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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ℹ️ About

Available offline

EMERGENTHeme/Onc

Tumor Lysis Syndrome

Massive cell death → release of intracellular contents (K⁺, PO₄, uric acid, nucleic acids). Occurs 12–72h after chemo initiation. Highest risk: high tumor burden + rapidly proliferating cancers (ALL, Burkitt, DLBCL). Kills via hyperkalemia, AKI, and cardiac arrest.

🔍 Overview

Cairo-Bishop Criteria Cairo-Bishop Classification, 2004

Laboratory TLS: ≥ 2 metabolic abnormalities within 3 days before or 7 days after chemo. Clinical TLS: lab TLS + organ damage (AKI, arrhythmia, seizure).

Lab	Direction	Mechanism	Danger
Potassium	↑↑	Released from lysed cells	Cardiac arrhythmia → VF → death. Most immediately lethal.
Phosphate	↑↑	Released from lysed cells	Binds calcium → calcium phosphate deposition in kidneys → AKI
Calcium	↓↓	Bound by elevated phosphate	Seizures, QT prolongation, tetany
Uric acid	↑↑	Purine breakdown from nucleic acids	Crystal deposition in renal tubules → AKI

High-Risk Cancers

Highest risk: ALL (especially B-cell), Burkitt lymphoma, DLBCL (high LDH, bulky disease)
Moderate risk: AML (high WBC > 100K), CLL treated with venetoclax
Lower risk: most solid tumors (rare but can occur with highly chemo-sensitive tumors)

🚨 Management

Prevention (Before Chemo)

Intervention	Dose	Notes
Aggressive IVF ALL PATIENTS	2–3 L/m²/day NS (goal UOP 2 mL/kg/hr)	Start 24–48h before chemo. Dilutes uric acid + phosphate. Most important prevention.
Allopurinol (Zyloprim) MODERATE RISK	300–600 mg PO daily	Prevents new uric acid formation (xanthine oxidase inhibitor). Does NOT break down existing uric acid. Start 1–2 days before chemo.
Rasburicase (Elitek) HIGH RISK	0.2 mg/kg IV × 1 dose (or fixed 3–6 mg)	Recombinant uricase -rapidly breaks down existing uric acid. Works within hours. Rasburicase TLS Trial, 2001 CONTRAINDICATED in G6PD deficiency (hemolytic crisis -produces H₂O₂). Check G6PD before giving if possible. Falsely lowers uric acid if sample is not kept on ice.

Treatment of Established TLS

Hyperkalemia: treat per hyperkalemia protocol (calcium, insulin/glucose, patiromer (Veltassa)/Lokelma, dialysis if refractory)
Hyperphosphatemia: phosphate binders (sevelamer, aluminum hydroxide short-term), aggressive IVF, dialysis if severe
Hypocalcemia: only treat if symptomatic (seizures, tetany, QT prolongation). Do NOT aggressively replete calcium -it worsens calcium-phosphate precipitation in kidneys
Hyperuricemia: rasburicase (if not already given), aggressive IVF
AKI: IVF,

🧪 Workup

Workup

K⁺, PO₄, Ca²⁺, uric acid, Cr -the "TLS panel." Check q6-8h starting 12-24h before chemotherapy in high-risk tumors. Cairo-Bishop criteria: lab TLS = ≥ 2 of: K⁺ ≥ 6, PO₄ ≥ 4.5, Ca²⁺ ≤ 7, uric acid ≥ 8 (or 25% change from baseline).
LDH -reflects tumor cell lysis and disease burden. Markedly elevated LDH pre-chemo = high TLS risk.
Cr + BUN -AKI from uric acid crystallization in renal tubules (urate nephropathy) and calcium-phosphate precipitation.
ECG -critical. Hyperkalemia (peaked T waves, widened QRS → fatal arrhythmia) and hypocalcemia (QTc prolongation → torsades). Get ECG before and after each lab check.
Urine output -track hourly. Target ≥ 2 mL/kg/hr with aggressive hydration. Oliguria = urate nephropathy → may need dialysis.
G6PD level -check BEFORE giving rasburicase. Rasburicase causes severe hemolytic anemia in G6PD-deficient patients (hydrogen peroxide accumulation). Prevalence: ~10% in African American males.
Risk stratification: High risk = ALL, Burkitt lymphoma, DLBCL with bulky disease + high LDH, WBC > 100K in AML. Intermediate = most AML, CLL with high WBC. Low = most solid tumors, indolent lymphoma.

