INTRODUCTION
The understanding of body water and electrolyte distribution is paramount in managing surgical patients with electrolyte derangements. These changes can occur preoperative, intra-operative and postoperative and the management is governed by adequate knowledge of the underlying mechanism and appropriate fluid therapy if indicated.
In a normal individual who has not undergone a surgical procedure, there are insensible physiological fluid and electrolyte losses, some of which are outlined in Table 1.1.
A normal individual consumes an estimated 2–3 L of water per day and consumes 3–5 g of salt per day both of which are regulated by the kidneys.
Normal Body Water and Electrolyte Distribution
Total body water (TBW) contributes to 40–60 percent of our total body weight. This may vary with age and sex of the individual. At birth, 80 percent of our body weight comprises of TBW which rapidly decreases with age. It is also known that the percentage of TBW in lean individuals is higher than elderly or obese individuals (10-20% lower). Young adult females also tend to have a lower percentage TBW (50%) compared to aged matched males.
The TBW is compartmentalized in the body with 2/3rd of it being intracellular and 1/3rd being extracellular. An example of TBW distribution in a 60 kg (50% of body weight) female is given in Table 1.2.
The chemical composition of fluid compartments is summarized in the Table 1.3.
The composition of electrolytes within each is governed primarily by the potassium, sodium, chloride and protein content. This is regulated by the ATP driven Na-K pump located within the cell membrane. Therefore, ions and protein movement is restricted, however, water is freely distributed across the compartments. As a result, if excess water is ingested it will be equally distributed amongst the compartments. On the other hand, if sodium containing fluids are given, this will expand the intravascular and interstitial volume.
Although there is free movement of water, the direction of flow into the respective compartments is dependant on the osmotic pressure within the compartment. The ultimate goal of water is to attain osmotic equilibrium.
Osmotic pressure is measured in osmoles (osm) or milliosmoles (mOsm). To calculate osmolality the following equation is used:
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The body tries to maintain the osmolality of the ECF and ICF at 290–310 mOsm and any change in the compartments will trigger movement of water across the semipermeable membrane to equalize the osmolalities. The usual travel of water is from a compartment with a low osmolality to a compartment with a relatively higher mOsm. As the calculation above implies that sodium is a major determinant of osmolality, one can say that net movement of water will usually be governed by changes in the concentration of sodium. This theory can be applied clinically when advising patients with hypertension (high intravascular volume) to reduce their salt intake.
ELECTROLYTE DISTURBANCES
Hyponatremia
A low sodium level is usually caused by either depletion of extracellular sodium or excessive dilution.1 The extracellular volume status is helpful in identifying the cause. In post-operative patients, hyponatremia is commonly a result of over-administration of fluid therapy or a physiological production of ADH as a result of intravascular volume depletion. Figure 1.1 summarizes the causes of a low sodium level.
Symptoms
- Headache, confusion, seizures
- Weakness, fatigue, lethargy
- Vomiting, diarrhea, salivation.
Signs
- Signs of raised intracranial pressure, altered deep tendon reflexes
- Oliguria
- Hypertension, bradycardia in severe cases.
- Coma.
Management
- If the patient is hypovolemic due to extrarenal losses, then slow correction Na with isotonic fluids is indicated. It is pertinent that Na levels are corrected slowly as rapid correction may result in permanent demyelination syndrome.2
- Over administration of sodium free fluids to post-operative patients is a common cause for hyponatremia, therefore, it is pertinent to review the amount and type of fluid input. Normal saline should be used in these situations. Hypertonic saline is rarely used as it can cause circulatory overload.
- Omit any drugs that may cause a low Na temporarily such as diuretics, proton pump inhibitors, ACE inhibitors.
- If the patient is euvolemic, SIADH should be considered. Note that an increase in ADH secretion postoperatively can be a normal physiological response and is a common cause for hyponatremia in these patients. However, SIADH should be considered. Management includes diagnosis via urinary Na and paired osmolalities of urine and serum and fluid restriction. It is also important to investigate and treat the underlying cause of SIADH.
