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O&P Library > Atlas of Limb Prosthetics > Chapter 27

Reproduced with permission from Bowker HK, Michael JW (eds): Atlas of Limb Prosthetics: Surgical, Prosthetic, and Rehabilitation Principles. Rosemont, IL, American Academy of Orthopedic Surgeons, edition 2, 1992, reprinted 2002.

Much of the material in this text has been updated and published in Atlas of Amputations and Limb Deficiencies: Surgical, Prosthetic, and Rehabilitation Principles (retitled third edition of Atlas of Limb Deficiencies), ©American Academy or Orthopedic Surgeons. Click for more information about this text.


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Chapter 27 - Atlas of Limb Prosthetics: Surgical, Prosthetic, and Rehabilitation Principles

Management of Pain in the Amputee

Maurice D. Schnell, M.D.
Wilton H. Bunch, M.D., Ph.D.

The goal of amputation surgery is to remove an often painful, functionless limb and to rehabilitate the amputee to a painless, functional state. The most common factor precluding successful outcome following lower-limb amputation is residual pain, which occurs in approximately 80% of patients at some point following a major extremity amputation. For the majority of these patients, this pain will gradually resolve. However, a significant number of amputees will have persistent limb pain that interferes with prosthetic usage.

Postamputation pain can be isolated to the residual limb or can occur as phantom pain. The physiologic mechanism for intrinsic stump pain and phantom pain is similar. The presence of preamputation pain, especially in dysvascular amputees, corresponds with the incidence of phantom pain in the immediate postamputation period but does not correspond to chronic phantom pain.

The treatment of chronic pain following an amputation is determined by the etiology of the pain. Obvious pathomechanical sources of pain such as degenerative arthritis of the knee in a transtibial amputation, ischemia in the residual limb in a dysvascular amputee, or a painful neuroma can be readily treated. Psychiatric factors may amplify amputee pain syndromes, yet personality disorders do not absolutely correlate with the incidence of phantom pain syndromes.

A large variety of surgical and nonsurgical methods exists for the treatment of postamputation pain. The survey of phantom pain treatment methods used by Veterans Administration hospitals, medical schools, and pain clinics showed that at least 50 different modalities are currently utilized for the treatment of amputee pain. Only a few of these treatment methods were even moderately successful at long-term follow-up.An appropriate treatment regimen is dependent on a knowledge of the basic mechanisms involved in both central and peripheral pain.

INTRINSIC CAUSES OF PAIN

Pain Mechanisms

Pain is a phenomenon that consists of complex circuits of cellular communication and integration elicited by stimulation of peripheral tissues such as skin, joints, tendon, ligaments, and viscera. It is a personal experience, differing somewhat from one individual to another as influenced by cultural experiences, personal attention, the importance of a specific situation, and other cognitive activities. Although there is no evidence of control mechanisms affecting the sensitivity of peripheral nerve receptors, pain is not simply a transmission of a neural message, but rather a reaction that involves interpretative processes within the central nervous system.

Several types of peripheral nervous receptors have been identified: mechanoreceptors, thermoreceptors, and nociceptors, or pain receptors. Mechanoreceptors and thermoreceptors consist of either free nerve endings or specialized capsulated receptors (Pacini and Ruffini endings, Merkel spots, and Iggo corpuscles). Impulses from these low-intensity receptors are carried by large myelinated fibers. The thermoreceptors and mechanoreceptors are characterized by a low threshold for certain stimuli. For example, thermoreceptors have a distinct sensitivity to high and low skin temperatures but can be excited by firm pressure. On the other hand, nociceptors have a high threshold to an appropriate stimulus and a relatively small field of reception. The two subclasses of nociceptors are thermal nociceptors and mechanical nociceptors. These receptors are terminal endings of small myelinated and nonmyelinated fibers and are activated by intense mechanical stimulation and low (less than 15C) or high (above 50C) temperatures.

There is considerable controversy regarding the existence of specific chemoreceptors. Although past studies have failed to substantiate unique chemoreceptors, there is abundant evidence from experimental work that extracellular chemical substances (such as bradykinin, histamine, and prostaglandins) released into extracellular fluid following tissue damage secondary to injury or disease act in some way to produce pain.

Once depolarization is initiated, the generated action potential flows along sensory nerve fibers to superficial and deep cutaneous complexes and ultimately to the dorsal root ganglion, where cell bodies of the afferent neurons are located. The axons of the ganglion cells enter the apex of the dorsal horn of the spinal cord and terminate in a complex array of synaptic arrangements (Fig 27-1.). The dorsal horn has been divided into six laminae on an anatomic and functional basis. Sensory input from the periphery is roughly distributed according to fiber size. The large myelinated fibers give off a collateral, which enters the dorsal horn and forms synaptic connections with cells and various laminae, especially laminae II and III. The small myelinated sensory afferent fibers proceed into the Lissauer tract, where they divide into ascending and descending divisions extending over one and two segments and establish synapses with marginal neurons and gelatinosa cells (Fig 27-2.).

The long ascending afferent pathways are formed by axons of neurons from laminae I, IV, V, and VI. The majority of these axons ascend in the contralateral spinothalamic tract. Some fibers arising from lamina V cells enter the dorsolateral and ventrolateral white matter both ipsilaterally and contralaterally to join the spinothalamic tract (Fig 27-3.).

The spinothalamic system is composed of two divisions: the neospinothalamic tract and the paleo-spinothalamic tract. The neothalamic system is characterized by long fibers that make direct connections to the ventrolateral and posterior parts of the thalamus. The third relay of fibers at the thalamic level is relayed to the postcentral gyrus, which represents the primary somatosensory cortex of the brain. This system provides rapid transmission of somatosensory information regarding the location of peripheral stimulation in space, time, and intensity. Although it has only three neurons involved in its transmission, the system sends numerous collaterals to the paleospinothalamic system, which ascends medially to it.

The paleospinothalamic system is associated with short fibers that project to the reticular formation, the pons, and the midbrain. It then connects with the medial intralaminar thalamic nuclei and from there to the limbic forebrain, hypothalamus, and other diffuse areas of the brain. This older system has frequent synapses and slow transmission. Functionally, it provokes a non-discrete, deep unpleasant sensation that motivates the individual into action. Also, it is involved with supra-segmental reflex responses that play a role in respiratory, circulatory, and endocrine functions of the organism.

Another important projection system for transmission of pain is the lemniscal system. It consists of large alpha fibers that enter the dorsal root and pass cephalad through the dorsal columns to synapse with the nucleus gracilis and cuneatus in the medulla. Second-order neurons cross the medulla and ascend in the medial lemniscus to the ventral and medial thalamus.Finally, third-relay neurons project through the internal capsule and corona radiata to the sensory cortex. The large, fast-conducting fibers of this system carry information concerning touch, pressure, vibration, and proprioception. Moreover, the lemniscal system assists in central analysis, assessment, and localization of sensory messages and then modulates, through corticifugal impulses, the sensory input before the action system is activated.

More recently other ascending pathways have been recognized as being important in the study of pain. The spinoreticular multisynaptic ascending system, the spinocervicothalamic system (SCT), the dorsal intra-cornu tract, and other propriospinal systems may play a role in the transmission of nociceptive impulses. Information regarding these alternate systems is sketchy, and their precise function in pain has not been described.

During the past 20 years investigators have attempted to unravel the complexities of the poorly understood, although extremely important inhibitory and facilitory mechanisms of pain acting at all levels of the central nervous system. Dorsal horn cells are modulated by peripheral sensory input. Lamina I cells are inhibited by stimulation of the sensitive mechanoreceptors and high-threshold afferents near the excitatory receptive field but are strongly excited by high-intensity thermal and mechanical stimuli. In contrast, lamina V cells have a wide range of inputs from skin, subcutaneous tissue, muscle, viscera, and other deep structures and are quite responsive to noxious stimuli in their respective field. Inhibition of lamina V cells is produced by stimulation of low-threshold afferents at the periphery of the receptive field.

In addition to local and segmental factors that participate in modulation of sensory information from the periphery to the brain, supraspinal descending neural systems strongly influence synaptic transmission in the dorsal horn and along the course of the ascending somatosensory tracts. The pyramidal tract, rubrospinal tract, and reticulospinal tract have been shown to inhibit firing of the cells in the dorsal horn and other parts of the spinal cord. The descending fibers from the cortex of the brain affect transmission in the thalamus, reticular formation, and dorsal-column relay station. Other fibers from each of these structures descend to lower relay stations and influence their transmission.

