Part 1

Preface
This is the third edition of Ain Shams University Textbook of Surgery for Medical
Students. The name of the book is changed from “Notes” to “Textbook”, as we
believe the new name is a real description of the book, it is a textbook for medical
students. This edition is totally revised and re-edited so much so that some parts
of the book are totally rewritten. We aimed at explaining every subject of the book
in simple words to help medical students understand what they are reading and
not simply to archive medical knowledge in their minds. The illustrations that we
added to the text also help to achieve the goal from reading the book, that is
understanding medicine rather than archiving medical knowledge. The names of
the chapters are generally kept the same as previous editions, however, some new
chapters are added such as the chapter of bariatric and metabolic surgery. The
principles of operations are described in corresponding chapters but operative
details are beyond the scope of this book.
Editors
Ahmed Abdel Aziz Abou Zeid

Head of General Surgery Department
Adel Abdel Aziz Ewada

Professor of General Surgery
Acknowledgement
The editors are greatly indebted to all staff members of the Department of Surgery,
Ain Shams University, who contributed to writing this book. Without their efforts
and dedication, this book would never have come to light. Many thanks are also
due to contributing staff members from the Departments of Urology, Orthopedic
Surgery, Plastic Surgery, Neurosurgery, Vascular Surgery, Pediatric Surgery,
Cardiothoracic Surgery, Anaesthesia and Oncology, whose contributions aided in
completing the chapters of this book, making it a complete and comprehensive
textbook of surgery for medical students. The editors never forget the late
Professor of Surgery, Abo Bakr El Sedik Mostafa, who was the first to adopt the
idea of inviting all staff members of the Department of Surgery, Ain Shams
University, to share in writing a textbook for medical students. The great effort that
he made to fulfill this goal was completed by Professor Emam Fakhr, Professor
Alae Abdalla and Professor Nabil Saber, Professors of Surgery, Ain Shams
University, and two editions of the book were published over the last few years
when they chaired the Department of Surgery. We thank them all.
Table of Contents
Chapter 1 (Metabolic response to Surgery) ………..……………………………………………….……………. 1
Chapter 2 (Haemorrhage, Shock, Blood transfusion) …………………………………………………………. 5
Chapter 3 (Fluid, Electrolytes & Acid-Base Balance) ……………………………………………….…………. 25
Chapter 4 (Surgical Nutrition) …..………………………………………………………………………………………. 45
Chapter 5 (Surgical Infections) ….………………………………………………………………………………………. 53
Chapter 6 (Hand Infections) ……..………………………………………………………………………………………. 68
Chapter 7 (Preoperative Assessment & Preparation) ……..…………………………………………..……. 82
Chapter 8 (Wound & Wound Healing) …………………………………………………………………..…………. 90
Chapter 9 (Postoperative Care & Complication) …………………………………………………………..…. 100
Chapter 10 (Cysts, Tumours, Sinuses & Fistulae) ………………………………………………….…………. 109
Chapter 11 (Abdominal wall & Hernias) …………….……………………………………………………………. 125
Chapter 12 (Anaesthesia & Perioperative Care) …………………………………………………..…………. 143
Chapter 13 (Surgical Oncology) ………………………………………………………………………………………. 153

Part I (Basic Surgery); Chapter 1 (Metabolic response to Surgery)
METABOLIC RESPONSE TO INJURY

AND MULTIPLE ORGAN DYSFUNCTION
Surgery, trauma and infection disturb the normal body physiology. Minor injury or infection
leads to localized inflammatory response that is beneficial to the body, while major injury or
infection leads to an exaggerated systemic inflammatory response that might be harmful to
the body called systemic inflammatory response syndrome or (SIRS). SIRS affects every
body system and organ and can eventually lead to multiple organ dysfunction syndrome or
(MODS). MODS is a major cause of death in surgical patients and it is the most common
reason for surgical patients to stay longer than 5 days in intensive care. Understanding
these responses is essential to plan the appropriate intervention.
Systemic inflammatory response syndrome (SIRS)
Major adverse event such as major trauma, major operations, and major infection can
cause major cell damage. SIRS is defined as an inflammatory state affecting the whole
body in response to severe infectious or non-infectious insult. SIRS is initiated by the
circulation of the noxious products of cell damage in the circulation. These include:
- Inflammatory cells (macrophages and neutrophils)
- Cytokines (IL8, TNF-α, IL1 and IL6)
- Pro-inflammatory substances (prostaglandins, kinins, complement, proteases and free
radicals)
- Anti-inflammatory substances (anti-oxidants, protease-enzyme inhibitors and IL10)
- Complement
- Bacteria, bacterial products and toxins
Such products are injurious to the capillary endothelium and their free circulation in blood
can cause generalized endothelial damage. The capillary pores all over the body widen and
the microcirculation will become “leaky”. Big protein molecules, that are normally confined
to the intravascular space, will leak to the interstitial space dragging fluid with them causing
hypotension, generalized hypoperfusion and oedema (see shock). MODS will eventually
happen. Early on, the condition may be reversible, however later, irreversible organ failure
will lead to death.
Causes of SIRS
- Major trauma
- Major operations
- Haemorrhage
- Fluid loss and dehydration
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- Infection, inflammation, major sepsis, endotoximia

- Major cardiovascular events
- Hypoxia
- Ischaemia and ischaemia–reperfusion injury (see shock)
In SIRS, two or more of the following criteria is met:
1- Temperature ≥38°C (100.4°F) or ≤36°C (96.8°F)
2- Heart rate ≥90 beats per minute
3- Respiratory rate ≥20 breaths per minute or
4- PaCO2 ≤32 mmHg or the need for mechanical ventilation
5- White blood cell count ≥12,000/μL or ≤4000/μL or ≥10% band forms
Extra factors that contribute to the occurrence or worsening of SIRS
• Fall in Intra-vascular volume
• Hypothermia
• Pain
• Psychological Stress
• Starvation
Multiple organ dysfunction syndrome (MODS)
SIRS will eventually lead to MODS that is defined as progressive dysfunction of two or
more major organ systems in a critically ill patient making it impossible to maintain
homeostasis without external support. The sequence of individual organ failure in MODS
often follows a predictable pattern with pulmonary failure occurring first, followed by hepatic,
intestinal, renal and finally cardiac failure. Manifestations of organ failure in MODS are:
- Pulmonary failure: Acute (formerly ‘adult’) respiratory distress syndrome (ARDS).
- Hepatic failure: Rising bilirubin, serum glutamic oxaloacetic transaminase (SGOT) and
lactate dehydrogenase (LDH)
- Intestinal failure: - Bacterial translocation
- Stress ulcer causing gastrointestinal haemorrhage requiring blood
transfusion.
- Renal failure: Rising serum creatinine and low urine output
- Cardiac failure: Low cardiac output and hypotension.
- Cerebral failure: Altered mental states
- Disseminated intravascular coagulopathy (DIC).
The mortality of MODS is related to the number of failing organs: mortality is 60% with two
organs and more than 90% with three failing organs.
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Components of the Metabolic Response to Injury

The components of the metabolic response to injury include
- Acute inflammatory response and cell damage
- Effect on blood vessels and microcirculation
- Effect on afferent nerves and sympathetic activation
- Endocrine response to injury
All these factors will be discussed in details in shock.
SIRS and MODS in surgery
Many surgical diseases or complications can lead to SIRS and MODS. Examples are
severe acute pancreatitis, bowel anastomotic leak, major trauma, limb ischaemia,
necrotizing fasciitis and others. Organ dysfunction often begins insidiously. If active
resuscitation and treatment are not started promptly, by 7–10 days MODS will be
established and the prognosis becomes substantially worse.
Prevention and treatment of SIRS and MODS
Prevention of SIRS and MODS is achieved by reducing the level of circulating injurious
inflammatory mediators and limiting the period of stress. This can be achieved by
eliminating the factors predisposing to the syndrome and improving the delivery of host
body defences to the tissues. Prevention is achieved by:
- Appropriate use of prophylactic and therapeutic antibiotics
- Proper clinical judgement and early diagnosis before MODS is established
- Proper surgical technique (effective excision of necrotic tissue, minimizing bacterial
contamination, avoiding accumulation of postoperative fluid collections (serum or blood)
- Surgical complications with septic potential should be treated early (e.g. drainage of
abscesses, exteriorizing leaking anastomoses). It is often better to perform a laparotomy on
suspicion and find it normal than to ‘wait and see’ and risk rapid deterioration and death.
- Adequate and early fluid resuscitation in patients with hypovolaemia
- Maintaining tissue oxygenation by supplemental oxygen or assisted ventilation as
required.
- Rapid resuscitation and early definitive treatment of major injuries
- Early and thorough excision of necrotic and infected tissue
- Rapid cardiovascular resuscitation and prevention of shock
- Nutritional support, by supplemental oral feeding, fine-bore nasogastric tube, feeding
jejunostomy, gastrostomy or by parenteral feeding (see chapter of Nutrition). Enteral
feeding is preferred to nourish enterocytes and colonocytes. This helps prevention of
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intestinal bacterial translocation. Glutamine, arginine and omega-3 fatty acids are believed
to be important.
- Proper pain control
- Correction of any psychological stress
- Warming patients and avoiding excess heat loss
There is no specific treatment for established multiple organ failure. Management is by
supporting organ systems with ventilation, cardiovascular support and
haemofiltration/dialysis until there is recovery of organ function.
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Part I (Basic Surgery); Chapter 2 (Haemorrhage, Shock, Blood transfusion)
HAEMORRHAGE
Definition:
Haemorrhage is the escape of blood outside the circulatory system through the damaged wall of
blood vessels.
Aetiology:
1- Injury to a blood vessel due to mechanical or surgical trauma.
2- Involvement of blood vessels in surrounding pathology such as an overlying benign ulcer (e.g.
duodenal ulcer eroding the gastroduodenal artery) or cancer (e.g. colon cancer eroding colonic wall
vessels)
3- Congenital or acquired haemostatic defects (Haemorrhagic Diathesis) This can increase the
amount of traumatic and pathological bleeding, or it can cause bleeding after minor or unnoticed
trauma (spontaneous haemorrhage).
Types Of haemorrhage:
A – According to the type of bleeding vessel:
1-Arterial haemorrhage; is characterized by bright red jets of blood that rise and fall with pulse.
2-Venous haemorrhage; is characterized by dark red steadily flowing blood. Venous bleeding can
be severe when large veins are opened or with high venous pressure.
3- Capillary haemorrhage; is characterized by bright red ooze of blood from a wide surface area.
B- According to the timing of haemorrhage in relation to trauma:
1- Primary haemorrhage: Occurs at the time of injury or during operation.
2- Reactionary haemorrhage: Occurs within the first 24 hours after trauma or operation. It is
caused by slipping of improperly tied ligature or dislodgment of a clot from a blood vessel. The latter
is predisposed to by factors to such as normalization of arterial blood pressure after surgery, and
postoperative increase in venous pressure due to cough or vomiting.
3- Secondary haemorrhage: Occurs 7-14 days after trauma or surgery and it is caused by sloughing
of the wall of a vessel precipitated by factors such as infection (e.g. after haemorrhoidectomy),
pressure necrosis from drains and malignancy. It can be fatal if a large artery is involved (e.g.,
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bleeding from the carotid artery after sloughing of the skin flaps of a radical neck dissection).
C- Revealed (External) versus concealed (Internal) haemorrhage:
Revealed or external haemorrhage is visible. It can occur through skin wounds or from body
orifices (e.g. epistaxis and haematemesis)
Concealed or internal haemorrhage is invisible. It can occur in body cavities (e.g., haemoperitoneum
and haemothorax), or in interstitial tissue (e.g. haemorrhage around fractures).
D- Acute versus chronic haemorrhage
Acute haemorrhage means loss of blood in a short period of time. If considerable, it can lead to
hypovolaemic shock. Common causes of acute haemorrhage are accidental and surgical trauma,
gastrointestinal bleeding, and obstetric bleeding.
Chronic haemorrhage means loss of blood over a long period of time. If improperly treated, it causes
anaemia. Common causes include bleeding from chronic peptic ulcer and gastrointestinal
malignancies.
E- Surgical and non-surgical haemorrhage

Surgical haemorrhage can be controlled by intervention, whether surgical operation or non-surgical
intervention (e.g. angioembolisation and endoscopic control of haematemesis). Non-surgical
haemorrhage is the general ooze from a raw surface due to coagulopathy. It cannot be stopped by any
intervention. It requires correction of the coagulation abnormalities.
Physiologic response to haemorrhage

The physiologic response to haemorrhage has two aims: 1. To stop bleeding and 2. To maintain
effective circulatory volume, the latter is directed to the perfusion of important organs and tissues
(heart and brain) at the expense of less important organs and tissues (skin, skeletal muscle and
splanchnic area).
A. Physiologic response to stop bleeding:
• Vasoconstriction and retraction of the intima of the injured vessel.
• Formation of the platelet plug.
• Activation of blood coagulation mechanism.
These mechanisms occur in sequence. They are more effective when the vessel is completely
transected than when there is a side tear, and in traumatic than in pathological cases when
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constriction of the vessel may be hindered by inflammatory or degenerative changes in the vessel
wall or in its surroundings, e.g., the fibrous tissue in the base of a bleeding chronic peptic ulcer.
B. Physiologic response to maintain effective circulatory volume:
This is achieved by neural factors, endocrine factors and improved transcapillary refill:
1. Neural factors: Hypotension decreases stimulation of arterial baroreceptors (in the aortic
arch and carotid sinus) and atrial stretch receptors leading to reduction of the normal inhibitory
discharges in the vagus and glossopharyngeal nerves to the vasomotor center. The sympathetic
system is thus stimulated resulting in:
- Constriction of veins, which normally contain two-thirds of the blood volume. This displaces blood
from the capacitance side of the circulation into the heart.
- Constriction of arterioles raises the peripheral resistance. This involves mainly the arterioles of the
skin, skeletal muscle, and splanchnic area. Perfusion of the heart and brain is maintained because
their metabolic needs override the alpha-adrenergic vasoconstrictor discharge.
- Increased rate and strength of cardiac contraction.
2. Endocrine factors:
- Hypotension stimulates catecholamine discharge from the adrenal medulla and from the nerve
endings throughout the autonomic nervous system. They increase the heart rate and myocardial
contraction and cause constriction of the arterioles of the skin, kidney and viscera.
- The metabolic hormones ACTH, cortisol, growth hormone and glucagon are increased. Insulin
release is inhibited by adrenaline and noradrenaline.
- Activation of the renin-angiotensin aldosterone system. The juxtaglomerular cells of the afferent
renal arterioles secrete renin in response to renal hypoperfusion. Renin splits angiotensinogen to
angiotensin I which is converted to angiotensin II by a converting enzyme in the lung. Angiotensin II
is a powerful vasoconstrictor and stimulates sodium and water retention by a direct action on the
kidney as well as indirectly through release of aldosterone from the zona glomerulosa of the adrenal
cortex.
N.B. Angiotensin-mediated vasoconstriction takes some 20 minutes to occur, whereas baroreceptor-
vasoconstriction occurs within seconds.
- Release of the antidiuretic hormone (vasopressin). Blood loss greater than 10% stimulates ADH
release. ADH increases the permeability of the renal collecting tubules allowing water absorption
into the hypertonic renal medullary interstitium. With severe haemorrhage high levels of ADH also
cause vasoconstriction.
3. Transcapillary refill. Reduction of blood volume and constriction of arterioles causes a fall
in capillary hydrostatic pressure and promotes movement of fluid from the interstitium into the
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capillaries. The resulting haemodilution increases the blood volume and lowers its viscosity, thus
improving effective circulatory volume.
Clinical picture of haemorrhage

Manifestations of haemorrhage depend on the amount of blood lost, the rate of loss and the patient’s
cardiovascular reserve. Thus, loss of only 500 ml of blood may cause myocardial infarction in a
patient with coronary artery disease, whereas in a healthy young adult, losses greater than 1500 ml
may not even lower the systolic blood pressure. The following are the clinical manifestations of
haemorrhage (and hypovolaemia):
Symptoms:
1. Weakness and fainting especially when standing.
2. The patient feels cold and thirsty.
3. Haemorrhage may be evident (e.g. haematemesis, melena, bleeding external wound)
Signs:
1. The patient is pale (due to constriction of skin blood vessels) and looks tired. The extremities are
cold (again due to constriction of skin blood vessels) and clammy, the veins are collapsed and the
capillary refill is slow. With decreasing cerebral perfusion, the mental status may vary from anxiety
to drowsiness, but the patient usually remains alert.
2. Pulse and blood pressure. With mild blood loss (less than 500 ml), the pulse and blood pressure
may remain normal, thanks to the efficient compensatory mechanisms. With more blood loss,
tachycardia develops but the blood pressure remains stable. With further blood loss, however, the
compensatory mechanisms can no longer maintain the blood pressure and progressive hypotension
develops.
3. The pulse pressure decreases leading to a thready pulse.
4. There is tachypnea and air hunger.
5. There is hypothermia. Hypothermia predisposes to coagulopathy and it should be avoided. It can
be aggravated by resuscitation by cold intravenous fluids.
6. Oliguria results from diminished renal perfusion.
Classification of haemorrhage and estimating blood loss:

The adult’s blood volume is 5 liters (70 ml/Kg in adults and 80 ml/Kg in children). Four classes of
haemorrhage are recognized
Class 1 < 15% of blood volume is lost
Class 2 15–30% of blood volume is lost
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Class 3 30–40% of blood volume is lost

Class 4 > 40% of blood volume is lost
In any patient with haemorrhage, it is of vital importance to have a rough estimate of the amount of
blood loss. This can be determined from:
1. Clinical data. The more the amount of blood loss, the more severe is the clinical picture.
2. Type of injury. Haematoma around a closed fracture of the tibia contains 500-1500 ml of blood,
that around a fractured shaft of femur, 500-2000 ml, that in fractured pelvis, 2000-3000 ml.
Haemorrhage in abdominal or thoracic cavities can accommodate even more amount of blood.
3. Blood loss at operation is calculated by addition of the amount of blood in the suction reservoir
and the amount mopped up by the swabs.
Management of Haemorrhage
Haemorrhage must be recognized and managed aggressively to reduce the severity and duration of
shock and avoid death and/or multiple organ failure. The first priority is to arrest bleeding. Although
necessary as supportive measures to maintain organ perfusion, attempting to resuscitate patients who
have ongoing haemorrhage by fluid or blood transfusion will increase the blood pressure that will
merely increase bleeding from the site, and fluid therapy cools the patient and dilutes available
coagulation factors. Thus, operative haemorrhage control should not be delayed and resuscitation
should proceed in parallel with surgery.
A. Immediate resuscitative maneuvers

1. Stop external haemorrhage: Different measures can be done to stop external haemorrhage
- Direct pressure can be applied on the bleeding site. Pressure can be maintained manually by a
sphygmomanometer cuff or by a bandage. Tourniquet is contraindicated because of its complications
unless the limb is going to be amputated.
- Balloon tamponade can stop haemorrhage from oesophageal varices.
- A bleeding cavity can be packed e.g. packing the nose in epistaxis.
- Elevation of the limb above the heart level stops venous and decreases arterial bleeding.
2. Airway and breathing should be assessed and controlled as necessary.
3. A large bore cannula is inserted in a large peripheral vein, preferably in the upper limb, or by a cut
down on the long saphenous vein, if necessary. This is used for taking blood samples and for
intravenous infusion. The blood sample is tested for
- Blood group, cross-matching and preparation of blood.
- Coagulation profile is measured and corrected.
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- Complete blood picture and haematocrit are measured for initial assessment and
follow up. The initial haematocrit is often normal because RBCs and plasma are lost in the
same ratio. Some 4-6 hours later, the haematocrit level will show a reduction because of
haemodilution that is caused by movement of part of interstitial fluid into the circulation
and replacement of the lost blood by crystalloids.
4. Insert Foley’s catheter to monitor urine output
5. Identify the site of concealed haemorrhage. The aim of this step is to define the next step in
haemorrhage control (operation, angioembolisation, endoscopic control). At this point, according to
the degree of haemorrhage, a decision should be made whether to take the patient immediately to
intervention or to do investigations. The definitive management depends upon the cause of bleeding.
B. Investigations
Investigations must be appropriate to the patient’s physiological condition. Shocked patients and
those with exsanguinating haemorrhage might not be suitable for any investigations more than rapid
bedside tests. Patients who are not actively bleeding can have a more methodical, definitive workup
by CT, ultrasound ……etc.
C. Restore blood volume
Patients should be aggressively resuscitated and warmed to avoid coagulopathy. Full correction
should be the goal only after haemorrhage is controlled, before this correction aims at keeping the
vital data acceptable to avoid patient’s deterioration and to bridge the time gap until active
intervention to stop bleeding is taken.
Volume replacement depends on the class of the haemorrhage. Class I haemorrhage does not need
fluid replacement, class II needs to be corrected by crystalloids, class III and IV need blood
transfusion. The amount of fluid infusion is 3 times the estimated deficit to replenish the interstitial
fluid volume. Administration starts as bolus infusion for rapid correction of blood pressure then
fluids are given at slower rate. Failure to achieve adequate improvement indicates inadequate
replacement, continuing haemorrhage or associated pathology.
D. General care and monitoring
- Bed rest and analgesia
- Monitor pulse, blood pressure, temperature, urine output, CVP, ECG, haematocrit, blood gases and
blood lactate (index of anaerobic metabolism)
- A pulmonary artery catheter is required in complex situations to monitor the function of the left
side of the heart.
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Shock
Shock is the most common cause of death among surgical patients.
Definition of shock
Shock is defined as a systemic state of low tissue perfusion, which is incompatible with normal
cellular respiration. If perfusion is not restored in a timely fashion, cell death ensues.
Pathophysiology of shock
A. Effect of shock on cells
As perfusion to the tissues is reduced, cells are deprived of oxygen and must switch from aerobic to
anaerobic metabolism. In anaerobic metabolism, glucose is utilized to produce a little amount of
energy and lactic acid. The accumulation of lactic acid in the blood produces systemic metabolic
acidosis. The little amount of energy is not enough for normal cellular function that eventually
deteriorate. The Na/K pump of the cell membrane and intracellular organelles becomes inefficient,
sodium and water accumulate in the cell and the lysosomes release autodigestive enzymes that cause
cell lysis. Intracellular contents, including potassium, are thus released into the bloodstream.
B. Effect of shock on blood and microcirculation
As tissue hypoperfusion progresses, capillary circulation slows down causing activation of the blood
coagulation cascade and the immune system. Thus, Unnecessary coagulation of blood occurs all over
the body, this is called disseminated intravascular coagulopathy (DIC) and the natural body
coagulation factors will eventually become depleted, this is called consumption coagulopathy. There
will consequently be generalized bleeding tendency.
Hypoxia and acidosis activate complement and prime neutrophils, resulting in the generation of
oxygen free radicals and the release of cytokines. These molecules can injure the capillary
endothelial cells that become ‘leaky’. The result is leakage of large protein molecules from the
intravascular space to the interstitial space dragging with them huge amounts of fluid. This
aggravates the hypovolemia, and the resultant tissue oedema exacerbates cellular hypoxia.
C. Body defence mechanisms against shock
- The cardiovascular system

As preload and afterload decrease, the baroreceptors in the carotid sinus and aortic arch become less
stimulated resulting in increased sympathetic activity and release of catecholamines from the
sympathetic nerve endings and the adrenal medulla into the circulation. This results in tachycardia,
increased cardiac muscle contractility and systemic vasoconstriction, all are factors helping to
maintain the blood pressure. Vasoconstriction affects mainly blood vessels of the skin, muscle and
splanchnic area, while blood supply to vital organs (brain and heart) is preserved.
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- The respiratory system

The metabolic acidosis and increased sympathetic activity result in an increased respiratory rate and
minute ventilation to increase oxygen delivery to the tissues. Tachypnea also increases the excretion
of carbon dioxide, causing compensatory respiratory alkalosis.
- The renal system
Decreased perfusion pressure in the kidney leads to reduced filtration at the glomerulus and a
decreased urine output. The renin–angiotensin–aldosterone axis is stimulated resulting in further
vasoconstriction, increased sodium and water reabsorption and conservation of bicarbonate trying to
compensate for the metabolic acidosis.
- The endocrine system
The adrenal cortex secretes cortisol that causes sodium and water reabsorption in the kidney and
sensitises the cells to catecholamines. The renin–angiotensin systems is activated and vasopressin
(antidiuretic hormone) is released from the hypothalamus in response to decreased preload and
results in vasoconstriction and reabsorption of water in the renal collecting system.
D. Effect of shock on other systems
Shock affects all body systems. Ischaemia of the gastric and duodenal mucosa may produce
superficial ulcers, the so-called "stress ulcers" which may bleed. Translocation of bacteria and
endotoxins can occur from the lumen of the colon into the circulation through ischemic mucosa. This
can cause septic death in previously shocked patients even after resuscitation. ischaemic hepatic
dysfunction and elevated liver enzymes is a frequent component of shock.
E. Changes in arterial blood gases (ABGs) in shock:
- Low pH (lactic acidosis)
- Low P02 <70 mm Hg (respiratory distress then failure)
- Low PCO2 (hyperventilation and compensatory respiratory alkalosis)
- Low HCO3 (depleted buffers).
F. Ischaemia–reperfusion syndrome
After correction of the state of shock, the normal circulation is restored and products of cellular
damage (complement, neutrophils, microvascular thrombi, lactic acid and potassium) are flushed
back into the circulation where they can cause further endothelial damage in vital organs such as the
lungs, kidneys and myocardium leading to death. Reperfusion injury can also cause vascular
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dilatation and further hypotension. Reperfusion injury can only be attenuated by reducing the extent
and duration of tissue hypoperfusion.
G. Multiple organ failure
The result of prolonged tissue ischaemia and reperfusion injury is end-organ damage and multiple
organ failure. Multiple organ failure is defined as two or more failing organ systems (Table 1).
Multiple organ failure currently carries a mortality rate of 60%. There is no specific treatment for
multiple organ failure. Management is by supporting organ systems with ventilation, cardiovascular
support and haemofiltration/dialysis until there is recovery of organ function.
Table 1 Effects of organ failure
Lung Acute respiratory distress syndrome
Kidney Acute tubular necrosis and acute renal insufficiency
Liver Acute liver insufficiency
Clotting Coagulopathy
Cardiac Myocardial depression and heart failure
Stages of shock
A. Compensated shock
Early in shock, there is adequate compensation by body defence mechanisms to reduce blood flow to
non-essential organs (skin, muscle and gastrointestinal tract), and maintain adequate blood flow to
the kidneys, lungs and brain. This stage can be clinically occult and apart from tachycardia and cool
extremities, there may be no other clinical signs of shock. Despite this, systemic metabolic acidosis
and activation of humoral and cellular elements within the underperfused organs is building up. If
this state is prolonged, it can lead to multiple organ failure and death because of the ischaemia–
reperfusion effect described above.
B. Decompensated shock
Further loss of circulating volume overloads the body’s compensatory mechanisms and there is
progressive renal, respiratory and cardiovascular decompensation. In general, loss of around 15% of
the circulating blood volume is within normal compensatory mechanisms, while decompensation
starts with loss of 30–40% of the circulating volume.
C. Unresuscitatable (Irreversible) 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. Peripherally there is
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loss of the ability to maintain systemic vascular resistance and further hypotension ensues. The
peripheries no longer respond appropriately to vasopressor agents. Death is the inevitable result.
Types of shock
There are different types of shock. All types are characterised by systemic tissue hypoperfusion,
however, the initiating mechanism of tissue hypoperfusion differs from one type of shock to another.
Each type of shock also has its own specific treatment. Thus shock is classified into:
1. Hypovolaemic shock in which tissue hypoperfusion is caused by a reduced circulating volume.
Hypovolaemia may be due to loss of blood (e.g. haemorrhage), loss of plasma (e.g. burns and severe
inflammation as pancreatitis and peritonitis), or loss of fluids (e.g. decreased fluid intake, vomiting,
diarrhoea, diabetes insipidus and excessive sweating). One form of fluid loss is third-space loss. This
means that fluid is sequestered in the patient's own body, however the body is not making use of it.
Examples of third space loss include intestinal obstruction (fluid is sequestered in the gastrointestinal
tract) and pancreatitis (fluid is sequestered in the interstitial retroperitoneal space). Hypovolaemia is
probably the most common form of shock and is to some degree a component of all other forms of
shock.
2. Cardiogenic shock in which tissue hypoperfusion is caused by failure of the heart to pump blood
to the tissues. Causes of cardiogenic shock include myocardial infarction, cardiac dysrhythmias,
myocarditis, heart valve disease, blunt myocardial injury and cardiomyopathy. Cardiac insufficiency
may also be caused by myocardial depression resulting from endogenous factors (e.g. bacterial and
humoral agents released in sepsis) or exogenous factors, such as pharmaceutical agents or drug
abuse.
3. Obstructive shock in which tissue hypoperfusion is caused by reduction in preload secondary to

mechanical obstruction of cardiac filling. Common causes of obstructive shock include cardiac
tamponade, tension pneumothorax, massive pulmonary embolism and air embolus.
4. Distributive shock in which tissue hypoperfusion is caused by peripheral vascular dilatation and
low systemic vascular resistance. This type of shock is usually accompanied by high cardiac output.
Distributive shock occurs in
- Anaphylactic shock, where vasodilatation is caused by histamine release
- Spinal shock (neurogenic shock) in which there is sudden extreme vasodilatation caused by
sudden loss of the sympathetic tone that is normally responsible for peripheral vascular resistance.
This is seen in vertebral fractures causing high transection of the spinal cord and as a complication of
high spinal anaesthesia.
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- Vasovagal attack is a simple form of neurogenic shock. It is caused by hearing bad news,
watching unpleasant events or it may follow sudden severe painful stimuli as a blow to the testis or
larynx. There is extensive vasodilatation in the splanchnic area and excessive vagal stimulation of
the heart causing hypotension and bradycardia. There is temporary fall in the blood supply to the
vital centers and temporary loss of consciousness.
- Septic shock is a severe type of shock that is commonly seen in surgical practice and is
caused by severe sepsis such as peritonitis and necrotizing fasciitis. In septic shock, vasodilatation is
caused by the release of bacterial endotoxins and the activation of cellular and humoral components
of the immune system, both can cause endothelial damage and vasodilatation.
5. Endocrine shock occurs in hypothyroidism, hyperthyroidism and adrenal insufficiency. Tissue
hypoperfusion has different mechanisms in endocrine shock:
- Hypothyroidism causes disordered vascular and cardiac responsiveness to circulating
catecholamines. This causes bradycardia, decrease in cardiac output and peripheral vasodilatation.
There may also be an associated cardiomyopathy.
- Thyrotoxicosis may cause high-output cardiac failure and cardiogenic shock.
- Adrenal insufficiency (Addison’s disease) leads to shock as a result of hypovolaemia and a
poor response to circulating and exogenous catecholamines. The result will be a state of peripheral
circulatory failure, hyponatraemia and hyperkalaemia. Adrenal insufficiency is seen in Addison’s
disease and in patients receiving continuous cortisone therapy if they are subjected to any stressful
situation such as infection or surgery. In the latter situation, the adrenal cortex is suppressed by the
exogenous steroids and the patient develops severe shock due to failure of release of corticosteroids
necessary to cope with the stress from the suppressed adrenal cortex.
Notice that different types may coexist within the same patient. A trauma victim, for example, may
have blood loss from an injured viscus that produces hypovolaemic shock, in addition to blood
collection in the pericardium that causes cardiac tamponade and obstructive shock. In another trauma
victim hypovolaemic shock may be compounded by the development of neurogenic shock that is
caused by cervical spine fracture which severs the spinal cord. In the later phases of septic shock
there is hypovolaemia from third space fluid loss into the interstitial spaces and there may be
concomitant myocardial depression causing cardiogenic shock.
Clinical picture of shock
A. Symptoms and signs that are common to all types of shock
1. Mild shock
- Mild anxiety
- Tachycardia
15
- Tachypnoea
- The peripheries are cool and sweaty
- Prolonged capillary refill times
- Mild reduction in urine output

- Blood pressure is usually maintained although there is a decrease in pulse pressure.
2. Moderate shock
- Patients become drowsy and mildly confused.
- Urine output dips below 0.5 ml/kg/h.
- There is further tachycardia
- Blood pressure starts to fall
3. Severe shock
In severe shock there is profound tachycardia and hypotension. Urine output falls to zero and patients
are unconscious with laboured respiration.
B. Symptoms and signs that characterize certain types of shock
- Early in septic shock, the peripheries will be warm and capillary refill will be brisk because of
extensive peripheral vasodilatation (hyperdynamic or warm shock). In late phases of septic shock,
the patient will develop a classic picture of shock.
- Cardiogenic shock is characterized by congested neck veins and a high CVP. There might also be
evidence of pulmonary or systemic oedema.
- In anaphylaxis, the patient might develop bronchospasm, laryngeal oedema, and respiratory
distress.
- In neurogenic shock there is normal pulse rate or bradycardia and warm dry skin.
C. Pitfalls in clinical picture of shock
- Tachycardia might be absent in patients who are on β-blockers or who have implanted pacemakers.
A pulse rate of 80 in a fit young adult who normally has a pulse rate of 50 is very abnormal.
- 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 by dramatic increases in stroke volume and peripheral
vasoconstriction. Elderly patients who are normally hypertensive may present with a ‘normal’ blood
pressure for the general population but be hypovolaemic and hypotensive relative to their usual blood
pressure.
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Table 2 Cardiovascular and metabolic characteristics of shock

