Version May 2024
INTRODUCTION — Postoperative surgery patients are prone to electrolyte derangements related to the loss of blood and bodily fluids, the stress response to surgery, intravenous fluid administration, blood transfusion, and the underlying surgical disease.
The etiology, evaluation, and management of common electrolyte abnormalities following surgery are reviewed here. The estimation of fluid losses and correction of fluid volume deficits following surgery are discussed separately. (See "Overview of postoperative fluid therapy in adults".)
ETIOLOGIES OF POSTOPERATIVE ELECTROLYTE ABNORMALITIES
Fluid therapy — Electrolyte abnormalities observed in the postoperative period often result from the administration of intravenous fluids, fluid shifts, transfusion, and parenteral nutrition support. (See "Overview of postoperative fluid therapy in adults" and "Perioperative blood management: Strategies to minimize transfusions" and "Postoperative parenteral nutrition in adults".)
Crystalloid fluids — A variety of crystalloids are used in fluid resuscitation after surgery, including 0.9% sodium chloride, Lactated Ringer's (LR) solution, and balanced salt solutions such as Plasma-Lyte (table 1).
●Although the sodium concentration of 0.9% sodium chloride (154 mEq/L) is higher than the normal plasma sodium concentration, it equals the sodium concentration of the aqueous phase of plasma, which is the phase that is in osmotic equilibrium with the rest of body fluids. However, the chloride concentration of 0.9% sodium chloride is much higher than that of plasma because the solution contains no bicarbonate.
●The sodium concentration of LR (130 mEq/L) is lower than that of blood. LR also contains potassium, calcium, and lactate, a buffer that is metabolized by the liver to bicarbonate.
●The concentration of sodium in balanced salt solutions (eg, Plasma-Lyte, Normosol) is equivalent to that of blood. For example, Plasma-Lyte's sodium concentration is 140 mEq/L. Plasma-Lyte also contains potassium and magnesium, as well as acetate, a buffer that is converted to bicarbonate independent of the liver.
Depending upon the solution chosen, recipients of a large volume of intravenous crystalloid fluid may develop hyperchloremic metabolic acidosis and dilutional electrolyte deficiency (ie, hyponatremia, hypocalcemia, hypomagnesemia, hypokalemia).
●Hyperchloremia – Large volume 0.9% sodium chloride resuscitation generates a hyperchloremic metabolic acidosis and renal vasoconstriction, both of which contribute to unpredictable water retention and electrolyte derangement [1]. In many cases, acidosis can be avoided with the use of a solution containing less chloride than 0.9% sodium chloride, such as LR or Plasma-Lyte. However, balanced salt solutions are more expensive than LR, and LR has a subphysiologic sodium concentration (130 mEq/L), which may result in hyponatremia when given in excess. (See "Overview of postoperative fluid therapy in adults".)
●Hyponatremia – During and after surgery, surgical stress results in the release of antidiuretic hormone (ADH; ie, vasopressin). ADH acts in the kidney to retain water [2]. In normovolemic postsurgical patients, the administration of additional sodium (ie, 0.9% sodium chloride) can result in a paradoxical fall in sodium concentration because the sodium contained in these solutions is excreted in the urine, resulting in net retention of electrolyte-free water. As a result, hyponatremia is commonly observed in postsurgical patients. It can also occur if too much LR or a balanced salt solution is administered [3].
Mild postoperative hyponatremia generally resolves without specific intervention [1,2,4]. As the stress response dissipates and ADH secretion is suppressed by the low serum sodium concentration, the excess free water is excreted in the urine. If the serum sodium does fall below normal, the administered intravenous fluid should be changed to one with a higher sodium concentration (eg, from LR to 0.9% sodium chloride) to avoid worsening hyponatremia and its complications. (See "Overview of postoperative fluid therapy in adults" and "General principles of disorders of water balance (hyponatremia and hypernatremia) and sodium balance (hypovolemia and edema)".)
However, moderate or severe hyponatremia can occur. It is particularly common and worrisome in patients with brain injury (see 'Brain injury' below), but it has also been reported after minor elective surgical procedures [5]. In most cases, postoperative patients with hyponatremia related to the administration of hypotonic fluids will respond to isotonic or hypertonic fluids without event. In one review, the prevalence of hyponatremia <130 mmol/L during the first postoperative week was 4.4 percent (48 of 1088 patients) [6]. Most patients (94 percent) were receiving hypotonic fluids (eg, hypotonic sodium chloride or dextrose infusion); however, none of the patients had significant neurologic deterioration. Although uncommon, seizures and even fatal cerebral edema have been reported in postoperative patients [3,7]. If the serum sodium concentration rapidly falls below 130 mEq/L (eg, in the first 24 hours after surgery) and the patient has symptoms that might be attributable to the acute hyponatremia, the electrolyte disturbance should be evaluated and emergently treated. (See "Overview of the treatment of hyponatremia in adults".)
●Hypokalemia – In addition to ADH release in response to surgical stress, aldosterone is released in response to hypotension or hypovolemia (figure 1). It acts in the kidney to retain sodium and waste potassium. The degree of this hormonal response for a particular patient or type of surgery is highly variable, as is the degree of associated electrolyte derangement. Although intravascular volume is restored, potassium levels are unpredictably affected [2]. This process is compounded by the administration of supernormal sodium doses with intravenous fluid therapy during and after surgery [8]. (See "Causes of hypokalemia in adults".)
