Ch 18 Haemostasis Flashcards
What are the three main principles used to augment haemostasis?
Reduction of blood flow
Topical haemostatic agents
Antifibrinolysis
How long does it take to form a blood clot?
Approx 30 seconds for platelet aggregation
An additional 2-3min for cross-linking with the formation of a fibrin matrix
list some methods of reducing blood flow (5)
Pressure/tamponade
2mm sealed with electrocautery
Topical vasoconstrictors
(epinephrine/adrenaline/ephedrine, - Dilution factor rage 1:1000 to 1:100000 U/mL)
Hypotension/Hypothermia (reflex peripheral vasoconstriction)
Control of distant blood flow (Temporary or permanent ligation of major vessels)
List the vessels which can be permanently ligated
temporary?
Temporary to assist:
pringle maneuver
carotid (nasal, maxilla,brain)
renal
femoral (distal loss)
AOarta (cardiac sx, abdo loss)
vena cava (adrenelectomy)
What are the suggested temporary ligation time of the following vessels in normothermic animals
- Descending thoracic aorta
- Pringle maneuver
- Hepatic artery
- Splenic artery and vein
- Renal artery and vein
- Abdominal aorta
Descending thoracic aorta - 5-10min
Pringle maneouver - 10-15min
Splenic artery and vein - 15-20min
Hepatic artery - 30min
Renal artery and vein - 30min
Abdominal aorta - 30min
What systemic responses have been recorded in humans in response to tourniquet application and removal?
Application - increased in circulated blood volume, hypertension and hypercoagulopathy
Removal - Transient but marked hypotension, hypercapnia, increased cerebral blood flow and intracranial pressure
What tourniquet pressure will result in demyelination?
What is the recommended tourniquet pressure?
Above 1000mmHg
Recommended is 100mmHg above systolic pressure
What is the equation to calculate tourniquet pressure?
P=T/RW
Pressure = tension / radius of limb x bandage width
What is the maximum time for tounriquet application on limbs?
Not established»_space; maximum of 1.5-2hr
Energy stores depleted in 2-3hr, mitochondrial changes visible after 1hr and microvascular damage after 2hr
What are the three groups of haemostatic agents?
Mechanical (absorb blood and provide a matrix for clot formation)
Active (actively stimulate the normal processed of haemostasis)
Haemostatic sealants
List the main forms of mechanical haemostatic agents (5)
Gelatines (Gelfoam, Spongostan): Experimental absorption in 5 weeks
Collagens (b. Bovine): Mechanical but also enhances plt aggregation
Oxidised regenerative cellulose (surgicel): MOA not fully understood – dense gelatinous clot in contact with blood
Polysaccharides: i. Hydrophilic, dehydrates blood, stimulates plts and acts as mechanical barrier
Wax: mechanical barrier and tamponade (bone healing?)
absorb blood, tamponade, matrix for clot formation and stabilization; absorbable
List the main forms of active haemostatic agents
stimulate normal processes of hemostasis
Thrombin (FII > converts endogenous fibrinogen to fibrin)
Thrombin gelatin matrix
Alginates (seaweed derived protein. Releases Ca on contact with slaine or body fluids, activating the clotting cascade)
List three forms of haemostatic sealants
Human plasma-derived tissue sealant (Thrombin and fibrinogen)
Autogenous plasma-derived tissue sealant
Synthetic polymers (polyethylene glycol polymers or albumin)
Form a seal of vascular or dural defects without utilising endogenous haemostatic mechanisms at all
What are the 2 main groups of antifibrinolytics
Lysine analogues (aminocaproic acid, tranexamic acid) > bind plasminogen
Serine protease inhibitor - license suspended in UK due to safety concerns
Not licensed, dogs likely require higher doses than humans, NOT effective when there is a depletion of clotting factors or coagulopathy
2019 review
Primary hyperfibrinolysis occurs due to quantitative or qualitative abnormalities of the proteins involved in the regulation of the fibrinolytic pathway (Kolev and Longstaff, 2016).
Secondary hyperfibrinolysis describes hyperactivity of a normal fibrinolytic pathway, typically provoked by abnormal coagulation, or hyperfibrinolysis due to increased susceptibility of fibrin to lysis
It is important to note that even viscoelastic techniques are imperfect and may either fail to detect hyperfibrinolysis or conversely report hyperfibrinolysis in apparently healthy patients
Dx: Portable handheld viscoelastic analysers are now available and have been recently validated in both canine and feline patient
in Greyhounds is reported to be as high as 26%
typically associated with the surgical site, however in some Greyhounds bleeding may progress to a generalised haemostatic disorder requiring intensive care and blood product administration
absence of primary or secondary coagulation derangement combined with incidence of delayed post-operative haemorrhage is reduced in Greyhounds receiving antifibrinolytic drugs
