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.

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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EmergentRheumatology

SLE Flare

Lupus is the great mimicker. Flares can involve any organ. The most dangerous: lupus nephritis (Class III/IV/V), cerebral lupus, catastrophic APS, and diffuse alveolar hemorrhage. Labs: ↓ complement (C3/C4), ↑ anti-dsDNA = active disease.

🔍 Overview

Organ Involvement & Severity

Organ	Manifestation	Severity
Skin / joints	Malar rash, discoid rash, photosensitivity, oral ulcers, arthralgia/arthritis (non-erosive)	Mild -treat with hydroxychloroquine ± NSAIDs
Serositis	Pleuritis, pericarditis	Moderate -steroids, NSAIDs, colchicine
Hematologic	Autoimmune hemolytic anemia (Coombs+), leukopenia, lymphopenia, thrombocytopenia	Moderate to severe -steroids, IVIG if severe thrombocytopenia
Renal (lupus nephritis)	Proteinuria, hematuria, rising Cr, nephrotic/nephritic syndrome. Class IV (diffuse proliferative) is most common and most severe.	Severe -renal biopsy, pulse steroids + mycophenolate or cyclophosphamide
CNS (cerebral lupus)	Seizures, psychosis, stroke, transverse myelitis, cognitive dysfunction	Severe -pulse steroids + cyclophosphamide. Rule out other causes (infection, TTP, APS).
Pulmonary	Diffuse alveolar hemorrhage (DAH), shrinking lung syndrome, ILD, pulmonary HTN	DAH = life-threatening -pulse steroids + cyclophosphamide + possible plasmapheresis

Flare Markers

↓ C3 / C4 (complement consumed by immune complexes) -most sensitive marker of active disease
↑ Anti-dsDNA -correlates with lupus nephritis activity. Rising titers = impending flare.
↑ ESR with normal CRP -classic lupus pattern (CRP usually only rises in serositis or infection, not lupus flares). If CRP is high → think infection.
Worsening cytopenias -active disease. But also consider medication side effects.

ESR ↑ + CRP normal = lupus flare. ESR ↑ + CRP ↑ = infection until proven otherwise. This distinction is clinically useful for differentiating flare vs infection in SLE patients (who are immunosuppressed and infection-prone).

💊 Management

Treatment by Severity

Severity	Treatment
All patients (baseline)	Hydroxychloroquine (Plaquenil) 200–400 mg daily CORNERSTONE -reduces flares, organ damage, thrombosis, and mortality. Never stop. Annual eye exam for retinal toxicity.
Mild flare (skin, joints)	NSAIDs (short course) + topical steroids. Low-dose prednisone (≤ 7.5 mg/day).
Moderate flare (serositis, cytopenias)	Prednisone 0.5–1 mg/kg/day → taper. Add steroid-sparing: mycophenolate, azathioprine, or methotrexate.
Severe flare (nephritis Class III/IV, CNS, DAH)	Pulse methylprednisolone 1g IV daily × 3 days → prednisone 1 mg/kg. Then: mycophenolate (preferred for nephritis induction -ALMS, 2009) or cyclophosphamide (Euro-Lupus low-dose protocol for severe nephritis). Belimumab (anti-BAFF) for add-on in active lupus nephritis BLISS-LN, 2020. Voclosporin (calcineurin inhibitor) added to MMF for nephritis AURORA, 2021.

📋 Clinical Example -Lupus Flare Assessment & Management

Patient: 28F with known SLE, presents with fatigue, joint pain, malar rash, oral ulcers, Cr rising from 0.8 → 1.6 over 2 weeks.
Flare workup:
- Labs: CBC (cytopenias?), BMP (renal), UA with microscopy (RBC casts = lupus nephritis), protein/creatinine ratio, complement C3/C4 (low = active disease), anti-dsDNA (rising titer = flare), ESR/CRP.
- UA: 2+ protein, 25 RBCs, RBC casts → active lupus nephritis. Protein/Cr ratio 2.8 (>0.5 = significant proteinuria).
- C3: 45 (low), C4: 8 (low), anti-dsDNA: 1:640 (elevated) → serologically active.
Diagnosis: Class III/IV lupus nephritis until biopsy proves otherwise. Renal biopsy is MANDATORY -treatment depends on ISN/RPS class.
Treatment:
- Mild flare (skin/joints only): Hydroxychloroquine (Plaquenil) 200mg BID (NEVER stop -reduces flares, thrombosis, and mortality). Low-dose prednisone (Deltasone) ≤10mg/day.
- Moderate flare (serositis, cytopenias): Prednisone 0.5-1mg/kg/day, taper over weeks.
- Severe flare (nephritis Class III/IV): Pulse methylprednisolone (Solu-Medrol) 500-1000mg IV × 3 days → prednisone 1mg/kg → taper. Induction: mycophenolate (CellCept) 2-3g/day OR cyclophosphamide (ALMS, 2009 -myco = cyclo for induction). Add belimumab (Benlysta) per BLISS-LN.
- Maintenance: Mycophenolate (CellCept) 1-2g/day + hydroxychloroquine indefinitely.
Key: Hydroxychloroquine is the ONE drug every SLE patient should be on. Reduces flares, organ damage, and mortality.

