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Heme Flashcards

1
Q

How to eval and treat hemolytic anemia from G6PD def

What is G6PD def

A

enzymatic d/o that inhibits regeneration of glutathione in RBC making them more suceptible to oxidative damage reduced lifespan of RBC

Workup: Hct, increased reticulocyte count, unconjugatedbilirubin, peripheral smear (heinz body), urinalysis (hemosiderin, urobilinogen), haptoglobin decreased

Eliminate precipitating factors: hypoxia, acidosis, hypothermia, hyperglycemia, infection/stress, fava beans,

drugs: methylene blue, nitrofuranotin, chloramphenicol, high dose ASA, hydralazine, procanamdie, SNP

Avoid drugs that induce metemoglobinemia (methemoglobin produces significant volume of oxidizing agents: lido, benzocaine, prilocaine, SNP

administer fluid & mannitol (maintain UOP and free radical scavanging properties

transfusion if necessary

Antimalarial drugs: primaquine, pamaquine, chloroquine

Sulfonamides: sulfanilamide, sulfamethoxazole mafenide, thiazolesulfone, dapsone

Methylene blue, toluidine blue

Drugs causing methemoglobinemia: benzocaine, lidocaine, articaine, prilocaine

Certain analgesics: aspirin,

nitrofurantoin

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2
Q

What is DIC?

cause

What labs would confirm

tx

differentiate bwteen liver dz and DIC

A

Disseminated intravascular coagulopathy-uncontrolled thrombosis and fibrinolysis (overerwhelming its inhibitors AT3 and alpla 2 antiplasmin)–>depletion of factors and plts, micro and large vessel thrombosis

cause

instrinisc pathway: endothelial damage:immune complex, bacteria/virus, vasculitis, sepsis (lead to activation factor 12)

Extrinsic; release TF from AFE/abruption/fetall death, adenocarcinoma, HUS, trauma/burns

dx: defects must be detected in all 3 pathways of hemostasis:
1) low plt 2)elevated PT PTT 3), decreased AT3 levels, low fibrinogen <100, elevated D-dimer=FSP (result of plasmin degradation of crosslinked fibrin)

tx

  1. treat cause
    2) . FFP (replace factors, AT 3 and alpha 2 antiplasmin ) cryo (replace fibrinogen), plts
    3) heparin for clots?
    4) activated protein C? inhibits thrombin formation via 5a and 8a inhibition, also antiinflammatory agent
  2. TXA contraindicated
    - DIC precipitous decline in fibrinogen and plt
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3
Q

what is TRALI, pathophy

dx criteria

tx

A

Transfusion related acute lung injury-more common w plasma components

path: donor leukocyte antibodies lead to activation of neutrophils on pulm vascular endothelim –>endothelial damage capillary leakage
1. acute onset hypoxemia Pa02/Fi02<300, SP02<90%
2. pulm edema on CXR (b/l chest infiltreates) within 6 hrs of transfusion
3. absence of cardiac failure or fluid overload (PCWP<18)
tx: stop transfusion from this donor, support vent (low TV) No diuretics

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4
Q

TACO vs TRALI

A
  1. signs:

TRALI: normal-low BP, fever, transient leukopenia, +leukocyte antibody testing

TACO: HTN, JVD, edema

  1. fluid status

TRALI: normo-hypovolemic

TACO: hypervolemic–>diuretic

  1. cardiac fxn

TRALI: normal TACO: impaired, elevated BNP

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5
Q

Pathophys of SSD

when does polymerization occur

Hct goal

A

hemoglobinopaty in which mutation of chromosome 11 for beta chain. In presence of decreased oxygen tension, HBs polymerize an RBC take on deformed SS shape. Prone to hemolysis 15 days vs 120, microvascular occlusion of capillaries, ischemic end organ injury

PaO2 50 (PaO2 venous 40 75% sat), process also time dependent

Hct at least 30% and HBS <30-40% (leukoreduced)

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6
Q

COnsideration for SS pts

A

Preop: determine dz and severity

adequate hydration and pain control

Hct 40% and Hb SS<30% via simple or exchange transfusion

Intraop

avoid conditions that promote sickling-hypoxia, hypo/hyperthermia, hypovolemia, hypotension, acisosis, shivering

no tourniquet

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7
Q

SS head to toe

A

CNS: cerebral thrombosis, painful/vasoocclusive crises, deficits from stoke/seizures

Cardiac: CHFfrom chronic hypoxia, hemochromatosis, MI,

pulm: increased intrapulm shunting, ACS

GI: nonconjugated hyper bili from hemolysis, bile cholelithaisis,

renal: meduallary infarcts leading to isothenuria

Heme: splenic infarcts, aspetic necrosis, osteo, infection (asplenic), aplastic anemia(Parovovirus/folate decreased rbc production+ reduced life span (20 vs 120 days)–>profound anemia), transfusion, anemia

Endocrine: hemachromatosis-DI, hepatomegaly, adrenal insufficiency, hypothyroidism, hypopara

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8
Q

Goals w SSD

ACS tx

A

avoid hypoxia, hypercarbia, acidosis, anemia, hypotension

normothermia

ACS 1) oxygen, broncodilators, IS, chest physio 2) abx atypical and encapsuled org 3) pain control 4)correct anemia w simple transfusion or exchange

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9
Q

SS crises

A
  • painful/vasoocculsive
  • aplastic: infection or folate def
  • sequestration in spleen
  • hemolytic

ACS\

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10
Q

Conditons that promote sickling

A

anything that causes RBC hypoxia or lowerHg O2 affinity (Rightward shift)

  • hypoxemia, hypotension, hypovolemia,
  • hyperviscosity, vasoconstriction, hypothermia
  • acidosis, fever, increased 2,3,DPG, shivering
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11
Q

leukocyte reduced blood benefits

A
  1. reduce risk HLA and RBC allooimmunization, limit plt refractoriness
  2. CMV transmission
  3. febril non hemolytic transfusion rxn
  4. may limit immune suppression

  infectious risk associated with immunomodulation (TRIM)

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12
Q

Need to transfuse but no T&S

A

give type O RH neg blood- they have no A B D antigens on their surface. Switch to type specific when it become available. No longer throught that more than 10 units of O neg will result in significant amount of anti A and anti B antibodies tha will lead to incompatibility when pt own blood type is transfused. More of a concern w whole blood as contains significant amount of plasma whereas RBC do not

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13
Q

difference between type and screen and type and cross

A

T&S: typed for ABO and Rh antigens; mixes recipient plasma with pannel of commercial RBCs antigens to detect presence of known antibodies

T&C: mix recipient plasma with donor RBC to detect incompatbility

risk of hemolytic rxn

2/1000 type specific

6/10k T&S

5/10K for T&C

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14
Q

cell saver contraindications and relative

reduce risk how

A

absolute; mocrobial contamination of field, cancer surgery high risk of direct tumor manipulation and rupture

relative

hemoglobinopathy: SS thalassemia

  • contamination:
    • drugs not meant for systemic use-cholhexadine
    • clotting agents–>activate systemic coagulation
    • methy methacrylate–>hemodynamic changes
    • urine–>bacteremia
    • bowel contents–>bactermia
    • amniotic fluid–>DIC
    • pheo–>retransfusion of catecholamines
    • malignancy

many concerns minimal if processed, washed, admin through leukodepletion feliter

Pharmacological agents

  Clotting agents (Avitene, Surgicel, Gelfoam, etc.)

