Pisohamate Ligament Instability/Tear

INTRODUCTION

Pisiform ligament complex syndrome (PLCS) is peri-pisiform ulnar palmar wrist pain caused by injury or disease to the components of the pisiform ligament complex (PLC). The PLC consists of the pisiform bone, pisiform ligaments, and the flexor carpi ulnaris (FCU) tendon. Injury to the pisiform ligaments leads to varying degrees of pisotriquetral (PT) joint instability with subsequent arthrosis. Osteoarthrosis (OA) of the PT joint is a degenerative joint disease involving the articular surfaces of the pisiform and triquetrum. Primary OA of the PT joint is an uncommon disorder. Many arthritic disorders of this joint are post-traumatic in nature preceded by PT joint instability. Familiarity with the anatomy and biomechanics of the pisiform and PT joint ligaments is crucial for understanding its pathologic disorders.

ANATOMY

At birth, the pisiform is cartilaginous and later develops an ossification center. A secondary ossification center rarely forms, and its failure to fuse with the remaining bone results in an accessory ossicle named os pisiforme secundarium . In 1945, Michelson reported that ossification of the pisiform occurs at a mean age of 8 years and 9 months. By age 12, the bone is fully developed. Until such time, the pisiform normally has a fragmented appearance that could be mistaken for a fracture among children.

The pisiform is the smallest of the eight carpal bones. It is ovoid-spherical ( Fig. 51-1 ) and positioned palmar to the plane of the remaining proximal row of carpal bones ( Fig. 51-2 ). The pisiform is embedded within the FCU tendon and a soft tissue envelope and acts as a sesamoid bone similar to the function of the patella. The pisiform is the only carpal bone with only one articular surface (PT joint) and any tendinous insertion (FCU). The pisiform articulates with the triquetrum over its dorsal surface, and this joint appears to be separate from other carpal articulations. The radial aspect of the pisiform is the medial wall of Guyon’s canal, which is in proximity to the ulnar nerve and artery. The triquetrum is pyramid-shaped with three articular surfaces. Its smallest surface is palmar and oval and articulates with the pisiform.

The pisiform receives its blood supply from branches of the ulnar artery. Panagis and colleagues observed in a cadaveric study a robust blood supply to the pisiform and triquetrum. One to three small vessels enter both the proximal and distal poles of the pisiform. These vessels anastomose beneath the articular surface, creating a constant arterial ring. The reported incidence of pisiform avascular necrosis (AVN) is very low because the pisiform receives at least two nutrient arteries and has elaborate intraosseous anastomoses.

The articulation of the pisiform and triquetrum appears to be separate from other wrist articulations. In 1945, Kropp observed a communication between the PT joint and the radiocarpal (RC) joint in 76% of specimens. In a postmortem arthrography study, Weston confirmed the presence of communication between the PT and wrist joints. Viegas and colleagues also reported a communication between the proximal wrist joint and the PT joint in 88% of cadavers dissected.

Arthroscopically, four articulations in the wrist may be visualized; the RC, midcarpal, distal radioulnar, and PT joints. The PT joint is the smallest of these articulations. Direct arthroscopy of the PT joint is difficult because of its size and the potential risk of damage to the dorsal branch of the ulnar nerve. The PT joint, however, can be seen by indirect arthroscopy through its communication with the RC joint. Arya and colleagues found four arthroscopic connection patterns between the PT and RC joints. Type 1 is a thick synovial membrane covering the joint, making it impossible to visualize. Type 2 shows a thin synovial membrane covering the joint, allowing a silhouette of the pisiform to be seen but not the PT joint. Type 3 is a fenestrated synovial membrane, but the opening is too small to allow passage of the scope. Type 4 is the most common pattern and is without synovial membrane but has a large fenestration through which the arthroscope could be easily passed to visualize the PT joint.

Pevny and colleagues described 10 soft tissue attachments to the pisiform, which include the FCU tendon, extensor retinaculum, abductor digiti minimi, pisometacarpal (PM) ligament, pisohamate (PH) ligament, transverse carpal ligament, volar carpal ligament, ulnar collateral ligament, triangular fibrocartilage complex (TFCC), and PT joint fibrous capsule. Rayan and colleagues later elaborated on their initial description of the PT joint fibrous tissue capsule, adding that it has two components: the radial PT and ulnar PT ligaments. In addition, they accounted for the superficially located PH arcade, which has a pisiform attachment and gives origin to the hypothenar muscles and the soft tissue confluence toward which all soft tissues converge superficial to the pisiform ( Fig. 51-3 ). Hence, there are 12 soft tissue attachments to the pisiform. Yamaguchi and colleagues identified three types of PH and PM ligaments based on their attachment to the pisiform.

BIOMECHANICS

The FCU tendon is the main dynamic structure that acts directly on the pisiform, exerting forces in a proximal direction. It is unclear whether the abductor digiti minimi generates any forces to the pisiform. The pisiform seems to act as a lever by enhancing the function of the FCU muscle. The pisiform attachment to the hand and carpus through the PM and PH ligaments is the link that transmits forces distally. The PH ligament transmits FCU forces to the distal carpal row. Wrist extensors and radioulnar deviator muscles transmit forces indirectly to the pisiform.

There is substantial mobility of the pisiform during wrist motion that has been attributed to the lax nature of the PT joint capsule. Vasilas and colleagues measured the PT joint space in various wrist positions and found that in neutral position the PT joint space ranges between 1 and 4 mm and that with wrist flexion it widens and with extension it narrows. In a three-dimensional computed tomography (CT) scan study, Moojen and colleagues demonstrated that with wrist extension, the pisiform translates and presses against the distal part of the triquetrum, but moves away from the triquetrum during wrist flexion. With wrist radial deviation, the pisiform flexes and the triquetrum extends. With wrist ulnar deviation, the triquetrum deviates ulnarly and extends.

Jameson and associates used radiographs and fluoroscopy to evaluate the wrist kinematics in normal volunteers and found that the pisiform has several planes of motion relative to the triquetrum. These are described as (1) longitudinal glide proximally during wrist flexion and distally during extension, (2) coronal shift ulnarly during ulnar deviation and radially during radial deviation, (3) sagittal tilt with PT angle forming distally during wrist flexion and proximally during extension, and (4) axial translation anteriorly with increased PT joint space and posteriorly with extension.

Beckers and Koebke studied the mechanical strain at the PT joint and force transmission within the carpus. They suggested that the pisiform contributes to the stability of the ulnar column of the wrist by preventing subluxation of the triquetrum and by acting as a fulcrum while transducing forearm forces to the hand. They concluded that excision of the pisiform should be reevaluated. However, their conclusion has not been substantiated by clinical studies. It is uncertain whether pisiformectomy creates any adverse or substantial changes on the biomechanics of the ulnar wrist.

Biomechanical testing by Pevny and colleagues found that the strongest soft tissue attachments to the pisiform were located distally. The weakest soft tissue attachments were ulnar in location. With release of the transverse carpal ligament, no significant decrease in stiffness of the PT joint was observed in any direction tested. Therefore, transection of the transverse carpal ligament may not cause any clinical PT joint instability.

Rayan and colleagues, in an anatomic, biomechanical, and radiographic study, classified pisiform ligaments into primary and secondary stabilizers, depending on the degree of stability provided to the pisiform and the PT joint. The three primary stabilizers are the PH ligament ( Fig. 51-4 ), which provides stability against ulnar displacement; the PM ligament ( Fig. 51-5 ), which provides stability against proximal displacement; and the ulnar PT ligament, which provides stability against radial displacement of the pisiform. The secondary stabilizers are the radial PT ligament and the transverse carpal ligament. The radial PT ligament provides a mild stabilizing effect, and the transverse carpal ligament has a minimal stabilizing effect on the pisiform against ulnar displacement. The transverse carpal ligament was observed to have no attachments to the pisiform in 50% of specimens studied, and in the remaining 50% it was attached only to the distal 20% of the pisiform. Rayan and colleagues suggested again that division of the transverse carpal ligament during carpal tunnel release does not seem to have adverse clinical effects on PT joint stability.

