Hospital Medicine Unplugged

In this episode of Hospital Medicine Unplugged, we break down hyperaldosteronism—recognize fast, test smart, and treat to protect the heart and kidneys.
We start with the big picture: primary aldosteronism (PA) drives up to 10% of hypertension cases, especially resistant hypertension, and carries outsized risks—atrial fibrillation, stroke, MI, CKD—even when BP looks controlled. Aldosterone excess wreaks havoc via sodium retention, potassium wasting, and vascular fibrosis.
When to screen? Think resistant hypertension, hypokalemia, adrenal incidentaloma, family history of early-onset HTN or stroke, and hypertension + OSA. Order PAC, PRA, and ARR (cutoff ARR ≥30 with PAC ≥10 ng/dL). Correct K⁺ first, keep salt intake normal, and stop MRAs 4 weeks prior if feasible. False negatives lurk if meds interfere—substitute with noninterfering agents (e.g., verapamil, hydralazine).
Confirmatory testing (saline infusion, oral sodium load, fludrocortisone suppression, or captopril challenge) seals the diagnosis. Then, differentiate subtype: CT for masses but remember, AVS is gold standard for surgical candidates, ensuring you don’t miss bilateral disease masquerading as unilateral.
Treatment tracks:• Unilateral disease → laparoscopic adrenalectomy. Expect cure or major BP improvement + normokalemia. Better CV/renal outcomes vs meds.• Bilateral disease or non-surgical → MRAs (spironolactone 12.5–25 mg → titrate; or eplerenone 25–50 mg BID if intolerant). Add salt restriction and other antihypertensives as needed.
Therapeutic goals: normalize BP with fewer meds, correct K⁺ without supplements, and see renin rise—your marker of effective blockade.
New horizons: aldosterone synthase inhibitors (e.g., lorundrostat) and ENaC blockers may expand the toolbox for those who can’t tolerate MRAs.
Monitoring matters:• Acute phase—check BP, K⁺, renal function daily; continuous ECG if severe hypokalemia.• After surgery—watch for hypoaldosteronism; track BP, K⁺, renin.• On MRAs—monitor for hyperkalemia, gynecomastia, renal decline; titrate carefully.
If left untreated? Expect refractory HTN, hypokalemic arrhythmias, LV hypertrophy, AF, strokes, MIs, and CKD progression—risks up to 4–12x higher for AF and 2–4x higher for CV events than essential hypertension.
Key takeaway: screen aggressively, confirm carefully, localize accurately, and treat decisively. Whether by scalpel or spironolactone, targeted therapy prevents irreversible cardiac and renal damage.

In this episode of Hospital Medicine Unplugged, we tackle hospital-acquired pneumonia (HAP) and ventilator-associated pneumonia (VAP)—spot early, culture smart, treat right, and prevent relentlessly.
We open with the definitions: HAP = ≥48 h after admission in non-ventilated patients; VAP = ≥48 h after intubation. Both drive ICU stays, mortality, and costs, with Gram-negatives + MRSA leading the charge and MDROs reshaping therapy.
Risk factors: prior antibiotics, prolonged hospitalization, intubation, comorbidities (lung disease, diabetes, CKD, immunosuppression), and high local MDRO burden. Pathogenesis is microaspiration + impaired defenses + hospital flora colonization, amplified by invasive devices.
Diagnosis: need new/progressive infiltrate + fever/leukocytosis/purulent secretions or worsening oxygenation. Always get respiratory samples before antibiotics—sputum/ETA/BAL depending on setting. Molecular panels can speed ID and resistance calls, but stewardship is key. Biomarkers (CRP, procalcitonin) support, but don’t replace cultures.
Treatment:• Start empiric antibiotics promptly after cultures, not before.• Low MDRO risk → standard-spectrum (e.g., ceftriaxone, ampicillin-sulbactam).• High MDRO risk → cover Pseudomonas + MRSA, with dual antipseudomonal therapy only in severe illness or recent IV antibiotics.• De-escalate at 48–72 h based on cultures and clinical response.• Duration: 7 days (shorter courses safe if improving; extend if Pseudomonas, slow response, or complications).• Adjuncts: optimize PK/PD dosing in critically ill; consider inhaled antibiotics in refractory MDRO cases.
