Bleeding disorders are either acquired or congenital . The most common congenital bleeding disorders are von Willebrand's disease and hemophilia in dogs and hemophilia in cats.
Clinically, there is a difference in the manifestation of coagulopathy and platelet defects. Coagulopathy tends to have delayed hemorrhage after initial injury and persistent bleeding into deep layers of muscles and joints, whereas with platelet defects bleeding usually occurs immediately after injury and frequently involves blood oozing and seeping into the mucous membrane and skin.
Physical examination may reveal prolonged bleeding of the skin or mucosal surfaces. The history may also indicate excessive bleeding following intravenous catheterization, hematoma after trauma, abnormal bleeding or recurrent spontaneous bleeding during and/or after surgery.
Confirm an abnormal tendency to bleed by conducting laboratory tests.
Abnormal platelet function and numbers can be detected using buccal mucosal bleeding and platelet counts :
a. Normal buccal mucosal bleeding time in dogs and cats is between 2-4 minutes.
b. Normal toe nail bleeding time in dogs and cats is between 2-6 minutes.
c. A normal platelet count in dogs and cats is between 150,000 to 700,000/mm3. Values below 100,000/mm3 are likely to result in prolonged bleeding times.
d. In cats, platelet clumping is a commonly occurring problem regardless of how well the samples are collected. Platelet clumping in cats prevents accurate counts of the platelets and is likely to cause erroneous report by either machine or manually. In dogs, platelet clumping is less of a problem than that observed in cats.
Extrinsic pathway and common pathway defects can be tested by measuring prothrombin time (PT) . Most extrinsic pathway defects are acquired and frequently involve factor VII . This usually results from vitamin K interference or deficiency. Rodenticide toxicity in dogs and cats can also cause significant prolonged PT. Normal PT is between 5 to 7 seconds. A PT longer than 1.5 times normal range together with clinical history of abnormal systemic bleeding rodenticide should be suspected.
Intrinsic and common pathway defects can be tested by measuring APTT (activated partial thromboplastin time ) and ACT (activated clotting time ). However, ACT does not distinguish between platelet deficiency/dysfunction and defect in the appropriate coagulation factors. It may be desirable to measure the concentration of the individual coagulation factors to determine the exact cause and thus determine the most appropriate blood product.
Normal APPT is between 11-20 seconds. An intrinsic pathway defect is usually an inherited disorder with at least one defect existing in factor VIII, IX, XI, or XII.
Thrombin clotting time can be used to test for deficiency or dysfunction of fibrinogen.
Assays detect von Willbrand's (vW) disease and determine the significance as type 1, 2, or 3. Type 1 vW disease is characterized by low plasma vW factor with normal protein structure. Type 2 vW disease is typically associated with a low vW factor concentration and an abnormal protein structure. Type 3 vW disease is a complete vW factor deficiency where the concentration of the factor in plasma is undetectable.
Breed disposition for Type I vW disease is most prevalent in Airedale, Akita, dachshund, Doberman pinscher, German shepherd, golden retriever, greyhound, Irish wolfhound, Manchester terrier, Pembroke Welsh corgi, poodle, mixed breeds, other dog breeds, Himalayan cats. Type 2 vW disease is more prevalent in German shorthaired pointer and German wirehaired pointer. Type 3 vW disease tends to occur in Dutch Kooikerhondje, Scottish terrier, Shetland sheepdog, and mixed breeds.
Hemophilia A is characterized by a deficiency of coagulation factor VIII and hemophilia B is a deficiency of coagulation factor IX in dogs and cats.
The main concern for pre-operative preparation in the bleeding disorder patient is sufficient deficient factors or blood to ensure perioperative hemostasis. Therefore, if at all possible, bleeding disorder patients should be managed before anesthesia and surgery. The management includes removal of the causes of the acquired bleeding disorder, administration of blood or blood product therapy , and adjunctive drugs and fluid therapy . Particular care with intravenous fluid therapy should be taken to avoid exacerbation of the existing problem.
Remove or discontinue the agent(s) causing the drug-induced thrombocytopenia or acquired bleeding disorder, such as aspirin, non-steroidal anti-inflammatory drugs, or rodenticides.
Underlying causes such as uremia, liver dysfunction, neoplasia, sepsis, systemic infection, pyometra, gastric dilatation-volvulus, or intestinal obstruction are likely to induce a bleeding disorder. Intestinal obstruction and biliary stasis or blockage may result in vitamin K deficiency. Liver dysfunction impairs all coagulation factors.
Transfusion of whole blood or blood products (platelets and plasma) supplies the defective patients with functional platelets or with specific plasma factors.
For those patients with active bleeding or for prevention of intra-operative bleeding during a minor or short duration surgery, a single transfusion, of appropriate volume and type, before surgery may be sufficient.
For those patients undergoing a major or prolonged surgery, multiple transfusions beginning before surgery and continuing during surgery through recovery until 1-3 days after surgery are often necessary.
