In this episode of Hospital Medicine Unplugged, we tackle one of the most ethically charged and clinically challenging topics in inpatient care: the use of restraints in the hospital setting. When are restraints justified, why do we still use them so often, and what does the evidence actually show about benefit versus harm? We start by defining physical restraints—any device or method that limits a patient’s movement, from wrist and ankle restraints to vests, belts, bed rails, and enclosure beds—and chemical restraints, medications used primarily to control behavior rather than treat an underlying condition. We unpack why experts increasingly reject the term “chemical restraint,” emphasizing pharmacologic treatment of agitation aimed at calming, not sedating, patients while addressing root causes. Next, we explore why restraints are used: fall prevention, prevention of device removal, management of delirium or agitation, and protection of staff. But here’s the paradox—observational data consistently show higher rates of the very outcomes restraints are meant to prevent, including unplanned extubations, device removal, increased agitation, delirium, and longer ICU stays. We break down the scope of the problem. Nearly 1 in 10 hospitalized patients experiences restraint use, with rates approaching 40% of ICU encounters and even higher among mechanically ventilated patients. Use varies widely by setting, staffing, and culture—highlighting that restraint use is often system-driven, not patient-driven. The heart of the episode focuses on ethics and law. Restraints represent a profound restriction of liberty, and ethical use requires three conditions: medical appropriateness, informed consent (or a valid emergency exception), and use of the least restrictive option. We review federal regulatory requirements—restraints only for imminent harm, after less restrictive measures fail, time-limited orders, mandatory face-to-face evaluations, continuous monitoring, and early removal. We then confront the real harms. Physically: DVT, PE, aspiration pneumonia, fractures, pressure injuries, rhabdomyolysis, asphyxiation, and death. Psychologically: fear, loss of dignity, and PTSD, affecting up to 25–47% of patients after a restraint event. These risks rise with each additional day of restraint use. From there, we pivot to what actually works: alternatives. Multicomponent, non-pharmacologic strategies—reorientation, sleep hygiene, pain control, early mobility, family engagement, sitters, sensory optimization, and delirium prevention bundles like ABCDEF—reduce delirium and restraint use by 40–60% while improving outcomes. We close with practical takeaways: assess underlying causes first (pain, hypoxia, infection, withdrawal, delirium), use verbal de-escalation and environment before meds, reserve restraints for true emergencies, document meticulously, reassess relentlessly, and remove early. The bottom line: restraints are not benign, not preventive, and not routine care—they are a last resort in modern, patient-centered hospital medicine. Fast, evidence-driven, and ethically grounded—protect safety without sacrificing dignity.

In this episode of Hospital Medicine Unplugged, we tackle dementia with behavioral and psychological symptoms (BPSD) in the hospitalized patient—why it happens, how to assess it fast, and how to manage it safely without making things worse. We start with the big picture: BPSD affects >90% of people with dementia, often driving hospital admissions. Symptoms span agitation, aggression, psychosis, depression, anxiety, apathy, sleep disturbance, and disinhibition—and they’re not benign. In the hospital, BPSD is linked to longer stays, higher mortality, restraint use, staff injury, early institutionalization, and one-third of total dementia care costs. Next, we walk through the do-first inpatient assessment. Rule out delirium (acute onset, fluctuating attention), then hunt for reversible triggers: pain, constipation, urinary retention, infection, hypoxia, metabolic derangements, sleep disruption, and iatrogenic harm from polypharmacy—especially anticholinergics, benzodiazepines, and opioids. Collateral history is critical to establish baseline behavior. Use structured tools like CAM/4AT for delirium, PAINAD for nonverbal pain, and NPI or CMAI to quantify symptoms. The DICE approach (Describe–Investigate–Create–Evaluate) keeps management personalized and efficient. We emphasize that non-pharmacologic strategies are first-line—always. In the hospital, this means person-centered care: reorientation, sleep hygiene, early mobility, sensory optimization (glasses/hearing aids), hydration, toileting, nutrition, and calm communication. Caregiver- and staff-focused interventions have the strongest evidence, reducing both symptom burden and distress. Music therapy, tailored activities, exercise, massage/touch, and multicomponent delirium programs like HELP can meaningfully reduce agitation and prevent escalation. When symptoms threaten safety, we cover how to use meds sparingly and smartly. Before adding anything, do a medication cleanup. Pharmacotherapy is time-limited, lowest dose, shortest duration, and always paired with non-drug strategies.• Cholinesterase inhibitors can modestly improve BPSD over time.• Antipsychotics offer small benefits for severe agitation or psychosis but carry real risks—increased mortality, stroke, sedation, EPS, QT prolongation, and functional decline. No clear winner among agents. Use hours to days, reassess daily, and document risk–benefit discussions. Avoid dopamine blockers in Lewy body dementia; if unavoidable, extreme caution.• SSRIs help depression/anxiety; evidence for agitation is limited. Mirtazapine doesn’t help agitation.• Benzodiazepines and valproate are generally avoid.• Pain control matters—untreated pain fuels agitation. We close with hospital pearls: no routine drugs for delirium; antipsychotics only for dangerous behaviors refractory to non-drug care. Plan early for deprescribing—one-third of patients started on antipsychotics in the hospital leave on them unless you stop it. At discharge, communicate what worked: triggers, de-escalation strategies, sleep plans, toileting schedules, and a clear reassessment plan. Align care with goals, dignity, and function. Bottom line: Treat the cause, lead with non-pharmacologic care, reserve meds for safety, reassess relentlessly, and deprescribe early.

