production of serous fluid. This stage can be identified readily, for instance
with extradural abscesses. Granulations develop in the dura mater around the
abscess and this causes irritation of the pia-arachnoid layers which respond by
producing a serous effusion. If the abscess drains spontaneously or is drained
surgically the effusion gradually subsides and this serous meningitis settles.
If, however, the local infection is not controlled infection may then spread
into the pia-arachnoid layers. There is initially a cellular reaction to this
and polymorphonuclear leucocytes increase in number, and this is followed by the
appearance of bacteria in the cerebrospinal fluid and a purulent meningitis. The
disease may remain localized initially but with the purulent stage developing it
rapidly becomes diffuse. In some cases, in which the bacteria are virulent,
there is only a very brief serous phase before the onset of the purulent phase.
In an untreated or a rapidly progressive infection the surface of the brain
becomes affected causing a meningo-encephalitis and a widespread and usually
fatal cerebral dysfunction occurs.
The bacteria commonly associated with meningitis are Haemophilus influenzae,
streptococci and pneumococci. Occasionally Bacillus proteus or Pseudomonas
pyocyanea may spread from a chronic mastoid infection.
CLINICAL FEATURES. Headache and neck stiffness are the two cardinal features of
serous meningitis. The headache is severe and may be initially localized to the
side of the disease but later becomes generalized. There will be neck stiffness
and tenderness, most easily tested by lifting the patient's head off the pillow.
Photophobia may be present, occasionally associated with vomiting due to raised
intracranial pressure. The patient's initial conscious level may be normal but
usually there is slight confusion and irritability with occasional episodes of
drowsiness. There may be an initial rigor but often the temperature is slightly
elevated from 38°C to 38,5°C.
As the disease progresses and purulent meningitis supervenes so the headaches
become extremely severe. The neck becomes rigid, there is a positive Kernig's
sign (an inability to extend the knee with the hip flexed to 90o). There may be
severe neck pain. Photophobia is marked and there is frequent vomiting. The
level of consciousness varies but there is marked confusion, irritability with
occasional periods of excitement during which the patient may cry out or talk
incoherently. The reflexes are increased initially but later, as the condition
advances, may be reduced. There is a persistently high temperature (39,5°C to
40°C) with a fast and weak pulse.
In the final stages paralysis may develop and can affect various parts of the
body and the cranial nerves, especially the III-rd and the Vl-th, with the
production of squinting. Optic neuritis is frequently seen while the pupils are
contracted and equal and react sluggishly. Coma supervenes before death.
DIAGNOSIS. Meningitis has been aptly described as the great imitator and must be
diagnosed and treated at an early stage for the best chance of survival. The
definitive test is lumbar puncture which should be done at the earliest
opportunity, except in cases where there is doubt about the diagnosis. If the
clinical features suggest the possibility of a brain abscess urgent
neurosurgical advice should be sought. The features suggestive of a possible
brain abscess include variable morning headache as opposed to continuous
headache in meningitis, a slightly elevated temperature, intermittent
drowsiness, focal signs and neck stiffness without a positive Kernig's sign.
Computerized transverse axial tomography (CAT scan) is rapid and extremely
sensitive in detecting brain abscesses. If this is not available a radio-isotope
scan or arteriography may be required.
Lumbar puncture can reveal a great deal of information. The normal pressure of
the cerebrospinal fluid is 80-120 mm of water and in meningitis it is raised
(300-600). It is important that there should be no blood in the fluid sent for
examination, and therefore the first few drops should be allowed to escape. Four
cells per cc may be regarded as normal. If the fluid is under tension, but clear
and sterile, and the cellular content is not increased, the meningitis is still
at the serous stage. On the other hand, if the fluid is under pressure and is
turbid from the presence of leucocytes, purulent meningitis may usually be
diagnosed. If organisms are present in addition, there can be no doubt.
Biochemical examination of the cerebrospinal fluid in meningitis will show
diminished or absent glucose, raised protein and globulin, and lowered chloride.
TREATMENT. Without waiting to identify the organisms responsible parenteral
antibiotic therapy should be instituted. 2 to 3 megaunits of penicillin are
given 3-hourly, combined with 2g of sulphonamide 6-hourly. Swabs from the ear
and fluid obtained at lumbar puncture are cultured to discover the organisms and
determine their sensitivities, and antibiotic therapy is continued with the
appropriate drug until the cerebrospinal fluid and clinical examination are
normal. Other antibiotics routinely used include ampicillin and oxacillin,
cephazoline and occasionally gentamicin. Intrathecal penicillin IOOOO units in
5ml may be introduced is turbid. Surgery of the underlying ear disease should be
carried out when the patient's general state permits. Labyrinthectomy may be
required in the presence of concomitant suppurative labyrinthitis.
PROGNOSIS. An uncomplicated meningitis has a more favourable outlook than one
associated with a sinus thrombosis, brain abscess or labyrinthitis.
Brain abscess
Brain abscess is the commonest intracranial complication of ear disease making
up over one-third of the total numbers. Ear disease, on the other hand, is the
commonest cause of brain abscess and accounts in some series for about half the
total. Cerebellar abscesses nearly always arise from ear disease. Today the
overall mortality from brain abscesses is quoted at around 40%. The earlier the
diagnosis is made and treatment instituted, the more likely are the chances of
recovery, but there is a significant morbidity rate in the survivors in terms of
epilepsy. Suspicion and early diagnosis, therefore, are vital if the prognosis
is to improve.
PATHOLOGY. An abscess develops close to the site of the original infection, so
otogenic brain abscesses arise in the temporal lobes and the cerebellum. The
majority are associated with chronic otitis media although acute infections
account for a significant number. Cerebellar abscess is due to: (1) extension of
infection from the mastoid posteriorly and medially through the triangular area
bounded by the superior petrosal sinus above, the labyrinth and facial nerve
anteriorly, and the lateral sinus laterally - there is usually a preceding
extradural abscess; (2) septic thrombosis of the sigmoid sinus which is usually
associated with a perisinus abscess; (3) labyrinthitis.
Temporal lobe abscess, the more common abscess, is caused by spread of infection
through the roof of the middle ear or mastoid antrum, again frequently preceded
by an extradural abscess. The dura mater, pia arachnoid and brain become
adherent to the inflamed tissue, and after an initial local surface encephalitis
the infection spreads to the subcortical white matter. More rarely the abscess
is due to septic thrombosis of one of the pial veins of the temporal lobe or
cerebellum. Infection by this route, which is common in cases of acute
middle-ear suppuration, may result in multiple abscesses.
Once infection is established in the brain, if unchecked, it involves more
tissue which becomes necrotic and an abscess is formed. The presence of
infection stimulates oedema of the surrounding tissue and results in increased
intracranial pressure, distortion of surrounding structures and functional
disturbance of them. Continuing infection causes tissue destruction, a further
displacement of brain tissue across the midline and eventually death, usually
from mid-brain damage.
CLINICAL FEATURES. The symptoms and signs produced are due to three factors: (1)
increased intracranial pressure, (2) focal disturbance of function, (3) systemic
disturbance.
1. Increased intracranial pressure. Headache is the dominant symptom and is
usually generalized and worse in the morning. Vomiting often occurs, especially
in cerebellar lesions. Drowsiness, confusion and lethargy develop as pressure
increases and finally coma supervenes. Papilloedema may be present but its
absence does not rule out raised intracranial pressure. The temperature is often
subnormal in the early stages unless there is coexisting meningitis and the
pulse is often slow.
2. Focal signs. These are variable. Homonymous hemianopia is a valuable sign in
temporal lobe abscess, as is nominal dysphasia. Cerebellar abscesses give rise
to ataxia and nystagmus. In very ill patients these signs may be difficult to
elicit.
