What are the causes of HYPONATEMIA and it's treatment?

Answer 1

Background

Serum sodium concentration and serum osmolarity normally are maintained under precise control by homeostatic mechanisms involving stimulation of thirst, secretion of antidiuretic hormone (ADH), and renal handling of filtered sodium. Clinically significant hyponatremia is relatively uncommon and is nonspecific in its presentation; therefore, the ED physician must consider the diagnosis in patients presenting with vague constitutional symptoms or with altered level of consciousness. Irreparable harm can befall the patient when abnormal serum sodium levels are corrected too quickly or too slowly. The ED physician must have a thorough understanding of the pathophysiology of hyponatremia to initiate safe and effective corrective therapy. The patient's fluid status must be accurately assessed upon presentation, as it guides the approach to correction.

Hypovolemic hyponatremia

Total body water (TBW) decreases; total body sodium (Na+) decreases to a greater extent. The extracellular fluid (ECF) volume is decreased.

Euvolemic hyponatremia

TBW increases while total sodium remains normal. The ECF volume is increased minimally to moderately but without the presence of edema.

Hypervolemic hyponatremia

Total body sodium increases, and TBW increases to a greater extent. The ECF is increased markedly, with the presence of edema.

Redistributive hyponatremia

Water shifts from the intracellular to the extracellular compartment, with a resultant dilution of sodium. The TBW and total body sodium are unchanged. This condition occurs with hyperglycemia.

Pseudohyponatremia

The aqueous phase is diluted by excessive proteins or lipids. The TBW and total body sodium are unchanged. This condition is seen with hypertriglyceridemia and multiple myeloma.
Pathophysiology

Serum sodium concentration is regulated by stimulation of thirst, secretion of ADH, feedback mechanisms of the renin-angiotensin-aldosterone system, and variations in renal handling of filtered sodium. Increases in serum osmolarity above the normal range (280-300 mOsm/kg) stimulate hypothalamic osmoreceptors, which, in turn, cause an increase in thirst and in circulating levels of ADH. ADH increases free water reabsorption from the urine, yielding urine of low volume and relatively high osmolarity and, as a result, returning serum osmolarity to normal. ADH is also secreted in response to hypovolemia, pain, fear, nausea, and hypoxia.

Aldosterone, synthesized by the adrenal cortex, is regulated primarily by serum potassium but also is released in response to hypovolemia through the renin-angiotensin-aldosterone axis. Aldosterone causes absorption of sodium at the distal renal tubule. Sodium retention obligates free water retention, helping to correct the hypovolemic state. The healthy kidney regulates sodium balance independently of ADH or aldosterone by varying the degree of sodium absorption at the distal tubule. Hypovolemic states, such as hemorrhage or dehydration, prompt increases in sodium absorption in the proximal tubule. Increases in vascular volume suppress tubular sodium reabsorption, resulting in natriuresis and helping to restore normal vascular volume. Generally, disorders of sodium balance can be traced to a disturbance in thirst or water acquisition, ADH, aldosterone, or renal sodium transport.

Hyponatremia is physiologically significant when it indicates a state of extracellular hypoosmolarity and a tendency for free water to shift from the vascular space to the intracellular space. Although cellular edema is well tolerated by most tissues, it is not well tolerated within the rigid confines of the bony calvarium. Therefore, clinical manifestations of hyponatremia are related primarily to cerebral edema. The rate of development of hyponatremia plays a critical role in its pathophysiology and subsequent treatment. When serum sodium concentration falls slowly, over a period of several days or weeks, the brain is capable of compensating by extrusion of solutes and fluid to the extracellular space. Compensatory extrusion of solutes reduces the flow of free water into the intracellular space, and symptoms are much milder for a given degree of hyponatremia.

When serum sodium concentration falls rapidly, over a period of 24-48 hours, this compensatory mechanism is overwhelmed and severe cerebral edema may ensue, resulting in brainstem herniation and death.

Prehospital Care

Hyponatremia is necessarily a hospital-based diagnosis, but patients may exhibit signs of severe neurologic dysfunction during prehospital evaluation and transport.

* Address acute life-threatening conditions and initiate supportive care.
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* Establish reliable intravenous access and give supplemental oxygen to patients with lethargy or obtundation. In these patients, evaluate the possibility of hypoglycemia with a rapid glucose check. Administer intravenous glucose to hypoglycemic patients.
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* Administer standard prehospital anticonvulsant therapy to patients experiencing seizures. Seizures secondary to hyponatremia are unlikely to respond to this therapy, but it should be administered until a definitive diagnosis and therapy are available.
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* Intubate and initiate hyperventilation to reduce intracranial pressure in patients exhibiting signs of brainstem herniation (eg, obtundation; fixed, unilateral, dilated pupil; decerebrate or decorticate posturing) until a more definitive therapy can be initiated.
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* Avoid giving hypotonic intravenous fluids because they may exacerbate cerebral edema.

