An Emergency Medicine Broadsheet
·Phoenix·
Est. MMXXVI
Blue Fish Med · Today's Topic
Conversion Disorder
This diagnosis is common, easy to mishandle, and often triggered by a high-stakes neurologic mimic. Missing an organic cause harms patients; mishandling the conversation can lock in disability and repeat ED use.
A 29-year-old woman in scrubs sits on the ED stretcher with tear tracks drying on her cheeks, her left leg hanging limp while her right foot taps the bedrail. Her vitals are calm, her skin is warm, and her speech is halting but clear; she says the weakness “just came on” after a fight at work. She can’t explain why the leg won’t move, yet when someone drops a blanket, she flinches before she thinks about it. The chart already says “stroke rule-out,” but the bedside picture is not lining up — and the next move matters.
— What’s your move? Read on.
Before you read
What dangerous diagnoses still must be excluded before you make the call?
How do you avoid telling the patient “it’s just stress” while still giving a useful ED plan?
When to Think of It
Think of conversion disorder when neurologic symptoms are inconsistent, internally incongruent, or clearly nonanatomic: abrupt weakness with give-way strength, tremor that changes with distraction, non-epileptic shaking with preserved awareness, or sensory loss that does not map to a neuroanatomic pattern. It often follows stress, trauma, pain, or a psychiatric trigger — but the diagnosis is made by positive exam features, not by “nothing found.”
Sick or Not Sick
The single fork is: does this patient still need a workup for an acute neurologic, toxic, metabolic, or infectious emergency? If the answer is yes, continue the medical evaluation; if no and the exam is convincingly functional, shift to supportive diagnosis and disposition.
The First Fifteen Minutes
If stroke is possible (sudden focal deficit, aphasia, visual field cut, facial droop, persistent objective asymmetry) → activate stroke pathway immediately; manage per protocol, because functional symptoms do not protect against real stroke.
If seizure is ongoing or there is concern for status epilepticus (altered mental status, cyanosis, rhythmic activity, tongue biting, urinary incontinence, persistent postictal state) → lorazepam 2–4 mg IV (or midazolam 10 mg IM if no IV), because benzodiazepines stop true convulsions.
If hypoglycemia is present or not yet excluded → dextrose 25 g IV (e.g., D50W 50 mL IV) because glucose derangement can mimic focal neurologic disease.
If opioid or sedative intoxication is possible → targeted reversal only when indicated: naloxone 0.04–0.4 mg IV/IM/IN, titrate to ventilation, because overshooting can precipitate withdrawal; flumazenil is generally avoided except in rare, expert-guided cases.
If the exam is convincingly functional and life threats are excluded → provide calm reassurance, avoid repeated painful testing, give a clear explanation of symptoms as real and reversible, and engage social work / psychiatry when available, because validation reduces escalation.
Definitive Care & Disposition
There is no ED “cure.” The best care is a confident, nonjudgmental explanation, documentation of positive functional signs, and arrangement for outpatient neurology, psychiatry, or behavioral health follow-up. Admit only if there is another medical reason, unsafe ambulation, inability to care for self, or unresolved diagnostic uncertainty.
How This One Kills
The classic failure is anchoring on “psych” and missing a true stroke, seizure, spinal cord lesion, toxic ingestion, or hypoglycemia. The opposite miss is overtesting a clearly functional presentation and reinforcing illness behavior.
The Differential — What Else Looks Like This
Acute ischemic stroke — objective vascular-pattern deficit, and confusing the two risks thrombolysis delay or missed reperfusion.
Focal seizure with postictal weakness — transient deficit after a witnessed event, and confusing it with conversion can miss epilepsy.
Spinal cord compression — back pain, sensory level, urinary symptoms, and confusing it with conversion can miss a time-sensitive neurosurgical emergency.
Hypoglycemia — autonomic symptoms or altered mentation with rapid glucose response, and confusing it with conversion can be fatal.
The Second-Day Story
In older adults, conversion-like symptoms are less common and a new focal deficit should be treated as organic until proven otherwise. In younger patients, the presentation may be dramatic but inconsistent, with symptoms that worsen when observed and improve with distraction. Some patients present with mixed functional and organic disease, so the presence of functional signs does not end the medical evaluation if anything in the story is off.
