Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Coexisting Test 3 > Heme > Flashcards

Heme Flashcards

1
Q

What is anemia characterized by? Defined as?

A

Characterized as decrease in red cell mass

  • Manifests clinically as a reduced absolute number of circulating RBCs
  • No single lab value
    • Hematocrit (Hct) most often used indicator
    • Hemoglobin (Hgb) and RBC count

Defined as

  • Adult Women: Hgb <12 g/dL (normal 12-15.5 g/dL); Hct <36% (normal 37-47%)
  • Adult Men: Hgb <13 g/dL (normal 13.5-17.5 g/dL); Hct <40% (normal 42-52%)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What happens to oxygen carrying capacity and tissue oxygen delivery in anemia?

A

Oxygen carrying capacity and tissue oxygen delivery become impaired

  • RBCs contain hemoglobi–> defines the O2 carrying capacity
  • Anemia decreases O2 carrying capacity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How do you calculate arterial oxygen content?

A
  • CaO2=(Hgb x 1.39)SaO2 + 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 CaO2 is 16-20 mL/dL
  • Drop in Hgb from 15 g/dL to 10 g/dL results in a 33% decrease in CaO2!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are compensatory mechanisms for acute and chronic anemia?

A
  • Decreased blood viscosity- HCT is primary determinant of blood viscosity
  • Decreased SVR
    • vascular tone and blood viscosity
  • Increased cardiac output
    • Increased SV and heartrate
    • Can lead to high-output heart failure in chronic- severe anemia
  • Tissue redistribution of blood to organs with high extraction ratios
    • Myocardium, brain, kidneys
    • Results in pallor- especially in distal fingertips/toes
  • Kidneys secrete erythropoietin
  • Rightward shift on oxyhemoglobin dissociation curve
    • Increased 2,3 DPGà increases P50 (normal P50 is 27 mmHg)
    • Facilitates release of oxygen from Hgb to tissues; chronic compensatory mechanism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What causes shifts in oxygen hgb dissociation curve?

A

Right shift= release oxygen

  • Increased CO2
  • Acidosis
  • Increased 2,3, DPG
  • Exercise
  • Increased Temperature

(also, sickle cell anemia)

(CADET faces RIGHT)

Left shift= love oxygen

  • Decreased CO2
  • Alkalosis
  • Decreased 2,3, DPG
  • Decrease temp
  • CO

many unique hgb also cause left shift

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Anesthesia management for acute and chornic anemia?

A
  • Care must include measures specific to underlying disease as well as the state of anemia
  • Avoid disruption of the compensatory mechanisms aimed at maintaining O2 delivery to tissues
    • Avoid decreasing cardiac output
      • Example: drug induced cardiac depression (etomidate or high opioid induction technique)
    • Avoid leftward shift on the oxy-hemoglobin curve
      • Respiratory alkalosis/ hyperventilation
      • Abnormal hemoglobin (fetal hgb and carboxyhemoglobin)
      • Hypothermia
        • Decreased tissue O2 requirements may be beneficial but unpredictable- shivering can increase O2 requirement over time
  • Maximize O2 delivery
    • Increase FiO2, transfusion of PRBCs (remember CaO2 equation!)
  • Normovolemic hemodilution, intraoperative blood salvage, transfusion therapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

VA and anemia?

A
  • Volatile anesthetics less soluble in anemic patients
  • Results in accelerated uptake
  • HOWEVERà increased cardiac output
  • NO clinically detectable differences in the rate of induction of anesthesia or vulnerability to an anesthetic overdose in anemic patients or nonanemic patients
    • Until hgb < 4.3 g/dL.
  • problem with VA in anemic is r/t to cardiac depression that a VA can have
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is transfusion therapy based on in anemia?Goals of transfusion therapy?

A
  • Decision based on:
    • Hgb level
    • Risks of anemia balanced with risks of transfusion
    • Presence of co-existing diseases
    • Magnitude of the anticipated blood loss
  • Clinical judgment that that the O2 carrying capacity must be increased to prevent O2 consumption (VO2) from outstripping O2 delivery (DO2)
  • Goal of transfusion therapy
    • Increase oxygen-carrying capacity (PRBCs)
    • Correct a coagulation disorder (FFP, platelets, DDAVP, cryoprecipitate)
    • NOT to increase plasma volume!!!
  • No transfusion trigger
    • Old “10/30” rule–> no evidence to support
      • said that you transfuse if Hgb <10 or HCT <30
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are some tranfusiton consideraitons in anemia based on Hgb level? coexisting conditions?

A
  • Hgb level
    • Rarely indicated if Hgb >10g/dl (Hct 30%)
    • Almost always indicated if Hgb< 6g/dl (Hct 20)
    • If Hgb is between 6-10g/dl transfusion is based on the patient’s risk for complications and inadequate oxygenation
    • Chronic anemia generally well tolerated
    • Use of transfusion trigger of Hgb not recommended by 2006 ASA guidelines
  • Co-existing diseases
    • Chronic anemia most often due to underlying disease process
    • Identify and treat underlying disease
    • Coronary artery disease
      • Hgb <7 g/dL can lead to myocardial ischemia
        • Hct 28-30% may require blood transfusion with significant CAD especially with unstable coronary syndromes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Risk of RBC transfusions?

