Risk factors for hypoxic-ischemic encephalopathy in asphyxiated newborn infants.

OBJECTIVE: To determine the risk factors for hypoxic-ischemic encephalopathy (HIE) in asphyxiated newborn infants. MATERIAL AND METHOD: A retrospective study of 17,706 newborns, who were admitted to the Neonatal Unit of King Chulalongkorn Memorial Hospital, from July 1999 till the end of December 2000. 84 infants with perinatal asphyxia were enrolled in the present study. All of the possible risk factors that might have contributed to asphyxia were identified and recorded HIE was diagnosed based on the Modified Sarnat-Sarnat Score for the diagnosis of neonatal encephalopathy. The clinical data of the HIE group were compared with those of the HIE negative group. The categorical data were analyzed for statistical significance (p < 0.05) by Chi-square test or Fisher exact test, or Student t-test. The odds ratio and 95% CI were calculated for those with statistical significance. Stepwise multiple logistic regression analysis used to determine the independent factors that may predispose an infant to HIE. RESULTS: Inappropriate antenatal care (OR 9.4; 95%CI: 2.6-35.4), post-term gestation (OR 7.4; 95%CI: 1.4-34.8), vacuum extraction (OR 5.4; 95%CI: 1.1-26.8), male (OR 4.8; 95%CI: 1.3-19.1), prolapsed cord (p = 0.01) and 1 and 5-minute Apgar scores, (p < 0.0001) were significant risk factors for HIE. However, by multiple regression analysis, only a 5-minute Apgar score was significantly associated with HIE (p = 0.001). CONCLUSION: Sophisticated or expensive equipment is not necessary for the treatment of HIE patient. HIE depends mainly on adequate and effective supportive strategy. The delivery of high risk pregnancies, under obstetric facilities and with appropriate intervention and with good neonatal resuscitation, may prevent the perinatal asphyxia and thereby minimize the occurring of HIE.

Peritubular capillary flow determines tubulointerstitial disease in idiopathic nephrotic syndrome.

The spatial relationship between renal perfusion and nephronal structure was determined in 51 nephrotic patients consisting of 11 patients with steroid sensitive, minimal change (MC) nephrosis, 12 patients with steroid resistant, mesangial proliferative (MesP) nephrosis and without tubulointerstitial fibrosis (TIF), 11 patients with steroid resistant, MesP nephrosis and with low grade TIF and 17 patients with focal segmental glomerulosclerosis (FSGS). The intrarenal hemodynamic study revealed a unique correlation between renal perfusion and nephronal structure. A normal or slight reduction in peritubular capillary flow observed in MC or mild MesP nephrosis correlates with an intact tubulointerstitial structure. A moderate reduction in peritubular capillary flow observed in steroid resistant, MesP nephrosis induces a low incidence of TIF. A severe reduction in peritubular capillary flow denotes a higher incidence of TIF as that observed in nephrosis with FSGS. Thus, it is of notion that the reduction in renal perfusion precedes the development of tubulo-interstitial fibrosis and thereby supports the concept of renal perfusion as a crucial determinant of nephronal structure.

Tubular function and tubulointerstitial disease.

Tubular transport determined by the fractional excretion (FE) of filtered solutes was studied in 129 nephrotic patients; 72 patients with mesangial proliferation (MesP-NS) and intact tubulointerstitium (group 1), 13 patients with MesP-NS and superimposed tubulointerstitial fibrosis (TIF; group 2), 27 patients with mild focal segmental glomerulosclerosis (FSGS; group 3), and 17 patients with severe FSGS (group 4). In the 72 nephrotic patients with MesP-NS and normal tubulointerstitium (no TIF), tubular transport was intact (FE of sodium [FENa], 0.5 +/- 0.5; FE of calcium [FECa], 0.3 +/- 0.3; FE of phosphate [FEPO4], 14 +/- 13; FE of uric acid [FEUA], 9.8 +/- 5; FE of magnesium [FEMg], 1.3 +/- 0.5). In the 13 nephrotic patients with MesP-NS and superimposed TIF (4.9% +/- 2%), there was no difference in FE solutes from those in group 1 except for FEMg (3.3 +/- 0.9; P < 0.001). In the 27 nephrotic patients with mild FSGS (TIF, 28% +/- 9%), four of five variables of FE solutes (FENa, 1.2 +/- 0.7; P < 0.001; FECa, 0.9 +/- 0.8; P < 0.001; FEPO4, 17 +/- 12; P, not significant; FEUA, 16.5 +/- 8; P < 0.001; FEMg, 4. 1 +/-1; P < 0.001) were significantly different from those of patients with MesP-NS without TIF, and two of five variables (FECa, FEMg) were statistically different from those of patients with MesP-NS with TIF. In the severe category of FSGS (TIF, 69% +/-19%), all FE solutes were statistically different from the other groups (FENa, 4.8 +/- 3; FECa, 2 +/- 1; FEPO4, 47 +/- 24; FEUA, 37 +/- 18; FEMg, 12 +/- 6). Thus, the results imply that (1) normal tubular transport reflects an underlying intact tubulointerstitial structure, whereas tubular dysfunction indicates an underlying tubulointerstitial disease, and (2) FEMg is the most sensitive index to detect an early abnormality of tubular structure and function.