Back to Our Patient
Back to our 29-year-old woman in scrubs with sudden left leg weakness after an argument: she has give-way weakness, a positive Hoover sign, normal speech, no facial droop, normal glucose, and no headache, trauma, back pain, or sensory level. She is recognized as having a functional neurologic presentation only after stroke, seizure, and metabolic red flags are assessed and are not present; she is risk stratified as not sick from an ED-neurologic standpoint. In the first fifteen minutes, we avoid unnecessary escalation, explain that the symptoms are real and commonly triggered by stress but not under voluntary control, and arrange safe follow-up. She is discharged with return precautions for new objective neurologic symptoms and outpatient neurology/behavioral health referral.
Patient Presentation to Attending
How you’d present this patient on the floor — tight, pertinent positives and negatives, no rambling
“29-year-old woman with acute left leg weakness that started after an argument at work. She has no headache, trauma, back pain, speech change, facial droop, sensory level, or loss of consciousness, and her glucose is normal. On exam she has give-way weakness and a positive Hoover sign; her cranial nerves and mental status are intact, and the deficit is inconsistent with a vascular pattern. I’m concerned for a functional neurologic symptom disorder after excluding stroke and other emergent mimics. I’m not giving sedatives or more invasive testing right now; I’d like to document the positive exam findings, provide a nonjudgmental explanation, and arrange outpatient follow-up with strict return precautions.”
Study Directive
Practice identifying 3 positive functional exam signs from memory: Hoover sign, give-way weakness, distractible tremor.
Write a 30-second script for explaining functional neurologic symptoms without using “it’s all in your head.”
Review one stroke mimic case and list the red flags that should override a functional impression.
Build a one-page differential for acute unilateral weakness that includes stroke, seizure, hypoglycemia, spinal cord lesion, and conversion disorder.
A practical reference for ED-relevant FND/conversion disorder care: make a positive bedside diagnosis using internal inconsistency and rule-in signs, screen for neurologic emergencies, communicate the diagnosis nonjudgmentally, and arrange
More in Today's Issue
3 additional topics
2 of 4
Eating Disorders
Eating disorders kill through arrhythmia, electrolyte collapse, organ dysfunction, and suicide. The ED job is to spot physiologic instability early and...
0:00 / –:––AI‑generated audio
The Case
A 17-year-old girl in a hoodie keeps tugging her sleeves over her hands while her mother answers most of the questions. The ECG monitor flickers with a slow rate, and her cheeks are sunken enough that the shadows look carved in. She says she’s “fine,” but she won’t stand up without getting lightheaded, and the bathroom smell from home is suddenly easy to imagine. Nobody has said the words out loud yet, but the body is already telling the story.
Before You Read
What findings make an eating disorder medically dangerous today?
Which electrolyte and cardiac complications should you check before letting the patient leave?
What makes this a psychiatric admission, a medical admission, or both?
Why It Matters
Eating disorders kill through arrhythmia, electrolyte collapse, organ dysfunction, and suicide. The ED job is to spot physiologic instability early and prevent a catastrophic discharge.
When to Think of It
Suspect an eating disorder in adolescents and young adults with weight loss, restriction, binge/purge behavior, excessive exercise, bradycardia, orthostasis, amenorrhea, parotid swelling, dental erosion, calluses on knuckles, dehydration, or repeated vague GI complaints. Bulimia may look “normal weight” while still carrying dangerous electrolyte and arrhythmia risk.
Sick or Not Sick
The single call is: is the patient medically unstable from malnutrition or purging? Red flags include bradycardia, hypotension, orthostasis, syncope, hypothermia, QT prolongation, severe electrolyte abnormalities, dehydration, arrhythmia, or inability to safely eat/drink. If unstable, they need medical admission, often with psychiatric co-management.
The First Fifteen Minutes
Check glucose immediately if altered, weak, or syncopal → dextrose 25 g IV if hypoglycemic, because malnutrition can precipitate low glucose.
Obtain ECG and telemetry if bradycardic, purging, weak, syncope, or electrolyte concern, because QT prolongation and bradyarrhythmia can precede sudden death.
Replace electrolytes when low:
Potassium chloride PO/IV per severity and access, commonly 10–20 mEq IV per hour via peripheral line, or higher via central access per protocol; check institutional limits.
Magnesium sulfate 2 g IV for hypomagnesemia or QT prolongation, because magnesium stabilizes myocardium and helps correct refractory hypokalemia.
Phosphate replacement if low, with dosing per severity and route; check local protocol because formulations vary.
If severe agitation, delirium, or seizure occurs from metabolic derangement → treat the underlying abnormality first; benzodiazepines do not fix the cause.
