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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EmergentHeme/Onc

Sickle Cell

Functional asplenia makes these patients vulnerable to encapsulated organisms -fever is a medical emergency. VOC is the most common reason for hospitalization. ACS is the #1 cause of death. Hydroxyurea saves lives.

🔍 Overview

Acute Complications

Complication	Features	Management
Vaso-occlusive crisis (VOC)	Severe pain (bones, chest, abdomen) triggered by dehydration, cold, infection, stress	Aggressive pain control (IV opioids -PCA preferred), IVF (NS or D5 1/2 NS at 1.5× maintenance), incentive spirometry q2h (prevents ACS)
Acute chest syndrome (ACS)	New infiltrate on CXR + one of: fever, chest pain, cough, hypoxia, tachypnea. #1 cause of death in SCD.	Antibiotics (ceftriaxone + azithromycin -covers atypicals + encapsulated), exchange transfusion if severe (target HbS < 30%), supplemental O₂, bronchodilators, incentive spirometry
Stroke	Children: ischemic (large vessel). Adults: hemorrhagic more common. Sudden neuro deficit.	Exchange transfusion emergently (target HbS < 30%). Chronic transfusion program to prevent recurrence.
Splenic sequestration	Sudden splenomegaly + hemoglobin drop ≥ 2 from baseline + reticulocytosis. Mostly children (adults with HbSC).	Volume resuscitation + transfusion. Can be fatal within hours. Consider splenectomy after recovery.
Aplastic crisis	Parvovirus B19 → transient red cell aplasia. Hgb drops, reticulocyte count near zero.	Supportive. Transfuse if symptomatic anemia. Self-limited (1–2 weeks).
Priapism	Painful sustained erection > 4 hours. Urologic emergency.	IVF, analgesia, aspiration/irrigation by urology. Exchange transfusion if refractory. > 4h → ischemic → impotence risk.

Infections & Sepsis in Sickle Cell

Fever ≥ 38.3°C (101°F) in SCD = medical emergency. Functional asplenia → cannot clear encapsulated organisms. Start empiric ceftriaxone within 1 hour of presentation. Do NOT wait for cultures. Mortality from overwhelming post-splenectomy sepsis can be > 50% if delayed.

Why Are SCD Patients at Risk?

By age 5, most HbSS patients have functional asplenia from repeated splenic infarction (autosplenectomy). The spleen is the primary filter for encapsulated bacteria -without it, these organisms can cause fulminant sepsis within hours. This is the same risk as surgically asplenic patients.

Key Organisms

Organism	Clinical Scenario	Key Points
Streptococcus pneumoniae #1 KILLER	Bacteremia, pneumonia, meningitis	Most common cause of fatal sepsis in SCD. Can progress from well → dead in < 12 hours. Penicillin prophylaxis (age < 5) + pneumococcal vaccines (PCV13 → PPSV23) are essential.
Haemophilus influenzae type b	Bacteremia, pneumonia, meningitis	Second most common encapsulated pathogen. Hib vaccine has dramatically reduced incidence.
Neisseria meningitidis	Meningococcemia, meningitis	Fulminant course with purpura fulminans. Requires meningococcal vaccines (MenACWY + MenB).
Salmonella species OSTEOMYELITIS	Osteomyelitis -most common cause in SCD	In the general population, S. aureus is #1 for osteomyelitis. In SCD, Salmonella is #1 (infarcted bone is a perfect growth medium). Also causes bacteremia and GI infections.
Capnocytophaga canimorsus DOG/CAT BITE	Dog or cat bite, scratch, or saliva exposure	Gram-negative rod found in dog/cat saliva. In asplenic/functionally asplenic patients → fulminant sepsis, DIC, purpura fulminans, gangrene. Mortality 25–30% in asplenic patients. Treat with amoxicillin-clavulanate (bite prophylaxis) or piperacillin-tazobactam (if septic). Any SCD patient with a dog or cat bite needs immediate antibiotics and close monitoring.
Parvovirus B19	Aplastic crisis (NOT sepsis)	Infects erythroid precursors → transient red cell aplasia. Retic count drops to near zero. Self-limited but may need transfusion.

