Acquired limb deficiencies. 2. Perioperative management

Acquired limb deficiencies. 2. Perioperative management

S9 Acquired Limb Deficiencies. 2. Perioperative Management Geetha Pandian, MD, Mark E. Huang, MD, Daniel A. Duffy, DO ABSTRACT. Pandian G, Huang ME, ...

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Acquired Limb Deficiencies. 2. Perioperative Management Geetha Pandian, MD, Mark E. Huang, MD, Daniel A. Duffy, DO ABSTRACT. Pandian G, Huang ME, Duffy DA. Acquired limb deficiencies. 2. Perioperative management. Arch Phys Med Rehabil 2001;82 Suppl 1:S9-16. This self-directed learning module highlights recent advances in the evaluation and management of complications arising from diabetes and peripheral vascular disease leading to amputation. It is part of the chapter on acquired limb deficiencies in the Self-Directed Physiatric Education Program for practitioners and trainees in physical medicine and rehabilitation. This article includes discussion of comorbid conditions that may have an impact on the prosthetic rehabilitation of a transtibial amputee. It also offers essential information regarding perioperative management of an upper extremity amputee. Overall Article Objective: To review recent advances in the evaluation and management of complications arising from diabetes and peripheral vascular disease leading to amputation. Key Words: Amputation; Diabetes mellitus; Peripheral vascular disease; Foot ulcer; Rehabilitation. © 2001 by the American Academy of Physical Medicine and Rehabilitation 2.1 Objective: To develop a plan for evaluation and management of a 60-year-old diabetic man with a nonhealing foot ulcer. An estimated 16 million Americans suffer from diabetes, and 5% to 15% of these patients will undergo lower extremity amputation.1 Foot ulcer formation is one of the major risk factors for lower extremity amputation. In the United States, an estimated 15% of diabetic patients will develop a foot ulcer.1 Seventy percent to 80% of chronic foot ulcers will result in lower extremity amputation. The risk of ulcers and amputation increases with age and duration of diabetes for both type 1 and type 2 diabetes.1 Prognosis after amputation is generally poor, with 30% to 50% of first-time amputees requiring additional amputation within 1 to 3 years and a survival rate of only 50% in 5 years. Problems that lead to ulceration and amputation are peripheral neuropathy, peripheral vascular disease, and infection. Although various factors can lead to foot ulcers, Pecoraro et al2 reported neuropathy to be the leading cause in 61% of their patients with foot ulcer. Other potential causes were minor trauma, cutaneous ulceration, infection, ischemia, faulty wound healing, and gangrene. Distal sensory motor polyneuropathy affects up to 50% of persons who have had diabetes more than

From the Department of Physical Medicine and Rehabilitation, University of Texas Southwestern Medical Center, Dallas, TX (Pandian); Department of Physical Medicine and Rehabilitation, Virginia Commonwealth University, Richmond, VA (Huang); and Rehabilitation Services, Field Neuroscience Institute, Saginaw, MI (Duffy). Accepted November 1, 2000. No commercial party having a direct financial interest in the results of the research supporting this article has or will confer a benefit upon the author(s) or upon any organization with which the author(s) is/are associated. Address correspondence to Geetha Pandian, MD, Dept of Physical Medicine and Rehabilitation, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX 75390. 0003-9993/01/8203-6656$35.00/0 doi:10.1053/apmr.2001.22227

15 years and may be present in 12% of patients at the time of diagnosis.3 Patients who lose protective sensation sustain injuries from stepping on sharp objects, foreign bodies in footwear, and pressure necrosis from poorly fitting footwear. However, the most common mechanism of injury appears to be unperceived repetitive pressure along plantar bony prominences and over calluses. Classic neuropathic ulcers occur on the plantar surface of the foot, but ulcers can also occur over the medial and lateral borders of the foot and on the dorsal surface of the toes. See table 1 for risk factors for foot ulcers. GENERAL GUIDELINES FOR EVALUATION Neurologic Evaluation A thorough examination including deep tendon reflexes, sensory testing, and motor assessment should be performed on all patients. Traditional evaluation of sensory loss using a cotton swab, pinprick, or tuning fork is highly subjective and has poor interobserver reproducibility. Examination with a Semmes-Weinstein 5.07 monofilament is a highly reliable method for detecting and quantifying sensory impairment and provides excellent predictability for ulcer risk.4 Testing the dorsal and plantar surface of the toes and plantar metatarsophalangeal areas with just enough pressure to buckle the filament slightly provides information about discriminatory ability. Musculoskeletal Examination A comprehensive evaluation includes examination for trunk deviation, leg length discrepancy, joint deformity, and limitations in range of motion. All of these can alter gait and pressure distribution over the feet. Biomechanical alteration of the foot from intrinsic muscle weakness, limited joint mobility, and arthritic deformities increases the risk of ulceration. Limited ankle dorsiflexion due to gastrocsoleus tightness increases the forefoot plantar pressure and causes callus and eventual ulcer formation.5 It also causes stress on subtalar joints and can lead to midfood Charcot arthropathy. A Charcot foot may be completely immobile, with a collapsed midfoot, which makes the foot prone to high pressure and ulcerations. Over half of diabetic patients have hammer toe or claw toe deformity. Migration of the plantar fat pad distally is seen with claw toe deformity, which exposes the metatarsal head to increased plantar pressure. Increased plantar pressure leads to callus formation. Plantar calluses increase the local pressure by as much as 29% and are associated with an 11-fold higher risk for ulceration.6 Other biomechanical alterations, such as prior toe amputations, bunions, or hallux rigidus, should be noted. Nonenzymatic glycosylation of collagen and keratin that occurs in diabetic patients makes the skin and subcutaneous tissue less pliable and limits toe and foot mobility.7 Vascular Assessment Although peripheral vascular disease is an infrequent cause of ulcers (5%–7%), it plays a major role in wound healing. Atherosclerosis of the peripheral blood vessels is 2 to 3 times more common in persons with diabetes. Peroneal and tibial vessels are more commonly involved in diabetic patients than in the general population. Skin and subcutaneous fat tissue Arch Phys Med Rehabil Vol 82, Suppl 1, March 2001

