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Acute Carpal Tunnel Syndrome

Schnetzler, Kent A. MD

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Journal of the American Academy of Orthopaedic Surgeons: May 2008 - Volume 16 - Issue 5 - p 276-282
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Carpal tunnel syndrome (CTS) is a median nerve impairment secondary to chronic use injuries and systemic disorders (eg, diabetes, rheumatoid arthritis, amyloidosis). It is thought to be the most common of the chronic compressive neuropathies.1 Excellent reviews of CTS are available.2,3 Acute carpal tunnel syndrome (ACTS), which is much less common than CTS, is more often related to trauma and requires urgent surgical intervention to avoid serious sequelae. ACTS is characterized by unrelenting pain and dysesthesias in the median nerve distribution resulting from a rapid rise in pressure within the carpal tunnel. It can be differentiated from chronic CTS by the rapid onset of severe symptoms and by its progressive course over hours, rather than weeks or months.

Although not a separate anatomic compartment, the carpal tunnel behaves physiologically like a closed compartment, and compartment syndrome can develop within it. The carpal tunnel is intolerant of spaceoccupying lesions, and symptoms quickly ensue secondary to increased pressure within the tunnel. Etiologies of and predispositions to ACTS include hand, wrist, and carpal bone trauma; infection; rheumatologic, hemorrhagic, and vascular disorders; burns and thermal injury; high-pressure injection injuries; and several other uncommon disorders and injuries (Table 1). A mass effect appears to be common to many of these diverse etiologies. In each case, an intracompartmental pressure threshold is exceeded and epineural blood flow is compromised, producing pain and dysesthesias in the median nerve distribution. Early recognition and management of ACTS is necessary to preserve function of the median nerve. The distinction among chronic CTS, ACTS, and nerve contusion is significant. Although urgent surgical intervention in chronic CTS is seldom needed, rapid surgical management is required to perform nerve-sparing decompression in the patient with ACTS.4,5 Nerve contusion can be adequately treated with rest and close observation.

Table 1
Table 1:
Unusual Conditions and Pathologies Associated With Acute Carpal Tunnel Syndrome

Anatomy and Pathophysiology

The carpal tunnel is a small, relatively fixed-volume space normally occupied by the four superficialis tendons, the four profundus tendons, the flexor pollicis longus tendon, and the median nerve (Figure 1). Anomalous structures within the carpal tunnel are associated with both ACTS6 and chronic CTS. Some authors have characterized the carpal tunnel as a closed space.7 The volume of the carpal tunnel measures approximately 5 mL, with a cross-sectional area of approximately 185 mm2.8

Figure 1
Figure 1:
Transverse section through the carpal tunnel. The median nerve is the most superficial structure. A = ulnar artery, C = capitate, CT = carpal tunnel, fpl = flexor pollicis longus tendon, H = hamate, M = median nerve, P = pisiform, PCL = palmar carpal ligament, S = scaphoid, t = profundus and sublimis tendons, T = triquetrum, TCL = transverse carpal ligament, U = ulnar nerve, UT = ulnar tunnel. (Adapted from Szabo RM, Steinberg DR: Nerve entrapment syndrome in the wrist. J Am Acad Orthop Surg 1994;2:115-123.)

The carpal tunnel is surrounded by unyielding margins. It is bordered radially by the scaphoid, the trapezium, and the fascial septum overlying the flexor carpi radialis. Its ulnar border consists of the hook of the hamate, the triquetrum, and the pisiform. The dorsal border is formed by the carpal bones, and the volar border by the flexor retinaculum. This latter structure consists of the deep forearm fascia, the transverse carpal ligament, and the distal aponeurosis between the thenar and hypothenar musculature. The narrowest and most vulnerable part of this unyielding tunnel lies immediately below the transverse carpal ligament. Variations in the diameter of the carpal tunnel do occur. In addition to size variations, conditions that increase the contents of the carpal tunnel (eg, proliferative tenosynovium) can contribute to the etiologic process.

