ABP Pediatric Hematology-Oncology cheat sheet
ABP Pediatric Hematology-Oncology · Keep the key ideas within reach.
Hematology: Red Cell Disorders, Anemias, Hemoglobinopathies, and Bone Marrow Failure
WHO anemia thresholds at sea level: Hb <11.0 g/dL for 6–59 months, <11.5 g/dL for 5–11 years, <12.0 g/dL for 12–14 years, <12.0 g/dL for nonpregnant females ≥15 years, and <13.0 g/dL for males ≥15 years.
Corrected reticulocyte count = reticulocyte % × (patient Hct ÷ normal Hct); an elevated corrected count indicates marrow response to hemolysis or blood loss.
Mentzer index = MCV ÷ RBC count; a value <13 favors thalassemia trait and >13 favors iron deficiency, but iron deficiency and thalassemia can coexist.
Oral elemental iron is commonly dosed at 3–6 mg/kg/day; ferritin <12–15 ng/mL supports iron deficiency but ferritin rises with inflammation, so continue iron 2–3 months after Hb normalizes.
Hemolysis produces reticulocytosis, increased indirect bilirubin and LDH, and low haptoglobin; a positive direct antiglobulin test indicates immune-mediated hemolysis.
Sickle cell disease: penicillin V prophylaxis until age 5 years and hydroxyurea for recurrent pain, acute chest syndrome, or severe anemia reduce morbidity; transcranial Doppler screening identifies stroke risk.
Beta thalassemia major causes severe transfusion-dependent anemia after about 6 months; chronic transfusion plus iron chelation prevents iron overload, and splenectomy is reserved for increased transfusion demand.
Fanconi anemia is confirmed by increased chromosomal breakage with diepoxybutane or mitomycin C; Diamond-Blackfan anemia shows isolated reticulocytopenic anemia with normal platelets and white cells early in life.
Hemostasis and Thrombosis: Coagulation Disorders, Platelet Disorders, and Antithrombotic Therapy
PT/INR reflects the extrinsic and common pathways (factors VII, X, V, II, fibrinogen); aPTT reflects the intrinsic and common pathways (VIII, IX, XI, XII, X, V, II, fibrinogen).
A prolonged PT or aPTT that corrects on mixing suggests factor deficiency; failure to correct suggests an inhibitor such as a factor antibody or lupus anticoagulant.
Hemophilia A (factor VIII) and B (factor IX) severity: <1% severe, 1–5% moderate, >5% mild; replace missing factor for bleeding, and use desmopressin only for mild hemophilia A.
von Willebrand disease presents with mucocutaneous bleeding and abnormal platelet-function testing; desmopressin is used for type 1, and factor concentrate for type 3 or severe bleeding.
Childhood immune thrombocytopenia is usually acute and self-limited; treat with IVIG or corticosteroids for significant bleeding or platelets <20,000/µL, and avoid platelet transfusion unless bleeding is life-threatening.
DIC laboratory pattern: prolonged PT/aPTT, low fibrinogen, elevated D-dimer, and thrombocytopenia; treat the underlying trigger and give platelets or plasma for active bleeding, not solely to correct numbers.
Vitamin K deficiency bleeding is prevented by 1 mg IM vitamin K at birth; late VKDB occurs at 2–12 weeks, often with intracranial hemorrhage, and is treated with vitamin K and factor replacement.
Pediatric venous thromboembolism often has central-line or inherited thrombophilia risk; anticoagulation duration depends on provocation, and direct oral anticoagulants are used only per age-specific approval.
Oncology: Leukemia, Lymphoma, and Solid Tumors
ALL is the most common pediatric malignancy; central nervous system prophylaxis and risk-adapted systemic therapy are essential, and end-induction minimal residual disease is a powerful prognostic factor.
Suspect acute promyelocytic leukemia with t(15;17) in a child with AML and coagulopathy; start all-trans retinoic acid immediately without waiting for molecular confirmation because it reduces early hemorrhagic death.
Pediatric AML treatment uses intensive induction and consolidation; cytogenetics and molecular markers such as RUNX1::RUNX1T1, CBFB::MYH11, and KMT2A rearrangements inform risk.