A
  • Hep B, C, HIV and bacterial infections
  • Longer ICU and hospital length of stays
  • Increased rates of ventilator associated pneumonia and transfusion related acute lung injury
  • Hemolytic transfusion reactions
  • Higher mortality rates
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are some transfusion considerations based on EBL for sx procedures?

A

Expected blood loss for surgical procedure

  • <15% of total blood volume= no replacement therapy
  • 15-30% to total blood volume= can be replaced exclusively with crystalloids
  • >30% generally requires RBC transfusion to replace O2 carrying capacity
  • Massive transfusion (>50% blood volume replaced) RBC transfusion should be accompanied with FFP and platelets ratio of 1:1:1
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How to calculate allowable blood loss?

EBV of men, women?

How much does 1 unit increase Hgb and Hct?

What is the HCT of a unit PRBC?

A
  • Must consider all transfusion considerations!
  • ABL= EBV x (pts Hct – allowable Hct)
  • pts HCT
  • Hct can be replaced by Hgb
    • Hct and Hgb are RELATIVE measures–> above calculation assumes patient is euvolemic!
      • meaning not dehydrated! need good fluid volume on board to be accurate
  • Estimated Blood Volume
    • Men 75 ml/kg
    • Women 65 ml/kg
  • 1 unit PRBC increases Hgb 1 g/dL and Hct 2-3%
  • 1 unit PRBCs has hematocrit of 70%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What clinical signs will yous ee in pt with 20% EBV loss?

A
  • Tachycardia
  • orthostatic hypotension
  • CVP change

in 70 kg person, this is 1L blood loss

under anesthesia, you can mask many of these symptoms. listen to suction, look over drapes, etc.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What s/s do you expect to see in pt with 40% EBV loss?

A
  • Tachycardia
  • hypotension
  • tachypnea
  • oliguia
  • acidosis
  • restlessness
  • diagphoresis
  • EKG ischemia
  • CVP change

in 70 kg pt, this is 2 L

under anesthesia, you can mask many of these symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Will acute blood loss be shown automatically in labs?

A
  • In acute blood loss, hematocrit may be unchanged initially
    • Takes 3 days to reach plateau
  • Decreases in Hct >1% every 24 hours can only be explained by acute blood loss or intravascular hemolysis- have blood on board before OR or ready to give in room
  • Physiologic signs and symptoms of acute anemic may be masked under anesthesia
  • Watch the field (and listen to the suction)!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Acute blood loss management?

A

Monitoring

  • Invasive monitoring? (CVP, Arterial BP, +/- PA)
  • Foley- urine output

Induction

  • Ketamine/Etomidate
  • maybe just versed if really bad

Maintenance

  • May be unable to tolerate even modest levels of volatile anesthetics
  • Scopolamine, benzodiazepines, and opioids
  • Use vasopressors sparingly- treat the cause, don’t mask it!!
  • Keep warm
  • Watch surgical field for non-clotting blood- if pt oozy, think about giving PLT, FFP as well
  • Restoration of intravascular volume
  • Crystalloids
  • Colloid
  • Blood products!!!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What labs to monitor intraop when acute blood loss?

Postop expectations?

A

Monitor labs and watch the field for oozing

  • Coagulation (PT, PTT, INR)
  • CBC (Hct/Hgb, platelets)
  • Fibrinogen level
  • Serum calcium, and potassium levels
  • ABGs
  • Persistent metabolic acidosis reflects hypovolemia and inadequate O2 delivery to tissues
  • Base excess and lactic acid values

Post-operative

  • May require postoperative ventilation due to anticipated fluid shifts from resuscitation
  • Pulmonary edema
  • ARDS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is a massive transfusion?

What consequences is it associated with?

A

Defined as:

  • 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

Associated with several consequences due to property of blood, agents to preserve blood and storage

  • Hypothermia (use your fluid warmer!)
  • Volume overload
  • Dilutional coagulopathy (no clotting factors in PRBCs)
  • Decreased in 2,3 diphosphoglycerate (effects on oxyhemoglobin curve???)– LEFTWARD shift
  • Hyperkalemia due to K leak
  • Citrate toxicity (binds calcium leads to hypocalcemia)
  • Contains glucoseà converted to lactateà acidosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are some diseases that lead to chronic anemia?

A
  • Renal dx
  • cancer
  • HIV/AIDS
  • RA
  • Crohn’s
  • DM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is iron deficiency anemia?

A
  • Results in ineffective erythropoiesis
    • Microcytic, hypochromic anemia
    • Insufficient iron= insufficient amount of hemoglobin produced
  • In infants/small children: most common form of nutritional deficiency
  • Adults: reflects depletion of iron stores due to chronic blood loss
    • Gastrointestinal bleeds, menstruation, cancer
  • Typical Hgb 9-12 g/dL
  • Decreased serum ferritin concentration (<30 ng/mL)
  • Treatment is ferrous iron salts for >1 year
  • In cases of severe anemia may postpone elective surgery for up to 4 months in order for ferrous iron salts to improve hemoglobin levels (mainly severe CAD)
    • If unable to delay surgery longer than 3 weeks, IV iron preparations can be considered
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is Vitamin B 12 (pernicious anemia)

A
  • Essential for normal DNA synthesis results in macrocytic (large RBCs) anemia
  • Alcohol abuse, poor diet, intestinal malabsorption syndromes, long N2O exposure at high concentrations (Abusing N2O, not normal expsoure in OR)
  • Pernicious anemia
    • Hgb levels 8-10 g/dL with large RBC volume
    • Degeneration of the lateral and posterior columns of spinal cord
      • Symmetrical paresthesia, loss of proprioception and vibration in lower extremities
    • Unsteady gait, diminished deep tendon reflexes
    • Memory impairment and depression
    • Thick, large smooth tongue (airway!)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Anesthesia managemenet for B12 deficiencies?

