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Hematologic Pathology > Lecture 1 > Flashcards

Lecture 1 Flashcards

1
Q

All cells come from what single cell type in the bone marrow?

A

Pluripotent Hematopoietic Stem Cell (PHSC)

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2
Q

First cell that is identified as part (beyond stem cell) of red cell series is called?

A

PRO-ERYTHROBLAST

Various stages that you can see on the left - divides from Pro-erythroblasts to mature RBC (erythrocytes)

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3
Q

During the stages of RBC production, what specific steps take place?

A

1. The Nucleus condenses to a small size and then finally is reabsorbed within the cell or extruded from the cell

2. Endoplasmic Reticulum in the cell is Also reabsorbed

At this stage there can be remnants of Mitochondria* & the *Golgi Apparatus and that’s when you can see the Reticulocyte

During the RETICULOCYTE STAGE:

3. The cell actually travels from the bone marrow → the circulation/blood

4. Where it is then squeezed through the pores of the capillary membrane (diapedesis)

5. Then in 1 - 2 Days = The bluish/ blackish remnants disappear completely and the cell matures = ERYTHROCYTE

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4
Q

What is the reticulocyte concentration of a NORMAL blood smear?

A

Reticulocyte Count is LOW

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5
Q

What is the reticulocyte concentration of an ANEMIC blood smear?

A

RETICULOCYTE Count HIGH

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6
Q

What is the most important determinant of RBC production?

A

TISSUE OXYGENATION

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7
Q

Wat are some other factors that will stimulate an INCREASE in RBC production?

A
  1. High Altitude
  2. LOW PaO2
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8
Q

Define Hematocrit (HCT).

A

HCT is the Fractional Volume of RBC Mass

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9
Q

Define Hemoglobin (Hgb).

A

Hemoglobin is the Main “Blood Protein”

  • Carries oxygen
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10
Q

How to calculate HCT using Hgb?

A

Hgb X 3 = HCT

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11
Q

How does volume status effect HCT?

A

Hypovolemia = vasculature would be more HEMOCONCETRATED.

This individual may not have adequate O2 carrying capacity, even though the HCT is normal

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12
Q

What is the NORMAL RBC count for a Male?

A

Male

  1. 7 - 6.1 million cells per microliter (cells /mcL)
    (5. 2 Million cells /mcL)
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13
Q

What is the NORMAL RBC count for Females?

A

Female

  1. 2 to 5.4 million cells/ mcL
    (4. 7 Million)
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14
Q

What are the three blood indices and what information does it provide?

A

Indices: – describe size and the hgb concentration

  1. MCV (Mean Corpuscular Volume: Measures the average Size + Volume of RBC)
  2. MCH (Mean Corpuscular Hemoglobin)
  3. MCHC (Mean Corpuscular Hemoglobin Concentration)
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15
Q

What is NORMAL MCV (Mean Corpuscular Volume)?

A

★Normal: 80 - 100

Normocytic Anemia

If MCV Elevated then = MACROCYTIC Anemia

If MCV Decreased, then = MICROCYTIC Anemia (Small RBC)

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16
Q

What is NORMAL Mean Corpuscular Hemoglobin?

A

★Normal: 25 - 30 (Normochromic) Anemia

MCH < 25: Hypochromic Anemia

MCH > 30: Hyperchromic Anemia

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17
Q

What is NORMAL MCHC (Mean Corpuscular Hemoglobin Concentration)

A

★Normal: 30 - 35

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18
Q

What is Erythropoietin?

What stimulates Erythropoietin release?

Where is Erythropoietin formed?

A

Erythropoietin

Glycoprotein Hormone

Stimulates RBC production in hypoxia

Formed in the kidneys - 90%

Without Erythropoietin, RBC production WOULD NOT INCREASE

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19
Q

What are some other factors that stimulate Erythropoietin production?

A

Epinephrine

Norepinephrine

Prostaglandins

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20
Q

What are some Nutritional Requirements for RBC Production?

A

B-12

Folic acid

A DECREASE in either of these requirements results in a MACROCYTIC anemia – cells are LARGER than normal

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21
Q

What is the MAJOR FUNCTION of the RBCs?

A

To TRANSPORT HEMOGLOBIN

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22
Q

Define Anemia?

A

Anemia: DECREASED Oxygen Carrying Capacity

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23
Q

What is the Carbonic Acid Equation?

