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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2826_Библиотеки_им_академика_М_И_Перельмана.pdf
Gallstones 183
Biliary pain
Biliary colic is the term used for the pain associated with the temporary
obstruction of the cystic duct or CBD by a stone.
Clinical features
There are recurrent episodes of severe and persistent pain in the upper
abdomen which subsides after several hours. The pain may radiate to the
right shoulder and the right subscapular region and is often associated with
vomiting. Clinical examination is often normal.
Investigations
The diagnosis is usually made on the basis of a typical history and a US
showing gallstones. Increased serum alkaline phosphatase and bilirubin
during an attack support the diagnosis of biliary pain. The absence of inflammatory features (fever, white cell count and local peritonism) differentiates
this from acute cholecystitis.
Management
The treatment is with analgesics and elective cholecystectomy. Abnormal
liver biochemistry or a dilated CBD on US is an indication for pre-operative
MRCP. CBD stones identified on imaging are removed at ERCP or sometimes
at the same time as cholecystectomy.
Acute cholecystitis
Acute cholecystitis follows the impaction of a stone in the cystic duct or neck
of the gall bladder. Very occasionally, acute cholecystitis may occur without
stones (acalculous cholecystitis).
Clinical features
The initial clinical features are similar to those of biliary colic. However, over
a number of hours, it progresses to severe pain localized in the right upper
quadrant associated with a fever, tenderness and muscle guarding. The
tenderness is worse on inspiration (Murphy’s sign). Complications include
empyema (pus) and perforation with peritonitis. The diagnosis of acute cholecystitis is usually straightforward. The differential diagnosis is from other
causes of severe right upper quadrant pain.
Investigations
• White cell count shows leucocytosis.
• Serum liver biochemistry may be mildly abnormal.
• Abdominal US shows gallstones and a distended gall bladder with a
thickened wall. There is focal tenderness directly over the visualized gall
bladder (sonographic Murphy’s sign).
184 Liver, biliary tract andpancreatic disease
Management
The initial treatment is conservative, with nil by mouth, intravenous fluids,
pain relief and intravenous antibiotics. Cholecystectomy is usually performed
within 48 hours of the acute attack and always if complications (see above)
develop.
Chronic cholecystitis
Chronic inflammation of the gall bladder is often found in association
with gallstones. On US examination, this may appear as a small shrunken
gall bladder. There is no evidence that this produces any symptoms and
cholecystectomy is not indicated. Chronic right hypochondrial pain and
fatty food intolerance are likely to be functional in origin and gallstones an
incidental finding.
Acute cholangitis
This is an infection of the biliary tree and most often occurs secondary to
CBD obstruction by gallstones (choledocholithiasis). Other causes are benign
biliary strictures following biliary surgery or associated chronic pancreatitis,
PSC, HIV cholangiopathy and patients with biliary stents. Bile duct obstruction due to cancer of the head of pancreas or bile duct (cholangiocarcinoma)
can also cause cholangitis and this is more likely after ERCP. In the Far East,
parts of Eastern Europe and the Mediterranean, biliary parasites can cause
blockage and cholangitis.
Clinical features
The classic description of cholangitis with fever, jaundice and right upper
quadrant pain (Charcot’s triad) is not always present, although most patients
often have fever with rigors. Jaundice is cholestatic in type and therefore
urine is dark, the stools are pale and the skin may itch. Elderly patients may
present with non-specific symptoms such as confusion and malaise.
Investigations
• White cell count shows leucocytosis.
• Liver biochemistry shows a cholestatic picture with raised serum
bilirubin and alkaline phosphatase.
• Blood cultures are positive (E. coli, Enterococcus faecalis, sometimes
anaerobes) in about 30% of patients.
• US shows a dilated CBD and may show the cause of the obstruction.
• MRCP can further assess the site and cause of obstruction.
• ERCP is the definitive investigation and will also allow biliary drainage. It
will show the site of obstruction and the cause. Bile can be sampled for
culture and cytology (if a malignant cause is suspected).
The Pancreas 185
Management
Treatment of acute cholangitis includes resuscitation and volume replacement in shocked patients, pain relief, treatment of infection with appropriate
intravenous antibiotics and relief of obstruction by biliary drainage. In endemic
areas, primary parasite infection must also be treated.