A
  • Airway evaluation and plan (plan B!)
    • strawberry, dry tongue, easily friable by blade placement
  • Maintain adequate oxygenation
  • Avoid N20- oxidizes b12 in bone marrow, causes bone marrow suppression
  • RBC transfusion for life-threatening anemia in emergency and urgent surgeries (usually unnecessary)
  • May want to consider avoiding regional anesthesia or peripheral nerve blocks if paresthesia is present
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are hemolytic anemias?

A
  • Accelerated destruction (hemolysis) of erythrocytes
    • Increased levels of unconjugated bilirubinemia
    • Increased lactate dehydrogenase (LDH) level
  • Results in tissue hypoxia and hyperproduction of RBCs in the bone marrow
    • Immature erythrocytes
  • Disorders of red cell structure
    • Hereditary spherocytosis
    • Paroxysmal nocturnal hemoglobinuria
  • Disorders of red cell metabolism
    • G6PD deficiency
    • Pyruvate kinase deficiency
  • u
  • u
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is hereditary spherocytosis?

A
  • Autosomal dominate, most common hereditary hemolytic anemia in US
    • Abnormal RBC membrane protein compositionà cell becomes more rounded and fragile
  • Ranges from mild/clinically silent–>severe with life-threatening hemolysis and anemia
  • Splenomegaly and fatigue
  • Risk of hemolytic crisis with viral/bacterial infections
  • Gallstones and jaundice
  • Anesthetic management
    • Depends on severity and if hemolysis is stable or period of exacerbation
    • Avoid infections
    • Cardiopulmonary bypass and mechanical heart valves may lead to excessive hemolysis
      • OFF pump CABG may be safest
    • H/o splenectomy are at higher risk of arterial and venous thromboembolism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is paroxysmal nocturnal hemoglobinuria?

ANesthesia management?

A
  • Complement- activated RBC hemolysis
    • Stem cell disorder, presents during 2nd- 8th decade of life
    • Abnormalities or reduction in a RBC membrane protein
    • Life expectancy after diagnosis 10 years
    • Thought to be result of CO2 retention and subsequent acidosis
  • High risk for DVT due to complement activation
    • Hepatic and portal veins
  • Aplastic bone marrow
  • Anesthetic Management
    • Avoid respiratory depressants- prevent CO2 retention!!!
    • Avoid hypoxemia, hypo-perfusion and hypercarbia
    • Maintain hydration and DVT prophylaxis
    • If transfusion required: “washed” RBCs should be used to decrease complement activation
      • if you anticipate giving blood, order washed PRBC and order the blood EARLY (at least a night in advance)
      • washed prbc take awhile…
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is G6PD deficiency?

A
  • Phosphogluconate oxidative metabolic pathway
    • Normally counteracts environmental oxidants and prevents globin denaturation
    • In deficiency of G6PD enzyme, oxidative stress causes denaturation of Hgb which precipitates on the inner surface of the RBC membrane resulting in membrane damage and hemolysis
  • Most common enzymatic disorder of RBCs worldwide
    • African Americans, Asians and Mediterranean populations
  • Ranges from mild/no hemolysis (Class V and IV)à chronic hemolytic anemia (Class I)
  • Oxidative drugs, infection, ingestion of fava beans aggravate preexisting hemolysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Keys for anesthesia management of G6PD patient?

A
  • Tailor to severity and acuity of anemia
    • Class V, VI–> little anesthetic implications
  • Avoid risk of hemolysis
  • Avoid oxidative drugs
    • NSAIDs, Quinolones, Sulfa drugs
  • Avoid drugs that depress G6PD activity
    • Isoflurane, sevoflurane, diazepam, metoclopramide
  • Avoid Methylene blue!
    • Life-threatening if administered (hemolysis)
  • Avoid drugs that cause methemoglobinema (because its treated with methylene blue. also avoid NTG, SNP)
    • Lidcaine, prilocaine, benzocaine, silver nitrate
  • Avoid and aggressively treat conditions that cause significant oxidative stress
    • Hypothermia, Acidosis, Hyperglycemia, infections
  • Codeine, midazolam, propofol, fentanyl and ketamine are safe
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is pyruvate kinase deficiency?

A
  • Most common enzyme defect that results in congenital hemolytic anemia
  • Worldwide
    • Northern European descent and China
  • Less prevalent than G6PD deficiency but considerably greater occurrence of chronic hemolysis
  • Accumulation of 2,3 DPG
    • Shifts oxyhemoglobin curve to the right
    • High incidence of hemolysis in the spleen–> splenomegaly
    • Life-threatening, transfusion-requiring hemolytic anemia at birth
  • Chronic jaundice, gallstones
  • Splenectomy improves degree of hemolysis and may eliminate need for transfusions
    • increases r/f infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are some immune system induced hemolysis? infection induced?

