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Fluid, electrolyte, and acid-base disorders
Alterations of water, osmolal, and electrolyte content and distribution as well as acid-base disturbances are common in the perioperative period and rarely happen in isolation because they are inherently interrelated. They both affect and are affected by the function and stability of several organ systems. Central nervous system (CNS) impairment, cardiac dysfunction, and neuromuscular changes are especially common in the presence of water, osmolal, electrolyte, and acid-base disturbances. Several perioperative events can exacerbate such alterations ( Table 20.1 ). Management of patients with these disturbances is based on an assessment of the cause and severity of the condition, an understanding of the interrelationships among these disturbances, and an awareness of the patient’s comorbid conditions.
TABLE 20.1
Common Causes of Water, Osmolal, Electrolyte, and Acid-Base Disturbances During the Perioperative Period
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Abnormalities of water, osmolality, and electrolytes
Water and osmolal homeostasis
In the nonobese adult, total body water comprises approximately 60% of body weight (obesity decreases this proportion). Body water is divided into intracellular fluid (ICF) and extracellular fluid (ECF) compartments according to the location of the water relative to cell membranes ( Fig. 20.1 ). ECF consists primarily of an interstitial compartment (three-fourths of ECF) and an intravascular plasma compartment (one-fourth of ECF). Water shifts between compartments according to the balance of hydrostatic and oncotic pressure across membranes, and thus water homeostasis relies on the maintenance of osmolality within a narrow physiologic range. The integrity of living cells depends on preservation of water homeostasis as well as on the energy-intensive maintenance of intracellular and extracellular concentrations of ions termed electrolytes. These electrolytes, in addition to being a major determinant of both osmolality and acid-base balance, are responsible for electrical potentials across cell membranes. Changes in electrolyte homeostasis especially impact excitable cells in the CNS and musculature that rely on action potentials for rapid and organized transfer of information.
Water and osmolal homeostasis are predominantly mediated by osmolality-sensing neurons located in the anterior hypothalamus. In response to osmolal elevations, these neurons stimulate thirst and cause pituitary release of vasopressin (antidiuretic hormone). Vasopressin is stored as granules in the posterior pituitary and acts through G protein–coupled receptors in the collecting ducts of the kidney to cause water retention, which in turn decreases serum osmolality. Vasopressin receptors are also present in other tissues and, most noticeably for the anesthesiologist, are present in high density on vascular smooth muscle cells where they induce vasoconstriction. As a major site of vasopressin effects, the kidney is responsible for maintaining water homeostasis by excreting urine with large variations in total osmolality. Under normal circumstances, serum osmolality is tightly regulated by thirst and renal control of water excretion. The normal range of serum osmolality is 280 to 290 mOsm/kg.
The osmolality of serum represents the total number of osmotically active particles (i.e., solutes) per kilogram of solvent. When osmolality is assessed, a shorthand indirect measurement of expected serum osmolality can easily be calculated as 2[Na] + [Glucose]/18 + [Blood urea nitrogen (BUN)]/2.8, and this calculated value should always be compared with direct laboratory-measured actual osmolality. A significant difference in these values (known as an osmolal gap) should alert the clinician to the presence of unmeasured osmotically active particles. Increases in serum osmolality may be encountered as a result of free water depletion (e.g., dehydration or diabetes insipidus) or the presence of additional solutes (most commonly from ingestion of ethanol or other toxins, hyperglycemia, or iatrogenic administration of osmolal loads such as mannitol or glycine). Perioperative attempts to induce fluid shifts by deliberate administration of osmolal loads should take into consideration the patient’s preexisting serum osmolality to avoid extreme increases in serum osmolality (>320 mOsm/kg). Mannitol should not be administered to an intoxicated patient with elevated intracranial pressure, for example, without prior consideration of the preexisting effects of ethanol molecules and water diuresis on the osmolal state of the patient.
Although vasopressin is predominantly secreted in response to increased osmolality, its release is also stimulated by large isoosmolar decreases in effective circulating volume. In addition, the pain and stress of the perioperative period are upregulators of vasopressin release, and the stress response to critical illness can include water retention, oliguria, and dilutional hyponatremia ( Table 20.2 ).
