0195-5616/98 $8.00 + .00
OSTEOCHONDROSIS
OSTEOCHONDRITIS DISSECANS OF THE HUMERAL HEAD Spencer A. Johnston, VMD
Osteochondritis dissecans (OCD) of the humeral head is frequently identified as a cause of forelimb lameness in the dog. Surgical removal of the cartilage flap remains the preferred method of treatment in dogs demonstrating clinical signs of lameness and pain. This article will review the pertinent literature regarding humeral head OCD, present diagnostic and therapeutic options, and discuss surgical treatment of this condition. Etiology, pathophysiology, and radiographic diagnosis of osteochondrosis (OC) and OCD are discussed in detail in other articles in this issue. PATHOPHYSIOLOGY, PAIN, AND HEALING
OC is an abnormality of endochondral ossification in which the cartilage of the epiphysis fails to form subchondral bone. This results in thickened, abnormal cartilage which is susceptible to injury. 20 The site most commonly affected in the canine shoulder joint is the caudalcentral or caudal-central-medial region of the humeral head. The reason this area of the humeral head is predisposed to OC is not fully understood but may be related to an increased cartilage thickness in this region in the normal dog. 14• 43 It is believed that trauma (physiologic or supraphysiologic) from contact between the abnormal cartilage of the humeral head and the glenoid cavity of the scapula predisposes to vertical fracture of articular cartilage and formation of the cartilage flap characteristic of an OCD lesion. 14• 15• 3 3, 4 3 From the Department of Small Animal Clinical Sciences, Virginia-Maryland Regional College of Veterinary Medicine, Virginia Tech, Blacksburg, Virginia
VETERINARY CLINICS OF NORTH AMERICA: SMALL ANIMAL PRACTICE VOLUME 28 • NUMBER 1 • JANUARY 1998
33
34
JOHNSTON
It has been stated that pain associated with humeral head OCD results from synovial fluid contacting subchondral bone,37, 45 because dogs are rarely lame or show pain when thickened cartilage is present without a cartilage flap (OC) but show pain and lameness once vertical fracture of the articular cartilage occurs (OCD), 40 The origin of pain associated with joint disease is a complex subject, however. Joints are richly innervated, with nociceptors (pain receptors) present in the synovium, joint capsule, tendons, ligaments, periosteum, and subchondral bone, 3 Sensitization of nociceptors, which causes a decrease in nociceptive threshold, results from the action of biochemical mediators such as cytokines and prostaglandins which are present in diseased joints. Nociceptor stimulation occurs due to chemical stimulation by inflammatory mediators like bradykinin or from mechanical stimulation by movement or direct pressure. Chemical stimulation of nociceptors also augments the responsiveness of mechanoreceptors to mechanical stimuli. Because free nerve endings are present in subchondral bone, 22' 46 it is possible that pain associated with OCD is due to exposure of subchondral bone to inflammatory mediators present in the synovial fluid of the affected joint An alternative theory is that synovitis, which accompanies OCD,41 , 42 may not be severe enough to cause clinical signs of pain and lameness until cartilage fracture occurs. Cartilage fracture and exposure of subchondral bone may result in the release of microscopic cartilage fragments, and free cartilage fragments are known to cause synovitis. 21 If synovitis is present, pain may be due to either chemical or mechanical stimulation of nociceptors throughout all the tissues of the joint. Another potential source of pain is stimulation of nociceptors in subchondral bone due to motion between the cartilage flap and subchondral bone, or to altered mechanical loading and altered transmission of pressure to subchondral bone or other periarticular tissues. When a cartilage flap dislodges or is surgically removed, there is complete exposure of the subchondral bone to synovial fluid, yet pain and lameness rapidly abate. This suggests that motion between the cartilage flap and subchondral bone, or altered mechanical loading and altered transmission of pressure to subchondral bone or other periarticular tissues, has an important role in pain production. It is also possible that joint lavage associated with arthrotomy or arthroscopy and removal of the cartilage flap decrease the amount of cartilage debris and inflammatory mediators present in the joint, thereby decreasing synovitis. Joint lavage has been demonstrated to decrease pain in osteoarthritic joints when used as an isolated treatment. 6' 12, 16 Healing of osteochondral defects occurs by the production of fibrocartilage.2 Methods to stimulate fibrocartilage production include fullthickness curettage (removal of calcified cartilage and eburnated subchondral bone) and forage (the drilling of multiple, small holes in subchondral bone). The purpose of both techniques is to disrupt subchondral blood vessels and cause bleeding, which leads to fibrin clot formation over the exposed subchondral surface. Undifferentiated mesenchymal cells from the bone marrow enter the fibrin clot, differentiate
OSTEOCHONDRITIS DISSECANS OF THE HUMERAL HEAD
35
into chondroblasts and chondrocytes, and are responsible for forming fibrocartilage. 2 ' 35 Nevertheless, experimental evidence suggests that fullthickness curettage and removal of subchondral bone result in biomechanical changes and decreased quality of reparative tissue; 17 therefore, this procedure is not recommended. An alternative to full-thickness curettage is superficial intracortical debridement (abrasion arthroplasty). This technique involves abrasion of the subchondral surface just deep enough-usually 1 to 3 mm-to cause subchondral bleeding without disruption of the subchondral bone plate. There are conflicting results regarding the benefit of this technique in human beings with osteoarthritic joints. 2 Although no studies have been performed comparing the benefits of abrasion arthroplasty or curettage to those of forage for the treatment of OCD lesions in dogs, studies in rabbits suggest that forage provides better long-term results than abrasion arthroplasty, perhaps due to an anchoring effect of the reparative tissue in the multiple, small drill holes. 19 Irrespective of the method used, the fibrocartilage formed does not duplicate the composition, structure, or mechanical properties of normal articular cartilage. 