Shock

&

Blood
Transfusion

Dr Ashik Mahmud
MBBS , FCPS (Surgery)
 DEFINATION

Shock is a systemic state of low

tissue perfusion which is
inadequate for normal cellular
respiration.
 Classification of shock
There are numerous ways to classify shock.
Based on the initiating mechanism
◼ Hypovolaemic shock
◼ Cardiogenic shock
◼ Obstructive shock
◼ Distributive shock
◼ Endocrine shock
 Hypovolaemic shock
◼ Hypovolaemic shock is due to a
reduced circulating volume.

◼ Hypovolaemiamay be due to
Haemorrhagic or
Non-haemorrhagic causes.
 Hypovolaemic shock
Non-haemorrhagic causes include
◼ Poor fluid intake (dehydration)

◼ Excessive fluid loss due to vomiting,

diarrhoea, urinary loss (diabetes)

◼ Evaporation, or ‘third-spacing’ where

fluid is lost into the gastrointestinal tract and
interstitial spaces, as for example in bowel
obstruction or pancreatitis.
 Cardiogenic shock
◼ Primary failure of the heart to pump
blood to the tissues.
Causes of cardiogenic shock include
◼ Myocardial infarction
◼ Cardiac dysrhythmias
◼ Valvular heart disease
◼ Blunt myocardial injury and cardiomyopathy.
◼ Cardiac insufficiency may also be due to
myocardial depression due to endogenous factors
(e.g. bacterial and humoral agents released in
sepsis) or exogenous factors, such as
pharmaceutical agents or drug abuse.
 Obstructive shock
◼ In obstructive shock there is a reduction in
preload due to mechanical obstruction of
cardiac filling.
Common causes
◼ Cardiac tamponade

◼ Tension pneumothorax,

◼ Massive pulmonary embolus or air

embolus.
 Distributive shock
1. Septic shock
2. Anaphylaxis and
3. Spinal cord injury.
◼ Inadequate organ perfusion is
accompanied by vascular dilatation with
hypotension, low systemic vascular
resistance, inadequate after load and a
resulting abnormally high cardiac output.
◼ In anaphylaxis, vasodilatation is due to
histamine
 Distributive shock
Spinal cord injury there is failure of
sympathetic outflow and adequate vascular
tone (neurogenic shock).

Spinal Anaesthesia
 Endocrine shock
Endocrine shock may present as a combination of
1. Hypovolaemic
2. Cardiogenic or
3. Distributive shock.
Causes of endocrine shock
◼ Hypo and hyperthyroidism
◼ Adrenal insufficiency.
 Endocrine shock
◼ Thyrotoxicosis may cause a high-output
cardiac failure

◼ Adrenal insufficiency leads to shock due to

hypovolaemia and a poor response to circulating
and exogenous catecholamines.
 Severity of shock
According to compensation
◼ Compensated shock
◼ Decompensation

According to severity
◼ Mild shock
◼ Moderate shock
◼ Severe shock
 Mild shock
◼ Tachycardia
◼ Tachypnoea
◼ Mild reduction in urine output
◼ Patient may exhibit mild anxiety.
◼ Blood pressure is maintained
◼ Decrease in pulse pressure.
◼ The peripheries are cool and sweaty
◼ Prolonged capillary refill times (except in
septic distributive shock).
 Moderate shock
◼ As shock progresses, renal compensatory
mechanisms fail, renal perfusion falls and
urine output dips below 0.5 mL/kg per hour.

◼ There is further tachycardia, and now the

blood pressure starts to fall.

◼ Patients become drowsy and mildly

confused.
 Severe shock

◼ In severe shock, there is profound

tachycardia and hypotension.

◼ Urine output falls to zero and patients are

unconscious with laboured respiration.
 Consequences
of SHOCK

◼ RESUSCITATION

◼ UNRESUSCITATABLE SHOCK

◼ MULTIPLEORGAN FAILURE
 Unresuscitatable shock
◼ Patients who are in profound shock for a
prolonged period of time become
‘unresuscitatable’.
◼ Cell death follows from cellular ischaemia
and the ability of the body to compensate is
lost.
◼ There is myocardial depression and loss of
responsiveness to fluid or inotropic therapy.
 Multiple organ failure
◼ Multiple organ failure is defined as two or more
failed organ system
◼ Multiple organ failure currently carries a mortality
of 60 per cent
◼ Effects of organ failure
◼ Lung: Acute respiratory distress syndrome

