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Lecture 1kursk state medical university 6 страница



Infection in the middle ear commonly involves the mastoid by direct extension,

but other surrounding structures may be involved. This can occur by direct

spread through an area eroded by disease, or through a congenital dehiscence or

a fracture line. The other mode of spread is by thrombophlebitis of emissary

veins.

ROUTES OF INFECTION. From the middle ear and mastoid antrum infection may spread

in the following directions:

1. Medially to the labyrinth, through the oval window, round window or by

erosion of the horizontal semicircular canal. Occasionally there may be erosion

of the promontory or the other semicircular canals. Meningitis commonly occurs

in this way.

2. Superiorly towards the middle cranial fossa resulting in an extradural

abscess or in an abscess of the temporal lobe; meningitis occasionally results

from spread of infection by this route.

3. Posteriorly towards the posterior cranial fossa producing (a) an extradural

abscess between the sigmoid sinus and its bony wall (perisinus abscess) or in

abscess medial to the sinus, (b) septic thrombosis of the sigmoid sinus,

(c)meningitis beginning in the posterior cranial fossa, (d) cerebellar abscess.

4. Inferiorly through the floor of the tympanum producing a septic thrombosis of

the bulb of the internal jugular vein. In rare cases this may result in an

abscess developing below the petrous bone and formation of a parapharyngeal

abscess.

Complications are more likely to arise from chronic otitis media than from acute

otitis media and are conveniently divided into two groups - extracranial and

intracranial. They are not mutually exclusive, however, as one complication may

precede or lead to another, e.g. labyrinthitis may lead to meningitis or

mastoiditis may lead to an extradural abscess.

 

Complications of otitis media

 

Extracranial:

Mastoiditis

acute

masked

chronic

Petrositis

Retropharyngeal abscess

Labyrinthitis

circumscribed

diffuse

serous

purulent

Intracranial:

Extradural abscess

Lateral (Sigmoid) sinus thrombosis

Otitic hydrocephalus

Meningitis

Brain abscess

temporal lobe

cerebellum

Subdural abscess

Cortical thrombophlebitis

EXTRACRANIAL COMPLICATIONS

 

Acute mastoiditis

 

Mastoiditis is a complication of otitis media in which infection spreads from

the tympanic antrum to involve the bony walls of the cells of the mastoid

process. The infection may be acute or chronic.

AETIOLOGY. Acute mastoiditis arises from an acute otitis media by extension of

infection from the mastoid antrum to the air cells, and occurs therefore in a

cellular temporal bone. In many cases of acute otitis media infection, although

present in the cellular system, produces no bone destruction, but in severe

acute infections there is a greater inflammatory reaction resulting in pus

formation, increased tension, resorption of bone with loss of trabeculation and

the formation of an empyema. Eventually the inflammatory process may erupt

through the lateral surface to produce a subperiosteal abscess. An untreated

abscess may spread in several directions: (1) through the periosteum and skin

covering the mastoid process, (2) into the external meatus to simulate a

discharging furuncle, (3) through the medial aspect of the mastoid tip into the

digastric fossa (Bezold's mastoiditis), (4) through the posterior root of the

zygoma beneath the temporal fascia (zygomatic mastoiditis) causing slight oedema

of the upper eyelid as an early sign, (5) through the canal for the mastoid

emissary vein or through the temporo-occipital suture to form an abscess

posterior to the mastoid process, (6) beyond the confines of the middle-ear

cleft giving rise to intracranial complications.

SYMPTOMS. The symptomatology of the majority of cases of acute mastoiditis seen

in hospital practice has been modified or obscured by previous unsuitable or

inadequate antibiotic therapy. In acute otitis media pain behind the ear and

tenderness over the area of the mastoid antrum are commonly present but are

relieved by successful antibiotic treatment. Increasing pain, or the return of

pain, and increasing mastoid tenderness are therefore significant. Tenderness



occurs not only over the mastoid antrum but may be elicited on pressure over the

mastoid tip and posterior border. In an untreated case of mastoiditis discharge

from the ear will usually have increased with extension of the disease, but in a

"masked" case discharge may be absent and the perforation may have healed. Fever

is not marked in adults but may be high in children, in whom a rising pulse rate

is a potential danger signal. Deafness is present in most cases but varies in

severity. Local signs vary with the stage and extent of the infection.

