الفهرس 
EMBRYOLOGY OF THE PANCREASOnly 14 pages are availabe for public view
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Abstract
Acute pancreatitis is an inflammatory disorder of the pancreas, causing sudden and severe abdominal pain. The pancreas is an organ that lies in the back of the mid-abdomen. It is responsible for insulin production and the manufacture and secretion of digestive enzymes. Most attacks of acute pancreatitis do not lead to complications, and most people recover uneventfully with medical care. However, a small proportion of people have a more serious illness that requires intensive medical care. In all cases, it is essential to determine the underlying cause of acute pancreatitis and, if possible, to treat this conditions to prevent a recurrence.
Gallstone pancreatitis is the most common cause of AP. Because the gallbladder and pancreas share a drainage duct, gallstones that lodge in this duct can prevent the normal flow of pancreatic enzymes and trigger acute pancreatitis.
Alcoholic pancreatitis is seen more frequently in men. Ethanol causes spasm of the sphincter of Oddi, and more importantly, it is a metabolic toxin to pancreatic acinar cells. It also transiently decreases pancreatic blood flow, possibly causing focal ischemic injury to the gland.
As regards pathogenesis of acute pancreatitis, the principle mechanism for it is premature activation of the pancreatic enzymes within the pancreas 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.
Clinical diagnosis:
Symptoms of pancreatitis usually include severe constant epigastric pain radiating to the back and flanks and vomiting. Signs may include pyrexia, abdominal distension and peritonism. The classical signs of discoloration of the flanks (Grey-Turner’s sign), peri-umbilicus (Cullen’s sign) and inguinal ligament (Fox’s sign) are not always seen and are a result of retroperitoneal hemorrhage tracking along tissue planes. In addition, symptoms and signs of end-organ involvement may be evident, including respiratory distress, shock, oliguria, jaundice and delirium. It is also possible for SAP to be painless.
Laboratory diagnosis:
Amylase, lipase and trypsinogen are all enzymes derived from pancreatic acinar cells; they can be measured with relative ease. Serum amylase is most commonly used in clinical practice. Serum lipase has been recommended as the assay of choice when available. Lipase concentrations are increased for up to 14 days after onset of pancreatitis and appear to be more sensitive and specific than amylase.
Imaging diagnosis:
Imaging tests provide information about the structure of the pancreas, the ducts that drain the pancreas and gallbladder, and the tissues surrounding the pancreas. Imaging tests may include transabdominal ultrasound, Computed tomography scanning of abdomen, MRI and Magnetic resonance cholangiopancreatography.
Assessment of disease severity:
Accurate prediction of severity early in the course of disease offers potential benefits in that complications can be anticipated and detected early through the use of intensive monitoring and frequent clinical assessment, and early and aggressive therapies can be instituted to attempt to prevent these complications. Routine clinical assessment at the time of admission is associated with low sensitivities (<50%) in identifying patients with SAP. Therefore, alternative methods for assessing disease severity based on scoring systems, CT scanning, and serum markers have been widely studied. In addition to these methods, hemoconcentration and obesity have been reported to be predictive of severe disease.
Treatment:
The goals of treatment of acute pancreatitis are to alleviate pancreatic inflammation and to correct the underlying cause. Treatment usually requires hospitalization for at least a few days.
Mild pancreatitis usually resolves with simple supportive care, which entails monitoring, drugs to control pain, antiacid therapy and intravenous fluids. You may not be allowed to eat anything during the first few days, but most people can gradually resume eating within three to seven days.
Moderate to severe pancreatitis requires more extensive monitoring and supportive care. This is because severe pancreatitis can lead to potentially life-threatening complications, including damage of the heart, lung and kidneys. People with pancreatitis of this severity may be closely monitored in an intensive care unit.
During this time you may be given one or more of the following treatments:
• Intravenous fluids are given to prevent dehydration.
• Nutritional support in acute pancreatitis has been discussed in many researches and studies in the last decade and it had been shown that early nutritional support plays an important role in preventing serious complications and ensuring optimal recovery in patients with acute pancreatitis and malnutrition.
• Oral feeding should be started once the patients pain resolve. In patients with moderate to severe pancreatitis 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.
• About 30 percent of people with severe acute pancreatitis develop an infection in the damaged pancreatic tissue. Antibiotics can prevent infections and control infections that are already present. It has been settled that imipenem is the suitable choice.
• Acute pancreatitis is sometimes complicated by extensive damage and/or infection to the pancreatic tissue. In these cases, the damaged and/or infected tissue may be removed in a procedure referred to as a necrosectomy. Necrosectomy can be done as a minimally invasive procedure.
• The therapeutic role of ERCP in acute pancreatitis is manifold. It is often directed towards management of gallstone and microlithiasis related pancreatitis, pancreas divisum, sphincter of Oddi dysfunction, pancreatic ductal neoplasm or towards management of complications such as ductal disruption or debridement of pancreatic necrosis.
Complications:
Systemic complications include ARDS, multiple organ dysfunction syndrome, DIC, hypocalcemia (from fat saponification), hyperglycemia and insulin dependent diabetes mellitus (from pancreatic insulin producing beta cell damage).
Local complications include pancreatic necrosis, pseudocyst or abscess formation, splenic artery false aneurysms, hemorrhage from erosions into splenic artery and vein, thrombosis of the splenic vein and portal veins and progression to chronic pancreatitis.
Prognosis:
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 etiology of the attack of pancreatitis, and the causes must be looked for and excluded.