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54
Fig. 15.1: Neuroendocrine response
Manipal Manual of Surgery
• Hypothalamic activation of the sympathetic nervous
system, causes the release of adrenaline from the
adrenal medulla and noradrenaline from nerve
terminals.
• Increased release of growth hormone and glucagon.
• Posterior pituitary hormone arginine vasopressin
level increases.
To summarise, the levels of ACTH, cortisol, growth
hormone, adrenaline, and glucagon are increased
following injury, mainly because of activation of the
neuroendocrine pathway.
Immune Response (Fig. 15.2)
The immune system of the body may be subdivided into
the:
• Innate immune system, which mainly includes
macrophages.
• Adaptive immune system, which includes T and B
lymphocytes.
Immune responses are mediated by protein signalling
compounds called ‘cytokines.’ The immune response
to injury includes a proinflammatory and an antiinflammatory response.
The initial response to injury is proinflammatory,
which leads to:
• Pyrexia, due to action of proinflammatory cytokines
on the hypothalamus
• Propagation of the hypothalamic stress response
• Proteolysis in skeletal muscle
Section I • Basic Principles of Surgery
• Production of acute-phase proteins in liver
Fig. 15.2: Immune response
The proinflammatory cytokines are interleukin-1
(IL-1), tumour necrosis factor-α, interleukin-6 (IL-6), and
interleukin-8 (IL-8). Following this, to control a robust
proinflammatory response, endogenous anti-inflammatory mediators take action to check a potentially
exaggerated inflammatory and immune response.
Example: IL-4, IL-5, IL-9, IL-13, IL-10, IL-1 receptor
antagonist, soluble tumour necrosis receptors and
transforming growth factor-β are released into circula-
tion to counteract the proinflammatory cytokines,
thereby developing Th2-type counter-inflammatory
response. There is a delicate balance between the
proinflammatory and anti-inflammatory immune
responses. Unopposed proinflammatory response
leads to ‘systemic immune response syndrome’ (SIRS).
On the other hand, exaggerated anti-inflammatory
response results in “compensatory anti-inflammatory
response syndrome (CARS)” or “counter-inflammatory
response syndrome”. Excessive or prolonged elaboration of either of them may result in sepsis and/or
death.
Note on the stress response to surgery: Although in an
evolutionary perspective, the stress response allows an
injured animal to survive better by catabolizing stored
body fuels, the latest argument errs on the notion that
it is unnecessary in the current surgical practice and
the potential deleterious effects of an unopposed
response has already been discussed. The body’s
response to surgical stress per se is essentially the same
as to other stressors like trauma, but a few specific
factors affecting surgical response are noteworthy:
• Age: As the age increases, the hormonal response in
the postoperative period lasts longer.
• Nutrition and diet: Perioperative nutritional support,
particularly the degree of diet has an effect on
metabolic response to surgery.
Metabolic Response to Injury
55
• Surgical method: Pneumoperitoneum CO2 insuffla-
tion can cause both local and systemic effects, thereby
altering the metabolic response to surgery. Cytokine
synthesis from mesothelial cells was also found to
be less after laparoscopy as compared to open
surgery.
• Operative stress: Surgical trauma/stress is an
important factor determining the magnitude of
inflammatory and metabolic response to surgery.
• Intraoperative and postoperative thermoregulation
and the factors determining them like anaesthetic
drugs, open body cavities, age, etc. influence the
metabolic response to surgery.
• Type of anaesthesia: The ability of anaesthetic agents
and neural blockade to modify the metabolic and
neuroendocrine response has been enthusiastically
studied. For example, regional anaesthesia with local
anaesthetics, particularly epidural blockade is known
to have many beneficial effects such as reduced
thromboembolic event, pulmonary, cardiac and
gastrointestinal postoperative complications, thereby
modifying the metabolic response to surgery.
Summary of response to injury has been given in
Key Box 15.1.
Key Box 15.1
Points to Remember
Hormones whose levels rise following injury:
ACTH
GH
Glucagon
Cortisol
Adrenaline
Hormones whose levels fall following injury:
Insulin
Thyroid hormones
Testosterone
Proinflammatory cytokines:
IL-1
IL-6
IL-8
TNF-α
Anti-inflammatory cytokines:
IL-4
IL-5
IL-9
IL-13
TNF-β
1. Which hormone level does not rise during injury?
A. ACTH
Adrenaline
B.