Psychological factors play an important role in the total pain experience. Scientific data suggest that various emotional, motivational, cognitive, and affective factors can stimulate areas of the brain that have the ability to inhibit transmission of painful impulses at the spinal cord and various other levels of the neuraxis. Paradoxically, psychological factors can enhance the transmission of noxious impulses to the brain under certain conditions and consequently increase the severity of the pain problem.

To summarize, impulses from afferent fibers are not simply transmitted to the brain by a group of spinal cord cells that are specific for each type of afferent receptor. Rather, the situation is one of convergence, interaction, and control. The gate-control theory proposed by Melzack and Wall in 1965 (Fig 27-4.) is one of the basic pain theories used to explain the complex anatomic and physiologic mechanisms that perform this integration process. This concept of pain suggests that the substantia gelatinosa in the dorsal horn of the spinal cord functions as a gate-control mechanism that increases or decreases the transmission of neural impulses from peripheral fibers to the central nervous system. The somatic input is modulated by the gate mechanism before it promotes pain perception and response. The degree of modulation by the gate is determined by the relative activity in the large (A ) and small (A d and C) fibers and the descending influences from the brain. The neural areas that are responsible for pain perception and responses are only activated when the flow of neural impulses through the gate exceeds a critical level.

Phantom Sensation

In 1551, Ambroise Pare first described the phenomenon of phantom limb sensation. After the Civil War (1871), Silas Weir Mitchell wrote a classic essay on his experience with phantom sensation. His observations resulted from management of 90 amputees from the 15,000 individuals who were estimated to have lost limbs during the conflict. His work pointed out that phantom sensation, with its remarkably constant subjective pattern, is almost universally a sequela of a major amputation.

The term "phantom sensation" is usually reserved for those individuals who have an awareness of the missing portion of their limb in which the only subjective sensation is mild tingling. It is rarely unpleasant; in fact, the majority of amputees describe their phantom sensations as painless. The presence of this phenomenon is usually described in terms of numbness, pressure, position, temperature, or needles and pins. These sensations seem to vary in intensity in individual patients, and the type of sensation described differs with each.

Since the phantom sensation is a painless image, no treatment is necessary. However, consultation with the patient both in advance of amputation and postoperatively is imperative for acceptance of phantom limb sensation as an expected sequela to this type of surgery. The phantom limb may change in its position and character in response to an external stimulus such as wrapping the stump, use of a postoperative rigid dressing, or wearing a prosthetic device. Amputees should be warned that in instances of altered consciousness after the use of certain medications or arousal from a deep sleep there may be a momentary tendency to use the phantom limb for weight bearing or external support with the possibility of an associated injurious fall. Most amputees are aware of the phantom limb immediately after surgery. The pattern of the phantom sensation is usually the most distal portion of the limb, namely, the hand or foot. The extent to which the more proximal segments of the ablated limb are present varies widely among individual amputees. In some patients the limb progressively shortens, with telescoping of the segments proximal to the hand or foot. The duration of the sensation is a matter of years, with only rare instances of complete disappearance of the phantom limb.

Phantom Pain

In contrast to phantom limb sensation, the patient with phantom pain tends to fall into certain broad categories. The three most commonly described painful sensations are (1) a postural type of cramping or squeezing sensation, (2) a burning pain, and (3) a sharp, shooting type of pain. Many patients may complain of a mixed type of pain, but often the major sensation falls into one of these categories.

Variation in the degree of discomfort of the phantom sensation led Feinstein et al. to suggest "that the painful state may be an accentuation or exaggeration of the type of feeling ordinarily experienced in the painless phantom. Thus tingling or pins and needles may become a stabbing type of pain; temperature variations, a burning pain; and postural or positional abnormalities, a cramping pain."

Melzack has listed four major characteristics of phantom limb pain: (1) the pain endures long after healing of the injured tissues and may last for years; (2) trigger zones may spread to healthy areas, and stimulation of these zones will produce pain; (3) phantom limb pain is more likely in patients who have suffered pain in the limb for some time; and (4) phantom pain may be abolished by changes in somatic input.

The causal mechanism of phantom pain remains controversial. Peripheral nerve irritation, abnormal sympathetic function, and psychological factors all contribute to the pain in some manner, yet none of these mechanisms satisfactorily explains the phenomenon of phantom limb pain. Recently it has been proposed that there is a central biasing mechanism in which the reticular formation exerts a tonic inhibitory influence (bias) on transmission at all synaptic levels of the somatic projection system. When amputation surgery destroys a large number of sensory fibers to the reticular formation, the inhibitory influence is diminished. This results in self-sustaining neural activity at all levels that can be initiated by the remaining fibers. If the self-sustaining activity reaches a critical level, pain results.

In 5% to 10% of amputees, painful sensations may occur in the phantom limb from immediately after surgery to years later. They may be episodic or continuous and are variously described as shooting, burning, cramping, or crushing. The pain is usually localized to anatomic regions of the foot or hand because of their greater cortical representation. Exacerbations of phantom pain may be triggered by seemingly innocuous stimuli such as cooling, local heat, or dependent positioning of the stump. Yawning, micturition, defecation, or coughing may suddenly precipitate more severe pain. Emotional disturbances such as anxiety, depression, sleeplessness, and emotional stress can elicit painful attacks but are not the primary cause. In some patients pain can be stimulated by touch or pressing over sensitive areas of the stump called "trigger points." If phantom pain persists for long periods of time, the trigger zones may spread to other unrelated healthy areas of the body.

Although the management of phantom pain is exceedingly frustrating, the task can be made less onerous by a systematic approach to evaluation and subsequent treatment. Initially, a thorough examination of the stump is mandatory to eliminate other causes of stump pain such as adherent scars, neuromas, bursitis, tendinitis, joint contractures, vascular insufficiency, vasomotor and sudomotor disturbances, soft-tissue infection, tumors, or pathologic conditions of underlying bone. A vascular etiology for certain patterns of phantom pain has long been recognized. A consistent inverse relationship has been demonstrated between stump temperature in a painful stump in comparison to the contralateral asymptomatic limb, thus suggesting some correlation with blood flow. Especially in dysvascular amputees with chronic stump pain, a vascular evaluation should be performed, including transcutaneous Po2 determinations or Doppler flow studies. Occasionally, short-term treatment of phantom pain may be successful with the usage of certain drugs that increase peripheral blood flow such as (-blockers (propranolol). In addition, sympathectomy, which increases blood flow to a limb, may also decrease the burning sensation of phantom pain.

Simple treatment measures that create increased peripheral central input may provide at least temporary partial relief of the phantom pain. Certainly one of the more effective adjuncts to the treatment program is extensive use of the prosthesis. Other treatment modalities include gentle manipulation of the stump by massage or a vibrator, stump wrapping, baths, and application of heat with hot packs, microwaves, or ultrasound. Most of these noninvasive techniques are easily learned and can be carried out as a home treatment program without expensive equipment.

No singular drug has been proved effective in long-term control of phantom pain. The use of other than mild analgesic drugs may lead to a serious drug addiction.

Specific "trigger points" on or near the stump may be injected with local anesthetic agents in combination with aqueous steroid preparations. Occasionally, prolonged relief of phantom pain is obtained. However, all too frequently pain recurs at a later date, but repeat injections of the trigger point can be performed at will with little risk or morbidity to the patient.

Amputees with generalized tender areas in the distal portion of the stump that aggravate phantom pain sometimes obtain excellent and prolonged relief with repeated injections of local anesthetic and steroid preparations.

Although the sympathetic nervous system seems to contribute to phantom pain in some way, the success of sympathetic blockade in relief of agonizing phantom pain is unpredictable. At times, abnormal sympathetic manifestations such as excessive sweating, vasoconstriction, decreased skin temperature, or hypersensitivity to light touch may be relieved for prolonged periods by anesthetic block of the sympathetic ganglia. Unfortunately, the phantom pain may not be affected. The greatest success with sympathetic blockade seems to occur when this type of therapy is instituted soon after the onset of pain. Since sympathetic activity is not a major cause of phantom limb pain, surgical removal of a segment of the sympathetic ganglia rarely produces lasting relief of this frustrating pain.

