Introduction The specialty of the Ear, Nose and Throat (ENT) system is relatively young compared to certain medical practices. Even to function as a unified discipline, pioneers of the specialty had to wage a protracted struggle to surmount considerable hindrances. Initially confined to managing ear infections alone, the introduction of surgical intervention skills gradually led the specialty to adapt a unified approach. Furthermore, with improved technological advances, the specialty’s horizon for surgical intervention broadened enabling it to handle disorders of the face, head and neck.
As a result, the discipline has become alternatively to be known as the specialty of Oto-Rhino-Laryngology – Head & Neck surgery (ORL – HNS). This specialty deals with a system that: •Occupies a strategic location at the very entrance of the aero – digestive tract. •Performs, among other things, four main sensory functions: hearing, balance, smell and taste, •Is very closely related to the body’s certain vital organs ……… the CNS, Eyes and major blood vessels destined for the head and neck. •Frequently encounters most common disorders (20 – 30% of all cases) – an estimate of a typical primary practice.
The above facts obviously imply that the ENT system plays a very significant role for the survival of the individual. Therefore, exposure to and acquiring basic knowledge of the system, would be instrumental to the young medical practitioners. Aims This short attachment course is designed to accomplish the following aims: •To review essential ENT anatomy and physiology •To demonstrate the use and application of basic equipments employed in ENT practice. •To show and exercise methods in examining the ear, the nose, the throat, and the head and neck region. To present trainees with commonly encountered ENT disorders. •To orient trainees with practical approach in the management of ENT disorders:- ? Planning diagnostic approaches ?Considering most relevant differential diagnoses ?Enable design and initiate appropriate therapeutic measures. Identify and facilitate referral cases as early as possible. • To assess how much has been absorbed by the trainees regarding attitude, knowledge, examination skill, ability to diagnoses and manage common ENT disorders. • To stimulate enthusiast pursue the ENT practice. Objectives
By the end of this brief attachment to the ENT discipline it is hoped that the trainees will: •Have refreshed essential ENT anatomy and physiology •Be well-oriented to symptoms related to disorders of the ENT system and head and neck. •Have acquired the ability to differentiate normal from abnormal; and recognize the nature of abnormality. •Be able to relate symptoms and physical examination findings to specific disorders of the ear, nose and throat. • Be able to: ?Do appropriate investigations to confirm the diagnosis ?Do required basic procedure ?Give primary care treatment ?Design follow ups visits Plan referral for specialist’s care. The Ear 1. Structure and Function Structurally, the ear is considered to have three parts: the external ear, the middle ear and the inner ear. 1. 1 The external Ear This includes the pinna, the external auditory canal (meatus) and the tympanic membrane. 1. 1. 1. The Pinna (Auricle) is made up of a framework if elastic cartilage covered by skin. It lies between the temporomandibular joint (TMJ) anteriorly and the mastoid process posteriorly. The covering skin on its anterior surface is adherent to the perichondrium, but is more loosely attached posteriorly. . 1. 2. The External auditory canal is about 3cm long consisting of an outer cartilaginous (1/3) and inner bony (2/3) portions. The cartilaginous portion is covered and lies at an angle to the bony part. The skin over the outer part or portion contains hair follicles and cerumen (wax) secreting glands. 1. 1. 3. The tympanic membrane is the window to the middle ear. It is a translucent membrane and lies obliquely and is concave on the outside. It is divided into a small superior flaccida and a larger inferior tensa portions by the lateral process of the malleus.
The main landmark on the tympanic membrane is the handle of the malleus. 1. 2 The middle Ear (the tympanic cavity) This is an air – containing compartment, connected to the nasopharynx via the Eustachian tube. The entire middle ear cleft is lined by respiratory mucosa. The middle ear cleft comprises the eustachian tube, the middle ear cavity, and the mastoid air cell complex. It contains two elements vital to the conduction of sound to the inner ear, an ossicular chain and clean, moist warm air. The ossicular chain consists from outward inward of the malleus (hammer), incus (anvil) and stapes (stirrup).
The handle of the malleus is embedded in the tympanic membrane, while its head lies in the attic where it articulates with the incus. (Attic is the area of the middle ear cavity above the pars flaccida). The middle ear cavity is traversed by the cranial VII nerve and contains two small muscles: •stapedius and tensor tympani •Two muco-fibrous tissue recesses: the oval and round windows. Both located on the medial wall of the tympanic cavity, the round below the oval. The foot-plate of the stapes rests on the oval window by a mobile circumferential joint. 1. 2. 1 Important Relations to the middle Ear: Medial to the Eustachian tube lies the internal carotid artery. • Superior to the middle ear and to mastoid is the middle cranial fossa containing the temporal lobe of the cortex (cerebrum). •Posterior to the mastoid is the posterior cranial fossa containing the cerebellum separated from the mastoid by the sigmoid sinus. •Medial to the middle ear is the inner ear/labyrinth/ separated from it by cranial VII nerve. 1. 3 The Inner Ear (Labyrinth) The inner ear is embedded in the petrous part of the temporal bone. It is divided into two functionally separate receptor mechanisms: The cochlea – the acoustic (hearing) end organ and The vestibule and the three semicircular canals (The vestibule /equilibrium/) end organ Morphologically, the labyrinth is divided into a bony and membranous part. The openings from the tympanic cavity to the bony and membranous labyrinth are sealed off respectively, by the stapes footplate/the oval window/ and the round window membrane. 1. 3. 1 The fluid compartments of the inner ear The membranous part contains endolymph. Another fluid perilymph, contained in the bony compartment, encircles the endolymph contained by the membranous part.
The endolymph is a filtrate of perilymph, but has a completely different Na+ and K+ concentrations. The concentration of the Sodium and Potassium ions is believed to be kept constant by the epithelium of the stria vascularis. The endolymph passes via the endolymphatic duct to end up in a blind sac… saccus endolymphaticus which lies in the epidural space on the posterior surface of the petrous pyramid, close to the sigmoid sinus. The perilymph is the immediate substrate of the cochlea and vestibular sensory cells. It is formed by filtration from blood and partly by diffusion of the CSF. . 3. 2 The Mechanism of Hearing The tympanic membrane vibration, initiated by sound waves striking its outer surface, is relayed to the cochlear fluid, through the ossicular chain, thereby stimulating the hair cells. The difference in surface areas between the tympanic membrane and the stapes footplate (17:1) combined with the lever effort of the ossicles (1. 3:1), provide a transference enhancement of nearly 22. 1….. (17×1. 3). This ensures sound wave traversing the cochlear fluid, thus circumventing the mismatch created by the air to fluid media.