Hypovolaemia Cardiogenic Obstructive Distributive
Cardiac Low Low Low High
Vascular resistance High High High Low
Venous pressure Low High High Low
Mixed venous saturation Low Low Low High
Base deficit High High High High
RESUSCITATION
Immediate resuscitation manoeuvres for patients presenting in shock are to ensure a patent airway
and adequate oxygenation and ventilation. Once ‘airway’ and ‘breathing’ are assessed and
controlled, attention is directed to cardiovascular resuscitation.
A. Conduct of resuscitation
1. Once a shocked patient is received, IV access should be established, an oxygen mask is applied for
better oxygen delivery to the tissues and a urinary catheter is inserted to monitor the urine output.
Resuscitation should not be delayed in order to definitively diagnose the type of shock. Rapid
clinical examination will provide adequate clues to make an appropriate first determination.
2. If there is initial doubt about the cause of shock it is safer to assume the cause is hypovolaemia
and begin with fluid resuscitation, followed by an assessment of the response.
3. In patients who are actively bleeding (external or internal haemorrhage), it is counterproductive to
institute high-volume fluid therapy without controlling the site of haemorrhage.
4. Hypovolaemic shock caused by third space loss (e.g. bowel obstruction, peritonitis, burns) must be
adequately resuscitated before undergoing surgery because the additional surgical trauma can worsen
the hypovolaemia and shock.
5. Early immobilization of fractures and pain relief is important in shock management.
6. If analgesics are needed, the intravenous route is used because the vasoconstriction in the muscles
can lead to poor absorption of drugs after intramuscular injections.
7. Elevating both legs with maintaining the trunk in the supine position is the preferred position in
patients with hypovolaemic shock and distributive shock.
B. Fluid therapy
1. Intravenous access should be started immediately. This is achieved by inserting at least two short,
wide-bore catheters that allow rapid infusion of fluids as necessary.
17
2. The first step to be done after IV access is achieved is to take blood samples for blood
investigations, blood group and possible preparation of blood for transfusion.
3. IV fluids are given to correct the hypovolaemia and inadequate preload. They have priority on
inotropic and chronotropic drugs. Giving cardiac stimulants to an empty heart will exhaust the
cardiac muscle and rapidly deplete the myocardium of oxygen stores resulting in cardiac ischemia
and failure.
4. Central venous catheters are more appropriate for monitoring than fluid replacement therapy.
5. The type of IV fluid to be used depends on the type of shock. Blood is the best replacement in
haemorrhage after control of the source of bleeding. In other types of hypovolaemic shock and
distributive shock, crystalloid solutions (normal saline, Hartmann’s solution, Ringer’s lactate) and
colloids (albumin or commercially available products) can be given. There is no overt difference
between the two solutions, but colloids can maintain blood pressure a little bit longer than
crystalloids. Hypotonic solutions (e.g. dextrose) are poor volume expanders and should not be used
in the treatment of shock unless the deficit is free water loss (e.g. diabetes insipidus) or patients are
sodium overloaded (e.g. cirrhosis).
6. The rate and amount of fluid therapy depends on the severity of shock.
7. It is to be remembered that the oxygen-carrying capacity of crystalloids and colloids is zero. If
blood is being lost, the ideal replacement fluid is blood, although crystalloid therapy may be required
while awaiting blood products.
C. Vasopressor and inotropic support
- Vasopressor or inotropic therapy is not indicated as first-line therapy in hypovolaemia.
- Vasopressor agents (phenylephrine, noradrenaline, vasopressin) are indicated in distributive shock
states (sepsis, neurogenic shock), in which there is peripheral vasodilatation and a low systemic
vascular resistance, leading to hypotension despite a high cardiac output.
- In cardiogenic shock or when myocardial depression complicates a shock state (e.g. severe septic
shock with low cardiac output), inotropic therapy (dobutamine) may be required to increase cardiac
output and, therefore, oxygen delivery.
D. Special considerations in treatment of special types of shock
- Treatment of the cause of cardiogenic shock is of utmost importance, such as thrombolytic therapy
in myocardial infarction, control of arrhythmias and relief of cardiac tamponade by emergency
pericardiocentesis.
- Anaphylactic shock should be treated by intravenous hydrocortisone and antihistaminics.
Endotracheal intubation may be needed if laryngeal oedema and stridor are developing.
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- Patients on chronic steroids with suspected suppressed suprarenal glands should receive additional
doses of hydrocortisone intravenously prior to any surgical procedure. The treatment of an
established case needs large doses of IV hydrocortisone, saline infusions and treatment of the
predisposing factor, e.g., infection.
- In septic shock, fighting infection is done by:
(a) Eradication of sepsis, e.g., drainage of a huge abscess or peritonitis, or resection of

gangrenous bowel.
(b) Aggressive treatment with multiple and broad-spectrum antibiotics is started immediately
without waiting for the results of culture and sensitivity. A combination of cephalosporin,
aminoglycoside, and metronidazole can cover the usual organisms. When the results of culture are
available, one may change the antibiotic regimen.
Monitoring of patients in shock
- The minimum parameters to be monitored in shocked patients are the clinical parameters: pulse,
blood pressure, venous filling, capillary filling, urine output and level of consciousness
- More invasive monitoring is indicated in critical patients and patients in severe degrees of shock.
This includes:
- Electrocardiogram
- Pulse oximetry
- Central venous pressure (CVP) is a measure of the preload. The normal pressure is 5-10 cm
of water. It is measured by a catheter placed in the right atrium via the median-cubital vein, the
subclavian vein or the internal jugular vein. After placing the catheter, its position should be checked
by chest X-ray. The radiograph also serves to rule out pneumothorax due to accidental pleural injury
during its insertion.
- Repeated haematocrit and haemoglobin assessment
- Blood gases (Normal P02 is 80-100 mm Hg, normal PCO2 is 35-45 mm Hg)
- Invasive blood pressure measurement
- Cardiac monitoring using pulmonary artery catheters (invasive), or by using newer non-
invasive monitoring techniques such as doppler ultrasound, pulse waveform analysis and indicator
dilution methods.
- Base deficit and serum lactate.
- Mixed venous oxygen saturation is the percentage saturation of oxygen returning to the
heart from the body. It is a measure of the oxygen delivery and extraction by the tissues. It is
measured by samples from the central venous line. Normal mixed venous oxygen saturation levels
19
are 50–70%. Levels below 50% indicate inadequate oxygen delivery and increased oxygen
extraction by the cells.
Septic Shock
This is the most lethal type of shock and is recognized as one of the major killers in surgical practice.
It can occur in severe sepsis such as that seen in peritonitis, perforated viscus, bowel gangrene,
cholangitis and infected central venous catheter. The most common causative organisms are gram
negative bacilli, staphylococci and candida. Predisposing factors are all conditions which suppress the
immune mechanism such as old age, diabetes mellitus, corticosteroids therapy, chemotherapy,
malignancy, and HIV / AIDS. The bacterial endotoxin generated by the infecting organisms triggers
complex immunologic reactions that produce damaging products such as tumour necrosis factor
(TNF), interleukines, cytokines, free oxygen radicals and others. These products cause vasodilatation
of the arteries and arterio-venous shunting resulting in reduced peripheral resistance, diminished
oxygen delivery to the tissues, sluggish capillary circulation and DIC. There is also vascular
endothelial damage under the effect of cytokines, resulting in leakage of protein-rich fluid from the
circulation into the interstitial space causing oedema. You will notice that the sequence of events that
lead from hypoxia to cell death are the same as other types of shock, but they proceed at a faster rate
in septic shock. Moreover, if septic shock is inadequately treated heart failure takes place because of
the injurious effect of some cytokines on the heart. Adult respiratory distress syndrome (ARDS) is a
common sequel of septic shock.
BLOOD TRANSFUSION
Blood transfusion has become commonplace in different surgical disciplines. Since the first
successful transfusion in 1829, great advances have been made in the science and practice of blood
transfusion. Because the supplies of blood are limited, the use of blood and blood products must
always be judicious and justifiable in terms of clinical need.
Collection of blood
Blood is collected from healthy human donors. Before blood donation, screening of donors for some
diseases is routinely done to prevent potential harm to the recipient and the donor. The maximum
amount of blood that one can donate is 450 ml three times a year. Each unit is tested for evidence of
hepatitis B and C, human immunodeficiency virus (HIV1 and 2) and syphilis. ABO and Rhesus D
blood group is determined, as well as the presence of irregular red cell antibodies. The blood is then
processed into sub-components.
Whole blood and blood components
Whole blood is the term given to the total blood donated containing all the cellular blood elements
20
(RBCs, WBCs and platelets) in its plasma. Because of limited resources, whole blood can be
separated into different components to make the maximum benefit from the donated blood and to
help as much as possible number of patients. Thus, a unit of donated blood can be separated to
supply RBCs that will help a patient with anaemia, platelets that will help a patient with
thrombocytopenia, and plasma which is rich in coagulation factors that will help a patient with
coagulopathy. This is the trend now in blood transfusion and whole blood transfusion should be used
only in very limited situations.
Indications of blood transfusion
1. Whole blood
Whole blood transfusion should be limited to patients who are losing blood or those who have the
potential to lose blood. Examples of indications for whole blood transfusion are different types of
haemorrhage, preparation for major surgical procedures, intestinal strangulation and deep burns
where there is haemolysis. Fresh whole blood transfusion is rich in coagulation factors and platelets,
while stored blood lacks platelets and some coagulation factors. Fresh blood transfusion is also
indicated in patients with leucopoenia and agranulocytosis as a source of white blood cells.
2. Packed red cells
Packed red blood cells are red blood cells that are separated from other blood components. Each unit
is approximately 330 ml and has a haematocrit of 50–70%. Recent storage solutions increased the
shelf-life of packed red cells to 5 weeks at 2–6°C. Packed RBCs is used to treat anaemia and
haemolytic conditions
3. Fresh-frozen plasma
Fresh-frozen plasma (FFP) is whole plasma that is separated from fresh blood and stored at -40 : -50
°C. It has a very long shelf life of 2 years. FFP is rich in coagulation factors and it is used when there
is loss of plasma like in major burns and severe inflammation, or in bleeding secondary to deficient
coagulation factors such as bleeding in in cirrhotic patients. Rhesus D-positive FFP may be given to
a Rhesus D-negative woman.
4. Cryoprecipitate
Cryoprecipitate is a supernatant precipitate of FFP that is rich in factor VIII and fibrinogen. It is
stored at - 30°C with a 2-year shelf life. It is given in low-fibrinogen states or in cases of factor VIII
deficiency.
5. Platelets
Platelets are prepared as pooled platelet concentrate from more than one donor. 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 or with platelet dysfunction or those on antiplatelet therapy who
21
are bleeding or undergoing surgery.

6. Prothrombin complex concentrates
Prothrombin complex concentrates (PCCs) are highly purified concentrates prepared from pooled
plasma. They contain factors II, IX and X; factor VII may be included or produced separately. PCCs
are indicated for the emergency reversal of anti-coagulant (warfarin) therapy in uncontrolled
haemorrhage.
7. Fibrinogen is used in cases of DIC.
8. Autologous blood
It is possible for patients undergoing elective surgery to predonate their own blood up to 3 weeks
before surgery for retransfusion during the operation. Similarly, during surgery blood can be
collected in a cell saver; this washes and collects red blood cells, which can then be returned to the
patient.
Complications of blood transfusion
1. Incompatible blood transfusion (haemolytic reaction)
Haemolytic reaction can be divided into major haemolytic reaction and minor haemolytic reaction.
Major haemolytic reaction is a very serious complication of blood transfusion that can be fatal. It is
caused by ABO incompatibility where severe antigen antibody reaction occurs between the antigen
on the donor’s red blood cells and the antibodies in the recipient’s serum resulting in massive
intravascular haemolysis of the donor’s red blood cells. The haemolysed cells precipitate in the renal
tubules and cause acute renal failure. Minor haemolytic reaction is triggered by minor group
incompatibility and is usually mild and self-limiting. Some cases may occur due to transfusion of
already haemolysed blood if it is too old stored for more than three weeks or has been over heated.
Clinical picture of incompatible blood transfusion
- The reaction usually starts after giving about 50 ml of the blood
- Pain at the site of transfusion and in both lumbar regions
- Chest tightness and headache
- Muscle aches
- Rigors and fever
- Smoky urine
- Tinge of jaundice
- If the patient is doing surgery under general anesthesia, there is unexplained hypotension and
unusual oozing from the wound.
- Patient may develop acute renal failure.
Treatment includes:
22
- Stop the transfusion immediately and contact the blood bank

- Take a sample of blood from the patient to recheck his blood group.
- Keep the vein open by giving IV saline or dextrose 5%
- Give sodium bicarbonate solution (50 m Eq) intravenously aiming at alkalization of urine.
- Give 200 ml of 10% mannitol solution IV as a strong osmotic diuretic to prevent renal failure.
- If patient passes into oliguria, renal failure should be suspected and treated accordingly.
To prevent transfusion reactions, all transfusions are preceded by ABO and Rhesus typing of both
donor and recipient blood to ensure compatibility. Full cross-matching of blood takes 45 min in most
laboratories. The first 50 ml of blood should be given at a slow rate.
2. Febrile transfusion reaction
Febrile transfusion reactions are non-haemolytic reactions that are usually caused by antibodies
directed against donor’s leucocytes and HLA antigens. There is fever, chills or rigors. Febrile
reaction is not serious and it is treated by stopping the blood transfusion immediately and giving
acetaminophen (paracetamol). This form of transfusion reaction is rare with leuco-depleted blood.
3. Allergic reaction
This is rare and is caused by the presence of antigen in the transfused blood. It presents as urticarial
patches on different parts of the body. Laryngeal oedema or anaphylactic type of reaction may occur
in severe cases. Treatment is by stopping transfusion and giving antihistaminics and corticosteroids
in severe cases.
4. Transmission of diseases
The following diseases can be transmitted by blood transfusion
- Viral Hepatitis
- AIDS (HIV)
- Malaria
- Different bacterial infection. Bacterial contamination of blood may occur during blood collection
on donation or it may be a result of faulty storage (blood should be kept at 4oC to prevent bacterial
growth during storage, and it should not be left unused in room temperature)
5. Thrombophlebitis at the site of transfusion
6. Air embolism
7. Transfusion-related acute lung injury (TRALI)
It is rare but serious acute lung injury caused by antibodies in donor’s blood attacking the recipient’s
lung
8. Pulmonary micro-emboli
Micro aggregates may be formed in stored blood and may block the pulmonary capillaries. The use
23
of micro-aggregates blood filters for transfusion can prevent this hazard

9. Complications from massive transfusion
If 4 liters or more of blood is given, the following side effects may occur
- Circulatory over load.
- Metabolic acidosis if old stored blood is used
- Coagulopathy and DIC because stored transfused blood is deficient in platelets and coagulation
factors.
- Hypocalcaemia due to excess citrate which is used as anticoagulant in the transfused blood. It can
be avoided by prophylactic use of calcium gluconate injection.
- Hyperkalaemia if old blood is given. This can lead to cardiac arrhythmia and arrest.
- Hypothermia because the transfused blood is cold. It can be avoided if the blood is warmed before
transfusion
- Patients who receive repeated transfusions over long periods of time (e.g. patients with
thalassaemia) may develop iron overload and haemosiderosis
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Part I (Basic Surgery); Chapter 3 (Fluid, Electrolytes & Acid-Base Balance)
Fluid and electrolyte balance

Our body survives in a medium of water and electrolytes. The content, concentration and
pH of this medium is accurately adjusted so that the body organs function properly. Any
major derangement in this accurately adjusted system will result in serious disease and
even death. In the following chapter, the water, electrolytes and acid base balance of our
body will be explained.
Distribution of Body water/The fluid compartments
The total amount of body water in adults is about 45 liters which comprises 50-60% of the
total body weight. The female body contains less water than the male because it contains
more adipose tissue, which naturally contains less water. The body water is distributed
between two major compartments: the intracellular compartment and the extracellular
compartment. About 2/3 the body water (30 L) is present in the intracellular compartment,
and 1/3 (15L) in the extracellular compartment. The extracellular water is further subdivided
between the intravascular compartment (or plasma, 3L) and the interstitial fluid
compartment (water surrounding the cells, 12L).
The third spaces is a part of the interstitial compartment that is separated from the
circulation by a specialized epithelium, (e.g. the subarachnoid space, the peritoneum and
pleura). Body water is available for exchange and balances between different
compartments other than the third space
Composition of Fluid Compartments/The electrolytes
A- The electrolytes of the intracellular fluid compartment are:
- Principal cations are potassium and magnesium
25
- Principal anions are, phosphate and proteins

B- The electrolytes of the interstitial fluid compartment are:
. Principal cation is sodium
. Principal anions are chloride and bicarbonate
C- The electrolytes of the intravascular compartment (plasma) are:
. Principal cation is sodium
. Principal anions are chloride, bicarbonate and plasma proteins.
Notice that:
- The composition of intravascular and interstitial compartments is similar because of the
free exchange of fluids and electrolytes between both compartments through the capillary
pores.
- The concentration and composition gradient between the intracellular and interstitial
compartments is maintained by the active sodium-potassium pumps located in the cell wall.
This pump is working all the time keeping sodium outside and potassium inside the cells. In
case of pump failure, sodium will move inside the cells and potassium outside with serious
consequences. The sodium potassium pump utilizes energy from adenosine triphosphate.
26
- Water moves freely between different compartments, through the capillary pores (between
plasma and interstitial fluid) and through the semipermeable cell wall (between the
interstitial and the intracellular fluid). The aim of free water mobility is to keep the
concentration of electrolytes (or osmolarity) between the compartments equal. For example,
if sodium concentration in the extracellular fluid increases, the osmolarity of the extracellular
compartment will increase. Water will move from the intracellular compartment to the
interstitial space until osmotic equilibrium between compartments is achieved. This will
result in dehydration of the cells. On the other hand, if sodium concentration decreases in
the extracellular fluid, the osmolarity of the extracellular compartment will decrease. Water
will move inside the cells to normalize the extracellular sodium concentration and
osmolarity. This will result in swelling of the cells.
- Plasma proteins are present only in the intravascular compartment and are not free for
exchange with the interstitial fluid because the size of the capillary pores does not allow
them to pass outside the circulation. In case of leaking capillary pores, such as in
inflammation and SIRS, plasma proteins can escape to the interstitial fluid dragging water
with them from the intravascular compartment leading to hypotension, shock and tissue
oedema.
Water balance
The normal daily water requirement of an adult is about three liters. The volume of body
water remains constant by the accurate balance between body gain and body loss. Water
gain is obtained from:
- 800-1500 ml from exogenous oral fluid intake
- 500-700 ml from exogenous solid food.
- 250 ml from endogenous oxidation processes that takes place in the body.
Water is lost through:
- 1000-1500 ml in urine
- 100 - 300 ml in stools
- 600 ml insensible loss from skin and lungs
Electrolyte balance
The normal adult daily requirements of some important electrolytes are:
- Sodium (Na): 50-90 mM/day
- Potassium (K): 50-70 mM/day
- Calcium (Ca): 5 mM/day
- Magnesium (Mg): 1 mM/day
27
The daily requirement of electrolytes is obtained in food of a usual balanced diet that
contains 3 to 5 g of dietary salt. Electrolyte balance is maintained by:
1. The kidney which is capable of excreting as little as 1 mEq/d or as much as 5000 mEq/d
of electrolytes to achieve electrolyte balance. In patients with renal disease, electrolyte
balance can be very much disturbed. Serum phosphate levels are tightly controlled by renal
excretion.
2. Sweat is hypotonic, GI losses are isotonic to slightly hypotonic, both contribute little to net
gain or loss of electrolytes.
4. Serum calcium level is regulated by the parathyroid glands
Potassium metabolism
Total body potassium is about 3300 mmol. About 98% of the total potassium is present
inside the cells, 3/4 of this amount is found in the skeletal muscles. Intramuscular
potassium is mobilized to extracellular compartment with protein catabolism, exercise,
acidosis, muscle injury and crush syndrome. Although only 2% of the total body potassium
is located in the extracellular compartment, this small amount is critical to cardiac and
neuromuscular function; thus, even minor changes can have major effects on cardiac
activity. Daily requirement of potassium for a normal adult is about 1 m mol per kg body
weight (70 m mol daily). Fruits, milk and honey are rich sources. Excretion is mainly in
urine. Following any trauma, including surgical operations, there is a period of increased
excretion of potassium the urine. This will last for few days in a direct proportion to the
severity of the insult. The normal concentration of the potassium in the extra cellular fluid is
about 4 m mol/L.
Magnesium metabolism
Magnesium is the fourth most common mineral in the body and, like potassium, is found
primarily in the intracellular compartments. Approximately one half of the total body content
of 2000 mEq is incorporated in bone and is slowly exchangeable. Of the fraction found in
the extracellular space, one third is bound to serum albumin. Therefore, the plasma level of
magnesium may be a poor indicator of total body stores in the presence of
hypoalbuminemia. The normal dietary intake is approximately 20 mEq/d and is excreted in
both the feces and urine. The kidneys have a remarkable ability to conserve magnesium,
with renal excretion <1 mEq/d during magnesium deficiency.
Volume balance
Volume changes are sensed by osmoreceptors and baroreceptors. Osmoreceptors are
specialized sensors that detect even small changes in fluid osmolality and drive changes in
28
thirst and diuresis through the kidneys. Baroreceptors also modulate volume in response to
changes in pressure and circulating volume. The net result of alterations in renal sodium
excretion and free water reabsorption is restoration of volume to the normal state.
Disorders of fluid and electrolytes
Although isolated derangements in fluid and electrolytes can occur, it is much more
common for derangements to be combined. Disorders in fluid balance may be classified
into three general categories:
A. Concentration disturbance: means pure water or pure sodium gain or loss
B. Volume disturbance: means isotonic gain or loss of salt solution
C. Composition disturbance: means loss or gain of any other ion in the extracellular fluid
compartment
A. Water Depletion:
Causes
Pure water depletion is rare. It is caused by diminished intake either due to lack of
availability (e.g. a person lost in the desert) or difficulty or inability to swallow (e.g. patient
with oesophageal stricture). Pure water loss may result from increased loss from the lungs
after tracheostomy.
Consequences
Water depletion will result in increased concentration of sodium and osmolarity of the
intravascular and interstitial spaces. Water will be dragged from the intracellular
compartment resulting in cellular dehydration.
Clinical Picture
- Intense thirst and weakness.
- Decreased output of high specific gravity urine
Treatment
Increase intake of water and hypotonic solutions (dextrose 5%)
B. Water Intoxication
Causes
- Over-infusion of the hypotonic 5% dextrose solution
- Excessive absorption of water of colonic washout
- Excessive absorption of water of washout during transurethral resection of the prostate
(T.U.R.P.)
- Inappropriate secretion of antidiuretic hormone in some case of bronchial carcinoma,
chest infection and head injuries
29
Consequences
Water intoxication will result in hypo-osmolality of the extracellular compartment. Water will
move intracellularly. The cells will swell, might rupture and die.
Clinical picture:
- Nausea and vomiting.
- Drowsiness, weakness, convulsions and coma.
- Polyuria with diluted urine.
- Low PCV, serum sodium and electrolyte concentration.
Treatment
Restrict water intake, give diuretics, correct the cause, consider giving sodium and
hypertonic fluids
C. Extracellular volume deficit
This is the most common fluid disorder seen in surgical patients. It means isotonic deficit in
extracellular fluid. In other words, water and sodium are lost from the extracellular
compartment in nearly the same proportion.
Causes
- Loss of GI fluids (nasogastric suction, vomiting, diarrhea, or high output intestinal fistula)
- Sequestration of fluid in soft tissue injuries, severe sepsis, intestinal obstruction
- Loss of fluid from skin in burns
Consequences
Dehydration and shock (see chapter of shock)
Clinical picture
- Volume deficit can be either acute or chronic. Acute volume deficit is associated with
cardiovascular and central nervous system signs (see chapter of shock), whereas chronic
deficits display tissue signs, such as a decrease in skin turgor and sunken eyes, in addition
to cardiovascular and central nervous system signs.
- Elevated blood urea nitrogen level if the deficit is severe enough to reduce glomerular
filtration and hemoconcentration
- Urine osmolality usually will be higher than serum osmolality, and urine sodium will be low,
typically <20 mEq/L. Serum sodium concentration does not necessarily reflect volume
status and therefore may be high, normal, or low when a volume deficit is present.
Treatment
- Correction of the cause
- Replacement by isotonic solutions
30
D. Extracellular volume excess

It means isotonic increase in extracellular fluid. In other words, water and sodium are
increase in the extracellular compartment in nearly the same proportion.
Causes
- Iatrogenic by over-infusion of isotonic solutions
- Secondary to renal dysfunction, congestive heart failure, or cirrhosis.
Consequences and clinical picture
The plasma and interstitial volumes are increased. Water does not move inside the cells
because the concentration of electrolytes in the extracellular compartment does not
change. Excess volume is thus manifest as tissue oedema, pulmonary oedema and
cardiovascular overload. The CVP is increased and the neck veins will be distended.
Congestive heart failure may quickly develop.
Treatment
- Correct the cause
- Give diuretics
- Treat pulmonary oedema and heart failure if present
E. Hyponatraemia
Total body sodium contents is about 5000 mM which is stored mainly in the bones. A low
serum sodium level occurs when there is actual decrease in the amount of extracellular
sodium (Depletional hyponatraemia), or when there is excess of extracellular water with
normal amount of sodium (Dilutional hyponatraemia).
Causes of depletional hyponatremia
- Decreased sodium intake. This is rare
- Increased sodium loss in adrenal disease
- Volume loss with relative increased sodium loss than water loss in cases of
. GI losses (vomiting, nasogastric suction, intestinal obstruction, G I fistula especially
with high output)
. Skin loss in burns and excessive sweating
. Third space loss in peritonitis, pancreatitis
Causes of dilutional hyponatremia
- Excess extracellular water (explained above).
- Drugs that cause water retention such as the antipsychotics, tricyclic antidepressants and
angiotensin-converting enzyme inhibitors.
Consequences: Same as water intoxication (see above)
31
Clinical picture
· Anorexia, nausea, vomiting
· Weakness, fatigue, muscle cramps/twitching
. Headache, confusion, hyperactive or hypoactive deep tendon reflexes, seizures, coma
Treatment
- Correction of the cause
- Restriction of water intake
- Intravenous administration of isotonic 0.9 % sodium chloride solution
F. Hypernatraemia
Causes
- Following trauma or operation there is a variable period (usually 24 hours) of reduced
excretion of sodium from the body due to increased adrenocortical activity.
- Over-infusion of 0.9% saline solution in the early postoperative period
- Cushing syndrome, primary hyperaldosteronism (Conn`s syndrome), secondary
hyperaldosteronism in cases of liver cirrhosis
Consequences
Hypernatraemia will result in a hyperosmolar extracellular fluid compartment. This will
stimulate the thirst reflex and the patient will drink water that will correct the hypernatraemia
at the expense of increasing the extracellular volume (see above). Symptomatic
hypernatremia will occur only in patients with impaired thirst reflex or those with restricted
access to water. Symptoms are rare until the serum sodium concentration exceeds 160
mEq/L but, once present, are associated with significant morbidity and mortality. The
hyperosmolar extracellular compartment will draw water from the intracellular compartment
through the semipermeable cell wall. This will cause:
1. Cardiovascular overload
2. Cell dehydration most manifest in the CNS
Clinical picture
- Puffiness of the face is an early sign
- Pitting oedema
- Weakness
- High blood pressure
- In young infants, tense anterior fontanelle
32
- Central nervous system symptoms in the form of restlessness, lethargy, ataxia, irritability,
tonic spasms, delirium, seizures and coma. CNS dehydration can put traction on the
cerebral vessels and lead to subarachnoid haemorrhage.
Treatment
- Correct the cause
- Give diuretics
- Give water and hypotonic solutions (dextrose 5%)
- I f convenient, give water by mouth
G. Hypokalaemia
Causes
- Inadequate intake
- Infusion of potassium-free IV fluids or potassium-deficient TPN for long period
- Direct loss of potassium from GI fluid (diarrhea, vomiting, GI fistulae, ulcerative colitis and
villous rectal neoplasm)
- Excessive renal potassium excretion in hyperaldosteronism
- Prolonged use of some medications such as diuretics
- Metabolic alkalosis and insulin therapy for diabetic ketoacidosis can cause intracellular
shift of glucose and potassium
Clinical picture
- Slurred speech and confusion
- Depressed reflexes and muscles hypotonia
- Abdominal distension due to paralytic ileus
- Weakness of the respiratory muscles predisposes to chest infection
- ECG changes include prolonged Q T interval, depressed ST segment, flatting or inverted
T wave and arrhythmias (with digitalis therapy).
Treatment
- Give potassium chloride orally (for mild, asymptomatic hypokalemia)
- Give IV potassium (careful slow drip to avoid cardiac dysrhythmia and arrest. Caution
should be exercised when oliguria or impaired renal function is coexistent.
- In case potassium deficiency is due to magnesium depletion, hypomagnesaemia should
be corrected
H. Hyperkalaemia
Causes
- Increased intake of potassium supplements
33
- Blood transfusions
- Haemolysis, rhabdomyolysis, crush injury, gastrointestinal hemorrhage
- Acidosis
- Rapid rise of extracellular osmolality (hyperglycemia or mannitol)
- Impaired excretion due to presence of renal insufficiency or failure
- Prolonged use of potassium-sparing diuretics
Consequences
Hyperkalaemia makes the cells more excitable. The effects are primarily on cardiac muscle
GI, neuromuscular, and cardiovascular.
Clinical picture
- Numbness and tingling
- Tiredness and weakness
- Nausea and vomiting
- Palpitation, arrhythmia, bradycardia, hypotension and cardiac arrest.
- ECG shows wide QRS complex, high peaked T wave, flattened P wave, prolonged PR
interval (first-degree block) and ventricular fibrillation.
Treatment
- IV calcium gluconate (potassium antagonist that counter acts cardiac effects of
hyperkalaemia)
- IV sodium bicarbonate to induce alkalosis that encourages intra cellular shift of potassium.
- IV infusion of 20 gm dextrose with 10 units regular insulin to encourage intra cellular shift
of potassium.
- Ion exchange resins as sodium polystyrene sulphonate 50 gm enema
- If all measures fail, renal dialysis is indicated
- For all patients, exogenous sources of potassium should be removed.
I. Calcium abnormalities
See chapter of parathyroid gland.
J. Hyperphosphatemia
Causes
- Decreased excretion in case of impaired renal function is the most common cause
- Hypoparathyroidism and hypocalcaemia
- Unbalanced parenteral nutrition
- Excessive use of phosphorus-containing laxatives
- Endogenous mobilization of phosphorus in cell destruction as haemolysis, sepsis.
34
Clinical picture
- Most cases of hyperphosphatemia are asymptomatic
- Manifestations of the original disease such as renal failure
- Deposition of soft tissue calcium-phosphorus complexes in prolonged hyperphosphatemia
Treatment
Treatment of the cause
K. Hypophosphatemia
Causes
- Decreased phosphorus intake in malabsorption and malnutrition
- Administration of phosphate binders
- Intracellular shift of phosphorus in respiratory alkalosis, insulin therapy, and hungry bone
syndrome
Clinical picture
Manifestations of hypophosphatemia are usually absent until its level falls significantly.
Symptoms are related to adverse effects on oxygen availability for tissue and decrease in
high-energy phosphates. It can be manifested as cardiac dysfunction or muscle weakness.
Treatment is by correction of the cause and giving phosphorous supplements.
L. Hypermagnesemia and hypomagnesemia
Consequences
The magnesium ion is essential for proper function of many enzyme systems.
Hypomagnesemia can lead to persistent hypokalaemia and persistent hypocalcaemia.
Clinical picture
Manifestations are similar to hyper and hypocalcaemia (see chapter of parathyroid glands)
Treatment
Correction of the cause is important. Magnesium supplements are given in
hypomagnesemia. When hypokalaemia or hypocalcaemia coexists with hypomagnesemia,
magnesium should be aggressively replaced to assist in restoring potassium or calcium
homeostasis.
Acid-base homeostasis
Daily metabolism of the human body produces enormous amount of acid. Normal cell
metabolism depends on the maintenance of blood pH within very narrow limits. The normal
pH of the human body is 7.4 ± 0.04. Even relatively mild excursions outside this normal pH
35
range can have deleterious effects. Survival is almost impossible if blood pH falls below 6.8
or rises above 7.8.
Some basic concepts
1. What is an acid: An acid is a substance which releases hydrogen ions (H+) on
dissociation in solution. For example: hydrochloric acid (HCl) dissociates to hydrogen ions
-
and chloride ions (HCl=H++Cl ) and carbonic acid (H2CO3) dissociates to hydrogen ions
-
and bicarbonate ions (H2CO3=H++HCO3 ).
2. What is the strength of an acid: Strong acids (like hydrochloric acid and sulphuric acid)
release more hydrogen ions in solution than weak acids (like carbonic acid and acetic acid).
3. What is a base: A base is a substance which in solution accepts hydrogen ions. For
-
example, the base bicarbonate (HCO3 ) accepts hydrogen ions to form carbonic acid
-
(HCO3 +H+=H2CO3)
4. What is pH: pH is a scale of 0-14 of acidity and alkalinity. Pure water has a pH of 7 and is
neutral (neither acidic nor alkaline). pH above 7 is alkaline and below 7 acidic.
5. What is a buffer: A buffer is a solution of a weak acid and its conjugate base which
minimize the change in pH which occurs when strong acids are added by ‘mopping up’
hydrogen ions and converting the strong acid into weak acid.
Mechanisms controlling acid base balance in the human body
The endogenous acid load, that is a normal product of human metabolism, is efficiently
neutralized by three mechanisms that act together in harmony. These are the body buffers,
the lungs and the kidneys.
In blood, the principle buffer system is the weak acid, carbonic acid (H2CO3) and its
conjugate base, bicarbonate (HCO3-). If a strong acid, e.g. HCl, is added to the bicarbonate
buffer, the acid will dissociate into hydrogen ions and chloride ions (HCl=H++Cl-). The
hydrogen ions will be absorbed by the bicarbonate base forming the weak carbonic acid
(HCO3-+H+ = H2CO3). The weak carbonic acid does not release big amount of hydrogen
ions in solution and therefore the pH does not change as much as would have occurred in
the absence of the buffer.
It is to be noted that buffering is only useful in the short term because if hydrogen ions
continue to be added, all bicarbonate would eventually be consumed (converted to carbonic
acid), the buffering effect would no more exist and the pH would then fall sharply if more
acid were added. However, if carbonic acid could be continuously removed from the system
36
and bicarbonate constantly regenerated, then the buffering capacity and therefore pH could
be maintained despite continued addition of hydrogen ions. That is, in effect, what happens
in the body. In essence, the lungs ensure removal of carbonic acid (as carbon dioxide) and,
in the kidneys, carbonic acid dissociates to bicarbonate and hydrogen ions by the enzyme
carbonic anhydrase that is present in the renal tubules. The bicarbonate is reabsorbed into
blood and the hydrogen ions pass into the lumen of the tubule and are eliminated from the
body in urine.
Other important buffers include intracellular proteins and phosphates and haemoglobin.
It is important to note that the reactions described above can go in the reversed direction.
Thus, a rise in carbon dioxide concentration forces the reaction to the left with increased
formation of carbonic acid and ultimately hydrogen ions.
Body compensation in metabolic derangements
Acidosis is defined as presence of too much acid or too little base in blood resulting in
decreased pH. Alkalosis is defined as presence of too much base or too little acid in blood
resulting in increased pH. Metabolic acidosis or alkalosis are caused by imbalance in
production of acid or bases and their excretion by the kidneys. Respiratory acidosis or
alkalosis are caused by changes in CO2 exhalation due to lung or breathing disorder.
In case of presence of acid-base derangements, body compensation for such
derangements occur to restore the pH to normal. Compensation occurs by respiratory
mechanisms for metabolic derangements, and by metabolic mechanisms for respiratory
derangements. Metabolic acidosis stimulates the chemoreceptors to increase ventilation,
thus washing out CO2 resulting in compensatory respiratory alkalosis. On the other hand,
metabolic alkalosis decreases the activity of the chemoreceptors, thus depressing
ventilation, CO2 will be retained resulting in compensatory respiratory acidosis. Similarly,
the kidneys provide compensation for respiratory abnormalities by either increasing or
decreasing bicarbonate reabsorption and hydrogen ion excretion in response to respiratory
acidosis or alkalosis, respectively.
Table 3-1 Normal Values
pH = 7.4 ± 0.04
HCO3- = 22-25 mEq/L
pCO2 = 31-42 mmHg
pO2 = 80-110 mmHg
37
Table 3-2 Respiratory and Metabolic Components of Acid-Base Disorders

Acute Uncompensated Chronic (Partially
Compensated)
Type of pH PCO2 Plasma pH PCO2 Plasma
Acid-Base (Respiratory HCO3– (Respiratory HCO3–
Disorder Component) (Metabolic Component) (Metabolic
Component) Component)
Respiratory ↓↓ ↑↑ N ↓ ↑↑ ↑
acidosis
Respiratory ↑↑ ↓↓ N ↑ ↓↓ ↓
alkalosis
Metabolic ↓↓ N ↓↓ ↓ ↓ ↓
acidosis
Metabolic ↑↑ N ↑↑ ↑ ↑? ↑
alkalosis
Mixed ↓↓ ↑ ↓
acidosis
Mixed ↑↑ ↓ ↑
alkalosis
Metabolic derangements
Metabolic acidosis
Aetiology of Metabolic Acidosis
Endogenous acid production
- Ketoacidosis (excessive production of ketones hydroxybutyrate and acetoacetate in
diabetes)
- Lactic acidosis (excessive production of lactic acids due to anaerobic respiration in shock).
This is a common cause of metabolic acidosis seen in surgical patients.
- Renal insufficiency (Failure of excretion of the normal acid load by the kidneys)
Acid administration (HCl)
Loss of bicarbonate
- GI losses (diarrhea, fistulas)
38
- Ureterosigmoidostomy (implantation of ureter in the sigmoid colon after bladder resection).

