Fluid and Electrolyte Management

Fluid and electrolyte management is key to all phases of care in surgical patients, but assessment of fluid and electrolyte status can present challenges in surgical patients different from those found in other types of hospitalized patients. For example, patients who undergo prolonged abdominal surgeries can experience significant and unaccounted insensible fluid losses and fluid shifts. Insensible fluid losses refer to the body’s loss of water through nonvisible and unmeasurable means (e.g., evaporation from the skin and respiratory tract). These losses can have a significant affect on fluid and electrolyte balance, particularly in settings where accurate assessment and management of fluid status are crucial. Similarly, patients recovering from bariatric surgery or small-bowel resection can experience electrolyte abnormalities that are not common in other surgical scenarios.

This rotation guide focuses on general principles of fluid and electrolyte management, including preoperative optimization, intraoperative considerations, and postoperative management.

The topics in this rotation guide are organized as follows:

• Fluid Resuscitation

  • Common Intravenous Fluid Solutions Used in Hospitalized Patients

  • Fluid Choice

  • Fluid Administration

• Electrolyte Abnormalities

  • Sodium

  • Potassium

  • Calcium

  • Magnesium

  • Phosphate

More information on fluid and electrolyte management can be found in the following rotation guides:

• Resuscitation Fluids and Blood Transfusion (Adult Critical Care)

• Fluids, Electrolytes, and Nutrition (Neonatal Care)

• Sodium Homeostasis Disorders (Adult Nephrology)

• Calcium-Based Disorders (Adult Endocrinology)

Fluid Resuscitation

Fluid selection is an essential component of medical care. Both the initial decision to give fluid and the choice of fluids requires a careful history and physical exam, and consideration of clinical adjuncts such as laboratory tests and imaging.

Common Intravenous Fluid Solutions Used in Hospitalized Patients

Crystalloid solutions (e.g., lactated Ringer solution, normal saline) contain ions that are movable across membranes and confer a degree of osmolarity. Most surgeons prefer balanced crystalloid solutions (e.g., lactated Ringer) over unbalanced fluids (e.g., normal saline) due to modestly better outcomes in surgical patients.

• Lactated Ringer (LR) solution

  • Chloride concentration composition more closely approximates human plasma than normal saline (NS).

  • LR is hypotonic to plasma and preferred for patients with hypernatremia.

  • LR contains a physiologic concentration of potassium and limits the tendency to hypokalemia that may occur with infusion of a large volume of potassium-free solutions.

  • Maintenance LR has been associated with modest improvement in renal outcomes as compared with NS in patients who are not in an intensive care unit (ICU) and may be associated with a small mortality benefit in patients in an ICU.

• Normal saline (NS)

  • similar osmolarity as plasma water

  • hyperchloremic as compared to plasma

  • large volume can cause mild metabolic acidosis

  • less likely to lead to hyponatremia (e.g., preferred in patients with significant gastric losses and in patients with traumatic brain injury)

  • recommended over LR when mixed with some medications to avoid precipitation

• Plasmalyte

  • available as a fluid with similar ion concentrations as plasma but less commonly used due to its high cost

Colloid solutions (e.g., albumin) contain proteins or other large molecules that maintain intravascular oncotic pressure better than crystalloid solutions. Colloids do not easily pass outside of vasculature and therefore expand intravascular volumes better than crystalloids do (via oncotic pressure), without adding high total-body-fluid volume.

• Albumin is the most commonly used colloid solution in surgical patients.

• Other types of colloids can be used in certain practice settings:

  • Hydroxyethyl starches (HES) are synthetic colloids that can be used for volume expansion during surgery or trauma, or when patients have significant edema. However, their use has declined due to concerns about kidney function impairment and coagulopathy.

  • Dextrans are glucose polymers that theoretically improve microcirculatory blood flow. Dextrans are sometimes used in vascular surgery to prevent venous thrombosis, but they can also interfere with blood typing and crossmatching as well as promote bleeding.

  • Gelatin-based solutions are derived from bovine collagen and can be used as plasma volume expanders. They are rapidly metabolized and have short duration of action, making them suitable for short-term use (e.g., in an operative setting where rapid fluid turnover is expected).

  • Artificial colloids are new synthetic colloid preparations similar to those based on modified fluid gelatin or newer starches, designed to minimize adverse effects.

