The Daily Differential — Tuesday, July 7, 2026

Opioid Use Disorder and Dependence

OUD is common, deadly, and often presents to the ED through withdrawal, overdose, pain, or “just needing help.” The ED visit is a high-yield chance to reduce withdrawal, start evidence-based treatment, and prevent near-term overdose.

By the Blue Fish Med Desk Jul 7, 2026 · Phoenix

0:00 / –:–– AI‑generated audio

A 29-year-old man sits on the stretcher with a hoodie pulled tight, one sneaker still on, tapping his foot against the rail. He keeps glancing at the door, sweating through the collar despite the cool room, and asks twice if “this is going to take long.” His pupils are pinpoints, his jaw aches from grinding, and he says he used to feel “normal” only after a shot or a pill. He is not asking for a detox brochure; he is asking, in a roundabout way, for the storm in his body to stop — and you have not yet decided how.

— What’s your move? Read on.

Before you read

Which patients need symptomatic treatment only, and which should start medication for OUD in the ED?
What is the one disposition error that turns a treatable visit into a lethal relapse?

When to Think of It

Think OUD when the story is repeated use despite harm, escalating dose, failed cut-down attempts, cravings, or withdrawal-driven use. In the ED, it appears as diaphoresis, mydriasis, yawning, piloerection, abdominal cramping, diarrhea, anxiety, tachycardia, and a patient who “feels awful” after last use.

Sick or Not Sick

Sick vs not sick = any respiratory depression, altered mental status, polysubstance exposure, severe dehydration, suicidal intent, pregnancy with unstable use, or inability to reliably follow up. The key call is whether this is uncomplicated withdrawal/OUD appropriate for ED initiation and discharge versus complicated dependence requiring admission/monitoring.

The First Fifteen Minutes

If opioid withdrawal is present and patient wants treatment → buprenorphine/naloxone 8 mg/2 mg SL now when moderate withdrawal is clear, because partial agonism relieves withdrawal and reduces relapse risk. Reassess in 30–60 min; may repeat 4–8 mg/1–2 mg SL to a common ED total of 16 mg/4 mg SL (some patients need more; follow local protocol).
If withdrawal is mild or buprenorphine-precipitated withdrawal risk is high → clonidine 0.1–0.2 mg PO, because alpha-2 agonism reduces autonomic symptoms. Repeat 0.1–0.2 mg PO q6–8h PRN if BP tolerates.
For nausea/vomiting → ondansetron 4 mg ODT/IV, because it improves oral tolerance and symptom control.
For diarrhea → loperamide 4 mg PO once, then 2 mg PO after each loose stool (max 16 mg/day), because it reduces fluid loss and cramping.
For myalgias/arthralgias → ibuprofen 400–600 mg PO (if renal function/GI risk acceptable), because it treats inflammatory pain.
For anxiety/restlessness/insomnia → hydroxyzine 25–50 mg PO, because it can blunt adrenergic distress without respiratory suppression.
If severe dehydration from vomiting/diarrhea → isotonic fluids (e.g., 1–2 L LR or NS IV), because volume repletion improves symptoms and perfusion.
If naloxone reversal has unmasked withdrawal → treat the withdrawal, not just the overdose history; start buprenorphine once moderate withdrawal is present, because naloxone itself does not solve the dependence.
Provide naloxone for discharge: 4 mg intranasal spray, 1 spray in one nostril; repeat every 2–3 min if needed, because relapse and overdose risk are highest after partial abstinence.

Definitive Care & Disposition

Start medication for OUD when feasible: buprenorphine/naloxone in the ED plus a bridge prescription and rapid follow-up are preferred. Link to outpatient addiction care, harm reduction, fentanyl test strips where legal/available, and safer-use counseling. Admit if complicated withdrawal, concurrent serious medical illness, active suicidality, inability to care for self, pregnancy with instability, or severe co-ingestions. If methadone is used, verify local rules and arrange an OTP pathway; EDs generally do not provide ongoing methadone maintenance outside regulatory exceptions.

How This One Kills

Missing OUD means discharging a patient in withdrawal with only comfort meds — they often go straight back to use, then overdose after a period of lowered tolerance. The fatal error is treating the symptoms but failing to start or connect them to effective long-term therapy.

