Hand Surgery
1st Edition

Camptodactyly and Clinodactyly
Scott H. Kozin
Camptodactyly and clinodactyly are abnormal deviations of the fingers in the sagittal and coronal planes, respectively (1,2). Camptodactyly is a painless flexion contracture of the proximal interphalangeal (PIP) joint that is usually gradually progressive (3). There is no intraarticular or periarticular swelling. The metacarpophalangeal and distal interphalangeal joints are not affected, although they may develop compensatory deformities. The definition of camptodactyly has been expanded to include reducible (also known as flexible) and irreducible (also known as fixed) forms, which create disparity among reports (4,5). The physician must differentiate between flexible and fixed deformities, as different treatment algorithms apply.
Camptodactyly is believed to occur in less than 1% of the population, although most patients are asymptomatic and may not seek medical attention (1,6). Camptodactyly is bilateral in approximately two-thirds of the cases, although the degree of contracture is usually not symmetric (Figs. 1, 2 and 3). The fifth finger is most commonly involved (2,7). Other digits can be affected, although the incidence decreases toward the radial side of the hand (Figs. 4 and 5).
Camptodactyly has been divided into three categories (2,8,9). A type 1 deformity is the most common form and becomes apparent during infancy. The deformity is usually an isolated finding and is limited to the fifth finger. This congenital form affects men and women equally. A type 2 deformity has similar clinical features, although they are not apparent until preadolescence (Figs. 1, 2 and 3). This acquired form of camptodactyly develops between 7 and 11 years of age and affects women more than men (6). This type of camptodactyly usually does not improve spontaneously and may progress to a severe flexion deformity (1,10). A type 3 deformity is often a severe deformity that usually involves multiple digits of both extremities and is associated with a variety of syndromes. The extent of involvement between hands is often asymmetric. This syndromic camptodactyly can occur in conjunction with craniofacial disorders, short stature, and chromosomal abnormalities (Figs. 6 and 7) (Table 1) (1,2,4).
Hereditary Factors
Most cases of camptodactyly are sporadic in occurrence. However, camptodactyly can be inherited and is considered an autosomal-dominant trait with variable expressivity and incomplete penetrance (3,11,12). This terminology signifies familial propagation, although the camptodactyly may skip a generation (incomplete penetrance) and may not be present in full form (variable phenotype).
The forces around the PIP joint create a balance between flexion and extension. Any slight alteration in this equilibrium generates an imbalance and leads to a deformity. In camptodactyly, this inequity can result from an increase in the flexion force or a decrease in the extension force around the PIP joint. The resultant deformity is initially passively correctable (i.e., flexible or reducible camptodactyly) but often develops into a fixed or irreducible contracture over time. This concept of imbalance of the flexion-extension forces is the basis to understanding and treating camptodactyly (10,13,14 and 15).
The exact etiology that underlies camptodactyly remains unknown, and there is no consensus about the pathogenesis of the condition. Almost every structure around the PIP joint has been implicated as the principal cause or a contributing factor in the formation of camptodactyly (3,5). Proposed skin and subcutaneous tissue changes include a deficiency or contracture within the dermis and fibrotic changes within the subcutaneous tissue or fascia, or both (16,17). Conceivable periarticular alterations consist of contractures of the collateral ligaments or the volar plate, or


both (18). Possible musculotendinous anomalies involve abnormalities of the flexor tendons, intrinsic muscles (lumbricals or interossei, or both), and extensor apparatus (3,7,13,15,16,19,20,21,22,23,24 and 25). Potential abnormalities in the restraining ligaments around the finger include anomalies of the transverse or oblique retinacular ligaments (15). Plausible bone and joint deformities include atypical configurations of the PIP joint, specifically the head of the proximal phalanx and the base of the middle phalanx (17,26). Even an abnormality within the spinal cord at the eighth cervical and first thoracic nerve segments has been implicated as a potential cause of camptodactyly (3).
FIGURE 1. A 15-year-old girl with acquired camptodactyly that affects both small fingers.
FIGURE 2. Left small finger with proximal interphalangeal flexion deformity and compensatory metacarpophalangeal hyperextension.
FIGURE 3. Right small finger with a lesser degree of proximal interphalangeal flexion deformity.
FIGURE 4. A 14-year-old patient with camptodactyly that affects both hands and multiple digits.
FIGURE 5. Left hand with involvement of the long, ring, and small fingers.
FIGURE 6. A 16-year-old patient with orofaciodigital syndrome and type 3 camptodactyly that affects both hands.
FIGURE 7. Left hand with severe ring finger camptodactyly and small finger clinodactyly.
Craniofacial disorders
   Orofaciodigital syndrome
   Craniocarpotarsal dystrophy (Freeman-Sheldon syndrome)
   Oculodentodigital dysplasia
Chromosomal disorders
   Trisomy 13 through 15
Short stature
   Camptomelic dysplasia type 1
   Facial-digital-genital (Aarskog-Scott syndrome)
   Osteoonychodysostosis (Turner-Kieser syndrome)
   Cerebrohepatorenal (Zellweger syndrome)
   Jacob-Downey syndrome
The most prevalent anomalies that are associated with camptodactyly affect the flexor digitorum superficialis and intrinsic musculature (lumbricals and interossei) (3,10,16,17,21,25). The normal flexor digitorum superficialis of the small finger has considerable structural variability (17,27,28). The flexor digitorum superficialis muscle can originate from the tendon of the ring finger flexor digitorum superficialis or as a separate muscle belly. Generally, the tendon runs parallel with the index finger flexor digitorum superficialis, although it may course adjacent to the ring flexor digitorum superficialis. Less commonly, the superficialis to the small finger may be completely absent (27). In camptodactyly, the flexor digitorum superficialis tendon has been described as contracted, underdeveloped, or devoid of a functional muscle (3,11,15,16). The tendon may originate from the palmar fascia or the transverse carpal ligament instead of a muscle belly (3,10,24,25). This abnormal musculotendinous architecture cannot elongate during periods of rapid growth (i.e., infancy and adolescence), which creates a tenodesis effect and a subsequent PIP joint flexion deformity (Fig. 8).
An aberrant lumbrical muscle has also been implicated as the principal cause of camptodactyly (4,16,21). Similar to the flexor digitorum superficialis, the normal lumbrical to the small finger has considerable variability (29,30 and 31). The typical insertion into the extensor apparatus was found in 60% to 72% of anatomic specimens, with an abnormal insertion recognized in 17% to 35%. Furthermore, as much as 5% of specimens lacked the lumbrical muscle altogether. In camptodactyly, the lumbrical may have an abnormal origin or insertion, although a consistent anomaly has not been reported (4,16,21,23). An abnormal origin has been reported from the transverse carpal ligament or from the ring flexor tendons (23). Aberrant insertions are more common and include an attachment directly into the metacarpophalangeal joint capsule, onto the flexor digitorum superficialis tendon, into the ring finger extensor apparatus, or within the lumbrical canal (6,7,16,21). The deficiency of the lumbrical muscles leads to an intrinsic-minus deformity, which may lead to camptodactyly. This concept is supported by examination of the active PIP joint extension, with the metacarpophalangeal joint positioned in extension and flexion. In flexible camptodactyly, enhanced PIP joint extension during metacarpophalangeal joint flexion is often evident. This finding implies abnormal function of the intrinsic tendons and normal performance of the extrinsic tendons (6).
FIGURE 8. Diagram of tenodesis effect of abnormal flexor digitorum superficialis, which causes proximal interphalangeal (PIP) joint contracture during growth.
FIGURE 9. Palmar skin pterygium across camptodactyly of the small finger.
Persistent PIP joint contracture leads to secondary changes in the surrounding structures. The palmar skin may appear to bowstring across the PIP joint, similar to a pterygium (Fig. 9). Abnormal fascial bands can form beneath the skin, mimicking Dupuytren’s contracture. Consequential changes in the bone and joint configuration of the PIP joint can ensue as a response to continual joint flexion (3,4,17,25).
The type 1 or congenital form of camptodactyly presents with a flexion deformity that is noted at birth or during infancy (8,10,13). The type 2 or acquired form begins with a subtle deformity that is gradually progressive (Figs. 1, 2 and 3).

