Download MBBS (Bachelor of Medicine and Bachelor of Surgery) 4th Year (Final Year) ENT CSOM complications Handwritten Notes
OTOGENIC BRAIN ABSCESS
ROUTE OF INFECTION
direct extension of middle ear infection through the
tegmen or by retrograde thrombophlebitis.
Cerebellar abscess also develops as a direct
extension through the Trautmann's triangle or by
retrograde thrombophlebitis
BACTERIOLOGY
Aerobic
Anaerobic
pyogenic staphylococci
Peptostreptococcus
Streptococcus pneumoniae,
Bacteroides fragilis.
Streptococcus haemolyticus,
Haemophilus influenzae
Proteus mirabilis,
Escherichia coli and
Pseudomonas aeruginosa
PATHOLOGY
Brain abscess develops through four stages.
1. Stage of invasion (initial encephalitis)
Patient may have headache,low-grade fever, malaise
and drowsiness.
2. Stage of localization (latent abscess)
no symptoms during this stage. Nature tries to localize
the pus by formation of a capsule.
3. Stage of enlargement (manifest abscess)
Abscess begins to enlarge. A zone of oedema
appears round the abscess and is responsible for
aggravation of symptoms
Clinical features at this stage are due to:
(a) Raised intracranial tension.
(b) Disturbance of function in the cerebrum or
cerebellum,causing focal symptoms and signs.
Stage of termination (rupture of abscess).
An expanding abscess in the white matter of brain
ruptures into the ventricle or subarachnoid space
resulting in fatal meningitis
CLINICAL FEATURES
Symptoms and signs of raised intracranial tension
Headache.
Nausea and vomiting
Level of consciousness
Papilloedema
Slow pulse and subnormal temperature
Localizing features
(a) Temporal lobe abscess
Nominal aphasia.
Homonymous hemianopia.
Contralateral motor paralysis.
Epileptic fits.
Pupillary changes and oculomotor palsy.
(b) Cerebellar abscess
Headache
Spontaneous nystagmus
Ipsilateral hypotonia and weakness.
Ipsilateral ataxia.
Past-pointing and intention tremor
Dysdiadochokinesia.
INVESTIGATIONS
Skul X-rays
CT scan
X-ray mastoids or CT scan of the temporal bone for
evaluation of associated ear disease.
Lumbar puncture.
CT scan showing left-sided cerebel ar
abscess
CT scan of right-sided otogenic cerebral
abscess.
TREATMENT
MEDICAL
High doses of antibiotics are given parenterally.
Raised intracranial tension can be lowered by
dexamethasone, 4 mg i.v. 6 hourly or mannitol 20% in
doses of 0.5 g/kgbody weight
Neurosurgical.
Abscess is approached through a sterilefield.
Options include: (i) repeated aspiration through a burr
hole, (ii) excision of abscess and (iii) open incision
ofthe abscess and evacuation of pus.
LATERAL SINUS THROMBOPHLEBITIS
(SYN. SIGMOID SINUS THROMBOSIS)
It is an inflammation of inner wall of lateral venous
sinus with formation of an intrasinus thrombus.
AETIOLOGY
complication of acute coalescent mastoiditis, masked
mastoiditis or chronic suppuration of middle ear and
cholesteatoma.
PATHOLOGY
1. Formation of perisinus abscess.
2. Endophlebitis and mural thrombus formation.
3. Obliteration of sinus lumen and intrasinus
abscess.
4. Extension of thrombus.
1. Formation of perisinus abscess.
Abscess forms in relation to outer dural wall of the
sinus. Overlying bony dural plate may have been
destroyed by coalescent bone erosionor cholesteatoma.
Sometimes, it remains intact when route of infection
was by thrombophlebitic process.
2. Endophlebitis and mural thrombus formation.
Inflammation spreads to inner wall of the venous sinus
with deposition of fibrin, platelets and blood cells
leading to thrombus formation within the lumen of sinus.
3. Obliteration of sinus lumen and intrasinus
abscess.
Mural thrombus enlarges to occlude the sinus lumen
completely. Organisms may invade the thrombus
causing intrasinus abscess which may release infected
emboli into the blood stream causing septicaemia.