💊 Medications

Medications

Drug	Dose	Route	Notes
Rasburicase	0.2 mg/kg IV × 1 dose	IV	Treatment of established TLS -converts uric acid → allantoin (highly soluble) Rasburicase TLS Trial, 2001. Onset within hours. Contraindicated in G6PD deficiency (severe hemolysis). Must put blood sample on ice immediately (rasburicase degrades uric acid in tube → falsely low reading).
Allopurinol	300-600 mg PO daily (start 2-3 days before chemo)	PO	PROPHYLAXIS ONLY -does NOT treat established TLS. Xanthine oxidase inhibitor -prevents NEW uric acid formation but does not break down existing uric acid. Dose-reduce in CKD.
IV fluids (NS or D5W)	200-250 mL/hr (3 L/m²/day)	IV	Aggressive hydration is the foundation. Start 24-48h before chemo. Target UOP ≥ 2 mL/kg/hr. Promotes renal uric acid excretion + prevents crystal precipitation.
Sevelamer	800 mg PO TID with meals	PO	Phosphate binder for hyperphosphatemia. Avoid calcium-based binders (calcium carbonate, calcium acetate) -risk of CaPO₄ precipitation in tissues with already elevated PO₄ + Ca product.
Calcium gluconate	1-2g IV over 10-20 min	IV	ONLY for symptomatic hypocalcemia (seizures, tetany, QTc prolongation). Avoid routine correction -exogenous calcium + high PO₄ → tissue calcification.
Insulin + D50	10 units regular insulin + 25g dextrose	IV	For hyperkalemia. Intracellular potassium shift. Check glucose at 1h. Use alongside calcium gluconate for membrane stabilization if ECG changes.
Kayexalate or patiromer	15-30g PO or 8.4g PO	PO	GI potassium elimination for persistent hyperkalemia. Slow onset (hours). Not a substitute for insulin + calcium in acute setting.

📋 On Rounds

Why is rasburicase contraindicated in G6PD deficiency?

Rasburicase is a recombinant uricase that converts uric acid to allantoin. This reaction produces hydrogen peroxide (H₂O₂) as a byproduct. Normally, glutathione neutralizes H₂O₂. In G6PD deficiency, the pentose phosphate pathway cannot regenerate NADPH → cannot regenerate glutathione → H₂O₂ accumulates → oxidative hemolytic crisis (methemoglobinemia + hemolytic anemia). This is life-threatening. Screen for G6PD deficiency (quantitative assay) before giving rasburicase, especially in African, Mediterranean, and Southeast Asian patients. Use allopurinol or febuxostat instead.

Why is allopurinol NOT a treatment for established TLS?

Allopurinol is a xanthine oxidase inhibitor -it blocks the conversion of hypoxanthine → xanthine → uric acid. It prevents NEW uric acid formation but does NOT break down existing uric acid. In established TLS with already-elevated uric acid (e.g., UA = 14), you need rasburicase, which is a recombinant urate oxidase that directly converts existing uric acid → allantoin (soluble, easily excreted).

What electrolyte abnormality in TLS can you NOT aggressively correct and why?

Hypocalcemia -do NOT aggressively correct unless symptomatic (seizures, tetany, QTc prolongation with hemodynamic instability). In TLS, both calcium AND phosphate are abnormal: phosphate is very high from cell lysis, calcium drops because Ca²⁺ binds to the excess phosphate (calcium-phosphate precipitation).