Transcutaneous electrical nerve stimulation (TENS) has been reported as being successful in reducing phantom limb pain on a temporary basis. Even if this technique is only partially successful, it may reduce the patient's requirement for more potent analgesic drugs. This safe and simple technique of neuromodula-tion is designed to diminish chronic pain through low-level stimulation of large myelinated afferent fibers. Since the equipment is portable, patients are able to treat themselves at home. The intensity of stimulation and the length of each treatment session are individualized. The combined use of TENS and appropriate psychotherapy may represent one of the most realistic approaches to the management of phantom pain. However, a recent randomized study of TENS showed no difference in the relief of phantom pain with sham TENS units in comparison to active TENS units during their early postamputee period.

Further exploitation of the inhibitory action of large myelinated afferent fibers in peripheral nerves and the dorsal columns of the spinal cord has been attempted by implantable peripheral nerve stimulators and dorsal-column stimulators, respectively. Although both of these techniques have proved partially effective in the relief of chronic pain, they appear to be no more effective than TENS, which does not have the attendant potential surgical hazards.

Interruption of the anatomic pathways of somatosensory input has led to a wide range of ineffective surgical intervention at all neuroanatomic levels. Surgical procedures for sensory interference range from neurectomies at the periphery, rhizotomies, cordotomies, tractotomies to thalamotomies, cortical ablation, and lo-botomies. In general, the long-term results of these surgical procedures have been disappointing, particularly in view of the associated complaints and risks. Dorsal root entry zone procedures have shown good results in treating isolated phantom pain but poor results in combined stump pain and phantom pain. Therefore, surgical intervention has a well-defined yet limited role in the treatment of chronic amputee pain.

Phantom pain may be controlled or abolished by distraction conditioning, hypnosis, and other forms of psychotherapy. The Minnesota Multiphasic Personality Inventory is a useful means of evaluating the presence of depression, hypochondriasis, and other personality disorders that may be influencing the degree of phantom limb pain.

When considering the multiple treatment modalities suggested for control of phantom pain, it is quite apparent that none of these methods is highly efficacious. Therefore the treatment of every amputee afflicted with this difficult problem must be approached on an individual basis. The ultimate treatment program should consist of carefully selected treatment techniques combined with ongoing psychotherapy and counseling.

Neuromas

The development of a neuroma is a natural repair phenomenon that occurs in any transection of a peripheral nerve. During the repair phase of the nerve the axons lose their architectural parallelism and tend to turn back on themselves and combine with the fibrous repair tissue to form a small enlargement at the distal end of the nerve.

Surgeons have varied in their recommendations regarding the handling of peripheral nerves during the performance of an amputation. Some adhere strictly to gentle traction on the nerve, followed by its division with a sharp scalpel, allowing the nerve to retract several inches above the distal end of the stump. Other surgeons add a single ligature placed slightly proximal to the transection of the nerve to control bleeding from the nutrient vessels. They believe that the ligature per se adds little to the degree of neuroma formation. Virtually no one now advocates injection of a nerve with noxious substances such as alcohol, phenol, or radioactive isotopes.

The importance of neuroma formation lies in its size and location. If the neuroma is located well above the distal end of the stump and is buried in adequate soft tissue, pressure and traction will not be sufficient to produce any local symptoms. Moreover, large neuromas located superficially may not be symptomatic when covered by a carefully fitted prosthetic socket. The pressure of the socket wall can be so well distributed over a large surface area of the stump that no symptoms are elicited at the neuroma site. If the prosthesis does trigger discomfort by stimulation of the neuroma, relief of the socket will generally alleviate the pain.

Injection of the neuroma site with local analgesics and steroids may alleviate the pain. Since pain relief may be only temporary, several injections may be necessary before a lasting remission is obtained.

Large neuromas buried in a scar or located in an exposed position may be so symptomatic that the amputee is severely impaired. Although surgical excision is the treatment of choice, resection of neuromas has failed to yield uniform results. Commonly, relief of pain is quite transient due to the eventual development of a new neuroma. Some of these neuromas may be more easily handled by a proximal neurectomy rather than an extensive exploration of the stump.

Encasement of the nerve stump in a microporous filter sheath (H.A. Millipore) occluded by a Silastic rod has been recommended. Not only has this technique been effective in preventing some cases of recurrent symptomatic neuromas, but it has also decreased phantom limb pain in some patients as well. Similar results have been achieved by producing slow atrophy of the intact nerve above the level of transection. Prolonged nerve compression is obtained by turning a Silastic rod around the nerve trunk 20 to 40 times.

Reflex Sympathetic Dystrophy

Amputations as a result of trauma, particularly partial-hand and foot amputations, may be followed by severe unremitting pain that is entirely out of proportion to the injury or the apparent state of the limb. This burning pain, originally called causalgia, and its variants may be considered together as reflex sympathetic dystrophy.

The cause is thought to be an abnormal prolongation of the normal sympathetic response to injury. This produces vasospasm, hyperhidrosis, and erythema. The pain impulses to the cortex are amplified, and this causes intense discomfort.

In the early stages the remaining dorsal portion of the limb is swollen, warm, and erythematous. There is hyperesthesia, particularly to light touch, and extreme sensitivity to cold. These symptoms make wrapping and wound care extremely difficult.

After about 3 months, the swelling in the remaining digits becomes fusiform. Palmar nodules and fasciitis become evident. Fixed contractures are present because of the lack of active motion.

By 6 to 9 months after the injury, the skin is pale, cool, and dry. The joints are fixed. If pain is still a predominant feature, it is quite likely that it will be persistent indefinitely. One can only hope that this stage of the process is prevented by prior treatment.

Radiographs of the distal bones will show patchy osteopenia, particularly in periarticular areas. There is a loss of bone substance, with up to one third of the inner aspect of the cortex being resorbed. If a technetium 99m etidronate sodium (ethane-1-hydroxy-l, 1-diphos-phate [EHOP]) scan is performed, it will be positive before the bone resorption is visible on plane films.

The early treatment is interruption of the abnormal sympathetic reflex. This is done by sympathetic blocks such as a stellate ganglion block for the upper limb.These may be repeated daily until the pain subsides.

Transcutaneous electrical nerve stimulation has afforded pain relief for patients who have not responded to nerve block. Stilz et al. have shown an increase in cutaneous blood flow with a 1.5 to 2.5C rise in skin temperature with this technique. Nerve stimulation should be strongly considered for those patients whose pain persists after a stellate ganglion block.

Bursitis and Tendinitis

Although uncommon as sources of pain in the amputee, bursitis and tendinitis must be considered in the differential diagnosis of aggravating limb pain. Localized tenderness, slight swelling with mild erythema of the overlying skin, increased localized skin temperature, and occasional soft-tissue crepitation are signs of possible bursitis or tendinitis. Passive stretching of the suspected involved tendon should increase the pain significantly if tendinitis is present. Radiographs of the affected limb segment may demonstrate a calcific deposit in some cases of tendinitis.

Treatment may consist of any combination of several of the following modalities: (1) elimination of any activity that has produced overstress to the involved tendons or localized trauma to affected bursae, (2) rest through reduced use of the involved limb, (3) temporary discontinuance of the prosthesis, (4) possible rigid dressing immobilization for 14 to 21 days, (5) compression of swollen bursae by elastic wraps, (6) application of heat modalities to involved structures, (7) injection of bursae or tendon sheaths with local anesthetic agents combined with steroid preparations, (8) appropriate analgesic drugs, and (9) modification of the prosthetic socket to alleviate local pressure to the stump.

Pain Not Associated With an Amputation

The prosthesis draws the amputee's attention to the involved limb. Thus any pain in the limb may be immediately associated in the patient's mind with the amputation and the prosthesis. This is not always the case. A large number of upper-limb referred-pain syndromes are entirely independent of the amputation or the prosthesis. These need to be remembered and eliminated as the cause.

Referred pain from the neck may masquerade as limb pain. This may be due to cervical disk disease or osteoarthritis and foraminal narrowing. Similarly, lumbar disk disease may produce referred pain to an amputated lower limb. The various vascular and nerve compression syndromes in the neck and axilla are occasionally the cause of pain in an amputee. Cardiac pain may be referred to the limb after an amputation as well as before.

Finally, not all pain has an organic basis. Pain on the basis of a neurotic syndrome or unresolved anxiety may persist long after the wound is healed and the physician has assumed that the patient has completed the acceptance of amputation.

EXTRINSIC CAUSES OF PAIN

Lower Limbs

Syme Ankle Disarticulation

Two common problems that arise in the management of the Syme ankle disarticulate are (1) hamstring pressure when the patient is seated and (2) pain with or without associated skin breakdown over the anterodistal portion of the stump.

