Hemorrhage-and-Blood-transfusion pdf - dr ahmed saleem

Dr. Ahmed Saleem

FICMS

TUCOM / 3rd Year / 2015

HEMORRHAGE AND BLOOD TRANSFUSION

Hemorrhage is the escape of blood from the cardiovascular system, externally or internally.
Hemorrhage must be recognized and managed aggressively to reduce the severity and duration of shock
and avoid death and/or multiple organ failure. Hemorrhage is treated by arresting the bleeding – not by
fluid resuscitation or blood transfusion alone; attempting to resuscitate patients who have ongoing
hemorrhage without concurrent arresting of bleeding will lead to physiological exhaustion (coagulopathy,
acidosis and hypothermia) and subsequently death.

Pathophysiology

Hemorrhage leads to a state of hypovolemic shock. The combination of tissue trauma and hypovolemic
shock leads to the development of an endogenous coagulopathy called acute traumatic coagulopathy (ATC)
and it is associated with a four-fold increase in mortality. Ongoing bleeding with fluid and red blood cell
resuscitation leads to a dilution of coagulation factors which worsens the coagulopathy. In addition, the
acidosis induced by the hypoperfused state leads to decreased function of the coagulation proteases,
resulting in coagulopathy and further hemorrhage. The reduced tissue perfusion includes reduced blood
supply to muscle beds. Underperfused muscle is unable to generate heat and hypothermia ensues.
Coagulation functions poorly at low temperatures and there is further hemorrhage, further hypoperfusion
and worsening acidosis and hypothermia. These three factors result in a downward spiral leading to
physiological exhaustion and death. Medical therapy has a tendency to worsen this effect. Intravenous
blood and fluids are cold and exacerbate hypothermia. Further heat is lost by opening body cavities during
surgery. Surgery usually leads to further bleeding and many crystalloid fluids are themselves acidic (e.g.
normal saline has a pH of 6.7). Every effort must therefore be made to rapidly identify and stop
hemorrhage, and to limit physiological exhaustion from coagulopathy, acidosis and hypothermia.

Classification



According to the source:

 Arterial hemorrhage is recognized as bright red blood, spurting as a jet which rises and falls

in time with the pulse.

 Venous hemorrhage is a darker red, a steady and copious flow. The color darkens still further

from excessive oxygen desaturation when blood loss is severe, or in respiratory depression
or obstruction. Blood loss is particularly rapid when large veins are opened, e.g. common
femoral or jugular. Venous bleeding can be under increased pressure as in asphyxia, or from
ruptured varicose veins. Portal vein pressures are high enough to cause rapid blood loss,
especially in portal hypertension with esophageal varices. Pulmonary artery hemorrhage is
dark red (venous blood) at around 30 mmHg, whereas bleeding from the pulmonary veins is
bright red (oxygenated).

 Capillary hemorrhage is bright red, often rapid, ooze. If continuing for many hours, blood

loss can become serious, as in hemophilia.

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

According to the presentation:

 Revealed hemorrhage is obvious external hemorrhage, such as exsanguination from an open

arterial wound or from massive hematemesis from a duodenal ulcer.

 Concealed hemorrhage is contained within the body cavity and must be suspected, actively

investigated and controlled. In trauma, hemorrhage may be concealed within the chest,
abdomen, pelvis, retroperitoneum or in the limbs with contained vascular injury or
associated with long-bone fractures. Examples of non-traumatic concealed hemorrhage
include occult gastrointestinal bleeding or ruptured aortic aneurysm.



According to the time after insult:

 Primary hemorrhage is hemorrhage occurring immediately due to an injury (or surgery).
 Reactionary hemorrhage is delayed hemorrhage (within 24 hours) and is usually due to:

1.  Dislodgement of clot by resuscitation.
2.  Normalization of blood pressure and vasodilatation.
3.  Technical failure, such as slippage of a ligature.

 Secondary hemorrhage is due to sloughing of the wall of a vessel. It usually occurs 7–14 days

after injury and is precipitated by factors such as infection, pressure necrosis (such as from a
drain) or malignancy.



According to the causative pathology:

 Surgical hemorrhage is due to a direct injury and is amenable to surgical control (or other

techniques such as angioembolization).

 Non-surgical hemorrhage is the general ooze from all raw surfaces due to coagulopathy and

cannot be stopped by surgical means (except packing). Treatment requires correction of the
coagulation abnormalities.

Assessment of the blood loss

The adult human has approximately 5 liters of blood (70 mL/kg children and adults, 80 mL/kg neonates).
Estimation of the amount of blood that has been lost is difficult, inaccurate and usually underestimates the
actual value.

