Gallbladder And Pancreas Cholecystoses Complications Investigations Treatment Notes

Gallbladder And Pancreas Introduction

One may wonder why gallbladder and pancreas are discussed together!! Yes, biliary tract (gallbladder is an important part of that) ends after joining with pancreatic duct by opening into 2nd part of duodenum.

Read And Learn More: Gastrointestinal Surgery Notes

Gallstones, when they block/pass through ampulla of Vater, produce acute pancreatitis. An important surgical condition—surgical jaundice or obstructive jaundice can be discussed better only if you know gallbladder and pancreas.

• Any surgery involving sphincter of Oddi in the form of sphincteroplasty/or removal (as in Whipple’s pancreaticoduodenectomy), the gallbladder does not function and hence it needs to be removed.
• Embryologically, liver, biliary tree, ventral pancreas, gallbladder—all developed from a diverticulum on the ventral aspect of the foregut of the embryo.
• And gallbladder will be palpable in most of the cases of periampullary/carcinoma head of the pancreas.

Describe the applied anatomy of biliary system. Describe the clinical features, investigations and principles of management of diseases of biliary system.

Surgical Anatomy Of The Gallbladder And Bile Ducts

The gallbladder is a pear- or globular-shaped organ present in the right hypochondrium on the inferior surface of the liver, situated in the gallbladder fossa. It is about 8-12 cm long.

• Fundus: It is the dilated portion of the gallbladder adherent to undersurface of liver from which it can be separated easily.
• Neck: The narrow angulated distal portion of the neck is called Hartmann’s pouch—common site where stones occur and tend to stay for a long time (also called infundibulum of gallbladder).
• Gallbladder drains into the common bile duct (CBD) through cystic duct, which is 3 cm long. It is lined by cuboidal epithelium. There are prominent mucosal folds within the cystic duct due to the presence of prominent circular muscle fibres underneath.
• Its lumen is usually 1-3 mm in diameter. Contraction of gallbladder produces a functional valve called valve of Heister which prevents the migration of stone into the CBD. The wall of cystic duct is surrounded by a sphincter structure called sphincter of Lutkens. A spiral fold keeps cystic duct open for drainage of bile.

Cholecystohepatic Triangle or Calot’s Triangle Boundaries

• Lateral: Cystic duct and gallbladder
• Medial: Common hepatic duct
• Above: Inferior surface of right lobe of the liver. Calot’s triangle is dissected free of all tissue except for the cystic duct and artery, and the base of the liver bed is exposed—the critical view of safety—Strasberg et al.

Contents

• Right hepatic artery and its branch, the cystic artery
• Cystic lymph node of Lund.

Gallbladder Blood Supply

• Cystic artery, a branch of right hepatic artery, arises behind the common bile duct. Soon, it branches out over the surface of gallbladder.
• Cystic artery is an end artery. Multiple small veins from the surface of gallbladder join the liver surface. There is also a cystic vein, from the neck of gallbladder draining into portal vein directly. This explains early spread of gallbladder malignancy to the liver.

Gallbladder Lymphatics

1. Subserosal and submucosal lymph nodes drain into cystic lymph node of Lund and from here they drain into nodes in the hilum of liver and coeliac nodes.
2. Subserosal lymphatic vessels of gallbladder are also connected to subcapsular lymph channels of liver, which accounts for frequent spread of carcinoma gallbladder to the liver.

Bile Ducts Of the Anatomy

• Common hepatic duct (CHD) is formed by the union of right and left hepatic ducts. It is 3 cm long, receives cystic duct and continues as common bile duct (CBD).
• Common bile duct is about 8 cm long. It has four parts: Supraduodenal, retroduodenal, infraduodenal and intraduodenal. Along with pancreatic duct, it forms ampulla of Vater. Controlled by sphincter of Oddi, it ends by an opening into the second part of duodenum.

Physiology

Functions of the Gallbladder

• Reservoir for bile: Bile excreted by the liver is stored in the gallbladder as total of about 500 to 1000 ml per day. At fasting, the tone of sphincter of Oddi is high. Food contents in the duodenum stimulates release of cholecystokinin, which causes gallbladder to contract.
• Concentration: Bile is 98% water. Due to active absorption of water, sodium chloride and bicarbo¬nate, bile gets concentrated 5-10 times. Thus, a relative increase in bile salts, bile pigments, cholesterol and calcium occurs.
• Mucus secretion: It secretes about 20 ml mucus per day. Obstruction to the cystic duct causes mucocele of the gallbladder.

Bile

• Secreted from hepatocytes.
• pH is more than 7.0.
• 500-1000 ml/day, 98% is water.
• Concentrated in gallbladder because of absorption of water. Capacity of gallbladder is 40-50 ml.
• Fatty food stimulation releases cholecystokinin, which stimulates gallbladder to contract and at the same time, sphincter of Oddi to relax.
• It also has inorganic ions (more than plasma) and hence, severe electrolyte imbalance is seen in biliary fistula.
• Cholesterol, synthesised in the liver, gives rise to bile acids—cholic and chenodeoxycholic acids. They are metabolised in the colon to deoxycholic acid and lithocholic acids.
• Main function of bile acids in the bile is to maintain cholesterol in solution.

Chronic Cholecystitis

Recurrent attacks of cholecystitis will convert the gallbladder into a fibrosed, nonfunctioning, contracted, shrunken, small gallbladder. Gallbladder wall is grossly thickened. Stones are invariably present. Such patients present with classical fatty food intolerance. Murphy’s sign is positive.

They are diagnosed by ultrasound which reveals a small, contracted gallbladder. Oral cholecystography (OCG) used to be done to know the function of the gallbladder earlier.

Chronic Cholecystitis Treatment: Cholecystectomy

Cholecystoses

Cholecystoses Definition: Uncommon group of conditions affecting gallbladder in which there are chronic inflammatory changes and hyperplasia of all tissue elements.

Cholecystoses Types

1. Cholesterolosis (strawberry gallbladder): Aggregations of cholesterol crystals in the mucosa/submucosa. Yellow specks of cholesterol crystals are seen when
2. Cholesterol polyposis (gallbladder polyp): Polypoidal projections of mucosa in the gallbladder. Polyp longer than 1 cm or change in size require surgery.
3. Cholecystitis glandularis proliferans: Granulomatous thickening and hyperplasia of the gallbladder. All layers of gallbladder are thickened.
4. Diverticulosis of gallbladder.
5. Gallbladder wall with fistula.

Cholecystoses Clinical Features: Dyspepsia, upper abdominal discomfort, Murphy’s sign is positive.

Cholecystoses Management: Ultrasound to confirm the diagnosis followed by chole-cystectomy.

Mucocele

Mucocele: It occurs when there is a stone blocking the cystic duct and the bile is not infected.

• As a result of obstruction, all the bile within the gallbladder is absorbed and is replaced by the mucus secreted from gallbladder epithelium.
• Clinically, it results in a soft, fluctuant, globular mass in the right hypochondrium which moves with respiration. It needs cholecystectomy.

Empyema And Perforation Of Gallbladder

These are uncommon. Impacted stone, diabetes, viru-lent organisms precipitate pyocele and perforation. Patients present with high grade fever with chills and rigors, toxicity, high leucocyte count. Perforation can cause local abscess, if there are adhesions due to previous inflammation.

Perforation into the general peritoneal cavity is rare but produces diffuse biliary peritonitis which has a high mortality rate. Urgent laparotomy, aggressive resuscitation, good antibiotic cover may help in reducing mortality. At laparotomy, removal of gallbladder is difficult. Hence, drainage of the pus and cholecystostomy with removal of gallstones can be done.

Empyema and perforation of gallbladder are Three types:

1. 1. Localised perforation with pericholecystic abscess— managed by catheter drainage.
   2. Free perforation into peritoneal cavity and peritonitis—urgent laparotomy drainage.
   3. Hollow viscous perforation (duodenum).