The stumps of some Syme ankle disarticulates cannot tolerate full end bearing in the prosthesis. In such cases the proximal portion of the socket can be modified similar to a patellar tendon-bearing (PTB) socket with resultant distribution of partial weight bearing proxi-mally. With faulty socket design patients may complain of soreness and pressure over the posterior aspect of the knee. Usually the patient is relatively comfortable in the upright position but has significant discomfort when sitting with the prosthetic foot resting squarely on the floor.

Pressure on the biceps femoris and semitendinosus produces hyperemia of the skin in the area of the distal portion of these tendons. The involved skin and tendons are tender to palpation. If the pressure gradient increases, superficial skin ulceration may occur.

Lowering the posterior brim of the socket to a point just distal to the center of the patellar bar and increasing the flare of the brim are ordinarily ample to alleviate the hamstring pressure.

High floor reaction forces are generated between heel-off and toe-off, and these forces must be dispersed over a large enough area of the anterior portion of the stump to prevent pain and possible skin breakdown. The anterior trim line of the socket must be placed at the level of the inferior pole of the patella to provide an adequate area of interface between the anterior portion of the stump and the front of the prosthesis.

Transtibial (Below-Knee) Amputation

Common causes of prosthetic pain in the transtibial amputee are (1) excessive end bearing, (2) uneven skin pressure, (3) frictional skin loss, (4) loss of total contact, (5) hammocking phenomenon, and (6) inlet impingement. Evaluating the complaint of pain is simply a systematic process of ruling out each of these causes and then applying the appropriate solution for its correction.

Excessive End Bearing.-If end bearing is a source of limb discomfort, commonly specific physical signs are present on examination of the stump. Often a callus is located over the distal end of the tibia and/or fibula. Also, there may be palpable bursae over the distal end of the tibia or fibula as further evidence of end bearing.

When the prosthesis is applied, the stump descends too deeply into the socket. The addition of an appropriate number of stump socks to raise the stump from the distal portion of the socket should provide prompt symptomatic relief.

If a physical examination is inconclusive and the possibility of end bearing warrants further evaluation, other techniques will aid in the diagnosis. The simplest method is to put a small ball of clay in the bottom of the socket and ask the patient to walk. Clay that is severely compressed is a crude indicator of excessive load bearing at the distal end of the stump.

A more informative test is the use of a Brand micro-capsular stocking. This system is composed of cotton fabric with a polyurethane lining into which encapsulated blue dye has been sprinkled. A stump sock is constructed from the basic material and then placed carefully over the stump. Next, the prosthesis is applied, and the patient is asked to walk. With increasing gradients of pressure, the microcapsules of dye are ruptured, and there is a color change from light yellow to various hues of green to deep blue. The use of this stocking locates any area of pressure quite precisely, but the amount of pressure is only grossly quantified.

Other careful tests include radiographs of the stump through the socket, with or without dye contrast medium injected around the stump; thermography; thermistor studies; and the use of a transparent check socket. Although radiographs provide information solely in a static loading condition, they are helpful in determining the adequacy of total contact of the socket. This is particularly true if a contrast medium is injected between the interface of the stump and the socket wall.

The use of a clear check socket gives similar information, but under conditions of both static and dynamic loading. A clear check socket can be made from a plaster positive mold of the existing socket, and then the degree of end bearing can be analyzed by direct visualization and probing the stump surface through multiple holes drilled in the socket distally. If evidence exists of excessive loading of the distal end of the stump, a new cast should be taken of the stump from which a new transtibial prosthesis is fabricated. This can be preceded by the use of a second clear check socket to confirm total contact in the new socket.

Positive thermograms will demonstrate an increased skin temperature in the area of end bearing. Repeat thermograms after appropriate prosthetic adjustment should show a reversal of the temperature gradient toward normal at the end of the stump. Such evidence corroborates the resolution of excessive end bearing as a source of stump pain.

The most frequent reason for end bearing is a reduction in stump volume. Although this problem may be temporarily alleviated by adding more socks, there is a limit to which this solution may be used. A large number of stump socks will cause increased pressure on the stump at the inlet of the socket and may further complicate the existing problem by producing choking of the stump or skin pressure problems at the proximal end of the stump. If the patient is using a socket liner, exterior pads may be added at various locations on the liner to compensate for the stump volume loss. Again, the benefit in regaining improved socket fit through this technique may be offset by problems produced by increased skin pressure at the level of the adjustment pads. Unless the problem is easily resolved, in the long run it is preferable to fit the patient with a new socket.

Uneven Skin Pressure.-A common problem produced by an ill-fitting socket is uneven distribution of skin pressure over bony prominences. Frequently, involved areas are the head of the fibula, tibial tuberosity, distal pole of the patella, and distal ends of the fibula and tibia. Occasionally, the condyles of the tibia may show evidence of increased soft-tissue pressure.

Fluctuating stump volume is a major cause of unequal skin pressure distribution. With a reduction in stump size secondary to the loss of edema, muscle atrophy, or excessive weight loss, the intimate contact between the surface of the stump and the socket is altered. Thus the stump may shift slightly distally in the socket. Even minor distal displacement may apply forces of a higher magnitude over various surface contours.

Other causes of uneven skin pressure include excessive use of stump socks, increased stump growth, and increased stump volume due to muscle hypertrophy, weight gain, or edema. On physical examination there is significant erythema of the skin overlying involved bony prominences. Although this skin has good capillary refill, the redness will persist for several minutes to several hours after removal of the socket. Even with minimal skin changes, the patient is usually very specific about areas of tenderness and can point directly to the involved area. With higher pressure gradients, the skin may have a deep violaceous color and be tender to palpation. With the use of multiple stump socks, ridges or indentations in the skin from the weave of the stump sock material may be present in areas of high pressure. In amputees who persist in walking despite considerable discomfort, superficial skin ulceration or blistering may occur. If the skin has resisted breakdown, the area of involvement may respond by formation of a callus or corn. The distal portion of the stump may have chronic lymphedema with associated generalized rubor, both of which are secondary to choking because of the tight fit at the inlet of the socket.

When the patient dons the prosthesis, the stump may be in the socket to the proper depth, but the anteroposterior or mediolateral diameters may be very snug. Frequently, a large number of stump socks are being worn. The stump socks will elevate the stump from the socket with resultant loss of distal stump contact and alteration in the interface between the contours of the socket and stump surface.

The first step in evaluating this problem is checking the relative lower-limb lengths by comparing the level of the iliac crests in the standing position. If the patient is long on the prosthetic side, this may indicate that the stump is not in the socket to the proper depth. Removing a few of the stump socks might correct this misfit and substantially relieve the patient's discomfort during standing and walking.

If the patient's socket is too tight as a result of increased stump volume or limb growth, skin redness, localized tenderness, and vivid stocking marks will be present. The use of a microcapsular stocking will dramatically outline the areas of increased pressure. Radiographic studies are seldom necessary in this situation, unless the examiner is concerned about the adequacy of total contact at the distal end of the stump. More precise information regarding areas of specific skin loading can be determined by use of a transparent check socket.

An easy therapeutic as well as diagnostic tool is reduction of the thickness of the socket wall in areas of skin discoloration and pain. If the patient is comfortable in standing and walking after adjustment of the socket, the problem is both identified and resolved. If all conservative measures of socket readjustment fail, fabrication of a new total-contact socket may be the only solution.

Frictional Skin Loss.-Superficial frictional blisters are a deterrent to prosthetic comfort and effective gait training. This phenomenon is predominantly seen in new amputees. Possible underlying pathomechanics include (1) highly localized shear forces to skin over bony prominences, (2) immature epithelium in areas of secondary healing of the surgical incision, (3) obstruction of venous and lymphatic outflow with vertical positioning of the limb and resultant localized edema blebs in regions of secondary healing, or (4) the presence of an extension contracture of the knee.

Physical examination reveals a superficial blister or shallow ulcer with surrounding erythema. The skin appears thin, shiny, and immature. The lesion may be surprisingly devoid of significant tenderness. However, if the condition is not recognized and treated, the lesion will increase in size and be accompanied by progressive discomfort.

Slight alteration of socket fit due to increased stump volume is a common cause of this type of skin breakdown. Among new amputees variability in stump volume from day to day is a constant hazard. Despite extensive efforts toward excellent stump compression and judicious inspection of the limb during gait training, development of a skin blister or small ulcer is likely to occur even under the supervision of an experienced prosthetic team. The transient change in socket fit is subtle, and it is sometimes difficult to detect. Consequently, the combination of increased skin compression over localized areas of the stump surface along with alteration of socket fit and possibly greater shear stress secondary to piston action of the socket resulting from inadequate suspension will produce a friction blister or ulcer.

