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Disseminated intravascular coagulation
Synonym(s): DIC, Consumption coagulopathy
Introduction
- DIC is a thrombohemorrhagic condition; intravascular activation of blood coagulation system concurrently with activation of fibrinolytic system.
- Cause: variety of diseases, eg sepsis, neoplasia, immune mediated diseases (eg IMHA), inflammatory conditions (pancreatitis/trauma/heat stroke).
- Signs: bleeding, coagulopathy, hypovolemic shock.
- Intravascular coagulation results in thrombosis of vessels in many organs → organ failure = consumptive coagulopathy.
- Depleted supply of platelets and coagulation factors results in bleeding disorder/coagulopathy.
- Treatment: removal of underlying cause, maintain tissue perfusion and oxygen delivery to tissues, plasma blood products.
- Prognosis: depends on extent of organ injury, those patients with fulminant bleeding have a poor prognosis.
Print off the owner factsheet Disseminated intravascular coagulation (DIC) to give to your client.
Presenting signs
- Clinical signs vary from asymptomatic to signs of organ failure associated with microvascular thrombosis to fulminant bleeding (overt DIC).
- Signs compatible with thrombosis of organs; tachypnea/dyspnea associated with pulmonary thromboembolism, acute kidney injury, lateralizing neurological signs with cerebrovascular accident Cerebrovascular disease, hemorrhagic diarrhea secondary to mesenteric thrombosis.
- Severe and acute bleeding (petechial and ecchymotic hemorrhages, epistaxis, gingival bleeding, bleeding at venepuncture sites), intracavitatory bleeding, hypovolemic shock, overt clinical bleeding less commonly seen in cats.
- Signs associated with underlying disease, eg pancreatitis, neoplasia, sepsis, immune mediated hemolytic anemia Anemia: immune-mediated hemolytic.
Acute presentation
- Hypovolemic shock Shock: hypovolemic secondary to acute bleeding.
- Spontaneous bleeding.
- Acute kidney injury Kidney: acute renal failure, dyspnea.
- Sudden death.
Special risks
- Surgery: post-operative hemorrhage.
Pathogenesis
Etiology
- Neoplasia, eg lymphoma Lymphoma.
- Infectious diseases, eg bacterial sepsis secondary to panleukopenia Feline panleucopenia virus disease, FeLV associated Feline leukemia virus disease, FIP related vasculitis Feline infectious peritonitis.
- Inflammatory conditions, eg pancreatitis Pancreatitis, sepsis Shock: septic.
- Miscellaneous, eg heat stroke, shock Shock, autoimmune-mediated hemolytic anemia Anemia: immune-mediated hemolytic, post surgical.
Pathophysiology
- Platelets and coagulation cascades activated by various inflammatory, neoplastic and other conditions which result in cell damage and release of tissue thromboplastin or endothelial damage with exposure of collagen.
- Thrombi form in many organs → organ dysfunction/failure.
- Fibrinolytic system activated → increased fibrinogen degradation products (FDPs) in blood. FDPs = potent anticoagulants (by inhibiting platelet function + various factors within clotting cascade).
- Consumption of clotting proteins and platelets → bleeding tendency.
- Concurrent coagulopathy and thrombotic disease.
- Damage to endothelial surfaces or antigen-antibody complexes: damaged necrotic cells → release tissue thromboplastin → activate extrinsic pathway → platelet aggregation and activation of intrinsic pathway.
- Inflammatory/infectious/neoplastic disease → create areas of necrosis and exposed collagen → stimulates clotting.
- Clotting → formation of thrombi in capillaries, arterioles and venules in many organs → severe circulatory and respiratory insufficiency, neurological disturbances, renal failure, gastrointestinal problems, liver damage.
- Activated fibrinolytic system → fibrin dissolved → fibrin degradation products released into blood.
- Activated clotting and fibrinolytic systems → interact with kallikrein-kinin system → vasomotor disturbance → shock.
- Consumption of platelets and clotting factors → bleeding tendency.
Timecourse
- Acute form: 1-5 days.
- Chronic form: days to weeks.
Diagnosis
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Treatment
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Prevention
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Outcomes
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Further Reading
Publications
Refereed papers
- Recent references from PubMed and VetMedResource.
- Goggs R, Mastrocco A, Brooks M B (2018) Retrospective evaluation of 4 methods for outcome prediction in overt disseminated intravascular coagulation in dogs (2009-2014): 804 cases. J Vet Emerg Crit Care (San Antonio) 28(6), 541-550 PubMed.
- Bruchim Y, Aroch I, Saragusty J, Waner T (2008) Disseminated intravascular coagulation. Compend Contin Educ Vet 30(10), E3 PubMed.
- Estrin M A, Wehausen C E, Jessen C R et al (2006) Disseminated intravascular coagulation in cats. J Vet Intern Med 20 (6), 1334-1339 PubMed.
- O'Keefe D A & Couto C G (1988) Coagulation abnormalities associated with neoplasia. Vet Clin North Am Small Anim Pract 18 (1), 157-168 PubMed.
- Slappendel R J (1988) Disseminated intravascular coagulation. Vet Clin North Am Small Anim Prac 18 (1), 169-184 PubMed.
- Thomas J S & Green R A (1988) Clotting times and antithrombin III activity in cats with naturally developing diseases: 85 cases (1984-1994). JAVMA 213 (9), 1290-1295 PubMed.
Other sources of information
- Rudloff E & Kirby R (2009) Disseminated Intravascular Coagulation: Diagnosis and Management. In: Kirks' Current Veterinary Therapy XIV. Bonagura J C & Twedt D C (eds), Philadelphia: W B Saunders. pp 287-291.