Special Hand Disorders

Aneurysm, Thrombosis, and Embolism in Radial, Ulnar, and Digital Arteries

Through the continuation of the radial artery into the hand as the deep palmar arch and the ulnar artery as the superficial palmar arch, circulation to the hand is usually sufficient to allow the digits to remain viable despite most disease and injury. The superficial arch is complete in almost 80% of hands and incomplete in about 20%. The deep arch is complete in about 98% of hands. The radial artery usually provides most of the flow to three or more digits in 57% of hands, whereas the ulnar artery provides flow to three or more digits in almost 22%. Flow provided from both arteries equally is provided in almost 22%.

Ischemic problems in the hand can result from an aneurysm, thrombosis, or embolism in the radial, ulnar, or digital arteries. Arterial occlusive ischemia is associated with trauma from direct blows, instrumentation of the vascular tree for angiography, vascular access procedures, and systemic illnesses, such as atherosclerosis and various collagen vascular diseases.

Symptoms of ischemia, pain, sensory changes, skin discoloration, ulceration, and necrosis can be aggravated by smoking, activity, and exposure to cold. Physical findings include hand or digital pallor or cyanosis, skin ulceration, necrosis distal to areas of occlusion, sensory and possibly motor changes of affected nerves, coolness to palpation, tenderness over an aneurysmal or thrombotic mass, a palpable thrill through an aneurysm, and lack of flow through the affected artery, which is shown by the Allen test ( Figs. 70.1 and 70.2 ). Because of spasms in the distal vessels, this condition can be confused with other conditions, such as Raynaud disease. Plain radiographs, Doppler flow assessment, ultrasonography, pulse volume recordings, segmental arterial measurement, skin temperature measurement, radionuclide scanning, magnetic resonance angiography, and contrast angiography are helpful diagnostic measures. Angiography provides definitive information about the location and extent of the principal lesion and the presence of other circulatory problems in the upper extremity and in the face of ischemia should be the first choice of imaging technique. If no ischemia exists then Doppler ultrasound, CT angiography, and MR angiography are useful.

Although aneurysms may have atherosclerotic, mycotic, metabolic, and congenital origins, aneurysms seen in the hand and wrist usually are the result of trauma. Blunt trauma can cause true and false aneurysms (see Fig. 76.12 ), whereas penetrating trauma usually causes false aneurysms to form. The patient will present with a pulsatile and painful mass as well as possible cold intolerance.

Preoperative and intraoperative evaluations of the anatomy of the palmar vascular arch and of the quality of distal circulation are important when deciding between aneurysm excision alone and aneurysm excision with end-to-end repair and reversed vein graft arterial reconstruction. If the palmar arterial arch is complete, and distal circulation is adequate, as determined by pink distal skin color after release of the tourniquet or by pulse volume recordings showing a digital-brachial index of more than 0.7, repair or reconstruction usually is unnecessary. Conversely, if the palmar arterial arch is incomplete, or if the distal circulation is inadequate, the artery should be repaired or reconstructed with a reversed segmental vein graft ( Fig. 70.3 ).

Although usually related to occupational or recreational trauma, arterial thrombosis in the wrist, palm, and fingers also can result from arterial cannulation in the forearm. The ulnar artery is the vessel most commonly affected by trauma-related thrombosis, probably because of a relative lack of protection at the wrist and its exposure to repeated forceful impacts, such as when the ulnar side of the wrist is used as a hammer. Occupations in which this may be seen include auto mechanics, machinists, miners, butchers, and even firearm use in police officers. Sometimes the pain is severe, and sensibility is lost over the distribution of the ulnar nerve in the hand. Tenderness is present over the artery, and occasionally a feeling of fullness is described in the wrist and hand. Although possible, it rarely causes digital ischemia. The Allen test (see Figs. 70.1 and 70.2 ) is helpful in diagnosing thrombosis, but arteriography is diagnostic.

