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TRANSFUSION THERAPY Dr.Sajid Nomani Deptt. Of Emergency medicine, Peerless hospital and B.K.Roy research centre Kolkkata.

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Page 1: Transfusion therapy

TRANSFUSION THERAPY

Dr.Sajid NomaniDeptt. Of Emergency medicine,Peerless hospital and B.K.Roy research centreKolkkata.

Page 2: Transfusion therapy

???………….A mcqA 22 yr old man sustain multiple penetrating wounds to

upper rt.chest,his wounds are all above the nipple. He is

intubated,closed tube thoracostomy is performed, and

1500ml of blood has drained from rt.chest,2 liters of

crystalloid are infused. His BP is now 60/?,HR-160b/m

The most appropriate next step in managing this pt. is

a. Perform FAST

b. Obtain a CT chest

c. Perform an angiography

d. Arrange transfusion & transfer to OT.

e. Infuse colloids

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15thJune 1667 – Jean Baptiste Denys

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Early 1800’sFirst successful human-human transfusion

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1902– Karl Landsteiner

Won the 1930 Nobel Peace Prize

Isolated the A, B, & O blood types.

Type AB blood was identified two years

later.

Beginning of safe and effective transfusion medicine

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RELATIONSHIP BETWEEN BLOOD TYPE & ANTIBODIES

Blood type Antigen on RBC Can donate to

Antibodies in serum

Can receive from

A A A & AB ANTI B A ,O

B B B & AB ANTI A B ,O

AB A &B AB NONE A ,B,O

O NONE ALL ANTI A & ANTI B O

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Well, it gets more complicated here, because there's another antigen to be considered –

the Rh antigen.

• Rh was 1st identified of a rhesus monkey → rhesus factor

• A person with Rh factor on his RBC said to be Rh+ve• Will not make anti Rh antibodies

• A person with out Rh factor on his RBC said to be Rh –ve• This will produce anti Rh antibodies

• Rh incompatibility dangerous in pregnancy.

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Term &Definitions

BLOOD PRODUCT :Any therapeutic substance prepared from human blood

WHOLE BLOOD :Unseparated blood

BLOOD COMPONENT : A constituent of blood ,separated from Red cell concentrate

PRBC

FFP

PLATELETS

CRYOPRECIPITATE

→ Leucoreduced / Irradiated / washed

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Why Separation of blood components ????

• The storage life of whole blood is less than that of individual components

• Allows optimal survival for each component.

• Allows transfusing specific blood components.

• Several patients can be treated from one unit.

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Decision making

• Whom to transfuse?

• What to transfuse?

• How much to transfuse?

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So…whom you would transfuse !!!!

i. 23 yo asymptomatic, healthy woman with menorrhagia,Hb 8.0 g/dl,MCV- 72 fl

ii. 61 yo,k/c/o Htn,with severe gram negative sepsis – BP-100/70,cold periphery,AMS & Hb 8.0 g/dl.

iii. 54 yo woman post hemicolectomy Hb 8.0g/dl.

iv. 73 yo man presenting with acute upper GI bleed; BP 80/60, Pulse 120 thready – Hb 8.0 g/dl,MCV- 90fl

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Objectives of transfusion therapy

• Maintain blood volume

• Maintain O2 carrying capacity

• Maintain coagulation

• Red Cell Transfusion SHOULD not be solely used as a ‘plasma expander’ – but primarily as a method to increase oxygen carrying capacity.

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So…what is threshold for transfusion ???

• Difficult to set a transfusion threshold that holds true for all patients.

• Depends upon clinical status & co-morbidities.

• Use "10/30“ rule.

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STATEMENT

American society of Anaesthesiologists (ASA) state that:

“Red blood cell transfusion is rarely indicated when the hemoglobin concentration is greater than 10 g/dl and is almost always indicated when it is less than 6 g/dl”

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 Transfusion guidelines have been published by the following societies:

• American Society of Anesthesiology

• British Committee for Standards in Hematology

• Australian and New Zealand Society of Blood Transfusion

• Eastern Association for Surgery of Trauma (EAST) & American College of Critical Care Medicine of the Society of Critical Care Medicine (SCCM)

• European Society of Cardiology (ESC)

• AABB (formerly the American Association of Blood Banks)

• American College of Physicians

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Some recommended threshold

• Hgb <6 g/dL – Transfusion recommended .

