1. ANATOMY OF THE PHARYNX AND LARYNX
2. OTOGENIC INTRACRANIAL COMPLICATIONS
3. NONINFLAMMATORY EAR DISEASES: SENSORINEURAL HEARING LOSS, OTOSCLEROSIS, MENIERE’S DISEASE, SEROUS OTITIS MEDIA
The pharynx is the expanded portion of the alimentary tract lying between the oral cavity and the esophagus. It is also part of the respiratory tract, as it connects the nasal cavity with the larynx. The upper part of the pharynx, called the epipharynx, communicates with the nasal cavity through the choanae and is known as the nasopharynx.
The openings of the Eustachian tubes lying on a level with the posterior ends of the inferior nasal turbinates are to be found on the lateral walls of the nasopharynx. An accumulation of lymphadenoid tissue in the top part of the posterior wall of the nasopharynx forms the pharyngeal or third tonsil, consisting of 5-6 lobes, and diverging from a common centre. In children aged two or three years this tonsil is often hypertrophied, as they grow older it decreases in size and by the age of puberty consists of diffuse lymphadenoid tissue scarcely emerging over the surface of the mucous membrane covering the nasopharyngeal roof. A plane which is a backward extension of the hard palate separates the nasopharynx from the middle part of the pharynx, known as the mesopharynx or, more commonly, as the oropharynx (Fig. 67).
The oropharynx is bounded by the posterior and lateral walls continuous with the corresponding walls of the nasopharynx, and anteriorly it communicates with the oral cavity through the fauces. The fauces are bounded by the soft palate above, by the base of the tongue below and by the anterior and posterior palatine arches, otherwise called faucial pillars, on the sides.
Oropharynx: (7) posterior wall of pharynx, (1) uvula, (3) palatine tonsil, (4) anterior faucial pillar, (2) posterior faucial pillar, (7) soft palate
The pharynx contains well-developed lymphadenoid tissue which forms fairly large masses embedded on both sides between the faucial pillars, which are known as the first and second palatine or faucial tonsils. The letter’s free surface facing the pharynx contains numerous pit-like depressions, or crypts, running through the entire body of the tonsil (Fig. 68). The squamous epithelium which lines the free surface of the tonsil also lines the crypts. A similar accumulation of lymphadenoid tissue at the base of the tongue forms the lingual, or fourth, tonsil. The ring-like chain of lymphoid tissue made up of these four tonsils and the lymphatic follicles in the mucous membrane is known as the lymphoid ring of the pharynx.
The plane that extends backwards from the base of the tongue divides the oropharynx from the laryngopharynx, or hypopharynx, which lies below and directly opens into the esophagus. The lower portion of the pharynx opens into the larynx. The mucous membrane of the nasopharynx consists of a stratified, columnar, ciliated epithelium, while its other two departments are lined with a stratified squamous epithelium. The pharyngeal mucosa contains numerous mucous glands.
Fig. 68. Horizontal Midline Section, of Tonsil Showing Deep, Branched Crypts Surrounded by Isolated Follicles
The constrictor muscles lie under the pharyngeal mucosa and serve to contract the middle and lower portions of the pharynx and push food into the esophagus.
PHYSIOLOGY OF THE PHARYNX
The pharynx serves as a passage for air and food, and also as a resonating chamber for the voice. Because the digestive and respiratory tracts cross each other at the pharynx it has reflex mechanisms to regulate the passage of food and air. At rest, the nasopharynx is open to the oral cavity, whereas in swallowing and in the articulation of certain vowels and consonants the soft palate is pulled up against the posterior pharyngeal wall and firmly shuts off the nasopharynx from the oropharynx, so preventing food from getting into the nasopharynx and nose, which sometimes happens in paralysis of the soft palate, for example, following diphtheria.
The passage of the alimentary bolus is accompanied by closure of the larynx, which moves up slightly under the base of the tongue, whose pressure compressed the epiglottis against the narrow entrance to the larynx, whereupon the bolus is passed into the esophagus.
The pharynx which is studded with gustatory nerve endings on the soft palate and at the base of the tongue, also functions as the organ of taste and performs the protective function of reflex muscular contraction in response to sharp thermic and chemical irritation or to the entry of foreign bodies.
As to the exact function of the pharyngeal lymphoid ring, this is still a matter for discussion. Most authors adhere to the “protective theory”, that is, regard the tonsils and the other lymphadenoid structures as a protective barrier against bacterial infection. In pathological conditions, the tonsils with their crypts which always harbour microbes prove, on the contrary, to be an entryway for infection and so account for the causal relationship between inflammations of the tonsils and constitutional diseases. In essence, the function of the lymphadenoid structures of the pharynx cannot be separated from the function of similar follicular structures in other organs, like Peyer’s patches of the small intestine, which produce lymphocytes and presumably neutralize infectious toxins entering the blood. For this reason, the removal of pathologically altered tonsils, corroborated by everyday practice, should not lead to any substantial damage from the viewpoint of their functional value for the body as a whole.
The other parts of the lymphoid ring and the lymphadenoid structures of the digestive tract will compensate for the defective function of pathological tonsils as well as for their complete removal.
The functional examination of the oral cavity and nasopharynx, the process of chewing and deglutition excluded, essentially consists in a gustatory test by using sugar, quinine, common salt and vinegar solutions to determine the taste for sweet, bitter, salty and sour substances respectively. The solution is applied on a glass stick to either side of the tongue in turn, with the nose being firmly closed to shut off the sence of smell.
In view of their different nerve-supply systems, the anterior and posterior parts of the tongue should be examined separately. The residue of the earlier used solution must be washed out of the mouth before any further examination is made.
METHODS OF EXAMINING THE PHARYNX
The oral cavity and oropharynx may be examined by means of artificial and natural lighting.
The patient and the source of light are placed in the same position as for examination of the nose; the head mirror is used similarly. Examination of the oral cavity which is a necessary prelude to examination of the pharynx commences with inspection of the lips and vestibule of the mouth. A spatula, or tongue depressor, is used to retract, in turn, the corners of the mouth and to avert with a gentle tug the upper and lower lips in order to note the colour of the mucosa, detect scratches, ulcers or fistulas and to inspect the gums and teeth. The tongue, as well as the hard and soft palates, should also be inspected. The floor of the oral cavity is examined by using the spatula to push up the tip of the tongue. The parts which are examined next are the faucial tonsils and the posterior pharyngeal wall. Here, the spatula is used gently to push down the dorsum of the tongue. The spatula must not be inserted too far into the mouth, or else the gag reflex will be brought into play. The patient should not put out his tongue or hold his breath, as this will interfere with the examination.
A stubborn child who resists examination by clenching its teeth must be firmly fixed in the same position as in adenoidectomy (see Fig. 71). If it does not open its mouth for breathing when its nose is pinched, the spatula is inserted in the mouth corner, behind the posterior molar, and pushed as far as the base of the tongue. This will cause the child to gag and open its mouth, which enables the doctor to depress its tongue with the spatula in order to examine the pharynx.
Attention is paid to the soft palate with its axches, the mobility of the soft palate as well as to possible fistulas, scars or fissures in the roof of the mouth. The normal colour of the pharyngeal mucosa is pink-red or pink, whereas the uvula and the faucial pillars often have a deeper hue.
In examination of the faucial tonsils, attention is given to the colour of their mucous membranes as well as to their size, possible adhesions to the faucial pillars, and the contents of the tonsillar crypts.
For inspection of the free surface of the tonsils hidden between the faucial pillars, as well as of the contents of the crypts, the anterior pillar is pulled outwards with a spatula or a blunt hook, and the spatula is gently pressed on the anterior pillar to shift the tonsil from its bed and to express the contents of its deep depressions. When the laryngeal part of the pharynx is being inspected the tongue is firmly pressed down and outwards, preferably with a curved spatula or a postnasal mirror, as in laryngoscopy.
In examination of the oral cavity and pharynx, it is essential to note simultaneously the condition of the submaxillary region and the lateral parts of the neck to detect enlarged lymph nodes metastases or tumour outgrowths, phlegmons, etc.