3. Systemic disturbance. Although there may be little initial systemic upset as
the infection progresses the patient becomes very ill and emaciated. There is
pyrexia, loss of appetite, exhaustion and a furred tongue. There is raised ESR
and a polymorphonuclear leucocytosis. A severe rise in temperature often occurs
if an abscess ruptures into the ventricular system.
Temporal Lobe Abscess
This is more common than cerebellar abscess and gives rise to a typical clinical
picture.
CLINICAL FEATURES. Headache is common and is usually generalized. If there has
been a preceding extradural abscess the headache may be more severe on the
affected side and be associated with tenderness over the temporal lobe. The
headache classically is worse in the morning and it is exacerbated by coughing,
sneezing or straining. Vomiting is occasionally seen. Mental changes may be
minimal initially and consist of subtle changes in personality and mild
confusion. As the intracranial pressure increases, however, the patient will
become lethargic and listless, and then drowsy. Drowsiness is a danger signal as
it indicates early tentorial herniation and mid-brain compression. Papilloedema
may be present at this stage.
Nominal dysphasia is a feature of temporal lobe abscesses and it suggests
involvement of the speech area of the dominant cerebral hemisphere. The speech
area is located in the frontotemporal region and is usually on the left side of
the brain in a right-banded person and on the right side in a left-banded
person. The earliest focal sign is usually a homonymous hemianopia. If this sign
is present the patient has visual field defects affecting the same sides of both
retinas, and he will be unable to see objects on one side, i.e. to the right if
there is a lesion of the left temporal lobe. The defect is due to interruption
of the fibres of the optic radiation as they pass near the temporal lobe and, if
the lesion is small, it may present early as a superior quadrantic visual
defect. This test is elicited by standing in front of the patient and comparing
his visual fields with the examiner's. In an unconscious or drowsy patient the
sign may be elicited by flashing a light or a handkerchief near the eye and
trying to elicit the blink reflex and comparing the sides. An expanding lesion
may cause contralateral paralysis of limbs and even a hemiplegia if the internal
capsule is affected. Pupillary abnormalities and oculomotor palsies are
suggestive of transtentorial herniation and are danger signs. Epileptic fits are
not uncommon but, unless they are focal, are of little localizing value. Sudden
onset of coma associated with a high fever indicates that the abscess has
ruptured into the lateral ventricle and is of a grave prognostic significance.
Cerebellar Abscess
This abscess is less common than temporal lobe abscess by a ratio of 1 to 4 or
5.
CLINICAL FEATURES. Headache is again a feature and tends to be suboccipital and
may be associated with nuchal rigidity. Vomiting is common and papilloedema is
seen more often than in temporal lobe lesions. Confusion and drowsiness occur if
the intracranial pressure increases and will progress to coma and death if
untreated.
Truncal and limb ataxia gives rise to unsteadiness, and Romberg's test is
positive. Other signs of cerebellar disease are past-pointing and
dysdiadokokinesia. In the latter test the patient is asked to pronate and
supinate his forearms alternately. If there is unilateral cerebellar disease
present he will be unable to do the test efficiently on that side. Nystagmus is
usually present and is coarser and of greater amplitude than that due to
labyrinthitis. As a rule it is directed towards the affected side. Later signs
consist of a VIth nerve palsy and dysarthria.
DIAGNOSIS. Once suspected it is essential to obtain neurosurgical advice as the
investigation and treatment are neurosurgical. Lumbar puncture is
contra-indicated, even if a concomitant meningitis is suspected, because of the
risk of coning. The investigations carried out depend on local facilities but
they must be done with utmost urgency.
1. Plain skull radiography. This is useful as it may show a midline shift if the
pineal gland is calcified.