The Differential — What Else Looks Like This

Alcohol withdrawal — tremor, hallucinosis, and seizure risk with alcohol history; confusing it with opioid withdrawal misses benzodiazepine treatment and can be fatal.
Acute gastroenteritis — diarrhea/vomiting without the classic yawning, mydriasis, piloerection, and craving history; mislabeling it delays addiction treatment.
Sepsis — fever, hypotension, and tachycardia may overlap, but infectious source and toxic appearance point away from pure withdrawal; missing sepsis is catastrophic.
Benzodiazepine withdrawal — more prominent agitation, seizures, and delirium; confusing the two can lead to wrong medication and incomplete stabilization.

The Second-Day Story

Older adults, pregnant patients, and people with concurrent sedatives often do not read like classic withdrawal. Elderly patients may present as “weak,” anxious, or with nonspecific GI complaints rather than obvious yawning and piloerection; fentanyl exposure can make withdrawal timing erratic, and buprenorphine can precipitate symptoms if started too early. The clue is the pattern: repeated use to avoid feeling sick, plus objective autonomic signs and a consistent substance history.

Back to Our Patient

Back to our 29-year-old with sweating, pinpoints? Wait — pinpoints fit opioid intoxication, but his foot-tapping, yawning, diaphoresis, and “normal only after a shot or pill” story point instead to opioid withdrawal from OUD once the exam confirms autonomic symptoms and he reports last use hours to a day ago. He is not sedated or hypoventilating, so he is not sick in the overdose sense; he is a candidate for ED-initiated buprenorphine/naloxone once moderate withdrawal is confirmed, plus symptom control, naloxone on discharge, and rapid addiction follow-up. The move not yet made is the life-saving one: start treatment rather than simply padding the wait.

Patient Presentation to Attending

How you’d present this patient on the floor — tight, pertinent positives and negatives, no rambling

“29-year-old man with opioid use disorder here with 12 hours of worsening withdrawal symptoms after last fentanyl use, chief complaint ‘I feel awful and need help getting through this.’ He reports sweating, abdominal cramping, diarrhea, chills, and anxiety; he denies chest pain, fever, hallucinations, suicidal intent, or co-ingestants. On exam he’s anxious, diaphoretic, yawning repeatedly, with piloerection, mydriasis, tachycardia, and no respiratory depression or altered mental status. His vitals are otherwise stable and his COWS is in the moderate range. I think this is uncomplicated opioid withdrawal in a patient with OUD, and I’d like to start buprenorphine/naloxone in the ED, treat symptoms, provide naloxone, and arrange bridge follow-up for MOUD.”

Study Directive

Memorize the COWS elements and practice scoring two sample patients from memory.
Drill a one-minute ED buprenorphine start script: eligibility, withdrawal threshold, dose, reassessment, discharge plan.
Build a personal “withdrawal comfort” order set with doses for clonidine, ondansetron, loperamide, NSAIDs, and hydroxyzine.
Practice distinguishing opioid withdrawal from alcohol/benzo withdrawal and sepsis using 5 discriminating bedside findings.
Review your institution’s buprenorphine bridge and follow-up pathway today.

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Alcoholic ketoacidosis

AKA is an easily missed high-anion-gap acidosis in malnourished heavy alcohol users, often after a binge followed by poor intake and vomiting. It improves...

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The Case

A 46-year-old woman in a wrinkled sweatshirt is curled on her side under the exam light, one hand over her belly, the other clutching an emesis basin that smells faintly sour. She says she “can’t keep anything down,” has been drinking less because she ran out of money, and last ate “maybe two days ago.” Her breath carries a sharp, acetone-like edge, her pulse is fast, and the nurse hands you a glucose that is not as high as you expected. The next decision is whether this is just a hangover with vomiting — or a metabolic trap.

Before You Read

What lab pattern distinguishes alcoholic ketoacidosis from DKA and toxic alcohol ingestion?
Which single therapy stops ketone production fastest?
When is this patient too sick for the floor?

