and lateral to the femoral vein.

Dorsalis Pedis Artery
The dorsalis pedis artery is a less commonly used site for ABG sampling. It can be palpated lateral to the extensor tendon at the midfoot level. This site is generally reserved for specific clinical scenarios where other arteries are not accessible.

Each site has its unique anatomical landmarks and considerations, which should be carefully evaluated to ensure accuracy and minimize complications during the procedure.

Patient Preparation

Proper patient preparation is essential to ensure the accuracy of radial artery blood gas sampling and minimize patient discomfort or complications. Below are the key steps to prepare the patient for the procedure [16,17]:

Introduction and Identification
Begin by introducing yourself to the patient and confirming their full name. Verify that the details on the laboratory form match the patient’s identity to prevent errors.

Patient History and Consent
Inquire about any allergies, phobias, or a history of fainting during previous injections or blood collection. Clearly explain the purpose, benefits, and potential risks of the procedure in simple terms. Once the patient or their next of kin fully understands the information, obtain verbal consent. Note that written consent is not required unless mandated by institutional policy.

Procedure Steps

The following steps outline the procedure for radial artery blood gas sampling, as recommended by W.H.O. guidelines [16,17]:

Patient Introduction and Identification
Approach the patient, introduce yourself, and confirm the patient’s full name. Verify the details on the laboratory form to ensure accurate identification.

Patient Positioning
Place the patient in a comfortable supine position on a firm surface. For radial artery sampling, ensure the arm is resting comfortably with the forearm supinated and the wrist dorsiflexed at approximately 40°. A rolled towel or gauze roll can be placed under the wrist to improve comfort and elevate the radial artery to a more superficial position. Avoid excessive wrist extension to prevent interference from flexor tendons, which could make pulse detection challenging.

Assess Collateral Circulation
Perform a modified Allen test to assess collateral circulation of the radial artery. If the test fails, repeat it on the other hand. Once an adequate site is identified, note the anatomical landmarks for accurate needle placement. If re-palpation is required, ensure sterile gloves are worn.

Preparation of Equipment and Work Area
Perform hand hygiene, prepare a clean work area, and gather all necessary equipment. Don an impervious gown or apron and face protection if there is a risk of blood exposure.
Site Disinfection
Disinfect the chosen puncture site using an antiseptic skin solution such as chlorhexidine or povidone-iodine. Allow the area to air dry completely before proceeding.
Needle and Syringe Assembly
If the needle and syringe are not preassembled, prepare them by attaching the heparinized syringe to the needle and setting the syringe plunger to the required fill level recommended by the laboratory.
Needle Insertion
Hold the syringe and needle like a dart, with the needle bevel facing upward. Use your index finger to palpate the radial pulse, then inform the patient about the puncture. Insert the needle at a 30º–45º angle approximately 1 cm distal to the palpating finger to avoid contamination of the puncture site.
Blood Collection
Advance the needle into the radial artery until a flashback of blood is observed. Allow the syringe to fill passively with 2–3 mL of arterial blood without pulling back the plunger.
Needle Withdrawal and Hemostasis
After withdrawing the required amount of arterial blood, remove the needle while simultaneously applying firm pressure to the puncture site with sterile gauze. Maintain pressure until hemostasis is achieved. For patients without anticoagulation or coagulopathy, this typically takes 3–5 minutes, while anticoagulated patients or those with bleeding disorders or hypertension may require up to 10–15 minutes of continuous pressure. Avoid checking the puncture site prematurely, as this can increase the risk of hemorrhage or hematoma formation.
Needle Safety and Specimen Handling
Activate the needle safety mechanism to cover the needle or use a one-hand scoop technique to recap it. Dispose of the needle safely in a sharps container.
Sample Preparation
Expel air bubbles from the syringe, cap it, and roll the specimen gently between your hands to mix it without compromising the sample’s integrity. Cap the syringe securely to prevent air contamination or leakage during transport.
Labeling and Transport
Label the sample syringe appropriately and place it in a container with ice to preserve the sample. Transport it immediately to the laboratory, ensuring proper handling protocols are followed. Adhere to the recommended time frames for sample analysis to ensure accurate results:
- For samples held at 4°C: Analysis should be conducted within 60 minutes.
- For samples held at room temperature: Analysis should be conducted within 15 minutes.
Cleanup and Hygiene
Dispose of all used materials and personal protective equipment in accordance with hospital protocols. Remove gloves and wash hands thoroughly with soap and water or use an alcohol-based hand rub.
Patient Reassessment
Check the puncture site for ongoing bleeding or other complications. Apply additional pressure if necessary and thank the patient for their cooperation.
Special Considerations
In critically ill or unresponsive patients, explain the procedure to family members or next of kin if possible. Additionally, minimize air bubbles in the sample as they can distort gas readings by altering PaO2 and PaCO2 levels.
Use of Local Anesthesia (Optional)
Local anesthesia, such as lidocaine HCl 1% without epinephrine, may be administered subcutaneously to reduce discomfort [18, 19]. However, this step is not always necessary, as the pain from administering the anesthetic is often comparable to the pain of the procedure itself. If used, 0.5–1 mL of anesthetic should be injected to form a small dermal papule at the puncture site. Care should be taken not to distort the anatomy, and the clinician should aspirate before injection to confirm the needle is not inside a blood vessel.

Post Procedure Care and Recommendations

After completing the blood sampling procedure, appropriate post-procedure care is essential to ensure patient safety and minimize complications [16,17].

Closely monitor the patient for any new symptoms, such as changes in skin color, persistent or worsening pain, active bleeding, impaired limb movement, or altered sensation. Monitoring is particularly crucial for patients receiving anticoagulants or thrombolytic agents, as delayed re-bleeding can occur hours after the procedure.