Biliary drainage and/or clearance are usually achieved at ERCP with
or without sphincterotomy. The urgency of this procedure depends on the
clinical condition of the patient and the initial response to antibiotics. Stones
can be removed from the CBD. Alternatively, a stent can be placed in the
biliary tree to relieve obstruction, such as in patients with cancer of the head
of pancreas or CBD. Antibiotics are continued after biliary drainage until
symptom resolution, usually in 7–10 days.
Common bile duct stones (choledocholithiasis)
CBD stones may also be asymptomatic with no features of cholangitis
and present with abnormal liver biochemistry, usually with a cholestatic
picture. US will show gall bladder stones and may show the obstructed
CBD containing a stone. MRCP is more sensitive than transabdominal US
and it is sometimes performed if there is a high index of suspicion and
US is negative. An alternative technique for imaging the biliary system is
endoscopic US.
THE PANCREAS
The pancreas has both endocrine and exocrine functions. The islets
of Langerhans secrete several hormones directly into the bloodstream
(endocrine function) of which insulin and glucagon play crucial roles in the
regulation of blood sugar. The pancreatic acinar cells produce pancreatic
enzymes (lipase, colipase, amylase and proteases) which pass via the main
pancreatic duct into the duodenum and are involved in the digestion of fat,
carbohydrate and protein in the small intestine.
Pancreatitis
Pancreatitis is divided into acute and chronic. Acute pancreatitis occurs
on the backdrop of a normal pancreas and the pancreas returns functionally and structurally to normal after the episode. It occurs as isolated or
recurrent attacks. In chronic pancreatitis, there is continuous inflammation with irreversible structural changes. In practice, it is not always
possible to clearly separate acute from chronic forms because the
acute causes (if untreated) may eventually lead to chronic pancreatitis
and there may be relapses of the chronic condition (acute-on-chronic
pancreatitis).
186 Liver, biliary tract andpancreatic disease
Table 4.13 Causes of pancreatitis
Acute Chronic
Gallstones* Alcohol*
Alcohol* Tropical
Infections (e.g. mumps, Coxsackie B) Autoimmune (IgG4-related)
Pancreatic tumours Idiopathic
Drugs: azathioprine, oestrogens,
corticosteroids, didanosine
Iatrogenic: post-surgical, post-ERCP
Metabolic: hypercalcaemia,
hypertriglyceridaemia
Miscellaneous: trauma, scorpion
bite, cardiac surgery
Idiopathic (unknown cause)
ERCP, endoscopic retrograde cholangiopancreatography; IgG4, immunoglobulin G4.
*Commonest causes in the Western world.
Hereditary: trypsinogen and inhibitory
protein defects, cystic fibrosis
Acute pancreatitis
Acute pancreatitis is a disease of increasing incidence and it is associated
with significant morbidity and mortality. Most patients will recover from the
attack with only general supportive treatment, but 25% will develop severe
acute pancreatitis with multiorgan failure. About 20% of these patients may
die. The causes of acute pancreatitis are stated in Table 4.13.
Pathogenesis
It is thought that the final common pathway, regardless of the initiating cause,
is a marked elevation in intracellular calcium, leading to activation of intracellular proteases and the release of pancreatic enzymes. Acinar cell injury and
necrosis follows, which promotes migration of inflammatory cells from the
microcirculation into the interstitium. Release of a variety of mediators and
cytokines leads to a local inflammatory response and sometimes a systemic
inflammatory response that can result in single or multiple organ failure.
Clinical features
There is usually epigastric or upper abdominal pain radiating through to the
back, associated with nausea and vomiting. On examination, epigastric or general abdominal tenderness with guarding and rigidity is present. However, other
manifestations (coma, multiorgan failure) may dominate the clinical picture,
leading to a delay in diagnosis. Ecchymoses around the umbilicus (Cullen’s sign)
or in the flanks (Grey Turner’s sign) indicate severe necrotizing pancreatitis.
The Pancreas 187
Investigation
The purpose of investigation is to make a diagnosis, assess the severity and
determine the aetiology.
• Blood tests: A raised serum amylase or lipase, in conjunction with the
appropriate history and clinical signs, strongly indicate a diagnosis of
acute pancreatitis. A normal level of serum amylase occurs if the patient
presents late, at which time urinary amylase or serum lipase levels may
still be raised. Serum amylase may also be moderately raised in other
abdominal conditions, such as acute cholecystitis, perforated peptic
ulcer and intestinal ischaemia, but very high levels (over three times the
normal level) are diagnostic of pancreatitis. A number of routine blood
tests should be measured on admission and after 24 and 48 hours as
these are used to assess the severity of pancreatitis (Table 4.14).
