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.

Rhabdomyolysis -CK, Myoglobin & AKI -RoundsRx

🔍 Overview

Definition

Rhabdomyolysis: Skeletal muscle necrosis with release of intracellular contents (myoglobin, CK, potassium, phosphate, uric acid, LDH) into the circulation. Defined as CK > 5× upper limit of normal (typically > 1,000 U/L, often > 5,000–10,000 in clinically significant cases). CK levels > 10,000 carry a high risk of AKI.

Pathophysiology

Myocyte necrosis (any cause) → release of myoglobin into bloodstream → myoglobin filtered by glomerulus → in acidic urine, myoglobin precipitates as ferrihemate casts → direct renal tubular obstruction + oxidative injury to tubular epithelium + renal vasoconstriction → acute tubular necrosis (ATN) → AKI. Simultaneously, massive release of intracellular K⁺ → life-threatening hyperkalemia, and PO₄ release → hypocalcemia (calcium binds to damaged muscle and phosphate).

Common Causes

Trauma/crush injury -earthquakes, prolonged immobilization, surgery
Immobilization -found down (overdose, stroke, fall), prolonged surgery
Drugs of abuse -cocaine, amphetamines, MDMA, PCP, synthetic cannabinoids
Medications -statins (especially + fibrates or CYP3A4 inhibitors), daptomycin, colchicine, antipsychotics (NMS)
Seizures -prolonged/status epilepticus
Extreme exertion -marathon, military training, CrossFit (especially in heat)
NMS / Serotonin syndrome -see NMS vs Serotonin Syndrome
Heat stroke -see Heat Stroke
Metabolic -hypokalemia, hypophosphatemia, hypothyroidism, DKA
Infections -influenza, HIV, Legionella, group A strep

Clinical Example

Case

22M found down after a party (likely substance use + prolonged immobilization). Presenting with diffuse myalgias, dark brown urine, and oliguria. Labs: CK 45,000, K⁺ 6.2, Cr 3.4, Ca²⁺ 7.1, PO₄ 6.8, uric acid 12. UA: positive for blood on dipstick but 0 RBCs on microscopy (= myoglobinuria). ECG shows peaked T-waves.

🚨 Management

Treatment Protocol

The THREE killers in rhabdo: (1) Hyperkalemia -can be rapid and fatal, check K⁺ q4–6h. (2) AKI -from myoglobin-induced tubular necrosis. (3) Compartment syndrome -if a limb is involved, check compartment pressures.

Priority	Intervention	Details
1. Aggressive IV fluids	NS or LR at 200–300 mL/hr	Target UOP 200–300 mL/hr (much higher than standard resuscitation). Goal: dilute myoglobin and prevent tubular precipitation. Most patients need 6–10 L in first 24h. Foley catheter mandatory for strict I&Os.
2. Treat hyperkalemia	Calcium gluconate, insulin + D50, kayexalate/patiromer	Check K⁺ q4–6h. If K⁺ > 6.0 or ECG changes → calcium gluconate 1g IV for cardiac membrane stabilization → insulin 10 units + D50 for K⁺ shift → kayexalate or patiromer for removal. See Hyperkalemia.
3. Bicarb (controversial)	Sodium bicarbonate 150 mEq in 1L D5W	Goal: urine pH > 6.5 to keep myoglobin soluble. Controversial -theoretical benefit but no strong RCT evidence. May worsen hypocalcemia (alkalosis binds ionized Ca). Consider if urine pH < 6.5.
4. Compartment check	Measure compartment pressures	If limb injury involved or tense/swollen extremity. Pressure > 30 mmHg or within 30 mmHg of diastolic → emergent fasciotomy. Ortho/surgery consult.
5. Dialysis (if needed)	Continuous RRT (CRRT) preferred	Indications: refractory hyperkalemia, volume overload, severe acidosis, uremia. Standard HD does NOT clear myoglobin (too large). CRRT may have theoretical benefit.

Do NOT give calcium for hypocalcemia in rhabdo (unless symptomatic with tetany or ECG changes) -calcium deposits in damaged muscle and worsens injury. The calcium will correct on its own as muscles heal.

