**2. Acute pancreatitis**

AP is an acute inflammatory condition of the pancreas with histological acinar cells destruction. It has a wide spectrum of morphological and clinical manifestations and can result in local injury, systemic inflammatory response syndrome (SIRS) and organ failure [1, 2].

### **2.1 Epidemiology**

AP is one of the most common gastrointestinal diseases requiring acute hospitalization [3]. Its incidence is rising worldwide and ranges from 5 to 30 cases per 100,000 [1] and despite improvements in the diagnosis, management and treatment, the overall mortality rate of AP remains around 2–5% [4, 5]. The average length of hospital stay for AP is 8 days, with economic burden to patients and the health care system all around the world [6].

### **2.2 Etiology**

The most common causes of AP are gallstones (up to 40–70% of cases) and alcohol abuse (25–35%).

Migrating gallstones cause transient obstruction of the pancreatic duct leading to the blockage of pancreatic secretion and lysosomal dysfunction generating injury and inflammatory response. Alcohol abuse exerts its effects in a complex way that include direct toxicity and immunologic mechanisms: prolonged alcohol use (four to five drinks in a day over a period of more than 5 years) is required and the type of alcohol ingested does not affect the overall lifetime risk of alcohol-associated pancreatitis, that range from 2% to 5% in heavy drinkers ("Heavy" alcohol consumption is generally considered to be >50 g in a day).

In absence of gallstones or alcohol, other etiologies of AP (**Table 1**) must be ruled out.

The agent or condition causing AP is not always clear and sometimes there is only the evidence of factors known to be potential contributors of unexplained pancreatitis, such as smoke, obesity and diabetes. Accordingly, idiopathic AP has been defined as a condition in which the etiological cause is not detectable after an accurate anamnesis excluding any substance abuse, infections, metabolic disorders, genetic mutations and at least two second-level imaging techniques [endoscopic ultrasound and

*Management of Acute and Chronic Pancreatitis DOI: http://dx.doi.org/10.5772/intechopen.109115*


*\*Among patients undergoing ERCP.\*\*5–14% of patients with benign or malignant pancreatobiliary tumors present with AP.*

### **Table 1.**

*Causes of acute pancreatitis.*

magnetic resonance imaging (MRI)] to exclude abnormality of pancreatic gland, pancreatic or biliary and gallbladder lithiasis.

Any mass that obstructs the main pancreatic duct can cause AP: 5–14% of patients with benign or malignant pancreatobiliary tumors present with this scenario and pancreatic tumor should be suspected in any patient older than 40 years with idiopathic pancreatitis, especially those with prolonged or recurrent course [4–6].

### **2.3 Clinical signs and symptoms**

Patients with AP usually present with epigastric or left upper quadrant pain, usually described as persistent, severe and often radiating to the back, chest or flanks. The intensity of pain is not correlated to the severity of the disease. Patients experience pain relief when sitting forward or worsening when lying flat. Nausea and vomiting are also common, and sequestered fluid in the small bowel may lead to rapid and severe dehydration. Diaphragmatic irritation may cause hiccoughs. The presentation can also be dominated by shock with tachycardia, tachypnea, hypotension, anuria and mental status alteration. On the other hand, patients may be paucisymptomatic,

with few physical signs. Abdominal examination reveals epigastric tenderness and guarding; abdominal distension with paralytic ileus. Later signs may include mottled skin or livedo reticularis and lace-like purplish discoloration of the skin. Abdominal periumbilical ecchymosis (Cullen's sign) and ecchymosis of the flank (Grey Turner's sign) result from the diffusion of fat necrosis and inflammation associated with retroperitoneal or intra-abdominal bleeding [5].

### **2.4 Diagnosis**

The diagnosis of AP is made following the Revised Atlanta Criteria, a global consensus classification (generated in 1992 and revised in 2012) designed to standardize diagnosis, clinical assessment, evaluation, severity and complications of AP and to help the communication between clinicians.

Diagnosis of AP requires two of the following three features:


According to these criteria, it is important to underline that when the diagnosis of AP is established by abdominal pain and by increased serum pancreatic enzyme activities (clinical and laboratory criteria), the radiological findings (imaging criteria) are not required for making the diagnosis [3, 7].

In the majority of patients, routine use of CT or MRI is unwarranted as the diagnosis of AP is apparent and most have a mild, uncomplicated course. CT or MRI imaging should be reserved for patients in whom the diagnosis is unclear or who fail to improve clinically within the first 48–72 hours after hospital admission [6].

Contrarily, transabdominal ultrasound should be performed on admission in all patients with AP, to define the underlying etiology and to identify the presence of gallstones that are the most common cause of AP [3, 6].

Moreover, it is important to record the time interval between onset, first observation and hospital admission. In fact, the onset of AP is defined as the time of beginning of abdominal pain and not the time of admission to the hospital [7].

In an episode of AP, the enzyme secreted by the pancreas (amylase, lipase, elastase and trypsin) are released from acinar cells of the pancreas into the bloodstream at the same time, due to increased permeability following inflammation.

Amylase is an enzyme synthesized mostly by pancreatic acinar cells and salivary glands and in negligible levels by adipose tissue, gonads, fallopian tubes, intestinal tract and skeletal muscle. Humans product one specific isoenzyme, α-amylase, with two major isoforms specific to pancreas and to salivary glands that help to identify different cases of hyperamylasemia. In case of AP, serum amylase rises rapidly within a few hours after the onset, with peaks at 3–6 hours, half-life of 10–12 hours, persistent elevation for 3–5 days and decrease to normal levels over the next three to 7 days.

Lipase is an enzyme that has a higher specificity because is mainly produced by acinar cells of the pancreas; nevertheless, high serum level can be determined also in patient with renal insufficiency, appendicitis, diabetic ketoacidosis, inflammatory

bowel disease and intestinal obstruction. In AP, elevation of serum lipase arises within three to 6 hours with peaks at 24 hours following the onset of symptoms and persistent elevation up to 2 weeks, giving a larger diagnostic window in comparison to amylase.

Therefore, serum lipase appears to be more specific and remains elevated for a longer period than serum amylase after disease presentation. Moreover, lipase has a better degree of sensitivity and specificity in diagnosing AP, during both early and late phases of the disease (sensitivity of lipase and amylase tests ranges between 64–100% and 45–87%, respectively).

According to these evidences, current guidelines recommend the preference use of serum lipase for diagnosis of AP [2, 4, 6].

### **2.5 Classification**

The most commonly used classification system for AP is the "2012 revision of the Atlanta Classification and definitions" based on international consensus [8].

This classification identifies two types (Interstitial edematous pancreatitis and necrotizing pancreatitis), three grades of severity (mild, moderately severe or severe) and two phases (early and late) of AP.

### *2.5.1 Types of acute pancreatitis*

Two different types of AP have been characterized: Interstitial edematous pancreatitis and necrotizing pancreatitis.

**Interstitial edematous pancreatitis** is an acute inflammation of pancreatic parenchyma and peri-pancreatic tissues, but without recognizable tissue necrosis. Developed by the majority of patients (80–85%), it is characterized by diffuse (or occasionally localized) enlargement of the pancreas, due to inflammatory edema; the clinical symptoms usually resolve within the first week.

**Necrotizing pancreatitis** is, instead, the presence of inflammation associated with pancreatic parenchymal necrosis and/or peri-pancreatic necrosis. The natural history of necrotizing pancreatitis is variable and this scenario evolves over several days because necrosis can remain solid or liquefy, can remain sterile or become infected, persist or disappear over time. This explains why an early CT made for assessment of AP may underestimate the eventual extent of pancreatic and peri-pancreatic necrosis. Moreover, most evidence suggest no correlation between the extent of necrosis and the risk of infection and duration of symptoms and usually infected necrosis is rare during the first week. Developed by 15–20% of patients with AP, this type of evolution of AP has increased morbidity and mortality compared to patients with interstitial edematous pancreatitis [5, 7].

### *2.5.2 Severity of acute pancreatitis*

A preliminary overview of complications of AP is mandatory, because the comprehension of these terminologies is central to definition and stratification of severity.

• **Local complications**: acute peri-pancreatic fluid collection, pancreatic pseudocyst, acute necrotic collection (sterile or infected), walled of necrosis (sterile or infected), gastric outlet dysfunction, splenic and portal vein thrombosis, ischemic colitis, colonic necrosis, enteric fistulas, hemorrhages.


There are three degrees of severity of AP:


Usually, mild AP account for 80–85% of cases, while severe AP is reported in 15–30% of patients [6].
