25. 1 Acute pancreatitis
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PANCREATITIS
There are four types of pancreatitis, according to the classification of Marseilles (1963):
I. Acute pancreatitis — a single episode of pancreatitis in a previously normal gland.
II. Acute relapsing pancreatitis— recurrent attacks of acute pancreatitis with normalcy in the intervals between attacks and without permanent functional damage of the pancreas.
III. Chronic pancreatitis — irreversible destruction of pancreatic function with constant pain.
IV. Chronic relapsing pancreatitis— recurrent attacks of pain with frequent pain-intervals with progressive functional damage of the pancreas.
ACUTE AND ACUTE RELAPSING PANCREATITIS
'Acute pancreatitis' means acute inflammation superimposed on a normal gland and when such several episodes occur 'acute relapsing pancreatitis' is said to exist.
Pathogenesis.—
1. GALLSTONES AND CHOLEDOCHOLITHIASIS— Gallstones and alcohol are the two major conditions which can give aetiological explanation of no less than nearly 90% of cases of acute pancreatitis. Gallstones have been detected in 2/ds of the cases in private nursing homes whereas '/rd of cases in government institutions among low income groups. Just reverse is the incidence of alcoholic pancreatitis, which is more (approximately V,rds) in government institutions among low income groups.
The mechanism by which gallstones result pancreatitis is not very clearly known, (a) For quite a long time 'common channel theory' has given much importance in which bile reflux into the pancreatic duct as the two ducts join together to form the common channel before they open into the duodenum. But unfortunately bidirectional reflux i.e. bile flowing into the pancreatic duct and pancreatic juice into the bile duct has been observed in humans without pancreatitis. Active perfusion of normal bile into pancreatic duct at normal pressure does not cause pancreatitis. Moreover pressure in the pancreatic duct system is consistently higher than that in the bile duct system and that is why one cannot expect that bile will perfuse the pancreatic ducts. (b) Transient obstruction of the pancreatic duct by gallstones can result in pancreatitis. Transampullary migration of biliary calculi appears to be well established as an important cause of acute and acute relapsing pancreatitis. Several studies have indicated that choledocholithiasis can lead to the development of acute pancreatitis even in the absence of a common biliary-pancreatic channel Presumably the presence of an ampullary stone or oedema at the papilla can obstruct pancreatic duct outflow and thus results increase in pressure within the pancreatic duct system.
2. ALCOHOL. — The exact mechanism is also not known how alcohol can induce pancreatitis, (a) A direct toxic effect of alcohol on the pancreatic parenchyma has been postulated but could not find a solid base. (b) With prolonged alcohol intake protein is precipitated in pancreatic juice within the ductules leading to ductular obstruction and increased pressure within the ductules. (c) Duodenal inflammation induced by alcohol may produce some degree of duct obstruction, (d) Persistent vomiting may cause regurgitation of duodenal contents into the pancreatic ducts. Two mechanisms seen to give reasonable explanation how alcohol may cause acute pancreatitis — (e) alcohol stimulates pancreatic secretion by way of acid-induced secretion release, (f) Alcohol increases sphincteric tone at the ampullary region. So alcohol increases secretion against an unyielding sphincter. This seems to be the most reasonable explanation of how alcohol causes acute pancreatitis.
3. OBSTRUCTION.— It is obvious that some sort of obstruction of the pancreatic duct is required to produce acute pancreatitis. But deliberate ligation of the major pancreatic duct in the treatment of chronic relapsing pancreatitis has not caused acute disease. So duct obstruction must be associated with stimulation of pancreatic secretion.
Closed-loop duodenal obstruction with biliary exclusion is followed by fulminating type of acute pancreatitis. Obstructed duodenum may elaborate factors that may provoke pancreatic inflammation.
4. METABOLIC FACTORS.— (a) Hyperlipidaemia has got some relation with acute pancreatitis. Some patients with a geneticpredisposition to hyperlipidaemia and pancreatitis are often diagnosed in childhood.The second variety of hyperlipidaemia which causes pancreatitis is often diagnosed as idiopathic variety. In this case neutral fats are usually increased immediately before the onset of abdominal symptoms and return to normal when attack is over. Dietary-induced hypertriglyceridaemia may cause attacks of acute pancreatitis in alcohol ic patients. It seems that conversion oftriglycerides to toxic free acids within the pancreatic parenchyma by pancreatic lipase may be the cause of pancreatitis in hyperlipidaemia. Fat emboli may cause obstruction of the pancreatic duct and may cause pancreatitis.
(b) Hypercalcaemia and pancreatitis are often associated with. Hyperparathyroidism may reveal itself by repeated attacks of acute pancreatitis. Precipitation of calcium phosphate in the pancreatic duct will lead to obstruction alongwith increased pancreatic secretion to cause pancreatitis. Parathyroid function should always be investigated in any patient with pancreatitis of obscure cause.
(c) Haemochromatosis has been thought to produce pancreatic fibrosis and atrophy due to irritating property of deposited iron in the pancreas.
5 VASCULAR FACTORS.— Pancreatitis may be induced by injection ofmicrospheres of various sizes into the pancreaticoduodenal arteries in animals. These particles occlude the terminal arterial supply and produce local ischaemia. Sometimes in older patients who have widespread vascular obstruction from atherosclerosis and patients who have undergone cardiopulmonary bypass are sometimes seen with severe hacmorrhagic pancreatitis.
6. POSTOPERATIVE PANCREATITIS.— Following certain infra-abdominal operations pancreatitis may occur These operations are mainly on the stomach or on the biliary tract. After Billroth II partial gastrectomy afferent loop obstruction may cause pancreatitis. After common bile duct exploration, specially if a long-armed T-tube has been placed through the sphincter ofOddi pancreatitis may follow. Even after exploration of the common bile duct while passing dilator through the sphincter ofOddi one may injure the papilla causing oedematous swelling and even pancreatic duct injury, which will all cause pancreatitis During gastreclomy when the region of the head of the pancreas is being dissected injury will cause pancreatitis After splenectomy pancreatitis may result following operative injury to the tail of the pancreas It must be remembered that mortality rate of postoperative pancreatitis is quite high reaching about 50%
7. MISCELLANEOUS,— A wide variety of seemingly unrelated factors have been associated with the development of pancreatitis.
Certain toxins such as methyl alcohol, zinc oxide, cholinesterase inhibitors have been known to produce pancreatitis by pancreatic injury.
A few viral diseases e.g. mumps, echoviros infection, coxsackie virus infections, mononucleosis have been incriminated to cause pancreatitis.
A few drugs e.g. corticosteroids, phenformim, azathioprin, chlorothiazide, frusemide etc have been held responsible to cause pancreatitis.
A certain investigative procedures particularly ERCP may cause pancreatitis
Trauma, scorpion sting, porphyria, shock, vasculitis are a few factors which have some direct relation with pancreatitis. Autodigestion by activated intrapancreatic enzymes may lead to such pancreatitis
Pathology- The basic process in acute pancreatitis is one of autodigestion following activation of tiypsmogen. Activated phospholipase A and elastase are also held responsible to cause acute pancreatitis
The various pathological changes can be described under two heads,
(a) The PERITONEAL CAVITY comains blood stained exudates. The omental and subperitoneal fats show areas of fat necrosis Fat necrosis are duly opaque and yellow-white areas. These are mostly seen around the pancreas. In the greater omentum and in the mesentery such fat necrosis are abundantly seen. Focal areas offal necrosis that occur in the stromal, peripancreatic fat and throughout the abdominal cavity. In the oedematous stage, which is the wildest form the whole or part of the organ becomes oedematous. In necrotic and haemorrhagic varieties one may find haemorrhages and areas of necrosis in the gland. The retroperitoneal tissues around the pancreas are engorged with blood-stained fluid.
Sometimes fluid may accumulate in the lesser sac and when the condition gradually resolves fibrosis occurs which walls off such collection of fluid within the lesser sac. This is called pseudocyst of the pancreas. This occurs in about 12% of cases of acute pancreatitis. With migration of bacteria into such fluid collection, the condition may turn into abscess formation.
