- Email: [email protected]
Neutrophil chemotaxis in preterm infants with infections
468
Brief clinical and laboratory observations
different than those employed by Holroyde et al. We found a significant linear correlation of percent pocked erythrocyte and gestational age, with the most premature infants having the highest counts, in the range of postsplenectomized individuals. The correlation is less significant with birth weight. It appears that the infant's splenic R E function as assessed by this technique correlates better with gestational age than with birth weight; therefore, splenic function may be more a reflection of maturational factors rather than birth weight. We have observed a lower percentage of pocked erythrocytes in second trimester fetuses compared to premature neonates of 25- to 32-week gestation. The reason(s) for this must remain speculative but may include differences in fetal erythrocyte m e m b r a n e characteristics, or may be due to the time required ,for the acquisition of these m e m b r a n e pocks. The very short life span of these early fetal erythrocytes may not allow sufficient time for the development of these autophagic vacuoles. Holroyde and Gardner 1~ have demonstrated that pocks appear in transfused red cells in asplenic patients over the course of 15 to 20 days in adult patients. Our study indicated an increase in the percent of pocked cells in post-term infants; this may reflect placental insufficiency as pregnancy proceeds post-term. In post-term infants with birth weights less than 90% of term values, major organs have fewer cells than normal, with the abnormality most apparent in the spleen. 13 The apparent decrease in reticuloendothelial function in the postmature infants may be a consequence of fetal hypoxia and malnutrition, leading to a diminution in splenic size and functional capacity. The authors acknowledge the excellent care given by the nurses in the Newborn Special Care Unit. We also thank David Scott, Ph.D., for statistical advice and Debra Camputaro for assistance in preparation of the manuscript.
The Journal of Pediatrics March 1980
REFERENCES 1. Pearson HA, Johnston D, Smith KA, and Touloukian R J: The born-again spleen return of splenic function after splenectomy for trauma, N Engl J Med 298:1389, 1978. 2. Pearson HA, McIntosh S, Ritchey AK, et al: Developmental aspects of splenic function in sickle cell diseases, Blood 53:358, 1979. 3. Holroyde CP, Oski FA, and Gardner FM: The "pocked" erythrocyte-red cell surface alterations in reticuloendothelial immaturity of the neonate, N Engl J Med 281:516, 1969. 4. Ruttenberg HD, Neufeld HN, Lucas RV, Carey LS, Adams P, Andersen RC, and Edwards JE: Syndrome of congenital cardiac disease and asplenia, Am J Cardiol 13:387, 1964. 5. Dubowitz L, Dubowitz V, and Goldberg C: Clinical assessment of gestational age in the newborn infant, J PEDIATR 71:1, 1970. 6. Hobbins JC, and Mahoney M J: In utero diagnosis of hemoglobinopathies: Technique for obtaining fetal blood, N Engl J Med 290:1065, 1974. 7. Likhite VV: Immunological impairment and susceptibility to infection after splenectomy, JAMA 236:1376, 1976. 8. Ozsaylu S, Hosain F, and McIntyre PA: Functional development of phagocytic activity of the spleen, J PEDtATR 90:560, 1977. 9. Reade PC, and Jenkin CR: The functional development of the reticuloendothelial system. I. The uptake of intravertousiy injected particles by foetal rats, Immunology 9:53, 1965. 10. Acevedo G, and Mauer A: The capacity for removal of erythrocytes containing Heinz bodies in premature infants and patients following splenectomy, J PEmATR 63:61, 1963. 11. Padmanabhan J, Risemberg HM, and Rowe RD: HowellJolly bodies in the peripheral blood of full term and premature infants, Hopkins Med J 132:146, 1973. 12. Holroyde CP, and Gardner FM: Acquisition ofautophagic vacuoles by human erythrocytes: Physiological role of the spleen, Blood 36:566, 1970. 13. Naeye R: Structural correlates of fetal under nutrition, in Waisman MA, and Kern G, editors, Fetal growth and development, New York, 1970, McGraw-Hill Book Company, pp 241-252.
Neutrophil chemotaxis in preterm infants with infections F. Laurenti, M.D.,* R. Ferro, M.D., G. Marzetti, M.D., M. Rossini, B.A., and G. Bucei, M.D., Rome, Italy
From the Department of Pediatrics and from the CNR Respiratory Virus Centre of Rome. *Reprint address: Clinica Pediacrica Universititdi Roma, Viale Regina Elena 324, 00161, Rome, Italy.
