Ascites - principles of diagnosis and treatment Practical course in Internal medicine, 4. year GM I. Department of Internal medicine Faculty of Medicine, Comenius University & University Hospital Bratislava Summer semester 2019/2020 Ascites • Ascites describes the condition of pathologic fluid collection within the abdominal cavity • Word „ascites“ is of Greek origin (askos) - and means bag or sac • Healthy men have little or no intraperitoneal fluid, but women may normally have as much as 20 mL, depending on the phase of their menstrual cycle Ascites - etiology 3 2 5 Liver cirrhosis (ALD 60%, HBV/HCV infection 10%, cryptogenic 10% 10 Malignity Heart failure Tuberculosis Other 80 Ascites – etiology Portal hypertension Portal hypertension PRESENCE ABSENCE SAAG ≥ 11 g/l SAAG < 11 g/l • Hypoalbuminemia • Prehepatic • Nephrotic syndrome • Splenic or portal vein trombosis • Severe malnutrition • Schistosomiasis • Protein-losing enteropathy • Intrahepatic • Malignancy • Pre-/intra-/postsinusoidal • Liver cirrhosis • Infection • Alcohol liver diesease • Tuberculosis • Infective, autimunne, toxic, other ... • Spontaneous bacterial peritonitis • Liver metastases • Pancreatitis • Posthepatic • Polyserositis in systemic or • Budd-Chiari syndrome, veno- occlusive disease endocrinal disorders • Cardiac (hypothyreosis, connestive • Right heart failure tissue diseases, vasculitis ...) • Constrictive pericarditis • Meigs syndrome Ascites – patophysiology disturbance of the balance between the formation and absorption of free abdominal fluid ↓ Fluid absorption ↑ Fluid production Ascites – combination of mechanisms in liver cirrhosis Natural history of chronic liver disease 1. Latent - hidden disorder of water and sodium management - decreased peripheral vascular resistance, increased minute volume, ECT expansion, no edema, normal activity RAAS, ADH, SNS) 2. Positive sodium balance - inability to exclude Na load, ECT expansion, swelling, mild ascites, normal function of RAAS, SNS, ADH 3. Decompensation stage - bulky to tense ascites 4. Hepatorenal syndrome type 2 – compensatory mechanisms on maximum, refractory ascites 5. Hepatorenal syndrom type 1 - failure of compensatory mechanisms, collaps of Development of ascites in liver cirrhosis: circulation, severe hypotension ➢ 1-year mortality 40% and renal hypoperfusion ➢ Consider liver transplantation Peritoneal dialysis – „arteficial ascites“ Ascites – clinical features (1) • usual progressive development, rarely occurs suddenly • nonspecific dyspepsia, meteorism, abdominal disension, shortness of breath, movement problems • Inspection: • together with thin limb – Chvostek´s habitus • navel is diminished • striae • abdominal wall hernia • collaterals - caput medusae (consequence of portal hypertension and also because of compresion of vena cava inferior by large ascites) • edema of lower extremities Ascites – clinical features (2) • Palpation • undulation phenomenon (fluid wave test) positive if ascites > 10l • Abdominal percussion • shifting dullness (necessary to try different positions of patient) - positive if ascites > 1.5-3l • dull percussion above groin area (in contrast with e.g. urinary bladder enlargement, pregnancy, abdominal tumors) • Chest percussion - pleural effusion (in 85% right-sided) • caused by defects in the diaphragm, even in the absence of ascites (negative pleural pressure that sucks the peritoneal fluid into the pleural cavity) • Signs of underlying disease • Liver disease: enlarged liver, jaundice, spider angioma, palmar erythema • Heart failure: elevated jugular venous pressure • Malignacy: weight loss, lymphadenopathy Ascites – imaging techniques • on sonography the minimum detectable amount of ascites > 100 ml Ascites – classification (1) Tense ascites: abdominal wall tension, severe shortness of breath, pressure on vena cava inferior and renal vessels > indication for terapeutic paracentesis Ascites – classification (2) a) Simple (uncomplicated) b) Complicated • Refractory - inadequate response to diuretics, frequent recurrence, or when diuretic therapy is contraindicated Inštruktážne video • Spontaneous bacterial peritonitis = bacterial infection of ascites without a detectable, surgically treatable source of infection - etiology- chronic venostasis in the splanchnic region > dysfunction of intestinal barrier and motility> translocation of bacteria from bowel lumen to ascites • Hyponatremia • Hepatorenal syndrome - type 1 and 2 Ascites - diagnostics Any sudden Every new increase in onset of the amount ascites of ascites DIAGNOSTIC PARACENTESIS !!! LABORATORY ANALYSIS OF ASCITIC FLUID Ascites –paracentesis technique • Instruction video Ascites – paracentesis • Abdominal punction, Ascitic tap • Diagnostic/Terapeutic • Neither coagulopathies nor thrombocytopenia are contraindications • Ultrasound guidance – properly before first puncture, in case of atypically distributed ascites, presence of solid masses in abdominal cavity ... Samples od ascitic fluid are sent to: 1. Biochemical examination - pH, glu, total protein, ALB, LD, cholesterol, TAG, AMS, oncomarkers, ...? 