PE - Approach to Ascites Flashcards
List important negatives to mention in a patient w/ascites
1) Stigmata of chronic liver disease
- cirrhosis is most common cause of ascites
2) Signs of hepatic encephalopathy
- always present if reversible acute on chronic liver failure
- may be present if irreversible chronic liver disease
3) Jugular venous pressure for volume status
- low/normal JVP –> cirrhosis (systemic vasodilation)
- elevated –> CKD, heart failure, constrictive pericarditis, atrial myxoma
4) Generalized lymphadenopathy
1. infection (EBV, CMV, HHV-6, HIV, toxoplasmosis, Bartonella)
2. malignancy
3. hematological malignancy
4. SLE
5. sarcoidosis
5) Caput medusae
- occlude vessels below umbilicus
- blood flow away from umbilicus = portal HT
- blood flow towards umbilicus = IVC obstruction
Explain the mechanism of ascites in generalized lymphadenopathy
1) Involvement of retroperitoneal lymph nodes
2) Lymphatic drainage of abdomen impaired causing ascites
List the 6Fs of abdominal masses
1) Fat
2) Fluid
3) Flatulence
4) Feces
5) Flaming tumour
6) Fetus
Explain the mechanism of ascites in nephrotic syndrome
List some causes of nephrotic syndrome
1) Hypoalbuminemia in nephrotic syndrome causes loss of water into the extravascular space causing ascites
2) Causes of nephrotic syndrome include
1. Idiopathic
2. Rheumatoid arthritis
3. SLE
List some causes of hypoalbuminemia
1) Malnutrition
2) Nephrotic syndrome
3) Liver disease
List the common causes of ascites
1) Cirrhosis (75%)
2) Malignancy (10%)
3) Heart failure (3%)
4) Tuberculosis (2%)
5) Pancreatitis (1%)
Outline initial investigations to make the etiological diagnosis of ascites
Blood tests
1) LFT –> check for impaired liver function in cirrhosis
2) CBC –> PLT (thrombocytopenia suggest hypersplenism secondary to portal HT) PLT less than 50 may also be contraindication for further invasive procedures
3) INR –> ?less than 1.7-1.5
4) Prothrombin time –> assess liver function + coagulopathy
Abdominal USG
1) R/o hepatic or other intra-abdominal masses suggestive of malignancy
2) Splenomegaly suggests portal HT
3) Hepatic vein + portal vein Doppler to r/o thrombosis
Diagnostic paracentesis
1) Ascitic fluid albumin + total protein
2) Ascitic fluid differential WCC
3) Ascitic fluid gram stain + culture
4) Ascitic fluid cytology
Outline the method of classifying ascites
Serum ascites-albumin gradient (SA-AG)
SA-AG= serum albumin - ascific fluid albumin
- less than 11 = exudative
- more than 11 = transudative
Explain the pathophysiology of ascites and edema in cirrhosis
1) In cirrhosis, ascites only occurs after development of portal HT
2) Disturbed portal blood flow in cirrhotic liver causes fluid accumulation in peritoneum
3) Cirrhosis is a state of systemic vasodilation which also dilates splanchnic circulation –> increased blood flow through portal vein increases portal vein pressure –> further reduces effective circulating volume and blood pressure –> RAAS + sympathetic activation –> salt + water retention –> edema + ascites
Outline the initial management for ascites in cirrhosis
1) Dietary Na restriction –> reduce edema + ascites
2) Fluid restriction –> reduce edema + ascites
3) Diuretics –> w/aldosterone antagonists first then loop diuretics AFTER achieving appropriate Na levels
Explain the pathophysiology of hepatorenal syndrome
1) Hepatorenal syndrome can be considered the endstage of the spectrum of portal HT and ascites
2) Systemic vasodilation continually reduces effective circulating volume
3) This induces a vasoconstrictor response in which renal blood flow is reduced thus reducing GFR
4) Results in progressive renal impairment in end stage liver disease despite structurally normal kidneys