Bacterial, Viral, Fungal and Protozoal Infections

Surgical Site Infections
Dr.Maryam Jamil
M.B.B.S. , FCPS , MRCS ( Edin.)
Assistant Professor Of Surgery
Lahore Medical and Dental College, Lahore
Infection
The invasion of an organism's body tissues by disease-causing agents,

their multiplication, and the reaction of host tissues to the infectious
agents and the toxins they produce
Types of Infection
 Two main types
 Community-Acquired
 Hospital-Acquired
Community-Acquired
• Skin/soft tissue
• Cellulitis: Group A strep
• Abcess/furuncle: Staph aureus
• Necrotizing: Mixed
• Hiradenitis suppurativa:Staph aureus
• Lymphangitis: Staph aureus
Cellulitis
Furuncle
Necrotizing Fasciatis
Lymphangitis
Paronychia
Diabetic foot
Community-Acquired
• Viral
• Hepatitis
• HIV/AIDS
• Tetanus
Hospital-Acquired
Post-operative
• At the surgical site
• Systemic.
Intracranial complications of Dental
infections
• Occur as a result of direct spread of dental infection after dental
extraction
• Proceeds along fascial planes to the base of the skull, then traversing
the skull mainly through bloodstream to the intracranial cavity
• Majority after extraction of Maxillary teeth

Intracranial complications of Dental
infections
• pyogenic meningitis
• Subdural empyema
• Cerebral vasculitis
• brain abscess
• cavernous sinus thrombosis
Cavernous Sinus Anatomy
• Large venous space situated in the middle cranial fossa, on either
side of body of the sphenoid bone
• Each sinus is about 2 cm long and 1 cm wide
• Interior is divided into a number of spaces or caverns by trabeculae.

Cavernous Sinus Boundries
• Anterior - extends into medial end
of superior orbital fissure.
• Posterior - upto apex of
petrous temporal bone.
• Medial – Pitutary above and
• sphenoid below
• Lateral – temporal lobe and uncus
• Superior – optic chiasma
• Inferior - endosteal dura mater,
greater wing of sphenoid
Contents
• Superior to inferior (within the
• lateral wall of the sinus)
– oculomotor nerve (CN III)
– trochlear nerve (CN IV)
– ophthalmic nerve, the V1 branch of

the trigeminal nerve (CN V)
– maxillary nerve, the V2 branch
of CN V
•abducens nerve (CN VI) runs through •
• the middle of the sinus alongside the
internal carotid artery (with
sympathetic plexus)
• These nerves, except the CN V2, pass
through the cavernous sinus to enter the

orbital apex through
the superior orbital fissure.
Dangerous area of face
• •
flow of blood in all tributaries & communication
are reversible as they possess no valve
Spread of infection can lead to thrombosis
of cavernous sinus
The cavernous communicate with dangerous area
of face through 2 routes
 Superior opthalmic vein
 Deep facial veins , pterygoid plexus of vein
, emissary vein.
Spread of Infection to Cavernous Sinus
1. Infection of the upper lip, vestibule of the nose and eyelids 

spread by way of the
• angular, supraorbital and supratrochlear veins to the ophthalmic
veins. Commonest route of infection.
2. Intranasal operations on the septum, turbinates or ethmoid /
sphenoid sinus infection  through the ethmoidal veins.
3. Operations on the tonsil, peritonsillar abscess, surgery or
• osteomyelitis of the maxilla, dental extraction and deep cervical abscess

 spread by pterygoid plexus or by direct extension to the internal
jugular vein.
4. Involvement of the middle ear and mastoid with lateral sinus phlebitis or
thrombosis  retrograde spread through the petrosal sinuses to the
cavernous sinus.
.
Etiology
•Septic CST Hematologic

Infectious • Polycythemia rubra vera
• Acute lymphocytic leukemia
Aseptic CST
Trauma Malignancy
• Nasopharyngeal tumor
Post surgery
• Rhinoplasty
Other
• Cataract extraction
• Ulcerative colitis
• Basal skull (including maxillary)
• Dehydration
•Tooth extraction • Heroin
Septic Cavernous Sinus Thrombosis
• Most commonly results from contiguous spread of infection from the nose
• (50%), sphenoidal or ethmoidal sinuses (30%) and dental infections (10%).
• Staphylococcus aureus is the most common - found in 70% of the cases.
• Streptococcus is the second leading cause.
• Gram-negative rods and anaerobes may also lead to cavernous sinus
thrombosis.
• Rarely Aspergillus fumigatus and mucormycosis.

