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—decon

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.

In this episode of Hospital Medicine Unplugged, we blitz acute diverticulitis—spot it early, stage it right, treat what matters, and prevent the encore. We open with the why: ~200,000 US admissions/year and >$6.3B in costs. Risk stacks with age >65, obesity, NSAIDs/steroids/opioids, HTN/DM2, connective-tissue disease, and genetics. Patients roll in with LLQ pain, fever, leukocytosis, N/V. Do-firsts in the ED/ward: IV access, analgesia (acetaminophen first; minimize opioids; avoid routine NSAIDs), antiemetics, IV fluids, and labs (CBC, BMP, UA, CRP). CT A/P with IV contrast is the diagnostic gold standard—~99–100% sensitivity/specificity—to confirm diverticulitis and flag complications. Call the type:• Uncomplicated = localized inflammation, no abscess/perf/fistula/obstruction.• Complicated = any abscess, perforation, fistula, obstruction/stricture, peritonitis. Who needs a bed? Admit for complicated disease, high fever (>38.5°C), marked leukocytosis, can’t tolerate PO, immunosuppression, serious comorbidity, or no home support. Outpatient is reasonable for low-risk, imaging-confirmed uncomplicated cases with reliable follow-up. Treatment—build the supportive core:• Bowel rest → advance diet as tolerated in 2–3 days.• Antibiotics are not routine for all uncomplicated cases; reserve for high-risk (elderly, immunocompromised, persistent fever/WBC, severe comorbidity, pregnancy).• If antibiotics needed: IV ceftriaxone + metronidazole or ampicillin/sulbactam; step down to orals when improving. Typical 4–7 days (uncomplicated needing abx); 7–14 days (complicated)—tailor to response and source control. If the core buckles—manage complicated disease:• Abscess <3 cm: IV antibiotics alone.• Abscess ≥3 cm: Percutaneous drainage + IV antibiotics (success up to ~80%).• Generalized peritonitis, failed drainage, obstruction, or clinical deterioration: Urgent surgical consult; consider resection ± primary anastomosis vs Hartmann based on stability.• Re-image at 48–72 h if no improvement. Special populations you won’t want to miss:• Elderly: lower threshold for CT; antibiotics more often indicated; individualize operative decisions.• Immunocompromised: always treat with antibiotics, admit liberally, and involve surgery early; higher risk of rapid progression despite mild exam. Complication radar: abscess/phlegmon, perforation/peritonitis, fistula (look for pneumaturia/fecaluria), obstruction/stricture, bleeding, sepsis/AKI. Risk rises with CRP >140 mg/L, WBC >15 ×10⁹/L, extraluminal air/fluid on CT, long inflamed segment, and major comorbidity. Colonoscopy after the dust settles:• Complicated diverticulitis: schedule 6–8 weeks post-resolution (unless a high-quality colonoscopy was done within a year and no alarm features).• Uncomplicated: individualized—consider prior screening and symptoms; investigate early for alarm signs (weight loss, anemia, bleeding, change in caliber, persistent pain). Secondary prevention that sticks:• High-fiber, plant-forward diet, physical activity, weight optimization, avoid tobacco, and limit chronic NSAIDs (keep aspirin for CAD when needed).• No routine mesalamine, probiotics, or rifaximin—evidence doesn’t support them.• Elective surgery isn’t about episode counting; decide based on severity, smoldering symptoms, fistula/stricture, and patient goals. We close with the diverticulitis bundle: (1) confirm with contrast CT; (2) supportive care first (fluids, pain control, diet advance); (3) selective antibiotics—don’t overuse; (4) drain abscess ≥3 cm; (5) call surgery for peritonitis/obstruction/failed nonop care; (6) reassess at 48–72 h, re-image if stalled; (7) plan post-acute colonoscopy (complicated: 6–8 weeks); (8) lock in lifestyle prevention. Imaging-led, selective with antibiotics, decisive with source control—treat what’s complicated, spare what isn’t, and keep patients out of the readmit loop.

