Hyponatremia

Hyponatremia
Classification and external resources

Sodium
ICD-10 E87.1
ICD-9 276.1
DiseasesDB 6483
eMedicine emerg/275 med/1130 ped/1124
MeSH D007010

Hyponatremia (Brit. hyponatraemia) is an electrolyte disturbance in which the sodium concentration in the serum is lower than normal. Sodium is the dominant extracellular cation and cannot freely cross the cell membrane. Its homeostasis is vital to the normal physiologic function of cells. Normal serum sodium levels are between 135-145 mEq/L. Hyponatremia is defined as a serum level of less than 135 mEq/L and is considered severe when the serum level is below 125 mEq/L.[1]

Hyponatremia is most often a complication of other medical illnesses in which either fluids rich in sodium are lost (for example because of diarrhea or vomiting) or excess water accumulates in the body at a higher rate than can be excreted (for example in congestive heart failure, syndrome of inappropriate antidiuretic hormone, SIADH, or polydipsia). Regarding sodium loss as a cause of hyponatremia, it is important to note that such losses promote hyponatremia in only an indirect manner. In particular, hyponatremia occurring in association with sodium loss does not reflect inadequate sodium availability as a result of the losses. Rather, the sodium loss leads to a state of volume depletion, with volume depletion serving as signal for the release of ADH (anti-diuretic hormone). As a result of ADH-stimulated water retention, blood sodium becomes diluted and hyponatremia results.

Hyponatremia can also affect athletes who consume too much fluid during endurance events,[2] people who fast on juice or water for extended periods and people whose dietary sodium intake is chronically insufficient.

Contents

Frequency

Hyponatremia is the most common electrolyte disorder. Its frequency is higher in females, the elderly, and in patients that are hospitalized. The incidence of hyponatremia depends largely on the patient population. A hospital incidence of 15-20% is common, while only 3-5% of patients who are hospitalized have a serum sodium level of less than 130 mEq/L. Hyponatremia has been reported in up to 30% of elderly patients in nursing homes and is also present in approximately 30% of depressed patients on selective serotonin reuptake inhibitors.[3]

Symptoms

Symptoms of hyponatremia include nausea and vomiting, headache, confusion, lethargy, fatigue, appetite loss, restlessness and irritability, muscle weakness, spasms, or cramps, seizures, and decreased consciousness or coma. The presence and severity of symptoms are associated with the level of serum sodium, with the lowest levels of serum sodium associated with the more prominent and serious symptoms. However, emerging data suggests that mild hyponatremia (serum sodium levels at 131 mEq/L or above) was associated with numerous complications and undiagnosed symptoms.[4]

Many medical illnesses, such as congestive heart failure, liver failure, renal failure, or pneumonia may be associated with hyponatremia. These patients frequently present because of primary disease symptomatology and are diagnosed after presenting due to manifestations of other medical issues.

Neurological symptoms often show for extremely low levels of sodium. When sodium levels in blood become too low, excess water enters cells and causes the cells to swell. Swelling in the brain is especially dangerous because the brain is confined by the skull and is unable to expand. Neurological symptoms most often are due to very low serum sodium levels (usually <115 mEq/L), resulting in intracerebral osmotic fluid shifts and brain edema. This neurological symptom complex can lead to tentorial herniation with subsequent brain stem compression and respiratory arrest, resulting in death in the most severe cases. The severity of neurological symptoms correlates with the rapidity and severity of the drop in serum sodium. A gradual drop, even to very low levels, may be tolerated well if it occurs over several days or weeks, because of neuronal adaptation. The presence of underlying neurological disease, like a seizure disorder, or non-neurological metabolic abnormalities, also affects the severity of neurologic symptoms.

Examination

Examination should include orthostatic vital signs and an accurate assessment of volume status. This determination (i.e. hypervolemic, euvolemic, hypovolemic) often guides treatment decisions. A full assessment of medical comorbidity also is essential, with particular attention paid to cardiopulmonary and neurological components of the examination.

Types of Occurrence

The imbalance between sodium and water in blood may occur in three primary ways:

In Chronic hyponatremia sodium levels drop gradually over several days or weeks and symptoms and complications are typically moderate. Chronic hyponatremia is often called asymptomatic hyponatremia in clinical settings because it is thought to have no symptoms; however, emerging data suggests that “asymptomatic” hyponatremia is not actually asymptomatic.[5]

In Acute hyponatremia sodium levels drop rapidly, resulting in potentially dangerous effects, such as rapid brain swelling, which can result in coma and death.

