Polyuria resident survival guide: Difference between revisions
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===Diagnostic Approach=== | ===Diagnostic Approach=== | ||
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{{ | {{Family tree | | | | | | | | | | | | | A01 | | | | |A01='''Suspected hypotonic polyuria'''<ref name="pmid30779536">{{cite journal| author=Feingold KR, Anawalt B, Boyce A, Chrousos G, de Herder WW, Dungan K | display-authors=etal| title=Endotext | journal= | year= 2000 | volume= | issue= | pages= | pmid=30779536 | doi= | pmc= | url= }} </ref>}} | ||
{{Family tree | | | | | | | | | | | | | |!| | | | | }} | |||
{{ | {{Family tree | | | | | | | | | | | | | B01 | | | | |B01='''confirm presence of polyuria''':(>50ml/kg/24hrs or >3-4L/day)}} | ||
{{ | {{Family tree | | | | | | | | | | |,|-|-|^|-|-|.| | }} | ||
{{ | {{Family tree | | | | | | | | | | C01 | | | | C02 |C01=(polyuria confirmed):<br>'''measure urine osmolality'''|C02=(no polyuria/ or >800 mOsm/kg):<br>'''diabetes insipidus(DI)/primary polydipsia ruled out'''}} | ||
{{ | {{family tree | | | | | | | | | | |!| | | | | | }} | ||
{{ | {{Family tree | | | | | | | | | | D01 | | | | | | |D01=(<800 mOsm/kg:hypotonic polyuria confirmed:<br>'''measure serum sodium and plasma osmolality'''}} | ||
{{ | {{Family tree | | | | | | | | | | |!| | | | | | }} | ||
{{ | {{Family tree | | | | | | |,|-|-|-|^|-|-|v|-|-|-|-|-|.| | | }} | ||
{{ | {{Family tree | | | | | | E01 | | | | | E02 | | | | E03 | |E01=low normal or low serum sodium <150 mmol/L), plasma osmolality <280 mOsm/kg)<br>'''primary polydipsia'''| E02=normal serum <br>sodium/plasma osmolality: <br>'''indeterminate diagnosis'''| E03=high serum sodium>146 mmol/L), plasma osmolality>300 mOsm/kg):<br>'''central or nephrogenic DI'''}} | ||
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===Therapeutic Approach=== | ===Therapeutic Approach=== | ||
Revision as of 11:42, 27 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]
- Nocturnal polyuria (NP), characterized by overproduction of urine at night (more than 20%-33% of total 24-hour urine volume depending on age). It can be caused by intake, urological, nephrological, hormonal, sleep, and cardiovascular factors. [2]
Causes
Life Threatening Causes
Common causes [3] [2]
- The most common causes of polyuria are:
- Psychogenic polydipsia
- Diabetes insipidus DI (central and nephrogenic)
- Chronic kidney disease (CKD)
- Uncontrolled diabetes mellitus (DM)
- Nocturnal Polyuria (NP) can be caused by different medical conditions including:
- Congestive heart failure (CHF)
- Diabetes mellitus (DM)
- Obstructive sleep apnea (OSA)
- Peripheral edema
- Excessive nighttime fluid intake
- Abnormalities in antidiuretic hormone arginine vasopressin (AVP) secretion can cause overproduction of urine at night
- Nocturnal Polyuria Syndrome, in the absence of any medical condition, it can be due to impaired circadian release of Arginine vasopressin(AVP).
Diagnosis
- Water deprivation test combined with desmopressin administration is the diagnostic gold standard, it differentiates between the causes of the polyuria‐polydipsia syndrome.
- The c‐terminal portion of the larger precursor peptide of Arginine Vasopressin AVP (co-peptin), has been evaluated in the setting of polyuria‐polydipsia syndrome, can be useful for the differential diagnosis. [4]
Management
Diagnostic Approach
Therapeutic Approach
Do's
Don'ts
References
- ↑ 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.
- ↑ 2.0 2.1 Weiss JP, Everaert K (2019). "Management of Nocturia and Nocturnal Polyuria". Urology. 133S: 24–33. doi:10.1016/j.urology.2019.09.022. PMID 31586470.
- ↑ Wieliczko M, Matuszkiewicz-Rowińska J (2013). "[Polyuria]". Wiad Lek. 66 (4): 324–8. PMID 24490488.
- ↑ Nigro N, Grossmann M, Chiang C, Inder WJ (2018). "Polyuria-polydipsia syndrome: a diagnostic challenge". Intern Med J. 48 (3): 244–253. doi:10.1111/imj.13627. PMID 28967192.
- ↑ Feingold KR, Anawalt B, Boyce A, Chrousos G, de Herder WW, Dungan K; et al. (2000). "Endotext". PMID 30779536.
| Suspected hypotonic polyuria[5] | |||||||||||||||||||||||||||||||||||||||||||||
| confirm presence of polyuria:(>50ml/kg/24hrs or >3-4L/day) | |||||||||||||||||||||||||||||||||||||||||||||
| (polyuria confirmed): measure urine osmolality | (no polyuria/ or >800 mOsm/kg): diabetes insipidus(DI)/primary polydipsia ruled out | ||||||||||||||||||||||||||||||||||||||||||||
| (<800 mOsm/kg:hypotonic polyuria confirmed: measure serum sodium and plasma osmolality | |||||||||||||||||||||||||||||||||||||||||||||
| low normal or low serum sodium <150 mmol/L), plasma osmolality <280 mOsm/kg) primary polydipsia | normal serum sodium/plasma osmolality: indeterminate diagnosis | high serum sodium>146 mmol/L), plasma osmolality>300 mOsm/kg): central or nephrogenic DI | |||||||||||||||||||||||||||||||||||||||||||