Case Report
The Journal of Hand Surgery (Asian-Pacific Volume) 2017;22(3):359-362 • DOI: 10.1142/S0218810417720236
Acute Traumatic Swan Neck Deformity: A Case Report of the Oblique Retinacular Ligament Lesion
J Hand Surg Asian-Pac Vol 2017.22:359-362. Downloaded from www.worldscientific.com by UNIVERSITY OF AUCKLAND on 09/15/17. For personal use only.
Giuseppe Checcucci*, Marco Biondi†, Marina Faccio†, Piergiuseppe Zampetti‡, Mariarosaria Galeano§, Massimo Ceruso* *Department of Hand Surgery and Reconstructive Microsurgery, Azienda Ospedaliero-Universitaria Careggi, Florence, Largo Palagi, Florence, †Orthopaedic Clinic, University of Florence, Largo P. Palagi, Florence, ‡ Department of Orthopaedic Surgery, Ospedale San Jacopo, Pistoia, Via Pertini, Pistoia, § Unit of Plastic Surgery, University Hospital, via Consolare Valeria, Messina, Italy
Swan neck deformity (SND) can be the manifestation of an acute trauma. We present a case report of a young basketball player with an acute traumatic SND determined by the single ulnar oblique retinacular ligament rupture. The patient caught a ball directly upon the tip of his right’s hand middle finger into extension. He immediately presented a SND with impossibility to actively flex the proximal interphalangeal joint (PIPJ), while preserving active flexion and extension of the distal interphalangeal joint (DIPJ). Hyperextension of PIPJ was reducible with passive mobilization, thus allowing full passive range of motion. The SND was seen to be caused by the lesion of the ulnar oblique retinacular ligament (ORL) on its distal insertion, with consequent dorsomedial migration of the ulnar lateral band. The early surgical distal reinsertion of the ORL allowed the restoration of the original kinematics of the finger flexion-extension. Keywords: Finger deformity, Swan neck deformity, Mallet finger, Oblique retinacular ligament
INTRODUCTION Swan neck deformity (SND) consists in the hyperextension of proximal interphalangeal joint (PIPJ) and flexion of distal interphalangeal joint (DIPJ). As classified in 1979 by Zancolli,1) it is the result of the extensor or intrinsic tendon overactivity, the failure of the stabilizing structures of the palmar joint or a combination of both. For these reasons, SND can develop from abnormalities of the wrist, metacarpophalangeal joint, PIPJ or DIPJ.2) Zancolli divided SND into three fundamental types, depending on the cause of the deformity: extrinsic, in-
Received: Oct. 16, 2015; Revised: Feb. 5, 2016; Accepted: Feb. 9, 2016 Correspondence to: Marco Biondi Orthopaedic Clinic, University of Florence, Largo P. Palagi 1, 50139, Florence, Italy Tel: +0039-3332253624, Fax: +039-0557948065 E-mail: [email protected]
trinsic and articular. The etiopathogenesis can be traumatic or not traumatic. As described by many authors1,3,4) SND is the biomechanical result of many forces acting on the PIPJ, with a common factor: the dorsal migration of the extensor lateral bands. The dorsal migration of the lateral bands, in fact, determines a loss of excursion of the PIPJ, thus a loss of power of extension of the DIPJ. This causes the transmission of all the extensor forces to the base of the middle phalanx where the central slip is inserted, resulting in the hyperextension of the PIPJ. Furthermore, also the deep flexor tendon plays a role in contributing to the mechanism of the SND lesion. This is due to the pronounced curve at PIPJ that forces the tendon to enhance its flexor action over the DIPJ and to lose force over the PIPJ. Patients with swan neck deformity suffer from a considerable functional loss and a tight grip of the finger around an object is impaired. This is also a difficult problem addressed to the most hand surgeons, due to the
360
J Hand Surg Asian-Pac Vol 2017.22:359-362. Downloaded from www.worldscientific.com by UNIVERSITY OF AUCKLAND on 09/15/17. For personal use only.
Giuseppe Checcucci, et al. Lesion of the Oblique Retinacolar Ligament
Fig. 1. Patient presented a right hand’s middle finger SND with PIPJ hyperextension in presence of full active range of motion of the DIPJ. The terminal extensor and flexor apparatus were preserved.
