Surgery Prep Manual PDF

Prelims.indd 1 02-04-2015 14:06:36  Exam Preparatory Manual for Undergraduates Surgery Prelims.indd 1 02-04-2015 14:06:36 Prelims.indd 2 02-04-2015 14:06:36  Exam Preparatory Manual...

Prelims.indd 1 02-04-2015 14:06:36  Exam Preparatory Manual for Undergraduates Surgery Prelims.indd 1 02-04-2015 14:06:36 Prelims.indd 2 02-04-2015 14:06:36  Exam Preparatory Manual for Undergraduates Surgery A comprehensive review of surgery exam questions of various universities for undergraduates Gunjan S Desai Ronak Patel MS General Surgery MD Radiodiagnosis Delhi University Delhi University Co-authors Suhani Tushit Mewada MS General Surgery MCh Neurosurgery (Resident) Delhi University GB Pant Hospital, New delhi The Health Sciences Publisher New Delhi | London | Philadelphia | Panama Prelims.indd 3 02-04-2015 14:06:36  Jaypee Brothers Medical Publishers (P) Ltd Headquarters Jaypee Brothers Medical Publishers (P) Ltd 4838/24, Ansari Road, Daryaganj New Delhi 110 002, India Phone: +91-11-43574357 Fax: +91-11-43574314 Email: [email protected] Overseas Offices J.P. Medical Ltd Jaypee-Highlights Medical Publishers Inc Jaypee Medical Inc 83, Victoria Street, London City of Knowledge, Bld. 237, Clayton The Bourse SW1H 0HW (UK) Panama City, Panama 111 South Independence Mall East Phone: +44 20 3170 8910 Phone: +1 507-301-0496 Suite 835, Philadelphia, PA 19106, USA Fax: +44 (0)20 3008 6180 Fax: +1 507-301-0499 Phone: +1 267-519-9789 Email: [email protected] Email: [email protected] Email: [email protected] Jaypee Brothers Medical Publishers (P) Ltd Jaypee Brothers Medical Publishers (P) Ltd 17/1-B Babar Road, Block-B, Shaymali Bhotahity, Kathmandu Mohammadpur, Dhaka-1207 Nepal Bangladesh Phone: +977-9741283608 Mobile: +08801912003485 Email: [email protected] Email: [email protected] Website: www.jaypeebrothers.com Website: www.jaypeedigital.com © 2015, Jaypee Brothers Medical Publishers The views and opinions expressed in this book are solely those of the original contributor(s)/author(s) and do not necessarily represent those of editor(s) of the book. All rights reserved. No part of this publication may be reproduced, stored or transmitted in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, without the prior permission in writing of the publishers. All brand names and product names used in this book are trade names, service marks, trademarks or registered trademarks of their respec- tive owners. The publisher is not associated with any product or vendor mentioned in this book. Medical knowledge and practice change constantly. This book is designed to provide accurate, authoritative information about the subject matter in question. However, readers are advised to check the most current information available on procedures included and check information from the manufacturer of each product to be administered, to verify the recommended dose, formula, method and duration of administration, adverse effects and contraindications. It is the responsibility of the practitioner to take all appropriate safety precautions. Neither the publisher nor the author(s)/editor(s) assume any liability for any injury and/or damage to persons or property arising from or related to use of material in this book. This book is sold on the understanding that the publisher is not engaged in providing professional medical services. If such advice or services are required, the services of a competent medical professional should be sought. Every effort has been made where necessary to contact holders of copyright to obtain permission to reproduce copyright material. If any have been inadvertently overlooked, the publisher will be pleased to make the necessary arrangements at the first opportunity. Inquiries for bulk sales may be solicited at: [email protected] Exam Preparatory Manual for Undergraduates—Surgery First Edition: 2015 ISBN 978-93-5152-642-1 Printed at Prelims.indd 4 02-04-2015 14:06:36  Dedicated to All the wonderful students who are going to be future doctors and who are the sole inspiration for writing this book Prelims.indd 5 02-04-2015 14:06:36 Prelims.indd 6 02-04-2015 14:06:36  Foreword In the MBBS training program, while there is a lot of stress on acquiring knowledge and skills, there is not enough emphasis on teaching students in handling the present format of theory question papers. Even ‘good’ students find a disconcerting ‘disconnect’ between the teaching-learning methods and the examinations. In teaching even the residents embarking on surgical careers, many of my colleagues and I, serving on medical school faculties across the country, were also all too aware of this disconnect. This lovely book, expertly compiled by Dr Gunjan S Desai and his team, aims to bridge the gap between the standard teaching textbook and the theory questions that have to be answered by the student in his/her final summative examination. Finally, this book is not meant to replace the standard textbooks of surgery, and, accordingly is not a comprehensive discussion of all surgical diseases. For an in-depth knowledge of surgical pathology, diagnosis and treatment, all students and especially the students embarking on surgical careers must first be thorough with a standard textbook of surgery before attempting to master this book. I congratulate the authors on the successful outcome of their hard work and dedication, and hope the readers will find the book informative, useful and interesting to read. Shaji Thomas MS Director–Professor Department of Surgery Lady Hardinge Medical College New Delhi, India Prelims.indd 7 02-04-2015 14:06:36 Prelims.indd 8 02-04-2015 14:06:36  Words of Appreciation from the Masters in this Field It gives me pleasure to learn that two of my students, Dr Gunjan S Desai and his team, have written a book Exam Preparatory Manual for Undergraduates—Surgery for MBBS students preparing for final professional surgery examination. The book contains over 450 questions asked in various university examinations along with their answers in a simplified form. I am hopeful that the book is helpful to the readers especially during revision phase of their preparation for final professional surgery examination. I wish the authors and their readers all the best. Ajay Kumar MS MCh FAIS FICS Director, Professor and Head Department of Surgery Lady Hardinge Medical College New Delhi, India Prelims.indd 9 02-04-2015 14:06:36  Words of Appreciation from the Masters in this Field The book Exam Preparatory Manual for Undergraduates—Surgery is a combined effort made by a group of hard working, intelligent and competent residents from various fields of surgery. The book covers around 450 questions and answers along with over 100 illustrations covering various sections of surgery. I am confident and hopeful that the book turns out to be of great help for undergraduate students preparing for final professional examination. I praise the efforts made by the authors and wish their endeavor a grand success. UK Shrivastava MS FAIS DHA Former Professor