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PERIOPERATIVE MANAGEMENT, Pandian Table 1: Risk Factors for Foot Ulceration in Diabetics

Neuropathy Loss of protective sensation Muscle weakness Autonomic (dry, cracked skin) Vascular disease Poor glycemic control Deformities of the foot Claw toes Hammer toes Hallux valgus, rigidus Charcot foot Splay foot Limited mobility of the foot Heel cord tightness Contractures of toes Limited inversion and eversion

Abnormal gait Hip and knee arthritis Leg length discrepancy Plantar calluses Thick mycotic nails Plantar fat pad displacement Previous ulcers and amputation Amputation of contralateral limb Elevated activity profile Poor hygiene of the foot Improper foot wear Elderly living alone Blind or decreased vision Lack of education Lower socioeconomic status

atrophy, shiny skin, hair loss on feet and toes, thickened nails, and rubor are indicative of peripheral vascular disease. Lower extremity pulses should be palpated routinely. Absence of posterior tibial and dorsalis pedis pulses may indicate lower extremity ischemia and require further vascular evaluation and other noninvasive testing. Objective assessment of vascular status can be obtained by calculating the ankle-brachial index through the use of Doppler ultrasound arterial pressure analysis. However, in some diabetic patients, ankle-brachial index may not be reliable because of the presence of medial arterial calcinosis, which results in falsely elevated values. Although not routinely needed, measurements of systolic toe pressures and transcutaneous oxygen tension can predict outcome. Satisfactory healing can be predicted if the ankle-brachial index is over .45 and transcutaneous oxygen tension and absolute toe blood pressures are above 35 to 40mmHg.8 Management of Neuropathic Ulcers Initial assessment should focus on: (1) etiology of the ulcer; (2) ulcer size, depth, and involvement of deep structures; (3) presence of infection, purulent discharge, necrosis, and sinus tracts; (4) status of surrounding tissue, including presence of edema, callus, cellulitis, and abscess; (5) evidence of systemic infection; and (6) vascular status. Infection Infection in diabetic patients may not produce the usual systemic symptoms and signs of fever and leukocytosis, but it often produces recalcitrant hyperglycemia and malaise. Wound infections can be categorized as mild, moderate, or severe or as non–limb threatening or limb threatening. Non–limb-threatening infections include those with no sign of systemic toxicity, less than 2cm of cellulitis, and absence of deep abscess, osteomyelitis, or gangrene.9 Limb-threatening infections are characterized by the presence of extensive cellulitis, deep abscesses, osteomyelitis, gangrene, and systemic symptoms. Most mild infections are caused by aerobic gram-positive cocci such as Staphylococcus aureus or streptococci. Deeper limb-threatening infections are usually polymicrobial. Culture by superficial swab technique is not recommended, because both colonizing and infecting organisms are recovered. The recommended technique consists of obtaining a specimen by curettage from the base of the ulcer after de´bridement. If infection is suspected, broad-spectrum antibiotic coverage should be initiated Arch Phys Med Rehabil Vol 82, Suppl 1, March 2001

immediately, then modified as necessary based on culture results. A currently recommended oral regimen for non–limbthreatening infection includes 1 of the following agents: cephalexin, clindamycin, dicloxacillin, and amoxicillin clavulanate. For more serious infection, an oral regimen with a combination of a fluoroquinolone and clindamycin is recommended. Immediate hospitalization de´bridement, and parenteral antibiotic therapy are recommended for limb-threatening infections. Radiologic Examination Radiologic evaluation is recommended for wounds of long duration and if osteomyelitis is suspected. Plain radiographs can show subcutaneous gas, foreign bodies, fractures, neuroarthropathic changes, and cortical erosion, but these signs are neither specific nor sensitive for a diagnosis of osteomyelitis. When the diagnosis is in doubt and the patient is clinically stable, conservative management can be pursued with follow-up x-rays in 2 weeks. If the x-rays are still negative, osteomyelitis is unlikely.9 No test definitively differentiates osteomyelitis from acute Charcot arthropathy. Additional imaging studies such as technetium bone scans, indium-111labeled leukocyte scanning, and magnetic resonance imaging may be helpful but are expensive. A bone biopsy may be necessary for a definitive diagnosis of osteomyelitis, particularly if other studies do not clarify the diagnosis. Wound Care Sharp de´bridement of necrotic tissue and surrounding callus at frequent intervals on an outpatient basis promotes wound healing. De´bridement must extend to viable noninfected tissue. A general recommendation regarding use of whirlpool baths and various topical agents cannot be given because there are no controlled studies showing their effectiveness. A moist wound environment is encouraged. Recombinant platelet-derived growth factors, when used topically in conjunction with adequate off-loading, de´bridement, and control of infection, provide a modest benefit in healing rate and time.10 Additional randomized clinical trials are warranted to evaluate clinical efficacy of new technologies such as living skin equivalents, electrical stimulation, cold laser, and hyperbaric oxygen therapy. Off-Loading Effective treatment of neuropathic foot ulcer requires elimination of weight bearing. Foot ulcers generally do not heal if patients continue to put weight on their feet, which causes ongoing repetitive trauma that prevents healing. Among the limited number of proven effective strategies for off-loading, total-contact casting has been most extensively studied and proven effective. Plantar ulcers with adequate blood supply, without evidence of osteomyelitis or acute infection, can be managed with total-contact casting. This cast, as proposed by Brand11 for protecting neuropathic ulcers, differs from the typical orthopedic cast. A total-contact cast is minimally padded and carefully molded to the shape of the foot and leg with a heel for walking. It is designed to distribute the pressure over the entire surface of the foot and leg. The first cast is usually changed in 2 to 7 days, depending on the edema present when the cast was applied.12 Casting can reduce edema dramatically and can result in a loose cast that causes skin breakdown. After the first cast change, if there are no complications, another cast is applied and then changed every 7 days, depending on the adequacy of the fit. The patient mentioned in the Learning Objective can be effectively managed with total-contact casting. Applying the total-contact cast requires skill and experi-

