Professional Documents
Culture Documents
Platelet Coagulatio
disorders n factors
disorders Severity Related to factor level:
Site of bleeding Skin Deep in
mucous soft tissues <1%- Severe -> Spontaneous bleeding
membrane (joints, 1.5%- Moderate bleeding with mild injury
s (epistaxis, muscles) 5-25% - Mild Bleeding with surgery or trauma
gum, Complications Soft tissue bleeding
vaginal, GI Hemophilia
tract)
Petechiae Yes No Clinical manifestations (hemophilia A and B are
Ecchymoses Small, Large, indistinguishable)
(bruises) superficial deep Hemarthrosis (most common) -> Fixed joints
Hemarthrosis/muscl Extremely Common Soft tissues hematomas (e.g muscles) -> Muscle
e bleeding rare atrophy, Shortened tendons
Bleeding after cuts Yes No Other sites of bleeding -> Urinary tract, CNC,
& scratches neck (may be life-threatening)
Bleeding after Immediate, Delayed (1- Prolonged bleeding after surgery or dental
surgery or trauma usually 2 days) extractions
mild often
severe
Treatment of hemophilia A
Classification
Common clinical conditions associated with Intravascular clot
Disseminated Intravascular Coagulation Decrease platelets and schistocytes
Activation of both coagulation and fibrinolysis
trigerred by Disseminated Intravascular Coagulation
Treatment approaches
Sepsis Obstetrical Treatment of underlying disorder
complications Anticoagulant with heparin
Amniotic fluid Platelet transfusion
embolism Fresh frozen plasma
Abruption placentae Coagutlation inhibitor concentrate
Trauma Vascular disorders (ATIII)
Head injury Reaction to toxin (e.g
Fat embolism snake venom, drugs) Liver Disease and Hemostasis
Malignancy Immunologic disorders 1. Decreased synthesis II, VII, IX, X,XI
Severe allergic reaction fibrinogen
Transplant rejection 2. Dietary Vitamin K deficiency
(Inadequate intake or malabsorption
Disseminated Intravascular Coagulation 3. Dysfribrinogenemia
4. Enhacned fibrinolysis (decreased alpha-
Systemic activation of 2 antiplsmin
coagulation 5. DIC
6. Thrombocytopenia due to
hypersplenism
Presence of plasmin
FDP
Vitamin K deficiency due to warfarin overdose Smoking
Managing high INR values Drugs -> Birth Control high estrogen
Congestive Heart failure
Clinical situation Guidelines Central Venous Pressue (CVP) catheter
INR therapeutic-5 Lower or omit next Pacemake/Defibrillator placement
dose; Resume Neurological deficits CVA, MS, Spilnal
therapy when INR is cors
therapeutic Superficial vein thrombosis
Herediatry deficiencies Protein C/S,
INR 5-9; no bleeding Lower or omit next antithrombin III
dose; Resume
therapy when INR is Hypercoagulability: Risk Factors
therapeutic Recent surgery
Omit dose and give o Tissue factor exposure
vitamin K (1-2.5 mg especially orthopedic
po) o Total hip replacement 25% w/o
Rapid reversal; prophylaxis (3-4% fatal)
vitamin K 2-4mg po o Reduced 30-50% with
(repeat) prophylaxis
INR >9; no bleeding Omit dose, give o Traumatic hip fx: 50%
vitamin k 3-5 mg po; o Total knee replacement 60%
repeat as necessary Fractures or other traumas.
Resume therapy at
lower dose when INR Virchows Classic Triad
therapeutic
Three Major Elements that promote thrombosis
Hypercoagulability more deaths from clotting
than bleeding Endothelial injury
Decrease in blood flow
Killer Clots Imbalance between procoagulant and
anticoagulant
Myocardial infarction o (Hypercoagulable state)
Deep venous Thrombosis -> Pulmonary
Emboli Endothelial Injury
Cerebral vascular accidents Mechanical trauma
Thrombotic Emboli-sources Artherosclerosis (intrinsic pathway)
o Carotids Endotixins from bacteria
o Heart-Atrial fibrillation, CHF Proteases and cytokines of inflammation
Immune-autoimmune
Deep Venous Thrombosis/ Venous Thrombo Hypoxia
Embolism
Decreased in Blood flow
VTE risk Heart failure (HF) causes stasis
Malignancy Atrial fib/flutter
Trauma Myocardial infarction
Surgery- Extremity Immobilization
o Long travel and long flight o Advanced age (fibrinogen levels
economy class syndrome increase) OCP, pregnancy
o Casting o Surgery, trauma
o Bedridden (stroke Hypercoagulable state from other
Thrombophilia (hypercoagulable) disease
o Malignancy
Genetic: o Renal-nephrotic syndrome
o 5-8% of population has one o thick blood polycythemia,
genetic clotting disorder; 25- Sickle cell
50% will have F. V Leiden
AGE: at onset <50 years Treatment of Venous Thromboembolism
INDENTIFIABLE RISH FACTORS: may be Risk Stratify
none Low risk and clearly identifiable cause
o Frequently triggered by 2nd risk o 3 months oral anticoagulation
factor Medium risk
FAMILY HISTORY: frequently positive o 6 months oral anticoagulation
PAST HISTORYT: recurrent events High risk
Get in trouble when 2nd factor is o Life long anticoagulant with
present INR 2-3
Dabigtran- PRADAXA
Contraindications to Thrombolytics
History of hemorrhagic stroke <2
months
CNS neoplasm, AV malformations, or
aneurysm, or CNS surgery <<2 months
Severe uncontrolled hypertension (over
200/130 or complicated by
retinovascular disease or
encephalopathy)
Ongoing (active) bleeding
s/p recent significant surgery
known bleeding disorder
MI due to aortic dissection
Allergy t o agent planned
Many relative contraindications