Page 30 - Journal of Laparoscopic Surgery

10.5005/jp-journals-10007-1136
Kiran Somani, Dnyanesh M Belekar
REVIEW ARTICLE
Role of Minimal Access Surgery in Management

of Infective Pancreatic Necrosis

1 Kiran Somani, Dnyanesh M Belekar
2
1 Associate Professor and Unit Head, Department of Surgery, KJ Somaiya Medical College, Mumbai, Maharashtra, India
2 Associate Professor, Department of Surgery, KJ Somaiya Medical College, Mumbai, Maharashtra, India

ABSTRACT
Aim: To study various minimal access surgical techniques of pancreatic debridement for infected pancreatic necrosis (IPN).
Method: A review of literature is done using various search engines like Google, Yahoo, PubMed, etc. by using keywords: Pancreatic
necrosectomy, laparoscopic, endoscopic pancreatic necrosectomy.
This article reviews various methods of minimally access pancreatic necrosectomy (MAN) can be classified by the type of scope
used flexible endoscope, laparoscope, nephroscope and the route of access transperitoneal, transgastric, retroperitoneal. Each of the
scopes and access routes has its advantages and disadvantages.
Result and conclusion: Only few large series of cases of MAN have been published, rest are limited to case reports. There are no
comparisons of results, either with open surgery or among different minimal access surgeries but a body of evidence now suggests
that acceptable outcomes can be achieved and minimal access necrosectomy is technically feasible, well tolerated and beneficial for
patients when compared with open surgery.
Keywords: Infected pancreatic necrosis, Minimal access pancreatic necrosectomy.

INTRODUCTION failure of the pancreatic microcirculation leads to ischemia, which

The gold standard for treatment of infected pancreatic necrosis compounds the enzymatic and inflammatory injury and leads to
(IPN) is surgical debridement. It can be achieved by open and the full syndrome of necrotizing pancreatitis. During this first
minimal access surgical approaches. Open surgery for this week or two, in the so-called vasoactive phase, there is the
condition carries a mortality rate of up to 50%, 1,2 therefore, a release of proinflammatory mediators that contribute to the
number of such techniques have been developed. pathogenesis of pulmonary, cardiovascular and renal
Pancreatic necrosis is defined as a diffuse or focal area of insufficiency. This early systemic inflammatory response and
nonviable pancreatic parenchyma that typically is associated multiorgan dysfunction are found frequently in the absence of
3
with peripancreatic fat necrosis. Necrosis can be sterile or pancreatic infection. In the later septic phase, which occurs in
infected. IPN is the leading cause of death associated with some patients after 3 to 4 weeks, these systemic events occur
severe acute pancreatitis. The incidence of acute pancreatitis as a consequence of pancreatic infection.
varies from 10 to 40 per 100,000 population. The proportion of There are five routes by which bacteria can infect pancreatic
patients that develop pancreatic necrosis is approximately necrosis. These are as follows:
15 to 20%. Approximately, 40% of these patients go on to • Hematogenous through mesenteric vessels to the portal
develop infection of the necrosis. The overall mortality of circulation
edematous pancreatitis is 1% or less, that of sterile necrosis 5% • Transpapillary reflux of enteric content into the pancreatic
and that of infected necrosis 10 to 20% in centers of excellence. duct
• Translocation of intestinal bacteria and toxins via the
PATHOGENESIS OF IPN mesenteric lymphatics to the thoracic duct and the systemic
Pancreatic necrosis occurs within the first few days of the onset circulation
of acute pancreatitis. Out of all the patients who develop • Reflux of bacteriobilia via a disrupted pancreatic duct into
pancreatic necrosis, 70% have evidence of this by 48 hours of the necrotic parenchyma and
the onset of abdominal pain and all of them by 96 hours. The • Transperitoneal spread.
premature activation of proteolytic enzymes within the acinar Cultures of infected pancreatic necrosis yield monomicrobial
cells and interstitium of the lobule results in extensive necrosis flora in three-quarter of patients. Gram-negative aerobic bacteria
of acinar cells and the substantial interstitial and intravascular usually are responsible (e.g. Escherichia coli, Pseudomonas
accumulation and activation of leukocytes. spp., Proteus and Klebsiella spp.), and this strongly suggests
There are a number of factors that contribute to the failure an intestinal origin, but Gram-positive bacteria (e.g.
of the pancreatic microcirculation, which is evident histologically Staphylococcus aureus, Streptococcus faecalis and
as stasis and/or thrombosis of intrapancreatic vessels. The Enterococcus), anaerobes and occasionally, fungi also have

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