Diagnosis in Otorhinolaryngology , Notas de estudo de Enfermagem

Baixe Diagnosis in Otorhinolaryngology e outras Notas de estudo em PDF para Enfermagem, somente na Docsity! ER atado aa Diagnosis in Pd ryngolog An Illustrated Guide T. Metin Önerci Diagnosis in Otorhinolaryngology Contenti Preface In preparing the material for this book, I took the advice of my students who generously shared their views and opinions with me. I was told that it would be preferable to have images of the various diseases with legends describing the disease. Students would be able to learn and retain the infor- mation more successfully if the material was accompanied by pictures and schematic drawings. Recent advances in technology have made it possible to photograph regions that are difficult to view with the naked eye, such as the ear, nose, throat, nasopharynx, and larynx – all the areas of otorhinolaryngology. Such an illustrated text in this field is important and necessary for teaching purposes. In this book I tried to compile images of the basic conditions that are commonly seen in general practice and to give the reader a visual survey with a brief description of the condition. I added tables and schematic drawings in order to provide practical information. It is not the purpose of this book to be a comprehensive textbook, since many textbooks are already available with more detailed information of the conditions illustrated here. This book is primarily intended for medical students, family and general practitioners, and ENT trainees. It may also serve as basic reading material for those in allied specialties. I hope my colleagues find this book useful and it contributes toward their teaching purposes. Ankara, Turkey T. Metin Önerci Contents Chapter 1 Ear 1.1 Ear Anatomy 2 1.2 ENT Examination 8 1.3 The Pinna 14 1.4 External Ear Canal 18 1.5 Otitis Media with Effusion 24 1.6 Acute Otitis Media 28 1.7 Chronic Otitis Media 34 1.8 Facial Nerve Paralysis 41 1.9 Complications of Otitis Media 43 1.10 Hearing Loss 45 1.11 Otalgia 48 1.12 Temporal Bone Fractures 50 1.13 Tinnitus 52 1.14 Vertigo 54 Chapter 2 Nose 2.1 The Common Cold and the Flu 58 2.2 Rhinitis 60 2.3 Allergic Rhinitis 65 2.4 Nasal Vestibulitis and Nasal Furunculosis and Mucormycosis 69 2.5 Sinusitis 72 2.6 Complications of Sinusitis 79 2.7 Nasal Polyposis 87 2.8 Nasal Obstruction 92 2.9 Septum 97 2.10 Epistaxis 101 2.11 Traumas 104 2.12 Dacryocystorhinostomy 110 2.13 Tumors 112 Chapter 3 Throat & Neck 3.1 Acute Tonsillopharyngitis 122 3.2 Adenoids 126 3.3 Snoring 129 3.4 Temporomandibular Joint 132 3.5 Airway Obstructions 134 3.6 Hoarseness 137 3.7 Cysts 143 3.8 Parotid Tumors 147 3.9 Oral Cavity 151 3.10 Neck Masses 159 3.11 Neck Malignancies 168 1.1 Ear Anatomy 2 1.2 ENT Examination 8 1.3 The Pinna 14 1.4 External Ear Canal 18 1.5 Otitis Media with Effusion 24 1.6 Acute Otitis Media 28 1.7 Chronic Otitis Media 34 1.8 Facial Nerve Paralysis 41 1.9 Complications of Otitis Media 43 1.10 Hearing Loss 45 1.11 Otalgia 48 1.12 Temporal Bone Fractures 50 1.13 Tinnitus 52 1.14 Vertigo 54 C O N T E N T S T. Metin Önerci: Diagnosis in Otorhinolaryngology DOI: 10.1007 / 978-3-642-00499-5,  Springer-Verlag Berlin Heidelberg 2009 1 Chapter 1 EAR 4 Chapter 1 Ear Fig. 1.1.6 Due to the differences in the physical properties of air and water, sound vibrations in the air are largely reflected away from the surface of water (99.9% of the energy of air-borne sound is reflected away), with only 0.1% entering the water. Although the surface area of the tympanic membrane is 85–90 mm2, the effective vibrating area of the tympanic membrane is 55 mm2. The surface area of the foot- plate is 3.2 mm2. The ratio of the surface areas of the tympanic mem- brane and the footplate is 55/3.2 = 17.1. This represents the hydraulic ratio of the tympanic membrane and stapes footplate, producing an increase force at the oval window of 17 times for the human ear, since the sound pressure level is equal to the force divided by the surface area (P = F/a). The final transformer ratio of the human tympanic membrane and ossicular chain is the product of the lever ratio of 1.3 times the hydraulic ratio of 17, which equals 22. This gain compen- sates the loss due to the air–bone difference Fig. 1.1.5 False-color scanning electron micrograph (SEM) of the three smallest bones in the human body responsible for conduction of sound waves in the middle ear. At the top left is the malleus (ham- mer), which strikes the incus (anvil – right of malleus); the incus is joined to the stapes (stirrups), which conducts sound toward the inner ear. Sound waves enter the ear through the external auditory meatus and cause the eardrum to vibrate. Vibrations from the ear- drum are passed to the malleus and then the stapes via the incus. The stapes transmits the vibrations to the fluid-filled cochlea of the inner ear where the vibrations are converted to nerve impulses. Lever effect: the manubrium mallei is 1.3 times longer than the long pro- cess of the incus. This difference in the lengths of the manubrium mallei and long process of the incus contributes a lever factor of 1.3 to increase the intensity of the sound (visual photos) 1.1 Ear Anatomy 5 Fig. 1.1.8 The inner ear comprises the cochlea and the labyrinth. The labyrinth consists of three semicircular canals (superior, posterior, and lateral) and two otolithic organs (utricle and saccule). The utricu- lar duct and the saccular duct join to form the endolymphatic duct Fig. 1.1.9 The cochlea has three fluid-filled compartments: the scala tympani, the scala vestibuli, and the scala media, which contains the organ of Corti (courtesy of Paparella, Paparella otopathology lab director) a b c Fig. 1.1.7 (a–c) The temporal bone contains the ear. It has five parts: the bony external ear canal, the styloid process, the squamous por- tion, the petrous portion, and the mastoid process. There are suture lines between these various portions such as the petrotympanic fis- sure, petrosquamous suture, tympanosquamous suture, tympano- mastoid suture etc. The mastoid process is not present at birth, which makes the facial nerve very superficial E A R N O S E T H R O A T A N D N E C K 6 Chapter 1 Ear Fig. 1.1.10 Inner ear organ of Corti. Color SEM of a section through the human inner ear, showing the organ of Corti (spiral organ). At the top right can be seen four rows of hair cells, supported by pillar-like Dieter cells. Each hair cell contains up to 100 individual hairs. The hairs translate mechanical movement caused by their displacement by sound waves into electrical impulses, which are transmitted to the brain via the cochlear nerve (visual photos) Fig. 1.1.11 Sensory hair cells in the ear. Color SEM of hair cells in the cochlea, the inner ear’s auditory sense organ. The crescent-shaped areas across the center are numerous stereocilia, and are located on top of supporting hair cells. Sound waves entering the inner ear displace the fluid that surrounds the stereocilia, causing them to bend. This triggers a response in the hair cells, which release neurotrans- mitter chemicals that generate nerve impulses. The nerve impulses travel to the brain along the auditory nerve. This process can transmit informa- tion about the loudness and pitch of a sound. Magnification: ×2,000 when printed 10 cm wide (visual photos) 1.2 ENT Examination 9 Fig. 1.2.5 Audiometer to test hearing Fig. 1.2.4 Soundproof hearing test rooms Rinne (diseased ear) Weber Type of hearing loss Positive Not lateralized Normal hearing Positive Lateralized to the better ear Sensorineural hearing loss Negative Lateralized to the diseased ear Conductive hearing loss Negative Lateralized to the better ear Total sensorineural hearing loss Table 1.2.1 Tuning fork tests and type of hearing loss 125 250 500 1000 2000 4000 8000 -10 0 10 20 30 40 50 60 70 80 90 100 110 Is it m e S ev iy es i d B ( IS O - 1 96 4) Frekanslar (HZ) 750 1500 3000 6000 125 250 500 1000 2000 4000 8000 -10 0 10 20 30 40 50 60 70 80 90 100 110 120 Is it m e S ev iy es i d B ( IS O - 1 96 4) Frekanslar (HZ) 750 1500 3000 6000 125 250 500 1000 2000 4000 8000 -10 0 10 20 30 40 50 60 70 80 90 100 110 120 Is it m e S ev iy es i d B ( IS O - 1 96 4) Frekanslar (HZ) a b c Fig. 1.2.6 Audiograms. (a) Normal hearing curve, (b) hearing loss due to acoustic trauma, (c) conductive-type hearing loss due to otosclerosis E A R N O S E T H R O A T A N D N E C K 10 Chapter 1 Ear a Fig. 1.2.8 Auditory brain stem response test. (a) Illustration showing the organs of hearing and the cerebellum. Sound waves are chan- neled by the pinna (visible part of the ear) into the auditory canal (pink) toward the eardrum. The eardrum transmits the vibrations to three tiny bones, the malleus, incus, and stapes, in the middle ear. The stapes passes the vibrations to the inner ear structures (purple), the semicircular canals and the cochlea (spiral). Auditory sensations are picked up by the cochlear nerve (yellow) and transmitted to the medulla (brain stem), the thalamus, and ultimately the cerebral cor- tex (visual photos). (b) The source of potentials. (c) Normal auditory brain stem response with six waves from five different anatomic sites Tympanometry Tympanometry is an indirect measure of the mobility (com- pliance) of the tympanic membrane and ossicular chain under different pressures. The mobility of the tympanic membrane is greatest when the pressure on both sides of the tympanic membrane is equal. Compliance is reduced as air pressure is increased or decreased from normal. High acous- tic energy is applied in the ear canal, some of this energy is absorbed and the remainder is reflected back and received by the probe. When the mobility is decreased, the energy is reflected more than the normal. In ears filled with fluid, tym- panic membrane thickening, or ossicular chain stiffening, the reflected energy is greater than in normal ears. Fig. 1.2.7 Classification of tympanograms. (a) Type A: The curve peaks at 0 mm H 2 O, indicating no pressure difference exists between the middle ear and the external environment. (If the peak of the curve is lower than the normal type A curve, stiffening of the ossicu- lar chain is often associated. If the peak of the curve is very high, it suggests ossicular discontinuity). (b) Type B: The tympanogram is relatively flat or dome shaped. This shows little change in the reflec- tive quality of the tympano-ossicular system as air pressures change in the external canal. This type of tympanogram is generally associ- ated with middle ear fluid. (c) Type C: The peak of the curve occurs with higher negative pressures (maximum compliance is reached at negative pressures, meaning the pressure in the middle ear is nega- tive). This curve indicates eustachian tube dysfunction 1.2 ENT Examination 11 Anatomic localization Wave Cochlea, eighth nerve I and II Cochlear nucleus III Olivary complex IV Lateral lemniscus V Inferior colliculus VI Table 1.2.2 The source of the potentials (Fig. 1.2.8 a, b, c) Fig. 1.2.9 Dix Hallpike maneuver for benign positional vertigo. Bringing the head to the head-hanging position may cause vertigo and nystagmus Peripheral Central Latent period + – Adaptationa + – Fatiguea + – Table 1.2.3 Differential diagnosis in positional vertigo aVertigo adapts by holding the patient’s head in the same position; ver- tigo fatigues on repeated positioning. Fig. 1.2.10 (a, b) Temporal bone CT scans. External auditory meatus, middle ear cavity, attic, mastoid aircells, cochlea, semicircular canals, and internal acoustic canal (and falciform crest in the internal acous- tic canal) can be seen a b b c Fig. 1.2.8 (Continued) E A R N O S E T H R O A T A N D N E C K 14 Chapter 1 Ear 1.3 The Pinna b a Fig. 1.3.1 (a) Preauricular skin tags are generally unilateral. They can be removed before school age if they cause cosmetic deformities. (b) Cartilage remnants in front of the tragus Fig. 1.3.2 Preauricular fistulas are due to fusion abnormalities dur- ing embryogenic development of the auricle. Seventy-five percent of cases are unilateral. If the orifice of the fistula is narrow, the debris may occlude the orifice and cause secondary infection. The whole sinus tract should be removed surgically Fig. 1.3.3 Macrotia is a large pinna Fig. 1.3.4 Prominent ear. (a) Posterior view before the operation and (b) 3 months after the operation. In prominent ears, the fold of the antihelix is either absent or poorly formed and the angle between the posterior surface of the conchal cartilage and the cranium is over 300°. There is an autosomal dominant inheritance. It is also referred to as bat ears or lop ears. Prominent ears should be corrected before school age, between 4 and 6 years a b 1.3 The Pinna 15 a b c d e f Fig. 1.3.5 Abnormalities of the auricle range from minor abnormalities that require no treatment to total absence of the pinna. Since the embryo- logical development of the pinna is completely different from the middle and inner ear, it is not generally associated with middle and inner ear abnormali- ties. However, atresia of the external ear canal may accompany microtia. (a, b) In type I microtia deformity, the deformity is only limited to the helix and antihelix and it is a minimal deformity. (c, d) In type II there is severe deformity, although the remnant of the pinna is present. (e, f) In type III deformity there