• Hgb 6 to 7 g/dL – Transfusion generally likely to be indicated

• Hgb 7 to 8 g/dL – Transfusion should be considered in postoperative surg.pts.

• • Hgb 8 to 10 g/dL – Transfusion generally not indicated, but should be

considered for some populations (eg, those with symptomatic anemia, ongoing bleeding, acute coronary syndrome with ischemia)

• Hgb >10 g/dL – Transfusion generally not indicated except in exceptional circumstances

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• Transfusion Requirements in Critical Care (TRICC)

Hebert PC, et al. N.Engl J Med. 1999;340(6):409-17

A multicenter, randomized, controlled clinical trial of transfusion requirements in

critical care has demonstrated that you can adopt a

• transfusion threshold of 7 g/dL and maintain critically ill

patients between 7 and 9 g/dL

• Patients with acute MI and unstable angina may possibly

benefit from Hb> 8 g/dL

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Blood component…..Doses , Indications & Response

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component indication Approx / U typical doses

Doses effects

PRBC1 U=250ml

Acute ongoing hemorrhageSever symptomatic anaemia

RBC-80% Hct-70%

2 units or 15ml/kg

↑Hb-2gm/dl↑Hct-6%

Platelets1 U=250ml

<10000/mm3 in asymptomatic pt.<20000/mm3 in major bleeding<50000/mm3 for invasive procedure<100,000/mm3 with neoro/cardiac surgery

1 unit or 5 mL/kg

↑50,000/mm3 but less in many cases(↑consumption/Active thrombosis/Destruction due to plt.antibodies.)

3–6 x 1011

FFP1 U=250 ml

1 u of each coagl.factor & Fibrinogen-2mg/ml

Coagulation Factor deficiency, fibrinogen replacement, DIC, liver disease, exchange transfusion massive transfusion, warfarin overcoagulation effect

Cryoprecipi-tate

1U=50ml

Four units or 15 mL/kg

Raises most coagulation factors levels approx. 20%

Fibrinogen / factor VIII / vWF / factor XIII /fibronectin.

10 units or 1 unit/5 kg

Raises fibrinogen 75 milligrams/dL

Bleeding with a fibrinogen level of <100 milligrams/dLFibrinogen deficiency vonWillebrands DiseaseFactor VIII or XIII deficiency

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Special processing of RBC

leukocyte-reduced PRBCs•↓nonhemolytic febrile reactions.•↓ risk of virus transmission.•to prevent sensitization in pt. for bone marrow transplantation

Irradiated PRBCs should be considered in transplant patients, neonates, and immunocompromised patients

washed PRBCs•↓risk of anaphylaxis in IgA deficient pt.•↓risk of reaction in pt.with recurrent / severe allergic reaction to blood products.

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Massive Transfusion

• 10 units of PRBCs within a 24-hour period.

• Replacement of a blood volume equivalent within 24hr

• >10 unit within 24 hr

• Transfusion > 4 units in 1 hr

• Replacement of 50% of blood volume in 5 hrs

• A rate of loss >150ml/hr

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Importance of Massive Transfusion

• 39% of trauma related deaths – uncontrollable bleeding (Leading cause of preventable death)

• 2% of trauma patients – need massive transfusion

• Bleeding 2 main causes• Vascular injury (surgical)• Coagulopathy (non-surgical)

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Lethal triad

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So.....What is Haemostatic /damage control Resuscitation?

• A ground breaking concept!

• Prevents post traumatic coagulopathy

• Aims to reduce use of blood products in the intensive care phase.

Expert’s openion

RBC:FFP:PLT1:1:1

TraditionallyPLT: <50,000/mm3

FFP : INR >1.5Crypts : fibrinogen

<100ml/dl

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Evidence of Haemostatic Resuscitation

• Massive transfusion practices around the globe and a suggestion for a common massive transfusion protocol Debra L Malone, John R Hess, Abe Fingerhut ;The Journal of trauma. 01/07/2006; 60(6 Suppl):S91-6.

Suggested – RBC:FFP - 1:1

• Indications for early fresh frozen plasma, cryoprecipitate, and platelet transfusion in trauma

Lloyd Ketchum, John R Hess, Seppo Hiippala; The Journal of trauma. 01/07/2006; 60(6 Suppl):S51-8.

