Anemia Flashcards
(104 cards)
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?
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?
3
Q
Types of amenia
A
- Acute = Acute blood loss
-
Chronic
- Nutritional Hemolytic
- Aplastic
- Manifestation of another disease
- Abnormal RBC structure (SS, Thalassemia)
4
Q
What are the CLINICAL manifestations of amenia
A
Decreased oxygen carrying capacity and the accompanying decreased tissue oxygen delivery
5
Q
What defines O2 carrying capacity
A
Hgb.
Anemia decreases it.
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
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
8
Q
Calculation of arterial blood oxygen content
A
CaO2 = (Hgb x 1.39) SaO2 + PaO2 (0.003)
9
Q
Compensation mechanisms for anemia
A
- Increase CO
- Increase 2,3-DPG
- Increased P50
- Increase plasma volume
- Decreased blood viscosity = increased CO
- Decreased SVR
- Blood shunting to organs with higher extraction ratios
- Kidneys release EPO
10
Q
In anemia, the oxy-hemoglobin dissociation curve…
A
Shifts to the RIGHT
11
Q
Methemoglobin resembles a shift to
A
the LEFT
12
Q
Curve shifts to the right are seen with
A
Think of anything that increases metabolism → RBC will want to drop off Oxygen at the tissues
- Increased CO
- Acidosis = Decreased pH
- Increased 2-3 DPG
- Exercise
- Increased temeperature (sepsis)
- Hgb variants with decreased oxygen affinity (Sickle cell)
*
13
Q
Curve shifts to the left are seen with
A
Think anything that decreases metabolism →tissue does not need as much oxygen
- Decreased CO2
- Alkalosis = Increased pH
- Decreased 2/3 DPG
- Decreased temperature - hypothermia
- High oxygen affinity Hgb variants (Fetal Hgb)
(a leftward shift on someone that is dependent on a rightowrd shift may be a problem - we do this from hyperventilation and decreaseing temperature)
14
Q
Suspicion of anemia begins around
A
Hgb
(<11.5 g/dL in females)
(<12.5 in males)
15
Q
What is the most effective treatment for anemia
A
Treating the underlying cause
16
Q
Bonus- What are the maximum doses for Bupivacaine and Lidocaine?
A
- Bupivacaine- 2.5mg/kg
- Lidocaine- 4mg/kg (7 with epi)
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, hypothermia, or decreased CO (propofol)
Will intererfere with O2 delivery
18
Q
Anesthesia management and considerations for chronic anemia
A
Goal = AVOID disruptions of compensatory mechhanisms that are aimed at maintinging O2 delivery to the tissues!
- Indentify and treat underlying disease if possible
- Maximize O2 delivery- High FiO2
-
Avoid drug induced decreases in CO
- consider etomidate induction
- may want to use high opioid technique
- hydrate/avoid hypovolemia
- AVOID propofol, high amounts of IAs, STP
-
AVOID leftward shifts of the oxyhemoglobin disassociation curve
- no hyperventilation/respiratory alkalosis
- no hypothermia
-
Consder volitile anesthetics may be LESS soluble in plasma
- may have a faster induction, however, often OFFSET by the fact that these patients have and increased CO
19
Q
- How do volatile agent kinetics change in a patient with anemia?
- In an anemic patient, what often offsets the lower B/G coefficient in regards to inhaled agents
A
- Lower B/G coefficient
- faster on/off,
- may need less gas
Often offset by:
- Increased CO
- That’s Pharm and Coexisting colliding…
20
Q
The decision to transfuse is based on:
A
- The clinical judgment that the oxygen carrying capacity must be increased to prevent oxygen consumtion (VO2) from outstripping oxygen delivery (DO2)
21
Q
What are the two possible goals of transfusion therapy?
A
- Increase O2 carrying capacity
- Correct a coagulation disorder
22
Q
1 unit of RBCs will increase Hct by how much
A
3-5%
23
Q
Nutritional anemias
A
- Iron deficiency
- Folic acid deficiency
- B12 deficiency
- Chronic illness (infections, cancer, RF, DM, AIDS, connective tissue disorders)
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
25
B12-def. anemia (pernicious)- RBCs are? May result in? Anesthesia considerations?
