C-reactive protein:quantitative marker of surgical trauma and post-surgical complications in dogs: a systematic review

C-reactive protein (CRP) is a major acute phase protein showing increasing serum concentrations in dogs with systemic inflammation following e.g., surgery, trauma, infections, or neoplasia. CRP is a useful diagnostic marker of systemic inflammation in dogs and automated assays have been validated for reliable measurements for routine diagnostic purposes. In the present study available evidence for the use of CRP as a marker of surgery related systemic inflammation in dogs was reviewed and assessed. Two main themes were in focus: (1) canine CRP as a potential marker of postsurgical infectious complications and (2) canine CRP as a marker of the degree of surgical trauma. As outlined in the review several studies suggest that CRP is a useful marker for both purposes. However, the evidence level is limited and studies in the field are all affected by considerable risks of bias. Thus, further studies are needed in order to confirm the assumptions from previous studies and increase the level of evidence for CRP as a useful marker for detecting inflammation after surgery in dogs

Evaluation of the TEG(® )platelet mapping™ assay in blood donors

BACKGROUND: Monitoring of antiplatelet therapy in patients at cardiovascular risk is difficult because existing platelet function tests are too sophisticated for clinical routine. The whole blood TEG(® )Platelet Mapping™ assay measures clot strength as maximal amplitude (MA) and enables for quantification of platelet function, including the contribution of the adenosine diphosphate (ADP) and thromboxane A2 (TxA2) receptors to clot formation. METHODS: In 43 healthy blood donors, the analytical (CV(a)) and inter-individual variability (CV(g)) of the TEG(® )Platelet Mapping™ assay were determined together with platelet receptor inhibition in response to arachidonic acid (AA) and ADP. RESULTS: The CV(a )of the assay for maximal platelet contribution to clot strength (MA(Thrombin)) was 3.5%, for the fibrin contribution to clot strength (MA(Fibrin)) 5.2%, for MA(AA )4.5% and for MA(ADP )it was 6.6%. The MA(Thrombin )CV(g )was 2.8%, MA(Fibrin )4.7%, MA(AA )6.6% and for MA(ADP )it was 26.2%. Females had a higher MA(Thrombin )compared to males (62.8 vs. 58.4 mm, p = 0.005). The platelet TxA2 receptor inhibition was 1.2% (range 0–10%) and lower than for the ADP receptor (18.6% (0–58%); p < 0.0001). CONCLUSION: The high variability in ADP receptor inhibition may explain both the differences in response to ADP receptor inhibitor therapy and why major bleeding sometimes develops during surgery in patients not treated with ADP receptor inhibitors. An analytical variation of ~5 % for the TEG(® )enables, however, for routine monitoring of the variability in ADP receptor inhibition and of antiplatelet therapy

Exercise induced hypercoagulability, increased von Willebrand factor and decreased thyroid hormone concentrations in sled dogs

BACKGROUND: Sled dogs performing endurance races have been reported to have a high incidence of gastric erosions or ulcerations and an increased risk of gastro intestinal bleeding leading to death in some cases. In addition, these dogs also become hypothyroid during training and exercise. Canine hypothyroidism has been shown to correlate with decreased von Willebrand factor antigen and potentially increased bleeding tendency. Whether increased gastro intestinal bleeding risk is exacerbated due to changes in the hemostatic balance is unknown. The aim of this study was to investigate the hemostatic balance in sled dogs before and after exercise and in addition evaluate any correlation to thyroid status. Twenty sled dogs have been assessed in untrained and trained condition and immediately after exercise. The first sample was collected in the autumn following a resting period, and subsequently the dogs were exposed to increased intensity of training. After four months the peak of physical condition was reached and a 68 km long sled pulling exercise was performed. Samples were collected before and immediately after the exercise. Evaluated parameters were: plasma thromboelastographic (TEG) R, SP, α and MA, activated partial thromboplastin time (aPTT), prothrombin time (PT), fibrinogen, von Willebrand factor (vWf), D-dimer, platelet number, thyroid hormones, hematocrit and C-reactive protein (CRP). RESULTS: Exercise induced an overall hypercoagulable state characterized by significant decreases of TEG R and SP and an increase of α, increased concentrations of plasma vWf and decreased aPTT. In addition, a proinflammatory status was seen by a significant increase of serum CRP concentrations. Thyroid status was confirmed to be hypothyroid as training and exercise induced significant decrease of thyroxin (T4), free thyroxin (fT4) and thyroxin stimulating hormone (TSH) concentrations. Fibrinogen decreased significantly and PT increased. The training-induced changes showed correlation between T4, fT4 and aPTT and correlation between TSH and fibrinogen. Exercise-induced changes showed correlation between T4 and PT. CONCLUSIONS: Exercise was associated with a hypercoagulable state and an increase of vWf concentration in this group of sled dogs. Decreased thyroid hormone concentrations after training and exercise were confirmed, but were associated with increased and not decreased vWf in this group of sled dogs

Use of serum C-reactive protein as an early marker of inflammatory activity in canine type II immune-mediated polyarthritis: case report

BACKGROUND: Monitoring systemic inflammatory activity during steroid therapy of canine immune-mediated polyarthritis (IMPA) is difficult and mainly relies on clinical signs. CASE PRESENTATION: Canine serum C-reactive protein (CRP) was measured serially and blinded during a 27-week follow-up period of a case of Anaplasma phagocytophilia induced type II immune-mediated polyarthritis. CONCLUSION: WBC was, as expected, observed not to reflect the inflammatory activity during steroid treatment in a clinical useful manner, whereas, CRP is suggested a valuable unbiased marker of inflammatory activity during steroid treatment in this case

Mortality in virulent canine babesiosis is associated with a consumptive coagulopathy

The inflammatory response to infection can activate the coagulation system via complex interactions. If uncontrolled, this may lead to a consumptive coagulopathy, which has been identified as a major risk factor for poor outcome in both human and canine medicine. This study was undertaken to prospectively determine whether the presence of a consumptive coagulopathy in dogs with Babesia rossi infection is related to mortality. A prospective, cross-sectional, observational study was performed. Seventy-two client-owned dogs diagnosed with canine babesiosis were included. Diagnosis was confirmed by polymerase chain reaction and reverse line blot and dogs infected with Babesia vogeli or Ehrlichia canis were excluded. Blood samples were collected at admission. Coagulation factor-, antithrombin (AT)-, and protein C (PC) activity, prothrombin time (PT), activated partial thromboplastin time (aPTT), fibrinogen and Ddimer concentrations were measured. The mortality rate was 18% (13/72) and results between non-survivors and survivors were compared. The median activities of all the coagulation factors were significantly lower in the non-survivors compared to the survivors. The median PT and aPTT were significantly longer in the non-survivors compared to the survivors. The median AT activity was not significantly different; however, the median PC activity was significantly decreased in the non-survivors. The median D-dimer concentration was significantly higher in the non-survivors compared to the survivors. This study showed that dogs that died from B.canis infection suffered from a more severe consumptive coagulopathy compared to survivors, characterized by procoagulant activation, inhibitor consumption, and increased fibrinolytic activity.Department of Companion Animal Clinical Studies, University of Pretoria.www.elsevier.com/ locate/tvjlhb2013mn201