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Recommended by the Ministry of Public Health of Ukraine as a textbook
for students of institutions of higher medical education of the 4th
level of
accreditation, who master the discipline in English
1
2
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Authors: Y. Mitin, Y. Deyeva, J. Gomza, V. Didkovsky, L. Krinichko, A. Motailo, G.
Tereschenko, Y. Shevchuk
The main questions of diseases of the ear, nose, and throat are examined in the
textbook. The anatomy, physiology, pathology and treatment of ENT diseases are
described.
The classic and modern data of scientific investigations in different branches of
otorhinolaryngology are given.
The textbook is for students of institutions of higher medical education (the 3rd
–
4th
level of accreditation).
4
CHAPTER 1
General description and history of otorhinolaryngology
Otorhinolaryngology is a clinical discipline, which studies the morphology,
physiology and pathology of the ear, upper respiratory tracts and adjacent areas. The
term is derived from four Greek words: otos – ear, rhinos – nose, lагуngos – larynx
and logos – studies. The first letters of the words marking the main branches of the
speciality form the abbreviation ORL or LOR (in English-speaking countries – ENT).
Otorhinolaryngology studies norms and pathology of most analyzers: auditory,
vestibular, olfactory and gustatory. Disorders in analyzers activity decrease
occupational capability and working capacity causing depression of the person.
It should be noted that otorhinolaryngology is a surgical speciality, which
encompasses a large range of operations: on the ear, nose cavity, paranazal sinuses,
pharynx, larynx, and trachea.
Development of otorhinolaryngology as a separate discipline began in the
middle of the 19th
century. Before that, the treatment of a small number of known ear
diseases was taught in the course of surgery, and of diseases of the upper respiratory
tract – in the course of therapy. Anatomico-topographical unity of the ear, throat and
nose, their physiological correlation and practical application of endoscopy methods
in ENT research were the reasons for ENT diseases joining.
It is important to know the main stages of otorhinolaryngology development. In
1841 German doctor F. Ноfmаnn suggested to examine deep areas of the ear, nose
and throat using a mirror without a small round part of amalgam in the center. Later
doctor A.F. Trolch created a frontal reflector on its basis. In 1854 M. Garsia, a Spanish
singer and one of the most prominent teachers of singing, professor of the Paris
Conservatoire and Royal Academy of Music in London (Fig. 1) offered the indirect
laryngoscopy method. By means of using a laryngeal mirror M. Garsia studied the
physiology of singer’s voice. In a year this method was introduced into practice. Then
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the methods of postnasal (1859), anterior, and middle rhinoscopy were offered. Later
direct methods were developed: esophagoscopy (Kussmaul, 1868), direct
laryngoscopy (Kirsten, 1894), bronchoscopy (Killian, 1897), respiratory
bronchoscopy (Fridel, 1956), fibrobronchoscopy (Іkedа, 1969). Otosurgery was
founded by German doctor I. Schwartze, who offered mastoid process trepanation
(anthrotomy) in his work in 1873. Puncture of the maxillary sinus through the
inferior nasal meatus was first perfomed and described by M. Schmidt in 1888.
American G.W. Caldwell in 1893 and Frenchman H. Luc in 1897 independently
worked out the method of radical surgical intervention at chronic maxillary sinusitis.
In Ukraine, due to privat-docent courses in at several universities,
otorhinolaryngology was popularized and introduced into medical practice and
education. At the medical department of the Kyivievs Ssnt. Vladimir Volodymyr
Uuniversity some ENT diseases were mentioned during lectures on surgery, therapy
and other disciplines some ENT – diseases were mentioned. So, in 1860-–1862 the
first lectures on larynx diseases were given by Ddoctor of Mmedicine I. Lazarevich,
the associate professor of obstetrics I. Lazarevych (the course name of the academic
course was The " Respiratory Ttract and Iits Partsbranches Ddiseases and Llarynx
sufferingLesions") and lectures on ear diseases were given by Professor Yu.
Shymanovsky in a course on theoretical and operative surgery. From 1864 to 1866 L.
Marovsky lectured a privat-docent course on rhinology and laryngology, in 1864 he
was elected an associate professor of diagnostics and laryngoscopy. His works were
About Croup Treatment, About Deafness Reasons etc. From 1871 to 1880 M.
Uspensky lectured a privat-docent course on otiatrics, and then from 1882 to 1884 N.
Zuk delivered the course Throat Diseases.
Mykola Volkovych (1858–1928; Fig. 2), a surgeon and otorhinolaryngologist,
professor and academician, was the first in Ukraine to begin a systematic lecture
course on otorhinolaryngology. From 1889 to 1903 he conducted an elective course
on otorhinolaryngology at the medical department of the Kyivievs Ssnt. Vladimir
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Volodymyr Uuniversity. He was one of the first, who paid proper attention to the
study of upper respiratory tracts scleroma and took an active part in the study of
etiology, pathogeny and treatment of this disease. The scientist also introduced a
surgical direction in otorhinolaryngology development. He widely performed
operations on the paranasal sinuses and mastoid process. He was the first in Russia to
publish a report on two examples of larynx extirpation in case of cancer and develop
surgical treatment of chronic larynx stenoses.
Otorhinolaryngology was also developing in Odessa, Kharkiv and other cities
of Ukraine. In 1921 otorhinolaryngology became a required subject of medical
departments of universities, which was very important for the development of the
speciality.
The otorhinolaryngology department of the Kyiv Medical Institute was
originated in 1922, when Alexander Puchkovsky became the head of the department.
He graduated from the Petersburg Military Medical Academy. The scientist made a
great contribution to the development of otorhinolaryngology in Odesa. A.
Puchkovsky was a prominent Ukrainian scientist researching scleroma, tuberculosis
of the upper respiratory tracts, ENT-oncology, reconstructive surgery. The Kharkiv
otorhinolaryngology department was founded by professor S. Surukchi (1922), in
Dnepropetrovsk – by professor S. Kompaneyets (1921), in Lviv – by professor A.
Yurash (1908).
The appearance of fundamental works since the 20–30s was a considerable
contribution into the development of otorhinolaryngology in Ukraine. S.
Kompaneyets, A. Puchkovsky, and O. Kolomiychenko studied the questions of
diagnostics and treatment of purulent otitis and concomitant intracranial
complications. M. Horshak founded a school of head and neck oncology. G.
Trombitsky, M. Pitenko and S. Kompaneyets investigated the problem of regional and
professional ENT-pathology. Works of M. Volkovich, V. Drobotko, L. Zarytsky, V.
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Yaroslavsky, A. Puchkovsky, S. Myhailovsky played a great role in the study of
etiology, pathogeny, epidemiology, diagnostics and treatment of respiratory scleroma.
In 1924 the publishing of the Journal of Ear, Nasal and Pharynx Diseases
began. In 1930 in Kharkiv the Otolaryngology Research Institute was organized,
which existed for 25 years. Here the problems of tonsillitis, nose physiology and
pathologies, prophylaxis and treatment of deafness and hearing loss were studied. In
1960 the Kyiv Research Institute of Otolaryngology was opened. Professor O.
Kolomyichenko (Fig. 3), Corresponding Member of the Ukrainian Academy of
Sciences and Lenin Prize Laureate, was the initiator and director of this institute till
1974. Professor A. Tsyhanov, State Prize Laureate, succeeded Professor O.
Kolomyichenko at this position. Since 1985 Professor Dmytro Zabolotny,
Corresponding Member of the Ukrainian Academy of Medical Science, is the head of
the institute.
According to the data of 2006, there are approximately 3,650 otolaryngology
specialists in Ukraine and ENT-departments can treat about 8,600 patients.
8
CHAPTER 2
Clinical anatomy, physiology, and methods of researching the
auditory analyzer
The auditory analyzer is divided into a peripheral section, conduction
pathways, and a cortical center. The peripheral section is divided according to its
function into sound-conducting and sound-perceiving systems.
The sound-conducting system consists of the external, middle ear, peri- and
endolymphatic spaces of the inner ear, basal and vestibular membranes of cochlea.
The sound-perceiving system is the receptor of auditory analyzer represented by the
spiral organ (organ of Corti). The sound-conducting system delivers sound to the
receptor. The sound-perceiving system transforms mechanical vibrations into a
nervous impulse.
The peripheral section of the auditory analyzer anatomically consists of three
parts: the external, middle and inner ear (Fig. 4).
The external ear consists of the auricle and external acoustic meatus. The
auricle collects and directs sound waves into the external acoustic meatus. The
external acoustic meatus deliveres sound vibrations to the ear drum (tympanic
membrane). The external ear is innervated by the branches of the 5th
, 7th
and 10th
cranial nerves.
The middle ear consists of an air cavities system represented by the tympanic
cavity, mastoid process cells and auditory tube (otosalpinx) (Fig. 5).
The tympanic cavity has six walls. The external wall of tympanic cavity is the
eardrum, the internal one is the lateral wall of the inner ear, the superior wall is the
tegmental wall separating the tympanic cavity from the middle cranial fossa, the
inferior wall is a bone separating the tympanic cavity from the bulb of jugular vein.
In its middle the internal wall has a peak (promontory) formed by the base of cochlea.
Behind and above the promontory the oval window is located, which is closed by the
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base of stapes. Under and behind the peak there is a round window closed by the
secondary tympanic membrane.
In clinical practice the tympanic cavity is divided into 3 floors: the superior one
is epitympanum, the middle one – mesotympanum, and the inferior one –
hypotimpanum. The epitympanum is situated above the short malleus process (lateral
process); the mezotympanum is between the short process and the inferior wall of
external acoustic meatus; the hypotimpanum is a small cavity located below eardrum
attachment.
There are auditory ossicles (malleus, incus, stapes) and muscles in the drum
cavity, which form an anatomically and functionally united system. The malleus is
very tightly fixed with the manubrium to the eardrum, and its head is united with the
incus by means of an articulation and a ligament. The incus attaches to the head of
stapes with its long limb. The base of stapes is fastened in the oval window with a
round ligament. The chain of auditory ossicles decreases the amplitude of sound
vibrations and simultaneously increases the force of sound pressure on the oval
window.
The mechanism of sound conduction is realized due to the muscles of drum
cavity: m. tensor tympani and m. stapedius. These muscles have two functions:
adaptative and protective. The adaptive function is conditioned by reciprocal
innervation: if one muscle contracts, the other relaxes reflexively.
During muscle traction of tensor tympani the m. stapedius relaxes. It results in
the retraction of the eardrum into the tympanic cavity and pressure of the bases of
stape on the labyrinth. This causes an increase of internal labyrinth pressure and
prevents low and weak sounds penetration into the internal ear.
Due to reduction of m. stapedius and weakening of m. tensor tympani, the
stapes are pulled out to the drum cavities, which reduces internal labyrinth pressure. It
is an obstacle for the transmission of higher sounds but facilitates low and weak
sounds conduction. The protective function of these muscles is realized by
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simultaneous tetanic reduction of both muscles when very loud sounds take place. It
protects the labyrinth from loud acute sounds, because during this reduction the base
of stapes begins to turn round close to its longitudinal axis, but does not move inside
the internal ear.
The auditory tube (otosalpinx) is important in the mechanism of sound
conduction. This is the only organ, which connects the middle ear cavity with the
environment. The otosalpinx is a narrow canal, 30–38 mm long, which begins in the
front wall of drum cavity and ends with a pharyngeal opening in the cavity of the
nasal part of throat at the level of the back-end of inferior nasal concha. The auditory
tube consists of cartilaginous and bony parts. It balances the pressure in the tympanic
cavity. The otosalpinx is usually closed, it is opened during swallowing and yawning,
as a result air gets into the drum cavity. This function of the otosalpinx is named
barofunction. The otosalpinx performs two functions: draining and protective. The
protective function is realized by the stratified ciliated epithelium. The cilia blink in
the direction of the pharyngeal opening and that removes foreign parts from the
otosalpinx mucosa.
The mastoid process located abehind the auricle is a part of the temporal bone.
It contains a number of air cells, the biggest one called antrum. Mastoid air cells are
covered with the fibrous tunic with pavement epithelium. Air cells unite with one
another and also with the drum cavity.
The middle ear is innervated by branches of the facial, glossopharyngeal,
trigeminal nerves and from the carotic plexus.
The internal ear is an ear labyrinth in the thickness of temporal bone pyramid.
The ear labyrinth may be divided into three parts: the front part is the cochlea, the
middle one – the vestibule, and the back part – the semicircular canals (Fig. 6). There
is a bone labyrinth with a membranous labyrinth inside which repeats the bone
labyrinth form (Fig. 7). The membranous labyrinth is a sac containing high-
potassium, low-sodium fluid (endolymph). There is low-potassium and high-sodium
11
fluid (perilymph) between the bone labyrinth wall and the membranous labyrinth
wall. Within the cochlea there are three fluid-filled spaces: the scala media (filled with
endolymph), the scala tympani, and the scala vestibuli (both filled with perilymph).
The internal fluid spaces of the saccule, utricle, and semicircular ducts contain
endolymph. The vestibule contains two bony depressions – the spherical recess holds
the saccule, and the elliptical recess holds the utricle. The saccule and utricle consist
of supporting and hair cells covered with gelatinous otolithic membrane, which
contains a number of small calcium phosphate crystals (otoconia). There are three
semicircular canals – anterior, posterior and lateral. Each semicircular canal contains a
semicircular duct that has an ampullated and a nonampullated ends joined within the
utricle. The cochlea consists of 2 ½ turns, with a total average length of 32 mm. The
vestibular membrane separates the scala vestibule from the scala media, and the basic
membrane separates the scala media from the scala tympani. The receptor of the
auditory analyzer is the spiral organ (organ of Corti), wich is located on the basic
membrane. The spiral organ is a complex structure consisting of supporting cells,
three layers of outer hair cells and a single layer of inner hair cells. The hair cells
carry out the transformation of sound irritation (mechanical vibrations) into a nervous
impulse.
The mechanism of sound conduction is the following: sound vibrations are
concentrated by the auricle in the external acoustic meatus and through it reach the
eardrum. Eardrum vibrations pass to the chain of otosteons. Vibrations of the base of
stapes pass to the liquid environment of the internal ear, through it sound vibrations
reach the spiral organ.
The primary analysis of the sound, taking place in the internal ear, divides
complex sounds into parts, due to the perception of certain frequencies by definite
areas of the spirale organ. Mechanical energy of a sound wave is transformed into
electric energy in the hair cells of the spiral organ, which leads to nervous impulse
appearance. Then this impulse passes to the peripheral processes (dendrites) of bipolar
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cells and to the spiral neuroganglion (the first neuron of the auditory way). Then the
impulse goes to the cochlear nerve (ramus n. vestibulocochlearis) and through the
pontocerebellar angle reaches the myelencephalon. Here, in the ventral and dorsal
nuclei, the second neuron lies. Then the fibre partially decussates in the pons and goes
to the olive (the third neuron). Axons of the third neuron go to the back of the tectal
plate of the midbrain tegmen and the medial geniculate body (the fourth neuron).
Fibres of the fourth neuron end in the temporal lobe. Due to the partial decussation of
the second neuron axons, each cochlea has bilateral connection with the cortex.
An adequate irritant of the auditory analyzer is sound – periodic oscillation of
environment (air) molecules. There are several principles concerning the adequate
irritant of the auditory analyzer.
The 1st
principle – the auditory analyzer perceives sound frequencies of certain
range, which is named the auditory range (volume) of human ear. A person perceives
sounds with vibration frequency from 16 to 20,000 vibrations a second. The sound
with the frequency less than 16 vibrations a second is named infrasound, more than 20
KHz – ultrasound.
The 2nd
principle – the auditory analyzer has different sensitiveness to the
sounds of different frequency. Thus, our ear is the most sensitive to the sounds from
1,000 to 3,000 vibrations a second. These frequencies are named the range of
speaking frequencies because we mainly speak on these frequencies. Perception of
sounds decreases from this optimum area. At 200 to 10,000 vibrations a second the
threshold force of sound is 1,000 times bigger than of the sounds with 1,000 to 3,000
vibrations a second.
The 3rd
principle – a man is able to distinguish the pitch of sound. If this ability
is high, we talk about absolute hearing. In addition, the human ear is able to
differentiate sound intervals (the distance between two degrees of scale) and is also
sensitive to consonances and dissonances.
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All this together with musical memory makes an ear for music. All these
abilities of musical ear are possible to be developed. Fully natural is the rhythm
feeling.
The 4th
principle – a man is able to determine the location of the source of
sound. This phenomenon is named ototopics. Ototopics is explained by the presence
of two ears, in this connection it has the second name of binaural hearing.
To understand the auditory analyzer physiology and master methods of its
research one should know that the auditory analyzer gives a possibility to distinguish
sounds by pitch, intensity, and timbre.
The pitch of sound concerns its frequency: the number of oscillations a second
and is expressed in hertzs (Hz). The intensity of sound is represented by its strength
and is expressed in decibels (dB). Timbre chatacterizes the sound and depends on
overtones, because bodies oscillate not only fully but also partially.
Inspection of the ear includes examination of the auricle, palpation of the
auricle, tragus, mastoid process, leadthrough otoscopies, and also inspection of
auditory function.
Otoscopy is executed to determinate the state of the external acoustic meatus
and middle ear. Such research is perfomed by means of a frontal reflector and ear
watering-cans of different diameter or by applying a special device – otoscope.
If otoscopy is carried out using a frontal reflector one is to look through the
reflector opening with the left eye. Light source must be on the right side of the
patient. The patient must be seated in a definite position: his head should be bent to
the shoulder, which is opposite to the examined ear. During otoscopy the axis of the
acoustic meatus must be on the visual line. One must examine the width of the
external acoustic meatus to define the proper diameter of the watering-can before its
introduction. A watering-can with a proper diameter should be chosen to prevent
unpleasant sensations of the patient. Also, the external acoustic meatus must be
cleaned before examination if it is necessary.
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The watering-can must be taken with the index finger and thumb of the right
hand for right ear examination, and with the left hand – for left ear examination. Then
the auricle is pulled up and backwards with the other hand (in little children –
downwards and backwards), and with subtle rotatory motions the narrow end of the
watering-can is brought to the external auditory meatus. All the walls are examined by
careful pushing of the watering-can into the depth of the external meatus. Due to the
change of the inclination angle of the head it becomes possible to observe the
tympanic membrane (Fig. 8). A normal tympanic membrane looks like a pearl grey
oval membrane ≈ 8×9 mm in diameter and ≈ 0.1 mm thick.
It has special features:
1) in the center of the membrane there is a convexity;
2) above the convexity there is the malleus fold, which looks like a grey strip
during otoscopy;
3) in the upper part the strip trasforms into the malleus prominence, which is
formed by the short process of malleus;
4) anterior and posterior folds spread behind and in front of the malleus
prominence;
5) during otoscopy it is possible to observe a pyramid of light – corneal reflex
(cone of light) behind and in front of the convexity; the corneal reflex arises due to
light reflection from the shining surface of the tympanic membrane exactly in the
places where surface is perpendicular to light rays, which fall from the frontal
reflector.
The methods of hearing testing can be divided into 4 groups:
- the 1st
group – testing of hearing by speech. Hearing is explored by whisper and by
speech with normal loudness. A normal ear perceives whisper at an average distance
of 6–7 m;
- the 2nd
group – testing of hearing by means of tuning forks.
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The most informative experiments are the Byng’s, Federici’s, Veber’s, Rynne’s,
Schwabach’s, and Gellee’s ones.
Testing of hearing by means of speech and tuning forks is named acumetry;
- the 3rd
group – audiometry methods – methods, which test hearing by means of
electronic apparatus (audiometers).
Depending on the patient’s participation, audiometry is divided into subjective
and objective. At subjective audiometry the result depends on the answers of the
inspected. These methods include pure-tone audiometry and superthreshold
audiometry (the Lüsher’s test and SISI test research volume function), speech
audiometry, determination of auditory sensitivity to ultrasound.
Pure-tone audiometry is the basic and most widespread audiometry method.
Audiometry results are shown in an audiogram (Fig. 9). It is a graph, the horizontal
line of which represents sound frequency in Hz, and the vertical line – sound intensity
in dB. Zero level in an audiogram is standard norm. Research results are reflected in
an audiogram as two curves, which characterize sound perception through air and
bone. Pure-tone audiometry allows defining the type of hearing disorders: sound
conducting, sound perceiving or of mixed pathology.
Results of objective audiometry do not depend on the patient’s answers. Here
belong the following methods: impedometry (registration of acoustic resistance or
impedance of the middle ear), brainstem auditory evoked potentials (computer
audiometry), electrocochleography (registration of potentials arising in the cochlea
due to sounds), otoacustic emission;
- the 4th group – the use of conditional and unconditional reflexes. Unconditional
reflexes are used for approximate determination of hearing presence in babies. In
response to loud sounds due to the auropalpebral reflex the child’s eyelids close or
blink more frequently than usually. Due to the auropupillar reflex the child’s pupil is
narrow when sound irritation takes place and dilates when sound abates.
Game audiometry is based on the formation of conditional reflexes in children.
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CHAPTER 3
Clinical anatomy, physiology, and methods of researching the
vestibular analyzer
The vestibular analyzer performs the function of equilibrium of body both in the
state of rest and during motion. The receptors located in the vestibule (otoconic
apparatus) are responsible for the function of equilibrium in the state of rest, and the
receptors of semicircular canals (ampullary apparatus) are responsible for the function
of equilibrium during motion. Together they perform the statokinematic function. The
vestibular apparatus unlike other analyzers is never in the state of rest because
gravitational force constantly acts on it.
The vestibular analyzer, as well as other analyzers, consists of a peripheral part
(receptor), a conducting part with kernels in the brainstem, and a central part.
The vestibular analyzer receptors are located in the inner ear. In the saccules of
the vestibule (utriculus et sacculus) the otoconic apparatus is located as macula
utriculi and macula sacculi. The otoconic apparatus is accumulation of
neuroepithelial or sense cells located between supporting cells. From the upper part of
the sense cells hairs detach, which interlace and form loops. Microcrystals of calcium
salts – statoconia – are located in the loops (Fig. 10). All of them are soldered with the
jellylike substance and form the otolithic membrane (membrana statoconiorum). An
impulse arises in the receptor at tangential displacement of the otolithic membrane
(that is forward and downwards, backwards and downwards, parallel to the planes of
macula).
Any force is an adequate irritant of the otoconic apparatus that can cause
rectilineal acceleration:
1) beginning or ending of steady rectilineal motion, its acceleration or
deceleration;
2) centrifugal force;
17
3) change of head or body position in space;
4) gravitational force.
The excitability threshold of the otoconic apparatus is 0.001–0.03 g (g –
acceleration of gravity, which makes 9.8 m/s²).
In every semicircular canal on one of its ends there is an ampule with an
ampullar crest. On this crest there is a receptor named the ampullary apparatus. It
consists of sense neuroepithelial cells with hairs on the upper part and supporting
cells. The hairs of sense cells are covered with jellylike substance and form a brush
(cupula terminalis), which is displaced at endolymph motions (Fig. 11). As a result of
this displacement a nervous impulse arises in the sense cells.
Angular acceleration is an adequate irritant of the ampullary apparatus. The
excitation threshold of semicircular ducts is angular acceleration of 0.12–2 m/c².
In the sense cells of ampullary and otoconic apparatus peripheral nerve fibres
(dendrites) go from the bipolar nerve cells of the vestibule to the neuroganglion
(ganglion vestibulare), located in the internal acoustic meatus. Axons of bipolar cells
form the vestibular part of the 8th
cranial nerve, which enters the brainstem through
the pontocerebellar trigone and approaches the vestibular nuclei located in the
diamond-shaped fossa of medulla oblongata. There are four vestibular nuclei on each
side: medial, lateral, superior and inferior. The nuclei are joined by commissural
fibres. The vestibular ways have not been studied higher. It is known that the cortical
part is in the anterior part of the temporal brain part.
The apparatus promotes irritation transformation into reflexes, which can be
divided into three groups.
1. Vestibulosomatic – reflexes from the vestibular apparatus on the skeletal
muscles of neck, trunk, extremities, eyes. These reflexes are identified by the
Romberg’s sign, gait, coordination tests (finger-nose, indicator, knee-heel),
nystagmus.
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2. Vestibulovegetative – reflexes from the vestibular apparatus on the smooth
muscles of internals. These reflexes declare themselves by skin redness, increased
perspiration, change of cardiac and respiratory activity, nausea, vomiting, frequent
urination.
3. Vestibulosensory – reflexes conditioned by the connection of the vestibular
apparatus with the cortex of the large hemispheres. Normally these reflexes declare
themselves by a conscious feeling of location in space, vestibular illusion of
contrarotation; at a pathology dizziness and violation of spatial feeling are observed.
Nystagmus is one of the most valuable indexes, which characterize the state of
the vestibular analyzer. Nystagmus is involuntary rhythmic repeating movements of
the eyeballs. The following varieties of nystagmus are distinguished: vestibular –
arises at irritation of the receptors of vestibular analyzer nuclei and optokinetic –
arises at irritation of the visual analyzer (looking at the object, which is moving
evenly). A slow and a rapid components are distinguished in nystagmus. The slow
component of nystagmus is conditioned by the irritation of vestibular analyzer
receptors. The slow down movement of eyes in response causes the central reaction,
and the eyes return to initial position. It is a quick component of nystagmus of cortical
genesises. Nystagmus direction is the most evidently observed after the rapid
component. Three degrees of nystagmus are distinguished: the 1st
degree – nystagmus
appears at a glance to the quick component, the 2nd
degree – at a glance to the quick
component and straight ahead, the 3rd
degree – at a glance to the quick component,
straight ahead and to the opposite side.
When down movement of the hands and trunk arises opposite to the nystagmus
direction, it is named harmonic. Harmonic down movement of the hands and trunk is
characteristic of peripheral vestibular syndrome.
Methods of researching the vestibular analyzer
19
The tests characterizing the state of the vestibular analyzer are conducted in a
certain sequence. The analysis of the test results is to be conducted paying attention to
such two moments.
1. Changes characteristic of a labyrinth pathology (peripheral vestibular
syndrome) or of a pathology of the central parts of the vestibular analyzer (central
vestibular syndrome).
2. When we come to a conclusion that we are dealing with peripheral vestibular
syndrome, we must specify if it is contingently caused by irritation (hyperreflexia) or
oppression (hyporeflexia) of the right or left labyrinth.
A vestibulometry chart includes:
1) study of complaints and disease anamnesis;
2) research of spontaneous vestibular reactions;
3) experimental tests;
4) decoding and estimation of results.
Inspection of the patient begins with a careful study of complaints and disease
anamnesis. At a pathology of the vestibular analyzer this information quite often
influences the setting of diagnosis.
Dizziness consists in specific complaints, disordered sense of balance and
violated gait accompanied by nausea and vomiting. Under dizziness we understand
seeming rotation of surrounding objects. Systematized dizziness is characteristic of
peripheral vestibular symptom complex: the patient notes that objects swim from right
to left or vice versa.
It should be noted that in connection with anatomic adjacency of the receptors
of the auditory and vestibular analyzers in the internal ear typical complaints of
peripheral vestibular syndrome are of hearing impairment and sonitus. Thus, the
peripheral vestibular syndrome is also named the cochleovestibular syndrome.
Therefore at differentiation of peripheral and central vestibular syndromes hearing
must be tested.
20
The following group of tests is directed at the research of spontaneous
vestibular reactions: spontaneous nystagmus determination, research of spontaneous
missing, firmness of static equilibrium, motions with eyes closed.
To determine the presence or absence of spontaneous nystagmus the doctor sits
down against the patient, puts the index finger on the right or on the left at the
distance of 60–70 cm from the eyes at an angle of 45°. If spontaneous nystagmus is
observed, its characteristics are determined: the plane, direction, and amplitude; it is
either clonic (only the quick component is visible) or tonic (the slow component also
becomes visible). One should avoid extremely avert stare as the patient can develop
brief nystagmus motions (end-position nystagmus).
Position nystagmus is a variety of spontaneous nystagmus. It should be studied
as follows. At first nystagmus is to be explored in the patient in sitting or standing
posture. After this the patient is examined lying on the back, lying on the left and right
side, and lying on the back with the head thrown back. The doctor notes in what
position of the head nystagmus appears in the patient, changes of nystagmus
parameters depending on the position of the head. Position nystagmus can be of
peripheral and central origin. Nystagmus with abrupt changes of direction, rhythm
and amplitude regardless of the patient’s position is characteristic of central vestibular
syndrome.
Research of pressure nystagmus is of great value. Its onset is usually related to
the destruction of the bony labyrinth capsule at purulent otitis media, that is to the
labyrinth fistula. Therefore this phenomenon is also named the fistula symptom. The
bone defect, which has appeared, opens the membranous labyrinth. The change of
pressure in the external acoustic meatus and drum cavity is passed onto its wall
causing displacement of the endolymph and irritation of the vestibular analyzer
receptors.
This test is conducted as follows. The doctor sits down against the patient, who
is looking straight ahead. The doctor presses on the tragus with the index finger to the
21
right and to the left in turn. If the labyrinth is in normal condition, nystagmus is not
observed. If there is a fistula in the lateral semicircular canal, nystagmus is observed
accompanied by imbalance, nausea or vomiting.
The tests, which allow exposing spontaneous missing, are important tests of
determining spontaneous vestibular disorders, disturbance of static balance and gait.
The following tests are simple and informative: the test of outstretched arms,
indicator, finger-nose, and “writing test”.
The test of outstretched arms is conducted as follows. The patient is sitting with
the eyes closed and stretches the arms out in front of him.
The index fingers are aimed straight, the other fingers make fists. The doctor is
sitting against the patient holding the index fingers against the patient’s fingers,
observing the motions of the latter. A healthy man holds hands in such position
without any substantial displacements during a long period of time. A patient with a
labyrinth pathology moves both arms toward the slow nystagmus component
(harmonious deviation). At a pathology in the posterior cranial fossa the arm on the
affected side deviates to the side or inwards, on the unaffected side the arm keeps the
given position; in such a case nystagmus is directed to the side of affection
(disharmonious deviation).
The pointing test also characterizes the state of coordination. During this test
the patient is sitting holding the hands on the knees. At first with the eyes opened, and
then – closed he must touch with the index fingers the doctor’s index fingers. If a
labyrinth pathology is observed, the patient will miss in the direction of the slow
nystagmus component with both hands. Disharmonious declination of one hand
characterises central vestibular syndrome.
The finger-nose test is a variety of the pointing test. At labyrinth diseases the
patient misses in the direction of the slow nystagmus component.
The test of “vertical writing”, offered by Fukuda, is referred to spontaneous
tests. The patient is sitting at a table and writes a vertical column of ten figures “30”
22
(one under another) in such a way that the hand is not touching the paper. For the first
time the patient writes with the eyes opened (control), and then with the eyes closed.
Inclination of the column of figures, written with the eyes closed, more than by 10
testifies to the asymmetry of muscles tone.
The Romberg’s station test is used to determine the stability of static
equilibrium. In the Romberg’s position at labyrinth parafunction the patient falls on
one side, opposite to the direction of spontaneous nystagmus. At labyrinth
parafunction the change of the direction of falling is observed at the change of head
position. At cerebellum pathologies the change of head position does not influence the
direction of falling. The patient falls on the affected side only.
A change of the tone of extremities and trunk muscles arises if the vestibular
analyzer is affected, which is seen in the gait. Study the following gait types.
1) Walking along a straight line: first with the face forward, and then with the
back. At a labyrinth pathology, as well as in the Romberg’s position, the patient
inclines to one side, opposite to spontaneous nystagmus. At central vestibular
syndrome, nystagmus and patient’s inclination are observed in the direction of the
affected side, i.e. they are disharmonious.
2) Flank gait: with attached steps to the right and to the left. At a labyrinth
pathology the flank gait is not violated. If the cerebellum is affected, the patient can
not execute the flank gait in the direction of the affected side.
The next group of tests of researching the vestibular analyzer is experimental.
The most widespread methods of experimental irritation are caloric and rotatory types
of stimulation.
In clinical practice the method of caloric test by N. Blagoveshchenskaya is now
widely used. Infuse 60–100 ml of cold or hot water into the acoustic meatus during 10
s. By means of stop-watch determine the latent period of nystagmus: the time from
the beginning of water infusion to the appearance of the first nystagmic eye
movements. Normally the latent period is 20–30 s. Decrease of the latent period and
23
increase of the frank one (N = 40–60 s) testifies to hyperreflexia of the labyrinth
proper. And vice versa, increse of the latent period and reduction of the frank one
testifies to hyporeflexia.
The classic rotatory Barany test consists in uniform rotation of the patient in the
Barany arm-chair with the eyes closed during 20 s up to 10 turns. After the arm-chair
is stopped the duration and description of nystagmus are determined.
If condition of the ampula receptor is normal, the duration of postrotatory
nystagmus in the Barany test makes 20–30 s. Nystagmus duration less than 20 s
testifies to labyrinth hyporeflexia, more than 30 s – to labyrinth hyperreflexia.
The Barany test is simple and accessible, which made it rather widely used in
clinical examination. However, at quite strong supraliminal stimuli there are applied
such irritants that are not always tolerated well by the patient. In this connection other
rotatory methods have been offered, one of them being cupulometry.
Cupulometry is a method of researching threshold values of vestibular analyzer
reflexes arising in response to uniformly increasing superthreshold stimuli.
Cupulometry is to be conducted with an electric rotatory arm-chair with a sufficient
range of angular velocity – from 0 to 90–120º/s².
The visual method of nystagmus estimation is subjective and has certain
failings, which do not eliminate possible diagnostic pitfalls. In this connection the
objective method of electronystagmography registration is widely used at this time.
As a result of the conducted research of the vestibular analyzer a proper
conclusion can be made:
1) vestibular analyzer without pathology;
2) peripheral vestibular syndrome with hyporeflexia or hyperreflexia of one or
another labyrinth;
3) central vestibular syndrome.
Vestibulometry is used not only in clinical practice but also in vocational
aptitude test. Vestibulometry helps to determine if an individual is ready for certain
24
professions such as a driver, a pilot, a sailor or a cosmonaut. These professions require
estimating the state of the otolithic apparatus. People of these professions mainly deal
with prolonged influence of rectilinear accelerations, which irritate the statoconial
membrane.
Statoconial membrane density has been researched by means of tests of
otolithic reactions (OR) by V. Wojaczek and tests by K. Hilov on four-stem swing.
Otolithic reaction consists of four moments:
1. The patient is sitting in a special chair, closes his eyes and leans forward by
90º.
2. Five turns are conducted to the right or to the left in 10 s, after which the
ampulla receptor gets irritated.
3. After the chair is stopped, we do not change the patient’s position and after 5
s we expect irritation of the copular apparatus to diminish.
4. The patient is offered to open the eyes and rise. The change of the patient’s
position and his orientation show the adequacy of otolithic apparatus irritation.
Research results are estimated according to the V. Wojaczek’s Otolithic Reactions
Chart:
Somatic Reactions Vegetative Reactions
0 – no reaction
1 – insignificant displacement of the
body
2 – significant displacement of the body
3 – the patient falls
0 – no reaction
1 – subjective sensation of dizziness and
nausea
2 – paleness or redness, changes of
cardiac and respiratory activity
3 – nausea and vomiting
Estimation of OR results is important for delivering judgement concerning
vocational aptitude and readiness of people, whose professional activity depends on
the vestibular analyzer. We should consider the degree of evident vegetative reactions.
25
So, if OR test of the patient shows the second or third degree of reaction, the patient is
considered unfit for the occupation. Considerable displacement of the head and trunk
(3º of somatic reactions) without any vegetative reaction is not considered a
contraindication to professional activities provided that somatic reflexes are brought
to physiological end points by special training.
People of maritime and aviation professions experience a significant load on
the vestibular apparatus and the otolithic system in particular.
Therefore one-time research with the help of OR appears insufficient. Research
of otolithic apparatus sensitivity is a necessity for irritations cumulation. For this
purpose we use the K. Khilov’s test of balancing on the four-stem swing.
During the main part of the research the patient is sitting on a swinging
platform with the eyes closed. Swinging is conducted for 15 min. The time of
vegetative reactions (skin pallor, nausea, and vomiting) appearance is a sign of the
patient’s sensitivity to vestibular irritation. 4 degrees of cumulation are distinguished:
0 degree – vegetative symptoms are absent during 15 min of swinging;
I degree – nausea and vomiting appear in 15 min of swinging;
II degree – nausea and vomiting appear in 5–10 min of swinging;
III degree – vomiting appears during the first 5 min of swinging.
People, who got through 15 min of swinging with no obvious vegetative
symptoms, are considered resistant to statoconial membrane irritation. Nonpersistent
persons are those with the second and third degree of cumulation. Individuals, who
have the first cumulation degree, are subject to retest.
For more careful selection of candidates for aviation and space professions we
use the test of sensitivity to acceleration – the Coriolis’ test. Accelerations appear
when an individual is exposed to mutually perpendicular forces. They can be
produced by rotation of the patient vertically and horizontally at the same time. This
can be achieved by rotating the patient in a chair, asking him to continuously bow his
head forward and backwards or to the left and to the right. Thus, permanent angular
26
motions perpendicular to plane’s motion, for example in an aircraft, produce Coriolis
acceleration. To determine sensitivity to Coriolis acceleration the test of continuous
Coriolis acceleration cumulation in S. Markoryan’s modification was used (1966).
The patient revolves in an arm-chair at a speed of 1 turn a second with the eyes closed
and vertical head position. In the end of the 5th
turn against the background of steady
rotation the patient begins to flex the head from the right shoulder to the left one. The
patient must report if and when he starts feeling heat, cold, illusion of swinging, bad
general condition, vegetative discomfort (e.g. nausea). During rotation one should
start recording the results after the onset of vegetative disorders of the patient: face
skin paleness, appearance of cold sweat, swallowing movements, and vomiturition. If
any vegetative disorder appears in the patient, the test is stopped. Individuals, who get
through the test for longer than 3 min are considered apt for aerial, nautical and space
professions with their vegetative stability being good. Individuals, who got through
the test for less than a minute and started manifesting vegetative symptoms, are
considered inapt and unsuitable for any work with load on the vestibular system.
During occupational selection the type, amount and results of different tests are
regulated by specific orders and instructions from different organizations with
different assessment criteria for different professions.
27
CHAPTER 4
Ear diseases
4.1. Ear maldevelopments
There are maldevelopments of the external, middle and inner ear. However,
auricle maldevelopments are observed more frequently.
Possible anomalies are observed in the 1) auricle, 2) auricle, external auditory
canal, tympanic cavity, 3) external, middle ear; face bones defects also take place.
There are such auricle maldevelopments: macrotia – a large auricle; microtia –
a small, deformed auricle (Fig. 12, 13); anotia – absence of auricle; squarrose auricles
(Fig. 14); auricle appendages – small cutaneous formations, which are located in front
of the auricle and consist of skin, hypoderm and cartilage (Fig. 13); parotic fistulas,
which are frequently located near the base of the crus of helix (Fig. 15).
Auricle anomalies lead to cosmetic defects of the face often accompanied by
hypoplasia (Fig. 12) or agenesia of the external acoustic meatus, can combine with
middle ear hypogenesis.
Maldevelopments of the external acoustic meatus and middle ear lead to the
conductive type of hearing loss.
The treatment of ear maldevelopments is surgical. Plastic operations are to be
performed. In case of macrotia the auricle must be reduced to normal size. When
auricle microtia or underdevelopment is present, a new auricle is to be formed. If
atresia of the external acoustic meatus takes place, a new external auditory canal must
be formed.
4.2. Traumatic injuries of ear
4.2.1. Auricle wounds
There are distinguished traumas of the auricle and traumas of the external
acoustic meatus.
28
Auricle damages are subdivided into gunshot wounds, cut or lacerated wounds,
ruptures and burns. Often there are bite wounds as a result of a dog’s or human bite.
Sometimes partial or complete abruption of the auricle can take place. The external
auditory canal is often injured by different objects: spokes, matches, etc. It often takes
place during combing or ear cleaning.
Treatment. The sooner the injured patient comes to the hospital, the better
treatment results will be. First of all the initial surgical d-bridement of the wound is
conducted. The wound is washed with 3 % hydrogen peroxide, then dried with gauze
tampons. The skin around the wound is treated with iodine and alcohol. The wound
edges are jointed and sutured. In case of complete auricle abruption a plastic operation
is carried out. After it the sutures are processed with iodine or alcohol and a tight
aseptic bandage is applied. Tetanus antitoxin and tetanus vaccine are injected into the
patient. Antibiotics are prescribed. If the patient was bitten by an unknown dog, he
must take a complete course of inoculations against hydrophobia under observation of
an infection disease doctor.
4.2.2. Othematoma
Othematoma is accumulation of blood between the perichondrium and
auricular cartilage. It appears as a result of a blunt injury of the ear, but sometimes
spontaneously. It happens more often to boxers and wrestlers.
Clinical presentation. The auricle skin is purple. The auricle, especially in its
superior part, is thickened. The bulge is elastic, tense, more evident on the anterior
surface of the auricle. On this surface the perichondrium is less densely connected to
the cartilage. Fluctuation is observed. The patient complains of obtuse pain in this
area, sometimes sense shock of the auricle.
Treatment. The ear is processed with iodine or alcohol. Othematoma is
punctured, its contents are drained. A tight compressive aseptic bandage is applied. In
case of suppuration of othematoma contents it is incised. The cavity is washed with
29
antibiotic solution, a rubber drain is inserted with gauze tampons saturated with
hypertensive solution. An aseptic bandage is applied. Antibiotics prescription is
obligatory.
4.2.3. Auricular chondroperichondritis
Auricular chondroperichondritis is purulent inflammation of perichondrium
and auricular cartilage. More frequently it develops as a result of auricular hematoma
suppuration. It can take place after insect bites, burns, frostbite of the auricle.
Pseudomonas aeruginosa is often found by means of bacteriological investigation.
Clinical presentation. Intense pain in the auricle is observed. The auricle
becomes red and thick. The temperature of the patient’s body increases. In serious
cases pus appears between the perichondrium and cartilage. Purulent melting of the
auricular cartilage takes place. Dead tissue tears away, and as a result the auricle
deforms strongly and becomes shrunken.
Treatment. Broad spectrum antibiotics are prescribed. The abscess is incised,
cavities are washed with antibiotic solution. Rubber drains are put in. Gauze tampons
with hypertensive sodium chloride solution are applied to the ear. A pressure bandage
is applied on the ear. The cavities are washed daily with antibiotics to their complete
cleansing, aseptic salve dressings are applied. Such physiotherapeutic procedures as
ultraviolet radiation or therapeutic laser are used.
