# Seminar 14: Psychiatric Emergencies

## Emergency Medicine Clerkship

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## Learning Objectives

By the end of this seminar, students will be able to:

1. Conduct a comprehensive suicide risk assessment using validated screening tools and structured interviews, and determine the appropriate level of care from discharge with safety plan to inpatient psychiatric admission
2. Evaluate the acutely agitated patient using a systematic de-escalation framework and select appropriate pharmacologic interventions based on the suspected etiology
3. Differentiate organic from functional causes of acute psychosis through a focused medical workup, and recognize medical mimics that require treatment of the underlying condition
4. Apply involuntary commitment criteria when a patient presents an imminent danger to self or others and lacks capacity to make informed decisions about their psychiatric care
5. Diagnose neuroleptic malignant syndrome and serotonin syndrome as life-threatening medication-related emergencies and initiate appropriate treatment with dantrolene or cyproheptadine respectively
6. Recognize intimate partner violence through screening and behavioral indicators, provide safety assessment and resources, and fulfill mandatory reporting obligations

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## Seminar Outline

### Section 1: Suicide Risk Assessment

Suicide is a leading cause of death across multiple age groups and is the most feared adverse outcome in emergency psychiatry. The emergency physician must evaluate every patient with suicidal ideation, self-harm behavior, or concerning mental health presentations using a structured risk assessment framework. Risk factors for suicide are categorized as demographic, psychiatric, and situational. Demographic risk factors include male sex (which carries a higher completion rate), age (bimodal peaks in adolescents/young adults and older adults), white or Native American race, unmarried or divorced marital status, and unemployment. Psychiatric risk factors, which are the strongest predictors, include prior suicide attempts (the single strongest predictor of future completion), depression, bipolar disorder, schizophrenia, substance use disorders, and personality disorders, particularly borderline personality disorder. Recent discharge from a psychiatric hospital represents a period of markedly elevated risk.

The clinical interview for suicide risk assessment should explore multiple dimensions of suicidal thinking. The Columbia-Suicide Severity Rating Scale (C-SSRS) provides a standardized framework for assessing the intensity and progression of suicidal ideation, from passive thoughts of death (wishing to be dead or not waking up) through active suicidal ideation without a plan, active ideation with a plan, and active ideation with both a plan and intent to act. The specificity of the plan is an important risk modifier: a patient who describes a concrete method, has access to the means, has identified a time and place, and has made preparatory behaviors (writing a note, giving away possessions, putting affairs in order) is at substantially higher risk than one with vague, nonspecific ideation. Hopelessness, as measured by validated instruments, has been shown to be one of the strongest psychological predictors of eventual suicide, independent of the severity of depressive symptoms.

Protective factors should be assessed alongside risk factors to provide a more complete picture of the patient's overall risk profile. Strong social connections, including a supportive family, meaningful relationships, and community involvement, serve as important buffers against suicidal behavior. Religious or spiritual beliefs that provide a sense of purpose or a moral objection to suicide may be protective. The presence of dependent children creates a sense of responsibility that may deter suicidal behavior. Active engagement in mental health treatment and willingness to use coping strategies and safety resources suggest a capacity for help-seeking behavior. Cultural factors may influence both risk and protective factors, and clinicians should be attentive to culturally specific expressions of distress and protective factors.

Disposition decisions are guided by the overall assessment of risk, the patient's resources, and the availability of outpatient support. Patients at high risk for imminent suicide, including those with a specific plan and intent, access to lethal means, acute psychiatric illness, and inadequate social support, require inpatient psychiatric admission, either voluntarily or involuntarily when the patient refuses and meets commitment criteria. Patients at moderate risk may be appropriate for discharge with a safety plan if they have adequate social support, are willing to engage in outpatient treatment, and can agree to specific safety measures including means restriction (particularly restriction of access to firearms, which are the most lethal method of suicide). The safety plan should be developed collaboratively and include identification of personal warning signs, internal coping strategies, social contacts for distraction, professional crisis resources, and means restriction steps.

<image>Panel A: Risk factor classification showing demographic (male sex, age peaks, marital status), psychiatric (prior attempts, depression, substance use), and situational (recent psychiatric discharge, recent loss, access to means) categories with their relative contribution to overall risk. Panel B: Columbia-Suicide Severity Rating Scale progression from passive ideation through active ideation without plan, active ideation with plan, to active ideation with plan and intent, with corresponding risk levels. Panel C: Protective factors assessment showing social connections, religious beliefs, dependent children, treatment engagement, and cultural buffers with their respective mechanisms of risk reduction. Panel D: Disposition algorithm from risk assessment through high-risk (inpatient admission), moderate-risk (safety plan with means restriction and close follow-up), and low-risk (outpatient referral) pathways.</image>

### Section 2: The Agitated Patient

Agitation in the emergency department is a common and potentially dangerous presentation that requires rapid assessment and management to ensure the safety of the patient, staff, and other individuals in the treatment environment. The causes of agitation are broadly categorized as medical, substance-related, and primary psychiatric. Medical causes include delirium from any etiology (infection, metabolic derangement, hypoxia, intracranial pathology), pain, urinary retention, and medication toxicity. Substance-related causes include intoxication with stimulants (cocaine, methamphetamine), hallucinogens, phencyclidine, or alcohol, and withdrawal from alcohol, benzodiazepines, or opioids. Primary psychiatric causes include acute psychosis from schizophrenia or bipolar disorder, severe anxiety, and personality disorder-related emotional dysregulation. The clinician must always consider and exclude medical causes before attributing agitation to a primary psychiatric condition.