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ence. With total-contact casting, the healing time of the ulcer is generally 5 to 10 weeks.13 Other strategies for off-loading include bed rest, a bivalve cast, a Charcot restraint orthotics walker, a DH pressure relief walker,a and healing sandals.14 The major disadvantage of these removable devices is patient noncompliance in wearing them as prescribed. Total-contact casting and other off-loading devices should continue to be used until the wound is healed and then probably for another week or 2 to permit scar maturation. A slow transition from cast to shoe is recommended, and in the interim a total-contact sandal with a thick, molded insole can be used. Vascular insufficiency may be present when an ulcer fails to heal despite adequate de´bridement, off-loading, antibiotic therapy, and good metabolic control. In these cases, consultation with a vascular surgeon is indicated, because surgical revascularization may preserve the limb.

egies. Orthotics and shoes should be assessed for improper fit and corrected promptly. Anemia, smoking, peripheral edema, and other cardiopulmonary conditions can compromise the delivery of oxygen to the distal extremity. Poor tissue oxygen tension within the ischemic extremity leads to more frequent and more severe infections.16-18 One should determine whether the patient’s current medication profile includes treatment to lower blood viscosity (pentoxifylline, naftidrofuryl, buflomedil, alprostadil).19 These medications may improve blood flow to a degree, but there is as yet no medication that can safely and efficaciously both alleviate pain symptoms and prevent disease progression.20 In diabetic patients, peripheral vascular disease is more prevalent and more likely to be progressive. Diabetes specifically has a predilection for distal, small-diameter arteries.21

Management of Healed Foot Ulcers The most important strategy in preventing recurrent foot ulcers is patient education and appropriate foot care. Patients should be educated in the proper care of nails, not walking barefoot, daily foot inspection, foot mobility exercises, and application of moisturizing lotion immediately after a bath. Plantar calluses should be trimmed at regular intervals, preferably by a health care professional. The use of accommodative footwear with adequate toe box and molded insoles markedly reduces the incidence of wound recurrence. In cases of severe foot deformity, custom-molded shoes are required. Rigid rocker sole shoes are effectve in preventing recurrent forefoot plantar ulcers. In carefully selected cases, prophylactic foot surgery for correction of deformities may be useful.

EVALUATION OF VASCULAR INTEGRITY When the cross-sectional area of a blood vessel decreases by 75%, the patient will begin to show signs and symptoms of ischemia. Blood velocity within the stenotic segment increases, and poststenotic turbulence causes a loss of kinetic energy, which decreases forward flow.22 On physical examination, loss of palpable pulses and delayed capillary refill time reflect decreased blood flow. The Doppler and transcutaneous oxygen tension measurements are simple, noninvasive tools to assess vascular status. Doppler ultrasound detects blood flow and, when used in conjunction with blood pressure cuffs, can measure arterial pressure. The ankle-brachial index calculated for each foot is the highest ankle pressure divided by the highest arm pressure. Ankle-brachial indices are consistent with the following clinical diagnoses: normal (1.0 –1.2), claudication (0.5– 0.9), existing tissue loss that is unlikely to heal (⬍0.5), ischemic rest pain (⬍0.4), threatened limb (⬍.15), and irreversible ischemia (0.0).23 Transcutaneous oxygen measurements reflect tissue perfusion. Significant occlusive disease will cause these measurements to fall below 40mmHg. Measurement of tissue oxygen tension is not affected by incompressible calcified vessels and appears to be very sensitive in evaluating arterial occlusive disease during exercise.24,25 Once significant vascular pathology has been confirmed, one should identify the distribution of vascular occlusion. Duplex ultrasonography offers the advantage of anatomic imagery and flow velocity determination in the arterial system. It requires expensive machinery and highly skilled technicians. Color duplex imaging with real-time B-mode scanning permits identification of a vessel and its anatomic detail (eg, plaque characterization, intimal flap, mural thrombus, diameter measurements, direction of flow, presence of turbulence).26 Duplex scanning is the noninvasive test of choice in following progressive vascular disease; it enables the clinician to make serial measurements over time, especially after vein bypass grafting.27 Plethysmography detects the volume change during an arterial pulsation and can detect changes in flow by measuring the incremental change in pulse volume over time. Currently, the air-filled cuff is the most commonly used in the clinical setting. Variations include segmental plethysmography, which uses narrower cuffs; strain-gauge plethysmography, which uses electric resistance; and photoplethysmography, which correlates the intensity of light.24,28 Laser Doppler and dynamic capillaroscopy use light scatter characteristics to determine capillary blood flow. Although they may not adequately measure nutritive blood flow to the skin, they can be used to monitor success of revascularization procedures. Karanfilian et al29 have used transcutaneous oxygen tension levels and laser Doppler velocimetry as objective predictors of wound healing

CONCLUSION Limb- and life-threatening complications in patients with diabetes can be prevented by prompt treatment through an integrated interdisciplinary approach. All clinicians should form the habit of routinely examining the feet of their diabetic patients. A concerted effort by both the patient and the health care providers will help achieve the US Department of Health goal of 40% reduction of amputation rates. 2.2 Objective: To discuss management considerations for this patient when progression of disease threatens imminent amputation. Progression of vascular disease threatens imminent amputation. The clinician must evaluate the cause of progression to determine whether conservative measures can be implemented to delay or prevent progression. It is important to clearly define the vascular status of the limb to determine whether the patient may be a candidate for medical intervention and/or revascularization procedures to avoid amputation. If amputation is deemed inevitable, it is essential to determine the optimal level for definitive surgical amputation to (1) facilitate adequate healing, (2) preserve as much residual limb length as possible to maximize function, and (3) avoid prolonged hospitalization or surgical revision.15 CAUSE OF PROGRESSION Noncompliance, whether intentional or unintentional, may contribute to the progression of disease in a nonhealing limb ulcer. Poor vision, decreased cognition, depression, and comorbid medical conditions (eg, diabetes mellitus, congestive heart failure, chronic obstructive pulmonary disease, venous insufficiency, cellulitis) can compound the vascular compromise and reduce the patient’s ability to comply with management strat-

