Background

Both carpal tunnel syndrome (CTS) and distal radius fractures are among the most common diagnoses of conditions treated by hand surgeons and orthopedic surgeons. However, their relationship to each other is poorly understood. Distal radius fractures are the most common fractures seen in the emergency department, with an incidence of more than 640,000 per year in the United States. A bimodal distribution of distal radius fractures is seen, with one peak representing predominantly young male patients sustaining high-energy injuries and another peak representing predominantly elderly female patients sustaining low-energy fragility fractures. Common complications that occur following distal radius fractures include arthrosis, malunion, nonunion, tendon rupture, chronic regional pain syndrome (CRPS), ulnar impaction, loss of rotation, finger stiffness, and, rarely, compartment syndrome. Another known complication of distal radius fractures is median nerve compression at the wrist, or CTS. A review of 565 patients revealed immediate or delayed CTS as the most common complication with distal radius fracture. The time for onset of CTS after distal radius fracture can vary from a few hours to many years. CTS can be classified as idiopathic (or primary), secondary, and acute. Idiopathic (or primary) CTS is the most common form and results in a multifactorial manner presenting most commonly in the fourth to fifth decade resulting in progressive median nerve paraesthesias that is worsened with activity and flexed positioning of the wrist. Idiopathic CTS is also the most common complaint of the hand. Secondary CTS occurs from anatomic changes to the carpal tunnel, space-occupying lesions, and inflammatory conditions resulting in increased pressure within the carpal tunnel. Acute CTS is progressive in nature, develops rapidly, and consists of painful paraesthesias in the median nerve distribution of the hand.

Acute CTS has been reported to occur in 5.4% to 8.6% of all distal radius fractures. Secondary CTS can occur months to years after a distal radius fracture. This presentation is usually associated with a malunion or residual displacement of the distal radius fragment, chronic edema of the tenosynovium, prolonged immobilization in the Cotton-Loder position, and enlarging callus. The incidence of delayed CTS after a distal radius fracture is estimated to be 0.5% to 22%.

Diagnosis

The major complaints with CTS are numbness and paraesthesias in the median nerve distribution of the hand and weakness in thumb opposition. Physical examination will note possible paraesthesias in the thumb, index and middle fingers, and radial half of the ring fingers. Semmes-Weinstein monofilament testing is the most sensitive in detecting sensory threshold changes in CTS. Symptoms may be brought on with prolonged wrist flexion (Phalen’s test) or direct compression of the median nerve at the carpal tunnel (Durkan’s test). Strength testing may identify weakness in resisted thumb abduction and atrophy of the thenar musculature. In the setting of a distal radius fracture, CTS symptoms may be worsened with progressive deformity and swelling ( Fig. 1 ).

The risk of median nerve injury increases with progressive deformity and fracture displacement. Note the extent of deformity following complete dorsal displacement of the distal radius fracture. This patient was originally splinted in this displaced position and presented with progressive median nerve paraesthesias. However, following provisional fracture reduction, the paraesthesias resolved.

Diagnosis

The major complaints with CTS are numbness and paraesthesias in the median nerve distribution of the hand and weakness in thumb opposition. Physical examination will note possible paraesthesias in the thumb, index and middle fingers, and radial half of the ring fingers. Semmes-Weinstein monofilament testing is the most sensitive in detecting sensory threshold changes in CTS. Symptoms may be brought on with prolonged wrist flexion (Phalen’s test) or direct compression of the median nerve at the carpal tunnel (Durkan’s test). Strength testing may identify weakness in resisted thumb abduction and atrophy of the thenar musculature. In the setting of a distal radius fracture, CTS symptoms may be worsened with progressive deformity and swelling ( Fig. 1 ).

The risk of median nerve injury increases with progressive deformity and fracture displacement. Note the extent of deformity following complete dorsal displacement of the distal radius fracture. This patient was originally splinted in this displaced position and presented with progressive median nerve paraesthesias. However, following provisional fracture reduction, the paraesthesias resolved.

Pathophysiology

Dyer and colleagues thought that “acute CTS should be distinguished from median nerve dysfunction due to deformity or contusion: the former usually develops slowly over hours to days and progressively worsens, whereas the latter is present at the time of injury, often improves after manipulative reduction, and tends to improve within days to weeks.” The potential effects of unrecognized or untreated CTS are permanent dysfunction of the median nerve and possibly CRPS. Therefore, the clinician must act expeditiously if CTS symptoms arise.

Direct Median Nerve Injury

Other studies have proposed that direct trauma to the median nerve at the time of injury can be a cause of CTS after a distal radius fracture. Median nerve injury has been reported with volar cortical fragments directly injuring the median nerve after a fracture ( Fig. 2 ). The authors recommended early carpal tunnel release (CTR) with removal or reduction of the volar fragment. A displaced volar fracture fragment has also been implicated in tardy median nerve palsy. Such cases may present months after the injury as a result of direct pressure on the median nerve and/or alterations of the anatomy within the carpal tunnel.

Direct median nerve injury from the displaced volar cortical fragment is impinging on the median nerve. This patient presented with acute CTS requiring urgent decompression and fracture reduction.

What is the evidence?

