Hospital Medicine Unplugged

In this episode of Hospital Medicine Unplugged, we sprint through atrial flutter—spot the sawtooth, choose the fastest safe path to sinus, and keep strokes off the table.
We open with the do-firsts: confirm the rhythm and triage the “why.” Grab a 12-lead ECG—regular narrow tachycardia with classic sawtooth F-waves (atrial ~240–300 bpm, often 2:1 AV → ~150 bpm). Don’t confuse variable conduction with AF. Put the patient on telemetry; replete K/Mg (K ≥4, Mg ≥2). Hunt triggers (infection, hypoxia, decomp HF, stimulants, post-op). Get an echo to size up structure/valves; plan TEE if cardioversion and duration ≥48 h or unknown.
Acute decisions—match stability to action:• Unstable (hypotension, ischemia, pulmonary edema, shock): synchronized cardioversion now. Start 50–100 J biphasic (AP pads), escalate as needed.• Stable: pick rate vs rhythm based on symptoms, duration, and comorbids.– Rate control first line: β-blocker (esmolol/metoprolol) or diltiazem/verapamil; avoid NDHP-CCBs in HFrEF. Add digoxin as adjunct if needed. If decomp HF/hypotension, IV amiodarone can slow the ventricle.– Rhythm control when rate control is tough or symptoms/high stakes: synchronized cardioversion (near-certain success), or ibutilide 1 mg IV over 10 min (give Mg 2 g IV; strict QT monitoring) or dofetilide (inpatient initiation, QT monitoring). Class IC (flecainide/propafenone) can provoke 1:1 conduction—never give without AV-nodal blockade and avoid in structural heart disease.– Pre-excitation (WPW pattern): avoid AV-nodal blockers; urgent cardioversion.
Anticoagulation—same rules as AF: use CHA₂DS₂-VASc for long-term decisions. If duration ≥48 h or unknown, choose ≥3 weeks of therapeutic anticoagulation or TEE-guided cardioversion, and continue OAC ≥4 weeks post-cardioversion. Many hospitalized adults meet OAC criteria—don’t skip stroke prevention.
When to favor rhythm early: persistent rapid rates despite meds, ischemia/HF, poor tolerance, or procedural timing needs. A quick shock back to sinus simplifies everything.
Think definitive: CTI ablation for typical (isthmus-dependent) flutter is >90–95% effective with low risk—strong option after a first significant hospitalization or if recurrent. Expect incident AF (~50%) after flutter—monitor and keep OAC per risk, not just rhythm appearance.
ICU/complex plays: in decompensated HF or shock, cardiovert early; if meds needed, amiodarone is often the hemodynamically friendliest for rate control. Correct hypoxemia, fever, and volume—they’re gasoline on the circuit.
Special populations, quick hits:• HFrEF: β-blocker if stable; avoid diltiazem/verapamil; amiodarone for rate/rhythm if needed; early ablation is attractive.• Post-cardiac surgery: often transient—rate control, consider amiodarone/ibutilide if symptomatic; map/ablate for recurrent cases.• Pre-excited flutter: no AV-nodal blockers; shock or procainamide (if truly stable and expert-guided).
Procedure pearls (make it boring-safe): Anterior–posterior pad placement, sedation ready, sync ON, start low energy (flutter needs less than AF), and re-check rhythm + anticoagulation plan before leaving the bedside.
We close with the system moves: an atrial-flutter bundle that (1) auto-flags sawtooth at ~150 bpm and fires a cardioversion pathway for instability; (2) hard-stops electrolytes to K ≥4/Mg ≥2; (3) blocks NDHP-CCBs in HFrEF and blocks AV-nodal agents if pre-excitation seen; (4) offers ibutilide with QT/Mg guardrails and dofetilide inpatient-initiation checklist; (5) forces TEE-or-≥3-weeks-OAC when duration ≥48 h/unknown, and locks in ≥4 weeks post-CV OAC; (6) auto-consults EP for CTI ablation after first significant admission or recurrence; (7) adds AF-surveillance plan (patch/tele) and leaves OAC tied to CHA₂DS₂-VASc, not wishful thinking.
Fast, ECG-led, and stroke-savvy—see the sawtooth, fix the rate or flip the rhythm, and never miss the anticoagulation.

In this episode of Hospital Medicine Unplugged, we blitz inpatient atrial fibrillation (AF)—fix the trigger, pick rate vs rhythm, and prevent stroke—so you can move fast and safely.
