Polyuria resident survival guide: Difference between revisions
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* [[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]]), [[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> | ||
==Causes== | ==Causes== | ||
Revision as of 02:33, 16 October 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
- Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.
- Polyuria does not have life threatening causes.
Common causes [2] [3]
- The most common causes of polyuria are:
- Pregnancy
- Psychogenic polydipsia
- Central diabetes insipidus (CDI)
- Nephrogenic diabetes insipidus (NDI)
- Diabetes mellitus (DM)
- Chronic kidney disease (CKD)
- Urinary tract infection (UTI)
- Interstitial cystitis
- Nephrolithiasis
- Primary hyperparathyroidism
- Familial hypocalciuric hypercalcemia
- Hypercalcemia
- Hypokalemia
- Sickle cell disease (SCD)
- Stroke or neurological diseases
- Benign prostatic hyperplasia (BPH)
- Stress incontinence
- Medications:
- Overactive bladder
- Drinking alcohol or caffeine
Management
Shown below is an algorithm summarizing the approach to polyuria.
| Suspected hypotonic polyuria[4] | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| 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 | |||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Water deprivation test | Baseline plasma copeptin | Hypertonic saline infusion test | |||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Urine Osm >800 mOsm/kg | Urine Osm <300 mOsm/kg | Urine Osm 300-800 mOsm/kg | Plasma coprptin >4.9pmol/L | Plasma coprptin <4.9pmol/L | |||||||||||||||||||||||||||||||||||||||||||||||||||||
| Mild primary polyuria | Desmopressin administration | >21pmol/L | <2.6pmol/L | >2.6pmol/L | |||||||||||||||||||||||||||||||||||||||||||||||||||||
| (Urine Osmolality: 300-800 mOsm/Kg and <50% increase): Therapeutic trial with desmopressin | Nephrogenic DI(partial or complete) | Complete Central DI | |||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary polydipsia | Partial Nephrogenic DI | Partial Central DI | |||||||||||||||||||||||||||||||||||||||||||||||||||||||
| (Initial urine osmolality: 30 mOsm/kg and >50% increase after desmopressin): Complete Central DI | (Urine osmolality <300 mOsm/kg or <50% increase): Complete Nephrogenic DI | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Polyuria ❑ 24-hour urine volume >3L ❑ 24-hour urine volume >50 ml/kg | |||||||||||||||||||||||||||||||||||||||||
| Urine Osmolality >300mosmol | Urine Osmolality <300[5]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)[means that ADH release and effect are intact] ❑ 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 | |||||||||||||||||||||||||||||||||||||||||
| In the last 3 settings desmopressin 10mcg intranasal, or 4mcg SC/IV is administered ❑ Measure urine volume and urine osmolality every 30 minutes over the next two hours | |||||||||||||||||||||||||||||||||||||||||
| >100% rise in urine osmolality | 15-50% rise in urine osmolality after administration of exogenous desmopressin | <15% rise in urine osmolality | |||||||||||||||||||||||||||||||||||||||
| Complete central diabetes inspidous[6] | Partial central DI or partial nephrogenic DI[7] | complete nephrogenic DI or '''primary polydipsia''' | |||||||||||||||||||||||||||||||||||||||
| Check plasma and urine ADH[8]and copeptin prior to administration of exogenous ADH ❑ Increase in plasma/urine ADH in response to rising plasma osmolality excludes central DI ❑ Appropriate elevation in urine osmolality as ADH secretion is increased excludes nephrogenic DI ❑ Copeptin > 21.4 picomol/L differentiates Nephrogenic DI from other etiologies with 100% sensivity and specifity[9] | |||||||||||||||||||||||||||||||||||||||||
| Polyuria (Urine Output > 3L/d)[10] | |||||||||||||||||||||||||||||||||||||||||
| Urine Osmolality | |||||||||||||||||||||||||||||||||||||||||
| Uosm <100mOsm/kg (Water Diuresis) *Psychogenic Polydipsia *DI (central and nephrogenic) | Uosm =100-300mOsm (Mixed Polyuria) *Partial DI(central and Nephrogenic) *Simultaneous water and solute intake *CKD | Uosm >300mOsm/kg (Solute Diuresis) *Hyperglycemia *Azotemia *High solute intake intravenous fluids enteral and parenteral nutrition Exogenous supplements | |||||||||||||||||||||||||||||||||||||||
| Water Deprivation Test | 24-Hour Urine Collection (estimation of osmoles) *Urine sodium *Urine potassium *Urine glucose *Urine urea nitrogen *Other osmoles | ||||||||||||||||||||||||||||||||||||||||
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.
- ↑ Wieliczko M, Matuszkiewicz-Rowińska J (2013). "[Polyuria]". Wiad Lek. 66 (4): 324–8. PMID 24490488.
- ↑ 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.
- ↑ Feingold KR, Anawalt B, Boyce A, Chrousos G, de Herder WW, Dungan K; et al. (2000). "Endotext". PMID 30779536.
- ↑ Robertson GL: Diabetes insipidus. Endocrinol Metab Clin North Am 24:549–572, 1995.
- ↑ Zerbe RL, Robertson GL: A comparison of plasma vasopressin measurements with a standard indirect test in the differential diagnosis of polyuria. The New England journal of medicine 1981, 305(26):1539-1546.
- ↑ Miller M, Dalakos T, Moses AM, Fellerman H, Streeten DH: Recognition of partial defects in antidiuretic hormone secretion. Annals of internal medicine 1970, 73(5):721-729.
- ↑ Diederich S, Eckmanns T, Exner P, Al-Saadi N, Bahr V, Oelkers W: Differential diagnosis of polyuric/polydipsic syndromes with the aid of urinary vasopressin measurement in adults. Clinical endocrinology 2001, 54(5):665-671.
- ↑ Timper K, Fenske W, Kuhn F, Frech N, Arici B, Rutishauser J, Kopp P, Allolio B, Stettler C, Muller B et al: Diagnostic Accuracy of Copeptin in the Differential Diagnosis of the Polyuria-polydipsia Syndrome: A Prospective Multicenter Study. The Journal of clinical endocrinology and metabolism 2015, 100(6):2268-2274.
- ↑ Bhasin B, Velez JC (2016). "Evaluation of Polyuria: The Roles of Solute Loading and Water Diuresis". Am J Kidney Dis. 67 (3): 507–11. doi:10.1053/j.ajkd.2015.10.021. PMID 26687922.