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Examinations in Chronic Abdominal Conditions
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Digital Examination of Rectum
It is done to look for secondaries (Blumer shelf) in anterior aspect above the prostate level. It is nodular hard with free mucosa (not adherent). It suggests advanced malignancy. It is due to peritoneal spread. It is useful in Crohn’s disease (fissure in ano or fistula in ano), and other chronic conditions.
Pervaginal examination is a must in females
especially in lower abdomen masses and when Krukenberg tumour (Carcinoma stomach) of ovary is suspected.
Systemic Examinations
Examination of respiratory system, spine (for secon­daries or tuberculosis), central nervous system is essential (Figs 20.23 and 20.24).
Fig. 20.23: Psoas spasm causing hip in flexion due to
Investigations
Detailed investigations and discussions of different conditions are beyond the scope of this book. Students should refer SRBs Manual of Surgery, 3rd edn and Bedside Clinics in Surgery for in detail discussions.
Blood – Hb%, ESR, relevant tumour markers. Stool examination: Occult blood, steatorrhoea (fat),
creatorrhoea (muscle fibres seen in chronic pan­creatitis), mucous in stool, microscopy, culture.
Gastric Function Tests
Patient is overnight fasting; should not take any antacids and anticholinergics for 24 hours. Nasogastric tube is passed early morning and gastric juice is aspirated under fluoroscopy after confirming the tip of tube is at mid stomach level. Normally it is around 70 ml. If it is more it suggests pyloric stenosis or hypersecretion. Tube now is connected to low pressure 5 cm Hg suction to have continuous aspiration. Later one hour aspiration is collected. It is called as morning basal secretion. Free acid level means only HCl level; total acid level means HCl plus other acids in the stomach.
Dragstedt test: Gastric content is aspirated through continuous low pressure suction for 12 hours from
9. PM to 9. AM and the juice is collected. Normal volume is 400 ml. It is increased in duodenal ulcer due to vagal hyperactivity; increased very much more­than a litre in Zollinger-Ellison syndrome. Normal HCl level in this is 10–20 mEq. It is 40-80 mEq in duodenal ulcer (); 100-300 mEq in ZE syndrome (↑↑); 5-15 mEq in gastric ulcer (). Basal secretion is the secretion from the parietal cell mass in resting condition. It is < 5 mEq/hour normally; > 5 mEq in duodenal ulcer; 1-2 mEq in gastric ulcer. Peak/maximal secretion is secretion in one hour after stimulation. Stimulation may be using pentagastrin (now used)/ Kay’s augmented histamine/Hollander’s insulin. It gives maximal/ peak acid output.
Fig. 20.24: Examination of spine is essential.
Pentagastrin test: Initial basal secretion is collected. 6 µ gm of pentagastrin is injected IM/SC and 15 minutes gastric samples are taken for one hour . Peak/maximum acid output is assessed. Normal is 25-27 mEq; in gastric ulcer it is upto 15 mEq; in duodenal ulcer it is 35-38 mEq; in ZE syndrome it is > 60 mEq/very high; in carcinoma stomach it is very low.
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Kay’s augmented histamine test: After collection of basal fasting sample, mepyramine maleate 100 mg IM is injected to neutralise histamine side effects without interfering gastric effects. After 30 minutes, histamine acid phosphate 0.04 mg/kg is injected S/C. Free acid level (only HCl) is assessed. In stomal ulcer it is 30-35 mEq; in duodenal ulcer it is 30­40 mEq; in gastric ulcer it is less than 15 mEq.
Hollander’s insulin test: It is useful to assess post­operatively and confirm the completeness of vagotomy.
0.2 units/kg wt of insulin is injected IV to a fasting patient so as to create hypoglycaemia below 35 mg% which stimulates the parietal cells through hypothala­mus and vagus causing acid secretion. Patient with complete vagotomy will not show the increased acid level. Increase in acid secretion in first one hour is called as early response and if it is more than 30 mmols/L suggests incomplete vagotomy . Delayed response is between 1st and 2nd hours and is due to delayed gastrin release.
Chew and spit test: Nasogastric tube is passed. Patient chews a meal and spits it out to stimaulate acid production through vagus. Gastric contents are aspirated and studied for acid level.
