ELECTROLYTE IMBALANCE

Dr. Tarun Yadav

ABNORMALITIES OF WATER AND ELECTROLYTE HOMEOSTASIS

Total body water constituting approximately 60% of the total body weight in kilograms) is designated intracellular or extracellular fluid

Water in extracellular compartments is further subdivided into interstitial and intravascular fluid

Approximately 55% of total body water is intracellular, 37% is interstitial, and the remaining 8% is intravascular

COMPARTMENTS OF WATER INSIDE BODY

DISORDERS OF SODIUM

Normal serum sodium concentration is 136 to 145 mmol/L.

However, because serum sodium is measured as a concentration, serum sodium derangements can exist in the presence of increased, normal, or decreased total body sodium and/or increased, normal, or decreased total body water.

HYPONATREMIA

Na level below 135 mmol/L is called Hyponatremia.

Hyponatremia exists when water retention or water intake exceeds the ability of the kidneys to excrete a dilute urine.

Hyponatremia exists in approximately 15% of hospitalized patients.

SIGNS AND SYMPTOMS

SIGNS SYMPTOMS

Anorexia Abnormal sensorium

Nausea Disorientation/agitation

Lethargy Cheyne-Stokes breathing

Apathy Hypothermia

Muscle cramps Pathologic reflexes

Pseudobulbar palsy

Seizures

Coma, Death

DIAGNOSIS

Hyponatremia usually co-exists with hypo-osmolality except in two circumstances.

1. The addition of osmotically active solutes that are unable to cross cell membranes easily, such as glucose, mannitol, and glycine, causes water to move from the intracellular space into the ECF with a resultant decrease in the serum sodium concentration.

2. When the sodium concentration in measured in plasma and the solid phase of plasma is greatly increased as, for example, in severe hyperlipidemia or a paraproteinemic disorder, the measured sodium concentration will be falsely low. This is termed pseudohyponatremia.

3. Measuring sodium concentration in serum avoids this problem.

Once these two causes of hyponatremia have been excluded, the approach to the diagnosis of hyponatremia is to first evaluate ECF volume from the clinical presentation.

Then, urinary sodium concentration from a spot urine sample will further distinguish between etiologies.

Urinary sodium concentration (UNa) (mEq/L) in a spot urine sample. SIADH, syndrome of inappropriate secretion of antidiuretic hormone

TREATMENT

Treatment of hyponatremia involves withholding free water and encouraging free water excretion with a loop diuretic.

Administration of saline is only necessary if significant symptoms are present.

The rate of correction of hyponatremia depends primarily on whether the development of hyponatremia was acute, that is, occurred in less than 48 hours or was chronic.

Acute symptomatic hyponatremia must be treated promptly. Solute-free fluids are withheld and hypertonic saline (3% NaCl) plus furosemide is administered to enhance renal excretion of free water.

Serum electrolytes should be checked frequently and this treatment continued until symptoms disappear, which may occur before the serum sodium concentration returns to normal

Chronic symptomatic hyponatremia should be corrected slowly to avoid the risk of osmotic demyelination.

It triggers demyelination of pontine and extrapontine neurons and may result in quadriplegia, seizures, coma, and death.

The risk of osmotic demyelination is higher in patients who are malnourished or potassium depleted.

Guidelines for correction of chronic symptomatic hyponatremia call for an initial correction in the serum sodium of approximately 10 mEq/L.

Thereafter, correction should not exceed 1 to 1.5 mEq/L per hour or a daily maximum increase of 12 mEq/L.

Treatment of chronic asymptomatic hyponatremia requires treating the underlying cause of the electrolyte disturbance and fluid restriction.

Patients with hypervolemic hyponatremia secondary to congestive heart failure respond very well to a combination of angiotensin-converting enzyme inhibitor and loop diuretic.

MANAGEMENT OF ANESTHESIA

If at all possible, hyponatremia, especially if symptomatic, should be corrected prior to surgery.

If the surgery is urgent, then appropriate corrective treatment should continue throughout the surgery and into the postoperative period.

Frequent measurement of serum sodium is necessary to avoid overly rapid correction of hyponatremia with resultant osmotic demyelination or overcorrection resulting in hypernatremia.

If the treatment of hyponatremia includes hypertonic sodium infusion during surgery, it may be appropriate to infuse this via a pump while replacing losses due to the surgery with lactated Ringer's solution, normal saline, colloid, or blood as required.

Treatment of the underlying cause of the hyponatremia should also continue throughout the perioperative period.