 External hemorrhage is obvious, but it may be difficult to estimate the actual volume lost.
 In the operating room, blood collected in suction apparatus can be measured and swabs soaked in

blood weighed.

 The hemoglobin level is a poor indicator of the degree of hemorrhage as it represents a

concentration and not an absolute amount. In the early stages of rapid hemorrhage, the hemoglobin
concentration is unchanged (as whole blood is lost). Later, as fluid shifts from the intracellular and
interstitial spaces into the vascular compartment, the hemoglobin and hematocrit levels will fall.

Treatment should therefore be based upon the degree of hypovolemic shock according to vital signs,
preload assessment, base deficit and most importantly, the dynamic response to fluid therapy.

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Management



Identify hemorrhage
External hemorrhage may be obvious, but the diagnosis of concealed hemorrhage may be more
difficult. Any shock should be assumed to be hypovolemic until proved otherwise, and similarly,
hypovolemia should be assumed to be due to hemorrhage until this has been excluded.

Shock



Hypovolemia?



Hemorrhage?



Immediate resuscitative manoeuvres
  Direct pressure should be placed over the site of external hemorrhage.
  Airway and breathing should be assessed and controlled as necessary.
  Large-bore intravenous access should be instituted and blood drawn for cross-matching.
  Emergency blood should be requested if the degree of shock and ongoing hemorrhage warrants

this.



Identify the site of hemorrhage
Once hemorrhage has been considered, the site of hemorrhage must be rapidly identified. Note this
is not to definitively identify the exact location, but rather to define the next step in hemorrhage
control (operation, angio-embolization, endoscopic control).

 Clues may be in the history (previous episodes, non-steroidal therapy for gastrointestinal (GI)

bleeding) or examination (nature of blood – fresh, melaena; abdominal tenderness, etc.).

 For shocked trauma patients, the external signs of injury may suggest internal hemorrhage, but

hemorrhage into a body cavity (thorax, abdomen) must be excluded with investigations
appropriate to the patient’s physiological condition. Rapid bedside tests (US, X-ray) are more
appropriate for profound shock and exsanguinating hemorrhage than investigations such as
computed tomography (CT) which take time.



Hemorrhage control

 The bleeding, shocked patient must be moved rapidly to a place of hemorrhage control. This

will usually be in the operating room but may be the angiography or endoscopy suites. These
patients require surgical and anesthetic support and full monitoring and equipment must be
available.

 There should be no unnecessary investigations or procedures prior to hemorrhage control to

minimize the duration and severity of shock. This includes prolonged attempts to volume
resuscitate the patient prior to surgery, which will result in further hypothermia and clotting
factor dilution until the bleeding is stopped.

 Attention should be paid to correction of coagulopathy with blood component therapy to aid

surgical hemorrhage control.

 Surgical intervention may need to be limited to the minimum necessary to stop bleeding and

control sepsis. More definitive repairs can be delayed until the patient is hemodynamically
stable and physiologically capable of sustaining the procedure. This concept of tailoring the
operation to match the patient’s physiology and staged procedures to prevent physiological
exhaustion is called ‘damage control surgery’.

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BLOOD TRANSFUSION

Human blood replacement therapy was accepted in the late nineteenth century. This was followed by the
introduction of blood grouping (A, B, and O groups and Rh grouping). Whole blood was considered the
standard in transfusion until the late 1970s, when goal-directed component therapy began to take
prominence. This change in practice was made possible by the development of improved collection
strategies, testing for infection, and advances in preservative solutions and storage.

Blood and blood products

Blood is collected from donors who have been previously screened to exclude any donor whose blood may
have the potential to harm the patient, up to 450 ml of blood is drawn, a maximum of three times a year.
Each unit is tested for evidence of hepatitis B, hepatitis C, human immunodeficiency virus (HIV). The ABO
and Rhesus D blood group is determined. The blood is then may be processed into sub-components.



Whole Blood

 Banked whole blood: All blood for transfusion must be stored in special blood bank

refrigerators. Blood allowed to stand at high temperatures for more than 2 hours is in danger of
transmitting infection. At least 70% of the transfused erythrocytes remain in the circulation for
24 hours after transfusion and are viable. The changes in the red blood cells that occur during
storage include reduction of intracellular ADP and 2,3-diphosphoglycerate, which alters the
oxygen dissociation curve of hemoglobin and results in a decrease in oxygen transport. Although
all clotting factors are relatively stable in banked blood except for factors V and VIII, banked
blood progressively becomes acidotic with elevated levels of lactate, potassium, and ammonia.
The hemolysis that occurs during storage is insignificant.

 Fresh whole blood: refers to blood that is administered within 24 hours of its donation.

