Download - Gall Bladder

Surgical anatomy and physiology

The gall bladder is pear-shaped, 7.5-12 cm long, with a normal

capacity of about 50 ml, but capable of considerable distension in certain

pathological conditions. The anatomical divisions are a fundus, a body and a

neck that terminates in a narrow infundibulum. The muscle fibres in the wall

of the gall bladder are arranged in a criss-cross manner, being particularly

well developed in i ts neck. The mucous membrane contains indentations of

the mucosa that sink into the muscle coat; these are the crypts of Luschka.

The cystic duct is about 3 cm in length but variable. Its lumen is

usually 1-3 mm in diameter. The mucosa of the cystic duct is arranged in

spiral folds known as the valves of Heister. Its wall is surrounded by a

sphincteric structure called the sphincter of Lutkins. While the cystic duct joins

the common hepatic duct in its supraduodenal segment in 80 per cent of cases,

it may extend down into the retroduodenal or even retropancreatic part of the

bile duct before joining. Occasionally the cystic duct may join the right

hepatic duct or even a right hepatic sectorial duct.

The common hepatic duct is usually less than 2,5 cm long and is formed

by the union of the right and left hepatic ducts. The common bile duct is

about 7,5 cm long and formed by the junction of the cystic and common

hepatic ducts. It is divided into four parts:

• the supraduodenal portion, about 2,5 cm long, running in the free

edge of the lesser omentum;

• the retroduodenal portion;

• the infraduodenal portion lies in a groove, but at times in

a tunnel, on the posterior surface of the pancreas;

• the intraduodenal portion passes obliquely through the wall of the

second part of the duodenum where it is surrounded by the sphincter of Oddi. It

terminates by opening on the summit of the papilla of Vater.

The arterial supply of the gall bladder is critical. It is proposed that arterial

damage during cholecystectomy may cause ischaemia and result in postoperative

Knowledge is the highest power Nothing to stand before it. Pandi

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bile-duct stricture. The cystic artery, a branch of the right hepatic artery, is usually

given off behind the common hepatic duct. Occasionally, an accessory cystic

artery arises from the gastroduodenal artery.

Surgical physiology

Bile, as it leaves the liver, is composed of 97 per cent water, 1-2 per cent bile

salts, and 1 per cent pigments, cholesterol and fatty acids. The liver excretes bile at

a rate estimated to be approximately 40 ml/hour. The rate of bile secretion is con-

trolled by cholecystokinin which is released from the duodenal mucosa. With feeding

there is increased production of bile.

Functions of the gall bladder

The gall bladder is a reservoir for bile. During fasting resistance to flow

through the sphincter is high, and bile excreted by the liver is diverted to the gall

bladder. After feeding the resistance to flow through the sphincter of Oddi is

reduced, the gall bladder contracts and the bile enters the duodenum. These motor

responses of the biliary tract are in part effected by the hormone cholecystokinin.

The second main function of the gall bladder is concentration of bile by

active absorption of water, sodium chloride and bicarbonate by the mucous

membrane of the gall bladder. The hepatic bile which enters the gall bladder

becomes concentrated 5-10 times, with a corresponding increase in the proportion

of bile salts, bile pigments, cholesterol and calcium.

The third function of the gall bladder is the secretion of mucus -

approximately 20 ml is produced per day. With total obstruction of the cystic duct

in a healthy gall bladder, a mucocele develops on account of this function of the

mucosa of the gall bladder.

Incidence of gallstones

A 'fat, fertile, flatulent, female of fifty' is the classical sufferer from

symptomatic gallstones. Useful as this clinical memorandum is, it should be

tempered with the knowledge that cholelithiasis occurs in both sexes from

childhood to the centenarian. In men the disease tends to occur in the older age

groups at which point the incidence is equal to that of women. Stones are rarer in


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Africa and in southern India, but not in north India.

Causal factors in gallstone formation

The aetiology of gallstones is probably multifactorial. Factors implicated are:

(1) metabolic; (2) infective; and (3) bile stasis.

