Perforated peptic ulcer by Dr.K.AmrithaAnilkumar

PERFORATED PEPTIC ULCER
PERFORATION
DEFINITION
It is the terminology used for perforation of duodenal ulcer or gastric ulcer or stomal ulcer.
Otherwise all clinical features and management are similar.
Perforation is common in duodenal ulcer
Mortality is more in gastric ulcer perforation and perforation in elderly

1. e n love da Homoeopathy PERFORATED PEPTIC ULCER

2. PERFORATED PEPTIC ULCER

3. PERFORATED PEPTIC ULCER PERFORATION DEFINITION It is the terminology used for perforation of duodenal ulcer or gastric ulcer or stomal ulcer. Otherwise all clinical features and management are similar. Perforation is common in duodenal ulcer Mortality is more in gastric ulcer perforation and perforation in elderly

4. DUODENAL ULCER PERFORATED DUODENAL ULCER It is common in males (8:1) between 35–45 years of age group, but can occur in any age group. In 80% of cases, there is a history of chronic DU. In 20% cases, it is silent perforation. Perforation can occur in acute ulcers or in acute presentation of a pre-existing chronic ulcer. Perforation may be precipitated by steroids, analgesics (NSAIDs), alcohol, antimalarials . Overall incidence is 5%. Active ulcers perforate commonly. Duodenal ulcer with H. pylori infection causes perforation more commonly, especially in young individual NSAID- induced ulcer causes perforation in elderly.

5. Mortality in perforated duodenal ulcer is 10% (in gastric ulcer it is more—20%). STAGES OF PERFORATION Stage of chemical peritonitis: Once perforation occurs ↓ stomach contents escape into the peritoneal cavity ↓ The acid from the stomach causes chemical peritonitis ↓ leading to severe pain in epigastric region, vomiting, tenderness, guarding, rigidity, tachycardia, sweating. Stage of reaction (Stage of illusion): Peritoneum secretes lots of fluid ↓ to neutralise the escaped content ↓ and so temporarily the pain reduces,

6. ↓ and the patient feels better. ↓ This phase lasts for about 6 hours. Stage of diffuse bacterial peritonitis: After about six hours, bacteria from GIT (escape) migrate from the site of perforation causing diffuse peritonitis CLINICAL FEATURES PAIN Severe persistent pain in the epigastrium initially, later in the right side abdomen (as the inflammatory fluid spills along the right paracolic gutter) and finally becomes generalised. Pain is of sudden in onset, is due to contact of expelled gastric contents with the parietal peritoneum.

7. Pain often radiates to right scapular region. Pain becomes more on movements TENDERNESS Tenderness and rebound tenderness is seen (Blumberg sign) all over the abdomen. OTHERS Fever Vomiting Dehydration oliguria occurs. Patient is toxic, with tachycardia, hypotension, tachypnoea. Abdominal distension occurs. Guarding and rigidity, initially in the epigastrium but later all over the abdomen Dullness over the flank because of fluid. Obliteration of liver dullness—as a result of collection of escaped gas under the diaphragm.

8. Silent abdomen with absence of bowel sounds. Tenderness felt on per rectal examination. Often slow, small perforation presents with subacute features, but diffuse peritonitis eventually sets in 24–48 hours. Sometimes fluid from supracolic region ↓ slowly trickles down along the right paracolic gutter ↓ and collects in right iliac region ↓ causing pain and tenderness in RIF ↓ mimicking appendicitis.

9. Terminal stage: Oliguria Septicaemia Shock Hippocratic facies (sunken eyes, cold periphery and shallow rapid breathing, ill look) with MODS ( Multiorgan dysfunction syndrome ). INVESTIGATION Chest X-ray with abdomen in erect posture (plain X-ray): Shows gas under diaphragm in 70% of cases. In 30% of cases, there is no gas under diaphragm Ultrasound abdomen shows free fluid and often gas. Blood urea, serum creatinine, total count, electrolytes, are helpful.

10. CT scan abdomen is very sensitive investigation whenever there is absence of gas under diaphragm. It rules out other conditions like pancreatitis. Gastrograffin upper GI study also confirms the perforation. DIFFERENTIAL DIAGNOSIS Acute appendicitis ™ Acute pancreatitis ™ Acute cholecystitis ™ Ruptured aortic aneurysm ™ Myocardial infarction ™ Mesenteric ischaemia ™ Pneumonia

11. TREATMENT Patient is advised admission. IV fluids—Ringer lactate, normal saline, dextrose saline. Antibiotics—Cefotaxime, metronidazole, amikacin. Catheterisation. Ryle’s tube aspiration. SURGERY Emergency laparotomy through upper midline incision is done. All infected fluid is sucked out. Perforation is identified and closed with interrupted, horizontal sutures using either silk or vicryl . Omental patch is placed before suturing—it is called as Rosoe -Graham Operation

12. Peritoneal wash (toilet) using 5–10 litres of saline is given. Drain is placed and abdomen is closed, often if required with tension sutures. GASTRIC ULCER. PERFORATED GASTRIC ULCER Commonly ulcer in the lesser curve near the antrum perforates. Amount of gas escaped is more than the perforated DU. Malignancy should always be suspected and so biopsy from the edge is a must. Mortality in gastric ulcer perforation is high (20%).

