When to intubate in GCS?

GCS ≤ 8 requires intubation for airway protection. The patient cannot protect their own airway at this level of consciousness. Motor score is the most prognostically important component.

What is the best initial fluid for sepsis resuscitation?

Lactated Ringer's (LR) is the preferred resuscitation fluid. The SMART trial (2018) showed balanced crystalloids reduced death, new renal failure, and persistent renal dysfunction compared to normal saline.

When to start vasopressors in septic shock?

Start norepinephrine (first-line vasopressor) if MAP remains < 65 mmHg after initial 30 mL/kg crystalloid resuscitation, or earlier if patient is profoundly hypotensive. Do not delay pressors to complete full fluid resuscitation.

Why can serum uric acid be normal during acute gout?

During acute inflammation, IL-6 increases renal urate excretion and redistributes urate from plasma to tissues. Up to 40% of acute gout flares have normal serum uric acid. Joint aspiration with polarized microscopy is needed for definitive diagnosis.

How do you distinguish lupus flare from infection in SLE?

Key clues: CRP is low/normal in flare but elevated in infection. Complement (C3/C4) drops in flare but is normal/elevated in infection. Procalcitonin is elevated in bacterial infection but normal in flare. Anti-dsDNA rises in flare, stable in infection.

What is the difference between DKA and HHS?

DKA features acidosis (pH 600), hyperosmolality (> 320), and minimal ketosis -typically in Type 2 DM. DKA requires insulin drip; HHS requires aggressive fluid resuscitation first.

When to give tPA in acute ischemic stroke?

IV alteplase (tPA) can be given within 4.5 hours of last known well time in eligible patients. CT head must rule out hemorrhage first. For large vessel occlusion, mechanical thrombectomy can be performed up to 24 hours with favorable imaging.

What antibiotics for community-acquired pneumonia?

Inpatient non-ICU: ceftriaxone + azithromycin. ICU: ceftriaxone + azithromycin (add vancomycin if MRSA risk). Outpatient healthy: amoxicillin. Outpatient with comorbidities: augmentin + azithromycin or respiratory fluoroquinolone. Duration: 5 days if clinically stable for 48 hours.

How to interpret iron studies?

Iron deficiency: low ferritin (< 30), high TIBC, low iron, low transferrin saturation (< 20%). Anemia of chronic disease: normal/high ferritin (acute phase reactant), low TIBC, low iron. A ferritin of 50-100 in an inflamed patient may still represent iron deficiency.

What is the correction rate for hyponatremia?

Correct sodium no more than 8 mEq/L in 24 hours to avoid osmotic demyelination syndrome (ODS). For symptomatic severe hyponatremia with seizures, give 3% hypertonic saline 100-150 mL bolus over 10-20 minutes. If overcorrected, use D5W + DDAVP rescue protocol.

When to start antibiotics in meningitis?

Within 30-60 minutes. Do NOT delay antibiotics for LP or CT. Draw blood cultures, start empiric antibiotics (vancomycin + ceftriaxone ± ampicillin if > 50 or immunocompromised), then perform LP when possible. Dexamethasone should be given before or with the first antibiotic dose.

DOACs vs warfarin in antiphospholipid syndrome?

DOACs are contraindicated in APS. The TRAPS trial (2018) showed rivaroxaban was inferior to warfarin with more thrombotic events in triple-positive APS patients. Warfarin with INR target 2-3 is the standard for APS, indefinitely.

How to manage scleroderma renal crisis?

ACE inhibitors (captopril) are life-saving -start immediately and titrate aggressively. Do NOT hold for rising creatinine. Steroids > 15 mg prednisone per day precipitate scleroderma renal crisis. ARBs are NOT a substitute -evidence is only for ACEi.

What are the 4 pillars of heart failure treatment?

Guideline-directed medical therapy (GDMT) for HFrEF: (1) ARNI or ACEi/ARB, (2) beta-blocker (carvedilol, metoprolol succinate, or bisoprolol), (3) MRA (spironolactone or eplerenone), (4) SGLT2 inhibitor (dapagliflozin or empagliflozin). All four should be initiated and titrated to target doses.

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EMERGENTGI/Nephro

Hepatorenal Syndrome

AKI in cirrhosis after excluding other causes. Kidneys are structurally normal but functionally failing due to splanchnic vasodilation → systemic underfilling → renal vasoconstriction. Diagnosis of exclusion. Terlipressin FDA-approved 2022. Liver transplant is the only cure.

