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Coexisting 2016 > Anemia and coagulopathy > Flashcards

Anemia and coagulopathy Flashcards

1
Q

What are some questions you might want to ask in regards to hematology?

A

Have you ever had a blood problem? Anemia? Leukemia?

Any clotting problems? Lots of bleeding from cuts, nosebleeds, surgery, dental work?

Have you ever required a blood transfusion?

Has a family member/blood relative ever had a serious bleeding condition or clotting problem?

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2
Q

What common medications would make you concerned in terms of possible hematological problems?

A

Aspirin/NSAIDS, Vitamin E, Ginseng, Gingko, Garlic, Saw Palmetto. How often, how much, and last dose?

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3
Q

Types of amenia

A

Acute- Acute blood loss

Chronic-
Nutritional
Hemolytic
Aplastic
Manifestation of another disease
Abnormal RBC structure (SS, Thalassemia)
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4
Q

What are the CLINICAL manifestations of amenia

A

Decreased oxygen carrying capacity and the accompanying decreased tissue oxygen delivery

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5
Q

What defines O2 carrying capacity

A

Hgb.

Anemia decreases it.

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6
Q

Bonus- What are the B/G coefficients of the common volatile agents?

A 
N20- 0.47
Halothane- 2.3
Enflurane- 1.8
Isoflurane- 1.4
Sevoflurane- 0.69
Desflurane- 0.42
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7
Q

In anemia treatment, what two things must be considered

A

Treatment of the underlying cause, as well as the state of anemia itself

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8
Q

Calculation of arterial blood oxygen content

A

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

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9
Q

Compensation mechanisms for anemia

A

Increase CO
Increase 2,3-dpg
Increase plasma volume

Decreased blood viscosity
Decreased SVR

Blood shunting to organs with higher extraction ratios

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10
Q

In anemia, the oxy-hemoglobin dissociation curve…

A

Shifts to the RIGHT

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11
Q

Methemoglobin resembles a shift to

A

the LEFT

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12
Q

Curve shifts to the right are seen with

A

Decreased pH
Hgb variants with decreased oxygen affinity (fetal Hgb)
Increased 2,3-dpg
Increased Temp

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13
Q

Curve shifts to the left are seen with

A

Increased pH
High oxygen affinity Hgb variants
Decreased 2,3-dpg
Decreased Temp

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14
Q

Suspicion of anemia begins around

A

Hgb

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15
Q

What is the most effective treatment for anemia

A

Treating the underlying cause

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16
Q

Bonus- What are the maximum doses for Bupivacaine and Lidocaine?

A

Bupivacaine- 2.5mg/kg

Lidocaine- 4mg/kg (7 with epi)

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17
Q

In managing a pt with chronic anemia, what do we really want to avoid?

A

Disrupting their compensation methods. For example, most don’t do well with alkalosis.

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18
Q

Anesthesia considerations for chronic anemia

A

Maximize O2 delivery- high FiO2

Avoid drug induced decrease in CO- consider etomidate induction, high opioid maintenance, hydrate/avoid hypovolemia

Avoid left shifts- no hyperventilation, no hypothermia

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19
Q

How do volatile agent kinetics change in a patient with anemia?

A

Lower B/G coefficient, faster on/off, may need less gas

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20
Q

In an anemic patient, what often offsets the lower B/G coefficient in regards to inhaled agents

A

Increased CO (That’s Pharm and Coexisting colliding…)

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21
Q

What are the two possible goals of transfusion therapy?

A

Increase O2 carrying capacity

Correct a coagulation disorder

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22
Q

1 unit of RBCs will increase Hct by how much

A

3-5%

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23
Q

Nutritional anemias

A 
Iron deficiency 
Folic acid deficiency
B12 deficiency
Chronic illness (infections, cancer, RF, DM, AIDS, connective tissue disorders)
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24
Q

Iron deficiency anemia-
RBCs are?
Common causes in adults?

A

Microcytic (also hypochromic, right?)

