6.5: Electrolyte imbalances 

Electrolyte imbalances may be primary or seconday in origin. A primary electrolyte imbalance usually affects only one electrolyte and typically involves an abnormality in either the intake or output of the ion of interest. For example, a high salt diet can result in hypernatremia while some diuretics waste potassium and can cause hypokalemia. A secondary electrolyte imbalance is one resulting from an abnormality in some other physiological function. Secondary imbalances usually affect more than one electrolyte and are common with fluid imbalances since they occur as a result of concentration or dilution of body fluids. For example, in renal failure the kidneys fail to output urine and can result in increased concentrations of all electrolytes normally excreted in the urine. Secondary imbalances are usually detected by looking first for fluid imbalances. Skin turgor (tenting in dehydration and pitting in edema) is a good fluid balance indicator as are sudden weight changes, blood pressure abnormalities, and peripheral or pulmonary edema. Fluid imbalances often appear on laboratory reports as changes in hematocrit. A high hematocrit suggests a possible concentration of blood maybe due to dehydration while a low hematocrit can appear with fluid overloads. It is recommended to seek consultation to senior/physicians for management of patient with electrolyte imbalance before anesthesia plan. 

6.5.1 Sodium 

The daily requirement is 1-2meq/kg for adult, with normal dietary intake ranging between 100-200mEq/d. In contrast, preterm infants have large renal & intestine sodium losses and require 4 to 5 mEq/kg/day during the initial post natal period. Normal ECF concentration of sodium is 135-145 mEq/L. Regulation of the quantity and concentration of sodium is accomplished primarily by the endocrine and renal system. 

Imbalances in sodium homeostasis are common, and although the underlying mechanisms are poorly understood, the clinical manifestations can have significant implications for the anesthetist. The plasma sodium level is important, but it is equally important to evaluate the patient's state of hydration states. Therefore, patients should be assessed clinically in conjunction with their plasma and urinary sodium levels. 

6.5.1.1 Hyponatremia: Exists when plasma sodium concentration less than 135mmol/liter. The measured value represents the ratio of sodium to volume in the serum (or plasma). (Causes of hyponatremia listed in ANNEX III-A) 

Clinical manifestations: The general signs are those of dehydration and hypovolemia in sodium deficiency. Specific symptoms include: 

• The speed of onset of hyponatraemia is much more important in the manifestation of symptoms than the absolute Na+ value. 
• Rare if Na+ >125 mmol/litre. 
• Na+ 125–130 mmol/litre mostly gastrointestinal symptoms. 
• Na+ <125 mmol/litre-neuropsychiatric symptoms, mortality high if untreated. Signs include nausea and vomiting, muscular weakness, headache, lethargy, psychosis, raised intracranial pressure, seizures, coma, respiratory depression. 

Treatment: Treatment depends on the clinical manifestations and speed of onset: 

• Asymptomatic with long-standing hyponatraemia. Simple fluid restriction and reversal of precipitating factors. 
• Asymptomatic with acute onset hyponatraemia—treat as above. 
• Symptomatic (usually associated with rapid onset hyponatraemia): 
• Treatment required urgently in consultation with an endocrinologist/physician. 
• o Water restriction to < 1000- 1500 ml/d is usually successful in reversing hyponatremia when [Na+] is between 125 mEq/L and 135 mEq/L and patients are asymptomatic.. 
• o Hypertonic (3%) saline is most clearly indicated in patients who have seizure or patients in whom acute symptoms water intoxication develop secondary to intravenous fluid administration. In such case, 3% saline could be administered at a rate of 1-2 ml/kg/hr, to increase plasma sodium by 1-2 mEq/L/hr 
• o Diuretics may also be required, especially if seizures and/or cerebral oedema are present or if administration of saline does not bring about a spontaneous diuresis. Use mannitol 20% 500 ml or furosemide (frusemide) 20 mg IV. 
• Treat any underlying pathology concomitantly. 

Anesthetic implications 

• No elective surgery if Na+ <120 mmol/litre or if the patient shows signs of fluid balance disturbance, decreased levels of consciousness, seizures, or focal nervous system deficit. 
•  May need to deal with problem acutely intra-operatively, e.g. TURP syndrome (p. 628). 