In this episode of Hospital Medicine Unplugged, we tackle one of the most anxiety-provoking inpatient consults: acute facial weakness—Bell’s palsy or stroke? We break down how to tell them apart fast, why the distinction matters, and how to manage each safely in hospitalized patients. We start with the bedside exam that saves lives. Forehead involvement = peripheral (Bell’s palsy); forehead sparing = central (stroke)—until proven otherwise. Bell’s palsy presents with acute unilateral facial paralysis involving the forehead, often peaking within 72 hours, and may include post-auricular pain, altered taste, hyperacusis, or dry eye, without other neurologic deficits. Stroke typically hits suddenly, often spares the forehead, and comes with red flags like limb weakness, aphasia, gaze deviation, dysphagia, or altered mental status. We walk through the don’t-miss pitfalls: brainstem strokes that mimic a lower motor neuron pattern, bilateral facial weakness, gradual or progressive onset, recurrent ipsilateral palsy, hearing loss or vertigo, and facial palsy in post-op, ICU, immunocompromised, or cancer patients—all of which demand a lower threshold for imaging and expanded workup. Next, the inpatient diagnostic strategy. Suspect stroke? Activate the stroke alert—determine last known well, check glucose, perform a focused neuro exam, and get emergent CT/MRI. For classic Bell’s palsy, routine labs and imaging aren’t required, but in hospitalized patients consider MRI with contrast or CSF if there are atypical features, infection risk, multiple cranial nerves involved, or no improvement by 3–6 weeks. Treatment pearls you can use today:Bell’s palsy—start oral corticosteroids within 72 hours (prednisone 50–60 mg daily x5 days, then taper). This improves complete recovery (NNT ≈10). Antivirals alone don’t work; adding them to steroids may modestly reduce synkinesis, especially in severe paralysis. Eye protection is non-negotiable: artificial tears, nighttime ointment, and a moisture shield—early ophthalmology if exposure risk.Stroke—time is brain. Eligible patients get IV thrombolysis and/or mechanical thrombectomy based on time and imaging, with guideline-directed blood pressure control, antithrombotics, and early rehab. We close with prognosis and counseling. Bell’s palsy has a 70–85% complete recovery rate (higher with early steroids), but 25–40% may have residual weakness or synkinesis—plan follow-up at 3 months if recovery lags. Stroke outcomes hinge on severity and speed to reperfusion, making rapid recognition critical. Bottom line: Examine the forehead, hunt for red flags, image early when in doubt, protect the eye, treat fast, and never miss a stroke.

In this episode of Hospital Medicine Unplugged, we get practical about single vs dual antiplatelet therapy after ischemic stroke—who gets what, for how long, and when DAPT does more harm than good. We start by framing the landscape: noncardioembolic vs cardioembolic stroke, small-vessel vs large-artery disease, and why platelets are center stage in atherothrombotic stroke but not in AF-driven cardioembolism. Then we walk through who actually qualifies for DAPT: Minor noncardioembolic ischemic stroke (NIHSS ≤3) High-risk TIA (ABCD² ≥4) Select mild-to-moderate strokes (up to NIHSS 5) and large-artery atherosclerosis / intracranial stenosis, where data for intensified therapy are emerging. We lay out exact protocols you can copy into your order sets: Classic aspirin + clopidogrel: loading, maintenance, and how to transition cleanly to SAPT. Ticagrelor + aspirin: when to prefer it (e.g., CYP2C19 loss-of-function) and how to factor in the higher bleeding signal. Why triple therapy is a hard no. A big chunk of the episode is “how long is long enough?”: Why the real benefit of DAPT is front-loaded into the first 10–21 days. How CHANCE, POINT, THALES, and meta-analyses sharpen the message: short-term DAPT cuts early recurrence; longer DAPT mainly buys bleeding. Why most patients should land on ~21 days of DAPT, then SAPT indefinitely, and when 30–90 days might still make sense (e.g., intracranial stenosis, stenting protocols). We also spell out when NOT to use DAPT: Moderate–severe stroke with big infarcts and hemorrhagic risk Cardioembolic stroke (AF, LV thrombus, valvular disease) where anticoagulation wins Lacunar stroke, where SPS3 showed more bleeding without benefit Patients with high bleeding risk or prior GI bleed, thrombocytopenia, or hemorrhagic transformation ESUS and other gray zones where DAPT has no proven upside. Finally, we zoom out to long-term secondary prevention: Choosing between aspirin, clopidogrel, and aspirin–dipyridamole Why clopidogrel often has the best net clinical profile (similar efficacy, less major bleeding) How to build a stroke unit habit: NIHSS + ABCD² on arrival, early mechanism workup, tight DAPT stop dates, and defaulting back to SAPT instead of “set-and-forget” dual therapy. If you’ve ever wondered “Should this patient be on DAPT, for how long, and what am I risking?” this episode gives you a crisp, evidence-based playbook you can use on your next stroke admission.