**Macrocytic** (Megaloblastic bone marrow morphology)
**May result in:**
* Bilateral peripheral neuropathy
* Loss of proprioception/vibratory sensation in lower limbs
* Decreased tendon reflexes
* Unsteady gait
* Memory impairment/mental depression
**Anesthesia considerations:**
* Avoid regional blocks (neuropathys)
* Avoid N2O (binds B12)
* Maintain oxygenation
* Emergency correction for surgery is RBC transfusion
26
Causes of acquired hemolytic anemias
Immune Hemolysis and Infection
* Drug induced (High dose PCN, alpha- methyldopa)
* Disease induced (malaria, epsteen Barr)
* Sensitization of RBCs (Materna/fetal)
(particals released durring hemolysis can result in **DIC** and **hypersplenism**)
27
Folic acid deficiency anemia- RBCs are? May result in? Anesthesia considerations?
**Macrocytic** (Megaloblastic bone marrow morphology)
**May result in:**
* Smooth tongue (difficult intubation)
* Hyperpigmentation
* Mental depression
* Peripheral edema
* Liver dysfunction Severely ill patient
**Anesthesia considerations:**
* Thorough airway assessment-
* Have an alternative airway plan in place, often have **difficult airways**
28
Anesthesia considerations for folic acid def. anemia
* Thorough airway assessment-
* Have an alternative airway plan in place, often have **difficult airways**
29
**Glucose-6-Phosphate** **dehydrogenase** deficiency What is it? Who does it affect? What should you avoid?
**Form of hemolytic anemia**
* Most common enzymopathy; decreased G6PD activity leaves RBCs susceptible to **damage by oxidation**.
* Cell membranes have increased **rigidity** **of** **membranes** and there is **accelrated** **RBC** **clearance**
* Acute and chronic episodes.
* Most prevalent in: Blacks, Asians, Mediterranean populations
**Anesestetic consideratons:**
* **AVOID**: oxidative drugs (LAs, Benzos, Meth. Blue) **AVOID**: hypothermia, acidosis, hyperglycemia, infection
30
Pyruvate kinase deficiency
**Hemolytic anemmia**
* Deficiency of **glycolic** **enzyme**→ which converts **glucose** to **lactate**→ it is the primary pathway to **ATP** production →
* leads to **K+ leak**→ results in **rigid RBC** and **accelerated destruction**
* 2,3-dpg accumulates, causes **right** shift
31
Peri-op **risks** for hemolytic anemia
* Tissue hypoxia
* Increased infection risk if prior splenectomy
* Increased risk of venous thrombosis
32
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** **RBC** transfusions
* Caution with **methylene Blue** - can increase hemolysis!!!
*
33
Sickle cell anemia patho
* Inherited Single AA defect in the **ß-globin** chains
* Mutant **S hemoglobin** →**valine** substituted for a **glutamic** acid
* Hgb aggregates and forms **polymers** when exposed to **low O2** concentrations
34
Sickle cell anemia 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 african americans have the trait
35
SS disease
* Homozygous for SS trait
* **70-98%** Hgb S
* Chronic hemolysis, low O2 situations can lead to vaso-occlusive crisis
36
Pts with SS disease typically display what type of shift in the O-Hgb dissociation curve?
**Right shift**
37
Complications associated with SS disease
* Stroke
* heart failure
* MI
* Hepatic/Splenic sequestration
* renal failure
* High rate of peri-op complications
38
Sickle cell anemia crisis
* Life threatening
* Deoxygenation causes Hgb S to form insoluble globulin polymers
* Acute vaso-occlusive crisis
* Ischemia and organ infarcts
* very painful
* Stroke, renal failure, liver failure, splenic sequestration, PE
39
Anesthetic concerns for Sickle cell anemia
* Assess for organ damage,
* cardiac dysfunction,
* current infections
* Possible benefit from conservative transfusions preoperatively if having a high risk surg→ decrease Hgb S to less than 30% (diluted with Hgb A)
40
3 things that must be avoid in Sickle cell anemia
1. Hypoxia
2. Hypovolemia
3. Blood stasis
41
Periop planning for Sickle cell anemia
* O2
* 12 hours hydration
* **Caution** **with** **pre-med**
* ****avoid respiratory depression that can lead to acidosis
* Regional
* AGGRESSIVE pain management
* Strict aseptic technique, must avoid infections
* Avoid tourniquets
42
Is regional a good idea in SS?
* **Yes**! = advocated for!
* But must keep in mind:
* **Hypotension**
* **Blood stasis**
* **Compensatory vasoconstriction**
43
What is a potentially fatal post-op complication in Sickle cell crisis?
