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COEXISTING > ANEMIA & COAGULOPATHIES > Flashcards

ANEMIA & COAGULOPATHIES Flashcards

1
Q

anemia definition

A

decrease in red cell mass

  • women hgb <11.5; hct<36%
  • men hgb <12.5; hct<40%

decreases O2 carrying capacity

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2
Q

arterial oxygen content equation

A

CaO2 = (hgb*1.39)SaO2 + PaO2(0.003)

- hgb has biggest effect

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3
Q

compensatory mechanisms of anemia

A
  • decreased blood viscosity
  • decreased SVR (a function of vascular tone & blood viscosity)
  • increased CO (increased SV & HR)
  • tissue redistribution of blood to organs w/ high extraction ratios (myocardium, brain, kidneys – pallor occurs)
  • EPO renal secretion
  • oxyhemoglobin R shift (increased 2,3-DPG –> increases P50)
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4
Q

oxyhemoglobin dissociation curve: P50; P90

A 
P50 = 27mmHg
P90 = 60mmHg
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5
Q

R shift oxyhemoglobin dissociation curve

A

represents reduced affinity of Hgb for O2

things that indicate increased metabolic rate:

  • increased temp
  • increased [H+] (acidosis)
  • increased 2,3 DPG
  • sickle cell anemia
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6
Q

L shift oxyhemoglobin dissociation curve

A

represents increased affinity of Hgb for O2

things that indicate decreased metabolic rate

  • decreased temp
  • decreased [H+] (alkalosis)
  • decreased 2,3 DPG
  • CO
  • abnormal Hgb (metHgb, etc.)
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7
Q

Bohr effect

A

increasing CO2 concentrations in the tissues facilitates release of O2
(and thus the pick up of CO2)

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8
Q

Haldane effect

A

oxygenation of the blood in the lungs facilitates the RBC release of CO2

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9
Q

basic anesthesia management of anemia

A
  • determine underlying disease
  • determine “state” of anemia for that patient
  • don’t disrupt compensatory mechanisms (don’t decrease CO or L shift oxyhgb curve)
  • maximize O2 delivery
  • tx blood loss as necessary
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10
Q

in the compensated anemic patient, are rates of induction w/ volatiles changed?

A

NO

  • less soluble in anemia = faster induction
  • high CO in anemia = slower induction
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11
Q

considerations when thinking of transfusing

A
  1. Hgb (almost always if <6g/dl, consider b/n 6-10) **no transfusion trigger
  2. risks/benefits
  3. coexisting dz (ie CAD - keep hgb>7)
  4. anticipated EBL
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12
Q

goals of transfusion therapy

A
  1. increase oxygen carrying capacity

2. correct a coagulation disorder

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13
Q

risks of RBC transfusion

A
  • hep B/C, HIV, infections
  • longer ICU/hospital LOS
  • transfusion related acute lung injury
  • hemolytic transfusion rxns
  • higher mortality rates
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14
Q

EBL & replacement generalities

A

<15% of total blood volume = no replacement therapy

15-30% loss = replace 3:1 w/ crystalloids

> 30% loss = RBC transfusion to replace O2 carrying capacity

> 50% loss = massive transfusion = add FFP & platelets to the RBC replacement @ 1:1:1

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15
Q

normal adult blood volume

A 
men = 75mL/kg
women = 65mL/kg
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16
Q

allowable blood loss

A

ABL = [EBV*(hct - allowable hct)] / hct

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17
Q

what is the effect of 1U PRBC

A

increases hgb 1g/dL
increases hct 2-3%

1U has a hct of 70%

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18
Q

s/s associated w/ acute blood loss

A

tachycardia
orthostatic hypotension
CVP change

w/ 40% acute blood loss, additional s/s:

  • tachypnea
  • oliguria
  • acidosis
  • restlessness
  • diaphoresis
  • EKG ischemia