is no pinna. Generally the external ear canal is completely atresic. In some patients the lobule may be present. The optimum age for surgery is around 5 years, until the other auricle reaches its adult size and the costal cartilage development is sufficient to be used in reconstruction. It is also important to operate on children before school age Fig. 1.3.6 In the complete absence of the auricle, an auricular implant may give a natural appearance Fig. 1.3.7 Sebaceous cyst in the postauricular sulcus. Complete removal is necessary to prevent recurrences E A R N O S E T H R O A T A N D N E C K 16 Chapter 1 Ear ca b Fig. 1.3.12 (a) Neurofibromas of the pinna. (b) Axial CT image shows massive involvement of the deep tissue planes. (c) Cafe-au-lait spots, which are characteristic of NF1, are also frequently seen in patients with NF2. Neurofibromas may be solitary or may occur as part of neu- rofibromatosis in patients with Recklinghausen’s disease. Solitary neurofibromas should be excised if they cause functional or cosmetic problems. Since these tumors have malignant potential, any change in the behavior of the tumor such as sudden increase in size, pain etc. should warn the surgeon about the possibility of malignancy. Extensive surgery is required for massive tumours. Conservative management is the best option Fig. 1.3.11 Hemangioma at the auricle. These tumors may regress spontaneously. Steroid treatment for young patients under 1 year of age may be useful (Courtesy of TESAV) Fig. 1.3.10 A burn in the preauricular skin and pinna due to cleaning with pure antiseptic agent (Courtesy of TESAV) Fig. 1.3.8 A benign mass located in the anteroinferior part of the helix Fig. 1.3.9 Malignant tumor in the auricle 1.4 External Ear Canal 19 Fig. 1.4.3 (a, b) Cerumen may cover the tympanic membrane like a layer and may give the impression of a pathologic eardrum. After cleaning the cerumen, the normal tympanic membrane is seen b a Fig. 1.4.4 In some people there is excessive cerumen production. The cerumen is generally occluded in the narrowest part of the exter- nal ear canal at its midportion. These patients need periodic cleaning. Use of cotton swabs can push the cerumen deeper in the ear canal, which occludes the ear canal completely and makes removal more difficult a b Fig. 1.4.5 (a) Removal of cerumen is done either by an ear curette or syringing. Adequate visualization and exposure is necessary to avoid trauma. If the cerumen is not hard enough, it may be removed with suction after being softened by ear drops. (b) Water irrigation is another method. After the ear canal has been straightened by pulling the pinna backward and upward, water at body temperature is administered in the posterosuperior direction. The water passes between the ear canal and the cerumen and pushes the cerumen outward. If the tympanic membrane is perforated, ear irrigation should not be done E A R N O S E T H R O A T A N D N E C K 20 Chapter 1 Ear Fig. 1.4.6 Anterior wall of the external ear canal is prominent pre- venting the anterior part of the eardrum from being seen Fig. 1.4.7 (a, b) Exostoses may narrow the external ear canal and may cause debris and cerumen to collect behind them. They are generally seen in swimmers. They are bony, hard, and usually remain small and symptom free. They do not require any treatment unless they cause problems a b Fig. 1.4.8 External auditory canal stenosis in a diabetic patient due to recurrent ear canal infections and trauma 1.4 External Ear Canal 21 Fig. 1.4.9 Acute otitis externa. The ear canal is hyperemic and nar- rowed due to swelling. Manipulation of the auricle or tragus is painful Fig. 1.4.10 Acute otitis externa. The ear canal is slightly narrowed due to swelling and is full of cerumen and purulent material Fig. 1.4.11 (a, b) Otomycosis. Several fungi may cause infections in the external ear canal. The most common type is Aspergillus (A. niger or A. flavus). Candida may occasionally be the agent. Fungal hyphae may be seen in the external ear canal a b E A R N O S E T H R O A T A N D N E C K 24 Chapter 1 Ear 1.5 Otitis Media with Effusion Fig. 1.5.1 (a) Right ear. Otitis media with effusion. Air–fluid level can be seen behind the transparent tympanic membrane. (b) Left ear. Air bubbles within the tympanic cavity a b Fig. 1.5.2 Right ear. The tympanic membrane is vascularized and the transparency of the tympanic membrane is slightly diminished Fig. 1.5.3 Right ear: otitis media with effusion. In long-standing effu- sions the tympanic membrane has a dull or opaque appearance with vascularization on it 1.5 Otitis Media with Effusion 25 Fig. 1.5.4 Right ear. Otitis media with effusion. The tympanic mem- brane is opaque, has lost its transparency, is vascularized, and retracted. Please note that the light reflex is shorter and moved upward due to retraction of the tympanic membrane Fig. 1.5.5 Left ear. Otitis media with effusion. Retractions occur mostly in the weak parts of the tympanic membrane, such as the pseudomembranous parts or pars flaccida due to middle ear nega- tive pressures Fig. 1.5.6 Right ear. In long-standing effusions the retraction pock- ets most frequently develop in the posterosuperior part of the tym- panic membrane. The retraction pocket just behind the malleus handle is seen and its apex can be identified. The pocket is clean con- taining no debris. The membrane lies on the incus and stapes. Behind the translucent thinned tympanic membrane, the incudostapedial joint and stapes tendon are clearly seen Fig. 1.5.7 Right ear. Retraction pocket with debris in it E A R N O S E T H R O A T A N D N E C K 26 Chapter 1 Ear Fig. 1.5.11 Thick and sticky mucoid material obtained from the mid- dle ear in a patient with otitis media with effusion Fig. 1.5.8 Left ear. Adhesive otitis media. The tympanic membrane is thinned and lies on the promontorium. The short process of the mal- leus and malleus handle is more prominent due to retraction of the membrane. Fibrous annulus is clearly identified Fig. 1.5.9 Right ear. Otitis media with effusion due to nasopharyn- geal carcinoma. Amber color and retraction of the tympanic mem- brane. A unilateral otitis media with effusion in adults always necessitates a detailed search for nasopharyngeal carcinoma Fig. 1.5.10 Mucoid material in the external ear canal after myringo- tomy in otitis media with effusion 1.6 Acute Otitis Media 29 Fig. 1.6.3 Bullous myringitis in (a) the right ear and (b) the left ear. The malleus handle is hardly visible. Bullous myringitis is due to a viral or Mycoplasma pneumoniae infection of the tympanic mem- brane. There is severe ear pain, but no hearing loss. Draining the blebs may provide immediate relief from pain. Only the outer epithe- lial layer should be punctured. Complete puncturing of the tympanic membrane may result in perforation b a a b c Fig. 1.6.4 Acute otitis media, hyperemia stage. (a) Hypere mia in the attic region of the left ear; the patient complains of ear pain only for the last one hour (b) Hyperemia in the attic region and the posterosu- perior part of the tympanic membrane of the left ear; the patient com- plains of ear pain only for the last three hours (c) Hyperemia in the attic region and the posterosuperior part of the tympanic membrane of the right ear; slight bulging of the tympanic membrane has started E A R N O S E T H R O A T A N D N E C K 30 Chapter 1 Ear Fig. 1.6.5 Acute otitis media. Different phases of the exudative stage. (a) Bulging in the posterior half of the tympanic membrane (right ear). (b) Slight bulging of the tympanic membrane (left ear). (c) Due to bulging the malleus handle cannot be differentiated (right ear). (d) More severe bulging (right ear). (e) More severe bulging and opaque tympanic membrane (left ear). There is conductive-type hearing loss a b c d e 1.6 Acute Otitis Media 31 Fig. 1.6.8 Suppurative stage in acute otitis media (right ear). (a) Puru- lent material filling the external ear canal and preventing the drum from being seen. (b) The small perforations in the tympanic membrane are seen after cleaning the purulent material in the external ear a b Fig. 1.6.7 Acute hemorrhagic otitis media in the right ear. There is severe bulging associated with severe ear pain. Due to extensive bulging, white-colored epithelium is seen on the tympanic mem- brane. The malleus cannot be identified Fig. 1.6.6 Acute hemorrhagic otitis media in the right ear. Bulging of the tympanic membrane due to hemorrhagic purulent material in the middle ear E A R N O S E T H R O A T A N D N E C K 34 Chapter 1 Ear 1.7 Chronic Otitis Media Fig. 1.7.1 Left ear. In the posteroinferior part of the tympanic mem- brane there is a central perforation. The epithelium goes into the middle ear from the anterior and inferior edges of the perforation. Anterior to the manubrium mallei the tympanic membrane is calci- fied. In the posterosuperior quadrant the tympanic membrane lies on the incus and stapes Fig. 1.7.2 Left ear. A central perforation in the anterosuperior quad- rant of the tympanic membrane. Through the perforation the eusta- chian tube orifice and tympanosclerotic middle ear mucosa are seen. The tympanic membrane appears to be tympanosclerotic Fig. 1.7.3 Right ear. Central perforation in the anteroinferior quad- rant of the tympanic membrane. Pseudomembranous tympanic membrane in the anterosuperior quadrant. The middle ear mucosa and the tympanic membrane are tympanosclerotic. Just posteroinfe- rior to the umbo, the tympanic membrane is thickened by fibrous tissue and embedded with calcium. Tympanosclerosis is the collec- tion of collagen and calcium in the submucosal layer in the tympanic membrane or middle ear mucosa. It is a healing process of the body. Especially after ventilation tube insertion, white calcium deposits may be seen due to submucosal bleeding. Such tympanosclerotic plaques may be large enough to interfere with normal tympanic membrane function. In the middle ear mucosa it may cause fixation of the ossicles and may lead to conductive-type hearing loss Fig. 1.7.4 Left ear. Anteroinferior central perforation. At the postero- inferior location of the perforation, polypoid granulation tissue is present; the middle ear mucosa is hyperemic and edematous. There are calcified plaques in the tympanic membrane 1.7 Chronic Otitis Media 35 Fig. 1.7.5 Right ear. Central perforation with tympanosclerosis in the middle ear. The tympanic membrane tries to close the perforation and a pseudomembrane formation is seen Fig. 1.7.6 Right ear. The anterior part is tympanosclerotic. The filter paper used to close the perforation is transported out onto the exter- nal ear canal and a replacement membrane closing the perforation is seen; however, there is a very small perforation still remaining between the filter paper and the pseudomembrane Fig. 1.7.7 Left ear. Acute infection in a patient with chronic otitis media. Purulent drainage in the external ear canal. There is a 3-mm central perforation in the tympanic membrane. Anterosuperior to the perforation there is polypoid tissue formation. The middle ear mucosa is edematous and hyperemic Fig. 1.7.8 Right ear. Short process of the malleus and malleus handle can be seen. Just above the short process, attic perforation is seen. Posterior to the malleus handle, the tympanic membrane is severely retracted and lies on the promontorium and incudostapedial joint. The long process of the incus, lenticular process, incudostapedial joint, and stapes tendon are seen behind the adhesive and thinned tympanic membrane E A R N O S E T H R O A T A N D N E C K 36 Chapter 1 Ear Fig. 1.7.9 Correct instillation of ear drops. First, any debris or dis- charge in the external ear canal is cleaned. The auricle is pulled upward and backward. Subsequently, five to six drops (or more if needed) are introduced into the ear canal (help may be needed). Tragal massage may help the drops go into the middle ear. The patient is kept in that position for 2–3 min. Cotton wool is placed in the ear canal and can be removed 10 min later Fig. 1.7.11 Right ear. The tympanic membrane in the posterosupe- rior quadrant behind the malleus handle is retracted. The retraction pocket has cerumen and keratin debris and the apex of the retraction pocket cannot be identified Fig. 1.7.10 Right ear. Attic perforation above the short process of the malleus after cleaning the epithelial debris Fig. 1.7.12 Right ear. The tympanic membrane is retracted postero- superiorly toward the antrum area. The bone over the retraction pocket is destroyed. The incus is eroded. The epithelium at the apex of the retraction pocket is seen. The chorda tympani nerve is visible behind the thinned retracted tympanic membrane 1.7 Chronic Otitis Media 39 Fig. 1.7.20 Right ear. Nearly total tympanic membrane perforation. Short process of the malleus, malleus handle, long process of the incus, incudostapedial joint, stapes, and posterior crus of the stapes are seen. The mucopurulent material is seen around the footplate and in the round window niche Fig. 1.7.21 Left ear. Nearly total tympanic membrane perforation. Posterior to the promontory, round window niche; posterosuperior to the promontory, stapes, footplate, and stapes tendon; above the stapes, facial nerve canal; and in the anterosuperior part of the mid- dle ear, tensor tympani muscle are seen Fig. 1.7.22 Left ear. Marginal