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64
Decreased preload
Decrease in stroke volume
Hypotension and hypoperfusion
Manipal Manual of Surgery
• Pressure packing the middle thyroid vein during
thyroidectomy and the lumbar veins during lumbar
sympathectomy.
• A Sengstaken tube is used to control bleeding from
oesophageal varices—internal tamponade.
2. Position and rest
• Elevation of the leg controls bleeding from varicose
veins.
• Elevation of the head-end reduces venous bleeding
in thyroidectomy—anti-Trendelenburg position.
• Sedation to relieve anxiety—midazolam in titrated
doses of 1–2 mg intravenously may be given. This
may help control blood pressure and the consequent
bleeding.
3. Tourniquets
Indications
• Reduction of fractures
• Repair of tendons
• Repair of nerves
• When a bloodless field is desired during surgery
Contraindications: Patient with peripheral vascular
disease. (The arterial disease may be aggravated due
to thrombosis resulting in gangrene.)
Types:
• Pneumatic cuffs with a pressure gauge
• Rubber bandage
Precautions:
• Too loose a tourniquet does not serve the purpose.
• Too tight: Arterial thrombosis may occur, which
may result in gangrene.
• Too long (duration of application): Gangrene of the
limb.
Application of a tourniquet to control bleeding is not
advised unless pressure bandaging has not been helpful
because of possible ischaemia of the limb. Hence, if
applied, the time of application must be noted down.
Deflate as soon as possible within 45–60 minutes.
Complications
• Ischaemia and gangrene
• Tourniquet nerve palsy
1
4. Surgical methods to control haemorrhage
• Application of artery forceps (Spencer Wells forceps)
to control bleeding from veins, arteries and capillaries.
_____________________
1
In MS examination, a candidate was asked to examine a case of
radial nerve palsy. The patient had an injury to the wrist
4 months prior. The cut flexor tendons had been sutured. The
candidate could not correlate the radial nerve palsy to the injury
at the wrist. He failed! It was a case of tourniquet palsy.
Section I • Basic Principles of Surgery
• Application of ligatures for bleeding vessels.
• Cauterisation (diathermy).
• Application of bone wax (Horsley’s wax, which is
bee’s wax in almond oil) to control bleeding from
cut edges of bones.
• Silver clips are used to control bleeding from
cerebral vessels (Cushing’s clip).
• Surgical procedure: Laparotomy and splenectomy
for splenic rupture, hysterectomy for uncontrollable
postpartum haemorrhage, laparotomy for control
of bleeding from ruptured ectopic pregnancy.
HYPOVOLAEMIC SHOCK
• Loss of blood—haemorrhagic shock
• Loss of plasma—as in burns shock
• Loss of fluid—dehydration as in gastroenteritis
Features (Key Box 17.1)
The primary problem is a decrease in preload. The
decreased preload causes a decrease in stroke volume.
Clinical features depend on the degree of hypovolaemia,
and are similar to those of haemorrhagic shock. Severe
(Class III or IV) shock results in tachycardia, low blood
pressure, and decreased urine output.
The peripheries are cold and the patient may be
confused or moribund (see Pathophysiology of
haemorrhagic shock).
Treatment
• Replace the lost blood volume.
• The primary goal is to restore tissue perfusion and
oxygenation as early as possible.
• Crystalloids: If crystalloids are used to replace blood
loss, 1.5–2 times the lost volume need to be given.
Ringer lactate is the crystalloid of choice. Large
volumes of saline infusion may cause hyperchloraemic metabolic acidosis. 5% dextrose is not
used to expand the intravascular volume, as it is
hypotonic once dextrose metabolises.
• Colloids: When colloids are used to replace lost blood
volume, a volume equal to the lost volume may be
given. However, they are not preferred.
Key Box 17.1
Hypovolaemic Shock
Shock and Haemorrhage
65
• Crystalloids are preferred during the initial phase of
resuscitation. If a large volume of blood is lost, transfuse blood products. Please refer to the management
of hamorrhagic shock described earlier in this
chapter.
CARDIOGENIC SHOCK
The blood flow is reduced because of an intrinsic
problem in the heart muscle or its valves. A massive
myocardial infarction may damage the cardiac muscle
so that there is not much healthy muscle to pump blood
effectively. Any damage (especially acute) to the valves
may also reduce the forward cardiac output, resulting
in cardiogenic shock.
