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Did Pneumatic Tourniquet Use Contribute To Post-Op Compartment Syndrome And Neuropathy?

Surgeons have used pneumatic tourniquets for centuries to assist in hemostasis, resulting in faster operating times and better identification of anatomical structures. Mortality and morbidity are rare but can occur with improper tourniquet use. In this case study, the authors discuss the development of a lower extremity neuropathy after seemingly proper pneumatic tourniquet use during ankle surgery.

The U.S. Food and Drug Administration recognizes the pneumatic tourniquet as a Class I medical device, indicating minimal harm to the patient with routine use.1 When there is proper tourniquet application, it creates a bloodless surgical field that enhances the surgeon’s ability to identify anatomic structures and reduce intraoperative blood loss.1 Estimates suggest that over 15,000 surgical procedures occur daily that require the use of a pneumatic tourniquet.1 

Routine tourniquet use is not without risk of morbidity or even mortality with potential complications including compression neuropraxia, compartment syndrome, wound infection, wound hematoma, delayed recovery of muscle power, arterial hypertension, cardiorespiratory decompensation, rhabdomyolysis and cardiorespiratory decompensation.2 The rate of nerve injury associated with tourniquet use ranges from 0.1 to 7.7 percent.3 To assist in decreasing comorbidities and mortality related to tourniquet use, numerous studies have addressed appropriate tourniquet applications, duration of use, design and patient selection.1 

In this case study, we’ll take a closer look at a patient who developed a common fibular neuralgia after routine use of a high calf tourniquet during routine ankle surgery. 

When A Patient Experiences An Unexpected Complication After Tendon Repair

A 48-year-old healthy female presented to our clinic with for chronic right ankle pain and weakness after she had suffered an ankle sprain one year prior. She had two years of conservative treatment with no resolution of her symptoms. Magnetic resonance imaging (MRI) showed tendinosis and possible tearing of her peroneal tendons.  which had progressively worsened over a one year duration. Initial onset occurred after twisting her ankle several years prior which was treated with conservative therapy. Related symptoms included an aching pain along her peroneal tendons and lateral ankle ligament complex which was rated at 3/10 per the Visual Analogue Scale and aggravated by activity. Use of an ankle brace while ambulating decreased subjective symptoms. Standard radiographic images revealed an avulsion fracture of the distal lateral malleolus. Based on clinical examination peroneal tendonitis and lateral ankle ligament sprain was diagnosed and treatment consisted of continued use of ankle brace, a referral to physical therapy, and topical pain medications. At her 6 week follow up, she admitted to resolution of pain and was released from care. Two years passed before presenting for clinical evaluation of increased right ankle pain. Relief of symptoms were not achieved with previously implemented treatment plan.  A MRI obtained revealed peroneal tendinosis, anterior tibio-fibular ligament tear and tenosynovitis of the flexor hallucis longus and tibialis posterior. Based on the progression and chronicity of her symptoms with  and failure and exhaustion of conservative treatment, the patient and care team elected to proceed with surgical intervention.

The patient received a preoperative popliteal fossa and saphenous nerve block. The team placed her in the supine position with a pneumatic calf tourniquet set to 250 mmHg. After an initial semi-linear incision along the course of the peroneal tendons and dissection down to the peroneal tendons, we identified an intrasubstance tear of the peroneus brevis tendon. We debrided and retubularized this tendon in the usual manner. 

We closed the operative wound and applied dressings in the usual fashion. The pneumatic tourniquet deflation occurred at with an inflammation time of 68 minutes with the proper hyperemic response noted. We applied a modified Jones compression posterior splint with the foot slightly everted and the ankle at 90 degrees. Prior to patient discharge, all vital signs were stable and vascular status was intact to the right lower extremity. Post-operative instructions included for the patient to remain non-weightbearing to her right lower extremity. 

The first postoperative visit one occurred 10 days following her procedure without any notable complications. Her pain level was tolerable and she related no complications involving falls. We transferred her into a removable CAM boot at this time and instructed her to continue non-weightbearing to the right lower extremity. At three weeks post-procedure, her second post-operative visit, 25 days following her surgery, she called complaining of a new onset of pain, numbness and paresthesia in her right lower extremity, from her knee to her foot, which worsened at night but was constant. and had begun approximately four days prior to the visit. 