●Hypomagnesemia – Part of the stress response to surgery includes the release of aldosterone, which contributes to magnesium wasting in the kidney [9]. For the reasons discussed below, magnesium is repleted more aggressively in surgery patients. (See 'Amount' below.)
Transfusion — The effects of transfusion on the development of postoperative electrolyte abnormalities depend upon the amount given, the clinical status of the patient, the temperature of the blood when it is transfused, and the duration of blood storage [10-13]. Hyperkalemia may be observed after the transfusion of red blood cells. As stored red blood cells age, they lyse, leaking potassium into the extracellular fluid. In this way, older banked blood tends to contain more extracellular potassium. When citrate, a red blood cell additive, is administered, it may result in the chelation of serum electrolytes, resulting in hypokalemia, hypocalcemia, or hypomagnesemia [14-16]. Banked red blood cells exist in an anaerobic environment, leading to the production and accumulation of lactic acid. The transfusion of red blood cells provides an acid load of approximately 15 mEq per unit, the sum of the citric acid anticoagulant and red blood cell lactic acid production [10]. In the normal individual, the acid load of banked blood can be adequately accommodated by metabolic and respiratory mechanisms. However, when red blood cells are transfused rapidly or in a large volume, profound electrolyte derangement is often observed in conjunction with acid-base disorder. This is further exacerbated when the product is not warm. (See "Massive blood transfusion", section on 'Complications' and "Practical aspects of red blood cell transfusion in adults: Storage, processing, modifications, and infusion", section on 'Potential adverse effects of transfusion'.)
To a lesser extent, this also applies to autologous blood transfusion, which may be used during resuscitation in the trauma bay, intensive care unit, or operating room. Rapidly lost blood is collected, washed, and returned to the patient promptly. The washing process reduces the potassium and lactate content in the sample [17]. Conditioning older banked blood using similar autotransfusion technology has also been shown to decrease its potassium and lactate content [18,19]. (See "Surgical blood conservation: Intraoperative blood salvage".)
Related to parenteral nutrition or prescription error — Iatrogenic electrolyte derangement may result from errors in parenteral nutrition prescription, intravenous fluid prescription, or electrolyte replacement therapy (eg, potassium content). (See "Postoperative parenteral nutrition in adults", section on 'Prescription'.)
Fluid loss — Surgical diseases that result in abnormal bodily fluid losses can result in electrolyte disturbances.
Third-spacing fluid loss — Following surgery, approximately two-thirds of administered intravenous fluid extravasates into the extravascular space. This process is informally known as "third spacing" into the soft tissues, peritoneal cavity, or pleural cavity. As the patient recovers, the capillary leak resolves, and the fluid returns to the vascular space. Electrolyte deficits (hypokalemia, hypomagnesemia, hypocalcemia, hypophosphatemia) tend to follow this process in an unpredictable manner. (See "Overview of postoperative fluid therapy in adults", section on 'Third-spacing'.)
Gastrointestinal loss — The compositions of various bodily fluids are given in the table (table 2). Loss of a sufficient volume of fluid that is not adequately replaced can lead to electrolyte abnormalities. (See "Overview of postoperative fluid therapy in adults", section on 'Fluid resuscitation'.)
Postoperative ileus or intestinal obstruction is commonly observed in surgical patients and may lead to vomiting that requires nasogastric drainage. The loss of a large volume of gastric fluid, which contains hydrochloric acid, can lead to intravascular volume contraction, metabolic alkalosis, hypochloremia, and hypokalemia. The loss of fluid volume stimulates aldosterone production, which promotes water retention and potassium wasting in the kidney. To produce more acid, the stomach pumps additional bicarbonate into the serum. This excess bicarbonate is excreted in the urine as an unabsorbed anion that obligates excretion of potassium to maintain electrolyte neutrality.
The pancreas generates a bicarbonate-rich fluid. When pancreatic fluid is lost externally, as with a pancreatico-cutaneous fistula following pancreatic injury (accidental or surgical), it generates a metabolic acidosis as well as secondary derangements in potassium.
High-volume diarrhea, ostomy output, or enterocutaneous fistula drainage leads to unpredictable electrolyte derangements, including hypokalemia and hypomagnesemia.
Urinary loss — As the patient recovers from surgery, fluid returns to the vascular space and is evacuated by the kidneys. The mobilization of third-space fluid results in large-volume auto-diuresis, which is associated with potassium and magnesium wasting. Although there is no firm relationship that describes the volume of urine and expected level of electrolyte derangement, it is the author's experience that urinary outputs that exceed 30mL/kg/day during auto-diuresis are typically associated with deficits of potassium, magnesium, or phosphorus. When auto-diuresis is associated with recovering renal dysfunction, such as that which resulted from an obstructing kidney stone or hypovolemia-induced acute kidney injury following hemorrhage, this electrolyte wasting can be exaggerated.
Brain injury (accidental or surgical) can lead to arginine vasopressin deficiency (AVP-D), formerly called central diabetes insipidus (DI), syndrome of inappropriate ADH (SIADH), and cerebral salt wasting, which are associated with electrolyte derangements. In AVP-D, uncontrolled water loss leads to hypernatremia. In SIADH and cerebral salt wasting, hyponatremia may result [20]. Hyponatremia in head-injured patients can be highly problematic as it contributes to cerebral edema. Hypotonic fluids should not be administered to head injury or neurosurgery patients at risk for cerebral edema. In some cases, hypertonic 3% sodium chloride and vasopressin receptor antagonists are needed to manage SIADH-associated hyponatremia in head injury patients [21]. (See "Treatment of hyponatremia: Syndrome of inappropriate antidiuretic hormone secretion (SIADH) and reset osmostat".)