🔍 Overview

Definition & Classification

HRS-AKI (formerly Type 1): Rapid Cr rise > 0.3 mg/dL in 48h or doubling of Cr within 7 days. Median survival 2 weeks without treatment.
HRS-CKD (formerly Type 2): Gradual, stable Cr elevation. Often associated with refractory ascites.

Pathophysiology

Portal hypertension → splanchnic vasodilation (nitric oxide, other vasodilators)
→ Effective arterial underfilling → activation of RAAS, sympathetic nervous system, ADH
→ Renal vasoconstriction → decreased GFR
→ Kidneys are structurally normal but functionally failing
If you transplant these kidneys into a healthy person, they work perfectly

HRS is a diagnosis of EXCLUSION. You MUST rule out: hypovolemia (albumin challenge), ATN (urine Na > 40, muddy brown casts), obstruction (ultrasound), nephrotoxic drugs. If FENa < 1% and bland UA → think HRS.

🚨 Management

Stepwise Approach

Step 1 -Stop nephrotoxins

STOP all nephrotoxic meds, diuretics, beta-blockers, NSAIDs, ACEi/ARBs. These worsen renal perfusion.

Step 2 -Albumin challenge

Albumin 1 g/kg (max 100g) IV × 2 days. Rule out pre-renal AKI. If no Cr improvement → HRS.

Step 3 -Triple therapy (classic)

Midodrine (ProAmatine) 7.5–12.5 mg PO TID + Octreotide (Sandostatin) 100–200 mcg SQ TID + Albumin 25–50g IV daily. Splanchnic vasoconstriction + volume expansion.

Step 4 -Terlipressin (preferred if available)

Terlipressin (Terlivaz) 0.5–1 mg IV q6h + albumin. FDA-approved 2022 based on CONFIRM, 2024. First drug specifically approved for HRS.

Step 5 -TIPS

Transjugular intrahepatic portosystemic shunt -reduces portal pressure. Consider if appropriate candidate.

Definitive -Liver transplant

Liver transplant is the only cure. HRS often resolves after successful transplant because the underlying portal hypertension is corrected.

🧪 Workup

Test	Expected in HRS	Purpose
BMP	↑ Cr, ↑ BUN	Baseline and trending renal function
UA with microscopy	Bland (no casts, no cells)	ATN has muddy brown casts; GN has RBC casts
Urine Na	< 10 mEq/L	Very low urine Na = avid renal sodium retention
FENa	< 1%	Pre-renal physiology (kidneys structurally normal)
Renal ultrasound	Normal kidneys	Rule out obstruction
Hepatic panel, INR, albumin	Deranged (cirrhosis)	Confirm underlying liver disease severity
Diagnostic paracentesis	Rule out SBP	SBP is a common trigger for HRS

💊 Medications

Drug	Dose	Mechanism / Notes
Midodrine (ProAmatine)	7.5–12.5 mg PO TID	Alpha-1 agonist → splanchnic vasoconstriction
Octreotide (Sandostatin)	100–200 mcg SQ TID	Inhibits splanchnic vasodilation
Albumin 25%	25–50 g IV daily	Volume expansion + oncotic pressure support
Terlipressin (Terlivaz)	0.5–1 mg IV q6h	Vasopressin analog. FDA-approved for HRS 2022. Preferred over triple therapy if available.
Norepinephrine	0.5–3 mcg/kg/min IV drip	ICU alternative to midodrine/octreotide. More potent vasoconstrictor.

📋 On Rounds

Pimp Questions

What is the pathophysiology of hepatorenal syndrome?

Portal hypertension → splanchnic vasodilation (mediated by nitric oxide and other vasodilators) → effective arterial underfilling → baroreceptor-mediated activation of RAAS, sympathetic nervous system, and ADH → intense renal vasoconstriction → decreased GFR. The kidneys are structurally normal -if transplanted into a healthy recipient, they work perfectly. This is why liver transplant cures HRS.

Why do we give an albumin challenge before diagnosing HRS?

To rule out pre-renal AKI (hypovolemia). Cirrhotics are often volume-depleted from diuretics, GI losses, or poor intake. Albumin 1 g/kg (max 100g) × 2 days provides a structured volume challenge. If creatinine improves → it was pre-renal, not HRS. If no improvement despite adequate volume → diagnosis of HRS is supported. This step is required by diagnostic criteria.

What's new about terlipressin?

Terlipressin (Terlivaz) was FDA-approved in 2022 as the first drug specifically approved for HRS. The CONFIRM trial showed terlipressin + albumin improved verified HRS reversal vs placebo + albumin. Key safety concern: respiratory adverse events, especially in patients who are volume overloaded. Must monitor closely for pulmonary edema.

Why stop beta-blockers in HRS?