TABLE 20.2
Factors and Drugs Affecting Vasopressin Secretion
| Stimulation of Vasopressin Release | Inhibition of Vasopressin Release | Drugs That Stimulate Vasopressin Release and/or Potentiate Renal Action of Vasopressin |
|---|---|---|
| Contracted ECF volume Hypernatremia Hypotension Nausea and vomiting Congestive heart failure Cirrhosis Hypothyroidism Angiotensin II Catecholamines Histamine Bradykinin |
Expanded ECF volume Hyponatremia Hypertension |
Amitriptyline Barbiturates Carbamazepine Chlorpropamide Clofibrate Morphine Nicotine Phenothiazines Selective serotonin reuptake inhibitors |
ECF , Extracellular fluid.
In contrast to osmolal homeostasis, the homeostatic response to isotonic changes in total body water relies on juxtaglomerular sensation of changes in effective circulating volume and consequent changes in kidney renin excretion. Renin converts angiotensinogen into angiotensin I, which is converted to angiotensin II in the lung. Angiotensin II induces adrenal release of aldosterone, which promotes sodium reabsorption and potassium loss in the distal tubules and leads to increases in water resorption. Elevations in circulating volume also cause increased release of natriuretic peptides that promote a return to water homeostasis.
Fluid resuscitation in patients with hypovolemia necessitates consideration of the cause and severity of the hypovolemia and patient comorbid conditions. Crystalloid administration should take into consideration a patient’s electrolyte and acid-base balance as well as concerns regarding the acute cardiovascular effects of additional volume and the neurologic effects of changes in volume, osmolality, and glucose levels.
Regarding the choice of crystalloid solution in the absence of compelling physiologic patient needs, a recent large pragmatic clinical trial in critically ill intensive care unit (ICU) adults demonstrated a lower rate of the composite outcome of death, new renal-replacement therapy, or persistent renal dysfunction when using balanced crystalloid as opposed to normal saline.
Infusion of colloids, including blood products, should be done in the context of appropriate goals for hemoglobin concentration, platelet numbers, and coagulation factors and must take into consideration the course of any ongoing blood loss and the health status of the patient. Synthetic volume expanders have been advocated to achieve volume expansion with reduced tissue edema compared to crystalloids. However, there is no good evidence that they provide advantages in outcomes in comparison to appropriately balanced crystalloid solutions. Indeed, some have been associated with increased bleeding and a higher incidence of renal dysfunction in addition to their increased cost in comparison with crystalloids.
Disorders of sodium
As the ion with the highest concentration in the ECF, sodium contributes most of the effective osmoles to serum. This underlying connection between serum sodium concentration and osmolality is critical for understanding disorders of sodium homeostasis. Under normal circumstances, serum sodium concentration is maintained between 136 and 145 mmol/L, primarily by the action of vasopressin on water and osmolal homeostasis.
Variations in measured sodium concentration frequently occur along with derangements in total body water. Assessment and treatment of changes in sodium concentration must therefore consider osmolality as well as the total body water of the patient. Total body water can be increased, normal, or decreased in the context of derangements in sodium concentration, and the cause and treatment of serum sodium disorders depend on the osmolality and volume status of the patient.
Hyponatremia
Hyponatremia commonly exists in concert with hypoosmolality when water retention or water intake exceeds renal excretion of dilute urine. Hyponatremia exists in approximately 15% of hospitalized patients, most commonly as a dilutional effect in the setting of increased vasopressin release. In the outpatient setting, hyponatremia is more likely to be a result of chronic disease, and in heart failure it has been shown to be an independent predictor of 30-day and 1-year mortality.
Signs and symptoms
The signs and symptoms of hyponatremia depend on the rate at which the hyponatremia has developed and are less pronounced in chronic cases. In addition, younger patients appear to tolerate a decrease in serum sodium better than elderly patients.
