Hemostasis Explained

In biology, hemostasis or haemostasis is a process to prevent and stop bleeding, meaning to keep blood within a damaged blood vessel (the opposite of hemostasis is hemorrhage). It is the first stage of wound healing. Hemostasis involves three major steps:

Coagulation, the changing of blood from a liquid to a gel which forms the fibrin clots, is essential to hemostasis. Intact blood vessels moderate blood's tendency to form clots. The endothelial cells of intact vessels prevent blood clotting with a heparin-like molecule and thrombomodulin, and prevent platelet aggregation with nitric oxide and prostacyclin. When endothelium of a blood vessel is damaged, the endothelial cells stop secretion of coagulation and aggregation inhibitors and instead secrete von Willebrand factor, which initiates the maintenance of hemostasis after injury. These processes seal the injury or hole until tissues are healed.

Etymology and pronunciation

The word hemostasis (sometimes) uses the combining forms and, Neo-Latin from Ancient Greek Greek, Ancient (to 1453);: αἱμο- Greek, Ancient (to 1453);: haimo- (similar to Greek, Ancient (to 1453);: αἷμα Greek, Ancient (to 1453);: haîma), meaning "blood", and Greek, Ancient (to 1453);: στάσις Greek, Ancient (to 1453);: stásis, meaning "stasis", yielding "motionlessness or stopping of blood".

Steps of mechanism

Hemostasis occurs when blood is present outside of the body or blood vessels. It is the innate response for the body to stop bleeding and loss of blood. During hemostasis three steps occur in a rapid sequence. Vascular spasm is the first response as the blood vessels constrict to allow less blood to be lost. In the second step, platelet plug formation, platelets stick together to form a temporary seal to cover the break in the vessel wall. The third and last step is called coagulation or blood clotting. Coagulation reinforces the platelet plug with fibrin threads that act as a "molecular glue". Platelets are a large factor in the hemostatic process. They allow for the creation of the "platelet plug" that forms almost directly after a blood vessel has been ruptured. Within seconds of a blood vessel's epithelial wall being disrupted, platelets begin to adhere to the sub-endothelium surface. It takes approximately sixty seconds until the first fibrin strands begin to intersperse among the wound. After several minutes the platelet plug is completely formed by fibrin.[1] Hemostasis is maintained in the body via three mechanisms:

  1. Vascular spasm: Vasoconstriction is produced by vascular smooth muscle cells, and is the blood vessel's first response to injury. The smooth muscle cells are controlled by vascular endothelium, which releases intravascular signals to control the contracting properties. When a blood vessel is damaged, there is an immediate reflex, initiated by local sympathetic pain receptors, which helps promote vasoconstriction. The damaged vessels will constrict (vasoconstrict) which reduces the amount of blood flow through the area and limits the amount of blood loss. Collagen is exposed at the site of injury, the collagen promotes platelets to adhere to the injury site. Platelets release cytoplasmic granules which contain serotonin, ADP and thromboxane A2, all of which increase the effect of vasoconstriction. The spasm response becomes more effective as the amount of damage is increased. Vascular spasm is much more effective in smaller blood vessels.[2] [3]
  2. Platelet plug formation: Platelets adhere to damaged endothelium to form a platelet plug (primary hemostasis) and then degranulate. This process is regulated through thromboregulation. Plug formation is activated by a glycoprotein called von Willebrand factor (vWF), which is found in plasma. Platelets play one of major roles in the hemostatic process. When platelets come across the injured endothelium cells, they change shape, release granules and ultimately become ‘sticky’. Platelets express certain receptors, some of which are used for the adhesion of platelets to collagen. When platelets are activated, they express glycoprotein receptors that interact with other platelets, producing aggregation and adhesion. Platelets release cytoplasmic granules such as adenosine diphosphate (ADP), serotonin and thromboxane A2. Adenosine diphosphate (ADP) attracts more platelets to the affected area, serotonin is a vasoconstrictor and thromboxane A2 assists in platelet aggregation, vasoconstriction and degranulation. As more chemicals are released more platelets stick and release their chemicals; creating a platelet plug and continuing the process in a positive feedback loop. Platelets alone are responsible for stopping the bleeding of unnoticed wear and tear of our skin on a daily basis. This is referred to as primary hemostasis.[4]
  3. Clot formation: Once the platelet plug has been formed by the platelets, the clotting factors (a dozen proteins that travel along the blood plasma in an inactive state) are activated in a sequence of events known as 'coagulation cascade' which leads to the formation of fibrin from inactive fibrinogen plasma protein. Thus, a fibrin mesh is produced all around the platelet plug to hold it in place; this step is called secondary hemostasis. During this process some red and white blood cells are trapped in the mesh which causes the primary hemostasis plug to become harder: the resultant plug is called a thrombus or blood clot. The blood clot contains the secondary hemostasis plug with blood cells trapped in it. This is a necessary step for wound healing, but it has the ability to cause severe health problems if the thrombus becomes detached from the vessel wall and travels through the circulatory system; If it reaches the brain, heart or lungs it could lead to stroke, heart attack, or pulmonary embolism respectively.