Verbal de-escalation is the first-line intervention for the agitated patient and should be attempted before any pharmacologic or physical intervention when it is safe to do so. The principles of de-escalation include approaching the patient in a calm, non-threatening manner; speaking slowly and clearly; using a low, steady tone of voice; maintaining a safe distance (at least two arm lengths) while positioning oneself near an exit; avoiding aggressive postures, prolonged direct eye contact, and any physical contact; identifying the patient's needs and offering concrete options to restore a sense of autonomy; and setting clear, reasonable limits. Active listening and empathic acknowledgment of the patient's distress are among the most effective de-escalation tools. Offering food, water, blankets, and a quiet environment can address basic needs that may be contributing to agitation.

When verbal de-escalation is insufficient and the patient poses an imminent threat to safety, pharmacologic management is initiated. The goal is calm cooperation, not sedation to the point of unconsciousness. For patients in whom the cause of agitation is undifferentiated, the combination of a first-generation antipsychotic and a benzodiazepine is a well-established approach. Haloperidol 5 milligrams intramuscularly combined with lorazepam 2 milligrams intramuscularly is a commonly used regimen. Second-generation antipsychotics, including olanzapine 10 milligrams intramuscularly and ziprasidone 10 to 20 milligrams intramuscularly, offer effective alternatives with potentially fewer extrapyramidal side effects. In suspected alcohol withdrawal, benzodiazepines are the agents of choice, as neuroleptics lower the seizure threshold and should be avoided. For stimulant intoxication, benzodiazepines are preferred because antipsychotics may impair heat dissipation and worsen hyperthermia. Ketamine 4 milligrams per kilogram intramuscularly has emerged as an effective rapid-onset agent for severe, refractory agitation, though it requires closer airway monitoring.

Physical restraints should be used only as a last resort when all other measures have failed and the patient poses an imminent physical threat. The application of restraints must follow institutional protocols and regulatory requirements, including physician orders, documentation of the indication and alternatives attempted, regular reassessment at defined intervals (typically every 15 to 30 minutes), monitoring of restrained extremities for neurovascular compromise, and assessment of the patient's basic needs (hydration, toileting, positioning). Restraints should be removed as soon as the patient is no longer an imminent danger. A patient in restraints is at risk for aspiration, particularly when agitated and struggling, and should be positioned to minimize this risk. The clinician should maintain awareness of the patient's ongoing medical status, as restraint-associated complications include rhabdomyolysis, positional asphyxia, aspiration, and deep vein thrombosis.

<image>Panel A: Differential diagnosis framework for agitation showing medical causes (delirium, pain, urinary retention), substance-related causes (stimulant intoxication, alcohol withdrawal), and primary psychiatric causes (acute psychosis, mania, personality disorder) with key distinguishing features. Panel B: Verbal de-escalation technique illustration showing the clinician positioned near an exit at a safe distance, with annotations of recommended communication strategies including calm tone, active listening, and concrete option offering. Panel C: Pharmacologic management algorithm showing agent selection based on suspected etiology: haloperidol plus lorazepam for undifferentiated agitation, benzodiazepines for alcohol withdrawal and stimulant intoxication, antipsychotics for primary psychosis, and ketamine for refractory agitation. Panel D: Physical restraint protocol showing proper application technique, monitoring schedule, documentation requirements, and potential complications including positional asphyxia, rhabdomyolysis, and aspiration.</image>

### Section 3: Acute Psychosis

The evaluation of acute psychosis in the emergency department requires a systematic approach to differentiate primary psychiatric disorders from medical conditions that present with psychotic features. Primary psychiatric causes of psychosis include schizophrenia (particularly first-episode psychosis in young adults), schizoaffective disorder, bipolar disorder with psychotic features (manifesting as grandiose or paranoid delusions and hallucinations during manic or depressive episodes), and brief psychotic disorder. Medical causes that must be excluded include drug intoxication (stimulants, hallucinogens, phencyclidine, cannabis), drug withdrawal (alcohol, benzodiazepines), metabolic derangements (hyponatremia, hypoglycemia, hepatic encephalopathy, uremia), endocrine disorders (thyroid storm, adrenal crisis), central nervous system infections (meningitis, encephalitis), structural brain lesions (tumor, stroke, hemorrhage), seizure disorders (postictal psychosis, complex partial seizures), and autoimmune encephalitis (particularly anti-NMDA receptor encephalitis, which should be considered in young women with psychiatric symptoms, seizures, and movement abnormalities).

The medical workup for acute psychosis is essential to exclude organic causes and should include a focused history and physical examination, point-of-care glucose, urine toxicology screen, basic metabolic panel, complete blood count, thyroid function tests, urinalysis, and a pregnancy test in women of reproductive age. Additional studies are indicated based on clinical suspicion and include computed tomography of the head for new-onset psychosis, focal neurologic findings, or head trauma; lumbar puncture when central nervous system infection or autoimmune encephalitis is suspected; electroencephalography for suspected seizure activity; and specific toxicology testing when indicated. Clinical features that raise suspicion for an organic cause include acute onset without prior psychiatric history (particularly in patients over 40), visual hallucinations (which are more common in organic causes compared with the auditory hallucinations of schizophrenia), fluctuating level of consciousness, disorientation, abnormal vital signs, and focal neurologic deficits.

Emergency management of acute psychosis addresses both symptom control and safety. Antipsychotic medications are the mainstay of treatment. Haloperidol 5 to 10 milligrams intramuscularly or intravenously is a well-established first-generation agent with rapid onset and predictable efficacy. Second-generation antipsychotics including olanzapine and ziprasidone are effective alternatives. Benzodiazepines may be used as adjuncts for agitation and anxiety but do not treat the underlying psychotic process. The patient should be placed in a calm, low-stimulation environment, and one-to-one observation may be necessary for patients who are at risk for self-harm or elopement. Medical causes identified during the workup should be treated definitively, as psychosis resulting from an organic cause will not resolve with antipsychotic medications alone.

