www.najms.org North American Journal of Medical Sciences 2010 May, Volume 2. No. 5.

Review Article OPEN ACCESS

Acute pancreatitis
Bo-Guang Fan, MD., PhD., Åke Andrén-Sandberg, MD., PhD.*

*Department of Surgery K53, Karolinska University Hospital at Huddinge

Stockholm, Sweden.

Citation: Fan BG, Andrén-Sandberg Å. Acute pancreatitis. North Am J Med Sci 2010; 2: 211-214.
Availability: www.najms.org
ISSN: 1947 – 2714

Abstract
Background: Acute pancreatitis continues to be a serious illness, and the patients with acute pancreatitis are at risk to
develop different complications from ongoing pancreatic inflammation. Aims: The present review is to highlight the
classification, treatment and prognosis of acute pancreatitis. Material & Methods: We reviewed the English-language
literature (Medline) addressing pancreatitis. Results: Acute pancreatitis is frequently caused by gallstone disease or excess
alcohol ingestion. There are a number of important issues regarding clinical highlights in the classification, treatment and
prognosis of acute pancreatitis, and treatment options for complications of acute pancreatitis including pancreatic
pseudocysts. Conclusions: Multidisciplinary approach should be used for the management of the patient with acute
pancreatitis.

Keywords: Pancreatitis, acute, gallstone disease, alcohol ingestion, classification,

pancreatitis was made by Fitz in 1889, and until the most

Introduction recent Atlanta symposium in 1992, a morphological
Acute pancreatitis is a common disease with a high component has always been included [3]. Whereas Fitz
mortality[1] , and frequently caused by gallstone disease believed that the morphological features of severe disease
[1] or excess alcohol ingestion [2]. The diagnosis of acute were evidence of pancreatic haemorrhage and
pancreatitis is supported by an elevation of the serum disseminated fat necrosis, the morphological features of
amylase and lipase levels. The amylase level becomes severe disease in the original Atlanta classification were
elevated within hours of the development of pain and may pancreatic necrosis, abscess, and pseudocyst [4].
remain elevated for 3 to 5 days. Serum lipase has higher
specificity for pancreatic disease, but its level may be As stated by Petrov [4], there is an ongoing effort to revise
elevated in other conditions as well. Laboratory the 1992 Atlanta classification of acute pancreatitis in the
abnormalities encountered in acute pancreatitis include light of emerging evidence. From clinician's view,
hyperglycemia, hypocalcemia, leukocytosis, and mild persistent organ failure is predictive of death in acute
elevations of liver function test results. Ultrasound and pancreatitis. Local complications without organ failure are
magnetic resonance cholangiopancreatography are associated with morbidity, prolonged hospital stay but low
potentially valuable tests in the evaluation of acute mortality. However, the categorization of the severity of
pancreatitis, and are helpful in detecting stones in the acute pancreatitis is one of the key elements of the
common bile duct and directly assessing the pancreatic classification [4].
parenchyma.
A three category classification of severity of acute
In the following review, we highlight the classification, pancreatitis were recently designed. Hammel et al
treatment and prognosis of acute pancreatitis, and concluded that three new category classification of
treatment options for complications of acute pancreatitis. severity of acute pancreatitis identifies patients with high
morbidity and mortality (severe acute pancreatitis), high
Classification of acute pancreatitis morbidity without mortality (moderate acute pancreatitis)
The first attempt to classify the severity of acute and low morbidity without mortality (mild acute
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pancreatitis) [5]. The entity of moderately severe acute endocytic structures, together with lysosomes, zymogen
pancreatitis is characterized by local complications granules and elements of the endoplasmic reticulum, also
without organ failure. Mortality in moderately severe acute play an important role in the physiological Ca2+ signal
pancreatitis is similar to that in mild pancreatitis but generation that normally regulates enzyme and fluid
hospitalization prolonged like in severe pancreatitis. Local secretion from the exocrine pancreas [12] .
complications are defined as pancreatic necrosis or fluid
collections [6]. The pathogenic mechanisms underlying acute pancreatitis
are involved in two key pathologic acinar cell responses of
this disease: vacuole accumulation and trypsinogen
Histopathology of acute activation [14]. An increase in intracellular calcium is the
pancreatitis basis for activation of trypsinogen, via a co-localization of
Patients with pancreatic infection may have infected enzyms (cathepsin B), inducing the inflammation. There
necrosis, pancreatic abscess, and/or infected pseudocysts are three ways to die: necrosis, apoptosis and autophagy.
[7]. The microbes most frequently involved are Without autophagy there is very little active trypsin, but
gram-negative organisms including Escherichia coli, with autophagy there is shown a lot of cytosolic cathepsin
Enterococcus, and Klebsiella [8]. On the other hand, for B, as part of the caspace activation. Caerulein stimulation
the earliest histopathological changes of acute pancreatitis, causes caspace 3 activation, just as exogenous cathepsin B
Kovalska and co-worker [9] investigated intraoperative causes caspace 3 activation in permeable rat acinar cells
pancreatic tissue samples, and attempted to find possibility [15]. However, heat shock proteins protects against
to reparation of pancreatic tissue in nearest after severe caerulin-induced pancreatitis, and has effects on pancreatic
acute pancreatitis. Their study demonstrated that the most cancer. Heat shock proteins are chaperone proteins that
severe damages take place in exocrine part of the pancreas. protect living cells against injury-inducing stimuli [16].
Nerves and stroma appeared to be resistant to pancreatitis
associated damage. Stromal construction put on some Possible strategies for early
limitation to extension of the inflammation. Pancreatic
intralobular ducts have shown resistance to inflammation, treatment of acute pancreatitis
which has been proportional to their diameter. Langerhans A genetic study suggested that polymorphisms in toll-like
islands also have relative stability to inflammation [9]. receptor-4 might affect the risk of developing infections in
acute pancreatitis [17]. Studies of chronic pancreatitis have
Distinguish between infected and sterile pancreatic shown that specific neural receptors, transient receptor
necrosis is always challenging for clinical practice, potential vanilloid subtype 1, mediate pain responses in a
therefore, needle aspiration may be required [8, 10]. model of chronic pancreatitis [18].

The pancreatic zymogen, chymotrypsin C, can degrade

Pathophysiology of pancreatic pathologically activated trypsin in the acinar cell.
acinar cell in pancreatitis Inactivating mutations in chymotrypsin C have been
Pancreatic duct obstruction rapidly changes the reported to predispose to the development of chronic
physiological response of the exocrine pancreas to a pancreatitis, especially in those who are prone to alcohol
Ca2+-signaling pattern that has been associated with abuse [18]. In the early stage of the inflammation, not only
premature digestive enzyme activation and the onset of the enzymes changes but some special characters are
pancreatitis [11]. The pancreatitis starts with Ca2+ signal happened: such as increased permeability (local and/or
that are generated by stimulation with cholecystokinin systemic), nerve stimulation, decreased blood flow, and
(CCK) and acetylcholine. It is known that CCK stimulate acid environment.
also the mitochondria. A single local cytosolic Ca2+ last for
only a short while and probably a prolonged increase of Acute pancreatitis is a drastically dynamic disease in
the spikes are the basis for pathological states leasing to several organs, including cardiovascular system,
inflammation. Toxic CCK concentration elicts sustained pulmonary, renal, pancreatic necrosis or infarction, and gut
calcium elevations, which induces post-exocytic endocytic injury (bacterial translocation). Patients with severe acute
vaculoe formation. Trypsin is activated in these vacuoles. pancreatitis typically develop vascular leak syndrome,
Alcohol induces Ca2+ dependent intracellular trypsinogen resulting in hemoconcentration, hypotension, pulmonary
activation in the apical granular area via non-oxidative edema and renal insufficiency. Angiopoietin-1 and 2 are
metabolites, such as fatty acid ethyl esters and fatty acids autocrine peptides that reduce or increase endothelial
[12]. Intracellular trypsinogen activation is a crucial permeability, respectively. it was concluded that serum
initiating event in the development of acute pancreatitis, angiopoietin-2 levels are strongly associated with severe
but the specific organelle in which this process takes place acute pancreatitis and persistent organ failure. Admission
has been unknown [13]. Recent data demonstrate that the angiopoietin-2 levels accurately predict organ failure [19].
Ca2+ dependent trypsinogen activation occurs in
postexocytotic endocytic vacuoles [12]. These vacuoles Clinically, gallstone disease is still a common cause of
are acid due to a bafilomycin-sensitive vacuolar H+ acute pancreatitis. To prevent recurrence of acute
ATPase and have a very Ca2+ permeable membrane. Acid pancreatitis, cholecystectomy is recommended after first
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episode of gallstone pancreatitis and after two bouts of for continuous lavage. The most common complication is
idiopathic acute pancreatitis. However, cholecystectomy occlusion of the drains with debris. Therefore, lavage to
fails to prevent recurrence in acute pancreatitis without get rid of debris and infected materials is a option, and
gallbladder stones and sludge. These results do not support thorough supplementary treatment with tailored antibiotics
the recommendation for cholecystectomy in idiopathic and jejunal feeding is mandatory [25].
pancreatitis [20].
Pancreatitis-induced inflammatory exudates can get to a
spleen immediately. Clinical and radiological changes in
Management of pancreatic the spleen were estimated mostly by computer tomography
necrosis or ultrasonography. Spleen damages can be categorised as
Sterile pancreatic necrosis is typically managed infarct, subcapsular fluid collections, subcapsular
conservatively without drainage. It may be challenging to hematoma and abscess. The spleen changes in acute
distinguish between sterile and infected pancreatic pancreatitis are transgent, and thus primary conservative
necrosis, and therefore, some study suggested CT-guided treatment can be the strategy in most patients [26].
fine-needle aspiration as a diagnose of the infected
pancreatic necrosis. However, fine-needle aspiration is Conclusion
associated with significant risks, and patients with Acute pancreatitis is a common disease frequently caused
extensive pancreatic necrosis and low C-reactive protein by choledocholithiasis or excess alcohol ingestion. A three
should be observed. CT-guided fine-needle aspiration is category classification of severity of acute pancreatitis
indicated only when there is clinical suspicion of infection were recently designed. The management of acute
and CRP >55 mg/L [21]. pancreatitis is frequently challenging, and
multidisciplinary approach should be used for the
Timing for debridement of severe acute pancreatitis may management of the patient with acute pancreatitis.
take place in proper demarcation of viable tissues enabling
an easier and safer debridement. Severe organ failure
within the first week after attack, however, is closely
linked to infection making postponing of intervention
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