Rhabdomyolysis Following Bariatric Surgery—Nursing Accredited

| April 1, 2019

This is a complimentary continuing education activity for nurses. Earn 1.0 Contact Hour.

Course Instructions

To access post-test and obtain credit, visit https://tinyurl.com/BTCE-April2019 (This activity is approved for nurses only). Participants must read the designated article and take, submit, and pass the post-test by April 1, 2020. Participants must answer at least 70% of the post-test questions correctly to pass and receive credit for the activity. Upon successful completion of the post-test, participants will receive a PDF certificate, which can be downloaded immediately following the test or via email.

Course Overview

All healthcare providers involved in the perioperative management of the bariatric surgical patient should be familiar with the signs and symptoms of rhabdomyolysis. The risk factors for developing rhabdomyolysis, signs and symptoms, the diagnostic tests, and the management of this complication are discussed.

Course Description

This continuing education course is designed to educate, through independent study, integrated healthcare clinicians who care for patients with overweight or obesity, including the metabolic and bariatric surgical patient population.

Course Objectives

Upon completion of this program, the participant should be able to:

  • Identify bariatric patients at high risk of developing rhabdomyolysis.
  • Acknowledge the importance of intraoperative positioning and padding the patient
  • Identify the presenting signs and symptoms of rhabdomyolysis including postoperative pain and weakness in dependent muscles and the presence of dark urine and/or low urine output
  • Recognize the importance of immediately obtaining a serum CPK level if rhabdomyolysis is suspected, and if the CPK is greater than 1,000 IU/L, begin intravenous fluid resuscitation
  • Identify and treat electrolyte disturbances and/or other potential complications.

Target Audience

This accredited program is intended for nurses who treat bariatric and metabolic surgery patients.

Completion Time

This educational activity is accredited for a total of 1.0 contact hour (Nursing).

Accreditation Summary

This educational program is provided by Matrix Medical Communications. Provider approved by the California Board of Registered Nursing, Provider Number 14887. Activity approved for 1.0 contact hour.

Provider Contact Information

Emily A. Scullin Matrix Medical Communications, 1595 Paoli Pike, Suite 201, West Chester, PA 19380; Email: escullin@matrixmedcom.com


Tracy Martinez, RN, BSN, CBN

Program Director, Wittgrove Bariatric Center, Del Mar, California

A Message from the Department Editor

Dear Colleagues:

As practitioners, we follow detailed policies and procedures to safely prepare our patients for bariatric and metabolic surgery. Thankfully, the perioperative management is usually safe and efficient. However, recognition of and preparation for the unexpected is equally important. Dr. Brodsky provides us with a comprehensive clinical picture of the pathophysiology, assessment, recognition, treatment, and prevention of a potentially fatal surgical complication—rhabdomyolysis. Rhabdomyolysis is a serious syndrome caused by direct or indirect muscle injury. Individuals with severe obesity are at greater risk than the general population for developing rhabdomyolysis, and patients undergoing bariatric surgery are at an even higher risk for developing this dangerous complication. Its incidence might be higher than originally thought. We hope you enjoy this article and find the knowledge gained from participating in this educational activity to be useful when developing your own treatment protocols for rhabdomyolysis, with optimal patient outcomes. I want to thank Dr. Brodsky for sharing his expertise with us on this important topic.

My best to you,

Tracy Martinez, RN, BSN, CBN


by Jay B. Brodsky, MD

Dr. Brodsky is Professor (Anesthesia) of the Department of Anesthesiology, Perioperative and Pain Medicine, at Stanford University School of Medicine in Stanford, California.

Funding: This article is part of a continuing education activity financially supported by Medtronic (Minneapolis, Minnesota)

Disclosures: Dr. Brodsky reports no conflicts of interest relevant to the content of this article.


