Anemia and coagulopathy Flashcards
What are some questions you might want to ask in regards to hematology?
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?
What common medications would make you concerned in terms of possible hematological problems?
Aspirin/NSAIDS, Vitamin E, Ginseng, Gingko, Garlic, Saw Palmetto. How often, how much, and last dose?
Types of amenia
Acute- Acute blood loss
Chronic- Nutritional Hemolytic Aplastic Manifestation of another disease Abnormal RBC structure (SS, Thalassemia)
What are the CLINICAL manifestations of amenia
Decreased oxygen carrying capacity and the accompanying decreased tissue oxygen delivery
What defines O2 carrying capacity
Hgb.
Anemia decreases it.
Bonus- What are the B/G coefficients of the common volatile agents?
N20- 0.47 Halothane- 2.3 Enflurane- 1.8 Isoflurane- 1.4 Sevoflurane- 0.69 Desflurane- 0.42
In anemia treatment, what two things must be considered
Treatment of the underlying cause, as well as the state of anemia itself
Calculation of arterial blood oxygen content
CaO2= (Hgb*1.39)SaO2+PaO2(0.003)
Compensation mechanisms for anemia
Increase CO
Increase 2,3-dpg
Increase plasma volume
Decreased blood viscosity
Decreased SVR
Blood shunting to organs with higher extraction ratios
In anemia, the oxy-hemoglobin dissociation curve…
Shifts to the RIGHT
Methemoglobin resembles a shift to
the LEFT
Curve shifts to the right are seen with
Decreased pH
Hgb variants with decreased oxygen affinity (fetal Hgb)
Increased 2,3-dpg
Increased Temp
Curve shifts to the left are seen with
Increased pH
High oxygen affinity Hgb variants
Decreased 2,3-dpg
Decreased Temp
Suspicion of anemia begins around
Hgb <11.5 for females (Hct 36%)
What is the most effective treatment for anemia
Treating the underlying cause
Bonus- What are the maximum doses for Bupivacaine and Lidocaine?
Bupivacaine- 2.5mg/kg
Lidocaine- 4mg/kg (7 with epi)
In managing a pt with chronic anemia, what do we really want to avoid?
Disrupting their compensation methods. For example, most don’t do well with alkalosis.
Anesthesia considerations for chronic anemia
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
How do volatile agent kinetics change in a patient with anemia?
Lower B/G coefficient, faster on/off, may need less gas
In an anemic patient, what often offsets the lower B/G coefficient in regards to inhaled agents
Increased CO (That’s Pharm and Coexisting colliding…)
What are the two possible goals of transfusion therapy?
Increase O2 carrying capacity
Correct a coagulation disorder
1 unit of RBCs will increase Hct by how much
3-5%
Nutritional anemias
Iron deficiency Folic acid deficiency B12 deficiency Chronic illness (infections, cancer, RF, DM, AIDS, connective tissue disorders)
Iron deficiency anemia-
RBCs are?
Common causes in adults?
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
B12-def. anemia (pernicious)-
RBCs are?
May result in-
Macrocytic (Megaloblastic bone marrow)
Bilateral peripheral neuropathy Loss of proprioception/vibratory sensation in lower limbs Decreased tendon reflexes Unsteady gait Memory impairment/mental depression
Anesthesia considerations for pernicious anemia
Avoid regional blocks (neuropathys) Avoid N2O (binds B12) Maintain oxygenation Emergency correction for surgery is RBC transfusion
Folic acid deficiency anemia-
RBCs are?
May result in-
Same are B12
Smooth tongue Hyperpigmentation Mental depression Peripheral edema Liver dysfunction Severely ill patient
Anesthesia considerations for folic acid def. anemia
Thorough airway assessment- Have an alternative airway plan in place, often have difficult airways
Glucose-6-Phosphate dehydrogenase deficiency (hemolytic)- What is it? Who does it affect? What should you avoid?
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
Pyruvate kinase deficiency (hemolytic)
Deficiency of glycolic enzyme leads to K+ leak, results in rigid RBC and increased clearance.
