Rhabdomyolysis Following Bariatric Surgery

by Pedro Paulo Tanaka, MD and Jay B. Brodsky, MD

Dr. Tanaka is Visiting Associate Professor (Anesthesia), Stanford University School of Medicine, Stanford University School of Medicine, and Associate Professor (Anesthesia), Federal University of Parana, Curitiba, Brazil; and Dr. Brodsky is Professor (Anesthesia), Department of Anesthesia, Stanford University School of Medicine.

Introduction

As the readers of Bariatric Times are aware, surgery is the most effective method of losing weight and maintaining weight loss in extremely obese patients. Although morbidly obese patients were once considered a high-risk surgical population, numerous series have now demonstrated that morbidity and mortality following bariatric surgery is low, and significant postoperative complications are relatively rare. However, a potentially fatal postoperative complication, rhabdomyolysis (RML), is being increasingly recognized and reported after long-duration surgery in morbidly obese patients.

Background

Rhabdomyolysis (RML) results from injury to skeletal muscle and can occur in a variety of diseases, as well as from direct trauma (Table 1). When skeletal 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 very high concentrations of myoglobin are released, the kidneys can be overwhelmed and acute renal failure (ARF) can develop.

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 (as much as 12L) can leave the circulation and become sequestered in the edematous muscle. This fluid shift results in intravascular hypovolemia with hemodynamic instability, which further compromises 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 possible cardiac arrest. Phosphate also leaves the cells and results in hyperphosphatemia. Metabolic acidosis ensues from release of lactic acid and other intracellular contents into the circulation.

Purines from the damaged muscle are metabolized to uric acid producing hyperuricemia. Other potentially life-threatening complications include disseminated intravascular coagulation and local compartment syndrome.[1 ]

Risk Factors

The risk factors associated with RML and obesity surgery are listed in Table 2. Rhabdomyolysis is believed to be due to pressure injury to muscle during prolonged procedures with the patient in a non-physiologic position while on the operating table. Pressure-induced RML has been described in normal weight patients following surgery.[2-3] Morbidly obese patients are at a greater risk for injury than normal patients, especially when they are positioned inappropriately or inadequately padded.[4] The majority of cases of RML in obese patients have followed surgery in the supine or lithotomy positions, probably because bariatric procedures are performed in those positions. However, RML can complicate surgery in any operative position in an obese patient.[5]

Rhabdomyolysis usually is the result of unrelieved pressure injury to the lower limbs and the gluteal and lumbar muscles. Although long duration surgery is the major risk factor, other factors also contribute to RML. Super-obese (BMI>50kg/m2) male patients with hypertension, diabetes, and/or peripheral vascular disease, are believed to be at greatest risk.[6] These factors may be inter-dependent since surgery in super-obese patients is often more technically challenging and therefore operative time is longer. Time is not the only factor since RML has been reported in morbidly obese patients undergoing procedures as short as 70 minutes,[7] even with close vigilance and extra padding.[8]

To date, no study has considered whether the choice of anesthesia or intraoperative medications influence the development of RML. There is the intriguing suggestion that the popular anesthetic agent propofol may be a risk factor.[9] With very large doses, propofol can accumulate in fatty tissue and interfere with metabolism and energy production. The possibility that propofol can also influence muscle metabolism, rendering muscle cells more vulnerable to pressure and ischemic injury, has not been investigated. Statin drugs have also been suggested as a risk factor since these drugs have been associated with myopathy.[10] One study found no difference in the incidence of RML between bariatric surgical patients using cholesterol-lowering statin agents and those who did not, but the question has not been completely resolved.[11]

Symptoms

Sensory and motor nerves are most sensitive to ischemic changes from pressure damage, followed by muscle, bones, and skin. Local signs and symptoms are non-specific and include muscle pain, tenderness, swelling, bruising, and weakness.[12] Complaints of numbness and muscular pain are almost always present, but aggressive pain management may mask these symptoms and delay diagnosis. For example, there is a case report of a patient who complained of low back pain in the recovery room and was treated with narcotics.[13] That evening, urinary output dropped to 20ml/hr, and despite crystalloid resuscitation, he developed oliguric acute renal failure (ARF). The frequent use of epidural analgesia in the immediate postoperative period, especially after open bariatric procedures, has also contributed to late detection of RML.[11]