Abstract: Pressure-induced rhabdomyolysis (RML) is common following bariatric surgery. The release of intracellular contents into the circulation from muscle injury can lead to electrolyte disturbances, myoglobinuria with acute kidney injury, and cardiac dysrhythmias. Risk factors for intraoperative RML include inadequate padding and improper positioning of the patient’s body, long-duration surgery, male sex, super-obesity (body mass index [BMI]>50kg/m2), and/or the presence of preoperative hypertension, diabetes, and/or peripheral vascular disease. In the recovery room, patients might report feeling pain and tenderness in dependent muscles; however, pain management might mask these symptoms. Brown or “tea” colored urine might be the first sign of RML. A serum creatine phosphokinase (CPK) level greater than 1,000 IU/L is characteristic of RML. The mainstay of treatment is aggressive fluid administration, diuresis, and the correction of electrolyte imbalances. Late complications include renal failure requiring dialysis, disseminated intravascular coagulopathy, and compartment syndrome. Familiarity with the signs and symptoms of RML is important for all healthcare clinicians who treat patients who have undergone bariatric surgery. Immediate treatment following RML diagnosis is critical to avoid serious complications in this patient population.

Keywords: Rhabdomyolysis, bariatric surgery, creatine phosphokinase, myoglobinuria, pressure injury, acute kidney injury

Bariatric Times. 2019;16(4):12–16.


Introduction

Rhabdomyolysis (RML) is a condition caused by injury to skeletal muscle tissue that results in its breakdown and release of intracellular contents into the bloodstream. The muscle injury can be caused by direct trauma to the muscle tissue or pressure-induced ischemia to the muscle. There are also a number of hereditary and acquired conditions that can cause damage to skeletal muscle tissue and result in the development of RML.1 Pressure injury is the most common cause of intraoperative RML.

Although obesity had previously been associated with RML, it was not until the year 2003 that RML was first reported following bariatric surgery.2 Since then there have been numerous case reports and retrospective and prospective studies documenting a 6- to 77-percent incidence rate of RML in patients with obesity undergoing bariatric surgery.3

Etiological Factors

When striated muscle is damaged, the oxygen-binding protein pigment myoglobin is released into the systemic circulation. Myoglobin and its breakdown products are filtered out of the bloodstream by the kidneys. When high concentrations of myoglobin are released, the kidneys can be overwhelmed, which in turn results in acute kidney injury (AKI).

The disruption of the skeletal muscle membrane integrity allows an influx of electrolytes and extra cellular fluid into the damaged muscle. Large volumes of intravascular fluid can exit the circulation and become sequestered in the edematous muscle. This fluid shift can result in intravascular hypovolemia with hemodynamic instability, which can further compromise renal function. Chloride and calcium enter the injured cells causing serum hypocalcemia and calcium retention in the skeletal muscles and renal tissue. Potassium leaves the skeletal muscle, producing hyperkalemia, which can cause dysrhythmias and even cardiac arrest. Phosphate also leaves the cells and results in hyperphosphatemia. The release of lactic acid and other intracellular contents into the circulation causes a metabolic acidosis. Purines from the damaged muscle are metabolized to uric acid producing hyperuricemia.

In addition to AKI, other potentially life-threatening complications of RML include release of thromboplastin and tissue plasminogen into the blood from injured muscle, which makes the patient susceptible to disseminated intravascular coagulation, and local compartment syndrome from tissue swelling.

Risk Factors

Perioperative risk factors associated with RML are listed in Table 1. Although pressure-induced RML has been described in patients with normal weight who undergo surgery, patients with obesity are at a far greater risk, especially if they have been positioned inappropriately or if pressure points have been inadequately padded.4 RML has now been documented following every type of operation in patients with obesity placed in every type of surgical position.5–6 The majority of reported cases have occurred folllowing procedures in which the patient was placed in the supine or lithotomy position, which are typical positions used in bariatric operations.

