Page 1428 - Small Animal Internal Medicine, 6th Edition

1400 PART XIII Hematology

Carriers of the defect may be asymptomatic but usually thrombocytopenia is present (70,000-125,000/µL), which is
have prolonged clotting times in vitro. Certain factor defi- likely caused by an excessive consumption of platelets from
VetBooks.ir ciencies (so-called contact factors), including factors XII and protracted bleeding.
These animals usually require immediate transfusions of
XI, Fletcher factor (prekallikrein), and HMWK, are also
found in otherwise asymptomatic animals (i.e., no excessive
tion factors (and packed RBCs if the animal is anemic). It
bleeding) with a markedly prolonged aPTT. However, WFB or FFP (or cryopoor plasma) to replenish the coagula-
massive and often life-threatening postoperative bleeding may take 8 to 12 hours before vitamin K therapy appreciably
starting 24 to 36 hours after surgery is common in dogs with shortens the OSPT and subsequently decreases bleeding.
factor XI deficiency. Vitamin K is available in several forms, but vitamin K 1 is
Most dogs and cats with congenital coagulopathies are the most effective. It is available for oral or parenteral use.
treated with supportive and transfusion therapies; no other Intravenous administration of vitamin K is not recom-
treatments appear to be beneficial, but anecdotally, amino- mended because of the risk of anaphylactic reactions or
caproic acid may help control bleeding. There is ongoing Heinz body formation; intramuscular injections in a dog
research on gene therapy in canine models of hemophilia with a coagulopathy usually result in hematoma formation.
and other inherited coagulopathies. As with animals with Subcutaneous administration of vitamin K 1 with a 25-gauge
other congenital defects, dogs and cats with coagulopathies needle (loading dose 5 mg/kg, followed in 8 hours by 2.5 mg/
should not be bred. kg subcutaneously [SC] q8h) is preferred if the patient is
properly hydrated. Administration of oral loading doses of
VITAMIN K DEFICIENCY vitamin K 1 has been advocated for the treatment of dogs with
Vitamin K deficiency in small animals usually results from rodenticide poisoning (5 mg/kg with a fatty meal, then
the ingestion of vitamin K antagonists (e.g., warfarin, 2.5 mg/kg q8-12h); this is my preferred treatment. Because
diphacinone, brodifacoum, bromadiolone), although it can vitamin K is lipid-soluble, its absorption is enhanced if given
also occur as a consequence of malabsorption in dogs and with fatty meals. Animals with cholestatic or malabsorptive
cats with obstructive cholestasis, infiltrative bowel disease, syndromes may require continued subcutaneous injections
or liver disease. Four clotting factors are vitamin K– of vitamin K. In critical cases the OSPT should be monitored
dependent: factors II, VII, IX, and X. Proteins C and S, two every 8 hours until it normalizes.
natural anticoagulants, are also vitamin K–dependent. If the anticoagulant is known to be warfarin or another
Because of its clinical relevance, the following discussion first-generation hydroxycoumarin, 1 week of oral vitamin K 1
focuses only on rodenticide poisoning, which is relatively is usually sufficient to reverse the coagulopathy. However, if
common in dogs and extremely rare in cats. it is indanedione or any of the second- or third-generation
Most dogs with toxicity are evaluated because of acute anticoagulants, oral vitamin K 1 therapy must be maintained
collapse and a possible history of rodenticide ingestion. for at least 3 weeks and possibly as long as 6 weeks. Most
Coughing, thoracic pain, and dyspnea are also common. currently available rodenticides contain second- and third-
These dogs usually have clinical signs compatible with sec- generation anticoagulants. If the rodenticide ingested is
ondary bleeding, such as hematomas and bleeding into body unknown, the animal should be treated for 1 week, at which
cavities. The most common site of bleeding in dogs evaluated time vitamin K treatment is discontinued. An OSPT is then
at our clinic is the thorax; some dogs have superficial skin determined within 24 to 48 hours of the last dose. If the
bruising in areas of friction, such as the axilla or groin. Other OSPT is prolonged, therapy should be reinstituted and main-
abnormalities include pale mucous membranes, anemia tained for 2 more weeks and the OSPT reevaluated at the end
(usually regenerative if sufficient time has elapsed since the of this period.
acute bleeding episode), and hypoproteinemia. Sudden
death may occur as a result of central nervous system or
pericardial hemorrhage. MIXED (COMBINED) HEMOSTATIC
If the rodenticide has been ingested minutes to hours DEFECTS
before presentation, induced vomiting and the administra-
tion of activated charcoal may eliminate or neutralize most DISSEMINATED INTRAVASCULAR
of it. If the ingestion is questionable and no clinical signs of COAGULATION
coagulopathy are present (e.g., hemothorax, hemoabdomen, DIC, previously called consumptive coagulopathy or defibri-
bruising), determination of the OSPT is recommended. nation syndrome, is a complex syndrome in which excessive
Because factor VII is the shortest lived vitamin K–dependent intravascular coagulation leads to multiple-organ micro-
protein (circulating half-life, 4-6 hours), the OSPT is usually thrombosis (multiple organ failure [MOF]) and paradoxic
prolonged before spontaneous bleeding becomes evident. bleeding caused by the inactivation or excessive consump-
The typical hemostasis screen in a dog with symptomatic tion of platelets and clotting factors as a result of enhanced
vitamin K deficiency reveals marked prolongation of the fibrinolysis. DIC is not a specific disorder but rather a
OSPT and aPTT; this is one of the few clinical situations in common pathway in a variety of disorders. Moreover, DIC
which the OSPT is typically longer than the aPTT. The FDP constitutes a dynamic phenomenon in which the patient’s
test is positive in more than half of affected dogs and mild status and the results of coagulation tests change markedly,