In this episode of Hospital Medicine Unplugged, we dive into acute variceal bleeding—a high-stakes emergency in cirrhotic patients where seconds count and outcomes hinge on rapid, coordinated care. We start with the crash course in recognition and stabilization: ICU-level monitoring, two large-bore IVs, and cautious transfusion—targeting a hemoglobin around 7 g/dL to avoid portal pressure spikes and rebleeding. Protect the airway early; intubate if hematemesis or encephalopathy loom. Pharmacologic therapy doesn’t wait for endoscopy. Hit fast with octreotide (50 μg bolus → 50 μg/h infusion) or terlipressin/somatostatin if available, and start ceftriaxone 1 g IV daily to cover against bacterial translocation and sepsis. These moves—simple but evidence-based—slash early mortality and infection risk. Then comes the endoscopic moment: perform urgent EGD within 12 hours. Band the culprit—endoscopic variceal ligation (EVL) is first-line for esophageal varices, while cyanoacrylate injection (± coils) dominates for gastric or ectopic sites. Visualization gets a boost from IV erythromycin pre-procedure. If bleeding laughs in your face—bridge with balloon tamponade or self-expanding stent while prepping for TIPS. TIPS saves lives when all else fails or when the odds are stacked: Child-Pugh C (10–13) or B >7 with active bleeding—go early (within 24–72 hours). It decompresses the portal system, quells refractory bleeding, and buys survival time. Once the storm calms, secondary prophylaxis takes over. Combine nonselective beta-blockers (carvedilol preferred at 12.5 mg daily) with repeat EVL every 2–4 weeks until varices vanish. No monotherapy—combo therapy halves rebleeding and boosts survival. For gastric or ectopic varices, keep repeating glue injection or move to BRTO or TIPS if anatomy and expertise allow. Avoid the traps:• Overtransfusion—raises portal pressure.• Routine plasma/platelet correction—no proven benefit.• Early steroid use or unguarded sedation—risk spirals fast. Complications hit early and hard—shock, infection, encephalopathy, AKI, and early rebleeding top the list. Six-week mortality can reach 40% in advanced cirrhotics, but drops sharply with prompt vasoactive therapy, antibiotics, and endoscopic control. Predict death early: Child-Pugh C, MELD ≥19, active bleeding at endoscopy, transfusion >4 units, or renal/hepatic failure—each turns the curve downward. These patients may benefit from pre-emptive TIPS and aggressive ICU support. Special plays:• GOV1 (lesser curvature) → treat like esophageal varices (EVL).• GOV2/IGV1 (fundal) → cyanoacrylate injection ± coil; consider BRTO if available.• Ectopic varices → tailored endoscopic or radiologic therapy.• Non-cirrhotic portal hypertension (e.g., splenic vein thrombosis) → definitive fix may be splenectomy or stenting. We close with the system bundle that keeps patients alive:(1) Early airway + restrictive transfusion;(2) Immediate vasoactive + antibiotic therapy;(3) Urgent endoscopy (<12 h);(4) TIPS within 72 h for high-risk;(5) NSBB + EVL combo for secondary prevention;(6) Multidisciplinary follow-up with hepatology, radiology, and ICU care. Rapid, protocolized, and team-driven—control the bleed, decompress the pressure, and protect the liver. This is how you turn variceal crisis into survival.

In this episode of Hospital Medicine Unplugged, we tackle Prinzmetal’s (variant) angina—catch the transient ST changes, prove the spasm, stop the vasoconstriction, and prevent malignant arrhythmias. We open with the do-firsts: targeted history (rest pain, night/early-AM clustering, hyperventilation/cold/drug triggers), ECG during pain (repeat until you catch it), high-sensitivity troponin, and continuous ST-segment/telemetry because events are brief and dangerous. Call the diagnosis when you have the triad: nitrate-responsive rest angina, transient ischemic ECG changes (ST↑ ≥0.1 mV, ST↓, or new negative U waves in ≥2 leads), and documented coronary spasm (>90% transient constriction) spontaneously or with provocation (acetylcholine/ergonovine/hyperventilation) with prompt reversal by nitro. Rule-out matters: coronary angiography to exclude obstructive CAD (prognosis is worse if present) and to visualize reversible spasm; consider invasive coronary function testing when microvascular disease is suspected. Keep a broad differential (pericarditis, PE, aortic dissection, myocarditis). Risk stratify for monitored care when you see: recurrent/prolonged episodes, ventricular arrhythmias, high-grade AV block, syncope, hemodynamic instability, elevated troponin/MI, or significant comorbidity. Treatment—build the anti-spasm core:• First-line: Calcium channel blockers (CCBs)—dihydropyridines and/or non-DHP—titrate to suppress episodes.• Add: long-acting nitrates for recurrence control.• Acute relief: rapid-acting nitroglycerin at onset.• Refractory options: magnesium or alpha-blockers in select cases.• Vascular health: statins when atherosclerosis/endothelial dysfunction is present. Hard stops (don’t do this): β-blockers (can worsen spasm), high-dose aspirin, short-acting DHP CCBs, nitrates within 24–48 h of PDE-5 inhibitor use, and routine NSAIDs for pain. Monitoring that saves lives: continuous ST/arrhythmia surveillance to catch fleeting ischemia plus VT/VF or high-grade block; be ready for ACLS. Trend troponin if symptoms/ECG suggest injury. Use nitrates during provocation testing and keep reversal agents at hand. Provocation testing—when spontaneous capture fails: carefully performed acetylcholine/ergonovine challenge in the cath lab with immediate access to intracoronary nitro; a positive test reproduces angina + ischemic ECG + angiographic spasm with full reversal. Complications you can’t miss: MI from prolonged spasm, malignant ventricular arrhythmias, syncope, and sudden cardiac death. High-risk phenotypes (diffuse ST↑, aborted SCD) need aggressive suppression and electrophysiology input. Discharge plays (prevent the next hit): smoking cessation (most potent risk factor), avoid triggers (cocaine, triptans/ergots/serotonergic agents, sympathomimetics, cold exposure), optimize lipids/BP/diabetes, and ensure adherence to CCB ± nitrate with a clear action plan for SL nitro at symptom onset. We close with a hospital bundle: (1) capture the ECG during pain + continuous monitoring; (2) angiography to define anatomy and demonstrate reversibility; (3) CCB-anchored regimen with nitrates for backup; (4) strict β-blocker avoidance; (5) provocation testing when diagnosis is uncertain, with immediate nitrate reversal; (6) arrhythmia pathway for VT/VF/AV block; (7) trigger audit + cessation counseling; (8) targeted follow-up for recurrent events or suspected microvascular spasm. Bottom line: identify it fast, prove the spasm, treat with CCBs + nitro, monitor relentlessly, and remove the triggers—because in Prinzmetal’s, seconds count and rhythm kills.