C. Glucagon
D. Thyroxine
1. D 2. A
2. Albumin level decreases during stress because of:
A. Decreased production
B. Decreased intake
C. Liver failure
D. Increased microvascular permeability
Answers
Section I • Basic Principles of Surgery
16
Tissue Engineering
and Stem Cell Therapy
Step 1: Choosing cell sources
Step 2: Further differentiation
Step 3: Scaffolds
Step 4: Seeding
INTRODUCTION
Tissue engineering is a relatively new field but also a
mine of unfulfilled potential for treating various
diseases. Tissue engineering aims to generate cells/
tissues in laboratories that mimic human tissues as much
as possible because most human tissues hardly show
any regenerative capacity, so the only way to repair any
loss or damage acquired would be to replace it and hope
for ideal outcomes.
This process is broadly divided into two methods:
• In vitro: Cells and the scaffold carrying them (as
required) are developed outside the body and
implanted thereafter.
• In vivo: Cellular or cell-free scaffolds are implanted
into the body and promote regeneration and repair
by ingrowing into the body’s cells.
Tissue engineering is relevant for surgeons through the
myriad of possibilities that it offers, ranging from acting
as models for testing therapeutic efficacy to scaffolds
reconstructing or replacing areas with extensive skin or
soft tissue loss, cartilage loss, and blood vessels, cardiac
muscle, valves, hollow viscera, and pancreatic islets.
Future prospects may include solid organ replacement.
Biological sciences, material sciences, and engineering
contribute to different aspects of the research and
development of stem cells, ideal scaffolds, and
conducive environments.
Sources of cells for tissue engineering include fully
differentiated somatic cells and stem cells.
for
Step 5: Implantation
Applications
Issues and concerns
STEP 1: CHOOSING CELL SOURCES
Somatic Cells
Fully differentiated cells from normal tissues are grown
in vitro and are developed on a scaffold. These cells can
be obtained from the recipient by tissue biopsy
(autologous cells) or from unrelated donors (allogenic
cells). Examples include autologous chondrocyte
implantation for areas of deficient cartilage and smooth
muscle with uroepithelial cells for bladder wall
reconstruction. Autologous cells carry the advantage of
no risk of immune-mediated rejection
carry the disadvantages of needing immunosuppression
and limited in vitro proliferative ability, making it
impractical for larger volumes.
Stem Cells
These are undifferentiated cells with the unique ability
of infinite cell division and hence constant renewal. If
stimulated with appropriate growth factors, they can
also differentiate into specialised cell lines. These
features make stem cells the most attractive option for
regenerative therapies.
They are classified depending on where they are
derived from, namely embryonic stem cells, fetal stem
cells, adult or somatic stem cells, and induced pluripotent stem cells.
a. Somatic stem cells: In adults, there exists reserve of
stem cells (especially in rapidly proliferating systems)
to provide replacements at the end of their functional
lifespans or during damage or disease. These cells
are especially predominant in the gastrointestinal
56
. Allogenic cells
Tissue Engineering and Stem Cell Therapy
57
epithelium and bone marrow. However, they can
differentiate into a limited number of cell types and
hence are ‘multipotent’.
Examples include hematopoietic stem cells (mainly in
hematological malignancies), mesenchymal stem cells
(mainly for tissue engineering), and neural stem cells.
b. Mesenchymal stem and stromal cells (MSCs):
Mesenchymal stem cells or stromal cells resemble
fibroblasts and are obtained from bone marrow,
adipose tissue, or the umbilical cord.
These cells have the ability to adhere to plastic
surfaces and display certain cell surface markers.
They are typically used for their ability to differentiate
into mesodermal-derived cells, such as osteoblasts,
chondrocytes, adipocytes, and myocytes.
They can also express growth factors and hence have
both trophic and immunomodulatory properties.
They are usually obtained by bone marrow aspiration
from the iliac crest or by liposuction, following which
they are cultured in vitro or are differentiated into
desired cell types by the addition of growth factors.
The ease of obtaining these cells has made them an
attractive option, especially for treating burns and
repairing cartilage.
c. Embryonic stem cells: These are obtained from the
inner cell mass of blastocysts using unused embryos
created at the time of in vitro fertilization. These cells
are totipotent and give rise to all the cells of the body.