2,3-dpg accumulates, causes right shift
Peri-op risks for hemolytic anemia
Tissue hypoxia
Increased infection risk if prior splenectomy
Increased thrombosis risk
Pre-op planning for hemolytic anemia
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
SS- patho
Inherited
Single AA defect in either the alpha or beta chains
Mutant S hemoglobin likely to form aggregates when exposed to low O2 concentrations
SS trait carriers
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
SS disease
Homozygous for SS trait
70-98% Hgb S
Chronic hemolysis, low O2 situations can lead to vaso-occlusive crisis
Pts with SS disease typically display what type of shift in the O-Hgb dissociation curve?
Right shift
Complications associated with SS disease
Stroke, heart failure, MI, Hepatic/Splenic sequestration, renal failure
High rate of peri-op complications
SS crisis
Life threatening
Deoxygenation leads to Hgb S forming insoluble globulin polymers
Acute vaso-occlusive crisis, organ infarcts, very painful
Anesthetic concerns for SS
Assess for organ damage, cardiac dysfunction, current infections
Possible benefit from conservative preop transfusions with high risk surg
What is the ASA goal for Hct in SS
30%
3 things that must be avoid in SS
Hypoxia
Hypovolemia
Blood stasis
Periop planning for SS
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
Is regional a good idea in SS?
Yes, but must keep in mind-
Hypotension
Blood stasis
Compensatory vasoconstriction
What is a potentially fatal post-op complication in SS crisis
Acute chest syndrome. It typically occurs 2-3 days postop
What are the signs and symptoms of acute chest syndrome and how is it managed
Pleuritic chest pain, dyspnea, fever, acute pulmonary HTN
Transfuse to Hct 30%, give O2, antibiotics, inhaled bronchodilators, aggressive pain management
Thalassemia major patho and signs and symptoms
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
Iron overload in thalassemia leads to
Impaired growth, infertility (Pituitary) Hypoparathyroid Cardiomyopathy, HF Hepatic cirrhosis DM Hypogonadism
Some periop concerns with thalassemia
Difficult airway due to maxillary deformities, consider awake fiber optic
Adrenal insufficiency –> decreased vasopressor response
Liver dysfunction –> coagulopathy
Arrhythmias –> EKG
Right sided failure –> ECHO
Aplastic anemia is caused by
bone marrow failure
Bone marrow failure is caused by
Drugs, all kinds
Radiation
Infectious diseases
What does a CBC look like in aplastic anemia
RBCs < 3.5 million/mcL
WBCs < 2.5billion/L
Neutrophils < 200 cells/mcL
Platelets < 100,000
Aplastic anemia periop concerns
Often on immunosuppression- may need stress dose steroids
Reverse isolation
Prophylactic antibiotics
Hemorrhage
LV dysfunction due to high output state
Difficulty in cross-matching
Co-existing congenital abnormalities with aplastic anemia
Fanconi anemia in peds
Cleft palate
Cardiac defects
Induction in aplastic anemia
Consider preop transfusion
Hemorrhage possible with DVL
Avoid nasal intubation
Labile hemodynamic response to induction
Maintenance in aplastic anemia
PEEP will allow for lower FiO2
Avoid nitrous
Maintain normothermia
Emergence in aplastic anemia
Period with greatest O2 demands
Monitor coags post-op
Methemoglobinemia
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
Methemoglobinemia can be caused by
Nitrate poisoning
Toxic drug reactions, such as from prilocaine (throat spray)
Anesthesia considerations for methHgb
Messes with pulse ox-
at SaO2 over 85%, true value is underestimated
at SaO2 under 85%, true value is overestimated
Treatment for methHgb
O2
1-2mg/kg IV methylene blue as a 1% solution given over 3-5 minutes
Signs of 20% acute blood loss
40% blood loss
Tachycardia, Orthostatic hypotension, CVP changes
Tachycardia, hypotension, tachypnea, oliguria, acidosis, restlessness, diaphoresis
What kind of anesthetic technique might be required in someone with massive blood loss
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
Post-op, what would be a concern is a pt that received massive volume resuscitation
Pulmonary edema
ARDS
Define massive transfusion
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
Consequences of massive transfusion
Hypothermia Volume overload Dilutional coagulopathy Decreased 2,3-dpg Hyperkalemia Citrate toxicity (hypocalcemia)
Whats polycythemia
Expanded red cell mass and increased Hct, caused by-
Reduced volume
Excess RBC production
Chronic hypoxia
What problems can polycythemia cause? At what Hct does it become a major problem?
