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Dec 20, 2012 · sodium deficiencies in Just Want to Talk

Drug and Medication Use

Medications and drugs that cause hyponatremia are listed in Table 1. Some of the more common causes of medication-induced hyponatremia are diuretics and selective serotonin reuptake inhibitors (SSRIs). Most of the medications cause SIADH, resulting in euvolemic hyponatremia. Diuretics cause a hypovolemic hyponatremia. Fortunately, in most cases, stopping the offending agent is sufficient to cause spontaneous resolution of the electrolyte imbalance.

TABLE 1
Agents that Cause Hyponatremia
——————————————————————————–
Diuretics

Carbamazepine (Tegretol)

Chlorpromazine (Thorazine)

Vasopressin analogs

Indapamide (Natrilix)

Selective serotonin reuptake inhibitors

Theophylline

Amiodarone (Cordarone)

Ecstasy (3,4-methylenedioxymethamphetamine)

Dec 20, 2012 · sodium deficiencies in Just Want to Talk

The body maintains a careful balance of electrolytes like sodium, potassium and chloride within the cells as well as in fluid outside the cells like blood and body fluids. Sodium is necessary to carry out some important functions like maintaining blood pressure. It also helps to maintain the function of nerves and muscles. Sodium enters the body through food and fluid intake. The common salt or table salt contains sodium chloride and it is used not only for cooking but also in preservatives. The same sodium chloride also is the reason for the salinity of our oceans. Excess sodium is excreted by the kidneys via the urine. Sodium levels in the plasma are normally maintained at a level of between 135 to 145 mmol/L.

The condition in which plasma level of sodium falls to below 135 mmol/L is called hyponatremia. Hyponatremia causes movement of excess water in the cells, causing them to swell. The cells of the brain in particular are unable to cope up with this swelling since they are confined within the bones of the skull. Thus, many of the symptoms caused by hyponatremia, especially severe cases, are related to the brain.

When taking medication we must remember that some of the drugs cause hyponatremia as a side effect. Many among these bring about this effect by resulting in a condition called SIADH or Syndrome of Inappropriate Secretion of ADH. ADH (antidiuretic hormone) or vasopressin is a hormone secreted by a small gland near the brain called the pituitary. It plays an important role in water absorption from the kidneys and stimulates thirst. Thus, in conditions of dehydration, by increasing water absorption from the urine and stimulating thirst, it helps to maintain the water content of the body.

SIADH is a condition where the control of ADH secretion is lost and it is secreted independent of the need to conserve water. This results in water retention and subsequent dilution of sodium levels, leading to hyponatremia.

Symptoms of hyponatremia may be mild like:

Nausea, vomiting, headache, and muscle cramps, or Symptoms may be serious like alteration in mental status including confusion, seizures and coma.

If hyponatremia is diagnosed, a careful history should be taken from the patients or their caregivers to find out if the patients are taking any medications that could result in hyponatremia. Stopping the medication usually helps to solve the problem.

May 25, 2012 · sodium deficiencies in Just Want to Talk

Hyponatremia is an important electrolyte abnormality with the potential for significant morbidity and mortality. Common causes include medications and the syndrome of inappropriate antidiuretic hormone (SIADH) secretion. Hyponatremia can be classified according to the volume status of the patient as hypovolemic, hypervolemic, or euvolemic. Hypervolemic hyponatremia may be caused by congestive heart failure, liver cirrhosis, and renal disease. Differentiating between euvolemia and hypovolemia can be clinically difficult, but a useful investigative aid is measurement of plasma osmolality. Hyponatremia with a high plasma osmolality is caused by hyperglycemia, while a normal plasma osmolality indicates pseudohyponatremia or the post-transurethral prostatic resection syndrome. The urinary sodium concentration helps in diagnosing patients with low plasma osmolality. High urinary sodium concentration in the presence of low plasma osmolality can be caused by renal disorders, endocrine deficiencies, reset osmostat syndrome, SIADH, and medications. Low urinary sodium concentration is caused by severe burns, gastrointestinal losses, and acute water overload. Management includes instituting immediate treatment in patients with acute severe hyponatremia because of the risk of cerebral edema and hyponatremic encephalopathy. In patients with chronic hyponatremia, fluid restriction is the mainstay of treatment, with demeclocycline therapy reserved for use in persistent cases. Rapid correction should be avoided to reduce the risk of central pontine myelinolysis. Loop diuretics are useful in managing edematous hyponatremic states and chronic SIADH. In all instances, identifying the cause of hyponatremia remains an integral part of the treatment plan.

