Results Group 11-Final case Physical Exam Bonnie has a partial weight bearing left hind limb lameness. She has difficulty getting up, but can walk quite well once she is up. When she stands still she is barely toe touching on the left hind leg. There is effusion of the left stifle joint with a distention of the joint capsule on either side of the straight patella ligament. There is pain on manipulation of the stifle. Bonnie is quite overweight but she has no other abnormalities. Interpretation: The unilateral partial weight bearing lameness is consistent with a cranial cruciate ligament (CrCL) rupture. It has been nearly a week since the actual event, so while initially with an acute full rupture of the ligament a non-weight bearing lameness would be expected, this usually evolves into a partial weight bearing lameness with time. Joint effusion is a normal finding with CrCL rupture due to the influx of inflammatory mediators resulting in leaky capillaries. The immune system releases chemical mediators like histamine that cause vasodilation (redness and heat) and vascular permeability . Serous exudate rich in protein seeps out of the leaky capillaries (swelling). The histamine and other chemotactic factors attract phagocytes such as neutrophils and later monocytes to the area of inflammation (further swelling) to clean up the waste. The chemical mediators also irritate nerve endings in the joint capsule (pain and loss of function). Lysosomal enzymes from leukocytes can begin to digest the debris with in the joint. Obesity is important in this case because it increases load and stress on the supporting structures of the stifle. Therefore if there is a traumatic event or the CrCL is weakened, obesity increases the chances of rupture. Orthopedic Exam There is joint effusion in the left stifle joint. A joint tap was performed. While awake, no cranial drawer can be palpated in the stifle joints. While under sedation a 4 - 5 mm cranial drawer can be palpated in the left stifle, with less than 2 mm palpable in the right. The patellae appear correctly positioned and normally mobile. The collateral ligaments are intact. The hip joints do not have any palpable laxity or pain when run through a full range of motion. No other abnormalities could be found. Interpretation: All results of the orthopedic exam are consistent with CrCL rupture. The function of the CrCL is to constrain the stifle joint so as to limit the normal internal rotation and cranial displacement of the tibia relative to the femur, and to prevent hyperextension of the stifle. Therefore a rupture of the CrCL will present as a cranial drawer sign or cranial displacement of the tibia in relation to the femur when shearing force is applied to the stifle. When awake, reflexive tightening of muscles, tendons, and external ligaments in response to pain provide enough stability n to eliminate a cranial drawer sign. Under sedation, these structures relax and a cranial drawer sign can be elicited in the presence of a partial or full CrCL rupture. In this case, a 4-5mm cranial drawer sign was elicited under sedation indicating a complete rupture. The rest of the findings of the orthopedic exam localize the cause of the lameness to the stifle and rule out patellar and collateral ligament involvement in the etiology of the lameness. Specialty Exams Hematology VALUE RBC 6.0 HGB 15.4 HCT 41.1 MCV 72.6 MCH 24.6 MCHC 33.9 WBC 12.704 HI* Band 0.0 Lymph 0.84 Mono 0.112 Eosin 0.183 Baso 0 Platelets 287 Chemistry VALUE Glucose 122 BUN 18 Creatinine 0.9 Phos 3.3 Calcium 9.6 LO* TP 6.1 Albumin 2.4 LO* Globulin 3.7 ALT 48 ALKP 89 TBIL 0.13 Sodium 148 Chloride 115 Potassium 3.8 CO2 21 Anion Gap1 5.8 Cholesterol 283 Joint Fluid Analysis Reddish colored clear fluid. Good mucin clot. Cell count about 3500 per hpf, mainly neutrophils and monocytes. No bacteria seen Interpretation: There are a few minor changes on the hematology reports. There is a slight leukocytosis characterized by a neutrophilia with no left shift. There is no clear cause of this neutrophilia; however, there are three possible etiologies. First, it could be a stress related neutrophilia. Endogenous cortisol released in response stressors such as pain causes the demargination of neutrophils and an increased release from the bone marrow storage pool. Usually there will be a concurrent monocytosis, lymphopenia, and eosinopenia with a stress leukogram which are not present in this patient. Second, it could be normal for this patient. Reference intervals are designed to include 95% of the population, so this dog could be in that 2.5% above the upper reference limit. A third possibility is that there is an underlying chronic inflammatory process that has caused a granulocytic hyperplasia. This hyperplasia takes over a week to develop, so it is unlikely that the neutrophilia is caused by the torn CrCL. A slight stress leukogram is the most likely cause of the leukocytosis. The slight hypoalbuminemia also has no obvious cause. Again it could be that Bonnie is a part of the 5% of the population that is outside the reference interval for this chemistry, or Bonnie could be suffering from a mild glomerular disease that causes protein loss into the urine, but is not severe enough to cause an azotemia. The slight hypoalbuminemia does explain the slight hypocalcemia. Forty percent of calcium in the blood is bound by albumin, ten percent is associated with citrate and phosphate anions, and fifty percent is ionized and diffusible. Clinically, we measure the total amount of calcium in the serum, including all three. Patients with a hypoalbuminemia often exhibit a concurrent hypocalcemia. This hypocalcemia is not associated with clinical signs as hypoalbuminemia does not affect the concentration of biologically active ionized calcium in the plasma. The calcium level in the serum can be adjusted to reflect this phenomenon. The adjusted calcium level is 10.7 mg/dL, which is within the normal reference interval. The serum chemistry analysis is consistent with what would be expected for a CrCL rupture. The joint fluid analysis shows a reddish colored clear fluid with a mild increase in cellularity (mainly macrophages and neutrophils), a good mucin clot, and no bacterial organisms. The reddish color can be attributed to a traumatic tap or intra-articular hemorrhage. The former explanation is most likely in this case considering the clinical signs and the rest of the fluid analysis. Clear fluid indicates a low likelihood of inflammatory joint disease. The mild increase in cellularity is consistant with the mild inflammatory effusion seen several days following a CrCL rupture. A mucin clot test is a qualitative test of polymerization of hyaluronate in the synovial fluid. The good mucin clot further indicates a low likelihood of inflammatory joint disease. In general, the more inflamed the joint, the poorer the mucin clot. In addition, bacterial organisms were not seen, which eliminates septic arthritis from the rule out list. Radiographic Interpretation: The craniocaudal radiograph of the left stifle has a small opacity at the level of the proximal insertion of the medial collateral ligament on the femur. While this abnormality should be further examined, it is not likely that it plays a role in Bonnie's current lameness. Additionally,there is an apparent decreased joint space on the medial side of the stifle. Considering the lack of concurrent clinical findings (such as crepitus or clicking) of a medial meniscal tear, it is less likely this is the cause of the decreased joint space. A more likely reason for this is that the stifle is malpositioned, but the presence of a meniscal tear should be investigated during surgical repair of the ruptured CrCL. The rest of the radiograph is normal. The lateral radiograph of the left stifle shows a significant intra-articular effusion as evidenced by the compression of the infra-patellar fat pad. The rest of the radiograph is normal. The results of the radiographic analysis are consistent with an acute CrCL rupture.