Serious and early onset of hyponatremia in severe asphyctic newborns: answers

The common characteristics, symptoms, and signs in both cases are: They were both born via cesarean section because of fetal distress, both had severe perinatal asphyxia, both needed resuscitation, both were exposed to a severe hypotensive period, both had neonatal ascites, and both had severe and early onset hyponatremia.

Urinary ascites. The current diagnostic work-up of patients with neonatal ascites consists of ultrasonography and paracentesis. The biochemical analysis of the ascites fluid should confirm the diagnosis of its origin; creatinine, urea nitrogen, and potassium concentrations are higher than the plasma levels [1]. In our cases, simultaneous plasma and ascites chemistry showed that creatinine concentrations of the ascites fluid were higher than the plasma creatinine concentrations, and the sodium concentrations of the ascites fluid were lower than those of the plasma, indicating urinary ascites in both cases.

Figure 1 shows the posterolateral wall defect at the fundus of the bladder. Figure 2 confirms the transition of the contrast agent into the peritoneum from the posterior wall defect at the fundus of the bladder during the retrograde cystography.

Asphyxia is defined as a combination of hypoxemia, hypercapnia, and metabolic acidosis. More importantly, severe asphyxia is associated with ischemic adverse effects on one or more organs. Spontaneous non-obstructive rupture of the bladder may occur as a result of hypoxia and hypotension, signifying that the bladder fundus vascular circulation is sensitive to ischemia. In both our cases, rupture of the bladder occurred in the posterior fundus. This region is known to be very sensitive to ischemia and circulatory disorders, and is the anatomical region where spontaneous non-obstructive bladder rupture is most frequently seen [2]. Very much like the situation in our cases, in the literature, urinary ascites-associated hyponatremia usually displays acute onset (< 48 h) and is also generally severe. The explanation for this electrolyte abnormality is based on the peritoneal surface’s highly efficient semipermeable dialysis membrane properties, resulting in a state of autodialysis.

Clarke et al.’s explanation [3] was: The intraperitoneal urine and the extracellular fluid will equilibrate as a result of diffusion of water and solutes based on osmolality differences and concentration gradients. High urine osmolality will cause a shift of water into the peritoneal cavity. Sodium is a solute with a lower concentration in the urine than the plasma and this concentration gradient will move sodium from the plasma into the urine. Following this decrease in plasma and renal tubular sodium concentrations, the renin–angiotensin–aldosterone system is activated and increased tubular sodium reabsorption and decreased urinary sodium concentration occurs. This urine with a lower sodium concentration will then pass into the peritoneal cavity and result in further lowering of plasma sodium.