6.5.1.2 Hypernatremia 

Exists when plasma sodium is greater than 145 mmol/litre. (Causes of hypernatremia are listed in ANNEX III-B) 

Clinical manifestations 

• May have features of dehydration. 
• The rate of onset is important, slow onset is much better tolerated 
• CNS symptoms are prominent because of the hyperosmolar state (cellular dehydration). 
• Altered mental status, lethargy, irritability, restlessness. 
• Seizures, muscle twitching, spasticity, hyperreflexia. 
• Fever, nausea, vomiting, intense thirst. 
• Intracranial haemorrhage as a result of cerebral dehydration. 
• Prerenal failure secondary to decreased cardiac output. 

Treatment: Correction should be achieved slowly over at least 48 h, as rapid correction may lead to cerebral edema and convulsions. 

• Treat the underlying cause if possible. 
• Treat with oral fluids (water) if possible. 
• Sodium excess (hypervolemic): diuretics, e.g. furosemide (frusemide) 20 mg IV and 5% dextrose, dialysis if required. 
• Water depletion (euvolaemia): estimate the total body water deficit, treat with 5% dextrose. 
• Sodium deficiency (hypovolaemic): 0.9% saline until hypovolaemia corrected, then consider 0.45% saline. 
• Diabetes insipidus-keep up with urinary fluid losses and give desmopresssin 1–4 μg daily (SC/IM/IV). 

Anesthetic implications 

• No elective surgery if Na+ >155 mmol/litre or hypovolemic. 
• Urgent surgery—use invasive central venous pressure monitoring if volume status is uncertain or may change rapidly intra-operatively, and be aware of dangers of rapid normalization of electrolytes. 

6.5.2 Potassium 

Potassium (K+) is the major intracellular cation in the human body and plays a crucial role in the electrophysiology of cell membranes. Imbalances in potassium homeostasis can be of critical importance to the anesthetist. Measurements of plasma potassium can be sent to the laboratory (note that falsely elevated potassium will be seen with a hemolysed sample). Intracellular potassium concentration is normally 150mEq/L, while the extracellular concentration is only 3.5 to 5mEq/L 

6.5.2.1 Hypokalemia 

Hypokalemia is defined as plasma [K+] less than 3.5 mEq/L and can occur as a result of (1) an intercompartmental shift of K+ (see above), (2) increased potassium loss, or (3) an inadequate potassium intake (Table 28–8). Plasma potassium concentration typically correlates poorly with the total potassium deficit. A decrease in plasma [K+] from 4 mEq/L to 3 mEq/L usually represents a 100- to 200-mEq deficit, whereas a plasma [K+] below 3 mEq/L can represent a deficit anywhere between 200 mEq and 400 mEq. (Causes of hypokalemia are listed in ANNEX III-C) 

Clinical manifestations: 

• Nonspecific symptoms of Hypokalemia include nausea & anorexia. 
• Cardiovascular- dysrhythmias, ECG changes (delayed repolarization with ST segment depression, reduced height of the T wave and a widened QRS complex), digitalis toxicity potentiation, postural hypotension and impaired pressor responses. 
• Effects on skeletal & smooth muscle /muscle weakness, paralytic ileus/. 
• Measured (K) plasma concentration <3.5meq/L 

Treatment of Hypokalemia 

The treatment of hypokalemia depends on the presence and severity of any associated organ dysfunction. 

Significant ECG changes such as ST-segment changes or arrhythmias mandate continuous ECG monitoring, particularly during intravenous K+ replacement. Digoxin therapy—as well as the hypokalemia itself— sensitizes the heart to changes in potassium ion concentration. Muscle strength should also be periodically assessed in patients with weakness. 

Anesthetic management: 

• Before induction repeat plasma potassium & obtain an ECG for evaluation of cardiac rhythm. Monitor EKG throughout the operation. 
• It should be recalled myocardial contractility and postural hypotension. Pts are sensitive to cardiac depressant effects of volatile anesthetics. 
• During surgery I.V fluid should avoid glucose loads. 
• Add 10-20meq of KCL to every liter of I.V maintenance fluids 
• Exogenous Epinephrine is discouraged. 
• Excessive ventilation of the lung must be avoided. 
• The potential for prolonged responses to NDMR must be anticipated. 

6.5.2.2 Hyperkalemia 

Hyperkalemia exists when plasma [K+] exceeds 5.5 mEq/L. Hyperkalemia rarely occurs in normal individuals because of the kidney's tremendous capacity to excrete potassium. The sympathetic system and insulin secretion also appear to play important roles in preventing acute increases in plasma [K+] following potassium loads. 