A

CO2 + H2O —> H2CO3 —> H+ + HCO3

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24
Q

How does RBC contribute to the carbonic acid reaction?

A

RBC carries a large amount of Carbonic Anhydrase

An enzyme that catalyzes the reaction between CO2 + H2O to form Carbonic Acid

This reaction allows the blood to carry LARGE amounts of CO2, In the form of Bicarbonate Ions (HCO3-)

From the dissociation of carbonic acid to Bicarbonate Ions HCO3-

From the tissues to the lungs where it is converted back into CO2 and exhaled as waste

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25
Q

What is the lifespan of RBCs?

A

Lifespan of 120 days

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26
Q

What is the shape of a normal RBC?

A

Biconcave disk with a diameter of 7.8 microns

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27
Q

How much Oxygen can 1 g of Hgb carry?

A

1.39/ 1.34 ml/ O2

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28
Q

What are some causes of Anemia (decreased O2 capacity)?

A
  1. DECREASE in # RBC (quantitative decrease in normal Hgb)

Decrease in RBC production (bone marrow problems due to chemo or radiation)

Lysis of cells (premature destruction)

  1. Abnormalities in HGB (qualitative problem → Sickle Cell)

The RBC of the sickle cell disease are miss shaped.

They can clog small capillaries and cause ischemia

  1. Lysis of RBC – d/t a structural disorder - often inherited
  2. Disorders affecting RBC metabolism

Including the pathway of glycolysis:

G6PD Deficiency (glucose 6 phosphate dehydrogenase deficiency) = found mostly in African, Asian, middle eastern and Mediterranean descent

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29
Q

Define Sickle Cell disease?

A

Hemolytic Anemia, Inherited: autosomal recessive disease

-There is a substitution of a Valine for Glutamic Acid in beta-globin subunit (Hgb S instead of Hgb A)

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30
Q

What are some “triggers” that causes the formation of Hgb S?

A

Hemoglobin “S” Triggers:

Acidosis (acidotic environment)

Hypoxemia (Pa02 < 40 mmHg )

HypOthermic

HypOvolemic (dehydration)

As result of the trigger, those RBCs will have conformational change and sickle – elongating of red cell to sickle shape

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31
Q

What is the problem with the body forming Hgb “S”?

A

Problem: The sickled RBCs will clog up blood vessels.

This will cause an infarction in various organs that aren’t getting circulation/oxygenation that is needed

There can also be sequestration of RBC in the liver and spleen

Also, pain

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32
Q

What is the difference between the HOMOZYGOUS and HETEROZYGOUS forms of Sickle Cell Disease?

A

Homozygous form causes the disease

Heterozygous form is only the trait

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33
Q

What are some characteristics of the HOMOZYGOUS form of Sickle Cell Disease?

A

Presents early in life

Severe hemolytic anemia

Vaso-occlusive disease involving bone marrow, liver, spleen, kidney, CNS

Episodic crisis with bone and joint pain and can be associated with other illnesses

May be associated with concomitant illness

Severity and progression varied

Organ damage beginning in early childhood

Spleen may be infarcted

Renal medulla may be affected = so will lose our hyperosmotic medullary interstitium. Will lose ability to concentrate urine and CKD results

34
Q

What is the leading cause of morbidity & mortality in Sickle Cell Disease?

A

PULMONARY & NEURO Complications are leading cause of M&M in sickle cell disease

Acute chest syndrome = due to pulmonary infarct with infection

Neuro = CVA (infart or hemorrhagic)

35
Q

How does Sickle cell disease affect the Oxyhemoglobin Associative Curve?

A

Sickle cell anemia will shift the oxyhgb curve to the RIGHT

Associated with a P50 of 31 mmHg (normal is 27 mmHg)

36
Q

What are some characteristics of the HETEROZYGOUS form of Sickle Cell Disease?

A

Heterozygous form is responsible for sickle cell TRAIT

Usually are carriers, but rarely have clinical manifestations themselves

37
Q

What are some of the results of Sickle cell disease where RBCs are destroyed and decrease in functionality?

A

Patients can have:

  1. Low HCT
  2. Elevated bilirubin
  3. Jaundice
  4. Cholelithiasis
38
Q

What are some treatment options os Sickle Cell Disease?

