RUQ Pain Flashcards

1
Q

Mrs Cole is an overweight 38-year-old Caucasian woman who presents to accident and emergency (A&E) at 11 p.m. complaining of severe pain in the RUQ of her abdomen, nausea, and vomiting.
What is your differential diagnosis for this lady’s current presentation? Think anatomically of which structures might give you pain in the RUQ of the abdomen. Try to arrange your list of possible diagnoses in order of likelihood given this patient’s sex, age, and presentation.

A
Biliary colic
Cholecystitis
Duodenal ulcer
Pancreatitis
Basal pneumonia (irritating the right hemidiaphragm)
Ascending cholangitis
Gastric ulcer
Small bowel obstruction
Appendicitis
Hepatitis (autoimmune, infective, or drug-induced) 
Pyelonephritis
Ovarian pathology
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2
Q

Let us suppose that Mrs Cole was 68 years old, rather than 38 years old.
Would your differential diagnosis list change?

A

Yes, the likelihood of certain diseases would change considerably. In older patients, certain pathologies are relatively more common, such as pneumonia, cancer (e.g. cholangiocarcinoma), or vascular disease (aortic dissection, abdominal aortic aneu- rysm, inferior myocardial infarction). Of course, the differential would still include those diseases seen in a 38-year-old Mrs Cole.

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3
Q

What questions should you ask in a history to narrow your differential diagnoses?

A

Site of pain, and has it moved since it began?
Onset of pain – was it sudden or gradual, and did something trigger it?
Character of pain – stabbing, dull, deep, superficial, gripping, tearing, burning?
Radiation of pain – does the patient have pain elsewhere?
Attenuating factors – does anything make the pain better (position? medications?)
Timing of pain – how long has it gone on for, has it been constant or coming and going?
Exacerbating factors – does anything make the pain worse (moving? breathing?) Severity – on a scale of 0–10, where 10 is the worst pain ever (e.g. childbirth).
Once you have characterized the pain, you should ask:

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4
Q

What other questions should you ask once you have characterised the pain

A
  • Has the patient had any symptoms other than pain? (e.g. fever, weight loss). The reason is that certain other symptoms will help you refine your diagnosis. Thus, fever suggests an infective process and makes a myocardial infarction less likely. Significant weight loss over the preceding months may be due to a cancer, which is catabolic.
  • When did they last open their bowels or pass any flatus (wind)? A patient who hasn’t opened his or her bowels may be constipated, whilst a patient who isn’t even managing to pass wind (‘absolute constipation’) may be obstructed – a surgical emergency.
  • Have they noticed any change in their stool recently? (e.g. colour, floating, smelly). If the common bile duct is obstructed, bilirubin and fat-dissolving bile salts won’t reach the bowel and thus stools will be pale, floating, and smelly (steatorrhoea). If blood is entering the bowel lumen via a bleeding ulcer, the iron (haemoglobin) in the blood will be oxidized, making stools appear very dark, black, tarry, and smelly (melaena).
  • If they are female, are they pregnant? If the patient is a female of fertile age, you must exclude pregnancy, even if the patient insists they are not pregnant or sexually active. This is partly because radiography of a pregnant woman is legally irresponsible and partly because potentially fatal ectopic pregnancies are a major source of abdominal pain – even if pain in the RUQ would be an unusual presentation.
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5
Q

Mrs Cole’s pain is in the RUQ of her abdomen. It came on gradually 16 hours ago when she went to bed. It is deep, sharp, constant, and 8/10 in severity. She also gets the occasional sharp stabbing sensation on her back and she points to her right scapula very specifically (this is known as Boas’ sign). She has not found anything that makes it better or worse. She last opened her bowels before she went to bed but has been passing flatus this morning. She reports no significant weight change recently.
In the history, she also reveals that every couple of months, usually after a heavy, fatty meal, she develops a sharp, stabbing pain in the same area of her abdomen and which usually gets better after a few hours. Her past medical history includes heartburn (dyspepsia), which is well controlled with omeprazole (a proton-pump inhibitor, PPI). However, the pain this time ‘feels different’ and she feels ‘very sick’.
ust from this history, particular diagnoses become very likely. The next steps will be to examine the patient and arrange first-line investigations with the aim of confirming your suspected diagnosis and ruling out those diseases that would require urgent management (those in red in our differential list above).
What key features on examination would you look out for?

