ORIGINAL ARTICLE
Year : 2022 | Volume
: 21 | Issue : 2 | Page : 118--123
Clinical profile, etiology, and outcome of acute pancreatitis: Experience at a tertiary care center
ML Patel1, Radhey Shyam2, Virendra Atam1, Harish Bharti1, Rekha Sachan3, Anit Parihar4, 1 Department of Medicine, King George's Medical University, Lucknow, Uttar Pradesh, India 2 Department of Geriatric Mental Health, King George's Medical University, Lucknow, Uttar Pradesh, India 3 Department of Obstetrics and Gynaecology, King George's Medical University, Lucknow, Uttar Pradesh, India 4 Department of Radiodiagnosis, King George's Medical University, Lucknow, Uttar Pradesh, India
Correspondence Address:
M L Patel Department of Medicine, King George's Medical University, Lucknow, Uttar Pradesh India
Abstract
Background: Acute pancreatitis (AP) is an inflammatory process of the pancreas with varying degree of involvement of regional tissues. This was a population-based study on the incidence of AP. We aimed to determine the incidence, etiology, and outcome of AP. Materials and Methodology: This prospective study was conducted in the Department of Medicine, King George's Medical University, Lucknow, India, on 120 patients of AP. Clinical history, examination, and laboratory investigations were done. Severity of AP was assessed using the modified Atlanta classification. Results: A total of 120 patients comprising of 88 men (73.33%) and 32 women (26.66%) were recruited. The mean age of study participant was 36.96 ± 13.44 years. The most common presentation was abdominal pain followed by vomiting. The leading etiological factors were alcohol in 85 patients (70.8%) and gallstones in 25 (20.8%). It was idiopathic 5 patients (4.1%). Mortality was seen in three (2.5%) patients, all of which had severe pancreatitis. Patients with body mass index (BMI) ≥25 kg/m2, Hematocrit (HCT) ≥44% and C-reactive protein (CRP) ≥150 mg/l had an increased risk of developing a severe AP. Conclusions: Alcohol and gallstones were the most common etiological factors of AP, whereas HCT, CRP, and BMI were the useful predictors of severe pancreatitis.
How to cite this article:
Patel M L, Shyam R, Atam V, Bharti H, Sachan R, Parihar A. Clinical profile, etiology, and outcome of acute pancreatitis: Experience at a tertiary care center.Ann Afr Med 2022;21:118-123
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How to cite this URL:
Patel M L, Shyam R, Atam V, Bharti H, Sachan R, Parihar A. Clinical profile, etiology, and outcome of acute pancreatitis: Experience at a tertiary care center. Ann Afr Med [serial online] 2022 [cited 2023 Nov 29 ];21:118-123
Available from: https://www.annalsafrmed.org/text.asp?2022/21/2/118/349967 |
Full Text
Introduction
Acute pancreatitis (AP) is defined as the inflammation of the pancreatic tissue, characterized by parenchymal edema and necrosis caused by auto-digestion by its own glandular enzymes leading to multi-organ failure or death.[1] In the past few decades, there have been many advancements in the intensive care of patients with AP due to its association with high morbidity and mortality.[2] As per the Indian data, no multicentric studies available only sporadic data were analyzed, thus the exact prevalence could not be assessed. The incidence was calculated from the patients admitted at different tertiary care centers all over the country.[3]
For the management and prevention of recurrence of the disease, its etiology is to be as ascertained. The two most common etiological factors, namely alcohol and gallstones contribute 80% of the cases, with alcoholic pancreatitis being much more common.[4],[5],[6],[7] Recent recommendations state that the etiology of AP should be established in at least 80% of cases with not more than 20% being classified as idiopathic.[8] Planning the management and delivery of care for AP requires the knowledge of the etiology as well as severity of the disease.