ANATOMY OF THE LARYNX
The larynx is a part of the wind-pipe, the upper end of which opens into the pharynx, through which it communicates with the oral and nasal cavities, while its lower end continues as the lumen of the trachea. The larynx lies in the anterior portion of the neck on a level with the fourth and sixth cervical vertebrae. A broad ligament connects the larynx with the hyoid bone above.
The laryngeal skeleton is made of cartilage (Figs. 84 and 85). The basic cartilage is the cricoid which resembles a signet ring in shape. Its narrow part faces outwards, while its broad, so-called signet portion looks backwards. Above it lies the thyroid cartilage which consists of two * wings or alae joined together at an angle and forming a notch at their junction. As this portion of the thyroid cartilage is covered with skin alone, it may be easily felt with the fingers, and in men it protrudes at the front of the neck, and is known as “Adam’s apple”. On the upper surface of the posterior part of the cricoid there are two arytenoid cartilages with two processes at their base, namely, the muscular and the vocal. The vocal muscle is attached to the latter. In addition, the laryngeal aperture is covered by a special cartilage, known as the epiglottis, which is attached by ligaments to the upper margin of the notch in the thyroid cartilage. All the laryngeal cartilages are bound together by numerous ligaments as well as by their joints.
The true vocal cords comprising the paired vocal, or thyroarytenoid, muscle are prominent in the laryngeal space. The vocal cords are stretched between the inner surface of the thyroid cartilage and the vocal process of the arytenoid cartilage on the appropriate side. In respiration, the vocal cords form a triangular opening for the passage of air known as the rima glottidis or the glottis (Fig. 86). In phonation the vocal cords draw nearer together.
Above the true vocal cords lie the false vocal cords which are simply two folds of mucosa. Between the true and the false cords, on the sides, there are two slit-like pockets, the so-called Morgagni’s ventricles whose mucosa has numerous glands which moisten the vocal cords.
Fig. 84. Ligaments and Joints of Larynx (Front View)
(1)epiglottis; (2) lesser comu of hyoid bone; (3) greater cornu of hyoid bone, (4) opening in thyrohyoid membrane for passage of superior laryngeal nerve; (5) thyroid cartilage; (6) tracheal cartilages; (7) cricotra-cheal ligament; (8) cricoid cartilage; (9) conus elasticus; (10) middle thyrohyoid ligament; (11) corpus adiposum; (12) thyrohyoid membrane
(2) Fig. 87. Laryngeal Muscles posterior cricoarytenoid muscle; transverse interarytenoid muscle; (3) oblique interarytenoid muscles
Fig. 86. Larynx in Vertical Section
(1) epiglottis; (2) extrinsic thyroarytenoid muscle; (3) Morgagni’s ventricle, (4) true vocal cord; (5) cricoid cartilage; (6) false ligament; (7) thyroid cartilage;(8) glottis; (9) subglottic region; (10) trachea
The laryngeal muscles. These may be divided into the extrinsic and the intrinsic muscles. The former connect1 the larynx with other parts of the skeleton. They lift and lower the larynx, or fix it in a certain position.
Fig. 88. Laryngeal Muscles
(1)posterior cricoarytenoid muscle; (2) lateral cricoarytenoid ‘muscle; (3) Intrinsic thyroarytenoid muscle
The intrinsic muscles are attached to the inner and outer surfaces of the larynx and do not extend beyond its limits. It is these muscles that perform the laryngeal functions of respiration and voice production. In accordance with these functions, the intrinsic laryngeal muscles divide into the constrictors and the dilators of the glottis. The basic, respiratory function of the larynx is performed by one paired muscle, namely, the posterior cricoarytenoid muscle, or simply the posterior muscle (Fig. 87), the only muscle which dilates the glottis; all the other muscles directly or indirectly serve to close the glottis. The antagonist of the posterior cricoarytenoid muscle is the lateral cricoarytenoid muscle (Fig. 88) which draws the vocal cords together and, consequently, narrows the glottis. The interarytenoid muscles, the transverse and the oblique, bring the arytenoid cartilages together and close the posterior part of the glottis. The vocal cords are kept in tension by the above-mentioned vocal, or thyroarytenoid muscle. The anterior cricothyroid muscle tenses the vocal cords, since it is attached to the cricoid and thyroid cartilages and in contraction lengthens the larynx in the anteroposterior aspect. The laryngeal mucosa is composed of elastic fibres and covered with a ciliated columnar epithelium, excluding the true vocal cords, arytenoepiglottic ligaments, laryngeal surface of the arytenoid cartilages and interarytenoid space covered with a stratified squamous epithelium.
The larynx is innervated by two branches of the vagus nerve, namely, the superior and the inferior laryngeal; nerves. The former is prima-1 rily a sensory nerve which! supplies sensation to the entire! laryngeal mucosa. This nerve I also has one motor branch ex- tending to the anterior cricoary-1 tenoid muscle. The nerve sup-! ply to all other laryngeal muscles is through branches of the inferior laryngeal nerve.
The larynx is not only an organ for the passage of air but also for voice production. The sound is produced by the vibration of tense vocal cords during the passage of air in I expiration through the glottis 8 closed to a narrow chink.
METHODS OF EXAMINING THE LARYNX
Examination of the larynx is conducted by means of dired visual inspection or mirrorlaryngoscopy with a laryngeal mirror attached to the handle of another laryngeal instrument (Fig. 89).
In laryngeal examination the patient is asked to lean slightly forward and to put out his tongue which is then held in position with a square gauze throughout the remainder of the examination. The mirror is slightly warmed, glass side down, in the flame of an alcohol lamp or in hot water, so that it will not fog on the patient’s breath when inserted in the mouth.
The laryngeal mirror is placed in the mouth, mirror side down, at an angle of 45° to the horizontal, with its back surface pushing the uvula and soft palate backwards and upwards, care being takeot to touch the posterior pharyngeal wall to avoid the gagging reflex. At the same time, the patient is told to breathe quietly and drawl the sound “e-e-e-e-e-e”. This raises the epiglottis and the larynx can be viewed reflected in the mirror.
The epiglottis is the first organ visible and by changing the position of the mirror a thorough examination of all its parts can be made, after which the vocal cords and interarytenoid region are subjected to the same scrutiny. Examination of the larynx can be considered successful only when all of its parts have been inspected, and mobility of the vocal cords in quiet breathing and phonation (voice production) has been ascertained (Fig. 90). It should be remembered that in mirror laryngoscopy all anterior parts of the larynx will appear as if being above, and all the rear parts will be seen as if below. The lateral parts will not change their positions in mirror reflection (Fig. 91a, b).
The larynx can also be examined by means of direct laryngoscopy, in which inspection is made without a mirror. An angular spatula is firmly pressed against the back of the tongue to push it forward. The patient’s head is gradually tilted backwards to bring the oral cavityr pharynx and larynx in one straight line. In this position, the epiglottis, arytenoid cartilages and vocal cords may be examined in turn with the aid of an appropriate light. In modern practice, the angular spatula has been supplanted by a more convenient instrument called the laryngoscope. Laryngeal mirrors marked with the letter “K” on the reverse side may be kept in boiling water. Other types of mirror cannot resist boiling and are sterilized in antiseptic solutions of lysol or carbolic acid, washed in boiled water and wiped dry with a square of gauze.
OTOGENIC INTRACRANIAL COMPLICATIONS
OTOGENIC INTRACRANIAL COMPLICATIONS – The extension of an infection from the ear to intracranial space of a skull. In such cases the severe, sometimes fatal, diseases can develop.
nMeningitis;
nAbscess of a brain or cerebella;
nSigmoid sinus thrombosis (and otogenic sepsis);
nSubdural abscess;
nExtradural abscess;
nArachnoiditis of posterior cranial fossa
THE REASONS of OTOGENIC INTRACRANIAL COMPLICATIONS
nAcute purulent otitis media;
nChronic suppurative otitis media;
nMastoiditis;
nLabyrinthitis.