First-episode psychosis warrants particular attention in the emergency department because it represents a critical juncture for diagnosis, treatment initiation, and long-term prognostic implications. The typical age of onset for schizophrenia is late adolescence to early twenties, and first-episode psychosis often brings the patient to medical attention for the first time. A thorough medical workup is especially important in first-episode presentations because medical mimics have not yet been excluded by prior evaluations. Brain imaging with CT or MRI should be obtained to exclude structural pathology. Anti-NMDA receptor encephalitis should be considered in the differential diagnosis of young patients with psychiatric symptoms, as this treatable autoimmune condition can closely mimic a primary psychotic disorder. Substance-induced psychosis should be considered and may be distinguished by temporal association with substance use and resolution with abstinence, though chronic substance use can precipitate primary psychotic disorders.

<image>Panel A: Differential diagnosis of acute psychosis organized into primary psychiatric causes (schizophrenia, bipolar, schizoaffective) and medical causes (intoxication, metabolic, endocrine, CNS infection, structural, autoimmune), with key distinguishing features for each category. Panel B: Medical workup checklist for acute psychosis showing first-line studies (glucose, toxicology, BMP, CBC, TSH, urinalysis) and second-line studies (CT head, lumbar puncture, EEG) with their specific clinical indications. Panel C: Clinical features suggesting organic versus functional psychosis, comparing visual versus auditory hallucinations, fluctuating versus stable consciousness, presence versus absence of disorientation, and vital sign abnormalities. Panel D: First-episode psychosis evaluation pathway showing the enhanced workup including brain imaging, anti-NMDA receptor antibody consideration in young women, and substance-induced psychosis assessment with temporal association analysis.</image>

### Section 4: Involuntary Commitment

Involuntary psychiatric commitment is the legal process by which a patient who meets specific statutory criteria is compelled to receive psychiatric evaluation and treatment against their expressed wishes. The general criteria across most jurisdictions require that the individual has a mental illness and, as a result of that mental illness, poses an imminent danger to themselves or others, or is so gravely disabled that they are unable to meet their basic needs for food, clothing, or shelter. The imminent danger standard requires more than a remote or hypothetical risk; there must be evidence that the danger is likely to materialize in the near future without intervention. The clinical basis for the commitment determination should be supported by specific observations, statements, and behaviors documented in the medical record, not merely by the patient's diagnosis.

The emergency physician plays a central role in initiating the involuntary commitment process, as the emergency department is often the first point of contact for patients in psychiatric crisis. The specific legal procedures vary by jurisdiction, but the general framework involves the physician completing a certification or petition that documents the clinical findings supporting the commitment criteria, including the patient's mental status examination, observed behaviors, verbalizations indicating danger to self or others, and the patient's inability to care for themselves. A magistrate, judge, or designated hearing officer reviews the petition and authorizes the commitment. The initial emergency commitment period is typically time-limited (ranging from 72 hours to 10 days depending on the jurisdiction), after which the patient must either consent to voluntary admission or a formal commitment hearing must be held with legal representation.

Capacity assessment is a related but distinct concept from involuntary commitment and refers to the patient's ability to make informed decisions about their medical care. Four elements of decisional capacity are assessed: the ability to understand the relevant information (including diagnosis, treatment options, and consequences), the ability to appreciate how that information applies to their specific situation, the ability to reason about treatment options by weighing risks and benefits, and the ability to communicate a consistent choice. Capacity is decision-specific and may fluctuate over time; a patient may have capacity for some decisions but not others. Importantly, a patient's refusal of treatment, even when the clinician disagrees with the decision, does not in itself indicate lack of capacity. The assessment of capacity should be documented carefully, including the specific questions posed and the patient's responses.

The emergency physician must balance the patient's civil liberties against the duty to protect the patient and the public from imminent harm. The decision to involuntarily commit a patient carries significant legal and ethical implications and should not be made lightly. Patients who are intoxicated may meet commitment criteria temporarily but may no longer meet criteria once sober; these patients should be reassessed after a period of observation and sobriety. Patients who present with suicidal ideation in the context of interpersonal conflict but deny ongoing intent and have adequate coping resources may not meet the imminent danger standard. Documentation should be thorough and specific, recording the patient's statements, behaviors, mental status findings, the clinical reasoning behind the commitment decision, and any alternatives that were considered and rejected. Risk management strategies include psychiatric consultation when available, communication with family and support systems, and ensuring that the commitment process follows all applicable legal requirements.

<image>Panel A: Involuntary commitment criteria framework showing the three prongs: mental illness (documented psychiatric diagnosis or symptoms), imminent danger (danger to self, danger to others, or grave disability), and inability to make informed decisions about care. Panel B: Emergency commitment process flowchart from physician assessment through petition completion, judicial review, initial commitment period (72 hours to 10 days by jurisdiction), and subsequent formal hearing with legal representation. Panel C: Four elements of decisional capacity assessment (understand, appreciate, reason, communicate) with example questions for each element and documentation guidance. Panel D: Clinical decision scenarios showing patients who clearly meet commitment criteria (active suicidal plan with means), those who do not (suicidal ideation in context of intoxication that resolves with sobriety), and borderline cases requiring careful assessment and documentation.</image>

### Section 5: Neuroleptic Malignant Syndrome

Neuroleptic malignant syndrome is a rare but life-threatening idiosyncratic reaction to dopamine-blocking medications, most commonly antipsychotic drugs, with a mortality rate of 5 to 20 percent when recognized and treated appropriately, and substantially higher when diagnosis is delayed. The pathophysiology involves blockade of central dopamine D2 receptors in the hypothalamus (causing temperature dysregulation), the nigrostriatal pathway (causing rigidity), and the spinal cord (contributing to muscle rigidity and autonomic instability). All dopamine-blocking agents can precipitate the syndrome, including typical antipsychotics (haloperidol, chlorpromazine), atypical antipsychotics (olanzapine, risperidone, quetiapine), antiemetics (metoclopramide, prochlorperazine), and lithium. The syndrome may also occur after abrupt withdrawal of dopaminergic medications such as levodopa in Parkinson disease patients.

