Hematology & Immunology Part 2 Flashcards by Carol Dumond

Withdrawal of patient’s own blood in OR just prior to surgery (blood replaced w/ crystalloid).
-During the case, the patient is losing blood with a Hct of 24/25 instead of a Hct of 30. -If you KNOW patient is going to bleed, let them bleed out low Hgb blood, and then replace with their own blood
-Some patients can’t tolerate low Hgb - watch for coronary ischemia, cerebral changes (mentation)
-Large, orthopedic surgery and are healthy.

Acute Normovolemic Hemodilution

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Patient donates 2 units of blood, give erythro and iron so Hgb normal. Must be planned well in advance of surgery; consider pt underlying condition
-Pt must be able to tolerate lower Hgb (not kidney patients, AS, CAD, or anemic)
-Orthopedic surgeries
-Questionable value, very expensive, doesn’t prevent patients from getting transfusions of other blood

Autologous Donation

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Helpful to reduce bleeding and risk of transfusion for patients at risk of excessive bleeding

TXA and Amicar

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Has an immediate effect
-Misidentification of patient/blood specimen
-Donor ABO incompatibility
-Complement activation -> acute intravascular hemolysis (release of bradykinin, histamine, & serotonin) -> CV collapse

Acute Hemolytic Transfusion Rxn

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Fever, chills, flushing, chest/flank/back pain, hypotension, nausea, oliguria, anuria, hemoglobinuria, diffuse bleeding
-Difficult to detect in anesthetized patient - inc temp, unexplained tachycardia, dec BP, hemoglobinuria, bronchospasm, diffuse ooziness in field

S/Sx of Acute Hemolytic Transfusion Rxn

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Treatment: stop transfusion, maintain UOP 75-100 ml/hr, assay urine/plasma hgb conc, return blood to bank, prevent hypotension, recheck labeling

Acute Hemolytic Transfusion Rxn

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Mild reaction, Re-exposure issue (caused by antibodies to non-D antigens- either Kells, Kidd, or Rhesus)
-Clinical: low grade fever, mild jaundice, unexpected drop in Hgb
-Treatment: Supportive (monitor hgb, hydration, transfusion)

Delayed Hemolytic Rxn

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Post-multiple transfusions (develop alloantibodies to HLAs on donated blood leukocytes) → subsequent transfusions antibody attacks donor leukocytes
-Symptoms: fever, shaking chills, resp distress, anxiety, HA, myalgia
-Treatment: acetaminophen (leukoreduction may prevent these)

Febrile Non-hemolytic Transfusion Rxn

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Donor lymphocytes become engrafted, proliferate, & establish an immune response against the recipient → only w/ cell transfusions (RBC & plt)
Immunocompromised patients especially at risk

Transfusion Associated Graft vs Host

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S/Sx:
-progresses rapidly to pancytopenia (high fatality rate!)
-sloughing mucous membranes (Attacks fast dividing tissues -orally and in GI tract), profuse diarrhea, rash, hepatomegaly

Consider irradiated blood products in high risk (BMT recipients, Hodgkin’s dz, SCID, intrauterine transfusions, leukemia, transplant)

Transfusion Associated Graft vs Host

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Administration of allogeneic blood leads to immune suppression by modifications in T helper cell/suppressor ratio, changes in B cell fxn, down regulation of antigen presenting cells, decreased # circulating lymphocytes

May impact: accelerated recurrence of malignancy, increased mortality, increased rates of infection

Transfusion Related Immunomodulation (TRIM)

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When blood is stored, biologic substances accumulate (cytokines, complement, membrane lipid breakdown products) → produce inflammatory response → contribute to multi-organ dysfunction
Ex: in CV surgery patients w/multiple blood products, have inc ICU LOS

Transfusion Related Inflammatory Response

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Noncardiogenic pulmonary edema occurring after blood product administration
-Associated with anti-HLA antibodies -> leukocytes sequester in lungs -> mediators -> capillary endothelial damage -> inc capillary permeability

-Humoral response to stress primes granulocytes, causing lung sequestration

Transfusion Related Acute Lung Injury (TRALI)

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S/Sx: begins within 6 hours of transfusion! Dyspnea, chills, fever, pulmonary edema, pulmonary compromise, hypotension/hypertension