🧪 Workup

Laboratory Workup

CK (creatine kinase) -diagnostic. Serial q6–12h until trending down. Peak usually at 24–72h. CK > 5,000 = significant rhabdo risk for AKI.
BMP -K⁺ (hyperK!), Ca²⁺ (hypoCa), PO₄ (hyperPhos), Cr/BUN (AKI), bicarb (metabolic acidosis)
Urinalysis -dipstick positive for blood but NO RBCs on microscopy = myoglobinuria. This is a classic boards question. The heme pigment on the dipstick cross-reacts with myoglobin.
LDH -elevated (nonspecific muscle injury marker)
Uric acid -often elevated (cell lysis)
Coags (PT/INR, aPTT, fibrinogen) -DIC risk with severe rhabdo
Lactate -tissue hypoperfusion marker
Urine myoglobin -can confirm but not widely available and clears quickly. UA dipstick is adequate.
Toxicology screen -if etiology unclear (cocaine, amphetamines)
ECG -hyperkalemia changes (peaked T-waves, wide QRS)

AST/ALT Pattern in Rhabdo, Looks Like Hepatitis but Isn't

Rhabdo routinely produces ↑ AST (often 200–800 U/L) and ↑ ALT (smaller bump), with AST > ALT. AST is leaked from lysed myocytes, not made by injured liver (skeletal muscle is constitutively rich in AST; ALT is present in muscle but at lower concentration). If CK is high, attribute the LFT abnormality to muscle and don't chase viral hepatitis serologies. AST/ALT will trend down as CK drops.

Why it matters: A patient with AST 400 / ALT 250 / AST > ALT after a found-down event or seizure does not need a hepatitis B/C panel. Check CK first. Wasted serology workup delays the only thing that helps the kidneys, aggressive hydration to UOP 200–300 mL/hr.

Red flags that argue for true hepatic injury (look elsewhere if any are present): AST/ALT in the thousands without matching CK, ↑ INR, ↑ bilirubin out of proportion to CK, encephalopathy, or AST/ALT not tracking CK on serial labs (real liver injury usually means ischemic hepatitis from shock, drug-induced injury, or alcoholic hepatitis).

Myoglobin vs Hemoglobin, Same Heme but Different Fate

Both proteins contain heme, but their clinical signatures diverge sharply, and this is a common point of confusion:

Myoglobin → kidney → urine (causes AKI, not jaundice). Filtered freely by the glomerulus (~17 kDa, small enough to pass). In acidic urine it precipitates as ferrihemate casts → tubular obstruction + oxidative injury to tubular epithelium + renal vasoconstriction → acute tubular necrosis. This is why rhabdo presents with tea-colored urine and AKI, the myoglobin gets excreted in urine before it can be metabolized to anything else.

Hemoglobin → spleen → bilirubin (causes jaundice when pathologic). Senescent RBCs are phagocytosed by splenic macrophages. Heme oxygenase converts heme to biliverdin; biliverdin reductase converts biliverdin to unconjugated bilirubin, which then travels to the liver for conjugation and biliary excretion. This pathway accounts for ~80% of daily bilirubin production.

Why the distinction matters: Myoglobin technically can yield trace bilirubin via the same heme-oxygenase pathway (the chemistry is identical), but clinically it doesn't produce jaundice because it's excreted in urine first. If a rhabdo patient is jaundiced, look elsewhere, hemolysis (free hemoglobin overwhelming haptoglobin → bilirubin surge), ischemic hepatitis from shock (AST in the thousands, ↑ LDH, ↑ INR), or drug-induced hepatic injury. Don't blame the myoglobin.

💊 Medications

Rhabdomyolysis Medications

Drug	Dose	Route	Role
Normal Saline or LR	200–300 mL/hr	IV	FIRST-LINE -aggressive volume resuscitation to target UOP 200–300 mL/hr. LR may be preferred (less hyperchloremic acidosis) but avoid if K⁺ > 6.0 (contains 4 mEq/L K⁺).
Sodium bicarbonate	150 mEq in 1L D5W	IV infusion	Urine alkalinization (target pH > 6.5). Controversial -no RCT evidence of benefit. Consider if urine pH < 6.5.
Calcium gluconate	1–2 g IV over 10 min	IV	ONLY for hyperkalemia with ECG changes. Do NOT give for asymptomatic hypocalcemia.
Insulin (regular) + D50	10 units IV + 25g D50	IV	K⁺ shifting for hyperkalemia. Onset 15–30 min, lasts 4–6h.
Kayexalate / Patiromer	Kayexalate 30g PO; Patiromer 8.4g PO	PO	K⁺ removal (delayed onset). Patiromer preferred (fewer GI side effects).

Monitoring Parameters

Parameter	Frequency	Target / Action
Urine output	Hourly (Foley required)	Target 200–300 mL/hr. If not meeting target, increase IV rate. If oliguric despite adequate fluids → nephrology consult.
CK (creatine kinase)	q6–12h	Trend to peak and decline. Stop aggressive IVF when CK trending down and < 5,000.
BMP (K⁺, Ca, PO₄, Cr)	q6h initially	K⁺ is the most dangerous -check frequently. Cr trend for AKI progression.
Urine pH	q6h if giving bicarb	Target > 6.5 if alkalinizing urine.
Compartment checks	q2–4h if limb involved	Tense, painful, swollen limb → measure pressures → fasciotomy if > 30 mmHg.
Vitals	q4h floor, q1–2h ICU	Watch for fluid overload with aggressive resuscitation.