Ascites CHOs FINAL Year -2023 Dr. Brima Bobson Sesay Medicine Department-NU
OUTLINE:- Definition of ascites Causes of ascites Differential diagnosis of ascites Mechanism of cirrhotic ascites Clinical manifestations Investigations Complications of cirrhotic ascites Treatment of cirrhotic ascites Refractory Ascites Spontaneous Bacteria Peritonitis
Definition of ascites: - Accumulation of fluid within the peritoneal cavity.
Causes of ascites: Generalized Causes : Hepatic e.g. liver cirrhosis/Chronic Liver Dz. Cardiac e.g. congestive heart failure. Renal e.g. nephrotic syndrome. Nutritional e.g. severe malnutrition.
Causes of ascites: B) Local causes : Abdominal malignancy: mesothelioma or peritoneal metatasis . TB peritonitis. Bacterial or fungal peritonitis.
Classification of ascites: Ascites is better classified as: Portal hypertensive ascites: serum ascites albumin gradient (SAAG) more than 1.1 g/dl. e.g. hepatic and cardiac. Non-portal hypertensive ascites: SAAG <1.1 g/dl in renal, malignant and inflammatory (TB) ascites.
Types of ascites: Differential criteria between transudate and exudate ascites: Exudate Transudate Item > 1017 < 1017 Specific gravity > 2.5 g/dl < 2.5 g/dl Protein co nt ents > 0.5 < 0.5 Protein ascites/serum ratio > 200 IU/L < 200 IU/L Lactic dehydrogenase In association with infections, malignancy, or connective tissue diseases Cases of generalized anasarca due to hepatic, renal and nutritional causes Causes
Clinical manifestations: Symptoms: Insidious onset. Increased abdominal girth. Recent weight gain. Shortness of breath. Early satiety. Generalized abdominal pain.
Clinical manifestations: B) Signs: Physical signs suggestive of cirrhosis and portal hypertension (e.g., spider navei, palmar erythema, splenomegaly, or flapping). The patient is sallow, muscle wasting is profound, and the thin limbs with protuberant belly lead to the description of the patient as a spider man.
Clinical manifestations: B) Signs: The abdomen is enlarged (mainly in the flanks), the umbilicus is everted, protrusion of hernias, visible or distended abdominal wall veins (portal & IVC collaterals), the latter disappeared when ascites is controlled. Abdominal striae may develop. Ascites is mainly detected by percussion.
Clinical manifestations: C) Associations: Pleural effusion: due to diaphragmatic defect allowing ascites to pass into the pleural cavity, mainly right sided. Oedema usually follows ascites.
Investigations: A) Ultrasonography: It detects minimal ascites, encysted ascites. It shows the size of the liver, spleen, portal vein diameter, thus it can diagnose portal hypertension. It shows the echopattern and surface of the liver and thus can diagnose liver cirrhosis and tumours .
Investigations: B) Diagnostic paracentesis : Parameters: physical: color, aspect. Chemical: proteins, albumin (for SAAG). Cells: WBCs (PMNLs or lymphocytes), RBCs. Bacteriological: culture and sensitivity.
Investigations: Diagnostic paracentesis : Cirrhotic ascites straw, clear transudate (proteins <2.5 gm / dL ) SAAG is > 1.1 g/ dL . WBCs: usually less than 100/mm 3 with a predominance of mononuclear cells and a low number of PMNLs.
Investigations: C) Plain X-ray abdomen: shows diffuse ground glass appearance. D) Laparoscopy: It is highly diagnostic for TB lesions allowing biopsy, histopathology and culture which settles the diagnosis beyond doubt. Laparoscopy also show clearly the spleen, liver and allow for aimed biopsy if needed.
Treatment of cirrhotic ascites: 1. Bed rest. salt restriction. Diuretics: spironolactone (100 up to 400 mg/day) , frusemide (40 up to 160 mg/day). Therapeutic paracentesis is generally a 2 nd line treatment except for patients with marked and refractory ascites.
Refractory ascites: Definition: ascites that cannot be mobilized or prevented from recurring by medical therapy. It is divided into: Diuretic-resistant: ascites is not mobilized despite maximal diuretic dosage. Diuretic-intractable: development of diuretic-induced complications that preclude the use of an effective diuretic dosage.
Refractory ascites: Dietary history, use of NSAIDs, ACEIs or ARBs, and patient compliance with the treatment regimen must be reviewed before confirming the diagnosis.
Treatment of refractory ascites: Repeated large volume paracentesis (LVP) with or without IV salt free albumin. TIPS should be considered 2 nd line treatment, and reserved for patients who require frequent LVP. Liver transplantation.
Spontaneous Bacterial Peritonitis
SBP – Antibiotic Therapy I Initiate for PMN ≥ 250/mm 3 IV Cefotaxime 2g q8 hours or Ceftriaxone 2g q24hours Duration of therapy unclear 2 weeks suggested if Blood cultures(+) If repeat paracentesis at 48 hours shows PMN ≤ 250/mm 3 , then 5-7 days of treatment may be adequate
SBP – Antibiotic Therapy II Prophylactic antibiotics should also be prescribed indefinitely until ascites has eliminated Options include: -Bactrim DS 1 tab po 5 days/week -Cipro 750mg po q week