The inability of the carpal tunnel to expand with mass-occupying lesions or structures can lead to increased pressure within the tunnel. Analogous to a compartment syndrome, the final result of this increasing pressure is the cessation of blood flow caused by reduction in the pressure differential through the capillaries supplying the median nerve, leading to median neuropathy. Rydevik et al9 used an experimental rabbit model to demonstrate that acute compression of a nerve may cause persistent impairment of intraneural microcirculation via mechanical damage to blood vessels. Follow-up studies demonstrated the importance of the duration of nerve compression.10 Szabo4 reported that carpal tunnel pressures within 30 mm Hg of diastolic blood pressure can cause significant motor and sensory dysfunction, which suggests ischemia as a cause of conduction block. Therefore, a hypertensive patient may display symptoms of CTS only after carpal tunnel pressures have significantly exceeded those of a normotensive patient. Conversely, a hypotensive patient may demonstrate symptoms at significantly lower tunnel pressures than a normotensive counterpart. Decreased microvascular blood flow clearly plays a role in acute nerve compression.11 This hypothesis is supported by the correlation between nerve function and blood pressure. Compression of the nerve affects microcirculation, increases vascular permeability (leading to edema), and impairs axonal transport (all leading to nerve dysfunction).12

Any increase in pressure within the carpal tunnel may adversely affect median nerve perfusion. Proximal to the flexor retinaculum, the median nerve receives its blood supply from both the radial and ulnar arteries. If a median artery is present, it usually terminates in the distal forearm. Rarely, it accompanies the median nerve through the carpal tunnel.13 Thrombosis of a persistent median artery has been implicated in ACTS.14,15 Obstruction of venous return within the perineural and epineural plexuses can lead to anoxia and endoneural edema.16 Fluid can leak from disrupted endoneurial microvessels into the endoneurium. With an intact perineurium, this fluid leakage can increase endoneurial pressure and create a “mini” compartment syndrome within the fascicle.13,17 The magnitude of conduction blockage and edema are related to the magnitude and duration of the compressive force.18 Acute compression of a nerve can cause impaired intra- and extrafascicular circulation from mechanical injury of a specific nerve segment.9 Lundborg et al19 provided compelling evidence to support the ischemia theory. Using an armtourniquet, they showed that ischemia is a greater determinant of dysfunction than is mechanical deformation. The authors also found that nerve fiber viability is acutely altered at critical pressure between 60 and 90 mm Hg.

Swelling within the endoneurium can interfere with nerve function via alteration in an axonal ionic environment,19 and blockage of axonal transport can occur with pressures of 30 mm Hg that last for at least 2 hours.20 Time for recovery of normal transport was correlated with the magnitude of compression.21 Higher pressures resulted in changes in nerve function and structure.22 Lowpressure balloons placed adjacent to nerves quickly produced endoneural edema and persistent increase in intraneural pressure, which reduced function in a dose-dependent manner. The amount of endoneural edema appeared to be important.23 Experimental studies indicate a doseresponse curve, with a correlation between greater duration and pressure, and greater nerve dysfunction. A direct cause-and-effect relationship between carpal tunnel pressure and median nerve dysfunction was demonstrated in an animal model.24

The acuity and time-dependency of pressure increase within the carpal tunnel is another important determinant of median neuropathy. In a normal hand, pressure within the carpal tunnel is approximately 2.5 mm Hg. With wrist flexion or extension, maximum pressures remain well below 32 mm Hg, the average capillary refill pressure.25 However, with maximal flexion or extension, pressure increases to approximately 30 mm Hg. The earliest detectable manifestation of nerve compression occurs with reduction of epineural blood flow to between 20 and 30 mm Hg. Axonal transport is impaired, and the normotensive patient may experience paresthesia.26 Lim et al27 demonstrated a dose-responsive reaction during development of acute pressure-induced median neuropathy in a rabbit model. At higher compartmental pressures, progressively less time is required to produce conduction blockage.28 In another study, graded compression of the median nerve in the carpal tunnel affected grip force and tactile sensibility at various sensory nerve action potentials, but not in parallel with reductions in the sensory potentials.29


Potential etiologies of ACTS include wrist and carpal bone trauma, including fracture and fracture-dislocation; hemorrhagic, vascular, and bleeding disorders; chronic and acute rheumatologic conditions; and, less commonly, infection; anomalous anatomy; burn and thermal injury; and high-pressure injection injury. A patient with a chronic condition may develop ACTS, but as an associated pathology rather than as a direct result of the chronic condition.