Fig. 2. A dorsal curved approach showed a hematoma of the ulnar ORL insertion on the ulnar lateral band at middle phalanx.
Fig. 3. Suture of the ulnar oblique retinacular ligament to the ulnar lateral band.
complex definition, understanding and correction of the biomechanical mechanism.
not actively flex the PIPJ but could flex and extend actively the DIPJ confirming the anatomic integrity of the terminal tendon of the extensor apparatus. The external manipulation to prevent PIPJ hyperextension allowed the finger to be actively fully flexed demonstrating the integrity of the flexor apparatus, especially the flexor digitorum superficialis. An accurate preoperative ultrasonography examination showed a dorsomedial migration of the ulnar extensor lateral band with integrity of the volar plate, central slip, collateral ligaments, extensor terminal tendon and flexor apparatus. No alterations were found in DIPJ. No X-rays abnormalities were present. During the surgical procedure the patient underwent local anesthesia to allow passive and active movements. A curved dorsal approach to the middle finger was performed showing the presence of a hematoma on the ulnar side of the middle phalanx, where the oblique retinacular ligament inserts (Fig. 2). The dorsal migration of the ul-
CASE REPORT A 23 year old right-handed basketball player suffered from a ball injury upon the tip of his right hand’s middle finger into extension. At physical examination after three days a general joints laxity was revealed, with a clear SND middle finger lesion passively reducible. The patient was complaining of pain over the ulnar side of the middle phalanx. The active flexion of the finger showed a PIPJ hyperextension of 20° while the DIPJ was able to flex 0–35° actively. On active finger extension the PIPJ hyperextended 30° and DIPJ extended to 0° (Fig. 1). There was no fixed deformity, and the finger could be completely flexed with external manipulation. The joint was stable at ulnar and radial stress. The patient could
361
J Hand Surg Asian-Pac Vol 2017.22:359-362. Downloaded from www.worldscientific.com by UNIVERSITY OF AUCKLAND on 09/15/17. For personal use only.
The Journal of Hand Surgery (Asian-Pacific Volume) • Vol. 22, No. 3, 2017 • www.jhs-ap.org
nar lateral band over the middle phalanx and a narrowing of the Winslow’s rhombus were noted at the patient's attempts to move the finger. The distal extensor apparatus insertion on DIPJ presented anatomical integrity. Once the damage was determined and the ulnar oblique retinacular ligament was sutured to the lateral band, the normal anatomy and kinematics were restored (Fig. 3). A complete active flexion and extension of PIPJ and DIPJ were immediately recovered, without hyperextension of PIPJ (Fig. 4). The patient wore a splint with 30° flexion of PIPJ and free DIPJ for 3 weeks. After six months the patient was able to play basketball again without pain, deformities or reduction of ROM (Fig. 5).
Fig. 4. Patient underwent local anesthesia: full active range of motion of the middle finger was immediately restored after ulnar ORL reinsertion.
DISCUSSION As described by Zancolli,1) the SND results from an imbalance between the extensor and flexor forces acting on the PIPJ, with prevalence of extensor forces. On the basis of our clinical evaluation and surgical revision we are reporting the case of an acute, traumatic, articular SND. The literature reports only a few cases of traumatic SND,2) being all associated with mallet finger, volar plate rupture with or without PIPJ dislocation, or lesion of the flexor digitorum superficialis.5) All of these cases report SND as a late manifestation of the first injury. In fact, due to the contracture of the periarticular soft tissues the original injury usually takes time to show a SND, that takes even more time to be establish. In our case SND occurred immediately after the trauma, as a primary traumatic articular SND with no signs of acute mallet finger, in which the terminal extensor tendon presents anatomical disruption. Due to the correct direction of the radial lateral band the finger maintained its active extensor force on the DIPJ, but the dorsal migration of the ulnar lateral band caused the impossibility to actively flex the PIPJ, that hyperextended for the added force on the PIPJ. No case of primary traumatic acute SND caused by the single lesion of one of the oblique retinacular ligaments is reported in literature, but their involvement in the biomechanical causes of a SND is commonly accepted. As described by many authors6,7) the ORL originates from the periosteum of the middle third of the proximal phalanx and flexor sheath, including A-2 and C-1 pulley. It then passes between the transverse retinacular ligament and the Cleland’s ligament, volar to the axis of PIP joint. The insertion is located on the lateral extensor band of the middle phalanx. The action of the ORL
Fig. 5. Follow-up at 6 months. The patient maintained a normal kinematic of flexion and extension of his right hand’s middle finger and returned to play basketball without pain.