In adults, depletion of iron stores is caused by chronic blood loss (GI bleed, menorrhagia, cancer)

Most common form of nutritional anemia in children

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25
Q

B12-def. anemia (pernicious)-
RBCs are?
May result in-

A

Macrocytic (Megaloblastic bone marrow)

Bilateral peripheral neuropathy
Loss of proprioception/vibratory sensation in lower limbs
Decreased tendon reflexes
Unsteady gait
Memory impairment/mental depression
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26
Q

Anesthesia considerations for pernicious anemia

A 
Avoid regional blocks (neuropathys)
Avoid N2O (binds B12)
Maintain oxygenation
Emergency correction for surgery is RBC transfusion
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27
Q

Folic acid deficiency anemia-
RBCs are?
May result in-

A

Same are B12

Smooth tongue
Hyperpigmentation
Mental depression
Peripheral edema
Liver dysfunction
Severely ill patient
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28
Q

Anesthesia considerations for folic acid def. anemia

A

Thorough airway assessment- Have an alternative airway plan in place, often have difficult airways

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29
Q

Glucose-6-Phosphate dehydrogenase deficiency (hemolytic)- What is it? Who does it affect? What should you avoid?

A

Most common enzymopathy, leaves RBCs susceptible to oxidation. Acute and chronic episodes. Increased rigidity of RBCs, increased clearance.

Blacks, Asians, Mediterranean populations

Avoid oxidative drugs (LAs, Benzos, Meth. Blue)
Avoid hypothermia, acidosis, hyperglycemia, infection

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30
Q

Pyruvate kinase deficiency (hemolytic)

A

Deficiency of glycolic enzyme leads to K+ leak, results in rigid RBC and increased clearance.

2,3-dpg accumulates, causes right shift

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31
Q

Peri-op risks for hemolytic anemia

A

Tissue hypoxia
Increased infection risk if prior splenectomy
Increased thrombosis risk

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32
Q

Pre-op planning for hemolytic anemia

A

EPO often given for 3 days pre-op

Hgb acutely less than 8 or chronically less than 6 should be considered for transfusion

Ensure pre-op hydration, prophylactic transfusions

Caution with methylene Blue

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33
Q

SS- patho

A

Inherited

Single AA defect in either the alpha or beta chains

Mutant S hemoglobin likely to form aggregates when exposed to low O2 concentrations

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34
Q

SS trait carriers

A

1 normal, 1 abnormal gene

40% is S Hgb, 60% is normal

Usually non-symptomatic, about 5% will have hematuria and difficulty concentrating urine. No treatment needed.

8% of AA have the trait

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35
Q

SS disease

A

Homozygous for SS trait

70-98% Hgb S

Chronic hemolysis, low O2 situations can lead to vaso-occlusive crisis

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36
Q

Pts with SS disease typically display what type of shift in the O-Hgb dissociation curve?

A

Right shift

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37
Q

Complications associated with SS disease

A

Stroke, heart failure, MI, Hepatic/Splenic sequestration, renal failure

High rate of peri-op complications

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38
Q

SS crisis

A

Life threatening

Deoxygenation leads to Hgb S forming insoluble globulin polymers

Acute vaso-occlusive crisis, organ infarcts, very painful

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39
Q

Anesthetic concerns for SS

A

Assess for organ damage, cardiac dysfunction, current infections

Possible benefit from conservative preop transfusions with high risk surg

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40
Q

What is the ASA goal for Hct in SS

A

30%

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41
Q

3 things that must be avoid in SS

A

Hypoxia
Hypovolemia
Blood stasis

42
Q

Periop planning for SS

A

O2

12 hours hydration

Caution with pre-med, avoid resp. depression that can lead to acidosis

AGGRESSIVE pain management

Strict aseptic technique, must avoid infections

43
Q

Is regional a good idea in SS?

A

Yes, but must keep in mind-

Hypotension
Blood stasis
Compensatory vasoconstriction

44
Q

What is a potentially fatal post-op complication in SS crisis

A

Acute chest syndrome. It typically occurs 2-3 days postop

45
Q

What are the signs and symptoms of acute chest syndrome and how is it managed

A

Pleuritic chest pain, dyspnea, fever, acute pulmonary HTN

Transfuse to Hct 30%, give O2, antibiotics, inhaled bronchodilators, aggressive pain management

46
Q

Thalassemia major patho and signs and symptoms

A

Inability to form beta-globin hemoglobin chains

Hepatosplenomegaly 
Dyspnea, orthopnea
Infection risk
CHF, dysrhythmias
Bone malformations
Hemothorax
Spinal compression
Mental Retardation
Digitalis sensitivity
Increased RBC production
Jaundice
Iron overload
47
Q

Iron overload in thalassemia leads to

A 
Impaired growth, infertility (Pituitary)
Hypoparathyroid
Cardiomyopathy, HF
Hepatic cirrhosis
DM
Hypogonadism
48
Q