In this episode of Hospital Medicine Unplugged, we tackle hospital-focused TB—isolate fast, diagnose accurately, treat immediately, and coordinate with public health. We open with the do-firsts: airborne isolation (negative pressure + N95s), notify public health, obtain CXR and 2–3 sputums for AFB smear/culture, and run first-line NAAT (Xpert MTB/RIF or Ultra) to both confirm TB and detect rifampin resistance within hours. If no sputum: induce or test extrapulmonary samples; in HIV or the critically ill, add urine LAM and site-specific molecular testing. Isolation shortcuts that are safe: maintain airborne precautions until effective therapy + clinical improvement + serial negative smears; in low-probability cases, negative NAATs can shorten isolation per local protocol. Don’t forget source control of aerosols (patient masking for transport) and robust room engineering. Treatment—build the bactericidal backbone:• RIPE for drug-susceptible TB: isoniazid + rifampin + pyrazinamide + ethambutol for 2 months, then isoniazid + rifampin for 4 more (6 months total). Stop ethambutol once susceptibilities confirm. Start empirically when suspicion is high or illness severe—don’t wait on cultures.• DOT (inpatient → outpatient) to secure adherence and curb resistance.• Pyridoxine with isoniazid to prevent neuropathy. If resistance is on the table:• Triggered by prior TB, exposure to MDR-TB, high-prevalence regions, or early rifampin resistance on NAAT.• Send rapid molecular DST and culture-based DST on all isolates.• For MDR/XDR, pivot to all-oral regimens (e.g., bedaquiline-based ± linezolid/pretomanid) with expert consult—never add a single drug to a failing regimen.• Keep strict isolation until on effective therapy and improving. Special plays:• HIV: daily TB therapy, mind rifamycin–ART interactions (use rifabutin when needed). Start ART within 2 weeks if CD4 <50 (delay for TB meningitis). Co-trimoxazole when indicated; watch for IRIS.• Renal/hepatic disease: adjust dosing, close LFT/Cr monitoring; PZA, INH, and RIF drive hepatotoxicity risk.• Pregnancy: standard therapy generally safe; monitor toxicity closely.• Extrapulmonary TB: tailor diagnostics; steroids for TB meningitis or pericarditis. Monitoring that moves outcomes:• Monthly sputum culture until two consecutive negatives; repeat DST if still positive at 2–3 months.• Baseline → monthly LFTs, renal function; CBC if on linezolid; ECG/electrolytes if on bedaquiline.• CXR at baseline, ~2–3 months, and end of therapy to document response.• Screen and treat depression, malnutrition, substance use, and social barriers—these derail adherence. Complications to anticipate and preempt: respiratory failure, hemoptysis, ARDS, miliary/disseminated disease, and organ-specific EPTB (CNS, bone, GU). In HIV, be ready for IRIS after ART start—recognize early, manage inflammation, continue TB therapy. The hospital TB bundle: Isolate immediately and notify public health. CXR + sputum AFB/culture + NAAT (add LAM/extrapulmonary NAAT when appropriate). Empiric RIPE now, switch per DST. DOT handoff and discharge plan aligned with public health. Toxicity labs monthly; culture conversion tracking. ART timing and DDI management for HIV. Resistance pathway (rapid DST → expert-guided, bedaquiline-based regimen). Education + social supports to sustain adherence. Fast, infection-controlled, and outcome-focused—isolate early, test smart, treat today, and partner with public health to break transmission and deliver cure.

In this episode of Hospital Medicine Unplugged, we cut through hospital-focused amputation decisions—prioritize life over limb, align with patient goals, and plan for function from day one. We open with the do-firsts: stabilize sepsis and perfusion, control infection with source control, tighten inpatient glucose, and stage limb threat (WIfI, GLASS). Loop in vascular, ortho/plastics, ID, endocrine, rehab, palliative, and social/behavioral health—decisions are team sport. Call amputation when absolute indications hit: uncontrolled sepsis, nonviable extremity, or metabolic derailment from necrosis. Relative cues: failed revascularization, intractable pain, nonfunctional limb, or nonambulatory baseline where salvage won’t restore independence. The diagnosis-to-decision framework:• Shared decision-making: clarify best/worst/most likely outcomes; center values (comfort vs mobility, limb image vs prosthesis function).• Select the most distal level that will heal and maximize function. Minor (toe/transmetatarsal) when feasible; escalate only when biology or biomechanics demand it.• Primary amputation for survival threats; secondary after failed salvage.• Build the post-op plan before the first cut: pain pathway (regional + multimodal), dressing/edema control, early PT/OT, discharge destination, prosthetics timeline. Level matters—function follows the joint:• Toe/forefoot: preserves gait; watch for pressure transfer and recurrence.• Midfoot (Lisfranc/Chopart) & Syme: possible but orthotics-heavy; risk of equinus/imbalance.• Below-knee (transtibial): knee preserved → highest prosthesis use and independent ambulation.• Through-knee: niche; seating advantages for some.• Above-knee (transfemoral): highest energy cost, lowest community ambulation—choose only when required. Outcomes reality check:• Mortality is high (30-day through 5-year climbs with age/comorbidity and proximal level).• Function and quality of life track with walking ability and prosthesis use; depression/anxiety are common—screen and treat.• Rehab and prosthetics access drive return to home/work more than the incision itself. Medical optimization pearls:• Resuscitate, revascularize if feasible, then operate—don’t chase salvage that endangers life.• Glycemic target ~<180 mg/dL, statin + antiplatelet unless contraindicated, smoking cessation, nutrition up.• Culture-guided antibiotics; debride early; involve ID for bone/joint disease. When salvage still on the table:• Attempt only with hemodynamic stability, manageable infection, reconstructible perfusion/soft tissue, and reasonable expectation of a pain-free, functional limb.• Bail-out early if physiology worsens, tissue demarcates proximally, or function will be inferior to amputation. Psychosocial essentials:• Name the losses, normalize grief, and offer peer support.• Embed behavioral health for depression/PTSD risk; family engagement improves clarity and follow-through.• Document goals of care and revisit as the picture evolves. System moves that change outcomes: Default multidisciplinary pathway (vascular-ID-rehab-behavioral). Objective staging (WIfI/GLASS) at consult. Life-over-limb trigger for primary amputation when unstable. Level selection huddle with prosthetist input. CRP-/trend-guided antibiotic and dressing protocols. Early mobilization + rigid/semirigid dressings for edema control. Prosthetics fast-track and scheduled socket checks. Contralateral limb surveillance and PAD secondary prevention. Quality dashboards (30-day complications, time to prosthesis, 1-year mobility) for continuous improvement. We close with the takeaway: decide fast, decide together, and decide for the whole patient—survival first, then the most distal level that heals, wrapped in rehab, psychosocial support, and lifelong vascular prevention.

