You are on page 1of 32

Pembimbing: dr. Partodji, Sp.

Rad

Oleh:
1. Ira rahmawati
2. Pradnya Ayu
3. Limastani

KEPANITERAAN KLINIK RADIOLOGI 10 OKTEOBER 2017


INTRODUCTION
Acute mastoiditis develops if the infection is not controlled
by antibiotics

There is a blockage of the aditus ad antrum with inspissation


of exudate in the mastoid cells.

Build-up of suppurative exudates that cannot be released


either through the Eustachian tube or through a perforation
of the tympanic membrane

The pressure within the mastoid cavity increases.


Local spread of infection from the mastoids and middle
ear cleft may occur via four routes :

via the anatomical


Bone erosion Thrombophlebitis Periphlebitis
pathways
Subperiosteal abscess (Bezolds abscess)

Erosion of the outer cortical bone of the mastoid can result in an abscess forming
in the soft tissues of the head and neck. It can extend into the external auditory
canal, along the zygoma or into the periauricular soft tissues.
As it is not clinically apparent, the infection can track surreptitiously into the
parapharyngeal space and mediastinum with grave consequences.
Bezolds abscess only occurs in patients with a pneumatized mastoid process, and
is therefore rarely seen in young children.
Treatment bezold abscess

Treatment initially consists of intravenous


antibiotics. Surgical management is aimed at
relieving the pus and abscess.
However, in patients who fail to improve, with
advanced disease or intracranial extension,
mastoidectomy is indicated.
Figure 1 (a) Axial and (b) coronal reconstruction CT images of the mastoid. The
right mastoid air cells are well aerated and the fine bony septa are clearly visible.
In comparison the left mastoid cavity and middle ear are opacified. There is almost
complete loss of the mastoid bony septa, and there has been erosion though the
cortical wall of the mastoid into the middle cranial fossa. There is also soft-tissue
swelling overlying the left face and mastoid process.
Figure 2 (a) Axial, soft-tissue window and (b) axial, bone window CT images of
the head. A large fluid density lesion is seen overlying the right mastoid,
consistent with a subperiosteal abscess. Bone window images show complete
opacification of the mastoid air cells bilaterally as is often the case in young
children. However, resorption of bony septa is seen on the right and the outer
cortex of the mastoid bone has been eroded and breached, leading to the
formation of a superficial abscess.
Figure 3 Contrast-enhanced axial CT image of the head and neck. A large
Bezolds abscess is seen within the soft tissues of the neck deep to the
sternocleidomastoid. This had tracked down from an acute mastoiditis that had
eroded through the mastoid tip.
Epidural Abscess

Thrombophlebitis
Extra-axial
Subdural Empyema

Intracranial Complication Petrous Apicitis

Meningitis
Intra-axial
Cerebritis and Cerebral
abscess
Epidural Abscess
Epidural abscesses occur most commonly in the posterior fossa due to erosion
of the cortex of the posterior petrous pyramid, over the sigmoid sinus plate or
in Trautmans triangle.
Erosion of the sigmoid sinus plate may lead to an epidural abscess to form over
the sigmoid sinus, called a perisinus abscess.
These can be clinically silent and those caring for the patient should have a
high index of suspicion.
CT or magnetic resonance imaging (MRI) is necessary to detect them.
Figure 5 Contrast-enhanced axial CT
Figure 4 Contrast-enhanced axial CT
image of a larger, more complex right
image shows an enhancing epidural
epidural abscess without extracranial
abscess in the right posterior fossa.
extension and, therefore, clinically
There is also obvious extra-cranial
acute.
extension of the abscess in this case.
Figure 6 A small subtle left perisinus epidural
abscess was detected on this childs MRI,
performed for acute mastoiditis. This was not
visible on the preceding CT.
Thrombophlebitis

The presence of a perisinus abscess and erosion of the sigmoid sinus plate increase
the risk of sigmoid sinus thrombophlebitis and the development of thrombus,
which can propagate to other dural venous sinuses and the jugular vein.
This complication can be asymptomatic and, therefore, a high index of suspicion
should be maintained. Patients may also present with symptoms of hydrocephalus
or increased intracranial, hypertension, and venous sinus thrombosis may lead to
haemorrhagic venous infarct.
On unenhanced CT, a sinus thrombosis should be suspected if
there is an increased density within the sinus. By administering
contrast medium, the presence of thrombosis will be more
evident as a filling defect within the sinus.
At MRI the absence of a flow void on spin-echo sequences and
filling defect on gradient-echo or MR venography sequences
should alert the radiologist to the presence of thrombus.
Figure 8 (a) Axial T2-weighted MRI of the brain of the same patient from Fig 7. There is
heterogeneous high signal replacing the expected flow void within the right sigmoid sinus indicating
the presence of thrombus. (b) Contrast-enhanced T2-weighted coronal MRI of the brain of the same
patient from Fig 7 with acute mastoiditis. A filling defect is noted within the right sigmoid sinus in
keeping with venous sinus thrombosis. (c) An MR venogram of the same patient from Fig 7
demonstrates a lack of flow within the right sigmoid sinus and proximal jugular in keeping with
thrombosis.
Subdural empyema

a subdural empyema will usually manifest early with


meningism, focal neurological signs, seizure, or reduced
level of consciousness.