MASKED BY ANESTHESIA

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19
Q

hct changes w/ acute blood loss

A

takes 3 days to plateau, may not be reflective of current status

  • decreases in hct >1%/24hrs can only be explained by blood loss/hemolysis
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20
Q

anesthetic management of acute blood loss

A
  • monitoring = invasive?, F/C
  • induction = ketamine/etomidate
  • maintenance = may have to avoid volatiles & just use scopolamine, benzos, opioids
  • keep warm
  • watch surgical field for blood loss, oozing, non-clotting blood, listen to suction, ask.
  • restore intravascular volume = crystalloids, colloids, blood products
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21
Q

labs to monitor w/ acute blood loss

A 
coags
CBC (h/h, platelets)
fibrinogen
Ca++, K+ (RBC have citrate, binds Ca++; K+ leak occurs)
ABGs (met acidosis = hypovolemia)
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22
Q

definition of massive transfusion

A 
>10U of PRBC in 24hrs
-same as-
replacement of at least 1 blood volume in 24hrs
-same as-
replacement of 50% blood volume in 6hrs
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23
Q

consequences of massive transfusion

A
  • hypothermia (use fluid warmer!)
  • volume overload
  • dilutional coagulopathy (no clotting factors in PRBC)
  • 2,3 DPG decrease (none in PRBC)
  • hyperkalemia (K+ leak)
  • citrate toxicity
  • PRBC contains glucose –> converted to lactate –> acidosis
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24
Q

iron deficiency anemia

A

ineffective erythropoiesis
- microcytic, hypochromic anemia

usually infants/small children
adults = reflects depletion of iron stores 2/2 chronic blood loss (GIB, menstruation, CA)

tx = iron; postpone elective surgery x4 weeks if severe to allow for correction

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25
Q

pernicious anemia

A

B12 deficiency = impaired DNA synthesis

  • macrocytic anemia
  • 2/2 EtOH, poor diet, malabsorptive syndromes, whip-its

can also lead to degeneration of lateral & posterior spinal columns = symmetrical paresthesia, unsteady gait
**thick, large, smooth tongue

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26
Q

anesthetic management of pernicious anemia

A
  • AIRWAY management & plan B
  • maintain adequate O2
  • avoid N2O
  • transfusion if necessary
  • consider avoiding regional if paresthesia present
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27
Q

hemolytic anemia

A

accelerated destruction (hemolysis) of erythrocytes

  • increased levels of unconjugated bilirubin
  • increased LDH
  • immature RBCs

EX:

  • hereditary spherocytosis (impaired RBC structure)
  • paroxysmal nocturnal hemoglobinuria (impaired RBC structure)
  • G6PD deficiency (RBC metabolism disorder)
  • pyruvate kinase deficiency (RBC metabolism disorder)
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28
Q

hereditary spherocytosis

A

autosomal dominant
most common hereditary hemolytic anemia in US
- severity ranges
- risk of hemolytic crisis w/ infections
s/s = splenomegaly & fatigue, gallstones, jaundice

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29
Q

anesthetic management of hereditary spherocytosis

A

depends on severity & if hemolytic exacerbation is present

  • avoid infections
  • cardiopulmonary bypass & mechanical valves may = excessive hemolysis
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30
Q

paroxysmal nocturnal hemoglobinuria

A

complement activated RBC hemolysis

  • 20s-80s
  • abnormalities/reduction in RBC membrane protein
  • life expectancy after diagnosis = 10yrs
  • result of CO2 retention & subsequent acidosis (OSA)
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31
Q

anesthetic management of paroxysmal nocturnal hemoglobinuria

A
  • avoid respiratory depressants (acidosis)
  • avoid hypoxemia, hypoperfusion, hypercarbia (acidosis)
  • maintain hydration
  • DVT prophylaxis (high risk 2/2 complement activation)
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32
Q

G6PD deficiency (glucose-6-phosphate dehydrogenase)

A

phosphogluconate oxidative metabolic pathway

  • normally counteracts environmental oxidants & prevents globin denaturation
  • w/ deficiency, oxidative stress = RBC membrane damage & hemolysis
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33
Q

what is the most common RBC enzymatic disorder?