In this episode of Hospital Medicine Unplugged, we unpack contrast-induced nephropathy (CIN)—spot the risks, flood the kidneys (not the lungs), cut the contrast, and prevent a hospital-acquired AKI before it starts. We open with the do-firsts: identify high-risk inpatients—those with CKD (especially eGFR <30), diabetes, heart failure, advanced age, or prior contrast within 72 hours. Draw a baseline creatinine and estimate GFR pre-procedure; no shortcuts here. Intra-arterial studies (PCI, angiography) carry more risk than IV contrast CTs. Call CIN when you see a rise in creatinine ≥0.5 mg/dL or ≥25% from baseline within 48–72 hours post-contrast, after excluding other causes (hypotension, nephrotoxins, atheroemboli). The KDIGO AKI definition is now preferred—≥0.3 mg/dL increase within 48h or 1.5× baseline within 7 days, or urine output <0.5 mL/kg/h for ≥6h. Pathophysiology plays:Contrast agents inflict direct tubular toxicity and indirect medullary ischemia. They cause vasoconstriction via endothelin, blunt nitric oxide, increase oxidative stress, and heighten viscosity—all of which tank renal perfusion. Tubular epithelial injury → cell swelling, necrosis, obstruction, and reduced GFR. Medullary hypoxia seals the deal. Risk-stratify before you inject (any = high risk):• CKD (eGFR <60; highest if <30)• Diabetes (esp. with CKD)• Age >75, heart failure, volume depletion, hypotension• High contrast volume (>350 mL or >4 mL/kg), intra-arterial route, repeat studies <72h• Nephrotoxins (NSAIDs, aminoglycosides, IV amphotericin, diuretics)• Acute coronary syndromes or mechanical circulatory support during PCI Clinical course: Creatinine rises in 24–72h, peaks day 3–5, and normalizes in 1–3 weeks if reversible. Usually non-oliguric, but oligo/anuria = severe. Dialysis need is rare (<2%), but mortality spikes if required. Prevention—build the hydration backbone:• Isotonic saline (0.9%) at 1 mL/kg/h for 6–12h pre- and post-contrast (shorter 3+6h for urgent PCI).• Sodium bicarbonate (e.g., 250 mL 1.4% over 1h pre-, then 1 mL/kg/h for 6h post-) is an alternative, but not superior (PRESERVE, JAMA 2020).• Oral hydration ≠ enough for high-risk inpatients.• Hold nephrotoxins around the procedure.• Use the lowest feasible contrast volume and choose iso- or low-osmolar media.• Avoid repeat contrast studies within 72h. Adjuncts (evidence weak but low-risk):• N-acetylcysteine 600–1200 mg BID, start before and continue after—may help, can’t hurt.• High-dose statins (e.g., atorvastatin 80 mg) may lower CIN risk in PCI.• No role for dopamine, fenoldopam, theophylline, or prophylactic dialysis. If CIN develops:• Supportive only—maintain euvolemia, stop nephrotoxins, monitor urine and labs.• Dialysis only for standard triggers (refractory hyperkalemia, acidosis, overload, uremia).• No therapy reverses established CIN—time, fluids, and vigilance are your tools.• Recheck creatinine daily for 3–5 days, then space if stable. Key lab trends:Creatinine ↑ by ≥0.5 mg/dL or ≥25% within 48–72h → peaks day 3–5 → resolves by week 2.Early shifts (≥5% in 12h) predict persistent damage. NGAL and cystatin C rise earlier but aren’t yet routine. Hospital protocol that sticks: Screen: all contrast orders → auto-prompt for eGFR. Hydrate: isotonic saline 1 mL/kg/h (adjust in CHF). Hold: nephrotoxins 24h pre/post. Limit: contrast dose and repetition. Check: creatinine at 48–72h post-exposure. Document: CIN episode in EHR for future contrast precautions. System moves:Bundle prevention into radiology workflow—automatic hydration orders, contrast dose calculators, EHR alerts for eGFR <45, and follow-up creatinine flags at 48h. Bottom line—CIN is preventable, predictable, and high-stakes. Hydrate early, minimize contrast, skip the nephrotoxins, and track the creatinine curve. Prevention beats dialysis every time.