❓ What are the Cairo-Bishop criteria for tumor lysis syndrome?

Laboratory TLS = 2 or more of: (1) uric acid ≥ 8 or 25% increase, (2) K⁺ ≥ 6 or 25% increase, (3) PO₄ ≥ 4.5 or 25% increase, (4) Ca²⁺ ≤ 7 or 25% decrease. Clinical TLS = lab TLS + ≥ 1 of: Cr ≥ 1.5× ULN, cardiac arrhythmia, seizure, or death. Clinical TLS is what kills patients.

❓ Why can you NOT give rasburicase to G6PD-deficient patients?

Rasburicase converts uric acid to allantoin via an oxidation reaction that produces hydrogen peroxide (H₂O₂) as a byproduct. G6PD-deficient patients cannot generate adequate NADPH to neutralize H₂O₂ → severe oxidative hemolytic anemia + methemoglobinemia. Prevalence of G6PD deficiency: ~10% of African American males, common in Mediterranean and Asian populations. Must check G6PD BEFORE rasburicase.

❓ Why do you avoid calcium-based phosphate binders in TLS?

In TLS, both phosphate and calcium levels are deranged. Giving calcium-based binders (calcium carbonate, calcium acetate) adds exogenous calcium. When the calcium × phosphate product exceeds 60, calcium-phosphate crystals precipitate in tissues -kidneys (worsening AKI), heart, lungs, and soft tissues (metastatic calcification). Use sevelamer (non-calcium binder) instead.

❓ What is the difference between allopurinol and rasburicase in TLS?

Allopurinol = prophylaxis only. Xanthine oxidase inhibitor -prevents NEW uric acid formation but does NOT reduce existing uric acid. Start 2-3 days before chemo. Rasburicase = treatment. Recombinant urate oxidase -directly converts existing uric acid → allantoin (1000× more soluble). Works within hours. For established TLS, rasburicase is vastly superior.

❓ Which malignancies are highest risk for TLS?

Highest risk: Burkitt lymphoma (highest proliferation rate of any cancer), ALL (especially with WBC > 100K), DLBCL (with bulky disease + high LDH), AML (especially with WBC > 100K). Intermediate: most AML, CLL with high tumor burden, aggressive lymphomas. Low risk: most solid tumors (rare but described with small cell lung cancer, hepatocellular carcinoma).

Clinical Examples

📋 Case 1, TLS Prevention in High-Risk ALL

Patient: 19M newly diagnosed B-ALL, WBC 142K, LDH 2800, uric acid 9.8, Cr 1.4, K⁺ 5.2, PO₄ 5.8. Starting induction chemotherapy tomorrow.

Key findings: Very high TLS risk: ALL + WBC > 100K + elevated LDH + elevated uric acid + elevated PO₄ baseline. Cairo-Bishop criteria for laboratory TLS likely already met. Chemo will cause massive cell lysis.

Management:

Rasburicase 0.2 mg/kg IV × 1 dose (uricase, enzymatically degrades uric acid, onset within hours)
Aggressive IVF: D5W + NS at 200 mL/hr (target UOP > 2 mL/kg/hr, flushes uric acid and phosphate)
Do NOT give allopurinol if giving rasburicase (allopurinol prevents uric acid formation; rasburicase degrades existing uric acid, allopurinol is the backup, not add-on)
Monitor: BMP + uric acid + LDH + PO₄ q6h for first 72h after chemo starts
Dialysis standby if K⁺ > 6 refractory to medical management or Cr doubling

Teaching point: Rasburicase is contraindicated in G6PD deficiency, it generates hydrogen peroxide during uric acid degradation, causing hemolytic anemia. Always check G6PD before giving rasburicase. Also: rasburicase degrades uric acid in the blood tube ex vivo, send samples on ice for accurate levels.

