Polyuria resident survival guide: Difference between revisions
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==Treatment== | ==Treatment== | ||
'''Cranial diabetes insipidus''': | |||
* Cranial DI can be managed by desmopressin orally or Intranasal (rarely used). | |||
* Partial DI can be treated with a single nocturnal dose to prevent sleep loss due to nocturia, but complete DI requires 2-4 daily doses. | |||
'''Nephrogenic diabetes insipidus''': | |||
* Withdrawal of lithium therapy usually leads to reversal of lithium-induced diabetes insipid. It can persist for years after lithium withdrawal, usually indicating that the patient has developed interstitial nephritis secondary to lithium. | |||
* Thiazide diuretics reduce urine output by up to 50%, and indomethacin has also been used. Results are frequently unsatisfactory, treatment is directed at sufficient fluid intake to replace urinary losses. <ref name="pmid12617410">{{cite journal| author=Moore K, Thompson C, Trainer P| title=Disorders of water balance. | journal=Clin Med (Lond) | year= 2003 | volume= 3 | issue= 1 | pages= 28-33 | pmid=12617410 | doi=10.7861/clinmedicine.3-1-28 | pmc=4953350 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12617410 }} </ref> | |||
==Do's== | ==Do's== |
Revision as of 12:17, 11 August 2020
Overview
- Polyuria is defined as urine output more than 2 L/24 hours, or 30 ml/kg/24 hours. There are 3 pathophysiologic causes of polyuria: increased thirst (idiopathic, psychogenic polydepsia, hypothalamic disease, and medications), central diabetes insipidus (DI) (decreased secretion of arginine vasopressin (AVP)), and nephrogenic diabetes insipidus (DI) (renal resistance to AVP).[1]
Causes
Life threatening causes
Common causes
The most common causes of polyuria are: psychogenic polydipsia, diabetes insipidus (central and nephrogenic), chronic kidney disease and uncontrolled diabetes mellitus. [2]
Diagnosis
Approach to polyuria
Polyuria ❑ 24-hour urine volume >3L ❑ 24-hour urine volume >50 ml/kg | |||||||||||||||||||||||||||||||||||
Urine Osmolality >300mosmol | Urine Osmolality <300[3]mosmol | ||||||||||||||||||||||||||||||||||
Solute diuresis ❑ Glucose ❑ Mannitol ❑ Contrast media ❑ High protein intake ❑ Diuretics ❑ Medullary cystic disease ❑ Resolving ATN ❑ Resolving obstruction | |||||||||||||||||||||||||||||||||||
Water diuresis ❑ Primary polydipsia ❑ Diabetes inspidous | |||||||||||||||||||||||||||||||||||
Water restriction test OR administration of hypertonic saline 0.05 mL/kg/min for 2 h | |||||||||||||||||||||||||||||||||||
Water restriction test
❑ Overnight fluid restriction should be avoided ❑ Recommend the patient to stop drinking 2-3 hours before coming to clinic ❑ Meaure urine volume every hour ❑ Measure urine osmolality every hour ❑ Measure plasma sodium concentration every 2 hours ❑ Measure plasma osmolality every 2 hours | |||||||||||||||||||||||||||||||||||
Test endpoints in adults: ❑ Urine osmolality reaches normal value (above 600 mosmol/kg) ❑ The urine osmolality is stable for 2 or 3 successive hourly measurements despite a rising plasma osmolality ❑ Plasma osmolality >295-300 mosmol/kg ❑ Plasma sodium is 145 or higher | |||||||||||||||||||||||||||||||||||
Treatment
Cranial diabetes insipidus:
- Cranial DI can be managed by desmopressin orally or Intranasal (rarely used).
- Partial DI can be treated with a single nocturnal dose to prevent sleep loss due to nocturia, but complete DI requires 2-4 daily doses.
Nephrogenic diabetes insipidus:
- Withdrawal of lithium therapy usually leads to reversal of lithium-induced diabetes insipid. It can persist for years after lithium withdrawal, usually indicating that the patient has developed interstitial nephritis secondary to lithium.
- Thiazide diuretics reduce urine output by up to 50%, and indomethacin has also been used. Results are frequently unsatisfactory, treatment is directed at sufficient fluid intake to replace urinary losses. [1]
Do's
Don'ts
References
- ↑ 1.0 1.1 Moore K, Thompson C, Trainer P (2003). "Disorders of water balance". Clin Med (Lond). 3 (1): 28–33. doi:10.7861/clinmedicine.3-1-28. PMC 4953350. PMID 12617410.
- ↑ Wieliczko M, Matuszkiewicz-Rowińska J (2013). "[Polyuria]". Wiad Lek. 66 (4): 324–8. PMID 24490488.
- ↑ Robertson GL: Diabetes insipidus. Endocrinol Metab Clin North Am 24:549–572, 1995.