As a result of hair cells stimulation, a nerve impulse is produced in their neurons. Remember that within the endolymphatic compartment is a membrane /the basilar membrane/ which supports the hair cells. The hair cells are connected to neurons. The neurons in turn combine to form the auditory portion of cranial VIII nerve. Because of the tonotopic representation of sound waves according to frequencies in the cochlea, the basal ends respond to high frequencies while the apical ends to low frequencies. Each frequency in the sound wave thus stimulates a different part of the basilar membrane.
The auditory center (auditory cortex) receiving the nerve impulses, decodes into the sounds we hear and comprehend. NB: Hearing depends on the fulfillment of two conditions: •Sound wave conduction from an air medium to a fluid medium and, •The processing of sound waves by the sense organ, (The Organ of Corti) into the auditory nerves, then conveyed to the auditory center in the CNS, where they are categorically decoded!! 1. 3. 3 The maintenance of Balance (Equilibrium) The vestibular system (End Organ of Balance) consists of the three semicircular canals, the utricle and the saccule.
These structures have highly specialized hair cells embedded in a covering cap called cupola. Stimulation of the hair cells generates a nerve impulse – which occurs when the cap is displaced by acceleration (utricle), gravity (saccule) or rotation (semicircular canals). These nerve impulses will be interpreted as movement in the vestibular center – in the CNS. The most important sensory input into the balance system, besides the vestibular system, is vision; but muscle tone and joint proprioception from both the neck and limbs are also significant.
Regulation of eye movement in response to rotation, Nystagmus, is accomplished by the vestibulo–ocular reflex (VOR): a complex and extensive link in the brainstem between the vestibular and occulomotor reflex. (Nystagmus is a physiological response to rotation). All these sensory information are coordinated by the vestibular nuclei in the brainstem. From here, there are connections both to the cerebellum and the cerebrum. The cerebellum coordinates the body’s responses to the changes in sensory input. The cerebrum is thought to exert some overall control, but mostly concerned with our awareness of changes. . 3. 4 The Nerves of Balance and Hearing ( Stato-acoustic Nerve) The vestibular nerve and the auditory nerve constitute cranial VIII nerve. It passes to the brainstem via the internal auditory canal (meatus), together with cranial VII nerve. 1. 3. 5 The Facial Nerve The facial Nerve – cranial VII nerve follows a complex path from its origin in the brainstem, enters the internal auditory canal (meatus) alongside cranial VIII nerve passes over the cochlea. It then angles backwards in the middle ear towards the stylomastoid foramen.
Through the foramen, it exists from the temporal bone to enter the parotid salivary gland where it divides to innervate the muscles of facial expression. During its complex course injury or any pathological disorder may lead to its dysfunction. In such cases functional testing of its various branches may help localize the injury sites: •The greater superficial petrosal nerve transmits secreto-motor fibers to the lacrimal gland. •The chorda tympani nerve transmits secreto-motor fivers to the submandibular salivary gland and sensory fibers from the anterior 2/3 of the tongue. The motor nerve fiber to the stapedius muscle, involved in stapedial reflex. 2. Examination of the Ear Examination of the ear may sometimes be a very challenging task, more so when examining young children and certain grown-ups under stress. So adapting a step-wise and systematic approach with cool temper is advisable. Step 1: Begin by obtaining brief medical history pertinent to the presenting complaints. Step 2:- Observation : General examination of the head from the front: Focus on the ears. Are both ears in normal position? Low set and anteriorly displaced ears represent congenital abnormalities.
As there may be other more significant abnormality features: View from the sides. Focus on the ear. Are both ears normal? If no, what is the abnormality? Step 3:- examination of the external ear (Normality is determined by exclusion of abnormality) •Deformity ……. Congenital …….. Acquired – old or recent •Inflammatory swelling …… Mastoiditis …? abnormal middle ear ……Lymphadenitis …. Normal middle ear •Surgical scars: …………….? Mastoidectomy, tympanoplasty Step 4:- Examination of the Ear Canal (Normality is determined by exclusion of abnormality) •Look for foreign body, cerumen impaction. •Infection ….
Otitis externa …. Is it localized or generalized? •A defect in the posterior canal wall. •Others: exostoses, hyperkeratosis; stenosis or adhesion Step 5:- The tympanic membrane (Normality is determined by exclusion of abnormality) •Inflammation: As in acute otitis media •Retraction: As in otitis media with effusion/OME/ •Perforation: As in post-trauma. Active chronic otitis media – (CSOM) •Inactive chronic otitis media – (CNSOM) •Scarred tympanic membrane – a perforation healed by scarring •Others: uncommon conditions – uninfected cholesteatoma. Step 6:- The Hearing… preliminary assessment Normal hearing: Accurate response to whispered voice test – delivered at a distance of •In cases of abnormal Response ?Normal speech voice – when delivered as a distance of indicates moderate hearing impairment. ?Loud speech voice – severe hears impairment. ?Tuning fork (512 Hz): to distinguish the hearing impairment whether conductive or sensor neural. •Assessment of Hearing in babies should commence as early after birth as possible: ?Few weeks of age… blinking, listening to noise ?At about six months: Turning head to localize the source of round. ?At a 9 month: babbling and making other noises. At 1 year: responding to familiar words ?As 1 years: picking up or pointing to things ?At about 2years: ability to hear soft music Disorders of the Ear Ear disorders are better considered according to the anatomic classification, as this enables thorough and systematic coverage: The External Ear Pinnal Deformity Congenital:- Minor: – minor prominance (bath) ears -Pre-auricular sinuses (pits)…. debris may accumulate and if infected abscess may form that requires excision and drainage. Major: – Microtia severe deformity of pinna and stenosis or atresia of the canal. These may result in conductive hearing loss (CHL).