Cholesterol and mixed stones

Metabolic

Cholesterol, insoluble in water, is held in solution by a detergent action of bile

salts and phospholipids with which it forms micelles. Bile containing cholesterol

stones has an excess of cholesterol relative to bile salts and phospholipids, thus

allowing cholesterol crystals to form. Such bile is termed 'supersaturated , or

'lithogenic'. Bile cholesterol increases with age and is raised in women, particularly

those taking the contraceptive pill, in obesity and by clofibrate - a drug used in the

treatment of certain hyperlipoproteinaemias. The concentration of bile salts in bile

is reduced by oestrogens, and also by factors which interrupt the intrahepatic

circulation of bile salts (e.g. ileal disease, resection or bypass and cholestyramine

therapy). These conditions are all associated with an increased incidence of stones,

but there are still some people with cholesterol supersaturation who remain free of

stones, suggesting that there are other factors of importance.

Infection.

The role of infection in causing stones is unclear. Often bile from patients

with gallstones is sterile, but organisms have been cultured from the centres of

gallstones: the radiolucent centre of many gallstones may represent mucus plugs

originally formed around bacteria (Moynihan's aphorism: 'A gallstone is a

tombstone erected to the memory of the organism within it,). Helicobacter pylori

antigens have been isolated within gall bladders containing stones.

Bile stasis

Gall bladder contractility is reduced by oestrogens, in pregnancy and after

truncal vagotomy, situations in which the incidence of gallstones is increased.

Patients on long-term parenteral nutrition have a high incidence of stones. Lack of

good oral intake precludes the release of cholecystokinin, the hormonal stimulant


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of gall-bladder contraction released from the duodenal mucosa.

Pigment stones are seen in patients with haemolysis in which bilirubin

production is increased. Examples are hereditary spherocytosis, sickle cell anaemia,

thalassaemia, malaria and mechanical destruction of red cells by prosthetic heart

valves. Pigment stones are found in the ducts of patients with benign and malignant

bile duct strictures. Pigment stones in Oriental countries are associated with

infestations of the biliary tree by Clonorchis sinensis and Ascaris lumbricoides.

Escherichia coli is often found in the bile of these patients. This bacterium

produces the enzyme β-glucuronidase which converts the bilirubin into its

unconjugated insoluble form. These stones are often present throughout the biliary

tree including the intrahepatic ducts.

The effects and complications of gallstones

Stones are found throughout the biliary tract and their complications relate to

obstruction of the cystic duct, of the intrahepatic radicals or of the ampulla of

Vater. Obstructive complications may be aggravated by the presence of infection

leading to cholangitis and abscess formation. Nevertheless, gallstones can be

asymptomatic; it is estimated that between 85 and 90 per cent of patients who have

gallstones remain asymptomatic. In the UK the prevalence of gallstones at the time

of death is estimated to be 17 per cent and possibly increasing. Thus, the mere

presence of gallstones is not an indication for a surgical approach. For this reason

symptoms must be analysed with care. A typical patient may fulfil Saint's triad

having gallstones, diverticulosis of the colon and a hiatus hernia, yet with symptoms

that cannot be directly contributed to any of these. When considering management

of a patient with gastrointestinal symptoms it is important to take a specific history

and consider whether or not the pain from which the patient suffers is typical or not

of biliary tract disease.

Effects and complications of gallstones

• In the gall bladder: Silent stones; Chronic cholecystitis; Acute

cholecystitis; Gangrene; Perforation; Empyema; Mucocele; Carcinoma

• In the bile ducts: Obstructive jaundice; Cholangitis; Acute


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pancreatitis

• In the intestine: Acute intestinal obstruction ('gallstone ileus')

Acute cholecystitis

Pathology

About one-fifth of patients first present with acute cholecystitis; in about

one-third there is clinical or pathological evidence of previous chronic

cholecystitis. It is usually due to persistent impaction of a stone in the neck of the

gallbladder. The result is initially a chemical inflammation of the gallbladder wall

perhaps due to the mucosal toxin lysolecithin, produced by the action of

phospholipase on biliary lecithin. This is soon followed by bacterial infection.

Because the cystic duct is occluded the inflammatory process is particularly

aggressive and the gallbladder becomes acutely distended, with accompanying

lymphatic and venous obstruction. The serosa may be covered by a fibrinous

exudate and subserosal haemorrhage gives the appearance of patchy gangrene. The

gallbladder wall itself is grossly thickened and oedematous and the underlying

mucosa may show hyperaemia or patchy necrosis. Histologically, three grades of

inflammation are recognized: acute cholecystitis, acute suppurative cholecystitis,

and acute gangrenous cholecystitis. Rarely an abscess or empyema develops within

the gallbladder, while perforation of an ischaemic area leads to a pericholecystic

abscess, bile peritonitis, or a cholecystoenteric fistula.

