pancreatitis

ACUTE PANCREATITIS

ANATOMY


Acute pancreatitis is one of the rare but important cause of acute abdominal pain that needs hospital admission. Pathology: Oedematous pancreatitis, the most benign and usually resolve spontaneously, but may progress to more dangerous types. Necrotizing pancreatitis in which the damage reaches the acinar cells. Haemorrhagic type: The most serious and cause bleeding into pancrease.


Pathophysiology Acute pancreatitis is auto-digestion by protease enzyme as a result of premature activation of zymogen granules releasing which digest the pancreas and surrounding tissue. The normal pancreas has only a poorly developed capsule, and adjacent structures, including the common bile duct, duodenum, splenic vein and transverse colon, are commonly involved in the inflammatory process.


The severity of acute pancreatitis is dependent upon the balance between activity of released proteolytic enzymes and anti-proteolytic factors. like trypsin inhibitor protein .

CAUSES OF ACUTE PANCREATITIS

Common (90% of cases) Gallstones Alcohol Idiopathic Post-ERCP Rare Post-surgical (abdominal, cardiopulmonary bypass) Trauma



Drugs like: azathioprine, thiazide diuretics, L-asparginase, and sodium valproate. Metabolic (hypercalcaemia, hypertriglyceridaemia) Pancreas divisum Sphincter of Oddi dysfunction Infection (mumps, Coxsackie virus) Hereditary Renal failure Organ transplantation (kidney, liver) Severe hypothermia Petrochemical exposure

CLINICAL PICTURE

Severe, constant upper abdominal pain which radiates to the back in 65% of cases builds up over 15-60 minutes. Nausea and vomiting are common. There is marked epigastric tenderness, but in the early stages (and in contrast to a perforated peptic ulcer) guarding and rebound tenderness are absent because the inflammation is principally retroperitoneal.


Bowel sounds become quiet or absent as paralytic ileus develops. In severe cases the patient becomes hypoxic and develops hypovolaemic shock with oliguria. Discoloration of the flanks (Grey Turner's sign) or the periumbilical region (Cullen's sign) are features of severe pancreatitis with haemorrhage “Haemorrhagic pancreatitis”. The differential diagnosis includes a perforated viscus, acute cholecystitis and myocardial infarction.


The most important D. D. of acute pancreatitis are: Perforated viscus. Acute cholecystitis. Inferior myocardial infarction.

COMPLICATIONS OF ACUTE PANCREATITIS

COMPLICATIONS OF ACUTE PANCREATITIS



A. SYSTEMIC: 1. Systemic inflammatory response syndrome (SIRS): Due to increased vascular permeability from multi-causes. 2. Acute respiratory distress syndrome (ARDS). 3. Hyperglycaemia. 4. Hypocalcaemia. 5. Low serum albumin.

B. PANCREATIC: Necrosis. Abscess. Pseudocyst. Pancreatic ascitis and/or pleural effusion.

C. GASTROINTESTINAL: Upper GIT bleeding due to gastric, duodenal erosions or varices. Duodenal obstruction due to pressure by pancreatic mass. Obstructive jaundice due to compression of CBD. Rarely erosion into colon.

PROGNOSIS

1. Acute pancreatitis is usually mild and self-limiting, with minimal organ dysfunction and uneventful recovery. 2. In some patients, it is severe, with local complications such as necrosis, pseudocyst or abscess, and systemic complications leading to multi-organ failure. The mortality in this severe group is approximately 30%.

PANCREATIC PSEUDOCYST

Pancreatic pseudocyst is a localised peri-pancreatic collection of pancreatic juice and debris which usually develops in the lesser sac following inflammatory rupture of the pancreatic duct. The pseudocyst is initially contained within a poorly defined, wall of granulation tissue which matures over a 6-week period into a fibrous capsule.



Small intrapancreatic cysts and pseudocysts are common features of both acute and chronic pancreatitis; they are usually asymptomatic and resolve as the pancreatitis recovers. Pseudocysts greater than 6 cm in diameter rarely disappear spontaneously. Large pseudocysts cause constant abdominal pain, can produce a palpable abdominal mass and may compress or erode surrounding structures including blood vessels to form pseudoaneurysms.


Pancreatic ascites: occurs when fluid leaks from a disrupted pancreatic duct into the peritoneal cavity. Leakage into the thoracic cavity can result in a pleural effusion or a pleuro-pancreatic fistula.

diagnosis of acute pancreatitis

Elevation of S. amylase or lipase concentration: S. amylase (normal range is 50-300 U/L) elevated early in the disease and soon return to normal due to renal excretion. Mild to moderate elevation also occurs in other acute abdominal conditions like perforated DU, acute cholecystitis, intestinal obstruction, intestinal ischaemia and ruptured ovarian cyst. Urine amylase also may be measured. A persistently elevated serum amylase concentration suggests pseudocyst formation. .