Types

Hemostasis can be achieved in various other ways if the body cannot do it naturally (or needs help) during surgery or medical treatment. When the body is under shock and stress, hemostasis is harder to achieve. Though natural hemostasis is most desired, having other means of achieving this is vital for survival in many emergency settings. Without the ability to stimulate hemostasis the risk of hemorrhaging is great. During surgical procedures, the types of hemostasis listed below can be used to control bleeding while avoiding and reducing the risk of tissue destruction. Hemostasis can be achieved by chemical agent as well as mechanical or physical agents. Which hemostasis type used is determined based on the situation.[5]

Developmental Haemostasis refers to the differences in the haemostatic system between children and adults.

In emergency medicine

Debates by physicians and medical practitioners still continue to arise on the subject of hemostasis and how to handle situations with large injuries. If an individual acquires a large injury resulting in extreme blood loss, then a hemostatic agent alone would not be very effective. Medical professionals continue to debate on what the best ways are to assist a patient in a chronic state; however, it is universally accepted that hemostatic agents are the primary tool for smaller bleeding injuries.[5]

Some main types of hemostasis used in emergency medicine include:

Disorders

The body's hemostasis system requires careful regulation in order to work properly. If the blood does not clot sufficiently, it may be due to bleeding disorders such as hemophilia or immune thrombocytopenia; this requires careful investigation. Over-active clotting can also cause problems; thrombosis, where blood clots form abnormally, can potentially cause embolisms, where blood clots break off and subsequently become lodged in a vein or artery.

Hemostasis disorders can develop for many different reasons. They may be congenital, due to a deficiency or defect in an individual's platelets or clotting factors. A number of disorders can be acquired as well, such as in HELLP syndrome, which is due to pregnancy, or Hemolytic-uremic syndrome (HUS), which is due to E. coli toxins.

History of artificial hemostasis

The process of preventing blood loss from a vessel or organ of the body is referred to as hemostasis. The term comes from the Ancient Greek roots "heme" meaning blood, and "stasis" meaning halting; Put together means the "halting of the blood".[10] The origin of hemostasis dates back as far as ancient Greece; first referenced to being used in the Battle of Troy. It started with the realization that excessive bleeding inevitably equaled death. Vegetable and mineral styptics were used on large wounds by the Greeks and Romans until the takeover of Egypt around 332BC by Greece. At this time many more advances in the general medical field were developed through the study of Egyptian mummification practice, which led to greater knowledge of the hemostatic process. It was during this time that many of the veins and arteries running throughout the human body were found and the directions in which they traveled. Doctors of this time realized if these were plugged, blood could not continue to flow out of the body. Nevertheless, it took until the invention of the printing press during the fifteenth century for medical notes and ideas to travel westward, allowing for the idea and practice of hemostasis to be expanded.[11]

