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. This involves coagulation, blood changing from a liquid to a gel.
Intact blood vessels are central to moderating 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
endothelial injury occurs, the endothelial cells stop secretion of coagulation and aggregation
inhibitors and instead secrete von Willebrand factor which initiate the maintenance of hemostasis
after injury. Hemostasis has three major steps: 1) vasoconstriction, 2) temporary blockage of a
break by a platelet plug, and 3) blood coagulation, or formation of a fibrin clot. These processes
seal the hole until tissues are repaired.

Contents

 1Etymology and pronunciation

 2Steps of mechanism
 3Types
 4In emergency medicine
 5Disorders
 6History of artificial hemostasis
 7Research
 8References
 9External links

Etymology and pronunciation[edit]

The word hemostasis (/ˌhiːmoʊˈsteɪsɪs/,[1][2] sometimes /ˌhiːˈmɒstəsɪs/) uses the combining
forms hemo- and -stasis, New Latin from Ancient Greek αἱμο- haimo- (akin to αἷμα haîma),
"blood", and στάσις stásis, "stasis", yielding "motionlessness or stopping of blood".

Steps of mechanism[edit]
Further information: Coagulation

Aggregation of thrombocytes(platelets). Platelet-rich human blood plasma (left vial) is a turbid liquid. Upon
addition of ADP, platelets are activated and start to aggregate, forming white flakes (right vial)
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".[3] 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.[4] Hemostasis is maintained in the body via three mechanisms:

1. Vascular spasm (Vasoconstriction) - 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.[5][6]
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.[5][7]
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 as 'thrombus' or 'Clot'. Therefore 'blood clot' contains secondary hemostasis plug
with blood cells trapped in it. Though this is often a good step for wound healing, 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. However,
without this process the healing of a wound would not be possible.[3]

Types[edit]
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.[8]
Developmental Haemostasis refers to the differences in the haemostatic system between
children and adults.

In emergency medicine[edit]
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.[8]
Some main types of hemostasis used in emergency medicine include:

 Chemical/topical- This is a topical agent often used in surgery settings to stop bleeding.
Microfibrillar collagen is the most popular choice among surgeons [recent source?] because
it attracts the patient's natural platelets and starts the blood clotting process when it comes in
contact with the platelets. This topical agent requires the normal hemostatic pathway to be
properly functional.[9]
 Direct pressure or pressure dressing- This type of hemostasis approach is most
commonly used in situations where proper medical attention is not available. Putting
pressure and/or dressing to a bleeding wound slows the process of blood loss, allowing for
more time to get to an emergency medical setting. Soldiers use this skill during combat when
someone has been injured because this process allows for blood loss to be decreased,
giving the system time to start coagulation.[10]
 Sutures and ties- Sutures are often used to close an open wound, allowing for the injured
area to stay free of pathogens and other unwanted debris to enter the site; however, it is also
essential to the process of hemostasis. Sutures and ties allow for skin to be joined back
together allowing for platelets to start the process of hemostasis at a quicker pace. Using
sutures results in a quicker recovery period because the surface area of the wound has been
decreased.[11]
 Physical agents (gelatin sponge)- Gelatin sponges have been indicated as great
hemostatic devices. Once applied to a bleeding area, a gelatin sponge quickly stops or
reduces the amount of bleeding present. These physical agents are mostly used in surgical
settings as well as after surgery treatments. These sponges absorb blood, allow for
coagulation to occur faster, and give off chemical responses that decrease the time it takes
for the hemostasis pathway to start.[12]

Disorders[edit]
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[edit]

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".[3] 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.[13]

Research[edit]
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.[14]
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.[15]

References[edit]
1. ^ "Hemostasis". Merriam-Webster Dictionary. Retrieved 2016-01-21.
2. ^ "hemostasis". Oxford Dictionaries. Oxford University Press. Retrieved 2016-01-21.
3. ^ Jump up to:a b c Marieb, Elaine Nicpon; Hoehn, Katja (2010). Human Anatomy & Physiology (8th
ed.). San Francisco: Benjamin Cummings. pp. 649–50.
4. ^ Boon, G. D. "An Overview of Hemostasis." Toxicologic Pathology 21.2 (1993): 170-79.
5. ^ Jump up to:a b Alturi, Pavan (2005). The Surgical Review: An Integrated Basic and Clinical
Science Study Guide. Philadelphia: Lippincott Williams & Wilkins. p. 300.
6. ^ Zdanowicz, M (2003). Essentials of pathophysiology for pharmacy. Florida: CRC Press. p. 23.
7. ^ Li, Zhenyu (11 Nov 2010). "Signaling during platelet adhesion and activation". Arteriosclerosis,
Thrombosis, and Vascular Biology. 30: 2341–
2349. doi:10.1161/ATVBAHA.110.207522. PMC 3085271.
8. ^ Jump up to:a b Kulkarni Roshni (2004). "Alternative and Topical Approaches to Treating the
Massicely Bleeding Patient" (PDF). Advances in Hematology. 2 (7): 428–31.
9. ^ Aldo Moraci, et al. "The Use Of Local Agents: Bone Wax, Gelatin, Collagen, Oxidized
Cellulose." European Spine Journal 2004; 13.: S89-S96.
10. ^ 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. doi:10.1046/j.1524-4725.1999.99151.x.
11. ^ Kozak Orhan; et al. (2010). "A New Method For Hepatic Resection And Hemostasis: Absorbable
Plaque And Suture". Eurasian Journal of Medicine. 41: 1–4.
12. ^ Tahriri Mohammadreza; et al. (2011). "Preparation And Characterization Of Absorbable
Hemostat Crosslinked Gelatin Sponges For Surgical Applications". Current Applied
Physics. 11 (3): 457–461.
13. ^ "Wies, C. H. "The History of Hemostasis." Yale Journal of Biology and Medicine 2". 1929: 167–
68. PMC 2606227.
14. ^ 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. doi:10.1016/j.bcmd.2005.12.037.
15. ^ Mikhail, Sameh; Kouides, Peter (December 2010). "von Willebrand Disease in the Pediatric and
Adolescent Population". Journal of Pediatric & Adolescent Gynecology. 23 (6): S3–
S10. doi:10.1016/j.jpag.2010.08.005.