In the case of periostitis gentle palpation over the mastoid area may reveal

thickening of the periosteum on the affected side. Later there is oedema of the

soft tissues with displacement of the auricle downwards and outwards which is

often seen more easily from behind the patient. If a subperiosteal abscess forms

there is a fluctuant swelling behind the ear. Narrowing of the external meatus

due to sagging of the posterosuperior meatal wall is a significant finding on

otoscopy, which may reveal a perforated drumhead with pulsating discharge or an

intact one which has a thickened or full appearance. Patients generally look ill

and feel off colour and disinterested.

DIAGNOSIS. In some cases difficulty may arise in distinguishing between

mastoiditis and furunculosis of the posterior meatal wall. Considerable help in

arriving at a diagnosis of mastoiditis may be obtained from radiography of the

mastoids by comparing films of the affected and unaffected sides in different

views of the temporal bone. The radiograph shows the type of mastoid process and

the extent of cellular development. In early cases of mastoid infection, slight

blurring of the cellular outlines is present on the affected side and the

outline of the bony plate of the lateral sinus becomes more prominent.

Increasing opacity with pus formation is followed by loss of cellular outlines

or trabeculation, by destruction of bone proceeding eventually to formation of

an abscess cavity. The radiological appearances should at all stages be

correlated with the clinical manifestations and follow-up radiography is often

necessary.

Blood examination generally shows a polymorphonuclear leucocytosis and the ESR

is increased, except possibly in those patients who have had antibiotic

treatment.

TREATMENT. The incidence of acute mastoiditis has been greatly reduced since the

advent of antibiotic treatment. The majority of cases of acute suppurative

otitis media now resolve by early and adequate treatment with parenteral

penicillin combined, if necessary, with paracentesis. The presence of pus in the

middle ear may be associated with increased tension requiring relief by surgical

drainage.

When the clinical features of mastoiditis develop the patient should be confined

to bed and antibiotic administration commenced. Until pus from the ear is

available for bacteriological examination, penicillin should be given by

intramuscular injection starting with 1 million units (benzylpenicillin)

followed by 500000 units 6-hourly. Lack of improvement in the patient's

condition in 48 hours is an indication for a change of antibiotic or a cortical

mastoidectomy.

The indications for the cortical mastoid operation, also known as Schwartze's

operation, are: (1) continued pain and mastoid tenderness for more than 2 or 3

days despite antibiotic therapy in full dosage and adequate drainage by

paracentesis; (2) increasing constitutional signs, e.g. fever and rising pulse

rate; (3) copious pulsating discharge, rapidly refilling the meatus after

mopping out; (4) sagging of the meatal wall, increasing oedema over the mastoid

process or zygoma; (5) symptoms or signs of labyrinthine or intracranial

complication; (6) onset of facial paralysis; (7) persistent suppurative otitis

media for more than 2 weeks despite efficient treatment; (8) progressive

deafness.

 

Masked mastoiditis

 

This serious and treacherous condition, associated with an unresolved or latent

otitis media, is the result of inadequate treatment with antibiotics. Failure to

recognize the state of the infection and to apply vigorous treatment may result

in the development of an intracranial complication such as meningitis or lateral

sinus thrombosis. At the present time it occurs mostly after the administration

of oral penicillin given for too short a period of time and, in some cases, in

inadequate dosage.

