Hyponatremia causes: Difference between revisions

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{{Hyponatremia}}
{{Hyponatremia}}
{{CMG}}
{{CMG}}; {{AE}} {{Saeedeh}}
==Overview==
Hyponatremia is caused by either increase [[ADH]] action/ secretion or kidney function impairment. [[SIADH|SIAD]] is the most common cause of euvolemic hyponatremia. After [[SIAD]], [[polydipsia]], [[drugs]] and clinical disorders are the most encountered etiologies in clinical practice.


==Causes==
==Causes==
[[Image:Hyponatraemia Causes.png|left|thumb|400px|Causes of hyponatraemia]]  
'''''To review the mechanisms of developing hyponatremia, click [[Hyponatremia pathophysiology#Pathophysiology|here]].'''''<small>
An abnormally low plasma sodium level is best considered in conjunction with the person's plasma [[osmolarity]] and [[extracellular fluid]] volume status.
* '''<big>Etiologies of SIAD:</big>'''
{| class="wikitable"
! colspan="2" |'''<big>Conditions</big>'''
|-
!<big>Malignant disorders</big>
|'''Carcinoma:''' Lung ( [[small cell carcinoma]], [[mesothelioma]]), oropharynx, stomach, duodenum, pancreas, ureter, bladder, prostate, endometrium, [[thymoma]]
 
'''Lymphomas'''
 
'''Sarcomas:''' [[Ewing's sarcoma]]
 
'''Olfactory neuroblastoma'''
|-
!<big>Pulmonary diseases</big>
|'''Infections:''' [[Bacterial pneumonia]], [[viral pneumonia]], [[pulmonary abscess]], [[tuberculosis]], [[aspergillosis]]
 
'''Others:''' [[Asthma]], [[cystic fibrosis]], [[respiratory failure]], [[emphysema]], [[COPD]],[[coronavirus]] disease, positive-pressure ventilation
|-
!<big>CNS disorders</big>
|'''Infections:''' Encephalitis, meningitis, brain abscess, [[RMSF]], [[AIDS]], [[malaria]]
 
'''Vascular and SOP:''' [[Subarachnoid hemorrhage]], [[stroke]], [[brain tumors]], [[head trauma]]
 
'''Others:''' [[Hydrocephalus]], [[cavernous sinus thrombosis]], [[Multiple sclerosis]], Guillain–Barré syndrome, Shy–Drager syndrome,
 
[[delirium tremens]], [[Acute intermittent porphyrias|acute intermittent porphyria]], chronic psychosis, pituitary stalk section, transsphenoidal adenomectomy
|-
!<big>Other causes</big>
|'''Hereditary:''' Gain-of-function mutation of V2 receptors
'''Idiopathic'''
 
'''[[#Drugs cause hyponatremia|Drugs]]'''
 
'''Transient:''' [[Exercise]], [[general anesthesia]], nausea, pain, stress
|}
<br>
* Causes of '''<big>acute hyponatremia:</big> '''  (develops in < 48 hrs)
{| class="wikitable"
!Etiology
|-
|
* Post operative phase
* Transurethral or endoscopic procedure (mannitol, sorbitol, glycine)
* Colonoscopy preparation 
* Polydipsia
* Exercise
* Oxytocin
* Cyclophosphamide
* Ecstasy( 3,4-Methylenedioxymethamphetamine, MDMA)
* Thiazide
* Halopridol
* Recently started desmopressin, terlipressin, vasopressin
|}
<small>( Etiologies that cause hyperacute and acute hyponatremia are applicable to each category interchangeably depending on the onset of symptoms)</small>
<br>
* Causes of '''<big>Hyponatremia</big>''' based upon '''Serum Osmolality:'''
{| class="wikitable"
!Classification
!Serum Osmolality
!Etiology
|-
|'''<big>Hypertonic or Isotonic Hyponatremia</big>'''
|> 295 mOsm/kg
|[[Hyperglycemia]]<sup>‡</sup>, [[Mannitol]], [[Glycine]], [[Maltose]], severe [[azotemia]]  
|-
|'''<big>Isotonic Hyponatremia</big>'''
'''(Pseudohyponatremia)'''
|275 – 295 mOsm/kg
|Lab/blood draw error, Post TURP (bladder irrigation with osmotic solutions),
intravenous immunoglobulin (IVIg), Hyperlipidemia ( triglyceride, cholesterol ),
 
hyper paraproteinemia (monoclonal gammopathy of undetermined significance (MGUS),
 
multiple myeloma),
|-
|'''<big>Hypotonic Hyponatremia</big>'''
|< 275 mOsm/kg
|[[Glycerol]], [[Sorbitol]], Etiology depends upon volume status (Hypervolemic/ Euvolemic/ Hypovolemic)
|-
| colspan="3" |<small>[[Alcohol]], [[Urea]], Ethylen glycol  are ineffective osmoles, cause hyperosmolar isotonic serum but not hyponatremia.</small>
|}
<small>‡ Hyperglycemia causes osmotic diuresis results in a rise in serum  sodium concentration, on the other hand it leads to extracellular shift of water due to osmotic gradient which causes relative hyponatremia , depends on which effect is stronger, there would be hypertonicity or hypotonicity<ref>{{Cite journal
 
| author = [[A. I. Arieff]] & [[H. J. Carroll]]
 
| title = Nonketotic hyperosmolar coma with hyperglycemia: clinical features, pathophysiology, renal function, acid-base balance, plasma-cerebrospinal fluid equilibria and the effects of therapy in 37 cases


Most cases of hyponatremia are associated with reduced [[plasma osmolarity]]. In fact, the vast majority of adult cases are due to increased [[vasopressin]], i.e., [[anti-diuretic hormone]] (ADH). Vasopressin is a hormone that causes retention of water, but not salt. Hence, the patient with hyponatremia can be viewed as the patient with increased ADH activity. It is the physician's task to identify the cause of the increased ADH activity in each case.
| journal = [[Medicine]]


In patients who are volume depleted, i.e., their blood volume is too low, ADH secretion is increased, since volume depletion is a potent stimulus for ADH secretion. As a result, the kidneys of such patients hold on to water and produce a very concentrated urine. Treatment is simple (if not without risk) &nbsp;&mdash; simply restore the patient's blood volume, thereby turning off the stimulus for ongoing ADH release and water retention.
| volume = 51


Some patients with hyponatremia have normal blood volume. In those patients, the increased ADH activity and subsequent water retention may be due to "physiologic" causes of ADH release such as pain or nausea. Alternatively, they may have the Syndrome of Inappropriate ADH ([[SIADH]]). SIADH represents the sustained, non-physiologic release of ADH and most often occurs as a side effect of certain medicines, lung problems such as pneumonia or abscess, brain disease, or certain cancers (most often small cell lung carcinoma).
| issue = 2