perforation of the tympanic membrane in the posterior part. The remnant of the tympanic membrane is opaque and thickened. Ivory-colored cholesteatoma mass is filling the whole middle ear cavity Fig. 1.7.23 A cholesteatoma mass removed from the ear, measuring approximately 4 cm in diameter E A R N O S E T H R O A T A N D N E C K 40 Chapter 1 Ear Fig. 1.7.24 Left ear. Atticoantrotomy cavity after keratin debris has been cleaned. The head of the malleus and the short process of the incus are seen in the cavity. There is a central perforation of 2 mm in the anteroinferior part of the tympanic membrane Fig. 1.7.25 Right ear. View after Bondy mastoidectomy. The tympanic membrane is slightly vascularized and retracted. The cholesteatoma is marsupialized into the external ear canal by the atticoantrotomy oper- ation. Bondy mastoidectomy is performed in cases of cholesteatoma that develop from the attic region and extend to the antrum cavity. Since the cholesteatoma mass does not extend into the middle ear cavity, there is no need to open the middle ear cavity. The cho- lesteatoma is followed and marsupialized into the external ear canal Fig. 1.7.26 Left ear. After myringoplasty the grafted tympanic mem- brane is very well vascularized. In the anterior part the fibrous annu- lus and membrane remnant are seen 1.8 Facial Nerve Paralysis 41 1.8 Facial Nerve Paralysis a b Fig. 1.8.3 Ramsey Hunt syndrome. (a) Vesicles in the right auricle. (b) Right-sided facial nerve paralysis; temporal MR image shows enhancement of the right facial nerve denoting viral infection of the facial nerve (courtesy of Dr. Sarac) Fig. 1.8.2 Bell’s palsy. When the patient closes his eyes, the eye on the paralyzed side rolls up (Courtesy of TESAV) Fig. 1.8.1 Facial nerve paralysis due to facial nerve absence at birth (Courtesy of TESAV) E A R N O S E T H R O A T A N D N E C K 44 Chapter 1 Ear Disease Fever Neurologic findings CSF findings Mastoiditis +++ – – Petrositis ++ + – Lateral sinus thrombophlebitisa +++ – – Otitic hydrocephalus – ± Pressure over 300 Bacterial meningitis +++ + + Extradural abscess ± – – Subdural abscess + ± – Brain abscess + + + Table 1.9.2 Main symptoms in otogenic complications a Chills are a highly diagnostic symptom associated with lateral sinus thrombophlebitis Extracranial Acute mastoiditis Facial nerve paralysis Acute suppurative labyrinthitis Petrositis Intracranial Meningitis Intracranial abscess Extradural abscess Subdural abscess Brain abscess Lateral sinus thrombophlebitis Otitic hydrocephalus Table 1.9.1 Complications of middle ear infections a b Fig. 1.9.4 Right temporal lobe abscess in a chronic otitis media patient with cholesteatoma. (a) Coronal view, (b) axial view 1.10 Hearing Loss 45 1.10 Hearing Loss Fig. 1.10.3 In stapes surgery, the stapes suprastructure is removed and a hole is created in the footplate for a Teflon piston. The Teflon piston is placed in the footplate and hung on the long process of the incus which creates a bridge instead of the stapes (courtesy of Sennaroğlu) Fig. 1.10.2 Temporal bone section. Otosclerosis causing obstruction in the vestibular aqueduct and endolymphatic hydrops in all turns of the cochlea (courtesy of Paparella, Paparella otopathology lab director) Fig. 1.10.1 Inflammation in the labyrinth of a patient with total hear- ing loss following suppurative labyrinthitis (courtesy of Paparella, Paparella otopathology lab director) Fig. 1.10.4 Extruded metal piston in the external auditory canal in a patient who had undergone otosclerosis surgery in the past E A R N O S E T H R O A T A N D N E C K 46 Chapter 1 Ear b a Fig. 1.10.7 (a) Temporal MR image. Glomus jugulare tumor on the right side extending to the hypotympanum. (b) Angiography shows hypervascularized glomus tumor Fig. 1.10.5 Glomus jugulare. A pink–bluish silhouette of a glomus tumor behind the tympanic membrane Fig. 1.10.6 Glomus jugulare tumor extending out to the external auditory canal Fig. 1.10.8 Right ear. Through the tympanic membrane perforation, the glomus tumor is seen to be localized in the hypotympanum. It is in contact with the incudostapedial joint 1.11 Otalgia 49 Fig. 1.11.4 Earache may also be seen in laryngeal carcinomas E A R N O S E T H R O A T A N D N E C K 50 Chapter 1 Ear 1.12 Temporal Bone Fractures Fig. 1.12.1 Axial CT scan. Transverse temporal bone fracture on the left side. High-resolution CT scans of the temporal bone provide nec- essary information about the fracture. Audiometric examination helps in the diagnosis Fig. 1.12.2 In longitudinal fractures, a fracture line at the posterosu- perior part of the external ear canal may be seen Fig. 1.12.3 Traumatic tympanic membrane perforation. These perfo- rations are sometimes seen after a blow to the ear. To be sure that the perforation is really traumatic, the physician should check that the edges of the perforation are irregular and hemorrhagic 1.12 Temporal Bone Fractures 51 Fig. 1.12.4 Schematic representation of longitudinal and transverse fractures. Temporal bone fractures are classified into two main groups: longitudinal and transverse fractures. Longitudinal fractures are much more frequent, with the incidence of longitudinal fractures being four times greater than transverse fractures. Generally, tempo- ral and parietal blows are associated with longitudinal fractures. Since the areas of the foramina are relatively weaker parts of the skull base, fractures tend to occur in their vicinity. Longitudinal fractures start in the squamous portion and go to the middle ear through the poste- rior and superior walls of the external ear canal and then to the petrous apex. Generally, conductive hearing loss is accompanied by longitudinal temporal bone fractures. Facial nerve injury may occur at the geniculate ganglion area and is only seen in 15% of longitudinal fractures. Tympanic membrane perforation or bleeding into the mid- dle ear may also be seen. Transverse fractures generally occur due to frontal or occipital trauma. Since the blow comes from anterior-pos- terior or posterior-anterior direction, the fracture line occurs at a right angle to the axis of the petrous bone and the fracture line starts from the foramen magnum or jugular foramen and extends to the middle ear. It frequently affects the facial nerve and inner ear. Hemotympanum may be associated with transverse fractures, but tympanic membrane perforation is not seen. Temporal bone fractures do not always follow these general guidelines, and some fractures are mixed. These frac- tures are evaluated according to the type of lesion Longitudinal Transverse Frequency (approximate %) 80 20 Hearing loss Conductive Sensorineural Vertigo Rare Frequent Facial nerve paralysis Rare (10–15%) Frequent (50%) Table 1.12.2 Differential diagnosis between longitudinal and transverse temporal fractures Head is elevated 30° Gaita softeners are prescribed Diuretics such as diazomide are given to decrease the CSF pressure Wide-spectrum antibiotics are started as prophylaxis against meningitis No packing is done to the external ear canal Table 1.12.1 How to treat CSF fistula How to Make the Diagnosis of CSF Draining from the External Ear Canal If the fluid is collected on a filtered paper or on a gauze, it forms a halo around the circle of blood. If the fluid can be collected in a tube, beta-2 transferrin positivity indicates CSF leak. E A R N O S E T H R O A T A N D N E C K 54 Chapter 1 Ear 1.14 Vertigo Duration No hearing loss With hearing loss Seconds Benign paroxysmal positional vertigo Minutes Vertebrobasilar insufficiency Hours Endolymphatic hydrops (Meniere disease) Days Vestibular neuritis Labyrinthitis Weeks Intracranial pathologies Multiple sclerosis Acoustic neurinoma, psychogenic Table 1.14.2 Differential diagnosis in vertigo according to duration Onset of vertigo Character of vertigo, real vertigo, or dizziness Duration Relationship to the movements of the head Other associated symptoms, tinnitus, hearing loss etc. Table 1.14.1 Anamnesis in vertigo patient Fig. 1.14.1 Normal appearance of Reissner’s membrane and the tec- torial membrane (courtesy of Paparella, Paparella otopathology lab director) Fig. 1.14.3 Profound endolymphatic hydrops in all turns of the cochlea (courtesy of Paparella, Paparella otopathology lab director) Fig. 1.14.4 Intracanalicular acoustic neuroma and serous labyrinthi- tis in the vestibule and cochlea (courtesy of Paparella, Paparella oto- pathology lab director) Fig. 1.14.2 Hydropic Reissner’s membrane in one turn of the cochlea (courtesy of Paparella, Paparella otopathology lab director) 1.14 Vertigo 55 Peripheral Central Latent period + – Adaptation + – Fatigue + – Table 1.14.4 Differential diagnosis in central and peripheral positional vertigo Peripheral Central Unsteadiness Slight, moderate Severe Nausea, vomiting Severe Slight Hearing symptoms Frequent Rare Neurologic symptoms Rare Frequent Compensation Fast Slow Table 1.14.3 Differential diagnosis in central and peripheral vertigo a b Fig. 1.14.6 (a) Balancing stone from inner ear. Color scanning elec- tron micrograph of crystals of calcium carbonate on the surface of an otolith. An otolith or otoconium is a calcified stone that is found in the otolith organs of the inner ear. They are attached to sensory hairs, and, when the head tilts, the movement of the stones causes nerve impulses that form the basis of the sense of balance. In humans, oto- conia can range in size from 3 to 30 µm (millionths of a meter) across (visual photos). (b) Dix Hallpike maneuver. The patient is brought to the supine position from the sitting position with the head turned to one side. The maneuver is repeated on the opposite side. The pres- ence of nystagmus or any feeling of movement is recorded Fig. 1.14.5 Temporal bone section. Otosclerosis causing obstruction in the vestibular aqueduct and endolymphatic hydrops in all turns of the cochlea (courtesy of Paparella, Paparella otopathology lab director) E A R N O S E T H R O A T A N D N E C K 56 Chapter 1 Ear Fig. 1.14.7 Epley maneuver for benign paroxysmal positional vertigo (BPPV). The patient is brought to the Dix Hallpike position, with the head turned 45° to the affected side. The head is then turned to the opposite side. The patient’s head is held in each position for 30 seconds. The whole body and head is brought to the lateral decubitus position. The patient is brought to the starting position-sitting position Fig. 1.14.8 (a-c) Acoustic neuroma on the right side. MR imaging is particularly useful in diagnosing acoustic neuroma. The lesions enhance with gadolinium injection a b c 2.1 The Common Cold and the Flu 59   Common cold Flu Virus Rhinovirus Influenza Contagiousness Droplets by inhalation or touch Droplets by inhalation Onset 1–3 days after virus entrance Sudden Duration One week One week or more Frequency Children six to eight colds per year, adults two to four colds per year Once Symptoms Milder Weakened senses of taste and smell, cough, runny or stuffy nose, sneezing, scratchy throat Worse Fever (39°C or above), body aches, extreme tiredness, dry cough more common, headache, sore throat, chills, tiredness Complications No serious complications May have serious complications, pneumonia, bacterial infections May be fatal in elderly, immunocompromised, and chronically ill patients Treatment Acetaminophen Antihistamine and/or decongestant Adequate fluid intake (eight glasses of water or juice) Avoid smoking and alcohol Avoid caffeine and alcohol No antibiotics Acetaminophen Antihistamine and/or decongestant Adequate fluid intake (eight glasses of water or juice) Avoid smoking and alcohol Avoid caffeine and alcohol No antibiotics Table 2.1.3 Clinical features of the common cold and flu Close contact with people who have a cold should be avoided especially during the first few days when they are most likely to spread the infection Hands should be washed after touching someone who has a cold Fingers should be kept away from the nose and the eyes to avoid self-infecting the cold virus particles A second hand towel should be put in the bathroom for healthy people to use The environment should be humidified The nose and the mouth should be covered with a tissue when coughing or sneezing Table 2.1.4 How to prevent a cold E A R N O S E T H R O A T A N D N E C K 60 Chapter 2 Nose 2.2 Rhinitis Rhinitis is a clinical diagnosis and is defined as inflammation of the nasal mucosa with one or more symptoms of sneezing, itching, rhinorrhea, and nasal blockage lasting for at least 1 h on most days. All diseases causing rhinorrhea and nasal obstruction should be considered in the differential diagnosis of rhinitis. Fig. 2.2.1 Allergic rhinitis. Serous nasal discharge with hypertrophic, pale inferior turbinates Fig. 2.2.2 Acute rhinitis, early period. Right inferior turbinate mucosa is hyperemic and there is serous secretion Fig. 2.2.3 Upper respiratory tract infection, 6th day, mucoid nasal discharge Fig. 2.2.4 Right acute maxillary sinusitis. Purulent nasal discharge with draining to the nasopharynx through the middle meatus 2.2 Rhinitis 61 Fig. 2.2.5 Chronic sinusitis, purulent discharge in left nasal cavity Fig. 2.2.6 Eosinophilic mucin in a patient with nonallergic rhinitis with eosinophilia syndrome (NARES). The discharge is sticky, thick, and yellow-green Fig. 2.2.7 Cerebrospinal fluid (CSF) rhinorrhea. Coronal CT showing