The excess HCl present in urine is absorbed from the sigmoid colon mucosa, sodium is
excreted in place of hydrogen and bicarbonate is secreted in place of chloride
(hyperchlroraemic acidosis)
- Renal tubular acidosis
- Carbonic anhydrase inhibitor (failure of dissociation of carbonic acid to hydrogen ions and
bicarbonate ions in the renal tubules)
Treatment
Treatment of metabolic acidosis is treatment of the cause. In lactic acidosis, efforts should
be directed to restore tissue perfusion with volume resuscitation rather than to attempt to
correct the abnormality with exogenous bicarbonate. With adequate perfusion, the lactic
acid is rapidly metabolized by the liver and the pH level returns to normal. The overzealous
administration of bicarbonate can lead to metabolic alkalosis that can be associated with
arrhythmias that are difficult to treat.
Metabolic Alkalosis
Aetiology
Metabolic alkalosis results from the loss of fixed acids or the gain of bicarbonate.
Bicarbonate is always raised in metabolic alkalosis.
1. Excessive administration or ingestion of bicarbonate
- In antacid preparation, this is usually transient.
- Excess acetate in parenteral nutrition
- Excess citrate in blood transfusions
- Excess bicarbonate ingestion
- Milk-alkali syndrome
2. Abnormal loss of hydrogen ions, the bicarbonate ions which would otherwise be
consumed in buffering these lost hydrogen ions consequently accumulates in blood.
Excessive loss of hydrogen ions occurs in
- Excessive vomiting
- Excessive aspiration of gastric juice
- Pyloric obstruction
Unlike vomiting associated with an open pylorus, which involves a loss of gastric as well as
pancreatic, biliary, and intestinal secretions, vomiting with an obstructed pylorus results only
in the loss of gastric fluid, which is high in chloride and hydrogen, and therefore results in a
hypochloremic alkalosis.
39
3. Severe potassium depletion Potassium is the main intracellular anion. When it is lost,
hydrogen ions will be driven from the extracellular space to inside the cells to replace the
depleted potassium and this results in metabolic alkalosis.
4. Mineralocorticoids excess Bicarbonate is preserved at the expense of losing chloride in
urine (Chloride losing metabolic alkalosis)
5. Impaired bicarbonate excretion
- Decreased glomerular filtration
- Increased bicarbonate reabsorption (hypercarbia or potassium depletion)
The majority of patients with metabolic alkalosis will have hypokalemia because
extracellular potassium ions exchange with intracellular hydrogen ions and allow the
hydrogen ions to buffer excess HCO3–.
Treatment of metabolic alkalosis includes replacement of the volume deficit with isotonic
saline and then potassium replacement once adequate urine output is achieved.
Respiratory Acidosis
Respiratory acidosis is associated with the retention of CO2 secondary to decreased
alveolar ventilation. Because compensation is primarily a renal mechanism, it is a delayed
response. Examples of causes of hypoventilation are excessive use of narcotics, trauma to
the central nervous system or chest, COPD, pleural effusion, limited diaphragmatic
excursion from intra-abdominal pathology, abdominal distention.
Treatment of acute respiratory acidosis is directed at the underlying cause. Measures to
ensure adequate ventilation are also initiated. Patients may require endotracheal intubation.
Respiratory Alkalosis
In the surgical patient, most cases of respiratory alkalosis are acute and secondary to
alveolar hyperventilation. Causes include pain, anxiety, and neurologic disorders, including
central nervous system injury and assisted ventilation. Drugs such as salicylates, fever,
gram-negative bacteremia, thyrotoxicosis, and hypoxemia are other possibilities.
Hyperventilation and hypocapnia can cause an uptake of potassium and phosphate into
cells and increased binding of calcium to albumin, leading to symptomatic hypokalemia,
hypophosphatemia, and hypocalcemia with subsequent arrhythmias, paresthesias, muscle
cramps, and seizures.
Treatment should be directed at the underlying cause, but direct treatment of the
hyperventilation using controlled ventilation may also be required.
Fluid and electrolyte therapy
Parenteral Solutions
40
Fluids given by the IV route are commonly used in surgery to correct fluid, electrolyte and
acid base abnormalities. They are also used routinely during the period of postoperative
ileus, in intestinal obstruction and many other diseases and conditions such as pancreatitis.
The type of fluid administered depends on the patient's volume status and the type of
concentration or compositional abnormality present. The composition of the most commonly
used solutions is shown in Table 3-3.
Both lactated Ringer's solution and normal saline are considered isotonic and are useful in
replacing GI losses and correcting extracellular volume deficits. Lactate is converted into
bicarbonate by the liver after infusion, even in hemorrhagic shock.
Table 3-3 Electrolyte Solutions for Parenteral Administration

Electrolyte Composition (mEq/L)
Solution Na CL K HCO3– Ca Mg mOsm
Extracellular fluid 142 103 4 27 5 3 280–310
Lactated Ringer's 130 109 4 28 3 273
0.9% NaCl 154 154 308
D5 0.45% NaCl 77 77 407
D5W 253
3% NaCl 513 513 1026
D5 = 5% dextrose; D5W = 5% dextrose in water.
Sodium chloride is an ideal solution for correcting volume deficits associated with
hyponatremia, hypochloremia, and metabolic alkalosis.
The less concentrated sodium solutions, such as 0.45% sodium chloride, are useful for
replacement of ongoing GI losses as well as for maintenance fluid therapy in the
postoperative period. This solution provides sufficient free water for insensible losses and
enough sodium to aid the kidneys in adjustment of serum sodium levels. 5% dextrose
contains 50 g of dextrose per liter. It supplies 200 kcal/L. Dextrose is always added to
solutions containing <0.45% sodium chloride to maintain osmolality and thus prevent the
lysis of red blood cells that may occur with rapid infusion of hypotonic fluids. The addition of
potassium is useful once adequate renal function and urine output are established.
Alternative Resuscitative Fluids
A number of alternative solutions for volume expansion and resuscitation are available
(Table 3-4). Hypertonic saline solutions (3.5% and 5%) are used for correction of severe
sodium deficits.
41
Table 3-4 Alternative Resuscitative Fluids

Solution Molecular Weight Osmolality (mOsm/L) Sodium (mEq/L)
Hypertonic saline (7.5%) 2565 1283
Albumin 5% 70,000 300 130–160
Albumin 25% 70,000 1500 130–160
Dextran 40 40,000 308 154
Dextran 70 70,000 308 154
Hetastarch 450,000 310 154
Hextend 670,000 307 143
Four major types of colloids are available—albumin, dextrans, hetastarch, and gelatins.
Colloid solutions have high molecular weights and thus are retained in the intravascular
space for some time to increase the oncotic pressure and act as volume expanders.
Albumin is available as 5% and 25% solutions. Because it is a derivative of blood, it can be
associated with allergic reactions. Dextrans are available as either 40,000 or 70,000
molecular weight solutions. They lead to initial volume expansion due to their osmotic effect
but are associated with alterations in blood viscosity.
Preoperative Fluid Therapy
Changes in both fluid volume and electrolyte composition occur preoperatively,
intraoperatively, and postoperatively, as well as in response to trauma and sepsis.
The administration of maintenance fluids should be all that is required in an otherwise
healthy individual who may be under orders to receive nothing by mouth for some period
before the time of surgery. This does not, however, include replenishment of a pre-existing
deficit or ongoing fluid losses. The following is a frequently used formula for calculating the
volume of maintenance fluids in the absence of pre-existing abnormalities:
For the first 0 to 10 kg Give 100 mL/kg per day
For the next 10 to 20 kg Give an additional 50 mL/kg per day
For weight >20 kg Give an additional 20 mL/kg per day
For example, a 60-kg female would receive a total of 2100 mL of fluid daily: 1000 mL for the
first 10 kg of body weight (10 kg x 100 mL/kg per day), 500 mL for the next 20 kg (10 kg x
50 mL/kg per day), and 80 mL for the last 40 kg (40 kg x 20 mL/kg per day).
An alternative approach is to replace the calculated daily water losses in urine, stool, and
insensible loss with a hypotonic saline solution rather than water alone, which allows the
kidney some sodium excess to adjust for concentration. Although there should be no
42
"routine" maintenance fluid orders, both of these methods would yield an appropriate choice
of 5% dextrose in 0.45% sodium chloride at 100 mL/h as initial therapy, with potassium
added for patients with normal renal function. However, many surgical patients have
volume and/or electrolyte abnormalities associated with their surgical disease.
Preoperative evaluation of a patient's volume status and pre-existing electrolyte
abnormalities is an important part of overall preoperative assessment and care.
Postoperative Fluid Therapy
Effect of trauma and stress hormones:
• Tendency for salt and water retention and K loss
• IV maintenance needs: Most as 5% dextrose for first 24-48 hrs. then 50% 5%
dextrose solutions and 50% salt solutions.
• K is not needed for first 4 days because of big stores
The fluid requirements for healthy adult is about 3000 mL /day
• This must be adjusted according to temperature, losses, urine output..
• No K administered for the 1st four days
• Fluid chart is essential for IV fluid administration
• Empirically, we give IV fluids as follows:
• Glucose 5% 1000 mL
• Normal saline (0.9% saline) 1000 mL
• Ringer lactate 1000 mL
Postoperative fluid therapy should be based on the patient's current estimated volume
status and projected ongoing fluid losses.
Any deficits from either preoperative or intraoperative losses should be corrected. Ongoing
requirements should be included along with maintenance fluids. Third-space losses,
although difficult to measure, should be included in fluid replacement strategies.
In the initial postoperative period, an isotonic solution should be administered.
The adequacy of resuscitation should be guided by the restoration of acceptable values for
vital signs and urine output.
If uncertainty exists, particularly in patients with renal or cardiac dysfunction, a central
venous catheter or Swan-Ganz catheter may be inserted to help guide fluid therapy.
After the initial 24 to 48 hours, fluids can be changed to 5% dextrose in 0.45% saline in
patients unable to tolerate enteral nutrition.
If normal renal function and adequate urine output are present, potassium may be added to
the IV fluids.
43
Daily fluid orders should begin with assessment of the patient's volume status and
assessment of electrolyte abnormalities. But there is rarely a need to check electrolyte
levels in the first few days of an uncomplicated postoperative course.
All measured losses, including losses through vomiting, nasogastric suctioning, drains, and
urine output, as well as insensible losses, are replaced with the appropriate parenteral
solutions as previously reviewed.
Fluid Therapy of Isolated Clinical Cases:
Intestinal obstruction
• Hypovolemia (Isotonic depletion) or hypovolemia + mild hyponatremia
• Hypokalaemia more with more distal obstruction
• Metabolic acidosis because intestinal portion exceeds gastric portion losses although
both HCl & HCO are lost
• Correction of deficit: Isotonic soln. + K (half deficit over 4 hours)
• IV fluids: 3 portions Salt soln. + 1 portion 5% dextrose soln. + K
Pyloric obstruction
• Na & water loss: Isotonic loss
• Hypokalaemia (GIT losses + compensatory renal for hypochloremia + compensatory
hyperaldosteronism for Na depletion)
• Hypochloraemia
• Metabolic alkalosis
Treatment: Like intestinal obstruction but less salt (1:1 salt and dextrose solns.) & more KCl
for both K and Cl
44
Part I (Basic Surgery); Chapter 4 (Surgical Nutrition)
Surgical Nutrition
Malnutrition occurs in about 30% of surgical patients with gastrointestinal disease and in up
to 60% of those in whom hospital stay has been prolonged because of postoperative
complications. It is frequently unrecognized and consequently patients often do not receive
appropriate support. The aim of nutritional support in surgical patients is to identify those
patients at risk of malnutrition and to ensure that their nutritional requirements are met by
the most appropriate route and in a way that minimizes complications.
Metabolic response to starvation
■ Low plasma insulin
■ High plasma glucagon
■ Hepatic glycogenolysis
■ Protein catabolism
■ Hepatic gluconeogenesis
■ Lipolysis: mobilisation of fat stores
■ Adaptive ketogenesis
■ Reduction in resting energy expenditure (15–20 kcal kg–1 day–1)
Metabolic response to trauma and sepsis
■ Increased counter-regulatory hormones: adrenaline, noradrenaline, cortisol,
glucagon and growth hormone
■ Increased energy requirements (up to 40 kcal kg–1day–1)
■ Increased nitrogen requirements
■ Insulin resistance and glucose intolerance
■ Preferential oxidation of lipids
■ Increased gluconeogenesis and protein catabolism
■ Loss of adaptive ketogenesis
■ Fluid retention with associated hypoalbuminaemia
NUTRITIONAL ASSESSMENT
Laboratory techniques
There is no single biochemical measurement that reliably identifies malnutrition.
Body weight
- Weight loss: Unintentional weight loss of more than 10% of a patient’s weight in the
preceding 6 months is a good prognostic indicator of poor outcome.
45
- Body mass index (BMI): Defined as body weight in kilograms divided by height in meters
squared. A BMI of less than 18.5 indicates nutritional impairment and a BMI below 15 is
associated with significant hospital mortality.
Anthropometry
- Measurement of skinfold thicknesses estimates body fat
- Measurement of mid-arm circumference estimates muscle mass
Clinical
- This involves a focused history and physical examination, an assessment of risk of
malabsorption or inadequate dietary intake and selected laboratory tests aimed at detecting
specific nutrient deficiencies.
- Malnutrition Universal Screening Tool (MUST) is a five-step screening tool to identify
adults who are malnourished or at risk of undernutrition.
NUTRITIONAL REQUIREMENTS
Normal nutritional requirements of any individual includes macronutrients, carbohydrate, fat
and protein, together with vitamins, trace elements, electrolytes and water. Daily needs may
change depending on the patient’s condition.
Macronutrient requirements
Energy
The total energy requirement of a stable patient with normal or moderately increased
metabolic need is approximately 20–30 kcal/ kg/day. This amount of energy requirements
must be provided by carbohydrate, fats and proteins.
Carbohydrate requirements
The obligatory carbohydrate requirement that meet the needs of the central nervous system
and haematopoietic cells is 2 g/kg/day (100-200 g/day). Glucose is the preferred
carbohydrate source.
Fat requirements
The basal requirements for is 100–200 g/week. In addition to supplying energy, fat
containing nutrients supply us with essential fatty acids (fatty acids that cannot be
synthesized by the body.
Protein requirements
The basic requirement for nitrogen is 0.10–0.15 g/kg/day. In hyper-metabolic patients the
nitrogen requirements increase to 0.20–0.25 g/kg/day.
Vitamins, minerals and trace elements
46
These are all essential components of nutritional regimens. The water-soluble vitamins B
and C act as coenzymes in collagen formation and wound healing. Vitamin B12 is often
indicated in patients who have undergone intestinal resection or gastric surgery. Absorption
of the fat-soluble vitamins A, D, E and K is reduced in steatorrhea and the absence of bile,
at which situations they must be provided by the parenteral route. Sodium, potassium and
phosphate are all subject to significant losses in patients with diarrhoeal illness. Their levels
need daily monitoring and appropriate replacement. Trace elements act as cofactors for
metabolic processes. Magnesium, zinc and iron levels may all be decreased as part of the
inflammatory response. Supplementation is necessary.
Table of Monitoring feeding regimens
Daily:
Body weight
Fluid balance (amount of fluid taken by any route compared to that excreted by any route)
Full blood count, urea and electrolytes
Blood glucose
Electrolyte content and volume of urine and/or urine and intestinal losses
Temperature
Weekly (or more frequently if clinically indicated):
Urine and plasma osmolality
Calcium, magnesium, zinc and phosphate
Plasma proteins including albumin
Liver function tests including clotting factors
Thiamine
Acid–base status
Triglycerides
Fortnightly:
Serum vitamin B12
Folate
Iron
Lactate
Trace elements (zinc, copper, manganese)
NUTRITIONAL SUPPORT
The indications for nutritional support:
Any patient who has sustained 5–7 days of inadequate intake or who is anticipated to have
no intake for this period should be considered for nutritional support. This period may be
less in patients with pre-existing malnutrition. The provision of nutritional support is not
specific to certain conditions or diseases.
47
Types of nutritional support

Enteral nutrition
The term ‘enteral feeding’ means delivery of nutrients through the gastrointestinal tract. This
route should be used whenever possible. Enteral feeding can be achieved with oral
supplements (sip feeding) or with a variety of tube-feeding techniques delivering food into
the stomach, duodenum or jejunum. A variety of nutrient formulations that vary in energy
content, osmolarity, fat and nitrogen content and nutrient complexity are available for
enteral feeding.
Sip feeding
Many formulas are commercially available. Supplementary sip feeds are used in
malnourished patients who can eat and drink but whose appetites are impaired or in whom
adequate intakes cannot be maintained with. Sip-feeding techniques are associated with a
significant overall increase in calorie and nitrogen intakes.
Tube-feeding techniques
Enteral nutrition can be achieved using conventional or fine-bore nasogastric tubes
(Ryle’s), gastrostomy or jejunostomy. Gastrostomy tubes can be inserted surgically or
by using percutaneous endoscopic techniques (PEG). The choice of the method depends
on local circumstances and the surgeon’s preference. Conventionally, 20–30 ml are
administered per hour initially, gradually increasing to goal rates within 48–72 hours.
Feeding is discontinued for 4–5 hours overnight to allow gastric pH to return to normal.
Tube blockage is common and thus all tubes should be flushed with water at least twice
daily.
Nasogastric tubes
Nasogastric tubes are appropriate for short term feeding (few weeks) in the majority of
patients. Fine-bore feeding tube is preferable because it is less likely to cause gastric and
oesophageal erosions. There is a small risk of malposition into a bronchus during insertion.
The position of the tube should be checked using plain abdominal radiography or by
injecting a jet of air into the tube while hearing the bubbling sound in the stomach using a
stethoscope.
Gastrostomy
The placement of a tube through the abdominal wall directly into the stomach is termed
‘gastrostomy’. This can be created surgically at the time of laparotomy, however, the
majority are performed by percutaneous insertion under endoscopic control using local
anaesthesia (PEG=percutaneous endoscopic gastrostomy).
48
PEG is used in patients requiring enteral nutrition for prolonged periods of time (4–6 weeks)
because it minimizes the traumatic complications related to nasogastric tubes. Uncommon
complications of PEG include abdominal wall abscesses and sepsis around the PEG site.
Persistent gastric fistula necessitating surgical closure can occur on removal of a PEG.
Jejunostomy
In recent years the use of jejunal feeding has become increasingly popular. It is indicated
when the stomach is needed to be bypassed in feeding, such as in patients who have
gastric outlet obstruction, or in presence of gastric anastomosis e.g. after Whipple
operation. Jejunostomy entails creating a defect in the jejunum, which can leak or be
associated with tube displacement; both of these complications result in peritonitis.
Complications of enteral nutrition
Tube-related
■ Malposition
■ Displacement
■ Blockage
■ Breakage/leakage
■ Local complications (e.g. erosion of skin/mucosa)
Gastrointestinal
■ Diarrhoea
■ Bloating, nausea, vomiting
■ Abdominal cramps
■ Aspiration
49
■ Constipation
Metabolic/biochemical
■ Electrolyte disorders
■ Vitamin, mineral, trace element deficiencies
■ Drug interactions
Infective
■ Exogenous (handling contamination)
■ Endogenous (patient)
Parenteral nutrition
Total parenteral nutrition (TPN) is defined as the provision of all nutritional requirements by
means of the intravenous route and without the use of the gastrointestinal tract. Parenteral
nutrition is indicated when energy and protein needs cannot be met by the enteral
administration of these substrates.
The most frequent clinical indications:
Massive resection of the small intestine
Intestinal fistula
Prolonged intestinal failure for other reasons.
Route of delivery: peripheral or central venous access
TPN can be administered either by a catheter inserted in a central vein or via a peripheral
line. In the early days of parenteral nutrition, the only energy source available was
hypertonic glucose which had to be given into a central vein to avoid thrombophlebitis.
Recently, the identification of isotonic mixtures of carbohydrates, fats and amino acids that
provide the daily requirements of nutrients and energy enabled the development of
peripheral parenteral nutrition.
Peripheral
Peripheral feeding is appropriate for short-term feeding of up to 2 weeks. Nutrients are
administered through a short peripheral cannula that is replaced regularly. Peripheral
parenteral nutrition has the advantage that it avoids the complications associated with
central venous administration but suffers the disadvantage that it is limited by the
development of thrombophlebitis. Peripheral feeding is not indicated if patients already
have an indwelling central venous line or in those in whom long-term feeding is anticipated.
Central
Central venous catheters can be inserted via the subclavian or internal or external jugular
vein.
50
- Internal or external jugular veins cannulation is usually preferred because these vessels
are easily accessible. Their disadvantage is that the exit site is situated on the side of the
neck, where repeated movements result in disruption of the dressing with the attendant risk
of sepsis.
- The infraclavicular subclavian approach is technically more difficult, however, the catheter
lies flat on the chest wall, which optimizes nursing care.
- Access can be achieved via a catheter inserted into a peripheral vein and maneuvered
into the central venous system [peripherally inserted central venous catheter (PICC) line].
Their disadvantage is that when thrombophlebitis occurs the whole peripheral vein is
irrevocably destroyed.
Any central venous cannulation is associated with the risk of pneumothorax (caused by
pleural injury), and central venous or cardiac thrombosis (when the catheter tip lies in the
distal superior vena). Whichever technique is employed, a post-insertion chest radiograph
is essential before feeding is commenced to confirm the absence of pneumothorax and the
catheter position. The safest means of establishing central venous access is by insertion of
lines under ultrasound guidance; however, this will not be practicable for all cases.
- For longer term parenteral nutrition Hickman lines are preferable. These are often inserted
by a radiologist with fluoroscopic guidance or ultrasound. They incorporate a small cuff,
which sits at the exit site of a subcutaneous tunnel. This is thought to minimize the
possibility of line dislodgement and reduce the possibility of line sepsis.
Complications of parenteral nutrition
Related to nutrient deficiency
■ Hypoglycaemia/ hypocalcaemia/ hypophosphataemia/ hypomagnesaemia
(refeeding syndrome)
■ Chronic deficiency syndromes (essential fatty acids, zinc, mineral and trace
elements)
Related to overfeeding
■ Excess glucose: hyperglycaemia, hyperosmolar dehydration, hepatic steatosis,
hypercapnia, increased sympathetic activity, fluid retention, electrolyte abnormalities
■ Excess fat: hypercholesterolaemia and formation of lipoprotein X,
hypertriglyceridaemia, hypersensitivity reactions
■ Excess amino acids: hyperchloraemic metabolic acidosis, hypercalcaemia,
aminoacidaemia, uraemia
51
Related to sepsis
■ Catheter-related sepsis
■ Possible increased predisposition to systemic sepsis
Related to line
■ On insertion: pneumothorax, damage to adjacent artery, air embolism, thoracic duct
damage, cardiac perforation or tamponade, pleural effusion, hydromediastinum
■ Long-term use: occlusion, venous thrombosis
Hickman Catheter in place Jejunostomy tube in place
52
Part I (Basic Surgery); Chapter 5 (Surgical Infections)
Surgical Infections
Some important definitions:
Inflammation: body response to any noxious agent such as bacteria, viruses, trauma,
foreign body.
Colonization: presence of bacteria in or on a host without causing symptoms or signs, and
without eliciting immune response.
Infection: invasion of local tissues with microorganisms causing local symptoms and signs
and eliciting a sustained immune response.
Surgical infection: Infection induced by surgery or that could be treated by surgery
Systemic inflammatory response syndrome (SIRS): See chapter 1
Multiple organ dysfunction syndrome (MODS): See chapter 1
Sepsis or septicaemia: severe infection associated with SIRS
Severe sepsis: severe infection associated with SIRS and MODS
Septic shock: sepsis with cardiovascular collapse and shock
Irreversible septic shock: late stage of septic shock not responding to treatment
Virulence: strength of the organism to cause infection. Virulence depends on the qualities of
organisms of adherence, invasiveness and production of toxins. Invasiveness of
microorganisms may be enhanced by their ability to secrete enzymes (e.g. hyaluronidase
and streptokinase), avoid phagocytosis (e.g. encapsulation or spore formation), kill
phagocytes and their inherent resistance to lysosomal destruction.
Toxins substances secreted by the organism (exotoxins) or released upon their death
(endotoxins). Toxins may produce local tissue damage, like in gas gangrene, distant toxic
effects, like in tetanus, or activate cytokine systems to cause systemic sepsis.
Toxaemia: Endotoxins or exotoxins circulating in blood initiating systemic body response
Bacteraemia: transient circulation of bacteria in blood. Bacteremia is usually asymptomatic.
Pyaemia: circulation of pus and pyogenic organisms in blood leading to multiple remote
abscesses called pyaemic abscesses. Pyaemia is of two types:
- Systemic pyaemia affects the systemic circulation and pyaemic abscesses are found in
different parts of the body
- Portal pyaemia affects the portal circulation and pyaemic abscesses are found in the liver
Micro-organisms of surgical importance
Staphylococci
Staphylococci are gram-positive cocci, Staph. aureus is the main pathogenic strain. It is
part of normal human bacterial flora, with about 30% of the population being nasal carriers
and 10% carrying it on perineal skin. Staph. Aureus typically produces pustules, boils,
breast abscesses, wound infections and osteomyelitis. Its virulence is partly due to the
enzymes and toxins it produces. Few patients harbor virulent strains that produce a
powerful toxin called the toxic shock syndrome toxin (TSST-1). Infection with this strain
produces toxic shock syndrome with serious systemic effects such as hypotension, shock
and multi-organ failure.
Staph. epidermidis (formerly Staph. albus) is a universal skin commensal rarely causing
significant infection.
53
Most staphylococcus strains can produce the enzyme beta-lactamase (also known as
penicillinase) that make them resistant to penicillins. Resistance arise because of
injudicious use of antibiotics in bad family and hospital practice. Most strains remain
sensitive to a range of common antibiotics, e.g. the beta lactamase resistant flucloxacillin,
erythromycin, some cephalosporins and gentamicin.
Methicillin-resistant Staph. aureus (MRSA)
These are strains of Staph. aureus that are resistant to beta lactamase resistant antibiotics
mentioned above. They are only sensitive to parenteral glycopeptide antibiotics,
vancomycin and teicoplanin. MRSA now accounts for about half of all S. aureus isolates
in hospitals and in the community. Ward areas at greatest risk are burns units, intensive
care units, cardiothoracic, neonatal, orthopaedic and geriatric wards.
MRSA is not more pathogenic than other Staph aureus strains, however it is more difficult
to treat. A worrying development is the emergence of vancomycin insensitive Staph. Aureus
(VISA). Inappropriate use of vancomycin must be avoided to prevent selection of such
mutants. New antibiotics active against MRSA and VISA have been developed, including
linezolid (which can be given orally), daptomycin and tigecycline.
Streptococci
Streptococci are gram-positive cocci that harbor aerobic, anaerobic and microaerophilic
strains. According to the haemolysis patterns they produce on blood agar culture plates,
streptococci can be divided into alpha-haemolytic streptococci (cause partial haemolysis of
blood agar) or beta-haemolytic streptococci (cause complete haemolysis of blood agar).
Beta-haemolytic streptococci are grouped serologically from group A to group O.
Streptococci of particular surgical significance are:
1. Group A beta-haemolytic streptococci (Strep. pyogenes) is the main human pathogenic
streptococcus and is carried in the upper respiratory tract by about 10% of children but less
often by adults. It can cause cellulitis, lymphangitis, sore throat and rheumatic fever.
Highly invasive strains of Strep. pyogenes may cause necrotizing fasciitis. Exotoxins
produced by certain strains can lead to a life-threatening streptococcal toxic shock
syndrome, with fulminant soft tissue infection, shock, acute respiratory distress syndrome
and renal failure.
2. Group B beta haemolytic streptococci (Strep. agalactiae) is a common cause of serious
neonatal sepsis.
3. Group C and G beta haemolytic streptococci are occasional causes of cellulitis and
bacteraemia.
4. Alpha haemolytic Strept viridans is a normal oral commensals of low virulence but is the
most common organisms causing infective endocarditis.
5. Alpha haemolytic Strep. pneumoniae (pneumococcus) is the most common cause of
lobar pneumonia, otitis media, pneumococcal meningitis and acute exacerbations of
chronic bronchitis. In surgery, it can cause bronchopneumonia in susceptible post-surgical
patients, post head injury pneumococcal meningitis and post splenectomy pneumococcal
sepsis.
6. Strep. milleri is a microaerophilic strept that is often found in abscesses in the appendix
area, the liver, lung and brain.
54
7. Anaerobic streptococci are bowel commensals and may form part of the mixed flora in
intraperitoneal abscesses or infections associated with necrotic tissue, e.g. diabetic foot
ulcers.
Penicillin is the drug of choice for most streptococcal infections. Many streptococci are
also sensitive to macrolides (e.g. erythromycin, clarithromycin). Meningitis needs
alternative antibiotics such as ceftriaxone or vancomycin.
Enterococci
Enterococci are gram-positive cocci closely related to streptococci. Enterococcus faecalis
(formerly Strep. faecalis) is the most common species. Enterococci are part of the normal
bowel flora and may cause infection where bowel has been opened or else infect urinary or
genital tracts.
Penicillin, ampicillin, amoxicillin or vancomycin are used for enterococcal infections.
The cephalosporins are all ineffective. Vancomycin-resistant enterococci (VRE) are
usually low-grade pathogens infecting intravascular lines in transplant and haematology
patients and on ICUs. They are difficult to treat, but newer antibiotics linezolid, daptomycin
and quinupristin/dalfopristin are active against most strains.
Enterobacteriaceae
These are Gram-negative bacilli (rods) known as coliforms. They constitute 1% of
normal intestinal flora. Escherichia coli, Klebsiella, Enterobacter, Serratia and Proteus are
the most common organisms of this group. They are found most often in surgical bowel-
related infections e.g. peridiverticular abscess, acute appendicitis, strangulated bowel. E.
coli can cause Gram-negative sepsis and about 80% of urinary tract infections. Proteus is
a common cause of urinary tract infections but occasionally causes other surgical
infections, usually originating from the urinary tract.
Most coliforms are sensitive to second- and third-generation cephalosporins, (as
cefuroxime and cefotaxime) and gentamicin. Many are sensitive to fluoroquinolones
(ciprofloxacin, levofloxacin, moxifloxacin) but resistant strains are emerging. Resistant
strains produce enzymes ESBL (extended spectrum beta-lactamase) that destroy second-
and third-generation cephalosporins. The only active antibiotics are the carbapenems
(meropenem, imipenem, ertapenem) and amikacin. However, some strains produce
carbapenemase, leaving the old toxic antibiotics such as colistin as the only effective
treatment.
‘Non-surgical’ Enterobacteriaceae
Other members of the family Enterobacteriaceae cause primary bowel infections such as
typhoid & bacillary dysentery. Yersinia sometimes produces an acute ileal inflammation
which may mimic acute appendicitis and has a similar appearance to Crohn’s disease at
laparotomy. Campylobacter jejuni, the most common cause of food-borne infection, can
also cause a pseudo-appendicitis by initiating terminal ileitis and mesenteric lymph node
inflammation.
Pseudomonas
The aerobic gram-negative rod Pseudomonas aeruginosa is an uncommon cause of
surgical infection except in debilitated patients. Infection is commonly acquired in hospital
because the organism is commonly found on hospital and cleaning equipment and even in
chemical disinfectants and antiseptics. In about 10% of the population, Ps. aeruginosa is a
55
normal intestinal commensal. Pseudomonas is a common colonising organism in

longstanding wounds such as compound fractures, chronic leg ulcers and indwelling urinary
catheters. It can be recognized by its characteristic blue-green discharge. It colonises burns
and may become pathogenic with extensive burns, giving rise to fatal sepsis. It may be
responsible for hospital-acquired pneumonias in ventilated patients or for fatal systemic
sepsis in terminally ill patients.
Ps. aeruginosa is intrinsically resistant to most antibiotics. It is sensitive to
aminoglycosides (gentamicin and tobramycin), some extended-spectrum beta-lactam
antibiotics (ceftazidime or cefepime), the combination of piperacillin and tazobactam and
the carbapenems (imipenem or meropenem). The quinolones, ciprofloxacin and
ofloxacin, are the only orally effective agents. True infection must be distinguished from
colonization where treatment is not indicated.
Acinetobacter
Gram-negative coccobacilli that are strictly aerobic and are generally not pathogenic. Their
importance lies in causing infections in vulnerable patients, especially on ICUs, and their
high rate of intrinsic antibiotic resistance. The most commonly identified species is A.
baumanii.
Anaerobes
Form a major part of the GI tract flora, outnumbering E. coli and related coliforms by 1000
to 1. Many parts of the body are colonised by anaerobes, even those exposed to air,
including skin, mouth, upper respiratory tract, external genitalia and vagina. These
colonising organisms become important because surgery disrupts anatomical barriers to
allow contamination and infection. Anaerobic infection can be life-threatening and surgical
management is often required. Some anaerobes cause toxin-related diseases including
tetanus. The most commonly encountered anaerobes are:
➢ Gram-negative bacilli—Bacteroides fragilis and other Bacteroides species.
➢ Gram-positive cocci—Peptostreptococcus and microaerophilic streptococci
➢ Gram-positive bacilli—Clostridium spp. (spore forming), Actinomyces spp.
Bacteroides cause pyogenic infections after faecal contamination of the peritoneal cavity,
along with other gut commensals, and occasionally cause sepsis in debilitated patients.
Most anaerobes are highly sensitive to metronidazole, that can be given orally,
intravenously or rectally. Metronidazole is standard prophylaxis before appendicectomy and
large bowel surgery. Other antibiotics with broad anaerobic activity are co-amoxiclav
(Augmentin), piperacillin/tazobactam (Tazocin), the carbapenems (imipenem and
meropenem) and chloramphenicol.
Clostridia
Clostridia are Gram-positive rods widely distributed in soil and as intestinal commensals.
Clostridia form spores resistant to drying, heat and antiseptics and can survive for long
periods. They are mostly obligate anaerobes which can only proliferate in the absence of
oxygen. The main pathological effects are caused by powerful exotoxins. Those of surgical
importance are gas gangrene, tetanus and C. difficile pseudomembranous colitis.
Principles of treatment of surgical infections
Remove dead and devascularized tissue
56
Dead and devascularised tissue acts as a nidus of infection and is isolated from humoral
and cellular defence mechanisms and from circulating antibiotics. A vital first step in
treatment of any surgical infection is to remove infected necrotic tissue e.g. amputating
infected necrotic limb
Drain collections of pus.
Similar to dead and devascularized tissue, pus contained in an abscess is isolated from
body defences and antibiotics. Any abscess should be drained
Remove foreign bodies Micro-organisms colonize foreign bodies (e.g. cannulae,
prostheses, mesh) to hide from body defences.
Drain obstructed hollow viscera Static secretions in hollow viscera (e.g. obstructed common
bile duct, obstructed ureter) encourage micro-organism multiplication and proliferation. The
hollow viscus will eventually turn to be an abscess. Obstruction should be drained
Antibiotic therapy Antibiotics are administered in one of two ways, empirical or specific
antibiotic therapy. In either way, hospital and formulary guidelines should be consulted for
doses and monitoring of antibiotic therapy.
1. Empirical antibiotic therapy
In which the antibiotics are chosen according to the most likely pathogens and the hospital
antibiogram. This method is used if urgent treatment is of great importance. Before starting
empirical antibiotics, a swab or aspirate is taken from the infected material and sent for
culture and sensitivity testing.
2. Therapeutic antibiotic therapy
In which the antibiotics are chosen according to the results of culture and sensitivity. This
method is used if the treatment is not urgent. Also patients who started empirical antibiotics
should modify the antibiotic regimen once the results of culture and sensitivity are available.
Give nutritional support and improve the patient’s general condition
Major infection and sepsis result in severe catabolism often associated with
hypoalbuminaemia and malnutrition. Nutritional support either by enteral or parenteral
routes may be appropriate.
Rest
Again this decreases catabolism and helps the body to restore normal homeostasis
Common antibiotics used in prophylaxis and treatment of surgical infections

Penicillin
Benzylpenicillin has proved most effective against Gram-positive pathogens, including most
streptococci, the clostridia and some of the staphylococci that do not produce B-lactamase.
It is still effective against Actinomyces, which is a rare cause of chronic wound infection. All
serious infections, e.g. gas gangrene, require high dose intravenous benzylpenicillin.
Ampicillin and amoxicillin
These B-lactam penicillins can be taken orally or may be given parenterally. Both are
effective against Enterobacteriaceae, and the majority of group D streptococci. Their use is
now rare as there are more effective alternatives.
Flucloxacillin and amoxicillin/clavulonic acid
Flucloxacillin is a B-lactamase-resistant penicillin and is therefore of use in treating most
beta lactamase producing community-acquired staphylococcal infections. Clavulanic acid is
57
available combined with amoxicillin (Augmentin) and can be taken orally. Clavulonic acid
protects amoxicillin from inactivation by B-lactamase-producing bacteria
Mezlocillin and azlocillin
These are ureidopenicillins with good activity against species of Enterobacter and
Klebsiella. Azlocillin is effective against Pseudomonas, but all are susceptible to B-
lactamases.
Cephalosporins
There are several B-lactamase-susceptible cephalosporins that are of value in surgical
practice: cefuroxime, cefotaxime and ceftazidime are widely used. They are effective in
intraabdominal, skin and soft-tissue infections, being active against Staphylococcus aureus
and most Enterobacteriaceae. Ceftazidime is also effective against Pseudomonas
aeruginosa. Newer cephalosporins may be effective against organisms such as MRSA, but
their spectra are usually limited.
Aminoglycosides
Gentamicin and tobramycin have similar activity and are effective against Gram-negative
Enterobacteriaceae. Gentamicin is effective against many strains of Pseudomonas. All
aminoglycosides are inactive against anaerobes and streptococci. Ototoxicity and
nephrotoxicity may follow sustained high toxic levels.
Vancomycin
This glycopeptide is most active against Gram-positive bacteria and has proved to be
effective against MRSA, although vancomycin resistance (VRSA) is increasingly being
reported. It is ototoxic and nephrotoxic, so serum levels should be monitored.
It is effective against C. difficile in cases of pseudomembranous colitis.
Imidazoles
Metronidazole is the most widely used member of the imidazole group and is active against
all anaerobic bacteria. It is particularly safe and may be administered orally, rectally or
intravenously.
Carbapenems
Meropenem, ertapenem and imipenem are members of the carbapenems. They are stable
to B-lactamase, have useful broad spectrum anaerobic as well as Gram-positive activity
and are effective for the treatment of resistant organisms, such as ESBL resistant urinary
tract infections or serious mixed-spectrum abdominal infections (peritonitis).
Quinolones
Quinolones, such as ciprofloxacin, were active against a wide spectrum of organisms. Their
widespread use has been related to the development of resistant organisms, and their role
in treating surgical infection is limited.
Regimens of antibiotic use in surgery:
A. Prophylactic antibiotic: used to prevent occurrence of infection
B. Empirical antibiotic: see above
C. Therapeutic antibiotic see above
Types of surgical infections:
Specific surgical infections: These infections are caused by specific organisms causing
specific diseases. Specific surgical infections include gas gangrene, tetanus, erysipelas,
58
tuberculosis, leprosy, candidiasis, anthrax, actinomycosis and parasitic infestations

(bilharziasis, amoebiasis, hydatid disease, filariasis),
Non-specific surgical infections: These are non-specific diseases caused by non-specific
organisms. They include
1- Soft tissue infection: wound infection, boil, abscess, carbuncle, cellulitis, necrotizing
fasciitis, lymphangitis
2- Bone infection: osteomyelitis
3- Non-closteridial gas forming and gangrene inducing infection
4- Blood infection by micro-organisms or their products: toxaemia,
bacteremia, pyaemia, septicemia.
Abscess
Definition: An abscess is a collection of pus (formed of dead and
dying neutrophils plus proteinaceous exudate) walled off by a Abscess formation
zone of acute inflammation.

