ASCITES Clinicla Practice Guidlines.pptx

KnowHow4 2 views 29 slides Oct 12, 2025
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About This Presentation

ASCITes Clinical Practice Guidelines


Slide Content

ASCITES IN CLD Presenters: Dr T ooba B ukhari Dr S aad Facilitator: Dr U mair Khan S herwani

DEFINATION Ascites is the abnormal accumulation of fluid within the peritoneal cavity.

ETIOLOGY Cirrhosis [75 %] Most common cause of ascites and most common complication Malignancy [10%] TB[2%] Pancreatic ascites 1% Various causes 9%

SERUM ASCITIC ALBUMIN GRADIENT [SAAG] Difference between serum and ascitic fluid albumin concentration correlates directly portal pressure . If SAAG is greater than 1.1gm/dl, the pt has portal hypertension with 95% accuracy

Serum-to-Ascitic Albumin Gradient

INTERNATIONAL ASCITES CLUB GRADING SYSTEM Grade 1 Mild only detected on USG Grade 2: Moderate symmetrical distension Grade 3: Gross ascites with marked abdominal distention

Evaluation Of Patients With Ascites In CLD History Physical Examination Abdominal USG Lab assessment LFTS RFTS Serum and urine electrolytes Analysis of ascitic fluid

DIAGNOSIS OF ASCITES Diagnostic Paracentesis Any pt with new onset of ascites Cirrhotic pt admitted with ascites Cirrhotic pt with grade 2 ascites who have ; hepatic encephalopathy gastrointestinal hemorrhage sudden renal deterioration fever, abdominal pain

ASCITIC FLUID TESTING

GROSS APPEARANCE

PARACENTESIS Site: 5cm cephalic and 5cm medial to ASIS in left lateral side To avoid injury to inf erior epigastric vessel Complication: abdominal wall hematoma hemoperitoneum or bowel injury Contraindication : fibrinolysis or DIC

PROGNOSIS OF PATIENT WITH ASCITES Child Pugh Score MELD-Na Hyponatremia Low arterial pressure GFR Low renal sodium excretion Since the development of grade 2 or 3 ascites in patients with cirrhosis is associated with reduced survival, Liver Transplant should be considered as potential treatment option.

MANAGEMENT OF UNCOMPLICATED ASCITES Grade 1 and 2: Salt restriction moderate restriction of sodium intake (80-120mmol/day, corresponding to4.6-6.9g of salt). This is equivalent to no added salt diet with avoidance of prepared meals. Diets with very low sodium content (<40 mmol/day) should be avoided as they favor diuretic induced complications and can endanger pts nutritional status

MANAGEMENT OF UNCOMPLICATED ASCITES Diuretics: Pts with 1 st episode of grade 2 ascites should receive anti mineralocorticoid drugs alone , starting at 100mg /day with stepwise increases every 72h (in 100mg steps) to a max of 400mg/day if there is no response at lower doses. In pts who do not respond to anti mineralocorticoid , as defined by body weight reduction < 2kg/wk , or in pts who develop hyperkalemia , furosemide should be added at an increasing stepwise dose i.e 40-160mg/day.

Continued… Pts with long standing or recurrent ascites should be treated with combination of an anti mineralocorticoid drug and furosemide, the dose of which should be increased sequentially. During therapy, max wt. loss of 0.5 kg/day in pts without edema and 1kg/day with peripheral edema is recommended. Once ascites has largely resolved, the dose must be reduced to lowest effective dose. During the 1 st weeks of treatment pts should undergo frequent clinical and biochemical testing particularly on 1 st presentation.

Continued… Pts presenting with GI hemorrhage, renal impairment, hepatic enceph, hyponatremia or hypo/hyper-kalemia , these abnormalities should be corrected before starting diuretics. Diuretics should be discontinued if severe hyponatremia ( Sr . Na <125 mmol/L), AKI, worsening hepatic enceph or incapacitating muscle cramps develop. Furosemide should be stopped if severe hypokalemia occurs (<3 mmol/L ). anti mineralocorticoid should be stopped if severe hyperkalemia (>6mmol/L). Albumin infusion or baclofen administration (10mg/d), with a weekly increase of 10mg/day up to 30mg/day are recommended in pts with muscle cramps.

