Complicated acute pancreatitis

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Chapter 13

• Chemotherapy and radiotherapy may have benefit in the adjuvant setting but currently remain

investigational.

• The clinical presentation in distal cholangiocarcinoma is very similar to that of other periampullary

tumours.

• Similar to hilar disease, a preoperative tissue diagnosis is not necessary to proceed with surgical

resection.

• When possible, endoscopic palliation is the preferred method to relieve symptomatic jaundice in the

setting of unresectable disease.

• Hepatocellular carcinoma must be excluded in patients with an intrahepatic mass.

• Metastatic adenocarcinoma to the liver from a remote primary, such as lung, breast or

gastrointestinal, must be excluded.

• Similar to all other locations of cholangiocarcinoma, complete surgical resection of an intrahepatic

cholangiocarcinoma is the optimal treatment and only chance for cure.

• In gallbladder cancer, a cholecystectomy should be performed for adenomatous polyps >1 cm,

or those that are smaller but growing and changing in character. Cholesterol polyps and adenomyomatosis are not premalignant conditions.

• Complete surgical resection is the goal, whether the diagnosis is made preoperatively,

intraoperatively or after a non-curative laparoscopic cholecystectomy.

• In patients with invasion into the common bile duct, consideration should be given to neoadjuvant

chemotherapy prior to surgical exploration in an attempt to best select patients for potentially curative resection.

• Obstructive jaundice in the setting of gallbladder carcinoma portends poor survival and systemic

therapy should be considered prior to entertaining surgical resection.

Complicated acute pancreatitis

Euan J. Dickson C. Ross Carter Colin J. McKay

Introduction

Complications following acute pancreatitis occur on a spectrum of severity, complexity and chronology. The majority of patients with acute pancreatitis (AP) recover with simple supportive management including intravenous fluids and analgesia. Approximately 20%, however, develop severe acute pancreatitis with local and/or systemic complications. Of this subgroup, up to half will die as a result of complications of their disease.

Successful management of the patient with complications following AP is challenging and best undertaken by a multidisciplinary team. Decision-making is complex, multimodal therapy is often required and the hospital stay is likely to be protracted. Increasingly, these patients are managed, at least initially, in the base hospital. Early and regular discussion with a specialist unit is recommended and those patients who exceed local institutional capability should be considered for transfer.

Initial management

The initial management of acute pancreatitis is covered in the relevant chapter of the Core Topics in General and Emergency Surgery volume of this series and is addressed in several guidelines and consensus statements. The most recent and relevant of these is the International Association of Pancreatology/American Pancreatic Association Guidelines of 2013 (IAP/APA Working Group

This chapter will therefore focus on the

2013). management of complications of acute pancreatitis.

Key concepts

There are three key concepts in the current management of complications of acute pancreatitis (Box14.1).

Definitions and terminology in acute pancreatitis

The original Atlanta Classification of acute pancreatitis was published in 1993 to define the disease and clarify the terminology. Over the subsequent two decades, understanding of the correlation between clinical, radiological and pathological features has improved. This is largely as a result of advances in medical imaging technology and, in particular, contrast enhanced computed tomography (CECT).

The revised Atlanta Classification was published

in 2013 deficiencies and confusion inherent in the previous definitions. Two phases of the disease process are identified: early and late, arbitrarily defined as less than/more than 4 weeks from presentation. A third category has been added to disease severity, which is now classified as mild, moderate or severe (Box14.2).

The ability to interpret fluid collections and necrosis is critical to decision-making regarding management, particularly intervention. The revised Atlanta Classification of these local complications is a significant improvement over the original definitions. Local fluid collections are now defined based on time from presentation and content,

and sought to address the recognised

in an effort

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Complicated acute pancreatitis

Box14.1 • Complications of acute pancreatitis

1. Patient pathophysiology, rather than anatomy of disease,

determines the need for intervention. Serial clinical review identifies global trends in patient trajectory and guides management.

2. If intervention is considered necessary it should in

general be delayed for as long as possible (unless immediately life-saving) and is best avoided in the first 2 weeks following the index episode.