The contracture remains mild up to the age of 10 years and is rarely disabling. This small amount of flexion may go unnoticed by the patient and family, and a delay in seeking evaluation and treatment is common. Often, the specific onset of the PIP joint flexion is unknown. During the growth spurt of adolescence, the PIP flexion deformity progresses and can advance to 90 degrees (3,17,32). A gradual worsening of the PIP joint position can continue until 20 years of age (3). The main complaint of the patient and family is the angulation of the finger and the appearance of the hand. Pain is not a common complaint and may indicate an alternative diagnosis (Table 2).
Diagnosis Distinguishing feature
Pterygium syndrome Multiple pterygiums; usually includes the knee and elbow
Arthrogryposis Multiple joint involvement, waxy skin and underdeveloped musculature, ulnar deviation of the digits
Symphalangism No active or passive joint motion, absence of skin creases
Boutonnière deformity History of trauma and pain, joint swelling, reciprocal distal interphalangeal joint hyperextension
Beals’ syndrome (39,40) Congenital contractural arachnodactyly; kyphoscoliosis; external ear deformities; flexion contractures of the proximal interphalangeal joint, elbows, knees
Marfan syndrome Arachnodactyly without flexion contractures, loose ligaments, eye problems, dissecting aortic aneurysms
Juvenile palmar fibromatosis (mimics Dupuytren’s contracture) Metacarpophalangeal joint involvement, characteristic skin changes with nodules adherent to dermis
Trigger fingers Metacarpophalangeal joint involvement, palpable click on finger extension
Inflammatory arthritis Widespread joint involvement, swelling around joints or tendons
The history should search for other potential causes of a PIP joint flexion deformity, such as trauma, inflammatory arthropathies, and arthrogryposis (Fig. 10). The differential diagnoses are often excluded by an astute history and thorough physical examination (Figs. 11 and 12). There is an uncommon deformity in infancy that is termed late extenders that can be confused with camptodactyly (33). The child cannot fully extend the PIP joint of the involved fingers, but passive motion is complete. Splint application and therapy for passive motion result in a gradual restoration of extension. These children most likely have a hypoplasia of the extensor mechanism, similar to a congenital clasped thumb.
FIGURE 10. A 15-year-old girl with congenital contractural arachnodactyly that affects both hands.
FIGURE 11. An 11-year-old girl with Marfan syndrome that appears to be similar to camptodactyly.
FIGURE 12. Further examination of the hand reveals excessive laxity of the soft tissues.

The preoperative status of the digit dictates the recommended treatment. The active and passive motion of the PIP joint is recorded with a goniometer. A flexible deformity must be differentiated from a fixed flexion contracture. The end feel of a contracted PIP joint that is placed in extension is fundamental information that is pertinent to the proposed treatment. A rubbery or soft end point implies probable improvement with therapeutic modalities, such as stretching and splinting. Active PIP joint flexion is preserved in camptodactyly, and the patient should be able to make a full fist.
The examination requires individual inspection and careful inventory of the potential causes for the flexion deformity. The examination begins with an inspection of the skin, including its integrity, tenseness, and presence or absence of a pterygium. Occasionally, a fascial band can be palpated beneath the skin along the palmar aspect of the proximal phalanx (16). A fixed PIP joint flexion contracture implies shortening and thickening of the flexor tendon sheath, checkrein ligaments, or volar plate, or a combination of these (34). The amount of passive PIP joint extension is assessed while varying the positions of the wrist and the metacarpophalangeal joint. Flexion of the wrist and the metacarpophalangeal joint can often increase the amount of passive PIP joint extension (Fig. 13). This finding implies tightness of the extrinsic flexors, primarily the flexor digitorum superficialis.
A flexible deformity with an extension lag indicates the possibility of attenuation of the central slip. The central slip tenodesis test is useful to determine its integrity (35). In a normal hand, simultaneous flexion of the wrist and the metacarpophalangeal joints results in complete PIP joint extension. An extension lag during this maneuver infers central slip attenuation that may require augmentation at the time of surgery.
FIGURE 13. The 15-year-old patient who was depicted in Figure 1 with a decrease in proximal interphalangeal joint flexion posture during concomitant metacarpophalangeal joint flexion.
FIGURE 14. Almost full, active proximal interphalangeal joint extension is achieved when the metacarpophalangeal joint is held in flexion.
The degrees of active PIP joint extension should also be assessed with the metacarpophalangeal joint positioned in extension and flexion. Compensatory metacarpophalangeal hyperextension frequently develops in response to a PIP joint that is postured in flexion (Fig. 2). Holding the joint in flexion prohibits this abnormal posture. Full active extension during metacarpophalangeal positioning implies that hyperextension of the joint is a considerable part of the problem (Fig. 14). This assessment is similar to the Bouvier’s test for ulnar nerve palsy, which assesses the ability of the extrinsic extensors to achieve active PIP joint extension (36).
Isolated function of the flexor digitorum superficialis and flexor digitorum profundus to the involved digits must be assessed. The flexor digitorum superficialis of the small and ring digit can be interconnected. This anomaly prohibits independent PIP joint flexion of the small finger and is present in one-third of individuals (17). Therefore, inability to flex the PIP joint of the small finger while holding the remaining digits in full extension may not imply absence of the flexor digitorum superficialis (Fig. 15). The test should be repeated with liberation of the ring finger and a similar assessment of active PIP joint flexion (Fig. 16). This two-part evaluation prevents an erroneous conclusion regarding the absence of the flexor digitorum superficialis to the small finger. An independent flexor digitorum superficialis to the small finger is a potential donor for tendon transfer. A dependent flexor digitorum superficialis must be separated from the ring finger at the time of surgery to be a suitable donor for transfer.
Anteroposterior and lateral x-rays are routinely performed to assess the joint space configuration and the status of the

surrounding bones. The lateral x-ray is the most informative view to assess abnormalities around the PIP joint (Fig. 17). In long-standing cases, the x-rays are invariably abnormal, with changes on both sides of the joint secondary to the prolonged flexion deformity (2,10,17,37). The proximal phalanx head often loses its normal convexity and appears misshapen. The flexed middle phalanx base creates an indentation along the palmar neck of the proximal phalanx. The base of the middle phalanx can be subluxed in a palmar direction and may appear flat.
FIGURE 15. Apparent absence of the flexor digitorum superficialis function in the small finger.
FIGURE 16. Repeat testing with liberation of the ring finger reveals the interconnection of the flexor digitorum superficialis between the ring and small fingers.
FIGURE 17. Lateral x-ray of a small finger with camptodactyly with palmar subluxation and flattening of the middle phalanx base.
Differential Diagnosis
Multiple ailments present with a flexion deformity of fingers, and these diagnoses require consideration during the evaluation of a patient with suspected camptodactyly (Figs. 10 and 11) (Table 2) (1,2,4,38,39 and 40). The majority of these etiologies can be excluded by a thorough history and astute physical examination. Finger contractures that are associated with syndactyly, central deficiencies, or brachydactyly are not regarded as camptodactyly.
Conservatism is the tenet for treatment of mild camptodactyly. A contracture of less than 30 to 40 degrees does not create a functional handicap or interfere with activity of daily living (2,3,5,25). The patient should be instructed to accept his or her deformity and to avoid surgical intervention. Static splinting at night is recommended to prevent progression of the deformity and subsequent surgical intervention. The static splint is fabricated from a thermoplastic material and is affixed to the finger with Velcro straps.
The natural history of camptodactyly is no improvement or progression of the deformity in 80% of individuals (10). Severe involvement hinders various occupational and sporting endeavors, such as using a computer keyboard, playing a musical instrument, or wearing a baseball glove (Fig. 18) (1,3). This extreme flexion warrants treatment, although restoration of full motion is not a realistic expectation or a reasonable goal. Bony changes are not a contraindication to surgery, although the expected outcome is downgraded (4).
FIGURE 18. Severe camptodactyly creates difficulty in grasping large objects.

