Hepatobiliary Flashcards
- What is biliary colic?
Biliary colic is an acute abdominal pain caused by a transient obstruction of the gallbladder (usually by a gallstone in Hartmann’s pouch or the cystic duct and rarely due to a stricture or tumor.)
The pain presents severely in the RUQ or epigastric region and is not a true colic due to the typical pain pattern of rising to a plateau and then being continuous in nature.
It typically radiates as a band across the upper abdomen and to the inferior angle of the right scapula and it is associated with nausea, vomitting and sweating.
The pain occurs when the gall bladder attempts to contract against the obstruction and this contraction is stimulated further by CholeCystoKinin from the duodenum post prandially, especially with fatty food.
Investigations and Management:
• Blood tests (FBC, UEC, CRP, LFTs, Lipase)
• Abdominal USS – stones or sludge
• Analgesia (opioid drugs e.g. morphine or fentanyl)
• Nil by mouth
• NSAIDs and antispasmodics may also be helpful
• IV fluid resuscitation
• Cholecystectomy should be considered
Complications:
• Acute cholecystitis or chronic cholecystitis
• Acute pancreatitis
• Ascending cholangitis
• Mucocoele or empyema formation
• Carcinoma of the gallbladder
• Rarely – perforation or fistula formation
- What causes cholangitis?
Cholangitisis an infection of the biliary tract. It is caused by obstruction of the biliary tree, which may lead to bile stasis and subsequent bacterial infection. Clinically it is characterized by the Charcot triad, which consists of abdominal pain, fever, and jaundice, although jaundice is not always present. Sepsis and septic shock may develop as a complication of acute cholangitis.
• Cholangitis can be caused by - E coli, Klebsiella, Proteus, Enterobacter, Citrobacter infecting the biliary tract in cases of: o Choledocholithiasis o Surgical injury causing strictures o ERCP introduced gut bacteria o Biliary tumours o Radiation induced biliary injury
- What are the clinical features of cholangitis?
Charcots triad- RUQ pain, jaundice and fevers with rigors.
Reynolds pentad- charcots triad + shock (tachy and hypotension) + altered mental status.
Other clinical features include pale stool and pruritus.
Dx: - Requires evidence of inflammation + bile duct obstruction o Inflammation: Fever, leucocytosis, elevated CRP o Obstruction: Elevated liver enzymes USS/CT – dilation of CBD, gallstones
Mx:
- Initial resuscitation
o NBM, IV Fluids, Indwelling catheter (input/output),
Analgesia (opiates, NSAIDs)
- Initiate sepsis pathway as required
- Mx Infection:
o IV Abx – Ampicillin and Gentamicin - Mx obstruction:
o Urgent decompression
ERCP (within 24-48h) +/- sphincterotomy +/- biliary stone removal
Percutaneous transhepatic cholangiography (PTC)
Endoscopic ultrasound guided (EUS) drainage
Open surgical drainage
- Mx underlying cause:
o E.g. cholecystectomy, biliary stent
- What is cholecystitis?
Cholecystitis is inflammation of the gallbladder that most commonly occurs after cystic duct obstruction from cholelithiasis. This is known as calculous cholecystitis.
Acalculous cholecystitis is less common and seen primarily in critically ill patients.
The acute inflammation in cholecystitis is due to the increased intraluminal pressure and irritation from supersaturated bile.
Acute cholecystitis is suspected based on symptoms and signs.
The pain of cholecystitis is similar in quality and location to biliary colic but lasts longer (ie, > 6 h) and is more severe.
Vomiting is common, as is right subcostal tenderness. Within a few hours, the Murphy sign (deep inspiration exacerbates the pain during palpation of the right upper quadrant and halts inspiration) develops along with involuntary guarding of upper abdominal muscles on the right side. Fever, usually low grade, is common.
INVESTIGATIONS?
Transabdominal ultrasonography is the best test to detect gallstones. The test may also elicit local abdominal tenderness over the gallbladder (ultrasonographic Murphy sign). Pericholecystic fluid or thickening of the gallbladder wall indicates acute inflammation.
TREATMENTS?
Conservative Tx= NBM, IV fluids, analgesia (opiates, NSAIDs), IV ABx= ampicilin and gentamicin. ongoing low fat diet.
Surgical Tx= cholecystectomy, OR percutaneous cholecystectomy if pt has contraindications.
COMPLICATIONS?
- gangrenous cholecystitis (2-30%)- fundus as vascular supply compromised
- perforation (10%)- most common @ fundus. transient relief followed by peritonitis.
- cholecysto-enteric fistulas- most common to duodenum and hepatic flexure
- gallstone ileus- obstruction of distal ileum due to gallstone that has passed via a fistula- occurs more in elderly and presents as unexplained intermittent small bowel obs. AXR will show pneumobilia, intestinal obs and gallstone in unusual site.
- What techniques are available for treating common bile duct stones? Describe the technique briefly.
The techniques used to treat choledocolithiasis include:
- Endoscopic Retrograde Cholangio-Pancreatography (ERCP)
- LAPAROSCOPIC CBD EXPLORATION
- OPEN CBD EXPLORATION
ERCP involves sedating the patient and inserting a side viewing endoscope that is able to visualise the duodenal papilla. A small canula is then introduced into the biliary system and radiographic contrast is used to visualise the anatomy with fluoroscopy.
Interventions such as sphincterotomy, papillary balloon dilation, lithotripsy and stone collection via balloon and basket retrieval can also be done as part of ERCP to remove the stone.
In the laparoscopic approach basket retrieval can be done in 2 ways. trans cystic which is via the cystic duct and the transductal which is done via a choledochotomy.Unlike the transcystic approach, however, the choledochotomy allows the choledochoscope to be inserted retrograde into the common hepatic duct and right/left hepatic ducts, as well as anterograde into the common bile duct. A wire basket can be deployed via the operating channel of the choledochoscope to retrieve any stone in the entire biliary tree.
Open stone retrieval involves manual manipulation of the CBD. If this is not successful, balloon extraction can be performed and if this is unsuccessful choledochoscopy with wire basket retrieval is performed.
- What are the potential complications of ERCP?
The General complications include;
- anesthetic complications
- contrast allergy
- cardio respiratory issues (aspirations, pneumonia,MI)
- post operative nausea and vomitting
- pain
Complications specific to ERCP include:
- pancreatitis- can be due to injection of contrast up pancreatic duct and/or irritation of mucosa at the ampulla causing edema and obstruction.
- bleeding- from sphincterotomy or injury from instruments
- perforation- of oesophagus/stomach/duodenu/jejunum from endoscope OR CBD perforation from instrument.
- Infection- more specifically cholangitis- this can be due to the introduction of gut bacteria
- stricture formation due to inflammatory fibrosis and future stone recurrence
- What are the symptoms of biliary colic?
How can it be differentiated from acute cholecystitis clinically?
Symptoms of bilary colic include;
- RUQ/epigastric pain
- radiation to the right back inferior scapular
- diaphoresis
- N&V
- lasts less than 6 hours with no fever and peritoneal signs
- pain increases but plateaus
Acute cholecystitis can be differentiate clinically from biliary colic as it presents with :
- a fever
- peritoneal signs such as involuntary guarding
- positive murphys sign as opposed to biliary colic where there is no murphys sign because there is no gall bladder inflammation
- leukocytosis
- What are the common causes of painless obstructive jaundice in a 65yo person?
Painless obstructive jaundice is a hallmark of pancreatic cancer, yet several clinical and diagnostic features must be kept in mind. This is a cancer of the head of the pancreas that compresses on the CBD and causes obstructive jaundice.
Other differentials can include:
- choledocolithiasis that can present with a history of biliary colic but non tender gall bladder and progressive jaundice if the stone is impacted or fluctuant if the stone is mobile.
- cholangiocarcinoma- adenocarcinoma of biliary duct
- mets from another GIT cancer
some uncommon causes include;
- pancreatitis
- Mirizzi syndrome- gallstone in hartmanns pouch causing inflammation of gallbladder and extrinsic compression of an extrahepatic biliary duct
- peri-ampullary malignant tumors
- strictures of the common bile duct
- How might a person with pancreatic cancer present to their GP?
Common presenting features include;
- an age of onset between 60-80
- presence of risk factors (smoking, chronic pancreatitis, high alcohol consumption, obesity, T2D)
- belt shaped epigastric pain which radiates to the back
- Courvoisier sign- enlarged gall bladder and painless jaundice
- diarrhea (possible steatorrhea secondary to exocrine pancreatic insufficiency)
- thrombosis of unknown origin
- weight loss and anorexia
- fatigue and weakness
- nausea and vomiting
- Why does a tumour of the head of the pancreas cause jaundice? AND
What are the haematological consequences of biliary obstruction?
The common bile duct (CBD) passes through the head of the pancreas to join with the pancreatic duct before entering the duodenum.
A tumour of the head of the pancreas will cause extrinsic compression of the CBD, leading to obstruction of flow into the duodenum, backflow into the biliary system and leakage of conjugated bilirubin through tight junction between hepatocytes into the blood. Alternatively metastatic lymphadenopathy of the porta hepatis may also result in biliary obstruction. Jaundice is caused by elevated levels of bilirubin in the blood – for jaundice to be visible serum bilirubin needs to be > 30μmol/L (normal range is 3-17μmol/L)
Haematological consequences:
- Elevated conjugated bilirubin (>50%)
- Obstructive LFT pattern (elevated ALP and GGT, with smaller elevation of AST and ALT, GGT increase occurs earlier and persists longer)
- Hypercholesterolaemia (normally excreted in bile but now back flows into serum level)
- Prolonged Prothrombin Time (PT) due to malabsorption of vitamin K and other fat soluble vitamins (ADEK)
- Why or how do gallstones cause pancreatitis?
Small gallstones (<5mm) have the propensity to pass through the cystic duct and CBD and get lodged at the ampulla of Vater.
This leads to obstruction of the pancreatinc duct and prevents exocrine pancreatic excretion into the duodenum and also allows for reflux of bile into the pancreatic duct.
The onset of pancreatitis is due to inappropriate activation of pancreatic enzymes and autodigestion of the pancreas.
There are many pancreatic enzymes secreted but trypsinogen triggers a cascade of activation when it is activated by enterokinase in the duodenum to become trypsin. In the case of obstruction there is failure of the normal inhibitory processes that prevents trypsinogen from spontaneously activating to trypsin and this leads to activation of all the enzymes and subsequently autodigestion of the pancreas.
Once the autodigestion process is initiated the inflammatory process leads to:
- oedema, haemorrhage and eventually necrosis if left untreated
- cytokine production which leads to systemic inflammatory response syndrome (SIRS) and potentially acute respiratory distress syndrome (ARDS) and disseminated intravascular coagulation (DIC).
- the third space fluid losses can lead to renal failure if left untreated.
- What are the common causes of pancreatitis?
I- idiopathic (10-20%0
G- gallstones (35-40%)
E- ethanol (30%)
T- trauma
S- steroids
M- mumps and malignancy and other viruses
A- autoimmune (rare)
S- scorpion venom (rare)
H- hypertriglyceridaemia (1-4%) MORE SO PREGNANCY hypercalcemia, hyperlipidemia, hypothermia
E- ERCP (2-3%)
D- drugs (<1.5%) - FANS- frusemide, azathioprine, NSAIDs, steroids
- How do you assess the severity of an episode of pancreatitis when the patient is first being admitted to hospital?
Severity is an important indicator of mortality and facilitates management decisions.
There are several scoring systems available to predict which patients will develop severe disease, including the Ranson criteria, modified Glasgow scores, Balthazar system and the Revised Atlanta severity criteria.
These scoring system rely on clinical and laboratory findings to provide early warning of severity and indicate prognosis.
The revised atlanta score categorises severity into the following groups:
●Mild acute pancreatitis, which is characterized by the absence of organ failure and local or systemic complications
●Moderately severe acute pancreatitis, which is characterized by no organ failure or transient organ failure (<48 hours) and/or local complications
●Severe acute pancreatitis, which is characterized by persistent organ failure (>48 hours) that may involve one or multiple organs
At initial evaluation, the severity of acute pancreatitis should be assessed by clinical examination to assess for early fluid losses, organ failure (particularly cardiovascular, respiratory, or renal compromise), measurement of the systemic inflammatory response syndrome (SIRS) score.
A complete metabolic panel, serum calcium, complete blood count, serum triglycerides and lactate are all useful investigations to assess severity. Although measurement of serum amylase and lipase is useful for diagnosis of pancreatitis, serial measurements in patients with acute pancreatitis are not useful to predict disease severity, prognosis, or for altering management.
- What is the initial management of pancreatitis?
Start by assessing the patient’s need for resuscitation- ABCDE.
If the pt is stable the next step consists of supportive care with aggressive fluid resuscitation and regular assessments, pain control, and nutritional support.
Attention to adequate fluid resuscitation should be the first priority in addressing abdominal pain, as hypovolemia from vascular leak and hemoconcentration can cause ischemic pain and resultant lactic acidosis. Adequate pain control requires the use of intravenous opiates.
Patients with mild pancreatitis can often be managed with intravenous hydration alone since recovery occurs rapidly, allowing patients to resume an oral diet within a week. Nutritional support is often required in patients with moderately severe pancreatitis and almost invariably needed in patients with severe pancreatitis as they are unlikely to resume oral intake within five to seven days.
Nasojejunal tube feeding (using an elemental or semi-elemental formula) is preferred to total parenteral nutrition (TPN).
Prophylactic antibiotics are not recommended in patients with acute pancreatitis, regardless of the type or severity. Abx would only be needed if pt deteriorates and is septic or there is suspicion for infected necrotitis.
Patients with acute pancreatitis should be monitored closely in the first 24 to 48 hours. Patients with organ failure will need ongoing monitoring for other complications that might arise.
Vital signs, especially oxygen saturation should be monitored and supplemental oxygen administered to maintain arterial oxygen saturation of greater than 95 percent.
Urine output, electrolytes, serum glucose levels should all be closely monitored. Patients that are severe should be be managed in the intensive care unit and should be monitored for potential abdominal compartment syndrome with serial measures of urinary bladder pressures. Any further complications that arise should be managed and any appropriate consult with gastroenterolgy, surgery or other specialties should be considered.
- What are the potential late complications of severe, acute pancreatitis, late being 2 or 3 weeks after the start of the episode?
Late complications include:
- pancreatic insufficiency (malabsorption and DM)
- chronic pancreatitis
- pancreatic pseudocyt formation
- splanchnic venous ( unusual manifestation of venous thromboembolism which involves one or more abdominal veins (portal, splenic, mesenteric and supra-hepatic veins)
- enteric fistulas
- intestinal obstructions- (mechanical obstruction by inflamed pancreas, pericolitis or mesenteric throbosis due to inflammatory state.)
- walled off pancreatic necrosis
- pancreatic ascites
Infected pancreatic necrosis, ARDS, DIC and GIT bleeding are complications that can present both early and late.