Thrombosis leading to CAD, pulm HTN, CNS disorders
Hct > 55%
Hemophilia A- Severe, moderate, mild
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
Hemophilia A anesthesia considerations
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
Hemophilia B- Severe, moderate, mild
Severe- factor IX less than 1%, associated with severe bleeding
Moderate- factor IX 1-5%
Mild- factor IX 5-40%
Increased PTT
NORMAL PT
Hemophilia B anesthesia considerations
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
vWB disease patho and signs
Dysfunctional platelets
Bleeding time is markedly prolonged, may also have increased PTT
Commonly bleed from mucus membranes- epistaxis, easy bruising, menorrhagia, GI, gingival
vWB disease anesthesia considerations
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
What does ASA do to platelets
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
What other drugs can cause platelet dysfunction
Antibiotics- affect aggregation and adhesion
Volume expanders- dextran, hespan
Conditions under which platelets quit
Temp < 35c
pH < 7.3
Uremia
-Give vWF with cryo, DDAVP, platelets
Thrombocytopenia- what is it, signs and symptoms
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
Most common intra-op coagulopathy
Dilutional- platelets/coag factors get diluted with fluids, PRBCs (more than 10 units)
Surgical hemorrhage also causes fibrinogen release
Platelet defects can also be caused by
Radiation Chemo Toxic chemicals Thiazides, ETOH, estrogen CA Viral hepatitis B12/folate deficiency
DIC
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
DIC lab profile
Rapid decrease to <50,000 platelets Prolonged PT, PTT Fibrin split products Low antithrombin III Normal fibrinogen
DIC management
Transfuse platelets, FFP, fibrinogen, antithrombin III
Give heparin to block thrombin formation which stops consumption of clotting factors
What factors is PT sensitive to?
I, II, V, VII, X (normal 10-12 secs)
What factors is PTT sensitive to?
I, II, V, VII, IX, X, XI, XII (normal 25-35 secs)
What factors is ACT sensitive to?
I, II, V, VII, IX, X, XI, XII (normal 90-120 secs)
What factors is Thrombin time sensitive to?
I, II (normal 9-11 secs)
What is a normal fibrinogen?
160-350
What’s a normal bleeding time?
3-10 minutes
Vitamin K is needed for formation of which factors?
II, VII, IX, X
What is the lab profile for vitamin K deficiency? Treatment?
Prolonged PT
NORMAL PTT
Vitamin K (takes 6-24 hours for effect) FFP for acute bleeding
Anesthesia considerations for hypercoagulability
Early ambulation SubQ heparin Compression devices ASA IVC filter
Regional anesthesia is beneficial, but contraindicated if pt on LMWH
What is long-term anticoagulation therapy used for
Venous thrombosis Hereditary hypercoagulable states Cancer Mechanical heart valves A-fib
Antiplatelet therapy is indicated periop for what conditions? Which meds are commonly used?
Pts at high risk for CVA, MI, vascular thrombosis complications
ASA, PDE inhibitors, ADP receptor antagonists
How does warfarin work
Competes with vitamin K –> inhibits factor II, VII, IX, and X
What lab tests are needed for warfarin monitoring
PT/INR
How does heparin work
Directly inhibits thrombin and Xa by binding to antithrombin III
What lab tests are needed for heparin monitoring
PTT or ACT
Heparin can be reversed with
Protamine
How many days should warfarin be held pre-op and what should be checked
At least 5 and check an INR ONE day preop, if greater than 1.8, give 1mg vitamin K subQ
What should be done for someone on warfarin, but is very high risk for clotting
Start heparin 3 days after stopping warfarin, stop heparin 6 hours prior to surg