Barium/Contrast Studies
Barium meal X-ray: Barium meal X-ray is done using barium sulphate (95% w/v) solution of which 400– 600 ml is given orally . Gastrograffin is also often used. It is done in empty stomach. Microcrystalised barium sulphate solution is better. Procedure should be done under fluoroscopic guidance. Buscopan injection is given to the patient to delay the gastric emptying. Glucagon also can be used. Effervescent tablet (calcium carbonate and antifoaming agent) is given to the patient. 200 ml of barium sulphate solution is given to drink. X-rays are taken to get double contrast barium meal X-rays. Indications for barium meal X-ray—Duodenal ulcer—shows absent/deformed duodenal cap; Benign gastric ulcer—shows niche (due to ulcer) and notch (due to spasm); Gastric outlet obstruction; Carcinoma stomach—irregular filling defect; Carcinoma head of pancreas—pad sign;
Periampullary carcinoma – Fr ostberg reverse ‘3’ sign; Chronic duodenal ileus—obstruction at mid 3rd part
of the duodenum; Stomal ulcer—ulcer crater at stoma;
Duodenal diverticula–trifoliate duodenum; Trichobe­zoars; Gastric fistulas; Pseudocyst of pancreas– widened vertebrogastric angle.
Barium meal follow through X-ray is done as late films often after giving prokinetic agents like metoclo­pramide.
Enteroclysis (small bowel enema): It is visualisation of entire length of small intestine –to assess anatomical problems. Indications are small bowel diseases/ ileocaecal tuberculosis, stricture, small bowel tumours, partial obstruction and Crohn’s disease. Technique – Patient is prepared overnight with empty stomach and laxatives. Nasojejunal tube is passed. Prokinetic drug like metoclopramide is given. Microbarium sulphate solution (50% w/v) or gastrograffin or water soluble iodine dye solution is (500-800 ml) passed through the tube. Under fluoroscopic guidance X-rays are taken as required. Features such as narrowing, smooth/ irregular filling defect, localised dilatation, obstruction or features of specific conditions are looked for. In conditions like ileocaecal tuberculosis enteroclysis and barium enema X-rays are combined. Problems with enteroclysis are poor patient acceptance, and technical
better options to visualise the small bowel. When nasojejunal tube is not able to be passed barium meal follow through X-ray is done by taking late films of barium meal (Figs 20.25 to 20.28).
Fig. 20.25: Barium meal X-ray showing
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Fig. 20.26: Barium meal X-ray showing
Fig. 20.28: Trifoliate duodenum–late effect of chronic
the colorectum using a enema tube from an enema can. Patient will be initially in left lateral position and later in prone position. In children a Foley’s catheter with inflation is used to maintain the retention of enema. Procedure is often observed under fluoroscopy. Injection buscopan is injected (20 mg IV) to relax the colon. X-ray film is taken after complete filling. Patient is asked to evacuate the barium and later post­evacuation film is taken. Air is insufflated into the colon to get air contrast film. Additional dif ferent view films are taken to see the suspected area properly.
Fig. 20.27: Benign gastric ulcer showing
Barium Enema X-ray
Technique of barium enema X-ray-24 hours liquid diet, laxatives for two nights and enema on previous night are the required preparations for barium enema X-ray . About one litre of barium sulphate/microbarium sulphate solution (25% w/v) is infused per anally into
Indications for barium enema are carcinoma colon; Ileocaecal tuberculosis [combined with Enteroclysis;] Ulcerative colitis; Crohn’s disease; Ischaemic colitis; Colonic polyps; Intussusception; Congenital mega­colon; Gastrojejunocolic fistula; Congenital diaphrag­matic hernia (Bochdalek).
Different findings: a. Hirschsprung’ s disease: Barium enema is done to look for the extent of disease and three zones. Foley’s catheter should not be used while doing barium enema in case of Hirschsprung’ s disease. Here barium in dilute saline is used – not in water.
1. Distal immobile spastic segment, i.e. aganglionic zone. 2. A proximal, middle transitional zone of about 1-5 cm length with less, sparse number of ganglions (Cone). 3. A still more proximal, hypertrophied dilated segment is actually the normal ganglionic area.