2' 17 Furthermore, a relationship between the extent and type of repair tissue present and long-term results with respect to pain or lameness has not been established in animals or humans. 2 Other methods for resurfacing osteochondral defects are currently being explored. Options include the use of soft tissue grafts such as periosteum or perichondrium, cell transplantation using chondrocytes or undifferentiated mesenchymal cells, the use of growth factors to stimulate cartilage repair, and the use of biologically derived or artificial matrices to deliver growth factors and stabilize cells in the defect_Z, 17 Transplantation of articular cartilage using either autologous grafts or allografts is also being studied. 2' 17 Although the results using these techniques are variable and the procedures are experimental, they offer promise that surgical intervention may some day result in restoration of a normal articular surface. Use of continuous passive motion has been demonstrated to stimulate pluripotential mesenchymal cells to differentiate into hyaline-like articular cartilage, prevent the formation of adhesions, and increase the final range of motion of the joint. 31 , 32 Unfortunately, reparative cartilage formed by this or any other current treatment method does not persist and tends to deteriorate once weight bearing is resumed. 11 ' 17 Although the use of continuous passive motion is impractical in the dog, this work suggests that use of the limb without transmission of large loads across the joint (manual passive motion, swimming) may be beneficial following surgical treatment of OCD. INCIDENCE AND SIGNALMENT
The incidence of humeral head OCD in dogs has been reported as 0.22% for male dogs and 0.09% for female dogs presenting to veterinary
36
JOHNSTON
teaching hospitals in the United States.29 The largest study29 reports a male:female ratio of 2.24:1, and smaller studies report ratios ranging from 2:1 to 6:1.1, 13, 24, 27, 29, 36, 44 Humeral head OCD most frequently occurs in large- and giant-breed dogs, although some large-breed dogs, including the Doberman Pinscher, Collie, and Siberian Husky, are at low risk for this condition. 29 OCD of the humeral head has been reported in the cat-25 Onset of lameness associated with humeral head OCD generally occurs when an animal is from 4 to 8 months of age. The median age of onset identified from review of four studies that specifically listed the age of lameness onset ranged between 5 and 6 months. 4 ' 13, 24, 44 The median age recorded in other studies that reported age at presentation for surgery ranged from 7.0 to 9.5 months. 4' 5, 13, 24, 36, 42, 44 The reason for the difference in age between these two sets of studies could be due to owner delay in presenting the patient to a veterinarian for diagnostic evaluation of lameness or might relate to the recommendation given by many veterinarians that conservative management be attempted first in young dogs before proceeding to surgical intervention. Both of these factors are likely to be involved. It should also be noted that review of studies evaluating dogs with humeral head OCD indicates that approximately 17% of patients are 12 months old or older at the time of diagnosis or surgery.4, 5, 13, 24, 29, 36, 42,44 CLINICAL SIGNS
Affected dogs present with a weight-bearing lameness of varying severity. Lameness tends to worsen following exercise and frequently improves after a period of rest. A shortened forelimb stride may be noted due to reluctance to flex and extend the shoulder joint. A head bob may be seen, where the head is raised during weight bearing on the affected limb and lowered during weight bearing on the contralateral forelimb. If both forelimbs are affected equally, a head bob may not be seen; however, the stride will be shortened bilaterally, and the patient may be reluctant to stand or move. Physical examination will frequently reveal pain on extension and flexion of the shoulder joint. Most normal dogs tolerate full flexion and extension of the shoulder joint; however, dogs with humeral head OCD typically resist these manipulations, withdraw the limb, and may vocalize when the shoulder joint is flexed or extended. Manipulation of the shoulder joint may exacerbate the lameness. Mild atrophy of the supraspinatus, infraspinatus, and deltoideus muscles may be present and can be recognized because of prominence of the spine of the scapula. Joint swelling or effusion is difficult to appreciate because of the overlying musculature. Direct pressure over the tendon of the biceps brachii muscle may result in mild discomfort due to synovitis extending into the bicipital tendon sheath. Other developmental abnormalities of the canine forelimb such as elbow dysplasia (fragmented medial coronoid
OSTEOCHONDRITIS DISSECANS OF THE HUMERAL HEAD
37
process, ununited anconeal process, OCD of the medial humeral condyle) and panosteitis should be ruled out. DIAGNOSIS
Diagnosis is based on signalment, history, and the results of physical and radiographic examination. The mediolateral radiographic projection is the most useful view for making a diagnosis (Figs. 1, 2, 3, 4). The caudocranial view is useful when attempting to determine the location of a detached cartilage flap (joint mouse) (Figs. 3 and 4) but is rarely used to establish the initial diagnosis. Sedation greatly facilitates radiographic positioning. Even well-behaved dogs will resist restraint and will move when experiencing pain, and full extension of the forelimb-a pain-inducing manipulation for dogs with humeral head OCD-is necessary to provide diagnostic radiographs. The dog is positioned in lateral recumbency with the affected limb down, and the head and neck are extended. Traction is placed on the affected limb so that the shoulder is pulled cranially and ventrally to avoid superimposition on the thorax and neck. The opposite limb is retracted caudally to avoid superimposition of that shoulder on the
Figure 1. Mediolateral radiographic projection of the shoulder joint of a 9-month-old Mixedbreed dog. Note the flattening of the caudal portion of the humeral head and associated radiolucent defect of the subchondral bone (arrows). These findings are consistent with osteochondritis dissecans of the humeral head.
