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Home , Internal auditory meatus, Middle nasal concha, Superior nasal concha, Suprameatal triangle

Clinical Anatomy,

Physiology and Examination of the External and Middle Ear EXTERNAL EAR

The external ear includes the auricle and the external auditory meatus. The auricle has a complex configuration and is subdivided into two parts: the lobule, which is a skin duplicature containing adipose tissue, and the skin-covered cartilage. The skin on the posterior surface of the auricle can be folded, while on the anterior surface it adheres tightly to the perichondrium. Several projections are found on the auricle, namely, the helix, the antihelix, the tragus, and the antitragns. The tragus projects anterior to the external auditory meatus (Fig. 27). Pressure on the tragus causes pain in acute otitis externa and also in acute otitis media in infants because their external auditory meatus lacks the osseous part and is therefore shorter than in adults. Applying pressure on. the tragus actually means pressure on the inflamed tympanic membrane, which is necessary for a more accurate location of abnormality in this area (haematoma of the triangular fossa, lobular abscess, etc.).

Fig. 27. Auricle 1-helix; 2-entry to the exteraal auditory meatus; 3-antihelix; 4-tragus; 5-lobule; 6-antitragus

The normal height of the auricle corresponds to the length of the nasal bridge. Deviations from this norm to either side are microtia or macrotia. The auricle stands out prominently from the head and has a specific blood supply (the vessels of the anterior auricular surface lack a protective layer of fat). Therefore, when exposed to cold, vascular spasm develops, and the ear can easily be affected by frostbite. The auricle plays on important role in ototopia (the ability to locate a sound source) and performs a protective function. The complex configuration of a normal auricle facilitates retaining of dust particles in the outer portion of the auditory meatus. In patients with a deformed or completely lost auricle, dust reaches the tympanic membrane and, being deposited on it can induce inflammation. The auricle is to a certain degree important for the hearing acuity, and sometimes a person holds a cupped palm to the auricle to increase its area for letter perceiving of

1 weak sounds. The auricle narrows like a funnel to become continuous with the external auditory meatus. Its diameter varies, but this does not affect hearing (Fig. 28).

Fig. 28. External auditory meatuas

In infants of the first year of life the osseous part of the external auditory meatus is absent; only its cartilaginous part exists- The meatus of a child is 0.5-0,7 and of an adult 3 cm. The cartilaginous part of the auditory meatus is partly composed of the cartilaginous tissue; inferiorly it borders, on the capsule of the parotid gland. Inflammation can spread to the parotid gland through the transverse tissures (Santorini’s fissures) in the cartilaginous part of the inferior meatal wall. The cartilaginous part contains numerous glands that produce cerumen and fine hair follicles which may get infected in penetration of the pathogenic flora and cause a furuncle of the external auditory meatus. The cartilaginous part of the external auditory meatus forms a groove which is free from cartilage in the region of the posterosuperror wall. Therefore, this wall is usually incised during surgical manipulations to avoid perichondritis. The anterior wall of the external auditory meatus borders on the temporomandibular joint and during mastication this wall changes its position. If a furuncle occurs on this wall, every chewing movement intensifies pain, Due to close contact of the external auditory meatus with the temporomandibular joint, the anterior wall of the meatus fractures from a blow on the chin attended by skin rupture with possible consequent cicatricial obliteration of the meatus. Besides, this intimate anatomical relationship accounts for the development of some syndromes in otorhinolaryngology and dentistry. The bony portion of the external auditory meatus is lined with thin skin. There is a narrowing at the site where it becomes continuous with the cartilaginous part. If a foreign body passes beyond this narrowing, its removal is difficult. The superior wall of the bony portion borders on the ; the posterior wall borders on air-cells of the mastoid process and, particularly, on the antrum. That makes

2 understandable the development of a pathognomonic sign of acute inflammation in the mastoid process (mastoiditis), that is, sagging of the postero-superior wall in the bony portion of the meatus, which narrows its lumen due to developing periostitis. The skin of the external auditory meatus and the auricle are innervated by the mandibular nerve (the third division of the trigeminal nerve), and by branches of the vagus and the glossopharyngeal nurves. This explains the

Fig. 29, Innervatitm of the teeth and ear by the trigeminal nerve 1—inferior dental nerve; 2—mandibular nerve (the think brunch of the trigeminal nerve); 3— area of the temporomandibulur joint; 4 - tympanic plexus; 5—external auditory meatus; 6— trigeminal ganglion; 7—branches innervating the tongue and oral mucosa radiation of pain, e.g., parodontal inflammation of the eighth lower tooth causes severe pain in the ear on the involved side (Fig. 29).

MIDDLE EAR

The external auditory meatus ends in a tympanic membrane that separates it from the tympanic cavity. Changes in the tympanic membrane (eardrum or a drumhead) are informative of the pathological changes occurring beyond the membrane, in the middle ear, because the eardrum is part of the middle ear, and its is continuous with the mucosa of other parts of the middle ear. Therefore, the present or past disease leaves marks on the drumhead: scars, perforations, calcareous deposits, retraction, etc., that can sometimes persist throughout the patient's life. The eardrum is a thin, sometimes semi transparent membrane consisting of two parts; the greater tense (pars tensa) and the smaller flaccid part (pars flaccida) ( Fig. 30). There are three layers in pars tensa: the outer squamous epithelium, the inner of the middle ear), and the middle fibrous layer 3 consisting of radial and circular fibres closely interwoven with one another. The flaccid part is composed of two layers; the middle fibrous layer is absent.

Fig. 30. Right tympanic membrane 1—antero-inferior quadrant; 2—postero-inferior quadrant; 3 – anterosuperior quadrant; 4 - posterosuperior quadrant; 5 – pars flaccida; 6 – short process of the malleus; 7 – manubrium; 8 - light reflex

The position of the drumhead in an adult is oblique (450) with respect to the interior wall of the auditory meatus. This angle is more pronounced in children (20°). The auricle should therefore be pulled down and back during examination of the tympanic membrane in children. The eardrum is rounded, the diameter being approximately 0.9 cm. The normal eardrum is bluish-grey and slightly retracted into the tympanic cavity forming a depression in the centre called umbo. Different parts of the eardrum are positioned in a different way in relation to the long axis of the auditory meatus. The antero-inferior portion is more perpendicular to it; therefore, the cone of light reflected from this quadrant has its specific position when the drumhead is normal. This light reflex is of topographic and diagnostic importance. A structure extending downward and posteriorly is the manubrium (the handle of the malleus). The angle formed by the manubrium and the cone of light opens anteriorly, which helps to distinguish between the left and the right eardrums. At the upper end of the manubrium a small eminence, the size of a millet grain, stands out. This is a short process of the malleus from which the anterior and posterior malleolar folds extend anteriorly and posteriorly. The latter separate pars tensa and pars flaccida. The tympanic membrane is divided into four quadrants for the convenience of topology: anterosuporior, antero-inferior, posterosuperior, and postero-inferior (see Fig. 30). These quadrates are conventionally distinguished by drawing a line through the manubrium and a line perpendicular to the first one passing through umbo. The middle ear consists of three interconnected parts: the eustachian (auditory) tube, the tympanic cavity, and the mastoid air-cells. Their mucosa is continuous and inflammation, produces

4 corresponding changes in all of them. The tympanic cavity (or the tympanum) is the central portion of the middle ear and has a complex structure. Though, the tympanum is small (the volume of about 1 cm3), it performs important functions. There ore six walls in the tympanic cavity: the membranous (lateral) wall is the inner surface of the tympanic membrane except for its upper bony part called the epitympanic recess or attic; the anterior wall is called carotid because it contains a bony through which the internal carotid artery passes; the upper part of this wall has a foramen, leading into the pharyngotympanic (eustachian) tube, and a groove where the body of the tensor tympani muscle is embedded; the inferior (jugular) wall (or the floor) borders on the jugular bulb that sometimes protrudes markedly into the tympanic cavity; the posterior (mastoid) wall has a in its upper part which leads to a short canal connecting the tympanic cavity with the , the largest, and permanent mastoid cell; the medial (labyrinthine) wall is occupied mainly with a rounded prominence called the promontory corresponding to the basal cochlear turn (Fig. 31). Posteriorly and slightly above the promontory there is an oval window (fenestra vestibuli) and posteriorly and below it, a round window (fenestra cochleae). The canal for the is found along the superior margin of the wall. As the canal turns back, it borders on the superior edge of the oval window niche. Than it turns down, runs in the thickness of the posterior tympanum wall, and ends in the ; the tegmenlal wall (the roof) adjoins the middle cranial fossa. The auditory (eustachian) tube of an adult is about 3.5 cm long. It consists of the bony and cartilaginous parts. The tube opens into the lateral wall of the nasopharynx at the level of the posterior ends of ,thc nasal concliae. The tube is lined with the ciliated epithelium.

Fig. 31. The external, middle, end internal ear 1—auditory tube; 2—scala tympani; 3—scala vestibuli; 4 —round window with the secondary tympanic membrane; 5—jugular bulb; 6—parotid gland; 7—cartilage of the external

5 auditory meatus; 8—notch of the cartilage of the auditory meatus; 9—middle cranial fossa; 10— tympanic membrane; 11 —malleus; 12—incua; 13— stapes; 14—canal for the facial nerve; 15— frontal .semicircular canal; 16—saccule; 17—utricle; 18— (upper trunk of the auditory nerve); 19 —facial nerve; 20—; 21— (lower trunk of the auditory nerve)

The cilia move towards the nasopharynx to prevent infection of the middle ear cavity with nasopharyngeal microflora. Drainage is another function of the ciliated epithelium. The tube opens during swallowing, and the air passes from The nasopharynx into the middle ear. The pressure on either side of the tympanic membrane is thus equilibrated, which is important for normal functioning of the organ of hearing. The of infants under two is shorter and wider than in older children. The cellular system of the mastoid process varies, depending on. The properties of air-cells. The following structural types of the mastoid process are differentiated: pneumatic, sclerotic, and diploetic. The mastoid antrum is the largest air-cell that communicates directly with the tympanic cavity. The antrum borders on the , the sigmoid sinus, the middle cranial fossa, and the external auditory meatus (by its posterior wall where the canal for the facial nerve passes). Therefore, destructive processes in the antral walls evoke severe complications in the bordering regions. In adults, the mastoid antruin is 1 cm deep, and in infants it is close to the surface of the mastoid process. The imaginary projection of the antrum on the temporal is found in the Chipault (suprameatal) triangle. Being a mucoperiosteum, the mucosa of the middle ear does not contain glands, but during inflammation they may appear due to metaplasia. The innervation of the middle ear mucosa is complex. Many nerves concentrate in this small area. The tympanic plexus formed by the fibres of the tympanic nerve, branching away from the glossopharyngeal nerve (hence the otalgic signs during glossitis, and vice versa), and sympathetic fibres from the internal carotid artery can be found on the labyrinthine wall of the middle ear. The tympanic nerve leaves the tympanum through the tegmental wall as the lesser superficial petrosal nerve and reaches the parotid gland to innervate it with parasympathetic fibres. Besides, the middle ear mucosa is innervated by the fibres of the trigeminal nerve, which explains severe pain during acute otitis media (Fig. 32). The chorda tympani nerve originating from the facial nerve leaves the tympanum through the and joins the lingual nerve. The test of salt, bitter, and sour is perceived by the anterior two thirds of the tongue due to chorda tympani. Besides, it innervates the submaxillary and sublingual salivary glands with parasympathetic fibres. The facial nerve branches off to the stapedius muscle. In the region of the genu of the facial nerve, a small 6 branch, the greater superficial petrosal nerve, originates and runs through the groove on the anterior surface of the pyramid of the to innervate the lacrimal gland with its parasym pathetic fibres. As the facial nerve leaves the stylomaatoid formen, it forms a branching known as the pes anserinus. The facial nerve contacts intimately the parotid gland capsule, and its inflammation and tumour may produce pareses And paralyses of the nerve. The knowledge of topography of the facial nerve and its branches helps locate the site of its injury.

Fig- 32. Innervation of the tympanic cavity 1 —styloid process of the temporal bone; 2—facial nerve; 3—mastoid process; 4—round (cochlear) window; 5—chorda tympani nerve; 6—stapedius nerve; 7—oval (vestibular) window; 8—projection of the canal for the facial nerve; 9—geniculum; 10—greater superficial petrosal nerve; 11 —lesser superficial petrosal nerve; 12—sympathetic fibres from the internal carotid artery; 13—internal carotid artery; 14—glossophoryngeal nerve from which the tympanic nerve passes to the tympanum; 15—tympanic plexus on the medial wall of the tympanum

Therefore, a complicated innervation of the middle ear is closely related to the nerve supply of the maxillodental system, and there exists a number of pain syndromes that include ear and maxillodental pathology. The tympanic cavity contains the ossicular chain, including malleus (hammer), incus (anvil), and stapes (stirrup). This chain originates from the tympanic membrane and terminates in the oval window into which a stapedial footplate is set. The articulate with each other by means of joints. Two antagonist muscles are attached to the ossicular chain: the stapedius muscle pulls the stapes back from the oval window, while the tensor tympani muscle draws it inward. These muscles create a delicate equilibrium of the ossicular chain, which is decisive for the hearing function.

7 PHYSIOLOGY OF THE MIDDLE EAR It has already been mentioned that the auditory tube performs a protective function and ensures conduction of sounds to the cochlea nerve endings in the by

Fig. 33. Perilymph displacement from the veslibular to the cochlear window under the pressure of the stapedial footplate 1— vestibular window; 2—cochlear window equilibrating pressure in the tympanic cavity. The function of the ossicular chain, eardrum and oval and round windows is to transmit air vibrations that arise due to sound to the liquid medium, of the inner ear, the perilymph, so that it moves from the oval (vestibular) window to the round (cochlear) window ( Fig. 33), The eardrum perceives air vibrations in the auditory meatus. Due to its specific resonance properties, the eardrum does not practically absorb sound energy. The vibrations are amplified by the lever system of ossicles by about 27 times, which is necessary to transmit the sound energy from the air to a more dense medium the perilymph. This system is very delicate and can transmit vibrations whose wavelengths equal the diameter of the hydrogen molecule. The perilymph can move in the inner ear only when the membranes of both windows are mobile (see Fig. 33), If motion of the stapes in the oval window or of the membrane in the round window is hindered (for instance, in otosclerosis), there would be no displacement of the perilymph because liquids are almost non-compressible. Hearing disorders caused by the impairment of the sound- conducting apparatus develop. The tympanic membrane also acts as a shield protecting the membrane of the round window from direct pressure of a sound wave of the same phase. If the tympanic membrane is defective, sound pressure acting on both windows is almost the same, which hinders the displacement of perilymph,

8 EXAMINATION OF THE EXTERNAL AND MIDDLE EAR

The examination begins with interviewing that aims to define the nature and the site of pathology. Inspection and palpation of the external ear and mastoid process reveal their swelling and tenderness as a result of the postauricular lymphadenitis, furuncle of the external auditory meatus, or mastoiditis. Otoscopy is the main method of examination of the external auditory meatus and the tympanic membrane (Fig- 34). Aural specula or Siegle's otoscope are normally used. A microscope (x5 to x32) is sometimes necessary to visualize parts of the tympanic membrane (Fig- 35). Principles of otoscopy. The patient sits with the ear inspected towards the examiner who directs the light beam of the head mirror to the external auditory meatus. During examination of the right ear, the aural speculum is inserted into the curtilacinous part of the auditory meatus with the right hand; this auricle is pulled up find back by the left hand. To inspect the left ear, the examiner pulls the auricle by the right hand and inserts the speculum by the left hand. The specula vary in size to fit the diameter of the meatal opening. The inserted speculum can be gently moved in the meatus in order to inspect all parts of the tympanic membrane in detail. The examination of the tympanic membrane is informative when the examiner observes all the landmarks of the eardrum and notes possible changes in its tense and

Fig. 34. Otoscapy

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Fig. 35. Otomicroscopy flaccid parts (perforations retraction, the absence of the light reflex, etc.). Study of function of the auditory tube. Functional examination of the middle ear includes the demonstration of the auditory function and the tubal patency. The ventilation via the eustachian tube is necessary not only to equilibrate pressure in the middle ear (to maintain the functions of the ossicles and the tympanic membrane) but also to prevent otitis media. The tubal functional examination is therefore of great practical importance. The tubal patency is determined using special devices that draw-curves demonstrating the degree of patency. Aural pressure gauges designed by Voyachek, Svetlakov and Gerasimov are used to assess tubal patency. Several degrees of patency are distinguished. 1. The liquid level in the tube of the pressiire gauge changes during swallowing. 2. The liquid level is altered at the moment of swallowing with closed nose (the alae are held to the by the patient's fingers). 3. The liquid level changes when the patient blows his nose (with closed nose). 4. The liquid level changes when the eustachian tube is inflated with a Politzer bag. 5. The liquid level changes when the tube is inflated through a metal catheter passed into the pharyngeal orifice of the eustachian tube.

Auditory Analyzer. Structure of the Cochlea. Examination of the Hearing Function

The hearing function of the middle ear should be examined together with determination of the function of the cochlear portion of the inner ear. Therefore, anatomy and physiology of the cochlea should first be studied.

10 Cochlea

The cochlea is composed of a solid bone and two and a half turns (or coils). The basal turn of the cochlea forms a prominence in the tympanic cavity called the promontory. The coehlear turns wind around the osseous cone-shaped core (modiolus) from which the osseous spiral lamina (also having two and a half coils) projects. Two membranous walls project from the free edge of the lamina. They are called basilar (true) membrane and the vestibular (or Reissner's) membrane at an angle to the former. Thus, each coehlear coil is divided into two sections: the upper one, the scala vestibuli, originating from the anterior wall of the vestibule of the inner ear, and the lower one, the scala tympani, originating from the apex of the cochlea where the scala vestibuli connects with it through a small opening named helicotrema. The scala tympani ends at the fenestra cochleae covered by a secondary tympanic membrane. In the centre of the modiolus, there is the internal auditory meatus containing the trunk of the auditory nerve. The nerve fibres of the spiral organ (the organ of Corti) reach the auditory nerve. The membranous cochlea (coehlear duct) is filled with fluid known as endolymph; the scala vestibuli and the scala tympani contain perilymph. The spiral organ serves as a peripheral receptor of the auditory analyser; the conducting pathways are represented by the auditory nerve. The auditory cortex is located in the region of the transverse gyri of the temporal lobe. The spiral organ contains several groups of neuroepithelial cells: the hair cells (outer and inner), outer border and phalangeal cells which support the hair cells and contribute to their nutrition. The inner hair cells are believed to be responsible for the accurate localization of sound, while the outer cells provide a complex of sound sensations. Besides, the outer hair cells perceive weak sounds, and the inner cells, strong stimuli. It is noted that the outer hair cells are more susceptible to injury and their function in various pathological conditions of the inner ear is disturbed easier than that of the inner hair cells, i.e., the patient first complains of poor perception of weak sounds. It is important to note that the hair cells are sensitive to oxygen lack in the endolymph that washes these cells. The spiral organ is the structure where mechanical energy is converted into bioelectric one. Perilymph is moved by the stapedial footplate along the scala vestibuli to the helicotrema in the apical end of the cochlea and then along the scala tympani to the fenestra cochleae covered by the mobile secondary tympanic membrane. This vibrates the basilar membrane mounting the organ of Corti. Low-pitch sounds vibrate the basement membrane along its entire length (from the basal turn of the cochlea to-its apical end), while high-pitch sounds stimulate the basal portion of the cochlea where the membranous fibres

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Fig. 39. Air and bone sound conduction 1—sound-conducling apparatus (air conduction); 2—sound-perceiving apparatus (bone conduction are shorter, their tension and resilience being 100 times higher than near the helicotrema. According to the current theories, the sounds of different frequencies can stimulate only definite portions of the basilar membrane. This explains the ability of the ear to differentiate between sound frequencies and to discriminate the complicated external sounds. Therefore, the spiral organ is considered to perform the role of a detector, responding only to a specific external sound energy, and a converter of sound energy into nervous excitation. The sound energy enters the inner ear either by the aerial pathway (through the external auditory meatus, tympanic membrane, and ossicuiar chain) or by the bone pathway (the vibrate stimulated by the high-pitch, sounds and displace the perilymph due to compression of the bony labyrinth of the inner ear). Therefore, air and bone conduction are examined. The condition of air conduction characterizes the function of the auditory meatus, tympanic membrane, ossicular chain, windows of the labyrinth, and inner ear. Bone conduction, in which sounds reach the spiral organ through skull bones, characterizes the function of the final hearing receptors, auditory nerve, and auditory cortex (Fig. 36). Tests for hearing acuity are based on determining the individual ability to differentiate between sounds of various frequencies conducted through the ear and skull bones.

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EXAMINATION OF HEARING ACUITY

In diseases affecting the sound-conducting and sound-perceiving apparatus of the ear, the perception of speech or pure tones generated by a tuning fork or a special device, audiometer, is disturbed. The simplest method for preliminary examination of hearing acuity is the whispered (spoken) voice test. The patient stands sideways to the examiner who asks the patient to close the opposite ear with the finger and whispers the words containing sibilants and vocals. The examiner notes within what distance the patient perceives the words correctly taking into account that a person with normal hearing perceives whisper at a distance of 6-7 metres in ordinary conditions. Sometimes, a patient does not perceive wbisper; spoken voice is then used, which is usually perceived at a distance of 20-25 metres. More information concerning hearing acuity and the nature of disorders is gained by the tuning fork tests. The tuning fork was invented in 1711 by G. Shore and was first used in singing; since late in the past century the tuning fork has been used for hearing tests. Forks with frequencies of 128 and 2048 Hz are now commonly used. Tuning fork tests reveal quantitative and qualitative changes in the auditory analyser; they reveal lesion of the sound-conducting or sound-perceiving apparatus and determine the degree of their dysfunction.

The tuning fork tests are conducted with C128 tuning fork, according to the scheme given below. The Weber test (Figs. 37 and 38) reveals sound lateralization in the right or left ear. The prong of the vibrating fork is placed in the midline of the patient's vertex. The patient is asked to report in which ear (affected or normal) the sound is heard louder. If the patient says that

Fig. 37. Weber's test (the Fig. 38. In patient with conductive sound of a tuning fork is hearing loss the sound is heard heard in the region of the better by the involved ear and in vertex) patients with sound perceiving hearing loss, by the healthy ear

13 the sound is louder in the involved ear, this indicates the disorder of the sound-conducting apparatus of this ear. If the sound is heard better in the healthy ear, lesion of the sound- perceiving apparatus of the involved ear can be suggested. A healthy person hears the sound of the tuning fork in the region of the vertex (no sound lateralization occurs).

In the Rinne test (Fig. 39) the duration of sound generated by a C128 tuning fork is compared in the air and bone conduction (the examiner brings the tuning fork close to the auditory orifice or the fork is placed on the mastoid process). Using a stopwatch, the examiner determines the lime during which the patient hears a sound of the tuning fork with air and bone conduction. Normally, the air conduction is about twice as longer. The Rinne test is said to be positive in such cases. If the sound-conducting apparatus is disordered, the Rinne test is negative, i.e., the air conduction is shorter than or equal to bone conduction. Hearing Test Findings

The Schwabach test is used to examine the sound-perceiving apparatus. The examiner holds a vibrating C128

14 Fig. 39. Rinne's test, Comparison of sound perception with air and bone conduction tuning fork to the patient's forehead and asks him to signal when he stops hearing the tone. The examiner then holds the tuning fork to his own forehead and if the sound is still heard, the patient's bone conduction is impaired (the disorder of the sound-perceiving apparatus). The Gelle test demonstrates fixation of the stapes in the oval window in otosclerosis.

A C128 tuning fork is held to the patient's mastoid process. By occluding the patient's external auditory

Pig. 40. Audiometric examination of the hearing function in a sound-proof chamber meatus with the index finger, the examiner increases or lessens air pressure in it; a Politzer bag can be used for this purpose. The patient must report if he perceives an intermittent or continuous tone. If the sound is intermittent, the stapes is not fixed; the Gelle test is positive. The tone is continuous in the stapedial fixation in the oval window: the Gelle test is negative.

A C2048 tuning fork is used to determine the duration of sound perception through air and the ability of the receptor apparatus to perceive high-pitch tones. The findings are entered into a special table which demonstrates the nature and degree of hearing loss. Hearing function is tested in detail by audiometers (Fig. 40) that allow to obtain audiograms. The latter demonstrate graphically the lesion of the sound-conducting or sound- perceiving apparatus, or their combined affection (see Fig. 81b).

15 Vestibular Analyser. Anatomy, Physiology. Methods of Examination

The bony labyrinth. The receptors of the vestibular analyser are located in two portions of the inner ear—the bony vestibule and the three semicircular canals. The bony vestibule is a very small, almost spherical cavity. The anterior wall contains an opening leading to the scala vestibuli of the cochlea. On the lateral wall of the bony labyrinth facing the tympanic cavity is the niche of the oval window, which is occupied by the footplate of the stapes. The vestibular medial wall contains two recesses for the two membranous sacs—the utricle and the saccule. Through the five small openings in its posterior wall the vestibule communicates with the bony semicircular canals: horizontal (lateral), frontal (anterior), and sagittal (posterior) canals which are situated in three mutually perpendicular planes (Fig. 41). The membranous labyrinth repeats the configuration of the bony labyrinth. Each of the three semicircular canals has a dilated end (the ampulla) and a simple (non-ampullated) limb; both limbs open into the vestibule.

Fig. 41. Bony labyrinth 1 — bony cochlea; 2—round window (fenestra cochleae); 3— ampulla of the posterior semicircular canal; 4—non-ampullated end of the lateral semicircular canal; 5— ampulla of the lateral semicircular canal; 6—common non ampullated end of the posterior and anterior semicircular canals; 7—ampulla of the anterior semicircular canal; 8 -oval window (fenestra vestibuli)

Only the horizontal (lateral) canal has its own simple limb and opening; the anterior and posterior canals join to form a common limb that enters the vestibule. The membranous labyrinth contains receptors (Figs. 42, 43);

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Pig. 42. Structure of the ampullary Fig. 43. Structure of the otolithic crest (crista ampulluns) apparatus

1 - jelly-like substance; 2—pili of 1—statoconia; 2—jelly-like sub- the hair cells; 3—hair cells; 4 -fibres stance; 3—pili of the hair cells; 4— of the auditory nerve hair cells; 5—fibres, of the auditory nerve; 6—supporting cells their stimulation by the motion of the endolymph inside the membranous semicircular canals controls the position of the trunk, head, and limbs in space. Ewald's experiments (1853) have demonstrated that an adequate (or specific) stimulus for the neuroepithelium of the semicircular canals is the motion of endolymph; its motion in the direction of the ampullated end of the semicircular canal produces movement of the head and eyes to the side of the irritated ear; the reverse motion sets up the head and eyes lo the opposite side. The vestibular sacs also contain sensory epithelium whose fibres respond to linear acceleration—forth and back, up and down. The neuroepithelium of the semicircular canals is stimulated when the head is turned or tilted. The fibres of the pass to the vestibular sacs and the brush-like structure of the nerve fibres (called the crista) of the semicircular canals. The vestibular apparatus of the inner ear is connected with some organs and systems of the body.

