hematological system and diseases Flashcards
describe anemia
- deficiency of RBCs
- H&H: women- 11.5/36; men- 12.5/40
- decreased arterial O2 content
- right shift of oxyhgb dissociation curve (increased O2 to tissues)
- increased CO d/t decreased viscosity
- decreased tissue O2 leading to erythropoietin (EPO) stimulation and an increase in RBC production
what are the most common causes of anemia?
- iron deficiency
- chronic disease
- acute blood loss
what causes the oxyhgb dissociation curve to shift left?
- decreased temp (hypothermia)
- decreased 2-3 DPG
- decreased hydrogen ions (alkalosis)
what happens with a left shift of the oxyhgb dissociation curve?
-higher affinity for O2 and hgb binding
-less O2 to the tissues
“hangs on”
what causes the oxyhgb dissociation curve to shift right?
- increased temp (hyperthermia)
- increased 2-3 DPG
- increased hydrogen ions (acidosis)
what happens with a right shift of the oxyhgb dissociation curve?
-less affinity for O2 and hgb binding
-more O2 to tissues
“throws off”
describe the relationship between SaO2 and PaO2
- normal saturation is maintained anywhere within the normal range for PaO2 of 80-100 mmHg
- below 60 mmHg, (or below 90% saturation), saturation levels begin to drop rapidly
- this is the reason 90% is usually considered the lowest acceptable SpO2 reading
what is the minimal acceptable pre op hgb?
- age, chronic disease and anticipated surgical blood loss must be considered (pt. specific)
- hgb of 10 g/dL commonly used
what is considered peak O2 carrying?
hct of 30%
- less than 30%, decreased carrying capacity (anemia)
- more than 30%, increased viscosity
how much more do PRBCs increase hgb in contrast to whole blood?
2x more
how does chronic anemia effect the oxyhgb curve?
- increased 2,3 DPG, causing a right shift
- causing decreased affinity of O2 and hgb binding and more O2 to tissues
how does decreased temperature effect the oxyhgb curve?
- causes a left shift
- increased affinity, decreased O2 to the tissues
when should the anemic pt. be transfused?
- if normovolemic, transfuse when symptomatic
- transfuse with acute blood loss when hgb drops to 7 g/dL (hct 21), esp. with comorbidities
- consider normovolemic hemodilution or cell saver
describe the RBC structure
- bi-concave disc with no nucleus, no mitochondria, 33% hgb
- 2, 3 DPG and ATP provide intracellular energy
- life span: 100-120 days
- renal O2 sensors regulate EPO
- EPO stimulates RBC production in bone marrow
name some RBC structure disorders
- hereditary spherocytosis
- hereditary elliptocytosis
- paroxysmal nocturnal hemoglobinuria
describe hereditary spherocytosis and anesthesia implications
- abnormal membrane protein
- most common inherited hemolytic anemia
- 1/3 very mild
- 5% can have life threatening hemolytic crisis usually d/t infectious illness
- prone to cholelithiasis (gallstones)
- AIs: episodic anemia with infection and cholelithiasis
describe hereditary elliptocytosis and anesthesia implications
- abnormal membrane protein
- prevalent in areas with malaria
- heterozygous is mild
- homozygous can be severe
- AIs: like anemia
describe paroxysmal nocturnal hemoglobinuria and anesthesia implications
- abnormal membrane protein
- increased risk of venous thrombosis
- chronic hemolytic anemia
- life expectancy 8-10 yrs. after diagnosis
- AIs: anemia, hypercoagulability
what are some RBC metabolism disorders?
