Diagnosis, treatment, and prevention of lower extremity pain

Overview

In the United States, 36.5% of adults suffer from chronic lower extremity pain. Only a fraction of these patients are true candidates for peripheral nerve surgery. It is important to recognize the numerous causes of lower extremity pain, that these other somatic causes of pain can confound the presentation of peripheral nerve pain, and that some patients, who have no other explanation for their pain, will often present to the peripheral nerve surgeon as a last ditch effort to have their pain treated.

As a surgical specialist, the plastic surgeon is most commonly seeing patients with chronic lower extremity pain in the setting of prior surgery and/or trauma or compressive neuropathies. Multiple studies have shown that up to 50% of patients will experience chronic lower extremity pain after nonoperative lower extremity trauma, operative fixation of lower extremity fractures, lower extremity joint replacements, and other elective lower extremity surgery. While many studies have also reported that a large portion of those chronic patients will have a neuropathic component of their pain, not all patients have a peripheral nerve–mediated pain process that would benefit from operative intervention. Patients’ chronic pain could stem from scar tissue, poor soft-tissue padding or pliability over bony prominences or hardware, discomfort from surgical hardware, chronic wounds, etc. Even with patients with neuropathic pain, the pain may be from injury or scar tissue of small cutaneous nerve branches, rather than a major, named sensory or mixed nerve. It is important to evaluate for these other causes. Some patients may benefit from surgery to remove the hardware or scar tissue or improve the soft-tissue padding. Patients whose pain is mainly from one of those more somatic causes likely will not improve with peripheral nerve surgery.

The senior author is the director of the peripheral nerve institute of the regional hospital system and is sent surgical referrals from other specialists including orthopedic surgeons, vascular surgeons, general surgeons, other plastic surgeons, neurologists, and physical medicine and rehabilitation physicians. Even with a highly selective referral patient population, 79% of 365 patients with lower extremity peripheral nerve complaints were considered operative candidates for a symptomatic neuroma or compressive neuropathy. This highlights the importance of a thorough understanding of all the possible etiologies of chronic lower extremity pain and being diligent in one’s evaluation and diagnosis before considering operative intervention.

Symptomatic neuroma

Major sensory and mixed nerves have cell bodies in a dorsal root ganglion of a spinal nerve. The afferent axons run in a myelinated sheath formed by Schwann cells from their exit from the spinal canal to the distal nerve endings receiving sensory information from the cutaneous dermatome that nerve innervates.

A neuroma is a benign growth of nerve tissue. Following transection of a nerve, the axons of the proximal segment regenerate and sprout via growth cones in an attempt to achieve axonal continuity with the distal nerve segment ( Fig. 6.1.1 ). If axonal continuity is achieved, the stimulus for the secretion of neurotrophic factors that prompt axonal sprouting stops. If axonal continuity is not achieved, the axons of the proximal segment will continue to sprout and form a tangled mass of sprouting axons, Schwann cells, and fibrous scar tissue. This is called a terminal neuroma. The free nerve endings of this neuroma are prone to spontaneous depolarization, which is centrally interpreted as pain. Mechanical stimulation of the nerve endings can also trigger depolarization, which is why neuromas encased in a surgical scar or located superficially in a weight-bearing location are more likely to be symptomatic.

A neuroma in continuity is a special case in which a neuroma forms within a nerve that still has some degree of axonal continuity. This scenario arises when a completely transected nerve is able to achieve proximal–distal continuity of some of the axons, while the remaining axons fail to do so and thus form a neuroma, or in a partially damaged nerve such as a partial transection or a traction injury results in which some axons are unable to achieve continuity and form a neuroma. A neuroma in continuity can also present with decreased/altered sensation, pain, and/or loss of motor function, though presentations are often more variable as patients will have normal function of the intact axons.

Not all neuromas are symptomatic. When motor or mixed nerves are cut, the musculotendinous unit the motor fascicles innervated will no longer function, but the motor fascicles do not sprout and become painful in the manner that sensory fascicles do. Sensory and mixed nerves are more likely to become symptomatic, but this is not the case every time. It is important to have diagnostic criteria to properly define a symptomatic neuroma to guide diagnosis and treatment. Eberlin et al . performed a systematic review and proposed the following diagnostic criteria: (1) pain with three or more neuropathic characteristics; (2) symptoms in a defined neural distribution; and (3) a history of a nerve injury; plus one of the three findings: (1) positive Tinel sign over suspected nerve; (2) positive response to local anesthetic; and (3) diagnostic imaging demonstrating a neuroma ( Table 6.1.1 ).