of Surgery University College of Medical Sciences Dean and Head, Surgical Discipline, Faculty of Medical Sciences Chairman, Board of Research and Studies, University of Delhi Former Professor and Head, AIMST University, Government of Malaysia Prelims.indd 10 02-04-2015 14:06:36  Preface “Surgery has always been and would always be a tough job whether it is performing a procedure or learning how to perform it.” When I entered the final year of MBBS, I faced this sentence for the first time. And now that I am a surgeon, I know how true it is. The reason is also slightly more obvious now. Just as there is no single standard technique to a single procedure, there is no single standard book to meet the university exam requirements. My colleagues and I faced a great amount of difficulty in order to accumulate the material important for the final year MBBS university examination. Make the question lists of important questions, do peer reviews for the answers, search for authentic papers in net for answers and also the unauthentic material that we get hands-on during MBBS and finally when examinations came, we always thought that we were underprepared for the subject. The worst part of this exercise was not the reading part but the time that was spent in getting together the material to read. The guidance in clinics is given for the cases and the practical part of the examination but not much is taught about the theory examination, which actually is necessary for the concept building. It is towards this end that I thought of writing this book as an aid to university examinations so as to make an effort to compile and accumulate all the material under one common heading. This book focuses more on the concepts that have been integral to getting the required knowledge of surgery and at the same time have a good compilation of all the university examination questions and their answers from authentic references. So, I went in search of the appropriate people to help me in this herculean task and got together this splendid team of experts in this field and also experts at advising on the correct approach to master the concepts related to their field of interest in surgery. I thank all the team members for their hard work and contribution. Their insight in their sections in this book is definitely going to help everyone who uses this book. The topics in this book are important for the university examinations and also important topics have been given a prolonged discussion to aid in the understanding of the topics. Also, the important conceptual points on clinical topics have been included for the student’s benefit. I am sure that this book will be of great help to all the undergraduates, would save a lot of their time and effort and would make learning surgery fun. Gunjan S Desai Prelims.indd 11 02-04-2015 14:06:36  Acknowledgments We would like to thank the Almighty, our parents and family members, our teachers and all our seniors, colleagues and friends without whose support; this book would not have been possible. We also thank Shri Jitendar P Vij (Group Chairman), Mr Ankit Vij (Group President) and Mr Tarun Duneja (Director–Publishing) of M/s Jaypee Brothers Medical Publishers (P) Ltd, New Delhi, India, at the outset as without their support; this would have been a rather difficult task to accomplish. A special thanks also to Dr Sriram Bhat for contributing a few of the illustrations in this book. Prelims.indd 12 02-04-2015 14:06:36  Contents Section 1: General Surgery 1 ‰‰ Drawbacks of laparoscopy 40 ‰‰ Complications of laparoscopy 40 Wound Healing 3 ‰‰ Physiology of pneumoperitoneum 40 ‰‰ Mechanisms of wound healing 3 ‰‰ Diagnostic laparoscopy 43 ‰‰ Chronic nonhealing of a wound 5 ‰‰ NOTES (natural orifice transluminal ‰‰ Wound dressings 7 endosurgery) 43 ‰‰ Pressure sore 9 ‰‰ Therapeutic embolization 45 ‰‰ Keloids and hypertrophic scar 11 ‰‰ Surgical diathermy 46 ‰‰ Photodynamic therapy 48 Fluid, Electrolyte and Acid-Base Imbalance 12 ‰‰ Day case surgery 48 ‰‰ Normal water distribution in body 12 ‰‰ Robotic surgery 49 ‰‰ Hyponatremia 13 ‰‰ Hypernatremia 14 Surgical Infections 50 ‰‰ Hypokalemia 15 ‰‰ Generalized lymhadenopathy 50 ‰‰ Hyperkalemia 16 ‰‰ Tubercular cervical lymphadenopathy 50 ‰‰ Steps of diagnoses of an acid-base disorder 17 ‰‰ Drug-resistant TB 52 ‰‰ Metabolic acidoses 18 ‰‰ Ludwig’s angina 53 ‰‰ Metabolic alkaloses 19 ‰‰ Tetanus 54 ‰‰ Plasma expanders 19 ‰‰ Gas gangrene 56 ‰‰ Carbuncle 57 Metabolism and Nutrition 20 ‰‰ Madura foot 58 ‰‰ Endocrine and metabolic response to stress/ ‰‰ Anatomy of palmar spaces 59 surgery/injury 20 ‰‰ Acute paronychia and felon 61 ‰‰ Nutritional assessment 23 ‰‰ Hydatid cyst 62 ‰‰ Total parenteral nutrition 24 ‰‰ Entamoeba histolytica 62 ‰‰ Enteral nutrition 25 ‰‰ Actinomycosis 63 Blood Transfusion and DIC 27 Trauma and Damage Control Surgery 65 ‰‰ DIC (Disseminated intravascular coagulation) 27 ‰‰ Flail chest 65 ‰‰ Blood “substitutes” 29 ‰‰ Disaster management 66 ‰‰ Blood components 30 ‰‰ “Damage control” in surgery 67 ‰‰ Complications of blood transfusion 31 ‰‰ Faciomaxillary trauma 69 ‰‰ Plasmapheresis 33 Perioperative Surgery 72 SIRS, Shock and MODS 34 ‰‰ Intraoperative patient monitoring 72 ‰‰ Classification of shock 34 ‰‰ Postoperative fever 73 ‰‰ Septic shock 35 ‰‰ Prophylactic antibiotics in surgery 74 ‰‰ MODS (multiple organ dysfunction syndrome) 35 ‰‰ Probiotics, prebiotics and synbiotics 76 ‰‰ Hemmorhagic shock 38 ‰‰ Surgical site infection 78 ‰‰ Lethal triad 38 Surgery of the Salivary Glands 81 Basic of Surgical Technologies and Advanced ‰‰ Classification of salivary gland neoplasms 81 Surgery 40 ‰‰ Pleomorphic adenoma 81 ‰‰ Minimal access surgery 40 ‰‰ Warthin tumor 82 ‰‰ Advantages of laparoscopy 40 ‰‰ Superficial parotidectomy 83 Prelims.indd 13 02-04-2015 14:06:37  xiv Exam Preparatory Manual for Undergraduates—Surgery Miscellaneous General Surgery Topics of ‰‰ Necrotizing enterocolitis 157 Importance 85 ‰‰ Meconium ileus 157 ‰‰ Surgical audit and ethics 85 ‰‰ Mesenteric ischemia 159 ‰‰ Universal precautions 88 ‰‰ Superior mesenteric artery syndrome 162 ‰‰ FNAC and biopsy 90 ‰‰ Morbid obesity 163 ‰‰ Sterilization techniques 91 ‰‰ Abdominal tuberculosis 165 ‰‰ Hospital waste management 92 ‰‰ Adult intestinal obstruction 167 ‰‰ Tracheostomy 93 ‰‰ Suture materials 94 Large Intestine 171 ‰‰ Pain management in surgery 95 ‰‰ Inflammatory bowel disease 173 ‰‰ Lower GI bleeding 173 Medicine in Surgery 95 ‰‰ Sigmoid volvulus 175 ‰‰ ARDS 95 ‰‰ Diverticulitis (peridiverticulitis) 176 ‰‰ Diabetic ketoacidosis 99 ‰‰ Hirschsprung’s disease (congenital ‰‰ Adrenal insufficiency 102 megacolon) 177 ‰‰ Myxedema coma 105 ‰‰ Stomas in surgery 179 ‰‰ Thyroid storm 108 Appendix 182 Section 2: Gastrointestinal, ‰‰ Alvarado score and its significance 182 ‰‰ Types of appendicitis 182 Hepatobiliary and Pancreatic ‰‰ Appendicular lump 184 Surgery 111 Rectum and Anal Canal 185 Esophagus and Diaphragm 113 ‰‰ Anatomy of anal canal 185 ‰‰ Diaphragmatic hernias 113 ‰‰ Blood supply of the rectum 