A
  • Jaundice: most easily seen in the whites of the eyes (sclera); it is typical of dis- eases that block the common bile duct such as choledocholithiasis, ascending cholangitis, acute pancreatitis, pancreatic cancer, or cholangiocarcinoma.
  • Bruising and discoloration around the umbilicus and flank (Cullen’s sign or Grey Turner’s sign, respectively). Sometimes seen in severe pancreatitis.
  • A pulsatile and laterally expansile central mass. This indicates an abdominal aortic aneurysm.
  • Murphy’s sign: palpate the abdomen just below the tip of the right ninth cos- tal cartilage, apply pressure, and ask the patient to take a deep breath. This will cause the liver and hence gallbladder to descend and press against your fin- gers. If the gallbladder is tender it will cause the patient to arrest inspiration as the gallbladder strikes your fingers. This is strongly suggestive of an inflamed gallbladder (cholecystitis).
  • Peritonitis: the patient will lie very still, have a rigid and exquisitely tender abdomen, and exhibit guarding when you try to palpate lightly. There may be no bowel sounds. In the case of Mrs Cole, this would suggest perforation of a peptic ulcer or the gallbladder.
  • Signs of small bowel obstruction: a distended abdomen (which may be hard to appreciate in a patient with a high body mass index (BMI)) and absent or tinkling bowel sounds. If the bowel becomes strangulated, signs of peritonitis would predominate.
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6
Q

On examination, Mrs Cole is febrile (38.3oC) and tachycardic (108 bpm). Her cardiovascular and respira- tory systems are otherwise unremarkable. She is not jaundiced, has no hernias, and no palpable abdo- minal masses. Her abdominal aorta is palpable but does not feel laterally expansile. Her RUQ is tender to light palpation with a positive Murphy’s sign. A digital rectal examination in the presence of a female nurse reveals soft faeces in the rectum but no signs of blood.
Her history and physical examination are very typical of a particular diagnosis. The next step is to arrange first-line investigations that will confirm this diagnosis and help rule out other diagnoses that you should exclude because of their need for urgent management.
What investigations will you request?

A

Full blood count: the patient may be anaemic from a chronically bleeding gastric or duodenal ulcer. Her white cell count will be elevated if she has any inflammatory condition (e.g. cholecystitis, ascending cholangitis, or basal pneumonia).

Serum amylase (or lipase) levels: slight increases (200–600 U/L) in amylase levels are most commonly caused by pancreatitis, but also by various other pathologies such as bowel obstruction, mesenteric ischaemia, a posteriorly perforated duodenal ulcer, mumps, pancreatic carcinoma, or opiate medica- tions. However, very high amylase levels (>1000 U/L) or elevated lipase levels (>300 U/L) are almost exclusively found in pancreatitis. (The exact cut offs will depend upon your local laboratory protocols).

  • Liver enzymes: elevated levels of aspartate aminotransferase (AST) and ala- nine aminotransferase (ALT) suggest inflammation in the liver which could be due to viral hepatitis, autoimmune hepatitis, or obstruction of the common bile duct because of a gallstone, infection of the duct, tumour of the duct, inflammation of the pancreas or tumour of the pancreas. A raised alkaline phosphatase (ALP) level by itself can be due to increased bone breakdown (e.g. metastatic bone disease, Paget’s disease). However, a raised ALP level that is more elevated than AST/ALT levels and/or accompanied by a raised gamma-glutamyl transferase (GGT) level suggests obstruction of the com- mon bile duct.
  • Bilirubin: elevated levels of unconjugated bilirubin suggest that the liver can- not conjugate it fast enough, either because there is too much breakdown of haemoglobin into bilirubin (e.g. haemolytic anaemia), because of a hereditary deficiency of conjugating enzyme (e.g. Gilbert’s syndrome), intrahepatic (e.g. viral hepatitis) or extrahepatic (e.g. gallstones). Elevated levels of conjugated bilirubin suggest the liver is working (conjugating) but that there is obstruction of bile flow.
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7
Q

