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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_1841_Библиотеки_им_академика_М_И_Перельмана.pdf
LIST OF FIGURES
xxix
Figure 3.38 The residual liver regenerates to a volume similar to that pre-
resection. 137
Figure 3.39 Diffusely involved liver with bilateral metastases. 137
Figure 3.40 A right portal vein embolization to produce atrophy of the right
lobe and compensatory left-sided hypertrophy. 138
Figure 3.41 The atrophic right lobe is resected leaving the hypertrophied left
lobe. 138
Figure 3.42 Diffusely involved liver again with bilateral metastases. 139
Figure 3.43 A combination of wedge resections and ablations with a segmental
resection of Segments V and VI. 139
Figure 3.44 Investigation of a mass in the liver. 143
Figure 3.45 Management of a benign liver tumour. 146
Figure 3.46 Management of cystic liver lesions. 147
Figure 3.47 Investigation of a suspected hepatocellular carcinoma. 149
Figure 3.48 Treatment of hepatocellular carcinoma. 150
Figure 3.49 Management of colorectal liver metastases. 153
Figure 3.50 Management of unresectable colorectal liver metastases. 156
Figure 3.51 Management of carcinoid liver metastases. 158
Figure 3.52 A small number of lesions of similar sizes. Potentially curative
and operable. May be recurrent. 159
Figure 3.53 Dominant or single lesion. May have necrotic centre and
often located near a major hepatic vein. These patients
should be offered surgery for symptoms even if not potentially
curative. 159
Figure 3.54 Miliary disease. Multiple lesions of different sizes. Often additional
disease (peritoneal, lung, retroperitoneal). All investigations apart
from laparoscopy and ultrasound understage the disease. These
patients are inoperable. 159
Figure 3.55 Management of incidentally discovered neuroendocrine
metastases. 161
Figure 3.56 Management of symptomatic neuroendocrine liver
metastases. 162
Figure 3.57 Management of metastatic gastrointestinal stromal tumours
(GISTs). 163
Figure 3.58 Management of non-colorectal, non-neuroendocrine liver
metastases. 165
LIST OF FIGURES
xxx
Figure 3.59 Management of portal hypertension in the surgical patient. 167
Figure 3.60 Management of complications of portal hypertension. 168
Figure 3.61 Typical Denver shunt design. 169
Figure 3.62 The patient positioned for surgery, neck rotated to the left side,
and the chest and abdomen exposed. 170
Figure 3.63 Muscle splitting incision through the abdominal wall made
watertight with two ‘purse-string’ sutures. 170
Figure 3.64 The neck incision. 171
Figure 3.65 The jugular vein exposed. 171
Figure 3.66 The jugular end of the shunt is exposed in the neck and cut to
size. 172
Figure 3.67 Ascites allowed to empty until the pressure difference is 4cm
water above the heart with no further flow. 172
Figure 3.68 The end of the shunt is then inserted into the jugular vein and
screened to check the position. The tip should lie in the superior
vena cava just above the right atrium. 173
Figure 3.69 Pump position identified for future use by ‘tattooing’ the local
skin immediately over it. 173
Figure 3.70 The final shunt position. 174
Figure 3.71 The management of variceal bleeding. 176
Figure 3.72 The management of recurrent or refractory variceal
bleeding. 177
Figure 3.73 Intra-variceal injection of sclerosant. 178
Figure 3.74 Retroflexed endoscopy looking towards the gastro-oesophageal
junction. 179
Figure 3.75 View towards the gastro-oesophageal junction showing the
endoscope surrounded by gastric varices. 179
Figure 3.76 Injection sclerotherapy to all visible varices. 180
Figure 3.77 Needle slowly withdrawn while still injecting to seal the
tract. 180
Figure 3.78 Four-lumen tube inserted transorally after fully deflating the
balloons and liberal lubrication. 181
Figure 3.79 Distal (gastric) balloon inflated to 300mL and gentle traction
applied. The oesophageal balloon is then inflated to half way
between systolic and diastolic blood pressure. 182
LIST OF FIGURES
xxxi
Figure 3.80 A new tennis ball is cut halfway across and used to secure the tube
and provides a simple method of adjusting the tension while
preventing ulceration. Gastric and oesophageal secretions are
collected and the oesophageal balloon pressure is monitored
hourly. 183
Figure 3.81 Surgery in patients with cirrhosis. 184
Figure 3.82 Circular stapler positioned in the lower oesophagus. 186
Figure 3.83 Oesophagus is drawn into the stapler by tying the purse-string
sutures. The gun is closed and fired. This transects and
re-anastomoses the oesophagus. 186
Figure 3.84 The inferior vena cava is mobilized. 188
Figure 3.85 A ‘side-biting’ clamp is applied. 189
