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Iatrogenic severe hypernatraemia is a rare medical condition that may follow sodium overload such as after intravenous infusion of hypertonic saline, topical application of salt over burned areas, peritoneal irrigation with hypertonic solution during dialysis or complication of hydatic cyst rupture.1 It has been demonstrated that in both rats and humans, severe hypernatraemia may produce central pontine or extrapontine myelinolis and neuronal damage with an elusive pathogenetic mechanism. Different factors may affect the development of these brain lesions, such as age, patient preclinical conditions, level and duration of hypernatraemia and rapidity of its onset.1 2 The majority of patients exposed to severe hypernatraemia undergo major neurological complications including convulsive seizures, coma and death. Some patients survive with neurological sequelae.1
Here we report on a patient who acutely developed an extreme hypernatraemia, with serum sodium concentration of 200 mmol/l, due to peritoneal lavage with hypertonic saline solution after hydatid cyst rupture, yielding status epilepticus and coma. MRI detected cerebral lesions distributed along the limbic system network. A suggested hypothesis for the regional selective vulnerability of hypernatraemia-induced brain damage is discussed.
We report on a 58-year-old-woman who underwent laparoscopic excision of a hydatid cystic liver mass of 11 cm in diameter. She had a past medical history of alcohol abuse and was affected by type 2 diabetes, low-grading hepatitis C liver cirrhosis. The laparoscopic intervention was complicated by the intraperitoneal cyst rupture, followed by …
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