Supportive care: oxygen and ventilation as needed, fluids, hemodynamic support, physiotherapy, nutrition, and aspiration precautions. ICU transfer if hypoxemia, shock, or organ failure.
Prevention bundles:• Non-ventilated patients: daily oral care (mechanical brushing > chlorhexidine rinses), aspiration precautions (HOB 30–45°, dysphagia screening), early mobilization, sedation minimization, hand hygiene.• Ventilated patients: subglottic secretion drainage, closed suction, avoid routine circuit changes, minimize sedation, and elevate HOB. Selective digestive decontamination can reduce VAP/mortality but use cautiously (resistance risk).• System-wide: minimize unnecessary antibiotics/acid suppression, maintain vaccines, embed multimodal prevention.
Complications: ARDS, empyema, lung abscess, sepsis, septic shock, renal failure, cardiac events, thromboembolism, longer LOS, readmissions. Risk of complications climbs with age, comorbidities, aspiration, and inappropriate empiric therapy.
Prognosis:• NV-HAP mortality 11–22%; VAP and ventilated HAP 21–29%.• ICU HAP → +82% 30-day mortality; VAP → +38%.• 1-year mortality ~35–41% even in survivors.• MDRO infections, multilobar infiltrates, vasopressor use, or failed early response = poor outcomes.
Bottom line: spot early, culture before antibiotics, hit hard if risk factors, de-escalate fast, shorten duration, and prevent with bundles. That’s how you save lungs, save lives, and save antibiotics.

In this episode of Hospital Medicine Unplugged, we sprint through acute hepatitis—find the cause fast, stabilize early, risk-stratify smart, treat the etiology, and don’t miss ALF.
We open with the do-firsts: airway/breathing/circulation, focused exam (jaundice, asterixis, volume), and a broad lab bundle—AST/ALT, bilirubin, INR/PT, albumin, CBC, BMP, glucose, acetaminophen level, pregnancy test when relevant. Send viral serologies (HAV IgM, HBsAg + anti-HBc IgM, HCV Ab → HCV RNA, HEV IgM/RNA, HDV testing if HBV+). Image with RUQ ultrasound to exclude biliary obstruction and vascular issues. Flag precipitating drugs and toxins early.
Call the diagnosis and the risk: AH and viral hepatitis (A–E) dominate admissions. Use MELD, Maddrey DF, ABIC, Glasgow for alcohol-associated hepatitis (AH); reassess steroid response with the Lille score on day 7. For any patient with coagulopathy and encephalopathy, think acute liver failure (ALF) and call the transplant center early.
Supportive care—build the foundation:• Hemodynamics + glucose (avoid hypotonic fluids; prevent hypoglycemia).• Nutrition: aggressive protein/energy support; adjust for severe hyperammonemia.• Infection vigilance—low threshold to culture and treat; infections drive mortality in AH/ALF.• Manage HE, AKI, SIRS fast; avoid routine INR correction unless procedures planned.
Alcohol-associated hepatitis (AH) moves:• Corticosteroids: prednisolone 40 mg daily for 28 days if Maddrey ≥32 or MELD ≥20 and no contraindications (active infection, GI bleed, severe AKI, uncontrolled sepsis).• Day-7 Lille: non-responder → stop steroids.• Adjuncts (e.g., N-acetylcysteine) may add short-term benefit; evidence is limited—not standard alone.• Early liver transplant: consider in severe, non-responding patients after multidisciplinary evaluation and commitment to abstinence care.• Always pair with addiction medicine, withdrawal management, vitamins (thiamine), and alcohol cessation program.
Acute viral hepatitis plays:• Acute HBV: mostly supportive; antivirals (entecavir/tenofovir) for severe/fulminant disease or high-risk reactivation.• HDV: no proven acute therapy beyond HBV agents; investigational drugs not for ALF.• HCV: supportive in the acute setting; DAA therapy may be considered selectively.• HAV/HEV: supportive care; watch for ALF in vulnerable hosts (pregnancy for HEV).
ALF protocol—don’t blink:• ICU, early airway, head-of-bed up, tight sodium/glucose control, neuro-monitoring.• CRRT for hyperammonemia/AKI; consider high-volume plasma exchange when transplant isn’t imminent.• Use King’s College + MELD to guide transplant activation.