Based on her clinical symptoms, we made an initial diagnosis of neuralgia. We began treatment with oral gabapentin 300 mg taken nightly and physical therapy one week later. At six weeks post-op, the patient continued to have numbness and and paresthesia to the entire right foot up to her knee. She denied any help from the gabapentin. 

A physical examination revealed decreased muscle strength and hypersensitivity to light touch to her right foot and lower leg. Physical therapy helped with recovery of her tendon repair but yielded no change to her neurological symptoms. Referral to pain management ruled out complex regional pain syndrome (CRPS). The patient tried and failed amitryptiline and was intolerant to duloxetine (Cymbalta, Eli Lilly). 

In order to assess for potential areas of nerve entrapment or injury, we obtained nA nerve conduction velocity and electromyography (EMG) studies approximately 14 weeks after surgery. Results revealed a mild polyneuropathy affecting sensory and motor nerves without evidence of a localized neuropathy such as a tarsal tunnel syndrome or focal sensory neuropathy. The study suggested  smaller nerve fibers may have been affected and this led to the decision that a resolved compartment syndrome was the likely etiology of the polyneuropathy. 

At five months postoperatively, the patient showed recovery from her peroneal tendon surgery but still experienced continued paresthesia and numbness to the right foot and ankle, and up to the knee. The patient noted the pain at this point was tolerable with shoe and activity modifications.  

Tourniquet-Related Complications: What You Should Know

Complications arising after tourniquet use during lower extremity surgical procedures are rare but still occur. Based on results of a questionnaire survey in Norway, Odinsson and Finsen estimated that neurological complications associated with lower extremity tourniquet use occurred in one per 3,752 applications.4 In our case study, we are reporting a neurological complications occurring secondary to a likelpossible compartment syndrome that occurred three weeks after the surgical procedure. 

Compartment syndrome is a potentially serious complication, which can occurs once interstitial pressure in a closed fascial compartment increases to a level that impedes vascular flow, resulting in myoneural functional impairment and soft tissue necrosis.5 Normal compartment pressures allowing capillary perfusion range from zero to eight mmHg.6 Interstitial pressure increases above this range impair blood flow, leading to the associated complications.6 

Previous case studies report compartment syndrome occurring after tourniquet use.5,7,8 However, in our case study, the clinical presentation of compartment syndrome was not present in this patient directly following surgery. Classic presentation of compartment syndrome is described as pain out of proportion and pain upon passive stretching of the affected compartment with associated clinical symptoms of pallor, pulselessness and paresthesia of the affected extremity.5 

Compartment syndrome after lower extremity tourniquet application reportedly occurs after prolonged ischemia with reperfusion edema, direct muscle trauma secondary to repeated inflations of the tourniquet, and improper positioning.9 As we described in our surgical report, there was appropriate patient positioning on the operating table along with proper application, location and duration of a pneumatic tourniquet without repeated inflations. This patient did have regional anesthesia via a popliteal fossa and saphenous nerve block, which some suggest can delay the diagnosis of compartment syndrome.10

Pain is a cardinal feature of compartment syndrome, which analgesia can theoretically alter. Our patient did not begin to experience pain until approximately three weeks following her surgical procedure. Mar and colleagues reported on 32 of 35 patients who received epidural analgesia and had “classic signs” of compartment syndrome, which included pain out of proportion. They concluded that there was no convincing evidence that regional analgesia delays the diagnosis of compartment syndrome.10  

Peripheral nerves are composed and organized into connective tissue structures, forming a framework to provide protection and function to nerve fibers. These connective tissue structures include the endoneurium, perineurium and epineurium. The endoneurium surrounds individual nerve fibers. The perineurium envelopes fascicles or groups of endoneurium.11 Vessels in the epineurium are more vulnerable to compression trauma, resulting in permeability changes in comparison to endoneurium vessels. 

