In this episode of Hospital Medicine Unplugged, we break down hypertensive crisis—separating urgency from emergency, tailoring the pace of reduction, and choosing the right IV agent for the right patient.

We open with the definitions:

Why it matters: rapid BP reduction in urgency risks AKI, cerebral hypoperfusion, and longer stays—no benefit shown. In emergency, uncontrolled pressure fuels stroke, MI, aortic dissection, renal failure—time-sensitive management prevents irreversible injury.

Management pearls:

IV agent playbook (scenario-driven):

Monitoring that sticks:

Prognosis reality check:

Bottom line: check for organ damage, choose the right lane (urgency vs emergency), titrate carefully, tailor the IV agent to the scenario, and don’t overtreat stable patients. That’s how you save lives and avoid iatrogenic harm.

In this episode of Hospital Medicine Unplugged, we tackle enteral nutrition (EN) in hospitalized patients—screen early, start within 24–48 h when indicated, tailor the route and formula, and prevent complications like refeeding syndrome.

We start with the definitions and routes:

When to use EN? If the patient cannot meet needs orally and has no contraindication (e.g., obstruction, uncontrolled shock, ischemia, high-output fistula, massive GI bleed). EN beats PN—lower infections, cost, and complications. Indications include critical illness, dysphagia, neuro disease, GI/liver disease, cancer, COPD, CKD.

Timing:

Dosing & advancement:

Formula selection:

Administration methods:

Complications:

Special situations:

Bottom line: EN early, unless contraindicated. Screen for malnutrition, start low and advance as tolerated, choose standard formulas first, protocolize administration, monitor closely, and prevent refeeding and aspiration. That’s how you fuel recovery safely and improve outcomes.

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:

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:

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:

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:

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:

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:

Alcohol-associated hepatitis (AH) moves:

Acute viral hepatitis plays:

ALF protocol—don’t blink:

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:

Surgery & source control—when to cut:

Special populations you can’t miss:

Monitoring that sticks:

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:

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):

Treatment—build the anti-acid backbone for reflux esophagitis:

Eosinophilic esophagitis (EoE) moves:

Infectious & pill-induced:

ICU & hospital specifics:

Prevention & follow-up:

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):

Diagnostic road map:

Treatment—build the repletion core:

If the backbone buckles:

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:

Complications & pitfalls you don’t want to meet:

Research horizon:

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):

• B. Shift K⁺ into cells (on board within minutes):

• C. Remove K⁺ (definitive):

Etiology plays (treat the cause):

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:

Recurrence prevention:

Controversies & pitfalls you don’t want to meet:

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.

Second-line (10–30 min): established SE—levetiracetam, fosphenytoin, or valproate.

Refractory SE (30–60+ min): seizures persist after a benzo + one second-line ASD → ICU, intubate, start continuous EEG and anesthetic infusions:

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:

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.