In this episode of Hospital Medicine Unplugged, we sprint through cerebral venous sinus thrombosis (CVST)—diagnose fast, anticoagulate early (even with ICH), escalate wisely, and individualize duration.

We open with the do-firsts: therapeutic heparin now—LMWH preferred for predictable dosing and lower HIT risk; UFH is fine if procedures are likely or renal function is tenuous. Anticoagulate even when intracranial hemorrhage is present unless there’s a specific contraindication (e.g., massive hematoma with expansion risk, HIT/VITT). Get MRI/MRV (or CTV when MRI’s a no-go) to confirm site/burden and look for venous infarction/hemorrhage.

Transition & duration: once stable, switch to oral anticoagulation—DOACs or warfarin are both acceptable. Treat 3–12 months in most; extend or make indefinite with persistent risks (thrombophilia, active cancer, recurrent VTE). Don’t chase recanalization to set duration—radiographic changes ≠ outcomes.

When the course bends: endovascular therapy (mechanical thrombectomy ± local lytics) is not routine—reserve for clinical deterioration despite adequate anticoagulation or when anticoagulation is contraindicated, and do it in experienced centers. Decompressive hemicraniectomy can be lifesaving for impending herniation/refractory intracranial hypertension from large venous infarcts.

Seizures & ICP: start anticonvulsants after a first seizure (or with parenchymal lesions/high risk); no prophylaxis otherwise. For edema/ICP, skip glucocorticoids, acetazolamide, and mannitol—evidence doesn’t support them here; avoid dehydration that could worsen thrombosis.

Special situations you must not miss:

Monitoring that matters: tight neuro checks, watch for worsening headache, papilledema, seizures, encephalopathy. Trend CBC/platelets, coagulation, creatinine; surveil for bleeding. Repeat imaging if symptoms progress or to document status at 3–6 months (not to dictate duration).

Workup & risk framing: screen for provoking factors (OCPs, pregnancy, dehydration, surgery/immobility, infection, malignancy) and targeted thrombophilia testing once off acute-phase confounders. Counsel on risk modification (hormonal therapy, dehydration, prolonged immobility).

System moves for a safer pathway:

Anticoagulate on diagnosis (LMWH first line).

MRI/MRV or CTV to confirm, map thrombus, and detect venous infarct/ICH.

Early ICU/stroke-unit care for severe cases; manage seizures if they occur.

Oral anticoagulant transition with 3–12 mo default; longer when risks persist.

Reserve thrombectomy for refractory deterioration; decompress for herniation.

No routine steroids/diuretics for ICP; avoid prophylactic AEDs.

Tailor for HIT/VITT/pregnancy/cancer, and set a follow-up plan.

We close with the CVST mantra: treat the clot, not the bleed—start anticoagulation early, escalate selectively, individualize duration, and avoid therapies that don’t help. Most patients walk back to independence when we get these steps right.

In this episode of Hospital Medicine Unplugged, we sprint through hematuria in the hospital—classify fast, stabilize what’s dangerous, risk-stratify smartly, and image with purpose.

We open with the do-firsts: confirm gross vs. microscopic (≥3 RBC/HPF) on a proper urinalysis; repeat if contamination or a transient cause is likely. Don’t blame anticoagulation—it can unmask disease, not explain it away. Take a tight history (infection, stones, trauma/instrumentation, menstruation, exercise, meds, malignancy risks) and exam (vitals, bladder distention, CVA tenderness, external sources).

Red flags that change the room: clot retention/obstruction, hemodynamic instability, sepsis, AKI, coagulopathy, uncontrolled pain. Actions: large-bore catheter → manual/continuous bladder irrigation, resuscitate, cultures/antibiotics if infected, reverse coagulopathy when appropriate, and urgent urology.

Source matters—sort glomerular vs. nonglomerular:

Risk stratify for cancer:

Imaging that earns its keep:

Diagnostic pathway that sticks:

Confirm hematuria correctly; exclude UTI/contamination.

Classify (gross vs. microscopic) and triage red flags.

Microscopy to split glomerular vs. nonglomerular and gauge proteinuria.

Risk-adapted imaging (US vs. CT urography) + cystoscopy per risk.

Refer: nephrology for glomerular features; urology for malignancy risk, obstruction, persistent unexplained cases.

Follow up persistent microhematuria with a plan—don’t lose patients to the void.

