Wounds & Hemostasis
By C. Kohn, Waterford WI
Normal Blood Flow
 To have normal blood flow, blood must be kept at an exact
viscosity (thickness)
 Too thin, and the smallest cuts would cause a pet to bleed to
death
 Too thick, and the blood would not flow
 Anticoagulants keep the blood thin and allow it flow
under normal circumstances
 Injury changes the situation
 Blood must not be allowed to flow freely everywhere or the
wound would never heal
4 Types of Open Wound
 Abrasions-injuries destroying only surface layers of the
skin.
 Incisions- wounds produced by sharp instruments
 these types of cuts usually have smooth edges.
 Puncture Wounds- penetrations of the superficial (surface-
layer) tissue.
 Lacerations- cuts with irregularly torn edges.
o Slide courtesy of Texas A&M
Hemostasis
 The series of chemical reactions needed to stop bleeding is
called hemostasis
 Hemostasis has three steps
 Step 0: Injury
 Step 1: Vasoconstriction – blood vessels constrict (or
“shrink”) to slow blood flow at the site of injury
 Step 2: Platelet Plug formation – the wound is “corked”, or
covered with sticky platelets
 Step 3: Formation of a fibrin blood clot – a more sturdy
solution is created
Step 1: Vasoconstriction
 In vasoconstriction, the walls of
the blood vessels “shrink” to
reduce the size of the area that
blood can flow through.
 The muscles surrounding the
vessel will contract, shrinking the
vessel
Step 2. Platelet Plug Formation
 At the site of injury, collagen will
help platelets to stick to the site
of the injury
 Collagen is sort of like branches
that the platelets can grab onto
as they pass in the bloodstream
Platelets
 Platelets are formed in the bone marrow and live in your body’s
circulatory system for roughly a week
 Platelets aren’t really cells – they do not have a nucleus and cannot
divide
 Platelets do have a coat made of a particular protein that prevents a
platelet from sticking to anything other than injured tissue
 Platelets contain contractile proteins
(like those in your muscle cells)
 These proteins enable a platelet to
expand and contract
 Inside the platelet are special chemicals
that aid in the formation of the platelet
plug (explanation on next slide).
Clot Contraction & Repair
 About 30-60 minutes after a blood clot has formed, the
platelets within the clot contract
 Like muscle cells, platelet cells can shrink due to actin and
myosin contractile proteins
 This contraction pulls on the wound from the inside;
bringing the edges of the wound closer together
 The blood clot is temporary –
at the same time of contraction,
the tissue surrounding the damaged
site begin to divide and repair via
mitosis.
WBC
RBC
Platelet
Degranulation: A Feed Forward
Mechanism
 The platelets release granules that enable more platelets to
get stuck.
 The more platelets that get stuck, the more granules are
released the promote more platelets to get stuck.
 This is a “feed-forward” mechanism…the process becomes
stronger as it happens more.
Step 3: Coagulation
 The platelet plug will become reinforced
with a fibrin “mesh net”
 This fibrin net also traps red and white
blood cells in order to from a blood clot
over the site of the injury
 The red blood cells will form a solid “plug”
 The white blood cells will aid in fighting
infectious agents that are able to make it
inside the body.
Review: 3 Steps of Hemostasis
 1. Vasoconstriction – the muscles of the damaged blood vessel
contract to reduce the amount of blood flowing through it by
reducing the size of the blood vessel
 2. Platelet Plug Formation – collagen fibers protruding from
the site of the injury ‘catch’ platelets and form a plug. Platelets
contract and “shrink” the wound
 3. Formation of a Blood Clot – a fibrin “mesh” catches red
and white blood cells to form a clot and prevent infection.
o http://www.mhhe.com/biosci/esp/2002_general/Esp/folder_structu
re/tr/m1/s7/trm1s7_3.htm
Prevention of Infection
 Once bleeding has been controlled, the next step is stopping
infection
 The blood vessels that were constricted now dilate (open
up) to bring white blood cells rushing to the scene.
 The process in which the wound swells and becomes inflamed is
called inflammation.
White Blood Cells
 White blood cells engulf and destroy any germs that may
have gotten into the body through the open wound.
 This process of destroying germs creates heat
 This causes the trademark symptoms of serious wounds –
swelling, redness, tenderness, and heat.
 The worse the infection, the
greater the inflammation and heat.
Fibrinolysis
 2 days after clotting the fibrin mesh that holds the clot
together is dissolved
 This process is called Fibrinolysis
Source: thrombosisadviser.com
Stuff You Should Know: Warfarin
 Warfarin (or Coumadin) is a blood thinner.
 It was originally a rat poison, and is still widely used for this
method
 Rats that eat food laced with Warfarin die from blood loss
because their blood is unable to coagulate
 Warfarin, in much lower doses is one of the most widely
prescribed medications in the world.
 Warfarin can help dangerous clots from forming in heart attack
and stroke victims
 Warfarin is named for WARF, or the Wisconsin
Alumni Research Foundation.
 This is the agency that funds all research
at the University of Wisconsin.
Review
 What is necessary for normal blood flow? What is an anticoagulant?
 What are the four types of open wounds?
 What is hemostasis? What are the 3 steps of hemostasis?
 What is vasoconstriction and how does it happen?
 What is a platelet and how does it help a wound heal? How do they
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know where to go when there is an injury? How is a platelet different
from other kinds of cells?
What is a fibrin blood clot made from? (i.e. what is a scab?) How does
it form?
How does an open wound close?
Why do open wounds sometimes swell, become hot, and look red?
What is fibrinolysis?
How does a wound “know” how to heal?
What is Warfarin and what does it do?