Fever Workup in SCD

Blood cultures × 2 (before antibiotics -but do NOT delay antibiotics if cultures take time)
CBC with differential -WBC, Hgb vs baseline, reticulocyte count
CXR -rule out ACS and pneumonia
Urinalysis + urine culture -UTI common
CMP -check for end-organ damage
Empiric ceftriaxone 2g IV -covers encapsulated organisms. Add vancomycin if toxic-appearing, meningitis suspected, or local DRSP rates are high

Required Vaccinations

Vaccine	Schedule
PCV13 → PPSV23	PCV13 series in childhood. PPSV23 at age 2, booster at age 5, then q5 years. Both types needed.
MenACWY	Primary series + booster every 5 years (lifelong in asplenic patients)
MenB	2-dose or 3-dose series (depending on product)
Hib	Standard childhood series. If unvaccinated adult, give 1 dose.
Influenza	Annual -respiratory infections trigger ACS

Penicillin prophylaxis: Penicillin VK 125 mg PO BID (age < 3) → 250 mg PO BID (age 3–5). Recommended for all HbSS children through age 5. PROPS, 1986: reduced pneumococcal sepsis by 84%. Discontinuation after age 5 is debated -many hematologists continue longer in high-risk patients.

🚨 Management

VOC Pain Management

Pain is real and severe. Treat aggressively. These patients are NOT drug-seeking. Chronic opioid tolerance means they need higher doses than you'd typically give. Use a PCA.

IV opioids: PCA (patient-controlled analgesia) is preferred. Hydromorphone or morphine. Titrate to pain relief.
Multimodal: ketorolac 15–30 mg IV q6h (if no AKI), acetaminophen 1g IV q6h, lidocaine patch
IVF: NS or D5 1/2 NS at 1.5× maintenance. Avoid over-hydration (risk of ACS).
Incentive spirometry q2h while awake -prevents atelectasis → ACS. Most important preventive measure during VOC admission.
Transfusion: simple transfusion if Hgb < 7 or > 2 below baseline. Target Hgb ≤ 10 (higher viscosity worsens sickling).

Disease-Modifying Therapy

Drug	Mechanism	Key Notes
Hydroxyurea 1ST LINE	↑ HbF production → ↓ sickling. Also ↓ WBC (anti-inflammatory), ↑ NO, ↑ MCV.	Most important disease-modifying drug. Reduces crises by 50%, reduces ACS, reduces mortality. MSH, 1995. Offer to ALL patients with ≥ 3 crises/year (or any ACS/stroke). Teratogenic -contraception required.
Voxelotor (Oxbryta)	HbS polymerization inhibitor -stabilizes oxy-Hb state	↑ Hgb by ~1 g/dL. FDA-approved. Long-term outcomes still being studied.
Crizanlizumab (Adakveo)	Anti-P-selectin monoclonal antibody -blocks sickle cell adhesion to endothelium	SUSTAIN, 2017: reduced median annual crises from 2.98 to 1.63. IV infusion monthly.
L-glutamine (Endari)	Reduces oxidative stress in RBCs	PO BID. Reduced crises by ~25%. Second-line add-on.

