hemostasis occurs when blood is present outside of the body or blood vessels

7/27/2019 Hemostasis Occurs When Blood is Present Outside of the Body or Blood Vessels

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Hemostasis occurs when blood is present outside of the body or blood vessels. It is the instinctive

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,plateletsstick 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.[1]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 vessels epithelial wall being disrupted

platelets begin to adhere to the sub-endotheliumsurface. 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.[2]

Hemostasis is maintained in the body via three mechanisms:

1.Vascular Spasm- Damaged blood vesselsconstrict. Vascular spasm is the blood vessels' first

response to injury. The damaged vessels will constrict (vasoconstrict) which reduces the amount of blood

flow through the area and limits the amount of blood loss. This response is triggered by factors such as a

direct injury to vascular smooth muscle, chemicals released byendothelial cellsand platelets, and

reflexes initiated by localpain receptors. The spasm response becomes more effective as the amount of

damage is increased. Vascular spasm is much more effective in smaller blood vessels .[1]

2. Platelet plug formation -Plateletsadhere to damaged endothelium to form platelet plug (primary

hemostasis) and then degranulate. This process is regulated through thromboregulation. Platelet Plug

Formation: Platelets play one of the biggest factors in the hemostatic process. Being the second step in

the sequence they stick together (aggregation) to form a plug that temporarily seals the break in the

vessel wall. As platelets adhere to the collagen fibers of a wound they become spiked and much stickier.

They then release chemical messengers such asadenosine

diphosphate(ADP),serotoninandthromboxane A2. These chemicals are released to cause more

platelets to stick to the area and release their contents and enhance vascular spasms. As more chemicals

are released more platelets stick and release their chemicals; creating a platelet plug and continuing theprocess 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.[3]

The second stage of Hemostasis involves platelets that move throughout the blood. When the platelets

find an exposed area or an injury, they begin to form what is called a platelet plug. The platelet plug

formation is activated by a glycoprotein called theVon Willebrand factor(vWF), which are found in the

bodys blood plasma. When the platelets in the blood are activated, they then become very sticky so

allowing them to stick to other platelets and adhere to the injured area.[4][5]

There are a dozen proteins that travel along the blood plasma in an inactive state and are known as

clotting factors. Once the platelet plug has been formed by the platelets, theclotting factorsbegin creating

the platelet plug. When this occurs the clotting factors begin to form a collagen fiber called

fibrin.Fibrinmesh is then produced all around the platelet plug, which helps hold the fibrin in place. Once

this begins, red and white blood cells become caught up in the fibrin mesh which causes the clot to

become even stronger.[3]

3. Bloodcoagulation- Clots form upon the conversion offibrinogentofibrin, and its addition to the

platelet plug (secondary hemostasis). Coagulation: The third and final step in this rapid response