What imaging will you request

A
  • Erect chest radiograph: air under the diaphragm strongly suggests a perforated viscus such as a gastric or duodenal ulcer (but can also be a sign of recent abdominal surgery). Bear in mind that if this patient had suffered a perforated peptic ulcer we would have found signs of peritonism during the abdominal examination. A wide mediastinum and/or heart shadow can suggest aortic dissection. Don’t forget to do a pregnancy test before any radiography on a woman of fertile age, no matter how much they insist they cannot be pregnant – this not only rules out certain gynaecological pathologies (e.g. ectopic pregnancies) but is important from a patient safety and medicolegal point of view.
  • Abdominal radiograph: air on both sides of the bowel wall (Rigler’s sign) strongly suggests a perforated gastric or duodenal ulcer. Small bowel loops with a diameter >3 cm suggests small bowel obstruction (possibly in conjunc- tion with large bowel obstruction). Large bowel loops with a diameter >6 cm suggests large bowel obstruction. Not being able to see one of the two shadows caused by both psoas muscles may suggest retroperitoneal fluid (e.g. a rup- tured abdominal aortic aneurysm or pancreatitis).

• Ultrasound of pancreas, common bile duct, and gallbladder: an ultrasound can reveal tumours in the pancreas or a dilated common bile duct due to obstruction (upper limit of normal is 6–7 mm diameter). An inflamed gall- bladder (thick wall, fluid around it) may in some instances be apparent on ultrasound. Stones in the biliary tree should be visible if present.
15

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8
Q

Mrs Cole’s blood tests, and chest and abdomen radiography are all normal. The abdominal ultrasound reveals a common bile duct of normal diameter, no masses in the pancreas but a gallbladder with a wall measuring an average of 4.5 mm (normal is ≤3 mm).
In light of the history, examination, and first-line investigations, what is the most likely diagnosis? How does this explain her symptoms?

A

This is a classical clinical picture for someone with cholecystitis: a middle-aged, Caucasian female with RUQ pain, positive Murphy’s sign, fever, and a previous his- tory of pains in this area after heavy, fatty meals. The normal serum amylase levels rule out pancreatitis. The lack of jaundice or raised serum bilirubin suggest that there is no obstruction of the common bile duct. There were no signs on examina- tion suggestive of bowel obstruction or peritonism, and the abdominal and chest radiographs were normal, so small bowel obstruction or a perforated peptic ulcer are unlikely. The ultrasound did not reveal any pancreatic or common bile duct masses, suggesting that there is no pancreatic cancer nor cholangiocarcinoma. It did show a thick gallbladder wall suggesting it is inflamed.
Cholecystitis (chole = bile, cyst = bladder, -itis = inflammation) is inflammation of the gallbladder, caused in 95% of cases by a stone in the gallbladder. The gall- bladder has a chemical inflammation and this may lead to subsequent infection affecting the surrounding tissue. The inflamed gallbladder irritates the parietal peri- toneum, causing a constant pain. Irritation of the visceral peritoneum in the initial stages produces a poorly localized, dull, midline epigastric pain. As the irritation spreads outwards to the parietal peritoneum, the pain becomes sharply localized to the RUQ. The inflamed gallbladder can also irritate the liver capsule, which in turn can irritate the diaphragm above it. The diaphragm is supplied by nerve roots C3, C4, and C5 (‘3, 4, 5 keep the diaphragm alive’) which also supply sensation to the shoulder. The referred pain in the right scapula is believed to be because the central nervous system (probably the dorsal spinal cord, but perhaps the sensory cortex in the brain) confuses the incoming signals from the right shoulder and the right hemidiaphragm.

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9
Q

How will the team manage Mrs Cole’s cholecystitis?

A

When asked about management in exams, remember that you must start from the beginning and not dive into drugs or surgery. Thus, having assessed her need for resuscitation (Airway, Breathing, and Circulation, ABC), taken a full history, examined the patient, carried out first-line investigations, and suggested a diagnosis of cholecystitis, Mrs Cole’s therapeutic management can be divided into operative and non-operative:

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10
Q

Describe the non-operative management of Mrs.Cole

A

• Non-operative:
− Nil by mouth. Mrs Cole should avoid all food and have only sips of water.
This is partly to avoid food in the duodenum triggering gallbladder con- tractions and partly to prepare her if there is a need for surgery.
− Intravenous (IV) fluids. To avoid dehydration, as she is nil by mouth (apart from sips).
− Analgesia.Opioidsmaybenecessaryintheinitialstages,regularparaceta- mol will probably suffice later. Orally administered analgesics should be avoided if the patient is vomiting.
− Antibiotics. Broad-spectrum cover in accordance with local hospital guidelines. This will start to combat the infection if surgery is delayed and will reduce the risk of systemic or peritoneal infection as a consequence of the surgery.

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11
Q

Describe the operative management

A

• Operative: Mrs Cole should undergo a laparoscopic cholecystectomy to remove her inflamed gallbladder. Controversy exists over whether the best strategy is urgent laparoscopic cholecystectomy within the first 72 hours or treating the acute episode and then returning the patient for an elective chole- cystectomy 6–12 weeks later. The arguments in favour of the latter are that conversion rates from laparoscopic to open surgery are reduced. However, waiting for an elective procedure may mean that patients have repeat admis- sions in the interim – and this entails increased morbidity, expense, and lost time (for the patient).

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12
Q
Mrs Cole (from the above case) was admitted onto a surgical ward, and the admitting team opted not to perform an urgent laparoscopic cholecystectomy. During her stay in hospital for cholecystitis, Mrs Cole’s RUQ abdominal pain becomes worse. She also becomes jaundiced, her temperature rises to 40.1oC, and she starts to shake uncontrollably with rigors.
What are the complications of cholecystitis, and what has happened to Mrs Cole? How must she be managed?
A

Complications of cholecystitis include empyema (a collection of pus in the gall- bladder that will need draining), formation of a cholecystoduodenal fistula (a con- necting fistula between the gallbladder and small bowel, which allows bowel air into the gallbladder – seen on radiography – but also allows gallstones to travel into the small bowel, eventually getting stuck in the terminal ileum and causing ‘gallstone ileus’), or even gallbladder carcinoma. However, Mrs Cole has more likely devel- oped ascending cholangitis, which is characterized by Charcot’s triad of signs:
• RUQ pain
• Jaundice
• Fever with rigors

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13
Q

Describe ascending cholangitis

A

Ascending cholangitis (chole = bile, angio = vessel, -itis = inflammation) is inflam- mation of the common bile duct because of an infected stone in the common bile duct or due to spread from an infected gallbladder (cholecystitis). Inflammation in the common bile duct leads to it becoming obstructed, so that conjugated bilirubin can no longer drain through it, its build-up causing jaundice. Unlike cholecystitis, where the infection is confined to the gallbladder, in cholangitis the infection can easily spread up the common bile duct, into the liver, and thence into the systemic circulation – hence it being called ascending cholangitis. The presence of inflamma- tory markers in the systemic circulation leads to the swinging fever and rigors.

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14
Q

Describe the management of ascending cholangitis

A

Management of ascending cholangitis: ascending cholangitis is a surgical emer- gency that carries a high mortality (~10–30%) if intervention is not started early, because of the high risk of the infection spreading upwards to the liver and ulti- mately entering the circulation (sepsis). Management should include:
• Blood cultures should be taken to try and establish the identity and antibiotic sensitivities of the infective bacteria.
• Antibiotics. The patient should then be started on broad-spectrum antibio- tics (e.g. co-amoxiclav + metronidazole, but guided by local policy) until the exact antibiotic sensitivities of the bacteria are known.
• Endoscopic retrograde cholangiopancreatography (ERCP) drainage. The patient must have their blocked common bile duct physically drained via ERCP. An endoscope is passed via the oesophagus from the patient’s mouth into the duodenum. From here, a fine catheter is passed via the sphincter of Oddi and into the common bile duct, where the pus is drained and sent for culturing to determine the identity and antibiotic sensitivities of the infective
298
Right upper quadrant (RUQ) pain
Short case
Short cases 299 bacteria. ERCP carries a risk of making matters worse if the pus is accidentally
pushed upwards into the liver.
• Monitoring. Once the common bile duct has been drained, the patient is kept in hospital on antibiotics, nil by mouth, fluids (IV), and analgesia and the patient’s vital signs are monitored carefully for any signs of systemic infection (sepsis).

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15
Q

Mrs Cole mentioned in her initial history that she often suffered from a sharp, stabbing pain in her RUQ, typically a few hours after a fatty meal. The pain came and went over a period of several hours but always self-resolved within half a day.
What pathological process was Mrs Cole most likely describing?

A

Mrs Cole was probably suffering from bouts of biliary colic due to cholelithiasis (chole = bile, lithiasis = stone formation). About 20% of the population have small stones in their gallbladder, but in 90% of cases these cause no problems at all. In some people, however, the stones can irritate Hartmann’s pouch (where the gall- bladder meets the cystic duct) or the common bile duct, causing a sharp, stabbing pain which, despite being called ‘biliary colic’, is rarely a true colic (i.e. waxing and waning pain), as the pain is usually fairly constant. In most patients the gallstone eventually passes into the small bowel but in some the gallstone requires removal via ERCP.

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16
Q

Mr Goldstone is a 52-year-old restaurant manager who presents to his hospital with severe RUQ pain. The pain started a few hours after lunch and has been present since. He says that for the last month he has been suffering from a burning pain in his upper abdomen, often after meals. This time, the pain is stabbing in nature and much worse in severity. He has not opened his bowels since the pain started, about 4 hours ago. He has a past medical history of osteoarthrosis of his right hip, for which he takes regular NSAIDs (diclofenac) whilst he awaits his hip replacement. Examination reveals only a mildly ten- der RUQ. His faecal occult blood test (FOBT) is positive but his chest and abdominal radiographs are normal, with no distended bowel loops or air under the diaphragm.
What diagnosis is likely in this gentleman? How would he be investigated?

A

Mr Goldstone gives a history of upper abdominal burning pain for the last month, which is highly suggestive of a peptic ulcer (you cannot tell if it is gastric or duodenal from associations with meals and times of the day, contrary to myth). His positive FOBT suggests that blood may have entered the bowel (or that he has consumed a lot of red meat), and this combined with his more severe, stabbing pain suggests that Mr Goldstone may have developed a bleeding peptic ulcer. However, Mr Gold- stone’s age means that other causes of blood in the gut lumen (haemorrhoids, angi- odysplasia, large bowel cancer) must be considered too.
To investigate a positive FOBT, a digital rectal examination is essential, as this may reveal haemorrhoids, a rectal mass (rectal cancer?), melaena (dark tar-like stools, suggestive of an upper gastrointestinal (GI) bleed), or haematochezia (bright red stools, suggestive of a lower GI bleed). The next step would be to visualize the gut wall for sources of blood using endoscopy. An oesophagogastroduodenoscopy (OGD) will look at the oesophagus, stomach, and duodenum, whilst a colonoscopy will look at the entire colon. If both forms of endoscopy still don’t reveal the source of bleeding, one can consider looking for a bleed in the jejunum and ileum using either an abdominal computed tomography (CT) angiogram (which will only pick up relatively large bleeds), video capsule, or a red cell scan.
Mr Goldstone was admitted to hospital and underwent an OGD. This showed a bleeding duodenal ulcer just distal to the pylorus which was injected with adrena- line to stop the bleeding. Biopsies of the ulcer were positive for Helicobacter pylori but showed no signs of malignancy. Mr Goldstone went on to receive triple eradica- tion therapy for his ulcer: a PPI (e.g. omeprazole) and two antibiotics (e.g. amoxicil- lin and clarithromycin) for 1 week.

17
Q

What is biliary colic

A

Biliary colic occurs when the gallbladder attempts to contract against an obstruction – usually a gallstone at Hartmann’s pouch. At this stage the gallbladder is not inflamed or infected. Pain only lasts until the stone falls back into the gallbladder or is passed along the cystic duct and then common bile duct – but this can be anything from minutes to hours.

18
Q

What is cholecystitis

A

Cholecystitis: a significant proportion of patients presenting with biliary colic go on to develop acute chole- cystitis – at which point the gallbladder is inflamed (chole = bile, cyst = bladder, -itis = inflammation). If a stone impacts in Hartmann’s pouch or the cystic duct, the gallbladder may be full of bile that cannot escape. As water is absorbed by the gallbladder, the bile becomes very concentrated and irritates the gallbladder caus- ing a sterile, chemical cholecystitis. As the bile and gallstone cannot drain, they often become infected caus- ing an infective cholecystitis. Hence, both biliary colic and cholecystitis can be regarded as consequences of stones in the gallbladder (cholelithiasis; chole = bile, lithiasis = stone formation). Bowel rest (nil by mouth), antibiotics, and analgesia are sufficient in 90% of cases of cholecystitis, although many surgeons will opt for either urgent cholecystectomy or elective cholecystectomy at a later date to avoid repeated attacks.

19
Q

What is ascending cholangitis

A

Ascending cholangitis is usually a complication of choledocholithiasis (chole = bile, docho = duct, lithiasis = stone formation) – stone(s) in the common bile duct. These stones block the common bile duct causing jaundice, but they can also become infected by gut bacteria and the infection can spread via the liver into the circulation, causing high fever and rigors. This is the most serious presentation of gallstone disease and carries a mortality of about 15%. Ascending cholangitis may also occur if the common bile duct is blocked by a stricture (due to recent surgery) or a tumour, or if gut bacteria have been pushed up into the common bile duct by a doctor during an ERCP. Charcot’s triad of fever, RUQ pain, and jaundice is present. The patient needs urgent drainage of the common bile duct, broad-spectrum antibiotics, and careful monitoring in hospital for signs of sepsis.

20
Q

What is bile? How are bile salts conserved by the body?

A

Bile is made up of four main components:
• Water: although much of this is reabsorbed while bile is stored in the gallbladder
• Fat: mainly cholesterol and some phospholipids
• Bile salts: which serve to solubilize the fats in bile but also fats and fat-soluble vitamins (A, D, E, K) found in food
• Conjugated bilirubin: digested by gut bacteria into a brown pigment (stercobilin) which gives faeces its unique colour
Bile salts are absorbed from the terminal ileum and then travel back to the liver via the enterohepatic circula- tion. Bile salts may be recycled up to ten times each day.

21
Q

Both liver disease or a blocked common bile duct (obstructive jaundice) can cause patients to have prolonged blood clotting times, but administering parenteral (not oral) vitamin K will only correct the problem in one of the cases: which one and why?

A

Remember that the extrinsic arm of the clotting cascade, as measured by the prothrombin time (PT), relies upon the liver making clotting factors II, VII, IX, and X. This process depends on vitamin K which is fat soluble and therefore absorbed thanks to bile salts. Liver disease may result in an increased PT due to impaired syn- thesis of these clotting factors within the liver. By contrast, if the patient is suffering from a blocked common bile duct (obstructive jaundice) then there will be little or no bile salts reaching the gut and emulsifying fats. Thus there will be severely impaired vitamin K absorption from the terminal ileum, and this in turn impairs clotting factor synthesis.
An increased PT due to liver disease will not be corrected by the parenteral administration of vitamin K as the problem is the liver, not the lack of vitamin K. Conversely, parenteral vitamin K will correct a prolonged PT that is due to obstructive jaundice (because clotting factor synthesis is only being impaired by a lack of raw material – vitamin K, rather than impaired synthetic ability).

22
Q

What sorts of gallstones are there? Which groups of patients are prone to particular sorts of gallstones?

A

There are three main types of gallstones: approximately 5% are bile pigment stones, 20% are cholesterol, and 75% are mixed composition. Note that only about 10% of gallstones are radio-opaque and thus the vast majority will not show on plain abdominal radiographs. Contrast this with renal/ureteric stones, about 90% of which are radio-opaque.
Certain patients are predisposed to particular gallstones:
• Bile pigment stones: bile pigments are haemoglobin breakdown products and thus patients with haemolytic anaemias (such as hereditary spherocystosis, sickle cell disease, or G6PD deficiency) are predisposed to these sorts of stones. Long-term total parenteral nutrition (TPN) is also associated with pigment gallstone disease.
• Cholesterol stones: it is said that the classic cholesterol gallstone patient is a fair, fat, fertile female of forty (the five Fs). Some add ‘flatulent’ as a further alliterative compliment to the unfortunate patient. The use of oral contraceptive therapy further increases the risk of cholesterol stones. Patients with Crohn’s disease may suffer higher rates of cholesterol stones because the terminal ileum pathology impairs reabsorption and enterohepatic circulation of bile salts, thus making bile- based stones less likely.

23
Q

What are the potential consequences of gallstones?

A

Remember that gallstones usually cause no pathology – they may uneventfully pass down the biliary tree and then into the duodenum. Otherwise think anatomically. Stones may remain in the gallbladder and cause biliary colic, acute or chronic cholecystitis, a mucocoele (mucus-filled gallbladder), empyema (pus-filled gallbladder), or cholangiocarcinoma. Stones may pass into the common bile duct and block it (obstructive jaundice) or get infected (ascending cholangitis). If the stone travels down the common bile duct it may become lodged at the ampulla of Vater and thus cause acute pancreatitis. Lastly, the stone may cause gallstone ileus. This latter pathology causes some confusion and is worth elaborating on. When the gallbladder becomes inflamed, its neighbouring structures, namely duodenum, transverse colon, and omentum, may wrap around the gallblad- der to ‘wall off’ the inflammation. This raises the possibility of fistula formation. A stone that travels through a cholecystocolic fistula (to the large bowel) is unlikely to cause any problems, and will most likely be passed from the body with the next stool. However, if a stone passes through a cholecystoduodenal fistula (to the small bowel) it is liable to get stuck at the narrowest part of the intestinal tract – the terminal ileum. This represents a mechanical obstruction and the term ‘gallstone ileus’ is thus rather a misnomer as ileus usually refers to functional obstruction of the gut. Gallstone ileus can be diagnosed on a plain abdominal radiograph by looking for signs of small bowel obstruction, air in the biliary tree, and perhaps a stone at the terminal ileum (remembering that radio-opaque gallstones are rare).

24
Q

Explain why the consumption of fatty foods can exacerbate the pain of biliary colic and chronic cholecystitis.

A

Cholecystokinin (CCK) is released from the duodenum in response to fatty foods. CCK stimulates the secre- tion of digestive enzymes from pancreatic acinar cells, and also stimulates contraction of the gallbladder and relaxation of the sphincter of Oddi. These last two actions would release bile into the duodenum to aid with fat digestion and absorption. However, CCK-induced gallbladder contraction can exacerbate the pain of biliary colic and chronic cholecystitis. It would also accentuate the pain of acute cholecystitis, but you are unlikely to be eating if you have this disease!

25
Q

During cholecystectomy the surgeon will look for Calot’s triangle – what is it?

A

Calot’s triangle (see Fig. 15.1) is an anatomical zone used to define the usual path of the cystic artery, the cystic duct, and the common hepatic duct. It is essential to visualize and dissect this triangle during a chole- cystectomy so that one can be sure that one is ligating and cutting the cystic artery and cystic duct, and not the right hepatic artery, hepatic duct, or common bile duct. The superior border of the triangle is the liver, the inferior border is the cystic duct, and the medial border is the common hepatic duct. The cystic artery is a branch of the right hepatic artery, which usually passes behind the common hepatic duct. However, in about 25% of patients, the right hepatic artery passes in front of the common hepatic duct.

26
Q

Where would a gallstone need to be in order to cause obstructive jaundice?

A

Typically the stone would need to be in the common bile duct or the ampulla of Vater. However, it is worth remembering that a stone in Hartmann’s pouch (see Fig. 15.2) may also press extrinsically on the common bile duct (Mirizzi’s syndrome).

27
Q

What is Courvoisier’s law?

A

This ‘law’ states that if the gallbladder is palpable in the presence of jaundice then the jaundice is unlikely to be due to stones. The rationale is as follows: if the obstruction is caused by a stone in the common bile duct then the gallbladder is likely to be thickened and fibrotic (as the gallbladder is the source of the stone) and thus not distended and palpable, but rather shrivelled up. By contrast, if the common bile duct is obstructed for some other reason, such as a tumour, then the gallbladder is likely to be normal and it will dilate due to back-pressure. Note the phrasing of Courvoisier’s law – it does NOT state that if the gallbladder is not palpable then the jaundice is due to a stone. This is because it is perfectly possible for the gallbladder to be dilated (perhaps due to a distal tumour causing back-pressure of bile) but not palpable because it is obscured by the liver or layers of fat in the abdominal wall.

28
Q

What is an ERCP? What is the advantage of ERCP over MRCP? What are the complications of ERCP?

A

ERCP is endoscopic retrograde cholangiopancreatography. A side-viewing endoscope is passed via the mouth, past the oesophagogastric junction and pylorus, and down to the second part of the duodenum. At this point a fine catheter emerges from the endoscope and is passed through the duodenal papilla and into the ampulla of Vater. It is possible to inject contrast medium directly into the biliary tree, which is then visual- ized radiographically.
MRCP is magnetic resonance cholangiopancreatography. It enables detailed visualization of the biliary tree, but is purely a diagnostic procedure. ERCP has a therapeutic role as it is possible to both remove stones (using a Dormia basket) and perform endoscopic sphincterotomy (cutting the sphincter of Oddi with a fine diathermy wire in order to facilitate the passage of any stones within the common bile duct).
Aside from being a rather unpleasant procedure to undergo, the risks of ERCP include bleeding, perfora- tion of the biliary tree, cholangitis, and pancreatitis. There is about a 1–3% risk of pancreatitis and, for rea- sons that are not entirely clear, this pancreatitis carries a 20% mortality risk (which is higher than normal for pancreatitis).