Anorexia, nausea, and general malaise may occur early, but CNS signs and symptoms predominate later in the course and in acutely deteriorating cases of hyponatremia ( Table 20.3 ). As mentioned, hyponatremia usually occurs along with extracellular hypotonicity. The associated osmolal gradient allows water to move into brain cells, which results in cerebral edema and increased intracranial pressure. Brain cells may compensate over time by lowering intracellular osmolality by movement of potassium and organic solutes out of brain cells. This reduces water movement into the intracellular space. However, when adaptive mechanisms fail or hyponatremia progresses, CNS dysfunction can manifest as a change in sensorium, seizures, brain herniation, or death.
TABLE 20.3
Symptoms and Signs of Hyponatremia
| Symptoms | Signs |
|---|---|
| Anorexia Nausea Lethargy Apathy Muscle cramps |
Abnormal sensorium Disorientation, agitation Cheyne-Stokes breathing Hypothermia Pathologic reflexes Pseudobulbar palsy Seizures Coma Death |
Diagnosis
Although hyponatremia usually coexists with hypoosmolality, osmolality should be measured in all cases of hyponatremia, particularly to avoid overlooking a pathologic hyperosmolar state caused by dangerous concentrations of glucose or exogenous toxins, or iatrogenic infusions of osmolal loads.
In such hyperosmolal situations, plasma volume expands as interstitial and intracellular water migrate into the intravascular space, causing a relative dilution of the serum sodium concentration without a reduction in the amount of total body sodium. Total body water may be increased, unchanged, or decreased depending on the competing effects of water administered with the osmolal load and the likely presence of an osmotic diuresis.
In patients with normal osmolality, a pseudohyponatremia can be seen as a laboratory artifact in cases of severe hyperlipidemia or hyperproteinemia when plasma volume is increased in the presence of normal serum sodium concentrations. Measuring sodium concentrations in serum rather than in plasma avoids this misinterpretation of laboratory data.
Once the two situations of hyperosmolality and normal osmolality have been excluded, the approach to the diagnosis of hypoosmolal hyponatremia includes evaluation of the severity of the electrolyte derangement and the underlying volume status of the patient. Hypervolemic hyponatremia suggests the possibility of renal failure, congestive heart failure, or a hypoalbuminemic state such as cirrhosis or nephrotic syndrome. Euvolemic hyponatremia is commonly seen in the syndrome of inappropriate antidiuretic hormone secretion (SIADH) or in situations of habitual ingestion of hypotonic solutions (e.g., water), as seen in psychogenic polydipsia. Hypovolemic hyponatremia should prompt an investigation into the source of free water loss. This free water loss may be from renal losses (e.g., from diuretics, mineralocorticoid deficiency, or other salt-wasting nephropathy) or extrarenal losses (e.g., gastrointestinal [GI] losses or third spacing).
Often the clinical context of hyponatremia offers the principal clue to its cause. For example, massive absorption of irrigating solutions that do not contain sodium, such as during transurethral resection of the prostate, is a relatively common cause of intraoperative hyponatremia. When the clinical context does not lead to a diagnosis, urinary sodium concentration measured from a spot urine sample can help further differentiate among the various causes of hyponatremia ( Fig. 20.2 ).
Treatment
Treatment of hypotonic hyponatremia will depend on the volume status of the patient. In hypovolemic hyponatremia, appropriate volume resuscitation should be pursued, usually with normal saline. If renal sodium losses are suspected, mineralocorticoid deficiency and the possibility of adrenal insufficiency should not be overlooked. Cases of massive third spacing, such as often accompany pancreatitis or burns, require tailored resuscitation based on the totality of electrolyte and hematologic derangements.
In euvolemic or hypervolemic patients, treatment involves withholding free water and encouraging free water excretion with a loop diuretic. Administration of saline is necessary only if significant symptoms are present. In these as in all cases of hyponatremia, the rate of correction depends on whether the development of hyponatremia was acute (i.e., occurred in <48 hours) or chronic.