Features
• The primary problem is a decrease in contractility of
the heart. The decreased contractility causes a
decrease in stroke volume.
• Left ventricular pressures rise as forward cardiac output
reduces. The sympathetic nervous system is activated,
resulting in increased systemic vascular resistance.
• Clinically, the patient presents with tachycardia, low
blood pressure, and decreased urine output.
• The jugular venous pulse may be raised, and an S3
or S4 gallop may be present.
• The lung fields may show bilateral extensive crepita-
tions due to pulmonary oedema.
• The peripheries are cold, and the patient may be
confused or moribund.
Treatment
• The primary goal is to improve cardiac muscle
function.
• Oxygenation can be improved by administering
oxygen, either by a face mask or by endotracheal
intubation and ventilation as necessary.
• Inotropes improve cardiac muscle contractility.
• Vasodilators such as nitroglycerine may dilate the
coronary arteries and peripheral vessels, and improve
tissue perfusion. Lowering systemic vascular
resistance reduces impedance to forward cardiac
output (afterload). However, the patient must be
monitored closely to avoid excessive reductions in
blood pressure.
• Intra-aortic balloon pump or ventricular assist
devices may be used to augment cardiac output.
• If hypotension continues to be refractory, revascu-
larisation (surgical or interventional) or valve replacement may be considered on an emergency basis.
DISTRIBUTIVE SHOCK
In distributive shock, the afterload is excessively
reduced, thereby affecting circulation. Distributive
shock may occur in the following situations:
• Septic shock
• Anaphylactic shock
• Neurogenic shock
• Acute adrenal insufficiency
Septic Shock
athophysiology
P
• Sepsis is the response of the host to bacteraemia/
endotoxaemia.
• It may be produced by gram-negative or gram-positive
bacteria, viruses, fungi, or even protozoal infections.
• Severe sepsis may result in persistent hypotension
despite adequate fluid resuscitation.
• Local inflammation and substances (especially endo-
toxin) released from organisms activate neutrophils,
monocytes, and tissue macrophages. This results in
a cascade of proinflammatory and anti-inflammatory cytokines and other mediators, such as IL-1,
IL-8, IL-10, TNF-, prostaglandin E1, endogenous
corticosteroids, and catecholamines.
• This results in cellular chemotaxis, endothelial injury,
and activation of the coagulation cascade (Key Box 17
.2).
Features
• These substances produce low systemic vascular
resistance (peripheral vasodilatation) and ventri-
cular dysfunction, resulting in persistent hypotension.
• Generalised tissue hypoperfusion may persist
despite adequate fluid resuscitation and improvement in cardiac output and blood pressures. This is
due to abnormalities in regional and microcirculatory
blood flow. These abnormalities may lead to cellular
dysfunction, lactic acidosis (anaerobic metabolism),
and ultimately, multiorgan failure.
• Early phases of septic shock may produce evidence
of volume depletion, such as dry mucous membranes
and cool, clammy skin.
Key Box 17.2
Disturbance of Procoagulant–Anticoagulant Balance
Inflammatory response in sepsis activates tissue factor
which in turn activates coagulation
Fibrinogen is converted to fibrin
Lowered levels of natural anticoagulants such as
protein C, protein S and antithrombin III
Procoagulant—anticoagulant imbalance → diffuse
microvascular thrombi
Section I • Basic Principles of Surgery
66
Manipal Manual of Surgery
• After resuscitation with fluids, however, the clinical
picture is typically more consistent with that of hyper-
dynamic shock. Features include tachycardia, bounding pulses with a widened pulse pressure, a hyperdynamic precordium on palpation, and warm
extremities.
• Signs of possible infection depend on the source of
sepsis. These may include fever, localised erythema
or tenderness, consolidation on chest examination,
abdominal tenderness, guarding, rigidity, and
meningismus.
• Signs of end-organ hypoperfusion include tachy-
pnoea, cyanosis, mottling of the skin, digital
ischaemia, oliguria, abdominal tenderness, and
altered mental status.