Hypernatremia (Fig. 1.2)
As in hyponatremia, a high sodium level can be subdivided by the extracellular volume status. Commonly a high sodium level is usually a result of dehydration and low extracellular volume.
Symptoms
- Lethargy, thirst, weakness
- Restlessness
- Fever
- In severe cases altered conscious level
- Note that symptoms rare unless Na more than 160 mEq/l.
Signs
- Evidence of dry mucous membranes and dehydration
- Oliguria or increased urine output
- Fever, tachycardia
- Signs of Cushing's disease such as buffalo hump, centripetal obesity, moon face
- Evidence of CAH may include ambiguous genitalia.
Management
- Assess fluid volume status as mentioned previously.
- Monitor fluid input/output chart with daily weights.
- If hypovolemic, the most likely cause is dehydration due to extrarenal losses especially in patients postoperatively. Management involves fluid replacement with isotonic solutions and slow correction of Na to avoid cerebral edema.
- Certain medications can cause hypernatremia such as antacids with sodium bicarbonate, antibiotics such as ticarcillin, salt tablets, intravenous hypertonic saline and should be discontinued.
- If the patient is alert the consider restricting dietary sodium intake temporarily.
- If the above measure fail to correct the Na level one must consider other rare causes such as Cushing's disease, diabetes insipidus and underlying renal disorders.
Hyperkalemia
High potassium level is defined as a value above 5 mEq/L. Severe hyperkalemia is defined as any level above 7 mEq/L. The causes are summarized in Figure 1.3 but usually involves a physiological change of increased absorption, impaired excretion or excessive release from cells.2 A high potassium level with ECG changes is a medical emergency and should be treated promptly.
Symptoms
- Mild symptoms include diarrhea, lethargy, nausea and vomiting
- Weakness and paralysis may ensue
- Severe life-threatening symptoms may include chest pain, palpitations, altered conscious level.
ECG Findings
- Flattened P waves
- Prolonged PR interval
- Peaked tented T waves
- Widened QRS complexes
- Sine wave formation
- Arrhythmia such as ventricular fibrillation.
Management
High potassium can be life-threatening but easily correctable and there, at a cellular level, the main goal is to drive the extracellular potassium within the cells to protect cardiac conduction cells from the effects of a raised potassium level.
- If there are ECG changes or in acute severe cases of hyperkalemia, administration of calcium gluconate 10 ml (10%) is required. While administering this drug cardiac monitoring is needed and should be discontinued if bradycardia develops.
- The administration of insulin sliding scale with dextrose will drive the potassium into cells tem porarily (lasts approximately 4 hours).
- In acute situations nebulized salbutamol can also assist in shifting potassium.
- Calcium resins are used to reduce GI absorption of potassium. This is usually given at a 15 g dose orally three times a day but preparations and route vary.
- Treat the underlying cause to prevent recurrent hyperkalemia.
- Bicarbonate can be used in resistant cases with associated metabolic acidosis as high H+ ions causes a shift of potassium to the extracellular compartment.3
- Renal dialysis is usually considered when all medical therapies have been exhausted.
- Once the patient is stabilized assess the medication history and discontinue drugs that may precipitate hyperkalemia. These include potassium sparing diuretics, oral potassium tablets, ACE inhibitors and any other drugs that would precipitate renal failure.
- Ensure that a low potassium diet is encouraged until the potassium is in normal range.
Hypokalemia (Fig. 1.4)
Symptoms/Signs
- Fatigue, lethargy, anorexia
- Leg cramps
- Constipation
- Weakness, hyporeflexia and paresthesia
- Ileus.
ECG Findings
- U waves
- Flattened T wave
- ST segment changes
- Arrhythmias and eventually cardiac arrest
Management
- A potassium level below 3 mEq/L potassium replacement should be administered at 20–30 mEq/L with ECG monitoring in severe hypokalemia.
- Potassium levels 3 to 3.5 mEq/L can be replaced orally or intravenous.
- Some patients may be resistant to potassium replacement and in these patients, magnesium levels must be checked as they often co-exist. It will be difficult to correct low potassium if the magnesium level is not corrected first.4
- It is also pertinent to omit any drugs that may aid the depletion of potassium temporarily.
