**1. Introduction**

Pancreatic necrosis is the presence of nonviable pancreatic parenchyma or peripancreatic fat which may be localized or diffuse. It is classified radiologically according to the Atlanta Criteria as an acute necrotic collection (ANC), which is defined as a non-encapsulated area of necrosis, or as walled-off necrosis (WON), which is encapsulated [1]. Although pancreatic necrosis may result from trauma, malignancy, or chronic pancreatitis, the most common cause is acute pancreatitis; 20% of patients with acute pancreatitis develop necrosis. For patients who develop necrosis, the mortality rate is 15–30% [2]. Surgery has historically been the primary treatment for pancreatic necrosis. However, the superior outcomes associated with new, less invasive techniques have narrowed the scope for surgical intervention. Despite these shifts in practice, surgical care remains an important tool for the treatment of pancreatic necrosis.

## **2. Diagnosis and conservative management**

Although the diagnosis of pancreatitis is generally clinical, the primary diagnostic tool for pancreatic necrosis is the computed tomography (CT) scan. With this modality, normal pancreatic parenchyma is low attenuation, 40–50 Hounsfield units (HU), but increases with contrast to 100–150 HU. In comparison, areas of necrosis remain hypoattenuating, <30 HU [3]. MRI and endoscopic ultrasound are also used, but CT scan is considered to be the gold standard for diagnosis and characterization [4].

Regardless of the presence of necrosis, fluid resuscitation, and early nutritional support are paramount to the treatment of patients with acute pancreatitis. For patients who are able to tolerate enteral nutrition, there is a significant reduction in the rates of infected pancreatic necrosis, multiorgan failure, surgical intervention, and mortality when compared to patients who are given total parenteral nutrition (TPN) [5, 6]. Thus, prior to initiation of TPN, patients should be evaluated for tolerance of oral, nasogastric, and nasojejunal feeding. Route notwithstanding, nutrition should be addressed in the first 24–48 hours of admission for acute pancreatitis [7].

Sterile pancreatic necrosis does not have a specific clinical presentation, but is more common in patients with symptoms lasting more than 48 hours and with concomitant organ failure [8]. The morbidity and mortality associated with pancreatic necrosis is exacerbated by development of infection, which may result of seeding associated with bacteremia, colonic bacterial translocation, or direct contamination from a procedure (e.g. endoscopic retrograde cholangiopancreatography (ERCP) or surgery) [9]. The risk of infection correlates with the degree of necrosis. If more than 30% of the pancreatic parenchyma is necrotic, there is a 22% risk of infection. If 30–50% is necrotic, the risk of infection is 37%. If necrosis exceeds 50%, the risk of infection is 46% [10]. The signs and symptoms of infected pancreatic necrosis are similar to those of other types of infection, including: fever, leukocytosis, and worsening condition with optimal supportive care. Once the necrosis becomes infected, the incidence of organ failure increases, along with the risk of mortality [11].

Differentiating sterile from infected necrosis based on clinical presentation can be difficult. Patients with sterile necrosis can proceed to organ failure in similar fashion to patients with infected necrosis. Infection can be detected non-invasively on CT scan by looking for the presence of gas locules within the area of necrosis, suggesting microbial gas production. However, these findings are not always seen on CT, and fine-needle aspiration (FNA) may be necessary for definitive diagnosis. Multiple FNA aspirates may be required due to the 10% false negative rate of this test [12].

However, proof of infection on radiology or by tissue culture is not necessary to initiate treatment. If infection is strongly suspected due to clinical course, antibiotics are indicated regardless of radiologic or tissue diagnosis. If no antibiotic sensitivities are available from culture results, broad-spectrum antibiotics should be started. Due to the ability to penetrate the necrotic tissue, carbapenems are considered first-line treatment [13]. Prophylactic use of antibiotics has not been shown to impact the rate of developing infected necrosis, systemic complications, mortality, or need for surgical intervention and is not recommended [14–16].

Prior to any invasive management, a patient should be treated with optimal supportive care. This includes fluid resuscitation, nutritional support, and antibiotics, if infection is suspected. The need for invasive management of sterile pancreatic necrosis is rare, especially in acute phase. However intervention may be necessary during the late phase for protracted abdominal pain, obstruction, or, less often, for

failure of clinical improvement. Infected necrosis requires invasive intervention more often, both in order to gain source control and in order to resolve other noninfectious symptoms [17].