💊 Medications

Key Medications -Sickle Cell

Drug	Dose	Indication	Key Notes
Hydromorphone (Dilaudid)	0.5–1 mg IV q2–3h PRN or PCA	VOC pain	PCA preferred. Titrate to pain control. These patients have opioid tolerance -use adequate doses.
Ketorolac (Toradol)	15–30 mg IV q6h (max 5 days)	VOC adjunct	Avoid if AKI. Reduces opioid requirements. Hold if Cr rising.
Ceftriaxone (Rocephin)	2g IV q24h	Febrile SCD / ACS	Empiric coverage for encapsulated organisms. Combine with azithromycin for ACS.
Azithromycin (Zithromax)	500 mg IV/PO daily	ACS (atypical coverage)	Covers Mycoplasma, Chlamydophila -common ACS triggers.
Hydroxyurea DISEASE-MODIFYING	15–35 mg/kg/day PO	Chronic -all SCD patients	↑ HbF → ↓ sickling. Reduces crises, ACS, mortality. Teratogenic. Monitor CBC q4–8wk.
Penicillin VK	125 mg BID (age < 3) → 250 mg BID (age 3–5)	Prophylaxis (children)	Prevents pneumococcal sepsis. PROPS, 1986: ↓ sepsis by 84%.
Amoxicillin-clavulanate	875/125 mg PO BID × 5d	Dog/cat bite prophylaxis	Covers Capnocytophaga + Pasteurella. Start immediately -do not wait for signs of infection.
Folic acid	1 mg PO daily	Chronic -all SCD patients	Chronic hemolysis depletes folate stores. Prevents megaloblastic crisis.

📋 On Rounds

Why do you target Hgb ≤ 10 when transfusing SCD patients?

Sickle cell patients have adapted to chronic anemia -their blood viscosity is calibrated to a lower Hgb. Transfusing to a "normal" Hgb (> 10) increases whole blood viscosity → paradoxically worsens vaso-occlusion and can trigger more crises. The optimal target is Hgb ≤ 10 g/dL. In exchange transfusions, the goal is to dilute HbS to < 30% while keeping total Hgb ≤ 10.

Why is incentive spirometry so important during VOC admission?

Chest wall pain during VOC → splinting → atelectasis → local hypoxia → triggers sickling in pulmonary vasculature → acute chest syndrome. ACS is the #1 cause of death in SCD and often develops during VOC admissions. Incentive spirometry q2h while awake prevents atelectasis and is the single most effective ACS prevention strategy during hospitalization -more important than any medication.

A sickle cell patient presents with fever, DIC, and purpura after a dog bite 2 days ago. What organism?

Capnocytophaga canimorsus -a gram-negative rod found in dog and cat saliva. In functionally asplenic patients (like SCD), it causes fulminant sepsis with DIC, purpura fulminans, and gangrene. Mortality is 25–30% in asplenic patients. This is why any dog or cat bite in a sickle cell patient needs immediate prophylactic antibiotics (amoxicillin-clavulanate). If already septic → piperacillin-tazobactam or meropenem.

What is the most common cause of osteomyelitis in sickle cell disease?

Salmonella -NOT Staph aureus. In the general population, S. aureus is #1 for osteomyelitis. In SCD, repeated bone infarctions create an ideal environment for Salmonella seeding. This is a classic boards distinction. However, S. aureus is still the #1 cause of septic arthritis in SCD. Mnemonic: Sickle cell + bone = Salmonella.

When do you do an exchange transfusion instead of a simple transfusion in sickle cell?

Simple transfusion (give pRBCs to raise Hgb): VOC with Hgb significantly below baseline, symptomatic anemia, aplastic crisis (parvovirus B19), splenic sequestration. Target Hgb ≤ 10 (never higher -hyperviscosity).

Why is incentive spirometry so important in sickle cell crisis?

Acute chest syndrome (ACS) is the #1 cause of death in SCD during hospitalization. It develops when VOC-related pain → splinting (shallow breathing to avoid pain) → atelectasis → ventilation-perfusion mismatch → local hypoxia → more sickling in pulmonary vasculature → infarction → ACS. Incentive spirometry (IS) breaks this cycle -deep breaths recruit collapsed alveoli, prevent atelectasis, and maintain oxygenation.

Clinical Examples

📋 Case 1, Vaso-Occlusive Crisis (VOC)

Patient: 22F with HbSS, presents with severe bilateral leg and back pain 10/10, not relieved by home oxycodone. Temp 37.8°C, HR 108. WBC 15K, Hgb 7.0 (baseline 7.5), retic 12%. No new infiltrate on CXR.

Key findings: Typical VOC: severe pain in bones/joints, mild fever (from inflammation, not necessarily infection), slight Hgb drop. No ACS (no infiltrate, no hypoxia). Pain management is the primary intervention.

