Surgical Infections

• Cellulitis
• Necrotizing fascitis
• Gas gangrene
• Tetanus
• Osteomylitis
• Carbuncle
• Abscess
Cellulitis
 Cellulitis
 Acute spreading infection of the skin extending into
the subcutaneous tissue
 Etiology:
- Staph and Strep most common (MRSA)
- Pseudomonas
- M. catarrhalis
- H. influanza
 Risk Factors
Breaches in the skin for organism invasion
• Obesity
• Edema
– Venous insufficiency
– Lymphatic obstruction
• Fissured toe webs
– Maceration
– Fungal infection
• Inflammatory dermatoses – eczema
• Repeated cellulitis
• Subcutaneous injection or illegal drugs
• Previous cutaneous damage
All lead to breaches in the skin for organism invasion
M. catarrhalis Strep & Staph

Anaerobes

H Flu
MRSA
Generally due to:
- Previous trauma
- Underlying skin condition

Skin lesion: borders are not sharply

demarcated with erythema, tenderness,
warmth, edema
Fever - malaise - chills
Regional adenopathy
Bacteremia ~ 20%
 Bite wounds

 Infections of burns, wounds, or

underlying dematitis

 Diabetic wound infections

 Decubitus ulcers

 Surgical wound infections

BITE WOUNDS AND INFECTIONS
 ANIMAL
- Dog
- Cat
- Snake
- organisms will reflect habitat of animals
 HUMAN
- Occlusional bites
- Clenched-fist injuries

Generally a polymicrobial infection

 TREATMENT-Antimicrobial

 If strong suspicion of etiologic agent treat with

specific antimicrobial.

 If etiologic agent unknown:

- No underlying risk factors
1st generation ceph (cover Staph and Strep)
Alternative: if Pen allergic
- Erythromycin or Azithromycin (Azomax)
 Secondary Treatment of Cellulitis
• Elevation of affected part
• Compression stockings
• Treat underlying tinea pedis, eczema, trauma
• Keep skin well hydrated
• Incision and drainage
• Toilet
• Wound excision
• Wet to dry dressing
• Amputation?
 Necrotizing Fasciitis

It is a progressive, rapidly spreading,

inflammatory infection located deep to the
deep fascia with 2ry necrosis of the
subcutaneous tissue.
 Risk Factors
• Immunocomproession illnesses
e.g.: DM, Cancer, alcoholism, vascular
insufficiency, organ transplant, HIV or neutropenia.

• Trauma or foreign bodies in surgical wound.

• Idiopathic as scrotal or penile necrotizing fasciitis.

 Diffuse Necrotizing Infection
(flesh-eating)

Dangerous………………?
• Difficult to diagnose
• Extremely toxic
• Spread rapidly
• May lead to limb amputation
 Classification
Colistridial :

Necrotizing cellulitis
Myositis

Non-colistridial (microaerophilic streptococci. staphylococci.

aerobic gram –ve, anaerobes ( peptostreptococi –
bacteroids)

NECROTIZING FASCIITIS
Streptococcal gangrene
 Mortality & Morbidity
The overall morbidity & mortality is 70 – 80%

Fournier’s gangrene has a reported mortality as

high as 75%
 Signs/Symptoms of Nec Fasc

Local:
– Very early - pain out of proportion to
findings
– Early - Swelling & erythema
– Late - purpleish discoloration & blistering
– +/- Crepitus
– +/- 'dishwater' colored fluid drainage
– +/- tracking of erythema or tenderness

Systemic:
SIRS +, diarrhea and vomiting can occur
 Investigations

Lab: CBC, U&E, Glu, Creatinine, Blood &

tissue cultures, Urine analysis, &
ABG.
Imaging Studies:

X-ray  gas in the subcutaneous

fascia planes.
C.T.  demonstrating necrosis with
asymmetric fascial thickening
& gas in the tissues.

MRI.
 Red Flags

patient's score

HIGH (>75%)
probability of
Nec Fasc.
 Management
Necrotizing Fasciitis is a surgical emergency!
If streptococci are the identified major pathogens, the
D.O.C is Penicillin-G with clindamycin as an
alternative.

