Coagulopathy

Coagulopathy (also called a bleeding disorder) is a condition in which the blood's ability to coagulate (form clots) 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]}

Coagulopathy
Other names	Bleeding disorder
Platelets
Specialty	Hematology

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 or thrombophilia.

External Research:

- Hematologic and coagulopathy parameter as a survival predictor among moderate to severe COVID-19 patients in non- ICU ward: a single-center study at the main referral hospital in Surabaya, East Java, Indonesia

Signs and symptoms

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 or stool, double vision, severe head or neck pain, repeated vomiting, 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]}

Mechanism

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 as hemophilia and Von Willebrand disease, can cause a reduction in clotting factors.^[2]

Anticoagulants such as warfarin will also prevent clots from forming properly.^[2] Coagulopathy may also occur as a result of dysfunction or reduced levels of platelets (small disk-shaped bodies in the bloodstream that aid in the clotting process).

Acute traumatic coagulopathy

In 2003, Karim Brohi, Professor of Trauma Sciences at Queen Mary University of London, first introduced the term Acute Traumatic Coagulopathy (ATC),^[3] establishing that coagulopathy induced by trauma results in:

• more severe bleeding
• multi-organ failure
• high mortality

Treatment

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]}

Critical care

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]}

• Blood plasma
• Prothrombin complex concentrate, factor XIII, and fibrinogen
• Fibrinogen with tranexamic acid

The use of tranexamic 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-related acute lung injury, acute respiratory distress syndrome, multiple organ dysfunction syndrome, major hemorrhage, and venous thromboembolism.^{[citation needed]}

Laboratory findings in various platelet and coagulation disorders^{[citation needed]}

Condition	Prothrombin time	Partial thromboplastin time	Bleeding time	Platelet count
Vitamin K deficiency or warfarin	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 in amyloid 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

See also

• Trauma triad of death
• Hypocoagulability
• Hypercoagulability

References

1. Hunt BJ (February 2014). "Bleeding and coagulopathies in critical care". The New England Journal of Medicine. 370 (9): 847–859. doi:10.1056/NEJMra1208626. PMID 24571757.
2. Spahn DR, Bouillon B, Cerny V, Coats TJ, Duranteau J, Fernández-Mondéjar E, et al. (April 2013). "Management of bleeding and coagulopathy following major trauma: an updated European guideline". Critical Care. 17 (2): R76. doi:10.1186/cc12685. PMC 4056078. PMID 23601765.
3. Brohi K, Singh J, Heron M, Coats T (June 2003). "Acute traumatic coagulopathy". The Journal of Trauma. 54 (6): 1127–1130. doi:10.1097/01.TA.0000069184.82147.06. PMID 12813333. S2CID 7583542.
4. Shakur H, Roberts I, Perel P (2010). "Tranexamic acid for trauma – Authors' reply". The Lancet. 376 (9746): 1050–1051. doi:10.1016/S0140-6736(10)61479-1. ISSN 0140-6736. S2CID 54321951.