25. 1 Acute pancreatitis

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Old Marseilles Classification (1963):

1. Acute pancreatitis

2. Recurrent (or relapsing) acute pancreatitis

3. Chronic pancreatitis

4. Recurrent (or chronic relapsing) pancreatitis

New Marseilles Classification (1984):

1. Acute pancreatitis:

a. Mild b. Severe.

2. Chronic pancreatitis

1. With focal necrosis.
   
2. b. With segmental or diffuse fibrosls.
   
3. c. With calculi.
   

Acute Pancreatitis

Acute pancreatitis is the acute inflammation of the pancreas manifested by acute upper abdominal pain and characterised by raised levels of pancreatic enzymes in blood, urine and peritoneal fluid. It is the result of autodigestion of the pancreas by activation of its enzymes. The morphological changes in the pancreas range from oedema and swelling in the mild form to complete disruption, necrosis, and bleeding (haemorrhagic necrosis) giving rise to a retroperitoneal phlegmon in the severe forms. Depending upon the severity of the pathological changes, there will be local and systemic effects.

Aetiology

The two major causes are alcohol abuse and biliary disease. These account for roughly 80 per cent of the cases. The remaining 20 per cent comprise a wide variety of conditions

Hyperilpidaemia

Hypercalcaemia

Scorpion venom

Drugs

Ampullary tumours

Ascaris obstruction

Blind-loop obstruction

(Polya gastrectomy)

Penetrating and closed

abdominal trauma

Postoperative

ERCP and paplllotomy

Postoperative

(cardiopulmonary bypass)

Low perfusion states

Lumbar aortography

Atheroembolism

Perlarterltis nodosa

Mumps

Coxsackle virus

Alcohol To produce acute pancreatitis, chronic alcohol abuse is necessary. The first attack occurs after a 6 to 8 year period of heavy alcohol ingestion. The mode of action was thought to be by stimulation of pancreatic secretion together with spasm of the sphincter of Oddi, or duodenal inflammation and papillltis obstructing the outflow of pancreatic juice. This has, however, not been substantiated in experimental studies. It has been suggested that alcohol produces relaxation of the sphincter of Oddi and there is reflux of duodenal contents into the pancreatic duct through the relaxed sphincter and enterokinase activates the pancreatic enzymes. Prolonged alcohol ingestion has been known to increase the protein content of pancreatic secretion (protein plugs blocking the pancreatic duct).

Biliary pancreatitis The aetlologic mechanism most likely consists of transient obstruction of the ampulla of Vater and pancreatic duct by a gall­stone.

Other causes These account for 20% of the cases. Hypercalcaemia and hyperparathyroidism have been implicated in the aetiology of acute pancreatitis. It is thought that the increased calcium concentration in pancreatic juice due to hypercalcaemla may prematurely activate proteases and also facilitate precipitation of calculi in the ducts. In the recent studies, however, association has been found to be much less frequent. Hyperlipidaemia has been blamed as a causative factor but it is more usual to find it as an incidental factor in alcoholics.

The venom of black scorpion (Tityus trin(tat(s) found in Trinidad and Venezuela has been found to precipitate acute pancreatitis. A causal relationship has been suggested between the administration of steroids, thiazide diuretics and azathloprine. Mechanical factors which impede pancreatic flow as ampullary tumours, roundworms impacted in the ampulla or built-up pressure in the closed duodenal loop (following polyagastrectomy) produce acute pancreatitis. Direct trauma to the pancreas in abdominal injuries (more commonly blunt), opera­tions near the head of the pancreas (e.g. partial gastrectomy or sphincteroplasty), and ERCP or perendoscopic papillotomy are known to Induce acute pancreatitis. Reduced blood flow as in low perfusion states (hypotension or during cardiopulmonary bypass), lumbar aortography, atheroembolism and generalised arterial disease (like atherosclerosis and polyarteritis nodosa) can lead to acute pancreatitis. Viral infections like mumps probably damage the acinar cells.

Pathogenesis

Acute pancreatitis results from an initiating event which causes activation of pancreatic enzymes follo­wed by autodigestion of the pancreatic substance.