Distal radius fracture is likely the most frequent cause of traumatic ACTS secondary to compression of the median nerve caused by hemorrhage or edema.30 Volar displacement of fracture fragments or direct contact with the median nerve can result in direct nerve contusion or ACTS. Patients with contusion injuries typically had immediate sensory loss and nonprogressive symptoms,31 a finding that aids in distinguishing between these two conditions.

Graf and Dorn32 described attrition and rupture of the flexor pollicis longus tendon secondary to a scaphoid pseudarthrosis that led to ACTS. ACTS caused by rupture of the palmaris longus has been reported.33 Olerud and Lönnquist34 described ACTS associated with a nondisplaced distal pole of the scaphoid fracture and a nondisplaced ipsilateral 5th metacarpal base fracture. Prompt surgical decompression of a tense hematoma resulted in immediate pain relief, with near normal sensation in 12 hours and completely normal sensation in 3 weeks. Fracture healing was uneventful. We have observed ACTS in association with an isolated scaphoid fracture.

In a study by Brüske et al,35 ACTS developed in 11 of 128 distal radius fractures. Prompt recognition and surgical decompression combined with external fixation decreased the persistence of symptoms. In another study, ACTS developed in 2 of 109 displaced distal radius physeal fractures treated with manipulation under anesthesia.36 Marked initial malposition was a primary risk factor for development of complications. In patients with displaced distal radius fractures, carpal tunnel pressures measured before, during, and after closed reduction demonstrated acutely increased pressures and an “overt compartment syndrome.”37 Injection of local anesthetic into a fracture hematoma increases pressure within the carpal tunnel, as does volar flexion of the wrist.38

Other wrist and hand trauma resulting in ACTS has been noted, including fracture-dislocation of the wrist. Gong and Lu39 described several cases of metacarpal fractures complicated by ACTS. Weiland et al40 described volar fracture-dislocations of the second and third carpometacarpal joints associated with ACTS. Martinet et al41 reported on carpal bone fractures (other than the scaphoid) that resulted in ACTS. McClain and Wissinger42 described nine cases of ACTS related to a variety of causes, including transscaphoid perilunate dislocation, Colles fracture, and distal radius epiphyseal fracture. An unusual traumatic volar dislocation of the trapezoid previously unreported in association with ACTS was recently discussed.43 Three of 13 patients with distal row carpal fracture developed ACTS.44

Immobilization of the injured wrist and hand in positions of marked flexion also can cause ACTS by decreasing the volume of the carpal tunnel. Finger flexion and forearm supination, as well as wrist extension and flexion, can dramatically increase pressures within the carpal tunnel.13 As early as the 1930s, the common practice of immobilizing wrist fractures in marked flexion (ie, Cotton-loader position) was recognized as deleterious.2 In a study by Kuo et al,45 healthy volunteers with their wrists splinted in neutral experienced the least compression of the median nerve.

Gelberman et al46 reported that intracarpal canal fluid pressures increased with flexion of the wrist following immobilization of Colles fracture; 45 % of wrists had pressures >40 mm Hg with 40° of flexion. A decrease in carpal tunnel cross-sectional area with wrist flexion has been noted on magnetic resonance imaging scans.47 Trauma may result in contusion of the median nerve. It must be differentiated from injury secondary to nerve compression because treatment of these two distinct pathologies differs.4 A volarly displaced distal radius fragment may compress the median nerve against the proximal edge of the flexor retinaculum.48 ACTS is differentiated from nerve contusion by characteristic progression of symptoms resulting from elevated pressure caused by swelling and edema. A patient with nerve compression may need rest and observation, whereas one with ACTS requires urgent surgical intervention.4