Aetiology and causative organisms: Acute abscess formation particularly occurs in
response to certain pyogenic microorganisms that attract neutrophils but are resistant to
phagocytosis and lysosomal destruction. The main pyogenic organisms of surgical
importance are Staphylococcus aureus, some streptococci (particularly Strep. pyogenes),
Escherichia coli and related Gram-negative bacilli (‘coliforms’), and Bacteroides species.
Abscesses also form in response to localized tissue necrosis and to some organic foreign
bodies (e.g. wood splinters, linen suture material).
Natural history: Without treatment, abscesses eventually tend to ‘point’ to a nearby
epithelial surface (e.g. skin, gut, bronchus), and then discharge their contents. If the
injurious agent is thereby eliminated, spontaneous drainage leads to healing. If an abscess
is remote from a surface (e.g. deep in the breast), it progressively enlarges causing much
tissue destruction. Sometimes local defense mechanisms are overwhelmed, leading to
runaway local infection (cellulitis) and sometimes systemic sepsis.
Systemic effects: Even with small, well-localised abscesses, showers of bacteria may enter
the general circulation (bacteraemia) but are mopped up by hepatic and splenic phagocytic
cells before they can proliferate. This is responsible for the swinging pyrexia characteristic
of an abscess. Severe infection causing excessive cytokine responses spilling over into the
systemic circulation causes systemic sepsis and rapid clinical deterioration.
In the presence of an abscess, circulating neutrophils rise dramatically as they are released
from the bone marrow; thus, a marked neutrophil leucocytosis usually indicates a
pyogenic infection.
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The chronic state: The essence of managing any abscess is to establish complete
drainage, usually by incision or aspiration. If drainage of an abscess is inadequate and the
causative agent is not fully eliminated, the neutrophil response persists and pus continues
to be formed, resulting in a chronic abscess that continuously discharges via a sinus or
else ‘points’ and discharges periodically with the sinus healing over between times. A
chronic abscess wall consists of fibrous scar tissue lined with granulation tissue.
Causes of chronic abscesses include:
➢ Infected foreign bodies are probably the most common cause of chronic abscess.
Foreign bodies implanted during surgery (e.g. synthetic mesh for inguinal hernia
repair, prosthetic hip joint) may become infected and treatment entails removal of the
foreign body.
➢ Dead (necrotic) tissue can act as a foreign body, forming a nidus for infection. For
example, diabetes may be complicated by deep foot infections with necrosis of
tendon and bone leading to chronic abscesses and ulcers. Hairs deeply implanted in
the natal cleft skin may cause a pilonidal sinus or abscess. Chronic osteomyelitis is
associated with remnants of dead bone known as sequestra
➢ Inadequate abscess treatment and drainage
Organisation and repair: The most common sequel to acute inflammation is organisation,
in which dead tissue is removed by phagocytosis and the defect filled by vascular
connective tissue known as granulation tissue. This tissue is gradually ‘repaired’ to form a
fibrous scar. Sometimes the original tissue regenerates, i.e. rebuilds its specialised cells
and structure.
Treatment: The only effective treatment for abscesses is incision and drainage. Deep
abscess can often be localised and drained under the guidance of ultrasound or CT. This is
called percutaneous drainage of abscess. Failure to drain an abscess in the presence of
inappropriate and prolonged antibiotic therapy can result in a troublesome chronic abscess
or antibioma. Antibiotic therapy is appropriate if there is clinical evidence of systemic
sepsis.
Antibiotics and abscesses: If antibiotics are given to treat a fully formed abscess, they
seldom effect a cure because the drug cannot gain access to the bacteria within pus.
Nevertheless, antibiotics may halt expansion or even sterilize the pus; the residual sterile
abscess is known as an antibioma. It is advisable to administer antibiotics when draining
an abscess because of the associated sepsis and the risk of metastatic infection, especially
if the patient has a prosthetic device in situ or a damaged heart valve.
What is the collar stud abscess? It is a superficial collection of pus coming from hidden
deep pocket and communicating with acute inflammatory narrow track. The deep pocket
can be missed resulting in inadequate drainage.
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Carbuncle
Carbuncle is pathologically multiple adjacent boils and small abscesses communicating
with each other and opening in the skin surface by multiple sinuses. It is common in thick
skin of the back of the trunk and the back of the neck. It is common in diabetic patients
especially when diabetes is uncontrolled. It is mainly caused by staphylococci. Carbuncle is
treated by de-roofing of all abscesses, antibiotics according to result of culture and
sensitivity, and proper control of diabetes.
Carbuncle
Cellulitis
Cellulitis is a spreading infection of connective tissues that is often
caused by β-haemolytic Streptococcus. The invasiveness of this
organism is due to the production of hyaluronidase (that dissolves the
intercellular matrix) and streptokinase (that dissolves the fibrin
inflammatory barrier). Cellulitis may be accompanied by obvious
inflammation of the draining lymphatics (lymphangitis) and the draining lymph nodes
(lymphadenitis). There may also be associated septicaemia. Cellulitis is a common
complication of lymphoedema from any cause. There is usually no obvious entry site for
bacteria, the cellulitis tends to be low grade and brawny in nature.
Treatment of cellulitis is by immobilisation and elevation of the affected part, antibiotic
therapy, and drainage of any residual abscesses. Cellulitis complicating lymphedema is
usually slow to recover to antibiotic therapy. Compression stockings are a useful long-term
measure, but recurrence is common.
Erysipelas
Erysipelas is a type of superficial cellulitis with
lymphatic involvement. It is usually caused by Group
A Streptococcus. Antecedent trauma, bite or
dermatoses is common. The most common site to be
affected is the lower extremity. Lymphangitis and
constitutional manifestations are common.
Clinical picture:
• Abrupt onset of high fever, chills, malaise and nausea
• Area of erythema with burning develops over next 2 days
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• The affected area is a red, shiny, hot plaque with raised edge that is sharply
demarcated from the normal skin. The raised well, demarked edge, the vesicles
and serous eruptions differentiate erysipelas from cellulitis
Treatment Erysipelas usually needs hospital admission and bed rest. Penicillin G IV is the
antibiotic of choice. Imipenem is used in severe cases.
Necrotizing fasciitis
- Necrotizing fasciitis is a serious disease caused by bacterial infection of the subcutaneous
fat and fascia.
- Infection spreads rapidly along fascial planes leading to necrosis of subcutaneous fat and
fascia, but it does not spread to muscle (unlike clostridial and non-clostridial myonecrosis)
- Classically infection is caused by streptococci, but more commonly polymicrobial infection
is encountered including streptococci, anaerobes and gram negative organisms, also
grouped into tabloid term “flesh eating bacteria”.
- Clinically there is fever, pain, blood containing blisters, marked leukocytosis and septic
shock.
- Treatment is by early aggressive extensive surgical debridement of all dead and necrotic
skin and subcutaneous tissue, with systemic antibiotics and supportive IV fluids and
nutrition. Control of blood sugar in diabetic patients is essential. If aggressive treatment is
not started in time, death is inevitable.
Wound infections & surgical site infection (SSI)

This is defined as invasion of micro-organisms through the tissues broken down locally after
surgery. The infecting organisms are often part of the patient’s normal flora residing on his
skin, in bowel or respiratory tract. SSI can be superficial and or deep sited infections
Types of wounds according to susceptibility to infection
1. Clean wound is characterized by:
- No breech of the respiratory, gastrointestinal, female genital and infected urinary
tracts
- No breech of sterilization rules
- Absence of host source of infection
e.g. Wounds of mastectomy, thyroidectomy and hernia repair operations
2. Potentially contaminated wound is characterized by
- Breech of the respiratory, gastrointestinal, female genital and infected urinary tracts
without spill
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- Minor breech of sterilization rules

e.g. Appendectomy and cholecystectomy wounds
3. Contaminated wound is characterized by
with minor spill
- Major breech of sterilization rules
- Surgery in infected tissues
e.g. Colectomy with minor spill of stools
4. Dirty wound is characterized by
with major spill
- Surgery in a field of pus, stool, gangrene
e.g. Exploration for peritonitis or perforated viscus
Antibiotic use in different types of surgical wound:
1. Clean wounds: No need for antibiotic prophylaxis. Wound infection rate is 2% in both
2. Potentially contaminated wounds: Single dose of IV antibiotic prophylaxis given from
1 Hour before surgery to time of induction of anaesthesia and scalpel use. With this
regimen, rate of wound infection decreased from 30% to 10%.
3. Contaminated wounds: IV antibiotic as given in potentially contaminated wounds but
extends to 1-3 days postoperatively. With this regimen, rate of wound infection decreased
from 60% to 20%.
4. Dirty wounds: IV antibiotic as given in potentially contaminated wounds but extends to
3-5 days postoperatively. With this regimen, rate of wound infection decreased from 80% to
40%.
The choice of the antibiotic used for prophylaxis depends on:
- The type of flora that normally colonizes the site of surgery, e.g. cephalosporine cover
gram positive cocci that normally colonize the skin, colonic surgery need coverage against
anaerobes and gram negative organisms
- The pathogens that are present because of specific disease
- The hospital antibiogram

Predisposing factors to SSI:
A. Exogenous factors (factors unrelated to the patient)
- Improper sterilization of surgical instruments and equipment
- Breaching rules of infection control in the hospital
Wound infection (pus)
B. Factors related to surgery:
1. Type of surgery (clean, potentially contaminated, contaminated, dirty)
2. Wound hematoma and seroma
3. Leaving dead space after surgery
4. Presence of foreign body
5. Local tissue ischemia and edema
6. Poor surgical technique
7. Residual necrotic tissue Early wound infection
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C. Factors related to the patient:

1. Unfavorable local tissue condition
2. Diabetes mellitus
3. Immune depression (cancer, AIDS, chronic steroid therapy)
4. Shock
5. Obesity
6. Chronic illness
7. Presence of septic focus
How to prevent wound infection
1. Short preoperative inpatient period (to decrease colonization by hospital bacteria)
2. Improve the patient’s general condition
3. Treat any septic focus before admission to hospital
4. Antiseptic bath before surgery
5. Proper sterilization of instrument
6. Proper scrubbing of all surgical team
7. Proper operative room discipline and handling technique
8. Antibiotic prophylaxis
Principles of treatment of soft tissues infection:
• Rest
• Improve general condition
• Start empirical antimicrobials after taking culture
• Improve and remove predisposing local cause for infection
• Remove debris, foreign bodies necrotic tissue and pus
• Good wash by normal saline with avoidance of irritant chemicals
• Avoid per holes surgery in drainage
• Closure of dead spaces
• Proper wounds dressing in technique and frequency
Nosocomial Infections
Infections that are not present or incubated in a patient at the time of admission and are
acquired in the hospital are called nosocomial infections. Nosocomial infections may be
acquired by cross-infection from infected patients, from contaminated furnishings, or from
‘carriers’ among staff by inhalation, ingestion or through contamination of medical
equipment and devices such as intravenous cannulae or urinary catheters. These infections
are often caused by antibiotic-resistant bacteria such as methicillin resistant
Staphylococcus aureus (MRSA). Risk of such infections can be drastically reduced by the
simple measure of everyone in contact with patients cleansing their hands with alcohol
based gel between every patient contact. Known MRSA infected patients or carriers should
be isolated when in hospital. Patients having operations where infection carries very high
risk should ideally be treated in areas separated from sick patients, especially emergency
admissions from long term care institutions. Particular risk is associated with eye surgery,
joint replacements and prosthetic vascular grafts. Postoperative patients are at particular
risk of nosocomial infections as host defences are impaired by the surgical assault, and
physiological protective mechanisms are disrupted allowing infection to gain ascendancy.
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The surgical patient’s general resistance may be further impaired by malnutrition,

malignancy, rheumatoid disease, corticosteroids or other immunosuppressive drugs.
Common hospital acquired infections are pneumonias, urinary tract infections and central
lines infection.
Gas gangrene
Gas gangrene is caused by infection with the gram positive anaerobic spore forming bacilli
Clostridium perfringens (formerly C. welchii) and other anaerobes. These organisms are
normal inhabitants in the human and animal stools. They proliferate in necrotic tissue and
they secrete powerful toxins. Toxins spread rapidly and destroy nearby tissues, generating
gas in different tissue planes causing the characteristic sign of crepitus (‘crackling’) on
palpation and the typical X-ray appearance. Deep traumatic wounds involving muscle, and
wounds contaminated with soil, clothes or faeces are most susceptible. The condition is
very common in battle wounds. In surgical practice, the highest risk of gas gangrene is in
lower limb amputations for ischaemia (especially above knee amputations due to
infection from the patient’s stools) and in high-velocity gunshot wounds when associated
with bowel perforation. Gas gangrene occasionally occurs in surgical wounds when
ischaemic tissue is contaminated with bowel flora. Gas gangrene spreads rapidly, the
overlying skin turns black and within hours, necrosis spreads along muscle planes. Later
the skin breaks down and a thin, foul-smelling purulent exudate leaks out. Toxins are
absorbed and cause rapid clinical deterioration and death within 24–48 hours unless the
process can be halted by timely and vigorous intervention.
Treatment of gas gangrene:
Prophylaxis
C. perfringens is very sensitive to benzylpenicillin which should be given prophylactically
by injection as soon as possible after a traumatic injury involving muscle, or less than an
hour before ischaemic limb amputation (metronidazole is suitable for patients allergic to
penicillin).
X-ray showing Gas forming infection (gas gangrene).

Treatment
Treatment of established gas gangrene is urgent and must proceed vigorously for any hope
of survival. Treatment is with high doses of intravenous penicillin to kill organisms in viable
and vascularised tissue, and emergency radical excision of all necrotic tissue until healthy
65
bleeding tissue is reached. Surgery requires meticulous excision of all necrotic tissue
followed by packing of the wound rather than suturing. Further excisions are likely to be
needed and delayed primary closure performed when risk of infection is over, a few days
later. Hyperbaric oxygen therapy can raise oxygen tension in necrotic tissues, inhibiting
organism growth. The patient is placed in a high-pressure chamber with pure oxygen at
about 3 atmospheres for several hours daily. Shock is treated as essential and anti-gas
gangrene toxin serum infusion is given. Even with intensive treatment, the prognosis for
established gas gangrene is bad.
Tetanus
Tetanus is caused by the gram positive spore forming anaerobic bacillus Clostridium tetani.
The entry wound is often unrecognized, minute and deep, perhaps caused by a rose thorn
or splinter. The incubation period is from few hours to 3 weeks. The organism produces
exotoxin that inhibits choline esterase at motor endplate resulting in widespread tonic
muscular spasm. The local effects are unremarkable. The first signs are often acute
muscle spasms and neck stiffness or trismus (‘lockjaw’). If untreated, these progress to
opisthotonus (arching of the back due to extensor spasm). There can be also dysphagia,
spasm in facial muscles (Risus Sardonicus), generalised convulsions and eventually death
from exhaustion and respiratory failure several days later. Tetanus is now rare in developed
countries because of immunization with tetanus toxoid during childhood, followed by
boosters at 10-year intervals. If the immunisation status following a major contaminated
injury is unknown, benzylpenicillin should be given plus passive immunization with
tetanus immune globulin.
Prophylaxis against tetanus includes strict sterilization of surgical instruments, and the use
of antitetanic serum for street wounds in non-vaccinated individuals.
Treatment of established tetanus usually requires
- Isolation in quiet surroundings in ICU
- artificial ventilation with muscle relaxants and anticonvulsants
- Antibiotics (benzyl penicillin)
- Passive immunization with tetanus antitoxin
- Local wound care
In some developing countries, neonatal tetanus results from the practice of applying cow
dung as a dressing to the umbilical stump. Mortality remains high, especially in the elderly.
Pseudomembranous colitis
Pseudomembranous colitis is one of the most serious antibiotic-associated diarrhea. It is
caused by overgrowth of a toxigenic Clostridium difficile. Infection produces a thick fibrinous
‘membrane’ on large intestinal mucosa, within which the organism proliferates. Its toxins
cause a profound watery and sometimes bloody diarrhoea, leading to dehydration and
electrolyte loss.
Pseudomembranous colitis may develop after only a single dose of any antibiotic.
Cephalosporins and ciprofloxacin are now the most common cause. Diagnosis can be
made by sigmoidoscopy and biopsy, looking for the characteristic pseudomembrane, and
by detecting the specific toxin in the stool. C. difficile can also be cultured from the stool.
Although the organism is sensitive to penicillin, this fails to penetrate the pseudomembrane.
Oral metronidazole is usually effective but takes at least 2 days before clinical response is
66
observed. Relapses are common in the elderly and oral vancomycin, which is not
absorbed from the GI tract, can be employed or when metronidazole fails.
Endogenous sources of infection
Large bowel is a reservoir for bacteria and endotoxin which are normally safely contained. If
the intestinal barrier is breached by splanchnic ischaemia, poor luminal nutrition of
enterocytes or altered intestinal flora, translocation of bacteria into the portal circulation
can occur in as little as 30 minutes. If the liver Kupffer cells are also impaired, intestinal
bacteria and endotoxin are not prevented from reaching the systemic circulation in the
normal way. This endogenous source probably explains the 30% of patients who suffer
organ dysfunction without an obvious source of infection.
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Part I (Basic Surgery); Chapter 6 (Hand Infections)
Hand Infections
The hand is a complicated, highly sensate organ that is designed to manipulate the
environment, therefore, it has some prerequisites to function effectively. Thus the hand
should be flexible and strong, sensitive and pain free, with well coordinated function. The
five functions of the hand are:
General Considerations:
• Infections of the hand are most common in manual workers and housewives who
frequently suffer small abrasions or pricks in the course of their work.
• Blood borne infection is very rare.
• 80% of hand infections are caused by Staphylococcus aureus that usually causes
localized infections.
• Strept. pyogenes and gram-negative Bacilli are rare causes of hand infections. They
characteristically give rise to diffuse infections.
• Oedema of the dorsum of the hand is a common feature of any hand infection
irrespective of its site. It is a potent cause of subsequent stiffness of the digits.
• Unless the infection can be aborted at an early stage,
suppuration will follow. The early detection of pus and its
accurate localization are of cardinal importance.
• Anatomical Nomenclature
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The Clinical Picture of Hand Infection in General:

a. Systemic symptoms and signs of pyogenic infection:
Depending on the type and severity of infection, systemic symptoms such as fever,
rigors, tachycardia, and general feeling of being unwell might be present.
b. Local symptoms and signs:
- All or some of local symptoms and signs of inflammation might be present. These are
pain, redness, hotness, tenderness, swelling and limitation of active and passive
movements.
- Pain might be dull aching or throbbing, the latter indicates abscess formation. Fluctuation
is a late sign and you should not wait for fluctuation to drain any hand infection.
- The maximum point of tenderness indicates the origin of infection.
- The regional lymph nodes may be enlarged and tender.
General principles of treatment of hand infections:
[1] Antibiotic therapy:
• Start with empiric antibiotics against gram positive organisms. Change to proper
antibiotic after you receive results of culture and sensitivity pus. Antibiotics are continued till
healing occurs.
• In this early stage, local heat (Hot fomentations) can help.
[2] Position of the hand:
• Early in infection and after abscess drainage, the hand is
placed in the position of rest.
• Extension of the wrist 20-30o
• Flexion of the metacrpo-phalangeal joint 45-60o
• Flexion of the interphalangeal joint 15o
• Thumb is opposed with the pads of the fingers
After the acute stage of infection has passed, the hand must be
placed in the position of function.
• Extension of the wrist 20-30o
• Flexion of metacrpo-phalangeal joint 45o
• Flexion of proximal interphalangeal joint 90o
• FULL extension of distal interphalangeal joint
• Thumb is opposed with the tip of the index finger
[3] Elevation and hot fomentations
[4] Early recognition and drainage of pus:
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a. General anesthesia or local ring infiltration (only in distal infection of the fingers).
b. Tourniquet is used to achieve a bloodless field.
[5] Criteria of incisions for draining hand infections:
➢ Should be parallel, and never cross skin creases.
➢ Should be placed over the maximum point of tenderness or the site of abscess
pointing.
➢ Avoid midline incision over the digits, instead a midlateral incision is done.
d. A drain should be inserted, either a tube drain or a piece of gauze.
[6] Adequate after treatment:
➢ Regular wound dressing.
➢ The drain should be removed after 48 hours.
➢ Active hand movements are encouraged as early as possible. Physiotherapy may be
indicated.
Classifications and Types of hand infections:
I. Diffuse infections: Such as cellulitis and erysipelas.
II. Localised infection: These are classified into:
a. Infections of the skin and subcutaneous tissue, include:
1. Subcuticular whitlow
2. Subcutaneous whitlow
3. Volar space infection
Diffuse infection Localised infection
4. Apical subungual infection
5. Paronychia
6. Pulp space infection
7. Web space infection
8. Infected subungual hematoma
b. Infections of fascial planes (spaces) include:
1. Subaponeurotic space infection (superficial mid-palmar space infection)
2. Mid palmar space infection (deep mid-palmar space infection)
3. Thenar space infection
4. Forearm space (Parona space) infection
5. Superficial and deep dorsal space infection
c. Infections of the synovial sheaths:
1. Suppurative tenosynovitis (intrathecal whitlow) of the index, middle or ring finger
2. Ulnar bursitis
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3. Radial bursitis
d. Infections of bones and joints:
1. Suppurative arthritis
2. Osteomyelitis
In the following section, some of the important hand infections will be discussed.
(1) Subcuticular Whitlow:
It is defined as pus accumulating under the cuticle within the epidermis. It might be
communicating with deeper abscess to form a collar stud abscess.
Treatment:
The raised epidermis is removed and gentle probing is done for a track extending to a
deeper abscess, which if present it should be drained.
(2) Paronychia (50%):

It is infection of the tissues related to the hidden part of the nail. It is a common infection
representing 50% of all hand infections. It is either acute or chronic.
Acute paronychia: The organisms enter through a site of hang-nail or careless nail paring.
Clinical picture:
➢ There is severe pain with red, hot, tender swelling around, or at a part of the
nail fold. Infection may extend around the nail forming a U-shaped swelling.
➢ Later on, pus may extend under the nail.
Complications: Spread to the pulp space, or interphalangeal joint.
Treatment:
➢ Follow the general rules of treating hand infections
➢ Abscess drainage:
A. If pus is limited to one side: a small incision is made into the nail fold and Paronychia
raise a triangular flap over a drain. If the abscess is big, a small triangular
piece of skin overlying the abscess is removed to allow proper drainage.
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B. If pus is tracking all around the nail fold: a long incision is made at the nail fold to
evacuate the pus and to raise a rectangular flap of the skin over a drain.
C. If pus is under the proximal part of the nail (subungual): The proximal part of the nail
overlying the abscess should be excised.
Chronic Paronychia: It is a chronic infection that may persist for weeks or months.
The pain is slight and the nail fold is swollen, indurated and deformed. It is usually
due to fungal infection.
Treatment:
a. The hands should be kept dry
b. Use antifungal ointment dressing.
b. If this fails, excision of the nail or half of it is done with curettage of the nail bed.
Incision and drainage of ACUTE paronychia
(3) Pulp Space Infection (Felon) (25%):

Anatomy:
Pulp space is the subcutaneous compartment related to the palmar surface of the distal
phalanx. It is a closed space that only contains fat, no tendons and no synovial sheaths. It
is divided by fibrous septa extending from the skin to periosteum, into 10-12 compartments.
It is separated from the distal volar space by the deep fascia which splits to be attached to
the distal crease of the finger and the periosteum of the distal phalanx.
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Clinical picture:
➢ Severe localized pain in the pulp, with redness, tenderness and induration. Fluctuation
occurs late and do not wait for it.
Complications:
1. Necrosis of terminal 2/3 of the distal phalanx (this will be manifested after 2 weeks on
X-ray). Necrosis occurs because infection induces thrombosis in the digital arteries which
are end arteries.
2. Spread of infection to the nearby tendon sheath causing tenosynovitis or to inter-

phalangeal joint causing septic arthritis.
Treatment:
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a. In early cases:
A mid lateral straight incision is done over one side of pulp starting 0.5 cm distal to the
distal crease and stopping short of the top of the finger. It is deepened flush with the bone
to divide all the fibrous tissue septa.
b. Late cases:
1. A counter incision may be done on the opposite side of the pulp.
2. The mid lateral incision can be further extended across the tip of the nail to make a
hockey stick incision.
WHY midlateral incision?
1. The skin is less subjected to trauma thus it heals well
2. Incision avoids injury of digital vessels and nerves
3. A painful, tender midline wound might preclude proper finger function late after healing
Hockey stick incision

(4) Web Space Infection:
Anatomy:
The web spaces are the three triangular regions between the dorsal and
volar skin filled with loose fat that bulges between the divisions of palmar
fascia.
Each space is connected distally, with the corresponding proximal volar
spaces, and proximally, with subcutaneous tissue of the palm, superficial and
deep mid-palmar space and thenar space along the tunnel of lumbrical
muscles.
Etiology:
Pricks or infected blisters, or extension from infection of the proximal volar space of the
finger.
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Clinical picture:
Besides the general and local
symptoms and signs, the
characteristic sign is wide separation
of the related fingers.
Complications:
1. Spread to the deep mid palmar space.
2. Spread to the adjacent volar spaces.
3. Spread to the adjacent web.
Treatment:
➢ Abscess drainage
- Classically, drainage is done by a transverse incision over the palmar surface of the web
over the site of maximum tenderness and swelling, one cm from the free margin of the web
to avoid injury of the digital nerves and vessels.
- After drainage, press on the palm, if pus comes out this will indicate deep palmar space
infection which should be drained also.
- Longitudinal Counter Incision may be placed dorsally between the bases of the proximal
phalanges, a generous communication is established between the two incisions.
(5) Apical subungual infection:
• It arises from a prick beneath the nail causing infection of the space between the
subungual epithelium and the periosteum.
• It causes severe pain with little swelling.
• Tenderness in greatest just beneath the free edge of the nail
where pus comes out.
• Pus is drained by removal of a small v shaped piece from the center of the free edge
of the nail.
(6) Subaponeurotic (superficial mid palmar) space infection:
The subaponeurotic space (or the superficial mid palmar space) is the space that lies
between the palmar aponeurosis and flexor tendons.
Aetiology:
It is usually due to direct prick or abrasion in the palm. The formed abscess is usually collar
stud in shape with one loculus superficial to the palmar aponeurosis and the other one is
deep to the palmar aponeurosis.
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Clinical Picture:
Besides the general and local symptoms and signs, the characteristic sign is marked
oedema of the dorsum of the hand.
Treatment:
It is done via a transverse incision over the site of maximum tenderness. Then the floor is
explored and the opening in the aponeurosis is enlarged and the subaponeurotic space is
drained also via transverse incision in the palmar aponeurosis and a drain is left for 48
hours.
(7) Deep Mid Palmar Space Infection:
It is also called mid palmer space infection. The space is bounded
by the flexor tendons of the little, ring and middle fingers anteriorly
and the fascia covering the interossei muscles posteriorly.
Aetiology:
• Suppurative tenosynovitis of one of the related fingers.
• Extension from thenar or web space infection or via the
lymphatics from a superficial infection.
• Penetrating wounds.
Clinical Picture:
• The characteristic sign is marked oedema of the dorsum of the hand with semiflexion
of medial four fingers and obliteration of the concavity of the palm (Frog hand). The original
focus may be present, as web space infection or septic wound.
Treatment:
➢ Drainage through a transverse incision in the line of the flexion crease passing across
the middle of the palm. Palmar fascia is divided in longitudinal direction, to avoid digital
nerves & vessels.
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(8) Thenar Space Infection:

The thenar space is bounded anteriorly by the flexor pollicis and
flexor indices tendons, posteriorly by the fascia covering the
transverse head of the adductor pollicis muscle, medially by the
lateral boundary of the deep mid palmar space, and laterally by
the shaft of the first metacarpal bone and thenar muscles.
Aetiology:
Suppurative tenosynovitis of the index finger or thumb.
Extension from the midpalmar space infection.
Local Sings:
The characteristic local signs are
- Ballooning of the thenar eminence.
- Abduction of the thumb.
- Concavity of the palm is preserved.
- Marked oedema of the dorsum of the hand.
Treatment
Abscess drainage:
a. Classically, a dorsal incision done along the lower border of first interosseous
muscle.
b. Alternatively, incision as that for drainage of the radial bursitis of the palm.
(9) Forearm Space (Parona space) Infection:

Parona space is bounded anteriorly by the ulnar and radial bursae, posteriorly by the
pronator quadratus and interosseous membrane, on both sides by the deep fascia which is
attached to the radius and ulna. Distally it is connected with the deep mid palmar space.
Aetiology:
It is always secondary to ulnar or radial bursitis or mid palmar space infection.
Local Sings:
The characteristic local signs are:
1. The primary focus of infection is usually apparent.
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2. Marked swelling and tenderness over the lower part of forearm.

3. Flexion of both wrist and elbow.
Drainage:
It is done by a longitudinal incision starting 2 cm above styloid process of ulna, immediately
in front of its subcutaneous border.
(10) Suppurative Tenosynovitis

Anatomy of the synovial sheaths of the hand
• Each of the middle three fingers has a synovial sheath which extends from
the level of distal palmar crease of finger to the middle of the palm.
• The synovial Sheath of the Thumb and the Little Fingers extend distally as
others, but proximally they continue with radial and ulnar bursae, respectively.
• The Radial Bursa envelops the flexor pollicis longus tendon. Distally it is
continuous with synovial sheath of thumb, and proximally it extends under the flexor
retinaculum to end 3 cm proximal to the distal crease of the wrist.
• The Ulnar Bursa envelops the flexor tendons of the medial four fingers (much
wider than the radial bursa). It is continuous distally with the synovial sheath of the
little finger. It ends proximally 3 cm above the distal crease of the wrist.
• In 75% of patients the ulnar and the radial bursae are connected with each
other.
Aetiology:
1. Spread from a nearby focus.
2. Direct puncture wounds.
Clinical Picture:
➢ Localized Suppurative tenosynovitis of a finger:
The characteristic “Kanavel’s four cardinal signs” of the affected sheath are:
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1. Symmetrically swollen finger.

2. Semiflexion of the all joints of the affected finger (Hook sign).
3. Both active and passive movements are painful.
4. Tenderness along the whole sheath, especially over its proximal cul-de-sac.
➢ Radial Bursitis: The local signs are:
• Signs of tenosynovitis of the thumb.
• Tenderness over the flexor pollicis longus sheath.
• Tenderness and swelling above the flexor retinaculum.
• The other fingers are free.
Suppurative flexor tenosynovitis Suppurative flexor tenosynovitis Flexor tendon sheath

of the middle finger of the index finger hand infection
➢ Ulnar bursitis: The local signs are:

• Signs of tenosynovitis of the little finger.
• Moderate swelling at the palm.
• Marked oedema of the dorsum of the hand.
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• Flexion of the medial four fingers, which resist extension, especially at the
little finger and less at the index finger.
• Kanavel’s sign: The site of maximum tenderness is over the part of the
bursa lying between the transverse palmar creases.
Complications of Tenosynovitis:
1. Necrosis of the tendon (it can be suspected if there is a persistent discharge
from the wound after drainage).
2. Spread of infection to Parona space and joints.
3. Stiffness of the fingers.
4. Median nerve paralysis due to compression at the carpal tunnel (needs urgent
decompression).
Treatment:
Localized Suppurative tenosynovitis of a finger:
Two transverse incisions are done, one just distal to the distal
crease of finger and the other over the cul de-sac. The synovial
sheath is opened and drained. Fine catheter can be introduced
inside the sheath to be irrigated with saline solution.
If the discharge persists for more than one week after
drainage, the tendon should be explored and if it is not viable, the dead part should be
excised with transfixion of its proximal end to avoid spread of infection to the proximal
space.
Radial Bursitis:
Incision is done along the ulnar side of the thenar eminence on the palmar surface, stops 4
cm distal to the distal crease of the wrist.
Ulnar Bursitis:
Incision is done along the radial side of the hypothenar eminence, nerves and vessels to
the little finger are retracted and the bursa incised and drained.
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Compound Palmar Ganglion

• It is chronic tuberculous tenosynovitis of the ulnar bursa.
• It presents in young adult as painful swelling in the palm which
enlarges slowly. The palm concavity is obliterated, skin over it is
usually normal. It is warm, tender, cystic (if there is fluid inside) or firm
(if there is granulation tissue inside). There is fluctuation across the
flexor retinaculum between the palmar part of the ulnar bursa and its extension in the lower
part of the forearm. Sometimes nodules are felt inside.
• In advanced cases there is atrophy of the small muscles of the hand. Active and
passive movements of the fingers are painful.
• General signs of tuberculous toxaemia may present.
• Diagnosis is made by biopsy.
• Treatment: Antituberculous drugs with excision of the bursa (synovectomy).
Ingrowing Toenail
• Ingrowing toenail (embedded toe-nail) of the big toe, usually results from encasing
sweaty feet in tight shoes, and is encouraged by cutting the nail short and convexly.
• The side of the nail curls inwards and grows to form a lateral spike, which causes a
painful infection of the overhanging nail fold.
Treatment:
(1) Conservative measures: can be successful, in mild cases.
• The overhanging nail fold is pushed away and reduced in size by daily packing of the
lateral groove with gauze soaked in a mild antiseptic.
• Warm water salt soaks.
• Antibiotic ointment.
• Avoid wearing tight shoes.
(2) Surgical treatment:
• Excision of a wedge on the affected side including the granulations and 1/3 of the
nail and its bed. A tourniquet is essential. In extensive cases removal of the whole nail and
its bed is done.
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Part I (Basic Surgery); Chapter 7 (Preoperative Assessment & Preparation)
Preoperative Assessment and Preparation

Preoperative patient preparation is concerned with gathering information to put the best plan to
prepare the patient for surgery. The steps to achieve this are:
1. Gather and record concisely all relevant information
2. Devise a plan to minimize risk and maximize benefit for the patient
3. Consider possible adverse events and plan how to deal with them
4. Communicate to ensure that everyone (including the patient) understands the surgical plan
Essential steps in preoperative assessment and preparation:
1. History and examination
Take a good detailed history. Examination should include:
- General examination for: anaemia, jaundice, cyanosis, nutritional status, teeth, feet, leg ulcers or
any other source of infection
- Cardiovascular examination for: pulse, blood pressure, heart sounds, bruits, peripheral pulses,
peripheral oedema
- Respiratory examination for: respiratory rate and effort, chest expansion and percussion note,
breath sounds, oxygen saturation
- Gastrointestinal examination for: abdominal masses, ascites, bowel sounds, bruits, herniae,
genitalia
- Neurological examination for: conscious level, any pre-existing cognitive impairment or confusion,
deafness, neurological status of limbs
2. Routine preoperative investigations
- For simple operations under local anaesthesia, the following investigations are required
- Full blood count
- Random blood sugar
- Clotting screen
- Pregnancy test for female in child bearing period
- Hepatitis/human immunodeficiency virus serology
- Routine preoperative investigations for all patients undergoing operations under general
anaesthesia:
- Full blood count
- Fasting (Random) blood sugar
- Serum electrolytes
- Renal function tests
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- Liver function tests

- Coagulation profile (PT, PTT)
- Pregnancy test for females in the child bearing period
- Hepatitis/human immunodeficiency virus serology
- For patients above 40 years, the following investigations are added:
- Chest x-ray
- ECG
- Further assessment according to patient's condition and diseases specific to each system:
- Pulmonary function test
- Arterial blood gases
- Echocardiography
3. Investigation and treatment of any intercurrent or occult illness
Such as treating chest infection and investigating recent chest pain
4. Making special preparations for the particular operation
Such as colonic preparation for left colon surgery and vocal cord examination for thyroid surgery
5. Collecting pre-admission information about diagnosis and assessment of the risk of surgery
The risk of surgery depends mainly on 2 factors:
1- Type of surgery: major surgery carries more risk than minor surgery, emergency surgery carries
more risk than elective surgery.
2- Type of patient and associated diseases: a patient with cardiac, renal or liver dysfunction is more
risky to do surgery than a healthy patient.
The commonest way to assess the patient risk of surgery is the ASA (American Society of
Anesthesiologists) score:
- ASA class I: A normal healthy patient
- ASA class II: A patient with mild systemic disease that does not limit functional activity
- ASA class III: A patient with severe systemic disease that limits functional activity
- ASA class IV: A patient with severe systemic disease that poses a constant threat to life
- ASA class V: A moribund patient who is not expected to survive for longer than 24 h, either with
or without surgery
The addition of an ‘E’ denotes emergency surgery.
6. Hospital admission and fasting
- Usually, patients are admitted to hospital the same day or one day before surgery.
- If complex assessment or preparation is required, admission to hospital is done several days before
surgery.
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- In emergency and urgent surgeries, hospital admission is done immediately.