A

G6PD deficiency

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34
Q

classes of G6PD deficiency

A 
class I = chronic hemolytic anemia
to
Class V &amp; VI = mild/no hemolysis
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35
Q

what aggravates preexisting G6PD (ie causes more hemolysis)?

A

oxidative drugs
infection
fava beans

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36
Q

anesthetic management of G6PD deficiency

A

depends on severity & acuity of anemia

  1. avoid risk of hemolysis
  2. avoid oxidative drugs (NSAIDs, quinolones, sulfa drugs, N2O, NO)
  3. avoid drugs that depress G6PD (iso, sevo, diazepam)
  4. avoid methylene blue & metHgb causing drugs (methylene blue = life threatening rxn) (lidocaine?, prilocaine, silver nitrate)
  5. avoid/aggressively treat conditions that cause oxidative stress (hypothermia, acidosis, hyperglycemia, infections)
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37
Q

what is the most common enzyme defect that results in congenital hemolytic anemia?

A

pyruvate kinase deficiency

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38
Q

what is more prevalent, G6PD or pyruvate kinase deficiency? which has more hemolysis?

A

G6PD more prevalent; pyruvate kinase is more hemolytic

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39
Q

what is pyruvate kinase deficiency?

A

accumulation of 2,3-DPG = oxyhgb R shift.
high incidence of hemolysis in the spleen = splenomegaly (improved w/ splenectomy)
- life threatening hemolytic anemia @ birth; chronic jaundice, gall stones

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40
Q

what are some types of acquired hemolytic anemia?

A
  1. immune induced (sensitization of RBCs, disease or drug-induced)
  2. infection induced (ie malaria)
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41
Q

periop considerations w/ hemolytic anemia

A
  1. increased risk of tissue hypoxia
  2. h/o splenectomy = increased infection risk
  3. increased DVT risk 2/2 coag cascade activation
  4. often on EPO preop
  5. consider transfusion if acute hgb drop <8 or chronic <6
  6. PREOP HYDRATION, possibly preop transfusion
  7. caution w/ methylene blue admin
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42
Q

what is sickle cell disease?

A

homozygous inherited disorder of hgb S mutation = defective beta globulin chain (valine substitute for glutamic acid) in 78-90% of hgb

  • extreme states of deoxygenation –> Hgb aggregation & sickled shape cell
  • this can occlude small vessels (impairs O2 delivery)
  • higher rate of hemolysis; average RBC lifespan 10-20 days
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43
Q

complications of sickle cell disease

A
  • severe hemolytic anemia = end organ damage
  • splenic infarction by 10s = infection
  • renal = painless hematuria & loss of concentrating ability = CRF by 30-40s
  • pulmonary damage 2/2 chronic persistent inflammation
  • neuro = ischemia & hemorrhagic strokes
  • vaso-occlusive crises (episodic bone & joint pain associated w/ illness, stress, dehydration)
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44
Q

what is sickle cell crisis

A

life threatening, acute episode of hgb sickling in response to low O2 states

  • ischemia/infarctions of oragns
  • pain, stroke, liver/renal failure, splenic sequesteration, PE
  • ACS
  • PAIN
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45
Q

what is acute chest syndrome as associated w/ sickle cell crisis? tx?

A

can be fatal (typically 2-3 days postop)

  • PNA like; new pulmonary infiltrate w/ one complete lung segment
  • pulm vasc occlusion
  • pleuritic chest px, dyspnea, fever, acute pulm HTN

TX

  • transfusion/exchange transfusion
  • O2, N2O (pulm vasodilation)
  • abx; inhaled bronchodilators
  • aggressive px management
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46
Q

sickle cell trait - what is it and what are the implications for anesthetic management?

