Letters to the Editor
purate and inulin. These manipulations may have dropped the Po~ in the unstable RDS infants as would be suggested by preliminary reports of Dangman and associates.' Dropping the Po~ below 40 mm Hg may lead to decreased blood pressure, shock and renal failure. The hazards of urethral catheterization make it questionable as a tool in research in sick neonates. Paul R. Williams, M.D. Director, Neonatal Research William Beaumont Hospital 3601 W 13 Mile Road Royal Oak, MI 48072 REFERENCES 1. Guignard JP, Torrado A, Mazouni SM, and Gautier E: Renal function in respiratory distress syndrome, J PEDIATR 88:845, 1976. 2. Siegel SR, Fisher DA, and Oh W: Renal function and serum aldosterone levels in infants with respiratory distress syndrome, J Pediatr 83:854,1973. 3. Siegel SR: Personal communication. 4. Dangman BC, Hegyi T, Hiatt M, Indyk L, and James LS: The variability of Po~ in newborn infants in response to routine care, Pediatr Res 10:422, 1976 (abstr).
Reply To the Editor." We appreciate Dr. Williams' comments regarding fluid requirements in RDS patients. It was one of the practical conclusions of our study that fluid administration should be increased in these oliguric patients. We, however, do not agree with Dr. Williams' simple explanation for the differences between Siegel and associates' study ' and our observations/ Siegel found normal renal function and a blood urea nitrogen of 14 mg/dl in 11 preterm RDS infants studied between the twenty-fourth and the thirty-eighth hour of life. Nine of our patients also were studied before the thirtyeighth hour of life (mean age at the time of the clearance study: 27 hours). Fluid administration in these patients was similar to that in Dr. Siegel's study, but they had decreased renal function and elevated plasma urea. The mean value for plasma urea (44.9 _+ 8.6 mg/dl) was not significantly different form that observed in our total group of 20 RDS patients (49 _+ 5.2 mg/dl). Age can thus not account for the differences found between Dr. Siegel's and our patients. As discussed earlier, ~ the relative values of Pao_' and Aio.2 in Dr. Siegel's patients suggest mild impairment of respiratory function in his infants. We also observed normal renal function in less severe cases of RDS, and found a correlation between renal function and severity of the disease as assessed by roentgenograms and evolution of Pao.2. That a transient drop in Pao., could be induced by urethral catheterization or intravenous infusion o f inulin and PAH cannot be excluded! But to ascribe the renal insufficiency to these maneuvers only is not justified. Oliguria and low Pao._, preceded to these manipulations. Finally while the hazards of urethral catheterization cannot be
The Journal of Pediatrics Febraarv 1977
neglected, it must be recognized that standard inulin clearance remains the most reliable method'. ~ by which to assess renal function in neonates. Urethral catheterization i s - u n f o r t u n a t e l y essential for accurate measurement of urine output! J.-P. Guignard E. Gautier Department of Pediatrics Centre Hospitalier Universitaire Vattdois 1011 Lausanne, Switzerland A. Torrado University Children's Itospital Clinica Sta Teresa Cogmbra, Portugal REFERENCES 1. Siegel SR, Fisher DA, and Oh W: Renal function and serum aldosterone levels in infants with respiratory distress syndrome, J PEDIATR 83:854, 1973. 2. Guignard J-P, Torrado A, Mazouni SM, and Gautier E: Renal function in respiratory distress syndrome, J PEDtATa 88:845, 1976. 3. Torrado A, and Guignard J-P: Renal failure in respiratory distress syndrome (RDS) J PEDIA'rR 85:443, 1974. 4. Guignard J-P, Fawer C-L, Torrado A, Prod'hom L-S, and Gautier E: Maturation of glomerular filtration rate in the neonate, Proceedings of the ninth Annual Meeting of the European Society for Paediatric Nephrology, 1975 (abstr.). 5. Guignard J-P, Torrado A, and Gautier E: Assessment of renal function without urine collection, Proceedings of the tenth Annual Meeting of the European Society for Paediatric Nephrology, 1976 (abstr.).
