Principles of management of volkmann’s contracture
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This document discusses the principles of management of established Volkmann's ischaemic contracture. It begins with an introduction that defines Volkmann's contracture and notes it is a challenging condition to manage requiring a multidisciplinary approach. It then covers relevant anatomy, pathogenesis, classifications, principles of management in four phases including nerve decompression, contracture treatment, tendon transfers, and salvage procedures. Outcomes depend on factors like dexterity, hand strength, and sensibility regained. Early detection and treatment of acute compartment syndrome is key to preventing Volkmann's contracture.
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Principles of management of volkmann’s contracture
- 1. Principles of Management of Established VOLKMANN’S ISCHAEMIC CONTRACTURE Dr Arojuraye S.A National Orthopaedic Hospital, Dala - Kano
- 2. Outline Introduction Relevant anatomy Pathogenesis Classification Principles of Management Prognosis Conclusion References
- 3. Introduction VIC: Dysfunctional limb with varying amounts of deformity, stiffness & paralysis as a result of ischemia leading to irreversible muscle & nerve damage. Mgt is challenging, multidisciplinary ACS ► ↓capillary perfusion ► muscle & nerve damage ► necrosis ► fibrosis ► contracture
- 4. Introduction… Severe ischaemic insult may have 3 outcomes: Complete recovery Gangrene Middle course (contracture) Difference between gangrene & ischaemic contracture is not purely quantitative: Gangrene involves all tissues Contracture is “selective” (muscles & nerves)
- 5. Introduction… 1881: Richard von Volkmann (tight bandaging) 1922: Brook (venous obstruction) Leriche & Griffiths (arterial spasm) 1911: Bardenheur (forearm fasciotomy)
- 6. Introduction… Risk factors Decreased compartment size Constrictive Splint, Dressing Closure of fascial defect Circumferential Burn eschar Increased compartment content Humeral supracondylar # Forearm bones # Vascular injury, Bleeding diasthesis Infection
- 8. Pathogenesis 4hrs of ischaemia ► muscle necrosis Fibroblastic proliferation within muscle Adheres to surrounding structures Fixes muscle position Reduces excursion & mobility Stiffness & joint contracture Peripheral nerves (Ischaemia / Compression)
- 9. Pathogenesis… Deepest compartments FDP & FPL In mildest contracture FDP to ring & long fingers In severe contracture All four digits Less commonly affected FDS & Pronator teres
- 10. Pathogenesis… Upper limb Elbow flexion Forearm pronation Wrist flexion MCPJ extension IPJ flexion Thumb flexion & adduction Median & ulnar nerve neuropathy
- 11. Pathogenesis… Extremity may initially be flexible Chronic muscle imbalance & joint stiffness Fixed deformity from 20 joint capsule Ligament & skin contractures
- 12. Pathogenesis… Intrinsic muscle contracture Intrinsic-plus deformity Flexion (MCPJ) + Extension (PIPJ) Volkmann's contracture Intrinsic-minus deformity Hyperextension (MCPJ) + Flexion (PIPJ) Although the two entities may occur simultaneously, the resultant claw-hand deformity is determined by contracture of the more powerful extrinsic finger flexors
- 13. Classification Bunnell (1944): Simple / Severe Pedemonte (1948): Classic / Useless Merle D’ Aubigne (1955): With claw hand / Without claw hand Holden (1975): Ischaemia proximal / ischaemia at the same level
- 14. Classification… Seddon (1956), modified by Tsurge: Mild Moderate Severe
- 15. Classification… Mild (localized) Limited to extrinsic finger flexors Usually 2 or 3 fingers Hand sensibility & strength are normal Intrinsic muscles not involved Fixed joint contracture not present Usually occur in young adults Most are caused by fractures or crush injury
- 16. Classification…
- 17. Classification... Moderate Classic type Primarily affects FDP & FPL Occasionally FDS, FCR & FCU Wrist & thumb are flexed Claw hand deformity 20 nerve compression Commonly median Rarely radial
- 18. Classification…
