Coagulopathy | |
---|---|
Other names | Bleeding disorder |
Platelets | |
Specialty | Hematology ![]() |
Coagulopathy (also called ableeding disorder) is a condition in which the blood's ability tocoagulate (formclots) is impaired.[1] This condition can cause a tendency toward prolonged or excessive bleeding (bleeding diathesis), which may occur spontaneously or following an injury or medical and dental procedures.[citation needed]
Coagulopathies are sometimes erroneously referred to as "clotting disorders", but a clotting disorder is the opposite, defined as a predisposition to excessive clot formation (thrombus), also known as a hypercoagulable state orthrombophilia.
Coagulopathy may cause uncontrolled internal or external bleeding. Left untreated, uncontrolled bleeding may cause damage to joints, muscles, or internal organs and may be life-threatening. People should seek immediate medical care for serious symptoms, including heavy external bleeding,blood in the urine orstool,double vision, severe head or neck pain, repeatedvomiting, difficulty walking, convulsions, or seizures. They should seek prompt medical care if they experience mild but unstoppable external bleeding or joint swelling and stiffness.[citation needed]
The normal clotting process depends on the interplay of various proteins in the blood. Coagulopathy may be caused by reduced levels or absence of blood-clotting proteins, known as clotting factors or coagulation factors.Genetic disorders, such ashemophilia andVon Willebrand disease, can cause a reduction in clotting factors.[2]
Anticoagulants such aswarfarin will also prevent clots from forming properly.[2] Coagulopathy may also occur as a result of dysfunction or reduced levels ofplatelets (small disk-shaped bodies in the bloodstream that aid in the clotting process).
In 2003, Karim Brohi, Professor ofTrauma Sciences atQueen Mary University of London, first introduced the term Acute Traumatic Coagulopathy (ATC),[3] establishing that coagulopathy induced by trauma results in:
If someone has coagulopathy, their health care provider may help them manage their symptoms with medications or replacement therapy. In replacement therapy, the reduced or absent clotting factors are replaced with proteins derived from human blood or created in the laboratory. This therapy may be given either to treat bleeding that has already begun or to prevent bleeding from occurring.[citation needed]
One area of treatment is managing people with major bleeding in a critical setting, like an emergency department.[1] In these situations, the common treatment is transfusing a combination of red cells with one of the following options:[citation needed]
The use oftranexamic acid is the only option that is currently supported by a large, randomized, controlled clinical trial, and is given to people with major bleeding after trauma.[4] There are several possible risks to treating coagulopathies, such as transfusion-relatedacute lung injury,acute respiratory distress syndrome,multiple organ dysfunction syndrome, majorhemorrhage, andvenous thromboembolism.[citation needed]
Condition | Prothrombin time | Partial thromboplastin time | Bleeding time | Platelet count |
---|---|---|---|---|
Vitamin K deficiency orwarfarin | Prolonged | Normal or mildly prolonged | Unaffected | Unaffected |
Disseminated intravascular coagulation | Prolonged | Prolonged | Prolonged | Decreased |
Von Willebrand disease | Unaffected | Prolonged or unaffected | Prolonged | Unaffected |
Hemophilia | Unaffected | Prolonged | Unaffected | Unaffected |
Aspirin | Unaffected | Unaffected | Prolonged | Unaffected |
Thrombocytopenia | Unaffected | Unaffected | Prolonged | Decreased |
Liver failure, early | Prolonged | Unaffected | Unaffected | Unaffected |
Liver failure, end-stage | Prolonged | Prolonged | Prolonged | Decreased |
Uremia | Unaffected | Unaffected | Prolonged | Unaffected |
Congenital afibrinogenemia | Prolonged | Prolonged | Prolonged | Unaffected |
Factor V deficiency | Prolonged | Prolonged | Unaffected | Unaffected |
Factor X deficiency as seen inamyloid purpura | Prolonged | Prolonged | Unaffected | Unaffected |
Glanzmann's thrombasthenia | Unaffected | Unaffected | Prolonged | Unaffected |
Bernard–Soulier syndrome | Unaffected | Unaffected | Prolonged | Decreased or unaffected |
Factor XI deficiency | Unaffected | Prolonged | Unaffected | Unaffected |
C1INH deficiency | Unaffected | Shortened | Unaffected | Unaffected |