Emergency Department Care

The ED evaluation of patients with hyponatremia includes determining the cause and the chronicity of the hyponatremic state in order to direct appropriate therapy.

* Acute hyponatremia is less common than chronic hyponatremia and typically is seen in patients with a history of sudden free water loading (eg, patients with psychogenic polydipsia, infants fed tap water for 1-2 d, patients given hypotonic fluids in the postoperative period).
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o Acute evolution of hyponatremia leaves little opportunity for compensatory extrusion of CNS intracellular solutes.
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o The ultimate danger for these patients is brainstem herniation when sodium levels fall below 120 mEq/L.
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o The therapeutic goal is to increase the serum sodium level rapidly by 4-6 mEq/L over the first 1-2 hours.
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o The source of free water must be identified and eliminated.
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o In patients with healthy renal function and mild to moderately severe symptoms, the serum sodium level may correct spontaneously without further intervention.
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o Patients with seizures, severe confusion, coma, or signs of brainstem herniation should receive hypertonic (3%) saline to rapidly correct serum sodium level toward normal but only enough to arrest the progression of symptoms. An increase in serum sodium level of 4-6 mEq/L is generally sufficient.
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* Chronic hyponatremia is more common than acute hyponatremia.
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o Patients with mild symptoms and a serum sodium level of 125 mEq/L or less often have chronic hyponatremia.
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o These patients lack any history of sudden free water loading.
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* Chronic hyponatremia must be managed with extreme care.
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o Correction of chronic hyponatremia has been associated with the development of central pontine myelinolysis (CPM) characterized by focal demyelination in the pons and extrapontine areas associated with serious neurologic sequelae.
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o The pathophysiology of CPM is controversial. Initial data suggested that overly rapid correction of chronic hyponatremia might lead to the development of CPM. More recently, investigators note that CPM often develops when chronic hyponatremia is complicated by hypoxia. Thus, CPM may be a form of hypoxic encephalopathy associated with hyponatremia and not a complication of therapy.7 Until further data are available, management should include meticulous attention to adequate oxygenation and a gradual increase in serum sodium level to 120-125 mEq/L. Serum sodium level should not be allowed to reach normal levels or hypernatremic levels within the first 48 hours.
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o Symptoms of CPM (eg, dysarthria, dysphagia, seizures, altered mental status, quadriparesis, hypotension) typically begin 1-3 days after correction of serum sodium level.
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o The condition is often irreversible; slow, cautious correction of serum sodium level and maintenance of adequate oxygenation in these patients is important.
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o Patients with hypokalemia, female gender, or history of alcoholism or liver transplant seem to be particularly prone to develop CPM.8 Exercise extreme caution in treating hyponatremia in these subgroups.
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o The risk of CPM appears to be minimal in patients whose chronic hyponatremia is corrected at a rate of less than 0.5 mEq/L/h or 12 mEq/L/d.
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o Patients with chronic hyponatremia and severe symptoms (eg, severe confusion, coma, seizures) should receive hypertonic saline but only enough to raise the serum sodium level by 4-6 mEq/L and to arrest seizure activity.

+ Further correction should proceed at an overall rate that is no greater than 0.5 mEq/L/h or 12 mEq/L/d.
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+ Anecdotal reports suggest that therapeutic relowering of the serum sodium level with hypotonic fluids and desmopressin (DDAVP) may help avert neurologic sequelae in patients whose chronic hyponatremia is inadvertently corrected too quickly.
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* In treating patients with chronic hyponatremia and mild to moderately severe symptoms, consider the cause of the hyponatremic state. Patients are classified as having hypovolemic, euvolemic, or hypervolemic hyponatremia based on historical clues and physical examination.
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o Hypovolemic hyponatremia: Patients have decreased total body sodium stores. If symptoms are mild to moderately severe, treat with isotonic saline; monitor serum sodium levels frequently to ensure that serum sodium level increases no faster than 0.5 mEq/L/h or 12 mEq/L/d.
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o Hypervolemic hyponatremia: Patients have increased total body sodium stores. Treatment consists of sodium and water restriction and attention to the underlying cause.
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o Euvolemic hyponatremia: This implies normal sodium stores and a total body excess of free water. Treatment consists of free water restriction and correction of the underlying condition. Recently developed AVP (vasopressin) receptor antagonists show promise as effective and well-tolerated therapy for SIADH. Further studies are needed to better define their role in the treatment of hyponatremia associated with SIADH.

Answer 2

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Answer 3

Prolonged low sodium diets, excessive sweating during races, certain diuretics used to manage blood pressure and the treatment of congestive heart failure, and also excessive vomiting and diarrhea and just a few to start with. The treatment is based on the cause of the hyponatremia. It can range from a 5% sodium chloride IV solution to decreasing ones water intake. i hope this helps.

Answer 4

Hyponatremia is water intoxication most commonly. Too many people over drinking during runs or other long events like cycling.

You have to drink too much water to have it. One lady just died trying to win a radio contest.

Treatment with diuretics, or increase of salts in ER.

Answer 5

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Answer 6

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