Complications you must prevent: cerebral edema, infection/sepsis, AKI/HRS, hypoglycemia, ARDS, shock. These—not the transaminases—set the mortality curve.
System moves that stick: (1) standardized acute hepatitis order set (labs/viral panel/US + acetaminophen level); (2) steroid checklist for AH (indications/contraindications + Lille day 7 stop rule); (3) infection screen q24–48h in AH/ALF; (4) automatic transplant alert for ALF criteria; (5) nutrition + addiction consults on day 0; (6) discharge bundle: vaccinate (HAV/HBV as indicated), alcohol cessation plan, cirrhosis education, and close hepatology follow-up.
Fast, score-guided, and etiology-targeted—stabilize first, prove the cause, treat what you find, and escalate to transplant before the cliff.

In this episode of Hospital Medicine Unplugged, we sprint through osteomyelitis—spot early, culture smart, hit bugs hard, cut dead bone, mobilize the team.
We open with the do-firsts: risk scan (diabetes, PAD, trauma/surgery, prosthetics, IVDU, MRSA exposure), focused exam for focal bony pain, warmth, swelling, sinus tracts, and labs (ESR/CRP↑ > WBC). Get blood cultures if febrile or vertebral disease. MRI is your early, high-sensitivity imaging to map abscesses and necrotic bone. Definitive diagnosis = bone biopsy for microbiology + histopathology—avoid swabs/sinus cultures.
Epidemiology & bugs: S. aureus (MSSA/MRSA) dominates; add gram-negatives (esp. in trauma, healthcare exposure, IVDU), polymicrobial in diabetic foot, and Kingella in kids. Tailor to host, route (hematogenous vs contiguous vs direct inoculation), and local resistance.
Antimicrobials—build the targeted backbone:• Empiric (ill or vertebral): MRSA coverage (vancomycin or daptomycin) + broad gram-negative (ceftriaxone/cefepime or FQ when appropriate). Consider Pseudomonas if risk factors; anaerobes for diabetic foot.• Narrow fast when cultures/susceptibilities return: MSSA → cefazolin/oxacillin; MRSA → vanc/dapto/linezolid (watch tox); Kingella → β-lactams.• Duration typically 4–6 weeks (longer if chronic, residual infected bone, or vertebral).• IV-to-PO switch works in stable patients with source control and susceptible organisms—choose high-bioavailability, bone-penetrant agents (e.g., FQ ± rifampin for staph with hardware, clindamycin, linezolid, TMP-SMX + rifampin when appropriate). Monitor for tox and interactions (rifampin, linezolid).
Surgery & source control—when to cut:• Chronic disease, abscess, sequestrum, sinus tract, failure of medical therapy, or unstable hardware → operative debridement.• Hardware strategy: remove if loose/infected; consider DAIR (debridement, antibiotics, implant retention) if stable hardware, early infection, and good debridement.• Dead-space management with antibiotic beads/spacers; plan staged reconstruction with plastics/ortho for coverage.
Special populations you can’t miss:• Vertebral OM: ≥6 weeks targeted therapy; urgent surgery for neurologic compromise, epidural abscess with deficits, instability, or failure of antibiotics.• Diabetic foot OM: often polymicrobial—pair aggressive debridement, vascular assessment/revascularization, off-loading, and tailored antibiotics; shorter courses possible after clean-margin minor amputation.• Prosthetic-associated & fixation infections: consider rifampin-based combos for staph (if hardware retained and susceptibilities allow).
Monitoring that sticks:• Track pain, wound status, function, and ESR/CRP trends; falling CRP supports response.• Re-image only if not improving or to define complications.• Watch drug safety: vanc AUC/AKI, linezolid cytopenias/neuropathy, FQ tendinopathy/QT, rifampin interactions.
Complications—don’t blink: pathologic fracture, chronic draining sinus, epidural/psoas abscess, relapse, amputation (diabetes/PAD), sepsis. Early escalation changes trajectories.
System moves that raise your cure rate:(1) MRI early + two sets of blood cultures when indicated.(2) Hold broad-spectrum if stable until bone cultures (don’t sterilize the biopsy).(3) Pathogen-directed regimens with IV→PO plan and toxicity labs embedded.(4) Multidisciplinary board: ID + ortho + plastics + vascular + wound care + endocrinology.(5) Hardware algorithm (retain vs remove) + DAIR criteria.(6) DFO pathway: probe-to-bone, imaging, vascular workup, off-loading, staged debridements, targeted antibiotics, 6-month recurrence surveillance.(7) Discharge bundle: OPAT or oral step-down with clear stop date, lab monitoring schedule, glycemic control, smoking cessation, footwear/off-loading, and wound clinic follow-up.
Fast, culture-led, and scalpel-savvy—get the bug, get the bone, get the source, and get the team.

In this episode of Hospital Medicine Unplugged, we sprint through esophagitis—spot it fast, pin the cause, heal the mucosa, prevent complications.
We open with the do-firsts: identify alarm features (dysphagia, weight loss, GI bleed, IDA), review meds (bisphosphonates, NSAIDs, tetracyclines), immune status, tube size/position, and supine time. Frame the epidemiology for inpatients: ~1/3 of scoped inpatients have esophagitis, morbidity is meaningful, and higher short-term mortality usually mirrors comorbidity—not the mucositis itself. Prefer fine-bore NG tubes when you must feed.
Call the diagnosis: symptoms alone are messy. Endoscopy for alarms or refractory symptoms—grade erosions, biopsy to confirm EoE, rule out Candida/HSV/CMV, pill injury, Barrett’s, strictures, or malignancy. Add pH monitoring/manometry only when the picture stays hazy or before surgery.
Etiology plays (treat what you find):• Reflux (GERD)—most common inpatient cause.• EoE—eosinophilic infiltration; dysphagia/food impaction.• Pill injury—temporal to culprit med, worse if taken without water/lying down.• Infectious—Candida/HSV/CMV in the immunocompromised.• Don’t forget motility disorders and functional overlap.
Treatment—build the anti-acid backbone for reflux esophagitis:• PPIs first-line for symptoms + mucosal healing; H2RAs for mild or if PPIs can’t be used. Use the lowest effective dose long term; reassess need to avoid PPI baggage (infections, micronutrients).• Refractory? BID PPI, switch agents, add H2RA at night, alginates, or baclofen (careful selection).• Surgery (fundoplication) only for documented pathologic reflux with persistent symptoms on optimal therapy; endoscopic options are investigational.
Eosinophilic esophagitis (EoE) moves:• Start with PPI therapy (anti-inflammatory effects beyond acid).• Add topical steroids (swallowed fluticasone or viscous budesonide) for histologic remission.• Dietary elimination works but watch feasibility.• Endoscopic dilation for fixed rings/strictures or severe dysphagia.
Infectious & pill-induced:• Candida → systemic azoles; HSV/CMV → antivirals guided by histology/NAAT.• Stop/substitute offending pills; insist on water + remaining upright ≥30 min.
ICU & hospital specifics:• Stress ulcer prophylaxis only for true indications (coagulopathy, prolonged ventilation). IV acid suppression (PPI or H2RA) acceptable—no clear winner for prophylaxis.• For acute upper GI bleeding, IV PPI post-hemostasis to reduce rebleed.• Minimize supine time, elevate HOB, and choose fine-bore tubes to reduce mechanical injury/bile reflux.
Prevention & follow-up:• Lifestyle nudges: HOB elevation, no late meals, weight loss when relevant, trim trigger foods and tobacco.• Reassess need for chronic PPI; step-down/stop when safe (no erosive disease/Barrett’s).• Arrange follow-up for healing, stricture detection, and Barrett’s surveillance when indicated.
Complications—don’t miss them: UGIB, strictures, Barrett’s, rare perforation/fistula with aspiration risk—act early (endoscopic therapy, CT + surgical consult for suspected perforation).
System moves that stick: (1) triage by alarm features; EGD + biopsy when indicated; (2) default PPI-first for erosive disease with dosing/meal-timing education; (3) EoE pathway (PPI → topical steroid → diet ± dilation); (4) targeted infectious therapy after sampling; (5) medication stewardship to avoid pill injury; (6) ICU prophylaxis by criteria only; (7) tube care protocol favoring fine-bore and HOB elevation; (8) deprescribing and surveillance plan at discharge.
Fast, endoscopy-led, and cause-targeted—treat reflux with PPIs, tailor therapy to EoE/infectious/pill injury, protect the mucosa, and engineer the inpatient environment to prevent harm.

