Đang tải... (xem toàn văn)
(BQ) Part 1 book Logan turner diseases of the ear, nose, and throat has contents: Anatomy and physiology of the nose and paranasal sinuses, investigation of nasal diseases, acute rhinosinusitis and its complications,... and other contents.
the Nose, Throat and Ear: Head and Neck Surgery covers the whole of otolaryngology in 70 chapters This classic textbook has been completely updated and expanded to reflect the increasing sophistication of diagnostic and management skills All subspecialties are covered with the content grouped into five major sections: • Rhinology • Head and Neck • Otology • Paediatric Otorhinolaryngology • Radiology Each chapter in this new edition includes key learning points, up-todate references, and suggestions for further reading.The contributors are leaders in their respective fields – a virtual list of ‘who’s who’ of British otolaryngology head & neck surgery ABOUT THE EDITOR FRCS(ORL-HNS), FRCP(Ed), is a Consultant ENT Surgeon and Honorary Professor of Otolaryngology at Ninewells Hospital and the University of Dundee School of Medicine in Dundee, UK He has been a member of both the UK Higher Surgical Training Committee (SAC in Otolaryngology) and the Intercollegiate Specialty Examination Board in Otolaryngology Professor Hussain has examined for the Board (FRCS ORL), the Royal College of Surgeons of Edinburgh (FRCS Ed) and the ELEVENTH EDITION S Musheer Hussain, MBBS, MSc(Manc), FRCS(Ed & Eng), ELEVENTH EDITION LOGAN TURNER’S First published over 100 years ago, Logan Turner’s Diseases of DISEASES OF THE NOSE, THROAT AND EAR SURGERY, OTORHINOLARYNGOLOGY Intercollegiate Diploma in Otolaryngology (DOHNS) LOGAN TURNER’S DISEASES OF THE NOSE, THROAT AND EAR HEAD AND NECK SURGERY Hussain edited by S Musheer Hussain K18615 an informa business w w w c r c p r e s s c o m K18615_Cover_mech.indd All Pages 6000 Broken Sound Parkway, NW Suite 300, Boca Raton, FL 33487 711 Third Avenue New York, NY 10017 Park Square, Milton Park Abingdon, Oxon OX14 4RN, UK ISBN: 978-0-340-98732-2 90000 780340 987322 7/29/15 1:23 PM LOGAN TURNER’S DISEASES OF THE NOSE, THROAT AND EAR HEAD AND NECK SURGERY ELEVENTH EDITION LOGAN TURNER’S DISEASES OF THE NOSE, THROAT AND EAR HEAD AND NECK SURGERY Edited by S Musheer Hussain MBBS MSc (Manc) FRCS (Ed & Eng) FRCS (ORL-HNS) FRCP (Ed) Consultant ENT Surgeon and Honorary Professor of Otolaryngology, Ninewells Hospital and the University of Dundee School of Medicine, Dundee, UK CRC Press Taylor & Francis Group 6000 Broken Sound Parkway NW, Suite 300 Boca Raton, FL 33487-2742 © 2016 by Taylor & Francis Group, LLC CRC Press is an imprint of Taylor & Francis Group, an Informa business No claim to original U.S Government works Printed on acid-free paper Version Date: 20151022 International Standard Book Number-13: 978-1-4441-2885-7 (e-Book) 978-0-340-98732-2 (Paperback) This book contains information obtained from authentic and highly regarded sources While all reasonable efforts have been made to publish reliable data and information, neither the author[s] nor the publisher can accept any legal responsibility or liability for any errors or omissions that may be made The publishers wish to make clear that any views or opinions expressed in this book by individual editors, authors or contributors are personal to them and not necessarily reflect the views/opinions of the publishers The information or guidance contained in this book is intended for use by medical, scientific or health-care professionals and is provided strictly as a supplement to the medical or other professional’s own judgement, their knowledge of the patient’s medical history, relevant manufacturer’s instructions and the appropriate best practice guidelines Because of the rapid advances in medical science, any information or advice on dosages, procedures or diagnoses should be independently verified The reader is strongly urged to consult the relevant national drug formulary and the drug companies’ and device or material manufacturers’ printed instructions, and their websites, before administering or utilizing any of the drugs, devices or materials mentioned in this book This book does not indicate whether a particular treatment is appropriate or suitable for a particular individual Ultimately it is the sole responsibility of the medical professional to make his or her own professional judgements, so as to advise and treat patients appropriately The authors and publishers have also attempted to trace the copyright holders of all material reproduced in this publication and apologize to copyright holders if permission to publish in this form has not been obtained If any copyright material has not been acknowledged please write and let us know so we may rectify in any future reprint Except as permitted under U.S Copyright Law, no part of this book may be reprinted, reproduced, transmitted, or utilized in any form by any electronic, mechanical, or other means, now known or hereafter invented, including photocopying, microfilming, and recording, or in any information storage or retrieval system, without written permission from the publishers For permission to photocopy or use material electronically from this work, please access www.copyright.com (http://www.copyright com/) or contact the Copyright Clearance Center, Inc (CCC), 222 Rosewood Drive, Danvers, MA 01923, 978-750-8400 CCC is a not-forprofit organization that provides licenses and registration for a variety of users For organizations that have been granted a photocopy license by the CCC, a separate system of payment has been arranged Trademark Notice: Product or corporate names may be trademarks or registered trademarks, and are used only for identification and explanation without intent to infringe Visit the Taylor & Francis Web site at http://www.taylorandfrancis.com and the CRC Press Web site at http://www.crcpress.com Contents Foreword ix Preface xi Contributors xiii SECTION I THE NOSE 1 Anatomy and physiology of the nose and paranasal sinuses Tawakir Kamani and Anshul Sama Investigation of nasal diseases Carl Philpott Epistaxis Thushitha Kunanandam and Brian Bingham Acute rhinosinusitis and its complications Andrew C Swift and Adam J Donne Granulomatous conditions of the nose Joanne Rimmer and Valerie J Lund Chronic rhinosinusitis Robin Youngs The blocked nose Paul S White Allergic rhinitis Martyn L Barnes and Quentin Gardiner Facial pain Nick S Jones 10 Nasal and facial trauma Peter D Ross 11 Facial plastic surgery Tim J Woolford 12 Pituitary surgery John Hill and Sean Carrie 13 Smell and anosmia Emma McNeill and Sean Carrie 14 Tumours of the nose and sinuses Kim W Ah-See 13 23 31 41 51 61 69 77 85 93 101 111 119 v vi Contents 15 16 Specific chronic nasal infections Salil Nair Snoring and OSA in adults Bhik Kotecha 131 139 SECTION II THROAT/HEAD AND NECK 147 17 149 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 Anatomy of the larynx and pharynx Richard M Adamson and Safina Ali Investigation of pharyngeal disease Nimesh Patel Benign disease of the pharynx Stephen R Ell Infections of the pharynx Andrew Robson Investigations of laryngeal disease Meredydd Harries Infections of the larynx Michael S W Lee Tumours of the nasopharynx Nicholas D Stafford Tumours of the oropharynx Paul Pracy Tumours of the hypopharynx Jean-Pierre Jeannon Tumours of the oral cavity Philip McLoughlin Tumours of the larynx Kenneth Mackenzie Salivary gland disease Patrick J Bradley Thyroid disease Omar J Hilmi Benign diseases of the oral cavity Graham R Ogden Neck space infections Muhammad Shakeel and S Musheer Hussain Disorders of voice Samit Majumdar Vocal cord paralysis Conrad Timon and Emma C Cashman Laryngo-tracheal trauma Andrew Harris and Sanjai Sood Tracheostomy John Dempster Neck masses Vinidh Paleri and Hisham Mehanna Dysphagia Charles E B Giddings and Francis M Vaz 159 165 175 183 191 209 215 219 225 235 243 253 263 277 289 301 311 319 327 339 Contents vii 38 The parathyroid Muhammad Shahed Quarishi 347 SECTION III EAR 359 39 361 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 Anatomy and physiology Liam M Flood Tests for hearing Desmond A Nunez and Li Qi Tests for balance Peter A Rea and Jaswinder S Sandhu Diseases of the external ear Patrick M Spielmann and S Musheer Hussain Acute otitis media Aanand Acharya and Andrew Reid Chronic otitis media Joseph G Toner Complications of otitis media Duncan Bowyer Otosclerosis David E C Baring and Iain R C Swan Sensorineural hearing loss David K Selvadurai Tinnitus Julian A Gaskin, Owen Judd and Henry Pau Disorders of balance Rahul Kanegaonkar Cerebellopontine angle tumours Christopher J Skilbeck and Shakeel R Saeed Otological trauma Nashreen Banon Oozeer and John Crowther The facial nerve Somiah Siddiq and Richard Irving Otitis externa Simon A McKean and S Musheer Hussain Tumours of the middle ear Anil R Banerjee Implants in otology E Mary Shanks and Peter Wardrop 375 385 395 403 411 421 433 443 453 461 471 483 497 507 513 519 SECTION IV PAEDIATRICS 531 56 533 57 58 Tonsils and adenoids Peter J Robb Acute rhinosinusitis and complications Mary-Louise Montague Stridor and airway endoscopy David Albert and Yogesh Bajaj 543 553 viii Contents 59 60 61 62 63 64 65 66 67 68 69 Tracheostomy Ann-Louise McDermott and Joe Grainger Subglottic stenosis Peter Bull and Neil Bateman Tumours and cysts of the head and neck Fiona B MacGregor The deaf child S J Prowse and C H Raine Acute otitis media and mastoiditis Gavin Morrison Otitis media with effusion Matt Rollin and Antony A Narula Chronic otitis media C Martin Bailey Balance disorders in children Katherine Harrop-Griffiths Choanal atresia Haytham Kubba Obstructive sleep apnoea Ray Clarke Drooling S Musheer Hussain and Muhammad Shakeel 567 573 583 589 595 609 617 625 637 643 651 SECTION V MISCELLANEOUS 657 70 659 ENT head and neck radiology Thiru Sudarshan Index 691 Foreword Two years before the First World War began in 1914, Dr Porter, an Edinburgh otolaryngologist, wrote a book that became a ‘best-seller’ We not know how his career would have progressed, nor how his book would have developed, because he, like so many other young professional men, was killed before the end of the war Fortunately his Edinburgh colleagues revived the book the year after the war ended in 1919 under the editorship of Dr Arthur Logan Turner, who became President of the Royal College of Surgeons of Edinburgh Between then and 1982 there were nine editions; the contributing authors traditionally were the consultants in post at the time in the Edinburgh department of otolaryngology The tenth edition in 1988 was edited by Professor Arnold Maran who, like Dr Logan Turner, became a President of the Royal College of Surgeons of Edinburgh, and the edition he edited was also written by Edinburgh laryngologists Many plans for further editions were discussed, but they were in the years during which written works were being replaced by electronic publishing, and there was doubt about the value of an ‘old-fashioned’ text book During this period of uncertainty there were many ‘false starts’, and for a time it looked as if this historic book would disappear However, we are grateful to Musheer Hussain, who has had the perseverance to create a team of contributors to complete this eleventh edition So much time has passed and so many changes have occurred in the delivery of health care in Scotland that the authors of the chapters are now no longer confined to Edinburgh That in itself is a marker of the development of the delivery of health care in Scotland, where now every centre has a standard of excellence that was once confined to the big cities This new edition reflects the huge change that has occurred in the specialty since the last century Although otolaryngology was originally a specialty that was created in order to remove pus from bony boxes in the skull to avoid intracranial complications, it has morphed into a form that would be unrecognisable to the original innovators These changes are elegantly presented in this book, which now covers neuro-sensory deafness, head and neck cancer, paediatric airway disease, skull base surgery and the rhinological revolution brought about by the endoscope Should there still be a place for the printed word? My answer would be in the affirmative, because electronic publishing has not reached the point where instant access to a single topic is as easy as it is with the printed word Is there still a place for a single work on a whole specialty? My answer would again be in the affirmative, because 95% of that specialty is between these hard covers The more specialised areas are the domain of single-subject volumes, but in this book, the jobbing otolaryngologist will find most of the answers to everyday problems Professor Arnold A G Maran ix 344 Dysphagia nerves influencing the oral and pharyngeal phases of swallowing Typically, there are other focal neurological deficits, and the prognosis is one of gradual improvement with rehabilitation Chronic neurological diseases may have a more indolent presentation with progressive symptoms and reduction in function of swallowing, speech, and voice and increasing aspiration in combination with systemic neurological problems Signs may include dysphonia, dysarthria, tongue wasting, difficulty managing secretions, cranial nerve paralysis and limb weakness Investigations Investigations and mitigation of the underlying neurological condition in conjunction with neurologists are key Endoscopic assessment of swallowing and videofluoroscopy will inform decisions on the safety of oral feeding Management Regular re-evaluation of swallowing with speech and language therapy and dietician involvement is essential for keeping this group of patients swallowing safely After acute injury, exercises are helpful in the rehabilitation of swallowing; in conditions with progressive dysfunction, compensatory strategies such as posturing and supraglottic swallowing may allow oral feeding to continue Altering food consistencies is also helpful in preventing aspiration, as thicker consistencies are considered easier to manage Patients with a high risk of aspiration may need to cease oral feeding and have a gastrostomy tube inserted as a palliative measure ACHALASIA History and examination Oesophageal motility disorders include uncoordinated spontaneous and non-peristaltic ‘tertiary contractions’ (Figure 37.2) and ‘nutcracker oesophagus’ Achalasia is an oesophageal motility disorder characterized by aperistalsis in the body of the oesophagus and failure of relaxation of the lower oesophageal sphincter caused by impairment of the myenteric plexus of Auerbach’s inhibitory Figure 37.2 A contrast swallow demonstrating tertiary contractions neurones in the distal oesophagus An elderly patient may present with a long history of intermittent dysphagia with occasional aspiration and regurgitation; younger patients may experience retrosternal pain from dysmotility and spasm Investigations Contrast swallow tests may initially be normal until oesophageal dilatation and elongation occur in the later stages, revealing the classical findings of contrast retention with a tapering distal gastro-oesophageal segment into a closed sphincter, also described as a ‘bird’s beak’ (Figure 37.3) Oesophageal manometry is the standard for the diagnosis of achalasia, and gastro-oesophagoscopy is also performed to exclude an underlying malignancy Very rarely, similar appearances may also be found in Chaga’s disease (infection with the protozoan Trypanosoma cruzi) Management Gastroenterology expertise aids in the management of achalasia Calcium channel blockers, Botox injections into the lower oesophageal sphincter and sphincter dilatation or myotomy are the mainstay of management Aetiology / Pharyngeal pouch 345 Investigations Bedside assessment of swallowing, contrast swallow, videofluoroscopy and endoscopic evaluation of swallowing form the mainstay of investigations Management Early involvement of speech and language therapists is essential to diagnose and manage the acute and chronic manifestations of treatment During treatment, aggressive therapy and rehabilitation may reduce the need for long-term gastrostomy tube feeding Surgery in the form of dilatations of strictures of the pharynx and oesophagus may help with mechanical causes Figure 37.3 A contrast swallow demonstrating achalasia IATROGENIC History and examination A thorough history must be taken, including previous conditions, treatments including surgery and radiotherapy and current medications Disruption of swallowing may occur as a complication of a wide range of treatments delivered via multiple specialties Surgery to the head and neck, including posterior fossa neurosurgery, surgery to the spine and oncological surgery to the mouth, base of tongue, hypopharynx and oesophagus, may cause damage to the pharyngeal plexus, cranial nerves or muscles involved in deglutition Drug-induced dysphagia may occur by influencing oesophageal motility or by direct mucosal injury Radiotherapy given with or without chemotherapy agents in the oncological management of head and neck cancers is a well-recognized cause of acute and chronic dysphagia Chemoradiotherapy is often delivered under the premise of ‘organ preservation’, for example in cancer of the larynx that would otherwise be treated surgically with a laryngectomy Comparable survival rates can be achieved, but toxicity following chemoradiotherapy may give worse long-term functional outcomes and consequently reduced quality of life PHARYNGEAL POUCH History and examination A pharyngeal pouch, also known as Zenker’s diverticulum, is a propulsion outpouching of the hypopharynx (epithelium and lamina propria only) It develops between a weakness in the inferior constrictors (oblique fibres of thyropharyngeus and the cricopharyngeus muscle’s transverse fibres) This area, also known as Killian’s dehiscence, is an established weakened area that allows herniation, more commonly on the left It has also been proposed that the cricopharyngeal sphincter may have a higher than normal resting tone Frequently, it is elderly patients who present with regurgitation of undigested food, recurrent chest infections secondary to aspiration and halitosis in addition to dysphagia There may be no physical signs but occasionally borborygmi may be elicited by palpation of the neck as the pouch is emptied into the pharynx Investigations A contrast swallow will delineate the size and position of the diverticulum, with an opening into the cervical oesophagus usually placed high and anteriorly It is for this reason that endoscopy must be performed with care as the endoscope will naturally pass into the pouch, not the oesophagus 346 Dysphagia Management Management decisions are based around the symptoms and effects on quality of life; a small pouch with minimal symptoms may require no intervention A pouch causing symptoms or recurrent chest infections may require endoscopic division This is performed under general anaesthetic with a split pharyngoscope (Figure 37.4) whose arms are positioned with one in the pouch and the other in the cervical oesophagus Division of the interpositioned pharyngeal bar will not only divide the mucosa but will also divide the fibres of cricopharyngeus Patients in whom sufficient endoscopic access cannot be achieved may require an external approach, when the pouch is excised and the defect repaired In addition, a cricopharyngeal myotomy is performed to reduce the chance of recurrence The excised pouch should be sent for histology as there have been reports of carcinoma occurring within the pouch KEY LEARNING POINTS ●● ●● ●● ●● Dysphagia has a significant impact on quality of life Swallowing has a complex mechanism and occurs in three phases Malignancy must be excluded in progressive dysphagia A multispecialty approach is essential, with speech and language therapists and dieticians FURTHER READING Figure 37.4 Endoscopic appearances of a pharyngeal pouch Cook IJ Oropharyngeal dysphagia Gastroenterology Clinics of North America 2009; 38(3): 411–31 Domsic R Gastrointestinal manifestations of systemic sclerosis Digestive Diseases and Sciences 2008; 53(5): 1163–74 Richter JE Oesophgeal motility disorders Lancet 2001; 358(9284): 823–8 Schindler JS Swallowing disorders in the elderly Laryngoscope 2002; 112(4): 589–602 38 The parathyroid MUHAMMAD SHAHED QUARISHI Introduction 347 Embryology and surgical anatomy 348 Histopathology 348 Physiology 348 Clinical assessment 349 Management options 349 Primary hyperparathyroidism 349 Familial hyperparathyroidism 350 Secondary and tertiary hyperparathyroidism 350 Preoperative localization investigations 350 Sestamibi scintigraphy 351 Ultrasound scan 351 USS or MIBI, or both 352 CT, MRI and PET 353 Fine-needle aspiration 353 INTRODUCTION The parathyroid gland was the last major gland to be identified in the human body Richard Owen wrote about the parathyroid glands in 1862 in the ‘Transactions of the Zoological Society’ Primary hyperparathyroidism (pHPT) is the most common cause of hypercalcaemia in the outpatient population and second only to malignancy in the inpatient population It is usually characterized by elevated serum calcium with an unsuppressed parathyroid hormone (PTH) level The incidence of pHPT is estimated to be between and 50 per 10 000 and is more common in patients Venous sampling 353 Intraoperative localization techniques 353 Intraoperative PTH monitoring 353 Radio-guided parathyroidectomy 353 Frozen section 354 Methylene blue 354 Surgical approaches to pHPT 354 Local anaesthesia considerations 355 Failed initial exploration, persistent and recurrent hyperparathyroidism, and re-exploration 356 Parathyroid carcinoma 356 Key learning points 356 References 357 Further reading 357 over 45 years of age, with a male-to-female ratio of 1:3 The incidence of pHPT is increasing owing to early detection since the advent of multichannel serum auto analyzers identifying hypercalcemia in asymptomatic patients There are two types of pHPT One is sporadic (95 per cent), of which 80 per cent are solitary adenomas, 15–20 per cent due to glandular hyperplasia and per cent carcinoma Hereditary (5 per cent) are those associated with multiple endocrine neoplasia (MEN) Type Parathyroid surgery is becoming more popular and gradually establishing itself as the acceptable definitive treatment for pHPT.1 347 348 The parathyroid EMBRYOLOGY AND SURGICAL ANATOMY There are four parathyroid glands in total The parathyroid gland is about 5–7 mm in size, soft, mobile and has an average weight of 30–40 μg It is oval in shape, and the colour is variable from light yellow in older people to reddish-brown in younger patients, depending upon fat content and proportion of oxyphil cells Parathyroid glands are placed as a superior and inferior pair on the posterolateral aspect of each thyroid lobe, with the upper pair being more constant in position Parathyroid glands are derived from the endoderm of the third and fourth pharyngeal pouches The developing parathyroid cells may be arrested at any point during their migration from the neck to the mediastinum Supernumerary fifth glands have been reported in per cent of cases and are often found in thymic tissue The nerve supply is from fibres from the superior and middle cervical sympathetic ganglion or from the perivascular plexus of the thyroid gland The venous drainage of the gland is from the superior and middle thyroid veins, which drain the upper and central parts of the thyroid and parathyroid glands The inferior glands develop along with the thymus from the third branchial pouch and have their blood supply from the inferior thyroid artery In 50 per cent of cases the inferior glands are found around 1 cm inferior, lateral or posterior to the lower pole of the thyroid lobe They are on a ventral plane in relation to the recurrent laryngeal nerve, caudal to the inferior thyroid artery, where they cross the recurrent laryngeal nerve In 25 per cent of cases the inferior parathyroid gland may be found within the thyrothymic horn In the remaining 25 per cent of cases their position is very variable, located some distance lateral to the thyroid (12 per cent) or adjacent to the trachea Less often they may be situated ectopically in the mediastinal thymus below the suprasternal notch, near the carotid sheath, sometimes as high as the carotid bifurcation, and rarely the inferior gland may be intrathyroidal (0.5–4 per cent) The superior parathyroid gland is dorsal (deeper) to the recurrent laryngeal nerve in the coronal plane and is quite often symmetrical in position and shape In 80 per cent of cases the superior parathyroid gland is found adjacent to the cricothyroid junction, posterolateral to the upper half of the thyroid lobe and approximately 1 cm cephalic to the junction of the recurrent laryngeal nerve and the inferior thyroid artery The main blood supply is from the inferior thyroid artery, while in 35–40 per cent of cases it may also be from the superior thyroid artery In per cent of cases the superior parathyroid glands may be found in a retropharyngeal, retrolaryngeal or retroesophagal position In rare cases (1 per cent) they may be positioned above the superior pole of the thyroid or in the posterior mediastinum HISTOPATHOLOGY Parathyroid glands have a thin connective tissue capsule with multiple septa that divide them into lobules The stroma consists of islands of secretory cells interspersed with fat cells and a rich sinusoidal capillary network There are two cell types: ‘chief or principal cells’ and ‘oxyphil’ cells Chief cells are the predominant cell type in children and synthesize PTH The oxyphil cells are larger and their number increases with age In elderly patients there is a decrease in the number of chief cells with 60–70 per cent of the mass being occupied by fat cells The adenomatous portion of the parathyroid may consist predominantly of chief cells with a suppressed rim of ‘normal’ parathyroid tissue differentiating it from a hyperplastic gland Chief cell hyperplasia causes 15 per cent of all pHPT cases, and in 20 per cent of cases it is familial and may be related to MEN syndrome PHYSIOLOGY In pHPT the excess PTH is uninfluenced by other biochemical factors and is produced by either neoplastic or hyperplastic parathyroid parenchymal cells In secondary HPT chronic stimulation of the parathyroid gland leads to parathyroid cell Management options / Primary hyperparathyroidism 349 proliferation and usually reverts to normal once the stimulus is removed In chronic renal failure, low calcium and a high phosphate burden causes parathyroid proliferation There is also reduced responsiveness of calcium receptors to PTH secretion owing to metabolic acidosis during renal failure Prolonged use of lithium and vitamin D deficiency are related to secondary HPT In chronic renal failure, after prolonged stimulus the hyperplastic gland may become autonomous and may not revert to its normal state after the stimulus has been removed This results in ‘tertiary’ hyperparathyroidism Familial HPT is associated with MEN1, MEN2, neonatal severe hyperparathyroidism, hyperparathyroidism-jaw tumour syndrome, familial isolated hyperparathyroidism and autosomal dominant mild hyperparathyroidism The penetrance of the MEN1 gene is high (95 per cent), and along with multigland HPT is associated with pituitary tumours and pancreatic and gut carcinoids MEN2 has a mild hypercalcaemic picture and may require no treatment or removal of enlarged glands They are both linked to medullary thyroid carcinoma and pheochromocytoma CLINICAL ASSESSMENT Patients presenting to surgeons are typically referred by endocrinologists and have biochemically confirmed pHPT The majority of patients with pHPT are asymptomatic (80 per cent), and their hypercalcaemia is picked up incidentally on biochemical screening for other reasons These patients are then further evaluated with PTHassay, 24-hour urinary collection for calcium level and creatinine clearance/glomerular filtration rate (GFR) A raised PTH-assay, hypercalcaemia and hypercalciuria confirm the diagnosis of pHPT Few patients today would present with the classical rhyme of ‘bones, stones, abdominal groans and psychic moans’ described in the 1930s, which possibly implied late presentation Most symptomatic patients have non-specific complaints such as fatigue, lethargy, depression, loss of concentration and joint and bone pain The neurocognitive symptoms can mimic dementia in the elderly population Table 38.1 Causes of hypercalcaemia • Hyperparathyroidism: primary/secondary/ tertiary • Malignancy: breast, lung, PTH-secreting tumours, parathyroid carcinoma • Drugs: thiazide diuretics, Vitamins A and D, calcium, aluminum, lithium • Granulomatous lesions: sarcoidosis, tuberculosis, histoplasmosis • Excess calcium intake: milk alkali syndrome • Prolonged immobilization • Familial: MEN syndromes, familial hypocaliuric hypocalcaemia • Endocrine disorders: thyrotoxicosis, Addison’s disease Gastro-intestinal symptoms may include abdominal pain, chronic constipation, peptic ulceration and pancreatitis Recent studies report the incidence of nephrolithiasis (20 per cent) and hypercalciuria (40 per cent) of all patients with pHPT It is important to ask about risk factors for hyperparathyroidism (lithium therapy, neck irradiation) and investigate other causes of hypercalcaemia (Table 38.1) In young patients with pHPT, family history of MEN should be investigated MEN patients tend to have multiple gland disease and are managed differently from those with solitary adenomas In some cases, pHPT is associated with metabolic and potential cardiovascular manifestations, including diabetes, hypertension and left ventricular hypertrophy MANAGEMENT OPTIONS PRIMARY HYPERPARATHYROIDISM The treatment modality for pHPT may range from watchful waiting to surgical intervention The symptomatic patient should be offered surgery for a curative outcome The asymptomatic patients may be managed conservatively with adequate hydration, avoidance of thiazide diuretics and control of calcium and parathormone levels by treating with bisphosphonates 350 The parathyroid Table 38.2 Guidelines for parathyroid surgery in asymptomatic pHPT3 Serum calcium (>upper limit of normal) 24-hour urine for calcium Creatinine clearance Bone mineral density Age Patients for whom effective medical surveillance/ follow-up is not possible * 0.25 mmol/L Not indicated in the absence of renal stones/nephrolithiasis*