- Fasting before surgery is indicated to reduce the risk of pulmonary aspiration. The
recommendations are:
• 2 hours For clear liquids
• 4 hours For breast milk
• 6 hours For infant formula
• 6 hours For non-human milk
• 6 hours For light meal
7. Prophylactic antibiotics
Antibiotic prophylaxis is used to decrease the incidence of postoperative wound infections.
According to the type of operation, antibiotic prophylaxis is as follows:
- Clean operations No antibiotic prophylaxis
- Clean contaminated operations Single dose of antibiotic given one hour before start of
operation
- Contaminated and dirty operations Antibiotic prophylaxis is extended to 1-3 postoperative
days
Particularly significant is the risk of colonization of any artificial material implanted at the time of
surgery, such as in joint replacement surgery or arterial grafting. The choice of the antibiotic used for
prophylaxis depends on:
- The type of flora that normally colonizes the site of surgery, e.g. cephalosporine cover gram
positive cocci that normally colonize the skin, colonic surgery need coverage against anaerobes and
gram negative organisms
- The pathogens that are present because of specific disease
- The hospital antibiogram

8. Venous thromboembolism prophylaxis
Surgery is a risk for deep venous thrombosis and pulmonary embolism. The risk factors for
thrombosis are:
- Increasing age
- Significant medical comorbidities (particularly malignancy)
- Surgery in the pelvis, lower limbs and abdomen, e.g. prostatectomy, hip surgery, rectal cancer
surgery.
- Prolonged surgery
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- Surgery in pregnancy and puerperium

- Prolonged preoperative or postoperative immobility
- Dehydration
- Obesity
- Family/personal history of thrombosis
- Drugs, e.g. oral contraceptive pills
- Smoking
Operations are classified according to the frisk for venous thromboembolism as follows:
Low risk operations
- Minor surgery (less than 30 min), no risk factors, any age
- Major surgery (more than 30 min), no risk factors, less than age 40
- Minor trauma or medical illness
Moderate risk operations
- Major surgery (not orthopaedic or abdominal cancer), age more than 40, or other risk factor
- Major medical illness, trauma or burns
- Minor surgery, trauma or illness in a patient with positive family or personal history of venous
thromboembolism
High risk operations
- Major surgery of the pelvis, hip or lower limb
- Major surgery, trauma or illness in a patient with positive family or personal history of venous
thromboembolism
- Lower limb paralysis/amputation
Prophylaxis against thrombosis can be achieved by:
Mechanical methods
- Early mobilization
- Leg compression stockings
- Calf and foot pumps
Pharmacological methods
- Heparin and low molecular weight heparin
9. The signed consent
The person obtaining consent should be fully conversant with the planned surgery, including all
possible complications and alternatives. The stages in the consent process are:
- Ensure that the patient can take in, analyze and express their view
- Check the patient details (make sure you are talking to the correct patient)
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- Make sure that the patient understands who you are saying and what your role is
- Discuss the treatment plan and sensible alternatives
- Discuss possible risks and complications of surgery
- Discuss the type of anaesthetic proposed
- Give the patient time and space to make the final decision
- Check that the patient has no more questions
- Record clearly and comprehensively what has been agreed
10. Mark the operation site
11. Make arrangements with operating theatre staff
Inform the operation staff about
- The type of operation and any special arrangements needed.
- Expected duration for each operation
- Name, age, sex, ward, and proposed operation for each patient.
- The side of the body to be operated on
- Patient positioning
- Presence of infection, allergies and comorbidities
- Amount of bank blood ordered
12. Making arrangements with the anaesthesia staff
The pre-anaesthetic visit (see chapter of anaesthesia)
13. Plan for postoperative care, rehabilitation and convalescence
- The patient should be transferred safely after surgery from the operating theatre to his bed, under
the supervision of the anaesthetist and surgeon.
- A clear operative note should be written immediately.
- Postoperative instructions to be written in the patient file:
• Observations required and frequency, e.g. 4-hourly pulse and blood pressure measurements
for 24 hours
• Possible complications and action to be taken if complications occur, e.g. if blood loss
exceeds 500 ml in a drain call the surgeon
• IV fluids and drugs
• Time lines for patient recovery, e.g. when to mobilize, when to resume normal oral intake,
the need for physiotherapy, allowable movements, dressing changes.
. Discharge and follow-up details
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SPECIFIC PREOPERATIVE PROBLEMS

- Cardiovascular disease such as hypertension, ischaemic heart disease, recent myocardial infarction,
dysrhythmias and cardiac failure. Proper cardiologic consultation should be obtained
- Respiratory disease such as infection, asthma, chronic obstructive pulmonary disease, pulmonary
fibrosis. General factors that increase risk for postoperative pulmonary complications are increasing
age, low albumin level, prolonged recumbence, obesity, upper abdominal operations, thoracotomy,
heart failure, chronic steroid use and smoking.
- Smoking is the commonest cause to increase perioperative pulmonary complications. Smoking
increased carboxyhaemoglobin levels, decrease ciliary function and increase sputum production and
stimulation of CVS due to nicotine. Recommendations for pulmonary risk reduction are:
• Preoperative:
o Encourage smoking cessation for at least eight weeks
o Treat airflow obstruction in patients with COPD or asthma
o Administer antibiotics and delay surgery if respiratory infection is present
o Begin patient education regarding post-operative lung-expansion maneuvers
• Intraoperative:
o Limit duration of surgery to less than three hours
o Use spinal or epidural analgesia*
o Avoid use of pancuronium
o Use laparoscopic procedures when possible
• Postoperative:
o Use deep-breathing exercises or incentive spirometry
o Use continuous positive airway pressure (CPAP)
o Use epidural analgesia*
o Use intercostals nerve blocks*
- Anaemia and blood transfusion

■ Consider preoperative blood transfusion if haemoglobin level is less than 8 g dl–1
■ Consider carefully which products to use
■ Order and write up blood products clearly
■ Give the blood at a sensible time of day
■ Consider co-administration of a loop diuretic
■ Be prepared to treat any reactions rapidly
- Nutritional problems
• Enteral or parenteral nutrition should be given to some categories of patients e.g. protein
deficiency, malignancy, dysphagia, IBD, to improve their general condition.
• Some categories of patients need specific nutrition e.g. high carbohydrate diet for hepatic patients
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• Gastric aspiration and lavage might be needed e.g. patients undergoing gastric surgery and
patients with pyloric obstruction.
• Fluid and electrolyte balance chart and therapy if needed e.g. patients with dehydration, intestinal
obstruction and shock.
- Obesity
Obese patients carry increased risks of
■ Difficult intubation
■ Regurgitation and aspiration
■ Myocardial infarction
■ Cerebrovascular accident
■ Deep vein thrombosis and pulmonary embolism
■ Respiratory compromise
■ Poor wound healing/infection
■ Pressure sores
■ Mechanical problems – lifting, transferring, operating table weight limits
- Surgery in the jaundiced patient
Jaundiced patients carry the risk of:
■ Clotting disorders
■ Hepatorenal syndrome
■ Infection
- Surgery in cirrhotic patients
- Surgery worsens the liver condition in cirrhotic patients because of blood loss and the use of
hepatotoxic drugs especially anaesthetics. The risk increases with the length and magnitude of
operation. According to the Child’s class of cirrhotic patient, the mortality risk of surgery is as
follows:
Child class A 10% mortality
Child class B 31% mortality
Child class C 76% mortality
- laparoscopic procedures might decrease rates of complication in cirrhotic patients.
- Surgery in patients with renal impairment

- A patient with end stage renal disease frequently required additional attention in the preoperative
period especially in using nephrotoxic drugs and in fluid and electrolyte balance. Preoperative
dialysis might be required in some patients with chronic renal failure.
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- Surgery in Diabetic patients

Diabetic patients carry the following surgical risks:
- Increased risk of surgical wound sepsis
- Increased risk of systemic sepsis such as pulmonary septic complications and central venous line
infection
- Increased risk of cardiac ischemia, cerebrovascular ischemia and peripheral vascular ischemia
- Difficult diabetes control especially with prolonged fasting
- Renal complications
- Fluid and electrolyte disturbances
- Surgery in patients with thyroid disease:
Hypo or hyperthyroidism should be treated before surgery. In patients with huge goiter, further
imaging may be warranted.
- Coagulation disorders
- All drugs interfering with platelet function or coagulation should be stopped at appropriate time
before surgery
Platelet transfusion
Coagulation factors replacement
- Airway assessment and anticipated difficult intubation:
The following categories of patients are expected to have difficult intubation
- Obese patients
- Patients with short neck and small mouth
- Patients who can open their mouth to a limited extent
- Presence of soft tissue swelling at the back of the mouth
- Limitations in neck flexion or extension
Preoperative anaesthetic medications: See chapter of anaesthesia
DOCUMENTATION
Notes must be accurate and legible, entries dated and signed, and the doctor’s name identifiable.
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Part I (Basic Surgery); Chapter 8 (Wound & Wound Healing)
Wound
A wound is defined as a disruption of skin continuity by exogenous force or object. It may

be superficial or deep, open or closed, tidy or untidy, vitalized or devitalized, penetrating or
non-penetrating.
Types of wounds:
1. Abrasion: rubbed off superficial layers of skin after sheering injury

2. Cut wound a wound caused by sharp object with minimal blunt force such as a
street knife or a piece of broken glass. The wound usually has an irregular jagged edge.
3. Incised wound A neat cut wound usually caused by scalpel in surgical operations.
The wound edge is sharp and regular.
4. Lacerated wound is caused by blunt objects such as a stick or stone. The edge is
ragged, irregular with necrosis and tissue loss.
5. Puncture wound is caused by pointed sharp objects such as a nail or needle. The
wound is a tiny deep hole.
6. Stab wound is caused by sharp flat objects such as a knife or screw driver. The
wound is deep and commonly associated with deep organ injury
7. Gunshot wound: caused by gunshots. The edge of the inlet wound is burnt. There
may be also an exit wound. The tunnel between the inlet and exit contains foreign
materials and necrotic tissue. There is usually associated deep organ injury.
8. Crushed wound extreme pressure smashing the skin and underlying tissues with
marked soft tissue damage
9. Traction and avulsion wounds caused by traction force, usually big machines. The
wound is open with marked tissue damage
10. Degloving wound also caused by machines that pull forcefully a part of skin and
completely denuding an area of tissue from its skin covering.
11. Bruises and contusion: caused by blunt objects that cause intradermal bleeding
from minor capillaries with interstitial tracking. The overlying skin is bluish in colour and
tender.
12. Hematoma: blood collection under the skin or in deep tissues after blunt trauma.
13. Bite caused by the teeth of animal or human. It can cause tetanus and rabies. Snake
bites are poisonous.
14. Friction burn forceful sheering abrasion causing thermal injury.
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15. Thermal wounds

16. Stings caused by insects, spiders and scorpions. They can be poisonous.
Complications of wounds:
A. General complications:
Haemorrhage with hypovolaemic shock.
Acute renal failure when there is extensive muscle necrosis.
Compartment syndrome.
B. Local complication:
Infection
Associated tissue and organ injury such as flexor tendon injury in cut wound of the
wrist.
Scar formation with associated problems such as contracture, hyper pigmentation,
hypertrophic scar or keloid formation.
MANAGEMENT OF WOUNDS
A. Initial treatment:
- Life saving and supports are essential in cases of severe or multiple injuries
- Arrest any external bleeding
- Give empiric antibiotics and anti-tetanic serum or tetanus toxoid.
- Local assessment of the type and extend of the injury
- Do the required investigation if needed
B- Definitive treatment:
Using either local, regional or general anesthesia and includes:
1. Direct sutures:
Used in clean tidy incised wounds, which are recent (within 12 hours).
2. Debridement:
Used in untidy lacerated and contaminated wounds within the first 24 hours after the
injury. All contused, lacerated, damaged and devitalized tissues are excised leaving
only viable clean tissues.
Timing of suture application:
1- Primary sutures:
Applied at the time of injury when dealing with a clean surgical wound or recent wound.
2- Delayed primary sutures:
Are applied to doubtful or contaminated wounds or in late presentation after injury.
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The wounds are left open after surgical excision with delayed primary suture applied 5
to 7 days later.
3- Secondary sutures:
Are used where an infected wound is left open to granulate and only when it gets clean,
sutures can be applied.
4- Reconstruction:
If there is skin or tissue loss to be replaced and gaps to be bridged skin covers and
different types of grafts may be needed at any stage of management.
SUTURES
An ideal suture material would be:
a. Strong with a high tensile strength suitable for the site, type of tissues and purpose it is
applied for.
b. Flexible and can be easily tied with a secure knot.
c. It would excite minimal tissue reaction.
d. Would not serve as a nidus for infection
The suture materials are either:
Absorbable or non-absorbable: Absorbable sutures are absorbed by the body while
non-absorbable sutures are retained for very long time.
Natural or synthetic.
Monofilament or braided: Monofilament does not harbor bacteria and do not invite
infection while braided can harbor bacteria and thus can invite infection.
A. Absorbable sutures:
1. Synthetic absorbable: As Vicryl and Dixon.
These are polymers of glycolic acid or glycosides and lactides.
They are commonly used in different surgeries such as intestinal anastomosis,
subcutaneous tissue closure and in tying blood vessels.
They excite minimal tissue reaction and are absorbed by hydrolysis.
Its tensile strength is lost in about 100 days.
2. Natural absorbable: As Catgut.
Are made from the submucosa of the bovine intestine.
Being protein in nature, it excites considerable tissue reaction and it is absorbed by
the action of protoelytic enzymes.
Its use has largely been abandoned given the theoretical risk of transmission of
infections such as mad cow disease.
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B. Non absorbable sutures:

1. Synthetic non-absorbable: e.g. monofilament prolene (Polypropylene) and
braided Terylene and Dacron
Are inert materials which retain their tensile strength for a very long period or
indefinitely.
Commonly used in hernia repair, abdominal wound closure and vascular
anastomosis.
2. Natural non absorbable:
Silk:
Is braided protein which is easy to handle and tie.
Is relatively inert but excites a polymorphnuclear reaction in the tissues.
It looses its tensile strength in about 2 years.
Stainless steel:
It is a strong inert substance which does not harbor bacteria.
It is difficult to tie or manipulate and may sustain fractures.
Wound healing
Stages of Wound Healing
1. Initial inflammatory Phase
* This is the initial response of all tissues to injuries. This phase takes 3-5 days. The
aim is to establish haemostasis and mobilize the immune system that will complete
the healing process. This phase is composed of a vascular response and a cellular
response.
a. Vascular response
Vascular response is precipitated by many factors such as serotonin, histamine,
kinins, platelet activation factor (PAF) and complement. Initial vasoconstriction, platelet plug
and activation of the clotting cascade cause haemostasis. This occurs in 5-10 minutes. This
is followed by vasodilatation in the following 72 hours. Vasodilatation is responsible for the
signs of inflammation such as redness, hotness, and oedema.
b. Cellular response
The cells responsible for the cellular response are:
* Leucocytes:
- Migrate through the vessel wall by diapedesis stimulated by chemotactic factors.
- Liberate enzymes that facilitate the breakdown of debris and bacteria.
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* Macrophages:
- The main cell in wound healing.
- Release chemotactic and growth factors that activate and stimulate the division of
fibroblasts and new blood vessels.
- They are dominant 3 – 4 days after injury.
* Mast cells:
- Release histamine, heparin.
- May be involved in the breakdown of debris and removal of collagen.
2. Lag or Substrate Phase
* Starts 3 – 5 days after the original insult.
* This phase is characterized by removal of debris and migration of capillary fibroblasts
and endothelial cells to the wound site.
* Muco-polysaccharides provide the environment for collagen deposition and fiber
formation.
3. Proliferative Phase
* From 5 – 21 days.
* Healing by 1ry intention occurs in clean cut wounds closed by sutures that require small
amount of new tissue. Fibroblasts produce collagen to fill the minimal gap under the skin
and epithelial regeneration occurs from the edges of the wound to join them. The result is a
neat linear scar.
* Healing by 2ry intention occurs where there is tissue loss. It can take weeks to months.
Infection and foreign bodies affect the healing process adversely. Stages of healing by
secondary intention are:
- Granulation tissue grows from newly formed blood vessels, fibroblasts and collagen.
Healthy granulation tissue is beefy red in color, granular and with no offensive
discharge. Unhealthy granulation tissue is less vascular, edematous, hemorrhagic,
has sloughs.
- Fibroblasts produce collagen and ground substance (muco-polysaccharides and
glycosaminoglycans). Vitamin C acts as a co-enzyme for the hydroxylation of proline
to hydroxy-proline which matures the collagen fibers.
- Wound contraction means gradual wound shrinkage is an attempt to decrease the
area to be covered by epithelium. Epithelium creeps from all around the wound to
cover the granulation tissue. Wound contracture, (shrinkage of the scar after
complete healing and epithelialization) might occur.
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4. Remodelling Phase
Type III collagen formed during the proliferation phase is converted to type I, and
undergo extensive reorganization, the fibers become lined up along the stress lines
of the wound.
Scar tissue becomes softer, flat, and its color fades.
This stage may last for a year or more.
Unfavourable factors for Wound Healing:
Local:
* Infection
* Tissue edema
* Presence of necrotic tissue or foreign body
* Poor blood supply
Systemic:
* Old age
* Malnutrition: Proteins and vitamins (C-A-E), are essential for wound healing.
* Chronic diseases e.g. Diabetes mellitus, cancer delay wound healing.
* Vascular insufficiency.
* Radiation (because it induces end arteritis obliterans).
* Immunosuppression e.g. AIDS, chemotherapy.
* Smoking.
Complications of Wound Healing
Early
* Infection.
* Haematoma.
* Wound dehiscence and disruption.
Late
* Ugly scars.
* Hypertrophic scars.
* Keloids.
* Wound contracture.
* Malignant transformation (Marjolin ulcer)
Management of wounds
The management of wounds passes in stages, each following the other. The final goal of
wound management is to obtain a good quality healing with a nice scar.
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These stages are:

i- Primary wound care.
ii- Wound dressings.
iii- Surgical wound management.
i- Primary wound care:
* Wound cleansing: using liberal amount of antiseptics and normal saline.
* Wound debridement: where the foreign material implanted in the wound is removed.
* Wound excision: where the apparently dead parts of tissues are excised.
* Bleeding points are secured by electrocautry or ligatures.
ii- Wound Dressing:
The ideal wound dressing should have the following properties:
* Maintain a moist environment for healing.
* Remove excess exudates.
* Allow gaseous exchange.
* Impermeable to bacteria.
* Atraumatic on removal.
* Non-allergic.
* Comfortable and conformable.
* Protect against further trauma.
* Provide thermal insulation.
* Cost effective with a long half-life.
* Carrier for medications.
* Comes in a wide array of sizes and shapes.
iii- Surgical wound management:
1-Skin suturing:
This technique is used when there is minor skin defect.
2-Skin grafts and flaps:
These are used when there is extensive skin loss and/or other soft tissue or skeletal
loss. Skin grafts and flaps will be discussed in the section of plastic surgery.
Scars formation
A scar is the inevitable consequence of wound repair. The final phase of wound repair
is the process of remodelling and scar maturation.
The granulation tissue in the newly healed wound is gradually replaced by relatively
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cellular and vascular scar tissue composed of mature collagen with scattered fibroblasts.
As a result of the remodelling wound breaking strength increases until about 6 months
after the injury.
Wound contraction:
A contraction force is exerted in the collagen matrix that fills the wound space.
The contraction pulls normal tissue into the open area and achieves coverage with
reduction in the wound size.
Contraction should differentiate from contracture which is loss of tissue mobility caused
by a shrinking scar.
Hypertrophic scar:
In wounds with delayed healing due to infection the scar may remain in the remodelling
phase longer than usual producing a more cellular and more vascular scar than mature
scar.
There is increased collagen production over breakdown with collagen deposition but the
scar tissue never extends beyond the limits of the original wound.
A hypertrophic scar is itchy. It appears red, raised above the skin surface and tender.
With spontaneous maturation the scar becomes pale and flat.
The process of maturation of a hypertrophic scar can be accelerated by application of
pressure to its surface.
Keloid scar:
It occurs more frequent in oriental races and Africans.
May occur in any wound after healing which could be perfect with no complication.
It is extreme over growth of scar tissue that grows beyond the limits of original wound
and showing no spontaneous tendency to subside.
Local steroid injection may help in some cases of keloid formation.
The best result can be achieved with surgical excision and postoperative interstitial
radiotherapy otherwise recurrence in inevitable.
Types of wound healing:
1st intention: sutured regular wound non infected, linear scar
2nd intention: non-sutured healing gapped wounds, disfigured wide scar
3rd intention: healing of wound after secondary sutures less ideal scar
Factors affecting wound healing:
Systemic:
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• Nutrition
• Age
• Steroids
• Cytotoxic drugs
• Chronic liver disease
• Chronic renal disease
• Sepsis
Local:
• Blood supply
• Tension in tissues
• Infection of the site
• Method of wound closure
• Oxygen supply
• Irradiation
• FB
• Local debris and necrosis
Tidy wound: sharp instrument, no devitalized tissue, regular skin edge, clean cut and
incised, could be closed primarily in the 1st 6-8 hours 1st intention healing, tendons arteries
and nerves could be repaired, e.g. knife, glass, and surgical incisions
Untidy wound: marked soft tissue damage, crushed, avulsions, devitalized tissues, +or –
fractures, tendons, nerves, vessels are exposed and may be damaged but not divided,
need wound excision exposure, wash hemostasis and dressing derided, and cleaned from
FB and dressing without primary closure, 2nd intention healing.
Complications of wound healing

Early:
1. Hematoma
2. Seroma
3. Infection
4. Disruption
Late:
1. Hypertrophic scar
2. Keloid
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3. Chronic ulcer
4. Malignancy
5. Scar contracture
Ideal scar
1. Primary healing 1st intension
2. Clean incised wound
3. No dehiscence or infection
4. No tension
5. Langer line skin tension
6. Opposed edges
7. Eyelids, palms
8. Age
9. Sex
Adverse scar
1. Wrong direction
2. Stretched wound
3. Contracted wound
4. Tattooing
5. Stitch mark
6. Type of stitching
7. Pigmented area
8. Race
9. Type of stitch
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Part I (Basic Surgery); Chapter 9 (Postoperative Care & Complication)
Postoperative Care and Complications

Postoperative care
The aim of postoperative care is to provide the patient with as quick, painless and safe
recovery from surgery as possible. Postoperative care starts from the moment the patient is
received from the OR after surgery until he is discharged from hospital.
Postoperative care includes:
■ Ensuring patent airway, adequate breathing and circulation
■ Postoperative pain management
■ Regular monitoring of the vital signs including pulse, blood pressure, temperature and
respiration
■ Instructions for early mobilization and chest exercises
■ Monitoring the return of intestinal sounds and bowel motions and resuming oral feeding
■ Watching for the development of general complications and their management e.g. DVT,
pulmonary embolism, chest infections
■ Watching for the development of complications specific to particular operations and their
management e.g. leak after intestinal anastomosis, scrotal oedema after surgery for
hydrocele, neck haematoma and suffocation after thyroidectomy
Postoperative Complications
Post-operative complications are classified into:
1. Local wound complications
2. General postoperative complications
3. Complications specific to particular operations
A. Local Wound complications
1. Wound hematoma
Definition: Abnormal collection of blood under the incision
Etiology: imperfect hemostasis
Diagnosis: discoloration of the wound edges (purple/blue) with
blood leaking through sutures
Prevention: careful hemostasis
Treatment: depends on size and duration of the haematoma. Small hematomas may
resolve spontaneously but larger ones require evacuation. Regarding the duration,
hematomas occurring soon after surgery should be explored and evacuated with revision of
hemostasis (look for a spurter), late occurring hematomas within two weeks post
operatively will usually reabsorb spontaneously.
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2. Wound seroma
Definition: Collection of serum and liquefied fat under the incision
Clinically: It presents as a non tender swelling with no overlying erythema.
As it contains fluid, fluctuation test is positive. Seroma is more common in
obese patients and after surgical procedure that require dissection of skin
flaps e.g. mastectomy and incisional hernia.
Treatment: In many cases, seroma is treated conservatively. If large,
seroma can be aspirated. The aspirate is yellow in color and clear.
Persistent seroma may need operative exploration and drainage.
3. Wound Infection
Wound infection is a common postoperative complication. It is called Surgical Site Infection
(See chapter of Infections).
4. Wound dehiscence and evisceration
Definition: Wound dehiscence is defined as partial or total disruption of any or all layers of
the operative wound. In the abdomen, it is called burst abdomen. The
incidence of burst abdomen after abdominal operation is 2%.
Evisceration is defined as rupture of all layers of the abdominal wall with
extrusion of abdominal viscera.
Clinically; an intact skin does not exclude wound dehiscence because
the deeper layers may be disrupted. A sero-sanguinous discharge from the wound is an
alarming sign. Whenever you find it, you should locally explore the wound for dehiscence of
deeper layers.
Aetiology: Dehiscence and evisceration are mainly caused by improper surgical technique
e.g. closure of the wound under tension and too tight or too lose sutures. Factors that result
in poor wound healing are considered risk factors for wound disruption and evisceration,
e.g. wound infection, malnutrition, old age, steroid use, increased intra-abdominal pressure
and diabetes.
Treatment: Dehiscence can be treated conservatively, with proper wound care and
dressing to give time for healing by second intention and granulation tissue to form. In this
case, ventral hernia is anticipated. Dehiscence may require operative intervention to repair
the wound. Wounds can be repaired only in absence of overt infection or devitalized
tissues.
Evisceration, on the other hand, is a surgical emergency because of the possibility of
devitalization and injury of the exposed intestine, and possibility of spread of intra-
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abdominal infection. Once discovered, cover the intestine with sterile saline moistened
towel, and prepare the patient for operative exploration and repair.
In all cases, correction of the underlying cause is essential.
5. Incisional hernia
This will be discussed in the chapter of abdominal wall & Hernias
B. General post-operative complications
1. Postoperative Fever
Postoperative fever is common. A clue to its cause can be reached by knowing the
postoperative day of onset. Most cases immediately follow surgery and are self-limited, but
it is critical not to miss more serious aetiologies. The causes of raised temperature
postoperatively include:
- Fever within the first 48 hours after surgery: is caused by surgical trauma and lung
atelectasis. Trauma leads to the release of pyrogenic cytokines which act directly on the
anterior hypothalamus to release prostaglandins that mediates the febrile response. The
more traumatic the surgery is, the higher risk of postoperative fever. The magnitude of fever
is not a reliable marker of the severity of the condition. Fever usually resolves without
therapy.
- Fever on postoperative days 3–5: is usually caused by superficial or deep wound
infections.
- Fever on the 5th postoperative day: can be caused by:
1. Chest infection (especially in patients with preexisting COAD or if have been
mechanically ventilated). Chest infection can be bacterial, viral or fungal
2. Urinary tract infection (especially if the patient had a urinary catheter)
3. I.V. line infection (peripheral lines cause superficial thrombophlebitis or cellulitis while
central lines cause blood stream infection)
- Fever after one week: usually indicates serious complication such as anastomotic
leak, intracavitary collections and abscesses
- Common noninfectious causes of postoperative fever include:
1. Deep Venous thrombosis (DVT)
2. Wound heamatomas
3. Transfusion reaction
4. Pyrogenic reactions to drugs and infusions
5. Lung atelectasis
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- Causes of postoperative fever that require emergency management:

1. Surgical infections causing myonecrosis
2. Pulmonary embolism
3. Acute adrenal insufficiency
4. Malignant hyperthermia
Diagnostic approach:
The diagnostic workup of post-operative fever includes:
1. Asking the patient if he/she is having any pain (and where?), cough, dysuria, or any other
symptom which may help to localize the source of the fever.
2. A thorough physical exam of all body systems should be conducted, with emphasis on
lung auscultation, abdominal examination and noting lower extremity edema.
3. Look for erythema or drainage from the surgical incision(s)
3. Reviewing the patient's surgical and post-operative course
2. Reviewing any evidence of infection in catheters, cannulas, central lines…etc 3.

Reviewing the patient’s medications
4. Laboratory testing and imaging includes urine and blood cultures as well as a chest X-
ray.is generally deferred for evaluation of fever that occurs within the first 48 hours post-
operatively,
2. Deep Venous Thrombosis
This will be discussed in details in the section of vascular surgery.
3. Pulmonary complications
- Postoperative pulmonary complications are common. The most common complications
are atelectasis and pneumonia. Acute respiratory distress syndrome may affect severely ill
patients.
- Predisposing factors for postoperative pulmonary complications include general
anesthesia, smoking, and presence of chronic lung disease.
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Radiograph showing right upper lobe atelectasis Radiograph showing lower left lobe consolidation
Radiograph showing a right tension pneumothorax with tracheal deviation to the left
- Proper pre-operative evaluation and early post-operative ambulation are the most
important preventive measures
- The incidence of respiratory complications may be reduced by:
1. Using adequate analgesia, including epidurals, to reduce postoperative pain which
reduces the patient ability to do proper respiration
2. Analgesics that depress respiration, such as opioids, should be used carefully
3. Administration of oxygen using face masks or nasal prongs
4. Regular lung physiotherapy in patients with asthma and chronic obstructive airway
disease
5. Postponing surgery in patients with upper respiratory tract infections.
Causes of acute postoperative shortness of breath
■ Myocardial infarction and heart failure
■ Pulmonary embolism
■ Chest infection
■ Exacerbation of asthma or chronic obstructive airway disease
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4. Gastrointestinal Complications
▪ Postoperative ileus (see intestinal obstruction)
▪ GI bleeding
Aetiology:
- Mallory Wise syndrome due to excessive vomiting
- Gastritis due to stress of surgical trauma (Cushing’s ulcer)
- Gastritis due to the use of postoperative non-steroidal anti inflammatory drugs (NSAID)
- Specific cause after GIT operations, such as technical errors in intestinal anastomosis or
stapling.
Treatment: The source of bleeding in the upper gastrointestinal tract is usually detected
and treated endoscopically. Surgical control of intestinal bleeding is required in up to 40
percent of patients.
▪ Postoperative nausea and vomiting
Predisposing factors for nausea and vomiting in postoperative patients are:
• Poorly controlled pain
• Postoperative use of opioids and NSAID
• Abdominal operations and ileus
• Female sex;
• Surgery in young adults
• History of preoperative vomiting
• History of motion sickness or migraine
• Acute gastric dilatation.
5. Postoperative collapse or rapid general deterioration
Collapse can occur at any time of the postoperative course. Important causes of
postoperative collapse are:
a. Cardiovascular causes: such as
- Myocardial infarction
- Cardiac arrythmia
- Pulmonary embolism
- Stroke
b. Respiratory causes: such as
- Failure to reverse anesthesia. This occurs early after surgery
- Hypoxia due to respiratory depressant drugs
- Severe pneumonia
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c. Infective causes leading to SIRS and MODD such as

- Severe surgical site infection
- Neglected infection of central lines
d. Surgical causes: such as
- Acute blood loss caused by slipped ligatures
- Decompensation in unrecognized hypovolemia and dehydration
e. Metabolic causes: such as
- Hypo- or hyper-glycaemia in diabetics
- Electrolyte disturbances
- Adrenal insufficiency
f. Drug reactions and anaphylaxis
Sudden postoperative collapse is assessed by:
• Taking short history looking for an underlying related medical condition (diabetic with
hypoglycemia, cardiac who developed myocardial ischemia, allergy to a recently
administered drug…etc
• Rapid clinical evaluation “ABC Airway, Breathing, Circulation & consciousness, any
neurological changes”.
• Rapid review of charts for vital signs & fluid intake & output.
Assessment of Low blood pressure postoperatively
• Is the patient dehydrated?
• Has the patient had an epidural or spinal anaesthetic?
• Is the patient losing blood?
• Is the patient on too much morphine?
• Has the patient had a myocardial infarct?
The treatment depends on the underlying cause.
6. Cardiovascular Complications
▪ Uncontrolled hypertension
▪ Myocardial ischemia or infarction
This is the leading cause of death in any surgical patient. The key to treatment is
prevention
▪ Arrhythmias
It is defined as 30 seconds of abnormal cardiac activity. The key to treatment is to
correct any underlying medical condition that can predispose to arrhythmia such as
correction of hypoxia and electrolyte disturbances
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7. Renal Complications
Urinary retention
▪ Reflex retention due to postoperative pain frequently seen after anal operations.
▪ Also may occur after spinal or epidural anesthesia or use of some medication.
▪ Single catheterization is needed for relief, but Folly's catheter may be needed in
some cases.
Acute renal failure
▪ May occur due to pre-renal, intrinsic or post-renal causes
8. Complications of Thermal Regulation
Hypothermia
Defined as drop in temperature by 2°C. Hypothermia can lead to coagulopathy, platelet
dysfunction, increased risk of cardiac events, blood loss and SSI.
Malignant hyperthermia
This is a rare but fatal event caused by inherited autosomal dominant deficiency of the
enzymes controlling muscle contractions. It presents by fever, tachycardia, rigidity, cyanosis
with induction of anaesthesia after giving muscle relaxants. Treatment: Dantrolene is given
until symptoms subside.
9. Adrenal insufficiency, Hypothyroidism, Hyperthyroidism
See chapter of endocrine surgery
10. Neurologic Complications
▪ Drug induced neurological complications such as delirium, dementia, psychosis,
seizures
▪ Stroke and TIA
1. COMPLICATIONS RELATED TO SPECIFIC OPERATIONS
Gastrointestinal surgery
• anastomotic leakage;
• bleeding or abscess;
• ileus
Biliary surgery
Biliary leakage, stricture, jaundice
Chest surgery
All pulmonary complications, empyema, mediastinitis
Anal surgery
Anal stenosis, incontinence
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Neurosurgical operations
Disturbed level of consciousness, signs of increased intracranial tension, paralysis or
paresis.
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Part I (Basic Surgery); Chapter 10 (Cysts, Tumours, Sinuses & Fistulae)
Cysts, Tumours, Ulcers, Sinuses and Fistulae