Diagnosis

Patients present with acute upper abdominal pain that has often been present

for 2 or 3 days. Because the inflammation extends to the parietal peritoneum the

pain is well localized and it hurts the patient to move or to breathe. Patients feel

generally unwell, may have been febrile, and are anorexic. Physical signs vary with

the severity of the inflammation but there is usually some degree of fever and

tachycardia. Mild jaundice is present in 10 to 15 per cent of patients. Right

hypochondrial tenderness is invariable and there may also be guarding, rigidity,

and rebound tenderness. If the latter physical signs are subdued it may be possible


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to feel the gallbladder itself. Murphy's sign (inspiratory arrest during subcostal

palpation) is widely regarded as pathognomonic of cholecystitis. It is certainly

present in patients with established acute cholecystitis, but it only reflects

peritoneal inflammation in the right upper quadrant, other causes of which include

chronic cholecystitis, acute hepatitis, and a localized abscess around a perforated

duodenal ulcer. There is usually a clear distinction between acute cholecystitis and

biliary colic: this is important since the management is different.

In elderly patients acute cholecystitis may present more insidiously and the

frequent absence of typical physical signs results in a delay in diagnosis. In

addition, the incidence of complications is higher and the prevalence of

intercurrent illness combine to increase the mortality rate 10-fold. Acute

cholecystitis is uncommon in children, most of whom have gallstones, sometimes

as a complication of haemolytic disease. Acalculous cholecystitis occurs in

children with severe sepsis.

Differential diagnosis

Clinically it can be difficult to distinguish acute cholecystitis from acute

pancreatitis, acute appendicitis, acute pyelonephritis, perforation of a peptic ulcer,

and, occasionally, biliary colic. A raised white cell count and serum amylase level

may occur in several of these conditions, although patients with biliary colic rarely

have a leucocytosis. Urine should always be examined under the microscope for

pus cells and sent for culture if appropriate. One-quarter of patients have disturbed

liver function tests, but not all will have stones in the bile duct. There are rarely

any specific features of acute cholecystitis on plain radiology, but ultrasound may

localize the tenderness to the gallbladder and may demonstrate stones. Free air

under the diaphragm on a chest radiograph implies perforation of a viscus, usually

a peptic ulcer. A normal HIDA scan excludes acute cholecystitis.

Acute viral hepatitis can sometimes present as acute cholecystitis. The

acutely swollen liver is painful and tender but the systemic symptoms and the

onset of jaundice soon make the true diagnosis clear.


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Treatment

Acute cholecystitis resolves with conservative treatment in the majority of

cases. If admission to hospital is necessary patients require intravenous fluids,

analgesia, and suspension of oral intake. Vomiting is unusual, but if present

nasogastric aspiration is helpful. If the patient fails to respond intravenous

antibiotics are prescribed.

Most patients should be offered cholecystectomy, which should normally be

undertaken on the next convenient operating list. There is no advantage in letting

the acute illness subside and removing the gallbladder 6 weeks later except in a

patient who is unfit for surgery and whose condition could be improved by

waiting.

Complications

Empyema of the gallbladder.

An empyema of the gallbladder may be suspected clinically if the physical

signs and symptoms fail to improve on conservative management. In particular,

fever and right upper quadrant tenderness fail to abate, and there is a persistent or

increasing leucocytosis. With time the gallbladder becomes necrotic and ruptures,

resulting either in a localized abscess or in generalized peritonitis. An empyema is

really an abscess within the gallbladder and it must therefore be drained. The best

method is to insert a pigtail catheter into the gallbladder under ultrasound control,

as the gallbladder is usually adherent to the peritoneum of the abdominal wall. If

there is any doubt a transhepatic route for the catheter should be chosen.

Percutaneous drainage is clearly less disturbing for the patient, who is usually quite

ill and toxic. If it fails for any reason a conventional surgical approach must be

adopted. Occasionally a safe cholecystectomy can be performed by an experienced

surgeon. For everyone else a cholecystostomy is better.