We open with the do-firsts: vitals + hemodynamics, bedside ECG, labs (electrolytes, Mg, CBC, TSH when relevant), pulse oximetry/ABG, and a deliberate hunt for reversible triggers—infection, hypoxia, electrolyte derangements, volume shifts, ACS/PE, surgery, alcohol/withdrawal, stimulants. Treat the cause; the rhythm often follows.
Unstable? (hypotension, shock, ischemia, pulmonary edema) → immediate synchronized DCCV. While prepping: oxygen, gentle fluids/pressors as needed, avoid AV-nodal blockers if WPW suspected.
Stable? Rate or rhythm are both reasonable.• Rate control first for most: β-blocker (metoprolol, esmolol) or non-DHP CCB (diltiazem) if LVEF >40%. Add digoxin when hypotensive/sedentary/HFrEF. Target lenient HR <110 at rest; go stricter if symptoms or TIC (tachycardia-induced cardiomyopathy).• Rhythm control when symptoms persist, HF decompensation, poor rate control, newly diagnosed AF with CV risk, or patient preference. Options: electrical cardioversion (fast, effective), or drugs tailored to substrate: Class Ic (flecainide/propafenone) only if no structural/ischemic disease; amiodarone for structural heart disease/HF; sotalol/dofetilide (inpatient initiation, watch QT/renal). Early rhythm control can lower CV events in selected patients.• HFrEF tips: favor β-blocker ± digoxin for rate; avoid diltiazem/verapamil; consider catheter ablation early for symptom control and outcomes.
Cardioversion anticoagulation rules (no preexcitation/WPW):• AF >48 h or unknown: ≥3 weeks therapeutic OAC or perform TEE-guided cardioversion if no LA thrombus, then ≥4 weeks OAC after.• AF <48 h and low stroke risk: may cardiovert now; still continue OAC for ~4 weeks if risk factors exist.
Stroke prevention—don’t miss it. Use CHA₂DS₂-VASc to guide therapy; check HAS-BLED to modifiable risks—not to deny needed OAC. Prefer DOACs over warfarin for most nonvalvular AF (dose-adjust for renal function). Warfarin for mechanical valves or moderate–severe mitral stenosis. In sepsis, avoid routine acute anticoagulation (↑bleeding, no stroke benefit). LAAO is a niche option when long-term OAC is truly not possible.
Post-op AF (CABG/valve): β-blockers first; rhythm control (amiodarone or DCCV) if poorly tolerated; consider OAC for ~6–8 weeks if bleeding risk acceptable, then reassess.Pregnancy: DCCV is safe; for rate use β-blocker (not atenolol) or digoxin. Heparins preferred for anticoagulation; DOACs are avoided.
We close with the hospital bundle that sticks:
Screen & treat triggers (sepsis, hypoxia, electrolytes, ACS/PE, meds).
Default to rate control (β-blocker or diltiazem; digoxin add-on) with HR <110 unless symptomatic.
Escalate to rhythm control for symptoms, HF, or failure of rate—DCCV early; pick AA drug by substrate; consider ablation in HFrEF or recurrent.
Anticoagulation pathway: DOAC-first, valve disease exceptions; TEE vs 3-week rule before cardioversion; ≥4 weeks after.
Monitoring: telemetry, daily K/Mg goals (K ≥4.0, Mg ≥2.0), watch QT/AV block, drug-drug interactions.
Risk-factor remix: weight loss, BP control, OSA treatment (CPAP), diabetes optimization, alcohol moderation, exercise, smoking cessation—these cut AF burden and recurrences.
Discharge plan: clear OAC plan, rate/rhythm meds with doses, red-flags, follow-up ECG/Holter, renal/hepatic labs for drug safety, and referral to AF clinic when available.
Bottom line: Treat the trigger, stabilize the rate, choose rhythm wisely, and anticoagulate by risk. Build a system that’s fast, safe, and recurrence-proof—so your patients leave in rhythm (or with a controlled rate) and a plan that lasts.

In this episode of Hospital Medicine Unplugged, we sprint through hepatorenal syndrome–AKI (HRS-AKI)—exclude look-alikes fast, start albumin + vasoconstrictor early, watch the lungs, and loop in transplant.