362
J Hand Surg Asian-Pac Vol 2017.22:359-362. Downloaded from www.worldscientific.com by UNIVERSITY OF AUCKLAND on 09/15/17. For personal use only.
Giuseppe Checcucci, et al. Lesion of the Oblique Retinacolar Ligament
allows the stabilization of the lateral bands during the range of motion of the DIP and PIP joints, opposing to the dorsomedial migration of the lateral bands in finger’s extension and allowing their volar migration in flexion.8) Landsmeer9) and then Littler10) showed that the dorsal displacement of the lateral bands indicates a stretching or giving way of the oblique retinacular ligament. The ORL involvement in the biomechanical mechanism of SND is well described by Zancolli in a cadaveric experiment.1) After excised the oblique lamina on one side of the cadaver, He strongly pulled the long extensor tendon proximally. The lateral extensor tendon exaggeratedly migrated towards the finger dorsum, determining a SND and getting much closer the middle line of the finger than the lateral extensor tendon of the opposite side whose oblique lamina was intact. In this case report, the lesion of the ulnar oblique retinacular ligament caused the dorsal migration of the lateral band with narrowing of the Winslow’s rhombus, like described by Zancolli. The synergic action between extensor and flexor tendons was interrupted. The shorter direction of the ulnar lateral band added force to the central slip resulting in the hyperextension of the PIP joint. The acute SND was certainly aggravated by the patient's general laxity that did not oppose to the hyperextending forces over the PIP joint, where the capsule and the volar plate usually contrast these forces. The early surgical treatment confirmed the suspected lesion of the ulnar ORL to be the pathophysiological mechanism of this case of SND. The simple suture of the ulnar ORL to the ulnar lateral band restored the physiological kinematics, whereas the general laxity couldn’t justify alone the mechanism, and in particular the impossibility to actively flex the PIPJ by the patient. This case shows that a single lesion of the oblique retinacular ligament must be
taken into account in a picture of the SND lesion, especially when there is no history of PIPJ dislocation and no lesion of the terminal extensor apparatus on DIPJ.
REFERENCES 1. Zancolli E. Structural and dynamic bases of hand surgery. 2th ed. Philadelphia: JB Lippincott Company; 1979:1-81. 2. Sebastin SJ, Chung KC. Reconstruction of digital deformities in rheumatoid arthritis. Hand Clinic. 2011;27(1):87104. 3. De Salamanca EF. Swan-neck deformity: mechanism and surgical treatment. Hand. 1976;8(3):215-21. 4. Merrell G, Slade JF. Dislocations and ligament injuries in the digits. In: Wolfe SW, Hotchkiss RN, Pederson WC, Kozin SH editors. Green’s Operative Hand Surgery. Philadelphia. Elsevier Churchill Livingstone; 2011:291-32. 5. Portis RB. Hyperextensibility of the proximal interphalangeal joint of the finger following trauma. J Bone Joint Surg Am. 1954;36(6):1141-6. 6. Roemer, FJ. Hyperextension injuries to the finger joints. Am J Surg. 1950;80(3):295-302 7. El-Gammal TA, Steyers CM, Blair WF, Maynard JA. Anatomy of the oblique retinacular ligament of the index finger. J Hand Surg Am. 1993;18(4):717-21. 8. Shrewsbury MM, Johnson RK. A systematic study of the oblique retinacular ligament of the human finger. Its structure and function. J Hand Surg Am. 1977;2(3):194-9. 9. Landsmeer JM. A report on the coordination of the interphalangeal joints of the human finger and its disturbances. Acta Morphol Neerl Scand. 1959;2(1):59-84. 10. Littler JW. Restoration of the oblique retinacular ligament for correcting hyperextension deformity of the proximal interphalangeal joint. In: R.Tubiana editor. La Main Rhumatoide. Paris: Expansion Scientifique Francaise; 1966:39-42.
