Disseminated intravascular coagulation, commonly called DIC, is a common complication seen in emergency room (ER) or intensive care unit (ICU) pets. Patients don’t develop DIC as a primary cause. With DIC, the body is unable to clot normally.
Normally, the body’s ability to clot is complex and involves multiple stages: tissue factor, platelets, clotting factors, fibrin, and components that break down fibrin. With DIC, abnormal clotting typically results in either abnormally fast clotting (called hypercoagulablity) – where the body is predisposed to throwing microscopic blood clots, or abnormally delayed clotting (called hypocoagulablity) – where the body loses the ability to clot and uncontrollable, life-threatening bleeding may be seen.
There are several primary causes that can predispose the body to this blood clotting disorder:
- Cancer (e.g., hemangiosarcoma, etc.)
- Heat stroke
- Sepsis (abnormal bacteria entering the blood stream secondary to a severe infection)
- Septic peritonitis (secondary to abnormal bacteria in the abdomen, typically due to the intestines rupturing)
- Heartworm disease (which is why it’s so important to keep your dog on year-round heartworm medication)
- Gastric dilatation-volvulus (GDV)
- Immune-mediated diseases such as immune-mediated hemolytic anemia (IMHA) or immune-mediated thrombocytopenia (ITP)
- Snake bites
- Severe hemorrhage
Clinical signs of DIC include the following:
- Bleeding from the nose
- Blood in the eye
- Small pin-point bruising of the skin (called petechiae)
- Larger bruises (called ecchymosis)
- Increased heart rate
- Difficulty breathing
- Increased respiratory rate
- Abnormal bleeding from any orifice
Keep in mind that other clinical signs may be seen due to the primary disease. For more information on each specific disease (e.g., gastric-dilatation volvulus) please see the appropriate handout or blog on Our Site.
The diagnosis of DIC is based on a clotting test (typically called a “coagulation panel.”) There are several different types of clotting tests available to veterinarians, some being more complete and extensive than others. When testing for DIC, typically, three of these abnormal blood tests need to be run before the blood clotting disorder can be “defined” as DIC. Classically, it’s a low platelet count and prolonged prothrombin time (PT) and activated partial thromboplastin time (aPTT).
Types of blood clotting tests include the following:
- A platelet count: This test often comes with a complete blood count (CBC – see below). Normal platelet count ranges from approximately 200,000-300,000/µl. With DIC, the platelet count is always decreased below the normal range.
- A coagulation panel: This test often includes the prothrombin time (PT), activated partial thromboplastin time (aPTT), fibrinogen, and fibrin split products (FSP/fibrin) degradation products (FDP). With DIC, the PT and PTT are typically prolonged (i.e., elevated), while the fibrinogen levels are low. The FSP and FDP levels are typically elevated.
- D-dimers: D-dimers test for the presence of breakdown products of crosslinked fibrin. This is not a typical test that veterinarians have readily available.
Some other key diagnostic blood clotting disorder tests that need to be performed typically include the following:
- A CBC which looks at the red blood cell count, white blood cell count, and platelet count
- A biochemistry panel to assess kidney and liver function, protein, and electrolytes
- Chest and abdominal x-rays to look for presence of cancer or underlying disease
- Abdominal ultrasound to look at the architecture inside of the organs
- A urinalysis to rule out underlying infection, kidney function, etc.
Unfortunately, there’s no cure or specific treatment for DIC, aside from fixing the underlying primary problem (e.g., surgery for a GDV). If severe clotting problems are noted, a fresh frozen plasma transfusion can be given to help provide clotting factors to a patient. Likewise, aggressive intravenous (IV) fluids may be necessary to help hydrate the patient. Symptomatic supportive care typically includes hospitalization at a 24/7 facility for oxygen therapy, IV fluid therapy, blood pressure, and electrocardiogram monitoring. Frequent monitoring of the patient along with clotting tests, red blood cell count, and platelet count rechecks should be performed.
With aggressive care, the primary disease may be treatable, as long as the secondary side effects of DIC don’t result in life-threatening clotting abnormalities. Remember that with any disease or medical problem the sooner it is diagnosed, the sooner it can be treated.
If you have any questions or concerns, you should always visit or call your veterinarian – they are your best resource to ensure the health and well-being of your pets.
Causes of DIC in Dogs
DIC occurs secondarily to some other major problem in the body. In fact, DIC is common during the final stages of a variety of fatal conditions. Some of the conditions during which DIC is commonly seen in dogs are:
- Crushing injuries
- Splenic torsion
- Heartworm disease
- End-stage liver disease
- Immune-mediated hemolytic anemia
- Immune-mediated thrombocytopenia
Research for Your Health
The NHLBI is part of the U.S. Department of Health and Human Services’ National Institutes of Health (NIH)—the Nation’s biomedical research agency that makes important scientific discovery to improve health and save lives. We are committed to advancing science and translating discoveries into clinical practice to promote the prevention and treatment of heart, lung, blood, and sleep disorders, including DIC. Learn about the current and future NHLBI efforts to improve health through research and scientific discovery.