The clinical presentation of neuroleptic malignant syndrome is characterized by four cardinal features that develop over a period of hours to days. Hyperthermia, often exceeding 40 degrees Celsius (104 degrees Fahrenheit), results from hypothalamic thermoregulatory failure. Lead-pipe rigidity, a diffuse, severe muscular rigidity that persists throughout passive range of motion and does not demonstrate the cogwheeling pattern of parkinsonism, is the hallmark motor finding. Autonomic instability manifests as labile blood pressure, tachycardia, diaphoresis, and urinary incontinence. Altered mental status ranges from confusion and agitation to obtundation and coma. Laboratory findings include markedly elevated creatine kinase from sustained muscle contraction (often exceeding 1,000 U/L and frequently much higher), leukocytosis, metabolic acidosis, acute kidney injury from myoglobinuria, and elevated liver transaminases.

The treatment of neuroleptic malignant syndrome begins with immediate discontinuation of the offending dopamine-blocking agent and initiation of aggressive supportive care. Active cooling measures, including ice packs, cooling blankets, and evaporative cooling, are essential for managing life-threatening hyperthermia. Aggressive intravenous fluid resuscitation targeting urine output of greater than 1 milliliter per kilogram per hour is necessary to prevent acute tubular necrosis from myoglobin deposition. Benzodiazepines may help reduce rigidity and agitation. Dantrolene sodium, a direct-acting skeletal muscle relaxant that inhibits calcium release from the sarcoplasmic reticulum, is given at 1 to 2.5 milligrams per kilogram intravenously every 6 hours and is the specific pharmacologic treatment for the muscular rigidity and associated hyperthermia. Bromocriptine, a dopamine agonist, is administered at 2.5 milligrams orally or via nasogastric tube two to three times daily to restore central dopaminergic tone. Amantadine, another dopaminergic agent, is an alternative when bromocriptine is unavailable.

Monitoring and disposition require intensive care unit admission for all patients with confirmed or suspected neuroleptic malignant syndrome. Continuous cardiac monitoring is essential because autonomic instability places patients at risk for arrhythmias. Creatine kinase should be monitored serially, as persistently rising levels indicate ongoing muscle destruction and heightened risk for renal failure. Renal function and urine output are monitored closely, with urine alkalinization considered when myoglobinuria is significant. Electrolyte monitoring, particularly potassium and calcium, is important because rhabdomyolysis releases intracellular potassium, risking hyperkalemia and cardiac toxicity. Recovery typically occurs over 1 to 2 weeks after the offending agent is discontinued, though rechallenge with any antipsychotic must be approached with extreme caution, using a different agent class with a lower D2 binding affinity, starting at the lowest possible dose, and with close monitoring.

<image>Panel A: Pathophysiology diagram showing D2 receptor blockade in the hypothalamus (temperature dysregulation), nigrostriatal pathway (rigidity), and spinal cord (muscle rigidity and autonomic instability), with the list of causative agents including typical and atypical antipsychotics, antiemetics, and lithium. Panel B: Four cardinal features of neuroleptic malignant syndrome (hyperthermia exceeding 40 degrees Celsius, lead-pipe rigidity, autonomic instability, altered mental status) with typical laboratory findings including elevated CK, leukocytosis, and metabolic acidosis. Panel C: Treatment protocol showing simultaneous discontinuation of offending agent, active cooling, aggressive IV fluids, dantrolene dosing (1-2.5 mg/kg IV every 6 hours), and bromocriptine (2.5 mg PO/NG two to three times daily). Panel D: Monitoring and recovery timeline showing CK trending, renal function assessment, electrolyte monitoring, and the 1-2 week expected recovery period with guidance for cautious antipsychotic rechallenge.</image>

### Section 6: Serotonin Syndrome

Serotonin syndrome is a potentially life-threatening condition caused by excessive serotonergic activity at central and peripheral serotonin receptors, most commonly resulting from the combination of two or more serotonergic medications. The pathophysiology involves overstimulation of 5-HT1A and 5-HT2A receptors, and it exists on a clinical spectrum from mild symptoms to a fulminant, life-threatening crisis. Common precipitating drug combinations include selective serotonin reuptake inhibitors (SSRIs) combined with monoamine oxidase inhibitors (MAOIs), which is the most dangerous combination; SSRIs combined with tramadol, triptans, or dextromethorphan; and SSRI overdose in isolation. Other serotonergic agents that may contribute include serotonin-norepinephrine reuptake inhibitors, tricyclic antidepressants, linezolid (which possesses MAOI properties), fentanyl, methylene blue, and illicit drugs including MDMA (ecstasy) and lysergic acid diethylamide (LSD).

The clinical features of serotonin syndrome encompass three characteristic domains: neuromuscular hyperactivity, autonomic dysfunction, and altered mental status. Neuromuscular findings are the most distinctive and diagnostically useful, including clonus (sustained, rhythmic involuntary muscular contractions), which is the most characteristic finding; hyperreflexia, which is typically more prominent in the lower extremities; tremor; and muscular rigidity in severe cases. Autonomic findings include hyperthermia, diaphoresis, tachycardia, hypertension, mydriasis, and diarrhea. Mental status changes range from anxiety and agitation to confusion and delirium. The Hunter Serotonin Toxicity Criteria provide a validated diagnostic framework: in a patient taking a serotonergic agent, the diagnosis is confirmed by the presence of spontaneous clonus; inducible clonus plus agitation or diaphoresis; ocular clonus plus agitation or diaphoresis; tremor plus hyperreflexia; or hypertonia plus temperature above 38 degrees Celsius plus ocular or inducible clonus. The onset is typically rapid, occurring within hours of the precipitating medication change.