The autodigestion is initiated by a rise of trypsin activity within the pancreas and which in turn activates other pancreatic enzymes including elastase, phosphoUpase A and kallikrein. Kalllkrein is capable of producing the polypeptides — kallidin and bradykinin. These are vasoactive and cause vasodllatatlon and Increased vascular permeability. Locally, they cause inflammation and pain, and systemically, they cause shock.

Lipase causes fat necrosis while phosphollpase A causes destruction of cell membrane and converts the lecithin in bile to cytolecithin which is cytotoxic to pancreatic duct epithelium.

Clinical Features

The main symptom in acute pancreatitis is severe upper abdominal pain of sudden onset. This rises to a peak in a few hours and is commonly associated with shock. Radiation to the back is seen only in 50 per cent of the cases. The pain lasts on an average for 2 days, but may persist for a week or more. Vomiting and fever are characteristic.

Variable degree of shock is present. Respiratory distress and cyanosis are common. There is tenderness and guarding in the epigastrium. Peristalsis is feeble and the abdomen may be distended. Ecchymosis at the umbilicus (Cullen's sign) and flanks (Grey Turner's sign) due to retroperitoneal haemorrhage occurs only in a few. Sometimes a vague mass may be palpable in the epigastrium. Jaundice may be seen in some.

Diagnosis

When a chronic alcoholic or an old patient of gall­bladder disease is seized with sudden upper abdominal pain. the first diagnosis that comes to the clinician's mind is acute pancreatitis especially if accompanied by shock or respiratory distress, but any other possibility should also be borne in mind, complexed with fatty acids (liberated from retroperitoneal fat by lipase).

A plain abdominal film may show isolated dilatation of a segment of the gut (sentinel loop) consisting of jejunum, duodenum or transverse colon adjacent to the pancreas. The colonic ileus is characteristically seen as the "colon cut-off sign". It usually affects the splenic flexure and its Incidence has been reported as between 1 and 14 per cent of all cases of pancreatitis. The exact cause is unknown but it may be a visceral reflex mediated by the superior mesenteric plexus in the presence of retroperitoneal inflammation and/or transient colonic ischaemla.

Occasionally, radio-opaque gallstones will be apparent. Ultrasound may detect a pseudocyst and a CT-scan of the pancreas may show pancreatic oedema with extension of the Inflammatory process to adjacent extrapancreatic space, or pancreatic pseudocyst or abscess formation.

Prognosis

For the mild variety of the disease no therapy is needed. In order to elect the appropriate treatment, it is necessary to identify those in whom the disease will have a severe course and com­plications. The first attempt to grade the severity of acute pancreatitis was by Ranson and associates in 1974 and the parameters used are given in Table 42.3.

ТаЫ» 42.3: Ranson's criteria of severity of acute pancreatitis

At admission

1. Age

2.WBC count

3.Blood glucose

4.Serum LDH SGOT

During the Initial 48 hours

1.Haematocrit fall

2.Blood urea N, rise

3.Serum calcium level

4.PaO,

5.Base deficit

6.Estimated fluid sequestration (loss)

Investigations

The serum amylase concentration rises to more than 2'/a times the normal within 6 hours of the onset of an acute episode and declines again after 48 hours, returning to normal within 4 to 8 days. Values well above 1000 lU/dl are characteristic. Urinary amylase excretion is also raised and can provide evidence of pancreatic damage for up to a week after the serum amylase has begun to fall.

In severe pancreatitis, the serum calcium concentration may fall as a result of calcium being

Presence of three factors or less

Mild pancreatitis: Mortality 1 to 3 per cent Presence of more than three factors

Severe pancreatitis: Mortality 62 per cent

Compliocations

Pulmonary complications Pulmonary thrombi block the pulmonary microvasculature. There is diffuse alveolar damage with hyaline membrane formation. The pulmonary changes result in hypoxia with an arterial PaOg less than 60 mm Hg.

Shock The mechanisms which may cause shock are the following.

1. Exudation of oedema fluid into the pancreas.
   
2. Kinins cause vasodllatatlon and Increased vascular permeability. c. Haemorrhage into the pancreas causes further hypovolaemia.
   