Induction and maintenance of anesthesia in patients with hypovolemic hyponatremia are fraught with the risk of hypotension.

In addition to fluid therapy, vasopressors and/or inotropes may be required to treat the hypotension and should be made available prior to the start of induction.

Hypervolemic hyponatremic patients particularly those with heart failure may benefit from invasive hemodynamic monitoring to guide fluid therapy

TURP SYNDROME During TURP the irrigating fluid is a nonelectrolyte fluid containing

glycine, sorbitol, or mannitol, and this fluid may be absorbed rapidly via open venous sinuses in the prostate gland, causing volume overload, hyponatremia, and hypo-osmolality. This is known as TURP syndrome.

This syndrome is more likely to occur if resection is prolonged (>1 hour), if the irrigating fluid is suspended more than 40 cm above the operative field, or if the pressure in the bladder is allowed to increase above 15 cm H2O.

TURP syndrome manifests principally with cardiovascular and neurologic signs and symptoms.

Hypertension is common. Monitoring for development of this syndrome includes direct

neurologic assessment in the patient under regional anesthesia or measurement of serum sodium concentration and osmolality in the patient under general anesthesia.

Treatment consists of terminating the surgical procedure so that no more fluid is absorbed, diuretics if needed for relief of cardiovascular symptoms, and hypertonic saline administration if severe neurologic symptoms are present or the serum sodium concentration is less than 120 mEq/L.

HYPERNATREMIA

Hypernatremia, defined as a serum sodium greater than 145 mEq/L and is less common because the thirst mechanism is very effective.

Even in renal disorders of sodium retention or water loss, patients regulate their serum sodium within the normal range if they are able to drink water.

In the hospital setting, hypernatremia is most likely to be iatrogenic as a result of overcorrection of hyponatremia or treatment of acid-base disturbances with sodium bicarbonate.

Sodium is a functionally impermeable solute; it contributes to osmolality and induces the movement of water across cell membranes. Hence, hypernatremia is invariably accompanied by hyperosmolality and always causes cellular dehydration and shrinkage.

SIGNS AND SYMPTOMS

Symptoms Signs

Polyuria Muscle twitching

Polydipsia Hyperreflexia

Orthostasis Tremor

Restlessness Ataxia

Irritability Muscle spasticity

Lethargy Focal and generalized seizures

Death

The most prominent abnormalities in hypernatremia are neurologic.

Dehydration of brain cells occurs as water shifts out of the cells into the hypertonic interstitium.

Capillary and venous congestion and venous sinus thrombosis have all been reported.

As the brain cells shrink, cerebral blood vessels may stretch and tear, resulting in intracranial hemorrhage.

Mortality rates up to 75% have been reported in adults with severe acute hypernatremia (serum sodium > 160 mEq/L), and survivors of severe acute hypernatremia often have permanent neurologic sequelae

DIAGNOSIS

TREATMENT

Treatment will be determined by the severity and rapidity of development of hypernatremia and whether the ECF volume is increased or decreased.

In hypovolemic hypernatremia, the water deficit is replaced with normal saline until the patient is euvolemic and then the plasma osmolality is corrected with hypotonic saline or 5% dextrose solution.

In patients with hypervolemic hypernatremia, the primary treatment is diuresis with a loop diuretic, but if the cause of the hypervolemic hypernatremia is renal failure, then hemofiltration or hemodialysis may be needed.

The patient with euvolemic hypernatremia requires water replacement either orally or with 5% dextrose intravenously.

Acute hypernatremia should be corrected over several hours. However, to avoid cerebral edema, chronic hypernatremia should be corrected more slowly, over 2 to 3 days. Ongoing sodium and water losses should also be calculated and replaced.

MANAGEMENT OF ANESTHESIA

If at all possible, surgery should be delayed until the hypernatremia has been corrected.

Frequent serum sodium measurements will be required perioperatively, and invasive hemodynamic monitoring may be useful.

Hypovolemia will be exacerbated by induction and maintenance of anesthesia and prompt correction of hypotension with fluids, vasopressors, and/or inotropes may be required.

DISORDERS OF POTASSIUM

Potassium is the major intracellular cation. The normal total body potassium content depends on muscle mass and is maximal in young adults and decreases progressively with age.

Less than 1.5% of total body potassium is found in the extracellular space.

Extracellular potassium concentration is controlled by factors that regulate transcellular potassium distribution, while total body potassium is regulated principally by the kidneys.

