confluent. Ulceration takes place, leaving a snail-track ulcer of a dirty grey
colour. The cervical glands are enlarged, and there may be a skin eruption.
Tertiary syphilis does not appear as a gumma for some years after the initial
infection. A hard purplish swelling appears on the palate, posterior between the
epiglottis and the tongue, and so be overlooked unless a breaks down at its
centre to form a punched-out ulcer with a greenish-yellow base and red,
indurated edges.
Postsyphilitic complications are much less often seen now. They were prone to
follow hereditary syphilis when they appeared about the age of be considerable
cicatricial stenosis of the pharynx.
Symptoms. The chancre may not cause any symptoms. Secondary lesions cause only
slight pain in the throat, although some dysphagia may be felt when ulceration
takes place. Pain is rare in the tertiary lesions, and the patient may only
complain of a nasal speech or of food entering the nose while eating.
Diagnosis. It must be made from other lesions causing ulceration or membrane
formation. The primary and secondary stages are usually recognized, but the
gumma may be confused with Vincent’s infection or with carcinoma. Serological
tests and a biopsy will generally decide the question. Lupus also causes
destruction of the pharyngeal mucosa, but is more slow and is associated with
skin nodules.
Treatment. Treatment is that of syphilis, and should be undertaken by a
venerologist. Local hygiene is necessary and the highly contagious nature of the
mucuous patches must be explained to the patient.
TUBERCULOSIS
Laryngeal Tuberculosis
Symptoms. They include hoarseness and coughing persisting for several months and
pain on swallowing radiating to the ear.
Pathogenesis. Tuberculous laryngitis is almost always secondary to active
pulmonary tuberculosis. The infection is transmitted to the larynx by bacillae
contained in the sputum. The posterior part of the larynx, the interarytenoid
area, and the epiglottis are those most commonly affected. There is a danger of
perichondritis. Monocorditis may also be caused by a miliary tuberculous
deposit.
Diagnosis. Microlaryngoscopy in fresh cases initially shows reddish-brown
submucous nodules which are partly confluent. Later ulcerations or granulations
develop. Monocorditis is characterized by redness and thickening, occasionally
with small ulceration of one vocal cord. Other investigations include histology,
culture, radiography, and examination by an internist.
Differential diagnosis. It includes vasomotor monocorditis, nonspecific chronic
laryngitis, and carcinoma.
Treatment. Antituberculous treatment is given in cooperation with a chest
physician. Pain is treated by blocking the superior laryngeal nerve. The patient
must be isolated, and contacts are investigated. The disease is reportable.
Course and prognosis. Laryngeal tuberculosis is infectious. Mucosal lesions
often heal with no permanent effects on laryngeal function, but if the
tuberculosis has affected the laryngeal cartilaginous framework defects arise
during healing. The prognosis currently is good.
Tuberculosis of the pharynx
Acute miliary tuberculosis is the most common variety found in the pharynx, but
is a rare complication of the pulmonary lesion. It is characterized by minute
grey or yellow tubercles on the fauces or palate. These rapidly break down into
shallow ulcers which spread widely in the mouth and pharynx to cause pain on
swallowing, excess salivation, a throaty voice and rapid emaciation. The
diagnosis must be made from syphilis, in which pain is absent, and from
diphtheria, which is excluded by a throat swab and by a biopsy from the edge of
the ulcer. Treatment is by antituberculous therapy. The prognosis is improving,
but the miliary nature of the condition calls for a guarded outlook.
Tuberculosis of the Tonsil
Tuberculosis of the tonsil is now extremely rare, and it presents no
characteristic features. Attention is drawn to the tonsils by the diagnosis of
tuberculous cervical glands. The tubercle bacilli are presumed to reach the
glands via the tonsils, which may or may not remain infected. There is no means
of diagnosing this by clinical inspection, and the condition is discovered by
histological examination after tonsillectomy. This is the more unfortunate
because half of the tonsils so sectioned do not show evidence of tuberculosis.
It is, however, sound surgical practice to remove the tonsils from children who
have a tuberculous cervical adenitis rather than to leave potentially infected
tonsils in situ. Full antituberculous therapy should be started when the
diagnosis is made in the glands.