If vomiting or dehydration is significant → 0.9% normal saline IV bolus 1–2 L in adults as needed, because volume repletion improves perfusion and orthostasis.
If concern for thiamine deficiency, especially with prolonged poor intake or concurrent alcohol use → thiamine 100 mg IV before significant glucose-containing fluids when feasible, because it helps prevent Wernicke encephalopathy.
Definitive Care & Disposition
Medical admission is indicated for physiologic instability, severe electrolyte derangement, QT prolongation, syncope, ongoing purging with arrhythmia risk, or inability to maintain oral intake. Psychiatry, adolescent medicine, nutrition, and social work should be involved early; definitive treatment is multidisciplinary and longitudinal, not ED-based. Discharge only when medically stable, safe follow-up exists, and the patient can reliably eat/drink.
How This One Kills
The classic failure is focusing on weight alone and missing the unstable “normal-weight” purging patient with a dangerous potassium or magnesium deficit. The other miss is discharging a bradycardic, orthostatic adolescent because the family promises follow-up.
The Atypical Presentation
Men, older adults, athletes, and patients with higher body weight can still have clinically significant restrictive or purging eating disorders. Some present not with explicit body-image complaints but with syncope, palpitations, constipation, stress fractures, or repeated “electrolyte” visits. Adolescents may minimize symptoms, while parents may describe ritualized meals, bathroom trips, or hidden exercise.
Back to Our Patient
Back to our 17-year-old in the hoodie with bradycardia and orthostasis: the combination of restrictive intake, lightheadedness, sunken appearance, and likely purging behavior makes an eating disorder medically dangerous until proven otherwise. She is recognized by the malnutrition/purging phenotype, and she is risk stratified as unstable because the slow pulse and orthostatic symptoms could precede arrhythmia or collapse. In the first fifteen minutes, we check glucose, ECG, potassium, magnesium, phosphate, and hydration status, give thiamine if indicated, and correct abnormalities while placing her on telemetry. She needs medical admission with psychiatric and nutrition consultation rather than discharge.
Patient Presentation to Attending
“17-year-old female with restriction and possible purging who presents with lightheadedness and bradycardia. She looks malnourished, has orthostatic symptoms, and her family reports reduced intake and frequent bathroom trips after meals. I’m worried about an eating disorder with medical instability rather than simple dehydration, and I’ve already ordered ECG, glucose, electrolytes including magnesium and phosphate, and placed her on telemetry. My plan is admission for monitoring and repletion, with psychiatry and nutrition involved early.”
Study Directive
Memorize the ED instability criteria for eating disorders and recite them without notes.
Practice reading 3 ECGs: sinus bradycardia, prolonged QT, and U waves from hypokalemia.
Make a repletion plan for potassium, magnesium, and phosphate using your department’s protocol.
Learn a 30-second nonjudgmental script for discussing restriction/purging with adolescents and families.
Key Medications
Dextrose 25 g IV for hypoglycemia.
0.9% normal saline 1–2 L IV bolus for dehydration/orthostasis, titrated to response.
Magnesium sulfate 2 g IV for hypomagnesemia/QT prolongation; may repeat depending on level and renal function.
Potassium chloride: commonly 10 mEq IV per hour peripheral, sometimes 20 mEq IV per hour central with monitoring; verify with protocol.
Thiamine 100 mg IV before glucose-containing fluids when deficiency risk exists.
Phosphate replacement: dosing varies by severity and formulation; check institutional guidance.
High-Yield Pearls
BMI is not a safety check; electrolytes and ECG are.
Normal serum phosphorus can fall rapidly after refeeding, so “initially okay” does not mean safe.
Repeated “GI complaints” plus dental erosion or parotid swelling should trigger a purging history.
The Mimics
Inflammatory bowel disease — GI symptoms and weight loss with inflammatory markers, and confusing the two can delay psychiatric and nutritional treatment.
Hyperthyroidism — weight loss with tachycardia and heat intolerance, and confusing it with anorexia misses endocrine disease.
Depression — poor intake and weight loss, but eating-disorder cognitions and purging behaviors are the discriminators.
Malignancy — weight loss and fatigue, and confusing it with eating disorder can miss cancer; red flags are fevers, night sweats, focal findings, or progressive pain.
Board Question
A 19-year-old woman with presumed bulimia presents with weakness and palpitations. She has a normal BMI, but ECG shows QT prolongation and labs reveal hypokalemia. What is the most appropriate next step?