Renal dysfunction It is often the result of shock. The dysfunction at times may be due to an Increase In renal vascular resistance due to fibrin deposits In the glomerular capillaries.

Hypocalcaemla It is explained In most cases by a fall in serum albumin and, therefore, in protein bound calcium. In more severe cases the sequestration of calcium into areas of fat necrosis may be an additional factor.

Gastrolntestlnal haemorrhage It may be due to the following.

1. Gastric or duodenal stress related erosions
   
2. Direct involvement (erosion) of a major vessel
   
3. Rarely due to gastric varices which can occur in case of splenic vein thrombosis.
   

Skin and bone complications Subcutaneous fat necrosis may result in subcutaneous nodules In the limbs and trunk. Intramedullary fat necrosis in the long bones can cause painful osteolytic lesions.

Pancreatic pseudocyst It Is an encapsulated collection of fluid, containing high concentration of pancreatic enzymes (Fig. 42.3). About half of all cases of acute pancreatitis are complicated by the formation of pseudocysts, and quite a number of these resolve spontaneously. Majority of pseudo-cysts are seen between the second and fourth week.

Pancreatic abscess It implies pancreatic necrosis with secondary infection, usually occurring in the second week after an attack of acute pancreatitis. There is high fever and leucocytosls. The abscess Is frequently multilocular. Without early and adequate external drainage, the mortality is high due to sepsis or major bleeding. A relapse of fever and reappearance of leucocytosls Indicates that an abscess is developing. The mortality of an undralned abscess is very high.

Management and Prognosis

The course of pancreatitis varies from mild to fulminant and the management is organised accordingly. The criteria for assessing the severity of pancreatitis according to Ranson (Table 42.3) have already been enumerated.

The management of pancreatitis is by the "R" regime and Is as follows.

1. Rest to the patient Rest to the patient and relief of pain by pethldine are Important. Morphine is avoided.

2. Rest to the pancreas Oral feeds are withheld and nasogastric suction is done. Antlcho-llnergics are of no value.

3. Rest to the bowel Paralytic ileus Is managed

by continuous nasogastric aspiration.

4; Resuscitation

a. IV infusion is given to overcome the

hypovolaemia.

b. Blood, plasma or plasma substitutes may be necessary.

5. Renal Junction Urine output is monitored by an indwelling catheter and hypovolaemia corrected.

6. Respiratory support Mild hypoxaemla Is trea­ted by oxygen administration; close monitoring of PaOg is essential; and occasionally positive pressure ventilation may be of benefit.

7. Resist enzymatic activity Aprotinin (Trasylol) has been tried but has not been found to be beneficial. The same applies to glucagon. Peritoneal lavage has been found useful by some but it Is only indicated in very severe cases.

8. Resist infection Broad spectrum antibiotics which cover both aerobic gram-negative bacteria and anaerobic infections should be used.

9. Repeated examination It is necessary to evaluate the general and local signs at frequent intervals to assess the progress.

10. Repeated Investigations Serum calcium Is of great prognostic value and should be esti­mated dally. Intravenous calcium gluconate is indicated if it is low. Serum amylase level may not Indicate the severity of the disease but persistently raised serum amylase levels (after the general symptoms and signs have abated) may point to pseudocyst or pancreatic ascites. Repeated WBC count is necessary when there is persistent fever. Persistently raised serum flbrinogen level may Indicate smouldering disease and may herald disseminated intravascular coagulopathy (DIC). A major advance In the treatment of acute pancreatitis has been our ability to image the pancreas with ultrasound and more precisely with computed tomography (CT) scan.

Surgical Treatment

Most surgeons would avoid an operation so long as the patient is responding to general medical therapy and is Improving. However, when the diagnosis is uncertain or if the patient's condition is deteriorating on Intensive medical treatment, then operative exploration should be undertaken to be certain of the diagnosis, to rule out any other surgical condition which might mimic pancreatitis (perforated duodenal ulcer, mesenteric ischaemia, small bowel obstruction), and to debride or drain any areas of pancreatic necrosis.

