scholarly journals Acute Hyponatraemia Secondary to Cerebral Salt Wasting Syndrome in a Patient with Tuberculous Meningitis

1998 ◽  
Vol 26 (4) ◽  
pp. 420-423 ◽  
Author(s):  
L. K. Ti ◽  
S. C. Kang ◽  
K. F. Cheong

A 30-year-old HIV-positive man presented with acute hydrocephalus secondary to tuberculous meningitis, for which an external ventricular drain was inserted. He developed marked natriuresis in the postoperative period, which resulted in acute hyponatraemia (131 to 122 mmol/l) and a contraction of his intravascular volume. A diagnosis of cerebral salt wasting syndrome was made, and he responded to sodium and fluid loading. This case highlights the differentiation of cerebral salt wasting syndrome from the more commonly occurring syndrome of inappropriate anti-diuretic hormone secretion as the aetiology of the hyponatraemia.

2005 ◽  
Vol 59 (3) ◽  
pp. 306
Author(s):  
Ja Young Lee ◽  
Eun Sil Lee ◽  
Jae Hyong Lee ◽  
Eun Ju Lim ◽  
Hyoung Su Kim ◽  
...  

2004 ◽  
Vol 23 (9) ◽  
pp. 884-886 ◽  
Author(s):  
Shih-Ming Huang ◽  
Chu-Chin Chen ◽  
Pao-Chin Chiu ◽  
Ming-Fang Cheng ◽  
Ching-Lan Chiu ◽  
...  

2016 ◽  
Vol 03 (03) ◽  
pp. 205-210 ◽  
Author(s):  
Harshal Dholke ◽  
Ann Campos ◽  
C. Reddy ◽  
Manas Panigrahi

AbstractTraumatic brain injury (TBI) is on the rise, especially in today’s fast-paced world. TBI requires not only neurosurgical expertise but also neurointensivist involvement for a better outcome. Disturbances of sodium balance are common in patients with brain injury, as the central nervous system plays a major role in sodium regulation. Hyponatraemia, defined as serum sodium <135 meq/L is commonly seen and is especially deleterious as it can contribute to cerebral oedema in these patients. Syndrome of inappropriate antidiuretic hormone secretion (SIADH), is the most well-known cause of hyponatraemia in this subset of patients. Cerebral Salt Wasting Syndrome (CSWS), leading to renal sodium loss is an important cause of hyponatraemia in patients with TBI. Although incompletely studied, decreased renal sympathetic responses and cerebral natriuretic factors play a role in the pathogenesis of CSWS. Maintaining a positive sodium balance and adequate hydration can help in the treatment. It is important to differentiate between SIADH and CSWS when trying to ascertain a case for patients with acute brain injury, as the treatment of the two are diametrically opposite.


1996 ◽  
Vol 135 (2) ◽  
pp. 245-247 ◽  
Author(s):  
Stephen L Atkin ◽  
Anne Marie Coady ◽  
Michael C White ◽  
Bruce Mathew

Atkin SL, Coady AM. White MC, Mathew B. Hyponatraemia secondary to cerebral salt wasting syndrome following routine pituitary surgery. Eur J Endocrinol 1996;135:245–7. ISSN 0804–4643 A female aged 53 years was found to have a suprasellar lesion, which was shown to be a Rathke's cyst after removal by transsphenoidal surgery. She presented 16 days postoperatively, and following two grand mal seizures was found to be profoundly hyponatraemic (sodium 101 mmol/l). She was initially thought to have the syndrome of inappropriate antidiuretic hormone and was treated accordingly, but central venous pressure measurement revealed the hypovolaemia of cerebral salt wasting syndrome. The patient subsequently developed severe neurological sequelae after the correction of her hyponatraemia, following the development of extrapontine myelinolysis. Cerebral salt wasting syndrome is a rare cause of hyponatraemia following pituitary transsphenoidal surgery, which may mimic the syndrome of inappropriate antidiuretic hormone secretion. This case emphasizes the poor prognosis that may result from the rapid correction of profound hyponatraemia. SL Atkin, Michael White Centre for Diabetes and Endocrinology, Royal Hull Hospitals, 220-236 Anlaby Road, Hull HU3 2RW, UK


2018 ◽  
Author(s):  
Lea Orlik ◽  
Reto Venzin ◽  
Thomas Fehr ◽  
Karin Hohloch

Abstract Background: Cerebral salt wasting (CSW) is a rare metabolic disorder with severe hyponatremia and volume depletion usually caused by brain injury like trauma, cerebral lesion, tumor or a cerebral hematoma. The renal function is normal with excretion of very high amounts of sodium in the urine. Diagnosis is made by excluding other reasons for hyponatremia, mainly the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Case report: A 60-year-old patient was admitted to the emergency room with pain in the upper abdomen and visual disturbance two weeks after knee replacement. The patient was confused with severe hematoma at the site of the knee endoprosthesis. Laboratory values showed massive thrombocytosis, leukocytosis, anemia, severe hyponatremia and no evidence of infection. CT scan of the abdomen was inconspicuous. Head MRI showed no ischemia or bleeding, but a mild microangiopathy. A myeloproliferative neoplasm (MPN) was suspected and confirmed by bone marrow biopsy. Cerebral salt wasting syndrome was identified as the cause of severe hyponatremia most likely provoked by cerebral microcirculatory disturbance. The hematoma at the operation site was interpreted as a result of a secondary von Willebrand syndrome (vWS) due to the myeloproliferative neoplasm with massive thrombocytosis. After starting cytoreductive therapy with hydroxycarbamide, thrombocytosis and blood sodium slowly improved along with normalization of his mental condition. Conclusion: To the best of our knowledge this is the first description of a patient with CSW most likely caused by a microcirculatory disturbance due to a massive thrombocytosis in the context of a myleopoliferative neoplasm. Key words: Cerebral salt wasting syndrome, hyponatremia, myeloproliferative syndrome


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