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General surgery module SUR 312– block 6

Introduction to General Surgery

Objectives:

 To study the types & classifications of wounds, phases and complications of wound
healing (surgery department)

 To study principles of management of polytraumatized patient (surgery department)

 To study the types, classifications and presentation and management of hemorrhages

(surgery + anaesthesia departments)

 To study principles of organs transplantation. ( surgery department)

 To know the basic causes and presentations of hemostatic disorders in surgical patient
and how to control (surgery department)

 Study the basic pathophysiology, clinical presentation and management of various types
of shock; including hypovolemic, septic , neurogenic and anaphylactic shocks (surgery +
anesthesia departments)

 To study the important and common electrolytes and acid bases disturbances in surgical
patient and how to manage (surgery + anesthesia departments)

 To study cases of malnutrition in surgery and study the common types, principles,
formulae and complications of surgical nutrition (surgery + anesthesia departments)

 Study the common specific and non-specific surgical infections and common types of
organisms involved (surgery + microbiology departments)

 To study the common clinical presentations, investigations, complications and treatment

of common surgical infections (surgery department)

 To study basic principles, classifications, presentation and management of burn

(surgery department)

 To study basics of skin grafts in burn patient (surgery department)

 To study the common anomalies of the face as cleft lip and palate (surgery department)

 Common ulcer and malignancy of the mouth and tongue (surgery department)

 The salivary glands; types, etiology, clinical presentations, investigations and treatment
of common diseases (infections – stones – tumors)
 To study principles of different types, principles and complications of anesthesia
(anesthesia department)
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Cases
I. Infections

1. Wound infection

2. Cellulitis

3. Abcess

4. Hand infections ( acute pulp space infection – tenosynovitis – ulnar bursitis –

radial bursitis)

II. Burn

III. Salivary glands

1. Acute parotid abcess

2. Tumors of parotid

IV. Cleft lip and Cleft palate

V. Cancer tongue

Sharing departments in surgery module:

 Anaesthesia: principles of anaesthesia – fluids, electroytes & acid base disturbances in

surgery – shock – hemorrhage – nutrition in surgery

 Microbiology: common organisms in specific and non-specific surgical infections

References:

o USMLE surgical guidelines

o KASR AL-AINI Text book of Surgery

o Baily and Loves basics of surgery

o Current Text book of Surgery

o SCHWRTZ Principles of Surgery

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Wounds

WOUND: is a circumscribed injury which is caused by an external agent and it can

involve any tissue or organ.
It may be surgical or traumatic

Classification of the wounds

I- open wounds
1. Abrasions:
 An abrasion is scraping away of the superficial layers of the skin due to friction
with a hard rough surface.
 The wound is very painful due to exposure of the sensitive nerve endings.
 Abrasions require cleaning with a bland antiseptic and a non-adherent dressing.
 Fate: Good wound healing
2. Penetrating wound
 Caused by sharp pointed object
 These are caused by penetration of a pointed object as a knife.
 The wounds are deeper than long, so there is risk of vascular and or internal organ
injury

 The external opening is small and drainage is poor, thus encouraging infection.
 Wound healing is bad
3. Cut- incised wound
 Caused by Sharp object
 The wound is longer than deep, its edges are clean cut and regular and there is
no much tissue destruction.
 Healing is good. e.g. Surgical wound
4- Contused wound
 Caused by blunt trauma
 The edges are contused and irregular
 Bad healing process
5- Lacerated wound - Crush wound:

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 These are caused by severe trauma with blunt objects, as in motor car accidents
or falling from a height.
 Such wounds are irregular in shape, and the tissues are severely traumatized and
devascularized.
 They are usually heavily contaminated and so the risk of infection is high.
 Inflammatory edema will develop after a few hours and this will raise tension
inside the wound (especially if the wound is dosed) leading to secondary
ischaemia of the tissues
6. Missile wounds.
 These wounds are very serious as the bullet transmits its high kinetic energy to
the tissues.
 The kinetic energy of the missile is determined mainly by its velocity, and
secondly by its weight.
 high-velocity missile injuries (rifles) are much more serious than low-velocity
ones (pistols).
The tissues damage is the result of:
 Direct damage by the missile in its track.
 The Shock waves that precede the missile in its journey through the body.
 Temporary cavitational effect.
 If the missile strikes a bone, the fragments of shattered bone serve
as secondary missiles producing more damage

 Sometimes damage occurs in areas far away from the missile tract.

II- Closed wounds:

1. Contusions
 This is due to a trauma by a blunt object leading to extravasation of blood
through the injured capillaries.
 The injured area becomes painful and swollen.
 The contused area is at first bluish in colour due to the extravasated blood,
later the colour turns to brownish or green.
 Elevation of the contused area is advisable to minimize oedema

2. Hematoma:
 If the amount of bleeding is excessive, a haematoma forms.
 At first it is cystic, but it will clot within hours. Later, the hematoma will
liquefy.
 If a haematoma is small, it can be aspirated by a wide-bore needle, otherwise
it is evacuated by a surgical incision under aseptic precautions

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Classification of the wounds according to the bacterial

Contamination:

1- Clean wound (class I): in clean operation, with no infection –

risk of infection < 2 %.

2- Clean-contaminated wound (class II):

 Elective surgery into the gastrointestinal, urinary or respiratory tracts with no
significant spillage.
 Risk of infection 2-5 %.

3- Contaminated wound (class III):

 Open accidental wounds encountered within 4 hours.
 Gross spillage from the gastrointestinal tract.
 Septic operation  the microorganisms involved in the infection was in the
operation site before the operation,
 Acute accidental perforation, fistula, abscess
 Risk of infection 10 : 20 %

4- Heavily contaminated wound (dirty wound) (class IV):

 Traumatic wounds more than 4 hours.
 Purulent infection or necrotizing soft tissue infection.
 Perforated viscus accompanied by high degree of contamination.
 Risk of infection →up to 40%.
 Presence of foreign bodies or prosthetic material.
 Severe septic operation
 War wounds
 Gangrene, abcess, tissue necrosis

Phases of Wound Healing:

1. Inflammation phase:
 The damaged endothelial cells release cytokines (Histamine, serotonin,
and kinins cause vessel contraction, decrease in blood loss, and attract
neutrophils, the most abundant cells in the initial 24 hour.

2. Proliferative phase:
 The neutrophils remove cellular debris and release more cytokines acting

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as attracting agents for macrophages.

 Fibroblasts now migrate into the wound, and secrete collagen
New vessels formation occurs by 48 hours.
 The deposition of collagen and angiogenesis continues for up to 3 weeks.
 Myofibroblasts causes wound contraction
 Great increase in wound strength occurs during this phase.

3. Maturation phase and remodelling :

 Is the final phase and starts from the 3rd week and continues for up to 9
months.
 Wound contraction.
 This is where collagen maturation occurs, and the tensile strength
continues to increase up to 80% of normal tissue.

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Types of wound healing

1. Healing by primary intention: without any complications. Fibrin
cover the wound producing linear wound healing.
 This occurs where the wound edges have been closed.
 The closure can be with stitches, staples, or skin glue, or even with
tapes
 Used when there has been very little tissue loss.
 An example of wound healing by primary intention is a surgical clean
wound
2. Healing by secondary intention
 Used when there is considerable tissue loss, and in which the
edges cannot be brought together
 The wound show marked inflammation
 Large amount of granulation tissue filling the large defect.
 More fibrosis filling the gap and Wound contraction occurs
 It is liable for infection.
 The end result is ugly scar devoid of hair, sweat and sebaceous glands
3. Healing by tertiary intension:

 When a wound is intentionally kept open for 5 days to allow edema or

infection to resolve.
 At the end of this period if there are no signs of infection, delayed
primary sutures can be performed.
 These wound result in more scarring than wounds that heal by primary
intention but less than wounds that heal by secondary intention.

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Factors affects wound healing:

Local:
1. Infection
2. Foreign body: Chronic inflammation e.g plates, screws, mesh,…
3. Tissue Edema  elevated tissue pressure
4. Ischemia of the tissues as in chronic ischemia

Systemic:
1- Age: children and adults heal more quickly than the elderly
(scar tissue is less elastic).
2- D.M.: impairs healing, defective angiogenesis and increases rate of
infection
3- Presence of chronic diseases: chronic liver disease, as uraemia, jaundice, and
malignancy
4- Obesity: patients are at an increased risk of wound infection and slower healing
because adipose tissue usually has an inadequate blood supply.
5- States of malnutrition and vitamins ( A & C) and minerals deficiency
6- Smoking: limits the oxygen-carrying capacity of the blood.
7- Medications:
 Steroids decreases cell growth and blood supply respectively
 Chemotherapy
 Radiotherapy
 Prolonged use of antibiotics favors wound infection

Complications of wound healing:

I- Early complications:
 Seroma
 Hematoma
 Wound disruption and Wound dehiscence
 Superficial wound infection
 Deep wound infection

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II. Late complications:

 Hypertrophic scar
 Keloid formation
 Incisional hernia

Keloid and Hyperthrophic scar

1- The keloid
 Defined as an abnormal scar that grows beyond the boundaries of the
original site of skin wound (on healthy surrounding skin).
 They are florid lesions, grossly elevated, involve the normal surrounding skin
 Tender to touch, feel itchy and hot
 Treatment:
a. prevent delayed wound healing and wound infection
b. Small keloids (< 2 cm):
Intra-lesional injections with corticosteroids every 4- 6 weeks until
flattening occur.
c. Mechanical pressure by compression devices
Pressure may theoretically break up collagen bundles and soften the
keloid mass. Used for 6 months
d. Topical silicone gel sheets
e. Cryosurgery: The period required to achieve a significant
response, 2-10 sessions separated by 25 days.
f. LASER
g. Surgery: is associated with high recurrence rates

2- Hypertrophic scar:
 The hypertrophic scar is defined as a widened scar that does not
extend beyond the original boundaries of the wound
 Raised, initially red, do not involve the surrounding normal skin.
 Regress in size with time.
 Same treatment modalities as keloids
 Surgical treatment has good result.

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Keloid hypertrophic scar

Wound disruption and dehiscence: burst abdomen:

1) This affects about 2% of midline laparotomy wounds.

2) It is due to failure of wound closure technique.

3) It usually occurs between 7 and 10 days postoperatively.
4) It is manifested by sero-sanguinous discharge from the wound.
5) Sometimes the viscera is seen from the wound when complete dehiscence
occurs (burst abdomen).
6) The defect usually involves the whole wound.
7) Management:
 Sterile dressing to the wound,
 Fluid resuscitation
 Early return to theatre for re-suture under anaesthesia
……………………………………………………………………………………………….

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Management of Polytrauma

I-Primary survey

(I) Pre-hospital management:

1. Ensure patent airways + support the mandible forwards and suck any
secretions,F.B. and blood.

2. Control any apparent bleeding by compression, elevation... etc.

3. During transfer to the hospital avoid flexion of the spine which may leads to
dislocation in unstable spine injuries + cervical spine support.

4. Any wound is covered with sterile dressing

(II) Hospital care:

The American College of Surgeons developed the Advanced Trauma Life Support (ATLS)
which includes: primary and secondary surveys

 Primary survey
A: Air way maintenance.

B: Breathing.

C: Circulation → control bleeding + anti-shock measures.

D: Disability support any fractures + x-ray for fracture pelvis.

E: Exposure and Environment.

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(A) Airway maintenance:

1. Place the patient on his side and lower the head slightly to prevent aspiration.

2. Prevent backward falling off the tongue by an oropharyngeal airway.

3. Suck any secretion or blood in the mouth + proper oxygenation.

4. Tracheostomy or cricothyroidotomy if indicated.

5. In comatose patient → endotracheal tube and mechanical ventilation.

Indications of mechanical ventilation:

a. Respiratory rate > 45/min.

b. PO2 < 60mmHg.

c. Flail chest.

d. PCO> 45mmHg.

e. Respiratory center depression.

B- Breathing

- Proper chest examination to detect hemothorax, pneumothorax and flail chest with
immediate management to allow proper breathing.

- Correction of any type of pneumothorax (by insertion of intercostal tube) or

cardiac tamponade (needle pericardiocentesis).

- put chest tube when indicated.

C- Circulation
1- CONTROL HAEMORRHAGE whether external by direct compression or internal by
rapid diagnosis and exploration.

2- Management of hemorrhagic shock see shock

Central and peripheral lines are inserted - Ringer lactate solutions and blood
transfusion are started.
D- Disability
Common causes of neurological deficit related to trauma are (Head injury,
Hypoxia, Shock, Alcohol or Drug abuse).

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Neurological assessment:
A = ALERT
V = VOCAL STIMULI RESPONSE
P = PAIN ELICIT RESPONSE
U = UNRESPONSIVE

E) Environment:
 Clothes of the trauma victim are removed with large sharp scissors.

 Warmth using blankets to avoid hypothermia.

 Radiological assessment (after initial resuscitation)

 Plain x-ray for chest injuries and skeletal Injuries.

 History of any (AMPLE):

* Allergies.
* Medications.
* Past medical history
*Last meal (time).
*Events of injury.
 Insert of :
* Urethral catheter to monitor urine output unless there is evidence of
rupture urethra.
* Nasogastric tube to decompress the stomach preventing vomiting &
aspiration.

II-SECONDARY SURVAY

Assessment of all systems to detect all injuries.

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1. H eeding from orifices, CSF leak from nose or ear, fracture cervical spines,
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3. Abdomen to detect signs of intra-abdominal

haemorrhage (tenderness, rebound tenderness and
guarding rigidity)
4. Diagnostic peritoneal lavage (in blunt abdominal trauma in
comatosed patient or unexplained hypotension).
5. Limbs for vascular trauma, wounds or fractures.
6. Nervous assessment  pupils, Glasgow coma scale, motor and
sensory power assessment.