A
  • Immune system induced hemolysis
    • Sensitization of RBCs
    • Disease- induced
    • Drug- induced
  • Infection induced hemolysis
    • Malaria
      • Particles released during hemolysis can result in DIC and hypersplenism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Periop risks and concerns for hemolytic anemias?

A
  • ↑ risk of tissue hypoxia
  • If previous splenectomy may have ↑ risk of perioperative infection
  • Increased risk venous thrombosis due to activation of coagulation cascade
  • Erythropoietin is often prescribed for 3 days preoperatively
  • Acute drops in Hgb below < 8 g/dl and chronic reductions to below 6 g/ dl should be considered for transfusion
  • Preop hydration and prophylactic administration of RBCs have been advocated
  • Caution Methylene Blue administration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is sickle cell disease?

A
  • Inherited homozygous disorder of the hemoglobin molecule
  • Substitution of valine for glutamic acid on the beta globulin chain
  • Results in mutant hemoglobin (S)–> 70-98% Hgb is type S
  • Extreme states of deoxygenation–> Hgb aggregates forming a polymer distorting the erythrocyte’s membrane–>sickled cell shape
  • Cells sickle and occlude small vessels-> decreasing blood flow and oxygen delivery to tissues
  • Increased incidence of hemolysis resulting in average RBC lifespan of 10-20 days (normal 120 day lifespan)
  • Oxy-hemoglobin curve shifts to the right as compensation
32
Q

What are some compliations a/w sickle cell diseae?

A
  • Begins early in life, progression highly variable
  • Severe hemolytic anemia–> end- organ damage
    • Bone marrow, spleen, kidneys, CNS
  • Splenic infarctionà loss of splenic function within first decade of life–> infection!
  • Kidney–> painless hematuria and loss of concentrating ability–>chronic renal failure in third-fourth decade of life
  • Pulmonary damage due to chronic persistent inflammation
  • Neurologic complications include both ischemic and hemorrhagic strokes
  • Vaso-occlusive crises
    • Episodic painful bone and joint pain associated with concurrent illness, stress, dehydration
33
Q

What is a sickle cell crisis?

A
  • Life threatening
  • With de-oxygenation, Hgb S forms an insoluble globulin polymer
    • Acute episodic vaso-occlusive crisis
    • Ischemia / infarction of organs
    • Pain, stroke, renal failure, liver failure, splenic sequestration, PE
    • Very painful
    • Acute chest syndrome
34
Q

What is acute chest syndrome? s/s, txmt

A
  • Can be fatal (typically 2-3 days postop)

​S/S

  • Pneumonia-like, presence of new pulmonary infiltrate involving one complete lung segment
  • Pulmonary vascular occlusion
  • Pleuritic chest pain, dyspnea, fever (>38.5 C), acute pulmonary hypertension

Treatment:

  • Transfusion or exchange transfusion to Hct of 30%
  • Supplemental 02, inhaled nitric oxide (reduce pulmonary hypertension)
  • Antibiotics
  • Inhaled bronchodilators
  • Aggressive pain management
  • Monitor for pain crises, stroke, and infection
    • typically won’t see on OR table, but may help managing pain
35
Q

What is sickle cell trait?

A

Heterozygous carriers of sickle cell

  • Have one normal gene and one abnormal gene encoding hemoglobin S (genotype AS)
  • 40% of their Hgb is S/ 60 % is normal Hgb A
  • Usually do not develop anemia and or symptoms, requiring no treatment
  • 5% at some time have
    • Hematuria
    • Difficulty concentrating urine
    • Do not require pre-op transfusions
  • 8% African Americans have trait
  • no changes in anesthetic managmeent guidelines
36
Q

Risk factors for periop complications with sickle cell disease?

low/med/high risk sx for sickle cell patients?

A
  • High incidence perioperative complications
  • Risk factors
    • Advanced age, frequent severe sickling episodes, evidence of end-organ damage (low baseline O2 saturation, elevated creatinine, cardiac dysfunction, stroke), and concurrent infection
  • Surgical considerations
    • Low risk surgeries: extremity and minor procedures (inguinal hernia repairs)
    • Moderate risk: intraabdominal operations
    • High risk: intracranial, intrathoracic and hip replacement
37
Q

Periop risks and concerns for sickle cell disease? Transfusion guidance?

A
  • Look for evidence of organ damage, cardiac dysfunction, concurrent infection
  • May benefit from conservative transfusions with high risk surgery
    • Pre-operative transfusion to increase HCT to 30% without regard to ratio of sickle Hb to normal Hb
    • Major noncardiac surgeries may transfuse to goal of HbS <30% and cardiopulmonary bypass surgeries goal of HbS<5%
38
Q

What situatiosn should be avoided in sickel cell diseae?

A
  • Hypoxemia/acidosis
  • hypovolemia
  • stasis
  • hypothermia
39
Q

Anesthetic considerations for sickel cell diseae?