A

heterozygous “carriers” of sickle cell disease

  • genotype AS
  • 40% of hgb S; 60% hgb A (normal)
  • usually no anemia/symptoms, need no tx; 5% have some minor symptoms
  • don’t require preop transfusions
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47
Q

sickle cell disease: what are some factors that put these pts at high risk for periop complications?

A
  • advanced age
  • frequent sickling episodes; severe episodes
  • evidence of end-organ damage
  • concurrent infection
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48
Q

w/ sickle cell pts, avoid all situations that lead to:

A
  1. HYPOXEMIA/ACIDOSIS
  2. HYPOVOLEMIA
  3. STASIS
49
Q

preop management of the patient w/ sickle cell disease

A
  • supplemental O2
  • preop hydration x12hrs
  • caution w/ premeds that cause resp depression (acidosis risk)
  • regional for px control (although caution w/ stasis & hypotension –> compensatory vasoconstriction)
  • pain management
  • avoid infections
  • avoid tourniquets
  • keep pt warm
  • maintain high CO
  • take care w/ positioning to avoid stasis
50
Q

what is thalassemia major?

A

inability to form either alpha (a-thalassemia) or beta (b-thalassemia) globulin chains of hgb

  • deficit in O2 carrying capacity prompts high, defective RBC release –> aggregation & precipitation formation
  • severe anemia, often require repeated transfusions
51
Q

hallmarks of thalassemia major

A
  1. ineffective erythropoiesis
  2. hemolytic anemia
  3. hypochromia w/ microcytosis
52
Q

complications of thalassemia major

A
  • extramedullary hematopoiesis (bone marrow hyperplasia, stunted growth, osteoporosis, hepatomegaly) –> large max/frontal bones
  • hemolytic anemia (splenomegaly, CHF, dyspnea, orthopnea)
  • transfusion therapy (iron overload = cirrhosis, RHF)
  • increased infection risk w/ splenectomy
  • arrhythmias
  • spinal cord compression
53
Q

major organs (and implications) affected by iron overload

A
  1. pituitary = impaired growth, infertility
  2. thyroid = hypoparathyroidism
  3. heart = cardiomyopathy, cardiac failure
  4. liver = hepatic cirrhosis
  5. pancreas = DM
  6. gonads = hypogonadism
54
Q

what is thalassemia minor?

A

heterozygous trait for either alpha or beta globulin gene mutation
= mild anemia, normal RBC count

55
Q

anesthetic considerations of the patient w/ thalassemia major

A
  1. hemodynamic: CHF (+/- arrhythmias) common w/ severe anemia, low cardiac reserve, may want to avoid cardiac depressants
  2. hepatosplenomegaly (splenectomy? infection); coagulopathies (+/- regional)
  3. airway (maxillary overgrowth?)
  4. consider complications of iron loading from chronic transfusions
56
Q

what is methemoglobinemia?

A

when iron in Hgb is oxidized from ferrous (+2) to ferric (+3)

57
Q

what are the oxygen delivery implications w/ methemoglobinemia?

A

oxyhemoglobin dissociation curve is markedly shifted to the L = decreased O2 delivery to tissues

58
Q

what are normal methgb levels? what levels cause issues?

A 
normal = <1%
<30% = no compromise to tissue oxygenation
30-50% = symptoms of O2 deprivation
>50% = coma &amp; death
59
Q

what causes methgb?

A
  1. globulin chain mutations that favor hgb M formation (usually asymptomatic)
  2. mutations impairing the methgb reductase system (methgb levels <25%)
  3. toxic exposure to substances that oxidize normal hgb faster than reductase systems can convert back (infants at greater risk; LA, nitrates, NO)
60
Q

anesthetic management of methgb

A
  1. AVOID toxic levels of methgb-causing meds, especially in infants, hgb M, & G6PD deficiency
  2. pulse ox is unreliable (typically reads 85% whether it’s higher or lower)
  3. tx of toxic methgb:
    - avoid tissue hypoxia & further L shift of oxyhgb
    - O2
    - 1-2mg/kg methylene blue 1% over 3-5mins; repeat after 30mins
    - art line
    - correct acidosis
    - monitor EKG for ischemia
61
Q

what is aplastic anemia

A

bone marrow failures characterized by destruction of rapidly growing cells

causes:
- genetic disorders (fanconi)
- drugs
- radiation
- infectious process (viral hepatitis, epstein-barr, HIV, rubella, TB)