M I L L E R 1 first reported a striking defect in P M N chemotaxis in healthy newborn infants; Klein et aF established that this activity was reduced to about 20% of adult values. However, the chemotactic behavior in term and preterm
0022-3476/80/030468 +03500.30/0 9 1980 The C. V. Mosby Co.
Volume 96 Number 3, part 1
infants during bacterial infection has not been elucidated. The present study was designed to investigate this behavior in preterm infants. MATERIAL AND METHODS The study was carried out on 16 preterm infants (ten males) in the first two weeks of life. Five infants (Group 1: BW: mean 1,440 gin, range 1,000 to 1,980: GA: mean 30.4 weeks, range 28 to 34) had no infection during the period of observation. Five infants (Group 2: BW: mean 1,890 gm, range 1,000 to 2,500; GA: mean 32.4 weeks, range 28 to 36) had only surface infections (conjuncdval, pharyngeal, nasal, umbilical) confirmed by several positive bacterial cultures at different sites. None had clinical signs of severe illness or more than mildly abnormal blood findings, such as increased band cells, PMN vacuolization, toxic granulation, and megathrombocytes; blood cultures were negative for bacterial growth. The remaining six patients (Group 3; BW: mean 1,550 gm, range 1,120 to 2,480; GA mean 30.2 weeks, range 28 to 36) presented with proven sepsis, characterized by sclerema, apneic spells, bradycardia, vomiting, abdominal distension, gray color, hypotension, and acidosis. Blood changes typical of infection were marked, and blood cultures were positive for Klebsiella or Pseudomonas aeruginosa.
Abbreviations used PMN: polymorphonuclear leukocytes HPF: high-poweredfield CI: chemotacticindex (No. of PMNs/HPF) BW: birth weight GA: gestational age
The chemotactic assays were performed in the course of infection and in the previous or subsequent infection-free periods. Heparinized blood (10 units/ml) (arterial or venous) was used. Informed consent was obtained from the parents. The CI was measured with a modified Boyden method using a special chamber which allows several assays simultaneously.~ The upper compartment was filled with 1 • l0 s dextran-separated and washed PMNs; the lower one with endotoxin-activated pooled serum. Results were reported as mean number of PMNs/ HPF obtained by the reading of 10 random fields after 120-minute incubation. Each sample was tested in triplicate. In addition, PMNs of normal adult and preterm infants were incubated in sera from septic patients to detect possible inhibitors. The whole set of tests required no more than 2 ml of blood. The t test was used for statistical evaluation.
Brief clinical and &boratory' observations
GROUP
2
GROUP
469
3
CELLS/HPF
,oou CELLS fHPF
:J +
60
i L I
40 20
before
durinr
after
SURFACE INFECTION
before during after PROVEN SEPSIS
Figure. Changes of the CI in infants of Groups 2 and 3 in consecutive periods with and without infection. When more than one determination was available in each period, the mean value has been reported. The cross indicates one death.
RESULTS In the five infants of Group 1, a total of 15 determinations was performed in the first ten days of life. Observed values ranged between 13 and 38 PMNs/HPF. The mean value of the C] (taking only one average value for each case) was 23 _+ 10 (SD), Similar values were obtained in Groups 2 and 3 during the infection-free periods (Group 2: mean 23 + 9, range 12 to 35; Group 3: mean 26_+ 13, range 10 to 42). In Group 2, during surface infections, the CI was markedly and significantly higher than in infection free periods (mean 85 • 30, range 45 to 120; P < 0.005). In sharp contrast, when sepsis occurred in infants of Group 3, the CI fell almost to zero (mean 2 _+ 2~ range 0 to 6; P < 0.005). The changes of the CI in individual cases are illustrated in the Figure. Sera from septic patients failed to affect chemotaxis of PMNs from normal adults and from noninfected preterm infants. COMMENT In preterm infants without infection the CI was similar to previous findings in term neonates, ~ corresponding to about 20% of the adult values. A greater number of observations would be needed to ascertain possible differences in newborn infants with very low BW and GA. In adults with acute bacterial infections PMN chemotaxis is usually enhanced ~. ~ and may become defective
470
B r i e f clinical and laboratory observatiotz~
only in overwhelming infection, ~ possibly because of marked endotoxemia. 7 In contrast, in the present series of preterm infants the enhancement of P M N chemotaxis was observed only in patients with superficial infections and without demonstrable bacteremia, whereas in patients with proven sepsis a striking fall of the CI was constantly demonstrated. Presumably, this finding was not due to the presence o f humoral factors, since no inhibitoryeffect was observed after incubation of PMNs from healthy preterm infants and adults in sera from preterm infants with proven sepsis. The complete inactivation of chemotaxis observed by us in septic preterm infants is additional and striking evidence of the functional inability of the neonatal PMN, consistent with previous studies? ~ ~ ~ The failure of this cellular defense mechanism may be, in part, responsible for the less favorable prognosis of neonatal infection, and may represent a rational basis for P M N tranfusion in infected nonleukopenic newborn infants? ~ These preliminary results suggest that the determination of the CI in preterm infants with clinical and laboratory signs of infection may help in the discrimination between patients with mild, localized infection and those with actual sepsis. REFERENCES
The Journal o f Pediatrics March 1980
2.
