Upper GIT Surgery (PDF)

NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT Upper GIT surgery Esophagus ………………………………………………...…… 1 Bariatric surgery ………………………………………………. 15 Stomach ………………………………………………………... 21 Minimally invasive surgeries …………………………………. 42 Hepatobiliary surgery Gall...

NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT Upper GIT surgery Esophagus ………………………………………………...…… 1 Bariatric surgery ………………………………………………. 15 Stomach ………………………………………………………... 21 Minimally invasive surgeries …………………………………. 42 Hepatobiliary surgery Gall bladder ………………………………………………….… 47 Pancreas ……………………………………………………….. 60 Liver …………………………………………………………….. 75 Spleen ………………………………………………………….. 88 NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT1111 NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT Esophagus Gastroesophageal reflux disease 3 Hiatus Hernia 7 Esophageal Webs 7 Achalasia of the Esophagus 8 Esophageal Diverticula 10 Esophageal Tumors 11 Esophageal Perforation 14 1 NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT1111  NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT Upper esophageal sphincter (UES) Lower esophageal sphincter (LES) Anatomical sphincter Physiological sphincter below diaphragm “Cricopharyngeus ms” # above diaphragmSliding HH At rest in state of tonic contraction Pressure=15-25 mmHg by manometry Pharyngeal phase  Relaxation > 40 mmHg  Achalasia # Failure of this relaxation  Zenker’s 40year, Sex: ♂ = ♀ 1) Lower esophageal sphincter (LES) GERD presentations (3 classes of symptoms) Functional not an anatomical sphincter Components of LES: Typical symptoms Atypical symptoms Alarming S/S - Flutter valve effect of IAP on abdominal 1) Heartburn (80%) 1) Non-allergic asthma  need urgent oesophagus (2-3 cm)  luminal collapse - Pinch cock mechanism: The diaphragm Retrosternal burning (20%) upper endoscopy discomfort 1) Dysphagia - Sling smooth muscle at the gastric cardia. - Chronic cough 2) Regurgitation (60%) - Angle of His: Acute angle at which the M/C Extra esophageal 2) Odynophagia oesophagus enters the stomach. Effortless return of gastric symptom. 3) Early satiety - Rosette-like arrangement of the cardiac sour contents into the - Chest pain 30% gastric mucosal folds. pharynx without nausea, 4) Vomiting retching, or abdominal Mistaken for angina/MI 2) Anatomical barriers: 5) GI bleeding contractions Relieved by nitroglycerin Disruption of the phreno-esophageal 6) Fe def. anemia ligament is associated with Sliding hiatal 3) Water brash 2) Hoarsness hernia (HH) & loss of His angle. Hyper salivation 3) Pharyngitis 7) Unexplained (HH Size is proportional to LES relaxations frequency) 4) Belching 4) Dental erosions Weight loss 3) Esophageal clearance: 5) Late Dysphagia (20%) 5) Globus:Throat lump 8) Choking swallowing  salivary flow  esophageal Peptic stricture clearance (mechanical &chemical buffer) adenocarcinoma irrespective of swallowing 9) Continual pain 4) Delayed gastric emptying: (i.e. Pyloric ✓ Activities that worsen GERD: recumbent position (at night), bending over, fatty meal. stenosis, GOO, post vagotomy) ✓ In some cases, Extra esophageal symptoms (EERD) are the only symptoms present with  frequency of reflux + amount of gastric normal endoscopic studies (NERD). fluid available to be refluxed. Complications of GERD (presented by alarming S/S) 10% C/O of GERD symptoms, 5% have symptoms daily. 1) Erosive esophagitis: acute mucosal inflammation (40-60% of GERD symptoms) 2) Esophageal stricture: progressive mucosal scarring  fibrosis  luminal Physiologic Pathologic narrowing (peptic stricture of the lower end oesophagus). reflux episodes GERD 3) Barrett’s esophagus (BE) (Norman Barrett,1950): 10% Short lived Long lived - Normal squamous epithelium is replaced by metaplastic columnar mucosa  (Post prandial) simulate gastric mucosa or intestinal mucosa (characterized by mucin producing +ve/-ve symptoms not +ve Symptoms goblet cells) - This specialized intestinal metaplasia (SIM) is premalignant. requiring ttt requiring ttt - BE is the only known pdf for adenocarcinoma of the lower esophagus. No nocturnal symptoms Nocturnal symptoms (10% BE develop adenocarcinoma within 20 Y) – (More in white adult obese ♂) d.t. TLESR d.t. loss of barrier (Risk of adenocarcinoma in BE X40 risk normal persons) mechanism Pulse. 3 NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT1111  NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT Investigations 1) Upper Endoscopy, with biopsy 2) 24 Hours esophageal pH studies (Diagnose GERD – can’t diagnose NERD) Gold standard (Diagnose GERD & NERD) 1) Diagnosis GERD if erosive esophagitis is present 1) Diagnosis of GERD: After exclusion of other causes of erosive esophagitis as - Low pH < 4 in episodes > one hour/24 monitoring. eosinophilic & corrosive esophagitis (objective diagnosis) - Acid episodes co-inside with pain. 2) 20 - 40 % negative results in NERD. 2) Diagnosis of 3) A must in +ve alarm symptoms and chronic GERD - NERD / Atypical symptoms / non-responders to medical ttt. Value: Value: - Assess degree of esophagitis (A, B, C, D) - Assess the extent and severity of reflux. - Assess condition of cardia (competent or incompetent) Transnasal catheter is positioned 5 cm above endoscopically defined - Exclude HH, BE or carcinoma (Dysphagia) squamocolumnar junction OR manometrically at the upper limit of LES. 3) Impedance PH metry 4) Barium swallow (Trendelenburg position) 5) Esophageal manometry Diagnose No role In GERD diagnosis No role to diagnose GERD Alkaline reflux & Weak acid reflux (-ve results don’t exclude GERD) Value: Value: Value: Used for GERD patients on Can be used to diagnose - Assess esophageal muscular function medications. ✓ HH in (especially type II HH) - Assess low LES pressure < 10 mmHg ✓ Complicated anatomy (especially in (N= 15-20 mmHg) Redo cases) - Choose ideal type of fundoplication. ✓ Week peristalsis  partial wrap ✓ Good peristalsis  Complete wrap  HH by upper GIT endoscopy  24hr esophageal pH studies  Sliding HH by barium swallow NERD (non-erosive reflux disease) 20%-40% of cases Symptomatic patient/ -ve Endoscopy (no erosions) / GERD is documented by 24 hr pH metry. Pulse. 4 NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT1111  NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT Diagnostic evaluation Classic/typical symptoms (heartburn & regurgitation …) exist in the absence of “alarming symptoms”  GERD is diagnosed (Clinical Diagnosis) + initiate treatment with H2RA or PPI   Response in 2- 4 weeks No response after one month  (1) Change from H2RA to PPI – (2) Maximize dose of PPI   Response Inadequate response despite max. PPI dosage  Confirm diagnosis by: EGD - 24 Hr pH metry EGD = (Esophagogastroduodenoscopy) Treatment Conservative/ Medical ttt Surgery (Restore Valve Action) Endoscopic ttt Ttt of complications Goals of therapy Procedure: 1) Radiofrequency Benign Stricture 1. Alleviate / eliminate symptoms. Open/ Laparoscopic fundoplication application (Stretta) Regular endoscopic Balloon 2.  