If bilateral, urgent intervention is required. Acquired: – Lacerations, burns, etc . may produce defect and scarring. – Haematoma:- beneath the perichondium – if untreated causes cauliftower ear deformity. Haematoma should be incised evacuated. – Trauma involving the canal may cause fibrotic stenosis. As this interferes with the normal epithelial migration out of the canal, debris accumulates, acting as a focus for infection. If repeatedly manipulated/scratched/,keratin sloughs may accumulate which may lead to meatal obstruction, keratisis obturans.
Neoplasm May be benign and malignant. The most common malignant neoplasm involving the pinna … basal cell and squamous cell carcinoma (SCC). Any persistent ulceration has to be suspected!! Ear canal Impacted wax (cerumen):- Having some wax in the external part of the ear canal is normal. Increased wax accumulation hinders ear canal out- ward epithelial migration, the self-cleansing action. As ear wax consists of sebaceous and ceruminous gland secretion, combined with hairs and desquamated skin, its impaction may result in CHL. Removal maybe accomplished by careful syringing.
Otitis external: may be localized or generalized Localized … e. g. furuncle Generalized …with possible complications: cellulites, adenitis, perichondritis, necrotizing otitis externa. The cause could be infection: bacterial, fungal, viral or allergy (dermatitis). In a diabetic or immunocompromised patient, pseudomonas infection may rapidly spread into the surrounding temporal bone and beyond (necrotizing otitis externa) Symptoms & signs relate to the pathological process, its site and the extent. Symptoms include: itching /irritation/; pain, blocked ear; discharge.
Signs: may be one or a combination of the following: tenderness on manipulating the pinna or tragus; inflammation and swelling, localized or generalized; accumulation of debris; purulent discharge; conductive deafness; cellulitis; tender lymph nodes; swollen, tender and inflamed pinna, ulceration, granlulation tissue. Treatment: directed at the cause to abort anticipated complications. This may include: – Cleaning ……? Syringing – Installation of: ?Soothing preparations: glycerine/ichthmol, either as drops or soaked into wool wick gently inserted into the ear canal. ?Antiseptic ear drop. Anti–inflammatory – preferably steroid – containing drops in combination of antibiotics. ?Specific formularies: anti-fungal drops or creams. NB – Cellulitis requires antibiotics -Perichondntis : I. V antibiotics -Necrotising otitis external: High dose specific I. V antibiotics and surgical debridement. Foreign Bodies (FBs) A wide range of FBs (material, shape, size, etc) some how introduced into the ear canal, encountered more often in children. Un-intelligent manipulation may result in regrettable complications. So, before any attempt to remove: •Know the nature of the FB – material, shape, etc. •Assess its positioning Observe any traumatic scratch from a previous removal attempt. Is the tympanic membrane status known? •Have the instruments you would like to use ready? •Inform the patient what you have to do. The Middle Ear For a quick appreciation of the overall status of middle ear disorder, reference may be made to the following summary: Acute otitis media •More commonly occurs in young children,1 – 2 years of age; no age is immune. •Initiated by cold or viral induced URI •Secondary bacterial infection: H. infuenzae, Streptococcus pneumoniae, Streptococcus pyogenes – involving the mucous membrane of the middle ear cleft. Inflammation swelling obstructes the Eustachian tube; middle ear effusion/empyema/ ‘bulging’ the tympanic membrane, which may cause perforation. Complications more likely to occur if the infection is trapped in the mastoid air cells. Otitis Media with effusion Middle ear effusion develops when the Eustachian tube function is impaired, usually following an episode of URI/acute otitis media/. Ventilation failure may be due to: •Mechanical blockage due to tube mucosal edema •Excess mucus secretion the middle ear mucosa As a result, any residual air is absorbed, thus creating a negative middle ear pressure leading to accumulation of mucus.
This impairs both tympanic membrane vibration and the ossicular chain movement, causing a conductive deafness. In children, natural resolution may be expected, but there are two problems: •Impairment of the child’s speech and development. Insertion of a ventilation tube/grommet/ may be required. •The overstretched tympanic membrane may become atrophic that may lead to formation of a retraction pocket for cholesteatoma. In an adult with middle ear effusion, suspect a tumour in the nasopharynx!! Chronic suppurative otitis media Chronic discharging ears classified as active chronic otitis media. Causes include: •Common causes. Chronic suppurative otitis media (CSOM), the usual type – Cholesteatoma •The less common causes, like tuberculous otitis media Reasons of failure to resolve some cases of acute otitis media that have progressed as far as perforation are: 1. Colonization by colliform bacteria… (Proteus, Klebsilla, Escherchia coli, Pseudomonas). 2. Certain changes at perforation margins prevent closure of the perforation during the healing phase: A seal margin created by the squamous epithelium forming a junction with the mucosal layer. Thus, the perforation remains open long after the infection is controlled. This is inactive chronic otitis media.
Chronic middle ear infection with persistent perforation contributes to conductive deafness. The degree of deafness will be greater when there is: •Osteitis or erosion of the individual ossicle, or •Fixation of the ossicular chain by fibrous deposition during the healing phase. Treatment: – Aural toileting – Ear drop instillation -Supplementary antibiotics NB: The more frequently the ear is cleaned and appropriate ear drops instilled, the more effective the treatment likely to be. Cholesteatoma: This is a very destructive middle ear disorder, caused by accumulation of squamous epithelium and keratin debris in the middle ear.
It may result from a traction pocket of the tympanic membrane or in growth of squamous epithelium from a perforation margin. It is sometimes described as a result of ‘skin in the wrong place’. Cholesteatoma is classified as: Concerning cholesteatoma formation, there are three main hypotheses:- •The skin may arise from embryonic cell rests derived from surface ectoderm in the formation of otocysts •The skin may arise from invasion as invagination of external meatal skin. •The skin may arise from cell metaplasia. Whatever, the importance of cholesteatoma is the fact that it steadily increases in size at the expense of the surrounding tissues.