Transfusion of whole blood or blood products is necessary when the packed cell volume (PCV ) is less than 20 percent. Short duration anesthesia has been performed with chronic bleeding disorder patients of PCV less than 20 without significant consequence. However, if a longer duration of anesthesia and surgery are required, a whole blood transfusion is a must. Since not all blood products would be suitable for a patient with abnormally low PCV, it is prudent to consider non-surgical treatment options before performing invasive surgery for further blood loss.
Fresh or frozen plasma can be transfused at 6-12 ml/kg. Alternatively, fresh whole blood can be used instead.
Most dogs (40%) are type A negative and can be considered universal donors. For a single transfusion in a dog that has never received a transfusion, few reactions occur. However, if time allows, typing of the blood and cross matching is strongly advised.
A universal canine blood donor with blood type of DEA-1.1, DEA-1.2 and DEA-7 loci should be used for major blood transfusions in hemorrhagic shock or dogs that have received a blood transfusion in the past. Cross match of the donor red blood cells to recipient's serum (major match) or donor's serum to recipient's red blood cells (minor match) should be performed prior to major surgery to compare donor and recipient control red cells and serum.
Unlike in dogs, cats must be carefully matched before a blood transfusion .
As a general rule, fresh whole blood, packed red blood cells, platelet-rich plasma, fresh or frozen plasma can be administered at a rate of 6-12 ml/kg to treat patients with anemia, low platelets, coagulation factor defects or vW disease.
Plasma cryoprecipitate (1 U per 10 kg) is best for treating patients with hemophilia A, vW disease or fibrinogen deficiency, while cryosupernatent (6-12 ml/kg) is best for treating patients with hemophilia B or other coagulation factor deficiencies.
200 ml fresh frozen plasma produces only 1 U of cryoprecipitate.
In cases of vitamin K deficiency or antagonizing rodenticide toxicity , vitamin K (5 mg/kg) can be given subcutaneously in multiple sites. The therapy should be used together with blood or blood product transfusion for best outcome.
Desmopressin acetate (DDAVP ) is a drug to treat vW disease. DDAVP stimulates releases of vW factors from endothelial stores. The DDAVP is reported to increase 40% of vW factor concentrations in donor dogs (4). DDAVP can be administered via injection or intra-nasal spray at a dose of 1 µg/kg 30-60 minutes before collecting blood from a donor dog for a recipient with vW disease.
DDAVP (1 µg/kg, SC) can be given directly to animals with Type I or Type II vW disease 30 minutes before the surgery to increase the release of endothelial stores of the factors and may shorten the bleeding time.
Avoid placement of jugular venous catheters, arterial catheters, or performing epidural or regional anesthesia techniques (eg brachial plexus block) due to concern of hematoma formation.
Avoid procedures such as thoracocentesis, abdominocentesis or ultrasound guided organ biopsy (eg liver biopsy).
Use cautery, topical tissue adhesive, suture or pressure wraps for local injuries.
Intramuscular injection (IM) is best avoided although some human literature indicates that IM injections can be used safely in hemophilia patients as long as coagulation factors are brought to within normal ranges within 2 hours of the IM injection.
Intubation should be performed with special care to avoid oral and airway trauma and to avoid hematoma formation.
Even a skilled person should use a laryngoscope with blade and well-lubricated endotracheal tube for oral tracheal intubation.
Some practitioners use a slightly smaller endotracheal tube than normal, for a given patient, to minimize trauma during oro-endotracheal intubation.
Avoid face-mask or chamber anesthesia induction to prevent trauma to the lips, tongue, or facial region should a rough induction occur.
Avoid any procedures that tend to cause epistaxis. Nasal placement of the oxygen tubing should be manipulated very carefully to avoid trauma.
Extubation should be performed gently and the endotracheal tube inspected for any signs of blood. Suspicion of airway or oral bleeding should be immediately followed with observation of the oral cavity and airway to rule out significant bleeding, hematoma formation and obstruction of the airway, or aspiration of a blood clot.
Judicious use of anticholinergic agents (atropine or glycopyrrolate ) in brachycephalic breeds may reduce salivation and airway secretions, and therefore, avoid oral or airway suction during the recovery. If suction is necessary, avoid trauma to the oral mucosa and airway with careful manipulation with the aid of light source (eg a laryngoscope) under direct visualization.
Wingfield W E, Van Pelt D (1989) Abnormal bleeding. Vet Clin North Am Small Anim Pract 19, 1275-1286 PubMed.
Johnson C S, Tunentine M A, Krause K H (1988) Canine von Willebrand’s disease. A heterogeneous group of bleeding disorders. Vet Clin North Am Small Anim Pract18, 195.
Angelos M G, Hamliton G C (1986) Coagulation studies: prothrombin time, partial thromboplastin time, bleeding time. Emer Med Clin North Am 4, 95.
Sampson J F, Hamstra R, Aldrete J A (1979) Management of hemophiliac patients undergoing surgical procedures. Anesth Analg 58, 133-135.
Other sources of information
Brooks M (1999) Hereditary bleeding disorders in dogs and cats. Vet Med 555-564.