We open with the do-firsts: clinical diagnosis by exclusion—rule out hypovolemia, nephrotoxins, structural kidney disease. Pull diuretics/ACEi/NSAIDs, check UA/sediment (should be bland), kidney US (should look normal), and hunt triggers (SBP, GI bleed, overdiuresis). Albumin challenge (≈1 g/kg/day, max 100 g for 24–48 h): no renal improvement → HRS-AKI. Urine biomarkers (e.g., NGAL) may help ATN vs HRS but aren’t ready for routine.
Call AKI early using ICA criteria: ↑Cr ≥0.3 mg/dL/48 h or ≥1.5× baseline/7 d and/or low urine output. Don’t chase urine Na/FeNa alone (diuretics confound). Treat the precipitant (especially SBP: antibiotics + albumin).
Treatment—build the hemodynamic fix:• Albumin is adjunct, not a cure: after the initial challenge, continue 20–40 g/day with vasoconstrictor.• First-line vasoconstrictor: terlipressin (now FDA-approved) + albumin. Dosing: 0.5–2 mg IV q6h or continuous infusion; up to 14 days. Stop early if <25% Cr fall by day 4 at max tolerated dose.• Safety watch: respiratory failure/pulmonary edema risk—avoid large albumin loads, hold if SpO₂ <90%, be cautious in advanced ACLF or cardiopulmonary disease.• Validated alternative: norepinephrine (ICU, central line). Evidence supports noninferior HRS reversal and sometimes fewer AEs—great in shock or when terlipressin is contraindicated.• If IV agents unavailable: midodrine + octreotide + albumin (inferior; use only as a fallback).
Special plays & edge cases:• ACLF: higher grade → lower response, higher risk—expedite transplant evaluation.• Volume overload on therapy: down-titrate/hold albumin, reassess with POCUS (IVC/B-lines), pause terlipressin if hypoxemia.• SBP: treat and give albumin (1.5 g/kg day 1, 1 g/kg day 2) to prevent kidney failure.• RRT: bridge to liver transplant or for life-threatening indications; limited benefit in non-candidates—align with goals of care.• Transplant is the only definitive cure; consider SLK in persistent renal dysfunction.
Monitoring that matters:• Daily Cr, UOP, weights, electrolytes, oxygenation; infection surveillance.• Track congestion (exam + POCUS), and de-escalate albumin if lungs load up.• Define response (Cr to near-baseline); nonresponse by day 4 → switch strategies.
Medication pitfalls you don’t want to meet:• Over-infusing albumin → pulmonary edema.• Delaying vasoconstrictors waiting for full “workup.”• Using midodrine/octreotide first when IV options exist.• Stopping early despite improving Cr; or continuing blindly past day-4 nonresponse.
We close with the HRS bundle that sticks: (1) Exclude hypovolemia/nephrotoxins/structural disease fast; (2) Albumin challenge (24–48 h) → if no improvement, start vasoconstrictor + albumin; (3) Prefer terlipressin, use norepinephrine in ICU/shock or contraindications; (4) Hard stop/check at day 4 for response; (5) Prevent/ treat SBP (antibiotics + albumin); (6) Protect the lungs—watch SpO₂, CXR/POCUS, adjust albumin; (7) Early transplant activation ± RRT as bridge; (8) Multidisciplinary liver–kidney–ICU collaboration.
Bottom line: HRS-AKI is a race against time—diagnose by exclusion, pair albumin with the right vasoconstrictor, watch for respiratory hits, and escalate to transplant pathways early.

In this episode of Hospital Medicine Unplugged, we blitz cardiorenal syndrome (CRS)—define fast, subtype smart, decongest early, protect kidneys, and tighten the cardio–nephro handshake.
We start with the frame: CRS = bidirectional heart–kidney dysfunction where trouble in one organ triggers or worsens the other. Know the five plays: Type 1 (acute cardiorenal), Type 2 (chronic cardiorenal), Type 3 (acute renocardiac), Type 4 (chronic renocardiac), Type 5 (secondary/systemic). Classification isn’t trivia—it drives workup and therapy.
Pathophys in one breath: venous congestion > low forward flow; RAAS/SNS surge, vasopressin, inflammation & endothelial dysfunction; sodium avidity → diuretic resistance. CKD stacks the deck toward higher mortality and rehospitalization.