reinforces the platelet plug. Coagulation or blood clotting uses fibrin threads that act as a glue for the
http://en.wikipedia.org/wiki/Plateletshttp://en.wikipedia.org/wiki/Plateletshttp://en.wikipedia.org/wiki/Plateletshttp://en.wikipedia.org/wiki/Hemostasis#cite_note-marieb-1http://en.wikipedia.org/wiki/Hemostasis#cite_note-marieb-1http://en.wikipedia.org/wiki/Hemostasis#cite_note-marieb-1http://en.wikipedia.org/wiki/Endotheliumhttp://en.wikipedia.org/wiki/Endotheliumhttp://en.wikipedia.org/wiki/Endotheliumhttp://en.wikipedia.org/wiki/Hemostasis#cite_note-2http://en.wikipedia.org/wiki/Hemostasis#cite_note-2http://en.wikipedia.org/wiki/Hemostasis#cite_note-2http://en.wikipedia.org/wiki/Vascular_spasmhttp://en.wikipedia.org/wiki/Vascular_spasmhttp://en.wikipedia.org/wiki/Vascular_spasmhttp://en.wikipedia.org/wiki/Vasoconstrictionhttp://en.wikipedia.org/wiki/Vasoconstrictionhttp://en.wikipedia.org/wiki/Vasoconstrictionhttp://en.wikipedia.org/wiki/Endothelial_cellshttp://en.wikipedia.org/wiki/Endothelial_cellshttp://en.wikipedia.org/wiki/Endothelial_cellshttp://en.wikipedia.org/wiki/Pain_receptorshttp://en.wikipedia.org/wiki/Pain_receptorshttp://en.wikipedia.org/wiki/Pain_receptorshttp://en.wikipedia.org/wiki/Hemostasis#cite_note-marieb-1http://en.wikipedia.org/wiki/Hemostasis#cite_note-marieb-1http://en.wikipedia.org/wiki/Hemostasis#cite_note-marieb-1http://en.wikipedia.org/wiki/Platelethttp://en.wikipedia.org/wiki/Platelethttp://en.wikipedia.org/wiki/Platelethttp://en.wikipedia.org/wiki/Thromboregulationhttp://en.wikipedia.org/wiki/Thromboregulationhttp://en.wikipedia.org/wiki/Thromboregulationhttp://en.wikipedia.org/wiki/Adenosine_diphosphatehttp://en.wikipedia.org/wiki/Adenosine_diphosphatehttp://en.wikipedia.org/wiki/Adenosine_diphosphatehttp://en.wikipedia.org/wiki/Adenosine_diphosphatehttp://en.wikipedia.org/wiki/Serotoninhttp://en.wikipedia.org/wiki/Serotoninhttp://en.wikipedia.org/wiki/Serotoninhttp://en.wikipedia.org/wiki/Thromboxane_A2http://en.wikipedia.org/wiki/Thromboxane_A2http://en.wikipedia.org/wiki/Thromboxane_A2http://en.wikipedia.org/wiki/Hemostasis#cite_note-clemetson-3http://en.wikipedia.org/wiki/Hemostasis#cite_note-clemetson-3http://en.wikipedia.org/wiki/Hemostasis#cite_note-clemetson-3http://en.wikipedia.org/wiki/Von_Willebrand_factorhttp://en.wikipedia.org/wiki/Von_Willebrand_factorhttp://en.wikipedia.org/wiki/Von_Willebrand_factorhttp://en.wikipedia.org/wiki/Hemostasis#cite_note-ritta-4http://en.wikipedia.org/wiki/Hemostasis#cite_note-ritta-4http://en.wikipedia.org/wiki/Hemostasis#cite_note-ritta-4http://en.wikipedia.org/wiki/Clotting_factorshttp://en.wikipedia.org/wiki/Clotting_factorshttp://en.wikipedia.org/wiki/Clotting_factorshttp://en.wikipedia.org/wiki/Fibrinhttp://en.wikipedia.org/wiki/Fibrinhttp://en.wikipedia.org/wiki/Fibrinhttp://en.wikipedia.org/wiki/Hemostasis#cite_note-clemetson-3http://en.wikipedia.org/wiki/Hemostasis#cite_note-clemetson-3http://en.wikipedia.org/wiki/Hemostasis#cite_note-clemetson-3http://en.wikipedia.org/wiki/Coagulationhttp://en.wikipedia.org/wiki/Coagulationhttp://en.wikipedia.org/wiki/Coagulationhttp://en.wikipedia.org/wiki/Fibrinogenhttp://en.wikipedia.org/wiki/Fibrinogenhttp://en.wikipedia.org/wiki/Fibrinogenhttp://en.wikipedia.org/wiki/Fibrinhttp://en.wikipedia.org/wiki/Fibrinhttp://en.wikipedia.org/wiki/Fibrinhttp://en.wikipedia.org/wiki/Fibrinhttp://en.wikipedia.org/wiki/Fibrinogenhttp://en.wikipedia.org/wiki/Coagulationhttp://en.wikipedia.org/wiki/Hemostasis#cite_note-clemetson-3http://en.wikipedia.org/wiki/Fibrinhttp://en.wikipedia.org/wiki/Clotting_factorshttp://en.wikipedia.org/wiki/Hemostasis#cite_note-ritta-4http://en.wikipedia.org/wiki/Hemostasis#cite_note-ritta-4http://en.wikipedia.org/wiki/Von_Willebrand_factorhttp://en.wikipedia.org/wiki/Hemostasis#cite_note-clemetson-3http://en.wikipedia.org/wiki/Thromboxane_A2http://en.wikipedia.org/wiki/Serotoninhttp://en.wikipedia.org/wiki/Adenosine_diphosphatehttp://en.wikipedia.org/wiki/Adenosine_diphosphatehttp://en.wikipedia.org/wiki/Thromboregulationhttp://en.wikipedia.org/wiki/Platelethttp://en.wikipedia.org/wiki/Hemostasis#cite_note-marieb-1http://en.wikipedia.org/wiki/Pain_receptorshttp://en.wikipedia.org/wiki/Endothelial_cellshttp://en.wikipedia.org/wiki/Vasoconstrictionhttp://en.wikipedia.org/wiki/Vascular_spasmhttp://en.wikipedia.org/wiki/Hemostasis#cite_note-2http://en.wikipedia.org/wiki/Endotheliumhttp://en.wikipedia.org/wiki/Hemostasis#cite_note-marieb-1http://en.wikipedia.org/wiki/Platelets