IMAGING

Several radiographic modalities are available to help assess the pisiform, PT joint, and the surrounding soft tissues. Each imaging technique has unique capabilities in analyzing the pathology of the pisiform and surrounding structures.

X-ray views should be obtained with the wrist and forearm in certain positions for adequate pisiform screening. For optimal viewing, we recommend three semilateral dynamic images: full wrist extension with the forearm in 30 degrees of supination, neutral wrist position with 30 degrees of supination ( Fig. 51-6 ), and full wrist flexion (passive, optional) with 45 degrees of supination with the thumb fully abducted. These techniques show pisiform pathology, fracture, arthrosis, and instability. Instability can be assessed by measuring PT joint space, PT wedge angle, pisiform excursion, and PH distance compared with normal data or the contralateral side if necesary. Carpal tunnel views allow visualization of the pisiform from a different perspective, but these views are more difficult to carry out and not as useful as semilateral views.

Real-time fluoroscopy during wrist flexion and extension can provide additional information about PT joint stability when compared with the contralateral side. Tomography of the wrist can help identify loose bodies in the vicinity of the PT joint, but this technique is seldom used today. Bone scintigraphy may be helpful in diagnosing fractures of the pisiform or triquetrum and bony tumors. Its limitation is a difficulty in diagnosing PT arthrosis. Aiki and associates used bone scanning among other radiographic modalities to diagnose a case of triquetral malunion.

Arthrography has been used by some for diagnosing PT disorders. Direct PT arthrography and/or RC joint arthrography can evaluate PT joint intra-articular abnormalities. Pessis and associates described a simple and safe procedure for direct arthrography of the PT joint. They reported that 27% of their patients with ulnar-sided wrist pain did not have arthrographic communication between the RC and PT joints. Direct injection is therefore necessary for the dye to reach the PT joint. This approach prevents unnecessary injection of the RC joint and can provide pain relief when steroids and local anesthetic are injected into the joint after arthrography.

Trispiral CT offers the clinician a sophisticated imaging modality to identify tumors and especially fractures of the pisiform, triquetrum, and hook of the hamate. Because of its high sensitivity for detecting small radiopaque osteocartilaginous fragments, CT is useful for identifying loose bodies of the PT joint. Blum and colleagues reported that pisiform dislocation and osteochondral fractures of the triquetrum were best identified with CT scanning. Combining CT with arthroscopy allows more precise evaluation of the PT joint but is limited by these modalities’ inability to precisely visualize the surrounding soft tissues.

Magnetic resonance imaging (MRI) is useful for delineation of soft tissues, including the ulnar nerve. Amrami described MRI arthrography as a dynamic method of real-time visualization of the flow of contrast and bony relationships during motion. Magnetic resonance arthrography (MRA) combines joint distention by contrast injection and visualization of soft tissues, such as ligament tears and cartilage irregularities. In a cadaveric study, Theumann and associates compared MRI and MRA and made the following observations: cartilaginous lesions and osteophytes were easily identified and detected more often in the pisiform than in the triquetrum; communication of the PT joint with the radiocarpal joint was seen in 82% of the wrists; the extensor carpi ulnaris (ECU), fibrous capsule, and cartilaginous surfaces of the PT joint were better visualized with MRA than MRI; MRA allowed inspection of the PH and PM ligaments; and MRA improves visualization of PT joint OA.

ARTHROSCOPY

As techniques of wrist arthroscopy have become more sophisticated, it is possible to evaluate ulnar wrist pain with minimally invasive surgery. Standard wrist portals can be used to visualize the PT joint in 48% of patients, creating the opportunity for PT joint evaluation to be part of routine wrist arthroscopy. Slutsky has described a safe and standardized approach to the volar ulnar aspects of the RC joint. This portal assists in evaluating the ulnar sling mechanism and the dorsal radial ligament and assists in diagnosis and debridement of palmar lunotriquetral ligament tears. This portal is practical for thorough arthroscopic examination of patients with ulnar-sided wrist pain. Berger described arthroscopic visualization of the PT orifice distal and anterior to the prestyloid recess from a more ulnar portal, such as the 4/5 portal. The PT orifice varies in size and is located immediately anterior to the proximal articular surface of the triquetrum. With a properly positioned arthroscope, it is often possible to visualize the articular facet of the pisiform and the insertion of the FCU tendon.