The Journal of Hand Surgery (Asian-Pacific Volume) 2017;22(3):359-362 • DOI: 10.1142/S0218810417720236
Acute Traumatic Swan Neck Deformity: A Case Report of the Oblique Retinacular Ligament Lesion
J Hand Surg Asian-Pac Vol 2017.22:359-362. Downloaded from www.worldscientific.com by UNIVERSITY OF AUCKLAND on 09/15/17. For personal use only.
Giuseppe Checcucci*, Marco Biondi†, Marina Faccio†, Piergiuseppe Zampetti‡, Mariarosaria Galeano§, Massimo Ceruso* *Department of Hand Surgery and Reconstructive Microsurgery, Azienda Ospedaliero-Universitaria Careggi, Florence, Largo Palagi, Florence, †Orthopaedic Clinic, University of Florence, Largo P. Palagi, Florence, ‡ Department of Orthopaedic Surgery, Ospedale San Jacopo, Pistoia, Via Pertini, Pistoia, § Unit of Plastic Surgery, University Hospital, via Consolare Valeria, Messina, Italy
Swan neck deformity (SND) can be the manifestation of an acute trauma. We present a case report of a young basketball player with an acute traumatic SND determined by the single ulnar oblique retinacular ligament rupture. The patient caught a ball directly upon the tip of his right’s hand middle finger into extension. He immediately presented a SND with impossibility to actively flex the proximal interphalangeal joint (PIPJ), while preserving active flexion and extension of the distal interphalangeal joint (DIPJ). Hyperextension of PIPJ was reducible with passive mobilization, thus allowing full passive range of motion. The SND was seen to be caused by the lesion of the ulnar oblique retinacular ligament (ORL) on its distal insertion, with consequent dorsomedial migration of the ulnar lateral band. The early surgical distal reinsertion of the ORL allowed the restoration of the original kinematics of the finger flexion-extension. Keywords: Finger deformity, Swan neck deformity, Mallet finger, Oblique retinacular ligament
INTRODUCTION Swan neck deformity (SND) consists in the hyperextension of proximal interphalangeal joint (PIPJ) and flexion of distal interphalangeal joint (DIPJ). As classified in 1979 by Zancolli,1) it is the result of the extensor or intrinsic tendon overactivity, the failure of the stabilizing structures of the palmar joint or a combination of both. For these reasons, SND can develop from abnormalities of the wrist, metacarpophalangeal joint, PIPJ or DIPJ.2) Zancolli divided SND into three fundamental types, depending on the cause of the deformity: extrinsic, in-
Received: Oct. 16, 2015; Revised: Feb. 5, 2016; Accepted: Feb. 9, 2016 Correspondence to: Marco Biondi Orthopaedic Clinic, University of Florence, Largo P. Palagi 1, 50139, Florence, Italy Tel: +0039-3332253624, Fax: +039-0557948065 E-mail: [email protected]
trinsic and articular. The etiopathogenesis can be traumatic or not traumatic. As described by many authors1,3,4) SND is the biomechanical result of many forces acting on the PIPJ, with a common factor: the dorsal migration of the extensor lateral bands. The dorsal migration of the lateral bands, in fact, determines a loss of excursion of the PIPJ, thus a loss of power of extension of the DIPJ. This causes the transmission of all the extensor forces to the base of the middle phalanx where the central slip is inserted, resulting in the hyperextension of the PIPJ. Furthermore, also the deep flexor tendon plays a role in contributing to the mechanism of the SND lesion. This is due to the pronounced curve at PIPJ that forces the tendon to enhance its flexor action over the DIPJ and to lose force over the PIPJ. Patients with swan neck deformity suffer from a considerable functional loss and a tight grip of the finger around an object is impaired. This is also a difficult problem addressed to the most hand surgeons, due to the
360
J Hand Surg Asian-Pac Vol 2017.22:359-362. Downloaded from www.worldscientific.com by UNIVERSITY OF AUCKLAND on 09/15/17. For personal use only.
Giuseppe Checcucci, et al. Lesion of the Oblique Retinacolar Ligament
Fig. 1. Patient presented a right hand’s middle finger SND with PIPJ hyperextension in presence of full active range of motion of the DIPJ. The terminal extensor and flexor apparatus were preserved.