Acute symptomatic hyponatremia must be treated promptly. Solute-free fluids are withheld, and hypertonic saline (3% NaCl) and furosemide are administered to enhance renal excretion of free water. Serum electrolyte levels should be checked frequently and this treatment continued until symptoms disappear, which will likely occur before the serum sodium concentration returns to normal.
Chronic symptomatic hyponatremia should be corrected slowly to avoid the risk of osmotic demyelination. During the development of chronic hyponatremia, brain cells retain their normal intracellular volume as the serum sodium decreases by exporting effective osmoles. Approximately half of these effective osmoles are potassium ions and anions, and the remainder are small organic compounds. While hyponatremia is being corrected, brain cells must reaccumulate these effective osmoles or water will move out of the cells into the now relatively hypertonic ECF, causing cell shrinkage. Such shrinkage can trigger central pontine myelinolysis, which can 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 serum sodium concentration of approximately 10 mEq/L. Thereafter, correction should not exceed 1 to 1.5 mEq/L/hr or a daily maximum increase of 12 mEq/L.
Treatment of chronic asymptomatic hyponatremia should consider the underlying cause of the electrolyte disturbance. Appropriate sodium intake and volume restriction are often the cornerstones of treatment. Patients with hypervolemic hyponatremia due to congestive heart failure respond very well to the combination of an angiotensin-converting enzyme inhibitor and a loop diuretic.
Management of anesthesia
If at all possible, significant hyponatremia, especially if symptomatic, should be corrected before surgery. If the surgery is urgent, appropriate corrective treatment should continue throughout the surgery and into the postoperative period. Frequent measurement of serum sodium concentration 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 should be infused via a pump while losses caused by the surgery are replaced with standard crystalloid or colloid solutions 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 these should be available before the start of induction. Hypervolemic hyponatremic patients, particularly those with heart failure, may benefit from invasive hemodynamic monitoring to assess cardiac function and guide fluid therapy.
Transurethral resection of the prostate (TURP) syndrome
Benign prostatic hyperplasia is often treated surgically by TURP. This procedure involves resection via a cystoscope, with continuous irrigation of the bladder to aid visualization of the surgical field and removal of blood and resected material. The irrigating fluid is usually a nearly isotonic nonelectrolyte fluid containing glycine or a mixture of sorbitol and mannitol. This irrigating fluid can be absorbed rapidly via open venous sinuses in the prostate gland and can cause volume overload and hyponatremia. The constellation of findings associated with absorption of bladder irrigation solution is known as TURP syndrome. This syndrome is more likely to occur when resection is prolonged (>1 hour), when the irrigating fluid is suspended more than 40 cm above the operative field, when hypotonic irrigation fluid is used, and when the pressure in the bladder is allowed to increase above 15 cm H 2 O. TURP syndrome ( Table 20.4 ) manifests principally with cardiovascular signs of fluid overload and neurologic signs and symptoms of hyponatremia. Use of hypotonic irrigating solutions can also induce hemolysis because red blood cells encounter a significant influx of free water from hypotonic ECF. Hypertension and pulmonary edema are common. If a glycine irrigant is used, transient blindness can occur that is thought to result from the inhibitory neurotransmitter effects of glycine on several populations of retinal ganglion cells. Glycine breaks down into glyoxylic acid and ammonia, and excessive ammonia levels are themselves known to cause encephalopathy.
TABLE 20.4
Signs and Symptoms of TURP Syndrome
| System | Signs and Symptoms | Cause |
|---|---|---|
| Cardiovascular | Hypertension, reflex bradycardia, pulmonary edema, cardiovascular collapse | Rapid fluid absorption (reflex bradycardia may be secondary to hypertension or increased ICP) |
| Hypotension | Third spacing secondary to hyponatremia and hypoosmolality; cardiovascular collapse | |
| ECG changes (wide QRS, elevated ST segments, ventricular dysrhythmias) | Hyponatremia | |
| Respiratory | Tachypnea, oxygen desaturation, Cheyne-Stokes breathing | Pulmonary edema |
| Neurologic | Nausea, restlessness, visual disturbances, confusion, somnolence, seizures, coma, death | Hyponatremia and hypoosmolality causing cerebral edema and increased ICP, hyperglycinemia, hyperammonemia |
| Hematologic | Disseminated intravascular hemolysis | Hyponatremia and hypoosmolality |
| Renal | Renal failure | Hypotension, hyperoxaluria (oxalate is a metabolite of glycine) |
| Metabolic | Acidosis | Deamination of glycine to glyoxylic acid and ammonia |
ECG , Electrocardiogram; ICP , intracranial pressure; TURP , transurethral resection of the prostate.