- 19. Classification… Severe Affect forearm extensors & flexors Commonly due to brachial artery damage Often encountered: Loss of nerve function Malunion or nonunion Cutaneous scarring Contractures
- 20. Classification…
- 21. Principles of management (Preoperative) History Age Hand dominance Deformity + difficulty with using the hand Hx of trauma around the elbow Hx of care PMHx
- 22. Principles of management (Preoperative) Examination Wasting Deformity Scar Cord- like induration Neurologic deficit Fixed contractures +ve Volkmann sign Clinical photographs
- 23. Principles of management (Preoperative) Investigations Plain radiograph Angiography MRI Direct nerve stimulation Others FBC, U/E, GMX
- 24. Principles of management (Preoperative) Informed consent Pathogenesis Prognosis
- 25. Principles of management (Intraoperative) Anaesthesia Tourniquet Lighting Operating loops Antibiotic prophylaxis Appropriate instruments
- 26. Principles of management (Intraoperative) Fine instruments Tissue handling Haemostasis Wound irrigation Closure Dressing
- 27. Principles of management Mild (early) Normal hand sensibility & strength: conservative Passive & dynamic extension splinting Alternate passive & dynamic splints at 2-hour At night: extension splints Satisfactory outcome with early treatment Mild (late) Excision of infarcted muscle Lengthening the tendon
- 28. Principles of management… Moderate to severe (4 phases) Release of 20 nerve compression Treatment of contractures Tendon transfers for substitution / reinforcement Salvage procedure (bone)
- 29. Principles of management… (I) Release of 20 nerve compression Improvement is related to severity & duration Signs of gradual recovery: 12-month period Severe fibrosis & contracture (all 3 nerves) Median nerve can be constricted in Lacertus fibrosus 2 heads of Pronator teres Proximal arch of FDS Carpal tunnel
- 30. Principles of management… Release of 20 nerve compression… Ulnar nerve compression Incidence much lower Btw ulnar & humeral heads of FCU Radial nerve compression Rarely involved Under tendinous origin of supinator (arcade of Frohse)
- 31. Principles of management… (II) Treatment of Contractures Should be performed at the time of, or subsequent to, nerve decompression Infarct excision 6 months of splinting b4 surgery (Seddon) Postop immobilization (supination & extension) Flexor tendon lengthening or excision Z- lengthening of FDP, FDS, FPL, PT (Goldner) Disadvantage: weakness
- 32. Principles of management… (II) Treatment of Contractures… Should be performed at the time of, or subsequent to, nerve decompression Flexor pronator slide First described by Page in 1923 More effective than infarct excision Release the origins of PT, FCR, PL, humeral head of FCU, FDS, FPL.
- 33. Principles of management… (III) Tendon transfers Usually delayed till after nerve recovery After maximal contracture correction Phalen & Miller (1947) Digital flexion & thumb opposition ECRL → FDP, ECU → thumb opposition, EPB → ECUs Huber Abductor digiti minimi quinti opponenplasty Zancolli & Burkhalter Extensor indicis proprius opponenplasty
- 34. Principles of management… (IV) Salvage procedure Seldom necessary Proximal or distal carpectomy Radius & ulnar shortening Wrist or digital fusion
- 35. Principles of management… Outcome Dexterity Hand grip strength Sensibility Appearance
- 36. Conclusion VIC of the forearm is very common in our society Prevention is easier than treatment Community awareness might play a role Early detection & Rx of ACS is the key to prevention
- 37. References Richard HG, Michael JB. Management Of Volkmann's Contracture. In: Chapman MW. Chapman's Orthopaedic Surgery, 3rd Edition. Lippincott Williams & Wilkins 2001; 65: 1782 – 1791. Khan F, Cheema TA, Bhatti ZI. Volkmann’s ischemic contracture; Post-circumferential contracture of the forearm. Professional Med J 2014;21(3): 550-555. Holden CE. Pathology and prevention of Volkmann ischaemic contracture. J bone joint surg. 1979; 61 (3): 269 – 300. Nayagam S and Warwick D. Orthopedic Operations. In: Solomon L, Warwick D, Nayagam S. Appley’s system of Orthopedics and fractures. 9th Ed. Hodder Arnold 418.