PATHOLOGY AND VARIANTS OF PISIFORM LIGAMENT COMPLEX SYNDROME

In 1987, Paley and associates described symptomatic PT joints in 16 patients and made correlations between etiologic factors and pathologic diagnoses. They also performed a literature search and gathered pathologic-etiologic data from 216 cases. The information obtained was organized into four pathologic groups: primary OA, secondary OA, other arthritides, and FCU enthesopathy. The most common etiologies were acute and chronic trauma and instability. Paley and associates hypothesized that loss of integrity to the pisiform retinacular structures resulted in its instability followed by PT joint dysfunction. The senior author (GMR) of this chapter considers PLC syndrome as a spectrum that encompasses many pisiform and PT joint disorders, several of which can ultimately predispose a patient to PT OA.

Congenital anomalies of the pisiform and PT joint are rare and usually asymptomatic. An accessory ossicle of the pisiform—os pisiforme secundarium—can be mistaken for a fractured pisiform. Congenital absence of the pisiform is associated with ulnar deficiency and ectrodactyly. Pisohamate coalition is often bilateral and classified as complete or incomplete synostosis. The latter may become symptomatic requiring pisiformectomy.

Tumors of the pisiform and PT joint are rare. Vosburgh and Rayan reported a case of ganglion originating from the PT joint. Helal and Vernon-Roberts reported on intraosseous ganglion of the pisiform. Osteoid osteoma of the pisiform has been reported in one patient who required surgical removal of the nidus.

Because of its robust blood supply, avascular necrosis of the pisiform is a rare occurrence. Match described a patient who had painful pisiform enlargement and diffuse sclerosis that was attributed to avascular necrosis and who required pisiform excision. Pisiform avascular necrosis has been reported as an isolated condition or as associated with PT joint arthrosis and ganglion cyst.

FCU tendinopathy is a degenerative change within the FCU tendon substance near its insertion in the pisiform and can be a cause of peri-pisiform pain. According to Paley and colleagues, 44% of patients with ulnar palmar wrist pain were found to have FCU enthesopathy as the cause of symptoms. FCU tendinopathy seldom occurs in isolation and frequently is associated with other conditions, especially PT instability and PT OA. Therefore, diagnosing FCU tendinopathy must raise suspicion of other associated conditions.

Loose bodies of the PT joint may be associated with synovial chondromatosis. Chondromatosis of the PT joint synovial membrane may cause metaplastic foci on the surface of the membrane to become sessile, and then pedunculated, and finally to detach producing loose bodies. Loose bodies may form within the PT joint in response to trauma or may migrate from the RC joint. They may develop in the presence of a normal joint or in association with PT OA. Because of their cartilaginous nature, loose bodies of the PT joint cannot always be identified on radiographs. Normal and Steiner found that chondral bodies are visible radiographically in one third of cases and that bony erosions are seen in 30% of radiographs. Polster and associates suggested that CT can detect PT bony erosions that are not seen radiographically. MRI can show noncalcified and nonossified chondral bodies that are not evident by other imaging techniques. Treatment of symptomatic cases is by excision of the loose bodies and pisiformectomy when PT OA is encountered during surgery. Steinmann and Linscheid described eight patients who underwent excision of PT loose bodies. Routine radiographs revealed a loose body in only four patients. CT delineated all loose bodies. Nonoperative treatment failed in all patients. Three patients underwent loose body excision only, and five patients had PT joint degeneration and underwent additional pisiformectomy.

Pisiform fractures represent about 1% of carpal bone fractures and have a mechanism of injury similar to that of dislocations. This results in a transverse avulsion fracture from the proximal pull of the FCU tendon or a comminuted fracture from impaction against the triquetrum. Sagittal avulsion fractures may occur near the origin of the abductor digit minimi. Pisiform fractures can be displaced or nondisplaced or can be extra-articular or intra-articular. Most fractures are nondisplaced, but many are intra-articular. Pisiform fractures are often associated with other carpal fractures and ligament injuries and may be overlooked initially. Use of lateral x-ray with 30 degrees of supination or CT scan is helpful in the diagnosis. Severely comminuted and displaced intra-articular fractures may result later in malunion and PT OA. Triquetral fracture and malunion can also lead to PT OA. Painful post-fracture healing with near-anatomic radiographic alignment sometimes may be caused by occult malunion, malalignment of the PT joint, early post-traumatic PT arthrosis, or associated PLC injury and incipient pisiform instability.

