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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EMERGENTEM/Vascular

Acute Limb Ischemia

Surgical emergency. “Time is tissue.” The 6 P’s: Pain, Pallor, Pulselessness, Poikilothermia, Paresthesia, Paralysis. Start heparin IMMEDIATELY, call vascular surgery.

Overview

6 P’s

Pain, sudden, severe
Pallor
Pulselessness
Poikilothermia (cold)
Paresthesia
Paralysis (late = bad)

Rutherford Classification

Category	Status	Sensory	Motor
I	Viable	None	None
IIa	Marginally threatened	Minimal	None
IIb	Immediately threatened	Rest pain	Mild-moderate
III	Irreversible → amputation	Anesthetic	Paralysis

SURGICAL EMERGENCY. Start heparin IMMEDIATELY. Do NOT wait for imaging to anticoagulate.

Embolism vs Thrombosis

Feature	Embolism	Thrombosis (in-situ)
Onset	Sudden, dramatic (“bolt from the blue”)	More insidious (hours–days)
History	AF, recent MI, valvular disease, endocarditis	Known PAD, prior bypass/stent, claudication
Contralateral leg	Normal pulses	Often diminished pulses (bilateral PAD)
Location	Bifurcations (femoral, popliteal, aortic saddle)	At site of prior stenosis/graft
Collaterals	Absent (no time to develop)	Present (chronic disease)
Treatment	Embolectomy (Fogarty catheter)	Thrombolysis, angioplasty, or bypass

Clinical Pearl: Embolic ALI → look for AF on ECG (most common source). Always check both legs, normal contralateral pulses suggest embolism; diminished bilateral pulses suggest thrombosis on PAD.

Time-to-Intervention Urgency

Rutherford Class	Time Window	Intervention
I, Viable	Not immediately threatened	Heparin + elective angiography within hours
IIa, Marginally threatened	Hours (urgent)	Catheter-directed thrombolysis (tPA 0.5–1 mg/hr × 12–24h)
IIb, Immediately threatened	Minutes to hours (emergent)	Surgical embolectomy or bypass, NO time for thrombolysis
III, Irreversible	Too late for salvage	Amputation ± palliative care. Revascularization risks fatal reperfusion injury

Key Distinction: Rutherford IIa = thrombolysis OK (sensory loss only). Rutherford IIb = motor deficit present = go directly to OR for embolectomy/bypass. Do NOT waste time with catheter-directed thrombolysis.

Workup

ABI, CTA (if stable). Labs: CBC, BMP (K+), lactate, CK, coags
ECG for AF (common embolic source)
Do NOT delay heparin for imaging

Management

Step	Action
1	Heparin 80u/kg bolus → 18u/kg/hr IMMEDIATELY
2	Vascular surgery consult STAT
3	Catheter-directed thrombolysis, embolectomy, or bypass
4	Post-reperfusion: watch compartment syndrome → fasciotomy

Reperfusion Injury: After revascularization, watch for the “deadly triad”, hyperkalemia (cardiac arrest risk), rhabdomyolysis (CK >10,000, AKI), and metabolic acidosis. Aggressive IVF, monitor K+ q2h, consider empiric calcium gluconate and sodium bicarbonate.

Medications

Drug	Dose	Notes
Heparin UFH	80u/kg bolus, 18u/kg/hr	aPTT 60–80s. Prevents clot propagation
tPA (catheter-directed)	0.5–1mg/hr intra-arterial	Rutherford I–IIa. Takes 12–24h

On Rounds

Most common cause of ALI?

Embolism (AF most common source) and in-situ thrombosis (on atherosclerotic disease). Embolic = sudden, no prior claudication. Thrombotic = PAD history, more insidious.

What is the first medication to give in suspected ALI, and why?

Unfractionated heparin (UFH) 80 u/kg bolus → 18 u/kg/hr infusion. Prevents clot propagation distally and proximally while definitive intervention is arranged. Start BEFORE imaging, “time is tissue.”

How do you distinguish Rutherford IIa from IIb, and why does it matter?

IIa = sensory loss only, no motor deficit → catheter-directed thrombolysis is an option. IIb = motor deficit present (cannot wiggle toes) → must go directly to surgical embolectomy or bypass. Thrombolysis takes 12–24h and is too slow for IIb.

Name 3 clinical features that distinguish embolic from thrombotic ALI.

Embolic: (1) sudden onset with no prior claudication, (2) normal contralateral pulses, (3) known AF or recent MI. Thrombotic: (1) history of PAD/claudication, (2) diminished bilateral pulses, (3) prior bypass graft or stent.

What is the “deadly triad” of reperfusion injury after revascularization?

Hyperkalemia (can cause fatal arrhythmia), rhabdomyolysis (CK >10,000, myoglobinuric AKI), and metabolic acidosis (lactic acid washout from ischemic tissue). Treat with aggressive IVF, calcium gluconate, bicarbonate, and monitor K+ q2h.

When should you suspect compartment syndrome post-revascularization, and what is the treatment?

Suspect when there is tense swelling, pain out of proportion, and pain with passive stretch of compartment muscles. Compartment pressure >30 mmHg (or within 30 mmHg of diastolic BP) is diagnostic. Treatment is four-compartment fasciotomy of the affected leg.

Why is Rutherford III considered irreversible, and what is the danger of attempting revascularization?

