Abstract
With a growing prevalence of amputation in the United States—largely because of diabetes and dysvascular disease, and a sizable portion of those individuals living with pain—an understanding of amputation-related pain is becoming increasingly important among clinicians in primary care as well as across multiple specialties. Amputation presents unique and potentially challenging presentations of pain, with multiple potential etiologies. Although neuropathic pain syndromes are the focus of this text, nonneuropathic causes must also be addressed, as they can either occur concomitantly or be difficult to distinguish. Probably the most unique neuropathic amputation-related pain syndrome is the phenomenon of phantom pain; however, other neuropathic conditions exist as well. This chapter discusses the evaluation and treatment of amputation-related pain, which can occur in this patient population through all stages of recovery, from the immediate postoperative period on.
Keywords
Amputation, Cortical reorganization, CRPS, Neuroma, Phantom limb pain
Introduction
The prevalence of limb loss in the United States has been estimated to be approximately 1.6 million in 2005 and to increase to approximately 3.6 million by the year 2050. Up to 80% of amputations in the United States are secondary to dysvascular conditions such as diabetes and peripheral vascular disease. A significant number of patients with amputation have pain related to their amputation, with survey-based studies showing that up to 80% of patients have chronic pain. The location of the postamputation pain can generally be divided into residual limb or residual limb pain and phantom limb pain (PLP). PLP is a unique pain syndrome, consisting of pain or painful sensations felt in the missing body part. Residual limb pain is heterogenous in origin. This chapter presents a brief review of amputation-associated nonneuropathic pain conditions important in the differential diagnosis of pain after limb amputation.
Incidence
The prevalence of pain after amputation is variable. A survey of 914 patients found that 79.9% of patients have PLP and 67.7% have residual limb pain. Earlier surveys of American veteran patients with amputation show a similar prevalence of PLP in 78% of patients surveyed. This correlates with a more recent study, which shows a similar prevalence of PLP (79%) in patients with peripheral vascular disease 6 months after amputation. This study also showed a 51% prevalence of residual limb pain in the same time frame.
The onset of pain is variable, either appearing immediately after amputation or in the following months. In approximately half the patients, the pain improves with time, with Schley et al. describing improvements in phantom pain in 48.2% of patients and in residual limb pain in 47.5%.
Etiology
As it can be difficult for patients to describe the character, nature, or even the exact location of their pain, it is important to keep a broad differential diagnosis in mind. A proposed differential diagnosis can be found in Box 15.1 . PLP is discussed extensively in a following section of this chapter.
- •
Neuropathic pain
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Complex regional pain syndrome
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Peripheral neuropathy
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Radiculopathy
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Neuroma
- •
Phantom limb pain
- •
- •
Musculoskeletal
- •
Myofascial pain
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Fracture
- •
Osteoarthritis
- •
Contractures
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Heterotopic ossification
- •
Poor prosthetic fit
- •
- •
Infectious
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Herpes zoster
- •
Cellulitis
- •
Septic arthritis
- •
Osteomyelitis
- •
Folliculitis
- •
Dermatitis
- •
- •
Vascular
- •
Thrombus
- •
Peripheral vascular disease
- •
- •
Rheumatologic
- •
Rheumatoid arthritis
- •
Gout
- •
- •
Dermatologic
- •
Skin breakdown of the residual limb
- •
Incisional pain
- •
Choke syndrome
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Although the focus of this book is on neuropathic pain syndromes, a discussion of nonneurologic causes cannot be ignored, as they must be considered in the differential diagnosis. Identification of the etiology of pain in a patient with amputation is especially important, because along the spectrum of recovery from an amputation there may be any number of pain generators and the appropriateness of treatment approach and duration of treatment for each of those pain generators may differ.
Pain is a subjective experience, and both residual limb pain and PLP develop secondary to a variety of factors. It is unclear how many objective findings in the residual limb, such as neuromas or heterotopic ossification, contribute to the presence of PLP or how many interventions aimed at the residual limb are able to affect PLP. To further complicate matters, PLP, although not always related to prosthetic wear, may be elicited or exacerbated by poor prosthetic fit or discomfort with prosthetic wear. Although it is difficult to objectify PLP, it is generally easier to delineate many causes of residual limb pain with typical clinical and imaging findings.
