Surgery tutorials for medical students

bbinyunus2002@gmail.com Page 1
TUTORIALS
COMPILED
BY
DR BASHIR BIN YUNUS (MBBS, ZARIA)
SURGICAL RESIDENT
AMINU KANO TEACHING HOSPITAL

Contents
PART ONE
Surgical infections………………………………………………………………………………………
Wound and wound healing…………………………………………………………………………
Sutures ……………………………………………………………………………………………………..
Cutaneous ulcers………………………………………………………………………………………..
Fluid and electrolytes therapy……………………………………………………………………..
Shock ………………………………………………………………………………………………………….
Blood transfusion………………………………………………………………………………………
Hemostasis in surgery…………………………………………………………………………………
Nutrition in surgery…………………………………………………………………………………….
Metabolic response to trauma……………………………………………………………………
Perioperative management………………………………………………………………………..
Surgical prophylaxis…………………………………………………………………………………..
SCD and surgery………………………………………………………………………………………….
Diabetics and Surgery ……………………………………………………………………………….
HIV and the surgeon …………………………………………………………………………………
Obesity and surgery…………………………………………………………………………………..
Surgery in the elderly ……………………………………………………………………………….
Surgical hypertension……………………………………………………………………………….
Asepsis in surgery…………………………………………………………………………………….

Multiply Injured patient …………………………………………………………………………..
Cancer chemotherapy…………………………………………………………………………………
Radiotherapy ……………………………………………………………………………………………..
Use of drains in surgery……………………………………………………………………………
Diathermy……………………………………………………………………………………………………
Lacer …………………………………………………………………………………………………………
Tourniquet…………………………………………………………………………………………………
Minimal access surgery……………………………………………………………………………..
Principles of neonatal surgery……………………………………………………………………
Biopsy ……………………………………………………………………………………………………….
Prostate biopsy
Dialysis
Informed consent………………………………………………………………………………………
Day case surgery ………………………………………………………………………………………
Medical ethics …………………………………………………………………………………………..
Surgical audit…………………………………………………………………………………………….
PART TWO (Principles in management)
Upper GI bleeding …………………………………………………………………………………….
Urinary calculi…………………………………………………………………………………………..
Calculus cholecystitis ……………………………………………………………………………….
Typhoid ileal perforation………………………………………………………………………….
Surgical management of peptic ulcer disease………………………………………….
Fournier gangrene …………………………………………………………………………………..

Benign prostatic hyperplasia…………………………………………………………………….
Prostate cancer………………………………………………………………………………………..
Obstructive uropathy...………………………………………………………………………………
Gastric outlet obstruction ………………………………………………………………………..
Gastrostomy …………………………………………………………………………………………………
Hernia …………………………………………………………………………………………………………..
Intestinal fistula……………………………………………………………………………………………
Malignant ascites ………………………………………………………………………………………..
Malignant bowel obstruction ……………………………………………………………………..
Malignant hyperthermia ……………………………………………………………………………..
Chest trauma……………………………………………………………………………………………….
Abdominal injury ……………………………………………………………………………………….
Mass casualty ……………………………………………………………………………………………..
Regional anaesthesia ………………………………………………………………………………….
PART THREE
Operatives…………………………………………………………………………………………………
PART FOUR
Long case ………………………………………………………………………………………………….
OSCE…………………………………………………………………………………………………………..
Surgical instruments………………………………………………………………………………….
Radiographs……………………………………………………………………………………………..
PART FIVE (pathology and management)

Surgical tutor …………………………………………………………………………………………..
Past questions –
 Essay
 Orals
SURGICAL INFECTIONS
DEFINITIONS
Infection in which there is anatomic or mechanical problem that must be resolved
by operation or another invasive procedure to cure the infection.
Antibiotic are adjunct and are not substitute for indicated surgical therapy.
BACTERAEMIA; the transient invasion of the circulation by bacteria is known as
bacteraemia.
SEPTICEMIA; this implies prolonged presence of bacteria in the blood accompanied by
severe systemic reaction.
SYSTEMIC INFLAMMATORY RESPONSE SYNDROME (SIRS): The systemic
inflammatory response to a wide variety of severe clinical insults manifests by 2 or more
of the following conditions:
• Temperature greater than 38°C or less than 36°C
• Heart rate greater than 90 beats per minute (bpm)
• Respiratory rate greater than 20 breaths per minute or PaCO2 less than 32 mm Hg
• White blood cell count greater than 12,000/mL, less than 4000/L, or 10% immature
(band) forms
SEPSIS: This is a systemic inflammatory response to a documented infection.
SEVERE SEPSIS: This is sepsis and SIRS associated with organ dysfunction,
hypoperfusion, or hypotension.
SEPTIC SHOCK: Refers to severe sepsis which is not responsive to intravenous fluid
infusion for resuscitation and requires inotropic or vasopressor agent to maintain systolic
blood pressure.

CHARACTERISTICS IF SURGICAL INFECTIONS
(unlike medical infections)
- Damaged host defences (especially epithelial barrier)
- Immunological defects are global – trauma, nutritional deficiency, etc
- Pathogens are polymicrobial, both aerobic and anaerobic
- Pathogens often from endogenous flora (opportunistic) as well as from exogenous.
ORGANISMS COMMONLY ENCOUNTERED IN SURGICAL INFECTIONS
The organisms commonly encountered in surgical infections are the:
 Staphylococci;
o Staph. pyogenes causes boils, carbuncle, styes, septic hand, breast abscess,
osteomyelitis, wound sepsis, deep abscess, septicemia and pyaemia
o Staph albus non pathogenic though can cause low grade inflammation in
dead tissues
 Streptococci; the haemolytic(α and β) and the anaerobic are surgical concern.
The toxins produce include; haemolysin, leucocidin, fibrinolysin, erythrogenic toxin,
hyaluronidase, deoxyribonuclease. Β-haemolytic strept. E.g Strep Pyogenes causes
erysipelas, cellulitis, severe wound infection, tonsillitis, otitis media, scarlet fever,
puerperal sepsis. Α-haemolytic eg Strept. Viriadans cause intra oral and dental
infections, can contaminate burns or chronic skin ulcers, seed cardiac lesions
 Pneumococci; lobar pneumonia or with other organisms causing
bronchopneumonia; they may also produce otitis media, sinusitis, meningitis,
acute primary peritonitis in young girls and wound infection.
 Gram negative bacteria; E.coli, Pseudomonas, Proteus, Klebsiella, Haemophilus
Influenzae. The intestinal bacteria commonly encountered are Escherichia coli,
Pseudomonas, and Proteus organisms usually described as coliforms. In general,
those bacilli which do not ferment lactose eg Pseudomonas, proteus, salmonella
B.fragilis , V.cholerae are more pathogenic for man. In surgical practice, however, it
is the lactose fermenters eg Klebsiella, E. coli, Enterobacter ,which predominate.
o They infect wounds near the lower ileum and colon, the urinary tract and
bums.

o They are found in mixed infections and are commonly secondary invaders in
infections by staphylococci and streptococci
o They elaborate in their capsule a powerful endotoxin which causes pyrexia,
rigors and septic shock when released into the blood stream
Other gram negatives
 Klebsiella organisms are gram-negative rods usually responsible for pneumonic
lesions and hepatic abscesses but may produce wound infections especially after
transplantation procedures.
 Haemophilus influenzae often found in the healthy upper respiratory tract. It
causes acute epiglottitis, meningitis and bronchitis.
INFECTIONS OF SIGNIFICANCE IN SURGICAL PATIENTS
SURGICAL SITE INFECTION (SSI)
It is defined as infection present in any location along the surgical tract after a
surgical procedure within 3odays of procedure or up to 1 year after a procedure
that has involved the implantation of a foreign material.
Classification
 Incisional SSI
o Superficial- those involving only the skin and subcutaneous tissue
o Deep - those involving deep soft tissues of the incision (e.g. fascial
and muscle layers)
 Organ/space SSI - involves any part of the anatomy (e.g., organs or spaces)
manipulated
Criteria for defining an SSI as superficial
1. Infection occurs within 30 days after an operation.
2. The infection involves only the skin and the subcutaneous tissue adjacent to the
incision.
3. At least one of the following is present:
 a purulent discharge from the surgical site,
 at least one of the signs and symptoms of infection(pain, tenderness,
localized swelling, rednessor heat),
 spontaneous dehiscence of the wound or deliberate opening of the
wound by the surgeon (unless the culture results from the site are
negative),

 an abscess or evidence of infection on direct examinationor
reoperation, or histopathologic or radiological examination,
 diagnosis of infection by a surgeon or attendingphysician.
Deep incisional SSI
Criteria:
1. They occur within 30 days after surgery with no implant
(up to 1 year after surgery if an implant is left in place),
2. The infections involve deep soft tissues, fascia and muscle layers,
3. At least one of the following:
 Purulent drainage/organism isolated from an aseptically obtained culture.
 Fascial dehiscence or deliberate opening of the fascia by a surgeon due to
signs of inflammation.
 An abscess or other evidence of infection noted below the fascia during
reoperation, radiological examination or histopathology.
 A surgeon declares that a deep incisional infection is present.
Organ/space SSI
These infections involve any part of the anatomy, in organs and spaces other than the
incision, which was opened or manipulated during operation.
Criteria
1. The infection occurs within 30 days after surgery or within 1 year if an implant is
present and the infection seems related to the operation.
2. The infection involves a joint/organ/space, or anatomic structures opened or
manipulated during the operation.
3. At least one of the following:
 Purulent drainage from a drain placed into the organ/space.
 An organism is isolated from a culture sample obtained aseptically from joint fluid
or deep tissue.
 An abscess or other evidence of infection involving a joint, organ or space during
reoperation, radiological examination or histopathology.
 A diagnosis of an organ/space SSI by a surgeon

RISK FACTORS FOR DEVELOPMENT OF SURGICAL SITE INFECTIONS
PATIENT FACTORS
Older age
Immunosuppression
Obesity
Diabetes mellitus , malignancies, steroids
Chronic inflammatory process
Malnutrition
Peripheral vascular disease
Anemia
Radiation
Chronic skin disease
Carrier state (e.g., chronic Staphylococcus carriage)
Recent operation
LOCAL FACTORS
Poor skin preparation, Surgical technique
Contamination of instruments
Inadequate antibiotic prophylaxis
Prolonged procedure
Local tissue necrosis, foreign body
Hypoxia, hypothermia, hematoma,
MICROBIAL FACTORS
Prolonged hospitalization (leading to nosocomial organisms)
Toxin secretion
Resistance to clearance (e.g., capsule formation)
Remote site infection
Bacterial number, virulence, and antimicrobial resistance
Previous antibiotic therapy

Surgical Wound Classification According to Degree of Contamination
WOUND CLASS
DEFINITION
Clean (classI)  Surgically incised, no break of asepsis.
 An uninfected operative wound in which no inflammation is encountered
 lumen is not entered.
 Wounds are closed primarily and, if necessary, drained with closed drainage.
 Surgical wounds after blunt trauma should be included in this category if they
meet the criteria
 Infection rate <2%
 Eg herniorrhaphy, lump excision, thyroidectomy, total joint athroplasty, lipoma
excision
Clean-
contaminated
(classII)
 lumen is entered under controlled conditions and without unusual
contamination or minimal spillage
 rate of infection is 5-10%
 Eg Cholecystectomy, elective GI surgery (not colon), bladder surgery,
uninflamed appendectomy
Contaminated
(classIII)
 Open, fresh, accidental wounds. <4h
 operations with major breaks in sterile technique
 gross spillage from the lumen
 and incisions in which acute, nonpurulent inflammation is encountered are
included in this category
 Rate of infection is 15-20%
 Eg appendectomy for inflamed appendix, Colorectal surgery, bowel resection
for infarcted bowel,
Dirty (class IV)  Old traumatic wounds with retained devitalized tissue, perforated viscera,
abscess, fecal contamination, established infection b4 wound is made on skin.
 Infection rate <40%