Treatment: largely supportive (stop transfusion, O2/ventilation-low tidal volumes, rule out TACO-transfusion associated circulatory overload)

Prevention: universal leukoreduction, restriction of multiparous donors for plasma products (pregnant), HLA antibody testing

Transfusion Related Acute Lung Injury (TRALI)

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Estimate Blood Volume Calculation

Estimated Blood Volume = typical blood volume x patient weight

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Allowable Blood Loss Calculation

EBV x (hct initial - hct final) / hct initial

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Present if <30% of normal
-Rare bleeding disorder that can be inherited or acquired
-Mild: no evidence of regular/spontaneous bleeding
-Severe: relentless spontaneous bleeding (nasal, oral, GI, GU)
-Inherited subtypes: Type 1 (most common - mild to severe), Type 2, and Type 3 (near complete deficiency)
-Acquired: malignancy, autoimmune, hypothyroidism

Von Willebrand Disease (vWF)

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Failure to synthesize/secrete or accelerated clearance of vWF
-Unable to bind to receptors on plt surface to form the plt plug

Tx:
-Desmopressin (administer slowly to avoid hypotension, flushing, tachycardia, and HA). Can have tachyphylaxis - loss of efficacy with large, repeated doses
-TXA (antifibrinolytic)
-Factor VIII/vWF concentration
-Cryo
-Avoid anti-plt drugs

Von Willebrand’s Disease

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X-linked hematologic recessive disorder characterized by unpredictable bleeding patterns: affects mostly males, females carry the gene
-A: deficient factor 8 (Mild - severe)
-B: deficient factor 9 (Christmas Disease)

Hemophilia

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-Mild: factor levels 5-30%, bleed only after surgery/trauma
-Moderate: factor levels 1-5%, occasional spontaneous bleeding
-Severe (most common): factor levels <1%, frequent spont bleeding

Hemophilia A

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Exhibit spontaneous bleeding, muscle hematomas, join pain leading to progressive arthropathy → often requires orthopedic surgical intervention

Preop:
-Inhibitor screening/inhibitor assay done within 1 week of surgery
-Hematology consult
-Detailed coags
-Detailed factor replacement plan prior to DOS
-Plan for monitoring levels periop
-Elective procedures occur early in the day and week for availability of lab support and factor concentrates

Hemophilia

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No procedure is too minor for adequate hemostasis (ABG, dental procedures, etc)
Treatment:
-Viral inactivated plasma-derived or recombinant concentrates preferred over Cryo/FFP
-Hemophilia A: cryo preferred over FFP
-Hemophilia B: FFP
-Desmopressin: helpful w/ mild-mod Hemophilia A; no help w hemophilia B (overall varied response, difficult to predict)
-TXA & Amicar (antifibrinolytics)
-Factor 7a → directly activates 10 w/o participation of 8, 9, 11

Treatment of Hemophilia

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Hemostatic agent of last resort (for cardiac surgery, prostate surgery, intracerebral hemorrhage)
-Acidosis decreases efficacy
-Non Emergency 20-40 mcg/kg vs Emergent 41-90 mcg/kg
-Thrombotic complications have been reported (expensive!)

Factor 7a

Intravascular coagulation activation with microvascular thrombi formation.
-Consumptive: thrombocytopenia, clotting factor depletion, thrombosis, hemorrhage w/end organ damage
-Tissue Factor plays a central role
-Acute: complication of sepsis, postoperative state, OB, blood transfusion rxn, malignancy
-Chronic: tumors & large aortic aneurysm

Disseminated Intravascular Coagulation (DIC)

ID & eliminate underlying cause; no/minimal support if mild, asymptomatic, and self-limited; hemodynamic support as indicated; drug therapy is controversial; Blood Component Therapy (if active bleeding or high risk for bleeding): FFP, PLT, Cryo, Antithrombin 3 -OB: Delivery -Sepsis: ABX

Treatment for DIC

Hypercoagulability: inherited or acquired (CV disease) -Factor 5 Leiden: increased activity of factor 5 d/t activated protein C resistance -Most common inherited thrombophilia, Venous clotting > arterial clot -Routine screening not recommended; Mgmt w/ antithrombotic therapy