Differentiating serotonin syndrome from neuroleptic malignant syndrome is a common diagnostic challenge because both present with hyperthermia, altered mental status, and autonomic instability. The key distinguishing features are the timeline of onset and the neuromuscular examination. Serotonin syndrome develops rapidly, within hours of medication exposure, while neuroleptic malignant syndrome develops over days. The neuromuscular findings in serotonin syndrome are characterized by clonus, hyperreflexia, and myoclonus with relatively preserved or even increased muscle tone, whereas neuroleptic malignant syndrome produces lead-pipe rigidity with diminished reflexes. Serotonin syndrome is associated with serotonergic agents, while neuroleptic malignant syndrome is caused by dopamine-blocking agents. Bowel sounds are hyperactive in serotonin syndrome (due to serotonin's effects on gastrointestinal motility) but often decreased or absent in neuroleptic malignant syndrome. The creatine kinase is moderately elevated in serotonin syndrome but markedly elevated in neuroleptic malignant syndrome.

Treatment of serotonin syndrome begins with immediate discontinuation of all serotonergic agents, which alone is sufficient for mild cases, as symptoms typically resolve within 24 to 72 hours. Supportive care includes intravenous fluids, active cooling for hyperthermia, and benzodiazepines for agitation, seizures, and muscular hyperactivity. Cyproheptadine, a serotonin 5-HT2A receptor antagonist, is the specific antidote and is administered as an initial dose of 12 milligrams orally or via nasogastric tube, followed by 2 milligrams every 2 hours as needed. Cyproheptadine is only available in oral formulation. In severe cases with temperatures exceeding 41.1 degrees Celsius (106 degrees Fahrenheit), neuromuscular paralysis with a non-depolarizing agent and intubation may be required to abolish muscle hyperactivity and prevent further heat generation, as antipyretic medications (acetaminophen, ibuprofen) are ineffective because the hyperthermia results from muscular activity rather than a hypothalamic set point elevation. Intensive care unit admission is indicated for moderate to severe presentations.

<image>Panel A: Serotonergic medication interaction diagram showing SSRIs, MAOIs, SNRIs, TCAs, triptans, tramadol, dextromethorphan, linezolid, and illicit drugs (MDMA, LSD) with the most dangerous combinations highlighted. Panel B: Three clinical domains of serotonin syndrome (neuromuscular: clonus, hyperreflexia, tremor; autonomic: hyperthermia, diaphoresis, tachycardia, mydriasis; mental status: agitation, confusion, delirium) with the Hunter Serotonin Toxicity Criteria decision tree. Panel C: Side-by-side comparison of serotonin syndrome and neuroleptic malignant syndrome showing differences in onset (hours versus days), neuromuscular findings (clonus versus rigidity), causative agents, bowel sounds, and CK elevation. Panel D: Treatment algorithm showing discontinuation of serotonergic agents, supportive care with fluids and cooling, cyproheptadine dosing (12 mg initial then 2 mg every 2 hours), and the role of neuromuscular paralysis for severe hyperthermia exceeding 41.1 degrees Celsius.</image>

### Section 7: Alcohol Withdrawal

Alcohol withdrawal syndrome occurs when a person with chronic, heavy alcohol use abruptly reduces or stops drinking, resulting in a hyperadrenergic state from unopposed excitatory neurotransmission. The pathophysiology involves chronic alcohol-mediated potentiation of inhibitory GABA-A receptors and inhibition of excitatory NMDA glutamate receptors; when alcohol is suddenly removed, the adaptive upregulation of excitatory pathways and downregulation of inhibitory pathways produce a state of central nervous system hyperexcitability. Symptoms typically begin 6 to 24 hours after the last drink and follow a predictable temporal progression. Early withdrawal (6 to 24 hours) manifests as anxiety, tremor, diaphoresis, tachycardia, hypertension, insomnia, and gastrointestinal upset. Withdrawal seizures, which are typically generalized tonic-clonic, occur between 12 and 48 hours after the last drink and may be the first presenting symptom.

Alcoholic hallucinosis develops 12 to 48 hours after cessation and is characterized by vivid auditory, visual, or tactile hallucinations occurring in a patient who maintains a clear sensorium, distinguishing it from delirium tremens. The patient may describe hearing voices, seeing insects or animals, or feeling bugs crawling on the skin (formication). Delirium tremens is the most severe and dangerous manifestation of alcohol withdrawal, occurring 48 to 96 hours after the last drink, with a mortality rate of 5 to 15 percent if untreated. It is characterized by global confusion with fluctuating attention (delirium), visual hallucinations, severe autonomic hyperactivity with marked tachycardia, hypertension, fever, and diaphoresis, and psychomotor agitation. Risk factors for progression to delirium tremens include prior history of delirium tremens, prior withdrawal seizures, heavy daily alcohol consumption, concurrent acute medical illness, and abnormal liver function.

The Clinical Institute Withdrawal Assessment for Alcohol-Revised (CIWA-Ar) is the standard validated tool for assessing the severity of alcohol withdrawal and guiding pharmacologic treatment. The scale evaluates ten parameters: nausea/vomiting, tremor, paroxysmal sweats, anxiety, agitation, tactile disturbances, auditory disturbances, visual disturbances, headache, and orientation/clouding of sensorium, with scores ranging from 0 to 67. A score below 10 indicates mild withdrawal that may be managed with observation alone. A score of 10 to 18 indicates moderate withdrawal that benefits from pharmacologic treatment. A score above 18 indicates severe withdrawal requiring aggressive pharmacologic intervention. Symptom-triggered therapy, in which medication is administered based on CIWA-Ar scores rather than on a fixed schedule, has been shown to result in lower total benzodiazepine doses and shorter treatment durations compared with fixed-dose regimens.