Hyponatremia generally is defined as a plasma sodium level of less than 135 mEq per L (135 mmol per L). This electrolyte imbalance is encountered commonly in hospital and ambulatory settings.The results of one prevalence study in a nursing home population demonstrated that 18 percent of the residents were in a hyponatremic state, and 53 percent had experienced at least one episode of hyponatremia in the previous 12 months. Acute or symptomatic hyponatremia can lead to significant rates of morbidity and mortality. Mortality rates as high as 17.9 percent have been quoted, but rates this extreme usually occur in the context of hospitalized patients. Morbidity also can result from rapid correction of hyponatremia. Because there are many causes of hyponatremia and the treatment differs according to the cause, a logical and efficient approach to the evaluation and management of patients with hyponatremia is imperative.

Water and Sodium Balance

Plasma osmolality, a major determinant of total body water homeostasis, is measured by the number of solute particles present in 1 kg of plasma. It is calculated in mmol per L by using this formula:

2 × [sodium] + [urea] + [glucose]

Total body sodium is primarily extracellular, and any increase results in increased tonicity, which stimulates the thirst center and arginine vasopressin secretion. Arginine vasopressin then acts on the V2 receptors in the renal tubules, causing increased water reabsorption. The opposite occurs with decreased extracellular sodium: a decrease inhibits the thirst center and arginine vasopressin secretion, resulting in diuresis. In most cases, hyponatremia results when the elimination of total body water decreases. The pathophysiology of hyponatremia will be discussed later in this article.

Clinical Signs and Symptoms

Most patients with hyponatremia are asymptomatic. Symptoms do not usually appear until the plasma sodium level drops below 120 mEq per L (120 mmol per L) and usually are nonspecific (e.g., headache, lethargy, nausea).In cases of severe hyponatremia, neurologic and gastrointestinal symptoms predominate.3 The risk of seizures and coma increases as the sodium level decreases. The development of clinical signs and symptoms also depends on the rapidity with which the plasma sodium level decreases. In the event of a rapid decrease, the patient can be symptomatic even with a plasma sodium level above 120 mEq per L. Poor prognostic factors for severe hyponatremia in hospitalized patients include the presence of symptoms, sepsis, and respiratory failure.

Diagnostic Strategy

Figure 113 shows an algorithm for the assessment of hyponatremia. The identification of hyponatremia must be followed by a clinical assessment of the patient, beginning with a targeted history to elicit the symptoms of hyponatremia and exclude important causes such as congestive heart failure, liver or renal impairment, malignancy, hypothyroidism, Addison’s disease, gastrointestinal losses, psychiatric illness, recent drug ingestion, surgery, or reception of intravenous fluids. The patient then should be classified into one of the following categories: hypervolemic (edematous), hypovolemic (volume depleted), or euvolemic.

Assessment of Hyponatremia

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FIGURE 1

HYPERVOLEMIC HYPONATREMIA

Hyponatremia in the presence of edema indicates increased total body sodium and water. This increase in total body water is greater than the total body sodium level, resulting in edema. The three main causes of hypervolemic hyponatremia are congestive heart failure, liver cirrhosis, and renal diseases such as renal failure and nephrotic syndrome. These disorders usually are obvious from the clinical history and physical examination alone.

