PRE-TRANS FUSION TESTING

1       -Determination of recipient ABO group.

2       -Determination of  recipient Rh (D) type

3       -Determination  of recipient serum alloantibodies

4       -Crossmatch between patient serum & Donor RBCS

5       -Coomb s test: "not routine"

ABO         RBS                RBcs  Ab in serum

Group        Ag   

A               A                     Ant. - B

B               B                    Anti. - A

AB         A&B                 Neither

O            Nerther          AntiA & Anti. –B

6 - selection of blood product for transfusion:

#whole blood or RBcs:- all testing  needed

Rh + takes Rh- or Rh + 

Rh -   takes Rh –

#FFP or cyopr.   : same group ABO ,without rgard Rh

#plts :same ABO group pereferabl &Rh (same as whole blood.)

#Emergeny transfusion:

Bl group "o" : **Not give whole blood?

                         **female below 50 y.(give Rh – ebs)

Whole blood

                Packed  RBcs                                   plts   rich   plasma  

                       

                                                                  plts poor  plasma      plts

 

                                                                                     

Albumin         factor concentrate        ffp     cryoprecipitate       Ig (s)

whole blood transfusion:

*Indication: active bleeding (loss> 4o% of total blood)

                  Massive blood loss in sugery.

*one unit whole blood increases  Hgb by 1gmldl.

*Not used to supply  coagulation factors,Plts or Chronic anemia

Packed Rbcs:

*One unit increases Hgb by lgmldl

*Indication: chronic symptmatic anemia spesially  coronaryA.D.

                  Active bleeding  

*Not used to supply    Plts ,Adequate blood volume orcoauqulstion factors 

Random- donor plt concatenate:

1unit whole blood   gives bag of plts contains 70ml plasma

1unit      plts increases plts count by 5xl0⁹/L

Indication: 1- proplyact* no bleeding with plts<15-20xl0⁹/L* Before invasive operation with plts<50xl0⁹/L*Before invasive operation with abnormal plt functions

                 2- bleeding with plts<50xl0⁹/Lor abnormal plt functions

Not used in *plts disorders( uremia, Hyperglobulinemia ,VWD)

                    *Acceleratrd plt destruction *ITP

HLA matched plts

-by hemapharesis     - contain 3× 10¹¹ plts

-equal to 6:8 units radorn donor plt conc.

-Used in pt. need plts but refractory to plts Transfusion due to alloimmunization.

(against plts HLA Ag or Non HLA plts specific Ag)  

Factor Vlll concentcrate

hemophilia A

factor 1X  concentcrate

hemophilia B

hemophilia A wit inhibitors to factor Vlll

congenital decrease of factor Vll and X 

Cryoprecipitate

vwD, hypofibrinogenima, DIC

factor Vlll or lX deficiency

Albumin:-

1- Acute   volume    expansion

                       Hyov. Schock

                      Chronic Albumin depletion ( LC, Protein losing enteropathy)

2- longterm replacement (burn)

3- Cadiopulm. pypass priming

4- thesapeutic Plasmapharesis.

FFP.

-multiple coagul. facter (DIC ,Liver disease )

-Massive transfusion

-Specific coag. factor deficiency(antithrombin 111, ll, V, Vll)

 -warfarin overdose

Adverse  effects of transfusion:.

(1)            I mmune mediated adverse effects:-

1       Acute hemolytic transfusion reactions:

*Pathogenesis: transfusion of ABo incompatible whole bl. or RBcs

*c/p:. pain at tran. site, chest pain, back pain, fever, chills, nausia ,dyspnea ,oliguria hemoglobinuria, hypotension ,shock, excessive bleeding

*treatement- Discontinue

                    -Fluid &   diuretics :

                    - treat hypotension & promote Renal blood flow.

                     - treatDIC

Investigation: -indirect serum bilirub.increased

-LDH -direct antigloulin test (+)

2       Delayed hemolytic transfusion reaction

Pathogenesis. Immunization against RBS alloantigen

C/P:-

- Subclincal - unexplained  -Hgb decreased

-   Fever - chills - anemia -  Jundice

-   Hemoglobinuria

treatement: Renal function monitoring in Renal  diseased patient serious sequalae are infrequent.

Investigation: direct antigloulin test (+)

indirect antigloulin test (+)

3- febrile nonhemlytic transfusion reaction

Pathogenesis:

-        recipient develops cytotoxic antibodies against antigens on donor granulocyte, lymphocytes or platelets (leukoaggslutinins). Ag AB. interaction with complement activation, pyrogens release &fever.

                  -         Commonly seen in multitransfused pts.

C / p: -during or shortly after transfusion.

         -Fever chills or rigors

tretement: -Exclude hemolytic transf. reaction

    -         discontinue tran.

- Antipyretic.  

4- Non cardiogenic pulmonary oedama.

Pathogenesis:

Patient lenkoagglutinins leads to Ag – AB intcraction and leuckocytes aggregation  trarring  in pulmonary  Vasculature&increased vascular permeability.

C/P: fever ,chills, Acute pul. oedma.

         No evidence of lt ventricular dysfunction.

  tretement:- investigate causes of Apo

-        discontinue trans.

-        Rule out Acute hemolytic tran. reactions

-        I.V. steroids

-        Leukocyts free bl. products.

5- Allergic transfusion reaction

- **Urticarial reactions:

Pathogenesis:

Transfused soluble atopens (commm in those with history of allrgy), histamie release from IgE ore IgG coated mast cells.

C/P. pruritis – usually without fever

treatement . temporary interruption of trans.

Antihistaminics

**Anaphylactic reactions:

-   relatively rare – commm in IGA deficient pts

-   may occur after only small dose transfusion

tretement: stop transf.  ,tretement hypoten ,epinephrine

Prevention:- RBcs extensively washed &free of plasma

-   autologous donor program before elective surgery.

6       Allo imm unization:

Against alloantigenis compoments in blood products :

--- Allo immuniZation to RBcs Antigens:- (Acute or delayed hlytic reactions).

---Allo immuniZation to plts

*(Abs developed against plts associated HLA ,Ags leads to

Refractoriness to plts transfusion typically seen in multitramsfued pts ,tretement HLA matched plts.

*Abs develop againt plts specific Ags leads to

Neonatal alloimmune thrombocytopenia or Post transf. purpura: 5: 15 days after transf.tretement by plasma pharesis &   autologous transfusisn.

7- GVHD

c/p.

develop      30     days after transf.

fever                    ,liver dysfunction

diarrhea     ,         infections, pancytopenia.

* tretement:ATG,  steroids, methothexate.

Cyclosporine, bl. Products irradiation.

(2)  Infectious diseases transimission

*Viral:- hepatotropic, HCV,HBV,HDV

          -Herpes virus: CMV ,EBV

          Retro Virus:- HILV-1 (tropical Spastic  Parapares orAdult T cell leuk. Lymphoma.

                                -HIV (AIDS)

*Non Viral:

-Syphilis: (treponema pallidum)

-Brucellosis (brucella species)

                                                                  

-gram – ve  bact. Contamination             (Yersinia &E-coli)

-Malaria

-Chagas' disease (trypanosoma cruzi)

-Toxoplamosis (toxoplasma gondii)

-Babesiosis (babesia microti)

(3) Complications related to massive transfusion.

-Replacement of pt bl. Volume by stored bl. In less than 24  h.

-Necessary in trama, liver transplant, vascular surgery.

1- hemostatic abnormalities.

Dilution plts & coag. Factors in circulation. → DIC

tretement- replacement Of coag. factors &plts.

2- citrate toxicuty:

Hypocalcemia → cardiac dysfunction.

tretement: calcium.

3- hypothermia:

Massive tr. Of stored refrigerated bl. → candiac dysrrhythmia.

tretement– use warmer blovd.

4- K imbalance:

Hypokalemia If metabolic Alkalosis due to citsate.

Hyperkalemia. Due to ↑ plts & plasma k with storage. (uncommon)

5- Acid base imbalance:

Early → metabolic acidosis

Late → metabolic alkalasis

6. mechanical trauma  to BBs: → hemolysis.

(4) other Non immunologic complications.

1- circulatory overload:

In carliopulmanary compromised pts.

C/p: dyspnea ,cyanosis ,penipheral oedema.

tretement: discontinue, tretement overload,Slow infusion of single component.

2- hemosiderosis:

1unit RBCS → contain 200 mg iron.

Chronic Transf. → cardiac, endocrine&hepatic dysfunction.

tretement: iron chelating agents.

Alternatives to homologous blood Transfusion:

(1) Autologous bl. Transfusion:

Is: any bl. Component donated by intended recipient.

Benefits: (low risk of):

-   Alloimmunlzation

-   GVHD

-   Infections dis. transmission.

-   Febrile, hlytic, allergic reaction.

Categories:

(1) autologus whole bl. Or KBcs.

* preoperative donation:

- before elective surgery (anticipated  bl. loss)

- contraindication:

          - symptomatic angina, AS, Valvular HD.

          - recent seizures.

          - hematocrit ↓ 33%

          -

* Intraoperative hemodilution:

- in cardiopulmonary bypass procedure.

- 1 or 2 units of bl. Removed → replaced by colloid or crystalloid→ after surgery → transf. of autol. b1ood& diuretics (to ↓ plasma volume).

* Intra Operative bl. Salvage:

Ind.: anticipated intraoperative bl. Loss (cardiac, vascular, obest. surgry).

Contraind.: operations with gross contamination.

Complication: DIC, sepsis, henelysis, Embolism dissemination.

Teachniqe: aspiration of intraoperative  blood  At operation site,, contrifugation → wash RBs → reinfuse.

* post operative blood. salvage

Significant drainage form cavity as chest cavity drainge ,,collect blood during 24: 48 h postoenative → Filteration → reisfuse within 6h of collection

(2) Autologous plts transfusion.

Preoperative Collection by hemapharis → frozen for future use as anticipation of BM suppression during chemotherapy.

(3) autologous FFP or csuopercipitate.

Very uncommon indication.

(4) autologus concenterated fibrinogn.

Separated from autologus plasma.

(2) Growth factors:

Epo: ↑ RBs production& ↓ need RBs donation

GM- CSF or G – csf: stimulate hematopoiesis &used with BMT&chemotherapy.

(3) blood substitutes: