The adult respiratory distress syndrome occurred during aggressive therapy of extensive acute leukemia. The pathogenic mechanisms involved includes development of disseminated intravascular coagulation probably initiated by tissue factors from necrotic leukemic cells following chemotherapy. Awareness of the possibility of the complication is stressed.
CASE REPORTThis 18-year-old Mexican male presented with a ten-day history of abdominal pain, malaise, lethargy and fever. Two weeks prior to admission a single episode of epistaxis had occurred. On initial clinical assessment widespread firm peripheral lymphadenopathy and prominent hepatosplenomegaly were present.Admission data revealed hematocrit of 37%, total white blood count of 480,000/mms, 100% blasts, and platelet count 48,000/mms. Serum glutamic oxaloacetic transaminase (SCOT) was 630 mU/ml, lactic dehydrogenase (LDH) 11,700 mU/ml, alkaline phosphatase 482 m&/ml, bilirubin 2.1 mg/dl, creatinine 0.1 mg/dl, uric acid 15.1 mg/dl, phosphate, 2.0 mg/dl, calcium 10.3 mg/dl, albumin 4.2 g/dl. The entry chest x-ray showed mediastinal widening (Fig. 1).Within 12 hours he had become stuporose. Lumbar puncture revealed an opening pressure of 300 cmH20, protein 38 mg/dl, glucose 7 0 mg/dl and 2 WBC/mm3. Bone marrow aspirate (and biopsy) showed acute lymphoblastic leukemia. Chemother- apy designed to induce rapid remission because of central nervous system leukostasis was immediately instituted; the plan was duanomycin 100 mg I.V. for three days, cytosine arabinoside 140 mg I.V. every 12 hours for seven days, G-thioguanine 120 mg orally every 12 hours for seven days, vincristine 2 mg I.V. every seven days, and prednisone 60 mg QID for seven days.Considerable complications of therapy ensued as a hematologic response was achieved in two days, when the peripheral blood smear showed 200 white blood cells/mm*, 80% polymorphonuclear, and repeat bone marrow showed a few white and red cell precursors only. Progressive azotemia, hyperkalemia, hyperuricemia, and oliguria required dialysis, peritoneal initially (day 2), and hemodialysis thereafter. A profound coagulopathy (Quick time 37 seconds, partial thromboplastin time 120 seconds, fibrinogen 190 mg/dl, protamine sulfate positive, fibrin degradation products 80-120 mg/ml, platelet count 20,000/mma) developed but supportive therapy of platelet transfusions and fresh frozen plasma averted major bleeding problems. This problem subsequently diminished. Other acute complications included hypocalcemia and hypophosphatemia.By day 2 acute respiratory distress had ensued: an evanescent peripheral diffuse alveolar infiltrate developed on chest x-ray (though the mediastinum had narrowed considerably) and gas exchange rapidly and progressively deteriorated. Hypoxemia, not adequately responsive to high flow oxygen or intubation and mechanical ventilation, responded to the use of positive end expiratory pressure (PEEP). The pulmonary insufficiency was later further compromised by infection, with both sputum and blood cultures yielding Klebs...