Use of external fixation for the treatment of distal radius fractures with excessive wrist distraction may have important implications in the development of ACTS. In one study, the position of the distracted wrist had a considerable effect on carpal tunnel pressure. Extended wrist positions were associated with greater increases in carpal tunnel pressures, and flexed positions were associated with lesser increases in carpal tunnel pressures.49 In a cadaveric study, a relationship was found between wrist distraction and increased carpal tunnel pressures upon simulation of the distraction forces experienced with distal radius external fixation.50


Atraumatic causes of ACTS are rare, but several unusual etiologies have been described (Table 1). Hemorrhagic, vascular, and bleeding disorders are the most common atraumatic etiologies, including hemophilia,51,52 von Willebrand disease,53 oral anticoagulant use,54–57 rupture of the median artery,58 thrombosed aneurysm of an epineural vessel,59 calcification,60 and aneurysm61 or thrombosis14,15,62 of a persistent median artery. Bleeding can be intraneural in the overly anticoagulated patient,63 can occur into the carpal tunnel, or can be spontaneous, with no apparent cause. A patient who presents with ACTS associated with bleeding tends to have more severe pain, rapid onset of swelling, and neurologic symptoms that appear early and progress rapidly (ie, mass effect).2

Anomalous anatomy that crowds the carpal tunnel may predispose a patient to ACTS. Kono6 reported on ACTS resulting from anomalous flexor digitorum superficialis muscle bellies within the carpal tunnel. Symptoms occurred within 2 hours of internal fixation of a scaphoid fracture associated with transscaphoid perilunate dislocation. Ametewee et al64 described an anomalous flexor digitorum superficialis muscle adherent to the median nerve as the cause of ACTS. Multiplicity and frequency of anomalous structures within the carpal tunnel may be higher than previously anticipated.65


Careful clinical examination leading to prompt diagnosis and surgical treatment is critical to reducing or eliminating the sequelae of ACTS. Steadily progressive intense pain and dysesthesias or paresthesias in the median nerve distribution are characteristic of ACTS. Surgery to relieve pressure within the carpal tunnel performed up to 40 hours after the onset of symptoms has been shown to hasten the return of normal two-point discrimination to the hand. However, some patients with similar early return of function were released at just 4, 6, and 12 hours.5 Early release resulted in earlier and more complete return of function compared with patients released later and those with nerve contusion. In patients with delayed diagnosis and treatment, more adverse outcomes secondary to intraneural scarring have been reported,30,66 and return of function is delayed and more variable. Thus, early and accurate diagnosis combined with early decompressive surgery is advantageous for optimal results, including the avoidance of the undesirable long-term sequelae of median neuropathy.

In some patients with acute trauma, the median nerve is contused rather than compressed. The distinction between chronic CTS and ACTS has treatment implications; thus, it is also important to differentiate between acute median nerve contusion and ACTS.4 Nerve dysfunction with contusion appears early, whereas symptoms with nerve compression appear more gradually and progress as edema increases. With contusion injuries, sensory loss appears immediately and typically does not progress.31 Contusion requires only rest and observation, while acute median nerve compression requires surgical decompression. The patient may have difficulty recalling onset of numbness in the setting of acute trauma. When the patient cannot be observed in a controlled setting, specific instructions regarding worrisome progressive symptoms must be given. The physician should be alerted to a possible diagnosis of ACTS when a patient returns to the emergency department with worsening symptoms and neurologic dysfunction after wrist or hand trauma. Loss of twopoint discrimination (normal, ≤6 mm) with readings >15 mm generally indicate 100% sensory loss and can easily be incorporated into the clinical examination.