III-Investigations
1) Plain X-RAY SKULL and cervical spines for head trauma
2) C.T scan brain in unconscious patient
3) Chest X-RAY for thoracic injuries.
4) Abdominal U/S and CT for abdominal trauma and visceral injuries
5) Plain X-ray for suspected fractures
6) Lab.  CBC, LIVER AND RENAL functions

IV-Definite treatment:

1) Chest life threatening conditions  chest tube or thoracotomy as in

severe hemothorax, F.B. in chest or associated intra-thoracic injuries
2) Abdominal bleeding  rapid exploration and dealing with the
cause as splenectomy for rupture spleen.
3) Vascular injuries  ligation of small vessels and repair of big vessels
by re- anastomosis or grafting.
4) Fractures  reduction and fixation
5) Intracranial bleeding  evacuation in extradural or
subdural hematomas

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Principles of organ transplantation

A- Terminology of transplantation :
1- Autograft : Donor and Recipient same person
2- Isograft : Donor and Recipient identical twins ( NO rejection)
3- Allograft : Donor and Recipient are of same species but genetically different ( Human to
human )
4- Xenograft: Donor and recipient are of different species ( animal to human)

B- Immunity in transplantation :
The immune system discriminates between self and non-self-antigens and destroys the latter
whether a microbe, altered cell as tumour or a transplanted organ.
The Genetic identity of individuals is determined by certain glycoprotein molecules on the
surface of cells named Human Leucocyte antigens because they were first detected on the surface
of leucocytes.
There are 2 important types of HLA regarding transplantation:
1-Class I-HLA (A,B,C), present on the surface of all nucleated cells and platelets.
2-Calss II-HLA (DR, the most important for transplantation), present only in Antigen
presenting cells (APC) e.g. : macrophages and dendritic cells.
Foreign class I and class II antigens are capable of stimulating the recipient immune mechanism
and triggering lymphocytes sensitization starting rejection of the transplanted organ.

Steps of the rejection process:

HLA in the graft is processed by the antigen presenting cells of the Recipient.
The processed antigens are presented to the recipient T-cells which have special receptors for
antigens known as T-cell receptors.
The binding of the antigen to T-cell Receptor leads to the liberation of cytokines mainly IL-2 which
stimulates the entire cascade of T-cells , this leads to:
1-Activation of cytotoxic CD8 cells which destroy the graft.
2-Activation of B-cells which differentiate into plasma cells which secrete Allo-antigens that
attack antigens or graft cells.
3-Activation of Macrophages.

C-Types of Graft rejection: (Four types are Known)

1-Hyperacute rejection:
It leads to irreversible damage to the graft within minutes to hours after Reperfusion of the
transplanted organ.

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It is due to the presence of preformed antibodies against donor HLA or ABO blood group
antigens. These antibodies are present in the recipient due to sensitization from previous
transfusion, pregnancy, or transplantation.
This leads to damage of the endothelium with platelet activation , thrombosis and ischemic
damage.
If hyperacute rejection occurs, the graft must be removed. Hyperacute rejection can be prevented
by pre-transplant blood group matching and tissue typing cross matching.

2-Accelerated acute rejection:

This type of rejection is seen within the first few days after a transplant. It involves both cellular
and anti-body mediated injury.
It is likely when a recipient has been sensitized by previous exposure to antigens present in the
donor, resulting in an immunologic memory response.

3- Acute rejection:
This is the most common type. It can occur at any time, usually within the first six months post-
transplant, but up to many years later when doses of immunosuppressive drugs are reduced. It is
usually T-cell mediated, Clinically the manifestations are non-specific with fever, lethargy, pain,
and tenderness over the graft. Laboratory tests reveal deterioration of the graft function. A sure
diagnosis depends upon biopsy of the graft.

4- Chronic rejection:
It Develops slowly after months or more commonly years after transplantation. There is gradual
decline of graft function and, eventually , organ failure.
Biopsies show intimal hyperplasia of small and medium sized arteries , interstitial fibrosis, and
atrophy.
The cause is not clearly understood. Immune and non-immune factors may be involved. There is
no treatment that saves the Graft, A new one will be needed.

Minimizing Risk of rejection:

I-Histocompatibility testing:
Compatibility between donor and recipient immune systems is assessed before transplantation.
-ABO blood group matching
-HLA tissue typing. Recipient lymphocytes are tested to find out which HLA class-I and II
molecules are expressed.

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-HLA-antibody screening. Recipient serum is tested for antibodies targeted at non-self HLA
molecules, e.g., by mixing it with lymphocytes from a panel of HLA-typed donors.
-Tissue typing crossmatch, this is the final pre-transplant test when the above tests have
identified potentially compatible to determine if anti-donor HLA antibodies are present in
the recipient.

II-Immunosuppressive drugs :
Immunosuppressive drugs are used to prevent acute rejection and to reverse it when it happens.
Immunosuppressive therapy is divided into:
induction, maintenance, and withdrawal phases:
-Induction: starts during the transplantation procedure before the vascular clamps are removed
to allow reperfusion of the allograft. Intravenous steroids often combined with a biological
antibody as anti-thymocytic globulin are given and continued for several days to few weeks.
-Maintenance: starts after graft implantation. In most cases this consists of triple oral therapy
combining a calcineurin inhibitor, anti-proliferative and steroids to produce a balanced immune-
defiant state which aims to prevent rejection while minimizing the risk of infection and drug
toxicity.
-In withdrawal phase: all drug doses are gradually reduced as the risk of acute rejection
diminishes.
D- Sources of organs for transplantation:
Live donor : as in kidney or liver transplantation
Advantages : better pre-operative preparation, shorter ischemia time
Disadvantages : Small but significant mortality and morbidity risk for healthy Donor.

Cadaver Donors : ( Brain stem dead donors)

Advantages: Avoid complications to living healthy donor and multiple organs can be taken from
one cadaver and given to multiple patients.

The organ is removed from a patient with proved brain death, victims of intracranial haemorrhage
or head injury are the main source of donor organs.

Diagnosis of brain stem death:

1-Flat EEG
2-Patient must be in apnoeic coma, unresponsive and dependant on mechanical ventilation.
3-No pupillary response to light, direct or consensual.
4-No corneal reflex
5-Absent cough reflex via bronchial stimulation.
6-Absent vestibule-ocular reflex:
No eye movement upon injection of 50 ml of ice-cold water into each external auditory meatus

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All the previous tests should be repeated after 24 hours and should be
done by a separate physician not involved in the transplant procedure.

E- Specific organ transplantation :

1. Renal transplantation:

Indications : All cases of end stage renal disease which may be due to different
conditions as Diabetes mellitus , Hypertension, Lupus nephritis, obstructive
uropathy. Etc.
Technique : Graft placed Extra peritoneal in the iliac fossa especially the Right
iliac fossa
Anastomosis of Renal artery to external iliac or internal iliac artery
Anastomosis of Renal vein to External iliac vein
Anastomosis of ureter to Bladder under mucosal tunnel
Prognosis : Excellent ( 5 year : 90 % with living donor)
Complications ( Apart from rejection)
a-Renal allograft non-function: early poor function is usually due to reversible
acute tubular necrosis secondary to reperfusion injury.
b-Lymphocele from lymphatic leak in retroperitoneum.
C-Graft vessel thrombosis resulting in sudden cessation of urine output.
d-Urine leak : usually due to leaking ureterovesical anastomosis.

2. Liver transplantation:

Indications: All cases of end stage liver disease due to:

Various types of cirrhosis (alcoholic, post viral, biliary. Etc), biliary atresia which is
the leading indication in children, chronic viral hepatitis, sclerosing cholangitis and
Budd Chiari Syndrome.
Technique: Graft usually taken from Right lobe and placed in the same position
(orthotopic transplantation)
Anastomosis of vessels and bile ducts to their corresponding

Prognosis: Very Good ( 5 year : 50 % with living donor )

Complications:
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a-Primary Non-function (1%): Graft fails to function in presence of

patent vascular anastomosis.
b-Hepatic artery thrombosis.
c-Portal vein stenosis or thrombosis.
d-Biliary stricture.

3. Pancreatic transplantation:

Indications : Type 1 DM + Renal failure ( combined renal and pancreatic)

Patients with previous renal transplantation suffering from
sever DM endangering grafted kidney

Technique : 2 types : A- Vascularized Pancreatic transplantation (whole or

segment)
B- Islets of Langerhans transplantation ( still under
study but is very promising)
Prognosis : Good ( 1 year : 45 % with living Donor)
Complications:
Technical complications as arterial or venous occlusion or duct leakage.
Rejection
Pancreatitis
Complications of immunosuppression

4. Bone marrow Transplantation :

Indications : e.g. : Aplastic Anaemia , some types of Leukaemia
Technique : I- Suppression of the Recipients immune system by Chemotherapy
and whole body Irradiation to inhibit Rejection.
II-Bone Marrow of donor is aspirated from iliac crest and then
filtered and heparinized then infused intravenously to the
recipient
Prognosis : Very Good

5. Intestinal transplantation:

Indications : Intestinal failure ( defined as inability of the patient’s intestine to

sustain his nutritional needs) when Total parenteral Nutrition (TPN) can no longer
be used.
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Common causes of intestinal Failure :

I-Adults: Massive small intestinal resection due to mesenteric vascular occlusion ,
tumours, trauma , Crohn’s or radiation enteritis.
II-Children : Massive small intestinal resection because of gastroenteritis , midgut
volvulus, intestinal atresia or necrotizing enterocolitis.
TPN failure may be confronted in:
a-TPN associated severe liver disease
b-Loss of central venous access due to stenosis or thrombosis
c-Recurrent central venous catheter infection.

6. Heart and lung transplantation:

Indications for Heart transplantation: Ischemic cardiomyopathy beyond

revascularization (45%), Idiopathic Cardiomyopathy 55%
Indications for Single lung transplantation: Emphysema or pulmonary
fibrosis.
Indications for combined heart and lung transplantation : Damage of
both organs as with cystic fibrosis and patients with primary pulmonary
hypertension with severe left ventricular dysfunction.

Complications: 1-Complications of immunosuppression

2-Graft Rejection
3-Graft atherosclerosis

Hemostatic disorders in surgery

Proper hemostasis depends on:

1. Healthy vessel wall
2. Adequate number and proper functioning platelets
3. Adequate clotting factors

What causes bleeding disorders?

I. Vessel wall defect
II. Platelet defect
III. Clotting factors defects

I-Vessel wall defect: Vitamin C deficiency

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II- Platelet defects: Thrombocytopenia:

 Hypersplenism in portal hypertension with liver cirrhosis or fibrosis
 Drug induced thrombocytopenia (Thiazides – alcohol)
 Bone marrow depression as with chemotherapy, radiotherapy and some
viruses as AIDS
 ITP (Idiopathic Thrombocytopenic Purpura)
 ASPRIN – NSAIDS produce defective platelet function.

III- Clotting factors deficiency:

 Hemophilia A
o The most common
o Due to deficiency of factor VIII (congenital)
o Lab results: prolonged PTT
 Hemophilia B
o Due to deficiency of factor IX (congenital)
o Lab: prolonged PTT
 Other causes:
o Intake of heparin or oral anticoagulant
o Chronic liver disease decreases synthesis of clotting
factors due to deficiency of vitamin K absorption
o Mal-absorption: decreases vitamin K absorption.

Investigations for bleeding disorders:

1) Bleeding time (n = 2 – 8 min.)  measure for number and function of

platelets 2) Platelet count (n = 150,000 – 400,000)
3) Prothrombin time (PT): (n = 11 – 14 seconds) measure extrinsic
pathway of clotting
4) PTT: Measure intrinsic pathway (n = 25 -35 sc)
5) Measurements of clotting factors in cases of Hemophilias.

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Hemorrhage
Causes of hemorrhage:

1. Traumatic Injury
These include: Abrasion, Hematoma, Laceration, Incision, Puncture, Wound,
Contusion, Crushing Injuries
2. Medical condition; Blood can escape from blood vessels as a result:
A- Intravascular changes (e.g. ↑ blood pressure, ↓ clotting factors)
B- Intramural changes - changes arising within the walls of blood vessels
(e.g. aneurysms, vasculitis, V.V, oesophageal Varices)

Classification of bleeding:
I- A- Internal B- External

II- 1- Arterial 2- Venous 3- Capillary

A- Arterial bleeding:
1. Most serious
2. bright red blood,
3. spurting as a jet which rises and falls with the pulse
4. Less liable to clot
5. Large amount of blood can be lost in short time

B- Venous bleeding:
1. Dark red
2. Steady and copious flow.
3. Blood loss is rapid when large veins are opened
4. Easier control than arterial

C- Capillary bleeding

2. Bright red,
3. In the form of rapid ooze.
4. If continuing for many hours, blood loss can become serious, as in haemophilia
5. Usually not serious and easily controlled
6. Can clot and stop by itself

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Clinical picture of hemorrhage:

 History of the cause as trauma or bleeding tendency
 Sense of Coldness
 Thirst sensation
 Anxiety and irritability
 Evidence of external bleeding
 Increasing pallor
 Moist sweaty skin.
 Decreasing blood pressure,
 Increasing heart and respiratory rates
 Delayed capillary refill,
 Decreasing urine volume

Classes of hemorrhage:

Class I II III IV

Blood Up to 750-1500 1500-2000 >2000

loss(ml) 750

Up to 15 % 15-30 % 30-40 % > 40 %

Pulse rate <100 100-120 120-140 >140

Blood Normal Normal Decreased Decreased

pressure

Respiratory 14-20 20-30 30-35 > 35

rate

Urine output >30 20-30 5-15 Negligible

(ml/hr)

Fluid Crystalloid Crystalloid Crystalloid Crystalloid

replacement and and blood
blood

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Management of hemorrhage:
The goals of emergency management are to:
1- Control the bleeding,
2- Maintain adequate circulating blood volume for tissue
oxygenation 3- Prevent shock

A- Control external bleeding:

If a patient is hemorrhaging externally (eg, from a wound),

1. Direct, firm pressure is applied over the bleeding area or the involved
artery at a site that is proximal to the wound
2. A firm pressure dressing is applied, and the injured part is elevated to stop
venous and capillary bleeding if possible.