DIAGNOSIS. Many cases are referred to hospital because of the persistence of

pain, deafness, fever and discharge or because of the appearance of an intact

unresolved reddish drumhead. Others are seen on account of recurrence of these

symptoms after an apparent recovery. The persistence of deafness is an important

symptom. There may be mastoid tenderness and headache with a slight rise in

temperature. The drumhead is usually congested and full or thickened in

appearance. Mastoid radiographs show opacity or haziness with, in some cases,

loss of cellular outlines on the affected side.

TREATMENT. Admission to hospital for observation and adequate treatment is

necessary. Resumption of full antibiotic therapy is justifiable in the absence

of acute signs of mastoiditis, a watch being kept on the patient's general

condition, temperature chart, tympanic membrane, mastoid process and hearing. In

the absence of early signs of improvement, and whenever some doubt exists, a

cortical mastoidectomy is indicated, effective drainage of the middle ear

reducing the possibility of some permanent conductive deafness.

 

The Cortical Mastoid Operation (Schwartze's Operation)

 

The aim of this operation is to remove all infected mastoid cells. A postaural

incision is made, the mastoid bone is exposed and Shipo's triangle identified.

The cortex is removed using a drill, although where an abscess is present the

cortex will be soft and necrotic. Each group of cells is systematically explored

and cleared so as to leave an appearance. Particular attention is paid to

removing infection in the tip cells and the cells in the sinodural angle. If

necessary the zygomatic cells are removed. If the plates of bone overlying the

dura mater and the lateral sinus appear healthy they are not opened to expose

these structures, but unhealthy bone in these situations must be removed and the

dura and sinus wall examined for extension of disease. A swab of pus will be

taken routinely for culture and sensitivity, and any granulation tissue should

be sent for histological examination. The wound is sutured and a rubber drain is

left in the lower part of the incision. The drain is removed after 24 to 48

hours and the stitches are removed in one week.

Lack of healing or continued meatal discharge suggests that some infected cells

may have been missed or that spicules of infected bone have been left in the

cavity, and in either case the wound may have to be reopened.

 

Labyrintitis

 

This is a not uncommon complication of otitis media and, if suspected, must be

treated vigorously and promptly. Failure to do so may lead to total

sensorineural deafness or meningitis. The least severe form is circumscribed

labyrinthitis, also known as paralabyrinthitis, and this is easily the most

common type. Serous labyrinthitis is less common, but more serious. The least

common but most dangerous variety is purulent labyrinthitis which inevitably

leads to a total and permanent loss of vestibular and auditory function.

PATHOLOGY. Circumscribed labyrinthitis is almost invariably due to a fistula,

i.e. cholesteatomatous erosion of the bony capsule of the labyrinth, usually the

horizontal semicircular canal but occasionally the promontory or other canals.

Diffuse labyrinthitis may be an extension of the circumscribed type but it more

frequently follows invasion through the oval or round windows, especially the

former. It involves the peri- and endolymphatic spaces. Diffuse labyrinthitis

may be serous or purulent. In serous labyrinthitis there is a general

non-purulent inflammation of the labyrinth with occasionally a fibrinous or

serous exudate. In purulent labyrinthitis there is infiltration of the spaces by

polymorphs, pus cells and destruction of the vestibular and cochlear structures.

Occasionally the bony capsule becomes involved.

Labyrinthitis may follow an acute otitis media, tuberculous otitis media or

chronic otitis media. Other causes of labyrinthitis include trauma, bloodborne

infection, bacterial or viral, and meningitis.

CLINICAL FEATURES Circumscribed labyrinthitis. There may be an initial bout of

vertigo and deafness in the formative stage of the fistula. Once the fistula is

established the main complaint may be of intermittent vertigo brought on by

sudden movements, cold water or air in the ear or, in more advanced cases, by

moving the auricle. There is usually evidence of chronic otitis media on

otoscopy and the diagnosis is confirmed by demonstrating a fistula sign, but a

negative fistula sign does not rule out a fistula. There may be a slight

sensorineural hearing loss in addition to the conductive hearing loss due to the

otitis media.

