Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_1841_Библиотеки_им_академика_М_И_Перельмана.pdf
LIVER TUMOURS
163
Fig. 3.57 Management of metastatic gastrointestinal stromal tumours (GISTs).
Metastatic
GIST
Primary still
in situ
C kit negative
C kit positive
Secondary
presentation
C kit negative
Chemotherapy
Good response
Surgery if disease
progression
No/poor
response
Surgery if
operable
Surgery if
resectable
Surgery if primary
and metastases
resectable
LIVER
164
The initial surgery is usually directed at the primary bowel tumour, which
should be resected if possible. The liver is assessed by palpation and intraop-
erative ultrasound to determine the extent of tumour involvement and to
determine if the disease is potentially resectable. Follow-up with chemotherapy
(Glivec®) is instituted. If the metastases respond, a watching brief is main-
tained. If unresponsive initially, or when metastases escape control, then
surgical resection is performed if it is possible to remove all known disease
(Maehara et al ., 2008 ; Rehders et al ., 2009 ). If this is not possible, then debulking
has no useful role and should not be performed.
Non-colorectal, non-neuroendocrine metastases ( Fig. 3.58 )
With the low morbidity and mortality now associated with liver resection, the
concept of palliative or, rarely, potentially curative surgery for metastatic tumours
from non-traditional sites is not unreasonable. Small series have been reported
for liver resections for renal, breast, gastric, and lung metastases as well as deposits
from melanoma, sarcoma, and a range of rarer tumours (Metcalfe et al ., 2006 ).
Providing no other spread can be detected beyond the liver (the advent of
PET scanning provides significantly more confidence in this respect) and
appropriate period of observation has been observed then the principles of
resection that apply to colorectal or neuroendocrine deposits are appropriate.
The major difference in outcome for non-colorectal metastases lies in the fact
that they did not reach the liver via the portal circulation and metastases out-
side the liver are likely even if they cannot be detected. This is always going to
be a small group of patients as many of them will develop extrahepatic disease
prior to their resection or have it demonstrated during their investigations. For
the remaining few however the outcome is often surprisingly rewarding with a
significant prolongation of their survival, or very rarely, an apparent cure.
Benign conditions
Portal hypertension ( Figs. 3.59 and 3.60 )
Portal hypertension represents a significant challenge to physicians and sur-
geons. The condition is common in clinical practice with patients who have often
been ill for long periods and repeatedly presented as emergencies ( Table 3.2 ).
Many of the symptoms are intractable, surgery in these patients is technically
difficult, and the procedure and its timing must be chosen with extreme care
or the situation may be worsened.
Surgical involvement in these patients occurs in four situations:
◆
Ascites
◆
Oesophageal varices
BENIGN CONDITIONS
165
Fig. 3.58 Management of non-colorectal, non-neuroendocrine liver metastases.
Non-colorectal
non-neuroendocrine
metastases
Tumour likely to
progress slowly
Assess for
possible resection
Tumour likely to
behave
aggressively
Chemotherapy
likely to control
disease
progression
Trial of
chemotherapy
Observation
Ablation
Non-responder to
radiotherapy or
chemotherapy
Surgery only for
obstructive/
intractable
symptoms
LIVER
166
◆
Portosystemic shunting for problems not managed by other methods
◆
Left-sided portal hypertension and hypersplenism.
The aim in patients with portal hypertension should always be to perform
the safest procedure that is likely to be effective and to choose the procedure so
that if any further intervention (particularly liver transplantation) is necessary,
the initial surgery will not render this more difficult or impossible (portal vein
no longer available, major abdominal surgery). In these decisions about the
most appropriate approach, two factors are crucial: the site of the obstruction
to the portal flow and the patient’s general condition. The hospital facilities
will determine the surgical or endoscopic options and the patient’s condition
is assessed by one of the classification methods.
We still use the Child–Pugh classification ( Table 3.3 ) which is easy to use
and practical and together with an understanding of the cause and site of the
increased portal pressure, facilitates the logical choice of an endoscopic or
surgical procedure (Child and Turcotte, 1964 ; Pugh et al ., 1973 ).
Table 3.2 Causes of portal hypertension
Presinusoidal
Extrahepatic: portal vein thrombosis, splenic vein thrombosis
(pancreatitis, pancreatic tumour), myelofibrosis, arterioportal
shunt,tropical splenomegaly
Intrahepatic: schistosomiasis, congenital hepatic fibrosis and portal
infiltration (sarcoidosis), drugs and toxins, veno-occlusive disease
Sinusoidal
Cirrhosis
Postsinusoidal
Hepatic vein occlusion (Budd–Chiari syndrome), veno-occlusive
disease, congestive cardic failure
Table 3.3 Child–Pugh classification
Points
1 2 3
Bilirubin (mg/dL) < 2 2–3 > 3
Albumin (g/dL) > 3.5 2.8–3.5 < 2.8
Prothrombin time increase
(seconds)
1–3 4–6 > 6
Ascites Absent Slight/controlled diuretics Large/tense
Encephalopathy None Mild Significant
Grade
A B C
Total points
5–6 7–9 10–15
BENIGN CONDITIONS
167
Fig. 3.59 Management of portal hypertension in the surgical patient.
Portal
hypertension
Complicated
Uncomplicated
Surveillance
Treatment only for the
development of complications
• Varices
• Bleeding
• Hypersplenism
Treat
complications
if required
Bleeding
Generally
endoscopy
Other
complications
(see Section 3)
The options available include peritoneo-venous shunts, the treatment of
varices with balloons, sclerotherapy and devascularization procedures, porto-
systemic shunts, splenectomy, and liver transplantation. Judicious use of these
approaches will reduce morbidity and mortality and it is possible to control
symptoms for many years. Many patients with portal hypertension will not
require intervention and this should not be considered in a prophylactic set-
ting apart from maintenance sclerotherapy after variceal bleeding. When
symptoms are impossible to control medically, or complications are life threat-
ening, treatment is indicated and can be very effective.
Ascites
Ascites is common but when it becomes tense and has not responded to
maximum diuretics and a low sodium diet (allowing the serum sodium to drift
down) then peritoneo-venous shunting can be very effective. The high pres-
sure ascites is a transudate but shunts are also used for malignancy (ovarian
cancer) when the fluid is an exudate. As well as the extreme discomfort
that develops from the ascites, diaphragmatic splinting is common and
attempts to reduce pressure by aspirating or draining the ascites frequently
make matters worse by removing protein (6L drained contains 120–150g of
protein). Under these circumstances shunts are valuable and although the
advent of transjugular intrahepatic portosystemic shunt (TIPS) has certainly
reduced the number of patients requiring them, they also remain valuable
for other causes of intractable ascites, particularly ovarian malignancy.
A number are available but we favour the Denver shunt which has a chamber
which can be pumped and our experience is that if the shunts are working at
96 hours, they will almost invariably continue to do so and function long term
LIVER
168
Fig. 3.60 Management of complications of portal hypertension.
Upper GI bleeding
from varices
Anaemia
Endoscopic
treatment
Endoscopic
treatment
Recurrent
TIPS
Liver transplant
Stent/
devascularization
Tamponade/
endoscopic
treatment
Overt blood loss
Massive bleeding
Hypersplenism
Development of
varices
CT
endoscopy
Portal
hypertension
If severe and associated with variceal
bleeding may need splenectomy
(can produce portal vein thrombosis)
Refractory
ascites
Endoscopic
surveillance
Peritoneo-venous
shunt (TIPS) if
transplant
candidate)
Treatment of if
signs of bleeding
BENIGN CONDITIONS
169
(LeVeen et al ., 1974 ; Stanley et al ., 1989 ). The use of these shunts requires
considerable attention to detail before, during and after the operation.
Peritoneo-venous shunting
Preoperative management No aspiration or drainage of ascites should have
occurred for 3 weeks preoperatively as infected shunts can be rapidly fatal. The
choice of shunt is important and Denver shunts can come in different flow
rates and with a single or double valve ( Fig. 3.61 ). We always use an extra-high
flow, single-valve shunt for ascites in this situation.
Operative procedure ( Figs. 3.62 – 3.70 ) This is best performed under general
anaesthetic but is possible under local anaesthetic. If under a local anaesthetic,
particular care must be taken when mobilizing the internal jugular vein not to
include or put tension on the vagus nerve. Antibiotics are given at the begin-
ning of the procedure.
The procedure begins with a small (4–5cm) transverse incision below the
right costal margin.
Fig. 3.61 Typical Denver
shunt design.
LIVER
170
The muscles are separated down to the peritoneum and a small hole made
with a scalpel just large enough to admit suction. The ascites is removed until,
when lifting up the abdominal wall, the ascites laps around the wound. There
needs to be a sufficient pressure difference across the shunt to ensure it will
work but not sufficient to fluid overload the patient with the ‘intravenous
infusion’ when the venous end is implanted and flow commences. Two Prolene
purse-string sutures are inserted around the peritoneal defect and the shunt
Fig. 3.63 Muscle splitting
incision through the
abdominal wall made
watertight with two
‘purse-string’ sutures.
Fig. 3.62 The patient positioned for surgery, neck rotated to the left side, and the
chest and abdomen exposed.
BENIGN CONDITIONS
171
is inserted. The shunt is not flushed with heparinized saline but with ascitic
fluid. This is important as heparin is bonded into the inner surface of the shunt
and can be partially washed off with heparinized saline. The distal end of the
shunt is clamped and a small transverse neck incision is made 3–4cm above the
clavicle over the heads of sternocleidomastoid The jugular vein is identified
and slung and when sufficient length is mobilized and the posterior surface
examined to exclude inclusion of the vagus nerve then the upper end is ligated.
The shunt is then drawn through from the abdomen to the neck using a vascu-
lar tunnelling device. The chamber must be located over the costal margin so
Fig. 3.64 The neck incision.
Fig. 3.65 The jugular vein
exposed.
LIVER
172
that it can be pumped. We open the space over the lower costal margin with a
large clip and create a pocket for the chamber. The chamber is anchored to the
costal margin with two Prolene sutures through the custom-made holes at the
corners of the chamber. The upper two holes are not used. When this has been
done we check the function of the shunt by pressing it through the skin onto
the ribs and ensure a good flow and check that the pumping chamber is effec-
tive. The skin is then ‘tattooed’ with India ink and a 22-gauge needle over the
point that represents the most favourable to press the shunt. This will ensure
Fig. 3.67 Ascites allowed to empty until the pressure difference is 4cm water above
the heart with no further flow.
Fig. 3.66 The jugular end of the shunt is exposed in the neck and cut to size.