Hyponatremia
Hyponatremia
Tod Sweeney
William W. Dexter
Basics
Description
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Decrease in serum sodium concentration to <136 mmol/L
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Serum sodium concentration and serum osmolarity normally are maintained under precise control by homeostatic mechanisms involving thirst, antidiuretic hormone (ADH), and renal handling of filtered sodium.
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Increased serum osmolarity above normal (280–300 mOsmol/kg) stimulates hypothalamic osmoreceptors, which then cause increased thirst and circulating levels of ADH.
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Can be associated with low, normal, or high tonicity
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Effective osmolality or tonicity refers to the contribution to osmolality of solutes such as sodium and glucose that cannot move freely across cell membranes, thereby inducing transcellular shifts in water.
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Most common form is hypotonic (dilutional) hyponatremia.
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Excess of water in relation to existing sodium stores, which can be decreased, normal, or increased.
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Retention of water most commonly reflects presence of conditions that impair renal excretion of water.
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Less commonly caused by excessive water intake, with normal or near-normal excretory capacity.
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Hypertonic hyponatremia results from a shift of water from cells to the extracellular fluid that is driven by solutes confined in the extracellular compartments (as occurs with hyperglycemia or retention of hypertonic mannitol).
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Pseudohyponatremia is a form of iso-osmolar and isotonic hyponatremia identified when severe hypertriglyceridemia or paraproteinemia is present, which affects accurate laboratory measurement of sodium concentration.
Epidemiology
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Occurs in 10–40% of ultraendurance athletes after a race
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7% of healthy elderly persons
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Predominant gender: Male = Female.
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More common in the very young and very old, who are less able to experience and express thirst and less able to autonomously regulate fluid intake.
Risk Factors
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Elite endurance athletes who consume excessive fluids
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In marathoners, more common in women, slower runners, and finishers who maintain or increase their body weight
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Excess fluid losses (eg, excessive sweating, vomiting, diarrhea, GI fistulas or drainage tubes, pancreatitis, burns) that have been replaced primarily by hypotonic fluids
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Infants given inappropriate amounts of free water
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Thiazide diuretics, chlorpropamide, cyclophosphamide, clofibrate, carbamazepine, opiates, oxytocin, desmopressin, vincristine, selective serotonin reuptake inhibitors, or tolbutamide
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Those with history of hepatic cirrhosis, congestive heart failure, or nephrotic syndrome, who are subject to increases in total body sodium and free water stores
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Acute or chronic renal insufficiency in patients who may be unable to excrete adequate amounts of free water or those with salt-wasting nephropathy
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Syndrome of inappropriate ADH secretion (SIADH)
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Uncorrected hypothyroidism or cortisol deficiency
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Consumption of large amounts of beer or use of the recreational drug methylenedioxy-methamphetamine (“ecstasy”)
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NSAID use
Commonly Associated Conditions
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Hyponatremic encephalopathy associated with noncardiogenic pulmonary edema in healthy marathon runners
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Cerebral edema leading to brain stem herniation and death
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Permanent CNS dysfunction
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Central pontine myelinolysis characterized by weakness, muscle spasms, diplopia, confusion, delirium, or dysphagia
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Seizures
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Rhabdomyolysis
Diagnosis
History
Thorough past medical, past surgical, medication, and social history, with special attention to signs, symptoms, and differential diagnosis as listed above
Physical Exam
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Signs and symptoms:
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Varying range depending on the chronicity, cause, and the individual
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Overhydration in athletes characterized by edema of the hands with swelling of the fingers
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Anorexia
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Headache
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Muscle cramps
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Nausea and vomiting
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Difficulty concentrating
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Confusion
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Lethargy
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Agitation
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Obtundation
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Coma
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Status epilepticus
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Physical examination:
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Most abnormalities are neurologic in origin.
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Assess level of alertness.
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Assess degree of cognitive impairment.
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Depressed deep tendon reflexes, ataxia, asterixis, pathologic reflexes, or pseudobulbar palsy (bilateral hemiplegia, dysarthria, dysphagia)
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Look for signs of focal or generalized seizure activity.
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In patients with acute severe hyponatremia, signs of brain stem herniation may be apparent, including coma; fixed, unilateral, dilated pupil; decorticate or decerebrate posturing; and respiratory arrest.
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Diagnostic Tests & Interpretation
Imaging
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Measure serum sodium level, and always consider possibility of laboratory error or improper sampling technique.
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Measure blood urea nitrogen, creatinine, uric acid, urinary osmolality, and urinary sodium.
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Measure serum osmolality (low <280 mOsmol).
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If normal (280–285 mOsmol), measure blood sugar, lipid, and protein levels.
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If elevated (>280 mOsmol), measure blood sugar.
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If serum hyperglycemia is present, then serum sodium must be corrected by a factor of 1.6 mEq/L for each 100 mg/dL increase in serum glucose.
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Consider chest x-ray, electrocardiogram, head CT scan, or other laboratory work based on history and physical examination.