To ensure adequate treatment, we have to cover

aerobic & anaerobic bacteria.

The anaerobic coverage can be provided by

Metronidazole or 3rd generation cephalosporin's.
 Further In-Patient Care

• Surgical debridment.

• Fasciotomy.

• Amputation?
 Complications

• Renal Failure.

• Septic Shock with cardiovascular collapse.

• Scarring with cosmetic deformity.

 Summary
Remember, nec fasc is a surgical emergency and surgery is the
only definitive treatment!

Mortality is very high, but the earlier you catch it, the more life
and limb you save :
Abscess
 Cellulitis: initial stage of infection

• Diffuse, reddened, soft or hard

swelling that is tender to
palpation.
• Inflammatory response not yet
forming a true abscess.
• Microorganisms have just begun
to overcome host defenses and
spread beyond tissue planes.
True abscess formation
• As inflammatory response
matures, may develop a
focal accumulation of pus.
• May have spontaneous
drainage intraorally or
extraorally.
 Oral tissue examination
• Examine quality and consistency:
– Soft to fluctuant (fluid filled) to hard (indurated)
• Color and temperature determine the
presence and extent of infection
• Normal v abnormal tissue architecture:
– Distortion of mucobuccal fold
– Soft palate symmetric with uvula in midline
(deviation → involvement of lateral pharyngeal space)
– Nasal tip, nasolabial fold, circumorbital areas
Examination, con’t.

• Identify causative factors:

– Tooth, root tip, foreign body, etc.
• Vital signs should be taken:
– Temperatures > 101 to 102°F accompanied by an
elevated heart rate indicate systemic
involvement of the infection and increased
urgency of treatment.
Principles in Treatment of Oral and Paraoral
Infections

1. Remove the cause.

2. Establish drainage.
3. Institute antibiotic therapy.
4. Supportive care, including proper rest and
nutrition.
Pathways of spread of periapical abscess
into the vestibular soft tissue
Pathways of spread of submandibular space
infection from mandibular molar
Ludwig’s angina with bilateral involvement of
sublingual and submandibular spaces
Pathway of spread for buccal
space infection
 Abscess

• ALWAYS, ALWAYS
– Incision and drainage
Drainage
 Drainable Abscess >3cm
• Incision and drainage
• No blood cultures
• No aspirate culture
• NO ANTIBIOTICS
 Abscess
• CBC with diff
• Blood cultures
• Culture exudate
 Abscess –When to Add Antibiotics
• Drainable abscess >3cm
• Undrainable
• Multiple sites of infection
• Rapid progression in presence of cellulitis
• Systemic illness (fever, hypotension, tachycardia)
• Immune compromise
• Elderly
• Difficult to drain area (hand, face, genitalia)
• Lack of response to incision and drainage
• Septic phlebitis - multiple lesions
• Gangrene
 What is Tetanus?

 An infectious disease caused by

contamination of wounds from the
bacteria Clostridium tetani, or the
spores they produce that live in the
soil, and animal feces

 Greek words -“tetanosand teinein”,

meaning rigid and stretched, which
describe the condition of the muscles
affected by the toxin, tetanospasmin,
produced by Clostridium tetani
Sporulated Vegetative
 Causes
 Tetanus spores are found throughout the
environment, usually in soil, dust, and animal waste.

 Tetanus is acquired through contact with the

environment; it is not transmitted from person to
person.
 Methods of transmission

• C. tetani can live for years as spores in animal feces and soil.
As soon as it enters the human body through a major or
minor wound and the conditions are anaerobic, the spores
germinate and release the toxins.
• Tetanus may follow burns, deep puncture wounds, ear or
dental infections, animal bites, abortion.
• Only the growing bacteria can produce the toxin.
• It is the only vaccine-preventable disease that is infectious but
not contagious from person to person.
 Causes
The usual locations for the bacteria to enter the body:
 Puncture wounds (such as
those caused by rusty
nails, splinters, or insect bites.)
 Burns, any break in the skin,
and IV drug access sites are
also potential entryways for the
bacteria.
 Route of Entry
• Apparently trivial injuries
• Animal bites/human bites
• Open fractures
• Burns
• Gangrene
• In neonates usually via infected umbilical
stumps
• Abscess
• Parenteral drug abuse
 epidemiology
Tetanus is an international health problem, as
spores are ubiquitous. The disease occurs
almost exclusively in persons who are
unvaccinated or inadequately immunized.
Tetanus occurs worldwide but is more common
in hot, damp climates with soil rich in organic
matter.
More common in developing and under
developing countries.
More prevalent in industrial establishment,
where agricultures workers are employed.
Tetanus neonatorum is common due to lack of
 Incubation Period
• Varies from 1 day to several months. It is
defined as the time from injury to the first
symptom.
 Period of onset
• It is the time from first symptoms to the reflex
spasm.