Learn about the following ways the NHLBI continues to translate current research into improved health for people who have DIC. Research on this topic is part of the NHLBI’s broader commitment to advancing blood disorders and blood safety scientific discovery.
- Helping understand the biology of DIC. NHLBI-supported studies laid the groundwork for understanding DIC, which was critical for later studies on treatments for the condition. For example, studies in the 1980s determined that the clotting factor protein C, which prevents clots, is activated in DIC and plays a major role in controlling the disease. Having low levels of protein C, such as from gene mutations, makes people more likely to develop DIC if they have a bacterial infection it also is linked to poor health outcomes.
- Studying underlying factors in severe trauma cases. The Trans-Agency Research Consortium for Trauma-Induced Coagulopathy (TACTIC) research program was a partnership between the NHLBI and the Department of Defense to study the disruptions in the normal process of blood clotting that occur in people who experience severe trauma.
- Accelerating translation of discoveries into innovative approaches. The Vascular Interventions/Innovations and Therapeutic Advances (VITA) Program is a translational program that supports and accelerates early-stage development of promising diagnostics and treatments. The VITA Program seeks to address unmet clinical needs for vascular diseases, particularly in underserved medical communities.
- The NHLBI Research Workshop on Implementation Science in Critical Care. The NHLBI convened a workshop in 2016 to discuss opportunities and needs for implementation science research in critical care. The workshop covered critical illnesses including sepsis, a leading cause of DIC. Learn more about the workshop on implementation research in critical care.
In support of our mission, we are committed to advancing research into vascular diseases and clotting disorders, including disseminated intravascular coagulation, in part through the following ways:
- We perform research. Our Division of Intramural Research, which includes investigators from our Cardiovascular Branch, performs research on diseases such as DIC that affect the cardiovascular system, blood clotting, and blood vessels.
- We fund research. The research we fund today will help improve future health. Our Division of Cardiovascular Sciences and Division of Blood Disorders and Resources oversee much of the research we fund on vascular diseases and blood disorders. Search the NIH RePORTer to learn about research that we are funding on vascular diseases and clotting disorders.
- We stimulate high-impact research. The NHLBI Strategic Vision highlights ways we may support research over the next decade.
Learn about exciting research areas the NHLBI is exploring about DIC.
In a severe deficiency or functional defect of coagulation proteins, clinical signs appear at an early age. Marked reductions in activity of coagulation proteins essential to hemostasis are usually fatal. Animals may be stillborn if there is aminocaproic acid is effective to prevent or stop bleeding in affected dogs.
Liver Disease in Animals
Most coagulation proteins are produced primarily in the liver. Therefore, liver disease characterized by necrosis, inflammation, neoplasia, or cirrhosis often is associated with decreased production of coagulation proteins, anticoagulants, and fibrinolytic proteins. Because the various coagulation proteins have a relatively short half-life (4 hours to 2 days), mild to marked deficiencies can result in secondary to severe hepatopathies. The APTT and/or PT are prolonged in 50%–85% of dogs with severe liver disease, meaning that the factor activity is
Vitamin K Deficiency in Animals
Vitamin K is solubilized in mixed micelles before passive diffusion across the brush border. Fat malabsorption associated with inadequate amounts of bile salts (eg, biliary obstruction), lymphangiectasia, or severe villous atrophy may result in vitamin deficiency and coagulopathy owing to the lack of production of the functional vitamin K−dependent Factors II, VII, IX, and X.
Ingestion of Anticoagulant Rodenticides by Animals
Ingestion of certain rodenticides by dogs and cats causes a coagulopathy owing to the lack of production of functional vitamin K−dependent factors. Inactive precursor coagulation Factors II, VII, IX, and X are still produced by the liver, but γ-carboxylation of the inactive precursors does not occur, because the rodenticide inhibits the epoxide-reductase enzyme required for recycling of active vitamin K. There are two general classes of anticoagulant rodenticides: the coumarin compounds ( warfarin , coumafuryl, brodifacoum, and bromadiolone) and the indanedione compounds (diphacinone, pindone, valone, and chlorophacinone). The anticoagulant rodenticides are further divided into first- and second-generation based on their toxicity and half-life. In general, the half-life of the coumarins (up to 55 hours) is much shorter than that of the indanedione compounds (15–20 days). Various concurrently administered drugs and coexisting disease may exacerbate the toxicity of the ingested anticoagulant.