📋 Case 2, Established TLS with Hyperkalemia and AKI

Patient: 55M with Burkitt lymphoma, 24h after starting R-CHOP. K⁺ 7.1, PO₄ 8.4, uric acid 14.2, Ca 6.8, Cr 4.2 (was 1.0). ECG: peaked T waves, widened QRS. Oliguric.

Key findings: Clinical TLS (laboratory TLS + organ dysfunction): hyperkalemia with ECG changes + AKI + hypocalcemia (from calcium-phosphate precipitation in renal tubules). Life-threatening emergency.

Management:

Calcium gluconate 3g IV (membrane stabilization for hyperkalemia, do NOT correct hypocalcemia aggressively as this worsens Ca×PO₄ precipitation)
Insulin 10 U + D50 (shift K⁺), albuterol 20 mg nebulized
Emergent hemodialysis, most effective treatment for TLS with AKI (removes K⁺, PO₄, uric acid simultaneously)
Rasburicase 0.2 mg/kg IV if not already given
IVF if any UOP remaining; sevelamer for phosphate binding

Teaching point: In TLS, do NOT aggressively correct hypocalcemia unless symptomatic (tetany, seizures, QTc prolongation), giving IV calcium in the setting of hyperphosphatemia causes calcium-phosphate precipitation in kidneys and tissues, worsening AKI. Lower the phosphate first.

📋 Case 3, Spontaneous TLS Before Chemotherapy

Patient: 42F presents with fatigue, found to have WBC 280K with 92% blasts (AML). Before any treatment: K⁺ 6.4, PO₄ 6.8, uric acid 12.4, LDH 4200, Cr 3.1. Ca 7.2.

Key findings: Spontaneous TLS, occurs before any chemotherapy due to rapid tumor cell turnover and death from massive tumor burden. Seen in highly proliferative cancers with very high WBC or bulky disease.

Management:

Rasburicase 0.2 mg/kg IV STAT (most urgent, uric acid nephropathy is the primary driver of AKI in spontaneous TLS)
Aggressive IVF 200-250 mL/hr targeting UOP > 2 mL/kg/hr
Treat hyperkalemia aggressively (calcium gluconate, insulin/D50, dialysis if refractory)
Must still start chemotherapy, delaying treatment allows tumor to keep lysing spontaneously
Leukapheresis if WBC > 100K with leukostasis symptoms (addresses both leukostasis and TLS risk)

Teaching point: TLS can occur BEFORE chemotherapy in highly proliferative tumors. Any patient with WBC > 100K or LDH > 2× ULN should have TLS labs checked at presentation. Spontaneous TLS is actually a predictor of chemosensitivity, these tumors are dying fast on their own.

📣 Sample Presentation

One-Liner

"Mr. Park is a 52-year-old with newly diagnosed Burkitt lymphoma (WBC 180K) who developed K⁺ 6.8, PO₄ 8.2, uric acid 14.2, Ca²⁺ 6.8, and Cr 3.4 twelve hours after starting chemotherapy. Consistent with tumor lysis syndrome."

Key Points to Cover on Rounds

TLS -Cairo-Bishop criteria met (2+ lab abnormalities + Cr rise). Labs: K⁺ 6.8 (treated emergently -Ca gluconate, insulin/D50, albuterol), PO₄ 8.2 (sevelamer started, avoid Ca-containing binders → CaPO₄ precipitation), uric acid 14.2, Ca²⁺ 6.8 (symptomatic → Ca gluconate only if ECG changes, otherwise avoid). Treatment: rasburicase 0.2 mg/kg IV × 1 (G6PD checked and normal). Aggressive IVF at 200 mL/hr. Allopurinol stopped (rasburicase is treatment, allopurinol is prophylaxis only). Nephrology consulted -HD if refractory K⁺ or fluid overload. Labs q6h. Plan: continue aggressive hydration, rasburicase, electrolyte management.

