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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Hematology

Immune Thrombocytopenia (ITP)

Antibody-mediated platelet destruction. Diagnosis of exclusion. Most adults need treatment only if platelets < 30K or bleeding.

🔍 Overview

Overview

ITP is an autoimmune condition where IgG autoantibodies target platelet surface glycoproteins (GPIIb/IIIa, GPIb/IX), leading to splenic phagocytosis and accelerated platelet destruction. It is a diagnosis of exclusion -there is no confirmatory test. Incidence: ~3-4/100,000 adults/year. Primary ITP (80%) has no identifiable cause. Secondary ITP (20%) is associated with SLE, HIV, HCV, H. pylori, CLL, or medications (heparin → HIT, not ITP). Key principle: treat the patient, not the number. Many patients tolerate platelets of 20-30K without significant bleeding.

🧪 Workup

Workup

CBC with peripheral smear -isolated thrombocytopenia with large platelets (young, reactive). All other cell lines normal. If pancytopenia → think MDS, aplastic anemia, infiltrative process.
Peripheral smear -must review. Rules out pseudothrombocytopenia (platelet clumping from EDTA -redraw in citrate tube), schistocytes (TTP/HUS), blasts (leukemia), leukoerythroblastic picture (marrow infiltration).
HIV, HCV -required in all new ITP (secondary causes that change management)
H. pylori testing -stool antigen or breath test. Eradication can improve platelet count.
Direct Coombs (DAT) -Evans syndrome = autoimmune hemolytic anemia + ITP. If DAT positive → treat as Evans.
Immunoglobulins (quantitative Ig) -CVID can present with ITP
ANA -if SLE suspected (young woman with ITP)
Coags (PT/INR, aPTT) -should be normal. If abnormal → think DIC, liver disease, factor deficiency.
Bone marrow biopsy -NOT routine for typical ITP. Indicated if: age > 60 (rule out MDS), atypical features (other cytopenias, splenomegaly, lymphadenopathy), or refractory to first-line therapy.

🚨 Management

Management

Observation only if platelets ≥ 30K and no bleeding and no upcoming procedures -most patients don't need treatment. ASH Guidelines, 2019
First-line -Corticosteroids:
- Dexamethasone 40 mg PO daily × 4 days -preferred by many experts. Faster response, shorter course. Can repeat q2-4 weeks × 3-4 cycles. Wei, 2016
- Prednisone 1 mg/kg daily × 2-4 weeks → taper. Classic approach. Response in 70-80% but relapse rate ~60-80% after taper.
First-line adjunct -IVIG 1g/kg × 1-2 days: for active bleeding or platelets < 10K or pre-procedure. Fastest response (24-48h) but transient (2-4 weeks). Fc receptor blockade → reduced splenic phagocytosis.
Anti-D (WinRho) 50-75 mcg/kg IV: only for Rh-positive, non-splenectomized patients. Causes mild extravascular hemolysis that "distracts" the spleen. FDA black box: rare fatal intravascular hemolysis.
Second-line -TPO receptor agonists: Eltrombopag 50 mg PO daily or Romiplostim 1-10 mcg/kg SQ weekly. Stimulate megakaryopoiesis. ~80% response. Maintenance therapy -platelets drop when stopped. RAISE, 2011; EXTEND
Second-line -Rituximab 375 mg/m² weekly × 4: ~60% initial response but only ~20-30% sustained at 5 years. Best in younger patients with short disease duration.
Second-line -Fostamatinib (SYK inhibitor): 100-150 mg BID PO. For refractory ITP. FIT, 2018
Third-line -Splenectomy: ~65% long-term remission. Defer at least 12-24 months (spontaneous remission possible). Requires pre-op vaccines (pneumococcal, meningococcal, Hib) ≥ 2 weeks before surgery.
Emergency bleeding: Platelets + IVIG + methylprednisolone 1g IV + aminocaproic acid (antifibrinolytic). Consider emergent splenectomy if refractory.

💊 Medications

Medications

Drug	Dose	Route	Notes
Dexamethasone	40 mg daily × 4 days	PO	Preferred first-line. Can repeat q2-4 wk. Wei, 2016
Prednisone	1 mg/kg × 2-4 wk → taper	PO	Alternative first-line. 70-80% response. High relapse on taper.
IVIG	1 g/kg × 1-2 days	IV	Fastest response (24-48h). For bleeding or plt < 10K. Transient. Monitor for infusion reactions, aseptic meningitis.
Eltrombopag	50 mg daily (titrate 25-75)	PO	TPO-RA. Response in 1-2 wk. Monitor LFTs. Take on empty stomach (no dairy/Ca). RAISE, 2011
Romiplostim	1-10 mcg/kg weekly	SQ	TPO-RA. Titrate by platelet response. Risk of marrow reticulin fibrosis (reversible).
Rituximab	375 mg/m² weekly × 4	IV	Anti-CD20. 60% initial response, ~25% durable at 5y. Check HBV before. Arnold, 2007
Fostamatinib	100-150 mg BID	PO	SYK inhibitor for refractory ITP. SE: diarrhea, HTN, LFT elevation. FIT, 2018
Aminocaproic acid	4-5g load → 1g/hr	IV/PO	Antifibrinolytic for emergency bleeding. Adjunct to platelets.