4.2.4. Frostbite and burns of the auricle
Frostbite of auricle takes place under the action of very low temperature. It
happens more frequently than frostbite of other parts of body because the skin of
auricle is thin and there is no hypoderm.
There are differentiated three stages of frostbite:
1. Erubescence.
2. Formation of blisters with transparent contents.
30
3. Auricle necrosis.
Treatment. At the first stage of frostbite one should carefully rub the auricle
with alcohol and apply dry bulky dressing. At the second stage – conduct section of
blisters. The section is conducted in aseptic conditions. Then antiinflammatory
ointments are applied on the frost-bitten areas. In case of the third degree of frostbite
surgical d-bridement is conducted. Necrotizing areas are removed. One should
appoint antibiotics internally or parenterally depending on the patient’s weight.
Antiinflammatory ointments are used.
Auricle burns are caused by hot water, steam, molten metal, some chemical
substances, electric current.
Four degrees of burns are distinguished.
1. Erubescence.
2. Formation of blisters with transparent contents.
3. Necrotic patches.
4. Charred auricle.
Treatment. Burns of the 1st
–2nd
degrees are treated with antiinflammatory
aerosols. If the burn is of the 2nd
degree, section of blisters is conducted in aseptic
conditions. Antiinflammatory hormonal ointments are used. At burns of the 3rd
–4th
degrees burn shock is possible. Intensive anti-shock therapy is administered. Surgical
removal of necrotizing areas is conducted. Antiinflammatory ointments are used.
Antibiotics are administered.
4.2.5. Injuries of the internal and middle ear
Eardrum damage is the most frequent trauma occurring at peacetime. Eardrum
trauma can be direct or indirect. A direct eardrum trauma happens as a result of
foreign body removal, when the eardrum is injured with a pin or a match during
cleaning of the external acoustic meatus. Indirect eardrum ruptures may be caused by
31
basal skull fracture, a blow in the ear, jumps into the water from a height, rapid
decompression (in divers), petard explosion close by, etc.
Eardrum trauma can be accompanied by onset of a sudden acute pain in the ear,
noise, hearing loss. Otoscopy of the external acoustic meatus detects blood,
hemorrhages, eardrum perforation of different size and form. As a result of eardrum
rupture an infection that can result in the development of acute suppurative otitis gets
into the tympanic cavity.
In case of mastoid process damage infection penetrates the bone causing
osteomyelitis, which is accompanied by the clinical picture of acute mastoiditis.
In case of a middle ear trauma there can be a rupture of the auditory ossicles
chain resulting in hearing impairment of conductive type.
Possible traumas of the labyrinth are direct and indirect. At peacetime the
former are rarely observed, sometimes as a result of surgical interference on the
middle ear. There can be stapes dislocation in the oval window, an injure of the lateral
semicircular canal. Indirect traumas of the labyrinth are observed in case of basal
skull fractures, which include periotic bone fractures and injure of the great blood
vessels of the cranial cavity.
The clinical picture in case of basal skull fractures is characterized by the
syncopal state of the patient. It is possible to detect hemorrhages under the
conjunctiva and in the area of eyelids.
In case of longitudinal fractures of the periotic bone eardrum perforation takes
place, through which blood and cerebrospinal fluid flow. The function of the cochlear
and vestibular apparatus is slightly violated. In case of transverse fractures of the
periotic bone the cochlear and vestibular function is completely impaired and
facioplegia is observed.
Such patients require skull roentgenography, lumbal puncture, eyeground
inspection, and study of the functional state of the cochlear and vestibular apparatus.
32
The labyrinth can be also damaged as a result of acute atmospheric pressure
fluctuations – that is a barotrauma. It happens in divers, pilots of airplanes. Action of
intensive sound causes an acoustic trauma. The cochlea can be damaged during
operations on the middle ear. All this results in the development of sensorineural
hearing loss.
Treatment. Eardrum rupture needs careful adjustment of perforation edges.
With the help of the operating microscope the edges of the ruptured eardrum are
straightened and adjusted. Fibrin tape is applied above the adjusted edges to preserve
their integrity. A sterile turunda is introduced into the external auditory canal.
Antiinflammatory treatment is administered. Such microsurgical interference is
possible only during the first days after the trauma, until suppuration signs appear.
In case of mastoid bone injure surgical debridement is conducted with removal
of the broken bone. The wound is not sutured, it is treated by the open method.
Traumas of the labyrinth caused by basal skull fractures need careful
transportation of the patient. In hospital otorrhagia is stopped by introduction of
sterile turundas into the external auditory canal. In case of heavy bleeding or
meningitis signs surgical interference is conducted on the middle ear.
In case of an acoustic trauma of the labyrinth antineuritic complex therapy is
prescribed.
4.3. Foreign bodies of the external auditory canal
Foreign bodies are more frequently found in children, who push various objects
into the ear. In adults these can be pieces of matches, cotton wool, corn, metal parts,
etc. Different insects can get into the external auditory canal, e.g. cockroaches,
bedbugs.
Clinical presentation. Usually foreign bodies do not cause unpleasant
sensations. But if a foreign body is sharp, it can cause blood-tinged discharge from the
33
ear, pain. Especially acute pain arises if insects get into the ear. There can be cough,
dizziness. Foreign bodies are clearly seen during otoscopy.
Treatment. The ear is to be washed with warm water by means of the Janet’s
syringe. If washing is ineffective, the otolaryngologist removes the foreign body with
a blunt hook (Fig. 16). It is impossible to remove the foreign body with pincers
because this instrument pushes the foreign body deeper into the external auditory
canal.
If an insect gets into the ear, at first it is necessary to stop its movement. For
this purpose alcohol or warmed vegetable oil is applied into the ear by dropping. Then
the foreign body is washed out with a syringe.
4.4. Auricle diseases
4.4.1. External otitis
External diffuse otitis. Otomycosis
Generalized bacteriogenous inflammation of the external acoustic meatus skin
is named external diffuse otitis.
Etiology. The inflammation is caused by staphylococcus, streptococcus,
hemophilic bacillus, blue pus bacillus, etc.
Clinical presentation. Patients complain of pain in the ear, itch, burning. Pain
is less intensive than at a furuncle. Pain in the ear increases at mastication, opening of
mouth, pressure on the tragus – unlike middle otitis, at which pain increases at
pressure on the mastoid process. Origin of the disease is usually related to a
mechanical injury of the ear by a finger or pins, matches and other objects. Often
external otitis arises as a result of skin irritation by purulent discharge at middle otitis.
Otoscopy findings: the skin of the external auditory canal is hyperemic, infiltrated.
The external acoustic meatus is narrow. Transparent excretions, which are interfused
with deadened epithelium, can ooze from the skin. Then excretions can become
34
purulent and form a stinking mass, which fills the external auditory canal. Hearing
can get worse.
Treatment. Tableted antibiotics are administered during 7–10 days.
Antihistaminic and calcium preparations are prescribed. Local administration:
washing-out of the ear with disinfectant solutions. Then the ear is dried with cotton
wool and processed with antibacterial ointments on turundas. Physiotherapeutic
procedures are administered.
Otomycosis is external diffuse otitis caused by fungi.
Clinical presentation. Similar to ordinary external diffuse otitis, but pain is far
less evident. More apparent itch. Otoscopy: hyperemia and skin infiltration are less
evident. Characteristic presence of transparent excretions in the external auditory
canal, there can be yellow-brown or black stratifications on the skin of the external
auditory canal. Duration of the disease is protracted, persistent.
Treatment. Application of turundas with antifungal agents to the external
auditory canal is administered during 1 month. Ultraviolet radiation is prescribed.
Furuncle of the external auditory canal (external limited otitis)
A furuncle is inflammation of a hair follicle or an oil-gland. These appendages
of skin are located only in the membranous-cartilaginous part of the external auditory
canal, they are not present in its osseous part. Therefore, if inflammation takes place
in the osseous part, it is not furuncle but some other disease.
Etiology: bacterial flora, staphylococcus is found the most frequently. The
following factors contribute to disease development: decline of organism resistance,
mechanical irritation of the skin of the external auditory canal, especially in patients
with purulent discharge from the ear. Recurrent furuncles of the external auditory
canal quite often testify to the presence of diabetes and are a manifestation of general
furunculosis.
35
Clinical presentation. Patients complain of acute pain in the ear. Occlusion of
the external acoustic meatus with a furuncle or pus can injure hearing. Body
temperature rises. The regional lymph nodes located under the auricle and on the
mastoid can multiply.
There are 2 stages of the disease:
1. Infiltration stage.
2. Abscess formation.
Otoscopy shows a narrow external acoustic meatus, hyperemic, infiltrated skin
of a limited area of the membranous-cartilaginous part of the external auditory canal.
At the stage of abscess formation it is possible to see an eminence with a white apex
in the center of hyperemia; lancing of the furuncle can show pus in the external
acoustic meatus. Pressure on the tragus and opening of mouth are acutely painful.
Treatment. At the infiltration stage disinfectants on turundas are administered
locally as well as physiotherapeutic methods on the ear. At the stage of abscess
formation furuncle section, pus removal, washing-out of the furuncle cavity with
antibiotic solution are conducted (Fig. 17). Then the cavity is drained with a rubber
strip and gauze turundas saturated with hypertensive sodium chloride solution.
Antibiotics are given by a five-day course. Tableted antibiotics are administered.
4.4.2. Auricle eczema
Auricle eczema is one of local manifestations of a common skin disease –
eczema. This is a neuroallergic inflammation of surface layers of skin with evident
itch.
Clinical presentation. Small transparent blisters appear on the skin of the
external auditory canal and auricle. Then they burst, and on their place multiple small
erosions with abundant oozing lesion appear. After this crusts form on their place. The
acute process lasts 1.5–2 months. There can be chronic eczema.
36
Treatment is aimed at removing the irritating factor and treating concomitant
diseases. Antihistaminic preparations, depressants, calcium preparations, and ascorbic
acid are administered. Locally: antiseptic solutions and corticosteroid ointments are
applied.
4.4.3. Auricle erysipelas
This is an acute streptococcus disease of skin with formation of a sharply
limited inflammation focus. If the skin of the auricle and external acoustic meatus is
affected, we talk about auricle erysipelas.
Etiology: streptococcus, which penetrates through small skin lesions.
Clinical presentation. Body temperature rises. The auricle becomes very
hyperemic, somewhat infiltrated, the external auditory canal becomes narrow.
Treatment. Antibiotics of penicillin group are administered during 7–10 days.
Antiseptic ointments are applied locally. Physical procedures – ultraviolet radiation on
the auricle is administered.
4.4.4. Cerumen
Cerumen is earwax accumulation in the external auditory canal as a result of
surplus secretion of the earwax glands or violation of its normal evacuation. The
increase of earwax viscidity and exostosis promote violation of earwax evacuation
from the external auditory canal. Earwax can have admixtures of epidermis, which
peels as a result of inflammatory diseases of the skin of the external acoustic meatus.
Clinical presentation. Usually there are no evident symptoms. The patient has
to consult a doctor after water gets into the ear, when cerumen is soaked and swelled,
completely obstructing the external acoustic meatus. Hereupon the patient’s hearing
gets worse suddenly. There can be complaints of ear noise, sensation of pressure in
the auditory channel, or sensation of the voice echoed in the head – autophony.
Diagnostics is not difficult. Earwax is usually clearly seen at otoscopy.
37
Treatment. Washing-out of the external acoustic meatus is performed with the
Janet’s syringe. By drawing the auricle back and up, water sheet is directed at the
posterosuperior wall of the external acoustic meatus. Water must have the body
temperature not to cause thermal irritation of the labyrinth and cause no dizziness.
Usually earwax is easily washed. The external acoustic meatus is dried with cotton
wool. On the 2nd
–3rd
hour a turunda is introduced with antiseptic. If the first washing
does not appear effective, it is recommended to apply 3 % hydrogen peroxide by
dropping in the ear 2–3 times per day during 3 days, whereupon to repeat the
procedure.
It should be remembered that at dry perforation of the eardrum water can get
into the tympanic cavity and cause exacerbation of inflammatory process. Therefore
before washing the ear one should carefully obtain anamnesis and find out from the
patient whether there was some time with no purulent discharge from the ear. In such
a case washing is contraindicated and cerumen is removed with a blunt hook.
4.5. Diseases of the middle ear
4.5.1. Acute suppurative otitis media
Acute suppurative otitis media is acute purulent inflammation of the mucous
tunic of middle ear air cavities.
Typical features are:
1. It happens often.
2. Can result in evident loss of hearing.
3. Passes into chronic otitis.
4. Can lead to intracranial complications.
Etiology. Viruses and bacteria cause acute purulent otitis media. These are
viruses, which cause acute respiratory diseases, flu virus. Among bacteria it is more
frequent in all staphylococci, streptococci, pneumococci, hemophilic bacilli,
morhaxella.
38
Pathogeny. The disease develops against the background of depressed
organism resistance.
Infection gets into the middle ear in the following ways:
1. From the nasal cavity through the auditory tube. It often happens at acute
rhinitis.
2. Through the external auditory canal – when the eardrum is damaged. It takes
place at eardrum rupture as a result of a trauma (more frequently after a blow in the
ear; Fig. 18).
At fresh eardrum ruptures such help is rendered: under the operating
microscope the edges of the torn eardrum are adjusted to each other. They accrete
thereupon.
3. Through blood – hematogenic way. This way is basic at infectious diseases –
influenza, scarlatina, etc.
In the pathogenesis of acute otitis media the state of nose, paranasal sinuses,
and nasopharynx plays an important role. Chronic rhinitis, nasal septum deviation,
purulent sinusitis contribute to disease onset.
Clinical presentation. Acute suppurative otitis media is characterized by
stormy development. It has three stages:
1) nonperforated;
2) perforated;
3) reparative.
The symptoms of acute suppurative otitis media depend on the stage.
The 1st
stage. The basic complaint of the patient is pulsing, shooting, stabbing
pain in the ear. Pain is felt deep inside the ear. It is caused by the fact that pus forms in
the tympanic cavity. It holds apart the tympanic cavity walls, presses on the eardrum.
The patient’s condition gets worse. General weakness appears. Sleep and appetite get
worse. Body temperature rises to 38–39º C and higher. Inflammatory changes appear
in the blood test. Otoscopy findings: at first eardrum reddening appears (hyperemia;
39
Fig. 19). The eardrum becomes thick later. When much pus is accumulated in the
tympanic cavity, the eardrum bulges outside (Fig. 20).
The 2nd
stage. Perforation takes place at this stage – that is eardrum rupture.
Purulent discharge exudes from the ear. Pain gets better in the ear, general condition
improves, body temperature decreases. Otoscopy shows the pulsating reflex – pus
exudes through the perforation drop by drop synchronously with pulse.
The 3rd
stage. The inflammatory process subsides, purulent discharge stops.
The eardrum recovers normal color. Still, hearing impairment remains. Hearing is
restored slowly. Small perforation heals completely leaving no scars. Large
perforation can not be closed up.
In children acute otitis media arises more often. This is predefined by the
anatomic features of the children’s ear. The disease usually begins suddenly, at night.
Body temperature is very high – 39–40º C. The child feels uneasy, twists the head
round, seizes the affected ear with a hand. General condition gets considerably worse.
Babies can have vomit, gastroenteric upset.
At infectious diseases the clinical course of acute otitis media also has its
peculiarities. The severest changes in the ear are observed at scarlet fever. Necrosis
begins in the ear (Fig. 21, 22, 23). All middle ear structures disintegrate. The auditory
ossicles are destroyed. Excretions from the ear begin to stink. There is hemorrhagic
otitis at influenza. Blood accumulates in the tympanic cavity. Blisters with bloody
content form on the eardrum and osseous part of the external auditory canal (Fig. 24).
At tuberculous otitis there are numerous eardrum perforations, malodorous pus
(Fig. 25).
Treatment depends on the stage of the disease.
The 1st
stage. Home or bed rest is prescribed. At severe condition
hospitalization is administered. The diet is vitaminized, which is easily digested.
Antibiotics and vasoconstrictive nasal drops are administered. Analgesics are used.
Antihistaminic and calcium preparations are prescribed. Antibacterial ear drops are
40
used. At the beginning of the disease, when there is no pus in the tympanic cavity yet,
physiotherapeutic methods are applied. But when pus appears in the tympanic cavity,
physiotherapeutic procedures are contraindicated.
Severe pain in the ear, eardrum prolapse are indications to the auripuncture or
paracentesis (Fig. 26, 27). The eardrum is punctured with a special spear-shaped
needle. Pus is aspirated. Antibiotic solution is introduced with a syringe into the
middle ear cavity. Solution penetration into the nasopharynx testifies to the fact that
the otosalpinx is free. The patient admits that the taste of medicine appears in the
mouth or nose.
The 2nd
stage. At the perforating stage of otitis the ear is to be cleaned 2–3
times a day with dry cotton wool on an ear probe. Use 3 % hydrogen peroxide to
soften pus. Usually the ear is cleaned with an aspirator. After this antibacterial drops
on turundas are introduced into the ear. A turunda is to be brought deeply into the
external auditory canal, up to the eardrum.
The 3rd
stage. At the reparative stage treatment consists in rehabilitation of ear
functioning. Ear inflation is conducted as well as otosalpinx catheterization and
eardrums pneumomassage (Fig. 28, 29, 30).
4.5.2. Mastoiditis
Mastoiditis is a purulent inflammatory disease of the mastoid bone. More
frequently it arises as a complication of acute otitis media, or develops at exacerbation
of chronic otitis media.
Organism reactivity decrease is one of the factors of disease onset. Inefficient
treatment of acute otitis – too late auripuncture or paracentesis – also results in
mastoiditis development.
Clinical presentation. General and local symptoms of mastoiditis are
distinguished. General symptoms are the same as at acute suppurative otitis media.
Body temperature rises. The patient feels worse. Blood test shows inflammatory
41
changes. Unlike acute otitis, pain in the ear does not get better even when perforation
takes place. Pain is very intensive, pulsating. Local symptoms are the following.
1. Pain at pressure on the mastoid.
2. Slight swelling of the mastoid, sticking out auricle.
3. Otoscopy: purulent discharge increase. Pus pulsation recommences, pus
becomes thick. Characteristic symptom: overhang of the superoposterior wall of the
osseous part of the external auditory canal (Fig. 31).
4. Sometimes pus can break from the mastoid outside. Thus subperiosteal
abscess develops. It can result in formation of a fistula, through which pus will ooze.
There can be an atypical course of mastoiditis. Then there is no eardrum
perforation and purulent discharge from the ear.
In children of the first year of life the mastoid structure has peculiar features.
Therefore antritis is talked about – inflammation of the mucous tunic of the mastoid
cavity.
Valuable information for diagnosis verification is provided by CT or
roentgenography (Fig. 32).
Treatment. Conservative and surgical types of mastoiditis treatment are
distinguished. Conservative treatment is the same as at acute otitis media of the
second stage. Ear cleaning is conducted, disinfectants are applied by dropping into the
ear. Antibiotics prescription is obligatory, preferably intramuscularly.
Antiinflammatory medicines are administered, such as aspirin. Antihistaminic
medicines, vitamins, and calcium preparations are prescribed.
If these measures are ineffective, elective operation is to be conducted –
mastoid trepanation (mastoidotomy; Fig. 33, 34, 35, 36).
In case of subperiosteal abscess or development of intracranial complications
the operation must be conducted urgently, without waiting.
In children antritis is treated by mastoideocentesis – puncture of the mastoid
cavity with diagnostic and medical purposes.
42
4.5.3. Chronic purulent otitis media
Chronic purulent otitis media is a long-term inflammatory infectious disease
of the middle ear cavities, which has a clinical course with periods of remission and
exacerbation. Beginning of the disease is related to acute otitis the patient had in
childhood.
Disease outcome:
1. Hearing loss.
2. Facial paralysis, labyrinthitis.
3. Life-threatening ntracranial complications.
Etiology. Staphylococcus or mixed microbial flora, moulds.
Pathogenesis. High virulence of microorganisms and weakened resistance are
instrumental in transition from acute otitis to chronic. The presence of other
concomitant diseases is of great importance. The state of the nasal cavity, paranasal
sinuses and pharynx play a certain role. Quite frequently recurrent acute suppurative
otitis media passes to chronic.
Clinical presentation. Obligatory signs are as follows:
1. Long-term purulent discharge from the ear. The disease lasts for years.
2. Constant eardrum perforation with callous edges.
3. Hearing impairment, ear noise.
The disease may have two forms: mesotympanitis and epitympanitis.
Mesotympanitis is a benign form of chronic otitis. At mesotympanitis the
middle and inferior parts of the tympanic cavity are affected. Patients complain of
purulent discharge from the ear and hearing impairment. Pain in the ear appears only
in the period of exacerbation. General condition is not violated in the period of
remission. During exacerbation purulent discharge from the ears increases. Pain
appears in the ear, febricula. Body temperature rises. Blood test shows inflammatory
changes.
43
Diagnosis is determined on the basis of otoscopy. There is odourless
mucopurulent content in the external auditory canal. Sometimes excretions from the
ear can have objectionable odor. It happens in slipshod patients, because of bad ear
hygiene. After washing and careful care of the ear an unpleasant smell disappears.