  Irrigating solutions (betadine, antibiotics meant for topical use)

  Methylmethacrylate

Contaminants

  Urine

  Bone chips

  Fat

  Bowel contents

  Infection

  Amniotic fluid

Malignancy

Haematological disorders

  Sickle cell disease

  Thalassaemia

Miscellaneous

  Carbon monoxide (electrocautery smoke)

  Catecholamines (phaeochromocytoma)

  Oxymetazoline (Afrin)

Papaverine

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15
Q

Risks of cell salvage

A
  1. hemolysis/nephrotoxicity (high levelsof free hemoglobin)
  2. contamination (urine, amniotic fluid, fat bacteria, cancer cells)
  3. coagulopathy: hemodilution, contamination w procoagulants (activated coagulation factors)
  4. gas embolism if infusion bag in circuit w pt

unwashed more likely to contain debris and activated clotting factors

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16
Q

post esophagectomy complications

A

neuro: phrenic, vagal, larngeal nerve injury
cardiac: arrythmia, hypotension
pulm: aspiration, PNA, BPF, PE, ARDS (10-24%)

GI; anastomatic leak/dehis, complications of TPN

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17
Q

pathogenesis of acute porphyria

signs of attack

A

an enzyme in the heme bisynthetic pathway is deficient, resulting in overprodion of porphyrins. heme is the most abundant form for porhyrin used to make Hgb and cytoP450 proteins. production controlled by ALA synthestase

neuro: AMS, seziure, muscle weakness (peripheral neuropathy), cranial nerve dysfunctiom
cards: autonomic neuropathy-hemodynamic instability (HTN tachy),
resp: resp failure (bulbar paralysis)

GI: N/V abdominal pain

endocrine; electrolyte disburbances Low K, soidum calcium

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18
Q

How to reduce risk of porphyric crisis?

A
  1. minimize fasting (10% glucose in saline as source cards), dehydration, stress (anxiolytic), infection
  2. avoid drugs that could trigger crisis: barbituates (methohexital, penytoin), diazapam, ketorolac, etomidate?,

hydralazine, nefidipine

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19
Q

How to treat porphyric crisis

A

dscontinue any tiggering drugs

IV hydration w dextrose

hematin to inhibit ALA synthetase

neuro: if seziure/anxiety/pain control give midaz-not phenytoin /pain meds
resp: ensure oxygenation and ventilation
cards: control tachycardia HTN w BB

GI: N/V antiemetic, hydration, carb (10% dextrose)

refractory: admin hematin- suppressed ALA synthetase activitiy and thus productin prophyrin

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20
Q

PE for prophria

A

neuro: neuropathy, cranial nerve dysfuncton (bulbar), muscle weaknes (can be at risk of aspiration and resp weakness)
cards: autonomic NS instability (tachy and HTN), fluid imbalance

electrolytes imbalance

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21
Q

post op bleeding. What labs to order.

A

CBC, PT PTT INR, fibrinogen, Fibrin degradation products

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22
Q

etiology of uremic plt dysfxn

tx

A
  1. decreased VWF formation and release
  2. increased NO and prostacylin
  3. uremia induced anemia-decreased viscocity-decresed plt interaction w endothelail surfaces

tx.

DDAVP, cryo, plt

EPO for anemia

fastest most effective: remove uremic acid-hemodialysis

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23
Q

Thinks to consider when debating transfusion

A
  1. severity of anemia
  2. risk of excessive/ongoing blood loss
  3. comorbidites- CAD CHF
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24
Q

role of platlets in coagulation

secondary hemostasis

A

primary hemostasis-plt plug formation

  1. adhesion to subendothelial collagen via GP1b binding vwF
  2. activation shape change, expose GP2b/2a R that binds to fibinogen, degranulation
    - alpha granules: PF4, fibrinognen/fibonectin, factor 5,8,vwf
    - dense granules: ADP/ATP, calcium, serotonin
  3. aggregation via GP2b/3a allowing plt-plt binding via fibrinogen

formation of fibrin clot via instrinstic and extrinsic pathway

  • extrinisc 7a/TF–>10–>2–>1
  • instrinisc: 11–>9/8–>10 (12
    thrombin: activates 1, 13, 5,8, and factor 11 of instrinsic pathway
25
Q

What factors are not made in liver

A

TF (3)

4 (calcium)

8:vwF (endothelium)

