Sickle Cell Disease
Vaso-occlusive pain crisis, acute chest syndrome, and severe anemia — the most common life-threatening complications of SCD
Symptoms / Associated Sx
Vaso-occlusive crisis (VOC): Severe bone pain (long bones, back, chest, abdomen); bilateral symmetry; acute onset; no fever typically unless infection
Acute chest syndrome (ACS): New pulmonary infiltrate + fever + respiratory symptoms (cough, chest pain, hypoxia) — most common cause of death in SCD
Severe anemia: Acute fatigue, pallor, tachycardia (aplastic crisis — parvovirus B19; splenic sequestration crisis)
Jaundice (chronic hemolysis); splenomegaly in young children; functional asplenia in adults
Priapism (prolonged painful erection >4h — urologic emergency)
Denies
Prior episodes with different character (any atypical features warrant additional workup)
Fever without pain (raises infection as primary diagnosis — SCD patients are functionally asplenic)
Productive cough + fever without new infiltrate (rules out ACS — requires new chest X-ray finding)
Bilateral lower extremity edema (rules out DVT — though SCD patients have elevated DVT risk)
Social History (SHx)
Known SCD genotype (HbSS most severe; HbSC milder; HbS-β thalassemia), baseline Hgb and Hct, frequency of prior crises and hospitalizations, prior transfusions and alloimmunization history, hydroxyurea compliance, penicillin prophylaxis, vaccination history (asplenic), prior ACS, stroke, or priapism.
Main Etiology
HbS polymerization under deoxygenation → sickling → microvascular occlusion → ischemia and pain
VOC triggers: cold, dehydration, infection, stress, hypoxia, high altitude, alcohol
ACS triggers: fat embolism from bone marrow (during VOC), infection (S. pneumoniae, Mycoplasma, Chlamydia, viral), pulmonary sequestration
Aplastic crisis: parvovirus B19 infection (transient arrest of erythropoiesis)
Splenic sequestration: acute trapping of blood in spleen → acute anemia; usually in children
Most Common DDx
Infection / sepsis (SCD patients are functionally asplenic → encapsulated organism sepsis: S. pneumoniae, H. influenzae, N. meningitidis — fever in SCD = infection until proven otherwise; blood cultures + broad antibiotics)
Pneumonia (ACS mimic — new infiltrate + fever + cough; often indistinguishable from ACS; treat both simultaneously)
Pulmonary embolism (SCD patients have elevated VTE risk; dyspnea + hypoxia + pleuritic pain without infiltrate; CTPA if ACS not confirmed by CXR)
Acute abdomen — cholecystitis, appendicitis (SCD patients develop gallstones from chronic hemolysis; abdominal pain can be VOC or surgical — differentiate with ultrasound, CT, serial exams)
Acute stroke (SCD patients have elevated stroke risk — ischemic stroke; sudden neurologic deficits; CT head + MRI brain; exchange transfusion urgently)
Aplastic crisis from parvovirus B19 (acute Hgb drop without reticulocytosis; parvovirus B19 IgM positive; bone marrow recovery after 7–10 days; transfusion supportive)
DATA
CBC with differential (Hgb vs. baseline — compare to patient's known baseline; reticulocyte count)
Reticulocyte count (low in aplastic crisis; elevated in hemolytic crisis)
BMP (creatinine — SCD nephropathy common; electrolytes)
LFTs (hepatic sickling, sickle cell intrahepatic cholestasis, cholelithiasis)
LDH, indirect bilirubin, haptoglobin (hemolysis markers)
Blood cultures × 2 (fever in asplenic patient = sepsis workup mandatory)
UA + urine culture (papillary necrosis, UTI common)
CXR (new infiltrate → ACS; must compare to prior; obtain on admission for any respiratory or chest symptoms)
ABG or pulse oximetry (ACS — hypoxia assessment)
Type and screen (transfusion readiness; alloimmunization history critical)
Parvovirus B19 IgM (if aplastic crisis suspected — low Hgb + very low reticulocytes)
HbS/HbF% (if hydroxyurea patient — monitor HbF level)
Home Meds
Hydroxyurea (assess dose and compliance — increases HbF, reduces sickling frequency; continue)
Penicillin VK or amoxicillin prophylaxis (asplenic — ensure compliance; continue)
Folate 1 mg PO daily (continue — high turnover state)
Iron chelation (if on chronic transfusion program with iron overload)
Opioid regimen (assess baseline home opioid doses — essential for appropriate dosing in crisis)
Plan
Vaso-occlusive crisis (VOC):
IV fluids: D5 ½NS at 1–1.5× maintenance (avoid aggressive saline — promotes sickling; glucose helps)
Opioid analgesia: individualize based on patient's baseline regimen — hydromorphone 0.2–0.4 mg IV q3–4h PRN or PCA; morphine 0.1 mg/kg IV q3–4h; reassess pain q30–60 min
DO NOT under-dose opioids — pain crises are severe; undertreated pain is a major issue in SCD
NSAIDs: ketorolac 15–30 mg IV q6h × 5 days (useful adjunct if no renal contraindication)
Incentive spirometry (prevents hypoventilation → ACS)
Supplemental O2 only if hypoxic (SpO2 <95%)
Antihistamines (Benadryl) if opioid-induced pruritus; avoid in high doses (sedation)
Acute chest syndrome (ACS) — medical emergency:
