Tibial Fractures Causing Compartment Syndrome
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Open Tibia Fracture With Compartment Syndrome, J. DeLee and J. Stiehl, Clinical Orthopaedics and Related Research 160:175-184 (1981).
In this study of 104 open tibia fractures, six patients developed compartment syndromes in all four compartments of lower leg. The open wounds were small and would correspond to Grade II injuries using the Gustilo classification. Initial exam revealed no evidence of sensory deficit. In two cases the compartment syndrome was diagnosed prior to debridement; the average time between the injury and onset of symptoms was two hours. In the other four cases the diagnosis of compartment syndrome was made after initial wound debridement and fracture reduction; the average time from debridement to the development of symptoms was 4.75 hours. In none of these patients was the wound closed primarily.
All patients were noted to have a tense swollen leg with marked pain on muscle palpation in all compartments, and diminished sensation of the superficial and deep peroneal nerve. Five patients had decreased sensation in the posterior tibial nerve and four in the sural nerve. Muscle testing revealed extensor hallucis longus and extensor digitorum communis function to be weak or absent in all cases. Marked weakness of the toe flexors was evidenced in five cases. Although muscle strength had not been gradable on initial examination, progressive weakness in these muscles was evident. Muscle pain on passive plantar flexion of the toes was present in all six cases, whereas pain on passive dorsiflexion was present in only four. Distal pulses were palpable unless there was an associated vascular injury.
Fasciotomy was accomplished within eight to seventeen hours (averaging 12.5 hours after onset of symptoms).
If tissue pressure rises or arteriolar pressure decreases, the transmural pressure difference decreases. Blood flow decreases until at a critical tissue pressure there is no transmural difference and arterioles close. This will ultimately result in necrosis of all elements in the involved compartment.
Even in the presence of an open fracture, development of compartment syndrome is possible. The minimal size of the open wound may be the reasons the fractures do not spontaneously decompress. Physical examination, including neurologic and vascular tests immediately on arrival at the emergency room, is essential for documenting a developing compartment syndrome. The identification of the patient at risk will aid in early diagnosis. Comminution of fractures implies a great amount of energy absorbed at the fracture site. In addition, displacement of the fibular fracture confirms disruption of the interosseous membrane with associated severe soft tissue injury. This allows the fracture hematoma to extend into the posterior and lateral compartments with resulting increase in pressure. A displaced fibular fracture can result in peroneal artery laceration, another cause of increased compartment pressure. There are good drawings of this event.
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In this study, the diagnosis of compartment syndrome was based on clinical signs: (1) pain disproportionate to injury (2) palpably swollen compartments (3) pain on passive stretching of involved muscles (4) diminished simple touch perception (5) decreased strength of compartment muscles (6) hypoesthesia in sensory distribution of nerves in involved compartment.
Several methods have been advocated to accurately determine interstitial fluid pressure and diagnose compartment syndromes.
Tissue pressures were not used in this study. Increasing pain in muscle groups exaggerated with stretching, a definite loss of sensation and a decrease in muscle strength were sufficient to establish the diagnosis in these cases. In all six of our patients, results from the initial sensory examination were normal. Muscle strength, although initially ungradeable due to pain at the fracture site, had decreased prior to fasciotomy.
It is recognized that diminished arterial pulses are seen late in the development of compartment syndromes. Rarely does the tissue pressure rise high enough to completely obliterate the pulses. The absence of pulses should be an absolute indication for arteriography.
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In some studies 90% of muscle fibers evidence injury after eight hours of ischemia. Others found that 92% had residual functional impairment after 12 ours of ischemia. In our series, ischemia for a duration longer than 6 hours led to irreversible changes and permanent necrosis of tissues. The poorest results occurred in the four patients where fasciotomy was performed after initial debridement (there was an average delay of 12.5 hours from onset of clinical symptoms to fasciotomy). Those patients evidenced marked sensory deficit and a total active motion at the ankle of less than twenty degrees. In all patients active dorsiflexion of the toes or ankle was absent and plantar flexors either weak or absent. Such losses can be secondary to direct muscular injury at the time of fracture or to ischemic necrosis post-fracture. Inability to document the degree of muscle weakness in the fractured limb makes it difficult to determine the cause of post-fracture motor weakness.
Functional neurologic changes occur after thirty minutes of ischemia and irreversible changes occur after twelve to twenty four hours.
Ankle stiffness and decreased range of motion occurred in all patients. No amputations were indicated.
These people developed compartment syndromes in all four compartments of the lower leg. Four compartment syndromes are high energy injuries. The prognosis, especially with delay in diagnosis, is poor. Clinical symptoms include increasing muscle pain which can be exaggerated by stretching, loss of sensation, decrease in muscle strength, and palpably swollen compartments.
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If you or someone you know has suffered a tibial fracture that has lead to compartment syndrome, you may be entitled to compensation. Whether the medical mishap occurred at Pittsburgh hospitals such as UPMC Presbyterian Shadyside, St. Clair Hospital or elsewhere in Pennsylvania, the medical malpractice attorneys at Berger & Lagnese, LLC are here to help. Our office is located at 310 Grant St #720, Pittsburgh, PA 15219, and consultations can be scheduled either online or by calling (412) 471-4300.