The document provides information on the history and physiology of infection, along with definitions and classifications of various types of infections such as surgical site infections, sepsis, bacteremia, and abscesses. It traces the history of infection from ancient Egyptians and their mummification practices to modern discoveries like antibiotics. Key physiological defenses against infection like the immune system are described. Various infections affecting wounds, skin and deeper tissues are defined and explained.

1. Dr. Ravi Gadani
M.S.,F.M.A.S.

2. History
 4000 yrs Egyptians- mummification
 Hippocrates –wine /vinegar as antiseptic
 Galen 130-200A.D. -suppuration can cause recovery
 Nineteenth century rapid progress in field of infection
 Louis Pasteur (1822–1895)-microorganism responsible
for spoiling wine
 Joseph Lister (1827-1912)-phenol to irrigate wounds.
Started the era of anti sepsis
 Alexander Fleming (1881-1955)-Penicillin

3. Physiology
 Mechanical barrier-Intact epithelium
 Chemical-Low Gastric pH
 Humoral (antibodies, complement, opsonins)
 Cellular (phagocytic cells, macrophages , lymphocytes,
WBC)

4. Risk factors
 Malnutrition
 Metabolic diseases
 Immunosupression
 Colonization and translocation in GIT
 Poor perfusion
 Foreign body
 Poor surgical technique
 Size and pathogenicity of bacterial inoculum

5. Definations
 Wound infection-Invasion of organisms through tissue
following a breakdown of local and systemic host defenses.
 Surgical site infection -infected wound or deep organ space
 SIRS -Body’s systemic response to an infected wound
 Sepsis-systemic manifestation of SIRS with a documented
infection
 MODS -effect that the infection produces systemically
 MSOF -end stage of uncontrolled MODS

6. Definations of SIRS
• SIRS-Two of :
Hyperthermia(> 38c)/Hypothermia (<36c)
Tachycardia>90/min
Tachypnoea>20/min
WBC>12000/<4000
• SEPSIS-SIRS with documented infection
• SEVERE SEPSIS- Sepsis with evidence of one or more
organ failure

7. Bacteremia
 Bacteremia: presence of viable bacteria in the blood
stream (toxemia)
 Causes :
 Dental procedures
 Indwelling catheters
 Following gastrointestinal , cancer , oral surgeries
 Diagnosis – blood culture
 Prophylaxis- antibiotic coverage before any surgical
procedure- prosthetic valves
 Bacteremia invokes- immune system response (fever,
hypotention etc.)-sepsis or septicemia

8. Septicemia
 Presence of bacteria in the blood often associated with
severe infections which invokes a systemic immune
response
 Infections throughout the body- can lead to
septicemia
 Lung –pnuemonia, lung abscess
 Abdomen- liver abscess, severe gastroenteritis, colitis,
 Urinary tract- pyelonephritis, renal abscess
 Bone-osteomyelitis
 Central nervous system -meningitis
 Heart -endocarditis

9. Clinical features
 The person looks very ill
 Spiking fevers, chills, rigors
 Rapid breathing (tachypnoea)
 Rapid heart rate( tachycardia)
 The symptoms rapidly progress
 Shock with- fever or decreased body temperature
(hypothermia)
 Falling blood pressure
 Confusion or other changes in mental status, and blood
clotting problems- (petecheae and ecchymosis).
 There may be decreased or no urine output.

10. Sepitcemia

11. Tests that can confirm infection
 Blood culture
 Blood gases
 CBC
 Clotting studies
 PT
 APTT
 Fibrinogen levels
 CSF culture
 Culture of any suspect skin lesion
 Platelet count
 Urine culture

12. Treatment
 Septicaemia is a serious condition - requires an intensive
care unit (ICU) admission.
 Hydration
 Oxygen , ventilatory support
 Antibiotics are used to treat the infection.
 Plasma or other blood products may be given to correct any
clotting abnormalities.
 Outlook (Prognosis)
 Depends on the organism involved and how quickly the
patient is hospitalized and treatment begins. The death
rate is high -- more than 50% for some organisms.