In this episode of Hospital Medicine Unplugged, we hit the brakes on routine bridging—who actually needs LMWH/UFH when you stop warfarin, and who is safer with no bridge at all? We start by nailing the definition: bridging = temporarily swapping a long-acting oral anticoagulant (usually warfarin) for short-acting heparin (UFH/LMWH) during interruptions for procedures or bleeding. Then we zoom out to the core tension: tiny peri-procedural thromboembolic risk vs a 3–4× jump in major bleeding with bridging. We walk through thromboembolic risk stratification—AF with CHA₂DS₂-VASc, recent VTE timing, mechanical valves, and severe thrombophilia—and pair it with procedure and patient bleeding risk (neurosurgery vs dental work, HAS-BLED factors, renal/liver disease, prior bleeds). Then comes the evidence gut-punch: BRIDGE: in AF on warfarin, no reduction in thromboembolism, but major bleeding triples with LMWH bridging. Meta-analyses: no thrombotic benefit, big bleeding signal across mixed AF/VTE/mechanical valve cohorts. PAUSE & DOAC data: rapid onset/offset means DOACs almost never need bridging. From there we carve out the true bridging exceptions—the “maybe yes” group:• Mechanical mitral or older-generation mechanical valves• Very recent (<3 months) VTE or stroke/systemic embolism• Severe thrombophilia or high-risk cancer-associated VTE Everywhere else, guidelines increasingly say: “Don’t bridge.” Most AF, remote VTE, bileaflet mechanical AVR without extra risk factors, and all DOAC-treated patients go down a simple interrupt-and-restart pathway instead of heparin drips and syringes. We close with a practical, ward-ready playbook:• Step 1: Classify thromboembolic risk (AF/VTE/valve).• Step 2: Classify procedure + patient bleeding risk.• Step 3: If DOAC → timed hold based on drug + kidney function, no bridge.• Step 4: If warfarin and truly very high thrombotic risk → consider LMWH/UFH, but delay/avoid post-op therapeutic dosing when bleeding risk is high.• Step 5: Use prophylactic-dose LMWH as VTE prophylaxis, not as a stealth “mini-bridge.” By the end, you’ll have a clean mental algorithm for “bridge vs no bridge” that lines up with ACCP, AHA/ACC, and AF guidelines—less bleeding, same stroke protection, and far fewer unnecessary heparin shots.

In this episode of Hospital Medicine Unplugged, we run the inpatient anticoagulation playbook—pick the right drug, dose it safely, and dodge both clots and bleeds. We start with why we anticoagulate in hospital: VTE treatment and prophylaxis, AF stroke prevention, ACS, and valve/bridging scenarios—always walking the tightrope between thrombosis and bleeding. Then we map the four main drug classes:• DOACs as default for most nonvalvular AF and VTE—rapid onset, predictable PK, no routine monitoring, but no go in mechanical valves, APS, pregnancy, or severe CKD.• LMWH as the inpatient workhorse—VTE treatment and prophylaxis, cancer, pregnancy, lower HIT and osteoporosis risk, but renally cleared and only partially reversible.• UFH as the rescue drug—severe renal failure, high bleeding risk, need for rapid on/off, thrombolysis, or upcoming procedures.• Warfarin for the “can’t DOAC” crowd—mechanical valves, rheumatic MS, triple-positive APS, advanced CKD/liver disease—with INR targets, monitoring, and all the interaction baggage. From there we build a clinical decision framework:• Renal and hepatic function drive DOAC vs LMWH vs UFH vs warfarin.• Bleeding risk (HAS-BLED, IMPROVE) and prior GI bleed shape how hard you push.• Drug–drug interactions (CYP3A4/P-gp, polypharmacy, antiplatelets/NSAIDs) push you toward or away from certain DOACs or warfarin.• Extremes of body weight, procedures on the horizon, and the need for a reversal plan all feed into the choice. For VTE treatment, we compare:• Stable DVT/PE with good kidneys → DOAC first (EINSTEIN, AMPLIFY, Hokusai).