Hyperkalemia can result from (1) an intercompartmental shift of potassium ions, (2) decreased urinary excretion of potassium, or, rarely, (3) an increased potassium intake. (Causes of hyperkalemia listed in ANNEX III-D) 

Manifestation: 

Cardiovascular: 

• Earliest change (6-7mEq/L)-development of tall peaked T waves, & a shortened QT interval. 
• Plasma potassium (8-10mEq/L), abnormalities in depolarization become manifest as widened QRS complexes & eventual loss of the P wave. 
• Plasma potassium (>10mEq/L) is associated with ventricular fibrillation. 

Neuromuscular: Paresthesia, weakness, paralysis and confusion 

Treatment of hyperkalemia 

• Administration of 5-10 ml of 10% calcium gluconate or 3–5 mL of 10% calcium chloride over 10 minutes (max 20 ml). This has an immediate but transient stabilizing effect on the myocardial cells. 
• 50mls of 50% glucose +5-10units of Insulin as an intravenous bolus or infusion. Glucose and insulin will produce an immediate migration of potassium into the cells thus reducing the serum level 
• Nebulized salbutamol 2.5 - 5mg will assist in moving K+ into the cells. 
• Hyperventilation 

6.5.3 Calcium 

Calcium plays a crucial role in many biological functions, such as muscle contraction, neurotransmitter release, cardiac pace maker automaticity, coagulation, bone formation, etc. Total calcium is normally about 9-10 mg/dL. The ionized fraction of calcium is responsible for the majority of biological activity. The ionized calcium is normally about 4.5-5 mg/dL. 

6.5.3.1 Hypocalcemia: a measured value of ionized calcium <4.5mg/dL. The hallmark of hypocalcaemia is increased neuronal membrane irritability and tetany. Manifestations include paresthesias, confusion, laryngeal stridor (laryngospasm), carpopedal spasm (Trousseau's sign), masseter spasm (Chvostek's sign), and seizures. Biliary colic and bronchospasm have also been described. Cardiac irritability can lead to arrhythmias. Decreased cardiac contractility may result in heart failure, hypotension, or both. Decreased responsiveness to digoxin and -adrenergic agonists has also been reported. ECG signs include prolongation of the QT interval. (Causes of hypocalcemia listed in ANNEX III-E) 

Treatment of Hypocalcemia 

Symptomatic hypocalcemia is a medical emergency and should be treated immediately with intravenous calcium chloride (3–5 mL of a 10% solution) or calcium gluconate (10–20 mL of a 10% solution). 

Anesthetic consideration in hypocalcaemia: 

• Management of anesthesia designed to prevent further decrease in the plasma calcium concentration and to recognize and treat adverse effects of hypocalcaemia. 
• Monitor plasma calcium concentration, electrocardiograph, intra operatively. 
• Respiratory or metabolic alkalosis, rapid blood transfusion decreases the plasma ionized calcium concentration. 
• Intra operative hypotension may reflect the exaggerated cardiac depression produced by anesthetic drugs. 
• Response to nondepolarizing muscle relaxant could be potentiated. 
• Coagulation problems should be anticipated. 

6.5.3.2 Hypercalcemia 

Occur when serum calcium level greater than 10.5mg/dl. Serum calcium level below 12mg/dl is not associated with symptoms. Hypercalcemia often produces anorexia, nausea, vomiting, weakness, and polyuria. Ataxia, irritability, lethargy, or confusion can rapidly progress to coma. Hypertension is often present initially before hypovolemia supervenes. ECG signs include a shortened ST segment and a shortened QT interval. Hypercalcemia increases cardiac sensitivity to digitalis. Pancreatitis, peptic ulcer disease, and renal failure can also complicate hypercalcemia. (Causes of hypercalcemia are listed in ANNEX III-F) 

Treatment of Hypercalcemia: Symptomatic hypercalcemia requires rapid treatment. The most effective initial treatment is rehydration followed by a brisk diuresis (urinary output 200–300

mL/h) with administration of intravenous saline infusion and a loop diuretic to accelerate calcium excretion. 

Anesthetic consideration 

• The principles of anesthetic management are the maintenance of hydration & urine output with IV fluid containing sodium. 
• Avoid anesthetic drugs that induce fluoride nephrotoxicity. 
• Hyperventilation not advised. 
• The preoperative existence skeletal muscle weakness would suggest decreased dose requirement for muscle relaxants. 
• Continuous monitoring in ECG.