Thrombophilias

A reduction in RBC indices (Hgb, HCT, RBCs) that leads to a reduction in arterial O2 concentration and potentially decreased delivery to the tissues. Initially compensated by SNS activation and decreased blood viscosity -Right shift of Oxyhgb curve (release)

Anemia

Based on lost circulating blood volume, Hgb level, ongoing bleeding, and risk of end-organ damage

Perioperative Transfusion

Causes: -underproduction (bone marrow failure) -increased loss (bleeding) -hemodilution (physiologic anemia of pregnancy) -chronic disease (inflammation, tissue injury, infection, malignancy, renal failure) -destruction of cells (autoimmune, nonimmune, hemolysis) -deficiencies of RBC synthesis (folate, iron, B12, heme synthesis deficiency-thalassemia) Most common chronic anemia: iron deficiency, anemia of chronic disease, thalassemia, and ongoing blood loss.

Anemia

An autosomal recessive disorder for abnormal hgb (Hbg S). Hereditary hemoglobinopathy. -Trait: heterozygous, Hgb S range 30-50%, sickling occurs during PaO2 20-30 mmHg -Disease: homozygous, Hgb S >50%, sickling occurs during PaO2 30-40 mmHg

Sickle Cell Anemia

Triggered by hypoxemia, hypothermia, infection, dehydration, venous stasis, or acidosis. S/Sx: chronic hemolytic anemia, intermittent vaso-occlusion, severe pain, end organ damage

Sickle Cell Crisis

Tx: adequate hydration, monitor UOP and CVP (don't want them dry, avoid hypoxia, maintain normothermia, maintain normal acid-bas balance, adequate pain mgmt, caution with vaso-occlusive devices (tourniquets). -Avoid Hgb >10 -Consider transfusion to decrease Hgb S level to <30-50% if high risk -Surgical intervention for gallstones due to excessive bilirubin from rapid breakdown of sickled erythrocytes -Pressure stockings, SCDs, etc

Sickle Cell Anemia

Group of X-linked disorders resulting in RBC hemolysis w/ oxidative stress -Acute hemolytic episodes, severe newborn jaundice, common in African, Middle Eastern, Mediterranean, Asian population, mostly asymptomatic -Exposure to oxidative stress: infection, hypothermia, fava beans, meds (antimalarials, sulfonamides, nitrofurantoin, ciprofloxacin, methylene blue, antipyretic analgesics) → key is to avoid the stress!

Glucose-6-Phosphate Dehydrogenase (G6PD) Deficiency

An abnormally high Hct. -Can be relative d/t a reduction in plasma volume without inc in red cell mass (fasting) -NPO causes a dec in plasma volume, which can turn an asymptomatic person into one of hyperviscosity -Hct > 55-60% inc whole blood viscosity, which threatens perfusion by affecting flow to small blood vessels such as capillaries -Cerebral circulation is vulnerable to a reduction in flow -Inc risk of thrombosis

Polycythemia

Platelet count < 150,000. Causes: decreased production (bone marrow, folate deficiency, malignancy), sequestration (liver & spleen), increased destruction (immune & non immune mediated) → sepsis, DIC, TTP -Risk of bleeding = inversely r/t plt count → need higher count for regional -Transfuse only if clinically indicated. Ok to proceed if plt > 50,000.

Thrombocytopenia

Immune response to heparin w/ associated consequences → severe thrombosis, amputation, death. -Occurs with any heparin dose/route -Diagnosis is based on a >50% dec in plt count from baseline or <100,000 w/normal baseline -Positive assays -Thrombocytopenia, cutaneous abnormalities, and tachyphylaxis after Heparin

Heparin Induced Thrombocytopenia (HIT)

Stop heparin immediately -Consult hematology -Administer direct thrombin inhibitors (argatroban) -Artery or venous thrombosis compromising distal perfusion requires embolectomy or vascular bypass

HIT

Onset 1-4 days; mild thrombocytopenia resolves spontaneously, not associated w/ serious sequelae.