- glucose-6-phosphate dehydrogenase (G6PD) deficiency
- pyruvate kinase deficiency
describe glucose-6-phosphate dehydrogenase deficiency
- many affected mostly in Asia and the Mediterranean area
- can cause acute, chronic, or very mild hemolytic disease
- precipitated by drugs (forane, sevo, diazepam, lidocaine, prilocaine), infections, fava beans
- therapeutic methylene blue can be life threatening (use in methemoglobinemia, vasoplegic syndrome)
- AIs: dependent on degree of hemolysis; caution w/ pre-op infection and drugs known to precipitate crisis
- infection/sepsis major trigger
describe pyruvate kinase deficiency
- can cause life threatening congenital hemolytic anemia requiring exchange transfusion
- usually chronic with varying hemolysis
- splenectomy may prevent hemolysis
- AIs: dependent on degree of hemolysis; caution w/ pre-op infection and drugs known to precipitate crisis
- infection/sepsis major trigger
describe the hemoglobin molecule
- made up of alpha chains, beta chains, and heme groups
- each heme group binds an O2 molecule
- most disorders r/t amino acid substitution on alpha or beta chains
describe sickle S hgb (hgb SS) disease
- disorder of the beta chain
- membrane distortion causing clumping (sickling)
- homozygous (SS anemia): severe hemolytic anemia, vaso-occlusive crises, splenic and renal infarcts
- leading mortality and morbidity d/.t pulmonary and neuro complications (clots)
- children and adolescents: infarct CVAs
- adults: hemorrhagic CVAs
describe acute chest syndrome associated with hgb SS
- 2-3 days post op
- lobular pneumonia-like illness with severe chest pain, fever, tachypnea, cough
- very painful
- tx: transfuse, O2, analgesia, inhaled nitric oxide (vasodilates)
what interventions peri-op can help prevent acute chest syndrome?
- well hydrated
- well oxygenated
- warm
- usually bring in the night before and begin to hydrate while NPO and consult hematology to ensure hct is adequate prior to procedure
what are anesthesia implications for hgb SS?
- trait carries no increased risk
- old tx: aggressive intra-op transfusion
- current tx: pre-op transfusion to hct of 30%
- good pain management to decrease sickling/crisis trigger
- may be tolerant to pain meds
- **warm, wet, green: normothermia, hydration, oxygenation
what are other pathologies of hgb?
- sickle C hgb
- sickle beta-thalassemia
- misc
describe sickle C hgb (hgb C)
- 1/4 the prevalence of Hgb SS
- cellular dehydration leads to hemolytic anemia
- AIs: treat like anemia
describe sickle beta-thalassemia
- 1/10th the prevalence of hgb SS
- severity depends on hgb A (good hgb) levels (decreased hgb A leads to hgb SS symptoms)
describe miscellaneous hgb pathologies
- greater than 100 identified, most w/o complications
- hgb chain fragments and heme form Heinz bodies which destabilize RBC membrane
- level of Heinz body formation dictates degree of hemolysis
- can have hemoglobinuria and/or renal failure
- splenectomy reduces or eliminates symptoms
describe macrocytic anemias
- folate and B12 deficiency
- folic acid and B12 essential for DNA synthesis so high turnover tissue (bone marrow) quickly affected
- marrow precursors appear large and cannot divide (macrocytic)
- severe: impaired memory, peripheral neuropathies (not good candidates for regional; document well any current issues)
what are some causes of folate and B12 deficiency?
- prolonged N2O exposure: methionine synthetase inhibition causes impaired B12 activity (poor scavenging, inhalation inductions and uncuffed tubes on children)
- alcoholism and malabsorption lead to folate deficiency
what are treatments for macrocytic anemias?
- vitamin therapy (oral or IV)
- PRBCs
what are types of microcytic anemias
- iron deficiency: nutritional in children; chronic blood loss in adults
- thalassemia: defective globin chains
what are treatments for iron deficiency?
- iron
- EPO
- transfusion
describe different severities of thalassemia
- minor: usually clinically insignificant
- intermedia: more severe; can have hepatosplenomegaly, cardiomegaly, skeletal changes
- major: severe, life-threatening childhood anemia
describe effects of major thalassemia
- long-term transfusion therapy leads to iron overload, cirrhosis, right heart failure, and eventually requires chelation
- decreased CaO2 increases EPO, which increases the production of defective hgb causing inclusion bodies and RBC membrane damage
what are treatments and anesthesia implications for thalassemia?
- splenectomy helpful but increases risk of sepsis, esp. in children under 5 y/o
- bone marrow transplant
- AIs: dependent on severity of anemia; similar to hgb SS
describe hgb with increased O2 affinity
- left shift of oxyhgb D curve (decreased O2 to tissues)
- normal hct, mild tissue hypoxia, and increased EPO lead to polycythemia, increased viscosity, and hypercoagulability
what are anesthesia implications for hgb with increased O2 affinity?
