transfusion reactions evaluation & management

Evaluation and Managementof Hemolytic Transfusion Reactions

Raul H. Morales-Borges, MD

Medical Director, Blood Services

American Red Cross, Puerto Rico Region

Clinical: Acute Hemolytic Transfusion Reaction

• Fever

• Chills/Rigors

• Hypotension– Shock

• Pain-IV site

• Flank pain

• Chest pain

• Oliguria

• Renal failure

• DIC

• GI complaints– Nausea/vomiting (N/V)

Nonspecific

Acute Transfusion Reactionsin the Setting of Incompatible Transfusion

Differential Diagnosis• Pertinent positives• Pertinent negatives

Occam’s razor* does not always apply* All things being equal, the simplest

explanation is usually correct.Examples: Hyperhemolysis in Sickle Cell

DHTR with aplastic crises

Clinical: AHTR vs. SepsisAHTR• Fever• Chills/rigor• Pain-IV, flank, chest• Hypotension• Tachycardia• Shock• GI-N/V/diarrhea• Renal failure• DIC

Sepsis (Endotoxemia)• Fever• Chills/rigors• Chest pain• Hypotension• Tachycardia• Shock• GI-N/V/diarrhea• Renal failure• DIC

SystemicInflammation

5

Adverse Reaction Signs and Symptoms• Fever

– Increase in temperature of >1C (or 2F)

• Shaking chills• Pain

– Infusion site– Chest– Abdomen– Back

• Blood pressure changes– Hypertension– Hypotension cont’d

Adverse Reaction Signs and Symptoms• Respiratory distress

– Dyspnea– Tachypnea– Apnea

• Shock• Loss of consciousness

• Skin changes– Hives– Itching– Flushing cont’d

7

Adverse Reactions Signs and Symptoms

• Nausea and/or vomiting

• Generalized bleeding; DIC

• Darkened urine; Hemoglobinuria

• Apprehension; Sensations of impending doom• ANY adverse manifestation at time of transfusion

should be considered

8

Acute immune-mediated hemolysis

– Usually due to transfusion of ABO-incompatible red cells

– May begin after infusion of as little as 10-15 mL of blood

– Symptoms may be misleadingly mild

– Early recognition and vigorous treatment are critical

Acute immune-mediated hemolysis• Presentation may include any sign or

symptom, but most typically:– Fever (may be the only symptom); chills– Hemoglobinuria, hemoglobinemia– Hypotension– Back or flank pain; pain at infusion site– Generalized bleeding/DIC– Renal failure

Adverse Reaction

• Transfusion should be stopped

• Labels, forms and patient identification should be rechecked at the bedside

• Patient’s physician and blood bank should be notified immediately

• Maintain I.V. line with normal saline until medical evaluation completed

Adverse Reaction

• Collect post-transfusion samples and send to blood bank– Avoid traumatic venipuncture and mechanical

hemolysis

• Depending on facility policy, send blood product container, administration set and any attached fluids to the Blood Bank.

• Urine sample may be useful for evaluation

AHTR as Systemic Inflammatory RXN

Common Involvement Inflammatory ResponseAHTR TRALIFebrile SepsisAllergic Hypotensive

Capon, Goldfinger. Transfusion 1995:35;513-20

Reaction

Fever &/orchills/rigors

CardiovascularRespiratory

HemolysisNoFNHTR*

Other

AHTRBacterial

Other

YesTRALI

Hypotensive AHTR

Bacterial Anaphylactoid

Volume OverloadOther

*FNHTR = Febrile, non-hemolytic transfusion reaction

Reaction

Fever &/orchills/rigors

CardiovascularRespiratory

HemolysisNoFNHTR

Other

AHTRBacterial

Other

YesTRALI

Hypotensive AHTR

Bacterial Anaphylactoid

Volume OverloadOther

Complete clinical assessmentComplete clinical assessmentAncillary laboratory testingAncillary laboratory testing

Three Tiers of Investigation

First Tier• Clerical Check

- Bedside and Laboratory• Repeat ABO/Rh (pre/post)• Visual Check for Hemolysis• Direct Antiglobulin Test*