Numerous studies have speculated as to the causes of median nerve injury and median nerve compression after a distal radius fracture. In a retrospective case-control study by Dyer and colleagues reviewed orthopedic trauma and billing databases for all surgically treated fractures of the distal radius in a 5-year period at 2 level 1 trauma centers. After exclusion criteria were accounted for, the total cohort between the 2 centers included 50 patients. The proposed risk factors for acute CTS included injury mechanism (low-energy, high-energy, and crush injuries), open fracture, ipsilateral wrist injury, ipsilateral upper extremity injury, and multiorgan system injuries. The authors concluded that ipsilateral upper extremity trauma (with hand fractures excluded) and translation of the fracture fragments were significant predictors of acute CTS. Weaknesses of the study include its retrospective nature, selection bias that may be present at level 1 trauma centers, and the large percentage of patients excluded as a result of missing or inadequate prereduction radiographs.

Itsubo and colleagues also performed a retrospective study in which they evaluated onset patterns and causes of CTS after a distal radius fracture. In their review, treatment was closed reduction and cast immobilization in 75 wrists, external fixation in 9 wrists, closed reduction and percutaneous pinning in 7 wrists, open reduction and internal fixation in 10 wrists, and corrective radius osteotomy after closed reduction and cast immobilization in 4 wrists. Treatments for CTS included CTR in 68 wrists, CTR with corrective radial osteotomy in 5 wrists, corrective radial osteotomy alone in 2 wrists, and conservative treatment only (steroid injection or splinting) in 30 wrists. Based on the results of the review, the authors noted that patients in the acute-onset group were significantly younger and had a higher proportion of male patients compared with the other 2 onset groups. In addition, the incidence of a high-energy injury was significantly higher in the acute-onset group than in the other 2 onset groups. Based on radiographic classification, the authors also concluded that the incidence of AO type C fractures was significantly higher in the acute-onset group than in the other 2 onset groups.

Unlike the study by Itsubo and colleagues, Bienek and colleagues prospectively followed the outcomes of 60 patients who presented with distal radius fractures and developed peripheral nerve compression during a 5-year period. Of the 60 patients in the study, 12 patients had symptoms of CTS and the diagnosis was confirmed electrodiagnostically. Those 12 patients had significantly worse subjective scores than the 48 patients without CTS. The authors were not able to demonstrate a correlation between the occurrence of CTS and the fracture type according to the AO classification. In addition, correlation was not observed between radiographic end results (radial inclination, volar tilt, and radial shortening) and the occurrence of CTS.

Many authors have attempted to study the relationship between compartment pressure in the carpal tunnel and acute median neuropathy after a distal radius fracture. Dresing and colleagues measured compartment pressures in a prospective controlled study in 56 patients. Measurements were taken at initial presentation, immediately before and after reduction, and 1, 2, 4, 12, and 24 hours after reduction. Sixteen patients underwent primary surgery and 4 patients had secondary surgery. All wrists were positioned in 25° of flexion and 20° of ulnar deviation after reduction. These fractured wrists were all casted and the respective casts were all split. All fractures were also grouped into the appropriate AO classification for distal radius fractures. Three measurements were taken using an intracompartmental pressure monitor system, 5 minutes after insertion of the catheter. The highest peak pressure (mean of 44.3 mm Hg) was seen at the time of reduction and a second peak occurred 4 hours after reduction (mean 37.0 mm Hg). The highest pressure was observed immediately after reduction before splitting of the cast. A sudden drop in pressure was instantaneously observed after splitting and loosening of the cast. Four patients eventually developed CRPS. Three of these patients had significantly elevated carpal pressures during reduction or afterward. One female patient had pressures exceeding 80 mm Hg and required median nerve decompression along with open reduction and internal fixation. The authors were also able to conclude that AO A2-type fractures had a significantly lower carpal tunnel pressure at the time of admission (average 16.1 mm Hg) compared with A3-type (average 25.5 mm Hg) and C2-type (average 27.7 mm Hg; P = .01) fractures.

Similarly, Fuller and colleagues measured carpal tunnel pressures in 10 patients who underwent open reduction and internal fixation of a distal radius fracture through a volar approach during a 7-month period. Surgery was performed using a volar approach, with a slit catheter inserted under direct visualization on the radial aspect of the median nerve in the carpal canal. During layered closure of the wound, the catheter was brought out through the proximal end of the surgical wound and a volar plaster splint was applied. Carpal canal pressures were measured every 2 hours during the first 24 hours postoperatively, when the catheter was removed. The maximum recorded carpal canal pressure was 65 mm Hg in the only patient with fracture blisters. That patient had a trending decrease in pressures down to 31 mm Hg by the end of the study period. In addition, that patient never had signs of acute CTS. Of note, the same patient had a history of systemic hypertension, which may have offered a protective mechanism during his recovery. The general trend of the carpal canal pressures was a decrease during the 24 hours of monitoring. Most patients had carpal canal pressures less than the safe threshold pressure of 40 to 50 mm Hg proposed by Gelberman and colleagues. Based on their findings, Fuller and colleagues concluded that “routine prophylactic carpal tunnel release is not recommended after volar plating of distal radius fractures.”