Rhabdomyolysis After Prolonged Operations

Postoperative rhabdomyolysis is a rare event, particularly in oral and maxillofacial surgery (OMS) procedures and is rarely discussed in OMS literature. Rhabdomyolysis occurs when damaged muscle breaks down, releasing intracellular contents, including myoglobin and creatinine kinase (CK), into circulation. This produces a non-specific clinical syndrome including electrolyte disturbances, hypovolemia, metabolic acidosis, coagulopathies, and risk for acute kidney injury (AKI).

Presented are two cases of rhabdomyolysis following maxillofacial surgery. The first is a 30 year-old, overweight non-obese male who underwent a LeFort I osteotomy, bilateral temporomandibular joint arthroplasties with total joint prostheses and fat grafting, and genioplasty. Upon admission to the SICU after the 16-hour operation, two pressure sores and dark urine were noted. The second patient is a 19 year-old morbidly obese male who underwent a two-piece LeFort I osteotomy and bilateral sagittal split mandibular osteotomies. At the end of the 10-hour case, dark urine was noted. He had no evidence of pressure sores or other tissue breakdown. The purpose of this case series is to determine clinical trends of rhabdomyolysis and identify measures predicting clinic outcomes, risk factors and early intraoperative signs.   

The anesthetic records and postoperative data were reviewed and analyzed for both patients. In case one, total time of hypotensive anesthesia (systolic blood pressure (SBP)<90mmHg) was 6.75 hours and total time with SBP>40mmHg below his baseline (130mmHg) was also 6.75 hours.  Total fluid input was 9000mL of lactated ringers and 500mL of Hextend. Total fluid output was 1275mL of urine (average 0.95mL/kg/hr) and 900mL of blood loss. CK peaked 14 hours post-operatively at 39,500 U/L. Creatinine peaked on postoperative day (POD) 0 at 1.25mg/dL and BUN peaked on POD9 at 40mg/dL. In case two, total time of hypotensive anesthesia was 2.75 hours and total time with SBP>40mmHg below his baseline (also 130mmHg) was 2.75 hours. Total fluid input was 4800mL of lactated ringers. Total fluid output was 580mL of urine (average 0.43mL/kg/hr) and 450mL of blood loss. CK peaked 21 hours post-operatively at 115,840 U/L, while BUN and creatinine remained unchanged. Both patients were treated with aggressive fluid resuscitation, forced diuresis, and recovered fully.

In these cases, like most oral and maxillofacial surgical cases, the patients did not have significant risk factors for rhabdomyolysis aside from prolonged operative time; though both patients had borderline hypertension and the second patient had elevated body mass index (38.5). In both cases, rhabdomyolysis is likely due to direct muscle breakdown from the surgical table padding and prolonged surgical time, possibly exacerbated by insufficient fluid resuscitation and prolonged hypotension.   

In cases where prolonged surgical time is anticipated, procedures may be divided into two stages to avoid prolonged muscle compression. Routine intraoperative repositioning and pressure point checks are recommended, and postoperative measurements of the serum creatine kinase and serum creatinine levels for prolonged surgeries. If a diagnosis of rhabdomyolysis is confirmed, aggressive fluid resuscitation may prevent acute kidney injury. In these two cases, patient one had AKI with CK elevation to 39,500 U/L, while patient two did not have AKI, but had CK elevation greater than 100,000 U/L, thus in this small sample, there is no clear correlation between AKI and CK elevation. A prospective study of patients undergoing maxillofacial surgery is planned to determine if direct correlations exist between operative length, intentional hypotension, BMI and CK levels.

Scharman EJ, Troutman WG. Prevention of kidney injury following rhabdomyolysis: a systematic review. Ann Pharmacother. 2013;47(1):90-105.

Choi W, Samman N. Risks and benefits of deliberate hypotension in anaesthesia: a systematic review. Int J Oral Maxillofac Surg. 2008;37:687-703.