Treatment options include exploration of the artery and resection of the entire thrombotic mass, arterial reconstruction with artery or vein grafts, local and regional sympathectomy, and palliation with medical and psychological methods. The history, physical examination, and Allen test determine the initial diagnosis. If the Allen test is positive, thermography, temperature probes, Doppler studies, and pulse volume recordings are used to confirm the diagnosis. If a stellate ganglion or brachial block relieves symptoms, treatment is observation. A stellate or brachial block may relieve vasospasm in acute thrombosis threatening digital survival. If symptoms are not relieved, arteriography is done, and, at the same time, intraarterial medications (reserpine or tolazoline) usually are given. Arteriography establishes the diagnosis, identifies the extent of the thrombosis and vascular disease, and determines the probable success of surgery. Symptomatic treatment is indicated if vascular disease is generalized. If symptoms diminish after arteriography, the patient can be observed. Surgery is indicated if symptoms persist and if digital survival is in question. After the thrombosed segment has been resected, the proximal end is clamped and the tourniquet is released. If backflow is good and pulse volume recordings of the ulnar digits are normal, the vessel is ligated, and the wound is closed. If backflow is poor, with no pulsatile flow on digital plethysmography, vein grafting should be considered. Contraindications to vein grafting include erythrocytosis, patient refusal to modify the environment, and patient refusal to discontinue smoking. If vein grafting is indicated, the entire thrombosed segment should be resected until normal intima is seen with the operating microscope. A reversed vein graft harvested from the forearm is inserted (see Fig. 70.3 ). Vein grafting is contraindicated if there is inadequate peripheral “runoff” on the arteriogram. Persistent symptoms after surgery can be controlled conservatively by cessation of smoking, biofeedback techniques, and intermittent administration of intraarterial medications; sympathectomy can be used as a last resort.

The thrombosed mass may extend proximally in the forearm but rarely distally across the palmar arch to involve the more distal vessels; in the latter instance, complete resection may be impossible. Adequate resection relieves the spasm of the distal vessels, and symptoms usually improve; the circulation in the hand depends entirely on the radial artery, which usually is sufficient.

Radial artery thrombosis after cannulation has an incidence of about 10% to 18% after removal of the cannula; however, it is only symptomatic in about 5%. Spontaneous recanalization has been reported to occur in 35% of patients. If significant ischemia is present surgical thrombectomy and repair with a vein patch or graft is performed.

In rare cases, thrombosis of a patent median artery may cause pain of median nerve compression within the carpal tunnel. It should be considered in the diagnosis when acute pain in the hand is limited to the distribution of the median nerve.

Arterial lacerations in the wrist and hand are discussed in Chapter 63, Chapter and Chapter 63, Chapter 65 . Arterial emboli in the upper extremity account for 15% to 20% of all emboli. About 70% of emboli in the upper extremity are believed to be of cardiac origin (e.g., through atrial fibrillation or as postmyocardial infarction mural thrombi); the remainder are related to the subclavian artery. Usually, acute arterial embolism is signaled by pallor, cold sensation, ischemic pain, paresthesia, occasional paralysis, and loss of palpable or Doppler-sensed pulses. Treatment includes intravenous administration of heparin, Fogarty catheter embolectomy, and warfarin (Coumadin) therapy. If the embolus significantly obstructs flow and cannot be removed, intraarterial administration of streptokinase has been effective if given within 36 hours of thrombosis and if not contraindicated. Newer thrombolytic agents, such as reteplase and TPA, are also effective in the management of this problem.

Thermal Burns

Hands are involved in 80% of severe burns; however, life-threatening injuries and extensive body burns take precedence over hand burns. Assessment for inhalation injury is essential because mortality from burns with associated inhalation injury approaches 35%, whereas mortality from burns without inhalation injury is only approximately 4%. Burns are best managed in a specialized burn center and specific indications for transfer to a burn center are burns involving greater than 20% of total body surface area, inhalation injury, involvement of face, hands, feet, perineum, genitalia, and major joints. The rule of nines is used in estimation of burn size, with the surface area of the palm and fingers being 1% of the total body surface area. Other measures essential to early management include taking appropriate radiographs, establishing intravenous lines, administering tetanus prophylaxis and antibiotics, preparing for blood transfusion, and conducting a careful physical examination. Preserving viable tissue, preventing infection, controlling fibrosis, and avoiding deforming contractures also take high priority in the management of a burn injury in the hand.

Although the initial examination may be difficult because of pain and other injuries, an estimation of burn depth is necessary. Wilhelm Fabry in 1607 classified burns into first degree involving epidermis only, second degree involving the dermis, and third degree involving full-thickness skin. Tissue depth classification divided second degree burns into superficial second degree involving the papillary layer and deep involving the reticular layer. Fourth degree burns involve muscle, tendon, and/or bone ( Fig. 70.4 ). The judgment of the treating surgeon usually determines the estimation of burn depth. Superficial burns (first degree) produce no blisters; although they are erythematous, capillary refill is good, sensation is intact, and the dermis is unharmed. Treatment is symptomatic with soothing lotions and the burns usually heal spontaneously in 2 to 3 days without scarring. In superficial partial-thickness burns, some of the dermis is left intact, blisters may form, and capillary refill and sensation usually are present. They are quite painful since they involve nerve endings in the dermis; however, the blisters that are formed heal spontaneously in 10 to 14 days via re-epithelialization. Deep partial-thickness burns usually involve the entire dermis with minimal epithelial elements preserved. Capillary refill may or may not be present, but there should be some bleeding with pinprick; sensation usually is not intact; and thrombosed veins may be seen. These burns may heal spontaneously but very slowly and with considerable scarring. In deep burns (third and fourth degree) with dermal and subcutaneous necrosis, the skin appears leathery, brown to black, and no circulation or sensation to the skin is present. These cannot heal spontaneously.

The most important determination for limb survival is the adequacy of distal circulation, especially if the burn has a circumferential component. Interdisciplinary involvement is necessary and may include a burn team, pediatric surgeon, plastic surgeon, and hand therapist. Circulation of the upper extremity is considered adequate if the hand and fingers have rapid capillary refill and are pink, warm, and soft, and if pulsatile flow can be shown in the palmar and digital vessels with a Doppler probe. If the burn has a circumferential component with decreased distal perfusion (pale hand and fingers; decreased capillary refill; firm, cool hand and fingers; diminished flow shown by Doppler probe), immediate escharotomy should be considered. Intracompartmental pressures also should be measured, and if these are elevated, fasciotomies may be required. While perfusion is being assessed, the patient should receive adequate hydration with appropriate intravenous fluid replacement and monitoring of urinary output.

The depth of the burn, infection, and early management are major determinants of the functional and cosmetic outcome of hand burns. Other important factors are the location of the burn, the patient’s age, and the patient’s compliance with a rehabilitation program. There is agreement regarding the management of superficial hand burns and full-thickness and deeper burns. Superficial second-degree burns, if protected from additional injury and infection, should heal within 10 to 14 days with no significant impairment of hand function or cosmesis. Outpatient treatment usually is appropriate for these injuries. For partial-thickness burns (deep dermal, superficial full thickness), two approaches are advocated: (1) a “wait-and-see” method, with conservative treatment consisting of hydrotherapy, topical chemotherapy, and physiotherapy, and (2) an “operative” approach (in the first 3 to 5 days, as soon as practical), with tangential or full-thickness burn excision and early skin grafting ( Fig. 70.5 ). Advocates of conservative treatment believe that with close follow-up and good patient cooperation patients who are treated with topical antimicrobials (silver nitrate, silver sulfadiazine, mafenide acetate, povidone-iodine), hydrotherapy, and an organized rehabilitation program may achieve long-term functional and cosmetic results similar to patients who undergo early surgical treatment. The risks and discomfort of the surgical route are avoided. Falcone and Edstrom proposed an algorithm for management of hand burns that allows flexibility for appropriate, timely treatment, depending on burn depth and apparent wound healing ( Fig. 70.6 ).

Proponents of surgical treatment of partial-thickness hand burns cite as advantages (1) accurate determination of burn depth early in treatment, (2) earlier physiologic healing achieved by definitive debridement, closure, and skin grafting, (3) early and quicker rehabilitation, and (4) avoidance of excessive scarring and contractures associated with the “failed” conservative method. Tangential excision with skin grafting and full-thickness excision with skin grafting are two techniques used for treatment of partial-thickness hand burns. The advent of vacuum-assisted closure (VAC), with and without the use of skin substitutes, has made early surgical intervention a better choice.

The special characteristics of the soft tissues in the hand allow for what might be considered a combined approach to partial-thickness burns of the hand. Dorsal burns may benefit from early excision (within 14 days) allowing for protective coverage and early mobilization of the superficial extensor tendon mechanism and interphalangeal joints where extension contractures can be devastating to hand function. On the flexor surface, the flexor mechanism and joints are deeper and relatively better protected and may tolerate a delay of 3 weeks better than the dorsal structures.

For deep full-thickness burns (third and fourth degree), primary full-thickness excision of the burn wound with skin grafting is the appropriate treatment ( Fig. 70.7 ). For palmar hand burns, full-thickness skin grafts offer improved durability and elasticity with less scar contracture than split-thickness skin grafts. Plantar glabrous skin grafts have been shown to offer reliable coverage in pediatric patients. Split-thickness skin grafting meshed 1 to 1 is preferred for dorsal coverage. When tendons, nerves, vessels, ligaments, bones, and joints are damaged by thermal injury, measures in addition to burn wound excision and split skin grafting may be required. Dermal substitutes such as Integra followed by skin grafting at 2 to 4 weeks has proved useful. Stabilization of bones and joints with Kirschner wires, arthrodesis of destroyed joints, local and remote pedicled skin flaps, and free tissue transfers may be needed to preserve a viable, functioning hand. (For additional information, see Chapter 67 for fractures, Chapter 73 for arthrodesis, Chapter 65 for flaps, and Chapter 63 for microvascular flaps.)

