Page 1432 - Small Animal Internal Medicine, 6th Edition

1404 PART XIII Hematology

Sodium heparin is given in a wide range of doses. Follow- tapered gradually, over 1 to 3 days, to prevent rebound
ing are the four traditional dose ranges: hypercoagulability, a phenomenon commonly observed
VetBooks.ir • Minidose: 5 to 10 IU/kg SC q8h in humans.
Aspirin and other antiplatelet agents can also be given to
• Low dose: 50 to 100 IU/kg SC q8h
ulation. Doses of 0.5 to 10 mg/kg of aspirin given orally
• Intermediate dose: 300 to 500 IU/kg, SC or IV, q8h prevent platelet activation and thus halt intravascular coag-
• High dose: 750 to 1000 IU/kg, SC or IV, q8h every 12 hours in dogs and every third day in cats have
been recommended, although in my experience aspirin is
I use low-dose heparin in combination with the trans- rarely of clinical benefit. If it is used, the patient should be
fusion of blood or blood components. The rationale is closely watched for severe GI tract bleeding, because this
that this dose of heparin does not prolong the ACT or NSAID can cause gastroduodenal ulceration, which could
aPTT in normal dogs (a minimum of 150-250 IU/kg q8h be catastrophic in a dog with a severe coagulopathy such
is required to prolong the aPTT in normal dogs), and it as DIC.
appears to be biologically active in these animals, given that
some of the clinical signs and hemostatic abnormalities are Maintaining Good Parenchymal
reversed in animals receiving this dosage. The fact that it Organ Perfusion
does not prolong the aPTT or ACT is extremely helpful in Good parenchymal organ perfusion is best achieved with
dogs with DIC. For example, if a dog with DIC is receiving aggressive fluid therapy consisting of crystalloids or plasma
intermediate-dose heparin, it is impossible to predict, on expanders such as dextran (see Table 87.6). The purpose of
the basis of hemostatic parameters, whether a prolongation this therapy is to dilute out the clotting and fibrinolytic
of the aPTT is caused by excessive heparin administration factors in the circulation, flush out microthrombi from the
or progression of this syndrome. As laboratory tests for the microcirculation, and maintain the precapillary arterioles
determination of heparin levels become widely available, this patent so that blood is shunted to areas in which oxygen
may become a moot point. Until then, my clinical impres- exchange is efficient. However, care should be taken not to
sion is that if an animal with DIC receiving minidose or overhydrate an animal with compromised renal or pulmo-
low-dose heparin shows a prolonged ACT or aPTT, the intra- nary function.
vascular coagulation is deteriorating and a treatment change
is necessary. The use of low-molecular-weight heparin in Preventing Secondary Complications
dogs with DIC has been investigated. In an experimental As noted, numerous complications occur in dogs with DIC.
model of DIC in Beagles, high doses of low-molecular- Attention should be directed toward maintaining oxygen-
weight heparin resulted in resolution of the clinicopatho- ation by oxygen mask, cage, or nasopharyngeal catheter,
logic abnormalities associated with DIC (Mischke et al., correcting acidosis, eliminating cardiac arrhythmias, and
2005). preventing secondary bacterial infections. The ischemic GI
I recently used cryoprecipitate infusions to treat five dogs mucosa no longer functions as an effective barrier to micro-
with DIC successfully; three had hemangiosarcoma and two organisms, bacteria are absorbed and cannot be cleared
had gastric dilation-volvulus (GDV). Lepirudin, a novel by the hepatic mononuclear-phagocytic system, and sepsis
leech recombinant AT, has proved beneficial in preventing occurs.
MOF in an experimental model of sepsis with enteric organ-
isms in Greyhounds. However, this treatment is currently Prognosis
cost-prohibitive. The prognosis for dogs and cats with DIC is still grave. De-
If evidence of severe microthrombosis is present (e.g., spite the numerous acronyms for DIC coined over the past
marked azotemia, lactic acidosis, increase in liver enzyme few decades (e.g., “death is coming,” “dead in cage,” “dog
levels, multifocal ventricular premature contractions), in cooler”), most patients recover with appropriate treat-
dyspnea, or hypoxemia, intermediate- or high-dose heparin ment if the inciting cause can be controlled. In the retro-
can be used, with the goal of prolonging the ACT to 2 to spective study of DIC in dogs conducted at OSU-VTH,
2.5 times the baseline value, or normal if the baseline time the mortality rate was 54%; however, the mortality rate in
was already prolonged. TEG can also be used to monitor dogs with minor changes in the hemostasis screen (fewer
heparinization. If overheparinization occurs, protamine than three abnormalities) was 37%, whereas in dogs with
sulfate can be administered by slow intravenous infusion severe hemostatic abnormalities (more than three hemo-
(1 mg for each 100 IU of the last dose of heparin; 50% of static abnormalities) it was 74%. In addition, marked pro-
the calculated dose is given 1 hour after the heparin and longation of the aPTT and marked thrombocytopenia
25% 2 hours after the heparin). The remainder of the dose were negative prognostic factors. The median aPTT in
can be administered if clinically indicated. Protamine dogs that survived was 46% over the controls, whereas it
sulfate should be administered with caution because it was 93% over the controls in dogs that did not survive.
can be associated with acute anaphylaxis in dogs. Once Similarly, the median platelet count in dogs that survived
improvement in the clinical and clinicopathologic param- was 110,000/µL, and in dogs that did not survive it was
eters has been achieved, the heparin dose should be 52,000/µL.