EUVOLEMIC AND HYPOVOLEMIC HYPONATREMIA

Hyponatremia in a volume-depleted patient is caused by a deficit in total body sodium and total body water, with a disproportionately greater sodium loss, whereas in euvolemic hyponatremia, the total body sodium level is normal or near normal. Differentiating between hypovolemia and euvolemia may be clinically difficult, especially if the classic features of volume depletion such as postural hypotension and tachycardia are absent.

Laboratory markers of hypovolemia, such as a raised hematocrit level and blood urea nitrogen (BUN)-to-creatinine ratio of more than 20, may not be present. In fact, results of one study showed an increased BUN-to-creatinine ratio in only 68 percent of hypovolemic patients. Two useful aids for evaluating euvolemic or hypovolemic patients are measurement of plasma osmolality and urinary sodium concentration. Plasma osmolality testing places the patient into one of three categories, normal, high, or low plasma osmolality, while urinary sodium concentration testing is used to refine the diagnosis in patients who have a low plasma osmolality.

Plasma Osmolality Measurement

NORMAL PLASMA OSMOLALITY

The combination of hyponatremia and normal plasma osmolality (280 to 300 mOsm per kg [280 to 300 mmol per kg]) of water can be caused by pseudohyponatremia or by the post-transurethral prostatic resection syndrome. The phenomenon of pseudohyponatremia is explained by the increased percentage of large molecular particles, such as proteins and fats in the serum, relative to sodium. These large molecules do not contribute to plasma osmolality, resulting in a state in which the relative sodium concentration is decreased, but the overall osmolality remains unchanged. Severe hypertriglyceridemia and hyperproteinemia are two causes of this condition in patients with pseudohyponatremia. These patients usually are euvolemic.

The post-transurethral prostatic resection syndrome consists of hyponatremia with possible neurologic deficits and cardiorespiratory compromise. Although the syndrome has been attributed to the absorption of large volumes of hypotonic irrigation fluid intraoperatively, its pathophysiology and management remain controversial.

INCREASED PLASMA OSMOLALITY

Increased plasma osmolality (more than 300 mOsm per kg of water) in a patient with hyponatremia is caused by severe hyperglycemia, such as that occurring with diabetic ketoacidosis or a hyperglycemic hyperosmolar state. It is caused by the presence of glucose molecules that exert an osmotic force and draw water from the intracellular compartment into the plasma, with a diluting effect. Osmotic diuresis from glucose then results in hypovolemia. Fortunately, hyperglycemia can be diagnosed easily by measuring the bedside capillary blood glucose level.

DECREASED PLASMA OSMOLALITY

Patients with low plasma osmolality (less than 280 mOsm per kg of water) can be hypovolemic or euvolemic. The level of urine sodium is used to further refine the differential diagnosis.

High Urine Sodium Level

Excess renal sodium loss can be confirmed by finding a high urinary sodium concentration (more than 30 mmol per L). In these patients, the main causes of hyponatremia are renal disorders, endocrine deficiencies, reset osmostat syndrome, syndrome of inappropriate antidiuretic hormone secretion (SIADH), and drugs or medications. Because of their prevalence and importance, SIADH and drugs deserve special mention, and the author will elaborate on these causes later in the article.

Renal disorders that cause hyponatremia include sodium-losing nephropathy from chronic renal disease (e.g., polycystic kidney, chronic pyelonephritis) and the hyponatremic hypertensive syndrome that frequently occurs in patients with renal ischemia (e.g., renal artery stenosis or occlusion). The combinations of hypertension plus hypokalemia (renal artery stenosis) or hyperkalemia (renal failure) are useful clues to this syndrome.

