STBS
SHOCK HEMORRHAGE
AND BLOOD TRANFUSION
SHOCK
Shock is a systemic state of low tissue perfusion,
which is inadequate for normal cellular respiration.
With insufficient delivery of oxygen and glucose, and
cells switch from aerobic to anaerobic metabolism.
It is due to circulatory collapse and tissue hypoxia.
Causes
1. Hypovolemic Shock
Due to reduction in total blood volume. It may be due
to;
Hemorrhage
 External from wounds, open fractures.
 Internal from injury to spleen liver, mesentery or
pelvis.
Severe burns, which result in loss of plasma.
Peritonitis, intestinal obstruction.
Vomiting and diarrhea of any cause.
2. Cardiac Causes
Acute myocardial infarction, acute carditis.
Acute pulmonary embolism wherein embolus
blocks the pulmonary artery at bifurcation or one of
the major branches.
Drug induced.
Toxemia of any causes.
Cardiac surgical conditions, like valvular diseases,
congenital heart diseases.
Cardiac compression causes:
 Cardiac tamponade due to collection of
blood,pus, fluid in pericardial space which
prevents the heart to expand leading to shock.
 Trauma to heart.
3. Septic Shock
Is due to bacterial infection which release toxins
leading to shock.
CHAPTER
04
4. Neurogenic Shock
It occurs due to sudden anxious or painful stimuli
causing severe splanchnic vessel vasodilatation. Here,
patient either goes into cardiac arrest and dies or
recovers fully spontaneously.
5. Anaphylactic Shock
It is due to type 1 hypersensitivity reaction.
6. Respiratory Causes
Atelectasis (collapse) of lung.
Thoracic injuries.
Tension pneumothorax.
Anesthetic complications.
7. Other Causes
Acute adrenal insufficiency (Addison's disease).
Myxedema.
Pathophysiology
i. Cellular
As perfusion to the tissues is reduced, cells are
deprived of oxygen and must switch from aerobic to
anaerobic metabolism. Lactic acid is produced as a
result of anaerobic respiration; the accumulation of
lactic acid in the blood produces systemic metabolic
acidosis.
As glucose within the cells is exhausted, anaerobic
respiration ceases and there is a failure of Na+/k+
pump in the cell membrane and intracellular
organelles. Intracellular lysosomes release
autodigestive enzymes and cell lysis occurs.
Intracellular contents including potassium are
released into the bloodstream.
ii. Microvascular
Hypoxia and acidosis activate complement and
prime neutrophils, resulting in the release of
oxygen free radicals and cytokine release.
 STBS
SHOCK HEMORRHAGE AND BLOOD TRANFUSION
These mechanisms lead to injury of the capillary
endothelial cells, these in turn further activate the
immune and coagulation systems.
Damaged endothelium loses its integrity and
becomes leaky.
Spaces between the endothelial cells allow the fluid
to leak out and tissue edema occurs, exacerbating
cellular hypoxia.
iii. Systemic
Types of Shock
a. Cardiovascular
As preload and afterload decrease, there is a
1.Vasovagal Shock
compensatory baroreceptor response resulting
in increased sympathetic activity and release of
catecholamines into the circulation, this results in
tachycardia and vasoconstriction (except in the
sepsis).
2.Hypovolemic Shock (Commonest Type)
b. Respiratory
The metabolic acidosis and increased
sympathetic response result in an increased
respiratory rate and minute ventilation to
increase the excretion of C02 (and so produce a
compensatory respiratory alkalosis).
c. Renal
Decreased perfusion in the kidneys stimulates
renin angiotensin aldosterone axis, resulting in
further vasoconstriction and increased sodium
and water reabsorption by the kidney.
d. Endocrine
Vasopressin (antidiuretic hormone) is also
released from the hypothalamus in response to
decreased preload and results in
vasoconstriction and reabsorption of water in the
renal collecting system. Cortisol is also released
from the adrenal cortex, contributing to sodium
and water reabsorption and sensitizing the cells
to catecholamines.
3. Cardiogenic Shock
iv. Ischemia - Reperfusion Syndrome
During the period of systemic hypo perfusion,
cellular and organ damage progresses because of
the direct effects of tissue hypoxia and local
activation of inflammation. Further injury occurs
once normal circulation is restored to these tissues.
4 37
The cellular and humoral elements activated by the
hypoxia (complement, neutrophils, microvascular
thrombi) are flushed back into the circulation
