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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_1841_Библиотеки_им_академика_М_И_Перельмана.pdf
Fig. 1.1 Management of acute pancreatitis. CBD, common bile duct; CT, computed tomography; ERCP, endoscopic retrograde cholangiopancreatog-
raphy; EWS, early warning score; US, ultrasound.
Moderate
Dilated duct
no necrosis
Dilated duct
necrosis
ERCP
•
Removal stones
•
Stent
ERCP if fit
enough
Manage
complications
Non-dilated
CBD
necrosis
Severe
US/CT
Presentation
Severity assessment
scoring system
Ranson
Apache
early warning score (EWS)
Conservative
management
Mild
US & Early
cholecystectomy
for stones
PANCREAS
4
smaller group with no clear predisposing cause, the attacks will be recurrent
and these patients can present a considerable challenge.
Gallstones
The majority of cases of acute pancreatitis are due to gallstones (Mayer et al .,
1984 ; Lee et al ., 1992 ; Eatock et al ., 2005 ). In some parts of the world, alcohol
is believed to be more common but if a diligent search is made for stones
(analysis of bile and sieving the faeces), rates always rise and it is likely that
even in some of these areas that the ratio would be reversed (Neoptolemos
et al ., 1988a ; Ammori et al ., 2003 ). The first description of gallstone pancreati-
tis was probably in the 1880s, and in 1901 Opie described an impacted lower
common bile duct (CBD) stone in a fatal case of pancreatitis (Opie, 1901 ). In
the developed world, gallstones are now the major cause of acute pancreatitis,
and over the last decade guidelines have appeared suggesting approaches to
these patients. This includes mandatory admission to a high dependency
(HDU) or intensive care unit (ICU) in severe cases and the management of
the causative factors, particularly gallstone disease (UK Guidelines, 1998 ; Uhl
et al ., 1999 ; Runzi et al ., 2000 ). It is important to identify and treat impacted
stones or residual CBD stones. This may improve the outcome. However, bile
duct dilatation alone is not an indication of stone disease and may result from
compression of the bile duct within the head of an inflamed gland. With a
dilated duct, it is usually possible for an experienced ultrasonographer to iden-
tify a stone or draw conclusions from a dilated duct only above the intrapan-
creatic portion. When there is doubt, patients should not be subjected to
endoscopic retrograde cholangiopancreatography (ERCP) without additional
investigation by magnetic resonance cholangiopancreatography (MRCP) or
endoscopic ultrasound (EUS). In the situation where the duct is dilated and
the liver function tests are mildly abnormal the situation is more complex. In
many of these patients the liver function tests will settle after a few days and
this correlates with an improvement in their clinical condition (reduction of
C-reactive protein [CRP], resolution of ileus, etc.) and no intervention is
required. If liver function tests do not steadily improve within the first 4 days
then it is our policy to perform an ERCP. Any stone should be removed after
sphincterotomy and a stent always left in situ . A simple sphincterotomy will
not relieve the obstruction due to the compressed duct in the head of the
gland. Similarly, if the investigations reveal CBD calculi the patient should be
stented after stone extraction.
Following stenting for stone disease, the gallbladder can be difficult to man-
age acutely and unless there is concern about impending perforation or ongo-
ing infection (continued tenderness around the area of the gallbladder or signs
PANCREATITIS
5
of gallbladder wall pathology on ultrasound scanning), then we tend to either
plan a prompt cholecystectomy during the same admission or once the
patient is over the acute attack of pancreatitis, wait 6 weeks, and proceed to a
laparoscopic cholecystectomy. If the patient is very elderly or unfit then man-
agement by sphincterotomy with or without stenting, or stenting alone is fea-
sible and is successful in 75–80% of patients (Cotton et al ., 1987 ; Foutch et al .,
1989 ; Nordback, 1989 ; Soomers et al ., 1990 ; Kaw et al ., 2002 ). The remaining
patients will have to have their gallbladder removed due to ongoing symp-
toms. Following cholecystectomy we remove the stent at a separate procedure
5–6 weeks later.
