ACUTE SURGICAL INFECTION DR.A.KENSARAH

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ACUTE SURGICAL INFECTION DR.A.KENSARAH
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ACUTE SURGICAL INFECTION

• Non-Specific Acute Infection Specific Acute
  Infection

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Non-Specific Acute Infection

• Postoperative Wound Infection
• Cellulitis
  
• Erysipelas
  
• Boil (Furuncle)
  
• Carbuncle
  
• Hydradenitis Suppurativa
• Acute Abscess
  
• Acute Lymphangitis and Lymphadenitis
• Bacteraemia and Septicaemia

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Specific Acute Infections

• Tetanus
  
• Gas Gangrene
  
• Necrotizing Fasciitis
  

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Postoperative Wound Infections

• Are caused by the presence of contaminating
  microbes derived from
• Endogenous
  
• OR
  
  
• Exogenous

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Postoperative Wound Infection

• Predisposing Factors
  General
  
• 1- Poor general condition
  
• 2- Systemic disease
  
• 3- Drugs that cause immunosuppression

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Postoperative Wound Infection

• Local
  
• 1- Poor blood supply
  2- Poor surgical technique
  3- Presence of foreign bodies
  4- Nature of the operation
  5- Defect in sterilization
  technique in
• the operating theatre

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Types of surgical wounds

• Operative wounds are divided into three
  categories
  1- Clean The risk of infection is
  1-2
  2- Clean contaminated The risk of
  infection 2-5
  3- Contaminated The risk of infection is
  5-30

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Pathology

• Acute inflammatory stage with local
  vasodilatation and infiltration by polymorph
  nuclear leucocytes. This is
  followed by suppuration with purulent discharge

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Clinical Picture

• Wound infection usually appears between the fifth
  and tenth days postoperative
• Fever Pain in the wound
  Signs
  _
  swollen
  _tenderness
  _redness
  _fluctuant

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Differential Diagnosis

• Other causes of postoperative fever
• chest infection
  
• DVT
  
• UTI
  Other causes of wound swelling
  
• heamatoma

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Prophylaxis

• Improve the defense mechanism
• Control the predisposing factors
  Prophylactic antibiotics
  In bowel surgery, mechanical and
  chemical preparation of the bowel
• Meticulous surgery
  Operation in septic areas with
  heavily contaminated wounds should be left open

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Treatment

• Surgical drainage of the pus
• Antibiotics in invasive infections
• Look for hospital acquired infection

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Cellulitis

• Is an invasive non suppurative infection of the
  loose connective tissue
• Organism
• streptococci common
• staphylococci occasionally
• mix

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Clinical picture

• The affected area is red,indurated,hot and
  painful
• It spreads rapidly with ill defined edge
• The skin may be the seat of blisters
• Fever
• Lymphangitis in the form of red streaks
• No suppuration
• In severe cases patches of skin necrosis with
  sloughing of subcutaneous tissues

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Differetial Diagnosis

• Contact allergy
• Chemical inflammation
• DVT

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Treatment

• Rest and elevation of the affected part
• Antibiotic penicillin iv

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Erysipelas

• Is a rapidly spreading non-suppurative
• inflammation of the lymphatics of the
• skin caused by a specific strain of
• hemolytic streptococci

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Clinical Picture

• Toxemia
• Locally similar to cellulitis,but there
• are the following differences
  
• 1. The color of the skin is rose-pink
• 2. The edge is well defined
• 3. There may islets of inflammation
• beyond the spreading margin

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Complications

• 1. Facial erysipelas may lead to cavernous sinus
  thrombosis
• 2. Septicemia
• 3. Recurrent erysipelas may block the lymphatics
  leading to elephantiasis.

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Treatment

• Isolation
• Similar to cellulitis

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Boil Furuncle

• Is a staphylococcal infection of a hair follicle
  or a sebaceous gland.
• The common sites
• face, neck and axilla.
• Common in diabetics.

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Clinical Picture

• A small painful indurated swelling which is
• - red
• - hot
• - and very tender

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Treatment

• 1.Antibiotics.
• 2.Antiseptic.

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Carbuncle

• Is infective gangrene of the subcutaneous tissues
  usually secondary to infection by Staphylococcus
  aureus.
• It is common in immunocompromised patients as in
  diabetics.
• The common sites
• face, nape of the neck, and the back

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Pathology

• Infection usually starts in a hair follicle
• Extends to the subcutaneous fat where other hair
  follicles get the infection.
• Multiple areas of necrosis and thrombosis of
  blood vessels occur.
• Patches of skin undergo sloughing and separate
  from the underlying granulation tissue

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Clinical Picture

• There is usually sever toxemia.
• Starts as a painful induration of the skin and
  subcutaneous tissues.
• The skin is red.
• Swelling its central part becomes soft.
• Multiple areas of skin thin out and separate
  forming multiple sinuses.

