Acute respiratory failure (ARF) in an 11-year-old child with pre-T acute lymphoblastic leukemia (ALL) at the beginning of induction therapy was observed, connected with a pulmonary thrombosis and not with an infective origin. A systematic search for this pathology identified six other children with the same pulmonary complication, five of whom where in the early phase of acute nonlymphoblastic leukemia (ANLL) and one in induction therapy for ALL in marrow relapse. At the beginning of the symptomatology, all children presented severe hypoxia and hypercapnia, with no or minimal chest radiograph abnormalities and no clear hemodynamic involvement. In all patients the arteriography and nuclear imaging studies confirmed the diagnosis. The causes of the thrombi could be connected with neoplastic emboli after cell lysis and/or with the vascular damage resulting from antiblastic therapy. Intravenous urokinase treatment and respiratory assistance had been successfully carried out in six of seven children. Cancer 67:696-702,1991.ULMONARY COMPLICATIONS are frequent among P immunodepressed patients. ' Interstitial pneumonia and pulmonary infiltrates of infectious origin or related to the underlying disease are seen in the stages when immunodepression is greatest and when the systemic disease is invasive. They have considerable negative impact on prognosis.2The pulmonary pathologic features that tend to arise when certain antiblastic drugs are used in specific therapeutic protocols have been amply dealt with and the implications have been pointed Three years ago a patient was admitted to our intensive care unit with initial pre-T acute lymphoblastic leukemia

Pulmonary thromboembolism (PTE) in leukemic children undergoing intensive chemotherapy should be promptly recognized so that specific therapy can be started. Our experience with the two cases reported here has led us to propose guidelines for the treatment of initial PTE in a pediatric hematology unit. Two children with leukemia developed PTE, the first during the relapse for acute lymphoblastic leukemia and the second at the onset of acute promyelocytic leukemia. In both cases, the diagnosis of PTE was based on clinical assessment of sudden acute respiratory failure with positive pulmonary perfusional scintigraphy in spite of a negative chest X-ray. The subintensive supervision consisted of instrumental monitoring with the assistance of an intensive care anesthetist. The clinical monitoring was based on the serial registration of respiratory rate, cardiac rate, SaO2 and body temperature. The thrombolytic therapy, together with heparin prophylaxis, was successfully administered in the hematology ward without the need for intensive care support (i.e. mechanical ventilation). The success of the treatment was documented by the criterion of a return to the normal cardiorespiratory parameters a few hours after the start of the thrombolytic treatment. Furthermore, a chest CT scan in case 1 and an arteriography in case 2 confirmed the PTE-related hypoperfusion. On the basis of this experience, the authors point out that in the course of acute respiratory failure in leukemic children, the combination of a negative chest X-ray and a positive pulmonary perfusional scintigraphy (compared whenever possible with ventilatory scintigraphy) in the presence of a negative CT scan could be a reliable diagnostic tool for PTE. This pathology should be treated promptly and with specific therapy to avoid progression to a severe, massive PTE.