Introduction

Imagine a patient waking up from a lengthy spine surgery, only to reveal an unexpected complication: one side of their face swollen, the underlying muscle silently damaged. This was the reality for a 50-year-old obese male (BMI 35) who underwent an 8-hour neurofibroma resection in the prone position. Diagnosed with masseter muscle necrosis, this case underscores a rare but serious risk of prolonged surgery. While not directly caused by anesthesia, anesthesiologists play a pivotal role in its prevention and early detection.

This article explores the pathophysiology, differentiates it from anesthetic complications, and outlines the anesthesiologist’s role in managing such cases.

Reference

Chowdhry M, Hazani R, Collis G, Wilhelmi BJ. Masseter muscle hypertrophy and other mimickers of parotid gland enlargement: diagnosis and treatment. Ann Plast Surg. 2010;65(5):456–460. doi:10.1097/SAP.0b013e3181d87bd1

What Causes Masseter Muscle Necrosis?The Mechanism Unveiled

The masseter muscle, positioned adjacent to a surgical headrest in the prone position, is vulnerable during prolonged procedures. In obese patients, sustained pressure can exceed the tissue perfusion threshold (~32 mmHg). Once this occurs, blood flow halts and ischemia begins.

At the cellular level, hypoxia forces cells into anaerobic glycolysis, depleting ATP stores and impairing sodium–potassium pump activity. This results in calcium overload, uncontrolled enzyme activation, and myocyte necrosis. Venous congestion further amplifies acidosis and inflammatory responses.

The cascade typically develops silently during surgery, only to manifest postoperatively as facial swelling.

Reference

Gefen A. The biomechanics of sitting-acquired pressure ulcers in patients with spinal cord injury or lesions. Int Wound J. 2011;8(6):611–618. doi:10.1111/j.1742-481X.2011.00838.x

Is Anaesthesia to Blame?Separating Fact from Fiction

The use of succinylcholine (75 mg) in this case raised concern for malignant hyperthermia (MH). However, the absence of hypercarbia, rigidity, and hyperthermia excluded MH. Similarly, there was no laboratory evidence of rhabdomyolysis, such as elevated creatine kinase or potassium.

The clinical picture pointed instead to mechanical ischemia from prolonged facial compression. This differentiation is crucial for anesthesiologists: while drugs may raise suspicion, the true etiology here was positional and mechanical rather than pharmacological.

Reference

Larach MG, Gronert GA, Allen GC, Brandom BW, Lehman EB. Clinical presentation, treatment, and complications of malignant hyperthermia in North America from 1987 to 2006. Anesth Analg. 2010;110(2):498–507. doi:10.1213/ANE.0b013e3181c6b9b2

The Anesthesiologist’s ArsenalProactive Prevention Strategies

Although anesthesiologists do not directly cause masseter necrosis, they are frontline defenders against it. Preventive measures include:

• Pressure redistribution: Use of gel pads or specialized face pillows to distribute weight evenly.
• Vigilant monitoring: Frequent checks of head and facial position to prevent sustained compression.
• Intermittent offloading: Periodic repositioning to restore perfusion.
• Hemodynamic stability: Maintaining mean arterial pressure above 65 mmHg to optimize tissue oxygenation.

These measures are particularly important in obese patients and long-duration surgeries, where the risk is greatest.

Reference

Stark ME, Lehmann LW, McCusker SB. Ischemic myopathy: a rare complication of prolonged surgery in the prone position. J Clin Anesth. 1994;6(6):473–475. doi:10.1016/0952-8180(94)90074-4

Decoding the Ischemic Cascade

Skeletal muscle tissue can tolerate only limited ischemia. After 2–3 hours of continuous compression, microvascular occlusion deprives the tissue of oxygen and nutrients.

Key events in the ischemic cascade include:

• Calcium influx that activates destructive enzymes and damages cellular structures.
• ATP depletion impairing sodium–potassium pump activity, causing intracellular swelling and eventual cell lysis.

The consequence is necrosis followed by edema and inflammation, which typically presents postoperatively as unilateral facial swelling.

Reference

Oomens CWJ, Bader DL, Loerakker S, Baaijens FPT. Pressure induced deep tissue injury explained. Ann Biomed Eng. 2015;43(2):297–305. doi:10.1007/s10439-014-1202-6

The Power of Postoperative Vigilance

When unilateral facial swelling is noted postoperatively, anesthesiologists must consider a differential that includes:

• Venous congestion from prone positioning
• Allergic reaction to medications or materials
• Ischemic myopathy or compartment-like syndrome of the masseter muscle

In this case, prompt recognition and referral to plastic surgery confirmed masseter necrosis. This highlights the anesthesiologist’s critical role in postoperative assessment and communication with the surgical team.

Reference

Gawande A, Zinner MJ, Studdert DM, Brennan TA. Analysis of errors reported by surgeons at three teaching hospitals. Surgery. 2003;133(6):614–621. doi:10.1067/msy.2003.169

Conclusion

Masseter muscle necrosis is a rare but significant complication of prolonged prone surgeries, particularly in obese patients. Although not directly attributable to anesthesia, anesthesiologists are central to its prevention and detection.

Through optimal positioning strategies, pressure-relieving devices, vigilant monitoring, and postoperative assessment, anesthesiologists safeguard patients against this complication. This case underscores their role as both intraoperative guardians and postoperative sentinels of patient safety.

Reference

Berton C, Guérin C. Prone positioning and neuromuscular disorders: a double-edged sword? Intensive Care Med. 2020;46(5):981–983. doi:10.1007/s00134-020-05988-w