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Complications

• Local spread of infection.
• Pyaemia and septicemia.
• Cavernous sinus thrombosis
• Epidural abscess or meningitis

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Treatment

• 1.Antibiotics.
• 2.culture and sensitivity of the discharge.
• 3.control of diabetes.
• 4.surgical excision of sloughs.

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Hydradenitis Suppurativa

• Mixed staph. And streptococcal infection
• of the apocrine sweat glands, in the
• perineum or the axilla,produces multiple
• abscesses and pus discharging sinuses.

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Treatment

• Surgical drainage of abscesses.
• Antiseptic and antifungal applications.
• Surgical excision of the apocrine sweat-bearing
  skin following by skin grafting is essential.

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Acute Abscess

• It is a localized suppurative inflammation.
• It is caused by pyogenic organisms.
  The commonest are staphylococci that produce a
  coagulase enzyme.

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Pathogenesis

• The organism reach the tissues by
• - direct access through wounds, scratches and
  abrasions.
  
• - local extension from an adjacent focus
• - lymphatic spread.
  
• - blood spread.

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Pathology

• An abscess consists of three zones
• 1- A central zone of coagulative necrosis
• 2- An intermediate zone of granulation tissue.
  
  
• 3- A peripheral zone of acute inflammation.

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Sequlea

• Resolution.
• Pointing and rupture.
• Spread infection locally
  
• - by lymphatics or blood
• Chronicity.

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Clinical Picture

• Locally - painful tender mass
  -The covering skin is red, and oedematous
  -The draining lymph nodes are usually enlarged
  and tender
• Systemic -Fever
  -Malaise
  -Headache
  -Tachycardia
  
  -Anorexia

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When Pus Forms

• The fever becomes hectic.
• Skin shows pitting oedema.
• The pain becomes throbbing.

• The inflamatory reaction becomes localized
• Fluctuation test becomes positive.
• There is shooting leucocytosis

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Treatment

• Before suppuration
  - antibiotic, rest -hot application.
  
  -supportive general measures.
• After suppuration
  -adequate surgical drainage.
  -a specimen of the pus is sent for
  culture and sensitivity.
  -antibiotic if there is
  systemic manifestation.
  
  

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Acute Lymphangitis and Lyphadenitis

• Acute lymphangitisis due to infection of lymph
  vessels by organisms usually streptococci.
• Acute lymphadenitis is due to spread of
  infection along lymphatics from a septic focus in
  the drainage area to the lymph- nodes.

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Treatment

• Antibiotics.
• Hot applications.
• Surgical drainage if suppuration occurs.

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Bacteraemia

• Presence of bacteria which are NOT multiplying,
  in the blood.
• It usually follows
  - dental work.
  -instrumentation of the
  urinary tract
• It is hazardous in patients with
  -damaged heart valves.
  -prosthetic valves.
  -immunosuppression
• Prophylactic antibiotics is essential

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Septicemia

• The presence of multiplying organisms
• in the blood stream.

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Specific Acute Infections
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Tetanus

• It is a specific anaerobic infection that is
  mediated by neurotoxin of
• Clostridium tetani
• and leads to
• nervous irritability and tetanic muscular
  contractions.

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Aetiology

• Organism Clostridiuam tetani is
• gram positive anaerobic bacillus with a
• terminal spore giving the characteristic
• drum-stick appearance.

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Mode Of Infection

• 1. Wounds-hypoxic,containing devaitalized tissue
  or a foreign body.
• 2.Umbilical stump tetanus neonatorum

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Pathology

• The neurotoxin is an exotoxin produced locally
  and reaches the central nervous system along the
  blood stream, the motor nerves or both.
• When the toxin reaches the nervous system, it is
  fixed by the motor cells and can not be detected
  in the blood or CSF.
• The antitoxin can only neutralize the toxin
  before it gets fixed to the nervous tissue.

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• The toxin increases the exitability of the motor
  cells of the medulla and spinal cord, so
  slightest stimuli produce violent spasm.
• Death results from exhaustion, hyperpyrexia,
  heart failure, asphyxia or pneumonia.

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Clinical Picture

• Incubation period
  - In non-immunized is short from 24H to
  15 days.
  - In immunized is longer than
  11 days to several weeks or months.
• Symptoms during incubation period are vague such
  as tenderness, rigidity of the muscles,
  swelling at the site of wound, local twitches,
  restlessness, and an anxiety.

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• Tonic stage
  -Pain and tingling in the area of
  injury. -Limitation of movements of the
  jaw. -Spasm of the facial muscles.
  -Stiffness of the neck.
  -Dysphagia.
  
  -Laryngospasm.
  -Hesitancy in micturition.

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• Clonic stage
  -Reflex paroxysms of violent muscular
  contraction.
  -Relaxation is incomplete during the
  intervals between clonic contractions.
  -Spasm of the intercostal muscles and diaphragm
  lead to long period of apnea. -Temperature
  elevated with profuse sweating.
  -Marked
  tachycardia

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Laboratory Finding

• Polymorphnuclear leucocytosis.

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Prevention

• Immunization active with tetanus toxoid with
  routine childhood immunization, with booster
  injections every 7-10 years.
• Individuals who previously received three or more
  doses, the last within 10 years need a
  booster dose of tetanus toxoid.
• Those who received less than three doses
  -need a booster dose of tetanus toxoid and
  tetanus immunoglobulin passive.
• Individuals not previously immunized
  -need full immunization with tetanus
  toxoid and tetanus immunoglobulin.

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Treatment

• Neutralize toxin with TIG.
• Wound debridment.
• Avoid sudden stimuli.
• Muscle relaxant with mechanical ventilation may
  require tracheostomy.
• Aqueous penicillin G ,10-40 million units a day
  IV.
• Nursing.

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Gas Gangrene

• It is an acute spreading infection
• associated with gas formation and
• profound toxaemia caused by anaerobic
• spore-bearing bacilli of the clostridium
• group.

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Pathology

• Clostridia proliferate and produce toxins that
  diffuse into the surrounding tissue.
• The toxins destroy local circulation.
• This allows further invasion.

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Factors predisposing to gas gangrene

• Lacerated wounds involving bulky muscles.
• Presence of foreign bodies or devitalized
  tissues.
• Ischemia of muscles.
• Infection by anaerobic bacteria.
• As a complication of above knee amputation in
  patient with faecal incontinence.

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Bacteriology

• Organisms falls into two groups
• Saccharolytic organisms
  -Cl.welchii,-Cl.septicum,-and Cl.oedematiens
• Proteolytic organisms
  -Cl.sporogenes,-Cl.histolyticum and
  Cl.tertium.

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Clinical Picture

• The incubation period varies from few hours to
  few days.
• Generally the patient is pale, anxious, and
  apprehensive.
  -The temperature may be raised and
  there is marked tachycardia.
  -The hands are cold and clammy.
  -An icteric tinge may be present and there is
  oliguria.In severe case there is shock.
  
  

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• Locally -pain and numbness in the affected area.
  
  -swelling and there may be crepitus with gas
  bubbles.
  -A sanguineous dischrge of a
  characteristic odour.
  -The affected
  muscles brick red then greenish and finally black
  discolouration,do not contract,do not bleed if
  cut, the skin black.

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Prevention

• Adequate debridement of wounds.
• Antibiotics.
• Avoid tissue hypoxia.

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Treatment

• Wound management.
• Hyperbaric oxygenation.
• Antibiotics penecillin.

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Necrotizing Fasciitis

• It is an invasive infection usually caused by a
  mixed microbial flora including microphilic
  streptococci, staphylococci, Gram-negative
  bacteria and anaerobes,especially
  peptostreptococci, and bacteroids.

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Pathology

• The infectious process spreads along the fascial
  planes and results infectious thrombosis of the
  vessels passing between the skin and deep
  circulation.
• Superficial skin necrosis follows.
• Hemorrhagic bullae appear as the first sign of
  skin death.
• Fascial and subcutaneous fat necrosis involves
  wider area than the skin.

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Clinical Picture

• There are manifestations of toxemia with fever
  and tachycardia.
• The skin shows hemorrhagic bullae and necrosis
  surrounded by oedema and inflammation.
• Crepitus is occasionally present.

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Investigations

• Swab for culture and sensitivity
• At surgery oedematous, dull gray fascia and
  subcutaneous tissue with visible thrombi in
  penetrating vessels

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Prevention

• Adequate debridement of wounds
• Antibiotics

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Treatment

• Surgical
• Antibiotics
• Blood transfusion

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