1. ACUTE SURGICAL INFECTION DR.A.KENSARAH

2. ACUTE SURGICAL INFECTION
Non-Specific Acute Infection Specific Acute Infection

3. Non-Specific Acute Infection
Postoperative Wound Infection
Cellulitis
Erysipelas
Boil (Furuncle)
Carbuncle
Hydradenitis Suppurativa
Acute Abscess
Acute Lymphangitis and Lymphadenitis
Bacteraemia and Septicaemia

4. Specific Acute Infections
Tetanus
Gas Gangrene
Necrotizing Fasciitis

5. Postoperative Wound Infections
Are caused by the presence of contaminating microbes derived from :
Endogenous OR
Exogenous

6. Postoperative Wound Infection
Predisposing Factors: # General
1- Poor general condition
2- Systemic disease
3- Drugs that cause immunosuppression

7. Postoperative Wound Infection
# Local :
1- Poor blood supply Poor surgical technique Presence of foreign bodies Nature of the operation Defect in sterilization technique in
the operating theatre

8. Types of surgical wounds
Operative wounds are divided into three categories : Clean The risk of infection is 1-2% Clean contaminated The risk of infection 2-5% Contaminated The risk of infection is 5-30%

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

10. Clinical Picture
Wound infection usually appears between the fifth and tenth days postoperative
* Fever * Pain in the wound Signs: _ swollen _tenderness _redness _fluctuant

11. Differential Diagnosis
Other causes of postoperative fever
chest infection
DVT
UTI Other causes of wound swelling
heamatoma

12. 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

13. Treatment Surgical drainage of the pus
Antibiotics in invasive infections
Look for hospital acquired infection

14. Cellulitis
Is an invasive non suppurative infection of the loose connective tissue
Organism :
streptococci [common]
staphylococci [occasionally]
mix

15. 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

16. Differetial Diagnosis
Contact allergy
Chemical inflammation
DVT

17. Treatment Rest and elevation of the affected part
Antibiotic penicillin iv

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

19. 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

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

21. Treatment
Isolation
Similar to cellulitis

22. Boil [Furuncle]
Is a staphylococcal infection of a hair follicle or a sebaceous gland.
The common sites:
face, neck and axilla.
Common in diabetics.

23. Clinical Picture A small painful indurated swelling which is - red
- hot
- and very tender

24. Treatment
1.Antibiotics.
2.Antiseptic.

25. 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

26. 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

27. 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.

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

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

30. 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.

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

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

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

34. 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.

35. Sequlea Resolution. Pointing and rupture. Spread infection – locally
- by lymphatics or blood
Chronicity.

36. 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

37. 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

38. 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.

39. Acute Lymphangitis and Lyphadenitis
Acute lymphangitis:is 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.

40. Treatment Antibiotics. Hot applications.
Surgical drainage if suppuration occurs.

41. 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

42. Septicemia
The presence of multiplying organisms
in the blood stream.

43. Specific Acute Infections

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

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

46. Mode Of Infection
1. Wounds:-hypoxic,containing devaitalized tissue or a foreign body.
2.Umbilical stump: tetanus neonatorum

47. 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.

48. 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.

49. 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.

50. Tonic stage: -Pain and tingling in the area of injury
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.

51. Clonic stage: -Reflex paroxysms of violent muscular contraction
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

52. Laboratory Finding
Polymorphnuclear leucocytosis.

53. 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.

54. 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.

55. 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.

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

57. 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.

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

59. 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.

60. Locally: -pain and numbness in the affected area
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.

61. Prevention Adequate debridement of wounds. Antibiotics.
Avoid tissue hypoxia.

62. Treatment Wound management. Hyperbaric oxygenation.
Antibiotics: penecillin.

63. 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.

64. 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.

65. 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.

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

67. Prevention
Adequate debridement of wounds
Antibiotics

68. Treatment
Surgical
Antibiotics
Blood transfusion