frequency or recurrence and duration of Indications: to increase LES reflux dilatation under IV sedation GERD Intractable or non-responders barrier and X-ray control. 3. Promote healing of injured mucosa. (after 2-3 months, up to 6-12 2) Transoral 4. Prevent complications. months of medical ttt) Incisionless (TIF) Barret esophagus Therapy: Ccc or C.I of medical ttt. BE without dysplasia Fundoplication using 1) Drugs: Start with PPI or H2 blockers and Young or middle-aged patient May regress after endoscopic sewing alginates (coating effect), with prokinetics responding to PPIs but do not devices (Esophyx). fundoplication. for 3 mnths want long-term therapy. BE with low grade dysplasia 2) Changes in lifestyle & diet restriction: Patient preference Resection by endoscope - Stop smoking, Weight reduction, Wear Complicated reflux by Endoscopic mucosal resection loose fitting clothing. Recurrent Strictures after Endoscopic submucosal dilatation. dissection - Avoid spicy, high fat & acidic foods, BE (excluding high risk of Or chocolate, alcohol, caffeine, garlic & pepper. malignancy by biopsy). - Taking smaller, more frequent and drier Ablation by radiofrequency Alkaline reflux. or photodynamic therapy meals Regurgitation - Elevate head of the bed at night 6 inches. Incompetent LES Followed by - Avoid drugs  GERD (CCBs, αagonists, Symptomatic HH > 5cm fundoplication theophylline, nitrates, sedatives, NSAIDS) (Correct the anatomic defect + BE with high grade dysplasia - Avoid lying down within 3-4 hours after a wrap to treat associated reflux. Esophagectomy (30-40% meal Symptoms correlate to non-acid there is associated CIS). - Avoid bending or straining soon after meals. reflux while on max. PPI dose Pulse. 5 NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT1111  NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT H2-Receptor Antagonists (H2B) Proton pump inhibitor (PPI) Ranitidine 150-300 mg tab /Famotidine 20-40 mg tab (twice daily) Pantoprazole 40 mg / Esomeprazole 20-40 mg (daily) Used regularly or on-demand. 30-60 min prior to meals Both are equally effective in symptomatic ttt of GERD or healing of erosive esophagitis (Although acid secretion is almost zero) Competitively block the histamine receptors in gastric parietal Ccc of long-term treatment: (benefits outweigh the risks): cells, thereby preventing acid secretion Iron and magnesium deficiencies More effective than antacids for relieving GERD RTI and GIT clostridium difficile infection Faster healing of erosive esophagitis Acute interstitial nephritis & systemic Lupus. Laparoscopic fundoplication (success rate is 90%) Procedure: 1. Dissection of the gastroesophageal junction at the hiatus and tightening the crura (correcting the hiatus hernia) 2. Wrapping the gastric fundus around the intraabdominal portion of the oesophagus to recreate a flutter valve. Types fundoplication: Contraindications of fundoplication: Nissen 360o complete wrap. 1) Psychic patient, aerophagist 3) Severe motility disorders 2) Negative PH study 4) Aperistaltic esophagus (scleroderma). Short Floppy Nissen complete non tight, short wrap Toupet 270o incomplete or partial wrap. Factors predictive of successful outcome after fundoplication: 1) Abnormal 24-hour pH score +++ Dor Partial anterior wrap used after 2) Typical primary symptom Heller’s cardiomyotomy (achalasia ttt) 3) Clinical response to acid suppression therapy Complications of fundoplication (10-15%): occurring in the first year after the fundoplication Improve with time and need no treatment Must be clearly explained to the patient before obtaining consent. 10% of these complicated patients will require Redo surgery. 1) Dysphagia: (usually temporary) - Causes of persistent dysphagia: Tight crurae, slipped wrap or tight or long wrap - If persistent & not responding to dilatation  Redo surgery 2) Recurrent reflux: - Causes: Due to Lose wrap or disrupted wrap. - If persistent after one year  Redo surgery 3) Gas-bloat syndrome 10%: - Causes: Due to retained air and decreased ability to belch causing increased flatus and Early satiety. - Redo surgery. Pulse. 6 NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT1111  NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT Hiatus Hernia Occurs when the proximal part of the stomach passes through the diaphragmatic hiatus up into the chest. Gastro esophageal junction (GOJ) Type I (80%) Type II Type III: Combined Siding hiatal hernia Paraesophageal hiatal (rolling) hernia GEJ in chest GEJ in abdomen Type IV: C/P C/P Herniated other organ Usually asymptomatic. Silent until it becomes very large. with the stomach Symptomatic: GERD. Intermittent dysphagia. Vague cardiac symptoms due to pressure on the heart. Type V Occasionally bouts of hiccough (irritation of phrenic nerve). Recurrent HH after Complications: Strangulation & Perforation. Treatment: Always surgical (tightening the crura & fundoplication) operation Esophageal Webs ✓ Circumferential mucosal folds (or webs) in the esophagus may produce annular narrowing and cause dysphagia. ✓ Predispose to carcinoma in the long term. ✓ Etiology: 1. Esophageal Web Upper esophagus: Associated with Plummer –Vinson or Paterson–Brown-Kelly syndrome. C/P: Woman + Triad (Severe Fe deficiency anemia + Dysphagia + Atrophic glossitis) Ttt if symptomatic dilatation 2. Esophageal Web Lower esophagus: Secondary to GERD (Schatzki ring) Pulse. 7 NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT1111  NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT Achalasia of the Esophagus Uncommon primary oesophageal motility disorder (1:200000) Pathophysiology & Etiology Clinical Picture Complications Defect involving parasympathetic Age: young adults & elderly (main age groups) Aspiration causing shocking and coughing Auerbach’s myenteric plexus  Sex: ♂ = ♀ with recurrent chest infections. (at night) Inadequate relaxation of the LES C/O Esophageal diverticula at any level weak / absent esophageal body Dysphagia: Painless Squamous carcinoma (5% risk) peristalses To fluids and solids from the start. 15–20 Y after diagnosis of achalasia. Proximal oesophagus dilates with Halitosis. Weight loss accumulated fluid and solids. Regurgitation of food into the pharynx. Retrosternal pain (in severe cases). Investigations Upper GIT Endoscopy Esophageal Barium swallow Chest X-ray after preparation manometry under fluoroscopic screening Wide mediastinal Preparation: 1) High LES 1) Peristalsis waves shadow due to Fasting or Ryle aspiration as esophagus is pressure Tertiary contractions Uncoordinated dilated full of food residue. (= > 40mmHg) purposeless peristaltic waves. oesophagus Demonstration that fails to relax (Distinct from normal & 2ndry Absence of fundic 1) Typical appearance of achalazia on swallowing contractions) air bubble Capacious distal esophagus (with 2) Tertiary Lost peristalsis (in chronic history). Signs of chest food and fluid residue) contractions 2) Fundic air bubble: Absent. infections. Tight LES (may or may not pass tip 3) Lost peristalsis 3) Bird or Parrot Beak: Short smooth Fluid level in the of the endoscope except by gentle more chronic tapering of lower esophagus. oesophagus is pressure). history. 4) Sigmoid Esophagus (late cases) visible behind the 2) Visualize OGJ to exclude an occult heart. neoplasm misdiagnosed as achalasia (pseudoachalasia). Dilated esophagus Differential diagnosis: Other esophageal motility disorders: 1) Nutcracker esophagus: Coordinate peristalsis but with increased amplitude 2) Corkscrew esophagus = Diffuse esophageal spasm Incoordinate and segmental peristalsis with increased frequency. Tight LES 3) Cancer esophagus 4) Other causes of dysphagia:Post corrosive stricture, rolling HH, ….  Barium swallow, Cardiac achalasia Pulse. 8 NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT1111  NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT Treatment of achalasia: Four modalities of treatment. Aim of ttt: to relieve the functional obstruction and improve esophageal emptying. (directed at the palliation of symptoms and cannot change the underlying pathology) Pharmacotherapy & Botulinum injection 3) Pneumatic balloon dilatation 4) Surgery (Open – laparscopic) 1) Pharmacotherapy Method: Open: Heller’s Myotomy By medications that relax smooth 1) Endoscopic passage of inflatable In very early cases effective in 50% muscles and theoretically decrease graded pneumatic balloon under Method: LES pressure. fluoroscopic guidance. 1) LES is weakened by cutting its muscle They are of limited value and are NOT 2) Single dilatation of LES is done per fibers down to the mucosa recommended. session (serially up to 40 mm). 2) Better combined with antireflux 3) Repeat dilatation in 50% technique (anterior Dor or posterior as (efficacy  after two sessions) 2) Botulinum toxin local injection Toupet) Disadvantages: 3) Now mostly done laparoscopically. Method 50% will require further dilatation within 5Y Endoscopic injection of Neurotoxin Complications: Contraindication: from Clostridium botulinum into LES. Risk of perforation: serious ccc Megaesophagus > 7-8 cm Initially effective in 60-85% High risk of mortality. Require esophagectomy because the Disadvantages: esophagus becomes aperistaltic Post dilatation Gastrografin swallow is 1) Intense inflammatory reaction of GEJ mandatory after dilatation. Laparscopic: POEM with subsequent fibrosis due to Botox Contraindications: Not widely done. injection impair future surgical ttt. Conditions which  risk of perforation Peroral endoscopic myotomy 2) 50% of causes develop recurrent during dilatation: HH, Epiphrenic 1) Incision of mucosa symptoms  repeat injection. diverticulum.Megaesophagus > 7-8 cm. 2) Circular muscles are cut from inside using the endoscope 3) Repair the incised mucosa Laparoscopic Heller myotomy  LES before / after botulinum injection with Dor fundoplication Follow up: Periodic follow up by endoscop to exclude developing squamous carcinoma (precancerous condition). Pulse. 9 NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT1111  NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT Esophageal Diverticula Pulsion or Traction, depending on the mechanism that leads to their development Upper third Cervical diverticula (Zenker's diverticula) Epiphrenic diverticulum Site: Junction of pharynx and esophagus Frequently associated with achalasia Etiology: Diagnosis: Usually pulsion (high pressure)  mucosa bulges Barium swallow Lack of coordination between the inferior Endoscopy. constrictor muscle of pharyns and Esophageal manometry cricopharyngeus during swallowing. confirm achalasia (Point of relative weakness = Killian’s dehiscence) Clinical Picture: Treatment Regurgitation: of recently swallowed food or pills Based on size or symptoms. Choking may follow regurgitation 1. Small diverticulum: Halitosis: putrid breath odor. Not resected + endoscopic surveillance Dysphagia: long standing large diverticulum (pressure on the esophagus ) 2. Large diverticulum: Crepitus and double swallowing: due to outside Pressure on diverticulum. Diverticulectomy + Myotomy (associated Complications: achalasia) Myotomy at the opposite side that goes 1) Squamous carcinoma: due to mucosa irritation in Long standing cases. beyond the distal extent of the diverticulum. 2) Perforation (mainly iatrogenic during endoscopy)  zenker’s pouch  Epiphrenic diverticulum Pulse. 10 NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT1111  NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT Esophageal Tumors A) Benign Esophageal Neoplasms: M/C Leiomyoma Very very rare - Occurs in middle & distal 1/3. - Usually asymptomatic. B) Malignant Esophageal Neoplasms (SCC- Adenocarcinoma) SCC / Adeno carcinoma (M/C) - Incidence of SCC = Adenocarcinoma ( in las decades) Adenoid cystic tumors, sarcomas & APUDomas: rare Malignant melanoma < 1% of esophageal malignancies PDFs: No familial predisposition in both types PDFs to Squamus Cell Carcinoma (SCC) PDFs to Adenocarcinomas 1) Heavy alcohol intake (20 X greater risk) Barrett's esophagus (BE) 2) Smoking (5 X greater risk). Only known pdf for adenocarcinoma of lower esophagus. 3) Achalasia 10% BE develop adenocarcinoma within 20Y. 4) Esophageal web or esophageal diverticula (ch. irritation). Low grade  high grade dysplasia  adenocarcinoma 5) Low vitamins, fruit and vegetable intake. BE develop adenocarcinoma (X40 Normal) 6) Caustic burns (Post corrosive) Incidence of adenocarcinoma 7) Irradiation On top of Barrett's 0.5%/year. - Without Barrett's 0.07%/year. 8) Plummer-Vinson syndrome 9) China, Far East, and around the Caspian Sea d.t fungus which grows on food grain. Pathology Clinical Picture Mac: Fungating - Ulcerating – Stricture- Polyp Age: Uncommon before the age of 50 years. Mic: 1) Painful Dysphagia (classic symptom) SCC: Commonest along whole length of esophagus Onset: Gradual /Coarse: Progressive /Painful Adenocarcinomas: Lower 1/3 or 2/3 mostly on top of BE Early to solids and in late stage to liquids. Spread In advanced cases the patient can’t swallow his own saliva 1) Direct through the wall: 2) Associated history & symptoms of PDF To Adjoining organs: RLNs, trachea, aorta, diaphragm. 3) Odynophagia: Pain on swallowing 2) Lymphatic spread: 4) Hematemesis: rare Cervical, mediastinal or abdominal celiac LN 5) Hoarseness of voice: Recurrent laryngeal nerve infiltration. 3) Blood spread: Late 6) RTI, cough (aspiration or trachea-esophageal fistula) To lungs and liver – Bone & brain -rare- Physical examination: Only in advanced disease 4) Peritoneal implantation Signs of wasting, malnutrition and cachexia Prognosis : Advanced by the time of presentation Hepatomegaly due to metastases. 70% dying within a year and only 8% surviving 5 years. Virchow’s LN in left supraclavicular fossa Pulse. 