Carcinoma Of Gallbladder

Carcinoma Of Gallbladder: Long-standing gallstones can bring about squamous metaplasia of gallbladder epithelium and can cause carci¬noma of gallbladder. However, the incidence is very low. Hence, routine cholecystectomy is not advised for silent gallstones. Porcelain gallbladder is a precancer condition.

Cholecystoses Porcelain Gallbladder

• It occurs due to deposition of calcium carbonate in the gallbladder wall.
• Diagnosis can be made by plain X-ray of the abdomen.
• On ultrasound examination, calcification appears as hyperechoic semilunar structure with dense posterior acoustic shadowing.
• In case of difficulties, CECT can help to differentiate it from gallstones.
• Incidence of carcinoma gallbladder is around 1 to 5%.
• Prophylactic cholecystectomy is indicated.
• One should be ready to do hepatic resection, if required.

Cholecystoses Mirizzi Syndrome

1. Type 1: Compression of CBD without lumen narrowing.
2. Type 2: Compression of CBD with lumen narrowing.
3. Type 3: Compression causing CBD wall necrosis.
4. Type 4: Stone ulcerating into CBD resulting in chole- cystocholedochal fistula. It is treated by ERCP.

Laparoscopic Cholecystectomy

Laparoscopic Cholecystectomy It has become the most popular choice today. More than 95% of gallbladders can be removed through a laparo¬scope. Some principles and procedure of laparoscopic cholecystectomy are discussed below.

Laparoscopic Cholecystectomy Procedure

• 1 cm incision is made below the umbilicus, through which a pneumoperitoneum is maintained by CO₂ insufflation.
• Following this, a laparoscope is introduced and a camera is attached. Three small, 1 cm incisions are made in epigastrium and V cm in the right hypochondrium. These are used for suction, instrumentation, cauterisation, dissection, retraction purpose—dissection port.
• Gallbladder is mobilised by dissecting Calot’s triangle by isolating cystic duct and cystic artery. Retraction of Hartman’s pouch laterally opens up Calot’s triangle.

Thus, it gives a view of liver bed and two structures— cystic artery and cystic duct. It is called critical view of Strasberg.

• Cystic duct and cystic artery are clipped and gallbladder is removed using gallbladder-holding forceps and is brought outside through the epigastric port.
• Bleeding from liver is controlled using lasers/cautery.
• The procedure is done under general anaesthesia. It may take 1-3 hours depending upon the experience of the surgeon.

Laparoscopic Cholecystectomy Advantages

• Hospital stay is 1-2 days, recovery is very fast.
• Pain is minimal. Hence, mobilisation of the patient is much better and easy.
• It gives an acceptable and better cosmetic result.
• Complications such as adhesions and incisional hernia are rare.
• Conversion to open when
• Very badly contracted, fibrosed gallbladder.
• Very difficult gallbladder—Calot’s triangle anatomy is not defined well. Dissection may cause injury to the bile ducts and can cause stricture. Partial cholecystectomy is a safe alternative.

Medical Treatment Of Gallstones

 It is indicated for pure cholesterol stones only.

• Patient Selection
  • Patients with functioning gallbladder proven by OCG or scintigraphy.
  • Young, thin, female patients.
  • Tiny (<5 mm), translucent, floating stones.
• Drawbacks
  • Recurrence of stones once treatment is stopped.
  • Lifelong maintenance is needed.
  • After dissolution of the stones, lithotripsy or extra-corporeal shock wave lithotripsy should be done.

Types of Medical Treatment

1. Oral Dissolution Treatment
   • Drugs used: CDCA—chenodeoxycholic acid UDCA—ursodeoxycholic acid
   • Mechanism of action: They inhibit HMG-CoA, a rate-limiting step in the synthesis of cholesterol, thereby increasing the bile salt pool. UDCA also acts by decreasing cholesterol absorption in GIT.
2. Direct Contact Dissolution: MTBE—methyl tert-butyl ether is the drug which is given through a catheter placed in gallbladder percutaneously.
   • Drawbacks: Explosive and toxic, if it enters bile duct or duodenum.
   • Indications: High-risk patients with symptomatic stones, refusing surgery. The patient must have patent cystic duct (proven by OCG/scintigraphy).
   • Side effects: Haemorrhage and catheter displacement.

Thus we have completed gallstones and their complications in the gallbladder. Now we will study the complication of gallstones in the common bile duct, mainly obstructive jaundice.

Obstructive Jaundice (Surgical Jaundice)

Obstructive Jaundice (Surgical Jaundice) Definition: Jaundice that occurs due to obstruction to the outflow of bile is called obstructive jaundice.

• Since these cases have to be managed by surgical intervention, it is also called surgical jaundice.
• However, haemolytic jaundice cases are not obstructive but a few are managed by splenectomy hence it is called as surgical jaundice.
• Before we start a detailed discussion of obstructive jaundice, we will study anatomy of the pancreas. This is an important long case in the university examina¬tion. For a better understanding of obstructive jaundice, students are requested to understand various causes of obstructive jaundice which are given in the subsequent pages.

 

Describe the types, etiopathogenesis, clinical features, investigations and management of chronic pancreatitis. Also the various surgical modalities available for treatment of chronic pancreatitis.

Chronic Pancreatitis Definition: Diffuse inflammatory process of pancreas involving head, body and the tail resulting in permanent structural and functional damage to the pancreas.

Chronic Pancreatitis Causes

1. Alcohol: High alcohol consumption is the most frequent cause. Alcohol stimulates pancreatic secretion rich in protein. This forms plugs in the pancreatic duct and results in stasis of secretion and stone formation. Alcohol also causes spasm of sphincter of Oddi.
2. Idiopathic: It is common in Kerala, and was thought to be due to consumption of tapioca. It is also called Kerala pancreatitis or tropical pancrea-titis. It is now thought to be due to malnutrition. It is also called fibrocalculous pancreatic diabetes.
3. Hereditary pancreatitis: It is a genetic disorder transmitted as a Mendelian-dominant trait.
4. Cystic fibrosis: Generalised dysfunction of exocrine glands causes secretions to precipitate in the lumen.
5. Hyperparathyroidism favours precipitation of calcium intraductally. It can also activate pancreatic enzymes.
6. Autoimmune pancreatitis: Diffuse enlargement of pancreas and narrowing of pancreatic duct is seen. Autoantibodies may be present. IgG4 is increased. Multiple joint pains, salivary gland infections may give clue to the diagnosis.

Chronic Pancreatitis Pathology: There is destruction of pancreas by ductal sclerosis, ductal strictures, glandular fibrosis and calcification, both intraductal and parenchymal.

Chronic Pancreatitis Idiopathic Type

• Common in warm climates (Kerala)
• Common in young age
• High incidence of diabetes
• High incidence of stones in the duct
• Increased chances of parenchymal calcification
• Increased chances of pancreatic cancer

Chronic Pancreatitis Clinical Features

• Malabsorption occurs due to damage to exocrine glands resulting in steatorrhoea—10 to 15 stools per day, bulky, frothy, rich in fat, foul-smelling. Mal-absorption indicates late disease and results in weight loss. Creatorrhoea refers to excessive loss of protein.
• Obstructive jaundice can occur due to oedema of the head of pancreas. Later, fibrous constriction of CBD due to fibrotic indurated mass in the head region can cause jaundice by compressing the CBD.
• Pain abdomen—upper abdominal pain radiating to the back in the region of L1 and L2 due to retro-peritoneal inflammation. Pain may be severe, sometimes radiating to both right and left sides. The pain is due to multiple strictures in the pancreatic duct increasing the intraductal pressure. It is relieved on stooping forward.
• Exploratory laparotomy—many cases are diagnosed at laparotomy where irregularity and hardness involving the entire pancreas are seen. Exploration is done for some other pathology.
• Diabetes—incidence of diabetes is about 10-20%. It should be suspected in diabetic patients with pain abdomen.

