scholarly journals Cerebral salt wasting in a case of tubercular meningitis in a child

2017 ◽  
Vol 4 (6) ◽  
pp. 2217
Author(s):  
Kapil Bainade ◽  
V. Kotrashetti ◽  
Vijay Sonwane ◽  
Rizwan Ahmed ◽  
Prashant Abusaria
Keyword(s):  
Serum Sodium ◽  
Hormone Secretion ◽  
Final Diagnosis ◽  
Total Leukocyte Count ◽  
Fluid Restriction ◽  
Communicating Hydrocephalus ◽  
Cerebral Salt Wasting ◽  
Meningeal Enhancement ◽  
Inappropriate Antidiuretic Hormone Secretion ◽  
Salt Wasting

A 12-year-old female child presented with fever, headache, vomiting since 20 days and convulsions for 1 day. She was unimmunised and BCG scar was absent. Clinical examination showed signs of meningeal irritation, Kernigs sign and Brudzinkins sign with signs of raised intracranial tension. Fundus examination was suggestive of stage 2 papilledema. Her laboratory reports were normal on admission. LP was with hold in view of raised ICT. CT brain was done. S/O meningeal enhancement, mild communicating hydrocephalus with periventricular ooze, extra axial hyper densities in bilateral sylvian fissures along the tentorium (Basal Exudates) On day 3 of admission she had low serum sodium, serum osmolality High urinary sodium. While on lumbar puncture (LP) and cerebrospinal fluid (CSF) examination, CSF protein, and total leukocyte count (predominant lymphocytes) were all increased. On his 5th day of admission, her serum sodium was low and he had a normal urine output. Fluid restriction was tried in order to rule out syndrome of inappropriate antidiuretic hormone secretion (SIADH) but the patient did not respond to it. Keeping in view the above findings, a final diagnosis of tuberculous meningitis leading to cerebral salt wasting syndrome was made. The patient was started on anti-tuberculous therapy (ATT), IV Steroids, anticonvulsants, 3% NaCl and supportive treatment, to which she responded favourably and was later discharged. 

scholarly journals Hyponatremia in Acute Stroke Patients: Pathophysiology, Clinical Significance, and Management Options

2019 ◽  
Vol 82 (1-3) ◽  
pp. 32-40 ◽  
Author(s):  
George Liamis ◽  
Fotios Barkas ◽  
Efstathia Megapanou ◽  
Eliza Christopoulou ◽  
Andromachi Makri ◽  
...  
Keyword(s):  
Acute Stroke ◽  
Sodium Level ◽  
Hormone Secretion ◽  
Fluid Restriction ◽  
Hypertonic Solution ◽  
Stroke Patients ◽  
Volume Depletion ◽  
Management Options ◽  
Cerebral Salt Wasting ◽  
Inappropriate Antidiuretic Hormone Secretion

Background: Hyponatremia is frequent in acute stroke patients, and it is associated with worse outcomes and increased mortality. Summary: Nonstroke-related causes of hyponatremia include patients’ comorbidities and concomitant medications, such as diabetes mellitus, chronic kidney disease, heart failure, and thiazides. During hospitalization, “inappropriate” administration of hypotonic solutions, poor solute intake, infections, and other drugs, such as mannitol, could also lower sodium levels in patients with acute stroke. On the other hand, secondary adrenal insufficiency due to pituitary ischemia or hemorrhage, syndrome of inappropriate antidiuretic hormone secretion, and cerebral salt wasting are additional stroke-related causes of hyponatremia. Although it is yet unclear whether the appropriate restoration of sodium level improves outcomes in patients with acute stroke, the restoration of the volume depletion remains the cornerstone of treatment in hypovolemic hyponatremia. In case of hyper- and euvolemic hyponatremia, apart from the correction of the underlying cause (e.g., withdrawal of an offending drug), fluid restriction, administration of hypertonic solution, loop diuretics, and vasopressin-receptor antagonists (vaptans) are among the therapeutic options. Key Messages: Hyponatremia is frequent in patients with acute stroke. The plethora of underlying etiologies warrants a careful differential diagnosis which should take into consideration comorbidities, concurrent medication, findings from the clinical examination, and laboratory measurements, which in turn will guide management decisions. However, it is yet unclear whether the appropriate restoration of sodium level improves outcomes in patients with acute stroke.

scholarly journals Cerebral salt wasting in a patient with myeloproliferative neoplasm

2019 ◽  
Author(s):  
Lea Orlik ◽  
Reto Venzin ◽  
Thomas Fehr ◽  
Karin Hohloch
Keyword(s):  
Hormone Secretion ◽  
Myeloproliferative Neoplasm ◽  
Visual Disturbance ◽  
Mental Condition ◽  
Microcirculatory Disturbance ◽  
Volume Depletion ◽  
Severe Hyponatremia ◽  
Cerebral Salt Wasting ◽  
Inappropriate Antidiuretic Hormone Secretion ◽  
Salt Wasting

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 myeloproliferative neoplasm.

scholarly journals Cerebral salt wasting in a patient with myeloproliferative neoplasm

2019 ◽  
Author(s):  
Lea Orlik ◽  
Reto Venzin ◽  
Thomas Fehr ◽  
Karin Hohloch
Keyword(s):  
Hormone Secretion ◽  
Myeloproliferative Neoplasm ◽  
Volume Depletion ◽  
Severe Hyponatremia ◽  
Cerebral Salt Wasting ◽  
Inappropriate Antidiuretic Hormone Secretion ◽  
Salt Wasting ◽  
Cerebral Hematoma ◽  
Very High ◽  
Rare Metabolic Disorder

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).

scholarly journals Cerebral salt wasting in a patient with myeloproliferative neoplasm

2019 ◽  
Author(s):  
Lea Orlik ◽  
Reto Venzin ◽  
Thomas Fehr ◽  
Karin Hohloch
Keyword(s):  
Hormone Secretion ◽  
Myeloproliferative Neoplasm ◽  
Volume Depletion ◽  
Severe Hyponatremia ◽  
Cerebral Salt Wasting ◽  
Inappropriate Antidiuretic Hormone Secretion ◽  
Salt Wasting ◽  
Cerebral Hematoma ◽  
Very High ◽  
Rare Metabolic Disorder

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).

Subarachnoid Hemorrhage

2018 ◽  
pp. 44-53
Author(s):  
Sherry Hsiang-Yi Chou
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Complex Disease ◽  
Hormone Secretion ◽  
Delayed Cerebral Ischemia ◽  
Early Brain Injury ◽  
Neurogenic Pulmonary Edema ◽  
Cerebral Salt Wasting ◽  
Inappropriate Antidiuretic Hormone Secretion ◽  
Salt Wasting ◽  
Wasting Syndrome

Subarachnoid hemorrhage (SAH) affects over 30,000 Americans per year, leaves over half of its survivors in severe disability, and has a mortality rate of approximately 20%. SAH syndrome presents with a complex disease course and symptoms involving both the central nervous system (CNS) as well as extra-CNS systems. SAH may lead to early brain injury, cerebral vasospasm, and delayed cerebral ischemia, which increases SAH morbidity and mortality. SAH-related extra-CNS organ injuries include neurogenic stunned myocardium, neurogenic pulmonary edema, syndrome of inappropriate antidiuretic hormone secretion, cerebral salt wasting syndrome, systemic inflammatory response syndrome, fever, and venous thromboembolism, all of which require careful critical care management. Though multiple randomized trials in the recent years have not successfully identified any effective neuroprotective therapy in SAH, the overall SAH outcome has significantly improved over the past two decades.

scholarly journals Syndrome of inappropriate antidiuretic hormone secretion and cerebral salt wasting as the common causes of hyponatremia in tertiary care hospital