13. Pyaemia
 Pyaemia (or pyemia) is a type of septicaemia that
leads to widespread abscesses of a metastatic nature.
 It is usually caused by the staphylococcus bacteria by
pus-forming organisms in the blood.
 Apart from the distinctive abscesses, pyaemia exhibits
the same symptoms as other forms of septicaemia.
 It was almost universally fatal before the introduction
of antibiotics.
 Antibiotics and treatment of cause

14. Multiple pyaemic abscess liver

15. Classification of sources of
infection
 Primary : Acquired from community/endogenous
peptic perforation
 Secondary: Exogenous acquired from operation
theater ,ward , aseptic technique etc.

16. Classification
 Nonnecrotizing
infections involve
superficial structures
generally
 Necrotizing
infections involve
deep structures
generally

17. Non necrotizing infection Necrotizing infection

18. Wound Abscess
 Collection of pus in the body
 Three types
1. Pyogenic
2. Pyaemic
3. Cold abscess

19. Pyogenic abscess
 Commonest variety
 Spread
1. Direct infection due to penetrating wounds
 Thorn injury- abscess of sole of foot
2. Local extension from adjacent tissue
 Pyelonephritis– renal abscess
3. Lymphatics
 Lymphangitis of leg– abscess of inguinal group of
lymph nodes
4. Blood stream
 Appendicitis- liver abscess

20. Pyogenic abscess
Pathology
 Infection – cell death and liquaefaction
 Abscess cavity- filled with pus and lined by pyogenic
membrane
 Pyogenic membrane
 Dead tissue cells and granulation tissue
 Later converted to fibrous tissue with collagen fibres
 Occasionally cavity persists –contains sterile pus
within thick wall -antibioma

21. Abscess

22. Pyogenic abscess
 Clinical features
 Redness (rubor)
 Pain (dolor)
 Heat (calor)
 Swelling
 Impairment of function or functiolasea

23. Abscess

24. Investigation
 For deep abscess
 Ultrasound
 CTscan
 Isotope scan-

25. Treatment
 Drainage of pus
 Free liberal incision at maximun pointing area of pus
 Hiltons method
 Aspiration – percutaneously via USG, CT guided
 Send pus for culture sensitivity
 Antibiotics according to C/S

26. Pyaemic abscess
 Condition of multiple abscess due to infected emboli
in pyaema
 Secondary foci of suppuration in various parts of body
 Examples –
 Associated with- osteomyelitis, endocarditis,
 Acute appendicitis- portal pyaema- multiple liver
abscess

27. Pyaemic abscess
 Features
1. Multiple
2. Commonly in subfascial plane
3. Acute features – absent
4. Constitutional disturbances are tremendous
5. Can occur in viscera – spleen, liver, brain, heart
 Treatment
 Antibiotics
 Culture sensitivity
 Locate source of infection

28. Cold abscess
 Name- cold and non reacting in nature
 The caseation of tuberculous granulation tissue and its
liquefaction is a slow and insidious process, and is
unattended with the classical signs of inflammation—
hence the terms “cold” and “chronic” applied to the
tuberculous abscess
 Features of pyogenic abscess absent
 Only if secondarily infected- features of inflammation
present
 Other cause -Actinomycosis

29. Cold abscess- Pathology
 The wall of the abscess is lined with tuberculous
granulation tissue
 The inner layers of which are undergoing caseation
and disintegration
 Outer layers consist of tuberculous tissue which has
not yet undergone caseation.
 The abscess tends to increase in size by progressive
liquefaction of the inner layers, caseation of the outer
layers, and the further invasion of the surrounding
tissues by tubercle bacilli.

30. Clinical features- cold abscess
 The development - insidious
 The swelling may attain a considerable size without
the patient being aware of its existence
 The abscess varies in size from a small cherry to a
cavity containing several pints of pus.
 The usual course of events is that the abscess
progresses slowly, and finally reaches a free surface—
generally the skin.
 As it does so there may be some pain, redness, and
local elevation of temperature.

31.  Most common sites – neck and axilla
 Loin
 Chest wall
 Ends of long bones, joints
 Fluctuation swelling
 If the case is left to nature, the discharge of pus
continues, and the track opening on the skin remains
as a sinus.
 Secondary infection- patient – can have symptoms
similar to pyogenic abscess

32. Cold abscess –psaoas abscess extending
to groin

33. Cold abscess

34. Tubercular sinus

35. Cold abscess-treatment
 Anti tuberculous treatment
 Aspiration of non dependent part of abscess
 Excision of LN if no resolution inspite of treatment
with AKT

36. Cellulitis
 Cellulitis- Non suppurative inflammation spreading
along the subcutaneous tissue and connective tissue
planes
 Poor localization
 Causative organism
 Streptocooccus pyogenes ,
 B- haemolytic streptococci,
 Staphylococci.

