SURGERY

WERNER DE ALMEIDA LEITE

Fluid & Electrolyte Disorders - Part II : Disorders of sodium balance

Hypernatremia

All hypernatremic disorders are hyperosmolar .Hypernatremia can develop from excess water loss, frequently accompanied by an impaired thirst mechanism, inadequate volume replacement, inappropiate volume management after surgery, excessive use of diuretics, Diabetes Mellitus, insensible losses from the skin and respiratory tract ( those losses are hypoosmolar to plasma and average 800 to 1,000 ml per day in adults ), Acute Renal Failure and excessive enteral feeding. Less commonly, hypernatremia is due to hypertonic salt administration ( eg, accidental intravascular injection of hypertonic saline used for induction of abortion or use of large doses of sodium bicarbonate therapy during cardiac arrest).

**Major Causes of Hypernatremia**
Water loss Insensible losses Increased sweating-fever, exposure to high temperatures Respiratory infections Burns Renal losses Central Diabetes Insipidus Nephrogenic Diabetes Insipidus Osmotic Diuresis : Glucose, mannitol, urea Hypothalamic disorders Hypodipsia Resetting of osmostat (Primary Aldosteronism) Sodium Retention Administration of hypertonic NaCl or sodium bicarbonate Ingestion of sodium No absolute change in total body salt or water Water loss into cells (seizures, severe exercise, rhabdomyolisis)

Clinical Features

Typically, hypernatremia develops in adults as result from a chronic process and symptoms are usually associated with other conditions of other diseases.

Unless polyuria is present, Central Nervous System (CNS) and tissue signs characterize acute symptomatic hypernatremia, which include : Thirst (unless hypothalamic lesions are the cause), restlessness, weakness, seizures, delirium, maniacal behaviour and coma. CNS symptoms appear to be caused by an acute decrease in brain volume that causes rupture of cerebral veins, resulting in focal intracerebral and subarachnoid hemorrhage.

Hypernatremia is the only state in which dry and sticky mucous membranes are characteristic. A flushed skin, a red swollen tongue, decreased saliva and tears and fever may be also present.

CNS abnormalities begin when serum osmolality reaches 350 mOsm/Kg of water, being the mortality rate in adults with this disorder for more than 48 hours (serum sodium more than 160 mEq/l) round 60%.

Symptoms are more likely to occur with acute rises in plasma sodium concentration, whereas chronic hypertonicity generally produces fewer CNS manifestations, since brain cells accumulate ideogenic osmoles, which minimize the tendency for brain shrikage that results from increases in effective ECF osmolality. The generation of these solutes usually begins 4 hours after the onset of hypernatremia and stabilizes in 4-7 days. This must be accounted for when considering the therapy of hypernatremia, since rapid correction may cause cerebral edema.

Diagnosis

Hypernatremia is defined as a serum sodium concentration above 145 mEq/l . The diagnostic approach is based on an assessment of the ECF volume, urine volume, urine osmolality and urine sodium.

Hypernatremia with ECF volume expansion

It is usually seen in patients receiving hypertonic saline or sodium bicarbonate. There is a net sodium gain with urine volume, urine osmolality and urine sodium elevation. Mild hypernatremia can be seen with primary hyperaldosteronism ( increased and inappropriate production of aldosterone from the adrenal leading sodium retention with hypertension , suppression of plasma renin, and hypokalemia and its manifestations) and Cushing’s syndrome.

Hypernatremia with ECF depletion

Extrarenal losses : include GI (diarrhea) and insensible losses such as sweating, burns and exertional losses from the respiratory tract. Lactulose causes an osmotic diarrhea with loss of free water. Renal water-conserving ability is functioning and the urine volume is decreased, urine osmolality is high (>800 mOsm/Kg H2O), and urine sodium is low.