Beta-blockers (nadolol, propranolol, carvedilol) reduce cardiac output in cirrhotics who are already hemodynamically compromised. In the setting of HRS, the heart needs to maximize output to compensate for splanchnic vasodilation. Beta-blockers blunt this compensatory response → further reduction in effective arterial volume → worsening renal perfusion.

Clinical Examples

📋 Case 1, HRS-AKI After SBP

Patient: 58M with decompensated cirrhosis (Child-Pugh C), recently treated for SBP. Despite antibiotics and albumin, Cr rising from 1.2 to 3.8 over 4 days. UOP declining.

Key findings: Bland UA (no casts, no proteinuria). FENa < 1%. Urine Na < 10. No nephrotoxin exposure. No response to albumin challenge (1 g/kg x 2 days). Renal US normal.

Management:

Stop diuretics, beta-blockers, NSAIDs, and all nephrotoxins
Start midodrine 7.5 mg PO TID + octreotide 100 mcg SQ TID + albumin 25-50g IV daily
Consider terlipressin if available (FDA-approved 2022) CONFIRM Trial
Hepatology and transplant evaluation, liver transplant is the only definitive cure
Monitor for volume overload (terlipressin risk: respiratory events)

Teaching point: SBP is the most common precipitant of HRS. The kidneys in HRS are structurally normal, if transplanted to a healthy recipient, they work perfectly. The problem is splanchnic vasodilation causing renal vasoconstriction.

📋 Case 2, Differentiating HRS from ATN

Patient: 51F with cirrhosis, admitted with GI bleed and hypotension. Received NS resuscitation. Cr rising from 0.9 to 2.4. UA shows muddy brown casts.

Key findings: FENa 3.2%. Urine Na 45 mEq/L. Muddy brown granular casts on UA. This is ATN from hypoperfusion during the bleed, NOT HRS.

Management:

Supportive care, ATN typically recovers with time
Avoid further nephrotoxins (no contrast, no NSAIDs, no aminoglycosides)
Continue volume resuscitation as needed for the GI bleed
Monitor Cr trend, ATN typically peaks in 7-10 days then recovers

Teaching point: HRS = FENa < 1%, urine Na < 10, bland UA. ATN = FENa > 2%, urine Na > 20, muddy brown casts. This distinction is critical because HRS requires vasoconstrictor therapy while ATN is managed supportively.

📋 Case 3, Terlipressin for HRS-AKI

Patient: 62M with NASH cirrhosis, MELD 32. Cr 4.2, rising despite albumin challenge. Diagnosed with HRS-AKI. Listed for liver transplant but unlikely to receive organ in time.

Key findings: Failed albumin challenge. No other cause of AKI identified. Hemodynamically: MAP 58, tachycardic. Volume status euvolemic by exam.

Management:

Terlipressin 0.5 mg IV q6h (titrate up to 2 mg q6h if Cr not improving) + albumin CONFIRM Trial
Monitor closely for respiratory adverse events (pulmonary edema), key safety concern
Daily Cr, urine output, volume status assessment
TIPS consideration as bridge to transplant in select patients
Dialysis if refractory hyperkalemia, acidosis, or volume overload develops

Teaching point: Terlipressin (FDA-approved 2022) is the first drug specifically approved for HRS. It is a vasopressin analog that causes splanchnic vasoconstriction, redirecting blood flow to the kidneys. Key safety concern: respiratory events, especially in volume-overloaded patients.

Monitoring

Parameter	Frequency	Target / Action
Creatinine	Daily (q12h if ICU)	Trending improvement = therapy working. No response by 48–72h → escalate.
Urine output	Strict I&Os	UOP > 0.5 mL/kg/hr. Oliguria common in HRS.
MAP	Continuous or q4h	Target MAP > 65–70. Midodrine/terlipressin should improve MAP.
Daily weights	Daily	Fluid balance assessment
Hepatic panel	Daily	Underlying liver disease trajectory

⚡ Summary

Definition

AKI in cirrhosis. Diagnosis of exclusion. Bland UA, FENa < 1%, urine Na < 10.

Pathophys

Splanchnic vasodilation → underfilling → renal vasoconstriction. Kidneys structurally normal.

Step 1–2

Stop nephrotoxins/diuretics/BBs. Albumin 1g/kg × 2 days challenge.

Triple Therapy

Midodrine + octreotide + albumin. Classic regimen for HRS.

Terlipressin

FDA-approved 2022 (CONFIRM trial). Preferred if available. Watch for respiratory events.

Definitive

Liver transplant is the only cure. TIPS as bridge in select patients.