The diagnosis of biliary disease can be suspected on the basis of ultrasound studies of the gall bladder early in the acute attack and some may decide to extract the stone by endoscopic sphlncterotomy decompress the obstructed biliary system rather than opt for an open operation.

When laparotomy has been performed and moderate pancreatitis found, the pancreas is left undisturbed and if gallstones are discovered, a cholecystectomy or cholecystostomy performed.

If there Is evidence of pancreatic or peri-pancreatic necrosis with abscess formation or sepsis, the area of necrosis, and the abscess needs to be debrided and drained. Contrast enhanced CT-scan obtained early in the course of the disease Is studied for the presence of non-enhancing areas which Indicate lack of vascular perfuslon and reflect the extent of necrosis. Percutaneous needle aspiration of the necrotic area is used to detect the presence of infection. An infected necrotising pancreatitis benefits most by surgical therapy. At operation, the gastrocolic omentum should be divided and the pancreas should be thoroughly inspected, the retroperitoneal cavity entered and any areas of cystic fluid collections, pancreatic necrosis, or abscess drained externally. Pancreatic debridement should be thorough and aggressive to include all dead or necrotic tissue, while avoiding injury to the healthy tissue. After aggressive debridement the abdomen is closed with multiple drains. The patient is carefully followed and treated with antibiotics. If further signs of sepsis or pancreatic necrosis become evident, operation is indicated as often as three or four times to control and drain the infection.

Treatment of Local Complications of Acute Pancreatitis

Pseudocyst A pseudocyst complicates acute pancreatitis 5 to 6 times more often in alcoholics than in cases of gallstone pancreatitis. It usually follows a moderate or severe attack and develops In about 2 to 4 weeks. Ultrasound or CT-scan has been Invaluable in detecting and assessing the progress of a pseudocyst. About 50 per cent of pseudocysts resolve spontaneously. A pseudocyst should be followed for a period of several weeks to determine if it Is Increasing in size or resolving. It is necessary to drain a persistent pseudopancreanc cyst, and If this is delayed beyond 6 weeks there Is a real risk of haemorrhage. At present, there are several options for treatment.

a. Ultrasound/CT-scan guided aspiration can be performed but fluid may reaccumulate after such an aspiration but cysts can be repeatedly aspirated. However, this carries the risk of Infection.

3. If the cyst Is thick-walled (and this usually occurs by about 6 weeks) and lies behind the stomach (Fig. 42.3), It can easily be drained into the stomach creating a cystogastrostomy. Pseudocysts which present below the stomach or do not touch upon the posterior wall of the stomach should be drained into a Roux-en-Y loop of jejunum (cystojejunostomy).
   
4. Perendoscopic drainage with the diathermy snare. A communication can be established between the cyst and the stomach through the posterior wall of the stomach. The complication of this drainage most commonly includes upper gastrointestinal bleeding. The source of bleeding may be the insutured margins of the cystogastrostomy.
   

Pancreatic abscess This dreaded complication occurs in 1 to 5 per cent of patients with acute pancreatitis and is more common when associated with gallstones. It usually occurs by about the third week of illness, but sometimes it may develop late (3-4 months). Persistent abdominal pain, pyrexia. anorexia, weight loss, leucocytosis and an abdo­minal mass are suggestive of pancreatic abscess. The common organism is E. coll. Diagnosis Is made on ultrasonography or CT-scan. Pancreatic abscess must be drained. Today It is possible not only to aspirate these under ultrasound/CT-scan guidance but also to insert polyethylene catheters Into the abscess for percutaneous drainage. Most people favour open drainage under appropriate antibiotic cover. It will be necessary to leave multiple sump drains. If there is diffuse retroperitoneal sepsis, drains may have to be placed at different sites. Sometimes repeated operations may become necessary. The overall mortality from pancreatic abscess ranges from 22 to 57 per cent.

Chronic Pancreatitis

When pancreatic inflammation leads to permanent structural or functional damage, the term chronic pancreatitis is used.

Aetlopathogenesis

The disease has a worldwide distribution. It Is seen both In the affluent and the developing countries. The highest prevalence in the world seems to be In Kerala In India, where Geevarghese has reported

an Incidence of 5A7 per cent in autopsy studies (and 1.0—1.7 per cent of hospital admissions). The aetiology is multifactorial and is listed in Table 42.4.