A third group of patients with hyponatremia are often said to be "hypervolemic". They are identified by the presence of peripheral edema. In fact, the term "hypervolemic" is misleading since their blood volume is actually low. The edema underscores the fact that fluid has left the circulation, i.e., the edema represents fluid that has exited the circulation and settled in dependent areas. Since such patients do, in fact, have reduced blood volume, and since reduced blood volume is a potent stimulus for ADH release, it is easy to see why they have retained water and become hyponatremic. Treatment of these patients involves treating the underlying disease that caused the fluid to leak out of the circulation in the first place. In many cases, this is easier said than done when one recognizes that the responsible underlying conditions are diseases such as liver cirrhosis or heart failure&nbsp;&mdash; conditions that are notoriously difficult to manage, let alone cure.
| pages = 73–94


Hyponatremia can result from dysfunctions of the [[mineralocorticoid]] [[aldosterone]] (i.e. [[hypoaldosteronism]]) due to [[adrenal insufficiency]], [[congenital adrenal hyperplasia]], and some medications.
| year = 1972


It is worth considering separately, the hyponatremia that occurs in the setting of diuretic use. Patients taking diuretic medications such as [[furosemide]] (Lasix), [[hydrochlorothiazide]], [[chlorthalidone]], etc., become volume depleted. That is to say that their diuretic medicine, by design, has caused their kidneys to produce more urine than they would otherwise make. This extra urine represents blood volume that is no longer there, that has been lost from the body. As a result, their blood volume is reduced. As mentioned above, lack of adequate blood volume is a potent stimulus for ADH secretion and thence water retention.
| month = March


A recent surge in death from hyponatremia has been attributed to overintake of water while under the influence of [[MDMA]].  Also, Almond ''et al.''<ref>Almond CS et al. (2005) Hyponatremia among runners in the Boston Marathon. N Engl J Med, 352(15):1550-6. PMID 15829535</ref> found hyponatremia in as many as 13% of runners in a recent Boston Marathon, with life-threatening hyponatremia (serum Na below 120 mmol/L) in 0.6%.  The runners at greatest risk of serious [[water intoxication]] had moderate weight gain during the race due to excessive water consumption (see reference). Siegel ''et al'' <ref> Siegel AJ et al. (2007) Am J Med, 120(5):461.e11-7.
| pmid = 5013637
PMID 17466660</ref> recently found that in addition to over-zealous drinking, the cause of exercise-associated hyponatremia (EAH) is from an inappropriate secretion of the hormone arginine vasopressin, or antidiuretic hormone.  This excess hormone secretion prevents the kidneys from excreting the excess water in the urine.
 
}}</ref>.</small>   
* Causes of '''<big>Hyponatremia</big>''' based on '''volume status''' '''<ref name="GuillauminDiBartola2017">{{cite journal|last1=Guillaumin|first1=Julien|last2=DiBartola|first2=Stephen P.|title=A Quick Reference on Hyponatremia|journal=Veterinary Clinics of North America: Small Animal Practice|volume=47|issue=2|year=2017|pages=213–217|issn=01955616|doi=10.1016/j.cvsm.2016.10.003}}</ref> :'''
{| class="wikitable"
!Volume status
!Sodium status
!Causes
|-
|'''<big>Hypovolemic</big>'''
'''<big>Hyponatremia<ref name="Rondon-BerriosAgaba2014">{{cite journal|last1=Rondon-Berrios|first1=Helbert|last2=Agaba|first2=Emmanuel I.|last3=Tzamaloukas|first3=Antonios H.|title=Hyponatremia: pathophysiology, classification, manifestations and management|journal=International Urology and Nephrology|volume=46|issue=11|year=2014|pages=2153–2165|issn=0301-1623|doi=10.1007/s11255-014-0839-2}}</ref>'''
|
* total body water ↓
* total body sodium ↓↓
|
* '''GI loss:''' [[Vomiting]], [[Diarrheal|diarrhea]], tube drainage
* '''Insensible loss:''' [[Sweating]], [[burns]]
* '''Renal loss:''' Salt-wasting nephropathy (inappropriate loss of Na+-Cl– in the urine),
bicarbonaturia ( renal tubular acidosis, metabolic alkalosis), [[osmotic diuresis]], [[diuretic use]],


=== Pseudohyponatremia ===
[[cerebral salt-wasting syndrome]] ([[Stroke]] ,[[SAH]] ,↑ [[brain natriuretic peptide]] and ↑ renal sodium loss )
Certain conditions that interfere with laboratory tests of serum sodium concentration (such as extraordinarily high blood levels of [[lipid]] or [[protein]]) may lead to an erroneously low ''measurement'' of sodium.  This is called pseudohyponatremia, and can occur when laboratories use the flame-photometric and indirect (but not direct) ion-selective electrode assays.<ref>Weisberg LS. (1989) Pseudohyponatremia: a reappraisal. Am J Med, 86(3):315-8.  PMID 2645773 </ref><ref>Nguyen MK et al. (2007) A new method for determining plasma water content: application in pseudohyponatremia. Am J Phys - Renal, 292(5):F1652-6.  PMID 17299138</ref>  This is distinct from a true dilutional hyponatremia that can be caused by an osmotic shift of water from cells to the bloodstream after large infusions on [[mannitol]] or [[IVIG|intravenous immunoglobulin]].
* '''Third spacing of fluids :''' [[Pancreatitis]], [[hypoalbuminemia]], [[Small bowel obstruction]]


=== Hypoosmolar Hyponatremia ===
* '''Mineralocorticoid deficiency:''' [[Addison disease]] (primary)  
When the plasma osmolarity is low, the extracellular fluid volume status may be in one of three states:
====Low Volume====
Loss of water is accompanied by loss of sodium.
*Excessive [[sweat]]ing
*[[Burn (injury)|Burns]]
*[[Vomit]]ing
*[[Diarrhea]]
*[[Urine|Urinary]] loss
**[[Diuretic]] drugs (especially [[thiazide]]s)
**[[Addison's disease]]
**[[Cerebral salt-wasting syndrome]]
**Other salt-wasting [[kidney]] diseases