Affected animals may have bruising or hematoma formation over pressure points or in the nasopharynx after minor trauma from ingested hard or sharp particles. Bleeding into body cavities may occur, resulting in acute collapse. Often, the animals do not bleed within the first 24 hours after ingestion of the toxin. The APTT, PT, and ACT are usually prolonged. Factor VII has the shortest half-life of the vitamin K−dependent coagulation proteins therefore, the PT is often abnormal before other tests and can be used to monitor response to treatment. With acute ingestion, emetics, absorbents, and cathartics are used to minimize absorption. Vitamin K therapy is often initiated even in asymptomatic animals.
Vitamin K1, 2.5–3 mg/kg SC, is recommended for initial treatment of coumarin toxicity, followed by 1.25–2.5 mg/kg, PO, twice daily for 4–6 days, followed by measurement of PT 48 hours later. For other longer-lasting anticoagulants, treatment should be continued for another 14–30 days depending on the specific anticoagulant, if known.. The PT is repeated after treatment, and vitamin K can be stopped when it is normal. IV administration of vitamin K1 is not recommended, because anaphylactic reactions can result. Administration of vitamin K3 is not useful.
Disseminated Intravascular Coagulation (DIC) in Animals
Disseminated intravascular coagulation (DIC) is not a primary disease but occurs secondary to numerous underlying diseases, such as bacterial, viral, rickettsial, protozoal, or parasitic diseases heat stroke burns neoplasia or severe trauma. The underlying disease causes an uncontrolled systemic inflammatory response characterized by massive activation and consumption of coagulation proteins, endogenous inhibitors, fibrinolytic proteins, and platelets.
In the initial stage of DIC, the animal is hypercoagulable because of circulating inflammatory mediators that cause activation of hemostasis through increased exposure of TF and inhibitor consumption. With time, consumption of coagulation factors may lead to a hypocoagulable state with overt bleeding. Because of the progressive nature of DIC, the clinical findings vary considerably and range from no overt signs of disease, accompanied by no or perhaps only subtle changes in traditional hemostasis parameters (APTT, PT, d -dimer, fibrinogen, and platelet count), to clinical signs of organ failure, associated with microvascular thrombosis in vital organs, finally culminating in overt bleeding. The latter presentation is traditionally thought of as the characteristic DIC patient, in which there are also pronounced alterations in hemostasis parameters and a drop in the platelet count.
Thromboelastography can differentiate the stage of DIC in dogs. Dogs diagnosed in the hypercoagulable stage have a much better chance of survival than dogs diagnosed in the hypocoagulable stage. This is likely because of early and aggressive intervention through supportive and/or antithrombotic therapy while the underlying disease is treated. Aggressive treatment likely minimizes thromboembolic complications and delays or even prevents progression to overt signs.
In veterinary medicine, the laboratory diagnosis of DIC is not standardized, and the hemostatic function tests used are not consistent, but DIC is often diagnosed based on three or more abnormal hemostatic parameters such as APTT, PT, fibrinogen, d -dimer, platelet count, and RBC morphology, along with a predisposing disease. The increasing availability of thromboelastography has made definitive diagnosis possible. Postmortem fibrinolysis makes necropsy an insensitive diagnostic criterion.
Therapy first must be directed to diagnosing and treating the underlying disease. In addition, if the patient is hypercoagulable, heparin would be indicated. If hypocoagulability and bleeding are present, heparin is no longer indicated instead, fresh frozen plasma should be given. Supportive care with fluids and possible plasma expanders helps maintain effective circulating volume.
Animals with clotting factor abnormalities are likely to develop hematomas or bleed into body cavities or joints.
Significant inherited factor abnormalities often become evident at teething or after surgery.
Treatment of anticoagulant rodenticide toxicity may require 4–6 weeks of treatment with vitamin K1.
DIC is always secondary to another condition, and treatment must address that as well as the coagulopathy.
When you are injured, proteins in the blood that form blood clots travel to the injury site to help stop bleeding. If these proteins become abnormally active throughout the body, you could develop DIC. The underlying cause is usually due to inflammation, infection, or cancer.
In some cases of DIC, small blood clots form in the blood vessels. Some of these clots can clog the vessels and cut off the normal blood supply to organs such as the liver, brain, or kidneys. Lack of blood flow can damage and cause major injury to the organs.
In other cases of DIC, the clotting proteins in your blood are consumed. When this happens, you may have a high risk of serious bleeding, even from a minor injury or without injury. You may also have bleeding that starts spontaneously (on its own). The disease can also cause your healthy red blood cells to fragment and break up when they travel through the small vessels that are filled with clots.
Risk factors for DIC include:
- Blood transfusion reaction
- Cancer, especially certain types of leukemia
- Inflammation of the pancreas (pancreatitis)
- Infection in the blood, especially by bacteria or fungus
- Liver disease
- Pregnancy complications (such as placenta that is left behind after delivery)
- Recent surgery or anesthesia
- Severe tissue injury (as in burns and head injury)
- Large hemangioma (a blood vessel that is not formed properly)