Endocrine disorders are uncommon causes of hyponatremia. Diagnosing hypothyroidism or mineralocorticoid deficiency (i.e., Addison’s disease) as a cause of hyponatremia requires a high index of suspicion, because the clinical signs can be quite subtle. In either case, the serum levels of thyroid-stimulating hormone (TSH), cortisol, and adrenocorticotropic hormone (ACTH) should be measured, because hypothyroidism and hypoadrenalism can coexist as a polyendocrine deficiency disorder (i.e., Schmidt’s syndrome). Treatment of Schmidt’s syndrome involves steroid replacement before thyroxine T4 therapy to avoid precipitating an addisonian crisis.

The reset osmostat syndrome occurs when the threshold for antidiuretic hormone secretion is reset downward. Patients with this condition have normal water-load excretion and intact urine-diluting ability after an oral water-loading test. The condition is chronic—but stable—hyponatremia. It can be caused by pregnancy, quadriplegia, malignancy, malnutrition, or any chronic debilitating disease.

Low Urine Sodium Level

Patients with extra-renal sodium loss have a low urinary sodium concentration (less than 30 mmol per L) as the body attempts to conserve sodium. Causes include severe burns and gastrointestinal losses from vomiting or diarrhea. Acute water overload, which usually is obvious from the patient’s history, occurs in patients who have been hydrated rapidly with hypotonic fluids, as well as in psychiatric patients with psychogenic overdrinking.

Diuretic therapy, on the other hand, can cause either a low or a high urinary-sodium concentration, depending on the timing of the last diuretic dose administered, but the presence of concomitant hypokalemia is an important clue to the use of a diuretic.

May 13, 2012 · sodium deficiencies in Just Want to Talk

SODIUM METABOLISM

1. Extracellular fluid contains about 3000 mEq of sodium, which is the main osmotic component. An increase or decrease as small as 1% of the total extracellular fluid volume can have serious effects. About 30,000 mEq of sodium undergo filtration at the glomeruli each day.
2. Several factors are active in the regulation of sodium in the body.
a. Renin is the enzyme responsible for the conversion of antiotensinogen to angiotensin I. An angiotensin converting enzyme converts angiotensin I to angiotensin II. Angiotensin causes vasoconstriction as well as the secretion of aldosterone from the adrenal gland. Renal hypoperfusion, adrenaline and other catecholamines stimulate renin secretion from the juxtaglomerular apparatus of the glomeruli.
b. Aldosterone is a hormone that is controlled by the renin-angiotensin system and acts to increase reabsorption of sodium in the cortical collecting duct.
c. Dopamine from the kidney inhibits reabsorption in the proximal tubules.
d. Prostaglandins block reabsorption in the tubules and stimulate renal vasodilatation.
e. Atrial natriuretic peptide blocks reabsorption of sodium in the collecting duct.