Figure 3.86 The graft is anastomosed to the inferior vena cava. 189
Figure 3.87 The portal end of the graft is anastomosed. 190
Figure 3.88 Final position of the H-graft which lies in an oblique position. 190
Figure 3.89 Spleen displayed in preparation for initial splenectomy and
splenic artery and vein divided in the splenic hilum. 193
Figure 3.90 Management of a liver abscess. 196
Figure 3.91 Incision of the cyst after confirmation of simple nature with
intraoperative ultrasound. 199
Figure 3.92 The wall is sent for histological examination to confirm a simple
cyst rather than cystadenoma. 200
Figure 3.93 Management of suspected hydatid disease. 202
Figure 3.94 Management of polycystic liver disease. 205
Figure 3.95 a) Dominant cysts in left lobe of liver with larger but fewer cysts
on the right side. b) Resection of the left lobe and deroofing of
superficial cysts on the right side. 206
Figure 3.96 a) Extensive polycystic liver disease in both lobes. b) Fenestration
resection in both lobes of the liver. 207
Figure 4.1 The management of gallstones. 210
Figure 4.2 Peritoneum between liver and cystic duct incised. 213
Figure 4.3 Dissection without diathermy is used initially to define the
space. 214
Figure 4.4 Once cystic artery and duct are clearly seen, diathermy can be
used with care. 214
LIST OF FIGURES
xxxii
Figure 4.5 a) Abnormal right hepatic duct giving origin to the gallbladder.
b) Right sectoral duct entering the gall bladder c) Short cystic
duct. 216
Figure 4.6 Cystic duct clipped with a proximal locking clip on the duct and
three metal clips on the artery (two proximally and one
distally). 216
Figure 4.7 Gall bladder dissected free from the liver with diathermy and
removed (in retrieval bag if necessary). 217
Figure 4.8 Successful open cholecystectomy relies on excellent retraction.
Medial and inferior packing together with the retraction is vital.
An assistant is always helpful. 218
Figure 4.9 A digital Pringle manoeuvre helps identify a bleeding point. Blind
suture must never be used. 220
Figure 4.10 Digital examination of the gallbladder lumen often helps to
determine the position of the cystic duct. 221
Figure 4.11 The gallbladder can be subtotally resected and the remnant
treated by adequate drainage. 221
Figure 4.12 Cholangiography is used selectively. 222
Figure 4.13 The management of patients with gallstones and abnormal liver
function tests. 223
Figure 4.14 Stones in the bile duct at laparoscopic cholecystectomy. 226
Figure 4.15 Laparoscopic bile duct exploration via the cystic duct following
intraoperative cholangiography using a small incision made
transversely in the cystic duct. 227
Figure 4.16 A cholangiogram catheter is introduced and a fluoroscopic image
of the biliary tract obtained. 227
Figure 4.17 A choledochoscope can be passed through a dilated cystic duct
giving images of the dilated common bile duct. 228
Figure 4.18 A Dormia basket can be passed down the cystic duct to extract
common bile duct calculi and a completion cholangiogram taken
to confirm clearance. 228
Figure 4.19 Longitudinal bile duct incision. 229
Figure 4.20 Bile duct exploration with a Dormia basket. 230
Figure 4.21 Bile duct exploration with Fogarty balloon. 230
Figure 4.22 A T-tube is cut to size (a). A small ‘V’ is made at the apex of
the T-tube to aid removal from the bile duct at 2 weeks (b and c).
LIST OF FIGURES
xxxiii
In small bile ducts removal is further aided by guttering the
T-tube (d). 231
Figure 4.23 The T-tube is placed through the choledochotomy and the bile
duct closed with interrupted 4/0 PDS sutures. 232
Figure 4.24 At the end of the procedure the T-tube is brought out through the
abdominal wall, a tube drain is placed along side the bile duct,
and the wound is closed. 233
Figure 4.25 Mirizzi’s syndrome showing a gallstone eroding through the
gallbladder wall into the bile duct. 237
Figure 4.26 Management of postcholecystectomy problems. 239
Figure 4.27 Investigation of suspected gallbladder cancer. 245
Figure 4.28 Management of gallbladder carcinoma. 246
Figure 4.29 Gallbladder cancer in the fundus with involved hepatoduodenal
lymph nodes. 249
Figure 4.30 Gallbladder is removed and all the structures in the hepatoduodenal
ligament skeletonized. 250
Figure 4.31 Right hepatectomy performed with bile duct divided above the
pancreas and to the left of the confluence. 250
Figure 4.32 Roux-en-Y with anastomosis to the left bile duct. 251
Figure 5.1 Investigation of abnormal liver function tests. 254
Figure 5.2 Investigation and management of a biliary stricture. 256
Figure 5.3 Types of choledochal cyst. a) Normal biliary tract. b) Solitary
fusiform. c) Extra-hepatic supraduodenal diverticulum.
