Hematology Flashcards
Calculation for arterial O2 content
CaO2 = SaO2(Hgb x 1.39) + PaO2(0.003)
1.39 = O2 bound to hemoglobin SaO2= saturation of hemoglobin with O2 PaO2= arterial partial pressure of oxygen 0.003 = dissolved oxygen ml/mmHg/dl Normal O2 capacity is 16-20 mL/dL
Normal value for O2 content / capacity
16-20mL/dL
O2 carrying capacity is defined by the presence of
hemoglobin
More hemoglobin = more O2 carrying capacity
Causes of anemia
1. Acute • Acute blood loss 2. Chronic • Nutritional deficiency • Hemolytic anemia • Aplastic anemia • Manifestation of another disease • Abnormal structure of RBC • Sickle cell, thalassemias
Compensatory mechanisms involved in anemia
– Increased cardiac output
– Increased red blood cell 2,3-diphoshoglycerate (DPG)
– Increased P-50 (partial pressure of O2 at which Hgb is 50% saturated with O2)
– Increased plasma volume
– Decreased blood viscosity
– Decreased SVR (larger BV diameter allows more blood to flow through it)
– RIGHTWARD shift of Oxygen-Hemoglobin dissociation curve
– Redistribution of blood flow to organs with higher extraction ratio (ER) –> cardiac and brain cells
A shift to the right in the Hgb dissociation curve is associated with
- Facilitates release of O2 from
Hgb to tissues
- Hgb variants with O2 affinity
- Due to Acidosis
- Exercise
- Hypermetabolism and fever
- Increased 2,3 diphosphoglycerate (2,3-DPG)A shift to the left in the Hgb dissociation curve is associated with
- Inhibits release of oxygen from HGB to tissues
- Alkalosis
- Hbg variants that increase O2 affinity (carbon monoxide)
- Hypothermia
- Decreased 2,3 diphosphoglycerate (2,3-DPG)
Anemia is suspected in these values for men and women
– <12.5g/dl (males) hct 40%
– BUT, remember that Hgb and Hct are relative measurements (think about their context→ hemodilution, bleeding, pregnant, etc.)
What is the most effective treatment of anemia?
Treat the cause!
Remember that anemia is almost always the manifestation of another disease process
General anesthesia management for chronic anemia
- Maximize O2 delivery
– Consider ↑ FiO2
– Transfuse If necessary - Avoid drug-induced ↓ in C.O.
– Selection of induction agent (etomidate)
– Anesthetic technique (↑ opioid)
– Hydrate, if tolerated; avoid hypovolemia - Avoid conditions that favor a leftward shift of the oxyhemoglobin dissociation curve
– Avoid respiratory alkalosis, hypothermia, etc. - Consider your volatile anesthetics
– May be less soluble in plasma of anemic patient (b/c volatile anesthetics cling to the lipid layer of RBCs)
• This is more theoretical than actual, but may need to decrease your IA dose
– Consider that this decrease in solubility may be offset by the impact of increased cardiac output
Causes of iron deficiency anemia
o Disorder of hemoglobin resulting in reduced or ineffective erythropoiesis and microcytic RBCs
o Most common form of nutritional deficiency in children and infants
o In adults- reflects depletion of iron stores from chronic blood loss, which may be from:
• Gastrointestinal tract
• Menorrhagia
• Cancer
S/S of Pernicious Anemia and Anesthetic Considerations
S/S:
• Bilateral peripheral neuropathy (assess for this pre-op!)
• Loss of proprioceptive and vibratory sensations in lower extremities
• Decreased deep tendon reflexes
• Unsteady gait
• Memory impairment and mental depression
Anesthesia:
• Avoid regional blocks due to neuropathies
• Avoid nitrous oxide (b/c it inhibits methionine synthase –> necessary for mylin formation)
• Maintain oxygenation
• Emergency correction for imminent surgery is with red cell blood transfusions
S/S of Folic Acid (B9) Deficiency anemia and anesthetic considerations
S/S • Smooth tongue • Hyperpigmentation • Mental depression • Peripheral edema • Liver dysfunction • Severely ill patients
Anesthesia
• Note thorough airway exam →Oral manifestations may make airway management challenging due to changes in tongue texture, etc.
• Have an alternate airway management plan!
