Complication

Transfusion
4 Agustus 2015
DARAH SEGAR:
umurnya 4 - 6 jam, masih berisi trombosit dan semua faktor k

DARAH BARU:
umumrnya 3 -4 hari, masih berisi trombosit dan faktor-faktor k

DARAH SIMPAN
umurnya sampai 21 hari. Berisi eritrosit, albumin, dan faktor-
Physiologically, haemodynamic compensatory mechanisms m

it is generally recommended that replacement of blood

components be guided by laboratory tests.
 Indications for blood transfusion

● Whole blood: blood loss > 1500ml, better than

PRBC + FFP.
● PRBC: blood loss < 1000ml.
● FFP: deficiency of coagulation factor and
protein, massive transfusion.
● PLT: thrombocytopenia, massive transfusion.
Hemolytic transfusion reactions occur when the recipient's
immune system encounters antigens from donor blood.
Antibodies may form in response to these antigens,
resulting in destruction of donor red blood cells (RBCs),
with sequelae leading to clinical manifestations of fever,
hypotension, rigors, acute respiratory failure, and acute
renal failure.

The type and screen are the first pretransfusion

compatibility tests performed and are used to identify the
patient's ABO group and Rh type and to detect expected
and unexpected antibodies in the patient's serum,
respectively.
Serologic crossmatch Transfusion medicine An
agglutination test that determines donor-recipient blood
compatibility.

Crossmatch (compatibility test)

- Major crossmatch:
- Patient serum which may contain antibodies is cross-
reacted against the donor's red cells and
- Minor crossmatch:
- Patient RBCs are incubated with donor serum, this is of
less clinical significance; it reveals donor antibodies
against uncommon antigens–eg Cw, -Wra, -Lia
Minor crossmatches, in truth, are rarely performed, for two
main reasons: First, transfused blood is screened for
unexpected (non-ABO) antibodies, so performing a minor
crossmatch to make sure that there is no non-ABO
antibody to cause a problem doesn't make a lot of sense
(the exception, of course, being a very low-incidence
antibody that might not show up on an antibody screen).
Second, since the volume of transfused serum is generally
small in comparison to the patient's blood volume, minor
incompatibilities are usually not of great consequence (for
example, a group O red blood cell transfusion to a group A
recipient would have a minor crossmatch incompatibility,
but is not contraindicated due to the very small amount of
incompatible antibody present in the unit of red cells.
The crossmatch is the final step of pretransfusion testing as
a routine procedure. A portion of donor blood is combined
with patient plasma or serum and is checked for
agglutination, which would signify incompatible blood. This
important step, also known as major crossmatch, serves as
the last guard to ensure a safe transfusion.

The crossmatch is routinely used as the final step of

pretransfusion compatibility testing. It serves 2
purposes: (1) to serve as a final check of ABO
compatibility between donor RBCs (RBCs) and patient
plasma or serum and (2) to detect clinically significant
antibodies that may have been missed by the antibody
screening test.
To perform the serologic crossmatch, 2 samples must be
collected, as follows:

- Donor RBCs from a "segment of tubing originally attached

to the blood unit container"
- The patient's plasma or serum
 Transfusion Reactions

• ANY unfavorable consequence is

considered a transfusion reaction of
blood TX

• The risks of transfusion must be

weighed against the benefits
Complications of blood transfusion

Early
Haemolytic reactions
Immediate
Delayed
Non-haemolytic febrile reactions
Allergic reactions to proteins, IgA
Transfusion-related acute lung injury
Reactions secondary to bacterial contamination
Circulatory overload
Air embolism
Thrombophlebitis
Hyperkalaemia
Citrate toxicity
Hypothermia
Clotting abnormalities (after massive transfusion)
Late
Transmission of infection
Viral (hepatitis A, B, C, HIV, CMV)
Bacterial (Treponeum pallidum, Salmonella)
Parasites (malaria, toxoplasma)
Graft-vs-host disease
Iron overload (after chronic transfusions)
Immune sensitization (Rhesus D antigen)
 Transfusion Reactions
1. Acute (<24 hours) Transfusion Reactions - Immunologic
– Hemolytic; Febrile-non hemolytic; Allergic; Anaphylactic; Transfusion
Reaction of Acute Lung injury(TRALI)
2. Acute Transfusion Reactions - Nonimmunologic
– Hemolytic (Physical or Chemical destruction of RBC); Circulatory
overload; Air embolus; Hypocalcemia; Hypothermia
3. Delayed (>24 Hours) Transfusion Reaction - Immunologic
– Hemolytic ; Graft vs. Host Disease; Posttransfusion Purpura
4. Delayed Transfusion Reactions - Nonimmunologic
– Iron Overload
5. Infectious Complications of Blood Transfusion
Current risk of transfusion-related infection after a unit of
screened blood in the UK