The eardrum has almost normal color. Eardrum perforation is central. It means that
around the perforation the eardrum limbus is preserved (Fig. 37). Perforation can be
large. Then it is possible to examine the tympanic cavity through it. Pus and thickened
mucous tunic will be visible in the tympanic cavity. Granulations are possible. Large
granulation has the name of aural polyp. A polyp can be large, it can even block the
external auditory canal. This results in pus deposit in the middle ear cavities and leads
to complications. In such a case polyp removal is the first aid.
Hearing gets worse at mesotympanitis. Sound transmission is violated. It can be
determined by audiometry.
Epitympanitis (attic disease) is a poor quality form of chronic otitis. At this
form there is destruction of the bone walls of the middle ear cavities. It can lead to
severe complications. At epitympanitis the superior floor of the tympanic cavity is
necessarily affected. Other floors can also be affected. The main feature of
epitympanitis is affection of not only the mucous tunic of the tympanic cavity, but
also of the bony structures. Bone affection is named caries.
Patients have the same complaints as at mesotympanitis. Besides, they can
complain of headache and dizziness. In the period of remission general condition is
satisfactory. Temperature rises during exacerbation, pain appears in the ear. The
patient feels febricula. Purulent discharge from the ear increases. Blood test shows
inflammatory changes.
Diagnosis is determined on the basis of otoscopy. At epitympanitis there is pus
in the external auditory canal. The amount of pus is often small. Pus always has
unpleasant smell. It takes place as a result of bone caries. Unpleasant smell is the
same as at teeth decay. Abundant excretion at epitympanitis is observed in two cases:
44
first – at cholesteatoma suppuration; second – at extradural abscess, when pus is
accumulated between the bone and dura mater of brain. Excretions are abundant,
malodorous, appear shortly after ear cleaning. In such cases the ear must be operated.
Eardrum perforation at epitympanitis is marginal. It reaches the bony
eardrumtympanic ring. The perforation necessarily takes part in the superior part of
the eardrum (Fig. 38).
Epitympanitis is characterised by the presence of a passage in the epitympanic
recess. One should conduct perforation probing with the Wojaczek ’s probe. If there is
a passway, the probe easily falls into the attic.
One of epitympanitis complications is cholesteatoma – stratification of furfures
and cholesterol. It has a shell. Cholesteatoma in the ear is an inflammation product. It
often festers. The danger of cholesteatoma consists in bone destruction. Depending on
the direction of cholesteatoma growth it can ruin the Fallopian aqueduct, external
semicircular canal, superior wall of the tympanic cavity or mastoid. Then there is
facial paralysis, labyrinthitis or intracranial complications.
Roentgenological study helps to detect cholesteatoma. A roentgenogram of the
temporal bone is made in the Schuller’s view (Fig. 32, 39).
Ear affection at epitympanitis is more evident than at mesotympanitis. Except
for sound conduction violation, violation of sound sensation takes place. Audiometry
shows it.
In most patients chronic otitis media has an allergic component.
Complex research of a patient with chronic otitis media must include
consultations of a neurologist and an oculist. It is necessary to timely diagnose the
origin of intracranial complications. There must be conducted X-ray study of the
temporal bone and audiometry.
Treatment. Common medical measures include organism hardening. The
measures are taken to strengthen general reactivity of the organism. Calcium
45
preparations, vitamins, and antiallergic preparations are administered. Routine
common uviolizing, rational nutrition are recommended.
Antibiotics are used only at exacerbation of the process.
Necessarily inspect the nose, nasopharynx and pharynx, paranasal sinuses.
These organs are sanitized if it is necessary.
Local treatment of chronic otitis media consists of two stages.
1. Ear cleaning.
2. Introduction of medications into the tympanic cavity.
Before local treatment granulation and polyps are removed from the tympanic
cavity. Large granulation or ear polyps are removed with the conchotome, curet or
loop (Fig. 40). Small granulation is cauterized with silver nitrate.
The 1st
stage. Ear cleaning. 3 % hydrogen peroxide is applied by dropping into
the ear. Pus is removed with an ear probe and cotton wool. It is possible to wash pus
from the tympanic cavity with disinfectant solutions. For pus softening the ear is to be
washed with enzymes. At presence of large perforation, washing is carried out with
the Janet’s syringe. To wash the attic use the Hartman’s canula (Fig. 41). After
washing carefully dry the ear with an ear probe with cotton wool, or with a blunt
canula connected to an aspirator. Careful ear cleaning guarantees successful treatment.
The 2nd
stage. Introduction of medications into the tympanic cavity. Substances
are introduced into the tympanic cavity in such medical forms: 1) solutions (drops); 2)
powders; 3) ointments. Mainly these are exsiccants.
Alcoholic solutions of antiseptic preparations are used. Solutions of antibiotics
are administered upon obtaining results of ear microflora analysis on antibiotics
sensitivity. Astringents are used, e.g. 1–2 % nitric silver solution.
After ear cleaning it is possible to blow powders into the tympanic cavity: boric
acid, antibiotics, sulfanilamides. Insufflations are conducted carefully, not to inject
surplus powder.
46
Purulent otitis media of mycotic origin is an otomycosis variety. Antifungal
agents are used to treat it.
At allergic manifestations of otitis antiallergic and corticosteroid drops are
used.
To treat chronic otitis media varied physiotherapeutic procedures are used –
electrophoresis with antibiotics, 1–2 % solution of nitric silver solution. Ultraviolet
radiation and aeroionotherapy are applied on the ear. Mud therapy is used: mud
applications on the mastoid. Mud therapy application is possible only in the period of
remission. At otomycosis laser is used.
Medicinal substances, which are introduced into the ear, must be changed every
2–3 weeks. Durable use of alcoholic solutions is not advisable.
The main recommendation to patients with chronic otitis media – to protect the
ear from water. During bathing or washing of hair the patient must close the ear with
cotton wool soaked with vaseline, olive oil, or any other ointment.
The described treatment is used more frequently at mesotympanitis.
At epitympanitis it is also possible to begin with conservative treatment.
However, surgical method is basic in epitympanitis treatment.
One should distinguish two types of operations in the surgical treatment of
chronic otitis media.
1. Sanation operations. Radical operation is basic. It eliminates the purulent focus in
the ear. Its purpose is to prevent intracranial complications.
2. Hearing improvement operations – tympanoplasty. Five types of tympanoplasty are
distinguished by Wulstein.
4.5.4. Labyrinthitis
Labyrinthitis is a complication of acute and chronic otitis media. It is an
inflammatory infectious disease of the inner ear. Infection from the middle ear cavity
gets into the inner ear and causes an inflammatory process in it. Rarely labyrinthitis
47
can arise as a result of meningitis or an infectious disease (for example, epidemic
parotitis).
Etiology. The direct reason for labyrinthitis is microbes, which are causative
agents of acute and chronic otitis media. Necrotizing labyrinthitis usually arises at
tubercular or scarlatinal otitis.
Classification. Acute and chronic types of labyrinthitis are distinguished. There
are the following forms of acute and chronic labyrinthitis:
a) erosive;
b) purulent;
c) necrotizing.
Chronic labyrinthitis is subdivided into:
1) limited;
2) diffuse.
Diffuse labyrinthitis is a process, which affects all structures of the inner ear.
Limited – a process, which affects a part of the labyrinth only. Limited labyrinthitis
arises, when there is a fistula in the lateral semicircular canal. A fistula appears as a
result of caries.
We will describe labyrinthitis forms.
Limited labyrinthitis is observed at chronic otitis media complicated by caries
and cholesteatoma. The bony capsule of the lateral semicircular canal gradually
collapses and a fistula is formed.
Clinical presentation. Patients complain of periodic dizzinesses accompanied
by nausea or vomit, unbalance. Nystagmus can appear – rhythmic horizontal
twitching of the eyeballs. Nystagmus is directed at the affected ear. If dizziness is
present, the patient complains of rotation of surrounding objects or his own body in
one direction.
The symptom of fistula is another important sign. Nystagmus appears if the
tragus is pressed with a finger. This nystagmus is named pressure nystagmus. The
48
eyeballs begin twitching to the affected side. Sometimes nystagmus is caused by
cleaning of the ear with a cottonwool tampon. At this moment the patient feels
dizziness. The nystagmus caused by irritation of the labyrinth is accompanied by
dizziness, nausea and declining or falling to the side, opposite to the affected ear.
At limited labyrinthitis hearing is not necessarily impaired. Hearing loss
depends on the presence of inflammatory process in the middle ear. Vestibulometry
allows confirming the diagnosis.
After a sanation operation on the ear the process is usually stopped. Self-
recovery without operation is rarely observed.
Treatment of limited labyrinthitis. At exacerbation of the process bed rest,
antibiotics, sulfanilamides, and dehydratation are administered. Sanation operation is
conducted on the middle ear.
Acute diffuse serosal labyrinthitis can develop at acute middle otitis or
exacerbation of chronic otitis media.
Clinical presentation. The auditory and vestibular functions are violated.
Evident lowering of the ear is characteristic. Nystagmus appears. At first it is directed
at the affected ear, then it changes direction and to the opposite site. Dizziness, nausea
and vomit appear. Equilibrium is violated. Vestibular symptoms are most evident.
Dizziness increases and is accompanied by vomit at the change of head position. At
dizziness the patient feels rotation of objects or his body. Vestibulometry allows
confirming the diagnosis.
Treatment. Rest, antiinflamatory and dehydration therapy are administered. At
acute middle otitis medicinal treatment often leads to convalescence. At mastoiditis
and chronic otitis media routine surgical treatment is used. Sanation operation is
conducted on the middle ear. If it is not conducted, intracranial complications may
take place. Operation is conducted immediately against the background of antibiotic
treatment.
49
Acute diffuse purulent labyrinthitis. This form of labyrinthitis has an
extraordinarily severe clinical course and complications. It always ends with complete
loss of hearing and vestibular function. In addition, intracranial complications may
arise. Meningitis and cerebellum abscess can develop.
Clinical presentation. Beginning and clinical course of the disease are stormy.
Evident dizziness, nausea and vomit, acute balance disturbance, spontaneous
nystagmus are basic symptoms. Complete and irreversible loss of the auditory and
vestibular functions happens very quickly – that is the difference between purulent
and serosal labyrinthitis. At the beginning of purulent labyrinthitis nystagmus appears
directed at the affected ear, but already in a few hours nystagmus changes its
direction.
At unfavorable clinical course there can be complications – meningitis,
cerebellum abscess.
Treatment. Operation is conducted immediately against the background of
antibiotic treatment.
Necrotizing labyrinthitis is observed mainly at scarlatinal and tubercular
otitis, sometimes at rubeola. Due to antibiotics use it is observed rarely.
Clinical presentation of necrotizing labyrinthitis is similar to the clinical
presentation of purulent labyrinthitis, but the clinical course is severer.
Necrotizing labyrinthitis is an indication to operation on the ear with
interference on the labyrinth.
4.6. Otogenic intracranial complications and otogenic sepsis
Otogenic intracranial complications are severe, life-threatening diseases. They
arise because of penetration of infection from the ear into the cranial cavity. It takes
place in case of acute and chronic otitis media. Meningitis or meningoencephalitis
frequently arises against the background of acute purulent otitis media. More
frequently otitis is complicated by meningitis. Rarer abscesses of the brain and
50
cerebellum develop. Even rarer there are sigmoid sinus thrombosis and otogenic
sepsis. Sometimes there can be a few complications simultaneously, for example sinus
thrombosis and cerebellum abscess, or meningitis and abscess of the cerebral
hemispheres.
Etiology. The reason for otogenic intracranial complications is the same
microbes, which cause otitis. Staphilococci, streptococci, and pneumococci prevail in
case of acute otitis. In case of chronic otitis – also certain Proteus, Pseudomonas
aerogenosis, etc.
Pathogenesis. Depending on the stages of infection spread from the ear into the
cranial cavity abscesses may be located above the dura mater (extradural abscess) and
between the brain tunics (subdural abscess). The inflammatory process can pass to the
venous sinus. As a result sinus thrombosis forms. If infection penetration is deep,
disseminate meningitis develops. If the process spreads, the cerebrum tissue can be
affected.
It results in the formation of cerebral hemispheres and cerebellum abscesses
(Fig. 42). We will consider basic types of otogenic intracranial complications.
Otogenic disseminate purulent meningitis is brain tunic inflammation. The
arachnoid and vascular membranes are affected. The infection penetrates from the
middle and internal ear. Meningitis can arise due to other otogenic complications, for
example sinus thrombosis.
Clinical presentation. Headache is the most frequent and the first symptom of
otogenic meningitis. Headache is very intensive. The reason for this is intracranial
pressure rise. Any external irritation increases pain. For example, touching the
patient’s skin, loud sounds, bright illumination. Therefore such a patient must be
treated in certain conditions without such irritations. Nausea and vomiting are the next
symptoms. Frequently they appear at the height of headache and are not connected
with food intake. Quite often vomiting temporarily improves headache.
51
The general condition of the patient is grave. At later stages loss of
consciousness passing to delirium can appear.
Quite often patients assume the position of a gun cock or a hunting dog. They
lie on the side or on the back with bent feet and thrown back head. The patient
reflexively assumes the given position because it relieves headache.
Body temperature is permanent, it rises to 38.5–39° C and higher. Pulse is rapid
and corresponds to body temperature.
Meningitis is characterised by meningeal symptoms:
1. Neck muscles rigidity. The doctor places the hands under the patient’s
head and flexes it forward. In case of meningitis the patient’s neck flexes badly.
The chin does not reach the breastbone.
2. The Kernig’s symptom. The patient is lying on the back, legs bent in the
hip and knee joints. Try to unbend the leg in the knee joint. In case of meningitis
the leg can not be unbent completely.
3. The Brudzinski’s symptoms superior and inferior. During research of
neck muscles rigidity the patient’s legs are bent and pulled up to the abdomen. It is
the superior Brudzinski’s symptom. The inferior symptom: during extension of a
patient’s leg the other leg bends in the knee and hip joints.
In case of severe course of the disease there is observed eyeballs bulging,
differently sized right and left orbits.
Diagnostics. Blood test data of meningitis patients show inflammation signs.
During eyeground examination stagnation is determined.
Research of the cerebrospinal fluid taken by spinal puncture has a large value
for meningitis diagnostics. Characteristic fluid changes are found in meningitis
patiens.
Otogenic sepsis. In case of purulent middle ear inflammation, both acute and
chronic, infection is generalized, microbes get into the blood. There is sepsis. It is
more frequent as a result of sinus thrombosis.
52
Clinical presentation of otogenic sepsis and sigmoid sinus thrombosis. The
symptoms observed in case of this disease are divided into two groups:
1. General symptoms, characteristic of sepsis of any nature.
2. Local symptoms conditioned by sigmoid sinus affection.
General symptoms. One of the most expository sepsis symptoms is hectic
fever. There is rapid increase of body temperature to 39–41° C, accompanied by chill.
Then in a few hours temperature quickly (critically) falls. Temperature drops are
accompanied by profuse sweat. There can be several rises of temperature during the
day, therefore the patient’s temperature must be taken every 2 hours. Body
temperature of younger children is permanent. Pulse accelerates according to the rise
of body temperature. The patient’s skin is pale with a sallow tint. It can be sclera
jaundice.
There are changes characteristic of an inflammatory process in the blood test.
Bacterial inoculation of blood is very important. In case of sepsis microbes can be
found in blood. Blood for the test is to be taken during chill when body temperature
rises.
At otogenic sepsis microbes spread in the blood vessels and settle in other
organs. There are abscesses in the lungs, joints, subcutaneous adipose tissue, and
muscles. More frequently patients die from pulmonary complications.
Local symptoms: there is edema and pain of soft tissues on the posterior margin
of the mastoid, painful neck palpation on the affected side. Often the patient’s head is
flexed toward the injury.
Otogenic abscesses of the cerebral hemispheres and cerebellum are abscesses,
which appear in the brain and cerebellum because of purulent otitis media.
Clinical presentation. There are four stages of the clinical presentation of
abscess:
53
1. The initial stage lasts for 2–3 weeks. The inflammatory process is
characteristic. There are light meningeal symptoms: headache, sickness, body
temperature rise, nausea, and vomiting.
2. The latent stage also lasts for 2–3 weeks. At this stage all symptoms either
disappear generally, or declare themselves weakly.
3. The frank stage lasts for a few weeks. It is characterized by a large variety of
symptoms. The patient feels weakness, appetite absence, exhaustion. Body
temperature rises. Blood test shows inflammatory changes. However, these
manifestations are considerably less evident than in case of meningitis and sepsis.
There is headache, which increases during pattering with a finger on the skull above
the area, where abscess is located. There is nausea and vomiting, which are not related
to food intake. Pulse slows down to 45 bpm. The ophthalmologist determines
stagnation on the eyeground. Cervical muscles rigidity and the Kernig’s symptom can
appear.
If abscess is located in the cerebral hemispheres, there will be paresises and
paralyses of extremities. There can be facial paresis, when the face becomes
asymmetric. There are cramps and other neurological symptoms. The patient falls on
the side opposite to the affection. There can be dizziness. Hallucinations take place.
The patient’s speech is violated. Sometimes it becomes incomprehensible, just
senseless words. The patient can forget how to read and write.
There are such symptoms of cerebellum abscess. Muscle tone of extremities
decreases on the side of affection. The patient’s hand resists poorly during unbending.
During examination of walking and Romberg’s position the patient bends to the
affected side. Impossibility of flanking gait on the affected side is characteristic.
During the pointing test the patient can not touch the tip of nose with the hand. The
hand deviates to the affected side on the side of injury. There is spontaneous
nystagmus directed at the affected side.
54
Abscesses of the brain and cerebellum can lead to impairment of consciousness,
breathing and cardiac activity.
4. The terminal stage of brain abscess. It is the last stage of abscess. Usually
lasts for a few days and leads to patient’s death. Brain edema develops. The patient’s
condition gets worse sharply. Intoxication becomes more intensive. Breathing and
cardiac activity stops, the patient dies.
Diagnostics of brain and cerebellum abscess. There are such modern methods
of diagnosing these complications:
1. Echoencephalography.
2. Radioisotopic encephalography.
3. Computer tomography (CT) and magnetic resonance tomography (MRT).
Medical treatment of intracranial complications. Mainly otolaryngologists
and neurosurgeons administer medical treatment of patients with otogenic intracranial
complications. However, neurologists, internists, pediatricians, infectiologists, and
oculists must take an active part in the treatment.
Medical treatment of patients with otogenic intracranial complications includes
surgical interference and intensive drug therapy.
Surgical interference directed at removal of purulent nidus from the middle ear
and complication elimination. In case of acute purulent otitis media operation is
conducted – extended antromastoidotomy. In case of chronic purulent otitis media
extended radical surgery is performed. At otogenic meningitis the middle and
posterior cranial fossae are dissected during the operation.
If sigmoid sinus thrombosis and otogenic sepsis are present, an operation on the
ear is performed. The posterior cranial fossa is necessarily opened. The sigmoid sinus
is punctured. If it is necessary, the sigmoid sinus is opened and the blood clot is
removed.
In case of otogenic brain and cerebellum abscesses the otolaryngologist
conducts antromastoidotomy or a radical operation. Then he opens the posterior or
55
middle cranial fossa and punctures the brain tissue. After this the doctor opens the
abscess and inserts drainage tube in the needle direction. If abscesses are plural or the
abscess is located far from the affected ear, the abscess is opened by the
neurosurgeon.
Simultaneously with surgical treatment intensive drug therapy is administered.
1. Antibiotics are prescribed. Ceftriaxon, ceftazidime, vancomycin, metrogyl,
penicillin in large doses introduced in injections.
2. Antiedemics are introduced intravenously. These are haemodez-N, blood
plasma, albumen, mannitol, lasix, 40 % glucose solution, 10 % solution of sodium
chloride, hexamethylenetetramine (urotropin), 5 % solution of ascorbic acid, retinol
(vitamin A), hydrocortisone. Arterial pressure is controlled.
3. Antiallergic drugs are introduced intramuscularly. These include dimedrol,
pipolphen, suprastin, etc.
4. During psychomotor agitation sodium oxybutyrate and seduxen are
introduced intravenously with 40 % glucose solution.
5. In case of staphylococcus infection immunotherapy is conducted.
Antistaphylococcic immunoglobulin is introduced intramuscularly.
6. Cardiac glycosides, analeptical drugs, anesthetics (in case of necessity) are
administered.
7. All patients with otogenic meningitis suspected must undergo spinal
puncture. Antibiotics are introduced into the spinal canal in case of need.
8. Heparin, syncumar, and neodicumarinum are administered using the
guidance of coagulogram to treat sigmoid sinus thrombosis.
It is very important to fight against brain edema. Use mannitol, 40 % glucose
solution with insulin, magnesium sulfate, lasix intravenously. Steroids are
administered: prednisolone, hydrokortisone or dexamethasone. Introduce 5 % solution
of ascorbic acid, 10 % solution of calcium chloride intravenously. Introduce
56
aminophylline, trental intravenously to improve cerebral circulation. Introduce
sodium oxybutyrate, glutamic acid, thiopental sodium intravenously (slowly!).
4.7. NONPURULENT EAR DISEASES
These diseases include reflux otitis media, otosclerosis, sensoneural hearing
loss, Meniere’s disease.