Fluid Choice

Fluid choice influences the volume administered and affects outcomes. The composition of varying solutes can lead to metabolic changes. The following table compares the composition of body electrolytes and common fluids used for resuscitation and maintenance. This information can be used by physicians to compare the electrolyte composition of various intravenous (IV) solutions against normal plasma levels, aiding in the selection of the appropriate fluid therapy to correct or maintain a patient’s electrolyte balance.

Fluid Administration

Maintenance: Maintenance fluids address the patient’s physiological needs, encompassing sensible and insensible fluid losses. Sensible losses pertain to conventional forms of excretion, such as urination and defecation. Insensible losses pertain to less obvious fluid expenditure, including sweating and respiratory evaporation.

• The 4-2-1 rule is typically used to calculate maintenance rate for crystalloid fluids.

  • 4 mL/kg/hr for first 10 kg of patient weight

  • 2 mL/kg/hr for second 10 kg of patient weight

  • 1 mL/kg/hr for every kg above 20 kg of patient weight

    • Example: A 70-kg patient requiring maintenance fluids should receive IV fluids at a rate of 110 mL/hr [(4 × 10) + (2 × 10) + (1 × 50)] = 110 mL/hr

• Maintenance fluids are generally only used in patients who have reduced fluid intake (e.g., nothing by mouth [NPO] status, altered mental status leading to poor intake) or increased/dysregulated outputs (e.g., large wounds, burns).

• NS should be used in patients on certain medications (e.g., ceftriaxone) to avoid calcium precipitation from calcium-containing LR.

Resuscitation/replacement of fuid losses: Vital-sign changes and physical exam findings provide early clues of volume depletion in surgical patients. Read more on the administration of different types of fluids for resuscitation. The following special considerations should be kept in mind during fluid replacement:

• Special considerations:

  • In patients with oliguria, the fractional excretion of sodium (FENa) can be used to determine whether the renin-angiotensin-aldosterone system is active and promoting sodium retention (assuming the patient is not receiving diuretics).

    • The fractional excretion of urea (FEUrea) is a similar calculation that can be used for patients on diuretics.

  • In burn patients, LR should be used for fluid resuscitation due to its physiologic electrolyte concentrations and to prevent acidosis. Read more on fluid resuscitation in burn patients.

    • The Parkland formula (4 mL × %TBSA [total body surface area burned] × body weight [kg]) can be used to calculate the amount of LR. The Parkland formula calculates the total volume of fluid to be administered during the first 24 hours following presentation. Half the amount is given within the first 8 hours and the other half is given during the remaining 16 hours.

    • Adequate resuscitation is measured with urine output (0.5-1 cc/kg/hr in adults, 1-2 cc/kg/hr in pediatric populations), examination of acid-base status, and vital signs.

  • Neonatal and pediatric patients, and those on dialysis, are important to identify early in the preoperative period because of the following special considerations during fluid administration:

    • Neonatal and pediatric patients have increased surface area-to-body volume ratio, resulting in higher rates of insensible losses. Read more on administration of fluids in neonates.

    • Patients with kidney disease may not adequately excrete fluid by urination and are particularly susceptible to developing volume overload.

  • Fluids during surgery that involves acute blood loss (e.g., trauma or transplantation) necessitate administration of blood products over crystalloid or colloid solutions to avoid dilution of coagulation factors.

  • Insensible (incalculable) losses (not urine, blood, or stool) are usually 8-12 mL/kg/day but can increase to one liter per hour in open thoracic or abdominal surgery due to evaporation from the exposed pleural or peritoneal cavity.

Electrolyte Abnormalities

Many electrolyte derangements in surgical patients, particularly in the postoperative period, are preventable, treatable, or both when recognized promptly. Most deficiencies can be attributed to NPO status of patients before and after surgery, as well as changes in absorptive capacities due to resections of the alimentary tract. Eectrolyte derangements can be similar in surgical patients and nonsurgical patients, but the etiology and treatment in the acute and chronic settings may differ.

Sodium

Sodium regulation and homeostasis are important factors in many surgical patients. Read more on the normal regulation of sodium and signs and symptoms of sodium dysregulation in the Nephrology rotation guide.

Hypernatremia: Hypernatremia is defined as a sodium concentration >145 mmol/liter and usually reflects a water deficit.

