Syndrome of inappropriate antidiuretic hormone differential diagnosis: Difference between revisions

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==Differentiating Syndrome of inappropriate antidiuretic hormone from other Diseases==
==Differentiating Syndrome of inappropriate antidiuretic hormone from other Diseases==
[[SIADH]] must be differentiated from [[cerebral salt wasting]], [[ adrenal insufficiency]], [[hypopituitarism]], [[hypothyroidism]], [[psychogenic polydipsia]]<ref name="pmid27936532">{{cite journal |vauthors=Heidelbaugh JJ |title=Endocrinology Update: Hypopituitarism |journal=FP Essent |volume=451 |issue= |pages=25–30 |year=2016 |pmid=27936532 |doi= |url=}}</ref><ref name="pmid15241506">{{cite journal |vauthors=Hammer F, Arlt W |title=[Hypopituitarism] |language=German |journal=Internist (Berl) |volume=45 |issue=7 |pages=795–811; quiz 812–3 |year=2004 |pmid=15241506 |doi=10.1007/s00108-004-1216-5 |url=}}</ref><ref name="pmid25712898">{{cite journal |vauthors=de Fost M, Oussaada SM, Endert E, Linthorst GE, Serlie MJ, Soeters MR, DeVries JH, Bisschop PH, Fliers E |title=The water deprivation test and a potential role for the arginine vasopressin precursor copeptin to differentiate diabetes insipidus from primary polydipsia |journal=Endocr Connect |volume=4 |issue=2 |pages=86–91 |year=2015 |pmid=25712898 |pmc=4401105 |doi=10.1530/EC-14-0113 |url=}}</ref>
[[SIADH]] must be differentiated from cerebral salt wasting, [[ adrenal insufficiency]], [[hypopituitarism]], [[hypothyroidism]], and [[psychogenic polydipsia]]<ref name="pmid27936532">{{cite journal |vauthors=Heidelbaugh JJ |title=Endocrinology Update: Hypopituitarism |journal=FP Essent |volume=451 |issue= |pages=25–30 |year=2016 |pmid=27936532 |doi= |url=}}</ref><ref name="pmid15241506">{{cite journal |vauthors=Hammer F, Arlt W |title=[Hypopituitarism] |language=German |journal=Internist (Berl) |volume=45 |issue=7 |pages=795–811; quiz 812–3 |year=2004 |pmid=15241506 |doi=10.1007/s00108-004-1216-5 |url=}}</ref><ref name="pmid25712898">{{cite journal |vauthors=de Fost M, Oussaada SM, Endert E, Linthorst GE, Serlie MJ, Soeters MR, DeVries JH, Bisschop PH, Fliers E |title=The water deprivation test and a potential role for the arginine vasopressin precursor copeptin to differentiate diabetes insipidus from primary polydipsia |journal=Endocr Connect |volume=4 |issue=2 |pages=86–91 |year=2015 |pmid=25712898 |pmc=4401105 |doi=10.1530/EC-14-0113 |url=}}</ref>
   
   
{| class="wikitable"
{| class="wikitable"
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|[[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.
|[[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]]
*[[Nausea]] / [[vomiting]]
*[[Cramps]]
*[[Cramps]]
*[[Depressed mood]]
*[[Depressed mood]]
*[[Irritability]]
*[[Irritability]]
*[[Confusion]]
*[[Confusion]]
*[[ Hallucinations]].
*[[ Hallucinations]]
*[[Seizures]] ,[[stupor]] or [[coma ]]
*[[Seizures]] ,[[stupor]] or [[coma ]]
|
|
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|The patient is
|The patient is
*[[Hypovolemic]]  
*[[Hypovolemic]]  
*[[Hyponatremic]].
*[[Hyponatremia|Hyponatremic]]


|Treatment is with adequate  
|Treatment is with adequate  
*[[Hydration]] and
*[[Hydration]] and
*[[Sodium]] replacement.
*[[Sodium]] replacement
|-
|-
|[[Adrenal insufficiency]]
|[[Adrenal insufficiency]]
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*[[Orthostatic hypotension]].
*[[Orthostatic hypotension]].


