Primary polydipsia: Difference between revisions

From Wikipedia, the free encyclopedia
Content deleted Content added
No edit summary
+ref
Line 58: Line 58:
* [[Vasopressin receptor antagonist]]s, such as [[conivaptan]]<ref>{{Cite journal|last=Douglas|first=Ivor|date=2006-09-01|title=Hyponatremia: why it matters, how it presents, how we can manage it|url=https://www.ncbi.nlm.nih.gov/pubmed/16970147?tool=bestpractice.bmj.com|journal=Cleveland Clinic Journal of Medicine|volume=73 Suppl 3|pages=S4–12|issn=0891-1150|pmid=16970147}}</ref>
* [[Vasopressin receptor antagonist]]s, such as [[conivaptan]]<ref>{{Cite journal|last=Douglas|first=Ivor|date=2006-09-01|title=Hyponatremia: why it matters, how it presents, how we can manage it|url=https://www.ncbi.nlm.nih.gov/pubmed/16970147?tool=bestpractice.bmj.com|journal=Cleveland Clinic Journal of Medicine|volume=73 Suppl 3|pages=S4–12|issn=0891-1150|pmid=16970147}}</ref>
* [[Acetazolamide]], a [[carbonic anhydrase inhibitor]]<ref>{{Cite journal|last=Takagi|first=Shunsuke|last2=Watanabe|first2=Yutaka|last3=Imaoka|first3=Takefumi|last4=Sakata|first4=Masuhiro|last5=Watanabe|first5=Masako|date=2017-02-01|title=Treatment of psychogenic polydipsia with acetazolamide: a report of 5 cases|url=https://www.ncbi.nlm.nih.gov/pubmed/21242740?tool=bestpractice.bmj.com|journal=Clinical Neuropharmacology|volume=34|issue=1|pages=5–7|doi=10.1097/WNF.0b013e318205070b|issn=1537-162X|pmid=21242740|url-access=subscription}}</ref>
* [[Acetazolamide]], a [[carbonic anhydrase inhibitor]]<ref>{{Cite journal|last=Takagi|first=Shunsuke|last2=Watanabe|first2=Yutaka|last3=Imaoka|first3=Takefumi|last4=Sakata|first4=Masuhiro|last5=Watanabe|first5=Masako|date=2017-02-01|title=Treatment of psychogenic polydipsia with acetazolamide: a report of 5 cases|url=https://www.ncbi.nlm.nih.gov/pubmed/21242740?tool=bestpractice.bmj.com|journal=Clinical Neuropharmacology|volume=34|issue=1|pages=5–7|doi=10.1097/WNF.0b013e318205070b|issn=1537-162X|pmid=21242740|url-access=subscription}}</ref>
It is important to note that the majority of [[Psychoactive drug|psychotropic drugs]] (and a good many of other classes) can cause dry mouth as a side effect, but this is not to be confused with true polydipsia in which a dangerous drop in serum sodium will be seen.
It is important to note that the majority of [[Psychoactive drug|psychotropic drugs]] (and a good many of other classes) can cause dry mouth as a side effect, but this is not to be confused with true polydipsia in which a dangerous drop in serum sodium will be seen.<ref>{{Cite journal|last=Meulendijks|first=Didier|last2=Mannesse|first2=Cyndie K.|last3=Jansen|first3=Paul A. F.|last4=van Marum|first4=Rob J.|last5=Egberts|first5=Toine C. G.|date=2010-02-01|title=Antipsychotic-induced hyponatraemia: a systematic review of the published evidence|url=https://www.ncbi.nlm.nih.gov/pubmed/20082537|journal=Drug Safety|volume=33|issue=2|pages=101–114|doi=10.2165/11319070-000000000-00000|issn=1179-1942|pmid=20082537|url-access=subscription}}</ref>


== Other animals ==
== Other animals ==

Revision as of 22:37, 30 October 2016

Primary polydipsia
SpecialtyPsychiatry, clinical psychology Edit this on Wikidata

Primary polydipsia is a form of polydipsia[1] characterised by excessive fluid intake in the absence of physiological stimuli to drink, often due to the sensation of dry mouth. Primary polydipsia includes psychogenic polydipsia, which is caused by mental disorders, most often schizophrenia, although some forms of primary polydipsia are explicitly characterized as nonpsychogenic, such as in patients with autoimmune chronic hepatitis with severely elevated globulin levels.[2]