26
Q

How is coagulation regulation

how is fibrinolysis regulatied

A

various inhibitors

primary

  1. normal endothelium, production No and prostaglidin

secondary

  1. AT3 inibits: 12a 11a 9a 10a
  2. Protein C s inhibit 5,8,
  3. tissue factor pathway inhibitor inhibits TF/7a complex

secondary

  1. PAI inhibits TPA
  2. alpha 2 antiplasmin consume plasmin
  3. thrombi activated fibrinolytic inhibitor prevents plasminogen activation
27
Q

how is TEG measured

values

A

measures visoelastic changes via elasticity changes as detected by a piston in a slowly rotating cuvette

  1. R-time to initial clot formation (measures intrinsitic pathway
  2. K time from R to 20mm deflection
  3. alpha angle: measures rate of clot formation
  4. MA: max amplitude, measures clot strength
  5. A 60; amplitude at 60 min, measures clot retraction
28
Q

Examples of aquired quantitative and qualiatitive plt d/o

A

Aquired:

autoimmume (ITP, drug induced)

blood dilution

CPB

DIC

splenic sequestration

Qualitative

hypothermia, hydroxyethyl starch, uremia, CBP, liver dz

29
Q

thrombocytopenia, when to transfuse

A

depends on cause and expected response to transfusion, any ongoing coaguopathy, and type surgery

  • ITP transfusion wont have prolonged effect
  • minor surgery no signs of coagulopathy no need if 50k
  • major surgery plt should be around 70-100k
  • minor should have 50k
  • 20K at risk for sponateous bleeding
30
Q

Evaluate a bleeding d/o

A

H: ask about epistaxis, rectal bleeding, menorrhagia, hematuria, hemoptypsis,

NSAID ASA use

excessive bleeding w trauma, surgery, dental extraction, prior transfusion

P: look for petechiae and echymoses, arthrici changesn, signs liver dz or splenomegaly

31
Q

Causes of elevated PTT

A
  1. hemophilia A-factor 8 (sex linked recessive)-joint bleeding most common & hemophilia B (9(
  2. VWD
  3. heparin, coumadin
  4. liver dysfxn
  5. vit K def
  6. lupus anticoagulant
32
Q

anesthetic considerations for hemophilia A

why not FFP or cryo

what if ptt doesnt improve w factor 8 C

A

-Preop: determine severity via H&P and factor 8 level. activity of 50-100% required for surgery (DDAVP or factor 8::C 1-2 hrs bf incision

Intaop: avoid regional, careful positioning

postop: monitor for bleeding, half dose of factor 8C may need to be readmin every 12 hr
- decreased volume and infectious risk (crypo pooled from several donors
- antibody to/inhibiotr to factor 8 may be present

33
Q

most common coagulopathy

Should DDAVP used

tx

A

VWD-most have minimal to no sx (easy brusing, epistxsis. PT and PTT usually normal

PTT usually only decreased in severe cases in which depletion of VWF leads to decrease in factor 8 (carried by VWF)

  • Not all pts have clinical coagualopthy
  • Response different depending on type
    1: quantitiative defect
    2. 2b contraindicated thrombosis and thrombocyopenia may result
    3. complete deficiency

tx

  • DDAVP 1 hr preop to cause endothelial release
  • Humate P-factor 8C concentrate also contains vWF and preferred over cryo, pasturized –>viral inactivation
  • ineffective try cryo: infectious risk
  • FFP: volume (20cc/kg) +infectious risk (

-

34
Q

How does liver failure cause coagulopathy

A
  1. decreased synthesis of clotting factors
  2. failure to clear activated clotting factors, plasminogen activators
  3. splenic sequestration in liver
35
Q

Role vit K on coagulation

Who is at risk of vit K def

best test

A
  1. cofactor that catalyes the attachment of a carboxyl group to factors 2,7,9,10 protein C and S,
  2. malabs,oral abx, poor diet, coumadin, neonate
  3. PT since factor 7 has shortest half life and will be effected first
36
Q

Why does hypothermia cause coagulopathy

A
  1. plt sequestration in liver and spleen
  2. plt dysfunction from impaired plt thromboxane A2
  3. Interference with factor activity
  4. release of thromboplastins
37
Q
A
38
Q

Aquired factor def causes

A
  1. liver dz: failure to synthesis
  2. vit K def

dilutional

fibrinolysis: CBP, hypothesmia, prostate surgery (urokinase), TPA

hypothermia

heparin

39
Q

RBC processing

How long pRBC good for? plt

A
  • 500cc whole blood centrifuged to give 250 cc RBC (hct 70%) resuspended to volume 350 6C
  • RBC supernanent spun down to yeiled 70cc plt, stored at 24C
  • FFPremaining supernanent frozen (to avoid inactivation of 8 and 5)
  • cryo: collect gelantinous precipitate collected during slow thawing FFP
  • in CPDA 35 days ADSOL 42 days, plt 5
40
Q

-Risks of homologous/allogenic blood

Blood product modification

A

hemolytic transfusion rxn, transmitted dz (Hep c B, HIV HTLV), alloimmunization, immunosupression

  1. leukodepletion: prevent febrile rxn and alloimmunization
  2. irradiation: to prevent graft vs host
  3. CMV neg: for premature neonates, seroneg pregnant, immunocompromised
  4. washing- remove Iga
41
Q

Transfusion indications

A
  • RBCs: improve oxygen carrying capacity, symptomatic anemia
  • plt:treat coaglopathy associated w thrombocyopenia/pathia
    1. <100 and diffuse microvascular bleeding (+/-CBP_
    2. < 50K ad impending surgery or invasive procedure
    3. <20K in nonbleeding pt at risk for spontaneous bleeding
  • FFP:
    1. bleeding associated w factor def (hemophilia, DIC, ),
  • TTP, AT3 def
  • hemodilution

PT/PTT>1.5x normal in pt going to surgery or invasice procedure

reversal warfarin prior to emergency surgery and no time for vit K

diffuse microvascular bleeding

-cryp: hemophilia A, VWD, fibrinogen def (8 VWF, fibinogen, fibronectin 13)

42
Q

No blood for pt w rare blood type, what to do

A

H1 & H2 blocker steriods

type specific blood if available, if not, type O-

o- risk of hemolytic trasfusion rxn 1-2/1000

6/10k ts

5/10 tc

43
Q

Cause of acute hemolytic transfusion rxn

signs under GETA

tx

different from delayed

A
  • ABO incompatble blood
  • hypotension, tachycardia, fever, diffuse oozung (DIC) RF, ***hemoglobinuria if often only apparent sign***
  • stop transfusion
  • ABC-tx hypotension, fluid pressors
  • limit renal injury: mannitol lasix, bicarb (prevents tubular hemoglobin precipitation)
  • r/o couagulopathy
  • confirm diagnosis; retyped donor and recpipeint and crossmatcg, coombs, low haptoglobin,hemoglobinuria and hemoglobinemia, increased serum bili
  • acute are intravascular complement mediated whil delayed are mediated extravascular via RES (jaudice anemia fever)
44
Q

Transfusion reactions (GAIN FAT)

A
  1. febrile: host antibodies against donor neutrophils (most common)
  2. anaphylaxiss: IgA to IgA def pt (wash RBC)
  3. TRALI: fever hypoxia pulm edema , antileukocyte antibodies against host leukocytes in the lung
  4. graft vs host: donor lymphocytes attacking host (irradiation or leukocyte depltion filter
  5. in immunocompromised: improved renal graf surivival and decrease reoccurance of crohns; increased tumor reoccurance and post op infection
  6. alloimmunization
  7. hemolytic
45
Q

What is massive transfusion

complications

A

transfuison of 1-2 x the blood volume over 24 hr

coagulopathy (hemodilution)

hypothermia, acidosis/alkalosis, hyperK, hypocalcemia

volume overload, transfusion reaction

46
Q

Indications of DDAVP (3 causes)

SE:

A
  • Hemophilia A: works better when factor levels >5%
  • Type 1 and 2a VWD
  • uremia
  • hypotension, flushing, ADH relese and hyponatremia
47
Q

limitations of DDAVP

A

treatment for type 1 (not 2 or 3)

