Molly A. Wasserman, MD and Mamta Swaroop, MD, FACS
Ms. Jones is a 68-year-old female with a past medical history significant for hypertension and hyperlipidemia, now 2 years status post open sigmoidectomy for recurrent diverticulitis. She presents with a 3-day history of crampy abdominal pain, nausea, and 5 episodes of nonbloody, nonbilious emesis. She also reports a gradual onset of abdominal distension with obstipation. Her last bowel movement was 4 days ago and was normal. She has had associated anorexia and subjective fevers. Her medications include furosemide and atorvastatin.
On physical exam, her vitals are as follows—T: 101.5; HR: 120; BP: 140/90; RR: 16; O2: 99% on RA; and weight: 70 kg. Abdominal exam reveals absent bowel sounds, abdominal distension with diffuse tympany, and tenderness in the left upper and lower quadrants with no rebound or guarding. The remainder of the exam is normal. Labs are notable for a sodium level of 130, potassium of 2.8, and magnesium of 1.5.
1. Why are Mrs. Jones’ electrolytes abnormal?
2. What are the risks associated with leaving her sodium and potassium uncorrected?
3. What orders would you write to replete her potassium?
The ability to anticipate electrolyte abnormalities is of paramount importance in the treatment and management of the surgical patient. It will also be one of your primary responsibilities as a surgical intern. You will be expected to take care of all but the most severe abnormalities. It is important to know when and how to replace electrolytes, and when to alert the senior on service in the case of a severe and potentially life-threatening abnormality.
1. Fluids and electrolytes can be lost most commonly from the gastrointestinal tract (emesis, diarrhea, nasogastric tubes, enterocutaneous fistulas), from the genitourinary system (renal disease), from the skin (sweat, burns, fever), and from fluid shifts (third spacing, postoperative open abdomens, vacuum-assisted wound closure devices, hemorrhage). Electrolyte abnormalities may be worsened by a patient’s NPO status and the administration of intravenous fluids that are insufficient to meet the patient’s metabolic demands. Predicting losses and repleting the patient early is the best way to thwart electrolyte abnormalities. In the case above, this patient has had both diarrhea and emesis, most likely has not been able to replete her losses secondary to anorexia, and will be made NPO and receive a nasogastric tube as part of her initial treatment. All of these factors compound each other to cause this patient to be at high risk of having severe electrolyte abnormalities. Additional consideration must be given to the patient’s medications. As an example, loop diuretics (eg, furosemide) put the patient at risk of hypokalemia.
2. Table 43-1 depicts the common symptoms and signs of electrolyte abnormalities. As shown below, electrolyte disorders have a wide range of symptoms. Common among these are a delayed return of bowel function, muscle weakness and fatigue, cardiac dysfunction and dysrhythmias, seizures, and failure to wean from a ventilator.
Table 43-1. Symptoms and Signs of Electrolyte Abnormalities
3. It is important to memorize how to treat each of the most common electrolyte abnormalities.
Hyponatremia: Hyponatremia is defined as a serum sodium concentration <135 mEq/L. There are a variety of causes of hyponatremia in the surgical patient. ADH is elevated as a part of the normal stress response, and activation of inflammatory and stress cytokines (IL-1, IL-6, TNF-α) further increases ADH release. Fluid overload, high-output enterocutaneous fistulas, and aggressive diuresis may also result in hyponatremia. Initial treatment of hyponatremia involves determination of the sodium deficit and overall volume status:
where TBW = 0.6 × (weight in kg) for male and TBW = 0.55 × (weight in kg) for female.
In treating hyponatremia, it is important to determine the overall fluid status of the patient. Hypovolemic, hyponatremic patients can often be treated by rehydration with normal saline or Lactated Ringer’s solution. Conversely, euvolemic or hypervolemic patients who are asymptomatic are best initially treated with free water restriction. Symptomatic patients require administration of hypertonic saline. Overly aggressive treatment of hyponatremia will result in central pontine myelinolysis and possible permanent spastic quadriparesis and pseudobulbar palsy. As such, serum sodium should be repleted at a rate of <8 mEq/kg/day or 0.25 mEq/L/h.
Hypernatremia: Hypernatremia is defined as a serum sodium concentration of >145 mEq/L. It is less common in the surgical patient but may be seen in patients with increased insensible water losses (burns, tracheostomies), major GI losses (NG tube suction, diarrhea, emesis), administration of sodium (TPN, sodium bicarbonate infusion), and when hypotonic losses are replaced with isotonic solutions (eg, post resuscitation). As with hyponatremia, the initial step in the treatment of hypernatremia is determining the free water deficit:
Patients with severe (Na >160 mEq/L) or symptomatic hypernatremia should be treated with D5W or D5 0.45 NS to correct at a rate of less than 0.5 mEq/L/h. Once the free water deficit is calculated, the first half of the total deficit should be administered over the first 24 hours, and the second half over the subsequent 24 hours. Overly rapid correction may result in cerebral edema and brainstem herniation.