A preliminary period of nonoperative treatment is almost always attempted to resolve any fixed flexion deformity (8,15,25,41). Formal therapy is usually required to provide adequate stretching, splinting (static and dynamic), and even serial casting. A mild prolonged stretch is necessary to elongate the tight palmar structures and is followed by static splinting (8). Serial splinting or casting in incremental amounts of extension can lead to improvement of a PIP joint contracture. Dynamic splinting can be added to the treatment regimen, although static progressive splinting is often more efficacious in rigid deformities (1). In infants, the splints must be forearm based for adequate fit and to decrease the chances of removal (Fig. 19) (4). The amount of splint wear per day varies among reports concerning conservative management (15,25,41). Hori et al. (41) used dynamic splinting 24 hours per day for “a few months,” followed by 8 hours per day after correction was achieved. Miura et al. (15) requested the splint to be worn “day and night” but accepted 12 hours per day in young children. Benson et al. (8) recommended 15 to 18 hours of splint wear per day in the young infant and 10 to 12 hours per day as the child grew older. Irrespective of the initial splinting regimen, part-time splinting needs to be continued for a long period of time. Complete discontinuation of the splint should be delayed until the late teens or closure of the growth plate, which indicates cessation of longitudinal growth of the finger (1,15,41).
Operative treatment is reserved for a severe deformity that has not responded to conservative management. The operative treatment of camptodactyly reflects the perceived pathology, and multiple procedures have been recommended. Proposed surgical treatment includes division of some or all offending agents, including fascia, skin, tendons, tendon sheath, capsule, collateral ligaments (3,17,21,42); reconstruction or augmentation of the extensor mechanism (3,6,17); and bony procedures around the PIP joint (18,26).
There are numerous problems that must be addressed at the time of surgery. The first concerns are the amount of PIP joint contracture and the status of the periarticular structures. Preoperative stretching and splinting may have diminished the initial deformity, but residual contracture is common. The second issue is the altered balance around the PIP joint and the possibility of anomalous anatomy. These problems are not mutually exclusive, and both may be addressed by manipulation of similar anatomic structures. For example, a flexor digitorum superficialis transfer may relieve a PIP joint contracture and may restore balance between the flexion and extension forces.
FIGURE 19. An 8-month-old patient with camptodactyly of the long, ring, and small fingers who was treated with a forearm-based splint and dorsal strap to position the proximal interphalangeal joints in less flexion.
The PIP joint can be approached by using a palmar or mid-lateral incision, depending on the magnitude of the contracture and the status of the skin (6). The surgeon must decide whether a local skin rearrangement (e.g., Z-plasty) is adequate to accommodate a complete extension of the PIP joint or whether a supplemental skin graft is required (Fig. 20). A palmar longitudinal approach with Z-plasty lengthening is used for a mild to moderate flexion contracture (4,16,17). A full-thicknesss skin graft is selected for a severe PIP joint contracture. The incision is extended into the palm in a zigzag fashion for complete exploration of the

digit. The proximal extent of the dissection ends at the transverse carpal ligament. Skin shortage within the palm is not an issue, and Z-plasty lengthening is not required. Flexible camptodactyly without a fixed flexion can be approached with a mid-lateral incision over the digit combined with a zigzag incision in the palm.
FIGURE 20. Palmar longitudinal incision that is segregated into Z-plasties for moderate camptodactyly.
Deeper Dissection
The degree of the PIP joint contracture and the involvement of the periarticular structures dictate the extent of the release that is required. A graduated release of the offending agents is performed until adequate PIP joint extension is obtained. After the skin incision, any abnormal fascia and linear fibrous bands are released during exposure of the deeper structures (4,17). Additional release of the flexor tendon sheath, the flexor digitorum superficialis tendon, the checkrein ligaments, the collateral ligaments, and the palmar plate may be necessary to obtain sufficient extension (16,34).
The digit is explored for anomalous structures, with specific examination of the intrinsic muscles and flexor digitorum superficialis. Any anomalous origin or insertion of the lumbrical or interosseous muscles is resected (4,16,17). The lumbrical should be explored along its entire length to assess for any abnormality (Fig. 21). The lumbrical can insert directly into the metacarpophalangeal joint capsule, onto the flexor digitorum superficialis tendon, or into the ring finger extensor apparatus (Fig. 22). Traction to an anomalous lumbrical muscle does not result in PIP joint extension. An anomalous palmar interosseous muscle can pass into the ring finger, although partial division of the intermetacarpal ligament may be required to completely assess its course. The palmar interosseous is assessed, but diligent exploration is not always performed.
FIGURE 21. Isolation and exploration of the lumbrical to the small finger.
FIGURE 22. Resection of an abnormal lumbrical that is inserted into the metacarpophalangeal joint capsule.
The flexor digitorum superficialis tendon is identified proximal to the first annular pulley (Fig. 23). Traction is applied to the tendon in a proximal and distal direction to assess its excursion and insertion. Deficient proximal excursion with concomitant inability to flex the PIP joint indicates abnormalities of insertion. This requires release of the flexor digitorum superficialis tendon through a third annular

pulley window. Lack of distal excursion implies proximal pathology or aplasia of the muscle and necessitates excision of the flexor digitorum