AReassure her because normal weight excludes medical risk
BDischarge if she can tolerate oral intake
CAdmit for telemetry and electrolyte correction
DStart benzodiazepines for anxiety
Reveal answer
Correct: C
Purging patients can have life-threatening electrolyte disturbances despite a normal BMI. QT prolongation and hypokalemia require monitored correction because of sudden arrhythmia risk.
EM-focused review covering recognition, medical instability, electrolyte/QT complications, refeeding risk, and disposition thresholds for patients with anorexia, bulimia, and related eating disorders.
3 of 4
Refeeding Syndrome
Refeeding syndrome can cause arrhythmias, respiratory failure, seizures, and death after starvation or prolonged poor intake. The ED often sees the first...
A 54-year-old man with a gaunt face and a hospital wristband is finally eating again after days of starvation. He looks better than yesterday — more alert, more hopeful, and eager for breakfast — but the monitor now shows a slightly fast heart rate and the nurse notices he’s weaker getting out of bed. His tube feeds were advanced overnight, and the labs from dawn are sitting in the chart with a few quiet numbers already sliding the wrong way. The dangerous part has not come from not feeding him; it may come from feeding him too fast.
Before You Read
Who is high risk for refeeding syndrome before calories are increased?
Which electrolyte shift is the warning shot?
How do you restart nutrition without triggering collapse?
Why It Matters
Refeeding syndrome can cause arrhythmias, respiratory failure, seizures, and death after starvation or prolonged poor intake. The ED often sees the first deterioration after hospitalization, tube feeds, or abrupt nutrition restart.
When to Think of It
Think of refeeding syndrome in malnourished patients after prolonged fasting, anorexia, alcoholism, chronic illness, cancer, bariatric surgery, prolonged NPO status, or severe cachexia. Early clues are weakness, edema, tachycardia, confusion, dyspnea, or new arrhythmia after calories, dextrose, or enteral feeds are started.
Sick or Not Sick
The single fork is: has nutrition already been restarted in a patient at high risk, and are phosphorus, potassium, or magnesium falling? If yes, the patient is medically unstable and needs slow feeding plus aggressive electrolyte monitoring/repletion.
The First Fifteen Minutes
Check phosphate, potassium, magnesium, glucose, and ECG immediately in a high-risk patient starting feeds or glucose, because the syndrome is defined by intracellular shifts.
If hypophosphatemia is present → phosphate replacement per severity and route; dosing varies by local formulation and renal function, so use your protocol/reference.
If hypokalemia is present → potassium chloride repletion per severity; commonly 10–20 mEq IV per hour depending on access and monitoring.
If hypomagnesemia is present → magnesium sulfate 2 g IV, because magnesium repletion helps stabilize the myocardium and corrects refractory potassium loss.
If thiamine deficiency risk exists (malnutrition, alcoholism, prolonged poor intake) → thiamine 100 mg IV before carbohydrate load when feasible, because carbohydrate metabolism can precipitate Wernicke encephalopathy.
If hypoglycemic → dextrose 25 g IV, but be cautious: carbohydrate loads can worsen refeeding shifts if not monitored.
Definitive Care & Disposition
Management is slow nutrition advancement, frequent electrolyte checks, telemetry for significant abnormalities, and close coordination with nutrition and the admitting team. Severe hypophosphatemia, arrhythmia, respiratory weakness, or neurologic changes merit monitored admission or ICU depending on severity. Prevention is the real treatment: identify risk before calories rise.
How This One Kills
The classic failure is “he’s hungry now, so let’s feed fast,” followed by sudden hypophosphatemia, arrhythmia, and respiratory failure. Another miss is forgetting that IV dextrose can act like refeeding in a starved patient.
The Atypical Presentation
Patients may look improved initially as calories resume, which falsely reassures teams while phosphate is falling. The syndrome can also appear after dextrose-containing IV fluids or tube feed initiation, not just oral eating. In older or chronically ill patients, subtle confusion, weakness, or edema may be the first clue.
Back to Our Patient
Back to our 54-year-old man with a gaunt face and new weakness after tube feeds: he is recognized as high risk for refeeding syndrome because prolonged starvation plus rapid nutrition restart is the setup, and the falling labs are the clue. He is risk stratified as potentially unstable due to electrolyte shifts that can trigger arrhythmia or respiratory failure. In the first fifteen minutes, we check phosphate, potassium, magnesium, glucose, and ECG, replete deficits, give thiamine, and slow the feeding plan. He needs monitored admission with strict electrolyte surveillance and gradual caloric advancement.