186 ‰‰ Portal hypertension 116 ‰‰ Fissure-in-ano 187 ‰‰ Esophageal varices 118 ‰‰ Fistula-in-ano 189 ‰‰ TIPS 118 ‰‰ Pilonidal disease 191 ‰‰ Achalasia cardia 123 ‰‰ Rectal prolapse 192 ‰‰ Tracheoesophageal fistula 125 ‰‰ Hemorrhoids 193 ‰‰ Barrett’s esophagus 128 ‰‰ Anorectal malformations 195 ‰‰ Gastroesophageal reflux disease 128 ‰‰ Ischiorectal abscess 197 ‰‰ Zenker’s diverticulum 131 ‰‰ Esophageal perforation 133 Liver 198 ‰‰ Caustic/corrosive injury in upper GIT 135 ‰‰ Anatomy of liver 198 Stomach and Duodenum 137 ‰‰ Cystic lesions of liver 201 ‰‰ Stomach: Relevant anatomy 137 ‰‰ Amoebic liver abscess 202 ‰‰ Physiology of gastric acid secretion 139 ‰‰ Liver transplantation 204 ‰‰ Gastric outlet obstruction 140 ‰‰ Liver injury 205 ‰‰ Congenital hypertrophic pyloric stenosis 142 Gallbladder and Bile Duct 206 ‰‰ H. pylori and peptic ulcer disease 144 ‰‰ Postgastrectomy problems 149 ‰‰ Gallstones and complications 206 ‰‰ Upper GI bleeding 150 ‰‰ Cholecystitis 207 ‰‰ Obstructive jaundice 210 Small Intestine 151 ‰‰ Postcholecystectomy problems 213 ‰‰ Short bowel syndrome 151 ‰‰ Choledochal cyst 216 ‰‰ Enterocutaneous fistula 153 ‰‰ Hemobilia and bilhemia 217 ‰‰ Meckel’s diverticulum 154 ‰‰ Choledocholithiases 218 ‰‰ Intusussception 156 ‰‰ Biliary strictures 220 ‰‰ Neonatal intestinal obstruction 157 ‰‰ Courvoisier’s law 220 Prelims.indd 14 02-04-2015 14:06:37  Contents xv Pancreas 220 ‰‰ PCNL 292 ‰‰ Annular pancreas 220 ‰‰ Percutaneous nephrostomy 293 ‰‰ Acute pancreatitis 221 ‰‰ Urinary diversion 293 ‰‰ Pseudocyst pancreas 224 ‰‰ Renal TB 294 ‰‰ Insulinoma 225 ‰‰ Renal trauma 297 ‰‰ Prognostic scoring in pancreatitis 226 ‰‰ Hematuria 300 ‰‰ Cystic pancreatic neoplasms 228 ‰‰ Pyelonephritis 302 ‰‰ Pancreatic duct disruption 230 ‰‰ Pyonephrosis 304 ‰‰ Hydronephrosis 304 Spleen 231 ‰‰ Wilms’ tumor 305 ‰‰ Hypersplenism 231 ‰‰ Horse shoe kidney 307 ‰‰ Splenic injury 232 ‰‰ PUJ obstruction 308 ‰‰ OPSI 234 ‰‰ Classification of renal lumps 309 ‰‰ Complications after splenectomy 234 Urinary Bladder 311 Hernias 235 ‰‰ Bladder calculi 311 ‰‰ Meshes in hernia surgery 235 ‰‰ Bladder injury 312 ‰‰ Incisional hernia 237 ‰‰ Vesicovaginal fistula 313 ‰‰ Anatomy of umbilicus 239 ‰‰ Micturition reflex 315 ‰‰ Umbilical hernia 240 ‰‰ Neurogenic bladder 315 ‰‰ Open and laparoscopic anatomy of inguinal ‰‰ Incontinence 317 region 243 ‰‰ Chyluria 318 ‰‰ Direct and indirect hernia 247 ‰‰ Vesicoureteric reflux 319 ‰‰ Femoral hernia 251 ‰‰ Ectopia vesicae 320 Gastrointestinal Oncosurgery 253 Prostate 321 ‰‰ Esophageal cancer 253 ‰‰ LUTS 322 ‰‰ Carcinoma stomach 255 ‰‰ Benign prostatic hypertrophy 322 ‰‰ GE junction tumors 258 ‰‰ TURP 322 ‰‰ Small bowel adenocarcinoma 259 ‰‰ Postoperative urinary retention 325 ‰‰ Carcinoid tumor 259 ‰‰ PSA 327 ‰‰ Gastrointestinal stromal tumor 263 Testis and Scrotum 328 ‰‰ Colorectal cancer 265 ‰‰ Carcinoma anal canal 271 ‰‰ Development of testis 328 ‰‰ Hepatocellular carcinoma 271 ‰‰ Cryptorchidism 328 ‰‰ Carcinoma gallbladder 273 ‰‰ Testicular torsion 330 ‰‰ Cholangiocarcinoma 276 ‰‰ Epididymoorchitis 332 ‰‰ Pancreatic cancer 277 ‰‰ Varicocele 333 ‰‰ Pseudomyxoma peritonei 278 ‰‰ Hydrocele 334 ‰‰ Fournier’s gangrene 334 Miscellaneous 280 ‰‰ Differential diagnoses of a scrotal swelling 335 ‰‰ Burst abdomen 280 ‰‰ Phimoses and paraphimoses 336 ‰‰ Peritonitis 282 ‰‰ Vasectomy 337 ‰‰ Mesenteric cyst 283 ‰‰ Circumcision 338 Penis and Urethra 339 Section 3: Genitourology 285 ‰‰ Penile ulcer 339 ‰‰ Urethral injury 340 Kidney and Ureter 287 ‰‰ Urethral stricture 342 ‰‰ Renal calculi 287 ‰‰ Lasers in urology 343 ‰‰ Calculus anuria 289 ‰‰ Posterior urethral valve 344 ‰‰ ESWL 291 ‰‰ Proteinuria 345 Prelims.indd 15 02-04-2015 14:06:37  xvi Exam Preparatory Manual for Undergraduates—Surgery ‰‰ Male infertility 346 ‰‰ Omental transfer operations 414 ‰‰ Development of genitourinary tract 348 ‰‰ Endovascular management 415 ‰‰ Hypospadias 350 ‰‰ Diabetic foot 416 Uro-oncology 351 Peripheral Venous Diseases 419 ‰‰ Renal cell carcinoma 351 ‰‰ Anatomy 419 ‰‰ Urinary bladder cancer 355 ‰‰ Varicose veins 420 ‰‰ Carcinoma testis 357 ‰‰ Deep vein thrombosis 424 ‰‰ Carcinoma penis 361 ‰‰ Raynaud phenomenon 425 ‰‰ Carcinoma prostate 364 Miscellaneuos Topics In CTVS 426 Section 4: Neurosurgery 367 ‰‰ Thoracic outlet syndrome 426 ‰‰ Lymphedema of lower limb 426 ‰‰ Physiology of CSF and its circulation 369 ‰‰ Hodgkin’s and non-Hodgkin’s lymphoma 430 ‰‰ Hydrocephalus 369 ‰‰ Unilateral lower limb edema 431 ‰‰ Criteria for brain death 373 ‰‰ Head injury pathophysiology 374 ‰‰ Glasgow coma scale (GCS) 376 Section 6: Breast and ‰‰ Monitoring of a head injury patient 376 Endocrine Surgery 435 ‰‰ CT scan in a patient with head injury 376 ‰‰ Management of head injury 378 Breast 437 ‰‰ Epidural hematomas 380 ‰‰ Blood supply and lymphatic drainage 437 ‰‰ Subdural hematoma 382 ‰‰ Nipple discharge 438 ‰‰ Spina bifida 384 ‰‰ ANDI (Aberrations of normal ‰‰ Functional neurosurgery 386 development and involution) 440 ‰‰ Stereotactic surgery 387 ‰‰ Mammary duct ectasia 441 ‰‰ Neurofibroma 389 ‰‰ Phylloides tumor 441 ‰‰ Intracranial space occupying lesions 390 ‰‰ Paget’s disease of nipple 442 ‰‰ Gynecomastia 443 Section 5: Cardiothoracic and ‰‰ LCIS and DCIS 444 Vascular Surgery 393 ‰‰ Triple breast assessment 446 ‰‰ Risk factors for breast cancer 446 Cardiac and Thoracic Surgery 395 ‰‰ Breast conservative surgery 447 ‰‰ Empyema thoracis 395 ‰‰ Management of locally advanced ‰‰ Pneumothorax 396 breast cancer 449 ‰‰ Hemothorax 398 ‰‰ Breast reconstruction 451 ‰‰ Cardiac tamponade 399 Thyroid 454 ‰‰ Cardiac arrest 400 ‰‰ Intercostal drainage 401 ‰‰ Embryology of thyroid and parathyroid 454 ‰‰ Thyroglossal cyst and fistula 455 Peripheral Arterial Disease for Lower Limb 403 ‰‰ Classification of thyroid swellings 456 ‰‰ Anatomy 403 ‰‰ Papillary thyroid cancer 457 ‰‰ Risk factors 403 ‰‰ Follicular thyroid cancer 459 ‰‰ Clinical features and investigations 404 ‰‰ Medullary thyroid cancer 460 ‰‰ Acute lower limb ischemia 404 ‰‰ Solitary thyroid nodule 461 ‰‰ Gangrene 408 ‰‰ Grave’s disease 462 ‰‰ Management 409 ‰‰ Complications of thyroidectomy 464 ‰‰ Critical limb ischemia 409 ‰‰ Buerger disease 411 Parathyroid and Adrenal 465 ‰‰ Amputation 412 ‰‰ Primary hyperparathyroidism 465 ‰‰ Sympathectomy 414 ‰‰ Adrenal incidentaloma 466 Prelims.indd 16 02-04-2015 14:06:37  Contents xvii Section 7: Surgical Radiology 469 ‰‰ Central venous pressure monitoring 539 ‰‰ Computed tomography (CT) 471 Skin 540 ‰‰ Ultrasound 473 ‰‰ Premalignant skin lesions 540 ‰‰ Doppler ultrasound 476 ‰‰ Squamous cell cancer 540 ‰‰ Magnetic resonance imaging (MRI) 478 ‰‰ Basal cell carcinoma 541 ‰‰ PET scan 481 ‰‰ Pigmented nevus 546 ‰‰ Intravenous pyelography (IVP) 484 ‰‰ Melanocytic nevi 546 ‰‰ Micturating cystourethrogram (MCU) 487 ‰‰ Malignant melanoma 547 ‰‰ ERCP 488 ‰‰ MRCP 491 Burns and Plastic Surgery 549 ‰‰ Radioisotope bone scan 493 ‰‰ Skin grafts and flaps 549 ‰‰ Thyroid scan 496 ‰‰ Phases of ‘take’ of graft 549 ‰‰ DMSA and DTPA scan 499 ‰‰ Types of burns 553 ‰‰ Mammography and BIRADS 