hypernatremia
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Etiology
- excessive loss of free water (most common)
- sweating - fever
- diarrhea
- diuretics concurrent with fluid restriction
- osmotic diuresis
- diabetes insipidus
- loss of urine-concentrating ability
- polyuric phase of acute tubular necrosis (ATN)
- postobstructive uropathy
- hypercalcemia
- hypokalemia
- lack of thirst
- excessive sodium intake
- incorrect reconstitution of infant formula
- high osmolar enteral feedings
- use of NaHCO3 in cardiopulmonary resuscitation
- hypertonic diasylate
- table salt ingestion
- hypothalamic dysfunction (impaired pituitary secretion of ADH)
- shift in hypotonic water from intracellular to extracellular space
- adrenal hyperfunction
- Cushing's disease
- primary hyperaldosteronism
- mild hypernatremia
- predisposing factors
Pathology
- hyperosmolarity
- total body water loss
- blunted thirst mechanism or inability to ingest water sufficient to replenish losses
- impaired pituitary secretion of ADH
Clinical manifestations
- symptoms appear with [Na+] > 155-160 meq/L
- central nervous system
- lethargy
- muscle weakness
- confusion
- seizures & irritability in infants
- intracerebral or subarachnoid hemorrhage
- rupture of cerebral veins secondary to changes in brain volume
- coma
- death
- thirst may go unrecognized secondary to decreased state of consciousness
- symptoms related to rate of change of sodium concentration
- acute hypertonicity leads to neuronal shrinkage
- during chronic hypernatremia, cellular adaptation occurs
- signs of dehydration
- hypotension
- tachycardia
- poor skin turgor
- sunken eyes
- may not be recognized in the elderly
- generally associated with systemic disorder
Laboratory
- serum chemistries
- appropriate tests for underlying systemic disorder
- free water deficit = total body water x (140/Na+ - 1)
- total body water in liters = 0.6 x weight in kg
- free water clearance (in liters)
- urine volume x (1 - (urine Na+ + urine K+)/serum Na+)
- urine osmolality
- maximally concentrated with inadequate water intake
- in the elderly, this may be only 600-800 mosm/kg (500-700)[7]
- inappropriately dilute urine in patients with renal water loss (i.e diabetes insipidus, hyperglycemia of diabetes mellitus)
- maximally concentrated with inadequate water intake
- lumbar puncture
- increased CSF protein
- few if any WBC in CSF
- not necessarily indicated
Complications
- cerebral edema & seizures may occur with excessively rapid correction of hypernatremia
- survivors often show neurologic sequelae
Management
- correct hypernatremia over 48-72 hours
- acute hypernatremia may be treated more rapidly
- 5% dextrose titrated to serum sodium of 140-145 meq/L over 24 hours[10]
- add free water deficit + free water clearance + 10 mL/kg/day to determine water deficit (see Laboratory above)
- rate of correction < 0.5 meq/l/hour
- time period necessary to correct free water deficit: (measured [Na+] - desired [Na+]) / 0.5 meq/L/hr
- no more than 1/2 of the calculated water deficit should be given in the 1st 24 hours[3]
- < 10 meq/L should be corrected in the 1st 24 hours to prevent cerebral edema[3]
- acute hypernatremia may be treated more rapidly
- replacement fluids
- correct hypovolemia (hypotension) with normal saline or lactated ringers
- hypotonic fluids appropriate after hypovolemia (hypotension) corrected
- water
- D5W
- 1/2 normal saline
- generally decreased level of consciousness dictates IV replacement
- replacement may be oral if patient is awake
- water treatment of choice orally or by NG-tube[3]
- hypotensive or tachycardic patient
- normal saline or lactated ringers may be used initially
- frequent electrolyte measurements to determine response to therapy
- diabetes insipidus (impaired pituitary secretion of ADH) is treated with desmopression (intranasal or oral)
More general terms
Additional terms
References
- ↑ Saunders Manual of Medical Practice, Rakel (ed), WB Saunders, Philadelphia, 1996, pg 677-78
- ↑ Mayo Internal Medicine Board Review, 1998-99, Prakash UBS (ed) Lippincott-Raven, Philadelphia, 1998, pg 600-601
- ↑ 3.0 3.1 3.2 3.3 Medical Knowledge Self Assessment Program (MKSAP) 11, 15, 16, 17, 18, 19. American College of Physicians, Philadelphia 1998, 2009, 2012, 2015, 2018, 2021.
Medical Knowledge Self Assessment Program (MKSAP) 19 Board Basics. An Enhancement to MKSAP19. American College of Physicians, Philadelphia 2022 - ↑ Pokaharel M, Block CA. Dysnatremia in the ICU. Curr Opin Crit Care. 2011 Dec;17(6):581-93 PMID: https://www.ncbi.nlm.nih.gov/pubmed/22027406
- ↑ Alshayeb HM, Showkat A, Babar F, Mangold T, Wall BM. Severe hypernatremia correction rate and mortality in hospitalized patients. Am J Med Sci. 2011 May;341(5):356-60. PMID: https://www.ncbi.nlm.nih.gov/pubmed/21358313
- ↑ Adrogue HJ, Madias NE. Hypernatremia. N Engl J Med. 2000 May 18;342(20):1493-9. Review. PMID: https://www.ncbi.nlm.nih.gov/pubmed/10816188
- ↑ 7.0 7.1 Geriatric Review Syllabus, 9th edition (GRS9) Medinal-Walpole A, Pacala JT, Porter JF (eds) American Geriatrics Society, 2016
Geriatric Review Syllabus, 11th edition (GRS11) Harper GM, Lyons WL, Potter JF (eds) American Geriatrics Society, 2022 - ↑ Sam R, Feizi I. Understanding hypernatremia. Am J Nephrol. 2012;36(1):97-104. Epub 2012 Jun 27. Review. PMID: https://www.ncbi.nlm.nih.gov/pubmed/22739333 Free Article
- ↑ Lindner G, Funk GC. Hypernatremia in critically ill patients. J Crit Care. 2013;28(2):216.e11-20 PMID: https://www.ncbi.nlm.nih.gov/pubmed/22762930 https://www.sciencedirect.com/science/article/abs/pii/S0883944112001621
- ↑ 10.0 10.1 NEJM Knowledge+ Nephrology/Urology
- ↑ Seay NW, Lehrich RW, Greenberg A. Diagnosis and management of disorders of body tonicity-hyponatremia and hypernatremia: core curriculum 2020. Am J Kidney Dis. 2020;75:272-286. PMID: https://www.ncbi.nlm.nih.gov/pubmed/31606238