Hyponatremia (A Short Review) by DG Ghalan Hypernatremia Introduction
It is anelectrolyte disturbance that is
defined by an elevated sodium level in the blood. Hypernatremia is generally not caused by an excess of sodium, but rather by a relative deficit of free water in the body. For this reason, hypernatremia is often synonymous with the less precise term,dehydration Water is lost from the body in a variety of ways, including perspiration, insensible losses from breathing, and in the feces and urine. If the amount of water ingested consistently falls below the amount of water lost, the serum sodium level will begin to rise, leading to hypernatremia. Rarely, hypernatremia can result from massive salt ingestion, such as may occur from drinking seawater. Ordinarily, even a small rise in the serum sodium concentration above the normal range results in a strong sensation of thirst, an increase in free water intake, and correction of the abnormality. Therefore, hypernatremia most often occurs in people such as infants, those with impaired mental status, or the elderly, who may have an intact thirst mechanism but are unable to ask for or obtain water. Etiology (1.)Hypovolemic Inadequate intake of water, typically in elderly or otherwise disabled patients who are unable to take in water as their thirst dictates. This is the most common cause of hypernatremia. Excessive losses of water from the urinary tract, which may be caused by glycosuria, or other osmotic diuretics. Water losses associated with extreme sweating. Severe watery diarrhea (2.) Euvolemic: Excessive excretion of water from the kidneys caused bydiabetes insipidus, which involves either inadequate production of the hormone, vasopressin, from the pituitary gland or impaired responsiveness of the kidneys to vasopressin. (3.) Hypervolemic: Intake of a hypertonic fluid (a fluid with a higher concentration of solutes than the remainder of the body). This is relatively uncommon, though it can occur after a vigorous resuscitation where a patient receives a large volume of a concentratedsodium bicarbonate solution. Ingesting seawater also causes hypernatremia because seawater is hypertonic. Mineralcorticoid excess due to a disease state such as Conn's syndrome or Cushing's Disease Symptoms:
Clinical manifestations of hypernatremia
can be subtle, consisting oflethargy, weakness, irritability, and edema. With more severe elevations of the sodium level, seizures and coma may occur. Severe symptoms are usually due to acute elevation of the plasma sodium concentration to above 158 mEq/L (normal is typically about 135-145 mEq/L). Values above 180 mEq/L are associated with a high mortality rate, particularly in adults. However such high levels of sodium rarely occur without severe coexisting medical conditions. Treatment:
The cornerstone of treatment is
administration of free water to correct the relative water deficit. Water can be replaced orally or intravenously. However, overly rapid correction of hypernatremia is potentially very dangerous. The body (in particular the brain) adapts to the higher sodium concentration. Rapidly lowering the sodium concentration with free water, once this adaptation has occurred, causes water to flow into brain cells and causes them to swell. This can lead to cerebral edema, potentially resulting in seizures, permanent brain damage, or death. Therefore, significant hypernatremia should be treated carefully by aphysician or other medical professional with experience in treatment ofelectrolyte imbalances. Hyponatremia Introduction:
It is an electrolyte disturbance in which
the sodium concentration in the serumis 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. 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, orpolydipsia). 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. 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,people who fast on juice or water for extended periods and people whose dietary sodium intake is chronically insufficient. 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. 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) is associated with numerous complications and undiagnosed symptoms. 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
(I) Hypervolemic hyponatremia:
excess water dilutes the sodium concentration, causing low sodium levels. Hypervolemic hyponatremia is commonly the result of kidney failure, heart failure or liver failure. (II) Euvolemic hyponatremia: normal water levels are combined with low sodium levels. This condition is commonly due to chronic health conditions, cancer or certain medications. (III)Hypovolemic hyponatremia: water and sodium levels are both low. This may occur, for example, when exercising in the heat without replenishing fluid electrolytes or with marked blood loss. 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. 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: Syndrome of inappropriate anti-diuretic hormone (SIADH). In this condition, high levels of the anti-diuretic hormone (ADH) are produced, causing the body to retain water instead of excreting it in urine. Cirrhosis. Liver disease can cause fluids to accumulate in the body. Kidney problems. Kidney failure and other kidney diseases can render the body unable to efficiently remove excess fluids from the body. Congestive heart failure. This condition causes the abdomen and lower extremities to retain fluids. Water pills (diuretics), especially thiazide diuretics. Diuretics work by making the body excrete more sodium in urine Consuming excessive water during exercise (exertional hyponatremia or exercise-associated hyponatremia (EAH)).Because sodium is lost through sweat, drinking too much water during endurance activities, such as marathons and triathlons, can dilute sodium content in blood. Hormonal changes due to adrenal gland insufficiency (Addison’s disease). Adrenal glands produce hormones that help maintain the body’s balance of sodium, potassium and water. Hormonal changes due to an under active thyroid (hypothyroidism). Primary polydipsia. In this condition, thirst increases significantly, causing a person to drink excessive amounts of fluid. Certain medications. Some medications, particularly selective serotonin reuptake inhibitors and some pain medications, cause a person to urinate or perspire more than normal. The recreational drug MDMA. This amphetamine causes a ripple effect on the body’s ADH and water levels that—especially in combination with heavy drinking—increases the risk of severe and even fatal cases of hyponatremia. Chronic, severe vomiting or diarrhea. This causes the body to lose fluids and electrolytes, including sodium. Dehydration. In dehydration, the body loses fluids and electrolytes. Diet. A low-sodium, high-water diet can disturb the proper balance between sodium and fluids in the blood. Excessive intake of diuretics, including beer, can have the same effect. Risk Factors:
Age. Low blood sodium is more common in
older adults. Contributing factors include age- related changes and a greater likelihood of developing a chronic disease that impairs the body’s sodium balance. Diet. A person may be at an increased risk of hyponatremia if he is following a low-sodium diet, especially in combination with drinking diuretic beverages. Intensive physical activities. People who drink too much water while taking part in marathons, triathlons, Iron Man competitions and other long-distance, high-intensity activities are at an increased risk of hyponatremia. Climate. New exposure to hot weather can increase the amount of sodium a person loses through sweating. Certain drugs. Medications that increase risk of hyponatremia include thiazide diuretics and selective serotonin reuptake inhibitors and pain medications that cause a patient to urinate or perspire more than usual. In addition, the recreational drug MDMA has been linked to fatal cases of hyponatremia. . Complication:
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 the incidence of hyponatremia in elderly patients with large-bone fractures was more than double that of non-fracture patients. Recent work by Verbalis etc 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. (Reference: Wikipedia) Thank you For any suggestions – ghalan_raj@yahoo.com