Patient Presentation to Attending
“54-year-old malnourished man with recent restart of tube feeds now has weakness and mild tachycardia. He was starved for several days and his labs are trending down, especially phosphorus, with concern for refeeding syndrome. I’ve ordered ECG, phosphate, potassium, magnesium, and glucose and started thiamine while coordinating slower nutrition advancement. He needs telemetry and close electrolyte repletion because of arrhythmia risk.”
Study Directive
Draw the intracellular shift diagram for refeeding syndrome from memory.
List 5 high-risk states for refeeding and rehearse them aloud.
Build a monitoring schedule: what labs to check at baseline, 6 hours, 12 hours, and 24 hours in your ED/admitting workflow.
Compare refeeding syndrome to DKA treatment shifts and explain the difference.
Key Medications
Thiamine 100 mg IV before carbohydrate load when feasible in high-risk malnutrition/alcohol use.
Magnesium sulfate 2 g IV for hypomagnesemia; may repeat based on level/renal function.
Potassium chloride commonly 10–20 mEq IV per hour with monitoring; verify limits.
Phosphate replacement: dosing depends on serum level, route, and product; check protocol due to variability.
Dextrose 25 g IV for hypoglycemia, but monitor closely in high-risk refeeding patients.
High-Yield Pearls
Phosphate is the classic “canary in the coal mine,” but potassium and magnesium often fall with it.
Dextrose alone can trigger the same physiology as feeding.
Edema after refeeding is not reassurance; it can be part of the syndrome.
The Mimics
Simple dehydration — improves with fluids and lacks the characteristic electrolyte collapse after calories.
Sepsis — can cause weakness and tachycardia, but the trigger is not refeeding and labs point to infection.
Heart failure — edema and dyspnea overlap, but the clue is recent nutrition restart in a malnourished patient.
Alcohol withdrawal — tremor and autonomic symptoms can overlap, but refeeding centers on phosphate/potassium/magnesium drop after carbohydrate exposure.
Board Question
A cachectic patient with prolonged poor intake is started on enteral feeds and returns 24 hours later with weakness and edema. Labs show phosphorus 1.1 mg/dL, potassium 3.0 mEq/L, and magnesium 1.4 mg/dL. What is the best next step?
AIncrease calories to reverse catabolism
BStop all nutrition permanently
CReplete electrolytes, give thiamine, and slow caloric advancement with monitoring
DGive naloxone and discharge
Reveal answer
Correct: C
This is classic refeeding syndrome. Treatment is not abandoning nutrition; it is cautious refeeding with phosphate, potassium, magnesium replacement and thiamine, while monitoring closely for arrhythmia and respiratory compromise.
Provides practical consensus guidance for ED-to-inpatient care: screen malnourished or prolonged-starvation patients, give thiamine and electrolyte repletion early, restart calories cautiously, and monitor phosphate, potassium, and magnesiu
Alcohol withdrawal can progress quickly from tremor to seizures to delirium tremens, which is life-threatening without prompt treatment. ED management...
A 46-year-old man in a wrinkled T-shirt smells faintly of old beer and sweat, sitting too still on a gurney with a tremor in both hands that makes the cup in his lap rattle. His wife says he’s “cutting down,” but he hasn’t slept and keeps asking the same question about the day and the time. On the monitor, his pulse is climbing; he squints at the fluorescent lights and says the room feels “too bright.” The chart already hints at the diagnosis, but the dangerous part is deciding what happens next.
Before You Read
Is this uncomplicated intoxication, withdrawal, or a complication like seizure or delirium tremens?
What medication treats withdrawal best, and when should you add adjuncts?
Who needs admission, telemetry, or ICU?
Why It Matters
Alcohol withdrawal can progress quickly from tremor to seizures to delirium tremens, which is life-threatening without prompt treatment. ED management hinges on recognizing the syndrome early and treating to prevent escalation, not just calming the patient.
When to Think of It
Suspect withdrawal in a patient who recently reduced or stopped heavy alcohol use and now has tremor, anxiety, diaphoresis, tachycardia, hypertension, nausea, agitation, insomnia, hallucinations, or seizures. Intoxication is different: slurred speech, ataxia, somnolence, and odor of alcohol, often without the autonomic hyperactivity of withdrawal.
Sick or Not Sick
The single fork is: is the patient in withdrawal with autonomic instability, hallucinations, seizures, delirium, or a history of severe withdrawal? If yes, treat aggressively and admit; if no, uncomplicated mild symptoms may be managed with observation and a safe plan.