• An incubation period of 4 days or less

or
• A period of onset of less than 48 hr is
associated with the development of severe
tetanus.
•Initially binds to
peripheral nerve
terminals
•Transported within the
axon and across synaptic
junctions until it reaches
the central nervous
system.
•Becomes rapidly fixed
to gangliosides at the
presynaptic inhibitory
motor nerve endings,
then taken up into the
How the toxin acts?
Blocks the release of inhibitory
neurotransmitters (glycine and
gamma-amino butyric acid)
across the synaptic cleft, which
is required to check the nervous
impulse.
If nervous impulses cannot be
checked by normal inhibitory
mechanisms, it leads to
unopposed muscular contraction
and spasms that are
 Tetanus prone wound
• A wound sustained more than 6 hr before
surgical treatment.
• A wound sustained at any interval after injury
which is puncture type or shows much
devitalised tissue or is septic or is
contaminated with soil or manure.
 Clinical features
 Risus sardonicus: Contraction of the muscles at the angle of
mouth and frontalis
 Trismus (Lock Jaw): Spasm of Masseter muscles.
 Opisthotonus: Spasm of extensor of the neck, back and legs to
form a backward curvature.
 Muscle spasticity
 Prolonged muscular action causes sudden, powerful, and
painful contractions of muscle groups. This is called tetany.
These episodes can cause fractures and muscle tears.

 If respiratory muscle is involved – apnoea.

The back muscles are more
powerful, thus creating the arc
backward

“Oposthotonus” by Sir
Charles Bell, 1809.

Baby has neonatal tetanus with

complete rigidity
 Signs and Symptoms
Other symptoms include:
 Drooling
 Excessive sweating
 Fever
 Hand or foot spasms
 Irritability
 Swallowing difficulty
 Uncontrolled urination or defecation
 Diagnosis
 There are currently no blood tests that can be used to
diagnose tetanus. Diagnosis is done clinically.

Differential Diagnosis
 Masseter muscle spasm due to
dental abscess
 Dystonic reaction to phenothiazine
 Rabies
 Hysteria
 Principle of Treatment
• 1. Neutralization of unbound toxin with
Human tetanus immunoglobulin
• 2. Prevention of further toxin production by
-Wound debridement
-Antibiotics (Metronidazole)
 3. Control of spasm
- Nursing in quiet environment
- avoid unnecessary stimuli
- Protecting the airway
 4. Supportive care
- Adequate hydration
- Nutrition
- Treatment of secondary infection
- prevention of bed sores.
 Prevention

 Tetanus is completely preventable

by active tetanus immunization.

 Immunization is thought to provide

protection for 10 years.

 Begins in infancy with the DTP

series of shots. The DTP vaccine is
a "3-in-1" vaccine that protects
against diphtheria, pertussis, and
tetanus.
 Prevention
 Can be achieved by active immunization by tetanus
toxoid (5 doses – 0 day, 1 month, 6 month, 1 year, 1
year).
 Older teenagers and adults who have sustained
injuries, especially puncture-type wounds, should
receive booster immunization for tetanus if more
than 10 years have passed since the last booster.

 Clinical tetanus does not produce immunity to further

attacks. Therefore, even after recovery patients must
receive a full course of tetanus toxoid.
 GAS
GANGRENE
• It is a rapidly progressive, potentially fatal condition
characterized by widespread necrosis of the
muscles and subsequent soft-tissue destruction.