Five neural arcs that are responsible for these connections are distinguished: (1) vestibulooculornotor; (2) vestibulospinal; (3) vestibulocerebellar; (4) vestibulovegetative; (5) vestibulocortical. These connections explain the symptoms and clinical manifestations that arise in abnormality of the vestibular apparatus.

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EXAMINATION OF THE VESTIBULAR FUNCTION

Examination of the patient with suspected vestibular disorders should be done step by step, beginning with simple tests. The planned interviewing can elicit specific labyrinthine symptoms (dizziness, nausea, vomiting, unsteady gait), which prove the connections that exist between the vestibular analyser and the , vegetative centres, and skeletal muscles. Demonstration of a spontaneous nystagmus. Nystagmus is a condition in which the eyes are seen to move in a more or less rhythmical manner from side to side, up and down, or in a rotary manner from the original point of fixation. Vestibular nystagmus has two components: the slow component and the rapid component. The test described below can elicit a nystagmus. The patient is asked to fix his eyes on the object or on the examiner's finger at a distance of 30 cm from the patient's . The linger is then moved to the right or to the left, and the examiner observes excursions of the eyeballs. The direction of nystagmus is determined by the direction of its rapid component: nystagmus to the right means that the rapid component is to the right. The nystagmus noted only when the eyes look in the direction of the rapid component is called the first-degree nystagmus. If the nystagmus continues when the eyes look straight ahead, this is a second-degree nystagmus. The nystagmust which persists when the eyes look in the direction of the slow component of nystagmus, is the third-degree nystagmus. The rapid component of nystagmus indicates the side of the overexcited labyrinth. Pointing tests (finger-nose test, finger-to-finger test). Finger-nose test. The patient with the eyes closed is instructed to move arms apart and then try to touch the tip of the nose with the point of the right and left index fingers. If a labyrinth is overexcited, the patient is unable to do it, and both hands deviate to the side of the slow nystagmus component, i.e., to the healthy ear. When there is a pathological condition in the region of the posterior cranial fossa, only one patient,s hand will deviate to the side of the lesion. Finger-to-finger test. The patient keeps eyes closed, both arms are lying on the knees. The examiner places two index fingers (spaced at a distance of 20 cm) 40-50 cm above the patient's laps. The patient is asked to raise both hands and bring the index fingers to the examiner's fingers, if the right labyrinth is overexcited, the patient's both hands will deviate to the side of the left ear (i.e., to the slow component of nystagmus). If the postorior cranial fossa is involved, only one patient's hand will deviate toward the affected side. Test for adiadochokinesia. The patient is asked to close the eyes and quickly perform supination-pronation movements. When the labyrinth is involved, the adiadochokinesia is absent, i.e., the speed and the amplitude of movements of both hands are the same. Adiadochokinesia is 18 revealed in patients with posterior fossa lesions: The hand on the involved side performs low, sometimes arrhythmical movements. Thus, these simple labyrinthine tests demonstrate impairment of the labyrinth and help dlfferentiate between the lesion of the labyrinth and those of the posterior cranial fossa (arachnoiditis, cerebellar abscess). The demonstration of gait. It has already been mentioned that an unsteady gait is a specific symptom of vestibular disorders. The patient is asked to close the eyes and try to go straight ahead to a distance of about six meters. If the right labyrinth is overexcited, the patient deviates to the left, in the direction of the slow component of nystagmus; the rapid component directed to the right also indicates the overexcited right labyrinth. Sideways walking, i,e., the movement to right or left side by setting one leg to the other, is also tested in patients with their eyes closed. Patients with vestibular disorders can perform this test, while patients with lesion of the posterior fossa perform it with difficulty, or are unable to move in the direction of the involved side. The Romberg test. The patient is asked to stand up, stretch his hands forward, with the eyes closed and the feet placed together. If, for instance, the right labyrinth is overexcited, a tendency to fall to the side of a good ear will be noted. Alteration in head position changes the direction of falling. In patients with lesion of the posterior cranial fossa, the direction of falling does not depend upon the head position. The caloric test. The test is based on the physical properties of the liquid molecules to descend under the effect of cold and rise during heating. A cold or warm water is introduced into the external audilory meatus to cause the endolymph molecules in the semicircular canals to flow toward the ampullated end or in the opposite direction. During this test the extent of overexcitement of the right and left labyrinths (separately) is determined by comparing the duration of the resultant nystagmus, its degree, the amplitude of the eyeball oscillations, and the manifestation of vegetative reactions (sweating, nausea, pallor, etc.) with the known normal indices and by comparing the results of the tests in thts right and left ears. Artificial stimulation of the frontal (anterior), satgittal (posterior), or horizontal (lateral) semicircular canals is possible, depending upon the patient's head position (inclined forward or backward, or tilted sidewise to the patient's shoulder). Caloric stimulation of the lateral semicircular canals is usually performed. To that end, the patient's head is tilled back to set the ampullae of the lateral semicircular canals in the uppermost position. Such optimal conditions provide motion of the eudolymph from the ampulla (cold caloric, testing) or toward the ampulla (warm caloric testing). The patient is then examined for nystagmus; 100 ml of cold water (20°C) are douched on the posterosuperior wall of the external auditory canal. Horizontal nystagmus normally occurs in 20 seconds; the rapid component (the measured duration is 60-120 seconds) is in the opposite direction (endolymph flow from the ampullated end). Any deviation will suggest inhibition or overoxcitemeiit of the labyrinth stimulated. The rotation test. Like the previous test, it reveals the inhibition or overexcitement, of the 19 labyrinth. The test is based on the Ewald phenomenon: movement of the endolymph toward the ampullated end produces nystagmus (rapid component) in the direction of the stimulated ampulla; movement from the ampullated end produces nystagmus in the opposite direction. The patient is seated in a special revolving chair with the head tilted 30 degrees forward (the lateral semicircular canals are in the plane of rotation); eyes are closed. The chair is turned clockwise at a speed of 10 turns in 20 seconds, then it is stopped suddenly, and the resultant nystagmus and also the extent of the patient's head and trunk deviation are estimated. If the vestibular sensitivity is normal, the duration of post-rotational nystagmus is 20 seconds. Five minutes later the patient is rotated in the reverse direction, and the reactions are compared. The fistula test. By pressing the tragus of the patient's examined ear with the thumb, the examiner increases pressure in the tympanic cavity and observes the resultant nystagmus and a feeling of dizziness. These symptoms are present (a positive test) when there is a fistula in the wall of a semicircular canal. If the test is positive, the increased compression of air in the auditory canal and tympanic cavity causes the nystagmus toward the examined ear, and rarefaction excites the nystagmus toward the opposite side.

20 Clinical Anatomy,

Physiology and Examination of the Nose, and

Nose According to the clinical anatomy, the nose comprises the external nose and the . EXTERNAL NOSE The shape of the external nose can be compared with a trihedral pyramid, with the base facing posteriorly. The upper narrow part of the external nose bordering the forehead is called the root of the nose. It is continuous downwards with the dorsum or the bridge of the nose ending by the tip of the nose. The lateral surfaces of the external nose are known as the wings (alae) of the nose. Determination of the focus of pathology requires such a division of the external nose.

Fig. 1. Skeleton of the external nose 1-nasal bones; 2-frontal maxillary process; 3-triangular cartilage; 4-greater alar cartilage; 5-lesser alar cartilage.

The free lower margins of the wings, together with the mobile part of the nasal septum, are shaped so as to form the lying in the horizontal plane. The skeleton of the external nose (Fig. 1) includes the two (right and left) nasal bones. They are very thin and join in the midline to form the upper part of the dorsum. They articulate by their upper serrated edges with the nasal processes of the and laterally with the frontal maxillary processes to form the sloping sides of the nose. The cartilaginous part of the external nose consists of paired lateral (triangular) and the greater and lesser alar cartilages. The skin of the root, dorsum, and sides of the nose is thin, mobile, and can therefore be widely used in various plastic operations. The skin covering the wings and the tip of the nose is, on the contrary, intimately attached to the underlying tissues and cannot be gathered in folds. There are numerous sebaceous glands in the skin of the nasal tip and wings the chronic inflammation of which or obstruction of their excretory ducts causes acne. This region of the external nose also contains numerous sweat glands.

21 The blood supply to the external nose, especially the outflow of venous blood, has some specific features. The skin of the external nose receives blood from the facial artery. Its terminal branch known as the angular artery (in the region of angle of the eye) joins with the branch of the ophthalmic artery, the dorsal artery of the nose. At the tip of the nose the arteries form a rich vascular network ensuring adequate supply of arterial blood to this region, which explains rapid wound healing and easy bleeding in injuries. The external nose (the tip and wings) and the upper lip are drained of venous blood through the facial vein which continues as the superior ophthalmic vein emptying into the cavernous sinus located in the middle cranial fossa. The development of a furuncle in this area is therefore very dangerous because clots of pus may spread via the veins from the nose to the cranial cavity with subsequent occurrence of sepsis. The lymph is drained through the lymphatic vessels which run together with the arteries and veins in this area. At the level of the oral fissure, they pass into the subcutaneous fat and empty into the submaxillary lymph nodes. Some lymphatic vessels terminate in deep and superficial cervical nodes. This should be taken into consideration if lymphadenitis develops in these areas. The innervation of skin of the external nose includes the ophthalmic and maxillary branches of the trigeminal nerve.

NASAL CAVITY The cavity of the nose is divided by the nasal septum into two, usually asymmetric, parts called the right and left halves of the nose. Anteriorly, the nasal cavity communicates through the with the external environment, and posteriorly, through the posterior nares, or choanae, with the upper part of the pharynx, the nasopharynx. Each half of the nasal cavity has lateral and medial walls, a roof and a floor. The nasal cavity begins with the vestibule. As distinct from other parts, the vestibule is lined with skin covered with many nasal hairs (vib-rissae) which are a kind of filter that retains large (lust particles during nasal breathing.

Fig. 2. The lateral nasal cavity 1- anterior end of the inferior conchae; 2-orifice of the nasolacrimal duct; 3-inferior ; 4-anterior end of the middle ; 5- ; 6-orifice of the frontal sinus; 7-orifices of the anterior and middle ethmoid air-colla; 8-orifice of the ; 9- ; 10-orifices of the posterior ethmoid air-cells; 11-orifice of the sphenoid 22 sinus; 12-; 13-pharyngeal tonsil; 14-mouth of the auditory tube Three elevations, called the conchae, situated one above the other, are clearly seen on the lateral wall of the nasal cavity (Fig. 2). The inferior (the largest) roncha is formed by an independent bone, while the middle and superior conchae are parts of the . A slit-like passage beneath each of the three conchae is called the nasal meatus. Three nasal meatuses are named according to the conchae that overlie them: the inferior, middle mid superior. The space between the free surface of the conchae and the nasal septum is known as the common nasal meatus. Besides the bony tissue, the submucous coat of the nasal conchae contains varicose venous plexuses (a peculiar cavernous tissue) where the fine arterioles enter the venules of a larger diameter. This enables the nasal conchae to swell and narrow the lumen of the common nasal meatus in response to certain irritating effects, thus providing a longer contact of the inspired air with the blood-filled mucous membrane. The nasolacrimal duct through which the tears are conducted opens into the nasal cavity under the anterior end of the concha into the inferior nasal meatus. Most of the paranasal sinuses (maxillary, frontal, anterior and middle cells of the ethmoid labyrinth) open into the middle meatus which is therefore called the 'mirror of the paranasal sinuses' because a suppurative catarrhal condition is manifested by a characteristic discharge in the middle nasal meatus.

Fig. 3. Nasal septum 1-septal cartilage; 2-perpendicular plate of the ethmoid bone; 3-vomer

The medial wall of the nasal cavity is formed by the nasal septum made up of three bony elements: the perpendicular plate of the ethmoid bone, the vomer and the nasal crest of the maxilla; it also includes the septal (quadrangular) cartilage and a portion (mobile part of the nasal septum) situated in the vestibule and consisting of skin duplicature. The vomer is an independent bone having the shape of an irregular quadrangle. Interiorly it articulates with the nasal crests of the maxilla and the palatine bone. Its posterior edge separates the right and left choanae. The upper edge of the septal cartilage forms the lower portions of the nasal bridge. This should be borne in mind in surgical correction of the deviated nasal septum because high resection of the septal cartilage may cause retraction of the bridge (Fig. 3). 23 In infants (usually under 5) the nasal septum is straight, but as the child grows, it becomes deviated due to uneven growth of the bony and cartilaginous parts of the septum. In adults, more often in men, a deviation of the nasal septum occurs in 95 per cent of cases. The roof of the nasal cavity in its anterior parts is formed by the nasal bones and in its middle part, by the of the ethmoid bone. It is the narrowest portion of the roof (about several millimetres wide). This wall is very thin and can be damaged by careless surgical manipulations in the nasal cavity. Liquorrhoea nasalis and meningitis (in case of infection) can thus be provoked. The roof has 25-30 small perforations through which pass the fibres of the , anterior ethmoidal nerve, and the vein accompanying the anterior ethmoidal artery (the cause of possible severe nasal bleeding). The floor of the nasal cavity separates it from the oral cavity. It is made up of the palatine process of the maxilla and the horizontal plate of the palatine bone. The floor of the nasal cavity in an adult is 12-15 mm wide; in a newborn, 7 mm. Posteriorly, the nasal cavity communicates with nasopharynx through the choanae. In newborns, they are (1x6 mm in size and have a triangular or round shape; their size doubles by the age of ten. The nasal meatuses in infants are narrowed by the nasal conchae. The is closely adjacent to the floor of the nasal cavity. Therefore, even a minor inflammation of the can cause complete obstruction of nasal breathing, and the child is unable to suck the breast. The nasal mucosa lines two conditionally separated zones: olfactory and respiratory. Along its entire course the mucosa of the respiratory zone is firmly attached to the underlying bony and cartilaginous formations; it is about 1 mm thick. The submucous layer is absent. The nasal mucosa contains ciliated epithelium and a large number of goblet and basal cells. The surface of a cell has 250-300 cilia which vibrate at a rate of 160-250 per minute. The cilia vibrate in the direction of the posterior parts of the nose, toward the choanae. During inflammation, the ciliated cells can transform into goblet cells und, like them, produce nasal mucus. The basal cells promote regeneration of the nasal mucosa. Normally, the nasal mucosa secretes about 500 ml of fluid a day, which is necessary for normal functioning of the nasal cavity. Inflammation greatly intensifies the mucosal secretory function. The mucosa of the nasal conchae overlies the tissue made up of a dense network of dilated veins (resembling a cavernous tissue). Rich smooth muscles of the venous walls are innervated by the fibres of the trigeminal nerve. Stimulation of its receptors can, promote swelling or shrinkage of the cavernous tissue, mainly of the inferior nasal conchae. A special area of about 1 cm2 abundantly supplied with particularly venous blood can be distinguished on the anterior part of the nasal septum. It bleeds easily and is called Kiesselbach's area-the common site of nosebleed (Fig. 4).

24

Tig. 4. Common site of nosebleed (Kiesselbach's area) (1)

The olfactory zone is located in the upper part of the middle concha, the entire superior concha and the upper part of the nasal septum opposite to it. The axons (non-medullated fibres) of the olfactory cells in the form of 15—20 fine nervefibres pass through the openings of the cribriform plate into the cranial cavity to enter the olfactory bulb. The dendrites of the second neuron join the nerve cells of the olfactory trigone and reach the subcortical centres where the fibres of the third neuron originate and stretch to the pyramidal neurons of the cortex, the central part of the olfactory analyser, near the paraterminal gyrus. The external carotid artery supplies blood to the nasal cavity through one of its terminal branches, the maxillary artery. The latter gives rise to the sphenopalatine artery entering the nasal cavity through the approximately at the level of the posterior end of the middle concha. It supplies blood through its, branches to the lateral wall of the nose and the nasal septum. Through the incisive canal it communicates with, the greater palatine and superior labial arteries. In addition, the anterior and posterior ethmoidal arteries enter the nasal cavity; they arise from the superior ophthalmic artery which is a branch of the internal carotid artery. Thus, both the internal and external carotid arteries supply blood to the nasal cavity; therefore, ligation of the external carotid artery sometimes fails to arrest persistent nosebleed. The veins of the nasal cavity pass superficially along-wide the corresponding arteries and form several plexuses in the mucosa of the nasal conchae and the septum one of which, Kiesselbach's plexus, is described above. There is also a plexus of larger veins in the posterior parts of the nasal septum. From the nasal cavity the venous blood drains in several directions. It passes from the posterior parts of the nasal cavity to the pterygoid venous plexus connected with the cavernous sinus in the middle cranial fossa. This can promote the propagation of infection from the nasal cavity and the nasopharynx into the cranial cavity. From the anterior parts of the nasal cavity the venous blood passes to the superior labial and angular veins opening through the superior ophthalmic vein to the cavernous sinus. Therefore, a furuncle of the nasal vestibule may become the cause of infection spreading to the 25 cranial cavity. Interconnection between the anterior and posterior veins of the ethmoidal labyrinth and the orbital veins is of great importance because it may be one of the underlying causes of orbital inflammation. Furthermore, a branch of the anterior ethmoidal vein passes through the cribriform plate into the anastomosing with I In) veins of the pia mater. Severe complications such as thrombophlebitis of the maxillofacial region, thrombosis of the orbital veins and cavernous sinus, and sepsis may develop due to the abundant vascular network with numerous anastomoses in the bordering regions. The lymphatic vessels drain lymph to the posterior parts of the nasal cavity; they pass into the nasopharynx, superior and inferior to the pharyngeal openings of the auditory tubes, and enter the retropharyngeal lymph nodes lodged in a loose cellular tissue between the prevertebral fascia and the cervical fascia proper. Some lymphatic vesels of the nasal cavity terminate in the deep cervical lymph nodes. Suppuration of the lymph nodes associated with inflammation in the nasal cavity, paranasal sinuses and the middle ear can cause the retropharyngeal abscesses in children. The sites of metastases of malignant tumours of the nasal cavity and the ethmoid labyrinth are specific and related to the character of lymphatic drainage: the lymph nodes swell by the course of the internal jugular vein. Innervation: in addition to the olfactory nerve (described above), the sensory fibres of the ophthalmic and maxillary nerves (the first and the second division of the trigeminal nerve) supply the nasal mucosa. The peripheral branches of these nerves innervate the and teeth anastomosing with each other. Therefore, pain may radiate from the nasal cavity to the teeth and vice versa, because both these areas are innervated by the trigeminal nerve.

Paranasal Sinuses

The paranasal sinuses are air-filled cavities located near the nasal cavity and communicating with it. There are four paranasal sinuses on each side of the head: maxillary (or antrum of Highmore), frontal (only one frontal sinus can sometimes be developed, or both sinuses are missing); the ethmoid cells, and the sphenoid sinus (separated by the partition into two halves). The paranasal sinuses begin developing during the 9th-10th week of gestation. Newborns have only the maxillary and ethmoid sinuses; the frontal and sphenoid sinuses develop by the sixth or eighth year of life.

26 MAXILLARY SINUS

The maxillary (Highmore's) sinus is the largest of all sinuses which lies within the body of a maxilla. In a newborn, it is a fissure confined between the anterior wall of the sinus, infraorbital margin, and the alveolar process (Fig. 5). It is 7 to 14 mm long, and 5 to 10 mm high. By the end of the first year of life, the sinus is rounded; its size gradually grows with the growth of the facial skeleton, and at the age of 6-7 the sinus acquires the shapes of a polyhedron observed in adults. After the formation of permanent teeth the sinus grows to the full size (by the age of 15 to 20). In adults its volume measures from 15 to 20 cm3. The anterior wall is slightly retracted; in Mongoloids the retraction is more marked. This wall extends from the infraorbital margin to the alveolar process.

Fig. 5. Size of the maxillary sinus depending on age 1-newborn; 2-1-year-old infant; 3-4-year-old child; 4-7-year-old child; 5-12-year-old child; 6—adult

The infraorbital canal opens 0.5-1 cm below the infraorbital margin. A vascular nerve bundle consisting of the maxillary nerve (the second division of the trigeminal nerve), the corresponding artery and vein emerges from the canal. Below the , there is a pronounced depression of the anterior wall-the canine fossa-the thinnest place at the level of the second premolar, which is most suitable for surgical opening of the maxillary sinus. The bone of the anterior wall is quite dense and spongy. Persistent blooding during the operation in therefore possible. The superior wall, the roof of the sinus, separates it from the orbit. On the surface of the wall lies a canal (sometimes a semicanal) which opens into the maxillary nerve and contains the maxillary nerve and vessels. Therefore, pathological conditions of the sinus may affect this vascular-nerve bundle. The inferior wall of the infraorbital nerve canal protrudes into the sinus in the form of a 27 prominence. The mucosa sometimes only slightly covers the infraorbital nerve. The superior wall of the sinus is very thin and may easily become carious due to inflammation or a tumour which can therefore extend to the orbit. The anterior internal margin of the superior wall joins with the lacrimal bone and takes part in the formation of the superior orifice of the nasolacrimal duct. Posteriorly, the superior wall borders with the papyraceous lamina separating the orbit from the ethmoid cells. The external wall of the nasal cavity is the internal wall of the sinus. The nasolacrimal duct passes in its anterior portion and opens into the inferior nasal meatus (Fig. 6).

Fig. 6. Correlation between maxillary sinuses, alveolar processes, and orbits 1—maxillary sinus; 2—orifice of the maxillary sinus; 3—ethmoid labyrinth; 4—orbit; 5— nasal septum; 6—; 7—common nasal meatus; 8—inferior nasal concha

The orifice of the maxillary sinus, which is almost under the roof, opens into the middle nasal meatus. Therefore, the maxillary sinus is best drained in the lying position. The external posterior wall is oblique and corresponds to the maxillary tuber facing the . The branches of the superior alveolar nerves pass in the superior portion of the external posterior wall. This is the site for administration of local anaesthetics for 'tuberal' anaesthesia in operations on the maxillary sinus and extraction of the corresponding teeth. The posterosuperior angle of this wall closely approaches the group of posterior ethmoid cells and the sphenoid sinus. The close proximity of the wall to the pterygopalatine fossa lodging the main trunk of the second division of the trigeminal nerve (the maxillary nerve), maxillary artery, and venous plexus connected with the orbit and cavernous sinus of the may promote the spread of pathology from the maxillary sinus to this region. The inferior wall (the floor) of the sinus is made up of the alveolar process of the maxilla (Fig. 7). Usually the floor extends from the alveole of the second premolar to the second molar alveole. Less frequently it is found between the first premolar and the third molar (wisdom tooth).

28

Fig. 7. Correlation between the teeth and floor of the maxillary sinus. a - lateral view; b - top view

Anatomical investigations show that the position of the floor of the maxillary sinus in an adult in relation to the floor of the nasal cavity varies. Thus, in 42.8 per cent it in lower than the floor of the nasal cavity; in 17.9 per cent it is above it, and in 39.3 per cent, occupies the some level. This should be taken into consideration in radical operation on the maxillary sinus when creating a passage to the nasal cavity in the area of the inferior nasal meatus. The tips of the tooth roots and the alveoli are usually near the sinus if the position of the sinus floor is low. In 45.5 per cent of cases the alveoli of the first and second molars are separated from the mucosa of the maxillary sinus by a very thin (0.5 mm) bony plate. Sometimes the root tips can be clearly seen in the cavity of the sinus. In such cases they are covered only by the mucous membrane. The maxillary sinus is then more susceptible to odontogenic infection, and the extraction of the mentioned teeth may cause a stable perforation through which food can penetrate from the mouth into the maxillary sinus. As a rule, the left and right sinuses are symmetrical, but the anomalies are encountered which include cases where the maxillary sinus is divided by partitions into several chambers. This creates difficulties in treatment o£ patients with maxillary . The mucosa of the maxillary sinus is continuous with that of the nasal cavity. It is very thin (can be compared with the cigarette paper). Being a mucoperiosteum, the mucous membrane closely adheres to the underlying bony tissue. Its absorbing capacity is high, and the lymphatics is extensive; the glands are few.

FRONTAL SINUS

The frontal sinus is located in the thickness of the frontal bone. The sagittal section of the skull shows the triangular shape of the sinus. The sinuses are rarely symmetrical: one sinus may be smaller, or even absent. One or both frontal sinuses are absent in 5-10 per cent of cases. The anterior wall is the thickest (from 5 to 8 mm). The obliquely positioned posterior (cerebral) wall separates the frontal sinus from the anterior cranial fossa. It is a thin but strong solid bone. The inferior wall separates the frontal sinus from the orbit; it is also very thin. Its size varies according to the size of the frontal sinus: the wall may cover the entire surface of the orbital roof and reach the lesser wings of the . The frontal sinus then borders on the sphenoid 29 sinus, the optic foramen, and reaches the middle cranial fossa. If both sinuses are present, they are separated by a thin bony partition which can deviate from the midline to each side. The sinus communicates with the nasal cavity through a thin tortuous which opens in the anterior portion of tlie middle nasal meatus (Fig. 8). The mucous membrane of the frontal sinus is similar to that of the maxillary sinus. It is lined with the ciliated epithelium that propels secretion through the frontonasal duct.

Fig. 8. Passages between the paranasal sinuses and nasal cavity 1- a probe passed into the maxillary sinus; 2—a probe passed into the frontal sinus through the frontonasal duct; 3—a probe passed into the sphenoid sinus; 4—orifice of the nasolacrimal duct; 5— mouth of the auditory tube; 6—sphenoid sinus; 7—frontal sinus

ETHMOID LABYRINTH

The ethmoid labyrinth has a complicated structure consists of a large number of air-cells situated in the saggital plane. The number of cells varies from 8 to 20 cells on each side. The cells open into the middle nasal meatus (anterior and middle cells) or into the superior nasal meatus (posterior cells). Mucosa of the ethmoid labyrinth is similar to that of other sinuses. The anatomo-topographical properties of the ethmoid labyrinth facilitate the spread of pathology from the sinus to the orbit, cranial cavity, and optic nerve. For a better understanding of the air-filled ethmoid labyrinth structure, it should be described in more detail. The ethmoid bone includes a perpendicular plate extending to the anterior cranial fossa in the form of and forming the bony part of the nasal septum, cribriform plate, orbital plate, separating air- cells from the orbit, and superior and middle nasal conchae.