Monitoring for the development of TURP syndrome includes direct neurologic assessment in patients under regional anesthesia and measurement of hemodynamics, serum sodium concentration, and osmolality in patients under general anesthesia. Treatment consists of terminating the surgical procedure so no more fluid is absorbed, administration of loop diuretics if needed for relief of cardiovascular symptoms, and administration of hypertonic saline if severe neurologic symptoms or signs are present or the serum sodium concentration is less than 120 mEq/L.
Hypernatremia
Hypernatremia is defined as a serum sodium concentration above 145 mEq/L. It is much less common than hyponatremia because the vasopressin-driven thirst mechanism is very effective in responding to the hypertonic state of hypernatremia. Even in patients with renal disorders of sodium retention or severe water loss, patients will regulate their serum sodium concentration close to or within the normal range if they have access to water. Therefore hypernatremia is much more likely to be seen in the very young, the elderly, and those people who are debilitated, have altered mental status, or are unconscious.
In the perioperative setting, hypernatremia is most likely a result of iatrogenic overcorrection of hyponatremia or treatment of acidemia with sodium bicarbonate. Free water losses from diabetes insipidus and extrarenal GI losses may also lead to hypernatremia. Because sodium is the major contributor to ECF osmolality, hypernatremia induces the movement of water across cell membranes into the ECF. Hypernatremia and the associated hyperosmolality will always lead to cellular dehydration and shrinkage.
Signs and symptoms
Signs and symptoms of hypernatremia can vary from mild to life threatening ( Table 20.5 ). The earliest signs and symptoms include restlessness, irritability, and lethargy. As hypernatremia progresses, muscular twitching, hyperreflexia, tremors, and ataxia may develop. The signs and symptoms progress as the osmolality increases above 325 mOsm/kg. Muscle spasticity, seizures, and death may ensue. The very young, the very old, and those with preexisting CNS disease exhibit more severe symptoms at any given serum sodium concentration or degree of hyperosmolality.
TABLE 20.5
Symptoms and Signs of Hypernatremia
| Symptoms | Signs |
|---|---|
| Polyuria Polydipsia Orthostasis Restlessness Irritability Lethargy |
Muscle twitching Hyperreflexia Tremor Ataxia Muscle spasticity 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 as well as venous sinus thrombosis have all been reported. As the brain cells shrink, cerebral blood vessels may stretch and tear, which results in intracranial hemorrhage.
Usually the signs and symptoms are more severe when hypernatremia is acute rather than chronic and when excessive elevations in serum sodium levels are present. Mortality rates of up to 75% have been reported in adults with severe acute hypernatremia (serum sodium concentration >160 mEq/L), and survivors of severe acute hypernatremia often have permanent neurologic deficits. During the development of chronic hypernatremia, brain cells generate idiogenic osmoles that restore intracellular water in spite of the ongoing hypernatremia and protect against brain cell dehydration. If chronic hypernatremia is corrected too rapidly, these idiogenic osmoles predispose to the development of cerebral edema.
Diagnosis
The diagnosis and treatment of hypernatremia should focus on the severity of the derangement and the volume status of the patient. The presence of hypervolemia, euvolemia, or hypovolemia dictates the appropriate diagnostic and treatment modalities ( Fig. 20.3 ).
In hypovolemic hypernatremia the patient has lost more water than sodium via renal or extrarenal routes. This may occur as a result of excessive diuresis, GI losses, or insensible fluid losses from burns or sweating.
