The fibrinolytic system is activated concurrently with coagulation; it regulates haemostasis and prevents thrombosis by restricting clot formation to the area of vascular injury and dismantling the clot as healing occurs. Dysregulation of the fibrinolytic system, which results in hyperfibrinolysis, may manifest as clinically important haemorrhage. Hyperfibrinolysis occurs in cats and dogs secondary to a variety of congenital and acquired disorders. Acquired disorders associated with hyperfibrinolysis, such as trauma, cavitary effusions, liver disease and Angiostrongylus vasorum infection, are commonly encountered in primary care practice. In addition, delayed haemorrhage reported in greyhounds following trauma and routine surgical procedures has been attributed to a hyperfibrinolytic disorder, although this has yet to be characterised. The diagnosis of hyperfibrinolysis is challenging and, until recently, has relied on techniques that are not readily available outside referral hospitals. With the recent development of point‐of‐care viscoelastic techniques, assessment of fibrinolysis is now possible in referral practice. This will provide the opportunity to target haemorrhage due to hyperfibrinolysis with antifibrinolytic drugs and thereby reduce associated morbidity and mortality. The fibrinolytic system and the conditions associated with increased fibrinolytic activity in cats and dogs are the focus of this review article. In addition, laboratory and point‐of‐care techniques for assessing hyperfibrinolysis and antifibrinolytic treatment for patients with haemorrhage are reviewed.

https://onlinelibrary.wiley.com/doi/epdf/10.1111/jsap.13068

A review of hyperfibrinolysis in cats and dogs.

Acute hemorrhage in small animals results from traumatic and non-traumatic causes. This review seeks to describe current understanding of the resuscitation of the acutely hemorrhaging small animal (dog and cat) veterinary patient through evaluation of pre-clinical canine models of hemorrhage and resuscitation, clinical research in dogs and cats, and selected extrapolation from human medicine. The physiologic dose and response to whole blood loss in the canine patient is repeatable both in anesthetized and awake animals and is primarily characterized clinically by increased heart rate, decreased systolic blood pressure, and increased shock index and biochemically by increased lactate and lower base excess. Previously, initial resuscitation in these patients included immediate volume support with crystalloid and/or colloid, regardless of total volume, with a target to replace lost vascular volume and bring blood pressure back to normal. Newer research now supports prioritizing hemorrhage control in conjunction with judicious crystalloid administration followed by early consideration for administration of platelets, plasma and red blood during the resuscitation phase. This approach minimizes blood loss, ameliorates coagulopathy, restores oxygen delivery and correct changes in the glycocalyx. There are many hurdles in the application of this approach in clinical veterinary medicine including the speed with which the bleeding source is controlled and the rapid availability of blood component therapy. Recommendations regarding the clinical approach to volume resuscitation in the acutely hemorrhaging veterinary patient are made based on the canine pre-clinical, veterinary clinical and human literature reviewed.

/pdf/volume-resuscitation-in-the-acutely-hemorrhaging-patient-4i00c5g57z.pdf

Volume Resuscitation in the Acutely Hemorrhaging Patient: Historic Use to Current Applications.

Objective: To evaluate the incidence of tranexamic acid (TXA)-induced nausea and vomiting after the prophylactic use of 2 antiemetics, ondansetron and maropitant, compared with saline.
Design: Prospective, blinded, placebo-controlled, randomized, crossover study.
Setting: University research facility.
Animals: Eight adult, purpose-bred Beagles.
Intervention: Dogs received 3 treatments on 3 occasions with a 3-week washout period. Either maropitant (1 mg/kg), ondansetron (0.2 mg/kg), or saline solution was given intravenously in equal volumes, followed 10 minutes later by 50 mg/kg IV TXA. A blinded observer evaluated the dogs for signs of vomiting and nausea for 30 minutes. The severity of nausea was assessed with a visual analog scale (VAS) and recorded at baseline before TXA, and at the end of 3 observational periods: 0-5, 5-15, and 15-30 minutes after TXA. A generalized linear mixed effect model was used to assess for group and period effects. Statistical significance was set at P<0.05
Measurements and main results: None of the dogs vomited after maropitant. Emesis occurred in 5 out of 8 dogs (62.5%), a median (range) of 1 time (1-2) after ondansetron and 1 time (1-3) after saline. There was a significant effect on vomiting of maropitant against saline (P < 0.0001) but not for ondansetron against saline (P = 0.53). The highest nausea VASs were recorded during the first 5 minutes after TXA with a significant reduction of VAS variability in the maropitant group (P = 0.003). The effect of maropitant and ondansetron against saline on the severity of nausea was not statistically significant (P = 0.069).
Conclusion: The neurokinin 1 receptor antagonist maropitant at the dose used, administered IV 10 minutes before 50 mg/kg TXA, was effective in preventing vomiting compared with ondansetron and placebo. Our results support the prophylactic IV administration of maropitant in dogs that are scheduled to receive TXA.

https://onlinelibrary.wiley.com/doi/epdf/10.1111/vec.12954

Prospective, controlled, blinded, randomized crossover trial evaluating the effect of maropitant versus ondansetron on inhibiting tranexamic acid-evoked emesis.