where they cause further endothelial injury to
organs such as the lungs and kidneys. This leads to
acute lung injury, acute renal injury, multiple organ
failure and death. Reperfusion injury can currently
only be attenuated by reducing the extent and
duration of tissue hypoperfusion.
It is sudden dilatation of peripheral and splanchnic
vessels causing reduced cardiac output and
shock. Often it may be life threatening due to hypoxia.
Hypovolemic shock is caused by a reduced circulating
volume; hypovolemia may be due to hemorrhagic or
non hemorrhagic causes.
i. Non - Hemorrhagic Shock
Due to:
Poor fluid intake (dehydration).
Excessive water loss because of vomiting,
diarrhea, urinary loss.
Evaporation and third spacing seen in bowel
obstruction or pancreatitis.
Burns.
ii. Hemorrhagic Shock
Due to:
Injury to the liver, spleen.
Bone fractures.
Hemothorax.
Vascular injury.
Severe bleeding on table during surgeries of
thyroid, liver, portal vein or major vessels.
Occurs when 50% of ventricular wall is damaged by
infarction. It also leads to pulmonary edema and
hypoxia, further worsening cardiac damage. Acute
massive pulmonary embolism from a thrombus or
an air embolism (50 ml of air), obstructing more
than 50% of pulmonary vasculature leads to severe
shock and sudden death.
 38 4 SHOCK HEMORRHAGE AND BLOOD TRANFUSION
Tachycardia, hypotension, pulmonary edema,
raised JVP, gallop rhythm are the features.
4. Obstructive Shock
In obstructive shock there is a reduction of preload
because of mechanical obstruction of cardiac filling.
Common causes of obstructive shock are:
 Cardiac tamponade.
 Tension pneumothorax.
 Massive pulmonary embolism.
 Air embolism.
5.Distributive Shock
Distributive shock describes the pattern of
cardiovascular responses characterizing a variety of
conditions including septic shock, anaphylaxis and
spinal cord injury.
i. Neurogenic Shock
It is usually due to spinal cord injury which causes
dilatation of splanchnic vessels.
ii. Septic Shock
Septic shock may be due to gram positive
organisms, gram negative organisms, fungi,
viruses or protozoal origin.
Gram -ve septicemia / Gram -ve septic shock is
called as endotoxic shock. It occurs due to gram
negative bacterial infections commonly seen in:
 Strangulated intestines.
 Peritonitis.
 Gastrointestinal fistula.
 Biliary and urinary infections.
 Pancreatitis.
 Major surgical wounds, diabetic wounds and
crush injuries.
Stages of septic shock
a. Hyperdynamic (Warm) Shock:
This stage is reversible stage.
Patient is still having inflammatory response and so
presents with fever, tachycardia, and tachypnea.
Pyrogenic response is still intact.
Patient should be treated properly at this stage.
Based on blood culture, urine culture (depending
on focus of infection) higher antibiotics like third
generation cephalosporins, aminoglycosides, and
metronidazole are started.
STBS
The underlying cause is treated like draining the
pus, laparotomy for peritonitis, etc.
Ventilator support with ICU monitoring may
prevent the patient going for the next cold stage of
sepsis.
b.Hypodynamic Hypovolemic Septic Shock (Cold
Septic Shock)
Here pyrogenic response is lost.
Patient is in decompensated shock.
It is an irreversible stage along with MODS (multi
organ dysfunction syndrome) with anuria,
respiratory failure (cyanosis), jaundice (liver
failure), cardiac depression, pulmonary edema,
hypoxia, drowsiness, eventually coma and death
occurs (irreversible stage).
iii. Anaphylactic Shock (Vasodilation Due to
Histamine Release)
Injections penicillins, anesthetics, stings
venoms, and shellfish may be having antigens
which will combine with IgE of mast cells and
basophils, releasing large amount of histamine
and SRS-A (slow releasing substance of
anaphylaxis). They cause bronchospasm,
laryngeal edema, respiratory distress,
hypotension and shock. Mortality is 10%.
Rashes all over the body are commonly
observed.
Anaphylactic Shock (summary)
Sudden onset.
Distributive shock pattern.
Bronchospasm, laryngeal edema.
Generalized rashes and edema.
Hypotension, feeble pulse.
Mortality 10%.
To start adrenaline 100 ug IV, steroids, IV fluids,
oxygen with foot end elevation.
Ventilator in severe cases.
Cardiac massage, defibrillation.
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SHOCK HEMORRHAGE AND BLOOD TRANFUSION 4 39