- hct greater than 55% may require pre-op exchange transfusion
- hemoconcentration from NPO time must be avoided
- hemodilution and blood loss can cause even less O2 to tissues
- Chesapeake, J-Capetown, Kemsey, Creteil
describe methemoglobinemia
- causes: globin mutation, inefficient or overwhelmed reductase system, toxins
- ferrous iron (Fe++) oxidized to ferric (Fe+++) state causing a left shift of the oxyhgb D curve which leads to severe hypoxia
- normally controlled by an RBC reductase enzyme system
- less than 30%: little compromise
- 30-50%: symptomatic hypoxia
- greater than 50%: coma and/or death
- cyanotic appearance with adequate PaO2 (hgb is hanging on to O2 so cant get to tissues)
what is treatment of methemoglobinemia?
- IV methylene blue
* only effective with normal G6PD function
describe aplastic (Fanconi) anemia
-severe pancytopenia presents in children and young adults
-leukemia and other malignancies later in life
-can be chromosomal (autosomal recessive), dose-dependent drug/radiation induced, viral, cancer induced
(usually reversible if drug, radiation, or viral induced)
-chloramphenicol and viral hepatitis can cause irreversible anemia
what are anesthesia implications for aplastic anemia?
- transfuse for significant anemia, thrombocytopenia
- antibiotic coverage d/t immunocompromise
describe polycythemias
- increased RBC mass and hct
- tissue oxygenation best at hct 33-36% or hgb 11-12 g/dL
- hct greater than 50%: increased viscosity, decreased flow (esp. cerebral)
- hct 55-60%: HAs, fatigue; seen with chronic lung disease
- hct greater than 60%: life threatening; loss of organ perfusion and thrombosis
what are anesthesia implications for all polycythemias?
- pre-op phlebotomy if severe
- may be hypercoagulable with paradoxical DIC like bleeding
- good fluid management; caution with NPO time (dehydration)
- hemodilute pt.
describe polycythemia vera (PV)
- “primary” and chromosomal
- increased RBCs, WBCs, and platelets
- usually appears after 50 y/o
- thrombosis, usually cerebral, often 1st event
- PV leads to acquired von Willebrand’s, causing consumptive coagulopathy, abnormal clotting, and increased bleeding
- high M&M d/t thrombi, cancer, myelofibrosis, leukemia
how is polycythemia vera treated?
-phlebotomy and/or hydroxyurea
what are 2 secondary polycythemias?
- hypoxia induced
- EPO induced
describe hypoxia induced polycythemia
- living at greater than 7,000 ft.: usu. clinically insignificant high hct; acute or chronic “mountain sickness” with HAs, N/V, cerebral edema
- cardiac disease: esp. congenital right to left shunts with associated cyanosis; low CO states lead to EPO stimulation
- pulmonary disease: pickwickian syndrome (morbid obesity with hypoventilation
- methemoglobinemia
describe EPO induced polycythemia
- renal disease and EPO secreting tumors
- athletic “doping”
list the clotting factors
I. fibrinogen II. prothrombin III. thromboplastin (tissue) IV. calcium V. proaccelerin VII. proconvertin VIII. antihemophilic IX. Christmas X. Stuart XI. thromboplastin (plasma) XII. Hageman XIII. fibrin-stabilizing
what are the 3 phases of the new coagulation model?
- initiation phase
- amplification phase
- propagation phase
describe the initiation phase of the coagulation model
- vessel damage
- tissue factor (TF) release which binds with VIIa
- conversion of X to Xa
- small amount of thrombin
describe the amplification phase of the coagulation model
the small amount of thrombin begins to activate:
- platelets
- V
- XI
describe the propagation phase of the coagulation model
- VIII, IX, and calcium on platelets
- activation of X while thrombin activates platelets, V, VII
- VIIIa-IXa complex
- VIIIa-IXa complex switches reaction to intrinsic (Xase) pathway
- 50x more efficient at Xa generation
- increased Xa leads to large amount of thrombin
- thrombin converts fibrinogen to fibrin
describe factor disorders of the initiation phase
- fVII: rare, variable severity, most asymptomatic
- prolonged PT, normal PTT
- tx: FFP, fix complex, recombinant fVII (Novo7)
- fX, fV, fII (prothrombin): severe deficiencies rare
- prolonged PT and PTT
- tx: FFP, concentrates
what are disadvantages of FFP use?
- large volume needed to significantly increase factor levels
- caution with CV pts./overload
what are disadvantages of concentrates?