The diseases have such symptoms:
1) hearing disorder;
2) ear noise;
3) no signs of purulent ear inflammation.
At the same time these diseases substantially differ from one another.
4.7.1. Reflux otitis media. Secretory otitis media
The basic cause of the disease is auditory tube dysfunction.
Reflux otitis media is characterized by inflammation of the mucous membrane
of the middle ear, auditory tube obturation, loss of hearing, and (quite often) presence
of liquid in the middle ear.
Pathogenesis. The auditory tube connects the middle ear and the nasal cavity.
Various inflammatory diseases of the nasal cavity, like rhinitis, sinusitis, adenoid
affection, may result in reflux otitis media. Swelling of the auditory tube mucosa
obstructs air flow passing through the tube to the tympanic cavity. As a result,
pressure in the tympanic cavity becomes negative, tympanic membrane bending
forms, the middle ear mucosa swells. Quite often this causes production of liquid,
called exudate, in the ear cavity. Exudate accumulates in the middle ear, developing
secretory otitis media. The allergic component plays an important part in the
development of secretory otitis media. Persistance of secretory otitis media may lead
to the formation of adhesions in the tympanic cavity, developing adhesive otitis.
57
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Ent book

  • 1. Recommended by the Ministry of Public Health of Ukraine as a textbook for students of institutions of higher medical education of the 4th level of accreditation, who master the discipline in English 1
  • 2. 2
  • 3. 3
  • 4. Authors: Y. Mitin, Y. Deyeva, J. Gomza, V. Didkovsky, L. Krinichko, A. Motailo, G. Tereschenko, Y. Shevchuk The main questions of diseases of the ear, nose, and throat are examined in the textbook. The anatomy, physiology, pathology and treatment of ENT diseases are described. The classic and modern data of scientific investigations in different branches of otorhinolaryngology are given. The textbook is for students of institutions of higher medical education (the 3rd – 4th level of accreditation). 4
  • 5. CHAPTER 1 General description and history of otorhinolaryngology Otorhinolaryngology is a clinical discipline, which studies the morphology, physiology and pathology of the ear, upper respiratory tracts and adjacent areas. The term is derived from four Greek words: otos – ear, rhinos – nose, lагуngos – larynx and logos – studies. The first letters of the words marking the main branches of the speciality form the abbreviation ORL or LOR (in English-speaking countries – ENT). Otorhinolaryngology studies norms and pathology of most analyzers: auditory, vestibular, olfactory and gustatory. Disorders in analyzers activity decrease occupational capability and working capacity causing depression of the person. It should be noted that otorhinolaryngology is a surgical speciality, which encompasses a large range of operations: on the ear, nose cavity, paranazal sinuses, pharynx, larynx, and trachea. Development of otorhinolaryngology as a separate discipline began in the middle of the 19th century. Before that, the treatment of a small number of known ear diseases was taught in the course of surgery, and of diseases of the upper respiratory tract – in the course of therapy. Anatomico-topographical unity of the ear, throat and nose, their physiological correlation and practical application of endoscopy methods in ENT research were the reasons for ENT diseases joining. It is important to know the main stages of otorhinolaryngology development. In 1841 German doctor F. Ноfmаnn suggested to examine deep areas of the ear, nose and throat using a mirror without a small round part of amalgam in the center. Later doctor A.F. Trolch created a frontal reflector on its basis. In 1854 M. Garsia, a Spanish singer and one of the most prominent teachers of singing, professor of the Paris Conservatoire and Royal Academy of Music in London (Fig. 1) offered the indirect laryngoscopy method. By means of using a laryngeal mirror M. Garsia studied the physiology of singer’s voice. In a year this method was introduced into practice. Then 5
  • 6. the methods of postnasal (1859), anterior, and middle rhinoscopy were offered. Later direct methods were developed: esophagoscopy (Kussmaul, 1868), direct laryngoscopy (Kirsten, 1894), bronchoscopy (Killian, 1897), respiratory bronchoscopy (Fridel, 1956), fibrobronchoscopy (Іkedа, 1969). Otosurgery was founded by German doctor I. Schwartze, who offered mastoid process trepanation (anthrotomy) in his work in 1873. Puncture of the maxillary sinus through the inferior nasal meatus was first perfomed and described by M. Schmidt in 1888. American G.W. Caldwell in 1893 and Frenchman H. Luc in 1897 independently worked out the method of radical surgical intervention at chronic maxillary sinusitis. In Ukraine, due to privat-docent courses in at several universities, otorhinolaryngology was popularized and introduced into medical practice and education. At the medical department of the Kyivievs Ssnt. Vladimir Volodymyr Uuniversity some ENT diseases were mentioned during lectures on surgery, therapy and other disciplines some ENT – diseases were mentioned. So, in 1860-–1862 the first lectures on larynx diseases were given by Ddoctor of Mmedicine I. Lazarevich, the associate professor of obstetrics I. Lazarevych (the course name of the academic course was The " Respiratory Ttract and Iits Partsbranches Ddiseases and Llarynx sufferingLesions") and lectures on ear diseases were given by Professor Yu. Shymanovsky in a course on theoretical and operative surgery. From 1864 to 1866 L. Marovsky lectured a privat-docent course on rhinology and laryngology, in 1864 he was elected an associate professor of diagnostics and laryngoscopy. His works were About Croup Treatment, About Deafness Reasons etc. From 1871 to 1880 M. Uspensky lectured a privat-docent course on otiatrics, and then from 1882 to 1884 N. Zuk delivered the course Throat Diseases. Mykola Volkovych (1858–1928; Fig. 2), a surgeon and otorhinolaryngologist, professor and academician, was the first in Ukraine to begin a systematic lecture course on otorhinolaryngology. From 1889 to 1903 he conducted an elective course on otorhinolaryngology at the medical department of the Kyivievs Ssnt. Vladimir 6
  • 7. Volodymyr Uuniversity. He was one of the first, who paid proper attention to the study of upper respiratory tracts scleroma and took an active part in the study of etiology, pathogeny and treatment of this disease. The scientist also introduced a surgical direction in otorhinolaryngology development. He widely performed operations on the paranasal sinuses and mastoid process. He was the first in Russia to publish a report on two examples of larynx extirpation in case of cancer and develop surgical treatment of chronic larynx stenoses. Otorhinolaryngology was also developing in Odessa, Kharkiv and other cities of Ukraine. In 1921 otorhinolaryngology became a required subject of medical departments of universities, which was very important for the development of the speciality. The otorhinolaryngology department of the Kyiv Medical Institute was originated in 1922, when Alexander Puchkovsky became the head of the department. He graduated from the Petersburg Military Medical Academy. The scientist made a great contribution to the development of otorhinolaryngology in Odesa. A. Puchkovsky was a prominent Ukrainian scientist researching scleroma, tuberculosis of the upper respiratory tracts, ENT-oncology, reconstructive surgery. The Kharkiv otorhinolaryngology department was founded by professor S. Surukchi (1922), in Dnepropetrovsk – by professor S. Kompaneyets (1921), in Lviv – by professor A. Yurash (1908). The appearance of fundamental works since the 20–30s was a considerable contribution into the development of otorhinolaryngology in Ukraine. S. Kompaneyets, A. Puchkovsky, and O. Kolomiychenko studied the questions of diagnostics and treatment of purulent otitis and concomitant intracranial complications. M. Horshak founded a school of head and neck oncology. G. Trombitsky, M. Pitenko and S. Kompaneyets investigated the problem of regional and professional ENT-pathology. Works of M. Volkovich, V. Drobotko, L. Zarytsky, V. 7
  • 8. Yaroslavsky, A. Puchkovsky, S. Myhailovsky played a great role in the study of etiology, pathogeny, epidemiology, diagnostics and treatment of respiratory scleroma. In 1924 the publishing of the Journal of Ear, Nasal and Pharynx Diseases began. In 1930 in Kharkiv the Otolaryngology Research Institute was organized, which existed for 25 years. Here the problems of tonsillitis, nose physiology and pathologies, prophylaxis and treatment of deafness and hearing loss were studied. In 1960 the Kyiv Research Institute of Otolaryngology was opened. Professor O. Kolomyichenko (Fig. 3), Corresponding Member of the Ukrainian Academy of Sciences and Lenin Prize Laureate, was the initiator and director of this institute till 1974. Professor A. Tsyhanov, State Prize Laureate, succeeded Professor O. Kolomyichenko at this position. Since 1985 Professor Dmytro Zabolotny, Corresponding Member of the Ukrainian Academy of Medical Science, is the head of the institute. According to the data of 2006, there are approximately 3,650 otolaryngology specialists in Ukraine and ENT-departments can treat about 8,600 patients. 8
  • 9. CHAPTER 2 Clinical anatomy, physiology, and methods of researching the auditory analyzer The auditory analyzer is divided into a peripheral section, conduction pathways, and a cortical center. The peripheral section is divided according to its function into sound-conducting and sound-perceiving systems. The sound-conducting system consists of the external, middle ear, peri- and endolymphatic spaces of the inner ear, basal and vestibular membranes of cochlea. The sound-perceiving system is the receptor of auditory analyzer represented by the spiral organ (organ of Corti). The sound-conducting system delivers sound to the receptor. The sound-perceiving system transforms mechanical vibrations into a nervous impulse. The peripheral section of the auditory analyzer anatomically consists of three parts: the external, middle and inner ear (Fig. 4). The external ear consists of the auricle and external acoustic meatus. The auricle collects and directs sound waves into the external acoustic meatus. The external acoustic meatus deliveres sound vibrations to the ear drum (tympanic membrane). The external ear is innervated by the branches of the 5th , 7th and 10th cranial nerves. The middle ear consists of an air cavities system represented by the tympanic cavity, mastoid process cells and auditory tube (otosalpinx) (Fig. 5). The tympanic cavity has six walls. The external wall of tympanic cavity is the eardrum, the internal one is the lateral wall of the inner ear, the superior wall is the tegmental wall separating the tympanic cavity from the middle cranial fossa, the inferior wall is a bone separating the tympanic cavity from the bulb of jugular vein. In its middle the internal wall has a peak (promontory) formed by the base of cochlea. Behind and above the promontory the oval window is located, which is closed by the 9
  • 10. base of stapes. Under and behind the peak there is a round window closed by the secondary tympanic membrane. In clinical practice the tympanic cavity is divided into 3 floors: the superior one is epitympanum, the middle one – mesotympanum, and the inferior one – hypotimpanum. The epitympanum is situated above the short malleus process (lateral process); the mezotympanum is between the short process and the inferior wall of external acoustic meatus; the hypotimpanum is a small cavity located below eardrum attachment. There are auditory ossicles (malleus, incus, stapes) and muscles in the drum cavity, which form an anatomically and functionally united system. The malleus is very tightly fixed with the manubrium to the eardrum, and its head is united with the incus by means of an articulation and a ligament. The incus attaches to the head of stapes with its long limb. The base of stapes is fastened in the oval window with a round ligament. The chain of auditory ossicles decreases the amplitude of sound vibrations and simultaneously increases the force of sound pressure on the oval window. The mechanism of sound conduction is realized due to the muscles of drum cavity: m. tensor tympani and m. stapedius. These muscles have two functions: adaptative and protective. The adaptive function is conditioned by reciprocal innervation: if one muscle contracts, the other relaxes reflexively. During muscle traction of tensor tympani the m. stapedius relaxes. It results in the retraction of the eardrum into the tympanic cavity and pressure of the bases of stape on the labyrinth. This causes an increase of internal labyrinth pressure and prevents low and weak sounds penetration into the internal ear. Due to reduction of m. stapedius and weakening of m. tensor tympani, the stapes are pulled out to the drum cavities, which reduces internal labyrinth pressure. It is an obstacle for the transmission of higher sounds but facilitates low and weak sounds conduction. The protective function of these muscles is realized by 10
  • 11. simultaneous tetanic reduction of both muscles when very loud sounds take place. It protects the labyrinth from loud acute sounds, because during this reduction the base of stapes begins to turn round close to its longitudinal axis, but does not move inside the internal ear. The auditory tube (otosalpinx) is important in the mechanism of sound conduction. This is the only organ, which connects the middle ear cavity with the environment. The otosalpinx is a narrow canal, 30–38 mm long, which begins in the front wall of drum cavity and ends with a pharyngeal opening in the cavity of the nasal part of throat at the level of the back-end of inferior nasal concha. The auditory tube consists of cartilaginous and bony parts. It balances the pressure in the tympanic cavity. The otosalpinx is usually closed, it is opened during swallowing and yawning, as a result air gets into the drum cavity. This function of the otosalpinx is named barofunction. The otosalpinx performs two functions: draining and protective. The protective function is realized by the stratified ciliated epithelium. The cilia blink in the direction of the pharyngeal opening and that removes foreign parts from the otosalpinx mucosa. The mastoid process located abehind the auricle is a part of the temporal bone. It contains a number of air cells, the biggest one called antrum. Mastoid air cells are covered with the fibrous tunic with pavement epithelium. Air cells unite with one another and also with the drum cavity. The middle ear is innervated by branches of the facial, glossopharyngeal, trigeminal nerves and from the carotic plexus. The internal ear is an ear labyrinth in the thickness of temporal bone pyramid. The ear labyrinth may be divided into three parts: the front part is the cochlea, the middle one – the vestibule, and the back part – the semicircular canals (Fig. 6). There is a bone labyrinth with a membranous labyrinth inside which repeats the bone labyrinth form (Fig. 7). The membranous labyrinth is a sac containing high- potassium, low-sodium fluid (endolymph). There is low-potassium and high-sodium 11
  • 12. fluid (perilymph) between the bone labyrinth wall and the membranous labyrinth wall. Within the cochlea there are three fluid-filled spaces: the scala media (filled with endolymph), the scala tympani, and the scala vestibuli (both filled with perilymph). The internal fluid spaces of the saccule, utricle, and semicircular ducts contain endolymph. The vestibule contains two bony depressions – the spherical recess holds the saccule, and the elliptical recess holds the utricle. The saccule and utricle consist of supporting and hair cells covered with gelatinous otolithic membrane, which contains a number of small calcium phosphate crystals (otoconia). There are three semicircular canals – anterior, posterior and lateral. Each semicircular canal contains a semicircular duct that has an ampullated and a nonampullated ends joined within the utricle. The cochlea consists of 2 ½ turns, with a total average length of 32 mm. The vestibular membrane separates the scala vestibule from the scala media, and the basic membrane separates the scala media from the scala tympani. The receptor of the auditory analyzer is the spiral organ (organ of Corti), wich is located on the basic membrane. The spiral organ is a complex structure consisting of supporting cells, three layers of outer hair cells and a single layer of inner hair cells. The hair cells carry out the transformation of sound irritation (mechanical vibrations) into a nervous impulse. The mechanism of sound conduction is the following: sound vibrations are concentrated by the auricle in the external acoustic meatus and through it reach the eardrum. Eardrum vibrations pass to the chain of otosteons. Vibrations of the base of stapes pass to the liquid environment of the internal ear, through it sound vibrations reach the spiral organ. The primary analysis of the sound, taking place in the internal ear, divides complex sounds into parts, due to the perception of certain frequencies by definite areas of the spirale organ. Mechanical energy of a sound wave is transformed into electric energy in the hair cells of the spiral organ, which leads to nervous impulse appearance. Then this impulse passes to the peripheral processes (dendrites) of bipolar 12
  • 13. cells and to the spiral neuroganglion (the first neuron of the auditory way). Then the impulse goes to the cochlear nerve (ramus n. vestibulocochlearis) and through the pontocerebellar angle reaches the myelencephalon. Here, in the ventral and dorsal nuclei, the second neuron lies. Then the fibre partially decussates in the pons and goes to the olive (the third neuron). Axons of the third neuron go to the back of the tectal plate of the midbrain tegmen and the medial geniculate body (the fourth neuron). Fibres of the fourth neuron end in the temporal lobe. Due to the partial decussation of the second neuron axons, each cochlea has bilateral connection with the cortex. An adequate irritant of the auditory analyzer is sound – periodic oscillation of environment (air) molecules. There are several principles concerning the adequate irritant of the auditory analyzer. The 1st principle – the auditory analyzer perceives sound frequencies of certain range, which is named the auditory range (volume) of human ear. A person perceives sounds with vibration frequency from 16 to 20,000 vibrations a second. The sound with the frequency less than 16 vibrations a second is named infrasound, more than 20 KHz – ultrasound. The 2nd principle – the auditory analyzer has different sensitiveness to the sounds of different frequency. Thus, our ear is the most sensitive to the sounds from 1,000 to 3,000 vibrations a second. These frequencies are named the range of speaking frequencies because we mainly speak on these frequencies. Perception of sounds decreases from this optimum area. At 200 to 10,000 vibrations a second the threshold force of sound is 1,000 times bigger than of the sounds with 1,000 to 3,000 vibrations a second. The 3rd principle – a man is able to distinguish the pitch of sound. If this ability is high, we talk about absolute hearing. In addition, the human ear is able to differentiate sound intervals (the distance between two degrees of scale) and is also sensitive to consonances and dissonances. 13
  • 14. All this together with musical memory makes an ear for music. All these abilities of musical ear are possible to be developed. Fully natural is the rhythm feeling. The 4th principle – a man is able to determine the location of the source of sound. This phenomenon is named ototopics. Ototopics is explained by the presence of two ears, in this connection it has the second name of binaural hearing. To understand the auditory analyzer physiology and master methods of its research one should know that the auditory analyzer gives a possibility to distinguish sounds by pitch, intensity, and timbre. The pitch of sound concerns its frequency: the number of oscillations a second and is expressed in hertzs (Hz). The intensity of sound is represented by its strength and is expressed in decibels (dB). Timbre chatacterizes the sound and depends on overtones, because bodies oscillate not only fully but also partially. Inspection of the ear includes examination of the auricle, palpation of the auricle, tragus, mastoid process, leadthrough otoscopies, and also inspection of auditory function. Otoscopy is executed to determinate the state of the external acoustic meatus and middle ear. Such research is perfomed by means of a frontal reflector and ear watering-cans of different diameter or by applying a special device – otoscope. If otoscopy is carried out using a frontal reflector one is to look through the reflector opening with the left eye. Light source must be on the right side of the patient. The patient must be seated in a definite position: his head should be bent to the shoulder, which is opposite to the examined ear. During otoscopy the axis of the acoustic meatus must be on the visual line. One must examine the width of the external acoustic meatus to define the proper diameter of the watering-can before its introduction. A watering-can with a proper diameter should be chosen to prevent unpleasant sensations of the patient. Also, the external acoustic meatus must be cleaned before examination if it is necessary. 14
  • 15. The watering-can must be taken with the index finger and thumb of the right hand for right ear examination, and with the left hand – for left ear examination. Then the auricle is pulled up and backwards with the other hand (in little children – downwards and backwards), and with subtle rotatory motions the narrow end of the watering-can is brought to the external auditory meatus. All the walls are examined by careful pushing of the watering-can into the depth of the external meatus. Due to the change of the inclination angle of the head it becomes possible to observe the tympanic membrane (Fig. 8). A normal tympanic membrane looks like a pearl grey oval membrane ≈ 8×9 mm in diameter and ≈ 0.1 mm thick. It has special features: 1) in the center of the membrane there is a convexity; 2) above the convexity there is the malleus fold, which looks like a grey strip during otoscopy; 3) in the upper part the strip trasforms into the malleus prominence, which is formed by the short process of malleus; 4) anterior and posterior folds spread behind and in front of the malleus prominence; 5) during otoscopy it is possible to observe a pyramid of light – corneal reflex (cone of light) behind and in front of the convexity; the corneal reflex arises due to light reflection from the shining surface of the tympanic membrane exactly in the places where surface is perpendicular to light rays, which fall from the frontal reflector. The methods of hearing testing can be divided into 4 groups: - the 1st group – testing of hearing by speech. Hearing is explored by whisper and by speech with normal loudness. A normal ear perceives whisper at an average distance of 6–7 m; - the 2nd group – testing of hearing by means of tuning forks. 15
  • 16. The most informative experiments are the Byng’s, Federici’s, Veber’s, Rynne’s, Schwabach’s, and Gellee’s ones. Testing of hearing by means of speech and tuning forks is named acumetry; - the 3rd group – audiometry methods – methods, which test hearing by means of electronic apparatus (audiometers). Depending on the patient’s participation, audiometry is divided into subjective and objective. At subjective audiometry the result depends on the answers of the inspected. These methods include pure-tone audiometry and superthreshold audiometry (the Lüsher’s test and SISI test research volume function), speech audiometry, determination of auditory sensitivity to ultrasound. Pure-tone audiometry is the basic and most widespread audiometry method. Audiometry results are shown in an audiogram (Fig. 9). It is a graph, the horizontal line of which represents sound frequency in Hz, and the vertical line – sound intensity in dB. Zero level in an audiogram is standard norm. Research results are reflected in an audiogram as two curves, which characterize sound perception through air and bone. Pure-tone audiometry allows defining the type of hearing disorders: sound conducting, sound perceiving or of mixed pathology. Results of objective audiometry do not depend on the patient’s answers. Here belong the following methods: impedometry (registration of acoustic resistance or impedance of the middle ear), brainstem auditory evoked potentials (computer audiometry), electrocochleography (registration of potentials arising in the cochlea due to sounds), otoacustic emission; - the 4th group – the use of conditional and unconditional reflexes. Unconditional reflexes are used for approximate determination of hearing presence in babies. In response to loud sounds due to the auropalpebral reflex the child’s eyelids close or blink more frequently than usually. Due to the auropupillar reflex the child’s pupil is narrow when sound irritation takes place and dilates when sound abates. Game audiometry is based on the formation of conditional reflexes in children. 16