• Radiology: An erect chest X-ray is performed to exclude perforated
peptic ulcer as the cause of the pain and raised amylase. An abdominal
US is performed as a screening test to look for gallstones as a cause of
pancreatitis and may show swelling of the inflamed pancreas. A contrastenhanced spiral CT scan or MRI is performed in all but the mildest attack
of pancreatitis to confirm diagnosis, identify the presence and extent of
pancreatic necrosis (associated with organ failure and higher mortality)
and identify peripancreatic fluid collections. It is performed after 72 days,
as early CT may underestimate the severity of pancreatitis.
Management
The management of acute pancreatitis is summarized in Fig. 4.9. Assessment
of severity is essential; those predicted to have severe pancreatitis with a
protracted course should be managed in a critical care environment with
Table 4.14 Glasgow criteria for severity of acute pancreatitis*
Age
White blood cell count >15 × 109/L
Blood glucose >10 mmol/L
Serum urea >16 mmol/L
Serum albumin <30 g/L
Serum aminotransferase >200 U/L
Serum calcium <2 mmol/L
Lactate dehydrogenase <600 U/L
P
ao2
*Three or more factors present during the first 48 hours predict a severe episode and a
poor prognosis.
>55 years
<8.0 kPa (60 mmHg)
188 Liver, biliary tract andpancreatic disease
Clinical assessment
Predicted
severe disease
• Medical therapy (see mild)
• Consider nursing on HDU or ITU
• Prophylactic antibiotics
• Nasogastric or nasojejunal feeding
• ERCP within 48 h if gallstone pancreatitis
and/or cholangitis
Contrast-enhanced CT
scan/MRI within 3–7 days
Monitor for complications
Fig. 4.9 The management of acute pancreatitis. CT, computed tomography;
ERCP, endoscopic retrograde cholangiopancreatography; HDU, high-dependency
unit; ITU, intensive care unit; MRI, magnetic resonance imaging; NG, n a s o g a s t r i c .
vigorous fluid resuscitation, correction of metabolic abnormalities and
administration of therapies to improve outcome. Most attacks of pancreatitis
are mild with only minimal or no pancreatic necrosis and without systemic
complications. These patients usually recover within 5–7 days and need general supportive care only. In contrast, severe pancreatitis is associated with
failure of one or more organ systems, such as renal or respiratory failure, and
impaired coagulation with disseminated intravascular coagulation. Severe
attacks are usually associated with pancreatic necrosis on CT scan. Several
scoring systems are in use to predict those patients with severe pancreatitis:
Glasgow criteria (see Table 4.14), Ranson’s criteria and the acute physiology
and chronic health evaluation score (APACHE). Obesity and a CRP >200 mg/L
in the first 4 days are also associated with a worse outcome.
of severity of
pancreatitis
Predicted mild
disease
Medical therapy
Pain control
Nothing by mouth
Intravenous fluids
?NG tube
General supportive care
Early fluid resuscitation is essential and in severe pancreatitis 5 L or more of
crystalloid daily may be required to maintain adequate urine output (>0.5 mL/
kg body weight/hour). Supplemental oxygen is given and requirements are
guided by pulse oximetry and arterial blood gas measurement. Low molecular
weight heparin is administered as prophylaxis against deep vein thrombosis.
Electrolyte and metabolic abnormalities are corrected and a variable rate insulin infusion may be necessary for good control of blood sugar levels. Adequate
analgesia should be provided and a patient-controlled system of administration may be necessary if there is persistent pain. Morphine should be avoided
as it increases sphincter of Oddi pressure and may aggravate pancreatitis.
In patients with a predicted severe episode, there is little likelihood of oral
The Pancreas 189
nutrition for a number of weeks. Nutrition is provided via a nasogastric tube
or a nasojejunal tube (placed endoscopically) for patients who are intolerant
of nasogastric feeding due to exacerbation of pain or nausea and vomiting.