The severity of pancreatitis varies from mild and self-limiting to severe and fatal.[1] Severity is an important indicator of mortality and the need for intensive care, nutritional support, urgent surgical intervention, and antibiotic usage.[8] Various scoring systems have been devised for AP such as the Atlanta Criteria,[9] which relies on evidence of organ failure and/or local complications as well as Acute Physiology And Chronic Health Evaluation II (APACHE II).[10] Ranson et al.[11] and modified Glasgow[12] scores based on clinical and laboratory values that assess systemic inflammation and the Balthazar Score which is based on computerized tomography (CT) findings.[13] For the diagnosis and prognostication contrast-enhanced scoring system is good because it improves the identification at early stage with high sensitivity (100%) and accuracy (87%) by the detection of extended areas of necrosis within the pancreatic region.[13]
Severe AP occurred in 20% patients of AP with mortality rates of 10%–30%.[7] Patients with AP have a high risk of morbidity due to local complications include pancreatic pseudocyst, pleural effusion, peritoneal collection, and pancreatic necrosis with superimposed infection, which has the highest mortality rate of 30%.[13] The systemic complications are either single or multiorgan failure (MODS). Deaths from pancreatitis occurring during the first 2 weeks of the illness are due to multiple organ dysfunction syndrome (MODS),[14],[15],[16] whereas deaths after 2 weeks are generally caused by pancreatic necrosis with superimposed infection.[13] According to the recent guidelines, mortality from AP should be <10% overall and <30% in severe cases.[8] Furthermore, all patients with severe pancreatitis or with organ failure should be managed in the high dependency unit or intensive care unit.[8]
Due to the lack of prevalence data of the disease in our country, changing trends of severity, complexity of the disease, and changing trends in the outcome, prompted us to undertake this study with aim to determine the demographic profile, etiology, severity, and outcome of AP.
Materials and Methodology
This prospective study was conducted in King George's Medical University, Lucknow, Uttar Pradesh, India, for 1 year from August 2018 to July 2019 in the department of medicine in collaboration with the department of radiology. Ethical clearance was obtained from the Institutional Ethics Committee, Research Cell, King George's Medical University, Lucknow, and a written (or verbal) informed consent for participation was obtained from the patients (or their relatives). A total of 129 cases of AP were enrolled in this study. Nine patients were critically ill and not willing to stay further in the study, so they were excluded. All patients age >15 years and admitted in indoor and fulfilling two out of three criteria. (i) Abdominal pain characteristic of AP, (ii) serum amylase and/or lipase levels at least three times the upper limit of normal, and (iii) characteristic findings of AP on abdominal ultrasonography and/or CT scan were included in the study as per the Atlanta Classification 2012.[9]
Patients who were suffering from chronic pancreatitis based on their hospital records or had radiological findings of pancreatic calcifications, dilated pancreatic duct, areas of atrophy, and pseudo cysts were excluded from the study.
After detailed history and physical examination, laboratory investigations requested at the time of admission included arterial blood gas analysis, hematocrit, kidney function test, liver function test, serum electrolytes, serum amylase, serum lipase, and complete hemogram. Abdominal ultrasonography was done at the time of admission and contrast-enhanced pancreatic CT scan was done after 72 h of hospitalization.
Patients were subsequently examined daily, and relevant laboratory investigations such as complete hemogram, blood sugar, serum amylase, serum lipase, and serum calcium were done on every 48 h; bedside index for severity in acute pancreatitis (BISAP) was calculated within first 24 h of admission, while Ranson's score was evaluated within first 48 h of admission. Moreover, APACHE II score was evaluated for each patient after 72 h of admission were calculated.
Patients with mild AP had neither local complications nor organ failure. Patients with moderately severe AP had transient organ failure or local complications or both, whereas patients with severe AP had persistent organ failure. Organ failure was defined based on the Modified Marshall scoring system. A score of ≥2 for more than 48 h was considered as persistent organ failure, whereas a score of ≥2 for <48 h was considered transient organ failure. Local complications included pancreatic necrosis, acute fluid collections, pseudo cyst, acute necrotic collections, and walled off necrosis. All the patients were managed as per the standard protocol.
Statistical methods
The statistical analysis was done using IBM SPSS (Statistical Package for the Social Sciences) Version 21.0 Armonk, NY, USA; IBM Corp. Continuous variables were described as mean ± standard deviations at 95% confidence intervals. Categorical variables were presented as proportions. Student's t-tests, one-way analysis of variance, and Pearson Chi-squared tests were used in the univariate analysis to evaluate statistical associations. Multiple logistic regression was utilized to identify the independent predictors of mortality based on which odds ratios were calculated. Risk factors that are found to be significant in univariate analyses are considered in the multiple regression model. A two-sided P < 0.05 was considered statistically significant.
Results
During a period of 1 year, 12,338 patients were admitted in indoor wards. Out of these total 129 (1.04%) patients with acute abdomen, who were diagnosed with AP based on elevated serum amylase and/or lipase levels and radiological findings on ultrasound and CT abdomen were included in this study. Age of patients ranged from 14 to 70 years, with a mean age of 36.96 ± 13.44 years. Majority of the patients 62 (51.66%) were between 41 and 60 years. There were more males (75.6%) than females (24.4%) with a male-to-female ratio of 2.75:1. The mean body mass index (BMI) of patients was 24.73 ± 2.40 kg/m2 [Table 1].{Table 1}
The mean length of hospital stay was 10.30 ± 4.50 days for the entire study cohort. Based on the severity of AP, the mean length of hospital stay in patients with mild AP was 5.89 ± 2.30 days, 7.84 ± 3.84 for moderate AP, and 10.79 ± 4.98 for severe AP. Majority of the patients were successfully discharged 117 (97.5%) from the hospital after treatment of their acute condition while death occurred in 3 (2.5%) of the study population due to multiple organ failure. Out of the three patients who died during the study period, 2 (3.8%) patients had severe pancreatitis and 1 (3.3%) patient had moderate pancreatitis. Disease severity was determined on the basis of the BISAP score at the time of admission and after 48 h (based on CT severity index score). CT scan was performed in 90 cases, out of which 20 (22.2%) had mild AP, 25 (27.77%) had moderate AP, while 45 (50.0%) cases had severe form of the disease [Table 1].
Among etiological factors, alcohol was the most common cause found in 85 (70.8%) patients, followed by gallstones in 25 (20.8%), idiopathic in 5 (4.1%) patients, hypertriglyceridemia in 3 (2.5%), and one case (0.8%) each of autoimmune etiology and postendoscopic retrograde cholangiopancreatography AP. All (100%) of the patients had a history of abdominal pain. Other presenting symptoms and signs were nausea and vomiting in 66.7%, fever in 50%, jaundice in 37.5%, pleural effusion in 20.8%, ascites in 25%, and abdominal tenderness in 100% of the study population. In the subgroup analysis, jaundice, pleural effusion, and ascites were absent in mild AP [Table 2] and [Table 3].{Table 2}{Table 3}
The sensitivity, specificity, positive predictive value, and negative predictive value of BMI ≥25 kg/m2 in predicting acute severe pancreatitis at admission was 60%, 73.2%, 36.16%, and 80.20%, respectively. Serum C-reactive protein (CRP) level at the time of admission for the detection of severity of AP showed a sensitivity, specificity, positive predictive value, negative predictive value, of 70.61%, 92.45%, 75.5%, and 92.71%, respectively. Serum HCT level at admission for the detection of severity of AP showed the sensitivity, specificity, positive predictive value, and negative predictive value was 68.75%, 84.30%, 59.65%, and 91.20%, respectively [Table 4].{Table 4}
Discussion
AP is a relatively common disease with the incidence of 5–80 per 100,000 population worldwide. The spectrum of the disease is wide, varying from mild attacks with mild epigastric discomfort to multiorgan dysfunction and death. The mild attacks often go undiagnosed leading to recurrence. The overall mortality of AP is static at 1%–2% but increasing to 10%–30% in severe AP.[7] Although its prevalence varies in different countries and even indifferent areas of a given country, there has been a significant increase in the number of new cases in recent years.[17] Early diagnosis and prompt treatment are the mainstay of the therapy in AP to significantly decrease morbidity and mortality.
In this study, the mean age of the patients was 36.96 ± 13.44 years which is lower than the findings in the studies done by Negi et al.[18] and Raghu et al.,[19] that reported mean ages of 42.89 ± 12.5 years and 42.9 ± 15.9 years, respectively. Majority of the patients in our study were in the age group of 41–60 years (51.66%) followed by patients between 14–40 years (31.66%) and 20 (16.66%) patients were above 60 years of age. Majority of the patients presented in the middle age, a period when alcohol consumption is more common especially in males; hence, the higher number of males than females presenting with AP. The male-to-female ratio of 2.75:1 recorded in this study is comparable with the studies of Uhl,[20] with a male to female ratio of 1.85:1 and de Beaux et al.,[21] where male-to-female ratio was 1:6.1.
In our study, abdominal pain was the common presenting complaint in all patients (100%), and this is similar to what was reported by Negi et al.[18] and Rao[22] also reported similar pattern of vomiting, fever, and pleural effusion, as found in this study.
The male predominance of alcoholic pancreatitis in north India is likely due to the fact that alcoholism is quite common among middle age men. Negi et al.[18] in their study found alcohol as major cause of pancreatitis in 59.35% of their patients. Mukherjee et al.,[23] in their study reported alcohol as a major etiology of AP in Eastern India. Macro[24] observed that the most common etiology was alcohol consumption (39.3%) followed by gallstones (24.1%).
Out of the 120 patients in this study, 117 patients recovered and 3 patients died showing an overall mortality of 2.5%. All deceased patients had severe pancreatitis showing an overall mortality of 5.6%. This correlates with the study done by Bota et al.,[25] where overall mortality rate was 4.6%. Recent guidelines suggest that mortality from AP overall <10% overall.[8] This mortality rate of 2.5% in our study was significantly lower in comparison to large epidemiological studies of pancreatitis done in other countries.[7],[26]
In our study, with BMI >25 kg/m2, 48% of the patients had severe pancreatitis, 46.7% had mild to moderate pancreatitis, and 26.3% had mild pancreatitis. The sensitivity, specificity, positive predictive value, and negative predictive value of BMI ≥25 kg/m2 inpredicting acute severe pancreatitis at admission was 60%, 73.2%, 36.16%, and 80.20%, respectively. Our study is comparable to a study done by Negi et al.[18] who reported obesity as a risk factor for severe AP. Another study done by Chen et al.[27] showed that obese patients (BMI ≥25) had a significantly increased risk of severe AP compared with nonobese patients.
In our study, the evaluation of serum HCT level at admission for the detection of severity of AP showed the sensitivity, specificity, positive predictive value, and negative predictive value was 68.75%, 84.30%, 59.65%, and 91.20%, respectively. Brown et al.[28] reported comparable values for sensitivity, specificity, positive predictive value, and negative predictive value of 72%, 83%, 68%, and 85%, respectively. Our study is also comparable to the study done by Negi et al.[18] who found that the sensitivity, specificity, positive predictive value, and negative predictive value was 67.86%, 85.26%, 57.57%, and 90%, respectively.
In our study, serum C-reactive protein (CRP) level at the time of admission for the detection of severity of AP showed a sensitivity, specificity, positive predictive value, negative predictive value, of 70.61%, 92.45%, 75.5%, and 92.71%, respectively. Our results were comparable with study done by Gurda-Duda et al.[29] and Pongprasobchai et al.[30] Our study is also comparable with the study by Negi et al.[18] who found sensitivity, specificity, positive predictive value, negative predictive value, of CRP for predicting severity of illness was 67.86%, 93.67%, 76%, and 90.8%, respectively.
Limitation of study
This was a single-center study in tertiary care center, and findings may have been due to referral bias and not reflective of the community. Serum HCT and serum CRP were done only at the time of admission. Despite the limitation, the study provides an insight into the validity of the different prognostic indicators in the assessment of severity of AP.
Conclusions
In this study, it is found that BMI, serum CRP, and HCT might be used as prognostic factors in AP. Till date the conservative management is the main stay of treatment; therefore, timely establishment of diagnosis, etiology, and severity of the disease is crucial in the management and is the key for saving life in patients with severe AP.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
References
1 | Sakorafas GH, Tsiotou AG. Etiology and pathogenesis of acute pancreatitis: Current concepts. J Clin Gastroenterol 2000;30:343-56. |
2 | McKay CJ, Imrie CW. The continuing challenge of early mortality in acute pancreatitis. Br J Surg 2004;91:1243-4. |
3 | Tandon RK. Management of acute pancreatitis: Indian guidelines and protocols. Med Update 2013;23:267-70. |
4 | Kingsnorth A, O'Reilly D, Acute pancreatitis. BMJ 2006;332:1072-6. |
5 | Gislason H, Horn A, Hoem D, Andren-Sandberg A, Imsland AK, Soreide O, et al. Acute pancreatitis in Bergen, Norway. A study on incidence, etiology and severity. Scand J Surg 2004;93:29-33. |
6 | Baig SJ, Rahed A, Sen S. A prospective study of the aetiology, severity and outcome of acute pancreatitis in Eastern India. Trop Gastroenterol 2008;29:20-2. |
7 | Frey CF, Zhou H, Harvey DJ, White RH. The incidence and case-fatality rates of acute biliary, alcoholic, and idiopathic pancreatitis in California, 1994-2001. Pancreas 2006;33:336-44. |
8 | Working Party of the British Society of Gastroenterology; Association of Surgeons of Great Britain and Ireland; Pancreatic Society of Great Britain and Ireland; Association of Upper GI Surgeons of Great Britain and Ireland. UK guidelines for the management of acute pancreatitis. Gut 2005;54 Suppl 3:i1-9. |
9 | Banks PA, Bollen TL, Dervenis C, Gooszen HG, Johnson CD, Sarr MG, et al. Classification of acute pancreatitis – 2012: Revision of the Atlanta classification and definition by international consensus. Gut 2013;62:102-11. |
10 | Knaus WA, Draper EA, Wagner DP, Zimmerman JE. APACHE II: A severity of disease classification system. Crit Care Med 1985;13:818-29. |
11 | Ranson JH, Rifkind KM, Turner JW. Prognostic signs and nonoperative peritoneal lavage in acute pancreatitis. Surg Gynecol Obstet 1976;143:209-19. |
12 | Blamey SL, Imrie CW, O'Neill J, Gilmour WH, Carter DC. Prognostic factorsin acute pancreatitis. Gut 1984;25:1340-6. |
13 | Balthazar EJ, Robinson DL, Megibow AJ, Ranson JH. Acute pancreatitis: Value of CT in establishing prognosis. Radiology 1990;174:331-6. |
14 | Woodcock S, Siriwardena A. High early mortality rate from acute pancreatitis in Scotland, 1984-95. Br J Surg 2000;87:379-80. |
15 | Isenmann R, Rau B, Beger HG. Early severe acute pancreatitis: Characteristics of a new subgroup Pancreas 2001;22:274-8. |
16 | Buter A, Imrie CW, Carter CR, Evans S, McKay CJ. Dynamic nature of earlyorgan dysfunction determines outcome in acute pancreatitis. Br J Surg 2002;89:298-302. |
17 | Kim TN, Kim SB, Cho JH, Kim KH. Comparison of clinical courseand outcome of acute pancreatitis according to two main aetiologies: Alcohol vs. gallstone. Pancreatol 2014;14:S62. |
18 | Negi N, Mokta J, Sharma B, Sharma R, Jhobta A, Bodh V, et al. Clinical profile and outcome of acute pancreatitis: A hospital-based prospective observational study in Subhimalayan State. J Assoc Physicians India 2018;66:22-4. |
19 | Raghu MG, Wig JD, Kochhar R, Gupta D, Gupta R, Yadav TD, et al. Lung complications in acute pancreatitis. JOP 2007;8:177-85. |
20 | Uhl W. A randomized double blind, multi-centric trial of octreotide in moderate to severe acute pancreatitis. Gut 1999;45:97-104. |
21 | de Beaux AC, Palmer KR, Carter DC. Factors influencing morbidity and mortality in acute pancreatitis; an analysis of 279 cases. Gut 1995;37:121-6. |
22 | Rao S. Etiology, clinical profile, severity and outcome of acute pancreatitis in relation to bedside index for severity of acute pancreatitis BISAP and CT severity index (CTSI) scores. Int JMed Res Health Sci 2014;3:922-8. |
23 | Mukherjee D, Bhakta S, Lahiry S, Sinha R. Demographic profile of Acute Pancreatitis in Eastern India: A single centre experience. Asian J Med Sci 2017;8:24-9. |
24 | Macro S. Predicting acute pancreatitis severity: Comparison of prognostic scores. Gastroenterol Res 2011;4:216. |
25 | Bota S, Sporea I, Sirli R, Popescu A, Strain M, Focsa M, et al. Predictive factors for severe evolution in acute pancreatitis and a new score for predicting a severe outcome. Ann Gastroenterol 2013;26:156-62. |
26 | Chen Y, Zak Y, Hernandez-Boussard T, Park W, Visser BC. The epidemiology of idiopathic acute pancreatitis, analysis of the nationwide inpatient sample from 1998 to 2007. Pancreas 2013;42:1-5. |
27 | Chen SM, Xiong GS, Wu SM. Is obesity an indicator of complications and mortality in acute pancreatitis? An updated meta-analysis. J Dig Dis 2012;13:244-51. |
28 | Brown A, Orav J, Banks PA. Hemoconcentration is an early marker for organ failure and necrotizing pancreatitis. Pancreas 2000;20:367-72. |
29 | Gurda-Duda A, Kuśnierz-Cabala B, Nowak W, Naskalski JW, Kulig J. Assessment of the prognostic value of certain acute-phase proteins and procalcitonin in the prognosis of acute pancreatitis. Pancreas 2008;37:449-53. |
30 | Pongprasobchai S, Jianjaroonwong V, Charatcharoenwitthaya P, Komoltri C, Tanwandee T, Leelakusolvong S, et al. Erythrocyte sedimentation rate and C-reactive protein for the prediction of severity of acute pancreatitis. Pancreas 2010;39:1226-30. |
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