Infection & anticoagulation plays:

Admission triggers: retention, instability, sepsis, AKI, severe bleeding, coagulopathy, intractable pain, or inability to manage at home. In-house: I/O, bladder scans, trend hemoglobin/creatinine, and maintain VTE prophylaxis unless contraindicated.

Cost–quality compass:

We close with the hematuria mantra: stabilize first, classify precisely, let urine microscopy guide the lane, match imaging to risk, and scope the bladder when risk is real—because gross hematuria and high-risk microhematuria demand answers, not assumptions.

In this episode of Hospital Medicine Unplugged, we cut through ascending cholangitis—recognize fast, resuscitate early, hit bugs hard, drain the duct.

We open with the do-firsts: aggressive IV fluids, hemodynamic stabilization, early broad-spectrum antibiotics, and urgent source control planning. Loop in GI/advanced endoscopy, interventional radiology, surgery, and ICU from the start.

How to call it—diagnosis without delay: fever, RUQ pain, jaundice (Charcot’s triad) when present, plus labs of infection + cholestasis and imaging (US first; CT or MRCP if equivocal) showing ductal dilation/obstruction. Remember: the triad is insensitive—don’t wait for all three.

Stratify with Tokyo Guidelines because timing rides on severity:

Antibiotics—cover what’s common and what counts: Enterobacterales + Enterococcus, consider Pseudomonas/ESBL in healthcare-associated disease or prostheses. Typical choices: piperacillin–tazobactam for community-acquired without high-risk features; escalate to a carbapenem (± VRE coverage per local ecology) for severe/MDRO risk. Tailor to cultures. Duration is usually 3–5 days after source control.

Source control—the main event:

ICU & adjuncts that matter: blood cultures before antibiotics (when it won’t delay therapy), correct coagulopathy, manage vasopressors judiciously, watch for AKI and post-ERCP pancreatitis. Reassess daily: vitals, mental status, bilirubin/ALP/AST/ALT, WBC/CRP, renal function, lactate. If fevers or labs stall, re-image and re-drain.

Pitfalls you can dodge:

We close with the system moves—build a cholangitis bundle that: (1) screens with “fever + RUQ pain/jaundice or cholestasis” → STAT US (then CT/MRCP as needed); (2) gives antibiotics in triage; (3) auto-pages GI/IR/ICU for Grade II/III; (4) targets ERCP ≤48–72 h (sooner if severe) with a time-to-drainage KPI; (5) standardizes antibiotic narrowing to culture data; (6) bakes in post-ERCP monitoring and re-imaging triggers; (7) routes malignant/benign strictures to definitive follow-up after stabilization.

Bottom line: resuscitate, cover, and decompress—fast. Early ERCP changes outcomes; protocols make it reliable.

In this episode of Hospital Medicine Unplugged, we race through acute mesenteric ischemia (AMI)—recognize early, image fast, revascularize now, salvage bowel.

We open with the do-firsts: high-flow crystalloids, bowel rest + NG decompression, broad-spectrum antibiotics, and therapeutic anticoagulation (arterial/venous causes) unless contraindicated. Loop in surgery, vascular, interventional radiology, and ICU immediately.

Diagnosis that doesn’t dawdle:

Risk stratify (any = high risk): age >70, AFib or recent MI, diffuse atherosclerosis, shock/vasopressors, dialysis/cirrhosis/malignancy, hypercoagulable state, peritoneal signs, metabolic acidosis, CTA showing occlusion or non-enhancing bowel. High risk → parallel tracks (resuscitate + CTA + consults), not serial steps.

Definitive therapy—reperfuse early:

Operative pearls when bowel’s threatened:

ICU & postoperative plays:

What not to miss:

Medication and systems pitfalls:

Take-home: Think AMI early, scan fast, anticoagulate, and revascularize—preferably endovascular—while you resuscitate. Treat the cause, spare the bowel, and standardize the system to drive down deaths and recurrences.

In this episode of Hospital Medicine Unplugged, we sprint through syncope—recognize the dangerous few, spare the benign many, and let the ECG lead the way.

We open with the do-firsts: define it right—transient LOC from global cerebral hypoperfusion with rapid, spontaneous recovery. Sort into the big three: cardiac, reflex/neurally mediated, and orthostatic. Cardiac etiologies drive morbidity/mortality—find them fast.