The First Fifteen Minutes
Thiamine 100 mg IV early in heavy alcohol use, malnutrition, confusion, or before glucose when feasible, because it reduces risk of Wernicke encephalopathy.
Lorazepam 2–4 mg IV for withdrawal symptoms, repeated every 15–30 minutes to effect, or diazepam 5–10 mg IV / chlordiazepoxide 50–100 mg PO in appropriate patients, because benzodiazepines are first-line and prevent seizures/DTs.
Midazolam 5–10 mg IM/IV can be used when rapid control is needed and IV access is limited.
Phenobarbital 130–260 mg IV loading or repeated boluses may be used in some protocols for refractory withdrawal or benzodiazepine-sparing strategies; dosing varies, so follow institutional guidance.
Dextrose 25 g IV only if hypoglycemic, because alcohol use commonly masks low glucose.
Magnesium sulfate 2 g IV if hypomagnesemic or with arrhythmia/seizure risk, because magnesium deficiency worsens withdrawal complications.
0.9% normal saline IV if dehydrated, because volume depletion worsens tachycardia and orthostasis.
Definitive Care & Disposition
Severe withdrawal, seizures, delirium tremens, significant autonomic instability, or refractory symptoms require monitored admission, often stepdown/ICU. In uncomplicated withdrawal, oral benzodiazepine taper and linkage to addiction treatment may be appropriate if the patient is reliable and safe. Give thiamine, assess for liver disease, trauma, GI bleed, pancreatitis, and co-ingestions as indicated.
How This One Kills
The big miss is labeling withdrawal as “anxiety” or “just intoxication” until the patient seizes or enters delirium tremens. Another is giving glucose without thiamine in a malnourished drinker when Wernicke risk is high.
The Atypical Presentation
Older adults, patients with liver disease, and those taking beta-blockers may have blunted tachycardia or tremor and still be in significant withdrawal. Some patients deny use or minimize timing, so collateral history matters. Withdrawal can begin even with a measurable ethanol level if the level is falling from the patient’s usual baseline.
Back to Our Patient
Back to our 46-year-old man with tremor, tachycardia, and photophobia after cutting down alcohol: he is recognized as having alcohol withdrawal, not simple intoxication, because the autonomic hyperactivity and insomnia fit the syndrome. He is risk stratified as potentially unstable because his pulse is rising and he may progress to seizures or delirium tremens. In the first fifteen minutes, we give thiamine, start benzodiazepine therapy, check glucose and electrolytes, and reassess frequently for escalation. Depending on response and severity, he likely needs monitored admission or at least observation with a clear detox plan.
Patient Presentation to Attending
“46-year-old man with heavy alcohol use who cut down recently and now has tremor, tachycardia, insomnia, and photophobia. He’s more consistent with withdrawal than intoxication because he’s autonomically active and getting worse, not just sedated. I’ve given thiamine, started benzodiazepines, and checked glucose and electrolytes, and I’m reassessing for hallucinations or seizure risk. If he continues to need escalating doses or develops confusion, he’ll need monitored admission.”
Study Directive
Rehearse the CIWA-Ar features and match them to withdrawal severity.
Memorize a benzodiazepine starting-dose plan and one phenobarbital pathway used at your shop.
Practice distinguishing intoxication from withdrawal in 3 brief case vignettes.
Review the admission criteria for DTs and withdrawal seizures from your institution.
Key Medications
Thiamine 100 mg IV once early; many admit teams use higher doses for suspected Wernicke, but check local protocol.
Lorazepam 2–4 mg IV repeat q15–30 min to symptom control.
Diazepam 5–10 mg IV or 10–20 mg PO depending on severity and pathway.
Chlordiazepoxide 50–100 mg PO for mild/moderate withdrawal in appropriate patients.
Midazolam 5–10 mg IM/IV for rapid control if needed.
Phenobarbital 130–260 mg IV bolus strategies vary; verify protocol.
Magnesium sulfate 2 g IV if low or high-risk.
Dextrose 25 g IV for documented hypoglycemia.
High-Yield Pearls
Alcohol withdrawal is a diagnosis of timing plus autonomic hyperactivity.
A measurable alcohol level does not exclude withdrawal if the patient is falling from baseline.
Thiamine is cheap; missed Wernicke encephalopathy is not.
The Mimics
Alcohol intoxication — sedation and ataxia without the escalating autonomic hyperactivity of withdrawal.
