Complications of active COM
Labyrinthitis:
Introduction:
This is defined as an inflammatory disorder involving the inner ear / labyrinth. Clinically this condition causes disturbances of balance and hearing of varying degrees in the involved ear.
Causes:
1. Bacterial infections
2. Viral infections
3. Autoimmune causes
4. Vascular ischemic causes
Pathophysiology:
Anatomically labyrinth is composed of an outer osseous framework surrounding the delicate membranous labyrinth which contains the peripheral end organs of hearing and balance. Membranous labyrinth include:
1. Utricle
2. Saccule
3. Semicircular canals
4. Cochlea
The labyrinth lies within the petrous portion of temporal bone. It communicates with the middle ear via the oval and round windows.
Infecting organism may find their way into the inner ear via:
Pre-existing fractures
Oval window
Round window
Congenital dehiscence involving the bony labyrinth
Viral labyrinthitis: Is characterized by sudden unilateral loss of hearing and equilibrium. Vertigo is usually incapacitating and associated with vomiting. These patients are bed ridden. Vertigo usually subsides within 4-6 weeks. Hearing loss is confined to high frequencies and is sensorineural in nature. An attack of upper respiratory tract infection precedes the development of labyrinthitis. This condition should not be compared with vestibular neuronitis which involves only the vestibular nerves and spares the cochlear component. Varicella Zoster oticus is an unique form of viral labyrinthitis caused by reactivation of dormant varicella zoster virus. This reactivated virus is known to attack spiral ganglion.
Common viral causes of labyrinthitis:
1. Mumps
2. Measles
3. Rubella (congenital labyrinthitis)
4. Cytomegalovirus
Bacterial labyrinthitis: can be potentially caused by meningitis / otitis media. This could be caused by direct invasion of membranous labyrinth by the infecting organism (suppurative labyrinthitis) causing permanent destruction of vestibular and cochlear end organs. In patients with meningitis spread of infections can be bilateral since infections can travel via the CSF and involve the inner ear fluids through the internal acoustic meatus / cochlear aqueduct. Bacterial infections involving the middle ear cavity can enter the labyrinth via erosion of lateral canal which is commonly seen in patients with cholesteatoma. Treatment is usually directed against infecting organism and supportive therapy. Suppurative labyrinthitis is usually followed by labyrinthitis ossificans where the whole of the membranous labyrinth gets ossified. Labyrinthitis ossificans indicates a permanently dead labyrinth.
Common bacterial causes of labyrinthitis include:
1. S. pnuemoniae
2. Haemophilus influenza
3. Streptococcus
4. Staphylococcus
5. Neisseria
6. Bacteroids
7. Proteus
8. Moraxella catarrhalis
Serous labyrinthitis:
This is a potentially reversible disorder caused by diffusion of bacterial toxins into the inner ear via the inflamed round window membrane. Studies have shown that the permeability of the round window membrane is increased when there is inflammation. This may cause diffusion of bacterial toxins and immune mediators into the inner ear causing transient impairment of the inner ear functions.
Brain abscess:
Otogenic brain abscess always develop in the temporal lobe or the cerebellum ofthe same side of the infected ear. Temporal lobe abscess is twice ascommon as cerebellar abscess. In children nearly 25% of brain abscessesare otogenic in nature, whereas in adults who are more prone to chronicear infections the percentage rises to 50%. The routes of spread ofinfection has already been discussed above, the commonest being thedirect extension through the eroded tegment plate. Although dura ishighly resistant to infection, local pachymeningitis may be followed bythrombophlebitis penetrating the cerebral cortex, sometimes theinfection could extent via the Virchow - Robin spaces in to thecerebral white matter. Cerebellar abscess is usually preceded bythrombosis of lateral sinus. Abscess in the cerebellum may involve thelateral lobe of the cerebellum, and it may be adherent to the lateralsinus or to a patch of dura underneath the Trautmann's triangle.
Stages of formation of brain abscess:
Stage of cerebral oedema: This is infact the first stage of brain abscessformation. It starts with an area of cerebral oedema and encephalitis.This oedema increases in size with spreading encephalitis. Walling off of infection by formation of capsule: Brain attempts to wall off the infected area with the formation of fibrous capsule. This formation of fibrous tissue is dependent on microglial and blood vessel mesodermal response to the inflammatory process. This stage is highly variable. Normally it takes 2 to 3 weeks for this process to be completed.