• Often, a definitive diagnosis cannot be made on the
basis of initial clinical features; hence, empirical
treatment for several possible conditions should be
commenced.
Treatment
• Removal of the septic focus is an essential step, and
is a priority in the treatment of septic shock (e.g.
resection of gangrenous bowels, closure of perforation, appendicectomy).
• Early empirical antibiotic therapy should be
administered to treat the precipitating infection. This
must be given within the first hour of arrival.
• Supportive care: Oxygenation and, if necessary,
endotracheal intubation and mechanical ventilation
should be administered.
• Intravenous fluids: Restoration of intravascular
filling pressures must be done using crystalloids,
colloids, and blood as necessary. Crystalloids, such
as isotonic saline or Ringer’s lactate, may be used.
Large amount may be required, which may contribute to tissue oedema. Colloids restore intravascular
volume faster and remain longer in the central
circulation. However, they are expensive and often
used in patients with a high-risk of pulmonary
oedema (due to cardiac dysfunction) who may not
tolerate large volume of fluids. Avoid hetastarch, as
it may increase the risk of renal injury and mortality.
If the patient is anaemic, blood transfusions may be
required to raise haemoglobin levels to 8–10 g%.
• Vasoactive agents, such as norepinephrine, may be
used to produce vasoconstriction and raise the
systemic vascular resistance to normal. Dopamine,
dobutamine, or adrenaline may need to be added.
Vasopressin infusion may be useful in patients with
refractory shock. All these potent drugs are given as
infusions under careful and continuous monitoring
of blood pressure, as well as cardiac filling pressures
Section I • Basic Principles of Surgery
(central venous pressures).
Key Box 17.3
Summary of Septic Shock
Early diagnosis of septic shock
Empirical antibiotics initially
Appropriate antibiotics after culture and sensitivity
testing
Ultrasonography, CT scan, and chest X-ray are key
investigations
Treatment of source of infection
– Pneumonia
– Drainage of pus
– Closure of perforation
– Resection of gangrene
Early and aggressive resuscitation, supportive care and
close monitoring in intensive care unit (ICU).
Measure and monitor serum lactate. The aim is to eliminate
lactic acidosis with fluid resuscitation and better perfusion.
A 54-year-old lady was admitted to the casualty with
low blood pressure and dyspnoea since one day. She
had a history of fever, vomiting, and diarrhoea since
3–4 days, and was treated in a local nursing home.
When she got worse, was referred to our hospital. In
spite of fluid therapy, profound hypotension persisted,
and within half an hour of arrival to the casualty, she
suffered a cardiopulmonary arrest.
Her trachea was immediately intubated, cardiopulmo-
nary resuscitation (CPR) was given, and she was shifted
to the intensive care unit for further management. She
required high doses of dopamine, adrenaline, and
noradrenaline to maintain blood pressure. A blood gas
analysis showed severe metabolic acidosis (pH = 7.02,
PaCO2 = 35 mmHg, and HCO
–
= 12 mmol/L).
3
Considering the history, a diagnosis of septic shock
was made when she continued to have hypotension
even after her central venous pressures were normal.
Peritoneal dialysis was done, as she was in oliguric
renal failure. Haemodialysis was not possible, as she
was hypotensive and on inotropes. A search for a septic
focus was initiated. Ultrasound abdomen showed a
dilated kidney and an obstructed urinary system.
A DJ-stenting of the ureter, which was done to relieve the
obstruction, drained pus. Once the pus was drained,
appropriate antibiotics were given, and with continued
cardiorespiratory support, she showed steady improvement. She was gradually weaned off the ventilator and
inotropes, and was discharged from the hospital five
Shock and Haemorrhage
67
weeks later. At discharge, she was fully conscious, stable,
ambulant, and very grateful to the medical fraternity.
This case illustrates the importance of resuscitation,
cardiorespiratory support, removal of the septic focus,
and antibiotics in the treatment of septic shock.
Anaphylactic Shock
Features
It occurs on exposure to an allergen that the patient is
sensitive to. It may be pollen, foodstuffs, preservatives
in the food, or a medication. Anaphylactic shock that
occurs in the hospital is usually due to some drug
allergy (e.g. to penicillin). Latex allergy is also being
increasingly recognised.
