Ear, Nose, and Throat Handbook PDF

Students and Foundation Trainees in Otolaryngology (SFO UK) SFO UK ENT UK t/a BACO & BAO-HNS Royal College of Surgeons 35-43 Lincoln's Inn Field London WC2A 3PE +442074058371 [email protected] Ear, Nose and Throat: The Official Handbook for Medical Students and Junior Doctors By the Students and Foundation Doctors in Otolaryngology (SFO UK) Part of ENT UK Authors and Editors Alexander Yao Michaella Cameron Charlotte McIntyre John Allen Mamoona Khalid-Raja Jayesh Doshi Andrew Robson Dheeraj Karamchandani Roland Hettige Eamon Shamil Irfan Syed Nimesh Patel Contents Introduction Preface Foreword A Career in Ear, Nose and Throat Surgery Further Information Generic Skills in ENT General ENT History Ear Examination Nasal Examination Neck and thyroid status exam Cranial Nerve Examination Otology Ear Anatomy Dizziness and Vertigo Hearing Loss Tinnitus Facial Nerve Palsy Otalgia Otorrhoea Otitis Externa Acute Otitis Media Otitis Media with Effusion Chronic Otitis Media Cholesteatoma Rhinology Nasal Function and Anatomy Epistaxis Nasal obstruction Fractured Nose Septoplasty/Septorhinoplasty Rhinitis and Rhinosinusitis Allergic Rhinitis Non-Allergic Rhinitis Acute Rhinosinusitis Chronic Rhinosinusitis Nasal Polyps Other Sinonasal Lesions Cleft Lip and Palate Head and Neck Head and Neck Anatomy Facial Muscles Blood Supply to the Face and Neck The Major Salivary Glands Oral Cavity Topography of the Neck Fascial Layers of the Neck Nervous Supply of the Head and Neck Physiology of Swallowing Taking History of a Neck Lump Causes of Neck Lump Branchial Cysts Dysphagia Dysphonia Tonsillitis Pharyngeal Pouch Globus Pharyngeus Thyroid Masses Thyroglossal cyst or sinus Multinodular goitre Thyroid cancer Benign and Malignant Neoplasms of the Salivary Glands Carcinoma of the Oral Cavity Carcinoma of the Pharynx Carcinoma of the Nasopharynx Carcinoma of the Oropharynx Carcinoma of the Hypopharynx Carcinoma of the Larynx Laryngopharygeal reflux Snoring and Obstructive Sleep Apnoea ENT Emergencies Acute Airways Obstruction Epistaxis (Nose Bleed) Foreign body in the nose Nasal septum haematoma Foreign body in the ear Perforated tympanic membrane FB in the pharynx or oesophagus Deep neck space infections Penetrating neck trauma Medications in ENT Antibiotics Steroids Antihistamines Vestibular sedatives & Meniere’s disease Practical Procedures in ENT Nasal Cautery Anterior Nasal Packing Nasendoscopy Oto-Microscopy and Foreign Body Removal ENT Investigations Pure Tone Audiometry Audiogram Case Study 1 Audiogram Case Study 2 Tympanometry Hearing Tests In Children ENT Operations Grommet Insertion Middle ear and Mastoid surgery Tonsillectomy Adenoidectomy Functional Endoscopic Sinus Surgery Parotidectomy Thyroidectomy Neck Dissection Tracheostomy Introduction Preface ENT makes up a significant part of the clinical practice of general practitioners, paediatricians and emergency doctors although exposure to the specialty is often limited during undergraduate training. This “E-book” has been written to provide a practical guide to the day-to-day management of common ENT conditions and will be helpful to medical students and junior doctors as well as other clinicians that have exposure to ENT as part of their practice. It has been developed by the Students and Foundation Doctors in Otolaryngology group (SFO UK), which is part of ENTUK. The group aims to provide support for undergraduates in medicine and junior doctors with an interest in ENT. The content is based on a Delphi study that set out what the most important topics should be in an undergraduate ENT curriculum taking in to consideration guidance published in Tomorrow’s Doctors by the General Medical Council guidance. Congratulations to the authors and to my colleagues on the SFO UK committee for delivering an excellent and novel educational resource. A number of individuals have been instrumental in producing this E-book from conception to production. These include Alex Yao, Michaella Cameron, Charlotte McIntyre, John Lee Allen and Mamoona Khalid-Raja. I also wish to particularly thank the section editors Andrew Robson, Dheeraj Karamchandani, Roland Hettige, Eamon Shamil, Nimesh Patel & Irfan Syed as well as James Tysome & Victoria Ward (Elf-ENT) for allowing us to use many of their images. Mr Jayesh Doshi PhD FRCS (ORL-HNS) MMed Consultant Otolaryngologist Chairman of SFO UK committee (2018) Foreword Ear, Nose, and Throat (ENT), or otorhinolaryngology, is an important, interesting and diverse specialty. It covers a wide range of areas from the common, such as tonsillitis, to the highly specialised, including cochlea implantation, congenital airway disease, voice disorders, skull base and facial plastic surgery. Whether you become a GP or an A&E doctor, you will encounter ENT pathologies in abundance, some of which can be life threatening. Yet, students have limited exposure to the specialty within most undergraduate curricula. This book complements the national ENT curriculum written by ENTUK. Although not designed to be a comprehensive text, this book aims to provide you with the most important topics that you should know by the time you finish medical school and qualify as a foundation doctor. The book will also prove useful for foundation doctors wishing to refresh and review their ENT knowledge. Topics are presented systematically in an easy-to-read format suitable for short attachments. Students may also find it useful to use as reference material chapters explaining common medicines, investigations, procedures, and operations specific to ENT. ENT is a very hands-on specialty and ENT doctors are generally very approachable! So make the most of every opportunity to exude enthusiasm, watch and participate during your attachment! Professor Anthony Narula Consultant Otolaryngologist MA MB BChir FRCS FRCS (Ed) President of ENTUK (2016) A Career in Ear, Nose and Throat Surgery Ear Nose and Throat (ENT) surgery or Otorhinolaryngology offers an exciting and varied surgical career option. It has been described as a ‘cradle to grave’ specialty with a caseload ranging from a baby with hearing loss, teenager with allergic rhinitis to an elderly man with throat cancer. As there is no separate medical companion, ENT surgeons also manage the non-surgical care of their patients. Furthermore, once at registrar level, on calls can be done from home, which can be considered as particularly attractive. Subspecialties Head and Neck Surgery Otology Skull Base Surgery/Neuro-Otology Thyroid and Parathyroid Surgery Rhinology Facial Plastic Surgery Paediatrics Laryngology Typical working week 4 clinics a week 2 surgical sessions a week Light emergency work Multidisciplinary work with other specialties (audiology, speech and language therapist, endocrinologist, oncologists, plastic surgeons, maxillofacial surgeons and dermatologists) Further Information Approach your local ENT team! ENT UK: www.entuk.org Student and Foundation Trainees in Otolaryngology (SFO UK): http://sfo.entuk.org Association of Otolaryngologist in Training (AOT) : www.aot.ac.uk Royal College of Surgeons of England: www.rcseng.ac.uk British Association of Paediatric Otolaryngology (BAPO): www.bapo.org.uk British Rhinological Society (BRS) : www.britishrhinologicalsociety.org.uk British Otolaryngology & Allied Sciences Research Society (BOARS) https://www.entuk.org/boars-section Intercollegiate MRCS exams: http://www.intercollegiatemrcsexams.org.uk/new Generic Skills in ENT General ENT History Principles of history taking in ENT Good history taking is an essential skill to be maintained throughout your training. By building a good rapport, you will help the patient feel more comfortable about discussing his/her symptoms. It provides the opportunity to explore a patient’s concerns and expectations. After completing a thorough history, you should have a good idea of what the top differential diagnoses could be. Before starting Wash your hands Introduce yourself and ensure the patient is comfortable Maintain good eye contact and remember the importance of developing good rapport with the patient (and the parents if present) Structure of history taking Presenting complaint (PC) ‘How may I help you today?’ History of presenting complaint (HPC) ‘ When did this problem begin’ Enquire about the relevant risk factors and other specific questions relating to the presenting complaint. Do have a targeted list of questions for PCs related to “Ear”, “Nose”, and “Throat/Head Neck” (For targeted histories, go to the relevant sub sections of this booklet) Previous episodes - Severity, response to previous treatment and hospitalisation Past medical history (PMH) Birth History – Particularly important for ear conditions in children Drug history (DH) - Including over the counter medication and vaccinations Allergies Family History Social history (SH) - Do not forget to enquire about the impact that the presenting complaint has had on quality of life Systems review - Also enquire on any tendency to bruise or bleed easily At the end of the history Summarise the patient’s history to them. Clarify that you understood them correctly and whether there is anything else that they would like to mention. Ear examination Before starting Gel/wash your hands Introduce yourself and ensure the patient is comfortable Ask about any pain or tenderness The patient should be positioned on the chair and you should place yourself to the side of the patient. In children, positioning is even more important. Children should be sat across the parent/nurses lap, with the side of the head held to the chest by the carer’s hand (See Figure 1) Flailing arms can be secured with the carer’s other hand. Ideally, aim to examine children as opportunistically as possible and incorporate play as part of the examination. Figure 1: Correct positioning of a child for ear exam Inspection From the front: note the size, assess symmetry of the pinna. Are there differing degrees of protrusion? Is there an obviously abnormal pinna? For example, see Figure 2. Figure 2: Congenital Microtia of the External Auditory Canal Inspect each ear individually - Start with the normal ear Pre-auricular - Inspect for scars (previous parotidectomy or middle ear surgery), swelling (infection, parotid tumour), erythema (infection/ inflammation), sinuses, pits, fistulae Pinna - Note any signs of erythema, swelling (infection, haematoma) or tenderness Post-auricular - Move pinna anteriorly to inspect behind the pinna. Note any post-auricular scars. Acute and/ or painful swelling here suggests infection (mastoiditis or lymphadenitis) Examine the other ear. Note any difference. Otoscopy Ensure the otoscope has good magnification and illumination. Use the largest speculum that will fit comfortable in the external auditory canal (EAC) Start with the “normal” ear Gently pull the pinna upwards and backwards to straighten the ear canal to best visualise the tympanic membrane. In children, pulling the pinna downwards and backwards may provide better visualisation Hold the otoscope like a pencil and use your little finger as a fulcrum against the cheek to avoid injury should the patient move suddenly Inspect systematically Figure 3: Normal right tympanic membrane External auditory canal: Wax or discharge, erythema, swelling (infection, trauma) Tympanic membrane (See Figure 3): Is there a normal light reflex in the anteroinferior quadrant? Colour of drum - Normal is greyish & translucent. Pink/red colouring can mean infection/inflammation and white plaques can indicate tympanosclerosis. Position of drum - Retracted (cholesteatoma, infection), bulging (infection), perforation Ossicles: The malleus, incus and stapes can be seen sometimes through the tympanic membrane especially if there is a perforation. Pneumatic otoscopy can also be used to assess