Pain in Chronic Pancreatitis

• Parenchymal hypertension
• Perineural inflammation
• Ductal hypertension
• Pseudocyst formation
• Stenosis of bile duct

Chronic Pancreatitis Investigations

• Plain X-ray abdomen can demonstrate stones in the pancreatic duct or parenchymal calcification.
• USG can detect the stones, stricture, dilatation and associated cysts.
• ERCP
  • Ductal distension, ductal stricture
  • Dilated pancreatic duct (diameter of the normal duct is 2 mm)
  • Demonstration of stones—appear as regular filling defect.
• CT scan: It can reveal ductal anatomy, head mass, size and configuration of pancreas.

Chronic Pancreatitis Complications

• Obstructive jaundice due to a mass lesion in the head region
• Carcinoma of pancreas
• Pseudocysts
• Steroids in autoimmune pancreatitis

Chronic Pancreatitis Treatment

1. Conservative
   • Pain relief by analgesics, epidural analgesia, or splanchnic nerve block. Slow release opioid skin patches are useful.
   • Supplement pancreatic enzyme — diet should be low in fat and vitamin D supplements should be given.
   • Pancreatic enzymes not only help in treating exocrine insufficiency but they also denature CCK releasing peptide, thereby diminishing the release of CCK. Thus, pain is decreased. Six capsules of pancreatin are given.
   • Control diabetes, stop alcohol consumption and tobacco smoking, antioxidants may help.
2. Surgery
   • Surgery Indications
     • Unrelieved pain
     • Suspicion of carcinoma
     • Complications:
       • Ascites
       • Cysts
       • Abscesses
       • GI bleeding—left-sided, portal hypertension, pseudoaneurysm
       • Obstructive jaundice
       • Duodenal obstruction

Chronic Pancreatitis Types Of Surgery

1. Chronic pancreatitis involving tail of pancreas: Distal pancreatectomy with removal of spleen.

2. Diffuse chronic pancreatitis with dilated (large duct) pancreatic duct

• Duct is laid open widely, strictures are cut open, stones are removed and it is anastomosed to a loop of jejunum—longitudinal pancreaticojejunostomy (LPJ)—Puestow’s operation (Roux-en-Y jejunal segment). The duct should be at least 6 mm in diameter. Sutures hold very nicely because of fibrosis of pancreas. Pain relief is obtained in about 80% of the cases. Pancreatic fistula is a complication of this surgery. Majority of the fistulae close spontaneously.
• This is a bypass procedure which preserve endo-crine and exocrine functions.

3. Chronic pancreatitis with a head mass: In this situation, doubt arises whether it is malignancy or not. Even trucut biopsy and frozen section are not foolproof. Hence, pancreaticoduodenectomy is advised, provided experience of the surgeon is good and the mortality rate is less than 5%.

4. Chronic pancreatitis with bile duct obstruction: If malignancy is ruled out, a bypass procedure is the treatment of choice.

• Choledochojejunostomy is the ideal treatment.
• Pancreaticoduodenal resection (Whipple) can also be done (as mentioned above).

5. Chronic pancreatitis with duodenal obstruction: Here also, resection of the head mass or gastro-jejunostomy is the treatment of choice.

6. Chronic pancreatitis with ascites: Treatment of choice is Puestow’s operation (stenting may also relieve ascites).

7. Resection: A duodenum-preserving pancreatic head resection is called Hans Beger’s procedure. Head-coring procedure is called Frey procedure.

Chronic Pancreatitis Head-coring—Frey Procedure

• Pathologic key to recurrent pancreatitis is localised to pancreatic head. It is called pacemaker.
• It is located in the crucial triangle which has to be excised.
• Pain and recurrent pancreatitis will decrease after Frey procedure.
• Surgery can be done with minimum blood loss.
• Try avoiding injury to lower CBD—if necessary, CBD can be opened and a sound can be introduced.

Cholangiocarcinoma – Bile Duct Carcinoma

Enumerate the types, etiopathogenesis, clinical features, investigations and management of cholangiocarcinoma.

Cholangiocarcinoma Risk Factors

• Cholangitis—primary sclerosing
• Colitis—ulcerative
• Clonorchiasis
• Choledochal cyst
• Caroli’s disease
• Chemical carcinogens like thorium, nitrosamines, diosmin
• Patients having following diseases have increased risk of developing cholangiocarcinoma.
• It is an uncommon cause of obstructive jaundice.
• Elderly males >60 years are commonly affected.
• Obstructive jaundice is the presenting feature.
• Tender hepatomegaly is present due to congestion and may be due to cholangitis.
• Gallbladder is not palpable in cases of cholangio- carcinoma unlike in periampullary carcinomas.
• Cholangiocarcinoma at the bifurcation of the hepatic duct is called Klatskin’s tumour.

Cholangiocarcinoma Types

1. Perihilar is the most common, Klatskin’s tumour comes under this.
2. Intrahepatic (10%)
3. Distal (CHD-CBD) 25%

Cholangiocarcinoma Management

• Abdominal ultrasound, CT scan, ERCP will help in localising the site of obstruction. ERCP and stenting the CBD is indicated in inoperable cases. However, MRI is better.
• Treatment is difficult because most of the lesions are high up in the hilar region infiltrating the liver, portal vein, etc. Resection and hepaticojejunostomy or endoscopic stent placement are the treatment modalities available.
• Resection involves liver for hilar growth and for lower end growth.

Congenital Biliary Atresia

Aetiopathogenesis: A disease of unknown aetiology, though rare, is fatal. Viral aetiology and defective embryogenesis have been blamed for the development of biliary atresia.

Congenital Biliary Atresia Types

1. Type 1: Common bile duct is involved.
2. Type 2: Common hepatic duct is involved.
3. Type 3: Atresia of right and left hepatic ducts.

Congenital Biliary Atresia Clinical Features

• It presents as jaundice at birth or in the neonatal period.
• Due to absence of bile in the gut, meconium is not bile-stained. Hence, stools are pale.
• Gradually, due to backpressure, liver enlarges.
• Enlargement of the spleen may follow, if there is development of portal hypertension.
• Steatorrhoea, pruritus and clubbing are the other features.

Congenital Biliary Atresia Treatment

• Surgical drainage of bile is the only available treatment provided patent bile duct or radicle is seen. Anastomosis of Roux-en-Y loop of jejunum to the dilated bile duct or sometimes excision of bile duct tissue up to the liver capsule should be done followed by Roux-en-Y anastomosis. This is called Kasai’s portoenterostomy.
• Liver transplantation is the choice when there is atresia of the intrahepatic duct.

Congenital Biliary Atresia Complications

1. Recurrent cholangitis giving rise to hepatic fibrosis.
2. Biliary cirrhosis and portal hypertension.

Carcinoma Of Gallbladder

Carcinoma Of Gallbladder Incidence: It is common in North Eastern India. Occurs in elderly patients in their sixties/seventies.

Aetiology

• Gallstones: 80–90% of gallbladder cancers are associated with gallstones. Calcification of gallbladder is associated with carcinoma gallbladder. Porcelain gallbladder is a precancerous condition. Incidence of malignancy may range from 1 to 5% of cases.
• Chemicals: High incidence of gallbladder and biliary cancer is noted in people who work in rubber industries.
• Gallbladder polyp
• Dietary: Adulterated mustard oil for cooking is found to precipitate carcinoma gallbladder.

Pathology

• 85% of cases. It is usually adenocarcinoma. Undifferentiated carcinoma and squamous cell carcinoma may also occur. The tumour is most commonly nodular, infiltrates the entire gallbladder and adjacent tissues.
• Three types of adenocarcinomas have been identified: Nonpapillary adenocarcinoma, papillary adenocarcinoma and mucinous adenocarcinoma. Majority are nonpapillary adenocarcinoma.

Carcinoma Of Gallbladder Clinical Features

• Significant weight loss, jaundice and mass in the right upper quadrant are common presentations. Clinically, it is palpable as a hard irregular mass.
• A few cases can present as chronic cholecystitis with a mass or acute cholecystitis. Ultrasonography may diagnose as stones and they are subjected to cholecystectomy. During surgery or postoperatively, the diagnosis gets confirmed.
• Obstructive jaundice, bleeding, ascites are late features.