Therapies to reduce the severity or frequency
ofcomplications
Broad-spectrum antibiotics reduce the risk of infection of the necrotic pancreas and they are given from the outset. Early ERCP (within 48–72 hours)
and sphincterotomy improves the outcome in patients with biliary pancreatitis, evidence of cholangitis or a high suspicion of a CBD stone (dilated CBD or
CBD stone seen on US or jaundice). They can also be done when pancreatitis
is predicted to be severe. Surgical treatment is sometimes required for very
severe necrotizing pancreatitis, particularly if it is infected or complications
such as pancreatic abscesses or pseudocysts occur.
Complications
Acute complications include hyperglycaemia, hypocalcaemia, renal failure
and shock.
Chronic pancreatitis
Inappropriate activation of enzymes within the pancreas leads to precipitation of protein plugs within the duct lumen, forming a nidus for calcification.
Subsequent duct blockage leads to ductal hypertension and further pancreatic damage. This together with cytokine activation leads to pancreatic
inflammation, irreversible morphological change and/or permanent impairment of function. The commonest cause of chronic pancreatitis in most
developed countries is excess alcohol. Other causes are tropical chronic
pancreatitis, heredity, autoimmune causes and cystic fibrosis.
Clinical features
Epigastric abdominal pain (either intermittent or constant radiating through
to the back) is the commonest symptom. There may be severe weight loss
as a result of anorexia. Diabetes and steatorrhoea may develop due to
endocrine (insulin) and exocrine (lipase) insufficiency. Occasionally, jaundice
is the presenting symptom. This is due to obstruction of the CBD during its
course through the fibrosed head of pancreas. The differential diagnosis is
pancreatic carcinoma, which also presents with pain and weight loss and
may develop on the backdrop of chronic pancreatitis. Carcinoma should be
considered when there is a short history and localized ductal abnormalities
on imaging.
Investigations
The diagnosis of chronic pancreatitis is made by imaging (to demonstrate
structural changes in the gland) and metabolic studies which demonstrate
functional abnormalities.
190 Liver, biliary tract andpancreatic disease
• Radiology: A plain abdominal X-ray will show pancreatic calcification in
some cases. US and CT scan may show calcifications, ductal dilatation,
irregular consistency, an outline of the gland and fluid collections. CT is
a more sensitive test than US. MRCP and endoscopic US are sometimes
used if the diagnosis is not confirmed with other imaging tests. ERCP is
usually reserved for therapeutic (e.g. pancreatic stent placement) rather
than diagnostic purposes.
• Functional assessment: These tests are insensitive in early pancreatic
insufficiency. Faecal elastase, measured on a single random stoolsample,
is reduced. Other tests rely on measuring decreased concentrations
of the products of synthetic compounds such as fluorescein dilaurate
(pancreolauryl) or N-benzoyl-l-tyrosyl-p-aminobenzoic acid (NBT-PABA).
They appear in the urine after oral administration and intraluminal
hydrolysis by pancreatic esterases and gut absorption. Serum amylase
is not useful in the diagnosis of chronic pancreatitis but it may be
raised during an acute episode of pain. A raised blood sugar indicates
diabetes mellitus.
Treatment
The patient should be advised to stop taking alcohol. The pain may require
opiates for control but they have an attendant risk of addiction. Surgical
resection combined with drainage of the pancreatic duct into the small bowel
(pancreaticojejunostomy) is of value for severe disease with intractable pain.
Pancreatic strictures or stones are sometimes amenable to endoscopic treatment with ERCP. Persistent pseudocysts are drained endoscopically into the
stomach or by surgical drainage. Pancreatic enzyme supplements are useful
for those with steatorrhoea and may reduce the frequency of attacks of pain
in those with recurrent symptoms. Diabetes requires appropriate treatment
with diet, oral hypoglycaemics or insulin as appropriate.
CARCINOMA OF THE PANCREAS
Epidemiology
Pancreatic cancer is the fifth most common cause of cancer death in the
Western world. Men are affected more commonly than women, and the
incidence increases with age, with most cases occurring in patients over 60
years. Most are adenocarcinomas of ductal origin.
Aetiology
Hereditary (a dominant susceptibility gene in some families and other susceptibility genes in defined syndromes) and environmental factors (smoking
and obesity in particular) both contribute. Chronic pancreatitis is also premalignant, particularly in patients with hereditary pancreatitis.