They have a superior proliferative ability, but their
development has given rise to several ethical issues.
There are strict guidelines in place for their development, and the dominant view in most countries is
that their potential therapeutic benefits outweigh
their ethical concerns. However, these cells are
allogenic and have the problem of rejection. Advances
in nuclear transfer have paved the way for developing
pluripotent stem cells designed for the recipient.
d. Fetal stem cells: These are obtained from the tissues
of fetuses that have been aborted. They are also
pluripotent. Uses include cell therapy in diabetes
mellitus, spinal cord injuries, neurological disorders,
etc. However, they are also associated with several
ethical issues.
e. Induced pluripotent stem cells (iPSCs): This is based
on the principle that certain adult cells can be
reprogrammed to become pluripotent stem cells by
manipulating their genetic structure. This is achieved
by transferring specialized transcription factors (e.g.
OSKM reprogramming factors, Yamanaka factors)
via viruses to the cells of interest. This breakthrough
comes with several advantages.
First, it overcomes any ethical concerns associated
with embryonic stem cells. Second, it overcomes the
risk of rejection, as the cells obtained from the
recipient can themselves be reprogrammed and used
for therapy. Third, a tissue bank of iPSCs from
volunteer donors can be created.
However, the problem associated with the use of
potentially oncogenic viruses is a disadvantage.
Current research has focused on overcoming these
issues with the use of non-retroviral vectors and
virus-free transfer options. Newer advances in
CRISPR-Cas9 gene editing have also helped tailor
iPSCs for disease research.
f. Endothelial progenitor cells: They express surface
markers found in peripheral blood and are involved
in the development of vessels and blood cells.
STEP 2: FURTHER DIFFERENTIATION
Current research aims at the most ideal environment
that stem cells need to finally differentiate into cells and
tissues of interest. Efforts are currently focused on
creating an environment as close to the normal development process as possible. The growth factors, matrices,
and scaffolds used for various tissue types differ;
however, they usually follow the same sequence of
initial differentiation of iPSCs into either of the three
lineages of ectoderm, mesoderm, or endoderm, followed
by further differentiation, both of which are done in
vitro. They are used only after they are fully phenotyped
and assessed for functionality.
STEP 3: SCAFFOLDS
Scaffolds, which are physical support systems for stem
cells and their progeny, mimic the extracellular matrix
(ECM). They function just like the ECM does, allowing
cells to attach, providing necessary signals, and aiding
growth, migration, and nutrition, and are biocompatible
and non-immunogenic. Rigid and semirigid porous
scaffolds, into which stem cells are seeded, are used.
Scaffolds can be natural or artificial.
Natural Scaffolds
Human tissues and organs are processed using
detergents to remove cells, and the ECM left behind is
used. This is especially useful when the target tissue
being regenerated has a complex structure, such as
complex solid organs. These whole organs needed for
engineering are obtained from cadavers. Hence, their
disadvantage lies in their limited availability.
Artificial Scaffolds
There is a wide assortment of artificial scaffolds available, and they are ideally biocompatible, bioresorbable,
and biodegradable. They are made from both natural
Section I • Basic Principles of Surgery
58
Manipal Manual of Surgery
and synthetic materials, such as polysaccharides,
collagen, fibrin, polyglycolide, graphene, ceramics,
glasses, etc. The development of these scaffolds has been
furthered by the use of 3D printing and electrospinning
technology. They are usually porous and hydrophilic.
Composite scaffolds and ‘smart scaffolds’ that respond
to physical stresses are also being developed.
Scaffolds are commonly used to restore vascular
integrity and are now advanced to include angiogenic
growth factors as well.
STEP 4: SEEDING
Cells are typically incorporated into the scaffolds in vitro.
Techniques include static cell seeding, dynamic cell
seeding (uses rotation), magnetic cell seeding (uses
supramagnetic microbeads binding to cells), photopolymerized systems using UV light, vacuum seeding,
and bioreactor perfusion systems.
STEP 5: IMPLANTATION
The efficacy of the engineered tissue ultimately depends
on how well it integrates into the host tissue and
reproduces its functions. Hence, an integral part of
developing these tissues is postproduction testing in
similar stressful environments that are subjected to in
the body to ultimately ensure successful outcomes.