Vessel permeability changes occurring secondary to trauma lead to associated edema formation and accumulation. Prevention of endoneurial edema from draining into adjacent areas is due to a blood-nerve-barrier and a lack of lymphatic channels. A selective diffusion barrier prevents perineurial edema from draining into adjacent areas. Past studies suggest edema accumulation inside nerve fascicles create a “miniature compartment syndrome,” which could alter nerve function.12 A miniature compartment syndrome may affect or impair nerve function through a sustained increase in fascicle pressure, altering endoneurium fluid electrolyte composition or reducing blood flow to nerve segments.

Ochoa and team demonstrated that nerves directly beneath and near the tourniquet cuff edge could sustain injury due to external compression.13 This direct pressure can cause displacement of the nodes of Ranvier and myelin sheath invagination, which disrupts nerve conduction.13 The resulting damage may lead to partial or complete local conduction block, which is usually reversible within weeks or months. Nodes of Ranvier are essential components of nerve function that are located along peripheral nerve axons to increase conduction velocities.14 Compression from tourniquet application can displace nodes of Ranvier up to 300 nanometers from their original sites.13 Tourniquet-induced compression can affect larger nerve fibers responsible for motor function or smaller nerve fibers responsible for pain, temperature and autonomic function. 

Our case study reports a polyneuropathy affecting motor and sensory nerves with a likely etiology of a resolved compartment syndrome. Clinical presentation of a classic compartment syndrome was not present during this patient’s immediate postoperative period. Nerve injury resulting in polyneuropathy was most likely secondary to nerve injury from external compression via the pneumatic tourniquet. As we discussed, alteration in nerve function can occur from an increase in fascicle pressure secondary to edema accumulation or displacement of essential nerve components required for normal nerve function. 

If a patient experiences nerve-related injuries after surgery, proper evaluation and a thorough workup are warranted to determine the severity of injury. A nerve conduction study can confirm the lesion grade. Seddon classified nerve injuries into three grades, neuropraxia, axonotmesis and neurotmesis, based on the severity of lesion.16 

Sunderland later expanded this classification into five different nerve injury patterns.16 Neuropraxia, grade 1, is the mildest injury and produces a local nerve conduction block at the site of injury with normal nerve conduction proximal and distal to the injury. There is no associated injury to the surrounding nerve tissues. Axonotmesis, or grade 2, is when demyelination occurs at the injured site, leading to Wallerian degeneration distal to the demyelinated segment.16 

Nerve regeneration is possible due to the preserved endoneurium and perineurium. If full functional recovery of the nerve occurs within three months after the injury, it is classified as a neuropraxia. However, if recovery occurs at a rate of one inch per month, one should classify the injury as axonotmesis. Evidence of fibrillation and denervation potentials exist distal to the site three weeks following the injury. Recovery is spontaneous and complete with axonotmesis injuries, but can take weeks to years.17 Damage to the endoneurium without damage to the epineurium can occur in grade 3 injuries. Damage to the myelin, endoneurium, perineurium and axon indicates a grade 4 injury. Grade 5 injuries consist of complete transection of the nerve.16   

Concluding Thoughts

Nerve- related injuries during surgery can create a complex postoperative course. If questionable nerve symptoms do occur, proper workup is warranted to determine the diagnosis and severity of the damage. Treatments range from oral and topical medications to surgical neurolysis. This case study shows our patient developing polyneuropathy that was likely due to a resolving compartment syndrome occurring three weeks after seemingly proper surgical use of a calf tourniquet. If a patient displays the appropriate symptoms, a high suspicion for compartment syndrome is warranted.  

Dr. Sigur Long is a Foot and Ankle Surgery Attending in the Department of Orthopaedics at Wake Forest Baptist Health in Winston-Salem, N.C. 

Dr. McCann recently completed his Podiatric Medicine and Surgery Residency at Wake Forest Baptist Medical Center in Winston-Salem, N.C. He will soon begin practice at the Medical University of South Carolina Hospital in Florence, S.C. 

Online Exclusives
By Christina Sigur Long, DPM and Michael McCann, DPM
References
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