Diagnosis

Diagnostic considerations

Primary polydipsia is a diagnosis of exclusion and diagnosis may be the result of elimination of the possibility of diseases causing polydipsia, such as diabetes inspidus.[3] Diagnosis may be complicated by the fact that chronic compulsive drinking may impair the response of the kidneys to vasopressin, thus reducing the ability of the kidneys to concentrate the urine.[4] This means that psychogenic polydipsia may lead to test results (e.g. in a water restriction test) consistent with diabetes inspidus or SIADH, leading to misdiagnosis.[5]

Dry mouth is often a side effect of medications used in the treatment of some mental disorders, rather than the underlying condition.[6] Such medications include antipsychotics, antidepressants, anticonvulsants, alpha agonists and anticholinergics.[7] It should also be ensured that the thirst isn't caused by diuretic use (particularly thiazide diuretics), MDMA use, excessive solute intake or chronic alcoholism. The following conditions should also be excluded: diabetes insipidus, cerebral salt wasting, pseudohyponatraemia, SIADH, mineralcorticoid deficiency, salt-wasting nephropathy, nephrotic syndrome, chronic heart failure and cirrhosis.[8]

Patient profiles

Psychogenic polydipsia is found in patients with mental illnesses, most commonly schizophrenia, but also anxiety disorders and rarely affective disorders, anorexia nervosa and personality disorders. It may also be found in people with developmental disorders, such as those with autism.[9] These patients, most often with a history of mental illness, show a shrunken cortex and enlarged ventricles on an MRI scan, which makes differentiation between psychogenic and physiological cause difficult.[10] While psychogenic polydipsia is usually not seen outside the population of those with serious mental disorders, it may occasionally be found among others in the absence of psychosis, although there is no existent research to document this other than anecdotal observations. Such persons typically prefer to possess bottled water that is ice cold, consume water and other fluids at excessive levels.[medical citation needed]

Signs and symptoms

Signs and symptoms of psychogenic polydipsia include:[11]

  • Excessive thirst and xerostomia, leading to overconsumption of water
  • Hyponatraemia, causing headache, muscular weakness, twitching, confusion, vomiting, irritability etc., although this is only seen in 20% - 30% of cases.[12]
  • Hypervoelemia, leading to oedema hypertension and weight gain (due to the kidneys being unable to filter the excess blood)[10] in extreme episodes
  • Tonic-clonic seizure[13]
  • Behavioural changes, including fluid-seeking behaviour; patients have been known to seek fluids from any available source, such as toilets and shower rooms.[10][14]

The most common presenting symptom is tonic-clonic seizure, found in 80% of patients.[15] Psychogenic polydipsia should be considered a life-threatening condition, since it has been known to cause severe hyponatraemia, leading to cardiac arrest, coma and cerebral oedema.[11]

Treatment

Treatment for psychogenic polydipsia depends on severity and may involve behavioural and pharmacological modalities.[16]

Acute hyponatraemia

If the patient presents with acute hyponatraemia (severe dehydration) caused by psychogenic polydipsia, treatment usually involves administration of intravenous hypertonic (3%) saline until the serum sodium levels stabilise to within a normal range, even if the patient becomes asymptomatic.[17]

Fluid restriction

If the patient is institutionalised, monitoring of behaviour and serum sodium levels is necessary. In treatment-resistant polydipsic psychiatric patients, regulation in the inpatient setting can be accomplished by use of a weight-water protocol.[18] First, base-line weights must be established and correlated to serum sodium levels. Weight will normally fluctuate during the day, but as the water intake of the polydipsic goes up, the weight will naturally rise. The physician can order a stepped series of interventions as the weight rises. The correlation must be individualized with attention paid to the patient's normal weight and fluctuations, diet, comorbid disorders (such as a seizure disorder) and urinary system functioning. Progressive steps might include redirection, room restriction, and increasing levels of physical restraint with monitoring. Such plans should also include progressive increases in monitoring, as well as a level at which a serum sodium level is drawn.