• Cancer-associated VTE → DOACs vs LMWH: DOACs now common, but LMWH still preferred for GI/GU tumors or very high bleeding risk.• Severe CKD or tenuous bleeder → UFH infusion with aPTT-guided titration and protamine in your back pocket.• Mechanical valves or APS → warfarin with bridging. For VTE prophylaxis, we keep it practical:• LMWH (enoxaparin/dalteparin) as first-line in most medical/surgical inpatients.• UFH for CrCl <30 or when you need a super short half-life.• DOACs (rivaroxaban, betrixaban) as select tools for extended prophylaxis, not routine inpatient starters.• Warfarin stays out of acute prophylaxis. We also tackle cardiology use cases:• UFH (or bivalirudin) for ACS/PCI.• Enoxaparin as an alternative in NSTE-ACS/unstable angina when managed medically.• DOACs and warfarin move to the long-game: AF, LV thrombus, and post-ACS patients who need both antiplatelets and anticoagulation. Finally, we walk through special populations:• Severe CKD → UFH first; dose-reduced LMWH or off-label apixaban only with eyes wide open.• Morbid obesity or very low weight → how we think about fixed-dose DOACs, weight-based LMWH, and when to consider anti-Xa levels.• Pregnancy → LMWH only, no DOACs or warfarin.• Cancer → choosing between DOACs and LMWH based on tumor site, bleeding risk, kidneys, and patient preferences. We close with a bedside checklist: define the indication, check kidney/liver function, estimate bleeding risk, scan the med list for interactions, ask “how fast do I need on/off?”, then lock in an agent, dose, monitoring plan, and a clear reversal strategy. Right drug, right patient, right moment—while keeping both clots and bleeds off your service list.

In this episode of Hospital Medicine Unplugged, we unpack iron deficiency anemia (IDA) and anemia of chronic disease/inflammation (ACD/AI)—absolute iron depletion versus hepcidin-driven iron lock-down, and why that distinction matters on the wards. We sprint through the core physiology: IDA runs on empty iron stores—low ferritin, low TSAT, low hepcidin, microcytosis. ACD/AI keeps iron trapped inside macrophages—normal/high ferritin, low TSAT, low transferrin, high hepcidin—producing a functional deficiency despite adequate stores. Diagnosis starts with the do-first labs: CBC with indices, smear, ferritin, serum iron, TIBC, TSAT, CRP, ± soluble transferrin receptor (sTfR) and reticulocyte Hb. Ferritin <30 ng/mL screams IDA, but in inflammation we need a higher cutoff (<100). sTfR high = IDA; normal = ACD/AI. Hepcidin stays low in IDA, high in ACD. Symptom patterns help but aren’t definitive: IDA brings classic iron-depletion clues (pica, restless legs, glossitis), while ACD/AI blends into the underlying chronic disease. Overlap syndromes blur the picture—ferritin “normal,” TSAT low, inflammation high—the most common and the most misdiagnosed group in the hospital. Management stays principle-driven:• Treat the cause first—stop the bleed, fix malabsorption, control inflammation.• Replete iron: oral every-other-day for pure IDA; IV iron for inflammation, malabsorption, or rapid repletion needs.• ACD/AI leans on underlying disease control; ESA therapy only in selected CKD/cancer patients.• Overlap syndromes? Think IV iron early; oral will fail against hepcidin. Risk matters: anemia on admission predicts longer stay, higher readmission, and higher mortality. The sickest group—older adults with multiple comorbidities—often has mixed pathology and needs aggressive evaluation and structured follow-up every 3–6 months with CBC and iron studies. We close with future directions: hepcidin antagonists, HIF-PH inhibitors, and precision biomarkers (hepcidin, sTfR) that may finally crack the code of inflammation-mediated iron restriction. For now, stick to the fundamentals: identify absolute vs functional deficiency, interpret ferritin through the lens of inflammation, choose the right route for iron, and never overlook an “inappropriately normal” ferritin.