* may be pos or neg withimmune hemolysis due to RBC destruction

Second Tier• Repeat ABO/Rh units• Repeat antibody screen• Repeat special antigen typing• Full crossmatch

• pre/post-reaction specimens

Third Tier• “Blood Bank Voodoo”

• enhanced techniques

• Clinical findings/history• Contributing factors• Ancillary tests-hemolysis• Other pertinent testing• Monitoring and treatment

19

Common Causes of Acute Adverse Reactions - Immunologic

• RBC incompatibility, i.e., RBC antibody• Antibody to plasma proteins

• Antibody to donor leukocytes

• Donor antibodies to patient leukocytes

20

Common Causes of Acute Adverse Reactions – Non-Immunologic• Volume overload

• Bacterial Contamination

• Physical or chemical destruction of RBCs– Incompatible solutions or medications– Excessive heat– Freezing

21

Laboratory Investigationof Transfusion Reactions

Laboratory Evaluation

Immediate Investigation:

• Check for Clerical Errors

• Check for Hemolysis

• Check DAT for evidence of blood group incompatibility

Clerical Errors

• The risk of getting the wrong unit of blood exceeds all transmissible disease risks combined.

• 1990-1999 data: 1 in 19,000 units was administered to other than the intended recipient – 51% errors at patient care area– 29% errors in Blood Bank– 15% multiple, sequential errors

Linden JV, Wagner K, et al. Transfusion 2000Linden JV, Wagner K, et al. Transfusion 2000

Transfusion Complications

Dzik WH. Transfusion 2003;43:1190-1199

Checking for Clerical Errors• Was the blood transfused

to the intended recipient?• Was the correct unit

tagged?• Was the correct unit

issued?• Was the correct sample

used for testing?

Visual Examination for Hemolysis

• Plasma from post-transfusion sample is inspected for hemolysis– May appear pink to red if significant hemolysis

has occurred in previous few hours– May appear deep red/brown or yellowish if

hemoglobin has metabolized to bilirubin– Increase in bilirubin may begin as early as 1 hour

after reaction, peaks in 5-7 hours and returns to normal within 24 hours (assuming normal liver function)

Visual Inspection for Hemolysis

Direct Antiglobulin Test

• Used as serologic check for incompatibility

• Perform on post-transfusion specimen; test pre-transfusion DAT for comparison

• DAT is likely to be positive if incompatible rbcs or incompatible plasma was transfused

Direct Antiglobulin Test

• Incompatible red cell transfusion:

– DAT may have a mixed-field appearance

– If transfused cells were rapidly destroyed, post-reaction DAT may be negative

– Time sample drawn is important, should be collected ASAP after reaction occurs

– Type of AHG employed may affect results

Additional Evaluation – When?

• If any of initial checks and tests give positive or suspicious results

• Clinical presentation is consistent with a Hemolytic Transfusion Reaction (HTR)

Repeat ABO grouping

• Standard 7.4.2.1 [26th edition]

“For suspected hemolytic transfusion reactions…, a repeat ABO group determination shall be performed on the post-transfusion sample.”

Also repeat ABO testing on pre-transfusion sample and blood from transfused unit or attached segment.

ABO grouping discrepancies

• Error in patient/sample identification– Pretransfusion sample mislabeled– Sample mix-up in the laboratory– Transfusion given to wrong patient

• Error in original ABO-group interpretation– Recording error– Problem solving incorrect

• Error in blood product labeling

Additional InvestigationNon-Immune Acute Hemolytic Reaction:

• Examine blood in container and lines for abnormal appearance, hemolysis

• Check records for any incompatible fluids or medications which may have been administered with blood

• Interview transfusionist/check records for details (use of infusion devices, blood product handling, etc.)

ContCont’’dd

Additional Investigation

Causes of Non-Immune Acute Hemolysis

• Defective blood warmers or infusion pumps

• Use of small bore catheters and/or pressure cuffs for infusion

• Improper storage (too warm, too cold)– Use of solid ice or dry ice– Use of microwave ovens, heating pads, room

heaters, hot water, etc. to warm blood

ContCont’’dd

Additional Investigation

Causes of Non-Immune Acute Hemolysis• Incompatible fluids, solutions or medications given

with blood, especially Lactated Ringer’s, 5% Dextrose, and hypotonic saline solutions.