Some periop concerns with thalassemia

A

Difficult airway due to maxillary deformities, consider awake fiber optic

Adrenal insufficiency –> decreased vasopressor response
Liver dysfunction –> coagulopathy
Arrhythmias –> EKG
Right sided failure –> ECHO

49
Q

Aplastic anemia is caused by

A

bone marrow failure

50
Q

Bone marrow failure is caused by

A

Drugs, all kinds
Radiation
Infectious diseases

51
Q

What does a CBC look like in aplastic anemia

A

RBCs

52
Q

Aplastic anemia periop concerns

A

Often on immunosuppression- may need stress dose steroids

Reverse isolation

Prophylactic antibiotics

Hemorrhage

LV dysfunction due to high output state

Difficulty in cross-matching

53
Q

Co-existing congenital abnormalities with aplastic anemia

A

Fanconi anemia in peds

Cleft palate

Cardiac defects

54
Q

Induction in aplastic anemia

A

Consider preop transfusion
Hemorrhage possible with DVL
Avoid nasal intubation
Labile hemodynamic response to induction

55
Q

Maintenance in aplastic anemia

A

PEEP will allow for lower FiO2
Avoid nitrous
Maintain normothermia

56
Q

Emergence in aplastic anemia

A

Period with greatest O2 demands

Monitor coags post-op

57
Q

Methemoglobinemia

A

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

This creates a marked LEFT shift

Normal level is 1%

at 30-50% pt will display signs of oxygen deprivation, brownish colored blood

Over 50% can lead to coma and death

58
Q

Methemoglobinemia can be caused by

A

Nitrate poisoning

Toxic drug reactions, such as from prilocaine (throat spray)

59
Q

Anesthesia considerations for methHgb

A

Messes with pulse ox-
at SaO2 over 85%, true value is underestimated
at SaO2 under 85%, true value is overestimated

60
Q

Treatment for methHgb

A

O2

1-2mg/kg IV methylene blue as a 1% solution given over 3-5 minutes

61
Q

Signs of 20% acute blood loss

40% blood loss

A

Tachycardia, Orthostatic hypotension, CVP changes

Tachycardia, hypotension, tachypnea, oliguria, acidosis, restlessness, diaphoresis

62
Q

What kind of anesthetic technique might be required in someone with massive blood loss

A

Ketamine/Etomidate induction

May be unable to tolerate any IA, may need scopolamine, benzo, opioid mix

Keep warm, use pressors sparingly, watch for non-clotting blood

63
Q

Post-op, what would be a concern is a pt that received massive volume resuscitation

A

Pulmonary edema

ARDS

64
Q

Define massive transfusion

A

More than 10 units PRBCs in 24 hour period
Replacement of at least one blood volume in 24 hours
50% blood volume replacement in 6 hours

65
Q

Consequences of massive transfusion

A 
Hypothermia
Volume overload
Dilutional coagulopathy
Decreased 2,3-dpg
Hyperkalemia
Citrate toxicity (hypocalcemia)
66
Q

Whats polycythemia

A

Expanded red cell mass and increased Hct, caused by-

Reduced volume
Excess RBC production
Chronic hypoxia

67
Q

What problems can polycythemia cause? At what Hct does it become a major problem?

A

Thrombosis leading to CAD, pulm HTN, CNS disorders

Hct > 55%

68
Q

Hemophilia A- Severe, moderate, mild

A

Severe- Factor VIII less than 1%, diagnosed in childhood, frequent spontaneous hemorrhages in joints, muscles, organs

Moderate- Factor VIII 1-5%, less severe, but still increased risk of bleeding in surg, fewer joint problems

Mild- Factor VIII 6-30%, often undiagnosed until adulthood, increased bleeding risk in major surg

Increased PTT

NORMAL PT

69
Q

Hemophilia A anesthesia considerations

A

Must bring factor VIII levels to near normal

50-60u/kg IV initially, half life of 12 hours. 25-30u/kg every 8 to 12 hours as maintenance. May need to continue up to two weeks post up.

DDAVP is also effective at correcting for surg

70
Q

Hemophilia B- Severe, moderate, mild

A

Severe- factor IX less than 1%, associated with severe bleeding

Moderate- factor IX 1-5%

Mild- factor IX 5-40%

Increased PTT

NORMAL PT

71
Q

Hemophilia B anesthesia considerations

A

Dose of 100u/kg needs to be given prior to surg. Half life is 18-24 hours, so 50% of original dose needs to be given every 12-24 hours to keep levels about 50%.

Treatment can result in increased thromboembolic events

72
Q

vWB disease patho and signs

A

Dysfunctional platelets

Bleeding time is markedly prolonged, may also have increased PTT

Commonly bleed from mucus membranes- epistaxis, easy bruising, menorrhagia, GI, gingival

73
Q

vWB disease anesthesia considerations

A

Avoid messing with the nose

DDAVP 0.3mcg/kg in 30-50ml NS over 10-20 minutes (can produce tachycardia and hypotension)

Can also give 300mcg nasally divided between each nostril

Cryo more reliable for severe bleeding or surgical prophylaxis

74
Q

What does ASA do to platelets

A

Inhibits aggregation for life of the platelet, prolongs bleeding time 2-3x within 3 hours of ingestion

Aggregation can be abnormal for up to 10 days

75
Q

What other drugs can cause platelet dysfunction

A

Antibiotics- affect aggregation and adhesion

Volume expanders- dextran, hespan

76
Q

Conditions under which platelets quit

A

Temp

77
Q

Thrombocytopenia- what is it, signs and symptoms

A

Low platelet count, approximately 1/3 of platelets sequestered in spleen

Petechial rash, nose bleeds, GI bleeds, bruising

Need >50,000 for major surg

A six pack of platelets should increase platelets by about 50,000

78
Q

Most common intra-op coagulopathy

A

Dilutional- platelets/coag factors get diluted with fluids, PRBCs (more than 10 units)

Surgical hemorrhage also causes fibrinogen release

79
Q

Platelet defects can also be caused by

A 
Radiation
Chemo
Toxic chemicals
Thiazides, ETOH, estrogen
CA
Viral hepatitis
B12/folate deficiency
80
Q

DIC

A

Excessive deposits of fibrin/ impaired fibrin degradation

Bleeding results from microemboli formation that consumes clotting factors

Associated with sepsis, trauma, cancer, OB complications, vascular disorders, immune disorders

81
Q

DIC lab profile

A

Rapid decrease to

82
Q

DIC management

A

Transfuse platelets, FFP, fibrinogen, antithrombin III

Give heparin to block thrombin formation which stops consumption of clotting factors

83
Q

What factors is PT sensitive to?

A

I, II, V, VII, X (normal 10-12 secs)

84
Q

What factors is PTT sensitive to?

A

I, II, V, VII, IX, X, XI, XII (normal 25-35 secs)

85
Q

What factors is ACT sensitive to?

A

I, II, V, VII, IX, X, XI, XII (normal 90-120 secs)

86
Q

What factors is Thrombin time sensitive to?

A

I, II (normal 9-11 secs)

87
Q

What is a normal fibrinogen?

A

160-350

88
Q

What’s a normal bleeding time?

A

3-10 minutes

89
Q

Vitamin K is needed for formation of which factors?

A

II, VII, IX, X

90
Q

What is the lab profile for vitamin K deficiency? Treatment?

A

Prolonged PT

NORMAL PTT

Vitamin K (takes 6-24 hours for effect)
FFP for acute bleeding
91
Q

Anesthesia considerations for hypercoagulability

A 
Early ambulation
SubQ heparin
Compression devices
ASA
IVC filter

Regional anesthesia is beneficial, but contraindicated if pt on LMWH

92
Q

What is long-term anticoagulation therapy used for

A 
Venous thrombosis 
Hereditary hypercoagulable states
Cancer
Mechanical heart valves
A-fib
93
Q

Antiplatelet therapy is indicated periop for what conditions? Which meds are commonly used?

A

Pts at high risk for CVA, MI, vascular thrombosis complications

ASA, PDE inhibitors, ADP receptor antagonists

94
Q

How does warfarin work

A

Competes with vitamin K –> inhibits factor II, VII, IX, and X

95
Q

What lab tests are needed for warfarin monitoring

A

PT/INR

96
Q

How does heparin work

A

Directly inhibits thrombin and Xa by binding to antithrombin III

97
Q

What lab tests are needed for heparin monitoring

A

PTT or ACT

98
Q

Heparin can be reversed with

A

Protamine

99
Q

How many days should warfarin be held pre-op and what should be checked

A

At least 5 and check an INR ONE day preop, if greater than 1.8, give 1mg vitamin K subQ

100
Q

What should be done for someone on warfarin, but is very high risk for clotting

A

Start heparin 3 days after stopping warfarin, stop heparin 6 hours prior to surg

Coexisting 2016 (12 decks)

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