Carcinoma Of Gallbladder Staging

• Tumour (T)
  • TX Primary tumor cannot be
  • T0 No evidence of primary tumor
  • Tis Carcinoma in situ
  • T1 Tumor invades lamina propria or muscular layer
  • T1a Tumour invades lamina propria
  • T1b Tumour invades muscular layer
  • T2a Tumour invades the perimus- cular connective tissue on the peritoneal side without involving the serosa
  • T2b Tumour invades the perimus- cular connective tissue on the peritoneal side without involving the liver
  • T3 Tumour perforates the serosa (visceral peritoneum) and/or directly invades the liver and/or one other adjacent organ or structure, such as the stomach, duodenum, colon, pancreas, omentum, or extrahepatic bile ducts
  • T4 Tumour invades main portal vein or hepatic artery or invades at least two extra- hepatic organs or structures
• Metastases (M)
  • M No distant spread assessed
  • M1 Distant spread
• Nodes (N)
  • Nx Regional lymph nodes cannot
  • N0 Regional lymph node metastasis
  • N1 Metastases to 1 -3 lymph nodes
  • N2 Metastases to >4 lymph nodes
• Stagging
  • Stage 0—Tis, N0, M0 be assessed
  • Stage 1—T1, N0, M0
  • Stage 2A—T2a, N0, M0
  • Stage 2B—T2b, N0, M0
  • Stage 3A—T3, N0, M0
  • Stage 3B—T1 to T3, N1, M0
  • Stage 4A—T4, N0 or N1, M0
  • Stage 4B—Any T, N2, M0; Any T, any N, M1

Carcinoma Of Gallbladder Investigations

• CA 19-9 is elevated in 80% patients.
• Ultrasonography and endosonography are very useful investigations. Ultrasonography-guided FNAC can be done for histological diagnosis in suspected cases of gallbladder mass.
• CT scan is useful for staging—lymph nodes meta¬stasis in the liver.
• ERCP, if there is obstructive jaundice to localise the exact site and nature of obstruction.
• Diagnostic laparoscopy. If peritoneal metastasis is present, it is not worth resecting.
• MRCP can be done. It visualises bile duct better than CT scan.

Carcinoma Of Gallbladder Treatment

• If gallbladder cancer is found at cholecystectomy and if mucosa alone is involved, then cholecystectomy is sufficient.
• If gallbladder wall is involved, then extended chole-cystectomy is done.
• Radiation has very small benefits.
• Chemotherapy also has been tried. 5-FU, mitomycin C, doxorubicin are the drugs used.

Carcinoma Of Gallbladder Extended Cholecystectomy

Carcinoma Of Gallbladder Prognosis: In general, five-year survival is very poor. Aggressive surgery and complete clearance give best result.

Gallbladder Cancer is the Worst, Why?

• Biologically very aggressive cancer (unlike basal cell cancer, carcinoma colon, etc.)
• High incidence of lymphatic spread
• Easily spreads into liver by direct infiltration
• Spreads by blood, neural, intraperitoneal routes
• Intraductal extension into CBD causes obstructive jaundice
• Infiltration into stomach, colon, duodenum and liver can occur because of its location
• Radiation and chemotherapy is rarely of any benefit

Carcinoma Of Gallbladder Rare or Uncommon Causes of Obstructive Jaundice: Parasites such as ascariasis, Clonorchiasis sinensis and biliary hydatid can give rise to obstructive jaundice. Thus, we have discussed various causes of obstructive jaundice. Students should be able to differentiate between all these different causes and to offer an appropriate diagnosis in the examination. Each of these short topics can be asked as short notes in the theory paper and short cases.

Endocrine Tumours Of The Pancreas

These tumours are members of APUDOMA arising from APUD (Amine Precursor Uptake Decarboxylation) cells. They are neuroectodermal in origin. Accordingly, following tumours can occur.

Endocrine Tumours Types

• Sporadic: Usually occurs as a single tumour.
  
• Familial: Occur with other adenomas as in multiple endocrine neoplasia syndrome—MEN Type 1: Pituitary, parathyroid, pancreatic adenoma

Insulinoma (β-Cell Tumour)

Most common functioning islet cell tumour. Majority of the insulinomas occur in the tail and body of pancreas and majority of them are benign, one- third are malignant and one-third are multiple. It can be a single adenoma, can be due to diffuse hyperplasia or due to carcinoma.

Clinical features are that of hypoglycaemia.

• In early stages, it can mimic a duodenal ulcer. Due to hypoglycaemia, hunger pain develops and a tendency to ask for food is present.
• As it becomes severe, giddiness, dizziness, syncopal attacks, blurring of vision and diplopia can occur.
• Late stages—epilepsy, semiconsciousness and coma.

Persistent Hypoglycaemia—Causes

• Insulinoma
• Hepatoma
• Hepatocellular damage
• Hypopituitarism
• Addison’s disease
• Large mesenchymal tumour

Whipple’s Triad of Insulinoma

1. Attack of hypoglycaemia in morning hours, in the fasting state.
2. Symptoms are relieved on taking glucose.
3. Blood sugar in the fasting state is less than 45 mg% during the attack.

Insulinoma Investigations

1. Serum insulin levels done by immunoassay method are found to be very high. Proinsulin levels and C- peptide level are also very high.
2. Persistent hypoglycaemia—blood sugar level of less than 50 mg/dl relieved by glucose is suggestive of insulinoma.
3. USG and CT scan of abdomen can demonstrate the tumour, if it is more than 2 cm. (Intraoperative ultrasound is a useful test.)
4. Selective angiography will demonstrate tumour blush as majority of them are very vascular.

Insulinoma Treatment

• Enucleation is the treatment of choice.
• Resection of the tumour and if necessary distal pancreatectomy can also be done in selected patients.
• Diazoxide is given to suppress insulin release.
• For inoperable islet cell carcinoma, streptozocin is the best chemotherapeutic agents.

Insulinoma—interesting most

• The most common functioning islet cell tumour of pancreas
• Mostly are single (75%)
• Mostly multiple in ‘MEN’ syndromes
• Mostly benign (70%)
• Mostly occur in tail and body of pancreas
• Mostly present as bizarre behaviour confusing type due to hypoglycaemia
• Most useful diagnostic test—very high (disproportional) levels of insulin during fasting hypoglycaemia
• The most important test to localise the tumour before surgery is CT/MRI
• The most important test to localise at surgery is intra-operative ultrasound
• Mostly they can be enucleated when occur in the head
• Most insulinomas are small, less than 2 cm

Gastrinoma (Zollinger Ellison Syndrome)

Two types are recognised.

1. Type 1 (rare): These have antral G cell hyperplasia, wherein gastrin is stored. Hypergastrinaemia with chronic peptic ulceration is a feature. Pancreas is normal.
2. Type 2: May be due to an ulcerogenic, non-β-islet cell tumour or sometimes diffuse hyperplasia of the islet cells. Tumour secretes gastrin and is usually found in the tail of the pancreas. 50% of them are malignant
   • Intractable peptic ulceration, hypergastrinaemia with massive acid hypersecretion of up to 500 ml/hr can occur.
   • Diarrhoea, steatorrhoea and hypokalaemia occur due to acid irritating the small bowel activity.

Gastrinoma Site: It commonly occurs in the gastrinoma triangle also called Passaro’s triangle. Following three points form Passaro’s triangle.

1. Junction of the cystic duct with the common bile duct.
2. Junction between head and neck of pancreas.
3. Junction between second and third parts of the duodenum.

Gastrinoma Diagnosis

1. Endoscopy will show prominent mucosal folds and large amount of acid in the stomach.
2. Serum gastrin is increased above normal levels (normal value <150 ng/dl).
3. CT scan and arteriography may localise the tumour.