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in diabetic patients. Cost limits the routine use of such technology. After a significant disruption of blood flow and the extent of the vascular pathology have been identified, options for revascularization versus surgical intervention should be addressed and should include the patient’s input. The options include limb amputation versus interventional techniques such as vascular reconstruction, vascular bypass, balloon angioplasty and atherectomy, endovascular stenting, and thrombolytic therapy.30 The specific vascular lesion(s) must be visualized for appropriate application of the newest advances in endovascular therapeutics, including balloon angioplasty, lytic therapy, balloon thrombectomy, and atherectomy. The magnified, real-time, 360° luminal view provided by angioscopy allows the surgeon to delineate the specific type of luminal disease present and to tailor the therapeutic intervention to that specific problem. The angioscope can be used to guide endovascular instrumentation, including thrombectomy catheters, guide wires, valvulotomes, forceps, and scissors.31 Intravascular ultrasound can identify 4 basic plaque components, particularly with the higher-frequency transducers, based on their echo properties. Echolucent areas correspond to regions of lipid deposit. Soft echoes disclose fibromuscular tissue, intimal proliferation, and areas of dispersed lipid. Bright echoes (dense) reflect collagen-rich tissues. Areas of acoustic shadowing correlate with calcified tissue. Intravascular ultrasound in general is less sensitive than angioscopy for characterizing the nature of intravascular thrombus, but it is easier to perform.31 Appropriate candidates for balloon angioplasty must have symptoms directly attributable to the occlusive arterial lesion. A lesion length less than 10cm responds best to balloon angioplasty. Longer segments or ulcerated lesions are less suitable.32 Localized fracture by the balloon of the calcified atherosclerotic plaque and dissection of the underlying media dilates the affected artery. A higher rate of calcification of the atheroma improves the success of balloon angioplasty but increases the risk of intimal rupture and vessel injury. Endoluminal stents were developed to deal with the limitations and complications of balloon angioplasty. Use of stents is favored for the following situations: (1) restenosis within 90 days of balloon angioplasty, (2) chronic iliac occlusion, (3) acute occlusions during balloon angioplasty, (4) a significant residual gradient following balloon angioplasty, (5) dissections longer than the angioplasty site, and (6) 30% or greater residual stenosis after balloon angioplasty.33 The primary objectives of the infusion of a fibrinolytic agent (streptokinase, urokinase, tissue plasminogen activator, prourokinase, acylated streptokinase activator complex) are to dissolve the occluding thrombus, restore perfusion, and allow evaluation of the underlying cause of the arterial or graft thrombosis. Arteriography is considered the gold standard for the definitive analysis of vascular status. Its limitations include cost, risks, and discomfort. Arteriography evaluates structure but not function, and it may inaccurately assess the length of occlusion or the vessels immediately proximal and distal to an occlusion.34 Magnetic resonance angiography is an alternative, noninvasive imaging modality that avoids the complications of arterial puncture, eliminates the risk of contrast-induced renal failure, and has a higher sensitivity than contrast angiography in the identification of severe peripheral arterial occlusive disease.35 Arch Phys Med Rehabil Vol 82, Suppl 1, March 2001

CONCLUSION A patient with progressive vascular disease may be in danger of eventual limb amputation. However, careful assessment of factors contributing to the progression may allow conservative intervention to delay the progression. In addition, there are now multiple means of assessing the severity and extent of vascular occlusion. These diagnostic assessments of a patient’s vascular integrity help determine if a patient is best served by medications, revascularization procedures, or amputation. If amputation is selected, they help determine the optimal level for healing and function. 2.3 Objective: To anticipate the impact of common comorbidities in this patient following transtibial amputation. PERIPHERAL VASCULAR DISEASE Peripheral vascular disease and diabetes account for 90% of all amputations in the elderly.36 There are many categories of peripheral vascular disease, such as atherosclerosis, acute and chronic venous insufficiency, thromboembolic disease, and vasospasm. However, the main reason for amputation in peripheral vascular disease is arterial insufficiency from atherosclerosis.37 Because atherosclerosis is usually symmetric, one should always be vigilant for signs of ischemia or open wounds in the contralateral limb. Vascular claudication of the sound limb may have an impact for functional mobility; thus, monitoring for signs of claudication will help establish exercise guidelines. Progression of vascular disease may limit the ability for prosthetic use; however, early rehabilitation and prosthetic intervention may allow a patient with an existing amputation to increase functional skills before a second one is needed.38,39 The vascular disease itself may compromise wound healing. Failure to heal after amputation is believed to occur in 3% to 29% of patients.36 Methods to enhance wound healing include proper nutrition, antibiotic treatment in the case of infected leg ulcers, and edema management. As opposed to traumatic amputations, in which fitting may occur any time from immediately postoperatively to 2 to 3 weeks after surgery, dysvascular patients in general have delayed temporary prosthetic fitting because of their poor wound healing. Patients may have fitting delayed 6 to 10 weeks after amputation to allow proper healing of the residual limb and resolution of edema.40 However, in uncomplicated cases with good wound healing, fitting may be performed 3 to 4 weeks postoperatively. Appropriate limb management in the case of transtibial amputation includes a rigid cast immediately postoperatively, followed by a rigid removable dressing to decrease edema, promote wound healing, and protect the residual limb.41 Exceptions are cases of suspected deep infection in the residual limb and wounds with areas left to heal by secondary intent. In the transfemoral amputee population, edema management may be done by using a compression stockinette with a waist suspension belt and eventually a light-duty stump shrinker that is measured for fit. Immediate postsurgical prosthetic fitting has theoretical advantages of earlier prosthetic fitting, resolution of edema, and decreased pain, but it may also lead to increased complications in wound healing. This approach was favored at one time but is no longer recommended unless skilled personnel are available for casting and monitoring of the wound postoperatively.40 DIABETES Diabetes is a significant comorbidity seen in cases of vascular limb amputation. Diabetes has been shown to accelerate atherogenesis, and it is an independent risk factor for coronary