fracture line in the fovea ethmoidalis of anterior ethmoid area E A R N O S E T H R O A T A N D N E C K 64 Chapter 2 Nose Antihypertensives Reserpine Guanethidine Phentolamine Methyldopa ACE inhibitors Alpha adrenoreceptor antagonists Topical ophthalmic beta blockers Chlorpromazine Aspirin Nonsteroidal anti-inflammatory agents Oral contraceptives Topical decongestants (rhinitis medicamentosa – long-term use of cocaine and nasal drops or sprays) Table 2.2.4 Drugs that can induce rhinitis Skin prick tests Specific IgE measurements Nasal smear Nasal provocation tests Histamine/methacholine Allergen Rhinomanometry Acoustic rhinometry CT, MR imaging Biopsy, electron microscopic examination Sweat test Table 2.2.3 Diagnostic tests for rhinitis   Seasonal Perennial Perennial nonallergic Time of year Seasonal Perennial Perennial Age of onset 10–20 10–20 Adulthood Prominent symptom Rhinorrhea, sneezing, itching Rhinorrhea, sneezing, itching Rhinorrhea, blockage Eye symptoms Common Uncommon Not present Nasal cytology EO (Eosinophil) EO EO/NT (Neutrophil) Allergens Pollens Dust mite, moulds, animal Negative Polyps Uncommon Uncommon Frequent Table 2.2.5 Diagnostic features of noninfectious rhinitis Fig. 2.2.12 Classification of rhinitis Rhinitis OthersChronicAcute Infectious rhinitis Nonallergic Rhinitis NARES Perennial Seasonal Allergic rhinitis 2.3 Allergic Rhinitis 65 2.3 Allergic Rhinitis Allergy is an inappropriate and harmful immune response to a normally harmless substance. Generally, allergens are proteins that do not cause any reactions in nonatopic individuals. What is atopy? Atopy is an inherited predisposition to produce IgE anti- bodies to certain substances. What is the difference between atopy and allergy? Atopy is the genetic predisposition to produce IgE anti- bodies. To develop allergy, stimulation of the cells of the immune system to produce IgE antibodies is needed. Although almost 25–30% of the population is atopic, not every atopic person develops allergy. Environmental factors are important in the development of allergic disease. Allergic Reaction Allergens enter the body through the airways, the gastroin- testinal tract, or the skin. In atopic patients an allergen is rec- ognized as being foreign to the immune system. B cells are stimulated to produce specific IgE antibodies. These IgE antibodies bind to the surface of mast cells. On subsequent exposures, the allergens bind to the IgE antibodies. Bridging two IgE antibodies makes the mast cell degranulate and the mast cell releases histamine and other cytokines that cause allergic reactions. Early Response The early response is initiated after bridging of IgE antibod- ies on the mast cells. Mast cells release mediators such as histamine, prostaglandins, leukotrienes, platelet-activating factor, and bradykinin. These mediators cause vascular dila- tation, increased permeability, and attract inflammatory cells into the tissues starting the inflammation. The early response is characterized by sneezing, rhinorrhea, bronchoconstric- tion, and increased bronchial responsiveness. Late Response The mediators released from mast cells attract inflammatory cells such as eosinophils, lymphocytes, neutrophils, and monocytes into the tissues. Therefore, the late response is a cell-mediated response. The late response is characterized by prolonged mucus secretion, edema formation, and bronchial hyperresponsiveness. Fig. 2.3.1 (a, b) Allergic rhinitis. The turbinates are pale, bluish, and swollen. Watery serous secretion is seen in both nasal passages a b E A R N O S E T H R O A T A N D N E C K 66 Chapter 2 Nose Fig. 2.3.7 Allergic conjunctivitis, erythema, and edema of the con- junctival mucosa, and watering. Limbal elevation can be identified (courtesy of Kıratlı D) Fig. 2.3.3 Supratip crease. Horizontal line in the supratip area due to repeated use of allergic salute Fig. 2.3.5 Skin prick test Fig. 2.3.6 Items that should not be present in the room of an allergic child Fig. 2.3.2 Allergy salute is a very common sign of allergic rhinitis in children Fig. 2.3.4 Long, silky eyelashes in an allergic child 2.4 Nasal Vestibulitis and Nasal Furunculosis and Mucormycosis 69 2.4 Nasal Vestibulitis and Nasal Furunculosis and Mucormycosis Infection of the skin of the nasal vestibule is termed nasal vestibulitis. It may be secondary to constant rhinorrhea, nose picking, or viral infections such as herpes simplex and her- pes zoster. Foreign bodies frequently cause vestibulitis in children due to purulent discharge. Nasal furunculosis is Staphylococcus aureus infection of the hair follicles. Nose picking is a frequent cause of furunculosis. Topical and if necessary systemic antibiotics are prescribed. The patient should be instructed not to squeeze out pus from this area. Since the veins draining this area are valveless and directly join the cavernous sinus, there is a potential risk of spreading infection to the cavernous sinus via these facial veins. Eczema may also mimic vestibulitis. In these cases steroid base ointment may help the patient. In persistent vestibulitis, neoplastic diseases such as basal cell or squamous cell carci- noma should be kept in mind. Fig. 2.4.1 Nasal vestibulitis on the left side. Note the slight edema and hyperemia as well as excoriation of the skin on the left side Fig. 2.4.2 If not treated, the infection in the nasal vestibule may spread to the upper lip. The upper lip on the right side appears hype- remic and edematous Fig. 2.4.3 Furunculosis in the nasal vestibule with spread of the infection to the nasal tip and dorsum Fig. 2.4.4 Infection starting as nasal vestibulitis with spread of infec- tion to the nasal dorsum and right periorbital area E A R N O S E T H R O A T A N D N E C K 70 Chapter 2 Nose Fig. 2.4.5 Venous drainage of the nose. (a) frontal view, (b) Lateral view. Since the veins draining this area are valveless and directly join the cavernous sinus, there is a potential risk of spreading infection to the cavernous sinus via these facial veins. This area of the nose is termed the danger triangle. Squeezing the pus from this area should be avoided a b Fig. 2.4.6 Constant rhinorrhea and the need to wipe the nose due to allergic rhinitis have resulted in vestibulitis Fig. 2.4.8 Hyperemia and edema in the columella and nasal tip mim- icking severe vestibulitis secondary to squamous cell carcinoma infil- tration. The neoplastic lesion is filling the left nasal passage Fig. 2.4.7 Right alar rim. Basal cell carcinoma with slight hyperemia around it. In persistent vestibulitis, neoplastic diseases such as basal cell or squamous cell carcinoma should be kept in mind 2.4 Nasal Vestibulitis and Nasal Furunculosis and Mucormycosis 71 Fig. 2.4.10 Mucormycosis in a child with leukemia. Gross tissue necrosis with a black eschar is characteristic of mucormycosis Fig. 2.4.9 Mucormycosis in a diabetic patient. Mucormycosis may infect different areas of the body, but the most frequent fatal form is the rhinocerebral form. (a) Necrotic areas on the face, (b) black necrotic areas in the nasal mucosa, (c) and after removal of necrotic area in the nose a b c Fig. 2.4.11 (a, b) Mucormycosis in an immunocompromised child. The disease progresses rapidly with extension of tissue necrosis out of the nose into the orbit and face. Local management requires wide deb- ridement of necrotic tissue with a margin of normal-appearing tissue (Courtesy of TESAV) a b E A R N O S E T H R O A T A N D N E C K 74 Chapter 2 Nose Fig. 2.5.5 Nasal discharge. (a) Mucoid drainage after common cold; (b) purulent drainage in the inferior meatus; (c) postnasal purulent drain- age; (d) allergic mucin: viscid, thick yellow–green drainage, generally eosinophilic a b c d 2.5 Sinusitis 75 Fig. 2.5.6 Waters view showing right acute maxillary sinusitis. There is an air–fluid level in the right maxillary sinus Fig. 2.5.7 Transillumination of the frontal sinus. In frontal sinusitis the frontal sinus fails to transilluminate Fig. 2.5.8 (a) Coronal CT shows bilateral maxillary sinusitis; (b) 15 days after starting medical treatment the sinuses appear to be normal a b Fig. 2.5.9 Maxillary sinus irrigation. An opening is created via the infe- rior meatus between the nose and maxillary sinus or via canine fossa E A R N O S E T H R O A T A N D N E C K 76 Chapter 2 Nose Fig. 2.5.10 The purpose of endoscopic sinus surgery is to restore ventilation and drainage of the paranasal sinuses. (a) Preoperative and (b) postoperative view Fig. 2.5.11 (a) Epithelized sinuses and normal mucosa of the sinuses after endoscopic sinus surgery. (b) Coronal CT after surgery shows that all sinuses are clean and ostia are open a b Fig. 2.5.12 Coronal paranasal sinus CT showing previously per- formed bilateral Caldwell-Luc operation. Note that both nasoantral windows in the inferior meatus are widely open ER atado aa Diagnosis in Pd ryngolog An Illustrated Guide T. Metin Önerci Diagnosis in Otorhinolaryngology Contenti Preface In preparing the material for this book, I took the advice of my students who generously shared their views and opinions with me. I was told that it would be preferable to have images of the various diseases with legends describing the disease. Students would be able to learn and retain the infor- mation more successfully if the material was accompanied by pictures and schematic drawings. Recent advances in technology have made it possible to photograph regions that are difficult to view with the naked eye, such as the ear, nose, throat, nasopharynx, and larynx – all the areas of otorhinolaryngology. Such an illustrated text in this field is important and necessary for teaching purposes. In this book I tried to compile images of the basic conditions that are commonly seen in general practice and to give the reader a visual survey with a brief description of the condition. I added tables and schematic drawings in order to provide practical information. It is not the purpose of this book to be a comprehensive textbook, since many textbooks are already available with more detailed information of the conditions illustrated here. This book is primarily intended for medical students, family and general practitioners, and ENT trainees. It may also serve as basic reading material for those in allied specialties. I hope my colleagues find this book useful and it contributes toward their teaching purposes. Ankara, Turkey T. Metin Önerci Contents Chapter 1 Ear 1.1 Ear Anatomy 2 1.2 ENT Examination 8 1.3 The Pinna 14 1.4 External Ear Canal 18 1.5 Otitis Media with Effusion 24 1.6 Acute Otitis Media 28 1.7 Chronic Otitis Media 34 1.8 Facial Nerve Paralysis 41 1.9 Complications of Otitis Media 43 1.10 Hearing Loss 45 1.11 Otalgia 48 1.12 Temporal Bone Fractures 50 1.13 Tinnitus 52 1.14 Vertigo 54 Chapter 2 Nose 2.1 The Common Cold and the Flu 58 2.2 Rhinitis 60 2.3 Allergic Rhinitis 65 2.4 Nasal Vestibulitis and Nasal Furunculosis and Mucormycosis 69 2.5 Sinusitis 72 2.6 Complications of Sinusitis 79 2.7 Nasal Polyposis 87 2.8 Nasal Obstruction 92 2.9 Septum 97 2.10 Epistaxis 101 2.11 Traumas 104 2.12 Dacryocystorhinostomy 110 2.13 Tumors 112 Chapter 3 Throat & Neck 3.1 Acute Tonsillopharyngitis 122 3.2 Adenoids 126 3.3 Snoring 129 3.4 Temporomandibular Joint 132 3.5 Airway Obstructions 134 3.6 Hoarseness 137 3.7 Cysts 143 3.8 Parotid Tumors 147 3.9 Oral Cavity 151 3.10 Neck Masses 159 3.11 Neck Malignancies 168 1.1 Ear Anatomy 2 1.2 ENT Examination 8 1.3 The Pinna 14 1.4 External Ear Canal 18 1.5 Otitis Media with Effusion 24 1.6 Acute Otitis Media 28 1.7 Chronic Otitis Media 34 1.8 Facial Nerve Paralysis 41 1.9 Complications of Otitis Media 43 1.10 Hearing Loss 45 1.11 Otalgia 48 1.12 Temporal Bone Fractures 50 1.13 Tinnitus 52 1.14 Vertigo 54 C O N T E N T S T. Metin Önerci: Diagnosis in Otorhinolaryngology DOI: 10.1007 / 978-3-642-00499-5,  Springer-Verlag Berlin Heidelberg 2009 1 Chapter 1 EAR 4 Chapter 1 Ear Fig. 1.1.6 Due to the differences in the physical properties of air and water, sound vibrations in the air are largely reflected away from the surface of water (99.9% of the energy of air-borne sound is reflected away), with only 0.1% entering the water. Although the surface area of the tympanic membrane is 85–90 mm2, the effective vibrating area of the tympanic membrane is 55 mm2. The surface area of the foot- plate is 3.2 mm2. The ratio of the surface areas of the tympanic mem- brane and the footplate is 55/3.2 = 17.1. This represents the hydraulic ratio of the tympanic membrane and stapes footplate, producing an increase force at the oval window of 17 times for the human ear, since the sound pressure level is equal to the force divided by the surface area (P = F/a). The final transformer ratio of the human tympanic membrane and ossicular chain is the product of the lever ratio of 1.3 times the hydraulic ratio of 17, which equals 22. This gain compen- sates the loss due to the air–bone difference Fig. 1.1.5 False-color scanning electron micrograph (SEM) of the three smallest bones in the human body responsible for conduction of sound waves in the middle ear. At the top left is the malleus (ham- mer), which strikes the incus (anvil – right of malleus); the incus is joined to the stapes (stirrups), which conducts sound toward the inner ear. Sound waves enter the ear through the external auditory meatus and cause the eardrum to vibrate. Vibrations