1. Surgical Infections
Dr. Zaid Muwafaq
MRCS .England
FJMC/ Surgery. Jordan
HSM/Surgery .Jordan

2. Definition
Infection :
Invasion of microorganism to the healthy tissue
producing inflammatory reaction

3. Pathogenesis and bacteriology
Microorganisms usually prevented from causing
infection in tissues by intact epithelial surface,
mainly the skin.
Protective mechanism includes:
1- Chemicals: low PH gastric juice.
2- Humoral: antibodies, complements and opsonin.
3- Cellular: phagocytic cells, macrophages,
polymorphnuclear cells and killer lymphocytes.

4. Host response can be
weakened by several factors:
1-Metabolic: malnutrition (including
obesity), diabetes, uremia and jaundice.
2- Disseminated disease: cancer and acquired
immune deficiency syndrome(AIDS).
3- Iatrogenic: radiotherapy,
chemotherapy and steroids.

5. The chance of developing
infection is also determined by:
1-the pathogenicity of the organisms present
and the size of bacterial inoculum.
2- Devitalized tissues, excessive dead space
or hematoma, all the result of poor surgical
technique increases the chance of infection.

6. Diagnosis
1-History
2-Clinical examination
Clinical features of acute
inflammation :
calor(heat) +rubber (redness),
dolour (pain)+ tumour (swelling)
+ function laesa
(loss/impairment of function)
3-Laboratory investigation /
Radiology imaging.

7. Complication
An infection may resolve
spontaneously, or it may
1- destruct tissues.
2- abscess, which may rupture
spontaneously.
3- sinus or fistula formation.
4- spreading infection
death of tissue(gangrene),
with it systemic effect.
5- bacteremia, septicaemia,
septic shoch, multiorgan
failure ,disseminated
intravascular coagulopathy
and death.

8. Treatment
Source Control:
- draining an abscess
- resecting or débriding dead tissue
- diverting bowel, relieving obstruction, and
closing a perforation.
Antibiotic treatment of a surgical infection
without this mechanical solution will not
resolve the infection. (adjunctive therapies).

10. 1- Acute nonspecific
surgical infection

11. . wound infection:
invasion of organisms
through tissues
following breakdown of
local or systemic host
defense.
SSI Are infection of the tissues, organs, or spaces
exposed by surgeons during performance of an
invasive procedures.
Post operative wound infection,
Surgical Site Infection(SSI)

12. Classification
Superficial surgical site
infection: infection of
surgical wounds.
Deep surgical site
infection: infection in the
deeper musculofascial
layer or organ spaces
infection.

13. Major surgical site infection: discharge
significant quantities of pus either
spontaneously or need surgical drainage
+local signs of infection patient + systemic signs;
tachycardia, pyrexia and raise WBC count.
Minor surgical site infection: may discharge
pus or infected serous fluid (-ve systemic
signs).

14. Treatment of surgical site
infection
Minor may resolve spontaneously by frequent
dressing change ,may require drainage.
Major :drainage of pus, May require debridement
(removal of dead devitalized tissue)
+Systemic antibiotic.

15. Cellulitis and Lymphangitis
- Is non suppurative invasive
infection of tissues with poor
locatization + cardinal signs
of inflammation.
-It is spreading infection
(B-haemolytic streptococci ,
staphylococcus ,
C. perfringens).
-Tissue destruction, gangrene and ulcer
may follow which are caused by release
of proteases and allow spread of
infection.

16. Clinical features
. well demarcated area of
inflammation (hot ,red
,tenderness ,swelling and
impairment of function)
• malaise, chills,fever,rigors and
a raised white cell count
• If not rapidly treated it can
progress to lymphangitis and
lymphadenitis

17. • Localized areas of skin necrosis may occur

18. Predisposing factors include:
o Lymphoedema
o Venous stasis
o Diabetes mellitus
o Surgical wounds
Management
• Rest and elevation of the affected limb
• Antibiotics (orally/ intravenous)
(Benzylpenicillin and flucloxacillin)
Lymphangitis is part of a similar process and presents
as painful red streaks in affected lymphatics.It is
associated with painful lymph node groups in the
related drainage area.