A

Treatment

AIMED at avoiding crisis, relieving symptoms and prevent complications

  1. Exchange transfusion
  2. Hydroxyurea

A medication that when taken daily reduces episodes of painful crisis and Acute Chest Syndrome (ACS) and reduces hospitalizations and transfusions

Stimulates fetal hgb production (found in newborns that prevent formation of sickle cells)

Increases risk of infection and long term use may cause problems alter on – more research needed

  1. Bone marrow transplant

Only potential cure

Usually preserved for people <16 years; as the risk increase with age

39
Q

What is the difference between the HOMOZYGOUS form and the HETEROZYGOUS form in regards to morbility and mortality peri-operatively?

A

Heterozygous vs Homozygous

Trait – no increase in periop M&M (hetero)

Disease – increases periop M&M! (homo)

40
Q

What are some risk factors that will INCREASE mobidity and mortality of sickle cell patients peri-operatively?

A

Risk factors

Age

Frequency of hosp/transfusions

Organ damage

Infection

Type of surgery

41
Q

What types of surgery will have an INCREASED mobidity and mortality risk for sickle cell patients?

A

Low risk:

Inguinal hernia

Extremity surgery (with exception of hip surgery)

Moderate risk: intraabdominal (including cholecystectomy)

High risk:

Intercranial

Intrathoracic

Hip surgery

Among orthopedic procedures, hip surgery (including hip replacement) has considerable risk of complications, including excessive blood loss in more than 70% of patients!

19% of patients have sickle cell crisis perioperative with hip surgery

42
Q

What are the goals of Hgb and HCT that you would like to see peroperatively in sickle cell patients?

A

HCT of 30%,

Hgb 10

– would like at least 50% of that hemoglobin to be Hgb A (but you can’t test this practically) Hgb S should be less than 40%

43
Q

Ig Hgb and HCT are BELOW the advised levels for a sickle cell patient peroperatively, do we administer a blood transfusion?

A

NO. Aggressive periop transfusion used to be what they did, but that had changed and showed no benefit. Risk of transfusion outweigh benefits often

44
Q

What are some factors to AVOID to DECREASE the right of sickling of RBCs?

A

Avoid to DECREASE the risk of RBC Sickling

  1. Dehydration / HypOvolemia

Maintenance x 1.5 for 12 hours pre op

  1. Hypotension & low flow situations
  2. Hypoxemia
  3. Acidosis
  4. Hypothermia
  5. Tourniquets are NOT contraindicated per readings, but some people say they should be avoided

Aggressively manage hypoxemia, acidosis, hypothermia, and PAIN (can exacerbate the disease)

45
Q

What is Acute Chest Syndrome in Sickle Cell Disease?

A

Acute chest syndrome is a term used to cover conditions characterized by chest pain, cough, fever, hypoxia (low oxygen level) and lung infiltrates.

A. Develops 2-3 days post op

B. Treat aggressively – focus on oxygenation, analgesia

C. Transfusions may be beneficial to improve oxygenation, correct O2 carrying capacity. CORRECT ANEMIA

D. Careful extubations

Make sure patient oxygenating well and have supplemental oxygen post op for 12- 48 hours

E. Hydration: take maintenance requirements and multiply by 1.5 and give for 12 hours pre-op

F. Nitric Oxide could help to decrease pulm HTN and improve oxygenation but not always available

46
Q

As anesthesia providers, how do we avoid acidosis, hypoxemia, or hypothermia?

A

Fluid Warmer, Bair Hugger

Avoid HYPERCARBIA or HYPOXEMIA

Avoid sedation all together or at least consider if they need it or not

47
Q

What is Ineffective Erythropoiesis?

What are two major causes?

A

Ineffective Erythropoiesis is immature death of RBCs due to a

Etiologies:

  1. Nutritional Deficiencies of Folate Acid or B12 Vitamin
  2. Thalassemia
48
Q

What is the pathology of a Folate and B12 deficiency?

A

FOLATE & B12 are REQUIRED in normal DNA Synthesis

In deficiency, the bone marrow is one of first areas affected

Cells that are precursors to adult RBCs in the bone marrow become LARGE and can’t complete the process of cell divisions

49
Q

What type of anemia develops from a Folate and B12 deficiency?

A

MACROCYTIC/ MEGALOBLASTIC Anemia –

LARGE RBCs

The bone marrow is referred to as “MEGALOBLASTIC” because there are so many large cells within it.

