Mirizzi syndrome is defined as common hepatic duct obstruction caused by extrinsic compression from an impacted stone in the cystic duct or infundibulum of the gallbladder. Patients with Mirizzi syndrome can present with jaundice, fever, and right upper quadrant pain. Mirizzi syndrome is often not recognized preoperatively in patients undergoing cholecystectomy and can lead to significant morbidity and biliary injury, particularly with laparoscopic surgery. Acute presentations of the syndrome include symptoms consistent with cholecystitis.
Surgery is extremely difficult as Calot’s triangle is often completely obliterated and the risks of causing injury to the common bile duct (CBD) are high.
Multiple and large gallstones can become impacted in the Hartmann’s pouch of the gallbladder, leading to chronic inflammation – which leads to compression of the CBD, necrosis, fibrosis, and ultimately fistula formation into the adjacent common hepatic duct (CHD). As a result, the CHD/CBD becomes obstructed by either scar or stone, resulting in obstructive jaundice. It can be divided into four types.
Type I – No fistula present
Type IA – Presence of the cystic duct
Type IB – Obliteration of the cystic duct
Types II–IV – Fistula present
Type II – Defect smaller than 33% of the CHD diameter
Type III – Defect 33–66% of the CHD diameter
Type IV – Defect larger than 66% of the CHD diameter

Simple cholecystectomy is suitable for type I patients. For types II–IV, subtotal cholecystectomy can be performed to avoid damage to the main bile ducts. Cholecystectomy and bilioenteric anastomosis may be required. Roux-en-Y hepaticojejunostomy has shown good outcome in some studies.

In most cases, the treatment of choice for acute cholecystitis is cholecystectomy performed early in the illness. The procedure can be carried out laparoscopically even when acute inflammation is present. Delayed surgery particularly around five to seven days after presentation is much more technically challenging and is often best deferred.

Up to 24% of women and 12% of men may have gallstones. Of these, up to 30% may develop local infection and cholecystitis. The classical symptom of cholecystitis is colicky right upper quadrant pain that occurs postprandially. Others include swinging pyrexia, and general feeling of being unwell. They are usually worst following a fatty meal when cholecystokinin levels are highest and gallbladder contraction is maximal.

Murphy’s sign is positive on examination. The standard diagnostic work-up consists of abdominal ultrasound and liver function tests. For management, cholecystectomy should ideally be done within 48 hours of presentation. In patients unfit for surgery, percutaneous drainage may be considered.

Pancreatitis is inflammation of the pancreas with variable involvement of regional tissues or remote organ systems. Acute pancreatitis (AP) is characterized by severe pain in the upper abdomen and elevation of pancreatic enzymes in the blood. In the majority of patients,
Biliary pancreatitis should always be treated eventually with a cholecystectomy after the process has subsided.
Feeding should be introduced enterally as the patient’s anorexia and pain resolves.
The use of nasogastric aspiration offers no clear advantage in patients with mild AP, but is beneficial in patients with profound pain, severe disease, paralytic ileus, and intractable vomiting.
AP is a mild, self-limiting disease that resolves spontaneously without complications. Patients can be initiated on a low-fat diet initially and need not invariably start their dietary advancement using a clear liquid diet. Systematic reviews and meta-analyses have shown that administration of enteral nutrition may reduce mortality and infectious complications compared with parenteral nutrition. Although the ideal timing to initiate enteral feeding remains undetermined, administration within 48 hours appears to be safe and tolerated.

This individual has acute cholecystitis. This is demonstrated by well-localized pain in the right upper quadrant, usually with rebound and guarding; frequent presence of fever and peritonism. Ultrasonography is the procedure of choice in suspected gallbladder or biliary disease. A bile duct measuring 4mm is usually normal.
Once gallstones become symptomatic, definitive surgical intervention with cholecystectomy is usually indicated (typically, laparoscopic cholecystectomy is the first-line therapy at centres with experience in this procedure).

Advances in endoscopy have suggested wider use of ERCP, which in the past was mostly restricted to the treatment of biliary fistulas and to patients with associated medical disease. Several series in literature demonstrate that ERCP with stenting for major bile duct injuries in the form of incomplete strictures has comparable efficacy with surgery and lower rates of morbidity and mortality, but few give long-term results.