A
  • Supplemental O2
  • Preoperative hydration for 12 hours prior to surgery
    • if they were not admitted the night before, find them first thing in preop and start giving fluid!
  • Pre-med
    • avoid respiratory depression leads to acidosis
    • may want to take over ventilation and don’t forget preoxygenation!
  • Regional anesthesia is advocated for pain control
    • concern with hypotension, stasis of blood flow, compensatory vasoconstriction
    • give fluid before regional and treat hypotension. helps to decrease crises
  • Aggressive pain management, may have tolerance
  • Avoid infections
  • Avoid tourniquets (but not contraindicated)
  • Keep patient WARM!
  • Maintain high cardiac output
  • Position to prevent stasis
40
Q

What is Thalassemia major?

A
  • Inability to form either ⍺ (⍺-thalassemia) or β (β-thalassemia) globin chains of hemoglobin
  • Severe- life-threatening anemia, often require repeated transfusions
    • with repeated transfusions, neeed T&C readily available prior to OR
    • Can have lots of abs to blood and change in blood type, making itdifficult to obtain blood in individuals
  • Hallmarks: ineffective erythropoiesis, hemolytic anemia and hypochromia with microcytosis
  • Chronic deficit in O2 carrying capacity–> max erythropoietin release–> increased unbalanced globin synthesis–> aggregation and precipitate formation–> membrane damage
    • Some cells destroyed in bone marrow –>ineffective erythropoiesis
    • Some escape into ciulation –> hemolytic anemia and hypochromia with microcytosis
41
Q

Complications of thallassemia major?

A
  • Extramedullary hematopoiesis–>bone marrow hyperplasia (maxillary bone and frontal bone), stunted growth and osteoporosis, hepatomegaly
    • can cause difficulty with intubation
  • Hemolytic anemia–> splenomegaly, CHF, dyspnea and orthopnea
  • Transfusion therapy–> iron overload–>cirrhosis and jaundice, right sided- heart failure, endocrinopathy–> chelation therapy
  • Increased risk infection (splenectomy)
  • Arrhythmias and very sensitive to digitalis
  • Spinal cord compression
    • note any paresthesias!
42
Q

What are some clinical sequelae of iron overload?

A
  • Pituitary- impaired growht, infertility
  • Thyroid- hypoparathyroidism
  • herat- CMP, cardiac fialure
  • Liver- hepatic cirrhosis
  • Pancreas- DM
  • Gonads- hypogonadism
43
Q

What is thalassemia minor?

A
  • Heterozygous state (trait) for either ⍺- globin or β-globin gene mutation
  • Mild to moderate microcytic anemia
  • Normal RBC count
  • no anesthesia implications
  • enough normla hgb that they’re ok
44
Q

Anesthetic management for thalassemia major?

A
  • CHF common with severe anemia
  • Cardiac arrhythmias due to heart failure
  • Hemodynamic compromise with induction agents if low cardiac reserve-use cardiac sparing drugs
    • etomidate, high dose opioid
  • Very sensitive to the effects of digitalis
  • Hepatosplenomegaly
  • Coagulopathy (? Regional Anesthesia)
    • not contraindicated, need to look at plt/coags and discuss plan with surgeon
  • Hypersplenism can result in thrombocytopenia and ↑ risk of infection
45
Q

Anesthetic management (r/t airway, and complications of iron loading from chronic therapy)

A
  • Potential difficult airway 2º to maxillary deformities
    • Consider awake fiber-optic intubation
  • Complications of iron loading from chronic therapy
    • Diabetes (Blood glucose monitoring)
    • Adrenal insufficiency (↓ response to vasopressors)
    • Liver dysfunction & Coagulation abnormalities
    • Hypothyroidism & hypoparathyroidism
    • Arrhythmias (ECG)
    • Right-sided Heart failure (ECHO)
46
Q

What is methemoglobinemia? % before you see effects?

A
  • Iron moiety in Hgb is oxidized from the ferrous (Fe2+) state to ferric (Fe3+) state
  • Methemoglobinemia moves the oxyhemoglobin dissociation curve markedly to the left–> little oxygen is delivered to the tissues (left= love)
    • Results in polycythemia
  • Normal RBC maintains methemoglobin levels <1% through the methemoglobin reductase enzyme system
  • Methemoglobin levels <30%= no compromise to tissue oxygenation
  • Methemoglobin levels 30-50%= symptoms of oxygen deprivation
  • Methemoglobin levels >50%= coma and death
47
Q

How do you develop methemoglobinemia?

A

Mechanisms of development:

  • Globin chain mutations favor formation of Hgb M
    • Resistant to reduction by methemoglobin reductase system
    • Hgb M carry brownish blue color that does not change to red when exposed to oxygen–> cyanotic appearance independent of PaO2
    • Usually asymptomatic
  • Mutations impairing methemoglobin reductase system
    • Methemoglobinemia levels <25%—> cyanotic appearance independent of PaO2
  • Toxic exposure to substances that oxidize normal Hgb iron at a rate that exceeds capacity of the normal reducing mechanisms
    • Infants at greater risk with oxidizing agents
    • Local anesthetics (prilocaine/benzocaine), nitrates and nitric oxide
48
Q

Anesthetic consideration for methemoglobinemia? What will the pulse ox read? Emergency treatment?