Similarly, hyponatremia from disordered ADH production may be observed in liver failure patients awaiting transplantation. These patients have a higher risk of morbidity, mortality, and worse survival after transplantation. The management of hyponatremia of liver failure differs from that of head-injury-associated SIADH. (See "Acute liver failure in adults: Management and prognosis".)
Following renal transplantation, allograft recovery often includes a phase of uncontrolled diuresis during which hypokalemia and hypomagnesemia commonly occur. Similarly, when a native kidney obstruction is relieved (eg, laser lithotripsy for an obstructing ureteral stone), diuresis and electrolyte wasting may result.
Brain injury — Hyponatremia is more commonly observed in patients with traumatic or surgical brain trauma. In a study of neurosurgery patients, hyponatremia was observed in 10 and 50 percent of patients, depending on the underlying condition. Accidental and surgical trauma to the brain more commonly result in the production of ADH, which leads to inappropriate fluid retention and dilutional hyponatremia. (See "Pathophysiology and etiology of the syndrome of inappropriate antidiuretic hormone secretion (SIADH)" and "Treatment of hyponatremia: Syndrome of inappropriate antidiuretic hormone secretion (SIADH) and reset osmostat" and 'Urinary loss' above.)
Related to tissue injury/ischemia and reperfusion — Mechanical tissue destruction and ischemia-induced tissue injury can cause tissue necrosis and cell lysis. The resulting cell injury may lead to the release of intracellular potassium into the bloodstream, causing profound hyperkalemia. With muscle injury, myoglobin is released into the circulation and can be nephrotoxic, further impairing potassium excretion. Phosphate released from cells leads to hyperphosphatemia and may also lead to calcium scavenging and hypocalcemia. When associated with significant muscle injury, these electrolyte disturbances are referred to collectively as part of a syndrome termed rhabdomyolysis. (See "Rhabdomyolysis: Epidemiology and etiology" and "Rhabdomyolysis: Clinical manifestations and diagnosis".)
Creatine kinase (CK) is often used as a biochemical marker of muscle damage. In general, increases in CK less than five times the normal value are unlikely to cause significant electrolyte abnormalities. However, the degree of CK elevation used to define rhabdomyolysis remains controversial [22,23].
Surgical trauma (ie, planned muscle division) results in muscle injury. Surgical patients can also experience muscle compression injury if improperly positioned in the operating room or if subjected to a prolonged period of immobility [24]. Patient positioning may also promote muscle ischemia by interrupting anatomic blood flow (eg, stirrups) or by compression (eg, pressure from security belts when patient is rotated into a lateral position). Generally, positions maintained for under two hours are unlikely to cause significant injury. However, patient factors, particularly obesity, may contribute to increased pressure, thereby leading to unanticipated muscle injury during shorter procedures, which has been demonstrated in a number of surgical populations [25,26].
Extremity injury (eg, crushed injury, electrical shock, open femur fracture) commonly leads to muscle injury and some degree of rhabdomyolysis. When a patient with crush injury is released from a crushing object, reperfusion may result in rapid-onset hyperkalemia and acidosis. Extensive bone and muscle injury with severe extremity injury often results in compartment syndrome, which, when released, can lead to rhabdomyolysis-induced renal failure and metabolic derangements [27]. (See "Severe crush injury in adults" and "Crush-related acute kidney injury".)
Acute tissue ischemia, such as in cases of thromboembolism to an extremity, can result in extensive muscle ischemia prior to limb salvage surgery. In such cases, rhabdomyolysis and its associated electrolyte abnormalities are commonly observed [28]. Blood flow to an extremity may be purposefully interrupted with a tourniquet or clamp for short periods of time to prevent blood loss during a planned surgery (eg, arm tourniquet during carpal tunnel release). Release of the tourniquet/clamp can also be associated with reperfusion of ischemic tissue. However, in such controlled settings, it is uncommon for this to result in significant electrolyte abnormalities unless the ischemia time is longer than usual.
Ablative or embolic procedures, such as for liver tumors, also result in acute tissue ischemia. With tumor ablation, rarely, tumor lysis syndrome may be observed. Tumor lysis syndrome is well described in case reports in patients who undergo transarterial chemoembolization of large liver tumors, although "large" is not well defined. In these cases, hyperkalemia, hyperphosphatemia, and hypocalcemia may be observed [29]. (See "Tumor lysis syndrome: Prevention and treatment".)
Refeeding syndrome — Many surgical diseases are associated with preoperative malnutrition, including malignancies (eg, colon, lung, esophageal carcinoma), chronic organ dysfunction, and inflammatory conditions (eg, pancreatitis, colitis). As malnourished patients recover from surgery and resume dietary intake, they are at risk for refeeding syndrome, a collection of electrolyte derangements associated with a massive intracellular shift of electrolytes. Hypophosphatemia is commonly observed as extracellular phosphate is rapidly taken into the cells to generate adenosine triphosphate (ATP).
Hypokalemia and hypocalcemia are also commonly observed. Malnourished patients should be closely monitored for clinical and laboratory evidence of refeeding syndrome when their nutritional intake is resumed. (See "Anorexia nervosa in adults and adolescents: The refeeding syndrome" and "Postoperative parenteral nutrition in adults".)