• The only approved solution for infusion with blood is 0.9% sodium chloride injection, USP (normal saline). 5% albumin may be used with physician approval.

Additional Investigations

• Antibody Elution

• Antibody Screen: on post, repeat pre

• Crossmatch

– On pre and post

– With AHG, esp. if not done previously

• Repeat Antigen typings on donor red cells (if applicable)

• Examination of urine specimen

Hemoglobinuria vs Hematuria

S.G. Sandler, D.A. Sandler. Emedicine.com 2003

Antibody Elution

• Removal of red-cell-bound antibody

• Common techniques include alteration in pH, heat, organic solvents, detergents, sonication

• Heat and sonication methods not suitable for recovering IgG antibodies; not recommended for investigation of HTR

Antibody Elution

• May be helpful even when DAT is negative

• Test eluate for presence of antibody with:

– Antibody screen

– A1 and B cells (when appropriate)

– Cells from transfused donor units

– DAT negative, pre-transfusion autologous cells (if possible)

Antibodies other than ABO• Repeat antibody screen and crossmatches

– Use segment from container– Test through AHG-phase– May want to use different test methods, phases

• Type post-transfusion sample for corresponding antigen– May help determine if incompatible cells were

eliminated or if some are still in circulation

Other Tests• Markers of hemolysis:

– Lactate dehydrogenase (LDH)– Bilirubin– Haptoglobin

• Most useful if pre- and multiple post-reaction values are available

• Rising indirect bilirubin is associated with extravascular hemolysis and HTR caused by non-ABO antibodies

ContCont’’dd

Other types of reactionsDelayed (>24 hours)

– Decreasing Hgb/Hct level, or absence of anticipated post-transfusion elevation

– Mild to moderate jaundice– Laboratory evidence of increased cell destruction

(increased bilirubin, LDH, etc)– Fever– Hemoglobinuria– Demonstration of previously undetected rbc

alloantibody in plasma or eluate

Non-Hemolytic reactions

Anaphylactic ReactionsConfirmed by demonstration of anti-IgA in the

patient’s plasma or serum. Test is available in specialized reference laboratories.

Screening for IgA deficiency should be the initial study. Most patients with IgA-related anaphylaxis have been IgA deficient.

Subclass or allotype-specific antibodies may develop in patients with normal IgA levels

Non-Hemolytic reactionsBacterial Contamination

– Onset typically rapid, occurring within 30 minutes of completion of transfusion

– More common in components stored at RT

– Examine returned unit for abnormal appearance (brownish or purple discoloration, clots, muddy appearance)

– Gram’s stain and Culture of blood bag contents should be performed if clinical presentation suggests bacterial sepsis

Non-Hemolytic reactionsTRALI

– 3rd leading cause of transfusion-associated death (CBER, FY2001 and FY2002)

– Suspect TRALI with any respiratory distress occurring during or following blood or blood component transfusion

– Notify facility that supplied blood component; test remaining product or donor sample for antibodies to HLA and/or granulocyte antigens

– Crossmatching donor sera with recipient lymphocytes or granulocytes can provide supportive evidence

Non-Hemolytic reactionsFebrile, Non-Hemolytic (FNHTR)

– Typically present with fever/chills towards ends of transfusion

– May be due to recipient antibody to donor WBC antigen

– May also be caused by infusion of cytokines released from WBCs during storage of component

– Since fever may be initial symptom of acute HTR or septic reaction, prompt attention is warranted to r/o life-threatening reaction

Non-Hemolytic reactionsUrticarial / Allergic (1% of transfusions)• Usual presentation: Hives, itching, flushing

• Hypersensitivity immune response

• If symptoms limited to urticaria, may restart unit after administration of antihistamines per physician order.

• Report to blood bank; repeated urticarial reactions will be evaluated to determine if washed blood products are required.