superficialis. In these instances, the tendon is traced into the palm and is released from its abnormal site of origin.
FIGURE 23. Isolation of the flexor digitorum superficialis tendon proximal to the first annular pulley and assessment of available excursion.
FIGURE 24. Division of the flexor digitorum superficialis through a third annular pulley window.
Tendon Transfer
The presence of distal excursion in the flexor digitorum superficialis makes the tendon suitable for transfer. The preoperative status of the flexor digitorum superficialis is an important consideration. An independent flexor digitorum superficialis to the small finger can be transferred without further dissection. However, a dependent flexor digitorum superficialis must be separated from the ring finger to become a suitable donor for transfer. Failure to achieve independent function is a relative contraindication to transfer of the small-finger flexor digitorum superficialis tendon.
Transfer of the flexor digitorum superficialis tendon to the extensor apparatus lessens the PIP joint flexion force and augments PIP joint extension (3,4,16). The flexor digitorum superficialis tendon is transected just distal to the PIP joint through a third annular pulley window (Fig. 24). The tendon is withdrawn into the palm proximal to the first annular pulley (Fig. 25). The lateral band and central slip are isolated over the dorsum of the digit (Fig. 26). A tendon passer is placed from dorsum of the finger into the lumbrical canal, beneath the intermetacarpal ligament, and into the palm (Figs. 27 and 28). The tendon passer is used to grasp the flexor digitorum superficialis tendon and to guide the tendon through the lumbrical canal (Figs. 29 and 30). The flexor digitorum superficialis tendon is attached to the lateral band and central slip via a weave technique. The tendon is tensioned with the metacarpophalangeal joint positioned in 30 degrees of flexion and the PIP joint held in full extension. A tendon braider facilitates the passage of the flexor digitorum superficialis tendon through the extensor mechanism. The coaptation sites are sutured with a nonabsorbable braided polyester stitch.
FIGURE 25. The divided flexor digitorum superficialis tendon is pulled into palm. A vessel loop is placed around the flexor digitorum profundus tendon.
FIGURE 26. Isolation of the lateral band and the extensor mechanism.
When the flexor digitorum superficialis tendon of the small finger is anomalous, an alternative donor for transfer is necessary. The flexor digitorum superficialis tendon from the adjacent ring finger can also be harvested and passed into the small finger extensor apparatus. In instances of multidigit camptodactyly, numerous flexor digitorum superficialis tendons can be used as donors. The flexor digitorum superficialis tendon can also be split and transferred into two adjacent digits, similar to a modified Stiles-Bunnell transfer (43).
FIGURE 27. The tendon passer is placed from the extensor surface through the lumbrical canal.
FIGURE 28. The tendon passer is positioned in the palmar incision.
After tendon transfer, the skin is closed using a Z-plasty or an application of a full-thickness skin graft (Fig. 31). The extremity is immobilized with the wrist in neutral, the metacarpophalangeal joints in 70 degrees of flexion, and the interphalangeal joints straight. Kirschner wire fixation of the PIP joint is controversial. Prolonged wire fixation can lead to loss of finger flexion and restricted grasp. In contrast, no internal fixation can foster early recurrence of the flexion deformity. The choice is usually made at the time of surgery and depends on the degree of preoperative PIP joint contracture, the ease of obtaining extension, and the end feel of the joint in extension (Fig. 32). If Kirschner wire fixation is chosen, the duration is limited to 3 weeks.
Alternative transfers have been described to restore PIP joint extension. The extensor indicis proprius tendon is accessible and expendable and can be rerouted through the lumbrical canal (44). The tendon is braided into the radial intrinsic or central slip, and tension is adjusted with the central slip tenodesis test.
FIGURE 29. The tendon passer grasps the flexor digitorum superficialis tendon.
FIGURE 30. The flexor digitorum superficialis tendon is pulled through the lumbrical canal toward the extensor mechanism.
Postoperative Care
Three weeks after surgery, the cast is removed, and the sutures are removed. A thermoplastic splint is fabricated with the wrist in neutral, the metacarpophalangeal joints in 70 degrees of flexion, and the interphalangeal joints straight. Another option is to use an ulnar wristlet sling that maintains the metacarpophalangeal joint in flexion and encourages PIP joint extension (Fig. 33) (45). The splint and the wristlet attempt to position the metacarpophalangeal joint in flexion to enable the extrinsic extensors to extend the PIP joint until the intrinsic tendon transfer is capable (Fig. 34). In addition, metacarpophalangeal joint flexion slackens the transferred flexor digitorum superficialis and protects the tendon transfer.
At this time, therapy is initiated with the focus on scar management and teaching the patient to activate the transferred tendon consistently. Scar massage should be with lotion to decrease the friction over the surgical site. The superficial (incision) and the deeper scar around the tendon transfer should be addressed. If the patient appears to have

signs of hypertrophy of the incision, the therapist may consider the use of supplemental products, such as a silicone gel or elastomer pad. This treatment provides prolonged pressure and may facilitate better organization of collagen (46,47). Ultrasound is another modality that can encourage tissue mobilization, although this technique is usually reserved for recalcitrant scar formation after the tendon transfer has healed (6 to 7 weeks after surgery).
FIGURE 31. Z-plasty closure after camptodactyly release and reconstruction.
FIGURE 32. Kirschner wire fixation after proximal interphalangeal joint release and flexor digitorum superficialis tendon transfer.
FIGURE 33. Ulnar wristlet that holds the metacarpophalangeal joint in flexion. The distal interphalangeal joint is splinted to concentrate the flexor digitorum profundus action on proximal interphalangeal joint flexion.
FIGURE 34. The ulnar wristlet positions the metacarpophalangeal joint in flexion to protect the intrinsic transfer and to allow extrinsic proximal interphalangeal joint extension.
Early tendon gliding is the most efficacious method to prevent deep scar formation that can limit motion. The patient must learn to consistently fire the transferred muscle without compensatory motion from adjacent musculature. During the first several days, the therapist attempts to palpate an isolated contraction of the transfer in an antigravity plane. The connection is often taught by having the patient complete the original function of the transferred muscle in an isometric manner. For example, the patient may be cued to attempt isolated PIP joint flexion of the donor digit, which should activate the flexor digitorum superficialis tendon and should yield PIP joint extension. If the patient is unable to isolate the transfer, biofeedback may be helpful in the reeducation process. As the patient achieves a consistent contraction, therapy may progress to functional activities that use PIP joint extension.
During week 6, the patient may engage in some light resistive strengthening. If the patient is firing the transfer, the splint may be removed during the day except during strenuous activity that places the tendon transfer at risk for rupture. During weeks 7 and 8, more resistance may be added to the strengthening program. The intrinsic transfer should be protected for at least 12 weeks after surgery (6,45). Subsequently, the splint is discontinued for all activity, and unrestricted use is allowed. Prolonged nighttime splinting until the late teens is required to prevent recurrence (15).
Salvage Procedures
Severe flexion deformity of the PIP joint with secondary bony changes is often not amenable to contracture release