Editor's Notes
- Acute compartment syndrome produces high interstitial tissue fluid pressures that can reduce capillary perfusion below the level necessary for tissue viability. If the compartment syndrome is sustained or untreated, ischemia results in irreversible muscle and nerve damage. Muscle then undergoes necrosis, fibrosis, and contracture. Concomitant nerve injury results in further muscle dysfunction, sensibility deficits, or chronic pain. The result is a dysfunctional limb with varying amounts of deformity, stiffness, or paralysis, known as Volkmann's ischemic contracture.
- The basis for VIC is compartment syndrome that can develop from swelling of the muscles and soft tissues that are contained in a tight osteofacial compartment. Due to this swelling, intracompartmental pressure rises sufficiently to cause blockage of capillary 2 perfusion . Muscle necrosis occurs after 4 hours of ischemia which is followed by fibroblastic 3 proliferation within the muscle infarct . Necrosed muscle mass become fixed by adhering to surrounding structures thereby reducing their 4 excursion and mobility . Peripheral nerves are secondarily compressed by surrounding necrotic muscle mass. This neuropathy can also lead to chronic pain, paresthesias and loss of limb 5 sensibility apart from motor paralysis
- In 1881, Richard von Volkmann first described this condition, noting paralysis and subsequent limb contracture that followed the application of tight, constricting bandages to an injured limb. In 1922, Brooks described a similar condition and believed venous obstruction was a factor in the contracture formation. Arterial spasm or injury were subsequently indicated as causes by Leriche and Griffiths (32,49). In an attempt to prevent the contracture described by Volkmann, Bardenheur in 1911 discussed the use of forearm fasciotomy .
- Muscle undergoes necrosis after 4 hours of ischemia produced experimentally by application of a tourniquet. With prolonged ischemia, muscle necrosis leads to fibroblastic proliferation within the muscle infarct. A variable amount of longitudinal and horizontal contraction may progress over a 6- to 12-month period following the ischemic insult. The necrotic muscle adheres to surrounding structures, fixes muscle position, and reduces excursion and mobility. Limitation of muscle excursion may lead to loss of joint motion with subsequent joint contracture. Peripheral nerves in the vicinity can also be injured from the original ischemic insult, as well as from subsequent compression resulting from muscle fibrosis, or from the chronic stretch of limb deformity. The developing fibrosis may surround, tether, or impinge on adjacent peripheral nerves, leading to local compression. Hyperflexion at the elbow or wrist can lead to secondary neuropathy of the ulnar nerve or the median nerve, respectively. In addition to the associated motor loss, neuropathy following ischemic contracture can lead to paresthesia, loss of limb sensibility, and chronic pain.
- The deepest compartments, especially those adjacent to bone on the volar forearm, usually have the highest interstitial pressure during an acute compartment syndrome. Subsequent injury that leads to ischemic necrosis is most marked in these deep compartments, more commonly involving the flexor digitorum profundus and flexor pollicis longus. In the mildest contractures, only part of the flexor digitorum profundus undergoes necrosis, usually to the ring and long fingers. In severe contractures, all four digits are involved. The flexor digitorum superficialis and pronator teres are generally less severely affected. In the most severe cases, the wrist flexors, the wrist and digital extensors, and the compartments proximal to the elbow may also undergo varying degrees of fibrosis and contracture
- When the forearm, hand, and arm are significantly involved, the deformity in the upper extremity often consists of varying amounts of elbow flexion, forearm pronation, wrist flexion, thumb flexion and adduction, digital metacarpophalangeal (MP) joint extension, and interphalangeal joint flexion (Fig. 65.3). The MP joint extension and proximal interphalangeal joint flexion give rise to a claw hand deformity.
- The extremity may initially be flexible, especially in milder cases. Chronic muscle imbalance and lack of joint motion may ultimately lead to fixed deformity from secondary joint capsule, ligament, and skin contracture.
