This retrospective study was performed to assess the epidemiological characteristics of acute pancreatitis in patients treated at a Clinic in Kosovo. Determining the anatomopathological form of acute pancreatitis and evaluating the methods applied for its diagnosis and treatment was one of the basic goals of this study. Another objective of this study was to detect eventual deficiencies in the diagnosis and treatment of acute pancreatitis.
The retrospective analysis of the medical documentation of 29 patients who were hospitalized, diagnosed and treated due to acute pancreatitis and its complications, in the departments of Abdominal Surgery at the University Clinical Center in Prishtina, in the period January 2001-December 2002.
Due to acute pancreatitis and its complications, 29 patients were treated. Of these, 17 were male (58.6%) and 12 were female (41.4%). Of the 24 cases with acute pancreatitis, 23 of them (95.8%) were cases with acute edematous pancreatitis and 1 patient (4.2%) with acute necrotic pancreatitis. Due to complications, 6 patients (20.7%) were treated. Of these, 5 cases were treated due to pancreatic pseudocyst and 1 case due to acute necrotic pancreatitis. In all cases, from the first day of hospitalization, antibiotics were applied. All cases with complications are treated surgically.
Keywords: acute pancreatitis, pancreatic necrosis, edematous pancreatitis
Contents
Abbreviations
ABSTRACT
1. INTRODUCTION
1.1. Review data for acute pancreatitis
1.1.1. Etiology of acute pancreatitis
1.1.2. Pathogenesis
1.1.3. The role of activated phagocytes
1.1.4. Cytokines
1.1.5. Diagnosis of acute pancreatitis
1.1.6. Prognostic indicators
1.1.7. Laboratory tests
1.1.8. Types of acute pancreatitis
1.1.9. Complications of acute pancreatitis
1.1.10. Trends of contemporary treatment of acute pancreatitis
2. THE AIMS OF THE STUDY
3. MATERIAL AND METHODS
4. RESULTS
4.1. General data for the sample
4.2. Methods used to diagnose the disease
5. DISCUSSION
6. CONCLUSIONS
7. REFERENCES
Abbreviations:
AP-Acute pancreatitis
SIRS-Systemic Inflammatory Reaction Syndrome
ERCP-Endoscopic retrograde cholangio-pancreatography
ECHO-transabdominal echosonography
PMN-Polymorphonuclear
IL - Interleukin
alpha-FTN: alpha factor of tumor necrosis
APACHE –acute physiologic and chronic health evaluation
LDH - Lactate dehydrogenase
AST –Aspartate-aminotransferase
ALT-Alanine aminotransferase
ABSTRACT
Introduction: Acute pancreatitis is a complex disease. In 80-90% of cases develops edematous form of pancreatitis, a form that is associated with minimal organ dysfunction and is characterized by a rapid convalescence. However, in 15-20% of cases acute necrotic pancreatitis develops a form that is implicated in local and systemic complications. The course of acute necrotic pancreatitis develops in two stages. In the first stage (the first two weeks), extensive pancreatic inflammation and necrosis are followed by systemic inflammatory response syndrome, which, within the first week, can worsen to multiorgan dysfunction syndrome. About 50% of deaths in the first week are due to multiorgan failure. The second stage begins after the second week and is characterized by the development of pancreatic necrosis infection and the formation of fluid collections. Pancreatic necrosis infection attacks about 40-70% of patients with acute necrotic pancreatitis. It is an important risk factor, affecting the rate of systemic complications and mortality. Despite advances made in the diagnosis and treatment of this disease, mortality in patients with pancreatic necrosis infection is still high, 20-50%. The application of relevant diagnostic and therapeutic methods, the identification of patients who are at risk of developing complications is an essential procedure for the correct and successful management of patients with acute pancreatitis.
The aims of the study: This retrospective study was performed to assess the epidemiological characteristics of acute pancreatitis in patients treated at our Clinic. Determining the anatomopathological form of acute pancreatitis and evaluating the methods applied for its diagnosis and treatment was one of the basic goals of this study. Another objective of this study was to detect eventual deficiencies in the diagnosis and treatment of acute pancreatitis.