3. Each intervention carries risk and benefit – therapeutic

gain is maximised when the intervention is limited to that which is absolutely necessary (the ‘step-up approach’). Radiological, endoscopic and other minimally invasive techniques are replacing major open surgical intervention.

Box14.2 • Revised Atlanta Classification (2012)

Mild acute pancreatitis

– no organ failure, local or systemic complications and

usually resolves within a week

Moderately severe acute pancreatitis

– transient organ failure, local complications or exacerbation

of comorbid disease

Severe acute pancreatitis

– persistent organ failure (duration >

48 hours)

as acute peripancreatic fluid collections (APFC), pseudocyst, acute necrotic collection (ANC) and walled-off necrosis (WON). Collections may be sterile or infected. The management of each of these differs and is outlined below with the updated definitions.

Acute peripancreatic fluid collection (APFC)

In the early stages of acute pancreatitis, up to 25% of patients will develop a fluid collection in the peripancreatic region. On contrast-enhanced computed tomography (CECT), APFCs are illdefined, homogeneous and may be multiple. Pancreatic vascular perfusion on CECT is normal, and there should be no necrotic material (e.g. peripancreatic fat) within the collection. Most acute fluid collections remain sterile, usually resolve without intervention and are of little clinical significance. There are, however, significant risks associated with aspiration and especially external drainage. These unnecessary interventions may introduce infection. Whilst most APFCs resolve spontaneously, a small number may persist beyond 4weeks and develop into a pancreatic pseudocyst.

Pancreatic pseudocyst

A pancreatic pseudocyst refers specifically to a fluid collection with no solid component persisting beyond 4 weeks of presentation. It

is predominantly in the peripancreatic tissues, although it may be partially or wholly within the pancreatic parenchyma. With time a well-defined wall will develop. Most post-acute collections described as pseudocysts are actually walledoff necrotic collections with a relatively minor volume of necrosis. Persistence of an acute fluid collection beyond 4 weeks is thought to result from disruption of the main pancreatic duct or its side branches, and the fluid within has a very high amylase content. Disruption of the duct will only occur following necrosis of either the duct or parenchyma and pancreatic necrosis must be present by definition. Therefore, a pancreatic pseudocyst is extremely rare in acute pancreatitis and most persistent collections should be thought of and managed as walled-off necrotic collections. CECT often underestimates the degree of solid material and MRI or EUS may be required to determine the volume of necrosis.

Asymptomatic or small pseudocysts do not require treatment, and many will eventually resolve spontaneously. Acute pseudocysts are most commonly retrogastric, and may or may not communicate with a disrupted pancreatic duct. Three-quarters will be associated with a mild to moderate hyperamylasaemia.

Necrosis

The revised Atlanta Classification dichotomises necrosis according to the phase of the disease process, with an arbitrary cut-point at 4weeks.

Acute necrotic collection

Acute necrotic collection (ANC) is the terminology used to describe a fluid collection with a solid necrotic component within the first 4 weeks following presentation. The fluid and solid components occur in variable proportions. It is therefore distinct from an APFC, which contains fluid only. The necrotic process may involve both the pancreas and peripancreatic tissues. On CECT these collections may be multiple, ill-defined and loculated.

Walled-off necrosis

Walled-off necrosis (WON) also contains necrosis but occurs later in the disease process (after 4weeks). On CECT it has a well-defined, mature, enhancing wall of reactive tissue and contains fluid and solid necrotic material. The nomenclature of this entity has perhaps undergone the greatest number of revisions over the last few decades and these are not revisited here in an effort to minimise confusion. WON can also occur at multiple sites, which may or may not communicate with each other, and can extend to more distant areas including the mesentery, making access challenging.

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245

Chapter 14

Sterile and infected collections

As will be discussed later, the development of infection within a collection has a profound effect on the clinical course and the need for intervention. All collections can become infected but this is unusual in the absence of necrosis, and infected acute fluid collections or pseudocysts are rare. Sepsis almost universally presents as an infected ANC or infected WON, the management of which will be discussed in a subsequent section. Infection may occur at any stage but is most frequent in the second and third weeks following presentation, and may be suspected through clinical deterioration, usually associated with a rising inflammatory response, and should prompt urgent CT.