11 NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT1111  NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT Investigations Dysphagia or odynophagiain a middle-aged or elderly patient  urgent investigation to exclude carcinoma N.B: After diagnosing proceed to investigations for staging to decide if the tumor is potentially curative or not A) For primary lesion B) For staging & to assess operability C) Assess patient fitness 1) EsopgagoGastros- 1) CT scan of chest and abdomen: to assess CVS function Duodenoscopy (EGD) + Local invasion of surroundings ECG Metastases to regional LN - Metastases to liver or lungs Echocardiography biobsy 2) Endoscopic ultrasound (EUS): Cardiopulmonary exercise EGD=Upper GIT testing endoscopy) a) Most sensitive test for determining the: Pulmonary function test: biopsies from any Depth of tumor penetration (T staging) Must be done for all patients suspicious areas. Presence of enlarged periesophageal LN (N staging). preoperatively. 2) Barium swallow b) EUS-guided LN biopsy. Fitness for thoracotomy Irregular Stricture. 3) Staging laparoscopy Spirometry and blood Shouldering & rat tail Lower 1/3 tumors: To assess Peritoneal or visceral gases appearance. metastases not seen on CT scan. FEV1 < 2 L  unlikely to Middle 1/3 tumors: to assess the pleural cavity tolerate single lung 4) Bronchoscopy: Exclude invasion of the trachea or bronchi ventilation during Indications: thoracotomy. Cancers of the middle & upper third of the thoracic  EUS: Distal adenocarcinoma esophagus (tumor at or above carina) Performed only if no evidence of M1 disease 5) PET scan: Fluorodeoxyglucose positron emission tomography) (FDG-PET): rarely needed for any metastases  Bairam swallow: Esophageal carcinoma: irregular stricture & rat tail appearance.  Endoscopy: Esophageal carcinoma Pulse. 12 NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT1111  NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT Treatment I) Palliative treatment II) Neoadjuvant therapy + Curative: Surgery (Esophagectomy) +/- Adjuvant thrapy Indications: Lesions Lesions below the carina Very low tumors 1) Systemic advanced disease at or above the carina (lower two third tumours) (Siewert type I) with metastases Three-stage esophagectomy Two-stage esophagectomy One field oesophago- 2) Locally advanced tumor with (McKeown operation) (Ivor-Lewis operation) gastric resection infiltration of big vs or trachea A) Incisions Oesophago-gastric 3) Bad general condition 1) Left cervical incision to 1) Right thoracotomy (or resection 4) Poor PFts. mobilize cervical oesophagus. thoracoscopy) to mobilize via 5) Cancer cervical esophagus 2) Right thoracotomy (or the thoracic oesophagus. Laparotomy (Radiotherapy is the main ttt thoracoscopy) to mobilize (Divided up at the level of the or left thoraco- and not surgery) thoracic oesophagus. azygous vein) abdominal incision Palliative measures include: 3) Laparotomy to mobilize the 2) Laparotomy to mobilize the + 1) Endoscopic Stenting with abdominal oesophagus & abdominal oesophagus & Esophago-gastric self-expandable metallic allow the stomach to be allow the stomach to be or esophago-jejunal stent: Best palliation. mobilized and fashioned into a mobilized and fashioned into Anastomosis Instructions after insertion: conduit. a conduit. Food has to be liquid. (Nearly entire esophagus resected) Fizzy drinks after eating to B) Abdominal & mediastinal LN are removed (radical operation) keep it clean C) Anastomosis (Gastric conduit + remaining part of esophagus) PPI for reflux. Remaining part: Remaining part: 2) Other palliative measures Cervical part in the neck Thoracic part in the thorax Laser photocoagulation No risk of mediastinitis if RISK of mediastinitis & high Brachytherapy anastomotic leakage occurs mortality if anastomotic leakage No palliative esophagectomy i.e.: Cervical anastomosis is occurs. i.e. McKeown operation Surgical resection aims only to cure. safer than an intrathoracic one preferred for lower 2/3 tumours Neoadjuvant therapy: Chemotherapy +/- Radiotherapy (chemoradiotherapy): to shrink or downsize the tumor. Adjuvant therapy: Chemo+/-radiotherapy following surgery in some patients. Organs of reconstruction after oesophagectomy: 1) Stomach: ✓ Is the preferred organ (getting its blood supply from the gastro-epiploic arcade). ✓ The short gastric vessels are sacrificed. 2) Colon: based on arc of Riolan & can reach the neck) 3) Jejunum (reaches only below carina) Pulse. 13 NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT1111  NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT VIP Note: Transhiatal esophagectomy: done through an abdominal and left cervical incisions. No mediastinal lymphadenectomy is done so it is not a radical operation. Complications of esophagectomy Siewert classification of adenocarcinomas of GEJ Early postoperative Late postoperative Adenocarcinoma of distal part of the esophagus. Type I Tumor center is located 1–5 cm above the GEJ 1) Leakage: 1) Anastomotic stricture with Fatal - risk of mediastinitis. dysphagia. Tumor center is located 1 cm above 2) Respiratory Ccc 2) Anastomotic site fistula. Type II or 2 cm below the GEJ Pneumonia - lung collapse. 3) Early satiety. Type III Tumor center is located 2–5 cm below the GEJ. 4) Reflux & Lung abscess 5) Oesophago-pleural fistula 6) Recurrence and metastasis  BE  Low grade dysplasia High grade dysplasia Adenocarcinoma  Esophageal Perforation Causes: 1) Iatrogenic during endoscopy especially when therapeutic like during insertion of stent (Most common cause) 2) During surgical operations like Heller’s myotomy or sleeve gastrectomy. 3) Spontaneous (Boerhaave’s syndrome) Investigations: CT with contrast findings. Lines of treatment: ✓ Nowadays Stenting is 1ry line of ttt for thoracic and abdominal perforations whether the patient is fit or not for surgery. ✓ Inserted alone or associated with drainage of the contaminated cavity (chest or abdomen) according to GC of the patient and CT with contrast findings. For minor leaks Healthy and early Late cases If diseased. Drainage alone Drainage + 1ry reinforced Exclusion or resection with Esophagectomy with repair diversion immediate reconstruction Pulse. 14 NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT1111 NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT Bariatric surgery Grades of obesity 16 co-morbidities of obesity 16 Laparoscopic adjustable gastric banding 17 Gastric Plication 17 Vertical band gastroplasty (VBG) 17 Sleeve Gastrectomy 18 Roux-en-Y gastric bypass 19 One Anastomosis Gastric bypass 19 Bilio-pancreatic diversion 20 BPD with duodenal switch DS 20 15 NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT1111  NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT Grades of obesity Medical complications (co-morbidities of obesity) According to BMI 1) Type II DM Normal 18.5-24.99 2) Hypertension Overweight 25-29.99 3) Hypertriglyceridemia & hypercholesterolemia Simple obesity 30-34.99 4) CVS: Coronary artery disease & congestive heart failure Severely obese 35-39.99 (no comorbidities) 5) Respiratory: asthma, obstructive sleep apnea. Morbid obesity ≥ 35+ comorbidities or ≥ 40 6) GIT: Gall stones, GERD & NASH. Super obesity ≥ 50 7) Urologic: (eg, stress incontinence) 8) Locomotor: back strain; disc disease; weightbearing osteoarthritis Other grading system: 9) Venous: DVT & lymphatic diseases Class I obesity 30-34.99 10)Dermatological: Skin crease disease Class II obesity 35-39.99 11)Infertility 12)Psychological problems & depression Class III obesity ≥ 40 13)Socio-economic 14)Cancer risk (colon, breast, endometrial, gallbladder)  Indications of bariatric surgery 1) BMI ≥ 40 2) BMI ≥ 35 with obesity-associated comorbidities 2nd consensus meeting on surgery for type 2 DM, London 2015 Hypertension, hypertriglyceridemia & hypercholesterolemia Metabolic surgery is recommended as an option in Severe Type II diabetes mellitus. BMI ≥ 30 + type 2 DM & metabolic syndrome. Pickwickian syndrome. Obesity-related cardiomyopathy & cardiac disease Metabolic syndrome: Clustering of at least 3 of the 5 Severe sleep apnea. 1) central obesity Osteoarthritis interfering with lifestyle. 2) High blood pressure 3) Additional important factors: 3) High blood sugar Age 10-65 4) high serum triglycerides, Previous failed weight loss attempts 5) Low serum high-density lipoprotein (HDL). Patients are motivated and well informed Patients are free of significant psychological disease Metabolic syndrome No history of substance abuse Increases the risk of heart disease, stroke & type 2 diabetes. Patients are generally fit for anesthesia and surgery Patients should for long life follow up Pulse. 16 NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT1111  NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT Types and indications of bariatric surgery Restrictive surgery Malabsorptive surgery Combined restrictive and Sleeve gastrectomy (M/C) Bilio-pancreatic diversion (BPD) malabsorptive Vertical band gastroplasty (VBG) BPD with duodenal switch (DS) Types of Roux-en-Y gastric bypass Laparoscopic adjustable gastric Jejunoileal bypass (JIB) Surgery (RYGB) & LRYGB banding (LAGB) (obsolete) Mini Gastric bypass & Intragasric balloon laparoscopic mini gastric Gastric placation (stopped now) bypass (LOAGB). 1) Bulk eaters. 1) Sweet eaters 2) BMI < 50 2) BMI > 50 3) Above 60 years. 3) Failed restrictive surgery Indications 4) Unreliable patient as regards 4) Metabolic syndrome & Diabetes supplements for life. (Indicated: RYGB, OAGB, DS) A) Restrictive surgery 1) Laparoscopic adjustable gastric banding (LAGB) 2) Gastric Plication (Now nearly stopped) Adjustable bands (employed a subcutaneous reservoir) Infolding (imbrication) of the mobilized greater curvature used to introduce saline via a tube connected to the band in without resection to reduce stomach volume by placement Procedure order to control the band's diameter. (was done by an of rows of nonabsorbable sutures external non-adjustable gastric banding) No F.B. is used No gastric resection/bypass Safest bariatric procedure Adv No use of staplers Minimal risk of leakage Potentially reversible Ccc Band slipping – dilatation - erosion & infection Difficulty of revisional surgery GERD, aspiration & esophageal dysmotility Inadequate long term & Inadequate long-term weight loss which (main cause weight loss & weight disadv. of drop of its use worldwide from 27% to 70% excess weight) ✓ Variable weight regain due to dilatation of pouch and stoma. outcome ✓ Remnant stomach is not accessible to endoscopy ✓ Dodenum & the route for ERCP is closed. ✓ High incidence of resolution of GERD after LRYGB. LRYGB OAGB Marginal ulcers Same incidence Same incidence Internal hernias More common Very rare Nutritional deficiencies Less severe More severe Metabolic S & D.M Superior in resolving them Outcome of weight loss Same Same Revision & Reverse Easier Anastomotic leakage 2 anastomoses Incidence from one anatomists Dumping & CCC Same Same Pulse. 19 NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT1111  NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT C) Malabsorptive surgery (2% of bariatric surgeries) Bilio-pancreatic diversion (BPD) BPD with duodenal switch DS Gastrectomy Partial Sleeve (56 F) bougie Dumping present No (pylorus preserved) Length of common 50 cm 100cm channel limb Outcomes of both: Volume of food returns to pre-operative levels and Malabsorption maintains the weight loss. High incidence of metabolic and nutritional ccc (need close and life-long follow-up): uncommon surgery despite excellent long-term outcomes for weight control and resolution of comorbidities. Pulse. 20 NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT1111 NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT STOMACH Acute Gastric Dilatation 23 Acute Peptic Ulcer 23 Stress Ulcers 23 Chronic Duodenal Ulcer 24 Chronic gastric ulcer 24 Bleeding peptic ulcer 29 Perforated peptic ulcer 29 Gastric outlet obstruction (GOO) 31 Pyloric Stenosis (Pyloric obstruction) 32 Tumors of the Stomach Benign Tumors (gastric polyps) 33 Adenocarcinoma 33 Gastric Lymphoma 37 Gastrointestinal Stromal Tumor 37 (GIST) Gastric Sarcomas 37 Chronic Duodenal Ileus 38 Gastric Volvulus 38 Haematemesis 39 Mallory–Weiss tear 40 Dieulafoy Gastric Lesion 40 Portal gastropathy 40 Aortic enteric fistula 40 Postgastrectomy Syndromes 41 21 NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT1111  NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT Surgical physiology Proximal 3/4 (Parietal cell area) Distal 1/4 (Antral area) Oxyntic (parietal) cells: Absent parietal and chief cells. secrete HCl & intrinsic factor. G cells: secrete gastrin (Part of APUD Chief cells: secrete pepsinogen. system of endocrine cells. Throughout the whole stomach 1) Argentaffin = enterochromaffin-like (ECL) cells: secrete histamine. 2) D cells: secrete somatostatin. Nerve supply of the stomach Parasympathetic nerve supply: Vagus nerve. Sympathetic nerve supply Acid secretion and gastric motility. They carry visceral pain sensation. Reaches stomach via anterior "Lt." & Posterior "Rt." Vagi. From the greater splanchnic nerves reaching the coeliac Each nerve trunk gives off a branch before continuing parallel to ganglion. the lesser curve (Nerve of Latarjet that ends in pylorus) Hepatic branch (branch of the anterior vagus)  liver Coeliac branch (branch of posterior vagus) coeliac plexus to share in the innervation of the gut to the mid transverse colon. Hydrochloric acid secretion Gastric secretion in response to eating is described in three phases. Cephalic phase: mediated by vagal stimulation. It is provoked by the sight, smell, or thought of food. Vagal stimulation  - Direct effect on parietal cellsHCL secretion. - Gastrin release from the G cells of the antrum. Gastric phase: mediated by Gastrin. Provoked by: Factors that cause gastrin release (Antral distension by food - Alkaline medium of antrum - Vagal stimulation) Gastrin  (+) ECL cells histamine (+)parietal cells HCL Intestinal phase: Mediated by secretin Acidification of the duodenum  production of secretin (from duodenum) Secretin: (-) gastric acid secretion (+) production of HCO3 by the pancreas. Pulse. 22 NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT1111  NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT Acute Gastric Dilatation Def.: PDFs: Inv: - Enormous acute dilatation of Follow major surgery, major trauma and Plain X-ray abdomen in erect position. stomach with atonic gastric wall. major burns. TTT: - The stomach occupies most of the C/P: - Nasogastric suction, abdomen and pelvis  sequestration of - Tachycardia & dehydration. - Fluid replacement lot of fluid  hypovolaemia. - Distended upper abdomen. - proper treatment of the original cause. - High mortality and rare - A succession splash can be elicited. Acute Peptic Ulcer (Acute Gastritis = Gastric Erosions) Definition: Multiple erosions in the mucosa of the stomach Treatment: and duodenum 1) Stopping the offending drug or agent. Causes: 2) Avoid spices, fat, coffee and any irritating food. Irritating agents, particularly aspirin and other NSAID, steroids 3) I.V. fluids instead of oral feeding (in severe cases). and alcohol. 4) Antacids, H2 blockers or PPI. Clinical Presentation: - continued for 4-6 weeks after the acute attack. - Acute pain and tenderness in epigastric region. 5) Manage hematemesis: - Blood transfusion - Nausea and vomiting can be present. - Endoscopic control of the bleeding points - Haematemesis can occur and be massive. - Total gastrectomy (rarely indicated, in life threatening Inv.: Upper GIT endoscopy. haematemesis that is not controlled by medical treatment. Stress Ulcers Curling ulcer: stress ulceration with major burns. Cushing ulcer: stress ulceration with head injury Etiology Treatment: - Ischemia of the gastric mucosa is the inciting event. As acute gastritis + correct underlying cause. - Exposure to stressful conditions such as: major surgery, Prophylaxis: major acute illness, extensive burns and sepsis. H2 blockers or PPI can be given in patients exposed to stress. Pulse. 23 NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT1111  NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT Chronic Duodenal Ulcer Chronic Gastric Ulcer Inciden. More common Less common. Age, sex 4th decade, More common in Men (M:F=5:1) Elderly, More common in Men (M:F=2:1) & Low SEC Behavior Not associated with malignancy May be malignant (considered malignant UPO) Etiology Factors associated with  gastric acidity and  stress Damage to the gastric mucosal barrier 1) A large parietal cell mass: ( Most important factor) d.t. Genetic predisposition & blood group "O". 1) Bile reflux to the stomach (Reflux biliary gastritis) 2) Helicobacter pylori infection: 2) Atrophic gastritis secretes urease  splits urea liberation of ammonia 3) Helicobacter pylori infection (a powerful alkali)   gastrin from G cells. (gram -ve spirochaetes (helical=curved rods) motile 3) Endocrinal causes: bacterium) - Zollinger-Ellison's syndrome. 4) Drugs: such as NSAIDs, salicylates, steroids and - Hyperparathyroidism & hyperCa  gastrin release. alcohol - MEN syndrome type I (Wermer's syndrome). 5) Cigarette smoking 4) Liver cirrhosis: (-) inactivation of gastrin & histamine. 5) NSAIDs, Smoking, spicy food & alcohol consumption. Patho. - Number Usually single (Kissing ulcers if two ulcers occur one the anterior the other on the posterior wall) - Size Usually small < 1cm larger up to 2 cm - Site - 1st inch of 1st part of the duodenum (duodenal bulb) - More common on the lesser curve (especially at the - More common on the posterior wall: because of incisura angularis) "Magenstrasse ulcer ". mechanical jet action of acid chyme. - Malignant ulcer is more common in the greater curve & - saddle-shaped ulcer: ulcer occupies the anterior, > 2 cm superior & posterior aspects of the bulb. - Shape Irregular due to fibrosis with - Edge Punched out or sloping edge. - Floor Covered by a thin layer of granulation tissue - Base Indurated base which penetrates the muscle coat. - Margin Congested edematous margin with convergence of the mucosal folds towards the ulcer. Gross appearance of the ulcer at operation Types of G.U. - Indurated localized part of the duodenum Type I M/C occurs at the body on the lesser curvature - Delicate vascular adhesions with the surroundings. Type II Ulcers occur in association with a D.U. - White scarring of the serosa at the site of the ulcer. Prepyloric ulcer (pyloric channel within 3 cm of - +ve "stippling sign": Petichial hge after rubbing the serosa Type III pyloric sphincter) over the ulcer by a piece of gauze. Type IV Proximal gastroesophageal ulcer DD Chronic calcular cholecystitis (CCC) Occur throughout the stomach & associated with Type V GERD the chronic use of NSAIDs Pulse. 24 NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT1111  NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT Chronic Duodenal Ulcer Chronic Gastric Ulcer C/O Pain (Burning or deep-seated boring in the epigastrium – referred to back), Vomiting, Periodicity - 2 hrs after meal: due to acid chyme passing on the 15-30 min after meal (immediately) ulcer following gastric evacuation. Pain - At night (Hunger pain) Relieved by eating Relieved by vomiting. Pain is worse after spicy food or use of condiments. Vomiting Rare (common if pyloric stenosis occurs) Common & is self-induced Periodicity Well-marked Less marked Periods of activity are work, worry, spring & autumn Periods of quiescence: patients are quite healthy. Appetite Good Good but afraid to eat Weight Weight gain Weight loss. +++ +/- Water-brash & heart burn +/- Melaena and haematemesis O/E Localized epigastric tenderness to Rt. of the midline. Localized epigastric tenderness to the Lt of the midline. Pointing sign: patient localizes site of pain by 1 finger Inv. EGD “most accurate” - Barium meal – Diagnosis of H pylori – inv. for cause or ccc EGD ** Oesophago-Gastro-Guodenoscopy Oesophago-Gastro-Guodenoscopy “Most - Diagnose chronic duodenal ulcer or its ccc (Pyloric - Diagnose chronic gastric ulcer. obstruction). - Allows for multiple biopsies to rule out cancer accurate” - Biopsy from antrum to diagnose H. Pylori. - biopsies to examine for H. pylori. Barium Findings suggestive of D.U. Findings suggestive of G.U. Meal - Ulcer niche - Ulcer niche or crater. - Persistent flake of barium at the ulcer crater after - Converging of the gastric folds towards the ulcer “rarely evacuation of barium. used” - Fixed trifoliate deformity of the normally triangular duodenal cap in serial films. Mainly done to rule out GOO & show deformed pylorus Mainly done to rule out GOO (hour glass stomach) H. pylori a) Serology: ELISA & CFT. b) H. pylori fecal antigen test: Sensitive (94%) & very specific (98%). c) Carbon 13 urea breath test: expensive d) Rapid urease test (CLO test: Campylobacter-like organism test) e) Antral biopsy & sent for culture & staining: H. pylori is cultured on Skirrow's media & stained by Giemsa stain. Estimation of serum gastrin level, serum calcium CT & EUS: others If suspected Zollinger Ellison or hyper-parathyroidism. To exclude cancer if still suspected with negative biopsy. Pulse. 25 NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT1111  NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT Carbon 13 urea breath test Rapid urease test (CLO test) - Patients are asked to drink urea (usually with a beverage) labeled - The test is performed at the time of EGD. with a carbon isotope (C13 or C14). A - Biopsy of mucosa is taken from the antrum of the stomach. - Concentration of the labeled carbon is measured in the breath. - Placed into a medium containing urea and an indicator such as - High concentration of labeled carbon when urease is present in the phenol red. stomach. - Urease produced by H. pylori hydrolyzes urea to ammonia  pH of the medium from yellow (-ve) to red (+ve). Barium meal Duodenal ulcer Gastric ulcer A B  Endoscopic US of the stomach. A) 5 layers in the normal stomach. B) Gastric cancer invades gastric wall muscle. Fixed trifoliate deformity Converging of the gastric folds Gastric carcinoma of triangular duodenal cap towards the ulcer Normal GU Cancer  Endoscopy  CT scan: gastric cancer Pulse. 26 NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT1111  NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT Chronic Duodenal Ulcer Chronic Gastric Ulcer Treatment (Medical and surgical ttt)  Medical ttt (Main line of ttt after exclusion of cancer n G.U.) “Most ulcers will heal in 8–12 weeks.” 1) Eliminate irritants: Avoid ethanol, tobacco & NSAIDs 2) Antiulcer treatment 3) Eradication of H. pylori by triple therapy - Histamine (H2) blockers: Triple drug therapy consisting of: Famotidine 40 mg orally at bed time. 1) Metronidazole. - PPIs: 2) Amoxicillin, tetracycline or clarithromycin. Omeprazole 20 mg orally in the morning. 3) Bismuth compounds. - Sucralfate Quadruple drug therapy consisting of: can be added as a cyptoprotective drug 1), 2), 3) + PPI Disadvantages of medical TTT: High rate of recurrence (Main disadvantage in D.U) Regimen to prevent relapse: 2 schools A or B A) Interval therapy  Full dose regimen is given at times of maximum stress & periodicity B) Maintance therapy  small dose at bed-time long life. Surgical ttt Indications of surgery in D.U. Indications of surgery in G.U. 1. Failure to respond to medical therapy 1. Intractability: 2. The development of complications (perforation, uncontrolled - Ulcer fails to heal after 3 months of medical therapy bleeding or GOO) - Recurrence within a year despite adequate therapy. 2. Development of complications (uncontrolled bleeding, perforation, and gastric outlet obstruction). 3. Malignancy cannot be excluded. Surgical options Surgical options 1. Truncal vagotomy & drainage procedure Partial or subtotal Distal gastrectomy + Vagotomy 2. Truncal vagotomy and antrectomy Parietal cell Excision of (ulcer + ulcer bearing area) & reconstruction by 3. vagotomy (highly selective vagotomy) a) Gastroduodenal anastomosis (Billroth I gastrectomy) If the duodenum can be mobilized b) Gastrojejunal anastomosis (Billroth II gastrectomy) if the duodenum cannot be mobilized Vagotomy is added to distal gastrectomy when there is associated duodenal ulcer with expected hyperacidity. Pulse. 27 NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT1111  NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT Surgical options for treatment of Duodenal ulcers Goal of surgery is to reduce acid secretion by Interrupting vagal stimulation Or elimination of antral gastrin secretion Or both Truncal vagotomy Truncal vagotomy Parietal cell vagotomy & drainage procedure and antrectomy (highly selective vagotomy) - Effectively decreases acid secretion. - Trunkal anatomy: division of the - Only the gastric branches of the - Drainage procedure (pyloroplasty or hepatic and coeliac branches of vagus vagus nerve are divided to avoid S/E gastrojejunostomy). - Antrectomy causes excision of the of truncal vagotomy. - Pyloroplasty (M/C Heineke- Mikulicz) gastrin secreting region of the stomach) The pylorus is divided longitudinally - Many side effects and sutured transversely Impaired motility (functional obstruction) Maintained motility (iinervated pylorus)  Drainage procedure  Drainage procedure Recurrence Lowest recurrence rate High rate recurrence. Side effects of Truncal vagotomy: 1) Gallbladder stasis & gallstones 2) Distension 3) Post vagotomy diarrhea - Mild (common) / disabling problem (rare) - Usually improve during the first year after surgery 4) Gastric dysmotility, delayed gastric emptying 5) GERD vagotomy +antrectomy vagotomy +antrectomy Roux-en-Y 6) Duodenal ulcer recurrence: Due to: (Billroth I) (Billroth II), gastrojejunostomy, - Missed Criminal nerve of Grassi: (90 % of cases) 1 or 2 branches of the posterior vagus that originate above the GEJ in. - Inadequate drainage with antral stasis & gastrin stimulation. Post vagotomy Diarrhea not constipation (Though parasympathetic innervation): Division of the hepatic fibres of vagus  GB distension  contraction  Expels increased quantities of bile salts (More than the resorptive capacity of S.I. vagotomy and vagotomy and Parietal cell vagotomy.  diarrhea by direct action on the colon) pyloroplasty gastrojejunostomy Pulse. 28 NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT1111  NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT Other peptic ulcers 1. Stomal ulcers: (on the jejunal side of the stoma): After gastrojejunostomy or distal gastrectomy (Billroth II type) 2. Ulcer in Meckel’s diverticulum. Complications of P.U. Acute complications Chronic complications Bleeding peptic ulcer 1. Gastric outlet obstruction Perforated peptic ulcer: can occur in patients known to 2. Malignant transformation of peptic ulcer have chronic PU or it can be the first presentation. 3. Penetration. 4. Ulcer recurrence Bleeding peptic ulcer Perforated peptic ulcer Mortality in bleeding peptic ulcer is high (20-30%). Duodenal ulcers > Gastric ulcers (75% of perforated peptic  Risk of mortality: Elderly/ comorbidities / > 5 units ulcers are duodenal ulcers). of blood transfusion during hospital stay. Anterior duodenal ulcers > posterior duodenal ulcers. Pdfs Worry, Work & Stress Periods of periodicity Ulcerogenic diet (alcohol, smolking) & drugs (steroids & NSAIDs) Patho Pathology Pathologic stages & its correlation with C/P +c/P 1) Mild (common): 1) Stage of chemical peritonitis: Once perforation occurs From granulation tissue in the floor of the ulcer due to trauma Gastric acid escapes into peritoneal cavity from solid food. C/O O/E 2) Moderate: Sudden severe epigastric pain General: a. Due to erosion of small vessels in the wall of ulcer crater (Generalized) + mild vomiting Tachycardia, hypotn sweating 3) Severe & may be fatal: Radiation: Due to erosion into a major vessel such as the back & right scapular region Local: gastroduodenal artery in a posterior duodenal ulcer.  movements and respiration. T RT GR Bleeding from erosion of gastro duodenal artery is severe, torrential and almost always needs early surgical 2) Stage of reaction (Stage of illusion): lasts for about 6 hours intervention. Gastric acid is diluted by peritoneal fluid secreted by peritoneum. All S/S temporarily improve and the patient feels better Clinical Picture: Only tachycardia persists. Haematemesis and melaena. 3) Stage of diffuse bacterial peritonitis: after 6 hrs Picture of shock: Pallor, tachycardia, hypotension, Bacteria from the site of perforation migrate diffuse peritonitis. tachypnoea, sweating, dry tongue, cold periphery. The patient becomes worse:  Pain returns  Repeated vomiting due to paralytic ileus Progressive constipation. C/P of frank septic peritonitis is present (Mention, pge 72) Pulse. 29 NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT1111  NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT Bleeding peptic ulcer Perforated peptic ulcer Inv 1) Gastroscopy (EGD): Laboratory: Identifies bleeding ulcer CBC: Leucocytosis. Identifies bleeding that is unlikely to be controlled by Serum electrolytes & KFTs. endoscopy (ominous signs on endoscopy): Serum amylase: Moderate elevation. - Presence of spurting vessel ABGs: metabolic acidosis - Fresh clot covering the ulcer crater Radiological: - Visible oozing vessel 1) Plain X-ray lower chest & abdomen erect: - Vessel with pseudoaneurysm Air under diaphragm is diagnostic Forrest classification: For purposes of selecting patients 2) CT scan abdomen: for endoscopic treatment & estimating risk of rebleeding. If other conditions like acute pancreatitis is suspected. 2) Coeliac angiogram: in case of obscure bleeding. 3) Blood group and cross-matching. 4) serum electrolytes, blood urea, serum creatinine, platelet count, coagulation profile & Hbg Ttt A) Conservative measures: 70% A) Rapid preoperative preparation & resuscitation Correction of shock NPO & IV fluids Stomach wash: using 1: 200,000 adrenaline in cold saline Ryle’s tube & nasogastric suction through Ryle's tube. Urinary catheterization & fluid chart IV ranitidine 50 mg or Antibiotics (third generation cephalosporin & metronidazole). Pantoprazole 80 mg in 100ml dextrose saline every 6-8 hrs. Antiulcer treatment (PPIs I.V.) B) Endoscopic maneuvers: Correction of electrolytes & acid-base imbalance if present Cauterization using bipolar cautery, Laser or heater probe B) Emergency Surgery: Vessel clipping using haemoclips. 1) Laparotomy through upper midline incision is done. Sclerotherapy using ethanolamine oleate. 2) All infected fluid is sucked out and sample taken for C/S Submucus injection of epinephrine, absolute alcohol or 3) Perforation is identified and closed with omental patch polidocanol. (Rose-Graham Operation). C) Angiographic embolisation of gastroduodenal artery. 4) Peritoneal wash (toilet) using 5-10 litres of saline. D) Surgical intervention: To control massive hemorrhage 5) Drain is placed and abdomen is closed. Patient shocked on admission. C) Ttt of original cause and follow up Hemodynamically unstable patients despite resuscitation Vagotomy (as definitive treatment for ulcer) in the stage of Continued blood loss requiring > 6 units / 24 hr period. chemical peritonitis only. Presence of ominous signs on endoscopy. Antiulcer ttt is continued Principles of surgery include: Gastroscopy must be done after 12 weeks. 1. Control of bleeding vessel by over-sewing the bleeding point.  If fails  In perforated gastric ulcer Ligation of the main feeding vessel (gastroduodenal A) Good GC  Distal gastrectomy including ulcer area 2. Definitive surgery to treat the ulcer if the patient’s Risky GC  Closure with omental patch as perforated D.U. + condition allows biopsies to exclude malignancy. Pulse. 30 NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT1111  NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT Forrest classification of bleeding ulcers Clinical picture of frank septic peritonitis Acute hemorrhage Complaint:Pain - Repeated vomiting. - Progressive constipation. 1) Forrest I a Spurting hemorrhage Examination Forrest I b Oozing hemorrhage General Ex Local Ex Signs of recent hemorrhage Patient looks Inspection: Abdominal distension - Forrest II a Non bleeding Visible vessel toxic and diminished movement with respiration Forrest II b Adherent clot dehydrated. Palpation: GT RT GR Forrest II c Flat pigmented haematin on ulcer base Fever Percussion: Lesions without active bleeding Tachycardia Obliteration of liver dullness d.t. collection of Forrest III No signs of recent hemorrhage & clean ulcer Hypotension escaped gas under the diaphragm. base Auscultation: Tachypnea oliguria Silent abdomen from paralytic ileus septic shock DRE: Tenderness DD of Perforated P.U. 1) Acute appendicitis: At first: Fluid collects in supracolic compartment of peritoneal cavity Then spills to the infracolic compartment by way of the right paracolic gutter (the left closed by the phreno-colic ligament) Remain localized to the right iliac fossa (conflicting S/S and sometimes wrongly diagnosed as acute appendicitis) 2) Acute cholecystitis 3) Acute pancreatitis 4) Acute mesenteric ischaemia 5) Ruptured AAA 6) Acute myocardial infarction 7) Pneumonia Gastric outlet obstruction (GOO) Fibrosis of a chronic D.U.  Pyloric obstruction Fibrosis of a saddle shaped G.U.  Hourglass stomach  TTT by distal gastrectomy Pulse. 31 NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT1111  NOT FOR PRINT NOT FOR PRINT NOT FOR PRINT Pyloric Stenosis (Pyloric obstruction) Clinical Picture Electrolyte changes in pyloric stenosis C/O : 1) Hyponatraemia, hypokalaemia, hypomagnesaemia, 1) Long history of ulcer dyspepsia. hypochloraemia: These electrolytes are lost in vomitus. 2) severe & persistent Pain with feeling of fullness. 2) Metabolic alkalosis, tetany, paradoxical aciduria 3) Vomiting: Stomach: Copious vomiting at the end of the day Loss of HCL  Hypochloremic metabolic alkalosis. Projectile, non-bile stained (clear), containing fermented Kidney: undigested food of previous meals of foul odor & usually - The kidney secretes excess bicarbonate to control the frothy. alkalosis. Usually gives considerable relief of fullness & distension. - Large amounts of Na+ are excreted in the urine with HCO3 4) Loss of Periodicity, nausea & loss of appetite. - This associated hyponatraemia  (+) aldosterone  Na+ O/E: conservation at the expense of more renal loss of K+ 1) Epigastric fullness. (hypokalemia) 2) Peristaltic waves propagating from left to right. - To correct this hypokalemia  H+ is exchanged with K+ 3) Succusion splash.  paradoxical aciduria (after depletion of K+) 4) In severe cases: Patient is confused Tetany: as alkalosis   ionized Ca++ (gastric tetany) Investigations Treatment 1) Barium meal: (Soup dish appearance) Surgery or intervention is indicated in all cases. Hugely dilated stomach & the greater curvature is below the level of iliac crest. Preoperative preparation includes: Deformed pylorus.