37. Cellulitis
 Pathology
 Organism- wound, scratch, surgical incision
 Release of streptokinase ,hyaluronidase ,proteases
 Tissue destruction, ulceration, necrosis
 Symptom and signs
 Systemic signs-fever ,chills , rigors
 Swelling ,redness, but no localization
 Surrounding lymph vessels inflamed –streaks – LN
enlargement

38. Cellulitis

39. Cellulitis of thigh

40. Cellulitis
 Treatment
 Rest , elevation of part to reduce edema
 Antibiotics
 Anti inflammatory drugs
 If pus forms – incision and drainage

41. Lymphangitis
 Lymphangitis-painful red streaks in affected
lymphatic's often accompanied by enlarged lymph
nodes
 Treatment-antibiotics, anti inflammatory drugs

42. Boil (furuncle)
 Acute staphyloccocal infection of hair follicle with
perifolliculitis which proceeds to suppuration and
central necrosis
 Clinical features
 Painful indurated swelling
 Tenderness, with surrounding edema
 After few days –softening of center summit of which has
a small pustule
 Bursts- pus discharge- cavity forms which heals with
graulation tissue
 Blind boil – subsides with out suppuration

43. Boil
STYE

44. Boil
 Sites
 Back , neck
 Eye- stye
 Furuncle of external auditory meatus- very painful-
skin and tight attachment of cartilage
 Complications
 Cellulitis- immunity low
 Infect neighboring follicles
 Secondary- infect LN

45. Boil
 Treatment
 General improvement of health
 Pustule small- touch iodine – hastens necrosis
 Multiple boils – antibiotics
 Incision and drainage

46. Carbuncle
 Infective gangrene of the subcutaneous tissue due to
staphyloccocal infection. Gram negative and
streptococci may be found occasionally
 Sites
 Back, nape of neck
 Shoulders, cheek, dorsum of hands –rare sites
 Pathology
 Staphyloccocus penetrate deep inside the sub cut. tissue
 Series of communicating abscesses formed –discharge
by separate opening on surface
 Area of central necrosis surrounded by a rossete of small
areas of necrosis

47. Carbuncle
 Untreated cases continue to extend in the
subcutaneous tissue and open in the surface
 Clinical features
 Males, >40 yrs , diabetic
 Painful stiff swelling which spreads rapidly with
marked induration
 Skin red dusky and edematous
 Central part softens and multiple vesicles appear on
skin
 Vesicles turn into pustules

48. Carbuncle
 Pustules burst- pus discharge
 Produces a sieve like or cribriform like appearance
 Openings enlarge and produce –ulcer
 Floor – ash grey slough
 Slough separates- red granulation tissue
 Constitutional symptoms a/c to pts resistence

49. Treatment
 Improve the general health of the patient
 Antibiotics to be started
 Control of diabetes
 Culture and sensitivity report and anti biotics
accordingly
 Debridement if carbuncle is > two and half inches or
toxemia and pain
 Once granulation tissue formed then –STG, flap can be
done

50. Carbuncle

51. Debridement of carbuncle

52. Erysipelas
 Acute infection of the
lymphatics of skin or
mucous membrane
 Streptococcus
haemolyticus group
A(strep. Pyogenes)

53. Erysipelas
 Pathology
 Organism- minor wound, scratch
 Inoculation- area red slightly raised from the surface
 Margin is irregular
 Lymphatics become crowded with streptococci
 Characteristic cell –lymphocytes and monocytes // other
strep. Infection—polymorphonuclear leucocyte
 Absence of pus formation

54. Erysipelas
 Clinical features
 Predisposes to deilitating state or poor health
 Rose pink rash which extends to adjacent skin which
disappears on pressure
 Rash has sharply defined margins
 Vesicles appear and rupture- serous discharge
 Oedema
 No pus discharge
 Constitutional symptoms

55. Erysipelas
 Treatment
 Antibiotics
 Anti-inflammatory drugs
 Complications
 Sloughing and gangrene –rarely occurs
 Lymphedema may occur due to lymphatic obstruction:
eyelids, scrotum

