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Hyponatraemia and death or permanent brain damage in healthy children

Arieff, A. I. ; Ayus, J. C. ; Fraser, C. L.

BMJ, 1992-05, Vol.304 (6836), p.1218-1222 [Periódico revisado por pares]

England: British Medical Journal Publishing Group

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  • Título:
    Hyponatraemia and death or permanent brain damage in healthy children
  • Autor: Arieff, A. I. ; Ayus, J. C. ; Fraser, C. L.
  • Assuntos: Adolescent ; Adults ; Autopsy ; Brain ; Brain damage ; Brain Damage, Chronic - etiology ; Brain edema ; Child ; Child health services ; Child, Preschool ; Children ; Electrolytes ; Female ; Humans ; Hyponatremia ; Hyponatremia - complications ; Hyponatremia - epidemiology ; Hyponatremia - mortality ; Male ; Pediatrics ; Prognosis ; Prospective Studies ; Retrospective Studies ; Sodium ; Time Factors
  • É parte de: BMJ, 1992-05, Vol.304 (6836), p.1218-1222
  • Notas: PMID:1515791
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  • Descrição: OBJECTIVE--To determine if hyponatraemia causes permanent brain damage in healthy children and, if so, if the disorder is primarily limited to females, as occurs in adults. DESIGN--Prospective clinical case study of 16 affected children and a review of 24,412 consecutive surgical admissions at one medical centre. PATIENTS--16 children (nine male, seven female; age 7 (SD 5) years) with generally minor illness were electively hospitalised for primary care. Consultation was obtained for the combination of respiratory arrest with symptomatic hyponatraemia (serum sodium concentration less than or equal to 128 mmol/l). MAIN OUTCOME MEASURES--Presence, gender distribution, and classification of permanent brain damage in children with symptomatic hyponatraemia in both prospective and retrospective studies. RESULTS--By retrospective evaluation the incidence of postoperative hyponatraemia among 24,412 patients was 0.34% (83 cases) and mortality of those afflicted was 8.4% (seven deaths). In the prospective population the serum sodium concentration on admission was 138 (SD 2) mmol/l. From three to 120 inpatient hours after hypotonic fluid administration patients developed progressive lethargy, headache, nausea, and emesis with an explosive onset of respiratory arrest. At the time serum sodium concentration was 115 (7) mmol/l and arterial oxygen tension 6 (1.5) kPa. The hyponatraemia was primarily caused by extrarenal loss of electrolytes with replacement by hypotonic fluids. All 16 patients had cerebral oedema detected at either radiological or postmortem examination. All 15 patients not treated for their hyponatraemia in a timely manner either died or were permanently incapacitated by brain damage. The only patient treated in a timely manner was alive but mentally retarded. CONCLUSIONS--Symptomatic hyponatraemia can result in high morbidity in children of both genders, which is due in large part to inadequate brain adaptation and lack of timely treatment.
  • Editor: England: British Medical Journal Publishing Group
  • Idioma: Inglês
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