- The pathomechanics of the ischemic claw-hand deformity are complex. Although there may be an apparent similarity between the ischemic contracture and the intrinsic muscle contracture in some patients, the actual deformities are considerably different. Intrinsic muscle contracture results in an intrinsic-plus deformity, with flexion at the MP joints and extension at the proximal interphalangeal joints. Volkmann's contracture often leads to an intrinsic-minus deformity, with hyperextension at the MP joints and flexion at the interphalangeal joints. Although the two entities are associated and may occur simultaneously, the resultant claw-hand deformity is determined by contracture of the more powerful extrinsic finger flexors. A paradoxical situation of a claw-hand deformity with intrinsic tightness can exist (82). The intrinsic contracture may not become apparent until the extrinsic flexors have been released by a muscle slide, tendon lengthening, or tenotomy. Only then does intrinsic tightness become evident.
- Holden classified VIC of the limbs into two types. Type 1 involving a major artery, occurred proximal to the site at which ischemia subsequently developed (above the elbow). Type 2 where direct trauma to a limb and subsequent ischemia occurred at the same site 8 (below the elbow)
- A mild or localized contracture is limited to a portion of the deep extrinsic finger flexors, usually involving only two or three fingers. Hand sensibility and strength are normal. The intrinsic muscles are not involved, and fixed joint contractures are not present. Most mild types of ischemic contracture are caused by fractures or crush injuries to the forearm or elbow, and they usually occur in young adults
- Moderate contracture, the classic type, primarily involves the flexor digitorum profundus and flexor pollicis longus muscles. Less frequently, the flexor digitorum superficialis, flexor carpi radialis, and flexor carpi ulnaris are involved. The wrist and thumb become flexed and the hand assumes a claw-hand deformity from contracture of the long finger flexors. Secondary compression neuropathies may develop at specific locations where nerves pass beneath ligaments or fibrous arcades or through contracted muscles. The median nerve is most frequently compressed, usually at the lacertus fibrosus, pronator teres, or flexor digitorum superficialis, or within the carpal tunnel. The ulnar nerve may be compressed within the cubital tunnel or between the two heads of the flexor carpi ulnaris. The radial nerve is rarely involved, but it may be compressed at the arcade of Frohse or within the supinator muscle. Most moderate contractures are caused by a supracondylar fracture of the humerus. These fractures occur most commonly at 5 to 10 years of age
- Severe contractures affect forearm extensors as well as flexors. Complications, including loss of nerve function, malunion or nonunion of forearm fractures, and cutaneous scarring and contracture, are often encountered. The most common causes of severe contracture are prolonged ischemia secondary to brachial artery injury, and prolonged external compression secondary to drug overdose
- The treatment of mild contractures depends on the severity of the deformity and the time interval between injury and initiation of treatment. Contractures of the deep forearm flexors, with normal hand sensibility and strength, may be treated conservatively. Occupational therapy, including passive and dynamic extension splinting, is designed to maintain wrist and interphalangeal joint extension, to maintain or improve thumb web-space width, and to strengthen weak thumb intrinsic muscles. Alternate the use of bivalved pancake plaster casts or custom-molded synthetic orthoses with low-profile digital extension, and thumb opposition splints. A C-bar may be incorporated into the splint to maintain thumb position. In the early stages, have the patient alternate passive and dynamic splints at 2-hour intervals during the day and, at night, wear extension splints. Splinting techniques for Volkmann's contracture have been described in detail by Goldner (30). A satisfactory outcome can be expected when mild contractures are treated soon after their development using these techniques. Tsuge recommends operative treatment for mild contractures that are encountered late . If the contracture is limited to one or two digits and a cordlike area is palpable, simple excision of the infarcted muscle or lengthening of the involved flexor tendons is recommended. Perform excision of the infarcted muscle through a curved, longitudinal incision on the palmar forearm. Identify and protect the radial artery, median nerve, and ulnar artery and nerve. Retract the flexor digitorum superficialis and flexor carpi radialis radially, and the flexor carpi ulnaris ulnarly, to expose the flexor digitorum profundus. Isolate and excise the palpable, cordlike areas of indurated muscle. The flexor digitorum profundus of the ring and long fingers is most commonly affected. If the contracture is localized to the pronator teres, this muscle may be excised. If the contracture and induration involve three or four digits, flexor tendon lengthening may be required. Perform Z-lengthening of the involved tendons in the distal two thirds of the forearm. Begin the Z-lengthening incisions proximally, near the musculotendinous junctions, to ensure adequate tendon length for satisfactory correction. Repair the tendons using 4-0 nonabsorbable suture. Following the surgery, immobilize the forearm in supination, the wrist in extension, and the digits in the corrected amount of extension.
