In spite of advances in neonatal surgery, the mortality rate from diaphragmatic hernia (DH) remains high. Infants with the early onset of symptoms are at greatest risk and die of hypoxia in spite of successful repair of the defect. The objective of this study was to determine the incidence and to identify factors leading to hypoxemia and death in these infants. Of 21 infants born with DH in our hospital during the last 7 years, 13 had respiratory distress from birth. Nine (70%) of these 13 infants had persistent fetal circulation (PFC) which terminated in death in 6 (46%) infants. PFC was characterized by elevated right atrial pressure, hypoxemia in the descending aorta in spite of inhalation of 100% oxygen and evidence for right-to-left shunt at atrial or ductal levels. In patients who died, progressive hypoxemia and metabolic acidosis were accompanied by severe peripheral vasoconstriction, poor skin perfusion and systemic hypertension. In this study, PFC was the major cause of death in infants with DH. PFC occurred commonly and exclusively in infants whose symptoms were present at birth. Unless PFC is recognized early and reversed by vigorous treatment, the infants will die as a result of progressive hypoxemia and metabolic acidosis.

Effective treatment of cardiogenic shock (CS) as a result of severe perinatal asphyxia (PA) in preterm infants is dependent on its early recognition and differentiation from RDS. Four preterm infants weighing 1240-2300 g., G.A. 32-34 wks., who had abnormal fetal heart rate pattern and acidosis, developed CS shortly after birth. All were severely depressed at birth and required prolonged resuscitation. ECG, heart rate (HR) and variability, aortic pressure (ABP), right atrial pressure (RAP), core and toe-skin temperatures, arterial blood gases, glucose, calcium, and lactic acid (LA) were measured in all. Respiratory failure requiring assisted ventilation, tachycardia, decreased HR variability, hypotension, elevated RAP, decreased toe and core temperatures, markedly elevated LA and alveolo-arterial oxygen gradients were noted in each shortly after birth. Initial chest radiographs revealed cardiomegaly and diffuse alveolar and interstitial edema. One infant improved spontaneously while 3 infants required iso-proterenol infusion in the first 6 hours. One infant died of persistent CS while 2 infants responded dramatically showing reversal of abnormal findings listed above, enabling discontinuation of assisted ventilation within 24 hours. This data suggests that severe PA may result in myocardial dysfunction leading to CS in preterm infants. Although presentation of CS resembles HMD, it can be differentiated by chest X-rays, elevated RAP and markedly elevated LA. Early use of isoproterenol can reverse severe heart failure leading to rapid recovery.

A prospective study was undertaken to determine if urinary LDH isoenzyme assays could differentiate site of infection in patients with urinary tract infection. Thirty children, with a mean age of 6.1 years (23 female and 7 male), were assigned to control, cystitis or pyelonephritis categories based on clinical, laboratory and radiologic criteria. LDH isoenzyme concentrations were measured by a thin film agarose electrophoresis (Pol-E-Stret, Pfizer Co.) and expressed as % of I, II, III, IV and V. Of the 10 controls, one had isoenzyme IV and V in 1.2% and 2.3% concentrations. Of 11 patients with cystitis, one had isoenzyme IV and V in 2.6% and 1.3% concentrations. However, in all 9 patients with pyelonephritis, there was a significant percentage concentration of LDH IV (13.8 ± 8.08) and V (15.1 ± 9.8) activity in the urine. It was concluded that patients with pyelonephritis had significant concentrations of LDH IV and V iso-enzymes in their urine, unlike normal children or those with cystitis. The source of these enzymes is postulated to be the renal parenchyma itself as modified by the disease process. The diagnosis of site of infection could be made by measuring LDH isoenzyme IV and V concentration in all the patients with urinary tract infection.