Fig. 2. A dorsal curved approach showed a hematoma of the ulnar ORL insertion on the ulnar lateral band at middle phalanx.
Fig. 3. Suture of the ulnar oblique retinacular ligament to the ulnar lateral band.
complex definition, understanding and correction of the biomechanical mechanism.
not actively flex the PIPJ but could flex and extend actively the DIPJ confirming the anatomic integrity of the terminal tendon of the extensor apparatus. The external manipulation to prevent PIPJ hyperextension allowed the finger to be actively fully flexed demonstrating the integrity of the flexor apparatus, especially the flexor digitorum superficialis. An accurate preoperative ultrasonography examination showed a dorsomedial migration of the ulnar extensor lateral band with integrity of the volar plate, central slip, collateral ligaments, extensor terminal tendon and flexor apparatus. No alterations were found in DIPJ. No X-rays abnormalities were present. During the surgical procedure the patient underwent local anesthesia to allow passive and active movements. A curved dorsal approach to the middle finger was performed showing the presence of a hematoma on the ulnar side of the middle phalanx, where the oblique retinacular ligament inserts (Fig. 2). The dorsal migration of the ul-
CASE REPORT A 23 year old right-handed basketball player suffered from a ball injury upon the tip of his right hand’s middle finger into extension. At physical examination after three days a general joints laxity was revealed, with a clear SND middle finger lesion passively reducible. The patient was complaining of pain over the ulnar side of the middle phalanx. The active flexion of the finger showed a PIPJ hyperextension of 20° while the DIPJ was able to flex 0–35° actively. On active finger extension the PIPJ hyperextended 30° and DIPJ extended to 0° (Fig. 1). There was no fixed deformity, and the finger could be completely flexed with external manipulation. The joint was stable at ulnar and radial stress. The patient could
361
J Hand Surg Asian-Pac Vol 2017.22:359-362. Downloaded from www.worldscientific.com by UNIVERSITY OF AUCKLAND on 09/15/17. For personal use only.
The Journal of Hand Surgery (Asian-Pacific Volume) • Vol. 22, No. 3, 2017 • www.jhs-ap.org
nar lateral band over the middle phalanx and a narrowing of the Winslow’s rhombus were noted at the patient's attempts to move the finger. The distal extensor apparatus insertion on DIPJ presented anatomical integrity. Once the damage was determined and the ulnar oblique retinacular ligament was sutured to the lateral band, the normal anatomy and kinematics were restored (Fig. 3). A complete active flexion and extension of PIPJ and DIPJ were immediately recovered, without hyperextension of PIPJ (Fig. 4). The patient wore a splint with 30° flexion of PIPJ and free DIPJ for 3 weeks. After six months the patient was able to play basketball again without pain, deformities or reduction of ROM (Fig. 5).
Fig. 4. Patient underwent local anesthesia: full active range of motion of the middle finger was immediately restored after ulnar ORL reinsertion.
DISCUSSION As described by Zancolli,1) the SND results from an imbalance between the extensor and flexor forces acting on the PIPJ, with prevalence of extensor forces. On the basis of our clinical evaluation and surgical revision we are reporting the case of an acute, traumatic, articular SND. The literature reports only a few cases of traumatic SND,2) being all associated with mallet finger, volar plate rupture with or without PIPJ dislocation, or lesion of the flexor digitorum superficialis.5) All of these cases report SND as a late manifestation of the first injury. In fact, due to the contracture of the periarticular soft tissues the original injury usually takes time to show a SND, that takes even more time to be establish. In our case SND occurred immediately after the trauma, as a primary traumatic articular SND with no signs of acute mallet finger, in which the terminal extensor tendon presents anatomical disruption. Due to the correct direction of the radial lateral band the finger maintained its active extensor force on the DIPJ, but the dorsal migration of the ulnar lateral band caused the impossibility to actively flex the PIPJ, that hyperextended for the added force on the PIPJ. No case of primary traumatic acute SND caused by the single lesion of one of the oblique retinacular ligaments is reported in literature, but their involvement in the biomechanical causes of a SND is commonly accepted. As described by many authors6,7) the ORL originates from the periosteum of the middle third of the proximal phalanx and flexor sheath, including A-2 and C-1 pulley. It then passes between the transverse retinacular ligament and the Cleland’s ligament, volar to the axis of PIP joint. The insertion is located on the lateral extensor band of the middle phalanx. The action of the ORL
Fig. 5. Follow-up at 6 months. The patient maintained a normal kinematic of flexion and extension of his right hand’s middle finger and returned to play basketball without pain.