- Phase 1: Release of Secondary Nerve Compression Following muscle infarct, nerves may become compressed within a constricting cicatrix, or at specific anatomic locations where space is minimal. Secondary compressive neuropathies require attention in the earliest stages of treatment. Improvement of nerve function is related to the severity and duration of compression, as nerves may sustain compression for longer periods than muscle and still show some reversibility, particularly in sensory function. When continuity is maintained, nerves may show signs of gradual recovery over a 12-month period. If both fibrosis and contracture are severe, all three major forearm nerves may become constricted. Careful clinical assessment is essential before the first phase of treatment. Median Nerve Decompression Return of median nerve function is essential for restoring a useful functional extremity. This nerve lies in the center of the constricting cicatrix and may become compressed in four anatomic regions: the lacertus fibrosus, the pronator teres, the proximal arch of the flexor digitorum superficialis, and the carpal tunnel. Sensory and motor loss consistent with median neuropathy warrant aggressive management for decompression. Use an incision similar to that used for decompression of an acute forearm compartment syndrome . Begin the incision on the palmar aspect of the medial arm, about 2 cm proximal to the medial epicondyle. Extend it obliquely across the antecubital fossa to the mobile wad. Continue the incision longitudinally, curving slightly ulnarly to reach the palmar distal forearm. Extend the incision into the palm for carpal tunnel release. Locate the distal portion of the incision ulnar to the palmaris longus to avoid injury to the palmar cutaneous branch of the median nerve. Identify the median nerve in the proximal portion of the incision and trace it distally to the lacertus fibrosus. The lacertus fibrosus is a fascial extension of the biceps tendon and lies anterior to the median nerve at the elbow. Nerve compression occurs frequently in this area in the acute stages of a forearm compartment syndrome, and it may also occur in the later stages of contracture. If signs of proximal median nerve compression are present, release the lacertus fibrosus. Incise the fascia of the lacertus fibrosus in a longitudinal fashion along the course of the median nerve to allow complete decompression and exposure of the nerve. Continuing distally, the median nerve will pass between the two heads of the pronator teres muscle. Nerve compression can occur between these two heads. The ulnar head lies deep to the nerve, and the humeral head is superficial to the nerve. A tendinous band, which often lies along the deep head, may contribute to compression. Completely release the nerve throughout the entire length of its passage through the pronator teres. This often requires division of the humeral head of the pronator teres and division of any tendinous bands, deep or superficial, that may impinge on the nerve. Distal to the pronator teres, the median nerve continues beneath and within the fascia of the flexor digitorum superficialis muscle, passing deep to the arch formed by the ulnar and radial origins. The nerve is most frequently compressed beneath the fibrous origin of this muscle (72). Decompress the nerve by either incising the investing fascia or by dissecting the flexor digitorum superficialis from the underlying flexor digitorum profundus. Completely release the nerve from the investing fascia (72). Despite the proximal location of muscle necrosis in Volkmann's contracture, the incidence of median nerve compression in the carpal tunnel is high. Extend the incision for forearm decompression and expose the palmar fascia and transverse carpal ligament. Incise these structures to decompress the median nerve decompression from the distal arm to the midpalm. Ulnar Nerve Decompression