Clinical features.— The signs and symptoms of acute pancreatitis vary according to the degree of the disease. The different varieties of acute pancreatitis have been described as (a) acute oedematous type, (b) haemorrhagic pancreatitis and (c) necrotic pancreatitis.
SYMPTOMS.— The main symptom of oedematous pancreatitis is penetrating upper abdominal pain which often follows heavy meal. The pain is frequently located in the midepigastrium and often radiates to the back or even to the flanks. The patient's discomfort is often improved by sitting up and gets aggravated by lying down. In haemorrhagic and necrotic pancreatitis the pain is cramp in nature and excruciating in degree. The distressing pain is a very characteristic symptom of acute pancreatitis. Pain is sometimes felt in the right or left upper quadrant due to severe involvement of the head or the tail of the pancreas respectively. Pain is agonising and Moynihan described it is 'illimitable agony'.
Persistent and repeated vomiting with nausea is another characteristic symptom of acute pancreatitis. Retching is also common. Vomiting may even occur in empty stomach.
PHYSICAL EXAMINATION usually reveals a low grade fever and epigastric tenderness. There may be guarding and involuntary rigidity of the epigastric region. Signs of shock are quite common including sweating, tachycardia and hypotension. Abdominal distension is sometimes evident due to paralytic ileus and free fluid within the peritoneal cavity. Shock is usually due to loss of fluid and blood in the peritoneal cavity and retroperitoneal tissue as well as fluid loss through persistent vomiting. Moreover a myocardial depressant factor (MDF) is often released from the pancreas during pancreatitis and this also contributes to the shock. The shock may be partly due to circulating' kinins' which are formed by the action oftrypsin on the plasma proteins. Mild jaundice may occur in '/Uh of the cases and this is partly due to swelling of the head of the pancreas and excessive haemolysis of red blood cells which become more fragile in acute pancreatitis. Cyanosis may be seen, but is not a regular feature. Hypocalcaemia is a feature of this disease. Whether it is due to hypoalbuminaemia or unresponsiveness of the end-organ to parathormone or stimulation of thyrocalcitonin is something to be predicted. Some excess secretion ofglucagon is also noticed during pancreatitis and this also contributes to the hypocalcaemia. Lot of calcium is also wasted for formation of fat necrosis. Very occasionally patient may show carpopedal spasm from severe hypocalcaemia.
Paralytic ileus is limited in the beginning to the duodenum and proximal jejunum. The gas-filled solitary loop of proximal jejunum may be seen on straight X-ray as 'Sentinel loop'. Unless nasogastric aspiration is started, a total abdominal distension may be evident after 12 hours.
Discolouration of the skin is a characteristic finding of acute pancreatitis, though not a regular feature. Discolouration of skin around the umbilicus is known as Cullen 'ssign. Such discolouration of skin varies from slate blue to mottled yellowish brown colour due to ecchymosis and extravasated blood. It may be seen in the loins, when it is called Grey Turner's sign.
At the end of the 2nd week approximately 10 days after the onset of the disease, a tender palpable mass may appear in the epigastrium. This is the pseudocyst of the pancreas. If the mass appears after 3rd week, it is due to abscess formation.
Special Investigations.—
1. ELEVATED SERUM AMYLASE is a well established feature of acute pancreatitis. Although it may be stated that the higher the serum amylase level, the greater is the probability of acute pancreatitis, it is impossible to predict with accuracy either the diagnosis of acute pancreatitis or severity of an individual episode using only the level of serum amylase. Normal serum amylase level is 80 to 150 Somogyi units. 400 units or above is suggestive of acute pancreatitis and a level of 1,000 units or above more clearly speaks in favour of acute pancreatitis. The highest level is attained within 1 hour after the onset of symptoms. After that, the level gradually decreases and reaches normal level within 3 to 5 days. Apart from acute pancreatitis there are a few conditions which will also lead to high level of serum amvlase. These are : acute cholecystitis, common duct stone with or without cholangitis, alcoholism in absence of pancreatitis, intestinal obstruction, perforated peptic ulcer, intestinal gangrene, intracranial bleeding, ectopic pregnancy, carcinoma of pancreas, renal failure and mumps. After the use of drugs such as meperidine (Demerol) or morphine serum amylase level is also increased.