and tendon transfer. In these instances, bony realignment is the only method to correct the excessive flexion. This adjustment can be made by a dorsal closing wedge osteotomy of the proximal phalanx or a PIP joint fusion (chon-drodesis or arthrodesis). The osteotomy corrects the posture of the finger and shifts the arc of motion. The overall amount of PIP joint motion remains unchanged, which results in loss of full flexion and impaired grasp (2,26).
A PIP joint chondrodesis or arthrodesis can also be used to reposition the finger into a better alignment, although any remaining motion is sacrificed. A chondrodesis requires removal of the cartilage from the proximal phalanx head and the base of the middle phalanx. The physis of the middle phalanx is preserved to allow continued longitudinal growth. The PIP joint is placed in approximately 40 degrees of flexion, and percutaneous Kirschner wires are placed for internal fixation. An arthrodesis is performed in a similar fashion without preservation of the growth plate. Additional options for internal fixation are available, including tension band, interosseous wire, or screw (48,49,50,51 and 52).
Camptodactyly is difficult to treat and even more difficult to consistently achieve successful results. McCarroll (5) noted different preoperative findings among outcome reports after surgical reconstruction of camptodactyly. The most noteworthy differences concerned the presence or absence of a fixed PIP joint flexion deformity and the amount of active extension of the PIP joint when the metacarpophalangeal joint is positioned in flexion. In addition, many reports combine different types of camptodactyly into a single cohort, which confounds the outcome after treatment. These considerable differences obscure the surgical results, as fundamental differences in pathoanatomy may be present before the procedure.
Conservative treatment with splinting and passive stretching has resulted in an improvement in the amount of PIP joint contracture (8,15,25,41). Supervised therapy and a compliant patient are prerequisites to implementation of conservative management. The best results are obtained in a well-motivated patient with a mild deformity (25). Prolonged diligent splinting is necessary to achieve a satisfactory outcome. Hori et al. (41) reported on 24 patients (34 fingers) with small finger camptodactyly who were treated with a splinting regimen. The splints were worn 24 hours per day until adequate correction was obtained, followed by 8 hours per day until maturity. The average follow-up time was almost 4 years. Twenty fingers had almost full extension, nine had improved extension, three were unchanged, and two fingers were worse. The average flexion contracture improved from 40 to 10 degrees after treatment.
Benson et al. (8) treated 22 patients (59 digits) with a therapy program and reported their results at a mean follow-up of 33 months. Type 1 or infantile camptodactyly (13 patients or 24 PIP joints) improved from a 23-degree flexion contracture to 4 degrees shy of full extension. Type 2 or adolescent camptodactyly (four patients or five PIP joints) were relatively noncompliant with therapy and achieved minimal correction. Two patients underwent an attempt at surgical correction, and both digressed after the procedure, with a worsening of the PIP joint contracture. Type 3 camptodactyly (five patients or 30 PIP joints) possessed a diverse amount of deformity. Twelve PIP joints lacked at least 15 degrees of extension and improved to an average of 1 degree shy of full extension after the splinting protocol.
Multiple surgical procedures have been reported for camptodactyly. The technique is variable, and the results are scattered with respect to outcome. Smith and Kaplan (3) performed an isolated tenotomy of the flexor digitorum superficialis at the wrist or the hand in 12 fingers with camptodactyly. The site of transection had no effect on the amount of correction that was achieved. The flexion deformity decreased by at least 33% in all fingers without a loss in finger flexion strength. Unfortunately, the exact amount of PIP joint flexion is not discussed.
Jones et al. (6) reported on a small cohort of six patients who underwent severance of the flexor digitorum superficialis combined with transfer of the tendon to the extensor apparatus. The residual PIP joint contracture averaged 15 degrees (with a range from 0 to 25 degrees) without mention of any sacrifice in flexion.
Engber and Flatt (10) analyzed the treatment of camptodactyly in 66 patients. Thirty-four patients were evaluated only once and were excluded from the follow-up data. Fourteen patients were treated without surgery by various forms of stretching and splinting. Six patients improved, and eight progressed despite conservative treatment. Corrective and salvage types of surgery were performed on 24 hands to lessen the contracture. Twenty hands underwent release of the palmar structures with or without transfer of the flexor digitorum superficialis. Seven hands improved, six remained the same, and seven worsened after surgery. Slightly better results were noted when the flexor digitorum superficialis was transferred. Four hands underwent osteotomy or arthrodesis to better align the finger. The authors concluded that surgical intervention is not uniformly satisfying.
Siegart et al. (25) reviewed 57 patients with “simple” camptodactyly, although multiple digital involvement was common. Thirty-eight fingers were treated with surgery, and 41 digits were treated by therapy. Seven patients were unavailable for follow-up evaluation. The remaining patients had a mean follow-up of more than 6 years. Surgery consisted of release of the contracted structures with or without transfer of the flexor digitorum superficialis. Abnormalities of the lumbrical muscle were found in two patients, whereas eight patients had anomalies of the flexor digitorum superficialis. In ten patients, the PIP joint was pinned in extension. The results were classified according to the ultimate improvement in PIP joint extension without a

simultaneous loss of flexion (Table 3). In the operative group, there were 25 poor, six fair, seven good, and no excellent results. The overall improvement in extension was only 10 degrees, and ten patients lost a significant amount of flexion. An additional six patients developed ankylosis of the PIP joint. In the conservative group, there were six poor, eight fair, 27 good, and no excellent results. Seigart et al. (25) concluded that camptodactyly appears superficially to be a simple problem. In reality, however, it is a “long-term and frustrating problem to both patient and doctor.”
Classification Criteria
Excellent Correction to full extension with less than 15 degrees of loss of PIP joint flexion
Good Correction to within 20 degrees of full PIP joint extension or a more than 40-degree increase in PIP joint extension, with less than 30 degrees of loss of flexion
Fair Correction to within 40 degrees of full PIP joint extension or a more than 20-degree increase in PIP joint extension, with less than 45 degrees of loss of flexion
Poor Less than 20 degrees of improvement in PIP joint extension or less than 40 degrees of total PIP joint motion
PIP, proximal interphalangeal.
Adapted from Siegert JJ, Cooney WP, Dobyns JH. Management of simple camptodactyly. J Hand Surg 1990;15:181–189.
Ogino and Kato (24) encountered 35 cases of camptodactyly over a 14-year period. Surgical treatment was performed on six patients after failure of conservative treatment and a strong patient desire. The flexor digitorum superficialis was hypoplastic in five patients, without proximal continuity to its muscle belly. Preoperative active extension deficit averaged 71 degrees, and active flexion averaged 93 degrees. At a mean follow-up of 27.5 months, the active extension deficit improved to 23 degrees, and flexion diminished to an average of 80 degrees. The amount of PIP joint flexion contracture reduced from a mean of 57.5 degrees to 16 degrees.
McFarlane et al. (16,21) are fervent supporters of abnormalities within the intrinsic system as the principal defect that underlies camptodactyly. A series of 53 surgical patients were assessed for preoperative, operative, and postoperative data to ascertain the cause of deformity and the results of treatment. An abnormal lumbrical muscle was found in all cases, and flexor digitorum superficialis anomalies were also noted in nearly one-half of the patients. These abnormalities were found to be interdependent, and each had an adverse effect on outcome. Overall, the PIP joint contracture improved from 49 degrees to 25 degrees. The return of finger flexion was prolonged, and only 33% of the patients regained full flexion at 1 year. Positive predictors of outcome were a PIP joint contracture of less than 45 degrees and independent flexor digitorum superficialis function.
Smith et al. (17) assessed the surgical management of camptodactyly in a cohort of 16 patients (18 fingers) who were followed for a mean of 2.8 years (with a range from 8 months to 9 years). A unified surgical approach was applied to the majority of patients with a graduated release of contracted structures and a thorough assessment for anomalous elements. The results were classified according to Siegart et al. (25) with inclusion of parameters for extension and flexion (Table 3). Excellent or good results were reported in 15 fingers or 83% (six excellent and nine good). Two fingers were rated as fair, one was poor, and all had preoperative bony deformities. These satisfactory results are in direct contrast to the series that was reported by Seigart et al. (25). The dissimilar outcome between these series is difficult to explain but may be related to different durations of follow-up, patient compliance, underlying pathoanatomy, and surgical technique.
Koman et al. (13) reported on eight patients who were seen at birth with severe flexion deformities of multiple digits (27 fingers) without a predilection for the small finger. This cohort is distinctly different from other reports of camptodactyly. Many of these children had associated anomalies, including two children with arthrogryposis and one with Marfan syndrome. All patients underwent initial hand therapy and splinting. Surgery was performed on six children (20 digits) between 13 months and 8.5 years of age. Follow-up on all patients was longer than 2 years. Eight digits had surgery that was limited to the palmar aspect, with release of the contracted structures and lengthening of the flexor digitorum superficialis. Twelve digits had surgery on the palmar side, combined with reconstruction of the extensor mechanism on the dorsal surface. Reconstruction was performed by lateral band realignment and transfer of the flexor digitorum superficialis. No improvement was noted in the eight digits that underwent an isolated palmar approach. Ten of the 12 fingers that had a combined approach demonstrated less than 20 degrees of residual flexion deformity and a “functional” grasp and release. This group of children represents a subset of camptodactyly that appears to benefit from extensor mechanism reconstruction by lateral band realignment and transfer of the flexor digitorum superficialis to augment intrinsic power.
Surgery for camptodactyly is fraught with early and late complications. A higher incidence of surgical complications occurs in severe camptodactyly with a fixed deformity. Release of these contracted fingers can result in injury to the neurovascular structures from laceration, tension during extension of the digit, or subsequent scarring (25). Skin slough is also more common in digits with considerable contracture. After skin loss, exposure of the tendon may require valiant techniques for coverage, such as a cross-finger flap. These complications often have a deleterious effect on outcome.