Initial evaluation that actually moves the needle: history (context, prodrome, exertion/supine, palpitations, meds), focused exam with orthostatic BPs, and a 12-lead ECG. These three steps often make the diagnosis and set the risk. Add targeted labs only when the story points (bleed, ischemia, electrolyte error).

Risk stratify with bedside red flags—abnormal ECG, known structural heart disease/HF, exertional or supine syncope, no prodrome, age ≥60, palpitations preceding LOC, family hx SCD, persistent hypotension, anemia/bleeding. Use a validated tool (e.g., Canadian Syncope Risk Score) to sharpen 30-day risk and disposition. Low risk? outpatient with education. High risk or unclear? admit/observe with telemetry.

In-hospital diagnostics—be precise, not profligate:

Management—match therapy to mechanism:

Observation & monitoring plays: structured protocols for intermediate-risk patients reduce unnecessary admissions, speed testing, and keep outcomes steady. Keep telemetry until an arrhythmic cause is excluded or a diagnosis lands.

Pitfalls you don’t want to meet:

Prognosis reality check: reflex and orthostatic—generally benign (recurrence > mortality). Cardiac syncope—highest short-term risk (arrhythmia, MI, SCD): act swiftly, treat definitively. Unexplained after work-up—risk tracks with age, cardiac history, and ECG.

We close with the system moves—a syncope bundle that (1) auto-captures orthostatic vitals and ECG in triage; (2) runs CSRS to gate observation vs. admission; (3) defaults to telemetry + TTE only when cardiac features present; (4) blocks routine neuro/PE testing without triggers; (5) standardizes reflex/orthostatic counseling + med optimization; (6) fast-tracks pacer/ICD/EP for arrhythmic pathways; (7) embeds clear return precautions and follow-up on discharge.

History + orthostatics + ECG, risk before tests, and mechanism-matched therapy—that’s how you turn a fall into a plan.

In this episode of Hospital Medicine Unplugged, we sprint through pulmonary hypertension (PH)—confirm the hemodynamics, protect the right ventricle, keep PAH therapy on, and don’t confuse Group 1 with the rest.

We open with the do-firsts: classify and hunt triggers. PH is mPAP >20 mm Hg; PAH (Group 1) adds PAWP ≤15 mm Hg and PVR ≥3 WU. Identify precipitants fast—infection, arrhythmia, volume shifts, med nonadherence—and correct them early. RV function drives outcomes.

Diagnostic snap: TTE for RV size/function and left-sided clues; ECG/CXR; targeted CT; V/Q scan for CTEPH; labs incl NT-proBNP. Right heart cath (RHC) when classification is unclear or before PAH-targeted therapy. Goal: pre- vs post-capillary split and reversible causes.

Risk stratify for admission to monitored/ICU care when: RV failure, hypotension/syncope, severe hypoxemia, rising lactate, escalating diuretic need, arrhythmia, perioperative context, or interruption of prostacyclin infusions.

Treatment—build the RV-protective backbone:

PAH (Group 1) specifics—don’t miss the meds: Continue or promptly resume maintenance therapy (PDE-5i, ERAs, sGC stimulator, prostacyclin analogs). Never abruptly stop IV/SC prostacyclin—treat line issues like an emergency. Use combination therapy per risk; escalate (add prostacyclin or move to triple) if high-risk features persist after stabilization. Consider sotatercept as emerging add-on in select patients (specialist center).

Non–Group 1 PH: treat the cause

Periop/ICU plays: meticulous lines for prostacyclin; bridging plans for procedures; avoid air emboli, sudden PEEP jumps, and systemic vasodilators without RV support. Multidisciplinary care with PH center involvement improves outcomes.

Monitoring that matters:

Pitfalls you don’t want to meet:

We close with the system moves—a PH inpatient bundle that (1) flags RV failure early; (2) standardizes oxygen/diuresis/pressors/inotropes with RV-first targets; (3) auto-pages PH team for any prostacyclin patient or RHC-needed case; (4) locks in continuation of home PAH meds; (5) routes Group 4 to CTEPH workup; (6) embeds a ventilation/PEEP guardrail; (7) documents phenotype (pre vs post) before discharge with a clear escalation plan.

RV-centric, classification-driven, and therapy-continuous—stabilize the ventricle, treat the group, and never lose the line.

In this episode of Hospital Medicine Unplugged, we sprint through antiphospholipid syndrome (APS)—spot it early, anticoag fast, prevent recurrence, never miss CAPS.

