Coagulation: Surgical Prospective Flashcards
normal mechanism of hemostasis (3)
vascular phase
platelet phase
coagulation phase
what results when a blood vessel is damaged?
vasoconstriction
construction of the injured blood vessel is to diminish
blood flow
what occurs during the platelet phase? (3)
formation of a loose and temporary platelet aggregate at the site of injury
platelets bind to collagen
after the activation, platelets change their shape and in the presence of fibrinogen, aggregate to form the hemostatic primary platelet plug
through two separate pathways, the intrinsic and extrinsic, the conversion of — to — is complete
fibrinogen to fibrin
fibrin tightly binds to platelets to form a
clot
what forms during the coagulation phase?
formation of a fibrin mesh that tightly binds to the platelet aggregate, which gives rise t o amore stable hemostatic plug (clot)
clot dissolution
partial or complete dissolution of the hemostatic plug by plasma
factors affected normal hemostasis mechanism are dependent upon (5)
vessel wall integrity adequate numbers of platelets proper functioning platelets adequate levels of clotting factors proper function of fibrinolytic pathway
common tests performed to evaluate hemostasis (3)
Platelet Count (Complete Blood Count)
Bleeding Time
Coagulation Profile
PT
prothrombin time
APTT
activated partial thromboplastin time
INR
international normalized ratio
platelet function tests
Accurate measurement of platelet function is important for identifying patients with platelet dysfunction
platelet function tests may be recommended for those who
bruise easily, have excessive bleeding, or take medications after a stroke or heart attack that can alter platelet function; to detect resistance to aspirin or clopidogrel and before certain surgeries
clotting factor assays (2-12) measures
the levels or functional activity of one or more coagulation factors
normal platelet count
150,000-400,000 cells/mm3
thrombocytopenia (normal bleeding time)
100,000-140,000
mild thrombocytopenia (mild prolonged bleeding time)
50,000-100,000
severe thrombocytopenia (bleeding after minor trauma)
<50,000
spontaneous bleeding
<20,000
bleeding time is how long a
precise nick takes to stop bleeding
what does bleeding time provide an assessment of?
platelet function
normal bleeding time
2-9 minutes
platelet dysfunction bleeding time
9-15 minutes (prolonger thrombocytopenia)
what does PT time measure?
effectiveness of the extrinsic pathway
tests the rate of conversion of 7 tp 7a (extrinsic pathway)
normal PT time range
12-13 s
11-13.5 is also an accepted normal range
common causes of prolonger PT Time include (3)
Warfarin use
Vitamin K deficiency from malnutrition, biliary obstruction, malabsorption syndromes, or use of antibiotics
Liver disease, due to diminished synthesis of clotting factors
what does aPTT measure
effectiveness of the intrinsic and common pathway (measures intrinsic clotting of blood, congenital clotting disorders)
is aPTT or PTT more sensitive
aPTT is considered a more sensitive version and is used to monitor the patients response to heparin therapy
normal APTT
30-40 sec
aPTT more than 70 sex signifies
spontaneous bleeding
congenital deficiencies of intrinsic system clotting factors such as (6)
factors VIII, IX, XI, and XII, including hemophilia A and Hemophilia B
von willebrand disease is the most common
inherited bleeding disorder, affecting platelet function owning to decreased von willebrand factor activity
liver cirrhosis
the liver makes most of the clotting factors, including those that are vitamin k dependent ones
diseases of the liver may result in an inadequate quantity of clotting factors, prolonging the aPTT
vitamin k deficiency
the synthesis of some clotting factors requires vitamin K, so vitamin K deficiency results in an inadequate quantity of intrinsic system and common pathways clotting factors, as a result the aPTT is prolonger
heparin therapy inhibits the
intrinsic pathway at several points (prothrombin 2), prolonging the aPTT
Coumadin therapy inhibits the function of (3)
factors 1, 9, 10, prolongering aPTT
common causes of prolonger aPTT (6)
congenital deficiencies of intrinsic system clotting factors von willebrand disease liver cirrhosis vitamin k deficiency heparin therapy Coumadin therapy
INR formula
(patient PT/mean normal PT)^ISI
PT=
patient prothrombin time
MNPT=
the mean normal prothrombin time
ISI=
the international sensitivity index determined for each batch of thomboplastic reagents by manufactures
INR
“Modified” PT test, where the sample is “standardized” by using an ISI value (International Sensitivity Index) for the tissue factor used in each test. The ISI is usually between 1.0 and 2.0.