Differential Diagnosis
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Adrenal insufficiency and adrenal crisis
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Congestive heart failure and pulmonary edema
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Gastroenteritis
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Hypothyroidism and myxedema coma
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Renal failure, acute
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Renal failure, chronic
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SIADH
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Cirrhosis
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Nephrotic syndrome
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Psychogenic polydipsia
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Pseudohyponatremia
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Iatrogenic
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Medication related
P.317
Treatment
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Long-term treatment
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Acute treatment
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Triathlete considerations:
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Unconscious athlete should have bladder catheterized and should be moved promptly to a hospital for definitive management.
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For severe hyponatremia (<126 mEq/L), patient should not receive fluids either orally or intravenously, except perhaps 3% saline solution (these athletes usually are volume overloaded).
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For less severe hyponatremia (>130 mEq/L), watchful waiting is the cornerstone of therapy because most will self-correct.
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Calculations:
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Change in serum Na = (infusate Na – serum Na)/total body water + 1. Estimates effect of 1 L of any infusate on serum Na.
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Total body water (in liters) is calculated as a fraction of body weight.
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Fraction = 0.6 in children; 0.6 and 0.5 in nonelderly men and women, respectively; and 0.5 and 0.45 in elderly men and women, respectively.
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Normally, extracellular and intracellular fluids account for 40% and 60% of total body water, respectively.
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Additional Treatment
General Measures
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Airway, breathing, and circulation (ABCs)
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Establish IV access.
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Determine cause by history, physical examination, and laboratory data, and direct treatment accordingly.
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There is no consensus about the optimal treatment of symptomatic hyponatremia. Increase serum sodium rapidly by 1–2 mEq/L/hr over the 1st 1–2 hr for levels <120 mEq/L.
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Patients with seizures or impending brain stem herniation should receive 3% saline (see “Calculations” above) to accomplish rapid correction, but only enough to arrest progression of symptoms; usually 4–6 mEq/L is sufficient. Be aware of cardiac status with aggressive IV therapy.
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Patients with mild symptoms and serum sodium <125 mEq/L often have chronic hyponatremia and must be managed cautiously.
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Rapid increase in serum sodium can lead to central pontine myelinolysis, but risk appears minimal if correction is at a rate <0.5 mEq/L/hr or 12 mEq/L/day. Isolated cases of osmotic demyelination after correction at 9–10 mEq/L/day have been reported; therefore, maximum correction of 8 mEq/L/day is a more conservative approach.
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Hypovolemic hyponatremia with mild to moderate symptoms is treated with normal saline (see “Calculations” above), and frequent monitoring of serum sodium levels is important to assess rate of correction.
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Hypervolemic hyponatremia treatment consists of sodium and water restriction and attention to the underlying cause.
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Euvolemic hyponatremia treatment consists of free water restriction and correction of the underlying condition.
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Patients with severe, symptomatic hyponatremia should be admitted to an ICU, with close monitoring of serum sodium levels.
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Proper management of underlying cause with close clinical follow-up
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Discontinue medications known to be associated with hyponatremia.
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Clozapine appears to be effective in long-term treatment of schizophrenic patients with compulsive water drinking.
Ongoing Care
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Although uncertainty about the diagnosis occasionally may justify a limited trial of isotonic saline, attentive follow-up is needed to confirm the diagnosis before substantial deterioration occurs.
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Isotonic saline is unsuitable for correcting the hyponatremia of SIADH.
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Great vigilance is required to recognize and diagnose hypothyroidism and adrenal insufficiency, which tend to masquerade as SIADH.
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Presence of hyperkalemia always should alert the physician to the possibility of adrenal insufficiency.
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Patients with persistent asymptomatic hyponatremia require slow-paced management, but those with symptomatic hyponatremia must receive rapid but controlled correction.
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Education on fluid intake and appropriate placement of support stations was associated with a decreased incidence of symptomatic hyponatremia at ultraendurance sporting events.
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Hypotonic fluids and excessive isotonic fluids should be avoided after surgery.
Additional Reading
Adrogue HJ, Madias N. Hyponatremia. N Engl J Med. 2000;342:1581–1589.
Ayus JC, Varon J, Arieff AI. Hyponatremia, cerebral edema, and noncardiogenic pulmonary edema in marathon runners. Ann Intern Med. 2000;132:711–714.
Craig S. http://www.emedicine.com/emerg/topic275.htm (hyponatremia). http://dynamicmedical.com Hyponatremia (hypotonic)
Kugler JP, Hustead T. Hyponatremia and hypernatremia in the elderly. Am Fam Physician. 2000;61:3623–3630.
Noakes TD, Mayers LB. A guide to treating ironman triathletes at the finish line. Physician Sportsmed. 2000;28.
Speedy DB, Rogers IR, Noakes TD, et al. Diagnosis and prevention of hyponatremia at an ultradistance triathlon. Clin J Sports Med. 2000;10:52–58.
Codes
ICD9
276.1 Hyposmolality and/or hyponatremia
Clinical Pearls
In ultraendurance athletes, IV should not be used unless there are signs of dehydration, including cardiovascular instability.