◼ Kidney: Acute liver insufficiency

◼ Clotting: Coagulopathy

◼ Cardiac: Cardiovascular failure

 Monitoring for patients in shock
Minimum
◼ ECG
◼ Pulse oximetry
◼ Blood pressure
◼ Urine output
Additional modalities
◼ Central venous pressure
◼ Invasive blood pressure
◼ Cardiac output
◼ Base deficit and serum lactate
 RESUSCITATION
Airway assessment
◼ Ensure cervical spine immobilization
and check for vocal response
◼ Clear mouth and airway if obvious
foreign bodies
◼ Jaw trust and chin lift, if required

◼ Consider airway adjuncts

◼ If Glasgow Coma Score 8, consider a

definitive airway
 RESUSCITATION
Breathing
◼ Give 100 per cent oxygen at high flow
◼ Inspect/percuss and auscultate chest

◼ Check for tension pneumothorax and

immediately decompress if suspected
◼ Insert chest drain for
haemothorax/pneumothorax
◼ Major vessel bleeding within the chest
needs to be controlled
 RESUSCITATION
Circulation
◼ Check pulse and blood pressure

◼ Secure two large-bore cannulae, take

bloods and commence fluid
resuscitation
◼ Examine for evidence of blood loss and
treat accordingly
 Fluid therapy
◼ First-line therapy, therefore, is intravenous
access and administration of intravenous fluids.
◼ Access should be through short, wide-bore
catheters that allow rapid infusion of fluids as
necessary
◼ Crystalloid solutions (normal saline,
Hartmann’s solution, Ringer’s lactate) or
◼ Colloids (albumin or commercially available
products).
 Fluid therapy
◼ If blood is being lost, the ideal replacement
fluid is blood, although crystalloid therapy
may be required while awaiting blood
products.
 Vasopressor and inotropic support
◼ Vasopressor agents (phenylephrine, noradrenaline) are
indicated in distributive shock states (sepsis, neurogenic
shock)

◼ Where the vasodilatation is resistant to catecholamines

(e.g. absolute or relative steroid deficiency) vasopressin
may be used as an alternative vasopressor.

◼ In cardiogenic shock inotropic therapy may be required to

increase cardiac output and therefore oxygen delivery. The
inodilator dobutamineis the agent of choice.
 Dynamic fluid response
◼ 250–500 mL of fluid is rapidly given (over 5–
10 minutes) and the cardiovascular
responses in terms of heart rate, blood
pressure and central venous pressure are
observed.
◼ Patients can be divided into
◼ Responders

◼ Transient responders

◼ Nonresponders.
◼ Responders : have an improvement in their
cardiovascular status which is sustained. These patients
are not actively losing fluid but require filling to a
normal volume status.

◼ Transient responders have an improvement over the

next 10–20 minutes. These patients have moderate
ongoing fluid losses (either overt haemorrhage or
further fluid shifts reducing intravascular volume).

◼ Non-responders are severely volume depleted and are

likely to have major ongoing loss of intravascular
volume, usually through persistent uncontrolled
haemorrhage.
 Treatment
◼ To treat the cause
◼ ™
To improve cardiac function
◼ ™
To improve tissue perfusion
Treatment of shock
◼ ™irst stabilize the patient with initial
F
resuscitation
◼ ™
Next evaluate the patient for cause and
severity
◼ ™
Lastly treat the specific cause to achieve
cure
 Treatment
General management principles
◼ The Golden Hour

◼ Establish and maintain a clear airway

◼ Ensure adequate ventilation

◼ Oxygen to keep sats above 95%

◼ Adequate intravenous access

◼ Continuous cardiac monitoring

◼ Urinary catheter

◼ Recording of fluid balance

◼ Central venous monitoring

 Treatment
◼ Physiologically desirable position
◼ Maintain optimum temperature
◼ Blood gases
◼ Acid / base balance assessment
◼ Psychological and family support.
◼ Observation of response to treatment
◼ Inotropes and vasoconstricting drugs
◼ Treatment of underlying disorde
◼ Hypovolaemia is probably the most
common form of shock
◼ Evidence of venous hypertension with
pulmonary or systemic oedema may coexist
with the classical signs of shock.
◼ In distributive (septic) shock, the
peripheries will be warm and capillary refill
will be brisk, despite profound shock.
◼ Tachycardia may not always accompany
shock. Patients who are on beta-blockers or
who have implanted pacemakers are unable
to mount a tachycardia.
◼ Blood pressure : hypotension is one of the last
signs of shock. Children and fit young adults are
able to maintain blood pressure until the final
stages of shock.
◼ Elderly patients who are normally hypertensive
may present with a ‘normal’ blood pressure.
HAEMORRHAGE
Classification