When the squamous-lined choleteatomas have come in contact with bone, which may be eroded, the outcome depending on the part involved: •With the ossicles, conductive deafness •The facial nerve, facial nerve palsy •The semicircular canals, vertigo Treatment: surgery, aimed at eradicating the cholesteatoma and reconstructing the middle ear sound conducting mechanism. Mastoiditis This is a complication arising form middle ear cleft infection with a high risk of intracranial spread. It may manifest as extra-dural abscess, sigmoid sinus thrombosis, leayseral tube abscess, cerebellar abscess.
Mastoiditis occurs when the infection is trapped within the mastoid air cell system/mastoid air cells/ and then spreads into the surrounding bone to cause osteitis mastoiditis. As osteitis develops, the soft tissue over the mastoid becomes inflamed, resulting in retro-auricular swelling. This indicates the formation of a sub-periosteal abscess over the mastoid bone. Abscess formation may also extend anterioly towards the zygoma, or inferiorly in retromandibular area/Bezold’s abscess/. Treatment: -High dose intravenous antibiotics, preferably a combination of …? ntimeningeal regimen!! – urgent surgical intervention to decompress the mastoid abscess and eradicate the osteitic bone /cortical mastoidectomy/. Otosclerosis In otosclerosis, there is an overgrowth of “spongy” bone in the bony capsule of the inner ear. When the oval window is involved, the stapes becomes fixed, resulting in conductive deafness: •Probably of a genetic origin, frequently seen in European origin, less common in Asian, almost unknown in the African counter-parts •Present usually in the 20 to 40 age group •Occurs usually on one side Is occurs in women during pregnancy. Treatment: Surgical…. stapedectomy; the stapes is resected and replaced by piston-shaped prosthesis. In case of surgical contra-indication, wearing a hearing aid is the alternative. Unusual Middle ear Disease: TB to be considered when the tympanic membrane perforation is multiple with chronic suppurative otitis media Middle Ear Neoplasim: is rare! Benign neoplasim /glomus tumour, a chemodectoma/ may present like pulsatile tinnitus and an abnormal reddish tympanic membrane. Malignant neoplasims present with persistent severe pain in an ear full of granulation tissue.
The Inner Ear Disorders affecting both cochlea and vestibular components Trauma: Basal skull fracture (bleeding and CSF leakage from the internal auditory meatus. •May transect the temporal bone with disruption of the inner ear to cause: ? Permanent Deafness ?Vertigo /compensation may occur/ ?Occasional cranial VII Nerve palsy – requires surgical decompression. •Lesser degrees of head injury may cause Labyrinthine concussion. Labyrinthitis /perilymph of the inner ear communicates with the CSF/ •Rare, deafness as a complication may occur •vertigo may also manifest
Treatment: – Intravenous – antibiotics – Surgical – to eradicate middle ear disease – wide exposure of the labyrinth to facilitate drainage Acoustic Neuroma /Schwannoma/ Rare If it occurs, it involves both auditory and vestibular nerves in the intemal auditory canal, causing sensori-neural deafness and balance disorder /non specific/ Treatment: – stereo-tactic radiotherapy, or – surgical excision Disorder affecting the cochlea: – Sensorineural deafness /SNHL/ Potential causes: congenital, birth asphyxia, neonatal jaundice, intrauterine meningitis, ototoxic drugs.
Treatment: – Prevention – Directed at the cause Disorders affecting the vestibular system (vertigo) Causes: – vestibular neuronitis, meniere’s disease, benign positional vertigo, labrynthitis, vertebro-basilar insufficiency(VBI). Management: requires understanding the specific nature. Facial (cranial VII nerve) palsy In the developed world, its prevalence is about 1:500, majority benign. Its manifestation as upper and lower motor lesions, is well known. •Upper motor Neuron facial palsy occurs as part of a cerebrovascular accident affecting the motor cortex.
Diagnosis: – “Forehead sparing” •Lower motor neuron facial palsy Idiopathic Bell’s palsy: A diagnosis by exclusion. Its variation: Herpes zoster oticus/RamsayHunt Syndrome/, Shingles. Lesions erupt in and around the external auditory canal Treatment: – Directed at the specific cause to secure quick recovery. Delayed management may end up in residual complications. For Ramsay Hunt syndrome, Acyclovir is advised. The Nose and the PN Sinuses This is considered in three parts: the external nose, the nasal cavities and the PN sinus, and the postnasal space.
The external Nose The supporting structure of the nose organized in the shape of a pyramid, consists of bone, cartilage and connective tissues. The bony superior portion is formed by the projecting facial skeleton from both sides, joined by the formal processes at the interior cartilaginous portion consists of the upper lateral and alar cartilages. The shape, position and proportion of the bony and cartilaginous components remarkably influence both the form and cosmetics) harmony of the face as well as the function of the nasal cavity.
Blood Vessels of the external Nose that are of practical importance: •Facial Artery and its braches •Dorsal Nasal Artery, a branch of the ophthalmic a. Profuse bleeding from these vessels occurs following trauma, accidents or surgery. The angular vein: A retrograde infection from a furuncle of the upper tip of the nose, may spread via the ophthalmic vein to the cavernous sinus, causing cavernous sinus thrombosis. Nerve supply to the External Nose Sensory supply: 1 to 2 branches (divisions) of Cranial V Nerve Motor: cranial VII nerve
The Nasal cavity The interior of the nose is divided into two cavities by a median partition, the nasal septum. Each cavity opens anteriorly through the vestibule at the anterior nares and posteriorly, it communicates with the nasopharynx through the choanae. The nasal vestibule contains hair/ vibrissae/ bearing skin. The vestibules are separated by the columella, which forms the front end of the nose. The nasal cavities are lined by ciliated respiratory mucosa, containing mucus secreting glands which can produce 750ml of mucus daily.
This mucus blanket has both protective and cleansing functions and is continuously moved by the activities of cilia, the ciliary’s action The Nasal septum has a cartilaginous skeleton anteriorly and a bony component ( ) posteriorly and it is covered by adherent mucosa, with prominent blood vessels in its anterior-inferior 1/3 portion, ‘Little’s area’, a common site for nosebleed/Epistaxis/. This is also a site for vascular anastmosis/Kiesselbach’s Plexus/. The septum is often deviated to one or both sides. This may follow trauma, at birth or later in life.