3. Hematopoietic stem cells for bone marrow transplant
in hematological malignancies.
4. Adult stem cells for ischemic heart failure (trials).
5. Stem cells for perianal fistulas (trials).
6. MSCs for graft vs host disease (trials).
ISSUES AND CONCERNS
1. Safety concerns: Development of malignancy is an
issue with using pluripotent stem cells, and rigorous
post-development purification and assessment is
needed to ensure that all cells are differentiated. To
reduce the effects of oncogenic viruses, viral vectors
that do not integrate into the genome and non-viral
vectors can be used.
. Infection transmission: Adequate screening is a must.
2
3. Need for immunosuppression.
4. Risk of rejection.
5. Side effects of immunosuppression.
6. Inadequate data as the entire field still in its early
stages of development.
7. Ethical issues.
8. Cost of development.
REFERENCES
APPLICATIONS
1. Embryonic stem cells programmed to develop into
retinal pigment epithelium cells to treat age-related
macular degeneration (experimental). iPSCs have
also been used for the same.
. Somatic cell nuclear transfer to produce beta
2
pancreatic cells from stem cells (experimental).
1. Williams N, O’Connell P, McCaskie A. Bailey and Love’s
Short Practice of Surgery. 27th ed. CRC Press, pp. 33–41,
2018.
2. Townsend C, Beauchamp R, Evers B, Mattox K, Sabiston D.
Sabiston Textbook of Surgery. 21st ed. Elsevier, pp. 150–156,
2021.
3. Sultana N, Bandyopadhyay-Ghosh S, Soon C. Tissue Engineering Strategies for Organ Regeneration. CRC Press, 2020.
Section I • Basic Principles of Surgery
17
Shock and Haemorrhage
Shock
Hypovolaemic
Cardiogenic
Distributive (septic, anaphylactic, neurogenic,
acute adrenal insufficiency)
Obstructive (tension pneumothorax, cardiac
tamponade)
SU17.1: Describe pathophysiology of shock, types of
shock and principles of resuscitation including fluid
replacement and monitoring.
SU17.2: Describe clinical features of shock with
appropriate treatment.
SHOCK
Definition
Shock is defined as an acute failure of the circulatory
system to supply blood in sufficient quantities or under
sufficient pressure to the tissues. It is a syndrome
characterised by hypoperfusion and severe dysfunc-
tion of vital organs.
Pathophysiology
Whenever there is hypoperfusion due to any reason,
the body tries to compensate by releasing massive
amounts of catecholamines (fight or flight response).
This causes progressive vasoconstriction of cutaneous,
muscular and visceral circulation in an attempt to
preserve blood flow to the vital organs, the heart, brain
and the kidneys. The heart rate increases resulting in
an increase in cardiac output. Thus, in most cases,
tachycardia is the earliest sign of shock. The peripheral
vascular resistance also increases due to the catechola-
Haemorrhage
Classification
Pathophysiology
Management
Indicators of fluid responsiveness
Central venous pressure
IVC collapsibility index
Passive leg raising
mine release which in turn causes the diastolic blood
pressure to rise and helps to maintain organ perfusion.
These compensatory mechanisms are effective in the
early stages and are limited. In later stages, other
vasoactive hormones such as histamine, bradykinin, β
endorphins and other cytokines are also released. The
hypoperfusion results in deprivation of oxygen and
essential substrates at the cellular level causing a shift to
anaerobic metabolism and development of lactic acidosis.
With prolongation of shock, there is inadequate ATP
production and the cells begin to lose their normal integrity. The electrical gradient across the cell membrane gets
lost, the cell swells up eventually causing cellular death.
Types of Shock
• Hypovolaemic shock: Loss of fluids or blood
(haemorrhagic shock)
• Cardiogenic shock
• Distributive shock: Septic shock, anaphylactic shock,
neurogenic shock
• Obstructive shock: Tension pneumothorax, cardiac
tamponade, massive pulmonary embolism
Clinical Features
Fast and feeble pulse, cold and clammy peripheries, and
reduced urine output are prominent features of a person
59
60
Manipal Manual of Surgery
in shock. Depending on the stage of shock, the patient
may be lethargic, confused, restless, delirious or even
unconscious. The patient may develop tachypnea as a
response to hypoxia (due to hypoperfusion of tissues)
and lactic acidosis. The patient can show features
specific to the cause of shock (bleeding in haemorrhagic
shock, myocardial infarction in cardiogenic shock).
