Total Revision: Ear, Nose And Throat

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Total Revision:Ear, Nose and ThroatP Séamus PhillipsMA, BM, MRCS, DO-HNSSpecialist Registrar in OtolaryngologySouth Thames Region, UKandLydia BadiaFRCS (ORL-HNS)Consultant OtolaryngologistRoyal National Throat, Nose and Ear Hospital, London, UK

roductionThe DO-HNS ExaminationviiixxxixiiSECTION 1 – Essential Revision Notes1. Basic Sciences2. Audiology3. Otology4. Rhinology5. Head and Neck/Laryngology/Pharyngology6. Paediatric Otolaryngology329355369119SECTION 2 – Practice QuestionsSection 2A – EMQsExtended Matching Questions (EMQs)129Section 2B – MTFsMultiple True/False Questions (MTFs)159Section 2C – AnswersExtended Matching Questions (EMQs) – AnswersMultiple True/False Questions (MTFs) – Answers181197SECTION 3 – ENT ExaminationExamination of the EarExamination of the NoseExamination of the ThroatExamination of the Neck223231235239SECTION 4 – Clinical ScenariosClinical Scenarios241SECTION 5 – OSCE QuestionsOSCE Questions and Answers247Question Index333Index337v

SECTION1Essential Revision NotesCONTENTS1. Basic SciencesHead and Neck AnatomyInflammationMicro-organisms in ENT InfectionAssessment for TheatreWounds and Healing in ENTHaematologyAnalgesiaAnaesthesia for ENTOperating Equipment for ENT SurgeryImaging/RadiologyImmunologyPhysiology for ENTAids to VentilationClinical Governance and Audit32. AudiologyClinical Assessment of HearingEvoked Response AudiometryHearing AidsTinnitus293. OtologyEmbryological Origin of Ear StructuresExternal EarEar Canal and Tympanic MembraneMiddle EarInner Ear354. RhinologyAnatomy and Physiology of the NoseExternal Nose and VestibuleNasal CavityNasal Sinuses53

5. Head and Neck/Laryngology/PharyngologyEmbryology of the Head and NeckThe NeckPharynx and Oral CavityInfratemporal FossaLarynx and TracheaThyroid GlandParathyroid GlandsSalivary GlandsFacial NerveTrigeminal NerveForeign Bodies in the Pharynx/Larynx/Oesophagus6. Paediatric OtolaryngologyPaediatric AnatomyPaediatric ENT ConditionsPaediatric Hearing Tests and Screening69119

ESSENTIAL REVISION NOTESSECTION 11Basic SciencesHEAD AND NECK ANATOMYmedial pterygoid platelateral pterygoid platecarotid canalforamen ovaleforamen spinosumjugular foramenstyloid processhypoglossal canalstylomastoid foramenmastoid processforamen magnumFig. 1 The cranial fossa and nerves3

TOTA L R E V I S I O N : E A R , N O S E A N D T H R OATCranial nerves exit from various foramina in the skull (Table 1).ForamenExiting structuresOptic canalOptic nerveOphthalmic arteryOphthalmic veinOphthalmic division of trigeminal nerveOculomotor nerveTrochlear nerveAbducent nerveMaxillary division of trigeminal nerveMandibular division of trigeminal nerveLesser petrosal branch of glossopharyngeal nerveMiddle meningeal arteryInternal carotid artery passes across foramenGreater petrosal branch of facial nerveVestibulocochlear nerveFacial nerveAnterior compartment – glossopharyngeal nerveMiddle compartment – vagus nerve, accessory nerveHypoglossal nerveSpinal accessory nerve vical/posteriorauricular branches of facial nerveSuperior orbital fissureForamen rotundumForamen ovaleForamen spinosumForamen lacerumInternal auditory meatusJugular foramenHypoglossal canalForamen magnumStylomastoid foramenTable 1 Foramina at the base of the skull and exiting structures4

S E C T I O N 1 : E S S E N T I A L R E V I S I O N N OT E Smiddle meningeal arterysuperficial temporal arteryposterior auricular arterytransverse facial arteryoccipital arterymaxillary arterylingual arteryascending pharyngeal arteryfacial arteryinternal carotid arteryexternal carotid arterysuperior thyroid arterycommon carotid arteryFig. 2 The external carotid artery and its branchesINFLAMMATIONInflammation is the response of the body to various types of injury, including: neoplasticinfectivetraumaticautoimmune.The resulting inflammation can be: acute – with a rapid onset and limited duration, orchronic – with a prolonged response and continuous repair taking place.5SECTION 1The external carotid artery has a number of branches, which supply various structures inthe head and neck.

TOTA L R E V I S I O N : E A R , N O S E A N D T H R OATAcute inflammationThe classic components of the acute inflammatory response are: redness (rubor)swelling (tumor)heat (calor)pain (dolor)loss of function.The response is caused by: local vasodilatationexudation of fluid and proteinmigration of leucocytes into the injured area.The process is mediated by a number of chemical mediators: histaminecytokinesnitric oxideprotein components of plasma (complement system).The complement system is a cascade of proteins, mutually activated in sequence, resultingin the lysing of microbes by the membrane attack complex (MAC). The most critical stepis the activation of the C3 component: either by the classical pathway (triggered by an IgM or IgG antibody)or by the alternative pathway (triggered by exposure to the surface of the microbes).Two other systems, the kinin system and the clotting system, also play a part in the acuteinflammatory response.6

S E C T I O N 1 : E S S E N T I A L R E V I S I O N N OT E Salternative pathwayendotoxinaggregated Igactivated C1C3C5C3bC3aC5alyticpathwayC5bmembraneattack complexFig. 3 The complement systemChronic inflammationChronic inflammation is an ongoing but unresolved response to injury. Its characteristicsare: proliferation of blood vessels and connective tissuemigration of lymphocytes and macrophagesfibrosisongoing repairformation of granulomas.Granulomas are focal areas of inflammation with a group of macrophages at the centrethat transform into epithelial-like cells and are surrounded by a collar of lymphocytes and7SECTION 1classical pathwayAg–Ab complexes

TOTA L R E V I S I O N : E A R , N O S E A N D T H R OATplasma cells. The epithelioid cells may fuse to form ‘giant cells’. The inflammation mayproduce central caseating necrosis (classically in the case of tuberculosis (TB)) or may benon-caseating (most other chronic inflammations).Response to inflammationThis depends on: the body’s immune statusthe nature of the injuring agentthe site of the injury.After commencement of treatment, the response will also depend on choice of treatmentand effective removal of the initial stimulus.Infections may be classified as: conventional (infection in previously well individuals)conditional (infection in the presence of a predisposing factor)opportunistic (infection in an immunocompromised individual).Most infections encountered in the ENT situation are conventional.MICRO-ORGANISMS IN ENT INFECTIONBacteria in ENT infectionThe list below gives the classification of common bacteria encountered on a surgical ward,along with the situations in which some of them might be encountered in ENT.Gram-positive Gram-positive cocci Aerobic– staphylococci (clusters)– Staphylococcus aureus – wound infections, chronic suppurative otitis media(CSOM), acute sinusitis, furunculosis– S. epidermidis – normal skin commensal– streptococci (chains/pairs) – otitis externa– α-haemolytic streptococcus– Streptococcus pneumoniae – acute sinusitis, tonsillitis, acute suppurative otitismedia (ASOM)– S. viridans– β-haemolytic streptococcus – tonsillitis– Lancefield group A – S. pyogenes – acute sinusitis8

S E C T I O N 1 : E S S E N T I A L R E V I S I O N N OT E SLancefield group B – S. faecalis – dental infectionsAnaerobic– gut flora, Enterococcus faecalis – tonsillitis, quinsyGram-positive bacilli Aerobic– Corynebacterium diphtheriae Anaerobic– C. tetani– C. difficile– Actinomycetes israelii– Gram-negative Gram-negative cocci Aerobic– Neisseria meningitidis– Moraxella catarrhalis – acute sinusitis, ASOMGram-negative bacilli Aerobic– Pseudomonas aeruginosa – malignant otitis externa, tracheostomy infection– Campylobacter– Haemophilus influenzae – tonsillitis, epiglottitis, ASOM– Legionella– Escherichia coli – dental infections, tonsillitis, quinsy– Proteus– Mycobacterium tuberculosis – chronic ENT infections Anaerobic– Bacteroides fragilisAlong with bacteria, fungi and viruses may also play a part in ENT disease.Fungi in ENT infection Aspergillus fumigatus – this may cause fungal sinusitis, which is usually chronic butmay be acute in immunocompromised individuals.A. niger – along with the other Aspergillus organisms, this may cause fungal earinfections.Candida albicans – this may cause oral thrush.Viruses in ENT infectionViral infection may be the precipitant cause for a bacterial tonsillitis. The following specificviruses are also encountered in ENT practice: Respiratory syncytial virus (RSV) – leads to chest infections, mainly in children inwinter-time.9SECTION 1

TOTA L R E V I S I O N : E A R , N O S E A N D T H R OAT Human immunodeficiency virus (HIV) – infects cells carrying the CD4 antigen, such asmonocytes, macrophages and T-helper cells. More than half of patients may have headand neck manifestations such as otitis media, chronic rhinosinusitis, oropharyngealKaposi’s sarcoma, lymphoma, herpes, or neck infections.Herpes – herpes zoster infection may lead to facial pain. In particular, if it affects thefacial nerve, it may cause facial palsy. This is the Ramsay Hunt syndrome.Antibiotics for ENT infectionsThe principles of antibiotic use in ENT are the same as in any branch of medicine. Effortshould be made where possible to identify the causative organism before antibiotics arestarted. Some common ENT problems along with antibiotics indicated are given in Table 2.In all cases, erythromycin can be substituted for penicillin/amoxicillin if necessary.Acute tonsillitisQuinsy/peritonsillar abscessAcute otitis externaMalignant otitis externaAcute otitis mediaAcute sinusitisChronic sinusitisEpiglottitisCellulitisWound infectionPost-tonsillectomySystemic penicillin – amoxicillin is avoided because ofthe risk of inducing a rash in cases of glandular feverSystemic penicillin and metronidazole, with drainageTopical antibiotic drops with steroidsSystemic antibiotics, dependent on culture resultsSystemic co-amoxiclavSystemic co-amoxiclav or second-generationcephalosporinBroad-spectrum antibiotics initiallyChloramphenicol or third-generation cephalosporinSystemic flucloxacillin and penicillinDependent on wound cultureCo-amoxiclavTable 2 Common ENT infections and suggested antibioticsASSESSMENT FOR THEATREFitness for ENT theatre depends on the following factors: the nature of the operation and anaesthetic that will be giventhe urgency of that operationthe health of the patient preoperatively.10

S E C T I O N 1 : E S S E N T I A L R E V I S I O N N OT E SPreparation for theatreHistory of the patientThis should include a history of the complaint leading to the need for the operation andits current status. Note should also be made of smoking and drinking history, drug historyand family history.Full examinationThis should include auscultation of the heart and chest, and an ENT examination. Themouth should be examined as ENT operations often involve risk of damage to teeth – aloose tooth can be dislodged. Furthermore, pre-existing damage to teeth should bedocumented.Special investigationsHistory and examination may reveal the need for an electrocardiogram (ECG) (in thoseover 60 years or with a history of cardiac problems), a chest X-ray (in those with clinicalsigns of chest disease) or an echocardiogram (in those with clinical signs of heart failure,or unexplained heart murmurs). Cross-match, group and save, full blood count,electrolytes, thyroid function, sickle cell status and/or clotting may be appropriate,depending on the nature of the operation and the patient’s medical and drug history.Thromboembolic and antibiotic prophylaxisENT operations rarely require antithrombotic prophylaxis, but in a patient with a historyof thrombosis and likely immobility after an operation, mechanical and chemicalprophylaxis may be indicated: Mechanical – thromboembolism-deterrent (TED) stockings, early mobilisation.Chemical – low molecular weight heparin is the most common agent, which shouldbe discontinued 24 hours prior to administration or withdrawal of epiduralanaesthesia/analgesia to prevent bleeding into the epidural space.Antibiotic prophylaxis is rarely indicated in ENT surgery, but it may be necessary in patientswith previous cardiac problems, patients who are immunocompromised, or operationswhere infection is likely to be present in or around the operation site.ConsentIt is important that patients being treated are fully aware as far as possible of what interventions are being proposed for their condition. To a certain extent, patients give ‘implied’consent to basic actions such as history taking and examination by simply attending a11SECTION 1Preparation for theatre may include the following:

TOTA L R E V I S I O N : E A R , N O S E A N D T H R OATmedical facility. However, informed consent should be sought for any other intervention,as failure to do so may constitute an assault on the patient.The procedure of obtaining informed consent may or may not involve the signing of a form,but in all cases the principles remain the same. An explanation of the following should begiven: thethethethedetails of the procedureconsequences if the procedure is not carried outexpected experiences during and after the procedure, such as pain levelsrisks and potential side-effects, including a statistical likelihood if possible.There should be an opportunity to ask questions.Although it is often good practice to involve the family in any consent procedure, it is notmandatory. If an adult patient is not competent to give informed consent, the decision restswith the treating doctor to act in the patient’s best interests. In these cases, all decisionsmust be carefully documented. Treatment may also be given in emergency situationswithout consent, as long as it is given in the patient’s best interests. However, consent mustbe obtained as soon as the patient is capable of giving it.For patients under 14 years of age consent should be obtained from the parents, althoughof course the child should not be left out of the conversation – a special consent form existsfor the signature of the parents or appointed guardian (Form 3). For children aged 14 and15, the doctor taking consent must make a judgement about whether the child is able tounderstand fully the procedure they are about to undergo, and all its implications and risks.The doctor should document this so-called ‘Gillick competence’ if the child is to sign theconsent form.A consent document is not legally binding; rather it acts as some degree of proof that adoctor has explained to a patient the nature of the procedure they are about to undergoand the risks of doing so. At any stage a patient may change their mind about proceeding.There are certain situations where a doctor may treat without informed consent: A patient who is unconscious may be treated in their best interest, as long as no formof valid ‘advance directive’ exists to direct the medical personnel.Patients who are mentally incapable of making fully informed consent may be treatedin their best interest – a special consent form exists for this purpose (Form 4), which issigned by the doctor only.WOUNDS AND HEALING IN ENTWounds are created and repaired in the course of surgery, and it is essential to understandthe process of wound healing, which consists of three phases:12

S E C T I O N 1 : E S S E N T I A L R E V I S I O N N OT E S The commonest wounds in ENT surgery are of the face, an area that heals quickly giventhe right conditions. However, it is also an area about which the patient is highly sensitivewith regard to slight asymmetry or changes in alignment. So, for the best result, care mustbe taken in the positioning of facial incisions to put the least possible tension on the healingwound. The skin has natural tension lines, and incisions placed on these lines tend to healwith a narrower and stronger scar, leading to more favourable results. In the face and neckthey are most readily identified as the lines of wrinkling, and this fact can be used preoperatively to mark the best possible position for an incision.Delayed wound healingRisk factors for delayed wound healing can be classified as follows: Local risk factors – infection, haematoma, mobility, foreign body, dirty wound, surgicaltechnique, ischaemia.General risk factors – older age, cardiorespiratory disease, anaemia, obesity, diabetesmellitus, malnutrition, malignancy, steroids.Poor healing may result in wound dehiscence, ie the partial or total disruption of layers ofthe operative wound.ScarsAll wounds form a scar in the process of repair. However, the healing response maybecome exaggerated. If excessive scar tissue is formed but is limited to the site of theoriginal wound, a hypertrophic scar results. However, if the tissue extends beyond theboundaries of the original wound, a keloid scar results. Risk factors for hypertrophic andkeloid scars include: young ageblack skinmale sexgenetic predispositionsite – sternum, shoulders, head, neck13SECTION 1 Acute inflammatory response – a clot is formed around the wound, with vasodilatationand influx of inflammatory cells, in particular neutrophils in the first 24 hours. Then themacrophages become more important, continuing the process of phagocytosis andsecretion of cytokines (for example, transforming growth factor β (TGF-β), epidermalgrowth factor (EGF), platelet-derived growth factor (PDGF).Cell proliferation and deposition of extracellular matrix (proliferative phase) –fibroblasts secrete extracellular matrix and collagen; angiogenesis takes place, forminggranulation tissue. There is wound contraction due to the action of myofibroblasts.Remodelling of the extracellular matrix (maturation phase) – lasts for many monthsand leads to a gradual increase in the strength of the wound, up to a maximum of80%.

TOTA L R E V I S I O N : E A R , N O S E A N D T H R OAT wound tensiondelayed healing.It is rare to find malignant change in a scar – if present, this is usually a squamous cellcarcinoma, called ‘Marjolin’s ulcer’.Drains in ENTHead and neck surgery may result in wounds at risk of haematoma formation – if this isnear the trachea, airway compromise may result, eg after thyroid surgery. To avoid this,drains may be placed in the area to minimise dead space. Drains in ENT are usually closedand often attached to a suction system, such as a Redivac drain. In the case of largeabscesses, occasionally an open drainage system such as a Penrose or corrugated drain isleft in situ after incision of the abscess.HAEMATOLOGYHaemostasisHaemostasis is the cessation of bleeding, and involves a sequence of complex events: exposure of subendothelial tissuevasoconstrictionadherence of plateletsdegranulation of plateletsactivation of the coagulation cascadeplatelet plug with fibrin supportfibrinolysis and remodelling.Platelets are a key factor – they bind to subendothelial collagen via von Willebrand’s factor.They release their content(s), including fibrinogen and thromboxane A2. The coagulationcascade is also a crucial factor, and it is shown in Fig. 4.14

S E C T I O N 1 : E S S E N T I A L R E V I S I O N N OT E SSECTION 1intrinsic pathwayXIIsurface contactprekallikreinHMW-kininogenextrinsic pathwayXIIaXIVII tissue factorXIaIXCatalysesCa2 Ca2 IXacomplexes withVIIIa, Ca2 andphospholipidsXXaV co-factorinactivated byantithrombin IIIprothrombinthrombin (potent enzyme)fibrinogenactivation of protein CXIIIfibrincross-linked fibrinCa2 Fig. 4 The coagulation cascadeFibrinolysis is carried out by plasmin, which is converted from inactive plasminogen by anumber of factors, notably tissue plasminogen activator (tPA). Clotting time is measured by: activated partial thromboplastin time (APTT) – which measures the intrinsic as well asthe common pathwayprothrombin time (PT) – which me

Paediatric Anatomy Paediatric ENT Conditions Paediatric Hearing Tests and Screening. 1 Basic Sciences HEAD AND NECK ANATOMY 3 SECTION 1 ESSENTIAL REVISION NOTES medial pterygoid plate lateral pterygoid plate styloid process mastoid process foramen ovale foramen spinosum jugular foramen stylomastoid foramen foramen magnum carotid canal hypoglossal canal Fig. 1 The cranial fossa and nerves .

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