Patients with hypervolemic hypernatremia will show signs of ECF volume expansion, such as jugular venous distention, peripheral edema, and pulmonary congestion. The differential diagnosis includes a history of hypertonic fluid administration, oral intake of salt tablets, and endocrine abnormalities marked by excessive aldosterone secretion.
Euvolemic and hypovolemic hypernatremia occur secondary to water loss without salt loss and may be seen with either extrarenal pathologic conditions (e.g., GI tract losses or insensible losses from burns or sweating) or from renal losses (e.g., diabetes insipidus, loop diuretics, or osmotic diuresis).
As with hyponatremia, testing of a spot urine sample for sodium concentration and osmolality can help distinguish among the causes of hypernatremia (see Fig. 20.3 ).
Treatment
Treatment is determined by how severe the hypernatremia is, how rapidly it developed, and whether the ECF volume is increased or decreased.
In hypovolemic hypernatremia the water deficit is replenished with normal saline or a balanced electrolyte solution 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 unless the cause is renal failure, in which case hemofiltration or hemodialysis may be needed.
Patients with euvolemic hypernatremia require water replacement either orally or with 5% dextrose intravenously. Treatment of diabetes insipidus depends on whether there is a central deficit of vasopressin release or a renal insensitivity to vasopressin’s actions.
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 and its associated symptoms have abated. Frequent serum sodium measurement and urine output monitoring will be required perioperatively, and invasive hemodynamic monitoring may be useful to assess volume status. Hypovolemia will be exacerbated by induction and maintenance of anesthesia, and prompt correction of hypotension with fluids, vasopressors, and/or inotropes may be required. The volume of distribution of hydrophilic drugs will be altered in hypovolemia and hypervolemia. However, the accentuated hemodynamic responses to anesthetic drug administration are most likely a consequence of the vasodilation and negative inotropic effects of anesthetic drugs rather than the result of changes in their volume of distribution.
Disorders of potassium
Potassium is the major intracellular cation. The normal total body potassium content depends on muscle mass; it is maximal in young adults and decreases progressively with age. Less than 1.5% of total body potassium is found in the extracellular space. Therefore serum potassium concentration is more a reflection of factors that regulate transcellular potassium distribution than of total body potassium. Total body potassium is regulated over long periods of time, principally by the distal nephron in the kidneys; the distal nephron secretes potassium in response to aldosterone, which leads to an increase in urine volume and nonresorbable anions and metabolic alkalosis. More than 90% of potassium taken in by diet is excreted in the urine, and most of the remainder is eliminated in the feces. As the glomerular filtration rate decreases in renal failure, the amount of potassium excreted by the GI route increases.
Hypokalemia
Signs and symptoms
Signs and symptoms of hypokalemia are generally restricted to the cardiac and neuromuscular systems and include dysrhythmias, muscle weakness, cramps, paralysis, and ileus.
Diagnosis
Hypokalemia is diagnosed by the presence of a serum potassium concentration below 3.5 mmol/L and results from decreased net potassium intake, intracellular shifts, or increased potassium losses. 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 ( Table 20.6 ). If the hypokalemia is the result of potassium losses, a spot urinary potassium reading will guide the diagnosis to either renal or extrarenal causes. Appropriately low urine potassium concentrations in the setting of hypokalemia point to a normally functioning kidney in the setting of inadequate potassium intake or GI losses. Renal potassium losses are indicated by a spot urinary potassium value of more than 15 to 20 mEq/L despite the presence of hypokalemia. In cases of renal potassium loss, assessment of the transtubular potassium concentration gradient, hemodynamics, and acid-base status will further help to elucidate the diagnosis. Hypertension with hypokalemia is usually the result of a hyperaldosterone state. Renal losses in the setting of acidemia point to a diagnosis of renal tubular acidosis or diabetic ketoacidosis. Renal losses in the setting of alkalemia can indicate a response to diuretics or can be seen in genetic disorders such as Liddle syndrome (associated with hypertension and excess sodium resorption) or Bartter syndrome (which presents with polyhydramnios, normal to low blood pressure, and neonatal polyuria and polydyspsia with tubular effects similar to those of loop diuretics). Hypomagnesemia can also exacerbate renal potassium losses. Hypokalemia without a change in total body potassium stores can be caused by familial hypokalemic periodic paralysis.