Cysts
A cyst is defined as a collection of fluid in a sac. The word “cyst” is derived from the Greek
word that means “bladder”. A cyst can be true or false. The wall of a true cyst is lined by
epithelium or endothelium, while that of a false cyst is lined by fibrous or granulation tissue.
False cysts are sometimes called “pseudocysts”.
Classification of cysts:
A. According to the pathogenesis and nature of the sac
1. Dermoid cysts:
These are true cysts caused by the persistence of ectoderm in or its migration to unusual
location. The wall of dermoid cyst is formed of ectoderm and it contains paste-like material
formed of desquamated epithelial cells and keratin. There are different types of dermoid
cyst (see later).
2. Cysts of embryonic remnants:
They arise from embryonic tubules and ducts which normally disappear or are only present
as remnants after birth. e.g. cysts of the urachus and vitellointestinal duct.
3. Retention cysts:
They are due to the accumulation of secretions of a gland behind an obstructed duct e.g.
parotid cyst caused by accumulation of saliva behind a stone in the parotid duct.
4. Distention cysts:
They are caused by accumulation of secretions in ductless glands or tissue, e.g. cystic
dilatation of thyroid acini and cystic dilatation of ovarian follicles. Lymphatic cyst and cystic
hygroma are considered to be distension cysts.
5. Exudation cysts:
They occur when fluid exudes into an anatomical space that is already lined by endothelium
e.g., vaginal hydrocele and bursa.
6. Traumatic cysts:
Liquefaction of a hematoma may end up in a cyst lined by fibrous capsule. The cyst is
located between muscle, fascia, or subcutaneous planes and contain straw or brown
coloured fluid representing the liquefied haematoma and characterized by containing
cholesterol crystals. Aspiration of traumatic cysts is only of temporary value and complete
excision is usually needed to achieve cure.
7. Degeneration cysts:
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A tumour may degenerate to form fluid collection in its center. This is called cystic
degeneration of a tumour.
8. Cystic tumours:
Some tumours have cystic form, e.g. cystic teratomas, pancreatic cystadenoma and
cystadenocarcinoma.
8. Parasitic cysts:
These are encysted forms in the life-cycle of various worms e.g. hydatid cyst of Taenia
echinococcus in the liver and cysts of Trinchina spiralis in muscles.
B. Congenital and acquired cysts
Sequestration dermoid, tubulodermoid and cysts of embryonic remnants are congenital
cysts. All other types of cysts are acquired.
Clinical features of a cyst:
1. Cysts usually present as a swelling that has a smooth surface and spherical appearance.
2. They are usually painless however cysts may be painful when infection or haemorrhage
causes sudden increase in intracystic tension.
3. The swelling is fluctuant, however, a tense cyst feels solid.
4. Cysts containing clear fluid are brilliantly translucent.
5. Bedside aspiration can reveal the nature of the contents.
6. Depending on its site, a cyst may have specific signs and symptoms. For example, the
common bile duct may be obstructed by a choledochal cyst, a hydatid cyst may cause pain
by stretching the capsule of the liver and an ovarian cyst may compress pelvic veins and
the patient presents with varicose veins.
Complications of a cyst:
1. Infection:
Infected cysts are tense, painful and adherent to the surrounding tissues making their
surgical excision difficult. An abscess may form and discharge pus forming an ulcer or
sinus.
2. Haemorrhage:
Haemorrhage causes rapid painful increase in the size of a cyst. This is not uncommon in
thyroid cysts when the patient presents with difficulty in breathing because of pressure of
the cyst on the trachea.
3. Torsion:
Torsion may occur in cysts which are attached to neighboring structures by a vascular
pedicle. Ovarian dermoids are sometimes brought to notice in this way as acute abdominal
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emergencies. The cyst becomes gangrenous and turns to a purple then black colour as the
venous, and then the arterial supply is cut off.
4. Calcification:
This may follow haemorrhage, or infection, or it may be the result of reaction to a parasite,
e.g. hydatid cyst.
Cysts commonly seen in surgical practice
A. Sebaceous cyst
This is a type of retention cyst caused by obstruction a sebaceous gland duct with
inspissated sebum. The cyst is lined by epithelium and contains yellowish white sebaceous
material that consists of fatty acids, cellular debris and keratin.
Clinical Picture:
- Sebaceous cyst can occur anywhere in the body except in the palms and soles because
they do not contain sebaceous glands.
- The most common sites to be affected by sebaceous cysts are the face, scalp and
scrotum.
- Multiple sebaceous cysts can occur especially in the scalp and scrotum.
- It is slowly growing, hemispherical, painless, soft swelling which is neither hot nor tender.
The edge is well-defined. The most characteristic sign is the attachment of the cyst to the
skin at one point by a punctum which may be black in colour.
Complications:
1. Infection:
The cyst increases in size, becomes painful, tender and the overlying skin is red. The cyst
now contains odorous pus.
2. Ulceration:
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An infected cyst may rupture forming a surface ulcer, which resembles an epithelioma. This
is called Cock’s peculiar tumour.
3. Sebaceous horn:
The contents sometimes escape slowly from the duct orifice and dry in successive layers in
the skin forming a sebaceous horn.
Treatment:
- Excision by an elliptical incision that should include the punctum.
- Infected cysts are treated by antibiotics and hot fomentations. If it forms an abscess, it
should be drained and delayed excision is done after resolution of infection.
B. Dermoid cyst
Depending on the pathogenesis, there are different types of dermoid cysts:
1. Sequestration dermoid:
It is due to subcutaneous sequestration of part of the surface epithelium during embryonic
skin fusion. It appears as a cystic, smooth, rounded swelling along lines of skin fusion. The
cyst is not attached to the overlying skin, but it may be adherent to the deeper structures
and there may be indentation of the underlying bone.
Common sites of sequestration dermoid cysts are:
a- Midline of the body, especially in the neck. (sublingual and submental dermoid)
b- Inner and outer angles of the orbital margin (internal or external
angular dermoid).
c- Root of the nose.
d- Behind the ear (post auricular dermoid).
Dermoid cysts of the head may have intracranial communication through a bone
defect. Plain X-ray or C.T for the skull will show any small defects. An impulse on
cough may be detected if the communication is wide.
Submental drmoid Sublingual Dermoid Implantation Dermoid
2. Implantation dermoid:
It is due to implantation of epithelial cells into the subcutaneous tissue induced by skin
trauma. The hands of manual workers and ladies are the most common sites of
implantation dermoid. Implantation dermoids can also occur under surgical or traumatic skin
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incisions. History of pin prick, puncture wound or skin incision may be obtained. The cyst
presents as painless, smooth, subcutaneous swelling which is not attached to the overlying
skin.
3. Tubulodermoid:
It is due to distension of a remnant of the embryonic ducts. Examples of tubulodermoid are:
- Thyroglossal cyst (from the thyroglossal duct).
- Branchial cyst (from the cervical sinus).
- Post-anal dermoid (from the neurenteric canal).
4. Teratomatous dermoid:
It is a benign form of teratoma and usually occurs in the ovary and testis. The wall is made
of skin and the cyst contains, teeth, bone and cartilage.
Treatment of dermoid cyst:
Treatment of dermoid cyst is excision. Special care should be taken if there is intracranial
communication. In this case, neurosurgical consultation is needed.
C. Ganglion
Ganglion is the commonest hand and forearm swelling. Its origin is uncertain, but it is
probably caused by leakage (and subsequent fibrous encapsulation) of synovial fluid
through the capsule of a joint or tendon sheath. They are sometimes predisposed to by
injury.
Ganglia are localized, painless or slightly painful, tense cystic swellings containing clear
gelatinous fluid. They are smooth, fluctuant and translucent. They are not attached to the
overlying skin. Because of its attachment to the tendon, it can be moved only in the
direction perpendicular (and not parallel) to the tendon. Ganglion becomes fixed on
stretching the tendon or on contracting the muscle.
There are two types of ganglia; simple and compound ganglia
- Simple ganglion is more common and is commonly found on
the dorsum of the wrist and the foot. It is treated by excision, but
it occasionally resolves spontaneously. Recurrence rate is high.
D. Chronic Bursitis
A bursa is a normal anatomical structure that is present over bony prominences and
between tendons to allow sliding of the skin over the bone or the tendons over each other.
When a bursa is subjected to repeated pressure or injury, it swells and secretes fluid
between its layers. This is called chronic bursitis. Treatment of chronic bursitis is to avoid
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the causative factor. Excision might be needed in some cases. Common sites of chronic
bursitis are
- Prepatellar bursitis (housemaid’s knee) which is caused by prolonged kneeling on the
knee. It is associated with occupations such as carpet fitting and tiling.
- Infrapatellar bursitis (clergyman’s knee)
- Olecranon bursitis (student’s elbow)
- Semimembranosus bursitis: This bursa lies between the semimembranosus muscle and
the medial head of the gastrocnemius muscle. It usually presents in children as painful or
painless swelling on the medial side of the popliteal fossa. It is neither warm nor tender. It is
cystic in consistency and becomes more tense on extension of the knee. It is not attached
to the skin and moves from side to side when the knee is flexed. It usually disappears
spontaneously. Excision might be needed in some cases.
Prepatellar Bursitis Baker's Cyst
E. Baker’s cyst
It is herniation of the synovial membrane of the knee joint through a weak part of the
posterior surface of the fibrous capsule. It is usually secondary to osteoarthiritis. It is difficult
to be differentiated from semimembranosus bursitis, but it occurs in the midline. Treatment
is directed to the cause.
E. Adventitious bursa
Adventitious bursa forms as a result of prolonged pressure over bony prominences. The
term ‘adventitious’ means that the bursa is acquired and no
anatomical bursa was present at the site of the newly formed
cyst. One of the commonest of such bursae is that over the
medial aspect of the head of the first metatarsal bone in hallux
valgus (Bunion).
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TUMORS
A tumour, or neoplasia, is defined as a new uncontrolled proliferation of cells that has no
useful function.
Classification of tumours
A. Behavioural classification
Tumours are classified according to their behaviour into
1. Benign tumours
These are characterized by:
- They are formed of well differentiated cells that resemble adult cells.
- They grow slowly by expansion
- They can cause compression of surrounding tissues.
- They are encapsulated.
- They do not metastasize to distant organs.
2. Malignant tumours
These are characterized by:
- They are formed of incompletely differentiated cells of variable shapes
(pleomorphism).
- They grow rapidly by invasion
- They infiltrate surrounding tissues.
- They are not encapsulated
- They can spread (metastasize) to distant parts of body such as liver, lungs & bone.
- Majority of malignant tumours are associated with weight loss and a rapid downhill
path.
A malignant tumour arising from ectoderm or endoderm is called carcinoma, while that
arising from mesoderm is called sarcoma. Germ cell tumours arise from germ cells e.g.
teratoma, seminoma.
3. Intermediate tumours
These are tumours that behave in a manner different from benign and malignant tumours.
Thus they infiltrate the surrounding tissues but do not metastasize. Examples of
intermediate tumours are mixed salivary tumour and desmoid tumour.
4. Hamartoma
Hamartoma is defined as a developmental malformation consisting of a tumour-like
overgrowth of tissue proper to the part. It is not a true tumour. Exampels are hemagiomas
and neurofibroma.
B. Histological classification
Tumours can be classified according to their cell of origin as follows:
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1. Tumours of epithelial tissue

a- Papilloma
Papilloma is a benign tumour that arises from non-secretory epithelial tissue, e.g.
squamous epithelium of the skin and transitional epithelium of the urinary bladder. It
consists of a central core of connective tissue that contain blood vessels and lymphatics
and that is covered by epithelium specific to the part. Commonest sites are skin, tongue, lip,
vocal cords and wall of cysts (e.g. cysts of the breast and ovary).
b- Carcinoma
The malignant counterpart of papilloma is carcinoma, e.g. squamous carcinoma of the
tongue, transitional carcinoma of the urinary bladder. Chronic irritation of non-squamous
epithelium may cause squamous metaplasia which may end up in squamous carcinoma
(e.g. transitional epithelium of the renal pelvis by renal stones and columnar epithelium of
the gall bladder by gall bladder stones).
c- Adenoma
Adenoma is a benign tumour that arises from glandular tissue. Sometimes adenomas
secrete hormones e.g. parathyroid adenoma and pancreatic insulinoma. Sometimes they
contain large amount of fibrous tissue, hence they are called fibroadenoma e.g. breast
fibroadenoma. Cystic degeneration can occur in an adenoma e.g. pancreatic cystadenoma.
Adenomas arising from glands of mucous membranes are liable to become pedunculated,
e.g. pedunculated colorectal adenomatous polyps.
d- Adenocarcinoma
The malignant counterpart of adenoma is adenocarcinoma. Common sites of
adenocarcinoma are the colon and rectum, breast, endometrium, prostate, and thyroid
gland. The term carcinoma simplex is used when the cells are arranged in circumscribed
groups, with little or no glandular structure being recognizable, while the term colloid or
mucoid carcinoma is used when there is degenerative process developing in tumours
arising from mucin-secreting cells
2. Tumours of connective tissue tumours
Connective tissue tumours are also called soft tissue tumours. They comprise a group of
tumours that arise from supportive tissue of various organs and extraskeletal structures.
They include tumours of fibrous tissue, adipose tissue, skeletal muscles, blood vessels,
lymphatics and peripheral nervous system. The vast majority of soft tissue tumours are
benign, surgical excision of benign tumours is associated with very high cure rate. The
following is a brief note about some common soft tissue tumours:
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A. Lipoma
Lipoma is a slowly growing benign tumour arising from fat cells of adult type. It is the most
common benign tumour.
Classification of Lipoma:
- According to its structure:
- Pure lipoma: contains only fat cells
- Mixed lipoma: contains fat combined with other tissue e.g. fibrolipoma (contains fibrous
tissue), neurolipoma (contains nerve fibers, it is usually painful), haemangiolipoma or
naevolipoma (contains excessive amount of vascular tissue, it looks bluish, is softer than
pure lipoma, may be partially compressible and the overlying skin contains capillary
cutaneous haemangioma)
- According to presence or absence of capsule:
1. Encapsulated lipoma:
A fibrous tissue capsule encapsulates the tumour and sends trabeculae which divide the
tumour into lobules. There is also an outer false capsule formed by the surrounding tissue.
In between the two capsules there is a line of cleavage which facilitates the enucleation of
the tumour.
2. Diffuse lipoma:
It has no capsule. It is usually present in the neck. It is usually symptomless, however it can
be unsightly.
- According to the site:
1. Subcutaneous lipoma:
This is the commonest type of lipoma. It is common in the back, shoulder, buttocks,
forehead and limbs. Clinically it appears as a painless slowly growing swelling which may
attain a large size. It is soft in consistency. Its capsule is attached to the skin and therefore
dimpling of the skin over the tumour will be manifested especially on displacement of the
swelling (lobulation). Also, it has a well defined slippery edge (slips away from the palpating
fingers on pressure). The edge and the lobulation are the pathognomonic signs of
subcutaneous lipoma. It may be sessile or pedunculated and it can be single or multiple.
Dercum’s disease (adiposis dolorosa) is a disease characterized by tender deposits of fat,
especially on the trunk associated with multiple lipomatosis.
2. Subfascial Lipoma:
It lies deep to the deep fascia. It is common at the forehead. It is not attached to the skin
(no dimpling) and lobulation is difficult to be detected.
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3. Submucous Lipoma:
This is lipoma of the mucus membranes. Depending on its site, symptoms may arise
(respiratory obstruction in submucus lipoma of the larynx and intussusception in submucus
lipoma of the intestine).
4. Subperiosteal:
It arises deep to the periosteum of the flat bones (forehead) or long bones (as tibia).
5. Subserous:
Lies beneath visceral or parietal peritoneum, and sometimes beneath the pleura.
Retroperitoneal lipomas may grow to enormous sizes.
6. Subsynovial:
Arises from the fatty padding around joints especially the knee. It may be mistaken for
Baker’s cyst. Differentiated from Baker’s cyst as its consistency is constant whether the joint
is extended or flexed.
7. Inter-muscular and intra-muscular:
It arises between muscles or within the muscle, mainly in the thighs or around the shoulder.
The tumour becomes firmer on muscle contraction.
8. Intraglandular:
Arises inside glands as parotid gland and pancreas
9. Extradural:
It arises inside the spinal canal (never inside the cranium as there is no fat there) and may
result in pressure symptoms.
10. Intra articular
It arises inside the joints
Treatment: Surgical excision is indicated if a lipoma causing
trouble on account of its site, size, appearance or the presence of
pain
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B. Neurofibroma
Neurofibroma arises from the connective tissue of the nerve sheath. It may arise from
cranial or peripheral nerves. It can affect the nerve trunk, nerve branch or nerve endings.
Types of neurofibroma:
1. Solitary neurofibroma:
- It usually arises in subcutaneous tissue, but it can arise from any nerve.
- It appears as a firm, tender, well defined slowly growing swelling, that can be moved
across, but not along, the nerve from which it arises.
- Parasthesia or pain is likely to occur from pressure of the tumour on the nerve fibers.
- Cystic degeneration or sarcomatous changes may occur.
- Symptomatic neurofibromas are treated by excision.
2. Generalized neurofibromatosis (Von Recklinghausen’s disease of
nerves):
- It is inherited (autosomal dominant) disease
- It can affect any cranial, spinal or peripheral nerve
- There are multiple swellings of variable sizes that are present along the
axis of different nerves and in the skin. It may arise in the spinal canal and
cause spinal cord compression. If it arises from an intracranial nerve, it will
increase the intracranial pressure.
- There are cafe-au-lait patches of the skin, especially on the back
- Elephantiasis neuromatosa and plexiform neuroma may be present (see later).
- There are no sensory or motor paralysis.
- Sarcomatous changes may occur in one or more of the neurofibromas. Sarcomatous
change is suspected when there is rapid increase in size, fixity, pain, change in consistency
and overlying skin changes.
3. Acoustic neuroma:
- It affects the eighth cranial nerve.
- It extends into the cerebello-pontine angle, compressing the pons, cerebellum and cranial
nerves. It may cause deafness and increased intracranial tension.
- Surgical intervention aims at total excision with preservation of the neurological function,
which is difficult. Recently “gamma knife” radiosurgery has been used effectively in the
treatment of those tumours with great success
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4. Plexiform neurofibromatosis:
- This is a rare condition that usually affects the branches of the fifth
cranial nerve, but it may also occur in the extremities.
- The affected nerves become enormously thickened as a result of
myxofibromatous degeneration of the endoneurium.
- If it occurs in the face, the overlying skin sometimes hangs down in
pendulous folds (Pachydermatocele).
5. Elephantiasis neuromatosa:
- It is a rare condition, due to diffuse affection of the nerves of the skin and subcutaneous
tissue of the limb.
- The skin becomes coarse, dry and thickened resembling an elephant’s hide with great
thickening of the subcutaneous tissue. If the leg is affected, walking is usually difficult.
C. NEUROMA
True neuromas are rare. They comprise the following types:
- Ganglioneuroma: It consists of ganglion cells and nerve fibers. It arises in connection with
the sympathetic plexus, thus it is commonly found in the neck, thorax or retroperitoneal
tissue. It is treated by excision.
- Myelinic neuroma: It consists of nerve fibres only. It arises in connection with the spinal
cord or pia matter. It is treated by excision.
- Neuroblastoma: It is less differentiated, the cells being of an embryonic type. It occurs in
infants and young children. It is treated by excision with or without chemotherapy
D. NEURILEMMOMA (Schwanoma)
It arises from the neurilemmal sheath cells. It forms a lobulated, encapsulated,
soft swelling that displaces the nerve from which it arises. It is treated by
excision.
E. FIBROMA
True fibromas containing only fibrous tissue is rare. Most fibromas are
combined with other mesodermal tissues such as: muscle “fibromyoma”, fat “fibrolipoma”
and nerve sheaths “neurofibroma”. Treatment is excision.
F. Malignant soft tissue tumours
- Malignant soft tissue tumours are called sarcomas. Fibrosarcoma, liposarcoma,
rhabdomyosarcoma, synovioma are some common types.
- They are rare tumours accounting for less than 1% of the overall human burden of
malignant tumours and they carry a bad prognosis.
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- They differ from carcinomas in the facts that sarcoma usually arises in younger age and
that they disseminate rapidly via blood stream rather than by lymphatics.
- Pain, big size (more than 5 cm), rapid increase in size, position deep to the deep fascia
and recurrence after previous excision suggest that a soft tissue tumour is malignant.
- Because they are very vascular, they can be pulsatile or misdiagnosed as abscess
- MRI (magnetic resonance imaging) is the modality of choice for detecting, characterizing
and staging of soft tissue tumours.
- Biopsy (image guided biopsy in inaccessible tumours, incisional biopsy in big tumours,
excisional biopsy in small tumours) is performed if the clinical diagnosis is not definite.
- Treatment is by wide local excision. Sometimes amputation is needed. Skin flaps or grafts
may be needed for reconstruction. High grade soft tissue sarcomas may need radiotherapy
after excision. Usually chemotherapy has a limited role in the treatment.
G. Desmoid tumour
See chapter of abdominal wall.
3. Tumours of lymphatics (Lymphangioma)
A. Capillary lymphangioma:
- This is a congenital anomaly composed of localized dilatation of the
lymphatics of the skin or mucous membrane.
- It appears as a brown papule or wart-like projection, on which small vesicle
can be seen on examination by a lens (lymphatic naevi).
- Treatment is by surgical excision.
B. Cavernous lymphangioma:
- It is often associated with the preceding type and consists of masses of
lymphatic cysts. Cystic Hygroma
- It usually occurs in the neck or axilla (cystic hygroma).

- It may affect the lips (macrocheilia) or the tongue (macroglossia) producing sometimes
gross soft tissue swelling.
- Treatment is by surgical excision.
C. Lymphangiosarcoma
Lymphangiosarcoma is a highly malignant tumour that arises from lymphatic endothelium. It
can develop in lymphoedematous tissue (e.g. in lymphoedematous arm after modified
radical mastectomy
4. Tumours of blood vessels
A. Haemagioma and vascular malformations: discussed in the chapter of plastic surgery
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B. Glomangioma (Glomus tumour)

- A glomus is a specialized cutaneous arrangement composed of a tortuous
arteriole that communicates directly with a venule, the vessels being surrounded
with a network of small nerves. It regulates skin temperature and it is found in the
limbs especially the nail beds (subungal).
- Glomus tumour is a small, purple, compressible nodule, few millimeters in
diameter that is disproportionately painful in response to insignificant stimuli
(including cold exposure). Subungal varieties may be invisible causing paroxysmal digital
pain.
- They grow slowly, and do not become malignant.
- They are treated by excision.
C. Angiosaroma
- This is a rare, highly malignant tumour of the vascular endothelial cells.
- Proliferation is rapid with early systemic spread.
D. Kaposi’s Sarcoma
- This is a malignant, proliferative tumour of vascular endothelial cells.
- It usually occurs in immunocompromised patients such as after transplantation or patients
with HIV infection.
- It starts as a red-brown, indurated, plaque-like skin lesion that become nodular and
ulcerates.
- Treatment is by surgery and radiotherapy.
ULCERS
An ulcer is defined as discontinuation of an epithelial surface. Ulcer may be traumatic,

malignant, non-specific or caused by specific disease such as TB or syphilis. On doing
clinical examination for an ulcer, the following items have an impact on reaching a proper
diagnosis:
- Site: venous ulcer occur in the gaiter area of the leg, bed sores occur in pressure areas on
bony prominences.
- Size, rate of growth, recent change: a malignant ulcer may grow rapidly or show recent
change such as bleeding, change in shape or itching.
- Shape: Malignant ulcer has irregular shape, gummatous ulcer is usually circular.
- Edge: healing ulcers have sloping edge, malignant ulcers have raised everted edge
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- Margin: The margin is the surrounding area of the ulcer. Tuberculous ulcers have bluish
margin.
- Floor: The floor is that which can be seen by an observer. Malignant ulcers have
necrotic floor, healing ulcers have healthy pink floor of granulation tissue
- Base: The base is what can be palpated under the ulcer. Malignant ulcer has
indurated base.
- Discharge: Purulent discharge indicates infection, watery discharge occurs in
tuberculous ulcers.
- Draining lymph nodes: Hard draining lymph nodes indicate carcinoma.
- Pain: Non-specific and ischemic ulcers are usually painful, specific ulcers are
usually painless except in anal chancre of homosexuals.
- Vascular examination: Arterial examination in ischaemic ulcers and venous examination in
venous ulcers are helpful in the diagnosis.
Sinuses and Fistulae
- A sinus is a blind track connecting an epithelial surface with a cavity
- A fistula is an abnormal communication between two epithelial-lined surfaces.
Sinuses and Fistulae may be congenital or acquired.
1- Congenital:
Examples are pre-auricular sinus, branchial fistula, tracheo-oesophageal fistula
and arteriovenous fistula.
2- Acquired:
Usually follows inadequate drainage of an abscess. Thus, a perianal abscess
may burst on the surface and leads to anal fistula or sinus. Acquired
arteriovenous fistula is caused by trauma or operation for renal dialysis.
Acquired fistula or sinus can heal spontaneously, however this might not occur.
Non-healing of a sinus or fistula may be due to:
- Presence of a foreign body or necrotic tissue such as suture, hairs,
sequestrum.
- Inefficient or nondependent drainage of an abscess.
- Unrelieved obstruction of the lumen of a viscus or tube distal to the fistula.
- Epithelialization of the fistula or sinus track.
- Sinus or fistula caused by specific disease e.g. actinomycosis, cancer, Crohn’s disease.
- Ischaemia.
123
- The use of drugs such as steroids and cytotoxics.

- Malnutrition.
- Irradiation: Irradiated tissues have poor blood supply because of endarteritis obliterans
that is associated with irradiation, e.g. rectovaginal fistula after pelvic irradiation for cervical
cancer.
- High-output fistula, e.g. duodeno-cutaneous fistula.
Investigations and treatment of sinus and fistula:
- Bacteriological and cytological examination of the discharge, sinogram and fistulogram
using water based contrast medium such as gastrographin, C.T, MRI and biopsy can all
help in diagnosis. Treatment is directed towards the cause.
Pilonidal sinus and perianal fistula are presented in the following photos.
Stitch sinus:
This is commonly encountered. It is the result of non-absorbable suture material acting as a
focus to a small infection within the wound. These sinuses are more commonly
encountered after closure of a dirty or potentially contaminated wound than after clean
operations. They tend to persist over many months and produce an inconvenient
seropurulent discharge and pain. The incidence of stitch sinuses is diminished by ensuring
that knots are tied and buried away from the subcutaneous plane. Healing of a persistent
sinus requires the removal of the suture.
124
Part I; Chapter 11 (Abdominal wall & Hernias)
Abdominal Wall and Hernias
Disorders of the Umbilicus

•Umbilical infections: Patients with omphalitis may
present with purulent umbilical discharge or periumbil-
ical cellulitis. Although infections may be associated
with retained umbilical cord or ectopic tissue, infec-
tions are often related to poor hygiene. Pilonidal sinus
of the umbilicus can occur but it is rare.
•Umbilical granuloma: Chronic infection at the um-
bilicus can lead to formation of mass formed of granu-
lation tissue. Small umbilical granulomas usually re-
spond to silver nitrate application. Large umbilical
granulomas or those that persist after silver nitrate
Umbilical polyp
treatment require surgical excision.
•Vitello-intestinal duct remnants: Persistence of
all or portions of the Vitello-intestinal duct can result in umbilical fecal fistula, umbilical
sinus, cysts (Enterocystoma), congenital bands, and mucosal remnants, which become
everted outwards leading to formation of an umbilical polyp.
•Urachal remnants: The developing bladder re-
mains connected to the allantois through the urachus.
Remnants of this connection include a patent urachus,
urachal sinus, and urachal cyst. Umbilical polyps can
also be observed in association with a urachal rem-
nant.
•Umbilical hernia: Umbilical hernias result when
persistence of a patent umbilical ring occurs. Umbilical
hernias may spontaneously close, but many require
surgical repair.
•Tumours: Primary malignant tumours originating in
the umbilicus (Epithelioma) is rare, it is going to spread Umbilical hernia
by lymphatics to both axillary and inguinal lymph
nodes. Secondary malignant nodules can affect the umbilicus due to spread from GIT
carcinoma or from breast cancer (Sister Mary Josef nodules).
Desmoid Tumour
A desmoid tumor (sometimes referred to as aggressive fibromatosis) is a rare (3 per
million population) tumor that may or may not be part of a genetic syndrome such as fa-
milial adenomatous polyposis (FAP). Desmoid tumors are histologically benign fibrous
neoplasms originating from the musculo-aponeurotic structures throughout the body.
The term desmoid, coined by Muller in 1838, is derived from the Greek word desmos,
which means tendon like.
Desmoid tumors often appear as infiltrative, usually well-differentiated, firm over-
growths of fibrous tissue, and they are locally aggressive. The synonym aggressive fi-
bromatosis describes the marked cellularity and aggressive local behavior. This course
and the tendency for recurrence make the treatment of these relatively rare fibrous tu-
mors challenging.
Although desmoid tumors most commonly arise from the rectus abdominis muscle in
postpartum women and in scars due to abdominal surgery, they may arise in any skele-
125
tal muscle. Oral contraceptive use has been associated with the occurrence of this dis-
ease, these associations combined with the detection of estrogen receptors within the
tumour suggests a regulatory role for estrogen in this disease. The tumors tend to infil-
trate adjacent muscle bundles, frequently entrapping them and causing their degenera-
tion. Although fixation to musculoaponeurotic structures is apparent, the overlying skin
is normal. The myofibroblast is the cell considered to be responsible for the develop-
ment of desmoid tumors. Retroperitoneal neoplasms are more common in familial poly-
posis coli and Gardner syndrome after abdominal surgery than in other conditions
Histologically they resemble low-grade fibrosarcomas, but they are very infiltrative and
tend to recur even after complete resection.
MRI is the investigation of choice in these cases providing information regarding the
extent of the disease.
Treatment may consist of watching and waiting, complete surgical removal, radiation
therapy, antiestrogens and NSAIDs, or chemotherapy.
Rectus Sheath Hematoma

Abdominal wall trauma blunt or iatrogenic (careless surgical hemostasis) following ab-
dominal (open or laparoscopic) operations injuring the superior or inferior epigastric ves-
sels leading to formation of a painful tender swelling over the rectus muscle with overly-
ing skin ecchymosis. Treated by surgical evacuation of the hematoma and ligation of the
injured vessel.
Abdominal Wall Wound Disruption (Burst Abdomen)

Serious complication which may be fatal or may lead to the formation of incisional her-
nia. It may be due to presence of one or more of the following predisposing factors:
Preoperative:
• Poor healing power (malnutrition, diabetes, liver cirrhosis & corticosteroid therapy).
• Obesity.
• Chest problems (chronic obstructive pulmonary diseases).
• Nature of the primary disease for which the operation was performed as in cases of
peritonitis, neglected intestinal obstruction& abdominal wall malignancy.
Operative:
• Vertical more than transverse incisions.
• Muscle cutting more than muscle splitting incisions.
• Clumsy surgical technique with damage to muscles, vessels& nerves.
• Closure of the abdominal wall using absorbable sutures. It’s recommended to take
good bites on either sides of the abdominal wall using nonabsorbable sutures as pro-
lene.
• Insertion of foreign bodies like tube drains in the main wound.
Post-operative:
• Vigorous coughing due to bad recovery from anesthesia.
• Increased intra-abdominal pressure due to coughing, vomiting or hiccough.
• Abdominal distension due to prolonged paralytic ileus.
• Wound hematoma.
• Wound infection.
Burst abdomen usually occurs on the fifth to the eighth postoperative day it may be
partial when the deep layers burst but the skin remains intact or it may be complete rup-
ture. If the intestine prolapses out of the wound it is called evisceration but if it is retained
inside it is called dehiscence. A warning sign to the occurrence of burst is (the red sign)
where a serosanguinous discharge soaks the dressing.
126
Treatment:
1. Cover prolapsed bowel by a sterile dressing.
2. Insert nasogastric tube and start IV fluids& antibiotics.
3. Under general anesthesia the protruding loops are washed with saline and returned
to the abdominal cavity, spread the omentum over the intestine and close the ab-
dominal wall as one layer by through and through nonabsorbable sutures.
4. Abdominal binder support is helpful.
Incisional Hernia
About 10% of abdominal operations results in Incisional hernias. The incidence of this
iatrogenic type of hernia is not diminishing in spite of an awareness of the many causa-
tive factors, if more than one of the following factors coexist in the same patient, the like-
lihood of postoperative Incisional hernia is maximized.
1. Poor surgical technique.
2. Postoperative wound infection.
3. Old age patients.
4. General debility.
5. Obesity.
6. Postoperative pulmonary complications.
7. Placement of drains or stomas in the main wound.
8. Intra operative blood loss more than 1000ml.
9. Failure to close the fascia of laparoscopic trocar site over 10 mm size.
Incisional hernia may involve only a portion of the scar or there may be a diffuse bulge
of the whole length of the incision. The hernia will increase steadily and the surrounding
muscles will be pushed apart. Attacks of irreducibility or strangulation may occur if the
neck of the hernia is small.
Treatment: Small Incisional hernia should be treated by early anatomical repair since it
may cause bowel obstruction. Large hernia should be repaired by the use of tension free
mesh repair. In poor surgical risk patients symptoms may be controlled by an elastic ab-
dominal binder.
External Abdominal Hernia
Definition: It is protrusion of a viscus or part of a viscus within a peritoneal sac through a

defect in the abdominal wall at certain anatomical sites, Abdominal wall hernias occur on-
ly at sites where the aponeurosis and fascia are not covered by striated muscle, some
are common like inguinal,& umbilical, others are less common like femoral hernia and
some are rare types like lumbar, obturator & spigelian hernias.
Causes:
1. Congenital preformed sac: like unobliterated processus vaginalis leading to congeni-
tal inguinal hernia and unobliteration of the umbilical ring leading to congenital umbil-
ical hernia.
2. Acquired causes: like diseases causing increased intra abdominal pressure or caus-
ing weakness of the abdominal wall.
Structure:
Any hernia consists of three components these are; sac, coverings and contents.
1. Sac: It is the peritoneal pouch bulging out through the abdominal wall defect. It is
formed of a neck (its junction with the peritoneum), body and fundus.
2. Coverings: these are the different anatomical structures stretched over and cover-
ing the sac.
3. Contents: like the intestine, the omentum. Any abdominal viscus can come out in-
side the sac except the pancreas. Some hernias may contain special contents and
127
acquiring special names like Richter’s her-

nia containing part of the circumference of
the intestine, Littre’s hernia containing
Meckel’s diverticulum, Maydl’s hernia con-
taining two loops of the intestine while the
intermediate loop lies inside the peritoneal
cavity forming the shape of W that is why it
may be called hernia in W.
Diagnosis:
The hernia is diagnosed by the presence of a
swelling at one of the known anatomical sites of
hernia (inguinal, umbilical, epigastric, femo-
ral…), the swelling gives expansile impulse on
cough and is reducible. You may need to do
special tests like the internal ring test to know
the exact type of the hernia. A hernia containing
omentum feels like a doughy sensation while a
hernia containing intestine gives the characteris-
tic gurgling sound during reduction. Then you
have to assess if there is any complication of
this hernia and if there is any cause for in- Types of abdominal wall hernias
creased intra abdominal pressure or weak ab-
dominal wall in order to be considered during
treatment.
Treatment:
Early operation should be advised to avoid the occurrence of the hazardous complica-
tions of the hernia like strangulation, the use of truss should be avoided and it should be
kept only for patients unfit for surgery.
* Complications of Hernia:
1. Irreducibility: Failure to return the contents into the abdomen which may be due to
formation of adhesions within the sac or due to protrusion of more omentum within
the sac. Irreducibility predisposes to obstruction and strangulation that is why early
operative treatment is a must.
2. Obstruction (Incarceration): Occlusion of the intestinal lumen from without or from
within without affection of its blood supply, this may lead to symptoms of intestinal ob-
struction as vomiting, colics, abdominal distension and constipation. Locally the her-
nia becomes distended, irreducible but is still soft. Distinction between obstruction
and strangulation is difficult and is not advisable, it’s much safer to diagnose the case
as strangulation and immediate surgery should be performed.
3. Inflammation: Following the use of badly fitted truss, or if the hernia sac contains an
inflamed organ( appendix, Fallopian tube, Meckel’s diverticulum) The hernia is going
to be painful, tender with redness and edema of the overlying skin. Early operation is
essential as strangulation cannot be excluded.
4. Rupture: Due to external trauma as rough taxis.
5. Hydrocele of Hernial sac: This occurs when the contents return back inside the ab-
domen and then fail to reenter the sac due to narrowing of its neck. Serous fluid is
going to collect in the sac forming a cystic swelling.
6. Strangulation: The most serious complication, it occurs due to constriction of the
contents together with interruption of their blood supply, ending in intestinal gangrene
within 4-6 hours that may end the patient’s life.
 Incidence: It can occur at any age and it varies according to the type of the hernia
128
so we can find that it occurs in 25-30% of cases of femoral hernia, 15-20% of cases
of paraumbilical hernia and 3-5% of cases of inguinal hernia.
 Causes: Extrusion of new contents following straining or it may follow repeated at-
tempts at reduction producing edema. The constricting agent may be the neck of
the sac, bands of adhesions within the sac or an anatomical narrow structure out-
side the sac like the internal or the external inguinal ring or the sharp edge of the
Lacunar ligament.
 Pathology: At the site of the constriction ring direct traumatic gangrene in the wall
of the intestine may occur. The intestine proximal to the strangulated loop will be
obstructed with progressive distension and hyperperistalsis. The intestine distal to
the strangulated loop will be collapsed. The strangulated loop will undergo the fol-
lowing sequelae:
a. Venous obstruction: The veins will be occluded first leading to congestion of
the strangulated loop and distension with accumulating fluid and gases. Persis-
tent venous congestion leads to hemorrhage in the wall of the intestine, into its
lumen and outside its surface inside the hernia sac.
b. Arterial obstruction: Leading to devitalization of the wall of the strangulated
loop of intestine permitting the passage of its contents (fluid, blood& bacteria) to
the peritoneal sac which thus contain dark highly toxic fluid.
c. Gangrene: It usually starts at the site of constriction, then it affects the an-
timesenteric border of the strangulated loop and then the whole loop and its
mesentery become gangrenous and perforation of the loop may occur.
d. Peritonitis: Neglected cases will end in peritonitis and septic shock from spread
of the infection from the sac to the general peritoneal cavity with fatal outcome.
 Clinical picture:
1- General: The patient will present with the picture of acute intestinal obstruction
with colicky abdominal pains, vomiting distension, and absolute constipation, the
patient will be dehydrated and has the picture of hypovolemic shock. With the on-
set of gangrene and peritonitis in neglected cases the patient will have the picture
of septic shock and will develop paralytic ileus with disappearance of the colics.
2-Local: The fixed symptom is persistent pain at the site of the hernia, the patient
may also notice that the hernia became larger in size and that he cannot reduce it.
On examination the hernia is Tense, Tender, Irreducible, Impulse on cough is neg-
ative and there may be congestion and edema of the overlying skin.
 Treatment: Should be done by urgent surgery after proper preparation of the pa-
Strangulated hernia with gangrenous loop of small intestine
129
tient. Taxis (manual reduction of the strangulated hernia) should be avoided as it

may lead to serious complications.
Preoperative preparation should include sedatives, Ryle’s tube suction, IV fluids,
correction of electrolytes imbalance and IV broad spectrum antibiotics.
Principles of surgery for strangulated hernia:

1. Use generous incision planned to expose fundus of the sac first.
2. Make an opening in the fundus of the sac and evacuate (by the use of suction)
the toxic fluid inside.
3. Then divide the constriction ring to relief the strangulation.
4. The contents are pulled out and examined.
5. Deal with the contents as follows:
• Viable intestine is returned to the abdomen.
• The omentum should be excised.
• Gangrenous small intestine is treated by primary resection anastomosis.
• Gangrenous right side of the colon is treated by primary resection and anasto-
mosis.
• Gangrenous left colon is treated by exteriorization resection ( Paul-Mickulicz
double barrel colostomy).
• In case of a suspicious loop of intestine warm packs are applied and patient is
given pure oxygen for few minutes and reexamine the loop of intestine for its
viability and deal accordingly
6. Repair the hernia defect using nonabsorbable sutures like prolene.
Sliding Hernia
This is a type of hernia where a viscus or part of a viscus (urinary bladder, caecum,
sigmoid colon...) forms part of the wall of the sac. Usually the clinical picture is that of
an obese old male patient with long standing inguinal hernia. Typically after reduction of
the contents there is still residual swelling at the site of the hernia, and the patient may
have some urinary symptoms in cases of sliding bladder. During surgical treatment of
the hernia if you discover it to be sliding do not try to dissect the sliding viscus to pre-
vent its injury or devascularization. Free the sliding sac and viscus from the surrounding
structure and then push them back behind fascia transversalis by multiple inverting su-
tures (Bevan technique), and perform proper tension free repair using mesh repair.
130
Inguinal Hernias
Anatomy of the Groin

The surgeon must have a
comprehensive understanding of
the anatomy of the groin to
properly select and utilize vari-
ous options for hernia repair. In
addition, the relationships of
muscles, aponeuroses, fascia,
nerves, blood vessels, and
spermatic cord structures in the
inguinal region must be mas-
tered to obtain the lowest inci-
dence of recurrence and to
avoid complications. These ana-
tomic considerations must be
understood from both the anteri- or
and posterior approaches be-
cause both approaches are use-
ful in different situations.
From anterior to posterior, the Nyhus's classic parasagittal diagram of the right
groin anatomy includes the skin midinguinal region illustrating the muscular apo-
and subcutaneous tissues, be- neurotic layers separated into anterior and posteri-
low which are the superficial cir- or walls. The posterior laminae of the transversalis
cumflex iliac, superficial epigas- fascia have been added, with the inferior epigastric
tric, and external pudendal ar- vessels coursing through the abdominal wall medi-
teries and accompanying veins. ally to the inner inguinal canal.
These vessels arise from and
drain to the proximal femoral
artery and vein, respectively,
and are directed superiorly. If
encountered during operation,
these vessels can be retracted
or even divided when necessary
External Oblique Muscle and