Behavioural

Behavioural treatments may involve the use of a token economy to provide positive reinforcement to desirable behaviour.[16] Furthermore, cognitive therapy techniques can be used to address the thought patterns that lead to compulsive drinking behaviour. Success has been seen in trials of this technique, with emphasis on the development of coping techniques (e.g. taking small sips of water, having ice cubes instead of drinks) in addition to challenging delusions leading to excessive drinking.[19]

Psychogenic polydipsia often leads to institutionalisation of mentally ill patients, since it is difficult to manage in the community.[10] Most studies of behavioural treatments occur in institutional settings and require close monitoring of the patient and a large degree of time commitment from staff.[17]

Pharmaceutical

A number of pharmaceuticals may be used in an attempt to bring the polydipsia under control, including:

There are a number of emerging pharmaceutical treatments for psychogenic polydipsia, although these need further investigation:[23]

It is important to note that the majority of psychotropic drugs (and a good many of other classes) can cause dry mouth as a side effect, but this is not to be confused with true polydipsia in which a dangerous drop in serum sodium will be seen.[28]

Other animals

Psychogenic polydipsia is also observed in some nonhuman patients, such as in rats.[29]

See also

References

  1. ^ Saito T, Ishikawa S, Ito T, et al. (June 1999). "Urinary excretion of aquaporin-2 water channel differentiates psychogenic polydipsia from central diabetes insipidus". J. Clin. Endocrinol. Metab. 84 (6): 2235–7. doi:10.1210/jc.84.6.2235. PMID 10372737.
  2. ^ Tobin MV, Morris AI (April 1988). "Non-psychogenic primary polydipsia in autoimmune chronic active hepatitis with severe hyperglobulinaemia". Gut. 29 (4): 548–9. doi:10.1136/gut.29.4.548. PMC 1433532. PMID 3371724.
  3. ^ "Psychogenic polydipsia - Diagnosis - Approach". British Medical Journal. 5 May 2016. Retrieved 29 October 2016.
  4. ^ "Primary polydipsia - General Practice Notebook". GPnotebook. Retrieved 29 October 2016.
  5. ^ Zerbe, R. L.; Robertson, G. L. (1981-12-24). "A comparison of plasma vasopressin measurements with a standard indirect test in the differential diagnosis of polyuria". The New England Journal of Medicine. 305 (26): 1539–1546. doi:10.1056/NEJM198112243052601. ISSN 0028-4793. PMID 7311993.
  6. ^ Rippe, James M.; Irwin, Richard S. (2008). Irwin and Rippe's Intensive care medicine. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. p. 909. ISBN 0-7817-9153-7.
  7. ^ "Psychotropic-induced dry mouth: Don't overlook this potentially serious side effect". Current Psychiatry. 10 (12): 54–58. December 2011.
  8. ^ "Psychogenic polydipsia - Diagnosis - Differential diagnosis". British Medical Journal. 5 May 2016. Retrieved 29 October 2016.
  9. ^ "Psychogenic polydipsia - Theory - Aetiology". British Medical Journal. 5 May 2016. Retrieved 29 October 2016.
  10. ^ a b c d Hutcheon, Donald. "Psychogenic Polydipsia (Exessive Fluid seeking Behaviour)" (PDF). American Psychological Society Divisions. Retrieved 29 October 2016.
  11. ^ a b Gill, Melissa; McCauley, MacDara (2015-01-21). "Psychogenic Polydipsia: The Result, or Cause of, Deteriorating Psychotic Symptoms? A Case Report of the Consequences of Water Intoxication". Case Reports in Psychiatry. 2015: 1–3. doi:10.1155/2015/846459. ISSN 2090-682X. PMC 4320790. PMID 25688318.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  12. ^ de Leon, Jose; Verghese, Cherian; Tracy, Joseph I.; Josiassen, Richard C.; Simpson, George M. (1994). "Polydipsia and water intoxication in psychiatric patients: A review of the epidemiological literature". Biological Psychiatry. 35 (6): 408–419. doi:10.1016/0006-3223(94)90008-6.
  13. ^ Hedges, D.; Jeppson, K.; Whitehead, P. (2003). "Antipsychotic medication and seizures: A review". Drugs of Today. 39 (7): 551. doi:10.1358/dot.2003.39.7.799445. PMID 12973403.