More than 90% of the potassium taken in by diet is excreted in the urine, and the remainder is eliminated in the feces.

As the glomerular filtration rate decreases in renal failure, the amount of potassium excreted by the gastrointestinal route increases.

HYPOKALEMIA( <3.5 MEQ/L )

Hypokalemia is diagnosed by testing the serum potassium concentration, and the differential diagnosis requires determining whether the hypokalemia is acute and secondary to intracellular potassium shifts, such as might be seen with hyperventilation or alkalosis, or whether the hypokalemia is chronic and associated with depletion of total body potassium stores .

If the hypokalemia is suspected to be related to depletion of total body potassium stores, a spot urinary potassium will guide the diagnosis toward either renal or extrarenal causes.

Renal potassium losses will be associated with a urinary potassium greater than 20 mEq/L, and inadequate potassium intake or gastrointestinal losses of potassium will be associated with a urinary potassium of less than 20 mEq/L.

Hypokalemia without a change in total body potassium stores can be caused by familial hypokalemic periodic paralysis, treatment of megaloblastic anemia, and refeeding syndromes when malnourished patients are started on enteral feeding.

ECG CHANGES

CAUSES Hypokalemia Due to Increased Renal Potassium Loss    1. Thiazide diuretics, 2. Loop diuretics   3. Mineralocorticoids    4. High-dose glucocorticoids    5. High-dose antibiotics (penicillin, nafcillin, ampicillin)

  6. Drugs associated with magnesium depletion

 (aminoglycosides)    7. Surgical trauma    8. Hyperglycemia    9. Hyperaldosteronism

Hypokalemia Due to Excessive Gastrointestinal Loss of Potassium

1. Vomiting and diarrhea    2. Zollinger-Ellison syndrome  3. Jejunoileal bypass    4. Malabsorption    5. Chemotherapy    6. Nasogastric suction Hypokalemia Due to Transcellular Potassium

Shift1. β-Adrenergic agonists    2. Tocolytic drugs (ritodrine)    3. Insulin    4. Respiratory or metabolic alkalosis    5. Familial periodic paralysis    6. Hypercalcemia    7. Hypomagnesemia

SIGNS AND SYMPTOMS

TREATMENT

Treatment of hypokalemia is dependent on the degree of potassium depletion and the underlying cause.

If the hypokalemia is profound or associated with life-threatening signs, potassium must be administered intravenously.

The amount of potassium to be given depends on whether there are associated decreases in total body potassium.

Typically, 20 mEq of potassium can be administered over 30 to 45 minutes and repeated as needed.

Such rapid repletion requires electrocardiographic monitoring.

MANAGEMENT OF ANESTHESIA

The decision to treat hypokalemia prior to surgery depends on the chronicity and severity of the defect.

If total body potassium stores are suspected to be low due to chronic potassium loss, then it is unlikely that the administration of small aliquots of potassium immediately prior to surgery will make any significant difference in potassium balance.

However, it has been suggested that even small improvements in potassium balance may help normalize transmembrane potentials and reduce the incidence of perioperative dysrhythmias

It may be prudent to correct significant hypokalemia in patients with other risk factors for dysrhythmias such as those with congestive heart failure or on digoxin therapy.

It is also important to avoid further decreases in serum potassium concentration, such as by the administration of insulin, glucose, β-adrenergic agonists, bicarbonate, and diuretics, or by hyperventilation and respiratory alkalosis.

Because of the effect of hypokalemia on skeletal muscle, there is the theoretical possibility of prolonged action of muscle relaxants. Doses of neuromuscular blockers should be guided by nerve stimulator testing.

Potassium levels should be measured frequently if repletion is ongoing or changes due to drug administration or ventilation are expected.

HYPERKALEMIA

Hyperkalemia is defined as a serum potassium concentration greater than 5.5 mEq/L.

Hyperkalemia can be the result of changes in the transcellular movement of potassium or in total body potassium stores

In hospitalized patients, hyperkalemia is frequently the result of overzealous correction of hypokalemia.

CAUSES OF HYPERKALEMIA

Increased Total Body Potassium Content

Altered Transcellular Potassium Shift

Pseudohyperkalemia

Acute oliguric renal failure

Succinylcholine Hemolysis of blood specimen

Chronic renal disease

Respiratory or metabolic acidosis

Thrombocytosis/leukocytosis

Hypoaldosteronism Lysis of cells due to chemotherapy

Drugs that impair potassium excretion

Iatrogenic bolus

1. Triamterene2. Spironolactone3. NSAIDS

DIAGNOSIS

First step : rule out a spuriously high potassium level secondary to hemolysis of the specimen.

