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PANCREATITIS
33
As can be seen, our approach has simplified over the years; wash out and
drainage, Roux loop repair of severe isolated duodenal injuries or pancreatic
lacerations which involve the duct, and resection. Resection is generally a
Whipple’s procedure although distal or subtotal pancreatectomy would be
indicated for penetrating injuries to the left upper quadrant, which involved
the pancreas to the left of the portal vein, and were not appropriate for
drainage into a Roux loop.
Delayed presentation
Delayed presentation presents a rather different problem and patients are fre-
quently in a poor clinical condition making accurate assessment more diffi-
cult. The intraoperative assessment is severely hampered by oedema, local
inflammation, soiling, and infection. In these patients, we generally control
any leaks and bleeding and, after a thorough washout, initially do no more
than drain any suspect areas such as the pancreatic bed. Adequate drainage
and lavage almost inevitably improves and stabilizes the situation, allows
repeat investigations to see which areas are improving or resolving and also
identifies residual problem areas that require treatment. Our experience,
however, is that these patients frequently settle remarkably well and may
end up with a controlled fistula which can be dealt with secondarily, either
endoscopically or surgically.
Fig. 1.21 Roux-en-Y reconstruction. After oversewing the head of the gland, the
distal portion is drained into the Roux loop. The anastomosis is identical to that
following a Whipple’s procedure.
PANCREAS
34
Pancreatic fistulae
Pancreatic injury and consequent fistula formation can result from biopsies,
pancreatic surgery, and trauma and during non-pancreatic operations (left
nephrectomy, splenectomy, etc.) (Ridgeway and Stabile, 1996 ; Lin et al ., 2004 ).
If unrecognized, and consequently not drained, they can cause major morbid-
ity. Postoperative leaks after pancreatic surgery are generally drained and hence
controlled and cause surprisingly few problems apart from skin excoriation.
The difficulty with controlled leaks lies in their subsequent management.
With non-surgical leaks (biopsies, iatrogenic injuries, trauma), the treat-
ment should be surgical (Buccimazza et al ., 2006 ). The drainage has already
started and, by definition, caused clinical problems that allowed their recogni-
tion. Endoscopic procedures have no place at this stage. Even if it were possible
to immediately control the fistula, the drainage will already have caused
sufficient damage to require surgical treatment.
Management ( Fig. 1.22 )
All patients are given 100mcg of octreotide three times a day from presenta-
tion until the drainage is controlled. At operation, a clear view of the origin of
the leak must be obtained and the treatment will depend on whether there is
an established tract. In patients who require early treatment, such as after Tru-
cut biopsies or where there is inadvertent damage usually into the tail of the
gland, then an attempt at primary repair is reasonable. Biopsy sites can be
oversewn but if there is a suspicion of involvement of the major duct and post-
operatively drainage continues, ERCP and pancreatic ductal stenting is essen-
tial. Ductal stents in this situation are simply to allow free drainage by
rendering the pancreatic sphincter incompetent and should be short, small
5-French stents. When the tail is injured, the gland is mobilized and either
oversewn or, if it appears unhealthy due to the leakage or superimposed infec-
tion, 1–2cm should be resected with an appropriate stapler and then oversewn.
After a thorough washout, the leak must always be drained and we use two
medium tube drains. All injuries to the tail are treated in the same way as
biopsy leaks. If there is any evidence the leak is not controlled, a pancreatic
stent is inserted.
When drains are in situ after pancreatic surgery or surgery to address a leak,
drain fluid assay for amylase is extremely valuable. Levels in the main duct vary
from 80 000–180 000IU/L, in side branches from 10 000–80 000IU/L, and
from radicles and parenchyma usually 3000–10 000IU/L. Management based
on these figures must always take into account that a leak may not communi-
cate directly with a drain but may pool first and become diluted.
PANCREATITIS
35
Fig. 1.22 Management of pancreatic fistula.
Early
presentation
Late presentation
Clinically well
Conservative
management
Surgery for
continued leak in
fit patients
ERCP & stent
ERCP &
pancreatic stent
Surgery
Surgery rarely
necessary
Conservative
management &
assessment
MRCP + ERCP
Post surgical/
endoscopy
clinically unwell
Post surgical/
endoscopy
clinically well
Pancreatic
Fistula
No further
treatment
Clinically unwell
Unfit
Fit
Continues
Settles
Urgent assessment and
surgical exploration
with drainage
Persistent leak
Traumatic
As for
management
of pancreatic trauma
PANCREAS
36
Established fistulae
Established fistulae following surgical procedures to the pancreas which were
drained, or surgery and drainage for pancreatic injuries, require a different
approach (Voss and Pappas, 2002 ; Morgan and Adams, 2007 ). Some of these
will settle with ductal stenting at ERCP and use of a somatostatin analogue
(Fischer et al ., 2004 ; Le Moine et al ., 2004 ; Goasguen et al ., 2009). In cases that
do not settle, it is important to repeat all investigations and establish the site
and size of the leak. Leaks after pancreatic surgery are complicated by the asso-
ciated surgical procedure, which makes approaching the fistulae difficult. If
investigations suggest a small leak, then a period of nothing by mouth and
parenteral nutrition is worthwhile and, even in established fistulae, the major-
ity will settle. The remaining intractable fistulae can either be left alone or
treated surgically and will require discussion with the patient.
Many of these patients have had a severe and protracted illness or postopera-
tive course and do occasionally elect to have no further surgery. This is reason-
able if the volume of drainage is small and the skin can be kept in good
condition with stoma and skin care products. If surgery is required, the only
approach we use is identification of the fistula tract, following it as far as pos-
sible towards the source and then draining it into a Roux loop (Alexakis et al .,
2004 ). The anastomosis is the same as for a conventional bilioenteric anasto-
mosis (see ‘Biliary bypass procedure (hepaticojejunostomy)’).
Pancreatic tumours
The pancreas is a complex organ and not surprisingly can give rise to a number
of tumours. In addition to the usual epithelial tumours arising from the duct,
cystic tumours can produce diagnostic and management dilemmas. Tumours
also arise from the endocrine components of the gland and can in themselves
be difficult due to the fact that they may be benign or malignant, multiple or
single, frequently do not arise in standard sites, and may be hormonally active
(Solcia et al ., 1991 ; Klimstra and Adsay, 2004 ).
The most common presentation is still painless obstructive jaundice due to a
ductal adenocarcinoma arising in the head of the gland and the dismal outlook for
these tumours has changed little over the last 30 years. This colours the judgement
of clinicians and particularly non-specialists. It is crucial that all these patients are
investigated sufficiently to establish a clear diagnosis and ensure that other less
common (but still not rare) tumours with better outlooks are not missed.
Investigation
While ductal adenocarcinoma remains difficult to visualize and is frequently
under staged even today, other pancreatic tumours have yielded to the advance
PANCREATITIS
37
of technology (Menges et al ., 2000 ; Kalra et al ., 2003a , b ). Multislice CT
scanners are very reliable for cystic tumours and ultrasound and CT are
effective for endocrine lesions (King et al ., 1998 ). However, despite the detailed
images on CT scans, abnormalities of the lining of cystic tumours (which
are the crucial component in deciding how to manage these lesions) are
frequently not well seen and we favour additional laparoscopy with
intraoperative ultrasound. For endocrine tumours, EUS or laparoscopy
and intraoperative ultrasound again gives remarkably good images and the
assessment is generally very accurate (Gouya et al ., 2003 ; Anderson et al .,
2000 ). The combination of these modalities is reliable in determining whether
even small lesions are cystic, heterogeneous, or solid. The added advantage
of a laparoscopic approach is the ability to examine the peritoneal cavity
and liver thoroughly (a crucial element with the propensity of these tumours
to spread even when small) and perform biopsies if necessary. We have increas-
ingly found ourselves using this as a staging procedure but it also allows a
full assessment of the patient under a general anaesthetic. Even with a
normal preoperative workup we have found the response of the patients in
this age group is often unpredictable and anaesthetists will sometimes
reconsider their assertion that the patient is fit enough for major surgery
(Whipple’s procedure etc). The advantages of laparoscopy and intraoperative
ultrasound are:
♦
Give an excellent assessment of the tumour(s)
♦
Allow examination of the peritoneum, serosal surfaces and liver with bi-
opsy of any suspicious lesions
♦
Provide an assessment of fi tness to proceed to a major surgical procedure.
In our experience, the management of patients will change for one of these
reasons in 25–40% of patients and laparoscopy is consequently now a standard
part of our workup (Doucas et al ., 2007 ).
Pancreatic anatomy
Before proceeding to discuss the surgical management of pancreatic tumours,
knowledge of the development and anatomy of the pancreas is essential.
The pancreas is a complex organ and there is considerable variability which
is explained by its embryology. It has a number of intimate relationships
with important structures in the abdomen and in addition occupies a central
position.
Developmental anatomy ( Fig. 1.23 ) A number of pancreatic pathologies are
related directly or indirectly to the gland’s early development. Its formation by
the fusion of dorsal and ventral anlages with the merging of the two drainage
PANCREAS
38
systems introduces the possibility of a number of anatomical variants.
The dorsal anlage forms the cephalad part of the head of the gland together
with the body and tail, and the ventral anlage forms the remainder of the head
and the uncinate process.
This produces the main pancreatic duct (of Wirsung) and the minor or
accessory duct (of Santorini), which drains through the minor papilla or retro-
gradely into the main duct. Surprisingly congenital abnormalities, including
aplasia, annular pancreas (invading or encircling the wall of the second part of
the duodenum), and heterotopic pancreas (where tissue is found in the duo-
denal wall or rarely the mesentery, omentum, colon, or appendix) are very
uncommon. However, failure of fusion of the ducts (pancreas divisum) occurs
in about 10% of individuals (Yu et al ., 2006 ).
Surgical anatomy ( Fig. 1.24 ) Much of the difficulty relating to the presenta-
tion, investigation, and management of pancreatic problems arises from its
intimate relationship to the duodenum and major vascular structures. The
gland lies in the curve of the first three parts of the duodenum to which it is
firmly adherent, extending upwards from the right of the second lumbar
vertebra to the splenic hilum on the left at the level of the twelfth thoracic
vertebra. There is no distinct capsule which partly explains its friability and
this is compounded by its rich blood supply. The blood supply comes from
both the coeliac axis and SMA and the collaterals are plentiful.
The head and uncinate process are supplied from the gastroduodenal
artery superiorly through the anterior and posterior pancreaticoduodenal
branches. They run down and anastomose with the corresponding anterior
and posterior branches of the inferior pancreaticoduodenal artery which is a
branch of the SMA. The tail and body are supplied from the splenic artery as it
Fig. 1.23 Development of the pancreas from dorsal and ventral anlages. Fusion of
the two components produces the main and accessory pancreatic ducts and explains
the large number of variation.
PANCREATITIS
39
runs along the superior border (giving the dorsal pancreatic artery just after its
origin). Variations of the arterial supply are common (approximately one in
three), with the most important pattern being an anomalous origin of the
hepatic artery from the SMA (the right hepatic artery in 25% and common
hepatic artery in 5%). These variations must be recognized, not only in resec-
tional surgery, but also during a biliary bypass or any procedure requiring
mobilization of the CBD.
The venous drainage parallels the arterial supply but ends in the splenic,
SMV, and portal veins. The inferior pancreaticoduodenal veins often join to
form a single large wide tributary which drains to the SMV behind the unci-
nate process and can be troublesome if not recognized and treated with care.
Portal vein anomalies are rare and include drainage into the superior vena cava
(SVC) and running in front of the duodenum.
Lymphatic drainage is profuse and terminates in a large number of peripan-
creatic and retroperitoneal lymph nodes. There may be up to 150 in 11 groups
and much work has been done (particularly in Japan) to bring order to these
groups in an attempt to produce a system which it was hoped would guide the
surgical procedure in a rational way and improve survival (Fernandez-Cruz
et al ., 1999 ). Unfortunately these efforts have been unable to alter the poor
outcome of pancreatic adenocarcinoma and lymph node involvement, irre-
spective of the site, dramatically worsens the prognosis and is a contraindica-
tion to a curative resection (Cordera et al ., 2007 ).
Fig. 1.24 The rich blood supply and relationships of the pancreas account for the
complex nature of surgery to the gland.
PANCREAS
40
Benign (non-neuroendocrine) lesions ( Fig. 1.25 )
Benign tumours of the pancreas are relatively uncommon but with modern
imaging methods are being detected much more frequently. Those usually
encountered are the serous or mucinous cystadenomas or the intraductal
lesions such as papillary adenomas. The majority (40%) are the mucinous
variety and their malignant potential complicates the management of these
lesions considerably (Solcia et al ., 1991 ; Klimstra and Adsay, 2004 ). Rarer
tumours such as teratomas are solid and will almost inevitably only be
diagnosed after removal.
The problem with these lesions is differentiating them from their malignant
counterparts and the majority of cystic lesions will at some stage behave in an
aggressive fashion, either increasing in size or undergoing malignant change
(Wilentz et al ., 1999 ; Sarr et al ., 2001 ; Strobel et al ., 2003 ). Our policy in respect
to these has consequently changed and over the last few years the only lesions
we feel comfortable in observing are the genuine simple cysts on CT scanning,
where the contents are serous and when laparoscopy and ultrasound confirms
an absolutely smooth lining with no fronds, irregularities, or thickening of the
Fig. 1.25 Classification of non-neuroendocrine cystic pancreatic lesions.
Pancreatic
cystic lesions
No linking
Pseudocysts
Mucinous
epithelium
Clear cell tumours
Squamous lined
cysts
Cysts lined by
acinar cells
Degenerative
changes in solid
tumour
Cystic
lymphangioma
Lymphangioma
sarcoma
cystic teratoma
Pancreaticoblastoma
Cystic
Neuroendocrine
tumour
Solid
pseudopapillary
tumour
Cystic ductal
adenocarcinoma
Acinar cell
carcinoma
Serous
cystadenoma
VHL associated
pancreatic cysts
Lymphoepithelial
cysts
Mucinous cystic
neoplasms
Intraductal papillary
mucinous tumour
PANCREATITIS
41
wall (Le Borgne et al ., 1999 ). The rest of the lesions we treat as cystadenocar-
cinoma until proven otherwise (see Cystic tumours of the pancreas, p.41).
Cystic tumours of the pancreas ( Fig. 1.26 )
Cystic pancreatic tumours are often malignant but generally easy to see and
image (Adsay, 2007 ). They usually occur in the tail of the gland and have a
better outlook than solid tumours (Sidden and Mortele, 2007 ; Lack and
Albores-Saavedra, 2003 ; Brugge, 2008 ).
The usual varieties are serous or mucinous cystadenocarcinoma and cystic
carcinomas. Adenosquamous carcinomas and signet ring carcinomas are less
common. The clinical setting and radiological features are often very helpful
when assessing these lesions (see Tables 1.4 and 1.5 , and Fig. 1.27 ).
It is essential to differentiate from a pseudocyst but generally this is straight-
forward due to the lack of a clinical history of an acute attack and the appear-
ances on imaging. If doubt does exist, the MRCP/ERCP demonstrating
communication with the duct is very supportive of an inflammatory aetiology.
Unfortunately, in a significant proportion of pseudocysts it is not possible to
Table 1.4 Possible causes of cystic lesions of the pancreas and their characteristics
Intaductal papillary mucinous neoplasm Mucinous cystic neoplasm
Age range 70–80 years
Predominantly men
Premalignant
Communicate with pancreatic duct
Usually > 1cm
Usually in the head of the gland
Age range 40–60 years
Almost exclusively women
Few locules (usually < 6)
Peripheral calcification
Premalignant
No communication with duct
Usually < 5cm
Usually in the tail of the gland
Solid pseudopapillary tumour Serous cystadenoma
Mean age of 30 years
Predominantly female
Alternating solid and cystic areas
Chunky calcification
Malignant potential
No communication with the duct
Up to 10cm
Can occur anywhere in the gland
Median age approximately 60 years
Male to female ratio 1:3
Thin, small septae (‘honeycomb’)
Central calcification
Benign
No communication with the duct
Usually < 5cm
Central scar
PANCREAS
42
Fig. 1.26 Origin of pancreatic cysts.
Pseudocysts
Epithelial origin
Mucinous cystic
neoplasmas
Intraducal
papillary mucinous
tumour(IPMT)
Cystic ductal
adenocarcioma
Serous
cystadenoma
Exocrine origin
Acinar cell
carcinoma
Cystic pancreatic
tumours
Endocrine origin
Cystic
neuroendocrine
tumour
Mesenchymal
origin
Sarcoma
Lymphoma
Cystic
lymphangioma
True cysts (Von-Hippel-Lindau, cystic
fibrosis, lymphoepithelial cysts)
Unknown/mixed
origin
Solid
pseudopapillary
tumour
Pancreatico-
blastoma
Cystic teratoma
Giant cell tumour