Early use of FFP,PLT - ↓ incidence of coagulopathy

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Transfusion’s Complications

• Up to 20% may lead to some type of adverse reaction.

• Mostly within 24 h.

• Most are minor reactions./ don’t miss the life threatening

• Acute vs Delayed reaction.

• Infectious & non infectious.

• Difficult to recognized in Critically ill patient

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Acute Transfusion Reactions

• Hemolytic Reactions (AHTR)

• Febrile Reactions (FNHTR)

• Allergic Reactions

• TRALI

• Coagulopathy with Massive transfusions

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AHTR

1 to 4 per 1 million units transfused.

Most commonly by ABO incompatibility.

Transfused cells are destroyed

↓ ↓ ↓

Activation of the coagulation system

with DIC & release of Anaphylotoxins & other vasoactive amines

↓ ↓ ↓

• High fever/chills

• Hypotension

• Back/abdominal pain

• Oliguria / Hemoglobinuria

• Dyspnea

• Pallor

• requires a high degree of suspicion in critically ill

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What to do? If an AHTR occurs

• STOP TRANSFUSION

• A /B /C’s

• Maintain IV

• Give diuretic

• Blood & urine transfusion reaction workup

• Send remaining blood back to Blood Bank

Renal st-BUN/ Creat

Coagl.st-PT/aPTT/fibrinogen/plt.

Hemolysis-Bill/LDH/haptoglobin

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Febrile transfusion reaction

Commenst among all

1 per 300 units of PRBC infused & 20% of plt.infusion.

Result from a combination of recipient antibody against donor leukocytes and the release of cytokines that are produced during storage.

Pretreatment with acetaminophen can mask this reaction.

• Rise in patient temperature >1°C

(associated with transfusion without other fever precipitating factors)

• fever / chills,

• Headache / myalgias,

• Tachycardia /dyspnea /chest pain.

• difficult to differentiate from more serious hemolytic transfusion reaction or sepsis.

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What to do?If an FNHTR occurs

• STOP TRANSFUSION

• Use of Antipyretics

• Suspect and manage as AHTR

• Initially difficult to distinguish between the two.

• Use of Corticosteroids for severe reactions

• Use of Narcotics for shaking chills

• Future considerations

• May prevent reaction with leukocyte filter.

• Use single donor platelets

• Use fresh platelets.

• Washed RBC’s or platelets

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Transfusion Related Acute Lung injury (TRALI)

• Clinical syndrome similar to ARDS

• Transfusion related noncardiogenic pulmonary edema

• Usually after FFP & Platelets transfusion

• Rare but , most common cause of transfusion related death

• Caused by WBC antibodies present in donor blood that result in pulmonary leukostasis

• Occurs 1-6 hours after receiving plasma-containing blood products

• High mortality

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TRALI Criteria

• Acute onset dyspnea during or within 6 hours of

transfusion

• Clinical evidence of hypoxemia

• Bilateral infiltrates on frontal chest radiograph

• No evidence of left atrial hypertension (i.e. circulatory overload)

• Absence of other attributable causes

Treatment is supportive

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DELAYED REACTION

• Alloimmunization

• Transfusion Associated Graft Verses Host disease (GVHD)

• Iron Overload

• Transfusion Transmitted Infection

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Alloimmunization

• Can occur with erythrocytes or platelets• Erythrocytes

• Antigen disparity of minor antigens (Kell, Duffy, Kidd)• Minor antigens D, K, E seen in Sickle patients

• Platelets• Usually due to HLA antigens• May reduce alloimmunization by leukoreduction

(since WBC’s present the HLA antigens)

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Transfusion Associated GVHD

• Mainly seen in infants

• Etiology—Results from engraftment of donor lymphocytes of an immunocompetent donor into an immunocompromised host

• Symptoms—Diarrhea, skin rash, pancytopenia

• Usually fatal—no treatment

• Prevention—Irradiation of donor cells

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Etiology Estimated Frequency: One Infection per Number of Units Transfused

HIV-1 1 per 2–3 million

HIV-2 Unknown, but extremely low

Human T-cell lymphotrophic virus type I and II

1 per 640,000

Hepatitis B 1 per 100,000–200,000

Hepatitis C 1 per 1–2 million

Parvovirus B19 1 per 10,000

Bacterial sepsis 1 per 6 million platelet concentrates

  1 per 500,000 packed red blood cells

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• THANKS YOU