Lupus Vulgaris and Tuberculosis of the Nose
Lupus vulgaris is the name given to a slowly growing, indolent deep-skin
ulcerative condition caused by Mycobacterium tuberculosis which affects the
nasal vestibule, the septum and the ala. It is more common in females than
males, and is more often encountered than frank tuberculosis of the nasal
mucosa. If untreated it is slowly destructive, and can lead to gross and
embarrassing deformity. Tuberculosis of the respiratory part of the nose gives
rise to granulation tissue and ulceration with sanguineous mucopurulent
discharge.
Diagnosis. All granulomatous lesions of the nose, whether of the skin or the
mucosa, must be submitted for pathological examination. Sometimes the
histological picture is so characteristic that a firm diagnosis can be made, but
in cases of doubt material should be submitted for bacteriological culture for
M. Tuberculosis, and some help can also be obtained by carrying out a weak Heaf
test. There is frequently evidence of tuberculosis elsewhere in the body.
Treatment. It depends on the sensitivities of the organism, and usually takes
the form of a combination of two or more of the following drugs – streptomycin,
PAS, isoniazid, rifampicin and ethambutol.
Part 10
TRAUMAS, FOREIGN BODIES, HEMORRHAGES
IN THE EAR, NOSE, PHARYNX AND LARYNX
AND EMERGENT AID
TRAUMAS OF THE EAR
Trauma of the external ear
Every injury to the auricle and cartilaginous part of the external auditory
meatus may damage the perichondrium causing cartilaginous necrosis. Furthermore,
bacterial infection can cause perichondritis with partial or complete
destruction of the cartilaginous framework leading to a cauliflower ear or
atresia of the meatus. Patients with partial or complete amputation of the
auricle should be admitted immediately to the hospital along with the severed
part of the auricle. Even large, completely severed parts of the auricle may be
resutured by appropriate reconstructive techniques, provided the interval
between the injury and the operation does not exceed 1 h.
Sharp and blunt trauma requires extensive debridement, primary suture, and
antibiotic cover.
Hematoma of the auricle. This arises from closed blunt injury with dissection of
the skin and perichondrial layer from the cartilage, and the formation of a
subperichondrial hematoma.
Symptoms. Swelling on the lateral or medial surface of the auricle which may
have a bluish tinge and considerable pain is experienced.
Treatment. A wide incision is made along the anterior edge of the helix, and
necrotic tissue is removed by curettage. If necessary, a window is made in the
cartilage to allow the two perichondrial surfaces to adhere and to prevent
further accumulation of blood and serum between the cartilage and the
perichondrium. An oiled silk compression dressing is used for 1 week, and
antibiotic cover is given.
Repeated aspiration may cause a seroma or superinfection leading to
perichondritis.
If a hematoma is not treated, connective tissue organization, secondary
calcification, and deformity of the auricle occur leading to a cauliflower ear.
Frostbite
Grade 1 - cyanosis of the skin due to vascular spasm
Grade 2 - ischemia with formation of vesicles
Grade 3 - deep necrosis of tissue
Treatment. Sterile dressings, antibiotics, intravenous vasodilators. The part
must be kept dry.
Burns require the same treatment as burns of the skin; particular attention must
be paid to the close relationship between the skin and the cartilage.
Late complications include necrosis of the auricle and atresia or stenosis of
the external auditory meatus.
Temporal bone fracture
Pathogenesis. Direct fractures are caused by the effect of external violence
concentrated on a small surface, e.g., by gunshot wounds. The result is a
penetrating perforating fracture with brain damage. Indirect fractures are due
to diffused external violence. The course of the fracture may run either: (1)
along the pyramidal axis (i.e., a longitudinal fracture) extending into the
middle ear; (2) across the pyramid axis (i.e., transverse fracture) extending
into the bony labyrinth and the internal auditory meatus. In both cases the dura
may be torn, producing an open connection between the pneumatic system of the
temporal bone and the subarachnoid space of the cranial fossae. The patient is
then in danger of a latent infection ascending via the eustachian tube to the
meninges.
Symptoms of the longitudinal pyramidal fractures (mainly affecting the middle
ear):
- Hemotympanum.
- Tearing of the tympanic membrane.
- Bleeding from the external auditory meatus.
- A break in the contour of the anulus tympanicus.