38
jOHNSTON
Figure 2. Mediolateral radiographic projection of the shoulder joint of a 7-month old Irish setter with osteochondritis dissecans of the humeral head. The caudal border of the humeral head is irregular, and there is reduced radiodensity of the subchondral bone. A mineralized cartilage flap (arrows) is associated with the lesion.
shoulder of interest. Routine radiographic examination of the opposite shoulder is recommended, because humeral head OC often occurs bilaterally. The diagnosis of OC or OCD is confirmed by the presence of a radiolucent area on the caudal aspect of the humeral head (see Fig. 1). This radiolucent area corresponds to the region of the endochondral defect, where there is failure of cartilage to form normal bone. If the lesion is mild, slightly oblique views may accentuate the subtle defects. The cartilage flap of an OCD lesion is mineralized in approximately 26% of affected joints,:w allowing it to be seen on plain radiographs (see Fig. 2). Unmineralized attached or detached flaps are not visible on plain radiographs. Radiographic changes consistent with osteoarthritis (see Fig. 3) such as osteophyte production, increased subchondral bone density, and glenoid cavity or humeral head remodeling are noted infrequently in young dogs (< 1 year) but may be present in older dogs. Occasionally, mineralized joint mice are identified in the bicipital tendon sheath (see Figs. 3 and 4). These dogs are typically lame and painful; they respond dramatically to surgical removal of the joint mice. Arthrography is valuable for detecting joint mice within the bicipital tendon sheath (see Fig. 4) and caudal joint pouch and for identifying cartilage status (presence of a cartilage flap or thickened cartilage with-
OSTEOCHONDRITIS DISSECANS OF THE HUMERAL HEAD
39
Figure 3. Mediolateral radiographic projection (A) of the shoulder joint of a 3-year-old Golden retriever. Multiple radiodense ossicles are present in the bicipital tendon sheath (straight arrow) and the caudal joint pouch (small curved arrow). An osteophyte is present on the caudal margin of the glenoid (curved open arrow) and the caudal aspect of the humeral head (large curved arrow). Caudocranial radiographic projection (B) of the shoulder joint demonstrates that there are multiple radiodensities (arrows) located on the medial aspect of the proximal humerus. These radiodensities represent ossicles present in the bicipital tendon sheath.
out a dissecting flap); it also allows for the evaluation of joint effusion. 40· 41 Joint mice were identified in the bicipital tendon sheath in approximately 10% (8 of 76) of canine shoulders in which both arthrography and arthrotomy were performed.39 In only 12% (1 of 8) of canine joints with joint mice present in the bicipital tendon sheath were the joint mice identified on plain radiography. This study did not report the clinical signs of dogs with joint mice in the bicipital tendon sheath, and it did not include any dogs with joint mice in the bicipital tendon sheath that did not have surgical treatment. Therefore, the consequence of failure to remove nonmineralized joint mice in this location is unknown. Nevertheless, it is likely that dogs with undiagnosed and unremoved bicipital tendon sheath joint mice have a less than optimal response to treatment even if arthrotomy, including removal of the remaining cartilage flap and forage of the subchondral bone bed, is performed. UNILATERAL AND BILATERAL LESIONS
Humeral head OC or OCD may occur either unilaterally or bilaterally. Although affected dogs typically present with a unilateral lameness,
40
jOHNSTON
Figure 4. Mediolateral radiographic projection (A) and caudocranial (B) radiographs of the left shoulder joint of a 2-year-old Labrador retriever. Mild irregularities in density to the subchondral bone of the humeral head are evident and a small calcific density is noted adjacent to the area of irregular density in the humeral head (open arrow). In addition, a bony density is present on the medial aspect of the proximal humerus in a location that would be compatible with an ossicle in the bicipital tendon sheath. An arthrogram (C) was performed by injecting positive contrast agent into the shoulder joint. This contrast agent demonstrates the ossicle noted on the plain radiographs to be located in bicipital tendon sheath (arrows). (From Carrig CB: Diagnostic imaging of osteoarthritis. Vet Clin North Am Small Anim Pract 27:777, 1997; with permission.)