62
Q

drugs associated w/ bone marrow damage & subsequent aplastic anemia

A
  • abx
  • antidepressants (TCAs, lithium)
  • antiepileptics
  • anti-inflammatory
  • antidysrhythmics
  • antithyroidal
  • diuretics
  • antihypertensives (captopril)
  • antiuricemics
  • antimalarials
  • hypoglycemics
  • platelet inhibitors (ticlid)
  • tranquilizers
63
Q

anesthetic considerations w/ aplastic anemia

A
  • immunosuppressive therapy (stress dose)
  • reverse isolation
  • prophylactic abx
  • hemorrhage risk
  • LV dysfunction 2/2 hyperdynamic CO
  • coexisting congenital abnormalities
  • difficulty w/ cross matching blood products after multiple transfusions
64
Q

anesthetic management of aplastic anemia

A
  1. preinduction/induction
    - consider pretransfusion
    - avoid nasal intubation, possibility of airway hemorrhage w/ DVL
    - regional depends on coags
    - labile hemodynamic response to induction
  2. maintenance
    - hyperoxia depresses bone marrow, use PEEP instead of increased FiO2
    - avoid nitrous (bone marrow suprression)
    - maintain normothermia
  3. postop
    - oxygenate
    - monitor coag status
65
Q

what is polycythemia

A

expanded RBC mass & increased hct

- increases O2 carrying capacity BUT increases viscosity –> net decreased tissue perfusion

66
Q

causes of polycythemia

A
  • reduction in plasma volume (dehydration)
  • production of excess RBC (polycythemia vera)
  • chronic hypoxia (pulmonary dz, low CO, extreme obesity w/ hypoventilation, high altitudes)
  • increased EPO (renal dz, EPO secreting tumor)
67
Q

at what hct level does polycythemia cause problems? how to treat?

A

hct >55%

tx = phlebotomy

68
Q

4 steps of coagulation

A
  1. vascular spasm (TxA2)
  2. primary hemostasis (platelet plug) (adhere to vWF, activate, release ADP/TxA2 to activate other platelets)
  3. secondary hemostasis (fibrin mesh formation) (extrinsic or intrinsic pathway)
  4. fibrinolysis (plasminogen via tPA –> plasmin; breaks down fibrin)
69
Q

extrinsic pathway of coagulation cascade

A

when cascade is initiated outside of intravascular space; fast (12 seconds)

factors = III, VII
PT/INR

70
Q

intrinsic pathway of coagulation cascade

A

when cascade is initiated inside of intravascular space; slow (6mins)

factors = VII, IX, XI, XII
PTT/ACT

71
Q

factors involved in final common pathway

A

I, II, V, X, XIII

72
Q

what is factor IV

A

calcium

essential in all pathways

73
Q

how does heparin work

A

increases action of antithrombin III

  • -> inhibition of intrinsic pathway (measure via PTT/ACT
  • -> also works on common pathway via inhibition of activated factor X
74
Q

how does coumadin work

A

inhibits vitamin K factors (blocks extrinsic pathway (measure via PT/INR)
–> also inhibits intrinsic & common pathways