A spuriously high potassium level may also occur with thrombocytosis and leukocytosis due to leakage of potassium from the cells in vitro.

Hyperkalemia due to extracellular potassium shifts may be a result of acidosis, rhabdomyolysis, or administration of drugs such as succinylcholine.

If the increase in serum potassium is thought to be associated with increased total body potassium stores, then decreased renal excretion or increased extrarenal production of potassium is likely.

The urinary potassium excretion rate can aid in the differential diagnosis of hyperkalemia.

ECG CHANGES ECG: early – peaked T waves then

flat P waves, depressed ST segment, widened QRS progressing to sine wave and V fib

TREATMENT In Life threatening dysrhythmias or ECG changes

the treatment is aimed at antagonizing the effects of a high potassium on the transmembrane potential and redistributing the potassium intracellularly.

Calcium chloride or calcium gluconate is administered intravenously to stabilize cellular membranes.

Potassium can be driven intracellularly by the action of insulin with or without glucose. This will be effective within 10 to 20 minutes.

Other adjuvant therapies include sodium bicarbonate and hyperventilation to promote alkalosis and movement of potassium intracellularly.

Potassium driven intracellularly will eventually move extracellularly again after hours so therapy may be continued.

If the hyperkalemia is secondary to increased total body stores of potassium, then potassium must be eliminated from the body.

This can be achieved by a loop diuretic such as furosemide, an infusion of saline to encourage diuresis, or an ion exchange resin.

The primary potassium exchange resin in use is sodium polystyrene sulfonate (Kayexalate) given either orally or by enema.

Dialysis may be required to remove potassium in patients with poor renal function.

MANAGEMENT OF ANESTHESIA

Recommended serum potassium concentration be < 5.5 mEq/L for elective surgery.

It is preferable to correct hyperkalemia prior to surgery, but if this is not feasible, steps should be taken to lower the potassium immediately prior to induction of anesthesia by the methods indicated previously.

Potassium levels do not influence the selection of drugs for induction and maintenance of anesthesia.

Since succinylcholine increases serum potassium by approximately 0.5 mEq/L, it is best avoided.

The effects of muscle relaxants may be exaggerated if there is muscle weakness from the hyperkalemia.

Respiratory and metabolic acidosis must be avoided since either will exacerbate the hyperkalemia and its effects.

Intravenous fluids should be potassium free. Avoid Ringer's lactated solution (contains 4 mEq/L of potassium) and

Normosol (contains 5 mEq/L of potassium).

DISORDERS OF CALCIUM

Only 1% of total body calcium is present in the ECF. The remainder is stored in bone. Calcium in the ECF exists with 60% free or coupled with anions and thus filterable and the remaining 40% bound to proteins, mainly albumin.

Only the ionized calcium in the extracellular space is physiologically active.

Several hormones regulate calcium metabolism: parathyroid hormone, which increases bone resorption and renal tubular reabsorption of calcium; calcitonin, which inhibits bone resorption; and vitamin D, which augments intestinal absorption of calcium.

HYPOCALCEMIA

Hypocalcemia is defined as a reduction in serum ionized calcium concentration.

Binding of calcium to albumin is pH dependent, and acid-base disturbances can change the fraction and therefore the concentration of ionized calcium without changing total body calcium.

Alkalosis reduces the ionized calcium concentration, so ionized calcium may be significantly reduced after bicarbonate administration or with hyperventilation

SIGNS AND SYMPTOMS

Paresthesias Irritability Seizures Hypotension Myocardial depression. Laryngospasm can be life

threatening.

DIAGNOSIS

The most common causes of hypocalcemia are due to a decrease in parathyroid hormone secretion, end-organ resistance to parathyroid hormone, or disorders of vitamin D metabolism. These are usually seen clinically as complications of thyroid or parathyroid surgery, magnesium deficiency, and renal failure.

ECG CHANGES

TREATMENT

Acute symptomatic hypocalcemia with seizures, tetany, and/or cardiovascular depression must be treated immediately with intravenous calcium.

The duration of treatment will be dependent on serial calcium measurements. Treatment of hypocalcemia in the presence of hypomagnesemia is ineffective unless magnesium is also replenished.