tympanic membrane mobility – this modified otoscope has an air-tight seal when placed in the ear canal and a rubber bulb (similar to that of a sphygmomanometer) which the user can squeeze which alters the pressure within the ear canal Hearing tests These tests include the Pure Tone Audiogram (see Chapter: ENT Investigations - Pure Tone Audiogram). Examine a patient’s response grossly to your greeting. Can they hear you? Is there a hearing aid being used? (i) Free field speech testing Free field testing is a good screening tool for hearing loss Use of masking improves the accuracy of testing: Rub the tragus of the contralateral ear whilst performing this to prevent sound being heard in the contralateral non-test ear Use polysyllabic phrase (number or letter) e.g. ‘C5’, ‘37’ or motivational phrases in children e.g. ball, sweets, crisps Test normal ear first. Perform, in order of intensity at 60cm (arms length) and 15cm: whisper, conversational speech, loud voice. Patient should be able to repeat >50% of the letters/numbers correctly. If he/she can repeat: Whisper at 60cm – Hearing better than 30dB Whisper at 15cm – Hearing better than 35dB Conversational voice at 15cm - Hearing better than 55dB Loud voice at 60cm – Hearing worse than 75-90dB ii) Weber’s and Rinne’s tests These tests assess air conduction (AC) and bone conduction (BC) and are used to help delineate whether hearing loss is sensorineural (SNHL)or conductive (CHL) in origin. Weber’s test Figure 4: Weber’s test Vibrating 512Hz tuning fork applied firmly to the midline of the forehead, apex of head (see Figure 4) Ask the patient if he/she can hear a tone in the right ear, left ear or centre of the head The “louder” ear may be due to conductive hearing loss in that ear (sound travels through the bone), or sensorineural hearing loss in the other ear You can work out which this is by performing Rinne’s test. Rinne’s test Figure 5: Rinne’s test Place vibrating tuning fork with base on mastoid process (position 1, testing bone conduction). See Figure 5 Then move the tuning fork so its prongs are adjacent to (but not touching) the external auditory meatus (position 2, testing air conduction). Ask patient to tell you which is louder, when the fork is placed behind the ear or in front of the ear Position 2 is louder than position 1 in the normal ear (Positive Rinne), as an intact hearing apparatus of the external and middle ear amplifies sound. When position 2 is quieter than position 1, (Negative Rinne), this indicates external or middle ear disease affecting the air conduction Interpretation of Weber’s and Rinne’s test (AC= Air conduction, BC= Bone conduction, SNHL= Sensorineural hearing loss, CHL= Conductive hearing loss) Facial Nerve Examination See “Cranial Nerves Examination” section. Concluding Thank patient Wash hands In an exam setting, summarise findings to the examiner and mention extra tests that you may wish to perform: Rigid nasendoscopy - Useful to identifying nasopharyngeal pathology e.g. adenoids, carcinoma, Pure tone audiometry and tympanometry. Nasal Examination Before Starting Gel/wash your hands Introduce yourself, ask for permission to examine the patient and ensure they are comfortable. Ensure the examination area is well lit. Ask about any pain or tenderness Ask if they have had any previous surgery Inspection From the front: shape change, deviation from the midline, symmetry of one side to another, scars, skin changes It is often easier to split the nose into thirds when describing shape or deviations, (see Figure 6 and Figure 7). Figure 6: Separation of the nose into bony pyramid, cartilaginous pyramid and lobule. The upper third mostly composed of bony vault, middle third made up of dorsal septum and upper lateral cartilages, and lower third or nasal tip composed primarily of lower lateral cartilages, septum and soft tissue) Figure 7: Upper, middle and lower thirds of the nose. From the side (the side or dorsal profile of the nose): can comment on shape, hump (protruding bump) or collapse (sunken in), projection (how far the nose sticks out from the face) and rotation of the tip (whether the tip of the nose is pointing up or drooping down). When performing advanced assessment of the nose, e.g for cosmetic analysis, then angles and measurements of the nose in relation to the surrounding face become more important. From below – look for symmetry, deviations and scars of previous surgery. Palpation Skin envelope – feel the thickness of nasal skin (thinnest over bone, thicker sebaceous skin over lower nose) Tip Recoil – the tip of the nose is pushed in and the degree of resistance is assessed- lack of recoil may indicate lack of tip support Anterior rhinoscopy Examine the anterior internal nose with a Thudicum’s speculum and headlight (see Figure 8). How to hold a Thudicum’s speculum Figure 8: How to perform anterior rhinoscopy with a Thudicum’s speculum. The speculum is held from the tip of the index finger of the left hand with the tines facing the patient. The middle finger goes in the front and the ring finger behind, with the thumb pressed firmly on top to support the speculum. The hand is then twisted, and pressure is then used between the middle and ring fingers to open and close the speculum. The speculum is held like this so the rest of your hand does not obscure your view into the nose. Your contralateral dominant hand is then free to use instruments in the nose should you need to. It is important to ensure your light source is lined up with the nasal cavity. Look especially for these common pathological findings: Septal deviations (see Figure 9) Evidence of swelling (rhinitis causing enlarged inferior turbinates, oedema and clear rhinorrhoea- Figure 10) Septal perforations (holes in the cartilage – see Figure 11) Prominent blood vessels (see Figure 12) Polyps in middle meatus/nasal airway (see Figure 13) Figure 9: Septal deviation to the right Figure 10: Right Inferior Turbinate swelling due to allergic rhinitis Figure 11: Septal perforation when viewed through the right nasal airway. Figure 12: Prominent blood vessels overlying right Little’s area (anterior septum) Figure 13: Left-sided inflammatory nasal polyp Other nasal tests Nasal misting Perform nasal misting with a Lack’s cold metal tongue depressor (see Figure 14) Figure 14: Cold spatula misting test. The humidified expired air creates a mist on the cold metal tongue depressor. Due to its simplicity and lack of invasiveness, it is especially useful to assess bilateral nasal patency in paediatric patients. Cottles & Modified Cottles Test Perform Cottle’s & Modified Cottle’s Test using a Jobson-Horne probe/ear curette for external/internal nasal valve patency +/- alar collapse (Figure 15). Figure 15: Modified Cottle’s test Modified Cottle’s Test which involves placing a Jobson Horne probe under the lower end of the upper lateral cartilage and opening out the internal nasal valve (the narrowest point of the nasal airway) which can be narrowed by septal deviations, enlarged inferior turbinates or collapsed nasal cartilages. The original Cottle’s maneuver described pulling the side of the face outwards to try and relieve the nasal obstruction, but this was not always deemed a reliable method of assessment. Examine the oropharynx Examine oropharynx with a tongue depressor. Look for posterior cobble-stoning associated with chronic inflammation or infection/post nasal drip or large antro-choanal polyp. Perform Flexible Nasendoscopy (FNE) The use of modern flexible endoscopes allows a thorough assessment of the nasal cavity and drainage pathways of the paranasal sinuses. One can also pass the endoscope beyond the post nasal space to assess the oropharynx, larynx and hypopharynx. However, in this section, we will concentrate on the examination of the nasal cavity. There main areas of examination are as follows: Figure 16: Endoscopic view of the right anterior nasal cavity. Figure 17: Endoscopic view of the right middle metal region Figure 18: Endoscopic view of the right post-nasal space. The Eustachian tube orifice is where the middle ear drains down into the nasal cavity. The Fossa of Rosenmueller is an important place to check for pathology such as nasopharyngeal carcinoma. Neck and thyroid status exam Before Starting Wash your hands Introduce yourself and ensure the patient is comfortable Ask about any tenderness (does their voice sound normal?) Expose the neck adequately (ideally to the clavicles) Ensure that you are able to move around the patient. If not, the patient should be repositioned Inspection Assess from the front and both sides of the patient Note any neck asymmetry or obvious masses. Be able to describe gross features of the mass (size, neck level, overlying skin involvement and obvious pulsatility) Scars from previous radiotherapy changes, thyroid surgery, parathyroid surgery, neck dissection, tracheostomy Palpation Figure 19: Correct hand position for thyroid examination You should examine the patient from behind. You may be able to note proptosis of the eyes (Graves’ disease) Fingers are more sensitive than thumbs so use your fingertips to palpate neck, rolling tissues and compressing them gently (Figure 19) Ask the patient to swallow a sip of water. If the mass moves upwards with swallowing it suggests thyroid origin Ask the patient to stick out their tongue- a midline lump moving up suggests a thyroglossal cyst When noting any lump during palpation, describe the presence of the following signs: Tender (infection, inflammation i.e. thyroiditis) /non-tender Temperature- heat may indicate inflammation or infection Firm/soft Smooth/craggy. Can you feel multiple nodules? Fixity to the overlying skin or underlying tissues. Site of lump. Is it in the anterior or posterior triangle? Size of lump; often comparing the size of a lump to common fruits (eg grape, plum, bean) is helpful Examine the lymph nodes in the neck (anterior & posterior triangles) Begin in midline with submental lymph nodes. Progress on to submandibular nodes, pre/ post-auricular nodes, occipital nodes, anterior/posterior cervical chain Do not forget the supra- clavicular area Auscultation Auscultate the thyroid. A bruit is a sign of increased blood flow and may indicate hyperthyroidism Percussion Tap the superior part of the sternum for a large goitre extending retrosternally with percussions sounding stony dull. Thyroid status examination General Appropriately dressed Look sweaty? Hands and arms Examine for tremor (hyperthyroidism) by asking patient to put arms outstretched Inspect the nails for thyroid acropachy (similar to clubbing, hyperthyroid- see Figure 20), and palmar erythema (hyperthyroid) Feel the temperature of hands and presence of sweating (hyperthyroid) Take the pulse. Atrial fibrillation, tachycardia (hyperthyroid), bradycardia (hypothyroid) Figure 20: Thyroid acropachy. Face “Peaches and cream” complexion of hypothyroidism. Loss of outer 1/3 of eye brows (hypothyroidism) Graves’ ophthalmopathy (see Figure 21), proptosis, chemosis, and injection of sclera in severe disease Examine the eye movements for dysconjugate gaze (indicator of severe disease) Examine for lid lag (sympathomimetic effect of thyrotoxicosis) Figure 21: Proptosis secondary to thyroid eye disease Legs Inspect for pre-tibial myxedema which is present in hypothyroidism Check the ankle reflexes- brisk in hyperthyroidism, and the opposite in hypothyroidism Pemberton’s test Pemberton’s test is a test for a retrosternal goitre that may obstruct the thoracic outlet and superior vena cava. A positive sign is congestion of facial/neck veins and hoarse voice upon raising the arms. Concluding Thank the patient Wash your hands Summarise your findings to examiner Cranial Nerves Examination Before starting Introduce yourself and obtain consent Wash your hands Ask about