🏥 Rounds

Sample Presentation

Mrs. Patel is a 34-year-old woman presenting with 3 days of spontaneous bruising and petechiae on bilateral lower extremities. No mucosal bleeding, no epistaxis, no hemoptysis, no melena. No recent illness or new medications. No joint pains or rash. VS stable. Exam: scattered petechiae on shins, no splenomegaly, no lymphadenopathy. Labs: platelets 8K (previously normal 6 months ago), Hgb 13.2, WBC 6.8, peripheral smear shows large platelets with no schistocytes/blasts. PT/INR normal. HIV negative, HCV negative, H. pylori stool antigen negative. DAT negative.

Key Points: Isolated thrombocytopenia with large platelets and otherwise normal CBC + smear = classic ITP. Plt < 10K with mucosal bleeding risk → start IVIG 1g/kg + dexamethasone 40 mg × 4 days. No need for bone marrow biopsy in a young patient with typical presentation.

Pimp Questions

❓ What is the platelet threshold for treatment in ITP?

Platelets < 30K or any clinically significant bleeding, regardless of count. Treat the patient, not the number. Many patients tolerate 20-30K without bleeding. ASH Guidelines, 2019

❓ What must you always check on the peripheral smear before diagnosing ITP?

Rule out pseudothrombocytopenia (EDTA-induced platelet clumping -redraw in citrate tube), schistocytes (TTP/HUS/DIC), blasts (leukemia), and leukoerythroblastic picture (marrow infiltration). ITP should show large platelets and nothing else abnormal.

❓ When do you give IVIG vs steroids alone in ITP?

IVIG 1 g/kg for: active bleeding, platelets < 10K, or pre-procedure urgent platelet rise needed. IVIG works in 24-48 hours (fastest). Steroids alone are adequate for stable patients with plt 10-30K and no active bleeding. IVIG effect is transient (2-4 weeks).

❓ What is Evans syndrome?

Evans syndrome = autoimmune hemolytic anemia (AIHA) + ITP. Positive direct Coombs test + thrombocytopenia. More aggressive course than ITP alone. Often associated with SLE or lymphoproliferative disorders. Treatment: steroids, rituximab. Check DAT in all ITP patients.

❓ What vaccines are required before splenectomy for ITP?

Pneumococcal (PCV20 or PCV15 + PPSV23), meningococcal (MenACWY + MenB), and Haemophilus influenzae type b (Hib). Give ≥ 2 weeks before surgery. Post-splenectomy: lifelong risk of overwhelming post-splenectomy infection (OPSI) from encapsulated organisms.

❓ What are TPO receptor agonists and when do you use them?

Eltrombopag (oral, daily) and romiplostim (SQ, weekly) stimulate megakaryopoiesis via the thrombopoietin receptor. Second-line for chronic ITP failing steroids. ~80% response rate. Maintenance therapy -platelets drop when stopped. Monitor LFTs (eltrombopag) and for reticulin fibrosis (both). RAISE, 2011

❓ When do you perform a bone marrow biopsy in ITP?

NOT routine. Indications: (1) age > 60 (rule out MDS), (2) atypical features (other cytopenias, splenomegaly, lymphadenopathy, abnormal smear), (3) refractory to first-line therapy, (4) before splenectomy (some centers). In typical young-adult ITP with isolated thrombocytopenia, diagnosis is clinical.

❓ What is "wet purpura" and why is it important?

Wet purpura = hemorrhagic bullae (blood blisters) in the oral mucosa. It indicates a higher risk of serious hemorrhage compared to dry purpura (skin-only petechiae/ecchymoses). Wet purpura with plt < 10K is an indication for urgent treatment with IVIG + high-dose steroids.

Clinical Examples

📋 Case 1, Newly Diagnosed ITP with Severe Thrombocytopenia

Patient: 28F with petechiae on legs, gum bleeding, and menorrhagia × 1 week. Platelets 8K. WBC and Hgb normal. Smear: large platelets, no schistocytes. No splenomegaly. No meds.

Key findings: Isolated thrombocytopenia in a young woman with no other cytopenias and normal smear = classic ITP. Large platelets = increased marrow production (compensatory). No schistocytes rules out TTP/HUS.

Management:

Dexamethasone 40 mg daily × 4 days (preferred over prednisone taper, faster response, shorter course)
IVIG 1 g/kg × 1-2 days if wet purpura or active mucosal bleeding (raises platelets within 24-48h)
Avoid platelet transfusion unless life-threatening bleeding (transfused platelets destroyed immediately)
Hold anticoagulants, avoid NSAIDs, IM injections, contact sports
Check HIV, HCV, H. pylori (treatable causes of secondary ITP)

Teaching point: ITP is a diagnosis of exclusion, there is no confirmatory test. The goal is NOT a normal platelet count; it's a safe count (≥ 30K in most patients). Overtreating asymptomatic mild ITP causes more harm than the disease.