Preventive Measures for Surgical Site Infection
TIMING OF
ACTION
DETERMINANT IN WHICH THE PREVENTIVE MEASURE ACTS
Microorganism Local Patient
Preoperative Shorten preoperative
stay
Antiseptic shower
preoperatively
Appropriate
preoperative hair
removal or no hair
removal
Avoid or treat remote
site infections
Antimicrobial
prophylaxis
Appropriate preoperative hair
removal or no hair removal
Optimize
nutrition
Preoperative
warming
Tight glucose
control (insulin
drip)
Stop smoking
Intraoperative Asepsis and
antisepsis
Avoid spillage in
gastrointestinal cases
Surgical technique:
Hematoma/seroma
Good perfusion
Complete débridement
Dead spaces
Monofilament sutures
Justified drain use
(closed)
Limit use of
sutures/foreign bodies
Delayed primary closure
when indicated
Supplemental
oxygen
Intraoperative
warming
Adequate fluid
resuscitation
Tight glucose
control (insulin
drip)
Postoperative Protect incision for
48-72 hours
Remove drains as
soon as possible
Avoid postoperative
bacteremia
Postoperative dressing for 48-72
hours
Early enteral
nutrition
Supplemental
oxygen
Tight glucose
control
(insulin drip)
Surveillance
programs

ACUTE INFECTIONS
Cellulitis
Phlegmon
Abscess
Pustule, furuncle and carbuncles
Hydradenitis supprativa
Infective gangrene
Tetanus
Necrotizing Fasciitis
Erysipelas
CELLULITIS
This is a diffuse inflammation of the subcutaneous tissue resulting from invasion
by pyogenic bacteria. It spreads along subcutaneous tissues and fascial planes.
Usually due to infection with ß haemolytic streptococcus- strep.pyogenes
(commonest cause) or Staph. aureus .Both produce enzymes that degrade tissue
and allow spread of infection.
Anaerobic streptococci (peptostreptococci) are part of the normal flora of the
mouth and gastrointestinal tract. In contrast to other streptococcal wound
infections, these organisms produce a thin, brown discharge, often with
crepitation in the infected tissue (anaerobic cellulitis).
Clinical features
• Cellulitis usually presents with a well demarcated area of inflammation
• Redness, heat, swelling and pain are the cardinal signs of inflammation
• Usually associated with malaise, fever and a raised white cell count
• If not rapidly treated it can progress to lymphangitis and lymphadenitis
• Localised areas of skin necrosis may occur
• Predisposing factors include
o Lymphoedema
o Venous stasis
o Diabetes mellitus
o Surgical wounds
Management
 Rest and elevation of the affected limb andapplication of insulating dressings to
prevent heat loss arecomforting
 Antibiotics
 May initially be given orally
 Intravenous administration if no rapid improvement

 Benzylpenicillin and flucloxacillin are usually antibiotics of choice
where suppuration occurs surgical d rainage is indicated.
PHLEGMON
occurs when inflammation is relatively diffuse, i.e. like cellulitis, yet there are
small loci of necrotic tissue as well as multiple tiny pockets of pus. It is the
subsequent progression shortly to innumerable microscopic abscesses which
distinguishes a phlegmon from cellulitis. The usual causative organism is
staph. aureus, possibly in combination with virulent strains of Strep.
haemolyticus.
PUSTULE, FURUNCLE AND CARBUNCLES
These are forms of abscesses peculiar to the skin and result from infections of
hair follicles by Staph. Pyogenes. The tiny abscess thus formed is a pustule and
the inflammation may subside with egress of the bead of pus. The infection
frequently spreads to the surrounding subcutancous tissue before discharge of the
necrotic products and in this layer further extension may take place involving
several hair follicles. This is a typical boil or furuncle with a central core of
necrotic tissue which is discharged with the pus on ripening of the boil.
Carbuncles also result from infection of hair follicles but in areas such as the back
of the neck, back of the trunk, the hairy surfaces of the hand or fingers, the
lip and scalp, well-endowed with thick columns of subcutaneous fat projecting
around the follicles. Diabetics arc particularly prone to this complication. Word
meaning of carbuncle is charcoal. It is an infective ga11grane of skin and
subcutaneous tissue. Control of diabetes is essential using insulin. Antibiotics like
penicilhns, cephalosporins or depending on C/S is given. Drainage is done by a
cruciate incision and debridement or all dead tissue is done. Excision is done later.
Once wound granulates well, skin grafting may be required.
HYDRADENITIS SUPPRATIVA
It is a chronic infective and fibrous disease of the skin bearing apocrine sweat
glands. Apocrine sweat glands are coiled glands which open into the hair follicles.
Site of apocrine sweat glands:
• Axilla, Areola, Umbilicus, Groin, Perineum

Aetiology
• Obesity, smoking, Poor hygiene,Diabetes mellitus, Steroids.
Common bacteria involved are staphylococci, streptococci, staphylococcus
~aureus, propioni-bacterium acnes.
Clinical Features
Common in females 4 : 1.
Commonest site is axilla.
Multiple discharging sinusct., with nodules in the skin which is tender.
Induration due to fibrosis.
Investigation: Discharge study, Biopsy.
DDX: Tuberculous sinus, Malignancy (squamous cell carcinoma of skin).
Treatment
Antibiotics.
Excision of the involved area widely followed by skin grafting or flaps (radical
wound excision). Wounds in the affected area do not heal well by secondary
intention.
Antiandrogen drugs.
ABSCESS
Liquefaction of the dead tissue is produced by proteolytic enzymes contained in
the polymorphonuclear leucocytes and the mass of bacteria, leucocytes, exudate
and dying tissue residues thus formed is called pus. A pyogenic membrane of
granulation tissue soon forms separating the suppurating mass from the
contiguous normal tissues. (pyogenic abscess)
Other Types Pyaemic abscess, Metastatic abscess, Cold abscess due to chronic
infection like tuberculosis
Bacteria causing abscess
• Staph. aureus.
• Strept. pyogenes
• Gram-negative bacteria (E. coli, Pstudomonas, Klebsiella).
• Anaerobes.

Factors precipitating abscess formation
• General condition of the patient; nutrition, anaemia, age of the patient
• Associa1ted diseases: Diabetes, HIV, immununosuppression
• type and virulence of the organisms
• Trauma, haematoma, road traffic accidents
Clinical Features
Fever often with chills and rigors.
Localised swelling which is smooth, soft and fluctuant
Visible (pointing) pus.
Throbbing pain and pointing tenderness
Brawny induration around.
Redness and warmth with restricted movement around the joint
(Commonly cellulitis occurs first which eventually get localized to form abscess.)
Treatment
Abscess should be formed before draining. Exceptions for this rule are:Parotid abscess,
Breast abscess, Axillary abscess, Thigh abscess, Ischiorectal abscess
INFECTIVE GANGRENE
Gangrene is the death of large sections of tissue with superimposed putrefaction. It is
occasionally due to infection. It is either directly through microbial enzymes or indirectly
through thrombotic occlusion of blood vessels.
Infective gangrene is aerobic, anaerobic or synergistic. Aerobic gangrene; the causative
organisms are highly virulent strains of Strep. haemolyticus often occurring in epidemic
forms such as the classic hospital gangrene. A similar condition may result from certain
highly virulent strains of Staph. aureus - the scalded skin syndrome. P. aeruginosa
burn wound necrosis is another form of monobacterial aerobic gangrene.
Treatment: appropriate bactericidal chemotherapy and wide debridement of all necrotic
tissues.

Anaerobic gangrene/ Gas gangrene it is an infective gangrene caused by clostridial
organisms.
The causative organisms fall into two groups: those that breakdown starch or the
saccharolytic group (CI. Welchii or CI. Perfringens, Cl. novy, Cl. oedematiens, Cl. septicum)
and those which break down protein or the proteolytic group (Cl. Sporogenes and CI.
haemolyticus). The effects produce are as a result of exotoxins produced by organisms.
It usually takes two forms; clostridium myonecrosis (attacking muscles more serious
disease with high mortality) and clostridium welchii cellulitis (affecting subcutenous
tissue) commoner, not associated with cardiovascular disturbances.
Extensive necrosis of muscle with production of gas (hydrogen sulphide; nitrogen; carbon
dioxide) which stains the muscle brown or black. Usually muscle is involved from origin
to insertion. Often may extend into thoracic and abdominal muscles.When it affects the
liver it causes necrosis with frothy blood-foaming liver, is characteristic.
Clinical Features
 Symptoms develop rapidly appearing within 10 -12 h after the injury.
 Features of toxaernia, fever, tachycardia, pallor.
 Wound is under tension with foul smelling discharge (sickly sweety odour).
 Khaki brown colored skin due to haemolysis.
 Crepitus can be felt.
 Jaundice may be ominous sign and also oliguria signifies renal failure.
Prevention of gas gangrene
 Proper debridement of devitalised crushed wounds.
 Devitalized wou11ds should not be sutured.
 Adequate cleaning of the wounds with H2O 2 and normal saline.
 Penicillin as prophylactic antibiotic.
X-rays of the affected part may reveal in the soft tissues collections of gas which cannot
be demonstrated by palpation.
lnvestiga11ons
X·ray shows gas in muscle plane or under the skin.
LFT

Treatment
 Resuscitate; correct hypotension, anaemia
 Debridement
 Irrigation and pack with H2O2 soaked guaze
 Exhibition of antibiotics, usually penicillin in massive doses of up to 10
million units a day is essential. Clindamycin and metronidazole together
have been effective.
 Administration of gas gangrene serum
 Hyperbaric O2
SYNERGISTIC GANGRENE
It is the result of symbiotic infections from two or more bacterial species, and the
resultant lesion is far more fulminant than the regular lesion usually attributable to either
individual pathogen. The anaerobic partners are usually the primary pathogens
contributing the destructive enzymes. The aerobic organism extract the O2 from tissue
making it conducive for the anaerobes.
MeIeney's Gangrene or Cellulitis, a progressive recalcitrant ulcer produced by
symbiotic infections with the anaerobe Peptostreptococcus and the common
aerobe Staph. aureus.
Ulcerative gingivitis; Fusiformis bacillus and a spirochete.
Cancrum oris, or noma; Sets of gram-positive cocci and Bacteroides
melaninogenicus
Necrotizing fasciitis.; Combinations of coliforms, staphylococci, anaerobic
streptococci, peptostreptococci and Bacteroides species.
Fournier 's gangrene; Mixed aerobic-anaerobic organisms (including
Staphylococcus, micro-aerophilic Haemolytic streptococcus, E. coli, Fusobacterium
and Cl. welchi)
Treatment: antibiotics, debridement and hyperbaric O2

TETANUS
This is caused by a gram positive spore-forming obligate anaerobe, C. tetani, found in
the feces of humans and animals, and capable of prolonged survival in soil. Two exotoxins
are produced: tetanospasmin, a neurotoxin, and tetanolysin, a hemolysin.
PATHOGENESIS spores
Enters wound
Germinates in anaerobic media to releasing bacteria which multiply
Release of exotoxins
Tetanospasmin hemolysin
Hemolysis
Thru perineural sheath circulation
Enters the CNS, blocks toxemia (thru blood) blocks the NMJ by acting on the
cholinesterase at the anterior cholinesterase enzyme
horn cells
Causes hyperexcitability and aggravates the muscle spasm
reflex spasms of muscles
Once toxin fixed to the nerve
tissue, can no longer be neutralized
by antitoxin.

CLINICAL FEATURES
Symptoms
 Jaw stiffness –lockjaw (usu the 1st symptom), pain and stiffness in the neck
and back muscles
 Anxiousness, sweating
 Headache, delirium, sleeplessness
 Dysphagia
 Dyspnoea
Signs
 Trismus, due to spasm of masseter and pterygoids.
 Risus sardonicus (smiling facies), due to spasm of the facial muscle-
zygomaticus major. Looks as if patient is smiling.
 Neck rigidity.
 Spasm and rigidity of all muscles.
 Hyperreflexia.
 Respiratory changes-due to laryngeal muscle spasm, infection,
aspiration.
 Tonic-clonic convulsions.
 Abdominal wall rigidity often with haematoma formation.
 Severe convulsion may often lead to fractures, joint dislocations and
tendon ruptures.
 Fever and tachycardia.
 Retention of urine (due to spasm of urinary sphincter), constipation
(due to rectal spasm).
 Rarely carditis, can cause cardiac arrest. Steroid is helpful.
 Symptoms will be aggravated by stimuli like light, noise.
INCUBATION PERIOD
 Time between the entry of spore and appearance of first symptom.
 Usually 6-10 days.
 Shorter the incubation period worser the prognosis and more severe the
course of the disease.

PERIOD OF ONSET
 Time between appearance of first symptom and appearance of first
reflex spasm.
 Shorter the period of onset worser the prognosis and vice versa.
 If less than 48hrs, death is very likely
TYPES
 Generalized (commonest)
 Localized
 Cephalic
 Neonatal
DIFFERENT POSTURES IN TETANUS
 Opisthotonus: Posterior muscles are acting more, so backward
bending.
 Orthotonus: Straight posture. Both front and back muscles are acting
equally.
 Emprosthotonus: Forward bending as front muscles are acting more.
 Pleurosthotonus: lateral bending as lateral muscles act more.
STAGING OF TETANUS
 Mildly ill: Rigidity, spasm, trismus and different postures.
 Seriously ill: Spasm, rigidity, severe respiratory infections.
 Dangerously ill: Cyanosis with respiratory failure and tonic-clonic
convulsions.
CAUSE OF DEATH IN TETANUS
 Respiratory failure with aspiration pneumonia and ARDS
 Severe carditis--an ominous sign
 Mortality is 45-50%
PRINCIPLES FOR TETANUS PROPHYLAXIS
There are two types of immunization the active and passive. The active- toxoid- the dead
or modified organism introduce into the host body which stimulates the reticulo-
endothelial system to produce antibodies. More effective but it takes about 2-3 months to
be operational. The passive form- tetanus immune globuline- given to protect the

victim. It neutralizes the toxin, however it is less effective and may precipitate
anaphylaxis.
Toxoid administration; 0.5ml subcutaneously
 Traditionally ; day 1, 6weeks, 6month and every 10years
 Rapid method; day 1, day 4 and day 7. Using alum-precipitated toxoid.
Immunity is demonstrable in 28days.
Anti-tetanus serum: given IM, after a test dose of 0.1ml or 150 IU subcutaneously
 Human ATS 250IU
 Equine ATS 1500IU
TETANUS PROPHYLAXIS IN WOUND MANAGEMENT (see surgical
prophylaxis)
History of
tetanus
toxoid doses Clean, minor
wound
All other
wounds
Toxoid+ Immune
globulin
Toxoid+ Immune
globulin
Less than three
doses or
unknown
Yes No Yes Yes
Three or more
doses++
Yes if < 10 years
since last booster
No Yes if ≥ 5
years
since last
booster
No
Treatment ; aims of treatment are
 Halt production of toxin
 Neutralize circulating toxin
 Removing source of infection
 Controlling convulsion or spasms

 General supportive measures and prevention of complications
Treatment is multidisciplinary
GENERAL MEASURES
• isolation
• Avoid noise and light
• A TG 3,000 units 1M
• ATS-50,000 IM and 50,000 IV-After test dose
• Antibiotics like inj penicillin 20 lacs 6th hourly or metronidazole
• Inj tetanus toxoid 0.5 ml 1M - to deltoid muscle
• IV fluids with TPN
• Urinary catheterization
• Nasogastric tube is passed to prevent aspiration initially, later for feeding
• Regular suction of throat
• Nasal oxygen when required
SPECIFIC MEASURES
• IV diazepam 20 mg 6th hourly
• IV phenobarbitone 30 mg 6th hourly
• IV chorpromazine 25 mg 6th hourly
• Endotracheal intubation and ventilator support or Tracheostomy if there is
severe respiratory secretions
• Steroids
• Bronchodilators like deriphylline
• Wound care- debridement, drainage, and local injection of A TG, wound is
not closed primarily.
ERYSIPELAS
This arises from cutaneous infection with strains of Strep. Pyogenes with a predilection
for the lymphatics. Rose pink rash with cutaneous lymphatic oedema develop. Vesicles
are formed which form eventually ruptures discharge. Site of predilection include face,
orbit, scrotum and umbilicus in infant. Toxemia is always a feature. Milian ear sign is
use to differentiate it from cellulitis wherein in cellulitis the ear lobe is spared. The
condition is associated with poor hygiene. Treatment is with penicillin.

NECROTISING FASCITIS
It is spreading inflammation of the skin, deep fascia and soft tissues with extensive
destruction, toxaemia.
Types;
 Type 1-lt is due to mixed infection
 Type 11- lt is due to Strep Pyogenes, usually due to minor trauma like
abrasions.
 Occurs in immunocompromised patients
 Often diabetic, alcoholics or intravenous drug abusers
 Occurs at several characteristic sites
 Limbs after cuts, abrasions or bites
 Around postoperative abdominal surgical wounds
 In the perineum secondary to anorectal sepsis
 In the male genitalia (Fournier's gangrene)
• Polymicrobial infection involving the following:
 Facultative aerobes
 Streptococcal species or E. coli
 Anaerobes
 Exotoxins produce severe systemic toxicity
Clinical features
 Often presents similar to cellulitis
 Warning features include
o Severe pain - out of proportion to the clinical signs
o Severe systemic toxicity
o Cutaneous gangrene
o Hemorrhagic fluid leaking from a wound
MANAGEMENT
• Requires high clinical suspicion and early diagnosis
• Patients should be managed in high dependency unit
• Need fluid resuscitation and organ support
• Early surgical debridement is essential

• Requires excision well into apparently normal tissue
• Amputation or fasciotomies may be required
• Defunctioning colostomy may be required for perineal sepsis
• Antibiotic cover should include benzylpenicillin, metronidazole and
gentamycin
• Hyperbaric oxygen therapy may be of benefit.
NOSOCOMIAL INFECTION
(Hospital Acquired Infection)
It is an infection acquired because of hospital stay.
SOURCES
• Contaminated infected wounds.
• Urinary tract infection.
• Respiratory tract infection.
• Opportunistic infections.
• Abdominal wounds with severe sepsis spreading can occur from one patient
to another, through nurses or hospital staffs who fail to practice strict asepsis.
It is more common in
• Diabetics
• Immunosuppressive individuals
• Patients on steroid therapy a nd life-Supporting machines
• Instrumentations (indwelling catheter, IV cannula, tracheostomy tube)
• Patients with artificial prosthesis
ORGANISMS
 Staphylococcus aureus is the commonest organism causing hospital
acquired wound infection. Others are Pseudomonas, Klebsella, E.
coli, Proteus,
 Strept. pneumo, Haemophilus, Herpes,Varicella, Aspergillus,
Pneumocystis carinii are the commonest pathogens involved in hospital
acquired respiratory tract infection which spreads through droplets.
 Klebsiella is the commonest pathogen involved in hospital acquired UTI
which is highly resistant to drugs.

MANAGEMENT
Most of the time, organisms involved are multidrug resistant, virulent and hence, cause
severe sepsis.
• Antibiotics.
• Isolation.
• Blood, urine, pus for culture and sensitivity to isolate the organisms.
• Blood transfusion, plasma or albumin therapy.
• Ventilator support.
• Maintaining optimum urine output.
• Nutritional support.
PREVENTION
• Isolation of patients with bodly infected open wounds, severe RTI/UTI.
• Following strict aseptic measures in out and in ward by hospital attendants.
• Proper cleaning and use of disinfectant lotions and sprays for bedpans,
toilets and floor.
• The precipitating causes has to be treated, along with caring for proper
nutrition and improving the anaemic status by blood transfusion.

WOUND AND WOUND HEALING
Wound is a break in the integrity of the skin or tissues often which may be
associated with disruption of the structure and function.
CAUSES
o Mechanical agents
o Chemical agents
o Radiation energy
o Pathogenic micro-organism
TYPES /CLASSIFICATION
 Close- intact epithelial surface
o Contusion or bruise: injury to tissue subadjacent to surface
epithelium usually by blunt trauma. A subcutaneous
hematoma > 1cm is Ecchymosis
o Hematoma: is a localized collection of blood outside the blood
vessels, liquid or clotted within the tissue.
 Open- break or disruption of skin or epithelium.
o Incision; a wound created with sharp instrument usually
during surgery
o Abrasion; loss of superficial layers of the epithelium
o Laceration: irregular tear-like wounds caused by some blunt
trauma or sharp instrument.
o Avulsion; injuries in which a body structure is forcibly
detached from its normal point of insertion. May be complete
(no connection between the injured and its original site) or
partial (tenuous or strands of tissue connect the tissue to site)
o Puncture: caused by pointed instrument with small entry e.g.
nail puncture
o Penetrating or perforating ; penetrating wounds enter a body
cavity such as the chest or abdomen perforating wounds
entirely pass through an organ or cavity and are characteristic
of firearms or missile injuries.
o Amputation;
o Gunshot; caused by a bullet or similar projectile driving into
or through the body. There may be two wounds, one at the
site of entry and one at the site of exit.

RANK AND WAKEFIELD CLASSIFICATION
o Tidy wounds
o Incised
o Clean
o Healthy tissues
o Seldom tissue loss
o Untidy wounds
o Crushed or avulsed
o Devitalised tissues
o Contaminated
o Often tissue loss
SURGICAL WOUNDS (see page 7)
o Clean
o Clean contaminated
o Contaminated
o Dirty
ACUTE AND CHRONIC WOUNDS
Acute wounds heal in a predictable manner and time frame. The process occurs with few,
if any, complications, and the end result is a well-healed wound.
A chronic wound is a wound that does not heal in an orderly set of stages and in a
predictable amount of time the way most wounds do; wounds that do not heal within
three months are often considered chronic. E.g. chronic leg ulcer
SIMPLE OR COMPLEX WOUND
In simple wounds, only skin is involved. Complex wounds, vessels, nerve, tendons, or
bones are involved.
WOUND MANAGEMENT (acute wound)
o History – timing, cause, type of injury, nature of force
o Examination – site, size, shape and depth, involvement of neighboring structures
o Initial resuscitation may be required
o Primary closure depends on the time of presentation; presentation within the
“Golden hours”- 6-8hours are primarily sutured otherwise delayed.

TREATMENT PROCEDURE
o Debridement
o Strict asepsis
o Wound closure
o Gentle tissue handling
o Minimize blood loss
o General measures
o Tetanus prophylaxis
o Immobilization and elevation
o Broad spectrum bactericidal antibiotics
WOUND HEALING
Wound healing is the process by which damaged tissues of the body are repaired by living
tissue. It is a natural restorative response to tissue injury.
PHASES
o HEMOSTASIS AND INFLAMMATORY
o Hemostasis precedes and initiates inflammation, with the ensuing release of
chemotactic factors from the wound site.
o Exposure of subendothelial collagen to platelets results in platelet aggregation,
degranulation, and activation of the coagulation cascade. Platelet -granules release
a number of wound-active substances, such as platelet-derived growth factor
(PDGF), transforming growth factor beta (TGF-b), platelet-activating factor
(PAF), fibronectin, and serotonin. There is also release of basic fibroblast growth
factor(b-FGF) and epidermal growth factor (EGF), VEGF, IGF-1.
o The process;
 Start immediately after wounding and last 4-6days
 1st vasoconstriction
 2nd blood clot formation
 3rd platelet aggregation
 4th platelet degranulation- growth factors release, serotonin and other
chemo-attractants
 5th vasodilatation- plasma,plasma proteins, C5a and C3a are poured into the
wound
 6th chemotaxis

 Granulocytes -1st 48hrs, attracted by inflammatory mediators
 Monocytes –attracted by compliment, activated by fibrin, hypoxia,
acidosis, foreign body. Reach maximum at 24hrs and last for weeks.
 Macrophage- 3rd day. Activated macrophage are essential for
proliferation, mediate angiogenesis,
o DESTRUCTIVE PHASE (DEMOLITION)
 Immediately follows inflammatory phase
 There is removal of dead and dying tissues from the wound
 Neutrophils and monocytes migrate into the wound kill bacteria,
monocytes converts to macrophage.
 The inflammatory and destructive phases are the LAG phases during which
wound has no tensile strength. A preparation phase, where foundation of
repair is laid down . 4-6days may be prolonged by infection.
o PROLIFERATIVE (COLLAGEN OR FIBROBLASTIC PHASE)
 Tensile strength of wound increase. Rapidly from 1-6weeks and slowly upto
a year.
 1st angiogenesis
 2nd fibroblast formation
 3rd formation of granulation tissue
 4th re-epithelialization
o REMODELING (MATURATION PHASE)
 Start from weeks to years
 Blood vessels starts to disappear(endarteritis obliterans)
 The fibroblasts starts to disappear
 Type III collagen is gradually been replaced by type I
 Tensile strength of scar gradually increase
TENSILE STRENGHT OF A WOUND; the capacity of the cut edge of a wound to hold
together and resist disruption. Very slight in the lag phase(4-6days) bridge only by
epithelium. It rises sharply to with peak rate at 14-15th day corresponds to fibroplasia in
the wound. After 15th day, the tensile strength but at slower rate after 6th weeks, for a year.
Attains 50% of pre-injury state at 3years. Lag phase of rectus sheeth is 7days. Increases
steeply for 3months, then more gradually for 1 year.

COLLAGEN; structural proteins in the extracellular space synthesis by fibroblast.
Tropocollagen is the procollagen molecule. Helical structure with glycine at every third
position, hydroxyproline(most abuntant) and hydroxylysine. Vitamin C is required in
the hydroxylation of proline and lysine. Copper is required to hydroxylate lysine. The 4
common types; I, II, III, IV seen predominantly in ‘SCAB’ (skin, connective tissues or
cartilage, arteries and basement membrane) respectively.
TYPES OF WOUND HEALING
Healing by primary intention
Healing by secondary intention
Healing by tertiary intention
Healing by primary intention
 Wound edges opposed.
 Normal healing.
 Minimal scar
 Healing In a surgically incised wound
■ By secondary intention
 Wound left open.
 Heals by granulation, contraction and epithelialisation
 Increased inflammation and proliferation
 Poor scar
 Healing in a wound with much tissue loss.
■ By tertiary intention
 also called delayed primary intention
 Wound initially left open(4-5days)
 Edges later opposed when healing conditions favourable
 Heavily contaminated wound

FACTORS AFFECTING WOUND HEALING
Systemic
 Age
 Malnutrition
 Trauma
 Metabolic diseases
 Immunosuppression
 Connective tissue disorders
 Smoking
 Medications; Steroids, cytotoxic.
Local
 Mechanical injury
 Infection
 Edema
 Ischemia/necrotic tissue
 Topical agents
 Ionizing radiation
 Low oxygen tension
 Foreign bodies
 Site of the wound; pressure, repeated movement
COMPLICATIONS OF WOUND HEALING
 Wound infection, septicaemia.
 Chronicity
 Abnormal scars: hypertrophic scar, keloid.
 Contracture
 hyperpigmentation
 Implantation cyst
 Neoplastic change
 Weak scar
 Cicatrization

DIFFERENCE BETWEEN KELOID AND HYPERTROPHIC SCAR
KELOID HYPRETROPHIC SCARS
Genetic predisposition yes no
Site of occurrence chest wall, upper arm anywhere in the body,
ears, lower neck common in flexure areas
Growth continues to grow without growth limits for 6 month
time limit, goes beyond scar limit to scar tissue only.
and extends to normal skin.
Treatment poor response good response to steroid
Recurrence very high uncommon
Collagen synthesis 20 times more than normal 6 times than normal skin
skin,(type III thick ) (type III fine collagen)
Age adolescence and middle children
age
Sex commoner in females equal in both sex
Race more in blacks (15 times) no racial relation
Structure Thick collagen with increased Fine collagen with
epidermal hyaluronic acid increased alpha actin
Size of injury no relation, small healed scar related to size of injury and
can form large keloid duration of healing.
WOUND DEHISCENCE.
The partial or total disruption of any or all layers of the operative wound.
Define evisceration. Rupture of the abdominal wall and extrusion of the abdominal viscera.
FACTORS THAT PREDISPOSE TO DEHISCENCE
 Age > 60 years,
 obesity and increased intra-abdominal pressure,
 malnutrition,
 renal or hepatic insufficiency,

 diabetes mellitus, use of corticosteroids or cytotoxic drugs, and radiation have
been implicated in wound dehiscence.
 Infection also plays an important role; an infective agent is identified in more than
half of wounds that undergo dehiscence.
 Despite these excuses, the most important factor in wound dehiscence is the
adequacy of closure. Fascial edges should not be devitalized. Ideally the linea alba
sutures should be placed neither too laterally nor too medially. Excessive lateral
placement may incorporate the variable blood supply of the rectus abdominis
muscle and compromise fascial circulation. Excessive medial placement misses
the point of maximal strength at the transition zone between the linea alba and
rectus abdominis sheath. In addition, sutures should be tied correctly without
excessive tension, and suture material of adequate tensile strength should be
chosen.
WHEN DOES WOUND DEHISCENCE OCCUR
It may occur at any time after surgery; however, it is most common between the 5th and 10th
postoperative days, when wound strength is at a minimum.
SIGNS AND SYMPTOMS OF WOUND DEHISCENCE
 Normally a ridge of palpable thickening (healing ridge) extends about 0.5 cm on each side
of the incision within 1 week. Absence of this ridge may be a strong predictor of
impending wound breakdown.
 More commonly, leakage of serosanguineous fluid from the wound is the first sign.
 In some instances, sudden evisceration may be the first indication of abdominal wound
dehiscence.
 The patient also may describe a sensation of tearing or popping associated with coughing
or retching.
MANAGEMENT OF WOUND DEHISCENCE.
 If the dehiscence is not associated with infection, elective reclosure may be the
appropriate therapeutic course.
 If the condition of the patient or wound makes reclosure unacceptable, however, the
wound should be allowed to heal by second intention. An unstable scar or incisional
hernia may be dealt with at a later, safer time.
 Dehiscense of a laparotomy wound with evisceration is a surgical emergency with a
reported mortality of 10-20%.

o Initial treatment in this instance consists of appropriate resuscitation while
protecting the eviscerated organs with moist towels;
o the next step is prompt surgical closure. Exposed bowel or omentum should be
lavaged thoroughly and returned to the abdomen
o The abdominal wall should be closed; and the skin wound should be packed open.
Vacuum-assisted wound closure may be valuable in select cases.

SUTURES AND SUTURE MATERIALS
DEFINITION
A suture is a strand of material use in approximation of wound edges or ligation of blood
vessel.
PROPERTIES OF AN IDEAL SUTURE
• Adequate tensile strength
• Good knot holding property
• Should be least reactive (inert)
• Easy handling property
• Should have less memory
• Should be easily available and cost effective
CLASSIFICATION
 Absorbable (natural or synthetic)
These are broken down in the body and eventually absorbed by digestion by lysosomal enzyme of
white blood cells or by hydrolysis (synthetic absorbable sutures).
 Non-absorbable (natural or synthetic)
They effectively resists enzymatic digestion. They are used in tissues that heal more slowly, or if a
very secure tightening is required. They are either left in the body, where they become embedded
in the scar tissue, or they are removed when healing is complete.
NATURAL ABSORBABLE
o Catgut
o Plain catgut is derived from submucosa of jejunum of sheep.
o - It is yellowish white in colour.
o - It is absorbed by inflammatory reaction and phagocytosis-absorption time
is 7 days.
o - It is used for subcutaneous tissue, muscle, circumcision in children.
Chromic catgut is catgut with chromic acid salt.

- It is brown in colour.
- Its absorption time is 21 days.
- It is used for suturing muscle, fascia, external oblique aponeurosis, ligating
pedicles, etc.
o Collagen
This is produced from the collagen fibers from the bovine flexor tendon in
both plain and chromic form, and can be applied in the same fields as
surgical gut.
SYNTHETIC ABSORBABLE
o Polyglycolic acid
o Dexon (Polyglycolic acid) is synthetic absorbable suture material like
vicryl. It is creamy yellow in colour (braided).
o It has an excellent tensile strength (remaining unchanged for about 3
weeks) and excellent knot security. It is completely absorbed in 60-90
days.
o Polyglactin
o Vicryl (Polyglactic acid):
o - It is synthetic absorbable suture material.
o - It gets absorbed in 90 days.
o - Absorption is by hydrolysis.
o - It is violet in colour (braided).
o - It is multifilament and braided.
o - It is very good suture material for bowel anastomosis,
o suturing muscles, closure of peritoneum.
o Poly-p-dioxanone
o PDS (Poly Dioxanone Suture material) is absorbable suture material.
o It is creamy in colour with properties like vicryl.
o It is costly but better suture material than vicryl.
o The tensile strength on day 14 is 70%. Absorption is minimal up to 90 days,
but complete within 6 months.
o Maxon (Polyglyconate) monofilament.
o Monocryl (Polyglecaprone) monofilament.
o Biosyn (Glycomer) monofilament
NATURAL NON-ABSORBABLE
o Silk
o Silk is natural, multifilament, braided, non-absorbable suture material derived
from cocoon of silkwormlarva. It is black in colour. It is coated suture material
to reduce capillary action.

o Linen
o This is a twisted thread, which is weaker than silk; however, it is straightened
when wet. Therefore, it must be dipped into saline solution before use.
o Cotton
o This is made from twisted cotton fibers. It should also be dipped into saline
solution.
o Stainless steel
o This causes almost no tissue reaction. It is manufactured in monofilament and
twisted forms.
o It is rarely used because it is difficult to handle, it may break up and it can easily
cut tissues.
SYNTHETIC NON-ABSORBABLE
o Polyesters
o They give the strongest sutures, apart from surgical steel.
o monofilament (Miralene or Mirafil)
o braided, either uncoated (Dacron, Mersilene or Dagrofil), or coated with Teflon
(Ethiflex or Synthofil)
o Polyamide (Nylon)
o Its tensile strength for 1 year is 80%, for two 2 years is 70% and for 11 years 66% and
it causes only a minimal inflammatory response.
o Polypropylene
o Polypropylene (Prolene) is synthetic, monofilament suture material.
o It is blue in colour.
o It has got high memory. (Memory of suture material is recoiling tendency after
removal from the packet. Ideally suture material should have low memory.)
(Prolene mesh used for hernioplasty is white in colour).
o it causes only a minimal tissue reaction, it has a high tensile strength (100% for 2
years) and it holds knots better than most other synthetic materials.
o It can also be applied in infected fields.
NUMBERING OF SUTURE MATERIAL
2-Thick. For pedicle ligation.
1-
0-zero.
1-zero.
2-zero. For bowel suturing.
3-zero.
4-zero.
5-zero. For vascular anastomosis.

6-zero.
7-zero.
8-zero.
9-zero. For ophthalmic surgery. Requires operating microscope.
TYPES OF SUTURING
Interrupted
o Simple
o Vertical mattress
o Horizontal mattress
Continuous
o Simple
o Locked
o Subcuticular
o Purse-string
TYPES OF KNOT
Reef knot or Viennese knot
Granny knot
Surgeons knot

CUTENEOUS ULCERS
ULCER is a sustained breach in the continuity of the surface epithelium- skin and mucous
membrane.
PARTS
1. Margin the line of demarcation between the ulcer and the intact skin.
o Healing margin shows typical bluish line of growing epithelium which is squamous
without cornification. Margin of a healing ulcer shows 3 zones
 Outer –white
 Intermediate – blue
 Inner – red
o Spreading ulcer margin shows irregular in malignant and inflamed in infected.
o Chronic non-healing ulcer shows fibrous thick white margin without the bluish
growing epithelium. (NB; margin commonly stated in conventional books)
2. Edge is the mode of union between the floor and the margin of the ulcer.
 Slopping –healing, venous ulcers.
 Punched out – trophic ulcers eg syphilitic
 Undermined – tuberculous
 Raised – rodent or basal cell ca.
 Everted – squamous cell ca.
3. Floor the exposed surface of the ulcer. i.e the part which can be seen within the edge of
the ulcer.
 Healing ulcer shows pink or red granular granulation tissue
 Chronic ulcer shows pale flat and smooth granulation tissue
 Infected ulcer shows unhealthy granulation tissue- contains slough.
 Tuberculous ulcer has afloor with watery or apple jelly granulation tissue
 A floor may also show hypertrophic granulation tissue- sprouting flesh.
4. Base the area on which the ulcer rest. The base is palpated through the floor of the ulcer
for;
 Mild induration may be felt in any chronic ulcer
 Marked induration is almost diagnostic of malignant ulcer
 Mobility of the ulcer over the underlying structure
CLASSIFICATION
Specific
Non-specific
Malignant

SPECIFIC ULCERS
They are caused by specific organisms e.g. mycobacterium ulcerans bacilli, treponema pallidum or
Pertenue. The edge is characteristic for each type.
 Tropical ulcers; synergistically by the anaerobic Fusobacteria (Bacteriodes
fusiformis) and the aerobic Borrelia vincenti. Commoner in males, risk factors
include malnutrition, walking bare-footed. Over 95% occur in the lower part of the
leg. Organisms are transmitted by flies.
 Tuberculous; mycobacterium tb
 Burili ; mycobacterium ulcerans
 Syphilitic; (gummatous ulcer); Treponema pallidum
 Yaws; Treponema pertenue
(NB; see text for details of specific ulcers )
NON- SPECIFIC
They have essentially the same feature of a sloping edge, but the underlying aetiologies are
varied. They are the commonest ulcers.
1. Traumatic ulcers.
2. Pyogenic ulcers.
3. Ulcers of vascular origin:
(i) Venous (gravitational) ulcers.
(ii) Arterial ulcers.
(iii) Decubitus ulcers.
(iv) Pressure sores.
4. Neurotropic (trophic) ulcers:
(i) Leprosy.
(ii) Diabetic neuropathy.
(iii) Cord lesions.
(iv) Peripheral neuropathies.
(v) Syringomyelia.
5. Ulcers associated with metabolic or systemic disease:
(i) Diabetic ulcers.
(ii) Haemoglobinopathic ulcers.
(iii) Ulcers of spherocytosis.
(iv) Ulcers of ulcerative colitis.
MALIGNANT ULCERS
 Squamous cell ca
 Malignant melanoma
 Basal cell ca
 Kaposi sarcoma
 Penetrating malignant tumour

PHASES
A non- specific ulcer goes through the following phases
I. Acute or infective phase / extension
 In this the initial phase, the ulcer is painful
 The sloughing floor is covered with purulent discharge in which different types of
bacteria may be identified
 Base is indurated and fixed
 Surrounding skin is inflamed
II. Transition phase
 The slough separates, the pus drains,
 infection subsides, granulation tissue grows and the floor becomes clean and
pinkish-red.
 The edge, which is sloping, has a thin bluish-white layer of young epithelium
growing inwards.
 The surrounding skin is slightly hyperaemic or nonnal.
 Induration diminish
III. Reparative or healing phase
 The ulcer is now painless.
 The healthy granulation tissue fills the floor and the epithelium grows from the
edge at the rate of 1 mm/day to cover the floor.
IV. Chronic, indolent or callous phase
 Some ulcers may enter a chronic phase and remain unhealthy for a long time
because of secondary infection, defective circulation, poor general condition,
foreign body, lack of rest, malignant transformation.
 Unhealthy granulation tissue
 Offensive discharge, indurated base ragged edge and inflamed surrounding skin.
COMPLICATIONS OF NON-SPECIFIC ULCERS
1. Septicaemia
2. Lymphangitis
3. Lymphadenitis
4. Wasting
5. Tetanus
6. Lymphoedema:- Recurrent lymphangitis may lead to below-knee lymphoedema of varying
degrees.
7. Periostitis: - When the ulcer is close to bone, periostitis occurs and if persistent may lead to
new bone format ion at the base of the ulcer.
8. Malignant change:- Long-standing ulcers and unstable scars may undergo squamous
carcinomatous change.
9. Deformities of the foot or ankle may occur if deep tissues are involved in the fibrosis.

TREATMENT OF NON-SPECIFIC ULCERS
1. ACUTE ULCERS
1. In the acute phase, the patient is admined for bed rest and the footend of the bed
elevated.
2 Wound swab is done for gram staining, culture and sensitivity of any organisms
cultured.
3. Broad-spectrum antibiotics are started while awaiting the results of the culture and
sensitivity tests.
4. Tetanus booster dose is given to prevent tetanus infection.
5. The wound is cleansed regularly with normal saline. Acetic acid is effective for cleansing
wounds suspected infected with pseudomonas.
6. Crepe bandage is applied firmly from the toes to the knee to promote lymphatic and
venous drainage.
7. The affected limb is splinted in the position of function to prevent formation of
contracture.
8. Physiotherapy is started early to prevent wastage of muscle and contractures.
9. Once the ulcer becomes healthy, it is grafted with split skingrart.
10. Where there is an infected slough, appropriate antibiotics are started and the slough
removed either with saline soaks or by sloughectomy i.e. surgical excision of the slough.
The wound is then cleansed regularly until healthy granulation tissue is formed.
A wound swab is then taken for culture to rule out streptococcal infection before grafting
with split skin.
2. CHRONIC ULCERS
These ulcers may be excised and then grafted with split-skin graft or covered with a flap.
3. ADVICE AFTER DISCHARGE
 The patient is advised on foot hygiene.
 He is advised to use pressure dressing from the toes to the knee to
promote lymph and venous drainage where there is excessive
scarring.
 Farmers are advised to wear protective clothing and boots.
 The patient should seek prompt treatment for any abrasion to the
affected limb.
DIFFERENTIAL DIAGNOSIS OF AN ULCER
The diagnosis is arrived at after:
1. Careful history.
2. Clinical examination and
3. Investigations.
HISTORY
Mode of onset
Duration
Pain
Progress of the ulcer:
Painful regional lymph lIodes
Symptoms or past history suggestive of;
Diabetes

Tuberculosis
DVT
Varicose vein
Haemoglobinopathy
Neuropathy
Yaws
Syphilis
EXAMINATION
a. The ulcer
 Number
 Site
 Size
 Shape
 Edge
 Floor
 Base
 Discharge
 Surrounding skin
 State of local circulation
 Arterial pulsation of the limb
 State of innervation
 Regional lymph node
b. General physical examination
INVESTIGATIONS
I. Urine - for sugar and albumin.
2. Blood ,
(i) V.D.R.L. for syphilis.
(ii) Sugar level for diabetes mellitus
(iii) Haemoglobin genotype for haemoglobinopathy .
(iv) Haemoglobin level to exclude anaemia.
(v) Plasma protein levels
(vi) Mantoux test.
(vii) E.S.R.
3. Bacteriology of the ulcer - for special organisms;Mycobacteria, Fusobacteria, Borrelia
4. Radiology:
(i) Plain films of ulcer to see any bony changes or calcification.
(ii) Duplex Doppler scanning, arteriography or venography for vascular disorders.
(iii) Plain films of the chest should be done also if tuberculosis or malignancy is suspected.
5. Biopsy of ulcer - may be the final step in definitive diagnosis.
6. Other tests may be done as indicated by the probable cause of the ulcer e.g. Lepromin test in
suspected leprosy.

FLUID AND ELECTROLYTES
Fluid and electrolyte management is paramount to the care of the surgical patient. Changes in
both fluid volume and electrolyte composition occur preoperatively, intraoperatively, and
postoperatively, as well as in response to trauma and sepsis.
BODY FLUIDS
TOTAL BODY WATER- (TBW); Water constitutes approximately 50 to 60% of total body weight.
It is primarily a reflection of body fat. Lean tissues such as muscle and solid organs have higher
water content than fat and bone. TBW depends on age, sex, obesity. It is lower in the aged and
obese.
Male – 60% body weight
Female -50% .
TBW--60%
ICF40% ECF20%
 Intravascular(plasma) 4%
 Extravascular 16%
 Transcellular 1%
 Interstitial 15%
TBW in full term neonate 75%, ECF 35%. The ratio of surface area to weight in neonate is larger
with more insensible loss. In preterm, TBW is 95%. By the age of 2years, it is corrected to TBW
65%, ECF 20%.
BODY ELECTROLYTE
INTRACELLULAR;
K+
14Ommol/l the most important cation
Na+
8mmol/l
Mg2+
15mmol/l
Phosphate 26mmol/l
most important anions
Protein 9mmol/l
EXTRACELLULAR
Na+
135-145mmol/l most important cation Mg2+
0.7-0.9mmol/l

K+
3.6-5.2mmol/l Cl-
95-105mmom/l
Ca2+
2.1-2.6mmol/l HCO3
-
24-29mmol/l
24HRS FLUID AND ELECTROLYTE REQUIREMENT IN THE TROPICS
FLUID
 LOSS
Insensible loss 1700ml
Urine 1500ml
Faeces 200ml
Total 3400ml
 GAIN
Endogenous production
200ml
 NET 3200ml
Surgical patient usually requires parenteral and not likely to pass stool, hence 24hrs requirement is
3000ml. for 10
C rise in temperature, 12% of daily requirement is added to compensate for water loss in
sweating.
ELECTROLYTE
Na+
130-140mmol/l
Urine 114mmol/l
Sweat 10-16mmol/l
Faeces 10mmol/l
K+
60mm0l/l
Urine 50mmol/l
Faeces 10mmol/l
Sweat – negligible
As surgical patient is unlikely to pass stool, daily Na+
is 130mmol and K+
50mmol.
Energy should be replace since patient is on NPO, and body store of glycogen (400g ≈1600kcal) is used
up in the 1st
day of starvation, then 75-90% is provided from combustion of fat and protein. 100-150g of

exogenous glucose is given to reduce gluconeogenesis to the minimum and acidosis prevented. 2L of 5%
DW contains 100g of glucose. VitC100-200g essential for wound healing and scavenger of free radicals
Bcomplex aids protein and CHO metabolisms. Other mineral and trace element are add prolong treatment
DISTURBANCE OF FLUID BALANCE
Extracellular volume deficit is the most common fluid disorder in surgical patients and can be either
acute or chronic. Acute volume deficit is associated with cardiovascular and central nervous system signs,
whereas chronic deficits display tissue signs, such as a decrease in skin turgor and sunken eyes, in
addition to cardiovascular and central nervous system signs. The most common cause of volume deficit in
surgical patients is a loss of GI fluids from nasogastric suction, vomiting, diarrhea, or enterocutaneous
fistula. In addition, sequestration secondary to soft tissue injuries, burns, and intra-abdominal processes
such as peritonitis, obstruction, or prolonged surgery can also lead to massive volume deficits.
Dehydration is loss of water and electrolyte especially sodium. Acute dehydration is loss of ECF as in
intestinal obstruction, peritonitis, diarrhea . in chronic dehydration, there is loss of both ECF and ICF as
in GOO. There is loss of large amount of K+
.
Shock ensues with ECF loss ≥ 3.5L
Signs and Symptoms of Volume Disturbances
System Volume Deficit Volume Excess
Generalized Weight loss Weight gain
Decreased skin turgor Peripheral edema
Cardiac Tachycardia Increased cardiac output
Orthostasis/hypotension Increased central venous pressure
Collapsed neck veins Distended neck veins
Murmur
Renal Oliguria —
Azotemia
GI Ileus Bowel edema
Pulmonary — Pulmonary edema
Extracellular volume excess may be iatrogenic or secondary to renal dysfunction, congestive heart failure,
or cirrhosis.
FLUID AND ELECTROLYTE THERAPY
Extracellular volume deficit leads to loss of fluid and electrolyte and the principle of correction is through
 Correction of deficit

 Correction of ongoing loss
 Maintainace fluid
 Monitoring of treatment
Parenteral solutions
Commonly used are;
0.9% saline
Na+
154mmol
Cl-
154mmol
mOsmo 308
Ringer’s lactate
Na+
130mmol
K+
4mmol
Ca2+
4mmol
Cl-
111mmol
HCO3
-
27mmol
mOsmo 273
full strength darrows
Na+
124mmol
K+
36mmol
Cl-
104mmol
HCO3- 56mmol
mOsmo 320
4.3% glucose in 1/5 saline
Na 30.8mmol
Cl 30.8mmol
Glucose 43g
5% dextrose water

50g glucose
Correction of dehydration (deficit)
IV access secured, blood samples taken for U/ECr, PCV
Crystalloid are started ; ringers lactate, N/S IL for 30-45min
Pass urethral catheter, empty the urinary bladder, then monitor urine output
Then re-assess patient, if parameters(PR,BP, urine output ) inadequate, repeat IV fluid IL over 30-45min,
and reassess as appropriate upto 4L, then give frusemide. Otherwise if adequate, place on maintenance of
1L 8hrly.
During resuscitation, the following parameters are checked for;
 Hourly urine output 30-50ml/hr (0.5-1ml/kg/min)
 Half-hourly P.R and BP
 Skin tugor, moistness of tongue , fill of subcutaneous veins
 Frequent auscultation of the lungs and monitoring of JVP to prevent overhydration or quickly
diagnose and treat if occur.
 CVP 10-15mmHg
Maintenance
With correction of deficit and patient is making adequate urine, PR,BP,CVP all within normal limit,
patient is placed on daily maintenance. 1L 8hrly, 2L of 5%DW,1L of N/S and 3g of KCL added to the
fluid. However, ongoing loss is taken into consideration and added to the total maintenance fluid.
Ongoing loss
Ongoing GI losses such as N-G tube drainage, drainage from enterocutenous fistulae, diarrhea, vomiting
are estimated and added into maintenance fluid.
Monitoring
 Input –out put chart
 Serum U/ECr must be checked daily and deficiency corrected,12hly for critically ill patient.
 Reapeat Hb/PCV after rehydration and correct if depleted.
 State of hydration assessed daily; urine output of ≥ 1000ml is indicative of good hydration
 Monitoring for overload
o Frequent auscultation
o CVP

ELECTROLYTE DISTURBANCE
SODIUM
HYPONATREMIA-
serum sodium level of ≤130mmol/L. Manifest clinically when serum Na<125mmol/L
Symptoms; Irritability, cerebral oedema – headache, vomiting and convulsion, pulmonary
congestion, convulsion is seen in severe hyponatremia < 120mmol.
Causes; vomiting or N-G aspiration, diarrhea, internal fluid shift, enterocutenous fistulae,
excessive sweating, polyuria.
Treatment ; IV normal saline. Treat the cause. In the presence of cerebral oedema, IV diuretics is
given.
HYPERNATREMIA
Hypernatremia results from either a loss of free water or a gain of sodium in excess of water.
Like hyponatremia, it can be associated with an increased, normal, or decreased extracellular
volume.
Types of Hypernatremla
• Euvolemic (pure water loos)
• Hypovolaemic (among the loss of water and sodium, more water is lost than sodium)
• Hypervolaemic (both sodium and water gain but sodium gain is more than water gain).
Hypernatremia could either be hypervolemic(caused either by iatrogenic administration of
sodium-containing fluids, including sodium bicarbonate. Urine Na conc. > 20mEq/L),
normovolemic(result from renal causes, including diabetes insipidus, diuretic use, and renal
disease) or hypovolemic(nonrenal water loss from the GI tract or skin, although the same
conditions can result in hypovolemic hypernatremia<20mEq/L)
Management is restriction of saline and sodium. Treatment of pulmonary oedema.
Correction is slowly to prevent cerebral oedema and hyperglycemia. N/S then 1/2strength saline
and later 5% dextrose.

POTASSIUM
Normal value is 3.5-5.6mmol/L
Hypokalemia
Can occur suddenly in a diabetic coma patient treated with insulin and saline.
Gradual loss is seen in;
• Diarrhoea of any causes, villous tumour of the rectum, ulcerative colitis.
• After trauma or surgery.
• Pyloric stenosis with gastric outlet obstruction.
• Duodenal fistula, ileostomy.
• After uretero sigmoidostomy.
• Insulin therapy.
• Poisoning.
• Drugs like beta agonists
Clinical Features
• Slurred speech.
• Muscular hypotonia.
• Depressed reflexes.
• Paralytic ileus.
• Weakness of respiratory muscles.
• Cardiac arrhythmias.
• Inability to produce concentrated urine and so causes nocturia and polyuria.
ECG shows prlonged QT interval, depression of the ST segment and inversion of T wave,
prominent U wave, ectopic beats. Often hypokalaemia is associated with alkalosis. Serum
potassium will be decreased.
Treatment
o Deficit ×weight ×0.6
o Using KCl in 5% dextrose or N/S slowly under ECG monitoring
o Patient making adequate urine
o Not > 20mmol/hr
o Not > 40mmol/L
o Not >120mmol/day
o Not given in bolus.
HYPERKALEMIA
Serum K+ > 6mmol/L
Causes:

o Trauma
o Burns
o Sepsis
o Shock
o Acidosis
o Massive transfusion of old blood
o Excessive supplement
o Drugs : K sparing diuretics, ACE inhibitors, Aminoglycoside
Clinical features
o Nausea, vomiting, diarrhea, muscle weakness
ECG;
o peak T wave,
o absent P wave,
o widened QRS,
o ventricular arrhythmias,
o fibrillation, cardiac arrest.
Treatment
o Under ECG monitoring
o Sodium bicarbonate 80-100mmol over 10min to combat acidosis
o 10% calcium gluconate to prevent cardiac arrest
o Glucose under influence of insulin uses K to form glycogen;
10IU of soluble insulin in 1L of 5%dextrose is given IV or 100ml of 20% dextrose in
30min
o Ion exchange resin, calcium resonium 15-30mg 6hly or 30g rectally is given to exchange Ca for
K.
o Β-2 agonist eg neubulised or IV salbutamol increase uptake of K
o Hemodialysis or peritoneal dialysis.
HYPERMAGNESAEMIA
It is rare. Serum magnesium > 2.5 mEq/L
Causes
• Advanced renal failure treated with magnesium
containing antacids, diabetic ketoacidosis.
• Intentionally produced hypermagnesaemia while treating pre-eclampsia.

Clinical Features
• l.oss of tendon reflexes (commonest).
• Neuromuscular depression.
• Flaccid quadriplegia.
• Respiratoty paralysis.
• Somnolence.
• Hypotension.
HYPOMAGNESAEMIA
• Serum magnesium< 1.5 mEq/L
Causes
o Malnutrition, alcohol.
o Large GI fluid loss.
o Patients on total parenteral nutrition.
Clinical Features
o Hypereflexia.
o Muscle spasm.
o Parasthesia.
o Tetany.
It mimics hypocalcaemia. It is often associated with hypokalaemia and hypocalcaemia.
Two gram (16 mEq) of magnesium sulphate slow intravenously, in 10 minutes. Later maintenance dose
of 1 mEq/kg/ day as slow continuous infusion is given/ oral magnesium is needed.
CALCIUM
The vast majority of the body's calcium is contained within the bone matrix, with <1% found in the ECF.
Serum calcium is distributed among three forms: protein found (40%), complexed to phosphate and other
anions (10%), and ionized (50%). It is the ionized fraction that is responsible for neuromuscular stability
and can be measured directly. When total serum calcium levels are measured, the albumin concentration
must be taken into consideration:
Adjust total serum calcium by 0.8mg/dl for every 1g/dl decrease in serum albumin

Unlike changes in albumin, changes in pH will affect the ionized calcium concentration. Acidosis
decreases protein binding, thereby increasing the ionized fraction of calcium.
Daily calcium intake is 1 to 3 g/d. Most of this is excreted via the bowel, with urinary excretion relatively
low. Total body calcium balance is under complex hormonal control, but disturbances in metabolism are
relatively long term and less important in the acute surgical setting. However, attention to the critical role
of ionized calcium in neuromuscular function often is required
HYPERCALCEMIA
Hypercalcemia is defined as a serum calcium level above the normal range of 8.5 to 10.5 mEq/L (2.2-
2.6mmol/L)or an increase in the ionized calcium level above 4.2 to 4.8 mg/dL. Primary
hyperparathyroidism in the outpatient setting and malignancy in hospitalized patients, from either bony
metastasis or secretion of parathyroid hormone–related protein, account for most cases of symptomatic
hypercalcemia.
Anorexia, nausea/vomiting, abdominal pain, Weakness, confusion, coma, bone pain, Hypertension,
arrhythmia, polyuria, Polydipsia
ECG changes in hypercalcemia include shortened QT interval, prolonged PR and QRS intervals,
increased QRS voltage, T-wave flattening and widening, and atrioventricular block (which can progress
to complete heart block and cardiac arrest).
Treatment ; initial therapy – fluid and diuretics, bisphosphonate and calcitonin.
Treatment of the underlying cause.
HYPOCALCEMIA
Hypocalcemia is defined as a serum calcium level below 8.5 mEq/L or a decrease in the ionized calcium
level below 4.2 mg/dL. The causes of hypocalcemia include;
o pancreatitis,
o massive soft tissue infections such as necrotizing fasciitis,
o renal failure,
o pancreatic and small bowel fistulas,
o hypoparathyroidism,
o toxic shock syndrome,
o abnormalities in magnesium levels,
o tumor lysis syndrome
o malignancies associated with increased osteoclastic activity eg breast and prostate ca.
o massive blood transfusion with citrate toxicity.
Asymptomatic hypocalcemia may occur when hypoproteinemia results in a normal ionized calcium level.
Conversely, symptoms can develop with a normal serum calcium level during alkalosis, which decreases
ionized calcium. neuromuscular and cardiac symptoms do not occur until the ionized fraction falls below
2.5 mg/d.

paresthesias of the face and extremities, muscle cramps, carpopedal spasm, stridor, tetany, and seizures.
Patients will demonstrate hyperreflexia and may exhibit positive Chvostek's sign (spasm resulting from
tapping over the facial nerve) and Trousseau's sign (spasm resulting from pressure applied to the nerves
and vessels of the upper extremity with a blood pressure cuff).Hypocalcemia may lead to decreased
cardiac contractility and heart failure. ECG changes of hypocalcemia include prolonged QT interval, T-
wave inversion, heart block, and ventricular fibrillation.
FLUID AND ELECTROLYTE IN;
BURNS
TYPHOID PERFORATION
GASTRIC OUTLET OBSTRUCTION
PANCREATITIS
BURNS
Hyponatremia : Hyponatremia is a result of decreased sodium in the blood from the destroyed tissue
caused by burns on the body.
Hyperkalemia; Hyperkalemia happens to burn victims as a result of the destruction of cells and tissues.
TYPHOID PERFORATION
Perforation is usually preceded by diarrhoea with considerable loss of potassium (20-40mmol/L) and
limited intake of food. With perforation, paralytic ileus occurs with loss of more potassium in the
accumulating intestinal secretions. The peritoneal exudate. which may be 2-3litres, also has increased
Concentration of potassium- 10mmol/L Vomiting also causes loss of more potassium (9 mmol/L).
The potassium deficit is therefore considerable although it may be masked by dehydration. This deficit
should be corrected pre-operatively as soon as urine output has improved with vigorous fluid therapy.
Otherwise, cardiac arrhythmias and even death on the table may result.
GASTRIC OUTLET OBSTRUCTION
Both E.C F. and I.C. F. are lost. Hydrogen and chloride ions are also lost. Potassium is lost not only in the
vomitus but also in large amounts from the kidney as a result of increased aldosterone secretion to
conserve sodium. The patient therefore has hyponatraemia, severe hypokalaemia, hypochloraemia and
metabolic alkalosis in addition to water depletion. He needs dextrose saline or saline and potassium
chloride later.

PREOPERATIVE FLUID THERAPY
A surgical patient without deficit, preoperatively are on NPO and hence placed on daily maintenance
fluid; 3L in adult surgical patient as seen above. This is form of 2L of 5%D/W and 1L of N/S and 3g of
KCl if making adequate urine. Fluid and electrolyte deficit if present is corrected before placing on
maintenance.
Alternatively fluid maintenance is given as;
For the first 0 to 10 kg Give 100 mL/kg per day
For the next 10 to 20 kg Give an additional 50 mL/kg per day
For weight >20 kg Give an additional 20 mL/kg per day
INTRAOPERATIVE FLUID THERAPY
With the induction of anesthesia, compensatory mechanisms are lost, and hypotension will develop if
volume deficits are not appropriately corrected before the time of surgery. Hemodynamic instability
during anesthesia is best avoided by correcting known fluid losses, replacing ongoing losses, and
providing adequate maintenance fluid therapy preoperatively. Blood loss is measured , the is third space
loss. Although no accurate formula can predict intraoperative fluid needs, replacement of ECF during
surgery often requires 500 to 1000 mL/hr of a balanced salt solution to support homeostasis.
Maintaining acceptable vital signs and urine output.
Redistributive and Evaporative Surgical Fluid Losses
Degree of tissue trauma Additional fluid requirement
Minimal (herniorapphy) 2 ml/kg/hr
Moderate (cholecystectomy) 4 ml/kg/hr
Severe (bowel resection) 6 ml/kg/hr
POST OPERATIVE FLUID THERAPY
Postoperative fluid therapy should be based on the patient's current estimated volume status and projected
ongoing fluid losses. Any deficits from either preoperative or intraoperative losses should be corrected
and ongoing requirements should be included along with maintenance fluids. In the initial postoperative
period, an isotonic solution should be administered.
COMPLICATIONS OF FLUID THERAPY
Thrombophlebitis
High osmolality

Prolong use of same needle or cannula and vein
Infection
Leakage of fluid around the vein
Endothelial injury
Local sepsis
Septicemia
Overloading
Air embolism
Pyrogenic reaction

SHOCK
DEFINITION
Shock is the clinical manifestation of failure of cellular function due to inadequate tissue
perfusion and consequent cellular hypoxia resulting from a reduction in the effective circulating
blood volume.
It the most common cause of death amongst surgical patient. Hence every surgeon must
understand the pathophysiology, diagnosis as well as priority in the management.
CLASSIFICATION
• Hypovolemic
• Cardiogenic
• Septic
• Neurogenic
• Anaphylactic
Hypovolemic shock; There is reduction in the actual blood volume. It may result from
Hemorrhagic (commonest)- could be internal or external bleeding
Loss of plasma as occurs in extensive bums or peritonitis.
Loss of Extracellular Fluid as occurs in intestinal obstruction, diarrhoea, peritonitis and
vomiting
Cardiogenic shock;
Impaired function of the heart causes reduced cardiac output and so to reduced effective
circulating blood volume. It is commonly due to myocardial infarction or contusion, cardiac
tamponade, sepsis and obstruction to blood flow from the heart by massive pulmonary embolism
or tension pneumothorax
The other forms (septic, neurogenic and anaphylactic) of shock results from peripheral
vasodilatation and pooling of blood resulting in reduction in effective circulating blood volume.
Total spinal anaesthesia, spinal injury-vasovagal syndrome, are causes of neurogenic shock.
PATHOPHYSIOLOGY
The cellular changes; in shock, there is cellular hypoxia, leading to decrease ATP production
(3ATP rather than 38) resulting in decrease efficacy of Na-K pump, with subsequent leakage of K
out cells and movement of Na into the cells along with water and the cells swell. The
concentration of cyclic AMP falls and the affect the actions of hormones on cell. With further
reduced energy production, there is release of lysosomal enzymes and proteases with causes lysis
of the cell with inflammatory responses.

The stages of shock; the stages are illustrated using haemorrhagic shock
Early stage; The average adult person has 4-5L of blood (75-80ml/kg) and 25 per cent (1000ml)
must normally be lost before shock appears. With blood loss, there is stimulation of the
baroreceptors which in turns sends inhibitory stimulus to the cardio-inhibitory (a center that
reduces the activity of the heart, via reduced vagal activity) center and the vasomotor center
(increases sympathic out flow via adrenaline release). There is subsequent vasoconstriction,
increase venous return, increase heart rate and contraction, and bronchiolar relaxation.
Middle stage; with continued bleeding or inadequate resuscitation, there is diversion of blood
from peripheral and splanchnic to vital organs (heart and brain). Reduction of renal perfusion
leads to release of renin from the juxaglomerular cells which causes conversion of
angiotensinogen to angiotensin I, this is further converted in the epithelium of the lungs to
angiotensin II. Angiotensin II – causes vasoconstriction, release aldosterone which causes
reabsorption of sodium and water, release of ADH, stimulates thirst center, stimulates sympathetic
out flow.
Splanchnic vasoconstriction causes mucosal ischemia, with depression of the barrier and bacterial
transmigration into the systemic circulation. (link between hemorrhagic and septic shock)
Late stage; the stage of decompensation. Compensatory mechanisms break down and the
circulation fails. Further blood loss reduce coronary and cerebral perfusion. There is cardiac
failure, venous pooling of blood, capillary damage from back pressure and impaired cerebral
function resulting in confusion, restlessness, coma and death.
CLINICAL FEATURES
1. Rapid, weak and thready pulse
2. Low or unrecordable blood pressure
3. Skin and mucous membrane is cold and clammy (except in distributive shock
where skin is warm). Mucous membrane is pale, cyanotic and collapse
4. Rapid and deep respiration (air hunger)
5. Confused, restless, apathetic or comatose, blurred vision
6. Decrease Urine output or anuria
7. Severe thirst
8. Subnormal temperature
9. MODS
MANAGEMENT OF A PATIENT IN SHOCK;
Categories;
a) Those who respond to treatment
b) Those who respond and relapse
c) Those who donot respond; a and b may require surgery to control bleeding

Resuscitation;
1. Control bleeding
2. Elevate the foot of the bed
3. Fluid replacement; secure iv access with widebore cannula. Take samples for hemogram,
GXM, U/ECr.
 Crystalloid (readily available); 1L of N/S or R/L is started over 30-45min, the re-
assess the PR, BP, urine output, CVP, if still deranged, repeat fluid up to 4L. (blood
must have been ready- in hemorrhagic shock. Otherwise septic shock in non-
hemorrhagic)
 Blood; in severe blood loss, crystalloid shows only transient improvement. Blood
is cross matched and transfused. Occasionally uncrossed matched blood is given to
save life.
 Blood substitute; in absent of blood, colloids; human albumin(most
physiologic), fresh frozen plasma, dextran 110 or 70, haemacel, gelofusine,
and hetastarch
4. Oxygen; oxygen supplements is given. Blood gases are monitored regularly and PO2
maintained between 80-100mmHg. If PO2 falls below 60mmHg and the PCO2 rises above
45mmHg, then ventilatory support is necessary.
5. Drugs
 Morphine; if patient is in pains, may be given 10mg 1v
 Vasodilators; after adequate fluid therapy, and normal CVP, but perfusion remains
inadequate;
i. Dobutamine; b-vasodilator, decreases pulmonary and systemic resistance
thereby better blood flow and O2 delivery.
ii. Isoproterenol; b-adrenergic; peripheral vasodilatation, increase force of
contraction of the heart.
iii. Dopamine; a precursor of nor-adrenaline, it acts on b1 and a-adrenergic
receptors.
 Hydrocortisone
 Naloxone
 Mannitol
 Sodium bicarbonate
MONITORING
1. CLINICAL
a. Sensorium
b. Skin; warm and vein refill
c. Pink conjunctiva
d. Capillary re-fill
2. Urine output > 30ml/h
3. PR and BP every 15min

4. CVP normal 10-15 cmH2O
5. Lungs and jugular vein
6. Blood gases
NON-HAEMORRHAGIC HYPOVOLEMIC SHOCK
Extracellular (extravascular) fluid loss must be at least 6% of body weight to result into shock.
That is 3600ml of ECF
IRREVERSIBLE SHOCK
Shock that does not respond to treatment.
Causes; inadequate fluid replacement, continued blood loss, undetected organ injury, metabolic
acidosis, myocardial failure, septic shock, MODS.

SEPTIC SHOCK
Results from moderate to severe sepsis or tissue damage. It is considered as part of a spectrum
and a progression of SIRS (systemic inflammatory response syndrome).
DEFINATION OF TERMS;
Bacteremia : transient invasion of circulation by bacteria
Septicemia: prolonged presence of bacteria in the blood accompanied by systemic reaction
SIRS (systemic inflammatory response syndrome ): it is a syndrome characterized by the presence
of two or more of the following clinical criteria:
 Temperature(core) >38°C or<36°C
 Heart rate >90beats/min
 Respiratory rate >20b/min or PaC02 <32mmHg
 WBC >12000cells/ml or <4000cells/ml or >10%immature band forms.
 Sepsis: SIRS with a clearly established focus of infection
 Severe sepsis: sepsis associated with organ dysfunction and hypoperfusion.
 Septic shock: Refers to severe sepsis which is not responsive to intravenous fluid
infusion for resuscitation and requires inotropic or vasopressor agent to maintain
systolic blood pressure.
EPIDEMIOLOGY
4.6 cases/1000 persons in a study in US. 200,000 cases annually with 50% mortality. M>F(most
studies M=52-66%). Extreme of ages are more affected. 13th leading cause of death in US. Leading
cause of death in ICU.
AETIOLOGY
BACTERIA: gram –ve nearly 2/3, gram+ve 1/3. of the gram –ve, E.coli is the commonest.
GRAM -VE
 Klebsiella,
 Entrobacter,
 Serratia,
 Proteus,
 Mirabillis/Vulgari,
 Pseudomonas and
 Bacteroides
GRAM +VE
 Streptococci

 Staph
 Clostridia and Pneumococci
Viruses, Fungi and Parasites in a few especially the immuno-compromised.
SOURCE
 Endogenous –
 Skin- SSI
 urinary tract- UTI
 respiratory tract- LRTI
 GIT- bowel surgery, perforations
 Exogenous.
 surgical instruments
 drapes
 imaging machines
 staff
RISK FACTORS
 Age (<10 >70years)
 malnutrition,
 anemia,
 Primary disease: Malignancies, DM, CLD, CRF,
 Immunosuppression, Immunosupresssive agents,
 necrotic tissue
 hematoma
 poor surgical technique
 Catheriration
 Prolong hospitalisation
 Major surgeries, trauma, extensive burns
PATHOGENESIS
Micro-organisms or products of tissue damage stimulates production of pro-inflammatory
cytokines (TNF-α, IL-1β, IL-6, IL-8) which in turn stimulate production of secondary mediators
(PGI2, PGE2, TXA2, LT, PAF,NO, KININS, IL-1,IL-6, OXYGEN FREE RADICAL, PROTEASES.) of
inflammation in order to localize infection and limit proliferation.
The production of the pro-inflammatory cytokines is regulated to limit damage.
However in poorly controlled sepsis or extensive tissue damage, there is excessive inflammatory
response which is poorly regulated.

Anti-inflammatory and immunosuppressive cytokines IL-10 which aided by IL-4 inhibits the
activity of the pro-inflammatory cytokines to limit damage.
In severe sepsis they become immunosuppressive to patient.

Effects of secondary mediators
 Damage of vascular endothelium
 Vasodilation of microvasculature
 Activation of neutrophils(aggravates endothelial damage)
 Diminished force of cardiac contraction
 These ultimately lead to peripheral pooling of blood, extravasation of fluid,
hypotension, hypoxia
EFFECT OF COPLIMENT COMPONENT
 vasodilatation and increase permeability
 Endothelial damage
 C5a causes aggregation of platelet and leucocytes thereby acting as procoagulant leading
to DICnd shock

Pro-inflammatory cytokines reduces plasma levels of thrombomodulin, coagulation inhibitors like
protein S, protein C, and ATIII. Microvascular coagulatio results which worsens DIC.
Hence there is acute inflammation, vasculitis, haemorrhage, capillary thrombosis and necrosis are
seen in several vital organs.
Net effect:
 Maldistribution of blood flow at microvasculature
 Arteriovenous shuting O2 utilization
 Interstitial loss effective vol. Hypovolemia
 Myocardial depression
CLINICAL FEATURES
It could be in inn patients receiving treatment for another condition
EARLYSTAGE(compensated/warm shock )

 Not associated with hypovvolemia
 febrile (38.2-41°C )
 Shivering and malaise
 warm dry and flushed skin.
 hyperventilation
 rapid bounding pulse
 wide pulse pressure
LATE STAGE (decompensated/ cold shock)
 Hypovolemia with superimposed sepsis
 altered sensorium
 cold clammy skin
 Feeble pulse
 hypothermia, hypotension
 Oliguria
 Jaundice
 upper GI bleeding
 DIC
LOCALISING INFECTION
A good complete systemic examination is done to detect any focus of sepsis.
NOTE THAT RESUSCITATION TAKES PRECEDENCE OVER INVESTIGATIONS, WHICH
SHOULD NOT DELAY INTERVENTION
INVESTIGATION GOES HAND-IN-HAND WITH RESUSITATION
 FBC: there is leucocytosis after initial leucopenia. Throbocytopenia
 Septic work up; Blood culture, Sputum m/c/s, Urine m/c/s, Wound swab m/c/s,
Endocervical swab m/c/s or any exudate
 Based on suspected source; CXR, Abd-X RAY, Abd-pelvic uss, CT Scan of various sites
TREATMENT
Septic shock is a medical emergency that requires prompt and efficient resuscitation
If possible patient should be admitted to ICU
AIMS:
 Improve haemodynamic state
 Restore tissue perfusion thereby increase O2 delivery to tissue.
 Administer O2
 Combat the bacteria and cytokines

 Eliminate septic focus
RESUSCITATION
 FLUID (see above)
 Vasopressor ; After adequate fluid resuscitation or about 4L, with signs of fluid
overload(basal crepitation, high CVP) and persistent hypotension.
a. Norepinephrine – α & β ; 1st
line for septic shock refractory to volume
replacement .Vasoconstriction & reflex bradycardia 5-20mcg/min
 Dopamine – systemic vasoconstriction, inotropic, renal vasodilatation 2-20mcg/m
 OXYGEN ADMISTRATION
In a cleared and patent airway, O2 is delivered via a face mask to increase O2
saturation. Increasing uptake and delivery to tissue.
 ANTIBIOTIC
Give in large doses IV to combat infection. Empirical
IV Broad spectrum bactericidal & anerobe coverage (3rd generation cephalosporin)
Ceftriaxone 50-100mg/kg up to 2gm daily + Metronidazole 500mg 8hrly
 Steroids
 NSAID
 FREE REDICALS SCAVENGERS; superoxide dismutase, allopurinol, vitamin C, a-
tocopherol
 Glycemic control- soluble insulin (GKI) to maintain blood sugar – 80- 120mg/dl
has been found to ↓morbidity/mortality.
 PREVENTION OF FURTHER COAGULATION
• Atiii and C₁-estrase inhibitor
• Recombinant human activated protein C
• inhibits thrombosis and inflammation, promotes fibrinolysis, and
modulates coagulation and inflammation.
 SURGERY
• resuscitative & therapeutic
• If septic focus is responsible for the shock it should be dealt with as soon as
possible especially if respose to therapy is poor. E.g debridement, drainage
of abscess

NUTRITION IN SURGERY
 Introduction
 Nutritional requirements
 Cause of under nutrition
 Effect of malnutrition
 Nutritional assessment
 Nutritional support
 Future trends
INTRODUCTION
The process of utilizing exogenous substances for the production of energy and synthesis of new
tissues. It entails provision of water, electrolyte, vitamins and other nutrients. Nutritional status
determines the outcome of a surgical patient. Provision of adequate nutrition requires
appreciation that injured or septic patient requires higher nutrient than healthy one. Nutrition
support is aimed in timely manner. It is given via the safest route to minimize complication.
Terms;
Resting energy expenditure (REE); the energy expended by a person at rest in a thermoneutral
environment. Basal metabolic rate (BMR); the expenditure for an individual under standard
condition of 12-18hours fasting, recumbent at mental rest in thermoneutral environment. REE and
BMR usually differs by lessthan 10% but REE is higher because it include energy expenditure at
mental activity and other expenditure. REE in newborn 55Kcal/kg/day, in adult 20-30Kcal/kg/day.
NUTRITIONAL REQUIREMENT;
Adult Neonate/infant
Energy (kcal/kg/day) 20-25 90-120
Protein (g/kg) 0.7-1.5 2.5
Fat (g/kg) 1.5-2.0 4.0
Water(/kg) 45-50ml 125-150ml
Caloric contribution; CHO 55-60%, Fat 30-35%, proteins 5-10% and 1g of CHO delivers
4kcal(17j), 1g of protein 4kcal and 1g of fat 9kcal(38j)
Vitamins; vitamin A 5000iu weekly, K 5-10mg weekly, C 60-80mg daily, B12 500mcg weekly, folic
acid 3-6mg daily. Fat soluble vitamins ADEC, water soluble B, C and folic acid. B is produced by
gut bacteria, B12(cyanocobalamin) absorbed in the terminal ileum, folic is absorbed in the
duodenum
Minerals; zinc 5mg, cu 0.5-2.0mg, Mn 70-150mcg, Cr 40mcg, Se 70-150mcg

The energy requirement is increased in catabolic states;
Major elective abdominal surgeries or trauma by 10-30%, generalized peritonitis 15-50%, sepsis 50-
80% and burns 80-200%. If these requirements are not met by exogenous supplement, they will
be provided from endogenous alternative ways to the deterrent of the body.
Starvation; 1st 12hrs previous meal utilized and within 24 hrs body glucose store is depleted.
After 24hrs fatty acids and amino acids are being broken down (gluconeogenesis).Obligate use of
glucose (the CNS others; rbc, wbc, fibroblast, proximal convulated tubules) is gradually being
adapted to ketones. Increased secretion of counter regulatory hormones. Exaggerated hepatic
glucose production. Pro inflammatory cytokines are produced TNF, IL6. Plasma albumin
concentration falls rapidly. There is increased catabolic state depending on the severity of
injury/infection. 12% increase in BMR/degree rise in temperature.
Trauma and sepsis; there is increased counter-regulatory hormones- adrenaline, noradrenaline
and cortisone. Energy requirement increase (upto 40kcal/kg/day). N2 requirement increase.
There is insulin resistance and glucose intolerance. There preferential oxidation of lipids. There is
increase gluconeogenesis, loss of adaptive ketogenesis, fluid retention with hypoalbuminemia.
CAUSES OF UNDERNUTRITION
DECREASE
INTAKE
INADEQUATE
ABSORBTION
EXCESSIVE LOSSES EXCESSIVE
DEMAND
starvation
poverty
anorexia
nervosa
hyperemesis
cancer
sepsis
liver disease
dysphagia
alcoholism
git
obstruction
short bowel syndrome
major gastric resection
motility disorders (
irritable bowel
syndrome)
pseudo obstruction
(ogilvie syndrome)
GIT fistula
malabsorbtion states
inflammatory bowel
disease
protein loosing
enteropathy
Hypercatabolicstates
burns
sepsis
trauma
surgical stress

EFFECTS OF MALNUTRITION
 Impaired mental function: Apathy, fatigue, poor cognition
 Impaired muscle function: Respiratory failure
 Impaired immune function: Increased incidence of infection
 Miscellaneous: Impaired thermogenic response, Impaired wound healing
NUTRITIONAL ASSESSMENT
Aim; identify patient who are at increased risk of post-operative complication due to malnutrition
and where possible, to improve nutritional status through intervention.
Methods;
Clinical
Anthropometry
Laboratory evaluation
Clinical
detailed history and examination
HISTORY
Vomiting, difficulty in swallowing, diarrhea.
Medical history of DM, AIDS, chronic liver dx, chronic kidney dx
Surgical history of abdominal operation
Drug history; chemotherapy.
Dietery hx; 24hr dietery recall.
CLINICAL EXAMINATION
Acutely or chronically ill looking.
Wasted, sunken eyes, palor, silky hair,chelosis, pedal aodema
Cvs; displaced apex beat , haemic murmurs
Abdomen; stomas, fistula, abdominal masses, hepatomegaly.
Rectal examination; perineal fistula, pale stools
Nervous system; neuropathies

SUBJECTIVE GLOBAL ASSESSMENT
5 features in the history
 Weight loss in the past 6months
 Dietary intake
 GI symptoms
 Functional status or energy level
 Metabolic demands
4 features in physical examination
 Loss of subcutaneous fat
 Oedema
 Ascites
 Muscle wasting
ANTHROPOMETRIC
Body mass index (BMI); 18.5-24.9kg/m2
Interpretation
 Severely underweight-<16.5
 Underweight-16.5-18.4
 Normal weight-18.5-24.9
 Overweight-25-29.9
 Obesity grade 1; 30-34.9
 Obesity grade 2; 35-39.9
 Obesity grade 3; >40
 Superobesity >50
Ideal body weight; using Devine formula
 Men:50kg+ 2.3kg for every inch over 5ft
 Women:45.5kg +2.3kg for every inch over 5ft.
Mid arm circumference, Triceps skin fold thickness, waist hip ratio,
LABORATORY EVALUATION
1. Serum protein concentration
a. Total protein
b. Albumin; <3.5g/dl, t ½ 21days
c. Prealbumn; for acute changes t ½ 3days

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