Mucocele of the gallbladder

A mucocele of the gallbladder forms when a stone impacts in the cystic duct

but bacterial infection does not occur. Bile is reabsorbed but the epithelium

continues to secrete mucous, and the gallbladder becomes distended. It is easily


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palpable and may even be visible, but it is not tender. Such patients have somewhat

subdued but nevertheless persistent symptoms, often including distressing nausea.

If infection does occur an empyema may develop rapidly. In either circumstance a

cholecystectomy is required. Rarely a mucocele of the gallbladder may perforate.

Although pseudomyxoma peritonei has been reported to follow rupture of a

mucocele it probably only follows rupture of a cystadenoma or

cystadenocarcinoma of the gallbladder.

Management of gallbladder stones

The first successful cholecystectomy was performed by Langenbuch in

1882, and since then the operation has become the standard treatment for

gallbladder stones. It is both safe and effective by modern surgical standards.

However, there are deaths and complications following the operation and it takes 6

to 8 weeks to recover following a conventional open operation. An alternative to

surgery would clearly be useful. Our understanding of the biochemistry of

gallstone formation first led to the development of drugs which dissolve

cholesterol gallstones. Further developments have produced a bewildering array of

methods for removing or dissolving stones without the disadvantages of surgery.

Operative technique

The principles of the operation are the same whichever surgical approach is

used. They are to isolate, occlude, and divide the cystic artery and the cystic duct,

and then to remove the gallbladder from the liver bed. A peroperative

cholangiogram helps to delineate the biliary anatomy and to identify stones in the

bile duct: the operation is best performed on an operating table suitably adapted for

cholangiography. General anaesthesia with good relaxation provides the best

exposure.

Cholecystostomy

Surgical drainage of the gallbladder is rarely necessary: percutaneous

ultrasound-guided drainage can now achieve the same result with less disturbance

to the patient. On the other hand the surgeon may embark on an urgent

cholecystectomy only to realize that the pathology is too severe to allow a safe


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operation. In these circumstances it is much better simply to drain the gallbladder

with a large tube after removing all the stones, allow the inflammation to settle and

to remove the gallbladder 6 weeks later.

The postcholecystectomy syndrome

Persistent or recurrent symptoms, excluding early operative complications,

are common after cholecystectomy and may be due to a number of conditions. In

one prospective study 50 per cent of patients had symptoms 1 year after a

cholecystectomy. Fortunately the majority of patients have only mild complaints

and often do not seek medical advice. Severe symptoms occur in 5 to 10 per cent

of patients. They are more common in middle-aged patients with a long

preoperative history and those who had a normal gallbladder removed. Upper

abdominal pain and dyspepsia are common and may be acute and severe. Two-

thirds of these patients experience symptoms similar or identical to those

experienced before surgery.

When a patient presents with recurrent symptoms the first cause to exclude

is a retained or recurrent stone in the bile duct. This accounts for about one-third of

the patients. In a further one-third another cause, such as pancreatic or liver

disease, peptic ulceration, or the irritable bowel syndrome, is found, and the

original diagnosis of gallbladder disease was probably wrong.

Some patients, particularly those in whom the gallbladder was normal, have

often had other intra-abdominal organs such as the appendix or the uterus removed.

They may show symptoms of anxiety or depression, and they tend to focus a lot of

attention on relatively mild symptoms. It is important to exclude the presence of

objective organic disease in the biliary tract as far as possible, and then to offer

these patients treatment for the underlying problem. Further surgery, including

endoscopic sphincterotomy, should be avoided. Even after all the appropriate

investigations have been done, no satisfactory cause for the symptoms is found in

about one-quarter of such patients.


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Stones in the bile duct

Stones in the bile duct may lie dormant for many years and only come to

light because of an episode of pain, jaundice, or cholangitis. They may also be

discovered by ultrasonography during investigation for stones in the gallbladder or

by cholangiography during cholecystectomy. Between 8 and 15 per cent of patients

with stones in the gallbladder also have stones in the ducts (choledocholithiasis).

The incidence increases with age: one-quarter of patients over 60 years of age have

stones in both sites. In patients from the West, most stones are found in the

common bile duct, whereas in the East hepatic duct stones are more usual.