• Causes: In surgical patients, causes include diuretic medications, diabetes insipidus, trauma, emesis/diarrhea, and even paraneoplastic syndromes. Hypernatremia can also result from excess sodium intake from sodium-containing medications without sufficient water intake in patients who have diminished thirst or ability to drink (e.g., intubated patients).

• Complications: Neurologic complications include severe hypernatremia, which can result in shrinkage of the brain and cause venous bleeding

• Treatment: Slow correction is not required in adults but physicians must have a low threshold to consult nephrology for help with titration.

  • A table summarizing the calculation for infusions to correct hypernatremia can be found here.

Hyponatremia: Hyponatremia is defined as a sodium concentration <135 mmol/liter and reflects water in excess of sodium in the blood. See a helpful algorithm for determining the cause of hyponatremia.

• Causes: In the surgical setting, hyponatremia most commonly is associated with hypovolemia coincident with intake of dilute fluids. Although the entirety of causes are beyond the scope of this guide, patients with common surgical issues are predisposed to developing hyponatremia from the following:

  • Gastrointestinal (GI) and blood losses: Patients with hypovolemia due to vomiting, diarrhea, or hemorrhage become hyponatremic with intake of dilute fluids (oral or IV) due to appropriate relase of vasopressin and renal retention of water.

  • Syndrome of inappropriate antidiuretic hormone secretion (SIADH): Major surgery and anesthesia are risk factors for SIADH, which leads to retention of excess water.

• Complications: Cerebral edema can lead to seizures, altered mental status, and even brain-stem herniation/death in extreme cases.

• Treatment: Management is directed at the etiology.

  • In the setting of volume depletion, colloid or isotonic crystalloid should be given. Once volume depletion is treated, the stimulus for vasopressin is removed and the kidneys can excrete excess water. The serum sodium in this setting may increase rapidly and may require intervention to slow the rate of correction.

  • In the setting of SIADH, hypertonic saline can be infused slowly to provide solute to help excrete excess water.

  • Calculate as a “sodium deficit” using the serum sodium level and estimated total body water (TBW, 0.6 × body weight for male patients, and 0.55 × body weight for femal patients). The formula is as follows: Na deficit=140−Serum Na × TBW

  • Correction of hyponatremia should be slow, with a goal of 6 mEq/day or 0.25 mEq/hour.

Potassium

Hyperkalemia: Hyperkalemia is defined as a serum potassium level >5.5 mEq/liter, although the laboratory value for the upper limit of normal may be slightly lower. Hyperkalemia is common in surgical patients both intraoperatively and postoperatively. Severe hyperkalemia can be life-threatening.

• Causes: Many surgical patients are at risk for hyperkalemia. The causes are extensive and include the following:

  • release of potassium from cell lysis, as with rhabdomyolysis or ischemia-reperfusion injury

  • pancreatic insufficiency or diabetes mellitus (due to lack of or resistance to insulin), which put patients at risk since insulin helps shift potassium into muscle cells

  • iatrogenic causes due to medication administration

  • acidosis contributing to hyperkalemia, as potassium shifts into serum in exchange for intracellular movement of hydrogen ions

  • volume depletion, acute kidney injury, and chronic kidney disease, which all limit renal excretion of potassium

  • high potassium values occurring in the setting of red blood cell (RBC) lysis related to phlebotomy or laboratory handling

• Complications: Hyperkalemia can lead to symptoms of muscle weakness and life-threatening arrhythmias.

• Treatment: Urgent electrocardiogram (ECG) is essential to the workup of hyperkalemia, as changes in cardiac electrical activity (e.g., peaked T waves) confirm that hyperkalemia is not a laboratory artifact.

  • Acute treatment of hyperkalemia with ECG changes focuses on shifting potassium intracellularly, as well as preventing the cardiotoxic effects of hyperkalemia.

    • initial treatment: 1-2 grams of calcium gluconate administered over 3 minutes to stabilize cardiac membranes and allow for time to correct the cause of hyperkalemia

    • subsequent acute treatment: 10 units of regular insulin to move potassium intracellularly followed by one ampule of 50% dextrose (D50) to limit the risk of hypoglycemia

    • sodium bicarbonate infusion: can be used in the presence of evidence of acidemia

    • a beta-agonist (e.g., albuterol)

    • acute treatments: do not decrease the total amount of potassium in the body and should be followed by more-definitive treatments (e.g., oral sodium polysterene and loop diuretics)

  • Definitive treatment increases renal and GI excretion of potassium using furosemide and a potassium binder.