Material and methods: The retrospective analysis of the medical documentation of 29 patients who were hospitalized, diagnosed and treated due to acute pancreatitis and its complications, in the departments of Abdominal Surgery at the University Clinical Center in Prishtina, in the period January 2001-December 2002. In the patient’s documents are analyzed: anamnesis, laboratory-biochemical analysis, radiological examinations, temperature lists and surgical interventions performed in patients with complications of acute pancreatitis.
Results: Due to acute pancreatitis and its complications 29 patients were treated. Of these, 17 were male (58.6%) and 12 were female (41.4%). Of the 24 cases with acute pancreatitis, 23 of them (95.8%) were cases with acute edematous pancreatitis and 1 patient (4.2%) with acute necrotic pancreatitis. Due to complications, 6 patients (20.7%) were treated. Of these, 5 cases were treated due to pancreatic pseudocyst and 1 case due to acute necrotic pancreatitis. The most attacked age group was 45-64 years old. Blood amylase was determined in only 17 patients (58.6%), while in urine it was determined in 6 patients (20.7%). Even other routine tests such as: leukocytes, Htc, glycemia, albumin, electrolytes, etc., were not determined in most patients.
Pulmonary X-ray and native abdominal X-ray were not performed in most cases. Abdominal ECHO was performed in 13 patients (44.8%).
In all cases, from the first day of hospitalization, antibiotics were applied. Gentamicin and ampicillin were the most commonly prescribed antibiotics. All cases with complications are treated surgically. In 3 out of 5 cases with pseudocysts of the pancreas, internal drainage was performed, while the last 2 were treated with external drainage, respectively cyst extrusion. The patient with necrosis underwent conventional necrosectomy and drainage.
Conclusions: The only cause of acute pancreatitis in our patients is biliary calculi. This finding is based more on anamnestic data and physical examination than on confirmation by relevant diagnostic methods. Diagnosis of acute pancreatitis in our patients is based on clinical presentation, laboratory tests and radiological examinations, where clinical presentation dominates over other diagnostic procedures. Deficiencies are evident in both the diagnosis and treatment of patients. Deficiencies in the diagnosis of acute pancreatitis are more pronounced than those in its treatment.
1. INTRODUCTION
Acute pancreatitis (AP) is an acute chemical, enzymatic inflammation of the pancreas, which can lead to autodigestation of the pancreas and adipose tissue, mainly retroperitoneal, by activated pancreatic enzymes and all this can be accompanied by bacterial infection (1, 2).
Based on the Atlanta criteria (1), AP is divided into:
- Acute edematous pancreatitis
- Acute necrotic pancreatitis
According to these criteria, acute edematous pancreatitis is defined as a form of pancreatitis that is associated with minimal organ dysfunction and is characterized by a rapid convalescence, while severe form of pancreatitis is considered where local and systemic complications are present. Local complications include: necrosis infection, abscess, or pseudocystic formations (1).
Acute necrotic pancreatitis develops in 15-20% of cases. It is now known that acute necrotic pancreatitis is a progressive disease and its course develops in two stages. In the first stage (first two weeks), extensive pancreatic inflammation and necrosis are followed by systemic inflammatory response syndrome (SIRS), which, in the first week, can worsen to multiorgan dysfunction syndrome. The release of proinflammatory mediators is thought to contribute to the pathogenesis of SIRS, a syndrome which is associated with pulmonary, cardiovascular and renal failure. Proinflammatory mediators include pancreatic proteases, cytokines, O 2 free radicals, etc. (3,4).
SIRS, in most cases, also develops in the absence of pancreatic necrosis infection. About 50% of deaths in the first week are caused by multiorgan failure (5,6,7).
Phase II begins after the second week, a phase characterized by the development of pancreatic necrosis infection and the formation of fluid collections (4,5,8).
Pancreatic necrosis infection develops in the second and third week of the disease, in 40-70% of patients with acute necrotic pancreatitis (7.8). This infection is an important risk factor, affecting the rate of systemic complications and mortality. Most microorganisms that causes infections are of enteric origin.
It has been demonstrated that organ failure develops in 50% of patients with pancreatic necrosis and that the extension of pancreatic necrosis is not correlated and does not influence organ failure. The lungs are the first to suffer complications, up to their insufficiency (9).
One study found that lung insufficiency was present in 21% of cases, renal insufficiency in 44.6%, cardiovascular insufficiency in 28.4% and coagulopathy in 7.1% of cases (10.11).
In recent years, changes in the understanding of pathophysiological factors along with technological advancements, have thankfully impacted on improving the management of these patients. However, despite these advances, mortality in patients with necrotic infection and organ failure as a consequence is still high, around 20-50% (8,9,11).
Given the complexity of this disease, the application of relevant diagnostic and therapeutic methods, the identification of patients who are at risk of developing complications, is essential for the correct and successful management of patients with acute pancreatitis (8).
The object of our study is the evaluation of diagnostic methods and therapeutic principles applied for the management of our patients with AP, identification of possible deficiencies in diagnosis and treatment and proposal of appropriate measures, in accordance with the contemporary strategy for diagnosis and treatment of patients with acute pancreatitis.
1.1. Review data for acute pancreatitis
1.1.1. Etiology of acute pancreatitis
The causes of acute pancreatitis are numerous. They can be grouped into metabolic, mechanical, vascular, and infectious agents (1,2).
Causes of acute pancreatitis:
- Mechanical obstruction of the pancreatic duct (with calculus)
- postoperative and posttraumatic pancreatitis
- ERCP
- obstruction of the pancreatic duct with tumors
- acute consumption of alcohol
- hyperlipoproteinemia-type I, IV, V
- hypercalcemia
- genetic abnormalities of metabolism
- some drugs
- periarteritis nodosa
- atherosclerosis
- parotitis virus
- coxakie viruses etc.
However, the most common causes of acute pancreatitis are: biliary calculi, alcohol, hyperlipoproteinemia, ERCP, operative trauma, and blunt trauma. In 80% of cases, the causes of acute pancreatitis are biliary calculi and alcohol (12).
In some regions (England and Asia) biliary calculi predominate, while in the US, alcohol is the dominant cause of acute pancreatitis (13). In 10-30% of cases, the causes cannot be detected.
It has been found that some patients have a genetic predisposition to acute pancreatitis (13). In this regard, it has been documented that this predisposition is inherited predominantly autosomally and is due to mutation of the corresponding gene for trypsinogen1, which results in premature activation of trypsinogen1 (14).
1.1.2. Pathogenesis
The main function of pancreatic acinar cells is the synthesis of digestive enzymes (trypsinogen, chymotrypsinogen, proelastase, procarboxypeptidase A and B and profosfolipase A2) and their secretion in the duodenum (15,16).
The conversion of inactive trypsinogen to active trypsin, in the duodenum, is catalyzed by enterokinase (17). Trypsin is the major enzyme that activates other proenzymes, including its precursor, trypsinogen (18).
The synthesis and secretion of these enzymes in inactive form, the synthesis of trypsin inhibitors in the pancreas and the presence of trypsin inhibitors in the blood (alpha1-antitrypsin, alpha2-macroglobulin), constitute the main defense mechanism, which prevents its premature activation and damage pancreas, including auto- digestion as a consequence (19).
However, as a result of the impact of the biliary calculus distally from the junction of the pancreas and the pancreatic duct, bile reflux is enabled in the pancreatic duct, where due to increased pressure leads to rupture of the ductal epithelium and penetration of pancreatic enzymes into the pancreas. Bile fluid plays an important role in the activation of these enzymes. Also, the passage of bile calculus through the papilla can traumatize it, which as a result causes edema of the papilla, and consequently stasis of bile and pancreatic fluid. During the passage of biliary calculus through the papilla, duodenopancreatic reflux is enabled activation of trypsinogen by intestinal enterokinase.
The explanation of the pathogenesis of acute alcoholic pancreatitis is based on the fact that alcohol influences the secretion of denser, more viscous pancreatic fluid, since it leads to protein precipitation and consequently inhibition of the flow of pancreatic fluid. Also, alcohol in the liver, under the action of alcohol-dehydrogenase is converted to acetaldehyde. It has been experimentally found that acetaldehyde injection causes acute pancreatitis. Alcohol is thought to have a direct toxic effect on acinar cells (17,19).
Digestive pancreatic enzymes explain part of the pathogenesis of acute pancreatitis. The release and action of pro-inflammatory mediators is another important mechanism.
In severe forms of pancreatitis, SIRS develops in the first week, a syndrome that is nonspecific for pancreatitis. This syndrome also develops in patients with sepsis, after burns, etc., conditions that are not influenced by the activation of pancreatic enzymes (20). This explains and supports the fact that in the pathogenesis of acute pancreatitis, in addition to enzymes and their action, other factors are involved, primarily proinflammatory cytokines (21).
Frequent complication of SIRS is dysfunction of organic systems, including lung damage, kidney failure, etc. (20).
1.1.3. The role of activated phagocytes
Activation of monocytes (mononuclear macrophages) and PMN granulocytes has been found to be an early occurrence of necrosis and plays an important role in disease progression, from a local necrotic inflammation to SIRS (22). Leukocyte activation influences their aggregation and increases the production of cytokines and other inflammatory mediators (prostaglandins, leukotrienes, thromboxane, platelet activating factor, O2, NO free radicals, and proteases — cathepsin and elastase) (23).
Bacterial endotoxins are potent activators of mononuclear phagocytes and induce the secretion of proinflammatory cytokines (IL-1, IL-6, IL-8, the alpha-factor of tumor necrosis) (24). Monocyte activation and increased secretion of proinflammatory cytokines are associated with the development of systemic complications of acute pancreatitis (21).
Excessive stimulation of PMNs plays an important role in aggravating acute pancreatitis, thus contributing to local destruction and systemic complications (25). Tissue damage by PMNs occurs through the formation of free radicals and the degranulation of proteolytic enzymes (elastase) (26). PMNs synthesize and release, together, pro- and anti-inflammatory cytokines (27).
1.1.4. Cytokines
Based on proinflammatory cytokines, SIRS can be categorized into three grades:
Grade I: Involves the production of cytokines as a reaction to local damage and infection.
Stage II: Protective release of cytokines into the systemic circulation.
Stage III: Characterized by homeostasis imbalance, accompanied by a massive systemic reaction, where cytokines now play a destructive rather than protective role.
Cytokines are low molecular weight proteins. They are secreted by different cell types, where leukocytes (monocytes and PMNs) play a dominant role (28).
IL-1 and alpha-FNT are primary inducers of IL-6 and IL-8 production, which are co-produced in patients with AP. Proinflammatory cytokines induce cell molecular adhesion, locally and systemically, increase capillary permeability, induce leukocyte adhesion and extravasation, and play an important role in the systemic manifestations of AP, including multiorgan dysfunction (21).
Alpha-FNT is thought to be one of the main mediators of inflammation and its concentration in serum correlates with the severity of the disease (29,30). Sometimes, it cannot be detected in serum, because its half-life is short and it is also broken down by neutrophil elastase, the values of which are high in AP (31).
IL-1 stimulates the secretion of IL-2 by T-lymphocytes. It has been found that IL-2 values are increased in AP. IL-6 is released by monocytes, macrophages and endothelial cells. Its serum values have been found to correlate with the severity of the disease. These values are increased 24-36 hours before those of C-reactive protein (32).
IL-8 is synthesized by mononuclear phagocytes and endothelial cells. It is believed to play a significant role in the development of organ dysfunction, particularly in acute lung damage (22).
IL-10 is the most important anti-inflammatory cytokine secreted by T-lymphocytes, monocytes and macrophages. Introduces an "endogenous" feedback factor that regulates the production of proinflammatory cytokines. IL-13 is synthesized by T-lymphocytes but not by monocytes and similar to IL-10 inhibits the secretion of proinflammatory cytokines (33).
Many studies suggest that cytokines activated by the 1beta-converting interleukin enzyme play an important role in the course of acute pancreatitis. In mice, pharmacological inhibition of this enzyme was performed experimentally and it was found that mortality, in the first week, decreased from 87.5% to 38.9% (34).
It has also been found experimentally that phospholipase A2 induces alveolar macrophages to release NO, a compound that affects lung damage in AP. These lung lesions were prevented by administration of the A2-quinacrine phospholipase inhibitor (35).
Using leukocyte labeling with Tc-99m, low leukocyte activity and their accumulation only in the pancreas in edematous forms of pancreatitis was ascertained. Whereas, in necrotic AP, Le activity was very intense and they accumulated not only in the pancreas but also in the lungs (36).
1.1.5. Diagnosis of acute pancreatitis
1.1.5.1. Clinical presentation
Diagnosis of acute pancreatitis is not an easy thing, as there is no specific clinical sign for acute pancreatitis. The most common symptoms are: pain in the upper abdomen, tenderness, fever, nausea, vomiting, ileus and jaundice (13).
In 1-3% of cases ecchymosis occur in the lumbar region (Gray-Turner sign) and periumbilical region (Cullen sign). However, none of these clinical signs predict the severity of the disease (37).
In the first days after the onset of the disease, patients with necrotic AP develop SIRS, which is characterized by fever, tachycardia, and tachypnea (30).
1.1.5.2. Biochemical diagnosis
Amylase: Traditionally, the biochemical diagnosis of AP is based on the determination of serum and urine amylase activity, whose activity increases in serum within 2-12 hours after the onset of symptoms. After 12-72 hours it reaches the highest values and in uncomplicated cases normalizes within 3-5 days (38). It has a sensitivity of 75-92% and specificity 20-60%. However, 19% of patients with AP have normal amylase values (15).
There are two types of amylase isoenzymes: P-isoamylase and S-isoamylase. 35-45% of amylase is P-isoamylase. In addition to the pancreas, amylase is also synthesized in the salivary glands, liver, kidneys, small intestine. Also some tumors such as: carcinoma of the: bronchi, esophagus, breast, ovary, etc., synthesize amylase (1,5).
The diagnosis of acute pancreatitis is almost certain if the amylase levels in the blood are three times higher than normal. Total amylase values return to normal values faster than those of pancreatic amylase. If amylase values are slightly elevated while trypsinogen is normal, then acute pancreatitis is ruled out. Simultaneous determination of amylase in blood and urine has greater diagnostic value, because amylase in blood increases more rapidly, while amylase in urine remains longer increased in the acute phase. This helps to make the retrograde diagnosis as well. Increased urinary amylase values persist even after clinical improvement (5).
Hyperamylasemia also occurs in some other diseases such as: acute cholecystitis, perforated duodenal ulcer, upper intestinal obstruction, embolism and mesenteric thrombosis, intestinal strangulation, dissecting aortic aneurysm, rupture of the aortic aneurysm, etc. In these cases, emergency ECHO, eventually CT, help determine the diagnosis (5,7,8).
Lipase: Lipase values begin to increase 4-8 hours after the onset of symptoms, reach a maximum after 24 hours, and normalize after 8-14 days. This biochemical test has a sensitivity of 86-100% and specificity 50-99%. Although lipase may also originate in the stomach, an increase in its values 5 times above normal is considered a sure sign of acute pancreatitis (38).
Trypsin: It is the major protease in human pancreatic fluid. It is secreted by exocrine cells as a proenzyme and activated in the duodenum by enterokinase.
There are two isoenzymes of trypsinogen: trypsinogen1 and trypsinogen2. In AP, trypsinogen2 values are higher than trypsinogen1.
Determination of trypsinogen2 in serum and urine as well as measurement of trypsin2-alpha1-antitrypsin complex have been shown to be potent markers for the diagnosis of AP (39).
The trypsinogen urinary strip test2 is a simple, rapid and successful test for identifying patients with AP retro and prospectively (39). However, trypsin determination is not yet routinely applied (38,39).
C-reactive protein: It is the most sensitive and important nonspecific reactant of the acute phase of inflammation and necrosis. However, its values increase after 48-72 hours, so it has no early prognostic role, but can serve for dynamic evaluation of the disease (40).
1.1.5.3. Radiological examinations
Abdominal ECHO is important for evaluating bile ducts, detecting biliary calculus, and confirming biliary obstruction. It is also a method for dynamic evaluation of patients with local complications such as pseudocystic formations and abscesses.
Contrast-enhanced CT has 100% diagnostic specificity. With this method it is possible to detect pancreatic necrosis and other complications. However, in 8-28% of cases with AP, mainly with acute edematous pancreatitis, the CT image obtained is normal (41).
