Case presentation

    Sickle cell anaemia

    A small, pale, jaundiced child with frontal bossing and no palpable spleen — presenting HbSS in steady state, the acute crises with their emergency orders, hydroxyurea and prophylaxis, stroke screening, and the ethics of refused transfusion.

    Pediatrics
    Haematology and oncology
    All colleges

    Presentation

    Good morning, sir. I examined Fatima, an 8-year-old girl with sickle cell anaemia diagnosed at 9 months after painful swelling of her hands and feet. She has had three blood transfusions and two admissions for painful crises this year. She is small, with weight and height below the 3rd centile. She has frontal bossing and prominent upper jaw bones. She is pale and her sclerae are mildly icteric. She is not cyanosed, clubbed or in distress, and there are no leg ulcers. The pulse is 104 and regular; the precordium is hyperactive with a soft grade 2/6 ejection systolic murmur at the left sternal edge, and no signs of heart failure. The liver is 3 cm below the costal margin, firm and non-tender, and the spleen is not palpable. There is no focal neurological deficit and her hips move fully. I would like to complete my examination by checking her oxygen saturation, blood pressure and urine for protein.

    Diagnosis

    Sickle cell anaemia (HbSS) in steady state, with chronic haemolytic anaemia, marrow expansion, growth faltering and probable functional asplenia.

    Differential diagnoses

    • HbSC disease — milder anaemia, spleen often still palpable, proliferative retinopathy, avascular necrosis
    • Sickle–beta-thalassaemia — microcytic indices, persistent splenomegaly
    • Beta-thalassaemia major — severe microcytic anaemia from infancy, massive hepatosplenomegaly, transfusion dependence
    • Hereditary spherocytosis — spherocytes, splenomegaly, family history, normal haemoglobin electrophoresis
    • G6PD deficiency — episodic haemolysis after triggers, normal between episodes
    • Hyperreactive malarial splenomegaly — massive spleen, raised IgM, responds to antimalarial prophylaxis

    Investigations

    TestWhat you expect or look for
    Full blood count and reticulocytesHaemoglobin 6–9 g/dL in steady state, reticulocytosis, raised white cells and platelets
    Blood filmSickle cells, target cells, Howell–Jolly bodies (hyposplenism), nucleated red cells
    Haemoglobin electrophoresis or HPLCHbS about 80–95%, HbF raised, no HbA
    Parents' genotypesBoth carriers; for genetic counselling
    Bilirubin, LDHRaised unconjugated bilirubin and LDH — haemolysis
    Urea, creatinine, urine protein-to-creatinine ratioSickle nephropathy
    Liver function, abdominal ultrasoundGallstones, liver disease
    Transcranial Doppler (yearly from 2 to 16 years)Velocity 200 cm/s or more means high stroke risk
    EchocardiographyPulmonary hypertension (tricuspid regurgitant jet)
    Hip X-ray or MRIAvascular necrosis
    Eye examinationRetinopathy (mainly HbSC)
    FerritinIron overload in transfused children
    Blood group with extended red cell typing; hepatitis B, C and HIVBefore transfusion; transfusion-transmitted infections

    Acute complications

    CrisisRecognitionEmergency treatment
    Vaso-occlusive painBone, chest or abdominal pain; dactylitis under 3 yearsAnalgesia within 30 minutes (paracetamol, ibuprofen, IV morphine 0.1 mg/kg), fluids at 1–1.5 × maintenance, warmth
    Acute chest syndromeFever, cough, chest pain, hypoxia and a new infiltrate on X-rayOxygen, IV cephalosporin plus a macrolide, analgesia, incentive spirometry, transfusion (simple or exchange)
    Splenic sequestrationSudden pallor, enlarging spleen, haemoglobin falls by 2 g/dL or more, shock; usually under 5 yearsRaise the foot of the bed, ABC, oxygen, 10–20 mL/kg saline for shock, transfuse 5–10 mL/kg red cells, mark the spleen edge
    Aplastic crisisPallor, fatigue, low reticulocytes; parvovirus B19Transfusion; isolate from pregnant staff
    HyperhaemolysisWorsening jaundice and anaemia with high reticulocytes; malaria, G6PD deficiencyTreat the cause; transfuse if needed
    StrokeHemiparesis, aphasia, seizures, reduced consciousnessUrgent exchange transfusion to HbS below 30%, imaging
    SepsisFever above 38.5 °CImmediate IV ceftriaxone after cultures — an emergency
    PriapismPainful erection over 2–4 hoursAnalgesia, fluids, urology — aspiration