Good U/S of the pancreas may confirms the diagnosis of pancreatitis. U/S also shows evidence of gallstones if present CT scan: Useful in diagnosis and confirming viability of the pancreas. Plain X-rays are taken to exclude other diagnoses such as perforation or obstruction and to identify pulmonary complications. Biochemical and haematological tests: like albumin, glucose, urea, ALT, lactic dehydrogenase, S. calcium, WBC count, C-reactive protein and Po2. (These are of prognostic value).


The presence of gas within necrotic material suggests infection and impending abscess formation, in which case percutaneous aspiration of material for bacterial culture should be carried out and appropriate antibiotics prescribed. Involvement of the colon, blood vessels and other adjacent structures by the inflammatory process is best seen by CT.


serial assessment of C-reactive protein (CRP) is a useful indicator of progress. It is worth noting that the serum amylase concentration has no prognostic value.

MANAGEMENT OF ACUTE PANCREATITIS

The initial management : analgesia: Pethidine (but not morphine) may be needed for severe pain. Correction of hypovolaemia using normal saline and/or colloids. All severe cases should be managed in intensive care unit. A central venous line or Swan-Ganz catheter and urinary catheter are used to monitor patients with shock.


5. Hypoxic patients need oxygen and patients who develop adult respiratory distress syndrome (ARDS) may require ventilatory support. 6. Hyperglycaemia is corrected using insulin. 7. it is not necessary to correct hypocalcaemia by intravenous calcium injection unless tetany occurs. 8. Nasogastric aspiration is only necessary if paralytic ileus is present.


9. Enteral feeding via a naso-enteral tube should be started at an early stage in patients with severe pancreatitis because a. They are in a severely catabolic state and need nutritional support . b. Enteral feeding decreases endotoxaemia and so may reduce systemic complications.


10. Prophylaxis of thromboembolism with low-dose subcutaneous heparin is also advisable. 11. Prophylactic, broad-spectrum intravenous antibiotics such as imipenem or cefuroxime may improve outcome in severe cases.

ADVERSE PROGNOSTIC FACTORS IN ACUTE PANCREATITIS(GLASGOW CRITERIA)

Serum calcium < 2 mmol/l (8 mg/dl) (corrected) S. Glucose> 10 mmol/l (180 mg/dl) S. Urea > 16 mmol/l (45 mg/dl) (after rehydration) Alanine aminotransferase (ALT) > 200 U/l Lactate dehydrogenase (LDH) > 600 U/l

SPECIFIC THERAPY

Patients who present with cholangitis or jaundice in association with severe acute pancreatitis should undergo urgent ERCP to diagnose and treat choledocholithiasis. In less severe cases of gallstone pancreatitis, biliary imaging (using MRCP) can be carried out after the acute phase has resolved.


If the liver function tests return to normal and ultrasound has not demonstrated a dilated biliary tree, laparoscopic cholecystectomy with an on-table cholangiogram is appropriate because any common bile duct stones have probably passed. When the operative cholangiogram detects residual common bile duct stones, these are removed by laparoscopic exploration of the duct or by post-operative ERCP. Cholecystectomy should be undertaken within 2 weeks following resolution of pancreatitis to prevent further potentially fatal attacks of pancreatitis.

CHRONIC PANCREATITIS

Definition: Chronic pancreatitis is a continuous, prolonged, inflammatory and fibrosing process of the pancreas with irreversible morphologic changes resulting in permanent endocrine and exocrine pancreatic dysfunction Acute pancreatitis and chronic pancreatitis are different disease processes, and most cases of acute pancreatitis do not result in chronic disease.

Causes of chronic pancreatitis

The main causes of chronic pancreatitis include the following: 1. Alcoholism: Changes appear to develop slowly and may develop after excessive alcohol consumption for 10 years or more. Alcoholism is associated with chronic pancreatitis in 60-90% of patients. 2. Idiopathic: Etiology is idiopathic in 10-40% of patients. 3. Hereditary causes: Hereditary pancreatitis is an autosomal dominant disorder. Symptoms usually appear in the patient's first decade of life, and eventually lead to both exocrine and endocrine pancreatic dysfunction.


4. Autoimmune conditions: Autoimmune pancreatitis is a rare condition that is often seen in patients with primary sclerosing cholangitis. 5. Congenital causes: A congenital abnormality of fusion, pancreas divisum, can cause chronic pancreatitis 6. Cystic fibrosis: This disease is associated with pancreatic atrophy and chronic pancreatitis 7. Other conditions: Hyperlipidemia, hyperparathyroidism, and uremia can cause chronic pancreatitis.

PATHOLOGY

Pathologically chronic pancreatitis can be classified into 3 categories: (1) Chronic calcifying pancreatitis (almost always related to alcoholism), (2) Chronic obstructive pancreatitis the pancreatic duct is dilated, and the pancreas is normal in size, atrophic, or focally and/or globally enlarged.


A variety of factors are implicated in chronic obstructive pancreatitis; these include Ductal obstruction due to ampullary stenosis, inflammatory or neoplastic causes. Surgical ductal ligation, Fibrosis due to a pseudocyst as a complication an episode of acute pancreatitis.