502 ‰‰ Assessment of burns 553 ‰‰ FAST 503 ‰‰ Prehospital care 554 ‰‰ Radiological features of acute intestinal ‰‰ 40% TBSA burns management 554 obstruction 510 ‰‰ Inhalational injuries in a burn patient 554 ‰‰ Barium swallow in esophageal disorders 513 ‰‰ Pathophysiology of thermal burns 557 ‰‰ Development of lip and palate 558 Section 8: Miscellaneous Topics 523 ‰‰ Cleft lip and cleft palate 558 Anesthesia 525 Head and Neck Surgery 560 ‰‰ Pre-anesthetic medication 525 ‰‰ Anatomy of neck 560 ‰‰ ASA grade 525 ‰‰ Epulis 562 ‰‰ Muscle relaxants 526 ‰‰ Adamantinoma 562 ‰‰ Mivacurium 526 ‰‰ Premalignant lesions of the oral cavity 564 ‰‰ Succinylcholine 526 ‰‰ Cystic hygroma 565 ‰‰ Regional anesthesia 528 ‰‰ Hemangioma 566 ‰‰ Spinal regional anesthesia 530 ‰‰ Branchial cyst and fistula 567 ‰‰ Local anesthetic drugs 530 ‰‰ Ranula 568 ‰‰ Epidural anesthesia 531 ‰‰ Epidural analgesia 531 Oncosurgery Basics 569 ‰‰ Brachial plexus block 533 ‰‰ Immunotherapy in cancer 569 ‰‰ Caudal block 533 ‰‰ Immunosupressants drugs 571 ‰‰ Cervical blocks 534 ‰‰ Cancer prevention 573 ‰‰ Nerve block and field block 535 ‰‰ Tumor markers 574 ‰‰ General anesthetic drugs 535 ‰‰ Oncogenes 575 ‰‰ Halothane 535 ‰‰ Tumor suppressor genes 576 ‰‰ Propofol 535 ‰‰ Sacrococcygeal teratoma 577 ‰‰ Postoperative ventilation 537 ‰‰ Complications of general anesthesia 538 Further Reading 579 Prelims.indd 17 02-04-2015 14:06:37 Prelims.indd 18 02-04-2015 14:06:37  How and When to Prepare for University Examination: An Overview Before we begin the journey into the field of surgery, we would like to congratulate all the readers to reach this stage in their medical career. The final year of MBBS is a tough year in all aspects of health—mental, physical and emotional and to remain healthy, you need proper planning and a good schedule to study and relax at appropriate times. This book is a long sought solution to remaining “healthy” while preparing one big aspect of your final year—surgery: The subject with maximum mortality and morbidity in the MBBS field. Also, the subject is asked in different ways in examination and often is found tough to conquer. We are giving a schema to tackle this subject and this section is followed by all the important topics worth revising before examination and for entrance examination. The best way to start the subject is to start as early as possible. Whenever you read any subject in MBBS, you need to decide two books for that subject—one with the details and one to get you through the examination. The book with details should be good enough to give you the basics and a grasp of subject with in-depth discussion of all the topics important for learning the subject. On the other hand, you also need a book to help in rapid revision and quick accumulation of various exam-oriented topics in the subject according to the university examination scheme to get you through the examination. Love and Bailey/Schwartz/Sabiston Textbook of Surgery are considered standard descriptive books of surgery and are excellent to gain in-depth knowledge of the field but difficult to digest and revise at examination time. The list also extends to include SRB’s Manual of Surgery, Manipal Text of Surgery, Das Concise Text of Surgery and many more. These books are descriptive and provide excellent insight regarding most of the topics of surgery even for postgraduates. This creates a rather difficult situation because both undergraduates and postgraduates are than reading the same basic material which does not seem right... Isn’t it? Especially during examination, when you have to revise the book that you have first read, Harrison in Medicine and Bailey in Surgery, it is a tough task to complete, also with the thought in mind that you have other subjects to look after. So, it is our advise to keep one textbook that suits you from the above options as a reference and this book since you start reading surgery and not just as a last resort book as this will help in rapid revision during the examination as well as necessary in-depth discussion of important topics as per undergraduate level. How this book will help you in your preparation of surgery? yy It will help you in gaining the requisite knowledge of all important topics of the field of surgery as per the last 10 years of university papers as well as recent topics, which are prospective questions in the years to come. yy This book also will provide you with the important and less frequently dealt topics of Anesthesia and Radiology that are not discussed in descriptive books and that need to be searched at examination times and create unnecessary waste of time and stress. Prelims.indd 19 02-04-2015 14:06:37  xx Exam Preparatory Manual for Undergraduates—Surgery yy Also, all the answers are from latest editions of best surgical books so as to help you in clearing the surgery part of your MCQ preparation. yy Because of the concise nature, it will help in rapid revision and will save time for other subjects. So, begin early, read a descriptive book and a question-answer pattern book like ours to quickly revise and orient yourselves to all the important topics of the subject. This pattern of studies will give you the necessary confidence that you know the basics and also be equipped to clear the examinations without much duress. Apply this pattern to all the subjects to gain maximum benefit. Prelims.indd 20 02-04-2015 14:06:37  SECTION General Surgery 1 yy Wound Healing yy Fluid, Electrolyte and Acid-Base Imbalance yy Metabolism and Nutrition yy Blood Transfusion and DIC yy SIRS, Shock and MODS yy Basic of Surgical Technologies and Advanced Surgery yy Surgical Infections yy Trauma and Damage Control Surgery yy Perioperative Surgery yy Surgery of the Salivary Glands yy Miscellaneous General Surgery Topics of Importance yy Medicine in Surgery Ch-1.indd 1 02-04-2015 11:30:55 Ch-1.indd 2 02-04-2015 11:30:55  Section 1: General Surgery 3 WOUND HEALING Q1. Write a note on mechanisms of wound healing. What are the phases of wound healing? Discuss in brief. Enumerate the phases and types of wound healing. Ans. Wound means the disruption of cellular and anatomic continuity of tissue. Goals of wound healing: yy Regeneration (recovery of full structure and function without scarring) yy Seen only in bone and liver. Phases of wound healing 1. Inflammation (1–3 days) yy Hemostasis, chemotaxis, epithelial migration yy Form fibrinous exudates/eschar yy Chronic wounds become stalled in this phase 2. Proliferation (3 days to 3 weeks) yy Proliferation of endothelial cells, smooth muscle cells and fibroblasts yy Granulation tissue 3. Maturation (3 weeks onwards) yy Contraction of wound edge yy Scar and scar remodelling Phase 1 yy Tissue injury causes activation of stromal cells and keratinocytes which on activation release macrophage chemoattractant protein (CCL 2), interleukin 8 (CXCL 8), CXCL 4,10 which are potent chemotactic for neutrophils yy Of these, CCL2, CXCl8 and 10 are elevated chronically in chronic wounds therefore keeping it in inflammatory phase. yy Interleukin 8 is low in fetal wounds which accounts for healing of wound with minimal inflammation and no scarring in fetal age yy C5a, leukotriene B4, C4 and D4 directly and via release of platelet aggregating factor from endothelium (thrombin mediates the stimulation of the endothelial cells to secrete PAF, interleukin1 and TNF) cause adhesion of the chemoattracted neutrophils. Interleukins and TNF are also released from monocytes and macrophages which also aid in this process yy Next after adhesion is migration of cells in extracellular matrix. Migration has phases of adhesion, spreading, contraction and retraction which are mediated by collagen, laminin and fibronectin in ECM with integrans on the cells yy Thus, by this mechanism, neutrophils finally reach the wound and mediate intracellular bacterial killing yy The role of these PMNs is only removal of contamination. It has no effect and no role in the process of wound healing. One important event in this phase is of epithelialisation which has the phases of detachment migration, proliferation, differentiation and stratification and is mediated by EGF, KGF and TGF alfa. Ch-1.indd 3 02-04-2015 11:30:55  4 Exam Preparatory Manual for Undergraduates—Surgery Phase 2 yy Macrophages are the effector cells of this phase yy Bacterial products, complement degradation products, C5a, thrombin, fibronectin, collagen, TGF beta and PDGF BB are all chemotactic for macrophages. Thus, the macrophages reach the wound site and mediate effects as follows: –– Macrophages release interleukin 2, collagenase, elastase and in the presence of lipopolysaccharide, macrophage releases free radicles and mediate phagocytosis –– It releases FGF, VEGF, TNF alfa and stimulates endothelial cell proliferation and angiogenesis –– It also releases PDGF, EGF, IGF-1 and TGF beta and stimulates fibroplasias and collagen, elastin and glycosaminoglycan synthesis –– It induces apoptosis of PMN –– Releases IL1 alfa and therefore produces a febrile response. yy Lymphocytes –– T lymphocytes induce fibroplasias by releasing TGF beta and TNF alfa –– They also release interferon gamma and mediate effects such as downregulation of prostaglandin synthesis –– Macrophage activation to release TNF alfa and IL1 –– Decrease collagen synthesis and keep macrophages in the wound –– Interferon gamma is thus another important mediator in chronic non healing wound –– B lymphocytes have no role in wound healing but are involved in downregulating wound healing once the wound closes. Two important events in proliferation phase are angiogenesis and fibroplasias Angiogenesis yy Activated endothelial cells degrade basement membrane of post capillary venules by release of plasmin and matrix metalloproteinases yy PDGF, TGF beta, FGF mediate migration of detached endothelial cells through these gaps and division resulting in tubule or lumen formation yy These tubules are then covered by deposition of basement membrane and capillary forms yy Important mediators include PECAM 1 which mediates endothelial cell-endothelial cell interaction and mediate cell-cell contact and beta1 integrin receptors which form tight junctions and stabilise the contacts developed by PECAM1 and lead to formation of capillaries, arterioles and venules yy Cell disruption and hypoxia are strong inducers of the angiogenic factors—VEGF (member of PDGF family) and PDGF are proangiogenic factors yy Timeline of angiogenesis –– FGF2 provides the initial angiogenic stimulus at day 3 –– VEGF provides delayed and prolonged stimulus between days 4 to 7 –– TGF alfa and EGF causes cell proliferation –– TNF alfa promotes formation of the capillary tube by increasing HIF 1 alfa which leads to increase in NO and VEGF during days 1 to 5. Ch-1.indd 4 02-04-2015 11:30:55  Section 1: General Surgery 5 Phase 3 –– PDGF and FGF causes fibroblasts to become active which are called stimulated fibroblasts or myofibroblasts which then mediate this phase –– Actin appears at day 6 after wounding, persists at high levels till 15 days and then disappears by 4th week –– Matrix metalloproteinases are important in wound remodelling and contraction of all these, MMP 3 (stromelysin) is particularly important –– Epidermodermal interface in healed wound is devoid of rete pegs and therefore have increased fragility and avulsion after minnow trauma. Types of wound healing yy 1st intention (Primary) healing: Well approximated edges of incised wound heal by this way yy 2nd intention (Secondary) healing: The wound is left open and allowed to heal on its own yy 3rd intention (Tertiary) healing (Delayed primary closure): The wound is initially left open for dressing and then closed after few days. Q2. Write a note on pathophysiology and management of chronic nonhealing wound/ulcer in lower limb. Enumerate the causes for the chronic nonhealing of a wound. Ans. Chronic wounds are wounds greater than 3 months. These are the wounds which fail to proceed to functional and anatomic integrity over a period of 3 months. Pathology yy Chronic wounds become stalled in inflammatory phase yy CCL2, CXCL 8 and 10 are elevated chronically in chronic wounds therefore keeping it in inflammatory phase yy Also increased levels of Interleukin 8, TNF alfa, Interleukin 1 and interferon gamma in these wounds along with increased MMP1,2,8,9 and decreased TIMP (inhibitor of matrix metalloproteinases) lead to decreased adhesion molecule expression, decreased cell migration, decreased growth factors and increased breakdown of products. yy This leads to increased inflammation and collagen degradation rather than collagen synthesis. Causes of nonhealing of wound yy Local infection is the most important factor to drive these mediators. Organism count >105/g or single beta hemolytic streptococci are the most detrimental factors hindering wound healing. Other important causes for chronic nonhealing of wound include: –– Hypoxia, anemia –– Diabetes due to repeated trauma, tissue hypoxia due to vasculopathy, decreased VEGF/PDGF and HIF 1 alfa –– Ionising radiation Ch-1.indd 5 02-04-2015 11:30:55  6 Exam Preparatory Manual for Undergraduates—Surgery –– Aging –– Malnutrition—hypoalbuminemia ( neonatal wound > adult wounds This is because of intrinsic fetal factors such as increased prolyl hydroxylase activity in fetal fibroblasts and extrinsic such as hyaluronan rich amniotic fluid yy Medication: Chemotherapy, steroids yy Local factors: Wound tension, foreign body, dead or devitalized tissue, excessive exudates. yy Nutritional status: Protein, zinc, vitamins, hypoalbuminemia (105 organisms/gram of tissue. For example, include zinc oxide, silver nitrate, bacitracin, neosporin, acetic acid and growth factors. Q5. What is pressure sore? Discuss its management. Ans. Definition: A sore area of skin that develops when the blood supply to it is cut off for more than two to three hours due to pressure on it and lack of movement. Main causative factors thus include: yy Mechanical effects of prolonged pressure yy Shearing forces yy Prolonged immobilization Grading NPUAP staging system for pressure ulcers I Intact skin with nonblanchable redness of a localized area, usually over a bony prominence II Partial thickness loss of dermis appearing as a shallow, open ulcer with a red-pink wound bed and slough may also appear as an intact or open/ ruptured serum-filled blister III Full-thickness tissue loss, subcutaneous fat may be visible, but bone, tendon or muscles are not exposed IV Full-thickness tissue loss with exposed bone, tendon or muscle Contd... Ch-1.indd 9 02-04-2015 11:30:55  10 Exam Preparatory Manual for Undergraduates—Surgery Contd... Unstageable Full-thickness tissue loss with the base of the ulcer covered by slough (yellow, tan, gray, green or brown) or eschar (tan, brown, or black) in the wound bed Deep tissue localized area of discolored, intact skin or blood-filled blister caused by injury damage to underlying soft tissue from pressure or shear Management General measures y Air mattress/water bed y y Frequent change of posture y y Avoiding soiling by incontinence or drooling y y Nutrition of patient should be taken care of y y Immunonutrition y y Protection of all pressure points by glove balloons y y Release and treatment of contractures y Grade 1 and 2—general measures and moist dressings will take care of most of these pressure sores. Options in treatment of grade 3 and 4 pressure ulcers As mentioned above, pressure sore grade 1 and 2 are managed with dressings and general supportive measures, whereas grade 3 and 4 usually require some form of reconstructive option once osteomyelitis or deep soft tissue infections are ruled out. Direct closure and skin grafting don’t serve much role in these grades of pressure sore. Options thus include Sacral Gluteus maximus myocutaneous flap Gluteal fasciocutaneous rotational or advancement flap Ischial Gluteus maximus myocutaneous flap Hamstring V-Y myocutaneous flap Posterior thigh flap based on inferior gluteal artery Trochanteric Tensor fascia lata advancement flap Rectus femoris flap Vastus lateralis myocutaneous flap Unsalvageable Hip disarticulation with tissue closure Intraoperative y During surgery in patients with spinal cord injury, especially T5 or higher, care y should be taken to avoid autonomic hyperreflexia while doing manipulation of pressure ulcer y Flaps should be larger than wound and suture line should be far away from pressure y points. Postoperative care y Air mattress for 7 to 10 days y y Care while position changes y Ch-1.indd 10 02-04-2015 11:30:55  Section 1: General Surgery 11 y Ischial flap—do not sit for 6 weeks y y Nutrition and muscle spasm control. y Q6. Write a note on keloids. Differentiate between keloid and hypertrophic scar. Ans. Keloid Hypertrophic scar y Genetic predilection is present y Not present y y y Predilection for darkly pigmented skin y No such predilection y y y No specific causative factors y Foreign body in wound, wound infection, y y suturing under tension predispose Pathology y Proliferation of immature fibroblasts and y Proliferation of mature fibroblasts and y y blood vessels with disordered collagen blood vessels and organized collagen synthesis synthesis y Increased expression of TGF beta 1 and y Hyperproliferation with normalisation on y y 2 with irreversible changes in extracellular removing the causative factors matrix production y Center of keloid lesions contain a paucity of y No such feature. Cells are uniformly y y cells distributed y Has increased vascularity y No increase in vascularity y y Clinical features y Females are more commonly affected y No sex predilection y y y Occurs more commonly in a triangular region y No site predilection y y bordered by both shoulders and sternum y Grows beyond the borders of the original y Confined to boundary of wound y y wound y Claw like extensions from the primary lesion y No extensions occur beyond the wound y y are common y Itchy lesions y Non-itchy lesions y y y Can be painful and tender y No pain or tenderness y y Natural history and prevention y Never regress spontaneously y Regress spontaneously after 6–8 months y y y Cannot be prevented y Can be prevented if causative factors are y y taken care of y Difficult to treat y Easy to treat y y y Recurrences are very common y Does not recur y y Common points y Both are hyperproliferation disorders with collagen abundance due to an imbalance between y collagen synthesis and degradation y Both have stretched collagen fibers along the same plane as epidermis y y Scars perpendicular to the direction of muscle fibers tend to be flatter and less chance of y hypertrophic scars. Contd... Ch-1.indd 11 02-04-2015 11:30:55  12 Exam Preparatory Manual for Undergraduates—Surgery Contd... Keloid Hypertrophic scar Prevention Postsurgery scar managemnt with silicone sheeting/triamcinolone acetonide at 6 weeks intervals/topical imiquimod cream or 5-Fluorouracil/pulsed dye lasers have the best outcome y First line treatment y − Triple therapy with surgery, steroid and silicone sheeting − − Excision pulsed dye laser − − Pressure therapy for 6 to 12 months − − Intralesional steroid − − Cryotherapy − − Combination of either of these − y Second line treatment y − Radiation − − Bleomycin therapy and tattooing − − Interferon alfa-2, intralesional verapamil with surgery and silicone sheeting − − Mederma gel (Onion extract gel with silicone) − FLUID, ELECTROLYTE AND ACID-BASE BALANCE Q7. Write a note on fluid balance in patients and surgery. Explain the normal water distribution in body. Ans. y Total body water—60% of total body weight in males and 50% of total body weight y in females (as females have more subcutaneous fat), most water is in skeletal muscles y Of the total body water y – 40% is intracellular – – 15% is interstitial [includes 2% transcellular (water in CSF and joint spaces)]. The – interstitial water has a rapidly equilibrating component and slowly equilibrating transcellular component – 5% intravascular (15% of this is arterial) – y Serum osmolarity = 2 sodium + urea/2.8 + glucose/18 (Normal—280–310 mosm/kg) y y The tendency of solute exchange is determined by osmolarity y y The tendency of water exchange is determined by tonicity y y Tonicity is thus relative osmotic activity of two solutions, e.g. azotemia is a hyperosmotic y condition but not a hypertonic condition y Therefore osmolarity of the extracellular fluid is determined primarily by sodium, y whereas the effective osmotic pressure between plasma and interstitium is determined by nondiffusible proteins and tonicity = 2 sodium + glucose/18 y Osmolar gap = measured – calculated osmolarity which is due to ethanol, methanol, y ethylene glycol and unidentified toxins y Major intracellular cations include potassium, calcium and major intracellular anions y include proteins and phosphates. y Major extracellular cation include sodium and anions include chloride and bicarbonate. y Ch-1.indd 12 02-04-2015 11:30:56  Section 1: General Surgery 13 Fluid losses and gain in body Intake 2000–2600 mL/day Urine 500–800 mL/day Insensible loss 600 mL/day (75% from skin, 25% from lungs) Stool 250 mL/day Important electrolyte values to remember In mEq/L Sodium Potassium H+ chloride Bicarbonate Osmolarity Sweat 50 5 50 50 0 Gastric 50 0 90 100 0 Bile 150 5 0 80 70 Pancreatic 150 5 0 80 110 Colon 120 30 0 80 30 Ileostomy 100 10 0 50 50 Diarrhea 50 50 0 20 40 Ringer lactate 130 4 0 109 Lactate 28, calcium 3 273 Normal saline 154 0 0 154 0 308 Q8. Enumerate the causes of hyponatremia. Discuss the clinical features and management of a patient with hyponatremia. Ans. Normal level—135 to 145 mmol/L Causes Sodium and water loss Euvolemic hyponatremia Water and sodium excess (Water >> sodium) Renal SIADH Nephrotic syndrome y Diuretics Hypothyroidism Congestive cardiac failure y y Mineralocorticoid deficiency Psychogenic polydipsia Cirrhosis y y Osmotic diuresis (Glucose, Glucocorticoid deficiency Acute and chronic renal failure y mannitol, urea) y Renal tubular acidoses y Extrarenal y Vomiting y y Diarrhea y y Burns y y Pancreatitis y y Rhabdomyolysis y Clinical features y Headache, confusion y y Weakness, fatigue, muscle cramps y y Anorexia, nausea, vomiting, watery diarrhea, lacrimation, salivation y y Hypertension, bradycardia, oliguria y Management y Hypovolemic hyponatremia: Isotonic saline administration y Ch-1.indd 13 02-04-2015 11:30:56  14 Exam Preparatory Manual for Undergraduates—Surgery y Euvolemic hyponatremia: Water restriction y y Hypervolemic hyponatremia: Sodium and water restriction y y Free water excess should be corrected first and then correction of low sodium y y If neurological symptoms are present, they should be treated with 3% saline y y Otherwise, treat with 0.9% saline and the rate of treatment should not exceed 12 mEq/L/ y day as rapid correction can lead to central pontine myelinolysis now better known as osmotic demyelination syndrome which can have both pontine and/or extrapontine myelinolysis which causes seizures, weakness, akinetic movements and finally permanent brain damage y Formula for sodium deficit calculation y y Sodium deficit = total body water (130 – measured) y Volume—sodium deficit/154 (saline in liters) Q9. Enumerate the causes of hypernatremia. Discuss the clinical features and management of a patient with hypernatremia. Ans. Causes Sodium and water loss Euvolemic hyponatremia Water and sodium excess (Sodium >> water) Renal Diabetes insipidus Primary aldosteronism y Loop diuretics Insensible losses from skin Cushing syndrome y y Osmotic diuresis (Glucose, and respiratory tract Hypertonic dialysis y mannitol, urea) Psychogenic hypodipsia Bicarbonate infusion Extrarenal y Diarrhea y y Burns y y Nasogastric aspirations y Clinical features y Restlessness, ataxia, lethargy, irritability, tonic spasm, delirium, coma y y Weakness, oliguria y y Dry sticky mucus membrane, red swollen tongue, decreased saliva and tears y y Tachycardia and hypotension y Management y Initially, water deficit should be corrected first then, hypernatremia correction is y decided by following formula: – Water deficit (liters) = total body water (sodium – 140)/140. – y Again, correction should not be done at a rate greater than 12 mEq/L/day. y Potassium balance is very important topic both for exams and for managing patients in clinics and therefore is explained in detail. Normal potassium homeostasis (Normal—3.5–4.5 mEq/L) y Total body potassium = 50 mEq/kg body weight. Extracellular is 2% of this and only y 0.4% is in plasma. Rest is intracellular. Ch-1.indd 14 02-04-2015 11:30:56  Section 1: General Surgery 15 y Therefore, 1 mEq/L change in potassium in serum is caused by either y – An intracellular deficit of around 200–400 mEq or – – Potassium excess of 100–200 mEq – y It is the value which is to be corrected to solve the patient’s problem. y Q10. Enumerate the causes of hypokalemia. Discuss the clinical features and management of a patient with hypokalemia. Ans. Causes Renal causes Extrarenal causes y Type I and II renal tubular acidoses y Diarrhoea y y y Acetazolamide y GI fistulas y y y Diabetic ketoacidoses y Villous adenoma y y y Uretrosigmoidostomy y Anorexia nervosa y y y All causes of metabolic alkalosis y Laxative abuse y y y Hypomagnesemia y Drugs y y y Bartter syndrome, Gitelman syndrome y Hypokalemic periodic paralysis y y y Hyperaldosteronism y Spurious hypokalemia: Extreme leucocytosis Redistributive hypokalemia: Theophylline toxicity, barium toxicity, insulin therapy, etc. Drugs causing hypokalemia: Aminoglycosides, amphotericin, cisplatin, foscarnet and ifosfamide Clinical features y Ileus, constipation y y Decreased reflexes, fatigue, weakness, paralysis y y Cardiac arrest and/or ECG changes as follows: y Flattened or inverted T waves, a U wave, ST depression and a wide PR interval. The prominent U wave is frequently superimposed upon the T wave and therefore produces the appearance of a prolonged QT interval. y Physiological variation: Potassium decreases by 0.3 mEq/L for every 0.1 increase in y pH above normal. Management y First step is restoration of volume y y Symptomatic hypokalemia: Give potassium 20 mEq IV over 1 hour under ECG guidance y for maximum 4 doses. Rate of correction should not exceed 20 mEq/hour in any case and if at all it is required, it should always be done through a peripheral venous line. Maximum tolerated limit for potassium correction under ECG guidance is 100 mEq/hr. y If still not corrected: Look for hypomagnesemia, as untreated hypomagnesemia can lead y to resistant hypokalemia which will not be corrected till the magnesium level is corrected. y Asymptomatic patients: Give oral syrup potassium chloride mixed with water, also add y coconut water, bananas and other potassium rich sources. Ch-1.indd 15 02-04-2015 11:30:56  16 Exam Preparatory Manual for Undergraduates—Surgery Q11. Enumerate the causes of hyperkalemia. Discuss the clinical features and management of a patient with hyperkalemia. Ans. Causes Spurious of hyperkalemia y Tight tourniquet y y Hemolysis y y Leucocytosis/thrombocytosis y Redistribution of hyperkalemia y Hyperglycemia y y Succinylcholine, digitalis y y Hyperkalemic periodic paralysis y High renin, low aldosterone y Addison disease y y Heparin and ACE inhibitors y Low rennin, low aldosterone y Hyporeninemic hypoaldosteronism y y Cyclosporine toxicity y End organ damage with high aldosterone Renal tubular damage due to: y Autoimmune—SLE, amyloidoses y y Hemolysis—sickle cell disease y y Drugs—spironolactone, triamterene and y amiloride Drugs causing hyperkalemia: Angiotensin receptor blockers, ACE inhibitors, digoxin, spironolactone, succinylcholine, heparin, cyclosporin, pentamidine, triamterene. Clinical features y Colic, diarrhea y y Nausea, vomiting y y Weakness, paralysis, respiratory failure y y Arrhythmias as follows: y Mild hyperkalemia (5.5–6.5 mEq/L) y Peaked T waves y y Prolonged PR segment y Moderate hyperkalemia (6.5–8 mEq/L) y Loss of P wave y y Prolonged QRS y y ST elevation y y Ectopics y Severe hyperkalemia (> 8 mEq/L) y Progressive widening of QRS complex y y Sine wave appearance y y Fascicular blocks/bundle branch blocks y y Ventricular fibrillations y y Asystole y Management y First step is restoration of volume. y Therapies y Calcium: Used only for arrhythmia stabilization. It has no effect on potassium level. It y should always be given with cardiac monitoring. 2 solutions : Calcium gluconate 10%=0.5 mL/kg slow IV injection or calcium chloride 10%=0.1–0.2 mL/kg slow IV injection. Ch-1.indd 16 02-04-2015 11:30:56  Section 1: General Surgery 17 y Salbutamol: [K+ sequestrant]. Given by nebulisation or IV y y Insulin/Glucose to be given at the same time (K+ sequestrant) y y Bicarbonate: In metabolic acidosis only y y Dialysis (K+ excretion) y y Kayexalate (K+ excretion) y Severe hyperkalemia Any patient with K+ >7.0 mEq/L or at risk of increasing and/or patient symptomatic and/or ECG disturbance: Manage with the following measures: y Calcium IV if ECG changes, salbutamol nebulization, insulin/glucose IV, bicarbonate IV y if metabolic acidosis y Dialysis y y Kayexalate (Polystyrene sulfonate) PR (if dialysis unavailable) y Moderate hyperkalemia Any patient with K 6 to 7 mEq/L, asymptomatic with normal ECG Manage with following measures: y Salbutamol nebulization, insulin/glucose IV, kayexalate (polystyrene sulfonate) PR or y oral, bicarbonate IV if metabolic acidosis Mild Hyperkalemia Any patient with K >5.5, asymptomatic with normal ECG Management y Stop K supplements y y Salbutamol nebulization, bicarbonate IV if metabolic acidosis. y Q12. Enumerate the parameters useful to decide acid-base disorders and give their normal values. Answer pH 7.35–7.45 PaO2 74–82 mm Hg PaCO2 35–45 mm Hg SaO2 >92% CaO2 16–20 vol % HCO3– 22–26 mEq/L Important buffering systems in body y Intracellular—proteins and phosphates y y Extracellular—bicarbonate-carbonic acid system y Q13. Discuss the steps of diagnoses of an acid-base disorder in a patient. Explain the mechanism of identification of an acid-base disorder and show its compensation mechanism. Ch-1.indd 17 02-04-2015 11:30:56  18 Exam Preparatory Manual for Undergraduates—Surgery Ans. Acid base imbalances are diagnosed as follows: 1st step: Identify the primary acid-base disorder (Mnemonic—ROME – Respiratoy has Opposite change between pH and pCO2 whereas Metabolic has Equal direction change between ph and bicarbonate) ABG pH PaCO2 HCO3 Compensation Metabolic acidoses Decrease N Decrease Decrease in PaCO2 Metabolic alkalosis Increase N Increase Increase in PaCO2 Respiratory acidoses Decrease Increase N Increase in HCO3 Respiratory alkalosis Increase Decrease N Decrease in HCO3 2nd step: Identify compensation as shown in the chart above 3rd step: See if gaps are present in case of metabolic acidoses y Anion gap y Unmeasured cations (UC) (Mn: PCM) Unmeasured anions (UA) (Mn: SOAP) Potassium, calcium and magnesium Sulphate, organic acids, albumin, phosphate Total – 11 mEq/L Total – 23 mEq/L Anion gap = UA – UC = 12 mEq/L = sodium – (chloride + bicarbonate) Adjusted anion gap = 2.5 (4.5 – albumin) + observed anion gap. High anion gap acidoses Normal anion gap acidoses Ethanol/ methanol/propylene glycol poisoning Proximal (Type 2), distal (Type 1) and Type 4 Salicylates Renal tubular acidoses Isoniazid toxicity Early renal failure Ketoacidoses (Diabetes/starvation/alcohol) Exogenous ammonium chloride or HCl Lactic acidoses Administration Uremia Diarrhea Carbonic anhydrase inhibitor therapy y Gap-gap in acidoses: It is calculated only when anion gap is present y Gap-gap = anion gap excess/bicarbonate deficit = (measured anion gap-12)/(24 – measured bicarbonate) y If gap-gap 1, it indicates co-existence of metabolic alkalosis with high anion gap acidoses. y Clinical features of acid-base imbalance are as shown in the table on the next page: Q14. Write a note on metabolic acidoses (above matter + following matter will make the SN). Ans. y First step is restoration of volume y y Management mainly aims at correction of the underlying cause y y Sodium bicarbonate is given only when ph < 7.1/sodium bicarbonate < 15 mEq/L y y Base deficit = 0.6 body weight (i.e. TBW) (15 – sodium bicarbonate) in mEq/L y y Half of this value is administered bolus and half added in the infusion form y y However, sodium bicarbonate has dubious role in management of metabolic acidoses y less severe than this and especially in patients with lactic acidoses. Ch-1.indd 18 02-04-2015 11:30:56  Section 1: General Surgery 19 Symptoms of acidoses Symptoms of alkalosis Headache, sleepiness, coma, dyspnea, Nausea, vomiting, muscle twitches, tremors, arrhythmias, nausea, vomiting, diarrhea, numbness, confusion, coma, tingling in hands seizures, weakness and feet. Q15. Explain: Metabolic alkaloses. Ans. Causes Chloride responsive Chloride unresponsive y Respond to chloride administration y Does not respond to chloride administration y y y Has low chloride in plasma and urine y Does not have low chloride in plasma and urine y y y Post-hypercapnea y Laxative abuse y y y Diuretic therapy y Bartter syndrome y y y Villous adenoma y Primary aldosteronism y y y Gastric aspirations y Cushing syndrome y y y Malignant or accelerated hypertension y Management y First step in management of any fluid electrolyte or acid-base disorder is the correction y of fluid abnormality, i.e. hypovolemia y Final management depends on correction of cause y y Chloride deficit = 0.3 body weight (100 – chloride level) y Volume to replace = chloride deficit/154 in liters of isotonic saline y H+ deficit = 0.5 body weight (actual – desired bicarbonate) y Volume to replace = H+ deficit/100 in 0.1N HCl. Q16. Write a note on plasma expanders. Ans. Rationale y Crystalloids redistribute after intravenous administration in a ratio of 1:3 that is for y 1 part that remains in the intravascular compartment, 3 parts go into the interstitium. For example, if 1 liter crystalloid is administered, 750 mL goes into interstitial space and 250 mL remain in intravascular space y Colloids on the other hand distribute 3:1, that is opposite of crystalloids and thus are y called plasma expanders. These are large molecules with poor diffusibility which create an osmotic pressure to increase fluid in intravascular space y Therefore to counteract blood loss, volume to be transfused y y Crystalloid—3:1 y y Colloid—1:1 y Plasma expanders include y 5% albumin y y 25% albumin (latest) y y 6% dextran y y 6% hetastarch y Ch-1.indd 19 02-04-2015 11:30:56  20 Exam Preparatory Manual for Undergraduates—Surgery Conflicts y No convincing evidence that colloids are better than crystalloids. y y No convincing evidence that one colloid is better than other colloid. y Adverse events y Decreases immunoglobulin response y y Decreases albumin production y y Decreases ionised calcium level y y Decreases response to tetanus toxoid y y Increases ECF volume deficit y y Dextran interferes with cross matching and it causes coagulopathy y y Hetastarch decreases vWF and factor 8c levels and causes coagulopathy y