Pressure measurement of the carpal tunnel with a wick catheter or the STIC device (Stryker, Kalamazoo, MI) can provide additional information to help distinguish ACTS from contusion (Figure 2). Using a pressure threshold of 40 mm Hg, Mack et al5 noted an average pressure of 52 mm Hg in four of five blunt wrist trauma patients with ACTS; normal pressures were noted in two patients with nerve contusion only. However, not all physicians have such equipment available, nor may all feel comfortable measuring pressures reliably in the carpal tunnel. Some physicians may advocate a nonsurgical trial of strict elevation and observation in the emergency department to alleviate symptoms. Others may forgo pressure measurements and elevation, and, when ACTS is suspected, may proceed directly to decompressive carpal tunnel release. Likewise, some physicians may feel comfortable casting patients who present with acute wrist trauma, while others never place a cast in the emergency department, instead advocating splinting in all cases. No matter the treatment algorithm chosen, the physician must be aware of and make a prompt diagnosis of ACTS.

Figure 2
Figure 2:
Carpal tunnel pressure measurement technique. The needle of the measuring device is inserted 1 cm proximal to the proximal wrist crease and slightly ulnar from the palmaris longus tendon. If the palmaris longus is absent, the needle can be inserted in-line with the long axis of the ring finger metacarpal. The needle is directed distally at a 45° angle and slightly radially, then advanced until it strikes the bony floor of the carpal tunnel. The needle is withdrawn a few millimeters to avoid erroneous readings caused by tissue blocking the needle lumen.5,31

Surgical Treatment

When ACTS is to be treated concurrently with surgical stabilization of wrist trauma (most often a distal radius fracture or fracture-dislocation), a careful preoperative plan addressing proposed incisions must be made. To decompress the carpal tunnel, a standard longitudinal or serpentine palmar incision can be made in line with the ring finger metacarpal. The decision to cross the wrist crease is dictated by surgeon preference. Regardless of the incision chosen and incision length, the surgeon must ensure that the carpal tunnel and, in most cases, distal forearm fascia are adequately decompressed. A longer incision that crosses the wrist crease and extends proximally may afford a better view of the contents of the carpal tunnel and allow for easier decompression, such as evacuation of a tense hematoma or constricting proximal structures (eg, antebrachial fascia).

Mack et al5 suggested the following treatment algorithm: (1) Consider ACTS in any patient with severe, progressive wrist pain and objective sensory dysfunction even after fracture reduction. (2) Treat the patient with nonsurgical measures (eg, elevation, cast or dressing release, observation) for 2 hours. If these measures fail to relieve symptoms, the surgeon should consider measuring carpal tunnel pressures directly with a wick catheter or other device to distinguish ACTS from nerve contusion. (3) When pressures exceed 40 mm Hg, carpal tunnel release should be done within 8 hours of onset of symptoms. To eliminate proximal constriction, the median nerve release should be extended proximally under the antebrachial fascia and superficialis muscles.

For wrist fractures treated with closed reduction and stabilization with percutaneously placed smooth wires, there is little difficulty in adding an incision to release the carpal tunnel. This is easily done concurrently with the original surgery. In the patient in whom ACTS develops later, carpal tunnel release can be performed as a second surgery. If a volar buttress plate is to be placed on the distal radius via a flexor carpi radialis incision, the incision can be extended in a sigmoid fashion to incorporate the carpal tunnel release, thus avoiding a narrow skin bridge and the risk of skin necrosis. When two separate or multiple incisions are required, the surgeon must ensure adequate skin bridges to avoid necrosis.


ACTS is often related to trauma, particularly distal radius fracture and fracture-dislocation of the wrist. However, nontraumatic etiologies of ACTS have also been reported. Early clinical recognition of ACTS is paramount because, unlike chronic CTS, the acute form requires prompt recognition and urgent decompressive surgery. It is important to differentiate between ACTS and nerve contusion because treatment is different for each. Symptoms of ACTS are similar to those of compartment syndrome and include intense and progressive pain with increasing dysesthesia and dysfunction. Persistent symptoms are likely related to acuity and duration of compression, leading to microvascular compromise and neural dysfunction.


Citation numbers printed in bold type indicate references published within the past 5 years.

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