Cardiovascular and Metabolic Characteristics Shock Index

of Shock It is the ratio of pulse rate to blood pressure. Normal is
Hypov- Cardio- Obstr- Distri- < 1.0. In shock, it reverses.
olemia genic uctive butive
Cardiac Output Low Low Low Low Clinical Monitoring
Vascular High High High High
Resistance a. Observation and Assessment of Person
Venous Pressure Low Low Low Low Restlessness, coldness, clamminess, cyanosis,
Mixed Venous Low Low Low Low
delayed capillary refill, and collapsed veins in hands
Saturation
High High High High
and feet indicate poor perfusion.
Base Deficit
Alertness, warmth, pinkness, rapid capillary refill
and distended veins indicate improvement.
Clinical Features of Shock
In Early Stages Tachycardia, sweating, cold b. Pulse
periphery, hypotension, Record the pulse rate and note any change in pulse
restlessness, air hunger, tachypnea, rate and character.
oliguria, collapsed veins.
In Late Stages Cyanosis, anuria, jaundice,
c. Blood Pressure
drowsiness.
Blood pressure gives a good indication of stroke
volume and therefore cardiac output.
Clinical Severity of Shock Diastolic pressure gives an indication of degree of
vasoconstriction and systolic pressure, the rigidity
1. Compensated Shock of main vessels in combination with
Compensated with mild tachycardia, normal blood vasoconstriction and stroke volume.
pressure, urine output, normal respiration and mild
lactic acidosis. d. Rate and Depth of Respiration
Persistent hyperventilation indicates that shock is not
2. Decompensated Shock being corrected adequately and it is a compensatory
Further loss of circulating volume overloads the mechanism going on to drop the PaCO2, so as to
body's compensatory mechanisms and there is
correct metabolic acidosis.
progressive renal, respiratory and cardiovascular
decompensation. Blood pressure is usually well
e. Urine Output
maintained and only falls after 30-40% of the
It is an indicator of renal blood flow, which is
circulating volume has been lost.
determined by cardiac output.
Paradox in severe sepsis:
3. Mild Shock
 Patient may pass 100-200 ml/hour inspite of
Mild shock with mild lactic acidosis, tachycardia,
being hypovolemic, often edematous and often
tachypnea and anxiousness. The peripheries are cool
with a high CVP and with pulmonary edema.
and sweaty with prolonged capillary refill times
 If fluids are restricted at this stage, BP and urine
(except in septic distributive shock).
output may fall suddenly.
4. Moderate Shock
f. Central Venous Pressure (CVP)
Moderate shock is with significant lactic acidosis,
This provides a simple method of assessing the
decreased urine, tachycardia, tachypnea, drowsiness
adequacy of patient's circulating volume and
and mild hypotension.
contractile state of myocardium.
Its response to small fluid challenge (200 ml of
5. Severe Shock
crystalloid or colloid) may assist in distinguishing
Severe lactic acidosis, anuria, tachypnea with gasping,
between cardiogenic and hypovolemic shock.
severe tachycardia, profound hypotension and
unconsciousness.
 40 4 SHOCK HEMORRHAGE AND BLOOD TRANFUSION
STBS