2020 ◽  
Vol 7 (4) ◽  
pp. 577
Author(s):  
Yogesh Pralhad Bade ◽  
Harishchandra Rameshchandra Chaudhari
Keyword(s):  
Antidiuretic Hormone ◽  
Tertiary Care ◽  
Hormone Secretion ◽  
Cerebral Salt Wasting ◽  
Common Cause ◽  
Inappropriate Antidiuretic Hormone Secretion ◽  
Salt Wasting ◽  
Antidiuretic Hormone Secretion ◽  
Common Causes ◽  
The Common

Background: Hyponatremia is a typical condition of electrolyte disturbance that may be euvolemic, hypovolemic or hypervolemic. Proper interpretation through laboratory tests helps to differentiate the types and causes of hyponatremia. This study was conducted to evaluate the syndrome of inappropriate antidiuretic hormone secretion (SIADH) and cerebral salt wasting (CSW) as the common causes of hyponatremia in tertiary care hospital.Methods: A prospective interventional study was conducted, including hyponatremia cases, admitted in NTU/ICU/CCU and other medical wards at Ruby Hall Clinic from August 2011 to December 2013.Results: Of 150 patients enrolled in this study, 33.33% patients were euvolemic, 34% patients were hypervolemic and 32.66% patients were hypovolemic. For the euvolemic patients, SIADH (68%) was the most common cause; whereas, CSW (34.39%) was the common cause for hypovolemic type of hyponatremia. Stroke was found to be the most common cause of SIADH (55.88%), Intra-cerebral bleeding was observed to be the most common causative factor between SIADH and CSW associated hyponatremia.Conclusions: Hyponatremia in central nervous system disorder patients frequently occurred due to SIADH and CSW. Most common cause of SIADH was stroke and for CSW it was intra cerebral bleed.

scholarly journals Mechanism, spectrum, consequences and management of hyponatremia in tuberculous meningitis

2019 ◽  
Vol 4 ◽  
pp. 189
Author(s):  
Usha K. Misra ◽  
Jayantee Kalita ◽  
Keyword(s):  
Natriuretic Peptide ◽  
Serum Sodium ◽  
Venous Pressure ◽  
Border Zone ◽  
Rapid Decline ◽  
Fluid Restriction ◽  
Cerebral Salt Wasting ◽  
Salt Wasting ◽  
Inappropriate Secretion ◽  
V2 Receptor

Hyponatremia is the commonest electrolyte abnormality in hospitalized patients and is associated with poor outcome. Hyponatremia is categorized on the basis of serum sodium into severe (< 120 mEq/L), moderate (120-129 mEq/L) and mild (130-134mEq/L) groups. Serum sodium has an important role in maintaining serum osmolality, which is maintained by the action of antidiuretic hormone (ADH) secreted from the posterior pituitary, and natriuretic peptides such as atrial natriuretic peptide and brain natriuretic peptide. These peptides act on kidney tubules via the renin angiotensin aldosterone system. Hyponatremia <120mEq/L or a rapid decline in serum sodium can result in neurological manifestations, ranging from confusion to coma and seizure. Cerebral salt wasting (CSW) and syndrome of inappropriate secretion of ADH (SIADH) are important causes of hyponatremia in tuberculosis meningitis (TBM). CSW is more common than SIADH. The differentiation between CSW and SIADH is important because treatment of one may be detrimental for the other; evidence of hypovolemia in CSW and euvolemia or hypervolemia in SIADH is used for differentiation. In addition, evidence of dehydration, polyuria, negative fluid balance as assessed by intake output chart, weight loss, laboratory evidence and sometimes central venous pressure are helpful in the diagnosis of these disorders. Volume contraction in CSW may be more protracted than hyponatremia and may contribute to border zone infarctions in TBM. Hyponatremia should be promptly and carefully treated by saline and oral salt, while 3% saline should be used in severe hyponatremia with coma and seizure. In refractory patients with hyponatremia, fludrocortisone helps in early normalization of serum sodium without affecting polyuria or functional outcome. In SIADH, V2 receptor antagonist conivaptan or tolvaptan may be used if the patient is not responding to fluid restriction. Fluid restriction in SIADH has not been found to be beneficial in TBM and should be avoided.

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