In this episode of Hospital Medicine Unplugged, we dive into hungry bone syndrome (HBS)—spot it early, replace hard, monitor relentlessly, and shorten the stay. We open with the do-firsts: check calcium, phosphate, magnesium, ALP, and PTH q6–12h in the first 48–72 hours post-op; screen symptoms (paresthesias, cramps, tetany) and get an ECG for QTc if calcium is low. In dialysis patients, sync labs with the dialysis schedule. Call the diagnosis when you see rapid, profound, and prolonged hypocalcemia (often Ca ≤7.5 mg/dL for >4 days) plus hypophosphatemia and hypomagnesemia after a sharp PTH drop (post-parathyroidectomy or thyroidectomy in thyrotoxicosis). Rising ALP over the first 1–2 weeks supports high bone turnover. Risk-stratify who will crash (any = high risk):• SHPT on dialysis (most common, most severe)• Very high pre-op PTH and ALP, long dialysis vintage, renal osteodystrophy, younger age, heavier gland mass• PHPT with severe hypercalcemia, big adenoma, radiologic bone disease, vitamin D deficiency• Thyrotoxicosis post-thyroidectomy with low BMD and high ALP• Consider comorbidity burden and published PTH/ALP-based risk scores to guide prophylaxis Management—build the replacement backbone:• IV calcium for symptoms, ECG changes, or severe hypocalcemia → calcium gluconate bolus then infusion, wean to high-dose oral calcium (often 3–6 g elemental/day, more if needed).• Active vitamin D early: calcitriol or alfacalcidol and add cholecalciferol to replete stores.• Magnesium matters: replace to mid-normal (hypomagnesemia blunts PTH action).• Go easy on phosphate: replete only if severe/symptomatic—overcorrection worsens hypocalcemia.• Dialysis patients: use higher-calcium dialysate, coordinate IV calcium around runs. If the backbone buckles:• Escalate calcium infusion rate, split oral doses across the day, and consider thiazide (if euvolemic, non-CKD) to limit calciuria.• For persistent losses, reassess Mg, vitamin D dosing, and exclude hypoparathyroidism (very low PTH + hyperphosphatemia points away from HBS). Etiology plays—treat the cause:• SHPT (CKD): ensure vitamin D analogs and optimize dialysis; manage renal osteodystrophy.• PHPT: confirm complete resection; replete vitamin D and calcium aggressively.• Thyrotoxicosis: keep magnesium topped up; anticipate transient high needs even with intact parathyroids. HBS vs post-op hypoparathyroidism—don’t mix them up:• HBS = low Ca, low PO₄, low Mg, PTH normal/low-normal, ALP ↑.• Hypoparathyroidism = low Ca, high PO₄, low PTH, Mg usually normal. Management differs. Monitoring & tapering that sticks:• Daily labs (sometimes q6–12h early) for Ca/PO₄/Mg/ALP; space as stable.• Trend ALP (peaks ~2 weeks) to anticipate duration.• ECG when Ca is low; watch for QTc.• Taper calcium and calcitriol slowly to avoid rebound hypercalcemia; set outpatient lab checks. Prevention & periop moves (esp. high risk):• Replete vitamin D pre-op when feasible.• Consider bisphosphonates selectively in PHPT with very high turnover (evidence evolving).• Have a standing postop protocol for high-risk patients: preprinted orders for labs, IV→PO calcium, calcitriol start, magnesium targets, and dialysis calcium bath adjustments. Medication pitfalls you don’t want to meet:• Under-replacing magnesium (keeps calcium low).• Over-replacing phosphate (drives calcium down).• Missing QTc prolongation.• Forgetting renal dosing and drug interactions with vitamin D analogs. We close with the system moves: a hospital HBS bundle that (1) flags SHPT/PHPT/thyrotoxicosis cases pre-op; (2) auto-starts calcitriol + calcium with Mg targets; (3) embeds q6–12h labs early; (4) differentiates HBS vs hypoparathyroidism with a PTH/PO₄ check; (5) standardizes dialysate Ca for dialysis patients; (6) maps a taper & follow-up plan before discharge. Bottom line—HBS is commonest after SHPT, fiercer with high turnover, and beatable with early recognition, aggressive but smart replacement, magnesium vigilance, and pro

In this episode of Hospital Medicine Unplugged, we take on pleural empyema in the hospital—recognize fast, drain early, cover smart, escalate on time—because delays and resistant bugs kill. We set the stage: hospital-acquired empyema hits harder than community-acquired (~47% vs ~17% mortality), driven by MRSA and Pseudomonas/Gram-negatives, poly-microbial mixes, and sicker hosts. Translation: broader empiric antibiotics, earlier drainage, lower threshold for surgery. Diagnosis you can’t miss: persistent fever, pleuritic pain, failure to improve on pneumonia therapy, and a new/large effusion. Ultrasound first (bedside, maps loculations, guides the tap), contrast CT to define split pleura/loculation or abscess, then diagnostic thoracentesis. Call it complicated when pus or pleural pH <7.20 (often with low glucose, high LDH)—that’s a drain now moment. Empiric antibiotics—match the source:• Community-acquired: ceftriaxone (or similar) + anaerobic coverage (e.g., metronidazole) or ampicillin/sulbactam.• Hospital-acquired/post-procedural: vancomycin + anti-Pseudomonal β-lactam (piperacillin–tazobactam or cefepime). Keep anaerobe coverage.• Avoid aminoglycosides in the pleural space; no intrapleural antibiotics. De-escalate to cultures but don’t drop anaerobes unless ruled out. Drainage—the make-or-break:• Small-bore, US-guided chest tube early for pus, low pH, large/loculated effusions.• If output stalls or loculations persist, go to intrapleural enzyme therapy (IET): tPA + DNase—combo beats monotherapy and cuts OR need.