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hematological system and diseases Flashcards

1
Q

describe anemia

A
  • 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
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2
Q

what are the most common causes of anemia?

A
  • iron deficiency
  • chronic disease
  • acute blood loss
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3
Q

what causes the oxyhgb dissociation curve to shift left?

A
  • decreased temp (hypothermia)
  • decreased 2-3 DPG
  • decreased hydrogen ions (alkalosis)
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4
Q

what happens with a left shift of the oxyhgb dissociation curve?

A

-higher affinity for O2 and hgb binding
-less O2 to the tissues
“hangs on”

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5
Q

what causes the oxyhgb dissociation curve to shift right?

A
  • increased temp (hyperthermia)
  • increased 2-3 DPG
  • increased hydrogen ions (acidosis)
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6
Q

what happens with a right shift of the oxyhgb dissociation curve?

A

-less affinity for O2 and hgb binding
-more O2 to tissues
“throws off”

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7
Q

describe the relationship between SaO2 and PaO2

A
  • 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
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8
Q

what is the minimal acceptable pre op hgb?

A
  • age, chronic disease and anticipated surgical blood loss must be considered (pt. specific)
  • hgb of 10 g/dL commonly used
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9
Q

what is considered peak O2 carrying?

A

hct of 30%

  • less than 30%, decreased carrying capacity (anemia)
  • more than 30%, increased viscosity
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10
Q

how much more do PRBCs increase hgb in contrast to whole blood?

A

2x more

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11
Q

how does chronic anemia effect the oxyhgb curve?

A
  • increased 2,3 DPG, causing a right shift

- causing decreased affinity of O2 and hgb binding and more O2 to tissues

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12
Q

how does decreased temperature effect the oxyhgb curve?

A
  • causes a left shift

- increased affinity, decreased O2 to the tissues

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13
Q

when should the anemic pt. be transfused?

A
  • 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
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14
Q

describe the RBC structure

A
  • 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
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15
Q

name some RBC structure disorders

A
  • hereditary spherocytosis
  • hereditary elliptocytosis
  • paroxysmal nocturnal hemoglobinuria
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16
Q

describe hereditary spherocytosis and anesthesia implications

A
  • 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
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17
Q

describe hereditary elliptocytosis and anesthesia implications

A
  • abnormal membrane protein
  • prevalent in areas with malaria
  • heterozygous is mild
  • homozygous can be severe
  • AIs: like anemia
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18
Q

describe paroxysmal nocturnal hemoglobinuria and anesthesia implications

A
  • abnormal membrane protein
  • increased risk of venous thrombosis
  • chronic hemolytic anemia
  • life expectancy 8-10 yrs. after diagnosis
  • AIs: anemia, hypercoagulability
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19
Q

what are some RBC metabolism disorders?

A
  • glucose-6-phosphate dehydrogenase (G6PD) deficiency

- pyruvate kinase deficiency

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20
Q

describe glucose-6-phosphate dehydrogenase deficiency

A
  • 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
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21
Q

describe pyruvate kinase deficiency

A
  • 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
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22
Q

describe the hemoglobin molecule

A
  • 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
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23
Q

describe sickle S hgb (hgb SS) disease

A
  • 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
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24
Q

describe acute chest syndrome associated with hgb SS

A
  • 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)
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25
Q

what interventions peri-op can help prevent acute chest syndrome?

A
  • 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
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26
Q

what are anesthesia implications for hgb SS?

A
  • 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
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27
Q

what are other pathologies of hgb?

A
  • sickle C hgb
  • sickle beta-thalassemia
  • misc
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28
Q

describe sickle C hgb (hgb C)

A
  • 1/4 the prevalence of Hgb SS
  • cellular dehydration leads to hemolytic anemia
  • AIs: treat like anemia
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29
Q

describe sickle beta-thalassemia

A
  • 1/10th the prevalence of hgb SS

- severity depends on hgb A (good hgb) levels (decreased hgb A leads to hgb SS symptoms)

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30
Q

describe miscellaneous hgb pathologies

A
  • 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
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31
Q

describe macrocytic anemias

A
  • 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)
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32
Q

what are some causes of folate and B12 deficiency?

A
  • 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
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33
Q

what are treatments for macrocytic anemias?

A
  • vitamin therapy (oral or IV)

- PRBCs

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34
Q

what are types of microcytic anemias

A
  • iron deficiency: nutritional in children; chronic blood loss in adults
  • thalassemia: defective globin chains
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35
Q

what are treatments for iron deficiency?

A
  • iron
  • EPO
  • transfusion
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36
Q

describe different severities of thalassemia

A
  • minor: usually clinically insignificant
  • intermedia: more severe; can have hepatosplenomegaly, cardiomegaly, skeletal changes
  • major: severe, life-threatening childhood anemia
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37
Q

describe effects of major thalassemia

A
  • 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
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38
Q

what are treatments and anesthesia implications for thalassemia?

A
  • 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
39
Q

describe hgb with increased O2 affinity

A
  • 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

40
Q

what are anesthesia implications for hgb with increased O2 affinity?