Hodgkin lymphoma shows Reed-Sternberg cells and often painless cervical or supraclavicular adenopathy; combined chemotherapy with response-adapted radiation reduces late effects.
Burkitt lymphoma is a highly proliferative B-cell tumor with MYC translocation; intensive multiagent chemotherapy and CNS prophylaxis are required, with tumor lysis prevention.
Neuroblastoma secretes catecholamines and is MIBG-avid; MYCN amplification, age, and stage determine risk, and high-risk disease uses intensive chemotherapy, surgery, radiation, and immunotherapy.
Wilms tumor presents as an abdominal mass; nephrectomy plus chemotherapy is standard, with radiation for advanced stage or unfavorable histology, and bilateral disease requires nephron-sparing approaches.
Leukocoria is the most common sign of retinoblastoma; germline RB1 mutation causes bilateral disease and second malignancy risk, and enucleation is used for advanced intraocular disease.
Tumor lysis syndrome causes hyperkalemia, hyperphosphatemia, hypocalcemia, and hyperuricemia; hydrate and use rasburicase for high uric acid risk, but avoid rasburicase in G6PD deficiency.
Transfusion Medicine and Hematopoietic Stem Cell Transplantation
Packed red cell transfusion of 10–15 mL/kg typically increases hemoglobin by about 2 g/dL; use restrictive thresholds and transfuse for symptomatic anemia or significant bleeding.
Platelet transfusion is commonly 10–20 mL/kg or one apheresis unit in older children; prophylactic thresholds vary, often <10,000/µL when stable and higher before procedures or with bleeding.
Irradiate cellular blood products (25 Gy) for HSCT recipients, severe cellular immunodeficiency, and intrauterine transfusions to prevent transfusion-associated graft-versus-host disease.
Leukoreduced products reduce febrile nonhemolytic reactions and CMV transmission; CMV-seronegative products are an alternative for selected seronegative transplant or pregnant patients.
For suspected acute hemolytic transfusion reaction, stop the transfusion, maintain IV access, check patient and unit identification, send the unit and samples to the blood bank, and treat shock; do not restart the same unit.
Autologous HSCT uses the patient's own stem cells and has no graft-versus-tumor effect; allogeneic HSCT provides graft-versus-tumor immunity but risks GVHD and requires HLA matching.
Acute GVHD affects skin, gut, and liver within months of allograft; prophylaxis uses a calcineurin inhibitor plus methotrexate or mycophenolate, and first-line treatment is high-dose corticosteroids.
Neutrophil engraftment is ANC >500/µL for 3 consecutive days; platelet engraftment is platelets >20,000/µL without transfusion for 7 days; chimerism monitoring assesses donor engraftment.
Supportive Care, Complications, Survivorship, Palliative Care, and Psychosocial/Ethical Issues
Febrile neutropenia: fever ≥38.3°C once or ≥38.0°C sustained plus ANC <500/µL or <1,000/µL falling; obtain cultures and start anti-pseudomonal antibiotics within 60 minutes.
Tumor lysis syndrome: potassium high, phosphate high, calcium low, uric acid high; aggressive hydration and rasburicase are used for high risk, and rasburicase is avoided in G6PD deficiency.
Pneumocystis jirovecii prophylaxis with trimethoprim-sulfamethoxazole is used during intensive chemotherapy and for at least 6 months after HSCT; alternatives are selected for sulfa allergy.
Cumulative anthracycline dose increases cardiomyopathy risk; obtain baseline and serial echocardiograms and counsel survivors about late heart failure risk.
Offer fertility preservation before gonadotoxic therapy: sperm banking for postpubertal males, oocyte or embryo cryopreservation for females, and ovarian tissue cryopreservation in selected cases.
Survivorship care includes surveillance for secondary malignancy, cardiac and endocrine late effects, neurocognitive problems, and psychosocial needs, with a written care plan and transition to adult care.
Palliative care addresses pain, dyspnea, nausea, and goals of care alongside curative therapy; hospice focuses on comfort when disease-directed treatment is no longer beneficial.
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