Residual Limb Pain
Residual limb pain is heterogenous in nature, and there is no existing uniform categorization for residual limb pain, although various algorithms have been proposed. Incisional and musculoskeletal pain experienced immediately after amputation, similar to that experienced in other postsurgical conditions, is typically self-limiting postsurgical pain. This is treated in the same fashion as with other surgical procedures, with antiinflammatory and narcotic medications, as warranted.
Factors that are thought to contribute to the development of postamputation pain can be divided into presurgical, surgical, and postsurgical ( Box 15.2 ).
| Presurgical | Surgical | Postsurgical |
|---|---|---|
| Prior neuropathic pain in limb | Residual limb length | Residual limb shaping |
| Vasculopathy/claudication | Nerve resection | Edema control |
| Infection | Bone shaping | Desensitization |
| Musculoskeletal pain | Incision placement | Prosthesis fit |
| Psychosocial | Limb shape | Wound healing |
| Resection of unhealthy tissue | Psychosocial |
Preexisting pain syndromes are thought to presensitize the patient to the development of postamputation pain. Dysvascular limbs have higher complication rates of delayed wound healing, and chronic wounds are suggested to create a local painful structure, as well as upregulate central pain pathways.
Surgical technique can also significantly affect future pain and prosthetic fit. A limb that has not been adequately amputated to resect unhealthy tissue can result in recurrence of tumor, symptomatic vascular disease with the development of ischemic or neuropathic pain, or recurrence of infection and the formation of new wounds.
A short residual limb is more difficult to fit with a prosthesis. Improper angling of the resected bone edges can create an aggressive bone edge that creates pressure points on the subcutaneous tissues. Placement of the incision within the weight-bearing point of the limb can create pain and incision breakdown. Various resection techniques of peripheral nerves can possibly contribute to or reduce the formation of painful neuromas.
Postsurgical factors that affect the development of pain include compliance with wrapping for edema control and residual limb shaping, utilization of desensitization techniques, presence of delayed wound healing, and proper prosthesis fit.
Prosthogenic pain, or pain from prosthetic wear, can occur from poor prosthetic fit and/or suspension, or the presence of skin and soft tissue adhesion, which contribute to pain with skin traction or increased focal pressure. The resulting local mechanical stress can cause a variety of disorders, such as formation of bone bruises, adventitious bursa, local callusing, pressure breakdown of the skin, or traction pain. Persistent vascular disease in the residual limb can result in claudication. This can be difficult to distinguish from pain caused by the prosthesis. In both cases, pain tends to worsen with increased weight-bearing activity and metabolic demand. Heterotopic ossification and aggressive bone edge can both cause local pain in the residual limb and occur in a high proportion of residual limbs (up to 63% in traumatic amputees). Treatment of prosthogenic pain involves identification of the offending cause (e.g., poor fit or suspension). Vascular-related pain may be treated with the combination of medications to maintain perfusion, therapy, and revascularization procedures. An in-depth discussion of diagnostic strategies for these types of pain is beyond the scope of this chapter. Critically, identifiable and sometimes reversible causes of residual limb pain should be aggressively pursued.
Neurogenic pain can occur from a local injury to a nerve, such as a neuroma, and can be sympathetically mediated, as seen in certain cases of complex regional pain syndrome (CRPS). Radiculopathy or lumbosacral plexopathy or peripheral nerve lesions can result in radiating pain. Hyperalgesia is also common postsurgically. Nociceptive pain can radiate from the spine or adjacent joints.
Diagnosis
The diagnostic approach to postamputation pain first includes differentiation of whether the pain occurs in the residual limb or in the missing body part, whether it is associated or is independent of prosthetic wear.
Detailed history and physical examination, including careful characterization of the pain, are perhaps the most helpful in delineating neurogenic from nonneurogenic causes. It should be noted that both types of pain can be experienced concurrently, and attempts to address all pain generators should be made to optimize functional progress.