Benzodiazepines are the first-line treatment for alcohol withdrawal across all severity levels, acting by potentiating GABA-A receptor function to replace the inhibitory effects of alcohol. Long-acting agents such as diazepam and chlordiazepoxide are preferred for mild to moderate withdrawal because their active metabolites provide a smoother, self-tapering course. Lorazepam is preferred in patients with hepatic dysfunction because it does not undergo hepatic oxidative metabolism and therefore does not accumulate unpredictably in liver disease. For severe withdrawal and delirium tremens, aggressive intravenous benzodiazepine dosing is required, often at doses far exceeding those used in other clinical contexts. Phenobarbital, a long-acting barbiturate, is an effective second-line agent and may be used as an adjunct to benzodiazepines in benzodiazepine-resistant withdrawal or as primary therapy in some protocols, given at 130 to 260 milligrams intravenously. Thiamine (vitamin B1) must be administered before or concurrently with glucose-containing fluids in all patients with suspected alcohol use disorder to prevent Wernicke encephalopathy, which manifests as the triad of encephalopathy, oculomotor dysfunction, and gait ataxia.

<image>Panel A: Timeline of alcohol withdrawal progression showing early withdrawal symptoms (6-24 hours), seizures (12-48 hours), alcoholic hallucinosis (12-48 hours), and delirium tremens (48-96 hours) with symptom descriptions at each stage. Panel B: CIWA-Ar scoring tool showing the ten assessment parameters with severity levels: below 10 (mild, observation), 10-18 (moderate, pharmacologic treatment), and above 18 (severe, aggressive intervention). Panel C: Benzodiazepine selection guide showing diazepam and chlordiazepoxide for mild-moderate withdrawal in patients with normal hepatic function, lorazepam for hepatic dysfunction, and phenobarbital as an adjunct for refractory cases. Panel D: Wernicke encephalopathy prevention and treatment protocol showing thiamine administration before glucose, the classic triad (encephalopathy, oculomotor dysfunction, ataxia), and dosing recommendations.</image>

### Section 8: Substance Intoxication and Overdose

Opioid intoxication is the most immediately life-threatening substance overdose due to respiratory depression and is recognized by the classic toxidrome of depressed mental status, respiratory depression with slow or irregular breathing, and miotic (pinpoint) pupils. The risk of death is primarily from apnea and subsequent hypoxic cardiac arrest. Naloxone, a competitive opioid receptor antagonist, is the specific antidote and is administered at an initial dose of 0.04 to 0.4 milligrams intravenously, titrated to restore adequate respiratory drive without precipitating full reversal and acute withdrawal. Intranasal naloxone at 4 milligrams and intramuscular naloxone at 0.4 milligrams are effective alternatives when intravenous access is not available. A critical consideration is that naloxone has a shorter duration of action (30 to 90 minutes) than most opioids, particularly long-acting agents such as methadone, and patients may re-sedate after the naloxone effect wears off. Therefore, patients who require naloxone should be observed for an appropriate duration, typically 4 to 6 hours for short-acting opioids, and longer for long-acting agents.

Sympathomimetic intoxication from cocaine, methamphetamine, and synthetic cathinones (bath salts) produces a hyperadrenergic state characterized by agitation, psychosis, tachycardia, hypertension, hyperthermia, diaphoresis, and mydriasis. Severe complications include seizures, intracranial hemorrhage, aortic dissection, myocardial infarction, and rhabdomyolysis. Management centers on benzodiazepines as the primary therapeutic agent, addressing agitation, seizures, hypertension, and tachycardia simultaneously by reducing central sympathetic outflow. Active cooling should be initiated for hyperthermia, as temperatures exceeding 40 degrees Celsius can rapidly progress to multi-organ failure. Beta-blockers should be avoided in cocaine intoxication because unopposed alpha-adrenergic stimulation may worsen hypertension and coronary vasoconstriction. Nitrates and calcium channel blockers are preferred for cocaine-related chest pain and hypertension refractory to benzodiazepines.

Sedative-hypnotic intoxication, including benzodiazepine and barbiturate overdose, presents with progressive central nervous system depression ranging from somnolence to coma, respiratory depression, and hypotension. Flumazenil, a benzodiazepine receptor antagonist, is available but carries significant risks that limit its use: it may precipitate seizures in patients with chronic benzodiazepine use or co-ingestion of proconvulsant substances, and it may precipitate withdrawal in benzodiazepine-dependent patients. Therefore, flumazenil is generally reserved for iatrogenic benzodiazepine over-sedation in benzodiazepine-naive patients, such as reversal of procedural sedation. For most benzodiazepine overdoses, management is supportive with airway management, ventilatory support, and hemodynamic monitoring. Barbiturate overdose has no specific antidote and requires aggressive supportive care including mechanical ventilation for respiratory failure and vasopressor support for cardiovascular depression.

Hallucinogen and dissociative drug intoxication encompasses a broad category of substances with diverse mechanisms and clinical effects. Phencyclidine (PCP) produces a unique presentation of agitation, violence, nystagmus (which may be horizontal, vertical, or rotary), muscular rigidity, and apparent insensitivity to pain, making affected patients extremely difficult to manage and potentially dangerous to themselves and others. Management involves benzodiazepines for agitation and a calm, low-stimulation environment. LSD and psilocybin produce altered perception, visual hallucinations, and anxiety but rarely cause medical emergencies; reassurance in a calm environment (the "talk down") is usually sufficient. Synthetic cannabinoids (K2, Spice) may produce severe agitation, psychosis, tachycardia, and seizures. MDMA (ecstasy) produces a sympathomimetic picture with the additional risk of profound hyponatremia from a combination of excessive water intake and inappropriate ADH release, which may cause seizures and cerebral edema.