Improper socket fabrication can create skin breakdown. If the anteroposterior diameter of the socket is too large, during sitting the anterior wall of the socket will displace forward from the anterior surface of the stump and generate increased compression and shear forces over the anterodistal portion of the stump. This error can be compounded by inaccurate placement of the pivotal axis for the suspension straps on the medio-lateral aspect of the socket. If the posterior trim line is too high or there is an extension contracture of the knee, the stump will be levered upward from the distal end of the socket, and again, the forces against the anterodistal stump surface are significantly increased. Provided that stump volume control is not a problem, ulceration over the anterodistal surface of the stump should direct the clinicians attention to careful scrutiny of the anteroposterior diameter of the socket in the standing and sitting positions. While the patient is seated, the anterior wall of the socket can be forced backward against the front of the stump. By placing a hand inside the posterior wall of the inlet, one can determine the tightness of the anteroposterior diameter. At the same time the location of the pivot point of the suspension system should also be checked.

In the early stages of gait training recent amputees have difficulty controlling the forces against the stump by proper coordination of knee and body action. If a prosthetic foot with a firm heel wedge is used, the end of the stump may be thrust forward against the anterior socket wall as the patient attempts to control the prosthesis at heel strike with active knee extension. The resultant discomfort and potentially hazardous skin pressures can be corrected by switching to a softer heel wedge, increasing plantar flexion of the foot (or extension of the socket), or moving the foot forward.

The occurrence of a blister or ulcer should signal the discontinuance of the prosthesis until the lesion is healed. During this time proper stump wrapping must be done continuously. Range-of-motion and muscle strengthening exercises should be carried out at the knee and hip. Any design discrepancies of the socket should be corrected before the patient returns to walking. With closure of the lesion and gaining control of the stump volume, prosthetic training can be initiated with skin inspection at frequent intervals and graduated periods of stump loading until skin tolerance is achieved.

Loss of Total Contact.-Satisfactory total contact over the distal portion of a stump is difficult to maintain when stump shrinkage or loss of weight occurs. The use of multiple stump socks to maintain a proper fit at the inlet of the socket is insufficient to regain total contact over the lower portion of the stump. The patient may complain of excessive tightness about the knee while still feeling looseness in the distal portion of the socket. Subsequently, choking of the stump may occur with gradual development of lymphedema in the lower portion of the stump. Chronic edema encourages the development of stasis pigmentation and hemorrhagic papules and nodules of the distal portion of the stump. In some instances, the skin takes on a characteristic hypertrophic Assuring called verrucous hyperplasia. In individuals with vascular insufficiency, particularly those with diabetes mellitus, progressive lymphatic and venous outflow obstruction may produce a stasis ulcer at the distal end of the stump. Failure to recognize this condition and to take appropriate corrective steps will only lead to gradual worsening of the soft-tissue ulceration.

The first step in the remedy of this condition is removal of the ill-fitting socket and application of appropriate topical treatment combined with continuous stump wrapping. With re-establishment of proper limb volume and healing of the stasis ulcer, a new total-contact transtibial socket should be prescribed.

Hammocking Phenomenon.-A somewhat uncommon, but frustrating problem is the development of localized skin abrasion or ulceration produced by the hammocking effect of a stump sock. This peculiar problem is the result of two major factors. First, there is a lack of total contact over the distoposterior aspect of the stump. Second, because of snug anteroposterior and mediolateral diameters at the midportion of the socket, the stump sock is suspended at this level as the prosthesis is donned. Consequently, the posterior side of the stump sock is drawn tightly against the distoposterior aspect of the stump. Edema gradually develops in the lower portion of the stump with use of the prosthesis. The combined effect of the tight sock and stump edema is significantly increased compression and shear forces over the posterior flap that may produce a skin ulcer. The unusual location of this ulcer should be a clue to its possible cause. More definite proof of the cause can be obtained by radiographs through the socket and the use of a clear check socket taken from the existing prosthetic socket.

A temporary solution to the problem may be obtained by altering the anteroposterior and mediolateral diameters of the socket, the use of a Daw nylon sheath, and Silastic foaming of the distal aspect of the socket. The definitive solution is refitting the amputee with a new total-contact socket with proper dimensions.

Inlet Impingement.-If the posterior trim line of a transtibial socket is too high posteriorly or the channels for the biceps femoris and semitendinosus tendons are inadequate, discomfort may result from pressure being applied against the hamstring tendons or the skin of the popliteal area with increased flexion of the knee. The amputee complains of tenderness and chafing of the skin behind the knee and in the region of the biceps femoris or semitendinosus tendons. The discomfort is made worse by sitting or excessive bending of the knee. Physical examination reveals redness and chafing of the skin along the course of the involved tendon and associated point tenderness. The skin may have a superficial ulceration where the pressure is maximal. The diagnosis is self-evident by inspection of the relationship of the posterior aspect of the socket with the back of the knee and hamstring tendons as the knee is flexed. Elimination of the source of the problem can be achieved by lowering the posterior trim line or deepening the channels for the hamstring tendons.

Transfemoral (Above-Knee) Amputations

Prosthetic causes of pain in the transfemoral amputee include (1) excessive pressure on the ischial tuberosity, (2) adductor roll, (3) choking, (4) malalignment, (5) inlet impingement, (6) excessive end bearing, (7) pressure from a high anterior wall, and (8) a high medial wall. As in the transtibial amputee, one must systematically eliminate each of these problems as the cause of the patient's complaint.

Excessive Pressure on the Ischial Tuberosity.-Improper design of the ischial seat may result in significant discomfort with either standing or walking. Any decrease in stump volume that allows greater distal displacement of the stump results in increased compression and shear forces over the ischial tuberosity. The patient often finds that he can obtain transient relief of his discomfort by sitting or lying down. However, if the ischial seat is too wide, even sitting may produce ischial symptoms.

Localized tenderness and skin changes ranging from hyperemia to frank skin breakdown are the hallmark of ischial seat pressure. If the increase in pressure is gradual, the involved skin will respond by forming a typical callus.

Checkout of the socket fit reveals no obvious problems except firm contact of the ischial tuberosity against the ischial seat. When the patient is asked to stand with full weight bearing on the contralateral limb and then to shift the weight gradually onto the prosthetic side, the degree of compression against an examining finger between the tuberosity and the ischial seat is obviously high. Further corroboration of ischial seat pressure can be demonstrated with the use of a microcapsular stocking or thermography.

When the pressure over the tuberosity is marginal, the addition of more stump socks will elevate the stump slightly and distribute some of the load bearing to the surrounding gluteal musculature. In the case of a suction socket the prosthetist may apply a liner pad along the interior of the posterior wall that will tighten the anteroposterior diameter and accomplish the same purpose. Lowering the ischial seat or increasing its radius may produce effective results for some patients. If these simpler measures fail, a new total-contact transfemoral suction socket should be prescribed.

Adductor Roll.-With improper stump wrapping, increased stump volume, or unsatisfactory socket fit, a horizontal bulge of soft tissue, or adductor roll, may develop high on the medial aspect of a transfemoral stump. The size of this roll may eventually prevent the amputee from donning the prosthesis properly. If the roll is excessive, the patient may complain of pain and tenderness along the inferior border of the roll due to impingement against the upper edge of the medial wall of the socket.

An adductor roll causes a relative lengthening of the prosthetic limb and a variety of gait deviations. When standing, the iliac crest on the involved side is higher than on the contralateral side. The patient may be forced to circumduct the prosthesis or vault on the opposite lower limb to clear the foot during swing phase. Or the patient may walk with the limb in abduction to reduce the medial wall pressure against the adductor roll. Palpation confirms the position of the ischial tuberosity well above the ischial seat. The adductor roll is easily felt on the inside of the stump above the brim of the medial wall.

Examination following removal of the prosthesis reveals a somewhat firm, tender roll of soft tissue with a horizontal orientation in the adductor region of the thigh. Inspection of the inferior margin of the roll may reveal considerable erythema but rarely any evidence of superficial ulceration. Often there is associated brawny edema of the distal end of the stump with early stasis changes of the skin because of the loss of total contact distally.