Supplemental O2 to maintain SpO2 ≥95%; escalate to non-invasive ventilation or intubation if needed
Bronchodilators: albuterol nebulizer q4–6h (bronchospasm common)
Antibiotics (cover typical + atypical pulmonary pathogens): Ceftriaxone 1 g IV daily + Azithromycin 500 mg IV daily
Simple transfusion (Hgb <9 or mild ACS): transfuse to Hgb ~10 g/dL; match phenotypically to reduce alloimmunization
Exchange transfusion (severe ACS — rapidly worsening, Hgb ≥9, bilateral infiltrates, ICU): reduce HbS% to <30%; hematology + apheresis
Incentive spirometry; aggressive pain control (splinting → hypoventilation → ACS progression)
ICU if O2 requirement escalating or hemodynamically unstable
Severe anemia (aplastic or sequestration crisis):
Transfusion: pRBCs phenotypically matched; goal Hgb ~10 (aplastic) or raise to baseline +2 g/dL (sequestration)
Parvovirus B19 isolation precautions (aplastic crisis — immunocompromised contacts at risk)
Priapism (>4h): Urologic emergency — IV hydration + analgesia + aspiration/irrigation by urology; exchange transfusion if unresponsive; NOT ice or compression
Continue hydroxyurea throughout admission; do not hold
Continue folic acid; penicillin prophylaxis
Hematology consult for ACS, exchange transfusion decisions, or severe/refractory VOC
Trend CBC q12–24h; BMP; reticulocytes; LDH; CXR if ACS
PT/OT; incentive spirometry; ambulation when able
Discharge: Resume hydroxyurea; ensure adequate home analgesic plan; penicillin prophylaxis; folic acid; outpatient hematology within 1–2 weeks; ensure vaccinations current (pneumococcal, meningococcal, Hib, influenza); hydroxyurea dose optimization discussion
Red Flags
Fever in SCD = sepsis emergency → blood cultures + broad antibiotics immediately (ceftriaxone); do not delay for workup
ACS with O2 sat <90% or bilateral infiltrates → exchange transfusion urgently + ICU
Acute neurologic deficits (stroke) → CT head → MRI → exchange transfusion to HbS% <30% urgently; stroke team
Priapism >4h → urologic emergency → aspiration/irrigation; irreversible erectile dysfunction if untreated
Hgb acutely <5 or drop >2 below baseline → aplastic or sequestration crisis → transfuse phenotypically matched pRBCs immediately
Senior IM Resident Pearls
ACS is the leading cause of death in SCD — can develop during or after VOC due to hypoventilation from pain; incentive spirometry and adequate pain control are preventive
Hydroxyurea increases HbF production → reduces sickling frequency and severity; reduces ACS rate by ~50%, hospitalization rate, and mortality; compliance is the most modifiable factor
Phenotypic matching of transfused pRBCs (C, E, Kell antigens at minimum) reduces alloimmunization — critical because SCD patients receive many transfusions over their lifetime
Functional asplenia begins in the first years of life in HbSS — adults have NO spleen function; S. pneumoniae sepsis can be fulminant within hours; prophylactic penicillin and pneumococcal vaccination are life-saving
Common mistake: Under-treating pain in VOC — institutional opioid hesitancy leads to undertreated pain; patients often know their own pain regimen; use PCA and patient-reported outcomes
Common mistake: Stopping hydroxyurea during admission — continue throughout hospitalization; abrupt discontinuation worsens disease
Labs
CBC with differential
Reticulocyte count
CMP
Mg, Phos
LDH
Total/direct bilirubin
Haptoglobin
Type & Screen
HbS%
If Fever
Blood cultures x2
UA
Urine culture
RVP/COVID/Flu
Trending
CBC q12–24h
Retic daily
CMP daily
LDH daily
Bilirubin daily
Imaging
CXR on admission
Repeat CXR PRN for ACS
CT PE if PE suspected
CT head ± MRI brain if neurologic deficits
Meds – VOC
D5½NS 75–125 mL/hr (or 1–1.5× maintenance)
Hydromorphone 0.2–0.4 mg IV q3–4h PRN
ORMorphine 0.1 mg/kg IV q3–4h PRN
Ketorolac 15–30 mg IV q6h × 5 days
Ondansetron 4 mg IV/PO q6h PRN
Diphenhydramine 25 mg IV/PO q6h PRN
O₂ only if hypoxic (goal SpO₂ ≥95%)
Meds – ACS
Ceftriaxone 1 g IV q24h
Azithromycin 500 mg IV/PO daily
Albuterol neb q4–6h PRN
O₂ to maintain SpO₂ ≥95%
Blood Products
pRBC transfusion if symptomatic, Hgb <7, ACS, or acute drop >2 below baseline
Goal Hgb ~10
Exchange transfusion for severe ACS, stroke, worsening hypoxia, MOF
Consults
Hematology
ICU (if severe ACS)
Apheresis/Transfusion Medicine
Urology (priapism >4 hr)
Neurology/Stroke Team (neurologic deficits)
Monitoring
Telemetry
Continuous pulse ox
Strict I&O
Daily weights
Incentive spirometry q2h while awake
Ambulate TID
VTE Prophylaxis
Enoxaparin 40 mg SQ daily
ORHeparin 5000 units SQ q8h
Therapy
PT/OT eval and treat
RT for pulmonary hygiene
Discharge
Pain controlled on PO regimen
No oxygen requirement
Stable Hgb
Continue hydroxyurea
Folic acid 1 mg daily
Hematology follow-up 1–2 weeks
Red Flags
Fever → cultures + ceftriaxone immediately
ACS + worsening hypoxia → exchange transfusion
Stroke symptoms → exchange transfusion emergently
Priapism >4 hr → Urology STAT
Do not stop hydroxyurea