A
  • Avoid toxic levels of: local anesthetics (prilocaine/benzocaine), nitrates, nitric oxide especially in infants, patients with Hgb M and those with G6PD deficiency
  • Pulse oximetry is unreliable–> typically reads 85%
    • Methemoglobin absorbs red and infrared wavelengths equally; 1:1 ratio= 85%
    • Falsely underestimates SpO2 when SaO2 is >85%
    • Falsely overestimates SpO2 when SaO2 of <85%
  • Emergency treatment of toxic methemoglobinemia
    • Avoid tissue hypoxia and further left-ward shift on oxy-hemoglobin curve
      • SNP can cause methhemoglobinemia and moves oxy-hgb curve even further to the left!
    • O2 therapy
    • 1-2 mg/kg of intravenous methylene blue as a 1% solution in saline infused over 3-5 mins, may repeat after 30 mins
    • Arterial line to measure bp, methemoglobin levels and arterial blood gas
    • Correct acidosis
    • Monitor EKG for signs of ischemia
49
Q

What is aplastic anemia?

A
  • Aplastic anemia refers to bone marrow failure characterized by destruction of rapidly growing cells
    • RBC, WBC (neutrophils) and platelets
  • Marrow Damage or failure from:
    • Genetic disorders (Fanconi Anemiaà pancytopenia and acute leukemia)
    • Drugs (see table 24-1 Stoelting 7th ed) (next slide)
    • Radiation
    • Infectious process (viral hepatitis, Epstein-Barr virus, HIV, rubella, TB)
  • CBC/WBC/Platelet values can be extremely low
  • May need pre-op transfusion
  • Know pre-op medications and therapies
50
Q

Drugs associated with marrow damage?

A
  • table 24-1 Stoelting 7th ed) from previous slide
  • Antibiotics (chloramphenicol, penicillin, cephalosporins, sulfonamides, amphotericin B, streptomycin
  • Antidepressants (lithium, tricyclics)
  • Antiepileptics (dilantin, carbamazepine, valproic acid, phenobarbital)
  • Anti-inflammatory drugs (phenylbutazone, nonsteroidals, salicylates, gold salts)
  • Antiarrhythmics (lidocaine, quinidine, procainamide)
  • Antithyroidal drugs (propylthiouracil)
  • Diuretics (thiazides, pyrimethamine, furosemide)
  • Antihypertensives (captopril)
  • Antiuricemics (allopurinol, colchicine)
  • Antimalarials (quinacrine, chloroquine)
  • Hypoglycemics (tolbutamide)
  • Platelet inhibitors (ticlopidine)
  • Tranquilizers (prochlorperazine, meprobamate)
51
Q

Anesthetic management of aplastic anemia?

A
  • 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 2º high output state and fluid overload- ECHO may be needed
  • Co-existing congenital abnormalities
    • Fanconi anemia is the peds version
    • Cleft palate; cardiac defects
  • Difficulty cross-matching blood products after multiple transfusions
52
Q

Pre/.induction, maintenance and extubation guideliens for aplastic anemia?

A

Preinduction/induction

  • Consider transfusions before induction
  • Airway hemorrhage possible with DVL
  • Avoid nasal intubation
  • Regional Anesthesia depends on coagulation
  • Labile hemodynamic response to induction (avoid decreases in CO)

Maintenance

  • PEEP will facilitate use of ↓ FiO2 (hyperoxia depresses bone marrow)
  • Avoid nitrous oxide (bone marrow suppressant)
  • Maintain normothermia

Extubation and postoperative period

  • Period with greatest O2 demands
  • Monitor coagulation status
53
Q

Polycythemia review and managmeent?

A
  • Expanded red cell mass and increased Hct
    • Does increase oxygen-carrying capacity but increases blood viscosityà decreased tissue perfusion
  • Caused by:
    • Reduction in plasma volume (dehydration)
    • Production of excess RBC (polycythemia vera)
    • Chronic hypoxia (pulmonary disease, extremely low CO, extreme obesity with hypoventilation, high altitudes)
    • Increased erythropoietin production (renal disease and EPO secreting tumors)
  • Increased blood viscosity
    • Venous / arterial thrombosis leading to CAD, pulm HTN, CNS disorders
  • Usually minor, until Hct > 55%
    • Mild hypoxic polycythemia= no specific treatment
    • Phlebotomy- if very high, (>55%), consider canceling sx and phlebotimize
54
Q

What is hemophilia A?

A

X chromosome congenital factor VIII deficiency (intrinsic pathway affected)

Severe Hemophilia:

  • Factor VIII levels less than 1% of normal
  • Diagnosis as children due to frequent spontaneous hemorrhages in joints and muscles or organs

Moderate Hemophilia:

  • Factor VIII levels 1% to 5% of normal
  • Reduced severity of the disease
  • Increased risk bleeding with surgery/trauma
  • Less problems with joints and muscles

Mild Hemophilia:

  • Factor VIII levels as low as 6% to 30%
  • often undiagnosed until adulthood
  • Increased bleeding risk with major surgery

Significantly prolonged PTT /normal PT

55
Q

Anesthetic management for hemophilia A?