g. Pulmonary Capillary Wedge Pressure (PCWP)
It is a better indicator of both circulatory blood
volume and left ventricular function.
It differentiates between left and right ventricular
failure, pulmonary embolus, septic shock and
ruptured mitral valve.
h. Serial Blood Gases and Serum Electrolyte
Measurements
i. ECG
Differentiates cardiogenic shock from other types and
will reveal arrhythmias.
j. Chest X-Ray
May differentiate between pulmonary embolism,
mediastinal trauma and cardiac tamponade.
 Colloidal solutions: e.g. plasma protein fraction
(PPF), dextran, gelatin (haemacel).
4. Support Cardiovascular Function
a. Ionotropic Agents
They are most useful in reversing the effects of
cardiac depressant drugs (including anesthetics), or
for tiding over a patient until a metabolic
disturbance can be corrected or a mechanical
defect repaired.
b.Vasodilator Therapy
It is useful in cardiogenic shock, in patients with
pulmonary edema associated with low cardiac
output, and in shocked patients who remain
oliguric and vasoconstricted.

Investigations c. Diuretic Therapy

Blood CP, ESR. A powerful diuretic, e.g. frusemide (lasix) 40 80mg
Blood glucose. IV is required in cases of fluid overload.
Platelets, coagulation profile.
Urea, creatinine, electrolytes. 5. Ensure Adequate Oxygenation And Ventilation
Liver biochemistry. a. Maintain patent airway, which may need;
Blood gases. Oro-pharyngeal airway.
Acid base state. Endotracheal tube.
Blood cultures. Tracheostomy.
ECG. b. Administer oxygen.
Chest X-ray. c. Support respiratory function, which may need:
Continuous positive airway pressure.
Treatment Mechanical ventilation.

Treat Primary Problem

Hemorrhage
1. Control Hemorrhage
Classification
2. Treat Infection
Remove indwelling catheters.
1. Based on the Source of Bleeding:
Administer full doses of appropriate antibiotic.
Surgical exploration and drainage.
a. Arterial Hemorrhage
3. Restore Cardiac Output And BP It is bright red in color, spurting like a jet with pulse
of the patient.
Volume Replacement
This is essential in shock with hypovolemic state. b. Venous Hemorrhage
Circulating volume must be replaced quickly. It is dark red, steady and continuous flow.
Choice of fluid → Pulmonary arterial blood is dark red in color.
 Blood: should be given in shock from Pulmonary venous blood is bright red in color.
hemorrhage, as soon as possible.
STBS
SHOCK HEMORRHAGE AND BLOOD TRANFUSION 4 41

c. Capillary Hemorrhage 3. Based on the Type of Hemorrhage

Here bleeding is rapid and bright red. It is often
torrential due to continuous ooze. a. External (Revealed) Hemorrhage
It is visible external hemorrhage.
2. Based on the Time of Onset of Bleeding
b. Internal (Concealed) Hemorrhage
a. Primary Hemorrhage It constitutes internal hemorrhage, may occur
Occurs at the time of injury or operation. from;
Liver injury.
b. Reactionary Hemorrhage Spleen injury.
It occurs within 24 hours after surgery or after Fracture femur.
injury. Ruptured ectopic gestation.
Cerebral hemorrhage.
Precipitating Factors and Causes of Hemothorax.