Аgents of otogenic intracranial complications are viruses, Staphylococcus; Streptococcus; Pneumococcus – and dyplococcus; Protey; Pseudomonas aerogenoza; combination of microorganisms.
Paths of penetration of an infection to the intracranial space
nContact (or on a prolongation), through the holes in the bony walls of middle and inner ear (due to destructions) or through dehiscence in walls of temporal bone arises immediate contact inflammatory of the center with brain shells.
nHaemotogenic or lymphogenic, when the infection penetrates intracranial space from a blood or lymph.
nThrough the prephormed paths – peryneural or peri vascular when inflammatory the process is spreaded to intracranial space through channels, that naturally exist in temporal bone (where nerves, vessel pass) and dehiscence in walls of middle ear.
nLabyrinthogenic – through aqueducts of the inner ear.
Pathogenesis of OICC
Impairment of exudates drainage from middle or inner ear. Eustachian tube not capable to take out the exudates from the ear to nasopharynx, and outflow it through a tympanic membrane is hampered. Exudates or cholesteatoma are accumulated in a tympanic cavity or mastoid process’s cells, where the pressure is increased. That promotes a penetration of infection by different ways into intracranial space.
Due to contact mode of a penetration the infection to the intracranial space, the accumulation of pus or cholesteatoma in attic or antrum results in destruction of the upper wall of a tympanic cavity or antrum. Contaminated exudate spreads under a dura mater of middle cranial fossa, where extradural abscess is created. In a place of abscess dura mater varies, becomes penetrable for toxins and bacterias, which hitting in space between dura mater and arachnoidea, forms subdural abscess. The more deep penetration of infection in brain substance finishes in creation of brain abscess.
If inflammatory process penetrates in the skull: either through a posterior-internal wall of mastoid process, or through internal auditory canal, or through the aqueducts of inner ear. The inflammation process progresses in posterior cranial fossa with formation of perysinuses abscess or cerebella abscess.
The generalization of process, due to reduced resistance of macroorganism and high resistance of micro flora, develops meningitis, meningoencephalitis or sepsis. All intracranial complications can be mortal.
The doctors, which have taken part in diagnosis and in treatment of the patient with ICC:
nENT- physician;
nReanimation physician;
nNeuropathology physician;
nNeurosurgery physician;
nTherapy – physician;
nOphthalmology physician;
nInfection physician;
nPhtysiatry – physician;
nX-ray physician.
OTOGENIC MENINGITIS
Otogenic meningitis Inflammation of all brain shells otologyc origin . Can be serous or purulent . Three groups of symptoms:
Meningeal symptoms
Appears due to tension of spinal nerve roots to the dura mater. They are:
nRigidity of neck muscles – impossibility to get by a patient’s chin to physician’s thumb located on jugular fossa;
nKerning – impossibility to unbend a leg in a knee joint after simultaneous bending of knee and coccyx joints;
nBrudzinsky upper – when patient try to get by the chin to jugular fossa the patient’s knees are reduced to a stomach;
nBrudzinsky middle – during pressing by physician’s fists on patient’s symphis the knees are reduced to the stomach;
nBrudzinsky lower – during checking Kerning symptom – other leg are reduced to the stomach.
Brain symptoms
nAppears due to raising of spinal liquor pressure:
nDeterioration of consciousness (sopor, stupor or coma).
nSevere headache,
nNausea, vomiting,
nhyper aesthesia (light phobia, noise phobia, raising of tactile and temperature sensitivity).
nForced position of the patient: „ Raising cock” pose;
The common – intoxication symptoms
nFever, temperature curve – constant;
nTachycardia;
nTachypnoe;
nBlood hypertension
nHypo or anuria.
Additional methods of inspection
nBlood analysis: neutrophillic leycocytosis, accelerated SОЕ is expressed;
nSpinal punction – liquid implies under the increased pressure, it is muddy, and also contains to much cells elements, protein, sometimes – bacteria, contents of sugar and chlorides are reduced.
nBacteriological research of ear pus and spinal canal liquid shows the agent and its antibiotics resistance (to choice the adequate antibiotic therapy).
nX-ray of temporal bone.
nComputer tomography and magnet -nuclear resonance research – detection of cavities, filled with exudates in temporal bone.
Treatment
Urgent hospitalization in ЕNT -department, where urgent surgical procedure will performed (extended radical mastoidectomy). From usual mastoidectomy it differs by maximum wide disclosure of a dura mater of middle and posterior cranial fosses, and available mastoid cells. Postauricular wound is not closed to give possibility of cleaning of operational cavity and introduction medicines in operational wound. The intensive conservative therapy includes: treatment by antibiotics in maximum dozes, that penetrate through blood-brain barrier (including in spinal canal), massive des intoxication, de hydratation, hormones.
ABSCESS OF TEMPORAL LOBE OR CEREBELLA
nSuppurative inflammation of brain substance, which localized mainly in cerebellum or in temporal lobe.
nCan be multiple abscesses.
nQuite often caused by anaerobic infection
STAGES of ABSCESS of the BRAIN and CEREBELLA
1. The initial stage (2 weeks) is characterized by insignificant changing of the general patient’s, subfebrile temperature, increasing of headache on pathologic side, possible nausea and vomiting. The clinical patient’s state is like accution of chronic suppurative otitis media.
3. The transformation in manifest stage happens gradually or suddenly. Presentation of arising of mental changing: depression, apathy, dormancy, slow silent language, attack of sleepiness at preservation of consciousness. Also: diminution of a patient’s mass, vomiting, local painfulness during percussion on skull, lack of appetite, smell from a mouth. Temperature can be normal or subfebrile, deceleration of a rhythm of intimate reductions (bradycardia), leukocytosis. Neurological manifestation of the brain abscess is a paralysis of arm or leg on opposite side. In this stage in majorities of cases it is possible to do the previous diagnosis.
4. The terminal stage is characterized by coma, which develops due to progressing encephalitis, brain edema, diffuse meningitis or breaking of abscess in the cerebrum ventricles.
LOCAL sings of temporal lobe abscess
nAmnesty aphasia (Right hand patients with abscess, located in the left brain lobe, caot term noun),
nMotor aphasia (the patients can understand the language, but caot speak)
nSensory aphasia (the patients lose a possibility to understand the people’s language and himself language).
nAbscess in the not conducting brain lobe is exhibited by mental disorders – lose of criticism, euphoria or depression. That can be imperceptible.
General patient’s state is more severe, than in patient with temporal lobe abscess. Rough rotatoric nistagmus directed to a pathologic side. Significant deterioration of an equilibrium and coordination. For diagnostics of cerebella abscess is necessary to fulfill a finger – nose, finger-finger, or tests, the patient misses out only by the hand on a side of abscess disposition.
In tests on an equilibrium: Romberg pose – direction of a falling does not vary at position of the head; at a straight gate patient with the closed eyes the course deviates in the abscess side. Besides the sign cerebella abscess is positive test on adiadochokinetic (hand on pathologic side defeats) and muscles hypotonia on abscess side.
Additional inspection method
nCommon blood analysis: possible leukocyteosis, accelerated SОЕ;
nSpinal punction – liquid implies under the raised pressure, transparent, increased contents of proteins and insignificant pleocytosis.
nComputer tomography imaging and magnet -nuclear resonance research – allows to reveal the abscess in the substance of brain, and to estimate it size and localization.
nBacteriological research of ear pus and spinal canal liquid shows the agent and its antibiotics resistance (to choice the adequate antibiotic therapy).
nEchoencephalographia – dislocation of brain structures
Treatment
Surgical disclosure of the purulent center in temporal bone together with wide disclosure of a dura mater of middle or posterior cranial fossa (extended mastiodectomy or extended radical operation on the ear). Through an operational wound make a injection of brain substance on depth in
SINUS THROMBOSIS And OTOGENIC SEPSIS
Sinus thrombosis arises mainly due to at mastoiditis and epitympanitis. The accumulation of pus in air cells located near sigmoid sinus, reduces in destruction inner bony of a wall mastois and creation pery sinus abscess. In a place abscess the sigmoid sinus wall inflammated – develops peryphlebitis. Afterwards inflammatory the process passes on inner surface of sinus (endophlebitis). In a sinus lumen wall thromb is created, it gradually increases in sizes and obstructs the sinus. Due to inflammation thromb purulently fuses, and it contaminated parts by the blood current are delivered on all organism (septicopiemia or septicehaemy), creating the lesions of remote metastases (in the lungs, muscles, joints, interior organs and so on).
