Severe hypernatremia in a hospitalized child: munchausen by proxy

Abstract

An 8-week-old infant presented to a referring institution with profuse diarrhea and infectious enteritis for 1 week. He was initially treated for suspected Salmonella spp. sepsis and meningitis, because the organism was found in the stool, but the child's illness progressed, manifested by paroxysmal profuse diarrhea and increased urine output. After several weeks, he suffered a sagittal venous thrombosis and intracranial hemorrhage. Subsequently the child was transferred to a tertiary center for intestinal evaluation. The patient's diarrhea and excessive diuresis resolved, and his sodium normalized soon after transfer. Four days later, however, after his mother arrived, he immediately developed severe hypernatremia (serum sodium concentration [Na(+)] = 214 mEq/L), with resumption of diarrhea and excessive diuresis. A gastric aspirate during the crisis demonstrated an extremely high sodium content, [Na(+)] = 1416 mEq/L, consistent with salt intoxication. Surveillance of the mother revealed that she manipulated the indwelling nasogastric tube; confronted, she admitted to salt administration. This case describes one of the ways that Munchausen syndrome by proxy can manifest with profound neurologic sequelae, and highlights the need for close observation and swift intervention when sufficient cause is present.

Figure 1

MRI image of end-stage brain injury that resulted from (i) seizure at presentation, (ii) sagital venous thrombosis and (iii) hemorrhagic transformation of stroke. It is possible that wide fluctuations of serum sodium observed at the outside institution and our own contributed to the evolution of the brain injury observed.

Figure 2

Temporal profile of serum sodium concentration (lower line graph) and serum osmolality (upper line graph) through 15 days of admission at our institution.