ASCITES Flashcards
What is ascites?
Ascites = fluid within the peritoneal cavity, a common complication of cirrhosis.
What is the 3 underlying pathogeneses of ascites?
- Sodium & water retention: due to peripheral arterial vasodilation (2’ to nitric oxide, ANP & prostaglandins) causing a reduction in the effective blood volume. Low blood volume activates sympathetic nervous system and RAAS, promoting salt & water retention.
- Portal hypertension: local hydrostatic pressure leading to increased hepatic lymph production and transudation of fluid into peritoneal cavity.
- Low serum albumin: due to poor liver function, further reducing plasma oncotic pressure
What are the clinical features of ascites & tense ascites?
Abdominal swelling
Pain/discomfort
Severe pain (suspicious of SBP)
Peripheral oedema
Respiratory distress & difficulty eating in tense ascites
What are the precipitating factors of ascites?
Excess alcohol consumption
Infection/sepsis
HCC/splanchnic vein thrombosis
How do you confirm the diagnosis of ascites?
Shifting dullness confirms the presence of fluid.
When may you find a right-sided pleural effusion (rare) as a result of ascites?
Congenital diaphragmatic defect allows passage for ascites
Which investigations are carried out for ascites?
Diagnostic aspiration, aka ascitic tap (10-20ml) obtained for:
Cell count - high neutrophil count (>250cells) indicative of spontaneous bacterial peritonitis
Gram stain & culture
Protein measurement -
high serum-ascites albumin = portal hypertension;
low serum-ascites albumin = non-liver disease related abnormalities of peritoneum
Cytology - malignant cells
Amylase - to exclude pancreatitis ascites
What is the aim of managing ascites?
Reduce sodium intake and to increase renal sodium excretion => producing a net reabsorption of fluid from ascites into the circulating volume.
How do you manage ascites?
- Check electrolytes, creatinine (U&E) and eGFR rate on alternate days. Weigh the patient & measure urinary output daily.
- Dietary sodium restriction (40mmol in 24hrs)
- Fluid restriction (<1.5L/day)
- Drugs - Limit high in sodium & sodium retaining drugs ie antacids, antibiotics, NSAIDs and corticosteroids
- Diuretics - start spironolactone (aldosterone antagonist 100mg - works by correcting RAAS) => chronic admin results in gynaecomastia; Eplerenone does not produce gyaecomastia.
If response is poor, add furosemide
Aim of diuretic therapy is to produce a net loss of 700ml fluid in 24hours.
In which conditions would you see a high serum-ascites albumin gradient?
- Portal hypertension e.g. cirrhosis
- Hepatic outflow obstruction
- Budd-Chiari syndrome
- Hepatic veno-occlusive disease
- Tricuspid regurgitation
- Constrictive pericarditis
- Right-sided heart failure
In which conditions would you see a low serum-ascites albumin gradient?
- Peritoneal carcinomatosis
- Peritoneal tuberculosis
- Pancreatitis
- Nephrotic syndrome
How do you manage symptomatic tense ascites?
How much fluid can be removed?
Paracentesis for tense ascites or when diuretic therapy is insufficient.
Up to 20L can be removed over 4-6 hours, with albumin infusion.
What are the complications of paracentesis?
Hypovolaemia and renal dysfunction (when more than 5L is removed and in patients with worse liver function)
In patients with normal renal function and without hyponatraemia, hypovolaemia is overcome by infusing albumin.
How do you treat resistant ascites?
Using a TIPS (transjugular intrahepatic portosystemic shunt)
What are the causes of straw coloured ascitic fluid?
Malignancy (most common cause)
Cirrhosis
Infective i.e. Tuberculosis, after intra-abdominal perforation, spontaneous bacterial peritonitis in cirrhosis
Hepatic vein obstruction ie Budd-Chiari syndrome
Chronic pancreatitis
Congestive cardiac failure
Constructive pericarditis
What are the causes of chylous ascites?
Obstruction of main lymphatic duct e.g. by carcinoma - chylomicrons are present
Cirrhosis
What are the causes of haemorrhagic ascites?
Malignancy
Ruptured atopic pregnancy
Abdominal trauma
Acute pancreatitis
What is spontaneous bacterial peritonitis (SBP)?
How many people are affected?
A complication of ascites
18% of decompensated ascites patients affected - SBP should be suspected in patients with ascites who are deteriorating rapidly as pyrexia and pain absent.
Recurrence is common 70%
Which bacteria commonly results in spontaneous bacterial peritonitis?
How are they spread?
E.coli, klebsiella, enterococci
Haematogenous spread
How do you diagnose spontaneous bacterial peritonitis?
Diagnostic aspiration of ascites - raised neutrophil count in ascites evidence for SBP
How do you manage spontaneous bacterial peritonitis?
Start off with broad-spectrum then narrow down once organism is known. Albumin infusion.
What is porto-systemic encephalopathy?
Porto-systemic encephalopathy occurs secondary to cirrhosis.
It occurs in portal hypertensive patients due to spontaneous shunting or in those with surgical or TIPS shunts.
What is the underlying pathogenesis of porto-systemic encephalopathy?
In cirrhosis, portal blood bypasses the liver via collaterals and toxic metabolites (ammonia) pass directly to the brain to produce encephalopathy.
Ammonia leads to brain neurotransmitter imbalance.
Ammonia is produced by breakdown of protein by the intestinal bacteria.
What clinical features (signs & symptoms) are seen in chronic porto-systemic encephalopathy?
Chronically, affects personality, mood and intellect.
Symptoms:
Patient is irritable, confused, disorientated with slow & slurred speech.
Nausea, vomiting, weakness, hyper-reflexia, increased tone
Coma
Signs:
Fetor hepaticus (sweet smell/pear-drop smell of breath)
Course flapping tremor (asterexis)
Contructional apraxia (unable to write/draw a 5 pointed star)
Decreased mental function (trail making or number connection test)
What clinical features (signs & symptoms) are seen in acute porto-systemic encephalopathy?
Patient becomes increasingly drowsy and comatose
Which factors precipitate porto-systemic encephalopathy?
High dietary protein
GI haemorrhage
Constipation
Infection (ie spontaneous bacterial peritonitis)
Fluid electrolyte disturbance due to diuretic therapy or paracentesis
Porto-systemic shunt operations/TIPS
Progressive liver damage (cirrhosis, ascites)
HCC
How do you manage porto-systemic encephalopathy?
- Identify & remove precipitating causes
- Give purgation & enemas i.e. lactulose to empty bowels of nitrogenous substances
- Maintain nutrition
- Give antibiotics
- Stop/reduce diuretic therapy
- IV fluids
- Treat infection
- Embolise collaterals that bypass liver may improve liver blood flow and reduce encephalopathy but need to be carefully selected.
What is the prognosis of porto-systemic encephalopathy?
Acute porto-systemic encephalopathy in acute hepatitis failure = poor prognosis
In cirrhosis, chronic porto-systemic encephalopathy = adverse prognosis