2. The rate of URINARY AMYLASE EXCRETION has been found to reflect the amount of amylase released from the pancreas into the blood. Quantification of the urinary amylase in addition to serum amylase determination will increase diagnostic accuracy for acute pancreatitis. Moreover urinary amylase remains elevated for longer periods. Estimation of total amount of amylase in a 24-hour urine sample is more accurate than the concentration of the enzyme in the urine. The number of positive diagnosis of pancreatitis is doubled when the amylase output in the urine exceeds 300 units in 1 hours.
3. Elevation in the SERUM AND URINARY LIPASE activities is also associated with acute pancreatitis. Elevated serum lipase alongwith elevated serum amylase is more diagnostic.
4. PARACENTESIS and THORACENTESIS are helpful in acute pancreatitis. Increased amylase in the aspirated Iluid particularly in the pleural fluid is more diagnostic than in the abdominal fluid.
5. RADI0IMMUNOASSAY for determining trypsinogen, elastase and other pancreatic proteolytic enzymes released in the serum during an episode of pancreatitis is recently being tried with success.
6. HYPOCALCAEMIA is often associated with more virulent type of pancreatitis and in fact value less than 7.5 mg/100 ml indicates poor prognosis. Explanation of low serum calcium in virulent acute pancreatitis includes (a) deposition of calcium in the peripancreatic retroperitoneal tissues, (b) a loss of serum albumin, (c) inadequate parathormone response at the bone level, (d) excess calcitonin secretion and due to hyperglucagonaemia of pancreatitis. Hypocalcaemia may persist for many days.
7. E.C.G. ABNORMALITIES are also noticed in acute pancreatitis and may be due to electrolyte disturbances. Such abnormality includes varying degrees of depression of ST segment, prolongation ofQT interval and flattening of Т waves. But normal E.C.G. does not preclude the diagnosis of acute pancreatitis.
8. CERTAIN SERUM ENZYMES are found to be increased in acute pancreatitis.
Deoxyribonuclease I values are markedly elevated in the blood only in pancreatic necrosis. In oedema of the pancreas the value remains normal. So increased concentration of this enzyme in the serum will reflect the presence of pancreatic disease, but its sensitivity is less than the values of serum amylase.
Leucine Aminopeptidase (Lap).— A raised level of this enzyme is considered sensitive and reasonably specific index of hepatobiliary disease and pancreas, but differentiation is not possible.
Lecithinase A.— This enzyme has a greater concentration in the pancreas and this is concerned in converting lecithin to lysolecithin and cephalin to lysocephalin with release of fatty acids. Elevation of this enzyme in the serum correlates well with acute pancreatitis in the same manner as increased level of serum amylase and lipase.
9. STRAIGHT X-RAY of the abdomen may reveal pancreatic or biliary calcification, (i) A single dilated paralytic loop of small intestine known as 'Sentinel loop' only provides contributory evidence to the diagnosis. (ii) Distension of the duodenum of moderate degree may be revealed in this investigation. Occasionally air-fluid level may be detected in severe cases, (iii) There is often mild distension of the transverse colon due to vicinity of this organ to the inflamed pancreas, which maybe revealed in straight X-ray. The descending colon is usually collapsed. So air-filled distended transverse colon is seen to be cut-off suddenly and this is known as the 'cut-off sign'.
10. BARIUM X-RAY of the upper G.I. tract, if the patient's condition permits, may show an enlarged 'C-Loop' of the duodenum due to swelling of the head of the pancreas. On lateral films, the stomach may be seen displaced forward due to extensive peripancreatic oedema. Such anienor displacement is more obvious due to accumulation of fluid in the lesser sac.