Origin of common duct stones

Primary stones form within the bile duct. They are usually bilirubinate

stones of the soft brown type, and they are associated with biliary stasis due to

obstruction, infection, and the presence of foreign bodies such as food. In the

Orient they are generally caused by infection, sometimes associated with parasites

within the biliary tract. However, most common duct stones originate in the

gallbladder and migrate through the cystic duct into the common bile duct. These

secondary stones consist mostly of cholesterol and often grow in size within the

duct.

Clinical presentation

Although stones in the bile duct may be silent, the development of

symptoms is potentially serious; obstructive jaundice, ascending cholangitis, and

acute pancreatitis are all associated with major morbidity and mortality.

Less seriously, stones in the ducts may cause bouts of abdominal pain or

dyspepsia indistinguishable from symptoms of gallbladder disease or of

intermittent biliary colic with transient jaundice. Elderly patients with bile duct

stones sometimes present in apparently obscure ways with malaise, confusion,

collapse, or septicaemia. The cause is often only discovered when routine liver

function tests are found to be abnormal. Until recently stones in the bile duct were

most commonly discovered at operation. About one in every 10 patients

undergoing cholecystectomy was discovered to have stones in the bile duct and


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required exploration of the duct, although stones were only recovered in perhaps

two-thirds of the explorations. Nowadays most bile duct stones are diagnosed by

ultrasound and removed endoscopically before cholecystectomy, although surgical

exploration of the bile duct is still occasionally necessary.

Ascending cholangitis

Ascending cholangitis is still a fatal disease and it must be treated as a

medical emergency. Fortunately it is usually an easy diagnosis to make clinically,

as most patients present with the classic symptoms of epigastric pain, rigors, and

jaundice (Charcot's triad or Charcot's intermittent biliary fever). Elderly patients

sometimes present simply with septicaemia or collapse with little or no jaundice,

and rarely the origin of a Gram-negative septicaemia is eventually traced back to

the bile duct.

Pathology

Cholangitis is always associated with some degree of obstruction within the

bile duct: stones in the ducts are the cause in 80 per cent of cases. Many of the

patients are elderly. Cholangitis is a rare presentation of malignant biliary

obstruction, except in those with carcinoma of the ampulla. Patients with a benign

biliary stricture commonly experience recurrent episodes of cholangitis and they

always have bacteria in their bile, as do patients with an endoluminal prosthesis in

place. Patients with stones nearly always have a positive bile culture, whereas this

is only found in 10 per cent of patients with malignant jaundice.

Bacteriology

Most of the bacteria cultured from the bile in patients with cholangitis are

also found in the bowel. Escherichia coli, Streptococcus faecalis, and Klebsiella

species are the most common pathogens, but Staphylococcus, Pseudomonas, and

Proteus may occasionally be present. Anaerobic bacteria such as Clostridium

perfringens and Bacteroides fragilis, although rarely cultured from gallbladder bile,

are an important feature in cholangitis. Bacteria reach the liver in the portal vein

and are normally cleared there by the reticuloendothelial system. There is also

evidence of cholangiovenous reflux of organisms into the circulation when the


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systemic symptoms of cholangitis become apparent. More than one organism is

present in over half of all patients, and there is some evidence of synergy between

the aerobic and anaerobic organisms. Antibiotic treatment, which should always be

vigorous, must take account of the polymicrobial nature of most infections.

Treatment

The obstructed bile duct must be drained adequately, by the most effective

route, and as quickly as possible. However, the patient must first be resuscitated

with intravenous fluids and antibiotics. Antibiotic treatment of septicaemia will

produce improvement in the patient for a short period, but it will not cure the

patient unless the obstruction is relieved. Nowadays this can usually be achieved

by an endoscopic sphincterotomy, but occasionally conventional surgical drainage

is still necessary.

Complications

Progression of the septic process within the bile ducts can occur in two

separate ways. Sometimes pus develops within the ducts; intrahepatic abscesses

may also appear. These abscesses may rupture through the hepatic capsule and

give rise to intraperitoneal collections. Purulent cholangitis is often associated with

a degree of tension within the biliary system, and there is a gush of purulent bile

into the duodenum when the offending stone is released endoscopically.