Causes

Many possible conditions and lifestyle factors can lead to hyponatremia, including:

Risk Factors

The following factors may increase risk of hyponatremia:

Complications

Chronic hyponatremia can lead to such complications as neurological impairments. These neurological impairments most often affect gait and attention and can lead to falls, osteoporosis, and decreased reaction time.

Complications for chronic hyponatremia are most dangerous for geriatric patients. Falls are the leading cause of deaths related to injury among people 65 years or older. In a recent study[6] the incidence of hyponatremia in elderly patients with large-bone fractures was more than double that of non-fracture patients. Recent work by Verbalis et al[7] suggests that hyponatremia induces osteoporosis and found the adjusted odds ratio for developing osteoporosis to be 2.87 times higher among adults with mild hyponatremia compared to those without.

Acute hyponatremia can lead to much more serious complications including brain disease, brain herniation, cardiopulmonary arrest, cerebral edema, seizures, coma, and death.

Treatment

The treatment of hyponatremia often depends on the underlying cause. If a person is truly asymptomatic or has only subtle symptoms, little treatment other than water restriction may be required. In a setting of volume depletion, intravenous administration of normal saline may be effective.

Pharmaceutically, vasopressin receptor antagonists can be used in the treatment of hyponatremia, especially in patients with congestive heart failure or liver cirrhosis. A vasopressin receptor antagonist is an agent that interferes with the action at the vasopressin receptors. Vasopressin is also known as ADH, the anti-diuretic hormone.

A new class of medication, the “vaptan” drugs has been specifically developed to inhibit the action of vasopressin on its receptors (V1A, V1B, and V2). These receptors have a variety of functions, with the V1A and V2 receptors are expressed peripherally and involved in the modulation of blood pressure and kidney function respectively, while the V1A and V1B receptors are expressed in the central nervous system. V1A is expressed in many regions of the brain, and has been linked to a variety of social behaviors in humans and animals.

The “vaptan” class of drugs contains a number of compounds with varying selectivity, several of which are either already in clinical use or in clinical trials as of 2010

Unselective (mixed V1A, V2) Conivaptan

V1A selective Relcovaptan

V1B selective Nelivaptan

V2 selective Lixivaptan Mozavaptan Satavaptan Tolvaptan The V2-receptor antagonists tolvaptan and conivaptan allow excretion of electrolyte free water and are effective in increasing serum sodium in euvolemic and hypervolemic hyponatremia.[8]

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In animals

Sodium deficiency exists in grazing animals where soil sodium levels have been depleted by leaching. This is more common in mountainous regions. Agricultural science research conducted in the northern Thai highlands in the 1970s found that an endemic sodium deficiency masked all other nutrient deficiencies across all seasons and reduced productivity. Sodium supplementation increased liveweight gain by around 30% and also reproductive rates by around 30%. Simple salt supplementation is now recommended in this region and neighbouring mountains, as both a herd management tool and for increased productivity.[9]

See also

References

  1. http://www.mayoclinic.com/health/hyponatremia/DS00974
  2. http://sportsmedicine.about.com/od/hydrationandfluid/a/Hyponatremia.htm Hyponatremia and athletes
  3. Schrier, Robert W. "Does 'asymptomatic hyponatremia' exist?" Nature Reviews Nephrology. Vol 6, Apr 2010; p 185.
  4. Schrier, Robert W. "Does 'asymptomatic hyponatremia' exist?" Nature Reviews Nephrology. Vol 6, Apr 2010; p 185.
  5. Schrier, Robert W. "Does 'asymptomatic hyponatremia' exist?" Nature Reviews Nephrology. Vol 6, Apr 2010; p 185.
  6. Harminder, S. Sandhu et al. "Hyponatremia associated with large-bone fracture in elderly patients." Int Urol Nephrol (2009) 41:733-737.
  7. Ayus, Juan Carlos and Michael L. Moritz. "Bone Disease as a New Complication of Hyponatremia: Moving Beyond Brain Injury". CJASN ePress. Jan 14, 2010. 10.2215/CJN.09281209.
  8. Robert D. Zenenberg,Do, et. al (February 2010). "Hyponatremia: Evaluation and Management". Hospital Practice. 38 (1): 89–96. doi:10.3810/hp.2010.02.283. http://hosppract.com/index.php?article=283#none. 
  9. Lindsay Falvey (1979) 'Factors Limiting Cattle Production in the Northern Thailand Highlands'. Ph.D. Dissertation, University of Queensland, Australia.

External links