Acid-base imbalance — Acute changes in serum pH are commonly observed in the postoperative surgical patient and result in electrolyte abnormalities, including (see "Simple and mixed acid-base disorders" and "Approach to the adult with metabolic acidosis" and "Causes of metabolic alkalosis"):
●Metabolic alkalosis – This commonly results from volume contraction combined with gastric fluid loss in the postoperative patient. The classic scenario is the patient with a bowel obstruction who undergoes laparotomy, during/after which aggressive third-spacing of fluid into the peritoneal cavity and intestinal lumen leads to volume contraction. Emesis and nasogastric tube decompression lead to further large-volume loss of hydrochloric acid (HCl). As the stomach produces more HCl to replace this loss, it delivers bicarbonate (HCO3-) into the serum. In this manner, volume contraction and HCl loss generate a hypochloremic hypokalemic metabolic alkalosis. There is a very small amount of potassium in gastric fluid that is directly lost during vomiting and gastric tube decompression as well.
●Metabolic acidosis – This may result from large-volume blood loss and under-resuscitation. The commonly observed scenario is the patient with hemorrhagic shock from large surgical blood loss, which leads to reduced end-organ perfusion and lactic acidosis. This generates a "gap" acidosis. Conversely, a patient who undergoes a large volume of 0.9% sodium chloride infusion may experience hyperchloremic acidosis associated with the large chloride load. This generates a "non-gap" acidosis. Both of these types of acidosis lead to hyperkalemia.
●Respiratory acidosis – The typical scenario is the postoperative patient who receives excessive narcotic pain medication, which results in narcotic-induced respiratory depression, hypoventilation, hypercapnia, and subsequent respiratory acidosis and hyperkalemia.
●Respiratory alkalosis – This may develop following thoracic surgery or upper abdominal surgery in the patient who experiences severe incisional pain. To limit the pain, the patient takes quick shallow breaths, which leads to hypocarbia, respiratory alkalosis, and hypokalemia.
In the acute setting, mild changes in serum pH are managed at the cellular level through Na-H exchange, Na-HCO3 cotransport, Na-organic anion cotransport, and Na-K-ATPase on cell membranes [8]. The shift of potassium into cells is due to altered Na-K-ATPase activity, which is influenced by a variety of factors that are related to the stress response to surgery, including aldosterone secretion and adrenergic stimulation [30]. (See "Simple and mixed acid-base disorders" and "Overview of postoperative fluid therapy in adults", section on 'Physiologic stress response to surgery'.)
In states of acid production (eg, lactic acidosis during hemorrhagic shock), we observe a rise in serum acid, a fall in serum pH, and hyperkalemia. Conversely, a drop in serum acid leads to hypokalemia, with H+ shifting out of cells and K+ shifting into cells. It is important to note that lactic acidosis does not directly cause a shift of potassium out of the cells, but the associated tissue ischemia and acute kidney injury often results in hyperkalemia [31]. (See "Potassium balance in acid-base disorders".)
Underlying surgical diseases and their treatment — Patients who undergo surgery for the treatment of certain surgical diseases are prone to electrolyte abnormalities before, during, and after surgery.
Examples include hypercalcemia associated with hyperparathyroidism, hypokalemia associated with an adrenal aldosteronoma, and hyponatremia associated with ADH production by lung cancer. Postoperatively, the opposite derangement is often observed. As examples, following parathyroidectomy, hypocalcemia and hungry bone syndrome can ensue; after resection of an aldosteronoma, hyperkalemia caused by atrophy of the unaffected adrenal gland can occur. Hyponatremia associated with an ADH-producing tumor is expected to resolve after tumor resection. (See "Hungry bone syndrome following parathyroidectomy in patients with end-stage kidney disease".)
In addition, many medical therapies that are administered to surgery patients cause electrolyte derangements. Examples include:
●Calcineurin inhibitors (eg, for solid-organ transplant recipients) cause hyperkalemia.
●Potassium-wasting diuretics (eg, for heart failure patients) cause hypokalemia.
●Laxatives and enemas (eg, for patients with postoperative constipation) result in hypokalemia and hyponatremia.
●Glucocorticoids (eg, treatment of Crohn colitis) result in hypokalemia [32].
●Heated intraperitoneal chemotherapy (HIPEC; eg, for peritoneal carcinomatosis) is associated with hyponatremia [33].
●Succinylcholine administration during surgery can lead to hyperkalemia [24], particularly in patients with renal failure or crush injury, in whom hyperkalemia may persist and can be life-threatening.
LABORATORY MONITORING — Postoperative surgical patients undergoing the following treatments should undergo electrolyte monitoring on a daily basis:
●Continuous intravenous fluid administration
●Blood transfusion
●Fluid resuscitation (eg, fluid boluses for hypovolemia)
●Major organ dysfunction (cardiac, renal, hepatic)
●Head injury (eg, traumatic brain injury, neurosurgery)
●Continuous bladder irrigation
●Abnormal bodily fluid losses (eg, large-volume pancreatic fistula, high-output ostomy, gastric tube evacuation therapy)
●Large surface area wounds (eg, burn)
●Rhabdomyolysis
●Ileus
●Pancreatitis
For adult patients who receive in excess of 50mL/kg/day of intravenous fluids and/or blood products per day, more frequent monitoring is advised (every 6 to 12 hours). Similarly, when correcting electrolyte deficiencies or excesses, frequent monitoring is often warranted to confirm resolution of the disorder. Typically, the rate of electrolyte replacement therapy is limited by safety protocols, such that serum electrolyte monitoring every six hours is usually sufficient. As an example, to replace a 40 mEq potassium deficit at 10 mEq/hour by the intravenous route, it will take at least four hours to complete the replacement.