<image>Panel A: Opioid intoxication toxidrome (depressed mental status, respiratory depression, miotic pupils) with naloxone dosing algorithm showing initial dose of 0.04-0.4 mg IV titrated to respiratory drive, alternative routes (intranasal 4 mg, intramuscular 0.4 mg), and observation periods based on opioid duration. Panel B: Sympathomimetic toxidrome showing agitation, tachycardia, hypertension, hyperthermia, and mydriasis with the management approach centered on benzodiazepines, active cooling, and avoidance of beta-blockers in cocaine intoxication. Panel C: Flumazenil risk-benefit assessment showing appropriate use in iatrogenic over-sedation of benzodiazepine-naive patients versus contraindicated use in chronic benzodiazepine users and co-ingestion scenarios. Panel D: Dissociative and hallucinogen clinical features showing PCP with nystagmus and violence, LSD with altered perception, synthetic cannabinoids with psychosis, and MDMA with hyponatremia risk, with management approaches for each.</image>

### Section 9: Intimate Partner Violence

Intimate partner violence encompasses physical, sexual, psychological, and economic abuse perpetrated by a current or former intimate partner and is a significant public health problem that the emergency physician is uniquely positioned to identify and address. Approximately 1 in 4 women and 1 in 10 men experience intimate partner violence during their lifetime, though these figures likely underrepresent the true prevalence due to underreporting. Emergency department presentations that should prompt screening include injuries inconsistent with the stated mechanism, injuries in various stages of healing suggesting repeated trauma, frequent emergency department visits for vague complaints, delay in seeking care, and a partner who insists on being present during the examination and answers questions on the patient's behalf.

Screening for intimate partner violence should be performed routinely as part of the emergency department assessment. Simple, direct screening questions such as "Do you feel safe at home?" and "Has your partner ever hit, kicked, or physically hurt you?" have been validated for use in the emergency department setting. The patient must be interviewed alone, without the partner present, in a private setting, as the abusive partner's presence will prevent the patient from disclosing abuse. When intimate partner violence is identified, the clinician should express concern, validate the patient's experience, and avoid judgmental statements or pressure to leave the relationship, as the decision to leave is complex and carries its own risks, including an increased risk of homicide during the period immediately after separation. Documentation should be thorough, objective, and include direct quotes from the patient, detailed descriptions and measurements of injuries, and photographs with the patient's consent.

Safety assessment is the most critical component of the emergency department response to intimate partner violence. The Danger Assessment tool evaluates the risk of lethal violence and includes factors such as access to firearms (the strongest predictor of intimate partner homicide), escalating frequency or severity of violence, threats to kill, strangulation attempts (a strong predictor of future lethality), and controlling behaviors including stalking. Patients who are in immediate danger should be provided with the resources to access safety, including domestic violence hotline numbers, information about shelters, and assistance with safety planning. A safety plan addresses immediate steps for leaving safely, identification of a safe location, essential documents and items to take, and a communication plan for reaching help.

Healthcare providers are mandated reporters of suspected child abuse and elder abuse in all jurisdictions, and some jurisdictions also require reporting of intimate partner violence to law enforcement, though this varies considerably. The clinician must be familiar with the specific reporting requirements of their jurisdiction and should consult social work, patient advocacy, and legal resources when uncertain. Medical treatment should address all injuries comprehensively, with attention to the possibility of strangulation injury, which may present with subtle external findings but carry the risk of delayed airway compromise from laryngeal edema, carotid artery dissection, and anoxic brain injury. Follow-up resources should be provided, including referral to domestic violence advocacy services, mental health resources for trauma-related disorders including post-traumatic stress disorder, and legal assistance services.

<image>Panel A: Types of intimate partner violence (physical, sexual, psychological, economic) with emergency department presentation patterns that should trigger screening, including inconsistent mechanism, injuries in various stages of healing, and partner behavior during the visit. Panel B: Screening protocol showing the requirement for private interview without partner present, validated screening questions, clinician response framework (express concern, validate, avoid judgment), and documentation standards including photographs and direct quotes. Panel C: Danger Assessment factors showing access to firearms as the strongest predictor of lethality, escalating violence, strangulation attempts, threats to kill, and stalking, with the safety planning components for patients in immediate danger. Panel D: Resource and reporting flowchart showing mandatory reporting requirements (child abuse, elder abuse, jurisdiction-specific IPV reporting), social work and advocacy referrals, domestic violence hotline and shelter information, and follow-up mental health and legal resources.</image>

### Section 10: Other Psychiatric Emergencies

Panic disorder presents with recurrent, unexpected panic attacks characterized by the sudden onset of intense fear or discomfort accompanied by a constellation of somatic symptoms including chest pain, palpitations, dyspnea, diaphoresis, trembling, paresthesias, and a sense of impending doom. The emergency department evaluation must exclude medical causes of these symptoms, particularly acute coronary syndrome, pulmonary embolism, arrhythmia, thyrotoxicosis, and pheochromocytoma, before attributing the presentation to panic disorder. Reassurance that the symptoms are not life-threatening is itself therapeutic. Acute treatment with a short-acting benzodiazepine such as lorazepam or alprazolam provides rapid symptom relief, though long-term benzodiazepine use should be avoided due to the risk of dependence. Patients should be referred for outpatient psychiatric follow-up for consideration of SSRI therapy, which is the first-line maintenance treatment, and cognitive behavioral therapy, which has the strongest evidence base for long-term management.

Conversion disorder (functional neurologic symptom disorder) presents with neurologic symptoms including weakness, paralysis, sensory loss, seizure-like episodes (psychogenic non-epileptic seizures), blindness, or gait disturbance that are incompatible with recognized neurologic or medical conditions. The diagnosis requires positive clinical findings that demonstrate internal inconsistency, such as Hoover sign (involuntary hip extension of the "weak" leg when the patient flexes the contralateral hip against resistance), collapsing weakness (the "give-way" pattern), and la belle indifference (an unexpected lack of concern about the deficit). It is essential to avoid dismissing these patients as malingering or attention-seeking, as conversion disorder represents genuine distress and disability. The emergency department evaluation should include a focused neurologic examination and appropriate studies to exclude organic pathology, after which the patient should be referred for outpatient neuropsychiatric evaluation.

