Acute pancreatitis (AP) presents with a broad clinical and prognostic spectrum. Predicting AP severity is a challenging matter because no single scoring scale has reached consensus yet. Moreover, in the paediatric population, the use of adult-based clinical scoring scales such as Ranson, Glasgow modified, as well as the radiological scale of Balthazar computed tomography–based severity index (CTSI) is still under debate (1). An AP scoring scale specifically addressed to the paediatric population was proposed by DeBanto et al in 2002 (2). To date, these scores have only been evaluated in 2 studies (3,4) for Ranson, Glasgow, and DeBanto, and never for Balthazar in children with AP. Here, we present the results of our study on the usefulness of Ranson, Glasgow, DeBanto, and Balthazar scores in a paediatric population and discuss them in light of the literature.
We retrospectively collected data from children (n = 48) with AP admitted between January 2003 and December 2007 in 3 hospitals in southern France (Hôpital Timone Enfants, Marseille; Hôpital Nord, Marseille; and Hôpital des Enfants, Toulouse). The diagnosis of AP was made if the children had at least 2 of the following signs: acute abdominal pain, increased serum amylase or lipase (>3-fold of the upper limit range), and radiological records compatible with AP. In cases of repeated episodes of AP, only the first one was taken into account for the study. We evaluated the severity according to the criteria of the Atlanta symposium (5), like in previous studies (2–4). For each patient, we recorded clinical data used in the Ranson, Glasgow, and DeBanto scores, and C-reactive protein as a marker of inflammation. In addition, 17 patients underwent a computed tomography (CT) scan and the Balthazar score was calculated by the same radiologist (P.P.). The statistical analysis was performed with Wilcoxon, Fisher tests, and receiver operator characteristic (ROC) curves.
We collected data from 48 patients (23 boys and 25 girls), with a median age of 133 months (24.9–233.5), diagnosed as having AP. The causes were trauma (23%), idiopathic (23%), lithiasis (12.5%), virus (10.5%), hereditary (8.3%), medication (8.3%), postsurgery (6.2%), and in 6.2% other causes (hypertriglyceridemia [n = 1], autoimmune [n = 1], inflammatory bowel disease [n = 1]). Thirteen pancreatitis cases were defined as severe. Ten had local complications, mainly pseudocysts (9/10) and 1 necrosis, and 5 had systemic complications. Two patients experienced both local and systemic complications. Thirty-five patients were considered as mild cases. No death occurred. The 2 groups were similar for age and weight but differed for the hospital stay (30 vs 9 days, P < 0.001), for the digestive rest (20 vs 5 days, P < 0.001), for the use of antibiotic (P = 0.007), and parenteral nutrition (P < 0.001). Due to the retrospective methodology, some data for several items were missing in a few patients, but the 2 groups did not differ statistically for the number of collected parameters (Ranson, Glasgow modified, DeBanto), thus allowing comparison between the groups.
The mean scores were statistically different between severe and mild pancreatitis for each score. The area under the ROC curve was 0.699 (95% CI 0.508%–0.891%, P = 0.054) for the DeBanto score, 0.846 (95% CI 0.69%–1%, P = 0.001) for the Ranson score, and 0.774 (95% CI 0.584%–0.964%, P = 0.008) for the Glasgow score (Fig. 1). Sensitivity levels were 61.54%, 53.85%, and 53.8% and specificity levels were 88.57%, 91.18%, and 80.0%, respectively, for Ranson, Glasgow, and DeBanto scores. The 48-hour trough calcium and 48-hour rise in blood urea nitrogen (BUN), 2 isolated laboratory parameters included in the Ranson score, each had good sensitivity (83%) and specificity (100%). Isolated C-reactive protein (32 patients) and haematocrit (27 patients) did not differ significantly between mild and severe pancreatitis for their values or their 48-hour evolution. For the CT scan data of 17 patients (7 with mild and 10 with severe pancreatitis), the area under the ROC curve was 0.898 (95% CI 0.73%–1%, P = 0.011) and for a threshold of 4 the sensitivity was 80.0% and the specificity was 85.71%.
As reported in our study, children with AP in southern France present with similar causes when compared with children of other countries (6,7). Due to the presence of criteria that are inappropriate for paediatric scoring (eg, age), the 3 scores share half of the constituting parameters: admission white blood cells, 48-hour trough calcium, and 48-hour rise in BUN and LDH. It could explain the similarity of the results of the 3 scores. Ranson, Glasgow modified, and DeBanto scores discriminated between mild and severe pancreatitis with a good specificity but a low sensitivity. Thus, we confirm the observation of Suzuki et al (3) and Lautz et al (4) on the low sensitivity (approximately 50%) of the 3 scores. Lautz et al (4) isolated 3 laboratory parameters (white blood cells, 48-hour trough calcium, and 48-hour rise in BUN) as independent predictors of severe outcome. Our data confirm the usefulness of 48-hour trough calcium and 48-hour rise in BUN but not of C-reactive protein and haematocrit; however, because 48-hour trough calcium and 48-hour rise in BUN are part of the Ranson, Glasgow, and DeBanto scoring scales, their isolated or combined use can only achieve a poor sensitivity.
It seems likely that more specific pancreatic markers should yield better prognostic sensitivity. To date, none among lipase, amylase, or trypsin has been correlated with the severity of the disease. The only laboratory parameter reported to be associated with AP severity was the pancreatitis-associated protein (8), but to date it has not been used for severity scoring. The place of CT severity scoring is problematic. To our knowledge, the present study is the first to assess it in paediatric AP. Our data shows that CT severity scoring achieves good sensitivity and specificity. These findings are in agreement with previous studies in adult AP, which concluded to the superiority of the CT over clinical scoring scales (9–11); however, the limit is that severity (particularly local complications) is determined by means of radiological workup (12). Thus, the CT score is “judge and jury,” and at least in 1 study the hospitalisation stay was not correlated to the Balthazar score (13). Finally, the problem of radiation exposure, notably in the paediatric population, limits the use of the CT scan as a scoring system. This could be resolved by the use of ultrasound investigation (14), but such a score has yet to be defined, especially in children.
To date, 3 studies (Suzuki, Lautz, and ours) have confirmed that present clinical scoring scales had low sensitivity in children and cannot be used as predictors of outcome for paediatric AP. Isolated laboratory testing for WBC, calcium, and rise in BUN can bring the clinician information about the score (mainly good specificity) in an easier way. The place of the imaging-based scoring scale seems more promising but needs further investigation.
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