OSTEOCHONDRITIS DISSECANS OF THE HUMERAL HEAD
41
radiographic evaluation frequently demonstrates bilateral lesions. Bilateral radiographic lesions have been reported to occur in 20% to 85% of cases, but review of reported studies indicates that 50% of dogs presenting with humeral head OCD have radiographically detectable lesions bilaterally. 4• 5 • 8• 13• 24• 27• 29• 36• 42 Despite the radiographic appearance of bilateral lesions, most dogs demonstrated lameness in only one leg, with only 21% of dogs with bilateral radiographic lesions exhibiting clinical signs in both forelimbs. 4, 13, 27, 3o, 36, 4o, 42 The outcome of patients with radiographically identifiable lesions in the humeral head but no clinical signs has been examined. The most extensive work in this area has been done by van Bree. 40 In this study, bilateral shoulder arthrography was performed on 40 dogs with radiographically identified bilateral humeral head OCD lesions. A loose cartilage flap was identified in 37 dogs and a detached cartilage flap (joint mouse) was identified in 3 dogs. All of these patients had clinical signs of pain and lameness in the affected limb. Thirty-five of 40 dogs had a radiographic lesion in the contralateral limb that was not associated with clinical signs of pain or lameness. Further evaluation of the radiographic change in the contralateral joint of these 35 dogs revealed that 18 joints had evidence of thickened cartilage without a loose cartilage flap, 12 had a loose cartilage flap, and 5 had a detached cartilage flap (joint mouse). Further surgical treatment was required within 2 to 4 months in 6 of the 12 joints with a loose cartilage flap. No further surgical treatment of the contralateral joint was necessary in any other dog during a follow-up period of 1 to 7 years. This work suggests that signs of pain and lameness are associated with a loose cartilage flap or a detached cartilage flap. If a cartilage flap is present without the dog showing signs of pain and lameness, there is a 50% probability that surgical intervention will eventually be required. If a joint mouse is present and the patient is demonstrating clinical signs, surgical removal of the joint mouse will likely resolve the lameness. If a joint mouse is present in the caudal joint pouch and the patient does not exhibit clinical signs of pain and lameness, these signs are unlikely to develop later. SURGICAL AND CONSERVATIVE MANAGEMENT
Dogs demonstrating clinical signs associated with humeral head OCD will recover more rapidly with surgical treatment than dogs treated conservatively. 1• 8 The recovery period following surgery is approximately 1 to 2 months, with many dogs having clinically normal ambulation by the fourth postoperative week or sooner. The recovery period (assuming lameness resolves) following conservative treatment is approximately 7 months. 1• 8 Recovery following surgery is usually complete, with 75% (30 of 40) of patients showing no lameness, 22.5% (9 of 40) showing minimal lameness, and 2.5% (1 of 40) having consistent lameness at a mean interval of 3 years following surgery. 29 These studies support the recommendation for surgical treatment
42
JOHNSTON
in dogs presenting with clinical signs of pain and lameness and demonstrating radiographic changes consistent with OCD. The presence of clinical signs suggests that a vertical fracture of the articular cartilage has occurred. Once a cartilage flap is present, it is unlikely to reattach. The only way that clinical signs resolve (other than with surgical treatment) is if the flap dislodges. This has led Olsson23 to recommend that dogs with clinical signs of OCD be exercised vigorously so that the cartilage flap will be dislodged. Although detachment of a cartilage flap may lead to relief of clinical signs, cartilage fragments can migrate to the biceps tendon sheath, or they may accelerate or perpetuate the production of inflammatory mediators and degradative enzymes associated with osteoarthritis. This can result in continued or future lameness. One study that included eight joints with detached cartilage flaps revealed that three joints in which the joint mouse was not lodged in the caudal pouch required surgical removal of a detached flap to relieve pain and lameness, although five joints in which joint mice were in the caudal joint pouch had an excellent outcome without surgical intervention.40 Treatment of dogs with bilateral lesions is typically based on clinical signs. Although dogs demonstrating mild clinical signs in the contralateral limb can have a satisfactory outcome if treated conservatively, it is the author's recommendation that all dogs demonstrating clinical signs in an affected limb undergo surgery. Thus, if a dog has muscle atrophy, altered gait, or pain on extension or flexion (or both) of both shoulder joints and radiographic signs are consistent with OCD, surgical treatment is recommended for both shoulders. If a question exists regarding the severity of clinical signs or the significance of a radiographic lesion, arthrography is recommended. When clinical signs and radiographic lesions are present bilaterally, the author recommends operating on both sides concurrently. All dogs undergoing arthrotomy, especially those having concurrent bilateral arthrotomy, require appropriate analgesia in the immediate postoperative period. This includes narcotics in the form of opioid agonists such as morphine (0.5-1.0 mg/kg administered intramuscularly or subcutaneously every 2-6 hours) or oxymorphone (0.05-0.2 mg/kg administered intramuscularly or subcutaneously every 2-6 hours) or agonist/ antagonists such as butorphenol (0.2-1.0 mg/kg administered intravenously, intramuscularly or subcutaneously every 1-2 hours) or buprenorphine (0.005-0.02 mg/kg administered intramuscularly or intravenously every 4-8 hours). 9 Addition of an anxiolytic agent such as acepromazine (0.020.05 mg/kg administered once intravenously, subcutaneously, or intramuscularly) will frequently help to smooth recovery in these patients. Analgesics may be administered either pre- or postoperatively but definitely prior to recovery in order to provide the greatest analgesic effect. Following recovery from anesthesia, administration of a nonsteroidal anti-inflammatory drug such as carprofen (2.2 mg/kg administered orally every 12 hours) or a nonsteroidal anti-inflammatory drug/narcotic combination such as acetaminophen (300 mg) and codeine (60 mg) given
OSTEOCHONDRITIS DISSECANS OF THE HUMERAL HEAD
43
