MRCS A ESSENTIAL REVISION NOTES

Book 2

Edited by Claire Ritchie Chalmers BA PhD FRCS Catherine Parchment Smith BSc MBChB FRCS

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MRCS ERN VOL 1 prelims.indd 2 8/19/2016 12:10:03 PM Contents

Acknowledgements v

Preface v

Picture Permissions vi

Contributors vii

Introduction ix

Chapter 1 – Abdominal Surgery 1 Catherine Parchment Smith, Arin K. Sara and Ravinder S. Vohra

Chapter 2 – Surgery 337 Jenny McIlhenny and Ritchie Chalmers

Chapter 3 – Cardiothoracic Surgery 397 George Tse and Sai Prasad

Chapter 4 – Endocrine Surgery 465 Nicholas E Gibbins and Sylvia Brown

Chapter 5 – Head and Neck Surgery 521 Nicholas E Gibbins

Chapter 6 – Neurosurgery (Elective) 593 Paul Brennan

iii

MRCS ERN VOL 1 prelims.indd 3 8/19/2016 11:05:26 AM Chapter 7 – Transplant Surgery 627 Karen S Stevenson

Chapter 8 – Urological Surgery 647 Mary M Brown

Chapter 9 – Vascular Surgery 729 Sam Andrews

Abbreviations 803

Bibliography 807

Index 809

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Stomac Oesophagus 3.8 3.7 3.6 3.5 3.4 3.3 3.2 3.1 1.3 1.2 1.1 Abdominal w 2.9 2.8 2.7 2.6 2.5 2.4 2.3 2.2 2.1

Congenital abnormalitiesof Gastric car Complications ofpeptic P Ph Anatom Anatom the stomach Gastritis ulceration Oesophageal car Barrett’ Other benignoesophageal Oesophageal perfor Motility disorders Hiatus hernia Gastro-oesophageal reflux P Anatom Complications ofhernias Anterior abdominalw disorders disease oesophagus Hernias ain anddifficulty swallowing eptic ulceration h andduodenum ysiology oftheupperGItract

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106 105 A 96 89 77 66 64 60 60 10 55 53 53 51 49 48 44 40 37 37 31 3 3 bdominal Surgery K 5. 4. . S

Catherine Parchment Smith, 5.10 5.9 5.8 5.7 5.6 5.5 5.4 5.3 5.2 5.1 Biliar Li 4.10 4.9 4.8 4.7 4.6 4.5 4.4 4.3 4.2 4.1 3.10 3.9 aha Ravinder and S. Vohra ver andspleen

y tree andpancreas Other disordersofthepancreas Other pancreatictumours P Ph Anatom Other disordersofthebiliary Ph Anatom Pancreatitis tree Gallstones T Li Li Li Cirrhosis Clinical ev P Jaundice Ph Anatom disease Other conditionsofthe Congenital abnormalitiesof stomach andduodenum the duodenum ancreatic carcinoma he spleen ortal hypertension ver cysts ver infections ver masses PTER C ysiology ofthepancreas ysiology ofthebiliarytree ysiology oftheliver

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y ofthepancreas y ofthebiliarysystem y oftheliver

aluation ofliver

174 173 168 164 162 161 159 150 147 144 144 139 138 137 134 133 131 127 120 115 110 110 106 107 1 8/17/2016 2:29:56 PM 1

CHAPTER 1 6. Acute Abdomen 176 8. Large bowel 242 6.1 Acute abdominal pain 176 8.1 Symptoms of non-acute 6.2 Common acute abdominal abdominal disorders 242 emergencies 182 8.2 and physiology of the 6.3 Intestinal obstruction 195 colon 259 6.4 Peritonitis 205 8.3 Diagnosis of colorectal disease 263 6.5 Stomas 215 8.4 Inflammatory bowel disease 269 8.5 Benign colorectal tumours 280 7. Small bowel 222 8.6 Colorectal cancer 289 7.1 Anatomy and physiology of 8.7 Other colorectal conditions 307 the small bowel 222 7.2 Imaging and investigating the 9 Perianal conditions 310 small bowel 226 9.1 Anatomy and physiology of 7.3 Intestinal fistulas 227 the rectum and anus 310 7.4 Tumours of the small bowel 230 9.2 Haemmorhoids 313 7.5 Bleeding from the small bowel 234 9.3 Anal fissures 318 7.6 Intestinal ischaemia 235 9.4 Anorectal abscesses 319 7.7 Diverticula of the small bowel 238 9.5 Anorectal fistulas 322 7.8 Infectious enteritis 239 9.6 Pilonidal sinus 324 7.9 Radiation small-bowel injury 240 9.7 Pruritus ani 325 7.10 Short-bowel syndrome 240 9.8 Rectal prolapsed 327 7.11 Short-bowel bypass 241 9.9 Proctalgia fugax 330 9.10 Faecal incontinence 330 9.11 Anal cancer 333 9.12 Sexually transmitted anorectal infections 334

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ERN 2012.indb 2 8/17/2016 2:29:56 PM ERN 2012.indb 3 muscles. This isavestigial thinlayer ofareolartissueover fasciaDeep transverse bands. abdomen. Dermatomesarealsoarranged in The skin has horizontal Langer’s lines over the Skin nterior abdominal wall Layers abdominal of the wall 1.1 • • • • • • • • through several layers: anterior abdominalwall you willgo When you makeanincisioninthe Learning point Learning

Peritoneum Extraperitoneal fat Transversalis Muscles (dependingonincision) Deep fascia(vestigial) Superficial fascia Subcutaneous fat Skin A (Scarpa’s fascia) Superficial fascia Muscles • • • • Abdominal wall Abdominal • • • • • • on theincisionsite: The muscles you’ll passthroughdepend Learning point Learning sac-like covering forscrotum/labia) (forms tubularsheathforpenis/clitorisand Continuous withColles’fasciaover perineum mistaken forexternaloblique!) Very prominentinchildren (caneven be inguinal ligament Fuses withdeepfasciaofleginferiorto Absent above andlaterally Rectus sheath Pyramidalis Transversus abdominis Rectus abdominis Internal oblique External oblique and herniasand CTION S e

1 8/17/2016 2:29:56 PM 3

CHAPTER 1 Abdominal Surgery

• External oblique is a large sheet of muscle the nerves enter the sheath laterally and CHAPTER 1 CHAPTER fibres running downwards from lateral run towards the midline (so are disrupted in to medial like a ‘hand in your pocket’. Battle’s incision – see Figure 1.3) Medially, the external oblique becomes • Linea alba is a fibrotendinous raphe running a fibrous aponeurosis which lies over the vertically in the midline between the left rectus abdominis muscle (see below), and right rectus abdominis muscles. It is forming part of the anterior rectus sheath formed by the fusion of the external oblique, • Internal oblique is a second large sheet internal oblique and transversus abdominis of muscle fibres lying deep to the external aponeuroses. They fuse in an interlocking/ oblique and at right angles to it. Medially, interdigitating structure through which it forms a fibrous aponeurosis which splits epigastric hernias may protrude. The linea to enclose the middle portion of rectus alba provides an avascular and relatively abdominis as part of the anterior and bloodless plane through which midline posterior rectus sheath laparotomy incisions are made. It is easier • Transversus abdominis is the third large to begin a laparotomy incision above the sheet of muscle lying deep to the internal umbilicus, where the linea alba is wider, oblique and running transversely. Medially, thicker and better defined than below the it forms a fibrous aponeurosis which umbilicus contributes to the posterior rectus sheath • Pyramidalis is a small (4 cm long) lying behind rectus abdominis unimportant muscle arising from the pubic • Rectus abdominis and its pair join at the crest and inserting into the linea alba. It linea alba in the midline to form a wide lies behind the anterior rectus sheath in strap that runs longitudinally down the front of rectus abdominis. This is the only anterior abdominal wall. It lies within the muscle you go through in your lower rectus sheath formed by the aponeuroses midline laparotomy incision and it is not of the three muscles described above. It is as bloodless as the linea alba which it attached to the anterior rectus sheath, but underlies not to the posterior rectus sheath, by three tendinous insertions. These insertions are at the level of the xiphisternum, umbilicus Rectus sheath and halfway between (giving the ‘six-pack’ appearance in well-developed individuals!). Learning point The blood supply of rectus abdominis is through the superior epigastric artery (a terminal branch of the internal thoracic Any incision over rectus abdominis will artery) and the inferior epigastric artery (a go through the anterior rectus sheath. branch of the external iliac artery) which Arrangement of the rectus sheath is best anastomose to form a connection between considered in three sections: the subclavian and external iliac systems • Above the level of the costal margin (Fig. 1.1). The superior epigastric artery is • From the costal margin to just below the pedicle on which a TRAM flap is raised the umbilicus for breast reconstruction. The nerve supply • Below the line of Douglas to the recti is segmental from T6 to T12 and

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• Above the level of the costal margin: the • Below the line of Douglas: about 2.5 cm anterior rectus sheath is formed by the below the umbilicus lies a line called the external oblique aponeurosis only. There is ‘arcuate line of Douglas’ (Fig. 1.1). At no internal oblique or transversus abdominis this level, the posterior rectus sheath (ie aponeurosis at this level. Therefore there the posterior leaf of the internal oblique is no posterior rectus sheath and rectus aponeurosis along with the transversus

abdominis lies directly on the fifth to abdominis aponeuroses) passes anterior CHAPTER 1 seventh costal cartilages to rectus abdominis. Therefore, below the • From the costal margin to just below the arcuate line of Douglas there is no posterior umbilicus: the anterior rectus sheath is formed rectus sheath. Rectus abdominis lies directly by the external oblique aponeurosis and on transversalis fascia, which is thickened the anterior leaf of the split internal oblique here, and called the ‘iliopubic tract’. The aponeurosis. It is attached to rectus abdominis anterior rectus sheath is now formed by all by tendinous intersections. The posterior the combined aponeuroses of the external rectus sheath is formed by the posterior leaf oblique, internal oblique and transversus of the internal oblique aponeurosis and the abdominis muscles transversus abdominis aponeurosis

Figure 1.1 Sagittal section of the abdominal wall

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Figure 1.2 Surface CHAPTER 1 CHAPTER landmarks of the anterior abdominal wall

(A) Transpyloric line: halfway between jugular (5) Tubercle of iliac crest: 5 cm behind ASIS at L5. notch and pubic symphysis at L1; this plane (6) Inguinal ligament: running from ASIS to pubic passes through pylorus, pancreatic neck, tubercle. duodenojejunal flexure, fundus of gallbladder, (7) Pubic tubercle: tubercle on superior surface of tip of ninth costal cartilage, hila of kidneys; also pubis; inguinal ligament attaches to it, as lateral it is the level of termination of the spinal cord. end of the superficial inguinal ring. (B) Subcostal line: under lowest rib (rib 10 at L3). (8) Superficial inguinal ring: inguinal hernia comes (C) Intertubercular/transtubercular line: between out above and medial to pubic tubercle at point two tubercles of iliac crest (L5); note that plane marked (I); femoral hernia below and lateral to of iliac crests (supracristal plane) is higher (at pubic tubercle at point marked (F). L4). (9) Symphysis pubis: midline cartilaginous joint (D) Midclavicular line: through midinguinal point, between pubic bones. halfway between ASIS and symphysis pubis. (10) Pubic crest: ridge on superior surface of pubic (1) Xiphoid process: xiphisternal junction is at T9. bone medial to pubic tubercle. (2) Costal margins: ribs 7–10 in front; ribs 11 and (11) Linea alba: symphysis pubis to xiphoid process 12 behind; tenth costal cartilage is lowest at L3. midline. (3) Iliac crest: anterior superior iliac spine (ASIS) (12) Linea semilunaris: lateral edge of rectus crosses to posterior superior iliac spine (PSIS); highest costal margin at ninth costal cartilage (tip of point L4. gall bladder palpable here). (4) ASIS.