Bedside diagnosis—do-firsts and don’t-miss:• History + trend the eGFR, meds, and prior decompensations.• UA + urine sediment to rule intrinsic renal disease; check albuminuria/proteinuria.• BNP/NT-proBNP, Cystatin C for risk; watch electrolytes, BUN/Cr.• TTE for LV/RV function and filling pressures; consider renal US/Doppler and VeXUS POCUS for systemic congestion; CMR selectively.• True AKI vs pseudo-AKI: a small creatinine rise during effective diuresis can reflect hemoconcentration, not injury—don’t abort decongestion if the patient is clinically improving.
Risk & admit cues: refractory hypoxemia, rising JVP/edema, oliguria, shock/low MAP, refractory hyperK/acidosis, suspected Type 1 or 3 CRS, or diagnostic uncertainty.
Treatment—make decongestion the north star:• First-line: IV loop diuretic (adequate dose & frequency) with daily weights, I/O, urine Na, and electrolyte/renal panels. Aim for complete decongestion.• If resistance hits: sequential nephron blockade (add thiazide-type), consider MRA when safe, and natriuresis-guided up-titration.• Vasodilators/afterload reduction for high filling pressures with preserved BP; inotropes for low-output states or shock—short and targeted.• SGLT2 inhibitors & RAAS blockade: recommended in HF; initiate/continue with renal vigilance and pause only for hypotension, hyperK, or true AKI.• Refractory congestion: ultrafiltration, peritoneal dialysis, or acute RRT—select carefully and match removal rate to plasma refill.• Devices: consider CRT for dyssynchrony and mechanical circulatory support in advanced cases—heart help can be kidney help.
Monitoring that matters:• Trend congestion (exam, weights, VeXUS, echo signs), urine output/Na, and CR/BUN/electrolytes.• Expect and accept permissive creatinine bumps if hemodynamics and volume status are improving.• Reassess daily: diuretic plan, RAAS/SGLT2 status, K/Mg, and hemodynamics (noninvasive first; invasive if shock/ambiguity).
Etiology threads—treat the cause:• Sepsis (Type 5): source control + hemodynamics.• Renal-first hits (Type 3/4): correct nephrotoxins, ischemia, or GN; manage afterload/arrhythmias.• Cardiac-first (Type 1/2): guideline-directed HF therapy with congestion-first strategy.
Pitfalls to dodge: underdosing loops, stopping diuresis for mild Cr rise, ignoring RV failure/venous hypertension, delayed escalation to combo diuretics/UF, and premature RAAS/SGLT2 withdrawal without a clear reason.
We close with the hospital CRS bundle that sticks:
Classify type (1–5) and rule intrinsic kidney disease (UA/sediment, albuminuria, renal US).
Default to loop + natriuresis-guided titration; add thiazide-type early for resistance; consider MRA.
Track congestion multimodally (exam + weights + VeXUS ± TTE).
Guard rails: daily labs, K/Mg repletion, renal & hemodynamic checks.
RAAS/SGLT2 smart use—continue/initiate when safe; hold for hypotension, hyperK, true AKI.
Escalation pathway: UF/RRT for refractory overload or life-threatening derangements; CRT/MCS in select HF.
Team sport: cardiology + nephrology + ICU/pharmacy from day one; discharge with diuretic plan, labs, and early follow-up.
Bottom line: Congestion kills kidneys—decongest completely, use RAAS/SGLT2 wisely, monitor like a hawk, and move fast together.

In this episode of Hospital Medicine Unplugged, we cut through the Mallory-Weiss tear—spot it fast, stop the bleed, stabilize smart, and endoscope right.
We open with the why and who: a longitudinal mucosal laceration at the gastroesophageal junction, triggered by vomiting, retching, or sudden pressure surges. Alcohol, reflux esophagitis, hiatal hernia, NSAIDs, coagulopathy, and liver disease stack the odds. It’s uncommon but not benign—~7.5/100,000 hospitalized patients, with a small but high-risk subset landing in the ICU.
Presentation pearls: classic sequence—retching then hematemesis—appears in <1/3 of cases. Hematochezia or shock = severe bleed. Keep an eye on cirrhotics, dialysis patients, and the elderly—they hide blood loss until they crash.
Diagnosis: stabilize first, scope early. EGD within 24 hours confirms the tear and rules out ulcers, varices, or Dieulafoy’s lesion. Imaging? Rarely needed unless endoscopy fails or perforation’s on the table.
