Management of Acute Pancreatitis

Cianci P*, Giaracuni G, Vovola F, Tartaglia N, Fersini A, Ambrosi A and Neri V

Department of Medical and Surgical Sciences, University of Foggia, Italy

*Corresponding author: Cianci P, Department of Medical and Surgical Sciences, University of Foggia, Italy

Received: March 08, 2017; Accepted: March 16, 2017; Published: March 21, 2017

Short Communication

Acute pancreatitis is a disease characterized by inflammation of the pancreas associated with a systemic response due to auto-digestion of the gland and peripancreatic tissues. The disease can occur in mild form with simple tissue edema or severe form with local necrotizing inflammation and systemic complications as systemic inflammatory response syndrome (SIRS) and organ failure. The initial process which is the basis of acute pancreatitis is the activation of pancreatic enzymes that from their inactive form become activated enzymes, this process takes place in the parenchyma of the gland where typically does not occur. The most frequent causes are biliary obstruction and alcohol consumption that occurring in almost 80% of patients. In 20% of cases the etiology can be genetic (hereditary pancreatitis), obstructive (tumours, pancreas divisum, biliary pancreatitis), metabolic (hypercalcemia, hyperlipidemia), pharmacological. The etiologic assessment can be a guide to therapeutic program. A detailed history and a careful clinical examination may reveal the characteristic signs and symptoms of this disease: nausea, vomiting, tachycardia, tachypnea, hyperthermia, and upper abdominal pain radiated to the back with abdominal wall tenderness, and muscular rigidity of varying degrees. A left pleural effusion can be present. During auscultation, bowel sounds can be reduced or absent. The diagnostic criteria also include specific laboratory data such as increased values of pancreatic amylase and lipase. Serum amylase increases at the onset of the disease and decreases in a few days (3-5 days); on the contrary the lipase tends to remain elevated for longer. The increase level of serum amylase has not correlation with severity of pancreatitis. Liver function tests, fasting serum calcium and lipid profile contribute to define biliary etiology of pancreatitis. In the evaluation of acute pancreatitis and its clinical course, radiological examinations play a central role. Abdominal ultrasound (US) may demonstrate gallbladder lithiasis and/or gallstones, sludge, microlithiasis in the common bile duct (CBD) with its dilatation (>8mm) or a real impacted stone of the CBD. Contrast enhanced computed tomography (CT) and magnetic resonance imaging (MRI) are considered second-level exams, with the aim to evaluate the damage of pancreatic parenchyma, the involvement of pancreatic tissue, presence of fluid-necrotic collections and on the other hand the detection of bile stones, CBD dilatation. The last two give us the suspicion of biliary origin of pancreatitis.

In the majority of the patients (70-80%), the acute pancreatitis occurs as a mild – moderate disease; in the 20-30% shows a severe course. The critical forms shows a very severe disease with early hypoxaemia, progressive mulptiple organ dysfunction, compromised computed tomography severity index (CTSI), increased incidences of necrosis, infection, and sometime abdominal compartment syndrome (ACS). Therefore, these severe forms of pancreatitis have a short course and a high percentage of mortality up to 40%. The first phase (first two week) of severe acute pancreatitis typically manifests with an early toxic-enzymatic injury, SIRS, and a late phase (third and fourth week) characterized by septic complications of necrotic tissue and the appearance of peripancreatic fluid necrotic collections [1]. The first phase of pancreatitis can develop in most cases with disease quickly responsive to intensive care based on aggressive rehydration. The revision of the Atlanta criteria has Indicated that the pancreatic necrosis can be a risk factor for worsening of severe acute pancreatitis and some data from the literature suggest that it may occurs also with minimal pancreatic necrosis [2-48]. Mild pancreatitis has generally favorable evolution without mortality risk; in the moderate forms there is minimal risk of mortality. Predictive factors of severity, except clinical evaluation, may be divided into direct and indirect. The direct factors are based on morphological and anatomical compromission of the pancreas and assessed by imaging exams (US, CT, MRI). The indirect methods can be divided into mono factorial and multi factorial. The first can make the prognostic assessment by means of single laboratory marker (Table 1). These consist of several hepatic, urinary biochemical data that can be early detector of systemic inflammatory response and multi organ failure. Into these markers are reliable and very early CRP (C-reactive protein), TAP (urinary trypsinogen activation peptide), procalcitonin. The multi factorial prognostic scoring systems consist of Ranson and Glasgow scores, specific for the pancreatitis and APACHE II score which is not specific (Table 2). The new scoring systems meet the need to assess severity of disease within the first 24h. The Harmless Acute pancreatitis score [49], aims to identify the mild/ moderate pancreatitis. On the other hand there is the Bedside index of Severity in Acute pancreatitis (BISAP) [50] based on the evaluation of 5 criteria: blood urea nitrogen (BUN) > 25mg/dL, age >60 years, impaired mental status, SIRS and pleural effusion. For BISAP a score of > 2 is associated with a 10 fold increase in mortality risk. CT images obtained within 72 h of onset allow the use of CTSI and modified CT severity index (MCTSI) with Balthazar scoring for grading of acute pancreatitis and points for necrosis. The classification is based on morphological and functional feature: local or diffuse enlargement of the pancreas, pancreatic gland abnormalities, peripancreatic inflammation with pancreatic and peripancreatic fluid collections and areas of non-enhanced parenchyma (that is necrotic). The imaging evaluation should be integrated and completed always within 24-72 hrs by CT assessment of pancreatic size index (PSI), extra pancreatic inflammation on CT index score (EPIC) and extra-pancreatic score (EP) [51]. In summary the evaluation of severity of AP should employ several detector following the onset and development of acute attack. At the admission can be useful BUN, hematocrit, procalcitonin, chest x ray; at 24–48 h, BISAP, Ranson, Glasgow score, APACHE II; after the 48h MCTSI and CTSI. MRI provides images and pathological data overlappable to CT.

Table 1: Mono factorial markers of severity most recurrent in the literature.




  
     
    Sensibility
    Specificity
    Accuracy
    References
  
  
    CRP*
      (> 150mg/L at 24 and 48h)
    57-94.1%
    60-90%
    76-80%
    *[3-14]
  
  
    TAP*
      (increased at admission and after 12h)
    58-100%
    73-89.7%
    -
    *[3,12-18]
  
  
    Procalcitonin*
      (> 160 f mol/mL at admission)
      infected pancreatic necrosis marker
      altered permeability of gut barrier marker
    67-100%
    20-89%
    85%
    *[6,19-26]
  
  
    Hct*
      (at admission and after 24h)
      cut off: 43%M – 39%F
    61-74%
    38-45%
    -
    *[27-30]
  
  
    Hyperglycemia*
      (>125mg/dL)
      pancreatic necrosis index
      complication index
    83-100%
    49%
    -
    *[29,31-33]



Table 1: Mono factorial markers of severity most recurrent in the literature.

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Citation: Cianci P, Giaracuni G, Vovola F, Tartaglia N, Fersini A, Ambrosi A, et al. Management of Acute Pancreatitis. Austin Pancreat Disord. 2017; 1(1): 1003.

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	Sensibility	Specificity	Accuracy	References
Ranson	33-83%	79-98%	78-89%	[34-48]
Glasgow	33-83%	79-98%	78-89%
APACHE II > 7	52-62%	77-86%	-
APACHE II > 9	50-75%	69-72.4%	-