In this episode of Hospital Medicine Unplugged, we crack open Against Medical Advice (AMA) discharges—why patients walk, who’s at highest risk, what really happens after they leave, and how to respond in a way that’s ethical, patient-centered, and legally defensible. We start with the basics: AMA = patients leaving before the team thinks it’s safe. It’s only ~1–2% of discharges, but clustered in younger patients, men, people with substance use and psychiatric disorders, those who are uninsured, on Medicaid, or homeless, and especially anyone with a prior AMA history. We unpack how structural factors—poverty, racism, housing instability, insurance gaps—drive “noncompliance” more than patient personality. Then we lay out the consequences: ~2× higher 30-day readmissions, a 2×+ bump in mortality, tons of early bounce-backs within 24 hours, and hundreds of thousands of hospital days and dollars burned. We connect the dots: shortened LOS, interrupted treatment, no meds, no follow-up, and patients showing up sicker at a different hospital. From there we get practical at the bedside: Capacity, always first. We walk through the 4 pillars—understanding, appreciation, reasoning, choice—and how to optimize capacity by treating delirium, intoxication, withdrawal, pain, and metabolic derangements before you even think about AMA. Risk stratification by diagnosis: MI, sepsis, DKA, respiratory failure, trauma, psychiatric emergencies—what leaving early actually means for morbidity and mortality in each bucket. Find the modifiable drivers: undertreated pain, unmanaged withdrawal, nicotine craving, childcare, job loss fears, transportation, homelessness, mistrust, and prior bad experiences with the system. Communication is the pivot. We lean into nonjudgmental, empathic conversations, motivational interviewing, and de-escalation. We break down the AIMED framework—Assess, Investigate, Mitigate, Explain, Document—as a stepwise way to turn “I’m leaving” into “How can we make this safer?” without coercion or power struggles. For high-risk groups with OUD and other SUDs, we focus on what actually moves the needle: Early, in-hospital MOUD (buprenorphine/methadone) to cut AMA and readmissions. Aggressive pain and withdrawal management, not just PRN clonidine. Addiction consult services to initiate MOUD, link to OTPs/bridge clinics, and coordinate post-discharge care. We zoom out to operational fixes: better discharge communication, individualized discharge plans, streamlined prescriptions, solving basics like transportation and childcare, and targeted workflows in high-risk units (ED, medicine, psych). Then we get into documentation and legal protection—what has to be in the note so “AMA” actually means something: Explicit capacity assessment (by element). Concrete risks, benefits, and alternatives discussed (including partial treatment). What the team offered to mitigate harm (pain control, MOUD, rides, follow-up). The patient’s reasons in their own words. Why the team judged the plan clinically reasonable at the time. We stress the limits of AMA forms and why the contemporaneous narrative note, free of stigmatizing language, is your real medicolegal shield. Finally, we tackle ethics and high-risk scenarios: autonomy vs beneficence, when persuasion becomes coercion, the difference between capacity and legal competence, and how AMA is different for minors, patients on involuntary holds, or those with guardianships. We close with harm-reduction discharges—provisional prescriptions, naloxone, wound supplies, rapid follow-up—and how to welcome patients back after an AMA episode without shame or blame. Fast, structured, and equity-focused—identify who’s likely to leave, fix what’s fixable, communicate without stigma, build harm-reduction exits, document like it matters, and never confuse “AMA” with “we’re done caring.”

In this episode of Hospital Medicine Unplugged, we dive into evidence-based, hospital-focused management of resistant hypertension—a condition affecting up to 1 in 5 hypertensive adults and carrying ≥50% higher risk of MI, stroke, ESKD, and cardiovascular death. We start by drawing the line between true resistant hypertension (BP above goal despite 3 complementary agents including a diuretic, or controlled BP on ≥4 meds) and the look-alikes: refractory HTN (uncontrolled on ≥5 agents including an MRA) and malignant HTN (acute end-organ damage). In the hospital, we must separate chronic resistant HTN from acutely uncontrolled BP driven by pain, anxiety, missed meds, volume shifts, or acute illness. Our first task: rule out pseudoresistance. That means fixing measurement errors, restarting home meds, identifying nonadherence, assessing pain and volume status, and removing BP-raising drugs—NSAIDs, steroids, sympathomimetics, calcineurin inhibitors, erythropoietin, excess IV fluids, and more. We emphasize the ACC/AHA message: 20% of hypertensive adults regularly take interfering medications, and up to 41% of hospitalized patients miss home antihypertensives. Next, we confirm true resistance with out-of-office BP—home BP or, ideally, ABPM, since white-coat resistant HTN carries far lower long-term cardiovascular risk than true resistance. If the numbers hold, we move into systematic secondary evaluation: primary aldosteronism, OSA, renal parenchymal disease, renovascular disease, and medication-induced hypertension. Treatment opens with the guideline-backed triple therapy backbone:• ACE-I/ARB + long-acting CCB + thiazide-like diuretic (chlorthalidone/indapamide preferred).• Below eGFR 40–45: switch thiazides to loop diuretics, typically q12h dosing. Then we deploy the fourth-line star: spironolactone 25–50 mg, the most effective agent based on RCTs and network meta-analyses, cutting 24-hour SBP by ~7–9 mm Hg. But since 4–40% cannot tolerate spironolactone, we cover alternatives:• Amiloride (10–20 mg)—equally effective in trials• Eplerenone—better tolerated hormonally, less potent BP reduction• Consider finerenone in CKD with albuminuria (role in resistant HTN still emerging) For fifth-line therapy, we reserve beta-blockers, alpha-blockers, clonidine, and direct vasodilators—but hydralazine/minoxidil must be paired with a β-blocker + loop diuretic to blunt reflex tachycardia and fluid retention. We also break down renal denervation, which offers modest (~3–5 mm Hg) 24-hour SBP reduction but lacks long-term CVD outcome data. Aprocitentan, FDA-approved in 2025, adds another option, though edema (9–18%) limits use in volume-sensitive patients. CKD deserves its own playbook: resistant HTN is twice as common in CKD, thiazides lose power as GFR falls, and aldosterone excess plus sympathetic activation fuel volume-driven hypertension. We outline strategies including loop diuretics, cautious low-dose MRAs with potassium binders, and the evolving role of nonsteroidal MRAs. Throughout, we reinforce that intensive BP control matters. For resistant HTN, pooled SPRINT/ACCORD analyses show similar benefit from a systolic target <120 mm Hg—when tolerated—cutting major CV events and mortality. We close with a hospital-ready framework:• Fix pseudoresistance first—measurement, meds, volume, pain, interfering agents• Confirm with out-of-office BP• Screen systematically for secondary causes• Build the ACE/ARB + CCB + potent diuretic foundation• Add spironolactone, or amiloride/ eplerenone when needed• Use advanced agents and devices selectively• Individualize BP targets while avoiding overcorrection of asymptomatic inpatient BP spikes Volume control, aldosterone blockade, clean med lists, and accurate BP data—that’s how you turn apparent chaos into controlled, evidence-based management of resistant hypertension in the hospital.