Hypokalemia: Potassium is the dominant intracellular cation, and only 2% of total body potassium resides in the serum. Potassium balance is controlled by the renin–angiotensin–aldosterone axis. Hypokalemia is defined as a serum potassium concentration <3.5 mEq/L. Total body potassium levels may be depleted by decreased potassium intake, increased loss from the GI tract (NG tube, emesis, diarrhea), renal disease, catecholamine stimulation, and certain medications (insulin, diuretics). Signs and symptoms of hypokalemia include gastrointestinal ileus, generalized fatigue and weakness, cardiac arrhythmias, and renal insufficiency. ECG abnormalities include flattened T waves, depression of ST segments, prominent U waves, and prolongation of the QT interval (Figure 43-1).
Figure 43-1. ECG abnormalities seen in hypokalemia. (Modified, with permission, from Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J. Harrison’s Principles of Internal Medicine. 18th ed. New York: McGraw-Hill; 2012. Figure e28-24. <www.accessmedicine.com>. Copyright © The McGraw-Hill Companies, Inc. All right reserved.)
Treatment of hypokalemia consists of oral or parental potassium supplementation. Oral formulations are preferred if the patient is able to take medications orally or is undergoing active diuresis. Intravenous potassium can be administered to patients unable to take po or those with severe hypokalemia (<2 mEq/L) at a rate of 10 mEq/h at a concentration no greater than 40 mEq/L. If repleting through a central line, it is permissible to replete at 20 mEq/h. Potassium can also be added to maintenance intravenous fluids at a concentration of 20 mEq in 1 L of fluid. As a general rule, administration of 10 mEq KCl, in either IV or po formulation, will increase the serum potassium level by 0.1.
It is important to note that hypomagnesemia antagonizes correction of hypokalemia. As such, if the patient is concomitantly hypomagnesemic, correction with magnesium supplementation must occur before potassium supplementation will correct hypokalemia.
Hyperkalemia: Hyperkalemia is defined as a serum potassium concentration >5.5 mEq/L. Common causes of hyperkalemia include renal disease and a decreased ability to excrete potassium, crush injuries, rhabdomyolysis, ischemia–reperfusion injuries, adrenal insufficiency, succinylcholine administration, β-receptor agonists, digitalis, and excessive administration of intravenous fluids containing potassium. Early identification and treatment of hyperkalemia is imperative, as hyperkalemia has life-threatening consequences including cardiac arrhythmias and neuromuscular weakness leading to flaccid paralysis. EKG abnormalities include peaked T waves, QRS widening, shortened QT intervals, deepening of the S wave into a sinusoidal pattern, and ventricular ectopy followed by hypoexcitability presenting as asystole (see Figure 43-2). It can less commonly also lead to ventricular fibrillation.
Figure 43-2. ECG abnormalities of hyperkalemia. (Reproduced, with permission, from Knoop KJ, Stack LB, Storrow AB, Thurman RJ. The Atlas of Emergency Medicine. 3rd ed. New York: McGraw-Hill; 2010. Figure 23.45A. Photo contributor: R. Jason Thurman, MD. <http://www.accessmedicine.com>. Copyright © The McGraw-Hill Companies, Inc. All right reserved.)
Treatment of hyperkalemia consists of early stabilization of the myocardium and a temporary shift of potassium intracellularly, followed by elimination of potassium into the stool or urine. Initial temporizing treatment includes administration of 1 ampule of calcium gluconate, which acts to antagonize myocardial depolarization. Another temporizing treatment is the administration of sodium bicarbonate, especially if the patient is acidotic. Both measures antagonize the effects of hyperkalemia on the membrane potential and also facilitate the intracellular shift of potassium. Additionally, 10 U of insulin is given to shift potassium intracellularly. This is followed by 1 ampule of D50 to thwart the impending insulin-induced hypoglycemia.