Stabilization priorities:• 2 large-bore IVs, crystalloids, restrictive transfusion (Hgb <7 g/dL unless cardiac or massive bleed).• Reverse coagulopathy; correct platelets >50k, fibrinogen >120 mg/dL in liver disease.• Airway protection if vomiting or altered.• ICU admission for shock, cirrhosis, or hemodialysis.
Endoscopic game plan—mechanical first:• Band ligation or hemoclips = best-in-class. Both achieve >95% hemostasis with minimal recurrence.• Epinephrine injection is for temporary control—never solo for spurting bleeds.• Combination therapy (epi + clip) works when mechanical access is tough.• Nonbleeding tears? Observe, hydrate, PPI, discharge early if stable.• If all fails—angiographic embolization or surgery (rarely needed).
Medical and supportive backbone:• High-dose IV PPI → oral PPI transition once stable.• Hold NSAIDs, antiplatelets, anticoagulants unless high thrombotic risk.• Monitor for anemia, AKI, sepsis, and rebleeding.• Refeed early in stable, nonbleeding patients—delays don’t help.
Special populations:• Cirrhosis or coagulopathy: correct deficits, early endoscopy, and antibiotics if variceal source uncertain.• Hemodialysis: gentle fluids, watch for overload, early scope.• Massive bleeds: resuscitate, scope fast, consider mechanical endoscopy or TAE (transarterial embolization) if refractory.
Complications: bleeding anemia (26%), shock (3%), AKI, sepsis, and rare death (~2–3%). Rebleeding 2–12%, mostly in coagulopathic or cirrhotic patients.Prognosis: excellent for most; poor in the elderly, cirrhotics, and those with shock.
Prevention & long game:• Manage reflux, cut alcohol, stop NSAIDs.• PPI prophylaxis for high-risk inpatients or post-bleed.• Helicobacter pylori eradication if present.• Multidisciplinary care = fewer readmissions, shorter stays, and safer outcomes.
We close with the system moves:(1) Early EGD protocol for all upper GI bleeds.(2) Restrictive transfusion + airway safety bundle.(3) Mechanical-first endoscopic pathway (band or clip).(4) ICU triage for cirrhosis/dialysis/shock.(5) Post-bleed PPI and risk-factor modification.(6) Track hemoglobin + rebleed signs before discharge.
Fast scope, tight stabilization, and mechanical mastery—that’s how you keep Mallory-Weiss tears from turning catastrophic.

In this episode of Hospital Medicine Unplugged, we tackle portal hypertension in hospitalized cirrhosis—find it fast, control bleeding, dry the belly, clear the brain, and pick the right patients for TIPS and transplant.
We open with the diagnosis play: suspect it in cirrhosis with splenomegaly/ascites/varices. Gold standard is HVPG; CSPH = ≥10 mmHg. In real life, lean on liver stiffness + platelets for risk (rule-in ≥25 kPa or rule-out <20 kPa with high platelets), and confirm with varices on endoscopy or collaterals on imaging.
When blood hits the basin—acute variceal bleed—move fast:• Do first: large-bore access, type & cross, start vasoactive agent immediately (octreotide/terlipressin), give prophylactic IV antibiotics—prefer ceftriaxone, and restrict transfusion to Hgb ~7 g/dL (unless extenuating).• Endoscopy with band ligation within 12–24 hours.• Early TIPS for the high risk: Child-Pugh C ≤13 or Child-Pugh B with active bleeding, or if endoscopy/meds fail. This cuts rebleeding and improves survival.• Avoid routine plasma/platelets; correct coagulopathy only for procedures or active bleeding.
Between bleeds, prevent the next one:• Primary prophylaxis: NSBBs (propranolol, nadolol, carvedilol preferred for large varices) or banding if NSBB-intolerant.• Secondary prophylaxis: combo NSBB + band ligation after a bleed.
Ascites management that sticks:• Sodium <2 g/day.• Diuretics: spironolactone + furosemide, titrate carefully.• Large-volume paracentesis for tense/refractory ascites with albumin replacement.• Consider TIPS for refractory ascites in appropriate candidates.• Watch for hyponatremia and renal injury—dose-adjust and protect the kidneys.
Encephalopathy, SBP, and kidneys:• HE: find triggers, lactulose to 2–3 soft stools/day, add rifaximin for secondary prevention.• SBP: ceftriaxone plus IV albumin (1.5 g/kg day 1, 1 g/kg day 2); consider secondary prophylaxis after recovery.• HRS-AKI: albumin + vasoconstrictor (terlipressin or norepinephrine), catheterize to trend UOP; evaluate for TIPS in select cases and early transplant referral.