It may also be developmental. Such a deformity may need correction /septoplasty/. The lateral Nasal wall Each lateral nasal wall of the nasal cavity consists of three bony projections, the turbinates, arranged roughly in a staircase fashion. Going from below upwards, they are the inferior, middle and superior turbinates. Each is covered by a thin mucous layer, beneath which there is a rich vascular plexus which act as erectile tissues acting under The Autonomic Nervous System Control: sympathetic stimulation causing vasoconstriction and parasympathetic stimulation causing vasodilatation.
The turbinates increase the surface area for the air conditioning function of the nose: warming and humidification of the air during breathing. The inferior turbinate is the largest of all. Beneath each turbinate, is a trough-like opening, called a meatus/plural meati/. The most significant of all is the middle meatus, because into it drain/ empty many of the PN sinuses. The nosolacrimal duct opens anteriorly into the inferior meatus. The olfactory epithelium is situated above the superior turbinates in the roof of the nose. This serves are the primary site for olfactory perception. Remember that for olfaction to occur. he scent containing particles must reach the olfactory epithelium. What is unclear is what mechanism actually stimulates the olfactory /Cranial –I/ nerve. The Nasal cycle: For unknown reasons, the mucosa over the turbinates swells and shrinks. In addition, the degree of patency or obstruction of normal nose varies even from hour to hour and side to side. This is known as the nasal cycle. The PN sinuses The major portion of the facial selection is some what hollowed out by air containing cavitations. These are the PN Sinuses, four pairs, one on each side of the face, along the nasal passages.
They are: the frontal, the maxillary, the ethmoidal and the sphenoidal sinuses. The sphenoidal sinus, the most posterior of all opens into the posterior aspect of the nasal cavity above the choanae; the others open into the middle meatus. The anterior group/the frontal, the maxillary and the anterior ethmoids/ drain into a common trough known as the ostiomeatal complex. Functions of the PN Sinuses The function of PN sinuses is uncertain; suggestions however include that they •Lighten the skull •Resonate the voice •Strengthen the facial skeleton and •Act as shock absorber during violent below
The anatomic locations of the PN Sinuses, however, have important influence over the spread of infections or malignant diseases to neighboring structures: •Frontal sinus: orbit, anterior cranial fossa, saggital sinus •Ethmoidal sinuses: orbit (lamina) papyracea and anterior cranial fossa (cribriform plate) lacrimal sac, nasal cavity •Maxillary sinus: orbit, infra orbital nerve, teeth, nasal cavity, check •Sphenoidal sinus: internal carotid artery, optic nerve, cavernous sinus (containing cranial III, IV and VI nerves) and the 1st and 2nd divisions of Cranial V Nerve.
The Postnasal Space This is the space posterior to the nasal cavity and above the soft palate also known as the nasopharynx. The soft palate which separates it from the pharynx, relaxes to facilitate airflow and, tightens to close off the space to avoid regurgitation into the nose during swallowing. The adenoids ,when present, is situated centrally in the roof of the space. Examination of the Nose Examination of the nose needs to be conducted systematically and initiated by pertinent history retrieval. This is followed by a general assessment of the ace from the front, then progressing to the sides and finally reviewing from above, every time focusing on the nose:- •Does the nose look abnormal in relation to the rest of the face? If so what is wrong about it? •Look for its bony and cartilaginous components for asymmetry, deviation or depression, hump. •Check the alar cartilage for asymmetry (cleft lip or palate or deformity) •Assessment of the interior of the nose (nasal passages) requires a good light source and a nasal speculum •Evaluation of the nasal passages include: 1.
Symmetry: usually both nasal passages not fully symmetrical the septum is NOT perfectly central. As long as no breathing disturbance is encountered, minor asymmetry is acceptable. 2. Nasal mucosa should be assessed for crusts, muco-epithelial debris 3. Continue assessment sequentially including the septum, nasal floor, the lateral wall, and the nasal roof. 4. Look for secretion or discharge: If there is, what does it look like? ?Watery: consider CSF rhinorrhea ?Clear and mucoid: Viral rhinitis? Allergic rhinitis ?Mucopurulent: Bacterial /pyogenic/ rhinosinusitis If unilateral in a child, suspect a FB – If unilateral in an adult, suspect a tumour ? Blood stained: consider infection, a common cause for nosebleed or a tumour 5. What does the septum look like? ?Straight: Normal ?Deviated to side one; may be c – shaped, s-shaped. Is there spur? 6. Any mass in the nasal cavity? ?Nasal polyps, foreign body…… Disorders of the Nose 1. Vestibulitis and Impetigo The opening to the nasal cavities/the nostrils, or nasal vestibules/ are lined by hair–bearing skin. It is frequently subject to trauma, predominantly digital, as in nasal picking.
A breech of the skin surface may predispose to localized infection, furuncle in a hair follicle. It may also ulcerate. If the organism is staphylococci, this may spread to the surrounding skin (= impetigo). Other conditions encountered in this area include: -herpes simplex sores -warts -malignancy – in adults, in case of persistent ulceration In general, this area is considered as part of “the danger area” for infection. Backward/retrograde/ intracranial venous blood flow, via the angular vein, may be complicated by Cavernous Sinus Thromophlebits. Treatment: Urgent IV antibiotics 1.
Rhinitis: Inflammation of the lining mucosa of the nose with variable degree of nasal obstruction. Most commonly encountered is viral in origin. . The most common presenting symptom include: -Nasal obstruction – due to inflammatory nasal mucosal swelling -Sneezing – due to irritation to nasal mucosa -Rhinorrhoea – due to excessive mucosal production with impaired ciliary function Types: •Allergic Rhinitis •Non- Allergic Rhinitis •Atrophic Rhinitis 1. 1. Allergic Rhinitis This occurs in individuals exposed to or sensitized by an allergen. They undergo a type – I hypersensitivity reaction in the nasal mucosa.