    • The older potassium binder, sodium polystyrene sulfonate (SPS), has been associated with bowel necrosis and has fallen out of favor.

    • Sodium zirconium cyclosilicate and patiromer are approved by the U.S. Food and Drug Administration for chronic hyperkalemia, but these agents are now commonly used in the acute setting given the concerns related to SPS.

Hypokalemia: Hypokalemia is defined as serum potassium level below 3.5 mEq/liter.

• Causes: Surgical patients often become hypokalemic because of renal or GI losses.

  • Patients with high-volume emesis or nasogastric tube output can develop hypokalemic, hypochloremic metabolic alkalosis if they are not receiving a proton pump inhibitor (PPI). Renal excretion of excess bicarbonate leads to renal wasting of potassium.

  • Patients with diarrheal losses and excess laxative use can develop hypokalemia.

  • Infusion of large volumes of IV fluids such as NS without potassium leads to renal potassium losses.

• Complications:

  • Similar to hyperkalemia, hypokalemia affects cardiac electrical activity and can cause dangerous arrhythmias if not treated promptly.

    • ECG can reveal flattened T waves or the presence of U waves, which can be indicative of impending severe arrhythmias.

  • Patients undergoing GI surgery may be predisposed to decreased oral intake, gut dysmotility and ileus, or malabsorption after intestinal resection. Therefore, the different causes for hypokalemia may require alternative management solutions than in nonsurgical patients.

    • For example, although oral potassium has excellent bioavailability, patients who are NPO prior to or after surgery often require IV potassium for potassium repletion.

    • Bariatric surgical patients are particularly susceptible to hypokalemia and may be prophylactically repleted following surgery.

    • Patients are also often deficient in other electrolytes or vitamins, with hypomagnesemia being a common codeficiency.

    • Magnesium is a cofactor in many potassium transporters and must be repleted first so that potassium repletion is effectively absorbed.

• Treatment:

  • For both oral and IV potassium repletion, 10 mEq of potassium is expected to increase serum potassium concentration by 0.1 mEq provided there are no ongoing losses.

  • For example, in a patient with a potassium level of 3.3, 20 mEq of oral or IV potassium should improve serum potassium levels to 3.5.

  • Unlike hyperkalemia, calcium gluconate administration usually does not have a role in the acute treatment of hypokalemia.

Calcium

Hypercalcemia: Hypercalcemia is defined as total serum calcium levels >10.4 mg/dL, or ionized calcium concentration >5.6 mg/dL (>1.31 mmol/liter). Hypercalcemia can be acute or chronic, and signs and symptoms may present at much higher calcium levels in chronic hypercalcemia.

• Causes: Hypercalcemia is often caused by pathology that can be treated surgically, such as primary hyperparathyroidism due to parathyroid adenomas.

  • Parathyroid hormone (PTH), along with vitamin D, is a primary driver of increasing calcium levels in serum.

  • Hypercalcemia can be caused by malignancy due to bone metastases or dysregulation of calcium hormones including PTH, vitamin D, and calcitonin.

  • Additional causes include, but are not limited to, medication administration (e.g., hydrochlorothiazide), sarcoidosis, familial hypocalciuric hypercalcemia, and excess intake of calcium or vitamins D and A.

• Complications: Hypercalcemia can lead to altered mental status, nephrolithiasis, nausea/vomiting/constipation, arthralgias and osteoporosis, volume depletion, and polyuria.

• Treatment:

  • Initial treatment of hypercalcemia is administration of IV fluids (usually at least 200 mL/hour of normal saline) to promote excretion because it often leads to volume depletion. Loop diuretics can be administered in the setting of volume overload.

  • IV fluids can be followed by additional medications if the hypercalcemia is severe (>14 mg/dL).

    • Calcitonin or glucocorticoids can be administered to lower serum calcium levels.

    • Bisphosphonates such as zoledronic acid can also be used to treat hypercalcemia, particularly in hypercalcemia of malignancy. However, these medications often require at least 48 hours to take effect.

Hypocalcemia: Hypocalcemia is defined as a serum total calcium level <8.5 mg/dL (ionized calcium concentration <4.65 mg/dL or <1.16 mmol/liter), can be classified as acute or chronic, and as disorders associated with high and low parathyroid hormone.

