Inflammatory diseases of the eustachian tube should be dealt with. These

diseases include septal deformity, hypertrophy of the turbinates, and adenoidal

hypertrophy. Immediate tympanotomy should be carried out for barotrauma with

severe sensorineural deafness to allow the round window to be assessed so that a

possible rupture of the round window membrane can be repaired.

Acute acoustic trauma

There is an important basic difference between explosion and gunfire injuries.

The physical-acoustic properties of an explosion are qualitatively identical to

those of gunfire but are completely different quantitatively. In an explosion

there is a high-pressure wave but the shock wave lasts more than 1,5 ms. where

as with gunfire the peak of the pressure wave lasts less than 1,5 ms.

Symptoms. In blast trauma there is marked persistent earache, occasionally

bleeding from the affected ear, deafness, and tinnitus.

In gunshot trauma there is a short stabbing pain in the ear, a marked continuous

tinnitus, and deafness.

Pathogenesis. In both explosion and gunshot trauma, the cause is partly a direct

and mechanical one due to bleeding and partly an indirect metabolic effect on

the microcirculation causing partially reversible damage to the sensory cells of

the organ of Corti. In explosion trauma, ruptures of the tympanic membrane and

other middle ear lesions often occur.

Diagnosis. Only explosion injury causes abnormal otoscopic findings: also the

audiogram shows a sensorineural or mixed deafness. In gunshot trauma, there is a

notch at 4000 Hz, or a high-tone loss, and positive recruitment.

Treatment. Low-molecular-weight dextran is infused intravenously within 24 h of

the trauma if possible. A tympanoplasty must be carried out for middle ear

injuries.

Course and prognosis. Traumatic middle ear lesions usually heal without

complications or can be reversed by operation. The prognosis is good.

Inner ear lesions are partially reversible, but in certain patients there is

continuing degeneration of sensory cells and secondary increased degeneration of

the peripheral neurons.

Chronic noise trauma to the inner ear

In contrast to acute acoustic trauma, this disease is the result of damage to

the inner ear by weaker but more prolonged noise. Therefore, the severity of the

lesion depends not only on the sound pressure peaks of the noise, but also on

the exposure time and on the individual patient's sensitivity to the effect of

noise. Emotional factors also play a considerable part and produce autonomic

symptoms which have deleterious effects on the entire body.

Symptoms. Subjectively, there is a feeling of pressure in the ears and in the

head, a feeling of deafness, generalized tiredness and lack of concentration,

and often tinnitus. The subjective symptoms are often reversible since the

patient becomes used to the noise. Few patients are aware of the developing

deafness in the early phases. Objectively, a pure-tone audiogram initially shows

a notch at 4000 Hz, typically in both ears in chronic noise trauma. Later the

threshold for the lower frequencies rises, and finally the deafness spreads to

the speech frequencies. Further loss of hearing follows as a result of the

physiologic aging process. In the early phases of its development, chronic noise

deafness shows a certain tendency to recover when the patient is no longer

exposed, but with increasing exposure this ability decreases.

Pathogenesis. The ear may react to sounds depending on the intensity and

duration of exposure, in one of the following ways:

1. A physiologic adaptation of threshold may develop.

2. After more prolonged exposure, the ear may react by fatigue or by the

appearance of a temporary threshold shift (TTS), which can be related directly

to acoustic damage which is proportional to the exposure time and which has a

linear relationship with the sound intensity. The "physiologic" TTS usually

recovers within minutes and at the most 2 h after the end of exposure to the

noise.

3. A permanent threshold shift (PTS) may develop which is an expression of

pathologic fatigue and irreversible damage to the hearing organ. It is caused by

a metabolic decompensation of the sensory cells due to a disturbed balance

between supply and demand of energy metabolism. This is determined by increased

oxygen consumption or by decreased supply during permanent intensive acoustic

irradiation. The outer hair cells degenerate first, and the inner cells last.

Diagnosis. The deafness is of long standing, and a social history reveals

occupational or lifelong social habits which are responsible. A pure-tone speech

audiogram is important.

Differential diagnosis

Endogenous heredodegenerative sensorineural deafness in which there is a

positive family history

Infective-toxic damage to the inner ear and auditory nerve, particularly by

ototoxic antibiotics

Progressive sensorineural deafness in severe generalized diseases such as

diabetes, chronic nephritis, and hypertension

The limits of noise causing damage to the ear are as follows:

Equivalent continuous sound pressure in the range 85 to 90 (±2,5) dB and higher

must be regarded as damaging to the ear.

Single sound impulses exceeding a peak of 135 dB also damage the ear.

Treatment. Active methods of treatment to deal with the cause are not available.

If hearing in social situations becomes inadequate, a hearing aid should be

prescribed. Prophylaxis including the provision of hearing protectors is very

important.

Protection of hearing:

Elimination or reduction of noise by technical improvements to machinery

Protection of personnel against noise by ear protectors

Limitation of the time of exposure to noise and frequent rest periods

Medical prophylaxis against damage to the hearing prescribed by occupational

medical health personnel

Course and prognosis. The disease progresses to advanced deafness if protective

measures are ignored.

INJURIES TO THE NOSE AND FACE

Direct injury to the nose is common. It frequently occurs in sport, in falls in

toddlers, children and adults, and in motor accidents and criminal assaults.

In children fracture of the nasal bones is uncommon, when one considers the

frequency with which they injure their noses. Toddlers often fall while learning

to walk, with consequent injury, and children may suffer injury to the face in

falls, or by being struck by a swing. They may suffer extensive bruising with

ecchymosis, and not infrequently there is a subperiosteal effusion of blood over

the nasal bones, giving rise to a swelling which absorbs only slowly, and which

may leave a permanent unilateral deformity. In children, too, the cartilaginous

nasal septum may become dislodged, either out of its sulcus in the columella, so

that there is a caudal dislocation into the anterior nares, or out of its

attachment to the nasal crests of the maxillary or palatine bone, so that it

becomes deviated to one side or the other. If this dislocation is diagnosed

early enough following the accident, the cartilage may be repositioned under

anaesthesia. Again, children more frequently develop a septal haematoma or

abscess than a fracture of the nasal bones.

Fracture of the nasal bones

A direct blow to one side of the nose of sufficient force will produce a

fracture of the nasal bones with external deviation to the other side. The bone

on the side of the blow is fractured more posteriorly than the contralateral

nasal bone, so that the latter becomes impacted beneath the former. A glancing

blow tends to fracture the nasal bones at a similar anteroposterior level,

giving rise to a deviated hump deformity. A direct blow to the front of the nose

splays out the nasal bones, and impacts them on the nasal processes of the

maxilla, giving rise to a depressed bridge to the nose.

Any injury of sufficient force to cause a fracture of the nasal bones will