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Chapter 13
(see below). Management of these patients is complex and should be discussed with a specialist unit at
an early stage. Specific measures will be determined
by the clinical situation. However, therapeutic interventions are aimed at restoring tissue perfusion
as rapidly as possible. This is achieved initially with
volume resuscitation titrated to haemodynamic and
physiological response, rather than the early use of
vasopressors or inotropes in patients who are still intravascularly deplete. Acute dialysis for acidosis has
not been shown to improve outcome but is required
for established renal failure. Currently there is no
specific therapy to reverse respiratory failure other
than ventilatory support.
Specific medical management
There have been many attempts to introduce specific medical treatments for acute pancreatitis and
these broadly fall into the following categories.
Prevention of infection
In patients who survive the early, systemic complications of acute pancreatitis, secondary infection of
pancreatic necrosis is the most important late complication. Infection occurs in 30–40% of patients
with a minimum 30% pancreatic necrosis13 and
is responsible for the majority of late deaths from
acute pancreatitis. Secondary infection manifests
as escalating sepsis or a deterioration in organ failure scores, usually in the second (36%) and third
(71%) weeks of the illness.
The role of prophylactic antibiotics to prevent
secondary infection has been widely studied. The
most recent Cochrane review31 found no evidence
of a significant reduction in mortality with antibiotic prophylaxis and no difference in the incidence
of infected pancreatic necrosis. Even non-pancreatic
infections showed no significant difference with
antibiotic therapy. It was noted, however, that all
of the studies were underpowered and a definitive
answer to this question will require better quality
clinical trials. The most recent meta-analysis of 14
trials including 841 patients also found no evidence of benefit with antibiotic prophylaxis.
Prophylactic antibiotics should not be used in
the management of acute pancreatitis.
Nutritional support
There are two main, and very separate, considerations in determining the mode of nutritional support. Severe acute pancreatitis is often a prolonged
and profoundly catabolic illness, and there is no
doubt that, throughout the illness, nutritional integrity should be maintained – the question in these
30
32
31,32
patients is not whether nutritional support is
necessary, but rather how it can be best administered.
The second consideration relates to the potential
of modulating the disease process by the mode of
delivery, either through maintenance of host defences or through the use of immunomodulating
feeds. The first issue is a practical problem faced by
clinicians on a daily basis, the second remains somewhat speculative, with interesting but inconclusive
evidence so far. These will be dealt with separately.
Nutritional delivery in the patient with acute pancreatitis
The key study in this regard was the randomised
study of Kalfarentzos et al. in 1996, who randomised 38 patients with severe acute pancreatitis
to total parenteral nutrition (TPN) or nasojejunal
feeding.33 The most recent Cochrane review, including eight randomised trials, demonstrated a
reduction in mortality, systemic complications
and surgical intervention in patients given enteral
nutrition.
34
Most experience to date has been with enteral
feeding distal to the duodenojejunal flexure. More
recently, four randomised studies have shown nasogastric feeding to be a practical alternative to jejunal
feeding.35 All studies in this area are underpowered
and it is therefore difficult to recommend this feeding route in routine clinical practice.
It is important to recognise that there are situations where parenteral nutrition must be considered, such as where complex fistulas develop, and
sometimes a combination of enteral and parenteral
routes is required. Combined feeding is most commonly required when enteral feed is not adequately
absorbed, leading to intractable diarrhoea and fluid
losses.
Nutritional support should be by the enteral
route where possible.
34
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 the systemic
inflammatory response syndrome (SIRS). In a small
study from Leeds,36 the authors reported a reduction in the inflammatory response and organ failure
in those receiving enteral support, but unfortunately
there were only 13 patients with severe disease, limiting the validity of the conclusions. There have
been several trials comparing so-called ‘immunonutrition’ with standard enteral feeding in critically
ill patients, but so far no evidence of benefit has
250
Acute pancreatitis
been demonstrated in acute pancreatitis.37 Similarly,
there has been interest in the role of ‘probiotics’,
but a randomised trial from the Netherlands found
an increase in fatal complications in the probiotic
group, with an unexpectedly high incidence of intestinal necrosis.
38
Other medical therapies
Inhibition of pancreatic secretion
Pharmacological attempts to suppress pancreatic
function have included intravenous glucagon, somatostatin and, more recently, the somatostatin
analogue octreotide. On the basis of the available
literature there is no justification for the use of octreotide or any other pharmacological inhibitor of
pancreatic secretion in acute pancreatitis.
Inhibition of pancreatic enzymes
Many studies have evaluated the concept of supporting the endogenous antiprotease defence mechanisms. Randomised trials of intravenous aprotinin
(Trasylol), gabexatemesilate, intraperitoneal aprotinin, and both low- and high-dose fresh frozen
plasma (FFP) have shown no therapeutic benefit.
Inhibition of the inflammatory response
Following initial promising results with the
platelet-activating factor antagonist, lexipafant, a
multicentre, randomised, placebo-controlled study
of anticytokine therapy recruited 1518 patients.
This study recruited only those patients with symptoms of less than 48 h duration and was restricted
to those with predicted severe attacks. Not only was
there no difference in mortality between groups, the
incidence of local complications, length of ICU stay,
hospital stay and change in organ failure scores
were all similar in the three study groups.
The potential for other agents that modify the inflammatory response to influence outcome in acute
pancreatitis has only been assessed in experimental
models.
Role of ERCP
There have now been three published randomised
trials addressing this issue, and four smaller studies. Contradicting an earlier Cochrane review,39
the most recent meta-analysis40 has shown early
ERCP in patients with either predicted mild or severe acute biliary pancreatitis without acute cholangitis did not lead to a significant reduction in the
risk of overall complications and mortality. There
is no role for urgent ERCP in patients with mild
disease. All patients with jaundice who exhibit signs
of sepsis should undergo urgent ERCP and sphincterotomy as cholangitis may coexist with acute pancreatitis and hyperamylasaemia, but there appears
to be little role for early ERCP outside this scenario.
In the non-jaundiced patient there is no role
for urgent ERCP and sphincterotomy.
40
Definitive management issues
The definitive management issues may be considered as, firstly, those designed to prevent further
attacks once a mild attack has subsided, and secondly those specifically related to the management
of early and late complications.
Prevention of recurrent acute pancreatitis
Management of gallstones
The timing of cholecystectomy will obviously depend on the clinical situation. In patients recovering from mild acute biliary pancreatitis, definitive
management of the gallstones to prevent a further
attack should ideally be achieved during the same
admission, and certainly no later than 4 weeks following discharge from hospital.26 This will normally involve a cholecystectomy (laparoscopic or
open) with intraoperative cholangiography, or alternatively duct imaging by MRCP (or EUS) followed
by cholecystectomy. Elderly patients or those with
significant medical comorbidity may be managed by
an endoscopic sphincterotomy, although this may
not be as effective as definitive surgery in preventing further attacks.
In severe acute pancreatitis, interval cholecystectomy should be performed when the inflammatory
process has subsided and the procedure is potentially easier.
uncomplicated acute pancreatitis should be
achieved within 4 weeks of discharge from hospital.
Investigation of non-gallstone-associated pancreatitis
Following resolution of an attack of acute pancreatitis, an assessment of potential aetiological factors
is an important aspect of care, and a diagnosis of
idiopathic pancreatitis should be made in less than
20% of patients.26 Evaluation of the initial acute
attack should include an adequate history (alcohol/
drugs/familial), biochemical tests (liver function
tests/ lipids (hypertriglyceridaemia)/calcium) and biliary ultrasound. If these investigations are normal,
axial imaging (CT or MR/MRCP) may be appropriate to exclude a mechanical cause. Patients in whom
29
Definitive management of cholelithiasis in
251
Chapter 13
no cause is identified following these investigations
should be considered for EUS, as a cause will be
identified in the majority of cases.41 A cholecystectomy or biliary sphincterotomy is justified in patients with recurrent idiopathic pancreatitis in whom
microlithiasis or biliary sludge is identified. With the
increasing use of EUS in these patients, it is increasingly recognised that many of these patients will have
changes consistent with early chronic pancreatitis,41
rather than biliary microlithiasis as suggested by earlier studies. The prevalence of microlithiasis appears
to be higher in regions where gallstone disease is the
predominant aetiology.
Peripancreatic fluid collections
Management of an early fluid collection
In the early stages of acute pancreatitis, up to 25%
of patients with acute pancreatitis will develop a
fluid collection in the peripancreatic area identifiable on CT. In themselves, these collections are of
little significance and require no intervention. There
are significant risks associated with aspiration and
especially external drainage, in particular the development of secondary infection, fistula and recurrence, and they therefore cannot be recommended.
Aspiration or drainage of sterile acute fluid
collections should be discouraged.
Management of a pseudocyst
Management of pseudocysts is determined by an
understanding of the anatomy (based on CT), the
degree of necrosis (MR/EUS) and the clinical condition of the patient. As a general rule, definitive
management should be delayed until all organ dysfunction has resolved and can often be performed
simultaneously with management of cholelithiasis
(see above).
In our experience, it is helpful to characterise pseudocysts associated with acute pancreatitis as either
fluid predominant or necrosis predominant.
In each case the collection may be sterile or infected and associated with varying degrees of systemic disturbance. The size of the collection and its
relationship to adjacent structures, in particular the
stomach, are also important factors when considering treatment options.
Asymptomatic pseudocysts do not require treatment, and many will eventually resolve spontaneously. Acute pseudocysts are most commonly
retrogastric, and may or may not link to a disrupted
pancreatic duct. Three-quarters will be associated
with a mild to moderate hyperamylasaemia. In
symptomatic cysts, a conservative policy may be
warranted for up to 12 weeks from the onset of
acute pancreatitis. This policy is not, however, without risk as pseudocyst rupture, bleeding or abscess
formation may occur. The likelihood of resolution
is related, at least in part, to pseudocyst size. Should
conservative treatment fail, the options are percutaneous, endoscopic or surgical drainage.
Percutaneous drainage
Results of percutaneous drainage suggest wide
variation in success (40–96%)42 and the introduction of infection is a risk that must be considered.
In practical terms, the risk of pancreatic fistula limits this approach and there is evidence that it can
make subsequent surgical intervention more hazardous if this becomes necessary.43 In our practice
we restrict the use of percutaneous drainage to occasional patients with infected, fluid-predominant
collections, particularly where there is a degree of
systemic organ dysfunction. Increasingly, however,
endoscopic or laparoscopic drainage is employed.
Endoscopic drainage
The technique of endoscopic cystgastrostomy as first
described by Baron et al.,44 initially by blind puncture of a cyst bulging into the stomach wall using
a side-viewing endoscope, has been subsequently
refined using endoscopic ultrasound guidance. EUS
guidance enables drainage of cysts where no intraluminal bulge is present and also helps avoid intervening vessels. Further procedures may be required to
facilitate drainage, particularly where cysts are large
or where there is much necrotic debris, but we have
not found it necessary to pursue active endoscopic
necrosectomy in this group of patients. Where disruption of the pancreatic duct has occurred, transpapillary duct stenting can aid resolution. Baron and
colleagues have recently updated their experience
in 104 patients with walled-off pancreatic necrosis
with successful resolution in 95 patients (91%). The
mean time to intervention was 63 days and mean
duration of treatment was 4.1 months. The complication rate, mainly haemorrhage and perforation,
was 14%.
Surgical drainage of an acute post-inflammatory collection
Surgery may be considered as a primary mode of
intervention in selected patients, particularly for patients with large, necrosis-predominant collections
without infection or systemic organ dysfunction.
This can be readily achieved by a laparoscopic transgastric procedure, or a direct cyst-enterostomy, and
allows simultaneous laparoscopic cholecystectomy
where appropriate. In those patients in whom endoscopic drainage fails to achieve complete resolution,
or a cyst recurs, simple surgical drainage is rarely
45
252
Acute pancreatitis
an option as this often results from separation of
the head/body and tail of the pancreas due to prior
necrosis of the central pancreas – termed a ‘disconnected tail’. These patients often require a challenging
distal pancreatico-splenectomy.
Symptomatic or persistent pseudocysts following
acute pancreatitis should be managed in a specialist
unit where the full range of interventional procedures is available.
Failure of percutaneous or endoscopic
management is associated with the need for
complex surgery and should therefore only be
undertaken by or following consultation with a
pancreatic specialist.
43
Management of a pancreatic duct fistula
This complication most commonly follows prior
intervention for an acute post-inflammatory collection or infected necrosis, and manifests as persistent drainage of amylase-rich opalescent fluid,
in the absence of significant sepsis. Management
is similar to that of a communicating pseudocyst,
initially by transpapillary stenting where possible.
Intraperitoneal rupture of a pseudocyst can result
in pancreatic ascites or pleural effusion. More invasive management of a persistent fistula, either inaccessible or failing to respond to ductal stenting,
should be delayed by percutaneous or endoscopic
control, until the patient has made a full recovery,
and again often requires surgical resection (distal
pancreatico-splenectomy).
Management of necrosis
The management algorithm surrounding necrotising
pancreatitis has altered radically in the last 15 years
in response to evolving concepts, improved understanding and the development of minimally invasive
techniques, including percutaneous necrosectomy
and laparoscopic or EUS-guided cystgastrostomy,
as an alternative to conventional open debridement.
A multidisciplinary approach has evolved, and it is
now common for several techniques to be utilised in
an individual patient, as the indications and clinical
condition of the patient alter during the course of
the disease process.
The development of secondary septic complications
is the usual initiator demanding invasive treatment.
The choice of intervention technique is underpinned
by an understanding of the dynamic evolution of
post-acute, necrosis-associated collections in pancreatitis. 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
success of various approaches will be dependent on
the anatomical position and particularly the ratio of
solid to fluid components within the collection.
The process of maturation or ‘organisation’, with
separation and partial liquefaction of the solid
components within a collection, takes in excess of
12 weeks to complete, during which four stages can
be recognised:
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. Organised pancreatic necrosis (OPN) – good
separation of devitalised tissue within a fluidfilled 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.
The necrotic process associated with pancreatitis
tends to involve both the pancreatic parenchyma and
surrounding adipose tissue. Indeed, 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. Early
aggressive debridement in the absence of infection
has been advocated. However, mortality in this series
was 25% overall, and the only randomised study of
early versus late (> 12 days) necrosectomy was discontinued as a result of the mortality rate in the early
treatment group (56% vs. 27%).46 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.
There is no role for early surgical intervention
other than for the management of complications.
Management of sterile necrosis
The development of retroperitoneal necrosis secondary to acute pancreatitis is not in itself an indication for intervention. Pancreatic necrosis, where
sterile, can usually be adequately treated by conservative means.47 There remains debate regarding the
role of debridement in patients failing to respond
to conservative treatment. Early debridement does
not improve outcome; however, some specialists
advocate debridement in patients with continuing
organ dysfunction after several weeks, but this may
also be detrimental.48 The majority of sterile postinflammatory fluid collections progress into organised pancreatic necrosis, which can be managed with
253
Chapter 13
low morbidity and mortality, and our policy is to
delay intervention where possible. The management
of these patients is discussed in the section dealing
with fluid collections associated with necrosis.
Sterile necrosis should initially be treated
conservatively where possible, allowing delayed
definitive treatment.
Management of infected necrosis (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
protocol-driven management in the 1990s, aimed at
the early identification of secondary infection within
necrosis. The presence of a persistent SIRS response
made clinical differentiation between SIRS and sepsis
difficult and this led to CT- or US-guided fine-needle
aspiration (FNA) of the pancreatic or peripancreatic
collections as a diagnostic test. FNA was considered the
cornerstone of management as it was thought infected
necrosis mandated radical surgical intervention.
Our own approach has progressed from one based on
the presence or absence of infection to one based
on organ dysfunction. Infected collections, even those
containing gas, may be observed when the patient is
clinically well and recovering with conservative treatment. Patients with profound organ dysfunction in
whom we suspect secondary infection, with a drainable peripancreatic collection, will undergo percutaneous drainage aimed at sepsis control, with later
staged percutaneous or open management of the
necrosis as clinically appropriate, and we no longer
perform diagnostic FNA. Decision-making in these
patients is extremely difficult and is best carried out
within an experienced multidisciplinary team.
Methods of necrosectomy
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;
51–53
however, they remain
the method of choice in some countries.
Open laparotomy/debridement
The technique of pancreatic debridement involves
a wide exposure of the abdomen, usually through
a bilateral subcostal/rooftop incision. Both colonic
flexures are mobilised to expose the retroperitoneum and the lesser sac entered via the gastrocolic
omentum, or occasionally the transverse mesocolon. Pus is aspirated from the abscess cavity, leaving
the solid component behind, which is then removed
by ‘blunt finger’ dissection (Fig. 13.4). Tissue that
49,50
Figure13.4 • Solid necrotic material removed at open
necrosectomy by blunt finger dissection.
will not come away by finger teasing should be left
in situ to demarcate and subsequent removal at a
later procedure. The procedure may also include
a cholecystectomy, operative cholangiogram and
feeding jejunostomy.
Methods for postoperative management of the de-
bridement cavity after laparotomy are as follows:
• With drainage/‘closed packing’. Simple
drainage, often with multiple retroperitoneal
tube drains, was the conventional approach to
the postoperative management of the debrided
pancreatic and peripancreatic bed. Whilst
mortality was less than with resective procedures,
multiple second-look laparotomies were often
required for residual sepsis. The initial results of
Warshaw and colleagues reported respectable
mortality figures of 24% using this technique.
Their technique has been modified using multiple
soft Penrose drains containing cotton gauze
to pack the cavity following completion of the
necrosectomy.54 These are subsequently removed
at intervals, allowing the cavity to collapse
around the drains. Their reported mortality rate
using this technique is the lowest in the literature
(6.2%), although the series included patients
with sterile necrosis (11%) and pancreatic
abscess (39%), and only 14% had both sepsis
syndrome and a positive culture requiring early
intervention, which is indicative of the difficulties
in interpretation of the available literature.
254
Acute pancreatitis
• With open packing. Bradley and colleagues from
Atlanta have been the principal proponents of
the open laparostomy technique.55 In this, at
the conclusion of the debridement, the lesser
sac is packed with lubricated cotton gauze and
the abdomen left open, allowing planned reexplorations every few days until granulation
tissue forms. Enteric fistula and secondary
haemorrhage are not uncommon, and the
technique is rarely performed as a first option.
Surgical packing and planned re-operation is,
however, sometimes required to control blood
loss from the retroperitoneum following the
development of an intraoperative coagulopathy,
a lavage system being created, following
correction of the coagulopathy, at the time of
subsequent pack removal.
• With closed lavage. Postoperative closed
lavage as described by Beger et al.56 is the
most popular method for postoperative
sepsis control following open debridement,
the aim of the lavage being the continuous
removal of devitalised necrotic material and
bacteria. Several (four to six) large-diameter
tube drains are inserted in the lesser sac and
throughout the abdomen, and the abdomen
closed. Continuous lavage is then commenced,
our own preference being for CAPD dialysis
fluid (Dianil 7, Baxter Healthcare, potassium
free, Iso-osmolar) warmed through a blood
warmer and delivered at 500 mL/h. The
lavage is continued, for around 3–4 weeks on
average, until the return fluid is clear and the
patient has no residual signs of systemic sepsis.
This technique has been adopted with minor
variations by centres on both sides of the
Atlantic.
Minimally invasive approaches to infected necrosis
Minimally invasive surgery has been shown consistently to be associated with a lesser activation of
the inflammatory response than 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 widespread belief that
formal necrosectomy is required has recently been
challenged and there is evidence that patients can
resolve following simple percutaneous drainage or
following limited necrosectomy. The PANTER trial
and several prospective cohort series
51–53
have sug-
gested that by minimising the massive inflammatory
‘hit’ of open pancreatic necrosectomy, a minimally
invasive approach to the management of infected
pancreatic necrosis may lessen the risk of postprocedural organ failure, respiratory and wound
morbidity in these patients. However, there is as yet
no evidence that one minimal approach is superior
to another.
• Percutaneous drainage. Freeny et al.,57
combining aggressive CT-guided percutaneous
drainage with continuous post-drainage
lavage, showed that nearly half the pancreatic
abscesses may resolve. However, more than half
of these 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 small-diameter 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.
• Minimally invasive surgery. Simple
percutaneous or endoscopic drainage alone may
result in complete resolution; however, they
also have a useful role providing initial sepsis
control, associated with an improvement in
organ dysfunction. Careful drain management
is required to recognise drain blockage early
and to prevent recurrent sepsis. As a result of
the difficulties in maintaining drain patency,
we have developed a technique58 to allow
minimally invasive drainage, and in addition
removal of the necrotic component. This
involves the intraoperative dilatation of a
previously placed CT-guided percutaneous
drain tract and subsequent necrosectomy using
a urological rigid-rod lens system (Fig. 13.5).
Complete resolution of sepsis and necrosis
can occur without recourse to further surgery,
with a reduced need for postoperative organ
support compared to the open procedures.
In other centres as well as within our own
patient cohort, this technique has significantly
reduced mortality.52 The Dutch Pancreatitis
study group have popularised a video-assisted
retroperitonael debridement technique (VARD
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
255
Chapter 13
Figure13.5 • Percutaneous necrosectomy showing the
rod lens scope and a guiding catheter to ensure accurate
drain placement.
necrosis, to now being used as a ‘step-up’
approach should initial percutaneous drainage
fail to control sepsis. The Dutch group have
completed a randomised trial51 comparing
this minimally invasive two-stage ‘step-up’
approach with open necrosectomy and have
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.59 have reported the
dilatation of an endocyst-gastrotomy tract,
allowing insertion of the endoscope into the
retroperitoneum and subsequent piecemeal
debridement. More recently the use of multiple
transgastric cyst gastrostomy puncture sites
has been reported, allowing nasocystic lavage
and stent-assisted drainage through alternative
drainage sites with good sepsis control.
There is currently no evidence that one minimally
invasive technique has any advantage over another
and choice is often determined by local expertise
and resources.
60
of the abscess wall. The EUS-guided endoscopic
technique appears to be associated with a lower
morbidity and has a reported resolution of sepsis of
nearly 90%.61 Laparoscopic cyst gastrostomy may
be an effective alternative.
Specific late complications
Haemorrhage
Life-threatening haemorrhage may rarely occur
acutely in pancreatic necrosis within the first week
following presentation and requires mesenteric embolisation or surgical exploration. Haemorrhage is,
however, a relatively common problem following
prior necrosectomy as a postoperative reactionary haemorrhage due to a combination of having
a large raw surface, partly controlled sepsis and exposed major vessels, leading to reactionary haemorrhage (Fig. 13.6). Bleeding may be arterial or venous.
Urgent surgical intervention and ligation of proximal visceral vessels may be suggested; however, the
combination of haemorrhage and subsequent laparotomy frequently precipitates escalating organ failure and death. Angiography and embolisation, with
endovascular metal coils, is therefore the treatment
of choice.
Segmental portal hypertension and gastrointestinal haemorrhage
Splenic vein thrombosis is associated with up to
15% of patients dying with acute pancreatitis. In
those patients with thrombosis that survive the
acute attack, the splenic venous drainage diverted
through the short gastric vessels may result in patients developing large venous collaterals. Short
Management of pancreatic abscess
A pancreatic abscess by definition is an infected,
fluid-predominant acute collection (pseudocyst)
with little or no necrosis, and is therefore suitable for
minimally invasive drainage. The endoscopic technique of Baron described above has been used in this
situation with reasonably good effect, but there is a
significant risk of haemorrhage from blind puncture
256
Figure13.6 • CT scan showing large acute fluid
collection with a pseudoaneurysm (indicated by white
arrow) and haematoma (black arrow) within the collection.
Acute pancreatitis
gastric and lienocolic varices may make surgery on
late complications of an acute pancreatitic episode
hazardous. When necessary, splenectomy is curative. Despite the frequency of venous collaterals on
follow-up CT, late gastrointestinal haemorrhage
due to gastric varices is rare in practice.
in recurrent attacks of abdominal pain, sometimes
with hyperamylasaemia and with dilatation of the
distal duct system. Management of the stricture
may be by simple dilatation and temporary stenting, by surgical resection of the stricture along with
the pancreatic tail, or by surgical drainage of the
pancreatic duct system into a Roux loop.
Pancreatic duct stricture
Pancreatic duct stricture can occur following resolution of an attack of acute pancreatitis as a result
of local tissue damage and fibrotic repair. More
commonly, complete occlusion occurs, resulting in
a disconnected duct syndrome should a remnant
of viable tail remain, the treatment of which is described above. A pancreatic duct stricture may be
present on its own, or in association with a duct
disruption causing a pseudocyst or pancreatic fistula. Isolated pancreatic duct stricture can result
Gastric outlet obstruction
Gastric outlet obstruction resulting in persistent vomiting or high-volume gastric aspirates from nasogastric
suction may complicate up to 10% of patients with
severe acute pancreatitis. The recent trend towards
nasojejunal intubation has rendered this complication
less troublesome and the majority of patients can be
treated by nasoenteric feeding until the local oedema/
ileus settles. Occasionally, a gastroenterostomy is
required for long-standing gastric stasis.
Key points
• Initial assessment and resuscitation should take account of the multisystem nature of the disease,
and patients with organ dysfunction should be managed within a high-dependency environment.
• All patients with acute pancreatitis should have ultrasonic assessment of the biliary tree within 24 h
of admission.
• Prophylactic antibiotics are not recommended as part of standard management in patients with
acute pancreatitis, and when used should be for a defined period. No drug therapy has been shown
to be beneficial.
• Nutritional support should be by the enteral route where possible.
• In the non-jaundiced patient there is no role for urgent ERCP and sphincterotomy.
• Definitive management of cholelithiasis should be within 4 weeks of discharge, in uncomplicated cases.
• Failure of percutaneous or endoscopic management is associated with the need for complex surgery
and should therefore only be undertaken by, or following consultation with, a pancreatic specialist.
• There is no role for early surgical intervention other than for the management of complications.
• Sterile necrosis should be treated conservatively.
• Surgery for infected necrosis should aim to achieve the adequate and maintained control of sepsis.
References
1. McKay CJ, Evans S, Sinclair M, et al. High
early mortality rate from acute pancreatitis in
Scotland, 1984–1995. Br J Surg 1999;86(10):
1302–5.
2. Appelros S, Borgstrom A. Incidence, aetiology and
mortality rate of acute pancreatitis over 10 years
in a defined urban population in Sweden. Br J Surg
1999;86(4):465–70.
3. Halvorsen FA, Ritland S. Acute pancreatitis in
Buskerud County, Norway. Incidence and etiology.
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