HYPONATREMIA
Definition:
1 Hyponatremia is sodium level under 135 mEq/ml but is actually an excess of water
with no effect from the amount of total body sodium.
2 Hypotonicity is always associated with hyponatremia, whereas hyponatremia can be hyper-, iso- or hypotonic.
3 Hypertonic hyponatremia is caused by osmotically active particles in the extracellular fluid (such as glucose) and a shift of water from intracellular to extracellular fluid as a result. Thus, low serum sodium is accompanied by normal or high osmolality.
4 Isotonic hyponatremia is also called pseudohyponatremia since it is an artifact caused by high lipid or protein in the serum.
5 True hyponatremia is hypotonic with sodium is under 125 mEq/ml and serum osmolality under 250 Osm/kg.
6 Hyponatremia can further be divided into hypovolemic states (GI, renal or third-space losses), isovolemic states and hypervolemic states (CHF, nephrotic syndrome, cirrhosis).
Etiology:
1 Increased fluid intake – more than 1000 ml/hour is more than the body is able to excrete and so water concentration exceeds sodium concentration. This is seen in psychiatric patients with water intoxication or in patients given hypotonic fluids intravenously in large amounts. This is isovolemic hyponatremia.
2 Decreased excretion of water
a. Increased reabsorption in the proximal tubules may reduce the kidney’s ability to excrete water. This can be caused by hypoperfusion due to hypovolemia, or disease states such as congestive heart failure, cirrhosis, or nephrotic syndrome (hypervolemia). The urine is low in sodium, due to increased reabsorption also of sodium. BUN is high.
b. A GFR that falls to less than 10% of normal reflects a decrease in the kidney’s ability to deal with water excretion.
c. Increased reabsorption in the collecting tubules is caused by ADH secretion that is not osmotically stimulated. Urine sodium is normal, with high urine osmolality.
3 SIADH (syndrome of inappropriate ADH secretion) is non-osmotically induced and connected with various disorders of the CNS (tumors, trauma, psychiatric disturbances) and of the lungs (oat cell carcinoma, infection, bronchospastic disease). It is also seen with hypopituarism due to primary adrenal insufficiency or impaired ACTH secretion, and with various drugs, particularly chlorpropamide, clofibrate, carbamazepine, and thiazide diuretics. Idiopathic SIADH may occur in the elderly and is probably connected to increasing ADH secretion with age. One type of SIADH, called “reset osmostat” is seen in patients with chronic illness or malnutrition. The set point for sodium concentration is lowered and the body maintains that value. SIADH is isovolemic.
Manifestations:
1 Depend on the underlying problem.
2 Hyponatremia may cause edema of brain tissues. Acute hyponatremia may cause acute CNS dysfunction with obtundation, coma, seizures and even death. Prolonged hyponatremia may cause permanent CNS damage due to edema of brain cells.

Diagnosis:
1. Plasma is hypotonic and urine osmolality is more than 50-100 Osm/kg.
2. Urine sodium is high in SIADH, but low with edema or hypovolemic states.
3. Water loading test – the patient is given 20ml/kg of water over 20-40 minutes. 80% of this should be excreted within 4 hours with urine osmolality below 100 Osm/kg afterward. If not, the kidney’s ability to excrete water is impaired.

Principles of management:
1 The first step is to reduce fluid intake to about 700 ml/day.
2 The giving of hypertonic infusions such as 3% sodium chloride will increase tonicity of the extracellular fluid. Serum sodium concentration should be increased slowly, no more than 2 mEq/hr. Too rapid correction may cause central pontine myelinolysis. Since rapid volume expansion may cause pulmonary edema, usually a diuretic such as furosemide is given at the same time. The goal is to reach a serum sodium level of 125 mEq/ml. Further correction to normal values can be done more slowly. The formula used is:

(125 – current Na level) x total body water (which equals body weight x 0.6) = mEq of hypertonic saline needed

3 Furosemide given with saline will increase water excretion transiently.
4 Demeclocycline acts on ADH-controlled movement of water in the collecting tubule. Dose is 600-1200 mg/day and several days are required to show an effect. This drug should not be used in patients with kidney disease, heart failure or liver disease.

Prognosis:
1. Acute hyponatremia can cause increased intracranial pressure and brain
damage.
2. Chronic hyponatremia may have a permanent effect on cognitive functions – the theory is controversial.



HYPERNATREMIA

Definition:
1. Hypernatremia is clinically significant above 155 mEq/ml.
2. Hypernatremia is always hypertonic.

Etiology
1. Renal causes
a. Decreased effect of ADH
(1) central diabetes insipidus – failure of secretion or synthesis of ADH due to tumor, trauma, sarcoidosis or histiocytosis
(2) nephrogenic diabetes insipidus – high levels of ADH with no effect, due to renal disease, sickle cell anemia, urinary tract obstruction, hypercalcemia, hypokalemia, lithium or demeclocycline use.
b. Osmotic diuresis as in hyperglycemia – both water and sodium reabsorption are affected, but water losses are more than sodium losses.

