intrinsic coagulation pathway is stimulated by vascular endothelium injury such as:
- cell trauma (valve, IABP)
- sepsis
- shock
- ARDS
- hypoxemia, acidemia
- cardiopulmonary arrest
extrinsic coagulation pathway is stimulated by tissue injury, releases “tissue thromboplastin”
- extensive trauma
- OB emergencies
- mallignancies
- dissecting aortic aneurysm
- extensive MI
what does Coumadin do? how is it reversed?
inhibits conversion of prothrombin; vitamin K
what does heparin do? how is it reversed?
inhibits thrombin; protamine
what happens in disseminated intravascular coagulopathy (DIC)?
- activation of clotting (microembolism) with resultant consumption of clotting factors (hemorrhage)
is DIC more of a clotting/bleeding problem?
clotting
what causes DIC?
- endothelial damage - sepsis, hypoxemia, shock, ARDS, AAA, acidemia, cardiopulmonary arrest
- release of tissue thromboplastin - extensive trauma, malignancies, OB emergencies, dissecting aortic aneurysm
- factor X activation - acute pancreatitis, liver disease
- miscellaneous - massive transfusions, PE, hemolytic anemia, fresh H2O drowning, ASA poisoning
what labs can be seen with DIC?
- primary - **ELEVATED FSP (increased fibrinolysis), PT/PTT/INR; decreased platelets, fibrinogen, hct
- secondary - INCREASED D-DIMER, increased antithrombin III
what are normal fibrin split products (FSP) and fibrinogen levels?
FSP <10mcg/mL
fibrinogen 200-400mg/dL
how is DIC treated?
- treat cause
- vitamin K
- FFP, cryo, platelets
- low dose heparin
what causes heparin-induced thrombocytopenia (HIT)?
- immune (IgG) response
- results in thrombosis (white clots) that consumes platelets
what are some S/S of HIT?
- platelets <150K or drop 30-50%
- petechiae - early sign
- clots leading to PE, MI, stroke, amputation
how is HIT treated?
- stop heparin
- ELISA (enzyme-linked immunosorbent assay) test for heparin antibody presence
- start direct thrombin inhibitor and continue until platelets stabilize, monitor PTTs, argatroban
- warfarin
- platelets <10K, monitor for changes in LOC (intracranial bleed)
how is idiopathic thrombocytopenia purpura (ITP) diagnosed?
- only decreased platelets, rest of CBC normal
- drugs that lead to thrombocytopenia and other clinical conditions (lupus, chronic lymphocytic leukemia) are not present
what are S/S of ITP?
- expected: petechiae, purpura, easy bruising
- common: epistaxis, gingival bleeding, menorrhagia
- rare: GI bleeding, hematuria, ICH
- numerous differential diagnoses need to be r/o
what is plasmapheresis and what is it indicated for?
- filtering and separation of plasma from whole blood via semipermeable membranes; done via central line similar to catheters used for HD
- Guillain-Barre syndrome, myasthenia gravis, thrombotic thrombocytopenic purpura
what are contraindications for plasmapheresis?
- pt’s who can’t tolerate central line placement
- actively septic or hemodynamically unstable
- allergies to FFP or albumin
- heparin allergies; used as an anticoagulant during plasmapheresis
- hypocalcemia pos at risk for worsening b/c citrate is commonly used to prevent clotting and can potentiate hypocalcemia
what are some acute (within 24hrs) S/S of transfusion reactions?
- respiratory: tachypnea, dyspnea, wheezing, rales, stridor, hypoxia
- CV: tachy/bradycardia, hyper/hypoTN, JVD, arrhythmia
- immune: fever (>1C), chills, rigors
- cutaneous: pruritus, uticaria, erythema, flushing, petechiae, cyanosis
- GI: n/v
- pain: HA, chest, ab, back/flank, infusion site
- renal: red urine (hemolytic, non-antibody mediated)
how would you manage acute hemolytic reactions (antibody mediated)?
- anticipate hypotension, renal failure, and DIC
- prophylactic measures to reduce risk of renal failure may include vigorous hydration with crystalloid solutions, and osmotic diuresis with 20% mannitol
- if DIC is documented and bleeding requires treatment, transfusions of frozen plasma, pooled cryo, and/or platelet concentrates may be indicated
how would you manage acute hemolytic reactions (non-antibody mediated)?
- transfusion of serologically compatible, although damaged, RBCs usually does not require rigorous management
- diuresis induced by an infusion of 500ml of NS/hr or as tolerated by pt, until red urine subsides
