© 2024 JETIR February 2024, Volume 11, Issue 2 www.jetir.

org (ISSN-2349-5162)

A rare case of cerebral salt wasting syndrome

Dr Mohd Shahzad Shaikh1 Dr Mudassir Ansari1 Dr Shaikh Ashar1 Dr M Kulkarni1 2
From the Department of Medicine JIIUS IIMSR Medical College and Noor Hospital Jalna-431201
Maharashtra
INTRODUCTION

Hypotonic hyponatremia linked to hypovolemia that can result in hypovolemia is the enigmatic condition known as CWS. Renal sodium
loss of cerebral origin can be attributable to subarachnoid hemorrhage (SAH) and neuro-meningeal tuberculosis infection but can also result
from any form of cerebral aggressiveness. The syndrome of inappropriate antidiuretic hormone secretion (SIADH) is a disease that can also
account for hyponatremia following cerebral aggressiveness, making the diagnosis challenging. Given the treatment differences between the
two, differentiation between the two entities is still necessary.

In this article, we report the case of a patient admitted with headache, altered sensorium and loss of power in whom the diagnosis of CWS
was made secondary to cerebrovascular accident.

CASE PRESENTATION

We report the case of 60 year old patient with history of Diabetes and Hypertension for 10 years non-compliant to medication came to
emergency department with complaints of loss of power, altered sensorium and headache while assessing neurological deficit were present.
On physical examination there was decrease in consciousness with GCS E2M3V2 with the poor orientation to time, place and person On
admission BP was 110/70 heart rate was 100 beats per minute respiratory rate was 20 per minute patient Temperature was 36.1 SPO2 was
98% at room air and random blood sugar was 156 mg/dl.MRI Brain suggestive of frontal lobe temporal lobe infarct involving MCA territory
patient was admitted in ICU and Intubated to prevent aspiration and anti-platelets were started at the time of admission Sodium 115 serum
osmolality 260 mosm/l.

Hyponatremia was thought to be caused by dehydration. She was treated with 3% NS to correct her sodium level. Sodium level came back
to Normal.

On 7th day patient successfully extubated and patient regain consciousness and there was no deterioration of neurological status. Throughout
the 7 day of the admission in the ICU electrolytes were normal Urine output were around 3500 and input were 3000 and patient does not
show any sign of hyponatremia. Serum electrolytes and urine output were regularly monitored,10th day of admission blood pressure were
falling, and patient started complaining of hiccups. Further deterioration of the neurological conditions was noted. Serum sodium was found
to ben to be 115.Urine output was 5000 ml no change in the medication during mean time. Clinically patient was hypovolemic and not any
other significant history or life history that will cause recurrent hyponatremia not identifying and after the correction of the hyponatremia
the hypotension is also resolved. The potential causes of hyponatremia in this case were looked for SIADH was kept as differential cerebral
salt wasting syndrome was also considered because of history describing stroke other causes like hypothyroidism and adrenal insufficiency
rule out.

Day1 Day 4 Day 7 Day 10 Day 12 Day 14

Serum sodium 135 140 139 125 129 139
Serum potassium 4.0 4.1 4.2 4.0 3.9 4.6
Serum chloride 96 99 102 105 102 112
Ph 7.44 7.33 7.32 7.40 7.55 7.40
Hco3 24.0 25.0 24.0 21.0 23.0 22.0

JETIR2402147 Journal of Emerging Technologies and Innovative Research (JETIR) www.jetir.org b429
© 2024 JETIR February 2024, Volume 11, Issue 2 www.jetir.org (ISSN-2349-5162)

Pco2 43 45 39 42 40 41
Urine output ml 2900 3200 3400 4600 5600 3400

DISCUSSION

CSWS is defined as hyponatremia and decreased extracellular fluid volume brought on by intracranial illnesses that cause renal salt loss. In
the setting of multi spectrum CNS pathology most notably due to aneurysmal subarachnoid bleeding. In this case report we attempted to
demonstrate the correlation between stroke cerebrovascular disease and the rare presentation of CSWS. Differential diagnosis of
hyponatremia are central diabetes insipidus, SIADH , CSWS, adrenal insufficiency and hypothyroidism .All other causes were carefully
excluded .According to one theory brain natriuretic peptide is released after traumatic brain injury and acts on the collecting duct of the renal
tubule preventing sodium reabsorption and renin release another theory is that due to hypothalamic injury the sympathetic nerve system no
longer stimulates sodium absorption and renin release

The most important differential diagnosis of CSWS is SIADH as both present with hypotonic hyponatremia urine sodium more than 40 and
hyperuricemia However there fundamental difference lie in volume status urine output and serum urea level it is essential to differentiate
CSWS from its close ally that is SIADH as the treatments are opposite

CONCLUSION

We provide a case report of a 60-year-old female patient with CSWS; the exact mechanism by which intracranial illness induces CSWS
remains unclear. The primary goals of The two theories are depicted below

The most important differential diagnosis of CSWS is SIADH as both present with hypotonic hyponatremia urine sodium more than 40 and
hyperuricemia However there fundamental difference lie in volume status urine output and serum urea level it is essential to differentiate
CSWS from its close ally that is SIADH as the treatments are opposite

JETIR2402147 Journal of Emerging Technologies and Innovative Research (JETIR) www.jetir.org b430
© 2024 JETIR February 2024, Volume 11, Issue 2 www.jetir.org (ISSN-2349-5162)

CONCLUSION

We provide a case report of a 60-year-old female patient with CSWS; the exact mechanism by which intracranial illness induces CSWS
remains unclear. The primary goals of management are to replace ongoing urinary sodium loss with intravenous hypertonic saline solutions
and correct intravascular volume depletion using 0.9% sodium chloride and hyponatremia. Fludrocortisone/mineralocorticoid, which acts
directly on the renal tubules to increase sodium reabsorption, demonstrated a positive response in CSW.

CONFLICT OF INTEREST

We declare that there were no conflicts of interest in this study.

REFERENCES

1. Cerebral salt wasting syndrome. Harrigan MR. Crit Care Clin. 2001;17:125–138. [PubMed] [Google Scholar]

2. Causes and management of hyponatremia. Palmer BF, Gates JR, Lader M. Ann Pharmacother. 2003;37:1694–1702. [PubMed] [Google
Scholar]

3. Analysis of factors associated with hiccups based on the Japanese Adverse Drug Event Report database. Hosoya R, Uesawa Y, Ishii-
Nozawa R, Kagaya H. PLoS One. 2017;12:0. [PMC free article]

4.Bouchlarhem A, Haddar L, Berrichi H, Jabri M, Lachhab A, El houda Lamassab N, et al. Cerebral Salt Wasting Syndrome (CSW): An
unusual cause of hypovolemia a er spontaneous cerebral hemorrhage successfully treated with udrocortisone. Radiol Case Reports.
2022;17(1).

5. Mehta V, Sharma A, Sharma CB, Guria RT. Cerebral salt wasting induced hyponatraemia presenting as catatonia Clinical. J R Coll
Physicians Edinb. 2021;51(4)

JETIR2402147 Journal of Emerging Technologies and Innovative Research (JETIR) www.jetir.org b431