Catatonia is a psychomotor syndrome that can occur in the context of psychiatric disorders (most commonly mood disorders and schizophrenia), medical conditions, and substance use, and requires specific recognition because standard antipsychotic treatment may worsen the condition. The clinical features include stupor (lack of motor activity and unresponsiveness to external stimuli), mutism, posturing (maintaining postures against gravity), waxy flexibility (passive limb positioning maintained by the patient), negativism (opposition to instructions or attempts to move the patient), and echolalia or echopraxia. The Bush-Francis Catatonia Rating Scale provides a standardized assessment. The first-line treatment is a benzodiazepine trial, typically lorazepam 1 to 2 milligrams intravenously, with a positive response (improvement in catatonic features within 30 minutes) supporting the diagnosis and guiding ongoing treatment. Electroconvulsive therapy is the definitive treatment for refractory catatonia.

Excited delirium is a controversial but clinically recognized syndrome characterized by extreme agitation, violence, bizarre behavior, hyperthermia, insensitivity to pain, and unexpected sudden death, often in the context of stimulant intoxication, acute psychosis, or their combination. Patients with excited delirium may exhibit extraordinary physical strength and may be extremely combative, posing significant danger to themselves and others. The syndrome has been associated with prone restraint, Taser application, and other physical control measures by law enforcement, and has been cited as a contributing factor in in-custody deaths. Emergency management priorities include rapid sedation (ketamine intramuscularly has been increasingly used in the prehospital setting), active cooling for hyperthermia, continuous cardiac monitoring for arrhythmias, avoidance of prone positioning (which may contribute to positional asphyxia), and aggressive treatment of metabolic derangements including acidosis, rhabdomyolysis, and electrolyte abnormalities.

<image>Panel A: Panic disorder presentation showing somatic symptoms (chest pain, palpitations, dyspnea, paresthesias) with the required medical workup to exclude cardiac, pulmonary, and endocrine causes, and the treatment pathway from acute benzodiazepines to outpatient SSRI therapy and cognitive behavioral therapy. Panel B: Conversion disorder clinical signs including Hoover sign demonstration (involuntary hip extension during contralateral hip flexion against resistance), collapsing weakness pattern, and psychogenic non-epileptic seizure characteristics, with emphasis on positive diagnostic signs and avoiding dismissive terminology. Panel C: Catatonia clinical features (stupor, mutism, posturing, waxy flexibility, negativism) with the benzodiazepine challenge test showing lorazepam 1-2 mg IV with assessment of response at 30 minutes and the Bush-Francis Catatonia Rating Scale. Panel D: Excited delirium syndrome showing extreme agitation, hyperthermia, and pain insensitivity with management priorities of rapid sedation, active cooling, avoidance of prone positioning, and cardiac monitoring.</image>

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## Summary

- Suicide risk assessment evaluates demographic, psychiatric, and situational risk factors; prior suicide attempt is the single strongest predictor of future completion
- The Columbia-Suicide Severity Rating Scale provides a standardized framework for assessing suicidal ideation severity from passive thoughts to active intent with a plan
- Verbal de-escalation is the first-line intervention for agitation; pharmacologic options include haloperidol plus lorazepam for undifferentiated agitation and benzodiazepines alone for alcohol withdrawal and stimulant intoxication
- Acute psychosis requires medical workup to exclude organic causes; visual hallucinations, acute onset, and vital sign abnormalities suggest an organic etiology
- Involuntary commitment requires mental illness plus imminent danger to self or others or grave disability; capacity assessment evaluates understanding, appreciation, reasoning, and communication
- Neuroleptic malignant syndrome presents with hyperthermia, lead-pipe rigidity, autonomic instability, and altered mental status; treatment is dantrolene plus bromocriptine after stopping the offending agent
- Serotonin syndrome is distinguished from NMS by rapid onset (hours versus days), clonus rather than rigidity, and hyperactive bowel sounds; cyproheptadine is the specific antidote
- Alcohol withdrawal progresses from early symptoms through seizures to delirium tremens; benzodiazepines are first-line treatment, and thiamine must be administered before glucose
- Naloxone for opioid overdose should be titrated to respiratory drive; patients require observation for re-sedation because naloxone has a shorter duration than most opioids
- Intimate partner violence screening requires a private interview without the partner; access to firearms is the strongest predictor of intimate partner homicide

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## Key Terms

| Term | Definition |
|------|------------|
| Columbia-Suicide Severity Rating Scale | Standardized tool for assessing suicidal ideation from passive thoughts of death through active ideation with specific plan and intent |
| Neuroleptic malignant syndrome | Life-threatening reaction to dopamine-blocking agents characterized by hyperthermia, lead-pipe rigidity, autonomic instability, and altered mental status |
| Serotonin syndrome | Excessive serotonergic activity causing neuromuscular hyperactivity (clonus), autonomic dysfunction, and altered mental status from serotonergic drug interactions |
| CIWA-Ar | Clinical Institute Withdrawal Assessment for Alcohol-Revised, a 10-item scoring tool for assessing alcohol withdrawal severity |
| Delirium tremens | Most severe form of alcohol withdrawal occurring 48-96 hours after cessation, characterized by delirium, hallucinations, and autonomic hyperactivity |
| Decisional capacity | The ability to understand, appreciate, reason about, and communicate a decision regarding one's medical care |
| Catatonia | Psychomotor syndrome characterized by stupor, mutism, posturing, and waxy flexibility; treated with benzodiazepines and electroconvulsive therapy |
| Conversion disorder | Functional neurologic symptom disorder with symptoms incompatible with recognized neurologic conditions, diagnosed by positive clinical signs |

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*This content is subject to the [MIT License](https://opensource.org/licenses/MIT). © 2024–2026 Hibbert School of Medicine.*