orally at the dosage of 1 to 2 mg/kg (based on the codeine portion) every 8 hours will help provide analgesia and facilitate ambulation when administered for 3 to 5 days following surgery. An alternative method of providing analgesia is the use of fentanyl transdermal patches, with a 50-jJ-g/h patch applied to dogs weighing 10 to 20 kg, a 75-iJ-g/h patch to dogs weighing 20 to 30 kg, and a 100-1-1g/h patch to dogs more than 30 kg. 9 These patches are applied 12 to 24 hours prior to surgery so that adequate plasma concentrations of fentanyl are reached preoperatively and are effective for 3 days. Fentanyl transdermal patches provide the advantage of analgesia during recovery from anesthesia which extends into the postoperative period, although additional analgesia may be required in the immediate postoperative period. Regardless of the method of analgesia used, it is important to recognize that analgesia should not be withheld as a means of restricting activity postoperatively. Postoperative recovery, whether surgery is performed unilaterally or bilaterally, is usually rapid, with good ambulation returning within 1 to 2 weeks and normal or near normal ambulation returning within 1 to 2 months. SURGICAL APPROACH
The osteochondral defect is most frequently located in the caudalcentral or caudal-central-medial region of the humeral head. Because the standard surgical approaches are all performed, to varying degrees, from the lateral side, manipulation of the limb (extension, flexion, internal and external rotation) during the procedure is necessary. Preparation and draping of the entire limb is recommended to facilitate this manipulation. Manipulation of the limb and application of countertraction by a surgical assistant, when appropriate, will increase the ease with which the procedure can be completed. The three standard approaches to the canine shoulder are the cranialateral approach, the caudolateral approach (with variations on manipulation of the teres minor muscle and tendon), and the caudal approach. All allow adequate exposure of the caudal humeral head by an experienced surgeon. Complete descriptions of these approaches are found in surgical texts. 26• 28 The craniolateral approach has two variations: tenotomy of the infraspinatus muscle or acromion osteotomy and tenotomy of the infraspinatus muscle. Acromion osteotomy is not recommended due to postoperative morbidity. The caudolateral approach has multiple variations, including cranial retraction of the teres minor muscle, separation between the teres minor and infraspinatus muscles with caudal retraction of the teres minor muscle, and tenotomy of the teres minor and cranial retraction of the infraspinatus muscle. The caudal approach involves separation between the scapular head of the deltoideus muscle and the lateral head of the triceps muscle. Knowledge of regional anatomy will aid in making the skin incision
44
JOHNSTON
in the appropriate location for any of these approaches. An appropriately placed skin incision will decrease the amount of undermining of skin and subcutaneous tissue necessary to gain adequate exposure, thereby decreasing the chance of postoperative seroma formation. Self-retaining retractors such as Gelpi perineal retractors will aid in providing adequate exposure. Because the exposure using the caudolateral and caudal techniques is limited, the surgeon will frequently be working in a restricted space. Adequate lighting (overhead lighting that can be focused or use of a surgical headlamp) is a valuable aid to allow adequate visualization of tissues. Because exposure to the caudal-central region of the humeral head is the limiting factor with the surgical approach, studies have been performed comparing exposures attained with the craniolateral and caudolateral approaches as well as with two variations of the caudolateral approach. The craniolateral approach offers significantly greater exposure of the articular surface of the humeral head as compared with the caudolateral approach with cranial retraction of the teres minor muscle. 18 This may be advantageous if an assistant surgeon is not available. Postoperative force plate analysis on days 21 and 28, however, revealed that dogs undergoing the craniolateral approach had a peak vertical force (a measure of weight bearing) that was significantly less than that demonstrated by dogs operated on using the caudolateral approach. 18 A decreased range of motion was also noted on postoperative day 35 in dogs operated on using the craniolateral approach when compared with dogs operated on using the caudolateral approach. 18 A further consideration when choosing the craniolateral approach is that access to the caudal joint pouch for removal of joint mice may be limited. 26 Evaluation of two variations of the caudolateral approach determined that exposure to the articular surface of the humeral head was greatest with cranial retraction of the teres minor muscle as compared with caudal retraction of the teres minor muscle and cranial retraction of the infraspinatus muscle. 27 Although exposure using the caudolateral approach is less than that with the craniolateral approach, the region of the humeral head exposed is the area most frequently affected by an OCD lesion. Extension of the shoulder and internal rotation of the humerus are necessary to visualize and provide access to the OCD lesion when using a caudolateral approach. In the author's opinion, if an assistant is present, the caudolateral approach with cranial retraction of the teres minor muscle is the preferred approach as compared to the craniolateral approach or the caudolateral approach with caudal retraction or tenotomy of the teres minor muscle. This approach provides satisfactory exposure while creating minimal trauma and postoperative morbidity. A direct comparison between the craniolateral or caudolateral approach and the caudal approach has not been made. An advantage of the caudal approach is that it provides greater access to the medial portion of the joint cavity. The presence of a joint mouse in this area would be an indication for the caudal approach. In both studies per-
OSTEOCHONDRITIS DISSECANS OF THE HUMERAL HEAD
45