56. Impetigo
 Superficial infection
 Honey colored crusts
 Involves epidermis and
dermis

57. Surgical Site Infection
 Infection may occur within the surgical site at any
depth, starting from the skin itself and extending to
the deepest cavity that remains after resection of an
organ.
 Types
 Superficial SSI involve tissue down to the fascia .
 Deep SSI extends beneath the fascia but not
intracavitary
 Organ /space infection are intracavitory, but if related
directly to an operation are considered to be SSI

58. Surgical site
infection

59. Superficial surgical site infection
1. Purulent drainage
2. Organisms isolated from an aseptically obtained
fluid or tissue
3. At least one of the following signs or symptoms:
pain, tenderness, localized swelling, redness, and
superficial incision is deliberately opened by the
surgeon
4. Diagnosis of SSI by the surgeon or attending
physician

60. Superficial SSI

61. Deep SSI
 Purulent discharge from the deep incision
 Deep incision spontaneously dehisces or deliberately
opened by the surgeon with one of the signs: fever,
localized pain, tenderness,
 An abscess or other evidence of infection involving the
deep incision
 Diagnosis of deep SSI by a surgeon or attending
physician

62. Deep SSI

63. Organ /space infection
 Purulent drainage from a drain
 Organisms isolated from an aseptically obtained
culture or fluid in the organ/space
 An abscess or other evidence of infection involving the
organ or space
 Diagnosis of an organ /space SSI by a surgeon or
attending physician

64. Organ/space SSI

65. Wound classification
 Class 1- Clean
 Class 2- Clean Contaminated
 Class 3- Contaminated
 Class 4- Dirty

66. Class I Wound (Clean)
 Atraumatic wound
without
inflammation
 Do not enter GI, GU,
biliary, or respiratory
tract
 1.5% infection rate
 Lipoma, inguinal
hernia

67. Class II Wound
(Clean-Contaminated)
 Respiratory, GI, GU,
or biliary tract
entered under
controlled conditions
 7.5% infection rate
expected
 Cholecystectomy,
appendectomy –
subacute or chronic

68. Class III Wounds
(Contaminated)
 Traumatic wounds
 Breaks in sterile
technique
 Gross spillage from GI
tract
 Acute, nonpurulent
inflammation
 15% anticipated infection
rate

69. Class IV Wounds (Dirty)
 Old traumatic
wounds
 Devitalized tissue
 Clinical infection
present
 Perforated viscus
 40% expected
infection rate
 Peptic, enteric
perforation

70. Microbiology
S. aureus
S. epidermidis
Enterococcus
E. coli
Pseudomonas
klebsiella
Gr -ve
strept species
anaerobic
Gr +ve
19%
14%
12%8%8%
4%
15%
6% 3% 2%

71. Prevention of SSI
 Patient factors
 Surgeon factor
 Operation theater
 Intraoperative and post operative care

72. Avoiding surgical site infections
 Wash hands between patients
 Length of stay of patient should be minimum
 Preoperative shaving to be avoided
 Antiseptic skin preparation should be standardized
 Attention to theatre techniques and discipline
 Avoid hypothermia perioperatively and ensure
supplemental oxygen therapy post operatively

73. Prophylactic antibiotics
 Empirical cover against expected pathogens as per
hospital guidelines
 Single shot IV at induction of anaesthesia
 Repeat only if prosthesis/ long operative time
 Continue therapy if contamination
 Benzyl penicillin for cl. Gas gangrene infection
 Pts. With heart valve-protect against bacteraemia

74. Cefazolin
Cefuraxime
vancomycin
Cefazolin
Clindamycin
Gentamycin
Cefazolin or
Cefoxitin

75. Gastrointestinal and Colon surgery
Oral
Neomycin and metronidazole
IV = Cefoxitin or cefotetan
Cefazolin and metronidazole

76. Cardiothoracic surgery
Cefazolin
Cefuraxime
B-lactam allergy
vancomycin Or clindamycin
24-72 hrs

77. Treatment of SSI
 Tissue and pus culture should be taken for before
antibiotics is started
 Choice of antibiotics is emperical untill sensitivities
are available
 Drainage of pus
 Wounds best managed by delayed primary or
secondary closure
 Improve the general condition of patient