Surgery tutorials for medical students

[email protected]

TUTORIALS

COMPILED

BY

DR BASHIR BIN YUNUS (MBBS, ZARIA)

SURGICAL RESIDENT

AMINU KANO TEACHING HOSPITAL

[email protected]

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…………………………………………………………………………………….

[email protected]

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 …………………………………………………………………………………..

[email protected]

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)

[email protected]

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.

[email protected]

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.

[email protected]

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),

[email protected]

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

[email protected]

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

[email protected]

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%

[email protected]

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

[email protected]

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

[email protected]

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

[email protected]

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.

[email protected]

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.

[email protected]

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

[email protected]

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

[email protected]

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.

[email protected]

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.

[email protected]

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

[email protected]

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

[email protected]

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.

[email protected]

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

[email protected]

• 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.

[email protected]

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.

[email protected]

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.

[email protected]

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.

[email protected]

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

[email protected]

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.

[email protected]

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

[email protected]

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

[email protected]

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,

[email protected]

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%.

[email protected]

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.

[email protected]

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.

[email protected]

- 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.

[email protected]

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.

[email protected]

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

[email protected]

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

[email protected]

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

[email protected]

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.

[email protected]

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

[email protected]

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.

[email protected]

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

[email protected]

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 10C 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

[email protected]

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

[email protected]

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

[email protected]

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

[email protected]

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.

[email protected]

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:

[email protected]

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.

[email protected]

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

[email protected]

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.

[email protected]

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.

[email protected]

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

[email protected]

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

[email protected]

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.

[email protected]

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

[email protected]

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

[email protected]

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.

[email protected]

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

[email protected]

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.

[email protected]

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.

[email protected]

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

[email protected]

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 )

[email protected]

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

[email protected]

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

[email protected]

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

[email protected]

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

[email protected]

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

[email protected]

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

[email protected]

d. Transferrin; t ½ 10days

e. Retinol binding protein; t ½ 12-24hours

2. Total lymphocytes count < 1500/ml

3. immunological; delayed cutaneous hypersensitivity, lymphocyte blastogenesis, neutrophil

chemotaxis, compliment level

COMBINED ASSESSMENT

Nutritional risk index(NRI)

(15.19×albumin) + 41.7× (actual weight/ideal weight)

Well nourish > 100

Mild malnutrition 97.5-100

Moderate malnutrition 83.5-97.5

Severe malnutrition <83.5

INDIRECT CALORIMETRY; Using O2 consumption; respiratory quotient; 0.7-1.0 normal,

<0.7 underfeeding, >1.0 overfeeding.

NUTRITIONAL SUPPORT

GOALS

Preservation of lean body mass

Preserve or reverse nutrient deficiency

Help patient better tolerate treatment

Minimize nutrition related side-effect and complications

Maintain strength and energy

Protect immune function, decreasing risk of infection

Aid recovery and wound healing

Maximize quality of life

INDICATIONS

Recent loss of Wt. > 15%

Body Wt <80-85% of ideal B.W

Serum Album < 3g/dl

Serum Transferrin < 200mg/dl

Skin Anergy

Duration of starvation (5-7day)

Poor premorbid state

History of functional impairment.

[email protected]

Determination Of Requirement Of A Patient;

1. Harris-Bennedict equation

a. Male ; (66.47 + 13.75×weight + 5.0× height - 6.76 ×age)kcal/day

b. Female ; (66.51 + 9.56×weight + 1.85×height – 4.68×age)kcal/day

2. Total energy expenditure (TEE)= basal energy expenditure(BEE) × a stress factor

3. Resting energy expenditure (REE)= 1.44×(3.91 × vO2 + 1.10 × vCO2)–3.34×N2 excretion

4. Using stress level

a. No stress/minimal activity 20kcal/kg/day

b. Mild stress 30kcal/kg/day

c. Moderate stress 35kcal/kg/day

d. Severe stress 40kcal/kg/day

ROUTES OF ADMINISTRATION;

1. Enteral

2. Parenteral

Enteral

It entail the delivery of nutrient into gastrointestinal tract. Used in patient with

functioning GI tract.

Merit

More Physiologic

Gut barrier and immune function are better maintained

Less complications

Attenuate gut mucosal atrophy

Cheaper

The liver is not bypassed

Forms of enteral feeds;

Polymeric (blenderized diet)

Elemental diet (chemically defined)

Disease specific e.g hepatic aid.

Modular (supplemental diet).E.g Amino aid.

Techniques

Sip feeding/oral

Naso-enteral; Nasogastric tube, Nasoduodenal, Nasojejunal

[email protected]

Gastrotomy; Percutaneous endoscopic gastrostomy (PEG), Surgical

gastrostomy, Fluoroscopic gastrostomy

Jejunostomy; PEG-jejunal tube, Direct percutaneous endoscopic jejunostomy

(DPEJ), Surgical jejunostomy

Contra-indications

Intestinal obstruction

Gi bleeding

Severe diarrhea/vomitting

Enterocolitis

High output fistula

Severe pancreatitis

Complications

Tube related; Relates to feeding regimen

• Malposition

• Dislogdement/migration

• Aspiration

• Peritonitis

• Fistula formation

• Intestinal obstruction

• Tube fracture/blockage.

• Intolerance

• Hyperglycemia

• Enteric infection

• Severe diarrhea- hyperosmolar feeds

leading to dehydration and electrolyte

imbalance

PARENTERAL NUTRITION; It involves the delivery of nutrients via intravenous access.Non

physiological, has substantial complications and occasional mortality. Benefit must overweigh the

risk. Total Parenteral Nutrition(TPN): Is defined as provision of all nutritional requirements by

means of intravenous routes and without the use of GI tracts.

Hyperalimentation: Is the intravenous delivery of nutrients to a malnourished patient or patient

in hyper catabolic state in amount as high as 2.5 times his basal requirements in healthy state.

Indications;

GIT fistula ( high output)

Short bowel syndrome

Burns, severe trauma.

Renal failure

[email protected]

Hepatic failure

Mal-absorption synd

GIT anomalies in infants

Acute radiation enteritis

Prolonged ileus after major surgery

Contraindications

CVS instability

Feasibility of enteral feeding

Severe blood dyscrasia

Shock

Uncontrolled DM

Severe metabolic derangement

Techniques

Peripheral;

• Isotonic solution(around 300mosmol/L) fats

• Short period less than 2 wks

• Change site every 48hrs

Central

• Via Internal Jugular Vein or subclavian vein

• Hyperosmolar

• Prolonged nutrition

• Absence of adequate peripheral vein

Monitoring of TPN;

Daily; weighing, U/E, RBS and urinalysis

Twice weekly; Serum calcium, Phosphate , albumin and FBC

Weekly; LFT, lipid profile and serum Mg

Monthly; Serum vitB12, folate, iron, zinc and clotting profile

Complications;

1. Acute reaction to fat/A.A seen in 1-2% of pt xterised back pain shevering, fever vomiting

and headache.

2. Hyperosmolar solution causing:

- Thrombophlebitis

- Decreased myocardial contractility

- Osmotic diuresis

[email protected]

3. Sepsis – from contaminated solution or central venous catheter

4. Metabolic complications; Electrolyte imbalance e.g.Na, Hypocal>, mg,phos> refeeding

syndrome, Metabolic acidosis, Hypoglycemia – xss insulin/ ↓ glucose infusion,

Hyperglycemia – Rapid initiation of infusion/sepsis, Essential FA deficiency

5. Congestive cardiac failure

6. Technical complications

Early -

• Pneumothorax/haemothorax

• Arterial laceration

• Brachial plexus injury

• Hydrothorax

• Sympathetic effusion

• Thoracic duct injury

• Air embolism

• Catheter embolism

Late –

• Erosion of bronchus/Rt. Atrium

• Subclavian thrombosis (5 – 10%)- Remove catheter, antithrombotic

Rx.

• Septic thrombosis.

Advantages of parenteral nutrition

1. Survival rate is improved and morbidity reduced

2. Weight loss and tissue breakdown is minimized

3. Wound healing is enhanced

4. Resistance to infection and general immunity improved

5. Formation of blood element such as plasma proteins, red cells are maintained

Some clinical application of nutritional support

1. Gastrointestinal fistula

2. Bowel failure

3. Burns

4. Pancreatitis

NEW TREND

Immunomodulation; Addition of glutamine, omega 3 fatty acids, arginine and nucleosides, has

been shown to enhance immunity, wound healing, reduce infections and hospital stay.

Fistuloclysis; Reinfusion of effluents from an intestinal fistula into the distal segment.

[email protected]

FUTURE DIRECTION

Administration Of Anabolic Factors

Gut derived hormones

growth hormone

insulin like growth factor

anabolic steroids

cathecholamines

Inhibition Of Proteolysis

Pharmacolical agents

lessons from nature

[email protected]

BLOOD TRANSFUSION

Introduction

Indications for transfusion of blood and component

Types of blood transfusion

Collection and administration

Complications of blood transfusion

Massive blood transfusion

Alternative to blood transfusion

INTRODUCTION; Blood transfusion is the infusion of blood and/ or its product into the venous

system for therapeutic purposes. It should not be given without adequate reason because of its

potential hazards. Specific component deficiency should be infused to minimize hazards.

INDICATIONS FOR BLOOD TRANSFUSION

1. Whole blood;

a. Sudden blood loss of >25% blood volume

b. Exchange blood transfusion

c. Patient continue to bleed after receiving 4 units of packed cells

2. Packed cells

a. Patients with chronic anaemia

b. Elderly

c. Small children

d. Patients prone to fluid overload & cardiac failure, renal and liver failure.

e. Major operation in association with clear fluids

NB; 1unit raise Hb by 1g/dl in a 70kg adult

3. Platelet concentrate

a. Thrombocytopaenic patients undergoing operations

b. Patients undergoing chemotherapy for leukemia

c. Abnormal platelet function

d. Aplastic anemia.

e. Accelerated platelet consumption or destruction (eg, acquired immunodeficiency

syndrome, sepsis, disseminated intravascular coagulation).

f. Surgical indications (eg, cardiopulmonary bypass surgery or surgery in patients

recently treated with drugs which impair platelet function).

NB; 1unit of concentrate raise platelet count by 5-10×10⁹/L

4. Granulocytes concentrates;

a. Used in selected patients with sepsis and severe neutropaenia

5. Fresh frozen plasma

a. Deficiencies of coagulation factors or inhibitors of coagulation for which specific

concentrates are not available

[email protected]

b. Emergency treatment of warfarin overdose and vit. K deficiency when factor IX

complex concentrates is not available.

c. Treatment of TTP

d. Treatment of DIC

6. Cryoprecipitate;

a. Use in hemophilia

b. Hypofibrinoginemia

c. Von Willebrand’s disease.

NB; rich in factor VIII and XIII, fibrinogen and von Willibrand’s factor

7. Protein solutions and factor concentrates

a. Use in correcting the respective deficiency states

TYPES OF BLOOD TRANSFUSION

• Homologous (Allogenic ) Transfusion; infusion of blood collected from a donor

• Autologous Blood Transfusion; collection and subsequent re-infusion of patients own

blood. it prevents the transmition of infections and immunological complications

associated with homologous blood transfusion.

– Pre-operative autologous Blood donation (PABD)

– Acute isovolaemic Haemodilution (AIVH)

– Intra-operative Blood Salvage (IBS)

– Post-Operative Blood Salvage (PBS)

Pre-operative autologous Blood donation (PABD); Donates 1-5 units of his blood preop, to

replace blood loss intraop or postop. Donation should be 3-7 days apart, last one should not be

within 72 hours of the surgery. Initial HB > 10g/dl and PCV of >30%. Patients with bacteremia,

serious cardiac disease and sickle cell should be excluded. Elective surgeries. Ferrous sulphate,

recombinant erythropoietin are given to prevent anaemia.

Acute isovolaemic Haemodilution (AIVH); 1- 4 units of patient’s blood are removed just b4 the

operation. Replaced simultaneously with a crystalloid or colloid. 3ml of crystalloid for every 1ml of

blood. 1ml of colloid for every 1ml of blood. The blood is then re-infused during or after the

operation. Initial Hb > 12g/dl and should not fall beyond 9g/dl. PR, BP and urine output should be

monitored during the procedure. Blood collection is simultaneously replace by crystalloid or

colloid in a separate venous access.

Intra-operative Blood Salvage (IBS); Shed blood from a wound or body cavity is collected and

subsequently re-infused into the same patient. Used in ruptured ectopic pregnancy, ruptured

spleen, penetrating injuries, the shed blood is collected with a galipot into a kidney dish

[email protected]

containing anticoagulant. The blood is filtered into a bottle thru 4-6 layers of sterile gauze in a

funnel. The bottle is then sealed and the blood is re-infused.Hemolysed or infected blood should

not be used. Contra-indicated in tumour resection. Special machines are available. Blood

collected have a shelf-life of 6hours at room temp., and 24 hour at 4°C.

Post-Operative Blood Salvage (PBS); If postoperative blood loss is likely to cause

homodynamic instability and require blood transfusion. Useful in cardiac surgery, penetrating

chest injuries, some orthopedic procedures. Blood salvaged from cavities and joint spaces are re-

infused.

BLOOD DONATION & COLLECTION

Donors must be fit:

• Hb>12g/dl

• 18-65yrs & > 51kg

• No major surgery or blood donation in last 6/12

• No pregnancy or blood transfusion in last 12/12

• No clinical malaria in last 1/12

• No hypertention, splenomegaly, hepatomegaly, bleeding disorder or allergic conditions e.g

asthma

• Free of viral hepatiis, HIV, syphilis, trypanosomiasis, brucellosis

• No vaccination in last 3/12

• not in high risk group for HIV

COLLECTION; of blood should be into collapsible plastic bags containing 60ml citrate,

phosphate, dextrose, adenine. (CPDA) or CPD or saline,adenin, glucose mannitol (SAGM)

STORAGE;

• Whole blood: 2-6 ˚C

• Cryoprecipitate: -40 ˚C

• Platelet concentrate: 20-24 ˚C for maximum of 5 days.

EFFECTS OF STORAGE; WHOLE BLOOD AT 2-6 ˚C

=RBC:

• swells by 20%

• loses k+ into plasma

• ↓ATP & 2,3 DPG →↓viability.

• 1% of RBC is lost per day of storage

=WBC:

• not viable after 24 hours of storage.

[email protected]

=PLATELETS:

• no viable platelets after 24 hours.

=ELECTROLYTES:

• plasma K+ ↑ by 1 mmol/day

• plasma Na+ ↑

• No ionized ca2+

=CLOTTING FACTORS

• factos VIII & V ↓ rapidly after 24hours. No activity after 7/7

• factor X: no activity after 7/7

• factor IX: no activity after 14 days.

• factor VII: ↓ only after 14/7

• fibrinogen & factor ii: stable for 21 days

=PH: ↓from 7.2 at collection to 6.8 at 20 days

=PLASMA Hb: ↑during storage b/c of leakage from rbc

NH3:↑

ADMINISTRATION; should be based on accurate diagnosis & informed indication benefits to

outweigh risks. Informed consent is obtained from patient. ABO & Rh compatible blood should

be crossmatched with patient’s serum b/4 use. Blood to be transfused should be identified &

checked against patient’s name, group, hospital no. & ward. Secure iv access for blood transfusion

with large bore cannula under strict asepsis. Check vital signs b/4 & during the process. Exclude

air from giving set. Regulate rate according to patient & his needs observe patient regularly for

complications & treat accordingly. Untoward symptoms usually occurs during infusion of the

initial 100ml. The rate should therefore be initially 20-30drops/min i.e 2-3mls/min then increased

to 60-80drops after half an hour.

COMPLICATIONS;

Immediate complications:

• febrile non hemolytic rxn

• hemolytic rxn

• allergic or anaphylactoid rxn

• bacterial contamination

• circulation overload

• cardiac arrest

• air embolism

[email protected]

Delayed complications:

• thrombophlebitis

• delayed hemolytic rxn

• post transfusion thrombocytopenic purpura

• iron overload

• immunosuppression

• transmission of diseases:

viral hepatitis A,B,C,

malaria

syphilis

cytomegalovirus (cmv)

trypanosomiasis

brucellosis

infectious mononucleosis

HIV

parvo virus

MASSIVE BLOOD TRANSFUSION;

This is transfusion of >1/2 the patient’s blood volume in 1 hour or ≥ total blood volume (TBV) in

24hours

Most frequent indication is Hypovolaemic shock secondary to blood loss (haemorrhagic shock)

which can arise from;

trauma,

ruptured aortic aneurysm

massive GI haemorrhage,

liver transplant

exchange blood transfusion

PROBLEMS

technical & clerical errors → hemolytic rxns

circulation overload

cardiac arrhythmias & arrest due to:

• cold blood

• hyperkalemia

• hypocalcemia

• acidosis

Respiratory complications

[email protected]

Bleeding diathesis due to:

• thrombocytopenia

• deficiency of clotting factors v & viii

• hypocalcemia

Reduced O2 delivery due to ↓ 2,3 DPG

ALTERNATIVE TO BLOOD TRANSFUSION

REASONS;

Adverse reactions of blood transfusion

Costs and availability of BT

Religious reasons

TECHNIQUES;

Autologous blood transfusion

Blood substitutes

Decreasing surgical blood loss

Increasing rbcs production

BLOOD SUBSTITUTE; plasma and red cell substitute

Plasma Substitutes: fluids used to replace lost circulating blood vol.: they include

Colloids

• stable plasma protein

• albumin

• dextran 70, 110, 40

• synthetic gelatin colloids (haemacel, gelofusine)

• hydroxyethyl starch preparations (hetastarch, pentastarch)

Crystalloids

Red blood cell substitutes;

• Diaspirin cross-linked Hb solution

• Perfluorocarbons

• others: stroma free hb, encapsulated hb, recombinant dna deried hb.

CRYSTALLOIDS

Normal saline, ringer’s lactate, Hartman's solution. Readily available and cheap. Osmotic pressure

is low, diffuse thru all body compartments, only 30 % remains in the intravascular compartment

[email protected]

Hypertonic solns; 3% NaCl, 7.5% NaCl, hypertonic ringer’s lactate. Retained in the intravascular

compartment. They cause movement of intracellular fluid into the intravascular. May cause

dehydration, cerebral edema, hypernatremia

COLLOIDS

Contain HMW proteins as well as electrolytes. The proteins cannot diffuse through the capillaries

and remain intravascular, so they are good for volume replacement. Are not as readily available

and cheap;

Human Albumin Soln

Osmotic pressure is the same as that of plasma proteins therefore suitable as replacement fluid. It

replaces only albumin. Contains no Ig and coagulation factors. T1/2 short – 24 hours. It is

expensive

Dextran 70

Polysaccharides, MW 70,000. Osmotic pressure > that of plasma, retained in the vascular

compartment. Withdraws fluid from the extravascular compartment. Excreted by the kidney in 24

– 48 hours. May cause renal damage. Reduce platelets adhesiveness. Induces roulex formation and

so may interfere with blood GXM. Not very satisfactory for replacing blood volume.

Dextran 40

MW 40,000. More rapidly excreted, within 24 hours. It lowers blood viscosity

Hemacel; Contains degraded polypeptides. MW of 35,000. T1/2 4 – 6 hours. It does not interfere

with blood GXM. It does not impair renal function.Satisfactory for volume replacement

Gelofuscine; Modified gelatin. MW 30,000. No effect on clotting or blood GXM. Promotes

osmotic diuresis

Hetastarch; MW 200,000 – 400,000. T1/2 6 – 8 hours. 1 – 1.5L is given daily. May interfere with

coagulation.Valuable volume expander.

RBC SUBSTITUTES

Also known as artificial O2 carriers. Most are currently in clinical trial. Co-administered with

colloids and crystalloids

MODIFIED HB SOLUTIONS; Are solutions that have similar O2 carrying capacity and exchange

properties as RBC Hb. Originated from outdated human blood, genetic engineering, or of bovine

[email protected]

origin. Rapidly cleared from the circulation. Can cause renal failure.Not readily available in our

environment

PERFLUOROCARBON EMULSIONS

Compounds with high gas dissolving capacity (O2, CO2). Dissolve O2 which is released to tissues

by diffusion. After I.V administration they are taken up by the RES, slowly broken down and

released into the circulation. Finally excreted in the lungs by exhalation. Cause mild flu-like

symptoms. Decrease platelets count.

INCREASING RBCs PRODUCTION

• Hematinics; iron, folic acid, vit b12

• Erythropoitin

• IMPROVED NUTRITION; Optimize RBC mass b4 an operation

Iron ; Essential component of Hb. Necessary for erythropoiesis. Orally or parenterally

(i.v or i.m). Orally at a dose of 200mg/day. S.E gastric irritation. i.m is discouraged; pain at inj site,

staining of the skin. I.V: Iron dextran, iron sucrose. Used in Severe IDA, Intolerance of oral iron,

Ongoing blood loss, CRF, together with EPO, PABD S.E; anaphylactic rxns, headache,

hypersensitivity, urticaria, myalgia

Erythropoietin; Stimulates erythrocytes production, Usually given with iron

supplements. Administered i.v or sc. 300u/kg/day for 5 days, then on alternate days for 2 weeks.

Equivalent of 1 blood unit is produced by day 7 and 4 units by day 28. Usually started 10 – 21 days

b4 the surgery. S.E, Thrombosis, hypotension. It is Expensive and Not readily available in

developing countries

Nutrition ; Early enteral feeding Parenteral nutrition for patients who cannot be

fed. Protein supplementation

DECREASING SURGICAL BLOOD LOSS

• Pharmacological

• Non pharmacological

NON PHARMACOLOGICAL

• Meticulous surgical techniques,

• Patient positioning,

• Regional anaesthesia,

• Maintenance of normothermia,

• Microsampling,

• Quick trauma response

[email protected]

Meticulous techniques; Tourniquet, Ligation of vessels, Use of diathermy, Haemostatic agents;

trasylol, topical glues, Laparoscopic surgeries

Patient Positioning; Avoid venous engorgement from obstruction of the venous return. If

possible the surgical site should be elevated above the level of the right atrium, to improves

venous return

Regional Anaesthesia; Patients operated under R.A have been found to bleed less > G.A

The sympathetic blockade lowers the arterial BP

Maintenance Of Normothermia; Hypothermia; low ambient operating room temp, evaporation

from large body cavities, etc. Hypothermia impaired platelets function and Prolonged coagulation

enzymatic rxns leading to more bleeding. Use blankets, thermal suits, machine to warm i.v fluids

Microsampling;Minimal amount of blood required Microtubes, Microchemistry analyzers

Quick Trauma Response; Act quickly, Arrest bleeding, Apply other modalities of alternatives to

blood transfusion.

PHARMACOLOGICAL

• Aprotinin

• Tranexamic acid

• Desmopressin

• Recombinant coagulation products

• Vit K

Aprotinin; Antifibrinolytic agent. Inhibits generation of plasmin. Used in cardiac, vascular and

orthopedic surgeries.

Tranexamic Acid; Antifibrinolytic. Displace plasminogen from fibrin. Prostatectomy,

menorrhagia

Desmopressin; Improves platelet adhesion to site of vascular injury. Increases plasma level of

factor VIII and VWF

Recombinant Coagulation Products;Factor IX conc, factor VIIa conc, antihemophilic factor

concentrate. Used to manage bleeding in pts with hemorrhagic dxs; hemophilia, VW dx.

Vitamin K; For mgt of bleeding due deficiency of Vit k dependent clotting factors

[email protected]

HAEMOSTASIS

Introduction

Physiology

Abnormal hemostasis

Peri-operative control of bleeding

INTRODUCTION; Haemostasis is a complex mechanism that prevent or terminate blood loss

from a disrupted intravascular space, provides a fibrin network for tissue repair, and, ultimately

remove the fibrin when it is no longer needed.

PHYSIOLOGY; It is achieve via four interdependent processes;

Contraction of the injured vessel.

Endothelial cell secretion and interaction

Plugging of the vessel by platelets.

Coagulation of blood in the vessel

Contraction of injured vessel; Aided by Sympathetic reflex and Release of vasoconstrictors

(TXA2, serotonin and catecholamines). Platelets adhere to the walls of damaged vessels.

Endothelial cell secretion and interaction; the products of endothelial cells which promotes

Haemostasis include von Willibrand’s factor (causes platelet adhesion and aggregation),

thrombospodin (causes platelet aggregation), endothelin(vasoconstrictor), and tissue factor

(initiate extrinsic pathway)

Plugging of vessels by platelet; when a blood vessel wall is injured, platelets adhere to the

exposed collagen and von Willebrand factor in the wall via platelet receptors → Platelet

activation. Activated platelets release the contents of their granules including ADP and secrete

TXA2 →activates nearby platelets to produce further accumulation of more platelets (platelet

aggregation) and forming a platelet plug.

Coagulation of blood in the vessels; the fundamental reaction is conversion of soluble

fibrinogen by thrombin to soluble fibrin monomer which is then converted by thrombin in the

presence of calcium ions and thrombin-activated factor XIII to insoluble fibrin polymer. This is

via two pathways;

Intrinsic; The initial reaction is the conversion of inactive factor XII to active factor XIIa.

Factor XII is activated in vitro by exposing blood to foreign surface (glass test tube). Activation in

vivo occurs when blood is exposed to collagen fibers underlying the endothelium in the blood

vessels.

[email protected]

Extrinsic; Requires contact with tissue factors external to blood.This occurs when there is

trauma to the vascular wall and surrounding tissues. The extrinsic system is triggered by the

release of tissue factor (thromboplastin from damaged tissue), that activates factor VII. The tissue

thromboplastin and factor VII activate factor X.

[email protected]

PREVENTION OF FURTHER CLOTTING AND BREAKDOWN OF CLOTS; once haemostasis

have been achieved, there are processes which prevent further clot and breakdown of clot;

1. Prevention of further clotting;

a. Action of thrombin is limited by ;

i. Absorption of thrombin in the fibrin clot reduces the amout available for

further action

ii. Antithrombin III combine with thrombin to form inactive complex. It is

also potent inhibitor of factor IX, X and XI

iii. Fibrin degradation product(FDP). Inhibits thrombin.

b. Tissue factor pathway inhibitor (TFPI); product of endothelial cells, inactivates

TF/factor VIIa complex.

c. Protein C anti-coagulant pathway; inhibits factor V and VIII. Protein S act as co-

factor.

d. CI- esterase inhibitor neutralizes activated factor XIII, XI and plasma kallikrein

e. A2 macroglobin inhibits kallikrein, thrombin and activated factor X

f. Prostacyclne causes disaggregation of platelet

g. Nitric oxide is a powerful inhibitor of platelet activation and a potent vasodilator

2. Breakdown of fibrin clot(fibrinolysis); plasmin hydrolyses fibrin into fibrin degradation

product.

3. Phagocytic cells of reticulo-endothelial system also remove fibrin

ABNORMAL HAEMOSTASIS; excessive bleeding during and / or after operation

Platelet abnormality- quantitative (e.g thrombocytopenia) or qualitative(e.g Glanzman’s

disease.)

Deficiency of clotting factors

Anticoagulants

Vascular problems

CAUSES OF BLEEDIND DIATHESIS

1. PLATELET ABNORMALITIES

Platelet deficiency (thrombocytopenia); <150 × 10⁹/L. excess bleeding occurs in <50 ×

10⁹/L and spontaneous bleeding occurs in <20 × 10⁹/L

Types;

idiopathic i.e. primary seen in children and infants probably due

to immune deficience

[email protected]

secondary; causes include; d

drugs- sulphonamides,quinine, quinidine, phenacitin, cytotoxics,

cephalosporins, indomethacin, serdomid, para-aminosalysilic acid,

phenylbutazone,

infections; rubella, mumps, infectious mononeucleosis, HIV,

malaria, leishmania.

Hyperslenism

Some malignancies; acute leukemia, lymphoma, MM, bone

metastesis

Collagen disease; SLE, rheumatoid arthritis and dermatomyositis

Irradiation

Treatment;

If drug found, it is stopped and the operation delayed if not urgent

Idiopathic or hyperslenism- splenectomy

ITP- steroid oral for elective until platelet is normal. In emergency IV

immunoglobulin

Transfusion of platelet concentrate during operation in emergency or 2L of

fresh whole blood(i.e blood collected within 3hours)

Qualitative platelet dysfunction;

Congenital or acquired

Congenital; Bernard-soulier syndrome(BSS) and Glanzmann’s thrombasthemia(GT)

They are autosomal recessive

Common with consanguinity

BSS is due to defect in platelet adhesion and GT in aggregation

Present as spontaneous bruises, epistaxis, bleeding gums, petechiae, menorrhagia

BSS differs from GT by thrombocytopenia and giant platelet in the peripheral blood

Mgt; desmopressin(DDAVP) and recombinant factor activated factor VII, platelet

transfusion in severe hemorrhage.

Acquired; Aspirin ingestion and ureamia

[email protected]

Aspirin impairs aggregation, ADP release and TXA2 synthesis. If ingested within 7days of

surgery, excess bleeding may occur.

Ureamia increase levels of guanidinosuccinic acid and phenolic acid which impairs

platelet function. The defect improve after dialysis.

2. DEFICIENCY OF COAGULATION FACTORS

I. Hereditary

Haemophilia A

von Willibrand’s disease

Haemophilia B (christmas disease)

II. Acquired

Vitamin K deficiency

Ureamia

Massive blood transfusion

Disseminated intravascular coagulopathy (DIC)

HAEMOPHILIA A

Caused by deficiency of factor VIII

Symptoms occur when factor VIII activity is < 30%

Sex-linked recessive

Presents with subcut and intramuscular haematoma, haemarthrosis occasionally GI

bleeding, prolong bleeding from site of injury or surgery

• Clinical severity depends on extent clotting factor deficiency

<1% activity - severe disease with life-threatening bleeding

1-5% activity - moderate disease with post-traumatic bleeding

5-20% activity - mild disease

Laboratory findings

Factor VIII levels are; low; < 2u/dl (severe), 2-10u/dl moderate), > 10-30u/dl (mild) .

The bleeding and prothrombin times- PT are normal.

The partial thromboplastin time-PTT, a measure of intrinsic pathway is always

prolonged.

The clotting time is usually prolonged.

Treatment

• Bleeding episodes are treated with factor VIII replacement

[email protected]

• Given as either factor VIII concentrate or cryoprecipitate

• Bleeding usually well controlled if factor VIII levels raised above 20%

normal

• Desmopressin increases intrinsic factor VIII levels

• 5-10% develop antibodies to factor VIII

• Renders patients refractory to factor replacement therapy

von Willebrand’s disease; caused by deficiency of von Willibrand’s factor resulting in excessive

catabolism of factor VIII which leads to low circulatory levels. It is autosomal dominant. There is

an associated platelet dysfunction.

Laboratory findings;

Factor VIII level is low

BT and PTT are prolonged

PT is normal

Clotting time may be normal or prolonged depending on the factor VIII level

Impaired platelet aggregation with ristocetin

Reduced von Willebrand’s factor or ristocetin cofactor activity

Treatment

Desmopressin in mild cases

Severe cases are treated with factor VIII concentrate, cryoprecipitate, FFP, vWF

concentrate. In the absence of these fresh whole blood may be used

CHRISTMAS DISEASE (HAEMOPHILIA B)

Factor IX deficiency

Only PTT and clotting time are prolonged

Factor IX is low

Treatment is with double dose of factor IX

FFP or fresh whole blood can be used in the absent factor concentrate

VITAMIN K DEFICIENCY

In vitamin k deficiency there is impaired synthesis of factors- II, VII, IX, and X leading to

bleeding.

Causes of vitamin K deficiency

Obstructive jaundice and steatorrhoea

Malabsorption syndrome and high enterocuteneous fistulae

Hepatocellular disease

Prolonged broad-spectrum oral antibiotics

[email protected]

Warfarin therapy

Laboratory findings

INR is > 2

PTT is prolonged if factor X and II are severly depressed

Treatment

Vit K, 5mg IM, is administered daily for 3-5 days before operation. In an emergency, 10-

20mg Vit K given IV or IM will significantly correct the deficiency in 8-12h.

If it is not detected before operation and bleeding occurs. FFP 9-15ml/kg or fresh whole

blood 15-20ml/kg must be infused in less than I h.

UREAMIA

Coagulation screening tests are usually nonnal. The bleeding time, however, is prolonged due to

impairment of platelet function and platelet-vessel wall interaction. These abnormalities are

corrected by haemodialysis. IV. DDAVP 0.3-0.4u/kg reduces bleeding episode

MASSIVE BLOOD TRANSFUSION (see above)

DISSEMINATED INTRAVASCULAR COAGULOPATHY (DIC)

• Due to widespread intravascular activation of clotting cascade

• Causes a bleeding tendency due to consumption of clotting factors

• Presents with bruising or purpura

• Oozing from surgical wounds and venepuncture sites

Causes

• Severe (usually gram-negative or meningococcal) infection

• Widespread mucin-secreting metastatic adenocarcinoma

• Hypovolaemic shock

• Severe trauma

• Burns

• Transfusion reactions

• Eclampsia

• Amniotic fluid embolus

• Fat embolism

• Promyelocytic leukaemia

• Open heart surgery with extracorporal circulation

• Viperine venom

[email protected]

Laboratory findings

•

Thrombocytopaenia.

Prolonged bleeding time.

Prolonged partial thromboplastin time.

Clotting time is prolonged; the clot formed is small and is soon lysed.

Thrombin time is prolonged.

Hypofibrinogenaemia.

Factors V and VIII are markedly depressed.

Increased FDP and D-dimer levels.

A fibrinogen level below 10g/L and a platelet count below 100 x 10⁹/L are diagnostic.

Treatment;

The precipitating cause is treated or removed.

Fresh frozen plasma is transfused to correct hypovolaemia and provide coagulation

factors.

6 units cryoprecipitate is given if hypofibrinogenaemia is severe. It will also provide

coagulation factors.

6 units of platelet concentrate is given if the platelet count is < 100 x 10⁹/L.

Fresh whole blood may be given if FFP, cryoprecipitate and platelet concentrate are not

available.

[email protected]

ANTICOAGULANTS

Warfarin

Heparin

Aspirin

Warfarin; interferes with hepatic synthesis of vitamin K dependent clotting factors- II,VII,IX and

X, as well as protein C and S. peak plasma time 2-3days

Heparin; low dose inactivates factor Xa and inhibits conversion of prothrombin to thrombin.

High dose inactivates factors IX, X, XI, and XII and inhibits conversion of fibrinogen to fibrin.

Peak plasma time 2-4hours

Aspirin; see above

VESSEL WALL

congenital

Hereditary haemorrhagic telangiectasia

Ehlers-Danlos syndrome

Acquired

Drugs (e.g. steroids)

Sepsis

Trauma

Vasculitis

Infections; Typhoid, SBE, Meningococcal meningitis, Gram-ve septicemia

Scurvy

Purpura

PERI-OPERTIVE CONTROL OF BLEEDING TENDENCIES

PREOPERTIVE

History

Bleeding tendencies, from orifices

Prolong oozing or massive haemorrhage

Family history

[email protected]

Drug history; aspirin, warfarin, heparin

Examination

Petechiae, bruises, jaundice, lymphadenopathy, palmar erythema etc

Splenomegaly, hepatomegaly

Investigation

FBC ,bleeding time, clot reaction, PT, PTT, platelet function test, fibrinogen, FDP, D- dimer

estimation, bone marrow examination

COAGULATION TESTS

Prothrombin time (PT)

Tests extrinsic and common pathways

Thromboplastin and calcium are added to patient plasma

PT is expressed as ration (International Normalised Ratio = INR)

Prolonged in:

Warfarin treatment

Liver disease

Vitamin K deficiency

Disseminated intravascular coagulation

Activated partial thromboplastin time (APPT, KCCT)

Tests intrinsic and common pathways

Kaolin added to patient plasma

Prolonged in:

Heparin treatment

Haemophilia and factor deficiencies

Liver disease


Massive transfusion

[email protected]

Lupus anticoagulant

Thrombin time (TT)

Tests common pathway

Thrombin added to patient plasma

Converts fibrinogen into fibrin

Prolonged in:

Heparin treatment


Dysfibrinogenaemia

Bleeding time (BT)

Measures capillary bleeding

Prolonged in:

Platelet disorders

Vessel wall disorders

TREATMENT :-

Stopping anticoagulant therapy

Dialysis/renal transplant for CRF patient

EPO in CRF, Jehovah witness

Anti failure regimen in hepatic failure

Vitamin K in neonates, liver Dx

Control of HTN

Platelet, factor conc., desmopresson, FFP administration as applicable

GXM

[email protected]

INTRA-OPERATIVE

This can be achieve via:

Mechanical

Thermal

Chemical

Surgical

TYPE OF ANAESTHESIA

Type of agents to be used

GA Vs Regional Vs LA

Adequate/intensive monitoring of blood loss as well as PaO2

SKILLED SURGEON/ASSISTANT

Proper knowledge of anatomy

Proper knowledge on principles of surgery

ADEQUATE LIGHTENING: ENSURE PROPER VISUALIZATION

POSITIONING:

Trenderlenburgh

Reverse trenderlenburgh

Head tilt to 30 degrees or more in head and neck surgeries

Lateral tilt

MECHANICAL METHODS

Use of tourniquet with or without exsanguination

Direct pressure:

Finger pressure e.g nose pinching in epistaxis, direct pressure in scalp bleeding,

Pringles' maneuver

Pressure packs (wet or dry)

Use of swabs

Use of balloons eg catheter, Sensetaken-Blakemore tube, Minnesota

Elevation with evertion eg in scalp surgeries

Haemostat

[email protected]

Ligatures

THERMAL METHODS

Cold packs: causes vasospasm and endothelial adhesiveness, increases local

haematocrit; Risk of hypothermia, ventricular fibrillation and thrombocytopenia esp at

temp <35

Cold saline

Warm packs: controversial

Cautery

Diathermy

Cryosurgery : Extreme cooling of -20 to -180 is used. Causes cryogenic necrosis

through dehydration and lipid denaturation. Useful in neurosurgery and some

gynaecological procedures

Laser surgery

CHEMICAL AGENTS

They vary in their MOA. Some have vasoconstrictive effect, some anticoagulant, some

inert with hygroscopic ppties

Epinephrine : in tonsillectomy, epistaxis

Octreotide

Skeletal muscle in the past (introduced by Cushing)

Gel foam (gelatin foam): made from denatured animal skin gelatin. Improve action in

combination with thrombin

Oxycel & surgicel: both are oxidized cellulose materials. They combine with blood to form

artificial clot. Surgicel have antibacterial effect

Requires phagocytosis for removal in 1-4wks

Impairs wound healing

Microcrystalline collagen: same ppties with surgical

Fibrin glue: Have same ppties with body’s fibrin. Good for oozing blood from liver and

spleen surfaces

Bone wax: bees wax.

paraffin as softening agent

Ostene: water soluble. Made from alkylene oxide copolymer derived from ethylene &

propylene oxide

[email protected]

SURGICAL METHODS

Shunting eg portocaval, lienorenal

Resections

Splenic

Hepatic

renal

Grafting:

Venous graft

Synthetic graft

Dacron

Expanded polytetrafluoroethylene E-PTFE

POST-OP CONTROLOF BLEEDING

Dressing

Firm/gentle not to compress blood supply

Use of Vaseline gauze

Post-op monitoring of pts with bleeding tendencies by regular checking of clotting profile and

prompt treatment depending on the situation

FUTURE TREND

General aim is towards bloodless surgeries.

Microvascular surgery

Use of hemobag for modified ultrafilteration in ECMO during cardiac surgeries

Harmonic scalpels

Arterial embolisation

OPERATIONS ASSOCIATED WITH EXCESS BLEEDING

1. Prostatic surgery

2. Transplant surgery

3. Portocaval surgery

4. Extracorporeal circulation

[email protected]

METABOLIC RESPONSE TO TRAUMA

Characteristic series of local and systemic adaptive homeostatic responses by an organism

following cellular injury/trauma or sepsis aimed at restoring body’s pre-injury state.

Appropriate response maintains homeostasis and allows wound healing. Excessive response can

produce systemic inflammatory response syndrome (SIRS) and multiple organs dysfunction

syndrome (MODS).

ACTIVATION OF THE METABOLIC RESPONSE

Pain

Hypovolemia

Hypothermia

Infection

Hypoxia

CONTROL OF RESPONSE

Sympathetic nervous system

Acute phase(inflammatory) reaction

o Cytokines

o Acute phase proteins

Vascular endothelium and blood response

Endocrine response

PHASES OF RESPONSE

EBB

FLOW

EBB PHASE; The ebb phase corresponds to the period of severe shock. Immediately after

trauma and lasts 24-48 hours. Reversible by resuscitation. Priority is to maintain

life/homeostasis. There is decrease in the following;

Cardiac output

Oxygen consumption

Blood pressure

Tissue perfusion

Body temperature

Metabolic rate

FLOW PHASE; In the flow phase, the body is hypermetabolic, cardiac output and oxygen

consumption are increased, and there is increased glucose production. Lactic acid may be

normal. It is further subdivided into;

[email protected]

Catabolic phase- lasts for 3-10 days. There is fat and protein mobilization associated

with increased urinary nitrogen excretion, weight loss

Anabolic phase- lasts for 10-60 days. Restoration of fat and protein stores, weight

gain.

FACTORS INFLUENCING MAGNITUDE OF RESPONSE;

Nature and severity of injury

Nutritional status

Sepsis, underlying disease

Age- Sex

Environmental temperature

Treatment – timing, type and effectiveness

Drugs (Steroids, NSAIDS)

ATTENUATING FACTORS

Prompt correction of fluids and electrolytes

Analgesia and anaesthesia-spinal/epidural

Minimally invasive surgery

Use of prophylactic antibiotics

Wound debridement

Early enteral feeding

SUMMARY OF EVENTS

COMPLICATIONS

• SHOCK

• SIRS

[email protected]

• MOD/MODS

• DEATH

PRE AND POST-OPERATIVE CARE OF THE SURGICAL PATIENT

Introduction

Assessment of operative risk

Personal relationship

General preparation: History, PE, Investigation

Risk analysis of the patient vis-à-vis the surgery

Now patient is fit

Peri op care

Post op care

INTRODUCTION

The ultimate goal of preoperative, intraoperative and postoperative care of the surgical patient

is to reduce morbidity or mortality and to return the patient to desirable functioning

(premorbid state or better) as quickly as possible

I. Assessment of Operative Risk

A. Natural History

relative harm (risk)

relative good (benefit)

B. Stages of the disease- error in clinical staging produces the greatest number of

controversies regarding management

C. Clinical Judgment- deviations of standard treatment is associated with significant

increase in mortality and morbidity

D. Basic Factors Affecting Operative Risk

1. Age over 70 years

2. Overall physical status

3. Elective vs. emergency surgery

4. Extent of pathology

5. Associated illnesses

[email protected]

II. Personal Relationship

A. Genuine bond of communication and personal responsibilities.

B. Do not convey a sense of hurry and inadequate time for explanations.

C. Demonstrate skills to contribute to diagnosis and treatment.

D. Specific treatment.

E. Informed consent

III. General Preparation of the Patient

A. Psychological preparation

1. Pre-op steps should be enumerated, justified and explained.

2. Surgeons should not equivocate in discussing possible disfiguring operations.

HISTORY

Previous illness

Previous surgery and anaesthetic experience

Concurrent diseases

Drug therapy e.g prolonged use of steroids

Social hx: alcohol, smoking

EXAMINATION

Respiratory system: treat infections. Spirometry. BGA/PH checks

Cardiovascular system: anaesthesia reduces CO by about 20%. Note- predictors of

cardiac risk (MI, CCF, etc), pt’s functional capacity, the procedure to be carried out

Urinary system: Albumin, casts, cells, sugar, ketones, urea level

Gastrointestinal system: carious and loose tooth. Treat mouth infections. Stool exam

→deworm

Blood picture: CBC, Sickling test. Bld trx at least 3 days to time of surgery. May use parenteral

iron therapy or recombinant erythropoietin. For bleeding tendency/jaundiced pts-platelets,

prothrombin, bleeding and clotting time

Hydration and Nutrition: ↓ K → difficulties with reversal of muscle relaxants.

Malnutrition: BMI used (weight[kg]/ht2[m2])

[email protected]

Malnutrition may be evidenced by weight loss. For example, in the absence of dehydration,

loss of ≥ 10kg in the last 6 months or loss of 5% in the last month calls for closer review.

Also determine Lymphocyte count, Albumin(˂3.5gm/dl-treat), Prealbumin, total

proteins(˂5.4gm/dl-treat).

NERVOUS SYSTEM

Examine the tones. Check for conditions that may interfere with the anaesthetic agents-

myasthenia gravis, suxa in the presence of hyperkalemia may produce cardiac arrest, where

there is active demyelinating dx, a muscle spasm instead of relaxation and there may also be

malignant hyperpyrexia. It can influence the type of anaesthesia all together.

PSYCHOLOGICAL STATE

No two patients are exactly the same

May need to sedate them

MINIMUM INVESTIGATIONS

Hb, pcv, sickling, Urinalysis - albumin, sugar, casts, Stool for amoebae and worms

Hypertensives and pts ˃40yrs; Chest x ray, ECG, FBS

INVESTIONS DONE WHEN INDICATED; Fbc, Sickling electrophoresis, Blood group/ x

matching, Serum e/u, Chest x ray, ECG, Plasma proteins, PT, clotting & bleeding time, clotting

factors, G6PD, FBS, FBS

Other measures;

Obstructive Jaundice: adequate hydration, vit k, antibiotic prophylaxis.

?Bowel prep for colonic surgery

Treat infective skin lesions

Pts on steroids: Replacement dose- hydrocortisone or methylprednisolone

Assessment of risks- ASA

ASA 1- a normal fit patient

ASA 2-Mild systemic dx e.g. Hb AS, controlled bp,dm, mild asthma,

ASA 3- A pt with systemic dx that limits activity but not incapacitating. E.g renal dx pt on

dialysis

ASA 4- A pt with incapacitating systemic dx that is a constant threat e.g septic shock

[email protected]

ASA 5-Moribund.Not expected to live˃24hrs

ASA 6 – Brain dead organ donor

CHILDS-PUGH’S GROUPING OF SEVERITY OF LIVER DX

Childs-pugh’s grading: Interpretation

A. Less than 6 points: Good operative risk

B. 6-9: Moderate risk

C. Above 10: Poor risk

NOW THE PATIENT IS FIT FOR SURGERY

Consent

Bowel prep

Bladder

Empty stomach

Remove dentures

Pre anaesthetic med

Adequate labelling

Diabetics – may require special prep

PREPARING DIABETIC FOR OPERATION

I. Those on diet alone treat as normal pts

II. If on oral hypoglycaemics, stop the biguanides. Use sulphonylureas

III. Alberti regime: 500mls of 10% g + 10units of SI + 1gm of KCl to run for 4hrs. 2hrly

check of sugar and K. May use 5% d/w with 5 units of SI. Aim at 4-10mmol/l and 3.5-

4.5mmol/l for sugar and K respectively

IV. Some use sliding scale

PERIOPERATIVE CARE

Check equipments/drugs. Note that equipment may malfunction. The hands must not go to

“sleep” Adequate positioning.

Monitoring: anaesthetist, surgeon, nurses. The patient belongs to all

Blood loss estimation

Watch for and prevent; Hypothermia, Hypotension, Hypertension, Cardiac

arrhythmias, Cardiac arrest, Hypoxia, Asphyxia (combination of hypoxia and

hypercapnia and caused by respiratory obstruction)

[email protected]

POST OPERATIVE CARE

Determinants of outcome:

Basic pathology

Effect of surgery including blood loss

Duration of surgery

After effects of the anaesthesia

Complications during surgery

After surgery

Recovering room or icu. monitoring

Supervise mvt to ward on a trolley with sides

Control airway

Ward shd be prepared with relevant equipments e.g supplemental oxygen,etc

Adequate care on the ward e.g Oxygen, airway mgt, vitals, adequate pain mgt. take

care of the patient who is vomiting-position

Nutrition/Fluid

Urine

Ambulation

Use of low molecular weight heparin

Wound

Daily visits ± physiotherapy

Hb on 3rd day

Other investigations as required

Fluid; see chapter on fluid mgt

Pain mgt

Preventing circulatory stasis

Leg exercises

TED stockings (Thrombo Embolic Deterrent)

Early ambulation

Positioning

Anticoagulants

Fluid intake

[email protected]

WHAT COMPLICATIONS DO I WATCH OUT FOR?

Post-operative complications are untoward conditions occurring within 30 days of

operation, or after 30 days but directly related to the operation.

First few hours:

Respiratory insufficiency

Cardiovascular emergencies

Reactionary haemorrhage

Central nervous problems

Others e.g. hypothermia in the neonate

Complications after 24hrs;

Respiratory tract

o Atelectasis

o Pneumonia

o Hiccough

o Tracheobronchitis

o Pulmonary embolism

Cardiovascular

o secondary haemorrhage, MI, DVT, PE

Genitourinary tract

o Retention of urine, Acute renal failure, UTI

Gastrointestinal tract

o N/V, gastric dilatation, paralytic ileus, peritonitis, intra abd abscesses,

constipation, Diarrhoea, pseudomembranous colitis, Upper GI bleeding,

Jaundice

Central Nervous system

o Delirium

The wound; Haematoma, SSI, Wound dehiscence

Late complications

Incisional hernia

Mech int obst from bands and adhesions

[email protected]

CARDIAC ARREST

Sudden cessation of a demonstrable heart beat with no clinical cardiac output in a patient not

expected to die. Clinical death: pt stops breathing and the heart stops also

Brain death: when the brain undergoes irreversible damage from oxygen deprivation after

cardiac arrest. Usually 4-6 mins after an arrest

Causes of cardiac arrest;

Resp obstruction, asphyxia, hypercarbia

Severe haemorrhage leading to hypovolaemia

Shock

MI

Massive transfusion

Acidosis,

hyper or hypo K,

hypothermia

Tension pneumo, PE, cardiac tamponade

Making a diagnosis of cardiac arrest;

Absent pulsations in major peripheral arteries

Unconsciousness

Apnoea

Dilated unreactive pupil

Managing cardiac arrest

Airway opened

Breathing restored

Circulation begun

Definitive therapy(drugs, diagnosis, defibrillation, disposition)

POST-OP FEVER

- elevated temperature observed in post-op patients does not necessarily signal a serious

complication

[email protected]

- a specific cause is identified in 20% of patients with pyrexia during the initial 24 hours

- comprehensive clinical evaluation is essential

Common causes of Post op pyrexia; (also remember the 5 ‘W’s – wind, water, wound,

walk and wonder drugs)

Metabolic response to trauma

Infection or haematoma

Malaria

Lung collapse, pneumonia, bronchitis

Laryngo-tracheitis

Peritonitis/intra-abdominal abscesses

Complications at sites of IVF

Complications from blood transfusion

UTI

DVT

Injection abscess

Sickling crisis in sicklers

Pseudo membranous colitis

Non-infective causes of Post-op Fever

1. Disseminated malignancy

2. Transfusion reaction

3. Hematoma

4. Administration of irritant fluids or drugs, drug sensitivity

5. Acute pancreatitis

6. Thyroid storm

7. Pheochromocytoma

8. Dehydration

[email protected]

MGT OF POST OP FEVER

History, examination, investigation and then treatment

Factors influencing likelihood of post-op infection

1. Definite decrease in host resistance

increasing age

obesity/malnutrition

diabetic ketoacidosis

acute/chronic steroid use

immunosuppressive drugs

remote infections

2. Post op infection

3. Possible decrease in host resistance

some forms of cancer

radiation therapy

adrenocortical insufficiency

foreign body

early shaving of the operative site

4. No effect on host resistance

gender

race

controlled DM

acute nutritional deprivation

Operations benefiting from antibiotic prophylaxis

1. Head and neck surgery with open aerodigestive tract

2. Esophageal except hiatal hernia repair

3. Gastroduodenal except for complications of uncorrected hyperacidity

4. Biliary tract surgery

patients over 70 years old

acute cholecystitis.

[email protected]

choledochostomy

5. Bowel resection

6. Perforated or gangrenous appendicitis

7. Hysterectomy

8. Revascularization and prosthetic graft surgery

9. Orthopedic surgeries with implantation of prosthesis

OPERATIVE TECHNIQUE TO MINIMIZE INFECTION

Eliminate hair, if necessary, just prior to incision time

Effective skin preparation

Gentle and effective handling of tissues

Effective hemostasis

Eradicate dead space

Minimize operative time

Closed suction drain a distance from the incision

DISCHARGE

written and verbal instructions; regarding follow-up care, complications, wound care, activity,

medications and diet.

Give prescriptions and phone numbers.

Discuss actions if complications occur.

CONCLUSION

Adequate pre op, peri op and post care of the surgical patient is essential

The best surgeon is the surgeon that knows when not to operate

[email protected]

SURGICAL PROPHYLAXIS

All sciences or acts to prevent perioperative complications. Eg tetanus prophylaxis, antibiotics

and DVT prophylaxis

ANTIBIOTIC PROPHYLAXIS

Antibiotics are chemical agents, synthetic or products of microbes which damage bacteria

without harming the tissues. They are more effective in controlling established infection than

prophylaxis. Indiscriminate use results in ineffectiveness and development of resistance.

Guidelines for prophylaxis

Single preop dose is as effective as a full five days course in uncomplicated procedure

Should be administered with one hour prior to incision, preferably at induction of

anaesthesia

Should target anticipated organisms

Should not extend beyond 24hours

In prolonged procedure, should be repeated every 3hours.

Wound type;

o Clean wound – not use except in immunosuppressed, implant surgery, esp

vascular and cardiac surgeries, neurosurgical operations, excess blood loss.

o Clean contaminated and contaminated – use prophylaxis

o Dirty wound treat rather than prophylaxis.

Drug with low toxicity, long serum half-life, broad spectrum and low cost is use

DVT PROPHYLAXIS

Deep venous thrombosis is the formation of blood clot in one of the deep veins of the body

usually the lower limbs. The outcome is devastating; PE or venous gangrene. For optimal

prophylaxis, risk factors as well as risk categorization most be noted.

Risk factors

Patient factors;

Age >40years

Obesity

Varicose veins

Immobility(bed>3days)

Pregnancy

[email protected]

Pueperium

High dose oestrogen therapy

Previous DVT or PE

Thrombophilia

o Deficiency of antithrombin III, Antihospholipid antibody, lupus anticoagulant

Disease /surgical procedure

Trauma

Surgery esp. pelvic, lower limb

Malignancy

Heart failure

Recent MI

Paraplegia

Infection

IBD

Nephrotic syndrome

Polycythemia

Paraprotinemia

PN hemoglobinuria

Homocystinaemia

RISK CATEGORY (THRIFT consensus group)

High risk > 40%

• Major surgery

• Pelvic, hip fractures

• Major surgery in a patient with malignancy

• Major surgery in a patient with history of DVT or > 60years

• Lower limb paralysis or major amputation

Moderate risk 5-40%

• Major surgery in patient > 40years not in high risk group

• Major surgery or lower limb surgery in patient on oral contraceptives

• Major medical illness with prolonged immobilization

Minor risks <5%

• Minor surgery (<30min) with no risk factors

• Major surgery (>30min) in patient <40years or with no risk

[email protected]

PROPHYLAXIS

Preoperative

Weight reduction

Stoppage of OCP 1month prior to surgery

Identification of high risk – by risk categorization

Aspirin

Oral anticoagulants

Low dose subcut heparin

Dextran 70

Intraoperative prophylaxis

Epidural anaesthesia

Physical means

o Electrical calf stimulation

o External intermittent pneumatic compression of calf

o Passive leg exercise (foot pedaling machine)

Chemical means (as commenced preoperatively and continued until patient is mobile)

o Low dose subcut heparin

o Dextran 70

Post operatively

Pressure graduated elastic stockings

Early mobilization, massage and leg movt

Adequate hydration

NB; for established DVT, as confirmed by; Doppler, ascending contrast venography or

impedance plethysmography it is treated

I. Anticoagulant therapy

a. LMWH

b. Unfractionated heparin if LMWH not available

c. Warfarin (72hours before heparin is stopped )

II. Thrombolytic therapy

a. Streptokinase

b. Tissue plasminogen activator

III. Operative; venous thrombectomy, interruption of inferior vena cava- Greenfield filter.

[email protected]

TETANUS PROPHYLAXIS

Tetanus infection result from wound invasion by clostridium tetani- a gram positive spore

forming obligatory anaerobic bacillus. They produce exotoxins; most importantly the

tetanospasmin which affect the nervous system producing its characteristic clinical picture.

Clinical forms;

Generalized tetanus

Localized tetanus

Cephalic tetanus

Neonatal tetanus

Features

Trismus

Risus sardonicus

Muscle stiffness and pains- neck, back, abdomen and region of wound.

Opisthotonus in severe cases

Exhaustion and respiratory failure leads to death

There may be associated autonomic dysfunction

Prophylaxis

This is achieved by immunization. The active and passive forms. The active(toxoid) stimulate

the body to produce antibodies. More effective but takes 2-3months to be operational. The passive

uses preformed antibodies in form of human or equine tetanus immunoglobulin. It is

immediately operational but less effective and may precipitate anaphylaxis.

Immunization depends on;

Immune status of patient

Degree of wound contamination

Patients are categorized into;

Fully immunize- do not require prophylaxis

o Completed toxoid and booster within past 5years

Partially immunize

o Completed toxoid, but booster >5years <10years- give a dose of toxoid.

o Completed toxoid but booster > 10yers. For clean wound give toxoid, for dirty wound

give toxoid and immunoglobulin

Not immunize or immune status unknown

[email protected]

o Clean wound, give toxoid complete course. Dirty wound toxoid complete course

plus immunoglobulin

Active immunity

Traditional; 1ml of toxoid subcut/im start, 6weeks, 6months and every 10years

Rapid method (alum-precipitated toxoid); 1st, 4th and 7th day. Active immunity is

demonstrated in 28days.

Passive immunity

Human immune globulin. 250-500IU, Protective antibodies for at least 4-6weks.

Does not produce serum sickness

Anti tetanus serum ATS; 1500IU subcut after test dose. Use only when HIG not

available. has high risk for serum sickness. Protection 7-10days

NB; for established tetanus, treatment;

I. Neutralize toxin

Daily HTIG 500IU until 3000-6000 or start of ATS 200,000IU after a test dose.

II. Prevent further toxin production

Wound debridement

Antibiotics

III. Control spasms

IV. Management of autonomic dysfunction

V. Supportive care

[email protected]

SICKLE CELL DISEASE AND THE SURGEON

Sickle cell disease refers to a condition in which an individual has inherited two abnormal Hb

gene, at least one of which is haemoglobin S (HbS) and the resulting problem is attributed to the

sickling phenomenum. Eg HbSC, HbSD, HbSS.

Sickle cell anaemia is the most severe form of sickle cell disease characterized by inheritance of

two sickle haemoglobin(HbSS).

Surgery in a sickle cell disease is associated with higher morbidity and the management is

multidisciplinary. Improvement in outcome is seen with meticulous care and follow-up.

EPIDEMIOLOGY

Highest prevalence in tropical Africa and slave trade countries. In Nigeria, 2-3% of live birth have

SCA, 0.4%(1-4years), and 0.05%(>7years). Sickle cell trait affects 30% of northern Nigeria

population and 24% of southern population.

PATHOLOGY

Sickle cell haemoglobin gene is inherited as autosomal recessive. Normal haemoglobin has two

alpha and two beta chains. In sickle disease, single amino acid substitution occurs on beta chain.

Valine is substituted for glutamic acid at position 6. SCA is homozygous, sickle cell trait is

heterozygous. The resulting HbS is less soluble than HbA. When deoxygenated, the HbS

undergoes polymerization and forms characteristic sickle cell. There is premature distruction of

rbc, there is reduced oxygen carrying capacity and increased blood viscosity. Blockage of small

vessels results in vaso-occlussive events. Sickling may be precipitated by infection, fever,

dehydration, cold, hypotension, hypoxia, stress-trauma, exercise, sport, emotional disturbances.

Types of crisis; haemolytic, aplastic, sequestration and vaso-occlussive.

PRESENTATION TO A SURGEON

They could present as emergency or elective pathologies which could be sickle cell related or non-

sickle cell related as in other patients.

Sickle cell related problems;

Gastrointestinal tract;

Liver

Hepatomegaly with abnormal liver function.

Progressive liver damage is due to

i. Congestive hepatic crisis

ii. Cholestasis

iii. Viral hepatitis

[email protected]

iv. Intrahepatic obstructive jaundice –

Cholelithiasis :

i. pigment stones due to chronic haemolysis

ii. 6-49% in SCD

iii. 20% have stones in common bile duct

iv. Treatment : Conservative

Cholecystectomy

Spleen

I. Acute splenic sequestration - major cause of death in the first 2yrs of life.

Treatment = packed cells, Parent education. Splenectomy- (i) after

prophylaxis for pneumococcus + H.influenza.

II. Hypersplenism

-Increased spleen 4cm BLCM

-Hb <6.5g/dl

-Platelets <200 x 10⁹/L

-Reticulocytes >15%

-2 occasions 6/12 apart

Intestine

Extensive collateral circulation protects against sickling phenomenon.

Intestinal infarction - malaena, ileitis, peritonitis, adynamic intestinal obstruction

Mesenteric infarction mimicks acute abdomen

Genitourinary

PRIAPISM; painful sustained erection .

60% in pt <12yrs : sleep

Sickling in the corpora carvernosa - congestion of the penile outflow tracts.

2 types based on severity :

i. Short shuttering attacks <3hrs

ii. Major >24hrs

Conservative

Surgical -drainage by caverno-spongiosal shunt with trucut needles (via the glans)

Impotence due to penile fibrosis if >24hrs.

-Penile implants – difficult to trea - migration due to corpora cavernous fibrosis

[email protected]

Bones

Osteomyelitis

AVN

Secondary osteoarthritis

Coxa vara

Spontaneous hip fracture

Generalized osteoporosis

Soft and thin inner cortex

Skin and limbs

Commonest surgical problem

10% in W/Africa ; 2% in Hb SC

Peak incidence age group- 15-19yrs

90% in distal 1/3rd of the leg above the medial malleolus

30-50% are bilateral.

2-10cm, punched out appearance with raised edge.

Usually superficial + deep

The eye

Sluggish flow, intravascular sickling, occlusion of vessels:- necrosis-collateral

Stage 1- dilation + increased tortuosity of vessels.

Stage 2- AV nipping, micro aneurysms common btw small arterioles + venules

Stage 3- neovascularization

Stage 4-proliferative neovascularization of the vitreous

Stage 5- retinal detachment (fibrovascular detachment) - ocular changes are

common in HbSC.

Rarely require or benefit from therapy.

Scatter photocoagulation for early lesions

Pregnancy

Impaired placental bld flow

Spontaneous abortion

IUGR

Pre-eclampsia

IUFD

prevent severe anaemia, infection & VOC

Management

Elective caesarian section

[email protected]

MANAGEMENT

I. Pre-operative; aims to prevent the development of crisis by treating infection and avoiding

other precipitants, taking detail history, physical examination, investigation and adequate

optimization. NB; those presenting as emergency are resuscitated.

Investigations; genotype, FBC, septic work-up, CXR, GXM, U/ECr, others depends on the presenting

pathology

General measures;

Analgesia

Expand plasma volume: glucose, fructose.

Difficult IV access

Alkalinize blood: NaHC03, lactate

Anticoagulation -pts who are prone to embolism

Eliminate infective foci (respiratory, UTI), treat malaria

Blood transfusion - avoid increased viscosity

Anaemia

Hbss 6-10g/dl (steady state) (avg-8g/dl)

Hbsc 12g and above

HbSC thal 11g/dl

Hb Sf 10g/dl

Informed consent

First on the operation list

II. Intra-operatively

a. Anaesthesia; GA, regional (preferable). Adequate analgesia with pre-oxygenation.

b. Preoperative antibiotics

c. Position; reduced blood loss- limb elevation, reverse trendelenberg in head and neck

operation

d. Tourniquet; relatively contra-indicated(no exsanguination), adequate timing

e. Shortened operation time

f. Avoid sickling triggers ;

i. Dehydration- adequate rehydration

ii. Hypoxia : preoxygenation

iii. Hypotension : minimum drug doses

iv. Hypothermia- temperature regulation, warm fluids

v. Judicious blood replacement using fresh blood

g. Adequate monitoring – SPO2, BP, PR, TEMP., urine output.

III. Post-operatively

a. Continuous monitoring

b. Oxygen administration

[email protected]

c. Adequate analgesia

d. Adequate hydration

e. Temperature control

f. Early ambulation

IV. Follow-up

a. Effectiveness of treatment

b. Identify complications

c. Address concerns of patient

CURRENT TRENDS

Pain mgt

Infection control

Induction of fetal haemoglobin – hydroxyurea,

Haemopoetic cell transplant

Laparoscopic surgery

CONCLUSION

No surgeon is exempt. Appropriate preoperative evaluation minimizes intra- and post-operative

complications. Effective multidisciplinary management and identification of risk factors reduces

morbidity and mortality.

[email protected]

DIABETIC AND SURGERY

Introduction

Epidemiology

pathology

Presentations

Management

Conclusion

INTRODUCTION

Diabetes mellitus is metabolic disorder characterized by abnormality in insulin production and utilization

with resultant hyperglycemia and excessive fat and protein breakdown. The have glucosuria and RBS of

11.1mmol/L, FBS of >7mmol/L in two occasions or two hourly blood glucose after oral 75g glucose of

11.1mmol/L.

EPIDEMIOLOGY

Estimated about 171 million people suffer from DM worldwide. Surgical problems are more common in

diabetic than non-diabetic. 80% of diabetic are over 40years of age and surgical procedures are more

common in this age group. >50% would have one form of surgery or the other in their life time

PATHOLOGY

Diabetic complications results from interplay of vasculopathy (macroangiopathy and microangiopathy),

neuropathy and susceptibility to infection (impairment of cellular and humeral immunity).

PRESENTATION TO A SURGEON

They could present as elective or emergency with diabetic or non- diabetic related pathologies just like

other surgical patients.

Diabetic related problems;

Peripheral vascular insufficiency

o DM foot, DM hand syndrome

Retinopathies, cataracts

Infections

o cellulitis, carbuncle, abscess

o pyomyositis

o osteomyelitis

o moniliasis (vulvulitis and balanitis )

o tuberculosis

o UTI

[email protected]

PRE-OPERATIVE PREPARATION

Aims; to prevent ketosis and avoid hypoglycemia.

Details history and physical examination. Look for presence of complications e.g neuropathy,

retinopathy, hidden infections as well as autonomic neuropathy – postural hypotension, gastroparesis,

neurogenic bladder and erectile dysfuntion. As well as other co-morbidities eg hypertension

Investigation; Urinalysis, FBS, 2HPP, E/U +Cr, HbA1c, ECG, CXR, septic work-up, others depend on the

presenting pathology.

Other Perioperative considerations for elective setting include

Stopping cigarette smoking at least 2weeks before surgery

Prophylaxis against DVT

Antibiotics prophylaxis

First on list

All electrolyte derangement are corrected. Further preparation depends on;

Nature of operation- minor or major, elective or emergency

On what patient achieves control

Glycemic control of patient

Elective cases are admitted two days before operation and monitored serially for blood sugar. Elective

cases with uncontrolled sugar should be postponed until control is achieve

Minor surgery;

Patient controlled on diet on diet are only treated as normal patient but 1st on the list

Those on oral hypoglycemic drug should be taken off biguanides and sustained on short acting

sulphurnylurea. The agent may be omitted on the day of surgery

Those on long acting insulin (lante). Start an intravenous infusion of 5% DW early in the morning

of surgery and give half the usual dose of the long acting.

Major surgery

All forms of DM going for major surgery, those on oral hypoglycemic drug are stabilized on

soluble insulin for tight control. They are placed on NPO and commenced GKI on the morning of

the surgery with monitoring until post operatively when patient commences orally.

Emergency

Those going for emergency are resuscitated with IV fluids then IV soluble insulin bolus(10IU) and

in infusion(10IU/hr) until a serum glucose of ≤14mmol/L is achieved then placed on GKI or

[email protected]

sliding scale with continuous monitoring. NB; other components of resuscitation depending on

type of emergency

GKI- GLUCOSE-POTASSIUM-INSULIN infusion in a ratio of 10:10:10 or 5:5:5 that is 5% DW, 5mmol of K,

and 5IU insulin to run over 4hours with 2hourly monitoring of serum glucose and potassium.

Aims; to maintain a serum glucose of 4-10mmol/L and K of 3.5-4.5mmol/L

Two IV access is secured; one for the GKI and the other for the maintenance infusion.

If the serum glucose rise above 10mmol/L a bolus of soluble insulin is give 2IU per 2mmol/L rise.

Likewise if it falls below 4mmol/L GKI is stopped given only DW infusion.

The GKI is continue until patient is recommenced orally and placed on previous regimen.

INTRA-OPERATIVE MANAGEMENT

Anaesthesia; regional anaesthesia is preferable because it produces little metabolic disturbance. The

stress of general anaesthesia, surgery could predispose patient to hyper or hypoglycemia and

hypotension. These should be monitored throughout anaesthesia. As well as the serum potassium as

the GKI is continued.

POST-OPERATIVELY MANAGEMENT

The postoperative goal is to maintain blood glucose between 8.5-14mmol/L. insulin containing infusion

is continued with strict monitoring until commenced orally. The placed on previous controlled regimen.

CONCLUSION

The current high standard of surgical and anaesthetic technology make surgical outcome in diabetics

comparable to non-diabetic

[email protected]

PROSTATE BIOPSY

Indications;

DRE features of malignancy

Elevated PSA > 10ng/ml

o NB; 4-10ng/ml other parameters. Density 0.15ng/ml, velocity 0.75ng/ml/year, % free

PSA< 25%

Paraplegia in suspected CAP

Screening for prostate Ca in asymptomatic patient >50years(life expectancy >10years, family hx,

African-American> 45years)

Follow-up biopsy (3-6months) after diagnosis of PIN or ASAP

Contra-indications

Coagulopathy

Painful anorectal conditions

Severe immunosuppression

Acute prostatitis

Preparation of patient

Informed consent

Stop all anticoagulant

Prophylactic antibiotic

Cleansing enema

Analgesia

o Topical

o Local prostatic block

o Skin infiltration

Positioning

o left lateral decupitus position with the hips and knees flexed at 90°

o lithotomy

Technique

o transrectal prostate biopsy

TRUS guided ; sextant biopsy, extended core biopsy

o Transperineal

o Transurethral

[email protected]

[email protected]

Complications

o Post biopsy infection

o Bleeding

o Acute urine retention

o Hematuria

o Hemospermia

Histological types of prostate ca;

Adenocacenoma 85%

o Ordinary

o Mucinous

o Ductal aggressive

o Neuroendocrine

o Small cell

Transitional cell ca

Pure primary squamous cell

Sarcoma

Lymphoma

Gleasons grading ; sum of two most prominent grade

2-4 low grade

5-7 intermidiate

8-10 high grade

[email protected]

DIALYSIS; method of removing toxic substance(impurities and waste) from the blood when the kidneys

are unable to do so.

Methods;

Haemodialysis

Peritoneal

Functions;

Cleans the blood of accumulated waste product

Removes the by-products of protein metabolism(urea, Cr and uric acid)

Removes excessive fluids

Maintains or restores the buffer system of the body

Maintains or restores electrolytes levels

Indications

Clinical

o Uremic encephalopathy

o Uremic pericarditis

o Uremic nephropathy

o Pulmonary edema

o Refractory oedema

o Refractory hypertension

o Bleeding diathesis

Laboratory

o Urea ≥30mmol/L or daily raise of 5mmol/L

o Potassium ≥6.5mmol/L or daily raise of 1mmol/L

o Bicarbonate ≤10mmol/L

o Cr >600mmol/L or daily raise of 100mmol/L

[email protected]

Surgery tutorials for medical students

Health & Medicine

Transcript of Surgery tutorials for medical students