Reactionary Hemorrhage 4. Based on the Duration of Hemorrhage

Precipitating Factors Common Causes a. Acute Hemorrhage

It is sudden, severe hemorrhage after trauma,
 Coughing.  Thyroid surgery.
surgery.
 Vomiting.  Cholecystectomy.
b. Chronic Hemorrhage
 Straining.  Major abdominal It is a chronic, repeated bleeding for a long period
surgeries. like in hemorrhoids, bleeding peptic ulcer,
carcinoma cecum etc.
 Rise of Blood pressure.  Hydrocele surgery. Patient present with chronic anemia with
hyperdynamic cardiac failure.
 Restlessness.  Circumcision.
They are in a state of hypoxia.
 Venous refilling during  Tonsillectomy. It is corrected by packed cell transfusion, not by
recovery from whole blood itself. Cause has to be treated
anesthesia. accordingly.
 Slipping of ligature.  Clot dislodgement.
c. Acute on Chronic Hemorrhage
It is more dangerous as the bleeding occurs in
c. Secondary Hemorrhage individuals who are already hypoxic, which may
It occurs in 7-14 days after surgery. get worsened faster.

Common Causes 5. Based on Possible Intervention

Erosion of carotid artery by cancer (secondaries
in the neck). a. Surgical Hemorrhage
Hemorrhoidectomy. Can be corrected by surgical intervention.
Inguinal block dissection.
Sloughing off part of arterial wall. b. Non-Surgical Hemorrhage
It is diffuse ooze due to coagulation abnormalities
Precipitating factors of secondary hemorrhage and DIC.
Infection.
Pressure by drain or bone malignancy.
A ligature in an infected area.
 42 4 SHOCK HEMORRHAGE AND BLOOD TRANFUSION
STBS

Classification of Hemorrhagic Shock Swelling in closed fractures

(Circulatory Failure)  Moderate swelling in closed fractures of tibia =
500-1500 ml.
 Moderate swelling in fractured shaft of femur =
Class Blood Loss Features 500-2000 ml.
I. Up To 15% (< 750 ml) Normal. Swab weighing
II. Blood Loss 15 – 30% Pallor, thirsty,  In operation theatre, swabs are weighed before
(750 – 1500 ml) tachycardia. and after use, and the total so obtained (1 gm =
III. Blood Loss 30 – 40% Hypotension,
1 ml) is added to volume of blood collected in
(1500 – 2000 ml). tachycardia
suction or drainage bottle. However this is 20%
Oliguria, confusion.
Rapid pulse, low
less than acute blood loss.
IV. Blood Loss > 40% BP, anemia,
(> 2000 ml) unconsciousness, 4. Hemoglobin Level
mods. There is no immediate change in hemoglobin, but
within a few hours, the level is lowered due to
hemodilution. (Intracellular and interstitial fluid is
Clinical Features of Hemorrhage transferred to vascular compartment to prevent
Pallor. circulatory collapse).
Cyanosis.
Tachycardia. 5. Blood Volume Determinants
Tachypnea (air hunger). Hematocrit reading will give the ratio of plasma to red
Cold clammy skin due to vasoconstriction. cells, and thus the total blood volume can be arrived
Dry face, dry mouth and goose skin appearance at.
(due to contraction of arrector pilorum).
6. Measurement of Central Venous Pressure (CVP)
Rapid thready pulse.
Oliguria.
Features related to specific causes. Effects of Hemorrhage
Hypotension. Acute renal shutdown.
Empty veins. Liver cell dysfunction.
Thirst, tinnitus and blindness may occur. Cardiac depression.
Hypoxic effect.
Metabolic acidosis.
Signs Of Significant Blood Loss GIT mucosal ischemia.
Sepsis.
Pulse > 100 / min.
Interstitial edema, AV shunting in lung ARDS.
Systolic BP < 100 mmHg. Hypovolemic shock - multi organ dysfunction
Diastolic BP drop on sitting or standing > 10 mmHg. syndrome (MODS).
Pallor / sweating.
Shock index (ratio of pulse rate to blood pressure) > 1.
Treatment
Clinical Monitoring
A. Stop Blood Loss
1. Pulse Rate, Blood Pressure and Pulse Pressure
Record keeping is made at 15 or 30 minutes intervals
1. Pressure and Packing
during an emergency and thereafter 4 hourly.
Pressure dressing from anything handy which is
soft and clean.
2. Urine Output
Digital pressure.
Clothes-peg for epistaxis.
3. Measuring Blood Loss
Use of a double balloon in esophagus and
Blood clot
stomach to control the bleeding from esophageal
 Size of a clenched fist = 500 ml.
varices.
STBS
SHOCK HEMORRHAGE AND BLOOD TRANFUSION 4 43

