transfusion reactions evaluation & management
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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– [email protected]
• Ashford Medical Center
– Suite # 107
– Condado, San Juan
– Tel. 787-722-0412
– Fax 787-723-0554
– Cel. 787-354-0758– [email protected]
– ww.ihoapr.com