TABLE 20.6
Causes of Hypokalemia
Adapted from Gennari JF. Hypokalemia. N Engl J Med . 1998;339: 451–458.
| Hypokalemia Due to Increased Renal Potassium Loss Thiazide diuretics Loop diuretics Mineralocorticoids High-dose glucocorticoids Antibiotics (penicillin, nafcillin, ampicillin) Drugs associated with magnesium depletion (aminoglycosides) Surgical trauma Hyperglycemia Hyperaldosteronism |
| Hypokalemia Due to Excessive Gastrointestinal Loss of Potassium Vomiting and diarrhea Zollinger-Ellison syndrome Jejunoileal bypass Malabsorption Chemotherapy Nasogastric suction |
| Hypokalemia Due to Transcellular Potassium Shift β-adrenergic agonists Tocolytic drugs (ritodrine) Insulin Respiratory or metabolic alkalosis Familial periodic paralysis Hypercalcemia Hypomagnesemia |
Treatment
Treatment of hypokalemia depends on the degree of potassium depletion and the underlying cause. If the hypokalemia is profound or is associated with life-threatening signs, potassium must be administered intravenously. In the presence of paralysis or malignant dysrhythmias, the rate of potassium repletion can be as high as 20 mEq over 30 minutes (via an infusion pump) and repeated as needed. If a malignant dysrhythmia appears during potassium repletion, the rate of potassium administration may be the cause. Therefore electrocardiographic (ECG) monitoring is required whenever rapid potassium repletion is undertaken. In the setting of urgent potassium repletion, potassium solutions without dextrose are preferred. Otherwise the insulin secretion stimulated by the glucose will induce intracellular potassium transfer.
The enteral route of potassium repletion is preferred in cases of nonemergent potassium repletion to avoid the risks of high-dose intravenous (IV) potassium administration. If IV repletion is chosen in a nonemergency situation, it should proceed at a rate of less than 20 mEq/h. Peripheral infusion of a concentrated potassium solution will result in pain and/or inflammation at the IV site, so administration via a central venous catheter is preferred.
Management of anesthesia
Whether or not to treat hypokalemia before surgery is an ongoing subject of debate and depends on the chronicity and severity of the deficit. Because of the limitations on the rate of potassium repletion and the large total body potassium deficits that accompany chronic hypokalemia, safe repletion of total body potassium stores often requires days. Although total body depletion is variable in its relationship to serum potassium concentrations, chronic hypokalemia with serum concentrations of less than 3.0 mEq/L may require delivery of 600 mEq or more of potassium to achieve a normal total body potassium. It is therefore unlikely that administration of small aliquots of potassium immediately before surgery will make any significant difference in potassium balance. Moreover, such interventions carry the risk of inadvertent hyperkalemia that may exacerbate the risk of dysrhythmias in the perioperative period. However, it has been suggested that even small improvements in potassium balance may help normalize transmembrane potentials and reduce the incidence of perioperative dysrhythmias. Recommendations on this controversial issue are based more on expert opinion, clinical judgment, and local practice patterns than on evidence from peer-reviewed studies.
It may be prudent to correct significant hypokalemia in patients with other risk factors for dysrhythmias, such as those with congestive heart failure, those taking digoxin, and those with ECG evidence of hypokalemia. ECG abnormalities associated with potassium derangement are illustrated in ( Fig. 20.4 ). Classically, U waves are seen. Anesthetic management of patients with significant hypokalemia should prevent further decreases in serum potassium concentration by avoiding administration of insulin, glucose, β-adrenergic agonists, bicarbonate, and diuretics as well as by avoiding 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, as always, be guided by nerve stimulator testing.
Potassium levels should be measured frequently if repletion is ongoing or changes resulting from drug administration, surgical progress, or ventilation are expected.
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