Loss of motion after surgery is a serious concern and can be limited by diligent postoperative care. Release of the flexor digitorum superficialis tendon violates the tendon sheath and leads to scar formation. Immediate distal interphalangeal motion prevents adhesion formation around the flexor digitorum profundus tendon (4). A confounding factor occurs when a concomitant PIP joint release is required, which is notorious for loss of motion. To lessen the chances of losing flexion, the duration of PIP joint immobilization should be limited to 3 weeks. Lack of full extension is better tolerated than deficient flexion, and early mobilization fosters restoration of flexion (17). Despite early motion of the flexor digitorum profundus and the PIP joint, return of flexion is slow and may take 6 to 12 months (16). A small residual flexion deficit is common, but this amount must be minimized to prevent impairment in grasp. Complete ankylosis of the PIP joint has been reported after camptodactyly reconstruction (10,25). This complication is associated with attempts at remodeling the joint surface, which should be avoided (10).
Clinodactyly is more common than camptodactyly but is less problematic. The abnormal deviation is in the coronal or radioulnar plane (1,53). Clinodactyly typically affects the small-finger distal interphalangeal joint, and the deviation is usually in a radial direction (Fig. 35). A deviation of less than 10 degrees is so common that it may be considered normal (1,53). On occasion, clinodactyly can involve several digits (Fig. 36). The deformity is usually fixed, and there is no intraarticular or periarticular swelling.
FIGURE 35. Clinodactyly of the small finger with radial deviation of the distal interphalangeal joint.
FIGURE 36. Clinodactyly that affects both hands and multiple digits.
Incidence and Demographics
Clinodactyly is reported to occur between 1.0% and 19.5% of normal children, and most are bilateral (1,54). The exact incidence is probably higher, as most patients are asymptomatic and do not seek medical attention. Clinodactyly can be inherited and is considered an autosomal-dominant trait with variable expressivity and incomplete penetrance (53,54). Clinodactyly is also associated with many syndromes and chromosomal abnormalities, most notably Down syndrome, with an incidence between 35% and 79% (1,55,56,57 and 58). Thumb cli-nodactyly is also a prominent feature of Apert’s syndrome (59), Rubinstein-Taybi syndrome (60), diastrophic dwarfism (61), and triphalangeal thumbs (Fig. 37) (62).
FIGURE 37. A 5-year-old patient with Rubinstein-Taybi syndrome and associated thumb clinodactyly.

The normal alignment of the interphalangeal joints is perpendicular to the long axis of the bone. Clinodactyly is a deviation from this normal orientation. Typical clinodactyly is caused by malalignment of the distal interphalangeal joint that is attributed to inclination of the middle phalanx articular surface (1,53). The fact that the middle phalanx is the last phalanx to ossify may be a factor in its involvement in clinodactyly.
Abnormal deviation of a digit can be caused by other pathology. An anomalous orientation of the growth plate can alter the configuration of the phalanx and can cause coronal deviation of the finger (1,63). This condition is known as a delta phalanx, a longitudinal bracketed diaphysis, or a longitudinal epiphyseal bracket. This entity must be considered during the evaluation of a child with clinodactyly.
Clinodactyly has been classified according to the extent of the deformity and the presence or absence of associated findings (Table 4) (64). The complicated cases often have a concomitant rotational deformity (Fig. 38).
Typical clinodactyly presents with radial deviation of the small finger, which is noted at birth or during infancy (Fig. 35). The primary complaint of the patient and family is often related to the appearance of the finger rather than a functional problem. A thorough history is necessary to ensure that this represents an isolated anomaly and is not part of a syndrome.
The angulation of the distal interphalangeal joint is measured with a goniometer. The active and passive motion of the distal interphalangeal joint is assessed and recorded. The deformity is usually fixed, and only slight passive correction is achievable via opening of the joint space. The other fingers and thumb are assessed for coronal deviation or additional anomalies.
Classification Criteria
Simple Bony deformity of middle phalanx with less than 45 degrees of angulation (with a range from 15 to 45 degrees)
Simple complicated Bony deformity of middle phalanx with greater than 45 degrees of angulation (with a range from 45 to 60 degrees)
Complex Bony and soft tissue deformity with less than 45 degrees of angulation (with a range from 15 to 45 degrees, with syndactyly)
Complex complicated Bony and soft tissue deformity with 45 to 60 degrees of angulation with polydactyly or gigantism
Adapted from Cooney WP. Camptodactyly and clinodactyly. In: Carter P, ed. Reconstruction of the child’s hand. Philadelphia: Lea & Febiger, 1991.
FIGURE 38. An 8-year-old patient with complicated clinodactyly that is attributed to underlying macrodactyly.
X-rays of the affected part are a routine component of the evaluation. The alignment of the digits and the configuration of the bony constituents are assessed. An inclination of the middle phalanx articular surface is characteristic of typical or simple clinodactyly. However, the surrounding bones are scrutinized for anomalies that may contribute to the malalignment. A longitudinal epiphyseal bracket (also known as a delta phalanx or a longitudinal bracketed diaphysis) tends to occur in the phalanges (Fig. 39) (1,64,65). The longitudinal epiphyseal bracket represents a functioning physis and epiphysis along the side of the phalanx that courses in a proximal-to-distal direction. The surface that overlies the longitudinal physis is covered by articular cartilage, and active enchondral ossification occurs along the involved side of the phalanx (63). The abnormal growth plate may bracket part of or the entire phalanx. This orientation prevents appropriate longitudinal growth of the finger and may promote progressive angulation.
The longitudinal epiphyseal bracket is highly variable in morphology, and, before ossification of the epiphysis, the ultimate shape of the phalanx and the extent of the abnormal epiphysis and physis cannot be determined (53,63). Successive x-ray films reveal the specific configuration of the bone and growth plate. The longitudinal epiphyseal bracket tends to be C-shaped and is situated along the

shorter side of the bone (63). Magnetic resonance imaging can be used for early delineation of the longitudinal epiphyseal bracket (Fig. 40).
FIGURE 39. Thumb clinodactyly that is secondary to a longitudinal epiphyseal bracket.
Conservatism and observation are the mainstays of treatment for simple camptodactyly. Mild and moderate forms of clinodactyly do not require surgery. Corrective procedures are reserved for severe angulation with digital overlap during fist formation. Clinodactyly that is secondary to a delta phalanx requires treatment that is directed toward the abnormal growth plate (63,66,67). Clinodactyly that is associated with syndactyly, polydactyly, or macrodactyly necessitates treatment of the primary malformation (Fig. 38).
FIGURE 40. Magnetic resonance imaging of a C-shaped longitudinal epiphyseal bracket that involves both metatarsals.
In contrast to camptodactyly, splinting is not recommended for clinodactyly (1,53,63). The underlying deformity is a bony malformation, and it is unlikely that splinting would impart any benefit. In complex clinodactyly that is attributed to a longitudinal epiphyseal bracket, progressive angulation can occur over time. However, the rate of development and the magnitude of the deformity are unpredictable. This variation is related to the growth potential within the cells and the morphology of the bracket (63). Therefore, observation of the digit is preferred until progressive angulation is demonstrated or until skeletal maturity is reached.
Operative treatment is reserved for a severe deformity that interferes with function. The basic treatment is an osteotomy of the middle phalanx to realign the digit. A variety of surgical techniques have been described to complete this task. The exact procedure depends on the underlying etiology, the amount of deformity, the status of the soft tissues, and the surgeon’s preference.
In simple uncomplicated clinodactyly, a closing wedge osteotomy provides ample correction of the deformity (Fig. 41). The wedge is removed from the middle phalanx along the convex side of the deformity. A mid-lateral approach

