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.

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.

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.

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.

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.

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).

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.

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.

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.

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.