2. Extrarenal causes
a. Reduced fluid intake – the body loses water through urine and feces, as well as insensible losses via the skin and mucus membranes. A minimum of about 700 ml/day is necessary in cool climates, more in warmer areas.
b. Vomiting and diarrhea increase gastrointestinal losses.
c. Sweating and burns increase losses via the skin.

Manifestations:
1 Most of the volume decrease is in intracellular fluid, but there is also a slight decrease in extracellular fluid.
2 Urine volume is reduced in cases of extrarenal water losses and normal kidney function. Polyuria is seen with renal causes.
3 Young children and the elderly may show CNS depression with obtundation, coma or seizures. Intracranial or subarachnoid hemorrhages may result from the tearing of bridging veins as brain volume decreases.

Diagnosis
1. Water deprivation test – the patient is given no fluids from 20:00 for 14 hours at which point urine osmolality is tested. It should be greater than 800 Osm/kg. An injection of 5 units ADH is then given which normally does not further increase osmolality. ADH deficiency is suspected if osmolality does not reach 800 after 14 hours or increases by more than 15% after ADH is injected. With nephrogenic diabetes insipidus, the osmolality will be less than 300 with no increase after ADH injection.
2. Urine osmolality under 150 Osm/L is characteristic of a primary problem of water conservation. Urine osmolality over 150 Osm/L with polyuria is characteristic of osmotic diuresis.
3. Urinary concentrations of sodium, glucose and urea may help to determine etiology. Bicarbonate diuresis manifests with a urine pH exceeding 6.
4. Actual ADH levels may need to be assayed in plasma since urine osmolality does not reflect ADH levels in nephrogenic diabetes insipidus.

Principles of management:
1 Fluids, either intravenous as 5% dextrose or orally as water, should be given. Hemolysis may result if fluids given are hypotonic less than 150 Osm/L.
2 Thiazide diuretics reduce polyuria by stimulating reabsorption of sodium and water in the proximal tubule. They are effective in nephrogenic diabetes insipidus.
3 ADH or vasopressin may be given as a nasal spray, 10-20 mg every 12 hours.
4 Drugs that cause SIADH may be useful.

Complications: only if access to water is limited

May 13, 2012 · sodium deficiencies in Just Want to Talk

Hyponatremia is an important electrolyte abnormality with the potential for significant morbidity and mortality. Common causes include medications and the syndrome of inappropriate antidiuretic hormone (SIADH) secretion. Hyponatremia can be classified according to the volume status of the patient as hypovolemic, hypervolemic, or euvolemic. Hypervolemic hyponatremia may be caused by congestive heart failure, liver cirrhosis, and renal disease. Differentiating between euvolemia and hypovolemia can be clinically difficult, but a useful investigative aid is measurement of plasma osmolality. Hyponatremia with a high plasma osmolality is caused by hyperglycemia, while a normal plasma osmolality indicates pseudohyponatremia or the post-transurethral prostatic resection syndrome. The urinary sodium concentration helps in diagnosing patients with low plasma osmolality. High urinary sodium concentration in the presence of low plasma osmolality can be caused by renal disorders, endocrine deficiencies, reset osmostat syndrome, SIADH, and medications. Low urinary sodium concentration is caused by severe burns, gastrointestinal losses, and acute water overload. Management includes instituting immediate treatment in patients with acute severe hyponatremia because of the risk of cerebral edema and hyponatremic encephalopathy. In patients with chronic hyponatremia, fluid restriction is the mainstay of treatment, with demeclocycline therapy reserved for use in persistent cases. Rapid correction should be avoided to reduce the risk of central pontine myelinolysis. Loop diuretics are useful in managing edematous hyponatremic states and chronic SIADH. In all instances, identifying the cause of hyponatremia remains an integral part of the treatment plan.