Packing by means of rolls of wide gauze. Local Hemostatic Agents

Tourniquets.
Gelatin sponge (Gel foam).
Oxidized cellulose (surgicel).
2. Position and Rest Collagen sponge (Helistat).
Elevation of the limbs (employs gravity to reduce Microfibrillar collagen powder.
bleeding), e.g. in: Topical thrombin.
 Ruptured varicose veins. Bone wax (derived from bees wax + almond oil).
 Thyroidectomy, when patient is placed in Gelatin matrices.
reverse-Trendelenburg position (feet tilted Topical cryoprecipitate.
downwards).
Absolute rest.
Blood Groups and Cross Matching
3. Operative Techniques
Pressure by artery forceps or clips.
Ligation with the catgut, cotton, thread or silk. 1.ABO & Rhesus System
Coagulation with diathermy. These are strongly antigenic and are associated
Suturing of vessel. with naturally occuring antibodies in the serum.
Patches of vein or Dacron mesh may be used to The system consists of three allelic genes A, B, and
repair a vascular defect. O.
Whole or part of the bleeding viscus may be The system allows for six possible genotypes
excised, e.g. splenectomy. although there are only four phenotypes.
Blood group O is the UNIVERSAL DONOR type as it
contains no antigens to provoke a reaction.
Management Concepts Blood group AB is the UNIVERSAL RECIPIENT and
Confirm shock, hypovolemia and hemorrhage by can receive any ABO blood type as they have no
clinical assessment. circulating antibodies.
Immediate resuscitation by blood, oxygen, fluid. The rhesus D antigen is strongly antigenic and is
Identify the site of hemorrhage – ultrasound, present in 85% of population.
endoscopy, CT scan, diagnostic peritoneal lavage
Antibodies to the D antigen are not naturally
(DPL), blood tools.
present in the serum of remaining 15% of
Control of hemorrhage – surgery, endoscopic control,
therapeutic embolization. individuals.
Definitive treatment if any. Their formation can be stimulated by transfusion of
Sepsis control. Rh-positive red cells or they may be acquired during
Prevention of coagulopathy by fresh frozen plasma the delivery of an Rh (D)-positive baby.
(FFP), platelet concentrate, fresh blood.
Critical care management. Type You can give You can
End point resuscitation, fluid and electrolyte
management, prevention of organ failure. blood to receive blood
from
B. Restore Blood Volume A+ A+, AB+ A+, A-, O+, O-
This is accomplished by giving one of the following: O+ O+, A+, B+, AB+ O+, O-
1. Blood transfusion.
B+ B+, AB+B+, B-, O+, O-
2. Albumin 4.5%.
3. SAG M blood. AB+ AB+ Everyone
4. Saline. A- A+, A-, AB+, AB- A-, O-
5. Gelatin.
6. Dextran. O- Everyone O-
7. Plasma infusions. B- B+, B-, AB+, AB- B-, O-
AB- AB+, AB- AB-, A-, B-, O-
 44 4 SHOCK HEMORRHAGE AND BLOOD TRANFUSION
STBS