Gastrinoma should be Suspected in Following Situations

1. Unusual ulcer: Peptic ulcer not responding to intensive medical treatment.
2. Unusual recurrence: Multiple recurrences in spite of the treatment.
3. Unusual number: Multiple ulcers scattered in the GIT.
4. Unusual sites: Ulcers present in the 2nd part of duodenum, an ulcer just distal to the ligament of Treitz.
5. Unusual age: Sudden development of an ulcer in a young boy or in a very elderly patient.

Gastrinoma Treatment

1. Type 1: Partial gastrectomy to remove G cells-bearing area.
2. Type 2: If the tumour is small, removal of the tumour can be done (enucleation).
3. If the tumour is large, omeprazole 20 mg twice a day or somatostatin derivatives have been used to control acidity. Total gastrectomy is the last resort, if gastri¬noma is not found.

Glucagonoma

It arises from alpha cells producing glucagon. Around 90% are in the body and tail. Clinically, it presents with extensive necrolytic migratory erythematous rashes. Rashes occur due to low amino acid levels due to gluconeogenesis brought about by glucagon. Rashes involve legs and perineum.

• Age range is 20-70 years.
• This is common in women.
• Mild diabetes, weight loss, diarrhoea are the other features.
• Glucagon levels are increased in serum diagnostic.
• Localisation is by elective arteriography and CT scan.
• Treatment is enucleation.

Treatment Principles of Glucagonoma

• Correction of malnutrition by TPN (total parenteral nutrition).
• Treatment with somatostatin analogues.
• Enucleation is easy, if it is in the head.
• Considerable palliation, even if subtotal removal is achieved.
• Low dose heparin—before and after surgery— because of high risk of DVT—pulmonary embolism.
• Streptozocin and dacarbazine are the most effective chemotherapeutic agents.

Thus, endocrine tumours of the pancreas are rare but when they occur, they can present with varying clinical manifestations which confuse a clinician. A high index of suspicion is necessary. They may be benign but can be fatal, if left untreated.

Acute Pancreatitis

Describe the clinical features, principles of investigation, prognosis and management of pancreatitis.

Pancreatitis Definition: It is defined as acute nonbacterial inflammatory condition caused by activation, interstitial liberation and autodiges-tion of pancreas presenting as acute abdominal pain.

• Acute pancreatitis stings like a scorpion (produces severe pain).
• Acute pancreatitis drinks like a fish (produces dehydration).
• Acute pancreatitis eats like a wolf (pancreatic necrosis).
• Acute pancreatitis burrows like a rodent (produces fistula).
• Acute pancreatitis kills like a leopard (life-threatening).

Classifications

1. Marseille’s classification
2. Modified Atlanta classification

 

1. Marseille’s Classification
   1. Acute pancreatitis
   2. Acute relapsing pancreatitis
      • In both these conditions, pancreas returns back to normal.
   3. Chronic pancreatitis
   4. Chronic relapsing pancreatitis
      • In both these conditions, there is always permanent damage to the pancreas.
2. Modified Atlanta Classification: The latest classification which is used is given in Tables.

Aetiology

1. Alcohol abuse (40 to 50%): It is the major cause of acute pancreatitis in our country and is seen in about 50% of the cases. Alcohol stimulates pancreatic secretions rich in protein, forms protein plugs and results in obstruction to the pancreatic duct. Alcohol stimulates trypsinogen. It causes spasm of sphincter of Oddi. It also has direct toxic effect on the pancreas. Tobacco smoking contributes to its effects.
2. Biliary tract disease: Stone in the biliary tree (gallstone pancreatitis) is the major cause of acute pancreatitis in the Western world (40%). In our country, it may be responsible for pancreatitis in about 20–30% of patients.
3. Collagen vascular disorders: Autoimmune disease, such as polyarteritis nodosa, can be a causative factor in acute pancreatitis.
4. Drugs: Corticosteroids, tetracycline, oestrogens, azathioprine, valproic acid and diuretics can cause pancreatitis.
5. Endoscopic procedures: Sphincterotomy, cannulation of CBD or pancreatic duct, or basketing of stones from CBD can precipitate acute pancreatitis by duct disruption and enzyme extravasation.
6. Familial or genetic factors have been blamed for acute pancreatitis. Hereditary pancreatitis may be due to mutation of cationic trypsinogen gene. Symptoms begin in early childhood.
7. Hyperparathyroidism causing hypercalcaemia may stimulate pancreatic juices and can cause pancreatitis. It also facilitates precipitation of calcium in the ducts.
8. Hyperlipidaemia (>1000 mg/dl of triglycerides) can also cause pancreatitis. Dietary control can cure pancreatitis.
9. Hypothermia and hypotension can cause ischaemia to the pancreas resulting in acute pancreatitis.
10. Injury to the pancreas either postoperative or following penetrating injury can result in pancreatitis.
11. Infection: Viruses such as Mumps and Coxsackie can cause pancreatitis. Scorpion sting can also cause pancreatitic abnormality.
12. Ductal: Around 20%. Some of them are due to pancreatic divisum seen during ERCP. The opening of the minor papilla is inadequate for drainage of pancreatic juice.
13. Postoperative pancreatitis
    • It follows operations on CBD—open or laparo-scopic. More common after T-tube insertions (now it is less).
    • Sphincteroplasty, ERCP, stone extractions
    • Pancreatic biopsy
    • Gastrectomy (distal/total)
    • Cardiac surgery. Here risk factors are periopera-tive administration of calcium, postoperative hypotension, preoperative renal failure.
14. Idiopathic: It is seen in about 15% of cases. Even though, classified as idiopathic (no cause is found), they are founs to have sludge or gallstone undected by ultrasound examination

Quick Reference to Common Causes of Pancreatitis

• Pancreatitis in teens—suspect hereditary or APBDJ
• Pancreatitis in women—suspect gallstones
• Pancreatitis in males—alcoholic pancreatitis
• Pancreatitis with fleeting joint pains—autoimmune pancreatitis
• Pancreatitis with bony lesions/cysts—hyperpara-thyroidism
• Pancreatitis with fever—viral

Pathogenesis: Autodigestion is the final common pathway leading to pancreatitis, a few theories have been explained as possible factors for autogenesis.

1. Obstruction/secretion: Recurrent attacks of pan-creatitis as in chronic cases can be due to multiple strictures, stasis, resulting in autodigestion.
2. Common channel theory: In about 90% of cases, bile duct and pancreatic duct converge into ampulla of Vater. However, only in 10% of cases, they have common channel. Reflux of bile into pancreas has been blamed for ‘gallstone pancreatitis’. However, strong evidence is lacking.
3. Duodenal reflux: Activation of enzymes takes place in the duodenum through action of entero- kinase. Hence, it is postulated that duodenal reflux is one of the causes of acute pancreatitis.
4. Back diffusion: Back diffusion of pancreatic enzymes through the ductal epithelium is a possible factor, when damaged by alcohol/bile acids, etc.
5. Systemic sepsis: Organ failure
   • ARDS, renal failure
   • Endotoxins originate from bacteria.

Acute pancreatitis is an autodigestion following activation of trypsinogen. This is brought about by various agents mentioned above. It may also be due to reflux of bile into the pancreas. Trypsinogen is converted into trypsin. It acts and stimulates:

1. Lipase: Lipase splits the fat into fatty acids and glycerol. Fatty acids combine with calcium to form calcium soap. This is represented as fat necrosis seen in the omentum, subsynovial pockets of knee joint, etc. This also explains hypocalcaemia and tetany seen in acute pancreatitis.
2. Elastase: It digests the elastic fibres of the blood vessels resulting in rupture and haemorrhage into the peritoneal cavity.
3. Lysolecithinase: This is derived from the bile. It produces extensive tissue necrosis resulting in destruction of pancreas.
4. Prostaglandins, bradykinins, kallikrein, etc.: These are the inflammatory mediators. They produce profound hypotension, shock and collapse, due to loss of fluid in the retroperitoneum (3 space loss).
5. Extensive necrosis of pancreas: It produces MDF (myocardial depressant factor) which depresses ventricular contraction resulting in cardiac failure. Ultimate result is the development of multiorgan failure.