Tab 42.4; Aetiological factors In chronic pancreatit

Alcohol

Gallstones

Odditis

Congenital anomaly of the pancreatic duct

Protein malnutrition

Toxic factors

Infective factors

Hyperparathyroidism (hypercalcaemla)

Hereditary pancreatitis

Alcohol is the chief aetiological factor in the West. It appears to change the amount and content of pancreatic juice resulting in the formation of protein plugs within the pancreatic ducts, and thfcse get progressively calcified giving rise to calculi which occlude the ducts. The association with gallstones is less common in chronic pancreatitis than in acute pancreatitis. Obstructive lesions of the duct from slow-growing tumours, congenital anomalies of the duct or papillary stenosis can also give rise to chronic pancreatitis. In Kerala, chronic pancreatitis is more prevalent in areas where tapioca constitutes the staple diet. The glycosides in tapioca tuber when hydrolysed release hydrocyanic acid (HCN). Normally, this is detoxicated by combining with SH radicals derived from the amino acid methionine. The average diet in Kerala is deficient in proteins and the HCN liberated but not detoxicated, is responsible for the acinar damage. An association between pancreas divisum (nonfusion of the ducts of dorsal and ventral pancreas) and chronic pancreatitis has been reported. Undetected trauma may be a causative factor especially in pseudocysts. Hypercalcaemia has been associated with chronic calculous pancreatitis. Certain families are known to have several members affected by the disease, but no definite mode of inheritance is known.

Pathological Changes

Whatever the aetiology or the pathogenesis, the end result is the same. There is destruction of acinar tissue accompanied by chronic inflammatory cell Infiltration and fibrosls. The islets of Langerhans become encased in fibrous tissue but retain their function till late in the disease. There is atrophy of the ductal epithelium and alternate narrowing and dilatation of the duct with eosinophilic precipitates In the lumen, giving rise to "the chain of lakes" deformity. Calculus formation is frequently seen. Rarely, the inflammation may involve adjacent structures and give rise to duodenal or antral stenosis. At times the splenic vein may get thrombo-sed and this gives rise to left-sided portal hypertension and haematemesis. The infraduodenal portion of the common bile duct may be Involved in the flbrosis and may get narrowed producing obstructive jaundice. The disruption of the ductal system and slow escape of pancreatic secretions into the perlpancreatic tissues can lead to the formation of a pseudocyst. This can extend in the retroperi-toneum and sometimes even into the mediastinum or the pleural cavity. Sometimes it can rupture Into the peritoneum and give rise to pancreatic ascites.

Clinical Features

hi the West, the mean age of onset is about 40 years of age and it occurs more frequently in men. In Kerala, it starts early in life. The most prominent symptom is abdominal pain. The pain is more often felt in the upper abdomen, especially epigastrium and is of a dull boring character. In most patients it radiates to the back, and the patient may get some relief in the prone position. However, the pain may sometimes be colicky and is felt maximally in the umbilical region or right hypochondrium.

The symptoms may sometimes be due to the complications and are the following.

1. Pseudocyst giving rise to a mass in the abdomen

2. Pancreatic ascites causing abdominal distension

3. Obstructive jaundice due to scarring of the common bile duct

4. Segmental portal hypertension and haema­temesis due to splenic vein thrombosis and gastric varices

5. Vomiting due to antral duodenal stenosis due to spread of the Inflammatory process to the adjacent structures.

Diagnosis

Most patients present with upper abdominal pain and the differential diagnosis includes chronic peptic ulcer, chronic cholecystitis and malignancy affecting the stomach, liver and pancreas. Upper GI endoscopy, barium meal series, ultrasound/CT-scan and cholecystogram help in excluding these other causes.

In Kerala, the disease starts early in life and the typical patient is stunted in growth and emaciated, has ashen-grey hue of the lips and is a diabetic. Such a patient complaining of upper abdominal pain will enable one to make a "spot diagnosis" of the disease. Steatorrhoea is found in cases where pancreatic insufficiency has become severe.