from the ear- drum are passed to the malleus and then the stapes via the incus. The stapes transmits the vibrations to the fluid-filled cochlea of the inner ear where the vibrations are converted to nerve impulses. Lever effect: the manubrium mallei is 1.3 times longer than the long pro- cess of the incus. This difference in the lengths of the manubrium mallei and long process of the incus contributes a lever factor of 1.3 to increase the intensity of the sound (visual photos) 1.1 Ear Anatomy 5 Fig. 1.1.8 The inner ear comprises the cochlea and the labyrinth. The labyrinth consists of three semicircular canals (superior, posterior, and lateral) and two otolithic organs (utricle and saccule). The utricu- lar duct and the saccular duct join to form the endolymphatic duct Fig. 1.1.9 The cochlea has three fluid-filled compartments: the scala tympani, the scala vestibuli, and the scala media, which contains the organ of Corti (courtesy of Paparella, Paparella otopathology lab director) a b c Fig. 1.1.7 (a–c) The temporal bone contains the ear. It has five parts: the bony external ear canal, the styloid process, the squamous por- tion, the petrous portion, and the mastoid process. There are suture lines between these various portions such as the petrotympanic fis- sure, petrosquamous suture, tympanosquamous suture, tympano- mastoid suture etc. The mastoid process is not present at birth, which makes the facial nerve very superficial E A R N O S E T H R O A T A N D N E C K 6 Chapter 1 Ear Fig. 1.1.10 Inner ear organ of Corti. Color SEM of a section through the human inner ear, showing the organ of Corti (spiral organ). At the top right can be seen four rows of hair cells, supported by pillar-like Dieter cells. Each hair cell contains up to 100 individual hairs. The hairs translate mechanical movement caused by their displacement by sound waves into electrical impulses, which are transmitted to the brain via the cochlear nerve (visual photos) Fig. 1.1.11 Sensory hair cells in the ear. Color SEM of hair cells in the cochlea, the inner ear’s auditory sense organ. The crescent-shaped areas across the center are numerous stereocilia, and are located on top of supporting hair cells. Sound waves entering the inner ear displace the fluid that surrounds the stereocilia, causing them to bend. This triggers a response in the hair cells, which release neurotrans- mitter chemicals that generate nerve impulses. The nerve impulses travel to the brain along the auditory nerve. This process can transmit informa- tion about the loudness and pitch of a sound. Magnification: ×2,000 when printed 10 cm wide (visual photos) 1.2 ENT Examination 9 Fig. 1.2.5 Audiometer to test hearing Fig. 1.2.4 Soundproof hearing test rooms Rinne (diseased ear) Weber Type of hearing loss Positive Not lateralized Normal hearing Positive Lateralized to the better ear Sensorineural hearing loss Negative Lateralized to the diseased ear Conductive hearing loss Negative Lateralized to the better ear Total sensorineural hearing loss Table 1.2.1 Tuning fork tests and type of hearing loss 125 250 500 1000 2000 4000 8000 -10 0 10 20 30 40 50 60 70 80 90 100 110 Is it m e S ev iy es i d B ( IS O - 1 96 4) Frekanslar (HZ) 750 1500 3000 6000 125 250 500 1000 2000 4000 8000 -10 0 10 20 30 40 50 60 70 80 90 100 110 120 Is it m e S ev iy es i d B ( IS O - 1 96 4) Frekanslar (HZ) 750 1500 3000 6000 125 250 500 1000 2000 4000 8000 -10 0 10 20 30 40 50 60 70 80 90 100 110 120 Is it m e S ev iy es i d B ( IS O - 1 96 4) Frekanslar (HZ) a b c Fig. 1.2.6 Audiograms. (a) Normal hearing curve, (b) hearing loss due to acoustic trauma, (c) conductive-type hearing loss due to otosclerosis E A R N O S E T H R O A T A N D N E C K 10 Chapter 1 Ear a Fig. 1.2.8 Auditory brain stem response test. (a) Illustration showing the organs of hearing and the cerebellum. Sound waves are chan- neled by the pinna (visible part of the ear) into the auditory canal (pink) toward the eardrum. The eardrum transmits the vibrations to three tiny bones, the malleus, incus, and stapes, in the middle ear. The stapes passes the vibrations to the inner ear structures (purple), the semicircular canals and the cochlea (spiral). Auditory sensations are picked up by the cochlear nerve (yellow) and transmitted to the medulla (brain stem), the thalamus, and ultimately the cerebral cor- tex (visual photos). (b) The source of potentials. (c) Normal auditory brain stem response with six waves from five different anatomic sites Tympanometry Tympanometry is an indirect measure of the mobility (com- pliance) of the tympanic membrane and ossicular chain under different pressures. The mobility of the tympanic membrane is greatest when the pressure on both sides of the tympanic membrane is equal. Compliance is reduced as air pressure is increased or decreased from normal. High acous- tic energy is applied in the ear canal, some of this energy is absorbed and the remainder is reflected back and received by the probe. When the mobility is decreased, the energy is reflected more than the normal. In ears filled with fluid, tym- panic membrane thickening, or ossicular chain stiffening, the reflected energy is greater than in normal ears. Fig. 1.2.7 Classification of tympanograms. (a) Type A: The curve peaks at 0 mm H 2 O, indicating no pressure difference exists between the middle ear and the external environment. (If the peak of the curve is lower than the normal type A curve, stiffening of the ossicu- lar chain is often associated. If the peak of the curve is very high, it suggests ossicular discontinuity). (b) Type B: The tympanogram is relatively flat or dome shaped. This shows little change in the reflec- tive quality of the tympano-ossicular system as air pressures change in the external canal. This type of tympanogram is generally associ- ated with middle ear fluid. (c) Type C: The peak of the curve occurs with higher negative pressures (maximum compliance is reached at negative pressures, meaning the pressure in the middle ear is nega- tive). This curve indicates eustachian tube dysfunction 1.2 ENT Examination 11 Anatomic localization Wave Cochlea, eighth nerve I and II Cochlear nucleus III Olivary complex IV Lateral lemniscus V Inferior colliculus VI Table 1.2.2 The source of the potentials (Fig. 1.2.8 a, b, c) Fig. 1.2.9 Dix Hallpike maneuver for benign positional vertigo. Bringing the head to the head-hanging position may cause vertigo and nystagmus Peripheral Central Latent period + – Adaptationa + – Fatiguea + – Table 1.2.3 Differential diagnosis in positional vertigo aVertigo adapts by holding the patient’s head in the same position; ver- tigo fatigues on repeated positioning. Fig. 1.2.10 (a, b) Temporal bone CT scans. External auditory meatus, middle ear cavity, attic, mastoid aircells, cochlea, semicircular canals, and internal acoustic canal (and falciform crest in the internal acous- tic canal) can be seen a b b c Fig. 1.2.8 (Continued) E A R N O S E T H R O A T A N D N E C K 14 Chapter 1 Ear 1.3 The Pinna b a Fig. 1.3.1 (a) Preauricular skin tags are generally unilateral. They can be removed before school age if they cause cosmetic deformities. (b) Cartilage remnants in front of the tragus Fig. 1.3.2 Preauricular fistulas are due to fusion abnormalities dur- ing embryogenic development of the auricle. Seventy-five percent of cases are unilateral. If the orifice of the fistula is narrow, the debris may occlude the orifice and cause secondary infection. The whole sinus tract should be removed surgically Fig. 1.3.3 Macrotia is a large pinna Fig. 1.3.4 Prominent ear. (a) Posterior view before the operation and (b) 3 months after the operation. In prominent ears, the fold of the antihelix is either absent or poorly formed and the angle between the posterior surface of the conchal cartilage and the cranium is over 300°. There is an autosomal dominant inheritance. It is also referred to as bat ears or lop ears. Prominent ears should be corrected before school age, between 4 and 6 years a b 1.3 The Pinna 15 a b c d e f Fig. 1.3.5 Abnormalities of the auricle range from minor abnormalities that require no treatment to total absence of the pinna. Since the embryo- logical development of the pinna is completely different from the middle and inner ear, it is not generally associated with middle and inner ear abnormali- ties. However, atresia of the external ear canal may accompany microtia. (a, b) In type I microtia deformity, the deformity is only limited to the helix and antihelix and it is a minimal deformity. (c, d) In type II there is severe deformity, although the remnant of the pinna is present. (e, f) In type III deformity there is no pinna. Generally the external ear canal is completely atresic. In some patients the lobule may be present. The optimum age for surgery is around 5 years, until the other auricle reaches its adult size and the costal cartilage development is sufficient to be used in reconstruction. It is also important to operate on children before school age Fig. 1.3.6 In the complete absence of the auricle, an auricular implant may give a natural appearance Fig. 1.3.7 Sebaceous cyst in the postauricular sulcus. Complete removal is necessary to prevent recurrences E A R N O S E T H R O A T A N D N E C K 16 Chapter 1 Ear ca b Fig. 1.3.12 (a) Neurofibromas of the pinna. (b) Axial CT image shows massive involvement of the deep tissue planes. (c) Cafe-au-lait spots, which are characteristic of NF1, are also frequently seen in patients with NF2. Neurofibromas may be solitary or may occur as part of neu- rofibromatosis in patients with Recklinghausen’s disease. Solitary neurofibromas should be excised if they cause functional or cosmetic problems. Since these tumors have malignant potential, any change in the behavior of the tumor such as sudden increase in size, pain etc. should warn the surgeon about the possibility of malignancy. Extensive surgery is required for massive tumours. Conservative management is the best option Fig. 1.3.11 Hemangioma at the auricle. These tumors may regress spontaneously. Steroid treatment for young patients under 1 year of age may be useful (Courtesy of TESAV) Fig. 1.3.10 A burn in the preauricular skin and pinna due to cleaning with pure antiseptic agent (Courtesy of TESAV) Fig. 1.3.8 A benign mass located in the anteroinferior part of the helix Fig. 1.3.9 Malignant tumor in the auricle 1.4 External Ear Canal 19 Fig. 1.4.3 (a, b) Cerumen may cover the tympanic membrane like a layer and may give the impression of a pathologic eardrum. After cleaning the cerumen, the normal tympanic membrane is seen b a Fig. 1.4.4 In some people there is excessive cerumen production. The cerumen is generally occluded in the narrowest part of the exter- nal ear canal at its midportion. These patients need periodic cleaning. Use of cotton swabs can push the cerumen deeper in the ear canal, which occludes the ear canal completely and makes removal more difficult a b Fig. 1.4.5 (a) Removal of cerumen is done either by an ear curette or syringing. Adequate visualization and exposure is necessary to avoid trauma. If the cerumen is not hard enough, it may be removed with suction after being softened by ear drops. (b) Water irrigation is another method. After the ear canal has been straightened by pulling the pinna backward and upward, water at body temperature is administered in the posterosuperior direction. The water passes between the ear canal and the cerumen and pushes the cerumen outward. If the tympanic membrane is perforated, ear irrigation should not be done E A R N O S E T H R O A T A N D N E C K 20 Chapter 1 Ear Fig. 1.4.6 Anterior wall of the external ear canal is prominent pre- venting the anterior part of the eardrum from being seen Fig. 1.4.7 (a, b) Exostoses may narrow the external ear canal and may cause debris and cerumen to collect behind them. They are generally seen in swimmers. They are bony, hard, and usually remain small and symptom free. They do not require any treatment unless they cause problems a b Fig. 1.4.8 External auditory canal stenosis in a diabetic patient due to recurrent ear canal infections and trauma 1.4 External Ear Canal 21 Fig. 1.4.9 Acute otitis externa. The ear canal is hyperemic and nar- rowed due to swelling. Manipulation of the auricle or tragus is painful Fig. 1.4.10 Acute otitis externa. The ear canal is slightly narrowed due to swelling and is full of cerumen and purulent material Fig. 1.4.11 (a, b) Otomycosis. Several fungi may cause infections in the external ear canal. The most common type is Aspergillus (A. niger or A. flavus). Candida may occasionally be the agent. Fungal hyphae may be seen in the external ear canal a b E A R N O S E T H R O A T A N D N E C K 24 Chapter 1 Ear 1.5 Otitis Media with Effusion Fig. 1.5.1 (a) Right ear. Otitis media with effusion. Air–fluid level can be seen behind the transparent tympanic membrane. (b) Left ear. Air bubbles within the tympanic cavity a b Fig. 1.5.2 Right ear. The tympanic membrane is vascularized and the transparency of the tympanic membrane is slightly diminished Fig. 1.5.3 Right ear: otitis media with effusion. In long-standing effu- sions the tympanic membrane has a dull or opaque appearance with vascularization on it 1.5 Otitis Media with Effusion 25 Fig. 1.5.4 Right ear. Otitis media with effusion. The tympanic mem- brane is opaque, has