The treatment options involve


intravenous antibiotics followed by
otological and neurosurgical
intervention as described above
Petrous apicitis

Suppurative infection can occur in patients that have a pneumatized


petrous apex. It may present with ipsilateral pain and can occur in
parallel with acute mastoiditis or independently.

Focal meningitis of the dura overlying the petrous apex or


involvement of the Gasserian ganglion in Meckels cave may cause
deep facial pain in the trigeminal nerve distribution.
Petrous apicitis

Abducens nerve palsy may be seen if it is involved as it passes through


Dorellos canal. If both these symptoms are seen along with otorrhoea,
then Gradenigos eponymous

Involvement of the sympathetic plexus


adjacent to the petrous internal carotid
artery may induce Horners syndrome
Meningitis

Infection may spread to the meninges by direct


contact with the epidural abscess, haematogenous or
labyrinthine spread

Gross dural thickening may be seen on contrast-enhanced


CT, but MRI is by far the best method to assess for
meningitis

The affected dura will be seen to be slightly thickened


with subtle enhancement.
Meningitis

manifest as slight swelling indicated by subtle effacement

The brain may also be hyperaemic, suggested by increased


vascularity (Fig 9).
Figure 9.
Gadolinium-enhanced T1-weighted coronal image of the brain. This adult male patient had symptoms of left mastoiditis,
sepsis, headache, and confusion. The left dural reflection is seen to be thickened in keeping with meningitis. There is
subtle swelling of the left temporal lobe with effacement of overlying sulci and slightly increased vascularity d signs
indicating cerebritis and hyperaemia. Of note is a filling defect within the right sigmoid sinus. This was deemed to be an
arachnoid granulation, which can act as a false positive for thrombus.
Cerebritis

can be seen as ill defined high


T2 signal areas, which may
have little or no contrast
enhancement
Cerebral abscess

Abscesses may form in areas of cerebritis


temporal lobe, followed by the anterior portion of the lateral
lobe of the cerebellum.
CT:area of low attenuation signifying cerebral oedema, which
may show irregular Enhancement (FIGURE 11)
MRI: surrounding oedema, indicated by high T2 and fluid-
attenuated inversion recovery (FLAIR) signal.
Elderly male
patient with
acute
mastoiditis

CT-SCAN MRI
CT scan
mastoiditis with bony resorption of the tegmen, and a temporal
lobe abscess, which contained gas.
The abscess appeared to be contiguous with the mastoid air
cells, allowing the communication of air into the abscess cavity
(FIGURE 12.a)
Axial CT image of the head of an elderly male with right mastoiditis and
increasing confusion. Alow attenuation area is seen within the right
temporal lobe containing a fleck of gas (FIGURE 12.a)
MRI
Performed 3 days later
the right temporal lobe abscess was larger and communicated both with
the mastoid air cells and the temporal horn of the right lateral
ventricle.
The lateral and third ventricles contain virtually no cerebrospinal fluid
(CSF), having been mostly replaced by gas. The CSF was presumed to
have drained from the ventricular system through the mastoid and ear,
via the abscess (FIGURE 12b & C)
(b.) axial T2-weighted MRI image of the brain of the same patient performed 3 days later.
Breach of the ventricle places the patient at high
risk of developing ventriculitis
The patientwas noted to be immunosuppressed,
possibly due to sepsis-induced cytopaenia. This
may have explained the relative lack of
subependyma enhancement despite the likely
presence of ventriculitis.
Conclusion

Intracranial complications can be clinically silent and insidious in onset.


MRI enhanced with gadolinium, including MR venography, is the ideal as it
demonstrates the subtle intracranial abnormalities that may not be visible at CT.
MRI is often limited, and CT allows rapid assessment and remains the workhorse for
on-call imaging.
Contrast-enhanced CT demonstrates possible intracranial or neck soft-tissue
complications. High-resolution thin section through the temporal bone enables
appreciation of destruction of the fine bony septa of the mastoid air cells.
MRI ;intracranial complications are still suspected despite a negative CT.
THANK YOU
6/10/17

You might also like