Biomedical subjects
Publications and source records attributed to E T Bowe.
Leprosy occurs rarely in women of reproductive age. Until this report, the treatment of leprosy with dapsone has not been associated with any adverse fetal or neonatal side effects. We have reported what we believe to be the first case of neonatal hyperbilirubinemia after maternal dapsone therapy for leprosy.
Theca lutein cysts are benign neoplasms known to be associated with twins, molar pregnancy and erythroblastosis fetalis, but they are only rarely associated with a normal singleton pregnancy. Their natural course is postpartum spontaneous regression. Documented cases were noted because of abdominal pain or dystocia. This paper reports theca lutein cysts which were asymptomatic and were first noted ultrasonographically in a singleton gestation at term. In a few published cases and in a larger number of unpublished cases, apparent confusion as to the benign nature of these cysts has led to unwarranted bilateral oophorectomy. Asymptomatic theca lutein cysts undoubtably occur more commonly than they are reported. With the increasing use of ultrasonography and cesarean section, this condition probably will be observed more frequently in the future. At the time of laparotomy in late pregnancy with ovaries which appear pathological, tissue biopsy and evaluation is of critical importance in order to avoid unnecessary castration in this group of young women.
The role of the fetal kidney during impairment of placental exchange was studied in eight fetal lambs, intact in utero; a standard asphyxial insult for a period of 1 hour was produced by occluding the umbilical cord sufficiently to lower the fetal heart rate by 35 +/- 5 beats/min and the pH by 0.15 units. This asphyxial stress caused a fall in urine output from a control of 0.17 to 0.03 ml/kg/min and of glomerular filtration rate from 1.2 to 0.3 ml/min; release of the occlusion was followed by mild diuresis. The fall in urine output was accompanied by a rise in total primary solutes including concentrations of electrolytes; this rise continued for 1 to 2 hours following the release of the occlusion. Because of the low urinary output during the period of occlusion, there was a fall in excretion of electrolyte; an increase in net acid excretion occurred only after the release of the cord. These experiments show that, although the fetal kidney is capable of contributing to elimination of acid following compression of the cord, there may be an associated net loss of water and electrolytes.
Response of the fetal kidney to metabolic acidosis was studied in five fetal lambs, 115-125 days gestation, in order to evaluate the renal contribution to elimination of hydrogen ion during intra-uterine development. Experiments were conducted on healthy unanesthetized fetuses, intact in utero, with catheters implanted at hysterotomy into a fetal femoral artery and vein and into the bladder via the urachus, four or more days prior to the study. A metabolic acidosis was induced by infusion of isotonic lactic acid, 15 m mole/kg, intravenously over a period of 90 minutes. Serial arterial samples were taken and urine collected in fractions before, during and for three hours following the infusion, for measurements of pH, bicarbonate, lactate and electrolytes as well as urine output. During the infusion, urine pH fell from 6.65 to 6.25 and was 6.34 three hours later (Figs. 1 to 4, Tabs. III to IV). Lactic acid infusion caused a prompt increase in urine output from a mean rate of 0.12 to a maximum of 0.28 ml/kg/min at the end of the infusion, returning to control rates three hours later. Lactate excretion increased from 0.05 to a maximum of 4.6 mumole/kg/min at the end of infusion; titratable acid increased from 0.22 to a maximum of 4 muEq/kg/min; the rates of excretion of lactate and titratable acid were still higher than control at the end of three hours. Ammonia excretion increased from 0.21 to a maximum of 0.56 muEq/kg/min three hours after the end of infusion. The acid infusion caused a small but significant fall in excretion of bicarbonate. During the 90 minutes of infusion and over the following three hours, about 800 mumole lactate was excreted while net acid excretion over the same period was no more than half that amount. The diuresis was also accompanied by a net loss of sodium and chloride, the excretion of these ions increasing more than threefold following acid infusion; excretion of potassium decreased to one-third its rate prior to the infusion. During the 90 minutes of infusion, blood pH fell from 7.36 to 7.13, base deficit rose from 3.8 to 16.4 mEq/L and lactate rose from 2.2 to 14.8 mM/L; there was also a small but significant rise in both blood PCO2 and PO2 (Figs. 1 to 2, Tabs. I to II). During the following three hours of recovery, pH rose gradually to 7.29, base deficit and lactate fell to 7.4 mEq/L and 8.7 mM/L respectively. Since renal excretion of net acid and lactate was small, the decrease in blood base deficit and lactate levels during the recovery must therefore be mainly due to equilibration in various fetal compartments as well as placental transfer. These experiments indicate that, in the lamb fetus, intact in utero, the kidney although limited by immaturity of several mechanisms, is capable of responding to an acid load and thus can make a small contribution to fetal homeostasis. The increase in excretion of net acid is accompanied by loss of sodium and chloride in the urine.
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