13. Commonly they are prepyloric in position. Primary closure with an edge biopsy is commonly used. Distal gastrectomy, including ulcer area is better option if patient’s general condition is favourable. Posterior gastric ulcer perforation is often difficult to diagnose both clinically and radiologically . XRAY SIGNS Different signs in X-ray in perforation ™ Cupola sign —crescent shaped radiolucency under the diaphragm ™ Riglers sign —visualisation of both aspects of the bowel wall being outlined by gas on either side ™ Inverted V sign —gas on either sides of the falciform ligament ™

14. Football sign —collection of gas in the center of the abdomen like a foot ball ™ Triangle sign —gas between bowel loops AETIOLOGY Common in people with blood group O +ve. Stress, anxiety—‘hurry, worry, curry’. Helicobacter pylori infection is an important aetiology for duodenal ulcer (90%). NSAIDs, steroids. Endocrine causes: Zollinger -Ellison syndrome, MEN syndrome, hyperparathyroidism. Other causes: Alcohol, smoking, vitamin defi ciency . Dragstedt dictum: “No acid – No ulcer

15. PATHOLOGY Ulcer occurs in the first part of duodenum ↓ usually with in the first inch, ↓ involving the muscular layer ↓ Sites: In the bulb (bulbar)—95%. b. Post-bulbar (5%). ↓ Eventually it shows cicatrisation causing pyloric stenosis. ↓ Serosa overlying the site of duodenal ulcer ↓ shows petechial haemorrhages with speckled red dots ↓ appearing like sprinkled cayenne pepper ↓ Microscopically, ulcer with chronic inflammation ↓ with granulation tissue

16. ↓ gastric metaplasia of duodenal mucosa, endarteritis obliterans are visualised. ↓ Sometimes two opposing ulcers, i.e. over anterior and posterior surfaces of duodenum are present and are called as kissing ulcers. ↓ An anterior ulcer perforates commonly, posterior ulcer bleeds or penetrates commonly . CLINICAL FEATURES Water-brash, heart burn, vomiting may be present. Melaena is more common, haematemesis also can occur. Appetite is good and there is gain in weight. It decreases once stenosis develops. Eats more frequently without any restriction. Chronic duodenal ulcer can be uncomplicated or complicated .

17. Gastric ulcer Duodenal ulcer Pain after food intake Pain before food intake Periodicity less common Periodicity more common DIFFERENCE Differences between clinical features of gastric ulcer and duodenal ulcer Haematemesis more common Malaena more common Weight loss occurs Weight gain occurs Equal in both sexes Common in males

18. COMPLICATION Pyloric stenosis: Due to scarring and cicatrisation of first part of the duodenum. Bleeding (10%). Perforation (5%). Both acute and chronic ulcers can perforate. Anterior ulcers perforate. Residual abscess. Penetration to pancreas . INVESTIGATION Barium meal X-ray shows deformed or absence of duodenal cap (because of spasm). Appearance of ‘trifoliate’ duodenum is due to secondary duodenal diverticula which occurs as a result of scarring of ulcer .

19. Gastroscopy reveals the type, location of ulcer, narrowing if any. Biopsy also can be taken to look for the presence of Helicobacter pylori. Usually biopsies are taken from duodenum, pylorus, antrum, body, fundus, and confirmed by rapid urease test or C13 or C14 breath tests. Estimation of serum gastrin level, serum calcium level . DIFFERENTIAL DIAGNOSIS Carcinoma stomach (pylorus) ™ Dyspepsia due to other causes Hiatus hernia Oesophagitis Cholecystitis Chronic pancreatitis 

20. Aim of therapy: To relieve symptoms; to heal ulcer; to prevent recurrence. I. General measures: Avoid alcohol, NSAIDs, smoking, spicy foods Have more frequent food. II. Specific measures: Intragastric pH should be maintained above 5 . Drugs H2 Blockers Proton-pump inhibitors 3. Antacids : Neutralises the HCl to form water and salt and also inhibits peptic activity. Aluminium hydroxide and magnesium trisilicate are commonly used. Dose is 2 grams 2 hours after food.

21. 4.Sucralfate It is an aluminium salt of sulfated sucrose which provides a protective coat to ulcer crater thereby promotes healing. It inhibits peptic activity. 5. Anti-Helicobacter pylori regime: It is very useful, given for 7–14 days—later the proton- pump inhibitors are continued. Triple or quadruple (tetracycline, bismuth, tinidazole , pantoprazole) regimes are used 6. Colloid bismuth sulphate is a good drug for ulcer 7. Misoprostol (200 mg tid ) is the only prostaglandin agonist accepted

22. SURGERY Highly selective vagotomy (HSV). Selective vagotomy with pyloroplasty (SV + P). Truncal vagotomy with gastrojejunostomy (TV + GJ). Posterior truncal vagotomy with anterior seromyo tomy — Taylor’s operation . It can be done through laparoscopy. Vagotomy with antrectomy Posterior truncal vagotomy Linear gastrectomy with posterior truncal vagotomy through laparoscopy. REFERENCE SRB's Manual of Surgery by Sriram Bhat M 2. A Manual on Clinical Surgery by Das 3. A C oncise textbook of Surgery by Das

23. A Special Thanks To A Very Special Doctor