2. Computerized transverse axial tomography scan. A CT scan is the best
investigation if available. It is quick, non-invasive and extremely accurate in
localizing abscesses, especially when it is combined with iodine enhancement. As
well as delineating the abscess, intracranial shift, cerebral oedema and
hydrocephalus can all be demonstrated.
3. Electroencephalography. This can be of use.
4. Brain scan. Radio-active technetium is injected intravenously and the brain
scanned by a gamma camera. It is very valuable in supratentorial lesions and is
non-invasive.
5. Arteriography. This is still recommended as an important investigation
because it shows intracerebral shifts, avascular areas and areas of increased
vascularity. It is not without risk, needs a general anaesthetic, unless the
patient is comatose, and its accuracy can be doubtful.
TREATMENT. This is primarily neurosurgical. High doses of antibiotics which
cross the blood brain barrier are given parenterally. Some help may be obtained
from swabs from the offending ear. Once the abscess is localized it is drained
via a burrhole and this may be followed by repeated aspiration and instillation
of antibiotic. In some cases a craniotomy is performed and the abscess with its
capsule, if well defined, is removed.
In an emergency if there is no immediate neurosurgical help available and the
patient is deteriorating rapidly a temporary improvement may be obtained by
giving 500 ml of 20% mannitol intravenously combined with 4 g of dexamethasone.
This may reduce the cerebral oedema sufficiently to prevent coning and allow the
patient to be transported to a neurosurgical unit.
The causative ear infection should be dealt with as soon as the patient's
general condition permits. A radical mastoidectomy is recommended for chronic
disease and a cortical mastoidectomy for acute infections.
COURSE AND TERMINATION. If untreated a brain abscess ends fatally with
increasing drowsiness, stupor and eventually coma which continues until death.
PROGNOSIS. Even today the mortality for brain abscesses may be as high as 40%. A
further 40% are left suffering from some degree of permanent disability, usually
epilepsy. If there is meningitis associated with the brain abscess the prognosis
is worsened.
Subdural abscess
This is an extremely rare complication of otogenic infection and it is serious,
with a poor prognosis. The mode of spread is similar to other intracranial
infections but pus collects in the subdural space. This causes increased
intracranial pressure, midline shift and transtentorial herniation. The patient
is extremely ill, has severe headache and, as infection spreads to involve the
cerebral cortex, develops focal signs of hemiplegia or hemi-anaesthesia.
Drowsiness progresses rapidly to coma. Epileptic fits may start. Neurosurgical
referral is a matter of urgency and investigations are similar to those for
brain abscess.
The treatment consists of draining the subdural space and in some acute cases
this may have to be done on a presumptive diagnosis in order to save the
patient's life.
Part 6
DISEASES OF THE NOSE AND PARANASAL SINUSES
Deviation of the nasal septum
Very few individuals have a completely straight nasal septum. Deviations and
spurs vary from being slight and causing no trouble, to being gross and causing
complete obstruction of one nostril. People vary greatly in the degree to which
they suffer from deviations of the septum, some complaining bitterly of
unilateral nasal obstruction when only a slight abnormality is found, and not
infrequently a gross deviation is encountered as a chance finding, the patient
having no symptoms whatsoever. It is therefore necessary to be guided by
subjective symptoms when deciding on the advisability of operative interference.
Deviations may be of developmental or traumatic origin. The latter group may
additionally show displacement of the tip of the nose, and there may also be an
untreated fracture of the nasal bones. In most septal deviations, the convex
surface is towards the narrow side and the concave towards the other. The
inferior and middle turbinates on the concave side may be enlarged to compensate
for the widening of the airway, and this enlargement may in turn give rise to
symptoms such as secondary sinusitis. due to reduced airflow through the middle
meatus.
The caudal end of the septal cartilage should be inserted into the columella in
the midline. If there is caudal dislocation of the septum into one nostril,
there is frequently a convex displacement into the other nostril more
posteriorly. The inferior surface of the septal cartilage should be inserted
into the crest of the maxilla. If it is dislocated a spur is formed.