362
J Hand Surg Asian-Pac Vol 2017.22:359-362. Downloaded from www.worldscientific.com by UNIVERSITY OF AUCKLAND on 09/15/17. For personal use only.
Giuseppe Checcucci, et al. Lesion of the Oblique Retinacolar Ligament
allows the stabilization of the lateral bands during the range of motion of the DIP and PIP joints, opposing to the dorsomedial migration of the lateral bands in finger’s extension and allowing their volar migration in flexion.8) Landsmeer9) and then Littler10) showed that the dorsal displacement of the lateral bands indicates a stretching or giving way of the oblique retinacular ligament. The ORL involvement in the biomechanical mechanism of SND is well described by Zancolli in a cadaveric experiment.1) After excised the oblique lamina on one side of the cadaver, He strongly pulled the long extensor tendon proximally. The lateral extensor tendon exaggeratedly migrated towards the finger dorsum, determining a SND and getting much closer the middle line of the finger than the lateral extensor tendon of the opposite side whose oblique lamina was intact. In this case report, the lesion of the ulnar oblique retinacular ligament caused the dorsal migration of the lateral band with narrowing of the Winslow’s rhombus, like described by Zancolli. The synergic action between extensor and flexor tendons was interrupted. The shorter direction of the ulnar lateral band added force to the central slip resulting in the hyperextension of the PIP joint. The acute SND was certainly aggravated by the patient's general laxity that did not oppose to the hyperextending forces over the PIP joint, where the capsule and the volar plate usually contrast these forces. The early surgical treatment confirmed the suspected lesion of the ulnar ORL to be the pathophysiological mechanism of this case of SND. The simple suture of the ulnar ORL to the ulnar lateral band restored the physiological kinematics, whereas the general laxity couldn’t justify alone the mechanism, and in particular the impossibility to actively flex the PIPJ by the patient. This case shows that a single lesion of the oblique retinacular ligament must be
taken into account in a picture of the SND lesion, especially when there is no history of PIPJ dislocation and no lesion of the terminal extensor apparatus on DIPJ.
REFERENCES 1. Zancolli E. Structural and dynamic bases of hand surgery. 2th ed. Philadelphia: JB Lippincott Company; 1979:1-81. 2. Sebastin SJ, Chung KC. Reconstruction of digital deformities in rheumatoid arthritis. Hand Clinic. 2011;27(1):87104. 3. De Salamanca EF. Swan-neck deformity: mechanism and surgical treatment. Hand. 1976;8(3):215-21. 4. Merrell G, Slade JF. Dislocations and ligament injuries in the digits. In: Wolfe SW, Hotchkiss RN, Pederson WC, Kozin SH editors. Green’s Operative Hand Surgery. Philadelphia. Elsevier Churchill Livingstone; 2011:291-32. 5. Portis RB. Hyperextensibility of the proximal interphalangeal joint of the finger following trauma. J Bone Joint Surg Am. 1954;36(6):1141-6. 6. Roemer, FJ. Hyperextension injuries to the finger joints. Am J Surg. 1950;80(3):295-302 7. El-Gammal TA, Steyers CM, Blair WF, Maynard JA. Anatomy of the oblique retinacular ligament of the index finger. J Hand Surg Am. 1993;18(4):717-21. 8. Shrewsbury MM, Johnson RK. A systematic study of the oblique retinacular ligament of the human finger. Its structure and function. J Hand Surg Am. 1977;2(3):194-9. 9. Landsmeer JM. A report on the coordination of the interphalangeal joints of the human finger and its disturbances. Acta Morphol Neerl Scand. 1959;2(1):59-84. 10. Littler JW. Restoration of the oblique retinacular ligament for correcting hyperextension deformity of the proximal interphalangeal joint. In: R.Tubiana editor. La Main Rhumatoide. Paris: Expansion Scientifique Francaise; 1966:39-42.