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b.Carcinoma colon: Irregular filling defect; Apple core lesion especially on left side; Metachronous growths (growths in different parts of the colon) should be looked for – 5% common; Narrowing – left sided lesion. c. Ulcerative colitis: Loss of haustrations; Contracted smooth colon; Presence of pseudopolyps; Collar button ulcers–contiguous mucosal involve­ment; Hose pipe/pipe stem lesions; Increased presacral space more than normal (normal is < 1 cm); Reflux ileitis; Rectum is almost always involved. d. Ileocaecal tuberculosis - Pulled up caecum due to fibrosis and contraction; Obtuse ileo caecal angle (normal angle is acute); Hurrying of barium due to rapid flow – Stierlin
sign; Narrow ileum with thickened ileocaecal valve, Fleischner–inverted umbrella sign; Incompetent
ileocaecal valve; Ulcers and strictures in terminal ileum– napkin lesions; Gooseneck appearance – ileum hanging from fibrosed; pulled up caecum. e. Crohn’s disease: Aphthoid ulceration; Skip lesions; Rectum is not commonly involved; String sign of Kantor;
Cobble stone appearance–pseudosacculations; Raspberry/rose thorn appearance; Fistula or strictures. f. Sigmoid diverticula: Saw teeth appearance of
sigmoid colon – concertina like – serrated appearance; Champagne glass sign – partial filling of barium with stercolith inside the diverticula; Fistula to adjacent structures. g. Intussusception - Claw sign – coiled spring sign: pincer end; Empty right iliac fossa – mainly in plain X-ray abdomen with multiple air fluid levels (on ultrasound – target sign/pseudokidney sign/bull’ s eye sign). h. Ischaemic colitis: Thumb print sign in splenic flexure.
Fig. 20.29: Barium enema X-ray showing typical claw sign/
Other signs in barium enema X-ray: Stacked coin appearance due to submucosal haemorrhages in
Henoch Schonlein purpura; Scalloped edges in colon in pneumatosis intestinalis (Figs 20.29 and 20.30).
Hypotonic duodenography: It is same as barium meal X-ray but duodenal hypotonia is achieved by giving injection glucagon or buscopan so that air contrast hypotonic barium X-ray study shows better pictures.
Oral Cholecystography (OCG, Graham-Cole Test)
Patient is advised to have fat free diet for 3 days. Previous night 6 tablets of iopanoic acid (T elepaque) is given orally. Next morning plain X-ray abdomen is taken to visualise the gallbladder. Later fatty meal
Fig. 20.30: Barium enema X-ray showing growth
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is given and X-rays are taken at 10, 15, 30 and 60 minutes to see the change in the size of the gallbladder (which should be less in size compared to the earlier film, as the gallbladder contracts on stimulation if it is functioning normally) (Fig. 20.31). Smooth filling defect signifies non-opaque stone.
or using propofol anaesthesia. Patient is placed in prone position with the head turned towards right. After passing gastroduodenoscope, sphincter is identified and cannulated. Under visualisation 3 ml of water soluble iodine contrast is injected into the bile duct and pancreatic duct. When cannula goes upwards beside vertebra, it is in bile duct; and if cannula goes across the vertebra it is in pancreatic duct.
Indications—Malignancyirregular filling defect; Chronic pancreatitis—chain-of-lakes appearance; Congenital anomalies, stones (Fig. 20.32); Stricture of biliary tree; Choledochal cyst; For sampling of biliary and pancreatic juices for analysis and cytology; Brush biopsy from tumour site.
Fig. 20.31: Oral cholecystogram done to see the
Contraindications: Patients with serum bilirubin > 3 mg%, acute cholecystitis. OCG is not done now.
Intravenous cholangiography: It is done to visualise bile ducts and biliary tree, by injecting IV Meglumine ioglycamate (Biligram) and taking X-Ray abdomen. It can be combined with OCG. Problems with this method are poor visualisation, drug reaction. It is not very useful if serum bilirubin is >3 mg%.
Endoscopic Retrograde Cholangio­pancreatography (ERCP)
Through a side viewing gastroduodenoscope, sphincter of Oddi is cannulated, dye is injected and biliary and pancreatic tree is visualised. It is done under C-ARM guidance. It is done under sedation like midazolam
Fig. 20.32: ERCP showing stone in common bile duct.
Therapeutic uses—Extraction of biliary duct stone; Nasobiliary drainage; Stenting of tumour in the CBD or in the pancreas; Dilatation of the biliary stricture; Endoscopic papillotomy.
Complications – Pancreatitis; Duodenal injury; Cholangitis; Bleeding.
Relative contraindications—Acute pancreatitis; Previous gastrectomy; Altered prothrombin time
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(corrected by injection Vitamin K, FFP); Bleeding disorders.