Management:

IV opioids within 30 min of arrival: hydromorphone 0.5-1 mg IV q15-20min until pain controlled (PCA if repeated doses needed)
IV ketorolac 15-30 mg q6h (NSAID, reduces opioid requirement by 30-40%)
IVF: NS or D5-½NS at 1-1.5× maintenance (avoid overhydration → ACS risk)
Incentive spirometry q2h while awake (prevents ACS, the #1 killer during VOC hospitalization)
Avoid: under-treating pain (causes splinting → atelectasis → ACS), over-hydration, excessive supplemental O₂ (suppress erythropoiesis if not hypoxic)

Teaching point: Incentive spirometry is the most important nursing order in SCD, it prevents ACS. Pain management is not optional, undertreated pain → splinting → ACS → death. Treat pain aggressively and reassess frequently.

📋 Case 2, Acute Chest Syndrome

Patient: 28M with HbSS, admitted 2 days ago for VOC. Now develops fever 39.2°C, cough, pleuritic chest pain, SpO₂ 88% on RA. CXR: new RLL infiltrate. Hgb dropped 7.5 → 6.2.

Key findings: ACS = new pulmonary infiltrate + one of: chest pain, fever, hypoxia, cough. Developed during VOC hospitalization (classic, splinting → atelectasis → sickling → ACS). #1 cause of death in SCD during hospitalization.

Management:

Simple transfusion to Hgb 10 (if Hgb < 9 or dropping; avoid Hgb > 10 in SCD → hyperviscosity)
Exchange transfusion if severe (SpO₂ < 90% despite O₂, multilobar infiltrates, rapid deterioration), target HbS < 30%
Ceftriaxone 2g IV + azithromycin 500 mg IV (cover typical + atypical pathogens, infection triggers ~50% of ACS)
Supplemental O₂ to SpO₂ ≥ 95%, incentive spirometry, bronchodilators if wheezing
Continue pain management, do NOT reduce opioids just because ACS developed (pain → splinting → worsens ACS)

Teaching point: ACS and pneumonia are indistinguishable on imaging, treat for both. Exchange transfusion is the definitive treatment for severe ACS. Simple transfusion is sufficient for mild-moderate cases. Never let Hgb exceed 10 g/dL in SCD.

📋 Case 3, Stroke in Sickle Cell Disease

Patient: 8-year-old girl with HbSS presents with sudden right hemiplegia and aphasia. CT head: no hemorrhage. CT angiography: left MCA stenosis. Hgb 6.8, HbS 78%.

Key findings: Ischemic stroke from large-vessel vasculopathy, affects 11% of SCD children by age 20. Sickled RBCs damage endothelium → intimal hyperplasia → stenosis of large cerebral vessels (especially ICA and MCA).

Management:

Emergent exchange transfusion, target HbS < 30%, Hgb ~10 (do NOT wait, this is the #1 treatment)
IV tPA is NOT standard in SCD stroke (exchange transfusion is preferred and more effective for the underlying pathology)
Chronic transfusion program: monthly simple transfusions to maintain HbS < 30% indefinitely (reduces stroke recurrence from 67% to 10%)
Consider transition to hydroxyurea after 1+ year of transfusions (SWiTCH trial) if iron overload problematic
Transcranial Doppler (TCD) screening annually for all SCD children ages 2-16, abnormal velocity (> 200 cm/s) predicts stroke risk

Teaching point: TCD screening is one of the most impactful preventive measures in SCD, identifying high-risk children and starting chronic transfusions reduces primary stroke risk by 92% (STOP trial). Every SCD child needs annual TCD.

📣 Sample Presentation

One-Liner

"Ms. Brown is a 24-year-old with SCD (HbSS) presenting with severe bilateral leg and back pain rated 10/10, not relieved by home oxycodone. WBC 14K, Hgb 7.2 (baseline 8.0). No fever. Consistent with vaso-occlusive crisis."