- In postsurgical patients, fluid administration must include potassium especially in those who are kept nil by mouth, on insulin sliding scale and stoma patients.
Hypermagnesemia (Fig. 1.5)
- High magnesium levels are rarely seen in surgical patients unless they are known to have renal disease. In these patients, magnesium levels should be monitored closely. Any medications that may increase serum levels such as Mg containing antacids and laxatives should be avoided.
- Symptoms and ECG changes resemble those in hyperkalemia. Symptoms and signs ensue at a level above 6 mEq/L whereas at a level above 10 mEq/L can be fatal.
- Management includes fluid replacement with isotonic saline administration to enhance renal excretion. This management may be ineffective in patients with severe renal failure who would require dialysis.
Hypomagnesemia
Symptoms/Signs
- Tremors
- Delirium/confusion
- Seizures
- Hyperactive tendon reflexes
- Positive Chvostek's sign.
ECG Findings
- Prolonged QT and PR intervals
- ST segment depression
- Flattening or inversion of P waves
- Torsades de pointes
- Arrhythmias.
Management
- Magnesium depletion is a common problem amongst in-patients and those in the critical care units.5
- Magnesium replacements usually come in two preparations. These include sulfates and chlorides.
- Moderately low magnesium levels can be replaced by oral therapy.
- In more severe deficits parenteral replacement is appropriate and should be done cautiously to avoid over-replacement especially in patients with renal failure.
- It is useful to know that hypomagnesemia can occur along with a low potassium and calcium levels and therefore these electrolytes should corrected.
Calcium Homeostasis
- Calcium plays an important role in the neuromuscular function and at a cellular level. The majority of the calcium is stored in the skeletal system with only 1 percent in the extracellular fluid.
- Calcium is distributed as three forms: Ionized (40%), albumin-bound (50%) and anion-bound (10%).The serum calcium concentration (4.2-5.2 mEq/L) is regulated by three hormones chiefly vitamin D, parathyroid hormone and calcitonin. These hormones have direct and indirect effects on three major organ systems as shown in Figure 1.6.
- The acid-base balance also alters the calcium concentration. Acidosis increases the serum calcium concentration as it reduces the protein binding whereas low serum calcium is seen in alkalosis.
- The ionized calcium concentration is important in the postoperative surgical patient especially post-parathyroidectomy patients.6The disturbance, although transient can cause clinical signs and symptoms that would require correction.
- Figure 1.7 lists some of the important causes of calcium abnormalities.
Hypocalcemia
- Clinical manifestations include lethargy, abdominal and muscle cramps, carpopedal spasm and in severe cases convulsions are also seen.
- Important clinical signs to elicit are exaggerated tendon reflexes, Chvostek's sign (spasm on tapping the facial nerve) and Trousseau's sign (spasm resulting from a blood pressure cuff applied to the upper limb).
- QT interval prolongation and T wave inversion are seen on the ECG. In severe cases conduction blocks and arrhythmias are seen.
- Management initially involves investigating and correcting pH abnormalities. In patients with an acute transient low calcium level, intravenous calcium gluconate or chloride can be given while monitoring the ECG. In patients with chronic low calcium, oral vitamin D and calcium supplements can be given.
- Malignancies associated with increase osteoclastic activity can result in hypocalcemia as a direct result of increased bone formation.7
Hypercalcemia
- Clinical symptoms include fatigue, muscle weakness, depression, abdominal pains, constipation and nausea, and symptoms of renal calculi.
- Severe hypocalcemia (level above 12 mg/dL) is a medical emergency as it can cause coma and death.
- ECG abnormalities include shortened QT interval, prolonged PR and QRS, flattened T waves and in severe cases conduction blocks and cardiac arrest.
- Malignancy and parathyroid abnormalities account for the majority of symptomatic hypocalcemia.6
- Treatment initially involves aggressive fluid replacement to enhance the excretion. If this is ineffective then furosemide, IV pamidronate and IV sodium sulfate are methods of reducing serum calcium. Management depends on the protocols within the local trust/hospitals.
