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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Pulm/Rheum

Sarcoidosis

Non-caseating granulomatous disease affecting multiple organs. Lungs involved in 90%. Bilateral hilar lymphadenopathy on CXR is the hallmark. Young adults, especially African Americans. Lofgren syndrome = excellent prognosis.

🔍 Overview

Overview

Sarcoidosis is a systemic granulomatous disease of unknown etiology characterized by non-caseating granulomas in affected organs. The lungs are involved in ~90% of cases. Other commonly affected organs: skin (erythema nodosum, lupus pernio), eyes (anterior uveitis), liver (granulomatous hepatitis), heart (conduction abnormalities, cardiomyopathy), and nervous system (cranial nerve palsies, especially CN VII). Epidemiology: peaks at age 25-35, higher incidence and more severe disease in African Americans and Scandinavians.

Lofgren Syndrome

A specific acute presentation with an excellent prognosis (>90% spontaneous resolution): bilateral hilar lymphadenopathy + erythema nodosum + polyarthralgia + fever. So characteristic that biopsy is often NOT required for diagnosis. More common in young women.

Scadding CXR Staging

Stage 0 -Normal CXR
Stage I -Bilateral hilar lymphadenopathy (BHL) alone. ~60-80% spontaneous remission.
Stage II -BHL + pulmonary infiltrates. ~50-60% remission.
Stage III -Pulmonary infiltrates WITHOUT lymphadenopathy. ~30% remission.
Stage IV -Pulmonary fibrosis. Irreversible. Poor prognosis.

🚨 Management

Treatment Approach

Many patients need NO treatment -sarcoidosis is self-resolving in a large proportion of cases, especially Stage I and Lofgren syndrome. Observation alone is appropriate for asymptomatic patients with stable disease.

Indications for Treatment

Progressive pulmonary disease -worsening PFTs, increasing infiltrates
Cardiac involvement -heart block, cardiomyopathy, ventricular arrhythmias
Neurological involvement -cranial nerve palsies, CNS mass lesions, seizures
Hypercalcemia -from granulomatous production of 1,25-dihydroxyvitamin D
Disfiguring skin disease -lupus pernio
Significant eye disease -posterior uveitis, optic neuritis refractory to topical therapy
Renal involvement -nephrocalcinosis, nephrolithiasis from hypercalciuria

First-Line Therapy

Prednisone 20-40 mg daily x 4-6 weeks, then slow taper over 6-12 months. Total treatment duration typically 12+ months. Relapse rate is high (~30-50%) when steroids are tapered. NSAIDs can be used for mild arthralgia and erythema nodosum.

Steroid-Sparing Agents

Consider when: unable to taper below prednisone 10 mg/day, steroid side effects, or relapse on taper.

Methotrexate (Trexall) -most commonly used steroid-sparing agent. 10-15 mg weekly. Supplement with folic acid.
Azathioprine (Imuran) -alternative to MTX. 50-200 mg daily. Check TPMT before starting.
Mycophenolate (CellCept) -500-1500 mg BID. Used for refractory disease.

Refractory Disease

Infliximab (Remicade) -anti-TNF-alpha. Reserved for severe disease failing conventional therapy. Evidence strongest for lupus pernio and neurosarcoidosis.

🧪 Workup

Diagnostic Workup

CXR -Scadding staging (I-IV). Bilateral hilar lymphadenopathy is classic.
CT chest -better characterization of parenchymal disease, lymphadenopathy pattern
PFTs -restrictive pattern (decreased FVC, decreased DLCO). Obstructive pattern also possible with endobronchial involvement.
ACE level -elevated in ~60% but NOT diagnostic. Neither sensitive nor specific (see alert below).
Calcium -check serum calcium (hypercalcemia from granulomatous 1,25-vitamin D production)
24-hour urine calcium -hypercalciuria may be present even with normal serum calcium
CBC, BMP, LFTs -baseline; elevated alk phos suggests hepatic granulomas
ECG -screen for heart block (PR prolongation, bundle branch block). If abnormal, consider cardiac MRI or PET.
Ophthalmology exam -screen for uveitis (anterior > posterior), even if asymptomatic
Biopsy of accessible tissue -lung (transbronchial), skin, lymph node. REQUIRED for definitive diagnosis.