3.
4.
5.
6.
7. 8.
9.
10.
Klein RB, Fischer TJ, ~trd SE, et al: Decreased mononuclear and polymorphonuclear chemotaxis in human newborns~ infants and young children, Pediatrics 60:467, 1977. Laurenti F, Businco L, Barbato MB, et al: Familial defect of cellular chemotaxis: clinical and immunological effects of Levamisole therapy, Riv ltal Pediatr 4/6:571, 1978. Hill HR, Gerrard JM, Hogan NA, and Quie PG: Hyperactivity of neutrophil teukotactic responses during active bacterial infection, J Clin Invest 53:996, 1974. Mowat AG, and Baum J: Polymorphonuclear leukocyte chemotaxis in patients with bacterial infections, Br Med J 3:617, 1971. Clark RA: Disorders of granulocyte chemotaxis, in Gallin JI, and Quie PG, editors: Leukocyte chemotaxis: methods, physiology and clinical implications, New York, 1978, Raven Press, pp 329-356. Territo MC, and Golde DW: Granulocyte function in experimental human endotoxemia, Blood 47:539, 1976. Betlanti JA, Cautz BE, Yang MC, et al: Biochemical changes in human polymorphonuclear leukocytes during maturation, in Bellanti JA, and Dayton DH, editors: The phagocytic cell in host resistence, New York, 1975, Raven Press, pp 321-332. Anderson DC, Pickering LK, and Feigin RD: Leukocyte function in normal and infected neonates, J PEDIATR85:420, 1974. Laurenti F, La Greca G, Ferro R, and Bucci G: Transfusion of polymorphonuclear neutrophils in a premature infant with Klebsiella sepsis, Lancet 2 (8080):111, 1978.
1. Miller ME: Chemotactic function in the human neonate: humoral and cellular aspects, Pediatr Res 5:487, 1971.
Transient hyperamrnonemia in an early preterm infant Jean-Claude Le Guennec, M.D., Ijaz Aslam Qureshi, B.V.Sc., Ph.D., Harry Bard, M.D.,* Jean-Yves Siriez, M.D., and Jacques Letarte, M.D., Montreal, P.Q., Canada
HYPERAMMONEMIA as a consequence of an inherited defect of enzymes of the urea cycle can cause severe and fatal illness? Transient h y p e r a m m o n e m i a has recently been documented in preterm infants with very high levels of ammonia; these infants all had a characteristic neurologic depression? They were vigorously treated by either exchange transfusions or peritoneal dialysis, and four of five survived without apparent sequelae. We describe here the case of an early preterm newborn
From the Centre de Recherche Pkdiatrique and DOpartement de POdiatric, Universitb de Montrbal. *Reprint address: Service de Nkonatologie, Centre de Recherche Pkdiatrique, Hbpital Sainte-Justine, 3175 Chemin Sainte-Catherine, MontrOal, QuObec, Canada, H3T 1C5.
infant with h y p e r a m m o n e m i a m e m b r a n e disease.
and
severe
hyaline
CASE R E P O R T A 1,450 gm boy was born to a 22-year-old gravida 2, para 1 woman at 29 weeks of gestation. Respiratory distress developed very early after birth, requiring high concentrations of oxygen. Abbreviations used PRAGA: preterm infants of similar gestational age TAGA: term infants of appropriate gestational age The infant was transferred to our neonatal intensive care unit 21 hours after birth. The examination on arrival did not demonstrate a neurologic deficit. At 22 hours of age, because of deteriorating blood gas values, the infant required tracheal
0022-3476/80/030470+03500.30/0 9 1980 The C. V. Mosby Co.