lost its transparency, is vascularized, and retracted. Please note that the light reflex is shorter and moved upward due to retraction of the tympanic membrane Fig. 1.5.5 Left ear. Otitis media with effusion. Retractions occur mostly in the weak parts of the tympanic membrane, such as the pseudomembranous parts or pars flaccida due to middle ear nega- tive pressures Fig. 1.5.6 Right ear. In long-standing effusions the retraction pock- ets most frequently develop in the posterosuperior part of the tym- panic membrane. The retraction pocket just behind the malleus handle is seen and its apex can be identified. The pocket is clean con- taining no debris. The membrane lies on the incus and stapes. Behind the translucent thinned tympanic membrane, the incudostapedial joint and stapes tendon are clearly seen Fig. 1.5.7 Right ear. Retraction pocket with debris in it E A R N O S E T H R O A T A N D N E C K 26 Chapter 1 Ear Fig. 1.5.11 Thick and sticky mucoid material obtained from the mid- dle ear in a patient with otitis media with effusion Fig. 1.5.8 Left ear. Adhesive otitis media. The tympanic membrane is thinned and lies on the promontorium. The short process of the mal- leus and malleus handle is more prominent due to retraction of the membrane. Fibrous annulus is clearly identified Fig. 1.5.9 Right ear. Otitis media with effusion due to nasopharyn- geal carcinoma. Amber color and retraction of the tympanic mem- brane. A unilateral otitis media with effusion in adults always necessitates a detailed search for nasopharyngeal carcinoma Fig. 1.5.10 Mucoid material in the external ear canal after myringo- tomy in otitis media with effusion 1.6 Acute Otitis Media 29 Fig. 1.6.3 Bullous myringitis in (a) the right ear and (b) the left ear. The malleus handle is hardly visible. Bullous myringitis is due to a viral or Mycoplasma pneumoniae infection of the tympanic mem- brane. There is severe ear pain, but no hearing loss. Draining the blebs may provide immediate relief from pain. Only the outer epithe- lial layer should be punctured. Complete puncturing of the tympanic membrane may result in perforation b a a b c Fig. 1.6.4 Acute otitis media, hyperemia stage. (a) Hypere mia in the attic region of the left ear; the patient complains of ear pain only for the last one hour (b) Hyperemia in the attic region and the posterosu- perior part of the tympanic membrane of the left ear; the patient com- plains of ear pain only for the last three hours (c) Hyperemia in the attic region and the posterosuperior part of the tympanic membrane of the right ear; slight bulging of the tympanic membrane has started E A R N O S E T H R O A T A N D N E C K 30 Chapter 1 Ear Fig. 1.6.5 Acute otitis media. Different phases of the exudative stage. (a) Bulging in the posterior half of the tympanic membrane (right ear). (b) Slight bulging of the tympanic membrane (left ear). (c) Due to bulging the malleus handle cannot be differentiated (right ear). (d) More severe bulging (right ear). (e) More severe bulging and opaque tympanic membrane (left ear). There is conductive-type hearing loss a b c d e 1.6 Acute Otitis Media 31 Fig. 1.6.8 Suppurative stage in acute otitis media (right ear). (a) Puru- lent material filling the external ear canal and preventing the drum from being seen. (b) The small perforations in the tympanic membrane are seen after cleaning the purulent material in the external ear a b Fig. 1.6.7 Acute hemorrhagic otitis media in the right ear. There is severe bulging associated with severe ear pain. Due to extensive bulging, white-colored epithelium is seen on the tympanic mem- brane. The malleus cannot be identified Fig. 1.6.6 Acute hemorrhagic otitis media in the right ear. Bulging of the tympanic membrane due to hemorrhagic purulent material in the middle ear E A R N O S E T H R O A T A N D N E C K 34 Chapter 1 Ear 1.7 Chronic Otitis Media Fig. 1.7.1 Left ear. In the posteroinferior part of the tympanic mem- brane there is a central perforation. The epithelium goes into the middle ear from the anterior and inferior edges of the perforation. Anterior to the manubrium mallei the tympanic membrane is calci- fied. In the posterosuperior quadrant the tympanic membrane lies on the incus and stapes Fig. 1.7.2 Left ear. A central perforation in the anterosuperior quad- rant of the tympanic membrane. Through the perforation the eusta- chian tube orifice and tympanosclerotic middle ear mucosa are seen. The tympanic membrane appears to be tympanosclerotic Fig. 1.7.3 Right ear. Central perforation in the anteroinferior quad- rant of the tympanic membrane. Pseudomembranous tympanic membrane in the anterosuperior quadrant. The middle ear mucosa and the tympanic membrane are tympanosclerotic. Just posteroinfe- rior to the umbo, the tympanic membrane is thickened by fibrous tissue and embedded with calcium. Tympanosclerosis is the collec- tion of collagen and calcium in the submucosal layer in the tympanic membrane or middle ear mucosa. It is a healing process of the body. Especially after ventilation tube insertion, white calcium deposits may be seen due to submucosal bleeding. Such tympanosclerotic plaques may be large enough to interfere with normal tympanic membrane function. In the middle ear mucosa it may cause fixation of the ossicles and may lead to conductive-type hearing loss Fig. 1.7.4 Left ear. Anteroinferior central perforation. At the postero- inferior location of the perforation, polypoid granulation tissue is present; the middle ear mucosa is hyperemic and edematous. There are calcified plaques in the tympanic membrane 1.7 Chronic Otitis Media 35 Fig. 1.7.5 Right ear. Central perforation with tympanosclerosis in the middle ear. The tympanic membrane tries to close the perforation and a pseudomembrane formation is seen Fig. 1.7.6 Right ear. The anterior part is tympanosclerotic. The filter paper used to close the perforation is transported out onto the exter- nal ear canal and a replacement membrane closing the perforation is seen; however, there is a very small perforation still remaining between the filter paper and the pseudomembrane Fig. 1.7.7 Left ear. Acute infection in a patient with chronic otitis media. Purulent drainage in the external ear canal. There is a 3-mm central perforation in the tympanic membrane. Anterosuperior to the perforation there is polypoid tissue formation. The middle ear mucosa is edematous and hyperemic Fig. 1.7.8 Right ear. Short process of the malleus and malleus handle can be seen. Just above the short process, attic perforation is seen. Posterior to the malleus handle, the tympanic membrane is severely retracted and lies on the promontorium and incudostapedial joint. The long process of the incus, lenticular process, incudostapedial joint, and stapes tendon are seen behind the adhesive and thinned tympanic membrane E A R N O S E T H R O A T A N D N E C K 36 Chapter 1 Ear Fig. 1.7.9 Correct instillation of ear drops. First, any debris or dis- charge in the external ear canal is cleaned. The auricle is pulled upward and backward. Subsequently, five to six drops (or more if needed) are introduced into the ear canal (help may be needed). Tragal massage may help the drops go into the middle ear. The patient is kept in that position for 2–3 min. Cotton wool is placed in the ear canal and can be removed 10 min later Fig. 1.7.11 Right ear. The tympanic membrane in the posterosupe- rior quadrant behind the malleus handle is retracted. The retraction pocket has cerumen and keratin debris and the apex of the retraction pocket cannot be identified Fig. 1.7.10 Right ear. Attic perforation above the short process of the malleus after cleaning the epithelial debris Fig. 1.7.12 Right ear. The tympanic membrane is retracted postero- superiorly toward the antrum area. The bone over the retraction pocket is destroyed. The incus is eroded. The epithelium at the apex of the retraction pocket is seen. The chorda tympani nerve is visible behind the thinned retracted tympanic membrane 1.7 Chronic Otitis Media 39 Fig. 1.7.20 Right ear. Nearly total tympanic membrane perforation. Short process of the malleus, malleus handle, long process of the incus, incudostapedial joint, stapes, and posterior crus of the stapes are seen. The mucopurulent material is seen around the footplate and in the round window niche Fig. 1.7.21 Left ear. Nearly total tympanic membrane perforation. Posterior to the promontory, round window niche; posterosuperior to the promontory, stapes, footplate, and stapes tendon; above the stapes, facial nerve canal; and in the anterosuperior part of the mid- dle ear, tensor tympani muscle are seen Fig. 1.7.22 Left ear. Marginal perforation of the tympanic membrane in the posterior part. The remnant of the tympanic membrane is opaque and thickened. Ivory-colored cholesteatoma mass is filling the whole middle ear cavity Fig. 1.7.23 A cholesteatoma mass removed from the ear, measuring approximately 4 cm in diameter E A R N O S E T H R O A T A N D N E C K 40 Chapter 1 Ear Fig. 1.7.24 Left ear. Atticoantrotomy cavity after keratin debris has been cleaned. The head of the malleus and the short process of the incus are seen in the cavity. There is a central perforation of 2 mm in the anteroinferior part of the tympanic membrane Fig. 1.7.25 Right ear. View after Bondy mastoidectomy. The tympanic membrane is slightly vascularized and retracted. The cholesteatoma is marsupialized into the external ear canal by the atticoantrotomy oper- ation. Bondy mastoidectomy is performed in cases of cholesteatoma that develop from the attic region and extend to the antrum cavity. Since the cholesteatoma mass does not extend into the middle ear cavity, there is no need to open the middle ear cavity. The cho- lesteatoma is followed and marsupialized into the external ear canal Fig. 1.7.26 Left ear. After myringoplasty the grafted tympanic mem- brane is very well vascularized. In the anterior part the fibrous annu- lus and membrane remnant are seen 1.8 Facial Nerve Paralysis 41 1.8 Facial Nerve Paralysis a b Fig. 1.8.3 Ramsey Hunt syndrome. (a) Vesicles in the right auricle. (b) Right-sided facial nerve paralysis; temporal MR image shows enhancement of the right facial nerve denoting viral infection of the facial nerve (courtesy of Dr. Sarac) Fig. 1.8.2 Bell’s palsy. When the patient closes his eyes, the eye on the paralyzed side rolls up (Courtesy of TESAV) Fig. 1.8.1 Facial nerve paralysis due to facial nerve absence at birth (Courtesy of TESAV) E A R N O S E T H R O A T A N D N E C K 44 Chapter 1 Ear Disease Fever Neurologic findings CSF findings Mastoiditis +++ – – Petrositis ++ + – Lateral sinus thrombophlebitisa +++ – – Otitic hydrocephalus – ± Pressure over 300 Bacterial meningitis +++ + + Extradural abscess ± – – Subdural abscess + ± – Brain abscess + + + Table 1.9.2 Main symptoms in otogenic complications a Chills are a highly diagnostic symptom associated with lateral sinus thrombophlebitis Extracranial Acute mastoiditis Facial nerve paralysis Acute suppurative labyrinthitis Petrositis Intracranial Meningitis Intracranial abscess Extradural abscess Subdural abscess Brain abscess Lateral sinus thrombophlebitis Otitic hydrocephalus Table 1.9.1 Complications of middle ear infections a b Fig. 1.9.4 Right temporal lobe abscess in a chronic otitis media patient with cholesteatoma. (a) Coronal view, (b) axial view 1.10 Hearing Loss 45 1.10 Hearing Loss Fig. 1.10.3 In stapes surgery, the stapes suprastructure is removed and a hole is created in the footplate for a Teflon piston. The Teflon piston is placed in the footplate and hung on the long process of the incus which creates a bridge instead of the stapes (courtesy of Sennaroğlu) Fig. 1.10.2 Temporal bone section. Otosclerosis causing obstruction in the vestibular aqueduct and endolymphatic hydrops in all turns of the cochlea (courtesy of Paparella, Paparella otopathology lab director) Fig. 1.10.1 Inflammation in the labyrinth of a patient with total hear- ing loss following suppurative labyrinthitis (courtesy of Paparella, Paparella otopathology lab director) Fig. 1.10.4 Extruded metal piston in the external auditory canal in a patient who had undergone otosclerosis surgery in the past E A R N O S E T H R O A T A N D N E C K 46 Chapter 1 Ear b a Fig. 1.10.7 (a) Temporal MR image. Glomus jugulare tumor on the right side extending to the hypotympanum. (b) Angiography shows hypervascularized glomus tumor Fig. 1.10.5 Glomus jugulare. A pink–bluish silhouette of a glomus tumor behind the tympanic membrane Fig. 1.10.6 Glomus jugulare tumor extending out to the external auditory canal Fig. 1.10.8 Right ear. Through the tympanic membrane perforation, the glomus tumor is seen to be localized in the hypotympanum. It is in contact with the incudostapedial joint 1.11 Otalgia 49 Fig. 1.11.4 Earache may also be seen in laryngeal carcinomas E A R N O S E T H R O A T A N D N E C K 50 Chapter 1 Ear 1.12 Temporal Bone Fractures Fig. 1.12.1 Axial CT scan. Transverse temporal bone fracture on the left side. High-resolution CT scans of the temporal bone provide nec- essary information about the fracture. Audiometric examination helps in the diagnosis Fig. 1.12.2 In longitudinal fractures, a fracture line at the posterosu- perior part of the external ear canal may be seen Fig. 1.12.3 Traumatic tympanic membrane perforation. These perfo- rations