Clinical Features
•Characterized by multiple cranial neuropathies
•Clinical feature -
 General feature of infection – fever , rigors ,malaise, and severe frontal &
• periorbital pain.
 U/L exopthalmos & tender eye ball
 Oedema of eyelid & chemosis of conjuctiva
• Oculomotor feature –
 External opthalmoplegia
 Ptosis
 Slight exopthalmos
 dilated pupil with loss of accomdation reflex
• Impairment of ocular motor nerves, Horner’s syndrome and
sensory loss of the first or second divisions of the trigeminal nerve
in various combination
• The pupil may be involved or spared or may appear spared with
concomitant oculosympathetic involvement.
Complications
• Intracranial extension of infection may result in meningitis,

encephalitis, brain abscess, pituitary infection, and epidural and
subdural empyema.
• Cortical vein thrombosis can result in hemorrhagic
infarction.
• Extension of the thrombus to other sinuses can occur.
Cavernous Sinus on CT Head
Cavernous Sinus on MRI Brain
Cavernous Sinus on MRI Brain
Treatment
•Septic cavernous sinus thrombosis –
• The mainstay of therapy is early and aggressive antibiotic administration.
• Although S aureus is the usual cause, broad-spectrum coverage for gram- positive, gram-negative, and
anaerobic organisms should be instituted pending the outcome of cultures.
• Empiric antibiotic therapy should include a penicillinase-resistant penicillin plus a third generation
cephalosporin.
• Vancomycin may be added for MRSA.
• IV antibiotics are recommended for a minimum of 3-4 weeks.

• The indication of anticoagulation is still debated because of possible
bleeding complications and an eventual suppressive role of the thrombus on
the extension of the infectious thrombophlebitis.
• Although, no randomized controlled studies have been conducted, early anticoagulant

therapy may have a beneficial effect on mortality and morbidity, reducing oculomotor
sequelae, blindness, and motor sequelae as well as the risk of hypopituitarism. (studied
in only 7 cases)
• A Cochrane review found 2 small trials involving 79 patients who were treated
with anticoagulants.
• Limited evidence suggests anticoagulant drugs are probably safe and may be
beneficial for people with sinus thrombosis.
• Anticoagulation carries a significant risk of hemorrhage if cortical venous
infarction or necrosis of intracavernous portions of the carotid artery are
present.
• Anticoagulant is contraindicated in the presence of intracerebral hemorrhage
or other bleeding diathesis.
Prognosis
 100% mortality prior to effective antimicrobials
 Typically, death is due to sepsis or central nervous system (CNS)
• infection.
 With aggressive management, the mortality rate is now less than
• 30%.
 Morbidity, however, remains high, and complete recovery is rare.
 Roughly one sixth of patients are left with some degree of visual impairment,
and one half (50 %) have cranial nerve deficits.
Thank You

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Surgical Site Infections

The invasion of an organism's body tissues by disease-causing agents,

• Majority after extraction of Maxillary teeth

• Each sinus is about 2 cm long and 1 cm wide

• Interior is divided into a number of spaces or caverns by trabeculae.

– ophthalmic nerve, the V1 branch of

• These nerves, except the CN V2, pass

through the cavernous sinus to enter the

1. Infection of the upper lip, vestibule of the nose and eyelids 

• osteomyelitis of the maxilla, dental extraction and deep cervical abscess

•Septic CST Hematologic

• Staphylococcus aureus is the most common - found in 70% of the cases.

• Streptococcus is the second leading cause.

• Gram-negative rods and anaerobes may also lead to cavernous sinus

• Rarely Aspergillus fumigatus and mucormycosis.

• Intracranial extension of infection may result in meningitis,

• Vancomycin may be added for MRSA.

• IV antibiotics are recommended for a minimum of 3-4 weeks.

• Although, no randomized controlled studies have been conducted, early anticoagulant

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