Complications

The radial artery blood gas sampling procedure, although relatively safe, is associated with several potential complications. These complications and their preventive measures are detailed below [16]:

Arteriospasm and Temporary Arterial Occlusion
Arteriospasm can lead to temporary arterial occlusion, which may compromise blood flow to the affected limb. This can be prevented by helping the patient relax through clear explanations of the procedure, ensuring the patient is in a comfortable position, and using analgesia when necessary.
Excessive Bleeding or Hematoma Formation
Excessive bleeding or hematoma may cause compartment syndrome and subsequent limb ischemia. Prevention involves avoiding puncturing the far side of the artery, applying immediate and firm pressure at the puncture site for at least 3–5 minutes in non-anticoagulated patients, or 10–15 minutes for those on anticoagulants or with coagulopathy. Close monitoring is essential to ensure cessation of bleeding.
Nerve Damage
Nerve damage may occur during the procedure and can present as persistent pain or paresis. To minimize this risk, healthcare personnel should select an appropriate sampling site and avoid excessive redirection of the needle during the procedure.
Vasovagal Response or Fainting Episodes
A vasovagal response may lead to fainting or lightheadedness in some patients. This can be mitigated by ensuring the patient is in a supine position with their feet elevated.
Infection at the Puncture Site or Needle-Stick Injuries
Infection at the puncture site and needle-stick injuries pose risks to both patients and healthcare personnel. Strict adherence to infection prevention and control measures, such as using aseptic techniques and wearing appropriate personal protective equipment, is essential to prevent these complications.
Air or Thrombus Embolism
Air or thrombus embolism may occur if air bubbles are introduced during sampling or if an inappropriate syringe is used. This risk can be reduced by expelling air bubbles from the syringe and using a properly heparinized syringe during the procedure.
Anaphylaxis from Local Anesthetic Agents
Anaphylaxis may occur in response to local anesthetic agents. Taking a thorough patient history regarding previous allergic reactions or anaphylaxis is crucial before administering local anesthesia.
Specific Concerns for Femoral Sampling
In cases involving femoral artery sampling, be particularly cautious about bleeding complications. The larger caliber and deeper location of the femoral artery can allow significant blood accumulation without immediate clinical findings, increasing the risk of circulatory compromise.
Other Notable Complications
- Local Pain: May occur at the puncture site but can be minimized with proper technique and patient reassurance.
- Vessel Laceration: Can result in profuse bleeding, requiring immediate evaluation and management.
- Compartment Syndrome: A rapidly expanding hematoma may compromise regional circulation, necessitating prompt intervention. Symptoms include pain, paresthesias, pallor, absence of pulses, and persistent limb pain.
- Limb Ischemia: Caused by arterial occlusion, thrombus formation, or vasospasm, it may present as absent distal pulses, coldness, and skin discoloration.

Hints and Pitfalls

To optimize the accuracy and success of radial ABG sampling while minimizing patient discomfort and complications, the following considerations should be observed [20]:

Analgesia for Patient Comfort
For patients experiencing anxiety or pain during the procedure, cryoanalgesia can be applied by placing an ice bag on the wrist for 3 minutes before arterial puncture. Alternatively, 0.5–1 mL of lignocaine 1% can be injected superficially to create a small wheal at the puncture site 30–60 seconds prior to sampling. Care should be taken to avoid deeper or larger volume injections, which may distort the anatomy and hinder vessel identification.
Preventing Pre-Analytic Errors
ABG measurements are highly sensitive to pre-analytic errors, including:
- Presence of air in the sample, which can falsely elevate PaO2 and lower PaCO2.
- Collection of venous rather than arterial blood.
- Clotted samples due to improper anticoagulation, inadequate mixing, or exposure to air.
- Delays in sample analysis exceeding 15 minutes at room temperature or 60 minutes at 4°C.
Cooling Samples to Preserve Accuracy
If analysis is expected to be delayed beyond 15 minutes, samples should be stored in a container with crushed ice to reduce metabolic activity of leukocytes and platelets. This prevents oxygen consumption and the associated clinically significant fall in PaO2, particularly in patients with leukocytosis or thrombocytosis.
Impact of Air Bubbles
Air bubbles introduced into the sample equilibrate with arterial blood, artificially increasing PaO2 toward 150 mmHg and decreasing PaCO2 toward 0 mmHg. Careful handling is essential to avoid air contamination.
Use of Heparin as an Anticoagulant
Heparin must be added to the syringe to prevent clotting. Flushing the syringe with heparin leaves an adequate amount in the dead space to ensure anticoagulation without affecting ABG results. Excess heparin should be expelled, as it can alter pH (falsely low) and gas measurements (falsely low PaO2 and PaCO2).
Frequency of Sampling and Site Rotation
The frequency of ABG sampling should be dictated by the patient’s clinical status. Repeated sampling at the same site increases the risk of hematoma, scarring, and arterial damage. Alternative sites should be used, or an indwelling catheter may be considered for patients requiring frequent sampling.
Techniques for Unsuccessful Sampling
Avoid pulling back the syringe plunger during unsuccessful attempts, as this increases the likelihood of venous sampling. Instead, withdraw the needle slowly until it is just beneath the skin and reattempt. Successful arterial sampling is indicated by the passive filling of the syringe with bright red, pulsating blood.

Special Patient Groups

Performing ABG sampling in pediatric patients presents unique challenges due to their fear, anxiety, and anticipation of pain, which may result in uncooperative behavior [20]. It is crucial to explain the procedure thoroughly to both the child and their parents before starting, ensuring informed consent is obtained. Allowing parents to be present during the procedure can provide comfort to the child, but healthcare providers should be mindful of the possibility that the parent may faint. In some cases, physical restraint of the child may be necessary to complete the procedure, although this approach could potentially traumatize the child. An alternative to percutaneous arterial sampling is capillary blood sampling from the heel, which can be used for gas analysis when arterial access is unavailable or when the clinician is less confident performing an arterial puncture.

For infants, arterial blood can be obtained from the radial, brachial, or dorsalis pedis arteries, while the umbilical arteries are an option in newborns. The radial artery remains the site of choice. In these patients, a small-gauge butterfly needle is preferred over the standard needle and syringe used in adults. Unlike adults, continuous but gentle suction should be applied during the procedure, and the appearance of pulsating blood is a reassuring sign that the radial artery has been successfully punctured.

In obese, edematous, or pregnant patients, the anatomical landmarks for arterial puncture may be difficult to identify. In such cases, the use of ultrasound guidance is highly beneficial for locating the artery. Ultrasound not only improves the success rate of arterial access but also reduces potential complications associated with repeated punctures, such as injury to the vessel or surrounding tissues.

Both pediatric and pregnant populations require special attention due to their unique anatomical and physiological considerations. In pediatrics, fear and discomfort associated with the procedure can make the hospital experience traumatic, emphasizing the need for proper explanation, comfort measures, and, when appropriate, pain-reducing products. In pregnant patients, the challenges often stem from anatomical changes caused by fluid retention or increased body mass.