- increased risk of thrombus and DIC
- varying levels of specific factors with different commercially prepared concentrates
describe hemophilia A
- inherited factor VIII disorder
- X linked (usually seen in males)
- several mutations, most severe have fVIII activity less than 1% of normal
- usu. diagnosed in childhood d/t spontaneous hemorrhage
- frequent fVIII transfusion
- levels of 6-30% mildly affected but at risk for major bleeding with surgery
- prolonged PTT, normal PT
describe anesthesia implications with hemophilia A
- bring fVIII activity up to 100% pre-op (confirm w/ labs)
- half life of 12 hrs in adults, 6 hrs in children
- therapy to keep 50% activity or better must continue up to 6 wks post-op depending on procedure
- 30% develop inhibiting antibodies, making difficult to transfuse and treat (recombinants don’t reduce antibody formation)
describe hemophilia B
- fIX deficiency
- less than 1%, significant bleeding (clinically like hem A)
- 5-40% activity is very mild disease and my go undetected until surgery
- prolonged PTT, normal PT
describe anesthesia implications with hemophilia B
- caution with recombinant combos (PCCS- prothrombin complex concentrates)
- to get significant fIX, large amounts of combo needed, leading to thrombi, esp. in ortho cases
- use only pure fIX for Hem B
- collagen absorption of fIX requires doubling the higher dose, but half life much longer
describe acquired fVIII or fIX inhibitors
-up to 40% of severe Hem A develop circulating inhibitors to fVIII; much lower incidence in Hem B/fIX
-test: Mixing study called Bethesda essay
high responders: greater than 10 Bethesda U/mL inhibitors that peak and drop with factor replacement
low responders: maintain low level inhibition even with factor treatment
describe anesthesia implications for acquired fVIII or fIX inhibitors
- low responders: fVIII or fIX
- high responders: PCCs or Novo7 (fVIII or IX alone ineffective)
- Novo7 is current treatment of choice for acquired inhibitors
- may require Novo7 infusion (very expensive)
describe Rosenthal’s disease
- Factor XI disease
- more rare than hemophilias
- AIs dependent on severity of disease and history
- treat with PCCs or Novo7
describe fibrinogen disorders
- afibrinogenemia, hypofibrinogenemia, & dysfibrinogenemia
- severe bleeding w/ fibrinogen level less than 50 mg/dL
- normal 200-400 mg/dL
- more than 300 mutations w/ varying severity, many clinically insignificant
- some have tendency to form thrombi instead of bleeding
- AIs dependent on severity, bleeding, hx
- treat w/ cryoprecipitate (10-12 U to increase fibrinogen by 100 mg/dL
- thrombus formers need anticoagulant therapy
describe factor XIII disorder
- rare
- umbilical/circ bleeding at birth
- soft tissue bleeding in adults
- fetal loss is almost 100%
- treat w/ FFP, cryo, or several pre-op wks of concentrated fXIII (fibrogammin)
describe thrombocytopenia
- platelet disorder
- categorized as disorder of production, distribution, opr destruction
- minimal pre-op platelet count: minor procedure (20-30K), major (greater than 50k), neuro (greater than 100k)
- spontaneous bleeding occurs at less than 15k
- bad sign: petechial rash
how can platelet count be increased?
-1 U apheresis platelets or 4-8 U donor platelets will increase by 50k
what are some congenital platelet production disorders?
- hypoplastic thrombocytopenia with absent radius (TAR syndrome): severe (less than 30k) but slowly improves; often have bilateral radial deformities
- Fanconi’s Anemia: usu. diagnosed after 7 y/o; bone marrow transplant only cure
- May-Hegglin: large, dysfunctional plts. w/ Dohle bodies in WBCs
- Wiskott-Aldrich: eczema, immunodeficient; small, dysfunctional plts.
- autosomal dominant: large, dysfunctional plts., often with deafness and nephritis (Alport’s syndrome)
what are some acquired platelet production disorders?
-d/t bone marrow damage from radiation, chemo, toxins, ETOH, hepatitis, Vit B12 deficiency, malignancies (multiple myeloma, leukemia, lymphoma)
what are anesthesia implications for platelet production disorders?
- platelet transfusion
- treat cause of thrombocytopenia
what are the nonimmune platelet destruction disorders?
