Download - Adverse Effects of Plasma Therapy
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Adverse effects
ofPlasma Therapy
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Adverse Effects of Plasma Usage
VolumeAntibodies
and
other Proteins
CYTOKINESCELLUL
ARCONTE
NT
CONTAMINANTS
ORGANISMS
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It is Important to Diagnosebecause..
How To Manage?
What to do with current Transfusion?
What all investigations to be done?
When and How to give next transfusion?
Does the patient need any special blood
products in future?
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Immediate
Allergic Reactions
Anaphylactic/Anaphylactoid
Febrile Non Hemolytic Transfusion Reactions
Hemolytic Transfusion Reactions
TRALI
TACO
Bacterial Contamination
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Delayed
Transfusion Transmitted Diseases
Transfusion Related Immuno Modulation
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Rare with FFP
RBC ALLOIMMUNISATION
TA-GVHD
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FREQUENCY
Allergic-1 in 33 to 1 in 100
FNHTR-1 in 100
Anaphylactic -1 in 20,000 to 50,000
HTR-1 in 12,000-20,000 TRALI-1 in 5000-10,000
TACO-1 in 150
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Allergic Reactions
Type 1 immediate hypersensitivity reaction
Immediately after transfusion
Atopic individuals more prone
Histamine and leukotriene mediated
MILD
ALLERGIC
SEVERE
systemic
ANAPHYLACTIC
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Mechanism
IgE antibodies in recipient react withproteins in transfused plasma
IgE antibodies in donor Reacts with
proteins in recipient plasma Rarely due to chemicals in bag/tubing
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Treatment
Transfusion temporarily discontinued
IV /oral antihistaminic
Diphenhydramine 25-50mg
PM/CPM Resume within 30 minutes in presence of doctor
Develops generalised urticaria,hypotension,facial/laryngeal edema -discontinue
Adrenaline if needed
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Prevention
Premedication with anti histamine(oral/parenteral) -only for those with >2 episodes of allergic reactions
May be donor induced
Masks some hemolytic symptoms
25-50 mg Pheneramine/diphenhydramine half to 1 hrbefore transfusion
if found ineffective -hydrocortisone 100 mg Remove plasma by washing from other
products(RBC,Platelets)
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Anaphylactic/AnaphylactoidReactions
Rapid
Serious Life Threatening
Transfusion of Few ml is enough
Systemic nature and severitydifferentiates from allergic
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Difference
Anaphylactic
Allergen in plasma reacts with Ig E in recipient
Anaphylactoid Allergen in plasma reacts with non IgE
antibodies in recipient
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Anaphylactoid reaction due to IgAdeficiency
The best documented reason for anaphylactoid reactions
IgA deficient individuals-1 in 700
Reaction frequency lower- 1 in 20,000-50,ooo
Mechanism antibodies against IgA in recipients body Other protein deficiencies
Complement
VwF
Haptoglobin
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URTICARIA
GENERALISED ITCHING
PRURITUS
ANGIOEDEMA
COUGH
HOARSENESS OF VOICE
STRIDOR ,RESPIRATORY OBSTRUCTION
WHEEZING,
CHEST TIGHTNESS
CRAMPS
NAUSEA
VOMITING
DIARRHOEA
HYPOTENSION
TACHYCARDIA
ARRYTHMIA
CARDIAC ARREST
IMMEDIATE
DRAMATIC ONSET
SYSTEMIC&
CUTANEOUS
SYMPTOMS
OTHER CAUSES
SHOULD BE RULED
OUT
INVESTIGATIONS
NOT MUCH,MAINLY CLINICAL
TRYPTASE LEVELS
IgA LEVELS
SKIN
RESPIR
ATORY
ABDOMI
NAL
CARDIAC
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Management
STOP the Transfusion,should not RESTART
Medical emergency
Same for anaphylactic and Anaphylactoid
Adrenaline
.3-.5 ml , 1:1000 s/c or IM
Severe hypotension,laryngel edema/resp.failureIV 1:10000
Oxygen,B agonist &/theophylline
Maintain BP
Trendelenberg
Fluids,
Dopamine
CONSIDER COINCIDENTIAL
OCCURRENCE
MyocardiaI Infarction?PulmonaryEmbolism?
Or something else?
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PREVENTION
Saline washed blood components-RBC&Platelets
Plasma Transfusion -only If unavoidable
Only IgA deficient plasma should be given to IgA deficientindividuals
Screen the family members
WHAT TO DO WITH NON IgA
DEFICIENT RECURRENT SEVERE
ANAPHYLACTICS?
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HYPOTENSIVE REACTIONS IN ACEINHIBITOR USERS
Mimics Anaphylaxis
Metabolism Bradykinin in transfusedplasma/PPF/Albumin -inhibited by ACE
Inhibitor Activation by prekalleikrein activator in
plasma
A/s with large volumes TPE etc
Also seen in Certain leukoreduction filters
Dialysis membranes
Immunoabsorption columns
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Febrile NonHemolytic TransfusionReactions
Increase in body temperature of 1C or more
During or within several hours of transfusion
Unrelated to hemolysis, sepsis, or other known
causes of fever. Frequency 1 in 100
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SIGNS AND SYMPTOMS
Early in transfusion or delayed
Fever
Chills and Rigors
Important d/d bacterial contamination,HTR
RARELY..
HYPOTENSION
TACHYCARDIATACHYPNOEA,DYSPNOEA,CYANSIS AND COUGH
LEUKOPENIA
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MECHANISMS
1.Antibodies in recipient plasma (usually anti HLA)
Acts against transfused HLA carrying cells-Lymphocyte,Granulocyte,platelets.
Cytokine Release 2.Antibodies in donor plasma-Rare
Acts agains recipient cells
Cytokine release
3.Infusion of Cytokines already accumulated in plasmaduring storage.
H/O BLOOD TRANSFUSION
H/O PREGNANCY
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Treatment
Transfusion discontinued
IV line kept patent
Antipyretics Paracetamol
ANTIHISTAMINES Are not of Use-most FNHTRsdoesnt involve histamine release
Restart ?
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BACTERIAL CONTAMINATION
50-250 fold more risk than TTD
Important cause of transfusion morbidity and mortality
Immediate or hours later,depends on the load
Maximum with platelets-PC and PRP(room temperature) 1 in 1000
Staph epidermidis
Bacilleus cereus
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Frozen products
More with cryoprecipitate-cryobath
Pseudomonas cepacia
Pseudomonas aeruginosa
Less with frozen plasma-temperature
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Symptoms
Fever
Chills
Rigor
Tachycardia
Hypotension
Low back pain
SHOCK
DIC
Diagnosis
SEND THE UNIT FOR GRAM STAIN-
MAY NOT PICK UP CULTURE
BLOOD CULTURE OFPATIENT
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Treatment
Delay in diagnosis if symptoms occur hours later
Start IV antibiotics and other supportive treatment
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Prevention Blood bank
Careful donor selection,not even trace evidence of viremiaaccepted
Sterile phlebotomy
Diversion pouch Storage
Look for appearance of blood product-not useful much in plasma
Colour change
hemolysis
After thawing should not be kept outside>4 hrs Should not immerse in water for thawing
Take care when transporting
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Hemolytic Transfusion Reaction
IMMUNE
Donor antibodies
Alternate group
Error
Inventory
Infants
BMT Dangerous O
Irregular hemolysingantibodies in donor
NON IMMUNE
Lysed RBCs transfused
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TREATMENT
Stop and do not restart
PROMPT IDENTIFICATION AND TREATMENT
Send the unit and sample
Liberal fluids Keep urine flow rate 1ml/kg/hr
Furosemide 40-80 mg IV
Low dose dopamine
Antipyretics
No response ? Consult nephro
Watch for DIC
Document
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PREVENTION in case of plasmatransfusion
Careful in alternate groups-plasmareduction for other products
Titration whenever needed esp exchange
Minor cross match Donor selection
Avoid clerical and ID errors
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How to differentiate febrileReactions
FNHTR IHTR BACTERIALCONTAMINATION
FEVER,CHILLS FEVER,CHILLS FEVER,CHILLS
Mild to moderate subside
with antipyretic
All invg.NEGATIVE
ANTI HLA Ab +
Mild to Severe
MAY NOT RESPOND
DCT +
Ab screen positive
Mild to severe
May not respondto antipyretic
Evidence of HemolysisGRAM STAIN
CULTURE +
See the product
Other recipients
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TRALI
Non cardiogenic Pulmonary edema
1 in 5000 to 10,000
5-10% fatal
SIMILAR TO ARDS RDP
WBC
APHERESIS
FFP
CRYO
GRANULO
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TRALI
A /c respiratory insufficiency and sudden deterioration inlung function
Hypoxemia PaO2/FIO2
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Chest tightness
Breathlessness
Dry cough
Tachypnoea
Tachycardia
Hypotension
Widespread creps
on chestauscultation
Nausea
Dizziness
fever -may develop laterRigor -not always
Copious frothy tracheal exudate on
suction
Like lightly whipped egg white
Hall mark of severe TRALI
CHEST X RAY
Nodular ShadowingBAT WING pattern
(ARDS)
Hypoxia
Hypercapnea
Leukopenia
Anti HLA antibody
Normal BNP
PA occlusion Pressure less
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A Different Presentation
Typically with cellular components
Usually within 30 mt
Fever and chills
Transient respiratory dysfunction Pulmonary Edema Not always demonstrated
Hypertension not Hypo
Recovery within 1-2hrs
Anti HNA -2a?
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Mechanism of TRALI
Antibodies in donor react with recipient antigens
HLA class 1 or 11
HNA-neutrophil antigens
Antgens on Monocytes /pulmonarymacrophages/Platelets
Antibodies in Recipient reacts with donor antigens
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COMPLEMENT
Direct lung injury
C3 a C5a Histamine and serotonin
released from basophils&platelets
LEUCO
AGGLUTINATES
Clog the pulmonarycapillary bed
CAPILLARY DAMAGE
AND LEAK
INTERSTITIAL EDEMA
OF LUNG
FLUID IN ALVEOLAR
SPACE
TRALI
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2 HRS 24 HRS
TRALI
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Management
In all A /c pulmonary reactions transfusion should bestopped
TRALI-Should not be restarted even after symptomsabate
Correct hypoxemia
O2 therapy
Ventilatory assistance if necessary
Symptomatic Most patients recover within 2-4 days
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Prevention
Leuco reduced products
No need of special products if donorinduced-may not recur
Donor tracing-hence reporting isimportant
HLA crossmatch/antibody detection
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TACO-Transfusion AssociatedCirculatory Overload
More risk in
Cardiac insuffi ciency,
Renal impairment,
Chronic anemia. Restricted blood volumes-neonates
Elderly
More risk with rapid infusion
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SYMPTOMS AND SIGNS
Dyspnoea
Orthopnoea
Tachypnoea
Tachycardia Hyper tension
Crepitations
Raised JVP
ECG changes
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TREATMENT
Stop the transfusion.
If transfusion is critical use the slowest possiblerate
Sitting position Diuretics-(frusemide 40 mg)
O2 as needed
Severe overload
Phlebotomy ??!! Not prudent in anemia/hypoxemia
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PREVENTION
Rapid transfusion -into a patient who is not activelyhemorrhaging produces no benefit and can causeHarm
Infusion should be at a rate not to exceed 2 to 4mL/kg/hour
Patients at high risk of circulatory overload.
Rate should be lower (1 mL/kg/hour)
Furosemide can be given prophylactically
Aliquoting can be tried
Centrifugation and plasma removal
FEATURE TRALI TACO
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FEATURE TRALI TACO
BODY TEMPERATURE FEVER NO FEVER
BLOOD PRESSURE HYPOTENSION HYPERTENSION
RESPIRATORYSYMPTOMS
A/C DYSPNEA A/C DYSPNOEA
NECK VEINS UNCHANGED DISTENDED
AUSCULTATIONS RALES RALES,S3
CHEST RADIOGRAPHS DIFFUSE B/L
INFILTRATES
DIFFUSE B/L
INFILTRATES
P/A OCCLUSIONPRESSURE
18mm Hg
RESPONSE TO
DIURETICS
MINIMAL SIGNIFICANT
WHITE CELL COUNT TRANSIENTLEUKOPENIA
UNCHANGED
BNP 1200 pg/ml
LEUKOCYTES DONOR LEUKOCYTEANTIBODIES PRESENT
MAY/MAY NOT BEPRESENT
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SPECIAL SITUATIONS
Citrate toxicity
Hypothermia
Inhibitor formation
Air embolism-very rare now
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Transfusion TransmittedDiseases
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HIVHBV
HCV
HTLV
CMV
EBV
HHV-8
HAV
HEV
GBVParvovirus B 19
SEN
Torgue Teno Virus
DENGUE
LCMV
SARS
SFVWNV
COAGULASE NEGATIVESTAPH,S.AUREUS.B.CEREUS
SERRATIA
YERSINIA
ENTEROBACTER
E COLI
PSEUDOMONAS
PRIONS
TREPONEMA
PALLIDUM
BORRELIA
PLASMODIUM
BABESIA
LEISHMANIA
T.CRUZI
RICKETTSIAE
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HBV-1:65000-1 lakh
HCV-1:5 lakh
HIV-1:1,20000
Malaria -5-50/million
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Prevention
Avoid unnecessary transfusion
Use of latest screening technology in bloodbank
Careful donor selection Vaccination if available in risk population
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Transfusion RelatedImmunomodulation
Increased Recurrence of Resected Malignancies
Increased Risk of Postoperative BacterialInfection
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TRIM effects, postulated mediatorsof TRIM, and preventive strategies
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How to manage a TransfusionReaction
Stop the transfusion
Keep IV line open with saline
Try to diagnose the cause
Mild ?allergic/FNHTR R /o identification error
call BB and r/o clerical error
Restart within 30 mts if suspected allergic&
do not re start in case of suspicion manage according to provisional diagnosis
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Reaction Form
Name,IP,Ward,Unit
History of previous transfusions
Time of reception,time of transfusion Amount of transfusion
Reaction occurred at----hrs
Signs and symptoms
Clinical diagnosis of patients original disease Investigations sent
Enclose 3 cc plain and EDTA samples from a differentlimb
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Contra Indications
Absolute
Documented intolerance to plasma or itscomponents
IgA deficiency Relative
Cardiac failure,pulm.oedema
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Inappropriate use of Plasma
Inappropriate
Concerns-
Adverse Effects Conservation
Inability to provide adequate dose to thepatient
Not it l f or
rti l r occasion
Not ing it atiscorr ct or roper
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WHY?
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WHAT TO DO?
WE SHALL SORT OUTTOGETHER!
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BLOOD IS ALSO COSTLY!!!
BLOOD BAG
Screening
Cross matching
Others
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Inappropriate Use of Plasma
Hypovolemia
Hypoproteinemia
Correction of abnormal laboratory parametersin the absence of bleeding
Correction of single coagulation factordeficiency for which factor concentrate isavailable
Nutritional deficiency
Vitamin K deficiency when there is time to
correct with vit.K Wound infection
Treatment of immune deficiency states
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Hypovolemia
Upto 30% blood loss can be managed without blood
Non protein colloids can be used unlesscontraindicated
Even after >30% blood loss,RBC will suffice FFP only in the setting of massive transfusion
Co-Existing Coagulopathy as evidenced byabnormal PT,aPTT
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Hypovolemia-Non Haemorrhagic
First line Crystalloids
Colloids if unresponsive
Specific Need for albumin only if hetastarch,dextran
etc are contraindicated Albumin rapidly decreases even after administration
in septic shock
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C/c Hypoproteinemia
Causes Defective Albumin Production
Malnutrition Mal absorption Liver disease etc
Excessive loss thro excretion Nephrotic syndrome Protein losing enteropathy Cirrhosis
Increased protein catabolism
Thyrotoxicosis Pancreatitis Common in critically ill,c/c diseases Think of Analbuminemia HAS
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How to minimise
Determine the underlying cause and treat
Restrict for A/c complications of c/c hypoalbuminemia,largevolume paracentesis etc
Improve circulating protein levels by dietary means Hypoalbuminemia need not be corrected to completely
normal levels
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Plasma in Albumin Correction
Universally opposed
TTD risk
Difficult to give adequate correction with plasma
Deficit in gX2Xplasma volume inlitres
5x2X2.5=25 g
PV=.07XwtX(1-Hct)
500 ml
albumin5%=25g
1 U SDP=4-6g
SDP
25/6=4.2 UALBUMIN
1U
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Correction of factor Deficiency
Should not use plasma if a factor concentrateavailable
Proper timing can reduce the usage
Exposure to large number of donors needed toprovide adequate dosage
Cost benefit
Difficulty in procuring the donors
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Nutritional & immunodeficiencystates
Oral and parenteral nutritionalsupplements freely available
Immunoglobulins much saferand effective forimmunodeficiency states
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Wound Infection
Earlier studies have shown equivocal results
Slight benefit of correcting the albumin so as toreduce edema and tissue tension
An array of alternate options-Antibiotics
Inadequate dosing
TRIM
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Reconstitution of whole blood
Reconstitution was earlier used
To reduce viscosity
In trauma
Still used in exchange transfusion-plasmais indicated
Not justified in absence of coagulopathy
Rarely used these days
Indications of whole blood itself is rare
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