Local complications of acute pancreatitis are defined by time (< / > 4weeks) and by necrosis (present or absent).

Clinical patterns and complications

Complications of acute pancreatitis may be broadly considered as systemic or local. These are inextricably linked and both may be present to varying degrees.

The clinical progress of a patient with pancreatitis,

including the development of systemic or local complications is not a binary process but rather a dynamic continuum with the potential for rapid deterioration. Within this continuum, patterns of clinical behaviour are apparent.

Early phase complications (<

Systemic complications Organ failure

The majority of patients with clinically mild acute pancreatitis may be managed in a ward environment. Patients with evidence of clinical deterioration, and in particular those with persistent organ dysfunction, should be managed in a critical care environment. Early indication for critical care support is usually as a result of an uncontrolled systemic inflammatory response resulting in organ failure. Late deterioration requiring critical care support is often the consequence of inadequately controlled sepsis, which is a risk factor for lifethreatening haemorrhage, and often precedes terminal decline.

Severe acute pancreatitis is frequently associated

with organ failure. Respiratory, cardiovascular, renal and gastrointestinal dysfunction are the most commonly involved systems. Deteriorating organ function mandates critical care support in the high dependency unit (HDU) or intensive care unit (ICU).

4 weeks)

Respiratory failure should prompt early discussion with the critical care team. Whilst non-invasive respiratory support may be sufficient for some patients, others require early mechanical ventilation and the transition from one level of support to the other can be rapid.

Cardiovascular collapse is treated with aggressive volume resuscitation directed towards optimising tissue perfusion. This should include addressing both haemodynamic targets and parameters of cellular respiration. Acid–base balance, lactate and mixed venous oxygen saturation are helpful in assessing adequacy of volume restoration. Vasoactive support is often required as a bridge whilst restoring circulating volume.

Renal failure as a consequence of cardiovascular compromise and reduced perfusion is common. Management again involves prompt volume resuscitation and close attention to fluid balance. Dialysis may be required for fluid overload, hyperkalaemia or acidosis. Recovering renal function in this context is a helpful marker of global improvement in physiology.

Reduced visceral perfusion may also result in gastrointestinal dysfunction. Gastrointestinal blood flow is further compromised by splanchnic vasoconstriction, either as a consequence of shock physiology or secondary to exogenous vasoconstrictor support. This manifests as abdominal bloating, nausea and vomiting and has two significant clinical sequelae. Firstly, patients may be unable to tolerate enteral nutrition including nasojejunal feeding. Secondly, inadequate mucosal perfusion leads to breakdown of the intestinal barrier function and is associated with bacterial translocation and infection of pre-existing necrosis.

Deteriorating physiology should prompt early

critical care input regardless of ‘predicted severity’.

Intra-abdominal hypertension (IAH)

IAH is recognised as a contributing factor to organ dysfunction in the context of a variety of acute abdominal processes. Most of the literature to date focuses on trauma patients, but there is increasing interest in its role in patients with severe acute pancreatitis. There are data to suggest that raised intra-abdominal pressure (IAP) may be associated with disease severity, organ failure and mortality in severe acute pancreatitis.

There are, however, no data to suggest improved outcome following surgical decompression for raised IAP in acute pancreatitis, and indeed this may be harmful. Abdominal compartment syndrome (raised IAP with associated organ failure) should initially be managed medically according to existing guidelines.

A decision to proceed to decompressive laparostomy

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Complicated acute pancreatitis

may be made on an individual case basis within a multidisciplinary team setting, but there is currently no evidence base for this approach.

There is currently no evidence base for the role

of decompressive laparostomy in acute pancreatitis.

The role of ERCP in acute pancreatitis

There has been long-standing controversy over the role and timing of endoscopic retrograde cholangiopancreatography (ERCP) in gallstone pancreatitis, with conflicting results from randomised trials. However, there are now several meta-analyses of the randomised evidence clarifying the position.

5,6

There is no role for early ERCP in mild pancreatitis. Following complete resolution of mild gallstone pancreatitis there may be a role for ERCP and sphincterotomy as definitive management where cholecystectomy is precluded by comorbidity.