Distal pisiform dislocation was reported by Immermann in 1948, but there are no series or clinical studies published regarding pisiform dislocation or its sequelae. Pisiform dislocation occurs in isolation or in association with other injuries, such as distal radius fractures and hamate dislocations. The mechanism of injury is direct force on the heel of the hand, such as a fall on an outstretched hand or, less often, indirect force from wrist extension and proximally directed FCU muscle contraction. Most reported cases of dislocation have been distal or radial. The logical explanation for this trend is the strong nature of the supporting ligaments—both distally (PM ligament) and radially (PH ligament). Surgical treatment for acute pisiform dislocation has been described in two case reports as open reduction and temporary internal fixation and open reduction and reconstruction of the ligaments. After this treatment, both cases resulted in subluxation of the pisiform, with post-traumatic arthritic changes in one. Recurrent positional dislocation of the pisiform was reported by Ishizuki and associates to occur distal to the triquetrum when the wrist was extended to 45 degrees or more. The pisiform was reduced to proper joint congruity after 55 degrees of wrist flexion or more. Pevny and Rayan reported a case of recurrent radial dislocation of the pisiform. At surgery, the cause was found to be attenuation of the ulnar PT ligament, and pisiformectomy resulted in resolution of the patient’s pain.

Acute PT joint instability without dislocation is a common but unrecognized and under-reported cause of ulnar palmar wrist pain. Injuries of the PLC can be acute or chronic. Acute PLC injuries occur from two possible mechanisms. The first is direct trauma, caused by a fall on an outstretched hand. In this mechanism, the force directed to the pisiform is radial, proximal, or distal, depending on the wrist position and direction of the force that leads to displacement and deformation of its ligaments. The force, however, is not severe enough to cause pisiform dislocation. The second mechanism is an indirect injury, caused by wrist hyperextension with generation of opposing FCU tensile forces transmitted to the ligaments, including the PH ligament and to some degree the PM and ulnar PT ligaments, causing their elongation and partial disruption.

Matsumoto and colleagues reported rupture of the PH ligament at the time of simultaneous complete dislocation of both the hamate and pisiform bones secondary to a crush injury to the hand. Open reduction with internal fixation with Kirschner (K) wires was performed, but the patient had 50% less grip strength, compared with the unaffected hand, and diminished sensation along the ulnar nerve distribution. Jackson and Rayan encountered a case of avulsion fracture of the hamulus from its base by the PH ligament, caused by wrist hyperextension. Corten and colleagues reported digital flexor tendon rupture secondary to PT instability.

Chronic pisiform ligament instability may be a sequela of acute pisiform dislocation or inadequate treatment without immobilizing an acute PLC injury, or it may be caused by repetitive occupational or recreational activities ( Fig. 51-7 ). Repetitive direct compression on the pisiform and indirect shear forces from wrist motion can cause PLC instability. Repetitive wrist flexion combined with ulnar deviation probably inflicts tensile forces on the PLC. Any of the PLC components can be injured, but damage to the primary stabilizers (PH ligament, PM ligament, and ulnar PT ligament) of the PT joint is likely to produce more instability. The instability compromises the PT joint kinematics and predisposes to chondromalacia and degenerative changes ( Fig. 51-8 ). PT OA therefore is the end stage on the spectrum of PLCS. Subluxation of the PT joint without pisiform dislocation was noted in 12 of 40 patients who suffered a distal radius fracture. Radiographically, PT joint instability can be classified into three stages. Stage I, without radiographic findings; stage II, with altered normal parameters with or without subluxation; stage III, manifested as dislocation. However, chronic stage I instability without radiographic findings can be a cause of unremitting pain, which may require surgical treatment.