1. Based on the source of bleeding:

2. Based on the time of onset of bleeding
3. Based on the type of haemorrhage
4. Based on the duration of haemorrhage
5. Based on the possible intervention
 Based on the source of bleeding
◼ Arterial : is bright red in colour, spurting like
jet along with pulse of the patient.
◼ Venous : is dark red, steady and continuous
flow. femoral vein, jugular vein, other major
veins, varicose veins, portal vein, oesophageal
varices.
◼ Capillary : Here bleeding is rapid and bright
red. It is often torrential due to continuous ooze.
 Based on the time of onset of bleeding
◼ Primary : Occurs at the time of injury or
operation. Haemorrhage occurring immediately

◼ Reactionary : It occurs within 24 hours after

surgery or after injury (commonly in 4-6 hours).
1. Dislodgement of clot by resuscitation,
2. Normalisation of blood pressure and
3. Vasodilatation.
4. Reactionary haemorrhage may also be due
to technical failure, such as slippage of a
ligature.
 Based on the time of onset of bleeding

◼ Secondary : Secondary haemorrhage is due to

sloughing of the wall of a vessel.
◼ It usually occurs 7–14 days after injury
◼ Precipitated by factors such as infection,
pressure necrosis (such as from a drain) or
malignancy.
 Based on the type of haemorrhage
◼ Revealed haemorrhage : obvious external
haemorrhage, such as exsanguination from an
open arterial wound or from massive
haematemesis from a duodenal ulcer.
◼ Concealed haemorrhage : contained within
the body cavity and must be suspected, actively
investigated and controlled.
Liver injury , Spleen injury , Fracture femur ,
Ruptured ectopic , gestation , Cerebral
haemorrhage , Haemothorax
 Based on the duration of haemorrhage
◼ Acute haemorrhage : It is sudden, severe
haemorrhage after trauma, surgery

◼ Chronic haemorrhage : It is chronic repeated

bleeding for a long period like in haemorrhoids,
bleeding peptic ulcer, carcinoma caecum.
 Based on the possible intervention

◼ Surgical haemorrhage : can be corrected by

surgical intervention.
◼ Nonsurgical haemorrhage : is diffuse ooze
due to coagulation abnormalities and DIC.
Clinical Features of Haemorrhage
◼ Pallor, thirsty, cyanosis.
◼ Tachycardia, tachypnoea.
◼ Air hunger.
◼ Cold clammy skin due to vasoconstriction.
◼ Dry face, dry mouth and goose skin
appearance(due tocontraction of arrector
pilorum).
◼ Rapid thready pulse, hypotension.
◼ Oliguria.
◼ Features related to specific causes.
 Measurement of Blood Loss
◼ Clot size of a clenched fist is 500 ml.
◼ Blood loss in a closed tibial fracture is 500-
1500 ml ; in a fracture femur is 500-2000 ml.
◼ Weighing the swab before and after use is an
important method of on-table assessment of
blood loss.
◼ Hb% and PCV estimation.
◼ Blood volume estimation using radioiodine
technique or micro-haematocrit method.
 Measurement of Blood Loss
◼ Measurement of CVP or PCWP.
◼ Investigations specific for cause: U/S abdomen,
Doppler and often angiogram in vascular injury,
chest X-ray in haemothorax, CT scan in major
injuries, CT scan head in head injuries.
 Effects of haemorrhage
◼ Acute renal shut down
◼ L
™iver cell dysfunction
◼ Cardiac depression
™
◼ Hypoxic effect
™
◼ M
™etabolic acidosis
◼ GIT mucosal ischaemia
™
◼ Sepsis
™
◼ Interstitial oedema, AV shunting in lung ARDS
™
◼ Hypovolaemic shock MODS
™
 Management
◼ Identify haemorrhage
◼ Immediate resuscitative
manoeuvres
◼ Identify the site of haemorrhage

◼ Haemorrhage control
 Haemorrhage control
◼ This will usually be in the operating room
but may be the angiography or endoscopy
suites.
◼ These patients require surgical and
anaesthetic support and full monitoring and
equipment must be available.
◼ There should be no unnecessary
investigations or procedures prior to
haemorrhage control to minimize the
duration and severity of shock.
 Damage control surgery
◼ ‘Damage control’ or ‘damage limitation surgery’
is a concept that originated from naval strategy,
whereby a ship which has been damaged may
have minimal repairs needed to prevent it from
sinking, while definitive repairs wait until it has
reached port.
◼ Damage control surgery is the concept that in
the temporary surgical facility closest to the
injured, only the minimum amount of surgery
should be performed to allow safe transfer of a
patient to a definitive treating facility.
 Damage control surgery
◼ Damage control surgery is restricted to only two
goals :
1. Stopping any active surgical bleeding
2. Controlling any contamination.
Damage control resuscitation (DCR)
The four central strategies of DCR are
◼ Anticipate and treat acute traumatic
coagulopathy
◼ Permissive hypotension until haemorrhage
control
◼ Limit crystalloid and colloid infusion to
avoid dilutional coagulopathy
◼ Damage control surgery to control
haemorrhage and preserve physiology.
TRANSFUSION
◼ Transfusion : The transfer of blood or blood
components from one person (the donor)
into the bloodstream of another person (the
recipient)

◼ Infusion : the introduction of a substance

, such as a fluid,electrolyte, nutrient, or drug,
directly into a vein or interstitially by
means of gravity flow.
◼ Blood is collected from donors who have been
previously screened before donating, to exclude
any donor whose blood may have the potential
to harm the patient or to prevent possible harm
that donating a unit of blood may have on the
donor.
◼ 450 mL of blood is drawn

◼ A maximum of three times each year.

◼ Each unit is tested for evidence of hepatitis B,

hepatitis C, HIV-1, HIV-2 and syphilis.

◼ Donations are leukodepleted as a precaution
against variant Creutzfeldt–Jakob disease
(this may also reduce the immunogenicity of
the transfusion).
Indications for blood transfusion
◼ Acute blood loss, to replace circulating
volume and maintain oxygen delivery

◼ Perioperative anaemia, to ensure adequate

oxygen delivery during the perioperative
phase

◼ Symptomatic chronic anaemia, without

haemorrhage or impending surgery.
Whole blood
Whole blood transfusion has significant
advantages over packed cells as it is
coagulation factor rich and, if fresh, more
metabolically active than stored blood.
Packed red cells
◼ Packed red blood cells are spun-down and
concentrated packs of red blood cells
◼ Each unit is approximately 330 mL and has a
haematocrit of 50–70 per cent.
◼ Packed cells are stored in a SAG-M solution
(saline–adenine–glucose– mannitol) to
increase shelf life to 5 weeks at 2–6°C.

◼ Older storage regimens included storage in

CPD (citrate–phosphate–dextrose solutions)
which have a shelf life of 2–3 weeks.)
Cryoprecipitate
◼ Cryoprecipitate is a supernatant precipitate of
FFP and is rich in factor VIII and fibrinogen.
◼ It is stored at −30°C with a two year shelf life.

◼ It is given in low fibrinogen states or factor VIII

deficiency.
 Fresh frozen plasma
◼ Fresh frozen plasma (FFP) is the liquid
portion of human blood that has been frozen
and preserved after a blood donation and
will be used for transfusion.
◼ FFP was made within eight hours of
collection of blood. Approximately 200-250
mL in a unit.
◼ FFP is stored at <-18°C for up to twelve
months , seven years at < -65° C.
◼ Effective dose: 10-20 ml/Kg body weight
 Fresh frozen plasma
◼ Thawed prior to administration, 300 ml
taking approximately 20 min to thaw.
Once thawed it should be used within 2
h as there is exponential degradation of
the clotting factors at room temperature.

◼ FFP contains coagulation factors,

including the labile factors V and VIII
and the vitamin K-dependent factors II,
VII, IX and X.
Pretransfusion testing

◼ FFP Should be ABO-compatible with

recipient RBC

◼ FFP is given without regard to Rh status

of donor or recipient

◼ FFP transfusion does not require a

crossmatch (not enough RBCs)
 Clinical uses of FFP
◼ Bleeding patient and has significant coagulation
factor deficiencies
◼ Bleeding patients with hepatic failure
◼ Thrombotic Thrombocytopenic Purpura
(TTP)
◼ Prevent bleeding in patients with coagulation
factor deficiencies
◼ Warfarin reversal
◼ To correct abnormal clotting in patients with
DIC or those who have undergone massive
transfusion or cardiopulmonary bypass.
 Platelets
◼ Platelets are supplied as a pooled platelet
concentrate and contain about 250 × 109/L.
◼ Platelets are stored on a special agitator at 20–
24°C and have a shelf life of only 5 days.
◼ Platelet transfusions are given to patients with
◼ Thrombocytopenia
◼ Platelet dysfunction who are bleeding or undergoing
surgery.
◼ Patients on clopidogrel who are actively bleeding
and undergoing major surgery may require almost
continuous infusion of platelets during the course of
the procedure.
 Prothrombin complex concentrates
◼ Prothrombin complex concentrates (PCC) are
highly purified concentrates prepared from
pooled plasma.
◼ They contain factors II, IX and X. Factor VII
may be included or produced separately.
◼ It is indicated for the emergency reversal of
anticoagulant (warfarin) therapy in uncontrolled
haemorrhage.
Preoperative autologous transfusion
◼ It is possible for patients undergoing elective
surgery to predonate their own blood up to 3
weeks before surgery for retransfusion during
the operation.
◼ There are three kinds of autologous (derived
from the same individual).
◼ Intra- and postoperative cell salvage