ACE level is NOT a good diagnostic test for sarcoidosis. Sensitivity ~60%, specificity poor. Many false positives and false negatives. ACE inhibitors lower it (false negative), diabetes can raise it (false positive). Diagnosis requires tissue biopsy showing non-caseating granulomas PLUS exclusion of other causes (TB, fungal infection, lymphoma, berylliosis).

💊 Medications

Medications

Drug	Dose	Route	Notes
Prednisone 1ST LINE	20-40 mg daily x 4-6 wk, then taper over 6-12 months	PO	Start at higher dose for severe organ involvement (cardiac, neuro). Monitor glucose, BP, bone density.
Methotrexate (Trexall)	10-15 mg weekly	PO/SQ	Most common steroid-sparing agent. Add folic acid 1 mg daily. Monitor LFTs, CBC q4-8 weeks. Avoid in pregnancy (teratogenic). Vorselaars, Chest 2013
Azathioprine (Imuran)	50-200 mg daily	PO	Check TPMT before starting (homozygous deficiency = fatal myelosuppression). Monitor CBC regularly.
Mycophenolate (CellCept)	500-1500 mg BID	PO	Alternative steroid-sparing. GI side effects common. Monitor CBC.
Infliximab (Remicade)	3-5 mg/kg IV at weeks 0, 2, 6, then q4-8 weeks	IV	For refractory disease. Screen for TB before starting (anti-TNF reactivates latent TB). Baughman, AJRCCM 2006
Hydroxychloroquine	200-400 mg daily	PO	Useful for skin sarcoidosis, hypercalcemia, and fatigue. Annual eye exams for retinal toxicity.

🏥 Rounds

Pimp Questions

❓ Why is ACE level a poor diagnostic test for sarcoidosis?

ACE is produced by epithelioid cells in granulomas. However, it has sensitivity of only ~60% and poor specificity. ACE inhibitors lower the level (false negative), while diabetes, hyperthyroidism, and other granulomatous diseases can raise it (false positive). It should NEVER be used as a sole diagnostic criterion. Diagnosis requires tissue biopsy + exclusion of other causes.

❓ What is Lofgren syndrome and why is it important?

Lofgren syndrome is an acute presentation of sarcoidosis with the triad of: (1) bilateral hilar lymphadenopathy, (2) erythema nodosum, (3) polyarthralgia, often with fever. It has an excellent prognosis (>90% spontaneous resolution) and is so characteristic that biopsy is often not required for diagnosis. Treatment is usually supportive (NSAIDs for symptoms).

❓ How does sarcoidosis cause hypercalcemia?

Activated macrophages within sarcoid granulomas express 1-alpha-hydroxylase, which converts 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D (calcitriol). This extra-renal production is NOT regulated by PTH, leading to increased intestinal calcium absorption and hypercalcemia. Treatment: corticosteroids suppress macrophage activity. PTH is appropriately suppressed (unlike primary hyperparathyroidism).

❓ What cardiac manifestations should you screen for in sarcoidosis?

Cardiac sarcoidosis can cause: (1) conduction abnormalities -AV block (most common), bundle branch block, (2) ventricular arrhythmias -VT, sudden cardiac death, (3) cardiomyopathy -dilated or restrictive. Screen all patients with an ECG. If abnormal or symptomatic, pursue cardiac MRI (late gadolinium enhancement) or FDG-PET. Cardiac involvement is a leading cause of death in sarcoidosis.

❓ When do you NOT need a biopsy for sarcoidosis diagnosis?

Biopsy may be deferred in two scenarios: (1) Lofgren syndrome -the classic triad of bilateral hilar LAD + erythema nodosum + polyarthralgia is so specific that it is considered virtually diagnostic, (2) Asymptomatic bilateral hilar lymphadenopathy in a young patient with a classic CXR pattern and no concerning features for lymphoma or infection -though many clinicians still prefer biopsy confirmation.

Clinical Examples

📋 Case 1, Stage II Sarcoidosis with Multisystem Disease

Patient: 34-year-old African American woman with 3 months of dry cough, dyspnea, and painful shin nodules. Blurry vision OS.

Key findings: CXR: bilateral hilar LAD + reticular opacities (Stage II). PFTs: FVC 65%, DLCO 58%. Calcium 11.2. Ophthalmology: anterior uveitis. Biopsy: non-caseating granulomas, AFB/fungal negative.

