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.

Lab Interpretation -Diagnostic Patterns, Critical Values & Clinical Pearls -RoundsRx

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1. CBC Abnormalities

Lab	High	Low	Key Differentials
WBC	>11K: infection, steroids, stress, CML, leukemoid reaction	<4K: viral, meds (chemo, immunosuppressants), aplastic anemia, SLE, HIV	Bandemia >10% = left shift → suggests bacterial infection
Hemoglobin	>16.5 M / 15 F: polycythemia vera, chronic hypoxia, dehydration	See anemia workup below	MCV guides anemia workup
Platelets	>450K: reactive (infection/inflammation/iron deficiency), CML, ET	<150K: ITP, TTP/HUS, DIC, HIT, liver disease, meds, pseudothrombocytopenia ITP = Immune Thrombocytopenic Purpura TTP = Thrombotic Thrombocytopenic Purpura HUS = Hemolytic Uremic Syndrome DIC = Disseminated Intravascular Coagulation HIT = Heparin-Induced Thrombocytopenia	ALWAYS check smear if <50K. Rule out pseudothrombocytopenia (EDTA clumping)

2. Anemia Workup (by MCV)

MCV Category	Differential Diagnosis
Microcytic (<80)	Iron deficiency (most common), thalassemia, anemia of chronic disease, sideroblastic, lead poisoning
Normocytic (80–100)	Acute blood loss, ACD, CKD, mixed deficiency, bone marrow failure
Macrocytic (>100)	B12/folate deficiency, alcohol, liver disease, hypothyroidism, MDS, meds (methotrexate, AZT)

Iron Studies Interpretation

Condition	Ferritin	TIBC	Iron	% Sat
Iron deficiency	↓ (<30)	↑	↓	↓ (<20%)
ACD	↑ or normal	↓	↓	Normal or ↓
Thalassemia	Normal	Normal	Normal	Normal
Sideroblastic	↑	Normal	↑	↑

3. Hemolysis Workup

Finding	Expected in Hemolysis
LDH	↑↑ (released from lysed RBCs)
Haptoglobin	↓↓ (binds free hemoglobin → consumed)
Indirect bilirubin	↑ (from heme breakdown)
Reticulocyte count	↑ (bone marrow compensating)
Peripheral smear	Schistocytes (MAHA), spherocytes (autoimmune), sickle cells MAHA = Microangiopathic Hemolytic Anemia
Direct Coombs (DAT)	+ = autoimmune hemolysis, − = non-immune (TTP, DIC, mechanical)

4. Liver Panel

Pattern	AST/ALT	Alk Phos	Bilirubin	Interpretation
Hepatocellular	↑↑↑ (>1000)	Normal / mild ↑	Variable	Viral hepatitis, acetaminophen, ischemic hepatitis, autoimmune
Cholestatic	Mild ↑	↑↑↑	↑ (conjugated)	Biliary obstruction, PBC, PSC, drugs
Infiltrative	Normal / mild ↑	↑↑	Normal	Malignancy, granulomatous disease, amyloid
Mixed	↑↑	↑↑	↑	Drug-induced, sepsis

Liver Panel Pearls: AST:ALT >2:1 = alcoholic liver disease (De Ritis ratio). ALT > AST in most other causes. AST/ALT >1000 = “shock liver,” acetaminophen, viral, Wilson’s, autoimmune.