**Acute chest syndrome.**
It typically occurs **2-3 days** postop
44
What are the signs and symptoms of **acute chest syndrome** and how is it managed?
**Signs and symptoms of acute chest syndrome**
* Pleuritic chest pain
* dyspnea
* fever
* acute pulmonary HTN
**Treatment:**
* Transfuse to Hct 30%
* give O2
* antibiotics
* inhaled bronchodilators
* aggressive pain management
45
Thalassemia major patho and signs and symptoms
* **Inability to form alpah or beta-globin hemoglobin chains**
Signs and symptoms:
* Hepatosplenomegaly
* Dyspnea &orthopnea
* Infection risk
* CHF, dysrhythmias
* **Bone malformations** (Overgrown maxillae - difficult intubation!!!)
* Hemothorax
* **Spinal compression** (No epidurals or spinals)
* Mental Retardation
* Digitalis sensitivity
* Increased RBC production
* Jaundice
* Iron overload
46
Iron overload in thalassemia leads to
* **Pituitary**: Impaired growth, infertility
* Hypothyroidism & Hypoparathyroidism
* **Adrenal insufficiency** (decreased response ot vasopressors)
* **Heart**: Cardiomyopathy, Heart Failure, Arrhythmias and Rt sided heart failure
* **Liver**: Hepatic cirrhosis/coagualtion abnormalities
* **Pancrease**: DM (monitor blood glucose)
* **Gonads**: Hypogonadism
47
Some periop concerns with thalassemia
* **Difficult airway** due to maxillary deformities, consider awake fiber optic
* **Adrenal insufficiency**→ decreased vasopressor response
* **Diabetes** → monitor blood glucose
* **Liver dysfunction**→ coagulopathy and throbocytopenia
* **AVOID** regional
* (also note: they are **VERY** sensitive to the effects of **digitalis**)
* **Arrhythmias**→ EKG Right sided failure → ECHO
48
Aplastic anemia is caused by
1. **Bone marrow failure**
2. Which may be cased by:
1. Drugs (all kinds)
2. Radiation
3. Chemotherapy
4. Infectious diseases
49
What does a CBC look like in aplastic anemia
RBCs \< **3.5** x million/mcL
WBCs \< **2.5** billion/L
Neutrophils **\<200** cells/mcL
Platelets **\<100,00**/mcL
50
Aplastic anemia periop concerns
* Often on immunosuppression
* may need **stress dose steroids**
* **Reverse isolation**
* Prophylactic **antibiotics** d/t neutropenia
* **Hemorrhage** (GI and intercranial)
* **LV dysfunction** due to high output state
* **Difficulty in cross-matching**
* (have had multiple transfusions)
* Co-existing **congenital** abnormaliities
* (Fanconi anemia - peds- cleft palate and cardiac defects)
51
Co-existing congenital abnormalities with aplastic anemia
Fanconi anemia in peds
* Cleft lip/palate
* Cardiac defects
52
**Induction** in aplastic anemia
* Consider preop transfusion
* Airway Hemorrhage possible with DVL
* Avoid nasal intubation
* Consiter Regional
* Labile hemodynamic response to induction
53
Maintenance in aplastic anemia
* PEEP will allow for lower FiO2
* Avoid nitrous (immunosupression)
* Maintain normothermia
54
Emergence in aplastic anemia
* Period with greatest O2 demands
* Monitor coags post-op
55
Methemoglobinemia
1. Formed when iron in Hgb is oxidized from the **ferrous** to the **ferric state** (2+ to 3+)
2. This creates a marked **LEFT** shift
3. Normal level is **1%**
4. At **30-50%** pt will display signs of **oxygen deprivation**
* ****brownish colored blood
5. Over **50%** can lead to coma and death
56
Methemoglobinemia can be caused by
* Nitrate poisoning
* Toxic drug reactions
* such as from prilocaine (throat spray)
57
Anesthesia considerations for metHgb
* Messes with pulse ox- absorbs red and infrared light equally
* at SaO2 over **85%** → true value is **underestimated**
* at SaO2 **under 85%→** true value is **overestimated**
(just think the UNDER/OVER RULE!!!)
58
Emergency treatment for metHgb
* O2
* _Methylene Blue_ **1%** solution: **1-2 mg/kg** over **3-5 minutes**
* Mary repeat after 30 minutes
59
* Signs of **20%** acute blood loss?
* **40%** blood loss?
**20% acute blood loss:**
* Tachycardia
* Orthostatic hypotension
* CVP changes
**40% acute blood loss**
* Tachycardia
* (may have EKG chnages d/t change in O2 carrying capacity)
* hypotension
* tachypnea
* oliguria
* acidosis
* restlessness
* diaphoresis
60
What kind of anesthetic technique might be required in someone with massive blood loss?
1. Ketamine/Etomidate induction
2. May be unable to tolerate any IA
* may need scopolamine, benzo, opioid mix (trauma cocktail)
3. Keep warm
4. use pressors sparingly
* (not treating the problem!)
5. watch surgical field for non-clotting blood
61
Post-op, what would be a concern is a pt that received massive volume resuscitation
* May need post op ventilation
* Risk for Pulmonary edema and ARDS
62
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**
63
Consequences of massive transfusion
* Hypothermia
* Volume overload
* Dilutional coagulopathy
* Decreased 2,3-dpg
* Hyperkalemia
* Citrate toxicity (hypocalcemia)→hypotension
* Tissue hypoperfusion and lactic acidosis
64
Whats polycythemia
* Expanded red cell mass and increased Hct, caused by-
* Reduced volume (dehydration)
* Excess RBC production (polycythemia vera)
* Chronic hypoxia
65
What problems can polycythemia cause? At what Hct does it become a major problem?
**Increased blood viscosity poses risk for:**
* Thrombosis leading to CAD, pulm HTN, CNS disorders
* Hct **\> 55%** is problematic
66
Hemophilia A- Severe, moderate, mild
**Increased PTT NORMAL PT ........ FACTOR VIII**
* **Severe**-
* Factor **VIII** less than **1%**
* diagnosed in **childhood**
* freq. spontaneous hemorrhages; 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** surgery
67
Hemophilia A anesthesia considerations
* Must bring **factor** **VIII** levels to near normal (100%)
* 3500-4000U given: **50-60 U/kg** IV initially,
* half life of 12 hours.
* **25-30 U/kg** every **8 to 12 hours** as maintenance to keep the plasma levels of factor VIII . 50%
* May need to continue up to two weeks post up.
* DDAVP is also effective at correcting for surg
68
Hemophilia B- Severe, moderate, mild
**Increased PTT NORMAL PT ......... FACTOR IX**
* **_Severe_**
* factor **IX** less than **1%**
* associated with severe bleeding
* **_Moderate_**
* factor **IX 1-5%**
* **_Mild_**
* factor IX **5-40%**
69
Hemophilia B anesthesia considerations
* GIVE factor **IX** prior to surgery!!!
* 7000 Units (70kg) **= 100 U/kg**
* 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
70
vWB disease patho and signs
* Dysfunctional platelets (NORMAL plt count)
* Bleeding time is markedly prolonged (normal = 3-10 minutes)
* may also have increased PTT
* **Commonly bleed from mucus membranes-**
* ****epistaxis
* easy bruising
* menorrhagia
* GI
* gingival
71
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
72
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 1**0 days**
73
What other drugs can cause platelet dysfunction
* Antibiotics- affect aggregation and adhesion
* Volume expanders- dextran, hespan
* NSAIDS
74
Conditions that cause platelet dysfunction
* Hypothermia **\< 35˚C**
* Acidosis **\< 7.3**
* Uremia(renal disease)
* Liver disease
75
Thrombocytopenia- what is it, signs and symptoms
* Low platelet count
* approximately 1/3 of platelets sequestered in spleen
* Signs: 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**
76
Most common intra-op coagulopathy
* Dilutional- platelets/coagulation factors
* get diluted with **fluids** or **PRBCs** (more than 10 units)
* Surgical hemorrhage also causes fibrinogen release
77
Acquired Platelet defects can be caused by
* Radiation
* Chemo
* Toxic chemicals
* Thiazides,
* ETOH,
* estrogen
* Cancer
* Viral hepatitis
* B12/folate deficiency
78
DIC What is it? what is it associated with? Clinical symptoms?
* Destruction of platelets??
* 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
* Clinical symptoms are a consiquence of **thrombosis** and **bleeding**:
* microemboli accumulation in the pulmonary system
* organ damage
79
DIC lab profile
* Rapid decrease in **platelet** count \<50,000
* Prolonged **PT/PTT**
* Presence of **ELEVATED** **split fibrin degredation products**
* **LOW** plasma concentrations of **Antithrombin III**
* **NORMAL** fibrinogen levels
80
DIC management
* Transfuse:
* platelets
* FFP
* fibrinogen
* antithrombin III
* Give **heparin** to block thrombin formation → STOPS the consumption of clotting factors
* Hemodynamic and respiratory support
81
What factors is PT sensitive to?
