At the outset, the clinician must be aware of the pathologic conditions that occur secondarily as a result of acute pancreatitis. A relatively uncommon but potentially lethal complication is that of intraabdominal hemorrhage requiring immediate intervention.80 The local complications of necrotizing pancreatitis are pancreatic necrosis, pancreatic abscess, and pseudocyst formation81; the process also may have more remote effects, such as formation of multiple intraabdominal collections, colonic perforation,82 and even gallbladder necrosis83 and abdominal compartment syndrome.84 Aggressive early hemodynamic stabilization is probably the only rational way to prevent further hypoperfusion injury to the pancreas and the development of these complications. Institution of peritoneal dialysis via the percutaneous or minilaparotomy route accelerates early improvement in some patients but does not appear to offer any benefit in decreasing the likelihood of complications and death.85 Patients in whom retroperitoneal necrosis (fat or pancreatic) develops are at high risk for morbidity and death.6 Those in whom this complication does not develop usually will survive with appropriate supportive measures only.
Pancreatic and Peripancreatic Necrosis
Pancreatic necrosis consists of patchy devitalization of the pancreatic gland; it develops in a few days to weeks after the onset of the inflammatory process. The patient usually has abdominal pain, persistent fever (possibly low grade), and leukocytosis. CT scan with vascular enhancement may demonstrate local or diffuse areas of nonenhancement. Needle aspirates obtained at this stage will show no growth on culture if necrosis is present without infection.
Treatment of this entity is controversial. It is difficult to predict how many cases of pancreatic necrosis (without infection) will resolve spontaneously with simple supportive management and how many will develop sepsis and clearly require débridement. Undoubtedly, the condition does resolve in some patients, who clearly would not benefit from laparotomy. Every pancreatic surgeon has had the experience of extensively débriding sterile retroperitoneal necrosis, subjecting the patient to perhaps many future débridements (which then, of course, involve infected tissue), and wondering whether the original noninfected condition might have resolved spontaneously. In addition, many “sequestrectomies” performed for pancreatic necrosis likely are excisions only of necrotic fat and not of necrotic gland. No comparison of these two pathologic entities in terms of morbidity and mortality has been reported. A retroperitoneum with a well-perfused pancreas surrounded by necrotic fat may carry a different outlook than if the gland itself is compromised. Therefore, removal of uninfected necrotic fat only may be a fruitless and conceivably dangerous exercise.
It has been suggested that infection develops in only 40% of patients with pancreatic and peripancreatic necrosis.86 Because of this and the aforementioned fear that surgery in the sterile situation actually may cause more harm than good, we tend to avoid major débridement unless sepsis is confirmed. Therefore, if the patient remains stable hemodynamically, has only low-grade fever and leukocytosis, has CT findings that do not suggest extensive glandular necrosis and infection, and has a sterile percutaneous retroperitoneal sample, we continue with supportive management without intervention. However, the patient ultimately may require intervention even in the absence of gross septic parameters simply because of a prolonged “smoldering” course showing no clinical improvement (Fig. 85-1).
CT scan of patient with acute alcoholic pancreatitis and evidence of a retroperitoneal collection containing fluid and air bubbles. Aspiration and culture confirmed infection with gram-negative organisms, and the patient was managed eventually with surgical débridement, enteral nutrition, and antibiotic therapy.
The role of antibiotics in the patient with pancreatic necrosis or sepsis is similarly controversial.87–91 Antibiotics are required in patients who have pancreatic necrosis (with or without sepsis), but their purpose is to provide systemic protection rather than local treatment or prophylaxis. Patients with sterile necrosis usually receive broad-spectrum antibiotics for systemic protection while the intensivist monitors the retroperitoneum, although this treatment undoubtedly brings with it a risk of opportunistic infection, such as disseminated candidiasis in the acutely ill host. In recent years, the case for routine antibiotic usage in such patients has strengthened. Certain antibiotics such as imipenem actually penetrate the pancreatic parenchyma, achieving good tissue levels during acute pancreatitis. In several studies, significant reduction in the incidence of septic complications followed the routine use of broad-spectrum antibiotics, but the effect on mortality has been less predictable. One study92 showed that routine use of imipenem-cilastatin altered the bacteriology in severe acute pancreatitis from predominately gram-negative coliforms to predominately gram-positive organisms without altering the incidence of resistance or fungal superinfection.
Prophylactic antibiotics for the purpose of selective decontamination of the gastrointestinal tract may prevent translocation of bacteria to the inflamed pancreatic bed, presumably from the transverse colon.93–96 Patients who develop infected necrosis must be treated actively to prevent or manage bacteremia and frequently require surgical débridement and drainage; however, even that approach is being challenged by some anecdotal evidence that antibiotics alone or in conjunction with percutaneous drainage without surgery may be sufficient to treat some patients with aspiration-proven retroperitoneal sepsis.97–101 This strategy still may be difficult to accept for those intensivists who have treated patients who developed fatal opportunistic infections in the past after long-term antibiotic therapy.
Infected Necrosis and Pancreatic Abscess
Some patients with pancreatic and peripancreatic necrosis develop spontaneous infection of the necrotic tissue presumably because of direct contamination by bacteria from the transverse colon. Although some authors do not distinguish between infected necrosis and pancreatic abscess, others differentiate them on the basis of suitability for percutaneous drainage: Infected pancreatic necrosis usually requires extensive surgical débridement and possibly pancreatic resection because of solid necrotic areas, whereas a pancreatic abscess may require just percutaneous drainage if liquefaction has taken place, leaving little solid necrotic tissue.
Notwithstanding the more conservative approach described earlier in selected patients, established sepsis in the retroperitoneum generally requires intervention to avoid the sequelae of systemic infection. This fact has significant implications in the patient who is critically ill from a primary illness. The diagnosis of retroperitoneal sepsis, whether infected pancreatic necrosis or pancreatic abscess, is made by recognition of clinical deterioration, which may be more precipitous than with pancreatic necrosis and may be accompanied by more pronounced fever and leukocytosis, typical CT findings, and a positive percutaneous aspirate.59,102 When the patient is maintained on broad-spectrum antibiotics (with perhaps decreased immunosuppression in the transplant patient), preparations are made for surgical débridement. Although some cases may be amenable to percutaneous drainage only, as stated previously, in our experience, most require laparotomy.
Principles of Surgical DéBridement
The conventional indications for surgery in acute pancreatitis include failure of early medical management, unresolving gallstone pancreatitis, and pancreatic sepsis. In the critical care setting, aggressive supportive care has virtually eliminated the need for early operation. As stated earlier, a persistent gallstone pancreatitis may be treated effectively by early endoscopic sphincterotomy. Therefore, the main indication for surgery in the critically ill patient with pancreatitis is the late development of necrosis or sepsis.58,59
Recommended methods of surgical débridement vary considerably, and their description is beyond the scope of this chapter. The principles of the different approaches are similar, however; the critical steps are the recognition of the patient in whom débridement is appropriate and quick execution of the procedure, with excellent anesthesia and postoperative intensive care.
The timing of surgery for pancreatic sepsis is critical,103 in that early débridement (done usually within 3 weeks of the onset of clinical pancreatitis) may encounter poor demarcation between necrotic and healthy tissue, leading to oozing from partially devitalized tissue after necrosectomy. If a wait can be tolerated by the patient, a late laparotomy (at 3 to 6 weeks) is likely to involve the removal of well-demarcated necrosis (often in a single procedure rather than multiple operations).
Surgery should consist of wide débridement of all devitalized peripancreatic fat and pancreatic tissue, followed by adequate dependent drainage, which should be generous enough to allow drainage of thick, purulent, often particulate material.104,105 Since multiple operations for repeated abdominal toilet sometimes are required, some surgeons have advocated open packing of the abdomen in such cases.102,106
Our own preference is for radical excision of all necrotic and infected material followed by generous dependent sump drainage and closure of the abdomen, although some practitioners advocate closed lavage postoperatively.107 Intubation of the gastrointestinal tract (cholecystostomy, gastrostomy, and jejunostomy were advocated enthusiastically in the past108) is to be avoided in this septic setting. Temporary packing of the retroperitoneum and scheduled reoperation occasionally are necessary to control venous oozing from the bed of the necrotic tissue.
The extent of pancreatic resection varies depending on the degree of necrosis of the gland itself. Although some surgeons have recommended routine performance of major pancreatic resection,109,110 we débride the gland itself only if necessary; only necrotic portions are removed, and major anatomic dissections are avoided, if possible, in these often unstable patients.
The patient who suffers infected pancreatic necrosis and who requires intensive care, often multiple operations, and an extended hospital stay clearly will have a protracted convalescence. However, a recent quality-of-life study111 found that the survivors of this morbid disease could look forward to good quality of life.
With more frequent use of ultrasound and CT scanning in the early stages of pancreatitis, recognition of fluid collections in and around the lesser sac has become the rule rather than the exception. Most collections probably consist of inflammatory exudate, and in fact, most resolve as the pancreatitis settles (Fig. 85-2). The persistence of a lesser sac fluid collection (or of fluid in a variety of areas, such as the peritoneal cavity, the retroperitoneum, or even the mediastinum) implies a communication with a ruptured pancreatic duct system. A collection that develops thick, fibrous walls consisting of the surrounding stomach, colon, and mesentery properly can be termed a chronic pseudocyst. Diagnosis of such a condition does not mandate immediate treatment unless the pseudocyst becomes symptomatic, grows quickly, becomes infected, bleeds, or ruptures into the peritoneal cavity or adjacent bowel. In an already sick patient, a quickly enlarging or infected pseudocyst is best treated with percutaneous decompression or endoscopic pseudocyst drainage, whereas immediate surgery is required for bleeding or free rupture. Occasionally, transpapillary stent placement is useful if a direct communication exists between the main pancreatic duct and the pseudocyst.112 The presence of a large collection does not of itself necessitate percutaneous decompression; in fact, one group found that collections that were drained early had a significantly increased chance of later developing septic complications requiring surgery and a longer hospital stay.113 It also has been suggested that percutaneous treatment is effective for peripheral collections, whereas more centrally placed collections need operative decompression.114 Spontaneous rupture into the intestinal tract, a rare occurrence, can be treated expectantly in this setting if the patient is otherwise stable. The uncomplicated pseudocyst that is stable in size and is at least 6 weeks old (to allow the walls to “mature” enough to accept sutures) is conventionally drained internally at laparotomy; in the intensive care situation, percutaneous drainage can be done safely to avoid the dreaded complications, but it must be used with full knowledge that recurrence is frequent.
CT scan of patient with acute pancreatitis and acute pseudocyst formation. The dumbbell-shaped pseudocyst resolved gradually without internal or external drainage.