An organized plan of rehabilitation is important to the success of the treatment of the burned hand. The focus of rehabilitation in the early acute stage is wound care, edema control, and preservation of motion. After closure of the burn wound, a program including static and dynamic splinting, active and passive range-of-motion exercises, and control of scar and edema is pursued. Scar contractures may severely limit hand function, so rehabilitation should be aimed at prevention. Puri et al. recommended the preoperative use of splints in certain patients with thermal burn contractures. The rehabilitation plan depends on the needs of the individual patient and requires the participation of hand therapists, occupational and physical therapists, and physical medicine consultants. Many patients with severe and disfiguring burns require the emotional support of psychiatric and psychologic consultants.

Electrical Burns

Electrical burns frequently involve the upper extremity and involve working age males 95% of the time. The dominant hand frequently is injured, and 50% of these injuries result in amputation. Tissue damage can result from a combination of thermal, electrical, and metabolic cellular factors. The extent of injury is determined by the characteristics of the injuring current, including the voltage, amperage, and resistance of the tissues; the duration of contact with the current; and the patient’s susceptibility to it ( Fig. 70.8 ). Exposure to 1 to 2 mA causes a tingling sensation, 8 to 12 mA causes muscle contraction, and greater than 20 mA causes tetanic contractions exceeding the let-go threshold, causing prolonged exposure with dislocations and fractures. Although the skin damage caused by electrical injury may be the most impressive presenting finding, significant deep injury may be present as determined by the route the electrical current takes through the body. Maximal damage occurs in narrow anatomic zones such as the elbow, wrist, and fingers, which are called choke points. Electrical injuries may involve the central and peripheral nervous systems, the cardiopulmonary and peripheral vasculature, the musculoskeletal system, the kidneys, and the skin. Initial management is directed at resuscitation. Appropriate diagnostic measures include radiographs of potential fractures and dislocations; electrocardiogram; and serum chemistries to assess electrolytes and liver, renal, cardiac, and skeletal muscle injury. Urine myoglobin levels and arterial blood gases are measured as well. The extent of injury to all systems should be evaluated, ensuring satisfactory hydration and urinary output, because patients with electrical burns may require more fluid resuscitation than might be calculated based on the injury to the total body surface area. Urinary output of 50 to 100 mL/hr is preferable. Recognizing, stabilizing, and reversing the effects of cardiac injury and the nephrotoxic effects of myoglobinuria and hemoglobinuria also are important. Because of the potential for hemorrhage from damaged vessels, a tourniquet should be kept near the patient’s bedside.

In electrical burns of the hand and upper extremity, the initial evaluation should include a thorough examination of the entire body for skin and neuromuscular injury. Evaluation of circulation includes examination of skin color and warmth, palpation of peripheral pulses, and flow assessment with a Doppler probe. Skin burns may be the result of contact, flame, flash, or electrical arcing, or all of these may be factors. Contact burns have a central charred area surrounded by erythema. Flash and flame burns are thermal injuries, having the appearance of other thermal burns. Arcing burns usually are seen in the axilla, the antecubital fossa, and the distal forearm. There is no correlation between the size of the skin injury and the actual extent of injury.

Muscle injury is assessed clinically using the usual methods of palpation and evaluation of active motion and measurement of tissue compartment pressures. Extensive muscle damage may be undetectable in a clinical examination, and myoglobinuria may be a clue as to the extent of muscle injury. Other techniques that have been studied include technetium-99m pyrophosphate scanning, arteriography, and a xenon-133 washout technique. Deep injury also may be shown with gadolinium-enhanced MRI.

Patients with relatively minor electrical injuries may not require surgical treatment. For the management of more severe electrical injuries of the upper extremity, two methods are advocated. One method is immediate escharotomy, fasciotomy, and debridement of necrotic tissue, followed by repeat debridement until the wound is suitable for closure with skin grafts, remote flaps, or free tissue transfer. Decompression of peripheral nerves, including the median nerve at the carpal tunnel, is included in this initial procedure. Because tissue necrosis may not be clearly detectable for 24 to 48 hours after injury, some prefer a second approach in which decompression procedures are delayed unless decreased perfusion or increasing compartmental pressures are clearly evident. The extent and severity of the injury may make amputation inevitable. Mann et al. reported an amputation rate of 45% in patients who had decompression within 24 hours and a rate of 10% in patients undergoing delayed decompression and debridement. Management of severe injuries should proceed in a progressive manner. Decompression by escharotomy and fasciotomy, when indicated, should be performed, followed by thorough debridement of necrotic tissue, usually in a serial fashion, and coverage by means of skin grafting, a remote flap technique, or free tissue transfer. After a course of healing and rehabilitation, patients with electrical burns may require additional reconstructive procedures ( Fig. 70.9 ).