The reaction may be in the form of mild rashes, with
or without bronchospasm, or a full blown anaphylactic
shock, wherein the patient presents with rashes,
generalised oedema (including laryngeal oedema),
bronchospasm and hypotension, and if not treated in
time, cardiac arrest.
Treatment
Key Box 17.4
Risk Factors for Adrenal Crisis
Infection
Trauma or surgery
Adrenal gland or pituitary gland injury
Premature termination of treatment with steroids such
as prednisolone or hydrocortisone.
• Primary adrenal insufficiency (Addison’s disease)
• Secondary adrenal insufficiency (pituitary gland
injury, compression)
• Inadequately treated adrenal insufficiency.
Features
• Headache, profound weakness, fatigue, slow and
lethargic movement, joint pain.
• Nausea, vomiting, abdominal pain, high fever and
chills.
• Low blood pressure, dehydration, rapid heart and
respiratory rates, confusion or coma.
rimary
I. P
• Oxygen and, if necessary, endotracheal intubation
and ventilation.
• Adrenaline, 0.5–1 mg IM or 50–100 µg IV boluses, as
necessary, to maintain blood pressure.
• Intravenous fluids—isotonic saline or Ringer lactate
• Leg-end elevation of bed.
II. Secondary
• Chlorpheniramine maleate
• Hydrocortisone 100 mg intravenously
If facilities exist, take a 10 ml sample of blood to
analyse for serum tryptase levels. If raised, it confirms
anaphylactic reaction.
Neurogenic Shock
Causes: High spinal cord injury, vasovagal shock.
Features: Hypotension without tachycardia (more often
bradycardia) that may deteriorate to cause shock and
cardiac arrest.
Treatment: Intravenous fluids, inotropes, and vago-
lytics, as necessary.
Acute Adrenal Insufficiency
Risk Factors (Key Box 17.4)
Adrenal crisis occurs, if the adrenal gland is deteriorating, as in:
Treatment
• Care of airway, breathing, and circulation
• Intravenous fluids
• Hydrocortisone 100 mg intravenously every 6 h to
provide mineralocorticoid activity
• Treat the precipitating factor
• Antibiotics as necessary
OBSTRUCTIVE SHOCK
In obstructive shock, there is impedance to either inflow
or outflow of blood into or out of the heart. It may be
due to cardiac tamponade or due to tension pneumothorax.
Cardiac Tamponade
In cardiac tamponade, the pericardium is filled with
blood or fluid, which hampers venous filling as well as
outflow. Therefore, the cardiac output reduces drastically, even to zero. It is a medical emergency. Prompt
recognition and treatment can save lives.
Causes
• Injury to the heart due to trauma
• Perforation of vena cava or atrial walls during
cannulation or intracardiac procedures
• Rupture of ventricular or aortic aneurysm
• Postoperatively after cardiac surgery
Section I • Basic Principles of Surgery
68
Manipal Manual of Surgery
Pericarditis can lead to accumulation of fluid in the
pericardial sac. This pericardial effusion tends to occur
more slowly but can produce cardiac tamponade when
there is large amount of fluid accumulation. It can be
due to infections (bacterial or fungal), inflammatory
causes (uraemia, systemic lupus erythematosus,
rheumatoid arthritis), cancer or certain medications.
Features
• The filling pressures of the left-sided and right-sided
chambers equalise.
• Beck’s triad: Low blood pressure, muffled heart
sounds and distended neck veins.
• The patients also have pulsus paradoxus where there
is at least a 10% decrease in systolic blood pressure
with inspiration.
• This can lead to cardiac arrest.
Treatment
• This is a life-threatening condition and must be
treated immediately, especially when acute.
• Pericardiocentesis: Drain the pericardial cavity using
a wide bore needle, attached to a syringe. It is inserted
from the subcostal area, under the xiphoid process,
pointing towards the left shoulder with continuous
aspiration (Fig. 17.2). Use of ultrasound to perform
this procedure under vision improves safety and is
recommended.
• Decompression of the pericardial cavity allows
venous filling of the heart and forward flow. Blood
pressure improves immediately.
• Monitor electrocardiogram during this procedure.
Watch for arrhythmias that can occur, if the needle
stimulates the myocardium.
