CRANIAL CRUCIATE LIGAMENT INJURY
PRESENTATION & HISTORY A six-year-old male Staffordshire Bull Terrier weighing 23 kg was presented with intermittent left hind limb lameness of four weeks duration, non-responsive to NSAIDs.
CLINICAL EXAMINATION & INVESTIGATIONThe dog was in good general condition and slightly over-weight. Intermittent non-weight- bearing lameness on the left hind limb was noted. The toe rested on the ground when standing. When put in sitting posture the left limb was extended and slightly abducted. There was swelling at the left stifle and thickening of the medial collateral ligament. A cranial drawer sign and cranial tibial thrust could be demonstrated. Pain could be elicited on joint manipulation but was not the hallmark of the examination. The dog was sedated with butorphenole and metomidine. Examination under sedation supported a diagnosis of cranial cruciate ligament rupture and radiographs of both limbs were taken.
DIFFERENTIAL DIAGNOSISPatellar luxationHip dysplasiaOsteomyelitisSeptic arthritisFracturesOther soft tissue injury
PRE-OPERATIVE MANAGEMENT Routine haematology and serum chemistry were unremarkable. The dog was pre-medicated with morphine and ACP, and anaesthesia was induced and maintained routinely. Analgesia, intravenous fluids and antibiotic treatment were given and the patient prepared for surgery. The dog was transferred to sterile theatre and placed in a dorsal recumbent position, tilted to the right so that the lateral aspect of the left hind limb was uppermost.
SURGICAL PROCEDURE The surgical approach to the stifle was through a lateral incision (Piermattei, 1993). Using a stifle distractor, the joint was examined to investigate the damaged ligament and possible meniscal injury. The menisci were found to be intact. The medial meniscus was manipulated gently and slightly, to ensure that no lesion was missed (Bennett & May, 1991). Fibres from the damaged cranial cruciate ligament were removed using sharp scissors and a No.11 scalpel blade. The joint was irrigated and the joint capsule closed with 2/0 polydioxanone (PDS™ II, Ethicon) in a simple interrupted suture pattern. The biceps femoris muscle was retracted caudally to expose the lateral fabella. The tibialis cranialis muscle was periostally elevated from its attachment to expose the tibial tuberosity and facilitate drilling at its proximal end. A crimp system (Veterinary Instrumentation) was used to stabilize the joint laterally, running from the fabella through a hole made in the proximal tibial tuberosity. With the joint in a semi-flexed position, the nylon was tightened and the crimp crimped at the distal end. The joint was manipulated for stability before closure. The incision at the proximal tibialis cranialis muscle was sutured over the metal crimp to fibrous connective tissue at the tibial crest. The lateral facia of the stifle and facia-lata were sutured with 2/0 polydioxanone (PDS™ II, Ethicon) in a simple continuous pattern. The subcutaneous tissue was sutured with 3/0 polydioxanone (PDS™ II, Ethicon) in a simple continuous pattern and the skin was closed with 3/0 polyamide (Ethilon®, Ethicon) in a simple interrupted pattern.
POSTOPERATIVE CARE The limb was dressed with a four-layer pressure bandage to prevent swelling. The dressing was removed after two day at the first post-operative examination (Clark et al, 2001). Intravenous fluid therapy was discontinued after approximately five hours. The dog was discharged the same day. Complete rest was advised for 10 days followed by gradual re-introduction to exercise.
POST-OPERATIVE OUTCOME/COMPLICATIONS Barely perceptible (Grade I, Appendix B5) left hind limb lameness could be detected four weeks post-operative with no apparent pain on manipulation. The owner reported occasional lameness after long exercise only.
FOLLOW-UP A 6-week post-operative examination revealed normal gait and no pain on manipulation. The joint was stable and no resentment to flexion or extension was noted. Gradual return to uncontrolled exercise was allowed. Good sitting posture was noted, although the owner reported occasional limb extension when sitting.
DISCUSSION Cranial cruciate ligament (CrCL) injury is one of the most common causes of hind limb lameness in dogs (Arnockzy, 1980), leading to stifle instability, pain, and chronic lameness. Degenerative joint disease (DJD) is the usual outcome and is characterised by osteophytosis and articular erosions (Brinker et al., 1997). Miniscal damage is a common secondary finding (Flo, 1993). Numerous surgical techniques have been described to stabilise the CrCL-deficient stifle; however, no technique has been shown to consistently arrest the development or progression of DJD (Moor & Read, 1995). Objectives of surgery are to provide normal joint mechanics and stability, relief of pain, prevention of secondary meniscal tears and prevention of further DJD (Kirby, 1993).
Surgical treatment is broadly separated into three groups: intracapsular, extracapsular, and tibial osteotomy techniques (Slocum & Devina, 1984, 1993). Tibial osteotomy techniques do not provide stability of the stifle but rather alter the geometry of the joint to eliminate cranial tibial thrust, such that functional joint stability is achieved during weight bearing. Visualisation of both menisci is a critical aspect of CrCL surgery, irrespective of technique. Regardless of the surgical technique employed, approximately 85% of dogs show clinical improvement. However, many of these dogs will demonstrate intermittent pain or lameness. Post-operative management is an integral part of the treatment of CrCL rupture, and significant benefits in limb function occur when post-operative physiotherapy is performed.
In many dogs rupture appears to be secondary to a chronic degenerative process that weakens the ligament and causes premature failure. There is evidence to suggest that immunologic mechanisms may play a role in the pathogenesis of CrCL rupture, especially partial rupture. Further investigation is required to determine whether these immune or inflammatory responses in the CrCL synovial membrane are the primary factor in ligament rupture or if they develop secondary to ligament rupture and instability caused by trauma.