May 13, 2012 · sodium deficiencies in Just Want to Talk

Sodium plays a vital role in maintaining the concentration and volume of the extracellular fluid (ECF). It is the main cation of the ECF and a major determinant of ECF osmolality. Sodium is important in maintaining irritability and conduction of nerve and muscle tissue and assists with the regulation of acid-base balance. The average daily intake far exceeds the normal daily requirements. The kidneys are responsible for excreting the excess and are capable of conserving sodium during periods of extreme sodium restriction. The kidneys accomplish this primarily through regulation of water intake/excretion. If the serum sodium falls, the kidneys respond by excreting water. If the serum sodium increases (increased osmolality)—thirst center is stimulated–increased ADH release by the posterior pituitary—acts on kidney to conserve water. Aldosterone also plays a key role by regulating Na+/ECF volume. Its release causes the kidneys to conserve water and sodium which results in increased ECF volume. Because changes in serum sodium levels typically reflect changes in body water balance, gains or losses of total body sodium are not necessarily reflected by the serum sodium level.
Hyponatremia: (Serum sodium less than 136 meq/L)
Clinical indicators and treatment depend on the cause of hyponatremia and whether or not it is associated with a normal, decreased or increased ECF volume.
Signs and symptoms: neurologic symptoms usually do not occur until the serum sodium level has dropped to approximately 120-125 meq/L. Hyponatremia with decreased ECF volume: irritability, apprehension, dizziness, postural hypotension, dry mucus membranes, cold and clammy skin, tremors, seizures. Hyponatremia with normal or increased ECF volume: headache, lassitude, apathy, confusion, weakness, edema, weight gain, elevated blood pressure, muscle cramps, convulsions.
History and risk factors: diarrhea, fistulas, vomiting, NG suction, diuretics, adrenal insufficiency, skin losses (burns, wound drainage), other. Note: hyperlipidemia, hyperproteinemia, and hyperglycemia may cause a pseudo-hyponatremia. This must be ruled out before determining therapy. For every 100 mg/dl increase in glucose, the sodium is diluted by 1.6 meq/L.
Diagnostic tests: serum sodium will be less than 136 meq/L. Serum osmolality will be decreased except in cases of pseudo-hyponatremia, azotemia, or toxins that increase osmolality (example: ethanol). Urine specific gravity will be decreased because of the kidneys attempt to excrete excess water. Urine sodium: decreased (except in SIADH and adrenal insufficiency).
Collaborative management: The goal of therapy is to get the patient out of immediate danger (eg return the sodium level to greater than 120 meq/L) and then gradually return the serum sodium to a normal level and restore normal ECF volume.

May 13, 2012 · sodium deficiencies in Just Want to Talk

HYPONATREMIA CAUSES: An abnormally low plasma sodium level is best considered in conjunction with the person’s plasma osmolality and extracellular fluid volume status. Indeed, correct ascertainment of volume status, as well as determination of the presence or absence of edema, are both critical in establishing the cause of hyponatremia. As described above, a state of volume depletion leads to increased blood levels of ADH and thus water retention.

The greater the amount of water that is retained, the more the blood sodium will become diluted to cause worsening degrees of hyponatremia. The presence of edema indicates that blood volume has been lost insofar as fluid from the blood has shifted out into the peripheral tissues to cause the edema. In other words, edema is usually reflecting a state of blood volume depletion. As a result, edematous states are also associated with increased blood levels of ADH, water retention, and hyponatremia. In all cases of volume depletion-associated hyponatremia, it is important to note that retention of water ”per se”, such as that promoted by ADH, does not correct the volume depleted state.

In addition to volume depletion, there are other causes of increased ADH levels (and ultimately, therefore, of hyponatremia). These include nausea, pain, and opiate drugs such as codeine and morphine. Such factors often play a role in the hyponatremia that is frequently seen in hospitalized patients.

May 13, 2012 · sodium deficiencies in Just Want to Talk

Hypervolemic hyponatremia – both sodium & water content increase, but the water gain is greater

cirrhosis
congestive heart failure
nephrotic syndrome
massive edema of any cause