Polyuria resident survival guide: Difference between revisions

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==Overview==
==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).<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>
* 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), cranial diabetes insipidus (DI) (decreased secretion of arginine vasopressin (AVP)), and nephrogenic diabetes insipidus DI (renal resistance to AVP).<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>


==Causes==
==Causes==

Revision as of 11:11, 7 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), cranial 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

Do's

Don'ts

References

  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.
  2. Wieliczko M, Matuszkiewicz-Rowińska J (2013). "[Polyuria]". Wiad Lek. 66 (4): 324–8. PMID 24490488.
  3. Robertson GL: Diabetes insipidus. Endocrinol Metab Clin North Am 24:549–572, 1995.