A plain X-ray of the abdomen often reveals multiple pancreatic calculi Ultrasound of the pancreas shows enlargement of the pancreas with cysts and dilated ducts. CT-scan Is useful. ERCP can demonstrate stenosis of the papilla or duct anomalies, e.g. pancreas divisum. It also shows whether the common bile duct is narrowed by the pancreatitis, to determine whether biliary calculi are present. Moreover ERCP helps the surgeon to select a proper procedure based on dilatation or otherwise of the pancreatic duct.

Treatment

Medical treatment It consists of abstinence from alcohol, analgesics and substitution therapy for the exocrine and endocrine deficiencies.

1. Drainage procedures On ERCP, if the ductal system is dilated (more than 8 mm), a longitudinal pancreatlcojejunostomy (Puestow procedure) is appropriate. The duct is opened anteriorly from the tail into the head of the gland and anastomosed side to side to a Roux-en-Y segment of the proximal jejunum.
   
2. Surgical treatment Surgical treatment is princi­pally of value to relieve chronic intractable pain. In most cases it Involves a procedure that facilitates drainage of the pancreatic duct and resects diseased pancreas or achieves nerve block.
   

U the obstruction is at the duodenal papilla, sphincteroplasty should provide adequate drainage but more often the duct has multiple strictures and because this procedure gives less predictable results, it has been given up. It is carried out transduodenally or endoscoplcally.

2. Pancreatectomy In the absence of a dilated duct and if the disease is confined to one portion of the pancreas, a idealised excision of that part gives gratifying results (pancreatoduo-denectomy or distal pancreatectomy with pancreatojejunostomy). When the entire gland is affected and the duct system is not dilated, 95 per cent (or subtotal pancreatectomy) or total pancreatectomy will be the ideal treatment. However, these are major undertakings with greater mortality and morbidity.

3. Coeliac plexus block Coellac plexus block with alcohol injection provides relief of pain in some patients. The technique should probably be tried before major pancreatectomy is considered because the latter procedure is associated with a higher risk of immediate and late complications.

surgeon to select a proper procedure based on dilatation or otherwise of the pancreatic duct.

Treatment

Medical treatment It consists of abstinence from alcohol, analgesics and substitution therapy for the exocrine and endocrine deficiencies.

1. Drainage procedures On ERCP, if the ductal system is dilated (more than 8 mm), a longitudinal pancreaticojejunostomy (Puestow procedure) is appropriate The duct is opened anteriorly from the tail into the head of the gland and anastomosed side to side to a Roux-en-Y segment of the proximal jejunum.
   
2. Surgical treatment Surgical treatment is princi­pally of value to relieve chronic Intractable pain. In most cases it involves a procedure that facilitates drainage of the pancreatic duct and resects diseased pancreas or achieves nerve block.
   

If the obstruction is at the duodenal papilla, sphincteroplasty should provide adequate drainage but more often the duct has multiple strictures and because this procedure gives less predictable results, it has been given up. It is carried out transduodenally or endoscoplcally. Pancreaiectomy In the absence of a dilated duct and if the disease is confined to one portion of the pancreas, a localised excision of that part gives gratifying results (pancreatoduo-denectomy or distal pancreatectomy with pancreatojejunostomy). When the entire gland is affected and the duct system is not dilated, 95 per cent (or subtotal pancreatectomy) or total pancreatectomy will be the ideal treatment. However, these are major undertakings with greater mortality and morbidity.

Coeliac plexus block Coellac plexus block with alcohol injection provides relief of pain in some patients. The technique should probably be tried before major pancreatectomy is considered because the latter procedure is associated with a higher risk of immediate and late complications.

Prognosis

The success of operative treatment for chronic pancreatitis would depend on the correct choice of procedure, based on the nature and the extent of the pathological change as assessed by adequate evaluation. However, the longer the follow-up, the worse are the results. Patients with alcoholic pancreatitis of long duration who "have narcotic addiction are poor candidates for surgery and results are uniformly bad in such cases. Patients undergoing extensive resection eventually become malnourished due to the poor quality of residual pancreas. Diabetes mellitus Is inevitable after subtotal or total pancreatectomy. Attempts are being made for the autotransplantation of the resected segment of the pancreas (segmented transplantation) and of islet tissue harvested from the resected pancreas, with doubtful success.