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artery disease. In general, diabetic patients are 15 to 17 times more likely to have an amputation than the general population. Fifty to 70% of all amputations are a result of complications of diabetes mellitus. The mean 3-year survival of diabetic patients after major amputation is 25% to 50%.42 Diabetes also has an impact on wound healing, which delays prosthetic fitting in this population when compared with those without diabetes. Further complications from diabetes that may affect rehabilitation include diabetic retinopathy, diabetic nephropathy, and peripheral neuropathy. Diabetes affects the lower limbs symmetrically, with 28% of geriatric amputees receiving a second amputation at 2 years and 66% at 5 years.39 Edema management is especially pertinent in persons with end-stage renal disease, in which residual limb volume may vary from dialysis. Special attention to the wound is required in cases of diabetic patients with peripheral neuropathy, who may not sense increased areas of pressure or potential areas of skin breakdown. Furthermore, diabetic patients are prone to autonomic neuropathy, which can result in orthostatic hypotension as well as hypotension during exercise. Caution should be used when first mobilizing patients for therapy in the acute care hospital as well as when progressing to more intensive exercise in a rehabilitation setting. Another precaution when instituting therapy is exercise-induced hypoglycemia, which may be seen both during and after the exercise session and is related to the blood glucose level and the intensity of exercise. Symptoms of hypoglycemia or overexertion should be the end point for cessation of exercise, because diabetic patients may vary in their tolerance of various blood glucose levels. Proper blood glucose control in the perioperative period facilitates wound healing. Teaching proper diet, monitoring skin condition, and using necessary diabetic agents will maximize outcome and minimize complications resulting from diabetes. CORONARY ARTERY DISEASE Coronary artery disease is another common comorbidity, evident in over half of patients undergoing amputation. Fiftyfive percent have significant rhythm, ST-segment, or hemodynamic abnormalities during stress testing.42 This factor can affect a patient’s outcome because functional status is related not only to the level of amputation but also to the patient’s cardiopulmonary status.43 Ideally, physiologic testing (ie, exercise treadmill stress test) should be done preoperatively to assess for coronary artery disease. This provides excellent guidelines for maximum heart rate as well as target heart rates during exercise. However, a physiologic stress test is often impractical in these patients, because their mobility may be severely limited. In these cases, a pharmacologic stress test such as the dipyridamole-thallium stress test or the dobutamine stress echocardiogram may be appropriate for risk assessment before surgery. Alternative methods for postoperative testing include upper arm ergometry, air dyne bicycle ergometry, and rowing ergometry to determine a target heart rate for exercise and levels of ischemia.42 However, this usually requires a cardiac laboratory that specializes in alternative testing and testing of the disabled. In the case of a perioperative myocardial infarction, exercise intensity should be limited to 3 to 5 metabolic equivalents during the acute-care hospitalization, which would be similar to phase I cardiac rehabilitation. Proper cardiac precautions with monitoring of blood pressure and heart rate in therapy may help limit myocardial ischemia. Heart rate should not exceed 30 beats/min above resting for those on beta blockade therapy, and systolic blood pressure should not drop more than 15mmHg from resting.36 Therapists should monitor for symptoms of ischemia such as chest pain, dyspnea,

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nausea, and diaphoresis. Because diabetic patients may have silent ischemia, vigilance for other symptoms of ischemia is highly recommended. When seeing patients postoperatively, the physiatrist should take into consideration energy expenditure for mobility issues and also gait training and possible prosthetic fitting.39 This will minimize potential ischemic episodes from overexertion. Persons with lower limb amputations usually have the same rate of energy expenditure as able-bodied subjects because of a tendency to decrease their self-selected speed. For transtibial amputees, using a prosthesis results in lower energy expenditure than does axillary crutch walking. Vascular transfemoral patients using crutches may have comparable or greater energy expenditures when compared with those using a prosthesis.42 For poor prosthetic candidates, level, smooth-surface wheelchair propulsion offers a lower-energy-expenditure alternative to ambulation. However, one should be aware that energy expenditures increase significantly with uneven and carpeted surfaces.42 Power chairs should be considered when there are severe cardiovascular limitations. DEEP VENOUS THROMBOSIS Patients who have undergone amputation may be at increased risk for lower extremity deep venous thrombosis (DVT) and pulmonary embolism. This is due to multiple risk factors for DVT in this population, such as age, immobility before and after surgery, and the amputation surgery itself, which involves ligation of vessels on the amputated side. Furthermore, 25% to 30% of patients undergoing vascular surgery have an identifiable hypercoagulable state. The incidence of DVT has ranged from 2% to 67%,44 and more recent studies, some of which used appropriate DVT prophylaxis, showed an incidence between 12% and 17% using duplex ultrasound for detection.45,46 There may be a higher incidence of DVT in the bilateral amputee. Zickler et al47 have shown that 26% of patients with bilateral amputations performed within the same hospitalization may have DVT or pulmonary embolism. If DVT is suspected, imaging should be performed on both legs, because some investigators have shown an equal incidence of DVT between the amputated and the contralateral limb.45 If the DVT is on the amputated side, it is usually proximal and thus is at higher risk for propagation and embolization. An appropriate period of immobilization may be required before resumption of therapy. The test of choice remains the duplex ultrasound because of its high sensitivity and specificity and its noninvasiveness. Given these risks, it is important to use proper DVT prophylaxis. The current standard for surgical patients, subcutaneous heparin 5000U every 8 to 12 hours, is appropriate for this population as well.48 Additional prophylaxis may be required for patients who have additional risk factors for DVT. In these cases, low–molecular-weight heparin may be used, although the cost is much higher. In bilateral amputees, use of inferior vena cava filters may be considered.47 Warfarin is another alternative, especially for patients already receiving it for another indication, such as bypass graft patency. OTHER COMORBIDITIES Other comorbidities to be anticipated postoperatively include pain, congestive heart failure, delerium, and stroke.49 Pain can cause significant functional limitation in patients postoperatively. Adequate analgesia should always be sought to maximize functional status and minimize patient discomfort. Use of oral narcotic agents is preferred after the initial use of intravenous patient-controlled analgesia. Initially, a sustained controlled-release agent in conjunction with breakthrough pain Arch Phys Med Rehabil Vol 82, Suppl 1, March 2001