tenderness CN I: Olfactory nerve Informal: Ask about changes in smell sensation Formal smelling set test e.g. The University of Pennsylvania Smell Identification Test (UPSIT) CN II, III, IV, VI: Optic nerve, Oculomotor, Trochlear, Abducens Inspect for normal colour vision and normal eye movements as these functions can be affected by skull base tumours and orbital infections. Gradenigo’s syndrome is a complication of acute otitis media resulting in a triad of periorbital unilateral pain, diplopia secondary to VI nerve palsy, & petrositis. CNV: Trigeminal nerve Motor component Patient to clench teeth whilst you palpate the tone of the masseter and temporalis muscles. Open mouth- look for deviation. Tests the pterygoids Sensory component Ask the patient to close their eyes, and say ‘yes’ when they feel you touching them with cotton wool Touch the patient’s face on the left then right of the forehead, cheeks and mandible in turn to test the 3 somatic sensory divisions of the trigeminal: ophthalmic, maxillary and mandibular divisions respectively. Rarely tested in practice are the temperature and pain sensations in these distributions Both motor and sensory Corneal reflex. The afferent limb of this reflex is mediated by CNV. The efferent limb is mediated by CNVII Jaw jerk. Minimal or absent is normal. Brisk is pathological but may be present in younger patients CNVII: Facial nerve Inspect for facial tone- asymmetry Motor. Testing the branches emanating from the parotid Raise eyebrows. Note forehead wrinkles and whether this is forehead sparing or not. If there is no forehead sparing, this likely suggests a lower motor neuron palsy Screw up eyes tight. Puff out cheeks. Smile. Show teeth/grimace. Hyperacusis- due to loss of the dampening effect of nerve to stapedius. Loss of taste- due to loss of chorda tympani. Loss of these modalities depend of the location of facial nerve lesion. CNVIII: Vestibulocochlear nerve See “ear examination” section for further details: Free field testing / whisper voice tests Weber’s and Rinne’s test Pure Tone Audiometry CNIX, and CNX: Glossopharyngeal and Vagus nerve Open mouth, say “ahhhhh”. Uvula will deviate away from the side of the lesion. Assess voice (hoarseness) and quality of cough. Is there a bovine sounding coughing? Think recurrent laryngeal nerve palsy if abnormal (CNX) Swallowing. Gag reflex CNXI: Accessory nerve Shrug against resistance- testing trapezius Turn head- tests the sternocleidomastoid of the contralateral side. CNXII: Hypoglossal nerve Look for tongue atrophy Ask patient to move the tongue side to side. Protrude tongue- tongue tip deviates towards the side of the lesion Conclusion Thank the patient Wash your hands Summarise your findings to the examiner Otology Ear Anatomy The ear is subdivided into 3 main parts: 1) the external ear 2) the middle ear 3) the inner ear (Figure 22). Figure 22: External auditory canal and middle ear (Elf-ENT) The External Ear The external ear canal consists of the pinna (auricle) and the external auditory canal. Pinna (auricle) The pinna consists of elastic cartilage, thrown into folds (see Figure 23), and a fibrofatty lobule. It is supplied by the greater auricular nerve, lesser occipital and facial nerve. Figure 23: Anatomy of the pinna (reproduced with permission from Otolaryngology Houston, www.ghoryeb.com) Nerve supply of the pinna Lateral Anterosuperior – Auriculotemporal nerve (V3) Anteroinferior – Great auricular nerve (C2/3) Posterior – Lesser occipital nerve (C2) Conchal bowl and ear canal – Auricular branch of vagus nerve Medial Greater auricular nerve (C2/3) and lesser occipital nerve (C2) External Auditory Canal (EAC) It is an oblique tube - 3 cm in length. The outer 1/3 is cartilage, and inner 2/3 is bony Ceruminous glands only exist in the outer 1/3. These glands secrete wax The tympanic membrane forms the medial boundary of the canal. Clinical important point: Examining the EAC In adults, the outer third of the canal is directed superiorly and posteriorly as it runs medially. The inner two thirds of the canal is directed inferiorly and anteriorly. When examining the ear canal, you must pull the auricle superiorly and posteriorly to align the two portions. (In infants, pull the pinna (gently!) posteriorly) Blood supply of the external ear Auriculotemporal branch of superficial temporal artery Posterior auricular branch of the external carotid artery Clinically important point: Cauliflower ear The cartilage derives its nutritional support from the overlying perichondrium. Separation of the two layers (with blood, infection or inflammation often following trauma) may result in cartilage necrosis resulting in a cauliflower ear (see Figure 24) Figure 24: Cauliflower ear (reproduced with permission from Otolaryngology Houston, www.ghoryeb.com) Nerve supply of the external ear canal The auriculotemporal nerve and the auricular branch of the vagus nerve The Middle Ear The middle ear is an air-containing cavity held within the temporal bone and it is lined with mucous membrane. It also communicates with the nasopharynx via the Eustachian tube. The function of the middle ear is mainly to amplify and transmit sound energy. The tympanic membrane forms the lateral boundary of the middle ear cavity. It is a circular shape and roughly 1cm in greatest diameter. It is innervated on the outer surface by the auriculotemporal nerve and the auricular branch of the vagus. Figure 25 illustrates the component of the tympanic membrane. The membrane is normally greyish/ pinkish in colour. When the membrane is examined with an otoscope, the concavity of the structure produces a cone reflex in the anteroinferior quadrant. The tip of the handle of malleus forms the deepest concavity of the membrane called the umbo, which is where the cone of light radiates from. The pars flaccida is the weakest and most flaccid area of the tympanic membrane. It plays a vital role in the pathophysiology of cholesteatoma. The pars tensa forms the remainder of the tympanic membrane. Figure 25: A labelled picture of the left tympanic membrane The middle ear structures include: Ossicles – Malleus, incus and stapes (Figures 26, 27, 28). The malleus is the largest ossicle. The lateral process of the malleus is attached to the tympanic membrane. The head articulates with the body of the incus. The long process of the incus articulates with the head of the stapes. The stapes structure includes two limbs (anterior crus and posterior crus), which are attached to the oval window footplate The tensor tympanic and stapedius muscles: these are attached to the ossicles to regulate their movement Chorda tympani (provides taste to anterior two-thirds of the tongue) Facial nerve Pictures of the three middle ear bones: Figure 26: Malleus (reproduced with permission from Otolaryngology Houston, www.ghoryeb.com) Figure 27: Incus (reproduced with permission from Otolaryngology Houston, www.ghoryeb.com) Figure 28: Stapes (reproduced with permission from Otolaryngology Houston, www.ghoryeb.com) The Inner Ear The inner ear is located within the petrous part of the temporal bone. It is medial to the middle ear. Function of the inner ear: Cochlea - Transduction of energy from sound to electrical impulses, which are relayed and interpreted by the brain 3 Semicircular canals (superior, lateral and posterior) – Detect angular head acceleration Utricle and saccule – Detects linear acceleration forwards/backwards and up/down respectively Clinically important points: The average human can detect sounds ranging between 20 and 20,000 Hz The cochlear is tonotopic with high frequency sounds detected at the basal turn of the cochlear and low frequency sounds detected at the apex. The ability to detect high pitch sounds decreases in older humans (presbycusis) Dizziness and Vertigo Description True vertigo is most often associated with a sensation of ‘spinning’ and movement of the surrounding environment. It is important to distinguish this from the more generalised dizziness of disequilibrium. Epidemiology Male: Female ratio 1 : 3 Causes and Differential Diagnoses Once you have established that the symptom is that of true vertigo, it is imperative to ascertain the duration and frequency of attacks, as this is the key to reaching the correct diagnosis and determining if the disorder is most likely peripheral (pertaining to the ear) or central (brain). There are 3 common causes of vertigo originating from the labyrinth itself: Benign Paroxysmal Positional Vertigo (BPPV)- most common cause of true vertigo with typical age of onset 40-60 years Vestibular neuronitis Meniere’s Disease These can generally be differentiated by the duration or onset of the vertigo and by the presence or absence of associated audiovestibular symptoms Another common condition that is seen is vestibular migraine. Symptoms do not always include a headache and/or visual symptoms and can sometimes overlap (e.g. hearing loss) making it difficult to differentiate between conditions such as Menieres. Signs and Symptoms BPPV- Dix-Hallpike test positive. Rotatory vertigo on moving head Meniere’s – Rotatory vertigo associated with fluctuating hearing loss often with low frequency thresholds affected. Tinnitus usually gets worse during an attack. Patients classically get an aural fullness before onset of vertigo. Vestibular neuritis – Rotatory vertigo that is continuous for over 24 hours often associated with nausea and vomiting. Classically they are confined to bed and it takes several days to weeks to recover. Vestibular migraine – Rotatory vertigo can last minutes to hours to days. Classically associated with headaches/photophobia/visual disturbance\phonophobia but these are not always present. Investigations Full neurological examination Pure tone audiometry Dix-Hallpike test MRI of internal auditory meatus may be appropriate with asymmetrical sensorineural loss to exclude an acoustic neuroma Video head impulse testing (vHiT) – this is performed using specialist equipment and can be used to assess the function of the semi-circular canals by measuring visual ocular reflex (VOR) function. It takes around 15minutes to perform and is a quick and sensitive measure of labrythine function Treatment BPPV - Epley’s manoeuvre can be curative in up to 90% by repositioning of the displaced otoconia crystals. In persistent cases, Brandt-Daroff exercises may be advised. Surgical management is rarely required but posterior semi-circular canal occlusion is useful in resistant cases. Vestibular neuronitis – Treatment is expectant with anti-emetics during the acute phase Meniere’s Disease – There is a hierarchy of treatments depending on the severity of the disease and response to previous treatments. The underlying pathophysiology is thought to be endolymphatic hydrops. Therefore “pressure reducing” therapies include low salt diet, medications such as betahistine and diuretics although the evidence for these treatments is weak. Intratympanic injection of steroid or gentamicin is used for those that fail conservative management. Other treatment options include saccus decompression, labyrinthectomy and vestibular nerve section. Vestibular migraine – Common trigger factors include dehydration, foods (classically chocolate, cheese), anxiety and a poor sleep pattern. A symptom diary can help identify these. In those that do not respond to avoidance measures, there are a variety of migraine-preventative medications available. Hearing Loss Description Hearing loss may be unilateral or bilateral. Causes of Hearing Loss Conductive Hearing Loss Sensorineural Hearing Loss History Sudden vs gradual onset. Unilateral or bilateral. Associated otological or neuro-otological symptoms Investigations Pure Tone Audiogram (PTA) & Tuning fork tests (Rinnes & Weber) are complimentary to each other – should always be used