There are many chemistry assays available for analyzing serum electrolytes. A complete chemistry report includes the normal values for reference, which vary from one assay to the next. As an example, a serum potassium of 5.3 mmol/L may be high or normal depending on the assay's reference range.
In assessing serum calcium in postoperative patients, the use of ionized serum calcium is more useful than total serum calcium. The total serum calcium concentration changes in parallel with the albumin concentration. For many surgical patients, their serum albumin does not accurately reflect their current state due to malnourishment around the time of surgery. Also, serum total calcium and albumin are prone to dilution in large-volume resuscitation. As such, measurement of the ionized serum calcium more accurately reflects the true serum calcium in the postoperative patient, though it is a more expensive test. (See "Relation between total and ionized serum calcium concentrations".)
Indications for ionized serum calcium measurement include hypoparathyroidism after parathyroid or thyroid surgery, sepsis, pancreatitis, arrhythmia, severe acid-base disturbance, renal replacement therapy, and administration of calcium-binding drugs or chemotherapeutics [34]. As an example, for patients with pancreatitis who demonstrate calcium sequestration and saponification, serial serum ionized calcium measurements may be required. (See "Relation between total and ionized serum calcium concentrations".)
TREATMENT
Electrolyte replacement — To avoid complications of electrolyte deficiency in the postoperative period (eg, ileus, arrhythmia, seizure), deficiencies in serum potassium, magnesium, phosphate, and calcium should be identified and treated before the onset of symptoms of deficiency. There is no standardized practice for electrolyte repletion that is universally accepted in postoperative patients. (See "Clinical manifestations and treatment of hypokalemia in adults" and "Hypomagnesemia: Evaluation and treatment" and "Treatment of hypocalcemia" and "Hypophosphatemia: Evaluation and treatment".)
For most cases of mild hyponatremia following surgery, use of intravenous (IV) fluid that delivers more sodium (eg, 0.9% sodium chloride instead of 0.45% sodium chloride or Lactated Ringer's [LR] solution) is effective in preventing complications of hyponatremia. As with the treatment of hyponatremia in medical patients, the serum sodium should be raised by no more than 8 mEq/L in a 24 hour period to avoid osmotic demyelination syndrome (ODS). The risk of ODS is greatest in patients with a serum sodium of 120 mEq/L or less whose serum sodium has been low for 48 hours or more. However, hyponatremia may be poorly tolerated in patients with head trauma or following neurosurgery, and correction by 4 to 6 mEq/L within a few hours may be necessary. (See 'Fluid therapy' above and "Overview of postoperative fluid therapy in adults" and "Overview of the treatment of hyponatremia in adults".)
Goal — The goal of electrolyte replacement in the postoperative surgical patient is normal serum electrolyte levels. Arbitrary goals are practiced widely and are often based upon anecdotal experience. For patients with ongoing losses, the author targets the middle of the normal range, to prevent complications of electrolyte deficiency.
Because commercial metabolic panel assays vary from one hospital to the next, leading to inconsistent "normal range" values, it is important for the clinician to be familiar with the normal range for their lab. There is no agreed-upon definition of what constitutes mild, moderate, or severe electrolyte deficiency. In general, if an electrolyte value falls within 25 percent of its normal value for a given lab, that would be considered a mild-to-moderate deficiency by the author. For levels falling more than 25 percent below the normal value, that would be considered a severe deficiency. Life-threatening complications of electrolyte deficiency are typically observed when electrolytes fall into the severe deficiency range.
As an example, if the normal range for serum potassium in your hospital is 3.5 to 4.5 mEq/L and the patient's level is 3.1 mEq/L during fluid resuscitation, the goal serum potassium should be 4 mEq/L, as the patient is expected to have a small amount of ongoing loss with further fluid resuscitation.
Route — Electrolyte deficiencies can be replaced using an enteral or intravenous route. One or the other route of administration may be more appropriate depending upon the clinical situation.
●Intravenous replacement – Severe electrolyte deficiencies should be treated intravenously to ensure rapid and complete drug absorption. Intravenous agents are preferred until gastrointestinal absorption can be established with a trial of enteral intake. Some replacement agents are absorbed poorly and will not reliably raise the serum level quickly (eg, magnesium).
●Enteral replacement – Patients who are able to tolerate enteral intake can take enteral replacements. Enteral medications can be administered orally or via a nasogastric or nasoenteral tube. They are usually less expensive and easier to administer, but they take longer to be fully absorbed.
•Enteral replacement occurs slowly. For patients with moderate-to-severe deficiency, employ intravenous replacement for a more rapid correction to avoid complications.
•It is important to ensure that the patient will absorb the medication. Patients with high-output fistulas, stomas, or those who have had bowel resection may not absorb oral medications normally. Similarly, patients who are vomiting should not receive enteral medications, which may cause further vomiting (eg, potassium) and may not be reliably absorbed.
•Each of the enteral replacement agents may be poorly tolerated in postoperative patients for the following reasons:
-Potassium – Nausea, vomiting, abdominal pain.
-Magnesium – Laxative-like effects, poor bioavailability.
-Calcium – Tastes like chalk, constipation, nausea.