CLINIC of SINUS THROMBOSIS
Sever common condition of the patient, is exhibited first of all by deterioration of central nervous system functions (stupor, coma), septic body temperature (more then 1 day differential), ague, dense sweat, tachycardia, painfulness of mastoid process, magnification and painfulness of neck lymphatic nods, accelerated SОЕ. Sometimes on the foreground appear septic lesions of interior organs: lungs, heart, kidneys, liver, digestive tract and so on. Hemorrhages in interior organs sometime happen, also under the skin and mucous lining. The skin quite often gains yellow coloring.
Additional inspection methods
nCommon blood analysis: possible leukocyteosis, accelerated SОЕ;
nSpinal punction – liquid implies under the raised pressure, transparent, increased contents of proteins and insignificant pleocytosis.
nComputer tomography imaging and magnet -nuclear resonance research – allows to reveal the inflammatory lesioear or in the sigmoid sinus, and presence of thromb in it lumen.
nBacteriological research of ear pus and spinal canal liquid shows the agent and its antibiotics resistance (to choice the adequate antibiotic therapy).
nEchoencephalographia- dislocation of brain structures.
Treatment
In suspicion of sinus thrombosis the patient must be urgently transported to ЕNТ-department. After installation of the diagnosis it is necessary to perform immediately operation. In patient with acute otitis media the extended mastoidectomy is necessary, in patient with chronic suppurative otitis media – extended radical mastoidectomy operation on ear. The aim of surgical interference is to remove inflammatory lesions in temporal bone, to disclose the sigmoid sinus, and to remove obliterative thromb (if persist). Intensive conservative therapy: treatment by antibiotics, that penetrate through hematological-encephalitic barrier, in maximum dozes (including in spinal canal), massive des intoxication, de hydratation, hormones and anticoagulants.
Prognosis favorable at opportune and combined (surgical and conservative) treatment.
After-care on the patients with intracranial complications
nAfter-care on the patients with intracranial complications has especially important value. The general state of the patient is commonly very severe and requires singular attention of medical staff. A right after-care has not smaller value, than surgical treatment, in preservation of patient’s life.
nSuch the patient is necessary to put in separate small chambers with the blacked out windows (light phobia), to ensure full silence (noise phobia), comfortable temperature and strict bed condition.
nIs necessary to ensure constant supervision of the general patient’s state, his consciousness, temperature, palpitation, and these data in an hour are spelled in the temperature leaf. Transport such patients (on bandagings) only on wheeled bed.
Prophylaxis of intracranial complications
nConsists in opportune detection both right treatment of acute and chronic suppurative otitis media.
nMandatory operating treatment in cholesteatoma;
nEarly paracentesis of a tympanic membrane in patient with acute purulent otitis media
NONINFLAMMATORY EAR DISEASES: SENSORINEURAL HEARING LOSS, OTOSCLEROSIS, MENIERE’S DISEASE,
SEROUS OTITIS MEDIA,
SENSORINEURAL HEARING LOSS
Evaluation of the patient with sensorineural hearing loss
In the adult patient, hearing loss can be due to one of the following possibilities, assessed in broad categories:
1.
2. Vascular or hematologic diseases
3. , metabolic, or renal abnormalities
4. Normal aging processes
5. Endocrine dysfunction
6. Disorders of bone metabolism
7. Hereditary disorders
8. Autoimmune diseases
9. Disorders of unknown etiology
10. Trauma
11. Intoxication
If the onset of SNHL dates to childhood or infancy, in addition to the above, one must consider the factors of
History
• The hearing loss should first be assessed and categorized according to whether one or both ears are involved, the rapidity of onset and progression, fluctuation, and any associated symptoms such as tinnitus, aural fullness, and pain.
• The handicap perceived by the patient should be assessed.
• Medications at present or in past, especially potentially ototoxic medications.
• The general health status of the patient should be determined.
• Review of systems for endocrine, metabolic, autoimmune, or cardiovascular disorders is significant.
• The family history should be reviewed for any suggestions of hereditary or familial hearing loss.
Physical examination
• Tuning fork tests can suggest a possible conductive component.
• The complete head and neck examination can detect other neurologic defects, the stigmata of hereditary, signs of systemic disease.
Testing
Auditory
• A complete audiogram initiates the auditory and vestibular testing and suggests direction for further testing. These tests should include speech audiometry.
• Auditory Brainstem Responces (ABR) is indicated in certain situations such as suspicion of retrocochlear pathology or the testing of a patient thought to be malingering.
• Electrocochleography (ECoG) which is wave 1 of the ABR has limited indications. Otoacoustic emissions are still investigative and may find a niche in fluctuating hearing loss and early sensorineural hearing loss of specific cochlear pathology (distinguish from 8th nerve) as ioise induced hearing loss.
Vestibular testing
• Caloric Testing is obtained to quantify the deficit in the labyrinth and is expressed as a percentage function of the affected ear in comparison to the normal ear.
• Posturography is a more complete examination to test all 3 systems involved in balance: vestibular, visual, proprioceptive and their integration.
Radiographic Evaluation
Most cases of bilaterally symmetric SNHL will not require radiologic evaluation; however the following situations require radiologic investigations:
• 1. Suspicion of retrocochlear pathology
• 2. Evidence or suspicion of systemic or local pathology involving the temporal bone.
• 3. Suspicion of Vascular or other skull base lesions.
Laboratory testing
Routine:
electrolytes, CBC with differential, Thyroid function, lipid profile.
Specific:
1. Autoimmune tests for systemic disease or specific ear autoimmunity tests
2. Syphilis tests: FTA-ABS or western blot
3. Serologic tests for other infectious disease: lyme, HZV etc
Causes of sensorineural hearing loss
OTOTOXICITY
High risk patients for audiovestibular damage include:
1. Patients with impaired renal function, evident either before or during therapy.
2. Patients with elevated peak-and-trough serum levels of ototoxic drugs.
3. Patients with pre-existing sensorineural hearing losses, especially those resulting from ototoxic drugs.
4. Patients taking more than one ototoxic drug or those with a previous history of using ototoxic drugs.
5. Patients for whom a treatment course in excess of 14 days is planned.
6. Patients with symptoms suggestive of cochlear or vestibular toxicity that become evident during treatment.
7. Patients over the age of 65.
8. Patients taking any combination of an aminoglycoside antibiotic and a loop diuretic such as furosemide.
Ideally such patients should be screened with audiometric testing and vestibular testing and these tests should be followed with repeat examinations as results and treatment indicate. Medications that are known to cause ototoxicity should be replaced when this is feasible.
Overview of ototoxic agents
Aminoglycoside antibiotics
Aminoglycosides inhibit bacterial protein synthesis at the ribosomal level and are most active against gram negative aerobic infections. These agents are excreted unmetabolized in the urine and consequently their clearance is solely dependent on renal function.[1] Their half life in cochlear fluids is significantly higher than serum half life. Among aminoglycosides there is a different profile of cochlear or vestibular toxicity for each of these agents.[2] Typically cochleotoxic agents include kanamycin, tobramycin, amikacin and neomycin, while streptomycin is vestibulotoxic. Cochleotoxicity rates for each one of these agents varies in both absolute numbers and severity: 9% with amikacin, 18% with gentamicin, 15% with tobramycin and 3% with netilmicin.
Up to 50% of the hearing losses are either asymmetrical or unilateral. Partial or complete reversibility of the ototoxicity has been reported in up to 50% of affected patients and occurs within the first 6 weeks of discontinuation of the medication.[3-5]
Recovery is less likely if:
1. SNHL is delayed in onset
2. the SNHL is immediate in onset and progresses after drug discontinuation
3. the SNHL is greater than 25 dB
4. further therapy with aminoglycosides is required despite the detection of immediate toxicity.