together. Management of Hearing Loss Audiological Hearing aids for mild-to-profound hearing loss Surgical Tympanoplasty - Cartilage or temporalis fascia is used to repair a perforation in tympanic membrane. N.B. This surgery is normally done for recurrent ear infections or to waterproof the ear; hearing improvement often occurs when a perforation is closed but cannot be guaranteed. Stapedectomy - Prosthesis used to bypass fixed stapes/footplate in otosclerosis and allow transmission of sound into inner ear Bone anchored hearing aid – a transcutaneous or percutaneous device can be surgically implanted under general or local anaesthesia for a conductive, mixed conductive /sensorineural hearing loss or unilateral dead ear Cochlear implantation- There are specific NICE criteria for cochlear implantation which includes profound sensorineural hearing loss. However it may be of benefit in other patients – they require a multidisciplinary team assessment. Middle ear implant – suitable for conductive and mixed hearing loss Management of excessive ear wax Tinnitus Description Tinnitus is a term used to describe the perception of sound when no external sound is present. It is sometimes described, as ‘the sound of silence’ because all people, if they are seated in a completely quiet soundproofed room, will hear tinnitus. This noise is usually masked by the environmental sounds. It is said to be objective when apparent to the examiner and subjective when apparent to the patient only (more common). Epidemiology No identifiable cause is found in most cases of tinnitus. It is often associated with hearing loss. Types of Tinnitus Non- pulsatile tinnitus is typically referred to as a false perception of sound that is heard by the affected individual only (subjective). It is often described as a buzzing, high-pitched tone or a clicking or popping.It can be associated with noise induced hearing loss, presbycusis, Meniere’s disease, head injury, otitis media and drug related causes (e.g. salicylates, nonsteroidal anti-inflammatory drugs, loop diuretics) Pulsatile Tinnitus (4%) is defined by a sound heard by an individual that is synchronous with their heartbeat and is usually caused by turbulent blood flow that reaches the cochlear. It may be associated with a treatable cause. It can be classified according to the underlying causes which is usually vascular or non vascular. Causes of Pulsatile Tinnitus Vascular causes Atherosclerosis on the internal carotid artery. The eventual stenosis of the artery may predispose the individual to pulsatile tinnitus due to turbulent blood flow. Vascular malformations. Arterio- venous malformations/fistulas are abnormal communications between the arterial and venous system. It may be congenital or acquired- the latter being secondary to trauma or a result of venous sinus obstruction. Glomus tumours are rare hypervascular tumours arising from paraganglia cells. Glomus tympanicum are associated with Jacobson’s nerve around the promontory in the middle ear. Glomus jugulare are found along the jugular bulb and they involve the skull base and may extend in the middle ear. Non-vascular causes Paget’s Disease Otosclerosis Myoclonus. Myoclonus of the middle ear muscles or palatal muscles may cause objective tinnitus, which classically presents with a clicking noise rather than a vascular thrill. Investigations If unilateral and associated with hearing loss, MRI should be performed to exclude an acoustic neuroma. Pulsatile tinnitus may be investigated using MR or CT angiography. Carotid duplex scanning may also be helpful if carotid artery stenosis is suspected. Arteriography is also helpful in a limited number of cases but is associated with a small risk of CVA. Treatment The vast majority of time, the patient just needs reassurance that tinnitus is very common and that they will adapt to it. It tends to be worse at quiet times (e.g. at night when trying to sleep) and worrying about it generally makes the tinnitus worse. Address any underlying cause of the tinnitus in appropriate cases e.g. hypertension, carotid stenosis, side effect of medications For selected patients, behavioural therapy can be provided by audiologist/hearing therapist who introduce coping strategies and tinnitus retraining therapy (TRT). A noise generator can mask tinnitus if interfering with sleep A hearing aid may improve tinnitus if hearing loss is present through a masking effect Facial Nerve Palsy Description Temporary or permanent paralysis of the facial nerve (CN VII) Epidemiology Bell’s palsy (idiopathic in origin) is most common but is a diagnosis of exclusion (15-40 cases/100,000) M: F, 1:1 Causes and Differential Diagnoses of Facial Nerve Palsy Symptoms Dry painful eye, especially, if eye closure is impaired Drooling from side of mouth and difficulties with eating Psychological disturbance Signs Differentiate between upper and lower motor neurone (upper motor neuron has sparing of forehead) Test strength of each branch of the facial nerve using House- Brackmann classification of nerve palsy - Raise eyebrows, tightly close eyes, wriggle nose, puff out cheeks, show teeth. Bell’s phenomenon - White sclera visible as eyeball rolls upwards to protect cornea when eyelid does not close Otoscopy – cholesteatoma, Acute Otitis Media Head and neck examination - parotid tumour Complications of Facial Nerve Palsy Corneal scarring - Blindness if eye care advice not given Wasting of facial muscles, synkinesis Psychological Investigations Pure Tone Audiogram – Look for conductive hearing loss (cholesteatoma) or asymmetrical sensorineural hearing loss (cerebellopontine lesion e.g. acoustic neuroma) MRI scan if suspecting central cause Treatment General: Eye care, Artificial tears/tape eyelid shut. Referral to ophthalmology. Medical: Bell’s palsy/Ramsay Hunt syndrome - Oral steroids and oral antivirals although the evidence for oral antivirals in Bell’s palsy is lacking. Treatment needs to be started within forty eight hours to be effective. Surgical ( rarely indicated): Depends on cause but options include facial nerve grafting, facial re-animation if the function does not recover. Otalgia Description Otalgia is ear pain that can originate from the ear itself or can also be referred from elsewhere in the head or neck (see referred otalgia below) Epidemiology This is a very common presentation to primary care especially in young children. History Referred Otolagia Always ask about other general symptoms – There are several other causes of otalgia, not directly related to the ear (referred pain). It is important to enquire about dental, nasal and throat symptoms in order to identify these. It is particularly important to identify potential indicators of malignancy. Pain referred to the ear is a well-documented phenomenon. Any pathology involving the cranial nerves V, VII, IX, and X and the upper cervical nerves C2 and C3 can cause the sensation of referred otalgia. Trigeminal neuralgia is the most common cranial neuralgia linked to referred otalgia. Other causes of referred cranial neuralgia are described below. Otorrhoea Description The ear can discharge wax, pus, blood, mucus and even cerebrospinal fluid. Remember discharging wax should be reassured as normal. The common bacterial pathogens in a discharging ear that can cause an infection include: Pseudomonas aeruginosa Staphylococcus aureus Proteus spp. Streptococcus pneumonia Haemophilus influenza Moraxella catarrhalis In most patients with a discharging ear, the diagnosis can be made based on good history and examination. We will recap on a focused history taking for otorrhoea and then revise the possible differentials of this symptom in more detail. History Duration of discharge – If chronic, think chronic otitis media including cholesteatoma especially if unilateral Is there associated otalgia (ear pain)? Associated fever or systemic symptoms indicates an infective aetiology Is there associated hearing loss or dizziness? Do not miss a history of putting foreign bodies in the ear especially in children Facial nerve palsy - May occur with acute or chronic otitis media especially if the facial nerve is dehiscent along its course in the middle ear (10% of the population) Check for history of trauma - CSF otorrhoea Has there been any recent history of topical antibiotics? This can in itself cause discharge or predispose to antifungal ear infections if there is prolonged usage Differential diagnosis Otitis Externa Description Inflammation of the external auditory canal that can be acute or chronic Epidemiology An estimated 10% of people develop otitis externa in their lifetime and there is an increased risk after first episode. Hence, otitis externa is an extremely common presentation when on call for ENT or at the emergency ENT clinic. Risk Factors Swimming Warm/humid climates Underlying skin conditions e.g. eczema Immunosuppression e.g. diabetes Trauma e.g. excessive cleaning or scratching Hearing aids that reduce ventilation or introduce infection into the canal Causes Mostly bacterial: Pseudomonas aeruginosa, S. Epidermidis and S. Aureus. Otitis externa can be fungal. There is an increased risk after prolonged antibiotic courses. Symptoms Otalgia (ear pain) - especially on movement of the pinna or jaw. Can be severe. Pruritus (itching) Discharge Hearing loss Signs Pain on moving the pinna and/ or tragus. Pinna may be very tender indeed. If pain is out of proportion with examination findings, there is a history of diabetes or failure to respond to antibiotics, consider necrotising otitis externa which is a severe, potentially fatal progressive form of otitis externa. It is a non-neoplastic infection, which spreads to the bone and results in osteomyelitis of the lateral skull base. It can cause multiple lower cranial nerve palsies. It is almost exclusively unilateral. External auditory meatus swelling, erythema with purulent discharge (Figure 29) Tympanic membrane not always visible because of swelling Complete external auditory meatus obstruction possible If possible, examine the tympanic membrane for a perforation. It is possible to have a secondary otitis externa associated with otitis media Complications Peri-auricular cellulitis Necrotising otitis externa Investigations Swab the external ear canal for MC&S Urgent CT scan is required if necrotising otitis externa is suspected (Unilateral, severe ear pain, elderly and/or immunocompromised) Treatment Aural toilet (microsuction) Topical antibiotic and steroid ear drops e.g. ciprofloxacin (provides anti-pseudomonal cover) Insertion of a Pope wick helps the antibiotic come into contact with the canal wall and stents open a severely oedematous ear canal. The Pope wick looks like a small thin sponge and expands in the ear canal when wet. Admit for diabetic control, IV antibiotics and regular aural toilet if suspecting necrotising otitis externa Figure 29: Otitis Externa (Courtesy of Elef-ENT) Acute Otitis Media Description Acute otitis media is acute onset inflammation of the middle ear, usually of an infective origin. Otitis Media with Effusion (OME) may be a sequelea of acute otitis media but is regarded as a different, non-infective condition. Epidemiology Occurs at all ages, but much more common in infancy Risk Factors Lack of breastfeeding as a baby Attending nursery/day care Positive family history Age between 6-18 months Exposure to smoking Causes An upper respiratory tract infection (URTI) results in inflammation of the upper airways and swelling causes obstruction of the Eustachian tube. Ascending infection results in hyperaemia of the middle ear mucosa with production of a purulent exudate. This is called acute otitis media (AOM) Viral infections account for two thirds of cases of AOM. Respiratory syncytial virus, rhinovirus and enterovirus are the most common. Bacterial organisms include Streptococcus pneumoniae, Haemophilus influenza, and Moraxella catarrhalis. Symptoms Infants: fever, ear pulling, irritability, vomiting Children and adults: otalgia (ear pain), fever, generally unwell, hearing loss. If the tympanic membrane bursts the pain may suddenly improve, but a purulent discharge develops from that ear Signs Bulging tympanic membrane (Figure 30) Injected tympanic membrane If there is a perforation, there may be purulent discharge coming through. There may also be secondary otitis externa Figure 30: Bulging tympanic membrane in AOM (Courtesy of Elef- ENT) Complications Intratemporal: tympanosclerosis (white patch on the ear drum due scarring), hearing loss, tympanic membrane perforation, mastoiditis, labyrinthitis, facial nerve palsy Intracranial: meningitis, intracranial abscess, lateral sinus thrombosis, cavernous sinus thrombosis, subdural empyema. Investigations Consider swab for M, C &S if ear discharging Imaging (CT and/or MRI) if complications are suspected Treatment Analgesia (e.g. Ibuprofen) and anti-pyretics (e.g. Paracetamol) If failure to improve within 24-48 hours, consider prescribing oral antibiotics. A 10 day course of Amoxicillin is first line. If no improvement, switch to Co-amoxiclav. Otitis Media with Effusion (OME) Description This is a middle ear effusion (fluid) without the signs of infection. Also known as ‘glue ear’. Epidemiology Bimodal distribution at a peak at 2 years and 5 years of age. Prevelance is 20% and 15% respectively. 