-Phosphate – Typically a mix of sodium phosphate and potassium phosphate; nausea, vomiting, diarrhea, abdominal pain.
As examples of an appropriate route of administration in surgical patients:
•A patient recovering from parathyroid adenoma excision who is eating normally 24 hours after surgery can be expected to take calcium supplements orally to correct mild asymptomatic hypocalcemia.
•A patient who experiences a seizure due to severe hypomagnesemia after liver resection should receive intravenous magnesium sulfate because it is immediately effective. By comparison, enterally administered magnesium is poorly absorbed in the setting of postoperative ileus, and its bioavailability is poor.
Amount — The amount administered for replacement varies with the patient's size, volume status, renal function, and ongoing fluid losses.
For the adult patient weighing at least 50 kg with normal renal function and no active fluid/electrolyte loss:
●Potassium – Potassium chloride 20 mEq administered intravenously should raise the serum potassium by 0.1 to 0.2 mEq/L. As an example, if the laboratory's normal potassium is 3.5 to 4.5 mEq/L, and the patient's serum potassium is 3.2 mEq/L, the patient's level is within 25 percent of the normal range and would be categorized as mild. A replacement dose of potassium chloride targeting the middle of the normal range (4 mEq/L) would be 20 mEq for each 0.1 to 0.2 mEq/L below the goal. In this case, a total dose of 80 mEq of intravenous or enteral potassium chloride would sufficiently correct the potassium deficit. For patients with normal intestinal function, oral and intravenous potassium are bioequivalent.
To avoid potassium overdose, repeat the serum potassium level after the administration potassium prior to administering further potassium. To obtain an accurate level in the setting of enteral replacement, wait at least one hour after the dose is given to ensure complete absorption of the enteral dose prior to rechecking the serum potassium level. A common practice is to obtain a daily chemistry panel in the morning, which allows for the prescription and administration of potassium during the day. For mild derangements in the absence of ongoing loss, it is common to await the potassium level the following day before administering further potassium. For moderate-to-severe derangement or with ongoing loss, a more urgent result is warranted as further repletion is often needed.
●Magnesium – Hypomagnesemia needs to be corrected to facilitate normalization of hypokalemia and hypocalcemia. For this reason and the reasons described below, magnesium is repleted more aggressively in surgery patients:
•Magnesium reduces nausea, vomiting, and shivering after surgery, acting to relax muscle via the calcium channel effect.
•Magnesium sulfate also acts as an analgesic adjuvant in managing postoperative pain and has an anti-inflammatory effect [35,36]. Its analgesic property seems to be associated with the regulation of calcium influx into the cells or antagonism of N-methyl-D-aspartate (NMDA) receptors in the central nervous system.
•Magnesium contributes directly and indirectly to recovery from postoperative ileus. With reduced pain, patients use less opioid medication, which reduces opioid-related effects [37].
•In neurosurgery, magnesium is often used to help prevent seizure.
•In obstetrics and gynecology, magnesium is often used to help prevent eclampsia.
Due to the laxative effect of oral magnesium and its variable bioavailability, oral magnesium is not routinely used to replace magnesium deficiencies in surgical patients. For each 0.4 mg/dL below the target serum magnesium level, give magnesium sulfate 2 g (8 mmol) IV. For mild-to-moderate hypomagnesemia (level is within 25 percent of the normal value), an initial dose of 2 to 4 g (8 to 16 mmol) IV is typically used. For moderate-to-severe hypomagnesemia (level below 75 percent of normal level), a total dose of 4 to 8 g (16 to 32 mmol) IV may be needed. The dose should be reduced by 50 percent in patients with significant renal dysfunction [38]. Due to gradual redistribution of magnesium to tissue following intravenous administration, levels are not repeated until 8 to 12 hours or more after the dose. The regimen is repeated until the serum magnesium reaches the middle of the normal range.
A common practice is to obtain a daily magnesium level in the morning, which allows for the prescription and administration of magnesium during the day. For mild derangements in the absence of ongoing loss, it is common to await the magnesium level the following day before administering further magnesium. For moderate-to-severe derangement or with ongoing loss, a more urgent result is warranted as further repletion is often needed.
●Calcium – For each 0.15 mg/dL below the targeted ionized calcium level, administer 1 g (2.3 mmol) IV of calcium gluconate. We prefer measurement of ionized (ie, fraction unbound to plasma proteins) rather than total calcium (bound plus unbound) because it is a better indicator of functional calcium capacity in postoperative patients. In most cases, acute hypocalcemia is treated with intravenous therapy, and calcium gluconate is the preferred form for nonemergency replacement. For mild-to-moderate hypocalcemia (level is within 25 percent of the normal value), 1 or 2 grams (2.3 or 4.6 mmol) of IV calcium gluconate is typically given. The dose may be repeated after six hours based upon ionized calcium level.
For severe (level below 75 percent of normal) or symptomatic hypocalcemia, calcium chloride, which provides three times the amount of elemental calcium per gram (as compared with calcium gluconate), is preferred. An initial dose of 1 g IV calcium chloride (6.8 mmol) or calcium gluconate 3 g (6.9 mmol) is given initially for symptomatic hypocalcemia and repeated as necessary. Concentrated calcium solutions (especially calcium chloride) are extremely caustic to tissues and should be administered in a central vein to avoid tissue extravasation. If greater than 4 g (9.2 mmol) of calcium gluconate is administered, consider repeating the serum ionized calcium level before administering further replacement therapy.