Risk factors for ototoxicity include the presence of renal disease, longer duration of therapy, elevated serum peak and/or trough levels, advanced age, and concomitant use of other ototoxic medications, especially the loop diuretics furosemide and ethacrynic acid.[6-8]
Measures that should be taken to minimize the risk of cochleotoxicity include repetitive monitoring of serum peak and trough antibiotic levels and increasing the interval between successive antibiotic doses or courses of therapy to allow clearance of the drug from perilymph, especially in cases associated with renal failure.[1, 2]
Vancomycin
The intravenous administration of vancomycin has been linked with development of SNHL when serum levels have been equal to or greater than 30 mg/ml. It is excreted by the kidneys, and renal failure can prolong vancomycin half-life.[9]
Topical ear preparations
Otic preparations commonly used in the topical treatment of bacterial infections incorporate neomycin, polymyxin B, and propylene glycol; ophthalmologic preparations containing chloramphenicol or tobramycin are also used.
Conflicting clinical and experimental evidence exists regarding hearing loss as a consequence of ototopical preparations. These agents should be used with caution in patients with tympanic membrane perforations.
The loop diuretics furosemide and ethacrynic acid can produce transient reversible hearing loss which is associated with the presence of tinnitus and is seen when these agents are administered intravenously, especially in large doses. They are capable of producing synergistic ototoxicity when administered concomitantly with aminoglycosides. Ototoxicity from loop diuretics is best averted by using a slow rate of intravenous infusion, adjusting the dosage for renal failure appropriately and avoiding the concomitant use of aminoglycosides.[10, 11]
Cisplatin
Cisplatin which is nephrotoxic can also manifest ototoxicity as an irreversible, bilaterally symmetric, progressive SNHL that initially is most severe at the high frequencies. The hearing deficit is dose dependent and encompasses progressively lower frequencies and becomes progressively more severe. Similar to the aminoglycosides, cisplatin is concentrated by the inner ear. The risk of ototoxicity appears to be related more to the size of each dose rather than the cumulative amount of administered drug. Newer derivatives of this drug, such as carboplatin appear to possess less ototoxic potential.[6, 10, 12-14]
Nitrogen mustard
This alkylating chemotherapeutic agent has been associated with severe hearing loss when large doses are utilized. The loss is irreversible.[13]
Deferoxamine
Deferoxamine is an iron-chelating agent that prevents iron loading in thalassemias due to transfusions. High dose deferoxamine not only is capable of causing hearing loss but is occasionally involved in visual losses as well. The hearing loss is variable, involves high frequencies and is permanent.[10]
Other
By now, more than 150 medications have been recognized to have ototoxic potential. Other such medications include: salycilates and quinine posses this potential.[7, 15]
NEUROLOGIC DISORDERS
Multiple sclerosis
Hearing loss in multiple sclerosis is the result of demyelination within the cochlear nerve or in the brain. It is uncommon, presenting in approximately 4% of patients with MS and may recover in a period of months.[16-19] Tests of auditory function, especially ABR are sensitive to this type of hearing loss and imaging with MRI may show low signal intensity lesions in the brain stem at the inferior colliculus suggestive of a demyelinating process.[20, 21]
VASCULAR DISORDERS
Migraine
Migraine headaches are very common in the
HEMATOLOGIC DISORDERS
Sickle cell anemia
SNHL has been observed in up to 22% of patients experiencing a sickle cell crisis. The postulated mechanism is one of vascular insufficiency to the cochlea. This is frequently unilateral and reversible.[25]
Blood viscosity disorders
The rheologic characteristics of whole blood are determined by it s two principal constituents: plasma and RBC s. No evidence exists to link subclinical hyperviscosity states with hearing loss. However this mechanism has been postulated in cases of sudden SNHL of unexplained etiology. In addition, when hyperviscosity states are associated with hearing loss, as in SLE or cryoglobulinemia, the hearing loss is more dependent on autoimmune pathology.[26, 27]
INFECTIONS
In instances of chronic otitis media that has eroded the bony labyrinth to produce a fistula between the middle and inner ear sensorineural hearing loss in addition to conductive hearing loss is observed. This can be rapid and profound if there is purulent labyrinthitis or slowly progressive if there is serous labyrinthitis. [28, 29]
Rarely acute otitis media may lead to purulent bacterial labyrinthitis as well as meningitis. Both of these conditions may manifest as profound SNHL.[30]
Rocky Mountain spotted fever
Rocky Mountain spotted fever (RMSF) is an infection caused by Rickettsia rickettsii, and like Lyme disease, it is transmitted by a tick vector; fever, headache, and (petechial) rash are the classic symptoms. The systemic vasculitis that is associated with the infection is responsible for serious complications such as brain-stem or multifocal encephalitis, nephritis, and hepatic abnormalities with a mortality of 4%. The SNHL observed in this disease is seen as evidence of brain stem involvement by vasculitis. Immediate treatment with broad spectrum antibiotics is essential.[31]
Lyme disease is caused by the tick-borne spirochete Borrelia burgdorferi; both feral and domestic animals may harbor infected ticks. The protean manifestations of the full-blown disease include dermatologic, neurologic, musculoskeletal, and cardiac abnormalities. Lyme disease is known to cause facial paralysis and more recently has been implicated in otherwise unexplained SNHL. The hearing loss seems to be variable and often fluctuant. Partial responses to IV penicillin have been reported.[32, 33]
Meningitis
As discussed previously, meningitis is thought to produce deafness by affecting the blood supply to the cochlear nerve as a result of arachnoid inflammation. It has a variable rate of deafness which is dependent on the virulence of the bacterium and is complete and irreversible in most instances.[34-40]
DISEASES OF BONE
Otosclerosis
Occasionally otosclerosis will involve the labyrinth producing SNHL. The pathophysiologic mechanism of this is debated. Medical treatment with sodium fluoride, vitamin D and calcium has not proved unequivocally efficacious in this condition but is a treatment option in the absence of contraindications.[41-43]
Paget’s disease
Paget s disease is commonly found in individuals of old age. It is a disease that manifests increased focal metabolic turnover of bone. Patients with Paget s disease affecting their skull may have temporal bone involvement. Of these patient s approximately 50% will manifest hearing loss. The hearing loss may be sensorineural, conductive or mixed and is progressive. The treatment of Paget’s disease consists of calcitonin and etidronate disodium and occasionally this will halt or reverse the hearing loss.[44, 45]
AUTOIMMUNE DISORDERS
Autoimmune disorders can be associated with a variety of patterns and presentations of SNHL.