2. Microscopy + differential count (EDTA-tube) – amount of WBC, RBC ? 3. Cytological examination - presence of malignant cells? 4. Cultivation - basic, specific Ascites –paracentesis Ascites – laboratory diagnostic (1) Older terms: Transudate Exudate • low total protein level • high total protein (due • low LDH inflammation and malignancy) • normal glucose • high LDH • WBC <0.1 G / L • low glucose levels • low pH (<7.3) • High WBC > 0.1 G / L • Difference between total protein in serum and ascites <10 Ascites – laboratory diagnostic (2) SAAG = „serum-ascites albumin gradient“ = serum albumin level - albumin level in ascitic fluid Ascites – laboratory diagnostic (3) Rare causes of ascites: • Pancreatitis: • Lab: high AMS, total protein, WBC • Tuberculosis: • Lab: high total protein, lymphocytes • Chylous ascites: • In case of lymphatic duct damage • Etio: usually solid tumors, malignant lymphoma, rarely advanced cirrhosis • Lab: 2-8x higher TG (compared to plasma) • Haemoperitoneum: • Etio: solid tumors, iatrogenic bleeding • Lab: RBC in ascites> 50,000 / mm3 Ascites – microbial cultivation • Spontaneous bacterial peritonitis = bacterial infection of ascites without a detectable, surgically treatable source of infection • Lab: neutrophils in ascites > 0.250 (0.5) G / L (> 0.4 leu) • Cultivation of ascites - positive detection only in about 30-40% • Clinicall features: • often – mild or no symptoms • abdominal pain, nausea, vomiting, chills, mild fever, worsening of hepatic and renal lab. tests, encephalopathy, increase in ascites resp. failure of diuretic treatment, bleeding into GIT • Bakterascites: = transient, possible reversible colonization of ascites • Laboratory: Positive result of ascites cultivations, but neutrophils level <0.25 • (Secondary) bacterial peritonitis = usually secondary due GIT / abdominal wall perforation • Lab: Neu concentration particularly high, high total protein, low GLU and LD • Dg. - abdominal CT, therapy – usually surgical intervention required Ascites – therapy • causal treatment of the underlying disease • In case of portal hypertension • chronic therapy - non-selective B-blocker p.o. (carvedilol) • acute treatmenr (upper GIT bleeding) - terlipressin i.v. Smaller ascites • Rest on the bed • Elimination of hepatotoxic / nephrotoxic medication: ATB, NSAID • Maintaining a negative sodium balance 1. Decreased sodium intake ➢ restrict sodium intake to 1500-2000mg (5-7g NaCl) – unsalted diet ➢ restriction of fluid intake: < 1.5 liter is allowed, if serum Na <120 mmol/l - <1l 2. Diuretic therapy - increased renal excretion of sodium Diuretics in treatment of hepatic ascites Purpose of treatment: pt. without ascites at the smallest dose of diuretic < dose titration Limitations of diuretic therapy: severe hypoNa, hypoK / hyperK, renal failure, convulsions, hypotension a) Aldosterone antagonists: • blockade of Na-reabsorption in distal tubule and collecting ducts • more effective than loop diuretic, in ascites therapy they are diuretics of first choice ❑Spironolactone: • starting dose of 100mg / day, increased by 100mg at 7 day intervals up to 400mg / day • CAVE: slow onset (2-4 days), retention of K + (hyperkalaemia) ❑Amiloride (10-40mg daily): especially in the collecting ducts, less effective b) Loop diuretics • inhibition of Na-reabsorption in the ascending arm of the Henle loop • less effective, in therapy of ascites they are diuretics of second choice • they should be added into the combination with therapy of spironolactone if: • recurrent ascites • insufficient response to spironolactone (inadequate diuretic effect) • therapy with spironolactone is limited (hyperkalaemia, gynecomastia ...) ❑Furosemide: • starting dose of 40mg, increases by 7 days by 40mg up to 120mg / day • Spinolactone:furosemide ratio - 100: 40mg Large ascites • Therapeutic (large-volume) paracentesis • Albumin i.v. - always administered after collection> 5 liters of ascites (prevention of postparacentic circulatory dysfunction) Refractory ascites - ie. not responding to the maximum tolerated doses of diuretics • reduction of diuretic treatment • repeated paracentesis • TIPS - transjugular intrahepatic portosystemic shunt • reduces portal BP> improves GF and increases renal excretion of Na, reduces the need for paracentesis • does not improve survival compared to the repeated paracentesis, faster progression of encephalopathy • KI: renal failure, severe heart and lung disease, severe encephalopathy,