Intraoperative RML is usually due to pressure injury to the lower limbs and to the dependent gluteal and lumbar muscles. Super-obesity (body mass index [BMI]>50kg/m2), male sex, hypertension, diabetes, and peripheral vascular disease are important risk factors. Long-duration surgery is the biggest risk factor; however, RML has been reported in patients with morbid obesity undergoing procedures as short as 70 minutes.4,7,8

The choice of anesthesia can influence the development of RML. Propofol is the most commonly used anesthetic induction agent. When large doses are infused over time, propofol can accumulate in fatty tissue and interfere with metabolism. The pathophysiology of “propofol infusion syndrome” is thought to be caused by either direct mitochondrial respiratory chain inhibition or impaired mitochondrial fatty acid metabolism. Interference with energy production possibly renders muscle cells more vulnerable to pressure and ischemic injury. Propofol infusion syndrome is most often associated with RML and AKI in the critical care setting.9 Some investigators have postulated that propofol anesthesia is an important risk factor for patients undergoing bariatric surgery.10 A study of 30 patients with morbid obesity (mean BMI 43±3kg/m2) who underwent laparoscopic sleeve gastrectomy found no differences in CPK, troponin, blood urea nitrogen, and creatinine plasma concentrations at the end of the operation and at 24 hours between patients who received a propofol infusion for anesthesia and those receiving an inhalational general anesthetic.11

The muscle relaxant succinylcholine has been associated with RML in patients with myopathies and malignant hyperthermia, but there have been no reports linking succinylcholine to RML in patients who underwent bariatric surgery. Likewise, statin drugs have also been reported to lead to RML due to their association with myopathy.12 However, no differences were found in the incidence of RML between patients who underwent bariatric surgery using cholesterol lowering statin agents and those who did not.13

Signs and Symptoms

Sensory and motor nerves are the most sensitive to ischemic changes from pressure damage. Local signs and symptoms of RML include pain, tenderness, swelling, bruising and weakness. Numbness and muscular pain are frequently reported by patients with RML. Aggressive pain management can mask these symptoms and potentially delay diagnosis for several days following surgery.

Diagnostic Factors

The primary indicator of RML is a blood creatine phosphokinase (CPK) level that is five times greater than normal, or 1,000 IU/L. Elevated serum CPK by itself has no adverse effects but is a marker of muscle damage. Clinically significant muscle damage with kidney injury and electrolyte abnormalities are usually not present until CPK levels rise above 5,000 to 8,000 IU/L. Using this definition, the occurrence of RML following bariatric surgery is extremely common. One prospective study reported a six-percent incidence of RML in laparoscopic gastric banding patients (“short” procedures) and a 75-percent incidence following gastric bypass (“long” procedures) patients.7 Four patients undergoing open gastric bypass had CPK levels greater than 10,000IU/L. Increasing CPK levels were positively correlated with increasing BMI and with duration of operation. In another study, patients with CPK levels in the 1,050 to 8,000IU/L range had no muscle pain, weakness, or swelling, but all patients with CPK levels greater than 8,000IU/L experienced severe pain and motor dysfunction.14

The incidence of RML varies with different reports but it is always high in bariatric patients. The incidence of RML was 30.4 percent in another series of patients undergoing open gastric bypass.15 When the operating time was less than two hours, the incidence of RML was zero,16 while 26.5 percent of patients had postoperative CPK levels greater than 1,000IU/L when operating time was more than four hours.17 Length of time in one position increases the risk of pressure-induced muscle injury. Open bariatric procedures are usually longer than laparoscopic procedures. RML was diagnosed in 17 (77.3%) of 22 consecutive patients undergoing open gastric bypass. The mean value of postoperative CPK was 7,467.7IU/L, with CPK levels greater than 5,000IU/L in 40.9 percent of these patients.18

In one of the largest series comprising 480 patients with obesity, RML was diagnosed in 62 (12.9%) patients with CPK ranging from 1,191 to 37,400 IU/L. Once again, length of surgery was the most significant independent risk factor. The best cutoff value of surgical time as a predictor for development of RML in this study was 230 minutes.19 Aggressive therapy with fluids and diuretics started within 24 hours after surgery was more effective in relieving RML and muscle pain than a comparative retrospective group with a delayed diagnosis and therapy.