Brief clinical and laboratory observations
different than those employed by Holroyde et al. We found a significant linear correlation of percent pocked erythrocyte and gestational age, with the most premature infants having the highest counts, in the range of postsplenectomized individuals. The correlation is less significant with birth weight. It appears that the infant's splenic R E function as assessed by this technique correlates better with gestational age than with birth weight; therefore, splenic function may be more a reflection of maturational factors rather than birth weight. We have observed a lower percentage of pocked erythrocytes in second trimester fetuses compared to premature neonates of 25- to 32-week gestation. The reason(s) for this must remain speculative but may include differences in fetal erythrocyte m e m b r a n e characteristics, or may be due to the time required ,for the acquisition of these m e m b r a n e pocks. The very short life span of these early fetal erythrocytes may not allow sufficient time for the development of these autophagic vacuoles. Holroyde and Gardner 1~ have demonstrated that pocks appear in transfused red cells in asplenic patients over the course of 15 to 20 days in adult patients. Our study indicated an increase in the percent of pocked cells in post-term infants; this may reflect placental insufficiency as pregnancy proceeds post-term. In post-term infants with birth weights less than 90% of term values, major organs have fewer cells than normal, with the abnormality most apparent in the spleen. 13 The apparent decrease in reticuloendothelial function in the postmature infants may be a consequence of fetal hypoxia and malnutrition, leading to a diminution in splenic size and functional capacity. The authors acknowledge the excellent care given by the nurses in the Newborn Special Care Unit. We also thank David Scott, Ph.D., for statistical advice and Debra Camputaro for assistance in preparation of the manuscript.
The Journal of Pediatrics March 1980
REFERENCES 1. Pearson HA, Johnston D, Smith KA, and Touloukian R J: The born-again spleen return of splenic function after splenectomy for trauma, N Engl J Med 298:1389, 1978. 2. Pearson HA, McIntosh S, Ritchey AK, et al: Developmental aspects of splenic function in sickle cell diseases, Blood 53:358, 1979. 3. Holroyde CP, Oski FA, and Gardner FM: The "pocked" erythrocyte-red cell surface alterations in reticuloendothelial immaturity of the neonate, N Engl J Med 281:516, 1969. 4. Ruttenberg HD, Neufeld HN, Lucas RV, Carey LS, Adams P, Andersen RC, and Edwards JE: Syndrome of congenital cardiac disease and asplenia, Am J Cardiol 13:387, 1964. 5. Dubowitz L, Dubowitz V, and Goldberg C: Clinical assessment of gestational age in the newborn infant, J PEDIATR 71:1, 1970. 6. Hobbins JC, and Mahoney M J: In utero diagnosis of hemoglobinopathies: Technique for obtaining fetal blood, N Engl J Med 290:1065, 1974. 7. Likhite VV: Immunological impairment and susceptibility to infection after splenectomy, JAMA 236:1376, 1976. 8. Ozsaylu S, Hosain F, and McIntyre PA: Functional development of phagocytic activity of the spleen, J PEDtATR 90:560, 1977. 9. Reade PC, and Jenkin CR: The functional development of the reticuloendothelial system. I. The uptake of intravertousiy injected particles by foetal rats, Immunology 9:53, 1965. 10. Acevedo G, and Mauer A: The capacity for removal of erythrocytes containing Heinz bodies in premature infants and patients following splenectomy, J PEmATR 63:61, 1963. 11. Padmanabhan J, Risemberg HM, and Rowe RD: HowellJolly bodies in the peripheral blood of full term and premature infants, Hopkins Med J 132:146, 1973. 12. Holroyde CP, and Gardner FM: Acquisition ofautophagic vacuoles by human erythrocytes: Physiological role of the spleen, Blood 36:566, 1970. 13. Naeye R: Structural correlates of fetal under nutrition, in Waisman MA, and Kern G, editors, Fetal growth and development, New York, 1970, McGraw-Hill Book Company, pp 241-252.
Neutrophil chemotaxis in preterm infants with infections F. Laurenti, M.D.,* R. Ferro, M.D., G. Marzetti, M.D., M. Rossini, B.A., and G. Bucei, M.D., Rome, Italy
From the Department of Pediatrics and from the CNR Respiratory Virus Centre of Rome. *Reprint address: Clinica Pediacrica Universititdi Roma, Viale Regina Elena 324, 00161, Rome, Italy.