A combination of correct stump wrapping with modification of the prosthetic socket is quite likely to resolve the adductor roll problem. If the roll is small, drilling a hole in the distomedial aspect of the socket and using a pull-through sock to advance the proximal stump tissues into the socket will compress the roll against the medial wall. Subsequent atrophy of the roll provides an improved socket fit. When adductor roll is extensive, it is preferable to fit the amputee with a new total-contact quadrilateral socket and anticipate the fabrication of a second socket at a later date as the proximal end of the stump changes shape.

Choking.-Constriction of the proximal portion of a transfemoral stump impedes venous and lymphatic outflow from the remainder of the stump. Excessive use of stump socks, weight gain, musculoskeletal growth, and limb swelling are some of the causes of stump choking. Resultant stump abnormalities include the absence of stump sock markings over the distal part of the stump, along with associated palpable edema, generalized skin redness, and a possible adductor roll. If severe, the skin may show typical stasis changes that eventually lead to verrucous hyperplasia. Stasis ulceration may be a late-stage sequela, but it is rather uncommon.

Usually careful assessment of the amputee while wearing the prosthesis will suffice in elucidating the nature of the problem. Almost inevitably the stump is riding partially out of the socket. Therefore the ischial tuberosity is well above the ischial seat; the ipsilateral iliac crest is elevated, thus creating pelvic obliquity, and the patient walks with some type of gait deviation such as abduction of the hip, circumduction of the prosthesis, or vaulting on the intact limb.

If confirmation of the loss of total contact is necessary, a clay ball compression test, radiographs through the socket, or a microcapsular stocking are helpful techniques. Seldom is a clear check socket necessary.

The resolution of choking should be approached initially by improving the socket fit through removal of unnecessary stump socks, use of a pull-through sock, improved stump wrapping, socket relief, and foaming the lower end of the socket to regain total contact. If these measures are only partially effective, the definitive solution is fabrication of a new socket.

Malalignment.-In the short transfemoral amputee, the degree of adduction of the lateral wall should be as much as conditions permit. Also, the lateral wall must be precisely contoured to evenly distribute the socket pressures over the largest possible surface area during midstance. Despite careful socket design, the patient may complain of progressive pain and soreness over the distolateral aspect of the stump. To alleviate the concentration of forces in this area during walking, he must incline the trunk laterally over the prosthesis to shift the weight line closer to the support line. His base of support may be widened by abduction of the hip as well.

Examination of the stump reveals no striking features except for varying degrees of skin erythema and localized tenderness in the area of increased pressure. The socket fit is nearly always satisfactory. Use of a microcapsular stocking or thermography are the most practical means to verify the increased local pressure to the stump.

Alignment adjustment through reducing the adduction of the socket and out-setting the prosthetic foot usually eliminates this problem.

Inlet Impingement.-An occasional source of pain in the anteromedial aspect of the transfemoral stump is irritation of the upper portion of the adductor longus and gracilis muscles. This occurs when the adductors are impinged by a narrow adductor channel of the socket. Physical examination rarely demonstrates any evidence of change in the stump except for point tenderness over the adductor longus and gracilis. This finding should suggest the cause of the patient's complaints. A diagnostic as well as treatment method consists of routing the adductor channel to increase its size. With this modification the patient is frequently relieved of his pain.

Excessive End Bearing.-As in the transtibial amputee, the reduction of stump volume or a significant drop in body weight will change the socket fit dramatically. The stump is able to descend deeper into the socket since all total contact with the socket surfaces has been lost. The rate and magnitude of stump volume loss determine the degree of pain and associated soft-tissue changes in the distal end of the stump. The physical findings are comparable to those of a transtibial stump, namely, hyperemia of the skin with possible bursitis over the distal third of the femur, localized soft-tissue tenderness, callus formation, and occasional superficial ulceration.

Positive physical findings include (1) relative shortening of the prosthetic limb, (2) displacement of the ischial tuberosity forward and distal to the seat, and (3) gait abnormalities consisting of a rapid swing phase with reduced stride length of the uninvolved limb and a shortened stance phase on the prosthetic side. Patients with minimal end bearing may be more accurately diagnosed by a trial of additional stump socks, a clay ball compression test, microcapsular stockings, socket radiographs, or a clear check socket. In suction sockets or sockets with openings for pull-through socks, the stump may be evaluated both visually and manually.

The addition of more stump socks may be the only treatment required in amputees with mild end bearing. Relief of the distal end of the socket and lining the socket to decrease the anteroposterior and mediolateral diameters may suffice in moderate cases. In more advanced circumstances the best remedy is fabrication of a new total-contact socket.

Any associated skin ulceration can be treated with appropriate topical care and stump wrapping. The underlying bursitis often responds to the relief of socket pressure and stump wrapping. Aspiration combined with injection of a local anesthetic agent and a corticosteroid preparation administered under sterile technique will often eradicate a more persistent bursitis that has failed to respond to noninvasive treatment. In the small number of amputees who are greatly disabled by chronic bursitis, surgical excision may be necessary.

Pressure From a High Anterior Wall.-The purpose of the anterior brim of the socket is to maintain the ischium in proper relationship to the ischial seat to prevent discomfort with ischial weight bearing. This is accomplished by building the anterior brim 5 to 6.5 cm (2 to 2 in.) higher than the ischial seat, flaring the margin of the brim generously, and bulging the inner wall of the brim in the area of Scarpa's triangle. Ordinarily, the high front does not interfere with sitting or bending over, provided that there is no contact with bony prominences of the pelvis and a channel is provided for the rectus femoris muscle. However, an obese transfemoral amputee with a protuberant abdomen or massive pan-niculus may experience pinching of lower abdominal soft tissues with sitting or bending over. It is rare to have any difficulty with standing or walking.

Customarily, the socket fits well otherwise. When the patient sits or leans forward, palpation demonstrates high compression against the lower abdominal tissues. With the prosthesis removed, the only localizing signs are erythema of the skin, varying degrees of tenderness in the areas of pressure, and occasional small hemorrhagic lesions secondary to contusion of the skin. Judicious lowering of the anterior wall and increasing the flare of the brim usually provide prompt relief.

High Medial Wall.-In a properly fitted quadrilateral socket essentially no weight should be borne by the medial wall. The upper third of the medial wall should be flattened and the superior brim flared to prevent skin irritation. Although the medial wall should be as high as tolerated, it is usually 0.3 to 0.6 cm (1/8 to 1/4 in.) lower than the ischial seat. With pelvic tilt, excessive adduction of the socket, or too much length of the medial wall, the amputee will develop pain and tenderness in the region of the origin of the adductor muscles as well as along the pubic ramus. The patient compensates for these changes while walking by maintaining a wide base of support by abduction of the hip during both stance and swing phase. Relief is provided by lowering the medial wall and flaring the superior brim.

Summary

The major prosthetic causes of pain in the lower limb are volumetric changes, malalignment, and inlet impingement. Comparison and contrast are best summarized in Table 27-1..

Upper Limbs

Partial-Hand Devices

Strict adherence to the surgical dogma of preserving all possible segments of an injured hand may result in chronic pain compounded by significant functional problems. For example, digits afflicted with post-traumatic vasomotor changes secondary to altered sympathetic innervation can be detrimental to patients because of episodic pain associated with increased cold sensitivity. Should reflex sympathetic dystrophy or cau-salgia develop, the recovery of hand usefulness is obstructed, and the difficulty of fitting the patient with an appropriate orthotic or prosthetic device is definitely magnified. Massive damage to joints and their related tendons may virtually ensure extensive permanent functional loss and pain since associated vascular and neurologic recovery of the hand is marginal at best. Unfortunately, insufficient venous and lymphatic drainage creates chronic swelling of the hand, thus adding another factor that enhances hand impairment. Worse yet, poor skin coverage and diminished epicritical sensation further complicate functional retraining of an injured hand with or without a special device.

To maximize the rehabilitation process of an injured hand, critical decisions regarding the preservation of those segments of the hand that have a reasonable likelihood of regaining nonpainful, useful function must be made by the attending surgeon during initial treatment. If the patient fails to make satisfactory progress during the rehabilitative period, consideration should be given to secondary reconstructive surgery that would involve a higher functional amputation. Removal of part or all of a painful, functionless hand with subsequent replacement by a well-designed prosthesis is welcomed by most patients.

In general, partial-hand prostheses have satisfied neither the cosmetic nor the functional needs of the hand amputee. Faulty design, poor material properties (weight, thermal conductivity, surface friction characteristics, strength, durability, etc.), inadequate device suspension, reduction of sensory feedback, and possible restriction of proximal joint motion are only a few of the reasons for prosthetic failure.

