This study was designed to establish reference values of maximal static respiratory pressures in children and adolescents in our community, and compare them with previous studies. Participants were recruited from three schools (randomly chosen from those located in the metropolitan area of the city of Valencia) after appropriate consent. None of the participants had a previous history of pulmonary, cardiac, and/or skeletal abnormalities, and all of them had normal spirometry. Forced spirometry (Spirotrac III, Vitalograph) and maximal inspiratory (P(ImaxRV)) and expiratory (P(EmaxTLC)) pressure values (Sibelmed 163) were obtained by the same investigator, following national guidelines (SEPAR 1990).We studied 392 subjects (185 males, 207 females) whose ages ranged from 8-17 years. The reproducibility of measurements was investigated in a subgroup of 88 participants (randomly selected from the total sample, and stratified for age and gender) by means of the intraclass correlation coefficient (P(EmaxTLC), 0.98; P(ImaxRV), 0.95). P(EmaxTLC) and P(ImaxRV) values were significantly different between males and females (P < 0.0001) and were normally distributed. A stepwise, linear multiple regression model was built in each gender group (male/female) for the prediction of P(ImaxRV) and P(EmaxTLC) values. Independent variables (weight, height, and age) and their potential interactions were forced to enter the model in order to maximize the square of the multiple correlation coefficient of the resultant equation. This model turned out to be applicable (homoscedasticity, independence, and normality requirements) for P(ImaxRV) (in males and females) and for P(EmaxTLC) (in males but not in females). Variables included in the model were age and the product of weight and height. Their predictive power ranged between 0.21-0.51. In conclusion, P(ImaxRV) and P(EmaxTLC) values increase with age from 8 until 17 years. In all age groups, values were higher in males than in females. Weight, height, and age are included in the predictive equations for P(ImaxRV) (in males and females) and P(EmaxTLC) (in males). Their predictive value is similar to that reported by other authors and ranges between 0.21-0.51. This model is not suitable for the prediction of P(EmaxTLC) in females; the observed mean and range should be used instead.

Symptomatic pulmonary manifestations of Kawasaki disease (KD) are uncommon. However, epidemiologic, radiologic, and histologic studies have indicated that respiratory symptoms and findings occur in KD and suggest that the KD agent may have a respiratory portal of entry. We report on three young infants with KD who developed pulmonary nodules, in addition to coronary artery aneurysms. Two patients had pathologic specimens available, one from biopsy and the other from autopsy. The nodules had predominantly mononuclear cell infiltrates, which were within the lung parenchyma and infiltrating vessel walls. Immunohistochemical studies of the nodules, using antibodies to common leukocyte antigen (LCA) and factor VIII-related antigen, confirmed the inflammatory nature of the lesions and showed capillary proliferation. IgA plasma-cell infiltration was observed in the nodule, consistent with previous KD findings of IgA plasma-cell infiltration in the vessel walls, kidneys, pancreas, and upper respiratory tract. The two patients with nonfatal KD were treated with intravenous immunoglobulin and aspirin, with resolution of the nodules. We propose that when pulmonary involvement occurs in KD, it ranges from subclinical interstitial micronodular infiltrates to larger inflammatory pulmonary nodules. These pulmonary infiltrates and nodules likely reflect the host response to the etiologic agent of KD, and may resolve with the disease process. Recognition of this pulmonary complication of KD may enable cautious observation of such lesions for spontaneous resolution.

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Since the mid-1960s intrathecal chemotherapy (methotrexate [MTX], cytarabine [Ara-C], or both, plus hydrocortisone) has constituted the standard approach to prophylaxis and treatment of central nervous system (CNS) leukemia and lymphoma. Intrathecal chemotherapy-related neurotoxicity has been described in a variable proportion of patients. At least 35 cases of subacute myeloencephalopathy with transient or permanent paraplegia/quadriplegia after intrathecal chemotherapy have been reported. Different factors have been cited: high cumulative MTX dose, meningeal leukemia, cranial irradiation, and preservatives in MTX and Ara-C. A direct toxic effect of the intrathecal chemotherapy seems the most likely mechanism. Early imaging studies are usually normal. We describe a nonfatal case of permanent flaccid quadriplegia after the fourth triple intrathecal chemotherapy in a 6-year-old girl with acute lymphoblastic leukemia and no evidence of meningeal involvement. Six months after intrathecal chemotherapy, CNS magnetic resonance imaging showed severe atrophy of spine, cerebellum, and cerebral hemispheres. The outcome of reported cases is diverse. No treatment has been shown to reverse neurotoxicity. Among the cases reported in the literature, complete recovery of neurologic deficits was observed in 9 patients, partial recovery with variable sequelae in 6, no recovery in 8, and 13 patients died from the initial oncologic disease or neurotoxicity progression.

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