M I L L E R 1 first reported a striking defect in P M N chemotaxis in healthy newborn infants; Klein et aF established that this activity was reduced to about 20% of adult values. However, the chemotactic behavior in term and preterm
0022-3476/80/030468 +03500.30/0 9 1980 The C. V. Mosby Co.
Volume 96 Number 3, part 1
infants during bacterial infection has not been elucidated. The present study was designed to investigate this behavior in preterm infants. MATERIAL AND METHODS The study was carried out on 16 preterm infants (ten males) in the first two weeks of life. Five infants (Group 1: BW: mean 1,440 gin, range 1,000 to 1,980: GA: mean 30.4 weeks, range 28 to 34) had no infection during the period of observation. Five infants (Group 2: BW: mean 1,890 gm, range 1,000 to 2,500; GA: mean 32.4 weeks, range 28 to 36) had only surface infections (conjuncdval, pharyngeal, nasal, umbilical) confirmed by several positive bacterial cultures at different sites. None had clinical signs of severe illness or more than mildly abnormal blood findings, such as increased band cells, PMN vacuolization, toxic granulation, and megathrombocytes; blood cultures were negative for bacterial growth. The remaining six patients (Group 3; BW: mean 1,550 gm, range 1,120 to 2,480; GA mean 30.2 weeks, range 28 to 36) presented with proven sepsis, characterized by sclerema, apneic spells, bradycardia, vomiting, abdominal distension, gray color, hypotension, and acidosis. Blood changes typical of infection were marked, and blood cultures were positive for Klebsiella or Pseudomonas aeruginosa.
Abbreviations used PMN: polymorphonuclear leukocytes HPF: high-poweredfield CI: chemotacticindex (No. of PMNs/HPF) BW: birth weight GA: gestational age
The chemotactic assays were performed in the course of infection and in the previous or subsequent infection-free periods. Heparinized blood (10 units/ml) (arterial or venous) was used. Informed consent was obtained from the parents. The CI was measured with a modified Boyden method using a special chamber which allows several assays simultaneously.~ The upper compartment was filled with 1 • l0 s dextran-separated and washed PMNs; the lower one with endotoxin-activated pooled serum. Results were reported as mean number of PMNs/ HPF obtained by the reading of 10 random fields after 120-minute incubation. Each sample was tested in triplicate. In addition, PMNs of normal adult and preterm infants were incubated in sera from septic patients to detect possible inhibitors. The whole set of tests required no more than 2 ml of blood. The t test was used for statistical evaluation.
Brief clinical and &boratory' observations
GROUP
2
GROUP
469
3
CELLS/HPF
,oou CELLS fHPF
:J +
60
i L I
40 20
before
durinr
after
SURFACE INFECTION
before during after PROVEN SEPSIS
Figure. Changes of the CI in infants of Groups 2 and 3 in consecutive periods with and without infection. When more than one determination was available in each period, the mean value has been reported. The cross indicates one death.
RESULTS In the five infants of Group 1, a total of 15 determinations was performed in the first ten days of life. Observed values ranged between 13 and 38 PMNs/HPF. The mean value of the C] (taking only one average value for each case) was 23 _+ 10 (SD), Similar values were obtained in Groups 2 and 3 during the infection-free periods (Group 2: mean 23 + 9, range 12 to 35; Group 3: mean 26_+ 13, range 10 to 42). In Group 2, during surface infections, the CI was markedly and significantly higher than in infection free periods (mean 85 • 30, range 45 to 120; P < 0.005). In sharp contrast, when sepsis occurred in infants of Group 3, the CI fell almost to zero (mean 2 _+ 2~ range 0 to 6; P < 0.005). The changes of the CI in individual cases are illustrated in the Figure. Sera from septic patients failed to affect chemotaxis of PMNs from normal adults and from noninfected preterm infants. COMMENT In preterm infants without infection the CI was similar to previous findings in term neonates, ~ corresponding to about 20% of the adult values. A greater number of observations would be needed to ascertain possible differences in newborn infants with very low BW and GA. In adults with acute bacterial infections PMN chemotaxis is usually enhanced ~. ~ and may become defective
470
B r i e f clinical and laboratory observatiotz~
only in overwhelming infection, ~ possibly because of marked endotoxemia. 7 In contrast, in the present series of preterm infants the enhancement of P M N chemotaxis was observed only in patients with superficial infections and without demonstrable bacteremia, whereas in patients with proven sepsis a striking fall of the CI was constantly demonstrated. Presumably, this finding was not due to the presence o f humoral factors, since no inhibitoryeffect was observed after incubation of PMNs from healthy preterm infants and adults in sera from preterm infants with proven sepsis. The complete inactivation of chemotaxis observed by us in septic preterm infants is additional and striking evidence of the functional inability of the neonatal PMN, consistent with previous studies? ~ ~ ~ The failure of this cellular defense mechanism may be, in part, responsible for the less favorable prognosis of neonatal infection, and may represent a rational basis for P M N tranfusion in infected nonleukopenic newborn infants? ~ These preliminary results suggest that the determination of the CI in preterm infants with clinical and laboratory signs of infection may help in the discrimination between patients with mild, localized infection and those with actual sepsis. REFERENCES
The Journal o f Pediatrics March 1980
2.