These large RBCs are then released into circulation

50
Q

Anesthetic Implications:

Macrocytic/ Megaloblastic Anemia

A
  1. The decsion of anesthetic is influenced by presence of Neurologic changes

Some patients, especially with vitamin B12 deficiency, develop Neuro changes, so a regional anesthetic (spinal or epidural) would NOT be good choice

  1. N2O should be avoided!

INHIBITS the enzyme METHYLENE SYNTHETASE by IRREVERSIBLY oxidizing the cobalt atom on vitamin B12 from an active to inactive state

This triggers NERVE DEGENERATION, even short exposures can produce changes

This is somewhat analogous to the conversion of Hgb to Met Hgb and it triggers NERVE DEGENERATION

51
Q

What type of anemia develops from an Iron deficiency?

A

MICROCYTIC Anemia

  • SMALL RBCs
  • Just treated with iron replacement
  • Sometimes in those patients erythropoietin helpful before surgery
52
Q

What are some etiologies for MICROCYTIC Anemia?

A

Causes:

  1. Inherited Defects: Thalassemia
  2. Decreased Oxygen Affinity: Methemoglobinemia
53
Q

What is Thalassemia?

What are the two types?

A

Thalassemia: Defective globin chain production

One of the leading causes of microcytic anemia in kids and adults

Two types: Alpha and Beta

Have different geographic distribution

Beta Thalassemia – Africa and Mediterranean

Alpha Thalassemia – Southeast Asia

54
Q

What are the three classifications of Thalassemia?

A

Thalassemia Minor

Usually results in only a relatively minor anemia

HGB 10 - 14, chronic compensated anemia

Thalassemia Intermediate

Thalassemia Major

Severe life threatening anemia in first few months of life

Need long term transfusion therapy: To survive childhood,

55
Q

What are the anesthetic implications for Mild (Thalassemia Minor) and Severe (Thalassemia Major)?

A

Mild (Thalassemia Minor): chronic compensated anemia

If the patient chronically has anemia they would have adjusted to it and it isn’t as significant. Hgb 10 - 14 usually

Severe (Thalassemia Major): They can develop

Splenomegaly, Hepatomegaly, CHF, Mental retardation

Complications of iron overload from multiple transfusions:

Cirrhosis

Right sided heart failure

Endocrinopathies

56
Q

What is Methemoglobin?

A

Methemoglobin is a form of hemoglobin that has been oxidized, changing its heme iron configuration from the ferrous (Fe2+) to the ferric (Fe3+) state.

Unlike normal hemoglobin, methemoglobin does not bind oxygen and as a result cannot deliver oxygen to the tissues.

Methemoglobinemia can be congenital or acquired

57
Q

Is methemoglobin normal?

A

Normal RBC have 1% of Hgb that is methemoglobin

58
Q

What is the problem with HIGH levels of methemoglobin?

A

HIGHER LEVELS of methemoglobin is that it shifts the Oxyhemoglobin dissociation curve to the LEFT

So that LITTLE OXYGEN is released/ delivered to the tissues

59
Q

What are the classification of methemoglobin levels?

A

MetHgb level < 30% of total HBG =

Then there is really NO signs of oxygen deprivation

MetHgb level 30 – 50% of total HBG =

Patients start to show signs of oxygen deprivation

If MetHgb level > 50% of total HBG =

Then coma and death result

60
Q

What is the EMERGENCY TREATMENT of HIGH levels of methemoglobinemia?

A

Emergency treatment =

Give Methylene Blue 1% 1 - 2 mg/ kg over 3 - 5 min

61
Q

Anesthesia implications for methemoglobinemia?

A

Avoiding certain substances that will oxidize iron and result in the conversion of Ferrous → Ferric (Fe+2 → Fe+3), particularly in patients with a genetic mutation that favors methemoglobin formation

Hurricane Spray

Antibiotics (trimethoprim, sulfonamides and dapsone)

local anesthetics (especially artic​aine, benzocaine, and prilocaine)

aniline dyes

metoclopramide

chlorates

bromates

Ingestion of compounds containing nitrates (such as the patina chemical bismuth nitrate)

In otherwise healthy individuals, the protective enzyme systems normally present in red blood cells, rapidly reduce the methemoglobin back to hemoglobin and hence maintain methemoglobin levels at less than 1% of the total hemoglobin .

Exposure to exogenous oxidizing drugs and their metabolites (such as benzocaine, dapsone and nitrates) may accelerate the rate of formation of methemoglobin up to one-thousand fold, overwhelming the protective enzyme systems and acutely increasing methemoglobin levels.