Research

There is currently a great deal of research being conducted on hemostasis. The most current research is based on genetic factors of hemostasis and how it can be altered to reduce the cause of genetic disorders that alter the natural process hemostasis.[12]

Von Willebrand disease is associated with a defect in the ability of the body to create the platelet plug and the fibrin mesh that ultimately stops the bleeding. New research is concluding that the von Willebrand disease is much more common in adolescence. This disease negatively hinders the natural process of Hemostasis causing excessive bleeding to be a concern in patients with this disease. There are complex treatments that can be done including a combination of therapies, estrogen-progesterone preparations, desmopressin, and Von Willebrand factor concentrates. Current research is trying to find better ways to deal with this disease; however, much more research is needed in order to find out the effectiveness of the current treatments and if there are more operative ways to treat this disease.[13]

See also

Notes and References

  1. Boon, G. D. "An Overview of Hemostasis." Toxicologic Pathology 21.2 (1993): 170–179.
  2. Book: Alturi, Pavan. The Surgical Review: An Integrated Basic and Clinical Science Study Guide. Lippincott Williams & Wilkins.. 2005. Philadelphia. 300.
  3. Book: Zdanowicz, M. Essentials of pathophysiology for pharmacy. limited. CRC Press. 2003. Florida. 23. 9781587160363 .
  4. Li. Zhenyu. 11 Nov 2010. Signaling during platelet adhesion and activation. Arteriosclerosis, Thrombosis, and Vascular Biology. 10.1161/ATVBAHA.110.207522. 21071698. 30. 12. 2341–2349. 3085271.
  5. Kulkarni Roshni . 2004 . Alternative and Topical Approaches to Treating the Massicely Bleeding Patient . Advances in Hematology . 2 . 7 . 428–431 . 2012-04-26 . https://web.archive.org/web/20090106061129/https://www.clinicaladvances.com/article_pdfs/ho-article-200407-hem.pdf . 2009-01-06 . dead .
  6. Aldo Moraci, et al. "The Use Of Local Agents: Bone Wax, Gelatin, Collagen, Oxidized Cellulose." European Spine Journal 2004; 13.: S89–S96.
  7. Smith Shondra L. . Belmont John M. . Casparian J. Michael . 1999 . Analysis Of Pressure Achieved By Various Materials Used For Pressure Dressings . Dermatologic Surgery . 25 . 12. 931–934 . 10.1046/j.1524-4725.1999.99151.x. 10594624 .
  8. Kozak Orhan. 2010 . A New Method For Hepatic Resection And Hemostasis: Absorbable Plaque And Suture . Eurasian Journal of Medicine . 41 . 1–4 . etal.
  9. Tahriri Mohammadreza. 2011 . Preparation And Characterization Of Absorbable Hemostat Crosslinked Gelatin Sponges For Surgical Applications . Current Applied Physics . 11 . 3. 457–461 . 10.1016/j.cap.2010.08.031 . 2011CAP....11..457K . etal.
  10. Book: Marieb. Elaine Nicpon. Katja. Hoehn. Human Anatomy & Physiology. 8th. San Francisco. Benjamin Cummings. 2010. 649–650.
  11. Wies, C. H. "The History of Hemostasis." Yale Journal of Biology and Medicine . 1929. 167–168. 2606227. Wies. C. H.. The Yale Journal of Biology and Medicine. 2. 2.
  12. Rosen . Elliot D. . Xuei . Xiaoling . Suckow . Mark . Edenberg . Howard . 2006 . Searching for hemostatic modifier genes affecting the phenotype of mice with very low levels of FVII . Blood Cells, Molecules and Diseases . 36 . 2 . 131–134 . 10.1016/j.bcmd.2005.12.037. 16524747 .
  13. Mikhail . Sameh . Kouides . Peter . December 2010 . von Willebrand Disease in the Pediatric and Adolescent Population . Journal of Pediatric and Adolescent Gynecology . 23 . 6 . S3–S10 . 10.1016/j.jpag.2010.08.005. 20934894 .

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