CLINICAL PRESENTATION

Any age group can be affected, but chronic pancreatitis is unusual in children younger than 10 years. Most patients are aged 40-50 years. A slight male preponderance exists. The most common presentation of chronic pancreatitis, is abdominal pain. Pain can be episodic, lasting hours to days, or it can persist for months or even years. The pain is characteristically steady in the epigastrium, and it frequently radiates to the back.


2. Most patients lose weight during the course of the disease. This weight loss may be related to malabsorption due to pancreatic exocrine deficiency or the fear of eating, because food intake exacerbates the pain. Pain relieve may occur after alcohol drinking or leaning forwards. 3. On occasion, the disease process can be painless, and patients may present with steatorrhea, weight loss, or diabetes mellitus.



Complications


1. Chronic pancreatitis is a relapsing condition that presents with abdominal pain. As the disease progresses, the frequency and duration of episodes of abdominal pain increase. Consequently, the following complications could occur: 2. Narcotic addiction is a common problem because of the intractable pain. 3. Weight loss and malabsorption are also common. 4. pseudocyst and fistula formation


5. pseudoaneurysms of large arteries close to the pancreas. 6. Stenosis of the common bile duct. 7. Splenic and/or portal venous obstruction. 8. Diabetes can develop in 70-90% of patients with chronic calcific pancreatitis. 9. Pancreatic ascitis.

The most important D. D. of chronic pancreatitis is carcinoma of the pancrease.

INVESTIGATIONS


A. Tests to establish the diagnosis of chronic pancreatitis and to define the anatomy of pancrease: 1. A. Plain radiographs show pancreatic calcification in 25-59% of patients. This feature is pathognomonic for chronic pancreatitis. NOTES: On anteroposterior radiographs, the spine may mask small punctate calcification; therefore, additional oblique or lateral imaging may be indicated.


Plain abdominal radiograph shows calcification in the pancreas associated with osteomalacia secondary to malabsorption.



2. Gastrointestinal (GI) tract barium testing still has a place in the management of chronic pancreatitis. First, some patients with chronic pancreatitis present with atypical abdominal complaints, and initially, barium studies may be ordered. Second, complications from chronic pancreatitis may cause obvious changes in the GI tract.


Upper gastrointestinal tract barium study shows a reverse 3 in the duodenum due to chronic pancreatitis. Pancreatic carcinoma can have a similar appearance


3. Ultrasonography is the first modality to be used in patients presenting with upper abdominal pain, although the direct diagnosis of chronic pancreatitis is not always possible (the pancreas may appear normal even in the presence of advanced disease. In patients who are obese, excessive intraperitoneal gas may obscure the pancreas. Gas overlying the pancreas also can make visualization of the pancreas difficult). ).


Sonography can help in determining the cause of chronic pancreatitis (eg, calculus disease) and in assessing the complications of the disease (eg, pseudocysts, ascites, splenic/portal venous obstruction

U/S: shows a pseudocyst of pancrease

4. MRI, particularly MRCP, is a noninvasive technique. MRI provides excellent images that may show the changes in the diseased pancreas and also the complications of chronic pancreatitis. The use of secretin with MRCP can demonstrate pancreatic exocrine reserve. as well as dilated Santorini duct seen in pancreas divisum.


MRI scan through the tail of the pancreas shows a dilated tortuous pancreatic duct (arrow).



5. CT is excellent for imaging of the retroperitoneum, and it is useful in differentiating chronic pancreatitis from pancreatic carcinoma.

CT: shows an enlarged pancreas associated with punctate calcification

6. Retrograde Cholangiopancreatography (ERCP): Is the most sensitive imaging modality; it is used to show the ductal anatomy directly and when intervention (eg, stricture dilatation, stent placement) is contemplated


ERCP: Shows a dilated common bile duct (CBD) associated with a stricture of the lower CBD (not well shown on this image) and a dilated ectatic tortuous pancreatic duct.


7. Angiography is reserved for patients with suspected angiographic complications resulting from chronic pancreatitis


Angiographyshows an occluded splenic vein and a large peripancreatic collateral vein that drains into the portal vein


B. Tests of pancreatic function for exocrine and endocrine functions like: 1. collection of pancreatic juice after secretin injection. 2. PABA (pancreolauryl) test . 3. Faecal chymotrypsin or elastase. 4. Blood glucose test.



TREATMENT OF CHRONIC PANCREATIC


1. Alcohol avoidance is essential, although some patients try to relieve pain by drinking excessive alcohol which causes further pancreatic damages 2. Surgical procedures including partial pancreatic resection and pancreatico-jejunostomy. 3. ERCP procedures: including dilatation and stent insertion of main pancreatic duct and lithotripsy.


4. Medical treatment: Including enzyme replacement (exocrine function), treatment of diabetes mellitus by insulin therapy and the most important is pain reliving by giving different types of analgesics including narcotics which may lead to drug addiction. Pain may be relieved some times by giving oral pancreatic enzymes.. The medical treatment also includes vitamins and mineral replacement and treatment of malabsorption. 5. Management of complications.