e gargles, topical vasoconstrictors and admission for IV antibiotics. See Royal College Aud it 2003 www.rcseng.ac.uk/surgical_research_units/docs/National%20Prospec- tive%20Tonsillect omy%20Audit%20Final%20Report%202005.pdf o t s e s a e s i d T N E W O H \200 2009 1 Coblation uses a plasma \201 eld of Na+ created by passing a current through saline to vaporize and dis- sect adjacent tissue: surgical science at the cutting edge. It has less t issue-heating eff ect than diathermy. \200 Stridor Stridor is a musical noise heard in inspiration from partial obstruction at t he larynx or large airways. Sterto is an inspiratory noise like snoring, coming from pharyn x obstruction (its adjective is stertorous; commoner in the obese). \200\207Children \200 \231s airways are narrower and more readily deformed than adult airways, so obstruction hap pens faster and more dramatically. \200\207Look for other signs: swallowing diffi culty/dr ooling, pale/cyanosed, using accessory muscles of respiration; downward plunging of the tra chea with respiration (tracheal tug); all are grave signs and mean impending obstruction. C auses \200 Congenital: Laryngomalacia, web/stenosis, vascular rings. \200 In \202 amma tion: Laryngitis, epiglottitis, laryngotracheobronchitis, anaphylaxis. \200 Tumors: Haema ngiomas or papillomas (usually disappear with onset of 566 \200 immunity \200\224but may require laser treatment before). Trauma: Thermal/chemical \200\224or from intubation. \200 Miscellaneous: Airway or oesoph ageal foreign body; vocal cord paralysis. Laryngotracheobronchitis/croup is the leading cau se of stridor with a barking cough (much commoner than Severity grading of croup172 epiglot titis). 95% are viral, eg parain- 1 Inspiratory stridor barking cough \202 uenza (riba virin can help, eg in im- 2 Grade 1 + expiratory stridor munode \201 ciency). Bacteria (kl ebsiella; 3 Grade 2 + pulsus paradoxus diphtheria) & fungi are rare. If there is 4 Grade 3 + cyanosis or cognition \200\201 cough and no drooling, croup is almost always the diagnosi s. 173 Usually self-limiting; treat at home ( antibiotics). s e s a e s i d T N E Admit (eg to ITU) if severe. In children, CXR may show \200\230steeple sign \200\231 of a tap ering trachea. Give antibiotics, humidi \201 ed O2, + nebulized adrenaline (5mL 1:1000 , may buy time in severe disease needing ventilating), and dexa- methasone 150 g/kg PO sta t or budesonide 2mg nebulized. See also p158. \200 Acute epiglottitis is rarer than croup, eg Managing epiglottitis 9/106/yr, but mortality is high: 1% if respiratory \200 Take to ITU; don \200\231t examine distress. \200 : \200 \211\210 3 : 1. It \200\231s an emerg e ncy as respir- throat (causes resp. arrest) \200 O2 by mask till anaesthe- atory arrest can occur. Often, history is short, tist and ENT doctor arrive septicaemia is rapid, and co ugh is absent. Also: \200 Give nebulized adrenaline, sore throat (100%), fever (88%), dysp noea (78%), voice change (75%), dysphagia (76%), tender an- terior neck cellulitis (27%) , hoarse ness (21%), pharyn gitis (20%), anterior neck nodes (9%), 174 drooling (head for w ard tongue out), prefers to sit, refusal to swallow, dysphagia. Typical cause: Haemophilus (vaccination has reduced prevalence); Strep pyogenes. Laryngomalacia This is the main conge nital anomaly of the larynx ( 60%) appearing within hours of birth (or up to a few months). Immature and \202 oppy aryepiglottic folds and glottis \200\200 laryngeal collapse in i nspiration. Stridor may be most noticeable in certain positions, sleep, or if excited/upset . In 85%, no \200\224 is needed and symptoms usually improve by 2 yrs old. Problems may oc cur with concurrent laryngeal infections or with feeding. 175 Try surgery if severe. It can also develop in association with gastro-oesophageal re \202 ux disease. 176 Laryngeal par alysis accounts for 15 \200\22320% of all those with congenital laryn- geal anomalies. Caus e: Often unknown, but might be from vagal stretching at delivery. Unilateral: May manifest during the 1st few weeks of life with a hoarse, breathy cry that is aggravated by agitation , feeding diffi culties aspi- ration. \201\227: Supportive; most recover by 2 \200\2233 years. Bilateral: Inspiratory stridor at rest that worsens upon agitation signi \201 c ant respiratory distress. \201\227: may need urgent airway intervention (intubation, trach eotomy) surgery. 