1.1.6. Prognostic indicators
There are a number of prognostic systems that are applied to predict the severity of the disease and the prognosis of patients with acute pancreatitis. These systems are applied to identify patients who are potentially at risk of developing local and systemic complications, in order for these patients to undergo the treatment in intensive care unit as soon as possible.
Among the best known are: criteria according to Ranson (42), APACHE II system, Glasgow system according to Imrie, stratification based on CT according to Baltazar, etc.
According to Ranson, it takes 48 hours to complete the criteria. This system has a sensitivity of 73% and specificity 77%.
The mortality rate correlates with the number of positive criteria.
APACHE II system has a sensitivity of 77% and specificity 84%. It can be calculated within a few hours after hospitalization of the patient and can be repeated daily (43).
1.1.7. Laboratory tests
The tendency of the researchers was and is the discovery of a simple test for the stratification and prognosis of patients with acute pancreatitis.
Thus, trypsinogen2 concentration has been found to correlate with disease severity (39). The values of trypsin2-alpha1-antitrypsin increase in both edematous and necrotic forms, but these values are significantly higher in necrotic forms (39).
A simple marker for stratification is C-reactive protein. However, its values increase after 48-72 hours, so it has no early prognostic role but can serve for dynamic evaluation of the disease (40).
PTC (procalcitonin), a precursor of calcitonin, has been found to detect bacterial contamination of pancreatic necrosis (44). It has also been found that in necrotic AP the serum concentrations of phospholipase A2 are high.
Measurement of serum neutrophil elastase concentration, as a marker of neutrophil activity, has been used successfully to stratify patients with AP. However, this test is not currently routinely applied (45).
Serum values of proinflammatory cytokines have been found to correlate with disease severity (21). Thus, IL-6 values, 24 hours after the onset of the disease, were found to correlate with the mortality rate.
In one study, it was found that the concentration of alpha-FTN, IL-6 and IL-8 was higher in patients with systemic complications than in those without complications, while the concentration of IL-1 was the same in both groups (46).
Concentration of anti-inflammatory cytokines (IL-10, IL-11, IL-13) has been reported to reflect the severity of the disease and is considered a potent marker for early prediction of the prognosis of acute pancreatitis (47).
In conclusion, the most important cytokines for predicting disease severity are IL-6 and IL-8. However, their effectiveness and superiority over prognostic systems (Ranson, APACHE II, Glasgow, etc.) has not yet been fully evaluated (48).
Since there is still no single, simple test that would quickly and cost-effectively detect and predict acute pancreatitis, it is recommended that for the stratification and prognosis of AP as well as the identification of early complications the test combinations (50) are used.
1.1.8. Types of acute pancreatitis
1.1.8.1. Acute edematous pancreatitis
It is the most common form of acute pancreatitis. It occurs in 80-90% of cases. It is characterized by cellular and interstitial edema. Complications, in this form, are rare. Mortality is less than 2%.
Acute edematous pancreatitis is mainly treated conservatively (1.5).
1.1.8.2. Acute necrotic pancreatitis
In 15-20% of cases this form of acute pancreatitis develops. In addition to cellular and interstitial edema, necrosis of the pancreatic parenchyma also develops.
In the first week, in 25% of cases pancreatic necrosis infection develops, while in the third week, the infection is present in 50-60% of patients.
Bacterial infection develops in 40-70% of cases with acute necrotic pancreatitis (4).
1.1.8.3. Pathogenesis of pancreatic infection
The exact mechanism of the pathogenesis of pancreatic and peripancreatic necrosis infection is still not entirely clear. There are various pathways through which microorganisms are translocated to the necrotic tissue of the pancreas. However, bacterial translocation from the colon appears to be the cause of the infection.
Mucosal barrier insufficiency is considered to be the first stage that enables the migration of microorganisms into the lymphatics, blood vessels, ascites or directly into the pancreatic tissue. Some studies support the hypothesis that bacterial translocation occurs from the small intestine.
Prior to prophylactic application of antibiotics, gram-negative gastrointestinal bacteria predominated as the cause of infection. In 60-87% of cases the presence of monomicrobial flora of bacteria such as: Escherichia coli, Pseudomonas spp., Enterobacter, Bacteroides and Proteus.
Shock, intestinal ischemia, or trauma often result in mucosal disruption, as the enteric mucosal barrier breaks down. Mucosal disruption is the basic mechanism of bacterial translocation, followed by systemic infections and organ failure.
However, there are other routes of bacterial translocation, such as the hematogenous route, through the central venous lines (after local infection) or ascending from the duodenum to the major pancteatic duct (8).
1.1.8.4. Identification of pancreatic necrosis infection
There is no specific biochemical marker that diagnoses pancreatic necrosis infection.
C-reactive protein, when its value is above 150 mg / l, is an indicator of the presence of infection. However, it has not been found that there is a correlation between its values and necrosis infection.
Procalcitonin has been found to be a potent marker that reflects bacterial or fungal infection. Its values> = 1.8 mg / ml detect the presence of necrosis infection with a sensitivity of 94% and specificity 90%. However, Procalcitonin is a nonspecific marker and the interpretation of its values only makes sense if it becomes an integral part of other diagnostic procedures.
The gold standard for identifying necrosis infection is aspiration with fine Chiba needles, followed by ECHO or CT (51). The aspirated material is then stained according to Gramm or planted in culture (5,8,51).
1.1.9. Complications of acute pancreatitis
They can be local and systemic. The most common local complications are: pancreatic necrosis infection, pseudocysts and abscess.
Whereas, the most common systemic complications are: shock, lung insufficiency and renal insufficiency (52).
1.1.10. Trends of contemporary treatment of acute pancreatitis
In the absence of causal therapy, trends have been oriented towards identifying patients with severe forms of AP and organ dysfunction, in the hope that prompt, adequate, and specialized intervention can improve prognosis (53).
Identification of patients with necrotic AP, hospitalization and their treatment in the intensive care unit, administration of enteral nutrition, prophylaxis with antibiotics, have been found to reduce the rate of complications and mortality.
In the initial stage, all patients with AP are treated conservatively. Surgical treatment is indicated in patients with pancreatic necrosis infection and it is generally agreed that this treatment should be performed as late as possible.
Treatment of sterile pancreatic necrosis is, in most cases, conservative. However, there are still many controversial opinions about the treatment of sterile necrosis (51,52).
1.1.10.1. Immunomodulation
Since the role of activating proinflammatory leukocytes and cytokines is already known, the new treatment strategy is oriented towards preventing the activity of these mediators or blocking their synthesis.
In general, immunomodulators can be grouped into three categories:
- specific anticytokine antibodies
- inflammatory cytokines
- nonspecific immunomodulators (32)
In the early stage of AP, when SIRS predominates, the application of agents that inhibit the release or action of proinflammatory mediators is beneficial (21).
Grewal et al., have found that prophylactic treatment with anti-alpha-FTN antibodies has improved the prognosis of AP in experimental animals.
Blockade of IL-1 receptors with antagonist reduces pancreatic damage in experimental AP (21).
Application of IL-10 has been found to reduce disease severity and increase survival in artificially induced AP.
Administration of an IL-10 agonist and anti-IL-8 antibodies has been reported to reduce the activity and response of proinflammatory cytokines (32).
In the late stage of AP, when immunosuppression predominates, the application of immune stimulants (gamma-interferon) has been concluded to represent an encouraging step for patients and their prognosis (23).
In the future, the treatment strategy should focus on a multimodal combination therapy, which suppresses the excessive inflammatory reaction, while preserving the immune competence and antimicrobial protection (54).
2. THE AIMS OF THE STUDY
The aims of this study were to ascertain:
-Causes of acute pancreatitis
-Anatomopathological forms of acute pancreatitis
-Gender and age group most affected by acute pancreatitis
-Methods applied in the diagnosis of acute pancreatitis
-Principles of treatment of acute pancreatitis
-Early complications of acute pancreatitis and their treatment
-Deficiencies in the diagnosis and treatment of acute pancreatitis
3. MATERIAL AND METHODS
The medical documents of 29 patients who were hospitalized, diagnosed and treated due to acute pancreatitis and its complications in the departments of Abdominal Surgery at the University Clinical Center in Prishtina, in the period January 2001-December 2002, was retrospectively analyzed.
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