    Management

    Management is multidisciplinary and lifelong — haematologist, nurse specialist, psychologist, social worker, school and the family. I would counsel the parents on the disease, recognising emergencies, prevention of infection and crises, and the recurrence risk of 1 in 4 in each pregnancy.

    Non-pharmacological

    • Comprehensive sickle cell clinic follow-up
    • Good hydration; avoid extreme cold, overexertion and dehydration
    • Sleep under an insecticide-treated net
    • Teach parents to feel the spleen and recognise pallor, fever, breathing difficulty and weakness
    • Treat any fever of 38.5 °C or above as an emergency
    • Nutrition, school support, and psychological support for chronic pain

    Pharmacological

    • Hydroxyurea from 9 months of age — start at 20 mg/kg/day, increase by 5 mg/kg every 8 weeks to the maximum tolerated dose (up to 35 mg/kg/day), monitoring the blood count; reduces pain crises, chest syndrome, transfusions and deaths
    • Folic acid 5 mg daily
    • Penicillin V prophylaxis from about 3 months to at least 5 years: 62.5 mg twice daily under 1 year, 125 mg twice daily at 1–3 years, 250 mg twice daily from 3 years
    • Malaria chemoprophylaxis as per national guidelines (for example, proguanil daily)
    • Vaccinations: routine schedule plus pneumococcal polysaccharide vaccine from 2 years (repeated after 5 years), meningococcal, typhoid, hepatitis B and yearly influenza
    • Chronic transfusion with iron chelation (deferasirox) for stroke prevention; moderate-dose hydroxyurea where regular transfusion is not feasible

    Surgical and interventional

    • Splenectomy after recurrent sequestration or hypersplenism, ideally after 2 years of age and after vaccination
    • Cholecystectomy for symptomatic gallstones
    • Hip replacement or core decompression for avascular necrosis
    • Haematopoietic stem cell transplantation from an HLA-matched sibling — curative, available in a few centres in Nigeria and abroad
    • Gene therapies are approved in some countries but not yet accessible here

    Complications and follow-up

    • Stroke and silent cerebral infarcts; neurocognitive problems
    • Acute chest syndrome, pulmonary hypertension
    • Overwhelming pneumococcal sepsis; Salmonella osteomyelitis
    • Gallstones; leg ulcers; avascular necrosis of the hip
    • Sickle nephropathy — haematuria, proteinuria, enuresis, chronic kidney disease
    • Retinopathy; priapism; delayed growth and puberty
    • Iron overload and alloimmunisation from transfusion
    • School absence, depression, stigma; high cost of care

    Review every 3 months: growth, blood count, oxygen saturation and blood pressure, and yearly transcranial Doppler, urine protein, eye review and echocardiography in older children. Plan transition to adult care in adolescence.

    Examiner questions

    References

    • Kliegman RM, St Geme JW, Blum NJ, Tasker RC, Wilson KM, et al., eds. Nelson Textbook of Pediatrics. 22nd ed. Philadelphia: Elsevier; 2025.
    • National Heart, Lung, and Blood Institute. Evidence-based management of sickle cell disease: expert panel report, 2014. Bethesda: NHLBI; 2014.
    • DeBaun MR, Jordan LC, King AA, et al. American Society of Hematology 2020 guidelines for sickle cell disease: prevention, diagnosis, and treatment of cerebrovascular disease in children and adults. Blood Advances. 2020;4:1554–88.

    Updated September 18, 2026