are sometimes seen after a blow to the ear. To be sure that the perforation is really traumatic, the physician should check that the edges of the perforation are irregular and hemorrhagic 1.12 Temporal Bone Fractures 51 Fig. 1.12.4 Schematic representation of longitudinal and transverse fractures. Temporal bone fractures are classified into two main groups: longitudinal and transverse fractures. Longitudinal fractures are much more frequent, with the incidence of longitudinal fractures being four times greater than transverse fractures. Generally, tempo- ral and parietal blows are associated with longitudinal fractures. Since the areas of the foramina are relatively weaker parts of the skull base, fractures tend to occur in their vicinity. Longitudinal fractures start in the squamous portion and go to the middle ear through the poste- rior and superior walls of the external ear canal and then to the petrous apex. Generally, conductive hearing loss is accompanied by longitudinal temporal bone fractures. Facial nerve injury may occur at the geniculate ganglion area and is only seen in 15% of longitudinal fractures. Tympanic membrane perforation or bleeding into the mid- dle ear may also be seen. Transverse fractures generally occur due to frontal or occipital trauma. Since the blow comes from anterior-pos- terior or posterior-anterior direction, the fracture line occurs at a right angle to the axis of the petrous bone and the fracture line starts from the foramen magnum or jugular foramen and extends to the middle ear. It frequently affects the facial nerve and inner ear. Hemotympanum may be associated with transverse fractures, but tympanic membrane perforation is not seen. Temporal bone fractures do not always follow these general guidelines, and some fractures are mixed. These frac- tures are evaluated according to the type of lesion Longitudinal Transverse Frequency (approximate %) 80 20 Hearing loss Conductive Sensorineural Vertigo Rare Frequent Facial nerve paralysis Rare (10–15%) Frequent (50%) Table 1.12.2 Differential diagnosis between longitudinal and transverse temporal fractures Head is elevated 30° Gaita softeners are prescribed Diuretics such as diazomide are given to decrease the CSF pressure Wide-spectrum antibiotics are started as prophylaxis against meningitis No packing is done to the external ear canal Table 1.12.1 How to treat CSF fistula How to Make the Diagnosis of CSF Draining from the External Ear Canal If the fluid is collected on a filtered paper or on a gauze, it forms a halo around the circle of blood. If the fluid can be collected in a tube, beta-2 transferrin positivity indicates CSF leak. E A R N O S E T H R O A T A N D N E C K 54 Chapter 1 Ear 1.14 Vertigo Duration No hearing loss With hearing loss Seconds Benign paroxysmal positional vertigo Minutes Vertebrobasilar insufficiency Hours Endolymphatic hydrops (Meniere disease) Days Vestibular neuritis Labyrinthitis Weeks Intracranial pathologies Multiple sclerosis Acoustic neurinoma, psychogenic Table 1.14.2 Differential diagnosis in vertigo according to duration Onset of vertigo Character of vertigo, real vertigo, or dizziness Duration Relationship to the movements of the head Other associated symptoms, tinnitus, hearing loss etc. Table 1.14.1 Anamnesis in vertigo patient Fig. 1.14.1 Normal appearance of Reissner’s membrane and the tec- torial membrane (courtesy of Paparella, Paparella otopathology lab director) Fig. 1.14.3 Profound endolymphatic hydrops in all turns of the cochlea (courtesy of Paparella, Paparella otopathology lab director) Fig. 1.14.4 Intracanalicular acoustic neuroma and serous labyrinthi- tis in the vestibule and cochlea (courtesy of Paparella, Paparella oto- pathology lab director) Fig. 1.14.2 Hydropic Reissner’s membrane in one turn of the cochlea (courtesy of Paparella, Paparella otopathology lab director) 1.14 Vertigo 55 Peripheral Central Latent period + – Adaptation + – Fatigue + – Table 1.14.4 Differential diagnosis in central and peripheral positional vertigo Peripheral Central Unsteadiness Slight, moderate Severe Nausea, vomiting Severe Slight Hearing symptoms Frequent Rare Neurologic symptoms Rare Frequent Compensation Fast Slow Table 1.14.3 Differential diagnosis in central and peripheral vertigo a b Fig. 1.14.6 (a) Balancing stone from inner ear. Color scanning elec- tron micrograph of crystals of calcium carbonate on the surface of an otolith. An otolith or otoconium is a calcified stone that is found in the otolith organs of the inner ear. They are attached to sensory hairs, and, when the head tilts, the movement of the stones causes nerve impulses that form the basis of the sense of balance. In humans, oto- conia can range in size from 3 to 30 µm (millionths of a meter) across (visual photos). (b) Dix Hallpike maneuver. The patient is brought to the supine position from the sitting position with the head turned to one side. The maneuver is repeated on the opposite side. The pres- ence of nystagmus or any feeling of movement is recorded Fig. 1.14.5 Temporal bone section. Otosclerosis causing obstruction in the vestibular aqueduct and endolymphatic hydrops in all turns of the cochlea (courtesy of Paparella, Paparella otopathology lab director) E A R N O S E T H R O A T A N D N E C K 56 Chapter 1 Ear Fig. 1.14.7 Epley maneuver for benign paroxysmal positional vertigo (BPPV). The patient is brought to the Dix Hallpike position, with the head turned 45° to the affected side. The head is then turned to the opposite side. The patient’s head is held in each position for 30 seconds. The whole body and head is brought to the lateral decubitus position. The patient is brought to the starting position-sitting position Fig. 1.14.8 (a-c) Acoustic neuroma on the right side. MR imaging is particularly useful in diagnosing acoustic neuroma. The lesions enhance with gadolinium injection a b c 2.1 The Common Cold and the Flu 59   Common cold Flu Virus Rhinovirus Influenza Contagiousness Droplets by inhalation or touch Droplets by inhalation Onset 1–3 days after virus entrance Sudden Duration One week One week or more Frequency Children six to eight colds per year, adults two to four colds per year Once Symptoms Milder Weakened senses of taste and smell, cough, runny or stuffy nose, sneezing, scratchy throat Worse Fever (39°C or above), body aches, extreme tiredness, dry cough more common, headache, sore throat, chills, tiredness Complications No serious complications May have serious complications, pneumonia, bacterial infections May be fatal in elderly, immunocompromised, and chronically ill patients Treatment Acetaminophen Antihistamine and/or decongestant Adequate fluid intake (eight glasses of water or juice) Avoid smoking and alcohol Avoid caffeine and alcohol No antibiotics Acetaminophen Antihistamine and/or decongestant Adequate fluid intake (eight glasses of water or juice) Avoid smoking and alcohol Avoid caffeine and alcohol No antibiotics Table 2.1.3 Clinical features of the common cold and flu Close contact with people who have a cold should be avoided especially during the first few days when they are most likely to spread the infection Hands should be washed after touching someone who has a cold Fingers should be kept away from the nose and the eyes to avoid self-infecting the cold virus particles A second hand towel should be put in the bathroom for healthy people to use The environment should be humidified The nose and the mouth should be covered with a tissue when coughing or sneezing Table 2.1.4 How to prevent a cold E A R N O S E T H R O A T A N D N E C K 60 Chapter 2 Nose 2.2 Rhinitis Rhinitis is a clinical diagnosis and is defined as inflammation of the nasal mucosa with one or more symptoms of sneezing, itching, rhinorrhea, and nasal blockage lasting for at least 1 h on most days. All diseases causing rhinorrhea and nasal obstruction should be considered in the differential diagnosis of rhinitis. Fig. 2.2.1 Allergic rhinitis. Serous nasal discharge with hypertrophic, pale inferior turbinates Fig. 2.2.2 Acute rhinitis, early period. Right inferior turbinate mucosa is hyperemic and there is serous secretion Fig. 2.2.3 Upper respiratory tract infection, 6th day, mucoid nasal discharge Fig. 2.2.4 Right acute maxillary sinusitis. Purulent nasal discharge with draining to the nasopharynx through the middle meatus 2.2 Rhinitis 61 Fig. 2.2.5 Chronic sinusitis, purulent discharge in left nasal cavity Fig. 2.2.6 Eosinophilic mucin in a patient with nonallergic rhinitis with eosinophilia syndrome (NARES). The discharge is sticky, thick, and yellow-green Fig. 2.2.7 Cerebrospinal fluid (CSF) rhinorrhea. Coronal CT showing fracture line in the fovea ethmoidalis of anterior ethmoid area E A R N O S E T H R O A T A N D N E C K 64 Chapter 2 Nose Antihypertensives Reserpine Guanethidine Phentolamine Methyldopa ACE inhibitors Alpha adrenoreceptor antagonists Topical ophthalmic beta blockers Chlorpromazine Aspirin Nonsteroidal anti-inflammatory agents Oral contraceptives Topical decongestants (rhinitis medicamentosa – long-term use of cocaine and nasal drops or sprays) Table 2.2.4 Drugs that can induce rhinitis Skin prick tests Specific IgE measurements Nasal smear Nasal provocation tests Histamine/methacholine Allergen Rhinomanometry Acoustic rhinometry CT, MR imaging Biopsy, electron microscopic examination Sweat test Table 2.2.3 Diagnostic tests for rhinitis   Seasonal Perennial Perennial nonallergic Time of year Seasonal Perennial Perennial Age of onset 10–20 10–20 Adulthood Prominent symptom Rhinorrhea, sneezing, itching Rhinorrhea, sneezing, itching Rhinorrhea, blockage Eye symptoms Common Uncommon Not present Nasal cytology EO (Eosinophil) EO EO/NT (Neutrophil) Allergens Pollens Dust mite, moulds, animal Negative Polyps Uncommon Uncommon Frequent Table 2.2.5 Diagnostic features of noninfectious rhinitis Fig. 2.2.12 Classification of rhinitis Rhinitis OthersChronicAcute Infectious rhinitis Nonallergic Rhinitis NARES Perennial Seasonal Allergic rhinitis 2.3 Allergic Rhinitis 65 2.3 Allergic Rhinitis Allergy is an inappropriate and harmful immune response to a normally harmless substance. Generally, allergens are proteins that do not cause any reactions in nonatopic individuals. What is atopy? Atopy is an inherited predisposition to produce IgE anti- bodies to certain substances. What is the difference between atopy and allergy? Atopy is the genetic predisposition to produce IgE anti- bodies. To develop allergy, stimulation of the cells of the immune system to produce IgE antibodies is needed. Although almost 25–30% of the population is atopic, not every atopic person develops allergy. Environmental factors are important in the development of allergic disease. Allergic Reaction Allergens enter the body through the airways, the gastroin- testinal tract, or the skin. In atopic patients an allergen is rec- ognized as being foreign to the immune system. B cells are stimulated to produce specific IgE antibodies. These IgE antibodies bind to the surface of mast cells. On subsequent exposures, the allergens bind to the IgE antibodies. Bridging two IgE antibodies makes the mast cell degranulate and the mast cell releases histamine and other cytokines that cause allergic reactions. Early Response The early response is initiated after bridging of IgE antibod- ies on the mast cells. Mast cells release mediators such as histamine, prostaglandins, leukotrienes, platelet-activating factor, and bradykinin. These mediators cause vascular dila- tation, increased permeability, and attract inflammatory cells into the tissues starting the inflammation. The early response is characterized by sneezing, rhinorrhea, bronchoconstric- tion, and increased bronchial responsiveness. Late Response The mediators released from mast cells attract inflammatory cells such as eosinophils, lymphocytes, neutrophils, and monocytes into the tissues. Therefore, the late response is a cell-mediated response. The late response is characterized by prolonged mucus secretion, edema formation, and bronchial hyperresponsiveness. Fig. 2.3.1 (a, b) Allergic rhinitis. The turbinates are pale, bluish, and swollen. Watery serous secretion is seen in both nasal passages a b E A R N O S E T H R O A T A N D N E C K 66 Chapter 2 Nose Fig. 2.3.7 Allergic conjunctivitis, erythema, and edema of the con- junctival mucosa, and watering. Limbal elevation can be identified (courtesy of Kıratlı D) Fig. 2.3.3 Supratip crease. Horizontal line in the supratip area due to repeated use of allergic salute Fig. 2.3.5 Skin prick test Fig. 2.3.6 Items that should not be present in the room of an allergic child Fig. 2.3.2 Allergy salute is a very common sign of allergic rhinitis in children Fig. 2.3.4 Long, silky eyelashes in an allergic child 2.4 Nasal Vestibulitis and Nasal Furunculosis and Mucormycosis 69 2.4 Nasal Vestibulitis and Nasal Furunculosis and Mucormycosis Infection of the skin of the nasal vestibule is termed nasal vestibulitis. It may be secondary to constant rhinorrhea, nose picking, or viral infections such as herpes simplex and her- pes zoster. Foreign bodies frequently cause vestibulitis in children due to purulent discharge. Nasal furunculosis is Staphylococcus aureus infection of the hair follicles. Nose picking is a frequent cause of furunculosis. Topical and if necessary systemic antibiotics are