In this episode of Hospital Medicine Unplugged, we tackle opioid withdrawal on the inpatient ward—a syndrome that’s not usually lethal, but absolutely destabilizing, deeply uncomfortable, and a leading driver of patient-directed discharge. We open with why this matters now: fentanyl has changed everything. Its high potency and lipophilicity make withdrawal more severe, more unpredictable, and often prolonged, leaving standard opioid agonist approaches underpowered. Add in common polysubstance use—stimulants, benzodiazepines, xylazine—and clinicians must often manage multiple withdrawal syndromes in parallel. Diagnosis starts with timing: 8–12 hours after short-acting opioids, 8–24 hours after fentanyl, up to 30 hours after methadone. Patients present with the classic multisystem storm—autonomic activation (sweating, tachycardia, piloerection, dilated pupils), GI distress, myalgias, and intense craving. We rely on COWS and SOWS for objective tracking; SOWS often detects symptoms earlier, COWS guides treatment thresholds. But step one is simple: ask about withdrawal and treat it aggressively. Untreated withdrawal drives AMA discharges, worsens medical illness, and erodes trust. Starting MOUD early lowers AMA discharge risk by ~27%. Treatment goals are clear: rapid symptom relief, stabilize with opioid agonists, prevent complications, and set up continuity of care. Our backbone: opioid agonist therapy. • Methadone shines here—no need to wait for withdrawal, no risk of precipitated withdrawal, and a full agonist profile that suits high-tolerance fentanyl users. Standard starts (20–30 mg/day) often fall short in the fentanyl era; rapid inpatient titration is increasingly used safely under monitoring. Watch QTc and delayed respiratory depression. • Buprenorphine brings a stellar safety profile and easy outpatient continuation. But it demands mild–moderate withdrawal (COWS >10) to avoid precipitated withdrawal—still a real fear among fentanyl-exposed patients. Enter microdosing/low-dose induction, now routinely used to bridge patients onto buprenorphine without requiring abstinence. • Some centers use slow-release oral morphine for patients with QTc issues or previous induction failures, and emerging inpatient data support short-acting full-agonist opioids as adjuncts for severe fentanyl withdrawal when standard regimens aren’t enough. If patients decline opioid agonists, we move to symptom-targeted therapy: • Alpha-2 agonists (clonidine, lofexidine) reduce autonomic symptoms; lofexidine offers less hypotension.• GI agents (loperamide, ondansetron, dicyclomine) smooth out the abdominal churn.• NSAIDs/acetaminophen ease myalgias; trazodone or cautious benzodiazepine use can support sleep and anxiety.But remember—non-opioid therapy alone is inferior and reserved for patients who decline MOUD. The differential stays broad: alcohol or benzodiazepine withdrawal, stimulant intoxication, viral GI illness, thyroid storm, adrenal crisis, and sepsis, especially in people who inject drugs. Missing these can be disastrous, so vitals, exam, and targeted labs remain central. We close with the systems moves that make withdrawal care consistent and safe: normalize withdrawal screening, default to MOUD first, incorporate COWS/SOWS into nursing workflows, build fentanyl-aware induction pathways, manage concurrent withdrawals, and hard-wire outpatient linkage—OTP confirmation lines, buprenorphine follow-up, and harm-reduction resources. Fast, compassionate, and evidence-driven—treat withdrawal early, stabilize with MOUD, support symptoms, and never miss a life-threatening mimic.