The allergen bind to IGE on the surface of the mast cells within the mucosa. This leads to mast cell degranulation and the release of two kinds of mediators such as histamine. These cause vascular dilatation and mucosal oedema [nasal obstruction] mucosal irritation [sneezing] and mucus hyperscretion [rhinorrhoea]. Reflex stimulation of the parasympathetic nerves perpetuates the nasal congestion. Late mediators promote migration of eosinophils into the mucosa. These release substances such as – leukotrienes – responsible for persistent nasal congestions. The following may serve as a summary:
Types of Allergic Rhinitis – Two broad types of allergic Rhinitis. -Seasonal Allergic Rhinitis – predominantly due to pollen dust exposure -Perennial Allergic Rhinitis – commonly due exposure to house dust mites and animal dander. Proper history retrieving may assist to distinguish the two. Further investigations. •skin prick testing •Allergy assay Treatment include: •Avoidance •Anti-histamine – for acute reaction •Mast cell stabilizing agent . . . Na cromoglycate for seasonal rhinitis •Topical steroid nasal sprays. •Systemic steroids to ameliorate symptoms
Non-Allergic Rhinitis – This occurs in individuals exposed to irritants like dust, fumes, vapor pollutants reacting adversely – and with similar symptoms to those of allergic rhinitis, but with different complaints: dry nasal obstruction. This is known as vasomotor rhinitis, assumed to be due to parasympathetic over-activity. No IGE elevation, nor could specific allergies be identified Treatment: is often difficult!! Rhinitis Medicamentosa Individuals with persistent nasal congestion tend to abuse the use of nasal decongestant spray, developing “Rhinitis medicamentosa.
In such cases, a reactive vasodilatation occurs as the effect of vasoconstriction wears off. The tendency to reuse the spray continues. On further repetitive application, tachyphylaxis results, thus the chronic mucosal swelling causing continual obstruction. Atrophic Rhinitis The cause of atrophic rhinitis – is usually obscure. It is characterized by atrophy of the nasal mucosa, with crusting. Infection and ulceration of the mucosa beneath the crusts further damages the mucosa. A foul nasal odor (ozaena) develops. Treatment:- Decrusting and cleansing by irrigating lukewarm saline •Moistening by use of glycerin/ alcohol solution •Surgical procedure to reduce the nasal potency •Selective use of antibiotics. Sinusitis Literally, it means inflammation of the lining mucosa of the PN sinuses. It is usually initiated by a viral rhinitis, seen more frequently in children. The potential do develop sinusitis is when the drainage channels for the sinuses (the ostiomeatal complex) get obstructed or when there is impaired ciliary function. Treatment – includes antibiotics, topical nasal decongestant. Complications:
Complications related to sinusitis usually due to either to delayed or in- effective treatment. The main complications include:- •Orbital cellulitis – mainly from frontal and ethmoidal sinusitis •Cavernous Sinus Thrombosis – involvement of venous channels, •Chronic sinusitis – protracted symptoms of nasal obstruction, nasal stuffiness, mucopurulent nasal discharge or postnasal drip. This is mainly due to ineffective treatment of acute sinusitis. Nasal Polyposis The etiology of nasal polyp formation is unknown. (Polyp:– a protruding growth from a mucus membrane).
Nasal Polyp more commonly arises from the ethmiod sinuses. When an edematous reaction in the sinus mucosa causes it to fill the sinus and then protrude through the sinus opening (ostium), thus expanding within the nasal cavity. Polyp formation is associated: -more frequently with nasal allergy, and -rarely with ASA sensitivity Polyps most often are bilateral and may have choanal extensions . . . [antro-chianal polyp]. Nasal polyps commonly cause nasal obstruction and, sometimes, loss of sense of smell (anosmia), if they obstruct air flow to the olfactory area.
Treatment: -Systemic steroid augmented by topical steroid nasal spray -Surgical removal, plus topical steroid nasal spray – [if response to conservative treatment is poor]. -Sinus surgery – in persistent and/or/recurrent cases Nasal Septal Deviation Deviation /deflection) of the nasal septum to either side, is a common finding. Cause: trauma or developmental Symptoms: – Nasal obstruction – Recurrent nosebleed – Crust formation Treatment – surgical . . . septoplasty Nasal Trauma Trauma to the nose is common problem.
It may be blunt and only confined to the nasal framework or may be part of injury of facial skeleton. Proper management requires proper assessment of the severity nasal bone injury. Look for: -nasal bone fracture: local tenderness, swelling -skeletal displacement In addition obtain a PA and Lateral radiology view of the nasal skeleton. This is for proper assessment of the displacement. Additional views may better be taken which will service for future references, training or legal purposes. Treatment: Depends one the severity, the nature of the deformity. Manipulation to re-align the fractured pieces. (close reduction) better done a week or ten days after the date of the injury—– after swelling has subsided, before fibrin deposition occurs. -Rhinoplasty (Open Reduction) -Nasal packing: – (48 – 72hrs) – to keep reduced parts in place. -Antibiotics – week/10days. Choanal Atresia This is a condition in which the posterior nasal cavity openings fail to develop. In neonates, if it is bilateral, it is an emergency and requires urgent surgical intervention, since, neonates are obligatory nasal breathers. Diagnosis: – Direct endoscopy contrast radiogram Treatment:- surgical – to create the choanal opening – A stent tube introduced and held in positions for 2 – 3 weeks, to prevent stenosis. The Throat, Head and Neck Functional Anatomy and Physiology The head & neck is one of the most complex regions. For primary ENT care, it will be appropriate to limit the discussion to those clinically significant structures within the upper aero-digestive tract. The oral cavity – extends from the vermilion border of the lip to the circumvallate papillae – inferiorly, and the junction of the hard and soft palates, superiorly.
Posteriorly, it is continuous with the oropharynx through the anterior facial arch. The vestibule of the mouth – lies between the lip and the cheek, and the teeth and the alveolar process. Three significant structures within the oral cavity: 1. The dentition /teeth/: (20 deciduous; 32 permanent) 2. The openings of the salivary glands: 2. 1. The Stensen’s duct – for the parotid – on the inner surface of the cheek, adjacent to the 2nd upper molar. 2. 2. Wharton’s duct – for the submandibular gland – in the floor of the mouth on each side of the frenulum of the tongue. 3.