2. Blood Transfusion It is indicated in;

Indications
 Acute blood loss following trauma.
 During major surgeries abdominoperineal
surgery, thoracic surgery, hepatobiliary surgery.
 Following burns.
 In septicemia.
As a prophylatic measure prior to surgery.
Whole blood is given in acute blood loss.
Packed cells are given in chronic anemias.
Blood fractions are given in ITP, hemophilias.
When blood must be given in emergency, GROUP
O is given:
 O-negative=to females.
 O-positive=to males.
Donor Criteria
Donor should be fit without any serious disease
like HIV1 and HIV2 and hepatitis infections and
malaria.
Weight of donor should be more than 45 kg.
Collection of Blood
Blood is collected in a sac containing 75 ml of CPD
(Citrate, Phosphate, Dextrose) solution and stored in
o
special refrigerators at 4 C. CPD blood lasts for 3
weeks.
In Stored Blood
RBC's last for 3 weeks.
WBC's are destroyed rapidly.
Platelets also get reduced in 24 hours.
Clotting factors are labile and so their levels fall quickly.
Blood Fractions
1. Packed Cells
It is obtained by centrifuging whole blood at 2000
2300 g for 15 20 minutes.
It is used in chronic anemias, in old age, in children.
It minimizes the cardiac overload due to
transfusion.
0 0
It can be stored for 35 days at 1 C- 6 C.
2. Plasma
This is obtained in the same way as packed cells by
centrifugation.
 Burns.
 Hypoalbuminemia.
 Severe protein loss.
It can be fractionalized into different fragments,
such as:
a. Human Albumin 4.5%
It is obtained after repeated fractionations and can
0
be stored for several months in liquid form at 4 C.
b. Fresh frozen plasma (FFP)
Fresh plasma obtained, is rapidly frozen and
0
stored at 40 C. It contains all coagulation factors.
1 unit of FFP increases the clotting factors level by
3%. It can be stored for 2 years.
Rhesus D positive FFP can be transfused to
Rhesus D negative female.
Uses
 Severe liver disease with abnormal coagulation
function.
 Congenital clotting factor deficiency.
 Deficiencies following warfarin therapy, DIC,
massive transfusion.
c. Cryoprecipitate
0
When FFP is allowed to be unfrozen at 4 C, visible
white supernatant layer develops and is called as
cryoprecipitate which is rich in factor VIII and
fibrinogen and is used in the control of bleeding in
0
hemophilia. It is stored at minus 40 C and can be
stored for 2 years.
d. Fibrinogen
It is obtained by organ fluid fractionation of plasma
and is stored in dried form. It is very useful in DIC
and afibrinogenemia. It has risk of transmitting
hepatitis.
3. Platelet Rich Plasma
It is obtained by centrifugation of freshly donated
blood at 150-200 g for 15-20 minutes.
4. Platelet Concentrate
It is prepared by centrifugation of platelet rich
plasma at 1200-1500 g for 15-20 minutes.
Used in thrombocytopenia and drug (aspirin,
clopidogrel) induced hemorrhage.
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SHOCK HEMORRHAGE AND BLOOD TRANFUSION 4 45