11. ULTRASOUND and COMPUTED TOMOGRAPHY often give conclusive evidence as to the diagnosis of this disease. In acute pancreatitis, swelling of the gland, loss of internal echoes and loss of the clevage plane between the splenic vein and the pancreas may occur. Ultrasonography is the method of choice for diagnosing and following pseudocyst. Cysts as small as 1 cm can be found by this study.
Computed tomography also gives an indication to acute pancreatitis by changes in the size or shape of the organ, decreased density, loss of sharp peripancreatic soft tissue planes due to extension of the inflammatory process into the adjacent retroperitoneum. Appearance of pseudocyst can be easily dignosed by this technique.
\7,.Cholescintigraphy with IDA scan also gives a clue to the diagnosis of this condition.
TREATMENT— Surgery is always deferred in acute pancreatitis and the treatment of choice is conservative management. Any attempt to operation will carry a mortality rate more than 50%. It is now generally agreed that immediate operation is unwise, provided other acute surgical emergencies can be excluded.
Conservative management.— 1. MANAGEMENT OF SHOOK AND ELECTROLYTE IMBALANCE.— The most urgent requirement of the acutely ill patients is the prevention of shock and its treatment. Intravenous fluid is started immediately. The amount of fluid required is detected by the degree of severity. Careful monitoring of fluid balance by central venous pressure and hourly measurement of urinary volume assists accurate replacement. About 7,rd of the circulating blood volume may be sequestered as a result of acute pancreatitis. Plasma and dcxtran may be infused so long as the blood is not available. Blood transfusions are required when the haemoglobin concentration drops. Nothing is permitted by mouth so gastric aspiration should also be added alongwith invisible water loss through lungs and skin and estimated fluid loss from the disease should be considered totally. When there is hypocalcaemia calcium gluconate will need to be added to the parcnteral fluid. Similarly potassium may be supplemented when hypokalaemia is detected.
2. RELIEF OF PAIN.— As soon as the diagnosis is confirmed and the course of treatment is determined, the patient should be given relief of pain. Pain is v cry severe and agonising in acute pancreatitis, so it should be relieved as soon as possible. Moreover pain is frequently accompanied by vasoconstriction which may be harmful to the myocardium and may reduce the blood supply to the pancreas to convert simple oedema to necrosis. Morphine and pethidine, which are quite effective in relieving severe pain. cannot be given in acute pancreatitis as they cause spasm of sphincter of Oddi. Moreover, administration of morphine is frequently followed by nausea and vomiting. Demerol (Mependine hydrochloride) in a dose of 50 to 100 mg every 4 hours is considered to be the analgesic of choice because of its anticholinergic action. It may be used in combination with Papaverine (100 mg i ntravenously) or Nitroglycerine. One of the barbiturates or paraldehyde may be used. In only extreme cases bilateral paravertebral splanchnic block or epidural block may be necessary.
3. SUPPRESSION OF PANCREATIC SECRETIONS.— This has a great beneficial effect in the treatment of acute pancreatitis. This can be performed (i) by stopping everything by mouth, (ii) by nasogastric aspiration and (iii) by non-absorbable liquid antacid (preferably a combination of magnesium trisilicatc and aluminium hydroxide as a liquid gel). All these act by curtailing secreting stimulus. Cimetidine may be effective as an antacid, (iv) An adequate dose of anticholinergic drug such as probanthine 30 mg ever) 8 hours or atropine sulphate 0.4 to 0.8 mg every 4 hours intravenously is effective in reducing pancreatic secretion by decreasing vagal stimulus. Acetazolamine (Diamox) has been found to reduce the volume of pancreatic cxocrine secretion and bicarbonate concentration. A dose of 250 to 500 mg may be administered twice daily without any untoward effects. Glucagon is known to reduce exocrine pancreatic secretion and has been claimed by some surgeons to reduce the mortality rate. But its general acceptances is still awaited.