Tension Pneumothorax
Causes
• Lung injury due to trauma
• Ventilator-induced barotrauma
• Rupture of emphysematous bullae in a patient with
chronic obstructive pulmonary disease.
Features
• Profound cyanosis, distended neck veins
• Tachypnoea, dyspnoea, or respiratory arrest
• No air entry on the side of pneumothorax, hyper-
resonance to percussion
• Tachycardia, hypotension, and cardiac arrest
Treatment
• A wide (large) bore needle/cannula (needle thoraco-
stomy) must be inserted into the pleural cavity to
drain the air. Traditionally, it was advised that the
needle should be inserted in the midclavicular line
in the 2nd intercostal space on the affected side
(Fig. 17.3).
• However, in adults diagnosed to have a tension
pneumothorax, the current Advanced Trauma Life
Support (ATLS) guidelines advise that the needle is
inserted in the 5th intercostal space in the midaxillary line.
• This is followed by tube thoracostomy.
A massive pulmonary embolus is a differential diagnosis for
obstructive shock.
Section I • Basic Principles of Surgery
Fig. 17.2: Pericardiocentesis
Fig. 17.3: Needle thoracocentesis
Shock and Haemorrhage
INDICATORS OF FLUID RESPONSIVENESS
Measurement of CVP has been used traditionally as an
indicator of fluid responsiveness. The newer ones
include pulse pressure variation, systolic pressure
variation, stroke volume variation, inferior vena caval
diameter and passive leg raising.
CENTRAL VENOUS PRESSURE (CVP)
• Pressure in the intrathoracic great veins is called
central venous pressure.
• It is the same as right atrial pressure.
• Normal CVP is 2–6 mmHg in a person breathing
spontaneously. It is higher (8–12 mmHg) in a patient
who is receiving mechanical ventilation.
• CVP is used as a surrogate measure of blood volume.
A low CVP suggests hypovolaemia.
• In shock, measurement of CVP is useful for planning
proper fluid management. Thus, it is desirable to
monitor CVP while treating patients in shock.
• However, it must be remembered that CVP may also
be affected by contractility of the right ventricle,
changes in intrathoracic and intrapericardial
pressures. Thus, a high CVP does not always indicate
hypervolaemia. In such situations, other means of
fluid responsiveness such as pulse pressure variation
or systolic pressure variation, measurement of
inferior vena caval diameter can be used.
Method
• The internal jugular vein (IJV) or subclavian vein
are preferred routes of accessing the central veins
(Key Box 17.5).
• A 16-cm long IV catheter is introduced into the central
vein with the patient supine, head down, and neck
rotated to the opposite side (Fig. 17.4). Head down
position helps in engorging the vein. Ultrasound
guidance to cannulation is now considered the
standard of care. Seldinger’s technique is employed,
and the catheter is advanced up to the junction of the
superior vena cava and the right atrium (corresponding externally to the manubrium sterni).
• Aspirate through the lumen to check for free flow of
blood into the connecting tube.
Key Box 17.5
Access to Right Heart/Great Veins
Internal jugular vein
Subclavian vein
Median cubital vein
External jugular vein
69
Fig. 17.4: Right internal jugular vein cannulation
• The tube is connected to an electronic pressure
transducer. The ‘zero reference point’ must be at the
midaxillary level, if the patient is in supine position,
or at the manubriosternal joint, if he is in the semireclining position (45°). If the facility for using an
electronic transducer is not available, a saline manometer may be used.
• CVP must be measured at end-expiration when the
influence of intrathoracic pressure on CVP is minimum.
Uses
1. If CVP is low, venous return should be supplemented
by IV infusion, as in cases of hypovolaemic shock.
. When CVP is high, further infusion of fluids may
2
result in pulmonary oedema.
3. In cardiogenic shock, CVP may be normal or high,
and it is affected by the reduced ventricular
contractility. In such situations, therefore, it may not
accurately reflect intravascular volume.
