Consider when to be.
By CBC (Complete Blood Count).
150,000 – 400,000.
Until endothelium creeps covers stent for 6 weeks (1.5 months).
Subendothelial collagen.
ADP binds to P2Y12 Receptors found on platelets, leading to platelet aggregation. Thromboxane A2 leads to platelet activation and vasoconstriction.
Tissue damage.
Vasoconstriction, platelet plug formation, and tamponade by surrounding tissue.
Simple pressure, ligation, under-running suture, electrocautery, clips, laser, repair of injured large vessels, and topical hemostatic agents.
By generating heat which causes tissue coagulation.
Gelatin foams (Gelfoam), surgical cellulose (Surgical), fibrin sealants, and platelet sealants.
Platelet/vessel abnormalities, leading to superficial bleeding such as petechiae, purpura, easy bruisability, epistaxis, and menorrhagia.
DIC (Disseminated Intravascular Coagulation).
20,000 – 50,000.
Decreased concentration of all clotting factors except factor VIII and VWF, dysfibrinogenemia, and decreased antithrombin levels.
For drug-eluting stent: 6 months to 1 year. For bare-metal stent: > 1 month.
To digest the clot and restore vascular patency.
Septicemia, severe shock, trauma, burns, ABO incompatible transfusion, malignancies, obstetric accidents.
Spontaneous thrombosis and recurrent DVTs.
Leukemia, cancer infiltration, viral infection, and chemotherapy.
Immune-mediated (ITP), drug-induced (e.g., heparin, thiazides, and sulpha).
Hypersplenism.
Arteries contain more muscular fibers.
Thromboxane from platelet membrane phospholipid, ADP, serotonin, and thrombin.
Transfused platelets are similarly sequestered in the spleen.
Inadequate surgical hemostasis.
Jaundice and spider naevi.
150,000 - 400,000/uL.
Continued just do meticulous hemostasis during surgery, then stopped for 5 - 7 days for major surgery and 24 hours for minor surgery.
a. Extrinsic: initiated by activation of factor VII upon admixture of plasma and tissue factor. b. Intrinsic: initiated by activation of factor XII upon contact with a non-endothelial surface, more directly by activation of factor IX through activated factor VII.
It involves heparin, LMWH, glycoprotein IIb/IIIa inhibitors, or cangrelor, which is a short-acting P2Y12 inhibitor, and is used to bridge the gap when antiplatelets need to be stopped.
Increased levels of fibrin degradation products (FDP).
The physiological arrest of bleeding involving vasoconstriction, platelet plug formation, and fibrin deposition to form a stable clot.
Inadequate diet, prolonged broad-spectrum antibiotics, cholestatic jaundice, malabsorption, oral anticoagulants.
Measures the time of clotting through the extrinsic and common pathways involving factor VII and factors X, V, II, and fibrinogen.
Measures the time of clotting through the intrinsic pathway (factors XII, XI, IX, and VIII) and the common pathway.
Measures the time of clotting after thrombin is added to plasma and is sensitive to abnormalities of fibrin formation.
To detect decreased fibrinogen levels, which is indicative of Disseminated Intravascular Coagulation (DIC).
24 hours.
Excessive fibrinolysis or thrombolytic agents.
Formation of the fibrin clot.
Glycoprotein Ib.
Plasmin cleavage of cross-linked fibrin.
Fresh frozen plasma 3 - 4 units.
Treatment of the underlying cause, replacement of coagulation factors, platelet transfusion, blood transfusion, and heparin for large vessel thrombosis.
Diet and bacterial synthesis in the colon.
It is a co-factor.
Leads to easy bruising and increased traumatic bleeding. Prolongs PT and PTT.
Essentially normal, but a larger fraction of platelets is in the enlarged spleen.
To evaluate factor XIII deficiency, which is not detected by the PT or PTT.
24 hours.
2 to 4 days.
1 to 2 days.
Do PT & APTT and treat accordingly.
Patients with a personal history or a family history of abnormal bleeding, and patients with diseases or who receive medications that can interfere with hemostasis.
1 month before elective surgery.
Supply vW and cryoprecipitate.
Coagulation.
It is monitored by INR (International Normalized Ratio) to assess its effect, not prothrombin time, as it varies according to the device used.
Widespread activation of coagulation leading to consumption of coagulation factors and depletion of platelets.
PT, PTT, and platelet count.
Thrombocytopenia, prolongation of PT and PTT, low fibrinogen level, raised levels of FDP and D-dimers.
Adhere to exposed subendothelial collagen, release granule contents, and aggregate to form a plug that seals the bleeding vessel.
It has a vital role in blood coagulation.
It is less effective when a vessel is partially injured, in stiff atherosclerotic vessels, and in large veins with a poor muscle coat.
To assess the risk of bleeding during and after the surgery.
History.
Interstitial hemorrhage.
Fresh frozen plasma (FFP).
Because they use only plasma and not whole blood to provide their assessment of the patient's clotting status.
To measure all dynamic steps of clot formation using a whole-blood sample until eventual clot lysis.
Deficiency of a natural anticoagulant (antithrombin III, protein C or protein S).
For a personal or family history of spontaneous/recurrent thrombosis, arterial and/or venous, as well as obstetric history of recurrent miscarriages.
They are more prevalent than congenital ones and may be accompanied by hemostatic abnormalities.
It has a main effect on factor 7 only, not all Vit K dependent factors, due to its short half-life cycle.
By inhibitors such as antithrombin III and proteins C and S.
Fibrin degradation products (FDP).
Diffuse bleeding, widespread bruising, purpura, mucosal bleeding, and occasionally ischemic manifestations.
To raise platelet count above 50,000/uL.
4 to 6 hours before.
12 to 24 hours before.
3 to 5 days.
Less than 1.5.
Deep bleeding, such as hemarthrosis, hematomas in muscles, retroperitoneal or visceral bleeding, in addition to easy bruisability.
Congenital diseases like von Willebrand disease, uremia, hypothermia, and certain drugs.
It suggests von Willebrand disease (vW).
A hereditary disorder.
An acquired disorder.
10,000 - 20,000.
Give LMWH (Low Molecular Weight Heparin).
Deficiency of vW factor which enhances platelet adhesion and acts as a carrier to factor VIII, preventing its premature destruction. Affects both intrinsic and extrinsic pathways.
Positive history in maternal grandfathers, maternal uncles, or a brother.
Fibrinolysis, which breaks down the clot to restore vascular patency after bleeding has stopped.
It can raise the levels of factor VIII and vWF and shorten the bleeding time.
Pregnancy, estrogen use (HRT or contraception), and malignancy.
Liver disease, chronic renal failure, massive blood transfusion, and drug intake.
Further investigations called aggregometry are ordered.
Infusion of factor concentrate within 1 hour before surgery and for 10 days thereafter. Avoiding aspirin and NSAIDs, and avoiding IV injections. Vaccination against hepatitis B is needed due to repeated transfusions.
10,000 - 20,000/uL.
Take heparin.
Give bridging anticoagulation.
Standard DVT prophylaxis.
Manifestations are due to platelet and coagulation problems.
Manifestations vary from frequent episodes of spontaneous bleeding starting in childhood, <1% of factor activity. Bleeding occurs only after trauma or surgery (factor level 5-20% of normal). Patients are liable to recurrent hemarthrosis.