In this episode of Hospital Medicine Unplugged, we sprint through hypokalemia—define fast, find the source, replete safely, prevent rebounds.
We open with the do-firsts: confirm K+ <3.5 mmol/L (<3.0 severe), review meds (loop/thiazide diuretics, insulin, steroids), check GI losses, volume/BP, and get serum/urine electrolytes + acid–base. ECG if symptomatic or K+ ≤3.0. Distinguish renal vs extrarenal losses early with urine K+ (spot or 24-hr) and chloride.
Call the diagnosis and risk: hypokalemia is common in the hospital (>20%) and not benign—arrhythmias, weakness/paralysis, ileus, and death. Even mild deficits raise morbidity/mortality, especially in heart failure, CKD, and digoxin users. Rapid drops are riskier.
Pathophys plays (why K+ falls):• External balance: diet in, kidney/colon out; aldosterone drives distal secretion.• Internal shifts: insulin, β-agonists, alkalosis push K+ into cells.• Usual culprits: diuretics, vomiting/diarrhea or NG suction, renal tubulopathies, surreptitious laxatives/vomiting, hypomagnesemia.
Diagnostic road map:• Urine K+: <20 mmol/L → extrarenal/poor intake; ≥20 → renal wasting. UK/Cr, FEK, or TTKG help if needed.• If metabolic alkalosis + HTN, think mineralocorticoid excess (check renin/aldo). If alkalosis + normal/low BP, think diuretics or tubulopathies.• Always pair with Mg, acid–base, and medication review.
Treatment—build the repletion core:• Oral first for mild–moderate and intact GI: typically 20–40 mmol/day (mild) or 40–100 mmol/day in divided doses (moderate).• IV KCl for severe (<2.5), symptoms/ECG changes, or no PO: 10–20 mmol/hr (central line for higher rates; max 40 mmol/hr in ICU with continuous ECG). Avoid dextrose-containing fluids.• Expect variability: the classic “10 mEq → +0.1 mmol/L” often overestimates; median response ~+0.05 mmol/L per 10 mEq, and loop diuretics blunt the rise—dose accordingly.• Choose the salt wisely: KCl is default; use K-bicarb/citrate with metabolic acidosis or K-phosphate when phosphate is low.
If the backbone buckles:• Fix Mg first/with K+—hypomagnesemia makes hypokalemia refractory.• Ongoing renal K+ wasting? Add K-sparing diuretics (e.g., spironolactone, amiloride) and reduce offending diuretics if possible.• Persistent GI loss? Replace chloride and treat the cause.
Risk-stratify & admit when any: K+ <2.5, symptoms (weakness, paralysis), ECG changes/arrhythmia, rapid fall, digoxin use, significant comorbidity (HF/CKD), or inability to take PO. In-house: telemetry if severe or IV rates >10 mmol/hr, frequent labs, and address etiology.
Monitoring that sticks:• Mild (3.0–3.5, asymptomatic): recheck within 24 h.• Moderate (2.5–2.9) or symptoms/ECG: q4–6 h during active repletion.• Severe (<2.5) or IV infusion: q2–4 h with continuous ECG for higher rates.• Track renal function and Mg, avoid overshoot—iatrogenic hyperkalemia is real, especially in CKD or with large cumulative doses.
Complications & pitfalls you don’t want to meet:• Overcorrection → hyperkalemia/arrhythmias—titrate and trend.• Slow-release K+ tabs can cause GI irritation; favor microencapsulated forms.• Dextrose-containing IVs worsen hypokalemia via insulin surge.• Failure to document and recheck leads to missed targets and harm.
Research horizon:• Better dose–response tools under real-world meds (esp. loops).• Oral vs IV comparative outcomes across HF/CKD.• Role of dietary K+ in restoring and maintaining normokalemia in chronic care.
Fast, physiology-led, and safety-first—fix the cause, replete smart (PO when you can, IV when you must), correct Mg, and monitor like it matters.

In this episode of Hospital Medicine Unplugged, we power through hyperkalemia—confirm fast, monitor the heart, stabilize the membrane, shift K⁺ in, and remove K⁺ out—while fixing the cause and keeping RAASi on board when safe.