I, II, V, VII, X
| (normal 10-12 secs)
82
What factors is PTT sensitive to?
I, II, V, VII, X
**IX, XI, XII**
(normal 25-35 secs)
83
What factors is ACT sensitive to?
I, II, V, VII, X
**IX, XI, XII**
(normal 90-120 secs)
84
What factors is Thrombin time sensitive to?
I, II
| (normal 9-11 secs)
85
What is a normal fibrinogen?
**160-350**
86
What's a normal bleeding time?
3-10 minutes
87
Vitamin K is needed for formation of which factors?
II, VII, IX, X
88
What is the lab profile for vitamin K deficiency? Treatment?
* Prolonged PT
* NORMAL PTT
Treatment:
* **Vitamin K** (takes **6-24 hours** for effect)
* **FFP** for acute bleeding
89
Anesthesia considerations for hypercoagulability
Prevent thrombus, PE, DVT, blood clots
* Early ambulation
* SubQ heparin
* Compression devices
* ASA
* IVC filter
* Regional anesthesia is beneficial, but **contraindicated if pt on LMWH**
90
What is long-term anticoagulation therapy used for
* Venous thrombosis
* Hereditary hypercoagulable states
* Cancer
* Mechanical heart valves
* **A-fib**
91
Antiplatelet therapy is indicated periop for what conditions? Which meds are commonly used?
**Antiplatelet therapy indicated for:**
* Pts at high risk for **CVA**, **MI**, vascular **thrombosis** complications
**Medication used**
* **ASA**, **PDE** inhibitors, **ADP** receptor antagonists
92
How does warfarin work
* Competes with **vitamin K** →inhibits formation of vitamin K dependent clotting factors
* factor **II, VII, IX,** and **X**
93
What lab tests are needed for warfarin monitoring
**PT/INR**
94
How does heparin work
**INDIRECTLY** inhibits **thrombin** and **Xa** by binding to **antithrombin III**
95
What lab tests are needed for **heparin** monitoring
**PTT** or ACT
96
Heparin can be reversed with
Protamine
97
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 **1 mg** vitamin K subQ
98
What should be done for someone on warfarin, but is very high risk for clotting
* Start heparin 3 days after stopping warfarin
* Then stop heparin 6 hours prior to surg
* surgery can be safely performed if INR **\< 1.5**
99
what changes can interefere with O2 delivery to the tissues, or with compensatory mechanisms of an anemic patient?
1. Anything that shifts the curve to the left
* **decreasing CO** (Propofol causes BP to go down and can be detrimental in an anemic patient
* **Respiratory alkalosis** (hyperventilation /decreased PaCO2)
* Hypothermia
* **Abnormal hemoglobin** - fetal Hgb and carboxyhemoglobin (smokers))
100
What is P50
* the **partial pressure** at which **50%** of hemoglobin is saturated
* Usually around **26-28%**
* A **right** **shift** needs a higher partial pressure to sarurate **50%** (left shift = lower PP)
101
Relative partial pressures and oxygen saturation
At **40** mmHg **70%** of hemoglobin will be saturated
At **60** mmHg **90%** of hemoglobin will be saturated
102
Explain the steep part of the oxyhemoglobin disassociation curve
* there is a **rapid unloading** of O2 in response to a small change in the partial pressure of O2
103
What is acute treatment for acute blood loss
1. **Restore intervascualr volume first!!!**
* Colloid
* crystalloid
* Blood products (O2 carrying capacity)
2. **Monitor coagulation**
* (blood loss **decreases** **clotting** **factors**)
* PT, PTT, INR, CBC, PLT
* If you see oozing in the surgical field **CHECK FIBRINOGEN!!!**
3. Monitor serum **calcium** and **potassium** levels
1. **citrate** binds to calcium
2. **blood** **products** have high potassium and will have a higher contenct as the cells degrade
3. **Hypotension? may need some calcium!**
4. ABGs
* **_persistent metabolic acidosis_** reflects reflects **hypovolemia** and **decreased** **oxygen** **delivery** to the tissues
104
How is warfarin reversed?
Vitamin K
4-factor PCCs
FFP