19. Erysipelas
Erysipelas is a sharply
demarcated streptococcal
infection of skin, usually
associated with broken skin on
the face .
The area affected is
erythematous and
oedematous.
fever+leukocytosis.
broad-spectrum antibiotics

20. Boils
A boil, also called a furuncle, is a deep
folliculitis, infection of the hair follicle.
-Staphylococcus aureus

21. Boils are red lumps around a hair follicle that are tender, warm, and
very painful (signs of inflammation).
- pea-sized to golf ball-sized.
- yellow or white point at the center of the lump / discharge pus.
severe fever, swollen lymph nodes, and fatigue.
chronic furunculosis is recurring boil + Systemic factors that lower
resistance : diabetes, obesity, and hematologic disorders.

22. Treatment
Antibiotics against Staphylococcus aureus .
small boil burst and drain spontaneously
recurrent boils a systemic cause should be
looked for and treated.

23. Carbuncle(A carbuncle is made up
of several skin boils)
A carbuncle is a deeper
skin infection that
involves a group of
infected hair follicles in
one skin location.
-back of the neck,
shoulders, hips and
thighs.
-diabetes
-Staphylococcus aureus,
or Streptococcus
pyogenes.

24. swelling + signs of inflammation + one or more
openings draining pus. fatigue, fever and a
general discomfort.

25. Treatment
Antibiotic against gram positive bacteria, incision
and drainage of pus collection followed by
frequent dressing.

26. Hidradenitis suppurativa
This is a chronic inflammatory
disease of the apocrine
gland containing skin(axillary
and groin ).
Less common sites :scalp,
breast, chest and perineum.
Hidradenitis suppurativa
+obesity and smoking.
Women are 4x.
The pathophysiology involves follicular occlusion followed
by folliculitis and secondary infection with skin flora
(usually Staphylococcus aureus and Propionibacterium
acnes).

27. Clinically,patients develop tender, subcutaneous
nodules which may not point and discharge,
but usually progress to cause chronic
inflammation , suppurative skin abscesses,
sinus tracts .

28. Management
Patients should be
-advised to stop smoking and lose weight
-Symptoms can be reduced by the use of
antiseptic soaps, tea tree oil, non-
compressive and aerated underwear.
-Medical treatments include topical and oral
antibiotics and anti-androgen drugs.
-if abscess developed ,need drainage.

29. In selected cases, patients may require radical
excision of the affected skin and subcutaneous
tissue+ skin grafting or flap transposition .

30. Abscesses
• An abscess is collection of
pus within soft tissues
Pathology
• An abscess contains
bacteria, acute inflammatory
cells, protein exudate and
necrotic tissue,It is
surrounded by granulation
tissue (the 'pyogenic
membrane')
The pus is composed of dead
and dying white blood cells
• In superficial abscesses
o Staph. Aureus
o Strep. pyogenes
• In deep abscesses
o Gram negative species (e.g. E.
coli)
o Anaerobes (e.g. Bacteroides)

31. Clinical features
1- Superficial
abscesses include
infected sebaceous
cysts, breast and
pilonidal abscesses.
superficial abscess shows cardinal features of inflammation -
calor, rubor, dolor, tumor(Heat,Redness,Pain,Swelling)
After few days superficial abscess usually 'point' and are
fluctuant

32. 2-Deep abscesses like; diverticular abscess,
subphrenic abscess and anastomotic
leaks(inside the abdomen)
• Patients shows signs of inflammation
o Swinging pyrexia
o Tachycardia
o Tachypnoea
• Physical signs are otherwise difficult to
demonstrate
• Site of abscess may not be clinically apparent

33. Radiological imaging(Ultrasound and/or CT
scan) often required to make the diagnosis

34. Treatment
(adequate drainage)
• Should be performed under
general anaesthesia
• Antibiotics have little to offer as
tissue penetration is usually
poor
• Prolonged antibiotic treatment can
result in a chronic inflammatory
mass (an 'antibioma')
• Superficial abscesses open drainage
• For deep abscesses closed drainage

35. Open Technique
• Superficial abscesses can
usually be drained through
a cruciate incision
• Position of incision may
allow depended drainage
• Pus should be sent for
microbiology
• Loculi should be broken
down and necrotic tissue
excised
• A dressing should be
inserted into the wound