Organ Specific Autoimmunity
1. Cogan s syndrome
2. Autoimmune SNHL
Systemic Autoimmunity affecting the inner ear
1. Relapsing Polychondritis
2. Systemic Lupus
3. Polyarteritis Nodosa
4. Wegener s
5. Rheumatoid Arthritis
6. Bechcet s
7. Takayasu s arteritis
8. Cryoglobulinemia s
The hallmark of the organ specific autoimmunity is that it variably improves with immunosupression. Steroids are used as first line and cytotoxic agents such as methotrexate and cyclophosphamide as second line agents. Plasmapheresis is reserved for refractory cases.[26, 46-50]
PRESBYCUSIS
Presbycusis is the term used to describe the bilaterally symmetric deterioration of auditory function that appears to have no basis other than the general aging process of the cellular elements of the cochlea. The extent to which this SNHL reflects a genetically programmed deterioration as opposed to a manifestation of the accumulated insults of a lifetime of noise exposure, disease, and/or toxic exposure is not clear. Presbycusis manifests during middle age and beyond, but the causative degenerative processes may begin as early as the second or third decades of life. Genetic factors may well play a role in cochlear neuronal degeneration and atrophy of the stria vascularis. In presbycusis a determination of the utility and type of amplification for aural rehabilitation is essential. This depends on the speech audiometry scores, the severity of hearing loss and the slope of the audiometric curve.[43, 51-58]
CHRONIC RENAL FAILURE
Chronic renal failure, particularly in association with treatment by hemodialysis, has been associated with progressive, fluctuating, and sudden SNHL, which can affect either one or both ears. A multitude of confounding factors exist in these patients that include but are not limited to treatment with ototoxic drugs, underlying systemic autoimmune illness, other systemic illnesses, vascular problems, embolism, uremic toxins in circulation etc An effort to delineate these factors is necessary in the management of these patients.[59]
ENDOCRINE DISORDERS
Diabetes mellitus
There is no strong evidence to support the hearing loss observed in diabetic patients as being directly linked to diabetes mellitus. However, hearing loss of greater severity than what expected for the age of these patients is commonly encountered especially in the older groups and is attributed to diabetic microangiopathy.[60]
Hypothyroidism
Hypothyroidism has been associated with SNHL in approximately 25% of adults and in up to 50% of children with cretinism. Responses of the SNHL to thyroid hormone replacement therapy have been reported.[5]
METABOLIC DISORDERS
Hyperlipoproteinemia
Hyperlipoproteinemia has been associated with bilaterally progressive SNHL that may be reversible if dietary intake is altered. This has been shown in both human and animal studies. However it is difficult to estimate the importance of other variables such as hypertension and atherosclerosis associated with such dietary patterns.[27]
These disorders are considered here because they present with hearing loss later in life.
Usher’s syndrome
An autosomal recessive disorder with two variants. Patients are afflicted with SNHL and retinitis pigmentosa. The first variant exhibits normal vestibular function with progressively worsening hearing loss. The second variant is more severe and there is deafness and absent vestibular function at birth.[61-63]
Waardenburg’s syndrome
An autosomal dominant disorder with typical phenotypic characteristics: white forelock, dystopia canthorum, heterochromia iridis and in 20% of cases SNHL. Two variants are recognized: in the second variant the hearing loss is more severe and is exhibited in 50% of those afflicted.[64]
Osteopetrosis
A disorder of osteoclast function in which progressive osteosclerosis occurs with attendant narrowing of the skull foramina. The autosomal recessive form is malignant and the autosomal dominant form is benign. In the later two types of the disease are characterized. In both subtypes the internal auditory canal is narrowed with impingement of the auditory nerve.[65, 66]
Other types of hereditary hearing losses have been characterized depending on the onset of hearing loss as well as the progression and the slope of the audiometric curve among other audiometric characteristics.
DISORDERS OF UNKNOWN ETIOLOGY
Meniere s disease
This is a disorder of unknown etiology, which is characterized by the triad of episodic vertigo, hearing loss and the sensation of aural fullness. The condition presents unilaterally and initially typically affects the lower frequencies. The hearing loss becomes progressively worse but the vestibular symptoms improve as the reserve of the labyrinth diminishes with repeated exacerbations of the disease.[67-69] In long term follow up studies, up to 50% of patients with this disease eventually manifest bilateral involvement. Treatment is initially medical and aimed at stabilization of hearing and improvement of vestibular symptoms. It includes dietary salt restriction, diuretics and stress modification along with vestibular sedatives. A multitude of surgical procedures exist that are aimed at controlling the vertigo effectively. They are classified as those that spare hearing and those that sacrifice hearing.[70-75]
Sarcoidosis
Sarcoidosis is a granulomatous disease of unknown etiology with neurologic manifestations in 5%of that may include hearing loss and vertigo. The hearing loss is predominantly sensorineural due to central nervous system involvement in the form of an aseptic meningeal inflammation. This is distinct from the typical sarcoid lesions which present as granulomas.[76,
disease and is invariably not severe.[14] Vestibular complaints are more common in otosclerotic persons than in the general population, and they occur more often than most believe. Unsteadiness, frank short episodes of vertigo are encountered in 25% to 55% of untreated otosclerotic patients A distinction has to be made whether the vertigo is due to:
1. Meniere’s
2. Otosclerosis involving the inner ear
3. Postural imbalance secondary to simple otosclerosis
4. Other types of vertigo.
Meniere’s disease occurs concurrently with otosclerosis in approximately 4% of patients. The clinical picture resembles the added symptoms of Meniere’s disease and otosclerosis.[15-17]
Otosclerotic inner ear disease is more frequent than meniere’s and otosclerosis and is distinctly characterized by:
1. (1) episodic vertigo lasting 20 minutes to 6 hours, which may be a vague floating or semifainting sensation 2. absence of nystagmus during a spell 3. normal caloric response, which often reproduces a spell’s symptoms 4. no positional nystagmus 5. normal neurological examination.
Causes of dizziness and vertigo in simple otosclerotic patients are not completely understood. There is histologic evidence of endolymphatic hydrops in temporal bones affected by otosclerosis in multiple foci.[14, 18, 19]
Physical examination With malleus fixation, which should be excluded, the long process of the malleus is immobile and this is appreciated with pneumatic otoscopy Schwartze’s sign is hyperemia of the promontory mucosa from increased vashe tympanic membrane. This is secondary to hyperemia of the mucosa around the oval window.[14]
Audiometry
A progressive, predominantly conductive hearing loss is the major audiometric sign in otosclerosis. The audiometric tests vary according to the degree of the stapedial ankylosis and the degree of sensorineural (cochlear) involvement.[19, 20] Cochlear Otosclerosis In a substantial proportion of patients the otic capsule is involved in many sites. The oval window niche is the one that becomes clinically manifest in the majority of cases. However in a small fraction of otosclerosis patients, cochlear manifestations of progressive sensorineural hearing loss due to otospongiotic foci around the cochlear become evident.[11, 17, 18, 21]
Treatment Otosclerosis involving the footplate is treated by surgery. Stapedectomy or stapedotomy with a prosthesis to replace the stapes is used. In cochlear otosclerosis or in otosclerosis in an only hearing ear consideration for chelating agents or sodium fluoride must be given.[21-28]
Stapedectomy or stapedotomy is a very effective procedure in reversing the conductive hearing loss and has durable results. Complications with stapedectomy do occur, the most dramatic one being complete sensorineural hearing loss which occurs in approximately 1% of cases for relatively unknown reasons. Other potential problems include: vertigo, persistent conductive hearing loss, displaced prosthesis, post – stapedectomy granuloma.
Meniere’s Disease
Meniere’s disease, also called idiopathic endolymphatic hydrops, is a disorder of the inner ear. Although the cause is unknown, it probably results from an abnormality in the fluids of the inner ear. Meniere’s disease is one of the most common causes of dizziness originating in the inner ear. In most cases only one ear is involved, but both ears may be affected in about 15% of patients. Meniere’s disease typically starts between the ages of 20 and 50 years. Men and women are affected in equal numbers.
Symptoms of Meniere’s Disease
The symptoms of Meniere’s disease are episodic rotational vertigo (attacks of a spinning sensation), hearing loss, tinnitus (a roaring, buzzing, or ringing sound in the ear), and a sensation of fullness in the affected ear. Vertigo is usually the most troublesome symptom of Meniere’s disease, and is often debilitating. The patient feels that either she or the room is moving, and may experience severe nausea and vomiting. Attacks may vary considerably from one patient to another and from episode to episode. Sleepiness may follow for several hours, and the off-balance sensation may last for days.
There may be an intermittent hearing loss early in the disease, especially in the low pitches, but a fixed hearing loss involving tones of all pitches commonly develops in time. Loud sounds may be uncomfortable and appear distorted in the affected ear. The tinnitus and fullness of the ear in Meniere’s disease may come and go with changes in hearing, occur during or just before attacks, or be constant. The symptoms of Meniere’s disease may be only a minor nuisance, or can become disabling, especially if the attacks of vertigo are severe, frequent, and occur without warning.
