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Postoperative, prolonged and refractory cerebral salt wasting syndrome (CSWS) after severe head trauma - what should we do?


Pavelescu, D.; Dumitrascu, M.; Luca, Vasiliu I.; Mirea, L.; Grintescu, I.

European Journal of Anaesthesiology (EJA): June 2013 - Volume 30 - Issue - p 199–199
Intensive Care Medicine

Emergency Clinical Hospital of Bucharest, Dept of Anaesthesiology & Intensive Care, Bucharest, Romania

Background: CSWS usually devellops in the first week following brain insult and is defined by extracellular volume depletion due to excessive natriuresis in patients with intracranial disease; its duration is usually brief but it can last for several months

Case report: A 74 years old woman was admitted in ICU for polytrauma with multiple fractures (femoral, humeral, pelvic, rib fractures) and severe head trauma; the brain CT scan on admission showed subarachnoidal haemorrhage and temporal bone fracture At 3 p.o. days (femoral+humeral osteosynthesis) she developped progressive headaches, deteriorated consciousness and vomiting refractory to medical treatment.

Biochemical: Plasmatic Na level 98-102 mmol/l, glucose, blood urea, creatininenormal value, NT-proBNP 890 pg/ml, ADH< 2 ng/ml.

Urinary: Na level 180 mmol/l, osmolality 720 mosm/kgH2O, uric acid 399 mg/24 hours.

No hystory of hyponatremia, no medication-related hyponatremia, adrenal and thyroid functions tests-normal.

Clinically: Hypovolemia, high urinary output.

The diagnosis of CSWS was made; the clinical course was uneventful.

The treatment include NaCl molar (1 mmol/ml) supplementation, volume replacement therapy, methylprednisolon 32 mg/day.

Discharge day 62 with plasmatic Na 138 mmol/l, no i.v. Na supplementation. A second hit 2 weeks after discharge, conservative treatment with NaCl tablets, 1 gr NaCl each 4-6 hours.





Discussion: Traumatic brain injury may severely impair brain function; neuroendocrine dysfunction is an important complication Most TBI-associated hyponatremia are mild and asymptomatic, but in severe cases the differential diagnosis CSWS/SIADH, also difficult to make, is decisive for the treatment options.

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1. Sherlock M, O'Sullivan E, Agha A, et al. The incidence and pathophysiology of hyponatraemia after subarachnoid haemorrhage. Clin Endocrinol (Oxf) 2006;64(3):250-4
2. Vespa P. Cerebral salt wasting after traumatic brain injury: an important critical care treatment issue. Surg Neurol 2008;69(3):230-2

Learning points: The CSWS related hyponatremia had a prolonged and difficult recovery; till now there are few data concerning the therapeutic approach of chronic CSWS, requiring new research.

© 2013 European Society of Anaesthesiology