MANAGEMENT OF UNCOMPLICATED ASCITES GRADE 3 OR LARGE ASCITES LVP is first line therapy in, these pts, which should be completely removed in single session. LVP should be followed with plasma volume expansion to prevent PPCD. In pts undergoing LVP of >5L of ascites, plasma vol . expansion must be performed by infusing albumin(8g/L) . In pts undergoing LVP of <5L of ascites, the risk of developing PPCD is low. After LVP pts should receive minimum dose of diuretics to prevent re-accumulation of ascites. When needed LVP should be performed in pts with AKI or SBP.

CONTRAINDICATIONS OF PARACENTESIS Uncooperative patient Abdominal skin infection at proposed puncture site Pregnancy Severe coagulopathy Severe bowel distention

DRUGS CONTRAINDICATED IN ASCITES NSAIDS  sodium retention, hyponatremia and AKI. ACE Inhibitors, Angiotensin II antagonist or alpha1 adrenergic receptor blockers  renal impairment. Aminoglycosides  AKI.

REFRACTORY ASCITES Diuretic resistant ascites : Ascites that can not be mobilized or the early recurrence of which can not be prevented because of a lack of response to sodium restricted diet and the maximum dose of diuretics Diuretic intractable ascites : Ascites that can not be mobilized or the early recurrence of which cannot be prevented because of the development of diuretics induced complication that preclude the use of an effective diuretics dosage

REQUISITES OF REFRACTORY ASCITES Treatment duration : Intensive diuretic therapy for at least 1 week and a Na restricted diet of less than 90mmol/day. Lack of response : Mean weight loss of less than 0.8kg over 4 day and Urinary sodium output less than sodium intake Early ascites recurrence: Reappearance of grade 2 or 3 ascites within 4 weeks of initial mobilization Diuretic induced complications: hepatic enceph, renal impairment, hyponatremia, hypo- or hyperkalemia

TREATMENT OPTIONS FOR REFRACTORY ASCITES serial therapeutic paracentesis with albumin (1st line) peritoneal venous shunting (Alfa pump) TIPS liver transplant

TIPS TIPS correct sinusoidal hypertension Tips insertion is recommended in  recurrent ascites and refractory ascites. Ascites resolves in 70-90% of patient Reported high mortality Not recommended in pts. with Bil >3 PLT <75 * 10*3 Ch. hepatic enceph or current HE >grade2 Progressive renal failure Pulmonary HTN Patient of child C cirrhosis may not be benefit by tips due to high rates of encephalopathy and mortality

Automated Low Flow Pump subcutaneously implanted pump connected to catheter that transfer ascites from peritoneal cavity to bladder, from which it is eliminated in urine. Adverse effect: AKI (require close monitoring)

Liver Transplantation Patient with cirrhosis and ascites should be considered as potential candidate of liver transplant Predictor of poor survival Refractory ascites Previous SBP Arterial hypotension Hepatorenal syndrome

C OMPLICATIONS OF ASCITES HEPATIC HYDROTHORAX: Cardiopulmonary and primary pleural disease should be ruled out before diagnosing hepatic hydrothorax Diagnostic thoracocentesis should be performed when infection of pleural fluid is suspected 1 st line management  Diuretics and thoracocentesis In dyspnea  Therapeutic thoracocentesis Recurrent symptomatic hepatic hydrothorax  TIPS Refractory hepatic hydrothorax not amenable to LT or TIPS  Pleurodesis

MANAGEMENT OF VARICEAL HEMORRHAGE primary prophylaxis must be initiated upon detection of “high-risk varices” Small varices with red wale marks or C hild Pugh C  NSBBs Medium-large varices  NSBBs or EBL In pts with progressive hypotention or who develop bleeding, sepsis, AKI or SBP  NSBBs should be discontinued Antibioic prophylaxis is recommended in DCLD pts for 7 days ceftriaxone 1g/24h  1 st line, those already on quinolone prophylaxis or quinolone resistant bacterial infection In acute variceal bleed  terlipressin, somatostatin or octreotide for 5 days. 1 st line management  vasoactive drugs and band ligation with in first 12hrs Beta blockers and vasodilators should be avoided during acute bleeding episode

Management Of SBP

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