In this episode of Hospital Medicine Unplugged, we plug into evidence-based blood transfusion—who really needs blood, how much, and when a “top-up” quietly harms more than it helps. We start with the big pivot: why modern practice has moved to a restrictive transfusion strategy (Hb <7 g/dL for most hemodynamically stable adults) and what the RCTs and Cochrane data actually show. We walk through nuanced thresholds for cardiac and orthopedic surgery, preexisting cardiovascular disease, ICU patients, kids, and hematologic/oncologic populations, and flag key exceptions like GI bleeding and brain injury, where the rules bend. Then we zoom out to the menu of components: RBCs for oxygen delivery, platelets for thrombocytopenia, plasma for true coagulopathy, cryo/fibrinogen for hypofibrinogenemia, and whole blood in massive hemorrhage. We hammer home indications beyond “just the number”—symptoms, hemodynamics, rate of Hb drop, volume status—and when NOT to transfuse: mildly abnormal INRs, “just-in-case” platelets, and procedure prophylaxis that doesn’t move bleeding risk. Massive hemorrhage gets its own sprint: what actually defines a massive transfusion, when to trigger an MTP, why balanced 1:1:1 resuscitation (RBC:plasma:platelets) improves hemorrhage control, and how to layer in TXA, calcium, fibrinogen replacement, and viscoelastic testing (TEG/ROTEM) without drowning the patient in crystalloid. We unpack the dark side of blood: TACO, TRALI, acute and delayed hemolytic reactions, TA-GVHD, alloimmunization, and iron overload—and how restrictive thresholds, leukoreduction, irradiation, careful dosing, and slower infusion rates slash those risks. You’ll get a practical mental checklist for “this patient is getting worse during transfusion—now what?” Zooming up to the system level, we build a patient blood management (PBM) toolkit: Choosing Wisely-aligned thresholds, single-unit RBC default with “transfuse 1, then reassess,” EMR best-practice alerts, audit-and-feedback reports, and multidisciplinary transfusion committees that actually change culture and save thousands of units (and dollars). We close on ethics and patient-centered care: informed consent that’s real, not scripted, transfusion decisions in frail or terminally ill patients, and caring for Jehovah’s Witness and other transfusion-refusing patients using IV iron, ESAs, cell salvage, hemostatic agents, and meticulous blood conservation—respecting autonomy while still practicing high-value medicine. Restrictive, thoughtful, system-aware, and patient-centered—this episode is your playbook to give blood when it heals, withhold it when it harms, and always know why you’re hanging that unit.

In this episode of Hospital Medicine Unplugged, we take a rapid, evidence-packed tour through unintentional weight loss (UWL) in hospitalized patients—screen fast, diagnose with structure, separate fluid from true tissue loss, and never miss the reversible causes. We open with the do-firsts: screen within 24–48 hours using MUST, NRS-2002, SNAQ, or MST; older adults get the MNA-SF. Positive screen? Move straight into GLIM—you need ≥1 phenotypic + ≥1 etiologic criterion before calling malnutrition. Phenotypics: weight loss >5% in 6 months or >10% beyond, low BMI (<20 if <70 years; <22 if ≥70), or reduced muscle mass (BIA, DXA, CT, ultrasound).Etiologics: reduced intake/assimilation or inflammation/disease burden—the cytokine-driven catabolic engine that overrides normal starvation physiology. We highlight the epidemiology: UWL hits 20–50% of hospitalized older adults and drives higher mortality, LOS, functional decline, and readmissions—often independent of disease severity. Causes cluster into malignancy, GI disease, psychiatric disease, endocrine disorders, chronic infections, and a surprisingly large fraction (6–28%) with no clear etiology even after thorough workup. Then the diagnostic sprint: CBC, BMP/CMP, LFTs, ultrasensitive TSH, CRP/ESR, LDH, UA, and age-appropriate cancer screenings. Chest radiography + fecal occult blood testing are universal; abdominal ultrasound or CT follows red flags. GI symptoms trigger stool culture, O&P, C. diff, malabsorption labs, or endoscopy. Never trust albumin or prealbumin—they track inflammation, not nutrition. We hit the pitfalls hard: fluid shifts mimic weight loss, medications blunt taste and appetite, oral/dental disease gets missed, dysphagia hides in plain sight, and depression in older adults presents without sadness. EPI masquerades as IBS or celiac. Adrenal insufficiency is chronically underdiagnosed. Thyroid–diabetes interactions derail metabolic signals. Failure to screen early, recheck every 7–10 days, or document true intake leads to cascading errors. Management? Treat the cause and build the nutritional core. Energy 20–30 kcal/kg and protein 0.8–1.5 g/kg, tailored to inflammation severity. For confirmed malnutrition, dietitian-led counseling + fortified oral supplements improve outcomes across major RCTs. Medication reconciliation is mandatory; polypharmacy wrecks appetite. Address oral pain, dentition, dysphagia, and social barriers. We zoom in on hospital-acquired malnutrition—driven by fasting orders, mealtime interruptions, poor food service quality, inadequate feeding assistance, multimorbidity, and long LOS. Solutions use organizational muscle: protected mealtimes, dietitian-MD collaboration, patient-centered menus, protocolized swallow evaluation, early mobility, and automated rescreening. For complex cases, we pull in the consultants:• GI for EPI, celiac, IBD, structural lesions• Endocrinology for thyroid disease, diabetes interactions, adrenal insufficiency• Psychiatry for depression, appetite changes, cognitive decline• ID for TB, HIV, chronic infections• Nutrition for intake monitoring, body composition, and intervention planning We close with the system moves: a UWL bundle that (1) screen-within-48h defaults; (2) GLIM-confirmation pathways; (3) early imaging + stool studies when indicated; (4) intake-tracking dashboards; (5) medication-effect flags; (6) fluid-vs-tissue differentiation via calf circumference + composition tools; (7) 7–10-day reassessment; (8) multidisciplinary escalation; and (9) cause-specific tracks (malabsorption, malignancy, endocrine, psychiatric). Fast, structured, and inflammation-aware—screen early, diagnose precisely, distinguish fluid from tissue, treat the cause, and don’t let hospital factors sabotage recovery.