📋 On Rounds

How do you distinguish lupus flare from infection in an immunosuppressed SLE patient?

This is one of the hardest clinical questions in rheumatology. Key clues: (1) CRP: low/normal in flare, elevated in infection. (2) Complement (C3/C4): drops in flare, normal or rises (acute phase) in infection. (3) Procalcitonin: elevated in bacterial infection, usually normal in flare (though not perfect). (4) Anti-dsDNA: rising in flare, stable in infection

Why is CRP typically normal in a lupus flare but elevated in infection?

In most autoimmune flares, CRP remains low or normal because lupus inflammation is driven by type I interferons, which actually suppress hepatic CRP production. In contrast, bacterial infection drives IL-6 release → potent CRP stimulation in the liver → CRP rises markedly. This makes CRP a useful discriminator: CRP < 5 + low C3/C4 + rising anti-dsDNA = flare. CRP > 50 + normal complements = infection.

Why should hydroxychloroquine never be stopped in SLE?

HCQ is the only SLE medication proven to reduce mortality -and the effect is dose-independent (even low doses help). Benefits: (1) Reduces flare frequency by 50-60%, (2) Reduces thrombosis risk (important in APS overlap), (3) Improves lipid profiles, (4) Reduces renal damage progression, (5) Safe in pregnancy (one of few SLE drugs that is). Stopping HCQ increases flare risk by 2.5× within 6 months. Even during remission, continue HCQ.

What are the indications for renal biopsy in lupus nephritis?

Biopsy is indicated whenever there is evidence of renal involvement in SLE -it determines the ISN/RPS class (I-VI) which directly guides treatment. Indications: (1) Proteinuria > 500 mg/day (UPCR > 0.5), (2) Active urine sediment (RBC casts, dysmorphic RBCs), (3) Unexplained rising creatinine, (4) Combination of proteinuria + hematuria even if individually below threshold. Why biopsy matters: Class I/II (minimal/mesangial)

Clinical Examples

📋 Case 1, Lupus Nephritis Class IV

Patient: 24-year-old woman with known SLE presenting with bilateral LE edema, foamy urine × 2 weeks, and fatigue. BP 148/92.

Key findings: UPCR 3.8 (nephrotic range), UA: 25 RBCs/hpf with RBC casts. C3 42 (low), C4 6 (low). Anti-dsDNA 1:640 (rising). CRP 1.8 (low). Renal biopsy: Class IV with crescents.

Management:

Induction: mycophenolate 3g/day + prednisone 0.5-1 mg/kg ALMS, 2009
Alternative: IV cyclophosphamide Euro-Lupus, 2004
Continue HCQ (never stop). Consider belimumab BLISS-LN, 2020
ACEi/ARB for proteinuria and BP

Teaching point: Cannot predict nephritis class clinically, biopsy is mandatory. Class IV is most common and aggressive. Low CRP + low complements = classic SLE flare pattern.

📋 Case 2, SLE Flare vs Infection

Patient: 32-year-old woman with SLE on mycophenolate and prednisone 10 mg, presenting with fever 39.1°C, fatigue, worsening joint pain × 3 days.

Key findings: CRP 42 (elevated). C3/C4 normal. Anti-dsDNA stable. Procalcitonin 2.4. Urine culture: E. coli.

Management:

Infection, not flare, high CRP, normal complements, stable dsDNA, elevated procalcitonin
Treat UTI per sensitivities. Hold mycophenolate during infection.
Do NOT increase steroids. Resume MMF once cleared.

Teaching point: CRP low + C3/C4 low + dsDNA rising = flare. CRP high + C3/C4 normal + procalcitonin elevated = infection. When uncertain, cover both.