  • 17. CHAPTER 3 Clinical anatomy, physiology, and methods of researching the vestibular analyzer The vestibular analyzer performs the function of equilibrium of body both in the state of rest and during motion. The receptors located in the vestibule (otoconic apparatus) are responsible for the function of equilibrium in the state of rest, and the receptors of semicircular canals (ampullary apparatus) are responsible for the function of equilibrium during motion. Together they perform the statokinematic function. The vestibular apparatus unlike other analyzers is never in the state of rest because gravitational force constantly acts on it. The vestibular analyzer, as well as other analyzers, consists of a peripheral part (receptor), a conducting part with kernels in the brainstem, and a central part. The vestibular analyzer receptors are located in the inner ear. In the saccules of the vestibule (utriculus et sacculus) the otoconic apparatus is located as macula utriculi and macula sacculi. The otoconic apparatus is accumulation of neuroepithelial or sense cells located between supporting cells. From the upper part of the sense cells hairs detach, which interlace and form loops. Microcrystals of calcium salts – statoconia – are located in the loops (Fig. 10). All of them are soldered with the jellylike substance and form the otolithic membrane (membrana statoconiorum). An impulse arises in the receptor at tangential displacement of the otolithic membrane (that is forward and downwards, backwards and downwards, parallel to the planes of macula). Any force is an adequate irritant of the otoconic apparatus that can cause rectilineal acceleration: 1) beginning or ending of steady rectilineal motion, its acceleration or deceleration; 2) centrifugal force; 17
  • 18. 3) change of head or body position in space; 4) gravitational force. The excitability threshold of the otoconic apparatus is 0.001–0.03 g (g – acceleration of gravity, which makes 9.8 m/s²). In every semicircular canal on one of its ends there is an ampule with an ampullar crest. On this crest there is a receptor named the ampullary apparatus. It consists of sense neuroepithelial cells with hairs on the upper part and supporting cells. The hairs of sense cells are covered with jellylike substance and form a brush (cupula terminalis), which is displaced at endolymph motions (Fig. 11). As a result of this displacement a nervous impulse arises in the sense cells. Angular acceleration is an adequate irritant of the ampullary apparatus. The excitation threshold of semicircular ducts is angular acceleration of 0.12–2 m/c². In the sense cells of ampullary and otoconic apparatus peripheral nerve fibres (dendrites) go from the bipolar nerve cells of the vestibule to the neuroganglion (ganglion vestibulare), located in the internal acoustic meatus. Axons of bipolar cells form the vestibular part of the 8th cranial nerve, which enters the brainstem through the pontocerebellar trigone and approaches the vestibular nuclei located in the diamond-shaped fossa of medulla oblongata. There are four vestibular nuclei on each side: medial, lateral, superior and inferior. The nuclei are joined by commissural fibres. The vestibular ways have not been studied higher. It is known that the cortical part is in the anterior part of the temporal brain part. The apparatus promotes irritation transformation into reflexes, which can be divided into three groups. 1. Vestibulosomatic – reflexes from the vestibular apparatus on the skeletal muscles of neck, trunk, extremities, eyes. These reflexes are identified by the Romberg’s sign, gait, coordination tests (finger-nose, indicator, knee-heel), nystagmus. 18
  • 19. 2. Vestibulovegetative – reflexes from the vestibular apparatus on the smooth muscles of internals. These reflexes declare themselves by skin redness, increased perspiration, change of cardiac and respiratory activity, nausea, vomiting, frequent urination. 3. Vestibulosensory – reflexes conditioned by the connection of the vestibular apparatus with the cortex of the large hemispheres. Normally these reflexes declare themselves by a conscious feeling of location in space, vestibular illusion of contrarotation; at a pathology dizziness and violation of spatial feeling are observed. Nystagmus is one of the most valuable indexes, which characterize the state of the vestibular analyzer. Nystagmus is involuntary rhythmic repeating movements of the eyeballs. The following varieties of nystagmus are distinguished: vestibular – arises at irritation of the receptors of vestibular analyzer nuclei and optokinetic – arises at irritation of the visual analyzer (looking at the object, which is moving evenly). A slow and a rapid components are distinguished in nystagmus. The slow component of nystagmus is conditioned by the irritation of vestibular analyzer receptors. The slow down movement of eyes in response causes the central reaction, and the eyes return to initial position. It is a quick component of nystagmus of cortical genesises. Nystagmus direction is the most evidently observed after the rapid component. Three degrees of nystagmus are distinguished: the 1st degree – nystagmus appears at a glance to the quick component, the 2nd degree – at a glance to the quick component and straight ahead, the 3rd degree – at a glance to the quick component, straight ahead and to the opposite side. When down movement of the hands and trunk arises opposite to the nystagmus direction, it is named harmonic. Harmonic down movement of the hands and trunk is characteristic of peripheral vestibular syndrome. Methods of researching the vestibular analyzer 19
  • 20. The tests characterizing the state of the vestibular analyzer are conducted in a certain sequence. The analysis of the test results is to be conducted paying attention to such two moments. 1. Changes characteristic of a labyrinth pathology (peripheral vestibular syndrome) or of a pathology of the central parts of the vestibular analyzer (central vestibular syndrome). 2. When we come to a conclusion that we are dealing with peripheral vestibular syndrome, we must specify if it is contingently caused by irritation (hyperreflexia) or oppression (hyporeflexia) of the right or left labyrinth. A vestibulometry chart includes: 1) study of complaints and disease anamnesis; 2) research of spontaneous vestibular reactions; 3) experimental tests; 4) decoding and estimation of results. Inspection of the patient begins with a careful study of complaints and disease anamnesis. At a pathology of the vestibular analyzer this information quite often influences the setting of diagnosis. Dizziness consists in specific complaints, disordered sense of balance and violated gait accompanied by nausea and vomiting. Under dizziness we understand seeming rotation of surrounding objects. Systematized dizziness is characteristic of peripheral vestibular symptom complex: the patient notes that objects swim from right to left or vice versa. It should be noted that in connection with anatomic adjacency of the receptors of the auditory and vestibular analyzers in the internal ear typical complaints of peripheral vestibular syndrome are of hearing impairment and sonitus. Thus, the peripheral vestibular syndrome is also named the cochleovestibular syndrome. Therefore at differentiation of peripheral and central vestibular syndromes hearing must be tested. 20
  • 21. The following group of tests is directed at the research of spontaneous vestibular reactions: spontaneous nystagmus determination, research of spontaneous missing, firmness of static equilibrium, motions with eyes closed. To determine the presence or absence of spontaneous nystagmus the doctor sits down against the patient, puts the index finger on the right or on the left at the distance of 60–70 cm from the eyes at an angle of 45°. If spontaneous nystagmus is observed, its characteristics are determined: the plane, direction, and amplitude; it is either clonic (only the quick component is visible) or tonic (the slow component also becomes visible). One should avoid extremely avert stare as the patient can develop brief nystagmus motions (end-position nystagmus). Position nystagmus is a variety of spontaneous nystagmus. It should be studied as follows. At first nystagmus is to be explored in the patient in sitting or standing posture. After this the patient is examined lying on the back, lying on the left and right side, and lying on the back with the head thrown back. The doctor notes in what position of the head nystagmus appears in the patient, changes of nystagmus parameters depending on the position of the head. Position nystagmus can be of peripheral and central origin. Nystagmus with abrupt changes of direction, rhythm and amplitude regardless of the patient’s position is characteristic of central vestibular syndrome. Research of pressure nystagmus is of great value. Its onset is usually related to the destruction of the bony labyrinth capsule at purulent otitis media, that is to the labyrinth fistula. Therefore this phenomenon is also named the fistula symptom. The bone defect, which has appeared, opens the membranous labyrinth. The change of pressure in the external acoustic meatus and drum cavity is passed onto its wall causing displacement of the endolymph and irritation of the vestibular analyzer receptors. This test is conducted as follows. The doctor sits down against the patient, who is looking straight ahead. The doctor presses on the tragus with the index finger to the 21
  • 22. right and to the left in turn. If the labyrinth is in normal condition, nystagmus is not observed. If there is a fistula in the lateral semicircular canal, nystagmus is observed accompanied by imbalance, nausea or vomiting. The tests, which allow exposing spontaneous missing, are important tests of determining spontaneous vestibular disorders, disturbance of static balance and gait. The following tests are simple and informative: the test of outstretched arms, indicator, finger-nose, and “writing test”. The test of outstretched arms is conducted as follows. The patient is sitting with the eyes closed and stretches the arms out in front of him. The index fingers are aimed straight, the other fingers make fists. The doctor is sitting against the patient holding the index fingers against the patient’s fingers, observing the motions of the latter. A healthy man holds hands in such position without any substantial displacements during a long period of time. A patient with a labyrinth pathology moves both arms toward the slow nystagmus component (harmonious deviation). At a pathology in the posterior cranial fossa the arm on the affected side deviates to the side or inwards, on the unaffected side the arm keeps the given position; in such a case nystagmus is directed to the side of affection (disharmonious deviation). The pointing test also characterizes the state of coordination. During this test the patient is sitting holding the hands on the knees. At first with the eyes opened, and then – closed he must touch with the index fingers the doctor’s index fingers. If a labyrinth pathology is observed, the patient will miss in the direction of the slow nystagmus component with both hands. Disharmonious declination of one hand characterises central vestibular syndrome. The finger-nose test is a variety of the pointing test. At labyrinth diseases the patient misses in the direction of the slow nystagmus component. The test of “vertical writing”, offered by Fukuda, is referred to spontaneous tests. The patient is sitting at a table and writes a vertical column of ten figures “30” 22
  • 23. (one under another) in such a way that the hand is not touching the paper. For the first time the patient writes with the eyes opened (control), and then with the eyes closed. Inclination of the column of figures, written with the eyes closed, more than by 10 testifies to the asymmetry of muscles tone. The Romberg’s station test is used to determine the stability of static equilibrium. In the Romberg’s position at labyrinth parafunction the patient falls on one side, opposite to the direction of spontaneous nystagmus. At labyrinth parafunction the change of the direction of falling is observed at the change of head position. At cerebellum pathologies the change of head position does not influence the direction of falling. The patient falls on the affected side only. A change of the tone of extremities and trunk muscles arises if the vestibular analyzer is affected, which is seen in the gait. Study the following gait types. 1) Walking along a straight line: first with the face forward, and then with the back. At a labyrinth pathology, as well as in the Romberg’s position, the patient inclines to one side, opposite to spontaneous nystagmus. At central vestibular syndrome, nystagmus and patient’s inclination are observed in the direction of the affected side, i.e. they are disharmonious. 2) Flank gait: with attached steps to the right and to the left. At a labyrinth pathology the flank gait is not violated. If the cerebellum is affected, the patient can not execute the flank gait in the direction of the affected side. The next group of tests of researching the vestibular analyzer is experimental. The most widespread methods of experimental irritation are caloric and rotatory types of stimulation. In clinical practice the method of caloric test by N. Blagoveshchenskaya is now widely used. Infuse 60–100 ml of cold or hot water into the acoustic meatus during 10 s. By means of stop-watch determine the latent period of nystagmus: the time from the beginning of water infusion to the appearance of the first nystagmic eye movements. Normally the latent period is 20–30 s. Decrease of the latent period and 23
  • 24. increase of the frank one (N = 40–60 s) testifies to hyperreflexia of the labyrinth proper. And vice versa, increse of the latent period and reduction of the frank one testifies to hyporeflexia. The classic rotatory Barany test consists in uniform rotation of the patient in the Barany arm-chair with the eyes closed during 20 s up to 10 turns. After the arm-chair is stopped the duration and description of nystagmus are determined. If condition of the ampula receptor is normal, the duration of postrotatory nystagmus in the Barany test makes 20–30 s. Nystagmus duration less than 20 s testifies to labyrinth hyporeflexia, more than 30 s – to labyrinth hyperreflexia. The Barany test is simple and accessible, which made it rather widely used in clinical examination. However, at quite strong supraliminal stimuli there are applied such irritants that are not always tolerated well by the patient. In this connection other rotatory methods have been offered, one of them being cupulometry. Cupulometry is a method of researching threshold values of vestibular analyzer reflexes arising in response to uniformly increasing superthreshold stimuli. Cupulometry is to be conducted with an electric rotatory arm-chair with a sufficient range of angular velocity – from 0 to 90–120º/s². The visual method of nystagmus estimation is subjective and has certain failings, which do not eliminate possible diagnostic pitfalls. In this connection the objective method of electronystagmography registration is widely used at this time. As a result of the conducted research of the vestibular analyzer a proper conclusion can be made: 1) vestibular analyzer without pathology; 2) peripheral vestibular syndrome with hyporeflexia or hyperreflexia of one or another labyrinth; 3) central vestibular syndrome. Vestibulometry is used not only in clinical practice but also in vocational aptitude test. Vestibulometry helps to determine if an individual is ready for certain 24
  • 25. professions such as a driver, a pilot, a sailor or a cosmonaut. These professions require estimating the state of the otolithic apparatus. People of these professions mainly deal with prolonged influence of rectilinear accelerations, which irritate the statoconial membrane. Statoconial membrane density has been researched by means of tests of otolithic reactions (OR) by V. Wojaczek and tests by K. Hilov on four-stem swing. Otolithic reaction consists of four moments: 1. The patient is sitting in a special chair, closes his eyes and leans forward by 90º. 2. Five turns are conducted to the right or to the left in 10 s, after which the ampulla receptor gets irritated. 3. After the chair is stopped, we do not change the patient’s position and after 5 s we expect irritation of the copular apparatus to diminish. 4. The patient is offered to open the eyes and rise. The change of the patient’s position and his orientation show the adequacy of otolithic apparatus irritation. Research results are estimated according to the V. Wojaczek’s Otolithic Reactions Chart: Somatic Reactions Vegetative Reactions 0 – no reaction 1 – insignificant displacement of the body 2 – significant displacement of the body 3 – the patient falls 0 – no reaction 1 – subjective sensation of dizziness and nausea 2 – paleness or redness, changes of cardiac and respiratory activity 3 – nausea and vomiting Estimation of OR results is important for delivering judgement concerning vocational aptitude and readiness of people, whose professional activity depends on the vestibular analyzer. We should consider the degree of evident vegetative reactions. 25
  • 26. So, if OR test of the patient shows the second or third degree of reaction, the patient is considered unfit for the occupation. Considerable displacement of the head and trunk (3º of somatic reactions) without any vegetative reaction is not considered a contraindication to professional activities provided that somatic reflexes are brought to physiological end points by special training. People of maritime and aviation professions experience a significant load on the vestibular apparatus and the otolithic system in particular. Therefore one-time research with the help of OR appears insufficient. Research of otolithic apparatus sensitivity is a necessity for irritations cumulation. For this purpose we use the K. Khilov’s test of balancing on the four-stem swing. During the main part of the research the patient is sitting on a swinging platform with the eyes closed. Swinging is conducted for 15 min. The time of vegetative reactions (skin pallor, nausea, and vomiting) appearance is a sign of the patient’s sensitivity to vestibular irritation. 4 degrees of cumulation are distinguished: 0 degree – vegetative symptoms are absent during 15 min of swinging; I degree – nausea and vomiting appear in 15 min of swinging; II degree – nausea and vomiting appear in 5–10 min of swinging; III degree – vomiting appears during the first 5 min of swinging. People, who got through 15 min of swinging with no obvious vegetative symptoms, are considered resistant to statoconial membrane irritation. Nonpersistent persons are those with the second and third degree of cumulation. Individuals, who have the first cumulation degree, are subject to retest. For more careful selection of candidates for aviation and space professions we use the test of sensitivity to acceleration – the Coriolis’ test. Accelerations appear when an individual is exposed to mutually perpendicular forces. They can be produced by rotation of the patient vertically and horizontally at the same time. This can be achieved by rotating the patient in a chair, asking him to continuously bow his head forward and backwards or to the left and to the right. Thus, permanent angular 26
  • 27. motions perpendicular to plane’s motion, for example in an aircraft, produce Coriolis acceleration. To determine sensitivity to Coriolis acceleration the test of continuous Coriolis acceleration cumulation in S. Markoryan’s modification was used (1966). The patient revolves in an arm-chair at a speed of 1 turn a second with the eyes closed and vertical head position. In the end of the 5th turn against the background of steady rotation the patient begins to flex the head from the right shoulder to the left one. The patient must report if and when he starts feeling heat, cold, illusion of swinging, bad general condition, vegetative discomfort (e.g. nausea). During rotation one should start recording the results after the onset of vegetative disorders of the patient: face skin paleness, appearance of cold sweat, swallowing movements, and vomiturition. If any vegetative disorder appears in the patient, the test is stopped. Individuals, who get through the test for longer than 3 min are considered apt for aerial, nautical and space professions with their vegetative stability being good. Individuals, who got through the test for less than a minute and started manifesting vegetative symptoms, are considered inapt and unsuitable for any work with load on the vestibular system. During occupational selection the type, amount and results of different tests are regulated by specific orders and instructions from different organizations with different assessment criteria for different professions. 27
  • 28. CHAPTER 4 Ear diseases 4.1. Ear maldevelopments There are maldevelopments of the external, middle and inner ear. However, auricle maldevelopments are observed more frequently. Possible anomalies are observed in the 1) auricle, 2) auricle, external auditory canal, tympanic cavity, 3) external, middle ear; face bones defects also take place. There are such auricle maldevelopments: macrotia – a large auricle; microtia – a small, deformed auricle (Fig. 12, 13); anotia – absence of auricle; squarrose auricles (Fig. 14); auricle appendages – small cutaneous formations, which are located in front of the auricle and consist of skin, hypoderm and cartilage (Fig. 13); parotic fistulas, which are frequently located near the base of the crus of helix (Fig. 15). Auricle anomalies lead to cosmetic defects of the face often accompanied by hypoplasia (Fig. 12) or agenesia of the external acoustic meatus, can combine with middle ear hypogenesis. Maldevelopments of the external acoustic meatus and middle ear lead to the conductive type of hearing loss. The treatment of ear maldevelopments is surgical. Plastic operations are to be performed. In case of macrotia the auricle must be reduced to normal size. When auricle microtia or underdevelopment is present, a new auricle is to be formed. If atresia of the external acoustic meatus takes place, a new external auditory canal must be formed. 4.2. Traumatic injuries of ear 4.2.1. Auricle wounds There are distinguished traumas of the auricle and traumas of the external acoustic meatus. 28
  • 29. Auricle damages are subdivided into gunshot wounds, cut or lacerated wounds, ruptures and burns. Often there are bite wounds as a result of a dog’s or human bite. Sometimes partial or complete abruption of the auricle can take place. The external auditory canal is often injured by different objects: spokes, matches, etc. It often takes place during combing or ear cleaning. Treatment. The sooner the injured patient comes to the hospital, the better treatment results will be. First of all the initial surgical d-bridement of the wound is conducted. The wound is washed with 3 % hydrogen peroxide, then dried with gauze tampons. The skin around the wound is treated with iodine and alcohol. The wound edges are jointed and sutured. In case of complete auricle abruption a plastic operation is carried out. After it the sutures are processed with iodine or alcohol and a tight aseptic bandage is applied. Tetanus antitoxin and tetanus vaccine are injected into the patient. Antibiotics are prescribed. If the patient was bitten by an unknown dog, he must take a complete course of inoculations against hydrophobia under observation of an infection disease doctor. 4.2.2. Othematoma Othematoma is accumulation of blood between the perichondrium and auricular cartilage. It appears as a result of a blunt injury of the ear, but sometimes spontaneously. It happens more often to boxers and wrestlers. Clinical presentation. The auricle skin is purple. The auricle, especially in its superior part, is thickened. The bulge is elastic, tense, more evident on the anterior surface of the auricle. On this surface the perichondrium is less densely connected to the cartilage. Fluctuation is observed. The patient complains of obtuse pain in this area, sometimes sense shock of the auricle. Treatment. The ear is processed with iodine or alcohol. Othematoma is punctured, its contents are drained. A tight compressive aseptic bandage is applied. In case of suppuration of othematoma contents it is incised. The cavity is washed with 29