3.
4.
5.
6.
7. 8.
9.
10.
Klein RB, Fischer TJ, ~trd SE, et al: Decreased mononuclear and polymorphonuclear chemotaxis in human newborns~ infants and young children, Pediatrics 60:467, 1977. Laurenti F, Businco L, Barbato MB, et al: Familial defect of cellular chemotaxis: clinical and immunological effects of Levamisole therapy, Riv ltal Pediatr 4/6:571, 1978. Hill HR, Gerrard JM, Hogan NA, and Quie PG: Hyperactivity of neutrophil teukotactic responses during active bacterial infection, J Clin Invest 53:996, 1974. Mowat AG, and Baum J: Polymorphonuclear leukocyte chemotaxis in patients with bacterial infections, Br Med J 3:617, 1971. Clark RA: Disorders of granulocyte chemotaxis, in Gallin JI, and Quie PG, editors: Leukocyte chemotaxis: methods, physiology and clinical implications, New York, 1978, Raven Press, pp 329-356. Territo MC, and Golde DW: Granulocyte function in experimental human endotoxemia, Blood 47:539, 1976. Betlanti JA, Cautz BE, Yang MC, et al: Biochemical changes in human polymorphonuclear leukocytes during maturation, in Bellanti JA, and Dayton DH, editors: The phagocytic cell in host resistence, New York, 1975, Raven Press, pp 321-332. Anderson DC, Pickering LK, and Feigin RD: Leukocyte function in normal and infected neonates, J PEDIATR85:420, 1974. Laurenti F, La Greca G, Ferro R, and Bucci G: Transfusion of polymorphonuclear neutrophils in a premature infant with Klebsiella sepsis, Lancet 2 (8080):111, 1978.
1. Miller ME: Chemotactic function in the human neonate: humoral and cellular aspects, Pediatr Res 5:487, 1971.
Transient hyperamrnonemia in an early preterm infant Jean-Claude Le Guennec, M.D., Ijaz Aslam Qureshi, B.V.Sc., Ph.D., Harry Bard, M.D.,* Jean-Yves Siriez, M.D., and Jacques Letarte, M.D., Montreal, P.Q., Canada
HYPERAMMONEMIA as a consequence of an inherited defect of enzymes of the urea cycle can cause severe and fatal illness? Transient h y p e r a m m o n e m i a has recently been documented in preterm infants with very high levels of ammonia; these infants all had a characteristic neurologic depression? They were vigorously treated by either exchange transfusions or peritoneal dialysis, and four of five survived without apparent sequelae. We describe here the case of an early preterm newborn
From the Centre de Recherche Pkdiatrique and DOpartement de POdiatric, Universitb de Montrbal. *Reprint address: Service de Nkonatologie, Centre de Recherche Pkdiatrique, Hbpital Sainte-Justine, 3175 Chemin Sainte-Catherine, MontrOal, QuObec, Canada, H3T 1C5.
infant with h y p e r a m m o n e m i a m e m b r a n e disease.
and
severe
hyaline
CASE R E P O R T A 1,450 gm boy was born to a 22-year-old gravida 2, para 1 woman at 29 weeks of gestation. Respiratory distress developed very early after birth, requiring high concentrations of oxygen. Abbreviations used PRAGA: preterm infants of similar gestational age TAGA: term infants of appropriate gestational age The infant was transferred to our neonatal intensive care unit 21 hours after birth. The examination on arrival did not demonstrate a neurologic deficit. At 22 hours of age, because of deteriorating blood gas values, the infant required tracheal
0022-3476/80/030470+03500.30/0 9 1980 The C. V. Mosby Co.