In patients with severe disease, there is a subgroup that present with hyperamylasaemia, pain, jaundice and fever within 12 hours of presentation. Early recognition that these patients have organ dysfunction secondary to biliary sepsis rather than pancreatitis, the hyperamylasaemia being incidental, should prompt an ERCP and biliary decompression.

A management dilemma, however, exists in the subgroup of patients with acute pancreatitis and jaundice as it may be difficult to differentiate between the systemic inflammatory response syndrome (SIRS) driven by acute pancreatitis and ‘true’ cholangitis. There is a lack of clear evidence regarding the role of early ERCP in patients with pancreatitis and jaundice but without evidence of cholangitis. In addition, unnecessary ERCP carries risk and may be technically challenging in the context of duodenal and periampullary oedema. The majority of duct stones causing acute pancreatitis are expected to pass spontaneously, and it may therefore be helpful to observe these patients for 24–48 hours and then divide them into one of three groups to determine if there is a need for ERCP (Box14.3).

Box14.3 • ERCP algorithm for acute pancreatitis

1. Patients with resolving jaundice

– observe

2. Patients with persistent jaundice but clinically improving

– biliary imaging with MRCP or EUS

3. Patients with persistent jaundice and clinical

deterioration – ERCP and biliary decompression

ERCP, endoscopic retrograde cholangiopancreatography; EUS, endoscopy-guided ultrasound; MRCP, magnetic resonance cholangiopancreatography.

Early haemorrhage

In the era of early surgical debridement, the term haemorrhagic pancreatitis

was often used to describe the presence of blood within the necrotic pancreatic and peripancreatic tissue found at laparotomy. Active haemorrhage is, however, extremely rare in the acute phase in the absence of intervention.

Colonic ischaemia

Mesenteric vascular compromise is extremely common in severe acute pancreatitis, usually as part of global systemic hypoperfusion. Mucosal hypoperfusion has been postulated as a potential source of secondary infection of acute necrotic collections.

This is believed to be modulated through bacterial translocation as a result of a breakdown in the mucosal barrier. At laparotomy and debridement, the vascular integrity of the colon often appears questionable, leading to a relatively high incidence of colectomy. Full-thickness intestinal ischaemia is fortunately relatively rare, and is seen much less frequently in the minimally invasive era. Patchy full-thickness ischaemia may lead to fistulation with secondary sepsis (Fig.14.1). Defunctioning ileostomy may be required for sepsis control.

Late complications (>

4 weeks)

Management of collections associated

with acute pancreatitis Management of necrosis

As previously stated, intervention is usually required only for ANC or WON, the majority of acute fluid collections resolving spontaneously. The management algorithm for pancreatic necrosis has altered radically in the last 20years in response to evolving concepts, improved understanding of the disease process and the development of minimally invasive techniques. These techniques include percutaneous, and endoscopic drainage

10–12

14,15

laparoscopic13

procedures as an

alternative to conventional open debridement.

The necrotic process associated with pancreatitis tends to involve both the pancreatic parenchyma and surrounding adipose tissue. Significant quantities of necrotic peripancreatic tissue can be present with an essentially viable gland. Complications relate to the extent of the necrotic process, and in particular the extent of parenchymal necrosis.

It is key to recognise that the presence of necrosis in itself is not an indication for intervention. The previously held concept that recovery would not occur until almost complete removal of necrosis had been achieved

has been progressively challenged and the focus of intervention is now on the ‘adequate and maintained control of sepsis’. The PANTER

demonstrated that 35% of patients will resolve

trial completely without necrosectomy in the absence of

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247

Chapter 14

a b

Figure14.1 • Colonic ischaemia with fistulation. (a) Gas within acute necrotic collection in the head of pancreas,

oedematous colon and free intraperitoneal gas and fluid levels laterally. (b) Portal pyaemia with gas within the peripheral intrahepatic portal venous radicals.

sepsis. Given sufficient time, ‘organisation’ occurs – solid components within a collection are gradually broken down through enzymatic and phagocytic activity, and pancreatic necrosis may resolve completely with resultant fibrosis and atrophy.

Successful management involves individualised multimodal care, selecting the appropriate intervention and technique for each stage of the patient pathway. A multidisciplinary approach has evolved, and it is now common for several different techniques to be utilised in an individual patient. The choice of intervention is dictated by physiology, anatomy and timing of disease and is underpinned by an understanding of the dynamic evolution of postacute, necrosis-associated collections in pancreatitis. The success of various approaches will be dependent on the anatomical position of the collection and particularly the ratio of solid to fluid components.

The proess of maturation or ‘organisation’ takes in excess of 12weeks to complete, during which four stages can be recognised (Box14.4).

Historically, early aggressive debridement in the absence of infection was advocated. However, mortality

Box14.4 • Evolution of pancreatic necrosis/collections

1. True pancreatic necrosis – minimal separation of

devitalised tissue with a high solid/fluid ratio.

2. Transitional pancreatic necrosis with partial but

incomplete separation.

3. Walled-off necrosis (WON) – good separation of

devitalised tissue within a fluid-filled cavity and formation of a fibrous wall lined with granulation tissue.

4. Pseudocyst – almost complete resolution of any solid

component and a well-formed fibrous wall lined with granulation tissue.

in this setting was high, and the only randomised study of early versus late (>

12 days) necrosectomy18 was discontinued as a result of the mortality rate in the early treatment group (56% vs 27%). The general principle is now to withhold surgery in the early phase of disease, operating for complications ideally once the acute inflammatory insult has subsided.

Indications for intervention

There are three main indications for intervention: sepsis, symptoms or persistence of the collection over several months. Early drainage (<

6 weeks) may be potentially harmful by introducing infection into a poorly defined collection. Minimally invasive techniques often require sequential procedures within an established management protocol and should not be undertaken in isolation.

There is no role for the early drainage of acute collections in the absence of suspected sepsis. Clinical deterioration usually manifests through an escalation in the Early Warning Score,

along with a rise in biochemical or haematological markers of sepsis. Suspected sepsis mandates urgent CT confirmation of the diagnosis, resuscitation, antimicrobial therapy and prompt drainage for control. Of note, in the deteriorating patient with clinical evidence of sepsis, the absence of gas in a collection does not exclude infected necrosis. Although fine-needle aspiration of the collection to confirm or refute infection has been advocated,

the authors do not recommend it. In the patient with escalating SIRS or multiple organ dysfunction syndrome (MODS) and a drainable collection, percutaneous or endoscopic drainage should be performed within a step-up context, and positive culture of the aspirate is almost universally present.

A caveat exists where there is a clinical radiological

mismatch on CECT (i.e. the patient is well but there

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Complicated acute pancreatitis

protocol-driven management in the 1990s, aimed at the early identification of secondary infection within necrosis. The authors’ approach has progressed from one based on the presence or absence of infection to one based on time from onset, organ dysfunction and anatomical position of the collection.

Methods of sepsis control

The traditional approach to infected necrosis was open laparotomy/debridement. These approaches are falling from favour with increasing evidence that minimally invasive intervention may reduce morbidity/mortality; remains the method of choice in some countries.

however, open debridement

Figure14.2 • Radiological mismatch – extensive gas

within an acute necrotic collection following foregut fistulation in an otherwise clinically well patient.

is gas present in the collection, see Fig.14.2), and the possibility of spontaneous discharge of the collection into an adjacent hollow viscus should be considered. In this scenario, whilst bacterial colonisation of the collection will have occurred, spontaneous discharge may result in resolution without intervention.

Symptoms requiring intervention include pain, early satiety and gastric outlet obstruction, the latter two arising from the local mass effect of the WON in relation to the stomach. Intervention for symptoms is not required with the same degree of urgency and there is often a place for nutritional optimisation with enteral feeding to allow the WON to ‘mature’ or even resolve.

Persistence of WON over several months is a relative indication for intervention and should be balanced against the individualised risks of the proposed procedure. Once the decision has been made to intervene, the options include percutaneous, endoscopic, laparoscopic or surgical drainage. This choice is largely determined by institutional capabilities, patient physiology and the position of the WON relative to other structures, particularly the stomach.

There are three indications for intervention on collections: sepsis, symptoms and failure of resolution.

Minimally invasive approaches to infected necrosis

Minimally invasive surgery provokes a reduced inflammatory response when compared to equivalent open surgery, and there is experimental evidence suggesting that local sepsis and the inflammatory response may be lessened by a minimally invasive rather than an open technique.

The PANTER trial and several prospective cohort series have suggested that by avoiding the massive inflammatory ‘hit’ of open pancreatic necrosectomy, a minimally invasive approach to infected pancreatic necrosis may reduce the risk of post-procedural organ failure and wound morbidity.

17,21

However, there is as yet no evidence that one

minimally invasive approach is superior to another,

and the choice of modality is dependent on the anatomical position of the collection and the available local skills and resources.

Percutaneous drainage

Freeny et al.,

combining aggressive CT-guided percutaneous drainage (PCD) with continuous post-drainage lavage, demonstrated resolution of pancreatic abscesses in nearly 50% of patients. The remaining patients required subsequent surgical intervention for residual sepsis. Drain occlusion is common due to necrotic debris and repeated drains may be necessary. Simple drainage, even with smalldiameter drains, may be associated with complete resolution and within the PANTER trial

‘step-up’ arm, 35% of patients were successfully managed by small-bore (4-mm) percutaneous drainage alone.

Sepsis control in an infected acute necrotic or walled-off collection (early phase, 2–6weeks)

Infected pancreatic necrosis has previously been described as the most feared surgical complication of acute pancreatitis. This led to the development of

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Minimally invasive surgery

Control and prevention of recurrent sepsis is core to recovery. Inadequate control leads to failure to progress and an increased rate of secondary complications (e.g. bleeding). Enhanced percutaneous drainage (+/– percutaneous necrosectomy) aims to optimise sepsis control. Sequential drain tract dilatation

249

Chapter 14

allowing insertion of a large bore (30-Fr) doublelumen lavage system is the simplest ‘step-up’ approach over PCD. Formal debridement using a urological rigid-rod lens system can remove devitalised tissue and prevent drain blockage. In other centres as well as within our own patient cohort, this technique has significantly reduced mortality. The Dutch Pancreatitis Study Group have popularised a video-assisted retroperitoneal debridement technique23 (VARD) using a variation of the Fagniez technique

through a small, 5-cm incision in the left flank. Their management approach has evolved from being initially performed on all patients with infected necrosis, to now being used as a ‘step-up’ approach should initial PCD fail to control sepsis. The Dutch group has completed a randomised trial comparing this minimally invasive two-stage ‘step-up’ approach with open necrosectomy

and has shown a reduction in early organ failure (respiratory) and late morbidity, but the study was underpowered to address mortality.

Endoscopic necrosectomy

The principle of tract dilatation and minimally invasive necrosectomy has also been used with the endoscopic approach. Seifert et al.

have reported the dilatation of an endocyst-gastrostomy tract, allowing insertion of the endoscope into the retroperitoneum and subsequent piecemeal debridement. More recently, the use of multiple transgastric cystgastrostomy puncture sites has been reported, allowing nasocystic lavage and stent-assisted drainage through alternative drainage sites with good sepsis control. Lumen-opposing stents (Hot AXIOS) allow rapid decompression of necrosis-associated WON, and are often the

treatment of choice in a critically ill patient as this can be performed at the bedside in the ICU. It is essential that a post-drainage protocol is followed to prevent blockage of the cystgastrostomy with recurrent sepsis. Although extremely effective as an initial intervention, increased use has seen a relatively high incidence of stent-associated morbidity, with recurrent sepsis, haemorrhage and stent migration being described (Fig.14.3).

There is currently no evidence that one minimally invasive technique has any advantage over another and choice is often determined by institutional capability.

Open laparotomy/debridement

Although the method of choice in the 1980s, open surgery and debridement is now relatively uncommon in most UK specialist centres. As originally described, the complete exposure of the retroperitoneum, with mobilisation of both colonic flexures originally arose through the unavailability of adequate axial scanning. A more limited laparotomy focused on adequate drainage of acute necrotic or walled-off collections identified on CECT has been suggested by some as a superior alternative in a fit patient with no organ compromise (Fig.14.4). This may allow rapid recovery and avoid the repeated interventions and prolonged hospital stay associated with minimally invasive procedures. This approach is most appropriate where the collection has matured and complete separation of the necrosis has occurred. Fig. 14.4 illustrates the exposed SMA following open evacuation of haematoma following a bleed into a walled off necrotic cavity. Adequate and definitive drainage can

a b

Figure14.3 • Complications of EUS-guided cystgastrostomy. (a) Internal migration of SEMS; (b) intraluminal migration

with small bowel obstruction.

250

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Figure14.4 • Open necrosectomy following acute

haemorrhage managed by interventional radiological embolisation of a branch of the superior mesenteric artery, with loss of the head and uncinate process.

then be achieved through a single intervention, often draining a collection through the posterior wall of the stomach (cystgastrostomy). This can be performed at open surgery or by laparoscopy.

Where organisation is incomplete, usually as a result of early intervention being mandated for sepsis, incomplete debridement carries a high incidence of recurrent sepsis, and several methods of maintaining sepsis control following debridement have been described. The commonest approach is closed lavage, popularised by Beger, laparostomy

or closed packing28 approaches are

but open

equally effective, and the method of choice often reflects local experience.

Retrocolic/perineal/mesenteric necrosis

Peripancreatic extension of the necrotic process commonly follows fat planes into the small bowel or colonic mesentery. It may also extend extraperitoneally behind the colon and abdominal wall, occasionally reaching the perineum. Adequate drainage of mesenteric extension without compromising the vasculature can be challenging, and patience is often rewarded. Retrocolic extensions often require multimodal, minimally invasive access drainage at several sites and, particularly with horseshoe collections, the VARD approach can be particularly useful (Fig.14.5).

Open surgery has largely been replaced by minimally invasive alternatives, but may occasionally be required to achieve control of sepsis and/or bleeding.

Nutritional support

Acute pancreatitis, particularly in the context of complications, is often a prolonged and profoundly catabolic illness. Nutritional insufficiency should

Complicated acute pancreatitis

be anticipated and managed proactively. There are two important but distinct considerations: (1) the mode of nutritional delivery, and (2) the potential to impact the disease process through the use of immunomodulating feeds.

Nutritional delivery in the patient with acute pancreatitis

The traditional management of acute pancreatitis was to promote gut rest and address nutritional requirements parenterally, yet there is no evidence to support this. The early randomised studies of total parenteral nutrition (TPN) versus fasting, enteral feeding

demonstrated a negative effect of

TPN, as a result of TPN-associated side-effects.

A Cochrane review including eight randomised trials, demonstrated a reduction in mortality, systemic complications and surgical intervention in patients given enteral nutrition.

Most experience to date has been with enteral feeding

distal to the duodenojejunal flexure. More recently, nasogastric (NG)

31a

feeding has been shown to be a practical alternative to jejunal feeding. All studies in this area are underpowered but in the absence of definitive evidence it is reasonable to attempt this route prior to considering nasojejunal (NJ) tube support.

It is important to recognise that there are situations where parenteral nutrition must be considered. These include failure to meet nutritional requirements with enteral feeding, complex gastrointestinal fistulas and high output losses such as intractable diarrhoea. Occasionally, a combination of enteral and parenteral support is required, for example when enteral feed is not adequately absorbed. A multidisciplinary approach with nutrition team input is imperative, regardless of the route of feeding.

In summary, oral or enteric nutrition is the preferred route in acute pancreatitis. There is no requirement to fast patients with acute pancreatitis, assuming diet is tolerated. Normal diet may be augmented with commercially available nutritional supplements. If this is inadequate, NG feeding may be attempted followed by NJ support if this also fails. Finally, TPN should only be used when enteral options are exhausted or contraindicated for the reasons outlined above (Box14.5).

Disease modulation through content or mode of delivery

There has been interest in the role of the intestine in the pathophysiology of multiple organ failure in critical illness, with loss of gut barrier function potentially leading to endotoxaemia and SIRS. These are largely non-clinical data but a small study from the authors reported a reduction in the

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