Clinical Pancreatology for Practising Gastroenterologists and Surgeons. Группа авторов

14 How to Deal with Infected Pancreatic Necrosis?

       J. Enrique Domínguez‐Muñoz

       Department of Gastroenterology and Hepatology, University Hospital of Santiago de Compostela, Santiago de Compostela, Spain

Introduction

      Acute pancreatitis is frequently a mild disease. However, about one in every five patients develops a more severe disease with (peri)pancreatic necrosis. Early organ or multiorgan failure develops in severe disease, usually within the first week of onset, due to systemic inflammatory response syndrome. Late development of organ failure is usually due to sepsis secondary to infection of (peri)pancreatic necrosis. Infected necrotizing pancreatitis is therefore one of the most severe complications of acute pancreatitis and one of the greatest therapeutic challenges in this disease.

      Infected (peri)pancreatic necrosis was historically considered an indication for early open necrosectomy [1]. However, this approach was associated with a high rate of complications and death. Because of this, prevention of infection of pancreatic necrosis became the main therapeutic aim in acute necrotizing pancreatitis, and prophylactic administration of antibiotics, mainly imipenem, was included as part of the standard of care of these patients [2,3].

      Several landmark studies and publications over the last 15 years have led to a dramatic change in the management of patients with acute necrotizing pancreatitis.

Prevention of Infection of (Peri)pancreatic Necrosis

      Intestinal bacterial translocation is generally accepted as the main source of infection of pancreatic necrosis [18]. In fact, intestinal permeability is increased and splanchnic perfusion is impaired in severe acute pancreatitis [19,20]. In addition, the bacteria infecting pancreatic necrosis are mainly of intestinal origin [21]. Since antibiotic prophylaxis has failed to provide any benefit in acute necrotizing pancreatitis [4–9] and because it is definitely not recommended in clinical practice, avoiding intestinal bacterial translocation is the main aim in the prevention of infection of pancreatic necrosis.

Enteral nutrition is one of the pillars in the management of severe acute pancreatitis. This not only provides nutrients to a severely ill patient, but also maintains intestinal barrier function. Enteral nutrition improves luminal gut nutrition, enhances splanchnic blood flow, and may stimulate enteral motility, thus reducing the risk of intestinal bacterial overgrowth and bacterial translocation [22,23]. This explains, at least partly, why enteral nutrition is superior to parenteral nutrition in patients with severe acute pancreatitis in terms of infection of pancreatic necrosis, septic complications, and death [24,25].

      Enteral nutrition can be delivered through a nasogastric or a nasojejunal tube [26,27]. Based on the similar efficacy and safety of both routes, nasogastric feeding is generally preferred as the first step in clinical practice. Nasojejunal feeding is mainly reserved for patients with gastric outflow obstruction and those with intolerance to gastric feeding.

      Early initiation of enteral feeding was generally recommended in clinical practice for patients with predicted severe acute pancreatitis. However, recent clinical trials have shown that early feeding is not associated with a reduction in infection, persistent organ failure, or mortality [28,29]. Based on this, enteral feeding can be delayed and given on demand to patients who are unable to tolerate oral refeeding after 72 hours from onset of acute pancreatitis.

Diagnosis of Infected (Peri)pancreatic Necrosis

The presence of fever early in acute pancreatitis is usually secondary to the release of inflammatory mediators. Later, the development of clinical and laboratory markers of sepsis in the absence of any extrapancreatic infection (respiratory, urinary, venous catheter) is the basis for the diagnosis of infected pancreatic necrosis. The presence of gas within the (peri)pancreatic area on computed tomography (CT) confirms the diagnosis (Figure 14.1). In the absence of pancreatic gas bubbles, which occurs in up to 60% of patients [30], fine needle aspiration (FNA) may be required to confirm the diagnosis of infection within the pancreatic necrosis. However, culture of FNA samples produces false‐negative results in about 25% of cases and frequently does not modify the therapeutic approach in patients with sepsis [30]. In our center, FNA for culture and antibiotic resistance testing is only performed once drainage of the necrotic collection has been indicated based on clinical, laboratory, and imaging data.

      Finally, serum measurements of procalcitonin may be a valuable tool supporting the diagnosis of infected pancreatic necrosis in patients with acute necrotizing pancreatitis and without extrapancreatic infection [31,32].