Percutaneous Transhepatic Cholangiography (PTC)
It is done in case of severe obstructive jaundice under coverage of appropriate antibiotics and after control of any bleeding tendency . With the help of fluoroscopy , Chiba (university) or Okuda needle which is long, flexible, thin, blunt, without beveled end, is passed into the liver through right 8th intercostal space in midaxillary line. Once needle is in the dilated biliary radicle, bile is aspirated (sent for culture, cytology, analysis); and then water soluble iodine dye is injected into the same so as to visualise the dilated biliary radicles, also the site and extent of any obstruction (i.e. tumour, stricture). Procedure can be used for therapeutic stenting across the biliary tree through any obstruction either in the hepatic ducts or in the CBD into the duodenum. Complications: Bleeding, biliary leak, biliary peritonitis and septicaemia.
Magnetic Resonance Cholangio­pancreatography (MRCP)
MRCP is a non-contrast imaging method, better than ERCP as diagnostic tool in biliary and pancreatic diseases. T2 W1 images are used.
scopy; polyp removal; submucosal resection; for ERCP—diagnostic and therapeutic procedures.
Procedure: Gastroscopy is done following eight hours of fasting. After lignocaine spray into the oral cavity; gastroscope is passed gently down the oesophagus when the patient does the swallowing action. Once the scope is inside the stomach, air is inflated and different parts of the stomach are visualised. Fundus is visualised by retropulsion. Scope is passed through the pylorus to see 1st and 2nd parts of the duodenum. Looked for any pathology and if required biopsy is taken (Figs 20.33 and 20.34). Often midazolam sedation is beneficial to have an easy passage.
Complications: Bleeding, aspiration, perforation (rarely).
Gastroscopy
It is visualisation of interior of stomach, duodenum and oesophagus. It is used for diagnosing any pathology—Gastric ulcer; duodenal ulcer; gastritis; stomal ulcer; carcinoma stomach; oesophagitis; oesophageal varices. Biopsies from the suspected cases of malignancy or for Helicobacter pylori can be taken. Endosonography can be done to assess the staging, operability of carcinoma stomach or oesophagus. Fibreoptic flexible gastroduodenoscopy also can be used. Videoendoscopy is used not only for diagnosis but also mainly for therapeutic procedures. Both end viewing and side viewing gastroscopes are available. For therapeutic procedures and ERCP, side viewing gastroscope is required.
Therapeutic procedures: Variceal injection or ligation; Stenting of pseudocyst of pancreas through gastro-
Fig. 20.33: Gastroscopy is being done.
US Abdomen
It is very useful to identify gallstones, liver pathology. But not a good method for assessing the pancreas.
Radioisotope Scanning
Inorganic iodide is given orally 2 days prior to block the thyroid. I
99m
Technetium is administered. 10 minutes later
131
labelled serum albumin or
scanning is done in supine position. It is useful to find out focal and diffuse diseases; abscess like in
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Fig. 20.34: Endosonography of stomach.
liver or subphrenic space; inflammatory pathology.
75
Se-labelled methionine is used to scan pancreatic lesions. It is also useful in GI bleeding. Blood loss is measured with help of RBCs labeled with Cr51 which is injected intravenously.
in midepigastrium; Periodicity, haematemesis/melaena (25%) are other features.
Complications are – hour glass contracture, tea-pot deformity, erosion into left gastric/splenic arteries, perforation and malignant transformation. Risk of carcinoma is 6-23%. Patients with gastric ulcer treated with anti-ulcer drugs like proton pump inhibitor will become symptomatically better but ulcer heals partially and retains its potentiality to transform into carcinoma stomach. Giant gastric ulcer is benign gastric ulcer more than 3 cm in size. Benign ulcer occurs usually in the lesser curve whereas ulcer in greater curve is commonly malignant. Barium meal X-ray shows niche (ulcer crater) and notch on opposite side (due to spasm of circular muscle). Lesser curve ulcer is usually
benign; greater curve ulcer is commonly malignant
(Fig. 20.35).
Selective angiography of superior mesenteric artery
and inferior mesenteric artery is often helpful in detecting the site of bleed. Once identified, therapeutic embolisation can be used to control the bleeding. Bleeding of 0.5 ml/minute can be detected.
Diagnostic laparoscopy; laparoscopic ultrasound are also useful.