Infection Estimated risk per unit of transfused blood

- Hepatitis A Negligible
- Hepatitis B 1 in 100 000
- Hepatitis C <1 in 1 000 000
- HIV 1 and 2 <1 in 4 000 000
 Acute Transfusion Reactions
Immunologic

TX Reaction of Acute Lung Iinjury

Etiology:
• Acute onset of hypoxemia and pulmonary edema on
CX-RAY within 6 hrs of TX without evidence of
cardiac failure.
Mechanism’s
• Primary Suspect: Donor antibodies to recipient
WBCs
• Another cause: Biologically active lipids in the lungs
causing edema
Pathogenesis

- Two different mechanisms for the pathogenesis of TRALI

have been identified: immune (antibody-mediated) and non-
immune.
- Immune TRALI results from the presence of leucocyte
antibodies in the plasma of donor blood directed against
human leucocyte antigens (HLA) and human neutrophil
alloantigens (HNA) in the recipient. Antibodies present in the
recipient only rarely cause TRALI.
- In up to 40% of patients, leucocyte antibodies cannot be
detected in either donor or recipient.
- In these cases it is possible that reactive lipid products
released from the membranes of the donor blood cells act as
the trigger. This is known as non-immune TRALI.
Pathogenesis

The target cell in both forms of TRALI is the neutrophil granulocyte

On activation of their acute phase cycle, these cells migrate to the
Oxygen free radicals and other proteolytic enzymes are then relea
A pulmonary capillary leak syndrome develops with the exudation
The majority of reactions are severe, and often life threatening; 70
The mortality in non-immune TRALI is lower, and the syndrome is
 Transfusion Reaction of Acute Lung
Injury(TRALI)
• Symptoms
• Chills, fever, cough, cyanosis, hypotension,
increased difficulty breathing
• Prevention: For recipients : give male
products- For donors: watch/defer.
TRALI usually occurs within the first 2 hours following a
transfusion but has been reported up to 6 hours later.
It usually resolves within 24 -72 hours with supportive
therapy, including mechanical ventilation.

Of note, steroids and diuretics are not thought to be useful

in the management of these patients.

The mortality is quoted to be up to 10% and in fact it is the

third most common cause of transfusion related deaths.
The most common complications of transfusion are

- Febrile nonhemolytic reactions: Chill-rigor reactions

- The most serious complications, which have very high mortality rates, are:

Transfusion-associated circulatory overload

Transfusion-related acute lung injury

Acute hemolytic reaction due to ABO incompatibility

Early recognition of symptoms suggestive of a transfusion reaction and prompt reporting to th

The most common symptoms are chills, rigor, fever, dyspnea, light-headedness, urticaria, itc
If any of these symptoms (other than localized urticaria and itching) occur, the transfusion sh
The remainder of the blood product and clotted and anticoagulated samples of the patient’s b
Note : The unit in question should not be restarted, and transfusion of any previously issued u
Various definitions of massive blood transfusion (MBT)
have been published in the medical literature such as:

- Replacement of one entire blood volume within 24 h

- Transfusion of >10 units of packed red blood cells
(PRBCs) in 24 h
- Transfusion of >20 units of PRBCs in 24 h
- Transfusion of >4 units of PRBCs in 1 h when on-going
need is foreseeable
- Replacement of 50% of total blood volume (TBV) within 3
h.

In children, as a transfusion of more than 40 mL blood/kg

(blood volume of children older than neonates is
approximately 80 mL/kg)
 Definition of massive transfusion

● Massive transfusion is accompanied most frequently with

significant blood loss or shock.
● Although the volume of blood transfused may lead to a
variety of potentially serious problems, the duration and
severity of shock (hypoperfusion, acidosis, hypoxia) appears
to be the primary derterminant of mortality and morbidity.
 Initial Management

● Initial fluid resuscitation with colloid or crystalloid, which

begins to replete intravascular volume.
● Restoration of tissue oxygenation with RBC transfusion.
● Primary surgical treatment of bleeding source to achieve
hemostasis.
● Replacement of hemostatic components diluted during
massive transfusion.
oprecipitate and platelets units (random donor platelets) in ea
The complications associated with massive transfusion are d

- Number of units transfused

- Rate of transfusion
- Patient factors
Complications of massive transfusion include metabolic and
haemostatic abnormalities, immune haemolysis and air
embolism which can result in a patient presenting with
cardiac arrhythmia or cardiac arrest.

