Cerebral salt-wasting syndrome: Difference between revisions

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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.
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.
{| class="wikitable"
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Disease
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Causes
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Symptoms
! align="center" style="background:#4479BA; color: #FFFFFF;" + |Diagnosis and treatment
|- Diagnostic criteria of SIADH include:
|[[SIADH]]
|[[SIADH]] is a syndrome characterized by excessive release of [[Vasopressin|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 malnutrition|edematous]] disease like[[ cardiac failure]], [[liver cirrhosis]],[[ nephrotic syndrome]].
*Normal [[adrenal]] and [[thyroid]] function
|-
|[[Cerebral salt wasting syndrome]]
|[[ Cerebral salt wasting syndrome]] is defined as the[[ renal]] loss of [[sodium]] during [[Intracranial Bleeding|intracranial]] [[disease]] leading to [[hyponatremia]] and a decrease in extracellular [[fluid]] volume
*[[Trauma]]
*[[Tumor]]
*[[Hematoma]]
|The patient is
*[[Hypovolemic]]
*[[Hyponatremia|Hyponatremic]]
|Treatment is
*[[Hydration]] and
*[[Sodium]] replacement
|-
|[[Adrenal insufficiency]]
|[[Adrenal insufficiency]]
* [[ Mineralocorticoid deficiency]] is present. [[Secondary]] or [[tertiary adrenal insufficiency]] will  have preserved[[ mineralocorticoid]] 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 gland|adrenal]] insufficiency: ( [[Aldosterone]]) levels normal
*Most common causes are:
*[[Traumatic brain injury (TBI) ]]
*[[Panhypopituitarism]] 
*Tertiary [[Adrenal gland|adrenal]] insufficiency
*Exogenous[[ steroid]] 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. A[[ cortisol]] 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 gland|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]] of[[ hypopituitarism]] 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]] or[[ body hair]] in men
* [[Short stature]] in children
|
* [[History]] and[[ physical examination]], including [[visual field]] testing, are important.
The [[Treatment-resistant depression|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 competence|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 Skin|sensitive]] tool for [[Screening (medicine)|screening]],diagnosis and [[Treatment-resistant depression|treatment]] follow up, when[[ pituitary]] is normal.
*The [[drug]] of choice for treatment is [[Levothyroxine]]
|-
|[[Psychogenic polydipsia]]
| Also called as primary [[polydipsia]] is characterized by[[ polyuria]] and [[polydipsia]]. Causes are:
*Adverse effect of a [[medication]]
*Traumatic[[ brain]] injury
*[[Psychiatric]] disorders such as [[schizophrenia]]
* Defect in the [[hypothalamus]]
|
*[[Polyuria]]
*[[Polydipsia]]
*[[Confusion]]
*[[Lethargy]]
*[[Psychosis]]
*[[Seizures]] and
*Sometimes, even death
|Evaluation of[[ psychiatric]] 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 in[[ psychiatric]] patients should include:
*[[Fluid]] restriction and[[ behavioral]] and [[pharmacologic]] modalities.
*The water deprivation test is the [[gold standard]] test
|}
==References==
{{Reflist|2}}


==Treatment==
==Treatment==
The reason for the abnormality is different, and 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.  
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.<ref name="pmid11836078">{{cite journal |author=Betjes MG |title=Hyponatremia in acute brain disease: the cerebral salt wasting syndrome |journal=Eur J Intern Med |volume=13 |issue=1 |pages=9–14 |year=2002 |pmid=11836078 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0953620501001923}}</ref>
Sometimes, [[fludrocortisone]] (a [[mineralocorticoid]]) improves the hyponatremia.<ref name="pmid11836078">{{cite journal |author=Betjes MG |title=Hyponatremia in acute brain disease: the cerebral salt wasting syndrome |journal=Eur J Intern Med |volume=13 |issue=1 |pages=9–14 |year=2002 |pmid=11836078 |doi= |url=http://linkinghub.elsevier.com/retrieve/pii/S0953620501001923}}</ref>



Latest revision as of 00:27, 4 October 2017

Cerebral salt-wasting syndrome
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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
  • Urine sodium concentration>40mmol/litre
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 The patient is Treatment is
Adrenal insufficiency Adrenal insufficiency

Adrenal insufficiency can be

Common causes of primary adrenal insufficiency:

Chronic disease is characterized by

Acute addisonian crisis is characterized by:

The diagnosis of Addisons disease is made through rapid ACTH administration and measurement of 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:

Adrenal crisis:

Hypopituitarism Abnormality in anterior pituitary function

Etiology is as follows:

Signs and symptoms ofhypopituitarism vary, depending on the deficient

hormone and severity of the disorder,some of the symptoms may be as follows:

The treatment of permanent hypopituitarism consists of replacement of the peripheral hormones

Hypothyroidism Hypofunctioning of the thyroid gland due to multifactorial etiology ranging from congenital to autoimmune causes described below: Diagnosis of hypothyroidism is based on blood tests:
Psychogenic polydipsia Also called as primary polydipsia is characterized bypolyuria and polydipsia. Causes are: 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:


References

  1. 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

  1. 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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