SPHENOID SINUS

The sphenoid sinus lies inside the body of the sphenoid bone, posterior to the nasal cavity. The sinus is divided by the bony septum into two parts and opens into the superior nasal meatus. The pituitary, optic chiasm, and cavernous sinus are found near the sphenoid sinus. Branches of the external and internal carotid arteries supply blood to the paranasal sinuses. The knowldege of blood supply to the maxillary sinus is important for dental students. It is 30 accomplished mainly by the maxillary artery and its branches:

Fig. 9. Innovation of the maxillary mucosa and teeth 1—superior dental plexus (from the second branch of the trigeminal nerve); 2—infraorbital nerve; 3—superior dental nerve branching from the infraorbital nerve and innervating mucosa of the maxillary sinus, gingivae, and teeth; 4—trigeminal ganglion the posterosuperior dental artery supplies blood to the walls, periosteum and mucosa of the sinus, cheek and gingivae, and also the upper teeth; the anterosuperior dental artery (the branch of the infraorbital artery) carries blood to the internal wall of the sinus, the soft and hard palate. During the operation on the maxillary sinus a severe bleeding may originate from the site where the maxillary sinus and the nasal cavity are separated, this is receiving blood from the descending palatine artery. The lateral wall of the sinus should sparingly be removed because the sphenopalatine artery may otherwise be damaged. The veins of the maxillary sinus form numerous anastomoses with the veins of the orbit, nose, face and sinuses of the dura mater. The lymphatic vessels of the maxillary sinus serve as the routes by which the infection and metastases can spread, since they are closely connected with the lymphatic vessels of the nasal cavity, retropharyngeal and deep cervical lymph nodes. In addition, inflammation can extend by the lymphatic vessels running from the teeth because the lymphatic vessels of the dental alveoli anastomose with the vessels of the mucous membrane of the maxillary sinus. The mucous membrane of the paranasal sinuses is innervated by the first (the ophthalmic nerve) and the second (the maxillary nerve) branches of the trigeminal nerve (Fig. 9.).

The Role of Nasal Breathing

Normal functioning of the nasal cavity plays an important role in the infraction of humans with the environment. The inspired air changes as it passes through the nasal meatuses. It is moistened, warmed up, separated from dust particles, and considerably disinfected. This is accomplished not only by the mechanical ciliary action, by which the retained dust particles and microorganisms are carried to the nasopharynx, but also by the nasal secretion, containing mucin and lysozyme. 31 It has been proved that the number of micro organisms penetrating into the lower respiratory pathways during nasal breathing is ten times smaller than during breathing through the mouth. Impeded nasal breathing facilitates the onset of acute tonsillitis, acute respiratory diseases, bronchitis, and pneumonia. Free nasal breathing promotes normal gas exchange in the blood because in mouth breathing the absorbed oxygen amounts to only 78 per cent of the norm. Pro- longed shortage of oxygen may cause anaemia and inhibit physical and mental development. Blood and lymphatic vessels of the nasal cavity are closely connected with vessels of the brain. Impeded breathing may impair blood and lymph circulation in the nasal cavity, paranasal sinuses, cerebral tissue. This may result in tachycardia, high intracranial pressure, persistent headache, rapid fatigue, hypomnesia, emotional labiality, poor appetite, and the inability to concentrate. Persistent nasal obstruction may lead to various nervous disorders, bronchial asthma, and epileptiform seizures and nocturnal enuresis in children. Long-standing nasal obstruction in children promotes the development of mouth breathing which results in malformation of the chest and facial bones; the maxilla grows defective, its lateral sides tend to near, the hard palate becomes narrow and high-arched (the gothic palate). The floor of the nasal cavity rises, the nasal septum deviates, and malocclusion develops. The voice changes and becomes nasal. Normally, functioning olfactory analyser impedes the inhalation of air containing pollutants. The helps us to detect improper food. Thus, in addition to the respiratory function, the nose performs also the defensive, olfactory, and resonance functions.

EXAMINATION OF THE NOSE AND PARANASAL SINUSES

The inspection of the external nose, nasal cavity and paranasal sinuses begins with revealing the patient's complaints and taking the anamnesis. Then comes thorough examination of the nasal cavity. The condition of the paranasal sinuses can be judged by the appearance of the nasal cavity. The external nose. Special attention is paid to the shape of the external nose, possible deviation of the bridge from the midline, or its depression. If nasal fracture is suspected, the examiner palpates the external nose for which the index finger is placed on the bridge of the nose at its root, while the thumb and the middle fingers exert pressure on the sides of the nose. The bridge is inspected from the root to the tip to determine a depression or protrusion parts of the external nose, displacement of bone fragments, and presence or absence of crepitation at the side of fracture. The nasal cavity. No special tools are necessary to inspect the nasal vestibule, but use of a 32 head mirror is obligatory. In order to inspect the deep structures of the nasal cavity, the beam of light from the head mirror should bo projected into the nostrils to illuminate the nasal cavity. To perform the procedure with the help of a head mirror, the lamp is placed behind and to the right of the patient at the level or his ear. To adjust the head mirror, the student fixes it in such a way that its hole is directed in front of the pupil of the examiner's left eye. A sharp focus is maintained due to the adjustment of the head, mirror so that the examiner can see a brilliant spot on the patient's face through the hole. The right eye is closed up to this moment. Once the left eye is focussed, the examiner opens the right eye for binocular vision, i.e. the examination of the object by both eyes simulataneonsly, which is important for spatial perception. When the patient occupies a correct position, the student fixes the beam of light on the patient's nostrils, the up of the nose is tilted up by the thumb of the right hand, and four fingers are placed on the patient's head. The vestibule of the nose (a part of the nasal septum, the inner surface of the wings with vibrissae) is thus adequately inspected (Fig. 10). Tho next stage of examination-anterior rhinoscopy-is performed using a nasal speculum. The position of the patient and the examiner remains the same. The speculum is held in the left hand, while the right hand is placed on this patient's head; this allows to change its position where necessary. The correct way to hold the speculum is shown in Fig. 11. The beam of light is focussed on the patient's into which closed speculum is carefully inserted, its blades being gradually opened to lift the ala in the direction of the outer canthus. The patient's head position is erect. The examiner can inspect the anterior end of the inferior concha, the inferior nasal meatus, Kiessel bach's area of the nasal septum, and the inferior portion of the common nasal meatus. As the head of the patient, is tilted back, the examiner can inspect the middle concha, the middle nasal meatus, the superior portions of the common nasal meatus, and the larger part of the septum (see Fig. 11). To save the patient from unpleasant sensations, the speculum which is to be removed from the nasal cavity should be open.

33 Fig. 10. Anterior rhinoscopy: examination of the nasal vestibule

Fig. 11. Anterior rhinoscopy: position of the patient and examiner. Inspection of the anterior and middle parts of the nasal cavity

The inspection of the posterior parts of the nasal cavity—posterior rhinoscopy—is more complicated. The examiner should use the nasopharyngeal mirror and the tongue depressor. The examiner holds the tongue depressor (or spatula) in his left hand; the patient's mouth is opened. The blade of the spatula should not touch the root of the tongue, since it may cause the patient to gag. The nasopharyngeal mirror (faced upwards) is held in the examiner's right hand. The glass surface is warmed over an alcohol burner (to prevent fogging). The tongue is depressed, the mirror is placed over the soft palate, and the patient is asked to inhale through the nose. The vault of the nasopharynx, the posterior end of the nasal septum -the vomer, the posterior ends of the nasal conchae, the nasal meatuses, the openings of the auditory tubes lodged on the lateral wall of the nasopharynx are inspected (Fig. 12).

Fig. 12. Posterior rhinoscopy 1-posterior ends of the nasal conchae; 2-vault of the nasopharynx; 3- vomer

As it has already been noted, the condition of the paranasal sinuses can be assessed by the appearance of the nasal cavity.

34 X-rays taken in several projections give reliable information on the paranasal sinuses. The anteroposterior view is commonly used, which is valuable because it gives the whole picture of the paranasal sinuses (Fig. 13). The condition of the sinuses is assessed by their radiopacity. If the sinuses are as radiopaque as the orbits, no pathology is present (Fig. 14). Diaphanascopy and ultrasonography are the additional methods. Computed tomography helps locate tumours of the nose and paranasal sinuses. Lipiodol is used as a contrast medium (contrast roentgenography). The respiratory and olfactory functions are examined by a rhinopneumometer and an olfactometer. Olfactometers are devices for estimating the keenness of the sense of smell. A simple way to check patency of the nasal cavity is to bring a gauze thread to the patient's nostrils in turn and ask him to inhale

Fig. 13. Paranasal sinuses (anteroposterior view) 1—frontal sinus; 2—ethmoid cells; 3—maxillary sinus; 4—sphenoid sinus; 5—orbit

Fig. 14. X-ray picture of the paranasal sinuses {anteroposterior view) 1—fluid level in the left maxillary sinus 35 and exhale. Flutter of the thread indicates the condition of nasal breathing. The acuity of the olfactory sense is determined using a set of odorous substances that stimulate the endings of the trigeminal, glossopharyngeal, and olfactory nerves participating in the process of smelling. Spirit of ammonia, wax, valerian tincture, and hard soaps are commonly used in such tests.

Pharynx

The pharynx is a muscular tube extending from the base of the skull to the seventh cervical vertebra. Below this level it is continuous with the oesophagus. According to the anatomo-physiological features and from the clinical standpoint, the pharynx is subdivided into three parts: the nasopharynx, the oropharynx, and the laryngopharynx (Fig. 15). The conventional borderlines separating these parts are posterior extension of the hard palate and the horizontal line drawn through the upper edge of the epiglotlis. The nasopharynx is a small space behind the choanae. The pharyngeal tonsil is found on its vault, and the pharyngeal orifices of the pharyngotympanic tubes which open under the are seen on the lateral walls. Inferiorly, the nasopharynx communicates with the oropharynx which can be well examined. It includes the soft palate with the uvula, a visible part of the posterior pharyngeal wall, and the fauces. The latter are bounded by the root of the tongue, the tonsillar pillars between which the palatine (faucial) tonsils are located, and the soft palate. Thus, the fauces can be defined as the space formed by the above-mentioned structures, and the expressions such as 'the fauces are hyperaemic'. or 'the patches are seen in the fauces are therefore incorrect. The mucosa of the posterior pharyngeal wall contains elements of the lymphoid tissue which sometimes form visible prominences, the so-called granules. Besides, the lymphoid bands are found behind the posterior tonsillar pillars. The mucosa of the posterior wall of the oropharynx is lined with squamous epithelium and contains numerous glands. It is innervated by the glossopharyngeal nerve whose fibres running by the course of the blood vessels react to their dilatation during inflammation and cause pain and dryness in the throat (Fig. 16).

36

Fig. 15. Pharynx a—nasopharynx; b—oropharynx; c—laryngopharynx: 1—first tracheal ring; 2—cricoid cartilage; 3—thyroid cartilage; 4—hyoid bone; 5~hard palate; 6—upper edge of the epiglottis

The palatine tonsils are located in the oropharynx. Their pathological condition requires special attention on the part of physicians of various specialities since it may cause a number of common diseases. Each palatine tonsil is embedded in the depression on the lateral wall of the oropharynx, the tonsillar fossa, situated between the anterior and posterior tonsillar (faucial) pillars exhibited as muscular structures. The muscular tissue of the pillars is visible through the thin mucous membrane and the bright pink colour can be mistaken for hyperaemia. The palatine tonsil is a mass of the rcticular tissue with a large number of lymphocyte-containing follicles that underlie the mucosa. The free surface of the tonsil is medial and contains numerous mouths of the tonsillar crypts, which are tortuous tubes running into the depth of the tonsil. The follicles are embedded in the walls of these tubes. The reticular tissue surrounds the tonsillar stroma which is composed of connective tissue. The tonsillar 'pseudocapsule' is turned laterally and attached to the fascia of the pharyngeal muscles.

37

Fig. 16. Pharyngoscopic picture 1—root of the tongue; 2—anterior tonsillar pillar; 3—palatine tonsil; 4—posterior tonsillar pillar; 5—lateral hand; 6— soft palate; 7- uvula; 8—lymphoid granules; 9—posterior pharyngeal wall

The lymphatics of the palatine tonsils drain into the lymph nodes that are located on the anterior edge of the sternocleidomastoid muscles, on the line separating its upper and middle thirds. The palatine, pharyngeal, and lingual tonsils, together with accumulation of the lymphoid tissue in the region of the auditory tubes, are known as the lymphoid ring (Waldeyer's tonsillar ring). The important function of the palatine tonsils is formation of immunity. When the inflammation involves cellular spaces found near the pharynx, this may lead to severe complications. These areas are: (1) the peritonsillar space which surrounds the palatine tonsil and is tilled with loose cellular tissue; (2) the retropharyngeal space which is behind the posterior pharyngeal wall between the prevertebral fascia and the cervical fascia proper. In children, the lymph nodes draining lymph from the nasal cavity, paranasal sinuses, and middle ear are found inside the cellular tissue; (3) the parapharyngeal (or pharyngomaxillary) space which is closely related to the organs of the maxillodental system (Fig. 17).

Fig. 17. Parapharyngeal space and its boundaries 38 1—epiglottis; 2—root of the tongue; 3-palatine tonsil; 4—styloid process; 5—lower jaw; 6— parotid gland; 7—internal jugular vein; 8—internal carotid artery; 9—retropharyngeal space; 10— parapharyngeal space

Medially, it is bounded by the pharyngeal muscles, laterally—by the capsule of the parotid gland, anteriorly by the mandible and its muscles, posteriorly by the bodies of two cervical vertebrae, and superiorly by the skull base having minute holes through which pass the main vascular and nerve trunks. Inferiorly, the parapharyngeal and the retropharyngeal spaces communicate with the posterior mediastinum. The external carotid artery is responsible for blood supply to the pharynx. The palatine tonsils receive blood from the tonsillar artery.

EXAMINATION OF THE PHARYNX

Posterior rhinoscopy, the method of examination of the nasopharynx, was discussed above. In addition, the examiner may also palpate the nasopharynx by passing the right index finger behind the soft palate and pressing the patient's cheek between the teeth with the left thumb to prevent the patient from biting the examiner's finger. This method helps detect neoplasms, and determine the consistency of the tissue. X-ray examination of the nasopharynx in the lateral projection is sometimes resorted to.

Fig. 18. Pharyngoscopy

During the inspection of the oropharynx (pharyngoscopy) the examiner uses the tongue depressor (or spatula) which he/she holds in the left hand (Fig. 18). The tongue is pressed to

39 observe the colour of the mucosa, the appearance of the posterior pharyngeal wall, the tonsillar pillars, and the tongue. Using the right hand, the examiner positions the patient's head, as for the anterior rhinoscopy. If the necessity arises to inspect the contents of the tonsillar crypts, another tongue depressor is used. The examiner holds it in the right hand and presses the anterior tonsillar pillar posteriorly to express purulent detritus or plugs from the tonsil (Fig. 19).

Fig. 19. Expressing pus from the tonsillar crypts

Sometimes smear is taken from the tonsillar mucosa and the posterior pharyngeal wall. These sites in the oropharynx are touched by a sterile tampon which is then placed into a test tube. The hypopharynx is inspected during laryngeal examination. To abolish the increased gag reflex, the throat is irrigated with the xylocaine, trimecaine or cocaine solutions.

Oesophagus At the level of the seventh cervical vertebra the pharynx is continuous with the oesophagus, a muscular tube reaching 25 cm in adults. The cervical (upper), thoracic (middle), and abdominal (lower) parts of the oesophagus are distinguished. The constricted oesophageal mouth (the entry) is found behind the larynx. There are three physiological narrowings of the oesophageal lumen: at the entry to the oesophagus, at the point of intersection with the aorta, and the junction with the stomach. The muscular coat of the upper oesophageal wall is composed of striated muscle fibres whose strong and rapid contractions propel the bolus through the oesophagus to its lower portions. The muscular coat of the middle oesophagus is composed of mixed and the lower oesophagus of only smooth muscle fibres responsible for peristaltic movements of the oesophageai walls. The recurrent laryngeal nerves pass between the oesophagus and the trachea. Therefore, oesophageal tumours can cause the development of laryngeal pareses and paralyses. Oesophagoscopy is usually performed to examine the oesophagus. For this purpose general or local anaesthesia is used, and oesophagoscopes and

40 flexible fiberoptic instruments with distal or proximal illumination are now available. As a rule, roentgenograms must be taken prior to oesophagoscopy.

Clinical Anatomy, Physiology and Examination of the Larynx Larynx

The larynx is found on the anterior part of the neck between the hyoid bone and the trachea. It is a hollow organ formed by cartilages, ligaments, and muscles. Anatomically, the larynx is in close relation to the thyroid gland and its isthmus, the main cervical vessels, the pharynx, and the oesophagus. The laryngeal framework includes three unpaired, or large, and three paired, or small, cartilages (Fig. 20).

Fig. 20. Laryngeal framework 1—first tracheal ring; 2—cricoid cartilage; 3— arytenoid cartilage; 4— corniculate carlilage; 5— superior horn of the thyroid cartilage; 6—opening in the thyrohyoid membrane through which the neurovascular bundle passes; 7—hyoid bone; 8—thyrohyoid membrane; 9— epiglottis; 10— thyroid cartilage; 11 — arch of the cricoid cartilage

The unpaired cartilages are the cricoid, thyroid, and epiglottis. The cricoid cartilage is the lowermost of the laryngeal cartilages that joins with the first tracheal incomplete ring; it is considered to be the base of the larynx. It resembles a ring: there is an arch and a signet, hence the name (from Gr krikos ring). By means of joints it articulates with the next single thyroid cartilage which has two approximately quadrangular plates fused anteriorly to form an angle, the laryngeal prominence known as Adam's apple especially noticeable in men. By its superior horns extending upward from each plate, the thyroid cartilage joins the hyoid bone, and by the inferior horns it articulates with the cricoid cartilage. The third unpaired cartilage, the epiglottis, is the uppermost portion of the larynx; it can be seen when the root of the tongue is 41 pressed. While the cricoid cartilage is the base of the larynx, and the thyroid cartilage is its shield from the external pressure, the epiglottis is a cover that protects the rima glottidis from penetration of saliva and food during swallowing.

Fig. 21. Innervation of the larynx 1— right subclavian artery; 2—right recurrent laryngeal nerve; 3—external branch of the right superior laryngeal nerve; 4—right vagus nerve; 5—internal branch of the right superior laryn- geal nerve; 6—superior laryngeal nerve; 7— thyrohyoid membrane; 8—hyoid bone; 9—left superior laryngeal nerve; 10—external branch of the left superior laryngeal nerve; 11—thyroid cartilage; 12— left vagus nerve; 13—left recurrent laryngeal nerve; 14— left subclavian artery; 15— arch of the aorta; 16—cricoid cartilage

The paired cartilages are the arytenoid, corniculate, and cuneiform ones. The vocal cords and most intrinsic muscles (lateral cricoarytenoid, oblique arytenoid, transverse arytenoid, vocalis, and anterior cricothyroid) which close the rima glottidis, and the posterior cricoarytenoid muscle which dilates it, are attached to the arytenoid cartilages. The extrinsic laryngeal muscles include three paired muscles: sternohyoid, sternothyroid, and thyrohyoid innervated mainly by the vagus nerve. The laryngeal mucous membrane is continuous with the nasal and pharyngeal mucosa. The true vocal cords are lined with squamous epithelium, and other laryngeal structures, with ciliated epithelium. The submucous layer of the ventral surface of the epiglottis, the false vocal cords, and the infraglottic cavity are well developed. These are namely sites of laryngeal oedema which, in pathology, causes difficult respiration and swallowing. The superior thyroid artery (the first branch of the external carotid artery in the cervical region) supplies blood to the larynx. The larynx is innervated by the superior laryngeal nerve (the branch of the vagus) 42 penetrating into the larynx through the opening in the thyrohyoid membrane. The motor (external) branch of the superior laryngeal nerve innervates only the anterior cricothyroid muscle which tilts the thyroid cartilage anteriorly, thus making the vocal cords tense, which accounts for the voice timbre. Other laryngeal muscles are innervated by the recurrent laryngeal nerves. The left recurrent laryngeal nerve curves the aortic arch and then ascends to occupy the groove between the oesophagus and the trachea. The right recurrent laryngeal nerve arches over the subclavian artery and also ascends to innervate the laryngeal muscles (Fig. 21). The compression of or injury to these nerves causes respiration and phonation difficulties. According to the anatomo-clinical signs, the larynx is subdivided into three parts: (1) the upper part, the vestibule of the larynx, extends from the entry to the larynx to the vestibular folds; (2) the middle part levels with the vocal folds; (3) the lower part, the infraglottic cavity, extends from the vocal folds to the trachea. The first manifestations and early metastases of the malignant laryngeal tumour mainly depend on its location and thus determine the prognosis and early diagnosis of the new growth. The vestibular folds of the larynx are the duplicature of the mucous membrane. Vocal folds are based on the vocalis muscle. The whitish colour of the vocal folds is due to the compact layer of squamous epithelium on their upper surface and the underlying elastic membrane. There is a space between the vestibular and vocal folds known as the sinus of the larynx or laryngeal ventricle (Fig. 22).

Fig. 22. Laryngeal folds 1—epiglottis; 2—aryepiglotic folds; 3—laryngeal ventricle; 4—vocal fold; 5—infraglottic space; 6—vestibular folds

43 FUNCTIONS OF THE LARYNX

The larynx performs respiratory, protective, and voice-producing functions. The larynx is not a mere air-pipe, since it takes an active part in respiration by controlling inspiration, depending on the quality of air inhaled. Its reflexogonic zones control the inspiration depth, thus decreasing the inhalation of polluted air. When these zones are irritated by a foreign body (saliva, food, etc.), the laryngospasm instantly occurs, and the cough reflex appears. Voice is produced not only due to vibrations of the vocal cords as the expired air passes through them, but also due to the active contractions of the laryngeal muscles. The length and width of the vocal folds vary during phonation. Only the free edges or the entire folds can vib- rate during phonation, thus giving the specific timbre to the voice. The vocai folds are wider and longer in persons with a low voice (bass, contralto) than in persons with a high voice (tenor, soprano).

EXAMINATION OF THE LARYNX External examination can reveal laryngeal asymmetry when there is a neoplasm or inflammation of the cartilaginous tissue. Diagnostic examination also includes palpation of the larynx and its active displacement in the horizontal plane (absence of crepitation of cartilages displaced suggests a malignant tumour). Indirect and direct laryngoscopy are used to inspect the laryngeal cavity. Indirect laryngoscopy is conducted with the laryngeal mirror with a handle. Special instruments, laryngoscopes with autonomous light source, are used in direct laryngoscopy. Indirect laryngoscopy (Figs. 23, 24). The patient sits erect, and the source of light is set at the level of the right ear. At first the examiner focusses light on the head mirror; then the laryngeal mirror is warmed, and the patient is asked to protrude the tongue which is wrapped with a napkin and held in this position. The patient must deeply breathe through the mouth where the mirror is inserted (with its back side against the uvula) so that it touches

44

Fig. 23. Indirect loryngoscopy position of the laryngeal speculum in the oropharynx 1— laryngeal speculum; 2 – epiglottis the soft palate. The patient is asked to utter a long 'e'. The larynx can thus be inspected during respiration and phonation. The colour of the laryngeal mucosa and the vocal folds, their mobility and junction during phonation, and also their symmetrical movements are noted (Fig. 25).

Fig. 24. Indirect loryngoscopy

Topical anaesthesia is used in exaggerated gag reflex. The palatine mucosa, posterior pharyngeal wall, and the root of the tongue are sprayed with an anaesthetic. A probe with a cotton applicator moistened in an anaesthetic may be used. Sometimes indirect laryngoscopy is not sufficient to make the diagnosis. In such cases direct microlaryngoscopy performed in anaesthetized patient which a special microscope is used (Fig. 26)

45

Fig. 25. Larynx during indirect laryngoscopy a—respiration; b—phonation; 1—epiglottis; 2—aryepiglottic folds; 3—veslibular folds; 4— vocal folds; 5—apices of the arytenoid cartilages; 6—interarytenoid space

Fig. 25. Larynx during indirect laryngoscopy a—respiration; 6—phonation; i—epiglottis; 2—aryepiglottic folds; 3—veslibular folds; 4— vocal folds; 5—apices of the arytenoid cartilages; 6—interarytenoid space

Fig. 26. Microlaryngoscopy in an anaesthetized patient The x-ray examination, especially tomography performed in the frontal projection, is helpful to verify the diagnosis, since it allows to inspect 'the entire larynx.

46 Diseases of the External Ear

Frostbite of the auricle. The auricle is subject to frostbite because it stands out prominently from the head, and the blood vessels of its anterior surface lack a protective layer of subcutaneous fat. Like in a frostbite of the external nose, there are three stages: erythema, formation of bullae, and gangrene. Treatment is the same. Congenital malformations of the external ear. Annually, one infant par 10 000 is born in the USSR with develop, mental malformations of the external and middle ear. Otorhinolaryngologics and dentists make plastic reconstruction of the auricle; besides, otorhinolaryngologists perform operations that improve hearing in these patients. Reconstruction of the auricle with its complicated relief is a most laborious plastic operation. The following degrees of the auricle malformation are distinguished: microtia (only some fragments are available: a lobule, a part of the helix in the form of a cutaneous band) and anotia (absence of the pinna and external auditory canal). In both cases the auricle is repaired using the carcass of the available cartilage, plastic materials, and skin. Malformations of the ear are often combined with developmental anomalies of other organs, namely, absence of a kidney, phimosis, hypomastia, and congenital valve defect. Anomalous jaws, underdeveloped masticatory muscles and salivary glands, cleft lip and palate are also common. Along with plastic surgery aimed at repairing the auricle and external auditory canal, reconstructive surgery of the middle ear directed at improving the hearing function is also performed.