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medication provides the best pain control. Once steady-state pain relief has been achieved, reducing analgesic medications to the lowest effective dose schedule is optimal. Adjuvant pain agents may be useful to minimize narcotic usage, because older persons may be more susceptible to the side effects of narcotic pain agents, such as altered mental status, hypotension, respiratory depression, constipation, and ileus. Congestive heart failure can be seen postoperatively as a result of intravenous hydration during the perioperative period. The situation may be exacerbated if patients have not received their normal cardiac medications orally during this period. Careful weighing and accurate measuring of intake and output can help monitor for fluid overload. Delerium related to medications, change of environment, and effects of anesthesia can be seen postoperatively. Other possible causes include urinary tract infection, pneumonia, wound infection, pulmonary embolus, and electrolyte abnormalities. Polypharmacy is a serious problem in the geriatric population in general and minimizing sedating medications and other agents will help control this effect. Restoration of the sleep-wake cycle through use of sedating agents at night only may help patients return to their baseline mental status. Stroke is another cormorbidity and complication seen in this population. Postoperatively, a new cerebrovascular event should be considered in the differential diagnosis in patients with persistent altered mental status when other obvious causes have been excluded. This is especially true in patients with signs consistent with stroke, such as hemiparesis, ataxia, dysphagia, and aphasia. Patients with preexisting stroke have been discussed extensively elsewhere.39 2.4 Objective: To formulate a plan for the perioperative management of a construction worker with a transradial amputation. In contrast to lower extremity amputation in the adult, upper limb amputation usually occurs in young, otherwise healthy adult men as a result of a work-related accident. The most common level of amputation in the upper limb is transradial.50 Traditionally, upper extremity rehabilitation has been divided into 9 phases.51 The perioperative period focuses on the first 4 phases: preoperative, amputation surgery and reconstruction, acute postsurgical, and preprosthetic. Preoperatively, the major focus is communication with the patient and family regarding the impending surgery and expected outcomes. Consultation with the surgeon should initially focus on the feasibility of limb salvage versus amputation. Ideally, a peer with an upper extremity amputation would visit the patient to prepare him/her psychologially for the upcoming surgery. Furthermore, learning about the prosthetics to be used will give the patient a better sense of the expected outcome and the goals after surgery. If the amputation has to be performed emergently, such orientation should be provided as soon as possible after surgery. Levels of amputation should be discussed openly with the patient, as should the expected functional outcomes. There is no point in salvaging the hand if the metacarpal joints cannot provide adequate pinch, because this limits functionality. Furthermore, use of prosthetic thumbs is preferable in most patients, as opposed to pollicization or toe transfer to the hand, because patients may not desire further surgery and prosthetic thumbs may offer an adequate alternative.50 In general, transradial amputation offers a better prosthetic outcome, rejection rates being lowest for this level of amputation.52 The low rejection rate is probably related to the increased functionality offered by a prosthesis at this level. At other levels of amputation, a prosthetic device may not enhance Arch Phys Med Rehabil Vol 82, Suppl 1, March 2001

function significantly or it may become too cumbersome to operate. In the surgical phase, all possible length should be salvaged, especially if the dominant hand is involved and also in cases of bilateral amputations. A short transradial amputation may be lengthened with fibular grafts and free muscle flaps. Length is not optimal in cases of adult elbow or wrist disarticulations and presents a problem for cosmesis and for fitting a myoelectric prosthesis. The disarticulation creates a longer arm on the amputated side because of the need to incorporate the terminal device or elbow into the prosthesis. Amputation surgery should include myoplastic closure, with myofascial flaps brought over the end of the residual bone to provide a cylindric contour to the limb.50 Transected muscles should be kept close to resting length to help with prosthetic training and kinesthetic feedback. This measure also provides better soft tissue padding over the bone and fixes the bony lever arm. Primary closure, which allows rapid progression to prosthetic training, is preferred to delayed closure and skin grafting. However, this consideration needs to be balanced with the benefits of preserving length in the residual limb. The acute postsurgical phase focuses on control of edema, reduction of incisional and phantom pain, conditioning of remaining body segments, maintaining range of motion, and changing hand dominance for most activities. After surgery, the use of rigid dressings helps to control edema pain and to promote wound healing. There is little difference, with respect to long-term outcome, between immediate postsurgical fitting and early postoperative application of prostheses. In immediate postsurgical fitting, a plaster of paris rigid dressing is applied and a prosthesis is then attached over the cast.53 To attach the prosthetic components on the cast, 1 or 2 layers of stockinette are applied over dressing and the distal end is padded. A terminal device is mounted over the stockinette with adhesive tape and reinforced with coban or elastoplast to allow easy removal of components. The terminal device is controlled with standard Bowden cable and a figure-of-8 harness. A final covering of elastoplast is used to fix components in place while allowing easy removal. The underlying cast is changed weekly; however, it can be removed earlier at any time to inspect the wound if skin breakdown or infection is suspected. Immediate postsurgical fitting has been associated with decreased edema, decreased incidence of phantom and limb pain, increased prosthetic use and proprioception, and enhanced psychologic adaptation.54 Prosthetic training is begun when the patient is able to tolerate therapy. An alternative to rigid dressings is elastic wrapping. It may be used once the cast is removed and is applied every 4 hours in a figure-of-8 pattern; however, this is time consuming and demands a high level of expertise. One must not apply bandages too tightly proximally, to avoid distal swelling or a dumbbell-shaped residual limb. A more viable option is an elastic stockinette, such as the Compressogripb or Tubigrip,c which can also help with edema reduction. Reduction of postoperative and phantom pain is also important, as is discussed in more detail in Learning Objectives 2.3 and 4.3. During early phases of rehabilitation, emphasis is placed on scapulothoracic and glenohumeral joint mobility, especially the serratus anterior, trapezius, rhomboids, deltoid, biceps, and triceps. Other muscles of importance are the latissimus dorsi and the pectoralis major. The patient is taught scapular protraction/retraction and forward flexion at the glenohumeral joint; both are key movements in operating a manual-opening terminal device for a body-powered prosthesis. The practitioner should be mindful of painful neuromas that may increase patient discomfort and decrease the patient’s tolerance of forces generated when operating the prosthesis. With an upper