Uncommonly, oral calcium is used in conjunction with intravenous calcium, such as in patients with hypocalcemia following parathyroidectomy; in such a case, standing oral calcium doses are titrated up slowly with as-needed doses of intravenous calcium until the serum calcium normalizes. These patients will often remain on calcium replacement therapy for a prolonged period of time, hence the oral route for therapy.
●Phosphate – For each 0.4 mg/dL below normal, give 15 mmol of phosphate IV. Sodium phosphate is preferred for intravenous phosphate administration. Potassium phosphate is an alternative, but it delivers 22 mEq potassium in a fixed ratio with each 15 mmol phosphate dose. For mild-to-moderate hypophosphatemia (level within 25 percent of normal), 15 mmol of sodium phosphate IV is typically given. In symptomatic or severe hypophosphatemia (level below 75 percent of normal), an initial dose of 30 mmol IV sodium phosphate is given. Phosphate homeostasis is dependent upon kidney function; for patients with significant renal impairment (creatinine clearance [CrCl] <30 mL/minute), the phosphate dose should be reduced by 50 percent or more [38]. For moderate-to-severe derangement or during monitoring for refeeding syndrome, the serum phosphate level should be repeated two to four hours after the intravenous dose is completed. Individuals at risk for developing severe hypophosphatemia and refeeding syndrome (eg, malnourishment, anorexia, alcohol use disorder) require very close monitoring (ie, check serum phosphate level every 6 to 12 hours).
For patients with normal gut function, oral phosphate replacement (typically a mix of potassium phosphate-sodium phosphate) dose should be approximately tripled to equal the intravenous dose. As an example, 15 mmol intravenous sodium phosphate may be converted to oral therapy as 16 mmol oral potassium phosphate-sodium phosphate administered for three doses. Bioavailability of enteral phosphate supplementation is variable, and it can cause diarrhea. Commonly used enteral phosphate supplements include 250 mg (equivalent to 8 mmol) of phosphate per tablet. (See "Hypophosphatemia: Evaluation and treatment".)
Rate — The rate of electrolyte replacement should match the rate of loss to prevent progression of a mild/asymptomatic deficiency to a severe or life-threatening situation. For this reason, acute deficits and moderate-to-severe deficits should be replaced quickly, usually by intravenous route, to avoid complications of electrolyte deficiency. Infusion rates are typically limited for safety reasons and vary slightly by institution:
●Potassium – Potassium chloride may be given through a peripheral intravenous catheter at a rate of 10 to 20 mEq/hour in a low concentration (ie, 10 mEq per 100 mL) to minimize the caustic effects of potassium infusion on peripheral veins (ie, chemical thrombophlebitis) and to avoid transient severe hyperkalemia that can have serious consequences. In many institutions, central venous potassium infusion is limited to 20 mEq/hour to avoid inadvertent hyperkalemia. In emergency situations, 40 mEq/hour may be given centrally or peripherally (eg, through multiple lines). Potassium chloride infusions are available premixed in a minimum of 50 mL of non-dextrose fluid. Conversely, as much as 80 mEq of liquid potassium chloride can be administered into the stomach at once, and it will be rapidly absorbed in most patients except those with abnormal gut function. Caution is advised as this large quantity of potassium may induce vomiting and is often poorly tolerated. Instead, divided enteral doses of 20 mEq may be given several hours apart and are often better tolerated. (See "Clinical manifestations and treatment of hypokalemia in adults".)
●Magnesium – Magnesium sulfate is typically used for intravenous replacement therapy; 2 g (8 mmol) is mixed in 50 to 100 mL of fluid and infused over 30 to 60 minutes through a peripheral or central venous catheter, except in emergencies. In emergencies (eg, severe or symptomatic hypomagnesemia), 2 to 4 g (8 to 16 mmol) of magnesium sulfate diluted in 10 to 50 mL of sodium chloride can be given intravenously over 2 to 15 minutes. For patients with significant renal impairment (nonemergency), a slower infusion rate (ie, ≤1 g/hour) has also been suggested to improve efficiency of replacement. (See "Hypomagnesemia: Evaluation and treatment".)
●Calcium – In mild-to-moderate hypocalcemia, calcium replacement is typically given as 1 or 2 g (2.3 or 4.6 mmol) of IV calcium gluconate mixed in 50 mL of fluid and infused over 30 or 60 minutes through a peripheral or central venous catheter. The dose may be repeated as needed based on ionized serum calcium level. In severe symptomatic hypocalcemia, 1 g (6.8 mmol) of calcium chloride or 3 g (6.9 mmol) of calcium gluconate diluted in 50 mL of fluid can be infused over 10 minutes to rapidly control symptoms; this dose is repeated as necessary. Avoid rapid intravenous bolus of calcium, which can result in acute respiratory depression and asystole. Concentrated calcium solutions (especially calcium chloride) are extremely caustic to tissues and should be administered in a central vein to avoid extravasation. Effective replacement of calcium in severe or symptomatic hypocalcemia may require administration of calcium as a continuous infusion following the initial IV dose(s). Details are provided separately. (See "Treatment of hypocalcemia".)
●Phosphate – Intravenous phosphate (in the form of sodium phosphate or potassium phosphate) is typically diluted in 250 mL of fluid and infused at a rate of 4 or 5 mmol/hour through a central or peripheral venous catheter. As an example, 30 mmol sodium phosphate may be administered intravenously over six hours. Slow infusion of phosphate is preferred to decrease the risk of injury due to calcium-phosphate precipitate, which can result in acute kidney failure. In patients with severe hypophosphatemia and normal renal function, a maximum rate of 7.5 mmol/hour has been used.