In this episode of Hospital Medicine Unplugged, we tackle in-hospital falls—how often they happen, why they’re so devastating, and how to build a multifactorial, restraint-sparing prevention bundle that actually works at the bedside. We start with the scope: typical acute-care fall rates run 1.5–4.2 falls per 1,000 patient-days, with geriatric and medical units hit hardest. Up to half of fallers are injured; in older adults, major injuries are ~8× more common, with hip fractures, subdurals, and ICH driving longer LOS, readmissions, cost, litigation, and loss of trust. Add in Joint Commission sentinel event rules and CMS non-payment for fall injuries—and you’ve got a must-fix safety problem. Then we clean up the language: hospital falls as any unexpected descent to floor/lower level; we sort anticipated physiological (gait, weakness, meds), unanticipated physiological (delirium, new illness, syncope), and accidental (environmental). We walk through injury severity from none → minor → moderate → Major A/B/C → death, and zoom in on high-risk contexts: toileting, bed-exit, transfers, ambulation, peri-procedural. Next, we hit what’s modifiable in hospital:• Psychotropics and other FRIDs (benzos, antidepressants, antipsychotics, sedatives, opioids, insulin, antihypertensives, high ACB burden)• Orthostatic hypotension, gait/balance deficits, muscle weakness, vision loss• Delirium, sleep disruption, pain, and continence issues• Environmental and care-related factors: clutter, lighting, equipment, staffing, and unsupervised toileting For screening and risk strat, we ditch scored “fall risk” stickers and lead with brief admission screening (think CDC STEADI 3 questions) plus automatic high-risk flags (recent falls, injury, frailty, gait impairment). Anyone who screens positive gets multifactorial assessment: meds, orthostatics, gait/balance (TUG), cognition/delirium, vision, feet/footwear, continence, ADLs, and environment—using tools like Morse or Johns Hopkins to structure, not replace, clinical judgment. When a fall happens, we move fast: ABCs, head-to-toe for occult injury, neuro check, hip and spine, orthostatics, targeted labs and imaging. We ask the framing question: “If this were a healthy 20-year-old, would they have fallen?” If not, we hunt for underlying pathology—arrhythmia, infection, stroke, medication toxicity—and loop in PT/OT early. The core of the episode is the multifactorial bundle:• Medication review & deprescribing FRIDs; reschedule diuretics/antihypertensives away from night• Supervised exercise & mobility: strength, balance, functional training; no “bed rest by default”• Environmental optimization: lighting, clutter, bed height, grab bars, walking aids within reach• Delirium prevention/management: orientation, sleep hygiene, sensory aids, early mobilization• Toileting protocols: scheduled voids, timely assistance, prioritize bathroom & bed-exit safety• Nutrition & vitamin D where indicated• Patient, family, and staff education as a high-yield, low-tech intervention We zoom in on special populations—very old, cognitively impaired, Parkinson’s, post-op, rehab and ICU patients—where falls are frequent and injuries severe. Here we stress person-centered care, care-partner involvement, sustained exercise, and balancing the tension between mobility and risk aversion. Then we tackle the controversies: physical restraints, bed/chair alarms, sitters, and high-tech sensors. We review why the evidence shows little benefit and real harm—more delirium, more device removal, more meds, longer stays—and how guidelines are shifting towards least-restraint, engagement-based models instead of “alarm everything.” We close with the post-fall and QI playbook: standardized post-fall assessment, a quick bedside huddle, unit-level root cause analysis, and using tools like Fall TIPS-style bedside plans to translate risk factors into visible, actionable precautions. We outline how to build a falls bundle into yo

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.