normal INR range
0.8-1.2
normal therapeutic levels of coagulation
2-3.5
the INR target range is 2.5-3 in which circumstances? (5)
Atrial Fibrillation Ischemic Stroke, Transient Ischemic attack (TIA) , or systemic embolism Mitral Stenosis Planned Cardioversion After open Heart surgery
bleeding disorders are a group of conditions involving the
body’s clotting process
such disorders can lead to
heavy and prolonger bleeding after injury
bleeding disorders may be either (2)
congenital or acquired
the acquired bleeding disorders are more common than
congenital bleeding disorders
Hemophilias A and B and Von Willebrand’s disease constitute over –% of all congenital bleeding disorders
90
congenital bleeding disorders (2)
hemophilia A and B
hemophilia A
clotting factor 8 deficiency
hemophilia B
clotting factor 9 deficiency (Christmas disease)
the decreased levels of factor 8 and 9 affect the normal coagulation cascade and thus the
fibrin clot formation in impaired in these patients
prevalence of hemophilia A
1 in 10,000
prevalence of hemophilia B
1 in 50,000
hemophilia can be inherited in a sex linked recessive manner, but –% of all patients have no family history
25%
does hemophilia affect more males or females?
males (1 in 10,000)
females (1 in 100,000,000)
why is it more prevalent in males?
critical blood clotting gene is carried on the X chromosome
late bleeding following surgery or injury, nhemarthrosis and hematoma formation are
classic sequelae of these coagulopathies
an elevated APTT is seen when
factor 8 or 9 levels fall below 30-50% of normal
levels of hemophilia (3)
mild
moderate
severe
People with mild hemophilia (6% to 49% factor level) usually have problems with bleeding only after serious (3)
injury, trauma, or surgery
in many cases, mild hemophilia is not discovered until an injury or surgery or tooth extraction results in
unusual bleeding
the first of mild hemophilia episode may not occur until
adulthood
People with moderate hemophilia, about –% of the hemophilia population, tend to have bleeding episodes after injuries
15
people with moderate hemophilia may also experience occasional bleeding episodes without obvious cause. These are called
“spontaneous bleeding episodes”
severe hemophilia constitutes –% of the hemophilia population
60%
people with severe hemophilia have bleeding following an injury and may have frequent
spontaneous bleeding episodes, often into the joints and muscles
preoperative therapy involves giving
cryoprecipitate and factor 8 concentrates (hemophilia A) and factor 9 concentrates (hemophilia B)
cytoprecipitate is prepared from plasma and contains (4)
fibrinogen
von willebrand factor
factor 8
fibronectin
cryoprecipate is the only adequate fibrinogen concentrate available for
intravenous use
additional treatment considerations include the use of splints to retain the venous blood clots in their socket and the avoidance of block local anesthetic unless factors are at least
50% of normal
the use of vasopressin analogue demopressin is valuable in cases of mild disease as they cause a three to four fold increase in the
factor 8 coagulant activity
teeth can be extracted under the cover of (2)
epsilon-aminocaproic acid or tranexamic acid (both inhibit fibrinolysis)
von willebrands disease
a bleeding disorder I which a protein called von villebrand factor is missing or does not work well in the body blood system
consequently, defective von willebrand factor interaction between platelets and the vessel wall impairs
primary hemostasis
3 major types of VQD
type 1
type 2
type 3
type 1 VWD
A shortage of von Willebrandfactor (mild). (Between 70% to 80% of all cases)
Most common form or VWD?
type 1
type 2 VWD
A flawed von Willebrandfactor (usually mild)(Subclassifiedas Type-2A and Type -2B).