formed to evaluate the caudal approach, the authors commented that it was necessary to have an assistant manipulate the limb while the surgeon performed curettage of the OCD lesion on the humeral head?· 38 Creating complete luxation of the humeral head has been described to give maximal exposure of this structure. 10 Although superior access to the humeral head is provided using this technique, the lesion location with OCD of the humeral head is so specific that access to the entire humeral head is usually not necessary. Even though this technique seems to be excessively traumatic, the recovery time reported following this procedure was similar to that reported for the other surgical approaches.10 If a joint mouse or joint mice are identified within the bicipital tendon sheath, surgical removal is indicated to alleviate pain and lameness. This is performed through a craniomedial approach to the shoulder.26 Although this approach can be completed through the skin incision for the caudolateral approach if the skin is undermined, the extensive undermining required will predispose to seroma formation. A separate cranial skin incision over the region of the biceps brachii tendon helps to avoid this complication. Many dogs with joint mice in the bicipital tendon sheath have significant lameness which results in muscle atrophy. Occasionally, the joint mice are palpable within the tendon sheath prior to surgery, making the surgical approach relatively easy. The approach requires cranial retraction of the brachiocephalicus muscle and partial transection of the insertions of the superficial and deep pectoral muscles. If not palpable percutaneously prior to surgery, the joint mice are usually palpable following this surgical exposure, and an incision can be made directly over the joint mouse. Once the free fragments are removed, the tendon sheath is repaired using small-diameter (3-0 or 4-0), absorbable suture material. Arthroscopic treatment of humeral head OCD has been reported. 24· 41 · 42 Advantages of arthroscopy include a more thorough examination of the synovium and articular cartilage (including the articular surface of the glenoid, which is usually inaccessible with conventional arthrotomy), decreased soft tissue trauma, decreased operative time, and rapid postoperative recoveryY· 42 Although these advantages undoubtedly apply in the hands of an experienced arthroscopist, the availability and cost of equipment and training as well as the lack of significant morbidity with surgical arthrotomy all suggest that veterinarians will perform conventional arthrotomy in a majority of cases. SURGICAL MANIPULATIONS
The cartilage flap usually remains attached to the surrounding cartilage at the cranial or craniomedial extent of the lesion. This attachment can usually be broken and the flap removed by placing a thin instrument such as a Freer periosteal elevator between the subchondral bed and cartilage flap and applying a twisting motion. Alternatively, a
46
JOHNSTON
scalpel blade or bone curette can be used to detach the flap. This is done with caution to prevent iatrogenic damage to surrounding tissues. Once the cartilage flap is removed, the subchondral bed should be examined, and all cartilage not firmly attached to the subchondral bone is removed. A Freer periosteal elevator is useful for determining cartilage attachment. Although the bone-cartilage interface is normally quite firm and only considerable force will cause osteochondral separation in areas of normal tissue, probing the subchondral bed should be done with care to avoid unnecessary damage to the articular surface. The edges of the cartilage should be trimmed using a sharp bone curette so that they are perpendicular to the subchondral surface. Beveled edges inhibit filling of the defect with fibrocartilage. 30 Examination of the subchondral bed will reveal one of three presentations: (1) a roughened, bleeding surface consistent with exposed subchondral bone; (2) a roughened, dull white, soft surface consistent with reparative fibrocartilage; or (3) a hard, smooth, ivory-colored surface consistent with eburnated bone. If bleeding bone or reparative fibrocartilage is present, no further treatment is necessary, as healing occurs through the production of fibrocartilage which occurs if there is an adequate blood supply. If an eburnated surface is present, creating vascular access by curettage (abrasion arthroplasty) or forage will promote healing. If abrasion arthroplasty is performed, care should be taken to minimize the subchondral bone defect created while establishing vascular exposure. Once the cartilage flap has been removed and subchondral bone has been assessed and treated, the caudal joint pouch should be explored for the presence of joint mice. The joint is flushed with saline to remove any remaining cartilage fragments. The joint capsule is closed using 3-0 interrupted, absorbable sutures. The deltoideus fascia is apposed with 3-0 absorbable suture. The subcutaneous tissue is closed with 3-0 absorbable suture, with care taken to eliminate dead space by tacking down each successive layer. Routine skin closure completes the procedure. POSTOPERATIVE CARE
Recovery from surgery in which a muscle separation technique is used occurs relatively quickly. Dogs will frequently walk on the operated limb immediately postoperatively or within 1 to 2 days, have little lameness within 2 to 4 weeks, and be clinically normal by 1 to 2 months postoperatively if not sooner. Because rapid recovery of ambulation normally occurs, it is recommended that exercise be restricted to leash walks for a minimum of 4 weeks postoperatively in order to decrease stress placed on periarticular soft tissues and developing reparative fibrocartilage. Seroma formation is the most frequent complication of shoulder arthrotomy. Many factors contribute to seroma formation, including the amount of tissue undermining, hemostasis, inadequate closure of dead
OSTEOCHONDRITIS DISSECANS OF THE HUMERAL HEAD
47
space, and patient activity. In the author's opinion, tissue undermining and inadequate closure of dead space are the most frequent causes of seroma formation. Failure to close the joint capsule does not contribute to seroma formation. 34 Appropriate closure of dead space requires suturing of the deep fascia, subcutaneous tissues, and skin. The prognosis for recovery from humeral head OCD is good. Dogs with pre-existing degenerative changes are less likely to have an excellent outcome. Information regarding the progression of osteoarthritis in surgically treated limbs is sparse. Clinical experience suggests that radiographic changes consistent with mild to moderate osteoarthritis are present in many shoulder joints affected with humeral head OCD when they are examined years after surgical treatment and that these changes have minimal clinical significance.