Severe shock may progress to cardiac arrest.
Diagnosis
Shock is mainly diagnosed by the clinical features. The
patient will manifest with hypotension, tachycardia,
tachypnea, obtundation or abnormal mental status, cold,
clammy extremities, mottled skin, oliguria, metabolic
acidosis, and hyperlactatemia. History and physical
examination will lead to the diagnosis of shock and the
cause of shock. Arterial blood gas showing a base deficit
or high lactate values can reliably help in the diagnosis
of shock.
General Principles of Resuscitation
The diagnosis and treatment of shock is always
concurrent and treatment at any point must not be
delayed due to any ongoing test/investigation for a
good outcome. Monitoring should include clinical
examination as well as with a pulse oximeter, noninvasive blood pressure and electrocardiogram.
The basic management principle is to ensure better
perfusion and oxygen delivery to the tissues. Assess
ABC (airway, breathing and circulation).
Assess airway: A patient in shock could be obtunded
or even unconscious. Secure airway, if the patient is
unable to maintain his airway. Give oxygen.
Assess breathing: If the patient is apnoeic or is
tachypneic and is not maintaining adequate gas exchange,
one may need to initiate mechanical ventilation.
Assess circulation: Circulation is inadequate in
shock. The priority of resuscitation is to restore
perfusion. Obtain two large bore peripheral intravenous
access (18 or 16 G). Begin resuscitation with rapid
infusion of 500 ml to a litre of Ringer lactate or isotonic
saline. Continue resuscitation with intravenous fluids,
blood products or both as necessary and appropriate
for the cause of shock to restore perfusion.
In haemorrhagic shock, after the initial litre of
intravenous fluid, packed cell volume, fresh frozen
plasma and platelets will be needed to replace lost blood
volume. Type specific blood is preferred but in an
emergency, O–ve packed cells can be given. If the facility
is available, it is wiser to activate massive transfusion
protocol (MTP) for more appropriate usage of blood
products. A patient in hypovolaemic shock due to loss
Section I • Basic Principles of Surgery
of fluids (as in severe diarrhoea) will require fluid
replacement but may not need blood products to be
transfused. Timely resuscitation in the initial phases
includes infusion of appropriate quantity of isotonic
electrolyte solutions and blood. Definitive control of
haemorrhage and restoration of adequate circulating
volume are the primary goals of management in
haemorrhagic shock.
A patient in septic shock and anaphylactic shock will
also require intravenous fluids. However, a patient in
cardiogenic shock will require infusion of vasopressors
and inotropes. They are often given diuretics to prevent
or treat pulmonary congestion. A patient in obstructive
shock will need urgent relief of this obstruction. This
can be done easily for tension pneumothorax (needle
thoracostomy) and for cardiac tamponade (pericardiocentesis). However, it is more difficult to treat massive
pulmonary embolism.
End-points of Resuscitation
The initial end-points of resuscitation (to be achieved
within a few hours) are a heart rate of < 100/min, blood
pressure of 90/60 mmHg and an oxygen saturation of
93–95%. As perfusion improves, one must aim for
normalising homeostasis. The final end-point of
resuscitation is a normal base deficit (eliminate
metabolic acidosis). This should be achieved within
12–24 hours of admission.
Specific Treatment
Specific treatment for different types of shock depends
on the cause and is given in the appropriate section.
HAEMORRHAGE
CLASSIFICATION
I. Depending on Nature of the Vessel Involved
A. Arterial haemorrhage: The blood jets out and is
bright red in colour. Pulsation of the artery may be
seen. It can be easily controlled, as it is visible.
B. Venous haemorrhage: The blood does not jet out
but oozes. It is dark red in colour. It is non-pulsatile,
and difficult to control because the vein gets retracted.
C. Capillary haemorrhage: The blood does not jet out
but oozes out slowly. The blood is red in colour. It
becomes significant, if there are bleeding tendencies.
II. Depending on the Timing of Haemorrhage
A. Primary haemorrhage: This occurs at the time of
surgery.
