Acute Pancreatitis: Expected Presentation vs. Actual Case

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Table of Contents

Abstract
Introduction
Disease description
Actual patient case
Critical analysis and knowledge synthesis
Conclusion
References

Abstract

Pancreatitis is a disease that occurs when pancreatic enzymes are activated in the pancreas rather than the small intestine (Prior, 2009). The disease can be acute or chronic. This paper investigates the variation between the expected presentation and an actual case of acute pancreatitis. Main symptoms include epigastric pain, nausea, vomiting and diarrhea (Balthazar, 2002). Most common causes include gallstones, alcohol and metabolic disorders (Markel, 2009). Patient history, blood tests, ERCP and CT scan are main components of AP diagnosis. Treatment is usually done by administration of fluids, pain management and treatment for nausea. The patient in the case study was a male aged 45 years old and had a history of elevated cholesterol levels which was being managed using atorvastatin. The patient was also a habitual drinker. The patient was admitted suffering from upper abdominal pain nausea and vomiting (Balthazar, 2002). None of the probable causes of AP were established during the first episode. However, a mild lesion established during the second episode was able to confirm that the patient was suffering from acute pancreatitis associated with alcohol use. The patient was treated with meperidine to control pain in both episodes. Other non pharmacological therapies such as bowel rest and fluid replacement were offered.

There is a lot of literature concerning alcohol use and pancreatitis, however, the actual mechanism of interaction remains unknown. More research should be carried out to establish the missing information to improve the diagnosis of alcoholic pancreatitis.

Introduction

Pancreatitis can be described as a “disease that occurs when pancreatic enzymes are activated in the pancreas rather than the small intestine” (Markel, 2009, p. 1). Pancreatitis can occur due to several factors and result into varied symptoms. Acute pancreatitis can be described as a sudden attack that causes inflammation of the pancreas which is often associated with a severe upper abdominal pain (Prior, 2009). This paper seeks to compare and contrast expected presentation of the disease process and use of pharmacotherapeutics with the presentation and treatment witnessed with an actual patient case. The knowledge gained about the disease and drug treatment will then be synthesized through the creation of an appropriate case study of the selected disease process (Balthazar, 2002). In order to bring out a clear comparison only one form of pancreatitis (acute pancreatitis) will be discussed.

Disease description

As shown earlier, acute pancreatitis can be described as a sudden inflammation of the pancreas. Acute pancreatitis can have varied symptoms, the most common ones being: severe epigastric pain that radiates to the back; nausea, diarrhea, vomiting and loss of appetite; hemodynamic instability that may include shock; respiratory distress; tachycardia; and peritonitis (Balthazar, 2002).

The most common cause of acute pancreatitis include: gallstones; alcohol; metabolic disorders such as hereditary pancreatitis, hypercalcemia, hyperlipidemia and malnutrition; penetrating ulcers; abdominal trauma; malignancy; drugs such as steroids, sulfonamides, furosemides, thiazides; infections such as mumps, coxsackievirus, mycoplasma pneumoniae, ascaris and clonorchis; structural abnormalities such as choledochocele and pancreas divisum (Markel, 2009).

Other causes that are less common include long common duct; head and pancreas carcinomas; blockage of pancreatic flow by “ascaris; ischemia following bypass surgery; fatty necrosis;pregnancy; regular marathon running; cystic fibrosis; valproic acid; and aneroxia” (Prior, 2009, pp. 3).

In the diagnosis of acute pancreatitis, the physician requests for patient history regarding alcohol consumption and symptoms of gallstones. Blood tests are then ordered to confirm the cause of the symptoms. Laboratory tests that might be used in the diagnosis of acute pancreatitis include: serum amylase and lipase; liver function tests; blood calcium tests; blood glucose tests; complete blood count and urinalysis; chest and abdominal x-ray; ultrasound examination; endoscopic retrograde cholangiopancreatology (ERCP); and computed tomography (CT) scan (Tsigrelis & Pitchumoni, 2006).

To treat AP, the patient is hospitalized, and an intravenous administration of fluids is carried out to assist in the restoration of blood volume (Prior, 2009). Medication for pain and nausea are provided to ease symptoms (Markel, 2009). Food consumption is usually withheld until the symptoms have been completely suppressed. Antibiotics are usually prescribed in severe cases of acute pancreatitis (Enns & Baillie, 1999). Alcohol consumption should be discontinued even if it’s found not to be the cause of the disease. If gall stones are identified to be the main cause of the acute pancreatitis then the gall bladder should be removed to prevent future episodes. In patients who the cause has not been directly identified, other diagnostic testing should be carried out. Worldwide statistics indicate that gallstones are the commonest causes of acute pancreatitis (AP).

Actual patient case

A “male patient aged 45 years who suffers from elevated cholesterol levels visited the hospital complaining of upper abdominal pain, nausea and vomiting for five days ” (Chintanaboina, & Gopavaram, 2012). The patient did not indicate any history of intolerance to drugs. Prior to the presentation the patient had began to take atorvastatin to manage the cholesterol. The patient was admitted to regular alcohol consumption. Investigations conducted on admission established that his vital signs were stable with a remarkable upper abdominal pain. Liver enzymes such as bilirubin were found to be normal. The serum lipase and amylase were elevated three times above the normal level (Enns & Baillie, 1999).

A CT scan indicated a mild edema of the pancreas. The findings were similar to those established in patients suffering from acute pancreatitis. An ultrasound was conducted on the abdomen indicated that the patient had a normal biliary tree (Markel, 2009). Atorvastatin treatment was temporarily stopped when the patient was admitted. The patient was treated with intravenous fluids, bowel rest, and pain management and discharged from the hospital three days after showing remarkable improvement (Chintanaboina, & Gopavaram, 2012, p. 5). On discharge, his serum lipase level had gone back to the normal range and he had begun to tolerate normal diet. No correlation was directly established between acute pancreatitis and atorvastatin therapy or alcohol use. The patient was however advised to cut down on his alcohol consumption and atorvastatin was restarted at the time of discharge. The risks associated with alcohol consumption and atorvastatin use were discussed with the patient before he was discharged to go home.

The same patient was re-admitted two months later with same symptoms. Upon examination, it was established that his vital signs were stable with a remarkable physical examination for upper abdominal tenderness (Balthazar, 2002 ). His serum amylase and lipase levels were raised considerably. A CT scan showed that there was a slight acinar atrophy and fibrosis (Balthazar, 2002). The slight pancreatic mass lesion could be attributed to alcohol use (Prior, 2009). The patient indeed confirmed that he had continued to take alcohol after the first visit. Further differential investigations were carried out to rule out other possible causes. Findings “on serum IgG4 levels were within the normal range and this ruled out the possibility of autoimmune pancreatitis” (Chintanaboina, & Gopavaram, 2012). The patient responded well to “bowel rest, intravenous fluids and pain management” (Balthazar, 2002, p. 6). In both cases pain control was achieved by meperidine adminstration. Investigation conducted on the levels of serum lipase and amylase showed that the two had gone down considerably. Following a thorough review of the patient case, no direct evidence was established between atorvastatin use and the acute pancreatitis. Alcohol use was implicated due to the fact that the damage established during the second visit was consistent with those established in other alcohol related cases. The patient was therefore advised to stop alcohol consumption. Atorvastatin therapy was again restarted upon discharge from the hospital. No more episodes of chronic pancreatitis were experienced by the patient in the two months follow up.

Critical analysis and knowledge synthesis

The findings of the above case are consistent with expected presentation of the disease process of acute pancreatitis. The symptoms that have been identified in the above case (Upper abdominal pain, nausea and vomiting) are some of the commonest symptoms of acute pancreatitis (Chintanaboina, & Gopavaram, 2012). However, the identification of these symptoms is not conclusive as there are many other conditions that have such symptoms. As described in medical literature concerning the disease, all the differential investigations carried out during the first visit did not show a possible cause of acute pancreatitis. The recurrence of the disease within two months led to a keen interest in establishing the possible cause. The patient was on atorvastatin therapy and was also a habitual alcohol user. There is no enough evidence on the association between pancreatitis and statin therapy. The case, therefore, offers a challenge to the dominant literature regarding the evidence of alcohol to induce pancreatitis.

Literature searches coupled with the findings of the above case has facilitated the organization information regarding alcohol use and acute pancreatitis.

According to the available data, alcohol abuse continues to be a major cause of morbidity and the mortality around the world (Markel, 2009). The association between alcohol use and pancreatitis is not very well understood as compared to the association between alcohol and other well known diseases such as liver cirrhosis. A census carried out in the United States showed that pancreatitis causes an estimated 5,000 deaths annually. Out of this figure, acute pancreatitis accounts for approximately 85%, with the remaining 15% attributed to chronic pancreatitis (Prior, 2009). Chronic pancreatitis is more commonly associated with alcohol abuse compared to acute pancreatitis.

There is lack of strong evidence to link pancreatitis with alcohol abuse. For instance, research data indicates that less than 10% of all alcohol abusers develop clinically relevant inflammation of the pancreas (Enns & Baillie, 1999). It’s therefore assumed that certain individuals are more at risk of developing chronic pancreatitis compared to others. Initially, alcohol abuse was only associated with chronic cases of pancreatitis that often resulted into endocrine and exocrine dysfunction (Markel, 2009). However, as shown in the above case, alcohol abuse can result acute pancreatitis. The acute exacerbations caused by alcohol can be detected early to prevent disease progression into the chronic phase.

A lot of research has been carried out in regard to the link between alcohol and chronic pancreatitis. However, the pathophysiology is still being investigated and there is no proper explanation for the mechanism. A study conducted by the University of Liverpool once concluded that acute pancreatitis occurs due to the fact that alcohol stimulates the pancreas into the production of fatty acids and other substances (Enns & Baillie, 1999). Such substances have the ability to destroy cells and inhibit the capacity of the pancreas to produce its own energy. Available literature indicates that the occurrence of the pancreatitis associated with alcohol often takes place in men aged between 35 and 40 years (Prior, 2009). The initial disease presentation may take several years to appear and usually increases when alcohol consumption is increased or taken for a prolonged period. The patient in the current case experienced pancreatitis symptoms for about one week. Studies indicate that pain experienced in chronic pancreatitis often resolves in one week (Balthazar, 2002).

Usually, the treatment of acute pancreatic is designed according to the needs of a given patient, and depending on the symptoms. The patient in the current case was treated with intravenous fluids, bed rest and pain management. In majority of acute pancreatitis cases, treatment is offered through supportive care, which may include bowel rest, pain killers, replacement of lost fluids and abstinence from food consumption (Balthazar, 2002). The therapy offered aims at preventing the development of further systemic complications, such as the necrosis of pancreatic tissue. The patient in the above case study was treated with meperidine to control pain. Historically, meperidine has been used as a first line option in controlling pain during an episode of acute pancreatitis (Markel, 2009). This is due to the fact that other narcotics were thought to cause irritation of the pancreas due to increased levels of lipase and amylase. However, recent research has shown that narcotic treatment does not necessarily result into increased release of pancreatic enzymes. Following this establishment any analgesic can be used in the treatment of acute pancreatitis. These include morphine, hydromorphine and meperidine (Markel, 2009). Meperidine is still commonly used in the treatment of pancreatitis though it usually has a dosage ceiling (Prior, 2009). Apart from pain control, treatment also aims at managing complications such as necrosis of the pancreatic tissue and organ failure. In the current case, this was done using intravenous fluid administration. This method is however not well understood, especially in regard to alcohol induced pancreatitis (Markel, 2009).

Conclusion

This paper sought to compare and contrast expected presentation of acute pancreatitis process and use of pharmacotherapeutics with the presentation and treatment witnessed with an actual patient case. A critical analysis of the pathophysiologic and pharmacotherapeutic components of an actual client case has also been conducted (Chintanaboina, & Gopavaram, 2012). The knowledge gained about the disease and drug treatment has been synthesized through the creation of an appropriate case study of the selected disease process.

It has been established that alcohol induced acute pancreatitis is not very well understood (Markel, 2009). Following the findings of this report, it’s recommended that more research should be carried out to establish the exact mechanisms through which alcohol results into pancreatitis. If this is established then repeated cases of attack can be prevented through proper diagnosis of alcoholic pancreatitis.

References

Balthazar, J. (2002). Staging of acute pancreatitis. Radiologic clinics of North America, 40(6):1199-1209.

Chintanaboina, J.K. & Gopavaram, D. (2012). Recurrent Acute Pancreatitis Probably Induced by Rosuvastatin Therapy: A Case Report. Case Reports in Medicine. 2012(973279): 1-4. Web.

Enns, R., & Baillie, J. (1999). Review article: the treatment of acute biliary pancreatitis. Aliment pharmacol , 13:1379-1389.

Markel, A. (2009). Alcohol-induced Pancreatitis. Chicago: University of Illinois.

Prior, K. (2009). Alcohol and Pancreatitis. Web.

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