36. Closed Techniques
• Deep abscess can be
treated by ultrasound
/CT guided drainage

38. Definitions of infected states
_ SSI(surgical site infection) is an infected wound or deep organ space
_ SIRS(systemic inflammatory response syndrome) is the body’s systemic
response to severe infection
SIRS when Two or more of:
hyperthermia (>38°C) or hypothermia (<36°C)
tachycardia (>90/min, no b-blockers)
tachypnoea (>20/min) or Paco2<32 mmHg or mechanical ventilation
white cell count >12 × 109/l or <4 × 109/l
Sepsis is SIRS with a documented infection
Severe sepsis or sepsis syndrome is sepsis with new onset organ
failures (respiratory (acute respiratory distress syndrome),
cardiovascular ,renal (acute tubular necrosis), hepatic, blood
coagulation systems or central nervous system)
septic shock = sever sepsis + hypotension (follows compromise of
cardiac function and fall in peripheral vascular resistance)
multiorgan dysfunction syndrome= acute potentially reversible
dysfunction of 2 or more organs

39. Bacteraemia and sepsis
Bacteraemia : presence of bacteria in the blood stream.
Sepsis(septicaemia): proliferation of bacteria in blood stream
producing systemic inflammatory response syndrome.
Bacteraemia occur :
1-anastomotic breakdown (deep space SSI).
2-procedures undertaken through infected tissues (particularly
instrumentation in infected bile or urine).
3- bacterial colonisation of indwelling intravenous cannulae.
Sepsis accompanied by MODS may follow anastomotic breakdown.
Aerobic Gram-negative bacilli are mainly responsible, but S. aureus
and fungi may be involved, particularly after the use of broad-
spectrum antibiotics .

40. Bacteraemia is important when a prosthesis has
been implanted, as infection of the prosthesis
can occur.

41. 2-Acute specific surgical infections
A-Gas gangrene
This is caused by C. perfringens.
Gram-positive, anaerobic,
spore-bearing bacilli
in soil and faeces.
-military , traumatic surgery and colorectal operations.
Risk factor for development of gas gangrene:
1- immunocompromised,diabetic
2- have malignant disease ,particularly if they have wounds containing
necrotic or foreign material, resulting in anaerobic conditions.
3- Military wounds
The cavitation which follows passage of a missile through the tissues
causes a ‘sucking’ entry wound, leaving clothing and environmental
soiling in the wound in addition to devascularised tissue.

42. Clinical Picture
Infected wound with
severe local wound
pain and crepitus (gas
in the tissues).
The wound produces a
thin, brown, sweet-
smelling exudate.
Oedema and spreading
gangrene follow the
release of collagenase,
hyaluronidase, other
proteases and alpha
toxin.
Early systemic complications with circulatory
collapse and MSOF follow if prompt action is not
taken

43. Diagnosis mainly clinical .
XR may show gas in the
tissue, gram stain of the
discharge show the
bacteria.
Treatment
Aggressive debridement
of affected tissues (this
may be repeated as
required)+ large doses of
intravenous penicillin

44. In neonate (tetanus neonaturum) following the
use of cow dung on the umbilicus
B-Tetanus
following deep or penetrating
(civilian/military) wound and burn .
-developing countries.

45. Microbiology
• Due to Clostridium tetani,Gram-positive spore
forming rod.
Widely found in the environment and soil.It is
strict anaerobe that produces a powerful
exotoxins
Typically Infection produces few signs of local
inflammation.

46. Pathogenesis
• Germination of
spores in wounds
releases the
exotoxin(tetanospasmi
n).
The toxin affects nervous system and reaches
CNS via the peripheral nerves.
It acts on presynaptic terminals of nerves
(myoneural junctions and the motor neurones of
the anterior horn of the spinal cord) and
reduces the release of inhibitory
neurotransmitters (e.g. glycine)
resulting in excess activity of motor neurones
produces muscle spasm.

47. Clinical features
The entry wound may show a localised small area of cellulitis+/-
exudate
A short prodromal period, which has a poor prognosis, leads
to spasms in the distribution of the short motor nerves of the
face followed by the development of severe generalised
motor spasms including :
Facial muscle spasm produces trismus
Typical facial appearance = 'risus sardonicus',
Back muscle spasm produces opisthotomous
Eventually exhaustion and respiratory failure leads to
death
A longer prodromal period of 4–5 weeks is associated with a
milder form of the disease.