A

Factor VIII must be brought near normal (100%) for surgery

  1. Infusion of factor VIII concentrate
    • initial infusion of 50 to 60 U/kg (3500–4000 units in a 70-kg patient). Since the half-life of factor VIII is approximately 12 hours in adults, repeated infusions of 25 to 30 U/kg every 8 to 12 hours will be needed to keep the plasma factor VIII level above 50%.
    • Therapy must be continued for up to 2 weeks to avoid postoperative bleeding that disrupts wound healing
  2. FFP, cryoprecipitate
    • FFP has all coag factors except plt
    • cryo has VIII, XIII, vWF, fibrinogen!
      • ​also has smaller administration volume
  3. Desmopressin (0.3 mcg/kg IV) for mild Hemophilia A
    • Increases factor VIII threefold to fivefold
56
Q

What is hemophilia B?

A

Congenital factor IX deficiency

Severe disease

  • Factor IX levels of less than 1%
  • Associated with severe bleeding

Moderate disease

  • Factor IX levels of bleeding 1% to 5%

Mild disease

  • Factor IX levels of between 5% and 40%

Significantly prolonged PTT /normal PT

57
Q

Anesthetic management of Hemophlia B?

A
  • Recombinant/purified product of factor IX are used to treat mild bleeding episodes or as prophylaxis with minor procedures
    • can result in increase DVT because it’s an activated factor IX
  • Dose of 100 U/kg (7000 units in a 70-kg patient) needs to be administered
  • Half-life of 18 to 24 hours, so repeated infusions at 50% of the original dose every 12 to 24 hours are usually sufficient to keep the factor IX plasma level above 50%.
  • Increased risk of thromboembolic complications because these agents contain activated clotting factors
  • FFP
    • Cryo cannot be given because cryo does not contain factor IX (only VIII. XIII, vwf, Fibrinogen)
58
Q

What is von Willebrand dx?

Types?

lab levels?

A

Most common inherited disorder of PLATELET FUNCTION

  • Problem is either a quantity or quality issue with vWF
    • Type 1: Quantitative defect; Desmopressin will work!
    • Type 2: Qualitative defect; desmopressin has varied results
    • Type 3: virtual absence of vWF because endothelium lacks vWF; desmopressin has no effect
  • Mucus membrane bleeding common and results in:
    • Epistaxis
    • Easy bruising
    • Menorrhagia
    • Gingival and gastrointestinal bleeding
    • Type 3 will also see bleeding in muscles and joints
  • Platelet count normal
  • Bleeding time is markedly prolonged (normal is 3-10minutes); rapid platelet function assay (RPFA)
  • May have prolonged PTT (due to low levels of factor VIII)
59
Q

Von Willebrand Anesthetic Management?

A
  • Avoid nasal intubations or insertion of nasal trumpets
  • DDAVP therapy (Desmopressin) –mild bleeding or minor surgerym (type I and II only!)
    • IV 0.3 μg/kg diluted in 30 to 50 mL of saline and infused over 10 to 20 minutes to minimize side effects ( tachycardia and hypotension)
    • Intranasal 300-μg dose of intranasal DDAVP (Stimate nasal spray), administered by the application of 100 μL of a 1.5-mg/mL solution to each nostril
    • Short lived effect (12-24 hours); Repeated doses result in tachyphylaxis
  • Cryoprecipitate – more reliable for severe bleeding or surgical prophylaxis
    • Cryoprecipitate is a readily available and effective blood product that contains concentrated fibrinogen, vWF, and factors VIII and XIII
60
Q

What are some causes of drug inducd PLT dysfunction/inhibition?

A
  • ASA irreversible inhibition of cyclooxygenaseà inhibits thromboxane A2 (TxA2) synthesisà severely inhibits platelet aggregation
    • Bleeding Time is prolonged 2-3 minutes within 3 hours of ASA ingestion
    • Lasts the lifetime of platelet
    • Bleeding time returns to normal within 72 hours but aggregation may not return for normal for 7-10 days
  • NSAIDS–> reversibly inhibits platelet cyclooxygenase
  • Antibiotics
    • PCNs and cephalosporins
    • Critically ill patients at greatest risk of significant bleeding
    • Interfere with platelet adhesion, activation and aggregation
  • Volume expanders
    • Dextran interferes with platelet aggregation
    • Hydroxyethyl starch in excess of 2 L
61
Q

What are some other, non-drug induced causes of platelet dysfunction? Treatment?

A

Platelets become very dysfunctional in setting of:

  • Hypothermia (<35℃)
  • Acidosis (pH <7.3)
  • Uremia
  • Liver Disease

Treatment:

  • Desmopressin for mild-moderate dysfunction or mild risk of bleeding
  • Cryoprecipitate for vWF (essential in platelet adhesion)
  • Platelet transfusion- if problem with plt
62
Q

What is thrombocytopenia?

A
  • Low platelet count
    • Normal platelet count 150,000-450,000, lifespan 9-10 days
  • Approximately 1/3 platelets are sequestered in the spleen
  • Signs include petechial rash, bleeding from nose, GI tract, bruising
  • Platelet count >50,000 needed for major surgery to control bleeding
    • 20,000-30,000 appropriate for minor surgery
    • 100,000 for neurosurgical procedures/ neuraxial (regional) procedures
  • Each unit of apheresis platelets or six units of random donor platelets (six pack) should increase platelet count approx 50,000
63
Q

What is the most common cause of intraoperative coagulopathy?