Non-Hemolytic reactionsCirculatory overload

– Usually seen in patients with compromised cardiac or pulmonary status

– Difficulty breathing, cough, cyanosis, tachycardia, hypertension, headache, congestive heart failure

– Symptoms usually improve when infusion is stopped and patient is placed in sitting position

Transfusion Associated Circulatory Overload (TACO)

• The primary symptoms of TACO are: dyspnea, orthopnea, peripheral edema, and rapid increase of blood pressure.

• It is difficult to determine the incidence of TACO, but its incidence is estimated at about one in every 100 to 10,000 transfusions. The risk increases with patients over the age of 60 and patients with cardiac or pulmonary failure, or anemia.

• Transfusion Associated Circulatory Overload is easily prevented by closely monitoring patients receiving transfusions and transfusing smaller volumes of blood at a slower rate.

• Differentiation from TRALI: While both are related to transfusion medicine and both are important, TACO differs from TRALI in part by having longer hospital stays and increased morbidity.

• The hypotension seen with TRALI and the hypertension seen with TACO provides a clinical differentiation of the two.

Hemolysis: Laboratory Evidence

Acute Hemolysis

• Plasma/serum free hemoglobin

• Haptoglobin

• Lactate dehydrogenase (LDH)

• Bilirubin– Direct < Indirect Bilirubin

• Urinalysis

Interpreted Interpreted relative torelative to

overall overall liver liver

functionfunction

Free Hgb

Hgb-Haptoglobin+

Release RBC Enzymes

Plasma FreeHemoglobin

Haptoglobin

LDH(LD1 > LD2)

Intravascular Hemolysis

Hemoglobinuria

Kidney

Free HgbFree Hgb

HaptoglobinHaptoglobin

HemoglobinuriaHemoglobinuria

24 hr1-6 hr

INTRAVASCULAR (ACUTE) HEMOLYSIS

Duvall et al. Hemoglobin catabolism following an HTR in SS anemia. Transfusion 1974;14:382-387.

Free Hgb

Hgb-Haptoglobin

Kidney

Hemoglobinuria

Spleen

Heme

Biliverdin

Indirectbilirubin

Free Hgb

Hgb-Haptoglobin

Kidney

BilirubinuriaHemoglobinuria

Spleen

Heme

Biliverdin

Indirectbilirubin

LiverDirectbilirubin

HemoglobinHemoglobin

Cummins et al. Ann Clin Biochem 1997:24:109-110.

Day 7 Day 14

Directbilirubin

Indirectbilirubin

Direct > Indirect

EXTRAVASCULAR HEMOLYSIS

Day 0

Free Hgb

Hgb-Haptoglobin

Kidney

UrobilinogenBilirubinuria

Hemoglobinuria

Spleen

Heme

Biliverdin

Indirectbilirubin

Liver

Direct bilirubin

GU

TUrobilin

Hematology: Ancillary testing

• Complete blood count (CBC) with WBC differential– Appropriate response– Survival– Marrow response

• Peripheral blood smear

• Reticulocyte count

• Coagulation studies

Hgb

Hct %PLTWBC

WBC, left shiftBacterial

Complete Blood Count with WBC Differential

WBCTRALI

PLTHemolysis

TRALIBacterial

1 gm Hgb/unit RBC3% Hct/unit RBC

Indices (MCV, MCHC, MCH): MCV - reticulocytosis RDW - reticulocytosis MCHC - spherocytosis

NoHgb

Immune“hyperhemolysis”

BleedingHemodilutionNonimmune

Peripheral Blood Smear

AnisopoikilocytosisSpherocytesBasophilia

AABB has not reviewed this slide and expressly disclaims any liability arising from relying upon or using information contained herein. Please see the full disclaimer appearing on the Disclaimer slide of this presentation.

Reticulocyte Count

• DHTR, unexplained anemia• Marrow responsive to anemia?• Response appropriate?

Critical in hemoglobinopathies– Differential Diagnosis (DDx): DHTR

with marrow suppression

Coagulation Studies

Monitor for Disseminated Intravascular Coagulation (DIC)

• Platelet count

• Fibrinogen

• PT and aPTT

• D-dimer

Free HgbFree Hgb

12 hr 24 hr

FibrinogenFibrinogen

Platelet Platelet

0 hr

XIIXIIXIIaXIIa

XIXIXIaXIa

IXIXIXaIXa

VIIIaVIIIa

Intrinsic System

(aPT

T)

XXXaXaVaVa

Tissue FactorTissue FactorVIIaVIIa

Ext

rinsi

c S

yste

m (

PT

)

Tissue Damage

IIII IIaIIa

VIIIVIII

FibrinogenFibrinogen FibrinFibrin

Intrinsic Pathway

XIIXIIXIIaXIIa

XIXIXIaXIa

IXIXIXaIXa

VIIIaVIIIa

Intrinsic System

(aPT

T)

XXXaXaVaVa

VIIaVIIa

Ext

rinsi

c S

yste

m (

PT

)

IIII IIaIIa

VIIIVIII

FibrinogenFibrinogen FibrinFibrin

HgbCytokines

ex.TNF Monocyte

Tissue FactorTissue Factor

Extrinsic Pathway

ABO IncompatibleABO Incompatible

ABO Compatible

WB

C P

roco

agul

ant A

ctiv

ityWBC Procoagulant Activity Induced by

ABO IncompatibilityDavenport R, Polar TJ, Kunkel SL.

Transfusion 1994;34:943-9

Time (hours)

Unsensitized DogsUnsensitized Dogs

Sensitized DogsSensitized Dogs

The role of Disseminated Intravascular Coagulation in Shock Induced by Transfusion

of Human Blood in DogsTakaki A et al. Transfusion 1979;19:404-409.

Note abrupt immediate drop in platelet count in both sensitized and unsensitized dogs

5 min

Sensitized (Sensitized (aPTT)aPTT)

NonsensitizedNonsensitized

Sensitized Sensitized (( PT) PT)

Sensitized (Sensitized (fibrinogenfibrinogen)

(-) CHARGED SURFACE(-) CHARGED SURFACEex. COLLAGEN ex. COLLAGEN

XIIXIIXIIaXIIa

XIXIXIaXIa

IXIXIXaIXa

VIIIaVIIIa

Intrinsic System

(aPT

T)

XXXaXaVaVa

Tissue FactorTissue FactorVIIaVIIa

Ext

rinsi

c S

yste

m (

PT

)

Tissue Damage

IIII IIaIIa

VIIIVIII

FibrinogenFibrinogen FibrinFibrin

Coagulation AssaysPT, aPTT, fibrinogen

DD

EE

EEEE DD DD DD

DD DD DD DDEE EE

DD DD

ProtofibrilFibrin

Bundles of protofibrils(14-22n)

thrombin

a,bpeptides

Fibrinogen

Generation and Breakdown of Fibrin

DD EE DD

D E

DD

EE

EE

EE DD

DD

DD DD DD DD

DD

EE

EE

DD

DD

thrombin fibrinopeptide

1. Fall in Fibrinogen

2. Generation of fibrinopeptides a & b

Plasmin Plasmin plasminogen plasminogen

3. Generation of fibrin split products(FDP) and d-dimers

DD DDDDD-dimerD-dimer

D

Evaluation of DIC

DD EE DD

Renal: Ancillary TestingUrinalysis• Hemoglobinuria (NOT hematuria)• Urobilinogen (acute hemolysis)• Hemosiderin (chronic hemolysis)• RBC casts• Evidence UTI

– Leukocyte esterase– Nitrate– WBC, RBC

DDx

Renal Ancillary Testing

Monitor renal function

• Electrolytes

• Urine output– Daily weights

Etiology Acute Renal Failure in HTR

• Ischemic - Shock- Vasoconstriction afferent renal

arterieso Cytokine mediated (ex IL-1)o Nitric oxide absorption

• Hgb-induced nephrotoxicity

• Tubular obstruction

• All of the above

RBC Pigment Cast

AA

Loops of Henle stained with hemoglobin. Alsoshown is an isolated pigment cast of hemoglobin.

Loops of Henle

Sobatta& HammersteinHistology

Glomerulus

Proximal tubules

DeGowin and Warner, Arch Int Med 1938; 609-630.DeGowin and Warner, Arch Int Med 1938; 609-630.