Complications
1. Pneumothorax
2. Accidental carotid artery puncture
3. Haematoma in the neck
4. Bleeding
5. Air embolism
6. Infection
Dynamic indicators of fluid responsiveness such as
stroke volume variation, systolic pressure variation and
pulse pressure variation measure the changes in stroke
volume, systolic pressure or pulse pressure respectively
with changes in intrathoracic pressure. A variation more
than 10–13% indicates fluid responsiveness (the patient’s
haemodynamic parameters will respond to volume
infusion). This parameter is useful when patients are
being mechanically ventilated with a tidal volume of at
least 8 ml/kg body weight.
Section I • Basic Principles of Surgery
70
Manipal Manual of Surgery
Inferior vena cava diameter: This is a noninvasive
method of measurement of fluid responsiveness. It is
diameter with respiration (IVC collapsibility index) also
indicates fluid responsiveness.
measured using ultrasound at a point where it enters
the right atrium. Using M mode, the maximum and
minimum diameter are measured. If the IVC diameter
is <10 mm, the patient requires volume and if >25 mm,
the patient is reasonably full. A variability >25% in IVC
Passive leg raising: By about 30° will result in increased
venous return. An improvement in haemodynamics
with this reversible manoeuvre suggests need for
volume replacement.
PHOTOGRAPHS OF PATIENTS WITH SEPTIC SHOCK (Figs 17.5 to 17.10)
Fig. 17.5: Extensive gangrene Fig. 17.6: Necrotising fasciitis of upper limb Fig. 17.7: Chest X-ray in
septic shock patient
Fig. 17.9A: Intra-arterial blood pressure monitoring
Fig. 17.8: Faecal peritonitis Fig. 17.10: Septic shock patient
Fig. 17.9B: Pancreatic necrosis—necrosectomy specimen
1. Which of the following medications is least preferred
in the initial management of haemorrhagic shock?
A. Oxygen B. Ringer lactate
.
Packed cells D. Vasopressors
C
2. Which of the following solutions is best suited in
the initial management of hypovolaemic shock?
A. Normal saline
B.
Ringer lactate
C. Hydroxyethyl starch
Section I • Basic Principles of Surgery
D. Albumin
recovering
3. Characteristic features of septic shock include the
following except:
A. Hypotension B. Tachycardia
.
Oliguria D. Alkalosis
C
4. Hyperbaric oxygen is helpful in the following conditions except:
A. Carbon monoxide poisoning
Gas gangrene
B.
C. Decompression sickness
D. Before chemotherapy
Shock and Haemorrhage
71
5. Regarding central venous pressure:
A. Right internal jugular vein is the route of choice
B
. CVP is a reliable indicator of blood volume status
C. CVP remains constant with respiration
D. CVP is low in tension pneumothorax
6. The following is NOT a feature of cardiac tamponade:
A. Tachycardia B. Hypertension
C
. Muffled heart sounds D. High CVP
7. Which of the following is a good indicator of fluid
responsiveness in a spontaneously breathing patient:
A. Stroke volume variation
B. Inferior vena caval diameter
C. Systolic blood pressure
D. Heart rate
8. During haemorrhage, if the systolic blood pressure
is normal but diastolic blood pressure is high, the
patient may be in Class ______ shock.
A. I B. II
III D. IV
C.
13. The central venous pressure is high in which type of
shock?
A. Hypovolaemic shock
B
. Anaphylactic shock
C. Septic shock
D. Obstructive shock
14. Translocation of bacteria from which organ may lead
to multiorgan failure (and thus, this organ is called
‘motor of multiorgan failure’)?
A. Kidney B. Brain
. Gut D. Liver
C
15. The route of choice for administering adrenaline in
anaphylactic shock is:
A. Intramuscular B. Intravenous
. Subcutaneous D. Inhalational
C
16. Which is the blood product of choice in bleeding patients
with a fibrinogen concentration of <100 mg/L?
A. Packed cells B. Fresh-frozen plasma
. Platelets D. Cryoprecipitate
C
9. In haemorrhagic shock, if the patient has lost 30–40%
blood volume, he is in Class ______ shock.
A. I B. II
C. III D. IV
10. Tension pneumothorax is a reason for which of the
following types of shock?