Any bariatric patient who complains of buttock, hip, or shoulder pain in the postoperative period and who has an elevated serum CPK level greater than 1,000 IU/L is considered to have RML. Routine preoperative and postoperative measurement of serum CPK has been suggested since earlier diagnosis will lead to prompt treatment and a better prognosis. Patients who go on to develop renal failure from RML tend to have higher peak postoperative CPK levels and a slower decline of serum CPK levels than those who do not develop AKI.20

Myoglobin is the principle cause of AKI in RML. The proposed mechanisms for renal insult by myoglobin include tubular obstruction, oxidative injury, and vasoconstriction. Hypovolemia and acidosis contribute to the nephrotoxicity. Under normal circumstances, small amounts of myoglobin are present in blood. With increasing serum and then urine myoglobin levels, a visible pigmenturia (classically “tea” or brown colored urine) develops, although RML can occur with pink colored urine. RML should be suspected in the presence of brown urine, particularly in the absence of hemoglobinemia and hematuria. Myoglobin is cleared from the circulation more rapidly than CPK and, therefore, it is less sensitive for detecting RML, especially if suspicion of RML is delayed.

A urine myoglobin level greater than 3,000 nanogram per milliliter (ng/mL) is associated with an increased risk of AKI. Serum myoglobin levels were measured prospectively in 281 patients undergoing bariatric surgery. Increased levels were detected at four hours after surgery (124 ng/mL, range: 25–22,064 ng/mL). Patients with a BMI of 60 kg/m2 or greater and whose operation was longer than 160 minutes demonstrated the highest postoperative serum myoglobin levels and had a higher incidence of RML, AKI, and compartment syndrome.21

Other important diagnostic considerations in RML include hyperkalemia, hypocalcemia, hyperphosphatemia, hyperuricemia, and raised levels of other muscle enzymes, including lactate dehydrogenase, aldolase, aminotransferase, and carbonic anhydrase III. Metabolic acidosis can result from release of phosphate, sulphate, uric acid, and lactic acid from the muscle cell.

Prevention and Treatment

Prevention of intraoperative RML begins with careful padding of all pressure points and close attention to patient position. Special pneumatic beds with intermittent compression and inflation in the dorsal area have been used for patients after bariatric surgery.22 Changing patient position periodically during long procedures has also been recommended,23 but might be considered impractical for most operations. Minimizing operative time, ensuring adequate perioperative hydration, and close postoperative monitoring and observation are believed to be the most important considerations in preventing and recognizing perioperative RML.

Although adequate intra-operative fluid replacement is believed to reduce the risk of postoperative RML, there have been few studies of prophylactic fluid administration in high-risk bariatric patients. In one study, patients scheduled to undergo laparoscopic sleeve gastrectomy, adjustable gastric band, or Roux-en-Y gastric bypass operations were randomized into two groups. Subjects in group A (n=47) received 15 mL/kg total body weight (TBW) of IV crystalloid solution (mean: 1,900 mL, range: 1,600–2,154 mL) during surgery, while subjects in group B (n=53) received 40 mL/kg TBW IV fluid (mean 5,000 mL, range: 4,495–5,515 mL). Group B patients had significantly higher urine output in the operating room, in the post-anesthesia care unit, and on Postoperative Days 0 and 1. However, there were no statistical differences in CPK levels at any time between the two groups. The combined incidence of RML in this prospective study was seven percent though all procedures were relatively short: 147 and 149 minutes in groups A and B, respectively. Four patients in Group A and three patients in Group B developed RML, although only one patient in Group B (large volume infusion) had a CPK level greater than 5,000IU/L. Six of the seven patients had super-obesity (BMI>50 kg/m2), four had diabetes, and all had hypertension.24 Conservative (15 mL/kg) versus liberal (40 mL/kg) intraoperative IV fluid administration did not change the overall incidence of RML between these groups. Since the “conservative” fluid group received, on average, 1,900 mL of IV fluid during a 2.5-hour procedure, this volume might have been sufficient to reduce the risk of RML.