• Escalate to VATS for failure of medical therapy, thick peel, trapped lung, or advanced (organizing) stage. Early VATS shortens LOS and complications; thoracotomy for the rare, refractory cases or when VATS isn’t feasible. Risk tools & triage: RAPID score (Renal, Age, Purulence, Infection source, Dietary/albumin) spotlights patients who need aggressive upfront therapy and early surgical consult. Layer in SOFA/qSOFA if septic. What delays look like—and how to avoid them: atypical elders, sedation blunting exam, “treating pneumonia harder” without tapping the chest, and weekend/after-hours imaging gaps. Counterpunch with a protocol that auto-triggers US → thoracentesis → tube if pH <7.2/pus and pre-authorizes IET/VATS when drainage is inadequate. Supportive care that moves the needle:• Nutrition (hypoalbuminemia worsens outcomes), glucose control, DVT prophylaxis, analgesia that preserves ventilation.• Daily output + imaging reassessment; tube position checks and flush protocols.• ID + Pulm + Thoracic Surgery at the table from day one. Micro pearls: hospital bugs = MRSA, Pseudomonas, Enterobacterales, Enterococcus, anaerobes; community bugs = Streptococci (incl. anginosus group), S. aureus, anaerobes. Inoculate pleural fluid into blood culture bottles to boost yield; polymicrobial = think aspiration/anaerobes. We close with the Empyema Bundle:(1) Flag high-risk (HAP, malignancy, postop, diabetes, renal disease, high RAPID).(2) US at bedside → diagnostic tap on any moderate/large or complex effusion.(3) Empiric antibiotics matched to source (MRSA/Pseudomonas in HAP) + keep anaerobes.(4) Early small-bore tube for pus/pH <7.2/large locules.(5) tPA + DNase if drainage stalls within 24–48 h.(6) Early VATS for non-responders or organizing stage—don’t wait for day 5–7 failure.(7) Daily goal checks (fever, WBC/CRP, output, aeration) and culture-driven de-escalation.(8) Nutrition/DVT/oral care & lung expansion to speed recovery and cut readmits. Bottom line: source-control early, cover the right bugs, and escalate decisively. That’s how you beat hospital-acquired empyema—and keep lungs expanding, not organizing.

In this episode of Hospital Medicine Unplugged, we tackle hospital-acquired dysphagia—spot it early, screen systematically, intervene fast—to cut pneumonia, malnutrition, and mortality. We start with the big drivers: critical illness, intubation/mechanical ventilation, tracheostomy, prolonged stay, and neuro disease (esp. acute stroke). In the ICU, post-extubation dysphagia (PED) hits ~12–26%—higher after emergency admits, severe illness, and long ventilation or RRT. Mechanisms stack up: airway trauma, impaired sensorium, neuromuscular/ICU-acquired weakness. On the wards, stroke leads the pack (up to 78%), and older adults/dementia carry heavy risk and consequences. Why it matters: aspiration pneumonia, malnutrition/dehydration, longer LOS, higher costs, and higher mortality. Dysphagia is under-recognized and under-screened—especially after extubation. How we find it—screen, then scope:• Universal nurse-led screening before PO in stroke and after extubation in ICU. Fail = NPO + SLP.• Bedside tools (e.g., Yale, GUSS, TOR-BSST) flag risk but miss silent aspiration.• Instrumental testing when unclear or high-risk: VFSS (gold standard) or FEES (bedside, repeatable).• Separate oropharyngeal vs esophageal patterns: initiate EGD/barium/manometry when transport symptoms dominate. Management—protect the lungs, feed the patient, train the swallow:• NPO until safe plan; upright 30–45°, slow assisted feeding, small sips/bites.• SLP-led strategies: posture (e.g., chin tuck), pacing, exercises; reassess after any neuro change.• Diet texture & liquids per IDDSI—individualize thickened liquids (benefit ≠ universal; watch hydration).• Early enteral nutrition (NG/PEG) if unsafe or inadequate PO.• Oral care bundle to lower pneumonia risk.• Medication hygiene: limit sedatives/anticholinergics/opioids that blunt swallow or sensorium.• ICU specifics: routine PED screen post-extubation, cuff management, early mobility, and wean plans; avoid reflex “regular diet” orders after tube removal.• Stroke specifics: screen before first sip, rapid SLP + VFSS/FEES as needed, start rehab early, and adapt as deficits evolve.• Elderly/dementia: simplify mealtime environment, cueing, hydration prompts, goals-of-care; monitor for silent aspiration.• Esophageal causes: treat the cause—PPI/EoE diet, endoscopic dilation/oncologic workup, or motility therapy—while maintaining safe intake. Red flags for higher-level care: recurrent coughing/wet voice, oxygen dips with PO, recurrent pneumonia, failure of bedside screen, bulbar weakness, or new neuro deficits. Quality & safety pearls:• Screen everyone at risk, every time (stroke, post-extubation, neuro, frail).• Don’t “test with a tray.” A failed screen mandates NPO + SLP.• Instrumental confirmation guides targeted therapy and prevents over- or under-restriction.• Track hydration & calories—thickened liquids can quietly dehydrate patients.• Build order sets that auto-trigger SLP, dietitian, oral care, and aspiration precautions. We close with the Dysphagia Bundle that sticks:(1) Screen before PO (stroke/post-extubation/elderly/neuro).(2) Failed screen → NPO + SLP + VFSS/FEES pathway.(3) IDDSI diet + compensatory maneuvers with education at bedside.(4) Oral care, hydration checks, and med de-sedation.(5) Escalate to GI (EGD/esophagram/manometry) when esophageal features present.(6) Reassess after status changes; step-up/step-down diet based on data.(7) Discharge plan: home exercises, texture guidance, and follow-up SLP. Bottom line: screen early, instrument wisely, individualize diets, and rehabilitate relentlessly. That’s how you make dysphagia safer in the hospital—and keep aspiration off your problem list.

In this episode of Hospital Medicine Unplugged, we blitz Guillain–Barré Syndrome (GBS)—recognize early, monitor relentlessly, start immunotherapy on time, prevent complications. We open with the do-firsts in the hospital: admit all suspected GBS; check vital capacity (VC) & negative inspiratory force (NIF) at baseline and serially; continuous telemetry & BP for dysautonomia; early swallow screen to prevent aspiration. Move moderate–severe weakness or bulbar signs to a monitored/ICU setting. Diagnosis is clinical-first, tests support: rapidly progressive, symmetric weakness with areflexia/hyporeflexia; look for albuminocytologic dissociation on CSF and use NCS to subtype (AIDP vs axonal). Rule out mimics (myelitis, MG crisis, CIP/CIM, botulism, cord compression). Treatment—build the evidence-based core:• Immunotherapy for non-ambulatory or rapidly progressive patients: IVIg (2 g/kg over 5 days) or plasma exchange (PE; 4–5 exchanges over ~2 weeks)—equally effective for speeding recovery; do not combine (no added benefit).• Steroids don’t work for typical GBS; reserve for select immune–checkpoint–inhibitor cases with expert input.• For treatment-related fluctuations, a repeat course of the initial therapy can be considered in select cases. Supportive care that saves lives:• Airway & breathing: trend VC/NIF at least twice daily; intubate early if VC < 15 mL/kg, rapidly falling metrics, or bulbar failure.• Autonomic surveillance: watch for tachy/bradyarrhythmias and labile BP; temporary pacing may be needed in severe cases.• DVT prevention: LMWH or heparin + compression; turn, mobilize early.• Pain: prioritize non-opioid neuropathic agents; treat constipation, bladder retention.• Nutrition & skin: enteral feeding if unsafe swallow; meticulous pressure injury prevention.• Rehab starts day 1: PT/OT, respiratory physio, contracture prevention, patient/family education. Risk & disposition plays:• Up to 20–30% require ventilation—strongest predictor of poor outcome.• Autonomic dysfunction (~20%) can trigger malignant arrhythmias or BP swings—keep on monitors.• Complication shield: aspiration pneumonia, sepsis, PE/DVT, pressure injuries—anticipate and prevent.• Use EGRIS (respiratory insufficiency risk) and mEGOS (functional outcome) to triage level of care, counseling, and resource planning. Subtypes & nuance:• AIDP predominates in the West; AMAN/AMSAN (axonal) skew more severe and recover slower; Miller Fisher = ophthalmoplegia/ataxia/areflexia. Subtype by NCS may inform prognosis but doesn’t change first-line immunotherapy. Quality & safety pearls:• Don’t delay IVIg/PE for confirmatory tests if the patient is deteriorating.• Avoid PE when hemodynamically unstable from dysautonomia; prefer IVIg.• IVIg cautions: hyperviscosity/thrombosis risk—hydrate, monitor high-risk patients.• Combination IVIg+PE = no gain; early steroids = harm/no benefit in classic GBS. Prognosis talk track:• Most regain independent ambulation by 6–12 months, but ~20% have persistent disability; ~3–5% die despite care. Axonal subtype, older age, severe nadir, C. jejuni antecedent, and the need for ventilation worsen outlook. We close with the hospital bundle that sticks:(1) Admit all suspected; baseline VC/NIF/telemetry + swallow screen.(2) Default to IVIg or PE (one, not both), started early.(3) ICU for bulbar signs, rapid progression, dysautonomia, or EGRIS high-risk.(4) Airway algorithm with objective thresholds (VC <15 mL/kg, falling NIF).(5) Autonomic pathway: continuous monitoring → pacing capable environment.(6) Complication prophylaxis: DVT, pressure, aspiration, sepsis.(7) Rehab-on-admission with daily PT/OT and caregiver education.(8) Score and re-score (EGRIS/mEGOS) to guide expectations and follow-up. Fast recognition, monitoring that doesn’t blink, and timely IVIg or PE—that’s how you keep GBS safe in the hospital and set the table for recovery.