A. Hypovolaemic shock B. Obstructive shock
C. Distributive shock D. Septic shock
11. The drug of choice in anaphylactic shock is:
A. Adrenaline B. Histamine
C
. Promethazine D. Chlorpheniramine
12. The ‘zero reference point’ for arterial pressure
transducers in seated patients should be at the:
A. Level of the nipple
B. Level of the manubriosternal junction
C. Level of the xiphoid process
D. Level of the radial artery
17. Beck’s triad is a feature of:
A. Cardiac tamponade
B
. Tension pneumothorax
C. Pulmonary thromboembolism
D. Massive myocardial infarction
18. The following is NOT a feature of tension pneumothorax:
A. Reduced breath sounds
. Dullness on percussion
B
C. Low blood pressure
D. Hypoxia
19. Intra-aortic balloon pump is used in which type of
shock:
A. Hypovolaemic shock
. Obstructive shock
B
C. Cardiogenic shock
D. Septic shock
Answers
1. D 2. B 3. D 4. A 5. B 6. B 7. B 8. B 9. C 10. B
11. A 12. B 13. D 14. C 15. B 16. D 17. A 18. B 19. C
Section I • Basic Principles of Surgery
18
Blood Transfusion
Blood transfusion
Blood products
Complications of blood transfusion
SU3.1: Describe the Indications and appropriate use of
blood and blood products and complications of blood
transfusion.
BLOOD TRANSFUSION
Administration of whole blood or its components into
a patient is often necessary for various reasons. Since
the only available source of blood is by voluntary human
donation, which is scarce, whole blood is separated into
its components, namely packed red blood cells, fresh
frozen plasma, platelets, and cryoprecipitate. Some
coagulation factors may be isolated and separately stored
(e.g. factor VIII for administration into haemophiliacs).
Packed red cells are the most common blood products
used. Their transfusion increases the oxygen carrying
capacity of blood. Transfusion of one unit of packed cells
raises haemoglobin by approximately 1 g% in an adult.
Indications for Blood Transfusion (Key Box 18.1)
. Packed red cells are used to replace acute and major
I
blood loss in:
• Haemorrhagic shock
Key Box 18.1
Guidelines: When to Transfuse
Haemoglobin <7 g%: Transfusion of red cells is likely
to be associated with reduced mortality.
Haemoglobin 7–10 g%: The decision to transfuse
blood should be taken, only if there are clinical
symptoms and signs due to anaemia.
Haemoglobin >10 g%: Transfusion is not indicated.
Autologous transfusion
Bleeding disorders
Hyperbaric oxygen
• Major surgery—open heart surgery, gastrectomy
• Extensive burns
I
I. Packed red cells are also used to treat anaemia due to:
• Extensive burns
• Chronic blood loss—haemorrhoids, bleeding
disorders, chronic duodenal ulcer, etc.
• Inadequate production—malignancies, nutritional
anaemia
Platelet concentrates are administered to replace
III.
platelets in thrombocytopaenia. Fresh frozen
plasma is given to replace plasma volume as well
as Vit K dependent coagulation factors unresponsive to vitamin K replacement (e.g. liver disease, to
reverse effects of warfarin). Cryoprecipitate is used
to replace fibrinogen in patients with disseminated
intravascular coagulation.
IV. Whole fresh blood administration is described in
massive trauma with heavy blood loss, the rationale
being that the patient rapidly loses all components
of blood, so all components need to be replaced.
Thus, it makes sense to administer whole blood,
rather than individual components. However,
many blood banks are reluctant to allow whole
blood transfusion. This is to ensure that the
donated blood can be optimally utilised. In such
cases, red blood cells, fresh frozen plasma, and
platelets are given in a 1:1:1 ratio.
BLOOD PRODUCTS
acked Red Blood Cells (PRBC)
P
When whole blood is centrifuged, red blood cells settle
down and the platelet-rich plasma remains supernatant.
72
Blood Transfusion
73
The plasma is transferred to another bag, while preservative is added to red cells and the bag is sealed. Each
bag of packed cells contains approximately 250–300 ml
with a red cell concentration of 70%. Red cell transfusion
is required for patients whose haemoglobin is <7 g%
(e.g. patients undergoing chemotherapy, major surgery,
delivery, trauma, grossly anaemic neonates and infants,
sickle cell anaemia—especially in sickle cell crisis). Each
unit of packed cells should increase haemoglobin by
1 g% and haematocrit by 3%.