CONCLUSIONS
The caudal-central region of the humeral head is a common site for OCD. If clinical signs of pain and lameness are present along with radiographic changes consistent with OCD, surgical treatment is recommended. The caudolateral approach with cranial retraction of the teres minor muscle provides good exposure to the cartilage flap and subchondral defect and results in minimal postoperative morbidity. In dogs with clinical and radiographic evidence of bilateral humeral head OCD, concurrent bilateral surgery is appropriate and practical, particularly if the caudolateral approach is used. The long-term prognosis for recovery is good.
References 1. Birkeland R: Osteochondritis dissecans in the humeral head of the dog. Nord Vet Med 19:291, 1967 2. Buckwalter JA, Mankin HJ: Articular cartilage. Part II: Degeneration and osteoarthrosis, repair, regeneration and transplantation. J Bone Joint Surg Am 79:612, 1997 3. Caron JP: Neurogenic factors in joint pain and disease pathogenesis. In Mcllwraith CW, Trotter GW (eds): Joint Disease in the Horse. Philadelphia, WB Saunders, 1996, p 70 4. Cordy DR, Wind A: Transverse fracture of the proximal humeral articular cartilage in dogs. Pathol Vet 6:424, 1969 5. Craig PH, Riser WH: Osteochondritis dissecans in the proximal humerus of the dog. J Am Vet Radiol Soc 6:40, 1965 6. Edelson R, Burks RT, Bloebaum RD: Short-term effects of knee washout for osteoarthritis. Am J Sports Med 23:345, 1995 7. Gahring DR: A modified caudal approach to the canine shoulder joint. J Am Anim Hosp Assoc 21:613, 1985 8. Griffiths R: Osteochondritis dissecans of the canine shoulder. JAVMA 53:1733, 1968 9. Hansen B: Management of postoperative pain in dogs and cats. In Proceedings of the Predictable Pain Management North American Veterinary Conference, Orlando, FL, 1996, p 13
48
JOHNSTON
10. Howard PE: Luxation of the canine shoulder joint to maximize exposure for treatment of osteochondritis dissecans. Vet Surg 13:15, 1984 11. Hunziker EB, Rosenberg L: Articular cartilage repair. In Koopman WJ (ed): Arthritis and Allied Conditions, ed 13. Baltimore, Williams & Wilkins, 1997, p 2027 12. Ike RW, Arnold WJ, Rothschild EW, et al: Tidal irrigation versus conservative medical management in patients with osteoarthritis of the knee: A prospective randomized study. J Rheumatol 19:772, 1992 13. Jones DGC, Vaughan LC: The surgical treatment of osteochondritis dissecans of the humeral head of dogs. J Small Anim Pract 11:803, 1970 14. Kincaid S, Van Sickle 0: Regional histochemical and thickness variations of adult canine articular cartilage. Am J Vet Res 42:428, 1981 15. Kinzel GL, Van Sickle DC, Hillberry BM, et al: Preliminary study of the in vivo motion in the canine shoulder. Am J Vet Res 37:1505, 1976 16. Livesley PJ, Doherty M, Needoff M, et al: Arthroscopic lavage of osteoarthritic knees. J Bone Joint Surg Br 73:922, 1991 17. Mcilwraith CW, Nixon AJ: General pathobiology of the joint and response to injury. In Mcilwraith CW, Trotter GW (eds): Joint Disease in the Horse. Philadelphia, WB Saunders, 1996, p 317 18. McLaughlin R, Roush JK: A comparison of two surgical approaches to the scapulohumeral joint in dogs. Vet Surg 24:207, 1995 19. Menche OS, Frenkel SR, Blair B, et al: A comparison of abrasion burr arthroplasty and subchondral drilling in the treatment of full-thickness cartilage lesions in the rabbit. Arthroscopy 12:280, 1996 20. Mow VC, Setton LA, Ratcliffe A, et al: Structure-function relationships of articular cartilage and the effects of joint instability and trauma on cartilage function. In Brandt KD (ed): Cartilage Changes in osteoarthritis. Indianapolis, Indiana University School of Medicine, 1990, p 22 21. Myers SL, Flusser 0, Brandt KD, et al: Prevalence of cartilage shards in synovium and their association with synovitis in patients with early and endstage osteoarthritis. J Rheumatol 19:1247, 1992 22. Nixon AJ, Cummings JF: Substance P immunohistochemical study of the sensory innervation of normal