50% of OME resolves spontaneously within 3 months Causes Eustachian tube dysfunction. In children, the Eusatachian tube is smaller and more horizontal than in adults therefore middle ear ventilation is impaired. Thus commoner in cleft palate and other syndromic diseases affecting the face and skull base. Beware of the adult with a unilateral middle ear effusion. Nasopharyngeal tumours can block the drainage of the Eustachian tube and result in a middle ear effusion Symptoms May be asymptomatic in an infant. Parent may notice the child has hearing loss or behavioural problems. Signs Poor speech development Otoscopy: tympanic membrane will appear dull +/- a visible fluid level. If pneumatic otoscopy is performed the tympanic membrane will have poor compliance (Figure 31) Figure 31: Dull right tympanic membrane with visible fluid level (Courtesy of Elef-ENT) Investigations Pure tone audiogram – this will reveal a conductive hearing loss (i.e. air bone gap on PTA) Tympanometry will show a flat trace due to the reduced compliance of the tympanic membrane (i.e. ‘type b’ curve) In an adult with a unilateral middle ear effusion ensure that flexible nasoendoscopy (FNE) is performed to rule out a nasopharyngeal tumour Treatment Antibiotics are not advised as they have no benefit in OME Watch and wait – 50% of OME will resolve spontaneously within 3 months Hearing aid may be useful whilst waiting for the OME to spontaneously resolve Myringotomy and ventilation tube insertion. This is a small incision in the tympanic membrane with the insertion of a small ventilation tube. Once inserted, the grommet will usually self extrude after around 9 months. Grommet insertion can lead to tympanosclerosis (scarring of the tympanic membrane) and tympanic membrane perforation (if the TM fails to heal after the grommet extrudes N.B. more common if history of multiple grommet insertion) Adenoidectomy may reduce the recurrence rate of OME Chronic Otitis Media Description There are two types of chronic otitis media: Mucosal: A tympanic membrane perforation in the presence of recurrent or persistent ear infection. Squamous: Gross retraction of the tympanic membrane with formation of a keratin collection. (cholesteatoma) The disease may be active (infection present) or inactive (no infection present): Inactive mucosal: Dry perforation Inactive squamous: Retraction pocket, which has the potential to become active with retained debris (keratin) Active mucosal: Wet perforation with inflamed middle ear mucosa and discharge Active squamous: Cholesteatoma Mucosal Chronic Otitis Media Epidemiology May occur in children and adults Causes Chronic infection following development of a post-infective, traumatic or iatrogenic perforation Pathogens: most commonly Pseudomonas aeruginosa, Staphylococcus Aureus Symptoms Hearing loss Otorrhoea Signs Mucosal inactive: Dry perforation (Figure 32) Mucosal active: Wet perforation with middle ear inflammation Otorrhoea: May be present in active disease May develop secondary otitis externa due to the discharge Figure 32: Right TM perforation (Courtesy of Elef-ENT) Complications As for acute otitis media. Investigations Pure tone audiometry Ear swab for MC&S Treatment Aural toilet with microsuction ensuring that the whole tympanic membrane is visualised Antibiotic and steroid combination ear drops if infection is present Myringoplasty (also known as Type 1 tympanoplasty). This is the surgical repair of the tympanic membrane perforation using cartilage or fascia. It is indicated to prevent recurrent otitis media. Cholesteatoma Description Despite the name, a cholesteatoma is neither a tumour nor does it consist of cholesterol. Instead, it is an accumulation of benign keratinizing squamous cells which most commonly involves the middle ear. The squamous cells are hyperproliferating and secrete enzymes, which can be locally destructive (with potentially serious complications). It is commonly described as ‘skin in the wrong place’. Epidemiology Can occur in both children and adults but it usually has it’s origins in childhood chronic Eustachian tube dysfunction although congenital cholesteatoma accounts for around 5% of cases (see below). It is more common in males. Causes Congenital cholesteatoma results from persistent epithelial cell rests left within the middle ear during growth of the embryo and is diagnosed in children who have an intact tympanic membrane and no history of ear surgery Acquired cholesteatoma develops after birth. Eustachian tube dysfunction results in tympanic membrane retraction and once the retraction is deep enough keratin migration from the tympanic membrane to the external auditory canal can no longer occur and the trapped keratin develops into a cholesteatoma. Keratin debris can become infected and leads to a chronic ear discharge Symptoms Persistent/recurrent ear discharge despite topical antibiotics Unilateral hearing loss Signs Otoscopy should be performed and micro suction should be used to clear any wax to ensure that the whole TM is visualised paying particular attention to the superior part of the TM (attic area) There is a deep retraction pocket in the TM with keratinous debris within it. There may be granulations around the margins of the retraction pocket and it is very common for adjacent bony erosion to occur If there is secondary infection there will be discharge in the ear canal In congenital cholesteatoma, the tympanic membrane is usually intact but it may be bulging and a white pearly mass will be visible through the tympanic membrane Figure 33: Active squamous chronic otitis media in left ear: attic retraction with retained squamous epithelial debris (cholesteatoma) (Courtesy of Elef-ENT) Complications As per acute otitis media (see above) Investigations Pure tone audiometry CT scan of the temporal bone Treatment Surgical management unless the patient is not fit for surgery The aim of surgery is to remove the cholesteatoma sac and repair the tympanic membrane and any adjacent bony defect, to prevent recurrent discharge. The mastoid cavity is drilled to allow access to the middle ear and all of the cholesteatoma is removed. If there has been destruction of the ossicles, hearing can be reconstructed (ossiculoplasty) using a variety of techniques and the tympanic membrane is replaced with a graft Rhinology Nasal Function and Anatomy Nasal Function The primary function of the nose is ventilation. Other functions include: Humidification of inspired air and dehumidification of expired air Heating or cooling of inspired and expired air Filtering of large matter by vibrissae (small hairs) in the nasal vestibule Olfaction and pheromone detection Mucus production (mucociliary escalator: mucus traps particulate matter and carries it as far as the pharynx, where it is swallowed and then eliminated by the digestive system) Immune protection – lysosomes, immunoglobulin A (IgA), IgG and nitric oxide Ventilation of middle ear cleft via Eustachian tube Drainage of nasolacrimal duct Voice tract resonance Nasal Anatomy The anatomy of the nose can be subdivided into the external nose and the internal nasal cavity and paranasal sinuses. The external nose is attached to the forehead by the nasal bridge and extends towards a free tip. The anterior openings are called the nares or nostrils. The nares are bounded medially by the nasal septum. The skeleton of the external nose consists of bone in the upper third (nasal bones) and cartilages (upper and lower laterals and septum) in the lower two thirds. Clinically Important Point The skin overlying the cartilaginous portion of the external nose contains multiple pilosebaceous glands. Rhinophyma (see Figure 34) is a pathological hypertrophy of the glands, which results in an enlarged, red bulbous nose. It begins with rosacea, which worsens to acne rosacea. It is more common in white men between the age of 40 and 60 years of age. Figure 34: Rhinophyma in an elderly man (reproduced with permission from Otolaryngology Houston, www.ghoryeb.com) The Nasal Cavity The nasal cavity extends from the nares anteriorly, to the choanae posteriorly. The midline is partitioned by the nasal septum (see Figure 35), which itself consists of structures including the maxillary crest inferiorly and perpendicular plate of the ethmoid bone superiorly and vomer posteriorly. The nasal septum is rarely in the midline, but when significantly deviated, it can contribute to nasal obstruction, particularly if the deviation is anterior. Each half of the nasal cavity has a roof, floor, lateral and medial wall. The roof is formed by the body of the sphenoid, cribriform plate of the ethmoid, frontal bone, the nasal bone and the nasal cartilages. The floor is formed by the maxilla, palatine bone and upper surface of the hard palate. The medial wall is illustrated opposite. Figure 35: Bony and cartilaginous septum. (reproduced with permission from Otolaryngology Houston, www.ghoryeb.com) The lateral wall of the nasal cavity consists of a series of bony projections called turbinates (See Figure 36 below). The turbinates are covered by pseudostratified ciliated columnar epithelium and contain venous plexuses, which can engorge in response to external stimuli, neural and hormonal control. They have a role in humidifying and filtering inspired air. Figure 36: Left Inferior turbinate as viewed with the rigid endoscope. There are four major openings into the internal nasal cavity: Sphenoidal air cells drain into the spheno-ethmoidal recess. The posterior ethmoid sinuses drain into the superior meatus. The anterior ethmoid sinuses, fontal sinus, and maxillary sinuses drain into the middle meatus. The nasolacrimal duct drains into the inferior meatus. The olfactory nerve arises in the olfactory mucous membrane adjacent to the cribriform plate. The trigeminal nerve provides general sensation through the ophthalmic and maxillary divisions with nerve endings distributed throughout the mucosa. The arterial supply to the nasal cavity is derived from branches of the internal carotid artery (anterior and posterior ethmoidal arteries) and external carotid artery (facial artery, sphenopalatine artery). The arteries involved in the Little’s area (which lies in the antero- inferior part of the nasal septum) are the following: Anterior ethmoidal artery (from the ophthalmic