SYMPTOMS. Deviations of the nasal septum give rise to unilateral or bilateral
symptoms. If the presenting complaint is of nasal obstruction, this will usually
be found on the convex side. If the presenting symptom is of catarrh, or of
facial pain due to obstruction or infection of the sinuses, it may be associated
also with the concave side, where the enlarged turbinates are causing
obstruction. The patient may also present with chronic otitis media due to
malfunction of the auditory (Eustachian) tube, secondary to a deformed septum.
CLINICAL FEATURES. Inspection of the nose will easily reveal the pathology, and
note should be taken of whether there is caudal dislocation, whether a spur is
present and whether there is any compensatory enlargement of the turbinates. The
external nose should be examined, and an assessment made of whether it is truly
midline, and if not whether the displacement is of the nasal bones alone, of the
nasal bones and the tip combined or of the tip alone. An X-ray of the sinuses
may reveal radiological changes suggestive of infection, which could account for
increasing symptoms in middle age.
TREATMENT. An assessment should be made of the degree of the patient's symptoms,
correlated with the appearance of the septal deformity. If it is decided that
surgery is indicated, the choice is between a submucosal resection and a
septoplasty operation. The essential feature of the former is removal of the
deviated section of cartilage and bone. This can be safely achieved only if it
is possible to retain an adequate depth of septal support superiorly and
caudally to maintain the position of the nasal tip. This operation therefore
remains the one of choice when there is no caudal dislocation of the septum, and
the deviation is confined to the inferior two-thirds of the cartilage.
The essential features of a septoplasty operation are to free all the
attachments of the quadrilateral (septal) cartilage, to remove the "spring" of
the deflection and to reposition it in the midline, with minimal removal of
cartilage or bone. It is therefore indicated in patients with caudal dislocation
of the cartilage, and as a cosmetic procedure where there is associated
displacement of the tip of the nose. When deviation of the nasal bones is also
present, or a hump or saddle deformity is present, it forms part of a
septorhinoplasty. A septoplasty can be safely carried out in children, whereas a
submucosal resection operation is contra-indicated until growth of the facial
skeleton has ceased.
Folliculitis of the nasal vestibule (sycosis) and nasal furuncle.
SYMPTOMS. Increasing pain, marked sensitivity to pressure, and feeling of
tension in the tip of the nose is followed by reddening and swelling of the tip
of the nose, of the nasal ala, and of the upper lip. The area becomes edematous,
and the patient may have a fever. The swelling may begin to resolve before
suppuration occurs. Otherwise, a typical furuncle forms, containing pus and a
central necrotic cove.
PATHOGENESIS. A pyodermia, usually due to staphylococcal infection, arises from
the hair follicles of the nasal vestibule of the upper lip, often close to the
nasal tip. The disease is always limited to the skin and never affects the
mucosa.
TREATMENT. Antibiotic creams are applied to the nasal vestibule as long as the
disease remains a circumscribed folliculitis. Manipulation on the nose is
forbidden. If it is suspected that a furuncle is forming, high-dose oral or
parenteral antibiotics are given, possibly combined with local antibiotics. They
must be continued for several days after the symptoms have subsided (do not
discontinue too early or use too low dosage)! It may be necessary to prescribe a
fluid diet and voice rest to immobilize the tip of the nose and upper lib. Soaks
of alcohol or ice water are used on the external nose. It may be necessary to
admit to the hospital in severe cases.
A furuncle on the nose or upper lip must never be squeezed because of the danger
of spreading of the infection and of complications such as thrombophlebitis and
cavernous sinus thrombosis. The veins of the nose and upper lip drain to the
venous system of the neck via the facial vein, but also drain via the angular
and ophthalmic veins through the orbit to the cavernous sinus. It is important
to use Heparine for prophylactic of sinus thrombosis.