Authors

Gan Kiat Kee

Dr Gan Kiat Kee is an enthusiastic and passionate emergency physician from Hospital Sultanah Aminah Johor Bahru, Johor, Malaysia. He has obtained his medical degree from University Sains Malaysia and completed his post-graduate training in emergency medicine from the same university. He has special interest in acute trauma care and ultrasound guided procedures especially in ultrasound guided regional anaesthesia for pain management in trauma patient. He is also the founder for Emergency Department Regional Anaesthesia (EDRA) of his current working department. Owing to his great interest in simulation and bedside teaching, he has been appointed as adjunct lecturer by Clinical School Johor Bahru, Monash University Malaysia and has been active in teaching various life support.

Arif Alper Cevik, MD, FEMAT, FIFEM

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References

Hassan W, Martinez S. Arterial Blood Gas Sampling [ABG Machine Use]. In: StatPearls. Treasure Island, FL: StatPearls Publishing; 2024. Updated May 9, 2024. Accessed January 1, 2025. https://www.ncbi.nlm.nih.gov/books/NBK606112/
Danckers M. Arterial blood sampling for arterial blood gas analysis. Medscape. Updated February 29, 2024. Accessed January 1, 2025. https://emedicine.medscape.com/article/1902703-overview
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Reviewed and Edited By

Arif Alper Cevik, MD, FEMAT, FIFEM

Chest Pain (2024)

December 31, 2024January 1, 2025 ~ iEM Education Project Team ~ Leave a comment

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.

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:

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.
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.
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.
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.
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.
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:

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.
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.

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].

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

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.

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

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

Khaled Alaboud Alkheder

Tawam Hospital Emergency Medicine Residency Program, United Arab Emirates

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

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.
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.
Malik MB, Gopal S. Cardiac Exam. In: StatPearls. StatPearls Publishing; 2021. Accessed April 26, 2023. https://www.ncbi.nlm.nih.gov/books/NBK553078/
Resuscitation Council UK. The ABCDE approach. Resuscitation Council UK. Published 2021. Accessed April 26, 2023. https://www.resus.org.uk/library/abcde-approach
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.
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.
Ravindranath S, et al. Chest Pain in Children: A Review. Pediatrics. 2017;140(3):e20173032.
Baker R, et al. Pediatric Chest Pain: A Review of the Literature. J Emerg Med. 2020;58(5):738-746.
Glickstein JS, et al. Evaluating Chest Pain in the Pediatric Emergency Department. Pediatr Emerg Care. 2019;35(4):233-238.
Hoffman MK, et al. Chest Pain in Pregnancy: A Review. Am J Obstet Gynecol. 2020;222(5):453-460.
Hernandez AF, et al. Acute Coronary Syndrome in Pregnancy: A Comprehensive Review. Circulation. 2021;143(6):545-558.
Miller JM, et al. Noninvasive Cardiac Imaging in Pregnancy: Safety and Efficacy. J Am Coll Cardiol. 2019;73(2):234-243.
Bennett KJ, et al. Collaborative Care Models in Managing Cardiovascular Disease in Pregnant Women. Obstet Gynecol. 2022;139(4):678-689.
Hernandez AF, et al. Atypical Presentations of Myocardial Infarction in Older Adults. J Geriatr Cardiol. 2022.
McCarthy MJ, et al. Comorbidities and Outcomes in Elderly Patients with Chest Pain. Emerg Med J. 2023.
Huang WC, et al. Impact of Delayed Diagnosis on Outcomes of Chest Pain in Older Adults. Am J Emerg Med. 2021.
Lee JH, et al. Evaluation and Management of Chest Pain in Geriatric Patients. Clin Geriatr. 2023.
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.
Morrow DA, et al. Acute Coronary Syndromes: A Review of Current Guidelines. J Am Coll Cardiol. 2013;62(12):1103-1110.
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.
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.
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Reviewed and Edited By

Arif Alper Cevik, MD, FEMAT, FIFEM

Aortic Dissection (2024)

December 31, 2024December 31, 2024 ~ iEM Education Project Team ~ Leave a comment

by Sreenidhi Vanyaa Manian, & Elizabeth DeVos

You Have A New Patient!

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

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

What Do You Need To Know?

Importance

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

Epidemiology

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

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

Pathophysiology

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

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

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

Medical History

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

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

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

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

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

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

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

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

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

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

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

Physical Examination

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

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

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

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

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

Patients may present with:

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

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

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

Alternative Diagnoses

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

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

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

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

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

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

Acing Diagnostic Testing

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

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

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

63 - AD Stanford A suprasternal view + pericardial effusion

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

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

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

Risk Stratification

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

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

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

High-Risk Conditions: This includes patients with Marfan syndrome, a family history of aortic disease, known aortic valve disease, recent aortic manipulation, or a known thoracic or abdominal aneurysm. It is score of 1.
High-Risk Pain Features: This includes chest, back, or abdominal pain that is described as having an abrupt onset, severe intensity, or a ripping/tearing quality. The presence of such pain features also contributes a score of 1.
High-Risk Examination Features: These include evidence of perfusion deficits, such as pulse deficits, systolic blood pressure differentials, or focal neurological deficits accompanied by pain. Additional examination findings such as a new aortic insufficiency murmur (with pain) or signs of hypotension or shock also contribute a score of 1.