Acute [[addisonian]] crisis is characterized by :
Acute [[addisonian]] crisis is characterized by:
*[[Fever]]  
*[[Fever]]  
*[[ Hypotension]].
*[[ Hypotension]]  
|The diagnosis of [[Addisons]] disease is made through rapid [[ACTH]] administration and measurement of [[cortisol]].
|The diagnosis of [[Addisons]] disease is made through rapid [[ACTH]] administration and measurement of [[cortisol]].
*Lab findings include:
*Lab findings include:
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* Decreased [[facial]] or[[ body hair]] in men
* Decreased [[facial]] or[[ body hair]] in men
* [[Short stature]] in children
* [[Short stature]] in children
|The diagnosis is based on detailed investigation of symptoms of target endocrine gland function relative to the corresponding pituitary[[ hormone]] deficiency. The clinical manifestations of[[ hypopituitarism]] result from the degree of the specific hormone [[deficiency]].
|The diagnosis is based on detailed investigation of symptoms of target endocrine gland function relative to the corresponding pituitary[[ hormone]] deficiency  
The clinical manifestations of[[ hypopituitarism]] result from the degree of the specific hormone [[deficiency]]
A thorough and longitudinal [[history]] and[[ physical examination]], including [[visual field]] testing, are important.
A thorough and longitudinal [[history]] and[[ physical examination]], including [[visual field]] testing, are important.
Hypopituitarism may involve from one to all endocrine axes regulated by the pituitary
Hypopituitarism may involve from one to all endocrine axes regulated by the pituitary
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*[[ Growth hormone]]
*[[ Growth hormone]]
*[[Surgery]] and/or
*[[Surgery]] and/or
*[[ Radiotherapy]] to restore normal [[endocrine]] function and quality of life.
*[[ Radiotherapy]] to restore normal [[endocrine]] function and quality of life
*Patients with hypopituitarism require lifelong monitoring of serum hormone levels and symptoms of hormone deficiency or excess.
*Patients with hypopituitarism require lifelong monitoring of serum hormone levels and symptoms of hormone deficiency or excess  
*Long-term care and monitoring of patients with hypopituitarism requires a experienced [[endocrinologist]].
*Long-term care and monitoring of patients with hypopituitarism requires a experienced [[endocrinologist]]
|-
|-
|[[Hypothyroidism]]
|[[Hypothyroidism]]
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*Signs and symptoms are neither [[sensitive]] nor [[specific]] for the diagnosis.  
*Signs and symptoms are neither [[sensitive]] nor [[specific]] for the diagnosis.  
*TSH is the most sensitive tool for screening,diagnosis and treatment follow up, when[[ pituitary]] is normal.  
*TSH is the most sensitive tool for screening,diagnosis and treatment follow up, when[[ pituitary]] is normal.  
*The drug of choice for treatment is [[Levothyroxine]].
*The drug of choice for treatment is [[Levothyroxine]]
|-
|-
|[[Psychogenic polydipsia]]  
|[[Psychogenic polydipsia]]  
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*[[Psychosis]]
*[[Psychosis]]
*[[Seizures]] and
*[[Seizures]] and
*Sometimes, even [[Death]].
*Sometimes, even death
|Evaluation of[[ psychiatric]] patients with polydipsia warrants a comprehensive evaluation for other medical causes of polydipsia, polyuria,[[ hyponatremia]], and the syndrome of inappropriate secretion of antidiuretic hormone.  
|Evaluation of[[ psychiatric]] patients with polydipsia warrants a comprehensive 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:
*The management strategy in[[ psychiatric]] patients should include:


*[[Fluid]] restriction and[[ behavioral]] and [[pharmacologic]] modalities.  
*[[Fluid]] restriction and[[ behavioral]] and [[pharmacologic]] modalities.  
*The [[water deprivation test]] is the [[gold standard]] test.
*The [[water deprivation test]] is the [[gold standard]] test
|}
|}



Revision as of 20:47, 24 August 2017

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Vindhya BellamKonda, M.B.B.S [2]

Overview

SIADH consists ofhyponatremia, inappropriately elevatedurine osmolality, excessive urine sodium and decreased serum osmolality in a euvolemic patient without edema. These findings should occur in the absence of diuretic treatment with normal cardiac, renal, adrenal, hepatic and thyroid function.Hyponatremia occurs in about 30% of hospitalized patients and SIADH is the most frequent cause of hyponatremia. Differentiating hyponatremia due to SIADH from other causes of hyponatremia becomes essential to evaluate the treatment plan. Syndrome of inappropriate antidiuretic hormone must be differentiated from cerebral salt wasting , adrenal insufficiency, hypopituitarism, hypothyroidism,psychogenic polydipsia

Differentiating Syndrome of inappropriate antidiuretic hormone from other Diseases

SIADH must be differentiated from cerebral salt wasting, adrenal insufficiency, hypopituitarism, hypothyroidism, and psychogenic polydipsia[1][2][3]

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.
  • 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. The patient is Treatment is with adequate
Adrenal insufficiency Adrenal insufficiency ranges from mild nonspecific symptoms to life-threatening shock like condition.

An important distinction in these patients is the presence ofmineralocorticoid deficiency. Those with secondary or tertiary adrenal insufficiency will typically have preservedmineralocorticoid function due to the separate feedback systems. Adrenal insufficiency can be

Tertiary 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 Hypopituitarism is defined as the partial or complete loss of anterior pituitary function that can result from acquired or congenital causes.

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 diagnosis is based on detailed investigation of symptoms of target endocrine gland function relative to the corresponding pituitaryhormone deficiency

The clinical manifestations ofhypopituitarism result from the degree of the specific hormone deficiency A thorough and longitudinal history andphysical examination, including visual field testing, are important. Hypopituitarism may involve from one to all endocrine axes regulated by the pituitary In order of frequency: growth hormone deficiency>secondary hypogonadism>secondary hypothyroidism>secondary adrenal failure). 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:
  • 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 asprimary polydipsia is characterized bypolyuria and polydipsia. Causes are: Evaluation ofpsychiatric patients with polydipsia warrants a comprehensive 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. Heidelbaugh JJ (2016). "Endocrinology Update: Hypopituitarism". FP Essent. 451: 25–30. PMID 27936532.
  2. Hammer F, Arlt W (2004). "[Hypopituitarism]". Internist (Berl) (in German). 45 (7): 795–811, quiz 812–3. doi:10.1007/s00108-004-1216-5. PMID 15241506.
  3. de Fost M, Oussaada SM, Endert E, Linthorst GE, Serlie MJ, Soeters MR, DeVries JH, Bisschop PH, Fliers E (2015). "The water deprivation test and a potential role for the arginine vasopressin precursor copeptin to differentiate diabetes insipidus from primary polydipsia". Endocr Connect. 4 (2): 86–91. doi:10.1530/EC-14-0113. PMC 4401105. PMID 25712898.


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