Symptomatic neuromas of the lower extremity develop after surgery or trauma and can involve the sciatic nerve, femoral cutaneous nerves, saphenous nerve, sural nerve, common peroneal nerve (CPN), superficial peroneal nerve (SPN) and its branches in the foot/ankle, deep peroneal nerve (DPN), tibial nerve and its branches in the foot/ankle, and the digital and interdigital nerves. Symptomatic neuromas can form in any of these nerves after penetrating trauma or fractures around the course of the nerve. Certain surgical procedures are associated with iatrogenic nerve injuries. The anterior (AFCN) and medial (MFCN) cutaneous branches of the femoral nerve, saphenous nerve, and lateral femoral cutaneous nerve (LFCN) can be injured during vascular procedures in the groin. The LFCN can also be injured in procedures around the iliac crest, such as abdominoplasties and iliac crest bone grafts/flaps. The sciatic and saphenous nerves can be injured during knee replacement surgery. The CPN and lateral sural cutaneous nerves are at risk for injury during surgeries around the fibular neck, such as fractures and CPN decompression. The SPN and sural nerves are at risk for injury during surgeries for the lateral ankle, such as fractures, stabilization procedures, and SPN decompression. The tibial and saphenous nerves are at risk for injury during surgeries around the medial ankle, such as fractures, stabilization procedures, and tarsal tunnel decompression. The saphenous nerve is also at risk during greater saphenous vein graft harvest, while the sural nerve is at risk during lesser saphenous vein graft harvest and sural nerve graft harvest. Surgeries for foot and ankle fractures place the terminal branches of the five major nerves of the lower extremity at risk: calcaneal branches of tibial and sural, medial and dorsal intermediate cutaneous branches of SPN, DPN, and digital nerves. A review of 598 patients and 299 symptomatic neuromas of the lower extremity found that the most commonly involved nerves were the interdigital nerves (25% of the study population), sural nerve (22%), SPN (15%), and saphenous nerve (13%).

Symptomatic stump neuroma

One of the most common presentations of a symptomatic neuroma is in a patient with chronic post-amputation pain. By necessity, all the major sensory nerves are cut in a major lower extremity amputation and will form terminal neuromas. Depending on how the nerves were addressed at the time of amputation and intrinsic patient factors, some of these neuromas will be symptomatic, drastically decreasing quality of life.

Symptomatic amputation stump neuromas can affect any nerve at the amputation level, but they occur most commonly in the SPN and saphenous nerves for below-knee amputations (BKAs) and the sciatic nerve in knee disarticulation amputations (KDAs) and above-knee amputations (AKAs). Nerve-specific PLP can also involve any nerve but tends to correlate highly with a symptomatic neuroma of the same nerve. Not every patient with chronic RLP will have a symptomatic neuroma. Some 57.1% of patients who had a BKA with traction neurectomies of all nerves reported chronic RLP, but only 25.7% of those patients had symptomatic neuromas (rate of 14.6%). Furthermore, 52.3% of 44 patients undergoing peripheral nerve surgery for symptomatic stump neuromas and/or PLP after a BKA, KDA, or AKA were recommended to have soft-tissue and/or bony alterations of the stump at the time of peripheral nerve surgery. This highlights the importance of a thorough preoperative evaluation to identify whether a patient’s pain will benefit from peripheral nerve surgery, stump revision surgery, both, or neither.

Symptomatic neuromas can form in the digital, interdigital, and dorsal and plantar cutaneous nerves following digit and midfoot amputations. In the senior author’s experience, it is rare that peripheral nerve surgery is required after minor lower extremity amputations given that the vast majority of patients receiving these amputations have diabetes and the peripheral neuropathy rendered those involved nerves insensate preoperatively.

Phantom limb pain

Phantom limp pain (PLP) is the pain that amputees experience in the missing portion of their limb. The mechanism of PLP is not fully understood but is believed to be due to aberrant peripheral nerve changes such as excessive axonal sprouting of the terminal neuromas in addition to maladaptive CNS cortical reorganization that amplifies the pain response. The mechanisms that may lead to the development of PLP are believed to start immediately from time of amputation once the major nerves are cut. Up to 80% of patients with major limb amputations will experience PLP.

In a study of 199 patients with BKAs whereby traction neurectomies were performed on all identified nerves, 44.7% of the patients reported chronic PLP. Of those patients, only 28.1% had PLP in a specific nerve distribution (12.6% rate of nerve-specific PLP). Symptomatic stump neuromas and nerve-specific PLP are intricately linked. In that same study, 92% of the patients with nerve-specific PLP had a corresponding symptomatic neuroma, and 82.8% of patients with a symptomatic stump neuroma had PLP in the distribution of the involved nerves. The patients with PLP in a specific nerve distribution and a symptomatic neuroma of that nerve are the ones who are most likely to benefit from peripheral nerve surgery.

Complex regional pain syndrome

Complex regional pain syndrome (CRPS) is a chronic pain condition, usually of the extremities, characterized by extreme, debilitating pain in addition to autonomic dysfunction that results in local vasomotor and sudomotor changes such as temperature, color, and edema fluctuations and asymmetries and changes in the skin, hair, and nails. There are two types of CRPS. Type I is CRPS without evidence of nerve damage in the limb, usually secondary to non-specific trauma, and accounts for about 90% of cases. Type II is CRPS with a known nerve injury of the affected limb.

