ascitites + cirrhosis Flashcards
what is ascites
a localised, pathological collection of fluid within the peritoneal cavity
what are the 3 grades of ascites
- detectable by imaging only
- clinically detectable
- tense and obvious (can’t indent abdomen)
causes for abdominal distension (5 Fs)
fluid, fat, faeces, foetus, fat
what is ascites
localised, pathological fluid collection within the peritoneal cavity
3 grades of ascites
- detectable by imaging only
- clinically detectable
- tense and obvious (can’t indent abdomen)
what are some causes of stomach distension (5 Fs)
fluid; fat; faeces; foetus; fat
what is chylothorax
a rare but serious condition in which lymph formed in the digestive system (chyle) accumulates in your chest cavity
what is cirrhosis
Cirrhosis is permanent architectual change (scarring) of the liver caused by long-term liver damage
fibrosis vs cirrhosis
fibrosis can progress and regress due to the activity of stellate cells -> cirrhosis is a permanent change
what equation is used to determine fluid flux into interstitual space between arterioles and venules
starling equation
what system drives ascites
RAAS
how to work out if ascites is transudative or exudative
serum ascites abumen gradient - SAAG
- take blood sample
- take ascites sample
- measure the albumin levels of both
- calculate the SAAG (SAAG = (serum albumin) − (albumin level of ascitic fluid))
- if >1.1g/DL then transudate
what value must the SAAG be over for ascites to be transudative
> 1.1g/Dl
how does hepatic encephalopathy arise
- astrocyte swelling (build up of toxins not being removed by the liver e.g. ammonia, glutamine, manganese, drugs - benzodiazepines
- astrocyte dysfunction (mt. dysfunction, ROS, BBB leakage)
- neuronal dysfunction (altered gene expression, decreased Ach etc.)
- symptoms of hepatic encephalopathy
what is liverflap (asterixis) associated with
hepatic enceophalopathy -> occurs due to build up of toxins in the brain as liver can’t filter them
what is the new haven grading system (hepatic encephalopathy)
- Changes in behavior with minimal change in level of consciousness;
- Gross disorientation, drowsiness, possibly asterixis, inappropriate behavior;
- Marked confusion, incoherent speech, sleeping most of the time but arousable to vocal stimuli;
- Comatose, unresponsive to pain; decorticate or decerebrate posturing
causes of ascites
- liver disease - cirrhosis -> transudate
- heart failure (esp R side) -> transudate
- cancer -> exudate
4.
causes of cirrhosis
- alcohol
- hep C
- NAFLD
- primary cholangitis
- wilson’s disease (Cu metabolic disorder)
- haemochromatosis (Fe metabolic disorder)
what cardiac condition can cause hepatomegaly
cor pulmonale (R sided heart englargement due to lung/pulmonary pathology)
when is SAAG very high
in causes where there is a rise in sinusoidal/postsinusoidal pressure
if SAAG level is 1.1-2.5g/dL what is the likely cause (3)
portal hypertension causes
1. cirrhosis
2. late budd-chiari syndrome
3. massive liver metastases
if SAAG level is >2.5g/dL what is the likley cause (5)
post hepatic causes
1. congestive heart failure
2. constrictive pericarditis
3. early budd-chiari syndrome
4. IVC obstruction
5. sinusoidal obstruction syndrome
if SAAG level is <1.1g/dL what is the likley cause (5)
non portal hypertension cause
1. biliary leak
2. nephrotic syndrome
3. pancreatitis
4. peritoneal carcinomatosis
5. tuberculosis
what is ascitic fluid tested for in the lab (7)
- ascitic albumin
- ascitis cytology
- ascitic fluid cell count and culture
- triglycerides (if >200mg/dL then thought to be chylous)
- amylase
- bilirubin
- adenine deaminase (if thought to be TB)
causes of prehepatic portal vein hypertension (3)
- portal vein thrombosis
- splenic vein thrombosis
- massive splenomegaly
causes of hepatic portal vein hypertension (5)
presinusoidal
1. schistosomiasis
2. congenital hepatic fibrosis
sinusoidal
3. cirrhosis
4. alcoholic hepatitis
postsinusoidal
5. hepatic veno-occlusive disease
causes of post-hepatic portal vein hypertension (4)
- budd-chiari syndrome
- restrictive cardio myopathy
- constrictive pericarditis
- congestive heart failure
what is budd-chiari syndrome
an uncommon disorder characterized by obstruction of hepatic venous outflow - can be thrombotic or non-thrombotic -> portal hypertension
causes of inflammatory (non portal vein) hypertension (6)
- radiation
- pancreatitis
- retroperitoneal fibrosis
- sarcoidosis
- whipple’s disease
causes of post-operative (non portal vein) hypertension (4)
- AAA repair
- post-liver transplant
- retroperitoneal node dissection
- inferior vena cava resection
what is the main cause of ascites
cirrhosis
what does the presence of ascites indicate in a cirrhotic pt
marks decompensation (along with other signs e.g. jaundice etc.)
signs of liver decompensation (6)
- ascites
- jaundice
- variceal bleeding
- liver encephalopathy
- falling albumen
- coagulopathy
what is an ascitic pt at risk of
ascititc infection (sponatenous bacterial peritonitis)
what are the categories in the childs-pugh score (5)
- eceophalopathy
- ascites
- bilirubin (high is bad - >3 severe)
- albumin (low is bad - <2.8 severe)
- prothrombin time (>2.3 is severe)
in a normal liver is there a pressure gradient across the liver
no
when can it be said that portal hypertension is present
(Inferior Vena Cava pressure) - Portal Vein pressure <5mmHg
i.e. there is an increased gradient across the liver
what are the 3 blood supplies of the liver
- hepatic artery
- portal vein
- hepatic vein
why can the portal vein pressure increase
- more blood flow coming in
- block to flow (resistance)
pressure = resistance x flow
3 types of portal hypertension
- pre heptic
- hepatic
- post hepatic
variceal haemorrhage treatment
surgery - rubber bands to stop bleeding and allow for fibrosis of bleeding point
causes of increased resistance in portal hypertension (4)
early
1. cellular elements
2. organ contraction
late
3. scar (fibrosis)
4.nodules
3 complications of cirrhosis
- hepatocellular carcinoma
- immune system paresis (liver is v important for innate immune system)
- decompensation event
what is the arterial underfilling hypothesis (ascites)
the primary abnormality is inappropriate sequestration of fluid within the splanchnic vascular bed due to portal hypertension and a consequent decrease in effective circulating blood volume
arterial underfilling hypothesis (ascites) steps (8)
- increased intrahepatic resistance
- increased mesenteric blood flow
- portal pressure goes up
- reduced intrathoracic blood volume
- activation of vasoconstrictor mechanisms (NA, ADH, RAAS)
- retention of salt and water at kidney level
- increased venous pressure at capillaries of mesenteric system
- intraperitoneal accumulation of fluid
i.e. decreased blood intrathroacically leads to vasoconstriction and retention of water -> increased capillary pressure and accumulation of fluid
ascites mgx
diuretics - spironolactone/frusemide
no added salt
if ascites is diuretic resistant/patients cant tolerate them what is the mgx
large volume paracentesis - US guided drain of the fluid
what must be given to pt undergoing large volume paracentesis (ascites)
albumin - 2.5 L
why is large volume paracentesis only left in for 6hrs max
risk of infection
what is a TIPS shunt and when is it used (GI)
Transjugular intrahepatic portosystemic shunt - a procedure that involves inserting a stent (tube) to connect the portal veins to adjacent blood vessels that have lower pressure thus relieving pressure
used in ascites
what is a complication of ascites
spontaneous bacterial peritonitis
secondary prophylaxis for spontaneous bacterial peritonitis
Rifaximin
primary prophylaxis for spontaneous bacterial peritonitis
norfloxican - given if childs-pugh score is >9
what is AKI-HRS
Acute kidney injury and hepatorenal syndrome in cirrhosis -> a severe and often fatal complication of end‐stage liver disease
treatment of Hepato-renal syndrome
- volume expansion - albumin
- vasoconstrictors - (midodrine + octerotide) or NA/ADH/terlipressin
- dialysis - only if liver failure is reversible or the pt is a liver transplant candidate
oesophageal varices bleed mgx
medical emergency:
1. intravascular volume support -> IV fluids
2. blood transfusion (with the aim of keeping the haemoglobin around 70-80 g/L [7-8 g/dL])
3. Terlipressin (a vasopressin analogue), or somatostatin (or its analogue octreotide) should be initiated as soon as a variceal bleed is suspected
4. endoscopy -> Endoscopic variceal ligation or sclerotherapy
5. abx - ceftriaxone is cirrhosis
if bleed so large can’t be stopped by EVL, use a Sengstaken-Blakemore tube or a Danis stent until haemostasis is achieved