- Corticosteroids can be used in patients where the cause is sarcoidosis, vitamin D intoxication or Addison's disease.
- Plicamycin can be used in metastatic disease.
- Hemodialysis may be needed if there is refractory hypocalcemia or in renal failure patients with impaired excretion.
METABOLIC DISTURBANCES
Metabolic Acidosis
A metabolic acidosis is defined as a disturbance in the acid-base homeostasis resulting in acidosis. This can be due to overproduction of hydrogen ions, increased intake of acids or an increased loss of bicarbonate ions. The physiological response is to counteract this and restore homeostasis. This is done by the following methods:7
- Hyperventilation in order to remove more CO2 (Kussmaul respirations)
- Increased production/reabsorption of bicarbonate ions via kidneys
- Increase the secretion of hydrogen ions.
A lot can be determined by working out the anion gap in these patients. In normal individuals there is an anion gap of less than 12 mmol/l and is usually due albumin and the gap must be adjusted accordingly.8 Any value above this represents unmeasured ions which would be due to ingestion or generation within the body. The formula involves subtracting cations from anions:
Causes of a High Anion Gap Acidosis
- Lactic acidosis
- Diabetic ketoacidosis
- Ingestion of acids, e.g. methanol, ethylene glycol
- Salicylate poisoning
- Organic acid production in renal failure.
Causes of Normal Anion Gap Acidosis
- Loss of bicarbonate ions via kidneys, GI tract or fistulae
- Medications such as acetazolamide
- Renal tubular acidosis.
Of these causes lactic acidosis and GI tract losses post-surgery are the commonest causes. Lactic acidosis develops as result of reduce tissue perfusion resulting in the production of lactic acid which can be corrected once perfusion is restored. GI tract losses are above the normal insensible losses that occur in the body and bicarbonate ions are lost. The body maintains the anion gap by restoring chloride ions.
Metabolic Alkalosis (Fig. 1.8)
Metabolic alkalosis is a common problem amongst surgical patients as many of them are volume deplete postoperatively. In order to correct the metabolic alkalosis it is pertinent to fluid resuscitate these patients with normal saline and adequately replace potassium via KCL solutions as these patients are also chloride deplete. This will negate the need for the kidneys to reabsorb bicarbonate and will allow acid-base homeostasis.
Respiratory Alkalosis
Hyperventilation and loss of CO2 from the alveoli is the physiological phenomenon that results in respiratory alkalosis. It results in a high pO2, low pCO2 with or without metabolic compensation. This pattern of breathing can be seen in the following clinical scenarios:
- Pain, anxiety
- Early stages of septicemia
- Neurological disorders like head trauma, meningitis
- Medications such as salicylates
- Hypoxia
- Thyrotoxicosis.
Hyperventilation causes electrolyte shift into cells primarily potassium and enhances binding of calcium to albumin resulting in symptomatic hypocalcemia and hypokalemia. Treatment generally involves correcting the underlying cause.9
Respiratory Acidosis
Any illness that will cause the patient to hypoventilate will result in respiratory acidosis. This can be diagnosed by a high pCO2, low pO2 with or without metabolic compensation. The list below summarizes some of the causes:
- Lung related: Effusion, atelectasis, pneumonia, mucus plug, COPD exacerbation
- Postoperative pain: Intra-abdominal or thoracic preventing optimal lung expansion
- CNS pathology
- Abdominal distension/compartment syndrome.
Treatment involves correcting the underlying problem and optimizing lung expansion if possible. If medical therapy fails to recover the acidosis then invasive ventilation should be considered in the context of the clinical case.8
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Types of Parenteral Solutions (Table 1.4)
There are a number of different parenteral solutions used in practice. Ringer lactate and normal saline are isotonic solutions and are usually used to replace insensible losses. It is, however, important to bear a few points in mind when considering the type of fluid replacement:
- The volume deficit
- The electrolyte abnormality present postoperatively
- Any potassium deficit
- Replacement of any ongoing insensible loss.
Hypertonic solutions are reserved only in situations where there is severe hyponatremia. Care must be taken to correct Na level slowly in order to prevent cerebral pontine myelinolysis.