We open with the do-firsts: assess for acute thrombosis (venous/arterial/microvascular), pregnancy history, triggers (infection, surgery, anticoagulant interruption), and extra-criteria clues (thrombocytopenia, livedo, valvular disease, neuro). Send aPL panel—LAC, aCL, anti-β2GPI—knowing diagnosis requires ≥1 clinical event + persistent antibody positivity ≥12 weeks. Flag high-risk phenotypes: triple-positive and coexisting SLE.

Call the diagnosis when the clinical picture (thrombosis and/or pregnancy morbidity) pairs with persistent aPL. Support with imaging (US/CTPA/brain MRI), TTE for valves/emboli, and exclude mimics (HIT, DIC, TTP, endocarditis, inherited thrombophilia).

Risk-stratify admission: new/worsening thrombosis, organ dysfunction, pregnancy, suspected CAPS, severe thrombocytopenia, or complex comorbidity. In-house: daily CBC/chemistry, INR/anti-Xa as appropriate, renal/hepatic checks, and watch for microangiopathy.

Treatment—build the anticoagulation backbone:

If the backbone buckles (recurrent events despite therapeutic INR, intolerance, or special phenotypes):

CAPS—don’t miss it: rapid ≤1 week multiorgan small-vessel thrombosis (≥3 organs), thrombocytopenia/MAHA, precipitated by infection/surgery or anticoagulant withdrawal. Action: start “triple therapy” now—heparin + high-dose IV steroids + plasma exchange or IVIG. Add eculizumab or rituximab in refractory cases. Manage in ICU; send biopsies/hemolysis labs; culture aggressively; monitor for DIC.

Monitoring & tapering that stick:

Pitfalls you don’t want to meet:

Etiology plays (treat the cause/trigger):

We close with the system moves—an APS inpatient bundle that: (1) auto-orders LAC/aCL/anti-β2GPI with reflex repeat plan at 12 weeks; (2) defaults to UFH/LMWH → warfarin (INR 2–3); (3) hard-stops DOACs in triple-positive/high-risk; (4) flags CAPS triggers and fires a triple-therapy pathway; (5) embeds anti-Xa monitoring when LAC present; (6) routes pregnant/SLE patients to co-managed tracks with LMWH+ASA±HCQ; (7) builds discharge plans for indefinite anticoagulation, drug-interaction counseling, and follow-up aPL testing.

Fast recognition, heparin-first, VKA-anchored, steroid-sparing unless CAPS—treat triggers, protect pregnancies, and never miss catastrophic APS.

In this episode of Hospital Medicine Unplugged, we tackle cyclic vomiting syndrome (CVS) in the inpatient world—abort fast, hydrate smart, calm the gut–brain axis, and plan the relapse-proof discharge.

We open with the do-firsts: confirm the stereotyped episodes + symptom-free intervals (Rome IV vibe), rule out red flags (intracranial, obstruction, metabolic), grab labs (electrolytes, glucose, renal, LFTs, lipase) and start dextrose-containing IV fluids early. Keep the room dark, quiet, low-stimulus—sensory brakes matter.

Abortive therapy—hit hard, hit early (even mid-emesis): most adults need ≥2 agents.

Supportive care that changes the trajectory:

Target the comorbid drivers: treat anxiety, depression, migraine, autonomic dysfunction—they modulate episodes and recovery. Reduce cannabis and opioid exposure; cessation improves response to prophylaxis.

Imaging & tests—once, not endlessly: one-time upper GI imaging or EGD if never evaluated or atypical; avoid repeat studies for retching-induced lesions (e.g., Mallory–Weiss). Brain imaging only with neuro red flags. Skip gastric emptying during flares.

Severe/refractory pathway:

Discharge that prevents bounce-backs:

Pitfalls you don’t want to meet:

We close with a ward-ready bundle that (1) initiates dextrose-IVs + electrolytes early, (2) delivers a combo abortive cocktail (triptan + antiemetic ± sedation), (3) defaults to ketorolac for pain, (4) escalates to NK1 for refractory cases, (5) treats psych/migraine/autonomic comorbids, and (6) locks in prophylaxis and a personalized action plan before discharge.

Bottom line: Start fast, combine smart, sedate judiciously, avoid opioids, hydrate with dextrose, and discharge with prophylaxis + a plan.