Oral phosphate replacement is typically given in three or four divided doses through the day. Consider repeating the phosphate level after administering 45 or 60 mmol of oral phosphate (eg, with morning labs). Note that oral phosphate supplements include variable amounts of sodium and potassium. One commonly available phosphate tablet preparation (K-Phos Neutral) delivers 13 mEq sodium and 1.1 mEq potassium in a fixed ratio with 8 mmol of phosphate. Additional detail on oral products is available in the potassium phosphate-sodium phosphate drug monograph included within UpToDate. (See "Hypophosphatemia: Evaluation and treatment".)
Electrolyte excess — In most cases, identification and treatment of the contributing disease will help to correct the excess. The treatment for electrolyte excess in surgical patients is similar to that of medical patients. However, surgical patients are often not candidates for enteral therapies as they recover from surgery. Factors known to aggravate the electrolyte excess should be avoided (eg, hyperkalemic patient should not receive LR solution, which contains potassium; hyperphosphatemic patients should take a renal diet that is low in phosphate content).
●Hyperkalemia and hypercalcemia – For surgical patients with acute kidney injury and severe hyperkalemia, enteral/rectal sodium polystyrene therapy may not be an option, and emergency dialysis may be the best treatment. (See "Treatment and prevention of hyperkalemia in adults" and "Treatment of hypercalcemia".)
●Hyperphosphatemia – In most cases, hyperphosphatemia in the postoperative surgical patient is related to rhabdomyolysis from accidental or surgical trauma. Less commonly, it is observed in tumor lysis syndrome as well as acute on chronic renal failure associated with surgical disease. Enteral phosphate binders may not be an option. However, acute hyperphosphatemia is rarely life-threatening; emergency dialysis is not usually needed. (See "Overview of the causes and treatment of hyperphosphatemia".)
●Hypernatremia – Postoperative general surgery patients often suffer from an imbalance in intravascular sodium and water resulting from a combination of intravenous fluid administration, the hormonal response to surgery (ie, antidiuretic hormone, aldosterone), as well as by evaporative, gastrointestinal, or urinary electrolyte-free water loss. Minor elevations of sodium are easily corrected by decreasing the sodium content of the intravenous fluid (eg, switch from 0.9% sodium chloride to 0.45% sodium chloride or 5% dextrose in water) or by adding free water to enteral feeds. (See 'Crystalloid fluids' above and "General principles of disorders of water balance (hyponatremia and hypernatremia) and sodium balance (hypovolemia and edema)" and "Nutrition support in intubated critically ill adult patients: Enteral nutrition".)
Caution is advised in using the urine output alone in this assessment in patients with head injury, who may suffer from arginine vasopressin deficiency In cases of head injury, mild permissive hypernatremia is helpful in avoiding cerebral edema; in such cases, little to no correction is warranted. However, when correction is employed, fluid adjustment may be part of a broader approach to therapy, including the administration of vasopressin or receptor therapy [39].
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Fluid and electrolyte disorders in adults".)
SUMMARY AND RECOMMENDATIONS
●Postoperative electrolyte problems – Postoperative patients are prone to electrolyte derangements resulting from intravenous fluid therapy, transfusion, stress hormones, nutrition support, refeeding syndrome, acid-base abnormality, fluid loss, and tissue trauma. Excess urinary loss can occur with auto-diuresis during recovery from surgery or head trauma. The patient's underlying medical condition prompting the surgery and treatment of other medical conditions may also contribute to electrolyte derangement. (See 'Etiologies of postoperative electrolyte abnormalities' above.)
●Electrolyte monitoring – Postoperative patients with the following conditions and treatments should have their electrolytes monitored on a daily basis; more frequent monitoring may be indicated in cases of electrolyte deficiency or excess (see 'Laboratory monitoring' above):
•Fluid resuscitation
•Blood transfusion
•Severe organ dysfunction
•Traumatic brain injury
•Continuous bladder irrigation
•Abnormal bodily fluid losses
•Large surface area open wounds or burns
•Maintenance fluid therapy in patients who are not eating
•Postoperative ileus or bowel obstruction
●Electrolyte replacement – To avoid complications of electrolyte deficiency in the postoperative period (eg, ileus, arrhythmia, seizure), electrolyte deficiencies should be identified and treated. Electrolyte replacement to a goal of normal serum electrolyte levels (as defined for a particular institution) is a safe practice. For the patient with ongoing losses, target the middle of the normal range. (See 'Electrolyte replacement' above.)
●Route of administration – Electrolyte deficiencies can be replaced using the intravenous or enteral route. One or the other route of administration may be more appropriate depending upon the clinical situation. Although an enterally administered replacement is preferred for those with gut function, these may be poorly tolerated or not feasible in postoperative patients. For patients with moderate-to-severe electrolyte deficiency, intravenous administration provides reliable and rapid delivery. The amount and rates of administration are reviewed above. (See 'Route' above.)
●Electrolyte excess – Electrolyte excess in postoperative patients is often related to the underlying disease for which surgery was indicated and its treatment. Factors known to aggravate the electrolyte excess should be avoided. The treatment for electrolyte excess in surgical patients is like that of medical patients. However, surgical patients are often not candidates for enteral therapies as they recover from surgery. (See 'Electrolyte excess' above.)
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