B. Reactionary haemorrhage: This occurs within
6–12 hours of surgery. The usual causes are
hypertension in the postoperative period, violent
Shock and Haemorrhage
61
sneezing, coughing, or retching. For example, the
superior thyroid artery may bleed after thyroidectomy, if the ligature slips; hence, it is better to ligate
it twice.
C. Secondary haemorrhage: This occurs within 5–7 days
of surgery. It is due to infection which eats away
the suture material, causing sloughing of vessel
wall (e.g. bleeding within 5–7 days of surgery for
haemorrhoids).
III. Depending on the Duration of Haemorrhage
A. Acute haemorrhage: This occurs suddenly (e.g. oeso-
phageal variceal bleeding due to portal hypertension).
B. Chronic haemorrhage: This occurs over a period of
time (e.g. haemorrhoids/piles, chronic duodenal
ulcer, tuberculous ulcer of the ileum, diverticular
disease of the colon).
IV. Depending on the Nature of Bleeding
A. External haemorrhage/revealed haemorrhage (e.g.
epistaxis, haematemesis).
B. Internal haemorrhage/concealed haemorrhage
(e.g. splenic rupture following injury, ruptured
ectopic gestation, liver laceration following injury).
A patient who had undergone subtotal thyroidectomy for
toxic goitre was shifted to the postoperative intensive care
unit. Within 10 minutes, the nurse came to inform the
surgeon that 450 ml of blood was collected in the
‘Redivac’ suction bottle. The dressing was opened and
there was no large collection of blood in the surgical
wound. The presence of a large haematoma was thus
ruled out. The blood pressure (BP), which was previously
under control, had shot up to 210/110 mmHg postoperatively, possibly due to pain. Careful monitoring and
treatment reduced the BP to 140/90 mmHg. After
24 hours, the drainage was only 100 ml. The incision did
not need re-exploration. This case illustrates reactionary
haemorrhage due to hypertension.
PATHOPHYSIOLOGY OF HAEMORRHAGIC SHOCK
A loss of >30–40% blood volume results in a fall in blood
pressure, and gross hypoperfusion of the tissues and
vital organs, leading to haemorrhagic shock. Haemorrhagic shock can be classified as follows (American
College of Surgeons) depending on the amount of blood
lost and clinical features:
Classification of Haemorrhagic Shock
Class I
• When blood loss is <750 ml (<15% of blood volume),
it can be called mild haemorrhage.
• 60–70% of blood volume is present in the low-
pressure venous system (capacitance vessels). 10%
of the blood volume is present in the splanchnic
circulation.
• When there is blood loss, peripheral venoconstriction
takes place, which compensates for the loss of blood
volume by shifting some blood into the central
circulation. Some amount of blood volume correction
also occurs due to withdrawal of fluid from the
interstitial spaces.
• Apart from mild tachycardia and thirst, there may
be no other symptoms or signs suggesting hypovolaemia. The blood pressure, urine output, and
mentation are all normal.
Class II
• Loss of 750–1500 ml (15–30% of blood volume) results
in moderate shock.
• Peripheral venoconstriction may not be sufficient to
maintain circulation. Hence, adrenaline and noradrenaline (endogenous catecholamines) released
from the sympathoadrenal system cause powerful
vasoconstriction of both arteries and veins.
• Increased secretion of ADH causes retention of water
and salt. Thirst increases.
• Clinically, the patient shows a heart rate of 100–120
beats/minute and an elevated diastolic pressure. The
systolic pressure may remain normal.
• Urine output is reduced to about 0.5 ml/kg/h and
the capillary refill time is more than the normal
2 seconds. Extremities may look pale and the patient
is confused and thirsty.
Class III
• Loss of 1500–2000 ml (30–40% of blood volume)
produces Class III shock. All the signs and symptoms
seen in Class II haemorrhagic shock get worse.
• The patient’s systolic and diastolic blood pressures
fall and the heart rate increases to around 120 beats/
minute. The pulse is thready.
• The respiratory rate increases to > 20/minute. Urine
output drops to 10–20 ml/hour. The patient appears
pale and is aggressive, drowsy, or confused.
Class IV
• A blood loss of >2000 ml (>40% of blood volume)
results in Class IV shock. The peripheries are cold
and ashen.