INFLAMMATORY DISEASES OF THE EXTERNAL EAR

External otitis means inflammation of the external auditory canal. Diffuse and localized forms are distiguished. Pain, itching, and discharge from the are common in patients with diffuse inflammation. External otitis occurs due to trauma, for instance, as a result of scratching in diabetes patients. At present, microbial flora has changed: Staphylococcus aureus was the main pathogenic organism 25-30 years ago, while nowadays the maid microbes of the ear are Pseudomonas aeruginosa, Proteus vulgaris, and Escherichia coli. These microbiological shifts are accounted for by the wide use of various antibiotics that inhibit coccal flora and permit nonsen-sitive microorganisms to dominate. Furuncle of the auditory canal (otitis externa circumscripta). Furuncle is a type of localized external otitis occurring in the cartilaginous canal of the ear. Pain, which intensifies on pressure applied to the tragus, is typical. If the furuncle is situated on the

47 anterior wall of the auditory canal, pain also intensifies during mastication due to displacement of the wall bordering on the temporomandibular joint. The lymph nodes in front of the tragus and in the postauricular area become enlarged and tender. Acute inflammation may spread to the parotid gland through the fissures (Santorini's fissures) in the cartilaginous portion of the inferior meatal wall. Diffuse skin inflammation is associated with pain, swelling, release of secretion, and narrowing of the auditory meatus. Treatment. In patients with diffuse external otitis careful irrigation of the auditory canal and suction of pus are necessary. Desensitizing drugs are given orally or applied locally as ointments: a 2 per cent synthomycin emulsion and a 1 per cent polymyxin ointment if the aural discharge contains Pseudomonas aeruginosa. Physiotherapy is helpful: ultraviolet irradiation of the ear canal through the tube plus UHF therapy. Antibiotics (penicillin, 500 000 U, four times a day, tetracycline and oletetrin, 400 000 U, four times a day by injections), ointments (3 per cent aminoniated mercury and Vishnevsky's ointment applied on cotton wisps) are prescribed. If the furuncle is not ripe to break spontaneously for a long time, pain is severe and abscess develops, the furuncle should be incised. Otomycosis. Treatment depends on the genus of fungus—mould (Aspergillus niger) or yeast-like (Candida albicans). If mould fungi are found, nitrofungin is used (turundas impregnated with the drug are inserted into the external auditory meatus); gentian violet and quinosol also prove effective for local treatment. If yeast-like fungi are discovered, levorin ointment and Castellani,s paint are used locally. Among the drugs taken per os nystatin and decamin are recommended. Prior to therapy antibiotics are suspended, general invigorating therapy and group B and C vitamins prescribed. Since allergy may develop, hyposensilizing drugs are given.

FOREIGN BODIES OF THE EXTERNAL AUDITORY MEATUS

Various objects, e.g., metallic objects, cereal grains, and also small insects canal. may be found in the auditory

48

Fig. 71. Aural irrigation The patient complains of an obstacle in the ear, hearing loss, sometimes pain, especially if the foreign body has deeply penetrated and touches the eardrum. History findings are important to specify the diagnosis. Otoscopy helps finally identify the foreign object. Indispensable conditions for the first aid are as follows: an object may be removed only under direct visual control (through the ear speculum); appropriate instruments are needed; the patient's head should be reliably fixed. Otherwise, the patient's condition may be aggravated, and the auditory canal, drum, and auditory ossicles can be injured, while the foreign body remains in the ear. It is more convenient to remove a smooth foreign object using a special hook. Aural irrigation, using Janet's syringe, is also effective (Fig, 71). Fluid is directed along the posterosupeior Avail of the auditory canal.

TRAUMA OF THE EXTERNAL EAR

Close anatomical connections of the external car with the maxillodental system provide conditions for combined injuries. First aid in such cases must preserve not only the anatomical structure of the injured organ, but also promote restoration of its function. For instance, a person sustained a heavy blow on the chin in a car accident, and the head of the condylar process displaced backward. This caused injury not only to the articulating surface of the temporomandibular joint, but also to the anterior bony wall of the external auditory canal. Displacement of bone fragments is accompanied by narrowing of the auditory meatus, reduced hearing acuity, otalgia, and bloody discharge from the ear canal (Fig, 72). After blood clots are removed from the depth of the ear canal, bulging of bone fragments in its anterior wall may be revealed. It should be noted that otorrhagia develops also when the pyramid of the temporal bone is fractured, which requires additional examination (tomography included) of the temporal bone. A physician who renders emergency aid must arrest bleeding and do his best to

49 prevent further narrowing and atresia of the auditory canal and functional disturbance of the temporomandibular joint. The treatment includes reposition of bone splinters using an elevator, and ear canal tamponade with turundas impregnated with antiinflammatory ointments (synthomycin emulsion). Local anaesthesia with a 2 per cent novocains solution administered above the tragus is given. Prophylactic treatment with antitetanus serum and antibiotics are prescribed.

Fig. 72. Trauma to the auricle, external anuditory meatus temporomandibular joint A dentist must control restoration of the joint function. Traumas of the external ear may be accompanied by injuries to the parotid gland and facial nerve.

OTALGIA

Otalgia means intense, paroxysmal pain localized near the auricle or in the depth of the ear and unassociated with ear pathology. Among the underlying causes is pathology of the organs that have common innervation with the external and middle ear. Stimulation of nerve endings of the glossopharyngeal, trigeminal, and vagus nerves that take part in aural innervation may cause reflected pain in various parts of the car. Foci of irritation of these nerve endings may be located in the mucosa of the oral cavity, pharynx, and nose. Carious teeth (especially the eighth lower tooth), destructive changes of the tongue root and temporomandibular joint may cause sharp paroxysmal pain.

50 The patient always consults otorhinolaryngologist, since pain in the ear is the leading symptom. Only a planned interviewing helps reveal other complaints: carious tooth or diseases of the nasal cavity. Examination reveals adenoids, hypertrophred posterior ends of the inferior nasal conchae, and inflammatory conditions of the larynx, first of all, of the epiglottis. Therefore, examination of patients with otalgia by a neuropathologist and dentist is obligatory. Sometimes, sanation of the eighth lower tooth immediately relieves excruciating pain. Otalgia should be differentiated from some neurological syndromes that have similar clinical picture. Thus, patients with the Costen syndrome complain of tinnitus, pain in the ear, dizziness, hearing loss, headache in the vertex, pain and crackle mainly due to malocclusion of the temporomandibular joint. This causes the backward displacement of the articulating head: the neurovascular bundle that passes through the petrotympanic fissure is exposed to increased pressure. Treatment administered by a dentist saves the patient from painful sensations.

Acute Diseases of the Middle Ear

The diseases of the middle ear are varied and may include inflammation, sequelae of inflammation (cicatrices, adhesions, ossicular destruction) of dystrophic condition (otosclerosis). All diseases of the middle ear impair the hearing function and are therefore of great social importance. Prevention of hearing loss and restoration of the hearing function lake the leading place in otorhinolaryngology in this country.

ACUTE OTITIS MEDIA

Acute inflammation of the middle ear (auditory tube, tympanic cavity, and the air- cells of the mastoid process) is called acute otitis media which may be catarrhal or suppurative, depending upon the type or stage of inflammation. The routes of infection invasion are as follows: (a) tubal route through the eustachian tube from the nasopharynx; (b) haematogenic route through the blood stream in the presence of infectious diseases; (c) through the injured eardrum. Infection may invade the middle ear in measles or scarlet fever patients through the auditory tube whose ciliated epithelium stops functioning under the action of viruses of measles, influenza, etc. Acute otitis media is one of the most common infections, particularly in childhood. Respiratory diseases, adenoids, 51 chronic inflammation of the nasal cavity and paranasal sinuses, and decreased body resistance contribute to the occurrence of acute otitis media. The pathogenic flora is represented by cocci (streptococcus, pneumococcus). Three stages of the disease are distinguished: I, before perforation; II, perforation and otorrhoea, III, perforation and cessation of otorrhoea. Each of those stages is manifested by specific signs, both clinical and pathological; the treatment of each stage differs. Stage I. Complaints: blocked ear, severe pain in the ear radiating to the , vertex, occiput, and teeth. Pain is constant, quickly intensifies, attaining maximum within the first day. Sleep is deranged, the patient's general condition worsens, and the body temperature rises. Otoscopy: the eardrum looks different, the usual landmarks (manubrium and short process of the malleus and light reflex) are not observed. The drum becomes crimson and begins to bulge into the auditory meatus. Treatment. Warming compress (folded gauze soaked in sunflower oil, alcohol or eau- de-Cologne) is placed on the mastoid process, above and in front of the auricle. A hole is done in the folded gauze through which an auricle passes. Vasoconstrictive drops (ephedrine, adrenaline) should be instilled into the nose (the head is tilted back). Analgin, baralgin (in tablets), and antibiotics are given. Camphor oil and glycerol are instilled into the external auditory meatus. If pain does not subside in two days, but, on the contrary, intensifies without spontaneous rupture of the

Fig. 73. Paracentesis 1-site of incision; 2—paracentetic needle eardrum, the signs of complication develop: meningism, high fever. Paracentesis, i.e., opening of the tympanic cavity by incising the tympanic membrane, is necessary and is best done in the posteroinferior quadrant of the eardrum (the site of its maximum bulging) (Fig, 73). Paracentesis quickly aborts the inflammation. Moreover, it prevents spontaneous rupture of the tympanic membrane and formation of stable perforation, since even margins heal perfectly,

52 Stage II. Complaints: hearing loss, otorrhoea; pain lessens substantially and disappears gradually. Otoscopy shows a pulsating purulent discharge filling the external auditory meatus: pus overlying the dilated blood vessels pulaates together with the vessels. Perforation may be unseen, since it looks as a fissure, and the site of per-

Fig. 74. Inflation of tbe eustachian tube with a Pulitzer bag

Fig. 75. Ear catheterization 1—catheter inserted into the mouth of the eustachian tubc; 2-rubber bulb; 3—otoscope foration may be detected only by the oozing pus. The eardrum is thick and hyperaemic; its landmarks are not visible. Treatment, Warming compresses, vasoconstrictive nose drops, antibiotics with due account to flora sensitivity, and hyposensitizing agents are continued. Pus should be removed from the ear canal by cotton on a probe or by an electric suction apparatus, or a rubber bulb. Inflation by the Politzor bag (politzerization) or catheterization of the ear is necessary (Figs. 74, 75).

53 Politzerization. An olivs connected with a rubber bulb by a flexible tube is inserted into the patient's nostril. The doctor closes the other nostril by pressing the wing of the nose to the nasal septum. The patient is asked to say ‘one’ ‘two’, ‘three’. When the last word is pronounced, the rubber bulb is strongly compressed forcing air into the nasal cavity and nasopharynx. Since in pronouncing 'three' the soft palate is lifted and retracted, while the nasopharynx and oropharynx disjoin, the blown air enters through the mouths of the eustachian tubes into the middle ear. Ear catheterization is performed if politzerization fails. First, the mucosa of the nasal cavity, nasopharynx, and mouths of the eustachian tubes is anaesthetized, then a curved metal catheter is inserted into the nostril to reach the nasopharynx. The tip of the catheter must enter the mouth of the auditory tube. The otoscope connects the patient's and doctor's ear and helps control the air passage from the bulb into the middle ear through the catheter. Stage III. Otorrhoea stops as a result of treatment or spontaneously. Complaints: impaired hearing, autophonia, and tinnitus. Otoscopy: discharge is absent from the ear canal, the tympanic membrane acquires usual appearance and colour; the manubrium and short process of the malleus become visible. Later the eardrum becomes normally positioned, and the light reflex appears. Treatment. Regular inflation of the eustachian tube is continued. Physiotherapy (0-7 procedures of the UHF therapy on the area of the middle ear) and pneumornassage of the tympanic membrane to prevent adhesions and cicatrices in the tympanic cavity. Patients recover in 10-14 days if the disease runs the usual course. Restoration of the hearing function is the criterion of cure. Acute otitis media lakes a subacute or chronic form if treatment is inadequate, the flora is highly virulent, and the patient's general condition is poor due to avitaminosis, allergic status, and malnutrition. Sometimes, acute otitis media ia complicated by facial paresis and intracranial pathology. A condition known as mastoiditis is a common outcome. Mastoiditis is an acute suppurative inflammation of the middle ear accompanied by destruction of the mastoid bony elements. It is the destruction of the bony tissue of the mastoid process that differentiates mastoiditis from acute otitis media. This destruction may entail various complications as a result of destruction of the tegmen of the mastoid antrum, the wall separating the sigmoid sinus from the antrum, labyrinthine walls, and bony walls protecting the facial nerve. Increased virulence of microflora, inadequate treatment, insensitivity of flora to antibiotics and sulphanilamides, impaired body reactivity (actually, the same cases that convert acute otitis media into its subacute and chronic forms) facilitate the transition of 54 acute otitis media to mastoiditis. Symptoms. In the presence of acute otitis media, or somewhat later, pain in the ear and behind it intensifies. Pain is spontaneous or may increase on pressure applied to the mastoid tip and plane (planum mastoideum). Diminished hearing, tinnitus, increased otorrhoea (pus becomes thick and yellowish) are also characteristic. Body temperature rises to 38-39 0C The patient's general condition substantially deteriorates. Otoscopy, the pathognomonic Sign of mastoiditis is sagging of the posterosupurior wall of the external auditory meatus in its bony portion. This is associated with periostitis: suppuration of the mastoid antrum destroys its walls and spreads in various directions reaching periosteum of the planum mastoideum and posterior wall of the external auditory meatus. Thickening and swelling of the structures and sometimes rupture of an abscess confirm the diagnosis of mastoiditis (Pig. 76). The tympanic membrane is thick and hyperaemic, and pus oozes through the perforation. Examination of patients with pronounced mastoiditis reveals a specifically outstanding auricle, swelling and hyperaemia of the skin behind the ear. Pressure applied to the mastoid process, or tapping on it, produces pain. X-ray examination of the temporal bone shows clouding of the mastoid aircells filled with pus and destruction of some bony partitions forming these cells. If the diagnosis of mastoiditis is verified or only suspected, the patient must be hospitalized for the final diag- nosis or emergency surgery to preclude severe complications. Treatment is surgical (mastoidectomy). After the postaural skin is incised, the cortical layer of the mastoid is removed, First the mastoid antrum is found, then the mastoid air-cells are opened (Fig, 77).

Fig. 76- Mastoiditis. Possible extension of infection from the mastoid air-cells; 1—to the mastoid process; 2—into the antrum; 3—into the middle cranial fossa; 4-to the posterior wall of the auditory meatus; 5— under the sternocleidomastoid muscle

To preserve the hearing function, the posterior wall of the ear canal is left intact during operation, and the tympanic cavity is not opened because acute inflammation of the middle 55 ear is not related to considerable ossicular destruction. Acute otitis media in infants is characterized by specific features. It is seldom isolated and is practically always combined with abnormality of other organs and systems (rickets, pneumonia, acute respiratory diseases, frequent belching associated with the danger of food getting into the middle ear through a wide auditory tube). It is difficult to diagnose acute otitis media in infants, since history findings are absent. Observation of the child is decisive: the baby may cry when sucking his mother, but remain silent when fed from a spoon. Otoscopic findings are not trustworthy. When the baby cries, the eardrum may become hyperaemic in the absence of inflammation, and, vice versa, the eardrum may be dull and grey in acute inflammation of the middle ear. Pressure applied to the tragus may produce pain in a baby with acute otitis media, since the auditory meatus (which lacks the bone portion) is short, and pressure is actually applied to the inflamed tympanic membrane. Infants

Fig. 77- The cavity in the mastoid process after removal of pathologic tissues (the avails of the cavity are smoothed out; the mastoid air-cells are removed) with acute otitis media lie on the affected side, stretch hand out to reach the sick ear, and rub against the pillow. Since the mastoid process in infants is underdeveloped-and only the mastoid antrum is present, the condition during which the antral walls are destroyed is called arttritis, and the operation for this condition is known as antrotomy.

Chronic Diseases of the Middle Ear CHRONIC SUPPURATIVE OTITIS MEDIA

Chronic suppurative otitis media is a rather widespread disease that leads not only to hearing loss, and impairment of the vestibular function of the inner ear, but also to severe life-threatening complications. Among the characteristic signs of chronic otitis media are persistent tympanic perforation, constant or recurrent purulent ear discharge, and disturbed hearing. Chronic otitis may be considered an equilibrium between the forces of reparation and destruction, ie., 56 the body cannot manage the infection, while the infection is unable to activate inflammation. This means that the regenerative mechanisms in the focus of inflammation are upset, and the tissue destruction cannot be compensated. Concomitant diseases such as diabetes mellitus, vitamin C-, D-, and B-dificiency, upset metabolism, poor living conditions, and untimely and inadequate medical aid in patients with acute otitis media contribute to the development of chronic otitis media. Microflora of patients with chronic inflammation of the middle ear is diverse and variable. Pathology of the nasal cavity, nasopharynx, and paranasal sinuses maintains chronic con- dition in the middle car. Adenoids, which disturb drainage and ventilation of the eustachian tube, are revealed most frequently. Morphological changes in the mucosa include epithelial destruction, necrosis and fibrosis of the mucous membrane, presence of vasculites, infiltrations, granulations, and polyps. Clinically, two major forms of chronic otitis media are distinguished: mesotympanitis (chronic inflammation affects only the mucosa of the middle ear) and epitympanitis (mucosal changes concur with inflammation of the bony walls of the middle ear and the auditory ossicles).

MESOTYMPANITIS

Hearing loss and permanent or recurrent otorrhoea are typical for mesotympanitis. Otoscopy. Tympanic perforation varies in size, but does not involve the margin (annulus) of the eardrum. Perforation occupies some area of pars tensa of the eardrum. The mucosa visible through the perforation is hyperaemic, thick and covered by a large layer of viscid mucopurulent discharge (Fig. 78).

Fig. 78. Tympanic perforation in mesotympanitis 1—niche uf the round window; 2—the edge of perforation; 3—annulus

X-ray shows consolidation of the mastoid bone (without signs of destruction). Flora: Streptococcus, Proteus, and Pseudomonas aeruginosa. Treatment is in most cases conservative and aimed to arrest otorrhoea. Surgical closure 57 of perforation is required in cases of stable remission. Treatment always begins with revision of the nasal cavity and nasopharynx, and if abnormality is detected, they are subjected to sanation. The latter consists in inflation of the eustachian tube anae mization of mucosa of the nasal cavity and mouths of the auditory tubes, removal of ear discharge by suction or wiping with cottonwool, and instillation of ear- drops that inhibit bacteria, stimulate epithelization, consolidate mucosa, and reduce secre- tion. For this purpose, antibiotic solutions, a 3 per cent boric acid and 1 per cent salicylic acid alcohol solutions, 1 per cent dioxydine solution are employed. Powders containing antibiotics or other antimicrobial drugs are blown. Instillation of eardrops demands the removal of pus, drying the ear canal and tympanic cavity in order to facilitate the contact of mucosa with the drug. Eardrops are instilled in a patient lying on the uninvolved side. Drops should be warmed to body temperature and instilled (5 drops) in the ear canal. After that the pressure should be applied to the tragus to promote penetration of drops beneath the perforation, into the eustachian tube, and other parts of the middle ear. Antibiotics should be used only after the sensitivity of flora to a particular antibiotic has been determined. Vitamins A and C are widely used, Mesotympanitis may last for years and sometimes decades. Injections of antibiotics are indicated to patients with exacerbations provoked by penetration of water into the ear, by cooling, or influenza. Mesotympanitis normally does not lead to complications.

EPITYMPANITIS

Complaints. The patient usually complains of severe hearing loss, purulent foul- smelling (sometimes blood-tinged) ear discharge, headache in the temple, and vertigo when the ear is cleaned. Otoscopy demonstrates the accumulation of thick, greenish-yellow pus with offensive odour that occasionally is mixed with cholesteatoma masses. Perforation is found in pars flaccida, and is marginal (the perforation involves the margin of the eardrum to which the affected pan of the tympanic membrane belongs). Bone destruction of the upperportion of the tympanic cavity, epitympanic recess (attic), may be revealed. In the majority of cases, the perforation may involve. Tympanic a portion of pars tensa. Granulation tissue, polyps and opalescent cholesteatoma masses may also be observed (Fig. 79).

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Fig. 79. Tympanic perforation in epitympanitis 1—the margin of the tympanic membrane (annulus); 2—the edge of perforation; 3 – granulations; 4—damanged lateral wall of the attic

When the bone is destroyed in the horizontal (lateral) semicircular canal (its ampulla is near the entry to the mastoid antrum), pus contacts the wall of the exposed membranous labyrinth. The patient may then develop dizziness, vomiting, or may even fall at the moment the pus is removed, which indicates destruction of bony walls of the inner ear. X-ray may reveal foci of destruction of the temporal bone. Bone destruction of the middle and inner ear develops due to caries and the effect of cholesteatoma. Cholesteatoma is a tumour-like mass that forms in the middle ear in the presence of chronic destructive con- dition, which is typical for epitympanitis. Cholesteatoma grows slowly and eccentrically. While growing, it damages the surrounding tissues; compact bone of the ear labyrinth may also be affected. Cholesteatoma is composed of epidermal masses of which cholesterol is the basis and covered by a strong membrane. Cholesteatoma serves as an indication for surgery. Treatment may be conservative, but surgery should be preferred. The latter is used to provide sanation of purulent focus in the middle ear and prevent complications. Treatment includes removal of purulent secretion and necrotic masses from the middle ear to reduce and then arrest otorrhoea. This is accomplished by irrigation of the middle ear through a special cannula with solutions of enzymes (chymopsin, chymotrypsin), antibiotics, add boric acid alcohol solution (Fig. 80),

Fig. 80, Irrigation of epitympanum through perforation

59 1—attic cannula

Polyps and granulations growing into the external audilory canal through the perforation are removed under local anaesthesia by special tiny forceps and wire snares. The operation for epitympanitis is called radical mastoidectomy and is aimed at removing pathologic mucosa and bone of the middle ear and at creating in the mastoid process of a common cavity formed by the external auditory canal, tympanic cavity, and mastoid cavity after scraping out of the mastoid air-cells. Radical operation and destructive changes in the sound-conducting apparatus considerably impair hearing. Therefore plastic surgery known as tympanoplasty is also performed along with sanation. It’s aim is to restore sound conduction in the middle ear by creating an artificial tympanic membrane and sometimes an artificial ossicular chain. Depending on the extent of destruction of the conduction system in the middle ear, various types of tympanoplasty are employed. The flap for an artificial tympanic membrane is fashioned from the fascia of the temporalis muscle, the perichondrium, and other tissues. If epitynipanitis is diagnosed in the early stage, bone destruction is insignificant, and the hearing function is almost normal sparing surgery is resorted to: the operation is done through the endaural incision (modified radical operation) using the operating microscope.

Otogenic Complications

Otogenic intracranial complications are severe diseases whose outcome may be quite serious. Spread of infection into the cranial cavity is due to destruction of the bony walls separating the cranial cavity from the middle ear. Mastoiditis and chronic suppurative epitympanitis are the major causes of complications, e.g., otogenic meningitis, sub- and epidural ahscesses, cerebral and cerebellum abscesses, or sepsis.

OTOGENIC MENINGITIS

Through the destroyed tegmen tympani and the mastoid antrum infection spreads into the cranial cavity. Severity of symptoms depends on involvement of the meninges. The most characteristic signs of otogenic meningitis are as follows. 60 (1) violent diffuse headache in the presence of chronic otitis or its exacerbation; (2) projective vomiting as a result of increased intracranial pressure without preceding nausea; (3) positive sign of neck muscle rigidity (stiff neck); the patient is unable to reach the manubrium sterni with the chin. If an attempt is made by a doctor to forcibly bend the patient's head to the chest, the muscles of the neck become strained, and the patient's head raises together with the trunk; (4) the characteristic patient's position in bed is on the side with the head tilted back; legs are flexed in the knee-hip joints; hands are held between the legs; (5) positive Kernig's sign: the thigh of a supine patient is flexed in the knee-hip joint; then the patienttries to extend the leg, which proves difficult; (6) positive Brudzinski’s sign (neck sign): rigidity of the neck muscles is checked in a supine patient. As the head is raised, involuntary knee flexion occurs; (7) examination of the cerebrospinal fluid and technique of lumbar puncture: a special needle provided with a mandrin is used to puncture meninges between the third and fourth lumbar vertebrae to get into the spinal canal of an adult that lodges at a depth of 4-4.5 cm. After the mandrin has been removed, cerebrospinal fluid begins oozing through the lumen. The normal rate is 60 drops per minute. Higher rate or flow of the cerebrospinal fluid indicates elevated intracranial pressure. In the majority of cases the fluid of a meningitis patient is cloudy. Leucocytosis, increased amount of protein and chlorides indicate inflammation of the cerebrospinal fluid. Treatment includes emergency surgery with revision of the walls separating the middle ear from the cranial cavity, sanation of the purulent focus in the ear; administration of massive doses of antibiotics and detoxicating preparations: rheopolyghicin, haemodez, vitamins, and hyposensitizing drugs. If meningitis develops in the presence of mastoiditis, vast mastoidectomy is performed. Chronic otitis media is managed by radical operation on the middle ear.