177,178 IV dexamethasone \200 Visual diagnosis at naso- pharyngeal intubation \200 Blood/epiglottic culture \200 Find cricothyrotomy kit \200 IVI + penicillin G & ceftri- axone 2g/12h IV, p204 \200 Anti pyretic, eg ibuprofen 567 \200 Acute airway obstruction: management in adults \200 Let the patient sit/lie down in the position he is most comfortable. \200 Give O2 or Heliox (79% helium+21% O2; it \200 \231s less dense than air & O2 \200\230 more lam inar \202 ow in obstructed airways, and may reduce work of breathing, respiratory distress, and post-extubation stridor).179 \200 Nebulized racemic adrenaline. \200 Place an IV cannula, give dexamethasone or hydrocortis one IV. \200 Note O 2 saturation, respiratory rate, pulse and blood pressure. \200 Call t he on-call ENT registrar and anesthetist for help (eg via crash bleep). \200 Get the crash tracheostomy kit ready. \200 Brief history from relatives, keeping in view the common cau ses of stridor. \200 Do arterial blood gasses if possible without causing delay or stress. \200 When the stridor improves, do a \202 exible nasendoscopy (ENT registrar) to visual ize the airway,thereby getting an idea about the cause for stridor. \200 Get AP + lateral X-rays of neck & chest. www.clinicaljunior.com/entstridordoddi.html Note on needle cricothy rotomy (OHCM p786) in children \200\224jet O2 at 15L/min through a wide-bore cannula (14G) placed in the cricothyroid membrane: allow O2 in for 1 sec and exhalation (through partiall y obstructed upper airway) for 4sec. Useful in adults too. Fig 2. Relations of the epiglottis. s e s a e s i d T N E If a surgical cricothyrotomy is used (not in children <12yrs; see OHCM p786) a tracheostomy in theater is needed within 30min as jet insuffl ation oxygenates rather than ventilates, so CO2 builds up. Why is this child drooling? Drooling is often normal if <3yrs old (eg associated with teeth ing). So don \200\231t assume that drooling + stridor must mean epiglottitis if drooling pr edated the stridor (chronic causes below). Find out if oral incontinence is from \200\201c erebral control of oral function, hypersalivation, or an obstruction to swallowing. \200 \200 Angioedema/anaphylaxis (p237) \200 Rabies (OHCM p432) \200 Epiglottitis \200 Neur odisability, eg cerebral palsy, bulbar palsy ( \200\201 oro-motor control).180 \200 Muscl e problems (oesophageal dysmotility; cricopharyngeal achalasia) \200 Ingestion of a forei gn body, heavy metals, lithium, or caustic substances \200 Head and neck trauma to swallo wing structures \200 Enlarged tonsils or adenoids nasal polyps/rhinosinusitis/severe t onsillitis \200 Congenital lesions/nasal masses (eg an encephalocele or glioma).1 1 Other causes in adults: ill- \201 tting dentures, re \202 ux oesophagitis, Parkinson \200\231s, stroke, motor neuron disease. \201\227: \200\230SPIT \200\231: scopolamineet a l (anicholinergics \200\201 salivary \202 ow); physio/oral motor training ( palatal tra ining appli- ances), attending to head position, education and training, suction aids, bio- feedback and support; injections of botulinum toxin: gland excisions; transposition or exci sion of ducts.181 Hoarseness (dysphonia) Hoarseness entails diffi culty producing sound with change in voice pitch or quality ( \200\230breathy \200\231, \200\230scratchy \200\231, \200\230husky \200\231). \200\207Investigate hoarseness (esp. in smokers) lasting >3wks, as it is the ch ief (and often the only) presentation of laryngeal carci- noma (p570). Ask about: Gastro \200\223oesophageal re \202 ux (GORD), dysphagia, smoking, stress, singing & shouting. Voi ce overuse is a common cause (prevalence >50% in eg in teachers).183 Tests Laryngoscopy (to assess cord mobility, inspect the mucosa, exclude local causes); slow- motion videolaryngo stroboscopy/acoustic analy- sis (causes have characteristic vibration patterns). Speci \201 c causes Re \202 ux laryngitis (laryngo- pharyngeal re \202 ux (LPR): This is chroni c laryn- geal signs and symptoms associated with GORD. 15% of all visits to the ENT clinic s are because of LPR. Treatment: Twice daily proton-pump inhibi- tors for 2 to 4 months surgical fundoplication.184 Laryngitis: This is often viral and self-limiting, but there ma y be secondary infection with streps or staphs. It can also be secondary to GORD (see above ) or autoimmune disease, eg rheumatoid arthritis. NB: in chronic laryngitis (lasting >3 wks ), any bacteria found are likely to be colonizers only.185 Symptoms: Pain (hypopharyngeal, dyspha- gia; pain on phonation), hoarseness; fever. \201\227: Sup- portive. If necessary, give penicillin V 500mg/6h PO for 1 week. Steam inhalation may help. Chronic \200 Chondro sarcoma cord irritation from smoking chronic voice abuse \200 Relapsing polychondritis may cause Reinke \200\231s oedema (a gelatinous fusiform Emergency presentations enlargeme nt of the cords, also associated with \200 Epiglottitis (p566) hypothyroidism \200\224if c onservative treatment fails, \200 Aortic dissection laser therapy may help). \200 Anaphyl axis Functional disorders of speech articulation: (ie \200 Acid/alkali ingestion \200 Tra uma/foreign body cause unknown). Aphonia: Phonation yields no Get help to secure the airway . response (or a whisper) in seemingly normal cord adductors, eg in young women at times of stress (NB: there are many func- tional voice disorders which may result in laryngeal oede ma nodules.) A good diff erentiating test is to ask patients to cough (needs functional adductors). It is a diagnosis by exclusion, eg allergic reactions may cause sudden apho- ni a, so don \200\231t assume a functional disorder without laryngoscopy. Treatment: Speech th erapy is the best, with attention to emotional factors which may be present. Spasmodic dysp honia: Strained, eff ortful, hoarse voice + tremors, jerky voice onset, intermittent voice breaks, breathy spasms, hypernasality, failure to maintain voice.186 Children with function al speech disorders have diffi culty with speci \201 c speech sounds (eg /r/, /s/, /z/, /r /, /l/ and/or \200\230th \200\231). Try to distinguish articulation disorders from phonolo gical delay, consistent and varying ( \200\230inconsistent \200\231) phonological disorders and speech dyspraxia. Differential: Before saying \200\230no cause can be found \200\231, consider generalized in \201 l- trating entities of the larynx, such as hyperkeratosis ( \200\223smoking, alcohol abuse, pollution), leukoplakia, also granulomata, papillomata, pol yps, and cysts. 568 \200 Less common causes \200 Intrinsic: \200\201Lubrication, eg sicca syn.; laryngocoeles, gr anulomas: eg Wegener \200\231s \202\223; sarcoidosis; TB; syphilis. \200 Extrinsic pressu re: Goiter, carotid body tumor. 182 \200 Neoplasia: Pancoast synd; larynx or thymus cancer; lymphoma; glomus tympani- cum tumor ( \201 g 1, p552). Toxic: Vomit; fumesetc. \200 Injury causing arytenoid subluxation; CVP lines. Bacteria: Epiglottitis; diph - theria; abscess; aortitis. \200 CNS causes: Vagus lesion G uillain \200\223Barr ; myasthenia; other vocal cord pareses. \200 Endocrine: Acromegaly, Addison \200\231s, myxoedema. s e s a e s i d T N E Rarer causes \200 Mycotic aneurysm \200 Subclavian aneurysm \200 Malformations \200 Mucormycosis/fungi in HIV \200 Mucosal leishmaniasis \200 Hamartoma/haemangioma \200 Angioneurotic oedema \200 Gouty cricoarytenoiditis \200 Beh et \200\231s vasculitis o f vasa nervorum of laryngeal nrv. 569 Laryngeal nerve palsy The recurrent laryngeal nerve supplies the intrinsic muscles of the larynx (apart from cric othyroideus, external branch of the superior laryngeal n.) and is responsible for both abdu ction and adduction of the vocal fold. It originates from the vagus, with a complex course: on the left under the ligamentum art- eriosum, on the right under the subclavian artery, t urning back in a cephalic direction to run in the tracheo-oesophageal groove. In its passag e between the cricoid and thyroid cartilages it is vulnerable to compression from the cuff on an overin \202 ated endotracheal tube. Symptoms of vocal cord paralysis are: \200 Hoa rseness with \200\230breathy \200\231 voice with a weak cough. \200 Repeated coughing/as piration ( \200\223weak sphincter + supraglottic sensation \200\201). \200 Exertional dys pnoea (glottis is too narrow to allow much air \202 ow). NB: while s e s a e s i d T N E at rest the contralateral cord can compensate by increased abduction. In partial paralysis, cords are often \201 xed in the midline; in complete paralysis nerv e \201 bres supplying they are \201 xed mid-way ( \200\230paramedian \200\231; Semon \200\231s law: the abductors are more susceptible to damage, and the median position is due to unopposed adduction). 187 NB: the Wagner \200\223Grossman theory is discredited. Causes : 30% are cancers (larynx in 40%; thyroid, esophagus, hypopharynx, bronchus, or malignant node). 25% are iatrogenic, ie after parathyroidectomy, oesophageal, or pharyngeal pouch sur gery. Paralysis after thyroid surgery is seen in \211 5%, and is reversible in about 35%. 188 Other causes: CNS disease (polio; syringomyelia); TB; aortic aneurysm; 15% are idiopath ic( \211\210 \200\230neurotropic virus \200\231). Tests: CXR, barium swallow/meal, MRI, pan endoscopy. Treating non-malignant causes: Unilateral palsies can be compensated for by move ment of the contralateral cord, but may need formal medial ization in the form of bioplasti que injections, or a thyroplasty, eg Isshiki-type. 189 Reinner- v ation techniques: ansa ce rvicalis-to-recurrent laryngeal nerve (RLN, eg after damage during thyroidectomy); primary RLN anastomosis, ansa-to-RLN+ cri- cothyroid muscle-nerve-muscle pedicle, ansa-to-thyroaryt enoid implantation, 190 ansa-to-thyroarytenoid neuromuscular pedicle, hypoglossal-to-RLN. M ET Singer \200\231s nodules Singer \200\231s nodules are caused by vocal abuse (untrained sing ers in smoky at- mospheres). These are \201 brous nodules (often bilateral) at the juncti on of the anterior \205\223 and posterior \205\224 of the cords. This is the middle of th e membranous vocal folds (the posterior portion of the vocal fold is cartilage), and it may receive most contact injury during speech. \201\227: Speech therapy (if used early), or e xcision. Fig 1. Singer \200\231s nodule (rt). R.Herdman FRCS Vocal hygiene Don \200\231t whisper! Don \200\231t shout! \200 Drink plenty of \202 u ids (8 cups/day, but not tea, coff ee, alcohol, or cola). \200 Get plenty of sleep: tired ness kills the voice. \200 Avoid irritants (spicy foods, tobacco, smoke, dust, alcohol, a spirin gargles). \200 Avoid eating late at night, as indigestion may aff ect the voice. \200 Humidify your living and sleeping areas, eg damp towel on radiators, etc. \200 Don \200\231t suck medicated lozenges; these numb the throat, and menthol is dry- ! ! p u t u h s d n a g n i k o m s ing. You can keep your mouth moist by chewing pastilles or gum. \200 Steam inhalations ma y help when you are ill (add nothing to them). p o t S Head & neck squamous cancers (HNSCC) Tongue cancer: OHCM p230 \200\207Use a multidisciplin ary approach to investigation, diagnosis (imaging, histolotology, HPV virology1), stag- ing (example below), and treatment (organ sparing or radical?). Have a low threshold for refer ral whenever symptoms in the MINIBOX occur (esp. in smokers). Nasopharyngeal cancer ( \201 g 1) 25% of all cancers in China vs 1% in UK. As- sociations: \200 HLA A2 allele ( \200 \201survival with B17 & BW46) \200 HPV 1 \200 Epstein \200\223Barr (EBV)191 \200 Toba cco, formaldehyde, wood dust exposure192 \200 Weaning on to salted \201 sh (?N-nitroso carcinogens). Staging: T1 Nasopharynx, oropharynx, or nasal cavity T2 Parapharyngeal extens ion T3 Bony structures of skull-base/paranasal sinuses T4 Intracranial, cranial nerves, hyp opharynx, orbit, 570 \200 Pharynx Nasopharynx Oropharynx (inc. soft palate, tonsils & tongue base) Hypopharynx Larynx Supraglottis Glottis Esophagus Hypoglottis Vocal folds Fig 1. Anatomy of the head and neck. Symptoms of HNSCC \200 Neck pain/lump \200 Hoarse voice >6wks \200 Sore throat >6 wee ks \200 Mouth bleeding \200 Mouth numbness \200 Sinus congestion \200 Sore tongue \200 Painless ulcers \200 Patches in the mouth \200 Earache/eff usion \200 Lumps (li p, mouth, gum) \200 Speech change \200 Dysphagia; epistaxis s e s a e s i d T N E infratemporal fossa/masticator space N1 Unilateral cervical, unilateral or bilateral retroph- aryn geal nodes, above supraclavic ular fossa, \211 6cm in the greatest dimension. N2 Bilateral cervical above supraclavicular fossa \211 6cm N3 >6cm. N3b Supraclavicular fo ssa. Stage II=T1N1 to T2N0 \200\2231. Stage III=T12N2 to T3 N0 \200\2232. Lymph spread: Usu ally early to upper deep cervical nodes. Local spread may involve cranial nerves via the ju gular foramen. Signs: Diplopia, conductive deafness (Eustachian tube aff ected), cranial ne rve palsy (not I, VII, VIII), nasal obstruction, or neck lumps. \201\231 : Endoscopy/biops y; PCR for EBV. NB: submucosal spread may mean the area looks normal. Stage by MRI, eg with STIR sequence (=short tau inversion recovery; better than CT).193 \201\227: Radiotherapy is mainstay (intensity-modulated/IMRT may cause fewer SE, eg xerostomia and dysphagia)194 chemotherapy surgery (radical neck dissection). 3-yr survival for stage II: 100% (93% for stage III; 69% for stage IV, in one study; worse if EBV +ve).195,196 Oropharyngeal car cinoma is often advanced at presentation. \200 : \200 \211\210 5:1. Histol ogy: 85% are squamous. Typical older patient: Smoker with sore throat, sensation of a lump, referred ota lgia, and local irritation by hot or cold foods, with risk factors: chewing or smoking toba cco (alcohol alone is not a risk fac- tor but is synergistic with smoking). 30% of squamous pharyngeal tumors will have a 2nd primary within 10yrs. 20% are node +ve at presentation. Imag- ing: MRI with STIR (above) contrast-enhanced CT. 197 Surgery, eg with: jejunal \202 aps; tubed skin \202 aps (eg radial forearm or anterolateral thigh \202 aps); gastric pull-ups; trans oral laser, robotic surgery and partial laryngeal surgery. Radio- therapy ( eg intensity-modulated) may be 1st line if the tumor is T1 (<2cm) or T2 (>2cm but <4cm; NB: T3 is >4cm and T4 beyond oropharynx). Hypopharyngeal tumors are rare and are usually a dis ease of the elderly. They can present as a lump in throat, dysphagia for solids then \202 uids, or as neck lumps. The anatomic limits of the hypopharynx are the hyoid bone to the l ower edge of the cricoid cartilage: the 3 main sites are piriform fossa, 1 Note on human papilloma virus (HPV; oncogenic wart virus, one mode of transmission is sex ual, p272). Head & neck cancers may be caused by HPV; they occur in younger people, and car ry a better prognosis than those associated with smoking.198 Oral sex: HPV16 cancer risk re lates (partly) to number of partners. 199 Kissing: In those who had never had oral sex, ris k of harboring HPV increases if \211 10 lifetime or 5 recent open-mouthed kissing partners . HPV vaccination: (p272) If this prevented all ENT HPV +ve cancers, this would increase it s cost-eff ectiveness (and boys should get it too, esp. as HPV is overtaking smoking as the chief cause of these cancers). 200 post cricoid region, and the posterior pharyngeal wall. Note premalignant conditions: leuko plakia and Patterson \200\223Kelly \200\223Brown syndrome (Plummer \200\223Vin- son) \200 \224in which a pharyngeal web is associated with iron de \201 ciency, angular stomatitis, glossitis, and koilonychia: 2% risk postcricoid cancer. They are as- sociated with previous irradiation, smoking and alcohol, but not as clearly as laryngeal carcinoma. Treatment opt ions are radiotherapy and surgery in vari- ous combinations. The prognosis is poor with 60% mortality at 1 year. Squamous cell laryngeal cancer ( \201 g 1) Incidence: 2000/yr (UK). Typical old- er patient: Male smoker with progressive hoarseness, then stridor, diffi culty or pain on swallowing haemoptysis ear pain (if pharynx involved). Regular canna- bis users are at \200\200risk.201 Typical younger patient: HPV +ve.1 Sites: Supraglottic, glo t- tic, or subglottic. Glottic tumors have the best prognosis as they cause hoarseness earl ier (spread to nodes is late). Diagno- sis: Laryngoscopy+biopsy. HPV status; MRI staging.20 2 \201\227: Radical radiotherapy (eg IMRT above) or total laryngectomy block dissection of neck glands. There is debate about organ-sparing chemoradiotherapy VS laryngectomy, as well as laser vs radio- therapy for organ-sparing approaches. HPV +ve patients respond bett er to chemotherapy (2-yr survival 95% vs 62%), radiotherapy, and cetuximab. Recur- rence af ter radiotherapy: Partial \200\230salvage \200\231 laryngectomy for some appears to be saf e, eff ective, and gives reasonable preservation of laryngeal function.203 After total lary ngectomy: Patients have a permanent tracheostomy, so must learn oesophageal speech. If a vo ice prosthesis is \201 tted at surgery, reasonable speech is possible within weeks. Give pre-op counseling. Discharge: eg <10d post-op, with a plastic stent or metal cannula to kee p the tracheostomy open (discarded some weeks later). Excess secretions crusting around the stoma are common, needing meticulous attention \200\224humidi \201 ed stomal covers (e g Laryngofoam ) help here. Say to take care while having a bath, and to avoid \201 shing and deep water (unless expert training is to hand). Complications: Wound infection; pharyn gocutaneous \201 stula; stenosis; pneumonias; post-ra- diation hypothyroidism (monitor TS H); pharyngeal stenosis; nodal metastasis. 204 Rehabilitation/self-help: Suggest a laryngec tomy club. (UK: 0207 381 9993) Sinus squamous cell cancer ( 1% of all tumors) Typical patie nt: Middle- aged or elderly. Suspect when chronic sinusitis presents for the \201 rst tim e in later life. Early signs: Blood-stained nasal discharge and nasal obstruction. Later: C heek swelling, swelling or ulcers of the buccoalveolar plate or palate, epiphora due to a b locked nasolacrimal duct ( \201 g 2, p419), ptosis and diplopia as the \202 oor of the o rbit is involved, and pain in maxillary division of the trigeminal nerve. Local spread may be to cheek, palate, nasal cavity, orbit, and ptery- gopalatine fossa. Patients present lat e because epistaxis, obstruction and headache only occur with large tumors. Images: MRI/CT endoscopy (with biopsy) is best. NB: coronal CT is needed to show bone erosion (esp. aro und the cribriform plate).205 Differential histology: Squamous cell (50%), lymphoma (10%), adenocarcinoma, adenoid cystic carcinoma, olfactory neuroblastoma, or chondrosarcoma, benig n tumors.2 Treatment: Radiotherapy radical sur- gery. 5-yr and 10-yr overall survival ra tes are 77% and 66% respectively.206 571 s e s a e s i d T N E Fig 1. Laryngeal cancer along one vo- cal cord; it \200\231s just been biopsied, hence the bleeding. Rory Herdman FRCS 2 Inverted papillomas (of Ringertz) are the most important benign tumors of the sinuses. Th ey are exophytic masses that show distinctive epithelial invagination of the stroma without destroying the basal lamina. Total excision can therefore be diffi cult without taking wid e margins. Most signi \201 - cantly, 2% show malignant change and 10% have a synchronous c arcinoma. Dysphagia Dysphagia is diffi culty in swallowing: unless it is associated with a transitory sore throat, it is a serious symptom: \200\207Endoscopy is essential. Painful swallowing is termed \200\230odynophagia \200\231. Globus pharyngeus is a sensation of a lump in the throat, when not swallowing food, with no primary swallowing diffi culty. Prevalence: 6% \200 Association: Hoarseness; mood \200\201.207 Tests: En- doscopy (?hypopharyngeal cancer ; pharyngeal pouch laryngeal cyst). Cause: Unclear. In a few there is cricopharyngeal overa ctivity208 or \200\200acid exposure at the laryngopharyngeal junction, with normal gastro- oesophageal pH. 209 Treat- ment: Reassure. NB: it is worsened by anxiety, and stress can fo rm a vicious circle, but don \200\231t dismiss these patients as \200\230globus hystericus \200\231. 210 The patient As examination is typically normal (unless anemic), the history is central. Dyspep- sia? Weight loss? Lumps? 572 \200 Malignant causes \200 Oesophageal cancer \200 Pharyngeal cancer \200 Gastric cancer \200 Extrinsic pressure, eg from lung cancer or node enlargement Neurological causes \200 Bulbar palsy (OHCM p510) \200 Lateral medullary syn. \200 My asthenia gravis \200 Syringomyelia (OHCM p520) Other causes \200 Benign strictures \200 Pharyngeal pouch \200 Achalasiaet al (OHCM p240) \200 Systemic sclerosis \200 O esophagitis \200 Iron-de \201 cient anemia s e s a e s i d T N E 1 Can \202 uid be drunk as fast as usual, except if food is stuck? Yes: Suspect a stricture (benign or malignant). No: Think of motility disorders (achalasia, neurological causes). 2 Is it diffi cult to make the swallowing movement? Yes: Suspect bulbar palsy, especially if he coughs on swallowing. 3 Is the dysphagia constant and painful? Yes (either feature): Suspect a malignant stricture. 4 Does the neck bulge or gurgle on drinking? Yes: Suspect a pharyngeal pouch (food may be regurgitated). Tests FBC; ESR; barium swallow; rigid endoscopy with biopsy; oesophageal motility studies ( this requires swallowing a catheter containing a pressure transducer). CXR. Ambulatory pH s tudies have no proven value. Nutrition Dysphagia can cause malnutrition. Nutritional suppor t may be needed pre- and post-treatment, eg via a percutaneous endoscopic gastros- tomy (PE G) tube. Get expert (dietician \200\231s) help; see OHCM p586.211 Oesophageal carcinoma Thi s is associated with achalasia, alcohol, smok- ing, Barrett \200\231s esophagus (OHCM p708) , tylosis (a hereditary condition causing hyperkeratosis of the palms), Patterson \200\223B rown \200\223Kelly (Plummer \200\223Vinson) syn- drome. Post-resection 5-yr survival is poo r (OHCM p620). Benign oesophageal stricture Causes: oesophageal re \202 ux; swallowing cor - rosives; foreign body; trauma. Treatment: Dilatation (endoscopic or with bou- gies eg und er GA). Barrett \200\231s esophagus OHCM p686. Achalasia OHCM p240. Pharyngeal pouch These are a common cause of dysphagia with gurgling. Imaging: Via the endoscope; barium radiology ( \201 g 1) can help predict pouches that are unsuitable for stapling.212 Procedures: End oscopic stapling (NICE) in- volves stapling the bar of tissue that divides the pouch from t he esophagus. A specially designed endoscope gains access (under GA) to the bar and the ope n- ings of both the pouch and the esophagus. In one study, other procedures in- cluded endo scopic laser surgery, external excision, cricopharyngeal myotomy; and pharyngoscopy with di latation. Endoscopic stapling was abandoned in 15% (some declined further surgery).213 573 s e s a e s i d T N E Fig 1. Pharyngeal pounch (called Zenker \200\231s diverticulum in the USA) \200\234I \200 \231ve got this cough seems to get worse watching the news on TV \200\235. When we hear t his sort of absurdity, ask \200\234What are you doing before the News comes on? \200\235. \200\234Eating my dinner \200\235 At this point ask about dysphagia, choking, chronic c ough, regurgitation of undigested food, halitosis, weight loss, and aspiration. Listen to t he neck after eating: any gurgles? Any lateral fullness/swelling? Oesophageal mucosa is her niating backwards between cricopharyngeus and inferior pharyngeal constrictors. Typical pat ient: A man over 60. Incidence: 2/100 000/yr. Treatment: Surgery, eg day-case endoscopic st a- pling; note that \202 exible endoscopy can cause perfora- tion when a pouch is unsuspe cted; hence the need for barium imaging. 214 Reproduced from McGrath et al, QJM (2008) 101 (9): 747 \200\223748, with permission from Ox ford University Press. Facial palsy Arising in the medulla, and emerging between pons and medulla, the facial nerv e passes through the posterior fossa and runs through the middle ear before emerging from t he stylomastoid foramen to pass into the parotid. Le- sions may be at any part of its cours e. Branches in the temporal bone: 574 \200 1 The greater super \201 cial petrosal nerve (lacrimation). 2 Branch to stapedius (lesions above this cause hyperacusis). 3 The chorda tympani (supply taste to anterior \205\224 of the tongue) ( \201 g 1). Causes Intracranial: Brainstem tumors; strokes; polio; multiple sclerosis; cerebellopontine angle lesions (acoustic neuroma, meningitis). Intratemporal: Ot itis media; Ramsay Hunt syndrome; cholesteatoma. Infratemporal: Parotid tumors; trauma. Oth ers: Lyme disease; sarcoid; Guillain \200\223Barr ; herpes; diabetes; Bell \200\231s palsy ( \201 g 2). Examination and tests Lower motor neuron lesions can paralyze all of one sid e of the face; but in upper motor neuron lesions, the forehead muscles may still work (they are bilaterally represented). Brainstem lesions produce only muscle weakness and may be ac companied by VI nerve palsies. Loss of lacrimation (Schirmer \200\231s test p418), stapediu s re \202 ex, taste (electrogustom- etry detects) and \200\201submandibular saliva produc tion (cannulate ducts) imply nerve lesions proximal to the origin of the relevant branches. Examine the parotid and the ears to exclude cholesteatoma and zoster (Ramsay Hunt syndrome /herpes zoster oticus, p652). Consider temporal bone radiography (CT). Electromyography rev eals completeness of the lesion. In traumatic cases, examine the VII nerve. An incomplete p alsy will probably recover; complete palsy demands surgical exploration in the presence of discontinuity of the nerve canal on CT. Infection Otitis media causes a facial palsy in the presence of a dehiscent fa- cial nerve and has an excellent prognosis. When cholesteatoma is present ar- range emergency exploratory surgery. If rare acute necrotizing otitis extern a is the cause, IV antibiotics (eg ticarcillin) and local toilet are needed. Bell \200\231s palsy (20 \200\22330/100,000/yr). Cause: In \202 ammatory oedema from entrap- ment of VII in the narrow bony facial canal, eg as part of a viral polyneuropathy (herpes simplex or z oster, eg without vesicles) demyelination (V, X & C2 can be aff ected too). Onset is abr upt (eg after a nap; may be preceded by pain); the mouth sags, and dribbling, and watering (or dry) eyes occur + impaired brow- wrinkling, blowing, whistling, lid closure, cheek-pout ing, taste, and speech. Treatment: Protect the eye with glasses, and tape closed during sle ep, ide- ally with well- \201 tting plastic cover over moistened gauze. If recovery is exp ected to take months, consider lateral tarsorrhaphy. Instill arti \201 cial tears regularl y at slightest evidence of drying. There is good evidence that prednisolone helps, if given early1 (eg in 1st 24h, eg 20mg/8h for 5 days, tail off over next 5 days). High-dose aciclo vir or valaciclovir may also be indicated: see opposite. 215 Hooks & cheek plumpers improve appearance. Various facial reanimation procedures may be needed. Surgical exploration to c heck nerve continuity is controversial, but may be considered (graft with eg the lateral cu taneous nerve of the thigh). Prognosis: \205\223 get full recovery. \205\223 have incompl ete recovery of facial motor function (but don \200\231t have noticeable abnormalities.) Th e rest have permanent neurological and cosmetic abnormalities. 216 s e s a e s i d T N E 1 Many give steroids \200\230to reduce oedema \200\231 (esp. if <6 days since onset). Help ful studies: Hat & Shafshak217 showing that bene \201 t of steroids may be con \201 ned t o those treated in 24h of onset. Spontaneous recovery is good-ish anyway. For every 3 peopl e treated with steroids within 24h, 1 extra had a good recovery compared with no treatment; for ethical reasons, this study was not randomized. Older randomized stud- ies were inconc lusive, but did not look speci \201 cally at early treatment. Meta-analyzes support steroi ds. 218 575 s e s a e s i d T N E 8 Sphenopalatine ganglion 9 Superior maxillary nrv 10 Lacrimal gland 11 Large deep petrosal nrv 12 Vidian nerve 13 Nose & palate gland nrvs 14 Small petrosal nerve at geniculate gang lion 17 Auricular branch 18 Stylomastoid foramen 19 Lingual nerve \200\224visceral motor VII & t aste VII & general sensory to tongue (V3) 1 Facial nerve nucleus, deep in the reticular formation of lower pons 2 Spinal nucleus of V 3 Superior salivary nucleus 4 Solitary tract 5 Porus acusticus internus 6 Meatal foramen 7 Large petrosal nerve 20 Submandibular ganglion 21 Submandibular gland 22 Sublingual gland 15 Stapedial nerve 16 Chorda tympani Fig 1. Facial nerve branches. Reproduced from Oxford Handbook of Clinical Medicine, with permission Fig 2. Bell \200\231s palsy: the patient is trying to smile, but his right lower lid is dro oping, the naso-labial fold is slack, and the lips do not move. OUP data bank \200\207Wh enever you see someone with Bell \200\231s palsy within 3 days of its starting, ask about p reced- ing pain in the ear, stiff neck, or a reddish auricle: if these are associated with severe paralysis, the cause is likely to be zoster (without vesicles: zoster sine herpete) \200\224and high-dose antivirals eg valaciclovir 1g/8h PO for 7 are indicated, days 219 (+p rednisolone). If there are no prodromal features, zoster is less likely and lower doses of antivirals may be used (eg valaciclovir 500mg/12h PO for 5 days). Lumps in the neck \200\207Don \200\231t biopsy neck lumps! Refer any possibly malignant ne ck lump to ENT, where thorough assessment and search for a primary can be done, eg in a ded icated fast-track \200\2302-week rule \200\231 neck lump clinic220 with access to \201 n e- needle aspiration (FNA for cytology \200\224beware pulsatile lumps!) and CT/MRI (MRI is better). \200\207Culture any specimens for TB: don \200\231t put it all in formalin. Diagn osis \200 How long has the lump been present? If <3 weeks, lymphadenopathy from 576 \200 a self-limiting infection is likely, and extensive investigation is unwise. Which tissue layer is the lump? Is it intradermal? (eg from sebaceous cyst with a central punctum, or a lipoma.) If the lump is not intradermal, and not of recent onset, allow yourself to feel the intoxic ating pleasure of a hunt beginning over complex terrain. But remember \200\224you are vastl y outnumbered by a pack of diseases, so be cunning. The first step in this process is a pro per appreciation of anatomy. Midline lumps In patients <20yrs old, the likely diagnosis is a dermoid cyst, or, if it moves on protruding the tongue and is below the hyoid, a thyroglo s- sal cyst (a \202 uctuant lump developing in cell rests in thyroid \200\231s migration path; treated by surgery). If over 20, it \200\231s probably a thyroid mass, unless it is b ony hard, when the diagnosis may be a chondroma.221 Submandibular triangle (Below jaw; abov e anterior belly of digastric.) If <20yrs, self-limiting lymphadenopathy is likely. If >20, exclude malignant lym- phadenopathy (eg \201 rm and non-tender). \200\207Is TB likely? If it \200\231s not a node, think of submandibular salivary stone, tumor, or sialadenitis.2 22 Anterior triangle (Below digastric and in front of sternomastoid.) Nodes are common (see above): remember to examine the areas which they drain (is the spleen enlarged? \200\224th is may indicate lymphoma). Branchial cysts emerge under the anterior border of sternomastoi d where the upper \205\223 meets the middle \205\223; age <20. The popular theory is that they are due to non-disappear- ance of the cervical sinus (where the 2nd branchial arch gr ows down over 3rd and 4th) but this is not universally accepted. Lined by squamous epitheli um, their \202 uid contains cholesterol crystals. Treat by excision. Cystic hygromas (mac rocystic lymphatic malformations) arise from the jugular lymph sac and transilluminate brig htly. Treat by surgery or hypertonic saline sclerosant. Ca- rotid body paraganglionomas are very rare, move from side-to-side, but not up and down, and splay out the carotid bifurcat ion. They are \201 rm (softness is rare) and pulsatile, and do not usually cause bruits. They may be bilateral, familial, and malignant (5%). This tumor should be suspected in tumo rs just anterior to the upper third of sternomastoid. Diagnose by MRI. Treatment: extirpati on by vascular surgeon. If the lump is in the superoposterior area of the anterior triangle , is it a parotid tumor? (more likely if >40yrs). A laryn- gocele is an uncommon cause of a lump in the anterior triangle: it is painless, more common in males, and is made worse by blowing.223 Posterior triangle (Behind sternomastoid, in front of trapezius, and above the clavicle.) If there are many small lumps, think of nodes \200\224TB or viruses, eg HIV or E BV (infectious mononucleosis) or, if over 20yrs, consider lymphoma or metastases. The prima ry may be head and neck (eg tongue base, posterior nasal space, tonsils, etc) or bronchus, gut, breast, or gonad (in that order of likelihood). Cervical ribs may intrude here.224 Tes ts Ultrasound shows lump consistency. CT de \201 nes masses in relation to their anatomica l neighbors. Do virology and Mantoux test. CXR may show malignancy or reveal bilateral hila r lymphadenopathy, when you should con- sider sarcoidosis. Fine-needle aspiration (FNA, \201 g 7). s e s a e s i d T N E 577 Fig 1. Branchial cyst. Fig 2. Goiter. Fig 3. Infected cyst. s e s a e s i d T N E Fig 4. Deep cervical abscess. Figs 1 \200\2236 Bechara Ghorayeb. Fig 5. Lymph node metastases. Fig 6. Submandibular abscess. Suspicious neck node Fig 7. Pivotal role of \201 ne needle aspiration cytology (FNAC).225 Fig 8. Procedure for suspicious node if FNAC +ve. \201\205 EGA: examination under GA \201\205 LCUC: large cel l undiff erentiated ca \201\205 MDT: multidiscipli- nary team \201\205 SCC: squamous cell ca \201\205 US: ultrasound Reproduced from Balm et al Int J Surg Oncol, 2010. ENT mirror and/or endoscopic examination skin and thyroid examination Primary tumor FNAC 1 Negative Staging and treatment FNAC 2 Negative Positive Cystic \202uid Biopsy \200 Incisional \200 Excisional \200 True cut See \201gure below US-FNAC FNAC Positive SCC/LCUC Melanoma Thyroid carcinoma Lymphoma Merkel cell carcinoma Adenoca Skin cancer MDT ENT examination Skin cancer MDT Ultrasound thyroid Excision \200\223 \200\223 MRI/PET CT scan* EGA \200 Tonsillectomy + directed biopsies \200 Tonsillectomy + blinded biopsies (Nasop harynx, base of tongue, piriform sinus)