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

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

Management

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

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

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

Medications

Esmolol

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

Labetalol

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

Nicardipine

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

Diltiazem

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

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

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

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

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

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

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

Special Patient Groups

Pediatrics

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

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

Pregnant Patients

Geriatrics

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

When To Admit This Patient

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

Revisiting Your Patient

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

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

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

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

Authors

Sreenidhi Vanyaa Manian

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

Elizabeth DeVos

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

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References

Clouse WD, Hallett JW Jr, Schaff HV, et al. Acute aortic dissection: population-based incidence compared with degenerative aortic aneurysm rupture. Mayo Clin Proc. 2004;79(2):176-180.
Patel PD, Arora RR. Pathophysiology, diagnosis, and management of aortic dissection. Ther Adv Cardiovasc Dis. 2008;2(6):439-468.
Hiratzka LF, Bakris GL, Beckman JA, et al. 2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/STS Guidelines for the Diagnosis and Management of Patients with Thoracic Aortic Disease: Executive Summary. J Am Coll Cardiol. 2010;55(14):1509-1544.
Fattori R, Nienaber CA, et al. Aortic dissection and related syndromes. Nat Rev Cardiol. 2008;5(12):748-759.
Isselbacher EM. Aortic dissection: a review. J Am Coll Cardiol. 2005;46(4):733-742.
Upadhye S, Schiff K. Acute aortic dissection in the emergency department: diagnostic challenges and evidence-based management. Emerg Med Clin North Am. 2012;30(2):307-327.
Stanford W, Armstrong W, et al. Aortic dissection: classification and prognosis. Am J Cardiol. 1966;17(6):807-809.
Helman A. How to Diagnose Aortic Dissection Without Breaking the Bank. ACEP Now. November 2017. Available at: https://www.acepnow.com/article/diagnose-aortic-dissection-without-breaking-bank/. Accessed April 3, 2023.
Hackett A, Stuart J, Robinson DL. Thoracic aortic syndromes in the emergency department: recognition and management. Emerg Med Pract. 2021;23(12):1-28.
Carr D, Helman A. Episode 92 – Aortic Dissection Live from The EM Cases Course. Emergency Medicine Cases. Available at: https://emergencymedicinecases.com/aortic-dissection-em-cases-course/. Accessed April 3, 2023.
Hagan PG, Nienaber CA, Isselbacher EM, et al. The International Registry of Acute Aortic Dissection (IRAD): new insights into an old disease. JAMA. 2000;283(7):897-903.
Hiratzka LF, Bakris GL, Beckman JA, et al. 2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/STS Guidelines for the Diagnosis and Management of Thoracic Aortic Disease. J Am Coll Cardiol. 2010;55(14):e27-e129.
Nienaber CA, Clough RE. Management of acute aortic dissection. Lancet. 2015;385(9970):800-811.
Cannon JW, et al. Aortic dissection: a review. JAMA. 2021;325(19):1952-1963.
Alvi MA, et al. Aortic dissection presenting as stroke: a case series. J Stroke Cerebrovasc Dis. 2018;27(7):1983-1986.
Gaul C, Dietrich W, Friedrich I, Sirch J, Erbguth FJ. Neurological symptoms in type A aortic dissections. Stroke. 2007;38(2):292-297.
Amsterdam EA, Wenger NK, Brindis RG, et al. 2014 AHA/ACC Guideline for the Management of Patients with Non–ST-Elevation Acute Coronary Syndromes. Circulation. 2014;130(25):e344-e426.
Kearon C, Akl EA, Ornelas J, et al. Antithrombotic therapy for VTE disease: CHEST guideline and expert panel report. Chest. 2016;149(2):315-352.
Goldhaber SZ, Bounameaux H. Pulmonary embolism and deep vein thrombosis. Lancet. 2012;379(9828):1835-1846.
Caforio ALP, Pankuweit S, Arbustini E, et al. Current state of knowledge on aetiology, diagnosis, management, and therapy of myocarditis: a position statement of the ESC Working Group on Myocardial and Pericardial Diseases. Eur Heart J. 2013;34(33):2636-2648.
Graham AM, et al. Tension pneumothorax: a review of the literature. Emerg Med J. 2018;35(9):556-560.
Burch MG, et al. Esophageal rupture: a review of the literature. Surg Endosc. 2020;34(5):1952-1961.
Mason RJ, et al. Acute pancreatitis. N Engl J Med. 2019;380(6):561-570.
Baker CJ, et al. Aortic dissection: the stroke mimic. J Neurointerv Surg. 2017;9(7):675-679.
Hagan PG, Nienaber CA, Isselbacher EM, et al. The International Registry of Acute Aortic Dissection (IRAD): design and initial results. Circulation. 2000;102(18):2000-2006.
Gonzalez A, Kwan T, Pacheco E. Aortic dissection: a review of the literature and a case study. J Emerg Med. 2019;57(5):622-628.
Baker S, Kearney P, Casserly I, et al. Aortic dissection: a review of the literature. Emerg Med J. 2002;19(5):413-418.
Keller MS, et al. The Role of Echocardiography in the Diagnosis of Aortic Dissection. Emerg Med J. 2019;36(4):1-7.
Nishimura RA, et al. Transesophageal Echocardiography in the Diagnosis of Aortic Dissection. J Am Coll Cardiol. 2021;77(1):1-10.
Hagan PG, Nienaber CA, Isselbacher EM, et al. The International Registry of Acute Aortic Dissection (IRAD): new insights into an old disease. JAMA. 2000;283(7):897-903.
Sweeney RA, Mullen MG. Aortic Dissection: A Review for the Emergency Clinician. Emerg Med Clin North Am. 2021;39(1):1-16.
Kelley RE, Graham TC, Hirsch R, et al. Pediatric Aortic Dissection: A Review. J Pediatr Surg. 2021;56(5):879-884.
Graham TC, Hirsch R, Kelley RE, et al. Imaging of Aortic Dissection in Children. Pediatr Radiol. 2020;50(12):1724-1732.
Hirsch R, Graham TC, Kelley RE, et al. Aortic Dissection in Children: A Review of the Literature. Pediatrics. 2019;143(1):e20183434.
Harris LA, Hirsch MA, Stark JR, et al. Pregnancy-Related Aortic Dissection: A Case Series and Review. J Vasc Surg. 2016;64(2):466-471.
Baker SB, Stark JR, Hirsch MA, et al. Aortic Dissection in Pregnancy: A Review of the Literature. J Am Coll Cardiol. 2019;73(12):1452-1460.
Hirsch MA, Stark JR, Harris LA, et al. Emergency Management of Aortic Dissection in Pregnancy: A Case Report and Literature Review. Am J Emerg Med. 2020;38(1):232-234.
Miller DC, Stark JR, Harris LA, et al. Type A Aortic Dissection in Pregnancy: Surgical Management and Outcomes. Ann Thorac Surg. 2021;112(2):548-555.
Stark JR, Harris LA, Hirsch MA, et al. Obstetric Considerations in the Management of Aortic Dissection. Obstet Gynecol Clin North Am. 2018;45(2):233-245.
Davis SM, Harris LA, Hirsch MA, et al. Management of Aortic Dissection in Pregnant Patients. Obstet Gynecol. 2022;139(5):850-858.
Yuan SM. Aortic dissection during pregnancy: a difficult clinical scenario. Clin Cardiol. 2013;36(10):576-584.
Tsai TT, Nienaber CA, Eagle KA. Aortic dissection: a 2008 update. Circulation. 2008;117(24):2927-2935.
Fattori R, Cao P, De Rango P, et al. Aortic dissection: a review. JACC Cardiovasc Imaging. 2013;6(12):1343-1355.
Matsumura JS, Cambria RP, Dake MD, et al. Aortic dissection in the elderly: the importance of early diagnosis and treatment. J Vasc Surg. 2015;61(2):564-570.