A

Dilutional thrombocytopenia and dilution of pro-coagulants

  • Blood loss replaced with crystalloid, colloid and PRBCs which dilutes platelets and factors
    • Massive blood transfusions 10 or more units
  • Surgical hemorrhage causes the release of fibrinogen from hepatic stores
    • Fibrinogen levels <150mg/dl–> coagulopathy
  • Must give FFP to restore pro-coagulants, and consider platelets
64
Q

What is acquired defects in PLT production?

A

Failure in platelet production resulting from marrow damage

  • Radiation therapy
  • Chemotherapy
  • Exposure to toxic chemicals
  • Drugs such as thiazide diuretics, alcohol, and estrogen
  • Malignancies
  • Viral hepatitis
  • Vit B12 or folate deficiencies

May require platelet transfusions

65
Q

What is DIC?

A

Disseminated Intravascular Coag

  • Platelet destruction disorder- clotting all over the palce and then destroying clots all over, rapid depletion of coagulants (anti and pro)
  • Associated with clinical conditions
    • Sepsis
    • Trauma
    • Cancer
    • Obstetric complications
    • Vascular disorders
    • Immunological disorders
  • Excessive deposit of fibrin / impaired fibrin degradation throughout the vascular tree
  • Platelet consumption
  • Depression of the normal coagulation mechanisms
  • Clinical symptoms of DIC are a consequence thrombosis and bleeding
    • Micro emboli accumulation in pulm system
    • Organ damage
66
Q

DIC Mgmt?

A
  • No single lab test can establish or rule out the diagnosis
    • Rapid decrease in platelet count < 50,000
    • Prolonged PT, PTT
    • Presence of elevated split fibrin degradation products (D-dimers)
    • Low plasma concentrations of factor VIII
    • Decreased fibrinogen levels
  • Treatment is the management of the underlying clinical disorder that triggered the coagulation process
    • Transfusion of platelets, FFP, cryoprecipitate, RBCs (if indicated)
    • Heparin administration to block thrombin formation which blocks consumption of the other clotting factors and allows hemostasis to occur.
    • Hemodynamic/ respiratory support

PT should not be on table unless absolutely necessary!!!

67
Q

Vitamin K deficiency impact?

A
  • Vitamin K is necessary in the liver for factors II,VII,IX,X
  • Deficiency occurs in the presence of
    • Malnutrition
    • GI malabsorption
    • Antibiotic induced elimination of intestinal flora
    • Liver disease/Obstructive jaundice
    • Prolonged PT in presence of normal PTT (because of factor VII!)
  • Treatment:
    • Vitamin K (6-24 hours for full effect)
    • Fresh Frozen Plasma if active bleeding is present
68
Q

What are some causes of hypercoagulability d/o?

A
  • Congenital disorders
  • Acquired:
    • Malignancies
    • Pregnancy
    • Oral contraception
    • Nephrotic syndrome
    • Systemic lupus erythematosus
69
Q

Management of hypercoagulabiliyt d/o?

A
  • Anesthetic considerations:
    • Early ambulation
    • Subcutaneous heparin
    • Compression elastic stockings
    • ASA
    • Vena caval filter
    • Hydration- KEY!!!
  • Regional anesthesia beneficial, but may not be advised if on LMWH
70
Q

What are long-term anticoagulants used for? mgmt around sx?

A

Long term anti-coagulants used for :

  • Venous thrombo-embolisms
  • Hereditary hypercoagulable states
  • Cancer
  • Mechanical heart valves
  • Atrial fibrillation

Therapy poses problem when need surgery (risk of thrombosis vs risk of surgical bleeding)

71
Q

What is antiplatelet therpay used for? examples?

A
  • Indicated for pts at risk for CVA, MI, other vascular thrombosis complications
    • Aspirin
    • NSAIDS
    • PDE inhibitors
    • ADP Receptor antagonists
72
Q

What does coumadin/warfarin inhibit? monitor lebels? reversal?

A
  • Competes with vit K and inhibits synthesis of vit K-dependent clotting factors
    • II, VII, IX, and X
  • Monitored with PT and INR
  • Reversal with vit K, 4-factor PCCs, FFP
73
Q

Long term anticoag management of coumadin and heparin periop?

A

Management includes:

  • Hold Coumadin 5 days
  • Measure INR one day pre-op and if INR >1.8 give 1mg to 2mg Vitamin K SQ
  • Emergent reversal of Coumadin 5-8 ml/kg of FFP

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
74
Q

What does heparin inhibit? monitor levels? reversal? complication?

A
  • Indirectly inhibits thrombin and factor Xa by binding to AT-III
  • Monitor with PTT or ACT
  • Reversal is Protamine
  • Complication is HIT
    • (thromboembolic complications)
75
Q

Regional anesthesia with long-term anticoag?

LMWH? ASA/NSAIDS? Plavix? SQ hep? Coumadin?

A
  • Can develop spinal hematoma/hemorrhage
  • LMWH- +/- regional (stop 24 hours)
    • ​varies between providers. guidlines say 24 hours may be ok, but a lot of anesthesia providers do not feel comfortable with lovenox being administered and regional anesthesia
  • ASA/ NSAIDS- regional may be ok, as long as not using other anticoagulants
  • Plavix- no regional (stop 7 days)
  • SQ heparin- regional may be ok (recommend give after regional)
  • Coumadin- stop 5 days (INR <1.5)

Coexisting Test 3 (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions