Essentials of Surgical Pathology Vol 1 PDF

Mircea Pop  Viorel Dejeu  Dănuţ Dejeu  Cezar Badale Essentials of Surgical Pathology Vol. 1 Mircea Pop  Viorel Dejeu Dănuţ Dejeu  Cezar Badale Essentials of Surgical Pathology Vol. 1 Editura Universității din Oradea, 2010 Descrierea CIP a Bibliotecii Naţionale a României POP, MIRCEA E...

Mircea Pop  Viorel Dejeu  Dănuţ Dejeu  Cezar Badale Essentials of Surgical Pathology Vol. 1 Mircea Pop  Viorel Dejeu Dănuţ Dejeu  Cezar Badale Essentials of Surgical Pathology Vol. 1 Editura Universității din Oradea, 2010 Descrierea CIP a Bibliotecii Naţionale a României POP, MIRCEA Essentials of surgical pathology / Pop Mircea, Viorel Dejeu, Dănuţ Dejeu. - Oradea : Editura Universităţii din Oradea, 2010 Bibliogr. ISBN 978-606-10-0053-1 I. Dejeu, Viorel II. Dejeu, Dănuţ 616-089(075.8) Editura Universităţii din Oradea este recunoscută de CNCSIS, cod 149 Coperta: Alina Farcas Dedic aceasta carte tatalui meu, dr. Pop Mircea senior, fost director al spitalului municipal Marghita. Dragi studenţi, Această carte este scrisă in mod special pentru voi! Clinica Chirurgie II Zoltan Krisar, se doreşte a fi un creuzet al formarii voastre din punct de vedere medical şi in mod special, chirurgical! Dorim să păstrăm ştacheta ridicată, acolo unde a aşezat-o chiar intemeietorul şcolii chirurgicale orădene, doctorul Zoltan Krişar! Moştenirea lasată de acest om şi chirurg deosebit, ne obligă şi ne motiveaza să lucrăm împreună, ca şi echipă, pentru a vă oferi cele mai bune unelte practice şi teoretice in vederea edificării voastre in nobila profesie de medic. O educaţie completă inseamna o înrădăcinare in istoria medicinei, prin cunoaşterea temeliilor ei şi o privire atentă, mereu aţintită spre noile progrese şi descoperiri. O preocupare exacerbată pentru nou, in lipsa cunoaşterii temeliilor aşezate de antemergători duce la o perspectivă limitată, insuficientă, chiar la snobism medical. Deasemenea, lipsa unui spirit vizionar si cantonarea doar in trecut va duce finalmente la blazare si superficialitate. Din acest motiv, am incercat să realizăm o carte ce combină principiile de bază, ce rămân mereu valabile, cu cele mai noi abordari şi tehnici pe care medicina modernă le dezvoltă in pas tot mai grăbit. Această carte este o modestă contribuţie la dezvoltarea secţiei in limba engleza, a Facultăţii de Medicină şi Farmacie din Oradea. Sprijinim in continuare eforturile tinerei noastre facultăti, cu convingerea ca îşi va dobândi o binemeritată poziţie intre Universităţile de Medicină cu tradiţie, din ţară. Sperăm să vă fie de folos şi mai mult de atât, să fie o carte care să vă motiveze mereu la mai mult si să vă deschidă noi orizonturi! Mircea Pop ,,And if any man think that he knows anything, he knows nothing yet as he ought to know.” (1 Corinthians 8:2) 7 Content Chapter 1 The surgical pathology of the esophagus and diaphragm …….. 13 I. Anatomy ………………………………………………………………………………………………….. 13 II. Esophageal syndrome. Signs, symptoms and investigations ………………………. 14 III. Esophageal disorders ……………………………………………………………………………….. 17 1. Esophagitis ……………………………………………………….…………………………….. 17 A. Reflux esophagitis. GERD ………………………………………………….. 17 B. Non reflux esophagitis ……………………………………………………….. 20 2. Esophageal diverticulae ………………………………………………………………….. 20 A. Congenital ………………………………………………………………………….. 20 B. Acquired …………………………………………………………………………….. 20 3. Motility disorders ……………………………………….………………………………….. 21 Achalasia ……………………………………………………….…..………………….. 21 Diffuse oesophageal spasm …………………………………………………….. 21 Nutcracker oesophagus ………………………………………………………….. 21 Hypertensive LOS …………………………………………….…………………….. 21 Non‐specific motility disorders ………………..…………………………….. 21 4. Tumors ………………………………………….……………………………………………….. 21 A. Benign ……………………………………………………………………………….. 21 B. Malignant ………………………………………………………………………….. 21 IV. Diaphragmatic hernia ……………………………………………………………………………….. 27 1. Congenital …………………………………………..………………………………………….. 27 2. Traumatic ………………………………………..…………………………………………….. 27 3. Hiatus hernia ………………………………………………………………………………….. 29 Chapter 2 Surgical pathology of the stomach and duodenum ………………….. 33 I. Anatomy ………………………………………………………………..…………………………………….. 33 II. Peptic ulcer disease …………………………………………………………………………………….. 35 1. Signs, symptoms and investigations ……………………………………………….. 35 2. Treatment ……………………………………………………………………………………….. 38 3. Complications ……………………………………..………………………………………….. 39 A. Perforation ……………………………………………………………………….. 39 B. Hemorrhage ……………………………………………………………………….. 41 C. Stenosis …………………………………………………………………………….. 41 III. Tumors ……………………………………………………………………….…………………………….. 1. Benign …………………………………………………………………………………………….. 2. Malignant ……………………………………………………………………………………….. IV. Postgastrectomy syndromes …………………………………………………..……………….. V. Morbid obesity and bariatric surgery ……………………………………………..………….. 44 44 44 54 55 Chapter 3 The surgical pathology of the liver ………………………………………………….. 59 I. Anatomy …………………………………………………………………………………………………….. 59 II. Hepatic abscess ……………………………………….……………………………………………….. 60 1. Pyogenic ……………………………………………………………………………………….. 60 A. Microscopic …………………………………………………………………….. 60 B. Macroscopic …………………………………………………………………….. 60 2. Amoebic ……………………………………………………………………………………….. 62 III. Hepatic cysts ………………………………………………………….……………………………….. 64 1. Nonparasitic cysts ……………………………………………………………………….. 64 2. Echinococcal cysts ……………………………………………………………………….. 65 IV. Hepatic tumors ……………………………………………………………………………………….. 68 1. How do we diagnose a liver tumor? ………………………………………….. 68 A. Benign tumors …………………………………………………..…………….. 70 B. Malignant tumors ……………………………………………..…………….. 75 a. Primary tumors ……………………..…………………………….. 75 b. Metastatic tumors ……………..……………………………….. 78 Chapter 4 Biliary tract surgical pathology ………………………………………………………….. 79 I. Anatomy …………………………………………………………………………………………………….. 79 II. Benign diseases of the biliary tract......................................................... 81 1. Congenital …………………………………………………………………………………….. 81 2. Acquired ……………………………………………………………………………………….. 81 A. Gallstones ………………………………………………………………….. 82 B. Chronic calculous cholecystitis………………………………….. 86 C. Acute calculous cholecystitis……………………………………….. 87 D. Choldecolithiasis.................... …………………………………….. 91 E. Acute acalculous cholecystitis........................................ 94 F. Cholesterolosis ………………………………………………………….. 94 G. Biliary Dyskinesia ……………………………………………………….. 94 H. Acute cholangitis ……………………………………………………….. 95 I. Primary sclerosing cholangitis........................................ 96 3. Tumors ………………………………………………………………………………………….. 96 Chapter 5 The surgical pathology of the pancreas ……………………………………….. I. Anatomy …………………………………………………………………….……………………………….. II. Acute pancreatitis ……………………………………………………………………………………….. III. Chronic pancreatitis ……………………………….………………………………………………….. IV. Pancreatic pseudocysts ………………………….………………………………………………….. V. Pancreas tumors …………………………….………………………………………………………….. 107 107 108 115 124 125 Chapter 6 Small intestine and appendix surgical pathology .......................... 133 I. Anatomy …………………………….……………………………………………………………………….. 133 II. Crohn’s disease ……………………………….………………………………………………………….. 134 III. Toxic megacolon …………………………….………………………………………………………….. 137 IV. Short‐gut syndrome ……………………….………………………………………………………….. 139 V. Small‐bowel tumors …………………………..……………………………………………………….. 142 1. Benign tumors ………………………………….…………………………………………….. 143 A. Leyomioma …………………………….………………………..……………….. 143 B. Adenomas …………………………….…………………………………………….. 143 C. Polyposis syndromes …………………………….…………………………….. 143 2. Intermediate neoplasms …………………………….………………………………….. 144 3. Malignant tumors …………………………….…………………………………………….. 144 A. Adenocacinoma …………………………….……………..…………………….. 144 B. GISTs …………………………….…………………………………………………….. 147 VI. Ileocecal tuberculosis …………………………….………………………………………………….. 148 VII. Appendix …………………………….……………………………..…………………………………….. 150 1. Acute appendicitis …………………………….…………..……………………………….. 150 2. Neoplasm of the appendix …………………………….……………………………….. 152 Chapter 7 The surgical pathology of the spleen …………………………….……………….. 153 I. Anatomy …………………………….……………………………………….……………………………….. 153 II. Splenic function and physiology ………………………………..……………………………….. 155 III. Indications for splenectomy ………………………...…………..……………………………….. 155 IV. Spleen pathology ………………………………………….…………..……………………………….. 156 1. Splenic cysts ……………………………..…….…………..……………………………….. 156 2. Splenic abscess …………………………….………………..……………………………….. 157 3. Splenic infarction ……………………………...…………..……………………………….. 157 4. Splenic tumors ………………………………….…………..……………………………….. 158 5. Hypersplenism …………………………….…….…………..……………………………….. 158 6. Splenectomy ………………………….………….…………..……………………………….. 158 7. Specific postoperative complications …………………………………………….. 159 Chapter 8 Upper Gastrointestinal Bleeding …………………………….……………………….. 160 I. Definition …………………………….………………………………..…………………………………….. 160 II. Ethiology ……………………………….……………………………..…………………………………….. 160 III. Diagnosis …………………………….………..……………………..…………………………………….. 162 IV. Rockall numerical risk scoring system …………………………….…………………..…….. 165 V. Acute UGI bleeding – initial assessment protocol …………………………….……….. 166 VI. Management of acute non‐variceal upper gastrointestinal bleeding …..….….. 167 VII. Variceal upper gastrointestinal bleeding …..…………………………………………….. 170 Chapter 9 Abdominal trauma …………………….………………………………………………………….. 179 I. Generalities …………………………….………………………….……………………………………….. 179 1. Blunt abdominal trauma …………………………….………………………………….. 179 2. Penetrating abdominal trauma …………………………….……………………….. 179 3. Diagnosis ……………………………..…………………………………………………….. 179 A. DPL …………………………………………………………………………………….. 180 B. Ultrasound …………………………….………………………………………….. 180 C. CT …………………………….………………..……………………………………….. 181 II. Pancreatic trauma …………………………….……………………………………………………….. 184 III. Liver trauma …………………………….…………………….………………………………………….. 187 IV. Splenic trauma …………………………….…………..……………………………………………….. 191 V. Small bowels trauma ………………………………………………………………………………….. 194 VI. Colonic injuries …………………………….………………………………………………………….. 195 VII. Rectum injuries …………………………….………………………………………………………….. 195 Chapter 10 Exercise your knowledges ….…….………………………………………………………….. 196 Bibliography ………………………………….………………………………………………………….. 206 Chapter 1 The surgical pathology of the esophagus I. Anatomy The oesophagus is a muscular tube that transports food from the pharynx to the stomach. It is divided into three parts. • Upper: extends from the cricopharyngeus to the level of the carina. • Middle: extends from the level of the carina to halfway. between the carina and the oesophagogastric junction. • Lower: the remaining segment that joins the stomach. Fig. 1 Esophagus‐ anatomical divisions Clinically, the term 'cardia' is used to describe the junction between the oesophagus and stomach. It contains the squamocolumnar junction, which 13 forms the serrated Z line that marks an abrupt change from the tough pale squamous epithelium of the oesophagus to the columnar epithelium of the stomach. II. The esophageal syndrom Symptoms Chest Pain: it can simulate angina pectoris. Dysphagia: difficulty with swallowing, which may be associated with ingestion of liquids, solids or both. Most causes of dysphagia are oesophageal in origin. Heartburn: an aching, burning sensation felt behind the lower part of the sternum, caused by reflux of acid from the stomach into the oesophagus. Regurgitation: when fluid from the stomach flows back into the mouth producing a sour taste. It is frequently postural and indicates gastric reflux. Water brash: sudden secretion of a quantity of saliva into the mouth as a reflex response to reflux. Odynophagia: painful swallowing and usually indicates oesophagitis. Causes of dysphagia Mural Carcinoma of the oesophagus: progressive, weight loss and anorexia, anaemia. Reflux oesophagitis: preceded by heartburn, anaemia, nocturnal regurgitation. Achalasia: liquids > solids, frequent regurgitation, recurrent chest infections due to aspiration, long history, younger patients or old age. Tracheo-oesophageal fistula: recurrent chest infections, childhood (congenital), late adulthood (post trauma, deep X-ray therapy, malignancy). Caustic stricture: history of corrosive ingestion, chronic Scleroderma: slow onset, skin and hair changes. Chagas' disease: Trypanosoma cruzi, South America, colonic dysmotility. Intramural Foreign body: acute distress, marked retrostemal discomfort, difficulty in swallowing saliva. Extramural Pulsion divertikulum: intermittent symptoms and unexpected regurgitation. External compression: mediastinal lymph nodes, left atrial hypertrophy, bronchial malignancy. Investigation of dysphagia Any new symptom of progressive dysphagia should be assumed to be a carcinoma until proven otherwise. 14 Obstructive dysphagia is first experienced when 20-30% of the oesophageal lumen is lost; most patients usually present when 50% of the oesophageal lumen is compromised. All patients • Full blood count: anaemia more common with tumours than reflux • Liver function tests: exclude hepatic disease Oesophagogastroduodenoscopy • Moderate risk • Differentiates between tumour, reflux, stricture and achalasia • Allows biopsy and possible treatment (e.g. placement of endoprosthesis) Fig 2. Esogastroduodenoscopy with polyp resection Fig. 3 Esogastroduodenoscopy Barium swallow • Low risk • Good for detecting: 15 - fistula, reflux, high tumour - diverticulum - dysmotility - extrinsic compression: chest X-ray (AP and L) Its main value lies in the demonstration of an associated hiatus hernia and in detecting stricture formation. Fig.4 Thoracic X‐ray Fig. 5 Barium swallow showing stenosis CT-scan Chest and mediastinum It reliably assesses the extent of mural invasion and the size of the lesion. It is also used for the detection of distant metastases including pulmonary metastases but not small peritoneal deposits. Fig. 6 CT scan used for the detection of distant metastases including pulmonary metastases 16 Fig. 7 Fig. 6 CT scan used for the detection of distant metastases including pulmonary metastases III. Oesophageal disorders • • • • Esophagitis Oesophageal diverticulae Motility disorders Tumors 1. Esophagitis A. Reflux B. Non-reflux A. Gastroesophageal reflux disease DEFINITION Chronic symptoms or mucosal damage produced by the abnormal reflux of gastric contents into the esophagus. • Patients who have endoscopically documented mucosal damage are said to have reflux esophagitis. • Patients who have typical symptoms of GERD due to reflux of acid into the esophagus but do not have any mucosal damage are said to have nonerosive reflux disease (NERD). Pathophysiology The disease develops as a result of failure of the normal antireflux mechanisms, with chemical injury to the squamous lining of the oesophagus. 17 • • • The antireflux mechanisms include: competence of the lower oesophageal sphincter (LOS) 'complex'; oesophageal clearance of refluxed material; mucosal resistance to the damaging effects of the refluxate. Etiology • Primary weakness of the smooth muscle of the LOS. • Short length of the intra-abdominal segment of oesophagus. • Defective hormonal and neural control of the sphincter: most commonly dietary induced and transient. • Presence of a hiatus hernia. This results in a change of the pressure environment, shortening of the LOS and changes in the anatomy and reflexes of the gastric cardia. Approximately 50% of patients with reflux symptoms and 90% of patients with reflux esophagitis have a hiatus hernia. • Delayed gastric emptying: present in up to 40% of patients with GORD. CLINICAL FEATURES Typical symptoms of GORD: Heartburn Regurgitation Dysphagia. Symptoms are aggravated by posture and can be especially severe at night and after large meals and activities that increase intra-abdominal pressure,e.g. bending, stooping. Treatment In the first instance conservative: • designed to reduce chemical damage and improve oesophageal clearance. • avoidance of large meals, especially within 3 h of retiring to bed. • postural advice includes sleeping propped up by raising the head of the bed. • medical treatment is good at controlling heartburn but less effective at reducing regurgitation: » H2 receptor antagonists » Proton pump inhibitors (e.g. omeprazole, lansoprazole) Surgical treatment Approximately 10-15% of patients will be referred for antireflux surgery. The indications for surgical treatment are as follows: • Failure of medical therapy: includes failure to control symptoms despite high-dose of proton pump inhibitor therapy for 6 months. • Development of complications in young or fit patients and patients with high-grade oesophagitis from the outset; 18 • • • • Persistence of reflux in children beyond 2 years; Reflux after previous upper abdominal surgery; Atypical symptoms: respiratory, pharyngeal and dental problems; Patient preference, especially in young patients. The most commonly performed operations are: • loose (floppy) total fundoplication; • partial anterior fundoplication; • partial posterior fundoplication. -open or laparoscopic surgery Complications • Benign stricture of the oesophagus • Barrett's oesophagus (risk of adenocarcinoma) • Bleeding 19 Fig. 8 Esophageal mucosal displazia B. Non-reflux oesophagitis Corrosive Infective: Candida, Herpes virus Drug induced: tetracycline, non-steroidal antiinflammatory drugs, doxycycline, etc. Radiation: doses greater than 20-40 Gy to the mediastinum if combined with Adriamycin or actinomycin D; Specific disorders: Bullous dermatoses, Behcet's syndrome, Crohn's disease, aphthous oesophagitis. 2. Esophageal diverticulae A. Congenital B. Acquired: pulsion and traction • Pharyngo-oesophageal (Zenker's)diverticulum (secondary to cricopharyngeal dysfunction and less commonly to an oesophageal motility disorder). • Mid-thoracic diverticulae • Epiphrenic diverticulae 20 Simptoms • regurgitation • constant throat irritation, • gurgling noises during swallowing • chronic cough • recurrent chest infections due to aspiration Complications Perforation: (the most common complications) - cervical oesophagus: cervical phlegmon - thoracic oesophagus: mediastinitis - abdominal oesophagus: peritonitis Also: pain, tachycardia, fever, nasal voice, hematemesis, subcutaneous emphysema. Treatment Conservative - antibiotic - nasogastric tube - enteral/parenteral nutrition Operative - diverticulectomy 3. Motility disorders Achalasia Diffuse oesophageal spasm Nutcracker oesophagus Hypertensive LOS Non-specific motility disorders Achalasia is the most common primary oesophageal motility disorder and is caused by inflammation of the myenteric plexus, leading to fibrosis with decrease or loss of myenteric ganglion cells and selective destruction of noncholinergic, non-adrenergic inhibitory neurones. 4. Tumours of the esophagus A. Benign: Leiomyoma (whith a predilection for the lower oesophagus). B. Malignant: mostly carcinomas (squamous cell carcinoma and adenocarcinoma). 21 Fig. 9 Barium Swallow showing a smooth filling defect in mid‐esophagus Fig.10 Intraluminal aspect of esophageal tumor 22 Fig. 12 Lower esophageal stricture Fig. 11 Esophageal stenosis Epidemiology • Male/female ratio 5 : 1 • Age 50-70 years • High incidence in areas of China, Iran, Russia, Scandinavia and among the Bantu in South Africa. Aetiology • Alcohol consumption and cigarette smoking; • Chronic oesophagitis and Barrett's oesophagus; • Stricture from corrosive (lye) oesophagitis or human papilloma virus infection; • Achalasia; • Plummer-Vinson syndrome (oesophageal web, mucosal lesions of mouth and pharynx, iron-deficiency anaemia); • Nitrosamines. Pathology Macroscopically, the disease assumes one of three forms: • stenosing; • polypoid (fungating, protruded); • ulcerative (excavated). 23 • • Histological type: 90% squamous carcinoma (upper two thirds of oesophagus); 10% adenocarcinoma (lower third of oesophagus) Spread: lymphatics, direct extension, vascular invasion. Diagnosis Dysphagia may not be experienced until two-thirds of the oesophageal lumen is obliterated. Clinically • malnutrition • weight loss • regurgitation • occasionally aspiration • palpable cervical lymph nodes and hepatic or cutaneous metastases at presentation. Key investigations - Barium swallow - Endoscopy with biopsy and cytology. - CT and endoscopic ultrasonography (used to assess depth of invasion of the oesophageal wall and infiltration of adjacent structures by the tumour.) Staging TNM- most common Primar tumour (T) TX Primary tumour cannot be assessed TO No evidence of primary tumour Tis Carcinoma in situ T1 a Tumour invades lamina propria T1 b Tumour invades submucosa T2 Tumour invades muscularis propria T3 Tumour invades adventitia T4 Tumour invades adjacent structures Regional lymph nodes (N) NX Regional lymph nodes cannot be assessed NO No regional lymph node metastasis N1 Regional lymph node metastasis Distant metastasis (M) MX Presence of distant metastasis cannot be assessed MO No distant metastasis Ml Distant metastasis 24 Treatment • depends on the stage of the disease and the condition of the patient. • the aim of surgery is an R0 resection (complete macroscopic and microscopic removal of tumour) • treatment of patients who are unfit or have locally advanced disease is by chemoradiation. Non-operative treatment Radiotherapy • May be curative (radical) or palliative to relieve dysphagia and metastatic bone pain. • It can also be given as an adjunct to surgical treatment, either in the form of multimodality treatment or after oesophagectomy to improve locoregional control. Chemotherapy Several agents are used in combination treatment regimens for oesophageal cancer. These include 5-fluorouracil (5-FU), cisplatin, vindesine, mitomycin C, paclitaxel and etoposide. Multimodal treatment Radiotherapy plus Chemotherapy Palliation of advanced oesophageal cancer for the relief of dysphagia: Recanalization: photocoagulation endoscopic-guided fulguration followed by dilatation. Intubation: plastic tubes and selfexpanding metallic stents. Curative treatment Surgical resection is curative only if lymph nodes are not involved. Reconstruction is by gastric 'pull-up' or colon interposition. Fig. 13 Esophagectomy 25 Fig. 14 Gastric pull‐up Fig. 15 Gastric pull‐up tehnic 26 Fig. 16 Colon interposition Prognosis • Following resection, 5-year survival rate is about 15%; • Overall 5-year survival (palliation and resection) is only about 4%. IV. Diaphragmatic hernias 1. Congenital diaphragmatic hernia Posterolateral hernia (through foramen of Bochdalek: • due to persistence of the pleuroperitoneal canals. Parasternal hernia (through foramen of Morgagni or Magendie). 2. Traumatic diaphragmatic hernia Penetrating or blunt trauma to the abdomen and chest. 27 Fig. 17 Congenital diaphragmatic hernia Fig. 18 Diaphragm anatomy 28 Fig. 19 Traumatic rupture of diaphragm Signs and simptoms • intestinal obstruction, strangulation; • haemorrhage; • progressive cardiorespiratory insufficiency. 3. Hiatus hernia • type 1, axial or sliding: the gastro-oesophageal junction and a variable portion of the adjacent stomach slide upwards into the mediastinum carrying with them a peritoneal sac. • type 2, para-oesophageal: the fundus of the stomach rotates in front of the oesophagus and herniates through the hiatus into the mediastinum In large hernias the entire stomach and pylorus may be found within the chest inside a large hernial sac, which may also contain the spleen and transverse the colon. • type 3, mixed para-oesophageal and sliding. 29 Fig20. Hiatus hernia Fig.21 Axial hiatus hernia 30 Fig. 22 Hiatal hernia with intratoracic transversus colon Fig. 23 Hiatus hernia with intrathoracic gastric Surgical treatment • excision of sac; • reduction of hernia; • antireflux repair (fundoplication). 31 Fig. 24 Total fundoplicatio Nissen Fig. 25 Partial fundoplicatio Toupet (posterior) 32 Chapter 2 Surgical pathology of the stomach and duodenum I. Anatomy • • In adult life, stomach located T10 and L3 vertebral segment Can be divided into anatomic regions based on external landmarks: – 4 regions: • Cardia • Fundus • Corpus (body) • Antrum Fig.1 Stomach‐ anatomical divisions ` 33 Vasculature Fig. 2 Anatomical relations Lymphatic drainage • Proximal portion of the stomach drains along the lesser curvature first drains into superior gastric lymph nodes surrounding the Left Gastric Artery; • Distal portion of lesser curvature drains through the suprapyloric nodes; • Proximal portion of the greater curvature is supplied by the lymphatic vessels that traverse the pancreaticosplenic nodes; • Antral portion of the greater curvature drains into the subpyloric and omental nodal groups. Fig. 3 Lymphatic drainage 34 Nerve Supply – Left and Right Vagus Nerves descend parallel to the esophagus within the thorax before forming a peri-esophageal plexus between the tracheal bifurcation and the diaphragm; – From this plexus, two vagal trunks are formed before passing through the esophageal hiatus of the diaphragm. Fig. 4 Nerve supply‐ Anterior plexus Fig. 5 Nerve supply‐ Posterior plexus II. Peptic ulcer disease Peptic Ulcer Disease (PUD) represents a spectrum of disease characterized by ulceration of the stomach or proximal duodenum due to an imbalance between acid secretion and mucosal defense mechanisms. Pathogenesis Four etiologic factors are responsible for the vast majority of PUD. 1. Helicobacter pylori (H. pylori); 2. Nonsteroidal anti-inflammatory drug (NSAID); 3. Cigarette smoking; 4. Acid hypersecretion occurs in the majority of patients with duodenal ulcers. 1. Signs and symptoms Gastroduodenal disease produces varied symptoms described by the term ‘Dyspepsia'. 35 Definition: episodic or persistent abdominal symptoms, often related to the intake of food, due to disorders of the proximal portion of the digestive tract'. The symptoms included in this generic definition of dyspepsia are: • pain or discomfort in the upper abdomen; • nausea and vomiting; • early satiety; • epigastric fullness and regurgitation. There are two categories of dyspepsia: 1. Organic 2. Nonorganic (no demonstrable focal lesion) Based on the predominant symptoms: • ulcer-like; • reflux-like; • dysmotility-like; • non-specific. Investigations Endoscopy is necessary for certain groups: - age over 45 years; - patients who are H. pylori positive; - patients with a history of using non-steroidal antiinflammatory drugs (NSAIDs); - patients with alarm/sinister symptoms (loss of appetite, weight loss, bleeding). Barium contrast radiography Fig. 6 Peptic ulcer 36 Fig. 7 Peptic ulcer covered with fibrin Fig. 8 Peptic ulcer 37 Fig. 10 Typical aspect of duodenal ulcer Fig. 9 Typical aspect of gastric ulcer on barium swallow 2. Treatment Medical therapy Surgical therapy for uncomplicated peptic ulcer disease is exceedingly rare. Indications for elective operation for PUD: - failure of medical therapy; - inability to exclude malignancy; - complications. Surgical therapy options Gastric ulcers - wedge excision; - antrectomy with inclusion of the ulcer, depending on ulcer location; - truncal vagotomy is reserved for patients who are known to have refractory ulcer disease despite maximal medical management; this is rare today. Duodenal ulcers - three possibilities: (1) truncal vagotomy with pyloroplasty; (2) truncal vagotomy with antrectomy and Billroth I (gastroduodenostomy) or Billroth II (gastrojejunostomy) reconstruction; (3) highly selective vagotomy (HSV). 38 Fig. 11 Gastrectomy types 3. Complications A. Perforation - in both acute and chronic peptic ulcers; - NSAIDs are prone to cause peptic ulceration, with an increased risk of both perforation and bleeding; - acute perforations may also accompany stress, such as burns, multiple injuries, sepsis, etc.; - some perforated gastric ulcers are malignant. The moment of perforation - sudden excruciating epigastric pain; - tenderness with guarding; - initially localized to the upper abdomen but soon becomes generalized; - abdominal distension is a late feature and is due to paralytic ileus; - later, abdominal wall rigidity. Paraclinic diagnose - abdominal x-ray reveals free subdiaphragmatic gas in 80% to 85% of cases. 39 Fig. 12 Pneumoperitoneum Fig. 13 Pneumoperitoneum 40 Surgical therapy: Perforated gastric ulcers - simple wedge resection to eliminate the perforation and exclude malignancy. - if wedge resection of the ulcer cannot be performed due to its juxtapyloric location, multiple biopsies of the ulcer are taken and omental patching is performed. B. Hemorrhage Is the leading cause of death due to PUD, with associated 5% to 10% mortality Manifested as: Hematemesis may be fresh (in severe active bleeding or from ruptured oesophageal varices) or chemically altered (because acid digestion simulates 'coffee grounds'). Melena Indications for surgery - repeated episodes of bleeding; - continued hemodynamic instability; - ongoing transfusion requirement of more than 6 units of packed red blood cells over 24 hours; - more than one unsuccessful endoscopic intervention. Surgical treatment Bleeding gastric ulcers - unstable patients: biopsy followed by oversewing or wedge excision of the ulcer; - stable patients: may be candidates for antrectomy and vagotomy; Bleeding duodenal ulcers are usually located on the posterior duodenal wall within 2 cm of the pylorus and typically erode into the gastroduodenal artery. - unstable patients: duodenotomy and oversewing of the bleeding vessel; - stable patients: consideration should be made for a concomitant acid-reducing procedure for those who have failed or are noncompliant with medical therapy. C. Stenosis Can occur as a chronic process due to fibrosis and scarring. Localisations: -pylorus: resulting a pylorus stenosis and gastric outlet obstruction; -body of the stomach: creating two chambers like an hourglass. 41 Fig. 14 Hour glass stomach Fig. 15 Midbody stenosis Fig. 16 Hourglass stomach 42 Fig. 17 Gastric outlet obstruction Indications for surgical therapy persistent obstruction after 7 days of nonoperative management; recurrent obstruction. Surgical therapy - antrectomy to include the ulcer and truncal vagotomy; - pyloroplasty and vagotomy. - In exceptional instances, truncal vagotomy with gastrojejunostomy may be preferred in those patients whose pyloroduodenal inflammation precludes safe management with Billroth I or II reconstructions. Fig. 18 Distal gastrectomy 43 III. Tumors 1. Benign Gastric Tumors - less than 2%; - usually located in the antrum or corpus. Gastric polyps Hyperplastic polyps - 75% of gastric polyps; - risk of malignant transformation is minimal; - regenerative rather than neoplastic. Adenomatous polyps - neoplastic in origin; - polyps greater than 2 cm have a 24% incidence of malignancy; - surgical resection with a 2- to 3-cm margin of gastric wall. Fig. 19 Gastric polyp 2. Carcinoma of the stomach • The second most common fatal malignancy in the world (after lung cancer); • Commonest in Far East (Japan); • Incidence declining; • High mortality unless disease detected early. Aetiological factors Genetic • 10 per cent of patients have a family history of the disease, and there is slightly greater disease correlation between identical rather than fraternal twins. Environmental and dietary • polycyclic hydrocarbons; nitrosamines, etc. Helicobacter pylori, chronic atrophic gastritis, intestinal metaplasia and others. 44 Clinical presentation • symptoms are often vague, non-specific, and attributed to dietary indiscretion or indigestion; • Definite symptoms do not usually occur until the tumour is large enough to obstruct the lumen and cause disordered gastric function by invading a large segment of the wall, or bleeds; • The most common symptom is vague indigestion or upper abdominal/epigastric pain, followed by weight loss, nausea and vomiting, haematemesis and melaena, profound anorexia, early satiety, and flatulence; • true postprandial pain is relatively unusual in patients with gastric carcinoma; • If the tumour is at the cardia, over 60 per cent of patients will present with dysphagia. Investigations Laboratory Barium contrast CT Endoscopy Laparoscopy and laparotomy Fig. 20 Gastric mucosa dysplasia Early endoscopy is advised for patients over the age of 40 years with persistent dyspeptic symptoms. Macroscopic Pathology • Gross types – Polypoid – Ulcerative – Infiltrative (extreme is linitis plastica – “leather bottle stomach”) 45 Fig. 21 linitis plastica – “leather bottle stomach’’ Fig. 22 Gastric tumor • Vast majority are adenocarcinomas (95 %); • Arise on background of chronic gastritis, intestinal metaplasia, dysplasia; • Most cases advanced at presentation. Microscopy • Intestinal type (forms glands – like cancers of colon and oesophagus); • Diffuse type – dissociated tumour cells often containing a mucinous “blob” – signet ring cells; 46 Fig. 23 gastric exophytic tumor Fig. 24 Intestinal type Fig. 25 Diffuse type 47 Less common gastric neoplasms • Lymphoma • Gastrointestinal stromal tumour (GIST) Larger tumours with high mitotic rate tend to behave malignantly Stomach is commonest site. • Neuroendocrine (carcinoid) tumours. Carcinoids are tumours of resident neuroendocrine cells in gastric glands. Usually seen in context of chronic atrophic gastritis (driven by gastrin). Clinical behaviour variable. Fig. 26 Gastric lymphoma • Local infiltration (through wall of stomach to peritoneum, pancreas etc); • Lymphatic – local and regional lymph nodes; • Blood – liver, lungs; • Transcoelomic (across peritoneal cavity). Often involves ovaries (esp. signet ring cancer) – Krukenberg tumour. Staging T1 T2 T3 T4 Invades Submucosa Muscularis propia Serosa Adjacent organs 48 49 LN group 1 R cardiac 2 L cardiac 3 Lesser curvature 4 Greater curvature 5 Suprapyloric 6 Infrapyloric 7 L gastric artery 8 Common hepatic artery 9 10 11 12 13 14 15 16 50 Celiac artery Splenic hilar Splenic artery Hepatic pedicle Retropancreatic Mesenteric root Middle colic artery Paraaortic N0 No regional node metastasis; N1 Involved perigastric nodes within 3 cm of tumor; N2 Involved perigastric nodes >3 cm from tumor edge or involvement of left gastric, splenic, celiac, or hepatic nodes; N3 Involved middle colic artery and paraaortic nodes. Metastasis Distant metastasis The most common sites for distant metastatic spread are the liver (49 per cent), lung (33 per cent), ovary (14 per cent), bones (11 per cent), and cervical and supraclavicular (Virchow's) nodes (8 per cent). Patients with distant metastases have a very poor prognosis: 95 per cent of patients with liver involvement will die within 1 year irrespective of the treatment of the primary cancer. The surgical treatment Criteria for a curative resection: • no peritoneal, serosal, or hepatic involvement; • a gastric resection with a lymph-node dissection one level beyond that of pathological lymph-node involvement; • adequate resection margins is an 8- to 10-cm clearance proximally and distally in the unstretched stomach. (The Japanese Research Society for Gastric Cancer ) Lymphadenectomy D0 gastrectomy does not remove any lymph-node group; D1 gastrectomy removes those nodes in group I (N1), predominantly perigastric nodes, but leaves a large portion of the greater omentum; D2 gastrectomy has the same criteria for adequate gastric removal but includes lymphadenectomy to remove group-II (N2) nodes en bloc with the stomach. In general the entire greater omentum is removed, with the superior leaf of the transverse mesocolon, pancreatic capsule, and lesser omentum; D3 gastrectomy attempts to remove nodes in group III (N3), and involves pancreatic and splenic resection. The D2 gastrectomy is the usual form of treatment for operable gastric cancer. It is recommended as the principal form of treatment for both early gastric and advanced cancer. 51 fig. 27 The corelation between the tumor localization and the extend of the resection. 52 Distal Tumors 35% - Subtotal gastrectomy Midbody Tumors 15-30% - Total gastrectomy Proximal Tumors 35-50% - Roux-en-Y total gastrectomy Fig. 28 Fig. 29 Total gastrectomy with Roux en Y anastomosis 53 Fig. 30 Proximal subtotal gastrectomy Palliative surgery - Resections Bypass Fig 31 Palliative gastroenteroanastomosis Adjuvant and neoadjuvant therapy - Chemotherapy - Radiotherapy IV. Postgastrectomy Syndromes A. Dumping syndrome - result from the rapid emptying of a high-osmolar carbohydrate load into the small intestine; - gastric resection leads to the loss of reservoir capacity and the loss of pylorus function; - dumping syndrome is most common after Billroth II reconstruction. 54 Early dumping occurs within 30 minutes of eating and is characterized by nausea, epigastric distress, explosive diarrhea, and vasomotor symptoms (dizziness, palpitations, flushing, diaphoresis). Late dumping symptoms are primarily vasomotor and occur 1 to 4 hours after eating. The hormonal response to high simple carbohydrate loads results in hyperinsulinemia and reactive hypoglycemia. Symptoms are relieved by carbohydrate ingestion. Treatment - is primarily nonsurgical and results in improvement in nearly all patients over time. Meals should be smaller in volume but increased in frequency, liquids should be ingested 30 minutes after eating solids, and simple carbohydrates should be avoided. B. Loop syndromes - loop syndromes result from mechanical obstruction of either the afferent or efferent limbs of the Billroth II gastrojejunostomy. Afferent loop syndrome - severe abdominal pain and nonbilious emesis within the first few weeks after surgery - lack of bilious staining of nasogastric drainage in the immediate postoperative period suggests this complication (duodenal stump blowout). Efferent loop syndrome - intermittent obstruction of the efferent limb of the gastrojejunostomy; - abdominal pain and bilious emesis months to years after surgery. C. Alkaline reflux gastritis - most commonly associated with Billroth II gastrojejunostomy; - triad of constant (not postprandial) epigastric pain, nausea, and bilious emesis. D. Roux stasis syndrome E. Postvagotomy diarrhea F. Nutritional disturbances - in 30% of patients after gastric surgery; - iron, folate, vitamin B12, calcium, and vitamin D deficiencies. V. Bariatric surgery Morbid Obesity is a condition characterized by the pathologic accumulation of excess body fat. Body mass index [BMI = weight (kg)/height (m2)] equal to or greater than 40. Indications: Patients who have failed intensive efforts at weight control using medical means are candidates for bariatric surgery if they have 55 a body mass index greater than 40 or greater than 35 with weight-related comorbidities. Bariatric surgery procedures A. Restrictive procedures, which limit the amount of food that can be ingested. B. Malabsorptive procedures, which limit the absorption of nutrients and calories from ingested food by bypassing predetermined lengths of small intestine. - Adjustable gastric banding open or laparoscopic placement of a silicone band with an inflatable balloon around the proximal stomach at the angle of His. The band is connected to a reservoir that is implanted over the rectus sheath; advantages include safety, adjustability, and reversibility, whereas disadvantages include need for frequent postoperative visits; Excess weight loss is approximately 50%. Fig. 32 Gastric banding 56 Fig. 33 Components Roux-en-Y gastric bypass (RYGBP) - a 30-mL proximal gastric pouch is created either by transection or by occlusion using a stapling device; - a 1-cm-diameter anastomosis is then performed between the pouch and a Roux limb of small bowel; - excess weight loss of 70%; - the gold standard in bariatric surgery. Fig. 34 Roux en Y gastric bypass 57 Sleeve gastrectomy - 70% to 80% excess body weight loss at 1 year; - long-term outcomes and durability of this procedure remain unknown. fig. 35 Gastric sleeve resection Benefits of the bariatric surgery - Hypertension completely resolves in 62% of patients and resolves or improves in 79%; - Diabetes is completely resolved in 77% of patients and resolves or improves in 86%; - Obstructive sleep apnea resolves or improves in 85% of patients; - Hyperlipidemia improves in 70%; - The quality of life is markedly better; Reduced mortality rates in morbidly obese patients undergoing bariatric surgery compared to matched controls. 58 Chapter 3 The surgical pathology of the liver I. Anatomy Fig. 1 Macroscopic liver anatomy Liver segmentation Removal of segments II to IV is described as ‘left hepatectomy'; Removal of segments V to VIII, ‘right hepatectomy'. Fig. 2 Liver segmentation 59 Blood suply - 80 per cent of which comes via the portal vein; - 20 per cent via the hepatic artery; - venous drainage is by three, large, short, hepatic veins that pass posteriorly to the inferior vena cava. (the right, middle, and left); - drainage of bile occurs from the left and right hepatic ducts to the common hepatic and bile duct, and then to the second part of the duodenum. II. Hepatic abcess 1. Pyogenic 2. Amoebic 1. Pyogenic abcess Two general categories, based upon the size and distribution of the focal sites of inflammation, the acuity of clinical presentation, and the nature of the therapy that is required. A. Macroscopic abscesses are usually restricted to one lobe of the liver, are frequently single or confluent, present subacutely with symptoms of several days to weeks' duration, and require some form of primary drainage. B. Microscopic abscesses are multiple, widely distributed throughout the hepatic parenchyma, usually manifest themselves acutely over a few days, and require primarily medical therapy, with any surgery that is carried out being aimed at the underlying process, rather than the hepatic parenchymal inflammation. Fig. 3 Liver abscess 60 Etiology and pathogenesis Six general categories: 1. Biliary tract disease- due to cholangitis whenever bile flow is obstructed; 2. Portal vein pylephlebitis suppurative thrombophlebitis in the portal venous system that is secondary to intra-abdominal inflammatory processes; 3. Hepatic arterial infection Systemic bacteremias may occasionally seed the liver, resulting in either macro-scopic abscesses or, more commonly, miliary microabscesses; 4. Post-traumatic; 5. Direct extension of infection. Bacteriology The most common facultative organism isolated from liver abcess is Escherichia coli. The second most frequent isolate is Klebsiella pneumoniae. Anaerobic and microaerophilic organisms, either alone or in conjunction with aerobic organisms, are isolated from up to 60 per cent of pyogenic liver abscesses. Signs and symptoms Macroscopic liver abscesses: - are more subacute, developing over several days to weeks, with fever, night sweats, anorexia, weight loss, and malaise far more common than rigors and hypotension. Fever is present in 90 per cent of these patients with macroscopic liver abscesses; nausea, vomiting, and abdominal pain; and symptoms such as pleurisy, diarrhea, dyspnea, and cough; - abdominal tenderness, usually localized to the right upper quadrant, is the most common physical finding; - hepatomegaly is demonstrable in approximately 50 per cent of patients with macroscopic liver abscesses; - jaundice is uncommon, unless biliary obstruction is present. Microscopic liver abscesses: - usually have an acutely septic clinical presentation, with fever, rigors, and, not uncommonly, hypotension, as well as right upper quadrant discomfort that can be quite severe; - other manifestations depend upon the underlying condition producing the microabscesses: rapidly progressing jaundice in the presence of biliary tract disease; congestive heart failure if the systemic sepsis is associated with endocarditis. Laboratory tests - abnormal hematologic and liver function tests; - the most characteristic liver function test abnormality is an elevated alkaline phosphatase level(ALP), which is observed in more than 75 percent of these individuals. 61 Diagnostic evaluation Ultrasonography CT Fig. 4 Pyogenic abscess Treatment Medical - a 4- to 6-week course of parenteral antibiotics. Surgical - open surgical drainage of the abscess; - correction, whenever possible, of the underlying pathology that led to the abscess; - percutaneous drainage under CT or ultrasound guidance. 2. Amebic abscesses - amebic abscess should be considered in every case of solitary hepatic abscess; - amebiasis is caused by the protozoan Entamoeba histolytica. This parasite exists in two forms: an infective cyst stage and a trophozoite stage, which is the form that causes invasive disease. 62 Fig. 5 Amebic abscess Etiology and pathogenesis - initiated by the ingestion of E. histolytica cysts; - once these cysts reach the small intestine, motile trophozoites are released and migrate to the colon, where they proliferate along with the resident bacterial flora; - once intestinal infection is established, amebas may be carried to the liver via the portal vein. Clinical symptoms - persistent fever and right-upper-quadrant pain; - initial symptoms are non-specific: fever, anorexia, night sweats, malaise, nausea and vomiting, and weight loss; - typically the patients appear chronically ill, abdominal tenderness, and hepatomegaly; - elevated right hemidiaphragm, pleural effusion, and atelectasis are common. Diagnostic evaluation • Serologic testing: indirect hemagglutination test is positive in 90 to 95 per cent of patients with an amebic abscess. • Ultrasound • CT Treatment - most amebic abscesses are cured with a regimen of metronidazole 750 mg orally or intravenously three times per day, for 10 days; - most patients show a prompt therapeutic response to metronidazole, with defervescence and decreased abdominal pain within 3 or 4 days; - this response is useful for differentiating amebic and pyogenic abscesses in situations where serologic testing is unavailable or uninterpretable; - percutaneous drainage; - open drainage of large abscesses to facilitate more rapid healing. 63 III. Hepatic Cysts 1. Nonparasitic cysts 2. Echinococcal cysts Fig. 6 Liver cyst 1. Nonparasitic cysts - generally are benign - solitary or multiple Conduite: - asymptomatic cysts require no treatment; - symptomatic cysts can be unroofed operatively by either an open approach or, more recently, by laparoscopy. 64 2. Echinococcal cysts Fig. 7 Lifecycle of E. granulosus Clinical manifestations - the most common presenting symptoms and signs are right-upperquadrant abdominal pain and palpable hepatomegaly; - jaundice, fever, urticaria, anorexia and malaise, coughing, hydatidemesis, headache, neurological, urological, or musculoskeletal symptoms; - imaging by nuclear medicine scan, ultrasonography, CT scan, or MR scan can demonstrate the abnormality; - the cyst should not be aspirated as an initial test because aspiration can cause spillage of the organisms and spread the disease throughout the abdominal compartment. Hydatid cyst - they are usually single, but multiple cysts may occur; - the cysts increase in size, slowly, over many years; - the surrounding parenchyma is displaced, but not invaded; - surrounding the cyst is an outer layer of adventitia (pericystic layer), which does not belong to the parasite but represents host parenchyma compressed into a fibrovascular layer. 65 Fig. 8 Hydatid cyst - - the free floating and gravitating scolices within the cyst fluid are described as hydatid sand; continuous restructuring of the germinal layer by means of protrusion, invagination, and fragmentation leads to endogenous daughter cysts, and the original univesicular cyst is eventually filled by hundreds of daughter cysts of various sizes; the hydatid fluid, which is a crystal clear transudate of serum that acts as the amniotic fluid for the countless scolices floating within it; if released into the circulation, eosinophilia, urticaria, bronchospasm, or anaphylaxis may occur; usually grow in the dome of the right lobe in segments VII and VIII and tend to push the liver downwards. Fig. 9 Hydatid liver 66 Paraclinic exploration Skin test The Casoni skin test was used extensively some years ago. Now abandoned. Serological test (ELISA), indirect haemagglutination, the radioallergosorbent test, andimmunoelectrophoresis are also available. Liver function tests may be abnormal and biliary obstruction demonstrated by increased levels of alkaline phosphatase and direct bilirubin. Eosinophilia is present in only 25 to 35 percent . Radiology and ultrasound CT, MRI Treatment - is primarily operative; - the abdomen is explored, and before unroofing, the cyst cavity is aspirated with a closed system. - if there is no evidence of bile in the cyst aspirate, a scolecidal agent is instilled into the cavity. Choices include hypertonic saline, 80% alcohol, hypertonic glucose. A second cycle is performed after 5 minutes. - In patients with biliary communication, only hypertonic sodium chloride (10% to 20%) or 0.5% sodium hypochlorite should be used as a scolecidal agent because other agents may damage communicating bile ducts. - pericystectomy is excision of the cyst in the plane between the host pericyst and liver tissue. The remaining cyst cavity can be managed in a number of ways: - small to medium-sized, univesicular cysts may be emptied and closed primarily; - alternatively, the space can be reduced by infolding (capitonnage) and left open to the peritoneal cavity or closed around a drainage tube which is brought to the outside; - another good method to obliterate the cavity is to mobilize and introduce a well vascularized pedicle of omentum (omentoplasty). This provides excellent absorptive drainage of any secreted fluid; - marsupialization to the abdominal wall is not recommended because of poor results; - internal drainage with a Roux-en-Y jejunal loop may be used for deep-seated hepatic cysts with biliary connections. 67 IV. Hepatic tumors A. Benign tumors B. Malignant tumors 1. How do we diagnose a liver tumor? Clinical - initial complete history and physical examination (detection of advanced comorbid disease, such as cirrhosis, or more extensive tumor spread, usually extrahepatic metastases). Laboratory • complete blood count, platelet count; • serum electrolytes; • ‘liver function tests‘ should include: aminotransferases, alkaline phosphatase, bilirubin, and lactate dehydrogenase; • measurement of the albumin level, prothrombin time, and partial thromboplastin time; • levels of anti-hepatitis B antibody, hepatitis B surface antigen, and anti-hepatitis C antibody should be measured. If these hepatitis B and C screening studies are positive, they should be confirmed by quantitative assessment of viral DNA or RNA by polymerase chain reaction. Tumor markers -In the case of primary and metastatic liver tumors, the markers alpha-fetoprotein (AFP) and carcinoembryonic antigen (CEA) are the most useful; AFP (normal range 1 to 10 ng/ml) - Overall, elevation of a-fetoprotein above normal has a true-positive rate of 80 percent and a false-negative rate of 20 percent; - in patients with chronic viral hepatitis, especially those with established cirrhosis: the recommendations are for measurement of serum AFP level every 4 months, along with trans-abdominal hepatic ultrasound every 16 months; CEA (normal range 1 to 5 ng/ml) - the measurement of carcinoembryonic antigen levels is most commonly used in the management of colorectal cancer, even though this antigen may be elevated in other cancers such as breast and lung; - 85 to 90 per cent of patients with hepatic metastases of colorectal cancer (Duke's D) have elevated antigen levels. 68 Imaging studies Fig.11 Liver tumors Fig. 10 Liver tumor Fig. 12 Pet CT‐ liver tumor 69 Ultrasound CT MRI PET-CT A. Benign neoplasms 1.Hemangioma is the most common benign liver tumor - female-to-male ratio of 5 to 6:1; - their blood supply is derived from the hepatic artery; - microscopically, the tumor consists of multiple large vascular channels lined by a single layer of endothelial; - malignant degeneration does not occur. Fig. 13 Liver hemangioma - most hemangiomas are asymptomatic; -life-threatening hemorrhage is extremely uncommon even in large tumors but can be precipitated by needle biopsy; - most hemangiomas are treated safely with observation. Indications for intervention include: - symptoms, complications, and inability to exclude malignancy; In these select patients, the preferred treatment is surgical extirpation; (Regression after low-dose radiation therapy or embolization in select cases has been described also.) 70 fig. 14Ultrasound‐ liver hemangioma fig. 15 CT‐ liver hemangioma 2. Focal nodular hyperplasia (FNH) - currently, it is thought to represent a nonneop