Hyponatremia is one of the more common electrolyte abnormalities in clinical medicine. Some sources estimate that the number of patients who experience sodium levels of less than 135 meq/L can be as high as 30% of all hospitalized patients. Management of hyponatremia is important because severe hyponatremia can cause substantial morbidity and mortality. One article cited a 1986 study in which 27% of previously healthy women undergoing elective surgery died after developing acute hyponatremia (averaging 108 mmol/L). Morbidity and mortality from hyponatremia is significantly higher in patients with underlying disease processes.
Classification of hyponatremia may help to determine its causes. In general, hyponatremia is classified based on volume status. Causes of hypovolemic hyponatremia may include excessive sodium losses from the kidneys, the skin, or the GI tract and also includes “third spacing” of fluids. Causes of euvolemic hyponatremia may include etiologies such as SIADH and psychogenic polydipsia. Many conditions stimulate ADH production including angiotensin release, hypovolemia, increased serum osmolality, hypotension, opiates, caffeine, and stress. ADH may be inappropriately secreted due to CNS or pulmonary infections and due to multiple medications including most diuretics. Causes of hypervolemic hyponatremia may include fluid overload states such as CHF, pregnancy, cirrhosis, and nephrotic syndrome. Serum sodium levels may also be artificially low with increased levels of plasma proteins or lipids and with increased serum concentration of osmotically active chemicals such as glucose and mannitol.
Clinical manifestations of hyponatremia depend on multiple factors including the chronicity of the symptoms, the absolute level of sodium, and the patient's overall health. The most common manifestations of hyponatremia are CNS-related and include mental status changes such as lethargy, confusion, disorientation, and agitation. Other symptoms such as nausea, vomiting, and weakness can also occur.
Severe hyponatremia may result in cerebral edema, encephalopathy and death.
General management of hyponatremia
Management of hyponatremia should take into account the chronicity of the disease. When hyponatremia is acute, an osmotic shift of free water into brain cells occurs, resulting in varying degrees of cerebral edema. When hyponatremia occurs over more than 48 hours, brain cells have more time to adapt to osmotic fluid shifts and significant amounts of cerebral edema are therefore less likely.
One of the more difficult aspects of managing symptomatic hyponatremia is determining the proper rate of sodium repletion. Expert panel guidelines on the management of hyponatremia note that “optimal treatment strategies [for hyponatremia] have not been well defined.” Patients with acute hyponatremia generally exhibit more symptoms than those with chronic hyponatremia and usually tolerate more rapid correction of their sodium levels. On the other hand, patients with chronic hyponatremia often have fewer clinical symptoms are are more likely to develop complications from rapid sodium repletion. If hyponatremia is corrected too rapidly in a patient with chronic hyponatremia, the rapid osmotic shift can cause osmotic demyelination, otherwise known as central pontine myelinolysis.
Guidelines on the management of hyponatremia published in 2007 recommended sodium correction of approximately 8 mmol/L per day and approximate limits of sodium correction to less than 12 mmol/L in 24 hours and less than 18 mmol/L in 48 hours. However, these guidelines also cited one study showing that severe demyelinating brain lesions rarely occurred unless the rate of sodium correction was more than 25 mmol/L in 48 hours. Other sources recommend correcting symptomatic acute hyponatremia at rates of up to 2 mEq/L/hr and correcting symptomatic chronic hyponatremia at rates of up to 0.5 mEq/L/hr until the patient's serum sodium level reaches 120 mEq/L or rises by 10 mmol/L in 24 hours.
In this case a patient presented to the emergency department with severe hyponatremia. According to the expert testimony, the patient was falling and was having difficulty with her motor function. She was unable to walk and her speech was difficult to understand. Despite these symptoms, she was also noted to be conversing with her daughter in the room.
The patient had been having “flu-like symptoms” for the previous two weeks and had been vomiting for the previous 4 days. She complained of abdominal pain on one occasion during the emergency physician's evaluation.
In the ensuing lawsuit, the plaintiff expert witness made several assertions which included the following
After reviewing the expert’s testimony and the available literature in this case, the Standard of Care Panel came to the following conclusions.
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