Extremity injuries and surgery are the most common inciting events leading to CRPS. A review of 1043 patients with CRPS found that 42% had a traumatic fracture, 21% had traumatic injuries without a fracture, 12% had surgery, 7% had a peripheral nerve compressive neuropathy, and 7% had no clear inciting event. The overall incidence of CRPS after extremity trauma or surgery is low, however, at less than 1%. Risk factors include female gender, psychiatric diagnoses, alcohol use, recreational drug use, and higher household income. The actual pathophysiology of CRPS is still not fully understood but is characterized by an abnormal inflammatory response to injury with excessive cytokine release, increased sensitization of the PNS and CNS, and autonomic dysregulation.

A patient is given the diagnosis of CRPS if they meet the Budapest Criteria: (1) chronic pain disproportionate to any inciting event; (2) at least one symptom in three of the four categories of sensory disturbance, vasomotor abnormalities, sudomotor abnormalities, and motor deficiencies or trophic changes; (3) at least one sign in two of the four previously stated categories; and (4) no other diagnosis that better explains the patient’s symptoms ( Table 6.1.2 ).

Clinical history

A thorough history of the patient’s pain including onset, location, quality, frequency, severity, radiation, and alleviating and exacerbating factors should be obtained. One should ask if the patient had prior surgery on that extremity, how many, the types of surgeries, if the patient has any hardware or other prosthetic devices in the extremity, and for the operative notes to determine if a prior surgeon had identified a nerve, needed to sacrifice a nerve, and, if so, if any procedures were performed on such nerves. Similarly, one should ask about prior trauma to the extremity, the mechanism of injury (sharp, blunt, ballistic), any prior fractures and the initial radiographs demonstrating the location and displacement/angulation of the fracture, and the presence of foreign bodies and/or orthopedic hardware. Patients should be asked about the temporal relationship of their pain and their surgery and/or trauma.

The location, quality, radiation, and alleviating and exacerbating factors are important to assess as certain pain presentations are more consistent with peripheral nerve injuries. Pain that is confined to a dermatome of a named sensory or mixed nerve and/or radiates along that nerve’s distribution is likely to be indicative of a pathology of a peripheral nerve. Pain that is sharp, burning, sensitive to pressure, manipulation, or weight-bearing, has temperature sensitivities, and hypersensitivity is likely to be neuropathic in nature. In patients with prior trauma and/or surgery, a symptomatic neuroma should be suspected. In patients without prior trauma or surgery, a peripheral nerve tumor or a compressive neuropathy should be considered. In patients with suspected neuromas, one should ask about the quality of their sensation and how critical, to them, maintaining or restoring that sensation is as that may guide treatment options.

Sometimes, the presentation of a symptomatic neuroma is straightforward. More often, patients present with a complex picture where components of the pain are consistent with a peripheral nerve injury while others present with a vaguer picture, which makes determining whether or not they will benefit from surgery challenging. Patients with more diffusely located pain could have symptomatic neuromas, a more somatic cause of their pain, centralized pain, CRPS, or a combination. All patients should be assessed for symptoms consistent with CRPS, including hyperesthesia, skin color or temperature asymmetry between the extremities, edema, unprompted sweating, weakness, tremors, and changes in the quality or texture of the skin, hair, or nails.

Patients should be asked about the severity and frequency of the pain and how the pain impairs their quality of life. Chronic pain of the lower extremity can significantly affect functional mobility, and it is critical to ask patients what their baseline level of physical activity was and what level they currently are functioning at. There is a high prevalence of psychiatric conditions in patients with peripheral nerve pain, so one should ask if they are currently or have previously been treated by a psychiatrist, for what conditions, and what type of psychotropic medications they are taking. One should also ask if they are seeing a chronic pain specialist and what their current pain medication regimen is. Patients being prescribed pain medications from multiple providers should be referred to a chronic pain specialist. Patients should be asked what other non-invasive modalities or non-prescription substances they have tried for their pain.

Patients with major lower extremity amputations should be asked all the above questions. In addition, these patients should be asked about the presence and location of PLP. Patients with BKAs should be asked if they experience PLP in the dorsum of the foot (SPN/DPN), plantar foot (tibial nerve), medial instep (saphenous nerve), or lateral ankle (sural nerve). Patients with more proximal amputations should be asked if they experience pain in their anteromedial leg (saphenous), elsewhere in the leg (sciatic nerve), posterior thigh (PFCN), medial thigh (MFCN), or lateral thigh (LFCN). Patients with amputations should be asked about their prosthetic, how well it fits, if they regularly follow with a prosthetist, and if they are ambulatory and to what degree with their prosthetic.