Detection

The primary diagnostic indicator of RML is an elevated serum creatine phosphokinase (CPK) level. A value five times greater than normal is diagnostic of RML. One retrospective study reported elevated CPK levels in 4.9 percent of patients following bariatric surgery.[14] Patients with CPK levels in the 1,050 to 8,000IU/L range had no muscle pain, weakness, or swelling. However, those with a CPK level greater than 8,000IU/L all experienced severe pain and motor dysfunction.
In a prospective study of 49 consecutive bariatric surgical patients, 13 patients (26.5%) had postoperative CPK levels greater than 1,000IU/L.[15] The sole significant independent risk factor identified by logistic regression analysis was operative time greater than four hours. Higher ASA physical status and diabetes also tended to be associated with RML, but these factors failed to reach statistical significance in this small series.

Another prospective study that defined RML as a postoperative CPK level greater than 1,050IU/L (5x normal value) reported a six-percent incidence of RML in gastric banding patients (shorter procedures) and a 75-percent incidence in gastric bypass (longer procedures) patients.[6] Four patients undergoing gastric bypass had CPK levels greater than 10,000IU/L. Absolute CPK levels were positively correlated with BMI and with duration of operation.

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 1,000IU/L should be considered to have RML. Routine preoperative and postoperative measurement of serum CPK is probably a good idea since earlier diagnosis will lead to earlier 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 ARF.[16]
The other important chemical change seen in RML is myoglobinuria. Myoglobin is cleared from the circulation by the kidneys, and under normal circumstances a low plasma myoglobin level is maintained. Myoglobin first becomes detectable in the urine at serum concentrations as low as 250mg/ml. A visible pigmenturia (classically “tea” or brown-colored urine) is present, although RML can occur with pink-colored urine. Rhabdomyolysis should be considered in the presence of brown urine, particularly in the absence of haemoglobinemia and hematuria.

Other important biochemical findings in RML include hyperkalemia, hypocalcemia, hyperphosphatemia, hyperuricemia, and raised levels of other muscle enzymes, including lactate dehydrogenase, aldolase, aminotransferase, and carbonic anhydrase III (which is a very specific marker for skeletal muscle injury). Metabolic acidosis may result from release of phosphate, sulphate, uric acid, and lactic acid from the muscle cell.

Prevention and Treatment

Prevention of RML begins with careful intraoperative padding of all pressure points and close attention to patient positioning. Some clinicians suggest changing patient position hourly during prolonged surgery. Minimizing operative time, adequate perioperative hydration, and close postoperative monitoring and observation are obviously important. For extremely obese patients some recommend procedures be performed in two separate stages to reduce operative duration. Special pneumatic beds with intermittent compression and inflation in the dorsal area have been used for patients recovering from bariatric surgery.[17]

Treatment should be instituted once CPK levels increase beyond 5,000 IU/L. (Table 3) Therapy focuses on the prevention of ARF and the management of the life-threatening metabolic complications.

Adequate intraoperative fluid replacement may reduce the risk of postoperative RML. Following surgery, aggressive hydration with large volumes of intravenous fluids will flush myoglobin from the kidneys. Diuretics, 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 seven 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 1.5ml/kg/hr.[3]

Hyperkalemia is treated initially in the conventional manner.[9] Persistent oliguria or anuria may require dialysis.[18]

Any patient suspected of developing RML should be admitted to a critical care unit for intense 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. One case of RML was diagnosed on the fifth postoperative day after a gastric bypass procedure.[19]The patient had undergone an eight hour and 30 minute laparoscopic operation. In the immediate postoperative period, epidural pain medication probably masked muscle or nerve complaints. Following discontinuation of the epidural analgesia, the patient initially complained of upper limb weakness, with subsequent involvement of the lower limbs and difficulty with movement in bed. Only on the fifth day did severe gluteal and lower limb pain occur.

Compartment syndrome is another major complication of RML. Treatment of compartment syndrome by fasciotomy is controversial since surgery does decompress swollen muscle, but it also increases the risk of infection in the injured tissue.
Thromboplastin and tissue plasminogen released from injured muscle make the patient susceptible to disseminated intravascular coagulation.

Conclusion

Now that surgeons, anesthesiologists, and intensivists are aware that bariatric patients are prone to develop RML, this complication is being increasingly recognized. Attention to postoperative complaints of pain and weakness, dark urine, and/or low urine output is essential, and serial serum CPK levels should be obtained. Prompt diagnoses and aggressive therapy must be instituted early to avoid the potentially fatal complications of RML.

References
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