4. ANTIENZYME PREPARATIONS.— Theoretically inhibition ofproteolytic activity might affect the course of pancreatitis. Some of the deleterious effects of acute pancreatitis are caused by activation of pancreatic proteolytic enzymes and to liberation of biologically active polypeptides similar to bradykinin. The release of trypsin from the affected gland is capable of activating pancreatic Kallikrein another proteolytic enzyme w hich spills to vasoactive decapeptide Kallidin from a globulin. This peptide is a potent vasodilator and hypotensive agent. An antienzyme preparation shown to be effective toward trypsin and Kallikrein in both experimental and human acute pancreatitis is Trasylol. This has been extracted from bovine parotid glands. This agent inhibits trypsin, chymotrypsin, Kallikrein and plasmin. But it should be remembered that once the necrotic process is well established Trasylol becomes ineffective. So Trasylol has to be used at the earliest possible opportunity in a massive dose (1,00,000 units or more daily intravenously).
5. ANTIBIOTICS.— Being an infective process, effectiveness of an antibiotic is beyond doubt. Its effectivity is certainly more in acute fulminating pancreatitis. It will counteract superimposed infection, prevent wide spread peritonitis and suppurative complications. Broad spectrum antibiotics e.g. ampicillin or tetracyclin may be used for this purpose. Third generation Cephalosporin has been claimed to be highly successful in fulmination pancreatitis.
6. PERITONEAL LAVAGE.— Peritoneal lavage is quite effective in limiting the number of early deaths in severe acute pancreatitis, but is probably not capable of preventing late local sequel of pancreatic necrosis. It removes the toxic products of pancreatic inflammation. Its use is limited to those who continue to deteriorate inspite of the best conservative treatment and when the diagnosis is absolutely confirmed. A lower midline or left lower quadrant incision is used and the peritoneal lavage catheter is introduced by making a nick through the abdominal muscles. 2 Litres of standard peritoneal dialysis solution containing 1.5 g/100 ml glucose, 4 mEq. of potassium per litre and 500 USP units ofheparin are run in gravity during 30 minutes period. This fluid is then drained out by lowering the bottle to the floor in the next 90 minutes. The cycle is repeated every 2 hours for 72 hours. Cardiovascular and respiratory monitoring are imperative as introduction of this fluid into the abdominal cavity may have adverse effects on the cardiac output and pulmonary compliance.
Surgical Treatment.— Acute pancreatitis is mainly treated by conserative management and the role of surgery is extremely limited. INDICATIONS OF SURGERY are mainly five —
1. The main indication is uncertain diagnosis. Many conditions of acute abdomen resemble acute pancreatitis and some of them require immediate operation. So doubt in the diagnosis is the first indication of surgery in acute pancreatitis.
2. If abdominal exploration has been performed in acute pancreatitis beacause of inability to establish the diagnosis, a few surgeons are in the opinion that one may perform cholecysteclomy if there are stones in the gallbladder. With dilatation of bile ducts one may explore the bile duct. Whether such procedures do any better or simply increase morbidity and mortality in patients with acute pancreatitis is a question. Probably simple drainage of gallbladder or common duct maybe life saving in patients with pancreatitis andbiliary calculi with superimoposed cholangitis. Therefore if acute pancreatitis is resolving without complication in a patient with known biliary disease it is preferable to wait until the pancreatic disease is completely resolved before performing any corrective biliary surgery.
3. There is a controversial indication of surgery when the patients are progressively deteriorating inspite of best conservative management. It these cases sump drainage and peritoneal lavage may improve the condition of the patient. Even in these cases the role of surgery is questioned and probably should better be avoided.
4. In the jaundiced patient if the serum bilirubin level fails to recede even with improvement in the general condition of the patient, operative interference may be justified.
5. In case of local complications such as pseudopancreatic cyst or pancreatic abscess there is a definite role of surgery.
COMPLICATIONS OF ACUTE PANCREATITIS
1. Massive haemorrhage may account for fatality initially.
2. Development of pseudocyst occurs in about 12% of cases. Pseudocyst rarely appears before the 2nd week of the disease.
3. Pancreatic abscess formation is a fatal complication whose mortality rate is quite high approaching 100% ifclostridial organisms are the cause of infection. Such abscess usually does not appear before the 3rd week. Gradually a swelling appears in the epigastric region or in the left flank. This alongwith swinging temperature sliould arouse suspicion of abscess formation. An abscess should be drained retroperitoneally.