with elevation of the extensor apparatus allows adequate exposure of the middle phalanx. The wedge is configured with the base along the ulnar border of the finger and the apex along the radial edge. The amount of wedge resection can be planned before surgery or can be determined at the time of surgery. During surgery, a 0.035-in. Kirschner wire is drilled perpendicular to the shaft at the proposed osteotomy site in the diaphysis. A 25-gauge needle is placed into the distal interphalangeal joint in the coronal plane. The angle between the Kirschner wire and the needle subtends the configuration of the wedge. A second Kirschner wire is placed retrograde from the fingertip into the distal phalanx and across the distal interphalangeal joint. This wire serves as a joystick in the distal fragment and provides fixation after wedge osteotomy. The positions of the Kirschner wires and needle are confirmed by mini fluoroscopy.
FIGURE 41. Diagram of osteotomy along the convex side of the middle phalanx to realign the digit. k-wire, Kirschner wire.
The osteotomy is performed with a bone biter or small oscillating saw. The saw must have a fine kerf to prevent excessive bone removal. The first cut is performed along the Kirschner wire and is advanced two-thirds through the middle phalanx. The transverse Kirschner wire is removed. A second cut is carried out parallel to the needle, such that the wedge meets along the radial border of the digit. The periosteum and a portion of the cortex along the radial side are not disrupted to preserve some stability. The wedge of bone is removed, and the finger is angulated into ulnar deviation. This maneuver cracks the remaining radial cortex and aligns the finger. The longitudinal Kirschner wire is advanced across the osteotomy site to provide provisional stability. The position of the longitudinal Kirschner wire, the alignment of the digit, and the status of the osteotomy site are verified by mini fluoroscopy. Additional stability can be obtained by placement of a second Kirschner wire in an oblique direction.
In simple complicated clinodactyly, the amount of wedge resection can result in an excessive amount of shortening. An opening wedge osteotomy can be performed along the concave side to lengthen the digit (Fig. 42). The skin may require Z-plasty lengthening to accommodate the increase in length. This type of osteotomy is considerably more difficult than a closing wedge.
In complicated clinodactyly, the underlying malformation must be addressed. Syndactyly, polydactyly, and macrodactyly have their individual treatment regimens that manage the bone and soft tissue anomalies. Clinodactyly that is secondary to a longitudinal epiphyseal bracket is the most common cause of complicated syndactyly. Multiple procedures have been proposed to correct the underlying physeal abnormality (Fig. 43). In general, the longitudinal epiphysis is cut, and the growth plate along the convex side of the bone is ablated. The horizontal portion of the epiphysis must be preserved to allow for longitudinal growth. In mild deformities, a closing wedge osteotomy of the phalanx can be performed to realign the digit. An opening wedge provides simultaneous lengthening of the digit, and an autograft or allograft can be placed into the defect. A reversed wedge graft has also been described, which resects a wedge from the convex side and inserts the segment into the concave side (66). An opening or reverse wedge can lead to fusion of the graft across the horizontal portion of the epiphysis. This results in a physeal bar with partial or complete growth arrest and a recurrent angular deformity or a shortened digit. Irrespective

of the type of osteotomy, Kirschner wires are used for internal fixation until union.
FIGURE 42. Diagram of opening wedge osteotomy and Z-plasty of the skin to correct clinodactyly and to preserve length. k-wire, Kirschner wire.
FIGURE 43. Diagram of surgical options for clinodactyly that is secondary to a longitudinal epiphyseal bracket.
FIGURE 44. Diagram of a resection of the longitudinal growth plate and fat graft insertion for clinodactyly that results from a longitudinal epiphyseal bracket.
A prophylactic procedure has been described for young children with progressive deformity (63,67). The operation is performed when the child is approximately 3 years of age. A mid-lateral approach along the digit provides exposure to the apex of the longitudinal epiphyseal bracket. The longitudinal portion of the bracket is excised, and a fat graft is inserted to cover the ends of the split physis (Fig. 44). Over time, the digit gradually straightens as growth of the digit occurs through the horizontal portions of the growth plate.
Simple clinodactyly that is treated by wedge resection is a relatively straightforward operation. A closing wedge osteotomy can disturb the surrounding tendons and can cause adhesions around the tendons. The resultant limitation of motion can hinder hand function. In addition, the extensor tendons do not tolerate substantial shortening, and an extension lag can develop at the distal interphalangeal joint.
Surgery for complicated clinodactyly is more prone to problems. The longitudinal epiphyseal bracket is a difficult condition to treat. A misplaced osteotomy can inadvertently injure the horizontal portion of the growth plate, which leads to a growth disturbance and a shortened digit.
1. Flatt AE. Crooked fingers. In: Flatt AE, ed. The care of congenital hand anomalies, 2nd ed. St. Louis: Quality Medical Publishers, 1994:47–63.
2. Senrui H. Congenital contractures. In: Buck-Gramcko D, ed. Congenital malformations of the hand and forearm. London: Churchill Livingstone, 1998:295–309.
3. Smith RJ, Kaplan EB. Camptodactyly and similar atraumatic flexion deformities of the proximal interphalangeal joints of the fingers. J Bone Joint Surg 1968;50:1187–1203.
4. Kay SP. Camptodactyly. In: Green DP, Hotchkiss RN, Pederson WC, eds. Green’s operative hand surgery, 4th ed. Philadelphia: Churchill Livingstone, 1999:510–517.
5. McCarroll HR. Congenital anomalies: a 25-year overview. J Hand Surg 2000;25:1007–1037.
6. Jones KG, Marmor L, Lankford LL. An overview on new procedures in surgery of the hand. Clin Orthop 1974;99:154–167.
7. Courtemanche AD. Campylodactyly: etiology and management. Plast Reconstr Surg 1969;44:451–454.
8. Benson LS, Waters PM, Kamil NI, et al. Camptodactyly: classification and results of nonoperative treatment. J Pediatr Orthop 1994;14:814–819.
9. Weber FP. A note on camptodactylia (Landouzy) and Dupuytren’s condition. Med Press Circ 1947;217:453–454.
10. Engber WD, Flatt AE. Camptodactyly: an analysis of sixty-six patients and twenty-four operations. J Hand Surg 1977;2:216–224.
11. Scott J. Hammer-finger with notes of seven cases occurring in one family. Glasgow Med J 1903;60:335–344.
12. Welch JP, Temtamy SA. Hereditary contractures of the fingers (camptodactyly). J Med Genet 1966;3:104–113.
13. Koman LA, Toby EB, Poehling GG. Congenital flexion deformities of the proximal interphalangeal joint in children: a subgroup of camptodactyly. J Hand Surg 1990;15:582–586.
14. Millesi H. Camptodactyly. In: Littler JW, Cramer LM, Smith JW, eds. Symposium on reconstructive hand surgery. St. Louis: CV Mosby, 1974:175–177.
15. Miura T, Nakamura R, Tamura Y. Long-standing extended dynamic splintage and release of an abnormal restraining structure in camptodactyly. J Hand Surg 1992;17:665–672.
16. McFarlane RM, Classen DA, Porte AM, et al. The anatomy and treatment of camptodactyly of the small finger. J Hand Surg 1992;17:35–44.
17. Smith PJ, Grobbelaar AO. Camptodactyly: a unifying theory and approach to surgical treatment. J Hand Surg 1998;23:14–19.
18. Fèvre M. Les locages tendineux digitaux. (Doigts à resort et flexions des doigts par blocages tendineux dans les gaines digitales.) Rev Orthop 1936;23:137–142.
19. Inoue G, Tamura Y. Camptodactyly resulting from paradoxical action of an anomalous lumbrical muscle. Scand J Plast Reconstr Hand Surg 1994;28:309–312.
20. Magnusson R. La camptodactylie. Acta Chir Scand 1942;87:236–242.
21. McFarlane RM, Curry GI, Evans HB. Anomalies of the intrinsic muscles in camptodactyly. J Hand Surg 1983;8:531–544.
22. Millesi H. Zur Behandlung der Kamptodaktylie. Klin Med 1966;21:329–335.
23. Minami A, Sakai T. Camptodactyly caused by abnormal insertion and origin of lumbrical muscle. J Hand Surg 1993;18:310–311.
24. Ogino T, Kato H. Operative findings in camptodactyly of the little finger. J Hand Surg 1992;17:661–664.