Many skin findings are easily identifiable with observation and palpation. Adhesions or wounds can cause reproducible traction pain, which is typically associated with prosthetic wear. Neuromas present as a localized point of typically extreme pain with mechanical stimulation and may have a positive Tinel sign. They can frequently be palpated subcutaneously.
When the cause of pain is not so clearly identifiable, imaging modalities may be used to support or confirm a diagnosis. Plain radiography and CT scan can identify fractures, heterotopic ossification, and aggressive bony edge. Ultrasonography has been described since 1989 as a tool for neuroma identification and may be used for guided intervention. MRI can be used to identify neuromas, adventitious bursae, bone bruising, and stress fractures from prosthetic wear, as well as identify infection and recurrence of tumor in patients with cancer.
Diagnosis of PLP is clinical and is discussed in length later in this chapter. It is easily differentiated from residual limb pain as it occurs in the location of the missing body part.
Individual Diagnoses and Treatments
Treatment of postamputation pain is as heterogenous as the differential diagnosis.
The three true neuropathic syndromes in the patient with amputation include neuroma, PLP, and CRPS when its cause is neurologic.
Neuroma
Symptomatic neuromas are described to occur in 13%–32% of patients with amputation and represent the most common cause of residual limb pain. Spindle or fusiform-shaped neuromas appear at sites of friction or local pressure, whereas terminal end nerve trauma (such as after amputation) causes terminal or end bulb neuromas, with a mass of haphazard proliferation of Schwann cells, connective tissue, and axons. Many neuromas found on imaging are asymptomatic, whereas others can be exquisitely painful, significantly limiting the quality of life and ability to tolerate prosthesis wear.
Pharmacologic interventions include anticonvulsants such as gabapentin, antidepressants such as duloxetine, and opiates.
Interventional approaches to the treatment of neuroma include guided phenol denervation, pulsed radiofrequency denervation, and guided steroid injection into the neuroma. All approaches have been described with variable results. Studies are low powered and, at this time, evidence is preliminary.
Surgical approaches to treatment include resection and reimplantation into adjacent muscle, reimplantation into veins, and tibioperoneal short circuit techniques. Targeted muscle reinnervation, a novel nerve transfer technique, has been extensively studied as a technique to confer more intuitive control over myoelectric prostheses. It has also been suggested to reduce reformation of neuromas by providing an intact distal scaffold for nerve regrowth. These studies consist of small group sizes but have demonstrated good effects. Traction neurectomy has not been found to have favorable outcomes.
Other local treatments for chronic intractable pain have been reported, primarily as case reports or small series, including transcutaneous nerve stimulation, extracorporeal shock wave therapy, and peripheral neuromodulation with implantable nerve stimulators with promising results.
Other general and nonspecific pain management approaches to intractable neuromas are similar to those treating phantom pain but do not have high-power evidence in the treatment of neuromas specifically. They are summarized in Table 15.1 .
| Pharmacologic | Surgical | Injection | Psychologic | Other |
|---|---|---|---|---|
| Opiates | Rhizotomy | Nerve block | Biofeedback | Physical therapy |
| NSAIDs | Dorsal column stimulation | Lumbar sympathetic block | Cognitive behavioral therapy | Occupational therapy |
| Anticonvulsants | Residual limb revision | Stellate ganglion block | Transcutaneous nerve stimulation | |
| Antidepressants | Neurectomy/neuroma removal/wrapping | Trigger point injection | Mirror therapy/graded motor imagery | |
| Partial mu agonists | Sensory discrimination training | |||
| Multidisciplinary pain management programs |
CRPS
Complex regional pain syndrome has been described as occurring after multiple triggering events, including amputation. Although it can occur after amputation as a type 1 CRPS, it is possible that it occurs as a type 2 CRPS with underlying nerve damage; the incidence of this is currently not well defined. Conversely, amputation of the affected limb has been used as a treatment for recalcitrant CRPS with some success. However, reoccurrence of CRPS after amputation has been described in up to 24% of patients, and amputation as a treatment remains controversial.
The syndrome follows a similar course in patients who develop it secondary to amputation and nonamputation patients. CRPS etiology, diagnosis, and treatment are discussed extensively in other chapters of this text.
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