CLINICAL EXAMINATION & INVESTIGATIONThe dog was in good general condition and slightly over-weight. Intermittent non-weight- bearing lameness on the left hind limb was noted. The toe rested on the ground when standing. When put in sitting posture the left limb was extended and slightly abducted. There was swelling at the left stifle and thickening of the medial collateral ligament. A cranial drawer sign and cranial tibial thrust could be demonstrated. Pain could be elicited on joint manipulation but was not the hallmark of the examination. The dog was sedated with butorphenole and metomidine. Examination under sedation supported a diagnosis of cranial cruciate ligament rupture and radiographs of both limbs were taken.
DIFFERENTIAL DIAGNOSISPatellar luxationHip dysplasiaOsteomyelitisSeptic arthritisFracturesOther soft tissue injury
PRE-OPERATIVE MANAGEMENT Routine haematology and serum chemistry were unremarkable. The dog was pre-medicated with morphine and ACP, and anaesthesia was induced and maintained routinely. Analgesia, intravenous fluids and antibiotic treatment were given and the patient prepared for surgery. The dog was transferred to sterile theatre and placed in a dorsal recumbent position, tilted to the right so that the lateral aspect of the left hind limb was uppermost.
SURGICAL PROCEDURE The surgical approach to the stifle was through a lateral incision (Piermattei, 1993). Using a stifle distractor, the joint was examined to investigate the damaged ligament and possible meniscal injury. The menisci were found to be intact. The medial meniscus was manipulated gently and slightly, to ensure that no lesion was missed (Bennett & May, 1991). Fibres from the damaged cranial cruciate ligament were removed using sharp scissors and a No.11 scalpel blade. The joint was irrigated and the joint capsule closed with 2/0 polydioxanone (PDS™ II, Ethicon) in a simple interrupted suture pattern. The biceps femoris muscle was retracted caudally to expose the lateral fabella. The tibialis cranialis muscle was periostally elevated from its attachment to expose the tibial tuberosity and facilitate drilling at its proximal end. A crimp system (Veterinary Instrumentation) was used to stabilize the joint laterally, running from the fabella through a hole made in the proximal tibial tuberosity. With the joint in a semi-flexed position, the nylon was tightened and the crimp crimped at the distal end. The joint was manipulated for stability before closure. The incision at the proximal tibialis cranialis muscle was sutured over the metal crimp to fibrous connective tissue at the tibial crest. The lateral facia of the stifle and facia-lata were sutured with 2/0 polydioxanone (PDS™ II, Ethicon) in a simple continuous pattern. The subcutaneous tissue was sutured with 3/0 polydioxanone (PDS™ II, Ethicon) in a simple continuous pattern and the skin was closed with 3/0 polyamide (Ethilon®, Ethicon) in a simple interrupted pattern.
POSTOPERATIVE CARE The limb was dressed with a four-layer pressure bandage to prevent swelling. The dressing was removed after two day at the first post-operative examination (Clark et al, 2001). Intravenous fluid therapy was discontinued after approximately five hours. The dog was discharged the same day. Complete rest was advised for 10 days followed by gradual re-introduction to exercise.
POST-OPERATIVE OUTCOME/COMPLICATIONS Barely perceptible (Grade I, Appendix B5) left hind limb lameness could be detected four weeks post-operative with no apparent pain on manipulation. The owner reported occasional lameness after long exercise only.
FOLLOW-UP A 6-week post-operative examination revealed normal gait and no pain on manipulation. The joint was stable and no resentment to flexion or extension was noted. Gradual return to uncontrolled exercise was allowed. Good sitting posture was noted, although the owner reported occasional limb extension when sitting.
DISCUSSION Cranial cruciate ligament (CrCL) injury is one of the most common causes of hind limb lameness in dogs (Arnockzy, 1980), leading to stifle instability, pain, and chronic lameness. Degenerative joint disease (DJD) is the usual outcome and is characterised by osteophytosis and articular erosions (Brinker et al., 1997). Miniscal damage is a common secondary finding (Flo, 1993). Numerous surgical techniques have been described to stabilise the CrCL-deficient stifle; however, no technique has been shown to consistently arrest the development or progression of DJD (Moor & Read, 1995). Objectives of surgery are to provide normal joint mechanics and stability, relief of pain, prevention of secondary meniscal tears and prevention of further DJD (Kirby, 1993).
Surgical treatment is broadly separated into three groups: intracapsular, extracapsular, and tibial osteotomy techniques (Slocum & Devina, 1984, 1993). Tibial osteotomy techniques do not provide stability of the stifle but rather alter the geometry of the joint to eliminate cranial tibial thrust, such that functional joint stability is achieved during weight bearing. Visualisation of both menisci is a critical aspect of CrCL surgery, irrespective of technique. Regardless of the surgical technique employed, approximately 85% of dogs show clinical improvement. However, many of these dogs will demonstrate intermittent pain or lameness. Post-operative management is an integral part of the treatment of CrCL rupture, and significant benefits in limb function occur when post-operative physiotherapy is performed.
In many dogs rupture appears to be secondary to a chronic degenerative process that weakens the ligament and causes premature failure. There is evidence to suggest that immunologic mechanisms may play a role in the pathogenesis of CrCL rupture, especially partial rupture. Further investigation is required to determine whether these immune or inflammatory responses in the CrCL synovial membrane are the primary factor in ligament rupture or if they develop secondary to ligament rupture and instability caused by trauma.
Source...