◼ Acute normovolaemic haemodilution

◼ Preoperative autologous deposit (PAD).

 Transfusion reactions
◼ 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
haemolytic reaction.
◼ Severe immune-related transfusion reactions due
to ABO incompatibility
◼ Transfusion reactions from other antigen
systems are usually milder and self-limiting.
 Transfusion reactions
◼ Febrile transfusion reactions are non-haemolytic
and are usually caused by a graft-versus-host
response from leukocytes in transfused
components.
 Miss match blood transfusion
Sign
◼ Difficulties in breathing along with a feeling
oppression
◼ Chills and rigor

◼ Flushing followed by sweating

◼ Pain at the infusion site

◼ Nausea and vomiting

◼ Haematuria

◼ Urticaria
◼ Constricting pain in the chest and pain in the
lumbar region
◼ Flushing of the face and neck
◼ Anuria
◼ Cyanosis
 Management
◼ Management of acute hemolytic reactions is
both expectant and supportive
◼ Early recognition and interdiction of further
incompatible blood may be the single most
important step.
◼ Hypotension is usually managed by aggressive
fluid resuscitation.
◼ Dopamine infused at 3-5 micro g/kg per
minute.
◼ Immediate treatment of renal insufficiency
traditionally include mannitol 20% and diuretics
to maintain a minimal urinary output of 0.5
ml/Kg per hour
◼ Alkalinizationon of the urine is routinely
recommended
◼ Heparin administration in case of DIC , dose
5000 units immediately followed by a
continuous infusion of 1500 units/hour for 6-24
hours
◼ Use of blood components such as plasma ,
platelets and cryoprecipitate.
◼ Often ventilator support, defibrillator if
cardiac arrest occurrs is needed.
◼ Correction of acidosis, electrolytes is needed.
 Massive blood transfusion
◼ This is defined as transfusion of a volume
greater than the recipient's blood volume in
less than 24 h corresponding to that particular
age (In adult it is 5-6 litres, in infants it is 85
ml/kg body weight.) Or single trans fusion of
blood more than 2,500 ml continuously.
◼ Massive transfusion is used in severe trauma
associated with liver, vessel, cardiac,
pulmonary, pelvic injuries. Often it is required
during surgical bleeding (primary
haemorrhage on table) of major surgeries
Complications from massive transfusion
◼ Coagulopathy
◼ Hypocalcaemia
◼ Hyperkalaemia
◼ Hypokalaemia
◼ Hypothermia.
◼ Citrate toxicity
◼ Poor oxygen delivery—due to reduced 2,3 DPG
◼ Incompatibility and transfusion reactions
◼ Cardiac abnormalities such as ventricular
extrasystoles, ventricular fibrillation
 Blood substitutes
◼ Blood substitutes are an attractive alternative to
the costly process of donating, checking, storing
and administering blood and due to the
immunogenic and potential infectious
complications associated with transfusion.
◼ Blood substitutes are either biomimetic or abiotic.
◼ Biomimetic substitutes mimic the standard
oxygen-carrying capacity of the blood and are
haemoglobin based.
◼ Abiotic substitutes are synthetic oxygen
carriersand are currently primarily perfluorocarbon
based.
Uses
◼ In battlefield scenarios.

◼ Where HIV infection is more

◼ Rapid treatment of patients in trauma situation

◼ Jehovah Witnesses
Complications from a single transfusion
◼ Incompatibility haemolytic transfusion reaction
◼ Febrile transfusion reaction
◼ Allergic reaction
◼ Infection
◼ Bacterial infection (usually due to faulty
storage)
◼ Hepatitis B & C

◼ HIV

◼ Malaria
◼ Air embolism
◼ Thrombophlebitis
◼ Transfusion-related acute lung injury (usually
from FFP).
END