• Causes: Hypocalcemia with low PTH is commonly caused by hypomagnesemia or acquired hypoparathyroidism (often secondary to surgical removal of parathyroid glands or disruption of parathyroid blood supply during thyroidectomy).

• Complications: Watch for signs of neuromuscular abnormalities, such as perioral numbness/tingling, paresthesia, sensorineurium alteration, and even ECG changes in severe hypocalcemia.

• Treatment: Immediately following parathyroidectomy, patients must be closely monitored for signs of hypocalcemia (including paresthesias, Trousseau sign, and Chvostek sign).

  • Patients may receive prophylactic oral calcium postoperatively, titrated based on the patient’s intraoperative drop in PTH and postoperative calcium levels.

  • Patients with calcium levels >7.5 mg/dL should be treated with oral calcium and vitamin D to increase the absorption of oral calcium.

  • Patients with calcium levels <7.5 mg/dL should be given IV calcium gluconate and closely monitored with serial labwork and ECGs.

Magnesium

Hypermagnesemia: Hypermagnesemia is defined as serum magnesium levels >2.3 mg/dL; however, symptoms typically only appear at levels higher than 4.0 mg/dL.

• Causes: Hypermagnesemia is rare and typically accompanied by renal failure (because the kidneys can generally handle a large magnesium load).

  • Hypermagnesemia can occur in patients with trauma or burns, in the peripartum period (associated with magnesium prophylaxis for eclampsia), and in patients who are on hemodialysis.

• Complications:

  • The most common presenting symptom is altered mental status, specifically diminished attentiveness.

  • Severe hypermagnesemia can cause diarrhea, muscle weakness and diminished deep tendon reflexes, arrhythmias, and seizures.

• Treatment:

  • As with hypercalcemia treatment, treatment includes administration of normal saline at a rate of at least 200 mL/hour, as well as diuresis.

  • Severe hypermagnesemia may also require treatment with calcium gluconate to stabilize cardiac membranes.

Hypomagnesemia: Hypomagnesemia is defined as serum magnesium levels <1.4 mg/dL; however, symptoms are not usually seen until magnesium level is below 1.0 mg/dL.

• Causes: Surgical patients often become hypomagnesemic during massive resuscitation or in the setting of GI losses.

• Complications: The most dangerous complication of hypomagnesemia is torsades de pointes, a dangerous ventricular arrhythmia.

• Treatment:

  • Torsades de pointes requires magnesium infusion emergently.

  • Milder symptoms can be treated with oral magnesium. However, oral magnesium can cause significant diarrhea, and IV magnesium may be better tolerated (although rapid infusion of magnesium can lead to rapid renal excretion).

Phosphate

Hyperphosphatemia is defined as serum phosphate levels > 5.0 mg/dL.

• Causes: Alterations in phosphate homeostasis occur in postoperative patients due to the role of phosphate in energy metabolism and calcium regulation.

  • Hyperphosphatemia is frequently caused by renal failure and contributes to secondary hyperparathyroidism in this setting.

  • Postoperative hyperphosphatemia can also occur after parathyroid surgery and will correct itself without intervention if the parathyroidectomy was successful.

• Treatment: Begin treatment with administration of fluids and phosphate binders.

  • Aluminum hydroxide should only be used for severe hyperphosphatemia (>7 mg/dL) and should be discontinued in favor of other binders (e.g., calcium carbonate, calcium acetate, or non-calcium-based binders, such as sevelamer).

  • Hemodialysis may be necessary for refractory hyperphosphatemia.

Hypophosphatemia is defined as serum phosphate levels below 2.5 mg/dL.

• Causes: Postoperative patients can develop hypophosphatemia after major surgery due to increased energy expenditure (adenosine triphosphate [ATP] usage) during healing.

  • Hypophosphatemia is common after hepatic resections due to the significant metabolic demand of liver-tissue regeneration.

  • Other causes in surgical patients include malabsorption or poor intake.

• Complications: Symptoms range from weakness to respiratory failure and leukocyte, erythrocyte, and platelet dysfunction.

  • Severe hypophosphatemia can develop in the setting of refeeding syndrome and can be life-threatening and result in cardiopulmonary failure due to the sudden increase in serum insulin levels and generation of ATP.

• Treatment: Begin empiric phosphate repletion postoperatively after major surgery (e.g., hepatic resection).