Why It Matters

AKA is an easily missed high-anion-gap acidosis in malnourished heavy alcohol users, often after a binge followed by poor intake and vomiting. It improves rapidly with the right fluids and dextrose — but can also hide sepsis, pancreatitis, GI bleed, or toxic alcohol ingestion.

When to Think of It

Think AKA in a patient with chronic alcohol use, recent binge or abrupt decrease in intake, persistent vomiting, abdominal pain, dehydration, tachycardia, and anion gap metabolic acidosis with normal/low glucose. Ketones are present, but bedside urine ketones may underestimate beta-hydroxybutyrate.

Sick or Not Sick

Sick vs not sick = hemodynamic instability, altered mental status, severe acidemia, electrolyte derangements (especially K/Mg/Phos), or concern for another dangerous cause of anion gap acidosis. The key call is whether this is isolated AKA versus a toxic, septic, or surgical abdomen masquerading as AKA.

The First Fifteen Minutes

Thiamine 100 mg IV now before glucose, because it treats deficiency and reduces Wernicke risk.
Dextrose-containing isotonic fluids: e.g., D5NS or D5LR 1–2 L IV, because glucose stimulates endogenous insulin and shuts off ketogenesis.
If hypovolemic or initially unstable → NS or LR 1–2 L IV bolus, then switch to dextrose-containing fluids, because perfusion must be restored.
Potassium repletion if low or falling → KCl 20–40 mEq IV/PO depending on severity, because insulin surge from dextrose can unmask dangerous hypokalemia.
Magnesium sulfate 2 g IV if hypomagnesemic or torsades risk, because Mg deficiency is common and worsens arrhythmia risk.
Phosphate replacement if severely low/symptomatic (institutional dosing varies), because profound depletion can impair diaphragmatic and cardiac function.
Antiemetic: ondansetron 4 mg ODT/IV, because stopping emesis allows oral intake and recovery.
If withdrawal is present → symptom-triggered benzodiazepine per protocol, because untreated ethanol withdrawal can coexist and worsen course. Dosing varies; follow CIWA/local protocol.

Definitive Care & Disposition

Correct volume depletion, glucose deficit, and electrolytes; search for triggers such as pancreatitis, infection, GI bleed, or withdrawal. Most uncomplicated patients improve within hours and can discharge once tolerating PO, anion gap is closing, vitals are stable, and electrolytes are safe. Admit if severe acidosis, persistent vomiting, pancreatitis, bleeding, withdrawal, inability to take PO, or any alternate diagnosis needing treatment.

How This One Kills

The fatal miss is assuming “alcoholic patient + vomiting = simple dehydration” and not checking the anion gap, beta-hydroxybutyrate, or toxic alcohol differential. AKA can look like DKA, but giving insulin to the wrong patient or missing a toxic ingestion can cause harm.

The Atypical Presentation

AKA is often not dramatic. Elderly patients, patients with cirrhosis, and those partially treated with fluids may show only mild abdominal discomfort, weakness, or tachycardia, while the acidosis is already substantial. Glucose can be normal or mildly elevated, and urine ketones may be unimpressive because beta-hydroxybutyrate dominates. If the history suggests poor intake after alcohol use, trust the pattern and the chemistry, not the bedside vibe.

Back to Our Patient

Back to our 46-year-old with vomiting, poor intake, and a sour/acetone breath. Her labs show a high anion gap metabolic acidosis with normal glucose and elevated beta-hydroxybutyrate, and she is tachycardic but not hypotensive or obtunded — this is alcoholic ketoacidosis, not DKA. She is not sick enough for ICU if her electrolytes are manageable and the gap closes, but she does need thiamine now, dextrose-containing fluids, potassium/magnesium repletion, antiemetics, and evaluation for pancreatitis, GI bleed, infection, or withdrawal. If she can drink, her gap improves, and no alternate dangerous diagnosis is found, she can be discharged with AUD resources and return precautions.

Patient Presentation to Attending

“46-year-old woman with heavy alcohol use and several days of vomiting and poor oral intake, now with abdominal pain and tachycardia. She denies trauma, melena, focal infectious symptoms, or diabetes history. Exam shows dehydration, mild diffuse abdominal tenderness without peritoneal signs, and acetone-like breath; she’s alert but uncomfortable. Her labs show high anion gap metabolic acidosis, normal/low glucose, elevated beta-hydroxybutyrate, and electrolyte depletion without severe renal failure. This fits alcoholic ketoacidosis, and I’m starting thiamine, dextrose-containing IV fluids, electrolyte repletion, antiemetics, and screening for pancreatitis, withdrawal, or another trigger.”