B- Management of internal bleeding

Surgical intervention accordingly

Fluids replacement to maintain tissues perfusion and shock prevention:

1- Two large cannulas are inserted to provide a means for fluid and blood
replacement
2- Blood samples are obtained for cross-matching
3- Types of fluids:
a) Isotonic electrolyte solutions (eg, lactated Ringer’s, normal saline),
b) Colloids
c) Blood component therapy
……………………………………………………………………………………………………………….
Complications of blood transfusion:

1. Fever: pyrogenic reaction

2. Allergic reactions: itching and macular or papular rash. it’s likely to occur during
the transfusion or very shortly after.
3. Acute hemolytic reaction: This complication is rare, but is a medical
emergency. Patient gets symptoms like fever, rigors, nausea, and chest pain. The
urine might turn dark (indirect hyper-bilirubinemia).

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4. Anaphylactic reaction: severe form of allergy.This happens within minutes of

starting a transfusion and may be life-threatening. Patient experiences flushing and
swelling of the face, edema of the larynx, dyspnea, and hypotension.

5. Blood-borne Infections:
 HIV
 Hepatitis B and C viruses
 CMV
 Malaria
6. Hemochromatosis (iron overload): due to repeated blood transfusion
7. Acute Lung Injury: is a condition of severe pulmonary insufficiency following
blood transfusion. Developing within 4 hours of transfusion.
8. Volume over-load: due to massive transfusion picture of CHF.
9. DIC: Due to repeated blood transfusion
10. Hypothermia - Air embolism – citrate toxicity, Hypo, or hyperkalemia.
………………………………………………………………………………………………………

Shock
It means inadequate tissue perfusion that leads to impaired cellular
metabolism

Hypovolemic shock
It means shock due to diminished blood volume

Causes:
1- Loss of whole blood components as in Internal or external hemorrhage.
2- Loss of plasma as in burns, pancreatitis and peritonitis.
3- Loss of fluids and electrolytes as in severe vomiting and diarrhea.
Pathophysiology:
1- Sympathetic and adrenal gland stimulation  to shift blood from less
critical tissues as skin to more important tissues as heart and brain. Progressive
pallor and coldness

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2- Microcirculatory changes:
a) Constriction of pre-capillary sphincters  decreases tissue perfusion 
anaerobic metabolism  lactic acidosis  Metabolic acidosis
b) Disseminated intravascular coagulopathy (DIC)
c) Capillary leakage  loss of intravascular fluids to interstitial spaces 
more hypovolemic shock.
3- Decreased myocardial contractility
4- GIT ischemia  mucosal ulceration (stress ulcers) and bleeding.
5- Renal impairment and later pre-renal failure.

Clinical picture of hypovolemic shock:

 Evidence of the cause of shock as hemorrhage burn

 Patient feels cold and thirsty
 Cold skin and increasing pallor
 Weakness and loss of consciousness
 Tachycardia, hypotension, subnormal temperature and tachypnea.
 Clinical evidence of the cause (as signs and symptoms of intra-abdominal hemorrhage)

Management of shocked patient

1- Arrest blood loss:

a) Stop external bleeding by packing or compression
b) Stop internal bleeding by dealing with injured organ
(e.g. splenectomy in rupture spleen - repair of vascular injury – ligation of varices)
2- Restore volume loss guided by CVP and urine output
 Fluid replacement starting by lactated ringer solution used in class II
hemorrhage
 Blood transfusion after cross matching in case of marked hemorrhage as in class
III and IV ( hematocrit value less than 30 is an indication for blood transfusion).
 Colloid solution as dextran or plasma in case of insufficient blood or major burn

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3- Monitoring of shocked patient:

 Pulse, blood pressure and temperature, important to determine
success of replacement and severity of shock
 Monitoring of conscious level
 Insert urinary catheter to monitor urine output and adjust fluid
replacement. Adequate urine output indicates good
resuscitation.
 Insert central venous line to monitor amount of fluids given to the
patient and prevent volume overload
 Insert nasogastric tube to decompress the stomach
 ECG monitoring
 Repeated CBC to evaluate the hematocrit value and Hb level.
 Renal function tests to evaluate kidney perfusion.
 ABG to monitor PO2, PCO2 and pH

4- Oxygen therapy to improve PO2 and pH: oxygen is given for class II, III, & IV
5- Inotropic drugs as dopamine in severe cases of shock to increase
myocardial contractility.
6- Analgesic for pain as pain aggravates shock state.

Irreversible shock:
 Failure of improvement of hypovolemic shock despite adequate volume
replacement.
 Complete vascular collapse with persistent hypotension with evidence of multiple
organ failure.

Causes: 1- prolonged duration of hemorrhage

2- Massive hemorrhage with delayed
management. 3- Severe trauma with multi-organ
damage
4- Major burns
5- Old age - pre-existing cardiovascular illness
………………………………………………………………………………………………
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Septic shock
It is type of shock results from severe systemic infection

Aetiology:
I- Causative organisms:
a) gram –ve bacilli is the commonest.
b) Staphylococci
c) Candida
II- common sources:
a) Generalized peritonitis
b) Cholangitis
c) Genitourinary tract infection
III- Predisposing factors:
D.M , old age, immune-compromized….
Pathophysiology:
1- Endotoxins released from the gram –ve bacteria  release mediators from
macrophages  V.D. of the capillary beds and A.V. shunts  pooling of the
blood in the interstitial spaces  decreases peripheral resistance 
hypotension and tissues hypoxia.
2- DIC
3- Low PH (metabolic
acidosis)

4- Low PO2 (Hypoxia)

5- Low PCO2  due to hyperventilation

Clinical picture:

1- Early signs = hyperdynamic septic shock:

Fever – Warm flushed skin – Confusion – Hyperventilation Tachycardia.

2- Late signs = hypodynamic = cold septic shock:

Same as picture of hypovolemic shock
Complications of septic shock:
1- Myocardial depression
2- ARDS  Impaired gas exchange in the lungs  more hypoxia  respiratory
failure.
30
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3- Brain hypoxia and ischemia confusion and coma

4- Acute tubular necrosis of the kidney leads to renal failure

31
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5- Stress ulceration of the GIT from mucosal ischemia  GIT bleeding.

6- Hepatic cell necrosis  jaundice and liver failure.
Investigations:
1- CBC  leukocytosis
2- Blood culture to isolate the causative organism and for sensitivity.
3- Increased lactate level in the blood & decrease Na HCO3(metabolic acidosis)
4- Investigations to detect the cause of sepsis

Treatment
1) Monitoring of shocked patient  as before (look hypovolemic shock)
2) Cardiac , renal, liver and respiratory support
 Adequate volume replacement and dopamine administration
improve renal blood flow.
3) Treatment of the cause of sepsis  using aggressive antibiotic therapy and
better according to C/S

 Eradication of sepsis, e.g., drainage of a huge abscess or peritonitis, or

resection of gangrenous bowel.

 Aggressive treatment with multiple and broad-spectrum antibiotics is

started immediately without waiting for the results of culture and
sensitivity. The antibiotic choice is based on the possible suspected
organisms which in most cases are Gram-negative bacilli.

 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

Prognosis: mortality rates ranges from 25 - 90%

………………………………………………………………………………………………………………………………….

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Anaphylactic Shock
 This type of shock may follow administration of:
 Antibiotics especially penicillins
 Anaesthetics
 Intravenous sera and dextrans adminstration.
 The antigen unites with the antibodies leading to the release of large amounts of
histamine.
 The patient develops bronchospasm, laryngeal oedema, and respiratory distress.
 Massive vasodilatation occurs and leads to hypotension.
Treatment:
1. Intravenous crystalloid infusion.
2. Intravenous hydrocortisona
3. Anti-histaminics
4. Endotracheal intubation may be needed if laryngeal oedema and stridor are developing.

…………………………………………………………………………………………………………….

Neurogenic Shock
 In neurogenic shock there is paralysis of the vasomotor fibres leading to
peripheral pooling of blood and inadequate venous return. It may be due to:

1- Vasovagal attack.
 This is the simplest type of neurogenic shock.
 It is due to hearing bad news or watching an unpleasant event.
 It may also follow severe painful stimuli
 Two factors operate to produce the abrupt collapse:
i. The first is extensive vasodilatation in the splanchnic area causing a sudden
reduction in the peripheral resistance, a temporary loss of venous return
and a sudden fall in the blood supply to the vital centers.
ii. The second factor is excessive vagal stimulation of the heart which causes
bradycardia. The mere act of falling to the
ground as the individual faints, assists the venous return and helps
recovery.
2- Sudden extreme vasodilatation also occurs in patients suffering underwent a spinal
anaesthesia or deep general anaesthesia.
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Clinically:
 Hypotension,
 Bradycardia
 Warm dry skin.
Treatment
1. The patient should lie flat, elevation of the legs helps to increase the
venous return.
2. I.V. crystalloid solution as Ringers lactate.
3. Vasopressors may be given.
………………………………………………………………………………………………………………………..

Fluid and Electrolyte Balances in

Surgical Patients
● Electrolyte Distribution (meq/liter)

E.C. I.C. Function

• Sodium 142 10 * fluid balance, osmotic pressure

• Potassium 5 160 * Neuromuscular excitability &

acid- base balance

• Calcium 5 * bones, blood clotting

• Chloride 105 2 * fluid balance, osmotic pressure

• Bicarbonate- 24 8 * acid-base balance

Fluid disorders = Volume changes

A. hypovolemia / Dehydration

B. hypervolemia / Overhydration

34
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A. hypovolemia / Dehydration

Causes

• Hot weather-sweating is increased

• Fever-sweating + tachypnea
• Diarrhea -water is lost in the stool
• Vomiting - water is lost in the vomit
• Diabetes - the body produces more urine
• Kidney disorders- kidneys unable to concentrate urine as needed
• Diuretics- increase the of water and salt excretion

Clinical features

General

• Dry skin
• Tachycardia
• low blood pressure
• Low urine out put ( The kidneys try to conserve urine)
• Sunken eyes
Treatment: Involves replacing lost fluids.

………………………………………………………………………………………………………………

Disorders Of Electrolytes Balance

Hyponatremia
Causes:
• inadequate sodium intake in the diet,
• Excreting too much salt (in sweat or urine),
• Excess loss in recurrent severe vomiting as in gastric outlet obstruction
• Diuretics  may cause the kidneys to excrete more sodium than water, resulting in
a low sodium level
• poorly controlled diabetes
• heart failure,
• liver failure,
• Renal disorders
• High ADH levels

35
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• Over-hydration

36
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When a person drinks a lot of water without consuming enough salt (sodium
-
chloride), typically during hot weather when a person also sweats more.
- When large amounts of fluids that do not contain enough sodium are given
intravenously.
Symptoms:

Confusion, drowsiness, muscle weakness, and seizures

Treatment:

A low sodium level is restored to a normal by giving sodium and water Orally or
intravenously (sodium chloride solution)

--------------------------------------------------------------------------------------------------------

Hypernatremia
Causes: Dehydration

● Excessive loss of fluid without loss of salt

● Addition of excessive salt without proportionate fluid volume
Symptoms

● Typically  thirst is the first symptom.

● Weakness and sluggishness.
● A very high sodium level can cause confusion, paralysis, coma,
and Seizures
Treatment

1- Oral plain fluids - If the sodium level is slightly high.

2- Intravenous fluids - If the sodium level is very high.
Once the body's fluids are replaced, the high level of sodium returns to a normal
level.
…………………………………………………………………………………………………….
Hypokalemia
Causes
• Diarrhea
• Vomiting for a long time as in cases of pyloric obstruction.
• Entero-cutaneos fistulae
• Use of Diuretics
• Use of digoxin

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Symptoms:
A- Mild Hypokalemia  no symptoms.
B- Moderate Hypokalemia  fatigue, confusion, and muscle weakness & cramps
C- Severe Hypokalemia  Muscle paralysis and arrhythmias.
D- ECG changes

Treatment
● Potassium supplements by mouth as a tablet or liquid or eating foods rich
in potassium.
● Potassium-sparing diuretic: In People who use diuretics  reduces the
amount of potassium excreted .
● IV- K supplement in surgical cases
………………………………………………………………………………………………………………
Hyperkalemia
A high potassium level (hyperkalemia) is much more dangerous than a low
potassium level.
Causes
1- Renal failure

2- Diuretics as spironolactone and angiotensin-converting enzyme (ACE)

inhibitors (used in hypertension) reduce the amount of potassium
excreted by the kidneys.

Symptoms:
• Arrhythmia and ECG changes

Treatment:

• Stop eating potassium-rich foods and stop taking potassium supplements.

• Drugs that cause the body to excrete excess potassium, such as diuretics.

Frusemide: prevents potassium from being re-absorbed are given to reduce

the amount of potassium in the body.
………………………………………………………………………………………………………………………………..

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Hypocalcemia
Causes:
• A widespread severe sepsis.
• Hypo-parathyroidism: if the parathyroid glands are removed or damaged during
neck surgery.
• Deficiency of vitamin D. [Vitamin D helps the body absorb calcium]
• Certain drugs, such as the anticonvulsants (phenytoin).
• Sever pancreatitis, can result in a low calcium level.
Clinical Features:
• Weakness, numbness in the hands or feet.
• Confusion or convulsions
• Muscle twitching

• Tetany:
● Carpo-pedal spasm of the hand

● Chevostec sign of the face

Treatment:
● involves taking calcium supplements by mouth or I/V
● Vitamin D ● Treat the Cause
--------------------------------------------------------------------------------------------------------

Hypercalcemia
Causes:

a- Excessive intake – milk alkali syndrome

b- Excessive release of calcium into the blood:
● bone metastases
● Paget's disease.
● Sarcoidosis
● Hyper-parathyroidism in hyperplasia or adenoma

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Symptoms;

1- A slight increase in the calcium level may not cause any symptoms.

2- A very high level can result in dehydration because it causes the kidneys

to excrete more water.

3-A very high level can also cause loss of appetite, nausea, vomiting, and
confusion.

Treatment:
1- Intravenous fluids
2- Steroids
3- Calcitonin and bisphosphonates - given intravenously for short periods.
They decrease the amount of bone being broken down and decrease calcium
released into the blood.
4- Treat the cause of the high calcium level.
Tumor of parathyroid gland,  surgery
………………………………………………………………………………………………………………………………………………..
Acid-Base Balance
An important property of blood is its degree of acidity or alkalinity (blood PH).
What Is the Blood pH?
 Acidity and alkalinity are expressed on the pH scale, which ranges from 0 (strongly acidic) to 14
(strongly basic, or alkaline). A pH of 7.0, in the middle of this scale, is neutral. Blood is normally
slightly basic, with a pH range of 7.35 to 7.45. To function properly, the body maintains the pH
of blood close to 7.40.

 Acidosis and Alkalosis: There are two abnormalities of acid-base balance.

 Acidosis: The blood has too much acid (or too little base), resulting in a decrease in blood pH.
 Alkalosis: The blood has too much base (or too little acid), resulting in an increase in blood pH.
 Acidosis and alkalosis are not diseases but rather are the result of a wide variety of disorders.
 Acidosis and alkalosis are categorized as metabolic or respiratory, depending on their primary
cause.
 The blood's acid-base balance is precisely controlled, because even a minor deviation from the

40
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normal range can severely affect many organs.

 The body uses different mechanisms to control the blood's acid-base balance which are :
Role of the Lungs:
 One of the mechanisms which the body uses to control blood pH involves the release of carbon
dioxide from the lungs. Carbon dioxide, which is mildly acidic, is a waste product of the
metabolism of oxygen (which all cells need) and, as such, is constantly produced by cells.

 As with all waste products, carbon dioxide gets excreted into the blood. The blood carries carbon
dioxide to the lungs, where it is exhaled. As carbon dioxide accumulates in the blood, the pH of the
blood decreases (acidity increases).

 The brain regulates the amount of carbon dioxide that is exhaled by controlling the speed and depth
of breathing.

 The amount of carbon dioxide exhaled, and consequently the pH of the blood, increases as breathing
becomes faster and deeper. By adjusting the speed and depth of breathing, the brain and lungs are
able to regulate the blood pH minute by minute.

 Respiratory acidosis and respiratory alkalosis are caused primarily by changes in carbon dioxide
exhalation due to lung or breathing disorders.

Role of the Kidneys:

 The kidneys are also able to affect blood pH by excreting excess acids or bases. The kidneys have some
ability to alter the amount of acid or base that is excreted, but because the kidneys make these
adjustments more slowly than the lungs do, this compensation generally takes several days.

 Metabolic acidosis and metabolic alkalosis are caused by an imbalance in the production of acids or
bases and their excretion by the kidneys.

Buffer Systems:
 Another mechanism for controlling blood pH involves the use of buffer systems (naturally occurring
weak acids and weak bases), which guard against sudden shifts in acidity and alkalinity.

 The most important pH buffer system in the blood involves carbonic acid (a weak acid formed from
the carbon dioxide dissolved in blood) and bicarbonate ions (the corresponding weak base).

41
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Acidosis
It is excessive blood acidity.
Major Causes of Metabolic Acidosis
1. Diabetic ketoacidosis (buildup of ketones)
2. Drugs and substances such as acetazolamide, alcohol, aspirin, and iron
3. Lactic acidosis (buildup of lactic acid as occurs in shock)
4. Loss of bases, such as bicarbonate, through the digestive tract from diarrhea, an
ileostomy, or a colostomy
5. Kidney failure
6. Poisons such as carbon monoxide, cyanide, ethylene glycol, and methanol.
7. Renal tubular acidosis (a form of kidney malfunction).
 If an increase in acid overcomes the body's pH buffering systems, the blood will become acidic.
 As blood pH drops, the parts of the brain that regulate breathing are stimulated to produce faster
and deeper breathing. Breathing faster and deeper increases the amount of carbon dioxide
exhaled.
 The kidneys also try to compensate by excreting more acid in the urine, failure of the kidney
results in metabolic acidosis.

Respiratory acidosis:
develops when the lungs do not expel carbon dioxide
Major causes of Respiratory acidosis:
1. Lung disorders, such as emphysema, chronic bronchitis, severe asthma, pneumonia, or
pulmonary edema .
2. Sleep-disordered breathing
3. Diseases of the nerves or muscles of the chest that impair breathing, such as Guillain-Barré
syndrome or amyotrophic lateral sclerosis
4. Overdose of drugs such as alcohol, opioids, and strong sedatives

Symptoms
 People with mild metabolic acidosis may have no symptoms but usually experience nausea,
vomiting, and fatigue.

42
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 Breathing becomes deeper and slightly faster (as the body tries to correct the acidosis by
expelling more carbon dioxide).
 As the acidosis worsens, people begin to feel extremely weak and drowsy and may feel
confused and increasingly nauseated. Eventually, blood pressure can fall, leading to shock, coma,
and death.

 The first symptoms of respiratory acidosis may be headache and drowsiness.

 Drowsiness may progress to stupor and coma.
 Stupor and coma can develop within moments if breathing stops or is severely impaired .
Diagnosis
 The diagnosis of acidosis generally requires the measurement of blood pH in a sample of arterial
blood, usually taken from the radial artery in the wrist.

 Arterial blood is used because venous blood contains high levels of bicarbonate and thus is
generally not as accurate a measure of the body's pH status.
Treatment

 The treatment of metabolic acidosis depends primarily on the cause.

 For instance, treatment may be needed to control diabetes with insulin or to remove the toxic
substance from the blood in cases of poisoning.

 The treatment of respiratory acidosis aims at improving the function of the lungs. Drugs that open
the airways (bronchodilators, such as albuterol) may help people who have lung diseases such as
asthma and emphysema.

 Acidosis may also be treated directly. If the acidosis is mild, the administration of intravenous fluids
may be all that is needed.

 Rarely, when acidosis is very severe, bicarbonate may be given intravenously.

Alkalosis
 Alkalosis is excessive blood alkalinity caused by an overabundance of bicarbonate in the blood or a
loss of acid from the blood (metabolic alkalosis), or by a low level of carbon dioxide in the blood that
results from rapid or deep breathing (respiratory alkalosis).

 Major causes of metabolic alkalosis

1. Loss of acid from vomiting or drainage of the stomach
2. Overactive adrenal gland (Cushing's syndrome)
3. Use of diuretics (thiazides, furosemide, ethacrynic acid).
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Major causes of Respiratory alkalosis

1. Anxiety
2. Aspirin overdose (early stages)
3. Fever
4. Low levels of oxygen in the blood, Pain.
Symptoms and Diagnosis
 Alkalosis may cause irritability, muscle twitching, muscle cramps, or no symptoms at all. If the
alkalosis is severe, prolonged contraction and spasms of muscles (tetany) can develop.
 A sample of blood usually taken from an artery shows that the blood is alkaline.
Treatment
 Treat metabolic alkalosis by replacing water and electrolytes (sodium and potassium) while
treating the cause.
 Occasionally, when metabolic alkalosis is very severe, dilute acid is given intravenously.
 With respiratory alkalosis, usually the only treatment needed is slowing down the rate of
breathing.

 When respiratory alkalosis is caused by anxiety, a conscious effort to slow breathing may make
the condition disappear.
 If pain is causing the person to breathe rapidly, relieving the pain usually improve alkalosis.
 Breathing into a paper (not a plastic) bag may help raise the carbon dioxide level in the blood
as the person breathes carbon dioxide back in after breathing it out
………………………………………………………………………………………………………………
…………………………………………………………………………………………………………………..

Surgical Infections
Introduction:

 Wound and skin infections are the growth and spread of microbes, usually bacteria,
within the skin or a break or wound in the skin. These infections trigger the body's
immune system and cause inflammation and tissue damage within the skin or wound
and slow the healing process. The infection may spread to the deeper tissues beneath the
skin. This spreading infection is called cellulitis.

 The most common causative organisms associated with wound infections include
Staphylococcus aureus/MRSA, Streptococcus pyogenes, Enterococci and Pseudomonas
aeruginosa. Anaerobic bacteria such as Bacteroides and Clostridium species may cause
44
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deeper wound infections.

 Surgical site infections (SSIs) are defined as infections occurring up to 30 days after
surgery (or up to one year after surgery in patients receiving implants) and affecting
either the incision or deep tissue at the operation site. The responsible pathogens
originate from the patient's endogenous flora.

Staphylococci

 Staphylococci are Gram-positive spherical bacteria that occur in grape like-clusters and
are catalase positive.

 S. aureus and S. epidermidis are the major components of the normal flora of skin ,
nose and mucous membranes.

 Staphylococcus aureus :It causes a wide range of suppurative infections (pus-forming)

and toxic shock syndrome .They are Gram-positive spherical cocci, arranged in clusters
(grape like) non-motile, non-spore forming,facultative anaerobes .

 Virulence factors:

 Coagulase is an extracellular enzyme which which enables the enzyme protease to

convert fibrinogen to fibrin, this results in clotting of the blood. Coagulase is a
marker for identifying S. aureus. The bacteria protect themselves from phagocytic
and immune defenses by causing localized lesion.

 Surface proteins that promote adherence to host cell

 Production of extracellular enzymes and toxins that promote bacterial spread in

tissues mainly leukocidin, hyaluronidase, proteases, lipase and deoxyribonuclease
(DNase).

 Inhibition of phagocytic engulfment by protein A, catalase production and

capsule production

 Exotoxins that damage host tissues: several different types of protein toxins are
responsible for symptoms during infections

 Toxins with superantigen activity which stimulate T cells non-specifically and

release cytokines in large amounts, causing the symptoms of toxic shock

 Exfoliative toxins (ET): Responsible for scalding skin syndrome. It causes

separation within the epidermis.
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Resistance of S. aureus to antimicrobial drugs:

 Hospital strains of S. aureus are resistant to a variety of antibiotics except vancomycin.

The term MRSA refers to Methicillin (or multiple) resistant S.aureus. S.aureus strains
develop resistance to antibiotics through different mechanisms either by mutation or
production of beta lactamase enzyme.

 Resistance to antiseptics and disinfectants which help its spread in hospital environment.

Pathogenesis :
 S. aureus causes a variety of suppurative infections and toxin mediated diseases in
humans.

 Pyogenic diseases include :

1. Skin infections are very common e.g abscess ,severe necrotizing skin and soft
tissue infections are caused by MRSA strains.
2. Hospital acquired (nosocomial) infections: S. aureus is one of the major causes
of surgical wounds .

3. Septicemia: can originate from localized lesion especially wound infection.

 Source of infection: either endogenous from skin and nasal normal flora or exogenous
by contact .

Laboratory diagnosis: Specimen : pus.

1. Direct microscopic examination: Gram positive cocci in grape like clusters.
2. Culture: on blood agar: complete (beta) hemolysis.
3. Catalase test is an important test to discriminate between Staphylococci
and Streptococcus species
4. Typing of S .aureus is done for epidemiologic puposes, in hospital wound
infections outbreaks. This could be achieved by phage typing, plasmid analysis, PCR.

………………………………………………………………………………………………………………………
Streptococcus
 Streptococcus pyogenes is one of the most important human pathogen in
nose and throat .
 Group A Streptococci typically have a capsule composed of hyaluronic acid and
exhibit beta hemolysis on blood agar.

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 They are catalase negative. Streptococcus pyogenes is responsible of pyogenic

infections, toxic and immunological diseases.

Streptococcus virulence factors:

1- Adherence (colonization) surface macromolecules they include M protein

2- Enhancement of spread in tissues:
a. Hyaluronidase or spreading factor: hydrolyses hyaluronic acid in host tissues.

b. Streptokinase: activates plasminogen to form plasmin cause lyses of fibrin in clots and
thrombi.

3- Evasion of phagocytosis by capsule production , leukocidins ,streptolysin and nucleases.

4- Production of exotoxins and other systemic effects such as
a- Pyogenic Toxin A responsible for streptococcal toxic shock syndrome
b- Exotoxin B: is a protease produced in large amounts that rapidly destroy
tissue causing necrotizing fasciitis.

Pathogenesis: Streptococcus pyogenes one of the causes of suppurative and toxigenic diseases.

Source of infection: endogenous or exogenous

Suppurative diseases i.e. active infections associated with production of pus, occur skin,
and systemically.
1- Skin: could be in the form of
a. Cellulitis infection in subcutaneous tissues
b. Erysipelas: Acute superficial cellulitis of skin with lymphatic involvement;
face and lower extremities. There is fever and systemic toxicity.
c. Necrotizing fasciitis involves infection of the fascia and may proceed
rapidly to underlying muscle causing severe tissue destruction.
The organisms causing this diseases are known as flesh-eating bacteria.
2- Bacteremia: bacteria in the blood with mortality 40% or Septicemia (sepsis).

3- Systemic toxigenic diseases: Streptococcal toxic shock syndrome :

is caused by a few strains .The infection starts with minor soft tissue infection and

47
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rapidly progressive shock and multiorgan failure.

Laboratory diagnosis: Specimen taken could be wound and blood

1. Direct examination:
a. Gram positive cocci arranged in pairs or chains

b. Latex agglutination test by group A antibody

2. Direct culture on blood agar,the culture shows small, beta-hemolytic colonies.

3. Blood cultures are done in cases associated with bacteremia or septicemia
e.g necrotizing fasciitis

………………………………………………………………………………………………………………………
Non fermentative Gram negative bacilli

Pseudomonas:
 These bacteria are common inhabitants of soil and water.
 It is an opportunistic pathogen can cause a variety of systemic infections,
particularly in patients with severe burns and in immunosuppressed patients
 Pseudomonas aeruginosa is the fourth most commonly-isolated nosocomial
pathogen accounting for 10% all hospital-acquired infections.

 They are Gram-negative bacilli, motile, non-spore forming, aerobic,

 It needs simple nutritional requirements.
 Produce soluble exo-pigments: a yellow pigment pyoverdin and the blue
pigment pyocyanin, both combined to form green colour characteristic of P.aeruginosa.

Virulence factors include: pili, polysaccharide capsule, endotoxin, exotoxin A, leukocidin.

Resistance:
 P.aeruginosa is resistant to high concentrations of salts and dyes,
to weak antiseptics, and antibiotics.
 Resistanse of P. aeruginosa to antibiotics is by plasmids,formation of biofilm
and permeability barrier afforded by its outer membrane LPS.

Pathogenesis:

 The organism cause pyogenic infection. "Blue pus" is a characteristic of

suppurative infections caused by P.aeruginosa and is due to the exopigment
48
[Type here]

pyocyanin produced by the organism.

 Pseudomonas infections are both invasive and toxigenic.

Diseases: Infections occur in the following organs:

1. Skin and soft tissue infections: Wound infections and dermatitis.

2. Bacteremia and septicemia: Usually hospital acquired occur mostly in

immuno-compromised and severe burns.

Laboratory diagnosis: It is identified on the basis of its gram morphology, and growth
at 42° .Fluorescence under ultraviolet light is helpful in early identification
of P. aeruginosa in wounds

Epidemiology and control

 Pseudomonas aeruginosa is a common inhabitant on skin of some healthy

persons, throat and stool of non-hospitalized patients.

 Within the hospital, P. aeruginosa finds numerous reservoirs

such as disinfectants, respiratory equipment. Spread occurs from patient to
patient on the hands of hospital personnel, or by contact with
contaminated reservoirs.

 The spread of P. aeruginosa can best be controlled by infection

control precautions.

Treatment: Only a few antibiotics are effective against Pseudomonas,

including fluoroquinolones, gentamicin and imipenem

…………………………………………………………………………………………………………………..

Anaerobic spore forming gram positive bacilli

Clostridium
 They are large, gram-positive bacilli, spore forming organisms.
 Vegetative forms of Clostridia are strictly anaerobes present in soils and the
intestinal tracts of animals.
 Being spore forming they can survive in the environment for many years.
49
[Type here]

 They are considered as opportunistic pathogens.

 It include C. perfringens with other Clostridium causing gas gangrene and C. difficile.
 Also, they include C. tetani and C. botulinum that produce the most potent biological
toxins known to humans.

Clostridium perfringens : Gram-positive large bacilli ,non-motile and anaerobic.

Biochemical reaction:

1- Fermentation of sugar with production of large amount of acid and gas this is detected by
stormy clot fermentation test .
2- Production of a lecithinase,α-toxin, that precipitate the lipid content of the media .
3- The enzyme is detected by Nagler reaction where colonies are surrounded by opaque zones
when cultured on serum media or egg yolk media .

Pathogenicity determinants : C. perfringens produce:

1- Lecithinase, (phospholipase C) which the primary virulence factor.

The toxin hydrolyze lecithin (phopholipids) of host cells and is responsible
for gas gangrene and myonecrosis in infected tissues.The toxin is also hemolytic.
2- Theta toxin has hemolytic and rapid necrotizing effect but it is not lecithinase.
It induces inflammatory mediators (cytokines), necrosis factor, platelet activating
factor which may lead to shock.
3- Extracellular enzymes: neuraminidase, proteases, lipases, collagenase
and hyaluronidase are spreading factor.

Clinical diseases:
1- Gas gangrene or Clostridial myonecrosis:is a bacterial infection that produces swelling
of tissues due to release of gas, as a fermentation products. The incubation period of the
disease is 1-6 days. It is fatal. Two groups of Clostridia are responsible for the disease:
a- Saccharolytic Clostridium which include: C. perfingens, C. novyi and C. septicum

50
[Type here]

b- Proteolytic Clostridium which include: C. histolyticum, C. bifermentans and C. fallax

2- Other forms of tissue infections include:

a) Cellulitis with gradual onset and no toxaemia. The infecting organisms invade
only dead tissue with no spread of infection.It has good prognosis.
b) Superficial wound contamination: The least serious infections, involves
only necrotic tissue. It is caused by C. perfringens, with Staphylococci
or Streptococci.

Laboratory diagnosis:

Specimen: Swabs are collected in a special transport media.

a. Direct examination:Large gram positive bacilli,with absence of phagocytic

cells being destructed by toxins.
b. Culture: are done under aerobic and strict anaerobic conditions at 37ºC for
48 hours. Colonies isolated from anaerobic culture are identified by
morphology, culture on egg yolk agar and biochemical reactions.
Clostridium tetani:

 It is the causative agent of tetanus.

 The organism is found in heavily-manured soils, in the intestinal tracts and
feces of various animals.Carrier rates in humans vary from 0 to 25%,
and the organism is a transient intestinal flora.
Morphology: Gram-positive, long thin motile bacilli, produces bulging terminal spores
giving it a distinctive drum stick appearance.

Culture: It is a strictly anaerobe, grow on blood agar or cooked meat medium.

Antigenic structure: Single antigenic toxin is found in all strains.

Pathogenicity determinant:

a. Tetanospasmin: systemic-acting, plasmid-mediated A-B neurotoxin.

 The B domain is responsible for binding of the toxin to host cell neurons,
 and the A fragment is responsible for the neurotoxicity of the toxin.
 Binding is irreversible event. Tetanospasmin, acts centrally at the level
of the anterior horn cells of the spinal cord.
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[Type here]

 The effect of the toxin is to block the release of inhibitory neuro-transmitters.

b. Tetanolysin: hemolysin, may be important in local infection.
Laboratory diagnosis:
Diagnosis is clinical and treatment should start to stop production and absorption of toxin.
Bacteria are isolated from wounds in a minority of cases
Specimen: Deep wound swab
1. Direct examination: Gram stain smears revealed gram positive bacilli with
terminal bulging spore, drum-stick.
2. Culture: Done under anaerobic condition, on blood agar for 48-72hours.
Colonies producing beta hemolysis are identified by gram stain.

……………………………………………………………………………………………………………………….

Acute abscess
 An abscess is a localized suppurative inflammation.
 The commonest causative organisms are staphylococci that produce a
coagulase enzyme which helps to localize the acute inflammatory processes.

How acute abcess is formed?

1. Direct access through wounds, scratches, and abrasions, or along natural

passages such as lactiferous ducts.
2. Near by septic focus as osteomyelitis
3. Blood spread as in cases of bacteremia (e.g. pyogenic liver abcess)

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[Type here]

Pathology:

An abscess consists of three zones:

1. A central zone of coagulative necrosis which becomes forming an abscess

cavity containing pus and is composed of inflammatory exudate, dead
leucocytes, necrotic tissue and dead and living organisms.

2. An intermediate zone of granulation tissue forms a protective layer

against the spread of bacteria and their toxins.

3. A peripheral zone of hyperemia of healthy surrounding tissues.

Fate of acute abcess:

1. Resolution by conservative treatment

2. Spontaneous rupture (common)
3. Spread of infection locally to near by tissues – lymphatic – blood
4. Change into chronic abcess
Clinical picture:

 General : fever (hectic), anorexia, headache, malaise

 Local : cardinal features:
 swelling : throbbing pain – redness of overlying skin – pitting edema
 fluctuation is positive especially in subcutaneous abcess (don’t wait for
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fluctuation in some areas?)

 sometimes needle aspiration is done in unclear cases (reveals pus)

 enlarged tender regional lymph nodes

Acute abcess

Investigations:
i. CBC: leucocytosis
ii. Ultrasound in special cases
Treatment:
 The standard treatment is incision and drainage under anaesthesis
 The classic incision is on the most pointing point of the abcess,
dependent position
 Special techniques adopted in special sites as parotid or pulp space
 Division of internal septa to open the loculi to allow proper drainage
 Packing inside the cavity

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 drains might be required in big abcesses

 regular dressing
……………………………………………………………………………………………………………

Boil (furuncle)
Aetiology:
 This is a staphylococcal infection of a hair follicle or a sebaceous gland
 It is particularly common is the face, neck and axilla.
 Boils are more common in diabetics and whenever there is lack of personal
hygiene.

Clinical features
 Clinically a boil forms a small painful indurated swelling which is hot, red and
very tender.
 Necrosis of the central part occurs and pus is discharged

55
[Type here]

boil
Treatment
1. Antibiotics effective against staphylococci.
2. Icthiol ointment and HOT foments facilitate necrosis of the overlying skin and
escape of pus.
3. Alway suspect diabetes mellitus in patients who develop recurrent boils.
……………………………………………………………………………………………………………

Hydradenitis suppurativa

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[Type here]

Cause: Mixed Staph. and streptococcal infection of the apocrine sweat glands,
 Common in perineum and the axilla,

Clinically:

 produces multiple small abscesses and pus-discharging sinuses

 It tends to be chronic and results in fibrosis in the affected area
Treatment: difficult and takes long courses.
 drainage of abscesses followed by careful hygiene,
 local antifungal applications may be enough. Otherwise,
 excision of the apocrine sweat-bearing skin followed by skin grafting
is needed in resistant cases
……………………………………………………………………………………………………………

Cellulitis

Cellulitis is a spreading bacterial infection of the skin and subcutaneous

tissues.

Causative organisms: Staphylococci and Streptococci are the commonest organisms

Risk factors:

1- A cut or small puncture wound, or insect bite.

2- Chronic irritation of the skin. It may also appear in the skin near ulcers or
surgical wounds
3- Chronic leg edema as in DVT and V.V.
4- People who have diabetes, AIDS or those receiving chemotherapy.
5- Conditions with venous insufficiency as, obesity and pregnancy.

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Clinical picture:
1- High fever, rigors, headache and malaise

2- Cellulitis usually begins as a small area of pain, swelling, redness and hotness that
spreads to adjacent skin.

3- Tender swollen regional lymph nodes

Cellulitis
Investigations:

1- CBC  increased WBCs count

2- C/S of blood may reveal the causative organism

Treatment:

1- Antibiotics, especially derivatives of penicillin that are effective against the responsible
bacteria
2- Pain relief with analgesics
3- Elevation of the affected limb
………………………………………………………………………………………………………………………………
Erysipelas

* Is a form of skin and superficial dermal and subcutaneous infection.

* It is red and has a well demarcated and elevated edge.
* It is treated as cellulitis.

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Erysipelas

……………………………………………………………………………………………………………
Carbuncle
 It is a big abscess larger than a boil, usually with one or more openings discharging
pus onto the skin.
Aetiology:

Organism: * bacterial infection, most commonly Staphylococcus aureus, or

Streptococcus pyogenes.
* The case is infectious and may spread to other areas of the body, or other
people.

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Risk factors:
1- Poor hygiene.
2- Poor nutrition and depressed immunity, (diabetes and HIV).
3- Repeated friction from clothing or shaving.
Clinical picture:

1 - Fever
2 - A carbuncle is made up of several skin boils. The skin is red
3 - The infected area is filled with fluid, pus and dead tissue.
4 - Carbuncles may develop anywhere, but they are most common on the back and the
back of the neck.
5- Carbuncles of the dangerous ares of the face can lead to cavernous sinus thrombosis
6- it may be complicated by pyemia or septicemia
Treatment:

1- Broad spectrum antibiotics

2- Hot foments
3- Cruciate incision of the infected area and proper drainage and debridemen
(excision) of the necrotic tissues.

Carbuncles

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………………………………………………………………………………………………

Wound infection

 The most common form is superficial wound infection occurring within the first
week postoperatively.
 Usually caused by skin staphylococci.

Risk factors
1. Systemic factors
 Age extremes
 malnutrition
 hypovolemia
 poor tissue perfusion
 obesity, diabetes, steroids, and other immuno-suppressants

2. Wound characteristics :
 Non-viable tissue in wound, hematoma, or foreign material (eg, drains
and sutures),
 poor skin preparation (eg, shaving)
 Pre-existent sepsis (local or distant)

3. Operative :
 Poor surgical technique
 Long operation (> 2 hours);
 intraoperative contamination (eg. from infected theater staff and
instruments or inadequate theater ventilation),
 prolonged preoperative stay in the hospital
 The type of the procedure (clean, clean-contaminated, contaminated,
and dirty-infected).

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Clinical Presentation: traumatic or surgical wound

severe wound infection

 Surgical site infection :

 Usually appears between the fifth and tenth days post-operatively but may
sometimes appear earlier or later.
 Wound pain and postoperative fever are the earliest manifestations.
 The wound is swollen (sutures are dipping through the skin), tender and red.
 Fluctuant areas or crepitus can occasionally be felt.
 Discharge from the wound may be seen.
 Infections deep to the deep fascia may be difficult to recognize.
 They are associated with systemic signs of infection as fever headache and malaise.

Diagnosis: 1- CBC  leukocytosis

2- Wound culture and sensitivity
Treatment:
Recommendations to minimize surgical site infections
A- The patient:
1. Correct any predisposing factors as control of diabetes, stopping of smoking
2. correction of nutritional deficiency.
3. Operations are avoided in patients with active infections if possible.
4. Shaving or clipping the hairs just before skin incision.
5. Skin preparation with appropriate antiseptics.

B- The surgeon:
o Surgeon should have short nails and should scrub properly.
o Meticulous surgical technique by proper haemostsis, gentle handling of tissue and

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avoiding tight sutures or leaving dead space.

o Delayed primary closure of heavily contaminated wounds.
o Prophylactic antibiotics:
Wounds and postoperative infection can be avoided by using appropriate prophylactic
antibiotics.
To treat infected wounds:
o Antibiotics better according to culture and sensitivity
o Open the sutured wound to allow for proper wound drainage
o Surgical debridement of the infected wound to remove the dead and necrotic tissues
and leave drains inside.
…………………………………………………………………………………………………………….
Bacteraemia and septicaemia

Bacteraemia:
 denotes the asymptomatic presence of bacteria, which are not multiplying in the blood.
 Its significance is variable but it is usually harmless.
 It usually follows dental work and instrumentation of the urinary tract especially in the
presence of infection.
 Bacteraemia is hazardous in patients with damaged heart valves or with prosthetic valves
because micro-organisms may settle on these valves or prostheses causing severe damage.
Bacteraemia is also dangerous in patients with immunosuppression.
 Antibiotic prophylaxis is essential in such cases.
 It should be noted that Gram-positive bacteraemia is usually less significant than Gram-
negative bacteraemia.

Septicaemia:
 Means the presence of multiplying organisms in the blood stream plus leucocytosis.
 It usually denotes significant infection in which bacteria, bacterial toxins or inflammatory
mediators escape the control of the immune system, enter the blood stream and produce a
systemic response including chills, fever and sometimes pulmonary failure or shock.
…………………………………………………………………………………………………………………………..

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GAS GANGRENE
Myo-necrosis
It is a rapidly progressive, fatal condition characterized by widespread necrosis of the
muscles and soft-tissue.

Pathogenesis :
Causative organisms:

Clostridium species: spore forming, anaerobic, gram +ve bacilli

- Clostridium perfringens (most common)

- C. Novyi
- C. Septicum

How infection occurs?

 Severe trauma + vascular injury or severe muscle damage + create anaerobic
condition at the wound + infection with gas forming clostridia
 Multiplication occur  carbohydrate fermentation occur with gas production
 Release of toxins (lecithinase) and enzymes (collagenase, protease, lipase) that
produce more damage to the tissues and vessels and more ischemia and anaerobic
state
Risk factors:
1- Diabetes Mellitus, and blood vessel disease

2- Severe trauma: with laceration and devitalization of the tissues

Clinical presentation:
1- High fever, toxic look, bad general condition
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[Type here]

2- Picture of septic shock

3- Massive tissue destruction
4- Blackening of skin. Rapidly progressing gangrene
5- Severe pain around the wound.
6- Blisters with gas bubbles form near the infected area. Crepitation in tissues (gas)
and very bad odor discharge

Complications:
 Toxemia, septic shock,..
 Renal failure, and death

Gas gangrene

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Investigations:

I- Lab.
1. C/S from the discharge and anerobic culture
2. Lecithinase test

II- RADIOLOGICAL:

 Plain x-ray of the affected area reveals gas in the soft tissue

Plain x-ray: shows gas in the tissues

Management:

Prevention:
1. Cleaning the wound with hydrogen peroxide
2. Remove the contaminated material
3. improve circulation in patients with poor circulation
4. Antitoxin for G.G.
5. In high risk wounds give the patient penicillin 1.5 mega-units 4 hourly, or
Tetracycline
6. Antishock measures

Treatment:
1. High doses of antibiotic : Penicillin
 10 mega-units of benzyl penicillin daily for 5 days as four 6 hourly doses
 Tetracycline 0.5 g intravenously every 6 hours
2. The dead tissue is removed or limbs are amputated with delayed suturing
3. No vaccine
…………………………………………………………………………………………………………

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Tetanus
Causative agent: Clostridium tetani
 Gram-positive, rod-shaped (drum stick) bacilli
 Spore-forming, anaerobic.
 Found in soil, and in the intestinal tracts and feces of various animals.
 pathogenic to humans by the production of a potent toxin
(tetanus toxin or tetanospasmin)

Pathogenesis:

1. Clostridium tetani enters the human body through a major or minor wound and
when the condition is anaerobic, the spores germinate and release the toxin
2. The toxins Initially binds to peripheral nerve endings.
3. Transported within the nerves until it reaches the central nervous system.
4. Blocks the release of inhibitory neurotransmitters
5. leads to unopposed muscular contraction and spasms
Types of tetanus:
 local- cephalic,  rare types
 Generalized – neonatal  most common types

Clinical presentation: generalized type:

 Incubation period: 3-21 days, average 8 days
 Tetanic seizures (painful, powerful muscle contraction)
 if the muscle spasms affect the larynx or chest wall, they may cause asphyxia
 stiffness of jaw (also called lockjaw)
 stiffness of abdominal and back muscles (opistotonus)
 contraction of facial muscles (trismus)
 fever
 Spasms continue for 3-4 weeks,
 Death occurs when spasms interfere with respiration.

Investigations:
1. Culture of the wound site
2. Tetanus Antibody test

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Treatment:
1. Intensive treatment should be started soon, as respiratory paralysis may
advance rapidly.

2. Neutralize toxin with TIG. The dose in established cases is 3000-6000

units intramuscularly, given preferably in the proximal portion of the
wounded extremity or in the vicinity of the wound.

3. Repeated doses may be needed since the half-life of the antibody is about 3
weeks and established tetanus often lasts longer

4. Excise and debride the suspected wound under anaesthesia.

5. Surgery should be done after systemic serotherapy has been started.

6. The wound must be left open and may be treated with hydrogen peroxide.

7. The patient should be protected from sudden stimuli, unnecessary

movements and excitement.

8. Diazepam may reduce the dose of barbiturates needed to control spasms.

9. The patient with respiratory problems may require tracheostomy, since

mechanical ventilation, once it becomes necessary, must be continued for
weeks.

10. The patient should be intubated once respiratory problems appear

11. Aqueous penicillin G, 10-40 million units a day, by intermittent

intravenous bolus injection should be given to kill clostridial organisms
and prevent further release of toxin.

12. Nursing. The patient is isolated in a dark quiet room, and nutrition is
maintained by a nasogastric tube.

13. The bacteria are killed with antibiotics, such as penicillin thus further
toxin production is thus prevented.
14. The toxin is neutralized with shots of tetanus immune globulin, TIG.
Prognosis
The death rate is 30-60% in established tetanus with respiratory insufficiency.
Prevention:
1. In severely wounded persons  anti-tetanic globulins is given

2. Proper wound care and dressings regularly

3. DPT vaccine: given in infant with booster doses may be taken every 10 years
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……………………………………………………………………………………………………………

Hand infections
Classification
I- Cutaneous and subcutaneous infections.
a. Paronychia.
b. Subcuticular and subcutaneous whitlow.
C. Pulp space infection.
d. Web space infection,
II. Fascial spaces infection.
a. Midpalmar space infection.
b. Thenar space infection.
c. Hypothenar space infection.
d. Space of Parona infection.
III. Synovial sheaths infection.
a. Acute digital tenosynovitis.
b. Ulnar bursitis.
C. Radial bursitis.
IV. Bone and joint infections: osteomyelitis and arthritis

General principals of hand infections:

 Commonest organism involved is staph aureus

 Route of infection is commonly minor injuries, or punctures
 Infection is rapidly evolved and late management leads to
suppuration,and spread to regional lymph nodes

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 Common clinical presentation for all types of infection include pain, redness,
swelling, edema and pus pointing in late cases
 All cases require plain x-ray to detect foreign body or osteomyelitis of
underlying bones
 Treatment involves antibiotics, analgesics and early drainage if needed
 The hand is kept in the position of function (flexion of M.P.J & extension
of inter-phalageal joints.
…………………………………………………………………………………………………….

Acute Paronychia
- A paronychia is an infection of the cuticle area around the finger nail.
- Acute paronychia is caused by staph aureus

Clinically: presents with redness, swelling, pain, and later with pus
around the nail bed.

Treatment:
1- Early cases may be treated with hot soaks and antibiotics,

2- If pus is seen or suspected, drainage by lifting the cuticle and/or nail

is required also.

Acute paronychia local anaesthesia

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Drainage of Acute paronychia

Subcuticular whitlow:
 It means Subepithelial collection of pus .
 Drainage is by excision of the insensitive roof without anaesthesia.
……………………………………………………………………………………………………………

Pulp space infection = Felon

N.B.
 Pulp space is a closed space filled with fat, traversed by fibrous septa. The
phalanx lies posteriorly.
 The space is closed proximally by the insertion of the profundus tendon to the
palmar surface of the base of the distal phalanx
 Because of this anatomical peculiarity, infection of the pulp space causes severe
throbbing pain as there is very little space for the pus to expand the pulp space.
 The Digital artery is an end artery
 The digital artery gives separate epiphyseal branch before it reaches the space.
Compression of the digital artery by tense edema lead to thrombosis.
 So, if septic thrombosis occurs in the diaphyseal branch necrosis of the diaphysis
only occur.

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 Fortunately complete regeneration can be obtained from the undamaged

proximal part which is supplied by the epiphyseal branch

Route of infection:
1..Direct through pin pricks
2.Extension form other lesion e.g. paronychia
Clinical Picture:
1- Severe throbbing pain (closed space).
2- The pulp becomes hot, red, very tender and swollen.

Pulp space infection

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Complications:
1- Extension of the infection to the phalanx  osteomyelitis
2- Extension of infection to the skin  sinus
3- Compression and thrombosis of the vessels  skin & bone necrosis
4- Tenosynovitis and septic arthritis of the DIPJ

Treatment
 Most patients with a pulp abscess require surgical intervention.
 The selection of the incision depends on the location of the swelling, pointing of the
abscess, and location of maximal tenderness.
How to drain the pulp space infection?
1. Digital block with 1 % injection lignocaine.
2. If the abscess is already pointing to the skin:
 An incision is made over the pointing site removing a circular or
an elliptical segment of skin.
 All the loculi are broken and the wound packed with a gauge.

3. If the abscess is deep seated and not pointing to the skin:

 A lateral incision is made close to the free margin of the nail.

 The pus is drained and the wound is packed with gauze

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Lateral incision

It is preferred to the palmar incision

It is made on the non-contact surface of the digits.

Irrespective of the location, the incision should stop short of the DIPJ crease
proximally and the terminal portion of the tip distally.
……………………………………………………………………………………………………………

Web space infection

 The web spaces lie between the bases of the fingers in the distal part of the palm and
is filled with loose fat.
 Infection of a web space produces a swelling that leads to separation of the two
adjacent fingers.
 Spread may occur along the lumbricals to involve the midpalmar space.

Web space infection

Incision:
 A V shaped incision is made on the dorsal aspect in-between the fingers.

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 if the pus is pointing to the palmar aspect a second V shaped incision is made on
the palmar aspect and the pus is drained

……………………………………………………………………………………………………………

Mid-palmar Space infection

 The mid-palmar space lies between the flexor tendons and the lumbricals
anteriorly and the fascia covering the interossei and the metacarpal bones
posteriorly.

Diagnosis:
 The hand is grossly swollen. The normal hollow of the palm is obliterated and the
dorsum of the hand is also swollen.
 The movement of the middle and ring fingers may be painful.

How to drain?
 A transverse incision is made over the proximal or distal palmar crease or over the
site of maximal fluctuation (incision A).
 The abscess is drained by Hilton's method.
 A sinus forceps is entered through the palmar fascia parallel to the flexor tendons
and the blades are then opened to drain the pus.
 Avoid injury to the digital vessels, nerves, flexor tendons

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Types of incisions for drainage

……………………………………………………………………………………………………………….
Tenosynovitis
It means inflammation of the tendons’ synovial sheaths Notes:
 Flexor tendons sheaths surround the flexor tendons and are closed spaces.
 Extends from the mid-palmar crease to the DIPJ

 Flexor sheath of little finger continues proximally with the Ulnar bursa
 Flexor sheath of the thumb continues as Radial bursa

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Synovial sheaths of the hand

Causes of tenosynovitis:
1- Pin pricks or penetrating trauma of the
hand 2- Following pulp space infection

Causative organism: staph aureus

Clinical picture:

General: Fever may be present

Local : Kanavel’s 4 cardinal signs of tenosynovitis:

1- Severe pain on extension of the fingers
2- Symmetrical swelling of the finger
3- Flexion deformity of the finger
4- Tenderness over the tendon sheath
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Tenosynovitis

Complications: necrosis of the tendons in neglected cases

Treatment:
 IV antibiotics
 Elevation of the hand - Initially, until infection is under control
 Splinting - In “safe position”
 Urgent surgical drainage of the synovial sheath + broad spectrum antibiotics

Technique:
2 incisions drainage technique:
Through digital and palmar incisions Using long catheter irrigation and
drainage.

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……………………………………………………………………………………………
Ulnar Bursitis

The ulnar bursa: it envelops the tendons of FDS & FDP

 Presents in the mid palm
 Continues medially only with the synovial sheath of little finger
Diagnosis of infection of ulnar bursa
 Painful swelling in the palm and Edema in the dorsum of hand.
 The fingers are flexed and attempts of extension causes pain which is most
marked in little finger

Drainage :
 Skin and deep fascia are incised over the antero-medial aspect of the fifth
metacarpal bone (incision C) (see above figure)
 Dissection is done till ulnar bursa is seen
 The ulnar bursa is incised and pus drained out.
 A catheter is introduced into the bursa and the bursa irrigated with normal
saline to wash out the pus.

………………………………………………………………………………………………………………

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Radial Bursitis

 is the continuation of the flexor policis longus tendon sheath of the Thumb
 when infected the inflammatory signs and symptoms are limited to thumb

How to drain radial bursa:

 A vertical incision along the radial aspect of the proximal phalanx of
the thumb ( incision D)
 The tendon sheath of the flexor pollicis longus is incised.
 A probe is passed up through the sheath and a proximal incision is made along
the radial side of the wrist.
 A catheter is introduced into the tendon sheath and irrigated with saline.

………………………………………………………………………………………………

Burn
Types = causes:

1. Dry heat or fire burns normally causing varying areas of deep skin loss
2. Hot fluids or scalds with burns of a widespread more superficial nature
3. Fash burns of short duration but intense heat
4. Electrical burns
5. Chemical burns caused by chemicals and caustics.
6. Radiation burns, from common sunburn to high-energy radiation injuries.

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Classifications of burns
I- According to the Degrees of burns:

1- 1st degree
2- 2nd degree
3- 3rd degree
4- 4th degree
II- According to depth of burns:

 Superficial burn
 Mid dermal level
 Deep dermal burn
 Full thickness burns
III- According to burn surface area:
A- Major burn
B- Moderate burn
C- Minor burn

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1- 1 st degree burn:
● Depth of burn: is superficial (epidermis)

● Cause: momentary exposure to the burn agent and sunburn

● Clinically:

- Sharp and uniform pain

- Skin Blanches on pressure, red, pink, edematous, soft and peeling

● Healing: takes 7 days or more

2- 2 nd degree burn:

1- Depth: Partial thickness (epidermis + part of dermis)

2- Causes:
a) Exposure of limited duration to lower temperature (40- 55°C),
b) Scalds, flash burn without contact,
c) Weak chemical burn
3- Clinically:
- severe pain
- Skin is mottled red, moist, blanches on pressure,
- With vesicles, edema, serous exudate .
4- Healing:
14-21 days

3- 3rd degree burns

1- Depth : full thickness burn (epidermis + dermis)

2- Cause: long duration of exposure to high temperature, flame, electrical, or

chemicals.

3- Clinically: - painless to touch no blanching,

- pale white, charred, hard, dry, leathery, and loss of hair .

4- Healing: Requires grafting

4- 4th degree burns

1- Depth: underlying structures, (muscles, bones,..)
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2- Cause: prolonged duration of exposure to extreme heat, electrical, flame,

or chemicals.

3- Clinically: usually painless charred, ‘skeletonized’

4- Healing: needs amputation or fasciectomy

2 nd degree burn

3rd degree burns

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4th degree burns

A- Superficial burns = partial thickness burn

These will heal spontaneously by epithelialisation and can be divided into:

1- Epidermal burns:
 They affect only the epidermis = 1st degree
 Hyperaemia occurs due to the production of inflammatory mediators,
 They are painful and heal within 7 days

2- Superficial dermal burns = 2 nd degree burn

● It affects the epidermis and the superficial part of the dermis.
 the blister (vesicle) is the most important feature
 the sensory nerves are exposed and the wound is therefore extremely painful
 has a moist surface
 they heal within 14 days

B- Deep dermal = Full thickness burn

 3 rd degree burn or more
 The burnt area is white
 No vesicles or blisters
 Lack of sensation in the area
 No spontaneous healing

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Classification of burn according surface area: “Rule of Nine”

A- Major burn:
 Burn surface involvement of 25% body surface area or more.
 Full-thickness burns 10% body surface area.
 Deep burns of the head, hands, feet, and perineum.
 Inhalation injury.
 Chemical or high-voltage electrical burn.
B- Moderate burn:
 Burn area of 15-25% body surface area.
 Superficial partial-thickness
 Superficial Burns of the head, hands, feet or perineum.
C- Minor burns:
 Less than 15 % body surface area.
 Nothing involving the head, feet, hands or perineum.

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Effects of burns:

I- Local effects of burn

1- Inner most zone = zone of coagulation:

● Point of maximum damage of tissues.
● Irreversible tissue loss due to coagulation of the constituent proteins

2- Middle zone = zone of stasis

● The zone of stasis is characterized by decreased tissue perfusion.

● Loss of tissue in the zone of stasis will lead to wound deepening and widening.
● The main aim of burns resuscitation is to increase tissue perfusion and prevent
any damage becoming irreversible.

3- Outer zone = Zone of hyperemia

● It shows the state of vascular phenomenon
● There is V.D. of the blood vessels in this area

II- General complications of burns

 Loss of water, electrolytes (Na & K), proteins and heat due to
increased vascular permeability, which results in the formation of
oedema
 Hypovolemia (= shock phase = first 48 H)
 Neurogenic shock
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 Immunosuppression leading to infection

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 Impairment of barrier function of the gut leading to translocation of

bacteria  septicemia (it is therefore important to start oral feeding early)
 Mucosal ischemia  peptic ulcer  hematemesis
 Systemic inflammatory response affects the lungs resulting in Adult
Respiratory Distress Syndrome (ARDS).

Management of burn
A- Emergency burn care
The principles of first aid:

 To stop the burning process.

 To cool the burn wound.
 Cooling the surface of the burn is also an effective analgesic.
 Cooling the burn wound will only be effective if started within 3 hours of the injury.
 Do not use ice or ice water, it will deepen the tissue injury and increases the risk of
hypothermia.
 If the patient’s clothes are burning wrap him in a blanket.
 In a scald remove clothing rapidly, as soaked clothes act as reservoir of heat.
 Leave adherent clothing in place and cut around it to remove the non- adherent
clothing.
 Use cold running (tap) water for 10-20 minutes to stop the burning
process; the ideal temperature is 15-18 C (range from 8 till 25 C)
 Prevent hypothermia by well wrapping.
 Avoid the use of tight dressings in limbs with compromised circulation to
avoid ischemia.
B- Admission criteria
1- Age:
- Children TBSA > 8%
- Adults TBSA > 15%

2- Sites of burn:
 Head & neck
 Hands & feet
 Groin & axilla
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 Perineum

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 Circumferential burns of chest and limbs

3- Depth: full thickness burns TBSA > 5%

4- type of burn: electrical, chemical, inhalation burns.

C- Rapid assessment:

 Check airway & breathing, give O2 in adult with >30% TBSA burned,
 give 4-8 liter humidified O2 / minute
 Check pulse and capillary refill
 Check neurological status.
 Perform escharotomy (decompression) in full thickness circumferential burns of the
chest and limbs
D- Fluid replacement:
1- Estimate TBSA, use the “ RULE of 9 ”
2- Weigh the patient
3- In all burns < 10% TBSA give oral fluids
4- Give IV fluids in burns > 15% TBSA in adults
Type and amount of fluids:
 Use Ringer’s Lactate or sodium chloride 0.9% (NS).

 Formula to be used is ( 4 cc x weight in kg x % TBSA ).

How to give?
 1 st 8 hours------------1/2 the deficit

 2 nd 8 hours ---------- ¼ the deficit

 3 rd 8 hours------------¼ the deficit
 2 nd 24 hours ----------- 2500 - 3000 cc / 24 hrs

E- Pain relief  Give adequate analgesia, preferably morphine or pethidine.

F- Laboratory:
•• CBC
•• Urea, creatinine & electrolytes

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Burn wound care

1- Clean the burn wound:
a- By water showering to remove dirt, dressing etc.
b- Clean further by using (Savlon) or normal saline.
C- Open the blisters and remove loose tissue.
2- Early active debridement and SSG,
 Consider this treatment 5 days post burn in all patients with full thickness burns or
partial thickness burns of the hands.

3- delayed management
A - Exposure of the burn wound (open method)
B - Closed wound treatment (closed method)
A- Open method:
1- Cleaning the wound with normal saline or (Savlon)
2- Removing loose tissue and de-roof vesicles
3- Allowing the burn wound to dry and to form a crust ( 3 - 4 days)
4- Then, the wound can be cleaned twice daily with normal saline and apply
topical oint.
5- After 10-14 days the burn has healed or the slough will separate gradually
leaving a granulating wound surface which can be grafted
6- Low costs – more painful
B- Closed Method:
 In which dressings are used.
 The dressing is the barrier to infection
 An antibacterial Topical agent has to be added otherwise the dressing
will create a warm and moist environment which helps infection
 High costs – less painful

4- Closure of burn wound:

•• superficial dermal burns will heal within 10-14 days. (without graft)
•• deep burns will heal within 21 - 28 days.
•• any burn not healed after 21 to 28 day and larger than 3 cm in diameter may

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benefit from skin graft.

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•• Full thickness burns always require surgical closure (grafts)

•• All burns requiring skin cover should be grafted as soon as possible, this reduces the
chance of infection
•• Before skin graft is applied the wound should be clean, has healthy granulations and
not infected.

Types of skin graft:

1- SSG (split skin graft)
2- Full thickness graft
SSG (split skin graft)
 Is most commonly used
 Takes well
 The thinner the graft the better the take
 Can cover large areas.
Disadvantages
 Is cosmetically less satisfactory
 Shrinks in time up to 50%
Full thickness graft
 Takes with more difficulty.

 Is cosmetically better.

 Will shrink up to 20%.

Indications of skin graft:

 In defects larger than 3 cm in diameter
 When the burn hasn’t healed after 21 days
 Graft early in hand and facial burns

Best donor sites are:

1- For a SSG,  thighs, upper arms and flexor aspect of the forearm.
2- For a full thickness graft, post-auricular skin, supraclavicular Skin and the groin.
3- For a pinch graft, the thighs.

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Contraindications of a skin graft:

1- The burn wound is infected
2- Hypergranulation
3- The wound bed is fibrous without granulation
Causes of Graft failure
a. Infection
b. Bleeding (graft is lifted of its bed)
c. Anaemia
d. Movement (make sure the graft is fixed well)
e. Unhealthy granulations, hypergranulations or no granulations
------------------------------------------------------------------------------------------

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Surgery of the face and oral cavity

Development of the face
I- fronto-nasal process  Forms the Filtrum, middle upper lip, nasal tip, collumella and
premaxilla of the hard palate.

II- 2 maxillary processes  complete the upper lip + the hard

palate III- 2 mandibular processes  gives the lower lip + the
mandible

………………………………………………………………………………………………………………

Cleft lip
Etiology:failure of fusion between the fronto-nasal process and the maxillary
processes.

Types of cleft lip:

1- Unilateral or bilateral  85 % are unilateral

In bilateral type: ● Orbicularis oris attaches at the lateral cleft margins

bilaterally at the nasal ala
● Laterally displaced nasal ala
● Extremely short columella

2- Complete or incomplete:

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a) Incomplete: Muscle fibers of the orbicularis oris are often intact but hypoplastic

b) Complete: ● Columella is displaced to the normal side

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● Nasal ala on the side of the cleft is displaced

● Nasal tip is deviated towards the non-cleft side

3- Simple or alveolar: if limited to the lip only it is called simple and if involves
lip and alveolus it called alveolar type.

4- Complicated or non-complicated: if associated with cleft palate or not.

5- Upper or lower cleft lip.

complete cleft lip incomplete cleft lip

Bilateral cleft lip

Clinical picture and complications:

1- Disfigurement
2- Difficult suckling: Cleft lip alone usually does not cause feeding problems
3- Other anomalies may be present.

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Treatment:
Time: age of 3 months to allow proper suckling

Technique: Milliard rotation-advancement technique

1- Dissect lip from the maxilla
2- Bare the edges of the cleft by zigzag incision
3- The muscle is sutured first then the mucous membrane then at last the skin

Repair of cleft lip

Cleft Palate

Aetiology: failure of fusion between the fronto-nasal process and the 2

maxillary processes.

Palate formation:

1- The palate is formed by the primary palate and the secondary palate which are
separated by the incisive foramen
2- The primary palate is formed from FN process = pre-maxilla
3- The 1ry palate forms part of hard palate anterior to the incisive foramen
4- Secondary palate formed by fusion of the 2 maxillary processes (post.to the
incisive foramen)
Types:

Types of cleft palate:

(A) Incomplete cleft of soft palate

(B) Complete cleft of soft palate
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(C) Cleft of soft palate and secondary palate

(D) Cleft of soft palate and unilateral cleft of hard palate
(E) Cleft of soft palate and complete cleft of hard palate

A B C D E
Cleft palate
Clinical picture and complications:

1- Difficulty of speech of some letters as K, P,T,G and nasal tone of voice

2- Recurrent infections  recurrent pharyngitis, rhinitis and persistent
otitis media and effusion

3- Nutritional problems due to difficult suckling: Cleft palate limits the

ability to suck due to the common cavity between the mouth and the nose 
loss of weight

4- Teeth malformation:

 Hypoplasia
 Loss of teeth
 Mal-arrangement
 Malformation
Treatment:
Timing  at 9 – 12 months
Operation:
a) 2 release incisions are done in the muco-perioseum of the palate on both sides of
the cleft and create flaps.
b) The 2 flaps are closed together in front of the cleft to close it.

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Repair of cleft palate
…………………………………………………………………………………………..

Tongue ulcers
Types of tongue ulcers

Dental Aphthus Frenal T.B. syphilis Herpes

simplex
Cause sharp or Stress or Whooping Pulmonary syphilis Herpes
broken dyspepsia cough T.B. simplex
tooth Virus
Number Single Single or Single Multiple Chancre Multiple
multiple or snail
track
ulcers
Site Side of the Tip and Under Tip and Tip and Lips, k
tongue sides of surface of sides of sides of cheek &
tongue the tongue tongue tongue tongue

Edge Sloping Sloping Sloping Undermine Raised Hyperemic c

Floor Red White Red Pale Glistening Red
granulation granulation granulation granulation white granulation n
tissue tissue tissue tissue epithelium tissue
Pain Painful Painful Painful Painless painless Painful
Lymph Enlarged & Enlarged Enlarged & Enlarged & May be Enlarged &
Nodes Tender & tender tender matted enlarged Tender
Treatment Treatment of Treatment Treat. Anti-T.B Anti- Antiviral
the cause of the Whooping drugs syphylitic drugs
Cause cough Drugs

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Dental ulcer:
* It is precancerous condition  may turn malignant
* It can be treated by removing the broken or sharp tooth.
---------------------------------------------------------------
Malignant tongue ulcer

Cancer tongue
Pathology
Age:old age
Sex: males > females
Predisposing
factors
 Chronic superficial glossitis
 Dental ulcer & sharp tooth
 Smoking, spirits & spices
Sites :
 Tip of tongue 10%
 Dorsum of tongue  10%
 Lateral side  25%
 Under surface  10%
 Posterior 1/3  20%
Macroscopic:

1- Ulcer  raised, everted edge + hard base + necrotic

floor 2- Hard deep tongue fissure
3- Hard mass or nodule

Microscopic: squamous cell carcinoma

Spread of Cancer tongue:

I- Local:
 Tumours of the anterior 2/3
tongue to the under surface & floor of the mouth. Later spread to the gum and
mandible

 Tumours of the posterior 1/3  spread to the pharynx

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87
II- Lymphatic spread:
Tip of tongue  submental lymph nodes
Anterior 2/3 of tongue  submandibular L.N
Posterior 1/3  upper deep cervical L.N.
III- blood spread:
More from the posterior 1/3 of the tongue

Clinical picture of cancer tongue:

1- Ulcer in the tongue, mass or fissure
2- Pain in the tongue: due to infiltration of the lingual
nerve 3- Excessive salivation
4- Ankylo-glossia = tongue fixation
5- Dysphagia  more in posterior 1/3 tumours
6- Bad odour of the mouth
7- Voice changes
8- Neck mass due to enlarged cervical L.N
.
Complications: bronchopneumonia – bleeding — cachexia

Investigations:

Incisional biopsy from the ulcer

Treatment of cancer tongue:

I- Cancer tip of tongue: Wedge excision with safety margin

II- small cancer in lateral side of tongue  local excision 1.5 cm safety margin
III- Larger cancer in anterior 1/3 hemi-glossectomy
IV- posterior 1/3 cancer  radiotherapy
V- Cervical lymph nodes  removal by block neck dissection

Prognosis:
Anterior 2/3 cancers has better prognosis than posterior 1/3 cancers because it is more
differentiated, early presentation, accessible for treatment and delayed blood and
lymphatic spread.

----------------------------------------------------------------------------------------- -

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 Carcinoma of the lip

Pathology:
Age: > 60 years
Sex: males > females
Predisposing factors: leukoplakia – exposure to sun – syphilis
Sites: Lower lip  93% Upper lip  5%
Angles of the mouth  2%
Macroscopic picture:
1- Ulcer  raised everted edge + hard base + necrotic
floor 2- Malignant fissure
3- Malignant nodule
Microscopic picture: squamous cell carcinoma
Spread: 1- Local  other parts of the lip
2- Lymphatic  to sub mental and submandibular lymph nodes
Clinical picture:
1- Ulcer or nodule in the lip
2- Lymph node
enlargement
Treatment:
1- Radiotherapy
2- Surgical excision of the mass
……………………………………………………………………………………………………………

Cysts of the Floor of mouth

1- Ranula:
It is mucus retention cyst present in the floor of the mouth
Site: under the tongue on one side of the midline
- covered by mobile mucous membrane
- crossed by submandibular duct
- The swelling is not tender
- Present in children and young adults
- Size  1- 5 cm
- The swelling is fluctuant and trans-illuminates
- The swelling is not compressible

89
Treatment: partial excision = (de-roofing or marsupialization)

90
2- Sub-lingual dermoid cyst:

It is type of inclusion dermoid cyst due to entrapment of a piece of skin in the midline
during fusion of the mouth cavity

Age: common in young age (10 – 15 years)

Site: in the midline under the chin and may bulge inside the floor of mouth

- The swelling is painless

- The swelling is cystic and not compressible

Treatment: excision.

………………………………………………………………………………………………

Salivary glands
Important anatomical points:
 There are 3 pairs of major salivary glands; parotid, submandibular and sublingual
glands .
 The parotid gland contains the facial nerve, posterior facial vein and
external carotid artery (from superficial to deep).
 The parotid duct (Stensen's duct) opens opposite the upper 2nd molar tooth.
 The submandibular gland lays in the submandibular fossa and its duct
(Wharton's duct) opens in floor of the mouth.

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Branches of facial nerve
● Within the gland the nerve branches and rejoins to form a plexus within the parotid
gland
● The nerve branches then emerges from the parotid:
Temporal – Zygomatic – Upper buccal – Lower buccal – Mandibular –
Cervical

Branches of facial nerve

.......................................................................................................

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Diseases of salivary glands
 Congenital (sialectasis)
 Inflammations and infections
 Stones
 Tumors

Congenital Diseases : Sialectasis

 is the salivary gland's analogue of bronchiectasis, that is characterized by degeneration of the
alveolar and duct system. As a result they become dilated.
 The etiology is not known, but many cases are congenital and familial.
 The dilated ducts and alveoli are inadequately drained, and, thus, get infected
 It is commonly misdiagnosed as mumps parotitis

Infections
1. Acute; viral or bacterial.
2. Recurrent subacute or chronic.
3. Chronic infections as TB and sarcoidosis (rare).
4. Viral parotitis = Mumps, though diminishing in frequency because of the routine immunization,
is still the commonest cause of salivary gland swelling. Bilateral painful parotid gland swelling with
fever, in a child is the usual presentation. The disease is self-limiting.

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 Acute bacterial parotitis and parotid abscess
Causative organism: staphylococci

Routes of infection:

1- Parotid duct: that opens opposite the upper 2nd molar tooth

 In bad oral hygine

 Stone obstructing the duct orifice stasis &infection

2- blood: spread of infection to the gland from distant infection

3- Direct: through wound in the parotid area.

Complications:
1- Fistula formation on the skin of the face
2- Stone formation in the parotid gland

Clinical picture of parotid abscess:

1- High fever
2- Sudden severe pain in the side of the face
3- The pain increases with movement of the tempro- mandibular joint during eating or
speaking.

4- Swelling at the site of the parotid gland:

 Lies in front and below the ear.

 Around the ramus of the mandible
 Fills the gap between the angle of the mandible and mastoid process.
 The swelling is hot and very tender.
 The skin overlying is red.
 Contraction of the masseter muscle the swelling becomes prominent.
 The swelling cannot be felt bimanually.

5- Enlarged upper deep cervical lymph nodes

6- The duct orifice is red and shows discharge coming out.

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 Acute parotid abcess

Investigations:
1- CBC: leukocytosis
2- C.T.: parotid region shows inflammatory reaction and fluid inside the parotid.
Treatment:
1- Antibiotics and analgesics, hot fomentation and mouth washes for 48 hours.

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 2- Abscess drainage by Hilton method:

-Vertical skin incision  sinus forceps introduced closed horizontally inside

the gland then opened inside the gland then withdrawn opened to avoid
injury of the facial nerve branches.
……………………………………………………………………………………………………………..

Salivary stones
It is solid substances formed inside the salivary gland or duct

Salivary stones are more common in the submandibular gland than parotid:
Due to: 1- high mucous content of the submandibular secretion.
2- Submandibular duct opens against gravity slowstasis
3- Submandibular duct opens in the floor of mouth easily obstructed by food
particles.
Composition of the stones: cellular debris + mucus + calcium + magnesium +
phosphate.

Clinical picture:
1- dull-aching pain deep to the mandible increases with
eating 2- The patient may feel swelling deep to the mandible
3- The patient feels better when he presses over the gland and feels discharge comes out in
his mouth
4- The gland is felt in the submandibular triangle and can be felt bimanually and is tender
before and during eating
5- Duct stone can be felt in the floor of the mouth.

Submandibular duct stone

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Investigations:
1- Plain X-ray to the submandibular region shows the radio-opaque stone.
2- ultra-sound to submandibular region detects the stones.
3- Sialography to detect duct stricture.

Treatment:
1- Gland stone excision of the gland = submandibular Sialo-adenectomy

2- Duct stone  removed under local or general anaesthesia

…………………………………………………………………………………………………………………………………..

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 Tumors of the salivary glands
 Salivary neoplasms constitute 1.2% of all neoplasms and 5% of head and neck tumours.
 The majority of these neoplasms are benign and most commonly arise in the parotid gland.

Benign tumours:

I- Mixed parotid tumour = pleomorphic adenoma

Pathology:
 Age: 25 – 50 year
 Sex: females > males
 Site: 90% in parotid gland-----10% in other glands
The superficial lobe of parotid is affected in 90% and the deep lobe in 10%
 Macroscopically: regular well defined soft or cystic in consistency + Pseudo-
capsule
 Microscopically: adenoma + fibrous tissue + myxomatus tissue + psudo-cartilage
(pleomorphic stroma)
 Spread: no spread

Complications:
a- malignant transformation in 2-3% (the tumour rapidly increases in size
become fixed and painful with facial nerve paralysis).

b- High Recurrence after excision

Clinical picture:
a- very slowly growing painless parotid swelling over years
b- The swelling is well defined, soft or firm and mobile
c- The lymph nodes are not enlarged
c- The facial nerve is intact

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 Pleomorphic adenoma of parotid

Investigations:
1- C.T parotid region shows site and extent of the tumour
2- Frozen section or fine needle aspiration cytology

Treatment:
1- Superficial parotidectomy if the tumour arises from the superficial lobe with
preservation of facial nerve.
2- Total parotidectomy if the tumour arises from the deep lobe.
……………………………………………………………………………………………………………..

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 II-Adenolymphoma = Wartin’s tumour
It is a benign tumour of the parotid gland
Age: 50-60 years
Sex: male: female  7:1
Macroscopically: smooth, regular, well capsulated and soft in consistency
Microscopically: adenoma + lymphocytes
Clinical picture:
● Painless slow growing swelling
● Regular,mobile and well defined parotid swelling
● Lymph nodes are not enlarged
● The tumour never to turn malignant
Investigations:
1- C.T parotid region
2- Isotope scan  hot spot
3- Biopsy  Fine needle aspiration cytology
Treatment: superficial parotidectomy
………………………………………………………………………………………………………………

Carcinoma of the salivary gland

Pathology
Age: old age
Sex: males affected more than females
Sites: parotid gland 60% / submandibular & sublingual  40%

 The incidence of malignancy varies inversely with the size of the gland,
thus it occurs in 25% of parotid neoplasms, in 40% of submandibular
neoplasms, and in 70% of neoplasms of the sublingual and minor salivary
glands.

Macroscopically: the swelling is irregular, hard, ill-defined and fixed

Microscopically:
1- Mucoepidermoid carcinoma: the commonest variety and
commonly affects parotid gland ( it may be low, moderate or high

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 grade differentiation)
2- adenoid cystic carcinoma: commonly affects minor salivary
glands
3- adenocarcinoma
4- Malignant mixed parotid carcinoma on top benign pleomorphic adenoma
Spread:
I - Local

1- intra-glandular  involves the facial nerve, posterior facial vein

and external carotid artery

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 2- Extra-glandular  involves skin, mandible and internal jugular
vein and last 4 cranial nerves

II- Lymphatics
To upper deep cervical lymph nodes
III- blood
Lung, liver, bone and brain

Clinical picture:
1- Parotid swelling rapidly growing and painful
2- The swelling is hard and fixed
3- Facial nerve paralysis deviation of the angle of the mouth to the same side +
dribbling of saliva +inability to close the eye + accumulation of food in the mouth.

4- Anemia and loss of weight

5- Enlarged hard fixed cervical lymph nodes

Investigations:
1- C.T scan of the parotid region
2- Biopsy as fine needle aspiration
3- Frozen section during surgery
Treatment:
1- Radical parotidectomy

(Total parotidectomy and cervical lymphadenectomy)

2- Commando’s operation: parotidectomy + hemi-mandiulectomy + removal of the

lymph nodes

………………………………………………………………………………………………………………………………….
Differential Diagnosis of parotid swellings:
1. Extra parotid swellings
a. Lymph nodes (parotid or upper deep cervical ) sebaceous cysts, and lipomas
b. Mandibular and maxillary bone tumors may produce the appearance of a parotid enlargement.
C. Hypertrophy of the masseter is bilateral in most cases.
2. True parotid swelling that is caused by:
i. Inflammation
ii. Benign tumors
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iii. Malignant tumors

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CONTENTS:

Wounds .............................................................................. 3

Polytrauma ……………………………………………………………. 11

Hemorrhage ............................................................. 13

Shock .........................................................................................16

Fluid, Electrolytes, and acid base Balances …………….. 22

Surgical Infections ....................................................... 31

Burns and skin grafts ………………………………………………… 67

Diseases of the face and oral cavity ..................................... 79

Salivary glands diseases …………………………………………….. 90

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