• The pulse is thready and >120/minute. The blood
pressures are very low or unrecordable.
• The patient may be moribund.
• If persistent, other organs may get damaged:
Section I • Basic Principles of Surgery
62
Manipal Manual of Surgery
– Mucosal ulcerations, upper GI bleeding, absorption
of bacteria and toxins, bacterial translocation, and
bacteraemia
– Liver: Reduced clearance of toxins
– Kidney: Acute renal failure
– Heart: Myocardial ischaemia, depression
– Lungs: Loss of surfactant, increased alveolo-
capillary permeability, interstitial oedema, and
increased arteriovenous shunting result in acute
lung injury (ALI).
• Multiorgan failure consequent to haemorrhagic
shock is associated with a high mortality rate.
• Early diagnosis of bleeding and appropriate manage-
ment is crucial to improve survival and outcome.
MANAGEMENT OF HAEMORRHAGIC SHOCK
reatment—General Measures
I. T
• Hospitalisation
• A patient in haemorrhagic shock needs immediate
resuscitation to prevent or minimise damage to the
vital organs and tissues. Resuscitation and control of
haemorrhage should happen simultaneously.
• O-M-IV: First, provide oxygen, attach a monitor to
record vitals (heart rate, blood pressure, respiratory
rate, and oxygen saturation) and obtain two large
bore intravenous access.
• Remember O-M-IV for all critically ill patients: O for
oxygen, M for monitor, and IV for intravenous access.
Blood sample for investigations, blood grouping, and
cross-matching should be sent at this stage.
• Care of all critically ill patients begins with
A (airway), B (breathing), and C (circulation).
• Airway and breathing: Oxygen should be adminis-
tered by face mask to all patients who are in shock,
but are conscious and are able to maintain their
airway. If unconscious, endotracheal intubation and
ventilation with oxygen may be necessary.
Circulation
• Haemorrhage control (see below)
• Resuscitation and haemorrhage control must happen
simultaneously.
• Two large peripheral lines (18 or 16 G) are preferred
for initial resuscitation. Intravenous fluids, preferably
at 40–42°C (crystalloids—Ringer lactate, or
plasmalyte) are infused rapidly to restore volume.
• Send blood sample for investigations, blood
grouping, and cross-matching.
• Dextrose containing solutions are not recommended.
Infusion of large amounts of isotonic saline may cause
Section I • Basic Principles of Surgery
hyperchloraemic acidosis and is not recommended.
• Insertion of central lines is not recommended (unless
done by skilled personnel), as it takes much longer
to insert, requires expertise, and may be associated
with complications.
• External jugular venous access is another option for
quick transfusion of large amounts of fluids and
blood products.
• If a peripheral intravenous access is not available, an
intraosseous needle may be inserted to infuse fluids
into the bone marrow (Fig. 17.1). All infusions that
can be given intravenously can also be given intraosseously.
Intraosseous Cannulation
• The bone marrow of long bones is in direct
communication with the vascular tree and hence,
anything injected into the bone marrow will reach
circulation. Thus, when intravenous access is not
available and access to the circulation is required in
an emergency as in major trauma, burns, circulatory
arrest, intraosseous needles can provide rapid and
life-saving access to the circulation. This is most often
performed in children but can be done in adults also
in emergency circumstances.
– Contraindications: Fracture of the long bone being
punctured, previous puncture of the same bone
either at the same site or another site on the same
bone, infection at the site, b
urn at entry site and
inability to locate landmarks.
– Sites: Intraosseous puncture is most commonly
made at the upper end of tibia, one finger-breadth
below the tibial tuberosity on the medial surface.
The other sites are lower end of femur, lower end
of radius, manubrium sternum, iliac bone and the
calcaneus.
– Needle: A large bore needle is required. A bone
marrow aspiration needle with a guide such as
Jamshidi needle is best suited for this procedure.
Several others such as
Sur-Fast intraosseous needle,
Sussmane-Raszynski needle or the EZ-IO can be
used. If these are not available, any large bore
needle with stylet can be used for this purpose.