The tongue: Its body separated from its base by a V – shaped terminal sulcus, at its center being the foramen caecum – a remnant of the thyrglossal duct. The Pharynx This is a fibro-muscular tubular organ in continuity with the oral cavity. It is divided into the oropharynx, the nasopharynx and hypopharynx. The Nasopharynx This is the space above the soft palate, limited above by the skull base. It is also known us the postnasal space. The nasopharyx contains the adenoids and the openings for the eustachian tubes . The oropharynx: this ill – defined area lies between the nasopharynx above and the hypopharynx below.
It contains the posterior pharyngeal wall – composed of the prevertebral fascia and the bodies of the 1st and 2nd cervical vertebrae. The hypo-pharynx: This portion of the pharynx extends from the upper border of the epiglottis to the inferior edge of the cricoid cartilage. It opens to the larynx anteriorly. On each side of the larynx lie the funnel – shaped pyriform sinuses. It is the area of parting of the air and food passages. The Ring of Lymphoid Tissues A collection of lymphoid tissues encircles the upper aero-digestive tract. This includes the faucial tonsils, the adenoids the valecullae (lingual tonsils).
This ring of lymphoid tissues is described as the Waldeyer’s ring and is thought to contribute to the immunologic competence in the early days of life. The Larynx The laryngeal skeleton (the hyoid, the thyroid, the cricoid, and the arytenoids) may be felt in the neck. The laryngeal cavity is divided into – the supraglottis, the glottis and the subglottis. The leaf-shaped epiglottis projects upwards and is anchored to the inner surface of the thyoid cartilage where the vocal cords meet anteriorly. Embryologically, the larynx develops from a two – part anlage. -The supraglottis – from a buccopharyngeal bud. The glottis and subglottis from the tracheo- bronchial bud. The glootis is formed by the free edge of the true vocal cords /vocal folds/. The vocal cords include: The vocal ligament, the vocalis /thyroarytenoid) muscle, and the mucosal covering. Musculature of the larynx Two groups of muscle – internal /3-paired/ and a single external muscle act both synergistically and antagonistically to control the function of the larynx. They open and close the glottis to put the vocal cords under tension. Innervations of the larynx. The nerve supply of the larynx arise from cranial X nerve – the vagus: 1.
Superior laryngeal – dividing into: -sensory /internal/ branch – supplies the interior of the larynx down into the vagus nerve, and -motor/external/ branch – to the external crico-arytenoid muscle. 2. Recurrent laryngeal nerve. -provides motor supply to the rest of the ipsilateral intermal laryngeal muscles and to the contralateral inter-arytenoid muscle. -Sensory innervations to the laryngeal mucosa distal to the glottic cleft. NB: -The Left Recurrent Laryngeal nerve (RLN) loops around the aortic arch to reach the larynx in the groove between the trachea and sophagus. -The Right RLN passes around the Subclavian Artery and then runs upward between the trachea and esophagus Phonation Speech production has three phases: pulmonary, laryngeal and oral. -The pulmonary phase :- creates the energy flow with inflation and expulsion of air. This provides the larynx with a column of air. -The laryngeal phase The column of air provided by the pulmonary phase sets the vocal cords into vibrations of certain frequencies to create sound. -The oral /supraglottic/ phase: Modifies the sound so created in the laryngeal phase.
This modified sound represents the unique individual voice. Words are, thus, formed by the action of the pharynx, tongue, lips and teeth. The Swallowing Action The act of swallowing occurs in two phases: an oral and pharyngo – esophageal phases. The oral phase: Deals with displacing the food bolus backward by the pressure of the tongue. This is an active /voluntary/ phase. The pharyngeal and esophageal phase: this is an involuntary /inactive/ phase, and involves several steps, the most important of which is laryngeal elevation as this protects the airway against food entry.
To sum up, the laryngeal functions include: -Conduit for respiratory exchange -Sphincter to avoid aspiration -A reflex protective mechanism -Voice production -Thoracic fixation for effort The sense of taste The basic taste sensations are sweet, salty, sour and bitter. All other tastes are mixed sensations in which smell sensation is also integrated. The sensory organs for taste are the taste buds found mainly in the lingual papillae (vallate, foliate, fungiform) and the remaining scattered in the hard palate, posterior pharyngeal wall, the buccal mucosa, etc.
These fine gustatory hair cells must bath in saliva or other fluid to allow the sense of taste to be evoked . The sensory innervations for the perception of taste is provided by: -The chorda tympani, arising from Crania N VII. -The lingual nerve, from Cranial Nerves V and IX. (Trigeminal & Glossophayngeal). The salivary Glands There are 3-paired major and numerous minor salivary glands. The major paired salivary glands are: -The parotid -The submandibular and -The sublingual The minor salivary glands – estimated to number >100 – 1000.