LIMITED DURATion of 6-12 hr

tachyphalaxisis

48
Q

-type of blood that can be transfused depending on comptabiltiy

A

platelets do not need ABO but rh compatible for child bearing females (no Rh antigens, but ABO on surface, hemolysis rare)

FFP needs to be ABO but not rh

49
Q

How does heparin work

  • dose for CPB
  • dose promatmine
A
  • neg charged binds to AT3 and enhances its activity (inhibit 9,10,11)
  • 300-400U/kg, ACT 400-480 (PTT unable to quantify larger doses)
  • 1mg/100U
50
Q

How does ANH work (Acute normovolemic hemodilution)

contraindications

A

blood loss minimized by reducing the blood likely to be shed during the procedure.

Leads to decreased viscosity and increased CO. maintain adequate oxygen deliver: decreased Hct but increased CO

-Blood flow is increased to vital organs, or organs that have higher oxygen extraction ratios

Anemia –>increase 2,3-DPG, –>facilitates oxygen extraction by tissues.

  1. Anemia Hbg <11 Hct<33
  2. Impaired renal fxn-pt may no be able to excrete fluid load
  3. conditions that make increased CO undesireable- AS
  4. signficant pulm dz: oxygen delivery to tissues may be inadequate in setting of pulm and decreased oxygen content associated with ANH

5 preexisiting coagulopathy

  1. severe CAD, Cerebrovascular dz
51
Q

mechanism of HIT

A

-heparin binds to plt causing agglutination

anti-heparin IgG binds to complexes of PF4 and heparin

can consider plasmapheresis of antiheparin IgG

52
Q

Protamine rxn

A
  1. histamine release from mast cells
  2. anaphylasis IgE in pt w prior protamin exposure (NPH PZI), fish allergy, vasectomy

3, anaphylactoid: IgG mediated

  1. PHTN: heparin protamin complexes result in release of thromboxane A2 from pulm macrophages
  2. A/C
53
Q

mechanism of aminocaproic acid/TXA

A

-antifibinolytics: bind to lysine binding sites of plasminogen preventing to the conversion of plasminogen to plasmin and attachment to fibrinogen

SE: thrombosis (CI in DIC)

54
Q

contraindication to neuraxial

A

refusal

coagulopathy

infection at site

critical preload and afterload dependence

55
Q

How to reduce need for homologous transfusion

CI induced hypotension

A
  1. use lowest transfusion trigger that still provides adeuquate oxygen delivery: depends on coexisting dz, chronicity of anemia, and rapidity of anticipated loses. 7-9 usually acceptable for healthy pt, 10 for significant CAD
  2. intraop salvaging
  3. employ techniques that minimize blood loss: induced hypotension, isovolemic hemodilution, phamacology (NO, SNP, alpha blocks, BB, CCB)
    - severe anemia, hypotension or dz w inadewuate end organ perfusion (CAD, CVD)
  4. drugs tthat reduce transfusion: DDAVP, antifinrinolytics
56
Q

How does body compensate for anemia

A
  1. increase CO: decrease viscosity (decreased afterload, increase venois return and preload-starling)

2, increase O2 extraction: increase 2,3, DPG

57
Q

What is met Hbg

What causes it

dx

tx

A
  • excess of oxidized Fe3+ ferric hemoglobin-which has decreased ability to bind to Oxygen and results in left shift of oxy hemoboglobin curve
  • oxidizing agents- sulfonimides, nitrates, NO, SNP, benzocaine, prilocaine, G6PD def (inadequate reduced glutathione production which protects Hgb from oxidation)- def of enzyme responsible for oxidizing hemglobin

dx; cynaosis, sx tissue hypoxia (H/A dizziness), pulse ox 88

tx: mtheylene blue

58
Q

Plan for case expecting massive blood loss

A
  1. 2 large bore IV + central introducer
  2. rapid infusers + blood warmers
  3. Blood products in room
  4. cell salvage
  5. antifibrinolytics
  6. ANH

AW (15 decks)

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