Hospital Medicine Unplugged

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.