Disorders of the bovine upper limb (Proceedings)

Trauma

Fractures of the metatarsal/metacarpal regions commonly occur in food animal practice particularly in young calves. Factors such as whether the fracture is open or closed and whether vascular damage has occurred determine the prognosis. Generally, the classic mid-shaft metatarsal/metacarpal fracture heals well under a cast to immobilize the joint above and below the fracture. I generally don't encase the foot, but some do. I like to keep them in a cast for 4-6 weeks, however, in young growing calves, they may outgrow the cast so we'll bring them back in about 2.5 weeks to re-check, and if necessary, change the cast.

Fractures of the shaft of the ileum usually result in mild to moderate swinging limb lameness. The gait is altered rather than having a definitive pain response. These present with the "knocked down hip" in which there is asymmetry noted in the pelvic girdle. Cattle with severe muscle atrophy may create an optical illusion as to whether the tuber coxae is lower than the other side. Typically, rectal palpation reveals a palpable fracture line or a definitive indentation or lack of continuity in the shaft of the ilium. These tend to heal with strict stall confinement. The only consideration is what the fracture does to the width and depth of the pelvis. There may be some ramifications for future natural delivery of a calf.

Salter- Harris fractures of the distal physis of the metacarpus or metatarsus occur. These animals are not as lame as you would expect. Casting the limb up to the carpus or tarsus generally allows enough stabilization for healing.

Some fractures above the carpus and tarsus can be corrected with combinations of external or internal fixation. External fixation with pin casts or double cortex pins and a connecting rod are usually tolerated quite well. In addition, casting and incorporating a Schroder-Thomas splint in cases of distal tibial or radial/ulnar fractures can provide satisfactory results as well.

Commonly in show animals or other cattle with overly straight hind limbs present with "puffy" hock joints. This swelling is not warm to the touch or painful and the animals are not lame. The degree of swelling is generally symmetrical. Animals with overly straight hocks, especially bulls, over time get joint effusion just from "wear and tear". These cases are aided by drugs such as Adequan®, however, this is only a short term fix.

Femoral nerve paralysis

Femoral nerve paralysis is most commonly seen as a result of dystocia, and more specifically when the calves get "hip locked" for any length of time. These calves can't extend the stifle, and if it is bilateral, usually can't stand. These calves have a guarded prognosis. The calves, in addition to ensuring they have adequate passive transfer of antibodies, require physical therapy. If the owners are willing to do this, we usually give them about 4 weeks to show signs of improvement. The main differentials are bilateral hip luxation and lateral luxation of the patella.

Stifle injuries

Stifle injuries are most commonly a result of mounting mishaps, fighting, poor footing and falling, degenerative joint disease or ataxia from metabolic disease (ie: low calcium). Clinical signs of stifle injury or disease usually result in the following:

Avoids flexing the stifle

Hock and stifle tend to remain in a fixed position

The animal puts most of its weight on the toe

The unaffected legs are camped under the body to take weight off the affected leg

Periarticular and intra-articular joint swelling

Warm to the touch in cases of infection (gonitis)

Lameness in the foot may closely resemble stifle signs so make sure to start at the foot even though it may appear obvious that the stifle is involved. To tap the lateral femorotibial joint compartment for fluid analysis or lidocaine insertion the needle is inserted behind the lateral patellar ligament and directed caudally. The femoropatellar space can be reached by inserting the needle between the medial and middle patellar ligaments directing dorsally and caudally. Obviously, appreciating a cranial drawer sign in a large ruminant is difficult, however, sometimes joint instability may be observed by palpation at a walk. In cases of some duration, quadriceps and gluteal muscle atrophy may be noted. Crepitation in the hip can appear as if its coming from the stifle, therefore, evaluate the coxofemoral joint internally and externally.

Cranial cruciate ligament rupture

It seems as if more and more animals are presented with rupture of the cranial cruciate ligament. Clinical signs include acute onset of lameness that is usually 3-4/5. If the condition is chronic, the animal may be less lame and display signs of muscle atrophy. There is usually a certain degree of joint effusion in early cases, however, as the condition continues without correction, the joint capsule thickens making the effusion more difficult sometimes to appreciate.

The treatment options depend on the value and intended use of the animal. Salvage is the best option for animals with less value. For more genetically valuable animals, stall rest and anti-inflammatories may render a animal that is functionally able to endure semen collection or undergo embryo donation. Various surgical methods have been advocated for repair, however, the majority of cases are not benefited enough to warrant intervention due to the nature of ruminants and their tendency to not be very good patients (protecting the limb, etc.). We have had some success stories in animals that were very docile and amenable to therapy.