d) Intraduodenal diverticulum (choledochocele). e) Fusiform
intra- and extrahepatic cysts. f) Intrahepatic cysts (multiple in
Caroli’s disease). 257
Figure 5.4 Investigation of a dilated common bile duct. 261
Figure 5.5 Appearance of the bile duct in ampullary stenosis. The dilation
continues to the ampulla, the duct is uniformly enlarged, and the
pancreatic duct is normal. 262
Figure 5.6 Appearance of the bile duct obstruction in pancreatitis. The duct
is smoothly narrowed in its intrahepatic course and the pancreatic
duct is often abnormal. 262
Figure 5.7 For a small defect in the wall of the bile duct T-tube insertion is
satisfactory. 265
Figure 5.8 The management of a bile duct injury. 267
LIST OF FIGURES
xxxiv
Figure 5.9 Fogarty balloon passed down a T-tube into the duodenum,
inflated, and gentle traction applied to stop the bleeding. 268
Figure 5.10 Indications and complications of ERCP. 269
Figure 5.11 Endoscopic basket has grasped the stone, which cannot be
removed and the basket will not release. 270
Figure 5.12 Creation of an access limb. The afferent loop is left long, sutured to
the underside of the abdominal wall, and marked with metal
clips. 272
Figure 5.13 A modification of the traditional access loop to aid radiological
access. The proximal end of the loop is marked with two silicone
covered metal loops at right angles to each other. 272
Figure 5.14 Management of extrahepatic cholangiocarcinoma. 274
Figure 5.15 Upper-third bile duct tumour dissected free of surrounding
structures. 276
Figure 5.16 Once respectability is confirmed, the bile duct is divided above
the duodenum and mobilized from surrounding structures. 277
Figure 5.17 Portal vein and hepatic artery separated from the bile duct. The
left and right ducts are mobilized. 277
Figure 5.18 Frozen section defines the extent of the bile duct resection. 278
Figure 5.19 A Roux-en-Y anastomosis is performed to the right and left
hepatic ducts. 279
Figure 5.20 Intraoperative ultrasound is helpful and accurately locates the
dilated duct to segment III. 280
Figure 5.21 The segment III bile duct is opened and anastomosed to a Roux
loop. 281
Figure 5.22 A completed bilio-enteric anastomosis to segment III. 281
Figure 5.23 Use of intraoperative ultrasound to locate the dilated segment V
duct (after cholecystectomy) to decide whether it is suitable for an
anastomosis. 282
List of tables
Table 1.1 The early history of pancreatic studies 1
Table 1.2 Classification of pancreatic injuries 30
Table 1.3 Management of isolated and combined pancreatic and duodenal
injuries 31
Table 1.4 Possible causes of cystic lesions of the pancreas and their
characteristics 41
Table 1.5 Comparison of the findings in a pseudocyst and pancreatic cystic
tumour 43
Table 1.6 Important points to remember when assessing a cystic pancreatic
lesion for malignancy or malignant potential 45
Table 1.7 WHO classification of neuroendocrine tumours 53
Table 1.8 Malignant potential of the neuroendocrine tumours 55
Table 1.9 Presentation, sites, and malignant potential of gastroen-
teropancreatic neuroendocrine tumours (GEP–NETs) 56
Table 1.10 Pancreatic epithelial tumours and their malignant potential 57
Table 1.11 The development of pancreatic surgery for malignancy 82
Table 1.12 Main stages in the management of carcinoma of the head of the
pancreas 86
Table 3.1 CT, MRI, and red cell scan appearances of common benign liver
tumours and suggested management 145
Table 3.2 Causes of portal hypertension 166
Table 3.3 Child–Pugh classification 166
Table 3.4 Postoperative care of a peritoneo-venous shunt 175
Table 3.5 Protocol for management of a Minneapolis tube 185
Table 5.1 Surgical treatment of cholangiocarcinoma depending on site 275
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Section 1
Pancreas
The pancreas has fascinated physicians and surgeons for thousands of years
but most of its secrets eluded them until much more recently ( Table 1.1 ).
Details of the structure and function were only described in the last few centu-
ries and details didn’t emerge until even more recently. Herophilus, a Greek
surgeon, was the first to describe the pancreas but it was not until the 1600s
that Wirsung (1589–1643) described the pancreatic duct in a letter to Riola
(Wood, 1979 ).
Physiological descriptions also began to appear and, in 1671, Graaf investi-
gated the secretory properties of the pancreas. A number of further anatomical
discoveries were made by Vater (1684–1751) who was the first to recognize
and describe the ampulla, Santorini (1681–1737) who gave the first detailed
description of the orifices of the two ducts, naming them the superior and
main pancreatic ducts, and Oddi who, while working in Bologna in 1864,
demonstrated the control of the lower end of the bile duct by the sphincter
mechanism (Oddi, 1888 ; Boyden, 1936 ). Later that century the first descrip-
tion of pancreatitis appeared from Fitz (Fitz, 1889 ). The management of
Table 1.1 The early history of pancreatic studies
Herophilus: first person to describe the pancreas. Greek physician known as the father of
anatomy. Worked in Alexandria 1800 years before Leonardo Da Vinci started dissecting
human cadavers again. Fire destroyed all his work in 391 BCE (Hornblower and Spawford,
1999 )
1642: Wirsung, Johann Georg, 1589–1643. Prosector in Padua. Discovered the pancreatic
duct during dissection of a recently hanged man. Transferred his sketch to a copper plate
but was murdered by Giacomo Cambier a year later, allegedly in a dispute over who
discovered the pancreatic duct (Carter, 1998 ; Flati and Andrén-Sandberg, 2003 )
1671: Graaf, Regnier de, investigated the physiological functions of the pancreas by
examining the juice in dogs using an artificial fistula. Commented on the small quantity
and the alkaline nature and published ‘Tractus anatomico-medicus de succi pancreatici
natura et usu’ (Graaf, 1671 )
1889: Fitz, Reginald, studied at Harvard University. Was awarded a doctorate in 1868 and
then spent time in Vienna, Berlin, and Paris before settling in Boston. Taught pathology
at Harvard University and described three forms of pancreatitis. Believed fat necrosis was
a result (Fitz, 1889 )
PANCREAS
2
pancreatic disease in any of its guises can be very challenging and requires a
methodical approach. The particularly wide spectrum represented by pancrea-
titis makes this even more important. On one hand, the mild forms of both
acute and chronic pancreatitis may simply need identification, recognition of
aetiological factors, and symptomatic management. On the other hand, serious
forms may present as desperately ill patients transferred in after a prolonged
illness or patients in the clinic with disabling pain and no residual quality
of life. Increasingly, these patients are being referred to a specialist centre,
requiring a conclusive diagnosis, which can prove difficult to establish.
Pancreatitis
Pancreatitis used to be classified into a number of different groups thought to
correlate with clinical presentation. Over the last 30 years, the situation has
been refined initially with the Cambridge Marseille classification (Cambridge
symposium 1983 and Marseille symposium 1984) (Sarner and Cotton, 1984 ).
This classification was further refined at an international meeting in Atlanta in
1992 (Singer et al ., 1985 ; Bradley, 1993 ). Today, whilst a perfect classification
still eludes us, things have been further simplified and we recognize acute and
chronic pancreatitis as disease entities. Previous categories such as acute fluid
collection, pancreatic necrosis, pseudocysts, and abscesses are merely manifes-
tations of the disease and not separate groups. The one term that we shall refer
to that is widely felt to be obsolete is pancreatic phlegmon. We believe that this
is a localized inflammatory mass without abscess formation and is a specific
problem that can result in difficult patients with acute pancreatitis when the
process seems to stall and, while it fails to progress, the body’s natural defence
mechanisms fails to resolve it. In chronic pancreatitis, the processes which
involve particularly the head of the pancreas are the basis for central European
and American procedures such as the Beger and Frey operations (Frey and
Amikura, 1994 ; Beger et al ., 1999 ).
Acute pancreatitis ( Fig. 1.1 )
Acute pancreatitis is a life-threatening illness, fatal in 5–10% of patients at first
attack (Bradley, 1993 , 1997 ; Garcea et al ., 2008a ). The common causes remain
gallstones and alcohol in varying ratios, depending on geography and factors
such as obesity and social status. If neither of these causes can be identified
then the less common aetiologies (particularly hypercalcaemia, hyperlipidae-
mia, and medications) must be considered (Bank 1999 ; Dervenis et al ., 1999 ;
Isenmann and Beger, 1999 ; Buter et al ., 2002 ). In a very small number of cases
no cause will be found and there may be a presumed viral aetiology. In an even