Study Directive

Rehearse the AKA lab pattern from memory: AG metabolic acidosis, normal/low glucose, beta-hydroxybutyrate, dehydration.
Write a 5-step order set: thiamine → dextrose fluids → electrolytes → antiemetic → search for trigger.
Compare AKA vs DKA vs toxic alcohols on one index card.
Practice saying when you would admit an AKA patient: severe acidemia, persistent vomiting, withdrawal, pancreatitis, infection, or inability to take PO.

Key Medications

Thiamine: 100 mg IV before glucose; higher doses may be used if Wernicke is suspected, check institutional protocol.
Dextrose-containing fluids: D5NS or D5LR 1–2 L IV initially; repeat based on volume status and glucose.
Normal saline or LR: 1–2 L IV bolus if markedly volume depleted before switching to dextrose-containing fluids.
Potassium chloride: commonly 10–20 mEq/hr IV for significant hypokalemia with monitoring; oral dosing preferred if stable. Check local potassium replacement protocol.
Magnesium sulfate: 2 g IV over 1 hour typical for hypomagnesemia/arrhythmia risk.
Ondansetron: 4 mg ODT/IV q6–8h PRN.
Benzodiazepines for ethanol withdrawal: protocol-based dosing varies; follow CIWA/institutional guidance.

High-Yield Pearls

Normal glucose does not rule out a dangerous ketoacidosis in alcohol users.
Beta-hydroxybutyrate predominance can make urine ketones misleadingly low.
If the acidosis does not begin to improve quickly with dextrose and fluids, stop anchoring and look for another diagnosis.

The Mimics

Diabetic ketoacidosis — marked hyperglycemia and known diabetes favor DKA; confusing the two can lead to inappropriate insulin or missed alcohol-related malnutrition.
Toxic alcohol ingestion — osmol gap, visual symptoms, renal injury, or refractory acidosis should trigger this concern; missing it is catastrophic.
Pancreatitis — epigastric pain radiating to the back and elevated lipase; confusing it with isolated AKA misses a common trigger and admission need.
Ethanol withdrawal — tremor, agitation, diaphoresis, and hallucinations may coexist; failing to treat withdrawal can worsen morbidity.

Board Question

A 52-year-old man with alcohol use disorder has repeated vomiting after stopping food intake for 2 days. He is tachycardic, has a high anion gap metabolic acidosis, glucose 92 mg/dL, and elevated beta-hydroxybutyrate. Which treatment will most directly stop ketone production?

AInsulin infusion
BDextrose-containing IV fluids after thiamine
CSodium bicarbonate bolus
DFomepizole

Reveal answer

Correct: B

Dextrose stimulates endogenous insulin and suppresses lipolysis/ketogenesis; thiamine should be given first to reduce Wernicke risk. Insulin is usually unnecessary and can cause hypoglycemia; bicarbonate is not routine; fomepizole is for toxic alcohols, not AKA.

Recent Literature

Review or guideline Alcoholic Ketoacidosis: Etiologies, Evaluation, and Management
J Emerg Med, 2021 · cited 36×

A focused EM review of alcoholic ketoacidosis covering the classic presentation, anion-gap workup, and treatment priorities of dextrose-containing fluids, thiamine, electrolyte repletion, and avoiding reflexive insulin.
Recent clinical Elevated osmol gaps in patients with alcoholic ketoacidosis
Clin Toxicol (Phila), 2024 · cited 4×

AKA can produce an elevated osmol gap, so toxic alcohol ingestion should be considered but not assumed solely from the gap when the history and beta-hydroxybutyrate-driven ketoacidosis fit.

TheDaily Differential

Opioid Use Disorder and Dependence

When to Think of It

Sick or Not Sick

The First Fifteen Minutes

Definitive Care & Disposition

How This One Kills

The Second-Day Story

Study Directive

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