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Hyponatremia



Ovid: 5-Minute Sports Medicine Consult, The


Hyponatremia
Tod Sweeney
William W. Dexter
Basics
Description
  • Decrease in serum sodium concentration to <136 mmol/L
  • 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.
  • Increased serum osmolarity above normal (280–300 mOsmol/kg) stimulates hypothalamic osmoreceptors, which then cause increased thirst and circulating levels of ADH.
  • Can be associated with low, normal, or high tonicity
  • 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.
  • Most common form is hypotonic (dilutional) hyponatremia.
    • Excess of water in relation to existing sodium stores, which can be decreased, normal, or increased.
    • Retention of water most commonly reflects presence of conditions that impair renal excretion of water.
    • Less commonly caused by excessive water intake, with normal or near-normal excretory capacity.
  • 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).
  • 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
  • Occurs in 10–40% of ultraendurance athletes after a race
  • 7% of healthy elderly persons
  • Predominant gender: Male = Female.
  • 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
  • Elite endurance athletes who consume excessive fluids
  • In marathoners, more common in women, slower runners, and finishers who maintain or increase their body weight
  • Excess fluid losses (eg, excessive sweating, vomiting, diarrhea, GI fistulas or drainage tubes, pancreatitis, burns) that have been replaced primarily by hypotonic fluids
  • Infants given inappropriate amounts of free water
  • Thiazide diuretics, chlorpropamide, cyclophosphamide, clofibrate, carbamazepine, opiates, oxytocin, desmopressin, vincristine, selective serotonin reuptake inhibitors, or tolbutamide
  • 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
  • Acute or chronic renal insufficiency in patients who may be unable to excrete adequate amounts of free water or those with salt-wasting nephropathy
  • Syndrome of inappropriate ADH secretion (SIADH)
  • Uncorrected hypothyroidism or cortisol deficiency
  • Consumption of large amounts of beer or use of the recreational drug methylenedioxy-methamphetamine (“ecstasy”)
  • NSAID use
Commonly Associated Conditions
  • Hyponatremic encephalopathy associated with noncardiogenic pulmonary edema in healthy marathon runners
  • Cerebral edema leading to brain stem herniation and death
  • Permanent CNS dysfunction
  • Central pontine myelinolysis characterized by weakness, muscle spasms, diplopia, confusion, delirium, or dysphagia
  • Seizures
  • 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
  • Signs and symptoms:
    • Varying range depending on the chronicity, cause, and the individual
    • Overhydration in athletes characterized by edema of the hands with swelling of the fingers
    • Anorexia
    • Headache
    • Muscle cramps
    • Nausea and vomiting
    • Difficulty concentrating
    • Confusion
    • Lethargy
    • Agitation
    • Obtundation
    • Coma
    • Status epilepticus
  • Physical examination:
    • Most abnormalities are neurologic in origin.
    • Assess level of alertness.
    • Assess degree of cognitive impairment.
    • Depressed deep tendon reflexes, ataxia, asterixis, pathologic reflexes, or pseudobulbar palsy (bilateral hemiplegia, dysarthria, dysphagia)
    • Look for signs of focal or generalized seizure activity.
    • 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.
Diagnostic Tests & Interpretation
Imaging
  • Measure serum sodium level, and always consider possibility of laboratory error or improper sampling technique.
  • Measure blood urea nitrogen, creatinine, uric acid, urinary osmolality, and urinary sodium.
  • Measure serum osmolality (low <280 mOsmol).
    • If normal (280–285 mOsmol), measure blood sugar, lipid, and protein levels.
    • If elevated (>280 mOsmol), measure blood sugar.
  • 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.
  • Consider chest x-ray, electrocardiogram, head CT scan, or other laboratory work based on history and physical examination.
Differential Diagnosis
  • Adrenal insufficiency and adrenal crisis
  • Congestive heart failure and pulmonary edema
  • Gastroenteritis
  • Hypothyroidism and myxedema coma
  • Renal failure, acute
  • Renal failure, chronic
  • SIADH
  • Cirrhosis
  • Nephrotic syndrome
  • Psychogenic polydipsia
  • Pseudohyponatremia
  • Iatrogenic
  • Medication related

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Ongoing Care
  • 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.
  • Isotonic saline is unsuitable for correcting the hyponatremia of SIADH.
  • Great vigilance is required to recognize and diagnose hypothyroidism and adrenal insufficiency, which tend to masquerade as SIADH.
  • Presence of hyperkalemia always should alert the physician to the possibility of adrenal insufficiency.
  • Patients with persistent asymptomatic hyponatremia require slow-paced management, but those with symptomatic hyponatremia must receive rapid but controlled correction.
  • Education on fluid intake and appropriate placement of support stations was associated with a decreased incidence of symptomatic hyponatremia at ultraendurance sporting events.
  • 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


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