Type 2 VWD is less common than Type 1. It represents 20-25% of allcases.
type 3 VWD
A complete lack of von Willebrandfactor (more severe). Type 3 VWD is very rare. It affects about 1 in 500,000 people
in patients with VWD, injuries and surgery can lead to
serve bleeding
what should prompt the dentist to consider VWD? (3)
an elevated bleeding time, normal platelet count, and no history of asrpij or NSAID use
blood tests are available to measure (3)
bleeding time
von willebrand factor activity levels
won villibrand factor antigen
what can show a defect in a patient with VW factor
genetic testing
preoperative therapy is usually decided after consultation with a hematologist and varies according to
severity of the disease
factor 8 cryoprecipitate and desmopressin are often given with
aminocaproic acid preoperatively and then again postoperatively after a period of 3 to 5 days
desmopressin helps to increase the production of
VW factor
demopressin is contraindicated in
type 2B patients
tranexamic acid an also be used intreat of aminocaproic acid as an
inhibitor of fibrinolysis
the normal platelet count is usually about
150,000 to 400,000 per microliter
thrombocytopenia (decreased platelet count) elevates the
bleeding time
the cause of thrombocytopenia is either (2)
decreased platelet production or increase platelet destruction
the common causes of increased destruction include (3)
idiopathic thrombocytopenia purapura (ATP)
drug included ITP (quinidine)
transfusion related purapuras
decreased production occurs secondary to
myelosuppresion due to antieoplastic agents as well as radiation treatment
in a patient with platelets in the range of 50,000-100,000, minor surgery like single tooth extraction nd biopsies are usually
tolerated without the need for platelet transfusion
following tooth extractions, use of local hemostatic measure measures is useful as it
stabilizes the blood clot
local measures of hemostatic agents (2)
suturing the wound
pressure with oral packs
in patients with platelet count below 50,0000, appropriate hematologist consultation should be taken and pre-operative transfusion with platelets or fresh frozen plasma given to a patient before performing
any type of oral surgical procedure
acquired bleeding disorders are most often drug induced but can also be (2)
secondary to alcohol (alcoholics have thrombocytopenia secondary to hyperplenism)
virus induced liver disease (as the liver produces all coagulation factors except factor 8 and possibly factor 13, a history of serious liver disease can cause a possible coagulopathy)
vitamin k deficiency from broad spectrum antibiotic use or malabsorption syndromes may also induce a
coagulopathy
acquired platelet function defect
idiopathic thrombocytopenia purpura
acquired bleeding disorders (4)
drug induced
vitamin k deficiency
acquired platelet function defect
multiple myeloma
acquired bleeding disorders (6)
patient taking oral anticoagulants (Coumadin, “Pradaxa” dibigatran, “Xarelto” - tivaroxaban)
patients taking anti platelet like placid, clopidogrel, SAIDS
patients with leukemia
patients on chemotherapy
HIV patients with low platelets count
kidney failure
it is important to achieve proper hemostasis in all patients during oral surgical procedures, so as to prevent
excessive intra-operative and post-operative blood loss
for successful peri-operative hematological management of patients with bleeding disorders and those on blood thinners, we need to achieve the following (6)
Medical Consultation (If necessary)
Assessment of Laboratory Test results
Referral to Oral and Maxillofacial Surgeon
Withdrawal of anticoagulant /Antiplatelet treatment prior to surgery (Do’s and Don’ts)
Role of Bridging Therapy
Local Measures used to control bleeding (Gelfoam, Surgicel, Tranexamic Acid, Suturing, Pressure Packs)
the management of patients receiving anti platelet and anticoagulant therapy is a fundamental skill of the dentist that requires
continual re-education as new medication become available for anticoagulation
patients on oral anticoagulant/antiplatelet treatment are currently not recommended to
discontinues their medication prior to minor oral surgery procedures as this increases their risk of developing a thromboembolic episode
in these patients, we currently recommended using local measures to
control bleeding after surgery
however, if patient’s need major oral surgery procedures, then appropriate medical consultation with physician is sought and the anticoagulant/antiplatelet medication is withheld from patient a few day/days prior to surgery. in this situation, patients on Coumadin are
put on a bridging treatment with heparin prior to surgery
it is important to understand the fact that the decision to withhold the anti platelet/anticoagulant medication can only be made by
the physician and not the treating dentist
local measures: hemostatic agents (2)
suturing he wound
pressure with oral packs
usual dose of local measures to irrigate the wound with tranexamic acid 5%
5-10 mL up to 4x daily, it does not need to be further diluted
the mouthwash should be rinsed around inside the mouth thoroughly for two minutes and then
spat out
after you have used this mouthwash, do not
eat or drink for one hour