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sticky platelets. As the fibrin mesh begins to form the blood is also transformed from a liquid to a gel like

substance through involvement of clotting factors and pro-coagulants. The coagulation process is useful

in closing up and maintaining the platelet plug on larger wounds. The release ofProthrombinalso plays

an essential part in the coagulation process because it allows for the formation of a thrombus, or clot, to

form. This final step forces blood cells and platelets to stay trapped in the wounded area. Though this is

often a good step forwound healing, it has the ability to cause severe health problems if the thrombusbecomes detached from the vessel wall and travels through the circulatory system; If it reaches the heart

or brain it could lead tostroke,heart attack, orpulmonary embolism. However, without this process the

healing of a wound would not be possible.[1]

Types of Hemostasis[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

ofhemorrhagingis great. During surgical procedures the types of hemostasis listed below can be used tocontrol bleeding while avoiding and reducing the risk of tissue destruction. Hemostasis can be achieved

bychemical agentas well as mechanical or physical agents. Which hemostasis type used is determined

based on the situation.[6]

Hemostasis in emergency medicine[edit]

Debates still continue to rise on the subject of hemostasis and how to handle situations with large

injuries. If an individual did acquire a large injury resulting in extreme blood loss, then ahemostatic

agentalone would not be very effective. Medical professionals continue to debate on what the best

ways to assist a patient in a chronic state are; however, it is universally accepted that hemostatic

agents are the primary tool for smaller bleeding injuries.

[6]

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.

Microfibrillercollagenis the most popular choice among surgeons because it attracts the patients

natural platelets and starts the blood clotting process when it comes in contact with the platelets. This

topical agent requires normal hemostatic pathway to be properly functional.[7]

Direct pressure orpressure 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 only 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.[8]

Sutures and ties-Suturesare 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
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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.[9]

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 surgerytreatments. 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 .[10]

Disorders[edit]

The body's hemostasis system requires careful regulation in order to work properly; if the blood does not

clot sufficiently, bleeding disorders such ashemophiliacan result. Over-active clotting can also cause

problems;thrombosis, where blood clots form abnormally, can potentially causeembolisms, 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 acquiredas well, such as inHELLP syndrome, which is due to pregnancy, orHemolytic-uremic syndrome(HUS),

which is due to E. colitoxins.

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 theAncient Greekroots "heme" meaning blood, and "stasis" meaning halting; Put

together means the "halting of the blood".[1]

The origin of hemostasis dates back as far as ancient Greece;

first referenced to being used in theBattle 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 based off the study of Egyptian mummificationpractice, 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]

Hemostatic Research[edit]

There is currently a lot 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 ofgenetic disordersthat

alter the natural process hemostasis.[12]

Von Willebrand diseaseis 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-

progesteronepreparations,desmopressin, and Von Willebrand factor concentrates. Current research is
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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]

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hemostasis occurs when blood is present outside of the body or blood vessels

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