Diagnosing Meniere’s Disease
The physician will take a history of the frequency, duration, severity, and character of your attacks, the duration of hearing loss or whether it has been changing, and whether you have had tinnitus or fullness in either or both ears. You may be asked whether there is a history of syphilis, mumps, or other serious infections in the past, inflammations of the eye, an autoimmune disorder or allergy, or ear surgery in the past. You may be asked questions about your general health, such as whether you have diabetes, high blood pressure, high blood cholesterol, thyroid, neurologic or emotional disorders. Tests may be ordered to look for these problems in certain cases. The physical examination of the ears, and other structures of the head and neck is usually normal, except during an attack.
An audiometric examination (hearing test) typically indicates a sensory type of hearing loss in the affected ear. Speech discrimination (the patient’s ability to distinguish between words like “sit” and “fit”) is often diminished in the affected ear. An ENG (electronystagmograph) may be performed to evaluate balance function. This is done in a darkened room. Recording electrodes are placed near the eyes. Wires from the electrodes are attached to a machine similar to a heart monitor. Warm and cool water or air are gently introduced into each ear canal. Since the eyes and ears work in a coordinated manner through the nervous system, measurement of eye movements can be used to test the balance system. In about 50% of patients, the balance function is reduced in the affected ear. Other balance tests, such as rotational testing or balance platform, may also be performed to evaluate the balance system.
Other tests may be done as well. Electrocochleography (ECoG) may indicate increased inner ear fluid pressure in some cases of Meniere’s disease. The auditory brain stem response (ABR), a computerized test of the hearing nerves and brain pathways, computed tomography (CT) or, magnetic resonance imaging (MRI) may be needed to rule out a tumor occurring on the hearing and balance nerve. Such tumors are rare, but they can cause symptoms similar to Meniere’s disease.
Treatments for Meniere’s Disease
Diet and Medications for Meniere’s Disease
Drug therapy usually can provide only symptomatic relief. Vertigo can be eased by anticholinergic agents, such as atropine or scopolamine, by antihistamines such as diphenhydramine or meclizine, or by barbiturate drugs such as pentobarbital that provide general sedation.
A low salt diet and a diuretic (water pill) may reduce the frequency of attacks of Meniere’s disease in some patients. In order to receive the full benefit of the diuretic, it is important that you restrict your intake of salt and take the medication regularly as directed.
For patients with bilateral Mйniиre’s disease, treatment is more difficult. Sometimes surgical intervention on the most problematic ear will stop the majority of attacks. In the past, the antibiotic streptomycin was sometimes used in exceptionally large doses, which had the effect of destroying the balance mechanism while not affecting the hearing. Some patients are willing to endure having to use their tendon reflexes and their eyes to achieve balance (meaning they have no sense of balance in a completely dark room) in order to stop the attacks of vertigo.
Surgery for Meniere’s Disease
If vertigo attacks are not controlled by conservative measures and are disabling, one of the following surgical procedures may be recommended. Although there is no cure for Meniere’s disease, surgery can control the attacks of vertigo iearly all cases.
Labyrinthectomy and eighth nerve section are procedures in which the balance and hearing mechanism in the inner ear is destroyed on one side. This is considered when the patient with Meniere’s disease has poor hearing in the affected ear. Labyrinthectomy and eighth nerve section result in the highest rates for control of vertigo attacks.
Selective vestibular neurectomy is a procedure in which the balance nerve is cut as it leaves the inner ear and goes to the brain. Vertigo attacks are permanently cured in a high percentage of cases, and hearing is preserved in most cases.
The endolymphatic shunt or decompression procedure is an ear operation that usually preserves hearing. Attacks of vertigo are controlled in one half to two-thirds of cases, but control is not permanent in all cases. Recovery time after this procedure is short compared to the other procedures.
Other operations or treatments may be advised in some cases. For example, a prosthesis may be implanted to help drain the excess fluid that accumulates in the ear as an attack begins.
Lifestyle Changes to Help Meniere’s Disease
Avoid caffeine, smoking, and alcohol. Quitting smoking can help decrease the frequency and severity of Meniere’s attacks. Get regular sleep and eat properly. Remain physically active, but avoid excessive fatigue. Stress may aggravate the vertigo and tinnitus of Meniere’s disease. Stress avoidance or counseling may be advised.
Safety Precautions for Meniere’s Patients
If you experience vertigo without warning, you should not drive, because failure to control the vehicle may be hazardous to yourself and others. Safety considerations may require you to forego ladders, scaffolds, and swimming.
SEROUS OTITIS MEDIA
Clinical and functional anatomy The middle ear cleft is a continuous space that extends from the nasopharyngeal orifice of the eustachian tube to the furthermost mastoid air cells. The three main segments are the eustachian tube; middle ear (tympanum); and the air cells of the mastoid, petrosa, and related areas. The middle ear cleft is normally gas-containing and is highly variable in dimension, with each of the main segments delineated or constricted by narrow isthmi and subdivided by mucosal folds or by discrete, communicating cells.
Epithelial lining.[15] The mucosal lining of the middle ear cleft varies from the thick, ciliated, respiratory epithelium of the eustachian tube and anterior tympanum to the thin, relatively featureless cuboidal epithelium in the mastoid cells. In the middle ears of patients with
The risk factors for AOM and OME are discussed together because they represent two stages of the same disorder.[27, 28]
Pathophysiology of otitis media
The pathophysiology of
Acute otitis media AOM is a bacterial disorder with similar microbiology throughout the world. Studies suggest that viruses are implicated in the pathogenesis of this disease with being found anteceding AOM or concurrently with bacteria in the middle ear.[33]
In the current theory regarding the pathogenesis of otitis media the following events are thought to occur:[17, 29-32, 34, 35]
1. pathogenic bacterial colonization of the nasopharynx, possibly preceded by viral pathogenic alterations of the nasopharyngeal mucosa. These are found in the overwhelming majority of cases in the nasopharynx with similar microbiologic profiles for the middle ear.
2. the adenoid in the nasopharynx may serve as a reservoir of these pathogenic bacteria. During swallowing, the adenoid is elevated by the soft palate and, when large, may obstruct the posterior choanae and contribute directly to increased nasopharyngeal pressure and, thus, indirectly to reflux. Although improvement in eustachian tube function is noted after adenoidectomy, this does not relate to the size of the adenoid or the obstruction of the eustachian tube which it does not cause.
3. reflux of nasopharyngeal organisms into the middle ear via the eustachian tube. This is facilitated by blowing the nose or swallowing with an obstructed nose. In addition, anatomic factors such as the slope of the eustachian tube in relation to the horizontal plane in addition to the pliability may play an important role.
Otitis media with effusion. Bacterial While eustachian tube dysfunction is not the cause of acute otitis media, it is certainly the cause of otitis media with effusion. This most often the result of an acute otitis or recurrent acute otitis. Rarely it can be found de novo and then it is termed secretory otitis media, believed to be the result of allergic predisposition.[25] In the vast majority of younger childen OME is the unresolved stage of an AOM.[36] Pathophysiologically this represents a failure of the middle ear clearance mechanism. Factors that may be involved include ciliary dysfunction, mucosal edema and hyperplasia, viscosity of secretion, and, possibly, a middle ear/nasopharyngeal pressure gradient. Bacterial exotoxin causes a reversible paralysis of middle ear cilia and inflammatory edema can obstruct middle ear drainage.[35]
Many investigations have confirmed the finding that chronic middle ear effusion is not sterile, as previously hypothesized, and contains the same spectrum of microorganisms is found in acute effusions. Thus, the available evidence links chronic middle ear effusion, regardless of its clinical presentation, to bacterial infection.[37, 38]
Barotrauma
Barotrauma is a known cause of MEE. When middle ear pressure becomes rapidly lower than atmospheric pressure, a clear, watery transudate may form in the middle ear, which is known as serous OM.[39]
Cleft Palate
Sequelae
Recurrent episodes of
DIAGNOSIS
History
The first step in diagnosis is recognition of a problem by the child’s care giver. Older children will complain of earache, but infants become fussy, sleep poorly, and pull at the affected ear. In infants, a fever often heralds the onset of AOM, but this sign may be absent in older children. Many parents are alerted by the URI that often precedes the AOM. OME, on the other hand, may be completely asymptomatic. Often the child is so accustomed to reduced hearing sensitivity that parents become aware of the problem only after the child turns up the volume of the radio or television or becomes inattentive to normal conversation.[48-50]
Otoscopy
The classic signs of AOM are redness and bulging of the tympanic membrane. Erythema, hyperemia are seen initially and as effusion develops, drum mobility is decreased. In the severe case none of the usual landmarks may be visible. If the process continues to worsen, necrosis of the tympanic membrane occurs and the effusion passes into the ear canal through a typically pinpoint perforation.[50]
Massive necrosis of the drumhead is now rare, although necrotizing streptococcal infection is a known cause of permanent perforation. Pneumotoscopy can be utilized in situations where the presence of fluid behind the ear drum is not clear. Otomicroscopy using the operating microscope is used to visualize depth and three dimensional structure.[44]
Variants:
1. Myringitis: inflammation of ear drum, no effusion present
2. Bullous Myringitis: exquisitely painful, bullae on tympanic membrane visible with no evidence of effusion. Both conditions are treated just like acute otitis media.