- Step formation in the external auditory meatus, which should be differentiated
from posterior displaced fracture of the mandibular condyle.
- Middle ear deafness.
- Facial paralysis in about 20% of patients.
- Occasionally CSF otorrhea.
Diagnosis. This rests on otoscopic findings, radiographs including Schueller’s
view, tomograms, and possibly CT in patients with facial paralysis or CSF
otorrhea.
Symptoms of the transverse pyramidal fractures (mainly affecting the inner ear):
- Intact external auditory meatus.
- Intact tympanic membrane, possibly with a hemotympanum.
- Hearing loss.
- Vertigo.
- Spontaneous nystagmus beating to the healthy ear.
- Facial paralysis in about 50% of patients.
- Cerebrospinal fluid leak via the eustachian tube to the nasopharynx.
Diagnosis. This is based on otoscopic and functional findings, radiographs in
Stenver’s view and tomograms.
Treatment of longitudinal and transverse pyramidal fractures. The treatment is
dictated by the ever-present danger of otogenic meningitis. Therefore,
prophylactic antibiotics are given consisting of high-dose, long-term parenteral
broad-spectrum agents.
The temporal bone must be explored for early or late complications.
Indications for early otologic intervention:
- Early meningitis, treated by mastoidectomy.
- Bleeding from the sinus, treated by opening of the mastoid and packing or
ligature of the sinus.
- Persistent CSF otorrhea, treated by repair of the dura.
- Facial paralysis, treated by decompression.
- Depressed fracture of the external auditory meatus, treated by reconstruction
of the meatus because of the danger of secondary atresia.
- Gunshot wounds of the temporal bone, treated by debridement of the fragmented
area.
Indications for late otologic intervention:
- Antibiotic-resistant traumatic otitis media.
- Chronic mastoiditis, treated by mastoidectomy.
- Late facial nerve paralysis with symptoms of denervation, treated by facial
nerve decompression.
- Posttraumatic deafness, treated by tympanoplasty.
- Posttraumatic cholesteatoma, treated by radical mastoidectomy and
tympanoplasty.
Emergency surgery must certainly be carried out, as soon as the general
condition of the patient permits, for the indications detailed above.
Course and prognosis. The following complications are possible, especially as a
result of unsatisfactory treatment or missed diagnosis:
Early complications:
- Acute otitis media with mastoiditis.
- Extension of the above infection to the subarachnoid space causing early
meningitis or an infected labyrinthitis extending to the meninges.
Late complications:
- Chronic otitis media with mastoiditis.
- Late otogenic meningitis.
- Subdural abscess.
- Otogenic brain abscess.
- Posttraumatic cholesteatoma.
Labyrinthine concussion
Posttraumatic disorders of the inner ear function (deafness and dizziness) in
the presence of normal otoscopic and radiographic findings are included under
the term labyrinthine concussion.
Symptoms. These include tinnitus, unilateral or bilateral sensorineural deafness
with positive recruitment and high-tone loss or a notch at 4000 Hz, dizziness
especially on change of position or rapid movements of the head, and disorders
of balance.
Pathogenesis. This disease is usually due to organic mechanical damage to the
membranous labyrinth similar to acute acoustic trauma. Microfractures of the
labyrinthine capsule accompanied by bleeding into the peri- and endolymphatic
space and mechanical disturbances of the microcirculation causing degeneration
of the cochleovestibular sensory cells may also occur.
Diagnosis
Normal otoscopic findings
Normal radiographs in Schueller's and Stenver's views
A pure-tone audiogram showing a sensorineural deafness with a notch at 4000 Hz
or high-tone loss with recruitment
Vestibular provocation nystagmus in the presence of vertigo, and more rarely
spontaneous nystagmus, possibly reduced sensitivity to caloric stimulation
Differential Diagnosis
Acute acoustic trauma in which vestibular symptoms are absent
Posttraumatic psychogenic hearing loss in which the findings are inconsistent
and vestibular symptoms absent
Treatment. It includes intravenous low-molecular-weight dextran infusion,
provided that there is no general contraindication, e.g., hypertension or
allergy. Antivertiginous drugs are given for dizziness.