subchondral bone in the equine metacarpophalangeal joint. Am J Vet Res 55:28, 1994 23. Olsson SE: Pathophysiology, morphology, and clinical signs of osteochondrosis in the dog. In Bojrab MJ (ed): Disease Mechanisms in Small Animal Surgery, ed 2. Philadelphia, Lea & Febiger, 1993, p 777 24. Person MW: Arthroscopic treatment of osteochondritis dissecans of the canine shoulder. Vet Surg 18:175, 1989 25. Peterson CJ: Osteochondritis dissecans of the humeral head of a cat. N Z Vet J 32:115, 1984 26. Piermattei DL: An Atlas of Surgical Approaches to the Bones and Joints of the Dog and Cat, ed 3. Philadelphia, WB Saunders, 1993, p 99 27. Probst C, Flo G: Comparison of two caudolateral approaches to the scapulohumeral joint for treatment of osteochondritis dissecans in dogs. JAVMA 191:1101, 1987 28. Probst CW, Johnston SA: Osteochondrosis. In Slatter D (ed): Textbook of Small Animal Surgery, ed 2. Philadelphia, WB Saunders, 1993, p 1944 29. Rudd RG, Whitehair JG, Margolis JH: Results of management of osteochondritis dissecans of the humeral head in dogs: 44 cases (1982-1987). JAm Anim Hosp Assoc 26:173, 1990 30. Rudd RG, Visco OM, Kincaid SA, et al: The effects of beveling the margins of articular cartilage defects in immature dogs. Vet Surg 16:378, 1987 31. Salter RB: The physiologic basis of continuous passive motion for articular cartilage healing and regeneration. Hand Clin 10:211, 1994 32. Salter RB, Simmonds OF, Malcolm BW, et al: The biological effect of continuous passive motion on the healing of full-thickness defects in articular cartilage. An experimental investigation in the rabbit. J Bone Joint Surg Am 62:1232, 1980 33. Scherrer PK, Hillberry BM, Van Sickle DC: Determining the in-vivo area of contact in the canine shoulder. J Biomech Eng 101:271, 1979
OSTEOCHONDRITIS DISSECANS OF TilE HUMERAL HEAD
49
34. Schiller AG, Smith CW, Seaman WJ: Surgical treatment of osteochondritis dissecans without suturing the joint capsule. Veterinary Medicine Small Animal Clinician 73:50, 1978 35. Shapiro F, Koide S, Glimcher MJ: Cell origin and differentiation in the repair of fullthickness defects of articular cartilage. J Bone Joint Surg Am 75:532, 1993 36. Smith CW, Stowater JL: Osteochondritis dissecans of the canine shoulder joint: A review of 35 cases. J Am Anim Hosp Assoc 11:658, 1975 37. Story E: Prognostic value of arthrography in canine shoulder osteochondrosis (osteochondritis) dissecans. Vet Clin North Am Small Anim Pract 8:301, 1978 38. Tomlinson J, Constantinescu G, McClure R, et a!: Caudal approach to the shoulder joint in the dog. Vet Surg 15:294, 1986 39. van Bree H: Comparison of the diagnostic accuracy of positive-contrast arthrography and arthrotomy in evaluation of osteochondrosis lesions in the scapulohumeral joint in dogs. JAVMA 203:84, 1993 40. van Bree H:, Evaluation of the prognostic value of positive-contrast shoulder arthrography for bilateral osteochondrosis lesions in dogs. Am J Vet Res 51:1121, 1990 41. van Bree H, Van Ryssen B, Desmidt M: Osteochondrosis lesions of the canine shoulder: Correlation of positive contrast arthrography and arthroscopy. Vet Radio! Ultrasound 33:342, 1992 42. Van Ryssen B, van Bree H, Missinne S: Successful arthroscopic treatment of shoulder osteochondrosis in the dog. J Small Anim Pract 34:521, 1993 43. Van Sickle DC: Selected Orthopedic Problems in the Growing Dog. South Bend, IN, American Animal Hospital Association, 1975, p 29 44. Vaughan LC, Jones DGC: Osteochondritis dissecans of the head of the humerus in dogs. J Small Anim Pract 9:283, 1968 45. Whitehair JG, Rudd RG: Osteochondritis dissecans of the humeral head in dogs. Compend Contin Educ Pract Vet 12:195, 1990 46. Wojtys EM, Beaman DN, Glover RA, eta!: Innervation of the human knee joint by substance-P fibers. Arthroscopy 6:254, 1990
Address reprint requests to Spencer A. Johnston, VMD Department of Small Animal Clinical Sciences Virginia-Maryland Regional College of Veterinary Medicine Virginia Tech Blacksburg, VA 24061-0442