Treat underlying cause and give IV isotonic saline. It is important to note that sudden restoration of blood volume to normal will turn off the stimulus for continued ADH secretion. Hence, a prompt water diuresis will occur. This can cause a sudden and dramatic increase the serum sodium concentration and place the patient at risk for so-called "[[central pontine myelinolysis]]" (CPM). That disorder is characterized by major neurologic damage, often of a permanent nature.
* '''Excessive diuretic administration: ''' mostly thiazide diuretics
|-
|'''<big>Hypervolemic</big>'''
'''<big>Hyponatremia</big>'''
|
* total body water '''↑↑'''
* total body sodium ↑
|
* '''Renal disease:''' Acute or chronic kidney disease or injury
(due to relatively higher water versus salt intake and poor excretion), nephrotic syndrome
* '''Congestive heart failure'''
* '''Cirrhosis'''
* '''Iatrogenic'''
|-
|'''<big>Euvolemic</big>'''
'''<big>Hyponatremia</big>'''
|
* total body water ↑
* total body sodium ↔
|
* '''Drugs:''' [[Vasopressin]], [[diuretics]], [[antidepressants]], [[opioids]]
* '''SIAD:''' [[SIADH]] (Malignancy, central nervous system (CNS) disorders, pulmonary disease, or drugs,
postoperative nausea, pain, stress, neoplasia (common), trauma, pregnancy)


Because of the risk of CPM, patients with low volume hyponatremia may eventually require water infusion as well as volume replacement. Doing so lessens the chance of a too rapid increase of the serum sodium level as blood volume rises and ADH levels fall.
''',''' nephrogenic SIAD (Gain-of-function mutation of v2 receptors)
* '''High fluid intake:''' Physical activity, surgery, primary polydipsia, potomania, tea & toast diet
(caused by a low intake of solutes with relatively high fluid intake)
* '''Medical testing''' (excess fluid intake) ''':'''[[Colonoscopy]] or [[cardiac catheterization]]
* '''Hypothyroidism'''
* '''Hormonal:''' [[Glucocorticoid deficiency 1|Glucocorticoid deficiency]], [[pituitary failure]] (secondary), hypothalamic failure (tertiary)


====Normal Volume====
* '''Reset osmostat <sup>†</sup> :''' Drugs, pregnancy
* [[SIADH]]
* '''Iatrogenic'''
* [[Polydipsia|Primary polydipsia]]
|}
* [[Exercise|Exercise associated hyponatremia]]
''<small>† Altered sensitivity to serum osmolality by the hypothalamic osmoreceptors</small>''
* Nephrogenic syndrome of inappropriate antidiuresis
<br>
* [[Glucocorticoid deficiency]]
* <big>'''Drugs''' which cause '''hyponatremia:'''</big>
* [[Hypothyroidism]]
* Low sodium intake


The cornerstone of therapy for SIADH is reduction of water intake. If hyponatremia persists, then [[demeclocycline]] (an antibiotic with the side effect of inhibiting ADH) can be used.  SIADH can also be treated with specific antagonists of the [[antidiuretic hormone|ADH]] receptors, such as [[conivaptan]] or [[tolvaptan]].
{| class="wikitable"
!'''<big>Drug Mechanisms <ref name="LiamisMilionis200822">{{cite journal|last2=Milionis|first2=Haralampos|last3=Elisaf|first3=Moses|year=2008|title=A Review of Drug-Induced Hyponatremia|journal=American Journal of Kidney Diseases|volume=52|issue=1|pages=144–153|doi=10.1053/j.ajkd.2008.03.004|issn=02726386|last1=Liamis|first1=George}}</ref></big>'''
!'''<big>Drug Classification</big>'''
|-
!'''<big>Increase ADH secretion</big>'''
|'''Antidepressants:'''[[Tricyclic antidepressants]] ( [[Amitryptiline]],
[[Protriptyline]], [[Desipramine]]),[[Selective serotonin reuptake inhibitors]],


====High Volume====
[[Monoamine oxidase inhibitors]]
There is retention of water.
*[[Congestive heart failure]]
*[[Hypothyroidism]] and [[hypocortisolism]]
*[[Liver]] [[cirrhosis]]
*[[Nephrotic syndrome]]
*[[Psychogenic polydipsia]]


Placing the patient on water restriction can also help in these cases.
'''Antipsychotic drugs:''' [[Phenothiazines]] ([[Thioridazine]], [[Trifluoperazine]]),


Severe hyponatremia may result from a few hours of heavy exercise in high temperature conditions, such as hiking in desert areas, or from endurance athletic events when electrolytes are not supplied. (Such an incident notably happened to long-distance athlete Craig Barrett in 1998).
[[Butyrophenones]] ([[Haloperidol]])


===Common Causes===
'''Antiepileptic drugs:''' [[Carbamazepine]], [[Oxcarbazepine]], [[Sodium valproate]]
 
'''Anticancer agents:''' [[Vinca alkaloids]] ([[Vincristine]], [[Vinblastine]]),
 
Platinum compounds ([[Cisplatinum|Cisplatin]], [[Carboplatinum|Carboplatin]])
 
'''Alkylating agents:''' Intravenous [[Cyclophosphamide lyophilized|Cyclophosphamide]], [[Melphalan]], [[Ifosfamide]]
 
'''Miscellaneous:''' [[Methotrexate Sodium|Methotrexate]], [[Interferon]], [[Levamisole]], [[Pentostatin]], [[Monoclonal antibodies]], [[MDMA]], [[Nicotine]]
 
'''Opiates'''
|-
!<big>Increase ADH effect</big>
|'''Antiepileptic drugs:''' [[Carbamazepine]], [[Lamotrigine]]
'''Antidiabetic drugs:''' [[Chlorpropamide]], [[Tolbutamide]]
 
'''Anticancer agents:''' Alkylating agents (Intravenous [[Cyclophosphamide lyophilized|cyclophosphamide]])
 
'''NSAIDS'''
|-
!<big>Drugs affecting water and sodium homeostasis</big>
|'''Diuretics:''' [[Thiazides]], [[Indapamide]], [[Amiloride]], [[Loop diuretics]]
|-
!<big>Reset omostat <sup>‡</sup></big>
|'''Antidepressants:''' [[Venlafaxine]]
'''Antiepileptic drugs:''' [[Carbamazepine]]
|-
!<big>Vasopressin analogues</big>
|[[Desmopressin]], [[oxytocin]], [[terlipressin]], [[Vasopressin analogue|vasopressin]]
|}
<small>‡ ''Altered sensitivity to serum osmolality by the hypothalamic osmoreceptors''
<br>
</small>
 