In this episode of Hospital Medicine Unplugged, we cut through appendicitis—risk-stratify early, choose surgery vs. antibiotics deliberately, and match therapy to CT and patient factors.

We open with the do-firsts: focused history/exam, labs (CBC, CRP), pregnancy test when relevant, urinalysis, and CT A/P (gold standard in adults) to confirm and stage—high-risk CT flags include appendicolith, mass effect/phlegmon, or diameter ≥13 mm. Layer in frailty and peri-op risk tools (e.g., NSQIP) to personalize decisions in older/comorbid patients.

Call the stage to steer care:

Operate when the risk is high or the belly declares itself: generalized peritonitis, complicated disease, or high-risk CT features. Laparoscopic appendectomy leads on lower SSI, shorter LOS, and faster recovery vs open. Give pre-op antibiotics for all; post-op antibiotics are not needed in uncomplicated cases with source control. Close the stump with endoclips/suture/staple/endoloop—choose based on anatomy and resources.

Antibiotics-first is real—when the CT says it’s safe. For uncomplicated cases without high-risk imaging, offer a nonoperative pathway:

Shared decision-making is non-negotiable. For CT-confirmed uncomplicated disease, both appendectomy and antibiotics are acceptable. We walk through risks, benefits, recovery time, recurrence/late failure with antibiotics, and surgical complications—then align with patient values, life context, and risk tolerance.

Supportive care that matters: IV fluids, analgesia, antiemetics, early mobilization, diet advance as tolerated. Trend fever, pain, WBC/CRP, and reassess exam frequently. In complicated cases after source control, 3–5 days of antibiotics (short, culture-guided) usually suffice.

Controversies you’ll meet on call:

Discharge & follow-up plays:

Pitfalls you don’t want to meet:

We close with a ward-ready bundle that (1) defaults to CT-led staging, (2) auto-flags high-risk CT for surgery, (3) offers a structured antibiotics-first track for low-risk uncomplicated cases with 24–48 h checkpoints, (4) standardizes pre-op antibiotics and post-op stewardship, (5) embeds frailty/NSQIP to individualize care, and (6) builds follow-up and recurrence education into every discharge.

Bottom line: image early, risk-stratify precisely, and match the plan to the patient—laparoscopic appendectomy for high-risk or declared abdomens; antibiotics-first for selected uncomplicated cases with tight monitoring and honest talk about recurrence.

In this episode of Hospital Medicine Unplugged, we sprint through hypophosphatemia—spot it early, fix the shift, replenish smart, protect the diaphragm and heart.

We open with the essentials: phosphate <2.5 mg/dL (mild 2–2.5, moderate 1–1.9, severe <1). High-risk crowds: ICU, alcohol use disorder, refeeding, DKA treatment, post-op. Why we care: respiratory failure, myocardial dysfunction/arrhythmias, rhabdo/hemolysis, encephalopathy.

Mechanisms at a glance:

Do-firsts in the hospital: check serum phosphate in at-risk patients (especially when starting nutrition), and always pair with Mg/K/Ca and renal function. Remember: serum phosphate may undercall total body deficit in acute illness—treat the patient.

When to treat: <2.0 mg/dL, symptomatic, or any high-risk scenario (vented, refeeding, rhabdo, hemolysis, cardiac dysfunction). Individualize by severity, symptoms, kidneys, and concomitant electrolyte issues.

How to replete—enteral first if mild–moderate and gut works:

When to go IV (severe <1, symptomatic, no enteral route, ventilatory failure, rhabdo/hemolysis):

Monitoring that matters:

Special situations:

Pitfalls you don’t want to meet: treating the number without the context, ignoring magnesium, pushing K-phos into hyperkalemia, routine high-dose IV in CKD, and forgetting that respiratory alkalosis can tank phosphate even when stores are low-normal.

We close with a ward-ready bundle that sticks: (1) screen high-risk patients when feeds/insulin start; (2) stratify by symptoms + level; (3) oral first when you can, IV for severe/symptomatic; (4) pick K- vs Na-phos wisely; (5) co-replete Mg/K, protect Ca; (6) tight monitoring (phos/Ca/K/Mg/Cr); (7) fix the driver (refeeding plan, alcohol care, ventilator alkalosis, PTH/FGF23 issues). Restore ATP, lift the diaphragm, steady the rhythm—safe repletion saves function.