48. Prevention
• Tetanus can be prevented by:
o Active immunisation with
tetanus toxoid with booster
every 5-10 years
o Adequate wound toilet of
contaminated wounds
any patient with open traumatic
wound (if not immunized)
should receive toxoid with
benzylpenicillin.
If immunized should receive a
booster of toxoid (if last
immunisation >5 years).

49. Treatment
• In suspected cases:
o Passive immunisation with anti-tetanus immunoglobulin
o Adequate wound debridement
o Intravenous benzylpenicillin
o Relaxants may also be required, and the patient may
require mechanical ventilation in severe forms, which may
be associated with a high mortality in Intensive care
support
o Despite the use of ITU mortality is about 50%
The diagnosis is essentially clinical, Exudate from the
wound can be stained to show the presence of Gram-
positive rods

50. C-Necrotising fasciitis
Necrotising fasciitis results from a polymicrobial, synergistic infection, most
commonly a streptococcal species (group A b haemolytic) in combination
with Staphylococcus, Escherichia coli, Pseudomonas, Proteus, Bacteroides
or Clostridia.
80%have a history of previous trauma/infection and over 60 % commence in
the lower extremities.
Meleney’s synergistic gangrene(abdominal wall) and Fournier’s
gangrene(perineum) are all variants of a similar disease process .
Predisposing conditions include:
• diabetes;
• smoking;
• penetrating trauma;
• pressure sores;
• immunocompromised states;
• intravenous drug abuse;
• perineal infection (perianal abscess, Bartholin’s cysts);
• skin damage/infection (abrasions, bites, boils).

51.  Classical clinical signs include: oedema extending
beyond visible skin erythema; a woody hard texture
to the subcutaneous tissues; an inability to
distinguish fascial planes and muscle groups on
palpation; disproportionate pain in relation to the
affected area with associated skin vesicles and soft
tissue crepitus .
Early on, patients may be febrile and tachycardic,
with a very rapid progression to septic shock.
Radiographs should not delay treatment but if taken,
they may demonstrate air in the tissues.

52. Treatment
3- debridement as soon as possible until viable,
healthy, bleeding tissue is reached.
Early re-look and further debridement is advisable
together with the use of vacuum-assisted dressings.
Early skin grafting in selected cases may minimise
protein and fluid losses.
Mortality of between 30 and 50 per cent can be expected
even with prompt operative intervention.
1-urgent fluid resuscitation,
monitoring of haemodynamic
status
2-administration of high-dose
broad-spectrum intravenous
antibiotics.

53. Thank you

54. Exam. picture 1
What is the diagnosis?
Treatment?

55. Picture 2
Diagnosis?

56. Picture 3
Diagnosis?
Treatment?

57. 3- Chronic specific infection
A-Tuberculosis
Tuberculosis(Mycobacterium tuberculosis or Mycobacterium bovis)
is common throughout the world. It Causes significant morbidity
and mortality particularly in Africa and Asia .
Primary tuberculosis
• Usually a respiratory infection that occurs in childhood, results in
sub-pleural Ghon focus and mediastinal lymphadenopathy
(primary complex).Symptoms are often few,resolution of infection
usually occurs.
• Complications include:
o Haematogenous spread causing miliary TB affecting lungs,
bones, joints,
meninges.
o Direct pulmonary spread resulting in TB bronchopneumonia

58. Post-primary tuberculosis
Occurs in adolescence or adult life,
due to reactivation of infection or
repeat exposure. Reactivation may
be associated with
immunosuppression (e.g. drugs or
HIV infection)
It Results in more significant
symptoms. Pulmonary infection
accounts for 70% of cases of post-
primary TB.
Clinical features include cough,
haemoptysis, malaise, weight
loss and night sweats.
Infection of lymph glands results in
discrete, firm and painless
lymphadenopathy. Confluence of
infected glands can result in a
'cold' abscess.
Infection of the urinary tract can
cause haematuria and 'sterile
pyuria'

59. Investigations
If discharging sinus,discharge sent for ZN stain and culture.
• Repeated samples may be required
Microscopy
stained by Ziehl-Neelsen stain
• Negative microscopy does not exclude tuberculosis
Culture
Collect adequate specimens (e.g. early morning urine
x3),Concentration of specimen (e.g. centrifugation).
o Culture on Lowenstein-Jensen method at 35-37° for at least 6
weeks
Histology
• caeseating necrosis
• Tuberculous follicle consists of central caseaous necrosis
surrounded by lymphocytes, multi-nucleate giant cells and
epitheloid macrophages Multinucleated (Langhan’s) giant cell.