CEREBRAL ACSCESS

Cerebral abscess is one of the most severe complications of suppurative otitis media. Otogenic cerebral abscesses make up about 70 per cent of all cases with cerebral abscess. Epityrnpanitis causes abscesses of the brain and cerebellum in 70 per cent of cases. Males aged from 20 to 50 are commonly afflicted- Mortality rate is as high as 50 per cent. Inflammation propagates due to destruction of the bony walls separating the middle ear from 61 the middle and posterior cranial fossae. Haematogenic route of infection spreading into the white matter of the brain is also possible. Flora is diverse: streptococcus, Proteus, Escherichia cali, and Paeudomonas aeruginosa. Stages of the disease may develop as a result of response of cerebral vessels affected by this pathogenic flora which leads to the destruction of their walls. Thrombosis and ischaemia later occur in the brain, which leads to further tissue destruction, necrosis, and suppuration. A cavity of various size and shape (from oval to triangular) forms. Cerebral abscess may develop at a depth of 0.5 to 6 cm. Foul-smelling pus that fills the cavity may. be thick, dirty-brown or yellowish-green. More frequently abscess occurs in the temporal lobe of the brain or the cerebellar hemispheres. The diagnosis of cerebral abscess presents difficulty since early stages of the disease are manifested by symptoms simulating those of chronic suppurative otitis media or mastoiditis. Symptoms. Violent headache of various localization intensifying in movements of the head, projectile vomiting without preceding nausea and unassociated with food intake. The patient's general condition is severe, skin is pale, sometimes with an earthy hue; the face expresses suffering. Bradycardia is frequent, body temperature may elevatc, but usually it is normal. Red blood is unchanged, the white blood is characterized by leucocytosis. The patient may be irritable, or on the contrary, indifferent. Insomnia, bulimia (excessive appetite) or anorexia (lack of appetite) may concur. The tongue is dry and furred. Fundus oculi is marked by congestion, more frequent on the affected side. Focal symptoms are related to the involved left temporal lobe in the right-handers. Amnesic aphasia develops: the patient cannot name familiar objects. For instance, if a person is shown a pen and asked to name it, the answer will be: ‘‘it means... to write,- something to write with...’’. Sometimes, the counting and writing ability is affected. In patients with deeply-extended abscesses of the temporal lobe complete aphasia occurs; the patient can neither name the object nor pronounce the word designating it. Euphoria may be secondary to oedema of the frontal lobe of the brain. Reflexes of Babinski, Gordon and Oppenheim are positive. Bradycardia (45-50 beats per minute) may be a suggesting symptom. Localization of an abscess in the right temporal lobe is less demonstrative. Today, computed tomography is of great help to diagnose cerebral abscesses. Lumbar puncture indicates high intracranial pressure; other findings are inconstant. Violent headache, usually in the beck of the head, asynergia, and ataxia are characteristic of the cerebellar abscess, Adiudochokinesia on the affected side, a pronounced nystagmus towards the involved side, and deviation of the patient's finger on the side of the lesion are noted. 62 Treatment, Surgery includes sanation of the purulent focus to the middle ear (mastoidotomy or radical operation), opening of the posterior and middle cranial fossae, and puncture of the brain matter to reveal the abscesses. When the abscess is found, it should be incised, evacuated, and drained. Cooperation with neuropathologists, neurosurgeons, and therapeutists is necessary during active general therapy. The prognosis of the disease is doubtful.

OTOGENIC SEPSIS

The term sepsis (Gk sepsis putrefaclion) was proposed by Aristotle in thu fourth century B-C. to designate a disease associated with tissue damage (wound or puerperal fever) resulting in poisoning of blood. Till today, the problem of sepsis remains highly urgent in many brandies of medicine including otorhinolaryngology and stomatology. Sulphanilamides and antibiotics considerably reduced mortality from sepsis; nevertheless, sepsis of various aetiology (ologenic, oral, and others) presents a great problem. There is no specific pathogen of sepsis: strepto- and staphylococcus and Escherichia coli are found in cultures. Sepsis is a systemic infectious disease in which the patient specifically responds to permanent or recurrent presence of various microorganisms, or their toxins, in the blood. The infection is not accompanied by any specific conditions in the portae of infection or in the entire macro-organisim. Therefore, a local purulent lesion is present which, permanently or recurrently, releases microorganisms or their toxic metabolites (toxins) into the circulat- ing blood. Frequently, phlegmonous and necrotic conditions develop in the area of the infection portae. Otogenic sepsis is secondary to a suppurative condition in the middle ear, which is accompanied by erosion of the sigmoid sinus wall. First, periphlebitis and then sinus phlebitis (inflammation of a cerebral sinus) develops in the presence of which a parietal thrombus is formed from the local lesion of the inner endothelial layer of the wall. Next, the occluding thrombus is formed, which may fill not only the sigmoid sinus, but spread over the jugular vein. Suppurated thrombus releases microorganisms and their toxins into the venous blood stream, and the clinical picture of sepsis develops. Two forms of sepsis,

63 septicaemia and septicopyemia, are distinguished. In the latter case purulent metastases in tlie distant organs occur. Clinical picture consists of general and local symptoms. If a chill lasting from 15 to 45 minutes occurs, the temperature curve changes (the circadian variation 4-5 0C), and profuse perspiration appears, possible otogenic sepsis may be suspected in a patient with mastoiditis or chronic suppurative epitympanitis. The skin is often pale and looks as 'gooseflesh'; later it becomes yellowish. Sepsis is characterized by disintegration of erythrocytes, inhibited activity of the bone marrow, pronounced leucocytosis, and metastases. Infected microemboli are carried by blood: from the jugular vein to the superior vena cava, right atrium and right ventricle, and finally through the pulmonary artery to arterioles where they settle and promote the formation of abscesses. If the emboli bypass the lesser circulation, they may accumulate) in any organ (kidneys, joints, skin) also forming abscesses. Treatment. Symptoms of sepsis serve as indications for urgent surgery on the middle ear (mastoidotomy or radical operation with formation of a common cavity), sigmoid sinus, and sometimes on jugular vein to remove the suppurative thrombus. Massive antibacterial and detoxicating therapy are administered.

LABYRINTHITIS

Inflammation of the inner ear is called labyrinthitis. Infection invades the inner ear via the walls of the .semicircular canal a destroyed by caries or cholesteatoma. The ampulla of the lateral (horizontal) semicircular canal, which is the nearest to the cellular system of the mastoid (where destruction develops), is damaged more frequently. Labyrinthitis may be circumscribed and diffuse, serous and suppurative. Vertigo, which the patient experiences at rest or in motion, unsteady gait, fits of nausea and vomiting are typical. Circumscribed labyrinthitis is characterized by a fistula symptom: when the ear is cleaned from pus, the patient suddenly becomes dizzy with the head tilted sideways. Such patients have a lesion in the bony wall of the lateral semicircular canal: a slight pressure applied to the external auditory canal displaces the perilymph and stimulates the receptors of the semicircular canal. The patient with diffuse labyrinthitis experiences violent vertigo that may last for several hours and is accompanied by exhausting vomiting. Suppurative labyrinthitis may result in complete destruction of receptors of the vestibular and auditory analysers, i.e., areflexia of the involved side and total hearing loss occur. Clinical picture. The patient with suppurative acute or chronic otitis media develops

64 vertigo and unsteady gait. Objective symptoms: (1) spontaneous nystagmus is at first towards the involved ear (later, after suppression or death of the receptors, nystagmus changes to the opposite side and its rapid component is towards the healthy ear); (2) during a finger-nose test the patient's both fingers deviate to the side of the slow component, i.e., to the healthy ear; (3) in the Romberg test the patienl. shows a tendency to fall to the side of the good ear. Labyrinthitis is differentiated from the abscess of cerebellum. Treatment. Operation on the middle ear for sanation of a purulenl focus is indicated- Massive antiinflammatory (antibiotics, sulphanilamides) and dehydration therapy are required. Below is given the scheme of vestibulometry, 1. Character of vertigo 2. Spontaneous nystagmus ( + ), (—). Its characteristics 3. Spontaneous deviation of bands 4. Finger-nose test 5. Finger-to-finger test 6. Romberg's sign 7. Test for adiadochokinesia 8. Direct walking 9. Sideways walking 10. Caloric test 11. Rotation test 12. Fistula test

PARESIS AND PARALYSIS OF THE FACIAL NERVE

Facial paralysis may occur due to pathological condition of the middle ear (acute and chronic otitis or a tumour) and of the internal auditory meatus (acoustic neurinoma). The facial nerve may be paralysed outside The cranial cavity, us it passes near the parotid gland, and may respond to compression by the tumour or cicatrices in this area. These paralyses are referred to as peripheral. Central paralysis developing due to impairment of the facial nuclei also occurs. Clinical picture depends on a particular portion of the facial nerve involved: the nerve gives off branches to innervate the lacrimal gland, stapedius muscle, mimic muscles of the 65 face, submaxillary and sublingual glands responsible for the sense of taste in the anterior two thirds of the tongue. Examination of these organs reveals the site of compression or disruption of the nerve trunk: it can be inside the canal or outside the stylomastoid foramen. Damage to the facial nerve within the internal auditory meatus (in fractures of the skull base and acoustic neurinoma). The symptoms: (1) paralysis of the three branches of the facial nerve—a dropped angle of a mouth, a smoothed nasolabial fold, and inability to frown on the involved side; (2) dry eye due to the absence of tears (dysfunction of the lacrimal gland); (3) impaired perception of sweet, salt, and sour in the anterior two thirds of the corresponding side of the tongue; (4) hyperacusia —auditory hyperesthesia on the involved side provided the organ of hearing is not involved. This is associated with the fact that stapedius muscle does not function and does not oppose the tensor tympani muscle; under the influence of sounds the stapes is pressed into the oval window more abruptly to push the perilymph. Damage to the facial nerve canal in its horizontal portion (labyrinthine wall of the tympanic cavity) from the genu of the facial nerve to the level where the stapedius muscle nerve branches off, and in the descending vertical portion of tho facial nerve (the mastoid wall of the tympanic cavity) before branching off chorda tympani. All above-mentioned signs are present except dry eye on the involved side; the patient complains of excess tearing: innervation of the lacrimal gland is unaffected, but due to impossibility to close the eye, sucking action of the lacrimal sac weakens, and the tear does not enter the nasolacrimal duct. Damage to the facial nerve outside the stylomastoid foramen (the level of the parotid gland). One or all branches of the facial nerve are damaged, which leads to inability to frown, or close the eye; the mouth angle drops, the nasolabial fold smoothes down. Taste is not impaired, and hyperacusia is absent. Central facial paralysis. Its specific feature is the preserved ability to frown on the involved side, since the superior branch of the facial nerve receives impulses and is connected not only with the nucleus of its side, but also with the opposite nucleus: nuclear abnormality evokes all symptoms of paralysis except inability to frown on the affected side. Depending upon the side of lesion of the facial nerve, the underlying cause may be suspected and therapy chosen. Treatment includes either emergency surgery on the middle ear during inflammation, or decompression of the facial nerve in idiopathic paralysis (of obscure aetiology), or a conservative treatment using dehydration or antiinflammatory therapy, and also surgery on the parotid gland.

66 Non-Suppurative Diseases of the Middle and Inner Ear TYMPANOSCLEROSIS. ADHESIVE OTITIS

Side-effects of chronic suppurative otitis media include fibrosis in all parts of the middle ear, which leads to hearing disorders, The ossicles are immobilized by fibrous tissue, or the elements of conduction chain are destroyed (tympanic perforation, destruction of the stapes and malleus). Such postinflammatory changes in the middle called tympanosclerosis and adhesive otitis, complaint is reduced hearing. Audiogram reveals conductive loss: bone conduction curve is normal, while the air conduction curve is 30-50 decibels below the normal level. Conservators treatment of adhesive otitis is less elective (politzerization, ear catheterization, pneumomassage of the tightly-mobile eardrum through the external auditory canal, and drugs softening the fibrous tissue, e,g, lydase). Surgery inclines mobilization of the ossicular chain by the 'swinging’ method, replacement of the auditory ossicles (immobilized by fibrous tissue) by alloprostheses, restoration of integrity of the tympanic membrane (tympanoplasty) and stapedoplasty.

OTOSCLEROSIS

A considerable part of the world population suffers from this disease whose aetiology is unknown. Otosclerosis causes stable hearing loss and deafness; young women are mostly affected. Hearing loss develops at the age of 20-26; pregnecy, childbirth, and lactation evoke hearing loss or intensify it. Otosclerosis may be hereditary or familial disease. Hearing loss may bilateral and practically symmetrical. Otosclerosis has nothing in common with sclerosis in the pathoanatomic sense. By the reason now unknown, spongy bone grows by the edges of the oval window niche. This spongy tissue first interferes

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Fig. 81- Audiograms a—norm; b—pathology: 1 - otosclerosis; 2 - neuritis of the acoustic nerves

with free movement of the stapes and later arrests it completely. The spongy growth strengthens with time and the stapes can no longer transmit, sound oscillation to the inner ear. Deafness thus develops. Symptoms. Bilateral hearing loss, tinnitus, roaring, whistling, or other sounds in

68 the ear. The patient usually hears better in noisy environment. The disease occurs in the young age and gradually progresses. Otoscopy. There is no earwax in the auditory meatus, its skin is thin, the tympanic membrane is usually normal except somewhat thin. Audiograms demonstrate conductive hearing loss (Fig. 81). Treatment. Surgery includes various types of stapedoplasty: the stapes is replaced by a teflon or cartilaginous prosthesis, and ossicular chain mobility is thus restored

Fig. 82. Stapedoplasty 1—dissection of the stapedial crura; 2—removal of the stapedial crura; 3—a hole is drilled in the footplate; 4—teflon prosthesis; 5—a sfit is clone in the head of the prosthesis;

6—the head of the prosthesis is attached to the long crus of the incush and the piston is inserted into the hole (ossicular chain mobility is restored)

(Fig. 82). Today, stable hearing improvement is attained in 95 to 98 per cent of patients with otosclerosis following stapedoplasty.

MENIERE'S DISEASE

Functional disturbance of the inner ear unassociated with inflammation in the middle and inner ear is diagnosed today by physicians of various specialities. This vestibular affection may be due to various pathologies in the inner ear, e.g., haemorrhage, hydrops, vascular spasm, mainly of the . The main symptoms of this abnormality are paroxysmal vertigo, nausea, vomiting, and unsteady gait. In 1861 P. Meniere was the first to describe the clinical picture of a disease accompanied by a severe vertigo. Clinical picture. A person in complete health experiences suddenly severe vertigo and may fall being unable to maintain equilibrium. Nausea and later vomiting accompany this condition. Occasionally, before the fit, the patient feels tinnitus and unilateral blocked ear. A fit lasts from few minutes to an hour and longer. Usually, each next fit resembles the previous one. Nystagmus towards the good ear is noted. The patient's condition between the

69 fits is quite satisfactory except for the remaining tinnitus and progressive unilateral hearing loss following each fit. A fit may be provoked by an acute respiratory disease, overstrain, rise or fall in arterial pressure. Treatment. During the fit the patient must be placed in bed and annoying factors (bright light, noise) removed. To terminate vegetative reactions (nausea and vomiting), 1 ml of a 1 per cent atropine solution should be injected, and 1 ml of a 2 per cent novocaine solution administered in the anterior end of the inferior nasal concha. The drugs that decrease permeability of the vascular wall (pipolphen, dimedrol, calcium chloride) are given. Liquid intake is limited. Severe cases (status meniericus) should be treated surgically between the fits: vestibulocochlear nerve should be transected and endolymphatic sac drained.

NEURITIS OF THE ACOUSTIC NERVE

Damage to the perception apparatus of the ear including its cochlear receptors, and also conduction pathways and the central organ, is called neuritis of the acoustic nerve though inflammation is absent. Progress in industry, traffic, intense noise and vibration, the use of various chemicals in industry, agriculture and everyday's life entail greater incidence of diseases of the receptor apparatus and central nervous system. A number of complications due to viral infections such as influenza, parotitis, meningococcal meningitis, which cause stable hearing loss and even deafness, has drastically increased. Some toxic drugs, as well as cranial injuries, may cause hearing loss too (the type of neuritis of the acoustic nerve). The dentist must know the drugs used in dentistry that may provoke hearing loss and deafness, first of all, aminoglycosides (streptomycin, gentamicin, kanamycin, monomycin, and neomycin). This group of antibiotics is especially important since they can cause a sudden and irreversible hearing loss that may transform into deafness. Hearing loss progresses even after discontinuation of the drug. Besides, it may combine with vestibular damage It is reported, for instance, that streptomycin sulfate damages mainly the organ of equilibrium, while dihydrostreptomycin sulfate has a toxic effect upon the organ of hearing. Neomycin is the most toxic to the acoustic nerve. Ototoxic antibiotics accumulated by fluids of the inner ear cause degeneration of the hair cells of the organ of corti and damage the acoustic nerve fibres. The data on antibiotic ototoxicity are given in Table 2. TABLE 2. Antibiotic Ototoxicity

70

The following rules of prescribing these antibiotics must be followed by every physician: (1) strict indications; (2) accurate dosage (single, daily and course doses); (3) discontinuation of the antibiotics in patients with upset renal excretory function; (4) obligatory control of renal function; (5) contraindications for patients with hearing loss due to the inner ear pathology; (6) consideration of incompatibility of some ototoxic antibiotics since it leads to potentiation; (7) the patient must report the first symptorns of intoxication (tinnitus, hearing loss, vertigo); (8) contraindications for pregnant women in the first half of pregnancy to avoid the action of antibiotics on the foetal inner ear; (9) symptoms of ototoxicity include uni- or bilateral hearing loss, permanent and exhausting high-pitch tinnitus. The patient's history does not always state the underlying cause of hearing loss except for the trauma or preceding disease, or medication (antibiotics and diuretics). Sometimes, deafness may occur suddenly accompanied by pronounced vertigo. In cases of acute hearing loss the patient must be urgently hospitalized where timely aid may be effective. Otoscopy does not reveal any changes of the tympanic membrane which looks normal. Tuning fork tests and audiometry are decisive. An example of a record made during a hearing test in a patient with unilateral neuritis of the acoustic nerve is presented below.

71

Treatment is not effective; hearing can only be improved in treated cases where the degeneration of the cochlear receptors is absent. Drugs that stimulate transmission of nerve impulses in synapses (anticholinesterase preparations; nivalin, galanthamin, proserin, dibazol) should be given in combination with vitamins B (Bl, B6), adenosine triphosphoric acid (ATP), cocarboxylase, apilac, and others. If it is impossible to correct hearing loss caused by damage to conduction or perception apparatus, hearing aids amplifying sound or improving its conduction are required.

Diseases of the Nose Diseases of the External Nose

Developmental anomalies are commonly encountered in combination with deformities of the adjacent regions, particularly, the maxilo-dental system. Thus, a congenital cleft of the hard and soft palate (a wide-spread congenital malformation), which is associated with harelip, is accompanied by nasal deformity. The latter is rnore pronounced in patients with a

72 lateral fissure when the nostril on the affected side is more wide, and the external nose is asymmetric. Asymmetry of the nasal cavity is associated with a markedly deviated nasal septum, especially in its anterior portion. Such anomalies should be treated surgically in early childhood by cheilo-uranoplasty that repairs cleftpatate, corrects harelip, and forms the right shape of the nostril. This also prevents possible complications which may occur in the nasal cavity, paranasal sinuses, and middle ear. The older the child, the worse are the cosmetic and physiologic effects of cheilo-uranoplasty. Frostbite. The skin of the nose reacts to cold as follows: erythema (first degree), formation of bullae and crusts (second degree), and gangrene (third degree). In patients with superficial (first-degree) frostbite, an abrupt pallor of skin is the result of persistent vascular spasm in the tip and alae of the nose. The sensitivity may be impaired, mid a person does not feel any discomfort. Marked redness and swelling of the aose tip are manifest later; then comes tching and pain. In a second-degree frostbite, the skin becomes bluish-red, then bullae are formed with subsequent bursting and formation of crusts. When crusts fall off, the affected area undergoes epidermization. The third-degree frostbite is the most severe and rare. Tissues mummify and may separate when touched. Treatment. First aid includes gradual warming of the frostbitten site which is massaged with a soft cloth; compresses are applied later. Manipulations should be sparing to prevent damage to epidermis and infection. After bullae open and crusts are removed, ointment dressings should be applied to facilitate epidermization and to prevent infection, Rhinophyma. Tumour-like outgrowths of the skin composed of hypertrophied connective tissue, blood vessels, and sebaceous glands form on the tip of the nose and the alae. Rhinophyma disfigures the patient's face and can impede nasal breathing due to marked nodular swelling. Rhinophyma is encountered in elderly males. Treatment requires . Furuncle is a pustular lesion of the hair follicle, which is caused by staphylococci. Though a furuncle forms in the vestibule of the nose, its manifestations are well seen on the external nose. Reddening of the alar outer surface is followed by formation in the nose vestibule of a bright-red cone-shaped elevation mounting on swollen adjacent tissues. The furuncle breaks spontaneously in 3 to 4 days to release thick pus. A crater is formed in the wing of the nose due to the necrotlzation of tissues surrounding the hair follicle. Ripening of the furuncle is attended by painful tension in the ala and nose tip tissues. Treatment is conservative only (!). Squeezing or surgical incising of the furuncle is 73 forbidden because clots of pus can pass via the veins into the cranial cavity and the cavernous sinus to evoke sepsis. The treatment consists in application of ointment to the exlernal nose, or packing the nasal vestibule (near the furuncle) with gauze turundas impregnated with ointment. Broad-spectrum antibiotics (penicillin, oletetrin, and laevomy- cetin), and physiotherapeutic procedures (UHF- and ultraviolet therapy) are necessary. A 3 per cent ammoniated mercury ointment, synthomycin emulsion, and ichthyol ointment are effective. Severe cases must be hospitalized to follow up the patient and prevent com- plications.

Diseases of the Nasal Cavity

Deviation of the nasal septum. It has already been mentioned that the nasal cavity is divided by the septum into two usually asymmetric parts, the nasal fossae. The asymmetry is associated with the fact that in the majority of cases, particularly in males, the septum may deviate to either side and have projections in the form of spurs or ridges, which considerably narrow the common nasal meatus and cause nasal obstruction. Deviation of the septum is usually insignificant, and surgical correction is required only when nasal breathing through one or both nostrils is impeded. The nasal septum is normally straight, at birth and is believed to deviate during the growth of the facial bones or due to some exogenous factors (injury, pressure by a hypertrophied nasal concha, or a tumour, etc.). Septal deviation can be different: the septum may be entirely deformed and impinge on the nasal concha; it may be S-shaped, or deformed only in its cartilaginous or bony part. The most typical symptoms that may be caused by a deviated septum are as follows: unilateral nasal obstruction, persistent nasal discharge, impaired olfaction, sometimes nasal twang. The diagnosis is made by anterior rhinoscopy during which the septal deviation, narrowing of one nasal half and widening of the other is easily visualized. The deformity of the nasal septum may be a permanent concomitant sign of the cleft palate. Treatment. Indications for surgery are as follows: (1) impeded or absent nasal breathing on one side; (2) infeasibility of such sanative manipulations in the nasal cavity as polypectomy, ear catheterization, or opening of the maxillary antrum through the nose. Submucous resection is an operation for surgical correction of septal deformity. The surgery is performed under local anaesthesia. After an incision is made through the mucoperichondrium (on one side of the septum only) the latter is elevated over the entire surface of the cartilaginous part of the septum. Then the septal cartilage is cut through in the 74 line of the first incision; and the mucoperichondrium is elevated on the opposite side. The deviated part of the septal cartilage or a perpendicular plate is removed, and a mobile cartilage-free septum is positioned in the midline. The wound surfaces of both mucoperichondrial flaps are placed together and held by nasal packs impregnated with oil. A successful operation restores nasal breathing. Haematoma and septal abscess. These conditions develop after external injury and are sometimes accompanied by nasal fractures. Following blow to the nose, blood accu- mulates between the cartilage and the perichondrium to raise the mucoperichondrium on both sides of the septum. Impeded nasal breathing and nasal twang are among the symptoms of haematoma. The effused blood may suppurate and turn into an abscess in which case headache, fever, and chill concur. Treatment includes wide opening of haematoma, drainage, and anti-inflammatory drugs. To hold the elevated mucoperichondrial flaps to the cartilage, tight packing of the nose is necessary. An abscess, if any, is widely incised; the patient should be aware of possible sinking of dorsum of the nose due to destruction of the septal cartilage (if much time has elapsed since formation of the abscess). The pus must be evacuated, and antibiotics prescribed. The patient should be hospitalized.

Fig. 44. Compound fracture with injury to the skin

Nasal fractures. Fractures can be open, or compound, with injury to the skin (Fig. 44), and closed, or subcutaneous, with or without displacement of bone fragments. In addition to the nasal bones, the frontal maxillary processes can be damaged by a blow. External nose

75 deformity varies, depending on the direction of a blow (a hook or a frontal blow). Sometimes, the sloping side of the nose sinks on the side of the blow, in other cases the opposite slope is also displaced (Fig. 45); a frontal blow depresses the nasal bridge (flat nose). Depending on the patient's general condition and the type of fracture (compound or subcutaneons), the patient may be treated in out-patient conditions or hospitalized.

Fig. 45. Nasal fracture resulting from left hook

To determine the type of fracture, the external nose is examined, the nasal bridge and the slopes are palpated, and the anterior rhinoscopy is performed. Lateral x-ray is obligatory. In compound fractures, primary debridement of the wound is first done, and antitetanus serum is administered. The most optimum terms for the reposition of bone fragments are within five hours or in five days after injury because marked oedema of the surrounding soft tissues develops to hinder repositioning of bone fragments. Before the reposition, local anaesthesia is obtained by a subcutaneous injection at the nose root of 2 ml of a 2 per cent novocaine or trimecaine solution, or by a nasal mucosa spraying or application with a 10 per cent cocaine solution (Fig. 46). Repositioning of the bone fragments is done on a lying patient. Kocher's forceps in a rubber tubing (to avoid additional damage to the soft tissues of the nasal cavity) inserted into the common nasal meatus is used for the purpose. Special instruments, elevators, whose curvature follows that of the nose are also employed (Fig. 47a). Outstanding portions of the lateral wall of the nose are repositioned by thumb pressure, while the fingers hold the patient's face (Fig. 476). The replaced bone fragments are held in place by tight packing.

