8.2 Coagulopathies, Myelosuppression & Oncologic Complications

Coagulopathy Landscape in the PICU

Critically ill children develop bleeding and clotting disorders from immune platelet destruction, consumptive cascades, drug reactions, marrow failure, and cancer therapy. The CCRN Pediatric exam expects you to separate immune thrombocytopenia (ITP), disseminated intravascular coagulation (DIC), and heparin-induced thrombocytopenia (HIT), then layer myelosuppression complications — especially tumor lysis syndrome (TLS) and febrile neutropenia.

Immune Thrombocytopenia (ITP)

Immune thrombocytopenia (ITP) is antibody-mediated platelet destruction, often following a viral illness in previously healthy children. Platelet counts may fall below 20,000/uL while hemoglobin and leukocyte counts remain normal. Clinical picture is mucocutaneous: petechiae, purpura, epistaxis, gingival bleeding, and menorrhagia in adolescents. Deep tissue or joint bleeding is less typical than in hemophilia.

Most childhood ITP is self-limited, but PICU-level concern focuses on life-threatening hemorrhage, particularly intracranial hemorrhage (ICH) — heralded by severe headache, vomiting, neurologic change, or “wet purpura” (bullous oral hemorrhage). Management may include IVIG, corticosteroids, or other immunomodulation per hematology; platelet transfusion is reserved for life-threatening bleed because transfused platelets are rapidly destroyed unless the acute emergency demands them. Nursing priorities: neuro checks, fall precautions, avoid IM injections and rectal temperatures, soft toothbrush, and rapid escalation for neurologic red flags.

Disseminated Intravascular Coagulation (DIC)

DIC is a consumptive coagulopathy triggered by sepsis (especially meningococcemia and gram-negative infection), trauma, burns, malignancy, and severe hemolytic reactions. Systemic thrombin generation creates microthrombi that injure organs while platelets and clotting factors are consumed, so the child both clots and bleeds. Bedside clues include oozing from lines and mucosa, purpura fulminans, oliguria, and acral ischemia.

Treat the cause first — antibiotics and source control for septic DIC remain the decisive step. Product support targets active bleeding plus labs: FFP for prolonged PT/aPTT, cryoprecipitate for critically low fibrinogen, and platelets for severe thrombocytopenia with bleeding. Heparin is rarely first-line in bleeding-predominant pediatric DIC and is considered only in selected thrombosis-predominant pictures under specialist guidance.

Heparin-Induced Thrombocytopenia (HIT)

Although less common than in adults, HIT occurs in heparin-exposed children (including line flushes and ECMO circuits). IgG against heparin–PF4 complexes activates platelets, producing a prothrombotic state despite thrombocytopenia. Suspect HIT with a >50% platelet drop typically on days 5–10 of exposure (sooner if prior heparin), new thrombosis, and no clearer alternate cause. Actions that cannot wait for serology: stop all heparin (unfractionated, LMWH, and heparin-coated devices when feasible) and start a non-heparin anticoagulant (e.g., argatroban or another agent chosen for age, organ function, and institutional protocol). Avoid prophylactic platelet transfusion and early warfarin, which can worsen limb ischemia.

Myelosuppression and Oncologic Complications

Chemotherapy and hematologic malignancies suppress marrow lineages: anemia, thrombocytopenia, and neutropenia. Absolute neutrophil count (ANC) <500/uL (and especially <100/uL) marks profound infection risk because neutrophils are the primary defense against bacterial and fungal invasion.

Tumor Lysis Syndrome (TLS)

Tumor lysis syndrome follows rapid malignant-cell breakdown — spontaneously in bulky high-grade lymphomas/leukemias or shortly after induction therapy. Intracellular contents flood the plasma:

• Hyperkalemia → arrhythmias, peaked T waves, widened QRS
• Hyperphosphatemia → binds calcium
• Secondary hypocalcemia → tetany, seizures, prolonged QT
• Hyperuricemia → precipitation in renal tubules → acute kidney injury

PICU TLS bundle: continuous cardiac monitoring; vigorous IV hydration (often 2–3 L/m²/day when cardiac/renal status allows); urinary alkalinization only when specifically ordered and not if phosphate is already high; urate oxidase (rasburicase) or allopurinol per risk strata and G6PD status (rasburicase contraindicated in G6PD deficiency); frequent labs (q4–6h initially); kayexalate/insulin-glucose/calcium for dangerous potassium; and early nephrology for oliguric AKI or refractory electrolyte crises requiring dialysis. Never add potassium to fluids in active TLS.

Neutropenic Fever

Fever in neutropenia is an emergency because an unopposed bacterial infection can progress to septic shock within hours. Definitions commonly use a single oral temperature ≥38.3°C (101°F) or ≥38.0°C (100.4°F) sustained over one hour with ANC <500/uL (or expected to fall there). Immediate actions:

1. Rapid assessment for shock and focus of infection (lines, mucosa, perineum, lungs, abdomen).
2. Blood cultures from periphery and each lumen before antibiotics when obtainable without delay.
3. Broad-spectrum anti-pseudomonal antibiotics within 60 minutes (and preferably sooner).
4. Strict protective practices: hand hygiene, private room as indicated, avoid rectal manipulation, meticulous central-line care, and early consideration of antifungal coverage for persistent fever per oncology protocols.

Integrate family teaching: fever instructions at discharge, central-line emergency signs, and medication adherence for growth-factor or antimicrobial prophylaxis when prescribed. The exam rewards recognizing that time-to-antibiotic in febrile neutropenia and time-to-metabolic control in TLS are as critical as ventilator or vasoactive titration elsewhere in the PICU.