Page 597 - Cote clinical veterinary advisor dogs and cats 4th

270 Disseminated Intravascular Coagulation

• Any of the following may be apparent: col- ○ Schistocytes, keratocytes, or acanthocytes Drug Interactions
lapse, pallor, tachycardia, tachypnea, petechiae, (fragmented red blood cells) from shred- Avoid heparin, hetastarch, and dextrans, and
VetBooks.ir Etiology and Pathophysiology • Serum biochemistry profile, urinalysis: when coagulation times are prolonged due to
ding by intravascular fibrin strands or
ecchymoses, melena, epistaxis, icterus
platelet inhibitors (e.g., aspirin, clopidogrel)
microangiopathic hemolysis
severe factor and fibrinogen depletion or if there
• Two major pathways initiate DIC
○ Systemic inflammatory response with evidence of underlying disease; effects of is severe thrombocytopenia.
thromboembolism (renal, hepatic)
cytokine and coagulation cascade activa- • Chest and abdominal radiographs or ultra- Possible Complications
tion (e.g., sepsis, polytrauma) sound: evidence of underlying disease and/ • PTE
○ Release of procoagulant stimuli into or thromboembolism, hemorrhage • Thromboembolism (kidney, brain, pelvic
the vascular space initiates widespread • Coagulation testing: prolonged prothrombin limbs, liver, portal vein)
activation of coagulation (e.g., heman- time (PT), and/or prolonged activated partial • Hemorrhage (+/− anemia, hypovolemia)
giosarcoma, mammary carcinoma). thromboplastin times (aPTT), decreased • Organ dysfunction and death
• Systemic fibrin deposition is insufficiently fibrinogen (p. 1325)
balanced by opposing anticoagulant • D-dimer or fibrin/fibrinogen degradation Recommended Monitoring
mechanisms. product (FDP) concentration: typically • Serial platelet counts and coagulation times
○ Antithrombin depletion from consump- increased (pp. 1334 and 1342) every 24-48 hours
tion, degradation, and suppressed synthesis • Antithrombin activity: typically decreased • Monitor organ function and tissue
○ Protein C system: downregulated by (p. 1309) oxygenation.
proinflammatory cytokines • For heparin treatment, monitor for signs
• Fibrinolysis is concomitantly suppressed. Advanced or Confirmatory Testing of hemorrhage, falling platelet count, or
○ High plasminogen activator inhibitor levels • Reduced protein C or protein S activity excessive prolongation of in vitro clotting
impair fibrinolysis. • High concentration of thrombin to anti- time (UFH therapy).
• Subsequent depletion of coagulation factors thrombin complexes • A target prolongation of aPTT to 1.5-2
and prolongation of coagulation times or • A scoring system has been developed for times baseline is evidence of UFH high-dose
clinical hemorrhage dogs (Wiinberg et al., 2010). anticoagulant effect.
• Consumption of platelets and subsequent • Thromboelastrography or thromboelastom- • UFH and low-molecular-weight heparins
thrombocytopenia etry may help diagnose occult or chronic can be monitored by inhibition of factor
• Local thrombosis contributes to acido- DIC or identify hypercoagulability. Xa. In humans, the target range of anti-Xa
sis, ischemia, organ dysfunction, and activity = 0.3-0.7 U/mL (UFH) and for low-
tissue necrosis, which can perpetuate the TREATMENT molecular-weight heparin = 0.5-1.0 U/mL.
syndrome.
Treatment Overview PROGNOSIS & OUTCOME
DIAGNOSIS DIC is a secondary condition arising from a
serious underlying disorder. Treatment involves • Depends on the underlying condition and
Diagnostic Overview control of thromboembolism or hemorrhage extent of thromboembolism or hemorrhage
No single laboratory test is diagnostic for (whichever predominates) and management of • Fulminant or hemorrhagic DIC carries a
DIC. Early diagnosis of the thrombotic the primary disorder. poor to grave prognosis.
phase is especially challenging and requires
an elevated index of suspicion. Nonspecific Acute General Treatment PEARLS & CONSIDERATIONS
physical exam abnormalities (see above), • Always treat the primary condition.
especially together with a documented recent • Support adequate perfusion with intravenous Comments
decrease in platelet count and/or altered fluids as needed. • Laboratory diagnostics are insensitive for
coagulation parameters in a patient with • Oxygen therapy if indicated (pulmonary identifying early DIC.
a recognized risk factor, suggest the pos- disease including PTE) (p. 1146) • Development of DIC contributes to the
sibility of DIC. After clinical hemorrhage • Red blood cell transfusion in anemic patients morbidity and mortality of the primary
occurs, DIC is likely advanced to the overt (p. 1169) disease.
hemorrhagic phase and more difficult to treat • Fresh-frozen plasma (FFP) transfusion if • Treatment is challenging and no gold
effectively. fibrinogen and clotting factor depletion standard approach is known.
causes hemorrhage or if fibrinogen-deficient • Treatment becomes less rewarding late in
Differential Diagnosis patients require surgery (p. 1169). Repeated the disease process.
• Hemorrhagic DIC doses of FFP may be needed (10-15 mL/kg • Having an early suspicion that DIC may
○ Anticoagulant rodenticides IV q 8-12h). develop is important for selecting appropri-
○ Severe primary thrombocytopenia • Heparin should be considered if dyspnea ate diagnostic tests and for monitoring the
○ Inherited or acquired platelet dysfunction from PTE or organ failure from thrombosis patient.
(thrombocytopathia) occurs (p. 842).
○ Dextran or hetastarch administration ○ Regular unfractionated heparin (UFH) Prevention
(prolonged clotting times) 100-200 U/kg SQ q 8h or 15-25 U/kg/h Critical factors in preventing or ameliorating
○ Liver failure IV continuous rate infusion DIC are specific and aggressive corrections of
• Thrombotic DIC: organ failure or pul- ○ Low-molecular-weight heparin: daltepa- the primary disease.
monary thromboembolism (PTE) from rin (Fragmin) 100 IU/kg SQ q 12h or
cardiac disease, heartworm disease, tumor enoxaparin (Lovenox) 1-1.5 mg/kg SQ Technician Tips
emboli, or hypercoagulability associated with q 12h • If DIC is suspected, avoid jugular
antithrombin loss phlebotomy.
Chronic Treatment • When collecting blood samples from very
Initial Database DIC is always secondary, and treatment ill dogs, consider collecting a citrate sample
• CBC, platelet count, blood smear should be directed toward the primary for coagulation testing such as PT, aPTT, or
○ Thrombocytopenia typical condition. D-dimer.

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