prescribed. The patient should be instructed not to squeeze out pus from this area. Since the veins draining this area are valveless and directly join the cavernous sinus, there is a potential risk of spreading infection to the cavernous sinus via these facial veins. Eczema may also mimic vestibulitis. In these cases steroid base ointment may help the patient. In persistent vestibulitis, neoplastic diseases such as basal cell or squamous cell carci- noma should be kept in mind. Fig. 2.4.1 Nasal vestibulitis on the left side. Note the slight edema and hyperemia as well as excoriation of the skin on the left side Fig. 2.4.2 If not treated, the infection in the nasal vestibule may spread to the upper lip. The upper lip on the right side appears hype- remic and edematous Fig. 2.4.3 Furunculosis in the nasal vestibule with spread of the infection to the nasal tip and dorsum Fig. 2.4.4 Infection starting as nasal vestibulitis with spread of infec- tion to the nasal dorsum and right periorbital area E A R N O S E T H R O A T A N D N E C K 70 Chapter 2 Nose Fig. 2.4.5 Venous drainage of the nose. (a) frontal view, (b) Lateral view. Since the veins draining this area are valveless and directly join the cavernous sinus, there is a potential risk of spreading infection to the cavernous sinus via these facial veins. This area of the nose is termed the danger triangle. Squeezing the pus from this area should be avoided a b Fig. 2.4.6 Constant rhinorrhea and the need to wipe the nose due to allergic rhinitis have resulted in vestibulitis Fig. 2.4.8 Hyperemia and edema in the columella and nasal tip mim- icking severe vestibulitis secondary to squamous cell carcinoma infil- tration. The neoplastic lesion is filling the left nasal passage Fig. 2.4.7 Right alar rim. Basal cell carcinoma with slight hyperemia around it. In persistent vestibulitis, neoplastic diseases such as basal cell or squamous cell carcinoma should be kept in mind 2.4 Nasal Vestibulitis and Nasal Furunculosis and Mucormycosis 71 Fig. 2.4.10 Mucormycosis in a child with leukemia. Gross tissue necrosis with a black eschar is characteristic of mucormycosis Fig. 2.4.9 Mucormycosis in a diabetic patient. Mucormycosis may infect different areas of the body, but the most frequent fatal form is the rhinocerebral form. (a) Necrotic areas on the face, (b) black necrotic areas in the nasal mucosa, (c) and after removal of necrotic area in the nose a b c Fig. 2.4.11 (a, b) Mucormycosis in an immunocompromised child. The disease progresses rapidly with extension of tissue necrosis out of the nose into the orbit and face. Local management requires wide deb- ridement of necrotic tissue with a margin of normal-appearing tissue (Courtesy of TESAV) a b E A R N O S E T H R O A T A N D N E C K 74 Chapter 2 Nose Fig. 2.5.5 Nasal discharge. (a) Mucoid drainage after common cold; (b) purulent drainage in the inferior meatus; (c) postnasal purulent drain- age; (d) allergic mucin: viscid, thick yellow–green drainage, generally eosinophilic a b c d 2.5 Sinusitis 75 Fig. 2.5.6 Waters view showing right acute maxillary sinusitis. There is an air–fluid level in the right maxillary sinus Fig. 2.5.7 Transillumination of the frontal sinus. In frontal sinusitis the frontal sinus fails to transilluminate Fig. 2.5.8 (a) Coronal CT shows bilateral maxillary sinusitis; (b) 15 days after starting medical treatment the sinuses appear to be normal a b Fig. 2.5.9 Maxillary sinus irrigation. An opening is created via the infe- rior meatus between the nose and maxillary sinus or via canine fossa E A R N O S E T H R O A T A N D N E C K 76 Chapter 2 Nose Fig. 2.5.10 The purpose of endoscopic sinus surgery is to restore ventilation and drainage of the paranasal sinuses. (a) Preoperative and (b) postoperative view Fig. 2.5.11 (a) Epithelized sinuses and normal mucosa of the sinuses after endoscopic sinus surgery. (b) Coronal CT after surgery shows that all sinuses are clean and ostia are open a b Fig. 2.5.12 Coronal paranasal sinus CT showing previously per- formed bilateral Caldwell-Luc operation. Note that both nasoantral windows in the inferior meatus are widely open 2.6 Complications of Sinusitis 79 2.6 Complications of Sinusitis Although the incidence of complications of sinusitis decreased remarkably after the introduction of antibiotics, these com plications may still be life threatening. Compli- cations of sinusitis can be classified as local, orbital, and intracranial. The most popular example of a local complication is fron- tal bone osteomyelitis. Frontal sinusitis may cause osteomy- elitis of the anterior table of the frontal bone. The pus may collect between the bone and periosteum. This subperiosteal abscess is known as “Pott’s puffy tumor.” Orbital complica- tions are very frequently due to ethmoidal sinusitis. Especially in children, the lamina papyracea is dehiscent and infection can easily spread to the orbit. Osteomyelitis Frontal (Pott’s puffy tumor) Intracranial Epidural abscess Subdural abscess Cavernous sinus thrombosis Meningitis Brain abscess Orbital Inflammatory edema (periorbital cellulitis) Subperiosteal abscess Orbital cellulitis Orbital abscess Optic neuritis (cavernous sinus thrombophlebitis) Table 2.6.1 Complications of sinusitis Periorbital cellulitis Infection anterior to the orbital septum Orbital cellulitis Infection posterior to the orbital septum Subperiosteal abscess Pus collection beneath the periosteum and lamina papyracea Orbital abscess Pus collection in the orbit Cavernous sinus throm- bophlebitis Extension of infection to cavernous sinus Table 2.6.3 Stages of orbital complications of sinusitis Complication Extraocular muscle  impairment Visual acuity loss Inflammatory edema None None Subperiosteal abscess Minimal, in early stages; may limit eye mobility significantly in big abscesses None, very minimal in big abscesses Orbital cellulitis Minimal Minimal Orbital abscess Complete Severe Cavernous sinus thrombosis Complete, often bilateral Severe, often bilateral Table 2.6.4 Orbital complications, eye mobility vs. vision Osteitis (osteomyelitis in bones with bone marrow) Direct extension Congenital dehiscences Fracture lines from previous head traumas Venous extension Retrograde thrombophlebitis between the sinus mucosal veins and orbital and dural veins; Septic emboli in diploic veinsb Table 2.6.2 Extension routes of infection in sinusitisa aLymphatic spread plays no role in extension of sinus infections bThere are no valves in the veins connecting the orbit and sinuses (Breschet diploic veins) and this creates an easy route for extension of infection Fig. 2.6.1 Right preseptal cellulitis. It is seen particularly in children because of the dehiscences in the lamina papyracea. Sometimes when the ethmoid sinus is completely congested, periorbital swell- ing may occur due to obstruction of venous drainage E A R N O S E T H R O A T A N D N E C K 80 Chapter 2 Nose Fig. 2.6.2 Schematic drawing of orbital complications of sinusitis. (a) Preseptal cellulitis, (b) orbital cellulitis, (c) subperiosteal abscess, (d) orbital abscess, and (e) cavernous sinus thrombophlebitis a b Fig. 2.6.3 Left-sided subperiosteal abscess. (a) The eye globe is pushed anteriorly and is displaced laterally and inferiorly by the sub- periosteal abscess. The patient’s upper lid is swollen, and (b) he is unable to elevate his left upper eyelid. His eye movements are lim- ited in the upward and medial gaze. (c) Axial CT scan shows com- plete opacification of the left ethmoid cells. There is a large subperiosteal abscess lateral to the lamina papyracea. Very small bony dehiscences can be noted in the lamina papyracea; (d) axial and (e) coronal MR images demonstrate complete opacification of ethmoid sinuses and large subperiosteal abscess 2.6 Complications of Sinusitis 81 Fig. 2.6.5 Schematic representation of intracranial complications of frontal sinusitis. Purulent material may collect between the bone and dura (epidural abscess) or between the dura and the brain (subdural abscess) or in the brain (brain abscess) Fig. 2.6.4 Right orbital abscess due to ethmoiditis. Infection from the ethmoid sinuses may spread very easily via small dehiscences in the lamina papyracea into the orbit. External drainage may be required c d e Fig. 2.6.3 (continued) E A R N O S E T H R O A T A N D N E C K 84 Chapter 2 Nose Fig. 2.6.8 (a, b) Axial and coronal CT scans of frontal sinus mucocele. The ethmoid sinuses are completely opaque, and the posterior and superior wall of the frontal sinus is destroyed. Erosion of the roof of the orbit leads to orbital displacement inferiorly and laterally a b Fig. 2.6.9 Left-sided ophthalmoplegia. The eye globe does not move in any direction. (a) The left upper lid is ptotic; (b) left eye does not move in lateral direction; (c) left eye does not move in medial direction; (d) left eye does not move in inferior direction; (e) left eye does not move in superior direction. Superior orbital fissure syndrome is character- ized by the involvement of the 3rd, 4th, 6th, and ophthalmic branch of the trigeminal nerve. Vision is normal. In orbital apex syndrome, the optic foramen is also involved and there is loss of vision due to optic nerve involvement in addition to the superior orbital fissure syndrome a b c e d 2.6 Complications of Sinusitis 85 a b c Fig. 2.6.11 (a–c) Osteoplastic frontal sinus operation in a patient with frontal sinus osteoma. The anterior table of the frontal sinus is elevated. The periosteum is not separated from the anterior table and is pedicled on the bone. After removing the osteoma and clean- ing the pathology, the anterior table is placed back into the original position. Although this procedure is performed rarely, it provides a wide exposure in complicated diseases, trauma, tumor, or CSF fistula of the frontal sinus Fig. 2.6.12 Due to ethmoidofrontal mucocele, the right eye is pushed laterally and inferiorly. The eye globes are not at the same level Fig. 2.6.10 Supraorbital frontal cell in the lateral wall of the frontal sinus. If they do not cause any symptoms, there is no need for sur- gery. To treat these disorders, osteoplastic frontal sinus operation is necessary E A R N O S E T H R O A T A N D N E C K 86 Chapter 2 Nose Fig. 2.6.13 Medial rectus muscle injury on the right side during endoscopic sinus surgery. (a–d) There is strabismus to the lateral side and impaired mobility of the eye. (e) Axial CT scans show the injury (courtesy of Şener) a b c e d 2.7 Nasal Polyposis 89 Fig. 2.7.6 Diffuse eosinophilic nasal polyposis completely obstruct- ing the nasal passage Fig. 2.7.7 In eosinophilic diffuse nasal polyposis, the mucus is thick, viscid, and yellow-green. It contains many eosinophils. It is referred to as allergic mucin Fig. 2.7.9 Fungal ball in sphenoid sinus Fig. 2.7.8 Diffuse nasal polyposis. Diffuse eosinophilia is seen on his- tological examination (H&E) E A R N O S E T H R O A T A N D N E C K 90 Chapter 2 Nose a b Fig. 2.7.10 Kartagener syndrome. (a) Dextrocardia on chest X-ray; (b) diffuse bronchiectasia on axial CT scan Fig. 2.7.11 Nasal bone expansion due to extensive diffuse nasal polyposis in the younger patient. Rhinoplasty is needed to restore the appearance Fig. 2.7.12 Diffuse nasal polyposis completely filling the nasal pas- sages. On the left side, nasal polyps protrude from the nostril. The patient did not agree to the operation because of her fear of anesthesia Table 2.7.2 Treatment evidence and recommendations for postoperative treatment in adults with nasal polypsa Therapy Level Grade of   recommendation Relevance Oral antibiotics: short term < 2 weeks No data D Immediately postoperative, if pus was seen during operation Oral antibiotics: long term > 12 weeks Ib A Yes Topical steroids after Functional endoscopic sinus surgery (FESS) Ib (two studies one +, one −) B Yes Topical steroids after polypectomy Ib A Yes Oral steroids No data D Yes Nasal douche No data D Yes After Table 13.6 of European Position Paper in Rhinosinusitis and Nasal Polyposis, Suppl 20, 2007. Reproduced with permission of Rhinology aSome of these studies also included patients with Chronic Rhinosinusitis (CRS) without nasal polyps 2.7 Nasal Polyposis 91 2 symptoms: one of which should be nasal obstruction or discoloured discharge +/- frontal pain, headache +/- smell disturbance ENT examination including endoscopy (size of polyps) consider CT scan consider diagnosis and treatment of co-morbidities eg. ASA consider other diagnosis unilateral symptoms bleeding crusting cacosmia orbital symptoms: peri-orbital oedema displaced globe double or reduced vision ophthalmoplegia severe frontal headache frontal swelling signs of meningitis or focal neurological signs mild VAS 0-3 topical steroids (spray) moderate VAS >3-7 topical steroids (drops) severe VAS >7-10 oral steroids (short course) topical steroids) review after 3 months improvement continue with topical steroids review every 6 months no improvement improvement follow up douching topical ± oral steroids ± long term antibiotics no improvement CT scan surgery review after 1 month urgent investigation and intervention Table. 2.7.3 Treatment scheme for ENT specialists for adults with nasal polyps. After Fig. 13.5 of European Position Paper in Rhinosinusitis and Nasal Polyposis, Suppl 20, 2007. Reproduced with permission of Rhinology E A R N O S E T H R O A T A N D N E C K