Diagnosis of primary hyperfibrinolysis and in vitro investigation of the inhibitory effects of tranexamic acid in a group of dogs with sarcomas - A pilot study

In people, the antifibrinolytic drug tranexamic acid reduces bleeding and the need for blood products with both normal and exaggerated fibrinolysis without increasing the number of thromboembolic events. In dogs, in addition to prevention and treatment of bleeding, higher doses of tranexamic acid can be used to induce vomiting. The objective of this study was to evaluate the effect of a high dose of tranexamic acid on the coagulation of healthy Beagle dogs. A prospective trial was conducted in eight healthy Beagles receiving tranexamic acid for a concurrent trial evaluating different antiemetics. Rotational thromboelastometry (ROTEM) analysis (EXTEM, APTEM, FIBTEM, INTEM) was performed before and 30 minutes after intravenous administration of 50 mg/kg tranexamic acid. ROTEM parameters before and after tranexamic acid administration and between EXTEM and APTEM were compared with Wilcoxon matched-pairs signed rank test and data is presented as median (range). After tranexamic acid administration, FIBTEM clotting time became significantly shorter (p=0.03) from 37 s (28-124 s) to 33 s (27-40 s) and INTEM clot formation time significantly decreased (p=0.02) from 82 s (47-132 s) to 60 s (43-107 s). After tranexamic acid APTEM MCF was significantly weaker (p=0.01) with 45 mm (30-63 mm) than EXTEM MCF with 55 mm (43-69 mm) and than APTEM MCF before tranexamic acid with 55 mm (43-69 mm) (p=0.02). All other analysed parameters including maximum lysis did not change after administration of tranexamic acid. The administration of 50 mg/kg intravenous tranexamic acid resulted in small changes in ROTEM profiles without inducing a hypercoagulable clot. In conclusion, tranexamic acid can safely be administered to healthy dogs with normal coagulation profiles. As an additional finding, APTEM parameters measured in the current study do not support the use of this test in dogs

/pdf/effect-of-50-mg-kg-intravenous-tranexamic-acid-on-365yuaii7u.pdf

Effect of 50 mg/kg intravenous tranexamic acid on coagulation assessed by rotational thromboelastometry (ROTEM) in healthy Beagle dogs

OBJECTIVE To assess pharmacokinetics of tranexamic acid (TXA) in dogs and assess antifibrinolytic properties of TXA in canine blood by use of a thromboelastography-based in vitro model of hyperfibrinolysis. ANIMALS 6 healthy adult dogs. PROCEDURES Dogs received each of 4 TXA treatments (10 mg/kg, IV; 20 mg/kg, IV; approx 15 mg/kg, PO; and approx 20 mg/kg, PO) in a randomized crossover-design study. Blood samples were collected at baseline (time 0; immediately prior to drug administration) and predetermined time points afterward for pharmacokinetic analysis and pharmacodynamic (thromboelastography) analysis by use of an in vitro hyperfibrinolysis model. RESULTS Maximum amplitude (MA [representing maximum clot strength]) significantly increased from baseline at all time points for all treatments. The MA was lower at 360 minutes for the 10-mg/kg IV treatment than for other treatments. Percentage of clot lysis 30 minutes after MA was detected was significantly decreased from baseline at all time points for all treatments; at 360 minutes, this value was higher for the 10-mg/kg IV treatment than for other treatments and higher for the 20-mg/kg IV treatment than for the 20-mg/kg PO treatment. Maximum plasma TXA concentrations were dose dependent. At 20 mg/kg, IV, plasma TXA concentrations briefly exceeded concentrations suggested for complete inhibition of fibrinolysis. Oral drug administration resulted in a later peak antifibrinolytic effect than did IV administration. CONCLUSIONS AND CLINICAL RELEVANCE Administration of TXA improved clot strength and decreased fibrinolysis in blood samples from healthy dogs in an in vitro hyperfibrinolysis model. Further research is needed to determine clinical effects of TXA in dogs with hyperfibrinolysis.

Pharmacokinetics of tranexamic acid in healthy dogs and assessment of its antifibrinolytic properties in canine blood.

Inappropriate Secondary Erythrocytosis in a Dog With Renal Sarcoma.

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Pharmacokinetics of tranexamic acid in healthy dogs and assessment of its antifibrinolytic properties in canine blood.

Inappropriate Secondary Erythrocytosis in a Dog With Renal Sarcoma.