Serious and early-onset of hyponatremia in severe asphyctic newborns: Questions

Excerpt

A female newborn weighing 2,820 g was born at 38 weeks’ gestation via cesarean section because of fetal distress and breech presentation. The emergency cesarean section was performed due to a nonreactive nonstress test and fetal bradyarrythmia. Apgar scores were 2 in the first minute and 6 in the fifth minute. The neonate was intubated at the delivery room and transferred to the Neonatal Intensive Care Unit (NICU). Umbilical vein catheterization was performed, and 50 cc /kg per day of fluid therapy, inotropic support, and whole-body cooling treatments were commenced. The physical examination in the first postnatal day was similar to that at birth, except the for presence of abdominal distension. Urine output was 1.3 ml/kg per hour; plasma sodium (129 mEq/l) and creatinine levels (2.3 mg/dl) were abnormal. Abdominal ultrasonography (US) demonstrated a mild increase in renal echogenity and ascites. Renal functions were closely monitored, and an appropriate fluid–electrolyte therapy was implemented. Urine output was monitored by placing a urinary catheter. Diagnostic paracentesis was performed. Biochemical investigation of the peritoneal fluid revealed the following: creatinine 17.2 mg/dl, sodium 65 mEq/l (Table 1). A second US examination was performed while sterile saline was instilled in the urinary bladder via a catheter (Fig. 1). A temporary Tenckhoff catheter was placed into the peritoneum, and peritoneal drainage was performed. Following this treatment approach, plasma creatinine levels returned to normal but the daily amount of peritoneal drainage did not decrease; plasma sodium was <120 mEq/l. The patient was operated upon on the third day of hospitalization, and a 3-mm ruptured area found on the upper and posterior bladder wall was sutured. After the operation, plasma sodium level rapidly improved within 12 h (131 mEq/l) without replacement therapy.

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