Introduction

Carpal tunnel syndrome is a well-known compressive neuropathy of the median nerve characterized by chronic progression of pain and numbness over the radial 3.5 digits and thenar atrophy. If left untreated, advanced stages may result in permanent deficits. Rarely, adverse events or risk factors such as trauma, swelling, infections, inflammation, anomalous anatomy, coagulopathy, or tumors may acutely raise intracanal pressure and produce the same constellation of signs and symptoms but with rapid progression. In such cases, the rate and severity at which symptoms progress and the potential for devastating and lasting effects distinguish acute carpal tunnel syndrome (ACTS) as an important clinical entity.

Anatomy

The carpal tunnel is an hourglass-shaped conduit through which nine flexor tendons and the median nerve traverse to gain entry into the hand. With the exception of the transverse carpal ligament (TCL) volarly, the canal is otherwise surrounded by the bones of the carpus, which form the floor (dorsally) and the walls (radially and ulnarly).

Grossly, the inlet of the carpal tunnel can be approximated by the volar wrist crease and the outlet is marked by Kaplan’s cardinal line. Cross-sectional investigations by Cobb and colleagues have shown that the width of the tunnel proximally and distally is roughly 25 mm, whereas the narrowest region (at the level of the hamate) averages 20 mm. The depth has been measured at 12 to 13 mm at the proximal and distal ends, whereas the narrow region between the thickest part of TCL and prominent capitate is about 10 mm. The total volume is estimated to be 5 mL.

The TCL is suspended from the scaphoid and trapezium radially and the hamate and pisiform ulnarly. Just deep to the TCL, the most superficial structure is the median nerve, which usually courses just radial to the midline. The median nerve supplies the sensation the radial 3.5 digits, the thenar musculature, and the lumbricals of the index and middle fingers. Generally, the motor fascicles face the radial side. Specifically, the recurrent motor branch of the median nerve innervates the thenar compartment and has a variable anatomy, which has been described as extraligamentous (branching after the carpal tunnel), subligamentous (branching within the carpal tunnel), and transligamentous (piercing the TCL). The remaining contents of the canal include the four tendons of flexor digitorum superficialis and the four tendons of the flexor digitorum profundus, which are encapsulated by the ulnar bursa, and the flexor pollicis longus, which is encapsulated in the radial bursa.

Anatomy

The carpal tunnel is an hourglass-shaped conduit through which nine flexor tendons and the median nerve traverse to gain entry into the hand. With the exception of the transverse carpal ligament (TCL) volarly, the canal is otherwise surrounded by the bones of the carpus, which form the floor (dorsally) and the walls (radially and ulnarly).

Grossly, the inlet of the carpal tunnel can be approximated by the volar wrist crease and the outlet is marked by Kaplan’s cardinal line. Cross-sectional investigations by Cobb and colleagues have shown that the width of the tunnel proximally and distally is roughly 25 mm, whereas the narrowest region (at the level of the hamate) averages 20 mm. The depth has been measured at 12 to 13 mm at the proximal and distal ends, whereas the narrow region between the thickest part of TCL and prominent capitate is about 10 mm. The total volume is estimated to be 5 mL.

The TCL is suspended from the scaphoid and trapezium radially and the hamate and pisiform ulnarly. Just deep to the TCL, the most superficial structure is the median nerve, which usually courses just radial to the midline. The median nerve supplies the sensation the radial 3.5 digits, the thenar musculature, and the lumbricals of the index and middle fingers. Generally, the motor fascicles face the radial side. Specifically, the recurrent motor branch of the median nerve innervates the thenar compartment and has a variable anatomy, which has been described as extraligamentous (branching after the carpal tunnel), subligamentous (branching within the carpal tunnel), and transligamentous (piercing the TCL). The remaining contents of the canal include the four tendons of flexor digitorum superficialis and the four tendons of the flexor digitorum profundus, which are encapsulated by the ulnar bursa, and the flexor pollicis longus, which is encapsulated in the radial bursa.

Pathophysiology

The possible inciting events leading to ACTS are innumerable and include a variety of traumatic, hematologic, rheumatologic, anatomic, homeostatic, and infectious causes. However, the final common pathway seems to converge with the following sequence of events: a space-occupying lesion creates a mass effect, which increases intracanal pressures. The carpal tunnel behaves like a closed compartment, because the circumferential bony and ligamentous architecture are unyielding and further bounded by occlusive synovial tissue at the entry and exit. As the pressures increase to a threshold level, perfusion of the epineurium decreases and this causes ischemia. Tissue ischemia leads to nerve conduction block, endoneurial edema, and dysfunction of axonal transport, which manifest as the classic symptoms along the median nerve territory. Experiments in animal models have shown a dose–response relationship correlating the duration and severity of exposure to the level of nerve dysfunction and ability to recover. Case series have corroborated this assertion by citing permanent nerve damage in unrecognized or delayed cases.

Causes

Although considered a rare entity, a large number of case reports have described ACTS originating from a variety of sources. Traumatic injury causing hemorrhage remains the most common mechanism ( Fig. 1 ). However, an assortment of atraumatic causes is not uncommon (see later discussion). A comprehensive list of factors precipitating ACTS was gathered from case reports and is listed in Table 1 .

Distal radius fractures are the most common cause of an ACTS. ( A ) Comminuted distal radius with extensive dorsal displacement ( yellow arrow ) with a large cortical fragment angulated volarly. The patient presented with excruciating pain in the wrist and numbness in the radial 3.5 digits. ( B ) Volar cortical fragments ( yellow arrow ) displaced in this position can apply direct pressure on the median nerve as it enters the carpal tunnel. ( C ) Enlarged hemorrhagic condition of the median nerve on the postreduction image following gross fracture reduction and decompression of the carpal tunnel and the volar forearm fascia.

ACTS resulting from a distal radius fracture is the most classically described mechanism. The first description of carpal tunnel syndrome by Paget in 1853 involves median nerve compression following a distal radius fracture that “repaired by an excessive quantity of new bone.” Although the details of the onset or progression of median neuropathy in Paget’s patient are unknown, many reviews have reported distal radial fractures as a cause since the distinction between acute and chronic CTS was further defined. Frykman reported the incidence of ACTS following distal radius fractures ranges as 2.3%. However, subsequent authors have cited ranges from 0.2% to 21.3% percent. Following this injury, the mechanism leading to ACTS is hemorrhage into the carpal tunnel or the deep distal forearm at the fracture site.

In a retrospective case-control study, Ring and colleagues investigated risk factors that may herald impending ACTS and found that only fracture displacement was predictive. However, a threshold risk (as a percentage of translation) was only defined in one subgroup: females younger than 48 years old with greater than 35% translation. Other risk factors, such as age, gender, inclination, dorsal tilt, mechanism of injury, ipsilateral injury, or open wound were not significant risk factors.

Case reports have demonstrated that carpal bone fractures, dislocations, and fracture-dislocations have been implicated in the development of ACTS. Among those listed are injuries to the scaphoid, hamate and triquetrum, trapezoid, metacarpals, carpometacarpal joints, and transscaphoid perilunate dislocations. Furthermore, lacerations, burns, animal bites, and high-pressure injection injuries have necessitated carpal tunnel release in some patients.

Traumatic iatrogenic causes also deserve special consideration. Edema and hematoma formation following elective and traumatic surgery, excessive injection into the carpal tunnel for reduction, and hyper-flexion of the wrist in an external fixator or the Cotton-Loder position following reduction of a distal radius fracture are preventable insults that should be avoided.