Radiation Burns

In radiation burns or dermatitis caused by overexposure to roentgen rays, the skin becomes pale, dry, atrophic, and wrinkled, and scattered keratoses develop; the fingernails split longitudinally. Within weeks of exposure, itching, erythema, and blistering may be seen; later, painful ulcers may develop. The skin can become increasingly painful, and eventually narcotics may be indicated. Multiple squamous cell carcinomas may develop and cause ulceration. Such burns have caused physicians and other medical professionals to lose digits. These burns, typically on the dorsum of the fingers of the left hand, presumably are caused in the medical profession by holding roentgen cassettes or using the fluoroscope without protection. When breakdown of tissue, pain, or malignant change makes resurfacing of the hand necessary, the damaged skin is excised and split-thickness grafts are applied simultaneously. The area of excision should be generous, including even questionably involved skin; usually all dorsal skin from the wrist distally should be replaced. Malignant changes in the hand may require amputation.

Chemical Burns

Chemical burns to the hand usually result from spills, splashing, or immersion. Most chemical burns to the hand are superficial, requiring only first aid management, and the prognosis is good. It is important to remember, however, that certain chemicals carry a risk of systemic toxicity and even death. Circumferential burns of the hand are unusual. Sulfuric acid and alkali account for most chemical injuries. Acid burns usually progress until damaged tissue neutralizes the acid or the acid is neutralized by lavage or a neutralization treatment. Injury caused by alkaline substances may progress for long periods, resulting in extensive and deep liquefaction necrosis. Jelenko and Reilly and Garner reviewed the chemicals that burn and their recommended emergency treatment ( Fig. 70.10 ). Prolonged water lavage is best for most chemical burns, avoiding attempts to neutralize with either alkaline or acidic solutions. It should be started at the scene of injury and should last 20 to 30 minutes to bring the skin pH to near neutral. Lavage for longer periods of time may be necessary for severe acid burns and for alkali burns. Chemical injury from some agents requires specific management ( Table 70.1 ). Exposure of elemental lithium, potassium, and sodium to water causes ignition. Initial management includes mineral oil application, followed by water irrigation of particles remaining in the skin. Hydrofluoric acid, which is used in glass etching and petrochemical refining, results in continuing tissue damage because of the fluoride ion, which combines with calcium and magnesium in the tissues. Hypocalcemia may result if it involves more than 2.5% total body surface area. After initial water irrigation, application of a 2.5% calcium gluconate gel may be sufficient. If pain is not relieved promptly, injection of 10% calcium gluconate or magnesium sulfate deep to the lesions may be beneficial. For persistent pain, 10 cc of 10% calcium gluconate in 40 cc saline can be delivered as Bier block or intraarterially over 4 hours or until the pain is eliminated. Because phenol is not water soluble, removal with glycerol or polyethylene glycol has been recommended. White phosphorus particles may continue to smoke as long as they are exposed to air. Initial irrigation with a solution of 1% to 3% copper sulfate blackens the phosphorus particles so that they can be removed under water in a water bath. If the phosphorus is not irrigated first with copper sulfate, it may ignite on contact with water. Tar burns are best treated with an emulsifying agent such as Neosporin cream. Significant chemical burns seen late may require hospitalization and monitoring of the hand and digital circulation with Doppler probes and digital oximetry. If circulatory compromise results from a circumferential burn, decompression is indicated. Deeper chemical burns may require debridement and closure with skin grafts, pedicle flaps, or free tissue transfer. Recovery usually is prompt if surgical treatment is combined with a hand therapy rehabilitation program.

Frostbite

Frostbite injuries to the hands and feet account for about 90% of frostbite cases. Frostbite tissue damage seems to arise from direct cell death owing to freezing and anoxia caused early by vascular constriction and later by vascular thrombosis. Research by Heggers et al. found elevation of thromboxane and prostaglandin metabolites in frostbite blister fluid. In order of increasing degrees of damage, the following conditions develop: erythema, edema, vesiculation, necrosis of the skin, necrosis of deeper soft tissue, and necrosis of bone ( Fig. 70.11 ). Superficial frostbite results in relatively clear blisters, and deeper injuries may be anesthetic after thawing and form hemorrhagic blisters. The traditional categorization of frostbite into four degrees has not been as useful in determining results of treatment as has the designation of the injuries as superficial and deep ( Box 70.1 ).