A
  • 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
41
Q

describe methemoglobinemia

A
  • 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)
42
Q

what is treatment of methemoglobinemia?

A
  • IV methylene blue

* only effective with normal G6PD function

43
Q

describe aplastic (Fanconi) anemia

A

-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

44
Q

what are anesthesia implications for aplastic anemia?

A
  • transfuse for significant anemia, thrombocytopenia

- antibiotic coverage d/t immunocompromise

45
Q

describe polycythemias

A
  • 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
46
Q

what are anesthesia implications for all polycythemias?

A
  • pre-op phlebotomy if severe
  • may be hypercoagulable with paradoxical DIC like bleeding
  • good fluid management; caution with NPO time (dehydration)
  • hemodilute pt.
47
Q

describe polycythemia vera (PV)

A
  • “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
48
Q

how is polycythemia vera treated?

A

-phlebotomy and/or hydroxyurea

49
Q

what are 2 secondary polycythemias?

A
  • hypoxia induced

- EPO induced

50
Q

describe hypoxia induced polycythemia

A
  • 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
51
Q

describe EPO induced polycythemia

A
  • renal disease and EPO secreting tumors

- athletic “doping”

52
Q

list the clotting factors

A 
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
53
Q

what are the 3 phases of the new coagulation model?

A
  • initiation phase
  • amplification phase
  • propagation phase
54
Q

describe the initiation phase of the coagulation model

A
  • vessel damage
  • tissue factor (TF) release which binds with VIIa
  • conversion of X to Xa
  • small amount of thrombin
55
Q

describe the amplification phase of the coagulation model

A

the small amount of thrombin begins to activate:

  • platelets
  • V
  • XI
56
Q

describe the propagation phase of the coagulation model

A
  • 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
57
Q

describe factor disorders of the initiation phase

A
  • 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
58
Q

what are disadvantages of FFP use?

A
  • large volume needed to significantly increase factor levels
  • caution with CV pts./overload
59
Q

what are disadvantages of concentrates?

A
  • increased risk of thrombus and DIC

- varying levels of specific factors with different commercially prepared concentrates

60
Q

describe hemophilia A

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
61
Q

describe anesthesia implications with hemophilia A

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)
62
Q

describe hemophilia B

A
  • 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
63
Q

describe anesthesia implications with hemophilia B

A
  • 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
64
Q

describe acquired fVIII or fIX inhibitors

A

-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

65
Q

describe anesthesia implications for acquired fVIII or fIX inhibitors

A
  • 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)
66
Q

describe Rosenthal’s disease

A
  • Factor XI disease
  • more rare than hemophilias
  • AIs dependent on severity of disease and history
  • treat with PCCs or Novo7
67
Q

describe fibrinogen disorders

A
  • 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
68
Q

describe factor XIII disorder

A
  • 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)
69
Q

describe thrombocytopenia

A
  • 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
70
Q

how can platelet count be increased?

A

-1 U apheresis platelets or 4-8 U donor platelets will increase by 50k

71
Q

what are some congenital platelet production disorders?

A
  • 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)
72
Q

what are some acquired platelet production disorders?

A

-d/t bone marrow damage from radiation, chemo, toxins, ETOH, hepatitis, Vit B12 deficiency, malignancies (multiple myeloma, leukemia, lymphoma)

73
Q

what are anesthesia implications for platelet production disorders?

A
  • platelet transfusion

- treat cause of thrombocytopenia

74
Q

what are the nonimmune platelet destruction disorders?

A
  • disseminated intravascular coagulation (DIC)
  • thrombotic thrombocytopenic purpura (TTP)
  • hemolytic uremic syndrome (HUS)
  • HELLP syndrome
  • all can lead to widespread thrombus w/ end organ damage
75
Q

describe DIC

A
  • 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
76
Q

describe thrombotic thrombocytopenia purpura (TTP)

A
  • 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
77
Q

describe hemolytic uremic syndrome (HUS)

A
  • 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
78
Q

describe HELLP syndrome

A
  • 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
79
Q

describe anesthesia implications for TTP, HUS, and HELLP

A
  • 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
80
Q

what are autoimmune platelet destruction disorders?

A
  • 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)
81
Q

what are the types of heparin induced thrombocytopenia?

A
  • 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
82
Q

describe Type 2 of HIT

A
  • 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
83
Q

what are anesthesia implications with HIT?

A
  • 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)
84
Q

describe idiopathic thrombocytopenia purpura (ITP)

A
  • 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
85
Q

describe Von Willebrand’s disease (vWD)

A
  • 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
86
Q

what are anesthesia implications for Von Willebrand’s disease?

A
  • 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
87
Q

describe acquired platelet dysfunction

A
  • 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)
88
Q

describe anesthesia implications with platelet disorders

A
  • 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
89
Q

described inherited hypercoagulation disorders

A

(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
90
Q

describe acquired hypercoagulation

A
  • 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
91
Q

what are anesthesia implications for hypercoagulation?

A
  • 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
92
Q

what are anesthesia implications for long term anticoagulation?

A
  • 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”
93
Q

what are anesthesia implications for arterial hypercoagulation?

A
  • 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

advanced pathophysiology (3 decks)

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