We open with the do-firsts: repeat K⁺ to exclude pseudohyperkalemia; 12-lead ECG + telemetry; hunt triggers (AKI/CKD, meds, acidosis, tissue breakdown). Remember: no ECG changes ≠ safe—severe hyperkalemia can be silent.
Call it when serum K⁺ >5.0 mmol/L (often severe ≥6.0). High-risk hosts: CKD, HF, diabetes, RAASi/K-sparing diuretics, hospitalized/critically ill. Why it matters: arrhythmias & sudden death—risk climbs with rapid rises and higher K⁺.
Treatment—build the three-part stack:
• A. Stabilize the myocardium (now if ECG changes or K⁺ ≥6.5):Calcium gluconate 10% 10 mL IV over 2–5 min (repeat if QRS doesn’t narrow). In arrest/central line, calcium chloride is acceptable. Calcium doesn’t lower K⁺—it buys time.
• B. Shift K⁺ into cells (on board within minutes):Insulin 10 U IV + dextrose 25 g (consider 50 g or dextrose infusion in CKD; q30–60 min glucose checks—hypoglycemia is common).Albuterol 10–20 mg nebulized (additive; watch for tachyarrhythmia/ischemia).Sodium bicarb only if metabolic acidosis or TLS/DKA physiology—limited effect otherwise.
• C. Remove K⁺ (definitive):Loop diuretic if making urine.Potassium binders: prioritize patiromer or sodium zirconium cyclosilicate for non-emergent/bridging and RAASi maintenance; avoid routine SPS (variable efficacy; GI injury risk).Hemodialysis = fastest & most reliable for severe/refractory, ESRD/AKI, TLS/rhabdo, or life-threatening ECG changes.
Etiology plays (treat the cause):• Decreased excretion: AKI/CKD, hypoaldosteronism, low distal Na⁺ delivery.• Meds: ACEi/ARB/ARNI, spironolactone/eplerenone, amiloride/triamterene, NSAIDs, heparin, calcineurin inhibitors, trimethoprim, non-selective β-blockers.• Redistribution: acidosis, insulin deficiency (DKA), β-blockade, succinylcholine, tissue breakdown (TLS, rhabdo).• Increased intake: supplements, salt substitutes, PRBCs/TPN.• Pseudohyperkalemia: hemolysis, thrombocytosis, leukocytosis—repeat plasma K⁺ before you treat aggressively.
Monitoring & safety that sticks: trend K⁺ q1–2 h after temporizers (watch rebound), then q4–6 h as stable; continuous telemetry for severe cases; point-of-care glucose after insulin; reassess ECG after calcium/each step. Document timing—time-to-therapy saves myocardium.
Special situations:• ESRD/AKI: skip diuretics if anuric—dialyze early.• TLS/rhabdo: simultaneous aggressive K⁺ control + underlying-cause therapy.• DKA: insulin alone will fall K⁺—replace K⁺ once <5.0 and urine flows.• Pregnancy: avoid SPS; binder choice and dialysis per severity.• Digoxin toxicity: avoid IV calcium in classic “stone heart” concern—prioritize digoxin-specific Fab and temporizers.
Recurrence prevention:• Medication audit (de-risk combos, stop non-essentials), correct metabolic acidosis, tailor diet (focus on processed/animal K⁺; don’t over-restrict plant-based foods), and use patiromer/SZC to maintain RAASi in HF/proteinuric CKD.• Build a monitoring plan for CKD/HF/diabetes or prior hyperkalemia (e.g., check K⁺ within 3–7 days after RAASi/diuretic changes, then space out).
Controversies & pitfalls you don’t want to meet:• Under-dosing insulin or skipping glucose checks → hypoglycemia.• Overreliance on ECG—normal ECG doesn’t rule out danger.• Reflex SPS use despite GI risk and uncertain benefit.• Stopping RAASi permanently after a single episode—use binders/monitoring to preserve cardio-renal benefit when feasible.• Missing pseudohyperkalemia—treat the patient + lab context, not a single hemolyzed value.
We close with the system moves: a hyperkalemia bundle that (1) auto-repeats K⁺ if hemolysis suspected; (2) routes to telemetry for severe cases; (3) fires a calcium-insulin-albuterol pathway with glucose checks; (4) preloads dialysis for ESRD/AKI or ECG danger; (5) flags culprit meds and suggests safer alternatives; (6) offers patiromer/SZC order sets to keep RAASi on board; (7) embeds follow-up K⁺ monitoring and patient education.