PERIOPERATIVE MANAGEMENT, Pandian

extremity amputation, vision is essential because it will substitute for lack of sensation in prosthetic devices. Assessment of visual and cognitive skills may reveal deficits that can hamper prosthetic training. Training in 1-armed activities and changing hand dominance may decrease frustration. Psychosocial assessment and counseling with the patient and family is usually needed. Because of the traumatic nature of the injury, the rehabilitation team should monitor for signs of posttraumatic stress disorder. Peer counseling may be helpful to introduce the patient to prosthetic fitting and the possibilities of enhanced function and return to work with a prosthesis. However, peer counseling is not a substitute for professional psychosocial counseling. The preprosthetic phase focuses on limb maturation in preparation for definitive prosthetic fitting. This phase may last anywhere from 3 to 6 weeks. Goals include shaping and shrinking, desensitization, muscle strengthening, maintaining joint mobility, mastering 1-handed activities, and psychosocial support. Once stitches or sutures have been removed, patients are casted for a temporary or preparatory prosthesis. The primary goal is to fit the patient as quickly as possible. Some have reported that fitting should be done during the “golden period”—the first 30 days— because after 30 days acceptance of a prosthesis is significantly reduced.40 Others have found that fitting within 3 to 6 months is crucial.53 Once the wound is well healed, the patient is instructed in gently massaging the residual limb. Progressively increasing sensory stimuli, through pressure, tapping, stroking, and vibration, can help desensitize the limb and encourage recovery. For candidates for body-powered prostheses, the main focus is on mastering use of the cable system to operate the terminal device and the wrist unit. For candidates for an externally powered prosthesis, muscles should be identified that are suitable for controlling the prosthesis, depending on the number of expected contact sites for control. There may be 2 sites of control, one in the flexor group and the other in the extensor group, but single-site control can be achieved. The focus should be on individual muscle activation, sustaining muscle contraction, and modulating the force of muscle contraction. This will allow proper control of the myoelectric device. Occupational or hand therapists can work with the patient on 1-handed activities and on switching dominance for general tasks (eg, writing, handling utensils). If the patient progresses rapidly, early job assessment and vocational retraining can be done to expedite the patient’s return to work. Depending on the nature of the job, the patient may be able to return to work in some capacity with the temporary prosthesis. References 1. Mayfield JA, Reiber GE, Sanders LJ, Janisse D, Pogach LM. Preventive foot care in people with diabetes. Diabetes Care 1998;21:2161-77. *2. Pecoraro RE, Reiber GE, Burgess EM. Pathways to diabetic limb amputation: basis for prevention. Diabetes Care 1990;13:513-21. 3. Vinik AI, Holland MT, Le Beau JM, Liuzzi JF, Stansberry KB, Colen LB. Diabetic neuropathies. Diabetes Care 1992;15:192675. *4. Caputo GM, Cavanagh PR, Ulbrecht JS, Gibbons GW, Karchmer AW. Assessment and management of foot disease in patients with diabetes. N Engl J Med 1994;331:854-60. 5. Banks AS. A clinical guide to the Charcot foot. In: Kominsky SJ, editor. Medical and surgical management of the diabetic foot. St. Louis: Mosby; 1994. p 115-43. 6. Young MJ, Cavanagh PR, Thomas G, Johnson MM, Murray H, Boulton AJ. The effect of callus removal on dynamic plantar foot pressures in diabetic patients. Diabet Med 1992;9:55-7.

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7. Delbridge L, Ellis CS, Robertson K, Lequesne LP. Non-enzymatic glycosylation of keratin from the stratum corneum of the diabetic foot. Br J Dermatol 1985;112:547-54. 8. Giordano JM. Noninvasive vascular testing. In: Kominsky SJ, editor. Medical and surgical management of the diabetic foot. St. Louis: Mosby; 1994. p 53-70. *9. Consensus development conference on diabetic foot wound care: 7-8 April 1999, Boston, Massachusetts. American Diabetes Association. Diabetes Care 1999;22:1354-60. 10. Wieman TJ, Smiell JM, Su Y. Efficacy and safety of a topical gel formulation of recombinant human platelet-derived growth factor–BB (becaplermin) in patients with chronic neuropathic diabetic ulcers. Diabetes Care 1998;21:822-7. 11. Brand PW. The diabetic foot. In Ellenberg M, Rifkin H, editors. Diabetes mellitus: theory and practice. 3rd ed. New Hyde Park (NY): Medical Examination Publishing; 1983. p 829-49. 12. Helm PA, Pandian G. Prevention of amputation. Phys Med Rehabil State Art Rev 1994;8:9-26. *13. Helm PA, Walker SC, Pullium G. Total contact casting in diabetic patients with neuropathic foot ulcerations. Arch Phys Med Rehabil 1984;65:691-3. 14. Catanzariti AR, Haverstock BD, Grossman JP, Mendicino RW. Off-loading techniques in the treatment of diabetic plantar neuropathic foot ulcerations. Adv Wound Care 1999;12:452-8. 15. Burgess EM, Matson FA III. Determining amputation levels in peripheral vascular disease. J Bone Joint Surg Am 1981;63: 1493-7. 16. Knighton DR, Halliday B, Hunt TK. Oxygen as an antibiotic: a comparison of the effects of inspired oxygen concentration and antibiotic administration on in vivo bacterial clearance. Arch Surg 1986;121:191-5. 17. Panchenko E, Eshkeeva A, Dobrovolsky A, Titaeva E, Podinovskaya Y, Hussain KM, et al. Effects of Indobufen and pentoxifylline on walking capacity and hemostasis in patients with intermittent claudication: results of six months of treatment. Angiology 1997;48:247-54. 18. Giansante C, Calabresse S, Fisicaro M, Fiotti N, Mitri E. Treatment of intermittent claudication with antiplatelet agents. J Int Med Res 1990;18:400-7. 19. Haustein KO. State of the art—treatment of peripheral occlusive arterial disease (POAD) with drugs vs. vascular reconstruction or amputation. Int J Clin Pharmacol Ther 1997;35:266-74. *20. McNamara DB, Champioon HC, Kadowitz PJ. Pharmacologic management of peripheral vascular disease. Surg Clin North Am 1998;78:447-64. *21. Kontos HA. Vascular diseases of the limbs. In: Wyngaarden JB, Smith LH, Bennett JC, editors. Cecil’s textbook of medicine. 19th ed. Philadelphia: WB Saunders; 1992. p 360-3. 22. Zierler RE. Hemodynamic considerations in the evaluation of arterial disease by Doppler ultrasound. Clin Diagn Ultrasound 1990;26:13-24. 23. Bandyk DF. Noninvasive vascular laboratory in clinical practice. Echocardiography 1992;9:525-35. *24. Lavin RA. Noninvasive vascular evaluation. Phys Med Rehabil State Art Rev 1994;8:27-40. 25. Modesti PA, Boddi M, Gensini GF, Serneri GG. Transcutaneous oximetry monitoring during the early phase of exercise in patients with peripheral artery disease. Angiology 1990;41:553-8. 26. Gahtan V. The noninvasive vascular laboratory. Surg Clin North Am 1998;78:507-18. 27. Bandyk DF. Postoperative surveillance of infrainguinal bypass. Surg Clin North Am 1990;70:71-85. *28. Mannick JA, Coffman JD. Ischemic limbs: surgical approach and physiologic principles. New York: Grune & Stratton; 1973. p 68-72. 29. Karanfilian RG, Lynch TG, Zirul VT, Padberg FT, Jamil Z, Hobson RW. The value of laser Doppler velocimetry and transcutaneous oxygen tension determination in predicting healing of ischemic forefoot ulcerations and amputations in diabetic and nondiabetic patients. J Vasc Surg 1986;4:511-6. 30. Malone MD, Barber L, Comerota AJ. Clinical applications of thrombolytic therapy for arterial and graft occlusion. Surg Clin North Am 1998;78:647-73. Arch Phys Med Rehabil Vol 82, Suppl 1, March 2001