25. Siegert JJ, Cooney WP, Dobyns JH. Management of simple camptodactyly. J Hand Surg 1990;15:181–189.
26. Oldfield MC. Campylodactyly: flexor contracture of the fingers in young girls. Br J Plast Surg 1956;8:312–317.
27. Furnas DW. Muscle-tendon variations in the flexor compartment of the wrist. Plast Reconstruct Surg 1965;36:320–324.
28. Shrewsbury MM, Kuczynski K. Flexor digitorum superficialis in the fingers of the human hand. Hand 1974;6:121–133.
29. Basu SS, Hazary S. Variations of the lumbrical muscles of the hand. Anat Rec 1960;136:501–504.
30. Eyler DL, Markee JE. The anatomy and function of the intrinsic musculature of the fingers. J Bone Joint Surg 1954;36:1–9.
31. Mehta HJ, Gardner WU. A study of lumbrical muscles in the human hand. Am J Anat 1961;109:227–238.
32. Adams W. On congenital contraction of the fingers and its association with “hammer-toe”; its pathology and treatment. Lancet 1891;2:111–114,165–168.
33. Barton NE. Late extenders. In: Hand correspondence newsletter. Rosemont, IL: American Society for Surgery of the Hand, 1999:43.
34. Curtis RM. Capsulectomy of the interphalangeal joints of the fingers. J Bone Joint Surg 1954;36:1219–1232.
35. Smith PJ, Ross DA. The central slip tenodesis test for early diagnosis of potential boutonnière deformities. J Hand Surg 1994;19:88–90.
36. Omer GE Jr. Ulnar nerve palsy. In: Green DP, Hotchkiss RN, eds. Green’s operative hand surgery, 3rd ed. Philadelphia: Churchill Livingstone, 1993:1449–1466.
37. Currarino G, Waldman I. Camptodactyly. Am J Roentgenol 1964;92:1312–1321.
38. Beals RK, Hecht F. Congenital contractural arachnodactyly. A heritable disorder of connective tissue. J Bone Joint Surg 1971;53:987–993.
39. Ogino T, Kato H, Ohshio I, et al. Clinical features of congenital contractural arachnodactyly. Congen Anom 1993;33:85–94.
40. Zancolli E, Zancolli E Jr. Congenital ulnar drift of the fingers. Pathogenesis, classification, and surgical management. Hand Clin 1985;1:443–456.
41. Hori M, Nakura R, Inoue G, et al. Nonoperative treatment of camptodactyly. J Hand Surg 1987;12:1061–1065.
42. Hefner RA. Inheritance of crooked little finger (streblomicrodactyly). J Hered 1929;20:395–398.
43. Smith RJ. Tendon transfers of the hand and forearm. Boston: Little, Brown and Company, 1987:253–254.
44. Gupta A, Burke FD. Correction of camptodactyly. J Hand Surg 1990;15:168–170.
45. Smith RJ. Tendon transfers of the hand and forearm. Boston: Little, Brown and Company, 1987:119–120.
46. Gold MH. Topical silicone gel sheeting in the treatment of hypertrophic scars and keloids. A dermatologic experience. J Dermatol Surg Oncol 1993;19:912–916.
47. Widgerow AD, Chait LA, Stals R, et al. New innovations in scar management. Aesthetic Plast Surg 2000;24:227–234.
48. Carroll RE. Small joint arthrodesis in hand reconstruction. J Bone Joint Surg 1969;51:1219–1221.
49. Faithfull DK, Herbert TJ. Small joint fusions of the hand using the Herbert bone screw. J Hand Surg 1984;9:167–168.
50. Lister G. Intraosseous wiring of the digital skeleton. J Hand Surg 1978;3:427–435.
51. McGlynn JT, Smith RA, Bogumill GP. Arthrodesis of small joint of the hand: a rapid and effective technique. J Hand Surg 1988;13:595–599.
52. Teoh LC, Yeo SJ, Singh I. Interphalangeal joint arthrodesis with oblique placement of an AO lag screw. J Hand Surg 1994;19:208–211.
53. Ezaki, M. Angled digits. In: Green DP, Hotchkiss RN, Pederson WC, eds. Green’s operative hand surgery, 4th ed. Philadelphia: Churchill Livingstone, 1999:517–521.
54. Hersh AH, DeMarinis F, Stecher RM. On the inheritance and development of clinodactyly. Am J Hum Genet 1953;5:257–268.
55. Gerald B, Umansky R. Cornelia de Lange syndrome: radiographic findings. Radiology 1967;88:96–100.
56. Hefke HW. Roentgenologic study of anomalies of hands in 100 cases of mongolism. Am J Dis Child 1940;60:1319–1323.
57. Houston CS. Roentgen findings in the XXXXY chromosome anomaly. J Can Assoc Radiol 1967;18:258–267.
58. Snyder CC. Bilateral facial agenesis (Treacher-Collins syndrome). Am J Surg 1956;92:81–87.
59. Poznanski AK, Garn SM, Holt JF. The thumb in the congenital malformation syndromes. Radiology 1971;100:115–129.
60. Rubenstein JH. The broad thumbs syndrome- progress report 1968. Birth Defects 1969;5:25–41.
61. Stover CN, Hayes JT, Holt JF. Diastrophic dwarfism. Am J Roentgenol 1963;89:914.
62. Wood VE. Treatment of the triphalangeal thumb. Clin Orthop 1976;120:179–193.
63. Light TR, Ogden JA. The longitudinal epiphyseal bracket: implications for surgical correction. J Pediatr Orthop 1981;1:299–305.
64. Cooney WP. Camptodactyly and clinodactyly. In: Carter P, ed. Reconstruction of the child’s hand. Philadelphia: Lea & Febiger, 1991.
65. Poznanski AK, Pratt GB, Manson G, et al. Clinodactyly, camptodactyly, Kirner’s deformity, and other crooked fingers. Radiology 1969;93:573–582.
66. Carstam N, Theander G. Surgical treatment of clinodactyly caused by longitudinally bracketed diaphysis. Scand J Plast Reconstr Surg 1975;9:199–202.
67. Vickers D. Clinodactyly of the little finger: a simple operative technique for reversal of the growth abnormality. J Hand Surg 1987;12:335–345.