Course and prognosis. The disease usually settles rapidly in young patients and
those with normal circulation. Otherwise, the symptoms, especially those of loss
of cochlear function, only resolve incompletely. Irreversible vestibular defects
are compensated centrally. Cochleovestibular symptoms, especially dizziness,
often progress in elderly patients.
Direct injures to the middle and internal ear
Symptoms. Injury of the tympanic membrane is accompanied by momentary pain,
slight bleeding from the ear, and modest deafness.
In middle ear injuries, there is profuse bleeding, pain and deafness, a
pulsating sound in the ear, and occasionally facial paralysis.
In inner ear injuries, there is immediate tinnitus, deafness, dizziness, nausea,
and vomiting.
Pathogenesis. Damage to the tympanic membrane and the middle and internal ear
may be caused by introduction of pointed objects such as matchsticks,
toothpicks, knitting needles, hairpins, and twigs into the ear, by careless
removal of foreign bodies, by occupational injuries (hot cinders, welding
sparks), by acid burns, or by gunshot wounds.
Diagnosis. Otoscopic findings include a tympanic membrane perforation with
jagged, frayed, blood-streaked, and occasionally inrolled edges. Blood is found
in the external auditory meatus mixed with perilymph in injuries to the inner
ear. Conductive deafness is found in middle ear injuries, sensorineural
deafness, or mixed deafness if the inner ear is involved, and in severe lesions
there is complete deafness and spontaneous nystagmus to the sound side. An
immediate total peripheral facial nerve paralysis is found in fractures
involving the bony tympanic segment of the facial nerve canal.
A bullet may be localized by radiographs in Schueller's or Stenver's view or by
tomograms.
Treatment. In simple tympanic membrane rupture, the fragments of the membrane
are repositioned and splinted aseptically under the operating microscope.
Systemic prophylactic antibiotics are given.
Warning: Unsterile instruments should not be used in the ear, and the ear should
not be syringed.
Combined injuries of the tympanic membrane, middle ear, and inner ear are
subjected to immediate exploration of the middle ear cavity and labyrinthine
capsule under the operating microscope (tympanoplasty). A perilymph leak, e.g.
from the round window, is stopped by closing the labyrinthine fistula.
Prophylactic antibiotics are given. A simultaneous facial nerve paralysis is
treated by decompression of the facial nerve.
Course and prognosis. Simple injuries of the tympanic membrane and middle ear
usually heal smoothly and without functional deficit if they are treated in the
correct manner by an otologist. Involvement of the labyrinth is usually followed
by irreversible cochleovestibular failure. The prognosis for the facial
paralysis is very good if continuity of the nerve has been preserved.
Barotrauma
Symptoms. They include acute pain, pulsating noise in the ear, deafness, and
occasionally vertigo and disturbance of balance.
Pathogenesis. Sudden changes in air pressure, producing an absolute or relative
reduction of pressure in the middle ear, cause bleeding into the middle ear
mucosa and into the tympanic membrane, and on occasion even rupture of the
tympanic membrane and of the round window membrane. This may occur after rapid
decompression or recompression from a low- or high-pressure chamber, a rapid
dive from a great height in a nonpressurized aircraft, or after surfacing too
quickly from deepsea diving.
The disease is caused by a sudden closure of the tube which is compressed by the
rapid rise of atmospheric pressure or by the associated increase of tissue
pressure. After about 2 h of closure of the tube, the Valsalva maneuver and
politzerization are ineffective since mucosal edema and serous-hemorrhagic
exudate of the middle ear cavity have occurred due to the reduced pressure in
the middle ear. This disorder is called aero- or barotitis.
Diagnosis. This is made from the history, from the otoscopic findings which show
retraction of the tympanic membrane, occasionally subepithelial hemorrhage in
the pars tensa, transudate behind the tympanic membrane, or a hemotympanum, and
from the finding of conductive deafness.
Treatment. It includes decongestant nose drops, catheterization of the tube,
possibly paracentesis, analgesics, and oral anti-inflammatory agents.
Prophylaxis is important by avoiding flying and diving during inflammation of
the nasopharynx, nose, and paranasal sinuses. Anatomic deformities in the nose
and nasopharynx obstructing nasal respiration and favoring the development of
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
inevitably cause considerable soft-tissue swelling. This becomes marked very
quickly and resolves about 10 days after the injury. This soft-tissue swelling
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