Renal losses

Due to osmotic diuresis : Osmotic diuresis occurs commonly in uncontrolled glycosuria (as in diabetic ketoacidosis or in nonketotic hyperosmolar coma ) and may occur during mannitol administration . Since glucose and mannitol are restricted to the ECF, the serum sodium level is generally reduced in the early stages of osmotic diuresis, and the effective ECF osmolality is increased primarily by the impermeant non-sodium solute. In prolonged osmotic diuresis, net water losses may be sufficiently great that hypernatremia develops. Hypernatremia due to an osmotic urea diuresis can occur if large amounts of protein and amino acids are administered by nasogastric tube, or if tissue catabolism is great, as in burns.

Due to diabetes insipidus : If the urine volume is high with an osmolality less than 250 mOsm/Kg H2O ( or an urinary density less than 1,005 ) and glycosuria and proteinuria are absent, diabetes insipidus, either central (CDI) or nephrogenic (NDI), is the most likely diagnosis.

In CDI renal concentrating defects are absent, resulting this disorder either from destruction of the centers of ADH synthesis or from failure of the mechanisms effecting ADH release.

Trauma to the neurohypophysis, either accidental or as result of hypophysectomy, is the major identifiable cause of CDI. A second major cause is an intracranial tumor. Less frequent causes of pituitary diabetes insipidus are granulomatous lesions of the central nervous system, including tuberculosis and sarcoidosis. Finally, 30 to 40 per cent of all patients with CDI have no identifiable cause for the disorder.

Acquired NDI is characterized by renal tubular unresponsiveness to ADH being usually less severe than CDI , since the kidney mantains some urinary concentration capacity. NDI may be seen with lithium or demmeclocycline therapy, after relief of prolonged urinary obstruction or by volatile fluorocarbon anesthetics, such as methoxyflurane.

The differential diagnosis between NDI and CDI can be established by administering exogenous ADH. In those patients with intact mechanism for ADH production and release, the administration of exogenous ADH will not produce an increase in the maximal urine osmolality achieved via water deprivation, helping to distinguish complete or partial NDI from other polyuric syndromes.

Treatment

The acute treatment of hypernatremia depends on the degree of volume depletion. If there is evidence of hemodynamic compromise, treatment should initially be with isotonic saline, since its osmolality (308 mOsm/Kg) is often lower than that of the patient. Once hemodynamic stability is achieved, the remaining free water deficit should be corrected over a period of at least 48 hours, since the excessively rapid correction is dangerous, particularly in those patients with hypernatremia for more than 24 hours, as it may lead to lethargy and seizures secondary to cerebral edema.

Free water deficit is calculated to restore normal osmolality for total body water:

« Body water deficit (liters) = 0.5 ´ Current body weight ´ {( Plasma sodium/140) - 1} * 0.4 for females, elderly and cachectic patients

The formula above calculates the amount of water that must be added to return the plasma sodium concentration to 140 mEq/l. It does not include any isosmotic fluid deficit that is also frequently present when both sodium and water have been lost as with osmotic diuresis, and does not account for ongoing urinary and insesible losses. Thus, this equation should be used only as guide for water replacement, being serial determinations of plasma sodium required (each 4 hours). Insensible losses and urine output also need to be replaced continuously to produce a positive water balance.

The plasma sodium should be corrected at a rate not greater than 0.5 mEq/liter/hour in asymptomatic patients or 1.0 mEq/liter/hour in symptomatic patients. Hypotonic fluid should be administered with 5% dextrose and with 0.45% saline.

For Central Diabetes Insipidus, a synthetic analogue of vasopressin, dDAVP ( 1- deamino, 8-D-arginine vasopressin), provides antidiuretic activity for 8 to 20 hours with negligible pressor effect, which can be taken as a nasal spray, and is the current drug of choice. The drug is best started at night to find the lowest dose that will prevent nocturia. This dose, usually 5 to 10 µg, can be given twice daily or doubled as a single mornig dose. For patients having some residual ADH production, the oral hypoglycemic agent chlorpropamide may produce adequate amelioration of symptoms by stimulating ADH secretion and augmenting the activity of residual ADH in the collecting duct. Alternatively, aquous vasopressin can be administered by subcutaneous route at a dose of 0.05 to 0.1 units/Kg, repeating the dose, if necessary, each 4 or 8 hours.

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