Liquefaction necrosis:Infected brain within the capsule undergoes liquefactive necrosis with eventual formation of pus. Accumulation of pus cause enlargement of the abscess.
Stage of rupture:
Enlargement of the abscess eventually leads to rupture of the capsule containing the abscess and this material finds its way into the cerebrospinal fluid as shown in the above diagram. Cerebellar abscess which occupy the posterior fossa cause raised intra cranial tension earlier than those above the tentorium. This rapidly raising intra cranial pressure cause coning or impaction of the flocculus or brain stem into the foramen magnum. Coning produces impending death. If the walling off process (development of capsule) is slow, softening of brain around the developing abscess may allow spread of infection into relatively avascular white matter, leading to the formation of secondary abscesses separate from the original or connected to the original by a common stalk. This is how multilocular abscesses are formed. Eventually the abscess may rupture into the ventricular system or subarachnoid space, causing meningitis and death.
The mortality rate of brain abscess is around 40%, early diagnosis after the advent of CT scan has improved the prognosis of this disease considerably..
The bacteriological flora is usually a mixture of aerobes and obligate anaerobes. Anaerobic streptococci are the commonest organisms involved. Pyogenic staphylococci is common in children. Gram negative organim like proteus, E coli and Pseudomonas have also been isolated.
Clinical features:
The earliest stage where the brain tissue is invaded (stage of encephalitis) is marked by the presence of headache, fever, malaise and vomiting. Drowsiness eventually follow. These early features may be masked by the complications such as meningitis or lateral sinus thrombosis. If this stage progresses rapidly to generalised encephalitis before it could be contained by the formation of the capsule, drowsiness may progress to stupor and coma followed by death..Usually the period of local encephalitis is followed by a latent period during which the pus becomes contained within the developing fibrous capsule. During this latent phase the patient may be asymptomatic.
During the next state (stage of expansion) the enlarging abscess first cause clinical features due to the alteration of CSF dynamics, and site specific features may also be seen due to focal neurological impairment. The pulse rate slows with rising intracranial pressure,the temperature may fall to subnormal levels. Drowsiness may alternate with periods of irritability. Papilloedema is also found due to elevated CSF pressure.
Clinical features also vary according to the site of involvement. Hence thedifferences that are seen between the cerebral and cerebellar abscess.
Cerebral (Temporo sphenoidal abscess):
A cerebral abscess in the dominant hemisphere often cause nominal aphasia, where in the patient has difficulty in naming the objects which are in day to day use. He clearly knows the function of these objects. Visual field defects arise from the involvement of optic radiations. Commonly there is quadrantic homonymous hemianopia,affecting the upper part of the temporal visual fields, more rarely it may also involve the lower quadrants. The visual field loss are on the side opposite to that of the lesion. This can be assessed by confrontation method. Upward development affects facial movements on the opposite side, and then progressively paralysis of the upper and lower limbs. If the expansion occur in inward direction then paralysis first affects the leg, then arm and finally the face.
Cerebellar abscess:
The focal features associated with cerebellar abscess is weakness and muscle incoordination on the same side of the lesion. Ataxia causes the patient to fall towards the side of the lesion. Patient may also manifest intention tremors which may become manifest by the finger nose test. This test is performed by asking the patient to touch the tip of the nose with the index finger first with the eyes open and then with the eyes closed. The patient may often overshoot the mark when attempted with the eyes closed in case of cerebellar abscess. The patient may also have spontaneous nystagmus. Dysdiadokinesis is also positive in these patients.
Investigations:
CT scan and MRI scans are the present modes of investigation. Scan is ideally performed using contrast media. These scans not only reveal the position and size of the abscess, the presence of localised encephalitis can be distinguished from that of an encapsulated abscess.Associated conditions such as subdural abscess, and lateral sinus thrombosis can also be seen.
Lumbar puncture: Isfrought with danger because of the risk of coning. Lumbar puncture mustbe performed in these patients only in a neurosurgical unit whereimmediate intervention is possible if coning occurs.
Treatment:
involves use of large doses of antibiotics. Ideally the abscess shouldbe controlled neurosurgically and with antibiotics. After the patientrecovers mastoidectomy is performed to remove the focus of infection.Abscess can be drained by placement of burr holes, and excision of thenecrotic tissue along with the capsule.