• This is a dreaded consequence of inadequately

treated missile wounds, crushing injuries and high-
voltage electrical injuries.
 Causative agent
• Clostribium species – spore forming, Gram +ve

c.septicum

c.novyi
c. Perfringens
(mostly)
• They are present in the
soil and have also been
isolated from the human
gastrointestinal tract and
female genital tract.

• Non-clostridial gas-
producing organisms such
as coliforms have also
been isolated in 60–85%
of cases of gas gangrene.
 vegetative
cells multiply
Spores Carbohydrates
germinate Fermentation

Anaerobic
PATHOGENESIS Gas production
In tissues
environment Incubation period is
1-7 days

Distension of
Toxemia and tissues
death Interfering
Blood supply
Ischemia/
gangrene
 Pathogenesis

- Bacteria
- The toxins Examples of enzyme:
enters the (lecithinase) colagenases, proteases
broken skin or and enzyme and lipases
wound are produced
- These enzymes will
- Thebacteria are kill other host cell and
- Spores are grow and ferment extend the anaerobic
produced environment
the muscle
carbohydrate - Produce gases (nitrogen,
- The bacteria hydrogen sulphide and
carbon dioxide)
present in the anaerobic - Crepitant tissue
circulation tissue present
system ( destroyed tissue)
 Symptoms
• High fever
• Shock
• Massive tissue destruction
• Blackening of skin
• Severe pain around a skin of wound
• Blisters with gas bubbles form near the
infected area,
• the heartbeat and breathing become
rapid.
 Presentation
Crepitation in tissues,
sickly sweet odor discharge,
rapidly progressing necrosis,
fever, hemolysis, toxemia,
shock,
renal failure, and death
Lab. Investigations

Culture and sensitivity

Storming fermentation
Lecithinase test
G
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 Prevention
• Cleaning the wound
• Avoid the contaminated material
• improve circulation in
patients with poor circulation
• antitoxin
 Prevention
(1) Do a thorough wound toilet.
(2) In high risk wounds give the patient
penicillin 1.5 megaunits 4 hourly,
or tetracycline
 Treatment

• High doses of antibiotic : Penicillin

• The dead tissue is removed or limbs are

amputated

• No vaccine
10 megaunits of benzyl penicillin daily for 5
days as four 6 hourly doses.

Or
Tetracycline 0.5 g intravenously
or 1 g orally every 6 hours.

Clostridia not sensitive to metronidazole,

some other anaerobic bacteria are, so give
it.
 EXPLORATION

Do this in a septic theatre,

or even in the out-patient department,
and not where clean cases go for operation.
 AMPUTATION
Amputate under a tourniquet
Close the stump by delayed
primary suture
Myonecrosis of right leg
Myonecrosis of left foot
Stump of above knee amputation
• Patients should be admitted to ICU and
treated aggressively with careful monitoring.
• The role of HBO is not as clear as in
necrotising fasciitis but it is recommended in
severe cases if the facilities are available.
– increases the normal oxygen saturation in the
infected wounds by 1000-fold leading to
• Bacteriocidal effect,
• Improves neutrophil function,
• Enhanced wound healing
 C1

Ludwig’s angina
• Ludwig’s angina is a rapidly progressive,
potentially fulminant cellulitis
• involves the sublingual and submandibular
spaces
• typically originates from an infected or
recently extracted tooth
– lower second and third molars
Ludwig’s angina with bilateral involvement of
sublingual and submandibular spaces
 C1

• Spread of process superiorly and posteriorly elevates

floor of mouth and tongue.
• In anterior spread, the hyoid bone limits spread
inferiorly, causing a "bull neck" appearance
Am Fam Physician 1999;60:109-12
 C1

Predisposing factors
• dental caries
• recent dental treatment
• sickle cell disease
• a compromised immune system
• trauma
• tongue piercing

Am Fam Physician 1999;60:109-12

 C1

Etiologic Organisms
Atypical
Common
• Pseudomonas
Staphylococcus
• Escherichia
Streptococcus
coli
• Klebsiella
Bacteroides
• Enterococcus faecalis
• Candida
• Clostridium

Crit Care Clin. 2003;19:55-72

J Emerg Med. 1995;13:499-503
Abscess