If, after prosthetic fitting, the patient with a hand amputation complains of discomfort, every effort should be directed toward evaluation and elimination of all potential pain sources. Assessment of the adequacy of skin coverage is simple but absolutely essential. A tethered, noncompliant scar is unyielding to shear forces that produce definite skin tenderness and discomfort with possible associated skin breakdown. Careful inspection and palpation of the involved hand provide sufficient information to estimate the probable skin tolerance to compression and shear stress from a proposed prosthetic device. If it is questionable whether the skin can tolerate such forces directly, the device should be lined with Plastazote, Pelite, polyurethrane, or comparable materials that will protect the damaged skin surfaces.

The painful hand with increased cold sensitivity often manifests coolness, cyanosis, edema, and excessive sweating. These vasomotor and sudomotor disturbances are similar to those of sympathetic reflex dystrophy. Characteristic signs of Raynaud's phenomenon may be elicited by exposure of the hand to a cold environment. These amputees should be instructed to avoid any exposure of the hand to environmental temperatures below 10C without an insulated glove. Furthermore, all partial-hand devices used in a cold environment should be constructed of material with poor thermal conductivity and lined with a synthetic substance with excellent insulation properties.

Wrist Disarticulation

Almost without exception the major reason for pain in individuals wearing a wrist disarticulation prosthesis is irritation of the soft tissue over the ulnar and radial styloid processes. With any reduction of total contact in the region of the distal radioulnar joint, the distal end of the stump tends to rotate independently of the prosthetic wall during pronation and supination of the forearm. The torsion of the prosthesis creates a high shear force across the skin in the region of the radial and ulnar styloid processes. In addition to localized pain, repetition of these forces across the involved skin produces reactive hyperemia, localized soft-tissue tenderness, and possible skin ulceration.

Detection of the source of pain and irritation is often a simple matter of careful inspection of the distal end of the amputation stump. If localizing signs are scant, the use of a microcapsular stocking may demonstrate increased localized pressure in the region of the ulnar and radial styloids. Seldom is it necessary to resort to radiographs through the socket, clear check sockets, or thermograms.

Foaming of the distal end of the socket with Silastic to regain satisfactory total contact is usually adequate in relieving this problem. If the volumetric loss of the stump is high, it is preferable to fabricate a new wrist disarticulation socket. When the problem may be the result of increased soft-tissue edema or a tight distal socket, relief in the area of skin pressure provides an easy solution.

In those few patients with chronic skin problems despite frequent adjustments and redesigning of the wrist disarticulation socket, surgical revision of the stump may be necessary. In the presence of adequate skin flaps, resection of prominent ulnar or radial styloids can be accomplished without the loss of important radioulnar joint motion, which is critical to the preservation of forearm pronation and supination.

Transradial (Below-Elbow) Amputation

Three frequent causes of pain in the transradial prosthetic wearer are (1) pressure over the anterodistal end of the stump, (2) choking of the stump, and (3) inlet impingement.

Amputees with acquired short transradial stumps are vulnerable to high compression and shear forces across the anterodistal aspect of the stump when lifting heavy loads with the elbow in a flexed position. Conditions are only made worse by (1) poor total contact of the socket distally as a result of stump shrinkage, (2) inadequate soft-tissue coverage over the distal end of the radius and ulna, and (3) osteophyte formation or apposi-tional bone growth of the forearm bones.

Whatever the cause, the symptoms and signs are similar-localized stump pain, tenderness of the distal end of the stump, reactive hyperemia of the skin, possible presence of an underlying bursa, and occasionally a skin ulcer. A lack of total contact may result in edema and induration of the distal portion of the stump as well.

Careful inspection of the stump localizes the area of increased skin pressure. With the artificial limb applied, strong resistance during elbow flexion will usually produce discomfort at the distal end of the stump. Seldom is it necessary to use a microcapsular stocking, socket radiographs, or thermography to determine the nature of the patient's complaints. Roentgenograms of the stump are valuable, however, in the detection of offending osteophytes or excessive appositional bone growth in the juvenile amputee.

Treatment should be directed initially toward healing the skin ulceration and reduction of stump edema if present. Next, socket relief distally or foaming the end of the socket with Silastic may eliminate skin pressure. In certain patients, a new total-contact socket is required.

The juvenile amputee is faced with periodic loss of socket fit as a result of musculoskeletal growth. With increased circumference and length of the stump, the socket is too small to accept the entire stump. As a result, increased forces over the distal end of the stump create painful pressure symptoms that reduce the functional efficiency of the amputee. Recognition of an improper socket necessitates replacement with a properly fitted one.

Transradial amputees with stump soreness will often increase the number of stump socks to relieve pressure against the end of the stump. This leads to elevation of the distal portion of the stump from the end of the socket and obstructs venous and lymphatic outflow from the stump because of constriction of the proximal portion of the stump. The resultant choking of the stump is painful and may produce skin changes of the distal end of the stump.

Inspection of the stump reveals an absence of sock markings over the distal portion of the stump. The lower portion of the stump is swollen and tender. There may be generalized reactive hyperemia of the skin of the stump. The proximal portion of the stump may have stump sock indentations indicating increased skin pressures. With the prosthesis donned the olecranon lies above the trim line of the posterior aspect of the socket, and this indicates a loss of socket fit.

Removal of some of the stump socks will often achieve an improved fit of the socket. If edema prevents continued use of the socket, it may be necessary to resort to continuous wrapping for a few days. With elimination of the edema of the stump, satisfactory total contact and stump protection can be obtained by foaming the socket with Silastic. If a tight inlet is responsible for choking the stump, routing the socket walls will aid in opening the inlet.

A Minister socket may produce impingement of the humeral condyles or the olecranon during the application of a vertical traction force with the elbow flexed to 90 degrees or with the elbow in maximum extension. Since this type of socket must be designed with restriction of complete extension of the elbow to maintain adequate suspension, excessive traction in the extended position would be expected to produce some discomfort over the humeral condyles or olecranon with high axial loads. However, some amputees find that with active flexion of their elbow they feel pressure over these bony prominences. This leads to localized pain and skin changes that usually can be corrected by socket relief or alteration of trim lines without sacrificing good socket suspension. Failure to diminish elbow impingement by means of socket adjustments dictates fabrication of a new socket in greater extension.

Transhumeral (Above-Elbow) Amputation

As in the transradial prosthesis wearer, the magnitude of forces applied to the anterodistal aspect of the transhumeral stump is significantly increased with progressive loading of the prosthesis. If the stump is quite short, total contact is poor, or soft-tissue coverage of the stump is less than optimal, the symptoms and physical findings of the involved stump are identical with high soft-tissue forces over any bony prominence. Careful physical examination is usually adequate to identify the cause of the problem. If necessary, confirmatory tests with a microcapsular stocking, thermography, or radiographic studies can be performed. Prosthetic solutions include relief of the distal portion of the socket, foaming of the distal end of the socket to regain total contact, or fabrication of a new socket. Stump revision may be required in the presence of poor skin coverage, bony overgrowth of the humerus, or extreme soft-tissue redundancy.

In the short transhumeral amputation, the anteroposterior walls of the socket must be extended medially over a large portion of the shoulder joint to provide rotational stability. Excessive tightness of the anteroposterior diameter of the medial portion of the inlet will produce pressure against the skin along the edges of the socket brim. Altering the trim lines, heating and rolling the brim edges, or increasing the anteroposterior diameter of the inlet will eliminate the pressure problem.

Children with acquired transhumeral amputations are plagued by troublesome appositional bone growth of the humerus. The gradual lengthening of the humerus compresses the skin over the distal end of the bone against the bottom of the socket. Associated pain when wearing the prosthesis interferes with its optimal use. Soon skin changes appear and may be accompanied by a swollen bursa over the end of the bone. As discomfort increases, the child periodically removes the prosthesis or refuses to wear it at all.

Early in the evolution of the problem, removal of an existing socket liner and/or deepening of the end of the socket will provide temporary help. However, with further bony overgrowth, the amount of stump change exceeds the improvement obtained with socket adjustments. Now the treatment of choice is surgical revision of the stump, which includes excision of the bony overgrowth and removal of any bursa. Since appositional bone growth is unrelated to epiphyseal growth, epiphy-siodesis is absolutely contraindicated. This condition tends to recur periodically so that the child is likely to have several surgical procedures until reaching skeletal maturity when general bone growth ceases. A Silastic bone plug has been recommended to prevent recurrence of appositional bone growth. However, its use has not been widespread.