76

Fig. 46. Local anaesthesia of the external nose during repositioning of bone fragments

Nosebleed. A physician of any speciality can encounter nasal bleeding. Light or copious hleeding may be due to general or local causes. Bleeding may be recurrent, it can arise spontaneously or due to objective causes. Atherosclerosis, crises of essential hypertension, and some systemic diseases associated with congenital or acquired abnormality of the blood coagulation or vessels are among common causes of profuse nosebleed. Not infrequently, nasal bleeding accompanies acute infectious diseases (e.g., influenza) attended by high body temperature in the presence of which vascular permeability increases, and blood coagulation in impaired, Nosebleed may be caused by some hereditary abnormality, e.g., Rendu-Osler-Weber disease. This condition is characterized by

Fig. 47. Repositioning of bone fragments (a) using an elevator to raise the collapsed nasal slope, (b) by applying thumb pressure to the bulging nasal slope a hereditary degeneration of arterial capillaries whose walls in some portions may consist of 77 endothelium alone. Flask-shaped dilatation of capillaries thus occurs (telangiectases). Since the vascular wall in these portions is highly vulnerable, even a alight physical strain or elevation of blood pressure (e.g., in bending the head or while blowing the nose) may induce abundant and persistent nasal bleeding. Some diseases, such as thrombocytopenic purpura or haemophilia, can cause debilitating nosebleed. Local causes are significant in tbe genesis of nosebleed. Injury to the nose and the nasal mucosa, its atrophy, and vascular neoplasms of the nasal cavity and nasopharynx are the most common causes of nosebleed. In about 80 per cent of cases nosebleed originates at Kiesselbac.h's plexus that lies in the anterior part of the nasal septum. Severe haemorrhage occurs from the posterior and superior parts of the nasal cavity supplied with large-diameter blood vessels. Correct control of bleeding saves the patient from marked blood loss and repeated painful manipulations in the nasal cavity and preserves health-depending on the site of bleeding, its severity, and the underlying cause certain manipulations are performed to arrest and prevent it; 1) Mild nosebleed from the anterior part of the septum is easily controlled by holding the wings of the nose tight to the septum for 15-20 minutes, 2) The source of mild bleeding can be easily located. If Kiesselbach's plexus bleeds, a cotton ball soaked in an adrenaline or ephedrine solution is inserted into the nasal vestibule and pressed against the septum by the wing of the nose, 3) If the bleeding vessel is seen during rhinoscopy, cauterization of this site is carried out after local anaesthesia using electric cautery, stiver nitrate, or cryocoagulation. Anterior nasal tamponade. Anterior tamponade is necessary in persistent nasal bleeding. It is accomplished as follows: (a) instruments needed: nasal speculum; bayonet forceps; a gauze ribbon tampon or a pneumatic rubber tampon; head mirror; (b) the patient is in a sitting position; (c) a doctor takes 40-50 cm long tampon with a bayonet forceps holding it 4-5 cm from the and of the strip. Packing begins from the floor of the nasal cavity in tight layers, one over the other. To prevent sinking of the ribbon's end into the nasopharynx, which can irritate pharyngeal mucosa and stimulate the vomiting reflex, the first layer must be placed so that the end is outside the patients's nostril. For this reason it is recommended to hold the gauze strip at a distance of 4-5 cm from, the end (Fig. 48). It should be remembered that anterior tamponade is efficacious if packing is sufficiently tight. The tampon is thug less hygroscopic and won't absorb blood. The pack may be left in for no longer than 48 hours. To 78 prevent injury to the nasal mucosa while with drawing the pack, it is expedient to impregnate it with liquid petrolatum.

Fig. 48. Anterior tamponade (the peck is tighlly placed in in layer the anterior parts of the nusal cavity) Fig. 49. Measuring out a pad of proper size

Posterior tamponade. This procedure is more complicated. It is used in patients with severe nasal bleeding due to the above-mentioned causes, and after some surgical mani- pulations in the nasal cavity and nasopharynx that are associated with considerable blood loss (e.g., surgical removal of neoplasms). The procedure includes several steps; 1) the volume of the patient's nasopharynx is measured in order to select the pad of proper size. The volume is usually compared with that of the first two phalanges of the patient's thumbs put together (Fig. 49); 2) the doctor checks the strings for strength and the tampon for elasticity; 3) a thin rubber catheter is passed through the inferior nasal meatus on the involved side (or both sides) until it can be seen in the patient's open mouth behind the soft palate; 4) of the catheter is taken by pincers and pulled to a distance of 4-5 cm; 5) two strings by which the tampon is tied up are tightly attached to this end of the catheter in such a way that their length is not less than 20 cm; the third string is fixed to the opposite end of the pack (to withdraw the tampon); 6) the catheter with the two strings is pulled back through the nose; threads shorter 79 than 20 cm are not long enough to fix another gauze roller in front of the nose;

Fig. 50. Posterior tamponade 1—rubber tubes are passed through both halves uf the nose and the oropharynx; 2— two strings by which the nasopharyngeal pad is tied up are attached lo the tubes; 3— nasopharyngeal pack is tightly lied up; 4 — the string for withdrawing the pad from the nasopharynx; 5—the pack is in front of the nose; 6—nasopharyngeal pad closes the choannae

(7) the tampon is then pulled out by the two strings into the nasopharynx using the left band. Simultaneously, the right index finger inserted above the soft palate helps to seat the pack and press it against the choanae (Fig. 50). The third string is fixed on the patient's cheek by the adhesive tape; (8) sometimes before fixing the roller in front of the nose, anterior tamponade is performed. In the majority of cases posterior packing stops epistaxis. The tampon can be left in the nasopharynx for no longer than 48 hours to prevent severe complications in the middle ear (spreading of infection through the auditory tube from the tampon soaked with blood which, in this case, serves as a culture medium for multiplication of pathogenic bacteria). The tampon is romoved from the nasopharynx by the free end of the third string. Before this manoeuvre, the gauze roller in front. of the nose is cut off. Ligation of the external carotid artery. Sometimes posterior tamponade fails to stop epistaxis, and the external carotid artery should then be ligated. The dentist must also be able to perform this serious surgical manipulation. The procedure should be done for special indications. The physician must know the topography of the site, location of the vessels, nerves, muscles, and fasciae. It should be emphasized that at the level of the superior border of the thyroid cartilage the common carotid artery divides into the external and internal carotid arteries (carotid bifurcation). It serves as a landmark for incision which begins approximately near the mastoid process where the sternocleidomastoid muscle is 80 attached. The head of the patient in a supine position is sharply turned in the opposite direction, which helps locate the border of the sternocleidomastoid muscle. The incision made along the anterior border of the muscle is 6-7 cm long. After the skin and fatty tissue are cut, the anterior border of the muscle (invested in the fascial sac to prevent its displacement) is found. The next incision, of the same length, is made along the fascial sheath of the anterior border of the muscle. Then the sternocleidomastoid muscle is hooked backward, and the inner flap of the sheath becomes visible. It is cut by the incision line and a large vessel, a jugular vein, is exposed. Its posterior displacement exposes two carotid arteries, the external one, lying deeper, and the internal, situated more superficially. Only the external carotid artery ramifies on the neck, which distinguishes it from the internal carotid artery. The external carotid artery is ligated above the point where the superior thyroid artery originates. Foreign bodies. Various foreign bodies, either occasionally inserted through the nostril or penetrating from tho adjacent areas, e.g., an ectopic tooth, can be present in the nasal cavity. Foreign bodies situated in the common or inferior nasal meatuses can maintain chronic inflammation and simulato severe systemic diseases. Leeches that stuck to the nasal mucosa can, for instance, cause persistent haemoptysis which may be misdiagnosed as tuberculous or associated with tumour. If small foreign bodies remain in the nose for a long time, they may turn into nasal calculi, rhinolitlis, due to the adsorption of mineral components of nasal secretion on their surface. They can also cause persistent purulent nasal discharge. The diagnosis of a foreign body is based on the findings of anterior and posterior rhinoscopy performed with dehaematizing agents for better observation of various parts of the nasal cavity. X-ray examination is useful. Living foreign bodies are removed by instilling a concentrated sodium chloride solution into the nasal cavity. Inanimate foreign bodies (after local anaesthesia) are extracted with special hooks to prevent pushing of the foreign body into tho nasopharynx from, where it can pass to the trachea.

ACUTE CATARRHAL RHINITIS.

Acute catarrhal rhinitis is the most common disease a person may repeatedly have during the lifetime. Acute rhinitis (otherwise known as coryza or common cold) may occur as an independent pathological condition of the nasal cavity, or as a syndrome attendant to chill or some infections. Though common cold had been known from time immemorial, 81 neither clinicians nor theorists can explain its pathogenesis. The exposure to cold of various body areas, sometimes quite distant from the nose, is known to cause acute rhinitis. Common cold is therefore believed to be connected with reflex mechanisms responsible for the reaction of nasal mucosa to cold. In the majority of cases acute rhinitis actually occurs immediately or shortly after cooling of feet or the lumbar region for back). Thus, cold is a triggering mechanism of catarrhal rhinitis. Cooling of the lumbar region causes a stubborn spasm of renal vessels, which can affect the daily diuresis. The nasal mucosa with its enormous capacity to produce secretion is supposed to partly stabilize the liquid balance in blood and tissues. This is a reflex: action, and as a result of congestive hyperaemia of the nasal mucosa, serous fluid, which is a transudate absolutely devoid of proteins begins secreting through the walls of superficial vessels. This is the first phase of acute rhinitis. Profuse watery secretion induces maceration of epithelium and causes formation of micronssures. The defence mechanisms (leucocytes, macrophages) come into action; serous nasal discharge becomes purulent. Thus, according to the clinical picture and morphology acute rhinitis is subdivided into three stages: 1) The onset is manifested by dryness in the nose, a burning sensation and fever, pain during inspiration and expiration; all these symptoms are preceded by chill, 2) The stage of secretion occurs within one or two hours after the onset and is characterised by stuffy nose, headache, copious watery secretion, sneezing, malaise, and mild fever, 3) The third stage develops within several days or a week. The nose is stuffed; the nasal discharge is thick and purulent; malaise and headache are typical complaints of the patient. Treatment. Stuffy nose and nasal discharge need no special treatment. The prescription of certain drugs should be grounded pathogenetically. For instance, vasoconstrictors (ephedrine, naphthyzine, and others) are not helpful during the second stage of the disease. Keeping the bed warm (bed regimen), diuretics (acetylsalicylic acid, furosemide) and counterattractive measures (hot foot baths, mustard plasters to the calves) are advisable. Drops with menthol oil are recommended to protect nasal mucosa from excessive irritation by discharge, passing air; in addition, they improve nasal breathing. Small doses of vasoconstrictors should be instilled infrequently, otherwise drug addiction may develop. During the third stage (the stage of intensive purulence) sulphanilamide powders can be inflated and ointments applied, hyposensitizing agents (dimedrol, suprastin, pipolphen) are also necessary. 82 Common cold must not be regarded as a mild disease because the nose, paranasal sinuses, or other bordering areas, and also the middle ear may be involved. Acute rhinitis ends in recovery or transition into subacute and then chronic form that differs qualitatively from acute catarrhal inflammation.

CHRONIC RHINITIS Chronic inflammation of the nasal mucosa is a common disease strongly affecting the respiratory, olfactory, defensive, and resonance functions. Prolonged nasal obstruction provides conditions for involvement of the throat, ear, and maxillodental system. Diseases secondary to the impeded nasal breathing can be cured only after the nose function is normalized. Several types of chronic rhinitis are distinguished: (1) catarrhal; (2) vasomotor; (3) hyperplastic (or hypertrophic); (4) atrophic; (5) ozaena. Each type has its specific features which help to make the differential diagnosis. Chronic catarrhal rhinitis. The symptoms include permanent or recurrent bilateral nasal stuffiness, especially when the patient lies on his side or back. Nasal obstruction is accompanied by copious nasal discharge. The patient complains of fatigue, headache, and dryness in the mouth. History. The disease is secondary to acute catarrhal rhinitis due to many causes (e,g., inadequate treatment, the presence of adenoids). The disease may last from several months to many years or even decades. Clinical picture. The patient’s general condition is satisfactory, the body temperature is normal. Uni- or bilateral nasal obstruction is noted. Anterior rhinoscopy reveals hyperaemic mucosa of the nasal conchae which are swollen due to marked submucous oedema and dilat- ed paretic blood vessels. The mucus, sometimes viscid, accumulates in common and inferior nasal meatuses. A recurrent obstruction of either side of the nose is a characteristic sign of chronic catarrhal rhinitis. As a rule, the patients take vasoconstrictors for a long time whose effect is only temporary. Diagnosis. To differentiate between simple and other types of chronic rhinitis (true hypertrophy) adrenaline test is performed. In patients with chronic catarrhal rhinitis, nasal conchae markedly shrink, nasal meatuses become wide, and respiration normalizes two or three minutes following painting of mucosa with adrenaline. 83 Treatment. If there are adenoids in the nasopharynx, adenoidectomy is first performed. Local therapy alone is used including ointments that dry nasal mucosa, diminish secretion, and facilitate shrinkage of the nasal conchae. Astringents (silver nitrate) such as protargol and collargol may be instilled. Cryocoagulation, or electrocautery, is sometimes indicated. Complications. Otitis media and sinusitis occur. Nasal obstruction facilitates dental caries and gingivitis due to drying of mucosa and upset enamel nutrition. Chronic vasomotor rhinitis. Two forms of vasomotor rhinitis are distinguished - allergic and neurovegetative. They have similar clinical picture characterized by paroxysmal course, persistant stuffiness of the nose during paroxysms, attacks of sneezing, and copious transparent watery discharge. Besides, most patients complain of deranged sleep, poor olfaction and appetite. The patients are irritable, and their working capacity is decreased. The allergic form is associated with inhalation of various allergens to which a person is sensitized. This hypersensitivity may be congenital or acquired, sometimes induced by occupational factors: dust, chemicals, wool, feathers, etc. Hay fever, which occurs during pollination of grass and plants, is referred to the group of allergic rhinites (pollinosis). The neurovegetative form is noted in patients hypersensitive to cold (feet in particular). Between attacks, respiration is normal, and there is no watery discharge. Vascular reactions manifested by increased permeability of the vascular walls and transudation are typical for both forms of rhinites. The rhinoscopic picture is alike and characterized by marked oedema and alternation of cyanotic and pallid (oven whitish) mucosa. The nasal meatuses are strongly narrowed, the passage is practically absent, and transparent watery secretion is accumulated. To differentiate between these forms of rhinitis, an allergic history should be taken, nasal mucus tested for the presence of eosinophils (absent in patients with the neurovegetative form), and test for identification of allergens performed. Treatment includes general and local measures: nonspecific hyposensitization by pipolphen, suprastin, dimedrol, and calcium chloride that decrease permeability of the vascular wall. Naphthalan ointment is locally applied; novocaine block of the anterior and posterior ends of the inferior nasal conchae is helpful. Chronic hyperplastic rhinitis. This form is characterized by permanent enlargement of the nasal conchae due to either hypertrophied cells or their proliferation. Enlarged conchae narrow the nasal meatuses, mainly the common one, which impedes inspiration and expiration, causes congestion in the nasal conchae and hypersecretion of mucus. Symptoms are similar to those of simple catarrhal rhinitis. The distinguishing feature is 84 that the enlarged conchae scarcely shrink after adrenaline application. Treatment. Mild cases require painting of mucosa with astringents (collargol, protargol). Finally, galvanocautcery, cryocoagulation, ultrasound disintegration, or removal of the whole or a part of a concha by special instruments (conchotomy) are performed. All these measures are aimed at diminishing mainly the inferior enlarged conchae to facilitate air passage through the nasal cavity. Chronic atrophic rhinitis. This severe form may combine with atrophic changes in the pharynx, larynx, and nasopharynx. The degenerative changes of the nasal mucosa associated with congenital features of the mucous membrane, occupational hazards connected with dust air or drying effect of vapors of some chemicals are the underlying cause of atrophic rhinitis. Symptoms are severe dryness in the nose, crusting, nasal obstruction, purulent nasal discharge, and upset sense of smell. Clinical picture. Rhinoscopy reveals a specific picture—wide nasal meatuses, pale and thin mucous membrane, accumulation of yellow viscous secretion which dries into heavy crusts. Treatment is mainly symptomatic and aimed at moistening the nasal mucosa and removing of crusts. Drugs containing vegetable oils (mineral oils dry the mucosa) and iodine, which stimulates glandular secretion by irritating the mucosa, are employed, Lugol's solution is used for the purpose. Vitamin A preparations are given to facilitate regenerative processes, Ozaena is an atrophic rhinitis whose incidence is rare. It is characterized by atrophy of the nasal mucosa and turbinate bones due to which the nasal meatuses widen considerably (the posterior pharyngeal wall can be seen through the nose). The whole nasal cavity, in spite of its large size, may be filled with heavy green-yellow crusts with offensive odour. Patients themselves are anosmic owing to a severe atrophy of mucosa. Treatment is symptomatic and consists in removing crusts and irrigating the nasal cavity. Streptomycin and iron preparations are also used.

Diseases of the Paranasal Sinuses

Inflammation of mucosa of paranasal sinuses is called sinusitis. The disease is given its name, according to the sinus affected. Thus, the inflammation of the maxillary (the

85 largest) sinus is called maxillary sinusitis (or highrnoritis); that of frontal sinus—frontal sinusitis; ethmoid cells—ethmoiditis; and the sphenoid sinus—sphenoiditis. Infrequently, several sinuses are simultaneously involved, and the condition is called pansinusitis (sinuses on both sides are involved) or hemisinusitis (inflammation of sinuses on one side). According to the nature of inflammation in the sinus, the diseases are subdivided into purulent maxillary sinusitis, catarrhal maxillary sinusitis, allergic maxilla-ethmoiditis, and polypous maxillary sinusitis. Depending on the duration of inflammatory condition, acute, subacute, and chronic sinusitis are classified. In the majority of cases, sinusitis occur due to inflammation of the nasal mucosa, especially secondary to influenza, when ciliated epithelium activity is suppressed, and the nasal microflora penetrates the sinus. Thus, according to their aetiology, rhinogenous sinusites are distinguished. The maxillary sinus is of particular importance. It may be involved not only immediately after any type of rhinitis, but also due to the maxillodental pathology. In such cases a specific type of sinusitis, odontogenic maxillary sinusitis that requires special methods of examination and treatment, is distinguished. Intimate anatomical relation of the upper teeth to the maxillary sinus promotes the development of odontogenic maxillary sinusitis. Adults are mainly affected because of the specific development of Highmore's antrum during growth of the facial bones. The volume of the newborn sinus measures 0.15 cm3; in a two or three-year-old child the sinus volume is 1-5 cm3. In infants, the antrum is deeply positioned; its thick (0.5-0.8 cm) anterior wall contains the tooth germs, and cannot therefore be trephined. In early childhood, the canine teeth are the closest to the maxillary sinus. At the age of five or six, the second premolar and the first molar also grow close to the floor of the sinus. In a child over six, the growth of the maxillary sinus is accelerated due to resolution of the alveolar process from dental sacs. Sometimes, when the sinus is large and its floor is low the roots of the premolars and molars are separated from the mucosa of the sinus only by a very thin bony plate, or the dental root immediately contacts the mucous membrane and protrudes into the maxillary sinus. When the sinus is small, the thickness of the bony plate varies: for the second molar, it is 1,3 mm, for the third molar 2.3 mm, for the first premolar 7.6 mm, and for the canine tooth 7,1 mm. As is known, frontal sinusitis, ethmoiditis, and sphenoiditis are not odontogenic, but sometimes severe odontogenic highmoritis may induce inflammation of these sinuses. Pathological changes in the walls of the sinuses depend on the duration of the disease and the nature of inflammation. Acute conditions are characterized by mucosal 86 oedema, congestion, and marked hyperemia. Normal maxillary mucosa resembles cigarette paper. An inflamed mucosa is 20 times thicker and considerably narrows the maxillary cavity, which impedes its drainage. The patient develops headache and his general condition worsens. At the stage of acute inflammation of maxillary mucosa, exudate is formed (haemorrhagic and then purulent) due to thickening of mucosa and vascular compression. During chronic inflammation of paranasal sinuses, pathoanatomical changes depend on the nature of inflammation. Signs of allergic or inflammatory oedema and the formation of polyps and cysts may prevail. Chronic suppurative conditions (highmoritis, frontal sinusitis and ethmoiditis) and acute ones are witnessed by thickening of mucosa, its stable hyperaemia and congestion, and then in duration, fibrosis, and hyperplasia.

Acute Maxillary Sinusitis (Highmoritis)

Symptoms. Frontal headache, heaviness in the head, the pain radiating to the upper teeth, sometimes pain in the buccal area; unilateral nasal obstruction (if one sinus is involved), purulent or mucoid nasal discharge. History. The disease is associated with overcooling, acute or chronic rhinitis, acute respiratory disease, and influenza. Clinical picture. Chill marked fever, lassitude, and malaise are common. Anterior rhinoscopy reveals accumulation of mucoid or purulent secretion in the common and, mainly, middle nasal meatuses. A "string of pus" can bo seen running from under the middle concha. The nasal mucosa of the affected side is hyperaernic (especially in the area of the middle nasal meatus) and oedematous. Diaphanoscope. There is no red pupillary reflex on the affected side. X-ray examination. The x-ray pattern in the anteroposterior view reveals intense opacity (comparing with the orbits) of the maxillary sinus. Electroroentgenography is also a sufficiently informative method to reveal a pathological condition of the paranasal sinuses and their walls. Treatment is conservative and directed at improving drainage from the maxillary sinus by widening the natural ostium of the sinus. This is obtained by instillation of vasoconstrictors (adrenaline, napthyaine, sanorine, and ephedrine) applied preferably by the middle nasal meatus. General treatment includes antibacterial therapy (sulphanilamides, antibiotics) and hyposensitizing agents (dimedrol, pipolphen, and calcium chloride). 87 Physiotherapeutic procedures, such as UHP, ultraviolet irradiation, and electrophoresis, are used. In cases of a prolonged course of the disease, persistent headache, and other manifestations of intoxication, antral puncture is performed for diagnostic and therapeutic purposes. The sinus is punctured through the inferior nasal meatus. The procedure is simple and, if done correctly, does not induce complications. The puncture is performed as follows. 1. The nasal mucosa of the inferior meatus is anaesthetized by a 2 per cent xylocaine solution. If the drug is not tolerated, a 10 per cent dimedrol solution is used, 2. A cotton-tipped applicator moistened in adrenaline solution is placed into the middle nasal meatus to widen the natural ostium of the sinus. 3. Five minutes later, a special needle is passed under the inferior turbinate bone (where the bony wall is thinner) under visual control so that its tip is directed at the lateral angle of the eye. 4. After the puncture of the wall of the antrum, a syringe is attached to the needle, and the contents of the sinus are with drawn to determine the flora and sensitivity to antibiotics. Then the sinus is washed by disinfectant solutions, 5. As soon as the fluid becomes transparent, medicinal solutions (antibiotics, enzymes) are administered through the needle. The patient lies on the affected side for 30 minutes to prevent leakage of the solution through the ostium. Usually, the procedure ends successfully, but complications are possible: the needle contaminated with pus from the sinus may pass into the orbit with consequent orbital phlegmon; the tip of the needle may puss into the surrounding buccal soft tissues if the needle pierces the anterior wall of the sinus. Air embolism, collapse, and shock are also possible. Indications for antral puncture must therefore be scrupulously grounded, and all situations that may be assessed as contraindications (blood diseases, allergic reaction to drugs, psychic status of a patient) must be considered. A puncture is a stress for a patient. If two or more procedures are required, a polyethylene tube may be inserted into the antral wall during the first puncture. Repeated irrigations of the sinus and administration of drugs performed through this tube.

Chronic Form of Maxillary Sinusitis

Maxillary sinusitis can be a chronic disease, especially when associated with allergy and polyps. The conversion of acute highmoritis into its chronic form is promoted by recurrent exacerbations, deviated septum, hypertrophied nasal conchae, adenoids, reduced 88 immune defense forces, pathogenic flora, poor living and working conditions, and inadequate therapy. Symptoms include unit or bilateral nasal obstruction, offensive odour, nasal discharge (purulent, watery, mucoid), frontal headache that intensifies on bending and in the evening. This is explained by the patient's erect position during the daytime due to which the purulent discharge is not sufficiently drained through the natural ostium situated near the roof of the sinus. The accumulated pug stimulates the receptors of the antral mucosa (branches of the trigeminal nerve), which causes persistent headache and pain in the upper teeth. The patient often complains of lassitude and fatigue. History. As a rule, the patient notes the undulant course of the disease characterized by alternation of remissions and exacerbations. The disease may last for years, especially in mixed polypous-suppurative forms of highmoritis, and also in allergic patients. Clinical picture. Patient's general condition depends on the degree of nasal obstruction and intoxication, concomitant diseases (e.g., bronchial asthma), and intensity of suppuration in the sinus. Occasionally, chronic suppurative highmoritis affects the gastro-intestinal tract: the appetite fails, aud chronic gastric diseases persist. Anterior rhinoscopy demonstrates purulent discharge in the middle nasal meatus and polyps that occupy the middle and common nasal meatuses. The colour of mucosa depends on the condition: it is markedly hyperaemic in suppurative and cyanotic in allergic forms of the disease. Visible polyps always extend into the nasal cavity from the maxiliary and ethmoid sinuses. Polyps grow backward from the maxillary sinus and can reach 10 cm in length extending through the choanae into the nasopharynx. They are known as choanal polyps and are benign bluishgrey formations with a smooth surface. They grow on a pedicle and can be displaced by a probe. X-ray examination (anteroposterior view) not only reveals abnormality in the sinus but also specifies it: homogeneous shadow is typical for a suppurative form; parietal thickening of the lining mucosa is common for a catarrhal form, and spots are characteristic of the polypous form of highmoritis. Antral puncture verities the character of inflammation, provides material for a bacteriologic study, removes congestive purulent secretion which may be viscid, crumblike, or thick, and fetid. Diagnosis is made taking into account the obtained data. The disease may be classified as chronic purulent, chronic polypous, catarrhal, and allergic highmoritis. Complications usually occur during exacerbation with possible inflammation 89 spreading to the orbit. The second branch of the trigeminal nerve (the maxillary nerve) which is found on tho superior wall of the sinus may be involved. The upper teeth that closely contact the floor of the maxillary sinus may be affected. Treatment is mostly surgical including puncture, prolonged drainage of the sinus ( Fig. 51), polypectomy, and a radical operation (opening) of the sinus.

Fig. 51. Puncture and irrigation of the maxillary sinus 1 —needle inserted through the vault of the inferior nasal meatus; 2—a curved metal catheter inserted through the middle nasal meatus (natural ostium)

If repeated punctures (7 or 8 punctures wilh irrigations during two weeks) prove ineffective, a radical antrum operation is indicated during which pus and pathologically changed mucosa are removed. The main task of the operation is creation of a window (nasoantral window) from the maxillary sinus into the inferior nasal meatus. It allows adequate postoperative washing of the cavity and administration of necessary drugs: antibiotics and enzymes which thin purulent conglomerates on the antral walls and

facilitate their withdrawal. Stages of a radical operation are shown in Figs. 52, 53 and 54.