Stimulant intoxication — agitation and tachycardia, but usually with mydriasis, psychosis, and a stimulant history.
Sepsis — tremor and tachycardia can overlap, but fever, source, and infectious markers point away from withdrawal.
Head injury or intracranial bleed — altered mental status in a drinker may be trauma, and confusing the two can be fatal.
Board Question
A 50-year-old man with a long history of heavy alcohol use presents 12 hours after his last drink with tremor, diaphoresis, anxiety, and tachycardia. Which medication is first-line?
AHaloperidol
BLorazepam
CNaloxone
DFlumazenil
Reveal answer
Correct: B
Benzodiazepines are first-line for alcohol withdrawal because they treat the GABA deficit and reduce seizures and delirium tremens. Antipsychotics may worsen seizure risk, and naloxone/flumazenil are not indicated.
ED-specific GRACE guidance supports practical AUD care at the bedside, including screening, brief intervention/referral, and initiation of evidence-based treatment rather than treating intoxication alone.
A quick test of recall from prior editions. Commit to an answer before you check.
From yesterday's edition
A 36-year-old woman presents after syncope while taking escitalopram, hydroxyzine, and azithromycin for a respiratory illness. Her ECG shows a QTc over 560 ms with broad-based T waves and a pause-dependent premature ventricular beat. What’s the diagnosis, and the first move?
Check your answer
Long QT Syndrome. Stop QT-prolonging medications, correct K/Mg/Ca, place on telemetry, and treat torsades immediately if it occurs. Syncope, QTc >500 ms with symptoms, or congenital concern warrants admission or urgent cardiology input.
From the July 3 edition
Today, three days ago: Adenosine. What’s the adult ED dose, and the contraindication you’d most regret missing?
Check your answer
6 mg rapid IV push followed immediately by saline flush; if no conversion, 12 mg rapid IV push, may repeat 12 mg once. Use proximal IV/stopcock technique. Second/third-degree AV block or sick sinus without pacer, asthma/severe bronchospasm caution, irregular/polymorphic wide-complex tachycardia, preexcited AF.
From the June 26 edition
A 52-year-old woman presents with sudden maximal-intensity headache, vomiting, and neck stiffness. Noncontrast head CT shows blood in the basal cisterns. Which additional therapy most reduces the risk of delayed ischemic neurologic deficits?
AMannitol
BNimodipine
CDexamethasone
DPhenytoin prophylaxis
Reveal answer
Correct · B
Nimodipine. Nimodipine is given to patients with aneurysmal SAH because it reduces delayed ischemic deficits, likely through neuroprotective and vasospasm-related effects. Mannitol may be used for ICP crises, steroids do not help, and routine anticonvulsant prophylaxis is not the key disease-modifying therapy.
Journal Watch
From the FOAMed wire
Notable posts and reviews from the last week, ranked by relevance to today’s lead and source trust.
Welcome back to Rebel MIND, the podcast where we sharpen the person behind the practitioner. MIND stands for Mastering Internal Negativity during Difficulty. This series emphasizes productivity, provider performance, and team optimization to ensure we are at our best during...
Chris Nickson Followership Followership is a high‑impact teamwork competency: active, engaged clinicians who speak up, monitor teammates, and adapt fluidly between leading and following boost team performance — provided leaders, culture, and systems make those behaviours possible.
Podcast Picks
Two for the shift
Critical Care Perspectives in Emergency Medicine2026-05-23
Acute hypoxemic respiratory failure is a leading cause of ICU admission worldwide. Oxygen is first-line therapy for patients with acute hypoxemic respiratory failure and can be given via nasal cannula (NC), non-rebreather mask (NRB), high-flow nasal cannula (HFNC), or noninvasive ventilation (NIV). At present, the literature is inconsistent on which mode...
Source
Critical Care Perspectives in Emergency Medicine
Published
2026-05-23
Host
Critical Care Perspectives in Emergency Medicine, Critical Care Perspectives in Emergency Medicine
We kick off July with pieces on sepsis from Haney, peds fingertip injuries from Ilene, and a case of a cranky consult with Jan and Swami. Megan and Mel work through last month’s EMA papers 1. Mel's July Update 2....
Critical Care Corner
Matched to today’s topics
A critical-care reference from LITFL’s Critical Care Compendium, tied to today’s differential.
Refeeding syndrome is the resuscitation-phase trap in severe eating disorders and alcohol-related malnutrition: calories can precipitate hypophosphataemia, arrhythmias, respiratory failure, and collapse unless electrolytes and thiamine are anticipated.