- Ulnar Nerve Decompression The incidence of ulnar nerve compression is much lower than that of median nerve compression. It is often compressed at the elbow as it passes between the ulnar and humeral heads of the flexor carpi ulnaris. Decompress it if there are signs of ulnar neuropathy. Radial Nerve Decompression The radial nerve is rarely involved in compression neuropathies following Volkmann's contracture. Occasionally, however, it may require decompression as it passes under the tendinous origin of the supinator muscle (arcade of Frohse) or within the muscle itself. Nerve compression is manifested by motor loss of the digital and thumb extensors and the ulnar wrist extensors. Radial wrist extensor strength and radial nerve sensibility remain intact, as these neural branches arise proximal to the area of compression (10). To decompress the radial nerve, make a straight, longitudinal incision on the proximal half of the posterior forearm along an imaginary line extending between the lateral epicondyle and the radial styloid. Develop the interval between the extensor carpi radialis brevis and the extensor digitorum communis. This interval is most easily defined in the distal portion of the incision and should be developed here first and traced proximally. Retract the extensor carpi radialis brevis radially and the extensor digitorum communis ulnarly. Identify the supinator. Identify the radial nerve proximally where it enters the supinator. The nerve may be found to be compressed by the tendinous bands of the arcade of Frohse, by a vascular leash that crosses the nerve transversely in this region, or by the supinator muscle itself. Carefully divide the appropriate structures to decompress the nerve (10). Forearm nerve decompression should be undertaken as soon as the patient's condition permits. A nerve stimulator may be helpful for verification of conductivity, especially in heavily scarred areas. Early return of sensibility and a decrease in pain may be expected when decompression is undertaken in a timely manner. Motor function return, although variable, can progress over several days or weeks, depending on whether neuropraxia or axontemesis is present. If nerves are irreparably damaged or have lost continuity (neurotemesis), secondary excision of damaged segments and microsurgical repair or reconstruction may offer some return of nerve function. Alternatively, reconstruction may be accomplished with appropriate tendon transfers.
- Phase 2: Treatment of Contractures Elbow flexion, forearm pronation, wrist flexion, digital clawing, and thumb adduction are fixed deformities that develop over time. Procedures used to help correct established forearm contractures include infarct incision, flexor tendon lengthening or excision, and flexor pronator slide. These procedures should be performed at the time of, or subsequent to, nerve decompression. Infarct Excision Perform infarct excision 1 to 6 months after injury. Seddon recommends at least 6 months of preliminary splinting before contracture release. Excise the frequently encountered ellipsoid infarct through a long palmar forearm incision (80). Excise fibrotic muscle and contracted scar tissue. The deep digital flexors and thumb flexor are usually most extensively involved. The pronator teres and pronator quadratus may be released or, if they are fibrotic, excised. Gently manipulate the forearm and wrist into supination and extension, respectively, and immobilize in this corrected position following surgery. Flexor Tendon Lengthening Goldner has noted that infarct excision may not be necessary and advocates Z-lengthening of the forearm flexors proximal to the wrist (30). The flexor digitorum profundus, flexor digitorum superficialis, flexor pollicis longus, and pronator teres may be lengthened to accomplish digital and thumb extension, and forearm supination (6,30). If severe forearm fibrosis is encountered and digital contracture is severe, excise the flexor digitorum superficialis. The chief disadvantage of flexor tendon lengthening in the forearm is further weakening of an already weakened muscle. However, contracture release is usually functionally advantageous to the maintenance of maximal strength. Tendon transfers, if needed, may be performed at a later date. Flexor Pronator Slide The flexor pronator slide, first described by Page in 1923 (69), has gained wide acceptance. It has been shown to be more effective than infarct excision alone in obtaining a lasting correction. Make a skin incision on the medial side of the elbow, 6 cm proximal to the medial humeral condyle and extending to the junction of the middle and distal thirds of the forearm. Separate the subcutaneous tissue from the deep fascia on the ulnar and radial sides of the incision. Isolate the ulnar nerve at the level of the elbow and transpose it anteriorly. Proceed with systematic, complete operative detachment of the origins of the flexor muscles of the forearm. Dissect the muscles subperiosteally using a scalpel. Release the origins of the pronator teres, flexor carpi radialis, palmaris