Massive transfusion is an independent risk factor for

developing multi-organ failure.
Some of the complications of massive transfusion include:

- Hypothermia
- Dilutional coagulopathy
- Hypocalcaemia, hypomagnesaemia, citrate toxicity
- Lactic acidosis
- Hyperkalaemia
- Air embolism

http://www.transfusion.com.au
Usual Adult Dose for Hypocalcemia
Intravenous:

500 to 2000 mg (5 to 20 mL) IV one time at a rate not to

exceed 0.5 to 2 mL/min. The dose may be increased as
needed. The usual daily dosage ranges from 1000 to
15,000 mg (10 to 150 mL) in divided doses or as a
continuous infusion. Doses may be repeated every 1 to 3
days as needed and tolerated to normalize the serum
calcium level.

Usual Adult Dose for Exchange Transfusion

300 mg (3 mL) IV one time with each 100 mL of citrated
blood at a rate not to exceed 0.5 to 2 mL/min.
rations in PRBCs can range from 7 to 77 mEq/L depending on

depend on the underlying renal function, severity of tissue

injury and rate of transfusion.
At transfusion rates exceeding 100-150 ml/min, transient
hyperkalaemia is frequently seen.
Also, acidosis secondary to hypoperfusion may worsen
hyperkalaemia.
Targets of resuscitation in massive blood loss:

- mean arterial pressure (MAP) around 60 mmHg

- systolic arterial pressure 80-100 mmHg (in hypertensive - -
- Hb 7-9 g/dl
- INR <1.5; activated PTT <42 s
- Fibrinogen >1.5-2 g/L
- Platelets >50 × 109/L
- pH 7.35-7.45
- Core temperature >35.0°C
- Base deficit <3.0/lactates <2 mEq/L.

Indian J Anaesth. 2014 Sep-Oct; 58(5): 590–595.

New evidence in trauma resuscitation - is 1:1:1 the answer?

Timothy E Miller

Miller Perioperative Medicine 2013, 2:13

rage, PRBCs have a pH below 7.0, and each unit has an acid
Damage control resuscitation
The concept of damage control resuscitation (DCR) was proposed in the mid

Damage control resuscitation involves:

1. Rapid control of surgical bleeding

2. Early and increased use of red blood cells, plasma and platelets in a 1:1:1

3. Limitation of excessive crystalloid use

4. Prevention and treatment of hypothermia, hypocalcemia and acidosis

5. Hypotensive resuscitation strategies

Miller Perioperative Medicine 2013, 2:13

Activated factor VII: The role of recombinant activated factor
VII (rFVIIa) to manage uncontrolled bleeding is unclear.
- considered as a rescue therapy in patients with life-
threatening bleeding that is unresponsive to standard
haemostatic therapy.
- recommended dose is 200 μg/kg initially followed by
repeat dose of 100 μg/kg at 1 h and 3 h.
Antifibrinolytic agents:
Drugs like tranexemic acid may be useful in bleeding complic
Early administration of tranexamic acid in bleeding trauma pa

Cell salvage:
Can be extremely useful in unanticipated blood loss and in pa
This strategy is generally reserved for massive blood loss in o
 Preparation for massive bleeding

Preparation for massive bleeding

Large bore intravenous (IV) access: Two peripheral IV (14/16
In emergency situations, canulation of external jugular vein m
Warming devices: In-line fluid warmers and surface warmers
Continuous core temperature monitoring
Invasive arterial pressure monitoring
Adequate amount of colloid (gelatins), crystalloid, infusion sets
and IV calcium preparations
Communication with blood bank about emerging massive
blood loss situation
Adequate manpower for sending samples for investigations
and getting blood and blood products
Point-of-care testing is highly desirable: Arterial blood gas
(ABG) and thromboelastograph (TEG).
ABG with haemoglobin (Hb), electrolyte and lactate levels,
repeated hourly, are useful in directing therapy
Rapid infusion pumps or pressure bags to speed the fluid
infusion rate
Laboratory monitoring:
Laboratory values should be obtained frequently. Recommen

Thromboelastography (TEG) is test of the visco elastic prope

Rapid availability of results helps in timely intervention.

Indian J Anaesth. 2014 Sep-Oct; 58(5): 590–595.

Thank You
Citrate toxicity: 80 ml of citrate phosphate dextrose
adenine solution present in each blood bag contains
approximately 3 g citrate.

A healthy adult can metabolise this load in 5 min.However,

hypoperfusion or hypothermia associated with massive
blood loss can decrease this rate of metabolism leading to
citrate toxicity.
Whole blood is deficient in clotting factors and has high
levels of potassium, ammonia, and hydrogen ions.

Although it provides volume expansion along with

increased oxygen-carrying capacity, there can be volume
overload before the needed components are replenished

J Emerg Trauma Shock. 2011 Jan-Mar; 4(1): 103–108.

Postpartum haemorrhage:
Recent studies suggest that acquired fibrinogen deficiency
may be the major coagulation abnormality associated with
obstetric bleeding which may be compounded by dilutional
coagulopathy and hyperfibrinolysis.