FOAMED and Other Resources for Further Reading

Evaluation of the adult chest pain in the emergency department. https://www.uptodate.com/contents/evaluation-of-the-adult-with-chest-pain-in-the-emergencydepartment?search=aortic%20dissection&topicRef=8190&source=see_link#H18
Borloz, Matthew. Thoracic aortic dissection. SAEM. 2019. https://www.saem.org/about-saem/academies-interest-groups-affiliates2/cdem/for-students/online-education/m4-curriculum/group-m4-cardiovascular/thoracic-aortic-dissection
Kurabayashi M, Miwa N, Ueshima D, et al. Factors leading to failure to diagnose acute aortic dissection in the emergency room. J Cardiol. 2011;58(3):287-293.

Reviewed and Edited By

Arif Alper Cevik, MD, FEMAT, FIFEM

Hypernatremia (2024)

December 30, 2024December 30, 2024 ~ iEM Education Project Team ~ Leave a comment

by Theresa Nguyen

You Have A New Patient!

An 87-year-old male patient with a past medical history of hypertension, stroke, and depression presents to the ED with lethargy and altered mental status. He was brought in by his daughter, who states that she has been visiting him at the nursing home over the past three days, during which he has appeared progressively weaker and more confused.

The nursing home staff report that the patient has had poor oral intake and multiple episodes of non-bloody diarrhea. He has not been participating in his usual activities and appeared more lethargic today, which prompted his daughter to bring him to the ED.

Initial triage vital signs are as follows: BP 92/60, HR 134, RR 18, SpO₂ 99%, Temp 36.8°C.

Exam findings are notable for a cachectic elderly male who is not oriented to person or place. He appears clinically dehydrated, with dry mucous membranes and poor skin turgor with tenting. He is able to follow basic commands but appears weak and confused. Laboratory findings were notable for a sodium of 165 mEq/L, chloride of 120 mEq/L, potassium of 4.0 mEq/L, and creatinine of 2.1 mg/dL.

What is the diagnosis for this patient, and what additional labs, treatment options, and potential complications should be considered?

What Do You Need To Know?

Importance and Epidemiology

Hypernatremia is defined as a serum sodium ([Na+]) level greater than 145 mEq/L [1]. It is a common electrolyte abnormality seen in elderly, pediatric, and critically ill patients, as these populations are more prone to impaired thirst regulation [2]. Hypernatremia occurs due to net water loss, excess sodium intake, or a combination of both [1]. Accurate diagnosis and appropriate treatment are crucial, as both undercorrection and overcorrection of hypernatremia are associated with poor prognosis and a high mortality rate of 40–60%, which is often underappreciated [1].

Pathophysiology

Understanding hypernatremia requires comprehension of the main body fluid compartments as well as the basic concepts of normal body water balance [1]. Since sodium is important for maintaining extracellular fluid (ECF) volume, any change in ECF volume can result in increased or decreased sodium excretion in the urine. Sodium excretion is regulated by mechanisms such as the renin-angiotensin-aldosterone system [1]. When there is a rise in serum sodium, plasma osmolality also increases, triggering the thirst response and antidiuretic hormone (ADH) secretion. This leads to renal water conservation and the production of concentrated urine [1].

Severe hypernatremia occurs when serum sodium rises rapidly or exceeds 160 mEq/L [2]. Most patients will be symptomatic at this level due to central nervous system dysfunction. Hypovolemic hypernatremia is the most common presentation of hypernatremia seen in the ED, as net water loss accounts for the majority of cases [3]. Determining the patient’s volume status is one of the most important steps in managing hypernatremia. A thorough history, clinical exam, and laboratory testing are used in conjunction to establish the etiology of hypernatremia.

Medical History

As stated previously, a thorough history is essential to determining a potential etiology for hypernatremia and guiding management [1]. For example, patients who have sustained a traumatic brain injury may be more likely to have central diabetes insipidus (DI), while a patient with an underlying psychiatric condition on lithium may be more likely to have nephrogenic DI [1]. The timing of symptoms is also relevant in determining whether the hypernatremia is acute or chronic. Hypernatremia that develops within the previous 48 hours is considered acute, while patients with symptoms lasting longer than 48 hours or with unknown timing of symptom onset are considered to have chronic hypernatremia [1]. The severity of symptoms is determined by both the speed and magnitude of the Na+ change.

The history should include detailed information about the patient’s fluid and salt intake, urine output, past medical history, and current medications [4]. Medications often implicated in hypernatremia include loop diuretics, lithium, phenytoin, lactulose, aminoglycosides, mannitol, and hypertonic saline [3,5]. Ask about any recent head trauma or surgeries, such as pituitary macroadenoma removal. Patients may report polyuria, polydipsia, confusion, or generalized weakness. If the patient is altered, the caregiver or family member (if available) should be interviewed to determine any specific mental or behavioral changes that are acute.

Physical Examination

Assess the patient’s volume status by checking skin turgor and capillary refill, in addition to examining for edema or elevated jugular venous pressure [1]. Vital sign abnormalities may include tachycardia or orthostatic hypotension. Check for signs of trauma, burns, infection, or skin breakdown, which may contribute to insensible water losses.

Patients with underlying hypernatremia may present with a broad range of signs and symptoms, including lethargy, irritability, restlessness, altered mental status, poor skin turgor, hyperactive reflexes, and increased muscle tone [5]. Hypovolemic patients are usually tachycardic, with decreased capillary refill and peripheral perfusion, while hypervolemic patients may appear edematous and have rales on exam.

Perform a complete neurologic exam on all patients presenting with hypernatremia, as altered mental status, seizures, and a comatose state are associated with greater risk of morbidity and mortality [5]. Cerebral adaptation to hypernatremia generally starts on the first day and results in a reduction of brain volume that is reversed by water movement from the cerebrospinal fluid into the brain [1].

Check for somnolence, disorientation, increased muscle tone, or spasticity. Patients may often appear weak and lethargic.

Classifications of Hypernatremia & Alternative Diagnoses

Following the initial history and assessment as detailed above, patients with hypernatremia can be categorized into one of the following three groups depending on their volume status.

Hypovolemic Hypernatremia (Concomitant Loss of Water and Salt):

Patients with hypovolemic hypernatremia experience both a loss of water and salt, but with a relatively larger loss of total body water (TBW) [1]. This is most commonly due to gastrointestinal losses (e.g., diarrhea, vomiting), skin losses (e.g., burns or excessive sweating), and renal losses (e.g., intrinsic renal disease, mannitol, and loop diuretics) [5].

Patients with hypovolemic hypernatremia should first be given normal saline solution or lactated Ringer’s to restore volume, followed by hypotonic saline solutions (e.g., half-isotonic saline or quarter-isotonic saline). Hypovolemic hypernatremia is the most common presentation of hypernatremia seen in the ED [3].

Euvolemic Hypernatremia (Water Loss with Normal Salt Content):

This results from decreased TBW without any accompanying loss of salt [1]. Euvolemic hypernatremia is caused by extrarenal losses from the respiratory tract or skin (e.g., excessive sweating or fever), renal losses (e.g., central diabetes insipidus [DI] or nephrogenic DI), and other causes such as medications [5].

Medications often associated with euvolemic hypernatremia include lithium, amphotericin, phenytoin, and aminoglycosides [3,5]. Treatment for euvolemic hypernatremia is aimed at free water replacement, which can be provided orally or through intravenous glucose solution.

Diabetes Insipidus (DI): Also known as arginine vasopressin deficiency (AVP-D), DI is characterized by the passage of large volumes (>3 L/24 hours) of dilute urine [6]. The classic presentation of DI in the ED includes symptomatic hypernatremia (e.g., polyuria, polydipsia, lethargy, and weakness) and an inappropriately low urine osmolality (<300 mOsm/kg) [6].

DI refers to an absolute or relative antidiuretic hormone (ADH) deficiency and can be further classified into two major forms:

Central DI: Characterized by an absolute ADH deficiency caused by inadequate ADH secretion. Common etiologies include malignant diseases, head trauma, pituitary surgery, infiltrative diseases, or idiopathic conditions [6].
Nephrogenic DI: Characterized by a relative ADH deficiency due to a lack of renal response to ADH. Common etiologies include chronic renal insufficiency, polycystic kidney disease, hypercalcemia, hypokalemia, lithium toxicity, or familial diseases [6].

Hypervolemic Hypernatremia (Relative Water Deficit with Concomitant Gain in Salt):

This less common form of hypernatremia results from increased sodium with normal or increased TBW [1]. Hypervolemic hypernatremia often has an iatrogenic cause, such as hypertonic fluid administration (e.g., hypertonic saline, sodium bicarbonate, or total parenteral nutrition) in hospitalized patients [1]. It can also result from ingestion of saltwater or large amounts of salt, as well as mineralocorticoid excess (e.g., adrenal tumors or congenital adrenal hyperplasia) [4].

Patients with hypervolemic hypernatremia will often appear volume overloaded. Many of these patients may have conditions contributing to salt retention, such as congestive heart failure, liver dysfunction, renal disease, or hypoalbuminemia [1]. Treatment involves free water replacement and the use of diuretics such as furosemide to promote sodium excretion [4]. Diuretics should be titrated as necessary to maintain a negative fluid balance [3].

Acing Diagnostic Testing

Laboratory testing is another essential component for determining the causative factors of hypernatremia, especially in patients with altered mental status who cannot provide a thorough history [1]. Obtain a full set of serum electrolytes (including magnesium, calcium, and phosphate), liver function tests, renal function tests, urine electrolytes, and calculate serum osmolality. A serum osmolality of >430 mOsm/L is often associated with seizures and death [5].

The urine osmolality is one of the most useful initial tests to order, as it can further categorize the etiology and determine whether or not the renal water-concentrating ability is preserved [1]. If the urine osmolality is less than 300 mOsm/kg, this favors a diagnosis of central or nephrogenic DI. Desmopressin (DDAVP) should be administered to differentiate between the two types of DI. In patients with central DI, DDAVP will result in an increase in urine osmolality [1,6]. If the urine osmolality is high (greater than 800 mOsm/kg), this suggests that the secretion and response to AVP are normal, indicating preserved renal concentrating ability. In such cases, the hypernatremia is most likely due to extrarenal losses [1].

Imaging can also be useful in determining other etiologies of hypernatremia and ruling out potentially life-threatening conditions. Obtain a chest x-ray to rule out congestive heart failure, pneumonia, malignancy, pulmonary edema, and cardiomegaly as potential contributing disease processes. A non-contrast CT scan of the head is recommended in all patients with severe hypernatremia, especially if focal neurologic findings are present on exam. Hypernatremia results in traction on dural bridging veins and sinuses, which can lead to intracranial hemorrhage, most often in the subdural space [3]. Hemoconcentration from total body water loss may also lead to dural sinus thrombosis.

Risk Stratification

As mentioned previously, the severity of symptoms is often determined by both the speed and magnitude of the Na+ change. Acute symptoms are usually noted when Na+ >160 mEq/L [2]. Patients with acute hypernatremia are more likely to present with neurologic manifestations such as confusion, altered mental status, seizures, or ataxia. In cases of rapid and severe hypernatremia that develops over minutes to hours, there is an increased risk of acute intracranial hemorrhage due to the accompanying rapid decrease in brain volume, which causes rupture of cerebral veins [3].

Patients with chronic hypernatremia are typically less likely to exhibit neurologic symptoms due to the brain’s compensatory mechanisms. The brain can adapt by generating intracellular osmogenic compounds, which increase osmolality in the cells and thereby maintain brain volume, resisting shrinkage [1].

Management

The ED management of hypernatremia revolves around two key tasks: treating the inciting cause and correcting the hyperosmolality [1,3]. It is important to note that correcting sodium either too quickly or too slowly is associated with an increased risk of death and cerebral edema [3]. Therefore, the treatment of hypernatremia requires appropriate timing and a systematic approach. The classic recommendation for the management of hypernatremia is to replace the calculated free water deficit over 48 hours, with a decrease in serum Na+ not to exceed 0.5 mEq per hour (or 10–12 mEq total per 24 hours) [2,7].

ED management of hypernatremia can be further broken down into the following steps:

1) Resuscitate:

Following the initial evaluation, patients who are hemodynamically unstable should be resuscitated with intravenous fluids to stabilize abnormal vital signs [7]. The initial goal is to address the underlying hypovolemia and tissue hypoperfusion. Unless this is corrected, the body’s normal response will be to increase sodium concentration to maintain intravascular volume, which will worsen hypernatremia. Fluid resuscitation can be initiated with an isotonic fluid such as normal saline (0.9%) or lactated Ringer’s for volume repletion [2].