Serous labyrinthitis. This may follow circumscribed labyrinthitis or any of the

other causes mentioned. There is hearing loss, occasionally pain and tinnitus,

but the main feature is vertigo, associated with nausea and vomiting. There may

be a sensation of objects moving from the diseased to the healthy side, i.e.

nystagmus, towards the diseased side. The patient invariably is bed-ridden, at

least initially, and lies on the unaffected ear and looks towards the diseased

side because this reduces the vertigo. As a rule there is no pyrexia. Caloric

reactions, if tested after the acute phase, are diminished on the affected side.

 

Purulent labyrinthitis. The symptoms are similar to those of serous

labyrinthitis but the vertigo and vomiting may be more frequent and severe.

Nystagmus, although initially directed towards the diseased ear, soon changes

direction towards the good ear. Total deafness develops. Caloric testing should

not be done during the acute phase because it can exacerbate roe vertigo, but if

done later a canal paresis is commonly found on the affected side. There is no

pyrexia unless there is an intracranial complication.

TREATMENT Circumscribed labyrinthitis. Suspicion of labyrinthine erosion by

cholesteatoma or granulations is an indication for surgery. Tomography may show

labyrinthine erosion. The mastoid is cleared of disease by a modified radical

mastoidectomy. The fistula may be exteriorized if caused by cholesteatoma. In

some cases the cholesteatoma can be removed and the fistula is covered by

temporalis fascia.

Serous labyrinthitis and purulent labyrinthitis. Bed-rest is essential in the

initial stages. Sedation with labyrinthine sedatives is required, dimenhydrinate

(Dramamine), promethazine hydrochloride (Pipolphen) or prochlorperazine

(Novamine) being useful. Parenteral antibiotics in adequate dosage are required.

A combination of penicillin and a sulphonamide can be used empirically until

swab results are known. Most patients settle on this regime. If the

precipitating cause were an acute exacerbation of chronic otitis media this can

be dealt with subsequently. Occasionally a myringotomy will be required in acute

otitis media, and occasionally it is necessary to deal surgically with a

mastoiditis. In a few cases persistence of symptoms with evidence of

intracranial irritation may call for exploration and a labyrinthectomy.

Labyrinthectomy. This is now rarely done but may be required in suppurative

labyrinthitis. It is also indicated in an ear where the cochlear function has

been severely damaged by chronic otitis media and there is persistent vertigo.

Occasionally it is indicated in Meniere's disease. A radical mastoidectomy is

performed. The lateral semicircular canal is exposed and opened and the

membranous labyrinth removed. The oval and round windows are joined and the

contents of the vestibule removed by suction. Some authorities recommend opening

all three canals.

 

INTRACRANIAL COMPLICATIONS

 

There has been a marked reduction in incidence of these complications over the

past four decades, the reasons for this being the same as for extracranial

complications. When they do occur, however, their morbidity and mortality are

still high. Even today a person who has a brain abscess has a 40% chance of

dying from it. It is vital, in any suspected case of intracranial extension of

disease, to liaise closely with the neurosurgeons. The only exception to this

rule being a small extradural abscess where the diagnosis is made during the

course of exploratory mastoid surgery.

 

Extradural abscess

 

An extradural abscess consists of a collection of pus between the bone and the

dura mater. Unless it is opened and drained it is frequently followed by other

intracranial complications. It is more common in the posterior than in the

middle cranial fossa, in some cases forming between the lateral sinus and the

bone of the posterior cranial fossa (perisinus abscess). Extradural abscess

occurs more commonly in acute than in chronic middle-ear suppuration. In chronic

purulent otitis media it is met with chiefly in cases of cholesteatoma and in

acute exacerbations of chronic suppuration. The extent of the abscess varies

greatly; it may be quite small or, in chronic cases, it may attain a

considerable size.

CLINICAL FEATURES. The symptoms are rarely characteristic and the majority of

extradural abscesses are only discovered at the time of operation. The condition

is associated with deep-seated boring pain, tenderness on tapping over the

temporal region or posterior fossa, and rise of temperature. If the abscess is

large, there may be evidence of compression of the brain. There are rarely any

localizing symptoms although occasionally paresis of the VIth nerve may be

encountered.

DIAGNOSIS. This is not easy as a rule. The relief of pain by the spontaneous

evacuation of a large quantity of pus, or the aspiration of much pus by mopping

or aspiration through the external meatus, may suggest the diagnosis. The

continuation of pain, pyrexia and a raised pulse rate after operation for a

mastoid complication should suggest the probability of the presence of a

deeper-seated collection of pus.

TREATMENT. This consists in opening the abscess and evacuating its contents by

free removal of the bony wall. When the abscess is opened the pus flows out in a

pulsating manner. The affected dura mater may be covered with red "healthy"

granulations, or it may be greyish-green and slough-like. Removal of the

underlying bony wall should be continued until the whole abscess cavity has been

freely exposed. The cortical or the radical operation - according to

circumstances - is performed at the same time. The patient should be carefully

watched in order to detect the first signs of further intracranial

complications, e.g. sinus thrombosis, brain abscess or meningitis.

 

Lateral (sigmoid) sinus thrombosis

 

This condition used to account for about 30% of all cases of intracranial

complications in the pre-antibiotic era, but now it occurs much less frequently

and today makes up less than 10% of the total. About half of these are

associated with other intracranial complications, usually cerebellar abscess or

meningitis. It is still a dangerous condition which must be recognized as early

as possible and treated vigorously.

PATHOLOGY. The initial lesion is inflammation of the wall of the sinus secondary

to local infection. This can be due to local venous thrombophlebitis but it is

usually a result of an extradural perisinus abscess, which has sometimes been

present for a considerable time. It occurs in both acute and chronic mastoid

infections although more frequently in the latter. The local inflammation in the

wall of the sinus results in thrombus formation which can spread to involve the

whole lumen. In untreated or rapidly developing cases the thrombus may extend in

either direction to involve the superior petrosal sinus (rare), cavernous sinus

(rare), jugular bulb (common) or the internal jugular vein (rare). The thrombus

tends to stop where two vessels meet. If the thrombus becomes infected an

abscess can develop and this may result in pieces of infected clot breaking away

and being carried to other parts of the body.

A pyaemia therefore occurs and abscesses are set up in the lungs and other

organs. If the infection breaches the medial wall of the sinus, meningitis,

subdural abscess or brain abscess can develop.

CLINICAL FEATURES. Sinus thrombosis may run its course without symptoms,

particularly where antibiotics have been used, and be found later at a

definitive operation for the underlying chronic otitis media. The classical

presentation, now rarely seen, consists of the occurrence of chilly sensations

or rigors in which the temperature rises suddenly to 39,5 or 40oC and falls

again as rapidly, the fall being accompanied by profuse sweating. There may be

only one rigor daily, usually in the afternoon or evening, or several. There is

a concomitant rise in the pulse rate. A high evening temperature for several

days after a mastoid operation calls for exploration of the sinus. In the

intervals between the rigors the patient is free from symptoms, although in

advanced cases there is persistent pyrexia. Headache and vomiting occasionally

occur, the tongue is dry, there may be herpes on the lips, an enlarged spleen

and a congested optic disc. Lumbar puncture, which should only be done if a

brain abscess can be excluded, may demonstrate raised cerebrospinal fluid

pressure, particularly when complete occlusion is present. In such cases the

Tobey-Ayer test is positive. This consists of compressing the jugular vein of

the normal side which causes a rise of cerebrospinal fluid pressure in the

manometer connected to the lumbar puncture needle, while compression of the vein

on the affected side produces little or no rise in pressure. Occasionally oedema

is present in the neighbourhood of the mastoid emissary vein (Griesinger's

sign).

If the thrombosis extends into the neck torticollis may develop, and there may

be tenderness over the line of the jugular vein. Occasionally a cavernous sinus

thrombosis can occur. As a result of escape of portions of the clot into the

general circulation pneumonia or lung abscess may arise. If the particles are

small, metastatic abscesses may appear in other parts of the body, especially in

the subcutaneous tissues or in the bones and joints.

DIAGNOSIS. The conditions with which sinus thrombosis is most likely to be

confused are malaria, typhoid fever, bronchopneumonia and erysipelas. The

diagnosis of sinus thrombosis is suggested by the occurrence of rigors in the

course of middle-ear suppuration; it is more difficult if the condition is

complicated by the presence of meningitis or brain abscess, both of which must

be treated first. Examination of the peripheral blood will show a

polymorphonuclear leucocytosis. In severe infections a falling haemoglobin can

occur. Blood cultures are rarely of value.

TREATMENT. Early energetic antibiotic and anticoagulant therapy often makes

operative treatment unnecessary. The same antibiotic regime as for labyrinthitis

is recommended. When active surgical intervention is required this consists of

removing the primary focus of disease by performing a cortical mastoidectomy in

cases due to acute middle-ear suppuration, and a radical operation in cases of

chronic suppuration. If sinus thrombosis is present there is usually excessive

bleeding from the bone at the mastoid operation. In every case which shows

symptoms suggestive of extradural perisinus abscess or sinus thrombosis the

sigmoid sinus should be exposed until the healthy wall is seen. A healthy sinus

wall is blue in colour and it is easily compressed. If a perisinus abscess is

found and there are healthy granulations on the sinus wall, and if only one

rigor has occurred, it is advisable to leave the wound open and pack the cavity

with tampon. The sinus should be opened if there are persistent rigors or if the

wall of the sinus is greyish-yellow, brownish-green or slough-like at the first

or subsequent operations. Before opening, the sinus plate is removed to expose

the healthy sinus wall above and below the diseased area. Gauze packing is

inserted between the sinus and bone superiorly and inferiorly to reduce any

bleeding and the sinus is slit open. All necrotic thrombus and tissue are

removed until either healthy clot is identified or free bleeding occurs. The

sinus and cavity are packed with tampon and the wound left open to be closed at

a second stage some 7 days later.

Septic thrombosis can follow injury to the sinus during mastoid operations.

Injury to the wall should be treated by application of a piece of temporalis

fascia or muscle to arrest the bleeding. Should rigors occur postoperatively the

case is treated as a sinus thrombosis.

PROGNOSIS. The prognosis of sinus thrombosis is more favourable since the

introduction of antibiotics. It is more favourable than that of brain abscess if

an operation is performed before systemic infection has occurred, and if there

is no other intracranial complication. With antibiotics and timely surgery a

cure is to be expected.

 

Meningitis

 

This complication accounts for about one-third of all intracranial

complications, only brain abscess being more common. Even with the armamentarium

of antibiotics available today it can still be fatal and must be suspected in

all cases of otitis media where there are symptoms and signs suggestive of

intracranial spread of disease. Like the other complications of otitis media it

is decreasing in incidence.

PATHOLOGY. Meningitis is an infection of the pia mater which invests the brain,

the arachnoid mater which is closely adherent to the under surface of the dura

mater, and the cerebrospinal fluid which lies between these two layers. It can

occur during an acute infection but is more commonly associated with chronic

otitis media. There are several ways in which infection can reach the meninges:

(1) direct extension through the dura mater due to thrombophlebitis of

communicating veins, erosion by disease or surgery, or congenital or traumatic

dehiscences; (2) extension of disease from an extradural abscess or lateral

sinus thrombophlebitis; (3) extension of a suppurative labyrinthitis via the

cochlear aqueduct or the subarachnoid sleeve of the VIIIth nerve.

As in other infections there is often an initial inflammatory response with


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