In this episode of Hospital Medicine Unplugged, we discuss Wernicke–Korsakoff syndrome—spot it early, slam thiamine, stop the slide to irreversible amnesia. We open with the do-firsts: high clinical suspicion in anyone with alcohol use disorder, malnutrition, bariatric surgery, cancer, hyperemesis, or refeeding. Don’t chase labs; give thiamine now—before glucose—and correct magnesium to make the thiamine work. Clinical diagnosis that doesn’t miss: the classic triad (confusion, ophthalmoplegia, ataxia) is rare. Use Caine criteria (≥2/4: dietary deficiency, oculomotor signs, cerebellar dysfunction, altered mental state/memory). Do not delay for MRI or thiamine levels; imaging is supportive, not decisive. Pathophysiology in one breath: thiamine deficiency → mitochondrial failure → lactate build-up → selective injury (mammillary bodies, thalamus, periaqueductal gray). Alcohol compounds the damage by blocking absorption and utilization, so doses must be higher. Epidemiology & outcomes you’ll actually use: alcohol-related WE is common and progresses to KS more often, while non-alcohol cases are deadlier in-hospital. Most WKS is missed antemortem; once KS lands, profound anterograde/retrograde amnesia with confabulation is often permanent. Treatment—build the thiamine backbone fast:• Suspected WE: High-dose IV thiamine (e.g., 500 mg IV TID) for 2–3 days, then 250–500 mg IV daily for several days, followed by high-dose oral (e.g., 100–300 mg/day).• Magnesium repletion (target normal) to restore thiamine-dependent enzymes.• Nutrition + electrolytes (mind phosphate for refeeding).• Oral thiamine alone is inadequate in high-risk or symptomatic patients. If the backbone buckles:• Escalate/extend parenteral dosing if mental status, ocular signs, or gait don’t improve.• Manage agitation/delirium with low-dose agents; avoid sedating away the exam.• Consider MRI only when the diagnosis stays murky after treatment has started. Prevention plays that save neurons:• Prophylactic parenteral thiamine for all at-risk inpatients (AUD, malnutrition, ICU, post-bariatric, hyperemesis, prolonged NPO/TPN), especially before dextrose.• Order-set defaults: auto-add thiamine to alcohol withdrawal and refeeding pathways; bundle Mg and nutrition consults.• Nix low-value tests (routine serum thiamine) and educate teams that over-treating is safer than missing. KS reality check: once established, expect severe memory impairment and executive dysfunction; focus on rehab, safety, caregiver training, and secondary prevention (nutrition, AUD treatment) to reduce readmissions. We close with the system moves: a WKS bundle that (1) screens risk on admission; (2) fires immediate IV thiamine + Mg with nursing-driven protocols; (3) blocks glucose-first orders in high-risk patients; (4) standardizes dosing/taper with auto-stop reminders to avoid under- or over-treating; (5) tracks outcomes (time-to-thiamine, neuro recovery, readmission); (6) hard-wires prevention into alcohol withdrawal, oncology, ICU, and post-bariatric pathways. Fast, protocolized, and prevention-forward—treat first, test later. Thiamine saves brains; delay steals memories.

In this episode of Hospital Medicine Unplugged, we untangle type 1 vs type 2 NSTEMI—different mechanisms, different playbooks, different outcomes—and why hospital factors often tip the scales for type 2. We set the stage fast:• Type 1 NSTEMI = atherothrombosis—plaque rupture/erosion → thrombus. Classic chest pain, ischemic ECG, higher use of angiography/PCI, and evidence-based cardioprotective therapy (aspirin + P2Y12, anticoagulation, high-intensity statin, beta-blocker). Protocols are tight and fast.• Type 2 NSTEMI = supply–demand mismatch—no acute coronary thrombosis. Precipitants are hospital triggers: sepsis, anemia, hypoxia, tachyarrhythmia, perioperative stress, hemodynamic instability. Patients are older, multimorbid, with atypical symptoms and non-specific ECGs. Pathway variability and fragmentation are common—especially off cardiology services. Diagnosis without derailment:• Both need troponin rise/fall + ischemia, but context is king. Type 1 often shows larger, quicker deltas and focal wall-motion loss; type 2 shows modest troponin, diffuse stressors, and may lack a culprit lesion.• When uncertain, lean type 1 to avoid undertreatment—then reclassify as data clarifies. Management that matches mechanism:• Type 1: run the ACS bundle—DAPT, anticoagulation, high-intensity statin, early invasive strategy for high-risk, plus ACEi/ARB, MRA when indicated.• Type 2: treat the trigger first—oxygenation, rate/rhythm control, volume/pressure optimization, fix anemia/infection. Antithrombotics are not one-size-fits-all; reserve revascularization for proven obstructive CAD or ongoing ischemia. Start/optimize statin, beta-blocker, aspirin when CAD is present or likely. Plan CAD evaluation (often outpatient) once stable. Why type 2 fares worse:• Higher in-hospital and 1-year mortality, driven by comorbidity and illness severity, not stentable lesions.• Undertreatment and delays: less cardiology involvement, fewer invasive evaluations, and variable secondary prevention despite frequent underlying CAD. Close the gap—hospital moves that matter: Create a type 2 NSTEMI pathway: trigger checklists (sepsis/anemia/hypoxia/tachyarrhythmia), hemodynamic targets, and early echo. Default cardiology consult for diagnostic clarification and CAD strategy. Order sets that separate type 1 antithrombotic bundles from type 2 trigger-first care, with guardrails on DAPT/anticoagulation. Secondary prevention audit: statin/beta-blocker/aspirin started when CAD present or suspected; deprescribe when risk > benefit. Service-agnostic timers for serial ECG/hs-troponin and for escalation if pain/ischemia persists. Discharge plan for type 2: trigger control, meds reconciliation, outpatient CAD testing, and close follow-up. Bottom line: Type 1 is a coronary emergency; type 2 is a circulatory stress test you’re failing. Match the treatment to the mechanism, standardize the inpatient pathway for type 2, and you’ll cut noise, delays, and mortality.