While the above measures will help reduce the serum potassium level, the effects are only transient. More definitive correction requires that potassium be excreted from the body. This is facilitated by administration of a loop diuretic (furosemide) or a sodium–potassium exchange resin (Kayexalate). Refractory hyperkalemia may ultimately require hemodialysis. A common mnemonic to remember how to treat hyperkalemia is “C-BIG-K-D,” or “See BIG Potassium Drop”:
C: Calcium gluconate
B: Bicarbonate (if acidotic)
Hypomagnesemia: Magnesium is an intracellular cation that serves as a cofactor in enzymatic reactions and is essential for protein synthesis, energy metabolism, and calcium homeostasis. Hypomagnesemia occurs when serum magnesium levels are <1.6 mg/dL. In the surgical patient this most commonly occurs secondary to hemodilution, but may also occur with chronically poor po intake, steatorrhea, biliary and enteric fistulas, or chronic use of loop diuretics. Severe hypomagnesemia places the patient at risk for lethal ventricular arrhythmias. Magnesium repletion should be considered if the magnesium level falls below 2.0. This may be done orally with magnesium citrate if the patient is able to take it. However, large doses will result in diarrhea and thus po repletion is generally neither necessary nor recommended in the acute hospital setting. Intravenous administration of magnesium sulfate is a better route of repletion for patients with severe hypomagnesemia and those unable to tolerate po.
Hypermagnesemia: Hypermagnesemia is defined as a serum magnesium concentration >2.8 mg/dL. It is rare if the patient has normal kidney function, but may be seen in patients with burns, crush injuries, or those who require chronic hemodialysis. It may also be seen in pregnant women who are being administered magnesium sulfate as a tocolytic agent. Treatment starts with elimination of magnesium-containing medications. Calcium infusion at 5 to 10 mEq is administered to stabilize the myocardium, followed by normal saline to expand the intravascular compartment. Loop diuretics and hemodialysis may also be used to eliminate excess magnesium.
Hypophosphatemia: Phosphorus is an important molecule in energy metabolism and ATP generation. Hypophosphatemia is defined as a serum phosphate concentration <2.5 mg/dL. It can be the result of renal failure and excessive renal losses, GI losses, diuretic use, major hepatic resection, or intracellular electrolyte shifts as occur in refeeding syndrome. Symptoms are related to ATP depletion and include cardiac and respiratory failure. Repletion should be considered when levels fall below 2.0 mg/dL, and this may be administered as NaPO4 or KPO4 (depending on the potassium level).
Hyperphosphatemia: Hyperphosphatemia is defined as a serum phosphate concentration of >5.0 mg/dL. This is a rare postoperative occurrence but may be seen in renal failure, rhabdomyolysis, and tumor lysis syndrome. Treatment options include expanding the plasma volume with normal saline, administration of phosphate binders (aluminum-containing antacids), or, if severe and associated with renal failure, hemodialysis.
TIPS TO REMEMBER
Surgical patients are at risk for a variety of electrolyte disorders based on the pathophysiology of their disease states (emesis, diarrhea, NG tubes, fistulas, burns, trauma, wounds, etc) and anticipation of these abnormalities will greatly enhance treatment and management of these patients.
It is important to know the volume status in the hyponatremic patient, as treatment differs based on whether the patient is fluid overloaded or dehydrated.
Repletion of magnesium to normal levels is necessary before the patient will respond to potassium repletion.
Calcium rapidly stabilizes the myocardium in the hyperkalemic patient.
1. In the case presented above, what are Ms. Jones’ anticipated electrolyte abnormalities?
A. Hypernatremia, hyperkalemia
B. Hyponatremia, hyperkalemia
C. Hypernatremia, hypokalemia
D. Hyponatremia, hypokalemia
2. Ms. Jones’ chemistry panel revealed a serum sodium level of 130. How would you replete her deficit?
A. High-sodium diet
B. 2.5 L of 3% hypertonic saline over 48 hours
C. 2.5 L of NS over 24 to 48 hours
D. Free water restriction
3. Which of the following is the initial treatment of severe hyperkalemia?
A. Insulin 10 U
B. Calcium gluconate 1 ampule
1. D. Ms. Jones is hypovolemic and hyponatremic secondary to her GI losses. As a result, her renal plasma flow and GFR will be low, ultimately resulting in increased sodium reabsorption by the kidneys in exchange for potassium.
2. C. In order to replete her sodium, it is imperative to determine her actual sodium deficit. Using the equation for Na deficit (0.55 [weight in kg] × [140—serum Na]), her total Na deficit is 385 mEq. Using 0.9% NS for repletion (which has 154 mEq of Na per liter), she would require 2.5 L (385/154) to make up for her sodium deficit.
3. B. Calcium gluconate is the initial treatment of acute hyperkalemia. It stabilizes the myocardium, but is temporizing with effects lasting only 30 minutes. Insulin is also a rapid-acting and temporizing measure, but is second line. Both Kayexalate and dialysis are definitive treatments for hyperkalemia, and should be instituted as soon as the hyperkalemia has been acutely corrected with more rapid measures.