The red cells may be leucodepleted (white blood cells
removed) for use in patients requiring multiple transfusions to prevent development of antibodies to leukocytes or in those who are known to react to leucocytes.
The rate of blood or blood product administration
depends on the quantity and speed at which it is lost
from the body. Slow transfusion is indicated in those
with cardiac disease, renal dysfunction, severe chronic
anaemia, and in paediatric patients.
In semi-emergent situations (e.g. treatment of low
haemoglobin in patients awaiting surgery or delivery),
each bag of packed cells may be transfused slowly. The
initial 25 ml may be given slowly to check whether the
patient tolerates it. Thereafter, it can be transfused at a
rate of 3–4 ml/kg/h (approximately 1.5 h for a bag of
red cells). The red cells must be transfused within
4 hours of removing it from the refrigerator, as bacterial
growth may be promoted after that.
In emergent situations, red cells may be transfused
much faster in order to keep up with the loss. When
large amounts are transfused in a short period (see
section on massive transfusion), the effects of other
components, such as citrate, become significant.
Packed red blood cells must be both ABO and Rh
compatible unless the patient has life-threatening
massive bleeding, in which case O –ve packed cells may
be transfused.
Platelets
The bag containing platelet-rich plasma is again
centrifuged to express off the plasma so that the bag
with the remaining platelets can be sealed off. Each unit
10
(50 mL) should contain at least 5.5 × 10
platelets
(platelet concentrate), and each unit should elevate the
3
platelet count by 5–10,000 cells/mm
in a 70 kg person.
Platelets may be transfused prophylactically or for
therapeutic purposes.
Prophylactic platelet transfusion may be done when
the platelet count is <10,000 cells/mm
3
in oncology
patients. In patients who are at high risk of alloimmunisation (e.g. leukaemia), the threshold for platelet
3
transfusion is even lower at 5000 cells/mm
, whereas
in patients with clinical instability, the threshold may
3
be raised to 20,000 cells/mm
. Patients who need to
undergo major surgery or require invasive procedures,
such as spinal anaesthesia, liver biopsy, etc. generally
need their platelet count elevated to >50,000 cells/mm
However, patients requiring surgery in critical areas,
such as neurosurgery or ophthalmic surgery, will need
3
their platelet count raised to >1,00,000 cells/mm
.
Therapeutic platelet transfusion is required in patients
who are known to be thrombocytopenic and are actively
3
bleeding (platelet count <50,000 cells/mm
). The dose
of platelets may be calculated as follows: One unit of
platelets (60 ml) for every 10 kg body weight.
Platelets must be transfused within 4 hours of
commencing the infusion. ABO compatibility is not
required for platelets. Filters of 170–260 µ must be used
to transfuse platelets as with other blood components.
Fresh Frozen Plasma (FFP)
The remaining plasma (200–230 ml) may be stored in a
frozen form (called fresh frozen plasma) at –18°C for
one year. It needs to be thawed over half an hour before
use.
Fresh frozen plasma transfusion is indicated in
patients with prolonged INR >1.5 who are bleeding or
require surgery. FFP provides coagulation factors to
those who are actively bleeding and those on warfarin.
It is administered in a dose of 10–20 ml/kg body weight,
and must be ABO compatible. FFP must be transfused
as soon as possible after thawing, and definitely within
24 hours. A hanging unit must be transfused within
6 hours of commencement of transfusion due to risk of
bacterial contamination.
Cryoprecipitate
FFP may be further treated to produce cryoprecipitate,
which is rich in fibrinogen. Transfusion of cryoprecipitate (each bag contains 20 ml) is indicated in patients
with fibrinogen levels <1 g% (e.g. disseminated intravascular coagulation (DIC)). The dose is 0.2 units/kg
body weight, but usually 10 units are transfused initially
and repeated as necessary.
Important points to remember before transfusing blood
products
• Always obtain informed consent from patients or
immediate relatives (in emergent situations) prior to the
transfusion.
• Recheck the patient’s blood group and that of the
donor blood, preferably along with one other qualified
person, to ensure that the correct bag is being
transfused to the patient. The patient’s hospital number
and the blood bag number should also be checked.
Both people must sign on the transfusion report.
3
.
Section I • Basic Principles of Surgery