The main goals of treating severe crush injuries are debriding away devitalized tissue and filling any resultant dead space with vascularized tissue. In the authors’ experience, the most ideal methods for soft tissue coverage in treating crush injuries are the iliac flap, the adipofascial lateral arm flap, and the gracilis flap. Accompanying bone defects respond very well to free corticoperiosteal flaps. Digital defects often require the use of complete or subtotal toe transfer to avoid amputation and restore function to the hand.
Key points
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Microsurgery changes the prognosis of crush hand syndrome.
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Radical debridement should be followed by rigid (vascularized) bony restoration.
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Finally, bringing vascularized gliding tissue allows active motion to be restored.
Introduction
Severe crush injuries to the hand and fingers often carry an unavoidably bad prognosis, resulting in stiff, crooked, and painful hands or fingers. In follow-up, osteoporosis is often times seen on radiographs. A shiny appearance of the skin and complaints of vague pain may lead the surgeon to consider a diagnosis of reflex sympathetic dystrophy, to offer some “explanation” of the gloomy prognosis that a crush injury predicates. Primary or secondary amputations are the common end options of treatment.
In the authors’ experience, the prompt and precise application of microsurgical techniques can help alter the often dismal prognosis held by those suffering from severe crush injuries. To avoid the progression of a severely crushed hand to a useless hand, one should understand that the pathophysiology involved in the distal forearm, wrist, and metacarpal area is different from that in the fingers. Therefore, this article discusses the pathology and treatment of injuries involving the distal forearm, wrist, or metacarpal area and fingers separately.
Introduction
Severe crush injuries to the hand and fingers often carry an unavoidably bad prognosis, resulting in stiff, crooked, and painful hands or fingers. In follow-up, osteoporosis is often times seen on radiographs. A shiny appearance of the skin and complaints of vague pain may lead the surgeon to consider a diagnosis of reflex sympathetic dystrophy, to offer some “explanation” of the gloomy prognosis that a crush injury predicates. Primary or secondary amputations are the common end options of treatment.
In the authors’ experience, the prompt and precise application of microsurgical techniques can help alter the often dismal prognosis held by those suffering from severe crush injuries. To avoid the progression of a severely crushed hand to a useless hand, one should understand that the pathophysiology involved in the distal forearm, wrist, and metacarpal area is different from that in the fingers. Therefore, this article discusses the pathology and treatment of injuries involving the distal forearm, wrist, or metacarpal area and fingers separately.
Acute crush to the distal forearm, wrist, and metacarpal area of the hand
Clinical Presentations and Pathophysiology
Two striking features after a severe crush injury are
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The affected joints tend to stiffen and the affected tendons tend to stick.
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The undamaged structures distal to the area of injury usually get involved.
The trauma appears to have a “contagious” effect that spreads distally, similar to a fire spreading to the higher floors in a skyscraper. There is no satisfactory explanation as to why normal anatomy seemingly spared during the initial traumatic event should convert to abnormality. To most, the consequence, a frozen hand, is more devastating than the original injury, that is, a focal trauma in the forearm ( Fig. 1 ).
This traumatic event will cause localized devascularization in the forearm and result in healing by fibrosis locally. These facts, however, do not explain the end result of a frozen hand, which often is very painful. The authors attempted to reveal mysterious pathophysiology of the crush syndrome of the hand, but such attempts have not been fruitful.
In exploring the pathophysiology, the following questions can be posed: What causes a healthy tendon to be unable to glide? Or a normal joint to stiffen? Or an uninjured finger to deviate? Several factors can shoulder some of the blame: insufficient debridement, the presence of dead space that fills with debris or hematoma, unstable fixation, and poor coverage. The underlying commonality with these factors is that they contribute to the formation of an enormous amount of fibrotic and scarred tissue. All of them are responsible for a delay in the commencement of active motion, which leads to the loss of tendon gliding and joint stiffness. Muscle contracture, secondary to diagnosed or undiagnosed compartment syndrome, would drag the fingers into dysfunctional positions.
Within this chaotic milieu of diminished blood supply, hematoma, unstable fractures, and poor soft tissue coverage in severe crush injuries, it is easy to foresee that any contaminant could lead to one of the most dreaded complications—deep space infections. Fibrosis and contamination with or without infection result in the dismally functionless “frozen” hand. Furthermore, chronic, unremitting pain is a common component of this syndrome in its later stage. Although a handy acronym “CRPS1” (complex regional pain syndrome) could offer an easy explanation to the onset of pain, a more logical and clearer explanation is that the nerves are either unable to glide and thus causing pain without movement (neurodesis) or ischemic in the confines of heavy scarring. The discomfort is exhausting for the patient both physically and psychologically, and amputation may be needed as the endpoint treatment ( Fig. 2 ).
Management
With the diligent and quick application of the appropriate techniques, a surgeon can halt the progression from crush injury to frozen hand, illustrated in Fig. 2 . It is hoped that aggressive operative management will result in a better functioning hand in the setting of an admittedly devastating injury. Management keys are to address each of the factors that lead to the poor results. Because of the complexity in the decision-making process and the technical expertise required in the treatment, it is crucial that the utmost care be undertaken by a skilled team of surgeons. With minimal variations, management focuses on addressing the 4 pillars in the listed order:
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Debridement
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Bone management
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Neurovascular structures damaged
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Soft tissue defect
Radical Debridement
In the setting of a severe crush to the forearm and the hand, there is a large amount of devitalized or threatened tissue. The devitalized tissue is a nidus for an inflammatory response, creating a wound bed that heals primarily through the means of fibrosis. This results in a massive amount of scarring. Reducing the burden of dead or dying tissue is paramount to promoting the revascularization of bone as well as for aiding tendon gliding.