CYSTS OF THE PANCREAS

These are divided into true cysts which have an epithelial lining and pseudocysts which have no epithelial lining.

True Cysts These are either congenital or neoplastic.

Congenital

Congenital pancreatic cysts are rare and are usually associated with Inherited polycystic disease of kidneys, liver or spleen. The cysts are usually multiple but can be solitary. Microscopically, the lining is of flattened epithelial cells.

Neoplastic

Serous cystadenoma and mucinous cystic tumours are the two forms of neoplastic pancreatic cysts commonly seen.

Serous cystadenoma is a well-circumscribed tumour, most commonly in the tall of the pancreas in elderly patients. It may be asymptomatic.

Mucinous cystic tumours In the past have been. divided into mucinous cystadehomas and mucinous cystadenocarcinomas. Both have malignant potential and the capacity to recur.

These cysts occur mainly In middle-aged women, most commonly in the tall of the pancreas. Calcification, as seen on X-ray, is considered characteristic of the lesion. The cyst contains viscid mucus and papillary growths are seen on the inner surface. Histologically, the epithelial lining Is composed of mucus-secreting cells. The tumour can usually be resected and If resection Is complete, the prognosis is good.

Pancreatic Pseudocyst

Any lesion of the pancreas which leads to leakage of the pancreatic juice In the lesser sac, gives rise to collection of fluid and a pseudocyst. The cai are the following.

1. Acute pancreatitis Is the commonest cai Ultrasound suggests that about half of all a of acute pancreatitis are complicated by formation of pseudocysts, but most of th resolve spontaneously and in only 2 per c< the pseudocyst persists.

2. Blunt Injury to the pancreas is the n common cause. The cyst may develop after days to 1 year of the injury.

3. A pseudocyst may form during an acute e;

cerbation of chronic pancreatitis. The term psuedocyst denotes absence of epithelial lining whereas true cysts are lined epithelium. The cyst wall is initially thin t later it becomes thick and fibrous.

4. A pseudocyst may arise during the course chronic pancreatitis unrelated to an acu episode. In this case, it results from dilatation ofti ducts, secondary to an obstruction. Theepitheliu atrophies bringing it within the definition of pseudocyst. This type may remain within or gro beyond the confines of the pancreas.

Clinically, a pseudocyst develops 3-4 weeks after an acute episode of pancreatitis. The patient eitht fails to improve or symptoms return after a period с improvement. Pain Is common and persistent wit] low grade fever, nausea and vomiting. Jaundice ma. result from pressure on the common bile duct am gastric outlet obstruction may occur. An epigastri» mass is palpable and this may be differentiated fron a phlegmon (a mass of Inflamed and oedematouf tissue) by ultrasound.

Clinical Features

It is commonly seen in young adults. The patient presents with progressively enlarging cystic swelling in the epigastrium and mild pain radiating to the back. The pain is relieved by forward bending and in the knee-elbow position. A pseudocyst may appear more prominently on one side. In order of frequency, the pseudocyst projects (i) between the stomach and the transverse colon); (ii) between the stomach and liver; or (iii) behind or below the transverse colon. The swelling is localised, its-surface smooth and it cannot be moved (c.f. mesenteric cyst, ovarian cyst). It does not move with respiration. It is a tense cystic swelling and fluctuation cannot be ellcltated. There is often a transmitted pulsation of the abdominal aorta and which is much diminished In the knee-elbow position. A barium meal X-ray Is done and the lateral view shows an anteriorly pushed stomach.

Complications

The major complications are the following.

1. Infection may be caused by intestinal organisms and may follow ERCP. An Infected cyst should be drained externally as an emergency.