While it may seem counterproductive to administer a sodium-containing fluid to a hypernatremic patient, the goal is to restore homeostatic mechanisms of sodium balance before free water correction [2]. If the patient is not hypovolemic, use D5W for fluid resuscitation.

2) Investigate:

Evaluate for and treat the underlying cause of hypernatremia [2,7]. Review the patient’s weight, intake and output, and current medications. Consider potential etiologies of hypernatremia, such as electrolyte imbalances, gastrointestinal losses, diabetes insipidus, and others as described above. Look for potential sources of infection.

Obtain additional labs to help identify the etiology of hypernatremia and direct management. Rule out other electrolyte abnormalities, such as hypokalemia and hypercalcemia, which may point to renal causes of hypernatremia [3]. Calculate the serum osmolality (normal reference range: 275–295 mOsm/L), as elevations may correlate with the degree of symptoms [5]. Once the cause of hypernatremia has been identified, treat the underlying condition.

3) Rehydrate:

Water replacement should address the total body water (TBW) deficit in addition to any ongoing losses of water. Each liter of water deficit raises the serum Na+ by approximately 3–5 mEq/L [1]. Calculate the free water required to achieve the target sodium level [7]. The choice of replacement solution and infusion rates are critical factors to avoid overcorrection of hypernatremia.

It is essential to know the sodium concentration in different solutions to accurately correct water and sodium imbalances [3]. The sodium concentrations in commonly used solutions are listed below [3]:

0.9% NaCl: 154 mmol/L
Ringer’s Lactate: 130 mmol/L
0.45% NaCl: 77 mmol/L
5% Dextrose in water (D5W): 0 mmol/L

To determine the TBW and water deficit:

Calculate TBW:
The total body water (TBW) is estimated as 50% or 60% of lean body weight in women and men, respectively, which is why different correction factors are used in TBW calculation. Below are the recommended correction factors for calculating TBW based on age and gender [7]:

Children and adult males: 0.6 × weight (kg)
Adult females: 0.5 × weight (kg)
Elderly males: 0.5 × weight (kg)
Elderly females: 0.45 × weight (kg)

Calculate water deficit:
The water deficit as a function of sodium concentration is calculated using the formula [1,3]:
TBW deficit = TBW × [(serum sodium/140) – 1]

This equation approximates the amount of water required to decrease sodium concentration to 140 mEq/L [3]. Note that this equation does not account for ongoing water losses or coexisting isosmotic fluid deficits, such as in patients with ongoing vomiting or diarrhea.

Rate and Volume of Correction:

Once the water deficit has been calculated, determine the rate and volume of correction. Several free online calculators, such as those available on MedCalc, can be used as reference tools.

Acute hypernatremia: Do not lower sodium by more than 1–2 mEq/L/hr.
Chronic hypernatremia: The goal is to lower Na+ by 10–12 mEq over 24 hours [5].

Avoid rapid overcorrection of hypernatremia, as this can result in cerebral edema, especially in children, who are more prone to this complication. Many patients with hypernatremia will also have reduced extracellular fluid (ECF) volume and other electrolyte abnormalities, which may require hypotonic fluids.

Treatment of Central DI:

The main treatment modality for patients with central DI is to supplement ADH in the form of desmopressin (DDAVP) [1]. Patients with known central DI should be given desmopressin, which may improve symptoms.

The initial dose of DDAVP is 1–2 micrograms (administered orally, intranasally, subcutaneously, or intravenously) and then up-titrated as necessary to reach the goal sodium level [6].

Special Patient Groups

Pediatrics

Hypernatremia is predominantly seen in infants and the elderly population due to their impaired thirst regulation [1]. Infants and small children are more vulnerable to hypernatremia because of their greater insensible water losses and their inability to communicate their need for fluids and/or access fluids independently. Two common presentations for infants at risk of hypernatremia include those receiving inadequate hydration in the setting of gastroenteritis or ineffective breastfeeding [2]. Furthermore, premature infants are at higher risk due to their relatively small mass-to-surface area ratio and their dependency on caregivers for fluid intake [2].

In breastfed infants, a relevant history should focus on whether there is a successful latch at the start of breastfeeding, the frequency and duration of feedings, the mother’s sensation of milk letdown, and whether the infant appears satiated after feeding. Common symptoms of hypernatremia in infants may include lethargy, weakness, restlessness or agitation, and a characteristic high-pitched cry [3]. It is important to remember that the degree of dehydration can be underestimated in children with hypernatremia due to a shift of water from the intracellular space to the extravascular space [2]. Children are often more susceptible to adverse effects from rapid correction of hypernatremia.

Pregnant Patients

Pregnant patients may develop hypernatremia due to transient diabetes insipidus, which affects approximately 4 out of 100,000 pregnancies [6]. Between the eighth gestational week and midpregnancy, the metabolic clearance of ADH increases 4- to 6-fold because of an increase in the enzyme vasopressinase, which is produced by the placenta. Vasopressinase activity peaks in the third trimester, remains high during labor and delivery, and then falls to undetectable levels two to four weeks postpartum [6]. Transient DI is caused by an amplification of the normal pregnancy-related increase in vasopressinase levels. Patients generally report increased thirst and urinary output that are out of proportion to those normally seen in pregnancy.

Patients with preeclampsia or HELLP syndrome are at increased risk for transient DI of pregnancy [8]. Transient DI should also be considered in the differential diagnosis of severe hypernatremia in obstetric patients with restricted oral intake after a Caesarean section [8]. Treatment options for transient DI of pregnancy include desmopressin and free water replacement [6]. Transient DI typically resolves postpartum and does not usually recur in subsequent pregnancies.

Geriatrics

Hypernatremia is also a relatively common electrolyte disorder in the elderly and critically ill patients. Approximately 27% of patients admitted to an intensive care unit (ICU) develop hypernatremia of variable severity during their ICU stay [9]. Additionally, studies have found that hypernatremia is an independent predictor of mortality and length of stay after controlling for illness severity and other ICU-acquired conditions and complications [9]. Even mild hypernatremia, with serum sodium levels between 145 and 149 mEq/L, is associated with a 28% increase in mortality risk and a 19% increase in ICU length of stay [9].