75
Q

vitamin K dependent coagulation factors

A

II, VII, IX, X

protein C & S

76
Q

what does FFP contain

A

all coagulation factors, no platelets

77
Q

what does cyroprecipitate contain

A

fraction of plasma that precipitates once FFP is thawed

high concentrations of VIII, XIII, vWF, & fibrinogen

78
Q

what is desmopressin

A

synthetic ADH

stimulates the release of endogenous vWF & increases factor VIII activity

79
Q

what is hemophilia A

A

X-linked congenital factor VIII deficiency

80
Q

what is the different between mild, moderate, and severe hemophilia A

A

severe = <1% of normal VIII levels (childhood diagnosis)

moderate = 1-5% of normal VIII levels; less problems than severe, but still increased risk of bleeding w/ surgery/trauma

mild = 6-30% of normal VIII levels; often undiagnosed until adulthood; increased bleeding w/ major surgery

81
Q

anesthetic management of hemophilia A

A

bring factor VIII levels near 100% normal for surgery

  • infusion of factor VIII concentrate, 50-60U/kg
  • E1/2t factor VIII = 12hrs; thus may need to repeat
  • continue therapy x2 weeks to avoid postop bleeding
  • FFP, cryoprecipitate
  • desmopressin (0.3mcg/kg IV for mild hemophilia A)
82
Q

what is hemophilia B

A

congenital factor IX deficiency

83
Q

what is the difference between mild, moderate, and severe hemophilia B

A

mild = factor IX levels 5-40%

moderate = factor IX levels 1-5%

severe = factor IX levels <1%; associated w/ severe bleeding

significantly prolonged PTT/normal PT

84
Q

what are the lab findings in hemophilia A & hemophilia B?

A

B = prolonged PTT/normal PT

A = prolonged PTT/normal PT

85
Q

anesthetic management of hemophilia B

A
  • recombinant/purified factor IX to treat mild bleeding or as prophylaxis (100U/kg)
  • E1/2t = 18-24hrs, may need to repeat dose
  • increased risk of thromboembolic complications
  • FFP
86
Q

what is von willebrand’s disease?

A

most common inherited disorder of platelet function

different types, problem w/ either quantity or quality of vWF
type 1 = quantitative defect; desmopressin will work
type 2 = qualitative defect
type 3 = virtual absence of vWF b/c endothelium lacks vWF; desmopressin has no effect

87
Q

clinical findings in patients w/ von willebrand’s disease

A

mucus membrane bleeding = epistaxis, easy bruising, gingival bleeding, GIB

  • type 3 = bleeding in muscles & joints
  • menorrhagia

labs

  • normal platelet count
  • prolonged PTT
88
Q

what is normal beleeding time?

A

3-10mins

89
Q

anesthetic management of von willebrand’s disease

A
  • avoid nasal intubation/nasal trumpet insertion
  • DDAVP therapy for mild bleeding or minor surgery
  • – 0.3mcg/kg IV diluted in 30-50mL saline, infused over 10-20mins to minimize side effects
  • — 300mcg intranasal; 100microL of 1.5mg/mL solution to each nostril
  • cryo is more reliable for severe bleeding or surgical prophylaxis
90
Q

list the blood products that you could give to hemophilia A, B, and von willebrand’s diseaes

A

hem A = factor VIII, FFP, cryo, DDAVP

hem B = factor IX, FFP

vW = cryo, DDAVP

91
Q

drugs that induce platelet dysfunction or inhibition

A
  1. ASA (irreversible inhibition of COX–> decreased TxA2)
  2. NSAIDS (reversible COX inhibition)
  3. abx (PCN, cephalosporins –> interfere w/ platelet adhesion, activation, aggregation
  4. volume expanders (dextran, hydroxyethyl starch >2L)
92
Q

patient factors that can induce platelet dysfunction

A
  • hypothermia (<35)
  • acidosis (<7.3)
  • uremia
  • liver disease
93
Q

what is thrombocytopenia, what are s/s

A

low platelet count

s/s

  • petechial rash
  • nose bleeds
  • easy bruising
  • GIB
94
Q

what is normal platelet count & lifespan

A

150,000-450,000

lifespan 9-10 days

95
Q

what do you need the patient’s platelets to be for surgery

A

> 50,000

20,000-30,000 ok for minor surgery
100,000 for neurosurgery

96
Q

how much does one 6 pack of platelets increase the patient’s platelet count by?