5. Renal Panel

Lab / Ratio	Significance
BUN/Cr ratio >20:1	Pre-renal azotemia, GI bleed (protein load), high-protein diet
BUN/Cr ratio <10:1	Intrinsic renal, liver disease, malnutrition
*FENa <1%** *FENa = Fractional Excretion of Sodium	Pre-renal (kidneys retaining Na)
FENa >2%	Intrinsic renal (ATN, kidneys can’t retain Na) ATN = Acute Tubular Necrosis
*FEUrea <35%** *FEUrea = Fractional Excretion of Urea	Pre-renal (use if on diuretics, FENa unreliable)
Urine Na <20	Pre-renal
Urine Na >40	Intrinsic renal or SIADH

6. Coagulation

Lab	Measures	Causes of Prolongation
PT/INR	Extrinsic pathway (VII) → common	Warfarin, liver disease, vitamin K deficiency, DIC
aPTT	Intrinsic pathway (XII, XI, IX, VIII)	Heparin, hemophilia A/B, lupus anticoagulant, DIC
Both ↑	Common pathway (X, V, II, fibrinogen)	DIC, liver failure, massive transfusion
Mixing study corrects	Factor deficiency	Replace the missing factor
Mixing study doesn’t correct	Inhibitor present	Lupus anticoagulant, factor inhibitor

DIC Labs: ↑PT, ↑aPTT, ↓fibrinogen (<200), ↑D-dimer, ↓platelets, schistocytes on smear.

7. Cardiac Biomarkers

Marker	Elevated In	Interpretation Pearls
Troponin	MI, PE, myocarditis, HF, renal failure, sepsis, demand ischemia	Rise-fall pattern with delta = acute MI. Chronically elevated = CKD/HF
BNP / NT-proBNP	HF, cor pulmonale, PE, AF, sepsis	BNP >400 or NT-proBNP >900 strongly suggests HF. Age-adjusted cutoffs for NT-proBNP. Falsely LOW in obesity
CK / CK-MB	MI, rhabdomyolysis, myositis, strenuous exercise	Less specific than troponin for MI. CK >5× ULN in rhabdo

8. Inflammatory Markers

Marker	Key Points	High-Yield Values
ESR	Nonspecific. ↑ in infection, autoimmune, malignancy, anemia, pregnancy	Very high (>100): endocarditis, osteomyelitis, TB, myeloma, temporal arteritis
CRP	More specific than ESR. Rises/falls faster	↑ in infection, inflammation. <10 = mild, >100 = likely bacterial infection
Procalcitonin	More specific for BACTERIAL infection	<0.25 = unlikely bacterial, >0.5 = likely bacterial. Guides antibiotic de-escalation. NOT elevated in viral or autoimmune
Ferritin	Acute phase reactant, ↑ in inflammation regardless of iron status	Very high (>1000): HLH, adult-onset Still’s, liver disease, iron overload
LDH	Nonspecific tissue damage marker	↑ in hemolysis, lymphoma, liver disease, PE, PJP, TLS

9. Thyroid Function Tests

TSH	Free T4	Diagnosis
↑	↓	Primary hypothyroidism
↓	↑	Primary hyperthyroidism (Graves’, toxic nodule, thyroiditis)
↓	↓	Central hypothyroidism (pituitary / hypothalamic)
↓	Normal	Subclinical hyperthyroidism or sick euthyroid
↑	Normal	Subclinical hypothyroidism

10. ABG Interpretation (Step-by-Step)

Step	Action
1	pH <7.35 = acidemia, pH >7.45 = alkalemia
2	Check PaCO2: if same direction as pH → respiratory cause
3	Check HCO3: if opposite direction as pH → metabolic cause
4	Check compensation (Winter’s formula for metabolic acidosis: expected PaCO2 = 1.5 × HCO3 + 8 ± 2)
5	If metabolic acidosis: check anion gap (Na − Cl − HCO3, normal 12 ± 2)
6	If AG elevated: check delta-delta ratio (ΔAG / ΔHCO3). >2 = concurrent metabolic alkalosis. <1 = concurrent NAGMA* *NAGMA = Non-Anion Gap Metabolic Acidosis

AG Metabolic Acidosis (MUDPILES): M ethanol · U remia · D KA · P ropylene glycol · I soniazid/Iron · L actic acidosis · E thylene glycol · S alicylates

Non-AG Metabolic Acidosis (HARDUP): H yperalimentation, A ddison’s, R TA, D iarrhea, U reteral diversion, P ancreatic fistula