- disseminated intravascular coagulation (DIC)
- thrombotic thrombocytopenic purpura (TTP)
- hemolytic uremic syndrome (HUS)
- HELLP syndrome
- all can lead to widespread thrombus w/ end organ damage
describe DIC
- marked endothelial disruption leads to a consumptive coagulopathy w/ microvascular clotting (thrombi) causing bleeding
- can have severe thrombocytopenia w/ heavy bleeding, prolonged coag times or low grade w/ less bleeding
- etiology can be viral, bacteremic, d/t malignancy, chemo, vasculitis, AIDS
- most significant platelet destruction from TTP, HUS, HELLP syndrome
describe thrombotic thrombocytopenia purpura (TTP)
- platelet thrombi in microvasculature causing decreased platelets and hemolytic anemia
- frequent 5 symptoms: fever, renal insufficiency, low platelets, anemia, neuro symtpoms
- can be familial, idiopathic, chronic/relapsing, complication of bone marrow transplant, or drugs
- preeclampsia/HELLP syndrome causes postpartum TTP
describe hemolytic uremic syndrome (HUS)
- similar to TTP but usu. in children and secondary to E.coli infection
- may lead to acute renal failure that may require short or long term dialysis
- most recover spontaneously with less than 5% mortality
- adults and older children have higher mortality
- often require plasma exchange and/or hemodialysis
describe HELLP syndrome
- mild thrombocytopenia (70-150k) often seen in pregnancy d/t dilutional anemias
- 50% of preeclampsia leads to DIC like thrombocytopenia (20-40k)
- H: hemolysis
- EL: elevated liver enzymes
- LP: low platelets
- need BP control and delivery for regression of symptoms
- some progress to postpartum TTP and/or HUS which is life threatening w/ poor prognosis
- plasma exchange and/or immunoglobulins not very effective
describe anesthesia implications for TTP, HUS, and HELLP
- delay surgery if possible until coags normalized/underlying disorder controlled
- if part of DIC: plts., FFP, supportive therapy, treat underlying cause
- TTP or HUS: plts. for severe bleeding only (plt. transfusion can lead to thrombosis w/ organ damage)
- HUS: dialysis and/or pheresis for unresolving renal failure
- HELLP: plasma exchange if unresolved after delivery
what are autoimmune platelet destruction disorders?
- thrombocytopenia purpura: toxins, post-transfusion (antibody formation) or drug-induced
- heparin-induced thrombocytopenia (HIT): usu. d/t unfractionated heparin but can also be d/t LMW heparin (Lovenox)
what are the types of heparin induced thrombocytopenia?
- Type 1 (non immune): early therapy- heparin binds to plts. decreasing plt. life; usu. transient and mild
- Type 2 (immune mediated): heparin-plt. complex causes antibody formation which bind to platelet receptors causing plt. activation and clumping (procoagulation)
- heparin plot complex also increases thrombin, leading to thrombus and organ damage
- more common w/ bovine v. procine and more common in ortho
- increases risk of CVA, MI, death in coronary bypass pts. and unstable angina
describe Type 2 of HIT
- early onset (previous therapy) or delayed onset (after heparin D/C’d
- consider direct thrombin inhibitor (Pradaxa) for plt. drop of 50%
- acute HIT type 2 can occur if heparin resumed within 20 days
- symptoms of acute HIT: dyspnea, diaphoresis, HTN, tachycardia, risk of fatal embolus
what are anesthesia implications with HIT?
- D/C heparin (including LMW) immediately
- thrombotic events with HIT must be treated with direct thrombin inhibitor
- oral anticoagulation (warfarin) w/o direct thrombin inhibitor can cause increased thrombosis, necrosis, and gangrene
- reverse warfarin with Vit. K
- platelets for life threatening hemorrhage or bleeding into closed space
- steroid therapy for ITP-type clinical picture
- some pts. can tolerate very low plt. counts w/o transfusion
- special considerations for HIV/AIDS (zidovudine- AZT therapy; splenectomy
- HIT pts. for non elective CP bypass: anticoagulate w/ direct thrombin inhibitor (if elective, delay until HIT resolved)
describe idiopathic thrombocytopenia purpura (ITP)
- autoimmune (unrelated to drugs, infection, or autoimmune disease)
- diagnosis of exclusion
- most proceed to chronic thrombocytopenic state (20-100k)
- splenectomy may be helpful
- severe, acute episodes w/ bleeding treated w/ high-dose steroids
- for ER sugery or IVH, platelets, immunoglobulins
- pregnancy: treat significant thrombocytopenia during last few wks; neonatal plt. count usu. normal but may be low
describe Von Willebrand’s disease (vWD)
- congenital disorder affecting platelet function
- severe vWD w/ life-threatening bleeding is rare
- basic screening: PT, PTT, bleeding time, plt. count
- full vWD screen: fVIII activity and vWF acitivity to determine which Type
what are anesthesia implications for Von Willebrand’s disease?