Carcinoma of the Pancreas 191
Clinical features
Cancer affecting the head of the pancreas or ampulla of Vater. The classical
presentation is with painless jaundice as a result of obstruction of the common
duct and weight loss. On examination, there is jaundice with characteristic
scratch marks and a distended, palpable gall bladder (Courvoisier’s law: if
the gall bladder is palpable in a case of painless jaundice, it is not due to
gallstones). In gallstone disease, chronic inflammation and fibrosis prevent
distension of the gall bladder. There may be a central abdominal mass.
Cancer of the body or tail. In this case the patient presents with
abdominal pain, weight loss and anorexia. Diabetes may occur and there is
an increased risk of thrombophlebitis. However, patients may also present
with non-specific symptoms, e.g. an elderly patient with dyspepsia and
change in bowel habit.
Investigations
Diagnosis is made by US (which demonstrates dilated bile ducts and a mass
lesion) and/or contrast-enhanced spiral CT; the latter is a more sensitive
test particularly for body and tail tumours and is almost always necessary
to stage the cancer. MRI and endoscopic US is used for staging and for
diagnosis in difficult cases. ERCP is usually restricted to palliative treatment
(e.g. bile duct stenting in a jaundiced patient) but may provide a source for
cytology in making the diagnosis. The tumour marker CA19-9 is sensitive but
not specific for diagnosis. Serial measurements are more frequently used to
monitor response to treatment.
Management
Optimal management is by a multidisciplinary team approach with the
involvement of the palliative care team for advanced disease, particularly to
help with management of pain. Surgical resection offers the only hope of cure,
but few patients have resectable disease at diagnosis. Tumour adherence or
invasion into adjacent structures, particularly major blood vessels (locally
advanced disease), makes complete resection difficult, and these patients
are treated with combined chemotherapy and radiotherapy. Chemotherapy
also increases survival when used as an adjuvant to pancreatic resection.
Palliative treatment is often necessary to relieve obstructive jaundice (usually
by endoscopic placement of a stent across the obstructed distal CBD), gastric
outflow obstruction, and pain in patients with unresectable pancreatic cancer.
Prognosis
Overall, the prognosis is very poor. For the few patients who have had
surgical resection with curative intent, the 3-year survival is 30%–40%. The
median survival for treated patients with locally advanced disease is 8–12
months, and for patients with metastatic disease it is 3–6 months.
192 Liver, biliary tract andpancreatic disease
Cancer of the bile ducts
Like pancreatic cancer, cholangiocarcinoma is also a disease of the elderly
with a poor prognosis. It occurs more frequently in patients with primary
sclerosing cholangitis, congenital bile duct abnormality and infections with
liver flukes, e.g. Clonorchis sinensis. Presentation is usually with jaundice
secondary to bile duct obstruction or with metastatic disease. Imaging by US,
CT or MRI shows a bile duct stricture, a hilar mass or multiple metastases.
NEUROENDOCRINE TUMOURS OF THE PANCREAS
Islet cell tumours are rare and usually produce their clinical effects by secretion of hormones (Table 4.15). Non-functioning tumours present with pain and
weight loss. Circulating hormone concentrations, e.g. gastrin, can be measured
in the serum. High levels help to make the diagnosis. Most neuroendocrine
tumours express large numbers of somatostatin receptors and radiolabelled
somatostatin analogue scanning (
of tumour localization. Endoscopic US is also used for tumour localization.
Treatment is by excision of the primary tumour if possible. Symptomatic treatment (e.g. high-dose proton pump inhibitors for gastrinomas) and chemotherapy
or hepatic artery embolization is used for patients with hepatic metastases.
Table 4.15 Clinical syndromes resulting from neuroendocrine
tumours
Tumour Secreted
Gastrinoma
(Zollinger–Ellison
syndrome)
VIPoma
Glucagonoma
Somatostatinoma
hormone
Gastrin Duodenal ulceration –
Vasoactive
intestinal
polypeptide
Glucagon Migratory necrolytic
Somatostatin Diabetes mellitus,
111
In-labelled octreotide) provides a means
Symptoms Symptom
recurrent and severe
Diarrhoea – hypersecretion
of gastric acid inhibits
digestive enzymes
Severe watery diarrhoea
and hypokalaemia due to
stimulation of intestinal
water and electrolyte
secretion
dermatitis, weight loss,
diabetes mellitus, deep
venous thrombosis
gallstones, diarrhoea/
steatorrhoea
control
High-dose
proton pump
inhibitors
Octreotide
Octreotide
Octreotide