A

50,000

97
Q

what is the most common cause of intraoperative coagulopathy?

A

dilutional thrombocytopenia & dilution of pro-coagulants

98
Q

what are some reasons a patient could have acquired defects in platelet production?

A
  • radiation
  • chemotherapy
  • exposure to toxins
  • drugs (thiazides, alcohol, estrogen)
  • malignancies
  • viral hepatitis
  • vitamin B12 or folate deficiencies
99
Q

what is DIC

A

disseminated intravascular coagulation

  • excessive deposition of fibrin/impaired fibrin degradation
  • -> platelet consumption
100
Q

what is DIC associated with

A
  • sepsis
  • trauma
  • CA
  • obstetric complications
  • vascular disorders
  • immunologic disorders
101
Q

clinical symptoms of DIC

A

consequence of thrombosis & bleeding

- micro emboli accumulation in various systems = organ damage + impaired functioning

102
Q

diagnosis of DIC

A

no single lab test can establish or rule out the diagnosis

  • rapid decrease in platelet count <50,000
  • prolonged PT, PTT
  • elevated FDP (D-dimer)
  • low plasma [ ] of factor VIII
  • decreased fibrinogen levels
103
Q

treatment of DIC

A

management of underlying clinical disorder that triggered the coagulation process

  • transfuse platelets, FFP, cryo, RBCs if indicated
  • heparin gtt
  • hemodynamic/respiratory support
104
Q

reasons for vitamin K deficiency

A
  • malnutrition
  • GI malabsorption
  • abx induced elimination of normal intestinal flora
  • liver disease/obstructive jaundic
105
Q

lab results in vitamin K deficiency

A

prolonged PT

normal PTT

106
Q

treatment of vitamin K deficiency

A

vitamin K (6-24hrs for full effect)

FFP for active bleeding

107
Q

tests: what is normal bleeding time & what is it testing?

A

3-10 minutes

platelet function

108
Q

tests: what is normal PT and what is it testing?

A

10-12 seconds

VII, III (X, V, II, fibrinogen)

109
Q

tests: what is normal PTT & what is it testing?

A

25-35seconds

VIII, IX, XI, XII (X, V, II, fibrinogen)

110
Q

tests: what is normal ACT & what is it testing?

A

90-120secs
VIII, IX, XI, XII
- specifically used to monitor the action of heparin

111
Q

tests: what is normal thrombin time & what is it testing?

A

9-11 seconds

fibrinolysis, prolonged w/ low levels of fibrinogen

112
Q

tests: what is normal fibrinogen level?

A

160-350

113
Q

what are causes of hypercoagulability disorders?

A 
congenital disorders
acquired
- malignancies
- pregnancy
- oral contraception
- nephrotic syndrome
- SLE
114
Q

anesthetic considerations of hypercoagulability disorders

A
  • early ambulation
  • SubQ heparin
  • TEDs
  • ASA
  • vena caval filter
  • hydration
115
Q

who is possibly on long term anticoagulant therapy?

A
  • recurrent DVT
  • hereditary hypercoaguable states
  • CA
  • mechanical heart valves
  • afib
116
Q

periop management of patients on warfarin

A

hold x5 days preop

  • measure INR 1 day preop & if INR >1.8, give 1mg vitamin K subQ
  • emergent reversal = 5-8mL/kg FFP

if high risk

  • bridge w/ heparin 3 days after stopping coumadin
  • turn off heparin 6hrs prior to surgery
  • ok when INR <1.5
117
Q

heparin reversal

A

protamine

118
Q

long term anticoagulation and regional anesthesia

A
  • can develop spinal hematoma/hemorrhage
  • stop LMWH 24hrs prior
  • ASA/NSAIDS: regional may be ok on their own
  • stop plavix 7 days prior
  • heparin: regional may be ok
  • stop coumadin 7-10 days prior (INR <1.5)

COEXISTING (10 decks)

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