Aponeurosis
The external oblique muscle
fibers are directed inferiorly and
medially and lie deep to the sub-
cutaneous tissues. The aponeu-
rosis of the external oblique
muscle is formed by a superficial
and deep layer. This aponeuro-
sis, along with the bilaminar ap- Anatomy of the important preperitoneal structures
oneuroses of the internal in the right inguinal space.
oblique and transversus abdomi-
nis, forms the anterior rectus
sheath and, finally, the linea alba by linear decussation. The external oblique aponeuro-
sis serves as the superficial boundary of the inguinal canal. The inguinal ligament
131
(Poupart's ligament) is the inferior

edge of the external oblique apo-
neurosis and extends from the an-
terior superior iliac spine to the pu-
bic tubercle, turning posteriorly to
form a shelving edge. The lacunar
ligament is formed by the insertion
of the inguinal ligament to the pu-
bis. The lacunar ligament forms the
medial border of the femoral
space. The external (superficial)
inguinal ring is an ovoid opening of
the external oblique aponeurosis
that is positioned superior and
slightly lateral to the pubic tubercle.
The spermatic cord exits the ingui-
nal canal through the external in-
guinal ring.
Internal Oblique Muscle and
Aponeurosis inguinal ligament
The internal oblique muscle fi-
bers are directed superiorly and medialy in the upper abdomen; however, they run in a
transverse direction in the inguinal region. The internal oblique muscle serves as the
cephalad (or superior) border of the inguinal canal. The medial aspect of the internal
oblique aponeurosis fuses with fibers from the transversus abdominis aponeurosis to
form a conjoint tendon inserted in the pubic tubercle. The cremasteric muscle fibers arise
from the internal oblique and encompass the spermatic cord. These muscle fibers are
essential to the cremasteric reflex but have little relevance to hernia repairs.
Transversus Abdominis Muscle and Aponeurosis and Transversalis Fascia

The transversus abdominis muscle layer is oriented transversely throughout most of its
area; in the inguinal region, these fibers course in a slightly oblique downward direction.
The strength and continuity of this muscle and aponeurosis are important for the preven-
tion of inguinal hernia.
The aponeurosis of the transversus abdominis covers both anterior and posterior sur-
faces. The lower margin of the transversus abdominis arches along with the internal
oblique muscle over the internal inguinal ring to form the transversus abdominis aponeu-
rotic arch. The transversalis fascia is the connective tissue layer that underlies the anteri-
or abdominal wall musculature. The transversalis fascia, sometimes referred to as the
endoabdominal fascia, is a component of the inguinal floor. It tends to be more dense in
this area but still remains relatively thin.
The iliopubic tract is a continuation of the transverse abdominis aponeurosis and fascia
at the upper border of the femoral sheath. The iliopubic tract also forms the inferior crus
of the deep inguinal ring. The superior crus of the deep ring is formed by the transversus
abdominis aponeurotic arch. The iliopubic tract is located posterior to the inguinal liga-
ment, and it crosses over the femoral vessels and inserts on the anterior superior iliac
spine and inner lip of the wing of the ilium.
Cooper's Ligament
Cooper's ligament is formed by the periosteum and fascia along the superior ramus of
the pubis. This structure is posterior to the iliopubic tract and forms the posterior border
of the femoral canal.
132
Inguinal Canal
The inguinal canal is about 4 cm in length and is located 2 to 4 cm cephalad to the in-
guinal ligament. The canal extends obliquely between the internal (deep) inguinal ring
(opening in fascia transversalis ½ inch above the midpoint of inguinal ligament ) and ex-
ternal (superficial) inguinal ring ( triangular opening in the external oblique aponeurosis
½ inch above and medial to the pubic tubercle). The inguinal canal contains the spermat-
ic cord or the round ligament of the uterus.
The spermatic cord is covered by internal spermatic fascia, cremasteric muscle fibers
( supplied by the genital branch of the genitofemoral nerve),and external spermatic fas-
cia.The cord is composed of the testicular artery and accompanying veins, , the vas def-
erens, artery of the vas, the cremasteric vessels, the lymphatics, and the remnants of
processus vaginalis. The cremaster muscle arises from the lowermost fibers of the inter-
nal oblique muscle and encompasses the spermatic cord in the inguinal canal. The cre-
masteric vessels are branches of the inferior epigastric vessels. These vessels supply
the cremaster muscle and can be divided to expose the floor of the inguinal canal during
hernia repair without damaging the testis.
The inguinal canal is bounded superficially by the external oblique aponeurosis. The
internal oblique and transversus abdominis musculoaponeurosis form the cephalad wall
of the inguinal canal. The inferior wall of the inguinal canal is formed by the inguinal liga-
ment and lacunar ligament. The posterior wall or floor of the inguinal canal is formed by
the transversalis fascia and the aponeurosis of the transversus abdominis muscle.
Hesselbach's triangle refers to the margins of the floor of the inguinal canal. The inferi-
or epigastric vessels serve as its superolateral border, the rectus sheath at the lateral
border of rectus abdominis muscle as medial border, and the inguinal ligament as the
inferior border. Direct hernias occur within Hesselbach's triangle, whereas indirect ingui-
nal hernias arise lateral to the triangle. It is not uncommon, however, for medium and
large indirect inguinal hernias to involve the floor of the inguinal canal as they enlarge.
The iliohypogastric and ilioinguinal nerves and the genital branch of the genitofemoral
nerve are the important nerves in the groin area.The iliohypogastric and ilioinguinal
nerves provide sensation to the skin of the groin, the base of the penis, and the ipsilat-
eral upper medial thigh.
Diagnosis
A bulge in the inguinal region re-
mains the main diagnostic finding in
most groin hernias. Typically it in-
creases with straining and can be
reduced back to the abdomen.
There may be associated pain or
vague discomfort in the region, but
groin hernias are usually not ex-
tremely painful unless incarceration or
strangulation has occurred. In the
absence of physical findings, alter-
native causes for pain need to be
entertained. Occasionally, patients
may experience parasthesias relat-
ed to compression or irritation of
the inguinal nerves by the hernia.
The inguinal region is examined
with the patient in both supine and
133
standing positions. The examiner visually inspects and palpates the inguinal region, ob-
serving for asymmetry, bulges, or a mass. Having the patient cough or perform a Valsal-
va maneuver can facilitate identification of a hernia. A bulge identified below the inguinal
ligament is consistent with a femoral hernia.
Ultrasonography also can aid in the diagnosis. There is a high degree of sensitivity and
specificity for ultrasound in the detection of occult direct, indirect, and femoral hernias.
Other imaging modalities are less useful. Computed tomography (CT) of the abdomen
and pelvis may be useful for the diagnosis of obscure and unusual hernias as well as
atypical groin masses. Occasionally, laparoscopy can be both diagnostic and therapeutic
for particularly challenging cases.
Oblique (Indirect) Inguinal Hernia
Anatomy:
• The hernia defect is the stretched deep inguinal ring.
• The neck of hernia sac is found lateral to the inferior epigastric vessels.
• The hernia sac passes through the deep ring and lies inside the cord anterolateral to
the vas and vessels. It passes out through the external inguinal ring and may reach
down to the scrotum.
• The contents are usually small intestine, omentum or both.
• The coverings of the sac in the inguinal canal include the skin, subcutaneous tissue
formed of superficial fatty layer and deep membranous layer (Scarpas fascia), exter-
nal oblique aponeurosis, cremasteric muscle and fascia and the internal spermatic
fascia.
• The coverings in the scrotum include the skin, subcutaneous tissue formed of the
Dartos muscle, then all the three cord coverings the external spermatic fascia, cre-
masteric muscle and fascia and internal spermatic fascia.
Anatomical Types:
1. Congenital: Due to the persistence of the whole processus vaginalis, the testis lies
within the contents of the sac. If it occurs in an adult the hernia reaches down to the
bottom of the scrotum the first time it appears.
2. Adult hernia: May present by one of the following :
• Bubonocele: A small hernia sac is found inside the inguinal canal.
• Funicular hernia: The hernia sac passes out through the external inguinal ring and
reaches down to the neck of scrotum. The testis can be felt below the sac.
• Scrotal: Complete descent of the hernia down to the bottom of the scrotum. The
testis is separate from the sac and behind it
Clinical Picture:
• Usually the patient presents by an oblong shaped swelling that gives expansile im-
pulse on cough at the inguinal region (bubonocele), it may grow downwards to de-
scend inside the scrotum (inguino-scrotal), scrotal neck test can be done to differenti-
ate between the two types, in case of inguino- scrotal hernia you can feel the swelling
by holding the neck of the scrotum.
• The swelling is found above and medial to the pubic tubercle while femoral hernia is
found below and lateral to the pubic tubercle.
• Reduce the hernia (direction of reduction is upwards, backwards and laterally) then
ask the patient to strain you can see that the direction of descent of the hernia is
downwards, forwards and medially.
• Internal ring test is done to differentiate between oblique and direct inguinal hernia,
it’s done as follows:
a. The hernia swelling is reduced back by asking the patient to lie on his back and
relax his abdominal muscles, then push gently the swelling up and laterally,
make sure that the hernia is completely reduced.
b. The deep inguinal ring site is located (1/2 inch above the midpoint of inguinal lig-
134
ament) and occluded by your thumb.

c. Help the patient to stand up and ask him to cough, direct inguinal hernia will
bulge out in spite of the occlusion of the internal ring while oblique hernia will ap-
pear only after release of your thumb.
Direct Inguinal Hernia

• In general, direct inguinal hernia produces fewer symptoms than indirect hernia and
is less likely to become incarcerated or strangulated.
• The hernia defect is the stretched Hesselbach’s triangle.
• The neck of hernia sac is medial to inferior epigastric vessels.
• The hernia appears like symmetric circular swelling at the external ring.
• More common in older age group with weak abdominal muscles seen as positive
Malgaigne bulging.
• It may be bilateral.
• It gives expansile impulse on cough.
• It descends directly forwards
• Direction of reduction is directly backwards.
• The coverings of the peritoneal sac are: skin, subcutaneous fascia, scarpas fascia,
external spermatic fascia, stretched conjoint tendon and fascia transversalis.
• Internal ring test is negative.
Differentiating between direct and indirect inguinal hernias is of little importance since
most groin hernias should be repaired regardless of type.
Operative Repair
There are some technical aspects of operation common to all anterior repairs. Open
hernia repair is begun by making a transversely oriented linear or slightly curvilinear inci-
sion 2 to 3 cm above and parallel to the inguinal ligament. Dissection is continued
through the subcutaneous tissues and Scarpa's fascia. The external oblique fascia and
external inguinal ring are identified. The external oblique fascia is incised through the su-
perficial inguinal ring to expose the inguinal canal. The ilioinguinal and iliohypogastric
nerves are identified and mobilized to avoid transection and entrapment. The spermatic
cord is mobilized at the pubic tubercle by a combination of blunt and sharp dissection.
Improper mobilization of the spermatic cord too lateral to the pubic tubercle can cause
confusion in the identification of tissue planes and essential structures and may result in
disruption of the floor of the inguinal canal.
The cremasteric muscle of the mobilized spermatic cord is separated parallel to its fi-
bers from the underlying cord structures. The cremasteric artery and vein, which join the
cremaster muscle near the inguinal ring, are usually cauterized or ligated and divided.
When an indirect hernia is present, the hernia sac is located deep to the cremaster mus-
cle and anterior and superior to the spermatic cord structures. Incising the cremaster
muscle in a longitudinal direction and dividing it circumferentially near the internal ingui-
nal ring help expose the indirect hernia sac. The hernia sac is carefully dissected from
adjacent cord structures and dissected to the level of the internal inguinal ring. The sac
is opened and examined for visceral contents if it is large; however, this step is unneces-
sary in small hernias. The sac can be mobilized and placed within the preperitoneal
space, or the neck of the sac can be ligated at the level of the internal ring, and any ex-
cess sac excised. If a large hernia sac is present, it can be divided using the electrocau-
tery to facilitate ligation. It is not necessary to excise the distal portion of the sac. If the
sac is broad based, it may be easier to displace it into the peritoneal cavity rather than to
ligate it. Direct hernia sacs protrude through the floor of the inguinal canal and can be
reduced below the transversalis fascia before repair. A lipoma of the cord represents ret-
roperitoneal fat that has herniated through the deep inguinal ring and needs to be suture
135
ligated and removed.
Tissue Repairs
Although tissue repairs have largely been abandoned because of unacceptably high
recurrence rates, they remain useful in certain situations. In strangulated hernias where
bowel resection is necessary, mesh prostheses are contraindicated, and a tissue repair
is necessary. Available options for tissue repair include iliopubic tract, Shouldice, and
Bassini repairs.
The iliopubic tract repair approximates the transversus abdominis aponeurotic arch to
the iliopubic tract with the use of interrupted sutures.The repair begins at the pubic tuber-
cle and extends laterally past the internal inguinal ring. This repair was initially described
using a relaxing incision (see later); however, many surgeons who use this repair do not
perform a relaxing incision.
The Shouldice repair emphasizes a multilayer imbricated repair of the posterior wall of
the inguinal canal with a continuous running suture technique. After completion of the
dissection, the posterior wall of the inguinal canal is reconstructed by superimposing run-
ning suture lines progressing from deep to more superficial layers. The initial suture line
secures the transversus abdominis aponeurotic arch to the iliopubic tract. Next, the inter-
nal oblique and transversus abdominis muscles and aponeuroses are sutured to the in-
guinal ligament. The Shouldice repair is associated with a very low recurrence rate and a
high degree of patient satisfaction in highly selected patients.
The Bassini repair is performed by suturing the transversus abdominis and internal
oblique musculoaponeurotic arches or conjoint tendon to the inguinal ligament. This
technique was the most popular type of repair done before the advent of tension-free re-
pairs.
Tension-Free Inguinal Hernia Repair
The tension-free repair has become the dominant method of inguinal hernia repair
Recognizing that tension in a repair is the principal cause of recurrence, current practic-
es in hernia management employ synthetic mesh prosthesis to bridge the defect, a con-
cept first popularized by Lichtenstein. There are several options for placement of mesh
during anterior inguinal herniorrhaphy, including the Lichtenstein approach, the plug-and-
patch technique, or the sandwich technique with both an anterior and preperitoneal piece
of mesh.
In the Lichtenstein repair, a piece of prosthetic nonabsorbable mesh is fashioned to fit

the canal. A slit is cut into the distal, lateral edge of the mesh to accommodate the sper-
matic cord. There are various preformed, commercially available prostheses available for
use. Monofilament, nonabsorbable suture is used in a continuous fashion beginning at
the pubic tubercle and running a length of suture in both directions toward the superior
aspect above the internal inguinal ring to the level of the tails of the mesh. The mesh is
sutured to the aponeurotic tissue overlying the pubic bone medially, continuing superiorly
along the transversus abdominis or conjoined tendon. The inferolateral edge of the mesh
is sutured to the iliopubic tract or the shelving edge of the inguinal (Poupart's) ligament to
a point lateral to the internal inguinal ring. At this point, the tails created by the slit are
sutured together around the spermatic cord, snugly forming a new internal inguinal ring.
The ilioinguinal nerve and genital branch of the genitofemoral nerve are placed with the
cord structures and are passed through this newly fashioned internal inguinal ring.
The tension-free mesh repair has been modified from the original Lichtenstein repair.
136
surgeons, many secure both plug and patch with several monofilament nonabsorbable
sutures, especially for very weak inguinal floors or large defects.
The sandwich technique involves a bilayered device with three polypropylene compo-
nents. An underlay circular patch provides a posterior repair similar to the laparoscopic
approach, a connector functions similar to a plug, and an onlay patch covers the posteri-
or inguinal floor. This repair has been deemed the Prolene Hernia System (PHS). The
use of interrupted fixating sutures is not mandatory, but most surgeons place three or
four fixation sutures in this repair.
PHS (prolene hernia

system)
Recurrent Hernia
The repair of recurrent inguinal hernias is challenging, and results are associated with
a higher incidence of secondary recurrence. Recurrent hernias almost always require
placement of prosthetic mesh for successful repair. Recurrences after anterior hernia re-
pair using mesh are best managed by either a laparoscopic or open posterior approach
with placement of a second prosthesis.
Bilateral Hernias
The approach to repair of bilateral inguinal hernias is based on the extent of the hernia
defect. Simultaneous repair of bilateral hernias has traditionally been associated with a
recurrence rate approximately twice that of unilateral repair. The use of a giant prosthetic
reinforcement of the visceral sac (Stoppa repair), or the laparoscopic repair is appropri-
ate for simultaneous repair of bilateral inguinal hernias, although bilateral anterior repair
through separate incisions can be used.
137
FEMORAL HERNIA
Femoral Canal
This canal is found in the medial compart-

ment of the femoral sheeth it begins at the
femoral ring and reaches down till the saphe-
nous opening. The boundaries of the femoral
ring are the iliopubic tract and inguinal liga-
ment (Poupart’s ligament) anteriorly,
Cooper's ligament (iliopectineal) posteriorly,
Lacunar (Gimbernt’s ligament) medially and
the femoral vein laterally. The femoral ring is
filled with a pad of fat called the femoral plug.
A femoral hernia occurs through this space
and is medial to the femoral vessels
Femoral ring
A. Femoral ring as seen from inside the pelvis..B abnormal ob-

turator arterycrossing the lacunar lig.
Abnormal obturator artery: Normaly there is anastomosis between the pubic branch of
the inferior epigastric artery and the pubic branch of the obturator artery in cases of con-
genitally abscent obturator artery the pubic branch of the inferior epigastric artery be-
comes enlarged to replace the missed obturator artery and it’s called abnormal obturator
artery, it crosses over the lacunar ligament in order to reach the medial side of the
thigh.It may be injuried during cutting the lacunar ligament during surgical treatment of
strangulated femoral hernia.
A femoral hernia is more common in females it occurs through the femoral canal, it
produces a mass or bulge below the inguinal ligament. After coming out through the sa-
phenous opening it cannot grow in downward direction because of the attachment of
Scarpas Fascia to the Fascia Lata 4 cm below the inguinal ligament.On occasion, some
femoral hernias will present over the inguinal canal. In this situation, the femoral hernia
sac still exits inferior to the inguinal ligament through the femoral canal but ascends in a
138
Femoral hernias.
cephalad direction.The differentiation point between inguinal and femoral hernia is the
relation to the pubic tubercle, Femoral hernia is found below and lateral to the pubic tu-
bercle while inguinal hernia is found above and medial to it.
The coverings of the peritoneal sac of femoral hernia are the stretched femoral plug
layer, fascia transversalis, cribriform fascia, scarpas fascia, subcutaneous fat and skin.
A femoral hernia can be repaired using the standard Cooper's ligament repair, a
preperitoneal approach, or a laparoscopic approach. The essential elements of femoral
hernia repair include dissection and reduction of the hernia sac and obliteration of the
defect in the femoral canal, either by approximation of the iliopubic tract to Cooper's liga-
ment or by placement of prosthetic mesh to obliterate the defect. The incidence of stran-
gulation in femoral hernias is high; therefore, all femoral hernias should be repaired, and
incarcerated femoral hernias have the hernia sac contents examined for viability. In cas-
es of compromised bowel, the Cooper's ligament approach is the preferred technique
because mesh is contraindicated. When the incarcerated contents of a femoral hernia
cannot be reduced, dividing the lacunar ligament can be helpful.
Umbilical Hernia in Adults

Umbilical hernia in adults occur long after closure of the umbilical ring, it’s more com-
mon in women and is due to gradual yielding of the cicatricial tissue closing the umbilical
ring, or just around the ring (paraumbilical hernia) usually in the midline. Predisposing
factors include: Multiple pregnancies, obesity, ascites and large intra abdominal tumours.
The hernia sac may have multiple loculations due to formation of multiple fibrous tissue
adhesions at its fundus, umbilical hernia usually contain omentum but small and large
intestine may be present. The neck of the hernia is usually narrow compared to the size
of the herniated mass and incarceration and strangulation are common.
Treatment: Early surgical treatment is essential as strangulation is common, tension
free repair or mesh repair should be done.
Epigastric Hernia
An epigastric hernia protrudes through the linea alba between the xiphoid process and
umbilicus and are usually within 5 to 6 cm of the umbilicus. The hernia may develop
through an area of congenital weakness in the linea alba or through one of the foramina
of egression of the small para-midline nerves and vessels.. It’s estimated that about 3-
5% of the population have epigastric hernia and it affects young &middle aged men three
times more than in women. They are multiple in up to 20% of patients, and about 80%
139
are just off the midline. It usually starts by protru-

sion of the extraperitoneal fat without peritoneal
sac (fatty hernia of linea alba), it presents by
painless soft mass usually discovered accidental-
ly, irreducible and it gives no expansile impulse on
cough. In some cases it may produce pain out of
proportion to its size owing to incarceration of
preperitoneal fat. Repair usually consists of exci-
sion of the incarcerated preperitoneal tissue and
simple closure of the fascial defect.
Uncommonly, these defects can be sizable it’s

going to pull on the underneath peritoneum acquir-
ing a peritoneal sac (gives expansile impulse on
cough) and my further pull on the intra-abdominal
organs like the omentum, the stomach or the small
intestine. If symptomatic their presentation ranges
from mild epigastric pain and tenderness to deep Epigastric hernia site (midline above
burning epigastric pain with radiation to the back. and away from the umbilicus)
The pain may be accompanied by bloating, nausea
or vomiting. The symptoms often occur after a large
meal and may be relieved by reclining.
Epigastric hernias are better repaired because
the defect is small and fat that has herniated from
within the peritoneal cavity is difficult to reduce and
may be strangulated, in small defects anatomical
repair is enough while sizable defects require
mesh repairs.
Diastasis Recti
This condition is also known as Divarication of
recti occurs due to diffuse widening and attenua-
tion of the linea alba without a fascial defect. On large umbilical hernia
examination it appears as a fusiform linear bulge
between the two rectus abdominis muscles without
a discrete fascial defect. There is no risk of incar-
ceration, anatomical repair or mesh repair could be
done.
UNUSUAL HERNIAS
Spigelian Hernia
A spigelian hernia occurs through the spigelian
fascia, which is composed of the aponeurotic layer
between the rectus muscle medially and the semi-
lunar line laterally. Nearly all spigelian hernias oc-
cur at or below the arcuate line. The absence of
posterior rectus fascia may contribute to an inher-
ent weakness in this area. These hernias are often
interparietal, with the hernia sac dissecting posteri-
or to the external oblique aponeurosis. Most
spigelian hernias are small (1-2 cm in diameter) Huge strangulated umbilical hernia
and develop during the fourth to seventh decades
140
of life. Patients often present with localized pain in the area without a bulge because the
hernia lies beneath the intact external oblique aponeurosis. Ultrasound or CT of the ab-
domen can be useful to establish the diagnosis.
A spigelian hernia is repaired because of the risk for incarceration associated with its
relatively narrow neck. The hernia site is marked before operation. A transverse incision
is made over the defect and carried through the external oblique aponeurosis. The her-
nia sac is opened and dissected free of the neck of the hernia and either excised or in-
verted. The defect is closed transversely by simple suture repair of the transversus ab-
dominis and internal oblique muscles, followed by closure of the external oblique apo-
neurosis. Larger defects are repaired using mesh prosthesis. Recurrence is uncommon.
Obturator Hernia
The obturator canal is formed by the union of the pubic bone and ischium. This canal is
covered by a membrane pierced by the obturator nerve and vessels. Weakening of the
obturator membrane may result in enlargement of the canal and formation of a hernia
sac, which can lead to intestinal incarceration and strangulation. The patient can present
with evidence of compression of the obturator nerve, which causes pain in the medial
aspect of the thigh that increases on doing extension and adduction or medial rotation of
the hip. (Howship-Romberg sign),abscent adductor reflex in the thigh(Hannington-Kiff
sign) may be positive. Nearly one half of patients with obturator hernia present with
complete or partial bowel obstruction. Bedside ultrasonography can visualize the hernia
and pelvic CT will establish the diagnosis if necessary.
A posterior approach, either open or laparoscopic, is preferred. This approach provides
direct access to the hernia. Patients with compromised bowel should have a preperitone-
al open repair. After reduction of the hernia sac and contents, any preperitoneal fat within
the obturator canal is reduced. The obturator nerve can be manipulated gently with a
blunt nerve hook to facilitate reduction of the fat pad. The obturator foramen is repaired
with sutures or a small piece of prosthetic mesh, with care to avoid injury to the obturator
nerve and vessels.
Lumbar Hernia
Lumbar hernias can be either congenital or acquired and occur in the lumbar region of
the posterior abdominal wall. Hernias through
the superior lumbar triangle (Grynfeltt's trian-
gle) are more common. The superior lumbar
triangle is bounded by the 12th rib, paraspinal
muscles, and internal oblique muscle. Less
common are hernias through the inferior lum-
bar triangle (Petit's triangle), which is bounded
by the iliac crest, latissimus dorsi muscle, and
external oblique muscle. Weakness of the lum-
bodorsal fascia through either of these areas re
-sults in progressive protrusion of extraperito-
neal fat and a hernia sac. Lumbar hernias are
not prone to incarceration.
Huge lumbar hernia
Satisfactory suture repair is difficult because
of the immobile bony margins of these defects. Repair is best done by placement of
prosthetic mesh, which can be sutured to the margins of the hernia. There is usually suf-
ficient fascia over the bone to anchor the mesh.
Interparietal Hernia
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hernia that does not reach all the way to the subcutis, but only to the musculoaponeurotic layer.
Interparietal hernias are rare and occur when the hernia sac lies between layers of the
abdominal wall. Interparietal hernias most frequently occur in previous incisions.
Spigelian hernias are nearly always interparietal.
The correct preoperative diagnosis of interparietal hernia can be difficult. Many pa-
tients with complicated interparietal hernias present with intestinal obstruction. Ab-
dominal CT can assist in the diagnosis. Large interparietal hernias usually require place-
ment of prosthetic mesh for closure. When this cannot be done, the separation of com-
ponents technique may be useful to provide natural tissues to obliterate the defect.
Sciatic Hernia
The greater sciatic foramen can be a site of hernia formation. These hernias are ex-
tremely unusual and difficult to diagnose and frequently are asymptomatic until intestinal
obstruction occurs. The most common symptom is the presence of an uncomfortable or
slowly enlarging mass in the gluteal or intragluteal area. Sciatic nerve pain can occur, but
sciatic hernia is a rare cause of sciatic neuralgia.
A transperitoneal approach is preferred if bowel obstruction or strangulation is suspect-

ed. Hernia contents can usually be reduced with gentle traction. Prosthetic mesh repair
is usually preferred. A transgluteal approach can be used if the diagnosis is certain and
the hernia is reducible. With the patient prone, an incision is made from the posterior
edge of the greater trochanter across the hernia mass. The gluteus maximus muscle is
opened, and the sac is visualized. Either the muscle edges of the defect are reapproxi-
mated with interrupted sutures, or the defect is obliterated with mesh.
Perineal Hernia
Perineal hernias are caused by congenital or acquired defects and are very uncom-
mon. These hernias also may occur after abdominoperineal resection or perineal prosta-
tectomy. The hernia sac protrudes through the pelvic diaphragm. Primary perineal herni-
as are rare, occur most commonly in older, multiparous women, and can be quite large.
Symptoms are usually related to protrusion of a mass through the defect that is wors-
ened by sitting or standing. A bulge is frequently detected on bimanual rectal-vaginal ex-
amination.
Perineal hernias are generally repaired through a transabdominal approach or com-

bined transabdominal and perineal approaches. After the sac contents are reduced,
small defects may be closed with nonabsorbable suture, whereas large defects are re-
paired with prosthetic mesh.
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Part I (Basic Surgery); Chapter 12 (Anaesthesia & Perioperative Care)
Anaesthesia and Perioperative Care

What is anaesthiology?
Anaesthesiology is the medical specialty, which is concerned with patient assessment and provision
of anaesthesia, analgesia and life support for surgical procedures and childbirth. It is also concerned
with assessment and management of critically ill patients and for care of patients with acute and
chronic pain.
The anaesthesiologist has a vital role in the operating room, recovery room, surgical and medical
intensive care units, emergency room, delivery room, radiology and endoscopy suites, as well as many
other areas of the hospital. The anaesthesiologist is thus the peri-operative physician concerned with:
1. Evaluating the patient before the surgery (preoperative).
2. Intra operative control of pain and support of life functions.
3. Supervising patient care after surgery (postoperative).
4. Managing compromised surgical patients in the I.C.U.
Preoperative anaesthesiologist visit:
Preoperative visit aims to achieve the following goals:
1. Establishment of rapport (Doctor – patient relationship).
2. Evaluation and optimizing the general medical condition of the patient.
3. Choosing and planning safe anesthetic management.
4. Anticipation and minimizing anesthesia - related complications.
This pre-operative assessment is achieved by:
1. Proper history taking.
2. Proper clinical examinations.
3. Revising patients investigations.
History:
Most important points to be evaluated in history are
1. Personal history.
2. Current medical problems.
3. Scheduled operation (site, side and informed consent) and other known problems e.g.
Cardiovascular – Pulmonary – CNS – Endocrine or Hepatic.
4. Medication history for (Drug Allergies – Drugs interacting with anaesthetics – Drug inducing Liver
enzymes – Steroids – Anticoagulants, …….)
5. Special Habits (Smoking – Alcohol Intake).
6. History of previous anaesthesia – surgery.
7. Family History.
Examinations:
1. Vital signs.
2. Airway.
3. Heart and Lung.
4. CNS.
5. Other systems that appear to be affected by history.
Investigations:
Recommended routine preoperative investigations:
1. Complete blood count (CBC) and coagulation profile.
2. Blood glucose.
3. Renal function tests
4. Liver function tests.
5. ECG and chest X-ray for patients above 40 years or as anticipated by history.
6. Other specialized tests e.g.:
· Echocardiography for patients with cardiac dysfunction.
· Pulmonary function test for morbidly obese patients or patients with pulmonary diseases.
143
· Preparation:
Solving the medical problems before scheduling the patients for surgery e.g. hypertension,
hyperglycemia, hyperthyroidism, dehydration, …
· Premedication:
It is administration of drugs in the 1-2 hours before induction of anaesthesia:
Aims and objectives:
1. Anxiolytics (decreases anxiety and fear).
2. Amnesia.
3. Anti-sialogogue (to decrease salivary secretions).
4. Analgesia.
5. Prevention of autonomic reflex responses during anaesthesia.
6. Sedation.
7. Antiemetics.
8. Others e.g. antibiotics, anti-histaminics.
Typical regimen for premedication for adult patients:
1. Visit the patient the day before surgery.
2. Oral benzodiazepines the night before the surgery.
3. Fasting after midnight.
4. Intramuscular opioids if analgesia is required.
5. H2 receptor antagonists in patients at risk of aspiration.
6. Morning dose of concurrent medications.
General Anaesthesia
By definition, general anaesthesia is a triad of:
1. Hyponosis (unconsciousness).
2. Analgesia.
3. A degree of muscle relaxation.
Anaesthesiologists’ tools to achieve general anaesthesia are:
1. Drugs.
2. Equipments:
· Airway equipment.
· Anaesthesia machine.
· Anaesthesia ventilator.
· Monitors.
Anaesthesia drugs:
1. Anaesthesiologists might require the administration of 3-15 drugs during operations under general
anaesthesia.
2. The four basic categories of anaesthetic drugs:
· Intravascular induction agents: to provide rapid smooth induction of hypnosis e.g.: barbiturates –
non barbiturates.
· Gases and volatile liquids: they are given by inhalation to diffuse rapidly from the lungs to the
brain to maintain anaesthesia during surgical procedures e.g. nitrous oxide – halothane – isoflurane.
· Analgesics: include opioids as Morphine and its synthetic derivatives as Pethedine and non opioid
analgesics as NSAIDs.
Muscle relaxants and their antagonists: muscle relaxants act at the neuromuscular junction (NMJ)
by blocking the binding of acetylcholine to nicotinic acetylcholine receptors thus causing muscle
relaxation and flacidity. Muscle relaxants are of two types:
a) Depolarizing (short acting) muscle relaxants e.g. succinyl choline. They are rarely used nowadays
because of their rare but serious complications (succinyl choline apnea and malignant hyperthermia)
b) Non depolarizing (long acting) muscle relaxants e.g. atracurium – pancuronium are used during
144
long surgeries that require muscle relaxation to facilitate the procedure (eg. abdominal surgery and
orthopedic surgery)
Anaesthesia equipment:
1. Airway equipment: the airway in anaesthesized supine patient tends to be occluded by the falling
tongue and is liable for aspiration of secretions or vomitus. Anaesthiologist should ensure patent and
protected airway by oral airways, endotracheal tubes or laryngeal mask.
2. Anaesthesia machine: which is composed mainly of a flowmeter to adjust flow of gases and a
vaporizer for administration of volatile anaesthetics.
3. Anaesthesia ventilator: it is a machine that is used to apply mechanical ventilation to the patient.
4. Monitors: monitoring is of utmost importance during anaesthesia. This is because anaesthetic
agents produces reversible depression of CNS, which unfortunately extend to cardiorespiratory
functions. Thus monitoring of the cardiovascular and respiratory functions is essential as well as
monitoring body temperature and neuromuscular transmission.
· Cardiovascular monitoring is done by:
a) ECG.
b) Arterial blood pressure.
· Respiratory monitoring is done by:
a) Pulse oximeter (non invasive monitor for oxygenation).
b) End Tidal CO2 monitoring (ETCO2).
· Temperature monitoring: by Specialized probes (Thermistors).
· Neuromuscular monitoring: A device that stimulate a peripheral nerve and records the response
of the muscles supplied by it.
Steps of general anaesthesia include:
1. Induction.
2. Maintenance.
3. Recovery.
Induction:
Before induction of general anaesthesia, the anaesthetist should:
1. Apply intravenous access by insertion of intravenous cannula for fluid and drug administration.
2. Measure baseline vital signs e.g. heart rate, rhythm, arterial blood pressure, oxygen saturation.
Either intravenous, inhalational, intramuscular, rectal.
Maintenance:
1. Oxygen inhalational anaesthetics via endotracheal tube
2. Muscle relaxants.
3. Additional doses of narcotics.
4. Mechanical ventilation of paralyzed patients.
5. Close monitoring of vital data.
Recovery:
1. Discontinuation of inhalational anaesthetics.
2. Antagonism of muscle relaxants by neostigmine with atropine.
3. Discontinuation of mechanical ventilation.
4. Oro – pharyngeal suction.
5. Removal of endotracheal tube.
6. Transfer the patient to the post anaesthesia care unit (PACU) or surgical intensive care unit (SICU).
Complications of general anaesthesia:
They are rare to occur but may occur during:
1. Introduction.
2. Maintenance.
3. Recovery.
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Complications during induction of anaesthesia:

1. Complications of airway manipulation: e.g. failure to intubate, undetected oesphageal intubation,
laryngospasm, reflex bronchospasm, aspiration of gastric content.
2. Stress response to intubation: e.g. hypertension, tachycardia, arrythmias.
3. Complications of administration of intravenous drug: e.g. allergic drug reaction, histamine release
leading to bronchospasm and hypotension, injection of wrong drug, awareness during anaesthesia,
drug overdose leading to hypoventilation and hypotension.
Complications during maintenance of anaesthesia:
1. Inadequate fluid or blood replacement.
2. Nerve injury due to inappropriate patient position.
3. Undetected patient ventilator disconnection.
4. Corneal ulcer due lack of protective reflexes.
5. Malignant hyperthermia which is a rare but very serious complication.
Complications during recovery of anaesthesia:
1. Post – operative nausea and vomiting.
2. Sore throat from endotracheal tube replacement.
3. Inadequate recovery of muscle power.
Delayed complications of anaesthesia:
1. Muscle pain due to fasiculations caused by succinyl choline.
2. Halothane induced hepatotoxicity.
How to minimize complications associated with anaesthesia?
1. Proper preoperative evaluation and preparation.
2. Before induction of anaesthesia, the anaesthetist must:
· Check the equipment to be used.
· Prepare all drugs including emergency drugs.
3. Proper monitoring of the patient intraoperatively.
4. Call for help early when needed.
5. During crisis move rapidly but do not panic
Regional Anaesthesia
Many surgical procedures can be performed using local or regional anaesthesia thus avoiding the risks
of general anaesthesia. Local and regional anaesthetics also provide better postoperative pain control.
(Lidocaine)
Techniques of regional anaesthesia:
1. Block of sensory nerve endings:
· Topical: by applying local anaesthetics to mucous membrane e.g. eye or mouth.
· Infiltration: e.g. subcutaneous injection of local anaesthetics to block nerve endings.
· Local intravenous: by retrograde diffusion of a local anaesthetic after injection into a vein in a
tourniquet occluded limb.
2. Central Neuro axial block: two types are common:
a) Subarachanoid (spinal anaesthesia): by applying local anaesthetic solutions directly into the
CSF.
· Complications: hypotension – bradycardia – nausea and /or vomiting – headache – urinary
retention.
b) Extradural (epidural anaesthesia): where local anaesthetics are injected between the dura matter
and the periosteum lining the vertebral canal.
· Advantages over spinal anaesthesia:
1) Can be performed at various levels of the vertebral column.
2) Long duration as we can inject anaesthetics repeatedly via a catheter placed in the epidural space,
this covers the intra and postoperative periods.
146
Contraindications to neuro axial blocks:

1. Absolute:
a) Patient refusal.
b) Known allergy to local anaesthetic drugs.
c) Infection at site of needle insertion.
d) Bleeding and coagulation disorders.
2. Relative:
a) Hypovolaemia.
b) Systemic sepsis.
c) Low fixed cardiac output.
Post-operative care and pain management:
Post-operative care:
Either in PACU (Post Anaesthetic Care Unit) or SICU (surgery intensive care unit).
These units should be equipped with:
1. Oxygen source – suction facilities.
2. Basic monitoring.
3. Emergency drugs.
4. Experienced nurses and anaesthesiologist.
Patients are discharged from this care unit after fulfilling the following criteria:
1. Fully awake – breathing adequately with good O2 saturation on room air.
2. Stable hemodynamics.
3. Pain free.
Some Anaesthetic Considerations for Patients with Medical Problems:
In addition to the routine anaesthetic management, each of the following diseases has special
considerations:
1. Renal Impairment:
Most common is chronic failure (uremia).
Preoperative:
· Hypertension is common.
· Investigations:
a) Arterial blood gases: to detect hypoxia, acid base disturbance.
b) Serum electrolytes: hyperkalemia, hypocalcaemia.
c) ECG: ischemic changes, conduction defects.
· Preoperative detection and management of complications of dialysis: e.g. volume depletion,
hypokalemia, hypoproteinemia, hepatitis B and C virus detection from long history of dialysis.
· Premedication: all doses should be decreased.
Intra operative:
· Monitoring: Invasive arterial blood pressure, central venous pressure, blood pressure measurement
should be avoided in the arm with A-V fistula.
· Choice of anaesthesia:
a) Regional anaesthesia: proffered in minor surgeries but care for coagulopathies.
b) General anaesthesia: induction should be rapid to decrease risk of aspiration, intravenous canula
in collateral arm of A-V fistula, decrease doses of all drugs doe to hypoalbuminemia (so increase
free drugs) and acidosis (so increase drug entry to brain).
c) Maintenance as usual but with decreasing the doses of the used drugs.
Postoperative:
· Close observation to detect the postoperative renal failure (detected by oliguria), postoperative
apnea, hypoxia, and postoperative hypertension.
2. Chronic Liver Disease:
The most common is liver cirrhosis.
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Preoperative:
History, examination and investigation for:
a) GIT and liver:
· Portal hypertension (10 mmHg) and its treatment, assess degree of hepatic impairment.
· Measure the bilirubin and serum albumin level.
b) Circulatory system:
· Hyperdynamic circulatory state.
· Alcoholic cardiomyopathy.
c) Haematologic system:
· Anemia (treated by preoperative transfusion).
· Thrombocytopenia (treated by platelet transfusion).
· Coagulation factors deficiencies (treated by fresh frozen plasma).
· Complete blood picture, coagulation screen.
d) Respiratory system:
· Respiratory alkalosis.
· Decrease lung volume from ascites (treated by paracentesis).
· Arterial blood gases and chest X-ray are requested.
e) Renal system:
· Decrease renal perfusion.
· Hepatorenal syndrome (treated by preoperative hydration by intravenous infusion and preoperative
mannitol 100 ml to prevent renal failure).
· Urine output is collected in 24 hours to detect oliguria.
f) Fluid and electrolyte balance:
· Hyponatraemia < 130 meq/L (treated by water restriction).
· Hypokalemia < 3.5 meq/L (treated by K+ replacement).
· Hypoglycemia < 80 mg/dl (treated by dextrose I.V. infusion).
· Na+, K+, and fasting blood sugar are requested.
g) Hepatic encephalopathy:
· Avoid premedication to avoid CNS depression.
· Neomycin, lactulose and enema are given.
h) Infections:
· Extra-caution to avoid contact with blood and body fluids.
Intra operative:
a) Monitoring:
· Arterial blood gases.
· Invasive arterial blood pressure.
· Central venous pressure.
· Urinary output.
b) Choice of anaesthesia:
· Regional anaesthesia: Can be used provided that no coagulopathy, no hypotension.
· General anaesthesia:
1) Induction: rapid intubation should be done.
2) Maintenance:
* Avoid N2O due to intrapulmonary shunts.
* Decrease doses of opioids.
* Use short acting muscle relaxants.
* Ventilation should be controlled (to avoid hypoxia and to maintain normal PaCO2).
Postoperative:
· Close monitoring to detect hepatic encephalopathy, oliguria, blood pressure changes.
3. Hypertension:
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Preoperative assessment: as above.

a) Decision whether to delay or to proceed with surgery e.g. severity of pre-operative blood pressure
elevation and the presence of complication.
b) Severity and duration of hypertension.
c) Cause and type of hypertension.
d) Complications of hypertension: e.g.
· Renal impairment.
· Cerebrovascular accidents.
· Hypertensive retinopathy.
e) Preoperative drugs taken with its side effects:
· Antihypertensive drugs should be continued up to the time of surgery.
· Diuretics should be stopped 2 days before to avoid dehydration.
Pre-medications:
· To maintain ABP stable within 10-20% of preoperative level.
Postoperative Pain Management
Pain is often the patient’s presenting symptom & it can provide useful clinical information.
Pain should be relieved wherever you see patients (emergency, operating room and on the ward) and
anticipate the needs for pain management after surgery and discharge.
NB: Do not unnecessarily delay the treatment of pain; for example, do not transport a patient From
OR without analgesia.
Regimens available for postoperative pain control include:
1. Regional techniques: peripheral nerve block and neuro axial administration of local anaesthetics
are efficient and safe methods for postoperative pain management.
2. Parenteral analgesia:
· Long acting opioid & short acting opioid for severe pain.
· Short acting opioid & NSAIDs for moderate pain.
· NSAIDs for mild pain.
3. Non-Steroidal Anti-Inflammatory Drugs (NSAIDs): either oral or injectable with several
advantages over opioids with no hemodynamics effects or respiratory depression with minimal
nausea and vomiting.
4. Oral opioids: they cause less discomfort than injection but with delayed onset of action.
Classification of pharmacological management of pain
➢ Non-opioids
Non-steroidal anti-inflammatory drugs (NSAIDs)
➢ diclofenac (1 mg/kg)
➢ paracetamol (15 mg/kg).
➢ ibuprofen can also be given orally and rectally
➢ Opioids
➢ Strong opioids: morphine, pethidine, fentanyl, nalbuphine
➢ Weak opioids: tramadol
➢ Local anesthetics
➢ lidocaine, bupivacaine, …
Opiate analgesics
There are three situations where an opiate might be given
o Preoperatively
o Intraoperatively
o Postoperatively
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Opiates given pre- or intra-operatively have important effects in the postoperative period. Short
acting opiate fentanyl is used intra-operatively to avoid the prolonged effect opiates. Naloxone
antagonizes (reverses) all opiates, but its effect quickly wears off. Opiate analgesics should be given
cautiously if the age is less than 1 year. They are not recommended for babies aged less than 3
months.
Commonly available inexpensive opiates are pethidine and morphine. Morphine has about ten times
the potency and a longer duration of action than pethidine.
Dose:
Most usual given intramuscularly
Morphine:
– Age 1 year to adult: 0.1–0.2 mg/kg
– Age 3 months to 1 year: 0.05–0.1 mg/kg
Pethidine:
give 7–10 times the above doses if using pethidine
Patient Controlled Analgesia (PCA)
Self-administration of analgesics using a computerized pump by either the IV or epidural
route
Advantages Disadvantages
• Gold standard of POP therapies • Significant time and resources needed
• Enables the patients to titrate their • Staff programming of the PCA pump
own analgesia  the potential for medication errors
• No analgesic gaps • Potential for device malfunction
• High level of patient satisfaction
Epidural Analgesia
Injection of analgesics into the epidural space close to the spinal cord and spinal nerves
where they exert a powerful analgesic effect
• Very effective pain relief • Invasive

• Low doses of opioids →  side • Staff time and training
effects • High catheter failure rate (25%)
•  Stress response to surgery • Post-dural puncture headache
• Risk of spinal hematoma
Peripheral Nerve Blockade

Injection of local analgesics close to peripheral nerves to produce analgesia by blocking
pain impulses from the nerve
• Excellent analgesia • Staff time and training
• Targeted analgesia • Potential for infection, hematoma &
•  Systemic exposure to opioids local anesthetic toxicity
•  Adverse effects • Not useful for abdominal and
cardiothoracic procedures
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SURGICAL INTENSIVE CARE

Indications for ICU Admission
• Surgical: P.O. Brain tumor, cervical spine, cardiac surgery, associated medical condition…
• Preoperative: hemodynamically unstable (shocked, serious arrythmias) multiple trauma
• Trauma: Airway, Chest, Cardiac, Brain, Cervical spine, …
• Medical: Acute coronary syndrome, cerebro-vascular stroke, Hypertensive emergency,
Diabetic emergencies, Resp., cardiovascular, multi-organ dysfunction syndrome (MODS), …
• Combined
CARE OF SURGICAL ICU PATIENTS
• Monitoring
• Infection control
• Position & care to avoid bed sores
• Vascular lines, catheters, tubes, drains…
• Connected devices: ventilators, intra-aortic balloon pump...
• Nutrition:
- Route: enteral (oral, Ryle, gastrostomy, jejunostomy, ileostomy), parenteral
- Type: diabetic, liver, renal, respiratory.
- Amount
- Timing
CARE OF COMATOSED PATIENTS
Care to prevent suspected complications
• Bed sores
• Respiration: obstruction, infection, Aspiration
• Infection
• Malnutrition
• Deformities
CARE OF NEUROSURGICAL ICU PATIENTS
• Consciousness deterioration
• Fits
• Bleeding
• Fluid imbalance
• Other neurological deficits
CARE OF CARDIAC SURGERY ICU PATIENTS
• Dysrhythmias & heart block
• Cardiac Failure & pulmonary edema
• Bleeding & Tamponade
• Blood pressure changes
• Neurological complications
• Renal dysfunction
CARE OF INVASIVE DEVICES
CONTROL AND PREVENTION OF INFECTION
PREVENTION OF IATROGENIC COMPLICATIONS
Indications of Mechanical Ventilation

• Respiratory failure
• Delayed postoperative recovery
• Increased intra cranial pressure (ICP)
• Post CPR (Cardiac arrest)
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• Postoperative hemodynamically unstable patient

CRITERIA FOR DISCHARGE (The following should be assessed before ICU discharge)
• Conscious level
• Cardiovascular system
• Respiratory System
• Renal
• Surgically (controlled or stable)
• Metabolic
• Other organ functions
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Part I (Basic Surgery); Chapter 13 (Surgical Oncology)
Principles of Radiation Oncology

Introduction:
Radiation oncology uses ionizing radiation to treat cancer (and occasionally a few benign
conditions). Radiotherapy or radiation therapy (RT) was initially developed in conjunction with
diagnostic radiology but has evolved into a separate specialty. Currently, more than 50% of cancer
patients undergo RT at some point during the course of their cancer.
Most receive treatment with curative intent (definitive therapy). Patients with incurable disease
receive shorter courses of therapy to relieve cancer induced symptoms designed to minimize acute
side effects.
The acute side effects of RT are often milder than either chemotherapy or radical surgery; most
patients find it the easiest portion of their therapy. While ionizing radiation damages both normal and
cancerous cells, normal cells have greater capacity to repair this damage and carefully administered
treatment can eradicate cancer cells while relatively sparing the organ that harbors them.
For example, a laryngeal tumor and its draining nodes can be cured while sparing the voice and neck
muscles. Although RT can be used alone, it is often combined with surgery and/or chemotherapy in a
multimodality regimen that benefits from the unique advantages of each modality. Combined
modality therapy does run the risk of increased toxicity because of each treatment’s side effects, so
these regimens should be carefully designed and tested in clinical studies.
RT consists of two modalities: teletherapy and brachytherapy:

Teletherapy, utilizes x-ray or sub-atomic particle beams, delivered by a machine positioned a
distance (typically, a meter) from the patient.
Brachytherapy, utilizes radiation emanating from radioactive sources implanted inside the patient’s
body, either temporarily or permanently.
Both modalities have been in use for over a century.
In order to deliver safe and effective RT, the radiation oncologist must master five foundation
disciplines: clinical oncology, radiobiology, oncologic imaging, computer science and medical
physics.
Clinical Oncology
Effective practice of radiation oncology depends on a sound understanding of clinical oncology and
basic sciences. This knowledge must include:
* Principles of cancer pathology, medical oncology and surgical oncology
* Gross anatomy and radiographic anatomy
* Natural history of each cancer
* General clinical care of the cancer patients, including supportive care, management of cancer
symptoms and treatment effects
Radiobiology
Radiobiology studies the impact of ionizing radiation on biological molecules, living cells and
tissues. Whether an ionizing ray hits a molecule upon striking a cell is a random event. Statistically, a
ray is most likely to strike the most common molecule in the cell, water. The ionizing ray causes
water molecules to break apart into ion pairs, producing the highly reactive hydroxyl radical. Free
radicals bounce around in the cell, and may strike other molecules, usually water, causing a cascade
that increases the number and density of free radicals. Ultimately, one or more of these radicals may
randomly strike a molecule of DNA, resulting in single or double strand DNA breaks. Without
functioning DNA, the cancer cells cannot reproduce properly or repair themselves, and the cells
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transition to apoptosis. Apoptosis (programmed cell death) is the capacity of a cell to destroy itself if
its DNA is irrevocably damaged.
The body can usually repair single strand breaks, and sometimes can repair double strand breaks.
Lethal damage results in mitotic cell death; damage that can be repaired is called 'potentially lethal
damage'. Death of a cell line after lethal damage may take several mitotic cycles and therefore,
depending on cell cycle time, as long as several months. A cell is most sensitive to radiation when it
is undergoing mitosis; conversely, cells in G0 and the late S phase are relatively radioresistant. After
cell death, the body must resorb the cell remains, and scars may form. So, tumors usually shrink
slowly, and sometimes a mass will remain that is simply a scar.
RT traditionally has been fractionated, which means delivered in multiple small daily doses, to
maximize the effect on tumor cells and minimize the late effects on normal tissues. Acute side
effects are largely due to the effect of radiation on the rapidly dividing normal cells of the body, such
as skin and mucous membranes. Tumor cells are actively dividing, so tumors tend to respond in the
same way as normal cells that actively divide.
Due to very different pathophysiology, occurrence of acute effects does NOT predict for occurrence
of late effects. Late effects are largely due to microvascular damage that resembles that caused by
diabetes mellitus, loss of parenchymal cell function and scarring. It is important to remember that
late effects may occur many years after treatment.
The 4 R’s of radiobiology: reoxygenation, repair, redistribution, and repopulation are the reasons
radiation oncologists fractionate radiation.
Reoxygenation:
When a tumor is irradiated, the better-oxygenated cells in the periphery of the tumor deposit are
more likely to die. As these cells die during the course of therapy, O2 penetrates more deeply into the
tumor, and reach cells that had previously been poorly oxygenated. Hence, fractionated radiotherapy
results in the induction of radiosensitivity in cells that had originally been radioresistant by the
phenomenon of ‘reoxygenation’.
Repair
Potentially lethal damage is damage which may be repaired; both in tumor cells and most
importantly in normal, healthy, non-cancerous tissue within the radiation field. This process is felt to
be largely complete in about 6 hours. Repair decreases risk of late effects.
Redistribution
Redistribution refers to the movement of cells into different phases of the cell cycle. Since cells in
the late S phase and G0 are relatively resistant to radiation, multiple treatments enhance the chance
that any given cell will receive treatment during a sensitive phase in the cell cycle. Redistribution
makes radiation therapy more effective.
Repopulation
Hopefully, all tumor cells are encompassed by the treatment and much normal tissue is not. In that
case, normal cells can migrate from un-irradiated tissue into the target volume to replace damaged
cells. For example; skin cells will migrate into a denuded patch of skin, creating islands of normal
skin which will enlarge to cover the open area. Surviving normal cells in the field can repopulate by
cell division. Repopulation heals acute effects and also decreases risk of late effects.
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Unfortunately, surviving tumor cells can also repopulate by cell division; so interruptions or
extended treatment duration may decrease the probability of tumor control.
Organs that are organized in parallel (lung, kidney, liver) can tolerate the loss of large portions of
their volume, while linear organs (spinal cord) cannot. Respecting radiation tolerance of these latter
organs is very important. Exceeding tolerance of (sacrificing) portions of lung, liver or kidney is
acceptable, providing enough functional parenchyma is left to sustain the vital function of that organ
and the patient’s quality of life. For example, the volume of lung that can be safely sacrificed
depends on the pretreatment lung function.
A radiation oncologist aims to deliver an effective dose to the tumor, while delivering as low a dose
as possible to the surrounding normal tissue. Radiation dose is a very complicated concept, as it
depends not only on the total dose, but also fraction size, and treatment duration.
Medical Imaging
The effective delivery of radiation therapy has always required an anatomic target. Originally, the
target was defined by physical examination, plain radiographs, surgical findings (and metallic clips
placed during surgery).
The advent of CT, MRI and PET scanning has dramatically altered the treatment planning
process.3D Treatment planning is now done virtually, in the computer, using three-dimensional
imaging from CT image sets obtained with the patient immobilized in the treatment position. MRI
and can be fused into these planning CT scans, enabling precise tumor delineation and close
conformity to the shape of the tumor (3-D conformal RT) and technological advances in treatment
delivery allow precise localization of dose in small volumes of the target and surrounding normal
tissue, Intensity Modulated Radiation Therapy (IMRT). As a result of better imaging, more normal
tissue is spared irradiation.
Figure (1c- d-e): 1cTreatment planning CT of patient with brain metastases; no tumor is visible, but there is a
hint of edema in right occipital lobe (arrow). 1d. The same planning scan slice with MRI fused and displayed:
50% MRI, 50% CT. Notice tumor (red arrow) is now clearly visible in posterior portion of edema, which is
much more visible on the MRI image. 1e. MRI fused into treatment planning CT, with dosimetric lines
defining treatment, with 100% line (yellow) (prescription dose) covering target volume. Red dot is pixel
receiving maximum dose.
Images courtesy of the University of Massachusetts Medical School, Department of Radiation oncology
Computer Science
The great recent advances in radiotherapy (3D Conformal RT, Intensity Modulated RT- IMRT,
IGRT) would not have been possible without the explosion in computer technology. Today,
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treatment planning is done almost entirely by computer. Computers also control the actual treatment
delivery, including the positioning and motion of the leaves that shape and texture the treatment
beams. Multi-leaf collimators have replaced lead blocks for beam shaping and can move during the
actual treatment (IMRT). IMRT paints dose into the body, permitting tight control of dose
distribution within the body by shaping dose around critical structures and the tumor. This
technology enables even greater dose conformity and treatment of tiny volumes. This precision
allows for safe delivery of much higher doses than possible with traditional treatment planning and
delivery techniques.
Medical Physics
The physics of ionizing radiation is the final body of knowledge required. X-rays, heavy particles
(such as protons) and electrons are beams produced by machines; gamma rays are the product of
radioactive decay. Treatment of deep-seated tumors requires high-energy beam(megavoltage) that
have greater penetrating power, so dose delivered at depth falls off more slowly than with
kilovoltage radiation. Both the amount of skin sparing and the depth of penetration depend on the
energy of the megavoltage beam. Megavoltage x-rays have this greater penetration, are not
preferentially absorbed in bone, and do not deliver full dose to skin. This skin sparing effect is due to
build-up of the free radicals generated as the beam penetrates into tissue.
Stereotactic Radiosurgery (SRS) or Stereotactic Radiotherapy (SRT)

The advent of CT and MRI based 3-dimensional treatment planning has made it possible to focus
high doses of radiation accurately. SRS delivers an ablative dose of radiation in a single fraction,
destroying both tumor and tissue. SRT utilizes the same technology, but fractionates therapy into 2-
5 treatments, thereby taking advantage of the 4 R’s of radiobiology.
Precise target definition and patient immobilization are critical. Individually designed restraints are
used to assure patient positioning.
Principles of Systemic Therapy in Cancer Patients

If cancer were a strictly localized type of disease, local therapy, notably surgery and/or radiotherapy,
would be appropriate, with little need for systemic treatment, i.e. cancer drugs. However, one of the
hallmarks of many cancers is their propensity to invade or infiltrate neighboring tissue and
anatomical structures, and to spread via the bloodstream or the lymphatic channels.
Traditionally systemic therapy would be thought to be chemotherapy but the definition also includes
hormonal treatments, chemical adjuncts, immunotherapy and biological agents
Aim of systemic treatment:
Curative
Chemotherapy is given as the definitive treatment for cure, e.g. acute leukaemia, choriocarcinoma.
Adjuvant
Treatment is given after a definitive treatment such as surgery or radiotherapy with the aim of
destroying micrometastatic residual disease, and thereby increasing the chances of cure, e.g.
chemotherapy after surgery for breast cancer.
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Neoadjuvant
A treatment is given before a definitive treatment such as surgery to facilitate the procedure and/or
improve chances of cure, e.g. chemotherapy is given to patients with osteosarcoma prior to resection
and replacement with prosthesis.
Palliative
A treatment is given to improve the quality of life and symptoms of a patient without the intention of
cure. It may prolong the life of the individual but this is not necessarily the case. Quality of life is the
prime assessment
Types of systemic therapy:
1- Cytotoxic Chemotherapy:
Chemotherapy involves the treatment with cytotoxic chemicals to kill cancer cells. Chemotherapy
agents are divided into different categories according to their mechanism of action. The rationale
behind chemotherapy is the high proliferation rate of cancer cells compared with the non cancer cells
in the body (Chemotherapy inhibit or kill rapidly dividing cancer cells. This may be due to the drug
acting at a particular point in the cell cycle (cell cycle-specific) or is independent of the cell cycle
(cell cycle-non specific)
Cytotoxic agents often work best in combination rather than as single drugs, whereby care must be
taken to combine drugs with similar anticancer efficacy, yet distinct mechanisms of action and
resistance and different toxicity profiles.
Examples of tumors in which chemotherapy has a significant impact:
Cured with chemotherapy

• Childhood acute leukemia
• Testicular cancer
• Ovarian germ cell tumors
• Choriocarcinoma
• Wilms’ tumor
Associated with improved survival

• Breast cancer
• Osteosarcoma
• Ewing’s sarcoma
• Ovarian cancer
Common toxicities of cytotoxic chemotherapy:
a) Hematologic toxicity: Most chemotherapeutic agents are associated with transient bone marrow
suppression and neutropenia is one of the most significant dose-limiting complications of
chemotherapy (eg. Taxanes, mitomycin C). Thrombocytopenia is not uncommon (eg. Carboplatin,
bleomycin)
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b) Cardiotoxicity: Chemotherapeutic agents may cause direct injury to the heart, either acutely, in the
form of myocardial tissue injury or dysrhythmias, or in a delayed or chronic fashion associated with
congestive heart failure (eg. Anthracyclines, Paclitaxel)
c) Renal toxicity: Chemotherapy may affect the tubules, renal parenchyma, and renal vasculature (eg.
Cisplatin, Ifosfamide)
d) Hepatic toxicity: The liver is the site of metabolism of most chemotherapeutic agents and many
agents are directly hepatotoxic. Hepatotoxicity can be acute or chronic and is most often manifested
as an elevation of transaminases (eg. Docetaxel, mercaptopurine)
e) Gastrointesinal toxicity: Mucositis (eg. 5FU, MTX), diarrhea (eg. Irinotecan, 5FU), nausea and
vomiting (eg. Cisplatin, alkylating agents)
f) Pulmonary toxicity
e) Others: Ototoxicity, dermatologic, ocular
2- Hormone therapy
Hormone therapy involves the manipulation of the endocrine system through exogenous
administration of specific hormones, particularly steroid hormones, or drugs which inhibit the
production or activity of such hormones (hormone antagonists). Because steroid hormones are
powerful drivers of gene expression in certain cancer cells, changing the levels or activity of certain
hormones can cause certain cancers to cease growing, or even undergo cell death. Surgical removal
of endocrine organs, such as orchiectomy and oophorectomy can also be employed as a form of
hormonal therapy.
Hormonal therapy is used for several types of cancers derived from hormonally responsive tissues,
mainly the breast and prostate. Hormonal therapy may also be used in the treatment of paraneoplastic
syndromes or to ameliorate certain cancer- and chemotherapy-associated symptoms, such as
anorexia. The most famous example of hormonal therapy in oncology is the use of the selective
estrogen-response modulator tamoxifen for the treatment of breast cancer, although another class of
hormonal agents, aromatase inhibitors, now have an expanding role in postmenopausal disease
Common toxicities of hormone therapy:

a) Hot flashes
b) Osteoporosis (Aromatase inhibitors)
c) Bone aches and myalgia
3- Molecularly targeted therapy:

Over the past decades great advances were made to clarify the principles of the molecular and
cellular pathology of cancer. It has become clear that cancer mostly arises due to the stepwise
acquisition in cancer stem cells and their progeny of somatic mutations in key genes critical for the
governance of normal cellular homeostasis and the control of mitotic proliferation, cellular
differentiation, cell survival (including programmed cell death, or apoptosis) and perhaps autophagy
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Examples of therapeutic molecular targeting of cancer cells

Monoclonal antibodies
B‐cell lymphoma (CD20 antigen, Rituximab)
Colorectal cancer and head and neck cancer (EGFR, Cetuximab)
HER2 ‐positive breast cancer and gastric cancer (HER2 gene, Trastuzumab)
Diverse cancers (VEGF/VEGFR, Bevacizumab)
Small molecules (mostly tyrosine kinase inhibitors)
CML (BCR-ABL fusion protein, Imatinib)
Non-small cell lung cancer (EGFR, Erlotinib and gefitinib)
Non-small cell lung cancer (ELM–ALK fusion protein, Crizotinib)
Melanoma (BRAF V600E mutation, Vemurafenib)
Diverse cancers (VEGF/VEGFR and other targets, Sunitinib and sorafenib)
Common toxicities of molecularly targeted therapy
a) Cardiovascular toxicity (eg hypertension, bevacizumab)
b) Gastrointestinal toxicity (eg diarrhea, sorafenib)
c) Cardiotoxicity (eg ventricular dysfunction, trastuzumab)
d) Skin toxicity (eg acneiform eruption, cetuximab)
4- Immune therapy:
Several clinical observations underpin the view that disturbances of immune regulation play a pivotal
role in cancer pathology. The immune system may indeed have anticancer cell mechanisms, mostly
T‐cell mediated. Specific types of cancer may be particularly frequent in immunosuppressed hosts,
such as patients with uncontrolled human immunodeficiency virus (HIV)‐mediated disease or
immunosuppressed organ transplant recipients. A well established form of ‘immune therapy’
against cancer is allogeneic stem cell transplantation where an immune response mediated by donor
lymphoid cells, the graft-versus leukemia/ lymphoma effect, is thought to be important in producing
the favorable results of allogeneic transplantation in a number of hematological cancers. Recently,
novel antibody‐mediated approaches to modulate T-cell response to cancer cells have been shown
to be of value, notably in metastatic melanoma.
Common side effects of immunotherapy:
a) Fever
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b) Flu like symptoms
c) Fatigue
d) Nausea
5- Other agents:
Bone modifying agents (osteoclast inhibitors), such as bisphosphonates and denosumab significantly
reduce the frequency of skeletal-related events in patients with bone metastases from a wide variety
of cancer types
Side effects include: Hypocalcemia, nausea, nephrotoxicity, osteonecrosis of the jaw
ONCOLOGICAL EMERGENCIES
Objectives:
- To identify most common oncological emergencies
- To understand etiology and clinical picture of specific common oncologic emergencies
- To recognize treatment of specific described oncologic emergencies
Definition:
It is an acute condition caused by cancer or its treatment, requiring rapid intervention to avoid death
or sever permanent damage.
Etiology:
It could be due to the tumor itself, oncological treatment or due to new or pre-existing condition not
related to cancer e.g. diabetes mellites, hypertension, etc.
Types & pathogenesis of oncological emergencies:
a) structural (obstructive) emergencies e.g. superior vena cava obstruction, urinary or airway
obstruction and spinal cord compression.
b) Metabolic or hormonal emergencies e.g. hypercalcemia or SAIDH (syndrome of inappropriate
anti diuretic hormone secretion).
c) Emergencies due to treatment complications e.g. anaphylactic reaction, tumor lysis syndrome
and haemorrhagic cystitis.
Common oncological emergencies:
1. Superior vena cava obstruction (SVCO):
It results from partial or complete obstruction of blood flow through the superior vena cava vein to
the right atrium, causing sever reduction in venous return from the head, neck and upper extremities.
This obstruction may be due to compression, invasion, thrombosis or fibrosis of this vessel.
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It is encountered mainly (90%) in malignant tumors e.g. primary lung carcinoma mainly SCLC type,
non Hodgkin’s lymphoma and metastatic tumors. Less commonly (10%) encountered in benign
diseases like T.B. and iatrogenic causes like central venous lines or surgery.
Clinical picture of SVCO:
The duration of patient symptoms could range from few days up to several weeks. They include
headache, cough, chest pain and generalized weakness.
Examination reveals tachycardia, hypotension, jugular vein distention and dilated vein &collaterals
over chest wall.
Investigations:
Chest x ray: which may reveal mediastinal widening.
Doppler u/s of jugular or subclavian vein: could differentiate thrombus from extrinsic compression.
CT scan of chest.
Bronchoscopy and thoracoscopy.
Needle biopsy from mediastinal mass.
Treatment:
# Elevation of head of bed, oxygen supply, diuretics, steroids and bed rest could lead to symptomatic
improvement.
# Chemotherapy, mainly used for small cell lung cancer, NHL and germ cell tumor.
# Radiotherapy, used in an urgent way for life threatening symptoms /signs e.g. stridor and cerebral
edema. It also combined with chemotherapy in SCLC and NHL.
# SVC stenting used for tumors not sensitive for chemotherapy or radiotherapy.
2- Spinal cord compression:

It is due to compression of spinal cord in one or more sites due to the tumor itself or due to
extradural metastases. Most commonly seen with lung, breast and prostatic cancers which affecting
thoracic (70%), lumbosacral (20%) and cervical (10%) spinal cord.
Clinical picture; varies from localized back pain & tenderness up to motor and / or sensory loss and
less commonly autonomic dysfunction as urinary retention.
Examination includes; full neurological examination to reveal the deficits or the sensory level,
passive neck flexion test and gentle vertebral column percussion.
Investigations:
Plain x ray; reveals vertebral body compression or collapse.
CT & MRI of suspected area of spinal compression.
Treatment:
Steroids should be started immediately when spinal cord compression is suspected in a dose of 10
mg dexamethasone intravenously followed by 4 mg every 6 hours and could be higher doses.
Radiation therapy is needed for radiosenstive tumors especially in spinal instability, it is directed
towards affected spine and epidural involved area.
Surgery could be done in limited cases e.g. laminectomy.
3- Anaphylactic reactions:
It is encountered with some chemotherapeutic agents e.g. taxans, platinum and L–asparginase due to
fast infusion rates; it could be manifested from second course of treatment. Symptoms in the form of
urticaria, angioedema, chest tightness, bronchospasm and hypotension.
Management of anaphylactic reactions depends mainly on three issues; early recognition,
maintenance of airway patency and hemodynamic support. The acute management of anaphylaxis in
adults should start by removing the drug considered to be responsible for the reaction. Immediate
assessment of the airway and administration of epinephrine subcutaneously. Depending on severity
of condition, intravenous fluids injection particularly in case of hypotension. Steroids and
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antihistamines e.g. diphenhydramine 50 mg I.V. followed by 25- 50 mg every 4- 6 hours orally may
also be added . In resistant hypotension cases, intensive care unit management will be required.
4- Tumor lysis syndrome:

This complication seen with treatment of rapidly growing chemosensitive tumors e.g. Burkitt’s
lymphoma, acute leukemia and NHL after starting chemotherapy which lead to malignant cells lysis
and cell death with subsequent release of intracellular component into the blood stream of the
patient. It is a metabolic triad of hyperuricemia, hyperkalaemia and hyperphosphatemia which could
end by renal failure and hypocalcemia as secondary complications.
Clinical picture: the patient develops generalized weakness, myalgia together with nausea and
vomiting. Also symptoms might include dark urine, seizures, arrhythmias up to sudden death.
Investigations: include full electrolyte panel (Na, K, Ca, Ph, Mg levels), LDH level and ECG.
Management; prophylaxis is more important while treating such rapidly growing tumors. It include
vigorous pre hydration, metabolic monitoring and allopurinol 300mg /day which inhibits xanthine
oxidase enzyme and prevent new uric acid formation & hyperuricemia.
Active treatment:
-hydration by normal saline 3 L/m2 / day with monitoring urine output which should be at least 100
ml/h
-Oral sodium bicarbonate to avoid acidic urine unless contraindicated e.g. in sever hypertension.
-Allopurinol.
-Rasburicase which is recombinant form of urate oxidase preventing the development of
hyperuricemia in patient at high risk of having tumor lysis syndrome. It is shown to be superior to
allopurinol in controlling hyperuricemia is given in dose 0.20mg/kg/day for 3- 7 days starting day
before or same day of chemotherapy.
-Electrolytes correction.
- Dialysis is last step of management in case of renal failure, sever hyperphosphatemia (> 10.2 mg
/dl) with symptomatic hypocalcemia , persistent hyperkalemia , azotemia , hyperuricemia, oligo/
anuria or refractory acidosis or volume overload. In resistant cases treatment commonly done in
intensive care unit.
162

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Preface

Ahmed Abdel Aziz Abou Zeid

Adel Abdel Aziz Ewada

Chapter 1 (Metabolic response to Surgery) ………..……………………………………………….……………. 1

Chapter 2 (Haemorrhage, Shock, Blood transfusion) …………………………………………………………. 5

Chapter 3 (Fluid, Electrolytes & Acid-Base Balance) ……………………………………………….…………. 25

Chapter 4 (Surgical Nutrition) …..………………………………………………………………………………………. 45

Chapter 5 (Surgical Infections) ….………………………………………………………………………………………. 53

Chapter 6 (Hand Infections) ……..………………………………………………………………………………………. 68

Chapter 7 (Preoperative Assessment & Preparation) ……..…………………………………………..……. 82

Chapter 8 (Wound & Wound Healing) …………………………………………………………………..…………. 90

Chapter 9 (Postoperative Care & Complication) …………………………………………………………..…. 100

Chapter 10 (Cysts, Tumours, Sinuses & Fistulae) ………………………………………………….…………. 109

Chapter 11 (Abdominal wall & Hernias) …………….……………………………………………………………. 125

Chapter 12 (Anaesthesia & Perioperative Care) …………………………………………………..…………. 143

Chapter 13 (Surgical Oncology) ………………………………………………………………………………………. 153

METABOLIC RESPONSE TO INJURY

- Infection, inflammation, major sepsis, endotoximia

Components of the Metabolic Response to Injury

1- Injury to a blood vessel due to mechanical or surgical trauma.

A – According to the type of bleeding vessel:

B- According to the timing of haemorrhage in relation to trauma:

1- Primary haemorrhage: Occurs at the time of injury or during operation.

C- Revealed (External) versus concealed (Internal) haemorrhage:

D- Acute versus chronic haemorrhage

E- Surgical and non-surgical haemorrhage

Physiologic response to haemorrhage

Clinical picture of haemorrhage

Classification of haemorrhage and estimating blood loss:

Class 3 30–40% of blood volume is lost

A. Immediate resuscitative maneuvers

- The cardiovascular system

- The respiratory system

- Low pH (lactic acidosis)

- Low P02 <70 mm Hg (respiratory distress then failure)

- Low PCO2 (hyperventilation and compensatory respiratory alkalosis)

- Low HCO3 (depleted buffers).

3. Obstructive shock in which tissue hypoperfusion is caused by reduction in preload secondary to

- Prolonged capillary refill times

- Mild reduction in urine output

Table 2 Cardiovascular and metabolic characteristics of shock

(a) Eradication of sepsis, e.g., drainage of a huge abscess or peritonitis, or resection of

are bleeding or undergoing surgery.

- Stop the transfusion immediately and contact the blood bank

of micro-aggregates blood filters for transfusion can prevent this hazard

Fluid and electrolyte balance

- Principal anions are, phosphate and proteins

D. Extracellular volume excess

Table 3-2 Respiratory and Metabolic Components of Acid-Base Disorders

- Ureterosigmoidostomy (implantation of ureter in the sigmoid colon after bladder resection).

Table 3-3 Electrolyte Solutions for Parenteral Administration

Table 3-4 Alternative Resuscitative Fluids

Types of nutritional support

Hickman Catheter in place Jejunostomy tube in place

normal intestinal commensal. Pseudomonas is a common colonising organism in

Common antibiotics used in prophylaxis and treatment of surgical infections

tuberculosis, leprosy, candidiasis, anthrax, actinomycosis and parasitic infestations

zone of acute inflammation.

Wound infections & surgical site infection (SSI)

- Minor breech of sterilization rules

- The pathogens that are present because of specific disease

- The hospital antibiogram

C. Factors related to the patient: