gastro 3 Flashcards
what is biliary colic?
caused by gallstones passing through the biliary tree
what can gallstones cause?
gallstones can cause a spectrum of disease, from biliary colic to acute pancreatitis depending on the region of the biliary system involved.
what causes gallstones?
Bile is formed from cholesterol, phospholipids, and bile pigments (products of haemoglobin metabolism). It is stored in the gallbladder, before passing into the duodenum upon gallbladder stimulation.
Gallstones form as a result of supersaturation of the bile. There are three main types of gallstones:
Cholesterol stones – composed purely of cholesterol, from excess cholesterol production
There is a well recognised link between poor diet, obesity, and cholesterol stones
Pigment stones – composed purely of bile pigments, from excess bile pigments production
Commonly seen in those with known haemolytic anaemia
Mixed stones – comprised of both cholesterol and bile pigments
the stones lead to biliary stasis
what are the risk factors for gallstones?
traditionally the 5F’s
Fat - obesity is thought to be a risk factor due to enhanced cholesterol synthesis and secretion
Female - gallstones are 2-3 more likely in women. Oestrogen causes more cholesterol to be secreted into bile.
Fertile - pregnancy is a risk factor
Forty
Family history
other risk factors including: diabetes crohn's rapid weight loss e.g. weight loss reduction surgery drugs: fibrates, COCP
what are the clinical features of biliary colic ?
biliary colic occurs when the gallbladder neck becomes impacted by a gallstone. There is no inflammatory response, yet the contraction of the gallbladder against the occluded neck will result in pain
sudden, dull and colicky pain
RUQ pain but may radiate to epigastrium or back
the pain may be precipitated by consumption of fatty foods
nausea and vomiting
what is acute cholecystitis?
Acute cholecystitis describes inflammation of the gallbladder
develops secondary to gallstones in 90% of patients - acute calculous cholecystitis
the remaining 10% of cases are referred to as acalculous cholecystiti
what are the features of acute cholecystitis?
Right upper quadrant pain
May radiate to the right shoulder
Fever and signs of systemic upset
Murphy’s sign on examination: inspiratory arrest upon palpation of the right upper quadrant
Liver function tests are typically normal
Deranged LFTs may indicate Mirizzi syndrome - a gallstone impacted in the distal cystic duct causing extrinsic compression of the common bile duct
what is murphy’s sign?
Whilst applying pressure in the RUQ, ask the patient to inspire. Murphy’s sign is positive when there is a halt in inspiration due to pain, indicating an inflamed gallbladder. This can be achieved more accurately with an ultrasound, namely the sonographic Murphy sign.
what investigations would you perform for gallstones?
LFTs
FBC - elevated WBC suggestions inflammation from a complication of the gallstone
serum lipase and amylase - acute pancreatitis
abdominal USS - will show the stones, gallbladder wall will be thickened if there is inflammation, bile duct dilatation indicates possible stones in duct
*if USS inconclusive MRCP - magnetic resonance cholangiopsncreatography
what is another word for gallstones?
cholelithiasis
how do you manage biliary colic?
pain relief - paracetamol +/- NSAIDs +/- opiates analgesia
elective laparoscopic cholecystectomy within 6 weeks of first presentation
lifestyle factos - low fat diet, weight loss, exercise
what investigations would you perform for acute cholecystitis?
CT or MRI of abdomen - if sepsis is suspected request contrast enhanced CT or MRI abdominal USS FBC CRP bilirubin LFTs serum lipase or amylase blood cultures and/or bile cultures
how do you manage acute cholecystitis?
analgesia and antiemetics
fluid resus
antibiotic therapy such as co-amoxiclav +/- metronidazole
early laparoscopic cholecystectomy or percutaneous cholecystostomy for those not fit for surgery and not responding to antibiotics
what are the complications of gallstones?
Mirizzi Syndrome - A stone located in Hartmanns pouch (an out-pouching of the gallbladder wall at the junction with the cystic duct) or in the cystic duct itself can cause compression on the adjacent common hepatic duct. This results in an obstructive jaundice, even without stones being present within the lumen of the common hepatic or common bile ducts. Diagnosis is confirmed by MRCP and management is usually with laparoscopic cholecystectomy.
Gallbladder Empyema - A gallbladder empyema is when the gallbladder becomes filled with pus. Patients will become unwell, often septic, presenting with a similar clinical picture to acute cholecystitis. They are associated with significant morbidity and mortality. The condition is diagnosed by either US scan or CT scan. Treatment is via laparoscopic cholecystectomy (may require intra-operative drainage if tense gallbladder) or percutaneous cholecystostomy (if unsuitable for surgery).
Chronic Cholecystitis- Patients with chronic cholecystitis will typically have a history of recurrent or untreated cholecystitis, which has led to a persistent inflammation of the gallbladder wall. Patients present with ongoing RUQ or epigastric pain with associated nausea and vomiting. It can be diagnosed typically by CT imaging (or often noted on histology post-cholecystectomy). Management in uncomplicated cases is via elective cholecystectomy. Its main complications are gallbladder carcinoma and biliary-enteric fistula.
Bouveret’s Syndrome and Gallstone Ileus
Inflammation of the gallbladder (typically if recurrent) can cause a fistula to form between the gallbladder wall and the small bowel, termed a cholecystoduodenal fistula, allowing gallstones to pass directly into the small bowel (typically at the duodenum)
As a consequence, bowel obstruction can occur:
Bouveret’s Syndrome – a stone impacts in the proximal duodenum, causing a gastric outlet obstruction
Gallstone Ileus– a stone impacts at the terminal ileum (the narrowest part of the small bowel), causing a small bowel obstruction
what is it called when there are stones in the common bile duct ?
choledocholithiasis
this can result in obstructive jaundice
what is ascending cholangitis?
Cholangitis refers to infection of the biliary tract - typically E.coli
It is caused by a combination of biliary outflow obstruction and biliary infection. During an obstruction, stasis of fluid combined with elevated intraluminal pressure allows the bacterial colonisation of the biliary tree to become pathological.
what are the causes of ascending cholangitis?
occlusion of biliary tree
gallstones
ERCP
cholangiocarcinoma
other causes: ancreatitis, primary sclerosing cholangitis, ischaemic cholangiopathy, and parasitic infections
The most common infective organisms implicated in cholangitis are Escherichia Coli (27%), Klebsiella species (16%), and Enterococcus (15%).
what are the clinical features of ascending/acute cholangitis
RUQ/upper abdominal pain and tenderness
jaundice
fever
there may also be pruritus as a result of bile accumulation and pale stools with dark urine
charcot’s triad - jaundice, fever and RUQ pain
Reynold’s pentad - jaundice, fever, RUQ pain, hypotension and confusion.
what investigations would you perform for ascending cholangitis?
trans-abdominal USS
ERCP - gold standard
BLOODS FBC serum urea - raised in patients with severe disease serum creatinine - raised in severe disease ABG LFTs CRP blood cultures U&Es coagulation panel
how do you manage ascending cholangitis?
if acutely ill - patients may present with sepsis
- IV antibiotics - co-amoxiclav +/- metronidazole and fluids
ERCP with or without sphincterotomy and stenting within the first 12-48 hours to remove decompress biliary tree
what are the risks of ERCP?
bleeding 0.9%
duodenal perforation 0.4%
cholangitis 1.1%
pancreatitis 1.5%
what is liver cirrhosis ?
Liver cirrhosis is the result of chronic inflammation and damage to liver cells. When the liver cells are damaged they are replaced with scar tissue (fibrosis) and nodules of scar tissue form within the liver. This fibrosis affects the structure and blood flow through the liver, which causes increased resistance in the vessels leading in to the liver. This is called portal hypertension.
It is the pathological end stage of any chronic liver disease
what are the most common causes of liver cirrhosis?
most common causes: Alcoholic liver disease Non Alcoholic Fatty Liver Disease Hepatitis B Hepatitis C
rarer causes: Autoimmune hepatitis Primary biliary cirrhosis Haemochromatosis Wilsons Disease Alpha-1 antitrypsin deficiency Cystic fibrosis Drugs (e.g. amiodarone, methotrexate, sodium valproate)
what are the signs or liver cirrhosis?
- abdominal distension - secondary to ascites in portal hypertension - symptom of decompensated cirrhosis
- Jaundice and pruritus - secondary to reduced hepatic excretion of conjugated bilirubin into the biliary tree. Pruritus is secondary to impaired bile secretion
- blood in vomit, black stools - secondary to gastrointestinal haemorrhage from gastro-oesophageal varicies in portal hypertension
- hand and nail features - leukonychia, palmer erythema, spider naevi
- facial features - telangiectasia, spider naevi, jaundiced sclera
- abdominal features - collateral circulation, hepatosplenomegaly, distension (however the liver can shrink as it becomes more cirrhotic, splenomegaly is due to portal hypertension)
- gynaecomastia and testicular atrophy in males due to endocrine dysfunction
- bruising due to abnormal clotting
- caput medusae - distended paraumbilical veins due to portal hypertension
- asterixis - flapping tremor - in decompensated liver disease
what investigations would you perform for liver cirrhosis
- LFTs - will be deranged
- Gamma-glutamyl transferase GGT - elevated
- serum albumin - decreased (a marker of hepatic synthetic dysfunction)
- serum sodium - reduced - hyponatraemia is a common finding in cirrhotic patients with associated ascites and worsens as liver disease progresses
- prothrombin time - prolonged
- platelet count - reduced
enhanced liver fibrosis blood test - the first line for assessing non-alcoholic fatty liver disease - but currently not readily available
USS - may show
- Nodularity of the surface of the liver
- A “corkscrew” appearance to the arteries with increased flow as they compensate for reduced portal flow
- Enlarged portal vein with reduced flow
- Ascites
- Splenomegaly
Fibroscan - transient elastography - It helps assess the degree of cirrhosis, should be used to test for cirrhosis. NICE recommend retesting every 2 years in patients at risk of cirrhosis:
Hepatitis C
Heavy alcohol drinkers (men drinking > 50 units or women drinking > 35 units per week)
Diagnosed alcoholic liver disease
Non alcoholic fatty liver disease and evidence of fibrosis on the ELF blood test
Chronic hepatitis B (although they suggest yearly for hep B)
Endoscopy -Endoscopy can be used to assess for and treat oesophageal varices when portal hypertension is suspected.
CT and MRI scans -CT and MRI can be used to look for hepatocellular carcinoma, hepatosplenomegaly, abnormal blood vessel changes and ascites.
Liver Biopsy
what scores can be used for liver cirrhosis?
Child -pugh score – it is based on the presence of ascites, hepatic encephalopathy, serum bilirubin, albumin and clotting.
Model of end-stage liver disease - MELD - The MELD score is recommended by NICE to be used every 6 months in patients with compensated cirrhosis. It is a formula that takes into account the bilirubin, creatinine, INR and sodium and whether they are requiring dialysis. It gives a percentage estimated 3 month mortality and helps guide referral for liver transplant.
how is liver cirrhosis managed?
treatment for underlying chronic liver disease
monitor for complications
sodium restricition and diuretic therapy for ascites - spironolactone
Ultrasound and alpha-fetoprotein every 6 months for hepatocellular carcinoma
Endoscopy every 3 years in patients without known varices
High protein, low sodium diet
MELD score every 6 months
Consideration of a liver transplant
Managing complications
liver transplant
what are the complications of liver cirrhosis?
Malnutrition
Portal Hypertension, Varices and Variceal Bleeding
Ascites and Spontaneous Bacterial Peritonitis (SBP)
Hepato-renal Syndrome
Hepatic Encephalopathy
Hepatocellular Carcinoma
how do you manage malnutrition in patients with liver cirrhosis?
Cirrhosis leads to malnutrition and muscle wasting
to manage this:
Regular meals (every 2-3 hours)
Low sodium (to minimise fluid retention)
High protein and high calorie (particularly if underweight)
Avoid alcohol
why do patients with liver cirrhosis get portal hypertension and varacies?
The portal vein comes from the superior mesenteric vein and the splenic vein and delivers blood to the liver. Liver cirrhosis increases the resistance of blood flow in the liver. As a result, there is increased back-pressure into the portal system. This is called “portal hypertension”. This back-pressure causes the vessels at the sites where the portal system anastomoses with the systemic venous system to become swollen and tortuous. These swollen, tortuous vessels are called varices. They occur at the:
Gastro oesophageal junction
Ileocaecal junction
Rectum
Anterior abdominal wall via the umbilical vein (caput medusae)
Varices do not cause symptoms or problems until they start bleeding. Due to the high blood flow through varices, once they start bleeding patients can exsanguinate (bleed out) very quickly.
how do you manage stable varicies?
Propranolol reduces portal hypertension by acting as a non-selective beta blocker
Elastic band ligation of varices
Injection of sclerosant (less effective than band ligation)
Transjugular Intra-hepatic Portosystemic Shunt (TIPS) - allows blood to flow directly from the portal vein to the hepatic vein and relieves the pressure in the portal system and varices. This is used if medical and endoscopic treatment of varices fail or if there are bleeding varices that cannot be controlled in other ways.
how do you manage bleeding varacies?
Resuscitation
Vasopressin analogues (i.e. terlipressin) cause vasoconstriction and slow bleeding in varices
Correct any coagulopathy with vitamin K and fresh frozen plasma (which is full of clotting factors)
Giving prophylactic broad spectrum antibiotics has been shown to reduce mortality
Consider intubation and intensive care as they can bleed very quickly and become life threateningly unwell
Urgent endoscopy
Injection of sclerosant into the varices can be used to cause “inflammatory obliteration” of the vessel
Elastic band ligation of varices
Sengstaken-Blakemore Tube is an inflatable tube inserted into the oesophagus to tamponade the bleeding varices. This is used when endoscopy fails.
what investigations would you perform for varicies?
hepatic venous pressure gradient - will assess for clinically significant portal hypertension
FBC
Coagulation profile
oesophago-gastro-duodenoscopy OGD - will show dilated veins in the lower oesophagus
why do patients with cirrhosis get ascites?
Ascites is basically fluid in the peritoneal cavity. The increased pressure in the portal system causes fluid to leak out of the capillaries in the liver and bowel and in to the peritoneal cavity. The drop in circulating volume caused by fluid loss into the peritoneal space causes a reduction in blood pressure entering the kidneys. The kidneys sense this lower pressure and release renin, which leads to increased aldosterone secretion (via the renin-angiotensin-aldosterone system) and reabsorption of fluid and sodium in the kidneys. Cirrhosis causes a transudative, meaning low protein content, ascites.
how do you manage ascites?
Low sodium diet
Anti-aldosterone diuretics (spironolactone)
Paracentesis (ascitic tap or ascitic drain)
Prophylactic antibiotics against spontaneous bacterial peritonitis (ciprofloxacin or norfloxacin) in patients with less than 15g/litre of protein in the ascitic fluid
Consider TIPS procedure in refractory ascites
Consider transplantation in refractory ascites
why do patients with cirrhosis get spontaneous bacterial peritonitis and how does it present?
This occurs in around 10% of patients with ascites secondary to cirrhosis and can have a mortality of 10-20%. It involves an infection developing in the ascitic fluid and peritoneal lining without any clear cause (e.g. not secondary to an ascitic drain or bowel perforation).
Presentation
Can be asymptomatic so have a low threshold for ascitic fluid culture
Fever
Abdominal pain
Deranged bloods (raised WBC, CRP, creatinine or metabolic acidosis)
Ileus
Hypotension
how do you manage spontaneous bacterial peritonitis as a complication of cirrhosis?
Most common organisms
Escherichia coli
Klebsiella pnuemoniae
Gram positive cocci (such as staphylococcus and enterococcus)
Management of SBP
Take an ascitic culture prior to giving antibiotics
Usually treated with an IV cephalosporin such as cefotaxime
