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Management of ascites in cirrhosis BSG 2006. Definition Pathogenesis Diagnosis- asctitic fluid analysis Treatment- salt restriction/diuretic Therapeutic

Mar 26, 2015



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Management of ascites in cirrhosis BSG 2006 Slide 2 Definition Pathogenesis Diagnosis- asctitic fluid analysis Treatment- salt restriction/diuretic Therapeutic paracentesis TIPSS SBP Slide 3 Setting the scene Occurs in 50% of patients over 10yrs Associated with 50% mortality over two yrs Indicates the need to consider liver transplantation Mortality from cirrhosis is 12.7 per 100,000 population Approx 4% of population have abnormal LFT, 10-20% of those develop cirrhosis over 10-20yrs Slide 4 Uncomplicated ascites- not infected and not associated with HRS Refractory ascites- cannot be mobilised or early recurrence of which ( that is after therapeutic paracentesis) cannot be prevented by medical treatment Diuretic resistant ascites- refractory to dietary salt restriction and intensive diuretic treatment ( spironolactone 400mg and frusemide 160mg per day and salt restricted diet of less than 90mmol/day ( 5.2g/day) Diuretic intolerant ascites- refractory to therapy due to the development of diuretic induced complications Slide 5 Grading of ascites 1.Grade I: Only detectable by US 2.Grade II: Moderate symmetrical distension of the abdomen 3.Grade III: Marked abdominal distension Slide 6 Pathogensis Portal hypertension Sodium and water retention Slide 7 Role of portal hypertension PH increases the hydrostatic pressure with the hepatic sinusoid and favours transudation of fluid into the peritoneal cavity PH occurs as a consequence of structural changes within the liver in cirrhosis and increased splanchnic blood flow Slide 8 Progressive collagen deposition and nodule formation alter vascular architecture and increases the resistance to portal flow Collagen is formed within the space of Disse and sinusoids become less distensible Slide 9 Increased splanchnic flow because of vasodilation due to release of NO Slide 10 Slide 11 Increased resistance in the hepatic sinusoid Portal hypertension Congestion of capillary in intestine Endotoxaemia NO release Arterial vasodilation in both systemic and splanchnic circulation- systemic ( tachycardia increased stroke volume) and splanchnic ( increased portal flow- and more rise in portal pressure) Decrease in effective circulatory volume Activation of RAS system and sympathetic system- ( aldosterone increase promoting Na retention and secondary fluid retention to restore blood volume) Renal vasoconstriction to increase glomerular pressure- ultimately attempts at homeostasis fails- GFR starts to fall Slide 12 Sinusoidal endothelial cells form and extremely porous membrane almost completely permeable to macromolecule Old theory that low albumin is the cause of ascites is false as there is no oncotic gradient ( it works for peripheral oedema but not for ascites) Portal hypertension is critical to development to ascites and develops when wedged hepatic portal venous pressure is more than 12mm TIPSS relieves ascites by reducing portal hypertension though low albumin and cirrhotic liver persists Slide 13 Presinusoidal portal hypertension does not produce ascites ( portal vein thrombosis) Post sinusoidal portal hypertension does produce back pressure and cause similar haemodynamic changes and causes ascites ( hepatic vein thrombosis) Slide 14 1.Sinusoidal portal hypertension, in the presence of severe hepatic decompensation 2.Leads to splanchnic and systemic vasodilatation-role of NO 3.Decreased effective arterial blood volume 4.Activation of systemic vasoactive factors, such as the renin- angiotensin system, the sympathetic nervous system, and vasopressin aimed at restoring arterial filling pressure. 5.Renal vasoconstriction increases concomitantly (leukotrienes and endothelins), counterbalanced by the intrarenal hyperproduction of vasodilating prostaglandins. When this balance is lost renal hemodynamics worsens, and hepatorenal syndrome develops Slide 15 Cirrhosis75% Malignancy10% Heart failure3% TB2% Pancreatitis1% Slide 16 Blood tests- FBC/U&E/LFT/INR Ultrasound- liver/spleen/portal vein/LN Ascitic fluid analysis Slide 17 Abdominal paracentesis 15cm lateral to umbilicus Avoid enlarged spleen and liver Avoid sp and inf epigastric arteries No data to support use of FFP Most clinicians would give pooled platelets if Ascitic fluid neutrophil count and culture SBP is present in 15% patients admitted to hospital Ascitic neutrophil count of >250cells/mm3 is diagnostic of SBP in absence of perforated viscus or inflammation of intraabdominal organs RBC count is usually 50,000 In bloody ascites 50% no cause and 30% HCC Slide 20 The prevalence of occult ascitic fluid infection in asymptomatic outpatients undergoing large volume paracentesis for resistant ascites is low As a result, the routine culture of fluid during paracentesis in such patients is probably not warranted. Obtain a cell count and differential on