Treatment of RML should be instituted if CPK levels increase above 5,000 IU/L. Therapy initially focuses on the prevention of AKI and the management of the life-threatening metabolic complications. Early and aggressive volume resuscitation to restore renal perfusion and increase urine flow is the main approach for preventing and treating AKI in RML. The administration of large amounts of IV fluids dilutes nephrotoxins and promotes renal tubule flow, which in theory prevents the accumulation of myoglobin in the kidneys. Aggressive hydration with large volumes of IV fluids will flush myoglobin from the kidneys.

A diuretic, such as mannitol or furosemide, should also be instituted once the diagnosis of RML is made. Mannitol mobilizes interstitial fluid and increases renal tubular flow but can also deplete circulating volume. Urine should be alkalinized by infusion of sodium bicarbonate with an objective of achieving a urinary pH greater than 7 to increase the solubility of myoglobin. Acetazolamide can be used if arterial pH is greater than 7.45. The target for aggressive hydration and diuresis is a urine output of at least 2.5mL/kg/hr. Persistent oliguria or anuria might require dialysis. Additionally, an electrocardiogram should be obtained, and hyperkalemia should be treated initially in the conventional manner to avoid dysrhythmias.

Any patient suspected of RML should be admitted to a critical care unit for close monitoring and treatment. Although RML usually presents in the recovery room immediately following surgery, late presentation or perhaps more accurately late diagnosis, is not uncommon.25 Late development of RML has occurred weeks or even months after bariatric surgery and is associated with nutritional deficiencies. At least one patient has been reported to experience delayed onset of neurologic symptoms following bariatric surgery associated with clinical, biochemistry, and muscle biopsy findings consistent with RML and a malnutrition-related myopathy.26

Compartment syndrome is another major complication of RML, usually occurring in the lumbar and gluteal muscles.27 Treatment of compartment syndrome by fasciotomy remains controversial: though surgery can decompress swollen muscle, it can also increase the risk of infection in the injured tissue.

Conclusion

All members of the allied healthcare team involved in the care of bariatric surgery patients should be familiar with the signs and symptoms of RML. Attention to postoperative complaints of pain and weakness in dependent muscles and the presence of dark urine and/or low urine output are important indicators of RML, and serum CPK levels should immediately obtained from any patient who exhibits these symptoms. Routine monitoring of CPK levels following any bariatric surgical procedure over four hours might be one way to help ensure optimal patient outcomes. Prophylactic measures, prompt diagnosis, and aggressive treatment of RML are imperative to prevent the potentially fatal complications of RML.28

References

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  23. Wiltshire JP, Custer T. Lumbar muscle rhabdomyolysis as a cause of acute renal failure after Roux-en-Y gastric bypass. Obes Surg. 2003;13:306–313.
  24. Wool DB, Lemmens HJ, Brodsky JB, et al. Intraoperative fluid replacement and postoperative creatine phosphokinase levels in laparoscopic bariatric patients. Obes Surg. 2010;20:698–701.
  25. Abrao MA, Ferreira RG, Filho PAG, Lemer LC. Rhabdomyolysis in morbidly obese patient submitted to gastric bypass and during upper limb revascularization of pediatric patient. Case reports. Rev Bras Anestesiol. 2006;56:63–71.
  26. Rigney LA, El-Haddad C, Cappelen-Smith C, et al. Rhabdomyolysis as a late complication of bariatric surgery. J Neurol Sci. 2016;364:102–104.
  27. Pereira B, Heath D. Gluteal compartment syndrome following bariatric surgery: a rare but important complication. Ann Med Surg (Lond). 2015;4:64–66.
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