- dependent on type of acuity of procedure
- IV or nasal desmopressin (DDAVP), cryoprecipitate, vWF-fVIII (1: responsive to DDAVP; 2: response to DDAVP variable; 3: non responsive to DDAVP)
- treat severe bleeders like hemophilias
- commercial vWF-fVIII complex preferred over cryo to decrease the risk of infection
describe acquired platelet dysfunction
- myeloproliferative disease
- dysproteinemia
- liver disease
- drugs: ASA, foods, ABs (PCNs), dextran
- ASA: irreversible cyclooxygenase inhibition causing plt. thromboxane inhibition
- other NSAIDS cause reversible inhibition
- dextran interferes with aggregation (hetastarch safer)
describe anesthesia implications with platelet disorders
- absolute platelet count does NOT predict risk
- DDAVP works well for mild bleeding
- platelet transfusion required for heavy bleeding
- normal bleeding time and TEG may not predict surgical risk
- hypothermia (less than 35 C) and acidosis (less than 7.3 ph) lead to platelet dysfunction (including transfused plts.)
- ASA given greater than 2 hours pre-op will not affect transfused platelets
described inherited hypercoagulation disorders
(antithrombin III: most important defense to clot formation in healthy vessels
- hereditary antithrombin III deficiency: undesired clot formation in healthy vessels
- AIs: anticoagulate, maintain antithrombin III level over 80% for 5 days post op w/ concentrates
- hereditary protein C and S deficiency: thrombin restricted, causing risk of thrombus (C & S synthesis is Vit K dependent, so warfarin therapy can actually increase coagulability)
- AIs: may need FFP or prothrombin concentrates
- factor V leiden: resistant to inactivation causing to circulate longer and increase thrombin; mild to mod. risk of thrombus
- prothrombin gene mutation: similar risk to factor V leiden
- factor V leiden and prothrombin gene mutation much higher in European descent; rare in African and Asian
describe acquired hypercoagulation
- myeloproliferative disorders: polycythemia vera
- malignancies, esp. pancreas, colon, stomach, ovaries
- pregnancy, esp. w/ hx of thrombi, PE, obesity, bed rest
- pts. taking oral contraceptives, esp. w/ smoking, migraines, inherited hypercoagulability, have 30x higher risk of DVT, PE, cerebral thrombi
- nephrotic syndrome, esp. renal vein
- antiphospholipid antibodies such as w/ lupus can progress to catastrophic antiphospholipid syndrome w/ widespread thrombosis, ARDS, DIC, multi organ failure
what are anesthesia implications for hypercoagulation?
- early ambulation, elastic stockings, subQ heparin, outpatient warfarin
- must balance bleeding risk w/ problematic clotting risk
- ASA is poor prophylaxis
- pneumatic compression hose almost as good as heparin
- post-op heparin or warfarin for high risk pts.
- FDA advisory: avoid SABs and epidural anesthesia on pts. receiving heparin d/t increased risk of epidural bleeding; do not withhold post op anticoagulants to allow for epidural anesthesia
- vena caval filters
what are anesthesia implications for long term anticoagulation?
- minor procedure: no interrupted therapy
- bleeding risk must be balanced w/ post op clotting risk
- moderate to high risk pts., bridge w/ unfractionated or LMW heparin (D/C warfarin 5 days pre-op, start heparin 36 hrs. after warfarin D/C’d)
- stop heparin infusion 6 hrs. pre-op
- stop LMW heparin 18-30 hrs. pre-op depending on dose
- ASA recommendation for regional: D/C LMW heparin 12-24 hrs. pre-op depending on dose
- post-op: warfarin effects delayed 24 hrs. so resume immediately post-op unless high risk of bleeding; consider “bridging”
what are anesthesia implications for arterial hypercoagulation?
- post MI wall motion dysfunction: risk of thrombi (usu. treated w/ warfarin several months post MI)
- A fib needs long term warfarin therapy (CHADS scoring system for estimating a fib stroke risk)
- pts. w/ lupus antiphospholipid antibodies at high risk of arterial AND venous thrombi
- some procedures cause 100% risk of thrombi
- venous thrombi: 2 million/yr
- 150,000 die from PE