Upward fixation of the patella

Upper fixation of the patella occurs due to the fact that the medial femoral condyle is larger than the lateral condyle. This occasionally allows the medial patellar ligament to "catch" on the medial condyle preventing normal flexion of the joint. Trochlear malformation predisposes calves to this occurrence as does decreased muscle tone and poor conformation. Damage to the femoral nerve may also contribute in cases of trauma.

The condition is characterized by lack of swelling and a gait in which the limb is fixed in extension at the end of propulsion and beginning of anterior phase of stride. When the patellar ligament finally slips off its attachment to the medial condyle, the animal takes a normal stride and gait until the "catching" occurs again.

Treatment involves correcting the underlying cause if possible and doing a medial patellar desmotomy. This procedure is relatively straight forward. Clients should be counseled on the possible heritability of this condition (conformation problems, etc.)

Lateral luxation of the patella

Lateral luxation of the patella usually happens in younger animals due to either trauma to the medial patellar ligament or the femoropatellar ligament or congenital malformation of the trochlea and or patella. In calves, you have to rule out the possibility of femoral nerve paralysis, therefore, its helpful to inquire about a possibility of dystocia. These calves resemble rabbits in the hind limbs if bilateral. Diagnosis is by careful palpation. These calves can be treated with imbrication of the femoropatellar ligament and joint capsule, however, in my experience there is usually conformational problems that do not lend themselves to repair.

Coxofemoral luxation

Coxofemoral luxation can occur in any direction but most commonly is either cranio-dorsal or cranio-ventral. Cranio-dorsal luxation usually occurs in younger cattle as a result of a traumatic event. These animals are usually ambulatory and rotate the toe and stifle outward. Three points of reference to use to evaluate pelvic symmetry are the greater trochanter, the tuber coxae and the ischial tuberosity. Comparisons between sides in the distances between these points in cases of coxofemoral luxation are very helpful in diagnosing the condition. However, only radiographs can definitively differentiate between luxation and fractures of the femoral head and neck or physis. Crepitance upon palpation over the hip while manipulating the leg may aid in differentiating a fracture from luxation.

Treatment of true luxation is very much dependant upon duration. Luxations occurring within a few hours of presentation (which very rarely happens!) may be amenable to closed reduction. I've had one case in a 6 month-old calf in which this procedure worked well. She protected it well and was a quiet calf. Most of the ones I've seen pop right back out. Surgical repair is unsuccessful in my experience. Semen can be collected from bulls and embryos from cows in genetically valuable animals.

Cranio-ventral luxation usually occurs in older animals. Trauma, calving difficulties and lightning strike are reported potential etiologies of this condition.

These animals are usually recumbent, and the femoral head can also often be palpated in the obturator foramen or at brim of pelvis per rectum. Salvage is the only option with these animals.

Osteochondrosis (OC)

Osteochondrosis occurs in rapidly growing individuals due to a disturbance in cell differentiation and maturation in joint cartilage and metaphyseal growth plates. Normally, resting chondrocytes, under the control of somatotropin, form organized columns of cells in the proliferating zone. These cells differentiate in the zone of hypertrophy. The intercellular matrix calcifies under the influence of thyroxine. Following capillary invasion, osteogenic cells lay down a matrix on the calcified cartilage cores. This matrix becomes mineralized forming the primary spongiosa which is replaced by secondary spongiosa. In OC, the cartilage cells fail to differentiate. The hypertrophied zone of cartilage fails to calcify and is retained. This prevents capillaries from entering the abnormal cartilage and endochondral ossification does not occur. The cartilage in this region thickens and becomes a barrier to the supply of nutrients to the area. Necrosis ensues. The abnormally, thickened cartilage fissures, leading to the liberation of debris into the joint. In other words, the cartilage basically outgrows its blood supply, leaving islands of uncalcified cartilage which undergo necrosis in deeper layers. These areas "slough" if you will, and become joint "mice" or subchondral bone cysts. The occurrence of this condition seems to have increased with the push for performance and the genetic favoring of high-performance animals. One study several years ago reported the incidence of OC as 8.5% in feedlot cattle.1 A 1999 study looked at the hind limb bones from 46, 12 month-old bulls with no clinical signs. These bulls were from a bull test station. Forty-five out of forty-six of these bulls had lesions in the joints and/or growth plates. The stifle was involved in 37 cases and lesions consisted of OC of the articular-epiphyseal cartilage complex in 25.2