  • 30. antibiotic solution, a rubber drain is inserted with gauze tampons saturated with hypertensive solution. An aseptic bandage is applied. Antibiotics prescription is obligatory. 4.2.3. Auricular chondroperichondritis Auricular chondroperichondritis is purulent inflammation of perichondrium and auricular cartilage. More frequently it develops as a result of auricular hematoma suppuration. It can take place after insect bites, burns, frostbite of the auricle. Pseudomonas aeruginosa is often found by means of bacteriological investigation. Clinical presentation. Intense pain in the auricle is observed. The auricle becomes red and thick. The temperature of the patient’s body increases. In serious cases pus appears between the perichondrium and cartilage. Purulent melting of the auricular cartilage takes place. Dead tissue tears away, and as a result the auricle deforms strongly and becomes shrunken. Treatment. Broad spectrum antibiotics are prescribed. The abscess is incised, cavities are washed with antibiotic solution. Rubber drains are put in. Gauze tampons with hypertensive sodium chloride solution are applied to the ear. A pressure bandage is applied on the ear. The cavities are washed daily with antibiotics to their complete cleansing, aseptic salve dressings are applied. Such physiotherapeutic procedures as ultraviolet radiation or therapeutic laser are used. 4.2.4. Frostbite and burns of the auricle Frostbite of auricle takes place under the action of very low temperature. It happens more frequently than frostbite of other parts of body because the skin of auricle is thin and there is no hypoderm. There are differentiated three stages of frostbite: 1. Erubescence. 2. Formation of blisters with transparent contents. 30
  • 31. 3. Auricle necrosis. Treatment. At the first stage of frostbite one should carefully rub the auricle with alcohol and apply dry bulky dressing. At the second stage – conduct section of blisters. The section is conducted in aseptic conditions. Then antiinflammatory ointments are applied on the frost-bitten areas. In case of the third degree of frostbite surgical d-bridement is conducted. Necrotizing areas are removed. One should appoint antibiotics internally or parenterally depending on the patient’s weight. Antiinflammatory ointments are used. Auricle burns are caused by hot water, steam, molten metal, some chemical substances, electric current. Four degrees of burns are distinguished. 1. Erubescence. 2. Formation of blisters with transparent contents. 3. Necrotic patches. 4. Charred auricle. Treatment. Burns of the 1st –2nd degrees are treated with antiinflammatory aerosols. If the burn is of the 2nd degree, section of blisters is conducted in aseptic conditions. Antiinflammatory hormonal ointments are used. At burns of the 3rd –4th degrees burn shock is possible. Intensive anti-shock therapy is administered. Surgical removal of necrotizing areas is conducted. Antiinflammatory ointments are used. Antibiotics are administered. 4.2.5. Injuries of the internal and middle ear Eardrum damage is the most frequent trauma occurring at peacetime. Eardrum trauma can be direct or indirect. A direct eardrum trauma happens as a result of foreign body removal, when the eardrum is injured with a pin or a match during cleaning of the external acoustic meatus. Indirect eardrum ruptures may be caused by 31
  • 32. basal skull fracture, a blow in the ear, jumps into the water from a height, rapid decompression (in divers), petard explosion close by, etc. Eardrum trauma can be accompanied by onset of a sudden acute pain in the ear, noise, hearing loss. Otoscopy of the external acoustic meatus detects blood, hemorrhages, eardrum perforation of different size and form. As a result of eardrum rupture an infection that can result in the development of acute suppurative otitis gets into the tympanic cavity. In case of mastoid process damage infection penetrates the bone causing osteomyelitis, which is accompanied by the clinical picture of acute mastoiditis. In case of a middle ear trauma there can be a rupture of the auditory ossicles chain resulting in hearing impairment of conductive type. Possible traumas of the labyrinth are direct and indirect. At peacetime the former are rarely observed, sometimes as a result of surgical interference on the middle ear. There can be stapes dislocation in the oval window, an injure of the lateral semicircular canal. Indirect traumas of the labyrinth are observed in case of basal skull fractures, which include periotic bone fractures and injure of the great blood vessels of the cranial cavity. The clinical picture in case of basal skull fractures is characterized by the syncopal state of the patient. It is possible to detect hemorrhages under the conjunctiva and in the area of eyelids. In case of longitudinal fractures of the periotic bone eardrum perforation takes place, through which blood and cerebrospinal fluid flow. The function of the cochlear and vestibular apparatus is slightly violated. In case of transverse fractures of the periotic bone the cochlear and vestibular function is completely impaired and facioplegia is observed. Such patients require skull roentgenography, lumbal puncture, eyeground inspection, and study of the functional state of the cochlear and vestibular apparatus. 32
  • 33. The labyrinth can be also damaged as a result of acute atmospheric pressure fluctuations – that is a barotrauma. It happens in divers, pilots of airplanes. Action of intensive sound causes an acoustic trauma. The cochlea can be damaged during operations on the middle ear. All this results in the development of sensorineural hearing loss. Treatment. Eardrum rupture needs careful adjustment of perforation edges. With the help of the operating microscope the edges of the ruptured eardrum are straightened and adjusted. Fibrin tape is applied above the adjusted edges to preserve their integrity. A sterile turunda is introduced into the external auditory canal. Antiinflammatory treatment is administered. Such microsurgical interference is possible only during the first days after the trauma, until suppuration signs appear. In case of mastoid bone injure surgical debridement is conducted with removal of the broken bone. The wound is not sutured, it is treated by the open method. Traumas of the labyrinth caused by basal skull fractures need careful transportation of the patient. In hospital otorrhagia is stopped by introduction of sterile turundas into the external auditory canal. In case of heavy bleeding or meningitis signs surgical interference is conducted on the middle ear. In case of an acoustic trauma of the labyrinth antineuritic complex therapy is prescribed. 4.3. Foreign bodies of the external auditory canal Foreign bodies are more frequently found in children, who push various objects into the ear. In adults these can be pieces of matches, cotton wool, corn, metal parts, etc. Different insects can get into the external auditory canal, e.g. cockroaches, bedbugs. Clinical presentation. Usually foreign bodies do not cause unpleasant sensations. But if a foreign body is sharp, it can cause blood-tinged discharge from the 33
  • 34. ear, pain. Especially acute pain arises if insects get into the ear. There can be cough, dizziness. Foreign bodies are clearly seen during otoscopy. Treatment. The ear is to be washed with warm water by means of the Janet’s syringe. If washing is ineffective, the otolaryngologist removes the foreign body with a blunt hook (Fig. 16). It is impossible to remove the foreign body with pincers because this instrument pushes the foreign body deeper into the external auditory canal. If an insect gets into the ear, at first it is necessary to stop its movement. For this purpose alcohol or warmed vegetable oil is applied into the ear by dropping. Then the foreign body is washed out with a syringe. 4.4. Auricle diseases 4.4.1. External otitis External diffuse otitis. Otomycosis Generalized bacteriogenous inflammation of the external acoustic meatus skin is named external diffuse otitis. Etiology. The inflammation is caused by staphylococcus, streptococcus, hemophilic bacillus, blue pus bacillus, etc. Clinical presentation. Patients complain of pain in the ear, itch, burning. Pain is less intensive than at a furuncle. Pain in the ear increases at mastication, opening of mouth, pressure on the tragus – unlike middle otitis, at which pain increases at pressure on the mastoid process. Origin of the disease is usually related to a mechanical injury of the ear by a finger or pins, matches and other objects. Often external otitis arises as a result of skin irritation by purulent discharge at middle otitis. Otoscopy findings: the skin of the external auditory canal is hyperemic, infiltrated. The external acoustic meatus is narrow. Transparent excretions, which are interfused with deadened epithelium, can ooze from the skin. Then excretions can become 34
  • 35. purulent and form a stinking mass, which fills the external auditory canal. Hearing can get worse. Treatment. Tableted antibiotics are administered during 7–10 days. Antihistaminic and calcium preparations are prescribed. Local administration: washing-out of the ear with disinfectant solutions. Then the ear is dried with cotton wool and processed with antibacterial ointments on turundas. Physiotherapeutic procedures are administered. Otomycosis is external diffuse otitis caused by fungi. Clinical presentation. Similar to ordinary external diffuse otitis, but pain is far less evident. More apparent itch. Otoscopy: hyperemia and skin infiltration are less evident. Characteristic presence of transparent excretions in the external auditory canal, there can be yellow-brown or black stratifications on the skin of the external auditory canal. Duration of the disease is protracted, persistent. Treatment. Application of turundas with antifungal agents to the external auditory canal is administered during 1 month. Ultraviolet radiation is prescribed. Furuncle of the external auditory canal (external limited otitis) A furuncle is inflammation of a hair follicle or an oil-gland. These appendages of skin are located only in the membranous-cartilaginous part of the external auditory canal, they are not present in its osseous part. Therefore, if inflammation takes place in the osseous part, it is not furuncle but some other disease. Etiology: bacterial flora, staphylococcus is found the most frequently. The following factors contribute to disease development: decline of organism resistance, mechanical irritation of the skin of the external auditory canal, especially in patients with purulent discharge from the ear. Recurrent furuncles of the external auditory canal quite often testify to the presence of diabetes and are a manifestation of general furunculosis. 35
  • 36. Clinical presentation. Patients complain of acute pain in the ear. Occlusion of the external acoustic meatus with a furuncle or pus can injure hearing. Body temperature rises. The regional lymph nodes located under the auricle and on the mastoid can multiply. There are 2 stages of the disease: 1. Infiltration stage. 2. Abscess formation. Otoscopy shows a narrow external acoustic meatus, hyperemic, infiltrated skin of a limited area of the membranous-cartilaginous part of the external auditory canal. At the stage of abscess formation it is possible to see an eminence with a white apex in the center of hyperemia; lancing of the furuncle can show pus in the external acoustic meatus. Pressure on the tragus and opening of mouth are acutely painful. Treatment. At the infiltration stage disinfectants on turundas are administered locally as well as physiotherapeutic methods on the ear. At the stage of abscess formation furuncle section, pus removal, washing-out of the furuncle cavity with antibiotic solution are conducted (Fig. 17). Then the cavity is drained with a rubber strip and gauze turundas saturated with hypertensive sodium chloride solution. Antibiotics are given by a five-day course. Tableted antibiotics are administered. 4.4.2. Auricle eczema Auricle eczema is one of local manifestations of a common skin disease – eczema. This is a neuroallergic inflammation of surface layers of skin with evident itch. Clinical presentation. Small transparent blisters appear on the skin of the external auditory canal and auricle. Then they burst, and on their place multiple small erosions with abundant oozing lesion appear. After this crusts form on their place. The acute process lasts 1.5–2 months. There can be chronic eczema. 36
  • 37. Treatment is aimed at removing the irritating factor and treating concomitant diseases. Antihistaminic preparations, depressants, calcium preparations, and ascorbic acid are administered. Locally: antiseptic solutions and corticosteroid ointments are applied. 4.4.3. Auricle erysipelas This is an acute streptococcus disease of skin with formation of a sharply limited inflammation focus. If the skin of the auricle and external acoustic meatus is affected, we talk about auricle erysipelas. Etiology: streptococcus, which penetrates through small skin lesions. Clinical presentation. Body temperature rises. The auricle becomes very hyperemic, somewhat infiltrated, the external auditory canal becomes narrow. Treatment. Antibiotics of penicillin group are administered during 7–10 days. Antiseptic ointments are applied locally. Physical procedures – ultraviolet radiation on the auricle is administered. 4.4.4. Cerumen Cerumen is earwax accumulation in the external auditory canal as a result of surplus secretion of the earwax glands or violation of its normal evacuation. The increase of earwax viscidity and exostosis promote violation of earwax evacuation from the external auditory canal. Earwax can have admixtures of epidermis, which peels as a result of inflammatory diseases of the skin of the external acoustic meatus. Clinical presentation. Usually there are no evident symptoms. The patient has to consult a doctor after water gets into the ear, when cerumen is soaked and swelled, completely obstructing the external acoustic meatus. Hereupon the patient’s hearing gets worse suddenly. There can be complaints of ear noise, sensation of pressure in the auditory channel, or sensation of the voice echoed in the head – autophony. Diagnostics is not difficult. Earwax is usually clearly seen at otoscopy. 37
  • 38. Treatment. Washing-out of the external acoustic meatus is performed with the Janet’s syringe. By drawing the auricle back and up, water sheet is directed at the posterosuperior wall of the external acoustic meatus. Water must have the body temperature not to cause thermal irritation of the labyrinth and cause no dizziness. Usually earwax is easily washed. The external acoustic meatus is dried with cotton wool. On the 2nd –3rd hour a turunda is introduced with antiseptic. If the first washing does not appear effective, it is recommended to apply 3 % hydrogen peroxide by dropping in the ear 2–3 times per day during 3 days, whereupon to repeat the procedure. It should be remembered that at dry perforation of the eardrum water can get into the tympanic cavity and cause exacerbation of inflammatory process. Therefore before washing the ear one should carefully obtain anamnesis and find out from the patient whether there was some time with no purulent discharge from the ear. In such a case washing is contraindicated and cerumen is removed with a blunt hook. 4.5. Diseases of the middle ear 4.5.1. Acute suppurative otitis media Acute suppurative otitis media is acute purulent inflammation of the mucous tunic of middle ear air cavities. Typical features are: 1. It happens often. 2. Can result in evident loss of hearing. 3. Passes into chronic otitis. 4. Can lead to intracranial complications. Etiology. Viruses and bacteria cause acute purulent otitis media. These are viruses, which cause acute respiratory diseases, flu virus. Among bacteria it is more frequent in all staphylococci, streptococci, pneumococci, hemophilic bacilli, morhaxella. 38
  • 39. Pathogeny. The disease develops against the background of depressed organism resistance. Infection gets into the middle ear in the following ways: 1. From the nasal cavity through the auditory tube. It often happens at acute rhinitis. 2. Through the external auditory canal – when the eardrum is damaged. It takes place at eardrum rupture as a result of a trauma (more frequently after a blow in the ear; Fig. 18). At fresh eardrum ruptures such help is rendered: under the operating microscope the edges of the torn eardrum are adjusted to each other. They accrete thereupon. 3. Through blood – hematogenic way. This way is basic at infectious diseases – influenza, scarlatina, etc. In the pathogenesis of acute otitis media the state of nose, paranasal sinuses, and nasopharynx plays an important role. Chronic rhinitis, nasal septum deviation, purulent sinusitis contribute to disease onset. Clinical presentation. Acute suppurative otitis media is characterized by stormy development. It has three stages: 1) nonperforated; 2) perforated; 3) reparative. The symptoms of acute suppurative otitis media depend on the stage. The 1st stage. The basic complaint of the patient is pulsing, shooting, stabbing pain in the ear. Pain is felt deep inside the ear. It is caused by the fact that pus forms in the tympanic cavity. It holds apart the tympanic cavity walls, presses on the eardrum. The patient’s condition gets worse. General weakness appears. Sleep and appetite get worse. Body temperature rises to 38–39º C and higher. Inflammatory changes appear in the blood test. Otoscopy findings: at first eardrum reddening appears (hyperemia; 39
  • 40. Fig. 19). The eardrum becomes thick later. When much pus is accumulated in the tympanic cavity, the eardrum bulges outside (Fig. 20). The 2nd stage. Perforation takes place at this stage – that is eardrum rupture. Purulent discharge exudes from the ear. Pain gets better in the ear, general condition improves, body temperature decreases. Otoscopy shows the pulsating reflex – pus exudes through the perforation drop by drop synchronously with pulse. The 3rd stage. The inflammatory process subsides, purulent discharge stops. The eardrum recovers normal color. Still, hearing impairment remains. Hearing is restored slowly. Small perforation heals completely leaving no scars. Large perforation can not be closed up. In children acute otitis media arises more often. This is predefined by the anatomic features of the children’s ear. The disease usually begins suddenly, at night. Body temperature is very high – 39–40º C. The child feels uneasy, twists the head round, seizes the affected ear with a hand. General condition gets considerably worse. Babies can have vomit, gastroenteric upset. At infectious diseases the clinical course of acute otitis media also has its peculiarities. The severest changes in the ear are observed at scarlet fever. Necrosis begins in the ear (Fig. 21, 22, 23). All middle ear structures disintegrate. The auditory ossicles are destroyed. Excretions from the ear begin to stink. There is hemorrhagic otitis at influenza. Blood accumulates in the tympanic cavity. Blisters with bloody content form on the eardrum and osseous part of the external auditory canal (Fig. 24). At tuberculous otitis there are numerous eardrum perforations, malodorous pus (Fig. 25). Treatment depends on the stage of the disease. The 1st stage. Home or bed rest is prescribed. At severe condition hospitalization is administered. The diet is vitaminized, which is easily digested. Antibiotics and vasoconstrictive nasal drops are administered. Analgesics are used. Antihistaminic and calcium preparations are prescribed. Antibacterial ear drops are 40
  • 41. used. At the beginning of the disease, when there is no pus in the tympanic cavity yet, physiotherapeutic methods are applied. But when pus appears in the tympanic cavity, physiotherapeutic procedures are contraindicated. Severe pain in the ear, eardrum prolapse are indications to the auripuncture or paracentesis (Fig. 26, 27). The eardrum is punctured with a special spear-shaped needle. Pus is aspirated. Antibiotic solution is introduced with a syringe into the middle ear cavity. Solution penetration into the nasopharynx testifies to the fact that the otosalpinx is free. The patient admits that the taste of medicine appears in the mouth or nose. The 2nd stage. At the perforating stage of otitis the ear is to be cleaned 2–3 times a day with dry cotton wool on an ear probe. Use 3 % hydrogen peroxide to soften pus. Usually the ear is cleaned with an aspirator. After this antibacterial drops on turundas are introduced into the ear. A turunda is to be brought deeply into the external auditory canal, up to the eardrum. The 3rd stage. At the reparative stage treatment consists in rehabilitation of ear functioning. Ear inflation is conducted as well as otosalpinx catheterization and eardrums pneumomassage (Fig. 28, 29, 30). 4.5.2. Mastoiditis Mastoiditis is a purulent inflammatory disease of the mastoid bone. More frequently it arises as a complication of acute otitis media, or develops at exacerbation of chronic otitis media. Organism reactivity decrease is one of the factors of disease onset. Inefficient treatment of acute otitis – too late auripuncture or paracentesis – also results in mastoiditis development. Clinical presentation. General and local symptoms of mastoiditis are distinguished. General symptoms are the same as at acute suppurative otitis media. Body temperature rises. The patient feels worse. Blood test shows inflammatory 41
  • 42. changes. Unlike acute otitis, pain in the ear does not get better even when perforation takes place. Pain is very intensive, pulsating. Local symptoms are the following. 1. Pain at pressure on the mastoid. 2. Slight swelling of the mastoid, sticking out auricle. 3. Otoscopy: purulent discharge increase. Pus pulsation recommences, pus becomes thick. Characteristic symptom: overhang of the superoposterior wall of the osseous part of the external auditory canal (Fig. 31). 4. Sometimes pus can break from the mastoid outside. Thus subperiosteal abscess develops. It can result in formation of a fistula, through which pus will ooze. There can be an atypical course of mastoiditis. Then there is no eardrum perforation and purulent discharge from the ear. In children of the first year of life the mastoid structure has peculiar features. Therefore antritis is talked about – inflammation of the mucous tunic of the mastoid cavity. Valuable information for diagnosis verification is provided by CT or roentgenography (Fig. 32). Treatment. Conservative and surgical types of mastoiditis treatment are distinguished. Conservative treatment is the same as at acute otitis media of the second stage. Ear cleaning is conducted, disinfectants are applied by dropping into the ear. Antibiotics prescription is obligatory, preferably intramuscularly. Antiinflammatory medicines are administered, such as aspirin. Antihistaminic medicines, vitamins, and calcium preparations are prescribed. If these measures are ineffective, elective operation is to be conducted – mastoid trepanation (mastoidotomy; Fig. 33, 34, 35, 36). In case of subperiosteal abscess or development of intracranial complications the operation must be conducted urgently, without waiting. In children antritis is treated by mastoideocentesis – puncture of the mastoid cavity with diagnostic and medical purposes. 42
  • 43. 4.5.3. Chronic purulent otitis media Chronic purulent otitis media is a long-term inflammatory infectious disease of the middle ear cavities, which has a clinical course with periods of remission and exacerbation. Beginning of the disease is related to acute otitis the patient had in childhood. Disease outcome: 1. Hearing loss. 2. Facial paralysis, labyrinthitis. 3. Life-threatening ntracranial complications. Etiology. Staphylococcus or mixed microbial flora, moulds. Pathogenesis. High virulence of microorganisms and weakened resistance are instrumental in transition from acute otitis to chronic. The presence of other concomitant diseases is of great importance. The state of the nasal cavity, paranasal sinuses and pharynx play a certain role. Quite frequently recurrent acute suppurative otitis media passes to chronic. Clinical presentation. Obligatory signs are as follows: 1. Long-term purulent discharge from the ear. The disease lasts for years. 2. Constant eardrum perforation with callous edges. 3. Hearing impairment, ear noise. The disease may have two forms: mesotympanitis and epitympanitis. Mesotympanitis is a benign form of chronic otitis. At mesotympanitis the middle and inferior parts of the tympanic cavity are affected. Patients complain of purulent discharge from the ear and hearing impairment. Pain in the ear appears only in the period of exacerbation. General condition is not violated in the period of remission. During exacerbation purulent discharge from the ears increases. Pain appears in the ear, febricula. Body temperature rises. Blood test shows inflammatory changes. 43