<br>
===Causes by Organ System===
===Causes by Organ System===


{|style="width:80%; height:100px" border="1"
{| style="width:80%; height:100px" border="1"
|style="height:100px"; style="width:25%" border="1" bgcolor="LightSteelBlue" | '''Cardiovascular'''
| style="width:25%" bgcolor="lightsteelblue" ; border="1" | '''Cardiovascular'''
|style="height:100px"; style="width:75%" border="1" bgcolor="Beige" | [[Congestive heart failure ]]
| style="width:75%" bgcolor="beige" ; border="1" | [[Congestive heart failure ]]
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="lightsteelblue"
| '''Chemical / poisoning'''
| '''Chemical / poisoning'''
|bgcolor="Beige"| No underlying causes
| bgcolor="beige" | No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="lightsteelblue"
| '''Dermatologic'''
| '''Dermatologic'''
|bgcolor="Beige"| [[Burns]]
| bgcolor="beige" | [[Burns]]
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="lightsteelblue"
| '''Drug Side Effect'''
| '''Drug Side Effect'''
|bgcolor="Beige"| [[ACE inhibitors]], [[Ajuga nipponensis makino ]], [[Asenapine maleate]], [[Cefpodoxime]], [[Chlorpropamide]], [[Cyclophosphamide]], [[Desmopressin]], [[Diuretics]], [[Duloxetine]], [[Eslicarbazepine acetate]], [[Ethacrynic Acid]], [[Felbamate]], [[Fluvoxamine]], [[Interferon gamma]], [[Ixabepilone]], [[Losartan and Hydrochlorothiazide]], [[Nilotinib]], [[Nivolumab]], [[Nonsteriodal anti-inflammatory drugs ]], [[Oxcarbazepine]], [[Pramipexole]], [[Rifaximin]], [[Tiagabine]], [[Tolazamide]], [[Zonisamide]], [[Tolbutamide]], [[Vortioxetine]]
| bgcolor="beige" | [[ACE inhibitors]], [[Ajuga nipponensis makino ]] , [[Asenapine maleate]], [[Cefpodoxime]], [[Chlorpropamide]], [[Cyclophosphamide]], [[Desmopressin]], [[Diuretics]], [[Duloxetine]], [[Eslicarbazepine acetate]], [[Ethacrynic Acid]], [[Felbamate]], [[Fluvoxamine]], [[Interferon gamma]], [[Ixabepilone]], [[Losartan and Hydrochlorothiazide]], [[Nilotinib]],[[Nivolumab]]<ref name="HataSakaguchi2021">{{cite journal|last1=Hata|first1=Koichi|last2=Sakaguchi|first2=Chikara|last3=Tsuchiya|first3=Michiko|last4=Nagasaka|first4=Yukio|title=Abdominal pain as an initial symptom of isolated ACTH deficiency induced by nivolumab in a patient with malignant mesothelioma|journal=BMJ Case Reports|volume=14|issue=7|year=2021|pages=e243093|issn=1757-790X|doi=10.1136/bcr-2021-243093}}</ref>, [[Nonsteriodal anti-inflammatory drugs ]] , [[Oxcarbazepine]], [[Pramipexole]], [[Rifaximin]], [[Tiagabine]], [[Tolazamide]], [[Zonisamide]], [[Tolbutamide]], [[Vortioxetine]], [[Brivanib]] <ref name="pmidhttps://www.ncbi.nlm.nih.gov/pubmed/27167519">{{cite journal| author=Berardi R, Santoni M, Rinaldi S, Nunzi E, Smerilli A, Caramanti M | display-authors=etal| title=Risk of Hyponatraemia in Cancer Patients Treated with Targeted Therapies: A Systematic Review and Meta-Analysis of Clinical Trials. | journal=PLoS One | year= 2016 | volume= 11 | issue= 5 | pages= e0152079 | pmid=https://www.ncbi.nlm.nih.gov/pubmed/27167519 | doi=10.1371/journal.pone.0152079 | pmc=4864354 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27167519  }} </ref>, [[Cetuximab]] <ref name="pmidhttps://www.ncbi.nlm.nih.gov/pubmed/27167519">{{cite journal| author=Berardi R, Santoni M, Rinaldi S, Nunzi E, Smerilli A, Caramanti M | display-authors=etal| title=Risk of Hyponatraemia in Cancer Patients Treated with Targeted Therapies: A Systematic Review and Meta-Analysis of Clinical Trials. | journal=PLoS One | year= 2016 | volume= 11 | issue= 5 | pages= e0152079 | pmid=https://www.ncbi.nlm.nih.gov/pubmed/27167519 | doi=10.1371/journal.pone.0152079 | pmc=4864354 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27167519  }} </ref>
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="lightsteelblue"
| '''Ear Nose Throat'''
| '''Ear Nose Throat'''
|bgcolor="Beige"| No underlying causes
| bgcolor="beige" | No underlying causes
|-  
|-  
|-bgcolor="LightSteelBlue"
|- bgcolor="lightsteelblue"
| '''Endocrine'''
| '''Endocrine'''
|bgcolor="Beige"| [[Addison's disease]], [[Corticosterone methyloxidase type I deficiency ]], [[Diabetes mellitus]], [[Diabetic coma]], [[Glucocorticoid deficiency]], [[Familial hyperreninemic hypoaldosteronism type 2]], [[Hypothyroidism]], [[Mineralocorticoid deficiency]], [[Myxedema coma ]], [[Syndrome of inappropriate antidiuretic hormone ]], [[Thyrotropin deficiency]], [[18-Hydroxylase deficiency ]], [[Familial  hypoaldosteronism ]]
| bgcolor="beige" | [[Addison's disease]], [[Corticosterone methyloxidase type I deficiency ]] , [[Diabetes mellitus]], [[Diabetic coma]], [[Glucocorticoid deficiency]], [[Familial hyperreninemic hypoaldosteronism type 2]], [[Hypothyroidism]], [[Mineralocorticoid deficiency]], [[Myxedema coma ]] , [[Syndrome of inappropriate antidiuretic hormone ]] , [[Thyrotropin deficiency]], [[18-Hydroxylase deficiency ]] , [[Familial  hypoaldosteronism ]]
|-  
|-  
|-bgcolor="LightSteelBlue"
|- bgcolor="lightsteelblue"
| '''Environmental'''
| '''Environmental'''
|bgcolor="Beige"| No underlying causes
| bgcolor="beige" | No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="lightsteelblue"
| '''Gastroenterologic'''
| '''Gastroenterologic'''
|bgcolor="Beige"| [[Acute liver failure ]], [[Cirrhosis]], [[Congenital chloride diarrhea ]], [[Diarrhea]], [[Gastrointestinal fistula]], [[Ileus]], [[Necrotizing enterocolitis ]], [[Pancreatitis]], [[Peritonitis]], [[Vomiting]], [[Cystic fibrosis]]
| bgcolor="beige" | [[Acute liver failure ]] , [[Cirrhosis]], [[Congenital chloride diarrhea ]] , [[Diarrhea]], [[Gastrointestinal fistula]], [[Ileus]], [[complicated appendicitis]]<ref name="KimNassiri2015">{{cite journal|last1=Kim|first1=Dennis Y.|last2=Nassiri|first2=Nariman|last3=de Virgilio|first3=Christian|last4=Ferebee|first4=Michael P.|last5=Kaji|first5=Amy H.|last6=Hamilton|first6=Camille E.|last7=Saltzman|first7=Darin J.|title=Association Between Hyponatremia and Complicated Appendicitis|journal=JAMA Surgery|volume=150|issue=9|year=2015|pages=911|issn=2168-6254|doi=10.1001/jamasurg.2015.1258}}</ref>, [[Necrotizing enterocolitis ]] , [[Pancreatitis]], [[Peritonitis]], [[Vomiting]], [[Cystic fibrosis]]
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="lightsteelblue"
| '''Genetic'''
| '''Genetic'''
|bgcolor="Beige"| [[18-Hydroxylase deficiency ]], [[Bartter Syndrome type 4 ]], [[Cystic fibrosis]], [[Familial  hypoaldosteronism ]], [[Corticosterone methyloxidase type I deficiency ]], [[Familial hyperreninemic hypoaldosteronism type 2]], [[Congenital chloride diarrhea ]]
| bgcolor="beige" | [[18-Hydroxylase deficiency ]] , [[Bartter Syndrome type 4 ]] , [[Cystic fibrosis]], [[Familial  hypoaldosteronism ]] , [[Corticosterone methyloxidase type I deficiency ]] , [[Familial hyperreninemic hypoaldosteronism type 2]], [[Congenital chloride diarrhea ]]
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="lightsteelblue"
| '''Hematologic'''
| '''Hematologic'''
|bgcolor="Beige"| No underlying causes
| bgcolor="beige" | No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="lightsteelblue"
| '''Iatrogenic'''
| '''Iatrogenic'''
|bgcolor="Beige"| [[After pituitary surgery]], [[After surgery]], [[Ascitic tap]], [[Gastric drainage]], [[Hypotonic infusions]], [[Pleuracentesis]]
| bgcolor="beige" | [[After pituitary surgery]], [[After surgery]], [[Ascitic tap]], [[Gastric drainage]], [[Hypotonic infusions]], [[Pleuracentesis]], [[Tumor lysis syndrome]] (TLS) associated with pediatric hematologic malignancies, and managed with aggressive intravenous hydration can cause fluid overload (FO) and [[acute kidney injury]] (AKI). <ref name="FloodRozmus2021">{{cite journal|last1=Flood|first1=Kayla|last2=Rozmus|first2=Jacob|last3=Skippen|first3=Peter|last4=Matsell|first4=Douglas G.|last5=Mammen|first5=Cherry|title=Fluid overload and acute kidney injury in children with tumor lysis syndrome|journal=Pediatric Blood & Cancer|year=2021|issn=1545-5009|doi=10.1002/pbc.29255}}</ref>
 
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="lightsteelblue"
| '''Infectious Disease'''
| '''Infectious Disease'''
|bgcolor="Beige"| [[Malignant boutonneuse fever ]], [[Neonatal bacterial meningitis ]], [[Peritonitis]]
| bgcolor="beige" | [[Malignant boutonneuse fever ]] , [[Neonatal bacterial meningitis ]] , [[Peritonitis]], [[influenza]] and other respiratory viruses, [[HIV]] infection, [[Corona virus]] infections, [[community acquired pneumonia]] from bacterial (streptococcus pneumonia, legionella etc) <ref name="pmid32718076">{{cite journal| author=Królicka AL, Kruczkowska A, Krajewska M, Kusztal MA| title=Hyponatremia in Infectious Diseases-A Literature Review. | journal=Int J Environ Res Public Health | year= 2020 | volume= 17 | issue= 15 | pages=  | pmid=32718076 | doi=10.3390/ijerph17155320 | pmc=7432506 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32718076  }} </ref>
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="lightsteelblue"
| '''Musculoskeletal / Ortho'''
| '''Musculoskeletal / Ortho'''
|bgcolor="Beige"| No underlying causes
| bgcolor="beige" | No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="lightsteelblue"
| '''Neurologic'''
| '''Neurologic'''
|bgcolor="Beige"| [[Intracranial hemorrhage]], [[Subarachnoid hemorrhage]], [[Pituitary cancer]]
| bgcolor="beige" | [[Intracranial hemorrhage]], [[Subarachnoid hemorrhage]], [[Pituitary cancer]], [[ stroke]] <ref name="pmid31722353">{{cite journal| author=Liamis G, Barkas F, Megapanou E, Christopoulou E, Makri A, Makaritsis K | display-authors=etal| title=Hyponatremia in Acute Stroke Patients: Pathophysiology, Clinical Significance, and Management Options. | journal=Eur Neurol | year= 2019 | volume= 82 | issue= 1-3 | pages= 32-40 | pmid=31722353 | doi=10.1159/000504475 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=31722353  }} </ref>, [[Post traumatic brain injury]] [[hypopituitarism]] causing [[adrenal insufficiency]]. <ref name="AwanMat2021">{{cite journal|last1=Awan|first1=Nusrat Mehmood|last2=Mat|first2=Arimin|last3=Canavan|first3=Ronan|title=Retracing the tracks for SIAD: hyponatraemia due to post-traumatic brain injury hypopituitarism|journal=BMJ Case Reports|volume=14|issue=7|year=2021|pages=e242764|issn=1757-790X|doi=10.1136/bcr-2021-242764}}</ref>
 
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="lightsteelblue"
| '''Nutritional / Metabolic'''
| '''Nutritional / Metabolic'''
|bgcolor="Beige"| [[Hyperlipidemia]], [[Hyperproteinemia]], [[Hypoalbuminemia]], [[Low sodium diet]], [[Metabolic acidosis]], [[Diabetic coma]]
| bgcolor="beige" | [[Hyperlipidemia]], [[Hyperproteinemia]], [[Hypoalbuminemia]], [[Low sodium diet]], [[Metabolic acidosis]], [[Diabetic coma]]
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="lightsteelblue"
| '''Obstetric/Gynecologic'''
| '''Obstetric/Gynecologic'''
|bgcolor="Beige"| [[Pregnancy]]
| bgcolor="beige" | [[Pregnancy]], postpartum in patients with [[preeclampsia]] <ref name="HsuTong2021">{{cite journal|last1=Hsu|first1=Richard|last2=Tong|first2=Anna|last3=Hsu|first3=Chaur-Dong|last4=Takeuchi|first4=Kyousuke|title=Hypervolemic Hyponatremia as a Reversible Cause of Cardiopulmonary Arrest in a Postpartum Patient with Preeclampsia|journal=Case Reports in Obstetrics and Gynecology|volume=2021|year=2021|pages=1–3|issn=2090-6692|doi=10.1155/2021/8850725}}</ref>
 
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="lightsteelblue"
| '''Oncologic'''
| '''Oncologic'''
|bgcolor="Beige"| [[Pituitary cancer]]
| bgcolor="beige" | [[Pituitary cancer]]
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="lightsteelblue"
| '''Opthalmologic'''
| '''Opthalmologic'''
|bgcolor="Beige"| No underlying causes
| bgcolor="beige" | No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="lightsteelblue"
| '''Overdose / Toxicity'''
| '''Overdose / Toxicity'''
|bgcolor="Beige"| [[Water intoxication]]
| bgcolor="beige" | [[Water intoxication]]
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="lightsteelblue"
| '''Psychiatric'''
| '''Psychiatric'''
|bgcolor="Beige"| [[Psychogenic polydipsia]], [[Psychosis]], [[Self-induced water intoxication and schizophrenic disorders syndrome ]]
| bgcolor="beige" | [[Psychogenic polydipsia]], [[Psychosis]], [[Self-induced water intoxication and schizophrenic disorders syndrome ]]
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="lightsteelblue"
| '''Pulmonary'''
| '''Pulmonary'''
|bgcolor="Beige"| [[Cystic fibrosis]]
| bgcolor="beige" | [[Cystic fibrosis]]
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="lightsteelblue"
| '''Renal / Electrolyte'''
| '''Renal / Electrolyte'''
|bgcolor="Beige"| [[Acute  kidney disease]], [[Chronic kidney disease]], [[Diuresis]], [[Glucosuria]], [[Ketonuria]], [[Nephrotic syndrome]], [[Renal Tubular Acidosis]], [[Tubulointerstitial kidney disease]], [[Bartter Syndrome type 4 ]], [[Corticosterone methyloxidase type I deficiency ]], [[Renal failure]]
| bgcolor="beige" | [[Acute  kidney disease]], [[Chronic kidney disease]], [[Diuresis]], [[Glucosuria]], [[Ketonuria]], [[Nephrotic syndrome]], [[Renal Tubular Acidosis]], [[Tubulointerstitial kidney disease]], [[Bartter Syndrome type 4 ]] , [[Corticosterone methyloxidase type I deficiency ]] , [[Renal failure]]
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="lightsteelblue"
| '''Rheum / Immune / Allergy'''
| '''Rheum / Immune / Allergy'''
|bgcolor="Beige"| [[Addison's disease]], [[Nephrotic syndrome]]
| bgcolor="beige" | [[Addison's disease]], [[Nephrotic syndrome]]
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="lightsteelblue"
| '''Sexual'''
| '''Sexual'''
|bgcolor="Beige"| [[Cystic fibrosis]]
| bgcolor="beige" | [[Cystic fibrosis]]
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="lightsteelblue"
| '''Trauma'''
| '''Trauma'''
|bgcolor="Beige"| [[Burns]]
| bgcolor="beige" | [[Burns]]
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="lightsteelblue"
| '''Urologic'''
| '''Urologic'''
|bgcolor="Beige"| No underlying causes
| bgcolor="beige" | No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="lightsteelblue"
| '''Dental'''
| '''Dental'''
|bgcolor="Beige"| No underlying causes
| bgcolor="beige" | No underlying causes
|-
|-
|-bgcolor="LightSteelBlue"
|- bgcolor="lightsteelblue"
| '''Miscellaneous'''
| '''Miscellaneous'''
|bgcolor="Beige"| [[Beer potomania]], [[Ecstasy abuse ]], [[Factitious hyponatremia]], [[Hydration]], [[Massive edema]], [[Pseudohyponatremia]], [[Water Intoxication  ]], [[Hyperlipidemia]], [[Hyperproteinemia]], [[Hypoalbuminemia]], [[Exercise associated hyponatremia]]
| bgcolor="beige" | [[Beer potomania]], [[Ecstasy abuse ]] , [[Factitious hyponatremia]], [[Hydration]], [[Massive edema]], [[Pseudohyponatremia]], [[Water Intoxication  ]] , [[Hyperlipidemia]], [[Hyperproteinemia]], [[Hypoalbuminemia]], [[Exercise associated hyponatremia]]
|-
|-
|}
|}

Latest revision as of 13:48, 18 August 2021

Hyponatremia Microchapters

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

Overview

Hyponatremia is caused by either increase ADH action/ secretion or kidney function impairment. SIAD is the most common cause of euvolemic hyponatremia. After SIAD, polydipsia, drugs and clinical disorders are the most encountered etiologies in clinical practice.

Causes

To review the mechanisms of developing hyponatremia, click here.

  • Etiologies of SIAD:
Conditions
Malignant disorders Carcinoma: Lung ( small cell carcinoma, mesothelioma), oropharynx, stomach, duodenum, pancreas, ureter, bladder, prostate, endometrium, thymoma

Lymphomas

Sarcomas: Ewing's sarcoma

Olfactory neuroblastoma

Pulmonary diseases Infections: Bacterial pneumonia, viral pneumonia, pulmonary abscess, tuberculosis, aspergillosis

Others: Asthma, cystic fibrosis, respiratory failure, emphysema, COPD,coronavirus disease, positive-pressure ventilation

CNS disorders Infections: Encephalitis, meningitis, brain abscess, RMSF, AIDS, malaria

Vascular and SOP: Subarachnoid hemorrhage, stroke, brain tumors, head trauma

Others: Hydrocephalus, cavernous sinus thrombosis, Multiple sclerosis, Guillain–Barré syndrome, Shy–Drager syndrome,

delirium tremens, acute intermittent porphyria, chronic psychosis, pituitary stalk section, transsphenoidal adenomectomy

Other causes Hereditary: Gain-of-function mutation of V2 receptors

Idiopathic

Drugs

Transient: Exercise, general anesthesia, nausea, pain, stress


  • Causes of acute hyponatremia: (develops in < 48 hrs)
Etiology
  • Post operative phase
  • Transurethral or endoscopic procedure (mannitol, sorbitol, glycine)
  • Colonoscopy preparation 
  • Polydipsia
  • Exercise
  • Oxytocin
  • Cyclophosphamide
  • Ecstasy( 3,4-Methylenedioxymethamphetamine, MDMA)
  • Thiazide
  • Halopridol
  • Recently started desmopressin, terlipressin, vasopressin

( Etiologies that cause hyperacute and acute hyponatremia are applicable to each category interchangeably depending on the onset of symptoms)

  • Causes of Hyponatremia based upon Serum Osmolality:
Classification Serum Osmolality Etiology
Hypertonic or Isotonic Hyponatremia > 295 mOsm/kg Hyperglycemia‡, Mannitol, Glycine, Maltose, severe azotemia
Isotonic Hyponatremia

(Pseudohyponatremia)

275 – 295 mOsm/kg Lab/blood draw error, Post TURP (bladder irrigation with osmotic solutions),

intravenous immunoglobulin (IVIg), Hyperlipidemia ( triglyceride, cholesterol ),

hyper paraproteinemia (monoclonal gammopathy of undetermined significance (MGUS),

multiple myeloma),

Hypotonic Hyponatremia < 275 mOsm/kg Glycerol, Sorbitol, Etiology depends upon volume status (Hypervolemic/ Euvolemic/ Hypovolemic)
Alcohol, Urea, Ethylen glycol are ineffective osmoles, cause hyperosmolar isotonic serum but not hyponatremia.

‡ Hyperglycemia causes osmotic diuresis results in a rise in serum sodium concentration, on the other hand it leads to extracellular shift of water due to osmotic gradient which causes relative hyponatremia , depends on which effect is stronger, there would be hypertonicity or hypotonicity[1].   

  • Causes of Hyponatremia based on volume status [2] :
Volume status Sodium status Causes
Hypovolemic

Hyponatremia[3]

  • total body water ↓
  • total body sodium ↓↓
  • GI loss: Vomiting, diarrhea, tube drainage
  • Insensible loss: Sweating, burns
  • Renal loss: Salt-wasting nephropathy (inappropriate loss of Na+-Cl– in the urine),

bicarbonaturia ( renal tubular acidosis, metabolic alkalosis), osmotic diuresis, diuretic use,

cerebral salt-wasting syndrome (Stroke ,SAH ,↑ brain natriuretic peptide and ↑ renal sodium loss )

  • Excessive diuretic administration: mostly thiazide diuretics
Hypervolemic

Hyponatremia

  • total body water ↑↑
  • total body sodium ↑
  • Renal disease: Acute or chronic kidney disease or injury

(due to relatively higher water versus salt intake and poor excretion), nephrotic syndrome

  • Congestive heart failure
  • Cirrhosis
  • Iatrogenic
Euvolemic

Hyponatremia

  • total body water ↑
  • total body sodium ↔

postoperative nausea, pain, stress, neoplasia (common), trauma, pregnancy)

, nephrogenic SIAD (Gain-of-function mutation of v2 receptors)

  • High fluid intake: Physical activity, surgery, primary polydipsia, potomania, tea & toast diet

(caused by a low intake of solutes with relatively high fluid intake)

  • Reset osmostat † : Drugs, pregnancy
  • Iatrogenic

† Altered sensitivity to serum osmolality by the hypothalamic osmoreceptors

  • Drugs which cause hyponatremia:
Drug Mechanisms [4] Drug Classification
Increase ADH secretion Antidepressants:Tricyclic antidepressants ( Amitryptiline,

Protriptyline, Desipramine),Selective serotonin reuptake inhibitors,

Monoamine oxidase inhibitors

Antipsychotic drugs: Phenothiazines (Thioridazine, Trifluoperazine),

Butyrophenones (Haloperidol)

Antiepileptic drugs: Carbamazepine, Oxcarbazepine, Sodium valproate

Anticancer agents: Vinca alkaloids (Vincristine, Vinblastine),

Platinum compounds (Cisplatin, Carboplatin)

Alkylating agents: Intravenous Cyclophosphamide, Melphalan, Ifosfamide

Miscellaneous: Methotrexate, Interferon, Levamisole, Pentostatin, Monoclonal antibodies, MDMA, Nicotine

Opiates

Increase ADH effect Antiepileptic drugs: Carbamazepine, Lamotrigine

Antidiabetic drugs: Chlorpropamide, Tolbutamide

Anticancer agents: Alkylating agents (Intravenous cyclophosphamide)

NSAIDS

Drugs affecting water and sodium homeostasis Diuretics: Thiazides, Indapamide, Amiloride, Loop diuretics
Reset omostat ‡ Antidepressants: Venlafaxine

Antiepileptic drugs: Carbamazepine

Vasopressin analogues Desmopressin, oxytocin, terlipressin, vasopressin

‡ Altered sensitivity to serum osmolality by the hypothalamic osmoreceptors


Causes by Organ System

Cardiovascular Congestive heart failure
Chemical / poisoning No underlying causes
Dermatologic Burns
Drug Side Effect ACE inhibitors, Ajuga nipponensis makino , Asenapine maleate, Cefpodoxime, Chlorpropamide, Cyclophosphamide, Desmopressin, Diuretics, Duloxetine, Eslicarbazepine acetate, Ethacrynic Acid, Felbamate, Fluvoxamine, Interferon gamma, Ixabepilone, Losartan and Hydrochlorothiazide, Nilotinib,Nivolumab[5], Nonsteriodal anti-inflammatory drugs , Oxcarbazepine, Pramipexole, Rifaximin, Tiagabine, Tolazamide, Zonisamide, Tolbutamide, Vortioxetine, Brivanib [6], Cetuximab [6]
Ear Nose Throat No underlying causes
Endocrine Addison's disease, Corticosterone methyloxidase type I deficiency , Diabetes mellitus, Diabetic coma, Glucocorticoid deficiency, Familial hyperreninemic hypoaldosteronism type 2, Hypothyroidism, Mineralocorticoid deficiency, Myxedema coma , Syndrome of inappropriate antidiuretic hormone , Thyrotropin deficiency, 18-Hydroxylase deficiency , Familial hypoaldosteronism
Environmental No underlying causes
Gastroenterologic Acute liver failure , Cirrhosis, Congenital chloride diarrhea , Diarrhea, Gastrointestinal fistula, Ileus, complicated appendicitis[7], Necrotizing enterocolitis , Pancreatitis, Peritonitis, Vomiting, Cystic fibrosis
Genetic 18-Hydroxylase deficiency , Bartter Syndrome type 4 , Cystic fibrosis, Familial hypoaldosteronism , Corticosterone methyloxidase type I deficiency , Familial hyperreninemic hypoaldosteronism type 2, Congenital chloride diarrhea
Hematologic No underlying causes
Iatrogenic After pituitary surgery, After surgery, Ascitic tap, Gastric drainage, Hypotonic infusions, Pleuracentesis, Tumor lysis syndrome (TLS) associated with pediatric hematologic malignancies, and managed with aggressive intravenous hydration can cause fluid overload (FO) and acute kidney injury (AKI). [8]
Infectious Disease Malignant boutonneuse fever , Neonatal bacterial meningitis , Peritonitis, influenza and other respiratory viruses, HIV infection, Corona virus infections, community acquired pneumonia from bacterial (streptococcus pneumonia, legionella etc) [9]
Musculoskeletal / Ortho No underlying causes
Neurologic Intracranial hemorrhage, Subarachnoid hemorrhage, Pituitary cancer, stroke [10], Post traumatic brain injury hypopituitarism causing adrenal insufficiency. [11]
Nutritional / Metabolic Hyperlipidemia, Hyperproteinemia, Hypoalbuminemia, Low sodium diet, Metabolic acidosis, Diabetic coma
Obstetric/Gynecologic Pregnancy, postpartum in patients with preeclampsia [12]
Oncologic Pituitary cancer
Opthalmologic No underlying causes
Overdose / Toxicity Water intoxication
Psychiatric Psychogenic polydipsia, Psychosis, Self-induced water intoxication and schizophrenic disorders syndrome
Pulmonary Cystic fibrosis
Renal / Electrolyte Acute kidney disease, Chronic kidney disease, Diuresis, Glucosuria, Ketonuria, Nephrotic syndrome, Renal Tubular Acidosis, Tubulointerstitial kidney disease, Bartter Syndrome type 4 , Corticosterone methyloxidase type I deficiency , Renal failure
Rheum / Immune / Allergy Addison's disease, Nephrotic syndrome
Sexual Cystic fibrosis
Trauma Burns
Urologic No underlying causes
Dental No underlying causes
Miscellaneous Beer potomania, Ecstasy abuse , Factitious hyponatremia, Hydration, Massive edema, Pseudohyponatremia, Water Intoxication , Hyperlipidemia, Hyperproteinemia, Hypoalbuminemia, Exercise associated hyponatremia

Causes in Alphabetical Order


References

  1. ↑ A. I. Arieff & H. J. Carroll (1972). "Nonketotic hyperosmolar coma with hyperglycemia: clinical features, pathophysiology, renal function, acid-base balance, plasma-cerebrospinal fluid equilibria and the effects of therapy in 37 cases". Medicine. 51 (2): 73–94. PMID 5013637. Unknown parameter |month= ignored (help)
  2. ↑ Guillaumin, Julien; DiBartola, Stephen P. (2017). "A Quick Reference on Hyponatremia". Veterinary Clinics of North America: Small Animal Practice. 47 (2): 213–217. doi:10.1016/j.cvsm.2016.10.003. ISSN 0195-5616.
  3. ↑ Rondon-Berrios, Helbert; Agaba, Emmanuel I.; Tzamaloukas, Antonios H. (2014). "Hyponatremia: pathophysiology, classification, manifestations and management". International Urology and Nephrology. 46 (11): 2153–2165. doi:10.1007/s11255-014-0839-2. ISSN 0301-1623.
  4. ↑ Liamis, George; Milionis, Haralampos; Elisaf, Moses (2008). "A Review of Drug-Induced Hyponatremia". American Journal of Kidney Diseases. 52 (1): 144–153. doi:10.1053/j.ajkd.2008.03.004. ISSN 0272-6386.
  5. ↑ Hata, Koichi; Sakaguchi, Chikara; Tsuchiya, Michiko; Nagasaka, Yukio (2021). "Abdominal pain as an initial symptom of isolated ACTH deficiency induced by nivolumab in a patient with malignant mesothelioma". BMJ Case Reports. 14 (7): e243093. doi:10.1136/bcr-2021-243093. ISSN 1757-790X.
  6. ↑ 6.0 6.1 Berardi R, Santoni M, Rinaldi S, Nunzi E, Smerilli A, Caramanti M; et al. (2016). "Risk of Hyponatraemia in Cancer Patients Treated with Targeted Therapies: A Systematic Review and Meta-Analysis of Clinical Trials". PLoS One. 11 (5): e0152079. doi:10.1371/journal.pone.0152079. PMC 4864354. PMID https://www.ncbi.nlm.nih.gov/pubmed/27167519 Check |pmid= value (help).
  7. ↑ Kim, Dennis Y.; Nassiri, Nariman; de Virgilio, Christian; Ferebee, Michael P.; Kaji, Amy H.; Hamilton, Camille E.; Saltzman, Darin J. (2015). "Association Between Hyponatremia and Complicated Appendicitis". JAMA Surgery. 150 (9): 911. doi:10.1001/jamasurg.2015.1258. ISSN 2168-6254.
  8. ↑ Flood, Kayla; Rozmus, Jacob; Skippen, Peter; Matsell, Douglas G.; Mammen, Cherry (2021). "Fluid overload and acute kidney injury in children with tumor lysis syndrome". Pediatric Blood & Cancer. doi:10.1002/pbc.29255. ISSN 1545-5009.
  9. ↑ Królicka AL, Kruczkowska A, Krajewska M, Kusztal MA (2020). "Hyponatremia in Infectious Diseases-A Literature Review". Int J Environ Res Public Health. 17 (15). doi:10.3390/ijerph17155320. PMC 7432506 Check |pmc= value (help). PMID 32718076 Check |pmid= value (help).
  10. ↑ Liamis G, Barkas F, Megapanou E, Christopoulou E, Makri A, Makaritsis K; et al. (2019). "Hyponatremia in Acute Stroke Patients: Pathophysiology, Clinical Significance, and Management Options". Eur Neurol. 82 (1–3): 32–40. doi:10.1159/000504475. PMID 31722353.
  11. ↑ Awan, Nusrat Mehmood; Mat, Arimin; Canavan, Ronan (2021). "Retracing the tracks for SIAD: hyponatraemia due to post-traumatic brain injury hypopituitarism". BMJ Case Reports. 14 (7): e242764. doi:10.1136/bcr-2021-242764. ISSN 1757-790X.
  12. ↑ Hsu, Richard; Tong, Anna; Hsu, Chaur-Dong; Takeuchi, Kyousuke (2021). "Hypervolemic Hyponatremia as a Reversible Cause of Cardiopulmonary Arrest in a Postpartum Patient with Preeclampsia". Case Reports in Obstetrics and Gynecology. 2021: 1–3. doi:10.1155/2021/8850725. ISSN 2090-6692.
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