Bile duct injuries (BDI) can occur after many abdominal operations, e.g. liver surgery, gastrectomy, common bile duct (CBD) exploration. However, the majority of postoperative bile duct injuries (POBDI) occur during open or laparoscopic cholecystectomy. Despite increasing experience with laparoscopy, a review of 1.6 million cholecystectomies demonstrated an unchanging 0.5% incidence of bile duct injury, reported after many days post operation, of abdominal pain, bile leak, jaundice or cholangitis. Only 30% of injuries are recognized at the time of operation.
Bile duct injuries, particularly strictures, have traditionally been managed by surgical reconstruction (Roux-en-Y hepaticojejunostomy). The reported occurrence of symptomatic anastomotic strictures after long-term follow-up of surgical reconstruction ranges from 9-25 %. Surgery is definitely associated with significant morbidity and mortality. Endoscopic treatment has demonstrated results comparable to those achieved with surgery, with lower morbidity and mortality.

A CT scan with IV contrast is needed because a scan without contrast will exclude a perforated viscus but will not be able to determine the presence of pancreatitis.

Acute pancreatitis may be mild or life-threatening but it usually subsides. Gallstones and alcohol abuse are the main causes of acute pancreatitis. Severe abdominal pain is the predominant symptom.

For diagnosis of acute pancreatitis, serum lipase is both more sensitive and specific than serum amylase.
Serum amylase levels do not correlate with disease severity and may give both false positive and negative results. Three scoring systems are used to assess the severity of the disease, which are Glasgow pancreatitis score, Ranson criteria, and APACHE II scoring system.

Management options are as follows:
1. There is very little evidence to support the administration of antibiotics to patients with acute pancreatitis. These may contribute to antibiotic resistance and increase the risks of antibiotic-associated diarrhoea.
2. Patients with acute pancreatitis due to gallstones should undergo early cholecystectomy.
3. Patients with obstructed biliary system due to stones should undergo early ERCP.
4. Patients with infected necrosis should undergo either radiological drainage or surgical necrosectomy.

A pancreatic pseudocyst is a circumscribed collection of fluid rich in pancreatic enzymes, blood, and necrotic tissue, typically located in the lesser sac of the abdomen. Pancreatic pseudocysts are usually complications of pancreatitis, although in children they frequently occur following abdominal trauma. Pancreatic pseudocysts account for approximately 75% of all pancreatic masses.
Signs and symptoms of pancreatic pseudocyst include abdominal discomfort and indigestion.

Diagnosis of Pancreatic pseudocyst can be based on cyst fluid analysis:
Carcinoembryonic antigen (CEA) and CEA-125 (low in pseudocysts and elevated in tumours);
Fluid viscosity (low in pseudocysts and elevated in tumours);
Amylase (usually high in pseudocysts and low in tumours)

The most useful imaging tools are:

-Ultrasonography – the role of ultrasonography in imaging the pancreas is limited by patient habitus, operator experience and the fact that the pancreas lies behind the stomach (and so a gas-filled stomach will obscure the pancreas).
-Computerized tomography – this is the gold standard for initial assessment and follow-up.
-Magnetic resonance cholangiopancreatography (MRCP) – to establish the relationship of the pseudocyst to the pancreatic ducts, though not routinely used.

Acute cholangitis is a bacterial infection superimposed on an obstruction of the biliary tree most commonly from a gallstone, but it may be associated with neoplasm or stricture. The classic triad of findings is right upper quadrant (RUQ) pain, fever, and jaundice. A pentad may also be seen, in which mental status changes and sepsis are added to the triad.

A spectrum of cholangitis exists, ranging from mild symptoms to fulminant overwhelming sepsis. Thus, therapeutic options for patient management include broad-spectrum antibiotics and, potentially, emergency decompression of the biliary tree.
The main factors in the pathogenesis of acute cholangitis are biliary tract obstruction, elevated intraluminal pressure, and infection of bile. A biliary system that is colonized by bacteria but is unobstructed, typically does not result in cholangitis. It is believed that biliary obstruction diminishes host antibacterial defences, causes immune dysfunction, and subsequently increases small bowel bacterial colonization. Although the exact mechanism is unclear, it is believed that bacteria gain access to the biliary tree by retrograde ascent from the duodenum or from portal venous blood. As a result, infection ascends into the hepatic ducts, causing serious infection. Increased biliary pressure pushes the infection into the biliary canaliculi, hepatic veins, and perihepatic lymphatics, leading to bacteraemia (25-40%). The infection can be suppurative in the biliary tract.

Gallstone ileus accounts for 1-4% of all small bowel obstructions, predominantly affecting elderly females. This entity is associated with a mortality approaching 20% due to the associated comorbidities that are often present.
Principles of treatment include stone removal via enterotomy through a site proximal to that of the obstruction.
Decompression using a sucking apparatus with many large openings, inserted through an enterotomy, is a fast and suitable method. The danger of wound infection can be considerably reduced by careful technique and by antibiotics. Nevertheless, open suction should be used only when the peritoneal cavity is already infected, or when closed decompression by retrograde stripping into the stomach is not possible.

Acute pancreatitis is an inflammatory condition of the pancreas most commonly caused by biliary tract disease or alcohol abuse. Damage to the pancreas causes local release of digestive proteolytic enzymes that autodigest pancreatic tissue. Acute pancreatitis usually presents with epigastric pain radiating to the back, nausea and vomiting, and epigastric tenderness on palpation. The diagnosis is made based on the clinical presentation, elevated serum pancreatic enzymes, and findings on imaging (CT, MRI, ultrasound) that suggest acute pancreatitis. Treatment is mostly supportive and includes bowel rest, fluid resuscitation, and pain medication. Enteral feeding is usually quickly resumed once the pain and inflammatory markers begin to subside. Interventional procedures may be indicated for the treatment of underlying conditions, such as ERCP or cholecystectomy in gallstone pancreatitis. Localized complications of pancreatitis include necrosis, pancreatic pseudocysts, and abscesses. Systemic complications involve sepsis, ARDS, organ failure, and shock and are associated with a considerable rise in mortality.

The Ranson score is used to predict the severity of acute pancreatitis:
At admission
age in years > 55 years
white blood cell count > 16000 cells/mm3
blood glucose > 11.1 mmol/L (> 200 mg/dL)
serum AST > 250 IU/L
serum LDH > 350 IU/L

At 48 hours
Calcium (serum calcium < 2.0 mmol/L (< 8.0 mg/dL)
Haematocrit fall >10%
Oxygen (hypoxemia PO2 < 60 mmHg)
BUN increased by 1.8 or more mmol/L (5 or more mg/dL) after IV fluid hydration
Base deficit (negative base excess) > 4 mEq/L
Sequestration of fluids > 6 L

Interpretation If the score ≥ 3, severe pancreatitis likely. If the score < 3, severe pancreatitis is unlikely Or Score 0 to 2 : 2% mortality Score 3 to 4 : 15% mortality Score 5 to 6 : 40% mortality Score 7 to 8 : 100% mortality

In patients with liver tumours, it is crucial to detect and stage the tumours at an early stage (to select patients who will benefit from curative liver resection, and avoid unnecessary surgery). Therefore, an optimal preoperative evaluation of the liver is necessary, and a contrast-enhanced MRI is widely considered the state-of-the-art method. Liver MRI without contrast administration is appropriate for cholelithiasis but not sufficient for most liver tumour diagnoses.

ERCP serves as a primary therapeutic modality for management of biliary pancreatitis in specific situations: pancreatitis due to microlithiasis, specific types of sphincter of Oddi dysfunction, pancreas divisum, ascariasis and malignancy. It is important that her coagulation status is normalized prior to performing this procedure.

Chronic cholecystitis can be a surgical challenge due to an inflammatory process that creates multiple adhesions, complicates dissection, and can hamper recognition of normal anatomical structures. In such cases cholecystostomy can be performed in order to alleviate the acute symptoms. Tube cholecystostomy allows for resolution of sepsis and delay of definitive surgery. Interval laparoscopic cholecystectomy can be safely performed once sepsis and acute infection has resolved.

Mirizzi’s syndrome is a rare complication in which a gallstone becomes impacted in the cystic duct or neck of the gallbladder causing compression of the common hepatic duct, resulting in obstruction and jaundice. The obstructive jaundice can be caused by direct extrinsic compression by the stone or from fibrosis caused by chronic cholecystitis (inflammation).

Type I – No fistula present

Type IA – Presence of the cystic duct
Type IB – Obliteration of the cystic duct

Types II–IV – Fistula present

Type II – Defect smaller than 33% of the CHD diameter
Type III – Defect 33–66% of the CHD diameter
Type IV – Defect larger than 66% of the CHD diameter

Simple cholecystectomy is suitable for type I patients. This patient has type I because no fistula is present.

In patients with suspected gallstone complications, blood tests should include a complete blood cell (CBC) count with differential, liver function panel, and amylase and lipase. Up to 24% of women and 12% of men may have gallstones. Of these up to 30% may develop local infection and cholecystitis.

Acute cholecystitis is associated with polymorphonuclear leucocytosis. However, up to one third of the patients with cholecystitis may not manifest leucocytosis. In severe cases, mild elevations of liver enzymes may be caused by inflammatory injury of the adjacent liver.

Patients with cholangitis and pancreatitis have abnormal laboratory test values. Importantly, a single abnormal laboratory value does not confirm the diagnosis of choledocholithiasis, cholangitis, or pancreatitis; rather, a coherent set of laboratory studies leads to the correct diagnosis.

Choledocholithiasis with acute common bile duct (CBD) obstruction initially produces an acute increase in the level of liver transaminases (alanine and aspartate aminotransferases), followed within hours by a rising serum bilirubin level. The higher the bilirubin level, the greater the predictive value for CBD obstruction. CBD stones are present in approximately 60% of patients with serum bilirubin levels greater than 3 mg/dL.

If obstruction persists, a progressive decline in the level of transaminases with rising alkaline phosphatase and bilirubin levels may be noted over several days. Prothrombin time may be elevated in patients with prolonged CBD obstruction, secondary to depletion of vitamin K (the absorption of which is bile-dependent). Concurrent obstruction of the pancreatic duct by a stone in the ampulla of Vater may be accompanied by increases in serum lipase and amylase levels.

Repeated testing over hours to days may be useful in evaluating patients with gallstone complications. Improvement of the levels of bilirubin and liver enzymes may indicate spontaneous passage of an obstructing stone. Conversely, rising levels of bilirubin and transaminases with progression of leucocytosis in the face of antibiotic therapy may indicate ascending cholangitis with the need for urgent intervention. Blood culture results are positive in 30%-60% of patients with cholangitis.

Ileal resection may lead to bile acid malabsorption and an altered biliary lipid composition. A “bile acid deficiency” in the enterohepatic circulation with a relative excess of cholesterol and cholesterol supersaturated bile might ensue, causing cholesterol gallstone formation.

In patients with Crohn’s disease involving the small
intestine, the prevalence of gall-bladder stones is higher
than that in the general population. One hypothesis
for this increased risk is that bile acid malabsorption,
secondary to impaired active bile acid transport as a
consequence of ileal disease/resection, leads to a
reduction in the total bile acid pool size and an increase
in biliary cholesterol saturation. In patients with
ulcerative or Crohn’s colitis, or who have undergone
colectomy, the bile acid malabsorption is less than that
in those with ileal dysfunction or resection, but the risk
of gallstone formation is still increased, allegedly by the
same mechanism.

ERCP is a highly sensitive means of detecting pancreatic and/or biliary ductal abnormalities in pancreatic carcinoma. Among patients with pancreatic adenocarcinoma, 90-95% have abnormalities on ERCP findings.
ERCP is more invasive than the other diagnostic imaging modalities available for pancreatic carcinoma. ERCP also carries a 5-10% risk of significant complications. Because of this morbidity, it is usually reserved as a therapeutic procedure for biliary obstruction or for the diagnosis of unusual pancreatic neoplasms, such as intraductal pancreatic mucinous neoplasms (IPMN).
ERCP findings provide only limited staging information, but ERCP does have the advantage of allowing for therapeutic palliation of obstructive jaundice with either a plastic or metal biliary stent.

Complications of ERCP include pancreatitis, duodenal perforation, duodenal haemorrhage, infection, stent migration, and complications secondary to endoscopy. CT is performed if patients have severe abdominal pain, jaundice, elevated white blood cell count, and fever after ERCP.

A cavernous liver haemangioma or hepatic haemangioma is a benign tumour of the liver composed of hepatic endothelial cells. It is the most common liver tumour, and is usually asymptomatic and diagnosed incidentally on radiological imaging. Liver haemangiomas are thought to be congenital in origin. Several subtypes exist, including the giant hepatic haemangioma, which can cause significant complications. This large, atypical haemangioma of the liver may present with abdominal pain or fullness due to haemorrhage, thrombosis or mass effect. It may also lead to left ventricular volume overload and heart failure due to the increase in cardiac output which it causes. Further complications are Kasabach-Merritt syndrome, a form of consumptive coagulopathy due to thrombocytopaenia, and rupture.

As one of the benign neoplasms, the AFP level of hepatic cavernous haemangioma patients is not usually outside the normal range.