Normal kidneynondilated tubules

Kidney with AHTRdilated, distended tubules

DeGowin and Warner, Arch Int Med 1938; 609-630.DeGowin and Warner, Arch Int Med 1938; 609-630.

ControlPeriod

Infusion of Hemoglobin Leads to VasoconstrictionInfusion of Hemoglobin Leads to Vasoconstriction

126

148

15 gm Hgb

7893

SBPSBP

DBPDBP

HR 67

56

8.5%

8.3%

8.3%

Increases in systolic (SBP) and diastolic (DBP), with

decreases in heart rate (HR)Miller and McDonald, J Clin Invest 1951;1033-1040.Miller and McDonald, J Clin Invest 1951;1033-1040.

Ren

al B

lood

Flo

wU

rine 11.5 1.5 ml/min 4.687%

15 gm Hgb HemoglobinuriaHemoglobinuria 2.5 hrs

673

220 ml/min

67%

Pla

sma

Hgb 175 mg/dl

AABB has not reviewed this slide and expressly disclaims any liability arising from relying upon or using information contained herein. Please see the full disclaimer appearing on the Disclaimer slide of this presentation.

Exclude Nonimmune Hemolysis

• Examine tubing/blood set

• Review infusion sheet– Concurrent medications?– Incompatible solutions?– Use of blood warmer/infusion pump?– Flow rate/needle size?– Improper storage on-site?

Medical Etiologies Hemolysis• Hematologic Disorders

– Hemoglobinopathies– Congenital membrane defects– Malignancy: cold, warm AIHA– Microangiopathies, e.g., TTP, HUS, HELLP

• Cardiovascular– Artificial valves– Arterial-venous malformations

• Infections– DIC, C. perfringens, parasitic

Treatment of Hemolytic Transfusion Reactions

Treatment AHTR

• Stop transfusion

• Supportive care

• Monitor/treat shock

• Prophylaxis & tx acute renal failure

• Monitoring & tx DIC, bleeding

Treatment AHTR• If shock

– O2– Fluid resuscitation– Pressor support

• MAP > 60 mm Hg or SBP >90 mm Hg• Dopamine 2 < 5 mcg/kg/min

– Steroids• Methylprednisolone 125 mg q 6 hrs

Treatment/Prophylaxis: Kidney

• Hydration

• Diuretics

• Possibly sympathomimetic (Dopamine)– Renal perfusion

• Nephrology consult

Treatment: Kidney

Hydration

• Normal saline

• Goal >100 mL urine/hr

• If oliguric, consider addition of diuretics

• If anuric, restrict after 1 liter

Treatment: Kidney

Diuretics

• Loop diuretics (Furosemide/Lasix)

• Osmotic agents (Mannitol)

• Additive, synergistic effects

• Precautions – Not appropriate in all patients

Synergism with mannitoland furosemide

Linear Dose-response between urine production

and dose/kg BW.

Sirevella et al. Ann Thorac Surg. 2000

Loop diuretic• Acts at medullary portion of

ascending limb of Henle• Inhibits Na+, K+ readsorption

• Increase osmosis, H20 loss

Furosemide (lasix)

Ascending loopof Henle (medulla)

Furosemide Administration

Adults• 20-40 mg IV over 1-2 min• Can be repeated 2 hrs,

dose to effect• Do not exceed 1 gm/day

Renal Insufficiency• 2.5 < 4 mg/min IV infusion

Pediatric (Edema doses)• 1 mg/kg/dose IV q 4-12 hrs

Ref. DrugPoints

Monitor K+, Na+, glucoseUric acid, hx gout

Drug Interactions ACE InhibitorsCardiac glycosidesAminoglycosidesLithium Indomethacin

Mannitol • Non-metabolized sugar• Excreted by kidney• Is not readsorbed

• Osmotic loss of H2O

• 50 gm Mannitol = 1 liter shift H20

Mannitol/Osmitrol Administration

Adults• 200 mg/kg test dose over 3-5 min.

or 50-100 gm as single dose• 30-50 ml urine (1-2 hrs)