Pancreatitis Clinical Features

• Symptoms: Severe upper abdominal epigastric pain radiating to the back increases over a period of hours—illimitable agony is a characteristic feature. It is partially relieved on stooping and bending forwards (Mohammedan Prayer sign). A meal or alcohol triggers the pain.
  • Vomiting—frequent and effortless due to reflex pylorospasm.
  • Fever—low grade.
  • Haematemesis and melaena can occur due to necrosis of duodenum. It is a poor prognostic
• Pancreatitis sign.
  • Febrile, tachypnoeic patient in agony.
  • Cyanosis—improper perfusion of lungs.
  • Faint jaundice due to oedema of the head of the pancreas.
  • Features of shock—feeble pulse, tachycardia, hypo-tension, cold extremities.
  • Abdominal findings
    • Tenderness in epigastrium
    • Upper abdominal guarding and rigidity
    • Distension of the abdomen
    • Mass in epigastrium
    • Muscle guarding
    • Abdominal distension due to either accumulation of blood or fluid in the peritoneal cavity or due to paralytic ileus.
  • Cullen’s sign: Bluish ecchymotic dis-colouration seen around umbilicus (first described for ruptured ectopic pregnancy).
  • Grey Turner’s sign
    • Bluish discolouration in the flanks
    • Both these signs are due to peripancreatic and retroperitoneal haemorrhage and seepage of blood along fascial planes, into the anterior abdominal wall and spread through falciform ligament.
  • Evidence of respiratory signs: Tachypnoea, dullness, effusion, crepitations, rhonchi (pulmonary oedema, ARDS).

Pancreatitis Systemic Complications:

• Disseminated intravascular coagulation as evidenced by:
  • Platelet count <100,000 cells / cumm
  • Fibrinogen <1 g/l
  • Fibrin split products >80 μg/dl
• Metabolic disturbance (serum calcium <7.5 mg/dl)

Pancreatitis Local Complications

• Necrosis
• Abscess
• Pseudocyst

Pancreatitis Investigations

1. Haemogram (CBP): Hb% may be low due to haemorrhagic pancreatitis. Total count is raised above 15,000 cells/mm³ due to inflammation.

2. Blood for urea, creatinine to rule out renal failure.

3. Serum amylase (widely used test)-Normal levels are 40-80 Somogyi units.

• Increased Amylase Levels—Seen in
  • Acute pancreatitis and its complications
  • Parotitis
  • Afferent loop obstruction
  • Spasm of sphincter of Oddi
  • Biliary peritonitis—duodenal injuries
  • Mesenteric infarction
  • Ruptured ectopic gestation
• Values around 400 are suggestive and values more than 1000 Somogyi units are diagnostic of acute pancreatitis.
• It is increased in the first 24-48 hours and returns to normal within 3-4 days.
• Persistent high level of amylase in acute pancreatitis indicates:
  • Unresolving inflammation
  • Recurrent attacks of pancreatitis
  • Complications—pseudocyst, pancreatic abscess
  • Serum lipase levels—more specific but difficult to measure. Lipase is only secreted by pancreas.

4. Blood and urine sugar estimation: Glycosuria is present in almost 100% of patients.

5. Serum calcium levels: Hypocalcaemia is seen, due to hypoalbuminaemia or fat necrosis.

6. Total proteins are usually low, especially albumin.

7. Plain X-ray abdomen (erect position)

• Calcification suggests chronic pancreatitis.
• To rule out perforation of peptic ulcer.
• Sentinel loop sign—one dilated jejunal loop of intestine which is seen in the region of pancreas.
• Colon ‘cut-off’ sign refers to mild distension of transverse colon with collapsed descending colon.

8. Abdominal ultrasound—can demonstrate oede- matous pancreas, fluid in the abdomen or biliary tract disease.

9. Contrast enhanced CT scan of abdomen is done after 3-5 days in patients who fail to respond to conserva-tive treatment. If CT scan demonstrates infected necrosis, an urgent CT-guided FNAC is done and Gram stain is sent. If Gram stain is positive, it has to be treated urgently.

Indications for CT scan in acute pancreatitis

• Patients with severe pancreatitis
• When the diagnosis is in doubt
• Patients with organ failure
• Patients with sepsis
• Localised complications such as pseudocyst, pseudoaneurysms
• Clinical deterioration

Pancreatitis Prognostic Indicators/Criteria: There are several scoring systems available, a few important ones have been given below. Atlanta’s Criteria for Acute Pancreatitis is applied for organ failure. Ranson score is applied for severity prediction and Balthazar score is applied for CT severity index.

Atlanta’s criteria for acute pancreatitis: Organ failure as defined

• Shock (systolic blood pressure <90 mmHg)
• Pulmonary insufficiency (PaO2 <60 mmHg)
• Renal failure (creatinine level >2 mg/ dl after fluid resuscitation)
• GI bleeding (>500 ml/24 hr)

Balthazar-Ranson criteria for severity or computed tomography severity index (CTSI): Severe pancreatitis is defined by the presence of any evidence of organ failure or a local complication.

Pancreatitis Management: Almost always conservative. However, a few scoring systems have been followed. Early aggressive fluid replacement is the key in the management of acute pancreatitis.

Even though management principles of any acute abdomen includes nil per oral’ so as to give rest to the part, in cases of pancreatitis it has been divided broadly into three categories. It is desirable to know the treatment followed for these categories. It has been given in Table.

Those of you who find it difficult can remember at least a few fundamentals of managing acute pancreatitis. They are given in the form of simple headlines: ABCDEF

A: Aspiration with Ryle’s tube, to give rest to the pancreas in cases of vomiting (may be for one or two days).

B: Blood transfusion if Hb% is low, or albumin and amino acids if proteins are low.

C: Charts—increasing pulse, increasing temperature indicates pancreatic necrosis which requires different care

D: Drugs and fluids: Drug of choice in acute necrotizing pancreatitis is injection imipenem. Dose is 1 g intravenous infusion twice or thrice daily. It is given to reduce further damage to pancreatic and peripancreatic infections or to prevent progression to infected necrosis and multiorgan failure. Narcotic analgesics also can be given if pain is severe. Choice of fluid is Ringers’ lactate . It is given at the rate of 125-150 ml/hr. Blood urea nitrogen (BUN) and creatinine should be used as markers to predict intravascular volume depletion and correction. Fluid resuscitation should be instituted early in cases of pancreatitis because of third space loss resulting in severe hypovolaemic shock. Hypovolaemia is due to endothelial cell damage and increase permeability.

E: Exploratory laparotomy is done when patient is not improving or when there is a complication of pancreatitis such as pancreatic fistula or necrosis. With the advent of wonderful imaging techniques, surgical intervention is rarely being done in the initial phase of acute pancreatitis. With conservative treatment, majority will return back to normal by 3-5 days. Those who develop complications are dealt separately. Details are given later.

F: Fluid should be given early. Rapid infusion of 3-4 litres of Ringer lactate is used to treat hypovolaemic shock. Plasma or albumin may also be given.

Details of the important aspects of treatment of acute pancreatitis are given below.

1. Admission: All patients with acute pancreatitis should be admitted and basic charts such as temperature, breathing, pulse, blood pressure intake output abdominal girth are monitored. Those patients with frequent vomiting, require nasogastric tube insertion for aspiration. Make a note of intake and output charts and accordingly, fluid balance is maintained. Admission in ICU is recommended only in severe pancreatitis. Mild cases do not require oxygen supplementation. Early ARDS patients will require ventilator support and care in ICU.

2. Pain relief: It is very important because pain is severe, deep and penetrates to the back. NSAIDs (nonsteroidal anti-inflammatory drugs) such as paracetamol, and ibuprofen are started. If the pain relief is not happened, change over to powerful opioids, such as codeine. Still if pain persists, narcotic analgesics such as morphine or pethidine are recommended. Buprenorphine is better than pethidine because it is a long- acting analgesic and does not cause dependence. If pain is also due to stones in the CBD-gallstone pancreatitis, ERCP and extraction of stones is done.

3. Fluid: Fluid resuscitation in acute pancreatitis is an important step in resuscitation. Early aggressive hydration, defined as 250 to 500 ml/h of isotonic crystalloid solution (ideally lactated Ringer’s solution), should be given to all patients during the first 12 to 24 h. However, if patient has cardiovascular, renal, or other related comorbid factors, then the fluid volume should be controlled or reduced. Once fluid replacement is adequate, there will be reduction in Hct and BUN levels over the first 24 h, particularly if they were high at the onset. In the same fashion, pulse rate, temperature, respiratory rate, blood pressure and urine output are monitored. Patients undergoing volume resuscitation should also undergo continuous pulse oximetry, receive supplemental oxygen as needed. Bedside ultrasound guided assessment of diameter of Inferior vena cava also helps in assessing the fluid response. Passive leg raising is a simple bedside method to check for fluid response.

4. Nutrition: It is an important part of treatment in acute pancreatitis. If enteral or parenteral nutrition is given early in the treatment of acute pancreatitis, there is a lower risk of death than if no supplemental nutrition is given. Patients with mild pancreatitis can resume an oral diet as soon as their pain decreases say by 2 to 3 days after an attack of acute pancreatitis. Low- residue, low-fat, and soft diet are well tolerated and can be given. Idea is to decrease peristalsis activity because some degree of paralytic ileus exists even after 2 or 4 days. Early refeeding also seems to result in a shorter hospital stay.

The enteral route is preferred over parenteral route because of following reasons:

• Intestinal mucosal barrier is maintained.
• Prevents the intestinal atrophy, if patients are kept NPO for long period.
• Intestinal atropy can promotes translocation of bacteria, thus sterile necrosis can turn to infective necrosis.
• Parenteral nutrition requires central 4 catheters, thus the risk of infection of a catheter is present.
• Is less expensive.

A nasojejunal feeding tube is placed beyond the ligament of Treitz under radiological or endoscopic guidance. Reason being one can avoid stimulating the gastric phase of the digestive process. If one cannot insert nasojejunal tube, even nasogastric feeding should be initiated. Whenever nasogastric tube is inserted, the GE junction sphincter does not function well and there is also paralytic ileus. So, to avoid aspiration, head end of the patient should be elevated to about 30 degrees.

5. Antibiotics: In mild cases of acute pancreatitis and in sterile necrosis, they are not indicated. However, if patient has some other pathology such as respiratory or urinary tract infection, antibiotics are given accordingly. In cases of infected necrosis, usual organisms are gram-negative such as E. coli, Klebsiella, and anaerobes. Thus, carbapenems, fluoroquino¬lones, and metronidazole are recommended.

6. Role of surgery: There is no role for surgery in mild pancreatitis cases and also in cases of sterile necrosis after the treatment followed as mentioned above, if they improve no surgical line of treatment is required. Patients who develop infected necrosis (around 15-20 days) are carefully monitored and if they do not show improvement, percutaneous, retroperitoneal drainage of necrotic material, followed by pigtail catheter insertion is done. Same thing can also be done by retroperitoneal videoendoscopic drainage. If patients show complete relief, no surgery is required. This is also called initial part of step-up approach treatment because around 3-4 weeks of time, necrotic pancreas is not very well demarcated. However, if toxic features such as temperature, tachycardia, tachypnoea, hypotension, etc. are persisting and repeat CECT scans detect significant necrotic material, laparoscopic or open necrosectomy is done.

Pancreatic Necrosectomy—Lap/Open Method

• Ideally done 4-6 weeks later when sepsis is still present.
• CT-guided FNAC/bacterial culture is a must.
• A midline laparotomy is done.
• Lesser sac is entered.
• Thorough debridement of the dead tissue is done.
• All fluid and tissue should be sent for aerobic and anaerobic culture.
• Blunt dissection rather than sharp dissection is done to minimise bleeding.
• Antibiotics of choice should be carbapenems and quinolones.
• Ileostomy should be done for retrocolic necrosis.
• Cholecystectomy should be done for gallstone pancreatitis cases.
• Perfect haemostasis should be achieved using manual compression, sutures and ligatures.
• In cases of early necrosectomy, lesser sac is packed, reoperation done after 48 hours—zipper closure of the abdomen is used.
• Continuous lavage of the lesser sac and retroperitoneum is done.
• Other alternate methods are closed packing.
• Today all these cases are done through minimally invasive methods.
• Endoscopic necrosectomy, retroperitoneoscopic necrosectomy is also done.

Treatment of Gallstone Pancreatitis: If gallstone is obstructing the ampulla of Vater and causing pancreatitis, endoscopic sphincterotomy may be done within days. It has shown some benefit to the patients. After 2-3 weeks, once the jaundice subsides, cholecystectomy is recommended.

Acute Pancreatitis

• Lipase is a more reliable test because it is more pancreas-specific and remains elevated for long after onset of symptom
• However, amylase is widely used
• It is not necessary to demonstrate CBD stone to prove the diagnosis of gallstone pancreatitis. Often stone has passed into duodenum

Complications of Acute Pancreatitis

Systemic Complications of Acute Pancreatitis

1. Shock

• Hypovolaemia and hypoperfusion are the major factors responsible for renal failure. Due to collection of large amount of fluid in the third space—peritoneal cavity, pleural cavity and extra- vascular space, shock occurs. Fluid replacement with blood or albumin should be done at appro-priate time to treat the shock.
• Electrolyte abnormalities should be corrected.

2. Respiratory insufficiency: Factors responsible for this are given. Measurement of arterial blood gas values and administration of oxygen is enough in the initial stages. In late stages, pulmonary insufficiency needs to be treated with ventilatory support.

Respiratory Failure

• Abdominal distension and elevation of diaphragm
• Intravascular coagulation in the lung
• Lecithin present in the pulmonary surfactant is altered due to lecithinase resulting in defective capillary alveolar exchange
• Defective ventilation caused due to pain
• Left-sided pleural effusion not responding to treatment

3. Hypocalcaemia needs to be treated with calcium 4. It is due to hypoalbuminaemia and due to calcium soap.

4. Pleural effusion is treated by pleural tap (ultrasound- guided), if it is symptomatic.

5. ARDS, MODS: Some mediators, such as phosphatase, damage alveolar membrane of lungs causing ‘ARDS’. It manifests as respiratory failure.

Local Complications of Acute Pancreatitis

1. Pancreatic abscess

• It develops after 3-4 weeks of pancreatitis. Secondary infection in a pseudocyst results in pancreatic abscess. It usually points out on the left flank.
• It has to be drained by CT-guided aspiration.
• Laparoscopy may be necessary not only for the diagnosis but also as a therapeutic means for removal of necrotic pancreas.
• Otherwise, open drainage of the abscess is required.

2. Pseudocyst of pancreas (vide infra): This complication is encountered after 2nd week following an attack of acute pancreatitis. It is seen in about 20% of the patients.

3. Perforation of colon or stomach

4. Pseudoaneurysm resulting in massive upper gastro-intestinal or lower gastrointestinal bleeding. Bleeding into the pancreatic duct is called haemosuccus pancreaticus.

• This condition occurs due to enzymatic digestion of the blood vessels in the vicinity of pancreas. Thus splenic artery, gastroduodenal artery, etc. are commonly involved.
• It has very high mortality. Prompt angiography followed by embolisation is the treatment.
• Otherwise, laparotomy, ligation of pseudoaneurysm with or without intracystic ligation of the bleeders is the treatment.

Pseudocyst Of Pancreas

Pseudocyst Definition: Collection of amylase-rich fluid in the lesser sac, due to pancreatic pathology. Fluid collection in the first 4 weeks is an acute fluid collection. After 4 weeks, it becomes an acute pseudocyst.

Pseudocyst Aetiology

1. Following an attack of acute pancreatitis, it usually appears after 4 weeks, as upper abdominal swelling.
2. Blunt injury of abdomen causing a ductal disruption wherein the pancreatic duct in the region of body is crushed against vertebral body results in a pseudocyst.
3. Some cause of chronic pancreatitis may be associated with pseudocyst.

Pseudocyst Locations

1. Between stomach and transverse colon
2. Between stomach and liver
3. Behind or below the transverse colon

Classification of Pseudocyst

1. Type 1. Acute postnecrotic pseudocyst that occurs after an episode of acute pancreatitis and is associated with normal duct anatomy and rarely communicate with pancreatic duct.
2. Type 2. Post-necrotic pseudocyst that occurs after an episode of acute on chronic pancreatitis and have a diseased but not strictured pancreatic duct and there is communication between the duct and pseudocyst.
3. Type 3 (also called retention cyst) occurs in chronic pancreatitis, uniformly associated with a duct stricture and a communication between duct and pseudocyst.

Pseudocyst Clinical Features

1. Tensely cystic mass in the epigastrium, umbilical region or in left hypochondrium. Tensely cystic mass feels firm on palpation. Classically upper border of the mass is not felt.
2. Does not move with respiration because it is retro-peritoneal in location.
3. It may have transverse mobility.
4. It does not fall forwards.
5. Percussion: It gives a resonant note because of stomach or intestine anterior to it.
6. Transmitted pulsations from aorta can be felt.
7. If a Ryle’s tube is passed, it can be felt over the swelling. It is called Baid sign.
8. Depending upon the tension within the cyst, it can be tender or nontender.

Pseudocyst Investigations

1. USG/CT: It can detect size, location of cyst and wall thickness. Confirm that there is no neoplasm of the pancreas before doing cystogastrostomy.

2. Barium meal stomach: In a lateral picture, the stomach is pushed anteriorly and increased vertebrogastric interval is seen not done nowadays.

3. ERCP may demonstrate communication of the cyst with the duct (routinely not done).

Pseudocyst Treatment:

1. Conservative Line of Treatment

• Majority of the pseudocysts following acute pancreatitis resolve spontaneously within 3-4 weeks.
• Hence, regular ultrasound examination is done to observe the pseudocyst.

2. Surgery: Increase in size of cyst, severe pain, no response to conservative line of treatment are indications for surgery.

Surgery Cystogastrostomy

• Cystogastrostomy Indications: Pseudocyst in relation to head and body of pancreas.
• Cystogastrostomy Timing: Surgery is done after 6 weeks because that is the time required for the wall to become fibrous.
• Cystogastrostomy Size of the cyst should be at least 6 cm.
• Cystogastrostomy Procedure: Anterior gastrostomy is done and an incision in the posterior wall of stomach opens into the cyst cavity. The contents are drained, opening is enlarged and cut end of stomach in posterior wall is sutured to cut edge of cyst wall. After one week, the cyst collapses. For reasons not known, the food does not enter the cyst cavity. Size of cystogastrostomy stoma is about 6 cm. This procedure can also be done by endoscopic method.

Surgery Distal pancreatectomy: Cyst confined to the tail of the pancreas is treated with removal of the tail and the cyst.

Surgery Cystojejunostomy: By using Roux-en-Y loop can be done, for large cysts by suturing jejunal loop to the cyst in the most dependent area.

3. Endoscopic Drainage: This is easy, less invasive and ideal in draining acute pseudocysts. This procedure can also be repeated. However, chances of introducing infection are present. Endoscopic method of draining the pseudocysts is also being done for chronic cysts. Few importan points here are there should not be more than 3 mm gap between cyst and posterior gastric wall and at the site of incision in the posterior wall there should not be any varices.

Congenital Anomalies Of The Pancreas

Embryological Anatomy

• Pancreas is formed by fusion of ventral and dorsal buds. This will occur by 6 weeks. Malrotation of ventral bud causes annular pancreas.
• Ventral bud forms head and uncinate process.
• Ductal anomalies are given.

Annular Pancreas: It is a rare anomaly which occurs due to persistence of a portion of the ventral pancreatic anlage which fails to rotate. As a result of this, second part of the duodenum is surrounded by a thin rim of pancreatic tissue. Hence the name, annular pancreas.

• Persistent ventral ‘anlage’
• Neonatal or adult age
• Barium meal—obstruction to second part of duodenum
• Plain X-ray—‘double bubble’
• Duodenoduodenostomy is the treatment
• Never divide the annulus

Associated Anomalies: Intrinsic duodenal atresia or stenosis.

Annular Pancreas Clinical Features

• Neonatal type: It manifests early in life. It produces symptoms of acute intestinal obstruction with vomiting and inability to take food.
• Adult type: It manifests after the age of 20. Vomiting is bile-stained. Due to stasis in the pyloric antrum, features of duodenal ulcer may be present.

Annular Pancreas Investigations

• Plain X-ray abdomen: Double bubble appearance occurs due to dilated stomach and dilated proximal duodenum.
• Barium meal: X-ray can demonstrate obstruction to second part of duodenum.

Annular Pancreas Treatment: Duodenoduodenostomy is the treatment of choice. Otherwise, duodenojejunostomy can be done.

Annular Pancreas Differential Diagnosis

• Pyloric stenosis
• Wilkie’s disease (chronic duodenal ileus)

Ectopic Pancreas

• This condition is not uncommon.
• Occasionally, at laparotomy for unrelated conditions, a soft to firm irregular tissue or nodule is found on the intestinal surface.
• Biopsy of this may come later as ectopic pancreas. Most of them are asymptomatic.
• It may be found in the submucosa of the stomach, duodenum, small intestines, Meckel’s diverticulum or in the hilum of the spleen.

Ectopic Pancreas Complications

1. In the stomach: It may undergo cystic degeneration.
2. In the intestine: It can cause intussusception. Some-times, it may be the source of gastrointestinal bleeding.
3. In the Meckel’s diverticulum: Any of the complica-tions mentioned above.

Congenital Cystic Fibrosis

It is inherited as an autosomal recessive disorder. It is a generalised dysfunction of exocrine glands resulting in defective mucus secretion. Malabsorption due to pancreatic insufficiency is a feature. Pulmonary disease due to bronchiolitis occurs later .

Viscid Mucus—Conditions

• Meconium ileus
• Cystic fibrosis of pancreas
• Respiratory tract infection
• Increased Na⁺ loss in the sweat

Pathology; The viscid mucin which is produced results in obstruc-tion of the ducts and ductules. Stasis of pancreatic secretions, alveolar rupture due to increased pressure take place later. As a result of alveolar rupture, pancreatic enzymes leak outside resulting in pancreatitis.

Congenital Cyctic Fibrosis Clinical Features

1. At birth: Meconium ileus or meconium peritonitis is an important manifestation of cystic fibrosis of pancreas.
2. In infants: Recurrent respiratory tract infection in the form of bronchiolitis and bronchiectasis results in cough with expectoration and dyspnoea. Emaciation, steatorrhoea. Stools are pale and sticky.
3. Older children: Steatorrhoea, gross emaciation and wasting are the features. Due to poor nutritional status, cirrhosis of the liver with portal hypertension can be a feature.
4. In adult: Lucky survivors will suffer from gross wasting, diabetes, bronchiectasis, cirrhosis of the liver, sialoadenitis and choroiditis.

Congenital Cystic Fibrosis Investigations

• Normal contents of the electrolytes in the sweat: Na⁺—70 mmol/l, Cl^–—60 mmol/l, K⁺— 20 mmol/l.
• In these patients, sodium excretion may be three to four times more than normal.

Congenital Cyctic Fibrosis Treatment (Only Symptomatic)

1. Nutritional support
   • Fat intake should be low, protein should be increased.
   • Pancreatic enzyme preparations (5 to 10 g) are given two to three times per day, to supplement pancreatic enzymes.
2. Control infection: Respiratory tract infection is treated with antibiotics, bronchodilators, mucolytic agents, etc.
3. Role of surgery: Indicated in meconium ileus to relieve intestinal obstruction