Confirm fast, protect the heart, shift now, remove for keeps, fix the cause—and keep the kidneys & heart therapies rolling when you can.

In this episode of Hospital Medicine Unplugged, we blitz status epilepticus (SE)—recognize at 5 minutes, give a full benzo dose fast, load a second-line ASD without delay, and escalate to ICU infusions + EEG when needed.We open with the do-firsts (0–5 min): ABCs, oxygen, lateral positioning, monitors, IV/IO access, check glucose (give thiamine → dextrose if at risk), draw labs, consider tox screen, and don’t miss mimics. If persistent altered consciousness, order EEG early to uncover nonconvulsive SE.Diagnosis & triage: SE = continuous seizure ≥5 min or recurrent seizures without recovery. Includes convulsive and nonconvulsive phenotypes; the latter is subtle—EEG is essential. Etiology buckets: structural (stroke/ICH/tumor/TBI), metabolic (electrolytes, organ failure), withdrawal/intoxication, medication non-adherence, autoimmune/NORSE, infection. Etiology predicts outcome—hunt it while you’re treating.First-line (5–10 min): benzodiazepine—full dose, once, fast.• IV lorazepam 0.1 mg/kg (max 4 mg); or IV diazepam 0.15–0.2 mg/kg (max 10 mg).• No IV? IM midazolam 10 mg (or IN/buccal 0.2 mg/kg).Speed and adequate dosing beat agent choice. Repeat once if still seizing and move on.Second-line (10–30 min): established SE—levetiracetam, fosphenytoin, or valproate.• Levetiracetam 60 mg/kg (max 4.5 g), fosphenytoin 20 mg PE/kg (max 1.5 g PE), or valproate 40 mg/kg (max 3 g)—similar efficacy, choose by comorbidity/contraindications.• Levetiracetam/valproate favored in cardiac disease; avoid valproate in pregnancy or severe hepatic disease.• Consider lacosamide if alternatives limited.Refractory SE (30–60+ min): seizures persist after a benzo + one second-line ASD → ICU, intubate, start continuous EEG and anesthetic infusions:• Midazolam or propofol (titrate to seizure or burst suppression).• Watch for hypotension, infection, metabolic complications; protocolize weans to avoid withdrawal seizures.Super-refractory (>24 h after anesthetics): broaden playbook—ketamine, additional ASDs, immunotherapy for suspected autoimmune/NORSE, ketogenic diet, neuromodulation (VNS/ECT), selective inhaled anesthetics, and surgical options for focal, resectable sources. Multidisciplinary team is non-negotiable.EEG strategy that sticks: spot NCSE early; in refractory phases, continuous EEG guides infusion targets and catches breakthroughs. Diagnostic IV ASD trials under EEG can clarify ambiguous patterns.Setting-specific pearls:• Alcohol withdrawal: benzodiazepines are primary; thiamine before glucose; phenytoin doesn’t treat withdrawal seizures.• Pregnancy: benzos for emergent control; levetiracetam or fosphenytoin next; avoid valproate when possible; magnesium for eclampsia.• Older adults: same ladder, but dose-low/go-slow, mind renal/hepatic function and drug–drug interactions.Why the hurry? Prolonged seizures shift receptors (↓GABA, ↑NMDA), fuel neuronal injury and pharmacoresistance, and raise mortality (>20% in refractory cases). Early, protocol-driven care saves brain and life.Medication pitfalls you don’t want to meet: under-dosing benzodiazepines, stacking sedatives without airway planning, ignoring QT/hypotension with fosphenytoin/propofol, and forgetting EEG in the quiet, confused patient.We close with the SE bundle: (1) time-zero ABCs + glucose/thiamine; (2) full-dose benzo now; (3) immediate second-line load if still seizing; (4) early EEG (liberal for suspected NCSE); (5) ICU + continuous EEG + anesthetic infusion for refractory; (6) parallel etiology hunt (CT/MRI, labs, CSF/autoimmune as indicated); (7) structured wean and recurrence plan; (8) post-event counseling on adherence, triggers, and secondary prevention.Fast benzo, full load, early EEG, decisive escalation—that’s how you beat status.