Acute rhinitis
Symptoms. Since the common cold may be due to different organisms, the symptoms
are not uniform. In the common form, there is a dry prodromal stage with
generalized symptoms including chills and a feeling cold alternating with a
feeling of heat, headache, fatigue, loss of appetite, possibly subfebrile
temperature, but often a high temperature in children, as well as itching,
burning, a feeling of dryness in the nose and throat, and nasal irritation. The
nasal mucosa is usually pale and dry. The catarrhal stage usually a few hours
later with watery secretions, nasal obstruction, temporary loss of smell,
lacrimation, rhinolalia clausa, and worsening of constitutional symptoms. The
nasal mucosa is deep red in color, swollen, and secretes profusely. After
several days, the disease changes to a mucous phase. The generalized symptoms
begin to improve, the secretions thicken, the sense of smell improves, and the
local symptoms gradually regress. Resolution should be achieved within a week.
Secondary bacterial infection may occur. The secretion are then greenish-yellow,
and the disease resolves more slowly.
Initial catarrh occurs in influenza and infection with other types of viruses
such as parainfluenza, adenovirus, rheovirus, coronavirus, enterovirus,
myxovirus, and respiratory syncytial virus. The symptoms are as described above,
but are complicated by other manifestations such as involvement of the entire
respiratory tract, the gastrointestinal tract (causing diarrhea), the menings,
the pericardium, the kidneys, and the muscles.
Pathogenesis. The infection is caused by a rhinovirus. More than 100 types have
been isolated, belonging to the Picorna group. The disease may also be caused by
numerous other viruses. The incubation period of the rhinovirus is from 1 to 3
days. The disease is spread by droplet infection and is potentiated by cooling
of the body.
Diagnosis. Initially, it is often not clear whether catarrh is the initial
symptom or an accompanying symptom of a severe virus infection.
Treatment. There is no treatment for the basic cause. Symptomatic treatment
includes decongestant nose drops or oral decongestants. Antibiotics should only
be given for secondary bacterial infection, and culture and sensitivity tests
should be taken first. Steam inhalations, treatment with infrared lamps, and
analgesis and bed rest should be prescribed if necessary.
CHRONIC RHINITIS
Chronic catarrhal rhinitis
SYMPTOMS. The main symptom is nasal obstruction that fluctuates markedly in the
early stages and also alternates from side to side. Later, it is continuous and
severe and usually affects both sides. The secretions are tough, stringy,
colorless, and only rarely purulent. Postnasal catarrh is particularly prominent
with sniffles and compulsive clearing of throat. Other symptoms include
rhinolalia clausa, epiphora, secondary dacryocystitis, and secondary
pharyngitis. In severe cases, fatigue, sleeplessness, an unsteady or woozy
feeling in the head, and, occasionally, headache and a felling of pressure in
the head may occur. There is a general loss of psychological and physical
well-being.
PATHOGENESIS. Many causal factors are possible such as recurrent acute
inflammation with gradual irreversible to the mucosa; infection in the sinuses,
obstruction of nasal drainage due to enlarged adenoids or a nasopharyngeal
tumor, chronic inflammation due to tobacco smoke and dust, chemicals, acquired
toxins, persistent extremes of temperature, excessive and abnormal humidity.
DIAGNOSIS. The disease is long-standing, and the history often shows one or more
of the toxins named above. Examination shows a dark red and partially
bluish-violet swelling, affecting the inferior turbinate especially. The nasal
lumen is narrowed or obstructed. The thickened mucosa responds to decongestant
nose drops.
TREATMENT. Conservative. Any known or suspected etiologic agents should be dealt
with. Some medicines may need to be curtailed, drug overuse controlled, and the
patient may need endocrinologic investigation by an internist. Attention to the
environment and occupation may prove valuable. Symptomatic medical treatment by
decongestant nose drops, etc., is only of short-term benefit. In the long term,
uncritical symptomatic treatment not only is valueless but is even damaging.
Allergic rhinitis
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