The pancreas is an important source of digestive enzymes and fluids, and plays a critical role in regulating blood sugar levels through the production of insulin and glucagon (NDDIC, 2012). Should the pancreas become inflamed there is the risk that the digestive enzymes will become activated within the pancreas, resulting in self-digestion. This disease is known as pancreatitis and even mild cases require hospitalization. This essay will review what is known about pancreatitis in the United States and the clinical guidelines for diagnosis and treatment.
Pancreatitis Pathophysiology, Epidemiology, and Etiology
The digestive enzymes produced by a healthy pancreas are secreted into the small intestine as zymogens, which are enzymes that have their catalytic domain blocked by a peptide group (Berg, Tymoczko, and Stryer, 2002). The intestinal brush border cells secrete enteropeptidase, which removes the peptide blocking the catalytic domain of trypsin. Trypsin then activates the digestive enzymes secreted by the pancreas. This system helps to protect the pancreas and secretory duct system from the enzymes during synthesis and secretion. Should the pancreas become inflamed, this protective process can break down and both the pancreas and duct system can be degraded due to the activity of these enzymes. The exocrine and endocrine functions of the pancreas will suffer accordingly.
There are two categories of pancreatitis, acute and chronic (NDDIC, 2012). Acute pancreatitis is a sometimes life-threatening attack that occurs in a previously healthy person, whereas the chronic form of the disease is progressive and recurrent attacks (Andris, 2010). The acute form of the disease is primarily caused by gallstones and heavy alcohol consumption, while the chronic form is due to long-term, heavy alcohol consumption, genetics, or autoimmune disease. In the United States, approximately 210,000 individual will suffer the acute form of the disease each year (NDDIC, 2012), while the prevalence of the chronic form is believed to be comparatively rare (Braganza, Lee, McCloy, and McMahon, 2011).
The most common (95%) symptom patients exhibit when seeking care for pancreatitis is epigastric pain felt in the chest or back region (Andris, 2010). Patients may complain of a sudden onset of pain accompanied by nausea and vomiting. The inflammation may cause a fever, which may precede the onset of pain. The resulting hypovolemia can trigger hypotension, tachycardia, attenuated peripheral perfusion, and shock. The pain and other symptoms are sometimes exacerbated if the patient eats fatty foods, consumes alcohol, or stands in an upright position. By contrast, a fetal position, which relieves pressure on the pancreas, reduces pain levels.
Most patients (85-90%) with the chronic form of the disease will also present with epigastric pain (Braganza, Lee, McCloy, and McMahon, 2011). These patients will tend to be elderly and may present with steatorrhea, diabetes, or jaundice depending on the etiology. Many patients experience so much pain that they may have quit eating and could be showing signs of malnutrition. Patients with late stage disease may be addicted to analgesics and their personal and professional lives in disarray as a result.
Arriving at a diagnosis of acute pancreatitis generally depends on patients presenting with epigastric pain and vomiting, together with elevated levels of pancreatic enzymes in the blood (Sargent, 2006). If the patient presents shortly after pain onset, amylase levels will be elevated by 2 hours (Andris, 2010). However, 36 hours after the onset of pain amylase levels may have returned to baseline. For these patients, a diagnosis will depend on elevated lipase levels. Lipase levels will often remain elevated for at least two weeks and should be monitored during treatment to help confirm a diagnosis of pancreatitis. If either enzyme is three times normal levels, then pancreatitis is indicated. Laboratory tests should also include a full blood count, liver function, blood glucose, urea and electrolytes, coagulation screen, triglycerides, arterial blood gases, and C-reactive protein (Sargent, 2006). To rule out other causes, such as a bowel perforation or obstruction, the abdominal region should be imaged.
A diagnosis of chronic pancreatitis, in the absence of a long history of acute pancreatitis, depends on the same laboratory tests (Braganza, Lee, McCloy, and McMahon, 2011). Imaging studies are also important for arriving at a definitive diagnosis. A radiograph revealing pancreatic calcification will be positive in approximately 30% of patients. If this test is negative, contrast-enhanced multi-detector computed tomography (ceMDCT) will often reveal an enlarged, sausage-shaped gland. If the imaging results are negative or inconclusive, a secretin test can be performed if available; however, this test is rarely available and magnetic resonance cholangiopancreatography with secretin stimulation can be substituted. If this test is negative, an endoscopic ultrasound can be performed. If all of the imaging studies are negative, then other potential causes should be considered. Additional tests may be required for suspected autoimmune pancreatitis.
Table: Differential Diagnosis
(Banks et al., 2006)
(Braganza et al., 2011)
Mesenteric ischemia/infarction ceMDCT
Focal autoimmune disease biopsy
Gastric perforation ceMDCT
Pancreatic adenocarcinoma biopsy
Duodenal ulcer ceMDCT
Atypical cystic fibrosis
Biliary colic ceMDCT
Idiopathic large duct disease biopsy
Dissecting aortic aneurysm ceMDCT
Intestinal obstruction ceMDCT
Inferior wall myocardial infarction ceMDCT
An important prerequisite for treating acute pancreatitis is determining disease severity (Andris, 2010). This can be accomplished by assessing patient symptom severity, CT imaging, and the use of a severity index instrument. There are several instruments available that have been supported by empirical validity studies and each has proven to have strengths and weaknesses depending on the clinical constraints. The Ranson criteria, for example, was found to be best for predicting severe pancreatitis, while the CT severity index (CTSI) is best for detecting nectrotizing pancreatitis.
Once the severity of acute pancreatitis has been determined, a clinical management approach can be designed (Andris, 2010). The treatment of mild acute pancreatitis depends on resting the bowel and pancreas by enforcing a nothing by mouth status. Intravenous fluids and jejunum feeding are therefore required during this period, with the former important for resolving hypovolemia and promoting urine production (30 ml/h). Analgesics are commonly prescribed in combination with antimemetics for uncontrolled nausea and vomiting. For pain, hydromorphone, morphine, or fentanyl are recommended. Hyperglycemia will need to be managed and supplemental oxygen may be required to prevent hypoxia. Patients with gallstones will need to have them removed and in cases of suspected alcohol addition, be monitored for symptoms of withdrawal.
In patients with severe acute pancreatitis, hypovolemia is the primary concern (Andris, 2010). Fluid accumulation around the pancreas can lead to multiple organ failure and should two or more organs fail, the risk of mortality increases to almost 70%. Pulmonary involvement and failure is a common complication. Sepsis and pancreatic hemorrhage are also significant risk factors, especially in patients with necrotizing pancreatitis.
The recommended treatment approach for chronic pancreatitis is similar to mild acute pancreatitis, except the treatment period is indefinate (Braganza, Lee, McCloy, and McMahon, 2011). The primary concerns are pain management, exocrine and endocrine support, and addressing mental health needs. Only when these approaches fail to limit patient suffering, should endoscopic or surgical treatment be considered.
Analgesic use mirrors recommendations for controlling pain in cancer patients (Braganza, Lee, McCloy, and McMahon, 2011). The first line recommendations are paracetamol and/or a non-steroidal anti-inflammatory drug. This is often followed by an opioid drug like tramodol, which may be prescribed in combination with a neuroleptic antidepressant. Narcotic analgesics are not recommended and may even cause complications that result in increased levels of pain. Patients with autoimmune pancreatitis often benefit from steroid administration. A maintenance dose of prednisolone (5.0-7.5 mg/d) has been found to be effective in preventing relapse in these patients.