If no/little response• Second test dose• If no response, stop & re-evaluate

Pediatrics• 0.75 gm/kg over 3-5 min• If no response, stop

Contraindications Mannitol• Intracranial bleeding*• Pulmonary edema• Capillary leak syndromes• Heart failure*• Anuria• Increasing renal failure after

initiation• Dehydration

*Commonly used in cardiac surgery and neurosurgery

MonitorBlood pressureRenal functionFluid/electrolytes

DopamineSympathomimeticVasopressorVasodilator

Contraindications:Ventricular fibrillation Tachyarrhymias Pheochromocytoma

Vascular smooth muscleTitrate dose to desired effect• 0.5-2.0 mcg/kg/min IV

– Increase renal perfusion– No BP

• 2-5 mcg/kg/min IV– Increase renal perfusion– Increase cardiac output, BP

• > 5-20 mcg/kg/min vasoconstriction, urine output

Solution: 1 gm furosemideper 500 ml 20% mannitol

Rate: 0.3-0.4 ml/kg/hr

Dopamine Rate: 0.2-0.3 mcg/kg/min

Intermittent Diuretics

ContinuousInfusion

Siverella et al. Ann Thorac Surg 2000; 69:501

Prophylactic infusion of mannitol, furosemide and dopamine (Group B) significantly decreased the need for post-operative dialysis due to TCV surgery and pigment

nephropathy (Hgb, myoglobin).

Treatment: DIC

• Consider Heparin*

• Blood product support for bleeding

• Hematology consult

*If bleeding despite factor replacement

Heparin binds Antithrombin III (ATIII) & IIa (thrombin)Induces change enzyme conformation ATIIIIncreases ATIII inhibitory activity15-19 fold

ATIIIATIII ATIIIATIIIHeparin

bindingIIa Inhibition IIa

ATIII is broad serineProtease inhibitor

Inhibitor of multiplecoagulation factors in the extrinsic andextrinsic pathways

Heparin

Loading dose• 5000 units IV

Continuous drip• 500-1000 units/hr

Monitor• PTT > 1.5x nl range

Contraindications:• Cerebral hemorrhage• Recent neurosurgery• Recent eye surgery• Recent organ biopsy• Major arterial injury• Hx heparin-associated

– Thrombosis (HITT)– Thrombocytopenia

• Allergic hypersensitivity to heparin

Rise in fibrinogen after Rise in fibrinogen after giving heparingiving heparin

Heparin Treatment of Intravascular CoagulationAccompanying Hemolytic Transfusion Reactions.

Rock RC, Bove JR, Nemerson Y. Transfusion 1969

DIC following transfusion of 260 mls Group A blood toa Group O patient, treated with heparin

Heparin Treatment of Intravascular CoagulationAccompanying Hemolytic Transfusion Reactions.

Rock RC, Bove JR, Nemerson Y. Transfusion 1969

DIC following transfusion of 2 units Fya incompatible blood, treated with heparin.

Summary

• The importance of prompt recognition and reporting of suspected Transfusion Reactions cannot be over-emphasized.

• Assess reactions quickly and efficiently to rule out the most serious causes first

• Communicate results with responsible physicians so appropriate actions can be taken without unnecessary delay

Summary:• Stop transfusion

• Supportive care– Oxygen prn– Pressor support– Fluid resuscitation

• Renal – Hydration, diuretics, dopamine

• Coagulation– Blood product support; heparin

Future Transfusions

Assess risk vs. benefit

Consider limiting blood draws

Hematopoietic supportex. folate, erythropoietin, iron

References

• AABB Standards for Blood Banks and Transfusion Services, 26th ed.

• AABB Standards for Immunohematology Reference Laboratories, 6th ed.

• AABB Technical Manual, 16th ed.

THANKS’

Dr. Raúl H. Morales BorgesHematology/Oncology

• American Red Cross

– Biomedical Services

– PR Medical Center

– Tel. 787-759-8100

– Ext. 3873

– Dir. 787-993-3873

– Cel. 787-505-5814– Raul.Morales@redcross.org

• Ashford Medical Center

– Suite # 107

– Condado, San Juan

– Tel. 787-722-0412

– Fax 787-723-0554

– Cel. 787-354-0758– rmoralesborges@yahoo.com

– ww.ihoapr.com