artery) Sphenopalatine artery (from the maxillary artery) Greater palatine artery (from the maxillary artery) Superior labial artery (from the facial artery) Epistaxis It is not a trivial condition and can potentially be life threatening. If the patient is actively bleeding, see them in A&E Resus, not in an isolated treatment room without resuscitation facilities/help. History You may have to take a focused history whilst simultaneously resuscitating and stabilising the patient (establishing intravenous access, sending off the pertinent bloods and setting up IV fluids). Important points to remember are: Unilateral Predominance- which side did it start or more commonly comes from, which can then focus your assessment for the likely source. Anterior/Posterior – often patients can tell initially if it runs out the front first or down the back of the throat, which may guide further management Frequency – how often is it troubling them? How much blood loss has occurred – estimating blood loss can be notoriously difficult and bleeding from the nose can be very distressing. By focusing on common measures such as a teaspoon, a cupful, or a kidney dish full of blood can help prioritise your patient’s resuscitation requirements. Co-morbidities such as hypertension, cardiac history, anti- coagulant use and previous nasal surgical history can all have an effect on patient management. Antecedents – traumatic bleeding can have a different anatomical source to other forms of bleeding Management techniques, risk factors, smoker, occupation, allergy to nuts Examination Most epistaxis occur in Little’s Area (otherwise known as Kisselbach’s plexus), located in the anterior part of the septum where an anastomosis occurs between the branches of the internal and external carotid arteries. Initial management options for epistaxis include leaning forwards and pinching the soft part of the nose to apply pressure to the septum (not the bony part of the nasal bridge - Figure 37 and Figure 38). Sucking on ice cubes or applied to the forehead may help slow bleeding by causing vasoconstriction of the feeding vessels. The next step should ideally be identification of the bleeding point for cautery (see Cautery in Practical Procedures Chapter) Figure 37: Incorrect method of pinching the nose. Figure 38: Correct method of pinching the nose Surgical Management of Epistaxis If these measures fail to control the bleeding (or bleeding from more posteriorly in the nasal cavity is responsible), an endoscopic sphenopalatine artery ligation under general anaesthesia is undertaken (see Figure 39). Traumatic epistaxis (for example from a sports injury) is usually anterior and related to the anterior ethmoidal artery. Ligation of this is often performed through an external incision at the medial aspect of the orbit. When dealing with acute traumatic injuries of the nose, it is important to rule out a septal haematoma (Figure 40), which can starve the underlying septal cartilage of oxygen and cause ischaemic necrosis and cartilage loss, resulting in a saddle nose. It is therefore important to drain these at an early opportunity. Trauma to the front of the nose may cause one or both nasal bones to be displaced. Assessment of any nasal vault deformity should be made after 5 days once the swelling has subsided. There is a window of opportunity in the weeks after the injury for the nasal fracture to be reduced under local or general anaesthetic. When the cartilaginous septum is fractured, deformed or displaced it may be corrected with a septoplasty (cartilage remodelling) procedure. Figure 39: An endoscopic clinical photograph of the right Sphenopalatine artery being clipped in the back of the nose under general anaesthetic for epistaxis. 2 clips have been applied to the main branch. Nasal obstruction Causes of Nasal Obstruction There are a number of causes for nasal obstruction, many of which are beyond the scope of this chapter. More common, acquired causes of nasal obstruction can be classified as seen below. A thorough history, good clinical examination and tailored investigations will often reveal the underlying aetiology: Infectious – viral; bacterial or fungal infections causing rhinitis/rhinosinusitis Allergy – inflammation with or without nasal polyps Developmental - resulting in septal deviation, bony deviation or both; cleft lip Traumatic – same as above (+/- septal haematomas, perforations, etc) Iatrogenic – previous surgery (eg septoplasty) causing scar tissue (adhesions); residual septal deformities; mucocoeles Drugs – chronic use of decongestants (rhinitis medicamentosa); side effects of medication (eg. Beta-Blockers, oral contraceptive pill); cocaine abuse resulting in vasculitis or septal perforation Neoplastic – benign or malignant masses Inflammatory/Systemic Diseases – eg. Granulomatosis with Polyangiitis (GPA); Eosinophilic Polyangiitis (EPA/Churg-Strauss); Sarcoidosis; Cystic Fibrosis; Kartaganer’s Disease Fractured Nose Nasal fractures do not need to be X-rayed. If the patient is well and there is no epistaxis and no septal haematoma (a boggy swelling of the septum which is usually seen bilaterally and insensate when probed with a jobson-horn- see Figure 40) they can be sent home. If there has been no change in shape and no new nasal obstruction since the injury the patient does not need to be seen by ENT and can be discharged with advice. However, if the swelling and bruising are such that any deformity is obscured, then they should be reviewed in 5-7 days (once the swelling has subsided) in the ENT emergency clinic for assessment of the injury and discussion as to whether the patient wants to proceed to manipulation under anaesthetic. The patients will need to be consented and listed for an MUA (manipulation under anaesthesia- Figure 41) after seeing them in the SHO emergency clinic. The common risks for the procedure include pain, bleeding, the need to pack the nose, the need to wear a splint, bruising and failure to get the nose back to its original shape. If the clinician is confident, however, and the patient will tolerate it, a manipulation under local anaesthetic can be undertaken. Using a dental syringe infiltrate over the nasion down to bone and then either side of the nasal bones. Then firm pressure over the deformity will usually result in the bones being realigned into the midline. Patient selection is key to a successful procedure. They will need to wear a splint for 1 week which can be removed by the patient themselves or their GP practice nurse. If a septal haematoma is present, the patient must have this drained (in theatre) as soon as possible to prevent infection and subsequent destruction of the septal cartilage. This will lead to saddle deformity of the nose. They will need to be started on antibiotics to prevent secondary infection of the haematoma causing a septal abscess. Figure 40: Septal Haematoma after nasal trauma. This requires urgent drainage to avoid complications such as abscess and septal cartilage necrosis. Figure 41: Pre-operative image of trauma resulting in significant nasal deformity. Septoplasty/Septorhinoplasty When the underlying midline cartilaginous or bony septum is deviated, a septoplasty can be undertaken to remodel and improve the functional nasal airway. It is often performed under general anaesthesia, as a day-case procedure. It can also be performed to gain better access to the nose for other endoscopic procedures e.g. limited access for epistaxis surgery or for septal cartilage harvest for graft harvesting. A septorhinoplasty may be indicated if the septum and bony vault are deviated. This operation can be carried out via an external approach (via an incision in the columella) or endonasally. It can be performed for functional and cosmetic indications, and has important implications for both, so patients require appropriate pre-operative counselling. Both of these procedures, if indicated, are not done acutely after the nasal injury and would be done on an elective list often 6 -12 months after the initial injury. Rhinitis and Rhinosinusitis Description The term ‘rhinitis’ describes inflammation of the lining (mucous membranes) of the nose, characterized by nasal congestion, a runny nose, sneezing, itching and post-nasal drip. It can be usually divided into allergic and non-allergic causes. The term ‘rhinosinusitis’ describes inflammation of the lining of the nose and paranasal sinuses. It has a number of manifestations, the commonest symptoms being anterior or posterior rhinorrhea (runny nose or post-nasal drip), nasal blockage/congestion or obstruction, and facial headache or reduction in sense of smell. Allergic Rhinitis Description IgE-mediated Type 1- hypersensitivity reaction of the nasal mucosa. This condition can significantly affect quality of life with negative impacts on activities of daily living, school and work attendance. Epidemiology Allergic rhinitis (AR) is common and increasing in western populations. It can be associated with atopic disease such as eczema and asthma (1 in 3 patients with AR have asthma). There can be a family history noted. Causes Intermittent (previously known as seasonal)- e.g. grass/tree pollen (hay fever) – late Spring/Summer. Persistent (previously known as perennial)- e.g. house dust mite, moulds, dogs, cats Food allergens causing rhinitis – this is a controversial area and not fully proven but may be a contributory factor Symptoms Rhinorrhoea (seasonal) Nasal irritation /itching (seasonal) Sneezing (seasonal) Nasal obstruction (seasonal and perennial) Ocular symptoms e.g. itchy/watery eyes Signs Inflamed nasal turbinates and mucosa- bluish and pale hue to turbinate mucosa, watery nasal discharge and gross turbinate hypertrophy Investigations Clinical diagnosis can be made with a combination of history & examination The mainstay of investigation is the skin-prick allergy test (SPT), which can be done cheaply and quickly in clinic. Positive (histamine) and negative (saline) controls are inserted into the skin (dermis), along with solutions of the various common inhaled aero-allergens (Figure 42), eg grass and tree pollen, dog and cat dander. A positive result is a wheal response after 20 minutes (Figure 43). Resuscitation equipment should be ready in case of anaphylaxis. Contra-indications include severe eczema/dermatographism or anaphylaxis. Patients should avoid taking anti-histamine tablets for 72 hours prior to the test in case they mask a response. Serum RAST (Radio-allergosorbent test) is a blood test to find specific IgE to an allergen. There is no risk of anaphylaxis, but this is more expensive and takes time for the results. This may be also useful in children who may not tolerate SPT. Figure 42: Skin Prick Allergy Testing (SPT) Droplets of various allergen solutions are placed onto the forearm and the skin is punctured Figure 43: After 15-20 minutes the results can be shown by the positive wheal reaction Treatment General advice- avoiding allergen exposure. E.g. washing bed linen at high temperature to reduce house dust mite allergen burden Nasal douching and barrier ointments/creams Oral non-sedating antihistamine, eg. Loratidine, Cetirizine, Fexofenadine Intra-nasal steroids e.g. Fluticasone (Flixonase or Avamys nasal spray), Beclomethasone (Beconase Nasal spray), or Mometasone (Nasonex Nasal spray) - 1 – 2 sprays, once or twice a day titrated to the patient’s symptoms for a minimum of 4-6 weeks. Check formulary for appropriate prescribing ages. Intra-nasal steroid sprays are suitable for long-term use if tolerated. Escalation to steroid drops or oral steroids can be considered on rare occasions for severe symptoms, but caution must be taken over longer courses due to the numerous systemic side-effects. Combination steroid and anti-histamine nasal sprays (eg. Dymista manufactured and distributed by Mylan®) – prescribed by specialists as 2nd line topical management for more effective relief in allergic rhinitis due to the synergistic combination of medications. Leukotriene antagonists e.g. montelukast, (orally) useful if patients also have asthma Immunotherapy- Desensitisation therapy works by gradually increasing the exposure to an antigen. It can be given sublingual or via subcutaneous injection. Immunotherapy to grass pollens and house dust mite is available in a few specialist centres. Non-Allergic Rhinitis Description Inflammation of the nasal mucosa. Epidemiology Very common. Up to 50% of all cases of rhinitis in adults Causes Irritants: tobacco, pollution, cleaning products (occupational) Vasomotor: temperature changes- especially cold, dry air Gustatory: Spicy food Pharmacological: rhinitis medicamentosa (rebound nasal congestion following prolonged use of topical decongestants), substance abuse- cocaine Infection Systemic- Granulomatosis with polyangitis (GPA), sarcoidosis. Physiological- exercise, positional, hormonal Atrophic rhinitis Symptoms Nasal congestion, rhinorrhea, post-nasal drip, hyposmia Signs Nasal congestion and hypertrophic turbinates Investigations Allergy testing to exclude allergic cause Treatment Non-surgical treatment. Non-surgical treatment should always be tried and is the mainstay of treatment. General advice- avoidance of trigger, eg smoking cessation. Nasal douches and intranasal steroids Other: Ipratropium. Decongestants (short-term only) Surgical treatment Surgery is not a permanent, curative procedure as the underlying pathology is to do with the lining of the nose. However, surgery may help improve the nasal airway and allow better delivery of topical nasal steroids, which the patient will need to continue postoperatively. Turbinate reduction surgery for obstructing inferior turbinates. Vidian Neurectomy – cutting the parasympathetic nerve supply to the nose (rarely indicated). Acute Rhinosinusitis (ARS) Description Acute rhinosinusitis (ARS) is caused by symptomatic inflammation of the mucosal lining of the nasal cavity and paranasal sinuses. There is sudden onset of two or more symptoms, one of which should be either nasal blockage/obstruction/congestion or nasal discharge (anterior/posterior nasal drip): ± facial pain/pressure ± reduction or loss of smell; for 12 weeks. Can be divided into CRS with polyps or CRS without polyps. Epidemiology Common. CRS accounts for 85% of outpatient visits for rhinosinusitis in adults. Can follow ARS. Causes Multifactorial and still not fully understood: Allergic: Intermittent or Persistent. Other non-allergic causes – Occupational, Hormonal, Granulomatous/ Inflammatory, Infective (Viral, Bacterial, Fungal), Anatomical, Iatrogenic, secondary to medication (eg. Rhinitis Medicamentosa/Cocaine abuse) Symptoms and Signs The European Position Paper on Rhinosinusitis and Nasal Polyps (EPOS 2012) defines the diagnostic criteria for CRS below: Inflammation of the nose & sinuses causing 2 or more symptoms Nasal blockage/obstruction/congestion Nasal discharge (ant/post nasal drip) +/- facial pain/pressure +/- reduction/loss smell And either: Endoscopic signs of polyps, middle meatal oedema or mucopurulent discharge CT mucosal changes of the ostiomeatal complex/sinuses Investigations CT Sinuses. Can assess the extent of disease and provide anatomical detail for pre-operative planning (see Figure 46). Figure 46: CT Scan in coronal section showing bilateral maxillary sinusitis. R = Right side. Disease is worse on the left hand side mostly in the maxillary sinus and there is hypertrophy of the left inferior turbinate (reproduced with permission from Otolaryngology Houston, www.ghoryeb.com) Treatment Non-operative. Appropriate medical management should be attempted primarily, including: Saline Nasal Irrigation Nasal decongestants (short course only) Anti-histamines (if there is an underlying allergic component) Oral steroids with CRS with polyps – (caution with side effects), followed by topical therapy Topical Steroids with CRS without polyps- Drops include: betamethasone or fluticasone (A typical regime might be for a period of 4-6 weeks) Then switch onto maintenance intra-nasal cortico-steroid spray (INCS) such as fluticasone or mometasone for 3 months until review. Antibiotics – Certain antibiotics may help by their anti-bacterial and anti-inflammatory mechanisms. The true benefit of antibiotics in CRS is undergoing evaluation by ongoing trials. The EPOS guidance suggests macrolides are useful in non- polyp CRS when the IgE levels are not raised and the cardiac history has been taken into account due to possible effects on prolongation of the QT interval (e.g. Clarithromycin 500mg OD PO for 3 weeks). In polyp patients, the antibiotic of choice is Doxycycline (50- 100mg OD PO for 3 weeks) if tolerated. Local formulary guidance should be sought if patients are allergic to first line options. Operative: Functional endoscopic sinus surgery (FESS). The principles of FESS are to remove diseased tissue, relieve obstructions and to restore the normal function and anatomy of the paranasal sinuses. Often it can involve removing the bony septae obstructing the sinus outflows whilst preserving mucosa, to widen the sinus drainage pathways and increase access for subsequent topical medical therapies. Sinus surgery should be seen as an adjunct in the management of CRS where medical treatment alone has failed, rather than stand alone definitive treatment. Patient selection is key, and quality of life screening tools such as the SNOT-22 (Sino-Nasal Outcome Test of 22 questions) can help identify appropriately symptomatic patients who may gain benefit from surgery. Nasal Polyps Description Nasal polyps are very common and are typically bilateral. They typically present with symptoms of nasal blockage with or without a change in smell perception. They are benign. They include: Inflammatory/Allergic Polyps – sino-nasal polyposis, often multiple grey, oedematous polyps associated with CRS (see Figure 47) Antro-choanal polyp – single polyp arising from maxillary sinus extending out towards nasopharynx causing unilateral nasal obstruction. Figure 47: Clinical photograph of left nasal cavity showing inflammatory nasal polyps arising from the sinus drainage pathway (Middle Meatus) blocking nasal airway Treatment Medical Medical treatment involves some form of steroid-based treatment combined with nasal saline rinses. If there are no contra-indications, a typical regime might consist of a short course of oral steroids (Prednisolone 0.5mg per kg PO for 7 days with PPI cover), followed by intra-nasal steroid drops for 4-6 weeks, and subsequently a maintenance intra-nasal corticosteroid spray (INCS) such as Mometasone until further review. There is some evidence from the EPOS guidance that certain antibiotics are of added benefit if the levels of IgE in the serum are not raised (eg. Doxycycline). Surgical The principles of surgery for CRS with polyps are to establish good access for further medical treatment, when medical therapy alone has failed. Simple endoscopic nasal polypectomy or Functional Endoscopic Sinus Surgery (FESS) is usually performed under general anaesthesia and aims to remove the polyps and re-establish the natural drainage pathways of the paranasal sinuses. The extent of surgery will be governed by disease factors, patient factors and the experience of the operating surgeon. When consenting patients for surgery, certain risks should be included such as pain, infection, bleeding, the need to pack the nose, intra-cranial complications (CSF leak and meningitis), intra- orbital complications (double vision/blindness) and possible recurrence of polyps/sinus disease. Other Sinonasal Lesions Benign lesions Papilloma/Wart – verrucous lesion, commonly in nasal vestibule, often multiple and painless, presents with bleeding. Local excision is mainstay of treatment Pyogenic Granuloma – friable lesion that bleeds, usually from trauma often arising on septum. Commoner in pregnancy Other rarer pathology can have the appearance of a “unilateral nasal polyp” during nasal examination. Examples include Inverted Papilloma – benign but locally aggressive polyp that has a predisposition for recurrence if not completely cleared including its site of origin. Can rarely transform into malignancy over time (see Figure 48) Juvenile Nasopharyngeal Angiofibroma (JNA) – vascular benign tumour exclusively present in adolescent males (may have hormonal element). These are extremely rare but classically present with nose-bleeds and nasal obstruction in teenage boys. Embolisation and subsequent surgical removal (endoscopic or open depending on extent) is the mainstay of treatment. Meningoencephalocoele/glioma – herniation of intracranial contents through a weakness in skull-base containing meninges, brain (rarely functioning) or support tissue. Imaging with MRI needed before biopsy. Figure 48: Inverted papilloma right nasal cavity arising from lateral wall of nose Malignant Sino-nasal malignancies are rare but present late, resulting in a poor prognosis. Presenting symptoms include unilateral nasal obstruction, unilateral glue ear, bleeding, pain, neck lumps, unexplained weight loss, eye symptoms, headaches or cranial nerve deficits. The commonest are squamous cell carcinomas (see Figure 49 and Figure 50), adenocarcinomas (associated with wood-working) and nasopharyngeal carcinomas (arising from the nasopharynx) Imaging and histology are essential and the results are discussed in a multi-disciplinary team meeting, where recommendations for which treatment is best suited for the patient can be made. Treatment can be curative or palliative and may include surgery, chemotherapy (drugs), radiotherapy (ionizing radiation) or a combination of these. Nasopharyngeal cancers are commonly treated with radiotherapy or chemoradiotherapy. Figure 49: SCC of the Left Maxillary Sinus Figure 50: Endoscopic image of SCC Left Maxillary Sinus Cleft Lip and Palate Description A cleft is a gap or split in the upper lip and/or roof of the mouth (palate) resulting in an abnormal connection between the oral and nasal cavity. A cleft lip and palate is the most common facial birth defect in the UK, affecting around one in every 700 babies. It can range in severity from a submucous cleft (the muscles of the soft palate not fully joining) which may be relatively asymptomatic to a bilateral cleft lip and palate with immediate concerns at birth regarding airway and feeding. It can be an isolated occurrence or associated with other genetic and developmental abnormalities. Important Considerations Feeding – poor suction, lengthy feeds, nasal regurgitation, excessive air intake, poor airway protection and expending too much energy can cause failure to thrive. Bottles with special nipples can help improve this. Otologic – high incidence of glue ear and delayed resolution (poor Eustachian tube function secondary to abnormally developed palate muscles predisposes to middle ear effusions) means hearing assessment early on is a priority with onward referral for grommets or hearing aids. Speech/Swallow – speech and language therapy to combat problems with palate dysfunction and reflux Cosmetic – lip and nasal deformities will require addressing within 1st year of life and revision often required later as patient grows Dental – restoration / prosthesis may be required for normal function and cosmesis Psychology, Social Work & MDT – parental counselling and assistance is important starting pre-natally and ongoing throughout childhood. Paediatricians are often well placed to help co-ordinate global development. Figure 51: Unilateral left cleft lip and palate (Courtesy of Elf-ENT) Head and Neck Head and Neck Anatomy As medical students and junior doctors, being able to apply anatomy in a clinical context is important. You do not need to have an in depth knowledge of complex head and neck anatomy. Instead, being able to grasp the basic anatomy to inform your examination skills and interpretation of findings is more advisable. Facial Muscles Muscles develop from the second arch mesoderm and are attached to the dermis and arranged into sphincters, dilators and muscles of facial expression. The groups can be subdivided into muscles of mastication (nervous supply: trigeminal nerve) and muscles of expression (nervous supply: facial nerve). Orbicularis Oris A complex muscle which encircles the mouth Contraction of this muscle narrows the mouth and closes the lips It is most evident when performing the act of whistling Buccinator This quadrilateral muscle forms the muscular component of the cheek. It lies between the mandible and the maxilla It is the deepest muscle of the face It acts to prevent accumulation of food between the teeth and cheek Clinically important points: The temporalis muscle is covered by tough fascia. This fascia can be used to repair a perforated tympanic membrane (myringoplasty) The masseter is the most powerful muscle of mastication owing to the multipennate arrangement of its fibres The lateral pterygoid muscle is the only muscle of mastication which is attached to the temporomandibular joint The facial nerve has a long course from the brainstem to innervate the muscles of facial expression. Damage of this nerve results in facial weakness. Supranuclear lesions (e.g. stroke) spare the forehead, usually due to bilateral innervation. Infranuclear lesions produce a lower motor neuron paralysis with both upper and lower facial muscles- there is typically unilateral weakness. Paralysis to the orbital muscles occurs when there is damage to the facial nerve. Ptosis results with secondary consequences of exposure keratitis and corneal surface ulceration Inability to form facial expression on one side of the face can be the first sign of facial nerve damage Blood Supply to the Face and Neck External Carotid is a branch of the common carotid artery, which gives off several branches in the neck Mnemonic: “Some Anatomists Like Freaking Out Poor Medical Students!” describes the branches of the external carotid from most inferior to superior aspect: Superior thyroid artery (Anterior branch) Ascending pharyngeal artery (Ascending branch) Lingual artery (Anterior branch) Facial artery (Anterior branch) Occipital artery (Posterior branch) Posterior auricular artery (Posterior branch) Maxillary artery (Terminal branches) Superficial temporal artery (Terminal branches) Clinically Important Points The common carotid bifurcates at the level of the superior border of the thyroid cartilage The carotid sinus (baroreceptor) and carotid body (chemoreceptor) are located at the bifurcation The internal carotid artery has no branches. In surgery, at least 2 or more branches from the external carotid artery should be identified to distinguish it from the internal carotid artery when considering ligating the external carotid artery The Major Salivary Glands Parotid Gland Large serous salivary gland anterior and inferior to the ear. Saliva is drained via the Stenson duct which lies superficial to the masseter. After piercing through the buccinators, it enters the oral cavity opposite the 2nd upper molar tooth Submandibular Gland Mixed serous and mucous salivary gland. Closely related to and indenting the mandible Forms majority of saliva when not eating. The gland drains into the floor of oral cavity via Wharton’s duct, one to either side of the frenulum Sublingual Gland Mucous gland. It drains via multiple openings into the submandibular duct and sublingual fold in the floor of the oral cavity. Oral Cavity The main function of the oral cavity is to provide the ability for satisfactory mastication, including formation of a food bolus, drinking and breathing. Speech is also an important function. Dentition Adults have 32 teeth and children 20 (milk teeth). Teeth are important for mastication. They require saliva to ensure they remain healthy. Dental health can be affected by a variety of problems, not least a poor diet, smoking and alcohol. Poor oral health can have adverse consequences on general health. Complications of dental disease include submandibular abscesses, deep neck space abscesses and are part of the differential diagnosis of acute tonsillitis and peritonsillar abscesses. The oral cavity is bounded by (Figure 52): Anteriorly by the lips Posteriorly by the palatoglossal arches (anterior pillars of the fauces) Laterally by the teeth and cheeks. Inferiorly by the floor of mouth and mylohyoid Superiorly by the hard palate Figure 52: Oral cavity (reproduced with permission from Otolaryngology Houston, www.ghoryeb.com) Nerve Supply of the Tongue Clinically Important Points The surface of the tongue is covered with 3 types of coarse papillae called filiform, fungiform (which contain taste buds) and circumvallate papillae (which are aligned in V shaped formation dividing the anterior 2/3rds of the tongue from the posterior 1/3 of the tongue) The apex of the circumvallate papillae (foramen caecum) represents the embryological site of the thyroid gland. A lingual thyroid may present as a mass in this area if there is failure of migration Unilateral hypoglossal nerve palsy will result in deviation of the tongue towards the affected side with associated muscle atrophy. Ludwig’s angina is a necrotising cellulitis+/- abscess formation of the floor of mouth, which can extend into the neck and can be caused by dental root abscesses. It's most dangerous complication is a potentially life threatening airway obstruction due to the swelling within the mouth/neck. Topography of the Neck The regions are described as levels and assigned a roman numeral. It is particularly useful when describing the location of a neck lump. These levels can be divided into subdivisions but for the purposes of this handbook we have not discussed this. Figure 53: Levels of the neck (courtesy of Elf-ENT) The neck can also be divided into anterior and posterior triangles. The anterior triangle is bounded superiorly by the mandible, laterally by the sternocleidomastoid muscle and medially by the midline. The posterior triangle is bounded anteromedially by the sternocleidomastoid, inferiorly by the clavicle and posteriorly by trapezius muscle Fascial Layers of the Neck Superficial layer- This layer forms a thin sheet of fascia that encircles the platysma muscle. Deep Layer consists of 3 separate layers: Investing layer (external) (Figure 54)- It splits to invest the trapezius, sternomastoid and parotid, and its deeper layer invests the great vessels to form the carotid sheath. Pretracheal layer (visceral) (Figure 55)- covers the salivary glands, muscles, thyroid gland and other structures located in front of the trachea Prevertebral layer (internal) (Figure 56)- covers the prevertebral muscles. The interval between the pharynx and the prevertebral fascia is called the retropharyngeal space Figure 54: Investing layer of fascia (Image courtesy of Elef-ENT) Figure 55: Visceral layer of fascia (Image courtesy of Elef-ENT) Figure 56: Prevertebral layer of fascia (Image courtesy of Elef-ENT) Nervous Supply of the Head and Neck Physiology of Swallowing 1. Oral Stage (voluntary) Oral preparatory - Food bolus is formed and held in the anterior part of the oropharyngeal cavity. The oral cavity is closed posteriorly by the soft palate and tongue to prevent leakage into the pharynx Oral Propulsive - The dorsum of the tongue gradually propels the food bolus to the back of the oral cavity 2. Pharyngeal Stage (involuntary- CNIX) The soft palate elevates and closes the nasopharynx at the same time as the bolus comes into the pharynx- this prevents bolus regurgitation into the nasal cavity The larynx is closed, elevated and tucked under the base of the tongue to prevent aspiration. The pharyngeal constrictor muscles contracts from top to the bottom, squeezing the bolus inferiorly 3. Oesophageal Stage The food bolus enters the upper oesophageal sphincter, which includes the cricopharyngeus muscle. This muscle relaxes at the arrival of the food bolus Peristalsis propels the food bolus at a rate of 4cm/s towards the lower oesophageal sphincter which also relaxes Gravity aids peristalsis in the upright position Figure 57: Swallowing Physiology Taking History of a Neck Lump Opening How old are you? What do you do for a living? Why have you come to see me today? History of Presenting Complaint What made you notice the lump? How many lumps have you noticed? Where do you notice the lump? Has the lump changed in size? Is the lump always there or does the lump come and go? How long have you had the lump? Associated symptoms Has the lump been painful at all? Any sore throat? Have you had any difficulties swallowing? Have you had painful swallowing? Have you had any problems with breathing? Any coughs or colds? Have you noticed any blood? Have you noticed any weight change? Have you had any ear pain? Have you noticed any sweating at night/ temperatures? Has your voice changed? Past Medical and Surgical History - to include: Have you had any previous investigations for this neck lump Have you received any treatments for this lump Medication and Allergies Do you take any regular medications? Are you allergic to anything? Social History Ask about smoking & quantify Ask about drinking alcohol and quantify Red Flag Symptoms for urgent referrals (with or without a neck lump) Unexplained neck lump that has changed over a period of 3- 6 weeks Hoarse voice > 3weeks New onset dysphagia Unexplained persistent swelling in the salivary glands Otalgia > 4 weeks and normal otoscopy Unexplained persistent sore or painful throat Non healing ulcers White or red lesion in the mouth or oropharynx Causes of Neck Lump Commonest aetiology of lymphadenopathy relative to age Child / young adult: inflammatory > congenital > neoplastic Adult: inflammatory > neoplastic > congenital Older adult: neoplastic > inflammatory Branchial Cysts Description These present as upper neck masses in young adults, often in the third decade of life. They represent epithelial inclusions within lymph nodes.. They sometimes become infected. In middle aged and older adults consider cystic masses to be oropharyngeal or thyroid cancer metastasis until proved otherwise Investigations Neck ultrasound and fine needle aspiration cytology (FNAC). Cross sectional imaging is usually performed as well. Treatment Surgical excision. Dysphagia Description Dysphagia is difficulty in swallowing History Establish the level of dysphagia (pharynx, upper, mid or lower oesophagus Is it dysphagia mainly to solids, liquids, saliva? Ask about associated symptoms such as Hoarseness Odynophagia (painful swallowing) Otalgia Regurgitation Gastrointestinal bleeding Weight loss Are the symptoms progressing? Ask about risk factors for cancer of oesophagus & pharynx e.g. smoking and alcohol excess Refer to General Skills in ENT for notes on neck and thyroid examinations and oral examination. Causes of dysphagia Extraluminal (external pressure on the pharynx and oesophagus) Neck mass (e.g. retrosternal goitre) Vascular abnormalities (e.g thoracic aortic aneuryism, double aortic arch) Any type of mediastinal mass eg secondary cancer Lung cancer Intramural Causes (pharyngeal/ oesophageal) Motility problems Motor neuron disease/ Multiple sclerosis CVA Achalasia Oesophageal spasm Pharyngeal pouch Benign/malignant stricture Candidiasis Intraluminal Obstruction (oesophageal) Foreign body Oesophageal or pharyngeal cancer Candidiasis Oesophageal web/Plummer-Vinson syndrome Investigations FBC- may show iron deficiency anaemia

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