Health Promotion and Disease Prevention
Patients suffering from both acute and chronic pancreatitis should be advised to refrain from consuming alcohol, smoking, or eating fatty foods (Andris, 2010; Braganza, Lee, McCloy, and McMahon, 2011). Adopting a healthy lifestyle, especially in terms of nutrition, is highly recommended. For patients with chronic pancreatitis, there is substantial empirical support for micronutrient supplementation being effective in reducing pain and the frequency of attacks (Braganza, Lee, McCloy, and McMahon, 2011). Micronutrient supplementation includes methionine, vitamin C, and vitamin E and a commercial preparation called Antox is available in the United Kingdom. Micronutrient therapy and other diet modifications should be done under the advice of the treating physician and monitored through laboratory tests. Patients who suffer from substance abuse should also be referred to mental health services for a psychiatric evaluation. Relapse prevention will likely depend on how successful their recovery is.
Patients suffering from acute or chronic pancreatitis will benefit from any and all information that promotes reducing or eliminating the underlying causes of the disease (Andris, 2010; Braganza, Lee, McCloy, and McMahon, 2011). Accordingly, the suspected or known causes for their disease should be discussed in detail. This discussion may include information on how to recover from alcohol addiction, stop smoking, control diabetes, and control hypertriglyceridemia. For patients suffering from substance abuse, the importance of mental health services for preventing relapse should be discussed. Patients with autoimmune or ideopathic pancreatitis will require information specific to the etiology of their disease.
When relevant, the information provided to pancreatitis patients should emphasize lifestyle choices (Andris, 2010; Braganza, Lee, McCloy, and McMahon, 2011). Patients should be made aware of the belief that reducing or eliminating fatty foods, alcohol, and tobacco help prevent relapse. Patients could also be informed of the possibility that increasing the amount of antioxidant-rich foods may provide benefits beyond replacing unhealthy foods.
Patient fears about pancreatitis should be addressed and any misconceptions dispelled as soon as possible (Braganza, Lee, McCloy, and McMahon, 2011). The importance of continuity of care should be emphasized and the risks of analgesic addiction discussed at length.
The primary goals of treatment are supportive care during hospitalization and home recovery, reducing inflammation and necrosis, preventing and treating complications, and preventing relapse (Amerine, 2007). Patients with mild acute pancreatitis typically recover within five to seven days and are discharged from the hospital; however, patients with moderate to severe pancreatitis will demand continuous monitoring in the intensive care unit for the first 48 hours and therefore typically require a longer hospital stay. Given the severity of the disease and the long hospital stay, patients will need considerable support during the discharge process and may even require home services. However, acute pancreatitis relapse prevention depends on prolonged management of the disease for several months after discharge and the combined efforts of physicians, nurses, nutritionists, and mental health professionals to alter the underlying causes of the disease. For patients with chronic pancreatitis, disease management is an ongoing process.
Amerine, Emmie. (2007). Get optimum outcomes for acute pancreatitis patients. Nurse Practitioner, 32(6), 44-48.
Andris, Abby. (2010). Pancreatitis: Understanding the disease and implications for care. AACN Advanced Critical Care, 21(2), 195-204.
Banks, Peter A. And Freeman, Martin L. (2006). Practice guidelines in acute pancreatitis. American Journal of Gastroenterology, 101, 2379-2400.
Berg, J.M., Tymoczko, J.L., and Stryer, L. (2002). Biochemistry, 5th Edition. New York, NY W.H. Freeman. Retrieved 18 Feb. 2013 from http://www.ncbi.nlm.nih.gov/books / NBK22589/.
Braganza, Joan M., Lee, Stephen H., McCloy, Rory F., and McMahon, Michael J. (2011). Chronic pancreatitis. Lancet, 377, 1184-1197.
NDDIC (National Digestive Disease Information Clearinghouse). (2012). Pancreatitis. National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). Retrieved 18 Feb. 2013 from http://digestive.niddk.nih.gov / ddiseases/pubs/pancreatitis/.
Sargent, Suzanne. (2006). Pathophysiology, diagnosis and management of acute pancreatitis. Gastrointestinal Nursing, 15(18), 999-1005.
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