Key Points to Cover on Rounds

VOC -pain crisis. Pain management: IV hydromorphone 0.5 mg q2h PRN started within 30 min of arrival (multimodal: + ketorolac 15 mg IV + acetaminophen 1g). Incentive spirometry q2h while awake (prevents ACS). Hydration: D5 1/2NS at 125 mL/hr. Hgb 7.2 (baseline 8.0) → no transfusion yet (threshold 7, or if significant drop). No transfuse above 10 (hyperviscosity). CXR baseline -no ACS. Reticulocyte count 8% (appropriate). On hydroxyurea at home -continued. Plan: aggressive pain control, IS compliance, monitor for ACS (fever + new infiltrate + respiratory symptoms).

⚡ Summary

Summary

VOC Management

Multimodal pain: IV opioids (hydromorphone 0.5 mg q2h PRN) + ketorolac + acetaminophen. Treat pain within 30 min of arrival. IVF with D5 1/2NS.

ACS

Fever + new infiltrate + respiratory symptoms. #1 cause of death. Management: exchange transfusion, antibiotics (ceftriaxone + azithro), IS q2h, bronchodilators.

IS Compliance

Incentive spirometry 10 breaths q2h while awake -prevents ACS. Reduced ACS from 36% to 0% in one study IS for ACS Prevention Trial, 1995.

Transfusion Rules

Simple: for symptomatic anemia, Hgb significantly below baseline. Exchange: for ACS, stroke, multiorgan failure. Target Hgb ≤ 10 (hyperviscosity).

Hydroxyurea

Disease-modifying: increases HbF → reduces sickling. Reduces VOC frequency, ACS, transfusion needs, mortality. All adults with SCD should be on it.

Infection / Sepsis

Functional asplenia → vulnerable to encapsulated organisms. Fever ≥ 38.3°C = emergency → ceftriaxone 2g IV within 1h. #1 killer: S. pneumoniae. Osteomyelitis: Salmonella (#1, not S. aureus). Dog/cat bite: Capnocytophaga → fulminant sepsis/DIC.

Vaccines & Prophylaxis

PCV13 + PPSV23, MenACWY + MenB, Hib, annual influenza. Penicillin VK prophylaxis through age 5 PROPS, 1986. Dog/cat bites → immediate amoxicillin-clavulanate.

Stroke

Children: ischemic (large vessel) -transcranial Doppler screening annually age 2-16. High TCD velocity → chronic exchange transfusion program (secondary prevention).

📄 One Pager

Sickle Cell -Quick Reference Card

SICKLE CELL -AT A GLANCE

🔥 Fever: ≥ 38.3°C = emergency → blood cultures + ceftriaxone 2g IV within 1h. Functional asplenia = no time to wait.
💉 Pain (VOC): IV hydromorphone PCA + ketorolac + acetaminophen. Treat within 30 min. IVF D5 1/2NS 1.5× maintenance.
🫁 ACS: New CXR infiltrate + fever/cough/hypoxia. #1 cause of death. Ceftriaxone + azithro. Exchange transfusion if severe.
🩸 Transfusion: Simple if Hgb < 7 or ≥ 2 below baseline. Exchange for ACS/stroke/MOF. Target Hgb ≤ 10 (never higher!).
🦠 Bugs to know: S. pneumoniae (#1 killer), Salmonella (osteomyelitis), Capnocytophaga (dog/cat bite → fulminant sepsis).
💊 Hydroxyurea: All adults with SCD. ↑ HbF → ↓ crises, ACS, mortality. 15–35 mg/kg/day. Monitor CBC q4–8wk.
🌬️ IS q2h: 10 breaths every 2 hours. Prevents ACS. Most important thing you can do during admission.
💉 Vaccines: PCV13 + PPSV23, MenACWY + MenB, Hib, annual flu. Penicillin VK prophylaxis age < 5.

🧪 Workup

Workup

CBC + retic -Hgb vs baseline
Type & screen -extended phenotype matching
CXR -new infiltrate = ACS
Blood cultures if febrile
LDH, indirect bili, haptoglobin
TCD -stroke screening children 2-16