62
Q

Why are infants more susceptible to methemoglobinemia?

A

Infants under < 6 months of age have LOWER levels of a key methemoglobin reduction enzyme (the NADH-cytochrome b5 reductase) in their red blood cells.

This results in a major risk of methemoglobinemia caused by nitrates ingested in drinking water.

Dehydration usually caused by gastroenteritis with diarrhea, sepsis, and topical anesthetics containing benzocaine or prilocaine. Nitrates used in agricultural fertilizers may leak into the ground and may contaminate well water.

63
Q

What are the four major causes of HypOproliferation of RBCs (Aplastic Anemia)

A
  1. Fanconi’s Anemia – constitutional Aplastic Anemia
    - Autosomal Recessive disorder
    - Characterized by SEVERE PANCYTOPENIA = all cells in bone marrow are diminished
    - Usually shows up in 1st 2 decades of life (Birth - 20 y/o), and proceeds to acute leukemia
  2. Drugs & Radiation (chemotherapeutic drugs and other drugs)

As long as drug doesn’t irreversibly damage bone marrow, then full recovery is possible

Some drugs associated with severe and irreversible aplastic anemia:

  1. INFECTION → Aplastic anemia
    - Viral Hepatitis, Epstein Barr (EBP), HIV, TB
    - Usually reversible, but could produce fatal aplastic anemia
  2. Cancer mets to bone marrow can cause aplastic anemia as well (crowds out normal cells)
64
Q

What are some anesthetic implications for Aplastic Anemia (Hypoproliferation, Infection, Cancer)?

A
  1. Reverse Precautions! Usually all cell types are affected – susceptible to infections – WBC concern there
  2. Stress Steroids often beneficial
  3. Appropriate antibiotics
  4. Make sure we have a Type & Cross Match and adequate blood readily available
65
Q

What is polycythemia?

A

Too many RBC manufactured

Elevated HCT (Erythrocytosis)

  • Often due to compensatory response to sustained hypoxia

- Tissue oxygenation is optimal at HGB 11 - 12 g/dL

A HGB > 12 g/dL = INCREASE in VISCOSITY = DECREASE blood flow = DECREASE O2 delivery

66
Q

What is the effect of an INCREASED HCT (Polycythemia)?

A

HCT 50%: The effect is relatively minor

> 50%, then flow to key organs like the brain can be compromised

HCT < 55 - 60: patients may not have many symptoms

HCT > 55 - 60%: patients have headaches* and *easy fatigability

HCT > 60%: Viscosity can be life threatening due to the loss of perfusion to vital organs

67
Q

What are the two types of Polycythemia?

A

Primary Polycythemia = “Polycythemia Vera”

  • Stem cell disorder
  • Patients are at risk for both thrombosis* and *bleeding
  • Bleeding: they get an acquired von Willebrand disease
  • Thrombosis: obvious due to viscosity of blood

Secondary polycythemia

Chronic hypoxia

  • High altitudes
  • ↑ erythropoietin

↑ erythropoietin production: due to renal disease or erythropoietin secreting tumor

68
Q

What are the anesthetic implications for polycythemia?

A

Anesthesia implications

Give O2!

Pre-op phlebotomy

Know they are at risk for bleeding and thrombosis

69
Q

What is the normal WBCs?

A

Normal: 5,000-10,000 cells/L

70
Q

What are the different WBCs? What is the average percentage of them founf in blood?

A
  1. Poly = PM = Neutrophils - 40 - 60%

Most prevalent of WBC

Bands - Immature neutriphils

  1. lymphocytes 20 - 40%
  2. Monocytes 2-8%
  3. Eosinophils 1 - 4%
  4. Basosphils 0.5 - 1%

smallest amount!

71
Q

Define Leukemia.

What are the two types?

A

Leukemia: Uncontrolled WBC production

Abnormal proliferation of WBC from cancerous mutation.

Myelogenous (begin in Bone Marrow - polys, monos)

OR

Lymphogenous (lympocytic cells that begin in lymph nodes)

72
Q

What is the two types of Myelogenous leukemia?

What aretheir mortality rates?

A

Myelogenous - begin in Bone Marrow - Neutrophils, Monocytes

1. Acute myeloid leukemia (AML)

Complete, sustained remission in 70-80% of pts younger than 60 years

50% remission of patients older than 60years

2. Chronic myeloid leukemia (CML)

73
Q

What are the two types of Lymphogenous leukemia?