60. Skin tests
• Delayed hypersensitivity reaction used to
diagnose tuberculosis.The two commonest tests
are the Mantoux and Heaf test.
• Positive skin test are indicative of active infection
or previous BCG vaccination
Treatment
• First line chemotherapeutic agents are rifampicin, isoniazid and
ethambutol
• Given as 'triple therapy' for first 2 months until sensitivities
available
• Rifampicin and isoniazid are the usually continued for further 7
months
• Less than 5% of organisms are resistant to first-line agents
• Second line treatment includes pyrazinamide

61. B-Syphilis
Syphilis is a systemic sexually transmitted disease
(STD) caused by the spirochete, Treponema
pallidum.
Stages of syphilis:
1-Primary Stage
One or more chancres (usually firm, round,small, and
painless) appear at the site of infection (most
often the genital area) 10 to 90 days after infection
.The chancres heal on their own in 3-6
weeks.Patient is highly infectious in the primary
stage.
2- Secondary Stage
Rashes occur as the chancre(s) fades or a few weeks
after the chancre heals.
Rashes typically appear on the palms of the hands,
the soles of the feet, or on the face,but also may
appear on other areas of the body.
Sometimes wart-like “growths” may appear in the
genital area.
Rashes and syphilitic warts tends to clear up on their
own within 2-6 weeks,but may take as long as 12
weeks.Patient is highly infectious in the secondary
stage.

62. Latent stage:
patient is serosensitive ,has no symptoms.
within one year of onset of infection,(Early latent stage )the
patient is potentially infectious.
more than one year after onset of infection(Late latent
stage), patient is not infectious at this stage.
3-Tertiary stage(late stage)
Lesion in the skin and bone(gummas), internal organs,
central nervous system, and cardiovascular system.
Signs and symptoms of late stage of syphilis include
difficulty coordinating muscle movements,
paralysis,numbness,gradual blindness and dementia.
This damage may be serious enough to cause
death.the patient is not infectious at the late stage.
Syphilitic ulcers are typically painless, rubbery , indurated,
punched out ulcer.

63. Diagnosis :
-Dark-field examinations or direct fluorescent
antibody tests of chancre tissue are the
definitive
methods for diagnosing primary and secondary
syphilis.
-sequential serologic tests (e.g. VDRL, RPR).
Treatment
is by use of a long-acting penicillin.

64. Actinomycosis
Chronic infectious inflammatory condition
originating in the tissues adjacent to
mucosal surfaces caused mostly by
infection with A. israelii ,but others, A.
naeslundii, A. odontolyticus, A. viscosus,
A. meyeri also can cause human
actinomycosis.
most common recognized infections: oral
and cervicofacial regions.
The thoracic region, abdominopelvic region,
and the CNS also frequently can be
involved.
Actinomyces is normal inhabitants of some
areas of the GI tract of humans and
animals from the oropharynx to the lower
Bowel.
Lesions:
induration and sinuses
, abscess , tissue fibrosis.
In pus, the most characteristic form is the
sulfur granule .
The firm, fibrous masses are often
initially mistaken for a malignancy

65. Diagnosis:
(Identification of microorganism is difficult)
-History : slowly progressive lesion with history of trauma
predispose to mucosal invasion by actinomyces.
-Biopsies for culture and histopathology (multiple
sections )
Treatment
Treatment of choice: Penicillin G. Other antimicrobics
(tetracycline, erythromycin, clindamycin) are active in
vitro and have shown some clinical effectiveness
High doses of penicillin must be used and therapy
prolonged for 4 to 6 weeks or longer before any
response is seen.