  14. ^ Perch, Julia; O’Connor, Kevin M. "Insatiable thirst: Managing polydipsia". Current Psychiatry. 8 (7): 82.
  15. ^ Ferrier, I N (1985-12-07). "Water intoxication in patients with psychiatric illness". British Medical Journal (Clinical research ed.). 291 (6509): 1594–1596. ISSN 0267-0623. PMC 1418423. PMID 3935199.
  16. ^ a b Dundas, Brian; Harris, Melissa; Narasimhan, Meera (2007-07-03). "Psychogenic polydipsia review: Etiology, differential, and treatment". Current Psychiatry Reports. 9 (3): 236–241. doi:10.1007/s11920-007-0025-7. ISSN 1523-3812.
  17. ^ a b c "Psychogenic polydipsia - Management - Step by step". British Medical Journal. 5 May 2016. Retrieved 29 October 2016.
  18. ^ Bowen, L.; Glynn, S. M.; Marshall, B. D.; Kurth, C. L.; Hayden, J. L. (1990-03-01). "Successful behavioral treatment of polydipsia in a schizophrenic patient". Journal of Behavior Therapy and Experimental Psychiatry. 21 (1): 53–61. ISSN 0005-7916. PMID 2373769.
  19. ^ Costanzo, Erin S.; Antes, Lisa M.; Christensen, Alan J. (2016-11-01). "Behavioral and medical treatment of chronic polydipsia in a patient with schizophrenia and diabetes insipidus". Psychosomatic Medicine. 66 (2): 283–286. ISSN 1534-7796. PMID 15039516.
  20. ^ Lee, H. S.; Kwon, K. Y.; Alphs, L. D.; Meltzer, H. Y. (1991-06-01). "Effect of clozapine on psychogenic polydipsia in chronic schizophrenia". Journal of Clinical Psychopharmacology. 11 (3): 222–223. ISSN 0271-0749. PMID 2066464.
  21. ^ a b Kruse, D.; Pantelis, C.; Rudd, R.; Quek, J.; Herbert, P.; McKinley, M. (2001-02-01). "Treatment of psychogenic polydipsia: comparison of risperidone and olanzapine, and the effects of an adjunctive angiotensin-II receptor blocking drug (irbesartan)". The Australian and New Zealand Journal of Psychiatry. 35 (1): 65–68. ISSN 0004-8674. PMID 11270459.
  22. ^ Goh, Kian Peng. "Management of Hyponatremia - American Family Physician". www.aafp.org. Retrieved 2016-10-29.
  23. ^ "Psychogenic polydipsia - Management - Emerging treatments". British Medical Journal. 5 May 2016. Retrieved 29 October 2016.
  24. ^ a b Greendyke, Robert M.; Bernhardt, Alan J.; Tasbas, Hedy E.; Lewandowski, Kathleen S. (1998-04-01). "Polydipsia in Chronic Psychiatric Patients: Therapeutic Trials of Clonidine and Enalapril". Neuropsychopharmacology. 18 (4): 272–281. doi:10.1016/S0893-133X(97)00159-0. ISSN 0893-133X.
  25. ^ Shevitz, S. A.; Jameison, R. C.; Petrie, W. M.; Crook, J. E. (1980-04-01). "Compulsive water drinking treated with high dose propranolol". The Journal of Nervous and Mental Disease. 168 (4): 246–248. ISSN 0022-3018. PMID 7365485.
  26. ^ Douglas, Ivor (2006-09-01). "Hyponatremia: why it matters, how it presents, how we can manage it". Cleveland Clinic Journal of Medicine. 73 Suppl 3: S4–12. ISSN 0891-1150. PMID 16970147.
  27. ^ Takagi, Shunsuke; Watanabe, Yutaka; Imaoka, Takefumi; Sakata, Masuhiro; Watanabe, Masako (2017-02-01). "Treatment of psychogenic polydipsia with acetazolamide: a report of 5 cases". Clinical Neuropharmacology. 34 (1): 5–7. doi:10.1097/WNF.0b013e318205070b. ISSN 1537-162X. PMID 21242740.
  28. ^ Meulendijks, Didier; Mannesse, Cyndie K.; Jansen, Paul A. F.; van Marum, Rob J.; Egberts, Toine C. G. (2010-02-01). "Antipsychotic-induced hyponatraemia: a systematic review of the published evidence". Drug Safety. 33 (2): 101–114. doi:10.2165/11319070-000000000-00000. ISSN 1179-1942. PMID 20082537.
  29. ^ Falk, John L. (1969-05-01). "Conditions Producing Psychogenic Polydipsia in Animals*". Annals of the New York Academy of Sciences. 157 (2): 569–593. doi:10.1111/j.1749-6632.1969.tb12908.x. ISSN 1749-6632.

Further reading

  • Risk factors for the development of hyponatremia in psychiatric inpatients. Arch Intern Med. 1995 May 8;155(9):953-7. PMID 7726704
  • Efficacy of clozapine in a nonschizophrenic patient with psychogenic polydipsia and central pontine myelinolysis. Hum Psychopharmacol. 2002 Jul;17(5):253-5. PMID 12404683

External links