4. Extension of thrombus.
Though central part of thrombus breaks down due
to intrasinus abscess, thrombotic process continues
both proximally and distally. Proximally, it may spread
to confluence of sinuses and to superior sagittal sinus
or cavernous sinus, and distally, into mastoid emissary
vein, to jugular bulb or jugular vein.
CLINICAL FEATURES
1. Hectic Picket-fence type of fever with rigors.
This is due to septicaemia, often coinciding with
release of septic emboli into blood stream. Fever is
irregular having one or more peaks a day. It is usually
accompanied by chills and rigors. Profuse sweating
follows fall of temperature. Clinical picture resembles
malaria but lacks regularity. In between the bouts of
fever, patient is alert
2. Headache.
3. Progressive anaemia and emaciation.
4. Griesinger's sign. This is due to thrombosis of
mastoid emissary vein. Oedema appears over the
posterior part of mastoid.
5. Papil oedema.
6. Tobey?Ayer test.
This is to record CSF pressure by manometer and
to see the effect of manual compression of one or both
jugular veins. Compression of vein on the thrombosed
side produces no effect while compression of vein on
healthy side produces rapid rise in CSF pressure which
will be equal to bilateral compression of jugular veins.
8. Tenderness along jugular vein.
7. Crowe?Beck test.
Pressure on jugular vein of healthy side produces
engorgement of retinal veins (seen by
ophthalmoscopy) and supraorbital veins. Engorgement
of veins subsides on release of pressure.
INVESTIGATIONS
1. Blood smear is done to rule out malaria
2. Blood culture
3. CSF examination
4. X-ray mastoids may show clouding of air cells
(acute mastoiditis) or destruction of bone
(cholesteatoma)
6. Culture and sensitivity of ear swab.
5. Imaging studies.
Contrast-enhanced CT scan can show sinus
thrombosis by typical delta sign. It is a triangular area
with rim enhancement and central low density area is
seen in posterior cranial fossa on axial cuts. MR
imaging better delineates thrombus. "Delta sign" may
also be seen on contrast-enhanced MRI.
TREATMENT
1. Intravenous antibacterial therapy.
2. Mastoidectomy and exposure of sinus
A complete cortical or modified radical
mastoidectomy is performed, depending on whether
sinus thrombosis has complicated acute or chronic
middle ear disease. Sinus bony plate is removed
toexpose the dura and drain the perisinus abscess
3. Ligation of internal jugular vein.
It is rarely required these days. It is indicated when
antibiotic and surgical treatment have failed to control
embolic phenomenon and rigors, or tenderness and
swelling along jugular vein is spreading.
4. Anticoagulant therapy.
OTITIC HYDROCEPHALUS
It is characterized by raised intracranial pressure with
normal CSF findings.
It is seen in children and adolescents with acute or
chronic middle ear infections.
MECHANISM
Lateral sinus thrombosis accompanying middle ear
infection causes obstruction to venous return.
If thrombosis extends to superior sagittal sinus, it will
also impede the function of arachnoid villi to absorb
CSF.
Both these factors result in raised intracranial tension.
Symptoms
1. Severe headache, sometimes intermittent, is the
presenting feature. It may be accompanied by nausea
and vomiting.
2. Diplopia due to paralysis of VIth cranial nerve.
3. Blurring of vision due to papilloedema or optic
atrophy.
SIGNS
1. Papilloedema
2. Nystagmus due to raised intracranial tension.
3. Lumbar puncture. CSF pressure exceeds 300 mm
H2O (normal 70?120 mm H2O). It is otherwise normal
in cell,protein and sugar content and is bacteriologically
sterile.
TREATMENT
The aim is to reduce CSF pressure to prevent optic
atrophy and blindness. This is achieved medically by
acetazolamide and corticosteroids and repeated
lumbar puncture or placement of a lumbar drain.
Sometimes, draining CSF into the peritoneal cavity
(lumboperitoneal shunt) is necessary.
Middle ear infection may require antibiotic therapy and
mastoid exploration to deal with sinus thrombosis.
This post was last modified on 11 August 2021