Features of Chronic benign Gastric Ulcer
It may be due to atrophic gastritis, smoking, alcohol; Typical pain is more after taking food and is relieved by inducing vomiting. Vomiting per se as a symptom is seen in 15% cases. Appetite is normal but avoids food due to pain and so looses weight. Deep tenderness
Types of gastric ulcer (Daintree Johnson)
Fig. 20.35: Multiple ulcers in the stomach on
Features of Duodenal Ulcer
‘Hurry, worry, curry’—stress, anxiety are the basic aetiological factors; Common in blood group O positive; Helicobacter pylori infection is seen in more
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than 90% of duodenal ulcer. Other causes are NSAIDs, steroids, alcohol, smoking, hyperparathyroidism. Anterior ulcer perforates (2%); posterior ulcer bleeds (5%). Pain is typically in duodenal point. Haemate­mesis and melaena is more common. Patient has more appetite and eats more to relieve pain and so gains weight. Hunger pain, early morning pain, periodicity, water brash, melaena are other features. Complications are pyloric stenosis, bleeding, perforation and penetration into pancreas. Chronic duodenal ulcer will never turn into malignancy. Gastroscopy, biopsy for Helicobacter pylori is needed. Barium meal X-ray shows deformed or absent duodenal cap (Fig. 20.36).
Carcinoma Stomach
It is the captain of men of death. It is more common in Japan. It can be familial (Napolean family). H. pylori is the main causative agent. Diet (smoked fish), gastric polyp, pernicious anaemia, gastric remnant, smoking, alcohol, benign gastric ulcer, chronic gastritis are the other causes.
Clinical features: Recent onset of loss of appetite and weight; upper abdominal pain; vomiting with features of gastric outlet obstruction, i.e. (VGP+ve, auscultopercussion test, +ve succussion splash); Mass abdomen: Mass in pylorus lies above the umbilicus, nodular, hard, with impaired resonance, mobile, moves with respiration, all border well made out; Dysphagia when mass is in upper epigastrium; When it arises from the body of stomach, it may present as only mass abdomen. Along with jaundice, liver may be palpable with secondaries which are hard, nodular (50%) with umbilication. Ascites; +ve Troisier’s sign (Virchow’s node in neck) ; +ve rectovesical secondaries (Blumer shelf); +ve T rousseau sign - migrating thrombophle­bitis, also seen in carcinoma pancreas; anaemia, cachexia; haematemesis, malaena; occasionally carci­noma stomach can present as perforation to begin with. Rarely present as secondaries in the liver with silent primary in stomach. Secondaries in umbilicus, as sister Joseph’s nodules.
Fig. 20.36: Duodenal ulcer location.
Features of Gastric Outlet Obstruction
Pyloric stenosis is due to congenital/chronic duodenal ulcer/carcinoma pylorus. Hypochloremic, hyponatrae­mic, hypokalaemic, hypocalcaemic, hypomagnesemic metabolic alkalosis with paradoxical aciduria is typical. Persistent pain, vomiting, decreased appetite and loss of weight, without any periodicity, visible gastric peristalsis, positive succussion splash, positive auscultopercussion test are the special features. Barium meal X-ray shows—Absent duodenal cap, if it is due to cicatrised chronic duodenal ulcer; Greater curvature is below the level of iliac crest; Mottled stomach due to retained food particles which gives coated/mosaic appearance; Barium will not pass into the duodenum; Dilated stomach.
Classifications: Lauren’ s–intestinal, diffuse. Japanese (for early gastric cancer – involvement of mucosa or submucosa with or without lymph nodes) – protruded, superficial elevated or flat or depressed, excavated. Borrmann’s (for advanced cancer–involvement muscularis or serosa with or without lymph node spread) – polypoid; ulcerated with clear margin or without clear margin; diffuse; unclassified. Leather bottle stomach (Linitis plastica) is diffuse type of carcinoma of stomach with mother of pearl look with enormous proliferation of fibrous tissue in submucosa (Fig. 20.37).
Gallstones and Chronic Cholecystitis
Gallstones
Types: (1) Cholesterol stones are 6% common, often solitary . (2) Mixed stones are 90% common. It contains cholesterol, calcium salts of phosphate, carbonate,
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Fig. 20.37: Gastroscope view of bleeding
palmitate, proteins and are multiple, faceted. (3) Pigment stones: are small, black or greenish black, multiple, often they can be sludge like. Common in ‘Fat, Fertile, Forty , Flatulent, Female’. Common in western countries and in North East India.Effects of the gallstones: (a) In the gallbladder—Silent asymptomatic stones; Acute cholecystitis; Chronic cholecystitis; Empyema gallbladder; Perforation causing biliary peritonitis or peri cholecystitic abscess; Mucocele of gallbladder; Limey gallbladder; Carcinoma gallbladder. (b) In the CBD —Secondary CBD stones; Cholangitis; Pancreatitis; Mirizzi syndrome (compression of CBD by stone from cystic duct or cholecystocholedochal fistula). (c) In the
intestine—Cholecystoduodenal fistula causing gall­stone ileus and so intestinal obstruction.