longus, and the humeral head of the flexor carpi ulnaris, and then detach the flexor digitorum superficialis. Detach the ulnar head of the flexor carpi ulnaris and the broad origin of the flexor digitorum profundus from the anterior aspect of the ulna. Carry the dissection across the interosseous membrane and release the origin of the flexor pollicis longus from the anterior aspect of the radius. Take care to avoid injury to the interosseous artery, vein, and nerves when detaching the flexors from the interosseous membrane. Allow the muscles to slide distally 2–3 cm. The incision may be extended distally and the palmar wrist capsule and pronator quadratus released. Although P.1788 excision of the infarct and neural releases may be performed at the time of the flexor pronator slide, tendon transfers are performed secondarily (91,92). Postoperatively, immobilize the extremity for 2–3 weeks with the elbow at 90° flexion, the forearm supinated, and the wrist and digits extended. The flexor pronator slide has been criticized for the unpredictability of correction achieved, the risk of recurrence of deformity with growth, and the resultant decrease in grip strength, particularly at the distal interphalangeal joint (52,91,92). Despite these criticisms, the procedure has gained popularity and has been shown to be effective in achieving satisfactory to excellent results in a large group of patients with moderate to severe contractures.
- Phase 3: Tendon Transfers for Substitution and Reinforcement Among the most desirable functions to restore in patients with Volkmann's contracture are finger and thumb flexion and thumb opposition. Tendon transfers are usually delayed until nerve recovery has plateaued and the contractures have been corrected maximally with mobilization and splinting, or with operative releases. In 1947, Phalen and Miller described a series of tendon transfers designed to provide digital flexion and thumb opposition (73). Tendon Transfers Transfer the extensor carpi radialis longus to the flexor digitorum profundus, and transfer the extensor carpi ulnaris, lengthened by tendon graft, to the thumb for opposition (71,73). Excise the tendons of the flexor digitorum superficialis if they are nonfunctional. The extensor pollicis brevis may be used to reinforce the extensor carpi ulnaris–opponens transfer. Alternative transfers to augment thumb opposition include the abductor digiti quinti opponensplasty described by Huber (42,52) and the extensor indicis proprius opponensplasty described by Zancolli (100) and Burkhalter et al. (14). To reinforce thumb flexion, the brachioradialis may be transferred to the flexor pollicis longus (91,92). When flexor tendons have been weakened severely by previous Z-lengthening, reinforcement by transfer of the extensor carpi radialis longus to the flexor digitorum profundus, and transfer of the extensor carpi ulnaris to the flexor pollicis longus, can be performed (30).
- Phase 4: Salvage of the Severely Contracted or Neglected Forearm The procedures of Phases 2 and 3 usually provide satisfactory results, and further procedures are seldom necessary. Occasionally, however, additional measures may be required for satisfactory correction of the severely contracted or neglected forearm. Operations that have proved useful include proximal or distal row carpectomy, radial and ulnar shortening, wrist fusion, and digital joint fusion. Proximal or distal row carpectomy results in limb shortening that allows wrist extension while maintaining flexibility. In severe deformities, carpectomy may be performed before tendon transfer. If adequate donor muscles are not available for transfer, interphalangeal joint fusion can be performed. The stabilized limb can then function as a hook, which is generally superior to a prosthesis, especially if some sensibility is retained (30). Radial and ulnar shortening and wrist fusion are rarely indicated for the treatment or salvage of Volkmann's contracture.
- Post-circumferential VIC of the forearm is very common in our society. The prevention of this form of iatrogenic disaster is by no means easy. Community awareness through health education and conducting medical camps and seminars might play a role in decreasing the influence of TBS. Additionally, the occurrence of VIC can be reduced by early detection and treatment of compartment syndromes. If symptoms of c o m p a r t m e n t s y n d r o m e a r e p r e s e n t , decompression should be done immediately to restore microcirculation.