Fig. 17.1: Intraosseous cannulation
Shock and Haemorrhage
63
– Procedure: The limb to be used must be stabilized
using a pillow or roll. Under aseptic precautions,
the skin over the puncture site is anaesthetized
using 2 ml of local anaesthetic. The bone is held
steady with the nondominant hand and the needle
held in the palm of the dominant hand such that
the needle, wrist and elbow are in the same straight
line. The bone is punctured with a rotatory
movement through the skin and then the bone. Loss
of resistance indicates entry of the needle into the
marrow. Care must be taken not to penetrate the
opposite surface of the bone. The operator must
be careful and not place his hand in the needle path.
The marrow may or may not be aspirated from the
needle. A 10 ml syringe containing saline is
connected to the needle. If the saline can be injected
freely and without any extravasation, an infusion
of saline or Ringer lactate can be commenced
through the needle. A free flow of this solution may
be obtained but may need to be injected, if there is
resistance. Anything that can be given intravenously
can also be given by the intraosseous route.
– Care must be taken to check the correct position of
the needle. Puncture of the opposite surface of the
bone must be avoided to prevent leakage of fluid
through that hole into the tissues. The limb must
be observed closely for any swelling due to
extravasation. An intravenous access must be
secured as soon as possible and the intraosseous
line removed. Generally, an intraosseous line is
removed in a few hours’ time but it can be used up
to 48 hours.
– Complications: Infections at the site of insertion
such as cellulitis, osteomyelitis can occur due to
poor aseptic technique. Extravasation of fluid and
compartment syndrome can occur, if not carefully
watched. Fracture of the bone can also occur if
excessive force is applied during insertion.
• The American College of Surgeons classification
of haemorrhagic shock (as given above) may be used
as a quick guide to gauge the amount of blood loss.
If the patient is tachycardic (heart rate >120/min) and
hypotensive (systolic blood pressure is <90 mmHg),
the patient has Class III shock or higher and has lost
>30–40% blood volume.
• Remember that the numbers given above are a rough
guide. The actual clinical presentation may change
with comorbid illnesses, other injuries, or concurrent
medications.
• If infusion of 1–2 litres (in an adult) of Ringer lactate
has not been successful in returning the vitals to
normal values, the patient may have lost a large
amount of blood and may be having ongoing
bleeding. Such patients require transfusion of blood
products (packed cells and fresh frozen plasma).
• It may be necessary to activate massive transfusion
protocol (when available at the hospital), if the patient
is bleeding profusely. Replacing the lost volume and
controlling haemorrhage is important to restore
perfusion and prevent tissue damage.
• Most blood banks do not issue whole blood (as it is
uneconomical for a scarce commodity), and provide
component therapy. In an actively bleeding patient
who is in hypovolaemic shock, the ratio of packed
cells : fresh frozen plasma : platelets would be 1:1:1.
• Generally, typed and cross-matched blood is given.
However, if the shock is severe and the patient is in
Class IV shock, O –ve blood may be given as a lifesaving measure. Subsequently, cross-matching needs
to be done before giving type-specific blood.
• In cases where the haemostasis is not yet achieved,
volume infusion should be controlled to maintain
systolic BP at 80–90 mmHg till the bleeding can be
stopped. This is called ‘hypotensive fluid resuscitation’
or ‘permissive hypotension’.
• Use of a fibrinolytic agent like tranexamic acid 1 g
stat and then 8th hourly is advised to reduce bleeding.
• Once bleeding is controlled, infuse sufficient volume
to allow blood pressure to reach normal levels as soon
as possible (first phase of resuscitation).
• The second phase of resuscitation involves continua-
tion of fluid therapy to ensure the base deficit is
eliminated. This is important to ensure that the microcirculation is normal. This should happen within
12–24 hours (the earlier, the better).
• All through the resuscitation, it is important to
maintain patient’s body temperature (by using warm
air blowers, keep him covered). Hypothermia impairs
coagulation, increases bleeding, depresses respiration
and circulation, and increases the chances of infection.
• Use of inotropes and vasoconstrictors is not indicated,
as they may harm tissue perfusion.
• However, if inotropes have been started as a life-
saving measure, an attempt should be made to wean
them as soon as the volume status is corrected and
the patient is stable.
II. Treatment—Specific Measures
Control Haemor
1. Pressure and packing
• This is the method of choice to stop bleeding when
the bleeding site is accessible.
• Packing using roller gauze with or without adrena-
line to control bleeding from the nose and scalp.
rhage
Section I • Basic Principles of Surgery