Trichobezoar
It is hair-ball commonly seen in a stomach of females with psychiatric illness who swallow hair regularly.
It forms a ball like mass occupying the full stomach (Figs 20.38A and B).
Clinical features: Haematemesis; Gastritis; Loss of appetite; Perforation; occasionally mass in the epigastrium which can be molded. Barium meal is confirmative.
A
Chronic cholecystitis: It is chronically inflamed, thickened gallbladder, which is non-functioning and nondistending. Causes: Gallstones; Cholecystoses; Chronic acalculous cholecystitis.
Clinical features: 1. Pain in right hypochondrium may be colicky, or persistent. 2.Positive Murphy’s sign where, in sitting position during deep inspiration, patient winces with pain at the summit of the respiration while palpating in right hypochondrium. 3. Flatulent dyspepsia.
B
Figs 20.38A and B: Trichobezoar—endoscopic view and
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Chronic Pancreatitis
It is persistent progressive irreversible damage of the pancreas due to chronic inflammation. It can be chronic relapsing pancreatitis or chronic pancreatitis. It can be chronic non-calcifying or calcifying pancreatitis. Stones may be in the duct or in the parenchyma. Chronic pancreatitis is more common in males, common in Kerala South India (Induced by diet rich in T apioca).
Aetiology: Alcohol; stones in biliary tree; malnutri­tion, diet; hyperparathyroidism; hereditary (Familial hereditary pancreatitis); idiopathic; trauma; congenital anomaly, etc. (Pancreatic divisum).
Pathology: It shows atrophy of acini, hyperplasia of duct epithelium, interlobular fibrosis, calcifications, ductal dilatation, with strictures in the duct.
Clinical features: (1) Pain in epigastric region, persistent and severe, which radiates to back. This pain is due to irritation of retropancreatic nerves, or due to ductal dilatation and stasis, or due to chronic inflammation itself. (2) Exocrine dysfunction: Diarrhoea, asthenia, loss of weight and appetite, steatorrhoea (signifies severe pancreatic insufficiency), malabsorption, etc. (3) Endocrine dysfunction: Diabetes mellitus. (4) Mild jaundice is due to narrowing of retropancreatic bile duct and cholangitis. (5) Mass per abdomen, just above the umbilicus, tender, nodular , hard, felt on deep palpation, not moving with respira­tion, not mobile, resonant on percussion. Chronic
pancreatitis can lead to carcinoma pancreas.
Complications of chronic pancreatitis: Pseudocyst of pancreas; Pancreatic ascitis; CBD stricture; Duodenal stenosis; Portal or splenic vein thrombosis; Peptic ulcer; Carcinoma pancreas (Fig. 20.39).
Pancreatic Tumours
Classification
A: Exocrine tumours: Benign: Benign cystadenoma. It is rare. Malignant: (a) Adenocarcinoma in ampulla or periampullary region or head of pancreas. Periam­pullary carcinoma may consist any of the component
- duodenal mucosa, CBD, pancreatic duct component or all. Occasionally squamous cell carcinoma or combination of adenosquamous can occur. (b) Cystade­nocarcinoma of pancreas occurs commonly in body and tail of the pancreas, which usually attains a large size (5%). B: Endocrine tumours. C: Lymphomas.
Exocrine pancreatic tumours: Aetiology: Smoking; alcohol; high energy diet rich in fat; chronic pan­creatitis; familial pancreatitis.
Sites: Head and neck region; Ampullary and periam­pullary region; Body and tail.
Pathology: (a) 75% are adenocarcinoma, common in elderly people. Arising from primitive cells or acinar cells or duct cells. It is common in head, neck and ampullary region. Most often it begins as carcinoma in situ. (b) Cystadenocarcinomas occurs 1% of all pancreatic malignancies. They are large cystic tumours, which are slow growing, occurring in the body and tail of the pancreas. They are commonly papillary- cystic tumours. Occasionally mucinous cystic tumours are also seen.
Clinical features: Ampullary tumours mainly present with jaundice and weight loss. Carcinoma head and neck tumours present with weight loss and jaundice. Cystadenocarcinoma of pancreas present with pain, weight loss and mass.
Jaundice is of obstructive nature which is of short duration, severe, progressive, associated with pruritus (due to deposition of bile salts in the skin which releases histamine). Painless jaundice is seen in ampullary malignancies. In periampullary carcinoma necrosis of tumour occurs sometimes, as a result of which jaundice may reduce temporarily thus becoming intermittent.