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.

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 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.

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.

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.

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.

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.

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.

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.