They are scattered in the mucosal layers of the aero-digestive tract. About 100 – 1500ml saliva are secreted daily, 9% being water. Physical, chemical and mental states influence salivary production. Embryologically, the major salivary glands arise from solid ectoderm cell accumulation of the foregut, between the 4th – 8th weeks of gestation. The ducts become patent in the 22nd week of intrauterine life. The following table demonstrates certain features of the individual major salivary gland: Characteristic Features of The Major Salivary Glands:
Srl. No. Distinguishing featuresThe Parotid glandThe Submandibular glandThe Sublingual gland 1. Anatomic Location On the side of the face at angle of jawIn the floor of the mouth Oral floor mucosa 2Duct, orificeStensen’s duct Adjacent 2nd upper molar Wharton’s duct, floor of mouth Into Submandibular Gland duct 3Type of saliva secretion, Serous 30% Serous and mucus: 55-65%Mucosa 5% 4SizeThe largest 2nd largeThe smallest 5Calculus formation Less frequentMost frequentLeast, if at all Functions of Saliva: )Protective action – on the mouth, upper respiratory tract 2)Assists digestion: lubrication; starch splitting by amylase 3)Helps in the excretion of antigens and foreign material 4)Dental protection: formation and maintenance of dental enamel 5)Medication taste sensation. Examination of the throat, head and neck A stepwise approach is advisable: 1. general inspection 1. 1. The head and neck – asymmetry; deformity 1. 2. The face bony structures; soft tissue – asymmetry, deformity 1. 3. The lips – abnormality in appearance, movement 1. 4. Assessment of the mouth opening . 5. Tongue: Appearance; movement 1. 6. Assessment of the oral cavity: Look for any visible abnormality of buccal sulcus, dental arches. 2. Palpation: any palpable mass. If so, describe the mass in terms of site, size, consistency degree of tenderness 3. Mirror laryngoscopy. Disorders of the throat, head and neck The Mouth The mouth may present with certain lesions that may turn out to be sources of discomfort. As most of them are commonly encountered, proper evaluation is advised. 1. Ulcer •Aphthous /herpetic/ – Hydrcortisone emulent; Acyclovir may at times help!! •Traumatic •Allergic /Auto-immune •Infective: Stevens Johnson syndrome •Neoplastic 2. Swelling: •Polyps – cheek mucosa – repeatedly trained •Retention cysts: – ranula •Other cystic lesions •Neoplasm The tongue •Micro-, macro- glossia •Fissured tongue •Black hairy tongue •Median Rhomboids •Glossitis •Smooth tongue The teeth Any gross abnormality Pharynx: Pharyngitis Infective: – Viral, bacterial – Fungal – candidacies Non-infective – due to – Inhalation – Post-Radiotherapy Tonsillitis: – Exudative – Chronic and recurrent – /fever, general malaise, reduced appetite/.
Treatment: – Medical: Antibiotic analgesics – Surgical: Tonsillectomy Indications: – Recurrent infections (7, 5, 3 ) PersistentObstructivesleep apnea/OSA/: Adeno-tonsillar hypertrophy in children – if untreated, complications like core pulmonale ( RF) -Followingperitonsillarabscess/ quinsy/. -Asymmetric unilateral tonsil enlargement in an adult Quinsy:- A collection of pus /abscess/ in the tonsillar bed, outside the tonsillar capsule.
It is associated with: intense pain, dysphagia and muscle spasm leading to trismus( lockjaw) Treatment: – Incision and drainage /Risk of aspiration in neglected cases, if spontaneous rupture at night occurs/. – I. V antibiotics – May require admission to hospital – Frequent saline throat wash with luke-warm saline Para-pharyngeal abscess: Treatment: Incision and drainage – I. V antibiotics, with anaerobe coverage. Retro-pharyngeal abscess: May be due to retropharyngeal adenoids being infected, progressing to abscess formation. Lateral neck x-ray view reveals retropharyngeal soft tissue shadow.
Treatment: – An emergency, requiring urgent incision and drainage, UA, assisted by suctioning, head kept reclined – I. V antibiotics anaerobic coverage / In some adults, suspect TB!! / Infectious Mononucleosis /glandular fever/ Cause: Epstein – Barr Virus •Usually as severe membranous tonsillitis •Inflamed and enlarged tonsils •Marked cervical lymphadenopathy •? Hepatosplenomegally. Atypical lymphocytosis /Paul– Bunnel titers rising rapidly/ Treatment: symptomatic (Skin rash following ampicillin administration is a characteristic response!! /. Pharyngeal Pouch: In middle age male. /M : F = 4 – 1/
Corrosive ingestion •Accidental – more in children Treatment: NG tube feeding The Larynx Inflammatory: •Laryngitis •Acute laryngotracheobronchitis (ALTB) . . . Croup •Common in winter, specially in children under 2 yrs •Follows an acute viral URTIs •Grossly swollen and edematous laryngeal and tracheobronchial mucosa Treatment: – Steroid: Dexamethasone, 0. 6mg/Kg po, iv, or subcut – Nebulised epinephrine 2ml of 1:1000in 2ml N saline, or – Nebulised ventolin 1ml of 1: 1000 in 3ml N saline – Humidification/steamy environment/ soothes the harsh cough ? Tracheotomy Epiglottitis:- Acute epiglottitis is a localized infection of the upper part of the larynx. The epiglottis becomes severely swollen, thus obstructing the laryngeal inlet. – Etiology: Haemophilus influena type B/HIB/ – rapid onset of ‘quack-like’ cough, with impending airway Obstruction – Strider develops rapidly – The child tends to sit up, leaning forward to relieve the Airway (tripod position) Treatment: – Minimize the attempt to examine the throat, as this may induce spasm Emergency admission to hospital – Resume i. v antibiotics/Amoxicillin/ – Endotracheal intubation/tracheostomy/, for airway restoration Vocal Abuse •Acute abuse: shouting, screaming ? singer’s nodule (MID 1/3). Localized thickening •A generalized oedema – of Reinke’s space along both vocal cords Neoplasm: The larynx is the most common site of neoplasm, both benign and malignant Causes: – polyp – Recurrent laryngeal papilloma (HPV 6,11) Symptoms: hoarseness of voice, strider Treatment: Larvngoscopic extirpation
Malignant: Most commonly encountered is squamous cell carcinoma. General principles of management Diagnosis: suspicision, examination, biopsy; assess staging Treatment: – surgery and/or/; Radiotherapy – Total Laryngectomy – Voice Rehabilitation: Esoph,; TEF with speech value ( blom singer voice prosthesis ) Laryngeal Dysfunction Impairment of either sensory nerve supply to the mucosa or motor supply to the laryngeal muscles. Sensory loss may lead to chocking or aspiration on swallowing. Motor loss (RLN palsy) results in the affected vocal cord assumes a median position.
Other laryngeal disorders may arise in relation to certain disorders: •Hypothyroidism •Angioneurotic edema •Rheumatoid arthritis •Foreign bodies The head and Neck Neck lumps may arise from: 1. Skin and subcutaneous tissue: •sebaceous cysts, lipomas ,globus pharyngeous 2. Congenital Remnants •Dermoid cysts (mid line ) •Thyroglossal duct cysts (mid line ) •Branchial cysts (lateral ) •Cystic Hypgroma 3. Thyroid gland 4. The salivary glands 5. Inflammatory •Mumps •Calculus ? submandibular 6. Neoplasm •Squamous cell carcinoma ( 90%) •Adenocystic carcinoma 7. Traumas