Hypertonic saline solutions have been used in closed head injuries as it has shown to increase the cerebral perfusion, reduce cerebral edema and improve the overall outcome.9-11 This is not the case for trauma patients as hypertonic saline solutions have not shown to be more beneficial than isotonic solutions.12
The other subset of parenteral therapy is colloids and this includes albumin, gelatins and dextrans. These are primarily used to expand intravascular volume in post-operative shock. Albumin is derived from blood hence it can cause allergic reactions and it has been shown in studies that it may cause renal and pulmonary failure when used during hemorrhagic shock.13, 14 Gelatins are derived from bovine collagen whereas dextrans are produced by bacteria grown on sucrose media. Both are volume expanders but dextrans are now only used to reduce plasma viscosity.
SPECIAL CONSIDERATIONS
Burns
Burns involve damage to the epidermis, dermis or the subcutaneous tissue causing permanent disfigurement, pain and electrolyte imbalance. The severity depends on the cause, degree, body parts affected and the presence/absence of inhalation injury.15 Patient's age and co-morbidities can also influence the severity. There are four essential features in managing patients with thermal injury. These are prevention of burn shock by adequate fluid resuscitation, adequate ventilation, removal of necrotic tissue with wound closure and metabolic support. In this section we will concentrate on the fluid resuscitation needs.
Fluid resuscitation is a crucial step in managing a patient with thermal injury and an adequate fluid administration without causing overload can be difficult at times as these patients have burn associated edema which can be mistaken for overload to the inexperienced clinician. The physiological mechanism of adequate intravascular volume allowing optimal tissue perfusion can be disturbed in these patients.16, 17 Many texts describe urine output as the sole sensitive indicator in determining tissue perfusion. Lab studies have shown that kidneys are the first organs to experience hypoperfusion.18 Therefore, renal function and urine output are useful indicators in assessing organ perfusion. The extent of burns is determined by the rule of nines where body parts injured are expressed as a percentage (Fig. 1.9), with 9% for each limb, 9% for the head and neck and the remaining divided equally between the front and back of the body.
There are a number of resuscitation fluid formulae but the commonly used regime is the modified Brooke formula.19
Figure 1.10 summarizes the management.
The electrolyte abnormalities in burn injury patients occur in phases which are categorized as below:21-23
- Fluid accumulation phase: This occurs within 36 hours of the injury and causes fluid shift from the vascular compartment to the interstitial space causing high potassium, hyponatremia, hypovolemia, hypocalcemia and metabolic acidosis.
- Recovery phase: May cause further electrolyte disturbance due to inadequate dietary intake or enteral feeding.
Burns patients are prone to infected wounds, pulmonary edema, airway compromise and gastrointestinal complications such as Cushing's ulcer and paralytic ileus. Therefore, apart from correcting electrolyte abnormalities, one must undertake a thorough clinical assessment and manage any associated complications.
GASTRIC OUTLET OBSTRUCTION (GOO)
Gastric outlet obstruction is a pathological obstruction of the free flow of gastric contents into the duodenum. The causes include peptic ulcer disease, tumor, polyps, pyloric stenosis, or any extrinsic compression such as pseudocysts, gallstones.
Nausea and projectile vomiting are cardinal features of this surgical presentation. There may be associated abdominal pain. The characteristic electrolyte abnormalities include:
- Increased urea and creatinine levels
- Low potassium which may be severe
- Hypochloremic metabolic alkalosis due to acid (HCl) loss from the stomach.
Definitive treatment involves correcting the underlying cause for GOO; however, in the interim the electrolyte abnormalities must be corrected.
Biliary Fistula
Biliary fistulae are any abnormal communication with the bile duct system. They are usually internal as communication with the abdominal wall is rare. The fistulae are the result of chronic inflammation, adhesions and erosions of the visceral surfaces. This communication is usually with the gastrointestinal tract and is usually caused by gallstones,24 but can be due to bile duct malignancy, chronic cholecystitis and inflammatory bowel disease.25, 2610
Patients with this fistula present with abdominal pain, nausea, dyspepsia, steatorrhea and rarely gallstone ileus. Frequently they can cause electrolyte abnormalities. These include:
- Hyponatremia which can be profound in external biliary fistulae
- Hypokalemia
- Hypomagnesemia
- Malabsorption of fat soluble vitamins.