Tympanometry
Principle: plots the amount of energy reflected from the tympanic membrane as the pressure in the external auditory canal is varied from
Type B tympanogram occurs when the middle ear is filled with effusion.
The type A tympanogram has a sharp compliance peak between ±
The type C tympanogram usually has a sharp peak between -100 and
Audiometry
MEE that fills the middle ear usually results in a moderate conductive hearing loss. Small amounts of MEE may not alter hearing sensitivity. Many studies have shown the variable range of hearing loss in
TREATMENT
A. Acute otitis media
Antimicrobial therapy
Antimicrobial therapy is the mainstay of treatment in the
Type of Antibiotic
Tympanocentesis
Knowledge of the specific organism is important for selection of therapy in cases of AOM occurring in: (1) premature newborns (2) immunocompromised patients (3) patients with progression of symptoms and signs while receiving an appropriate antimicrobial (4) cases with intracranial infection (5) research subjects. The procedure is performed with an 18-gauge spinal needle attached to a 1-ml tuberculin syringe. No anesthetic is necessary. The needle is inserted into the anteroinferior quadrant of the tympanic membrane and the fluid aspirated into the needle. The needle hole closes too quickly for any significant drainage to occur, although the aspiration does temporarily decompress the middle ear.[49, 65, 66]
Myringotomy
Making an incision in the tympani membrane promptly relieves severe pain due to AOM but adds little to either remission of infection or clearance of MEE in cases of AOM treated with appropriate antibiotics. In complicated cases and when symptoms are severe, myringotomy should be performed without delay to provide material for culture and relieve symptoms.[48, 67, 68]
B. Recurrent acute otitis media
Prophylaxis
Low dose, once a day sulfisoxazole or amoxacillin are an effective way of preventing recurrent episodes of otitis in otitis prone children. This is empirically defined as more than 3 episodes in 6 months. Children who develop recurrent AOM while on prophylaxis are candidates for surgical management. Tympanostomy tubes will effectively prevent AOM recurrences, while adenoidectomy in this setting does not show conclusive results.[23, 46, 69-71]
Complications
The suppurative complications of AOM were not trivial in the preantibiotic era. Extension of the infection to involve the bone of the mastoid, soft tissues of the neck, meninges, and cerebral/cerebellar cortex were not uncommon. Because all severe cases of AOM have mucosal involvement of the mastoid, clouding of air cells on plain radiographs or CT scans is not unusual. The key sign of mastoid osteitis, namely demineralization of the air cell septae, lags behind the clinical findings. Once osteitis is diagnosed, mastoidectomy is generally warranted to remove the infected, ofteecrotic bone. In many of these cases, a subperiosteal postauricular abscess is present and surgery is performed for drainage of this pus and removal of the infected bone.[24, 30, 65, 68, 72-75]
Intra-cranial complications are more commoow in cases of chronic suppurative otitis media than in acute cases. Nonetheless, awareness of the possibility of meningitis, extradural abscess, or even brain abscess is an important part of the evaluation of patients with severe or neglected AOM.[76]
C. Otitis media with effusion
Antimicrobial therapy OME, as AOM, is also a bacterial disease, and the MEE is known to contain viable, pathogenic bacteria. Antimicrobial therapy is a logical choice, and the efficacy of this therapy has been determined in several reports. Pediazole has been found to clear 45% of cases by 1 month and 60% by 2 months. In other placebo controlled studies amoxacillin and sulfamethoxazole were shown to be efficacious.[16, 34, 45, 62, 66, 77]
Management of persistent OME
For children with asymptomatic OME discovered by screening or interval examination, a course of an appropriate antimicrobial is recommended, followed by at least a 1-month observation period. If signs of improvement are noted by otoscopy or tympanometry, a second course or additional observation may be warranted. If no change is seen at 1 month, surgical treatment may be considered.[49, 66]
Antihistamines and decongestants
Both antihistamines and decongestants have not been shown to affect the course of OME. If there is reason to utilize these medications, such as concurrent URI or rhinitis then they should be given.
Corticosteroids
The use of a short course of prednisone (1 mg/kg maximum dose) as a possible alternative to surgical therapy for treatment of persisting OME was studied by double blind placebo controlled trials along with antibiotics. The results are conflicting and therefore this form of treatment cannot be recommended at present.
Surgical therapy
Considerable controversy continues about the indications for surgical therapy. The debate centers primarily on duration of effusion and whether persistent effusion, with its attendant mild conductive hearing loss, is harmful to the child’s development. It has been proven by studies that even a small conductive hearing impairment is a risk factor for developmental impairment.[40-44]
It is undoubtedly true that this risk may be reduced through compensatory measures of parents, teachers, and the children themselves; but this reduction is difficult to identify and quantify. Therefore, reduction of morbidity by surgical therapy remains an important option for parents of affected children, who often elect surgical treatment for prompt remediation of the hearing loss and avoidance of long-term sequelae. For OME persisting more than 90 days in spite of adequate antimicrobial therapy, surgical treatment may be recommended for those children with persisting OME and hearing loss. Persistent effusion can be found for up to 3 years in 40% of cases and up to 5 years in 25% of cases.[47, 78, 79]
Other, more urgent indications for surgical intervention relate to structural abnormalities of the tympanic membrane that may lead to ossicular erosion or cholesteatoma. These indications are retraction pockets in contact with the long process of the incus or the stapes or pockets in which epithelial debris accumulates, thus heralding an incipient cholesteatoma.
Myringotomy
The results from this simple procedure have been disappointing. Most investigators and clinicians agree that if a child is to receive an anesthetic for such treatment, then tympanostomy tubes should be inserted or an adenoidectomy performed because the cost-benefit ratio for myringotomy and aspiration is too low to justify myringotomy as an independent procedure.
Tympanostomy tubes
Since their adoption as the standard of care, improved hearing and a decreased rate of recurrent AOM have resulted from their use in large numbers of cases. However, the complications of tympanostomy tubes including:
1. purulent otorrhea
2. permanent perforation
3. recurrent effusion
The risk of permanent perforation from the short-term tubes is about 1% and increases to a maximum of about 5% depending on the length of time the tube remains in place and the diameter of the tube. The factors that influence perforation have not been determined. The rationale for TT is prolonged ventilation of the tympanum. Replacement of the MEE by an aerated tympanum results in prompt return of hearing to preinfection levels in the vast majority of cases. Experimental evidence suggests that the mucosal hyperplasia of the tympanum will revert to a more normal condition with aeration.[47, 78, 79]
Adenoidectomy
The adenoid is a midline structure in the nasopharynx which attains considerable size by 7 months of age. It usually continues to grow up to the age of 5 years at which time it starts to involute. Adenoidectomy is a useful adjunct to treatment is selected cases. It is not recommended for every case of OME that requires PET placement.[80-83]
complications
1. Bleeding / 0.4%
2. Transient velopharngeal insufficiency (must examine for presence of occult cleft which would make this complication permanent)