What is the mortality rate?

A

Lymphogenous - began in Lymph Nodes

1. Acute lymphoblastic leukemia (ALL)

15% of adult leukemias

Chemo cures 70% of children

Chemio cures 25 - 45% of adults

2. Chronic lymphocytic leukemia (CLL)

25% of all leukemias

Rare in children

74
Q

The difference between nornal hematopoietic stem cells and those with leukemia?

A

Leukemia/ Cancerous cells divide rapidly

The expanding cell mass will squeeze out the normal cells in bone marrow and in other tissues.

As normal cells essentially are eliminated by cancerous cells rapidly proliferating, patients are effectively APLASTIC b/c don’t have good cells and have significant anemia!

Leukemia Cells can infect liver, spleen , meninges, lymphatics

b/c cells so rapidly dividing, using up all nutrients, so patient is fatigued from metabolic starvation

75
Q

What is the major cause of infections for those with leukemia?

A

BONE MARROW FAILURE is the cause of fatal infections

Because normal WBCs that fight infections not present

&

HEMORRHAGE b/c platelets are originally formed in bone marrow

76
Q

When are leukemia cells considered a “Lethal Mass”?

When does a patient begin to develop symptoms?

A

A kg (1012 power) of leukemic cells is a LETHAL MASS and a person does not develop symptoms until 109 power

77
Q

What is the MAJOR treatment of Leukemia?

What are the three drugs used?

A

CHEMOTHERAPY

Drugs used are primarily those that depress bone marrow

- Bleeding & Infection are likely complications

Also, destruction of the tumor can produce a uric acid load that can cause a Gouty Arthritis, and damage to the kidneys (nephropathy) “urate nephropathy”

Immunosuppression is a huge problem

Two drugs used are:

  1. Doxorubicin (Adriamycin)
  2. Bleomycin
  3. Vinca alkaloids
78
Q

What are some anesthesia implications of Doxorubicin (Adriamycin)?

A

Doxorubicin (Adriamycin)

2% of patients develop a chronic, cumulative dose related TOXICITY that manifests as Severe Cardiomyopathy

This can result in irreversible CHF that doesn’t respond to treatment – does not respond to inotropes

Can occur with a total dose as low as 250 mg/ m2 (body surface area)

At a HIGHER dose of 550 mg/ m2, the risk of that will increase to 20%

  • So important if we can get the records to find out what was the total dose of doxorubicin

** Also want ECHO pre-op on these patients

  • Symptoms of toxicity can appear up to 5 years later (not seen immediately)
79
Q

What are some anesthesia implications for Bleomycin?

A

BLEOMYCIN

Pulmonary toxicity/fibrosis 5-10% of patients

Greatest risk in elderly

& With patients with > 400 units total dose

Anesthesia Implications

1. Pulmonary Fibrosis gets worse with HIGH FiO2

  • You want to have FIO2 < 30% if possible!
  • You need to use “air” as a carrier gas
    2. Prefer to use colloid instead of crystalloid

crystalloid administration, can affect pulmonary status (colloids better!)

80
Q

What are some anesthesia implications for Vinca alkaloids?

A

VINCA ALKALOIDS

EX. Vincristine, Vinblastine

Can cause NERVE DAMAGE

Peripheral neuropathy, will manifest paresthesias in hands and feet

Can also cause Autonomic Neuropathy, SIADH

81
Q

Other than Chemotherapy, what is another treatment for leukemia?

A

BONE MARROW TRANSPLANT

  1. Autologous –the patients own cells used
  2. Allogenic – donor cells are used
    - In either case, the patient undergo HIGH DOSE radiation/chemo to completely abolish their own bone marrow
    - Bone marrow Is harvested from repeated aspiration from posterior iliac crest
    - At an appropriate time, they are infused via central line form central circulation to the bone marrow of the receipant
    - The time to engraftment is 10-28 days
    - The patient is usually in isolation during this time
82
Q

What are some anesthesia implications for a bone marrown transplant?

A

1. Usually General Anesthesia!

  • (transplant doesn’t require anesthesia, just CVL!)
    2. Avoid N20 b/c maybe causes Bone Marrow suppression
    3. Pre op – check their volume status
  • Past chemos and any coagulopathies
  • Hx of nausea/vomiting

Hematologic Pathology (1 decks)

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