At this final procedure it is our policy to perform a further formal sphincter-
otomy to ensure it is widely patent and also to check that the duct is clear.
If there were difficulties encountered at the initial ERCP because of multiple
stones and it was not possible to be certain that the duct was clear or there are
stones too large to be removed, then a decision has to be made about whether
to attempt to combine the clearance of the duct with the gallbladder surgery or
whether it is going to be possible to clear this at a repeat ERCP. This should be
done before the cholecystectomy, as it is undesirable to have removed the gall-
bladder and subsequently be unable to clear the duct endoscopically and so
require a further surgical procedure. If clearance cannot be successfully accom-
plished (which often depends on ERCP availability and expertise), the approach
to the bile ducts is the same for patients without pancreatitis (see Section 4).
Alcohol
Alcoholic pancreatitis is the second commonest cause of acute pancreatitis in
the developed world and in some areas of the USA and Scandinavia it is the
predominant cause (Ranson et al ., 1974 ; Kivilaakso et al ., 1981 ; Sainio et al .,
1995 ). The difficulty in these patients frequently lies not in the immediate
management but in establishing with confidence that alcohol is the cause of
the attack. A number of patients will present after drinking very large quanti-
ties of alcohol and in the absence of gallstones it is reasonable to assume that
the pancreatitis is secondary to this. In a significant group, however, the situa-
tion is less clear and they present having drunk some alcohol but also having
had a viral infection, other prodromal illness, or a change in medication. Under
these circumstances it is important to search for other causes, but generally in
the absence of gallstones none will be found. Causes such as hyperlipidaemia
and hypercalcaemia cannot be investigated in acute attacks, as they are almost
always abnormal as a result of the inflammation in the pancreas or systemic
effects secondary to the release of pancreatic enzymes. When alcohol is estab-
lished as the cause (often after repeated attacks, especially when alcohol
PANCREAS
6
consumption is excessive), then the patient must be counselled about the
dangers. It is, however, frequently impossible to persuade the patients to stop
drinking completely and an attempt should be made to modify their lifestyle to
discourage excess consumption (and for patients to be aware of the times
when this occurs in particular prolonged events such as weddings, Christmas
and New Year’s Eve, and other celebrations). In reality, however, a cohort of
patients is refractory to all advice in the long term and experience recurrent
attacks over many years.
Recurrent acute pancreatitis
Recurrent acute pancreatitis is only common in the alcoholic group. Removal
of the initial cause in patients with gallstones, drug-induced problems, hyper-
lipidaemia, or hypercalcaemia usually prevents further attacks. A small number
of individuals will, however, continue to get problems. In these patients, even
in the absence of demonstrated gallstones, we will perform laparoscopy with
intraoperative ultrasound. This frequently reveals microlithiasis but whether
this is cause or effect is impossible to say. In some patients it seems highly likely
that longstanding biliary obstruction caused by the narrowing of the bile duct
in the head of the pancreas has caused the gallstones, as these patients may
have had attacks over many years and had the gallbladder pathology been
responsible then one would expect it to be considerably more advanced with
demonstrable stones.
Our practice in these patients is to remove the gallbladder and this results in
the cessation of attacks in the majority. The remaining group where attacks
continue are difficult, and it seems likely (although not proven) that the gland
can in these patients be affected by a number of different combinations of
agents (viral and moderate alcohol, hyperlipidaemia and alcohol, etc.). If attacks
do continue after attempting a low-fat diet we would use exocrine supplements
regularly and re-investigate the patients to detect those rarer causes such as
pancreas divisum and previously undetected pancreatic ductal strictures.
This leaves a very small number of patients who continue to have frequent
problems with no clear precipitating event. We admit these patients and try
intravenous fluids and nil by mouth for 72 hours followed by an elemental diet
for 2 weeks. A satisfactory outcome is almost certainly due to the elemental
diet as ‘fluids and nil by mouth’ are standard treatment during acute admis-
sions and will therefore have previously been tried. We have only seen one
patient who subsequently relapsed after reverting to a ward diet. We treated
this patient with intravenous nutrition for 4 weeks. While attacks ceased they
recurred after reverting to enteral nutrition, but were not severe and were less
frequent.
PANCREATITIS
7
Inflammatory masses
These seem to be less common in Australia and England than in central Europe
and the USA where it is a more common sequela of both acute and chronic
pancreatitis.
In acute pancreatitis, inflammatory masses produce a generally unwell
patient with a raised CRP, white cell count, and a low-grade temperature.
Mechanical problems such as gastric outlet obstruction and obstructive jaun-
dice are almost inevitable and the combination of these problems produces
considerable difficulty. ERCP and stenting can treat obstructive jaundice,
although this can be technically difficult if the mass is large and distorting the
duodenum. Gastric outlet obstruction cannot be treated medically but patients
can often manage fluid or liquid diets. In their condition, however, this is fre-
quently insufficient to prevent continued loss of weight and hypoalbuminae-
mia (even if fine-bore feeding can be instituted at a reasonable rate). These
patients should be started on total parenteral nutrition (TPN) and, although
the evidence suggests that early enteral feeding is not harmful and may even
be beneficial, we favour at least trying a period of TPN alone (72–96 hours) to
see if this will abort the process. If this has no obvious effect then we will
initiate enteral fine-bore feeding as well and expect a protracted recovery
period, which can range from weeks to occasionally months. It is not our pol-
icy to perform surgery at an early stage to treat gastric outlet obstruction, as
only a small number of patients will fail to resolve as the inflammatory mass
subsides.
Pseudocysts
Pseudocysts are a common accompaniment of acute pancreatitis, particularly
when the attack is severe. Initial fluid collections frequently resolve leaving no
residual abnormality and this is particularly so if they are small (less than 5cm)
(Yeo et al ., 1990 ; Werner and Warshaw, 1997 ). Treatment should therefore
always be conservative (particularly with fluid outside the lesser sac) unless a
collection becomes complicated. In addition, while pseudocysts in the lesser
sac can be treated relatively easily by transgastric drainage into the stomach
endoscopically or surgically or even occasionally by simple aspirations, pseu-
docysts elsewhere are more difficult (Habashi and Draganov, 2009 ). They can
develop anywhere in the abdomen, even tracking down into a patent processus
vaginalis, and up into the chest (Dennison and Royle, 1984 ).
The traditional teaching is that no intervention should be undertaken for
at least 6 weeks until the wall has become sufficiently robust to withstand
manipulation, and unless infection intervenes, this is an important principle
(Werner and Warshaw, 1997 ; Tsiotos and Sarr, 1999 ; Nealon and Walser, 2002 ;
PANCREAS
8
Zein et al ., 2003 ). At this stage, even with larger pseudocysts, if there is no
mechanical problem we prefer to adopt a conservative approach and some of
these will still resolve as the patient’s general condition improves. Waiting also
makes the situation safer if intervention is required as the patient is then much
fitter.
When it appears that resolution is not occurring (8–12 weeks), we would
repeat the MRCP to see if there was any communication with the main pancre-
atic duct or a side branch. Such a communication makes it less likely that reso-
lution will occur but allows a potential therapeutic option with ERCP and
stent insertion into the pancreatic duct. Occasionally stents can be placed
through the pancreatic duct into the cyst to facilitate drainage but, more com-
monly, stenting the main pancreatic duct is all that is possible. This can, how-
ever, also be effective, probably by allowing free drainage of the pancreatic
duct. If these measures are unsuccessful, the options are a minimally invasive
or surgical approach.
Minimally invasive treatment ( Figs. 1.2 – 1.4 ) Lesser sac pseudocysts, which
require treatment, are usually suitable for a minimally invasive approach either
endoscopically with EUS or a combination of an endoscopic and percutaneous
approach. Patients may not be suitable if a very large pseudocyst displaces the
stomach so that it is not anterior (and can not be manipulated into position)
but this is simple to detect with ultrasound. We favour the combined method
where following gastroscopy and evacuation of the stomach, the radiologist
inserts a wire into the pseudocyst under ultrasound control (after aspiration
for culture) and this is followed by a double J stent.
The endoscopist inflates the stomach, checks the stent position, and ensures
drainage is adequate. Obviously infected or excessively thick contents may
require two stents. If aspiration reveals infected contents and there is concern
about the ability of the stent(s) to provide adequate drainage, this method
also allows an additional external drain to be left in for irrigation and imaging
(Van Sonnenberg et al ., 1989 ; Freeny et al ., 1998 ; Ferrucci and Mueller, 2003 ;
Naoum et al ., 2003 ).
Pancreaticocystgastrostomy ( Figs. 1.5 – 1.9 ) For an intra-abdominal pseudo-
cyst, the preparation and anastomosis for pancreaticocystgastrostomy or pan-
creaticocystjejunostomy are similar and differences arise only in the approach.
With a pancreaticocystgastrostomy, it is important to wait at least 6 weeks for
maturation of the wall of the cyst, which has to be approached through the
very vascular posterior aspect of the stomach.
A standard transverse incision is used, the abdominal cavity examined, and
any adhesions to the anterior wall of the stomach freed. We then ultrasound
PANCREATITIS
9
the cyst to ensure there are no major intervening vascular structures. We open
the anterior wall of the stomach through a vertical gastrotomy and after aspi-
rating and partially deflating the cyst to avoid spillage, insert a Foley catheter
and send the aspirate for microbiology.
Gentle traction on the Foley catheter lifts up the combined walls of the stom-
ach and pseudocyst and enables a 2–3cm disc to be excised and sent for histol-
ogy. With the stomach and pseudocyst walls together, there is often a thick
1.5–2cm of tissue to anastomose.
It is important initially not to remove the whole disc so that control is main-
tained and the posterior wall of the stomach cannot fall away. We begin by
excising about 90 degrees and start to anastomose posterior stomach wall to
pseudocyst wall. We use 3/0 polydioxanone (PDS) interrupted sutures and a
J-shaped needle can often be useful to ensure full thickness bites are achieved.
Fig. 1.2 Initial inspection
of the stomach to exclude
other pathology.
PANCREAS
10
All sutures are left long until about eight to ten have been inserted and the
disc excised. Lifting the sutures allows a careful examination of the area for
bleeding and confirmation that the full thickness of both walls has been incor-
porated. Further interrupted sutures may be necessary to ensure this is the
case. We then close the anterior stomach wall with two layers of continuous
3/0 PDS suture. After a thorough washout and insertion of two tube drains, the
abdomen is closed. We give octreotide and a proton pump inhibitor (PPI) in
the postoperative period. The octreotide ceases after 5 days but the patients are
sent home on the PPI. Oral intake is started at 3–4 days.
Pancreaticocystjejunostomy ( Fig. 1.10 ) Pseudocysts outside the lesser sac are
not suitable for an endoscopic or percutaneous approach. In these patients we
Fig. 1.3 Gastroscopy confirms the position of the pseudocyst and allows the stomach
to be collapsed to facilitate ultrasound examination.
PANCREATITIS
11
Fig. 1.4 Guide wire inserted into the pseudocyst under ultrasound control and the
double J stent(s) follows over the wire. The stomach is then reinflated to confirm the
position and ensure drainage is adequate.
Fig. 1.5 The pseudocyst is
identified and any viscera
adherent to the stomach
wall freed.
PANCREAS
12
Fig. 1.6 Anterior vertical gastrotomy after ultrasound confirmation of optimal
position.
Fig. 1.7 Suitable portion of the posterior stomach and fused anterior wall of the
pseudocyst identified; the pseudocyst contents are aspirated to reduce pressure and
contents sent for microbiology.