Imaging & surveillance you shouldn’t skip:• US with Doppler to look for portal vein thrombosis and to screen for HCC (pair with AFP per local protocol).• Endoscopic surveillance individualized by risk and noninvasive markers rather than one-size-fits-all scopes.
Who gets a shunt (and who doesn’t):• TIPS controls bleeding and ascites—great in the right patient, risky in the wrong one. Beware high MELD, severe liver failure, or significant cardiac disease (relative/absolute contraindications). Monitor post-TIPS for encephalopathy and shunt dysfunction.
Medication & system pitfalls:• Don’t over-transfuse—it raises portal pressure.• Start ceftriaxone early in variceal bleed.• Carvedilol can drop BP—titrate to tolerance.• Albumin after paracentesis when >5 L removed.• Avoid nephrotoxins (NSAIDs, IV contrast when possible).• Build order sets: vasoactive + antibiotic bundle for bleed, CRP/renal checks, and a TIPS early-evaluation pathway for high-risk bleeders.
We close with the big picture: portal hypertension is the engine of decompensation—catch it, treat bleeds aggressively, use NSBBs/banding wisely, control ascites, and pull the TIPS lever early in the patients who benefit. And never forget the destination for many: timely transplant evaluation once major-index complications appear.

In this episode of Hospital Medicine Unplugged, we blitz acute peptic ulcer bleeding—risk fast, resuscitate right, scope within 24 hours, secure hemostasis, run high-dose PPIs, and crush recurrence.
We open with the do-firsts: airway/breathing/circulation, 2 large-bore IVs, orthostatics, urine output, type & cross, and labs (CBC, BMP, INR/LFTs). Risk-stratify with Glasgow–Blatchford (GBS)—≤1 may go outpatient; everyone else is inpatient/urgent care.
Resuscitation that matters: balanced crystalloids, permissive targets while bleeding, and a restrictive transfusion strategy (Hb <7–8 g/dL; <10 g/dL if active CAD). Correct coagulopathy pragmatically; reverse only when it changes decisions.
Pre-endoscopic moves: start IV PPI immediately, consider IV erythromycin 250 mg 30–60 min pre-EGD to clear the field. No tranexamic acid. If cirrhosis/portal hypertension is on the table: prophylactic antibiotics + vasoactive therapy.
Endoscopy: within 24 hours after stabilization; sooner if unstable once perfusing. Treat high-risk stigmata (Forrest Ia/Ib/IIa/IIb):• Dual-modality is king—epinephrine + thermal or mechanical clips.• Over-the-scope clips (OTSC) and hemostatic powders are clutch for difficult or diffuse bleeding.• No therapy for clean base/flat spot; discharge planning starts now.
Post-EGD pharmacotherapy—build the acid-suppression backbone:• High-dose PPI for 72 h: 80 mg IV bolus → 8 mg/h infusion or 40–80 mg IV/PO BID. These regimens are equivalent.• Then step down: most get daily PPI; high-risk get BID x 10–14 days, then daily 2–4 weeks.
Monitoring & rebleeding: watch vitals q2–4h, H/H q6–12h for 24–48h, and the stool/NG story. Rebleed? → repeat endoscopy first. If failure or early re-rebleed, transcatheter arterial embolization; surgery if IR/EGD fail.
Etiology plays—prevent the encore:• H. pylori: test everyone (biopsy/stool/UBT), treat 14 days, confirm eradication off PPI (≥2 weeks) and antibiotics/bismuth (≥4 weeks).• NSAID/aspirin ulcers: stop the culprit when possible. If needed, switch to COX-2 + daily PPI. For secondary prevention, resume aspirin early after hemostasis.• Idiopathic ulcers: high-dose PPI 6–8 weeks, scrutinize meds/comorbidities, close follow-up.
Antithrombotics without fear:• Aspirin for secondary prevention—continue or restart early; mortality benefit outweighs modest rebleed risk.• Warfarin/DOACs: hold during active bleed; reverse selectively for life-threatening hemorrhage; restart promptly after hemostasis based on thrombotic risk (coordinate with cardiology/hematology).
Nutrition, level of care, disposition: early feeding after control is safe and shortens LOS. Step-down/ICU for major stigmata or instability (first 24 h). Low-risk ulcers can go home early with clear return precautions and a PPI plan.