Alternatively the sepsis may become systemic. Progressive renal and

cardiac impairment ensues, and patients develop septic shock. Dialysis or

haemofiltration may be required. Occasionally, the presenting feature of

cholangitis is complete renal failure or cardiovascular collapse; the mortality rate

in these patients is very high.

Acute pancreatitis

Acute pancreatitis is associated with gallstones. Impaction of a small stone

at the ampulla and occlusion of the pancreatic duct is a cause of pancreatitis in a

minority of patients. An early ultrasound examination of the biliary tract is

therefore essential in every patient who is admitted with acute pancreatitis,

particularly if there is any change in the liver function tests. A few have evidence


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of stones in the bile duct and an immediate endoscopic sphincterotomy and

extraction of the stone is well worthwhile in these patients, as it may abort the

episode of pancreatitis immediately. There is no evidence that the pancreatitis is

made worse by ERCP, although it is wise to avoid cannulating the pancreatic duct.

Investigation of common duct stones

The most important investigation is ultrasound examination of the liver, the

bile duct, the gallbladder, and the pancreas. It should be undertaken on the least

suspicion of stones or another obstructive lesion in the bile duct. The

ultrasonographer need only decide whether or not the bile ducts are dilated. The

normal common bile duct should not be greater than 7 mm in diameter when

measured on ultrasound. If the ducts are dilated, the patient has an extrahepatic

obstructive cause for his or her symptoms. If the ducts are not dilated it is unlikely

that there are stones in the bile duct, but there are two important exceptions to this

rule. If the examination is done very soon after a stone has entered the bile duct

there may have been insufficient time for dilatation to have developed. The

examination should be repeated 1 week later. In patients with cirrhosis of the liver

the intrahepatic bile ducts are simply not able to dilate. If there is clinical

uncertainty about the presence of a stone within the ducts a cholangiogram is

needed.

An experienced ultrasonographer can always detect dilation of the ducts,

but the site of the obstruction will only be identified in two-thirds of patients, and

the cause of the obstruction in one-third. Nevertheless stones and strictures can

sometimes be identified on ultrasound.

Before the introduction of ultrasound, biochemical markers of liver function

were important in differentiating surgical from medical jaundice. Their specificity

and sensitivity were very poor and they are now only of historical interest. The

main value of biochemistry nowadays is to quantify the severity and the duration

of an obstruction and to monitor the effects of treatment.

Computed tomography (CT) has a limited place in the imaging of common

duct stones. The ultrasound examination may raise the possibility of a malignant


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obstruction, and a CT scan may be obtained before ERCP. CT detects dilatation of

the ducts very reliably, and it is slightly better than ultrasound at identifying the

site and the cause of an obstruction.

The prothrombin time is a marker of coagulation and should always be

measured, even if the patient is not jaundiced. Patients with a prolonged

prothrombin time should receive vitamin K and may also require fresh frozen

plasma to correct a coagulation defect before embarking on an endoscopic

sphincterotomy.

Any patient who has any degree of jaundice and a fever must have blood

cultures taken before treatment with antibiotics. This may be the only opportunity

to identify an organism.

It can still be very difficult to differentiate medical from surgical causes of

jaundice and hepatitis occasionally develops in patients who also have stones in the

ducts. As soon as this is suspected the immunological markers for hepatitis must be

measured, and the laboratory must be warned.

Management of common duct stones

It is essential to determine whether the jaundice is due to liver disease,

disease within the duct such as sclerosing cholangitis or obstruction. Ultrasound

scanning, liver function tests, liver biopsy if the ducts are not dilated, and MRI

or ERCP will demarcate the nature of the obstruction. The patient may be ill. Pus

may be present within the biliary tree and liver abscesses may be developing. Full

supportive measures are required with rehydration, attention to clotting, exclusion

of diabetes and starting the appropriate broad-spectrum antibiotics. As soon as

resuscitation has taken place, relief of the obstruction is essential. Endoscopic

papillotomy is the preferred first technique with a sphincterotomy, removal of the

stones using a Dormia basket or the placement of a stent if stone removal is not

possible. If this technique fails, a percutaneous transhepatic cholangiogram can be

performed to provide drainage and subsequent percutaneous choledochoscopy.

Surgery, in the form of choledo-chotomy, is now rarely used for this situation as

most patients can be managed by minimally invasive techniques.


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Choledochotomy

If a stone (or stones) is present in the common bile duct, removal should

have priority over cholecystectomy. Should the patient be unfit for

cholecystectomy, or even cholecys-tostomy, the gall bladder should be removed

on a future occasion ('a living problem is better than a dead "cert ," -Grey

Turner). In particular, this may be the case in suppurative cholangitis. Recent

evidence suggests that subsequent cholecystectomy may not be necessary. After

endoscopic removal of stones, only 10 per cent of patients will have subsequent

problems with their gall bladder.

Supraduodenal choledochotomy

Most stones in the common bile duct can be removed by this route. If, as is

often the case, a stone can be felt, an attempt is made to manoeuvre it into a

position midway between the entrance of the cystic duct and the superior border

of the duodenum. The stone is steadied between the finger and thumb. The duct

is opened longitudinally directly on to the stone, enabling it to be removed by a

malleable scoop or Desjardin's gallstone forceps. The interior of the duct is then

explored upwards and downwards with the scoop for further stones.

When the stone cannot be felt, or cannot be manipulated into the optimum

position just described, 2 cm of the common bile duct is exposed, two stay

sutures are placed in the duct and a longitudinal incision into the duct is made

between them. Escaping bile is mopped up or removed by suction. Through this

opening it may be possible to identify the stones and remove them with a scoop

or forceps. A balloon catheter, similar to that used for embolectomy, and

irrigation of the ducts with saline are useful additional methods.

Choledochoscopy may be employed to confirm that all calculi have been

removed. Usually drainage of the common bile duct is carried out by means of a

T-tube; T-tubes should be made of latex or rubber and used only once - plastic

tubes are hardened by the bile and are difficult to remove. Latex and rubber

stimulate fibrinous adhesion of the omentum to liver and colon to form a safe

track. There is very little reaction to a plastic tube and therefore the risk of biliary


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peritonitis is greater. The transverse limb, shortened if necessary to about 5 cm

long, is inserted in the duct which is closed snugly about the vertical limb, using fine

catgut on an atraumatic needle. The long limb is brought out through a separate stab

wound laterally. The bile draining from the tube is collected in a plastic bag by

the side of the bed, its amount and character being noted. After 10 days the tube

may be clamped for increasing periods, and the absence of pain and jaundice and

the presence of bile in the stools indicate satisfactory flow into the duodenum.

Sodium diatrizoate is injected down the tube to obtain a cholangiogram, and if

there are no filling defects in a well-outlined duct, and the contrast enters the

duodenum freely, the T-tube can be removed. Subsequent bile drainage is

minimal and does not usually persist for more than 1 day.

Closure of the common duct without a T-tube

If this procedure is attempted, it is essential to provide drainage placed in

apposition to the common duct.

Transduodenal sphincterotomy.

In this operation the bile duct is approached across the duodenum and

through the ampulla. It is usually combined with a plasty. The duodenum is fully

mobilized and a longitudinal incision is made in the right lateral wall over the

ampulla. A probe is then passed into the bile duct and the ampullary sphincter is

divided with scissors. Fine catgut sutures are placed to appose the mucosa of the

bile duct to the duodenum and the stones are then extracted with Desjardin forceps.

The choledochoscope can be used to ensure that all the stones have been removed

and the duodenum is then closed. The advantage of this approach is that any

missed stone will pass spontaneously. The disadvantage is the risk of pancreatitis

from interference with the ampulla. Most patients who need a transampullary

approach to their bile ducts are better treated endoscopically.

Choledochoduodenostomy

Occasionally an alternative to closure of the common bile duct over a t-tube

after a supraduodenal exploration is a choledochoduodenostomy. Provided the bile

duct is more than 15 mm in diameter the operation is quick and easy to perform,


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and there are no worries about retained stones. The vertical incision in the common

bile duct is sutured to a longitudinal incision in the duodenum with a single layer

of stitches. Results in elderly patients are satisfactory, but in patients who have had

the anastomosis for a number of years recurrent cholangitis may develop. This is

known as the sump syndrome: infection arises from stones and vegetable matter

which collect in the retroduodenal portion of the bile duct between the anastomosis

and the ampulla. There may also be stenosis of the choledochoduodenostomy.

Endoscopic sphincterotomy of the ampulla and balloon dilatation of the

anastomosis may alleviate the symptoms, but treatment is not very satisfactory.

Biliary peritonitis

Percutaneous cholangiography is the most common cause of bile peritonitis,

although there is usually blood present as well. Provided the signs are localized

treatment can be conservative, although if there is a significant biliary obstruction

it is likely that the leak will persist. It is still wise to perform percutaneous

cholangiography only when it is also possible to relieve any obstruction, either

radiologically or at an operation within 12 h.

Occasionally the acutely inflamed gallbladder perforates and fills the

peritoneum with bile; this may also happen if a t-tube is removed too soon. Bile

peritonitis can be difficult to diagnose clinically because uninfected bile is often

not particularly irritant and the signs may be very subdued. Once the diagnosis is

made laparotomy is usually needed, but for smaller more localized collections, as

may occur after a percutaneous cholangiogram, ultrasound guided drainage may be

sufficient.

Biliary fistula

Leakage of bile from the biliary tract can occur from the liver, the

gallbladder, or the bile duct itself, and it may leak to the skin via the peritoneum or

to the bowel. Some fistulae are created deliberately, such as a

choledochoduodenostomy. Others develop from a pathological process, either from

surgical complications, from ulceration of a stone, or from drainage of pus into an

adjacent structure.


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External biliary fistula

The most common external fistula develops following surgery. Even after a

straightforward cholecystectomy there may be a little bile in the drain the

following day. Larger volumes of bile occasionally drain, presumably because the

tie on the cystic duct stump has slipped. Providing a stone has not been left in the

bile duct and that there is no other cause of biliary obstruction the volume will

decrease and the fistula will close spontaneously.

A t-tube in the common bile duct is technically a fistula. Normally a

cholangiogram will be performed before the t-tube is removed to confirm that there

is free flow into the duodenum; the fistula closes rapidly once the t-tube is

removed. Any delay in closure implies some degree of obstruction, such as a

residual stone, and an ERCP is necessary.

The late development of a fistula after an open cholecystectomy almost

always signifies unrecognized damage to the bile duct and comes to light after the

drainage of an abscess. These patients are usually ill and septic. They need careful

evaluation and investigation before any further surgical intervention. Biliary leaks

from the cystic duct stump are a complication of laparascopic cholecystectomy.

Placing a stent in the bile duct at ERCP normally stops these leaks at once.

Severe cholangitis occasionally leads to an intrahepatic abscess, which

ruptures first into the perihepatic peritoneum. Biliary peritonitis rarely ensues

because of surrounding adhesions, but when the abscess is drained externally a

fistula results. Such a fistula will only close when the proximal obstruction that

caused the cholangitis is removed or relieved. This may not be possible with a

malignant obstruction.

Any significant bile loss externally is accompanied by rapid fluid and

electrolyte depletion which must be vigorously replaced. If the patient will tolerate

it bile can be returned to the bowel via a nasogastric tube.


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Internal biliary fistula

Spontaneous internal fistulae are uncommon and are usually discovered at

cholecystectomy when a communication between the gallbladder and the

duodenum becomes apparent as Hartmann's pouch is dissected away from the

bowel. This usually results when a stone has ulcerated into the duodenum and

disappeared in the faeces. There are no specific symptoms to suggest that this has

happened, except when a large stone escapes and impacts in the terminal ileum,

giving rise to gallstone ileus. Rarely, the stone ulcerates into the stomach or the

colon. In the latter instance patients have profuse diarrhoea as the bile is irritant to

the colon.

The treatment is to remove the gallbladder and to close the hole in the

bowel. It is very rarely necessary to resect the bowel, but it is wise to leave a drain

in the wound.

Gallstones small bowel obstruction.

These tend to occur in the elderly secondary to erosion of a large gallstone

through the gall bladder into the duodenum. Classically, there is impaction about

60 cm proximal to the ileocaecal valve. The patient may have recurrent attacks

as the obstruction is frequently incomplete or relapsing due to a ball-valve

effect. A radiograph will show evidence of small bowel obstruction with a

diagnostic air-fluid level in the biliary tree. The stone may or may not be

visible. At laparotomy it may be possible to crush the stone within the bowel

lumen if it is soft, after milking it proximally. If not, the intestine is opened and

the gallstone disimpacted, milked back and removed.


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