Prognosis

The success of operative treatment for chronic pancreatitis would depend on the correct choice of procedure, based on the nature and the extent of the pathological change as assessed by adequate evaluation. However, the longer the follow-up, the worse are the results. Patients with alcoholic pancreatitis of long duration who • have narcotic addiction are poor candidates for surgery and results are uniformly bad in such cases. Patients undergoing extensive resection eventually become malnourished due to the poor quality of residual pancreas. Diabetes mellitus is inevitable after subtotal or total pancreatectomy. Attempts are being made for the autotransplantation of the resected segment of the pancreas (segmental transplantation) and of islet tissue harvested from the resected pancreas, with doubtful success.

CYSTS OF THE PANCREAS

These are divided into true cysts which have an epithelial lining and pseudocysts which have no epithelial lining.

True Cysts These are either congenital or neoplastlc.

Congenital

Congenital pancreatic cysts are rare and are usually associated with Inherited polycystic disease of kidneys, liver or spleen. The cysts are usually multiple but can be solitary. Microscopically, the lining is of flattened epithelial cells.

Neoplastic

Serous cystadenoma and muclnous cystic tumours are the two forms of neoplastlc pancreatic cysts commonly seen.

Serous cystadenoma is a well-circumscribed tumour, most commonly in the tail of the pancreas in elderly patients. It may be asymptomatic.

Muclnous cystic tumours In the past have been. divided into mucinous cystadenomas and mucinous cystadenocarclnomas. Both have malignant potential and the capacity to recur.

These cysts occur mainly in middle-aged women. most commonly In the tall of the pancreas. Calcification, as seen on X-ray, is considered characteristic of the lesion. The cyst contains viscid mucus and papillary growths are seen on the inner surface. Histologlcally, the epithelial lining Is composed of mucus-secreting cells. The tumour can usually be resected and If resection Is complete, the prognosis is good.

Pancreatic Pseudocyst

Any lesion of the pancreas which leads to leakage of the pancreatic juice in the lesser sac, gives rise to collection of fluid and a pseudocyst. The cai are the following.

1. Acute pancreatitis is the commonest cai Ultrasound suggests that about half of all ca of acute pancreatitis are complicated by formation of pseudocysts, but most of th resolve spontaneously and in only 2 per ce the pseudocyst persists.

2. Blunt injury to the pancreas is the n< common cause. The cyst may develop after days to 1 year of the Injury.

3. A pseudocyst may form during an acute e? cerbation of chronic pancreatitis. The term psuedocyst denotes absence of . epithelial lining whereas true cysts are lined epithelium. The cyst wall is Initially thin b later it becomes thick and fibrous.

4. A pseudocyst may arise during the course chronic pancreatitis unrelated to an acu episode. In this case, it results from dilatation oftt ducts, secondary to an obstruction. The epithellu] atrophies bringing it within the definition of pseudocyst. This type may remain within or gro' beyond the confines of the pancreas.

Clinically, a pseudocyst develops 3-4 weeks afte an acute episode of pancreatitis. The patient eithe fails to Improve or symptoms return after a period о improvement. Pain Is common and persistent witi low grade fever, nausea and vomiting. Jaundice ma} result from pressure on the common bile duct and gastric outlet obstruction may occur. An epigastric mass is palpable and this may be differentiated from a phlegmon (a mass of Inflamed and oedematous tissue) by ultrasound.

Clinical Features

It is commonly seen in young adults. The patient presents with progressively enlarging cystic swelling in the epigastrium and mild pain radiating to the back. The pain is relieved by forward bending and in the knee-elbow position. A pseudocyst may appear more prominently on one side. In order of frequency, the pseudocyst projects (1) between the stomach and the transverse colon (Fig. 42.3); (11) between the stomach and liver; or (ill) behind or below the transverse colon. The swelling is localised. Its-surface smooth and it cannot be moved (c.f. mesenteric cyst, ovarian cyst). It does not move with respiration. It Is a tense cystic swelling and fluctuation cannot be elicitated. There is often a transmitted pulsation of the abdominal aorta and which Is much diminished in the knee-elbow position. A barium meal X-ray Is done and the lateral view shows an anteriorly pushed stomach.

Complications

The major complications are the following.

1. Infection may be caused by Intestinal organisms and may follow ERCP. An infected cyst should be drained externally as an emergency.
   

Respiratory infection must be controlled by antibiotics.