Cerebral salt-wasting syndrome

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Cerebral salt-wasting syndrome (CSWS) is a disease featuring hyponatremia (low blood sodium levels) and dehydration in response to disease processes in or surrounding the brain.

Differentiating Cerebral Salt-Wasting Syndrome from other Diseases

It may be difficult to distinguish CSWS from the syndrome of inappropriate antidiuretic hormone (SIADH), which develops under similar circumstances and also presents with hyponatremia.

The main clinical difference between these two conditions is that of total fluid status of the patient: CSWS leads to a relative or overt hypovolemia, whereas SIADH is consistent with a normal to hypervolemic patient. ^[1]

Another useful point in differentiating CSWS from SIADH is a laboratory finding: random urine sodium concentrations tend to be >100 mEq/L in CSWS. SIADH rarely, if ever, leads to a random urine sodium of >100 mEq/L.

Cerebral salt-wasting syndrome must be differentiated from other causes of headache, polyuria and polydypsia.

Disease	Causes	Symptoms	Diagnosis and treatment
SIADH	SIADH is a syndrome characterized by excessive release of antidiuretic hormone (ADH or vasopressin) from the posterior pituitary gland or another source. The result is hyponatremia, and sometimes fluid overload	Nausea / vomiting Cramps Depressed mood Irritability Confusion Hallucinations Seizures, stupor or coma	Hyponatremia <135 mmol/l Effective serum osmolality<275mosm Urine sodium concentration>40mmol/litre Plasma uric acid <200;FeUrate>12% Absence of edematous disease likecardiac failure, liver cirrhosis,nephrotic syndrome. Normal adrenal and thyroid function
Cerebral salt wasting syndrome	Cerebral salt wasting syndrome is defined as therenal loss of sodium during intracranial disease leading to hyponatremia and a decrease in extracellular fluid volume Trauma Tumor Hematoma	The patient is Hypovolemic Hyponatremic	Treatment is Hydration and Sodium replacement
Adrenal insufficiency	Adrenal insufficiency Mineralocorticoid deficiency is present. Secondary or tertiary adrenal insufficiency will have preservedmineralocorticoid function owing to separate feedback mechanisms Adrenal insufficiency can be Primary Secondary Tertiary Common causes of primary adrenal insufficiency: Autoimmune Iatrogenic Drugs Adrenal hemorrhage Cancer Infection Congenital Secondary adrenal insufficiency: ( Aldosterone) levels normal Most common causes are: Traumatic brain injury (TBI) Panhypopituitarism Tertiary adrenal insufficiency Exogenoussteroid administration is the most common cause of tertiary adrenal insufficiency	Fatigue Muscle weakness Loss of appetite Weight loss Abdominal pain Diarrhea Vomiting Chronic disease is characterized by Weight loss Sparse axillary hair Hyperpigmentation Orthostatic hypotension. Acute addisonian crisis is characterized by: Fever Hypotension	The diagnosis of Addisons disease is made through rapid ACTH administration and measurement of cortisol. Lab findings include: White blood cell count with moderate neutropenia Lymphocytosis Eosinophilia Hyperkalemia Hypoglycemia Hyponatremia Morning low plasma cortisol. The definitive diagnosis is the cosyntropin or ACTH stimulation test. Acortisol level is obtained before and after administering ACTH. A normal person should show a brisk rise in cortisol level after ACTH administration. Management: The management of Addison disease involves: Gluocorticoid Mineralocorticoid Sodium chloride replacement. Adrenal crisis: In adrenal crisis,measure cortisol level,then rapidly administer Fluids Hydrocortisone
Hypopituitarism	Abnormality in anterior pituitary function Etiology is as follows: Pituitary tumors Sellar tumors Head trauma Infection Empty sella Infiltration Idiopathic Congenital	Signs and symptoms ofhypopituitarism vary, depending on the deficient hormone and severity of the disorder,some of the symptoms may be as follows: Fatigue Weight loss Decreased libido Decreased appetite Facial puffiness Anemia Infertility Cold insensitivity. Amenorrha Inability to lactate in breast feeding women Decreased facial orbody hair in men Short stature in children	History andphysical examination, including visual field testing, are important. The treatment of permanent hypopituitarism consists of replacement of the peripheral hormones Hydrocortisone DHEA Thyroxine Testosterone or oestradiol Growth hormone Surgery and/or Radiotherapy to restore normal endocrine function and quality of life Life long monitoring of serum hormone levels and symptoms of hormone deficiency or excess is needed in these patients
Hypothyroidism	Hypofunctioning of the thyroid gland due to multifactorial etiology ranging from congenital to autoimmune causes described below: Congenital Autoimmune Drugs Post surgery Post radiation Infiltrative e.g., amyloid	Fatigue Constipation Dry skin Weight gain Cold intolerance Puffy face Hoarseness Muscle weakness Elevated blood cholesterol level Bradycardia Myopathy Depression Impaired memory	Diagnosis of hypothyroidism is based on blood tests: T3(triiodothyronine) T4(Thyroxine) and TSH (thyroid stimulating hormone). Signs and symptoms are neither sensitive nor specific for the diagnosis. TSH is the most sensitive tool for screening,diagnosis and treatment follow up, whenpituitary is normal. The drug of choice for treatment is Levothyroxine
Psychogenic polydipsia	Also called as primary polydipsia is characterized bypolyuria and polydipsia. Causes are: Adverse effect of a medication Traumaticbrain injury Psychiatric disorders such as schizophrenia Defect in the hypothalamus	Polyuria Polydipsia Confusion Lethargy Psychosis Seizures and Sometimes, even death	Evaluation ofpsychiatric patients with polydipsia requires an evaluation for other medical causes of polydipsia, polyuria,hyponatremia, and the syndrome of inappropriate secretion of antidiuretic hormone. The management strategy inpsychiatric patients should include: Fluid restriction andbehavioral and pharmacologic modalities. The water deprivation test is the gold standard test

References

↑ Harrigan MR (1996). “Cerebral salt wasting syndrome: a review”. Neurosurgery. 38 (1): 152–60. PMID 8747964.

Treatment

The reason for the abnormality is different in CSWS and SIADH, so treatments are opposites: fluid restriction is used in SIADH, which would worsen cerebral salt wasting. Instead, CSWS is treated with fluids and correction of the low sodium.

Pharmacotherapy

Sometimes, fludrocortisone (a mineralocorticoid) improves the hyponatremia.^[1]

References

↑ Betjes MG (2002). “Hyponatremia in acute brain disease: the cerebral salt wasting syndrome”. Eur J Intern Med. 13 (1): 9–14. PMID 11836078.

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[pmid8747964-1] Harrigan MR (1996). “Cerebral salt wasting syndrome: a review”. Neurosurgery. 38 (1): 152–60. PMID 8747964.

[pmid11836078-2] Betjes MG (2002). “Hyponatremia in acute brain disease: the cerebral salt wasting syndrome”. Eur J Intern Med. 13 (1): 9–14. PMID 11836078.

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Cerebral salt-wasting syndrome

Overview

Differentiating Cerebral Salt-Wasting Syndrome from other Diseases

References

Treatment

Pharmacotherapy

References

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