4. It may cause obstruction of the common bile duct and even duodenum.
5. Collection of blood in the lesser sac though rare, is a dreaded complication. Sudden appearance of an epigastric swelling should be suspected in this line. This will require surgery and the clot should be evacuated immediately.
6. Acute renal failure is also a fatal complication of this disease. Presence of progressive azotemia and persistent oliguria, despite the correction of hypotension and dehydration, should be considered and treatment as acute renal insufficiency should be instituted.
7. Haematemasis and melaena may sometimes complicate this condition. It is often a complication of alcoholic pancreatitis. It cames'bad prognosis.
8. Pancreatic ascites may be seen. This may also be due to cirrhosis following alcoholism.
9. Acute psychosis is also a complication associated with acute pancreatitis among alcoholics.
10. Diabetes meltitus may occur as a sequel of acute pancreatitis. The frequency of diabetes increases with the number of attacks.
11. Chronic pancreatitis may develop as an aftermath of acute pancreatitis due to damage to the pancreatic tissue. This is a quiet progressive fibrosis leading to pancreatic insufficiency, which gives rise to steatorrhoea, nutritional deficiency and at times diabetes.
Subsequent management.— After recovery of acute pancreatitis after an interval of 1 month patients should be thoroughly investigated for presence of biliary tract diseases. Operation must be performed to cure such biliary diseases. This should be cholecystectomy for gallstones, exploration of bile duct for biliary calculi and sphincteroplasty. One may perform choledochoduodenostomy if there is chance of any remnant stones.
CHRONIC AND CHRONIC RELAPSING PANCREATITIS
The distinction between chronic pancreatitis and chronic relapsing pancreatitis is wholly clinical. In chronic relapsing pancreatitis inspite of progressive destruction of the gland, there may be asymptomatic periods of varying duration. In chronic pancreatitis there is no such asymptomatic period and the abdominal pain is continuous and unrelenting.
Though acute pancreatitis may turn into chronic pancreatitis, yet chronic pancreatitis should be considered as a separate disease entity from acute pancreatitis. In majority of cases chronic pancreatitis develops de novo without previous acute disease and the average age of patients with chronic pancreatitis is 10 years less than the average age of the patients with acute pancreatitis.
Pathogcnesis.— 1. Biliary tract disease.— Cholecystitis, calculous cholecystitis, choledocholithiasis, dysfunction or fibrosis of the sphincter of Oddi, benign and malignant growths of the ampulla of Vater are important aetiological factors. •
2. The common channel theory.— Many believe that the obstruction of the ampulla of Vater is the main cause of pancreatitis. So transduodenal sphincterotomy became one of the important treatments of this condition.
3. Chronic alcoholism has always been associated with chronic pancreatitis. It is often believed that the obstruction at the ampulla of Vater is a factor common to biliary tract disease and alcoholism. Alcohol presumably causes oedema and inflammation of the papilla of Vater by its local effects.
4. Hyperparathyroidism has often been associated with chronic pancreatitis.
5. Hyperlipidemia has often been seen in chronic pancreatitis.
6. Intrapancreatic duct obstruction at one or more sites can be demonstrated in many instances of chronic pancreatitis. Whether this represents a cause or an effect is to be found out. Due to alcoholism both in man and in experimental animal plugs of protein has been precipitated and often calcified in the ductal system of pancreas.
Pathology.— Histologically lobules of functional acinar and islet tissue are surrounded by thick band of fibrous tissue. Alternating areas of stricture and dilatation of the main ductal system is a regular feature. Calcification occurs in later stages. It is almost always intraductal and may be interstitial. Calcification and ductal distortion are common features of familial or genetic chronic pancreatitis.
Clinical features of chronic pancreatitis.— The patients are usually in their late thirties or early forties. A past history of chronic alcoholism and repeated attacks of pancreatitis may be received. Pain changes from intermittent to persistent and continuous. It is usually located in the epigastrium and characteristically radiates
The Small and Large Intestines