Shoulder Disarticulation

Achievement of proper prosthetic suspension and total-contact fit of the socket is difficult in the shoulder disarticulation amputee. The weight of the prosthesis tends to create a downward displacement and rotation over the acromion. Combined high compression and shear forces generated over the tip of the acromion cause localized pain and concomitant skin changes. Lining the involved portion of the socket wall with Plasta-zote, Pelite, or similar synthetic materials distributes the forces over a larger skin surface area, thus making the soft-tissue pressure more tolerable. Adjustment or redesigning the suspension system will also reduce the rotary action of the socket.

Meticulous socket design usually minimizes soft-tissue pressure problems over the anteroposterior aspect of the shoulder girdle. Subsequent alterations of tissue forces as a result of soft-tissue shrinkage, edema, or musculoskeletal growth can be managed by socket relief, socket lining, or increased socket dimensions by routing the socket wall.

Forequarter Amputation

Most of the discomfort associated with fitting a fore-quarter prosthesis is caused by uneven distribution of soft-tissue pressure. Suspension problems with this type of prosthesis are immense, and contouring the socket wall to accommodate uneven bony prominences and bulky soft tissues is most difficult. The use of the lightest possible prosthetic components minimizes the downward displacement of the device. Lining the socket wall with compliant synthetic materials improves soft-tissue pressure distribution. Considerable prosthetic discomfort may usually be prevented by adjustments of the trim lines; periodic checking of socket contact with the thoracic wall, base of the neck, and opposite shoulder region; and alteration of the suspension system.

References:

  1. Blankenbaker WL: The care of patients with phantom limb pain in a pain clinic. Anesth Analg 1977; 56:842-846
  2. Bonica JJ: Causalgia and other reflex sympathetic dystrophies. Postgrad Med J 1976; 53:143-148
  3. Bonica JJ: Neurophysiologic and pathologic aspect of acute and chronic pain. Arch Surg 1977; 112:750-761
  4. Brand PW, Ebner JD: Pressure sensitive devices for denervated hands and feet. J Bone Joint Surg [Am] 1969; 151:109-116
  5. Carron H, Weller RM: Treatment of post traumatic sympathetic dystrophy, in Bonica JJ (ed): Advances in Neurology, vol 4, Pain. New York, Raven Press, 1974
  6. Casey KL: Pain: A current view of neural mechanisms. Ami Sci 1973; 61:194-200
  7. Ersek RA: Transcutaneous electrical neurostimulation: A new clinical modality for controlling pain. Clin Orthop 1977; 128:314-324
  8. Feinstein B, Luce JC, Langton JNK: The influence of phantom limbs, in Klopsteg PE, Wilson PD (eds): Human Limbs and Their Substitutes. New York, McGraw-Hill, International Book Co, 1954, pp 79-138
  9. Ferguson JP, et al: Neurosurgical management of intractable pain. NC Med J 1973; 34:707-710
  10. Finsein V, Persen L, Lvlien M: Transcutaneous electrical nerve stimulation after major amputation. J Bone Joint Surg [Br] 1988; 70:109
  11. Foort J: The patellar-tendon-bearing prosthesis for below knee amputees: A review of technique and criteria. Artif Limbs 1965;9:4-13
  12. Frazier SH, et al: Psychiatric aspects of pain and the phantom limb. Orthop Clin North Am 1970; 1:481-495
  13. Hampton FL: Prosthetic principles in the lower extremity amputee. Orthop Clin North Am 1972; 3:339-347
  14. Henderson WR, Smyth GE: Phantom limbs. J Neurol Neurosurg Psychiatry 1948; 11:88-112
  15. Iacono R, Linford J, Sandyk R: Pain management after lower extremity amputation. Neurosurgery 1987; 20:496
  16. Iggo A: Pain receptors, in Bonica JJ, Procacci P, Pugni CA (eds): Recent Advances on Pain: Pathophysiology and Clinical Aspects. Springfield, Ill, Charles C Thomas Publishers, 1972
  17. Iggo A: The case for "pain" receptors, in Tanzen R, Keide WD, Herz A, et al (eds): Pain. Baltimore, Williams & Wilkins, 1972, pp 60-61
  18. Jensen T, Krebs B, Nielsen J, et al: Immediate and long term phantom limb pain in amputees: Incidence, clinical characteristics and relationship to preamputation limb pain. Pain 1985; 21:267
  19. Kerr FWL: Segmental circuitry and spinal cord nociceptive mechanisms, in Bonica JJ, Albe-Fessard D (eds): Advances in Pain Research and Therapy, vol 1. New York, Raven Press, 1976, pp 75-89
  20. Lim RKS: Neuropharmacology of pain and analgesia, in Lim RKS, Armstrong D, Pardo EG (eds): Pharmacology of Pain, vol 9. New York, Pergamon Press Inc, 1968, pp 169-217
  21. Loeser JD: Neurosurgical relief of chronic pain. Post Grad Med J 1973; 53:115-119
  22. Loeser JD, et al: Relief of pain by transcutaneous stimulation. J Neurosurg 1975; 43:308-314
  23. Long DM: External electrical stimulation. Minn Med 1974;57:195-198
  24. Melzack R: Central neural mechanisms in phantom limb pain, in Bonica JJ (ed): Advances in Neurology, vol 4, Pain. New York, Raven Press, 1974, pp 319-326
  25. Melzack R: Phantom limb pain: Implications for treatment of pathologic pain. Anesthesiology 1971; 35:409-419
  26. Melzack R: The Puzzle of Pain. New York, Basic Books Inc Publishers, 1973
  27. Melzack R, Wall PD: Pain mechanism: A new theory. Science 1965; 150:971-979
  28. Mitchell SW: Phantom limbs. Lippincott Mag 1871; 8:563
  29. Nathan PW: Pain. Br Med Bull 1977; 33:149-155
  30. Nielson KD, et al: Phantom limb pain. Treatment with dorsal column stimulation. J Neurosurg 1975; 43:301-307
  31. Parkes CM: Factors determining the persistence of phantom pain in the amputee. J Psychosom Res 1973; 17:97-108
  32. Radcliffe CW: Functional considerations in the fitting of above knee prostheses. Artif Limbs 1955; 2:35-60
  33. Radcliffe CW, Foort J: The Patellar-Tendon Below Knee Prosthesis Manual. Berkley, Calif, University of California, Biomechanics Laboratory, Department of Engineering, 1961
  34. Rexed B: The cytoarchitecture organization of the spinal cord of the cat. J Comp Neurol 1952; 96:415-496
  35. Riding J: Phantom limb: Some theories. Anesthesia 1976; 31:102-106
  36. Saris S, Iacono R, Nashold B: Dorsal root entry zone lesions for post-amputation pain. J Neurosurg 1985; 62:72
  37. Saris S, Iacono R, Nashold B: Successful treatment of phantom pain with dorsal root entry zone coagulation. Appl Neurophysiol 1988; 51:188
  38. Sherman R: Stump and phantom limb pain. Neurol Clin 1989; 7:249
  39. Sherman R, Sherman C, Gall N: A survey of current phantom limb pain treatment in the United States. Pain 1980; 8:85
  40. Sinclair WF: Below the knee and Syme's amputation prostheses. Orthop Clin North Am 1972; 3:349-357
  41. Stilz RJ, Carron H, Sanders DB: Reflex sympathetic dystrophy in a 6-year-old: Successful treatment by transcutaneous nerve stimulation. Anesth Analg 56(3): 1977; 53:438-443
  42. Sweet WH, et al: Stimulation of the posterior columns of the spinal cord for pain control: Indications, techniques and results. Clin Neurosurg 1974; 21:278-310
  43. Wall PD: Physiological mechanisms involved in the production and relief of pain, in Bonica JJ, Procacci P, Pagni CA (eds): Recent Advances on Pain: Pathophysiology and Clinical Aspects. Springfield, Ill, Charles C Thomas Publishers, 1974, pp 36-63
  44. Webster KE: Somesthetic pathways. Br Med Bull 1977; 33:113-120
  45. Whidden A, Fiddler MR: Pathophysiology of pain, in Ja-cox AK (ed): Pain: A Source Book for Nurses and Other Health Professions. Boston, Little Brown & Co Inc, 1977, pp 27-56
  46. Wilson ME: The neurological mechanisms of pain. A review. Anaesthesia 1974; 29:407-421

Chapter 27 - Atlas of Limb Prosthetics: Surgical, Prosthetic, and Rehabilitation Principles

O&P Library > Atlas of Limb Prosthetics > Chapter 27

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