Pleural effusion in histoplasmosis To the Editor." Weissbluth ~ reported a case of histoplasmosis with pleural effusion. We have seen a similar picture in a 9%-year-old boy who was hospitalized with persistent pneumonia. Nine days before admission he developed left pleuritic chest pain, dyspnea. fever, chills, night sweats, and a nonproductive cough. Three days before admission a chest radiograph revealed a left lower lobe infiltrate with a left-sided pleural effusion. He was begun on oral tetracycline with no resolution of symptoms. Upon hospitalization he denied recent travel or unusual exposures. Routine laboratory testing, cold agglutinins, an intermediate strength purified protein derivative and paired sera for influenza A and B were negative. The pleural fluid contained 2,200 lymphocytes and 20,000 red blood cells/mm ~, specific gravity was 1.034. Pleural fluid Gram and acid fast stains as well as cuttures for bacteria, tuberculosis, fungi, and viruses were negative. Countercurrent immunoelectrophoresis was negative for Slreptococeus pneumoniae and Hemophilus influenza, type b. A histoplasmin skin test was positive. Mycelial and yeast phase titers were 1:64
Volume 90 Number 2
Letters to the Editor
and 1:256, respectively, on the eighteenth day following hospitalization and 1:16 and 1:1024 on both the forty-fifth and eightieth days. During the month following admission the pleural effusion resolved. He continued to be active and gain weight. Chest radiographs three months after discharge revealed residual fibrosis with bilateral mediastinal adenopathy. The interpretation of the initial serology results was confused by the antecedent histoplasmosis skin test, but the fourfold rise in the yeast phase titer is diagnostic of histoplasmosis. ~ :' Because of the potential alteration in serologic values in addition to its questionable diagnostic value, the histoplasmosis skin test should not be utilized for diagnostic purposes.
Charles D. Ericsson, M.D. Larry K. Pickering, M.D. George W. Salmon, M.D. The University of Texas Medical School Department of Pediatrics Program in Infectious Diseases and Cfinical Microbiology 6400 West Cullen Houston, TX 77030
the five had a short benign course. Where histoplasmosis is endemic, it should be considered in the differential diagnosis o f pleural effusion, even though it is a relatively uncommon manifestation of this infection.
Helen F. Brickman, M.D. Assistant Professor of Pediatrics MeGill University, Montreal Department of Respiratory Function The Montreal Children's Hospital 2300 Tupper St. Montreal, Quebec Canada H3H 1P3 REFERENCES 1. Weissbluth M: Pleural effusion in histoplasmosis, J PEDIATR 88:894, 1976. 2. Palayew MJ, Frank H, and Sedlezky I: Our experience with histoplasmosis: An analysis of seventy cases with follow-up study, J Can Assoc Radiol 17:142, 1966.
Group C hemolytic streptococcal pharyngitis
REFERENCES 1. Weissbluth M: Pleural effusion in histoplasmosis, J PEDIATR 88:894, 1976. 2. Buechner HA, Seabury JH, Campbell CC, et al: Committee recommendations: The current status of serologic, immunologic and skin tests in the diagnosis of pulmonary mycoses, Chest 63:259, 1973. 3. Sigrest ML, Lummus FL, Campbell GD, et al: Effect of diagnostic skin testing on antibody levels for histoplasmosis, N Engl J Med 269:390, 1963.
To the Editor: The recent report by Dr. Weissbluth of pleural effusion in a child with acute histoplasmosis' reminded us of a similar case in our own experience, A 14-year-old male was admitted to the Montreal Children's Hospital on 4/4/72 because of malaise, fever, chest pain, and dyspnea of two days' duration. Radiography revealed a large left pleural effusion; the fluid was serosanguineous, sterile, and cytologically unremarkable. Radiographic follow-up a week later confirmed the rapid decrease in the effusion and demonstrated a mediastinal mass not previously evident. Tomography disclosed a 4.5 • 3 cm pear-shaped mass in the posterior midmediastinum that extended to the region of the left lower bronchus. There was also a lesion, 8 mm in diameter, in the left lower lobe, and a suggestion of pericardial effusion. Though cultures of sputum and bone marrow did not grow Histoplasma capsulatum, a diagnosis of histoplasmosis was made on the basis of a rise in complement-fixation titer from 1:32 before obtaining a strongly positive histoplasmin skin test, to a peak of 1:256. The titer declined to 1:64 five months later. Histoplasmosis has been recognized to be endemic in Montreal since an outbreak in 1963-1964 comprised several hundred active cases. Pleural effusion was reported in five out of 70 patients in a general hospital. One of the five was a ten-year-old child; each o f
To the Editor: We were interested to read the paper by Benjamin and Perriello' on an epidemic of group C hemolytic streptococcal pharyngitis, since we recently identified the same organism in three out of four members of a family, two of whom also presented with fever, sore throat, and exudative pharyngitis. There were no abnormalities on urinalysis. The two adolescents in the family had pharyngitis, their father had a hordeolum of the left eye which was surgically drained, but not cultured. He was treated with ampicillin. The mother was asymptomatic but had a positive culture. The ASLO titers in the family are shown in Table I. Routine Lancefield grouping of all non-group A hemolytic streptococcus, as suggested by the authors, was carried out. In order to ascertain the frequency of this disorder in our institution, all throat cultures taken over the previous 10-month period were reviewed. Only one additional case of group C hemolytic streptococci was cultured. It is of interest that this patient was also an adolescent who presented with exudative tonsillitis and fever. His ASLO titer was 166 Todd units. All patients responded
Case Adolescent Adolescent Mother Father
Initial ASLO titer
Positive Positive Negative Positive
Positive Positive Positive Unknown
166 250 333 166
Follow-up ASLO titer (10 days) 166 250 333 166