5. Prothrombin Complex Concentrate 3. Infections

These are derived from pooled plasma which Serum hepatitis.
contains factors II, IX and X; used in emergency HIV infection.
reversal of warfarin therapy in uncontrolled Bacterial infection.
hemorrhage. Malaria transmission.
Epstein Barr virus infection.
Cytomegalovirus infection.
SAG-M Blood Syphilis, yersinia.
Babesia microti infection.
A proportions of donations will have plasma removed Trypanosoma cruzi infection.
and will be replaced by crystalloid solution of SAG-M.
S --- Sodium chloride. 4. Air Embolism
A --- Adenine.
5. Thrombophlebitis
G --- Glucose anhydrate.
M--- Mannitol. 6. Coagulation Failure
Dilution of coagulation factors.
Advantages DIC.
This allows good viability of cells. Dilutional thrombocytopenia occurs in patients
It is very useful in anemias.But it is devoid of any with massive blood transfusion.
protein.
7. Circulatory Overload
Precaution Causing heart failure.
For every four units of SAG-M blood, one whole liter
blood has to be given. 8. Hemochromatosis
Later for every two units of SAG-M blood, one unit Occurs in patients with chronic renal failure receiving
(400 ml) of 4.5% human albumin has to be given. repeated blood transfusions.
Coagulation status and platelet count should be
checked regularly. 9. Citrate Intoxication
After grouping and cross matching, 540 ml of blood Causes bradycardia and hypocalcemia. For every four
is transfused in 4 hours (40 drops / min) using a units of blood, 10 ml of 10% calcium chloride or
filtered drip set. gluconate should be infused intravenously.
One liter of blood contains 350 mg of iron. Normal
excretion of iron is 1 mg / day. Iron overload can 10. Iron overload
occur after many transfusions. Iron excretion can be
increased by desferroxamine infusion.
Blood Substitutes
Complications of Blood Transfusion
1. Congestive Cardiac Failure 1. Human Albumin 4.5%
There is no risk of transmitting hepatitis.
2. Transfusion Reactions
Incompatibility, major and minor reactions with 2. Dextrans
fever, rigors, pain, hypotension. Dextrans are useful to improve plasma volume. They
Pyrexial reaction due to pyrogenic ingredients in are polysaccharides of varying molecular weight.
the blood.
Allergic reactions. a. Low Molecular Weight Dextran (Dextran 40)
Sensitization to leukocytes and platelets. Dextran 40 is very effective in restoring blood
Immunological sensitization. volumeimmediately. But small molecules are
readily excreted in the kidney so effect is transitory.
 46 4 SHOCK HEMORRHAGE AND BLOOD TRANFUSION
STBS

b. High Molecular Weight Dextran (Dextran 110 and Recycled Blood

70)
They are less effective but long acting, so useful to
have prolonged effect.
Precautions
Blood samples for blood grouping and cross
matching should be taken before giving dextrans as
it interferes with rouleaux formation of red cells.
Dextrans also interfere with platelet function and so
may precipitate abnormal bleeding.
Total volume of dextrans should not exceed 1000
ml.
In major surgeries if there is significant blood loss, then
patient's bled blood is carefully sucked out through a
sterile system and is filtered gain and reused to the
patients. This will reduce the number of transfusions.
Artificial Blood
1. Perfluorocarbon (Fluosoleda)
It is abiotic substitute as synthetic oxygen carrier.
It has got high affinity for O2.
It is inert.
It is biocompatible.

Massive Blood Transfusion 2. Stroma Free Hemoglobin

Biomimetic hemoglobin based substitute.
It is defined as replacement or transfusion of blood
equivalent to patient's blood volume in < 24 hours 3. Chelates which reverse bound 02
corresponding to that particular age (in adult it is Intra-Operative-Salvage of Blood: On table blood is
5-6 litres, in infants it is 85 ml/kg body weight.) or collected, washed, filtered and transfused. Used in
single transfusion of blood more than 2,500 ml trauma.
continuously.
Massive transfusion is used in severe trauma Erythropoietin Injection
associated with liver, vessel, cardiac, pulmonary, 1000-3500 units pre-operatively also used to
pelvic injuries. Often it is required during surgical increase the RBC count.
bleeding (primary hemorrhage on table) of major It is used in chronic renal failure (CRF) patients who
surgeries. are on hemodialysis. It is given twice weekly but it
is costly.
Adverse Effects of Massive Transfusion
Severe electrolyte imbalance High Yield Mnemonics
(hypocalcemia, acidosis).
Coagulopathy-altered platelet and coagulation
factors. Shock: types
Citrate toxicity. RN CHAMPS:
Hypothermia. Respiratory
Poor oxygen delivery. Neurogenic
Infections. Cardiogenic
Incompatibility and transfusion reactions.
Hemorrhagic
ARDS.
Anaphylactic
Metabolic
Autologous Blood Transfusion Psychogenic
A healthy individual with no infection and hematocrit Septic
≥ 30% can donate blood few weeks prior to any
elective surgeries which in turn can be used at the
time of surgery.