Fig. 52. Primary incision made in the supra dental fossa

Fig. 53. Periosteum is scraped off. anterior bony wall is opened in the area of the canine fossa

90 Fig. 54- A passage between the maxillary sinus and nasal cavity in the area of the inferior nasal meatus (1) (the bone of the anterior antral wall is removed); a thread passed through the window and nostril (2)

Features of Odontogenic Maxillary Sinusitis

The symptoms arc not always pronounced, especially in the presence of an oroantral fistula connecting the maxillary sinus with the oral cavity. In such cases the purulent discharge runs from the sinus and lessens the patient's subjective condition: the nasal breathing may be normal and headache is not severe as in rhinogenous maxillary sinusitis. Thus, the diagnosis of odontogenic maxillary sinusitis is not always timely and precise. A female patient attended a doctor for pronounced swelling and tenderness of the left chucks Earlier, the dentist opened abscesses in this region twice: the first time with the intraoral approach, and the second, with the extra-oral one. The examination of the patient revealed a pyonecrotic form of odontogenic maxillary sinusitis accompanied by destruction of the anterior antral wall. Sanation of the sinus and affected teeth led to a complete recovery. Among the underlying causes of odontogenic maxillary sinusitis are foreign bodies that penetrated into the sinus from the oral cavity (tooth-filJing material, fragments of

Fig. 55. Underlying causes of odontogenic maxillary sinusitis 1—collateral oedema of the mucous membrane of the sinus; 2— subperiosteal abscess; oedematous dental granuloma; 3 - foreign body; 4 - fistula; 5—osteitis; 6— parodontosis dental instruments, dental roots, turundas, etc.), dental granulomas, subperiosteal abscesses, and paradontosis ( Fig. 55). Mild frontal headache, purulent discharge from the oroantral fistula in the alveolar process, air passage into the oral cavity during nose blowing, penetration of food into the sinus, and offensive odour sensed fry the patient are the most typical signs of odontogenic maxillary sinusitis. A correctly taken history disclosing the patient's dental pathology and preceding

91 manipulations in the oral cavity is important for making a diagnosis. As a rule, an affected tooth (destroyed or treated) is detected. A hole leading to the sinus after tooth extraction and purulent discharge into the oral cavity through the fistula observed in the middle nasal meatus during anterior rhinoscopy are determined. Purulent discharge from the sinus is always foul-smelling. X-ray examination of the paranasal sinuses and orthopantomography determining the condition of "dental roots related to the sinus are the leading diagnostic methods for revealing odontogenic maxillary sinusitis. Sometimes, contrast study of the sinus is necessary with the help of iodolipol introduced through, a special needle or fistula.

Fig. 56. Scheme showing the closure of the fistula by a flap on a pedicle

X-ray demonstrates specific thickening of.the antral floor adjacent to the alveolar process. Treatment consists of sanation of the involved tooth and sinus itself. Treatment is normally surgical, though prolonged drainage occasionally proves effective since the oroantral passage can close spontaneously or following repeated application of iodine tincture. In addition, plastic closure of the fistula is.resorted to, but grafting is sometimes difficult. A variant of plastic closure of a fistula is shown in Fig. 56. Besides, the affected teeth must be devitalized, their root apices resected, and foreign bodies removed from the sinus. The affected mucosa of the sinus is excised. It is imperative to create a window between the antrum and nasal cavity in the region of the inferior nasal meatus for postoperative drainage and treatment of the sinus. Inflammatory Diseases of Other Sinuses

Inflammatory diseases of mucosa of the frontal sinus, ethmoid cells, and sphenoid sinus are not immediately related to abnormality of the maxillodental system. They have, however, much in common with. highmoritis, and specific manifestations of ethmoiditis, frontal sinusitis, and sphenoiditis must therefore be differentiated. Besides, these conditions themselves may entail severe complications of the orbit and cranial cavity.

92 Frontal sinusitis. It occurs in the presence of acute respiratory disease or influenza. Thickening of mucosa due to inflammatory oedema of the sinus impairs evacuation of the sinus contents through the nasofrontal duct into the middle nasal meatus. Active exudation and suppuration cause empyema of the frontal sinus. In acute frontal sinusitis or exacerbation of its chronic form, periostitis of the floor separating the sinus from the orbit may occur. Upper lid oedema develops, the eye may close completely, and sometimes pus bursts through the inner canthus of the eye to produce a fistula. Symptoms. Severe headache in the forehead and a feeling of heaviness. Anterior rhinoscopy may show purulent or mucoid discharge in the middle nasal meatus. X-ray demonstrates homogeneous darkening of one or both sinuses. Treatment. Acute condition is managed, first, by conservative treatment to achieve patency of the nasofrontal duct (instillation of vasoconstrictive nose drops, a 3 per cent ephedrine or naphthyzine solution); antioedematous drugs (dimedrol, pipolphen, suprastin), antipyretics, antibiotics, and sulphanilamides are also indicated. If the acute frontal sinusitis is complicated by periostitis or intracranial inflammation, urgent surgery is performed: the frontal sinus is opened, its walls revised, pathologically changed mucosa removed, and a passage between the sinus and nasal cavity created. Sluggish inflammation of the frontal sinus should be treated by trephination. The thick anterior wall of the sinus is opened by a special tool known as trephine. A metal cannula is then inserted for repeated irrigation of the sinus and administration of medicinal solutions (antibiotics and enzymes). Chronic forms resisting conservative therapy and complicated forms require a radical operation. Ethmoiditis. Inflammation of the ethmoid cells is commonly attended with inflammation of the maxillary and frontal sinuses. Symptoms. Nasal obstruction, purulent or mucoid nasal discharge, heaviness in the region of the nose root., and frontal headache. Clinical picture. Anterior rhinoscopy demonstrates swollen mucosa of the middle nasal meatus aud accumulation of pus. The polypous form of elhmoiditis is also charac- terized by small, multiple polyps that occupy the middle and common nasal meatuses. X-ray shows opacity of the ethmoid cells. Treatment is the same as that described for the above sinusites: improvement of drainage, polypectomy, and opening of the ethmoid cells. Complications include inllammation of the organ of vision: retrobulbar neuritis and orbital cellulitis. Sphenoiditis. It is encountered less frequently and is characterized by girdle headache; the pain is sometimes localized in the occiput. Pus from the sphenoid sinus flows down into 93 tho posterior portions of the nasal cavity and therefore may be detected only by posterior rhinoscopy. Lateral x-ray is decisive for the diagnosis of sphenoidilis. Suppurative sphenoiditis may cause such severe complications as meningitis and involvement of the optic nerve. Therefore, if sphenoiditis is suspected, every effort should be made to verify or exclude this condition. Sinusitis in children. The smaller the child, the thicker is the lining mucosa of the maxillary sinus and ethmoid cells. This explains its increased secretory function in children, which determines the frequency of sinusites and their specific course. In early childhood, the ethmoid cells are involved more frequently. According to the data obtained, highmoro-ethmoidites make up 18 per cent of paediatric morbidity. Though sinusites are common, paediatricians do not always diagnose them correctly. Exudative forms prevail, and the affection is usually bilateral. Infants tend to develop respiratory diseases in the presence of which epithelial desquamation of the nasal mucosa and the mucosa of paranasal sinuses caused by viruses facilitates the invasion of pathogenic microorganisms. Besides, adenoids in infants facilitate inflammation in the maxillary sinus and ethmoid cells. Acute highmoro-ethmoiditis easily responds to conservative treatment, but may cause complications such as orbital periostitis and phlegmon that require emergency surgery: opening and sanation of the sinuses.

Maxillary Cysts Inflammation of the maxillary mucosa is in 6 to 13 per cent of cases attended with maxillary cysts that are sometimes connected with dental abnormality. Such eases require timely differential diagnosis and adequate treatment. Cysts are found in all sinuses, but more often they occur in the maxillary sinus. Cysts developing as a result of dental pathology are divided into radicular (or dental) and follicular (or tubular) cysts. Radicular cysts primarily form about the root of a tooth. The inflammation then causes cystic granuloma that gradually enlarges, destroys the bony wall of the tooth socket, and penetrates into the sinus. The cystic contents may be serous and purulent. Follicular cysts (tubulocysts) are rare and associated with developmental anomaly of a tooth follicle. Retention cysts are the most common type of maxillary cysts. They result from the inflammatory diseases of the maxillary mucosa, obstruction to the excrulory ducts of glands, and dysfunction of their ciliated epithelium. Retention cysts are characterized by simultaneous occurrence of several cysts that can be situated on any wall of the sinus, but 94 more often they develop (like the odontogenic cysts) on the inferior, alveolar wall. The symptoms of maxillary cysts are often not pronounced and may be a chancy x-ray finding in the examination for some other disease (Fig. 57). The characteristic sign of a cyst is a round shadow in the sinus. Along with asymptomatic course of the disease, maxillary cysts can be manifested by specific signs. These include persistent headache in the forehead not associated with abnormality of the nasal cavity or pharynx. Sometimes unilateral nasal obstruction may concur. Diagnostic

Fig. 57. X-ray pattern (anteroposterior view) demonstrating a shadow of a cyst in the right maxillary sinus

puncture of the sinus, along with x-ray examination including tomography, are decisive in establishing a final diagnosis. If the cyst is large, a yellowish opalescent cystic fluid oozes through the lumen of the puncture needle. If headache subsides after drainage of the cyst, the sinus must be opened and the cyst capsule removed. The cyst may sometimes suppurate and produce signs typical for acute maxillary sinusitis. Treatment consists in extirpation of the suppurative cyst and creation of a passage between the sinus and nasal cavity (as in radical antrum operation). The patient's complaints, the size and genesis of a cyst suggest the method of and time for surgery.

95 Acute Inflammations of the Pharynx

Acute inflammations of the pharynx can be divided into two main groups—acute tonsillitis and pharyngitis which may be either independent or concomitant diseases.

Acute Tonsillitis

Acute tonsillitis is a common disease affecting mainly children and young adults; 75 per cent of the morbidity comprise persons aged under 30. According to a modern definition, acute tonsillitis is an acute systemic infectious-allergic disease with a severe lesion of the lymphadenuid tissue of the palatine tonsils. The pathogenic agent plays a decisive role in the onset and. course of the disease; therefore, a person may got infected by air-droplet route or a direct contact will a sick person. Being an infectious disease, tonsillitis produces the immunity; relapses of acute tonsillitis within a year suggest decreased immunity of a person. This should be borne in mind when selecting therapy. Cooling of the trunk, feet, and tonsillar mucosa are unfavourable factors facilitating the development of acute tonsillitis. Tonsillitis is commonly caused by the haemolytic streptococcus. Spirochaetes of the oral cavity, fusiform bacillus, and sometimes staphylococcus, viruses, and anaerobic microorganisms may also cause acute tonsillitis. Palatine tonsils are mostly affected; pharyngeal, lingual, and laryngeal tonsils are less commonly involved. Occasionally, acute tonsillitis is closely related to the pathological condition in the teeth and oral cavity; acute tonsillitis may combine with lesions of the gingival and buccal mucosa and accompany severe systemic diseases. Several types of acute tonsillitis are distinguished, depending upon severity of the condition and morphological changes in the tonsils. Catarrhal acute tonsillitis is the mildest form of the disease. Symptoms. Pain in the throat during swallowing of saliva or food. Pain is not severe and is usually bilateral. The patient complains of malaise, headache, and pain in the limbs; body temperature elevates to 37.0-37.5 0C. The onset is marked by sore and dry throat. Catarrhal acute tonsillitis usually combines with a catarrhal inflammation of the nasal and pharyngeal mucosa. Clinical picture. Pronounced hypcraemia of mucosa lining the tonsils, pillars, end soft palate is found by pharyngoscopy. The course is favourable and in 3 to 4 days the symptoms subside. Treatment includes warming compresses on the throat, warm ample drinks, alkaline gargles, hot foot baths, sulphanilamides, and bed rest.

96 Lacunar (caseous) acute tonsillitis is a severe disease involving tonsillar parenchyma. Streptococcus causes epithelial oedema in the depth of the tonsillar crypts (lacunae). Then necrosis of the superficial and deep epithelium develops, which is followed, by its desquamation and the formation of wound surfaces on the mucosa. Plugs of caseous matter are formed in the lacunae and their mouths; hence the name of the disease. Symptoms include severe pain in the throat on swallowing of food or saliva, headache, lassitude, malaise, chill, deranged sleep, and high body temperature (38-39 °C). Clinical picture. Examination of the oropharynx reveals oedematons and engorged palatine tonsils; their mucosa is hyperaemic and greyish-white patches cover the surface of the tonsil near the lacunar mouths. The enlarged lymph nodes located behind the angle of the mandible are tender to palpation. As the disease progresses, the deep nodes located along the course of the external jugular vein become responsive. Treatment in the same as in catarrhal acute tonsillitis. Antibiotics and hyposensitizing agents are also necessary. Bed rest and ample drinks to lessen intoxication are obligatory. Acute follicular tonsillitis is the most severe form of acute tonsillitis caused by streptococcus. Not only the surface of mucosa of the palatine tonsils but also their follicles are inflamed. Symptoms. The patient's general condition is the same as in acute lacunar tonsillitis. The general symptoms are more pronounced, and the body temperature rises to 40 0C and higher. Clinical picture. In addition to the engorged and hyperaemic palatine tonsils and surrounding tissues, pharyngoscopy reveals yellowish patches of suppurating tonsillar follicles in the presence of severe hyperaemia. Treatment is the same as in acute lacunar tonsillitis. Vincent's angina (ulceromembranous angina) is due to the symbiosis of oral spirochaete and fusiform bacillus which reside in the oral cavity in the presence of carious teeth and gingivitis. The characteristic feature of this disease is a quite satisfactory patient's general condition accompanied by vast destructive changes in the palatine tonsils. Occasionally, an ulcerated tonsil can be detected by chance, e.g., during a visit to a dentist. The ulcer may be large and cover almost the entire tonsil. An easily detachable greyish- yellow patch is seen at the base of the ulcer. As has been mentioned, the patient's subjective condition is good and the body temperature may be normal. Fetid breath is typical. Slightly tender lymph nodes behind the angle of the mandible and along the anterior margin of the upper sternocleidomastoid muscle are enlargod. The ulcerated tonsil and the patch at its base must be taken into consideration by the physician who has to differentiate Vincent's angina 97 from more dangerous diseases with similar symptoms, e.g., diphtheria, syphilis, or malignant tumour. A smear is taken for the bacteriologic study. The above-mentioned symbiosis of microorganisms is typical for Vincent's angina. Treatment includes gargles of dilute hydrogen peroxide and potassium permanganate solutions, painting the ulcer with iodine tincture, vitamins A and C, warming compresses on the throat and regional lymph nodes. The patient must be isolated and have individual crockery. Acute lingual tonsillitis is a very severe disease. Symptoms include sharp pain in the throat that radiates to the ear, nasal twang, foul breath, and high fever. The patient's general condition is critical. The some symptoms are characteristic of abscess of the tongue therefore the patient with acute lingual tonsillitis must be hospitalized. The advanced abscess is witnessed by unilateral swelling of the tongue, inability to protrude the tongue, very high fever, and a pronounced trismus. Patients with acute lingual tonsillitis are given intensive antiinflammatory therapy; the abscess is opened with a To-bold special knife.

TONSILLITIS IN PATIENTS WITH BLOOD DISEASES

Acute leukaemia. The lesions of oral and pharyngeal mucosa (gingivitis, stomatitis, and acute tonsillitis) are among the earliest signs of leukaemia. Patients may complain of increased gingival bleeding that resists conservative treatment and pain during swallowing. The lesions of the palatine tonsils in patients with acute leukaemia are manifested by ulcers with a dirty coat over the tonsillar surface. After removal of the coat, a bleeding surface is exposed. The patient's general condition is severe. Cervical, axillary, and inguinal lymph nodes are considerably enlarged. Clinical experience shows that total blood counts are necessary in all cases of tonsillar ulceration in order to establish a final diagnosis. Treatment. General: haematologic; antibiotics are used to protect the wound surface of the tonsil from microflora. Local: nitrofurazone, dilute hydrogen peroxide, and marigold solutions are used as a gargle. Analgesics (ana-esthesin) are recommended. Agranulocytosis. It is characterized by decreased number or even complete absence of granulocytes in the peripheral blood, sometimes due to the effect of some drugs (amidopyrine, norsulfazole, and acetyl salicylic acid). The onset of the disease is acute: body temperature sharply rises to 40 °C; chills and sore throat occur, Deep ulcers are formed over the tonsils, but not confined within their boundaries. The patient's general condition is grave. Granulocyte count is low; the tonsils are destroyed, and the breath becomes foul. Treatment. General: haematologic. Local therapy includes gargling with antiseptic solutions, powdering ulcers with anaesthesin, or their irrigation with cocaine solution. 98 Monocytosis. This blood disease is accompanied by necrotic changes of the palatine tonsils: tonsillar coats resemble diphtheritic membranes. Blood count that reveals increased number of monocytes permits to establish a correct diagnosis. The outcome of the disease is usually favourable.

PERITONSILLAR ABSCESS (QUINSY)

Inflammation of the peritonsillar cellular tissue is called quinsy or peritonsillar abscess. The condition is caused by spreading of inflammation from the tonsillar pa- renchyma or from the region of the eighth tooth (especially in difficult eruption with the 'hood1 symptom) onto the cellular tissue of the tonsil. Diffuse peritonsillar inflammation has its specific features (1) as a rule, it occurs soon after acute tonsillitis; (2) acute unilateral sore throat is accompanied by sharp deterioration of patient's condition: fatigue, insomnia due to severe sore throat with pain radiating to the ear, inabilily to eat or drink. There may be chills; body temperature rises to 39-40°C. Trismus and hypersalivation are present; the voice becomes nasal and the skin of the face grey. If the mouth of the patient can be opened, fetid odour is felt. Asymmetry of the soft palate due to displacement of one tonsil toward the midline is seen. There is a swelling and hyperaemia of the adjacent tissues above, laterally, and below the tonsil. Anterosuperior, anteroinferior, lateral, and posterior peritonsillar abscesses are distinguished, depending upon the location of abscess in the peritonsillar cellu- lar tissue. The lateral one is considered to be the most dangerous, since it may spread to the parapharyngeal (pharyngomaxillary) cellular space. Peritonsillar abscess belongs to emergency conditions. Prior to the formation of abscess, patients with difiuse suppuration of the peritonsillar cellular tissue should be given broad-spectrum antibiotics (injections are preferable because tablets are difficult to swallow). Antihistamines (pipolphen, suprastin, dimedrol), warming compresses on the neck, warm gargles (nitrofurazone and potassium permanganate), antipyretics (aspirin, amidopyriue), and analgesics (analgin, baralgin) are recommended. A ripe abscess must be opened as early as possible. The following rules should be observed to prevent possible severe complications:

99

Fig. 59. Intracutaneous of novocains to relieve trismus in peritonsillar abscess (1) the patient's mouth must be sufficiently opened. Patients with trismus should be given intracutaneous novocaine injections to the region of the mandibular angle on the involved side: using an insulin syringe, 3 ml of a 2 per cent novocaine solution are injected intracutaneously till the ‘intracutaneous bleb’ is formed over an area of 2,5 cm (Fig. 59). This injection not only removes trismus but also anaesthetizes the zone of abscess, which helps the patient to experience the procedure; (2) the abscess is incised at the most bulging site. To prevent damage to the adjacent large blood vessels, the point of the blade sbould be directed as shown in Fig. 60; (3) after opening the abscess, the patient's head must be bent to prevent passage of pus into the airways. Evacuation of the abscess cavity gives a rapid symptomatic relief; after a long thirst the patient pleads for water; (4) during 2 or 3 days following the operation, gargles with antiseptic solutions and adequate drainage are necessary. No additional treatment is required, as a rule.

Fig. 60. Scalpel position in. opening a peritonsillar abscess Since recurrent peritonsillar abscesses are regarded as manifestations of chronic tonsillitis, tonsillectomy is rcecominended during remission. In cases with odontogenic aetiology, the underlying cause must be eliminated. 100 Symptoms of tonsillites are given in Table 1.

Parapharyngeal and Retropharyngeal Abscesses These are diseases of odontogenic and rhinopharyngeal origin. Both are rare but present severe and dangerous complications of inflammatory conditions to the teeth, oral mucosa, parotid glands, and also of diseases of the nasal cavity and paranasal sinuses. Abscesses in the parapharyngeal and retropharyngeal spaces are associated with spread of infection through the lymphatic pathways into the lymph nodes draining lymph from the nasal cavity, nasopharynx, paranasal sinuses, auditory tube, teeth, and palatine tonsils. Retropharyngeal abscesses are common in early childhood, since in children over 5 these lymph nodes undergo atrophy. Retropharyngeal abscess in an adult may develop due to injury to the posterior pharyngeal wall (for instance, by a fish bone) and spreading of infection from carious teeth. Symptoms. Sore throat and difficult swallowing, impeded breathing, lockjaw, and dyspnoea. Cough is also noted in children. Diagnosis is easily established by pharyngoscopy (in the absence of lockjaw): a smooth overgrowth that descends to the lower pharynx is revealed on the posterior pharyngeal wall. Treatment. Urgent surgery is required. The surgeon inserts the left index finger into the child's oral cavity and reaches the soft wall of abscess. The blade of the scalpel is all wrapped in adhesive tape, except its lip. The blade should be guided by the surgeon's finger until the abscess is reached and incised. The child's head should then he turned quickly to prevent pus from entering the trachea. 101 Abscess opening is simpler in an adult: In a sitting patient, the abscess is opened under visual control. The abscess, which may extend to the sixth or seventh cervical vertebra, is then aspirated. A parapharyngeal (pharyngomaxillary) abscess may be due to inflammation of the palatine tonsils, peritonsillar cellular tissue, and also to pathological condition of the parotid glands and inflammation in the region of the co-ronoid process of the mandible. The disease takes a severe course with signs of violent intoxication. Latoral cervical pain, painful swallowing, and fever ore typical. Upper lateral parts of the neck are swollen, hyperacute, and lender to palpation. The swelling is firm. The danger of retropharyngeal and parapharyngeal abscesses is associated with possible spreading of suppuration to the mediastinum. Emergency hospitalization Js a must for opening the abscess by the external or intraoral incision (parapharyngeal abscess) or through the mouth (retropharyngeal abscess).

Acute Pharyngitis

It may he an independent disease, but frequently it is secondary to a catarrhal inflammation of the upper airways and is characterized by dry, burning, and sore throat. Unlike acute tonsillitis, sore throat in acute catarrhal pharyngitis is mostly felt during swallowing of saliva, while food swallowing is less painful. Besides, the patient complains of constant mucus flow by the posterior pharyngeal wall, which makes swalfowing frequent. The general condition is normal, and body temperature does not rise over 37 0C, Treatment. Warm antiseptic gargles and warming compresses on the neck (renewed at 4-hour intervals).

Chronic Diseases of The Pharynx

CHRONIC TONSILLITIS

The disease is commonly encountered among young people leading to prolonged disability due to frequent relapses and numerous complications of the viscera. Thus, chronic tonsillitis is not only a chronic inflammation of the lymphoid tissue of palatine tonsils; it is a complicated condition including local and general symptoms occurring in exacerbation and remission and in the presence of patient's autosensitization. The specific structure of palatine tonsils (deep tortuous crypts penetrating the tonsillar

102 parenchyma) creates conditions for the assimilation of foreign protein and toxins excreted by numerous microorganisms that get into the oral cavity with food and inhaled air. An allergic condition may thus develop in the presence of which inflammatory diseases develop in response to non-specific stimulation. In such cases local or general overcoofing that may be regarded as a non-specific stimulant results in inflammation in the palatine tonsils or distant organs— kidneys, myocardium, and joints (due to the body's sen- sitization). Tonsillitis creates unfavourable conditions for the drainage of tonsillar crypts since wound surfaces are formed due to epithelial desquamation, which leads to the formation of adhesions in the crypts. This impedes to a greater extent drainage of the crypts where food particles, epithelial debris, and microorganisms are accumulated providing conditions for torpid tonsillar inflammation along with patient's sensitization. The clinical picture is not always vivid. There are many symptoms the corumination of which may help diagnose a condition. Basic symptoms of chronic tonsillitis. (1) Symptoms and history: recurrent attacks of acute tonsillitis (2-3 or more times a year) with high body temperature; increased fatigue, non-motivated headache, subfebrile temperature in the evening between episodes of acute tonsillitis. The patient relates diseases of the heart and joints to the preceding attack of acute tonsillitis. Foul breath, swollen and tender lymph nodes below the angle of the mandible. (2) Objective findings: adhesions of the pillars to tonsillar mucosa (recurrent attacks of acute tonsillitis are accompanied by desquamation of the pavement epithelium, and conditions arise predisposing to adhesions), thick and hyperaemic tonsillar pillars due to the purulent discharge from the tonsillar crypts. The presence of liquid purulent detritus or numerous fetid purulent plugs in the crypts. Normally, peripheral blood undergoes no changes in remissions. In a specific instance not all the above-described symptoms may be pronounced. Sometimes the diagnosis is established by separate symptoms or when two or three of them are combined. Recurrent attacks of acute tonsillitis are an important criterion to validate the diagnosis, but chronic tonsillitis may also run without exacerbations. Two main types of chronic tonsillitis are dis- tinguished from the therapeutic aspect. Some cases can be treated conservatively, others require surgery. Example of chronic tonsillitis I. (1) Acute tonsillitis accompanied by elevated body tomperature recurs not more than twice a year without local or systemic complications, (2) The history of acute tonsillitis is absent, but examination of the tonsils reveals much pus and plugs in the crypts. Regional lymph nodes are enlarged. Example of chronic tonsillitis II. (1) Attacks of acute tonsillitis with high fever recur 103 more than twice a year; their course is severe (lacunar and follicular acute tonsillites). Conservative treatment fails—acute tonsillitis recurs at any season, but complications are absent. (2) Recurrent attacks of acute tonsillitis one of which is complicated by nephritis, rheumatic carditis, or some other disease. (3) History of acute tonsillitis is absent, but examination of the tonsils reveals accumulation of pus and plugs in the crypts. The patient suffers from rheumatic carditis. (4) The patient's history has several episodes of acute tonsilities one of which is complicated by a peritonsillar abscess. The fact that history helps identify chronic tonsillitis might be emphasized. Approximately in 80 per cent of cases, chronic tonsillitis causes acute nephritis or complications of a chronic nephritis, aggravates the disease are facilitates the transition of acute nephritis into its chronic form. Otorhinolaryngeal treatment, e.g., tonsillectomy, does not cure the patient from nephritis, but contributes to the efficacy of drug, diet and spa therapy of diseases of the kidneys, joints, and heart.

Fig. 61. Irrigation of tonsillar

Conservative treatment is aimed at sanation of tonsillar crypts and restoration of body's defense. Irrigation of tonsillar crypts wilh antiseptic solutions is popular, which removes purulent plugs, detritus, and necrotic masses from the crypts (Fig. 61), Physiotherapy includes UHF-therapy of the regional lymph nodes, low-frequency ultrasound, electrophoresis, ultraviolet irradiation, and others. Surgical treatment includes tonsillectomy (Fig. G2), cryosurgery (if there are contraindications, e.g., blood diseases, lor common surgery), and ultrasound.

