Pancreatitis

Synonyms :  Acute Pancreatitis

Clinical features, Diagnosis, Management, Prognosis, Nutrition, Herbs,

Pancreatitis refers to inflammation and damage of the pancreatic tissue that is usually classified into acute and chronic. Acute and chronic forms are distinguished from each other on the basis of structural (pathologic) criteria. In acute pancreatitis the gland is normal before the attack and can return to normal after resolution of the attack, whereas in chronic pancreatitis the gland is abnormal before or after attack, or both. This classification scheme does not depend on how rapidly symptoms appear or resolve, or on the severity of the symptoms (what would be expected from the terms acute and chronic). Thus, it may be impossible to distinguish an exacerbation of chronic pancreatitis from an attack of acute pancreatitis on clinical grounds alone. 

Acute Pancreatitis 

This is an acute condition resulting from the activation of the digestive proenzymes in the pancreatic duct system or even in the pancreatic glandular cells. The release of enzymes leads to necrosis of the pancreatic tissue and adjacent structures. About 50% of cases are associated with biliary disease (acute pancreatitis develops in 5% of all patients with gallstones) and about 20% with alcoholism while in rest no cause can be identified (idiopathic). However, it is controversial whether alcohol can cause acute pancreatitis in a normal pancreas. Most episodes of alcohol-associated pancreatitis occur in patients who have abused alcohol for many years. Thus, chronic pancreatitis is probably present at the time acute painful episodes begin. 

Risk factors for acute pancreatitis:

       alcohol (probably in the setting of mild chronic pancreatitis) by causing oxidative stress with free radical formation

       gallstones causing temporary impaction in the sphincter of Oddi before passing into duodenum

       local obstructive factors (duodenal diverticulum, stenosis of the papilla of Vater, carcinoma in the head of the pancreas)

       infections (mumps)

       hyperlipoproteinaemia (hypertriglyceridaemia)

       hypercalcaemia

       abdominal trauma 

The precise mechanism how pancreatic proenzymes are activated is not well understood and it can probably vary in different patients. It is believed that increased pressure in the pancreatic duct system may be the first event. The pathologic changes of acute pancreatitis strongly suggest autodigestion of the pancreatic tissue by inappropriately activated pancreatic enzymes. The tissue lesions appear to be the consequence of proteolysis, lipolysis, and damage of blood vessels. Normally, pancreatic enzymes are present in the cells in the proenzyme form and have to be activated, which occurs in the intestines under influence of enzyme enterokinase. Under normal circumstances pancreatic proenzymes and lysosomal enzymes are separated in pancreatic cells. It is possible that direct contact between these two is responsible for the activation of pancreatic proenzymes which then start to digest and damage pancreatic tissue. Activation of trypsin from trypsinogen is believed to be one of the initiating events. The activated enzymes so generated cause disintegration of fat cells and damage to the elastic fibres of blood vessels, which can explain fat necrosis (chalky-white patches scattered throughout the abdominal cavity and seen during surgery) and rupture of blood vessels with resulting haemorrhage.  

Later on after the removal of necrotic tissue by inflammatory cells, a pancreatic pseudocyst (pseudocysts have no epithelial lining in contrast to ‘real? cysts) might be formed from collection of pancreatic secretions walled of by granulation tissue, and with communication with pancreatic duct system. If infection with bacteria occurs, pseudocyst can be transformed into pancreatic abscess. 

Providing the patient survives the attack of acute pancreatitis all of the listed histologic changes in the pancreatis tissue are almost fully reversible with no residual damage left.

Clinical features:  < BACK TO TOP >

       There is usually sudden onset with severe pain in the epigastrium occurring within 12-24 hours following a large meal or alcohol bout.

       The pain is usually persistent (may last for few hours or even several days) and radiates through to the back, and may be described as the most severe pain ever experienced.

       Patients report that sitting up and leaning forward may reduce the pain, but coughing, sneezing, deep breathing and sudden movements may aggravate it (stretching of inflamed peritoneum).

       Nausea and vomiting are common.

       In severe cases patient’s condition worsens with increased respiratory rate (tachypnoea), dyspnoea (breathlessness) and hypoxaemia (low saturation of blood with oxygen) due to the damage of the lungs by enzymes (phospholipase A₂ can also degrade surfactant in the alveoli) and toxic material that get absorbed in blood (ARDS - adult respiratory distress syndrome); there can be fever and hypotension.

       Acute pancreatitis may be mistaken for acute cholecystitis, cholangitis, perforated peptic ulcer, myocardial infarction, bowel infarction or even appendicitis.

       Pseudocyst develops 1-2 weeks after the onset of pancreatitis and presents with persistent abdominal pain, nausea, vomiting and weight loss.

       In case of pancreatic abscess, patient’s condition deteriorates (3-5 weeks after the onset of acute pancreatitis) with severe abdominal pain, fever and weight loss.

Diagnosis:  < BACK TO TOP >

       Physical examination reveals epigastric tenderness with or without rigidity (guarding).

       Serum amylase activity is elevated first day of the disease and after that starts to fall due to renal clearance (amylase is a pancreatic enzyme which is released into the circulation in pancreatic damage). Persistently elevated amylase suggests the development of pseudocyst or pancreatic abscess.

       Tests which are even more specific for pancreas are serum lipase and pancreatic isoamylase (a form of amylase found only in the pancreas, sometimes referred to as amylase-P).

       Blood test shows leukocytosis and raised ESR rate, serum calcium level can fall due to formation of calcium soaps in the pancreas and peritoneal cavity.

       Ultrasound scanning and computed tomography are the most important in the diagnosis of the condition, especially to detect the development of pseudocyst, abscess or haemorrhage.

Management  < BACK TO TOP >

       Initially fluid replacement and relief of pain are important (pethidine [Pethidine] by intramuscular injections; morphine can cause constriction of the sphincter of Oddi and is better avoided).

       Careful monitoring of the respiratory function is carried out and oxygen is given if necessary.

       Stopping of oral feeding (intravenous feeding instead) with naso-gastric intubation and suction to prevent overaccumulation of fluid in the stomach and intestines due to reflex atony (ileus) of the gut. Ileus is always found in the acute phase and suction should be continued until gastrointestinal motility has returned. Suction of the gastric content can also help relieve vomiting.

       Surgery is an option in case of pancreatic abscess or cholecystitis of the gallbladder.

       Surgical resection of the pancreas may be carried out when necrosis is very marked but the mortality rate is high; clinical trials did not manage to demonstrate that this improves the outcome.

       Pseudocysts usually subside spontaneously in 4-6 weeks but if they fail to do so, surgical resection in treatment of choice.

       Prognosis depends upon the severity of the attack. Overall, the mortality is 10-20%, and death is caused by multiorgan failure, shock, secondary abdominal infection or the adult respiratory distress syndrome.

Prognosis  < BACK TO TOP >

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Nutrition < BACK TO TOP >

Nutrition that alleviate or prevent Pancreatitis :-
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Herbs < BACK TO TOP >

Herbs that alleviate or prevent Pancreatitis :-
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