Multiple factors, both individually and collectively are believed to play a role in the development of OCD. Rapid growth has been reportedly a predisposing factor in the development of osteochondrosis.3 This growth is the product of genetic selection for performance, therefore, it is difficult to elucidate whether hereditary or nutritional factors are the single most important factor. It is widely accepted that cattle on a high-energy ration are predisposed to develop OC.3 However, due to the relatively low incidence of OC reported in fast-growing cattle on commercial diets, the role of energy as a predisposing factor for OC is not well understood.4 Other nutritional factors thought to play a role in the predisposition and/or creation of OC include a Ca:P imbalance (P excess in high grain diets), P deficiency, Cu deficiency (also created by an excess of Mo, Zn, Fe or SO4) and Zn deficiency. Copper is required for cross-linking of collagen. Zinc deficiency has also been linked to interdigital dermatitis and foot rot. In addition, alterations in hormone concentrations have been demonstrated to cause OC.5 Although no particular breed has been identified as being predisposed to OC, numerous cases of OC have been reported in purebred cattle.3 However, this may be due to the fact that more of these cases are recognized because of the owners' willingness to pay for such diagnostics. Trauma may also contribute to the manifestation of clinical signs of OC due to the inferior quality of the cartilage. Therefore, excessively straight legged cattle are predisposed. Clinically, OC is reported almost three times more often in male cattle than female cattle.6 This may be unrealistic because males were generally considered more of an economic entity than cows when these studies were performed, therefore, they were subjected to more advanced diagnostic techniques.

In cattle, bulls on test and show animals are the cases we most commonly see. Generally, these animals are still growing (less than 2 years of age). The average age at which cattle demonstrate clinical signs from OC is 18-24 months.3 Origin of lameness varies depending upon the joints involved. Intra-articular analgesia may be very beneficial in localizing the lameness to one particular joint in cases that lack joint effusion. The lateral trochlear ridge of the distal femur is most commonly affected in cattle.6 Lesions have also been reported in the tarsus,7 shoulder,6 distal radius6 and phalanges.6 Clinical signs include discomfort, weight shifting, enlargement of ends of the long bones and reluctance to mount. Joint effusion may be present, but is not typically found with subchondral bone cyst lesions.

Differentials for young, growing cattle would include septic arthritis, trauma and synovitis. Definitive diagnosis is by ruling out other potential causes and radiographs. Sometimes radiographs may not show anything impressive, especially in the early course of disease. Subchondral bone cysts typically do not display joint effusion even though the animal is lame. Cystic lesions and dissecting flaps (joint mice) can be detected radiographically. Osteochondrosis commonly occurs bilaterally, therefore, we suggest radiographing the opposite joint if possible. Arthrocentesis and synovial fluid analysis often reveal a mild, nonseptic inflammation with mild to moderate increases in leukocyte counts and total protein.8

Treatment options include strict stall rest with use of NSAID's as needed. As mentioned earlier, I have had some success using glucosaminoglycans in an extra label fashion as used in equine. However, I could find no documented reports of efficacy in the literature for cattle. Evaluation and correction of the ration with regards to mineral, energy and protein content is indicated. Valuable animals could undergo arthroscopic "cleaning of the joint" to debride and remove osteochondral fragments and cystic beds. Means to prevent the disease include monitoring the Ca:P status of the ration as well as the Cu and Zn, restricting rations for breeding stock, providing adequate exercise and selecting appropriate genetics.

As for prognosis, varying degrees of success are reported. Cattle with OC, lameness and radiographic evidence of degenerative joint disease carry a guarded prognosis regardless of therapy.9 Clinically, conservative medical management was associated with more than 80% of the cattle being culled for refractory lameness according to one study.6 The culling occurred within 6 months of the diagnosis. In valuable animals, surgery should be considered because it has reportedly produced a more positive outcome.8

References

1. Jensen R, Park RD, Lauermann LH, et al (1981): Osteochondrosis in feedlot cattle. Vet Pathol 18:529-535.

2. Dutra F, Carlsten J, Ekman S (1999): Hind limb skeletal lesions in 12 month-old bulls of beef breeds. Zentralbl Veterinarmed A. 46(8):489-508.

3. Reiland S, Stromberg B, Olsson SE, et al (1978): Osteochondrosis in growing bulls: Pathology, frequency and severity on different feedings. Acta Radiol (Suppl)358:179-176.

4. Trostle SS, Nicoll RG, Forrest LJ, et al (1998): Bovine Osteochondrosis. Compendium for the continuing education of practicing veterinarians. 20(7):856-863.

5. Fischer AT Jr, (2002): Osteochondrosis. In: Smith BP (ed): Large animal internal medicine. St. Louis, Mosby p – 1088.

6. Trostle SS, Nicoll RG, forrest LJ, et al (1997): Clinical and radiographic findings of cattle with osteochondrosis: 26 cases. J Am Vet Med Assoc 211:1566-1570.

7. Baxter BM, Hay WP, Selcer BA (1991): Osteochondritis dissecans of the medial trochlear ridge of the talus in a calf. J Am Vet Med Assoc 198:669-671.

8. Todhunter RJ (1992): Diagnostic principles of joint disease. In: Auer JA (ed) Equine Surgery. Philadelphia, WB Saunders Co. pp - 866-882.