all samples of ascitic fluid while obtaining cultures only in symptomatic patients. Slide 21 Culture in sterile container will identify onlY 40% of cases of SBP Whereas culture in blood culture bottle will identify 72-90 % Gram stain and AFFB stain inappropriate Fluid culture for mycobacteria 50% sensitivity Slide 22 Cytology is 60-90% accurate in malignant ascites if several hundred ml of fluid is sent and concentration technique is used But it is not investigation of choice in HCC Slide 23 Previously transudate if >25g/L and exudate if >25g/L of protein Up to 30% of cirrhosis will be exudate if we use protein to categorize SAAG is far superior with 97% accuracy Eg Serum albumin 26 and ascitic albumin 11- so SAAG is 15- so high SAAG- previously called transudate SAAG>11g/L Cirrhosis Cardiac failure Nephrotic syndrome SAAG Slide 24 Amylase in pancreatic ascites Triglyceride in chylous ascites Bilirubin in post op ascites Slide 25 Treatment-bed rest No clinical data to back up the finding that upright position is asscociated with reduced GFR and reduced Na excretion and reduced diuretic efficacy Bed rest promote muscle atrophy and other complications and extends hospital stay So bed rest not recommended Slide 26 Treatment- salt restriction Typical UK diet has 150mmol/day- 15% added salt and 70% is manufactured salt Suggestion is no added salt diet and avoidance of prepared food So that patient gets 90mmol/day ( 5.2gm) Lowers diuretic requirement, faster resolution of ascites and shorter hospital stay Avoid high salt content of fluid and medicine except in HRS Slide 27 Treatment- water restriction No role in uncomplicated ascites Most hepatologists restrict fluid in ascites associated with hyponatraemia- but is illogical The downside is water restriction causes increase in the central effective hypovolaemia- more ADH- more water retension and further dilutional hyponatraemia So hepatologist including the authors of the BSG guidelines suggest further plasma expansion to inhibit ADH secretion Data emerging supporting use of specific vasopressin 2 receptor antagonists To be effective the intake should be less than urine output rather than arbitrary 1.5L/day If the serum sodium concentration does not increase within the first 24 to 48 hours, the degree of fluid restriction has been insufficient. Slide 28 Treatment- diuretic Spironolactone is drug of choice Aldosterone antagonist acting in distal tubule to increase natriuresis and conserve potassium Initial dose 100mg and increasing up to 400mg Lag of 3-5days Better natriuresis and diuresis than a loop diuretic Antiandrogenic effect- gynaecomazia- tamoxifen 20mg bd Hyperkalaemia frequently limits the use Slide 29 Treatment- diuretic Frusemide has low efficacy in cirrhosis Use only if 400mg of spironolactone fails to achieve weight loss Start at 40mg a day and increasing by 40mg every 3 rd day to max of 160mg Watch out for metabolic alkalosis and electrolyte disturbance Slide 30 Treatment- diuretic Stepped care approach Till oedema is present no need to slow down the daily weight loss Once oedema is resolved daily weight loss should be less than 0.5kg per day Over diuresis is associated with intravascular volume depletion, leading to renal impairment, hepatic encephalopathy and hyponatraemia 10% will have refractory ascites Dietary history to exclude salt ingestion- 24hr urinary Na excretion should be less than recommended intake Drug history - NSAID Slide 31 Problem with hyponatraemia Na 126-135 and normal creatinine Continue diuretic Do not water restrict Na 121-125 and normal creatinine Continue/? discontinue Na 121-125 and high Creatinine Stop diuretic and give volume expansion Na Controversy regarding normal saline Give only if renal function is worsening creatinine >150 or 120 and rising Gelofusion/Haemaccel/ 4.5% albumin all have 153mmol of Na per L This will worsen salt retention but better to have ascites than to develop HRS Slide 33 Therapeutic paracentesis Total paracentesis is associated with significant haemodynamic changes Large volume paracentesis causes marked reduction of IAP and IVC pressure- decrease in right heart pressure and This changes are maximal at 3hrs Slide 34 International ascites club recommend if 5L at dose of 8g/L of ascites drained ( 100ml of 20% albumin= 20gm, so 3L of ascites fluid removal needs 3x8=24 gm of albumin replacement = 125ml but we tend to round it to 100ml) So if >10L remember to give an extra 100ml of albumin 25% albumin can be given if the patient is hypervolemic while 5 percent albumin can be given if dehydration is suspected. Slide 35 Use Z technique- puncture site on the skin does not overlie the puncture site on peritoneum Left flank is preferrable to right flank After drain is out patient lie on opposite site Colostomy bag if continuous leakage ( some use purse string suture) As rapidly as possible- should not be left overnight No upper limit of 8 litres or maximum time of 6 hours has been mentioned in the guidelines Slide 36 10% of patients will have refractory ascites and will need paracentesis Followin