Refeeding Syndrome = a group of clinical findings that occur in severely malnourished individuals undergoing nutritional support.
Pharmacology Corner
Two drugs for the shift
One antimicrobial and one other ED workhorse — selected daily, with sources and last-reviewed dates so every dose is cross-checkable.
Antimicrobial of the Day
Clindamycin
Lincosamide antibiotic; toxin-suppressing protein synthesis inhibitor
Indication
Adjunctive toxin suppression in necrotizing fasciitis or streptococcal toxic shock; anaerobic and gram-positive coverage in selected dental, skin, and soft tissue infections; alternative in some beta-lactam allergy scenarios.
What’s your dose? — reveal dosing & cautions
ED Dose
600–900 mg IV q8h for severe infection. 300–450 mg PO q6–8h for outpatient SSTI/dental infections when appropriate.
Renal Adjustment
No renal dose adjustment.
Contraindications
Known clindamycin allergy; history of severe C. difficile is a major caution.
Interactions
Neuromuscular blockers may be potentiated; erythromycin antagonism possible in vitro.
Monitoring
Diarrhea/C. difficile risk, LFTs and CBC with prolonged courses, local resistance patterns for MRSA.
ED Pearl
In suspected nec fasc or streptococcal toxic shock, clindamycin is not there for coverage breadth — it is there to suppress toxin production while definitive source control happens.
For educational use only. Verify dosing against the FDA label and your institution’s pharmacy resources before administering.
ECG of the Day
Ischemia
Posterior STEMI
ST depression in V1–V3 with tall R waves and upright T waves is the mirror image of posterior wall infarction — flip the ECG and you are looking at a STEMI.
The Tracing
A 62-year-old woman with diaphoresis and back pain has an ECG that shows ST depression of 2 mm in V1 through V3 with notably tall R waves in V1–V2 and upright T waves in those leads. Inferior leads show subtle ST elevation of about 1 mm in II, III, and aVF. The triage interpretation reads 'anterior ischemia' and no STEMI alert is called. Posterior leads V7–V9, placed at the request of the senior physician, show 1.5 mm of ST elevation. The cath lab is activated.
Horizontal ST depression in V1–V3 (sometimes extending to V4) — the mirror image of ST elevation
Tall R waves in V1–V2 (R/S ratio > 1, R wave width often > 40 ms)
Upright T waves in V1–V2
Often accompanied by inferior STEMI findings (ST elevation in II, III, aVF) because the same RCA territory is involved
Confirm by placing posterior leads V7–V9: ≥ 0.5 mm ST elevation is diagnostic
Pearls
When you see anterior ST depression, ask whether the ECG is upside down. Flip the tracing mentally — depression becomes elevation, R waves become Q waves, and the diagnosis becomes obvious.
Posterior MI is most often part of an inferior or lateral infarct. If the inferior leads are abnormal, look harder at V1–V3.
Posterior leads add only 30 seconds at the bedside. Use them whenever V1–V3 show ST depression that you can't otherwise explain.
Pitfalls
The standard 12-lead ECG does not directly view the posterior wall, so the diagnosis is easy to miss without active suspicion.
Computer interpretation rarely calls posterior MI; many algorithms label it 'anterior subendocardial ischemia' instead.
An isolated posterior MI (no inferior or lateral involvement) is rarer but happens. Keep V7–V9 on the table when the story fits.
At the Bedside
Treat as STEMI. ASA and anticoagulation per local pathway, cath lab activation, posterior leads to confirm and document. Do not delay activation while obtaining V7–V9 if suspicion is high — the workflow runs in parallel.
For educational use only. Verify ECG interpretation against the LITFL entry and your institution’s practice before clinical decision-making.
Case of the Day
From the lead · Conversion Disorder
Self-Examination
Test Your Understanding
A 32-year-old woman develops sudden right arm weakness after a family conflict. CT head is negative. On exam, her arm drift improves when she is distracted, and she has inconsistent effort with normal reflexes and no facial droop. Which is the best next step?
AStart IV alteplase
BReassure her that symptoms are voluntary and discharge without follow-up
CProvide a clear explanation that symptoms are real, document positive functional signs, and arrange outpatient follow-up
DGive lorazepam and observe for postictal recovery
Reveal answer
Correct answer · C
Functional neurologic symptoms are diagnosed by positive exam features after emergent mimics are excluded, and the best ED management is a validating explanation plus follow-up. Calling the symptoms voluntary is harmful and usually worsens outcomes.