These are the 4 hereditary hemolytic anemias
- Hereditary spherocytosis
- Paroxysmal nocturnal hemoglobinuria
- Glucose-6-Phosphate Dehydrogenase Deficiency
- Pyruvate Kinase Deficiency
Hereditary spherocytosis
o Hereditary disorder affecting red cell membrane skeletal structure
o Lifelong hemolytic anemia
o Most common red cell membrane defect-disorder of membrane skeletal proteins -> cell more rounded, fragile, shortened circulation half-life (destroyed in spleen)
o Splenomegaly, fatigability, risk of episodes of hemolytic crisis, often precipitated by infections; risk of gallstones/ jaundice
Paroxysmal nocturnal hemoglobinuria (description and anesthetic considerations)
o Hereditary disorder of RBC structure
o Clonal disorder that arises in hemotopoietic cells with a reduction in membrane protein in RBCs
o Poor prognosis once diagnosed (8-10 years)
• Preoperative hydration and prophylactic administration of RBCs have been advocated
Glucose-6 Dehydrogenase Deficiency (description and anesthetic considerations)
o Disorder affecting red cell metabolism
o Most common enzymopathy- African Americans, Asians, Mediterranean populations-> G6PD activity decreases-> susceptible to damage by oxidation
o ↑ rigidity of membrane & accelerates clearance
• Affects approximately 10% of black males in U.S.
• Acute and chronic episodes of anemia
Anesthesia:
• Need to avoid exposure to oxidative drugs (methylene blue, IAs, benzos, etc)
• Avoid hypothermia, acidosis, hyperglycemia, infection
Pyruvate Kinase Deficiency
o Disorder affecting red cell metabolism
o Deficiency of glycolic enzyme which converts glucose to lactate & is primary pathway for ATP production->results in K+ leak-> ↑ rigidity & accelerates destruction
o Accumulations of 2.3-DPG in the RBCs cause right shift oxy-Hbg curve
Anesthetic Considerations for Hemolytic Anemias***
o ↑ risk of tissue hypoxia
o If previous splenectomy may have ↑ risk of perioperative infection
o Increased risk venous thrombosis due to activation of coagulation
o Erythopoietin is often prescribed for 3 days preoperatively
o Preop hydration and prophylactic administration of RBCs have been advocated
o Acute drops in Hb below < 8 g/dl and chronic reductions to below 6 g/ dl should be considered for transfusion
o Caution Methylene Blue administration
Patho of sickle cell disease
Mutant hemoglobin (S) due to valine substitution for glutamic acid on B-globulin chain-> Hgb aggregates & forms a polymer when exposed to low O2 concentrations
This can cause small vessels to be occluded
Lifespan of a RBC is sickle cell disease
12-17 days
Is sickle cell TRAIT, the patient is heterozygous for the gene, and __% of their Hgb is S, and __ % is normal Hgb A
40% = S 60% = Normal
Most patients are asymptomatic and does not pose risk for surgery or anesthesia.
In sickle cell DISEASE, the patient is homozygous for the gene and __% of their Hgb is Hgb (S) form
70-98%
Sickle Cell patients are at high risk for these complications peri-operatively d/t hemolysis and vasoocclusion
– Stroke – Heart failure – MI – Hepatic or splenic sequestration – Renal failure
Anesthetic Considerations for Sickle Cell Disease
**** Avoid all situations leading to…
1. Hypoxemia
2. Hypovolemia
3. Stasis
4. Hypothermia
5. Acidosis
• Look for evidence of organ damage, cardiac dysfunction, concurrent infection
• May benefit from conservative transfusions with high risk surgery
– ASA recommends pre-operative transfusion to increase HCT to 30%
• Goal of transfusion is to decrease Hgb S to less than 30% (Want to increase Hgb A levels) However, low risk procedures normally don’t need transfusion.
• Give Supplemental O2
• Preoperative hydration for 12 hours prior to surgery (decrease likelihood of hypovolemia/sickling)
• Pre-medication
o Avoid respiratory depression that can lead to hypoxia and acidosis
• Regional anesthesia is fine, although:
o Concern with hypotension
o Stasis of blood flow
o Compensatory vasoconstriction
• Aggressive pain management
• Avoid infections
What is sickle cell crisis and how is it managed?
• Life threatening complication
• As a result of hypoxia, Hgb S forms an insoluble globulin polymer
– Acute episodic vaso-occlusive crisis
– Ischemia / infarction of organs the danger
– Pain, stroke, renal failure, liver failure, splenic sequestration, PE
– Very painful
• Acute chest syndrome-can be fatal (typically 2-3 days postop)
– Pleuritic chest pain, dyspnea, fever, acute pulmonary hypertension
Anesthetic Management of Sickle Cell Crisis:
– Transfusion or exchange transfusion to hct of 30%
– Supplemental 02
– Antibiotics (to avoid infections)
– Inhaled bronchodilators (for the acute chest syndrome)
– Aggressive pain management
Characteristics of Thalassemia Major
- Inability to form beta-globin chains of hemoglobin
- Hepatosplenomegaly
- Dyspnea and orthopnea
- Infection risk
- Arrhythmias, CHF
- Skeletal malformations
- Growth failure and osteoporosis
- Hemothorax
- Spinal cord compression
- Mental retardation
- Very sensitive to digitalis
- Increased RBC production
- Jaundice
Iron overload may cause
Endocrine: Impaired growth, hypogonadism, infertility, hypoparathyroidism, DM
Heart: CM and CHF
Liver: cirrhosis
Considerations for thalassemia
• Potential difficult airway 2° to maxillary deformities
o Consider awake fiberoptic intubation
• Complications of iron loading from chronic therapy
o Diabetes (Blood glucose monitoring)
o Adrenal insufficiency (↓ response to vasopressors)
o Liver dysfunction & Coagulation abnormalities
o Hypothyroidism & hypoparathyroidism
o Arrhythmias (ECG)
o Right-sided Heart failure (ECHO)
• CHF common with severe anemia
• Cardiac arrhythmias due to heart failure
• Hemodynamic compromise with induction agents if low cardiac reserve-use cardiac sparing drugs
• Very sensitive to the effects of digitalis
• Hepatosplenomegaly
• Coagulopathy (? Regional Anesthesia)
• Hypersplenism can result in thrombocytopenia and ↑ risk of infection
Cause of aplastic anemia
– Marrow Damage from:
• Drugs
• Radiation
• Infectious process
Anesthetic Considerations for Aplastic Anemia
– May need pre-op transfusion
– Patients on immunosuppressive therapy
• Steroid “stress” dose should be considered
– Reverse isolation due to thrombocytopenia and increased risk of infection
– Prophylactic antibiotics due to neutropenia
– Hemorrhage (GI & Intracranial)
– LV dysfunction 2° high output state and fluid overload
– Co-existing congenital abnormalities
• Fanconi anemia is the peds version
• Cleft palate; cardiac defects
– Difficulty cross-matching blood products after multiple transfusions
– Preinduction/induction**
• Consider transfusions before induction
• Airway hemorrhage possible with DVL
• Avoid nasal intubation
• Regional Anesthesia
• Labile hemodynamic response to induction
– Maintenance**
• PEEP will facilitate use of ↓ FiO2
• Avoid nitrous oxide
• Maintain normothermia
– Extubation and Postoperative period**
• Period with greatest O2 demands
• Monitor coagulation status
What is methemoglobin?
Hemoglobin is normally Fe+2, but is now Fe+3
Methemoglobin will shift the curve to the
left
These factors can cause methemoglobinemia
- Nitrate poisioning
- Toxic reactions to drugs such as local anesthetic prilocaine
- Hurricane spray
Anesthetic Considerations for Methemoglobinemia
- Can influence the accuracy of pulse oximetry as methhemoglobin absorbs light equally in both red and infrared.
- At Sa02 of >85% underestimates the true value
- At Sa02 of <85% overestimates the true value
- Emergency treatment of toxic methemoglobinemia
* 02 therapy
* 1 to 2 mg/kg of intravenous methylene blue as a 1% solution in saline infused over 3 to 5 minutes.
* may be repeated after 30 minutes.
S/S of acute blood loss with 20% and 40% of EBV
20% EBV Loss
- Orthostatic hypotension
- Decreased CVP
- Tachycardia
40% EBV Loss
- Hypotension
- Tachycardia
- Tachypnea
- Oliguria
- Acidosis
- Restlessness
- Diaphoresis
What is the first fluid we go for to replace blood loss?
Crystalloids
What is the definition of a massive transfusion?
– Transfusion of > 10 units of RBC in 24 hour period
– Replacement of at least one blood volume in 24 hour period
– Replacement of 50% blood volume in 6 hour period
Complications of massive transfusion
– Hypothermia – Volume overload – Dilutional coagulapathy – Decreased in 2,3 DPG – Hyperkalemia – Citrate toxicity (binds calcium)
Polycythemia usually isn’t a problem until Hct >
55%
Hemophilia A is from a deficiency of factor ___, and causes a prolonged ____
VIII
PTT (However, PT will be normal)
Anesthetic Considerations for Hemophilia A
Factor VIII must be brought to near normal levels before the procedure.
Can achieve this with Factor VIII infusion and DDAVP
Hemophilia B is from a deficiency of factor ___, and causes a prolonged ____
IX
PTT (again, PT will be normal)
Anesthetic Considerations for Hemphilia B
Factor IX replacement
Characteristics of VonWillebrand’s disease
- Lack of vWF, which is needed for plt adhesion
- Platelet count normal
- Bleeding time is markedly prolonged (normal is 3-10minutes)
- May have prolonged PTT
- Skin and mucus membrane bleeding common
Anesthetic considerations for vWD
Replace vWF with Cryo or DDAVP
Medications that interfere with plt function
ASA (COX inhibitor that blocks the formation of thromboxane A2, which inhibits platelet aggregation)
Antibiotics (big impact on critically ill pts)
Volume expanders like hetastarch and dextran
Besides medications, these factors can also inhibit plt function
– Hypothermia (<7.3)
– Uremia
– Liver disease
Treatment for altered plt function
Replace vWF (Cryo or DDAVP) Transfuse plts
Platelet count >____ needed for major surgery to control bleeding and > _____ for intracranial procedures
50,000 for major surgery
100,000 for intracranial procedures
Surgical hemorrhage causes release of ____ from hepatic stores
Fibrinogen
Lab tests associated with DIC
– Rapid decrease in platelet count < 50,000 (factors being used up)
– Prolonged PT,PTT
– Presence of elevated split fibrin degradation products
– Low plasma concentrations of antithrombin III (we don’t want to release stuff that keeps us bleeding)
– Normal fibrinogen levels (released by the liver during detected hemorrhage)
Treatment of DIC
– Treat whatever triggered the DIC
– Transfusion of platelets, FFP, fibrinogen, Anti-thrombin III
– Heparin administration to block thrombin formation which blocks consumption of the other clotting factors and allows hemostasis to occur.
– Hemodynamic/ respiratory support
Anesthetic Considerations for those on long-term anticoagulation
– Hold Coumadin 5 days (we want the INR to be less than 1.8)
• Measure INR one day pre-op and if INR >1.8 give 1mg Vitamin K SQ
– If high risk without anticoagulation-
– Start IV or SQ heparin 3 days after stopping Coumadin
– Turn off heparin 6 hours prior to surgery
– Surgery can be safely performed if INR is <1.5
– Regional anesthesia `
This infection can cause hemolysis
Malaria
Overall in anemia, our goal is to avoid disruption of the compensatory mechanisms of anemia. These may include:
Increased CO
Decreased blood viscosity
Increased plasma volume
Increased 2,3-DPG
Increased P-50 (PaO2 when SaO2 is 50%)
Shift to the right of the dissociation curve
Redistribution of blood flow to organs with higher extraction ratios
Normal O2 carrying capacity is
16-20mL/dL
General anesthesia management goals for the patient with chronic anemia
1) Give enough O2
- FiO2
- Possible transfusion
2) Avoid drugs that will decrease CO
- Avoid propofol on induction
- Avoid hypovolemia
3) Avoid things that will shift the curve to the left (alkalosis, hypothermia, decreased 2,3-DPG)
4) Consider your volatile anesthetics (lower Hgb means lower solubility and decreased dose, but may be offset somewhat by higher CO)
Two origins or acquired hemolytic anemias
1) Immune mediated
- Drug induced (PCN reaction)
- Transfusion reaction
- Hypersplenism
2) Infection
- Malaria
Methemoglobin causes a marked shift to the
LEFT
These 3 things can cause methemoglobinemia
- Nitrate poisioning
- Toxic reactions to drugs such as local anesthetic prilocaine
- Hurricane spray
This is the emergency treatment for toxic methemoglobinemia
1 to 2 mg/kg of intravenous methylene blue as a 1% solution in saline infused over 3 to 5 minutes.
• may be repeated after 30 minutes.
Massive blood transfusion will have this effect on 2,3-DPG
It will decrease 2,3-DPG levels
Treatment of DIC
– Transfusion of platelets, FFP, fibrinogen, Anti-thrombin III
– Heparin administration to block thrombin formation which blocks consumption of the other clotting factors and allows hemostasis to occur.
– Hemodynamic/ respiratory support
We hold warfarin (coumadin) for __ days pre-op and we want INR to be less than ____
5 days
1.8
If not less than 1.8, we give 1mg of vitamin K SQ
If our patient can’t be taken off anticoagulation prior to surgery, how do we manage that?
– Start IV or SQ heparin 3 days after stopping Coumadin
– Turn off heparin 6 hours prior to surgery
– Surgery can be safely performed if INR is <1.5