📋 Case 3, SLE in Pregnancy

Patient: 29-year-old woman with SLE (class III nephritis in remission × 18 months) on HCQ and azathioprine, now 8 weeks pregnant. Anti-Ro/SSA positive.

Key findings: Stable disease. UPCR 0.15. C3/C4 normal. aPL negative.

Management:

Continue HCQ, safe, reduces neonatal lupus and flares
Continue azathioprine, safe (unlike mycophenolate, which is teratogenic)
Anti-Ro/SSA+ → fetal echo at 16 weeks for congenital heart block
ASA 81 mg at 12 weeks (preeclampsia prophylaxis)

Teaching point: Safe: HCQ, azathioprine, low-dose prednisone. Teratogenic: mycophenolate, cyclophosphamide, MTX. Anti-Ro requires fetal cardiac monitoring.

📣 Sample Presentation

One-Liner

"Ms. Johnson is a 28-year-old with SLE presenting with facial rash, pleuritic chest pain, and UA showing 2+ protein and 15 RBCs/hpf. Anti-dsDNA elevated, C3/C4 low. CRP 2.4 (low). Consistent with lupus flare with possible nephritis."

Key Points to Cover on Rounds

SLE flare -active serology (rising anti-dsDNA, falling C3/C4). CRP low (supports flare over infection). Organ involvement: skin (malar rash), serositis (pleuritic chest pain -CXR: small left pleural effusion), renal (proteinuria + hematuria → nephritis?). Urine protein/Cr ratio sent -UPCR 2.4 (nephrotic range). Nephrology consulted for renal biopsy (needed for class determination → guides treatment). Hydroxychloroquine continued (never stop -reduces flares, thrombosis, mortality). Prednisone 0.5 mg/kg started pending biopsy. If class III/IV → mycophenolate or cyclophosphamide induction. Plan: renal biopsy this week, continue HCQ + steroids, check for infection before immunosuppression.

Monitoring Parameters -DIC

Parameter	Frequency	Target / Action
Vitals	q4h floor, q1–2h ICU	HR, BP, RR, SpO₂, Temp -notify for significant deviations
Labs (BMP, CBC)	Daily AM or as indicated	Trend Cr, K⁺, WBC, Hgb -adjust treatment based on trajectory
Disease-specific markers	Per clinical context	See Overview and Management tabs for condition-specific targets
I&Os	Strict if volume-sensitive	UOP ≥ 0.5 mL/kg/hr. Net fluid balance guides diuresis or resuscitation.
Telemetry	Continuous if indicated	Arrhythmia detection. Discontinue when no longer indicated (reduces alarm fatigue).
Clinical response	Each assessment	Symptom improvement, functional status, appetite, mental status -the exam matters more than labs

Don't just order labs -act on them. Every lab should have a clear clinical question. If you wouldn't change management based on the result, don't order it.

🧪 Workup

See the Overview and Management tabs for topic-specific diagnostic evaluation.

💊 Medications

Key Medications -DIC

Refer to the Management tab for the full treatment algorithm with drug choices, dosing, and contraindications. Refer to the Antibiotic Guide if infectious etiology. Always check renal dosing and drug interactions.

First-line agents: See Management tab for evidence-based recommendations with trial citations
Renal adjustment: Check CrCl -see Antibiotic Guide renal dosing tab or Calculators for CrCl
Drug interactions: See Drug Interactions reference
Allergies: Always verify before prescribing. Document reaction type (rash vs anaphylaxis)

⚡ Summary

Summary

Diagnosis

EULAR/ACR 2019: ANA positive (entry criterion) + ≥ 10 points from clinical + immunologic domains. High-weighted: class III/IV nephritis, anti-dsDNA, low C3/C4.

Never Stop HCQ

Hydroxychloroquine reduces flares 50-60%, thrombosis, renal damage, and mortality. Continue lifelong. Eye exam annually after 5 years.

Nephritis Biopsy

Biopsy when proteinuria > 500 mg/day, active sediment, or rising Cr. Class determines treatment. Can't predict class clinically.

Treatment by Class

Class I/II: HCQ + monitoring. Class III/IV: induction (mycophenolate or cyclophosphamide + steroids) → maintenance (mycophenolate). Class V: immunosuppression if nephrotic.

Flare Markers

Rising anti-dsDNA + falling C3/C4 + rising CRP (low CRP in SLE suggests flare, not infection). Active urine sediment.

Pregnancy

Plan with rheumatology. HCQ safe (continue). Avoid mycophenolate, cyclophosphamide, MTX (teratogenic). Azathioprine is safe alternative.