Metabolic or respiratory alkalosis should be corrected. If metabolic or respiratory acidosis is present with hypocalcemia, then the calcium level should be corrected before the acidosis is treated because correcting an acidosis with bicarbonate or hyperventilation will only exacerbate the hypocalcemia.

Less acute and asymptomatic hypocalcemia may be treated with oral calcium supplementation and vitamin D.

MANAGEMENT OF ANESTHESIA

Symptomatic hypocalcemia must be treated prior to surgery, and every effort must be made to minimize any further decrease in serum calcium intraoperatively. This might occur with hyperventilation or administration of bicarbonate. Ionized calcium levels may be decreased by massive transfusion of blood containing citrate or when the metabolism of citrate is impaired by hypothermia, liver disease, or renal failure.

Sudden decreases in ionized calcium levels may be seen in the early postoperative period after thyroidectomy or parathyroidectomy and may cause laryngospasm.

HYPERCALCEMIA

Hypercalcemia results from increased calcium absorption from the gastrointestinal tract (milk alkali syndrome, vitamin D intoxication, granulomatous diseases such as sarcoidosis), decreased renal calcium excretion in renal insufficiency, and increased bone resorption of calcium (primary or secondary hyperparathyroidism, malignancy, hyperthyroidism, and immobilization).

SIGNS AND SYMPTOMS

Hypercalcemia is associated with neurologic and gastrointestinal signs and symptoms such as confusion, hypotonia, depressed deep tendon reflexes, lethargy, abdominal pain, and nausea and vomiting, especially if the increase in serum calcium is relatively acute.

Chronic hypercalcemia is often associated with polyuria, hypercalciuria, and nephrolithiasis.

DIAGNOSIS

Almost all patients with hypercalcemia have either hyperparathyroidism or cancer.

Primary hyperparathyroidism is usually associated with a serum calcium concentration less than 11 mEq/L and no symptoms, whereas malignancy often presents with acute symptoms and a serum calcium level greater than 14 mEq/L.

TREATMENT

Treatment of hypercalcemia is directed toward increasing urinary calcium excretion and inhibiting bone resorption and further gastrointestinal absorption of calcium.

Since hypercalcemia is frequently associated with hypovolemia secondary to polyuria, volume expansion with saline not only corrects the fluid deficit but also increases urinary excretion of calcium. Loop diuretics will enhance urinary excretion of sodium and calcium.

Calcitonin, bisphosphonates, or mithramycin may be required in disorders associated with osteoclastic bone resorption. Hydrocortisone may reduce gastrointestinal absorption of calcium in granulomatous disease, vitamin D intoxication, lymphoma, and myeloma. Oral phosphate may also be given to reduce gastrointestinal uptake of calcium if renal function is normal.

Dialysis may be required for life-threatening hypercalcemia. Surgical removal of the parathyroid glands may be necessary to treat primary or secondary hyperparathyroidism.

MANAGEMENT OF ANESTHESIA

Management of anesthesia for emergency surgery in a patient with hypercalcemia is aimed at restoring intravascular volume prior to induction and increasing urinary excretion of calcium with loop diuretics (thiazide diuretics should be avoided as they increase renal tubular reabsorption of calcium). Ideally, surgery should be postponed until calcium levels have normalized.

Central venous pressure or pulmonary artery pressure monitoring may be advisable in some patients requiring fluid resuscitation and diuresis as part of their perioperative treatment of hypercalcemia. Dosing of muscle relaxants must be guided by neuromuscular monitoring if muscle weakness, hypotonia, or loss of deep tendon reflexes is present.

DISORDERS OF MAGNESIUM

Magnesium is predominantly found intracellularly and in mineralized bone. Sixty percent to 70% of serum magnesium is ionized, with 10% complexed to citrate, bicarbonate, or phosphate and approximately 30% bound to protein, mostly albumin. There is little difference between extracellular and intracellular ionized magnesium concentrations so there is only a small transmembrane gradient for ionized magnesium. It is the ionized fraction of magnesium that is associated with clinical outcome.

Magnesium is absorbed from and secreted into the gastrointestinal tract and filtered, reabsorbed, and excreted by the kidneys. Renal reabsorption and excretion are passive, following sodium and water.

HYPOMAGNESEMIA

Some degree of hypomagnesemia occurs in up to 10% of hospitalized patients. An even higher percentage of patients in intensive care units, especially those receiving parenteral nutritional or dialysis, have hypomagnesemia. Coronary care unit patients with hypomagnesemia have a higher mortality rate that those with normal levels of serum magnesium

SIGNS AND SYMPTOMS

Signs and symptoms of hypomagnesemia are similar to those of hypocalcemia and involve mostly the cardiac and neuromuscular systems. Dysrhythmias, weakness, muscle twitching, tetany, apathy, and seizures can be seen. Hypokalemia and/or hypocalcemia that had been refractory to supplementation do respond after correction of hypomagnesemia.

DIAGNOSIS

Hypomagnesemia is most commonly due to reduced gastrointestinal uptake (reduced dietary intake or reduced absorption from the gastrointestinal tract) or to renal wasting of magnesium. These entities can be differentiated by measuring the urinary magnesium excretion rate. Much less frequently, hypomagnesemia is due to intracellular shifts of magnesium with no overall change in total body magnesium, to the “hungry bone syndrome” after parathyroidectomy, or to cutaneous losses.

TREATMENT

Treatment of hypomagnesemia depends on the severity of the deficiency and the signs and symptoms that are present. If cardiac dysrhythmias or seizures are present, magnesium is administered intravenously as a bolus (2 g of magnesium sulfate equals 8 mEq of magnesium), and the dose is repeated until symptoms abate. After life-threatening signs have resolved, a slower infusion of magnesium sulfate can be continued for several days to allow for equilibration of intracellular and total body magnesium stores. If renal wasting is present, supplementation must be increased to account for the magnesium lost in the urine.

Hypermagnesemia is a potential side effect of the treatment of hypomagnesemia so the patient should be monitored for signs of hypotension, facial flushing, and loss of deep tendon reflexes.

MANAGEMENT OF ANESTHESIA

Management of anesthesia in a patient with hypomagnesemia includes attention to the signs of magnesium deficiency, magnesium supplementation, and treatment of refractory hypokalemia or hypocalcemia if needed. If the hypomagnesemia is secondary to malnutrition or alcoholism, the anesthetic implications of these diseases must be considered.

Ventricular dysrhythmias should be anticipated and treated as necessary. Muscle relaxation should be guided by the use of a peripheral nerve stimulator since hypomagnesemia can be associated with both muscle weakness and muscle excitation. Fluid loading (particularly with sodium-containing solutions) and the use of diuretics should be avoided since the renal excretion of magnesium passively follows sodium excretion.

HYPERMAGNESEMIA

Hypermagnesemia (i.e., a serum magnesium concentration > 2.5 mEq/L) is much less common than hypomagnesemia because a magnesium load can be briskly excreted if renal function is normal.

Even patients with renal failure rarely have symptomatic hypermagnesemia unless there is a significantly increased dietary intake. However, milder elevations of serum magnesium are frequently found in intensive care unit and dialysis patient populations. Hypermagnesemia may be a complication of magnesium sulfate therapy for preeclampsia/eclampsia

SIGNS AND SYMPTOMS

Signs and symptoms of hypermagnesemia begin to occur at serum levels of 4 to 5 mEq/L and include lethargy, nausea and vomiting and facial flushing.

At levels above 6 mEq/L, there are a loss of deep tendon reflexes and hypotension. Paralysis, apnea, and/or cardiac arrest are likely if the magnesium level exceeds 10 mEq/L

DIAGNOSIS

Evaluation of hypermagnesemia involves determining renal function (creatinine clearance) and detecting any source of excess magnesium intake, such as parenteral infusion, oral ingestion of antacids, and magnesium-based enemas or cathartics. Once these have been excluded, less common causes of hypermagnesemia including hypothyroidism, hyperparathyroidism, Addison's disease, and lithium therapy can be considered.

TREATMENT

Life-threatening signs of hypermagnesemia may be temporarily ameliorated with intravenous calcium administration but may require hemodialysis.

Lesser degrees of hypermagnesemia can be treated with forced diuresis with saline and loop diuretics to increase renal excretion of magnesium.

MANAGEMENT OF ANESTHESIA

Invasive cardiovascular monitoring may be necessary perioperatively to measure and treat the hypotension and vasodilation of hypermagnesemia and to guide fluid resuscitation and ongoing replacement of fluids during a forced diuresis.

Acidosis exacerbates hypermagnesemia so careful attention must be paid to ventilation and arterial pH. Initial and subsequent doses of muscle relaxant should be reduced in the presence of muscle weakness and guided by a peripheral nerve stimulator.

Hypermagnesemia and skeletal muscle weakness are not uncommon causes of failure to wean from mechanical ventilation in the intensive care setting, especially in patients with renal failure.