📋 Case 2, Chronic Refractory ITP

Patient: 52F with ITP × 3 years. Failed steroids (relapsed after taper × 3), failed rituximab. Currently on romiplostim 5 mcg/kg weekly, platelets fluctuate 15-40K. Now needs hip replacement. Surgeon wants platelets > 50K.

Key findings: Chronic refractory ITP requiring pre-surgical platelet optimization. Bone marrow biopsy showed megakaryocytic hyperplasia (appropriate for ITP). No MDS features.

Management:

Increase romiplostim to 8-10 mcg/kg weekly (titrate to target > 50K for surgery)
Add IVIG 1 g/kg 1-2 days pre-op for rapid temporary boost
Platelet transfusion available in OR (transfuse only for active surgical bleeding)
Consider eltrombopag 50-75 mg daily as add-on or alternative TPO-RA
TXA 1g IV pre-op + 1g q8h × 3 days post-op (antifibrinolytic, reduces surgical bleeding)

Teaching point: TPO receptor agonists (romiplostim, eltrombopag) are the backbone of chronic ITP management. They work in ~80% of patients but require ongoing therapy, platelets drop when stopped. For surgery, combine TPO-RA dose escalation + IVIG for reliable platelet elevation.

📋 Case 3, ITP with Life-Threatening Intracranial Hemorrhage

Patient: 65M with known ITP (non-compliant with eltrombopag). Presents with sudden severe headache, vomiting, right hemiplegia. CT head: left basal ganglia hemorrhage with midline shift. Platelets 3K.

Key findings: ICH in the setting of severe thrombocytopenia, life-threatening emergency. Mortality of ICH with plt < 10K approaches 50%. This is one of the few situations where platelet transfusion is indicated in ITP.

Management:

Platelet transfusion: 2-3 adult doses STAT (even though destroyed rapidly, provides temporary hemostasis)
IVIG 1 g/kg IV STAT (raises endogenous platelets within 24-48h by blocking Fc receptors on splenic macrophages)
Methylprednisolone 1g IV daily × 3 days
TXA 1g IV (antifibrinolytic, stabilizes existing clot)
Emergent neurosurgery consult for possible decompressive craniotomy

Teaching point: ICH is the most feared complication of ITP (< 1% but devastating). In this scenario, transfuse platelets despite ITP, the immediate hemostatic need outweighs the short platelet lifespan. Combine with IVIG and steroids for sustained response.

Monitoring

Platelet count -q1-2 days during active treatment; weekly during titration; monthly once stable. Goal: ≥ 30K (not "normal").
Bleeding assessment -skin (petechiae, purpura, ecchymoses), mucosal (oral blood blisters = "wet purpura" = higher bleed risk), menorrhagia, epistaxis, GI, intracranial
Blood glucose -while on steroids (dexamethasone/prednisone)
LFTs -q2-4 weeks on eltrombopag (hepatotoxicity risk)
CBC with differential -monitor for new cytopenias (would suggest secondary cause or MDS)
Reticulin fibrosis -consider bone marrow biopsy if on TPO-RA > 1 year (rare reversible marrow fibrosis)
Infection screening -on immunosuppression (rituximab, chronic steroids). HBV reactivation monitoring with rituximab.

📋 Summary

Summary

Definition

Autoimmune platelet destruction. Diagnosis of exclusion. Isolated thrombocytopenia + large platelets.

Workup

CBC + smear (rule out pseudo, TTP, leukemia). HIV, HCV, H. pylori, DAT, coags. BMBx only if atypical.

Treat If

Plt < 30K OR bleeding. Goal: safe platelet count, not normal. Treat patient not number.

First-Line

Dexamethasone 40 mg × 4d or prednisone 1 mg/kg. IVIG 1g/kg if bleeding or plt < 10K.

Second-Line

TPO-RA (eltrombopag, romiplostim), rituximab, fostamatinib. Splenectomy = third-line.

Pearl

Wet purpura = high bleed risk. Evans = ITP + AIHA. Always check smear. Don't BMBx young typical ITP.

📄 One Pager

One-Pager

ITP

Immune Thrombocytopenia

Diagnosis

Isolated thrombocytopenia + large platelets on smear. Normal WBC/Hgb. Rule out: pseudothrombocytopenia (EDTA clumping), TTP (schistocytes), DIC (fibrinogen), HIT (heparin exposure), drug-induced. Check HIV, HCV, H. pylori, DAT.

Treatment Algorithm

Plt ≥ 30K no bleeding → observe. Plt < 30K or bleeding → dexamethasone 40 mg × 4d ± IVIG if severe. Refractory → TPO-RA (eltrombopag/romiplostim) or rituximab. Last resort → splenectomy (vaccinate first).

Key Drugs

IVIG 1g/kg (fastest, 24-48h, transient). Dexamethasone 40 mg × 4d. Eltrombopag 50 mg PO daily. Romiplostim 1-10 mcg/kg SQ weekly. Rituximab 375 mg/m² × 4. Aminocaproic acid for emergency bleeding.