CHRONIC PHARYNGITIS

Chronic pharyngitis is also a common disease; it comes at the head of the attendance list. The disease is characterized by a prolonged course and often is not ail-independent disease but concurs with other pathological conditions, mostly of the gastro-intestinal tract. 104 Chronic pharyngitis should not therefore be regarded as a local lesion

Fig. 62. Tonsillectomy a—first step; 1-5—sites for novocaine administration; 6—incision by the margin of the anterior pillar; b - second step: 7—the tonsil is by forcops and separated bluntly; c— third step: 8— separated tonsil is cut at its base with a snare of the pharyngeal mucosa, but an attempt should be made to relate it to the general causes. The latter can be revealed by the additional methods of examination which include gastrostomy and biopsy of gastric mucosa. Several varieties of chronic pharyngitis are distinguished: catarrhal, hypertrophic, and atrophic pharyngites. Despile morphologic differences, the patient's complaints are quite similar: a feeling of an obstacle in the throat, mild hut persistent, pain during swallowing of saliva, intensification of pain after taking spicy, hot, or cold food; a sensation of a foreign body in the throat, dryness or permanent flow of secretion by the posterior pharyngeal wall, and dry cough. Catarrhal pharyngitis. Hyperaemic and oedematous mucous membrane of the posterior pharyngeal wall and the presence of mucus are typical. These symptoms intensify during common cold or exacerbation of gastrointestinal diseases. Hypertrophic (granular) pharyngitis. Accumulation of lymphoid tissue in the form of large crimson granules and enlarged lymphoid bands behind the posterior tonsillar pillars are specific for the lateral hypertrophic pharyngitis. Atrophic pharyngitis is the most severe form of the disease. The patient complains of acute dryness in the throat combined with pain and the formation of crusts. Treatment is complex and directed at lessening the local manifestations and 105 eliminating the underlying cause. All patients with pharyngitis, regardless of its form, should be examined by the otorhinolaryngologist, neuropathologist, and gastroenterologist. Some occupational factors, such as dirty and extremely dry air and presence of gases irritating the mucosa, can affect the course of chronic pharyngitis. The properties of food (spicy, hot, or cold), smoking, or alcohol abuse are of particular importance. Local medication includes the drugs that help to moisten the mucous membrane of the posterior pharyngeal wall and abate the sensations which may be regarded as paresthesias— tickling and the feeling of a foreign body in the throat, etc. Chamomile and sage teas are recommended as gargles for prolonged use in patients with catarrhal pharyngitis. Alkaline gargles and silver nitrate preparations (protargol, collargol) are also used to render drying effect. The treatment of hypertrophic forms consists in electrocautery of hyperplastic parts; the method of cryodestruction is also used. The treatment of atrophic forms is mainly symptomatic and directed at lessening dryness and pain in the throat. A 1 per cent Lugol's solution is used for the purpose.

PHARYNGOMYCOSIS

Pharyngomycosis is a fungal infection of the pharyngeal mucosa. Patients do not usually present any complaints and may discover only by chance whitish-yellow cone- shaped formations elevated above the mucosal surface of the tongue, palatine tonsils, or tonsillar pillars. The disease is caused by Lspiethrix buccalis, a saprophytic fungus inhabiting the buccal cavity. Cornincation of the epithelium involves small parts of the mucosa where cone-shaped pillars. 2-3 mm high, occur that firmly adhere to the underlying tissue.They may be found on the tongue, soft palate, tonsils, and other parts of the oropharynx. Treatment includes decamin, 1 caramel four times a day for two weeks, and quinosol solutions as a gargle.

ADENOIDS

Hypertrophy of the pharyngeal tonsil (adenoids) comes first in the list of nasopharyngeal abnormalities, which is indirectly related to the pathological condition of the maxillodental system. Adenoids are most frequently encountered in children, i.e., in the period when facial bones are shaping toward the adult configuration and daring the period of 106 dentition. Therefore, nasal breathing must be unobstructed to prevent developmental anomalies of the hard palate and teeth. Adenoids may cause stable nasal obstruction, congestive mucosa of the nasal cavity and paranasal sinuses, and also persistent rhinites and otitis media. Symptoms include persistent nasal obstruction, chronic rhinites, headache, apathy, and deranged appetite. Pallor, apathetic facial expression, flattened nasolabial folds, and half- opened mouth with carious teeth are typical. Diagnosis is based on the history findings and child's appearance. Posterior rhinoscopy shows adenoids (formations with a rough surface) in the vault of the nasopharynx that obstruct the choanae. Besides, palpation of the nasopharynx is of great diagnostic value. It is done by the right index finger inserted into the nasopharynx behind the soft palate; sometimes lateral x-ray examination is helpful.

Fig. 63. Adenoids in or the Fig. 64. Adenoidectomy nasopharynx 1 - nasal septum; 2— tissue; 3—soft palate

vouH Three degrees of adenoid growths are distinguished: adenoids extend to the upper edge of the choanae; adenoids occupy a considerable part of the nasopharynx and half cover the vomer; III, adenoids completely obstruct the choanae (Fig. 63). The basic method to restore nasal breathing in patients with adenoids is surgery— adenoidectomy performed with the use of a special fenestrated knife called adenotome (Fig. 64). Timely adenoidectomy prevents development of diseases of the nasal cavity, paranasal sinuses, and maxillodental abnormalities (stomatitis, gingivitis, dental caries, and malocclusion).

107 FOREIGN BODIES OF THE PHARYNX

Foreign bodies mainly lodge in the oro and laryjigo-pharynx. Palatine tonsils are the most probable site where a foreign body can be deposited, A sharp and thin fish bone may penetrate into the thickness of the palatine or lingual tonsil, and orily 1 or 2 mm of the bone can be seen over the surface ol the tonsil. This causes discomfort, pain, and permanent retching. Sometimes adequate examination of the oro- and laryngopharynx can bo done only under anaesthesia of the mucosa. Foreign bodies are removed under visual control by special forceps.

FOREIGN BODIES OF THE OESOPHAGUS

Various foreign objects can be captured in the oesophagus. Removable dentures are the most dangerous foreign bodies since their claspers may be infected and damage the oesophageal wall to cause oesophagitis. In 80 per cent of cases, the foreign bodies settlo in the first narrowing of the oesophagus whose striated muscles rapidly and strongly contract to propel the bolus into the lower oesophagus. If a sharp foreign hody is captured, stimulated mucosal receptors cause muscular contractions of the upper oesophagus to aggravate the situation by strongly holding the foreign object. The diagnosis is based, on the patient's complaints (difficult swallowing of food and water, or the inability to do it, pain in the cervical region, sometimes radiating to the interscapular region). X-ray demonstrates a foreign body or contrast medium retained over it. Treatment consists in oesophagoscopy under general or local anaesthesia with extraction of the foreign body by special forceps.

Diseases of the Larynx

Laryngeal diseases, which may be connected with abnormality of the maxillodental system, mainly corns from injuries. Traumas of the jaws and pharynx cause stenosis that should immediately be corrected. Sometimes first aid is needed in laryngeal stenosis due to intolerance of some drugs used by a dentist, e.g., iodine tincture. Besides, some laryngeal inflammations of childhood may cause conditions that a physician of any speciality must be able to correct.

ACUTE LARYNGITIS 108

Acute laryngitis is a common disease of the laryngeal mucosa. As an independent disease, it may be produced by vocal overstrain, but in the majority of cases it is a component of acute upper respiratory infections and influenza. Occasionally, the disease may develop as a result of irritating action of industrial dust or gases. Mucosal changes in acute catarrhal laryngitis are characterized by oedema and pronounced hyperaemia of the entire larynx, which is especially visible in the true vocal cords. Normal vocal cords have thin edges and join tightly during phonation; inflamed cords are thick, their edges become flaccid, and the cords fail to strain and join closely during phonation. Accumulating in the lumen of the rima glottidis, the inflammatory secretion causes cough, which to a greater extent impedes junction of the vocal cords. Symptoms include change of voice, sore throat, and cough. Dysphionia (voice impairment) may vary in severity. The voice is rough, low, and hoarse. Aphonia (loss of voice) may develop. Laryngoscopy demonstrates diffuse hyperaemia over the entire larynx. Treatment includes sparing conditions for the voice. If the occupation is associated with vocal overstrain, the patient must be given a sick leave till the vocal function is completely restored. Diet is of great importance: cold, hot, or piquant food is forbidden. Warming of the laryngeal mucosa is accomplished by drinking warm milk and mineral water, and by warming compresses on the neck. Hot foot baths and vapour inhalations are included. Antibiotic aerosols, particularly penicillin aerosol are most effective. Alkaline inhalations soften the crusts and promote their separation; this, in turn, lessens the urge to cough. In patients with laryngeal oedema, drugs reducing permeability of the vascular wall (pipolphen, dimedrol, suprastin, and calcium chloride) are used; mustard plasters to the calves are also recommended.

CHRONIC LARYNGITIS

Three forms of the disease are encountered; catarrhal, hyperplastic, and atrophic. Disturbed vocal function is typical for all three forms. Occupational hazards, smoking, and vocal overstrain help maintain chronic inflammation in the larynx. High-temperature cigarette smoke dries mucosa of the larynx, trachea, and bronchi. In addition, it evokes congestive hyperaomia of the mucosa, thus maintaining inflammation with a large amount of sputum. The latter, in turn, provokes cough, especially in the morning because smoke suppresses the function of ciliated epithelium of the larynx, trachea, and bronchi, and therefore during the daytime the cough reflex is reduced; transportation of 109 the accumulated sputum to the infraglotic cavity is difficult. At night, ciliated epithelium restores its function to some extent and can transport sputum to the lower larynx to stimulate the cough reflex and facilitate expectoration. Cough may be violent since viscid sputum adheres to the walls and is expectorated with difficulty. Resultant microinjuries to the laryngeal mucosa also maintain inflammation. Chronic catarrhal laryngitis. Persistent, mild, and diffuse hyperaemia of the entire larynx, and moderate oedema are typical. Chronic hyperplastic (hypertrophic) laryngitis. Thickening of the vocal and vestibular folds, and of the interarytenoid mucosa is characteristic. Thick vocal cords fail to completely close the rima glottidis, Forcible work of muscles is required to constrict the rima glottidis. This leads to their overstrain and finally to persistent voice impairment. Thickening of the vocal cords may be diffuse and localized. ‘Singers’ nodules’ represent one of the forms of chronic laryngitis. They are formed on the free edge of vocal cords, which impedes junction. This form of laryingitis is usually associated with vocal abuse. Treatment combines drug therapy, lasercoagulation, cryodestruction, and surgery aimed to remove the hypertrophied foci. Microsurgical operations employing the microscope are the most efficacious in patients with 'singers' nodules'. Chronic atrophic (dry) laryngitis resists treatment, and only palliative therapy can be used. Dystrophy developing in the mucosa of the larynx, nose, pharynx, and trachea underlies this form of chronic laryngitis. This is a systemic disease of the mucous membrane. The patient's complaints include severe dryness and a feeling of a foreign body in the throat, voice impairment (up to aphonia), and recurrent crusts. The final diagnosis can be established after indirect laryngoscopy which reveals pale, exsangaineous, and thin mucosa; thin vocal cords fail to join in the midline: viscous yellowish sputum forms crusts in the lumen of the rima glottidis. Treatment. A special laryngeal syringe is used to administer solutions that moisten the mucosa, soften and separate crusts, and prevent mucosa from drying during breathing. These solutions may contain drugs that stimulate mucosa and thereby functioning of mucous glands. Alkaline inhalations facilitate expectoration of viscous sputum and soften crusts. Inhalations should be repeated during the daytime, and the patient can use portable inhalers atomizing oil preparations. Stationary inhalers are equipped with apparatuses that produce aerosols reaching not only the larynx and trachea but also small bronchi and alveoli. Medicinal aerosols become involved in the lesser circulation and bypass the liver to ensure their prolonged effect. It should be borne in mind that high temperature of aerosols affects 110 the pharmacological properties of drugs and the function of the ciliated epithelium of the trachea, bronchi, and larynx: epithelial cilia stop functioning at a temperature of 38 0C, while mineral waters used for inhalation become inactive at a temperature of 37-38 °C.

Acute and Chronic Stenosis of the Larynx. Stages of Stenosis and Emergency Aid

Pathological conditions leading to the narrowing of the lumen of rima glottidis present a special category of laryngeal diseases.

Acute Stenosis of the Larynx

Acute stricture of the glottis may be caused not only by Inflammatory diseases of the laryngeal mucosa but also occurs as a result of trauma or allergic oedema induced by intolerance of some drugs used in dentistry (antibiotics, iodine tincture, and others). An abrupt stenosis sometimes occurs—spasm of muscles dilating the rima glottidis develops due to the ingress of a foreign object (food, fluid, fragments of removable dentures, etc.). Obstruction of the glottis by food is infrequent in drunken persons: foreign bodies may be inhaled dire to the reduced control of reflexogenic zones of the oral cavity, pharynx, and larynx. Depending on the underlying cause of acute laryngeal stenosis, the physician takes either conservative or surgical measures. The ability of a physician to estimate the condition of the patient is of great importance. Therefore, the physician must be well familiar with the clinical picture of the disease, since the width of the rima glottidis is the sign that determines the clinical picture of laryngeal stenosis. An adult at rest normally inhales about 7 litres of air per minute; this volume contains 225 cm3 of pure oxygen. In patients with stenosis, the act of respiration (consisting of inspiration, physiological pause, and expiration) must undergo some transformation in order to inhale the adequate amount of air- Respiration is regulated automatically and depends upon the amount of carbon dioxide diluted in blood, which stimulates the respiratory centre. Increased amount of carbon dioxide in patients with stenosis changes their respiration—the necessary amount of air that must pass through the constricted rima glottidis makes the inspiration phase longer and the pause and expiration phase shorter. Thus, inspiratory dyspnoea (difficult inspiration) develops. Clinically, four stages of stenosis are distinguished and guide the physician in choosing proper measures to save the patient. 111

STAGES OF LARYNGEAL STENOSIS

Stage I (compensation). The patient tries to compensate for deficiency of air inhaled through the narrowed glottis. This slage is marked by slow (bradypnoea) and noisy respiration, prolonged inspiration, short physiological pause, short and abrupt expiration followed by another short pause and another long inspiration. A person at rest does not feel dyspnoea (exertional dyspnoea). This is a mild form of stenosis. Stage II (relative compensation). The patient, still manages to compensate for deficiency of air by activating accessory muscles, but this compensation is difficult. This stage is marked by pronounced inspiratory dyspnoea: difficult long inspiration, complete absence of the pause between inspiration and short violent expiration. Bradypnoea progresses. Retraction of the yielding intercostal spaces, supraclavicular and suprasternal fossae becomes vivid. The patient is forced to occupy sitting position with the head tilted back and hands leaning against the bed. The patient is excited and restless; acrocyanosis develops. Stage III (decompensation). The patient's anxiety is extreme. He may run about the room, tear his collar in an effort to facilitate the inhalation of air. The face is covered with sticky cold sweat, the eyes seern to be getting out from the orbits and express fright. First the face and then the neck and chest become cyanotic. Tachypnoea develops, but respiration becomes shallow and respiratory movements are scarcely distinguishable because the chest is practically immobile and only the laryngeal prominence(Adam's apple) rapidly moves up and down. Voice and cough are silent, pulse is rapid, the patient is conscious. Stage IV (asphyxia) is the terminal stage of laryngeal stenosis. Senses are lost or consciousness is confused, respiratory excursions are unnoticeable, or Cheyne-Stokes respiration develops. The skin is cyanotic and pallid. The heart continues contracting, the pupils are sharply dilated. Choice of emergency care in acute laryngeal stenosis depends on the stage of stenosis, Us cause (foreign ohject, oedema, trauma, false or diphtheritic croup), and the patient's condition. Emergency care in acute laryngeal stenosis may be conservative or surgical, Conservative measures are given to patients with. the first stage stenosis due to the inflammatory or allergic oedema of mucosa of the infragloltic space, the area of the arytenoid cartilages, interarytenoid space, and ventral surface of the epiglottis. It should be remembered that oedema of any part of the larynx may quickly extend to the vocal cords 112 and the infraglottic space; the patient with oedema of the larynx must therefore be urgently hospitalized. Treatment of laryngeal stenosis caused by oedema comprises the following procedures: (1) hot foot baths (the patient's legs are dipped into hot water to the knee level); (2) mustard plasters to the calves (plasters must not be wetted in hot water since they become ineffective); (3) diuretics (furosomide, lasix) lessening tissue oedema and drugs reducing permeability of the vascular wall (dimedrol, 10 per cent solution of calcium chloride intravenously, pipolphen, suprastin, hydrocortisone, and 40 per cent glucose solution); (4) vascular stimulants (1 ml of a 1 per cent lobeline); (5) antibiotic aerosols (200 000 U); (6) inhalations with humidified oxygen; (7) careful nasotracheal intubation in children. Preparations of morphine hydrochloride that inhibit the respiratory centre must not be used.

EMERGENCY SURGERV

Prompt and correct identification of the patient's condition (in the presence of extreme restlessness and progressing asphyxia) plus assessment of the possibilities at hand comprise the main difficulties encountered by the physician who renders first aid to the suffocating patient. Plethoric cervical veins and sometimes specific anatomy of the neck (excess subcutaneous fat, short neck) interfere with surgery. The physician must choose the technique of opening the airways. In the absence of conditions for a classic tracheotomy, a dentist must be able to perform surgery that saves the patient's life and allows transport to a hospital where tracheotomy is performed. The operation that can be performed in most inappropriate conditions (in traffic, in the street, in public places) is coniotomy. Coniotomy is making entry to the trachea through the cricovocal membrane (conus elasticus) which joins the arch of the cricoid cartilage and inferior margin of the thyroid cartilage. The conus elasticus covers a small depression between the margins of the thyroid and cricoid cartilages, which is well palpable in a patient with his head tilted back. Large blood vessels are absent in this area. The skin covers conus elasticus beneath which lies the infraglottic cavity. After incising the overlying skin and cricovocal membrane, one can 113 easily penetrate into the trachea in the absence of bleeding using any cutting instrument at hand (a kitchen-knife, blade, scissors, etc.) Non-collapsible (even of a small diameter) tube should then be inserted into airways through the created incision. This will allow the patient to breathe until tracheotomy (with the insertion of a cannula) is done. The danger of coniotomy lies in possible damage to the cricoid and thyroid cartilages and the mucosa of the infraglottic cavity, which can later provoke granulation, perichondritis and, consequently, narrowing of the infraglottic cavity due to fibrous tissue. This, in turn, causes narrowing of the trachea at late postoperative period. Therefore, this operation is regarded as an emergency one because the physician cannot do anything else under the given circumstances. Fixing the tube in place by any suitable means (even holding it in hand), the physician has a chance to transport the patient to a hospital where tracheotomy is carried out. To perform the procedure, the head of a sitting patient is tilted back, which helps to identify the site of a crico vocal membrane. Its determination is easier by a fingertip that slides along the anterior margin of the thyroid cartilage until gets into the depression. After the point is found, a stab horizontal incision through the skin and crico vocal membrane is done without local anaesthesia to save time, and the physician penetrates into the infra- glottic cavity. Posterior structures of the cavity should not be damaged. The inserted tube must not be wide, since otherwise it exerts excess pressure on the surrounding tissues and entails reactive inflammatory reaction. Figure 69 shows levels for tracheotomy.

Fig. 69. Levels for tracheotomy 1—coniotomy; 2—cricotomy; 3—superior tracheotomy; 4— inferior tracheotomy; 5—median tracheotomy

Tracheotomy has been known since antiquity as a method of saving patient's life in various diseases and injuries to the larynx. This operation still remains highly important nowadays: timely tracheotomy saves tho patient's life and promotes a complete cure. 114 Indications for tracheotomy include acute or subacute stenosis (acute respiratory-viral and other infections) and severe cranial injuries. It Is also used for inferior bronchoscopy, i.e., insertion of a bronchoscope through a previously created tracheostoma. Tracheostoma is placed according to the following rules. 1. The most common patient's position is supine, though in some cases tracheotomy is performed in a sitting patient with his head tilted back. First, for conveniency of manipulations, a bolster is placed under the patient's neck. The bolster is then moved under the patient's back to make easier manipulations on the trachea. At the onset of operation the bolster should not be placed under the patient's back since it impedes breathing even more. Only when the trachea is exposed and few seconds are left before its opening, the bolster may be placed under the patient's back. 2. Anaesthesia, Emergency tracheotomy is usually done under local anaesthesia. It asphyxia develops and the operation should be performed immediately, no anaesthesia is applied. For the planned operation intubation anaesthesia is rational, since artificial lung ventilation provides conditions for the most sparing surgical intervention. Novocaine or trimecaine solutions (1-2 per cent) are used for local anaesthesia. Figure 70 shows schematically the administration of topical anaesthetics.

Fig. 70. Scheme of novocaine administration (total anaesthesia) prior to tracheotomy

3. There are clear land marks on the anterior surface of the neck (the laryn geal prominence, arch of the cricoid cartilage, and suprasternal notch) above and below the incision site on the tracheal wall. The skin must he incised accurately by the midline, otherwise, the surgeon risks to miss the trachea. 4. The surgeon stands on the right of the patient during superior and median, tracheotomy, and on the left in inferior tracheotomy. In these positions it is convenient to 115 make incisions at various levels. 5. A 5 to 6 cm incision is made on the skin from the middle of the laryngeal prominence downward to the suprasternal notch, 6. The skin and subcutaneous fat are incised with a bellied scalpel (using a sharp- pointed scalpel is dangerous because its tip can. sink deep and damage not only the muscular tissue, but also the isthmus of the thyroid gland). Linea alba cervicalis (where the sternohyoid muscles join) is then found. If this line is seen in the wound after separation of the tissues, the direction is correct. 7. Linea alba should lie dissected all along its course. To prevent damage to the underlying isthmus of tho thyroid gland, this line should be dissected with scissors (not with a scalpel). Before that, approximately at the middle of the linea alba, the tissue is lifted by two forceps, and a transverse incision is made with scissors. A grooved probe is inserted into this incision upward and down ward, and the linea alba is dissected along this probe to the length of incision on the skin. 8. After Ihe muscles are drawn apart, Ihe plethoric isthmus of the thyroid gland covering the trachea is exposed, For a superior tracheotomy, the isthmus must be preliminarily mobilized by dissecting the fascia that holds it to the tracheal wall. Once the isthmus is pulled down by a blunt hook, the first tracheal rings are exposed. For an inferior tracheotomy, the isthmus is displaced superiorly, thus exposing the third, fourth, and fifth tracheal rings. 9. Absolute haemostasis is advisable before opening the trachea. To suppress the cough reflex, 1 ml of a 5 per cent cocaine or a 1 per cent dicaine solution should be instilled into the tracheal mucosa by piercing the band between the rings. During superior tracheotomy, the second and third rings are cut; in median tracheotomy, the third and the fourth; and in inferior tracheotomy, the fourth and fifth rings are dissected. Care is taken not to damage mucosa of the infraglottic cavity while dissecting the second ring during superior tracheotomy. Injury to the tissues of this area and prolonged presence of a tracheotomy tube provoke granulations with subsequent stable cicatrization that narrows the laryngeal lumen, as a result of which a patient may become a tube carrier for a long time. In laryngeal stenosis the trachea and larynx rapidly move up and down. This necessitates larynx fixation before dissecting the tracheal wall. To that end, the assistant puts a sharp single-toothed hook into the arch of the cricoid cartilage, pulls the larynx up and keeps in this position until the trachea is opened. 10. The tracheal rings are dissected with a sharp-pointed scalpel. Care should be taken not in damage the posterior tracheal wall. To that end, the belly of the scalpel should be 116 wrapped in wot cotton-wool with its tip left open to cut the tracheal wall to the depth of 0.5cm. After dissecting the two rings or band between them, a dilator is inserted into the wound. After dilalation of the wound, a tracheotomy tube, metal or plastic, of a corresponding diameter (Nos 1-5) is inserted. It consists of the inner and outer tubes which are necessary for postoperative care. When the inner tube is plugged with mucus, sputum, or crusts, it must be removed, while the outer tube remains in the trachea. After cleaning the inner tube is repositioned. The tracheotomy tube should be inserted as follows: grasping the flange of the tube between the index finger and thumb, il is first put across the patient's neck moving its tip to the stoma. When the tip of the tube enters the trachea, the tube should be turned to align with the neck axis and inserted into tho trachea. The tube should be tightly held in place, the strings must obligatorily be knotted to prevent their spontaneous undoing as a result of which the tube may slip out. The strings should be tied on the neck side so as not to bore the supine patient and to be easily controlled by the medical personnel. After a cannula has been inserted, the incision on the skin is sutured with one or two stitches above and below the tube. 11. The patient with a tracheotomy tube should be constant medical surveillance. During the first postoperative hours patient's respiratory movements must be watched, since it is difficult for the patient to adapt to unusual breathing through the cannula. In some cases the respiratory centre is stimulated by the administration of lobeline. Possible complications of tracheotomy. 1. Loss of orientation after incision of soft tissues. Severe bleeding due to injury to the isthmus of the thyroid gland. 2. Blood aspiration during hasty and unprepared dissection of the tracheal wall. A damage to the posterior tracheal wall and penetration into the oesophagus as a result of unreasonably deep incision in cases with in adequate fixation of the larynx and trachea. 3. The insertion of a tracheotomy cannula between this separated, but not dissected tracheal mucosa and the tracheal wall leads to tracheal obturation. 4. Subcutaneous emphysema in complete closure of the incised skin and disagreement between the size of wound in the tracheal wall and the diameter of cannula. During breathing and especially coughing the air penetrates into subcutaneous fat to cause emphysema. The latter first extends to the neck and face and then may spread over the chest. After emergency tracheotomy all efforts must be directed at eliminating the causes of acute stenosis.

117 Chronic Laryngeal Stenosis

This condition is controversial in otorhinolaryngology, since in the majority of cases chronic laryngeal stenosis may be caused by neoplasms, disordered innervation, and cicatrization. Stenoses may also be the result of traumas and burns of the larynx, which leads to inflammation of the laryngeal soft tissues and cartilages. The diagnosis of chronic laryngeal stenosis does not present difficulty: the severity of stenosis depends on the size of rima glottidis. Cicatricial tissue is removed surgically (cryode-struction, ultrasound, laser beam), and the laryngeal channel is then dilated by a T-tube. Treatment of patients with chronically stenosed larynx is aimed at restoration of spontaneous respiration through the mouth and nose.

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