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31. White JV, Eid I. Diagnostic and interventional angioscopy. Surg Clin North Am 1998;78:539-59. *32. Haji-Aghaii M, Fogarty TJ. Balloon angioplasty, stenting, and role of atherectomy. Surg Clin North Am 1998;78:593-616. 33. Cikrit DF, Dalsing MC. Lower-extremity arterial endovascular stenting. Surg Clin North Am 1998;78:617-29. 34. Cossman DV, Ellison JE, Wagner WH, Carroll RM, Treiman RL, Foran RF, et al. Comparison of contrast angiography to arterial mapping with color-flow duplex imaging in the lower extremities. J Vasc Surg 1989;10:522-9. 35. Owen RS, Carpenter JP, Baum RA, Perloff LJ, Cope C. Magnetic resonance imaging of angiographically occult runoff vessels in peripheral arterial occlusive disease. N Engl J Med 1992;326:1577-81. 36. Brown PS. The geriatric amputee. Phys Med Rehabil State Art Rev 1990;4:67-76. 37. Pandian G, Hamid F, Hammond MC. Rehabilitation of the patient with peripheral vascular disease and diabetic foot problems. In: DeLisa JA, Gans BM, editors. Rehabilitation medicine: principles and practice. 3rd ed. Philadelphia: Lippincott-Raven; 1998. p 1517-44. 38. Campbell WB, Ridler BM. Predicting the use of prostheses by vascular amputees. Eur J Endovasc Surg 1996;12:342-5. 39. Andrews KL. Rehabilitation in limb deficiency. 3. The geriatric amputee. Arch Phys Med Rehabil 1996;77:S14-7. 40. Leonard JA Jr, Meier RH III. Upper and lower extremity prosthetics. In: DeLisa JA, Gans BM, editors. Rehabilitation medicine: principles and practice. 3rd ed. Philadelphia: LippincottRaven; 1998. p 669-96. 41. Wu Y, Krick H. Removable rigid dressing for below-knee amputees. Clin Prosthet Orthot 1987;11(1):33-44. *42. Czerniecki JM, Gitter A. Cardiac rehabilitation in the lowerextremity amputee. Phys Med Rehabil Clin North Am 1995;6(3): 11-30. 43. Kurdibaylo SF. Cardiorespiratory status and movement capabilities in adults with limb amputation. J Rehabil Res Dev 1994; 31:222-35. 44. Barnes RW, Slaymaker EE. Postoperative deep venous thrombosis in the lower extremity amputee: a prospective study with Doppler ultrasound. Ann Surg 1976;183:429-32.

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45. Yeager RA, Moneta GL, Edwards JM, Taylor LM Jr, McConnell DB, Porter JM. Deep vein thrombosis associated with lower extremity amputation. J Vasc Surg 1995;22:612-5. 46. Fletcher JP, Batiste P. Incidence of deep vein thrombosis following vascular surgery. Int Angiol 1997;16:65-8. 47. Zickler RW, Gahtan V, Matsumoto T, Kerstein MD. Deep venous thrombosis and pulmonary embolism in bilateral lower-extremity amputee patients. Arch Phys Med Rehabil 1999;80:509-11. 48. Clagett GP, Anderson FA Jr, Geerts W, Heit JA, Knudson M, Lieberman JR, et al. Prevention of venous thromboembolism. Chest 1998;114:531S-60S. 49. Cutson TM, Bongiorni DR. Rehabilitation of the older lower limb amputee: a brief review. J Am Geriatr Soc 1996;44:1388-93. *50. Meier RH. Upper limb amputee rehabilitation. Phys Med Rehabil State Art Rev 1994;8:165-86. 51. Esquenazi A, Meier RH III. Rehabilitation in limb deficiency. 4. Limb amputation. Arch Phys Med Rehabil 1996;77:S18-28. 52. Wright TW, Hagan AD, Wood MB. Prosthetic usage in major upper extremity amputations. J Hand Surg Am 1995;20:619-22. 53. Esquenazi A. Upper limb amputee rehabilitation and prosthetic restoration. In: Braddom RL, editor. Physical medicine and rehabilitation. Philadelphia: Saunders; 1996. p 275-88. 54. Brenner CD. Prosthetic principles. In: Bowker JH, Michael JW, editors. Atlas of limb prosthetics. Surgical, prosthetic, and rehabilitation principles. 2nd ed. Philadelphia: Mosby; 1992. p 241-8.

*Key References.

Suppliers a. Royce Medical Co, 742 Pancho Rd, Camarillo, CA 93012. b. Knit Rite, Inc, 120 Osage, PO Box 3900, Kansas City, KS 66103. c. Seton Healthcare Group plc, Tubiton House, Oldham OL1 3HS, England.