When the crush injury involves the metacarpals, one has to consider debriding the interosseous muscles should they be devascularized and/or denervated. Most of the blood supply to the interosseous muscles enters proximally, and an injury to the carpal arch unavoidably impairs the arterial inflow into the deep muscles of the hand. In addition, compartment syndrome in the hand may occur with minimal clinical symptoms and remains difficult to diagnose. Such compartment release should occur with low suspicion to preempt future dysfunction.
When the crush injury occurs at the carpal level, severe derangement of the carpal architecture—including floating carpal bones, disruption of the deep carpal arches, and potentially hand devascularization—can be expected. Acute hand amputation is not rare, and late amputation due to deep hand infection is unfortunately common. Amputation is not surprising in this scenario, because the entire central portion of the hand is deprived of its arterial inflow, and potential interosseous muscle necrosis may occur if revascularization is needed.
Interestingly, simple debridement of this central devitalized tissue can lead to further problems because the dead space created may fill with blood upon release of the tourniquet. This central hematoma might become secondarily infected, and if not infected, it may still lead to the formation of densely fibrotic tissue, with both carrying an ominous prognosis. The only way the authors found to manage this central dead space is with coverage with a well-vascularized free muscle flap. The muscle flap contours well to the 3-dimensional defect and changes the local environment from scar formation to well-padded, well-vascularized tissue. A vascularized bone graft may be needed as a solution in selected cases ( Fig. 3 ).
Bone Injury or Defect
Typically, a crush injury does not cause simple fractures only, but rather a mixture of simple and comminuted fractures that are often characterized by cortical shattering and free cortical fragments. Primary or secondary bone loss after debridement is frequent. Furthermore, when the injury area includes a joint, the fracture may burst into small, nonfunctional pieces, making joint reconstruction impossible. Despite that specific fractures need different treatments, it is important to note, however, that achieving rigid fixation with minimally invasive techniques permits early commencement of active range of motion with tendon gliding and causes less local devascularization. In the metacarpals and phalanges, the authors usually achieve satisfactory results with the use of intramedullary cannulated screws, and stable fixation is achieved in minimal time with no dissection and devascularization of the tissue ( Fig. 4 ).
If minimally invasive techniques (eg, fixation with intramedullary cannulated screws) are not feasible for fracture fixation, then plate fixation is the next option. Both methods will allow for early motion, diminishing the risk of adhesions. It is not always possible to perform fixation with ideal results. When a joint has severe damage that prevents functional recovery, it is best to replace the joint. This especially applies when the joint injury occurs in the setting of severe soft tissue injury ( Fig. 5 ). Although this approach seems very aggressive, the reward is often a much better end result with overall less patient suffering and faster healing times. One should bear in mind that early rehabilitation is of the utmost benefit in all hand trauma cases and of even more benefit as the degree of injury increases.
Unlike crush injuries in metacarpal or phalangeal regions, major carpal injuries can rarely be fixed rigidly enough as to allow for early motion as the concomitant ligamentous injuries require prolonged immobilization times. If rigid fixation is unfeasible, then Kirschner wires and other devices are used as needed. Fortunately, at the wrist level, tendons adhesions are very forgiving, much the same as with zone III or IV flexor tendon injuries, and tolerate some delay in starting mobilization. Furthermore, with wrist immobilization, the fingers can still be allowed to move, preventing tendon adhesions at the wrist.
At the level of the distal radius, the preferred method of rigid fixation, especially with joint involvement, is with volar locking plates. When the fracture involves the shaft of the radius, multiple, shattered, devascularized fragments are commonly seen.
Very severe crush injuries often require a wide, and often both dorsal and volar, approach to appropriately manage the bony injury. This, in turn, creates an increased need for flap coverage. Although this may be a potential drawback, liberal usage of free tissue transfer will often benefit patients by virtue of the fact that the surgeon can better radically debride any tissue of dubious vascularity as well as for allowing the addition of subcutaneous tissue for better tendon gliding.
In any locations, cortical bone fragments devoid of periosteal connections are best debrided away and replaced with cancellous bone. This approach will speed up wound healing times without an increase in infection rates. When the defect is large, or when there is a large area of tissue devascularization, cancellous bone grafting alone will not ensure bony union or the bony healing is delayed. The cancellous bone grafting greatly interferes with the functional outcome in the authors’ experience ( Fig. 6 ).
For this reason, the authors advocate early use of vascularized bone transfer, which is preferable in this situation. Not only will vascularized bone promote rapid healing but also it will resist infection. When the defect is less than 3 or 4 cm, the authors’ preferred flap is the medial femoral condyle flap ( Fig. 7 ), but the skin island may have variations that may make it less preferential. A vascularized lateral scapular free flap can address both bone and soft tissue defects, but the skin on the back, like the iliac crest, is often too thick. The fibula has an innate problem of no guaranteed blood supply when used as small segments. In the senior author’s observation, the fibula flap only has a secondary role in treating small complex defects.