Colonic Diarrhea
Diarrhea is a change in bowel habit to become more loose and/or an increased frequency. It is also defined as stool weight in excess of 200 g/day and having more than 3 bowels movements a day. It is a common problem and its causes are vast. Diarrhea can be of acute or chronic in nature and is divided into the following types (with a few examples):
| - | Bacterial, viral and protozoal |
| - | Autoimmune, radiation and micro-scopic colitis |
| - | Colorectal, pancreatic and VIPoma |
| - | Thyrotoxicosis, carcinoid syndrome |
| - | Antibiotics, laxatives. Many other drugs have diarrhea as a side effect |
| - | Coeliac disease, Whipple's disease and tropical sprue. |
Diarrhea results in a number of electrolyte disturbances along with dehydration if the total output exceeds the total fluid intake. This results in the following electrolye disturbances:
- Hypokalemia
- Hyponatremia27
- Metabolic acidosis due to bicarbonate loss.
These are the major electrolyte abnormalities and replacement of the electrolytes should be prioritized by the severity of the disturbance and its effect on the body. Associated electrolytes such as magnesium levels can also be affected and therefore, it is pertinent to check and correct these.
Liver Cirrhosis
Cirrhosis is a histological change of normal liver tissue into fibrosed nodular liver as a result of chronic irreparable liver injury. There are a number of causes to chronic liver disease, however, alcohol and viral hepatitis are the leading causes worldwide.
Symptoms can develop and are usually a result of impaired hepatic synthetic function. This includes coagulopathy, hepatic encephalopathy and variceal bleeding. Cirrhosis is a major problem worldwide and with scarcity of transplants, many of them have recurrent admissions with complications of their illness. One of the factors that warrant medical review is electrolyte disturbance. The electrolyte disturbances are summarized during cirrhosis phase and post-liver transplant phase.
- Cirrhosis phase: Cirrhosis impairs the normal synthetic function of the liver resulting in a scarcity of albumin in turn resulting in a reduced oncotic intravascular pressure. This causes fluid shift into the extravascular space resulting in ascites, peripheral edema. These patients have a number of electrolyte abnormalities resulting from the disease as well as the diuretic therapy:
- Diuretic related hyponatremia, hyper/hypokalemia, renal impairment, hypomagnesemia and hypocalcemia.
- Hepatorenal syndrome causing renal impairment and refractory hyponatremia. Definitive treatment usually involved transplantation. Transjugular intrahepatic portosystemic shunting can be used (TIPS).
- Raised ammonia levels resulting in hepatic encephalopathy. This is precipitated by infection, constipation, medications, variceal bleeding, renal failure and a high protein diet.
- Other abnormalities include uremia and hypoglycemia.
- Liver transplantation phase: One must fulfill strict criteria in order to be eligible for a liver transplantation. Once eligible the workup for transplantation involves minimizing any perioperative and postoperative complications. A number of electrolyte disturbances can occur some of which are summarized below:
- Calcium: Hypocalcemia is evident preoperative however, severe hypocalcemia is evident postoperatively as the new liver metabolizes citrate, massive blood transfusion during transplant releases citrate. This is transient (36-48 hours) and should be treated with intravenous fluid replacement.
- Potassium: Hypokalemia is common preoperatively but immediately post-op the potassium level rises due to reperfusion, this however is transient (10 minutes). Later on hypokalemia may be a feature due to bile, ascitic and nasogastric drainage loss.
- Magnesium: Low magnesium is a feature throughout pre- and post-liver transplantation phases. Cyclosporin given postoperatively further increases renal magnesium loss.
- Sodium: Hypernatremia is a feature intra- and post-operatively as blood products are frequently administered. Overzealous correction of this can cause neurological signs also known as central pontine myelinolysis.
- Phosphate: Low phosphate levels are a feature post-operatively due to fluid administration, cyclosporine administration, carbohydrate administration.
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