Management:

Prednisone 40 mg daily × 4-6 weeks, then taper over 6-12 months
Topical steroids for uveitis (ophthalmology comanagement)
Methotrexate as steroid-sparing agent for prolonged therapy
ECG screening for cardiac sarcoidosis

Teaching point: Not all sarcoidosis needs treatment. Indications: progressive pulmonary disease, hypercalcemia, cardiac involvement, neurosarcoidosis, sight-threatening uveitis.

📋 Case 2, Lofgren Syndrome

Patient: 28-year-old Scandinavian woman with acute bilateral ankle pain, fever, and tender erythematous shin nodules × 1 week.

Key findings: CXR: bilateral hilar LAD (Stage I). Classic triad: BHL + erythema nodosum + polyarthralgia. ESR elevated. Calcium normal.

Management:

Biopsy NOT required, Lofgren syndrome is clinically diagnostic
> 90% spontaneous resolution within 2 years
NSAIDs for symptoms. Low-dose prednisone only if refractory.
Follow-up CXR in 3-6 months to confirm resolution

Teaching point: Lofgren syndrome has the best prognosis in sarcoidosis. Recognize the triad. Rarely needs immunosuppression.

📋 Case 3, Cardiac Sarcoidosis

Patient: 42-year-old man with known pulmonary sarcoidosis presenting with palpitations and near-syncope. ECG: new complete heart block.

Key findings: Cardiac MRI: late gadolinium enhancement in basal septum. LVEF 40% (was 55%). FDG-PET: active myocardial inflammation. No CAD on angiography.

Management:

Temporary pacing wire; evaluate for permanent pacemaker/ICD
Prednisone 40-60 mg daily for active cardiac sarcoidosis
Steroid-sparing agent (methotrexate or mycophenolate)
ICD if LVEF ≤ 35% or sustained VT
Guideline-directed HF therapy

Teaching point: Cardiac sarcoidosis is a leading cause of death. Screen ALL sarcoidosis patients with ECG. New AV block or unexplained cardiomyopathy → cardiac MRI or FDG-PET.

Sample Presentation

Ms. Davis is a 34-year-old African American woman presenting with 3 months of dry cough, progressive dyspnea on exertion, and bilateral ankle swelling. She also notes painful red bumps on her shins and bilateral ankle pain. CXR shows bilateral hilar lymphadenopathy with diffuse reticular opacities (Stage II). PFTs: FVC 65% predicted, DLCO 58% predicted. Labs: calcium 11.2, ACE level 85 (elevated), LFTs mildly elevated. Ophtho exam: anterior uveitis OS. Transbronchial biopsy: non-caseating granulomas. AFB and fungal stains negative.

Key Points: Classic Stage II sarcoidosis with multisystem involvement (lungs, skin -erythema nodosum, eyes -uveitis, liver, hypercalcemia). Treatment indicated given progressive pulmonary disease and hypercalcemia. Start prednisone 40 mg daily. Plan for steroid-sparing agent (MTX) given likely need for prolonged therapy.

Monitoring

PFTs -repeat every 3-6 months while on treatment. FVC and DLCO most useful for tracking disease activity.
CXR or CT chest -every 6-12 months depending on disease severity.
Serum calcium and 24h urine calcium -monitor for hypercalcemia/hypercalciuria, especially when tapering steroids.
Ophthalmology -annual screening even if asymptomatic. More frequent if active uveitis.
ECG -annual. Low threshold for cardiac MRI or PET if new symptoms (palpitations, syncope, dyspnea).
LFTs -monitor for hepatic sarcoidosis and drug toxicity (MTX, azathioprine).
CBC -for steroid-sparing drug monitoring (MTX, azathioprine, mycophenolate).
Bone density (DEXA) -if on prolonged steroids (>3 months prednisone >= 5 mg/day).
ACE level -some clinicians follow trends, but NOT useful for diagnosis or as sole marker of disease activity.

📋 Summary

Summary

Pathology

Non-caseating granulomas. Must exclude TB, fungal, lymphoma.

Classic CXR

Bilateral hilar lymphadenopathy. Scadding staging I-IV.

Treatment

Many DON'T need treatment. First-line: prednisone 20-40 mg. Steroid-sparing: MTX, AZA.

ACE Level

NOT diagnostic. Sensitivity 60%, specificity poor. Biopsy is required.

Lofgren

BHL + erythema nodosum + polyarthralgia + fever. Excellent prognosis. Biopsy often NOT needed.

Hypercalcemia

Granulomatous 1,25-vit D production. PTH suppressed. Treat with steroids.