Monitoring

K⁺, PO₄, Ca²⁺, uric acid, Cr q6-8h -for first 48-72h after chemo initiation. High-risk patients may need q4h monitoring initially.
ECG -before each lab check. Hyperkalemia (peaked T → wide QRS → sine wave) and hypocalcemia (prolonged QTc) are immediately life-threatening.
Urine output hourly -target ≥ 2 mL/kg/hr. Falling UOP = urate nephropathy or CaPO₄ precipitation → nephrology consult for possible dialysis.
LDH trending -should decline after initial surge. Persistent elevation → ongoing tumor lysis.
Fluid balance -aggressive IVF can cause volume overload, especially in patients with impaired renal or cardiac function. Daily weights + I/Os.
Dialysis indications: refractory hyperkalemia, severe oliguria/anuria, volume overload unresponsive to diuretics, symptomatic hypocalcemia with concurrent hyperphosphatemia (can't give Ca safely)
Ca × PO₄ product -if > 60 → high risk of metastatic calcification. Prioritize phosphate lowering.

⚡ Summary

Summary

Lab Criteria

Cairo-Bishop: ≥ 2 of: K⁺ > 6, PO₄ > 4.5, uric acid > 8, Ca²⁺ < 7 (or 25% change from baseline). Clinical TLS = lab TLS + organ dysfunction.

Prevention

Aggressive IVF 200-250 mL/hr + allopurinol (prophylaxis only). Rasburicase prophylaxis if high-risk (Burkitt, ALL with high WBC).

Treatment

Rasburicase (converts existing uric acid → allantoin, not allopurinol). Aggressive IVF. Patiromer/Lokelma for K⁺. Dialysis if refractory.

Do NOT

Don't give calcium for hypocalcemia unless symptomatic (increases CaPO₄ precipitation → renal damage). Don't give allopurinol for established TLS.

High-Risk Tumors

Burkitt lymphoma, ALL (high WBC), DLBCL, bulky tumors. Monitor: K⁺, PO₄, Ca²⁺, uric acid, Cr, LDH q6-8h after chemo initiation.

When to Dialyze

Refractory hyperkalemia, refractory hyperphosphatemia, volume overload, severe symptomatic hypocalcemia, worsening AKI despite treatment.

📄 One Pager

Oncology / Nephrology · One Pager

Tumor Lysis Syndrome

High K⁺ + high PO₄ + high uric acid + low Ca²⁺ + AKI after chemo. Prevention: hydration + allopurinol. Treatment: rasburicase + aggressive IVF + dialysis if refractory.

🧪 Diagnosis

Cairo-Bishop: ≥ 2 lab abnormalities (K⁺ > 6, PO₄ > 4.5, uric acid > 8, Ca²⁺ < 7) OR 25% change from baseline. Clinical TLS = lab TLS + organ dysfunction.

🚨 Treatment

Rasburicase 0.2 mg/kg IV (converts existing uric acid → allantoin). Aggressive IVF 200-250 mL/hr. Treat hyperkalemia emergently. Sevelamer for hyperphosphatemia. Dialysis if refractory.

⚠️ Do NOT

Don't give calcium for hypocalcemia unless symptomatic (increases CaPO₃ precipitation). Don't give allopurinol for established TLS (only prophylaxis). Check G6PD before rasburicase (hemolysis risk).

💊 Key Drugs

Rasburicase0.2 mg/kg IV × 1 (treatment)

Allopurinol300 mg daily (prophylaxis only)

IVF200-250 mL/hr NS or D5W

Sevelamer800 mg TID (for hyperPO₄)

⚠️ Pitfalls

Allopurinol for established TLS (doesn't break down existing uric acid)
IV calcium for hypocalcemia (CaPO₃ precipitation → renal damage)
Not monitoring labs q6-8h after chemo in high-risk tumors
Rasburicase in G6PD deficiency (hemolysis)