Type 1 HIT (non-immune mediated)

Onset 5-14 days; severe thrombocytopenia associated w thrombosis & serious sequelae -PF4 -IgG

Type 2 HIT (Immune mediated)

The leading cause of M&M after orthopedic surgeries (THA, TKA, pelvic Fx at highest risk) -Due to venous stasis, hyper coagulability, and vascular trauma -S/Sx: PE (dyspnea, cp, tachycardia, shock) and DVT (painful swelling of extremity, fever) Tx: -Anticoagulation w/heparin, LMWH, or oral -Prevent with early mobility/ambulation, compression stockings, SCDs

Thromboembolic Events

-Protects the body from a wide variety of pathogenic microbes: viruses, bacteria, prions, fungi, protozoa, abnormal self cells → ability to distinguish self from non-self!! -Innate (Natural) & Adaptive (Acquired) -Humoral response mediated by B lymphocyte antibodies circulating in blood & lymph -Cell-mediated response produced by phagocytes, T lymphocytes, & cytokines

Immune System

Intolerance to an immune system response to a foreign/environmental allergen exposure & onset of symptoms → type 1-5

Hypersensitivity

Immediate hypersensitivity occurs within 15-30 minutes -IgE mediated -S/sx: mild cutaneous, GI, bronchospasm, cardiopulmonary collapse -Can happen with NMBs (Succ > Vec > Roc > Pancuronium > cis-atracurium) Tx: Antihistamines and bronchodilators

Type 1 Hypersensitivity

Mediators: -IgE, Mast Cells, Basophils Drug allergy, hay fever, asthma

Type 1

Mediators: IgG, IgM, and Compliment Myasthenia gravis, blood transfusion

Type 2

Mediators: IgG, IgM, Neutrophils, and Compliment SLE, RA

Type 3 (Immune Complexes)

Mediators: T Cells, monocytes, macrophages, cytokines Poison ivy, transplant rejections

Type 4

Mediators: Humoral Antibodies Graves Disease

Type 5

Usually due to a Type 1 Rxn to a NMB. Tx: -Discontinue triggering agent -Trendelenburg -FiO2 100% ventilation -Epi (SC, IM, IV) -Fluids (NS/LR 10-30 mcg/kg bolus) Secondary Tx: -If epi unresponsive: vaso or norepi -Bronchospasm: beta 2 agonists (albuterol) -Preop beta blockade (glucagon) -Antihistamines: benadryl and ranitidine -Airway edema: corticosteroids After: -Serum tryptase <120 min -24 hr monitoring -Allergist consult

Intraoperative Anaphylaxis

-Excision of tumors may stimulate proliferation & metastasis of tumor cells -Disrupts blood vessels supplying tumor but allows tumor cells to enter systemic circulation -Angiogenesis increased post op: promotes tissue repair at surgical site but contributes to tumor growth/metastasis -Catecholamines promote angiogenesis (formation of new blood vessels)

Cancer Recurrence with Surgery

Causes depression of the immune system, increased incidence of SSI, earlier recurrence of cancer. -Irradiated or leukocyte-depleted blood products recommended; use of intraoperative cell savers may contribute to cancer recurrence (bc surgical blood contains tumor cells)

Perioperative Blood Transfusions and the Immunocompromised Patient

Increased susceptibility to infection secondary to depression of both innate & adaptive immune systems -Increased incidence of SSI & poor patient outcomes; BG 140-180 can attenuate effects on immune system

Hyperglycemia in Immunocompromised patients

Associated with increased blood loss, impaired wound healing, decreased immune function, increased need for blood transfusion

Hypothermia in Immunocompromised patients

Uncontrolled post op pain contributes to peri op immune suppression & tumor promoting effects of surgery → multimodal approach; opioids suppress NKC activity

Pain and the Immunocompromised patient

Regional Anesthesia attenuates surgical stress response and preserves normal immune function (!) -Associated with decreased cortisol levels, normal NKC activity, decreases opioid & volatile inhalation agent usage, amide LAs cytotoxic effects on cancer cells, lower incidence of SSIs

Regional Anesthesia

-Wash your hands & Strict aseptic technique -Maximum barrier precautions (scrub the hub!) -GA/regional/combined technique -Neuraxial block blunts the surgical induced neuroendocrine response associated with suppression of the immune system/heightened risk of infection. -Prophylactic abx administered 30 min before incision -Active warming measures to avoid hypothermia -Avoid perioperative hyperglycemia -Leukocyte poor & irradiated blood products used when transfusion unavoidable -Multimodal pain management!!

Anesthesia Care of the Immunocompromised Patient