الفهرس 
PHYSIOLOGY OF PANCREASOnly 14 pages are availabe for public view
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Abstract
Acute pancreatitis is considered a common surgical emergency. It ranges from mild attack to severe acute pancreatitis up to pancreatic necrosis and multisystem organ failure. So critical care, close observation should be taken toward these patients.
As regards pathogenesis of acute pancreatitis the principle mechanism for it is premature activation of the pancreatic enzymes within the pancrease that leads to organ injury and pancreatitis, also inflammatory mediators (IL-1, IL-6, TNF and others) should be taken in consideration as it causes increases in the pancreatic vascular permeability leading to hemorrhage, edema and eventually pancreatic necrosis.
As regards diagnosis of acute pancreatitis a triple assessment should be followed:
1. Clinical diagnosis
The patient with acute pancreatitis is presented mainly with pain, nausea and vomiting associated with multiple signs that may vary from mild tenderness to generalized peritonitis up to multisystem organ failure.
2. Laboratory diagnosis:
It should be started once working diagnosis of acute pancreatitis is started, S. amylase, lipase are the main diagnostic factors. However individual studies support the superiority of the lipase.
3. Imaging diagnosis
• Visualization of inflammatory changes within the pancreas provides morphological confirmation of the diagnosis.
• Many imaging devices are helpful in diagnosing acute pancreatitis (ultrasound, endoscopic ultrasound, computed tomography and more recently MRI and MRCP).
Severity of acute pancreatitis can be assessed
1. Clinically
2. Multifactorial system:
It includes multiple scoring system for assessment of severity of acute pancreatitis like Ranson’s criteria, Glasgow criteria, APACHE scoring system , BALI scoring system and BISAP scoring system.
3. New serum markers
• Recent researches has examined potential biological markers for predicting the severity and prognosis of acute pancreatitis.
• These includes IL-1, TNF, C. reactive protein, lactate dehydrogenase and other.
As regard management of acute pancreatitis it can be managed conservatively or surgically:
Recently new trends have been applied in the management of acute pancreatitis , nutritional support, antibiotic prophylaxis, surgical and laparoscopic management.
As regard antibiotic prophylaxis, recent studies showed that empiric antibiotic therapy to prevent secondary infection in acute pancreatitis has no benefit, and it is reasonable to initiate antibiotic treatment in patients with necrotizing pancreatitis:
• It has been settled that imipenem is the suitable choice.
• Limitation for the use of antibiotics is mainly due to their side effects especially increase rate of fungal infection, bacterial resistance more with gram +ve organisms.
Nutritional support in acute pancreatitis has been discussed in many researches and studies in the last decade and it had been shown that in patient with mild acute pancreatitis oral feeding should be started once the patients pain resolve.
In patients with moderate to severe pancreatitis beginning nutritional support as early as possible is more beneficial, optimally nasojejunal feeding with a low fat formulas should be initiated at admission.
However, TPN may be required in patients who are unable to maintain their caloric needs with enteral nutrition or because adequate jejunal access cannot be maintained. TPN should include fat emulsions in amounts sufficient to prevent essential fatty acid deficiency.
Early nutritional support plays an important role in preventing serious complications and ensuring optimal recovery in patients with acute pancreatitis and malnutrition.
Infected pancreatic necrosis is thought to be a result of bacterial translocation from the gastrointestinal tract. Breakdown of gut barrier integrity systemic and local immunosuppression from the early phase and bacterial overgrowth due to the decrease of gut motility.
Enteral nutrition appears to be clinically beneficial because it encourages the rapid return of normal gut function and reduces the cytokine generated stress response that occurs during an acute episode of pancreatitis.
Studies indicate that elemental dietary formulae, i.e., ones that are predigested, consisting of simple sugars and amino acids, have little stimulatory effect on the pancreas.
Studies documented that enteral nutrition is cheaper than parenteral nutrition in patients with acute pancreatitis.
Many studies showed significant evidence that the patients given enteral nutrition received fewer days of nutritional support than did the patients given parenteral nutrition and accordingly decrease length and cost of hospitalization.
The main indication for surgery in acute pancreatitis is infected pancreatic necrosis. Infection occurs in approximately 30-40% of patients with pancreatic necrosis.
The therapeutic role of ERCP in acute pancreatitis is directed towards management of gallstone and microlithiasis related pancreatitis, pancreas divisum, sphincter of Oddi dysfunction, pancreaticobiliary ascariasis, pancreatic ductal neoplasia or towards management of complications such as ductal disruption or debridement of pancreatic necrosis.
Other new measures in treatment of acute pancreatitis under research such as role of anticytokine therapy, low intensity laser radiation, protease inhibitors, antioxidant, heparin, H2 antagonist.
The overall mortality from acute pancreatitis has remained at 10-15% over the past 20 years. There is a clear responsibility before the patient is discharged to determine the aetiology of the attack of pancreatitis, and the causes must be looked for and excluded.