  • 44. Diagnosis is determined on the basis of otoscopy. There is odourless mucopurulent content in the external auditory canal. Sometimes excretions from the ear can have objectionable odor. It happens in slipshod patients, because of bad ear hygiene. After washing and careful care of the ear an unpleasant smell disappears. The eardrum has almost normal color. Eardrum perforation is central. It means that around the perforation the eardrum limbus is preserved (Fig. 37). Perforation can be large. Then it is possible to examine the tympanic cavity through it. Pus and thickened mucous tunic will be visible in the tympanic cavity. Granulations are possible. Large granulation has the name of aural polyp. A polyp can be large, it can even block the external auditory canal. This results in pus deposit in the middle ear cavities and leads to complications. In such a case polyp removal is the first aid. Hearing gets worse at mesotympanitis. Sound transmission is violated. It can be determined by audiometry. Epitympanitis (attic disease) is a poor quality form of chronic otitis. At this form there is destruction of the bone walls of the middle ear cavities. It can lead to severe complications. At epitympanitis the superior floor of the tympanic cavity is necessarily affected. Other floors can also be affected. The main feature of epitympanitis is affection of not only the mucous tunic of the tympanic cavity, but also of the bony structures. Bone affection is named caries. Patients have the same complaints as at mesotympanitis. Besides, they can complain of headache and dizziness. In the period of remission general condition is satisfactory. Temperature rises during exacerbation, pain appears in the ear. The patient feels febricula. Purulent discharge from the ear increases. Blood test shows inflammatory changes. Diagnosis is determined on the basis of otoscopy. At epitympanitis there is pus in the external auditory canal. The amount of pus is often small. Pus always has unpleasant smell. It takes place as a result of bone caries. Unpleasant smell is the same as at teeth decay. Abundant excretion at epitympanitis is observed in two cases: 44
  • 45. first – at cholesteatoma suppuration; second – at extradural abscess, when pus is accumulated between the bone and dura mater of brain. Excretions are abundant, malodorous, appear shortly after ear cleaning. In such cases the ear must be operated. Eardrum perforation at epitympanitis is marginal. It reaches the bony eardrumtympanic ring. The perforation necessarily takes part in the superior part of the eardrum (Fig. 38). Epitympanitis is characterised by the presence of a passage in the epitympanic recess. One should conduct perforation probing with the Wojaczek ’s probe. If there is a passway, the probe easily falls into the attic. One of epitympanitis complications is cholesteatoma – stratification of furfures and cholesterol. It has a shell. Cholesteatoma in the ear is an inflammation product. It often festers. The danger of cholesteatoma consists in bone destruction. Depending on the direction of cholesteatoma growth it can ruin the Fallopian aqueduct, external semicircular canal, superior wall of the tympanic cavity or mastoid. Then there is facial paralysis, labyrinthitis or intracranial complications. Roentgenological study helps to detect cholesteatoma. A roentgenogram of the temporal bone is made in the Schuller’s view (Fig. 32, 39). Ear affection at epitympanitis is more evident than at mesotympanitis. Except for sound conduction violation, violation of sound sensation takes place. Audiometry shows it. In most patients chronic otitis media has an allergic component. Complex research of a patient with chronic otitis media must include consultations of a neurologist and an oculist. It is necessary to timely diagnose the origin of intracranial complications. There must be conducted X-ray study of the temporal bone and audiometry. Treatment. Common medical measures include organism hardening. The measures are taken to strengthen general reactivity of the organism. Calcium 45
  • 46. preparations, vitamins, and antiallergic preparations are administered. Routine common uviolizing, rational nutrition are recommended. Antibiotics are used only at exacerbation of the process. Necessarily inspect the nose, nasopharynx and pharynx, paranasal sinuses. These organs are sanitized if it is necessary. Local treatment of chronic otitis media consists of two stages. 1. Ear cleaning. 2. Introduction of medications into the tympanic cavity. Before local treatment granulation and polyps are removed from the tympanic cavity. Large granulation or ear polyps are removed with the conchotome, curet or loop (Fig. 40). Small granulation is cauterized with silver nitrate. The 1st stage. Ear cleaning. 3 % hydrogen peroxide is applied by dropping into the ear. Pus is removed with an ear probe and cotton wool. It is possible to wash pus from the tympanic cavity with disinfectant solutions. For pus softening the ear is to be washed with enzymes. At presence of large perforation, washing is carried out with the Janet’s syringe. To wash the attic use the Hartman’s canula (Fig. 41). After washing carefully dry the ear with an ear probe with cotton wool, or with a blunt canula connected to an aspirator. Careful ear cleaning guarantees successful treatment. The 2nd stage. Introduction of medications into the tympanic cavity. Substances are introduced into the tympanic cavity in such medical forms: 1) solutions (drops); 2) powders; 3) ointments. Mainly these are exsiccants. Alcoholic solutions of antiseptic preparations are used. Solutions of antibiotics are administered upon obtaining results of ear microflora analysis on antibiotics sensitivity. Astringents are used, e.g. 1–2 % nitric silver solution. After ear cleaning it is possible to blow powders into the tympanic cavity: boric acid, antibiotics, sulfanilamides. Insufflations are conducted carefully, not to inject surplus powder. 46
  • 47. Purulent otitis media of mycotic origin is an otomycosis variety. Antifungal agents are used to treat it. At allergic manifestations of otitis antiallergic and corticosteroid drops are used. To treat chronic otitis media varied physiotherapeutic procedures are used – electrophoresis with antibiotics, 1–2 % solution of nitric silver solution. Ultraviolet radiation and aeroionotherapy are applied on the ear. Mud therapy is used: mud applications on the mastoid. Mud therapy application is possible only in the period of remission. At otomycosis laser is used. Medicinal substances, which are introduced into the ear, must be changed every 2–3 weeks. Durable use of alcoholic solutions is not advisable. The main recommendation to patients with chronic otitis media – to protect the ear from water. During bathing or washing of hair the patient must close the ear with cotton wool soaked with vaseline, olive oil, or any other ointment. The described treatment is used more frequently at mesotympanitis. At epitympanitis it is also possible to begin with conservative treatment. However, surgical method is basic in epitympanitis treatment. One should distinguish two types of operations in the surgical treatment of chronic otitis media. 1. Sanation operations. Radical operation is basic. It eliminates the purulent focus in the ear. Its purpose is to prevent intracranial complications. 2. Hearing improvement operations – tympanoplasty. Five types of tympanoplasty are distinguished by Wulstein. 4.5.4. Labyrinthitis Labyrinthitis is a complication of acute and chronic otitis media. It is an inflammatory infectious disease of the inner ear. Infection from the middle ear cavity gets into the inner ear and causes an inflammatory process in it. Rarely labyrinthitis 47
  • 48. can arise as a result of meningitis or an infectious disease (for example, epidemic parotitis). Etiology. The direct reason for labyrinthitis is microbes, which are causative agents of acute and chronic otitis media. Necrotizing labyrinthitis usually arises at tubercular or scarlatinal otitis. Classification. Acute and chronic types of labyrinthitis are distinguished. There are the following forms of acute and chronic labyrinthitis: a) erosive; b) purulent; c) necrotizing. Chronic labyrinthitis is subdivided into: 1) limited; 2) diffuse. Diffuse labyrinthitis is a process, which affects all structures of the inner ear. Limited – a process, which affects a part of the labyrinth only. Limited labyrinthitis arises, when there is a fistula in the lateral semicircular canal. A fistula appears as a result of caries. We will describe labyrinthitis forms. Limited labyrinthitis is observed at chronic otitis media complicated by caries and cholesteatoma. The bony capsule of the lateral semicircular canal gradually collapses and a fistula is formed. Clinical presentation. Patients complain of periodic dizzinesses accompanied by nausea or vomit, unbalance. Nystagmus can appear – rhythmic horizontal twitching of the eyeballs. Nystagmus is directed at the affected ear. If dizziness is present, the patient complains of rotation of surrounding objects or his own body in one direction. The symptom of fistula is another important sign. Nystagmus appears if the tragus is pressed with a finger. This nystagmus is named pressure nystagmus. The 48
  • 49. eyeballs begin twitching to the affected side. Sometimes nystagmus is caused by cleaning of the ear with a cottonwool tampon. At this moment the patient feels dizziness. The nystagmus caused by irritation of the labyrinth is accompanied by dizziness, nausea and declining or falling to the side, opposite to the affected ear. At limited labyrinthitis hearing is not necessarily impaired. Hearing loss depends on the presence of inflammatory process in the middle ear. Vestibulometry allows confirming the diagnosis. After a sanation operation on the ear the process is usually stopped. Self- recovery without operation is rarely observed. Treatment of limited labyrinthitis. At exacerbation of the process bed rest, antibiotics, sulfanilamides, and dehydratation are administered. Sanation operation is conducted on the middle ear. Acute diffuse serosal labyrinthitis can develop at acute middle otitis or exacerbation of chronic otitis media. Clinical presentation. The auditory and vestibular functions are violated. Evident lowering of the ear is characteristic. Nystagmus appears. At first it is directed at the affected ear, then it changes direction and to the opposite site. Dizziness, nausea and vomit appear. Equilibrium is violated. Vestibular symptoms are most evident. Dizziness increases and is accompanied by vomit at the change of head position. At dizziness the patient feels rotation of objects or his body. Vestibulometry allows confirming the diagnosis. Treatment. Rest, antiinflamatory and dehydration therapy are administered. At acute middle otitis medicinal treatment often leads to convalescence. At mastoiditis and chronic otitis media routine surgical treatment is used. Sanation operation is conducted on the middle ear. If it is not conducted, intracranial complications may take place. Operation is conducted immediately against the background of antibiotic treatment. 49
  • 50. Acute diffuse purulent labyrinthitis. This form of labyrinthitis has an extraordinarily severe clinical course and complications. It always ends with complete loss of hearing and vestibular function. In addition, intracranial complications may arise. Meningitis and cerebellum abscess can develop. Clinical presentation. Beginning and clinical course of the disease are stormy. Evident dizziness, nausea and vomit, acute balance disturbance, spontaneous nystagmus are basic symptoms. Complete and irreversible loss of the auditory and vestibular functions happens very quickly – that is the difference between purulent and serosal labyrinthitis. At the beginning of purulent labyrinthitis nystagmus appears directed at the affected ear, but already in a few hours nystagmus changes its direction. At unfavorable clinical course there can be complications – meningitis, cerebellum abscess. Treatment. Operation is conducted immediately against the background of antibiotic treatment. Necrotizing labyrinthitis is observed mainly at scarlatinal and tubercular otitis, sometimes at rubeola. Due to antibiotics use it is observed rarely. Clinical presentation of necrotizing labyrinthitis is similar to the clinical presentation of purulent labyrinthitis, but the clinical course is severer. Necrotizing labyrinthitis is an indication to operation on the ear with interference on the labyrinth. 4.6. Otogenic intracranial complications and otogenic sepsis Otogenic intracranial complications are severe, life-threatening diseases. They arise because of penetration of infection from the ear into the cranial cavity. It takes place in case of acute and chronic otitis media. Meningitis or meningoencephalitis frequently arises against the background of acute purulent otitis media. More frequently otitis is complicated by meningitis. Rarer abscesses of the brain and 50
  • 51. cerebellum develop. Even rarer there are sigmoid sinus thrombosis and otogenic sepsis. Sometimes there can be a few complications simultaneously, for example sinus thrombosis and cerebellum abscess, or meningitis and abscess of the cerebral hemispheres. Etiology. The reason for otogenic intracranial complications is the same microbes, which cause otitis. Staphilococci, streptococci, and pneumococci prevail in case of acute otitis. In case of chronic otitis – also certain Proteus, Pseudomonas aerogenosis, etc. Pathogenesis. Depending on the stages of infection spread from the ear into the cranial cavity abscesses may be located above the dura mater (extradural abscess) and between the brain tunics (subdural abscess). The inflammatory process can pass to the venous sinus. As a result sinus thrombosis forms. If infection penetration is deep, disseminate meningitis develops. If the process spreads, the cerebrum tissue can be affected. It results in the formation of cerebral hemispheres and cerebellum abscesses (Fig. 42). We will consider basic types of otogenic intracranial complications. Otogenic disseminate purulent meningitis is brain tunic inflammation. The arachnoid and vascular membranes are affected. The infection penetrates from the middle and internal ear. Meningitis can arise due to other otogenic complications, for example sinus thrombosis. Clinical presentation. Headache is the most frequent and the first symptom of otogenic meningitis. Headache is very intensive. The reason for this is intracranial pressure rise. Any external irritation increases pain. For example, touching the patient’s skin, loud sounds, bright illumination. Therefore such a patient must be treated in certain conditions without such irritations. Nausea and vomiting are the next symptoms. Frequently they appear at the height of headache and are not connected with food intake. Quite often vomiting temporarily improves headache. 51
  • 52. The general condition of the patient is grave. At later stages loss of consciousness passing to delirium can appear. Quite often patients assume the position of a gun cock or a hunting dog. They lie on the side or on the back with bent feet and thrown back head. The patient reflexively assumes the given position because it relieves headache. Body temperature is permanent, it rises to 38.5–39° C and higher. Pulse is rapid and corresponds to body temperature. Meningitis is characterised by meningeal symptoms: 1. Neck muscles rigidity. The doctor places the hands under the patient’s head and flexes it forward. In case of meningitis the patient’s neck flexes badly. The chin does not reach the breastbone. 2. The Kernig’s symptom. The patient is lying on the back, legs bent in the hip and knee joints. Try to unbend the leg in the knee joint. In case of meningitis the leg can not be unbent completely. 3. The Brudzinski’s symptoms superior and inferior. During research of neck muscles rigidity the patient’s legs are bent and pulled up to the abdomen. It is the superior Brudzinski’s symptom. The inferior symptom: during extension of a patient’s leg the other leg bends in the knee and hip joints. In case of severe course of the disease there is observed eyeballs bulging, differently sized right and left orbits. Diagnostics. Blood test data of meningitis patients show inflammation signs. During eyeground examination stagnation is determined. Research of the cerebrospinal fluid taken by spinal puncture has a large value for meningitis diagnostics. Characteristic fluid changes are found in meningitis patiens. Otogenic sepsis. In case of purulent middle ear inflammation, both acute and chronic, infection is generalized, microbes get into the blood. There is sepsis. It is more frequent as a result of sinus thrombosis. 52
  • 53. Clinical presentation of otogenic sepsis and sigmoid sinus thrombosis. The symptoms observed in case of this disease are divided into two groups: 1. General symptoms, characteristic of sepsis of any nature. 2. Local symptoms conditioned by sigmoid sinus affection. General symptoms. One of the most expository sepsis symptoms is hectic fever. There is rapid increase of body temperature to 39–41° C, accompanied by chill. Then in a few hours temperature quickly (critically) falls. Temperature drops are accompanied by profuse sweat. There can be several rises of temperature during the day, therefore the patient’s temperature must be taken every 2 hours. Body temperature of younger children is permanent. Pulse accelerates according to the rise of body temperature. The patient’s skin is pale with a sallow tint. It can be sclera jaundice. There are changes characteristic of an inflammatory process in the blood test. Bacterial inoculation of blood is very important. In case of sepsis microbes can be found in blood. Blood for the test is to be taken during chill when body temperature rises. At otogenic sepsis microbes spread in the blood vessels and settle in other organs. There are abscesses in the lungs, joints, subcutaneous adipose tissue, and muscles. More frequently patients die from pulmonary complications. Local symptoms: there is edema and pain of soft tissues on the posterior margin of the mastoid, painful neck palpation on the affected side. Often the patient’s head is flexed toward the injury. Otogenic abscesses of the cerebral hemispheres and cerebellum are abscesses, which appear in the brain and cerebellum because of purulent otitis media. Clinical presentation. There are four stages of the clinical presentation of abscess: 53
  • 54. 1. The initial stage lasts for 2–3 weeks. The inflammatory process is characteristic. There are light meningeal symptoms: headache, sickness, body temperature rise, nausea, and vomiting. 2. The latent stage also lasts for 2–3 weeks. At this stage all symptoms either disappear generally, or declare themselves weakly. 3. The frank stage lasts for a few weeks. It is characterized by a large variety of symptoms. The patient feels weakness, appetite absence, exhaustion. Body temperature rises. Blood test shows inflammatory changes. However, these manifestations are considerably less evident than in case of meningitis and sepsis. There is headache, which increases during pattering with a finger on the skull above the area, where abscess is located. There is nausea and vomiting, which are not related to food intake. Pulse slows down to 45 bpm. The ophthalmologist determines stagnation on the eyeground. Cervical muscles rigidity and the Kernig’s symptom can appear. If abscess is located in the cerebral hemispheres, there will be paresises and paralyses of extremities. There can be facial paresis, when the face becomes asymmetric. There are cramps and other neurological symptoms. The patient falls on the side opposite to the affection. There can be dizziness. Hallucinations take place. The patient’s speech is violated. Sometimes it becomes incomprehensible, just senseless words. The patient can forget how to read and write. There are such symptoms of cerebellum abscess. Muscle tone of extremities decreases on the side of affection. The patient’s hand resists poorly during unbending. During examination of walking and Romberg’s position the patient bends to the affected side. Impossibility of flanking gait on the affected side is characteristic. During the pointing test the patient can not touch the tip of nose with the hand. The hand deviates to the affected side on the side of injury. There is spontaneous nystagmus directed at the affected side. 54
  • 55. Abscesses of the brain and cerebellum can lead to impairment of consciousness, breathing and cardiac activity. 4. The terminal stage of brain abscess. It is the last stage of abscess. Usually lasts for a few days and leads to patient’s death. Brain edema develops. The patient’s condition gets worse sharply. Intoxication becomes more intensive. Breathing and cardiac activity stops, the patient dies. Diagnostics of brain and cerebellum abscess. There are such modern methods of diagnosing these complications: 1. Echoencephalography. 2. Radioisotopic encephalography. 3. Computer tomography (CT) and magnetic resonance tomography (MRT). Medical treatment of intracranial complications. Mainly otolaryngologists and neurosurgeons administer medical treatment of patients with otogenic intracranial complications. However, neurologists, internists, pediatricians, infectiologists, and oculists must take an active part in the treatment. Medical treatment of patients with otogenic intracranial complications includes surgical interference and intensive drug therapy. Surgical interference directed at removal of purulent nidus from the middle ear and complication elimination. In case of acute purulent otitis media operation is conducted – extended antromastoidotomy. In case of chronic purulent otitis media extended radical surgery is performed. At otogenic meningitis the middle and posterior cranial fossae are dissected during the operation. If sigmoid sinus thrombosis and otogenic sepsis are present, an operation on the ear is performed. The posterior cranial fossa is necessarily opened. The sigmoid sinus is punctured. If it is necessary, the sigmoid sinus is opened and the blood clot is removed. In case of otogenic brain and cerebellum abscesses the otolaryngologist conducts antromastoidotomy or a radical operation. Then he opens the posterior or 55
  • 56. middle cranial fossa and punctures the brain tissue. After this the doctor opens the abscess and inserts drainage tube in the needle direction. If abscesses are plural or the abscess is located far from the affected ear, the abscess is opened by the neurosurgeon. Simultaneously with surgical treatment intensive drug therapy is administered. 1. Antibiotics are prescribed. Ceftriaxon, ceftazidime, vancomycin, metrogyl, penicillin in large doses introduced in injections. 2. Antiedemics are introduced intravenously. These are haemodez-N, blood plasma, albumen, mannitol, lasix, 40 % glucose solution, 10 % solution of sodium chloride, hexamethylenetetramine (urotropin), 5 % solution of ascorbic acid, retinol (vitamin A), hydrocortisone. Arterial pressure is controlled. 3. Antiallergic drugs are introduced intramuscularly. These include dimedrol, pipolphen, suprastin, etc. 4. During psychomotor agitation sodium oxybutyrate and seduxen are introduced intravenously with 40 % glucose solution. 5. In case of staphylococcus infection immunotherapy is conducted. Antistaphylococcic immunoglobulin is introduced intramuscularly. 6. Cardiac glycosides, analeptical drugs, anesthetics (in case of necessity) are administered. 7. All patients with otogenic meningitis suspected must undergo spinal puncture. Antibiotics are introduced into the spinal canal in case of need. 8. Heparin, syncumar, and neodicumarinum are administered using the guidance of coagulogram to treat sigmoid sinus thrombosis. It is very important to fight against brain edema. Use mannitol, 40 % glucose solution with insulin, magnesium sulfate, lasix intravenously. Steroids are administered: prednisolone, hydrokortisone or dexamethasone. Introduce 5 % solution of ascorbic acid, 10 % solution of calcium chloride intravenously. Introduce 56
  • 57. aminophylline, trental intravenously to improve cerebral circulation. Introduce sodium oxybutyrate, glutamic acid, thiopental sodium intravenously (slowly!). 4.7. NONPURULENT EAR DISEASES These diseases include reflux otitis media, otosclerosis, sensoneural hearing loss, Meniere’s disease. The diseases have such symptoms: 1) hearing disorder; 2) ear noise; 3) no signs of purulent ear inflammation. At the same time these diseases substantially differ from one another. 4.7.1. Reflux otitis media. Secretory otitis media The basic cause of the disease is auditory tube dysfunction. Reflux otitis media is characterized by inflammation of the mucous membrane of the middle ear, auditory tube obturation, loss of hearing, and (quite often) presence of liquid in the middle ear. Pathogenesis. The auditory tube connects the middle ear and the nasal cavity. Various inflammatory diseases of the nasal cavity, like rhinitis, sinusitis, adenoid affection, may result in reflux otitis media. Swelling of the auditory tube mucosa obstructs air flow passing through the tube to the tympanic cavity. As a result, pressure in the tympanic cavity becomes negative, tympanic membrane bending forms, the middle ear mucosa swells. Quite often this causes production of liquid, called exudate, in the ear cavity. Exudate accumulates in the middle ear, developing secretory otitis media. The allergic component plays an important part in the development of secretory otitis media. Persistance of secretory otitis media may lead to the formation of adhesions in the tympanic cavity, developing adhesive otitis. 57