In the elderly population, the causes of hypernatremia tend to be multifactorial and include a decrease in thirst sensation, polypharmacy, and pre-existing comorbidities [10]. Renal function, concentrating abilities, and hormonal modulators of salt and water balance are often impaired in the elderly, making them more susceptible to hypernatremia and the associated morbidities and iatrogenic events involving salt and water [10]. The age-related decrease in TBW and concomitant impairment in thirst mechanisms also make elderly individuals more vulnerable to stresses on water balance [10]. By age 75 to 80 years, total body water content declines to approximately 50%, and even lower in elderly women. Providers should maintain a high index of suspicion for hypernatremia in elderly patients presenting from long-term care facilities, nursing homes, or after prolonged inpatient hospitalizations.

When To Admit This Patient

Patients with symptomatic hypernatremia or a serum sodium level greater than 150 mEq/L should be admitted to the hospital for further evaluation and treatment, as the free water deficit will generally need to be replaced gradually [1]. Those with severe neurological symptoms should be admitted to the ICU for regular neurologic exams. If available, a nephrology consult may be required for recommendations on dialysis and fluid regimens in more severe cases of hypernatremia. Sodium and electrolyte levels should be closely monitored every 2 to 4 hours during the acute phase of correction [2]. If a patient develops seizures during the course of treatment, this may indicate cerebral edema caused by rapid shifts in osmolality [2].

Hemodynamically stable and asymptomatic patients with mild hypernatremia from benign causes may be discharged with outpatient follow-up. Any medications contributing to the hypernatremia should be appropriately tapered or discontinued. Patients should be given specific instructions on the appropriate daily fluid intake and advised to avoid foods high in sodium (such as soy sauce, canned soups, chips, and processed foods) [1]. A plan should be in place to obtain follow-up sodium levels within 5 to 7 days or sooner if the patient becomes symptomatic.

Patients should also be instructed to return for any worsening fatigue, altered mental status, increased thirst, or confusion. Serum sodium and drug levels should be periodically monitored in patients taking medications known to cause nephrogenic DI. For elderly patients, a coordinated discharge plan involving the discharging physician, primary care physician, and nursing home staff is essential to prevent readmission due to hypernatremia [2].

Revisiting Your Patient

This case presents a common scenario where an elderly nursing home resident with poor oral intake presents to the ED with altered mental status and lethargy due to decreased oral intake and diarrhea. Vital signs are notable for tachycardia and hypotension, along with physical exam findings of dry mucous membranes and poor skin turgor. The patient was found to be hypernatremic, with a sodium level of 165 mEq/L and an elevated creatinine of 2.1 mg/dL. These findings are consistent with a clinical picture of hypovolemic hypernatremia.

Additional history obtained from the patient’s daughter and a review of nursing home records revealed medications that included lisinopril, aspirin, and sertraline. There were no recent medication changes, and the patient was still taking all of his medications despite the reported decrease in oral intake. Regarding his baseline mental status, the patient is typically communicative and usually awake, alert, and oriented to person, place, and time. He is now more confused and only oriented to person. There was no reported trauma or recent surgeries.

The patient was initially fluid resuscitated with 1 L of normal saline to stabilize the tachycardia and hypotension. Given the change in mental status, a head CT was performed, which did not show any acute intracranial hemorrhage or brain mass. A chest x-ray revealed no acute cardiac disease, focal consolidation, or pulmonary edema. Additional labs did not reveal any other electrolyte abnormalities. His serum osmolality was calculated to be 352 mOsm/kg, and his urine osmolality was elevated at >800 mOsm/kg.

Following initial fluid resuscitation, the patient’s calculated water deficit was estimated to be 5.35 L using the formula:
TBW deficit = TBW × [(serum sodium/140) – 1]
Using a weight of 60 kg:
(0.5 × 60 kg) × [(165/140) – 1] = 30 × (1.18 – 1) = 5.35 L

Given the patient’s altered mental status, degree of dehydration, and significant hypernatremia, he was admitted to the hospital for additional monitoring and fluid management. His IV fluids were adjusted to achieve a goal of decreasing the Na+ by 0.5 mmol/L/hr.

The patient responded well to treatment, and his confusion gradually resolved. He was discharged back to the nursing home within 3 days and did not experience any adverse outcomes.

Author

Theresa Nguyen

Dr. Theresa Nguyen is an Associate Professor of Emergency Medicine and the Director of the Center for Community and Global Health at Loyola University Medical Center in Maywood, IL. She also co-founded the Loyola Street Medicine program, which is dedicated to providing medical care and social outreach to individuals experiencing homelessness. Dr. Nguyen has international fieldwork experience in Haiti, Peru, Guatemala, Dominican Republic and Vietnam. Over the course of her global health work, Dr. Nguyen developed a strong interest in tropical diseases and obtained her Certificate of Knowledge in Clinical Tropical Medicine and Travelers' Health in 2014. Dr. Nguyen's current interests include ultrasound teaching in resource-limited settings, addressing language barriers, providing access to care for the homeless population, increasing awareness and education surrounding human trafficking, and international EM development.

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References

Muhsin SA, Mount DB. Diagnosis and treatment of hypernatremia. Best Pract Res Clin Endocrinol Metab. 2016;30(2):189-203.
Sonani B, Naganathan S, Al-Dhahir M. Hypernatremia. In: StatPearls. Treasure Island, FL: StatPearls Publishing; 2023. Updated May 20, 2023. Accessed June 19, 2023. https://www.ncbi.nlm.nih.gov/books/NBK441960/
Adrogué HJ, Madias NE. Hypernatremia. N Engl J Med. 2000;342(20):1493-1499.
Farkas J. Hypernatremia and dehydration in the ICU. The Internet Book of Critical Care. Published June 25, 2021. Accessed April 3, 2023. https://emcrit.org/ibcc/hypernatremia/
Liamis G, Filippatos TD, Elisaf M. Evaluation and treatment of hypernatremia: a practical guide for physicians. Postgrad Med. 2016;128(3):299-306.
Hui C, Khan M, et al. Diabetes Insipidus. In: StatPearls. Treasure Island, FL: StatPearls Publishing; 2023. Updated June 1, 2023. Accessed June 19, 2023. https://www.ncbi.nlm.nih.gov/books/NBK470458/
Ramzy MM. EM@3AM: Hypernatremia. emDocs. Published July 14, 2018. Accessed April 10, 2023. https://www.emdocs.net/em3am-hypernatremia/
Sherer DM, Cutler J, Santoso P, et al. Severe hypernatremia after cesarean delivery secondary to transient diabetes insipidus of pregnancy. Obstet Gynecol. 2003;102(5):1166-1168.
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Reviewed and Edited By

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