Advances in testing for infectious disease now make fresh whole blood another option. An
advantage to the use of fresh whole blood is that it provides greater coagulation activity than
equal units of component therapy.

 Autologous blood: It is possible for patients undergoing elective surgery to predonate their own

blood up to 3 weeks before surgery for retransfusion during the operation.



Packed red cells
Packed red blood cells are cells that are spun down and concentrated. Each unit is approximately
330 ml and has a hematocrit of 50–70%.



Fresh-frozen plasma
Fresh-frozen plasma (FFP) is rich in coagulation factors; it is removed from fresh blood and stored at
–40 to –50

C with a 2- year shelf-life. It is the first-line therapy in the treatment of coagulopathic

hemorrhage.



Cryoprecipitate
Cryoprecipitate is a supernatant precipitate of FFP and is rich in factor VIII and fibrinogen. It is stored
at –30

C with a 2-year shelf-life. It is given in low-fibrinogen states or in cases of factor VIII

deficiency.



Platelets
Platelets are supplied as a pooled platelet concentrates containing about 250 × 10

cells per liter,

have a shelf-life of only 5 days. Platelet transfusions are given to patients with thrombocytopenia or
with platelet dysfunction who are bleeding or undergoing surgery.

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Indications for blood transfusion

Blood transfusions should be avoided if possible and many previous uses of blood and blood products are
now no longer considered appropriate. The indications for blood transfusion are as follows:



Acute blood loss, to replace circulating volume and maintain oxygen delivery.



Perioperative anemia, to ensure adequate oxygen delivery during the perioperative phase.



Symptomatic chronic anemia without hemorrhage or impending surgery.

Blood groups and cross-matching

Human red blood cells have many different antigens on their cell surface. Two groups of antigens are of
major importance in surgical practice – the ABO and Rhesus systems.



ABO system
These are strongly antigenic and are associated with naturally occurring antibodies in the serum.
The system consists of three allelic genes – A, B and O – which control the synthesis of enzymes that
add carbohydrate residues to cell surface glycoproteins. Expression of the A and B genes results in
specific residues being added whereas the O gene is an amorph and does not transform the
glycoprotein. The system allows for only four phenotypes (O, A, B and AB). Naturally occurring
antibodies are found in the serum of those lacking the corresponding antigen. Blood group O is the
universal donor type as it contains no antigens to provoke a reaction. Conversely, group AB
individuals are ‘universal recipients’ and can receive any ABO blood type as they have no circulating
antibodies.



Rhesus system
The Rhesus D [Rh(D)] antigen is strongly antigenic. Antibodies to the D antigen are not naturally
present in the serum of those lack the antigen but their formation may be stimulated by the
transfusion of Rh-positive red cells or they may be acquired during delivery of a Rh(D)-positive baby.

Cross-matching

To prevent transfusion reactions, all transfusions are preceded by ABO and Rhesus typing of both donor
and recipient blood to ensure compatibility. The recipient’s serum is then mixed with the donor’s cells to
confirm ABO compatibility and to test for Rhesus and any other blood group antigen–antibody reactions.
Full cross-matching of blood takes 45 min in most laboratories. In more urgent situations, ‘type-specific’
blood is provided, which is only ABO/Rhesus matched and can be issued within 10–15 min. When blood
must be given in an emergency, group O (universal donor) blood is given (O– to female patients, O+ to male
patients). When prescribing and administering blood it is essential that the correct patient receives the
correct transfusion. Two individuals should check the patient details against the prescription and the label
of the donor blood. Provided that these principles are strictly adhered to the number of severe and fatal
ABO incompatibility reactions can be minimized.

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Complications of blood transfusion

Complications from blood transfusion can be categorized as those arising from a single transfusion and
those related to massive transfusion.



Complications from a single transfusion

 Incompatibility hemolytic transfusion reaction: If antibodies present in the recipient’s serum are

incompatible with the donor’s cells, a transfusion reaction will result. This usually takes the form
of an acute hemolytic reaction. Severe immune- related transfusion reactions caused by ABO
incompatibility result in severe and potentially fatal complement-mediated intravascular
hemolysis and multiple organ failure.

 Febrile transfusion reaction: They are non-hemolytic and are usually caused by a graft-versus-

host response from leucocytes in transfused components. There is fever, chills or rigors.

 Allergic reaction.

 Infection:

– Bacterial infection (usually as a result of faulty storage).
– Hepatitis.
– HIV.

 Air embolism.

 Thrombophlebitis.

 Transfusion-related acute lung injury (usually from FFP).



Complications from massive transfusion

  Coagulopathy.
  Hypocalcemia.
  Hyperkalemia.
  Hypokalemia.
  Hypothermia.

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