Rutherford III = anesthetic limb with paralysis, rigor, and mottling. Muscle is already necrotic. Revascularization at this stage causes massive reperfusion injury, washout of potassium, myoglobin, and lactate can cause cardiac arrest, DIC, and multi-organ failure. Primary amputation is indicated.

A patient has ALI and you find AF on ECG. After acute management, what long-term anticoagulation is needed?

AF-related arterial embolism requires lifelong anticoagulation. After acute heparin therapy and intervention, transition to a DOAC (apixaban, rivaroxaban) or warfarin (INR 2–3). Also consider rate vs rhythm control for the AF and evaluate for LA thrombus with TEE. RE-LY, 2009; ARISTOTLE, 2011

Clinical Examples

📋 Case 1, Embolic ALI from Atrial Fibrillation

Patient: 72F with known AF (not on anticoagulation, “refused warfarin”), presents with sudden onset left leg pain, pallor, and coldness 3 hours ago. No prior claudication.

Exam: Left leg pale, cool, no popliteal or pedal pulses. Sensation diminished over foot. Can still weakly dorsiflex toes. Right leg warm with normal pulses.

Classification: Rutherford IIa (sensory loss, minimal motor). Normal contralateral pulses + AF + sudden onset = embolic etiology.

Management:

Heparin 80 u/kg bolus → 18 u/kg/hr started immediately in ED
CTA confirms occlusion at left common femoral artery bifurcation (classic embolic location)
Vascular surgery performs Fogarty balloon embolectomy under local anesthesia
Completion angiogram shows restored flow. Pedal pulses return
Post-op: monitor for compartment syndrome, K+ q2h, CK trending
Long-term: Started apixaban 5 mg BID for AF (CHA₂DS₂-VASc = 4). Cardiology follow-up

Key lesson: Embolic ALI from AF is preventable with anticoagulation. Fogarty embolectomy is first-line for embolic ALI.

📋 Case 2, Thrombotic ALI in Peripheral Arterial Disease

Patient: 65M with history of PAD (prior right SFA stent 2 years ago), DM2, smoking. Presents with 18 hours of worsening right foot pain and numbness. Reports baseline 1-block claudication.

Exam: Right foot mottled, cool. No pedal pulses. Cannot dorsiflex toes (motor deficit). Left leg has diminished but palpable dorsalis pedis pulse.

Classification: Rutherford IIb (motor deficit). Bilateral diminished pulses + PAD history + gradual onset = thrombotic etiology (likely in-stent thrombosis).

Management:

Heparin bolus + infusion started immediately
Rutherford IIb with motor deficit → NO thrombolysis (too slow). Taken to OR emergently
Intra-op: thrombosed SFA stent with propagation into popliteal. Surgical thrombectomy + fem-pop bypass with reversed saphenous vein graft
Post-op: pedal pulses restored. CK peaked at 8,200. K+ 5.8 → treated with calcium gluconate + insulin/dextrose
Monitored for compartment syndrome, pressures remained <25 mmHg, no fasciotomy needed
Long-term: Dual antiplatelet (ASA + clopidogrel), statin, smoking cessation, DM optimization

Key lesson: Rutherford IIb (motor deficit) = go to OR, not cath lab. Thrombotic ALI in PAD often needs bypass rather than simple embolectomy.

📋 Case 3, Reperfusion Injury After Revascularization

Patient: 58M s/p emergent embolectomy for Rutherford IIb ALI (6-hour ischemia time). Pulses restored in OR. Four hours post-op, develops tense calf swelling, escalating pain, and oliguria.

Labs: K+ 6.4, CK 45,000, Cr 2.8 (baseline 1.0), pH 7.22, lactate 8.5, urine dark brown (myoglobinuria).

Diagnosis: Reperfusion injury with rhabdomyolysis, hyperkalemia, and metabolic acidosis. Tense calf = compartment syndrome.

Management:

Hyperkalemia: Calcium gluconate 1g IV (cardiac membrane stabilization), insulin 10 units + D50, kayexalate. Continuous telemetry for peaked T-waves
Rhabdomyolysis: Aggressive IVF (target UOP 200–300 mL/hr), sodium bicarbonate drip to alkalinize urine (target urine pH >6.5)
Compartment syndrome: Compartment pressures 42 mmHg → emergent four-compartment fasciotomy
ICU admission: Continuous renal replacement therapy (CRRT) initiated for refractory hyperkalemia and acidosis. CK trended downward over 5 days
Fasciotomy wounds closed with split-thickness skin graft at day 7

Key lesson: Reperfusion injury is the “second hit” after revascularization. Longer ischemia time = higher risk. Anticipate hyperK, rhabdo, and compartment syndrome. ICU monitoring is mandatory.

Monitoring

Parameter	Frequency
Pulse checks	q1h
Compartment pressures	Post-reperfusion. >30mmHg → fasciotomy
K+, CK, Cr	q4–6h post-reperfusion
aPTT	q6h

Summary

6 P’s

Pain, Pallor, Pulselessness, Poikilothermia, Paresthesia, Paralysis.

First Step

Heparin 80u/kg NOW + vascular surgery STAT.

Treatment

Thrombolysis, embolectomy, or bypass by Rutherford class.

Post-Reperfusion

Compartment syndrome, hyperK, rhabdo, acidosis.