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Contents of the rectus sheath • Segmental vessels from T7 to T12 • Rectus abdominis • Superior and inferior epigastric vessels (see • Pyramidalis Figure 1.1) • Segmental nerves CHAPTER 1 Layers of the abdominal wall divided in three common incisions

Midline laparotomy Kocher’s incision Gridiron appendicectomy incision Skin Skin Skin Subcutaneous fat Subcutaneous fat Subcutaneous fat Scarpa’s fascia Scarpa’s fascia Scarpa’s fascia Linea alba Medially: Anterior rectus sheath Rectus abdominis Posterior rectus sheath Laterally: External oblique External oblique Internal oblique Internal oblique Transversus abdominis Transversus abdominis Fascia transversalis Fascia transversalis Fascia transversalis Preperitoneal fat Preperitoneal fat Preperitoneal fat Parietal peritoneum Parietal peritoneum Parietal peritoneum

Diseases of the umbilicus Endometriosis Congenital Hernias • Cord hernias • Childhood (umbilical) • Gastroschisis • Adult (paraumbilical) • Exomphalos Fistula Tumours • Urinary tract (via urachal remnant) • Primary • Gastrointestinal tract (via vitelloin- • Benign (papilloma, lipoma) testinal duct) • Malignant (squamous cell carcinoma Suppurations [SCC], melanoma) • Primary • Secondary • Obesity • Breast • Pilonidal • Ovarian • Fungal infections • Colon (via lymphatic, transcoloemic and • Secondary direct spread along falciform ligament) • From intra-abdominal abscess

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Benign br 2.1 T 1.4 1.3 1.2 1.1 2.4 2.3 2.2

Benign breastlumps 2.1.1 Diagnosis ofbreastdisease History andexaminationofthe Ph Anatom 2.1.2 breast 2.1.3 2.1.4 2.1.5 2.1.6 Breast infectionandabscess Breast pain diseaseanddisc ysiology ofthebreast

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Jenny McIlhenny Ritchie and Chalmers

355 335 355 348 346 345 339 339 356 357 357 358 364 364 359 359 3 5 4

3.6 3.5 3.4 3.3 3.2 3.1 Br abnormalities Congenital andde 4.2 4.1 Male br 3 3.9 3.8 3.7 Breast Surgery .10 UKBreastScreeningProgramme east cancer

in breastcancer 3.6.1 T Prognostic featuresandstaging Diagnosis ofbreastcancer Risk factorsforbreastcancer P Breast cancerepidemiology 3.6.2 Gynaecomastia Male breastcancer 3.6.3 Ad Oncoplastic breastsurgery patients F ollow-up forbreastcancer athology andclassification reatment ofbreastcancer vanced breastcancer PTER C east disease

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CHAPTER 2 ERN 2012.indb 339 natomy breast axilla ofand the 1.1

A CTION S The breastThe e axilla. extends intothe deep fasciaand which pierces the (C) The axillary tail, (B) Sagittalsection. internal structure. removed toshow with skinpartially Anterior view of thebreast. (A) 2.1 Anatomy Figure 1 339 8/17/2016 2:30:27 PM

CHAPTER 2 Breast Surgery

Embryology of the breast and this ridge develops from ectoderm • The breast is a modified apocrine sweat at 5 weeks’ gestation, extending from gland the axilla to the groin (milk line). In • Ectoderm gives rise to the epithelial lining of humans it regresses to leave a nipple with the ducts and acini specialised epithelial cords which forms CHAPTER 2 CHAPTER • Mesenchyme gives rise to the supporting 15–20 lactiferous ducts tissue called the stroma • At puberty the lactiferous ducts proliferate • There is downward growth of ectoderm and the breast bud is formed (around age into underlying mesenchyme at 4 weeks’ 10) gestation • Nipple development occurs at around 12 • The breast develops from the mammary years ridge (first seen at 5 weeks’ gestation)

Anatomy of the breast

Learning point

• Extent: the breast extends from the second to the sixth rib, and from the midline to the midaxillary line. The axillary tail of Spence is a projection of the upper outer quadrant of the breast into the axilla. • Position: the breast lies anterior to the muscles of the chest wall: medial two-thirds on pectoralis major and lateral third on serratus anterior; the inferior aspect of the breast base also rests on the upper aspects of the external oblique abdominis and rectus sheath. It is separated from these muscles by the deep fascia. • Structure: the breast is composed of 15–20 lobules which open, via ducts, on to the nipple. Lobules drain into lactiferous ducts, which drain into lactiferous sinuses, the function of which is to store milk during lactation. The ducts of each lobule are lined with columnar or cuboidal epithelium, and the short excretory ducts (just beneath the nipple/areolar complex) are lined with squamous epithelium. • Suspensory ligaments: anterior projections of the deep fascia form the suspensory ligaments of Astley Cooper which divide the breast into lobules and connect the deep fascia to the skin • Arterial supply: lateral thoracic and thoracoacromial branches of the axillary artery, the internal thoracic (mammary) artery and the lateral perforating branches of the intercostal arteries • Venous drainage: via the internal thoracic, axillary and posterior intercostal veins • Nerve supply: intercostal nerves. Nipple sensation is from the fourth intercostal nerve • Lymphatic drainage: >75% to axillary nodes, <25% to internal mammary nodes • The nipple is anatomically in line with the fourth rib interspace (at the ) but its position varies with increasing age as a result of glandular descent or ptosis.

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Arterial supply of the breast There is considerable crossover of arterial supply and venous and lymphatic drainage across the breast.

Lateral breast Subclavian artery  Axillary artery  Lateral thoracic artery  Thoracoacromial artery (Also the superior thoracic and subscapular branches of the axillary artery to a lesser extent.) Lateral perforating branches of the intercostal arteries CHAPTER 2 Medial breast Subclavian artery  Internal thoracic (mammary) artery  Perforating branches (first to fourth intercostal spaces)

Venous drainage of the breast Lateral breast  Thoracoacromial vein  Lateral thoracic vein  Axillary vein  Subclavian vein Medial breast  Internal thoracic vein  Subclavian vein

Posterior intercostal vein: the posterior intercostal veins also receive tributaries from the ribs and communicate with the vertebral venous plexus via a valveless system; hence metastatic cells from breast cancer can spread to the ribs and thoracic vertebrae with relative ease.

Nerve supply of the breast • There is free communication of lymphatic • Sensory supply via cutaneous branches of channels across the breast (lateral to medial intercostal nerves of T4–6 and vice versa) • Also a sympathetic supply • There is an anastomosis of the lymphatics across the midline to the contralateral breast, and down the abdominal wall; Lymphatic drainage of the breast therefore lymphatic spread of breast • Studies using radiolabelled tracers demonstrate cancer can be to the opposite axilla, to the that 75–97% of the lymphatic drainage of the peritoneal cavity and liver and, rarely, to the breast drains to the axillary nodes inguinal nodes • Up to 25% drains to the internal mammary • The sentinel lymph node or nodes are nodes through the second to fourth believed to be the first node(s) in the axilla intercostal spaces to receive drainage from the breast (see Sentinel node biopsy)

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Anatomy of the axilla The axilla is the space between the upper arm Learning point and the thorax. The surface markings are the anterior and posterior axillary folds, formed by Contents of the axilla pectoralis major and latissimus dorsi respec-

CHAPTER 2 CHAPTER • Brachial plexus tively. It is pyramidal in shape, with the base • Axillary artery of the pyramid (the floor of the axilla) the most • Axillary vein superficial, and the apex deep, towards the root • Axillary fat pad, which contains of the neck (Figure 2.2). The axillary vessels and 20–30 axillary lymph nodes nerves pass through a space at the apex formed • Intercostal brachial nerves (sensory by the posterior clavicle, superior border of the nerves to skin of axilla) scapula and lateral border of the first rib. • Long thoracic nerve of Bell (motor nerve to serratus anterior) • Thoracodorsal trunk (the artery, vein and motor nerve supplying latissimus dorsi)

anterior Boundaries of the axilla • Anteriorly: pectoralis major and minor; subclavius at apex APEX posterior • Medial: serratus anterior on the chest wall (and first four ribs) • Lateral: coracobrachialis; short biceps tendon. These lie medial to the bicipital BASE groove of the humerus (sometimes called the intertubercular groove, as it lies between the greater and lesser tubercles), where the anterior and posterior walls of the axilla converge • Posterior: subscapularis superiorly; teres major; latissimus dorsi • Superior: axillary vein • Apex: clavicle; first rib; superior border of scapula • Floor (or base): axillary fascia covers the axillary floor between serratus anterior, pectoralis major and latissimus dorsi, converging at a point to meet the deep fascia of the arm Figure 2.2 The shape of the axilla

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Surger 2.4 2.3 2.2 2.1 1.1 Surger 1.2 1.10 1.9 1.8 1.7 1.6 1.5 1.4 1.3

Mitr Mitr Aortic regurgitation Aortic stenosis Cardiactr interventions P b Complications ofcoronaryartery isc Cardiac surgeryproceduresfor Cardiopulmonary b T during cardiacsurgery Intr cardiac surgery Preoperative considerations and revascularisation Indications forcoronaryartery disease Pathology ofischaemic heart ercutaneous coronary he mediansternotomy incision ypass graft y oftheheartvalves haemic heartdisease aoperative considerations al stenosis al regurgitation

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CHAPTER 3 ERN 2012.indb 399 athology of ischaemic 1.1 infarction (MI)never gettohospital. UK, 30% of patients who have a myocardial rates of diabetes, obesity and smoking. In the sation of the developing world, with increased prevalence israpidly risingduetothewesterni- due tomedicaladvances; however, worldwide western world. Survival isslowly improving causes ofmorbidityandmortalityinthe Ischaemic heartdiseaseisoneofthemajor • • • • of: caused by atherosclerosis,withthesteps The majority ofischaemic heartdisease is Learning point Learning

leading tocalcificationofthe plaque Chronic inflammatoryresponse, intimal thickening fibroblast proliferation, resultingin Smooth musclemigration and macrophages) Lipid accumulation(insubendothelial Endothelial dysfunction P heart disease heart Surgery for ischaemic ischaemic for Surgery • • • key steps: an area of research, but involves the following The pathological basis of atherosclerosis is still can beusefulinrevascularisation oftheheart. are relatively sparedfromthediseaseandhence The internalthoracic (mammary)arteries(IMAs) and rightcoronaryarteriesaretheworst affected). proximal leftanteriordescending,circumflex not theintramyocardial coronaryvessels (the Atherosclerosis affectstheepicardialvessels but in thecontextofchronic atherosclerosis. angina. Mostmyocardial infarctions (MIs)occur flow limitationon exercise, leadingto exertional severe, erodethe‘coronaryreserve’ andcause coronary stenoseswhich, when sufficiently heart disease(CHD)have advancing occlusive The vast majorityofpatientswithcoronary endothelial cellsleadingto microthrombi Platelet adhesiontothesurface of intimal thickening andatheromaformation triglycerides andcholesterol. Leadingto form theplasma–proteinscarrying Low-density lipoprotein(LDL)accumulation mechanisms andhyperlipidaemia hypertension, nicotine,immune to several riskfactors,mostimportantly Endothelial cellinjuryanddysfunction due heart disease heart CTION S e 1 399 8/17/2016 2:30:30 PM

CHAPTER 3 Cardiothoracic Surgery

formation and release of platelet-derived 2. Acute plaque rupture, in which the growth factor, which attracts monocytes to endothelium becomes fissured, exposing the area the thrombogenic plaque contents (lipids, • Low density lipoprotein (LDL) accumulation collagen and necrotic debris), and a clot form the plasma – plasma proteins carrying forms on top of the plaque causing acute triglycerides and cholesterol. Leading to coronary obstruction, resulting in an ‘acute intimal thickening and atheroma formation coronary syndrome’ (unstable angina, MI or • Monocytes/macrophages engulf cholesterol, acute coronary death) becoming foam cells, and also secrete The table opposite summarises the pathological CHAPTER 3 CHAPTER free radicals, which causes oxidation of and clinical features together with treatment circulating LDL options for stable and unstable angina and MI. • Further oxidised LDL is taken up by macrophages via their scavenger receptors, leading to release of interleukin-1 (IL-1) and 1.2 indications for tumour necrosis factor (TNF), stimulating coronary artery smooth muscle cell and fibroblast revascularisation proliferation • Fibroblasts lay down collagen and elastin which helps to form the mature athero- Learning point sclerotic plaque • Smooth muscle cells migrate from the When medical therapies are insufficient media to the intima and transform into to adequately control angina symptoms, secretory cells producing collagen, elastin revascularisation may be attempted. This and chemokines, which serve as important field is subject to rapid evolution as both mediators of the process percutaneous and surgical techniques • This chronic inflammatory response leads to improve. calcification of the plaque As coronary vascular disease is primarily managed by cardiologists and Initially, atherosclerotic plaques tend to percutaneous coronary intervention bulge outwards and so the vascular lumen is (PCI) has a lower risk of mortality and maintained. morbidity, surgery is largely offered • Luminal loss of <50% can usually be when PCI options are exhausted. Hence tolerated without causing symptoms the population undergoing coronary • Obstruction of 75% is associated with artery bypass grafting (CABG) is an older exertional angina population, with more severe disease. • 90% stenosis causes angina at rest

In the progression of atherosclerotic plaques, there are two potential outcomes: 1. Gradual progression of the plaque causing increasing luminal stenosis and decreasing exercise tolerance

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ISCHAEMIC HEART DISEASE: PATHOLOGY, CLINICAL FEATURES AND TREATMENT OF STABLE AND UNSTABLE ANGINA AND MYOCARDIAL INFARCTION

Coronary Stable angina Unstable angina Myocardial infarction syndrome (crescendo angina, subendocardial infarction) Pathology Coronary ’Fixed stenosis’ Acute plaque rupture or Acute plaque rupture or Stable plaque thrombosis thrombosis Myocardial Reversible ischaemia Reversible ischaemia Full-thickness infarction or minor infarction in watershed areas, eg subendocardium Clinical features Symptoms Chest pain and shortness Chest pain and shortness Sudden death, 30 of breath on exertion of breath on mild exertion minutes CHAPTER 3 Predictable exercise tolerance Decreasing exercise of severe central chest Symptoms relieved by nitrates tolerance pain and shortness of and rest Symptoms may or may not breath (except silent be relieved by rest or nitrates ischaemia, eg in diabetic patients) ECG changes ST depression in affected ST depression in affected ST elevation in affected territory territory. May have deep territory, leading to T-wave inversion Q waves Enzyme rises Nil Rise of troponin I carries Troponin I prognostic significance CK, LDH Arrhythmias Unlikely VF or VT likely VF or VT likely Management Acute GTN spray MONA (morphine, oxygen, MONA + clopidogrel Rest nitrates, aspirin) Medical Aspirin Anticoagulation PCI first line Anti-angina agents: Enoxaparin Thrombolysis if PCI β Blockers Heparin infusion not available within 90 Calcium channel blockers Abciximab minutes (streptokinase, Long-acting nitrates GP IIb IIIa inhibitors rTPA) Nicorandil Nitrates Risk factor modification: Nitrocine™ infusion Statin GTN infusion Stop smoking Statin Control hypertension Lose weight Modify diet PCI If symptoms difficult to If anticoagulation and First-line therapy control medically nitrates unsuccessful CABG If anatomy unsuitable for PCI If procedure unsafe for PCI Rarely

CABG, coronary artery bypass graft; GP, glycoprotein; GTN, glyceryl trinitrate; PCI, percutaneous coronary intervention; rTPA, recombinant tissue plasminogen activator; VF, ventricular fibrillation; VT, ventricular tachycardia.

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Pros and cons of PCI and CABG

PCI CABG Advantages Minimally invasive Reliable revascularisation Low morbidity Suitable for wide range of coronary lesions Acceptable to patients Ability to perform simultaneous procedures, Low immediate complication rates eg valve replacement Disadvantages Unsuitable for some coronary lesions (eg Major procedure

CHAPTER 3 CHAPTER left main stem – LM) Morbidity from sternotomy and conduit Early re-occlusion of angioplasty sites harvesting sites and in-stent thrombosis Late graft failure (especially saphenous vein) High rate of recurrence of symptoms Poorer ‘freedom from medication’ Requires cardiac surgical back-up in case of complications Burgeoning Drug-eluting stents Minimally invasive techniques technologies Wider range of suitable targets (LM) ’Off-pump’ techniques Total arterial revascularisation

1.3 Preoperative considerations and cardiac surgery

History taking before Learning point cardiac surgery Cardiac surgical procedures are major operations Usually performed in a pre-assessment performed on patients who have high levels of clinic, preoperative work-up before comorbidity. Preoperative investigations allow cardiac surgery for ischaemic heart physiological optimisation to reduce periop- disease includes: erative morbidity and mortality, either through • History alteration of medication or exclusion of other • Examination pathology. Therefore it is wise to see the patient • Investigations in a pre-assessment clinic about 1 week before • Adjustment of medications surgery. • Discussion of morbidity and mortality • Discussion of treatment options

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