Medication pitfalls you don’t want to meet: epinephrine monotherapy (never), under-dosed PPIs, premature endoscopy before resuscitation, and stopping secondary-prevention aspirin without a plan.
We close with the systems bundle that sticks:
Triage with GBS + ABCs + IV PPI ± erythromycin;
EGD ≤24 h with dual-modality for high-risk stigmata; OTSC/powders for select cases;
72-hour high-dose PPI (infusion or BID—equivalent), then tailored step-down;
Rebleed pathway: repeat EGD → IR embolization → surgery if needed;
Etiology track: test/treat/confirm H. pylori, NSAID strategy, idiopathic high-dose PPI;
Antithrombotic game-plan: early aspirin for secondary prevention, timely anticoagulant resumption;
Early enteral nutrition, targeted monitoring, and clear discharge instructions.
Fast, hemostasis-focused, and recurrence-proof—stabilize, scope, suppress acid, fix the cause, and never miss a rebleed.

In this episode of Hospital Medicine Unplugged, we take on acute peptic ulcer bleeding (PUB)—triage fast, stabilize smart, scope early, seal the vessel, and lock in acid suppression + secondary prevention.
We start at the door with risk stratification: use the Glasgow–Blatchford Score (GBS)—≤1 means very-low risk and potential outpatient management; everyone else gets admitted and prepped for urgent endoscopy. Pull CBC, chemistries, INR, type & cross.
Resuscitation that helps, not harms: large-bore IVs, balanced crystalloids, and a restrictive transfusion strategy—transfuse at Hgb <7–8 g/dL (consider <10 g/dL in active coronary disease). Aim for hemodynamic stability before the scope. Early enteral feeding once controlled shortens LOS.
Pre-endoscopic moves: start IV PPI immediately; give IV erythromycin pre-scope to clear the stomach (better visualization). Skip tranexamic acid. If the patient has cirrhosis, flip to the variceal bundle (antibiotics + vasoactive agents) while you clarify source.
Endoscopy timing & targets: perform within 24 hours (earlier only after stabilization in the unstable). Treat high-risk stigmata—active bleeding, non-bleeding visible vessel, adherent clot. Use dual-modality therapy (epi injection + thermal or clips) as your default. Deploy OTSC or hemostatic powder for difficult lesions or poor visualization. Clean base/flat spots? No therapy; plan early discharge.
Post-endoscopic pharmacotherapy (the acid wall): run high-dose PPI for 72 hours—either 80 mg IV bolus → 8 mg/h infusion or intermittent high-dose IV/PO (equally effective). Then step down: once-daily PPI for most; BID for 10–14 days in high-risk, then daily 2–4 weeks.
Monitoring & rebleeding rescue: watch closest in the first 72 hours—vitals, H/H every 6–12h, stool color, symptoms. Suspect rebleed? Resuscitate → repeat endoscopy (works ~75%). If bleeding persists, escalate to transcatheter arterial embolization (TAE); surgery if IR/endoscopy fail.
Etiology matters (prevent the sequel):• H. pylori: test everyone, eradicate if positive, and confirm cure (breath/stool ≥4 wks post-abx; off PPI ≥2 wks). Eradication slashes recurrence to near-zero.• NSAID/aspirin ulcers: stop NSAIDs; if indispensable, switch to COX-2 + PPI. For secondary-prevention aspirin, resume within 1–7 days post-hemostasis (cardiology input for DAPT).• Idiopathic ulcers: higher recurrence—longer PPI course (6–8 wks) and tight follow-up.
Antithrombotics without chaos: hold during active bleed, but restart early after hemostasis to avoid thrombotic events—continue/restart aspirin for secondary prevention and reintroduce anticoagulants promptly based on thrombotic risk (multidisciplinary call). Use PCC/vitamin K or specific DOAC reversal only for life-threatening bleeds.
Discharge playbook:• Low-risk endoscopic findings → early discharge with clear return precautions.• High-risk stigmata → observe ≥72 h with high-dose PPI, then taper.• Educate on red flags (melena, hematemesis, syncope), ensure H. pylori test-of-cure, review meds, and consider iron for anemia.
Bottom line: assess risk fast, resuscitate right, endoscope within 24h, use dual-modality hemostasis, and run high-dose PPI for 72h. Then fix the cause (H. pylori, NSAIDs, antithrombotics) to prevent the rematch.