Ascites Mai kadry Ascites Physiological 100-150 mm For lubrication Pathological accumulation of fluid within the peritoneal cavity: ❑ Free ❑ Non-Purulent Loculated ascites Most common cause Portal hypertension secondary to cirrhosis (80%) ❑ Malignant ascites ❑ Tuberculous ascites ❑ Sarcoidosis associated ascites Etiology of Ascites: SAAG Serum albumin conc. – ascetic fluid albumin conc. > 1.1 g/dL Portal hypertension ❑ ❑ ❑ ❑ < 1.1 g/dL Rare ❑ Meigs syndrome ❑ Vasculitis Cirrhosis (81%) Heart failure (3%) ❑ Peritoneum mesothelioma Hepatic venous occlusion *Budd-Chiari syndrome* Constructive pericarditis Peritoneal Non-portal hypertension ❑ ❑ ❑ ❑ ❑ ❑ Cancer Infection (TB) Pancreatitis Serositis Nephrotic syndrome Hereditary angioedema SAAG Serum albumin conc. – ascetic fluid albumin conc. > 1.1 g/dL Serum albumin conc. Ascetic fluid albumin conc. Transited < 1.1 g/dL Serum albumin conc. Ascetic fluid albumin conc. Exudate Fluid nature Transited Exudate Low protein content High protein content All cause of ascites with high SAAG ratio All cause of ascites with low SAAG ratio EXCEPT heart failure EXCEPT Nephrotic syndrome Mechanism of ascites formation: ❑ Hypoalbuminemia (Major factor) ❑ Portal hypertension (Localizing factor) ❑ Sodium and water retention ❑ Minor lymphatic obstruction Sodium and water retention Urinary sodium excretion < 5mmol/day Fluid accumulation Ascites Expansion of extracellular fluid volume Edema Theory for ascites formation: Peripheral arterial vasodilatation Cirrhosis Cytokines Inflammatory mediators Stimulate Nitric Oxide Vasodilator Portal Vasodilatation Systemic Effective arterial blood volume Systemic arterial pressure Hypovolemia/ Hypotension Tachycardia/ Hyperdynamic circulation RAAS Aldosterone ADH Sodium & water retention Angiotensin II • potent vasoconstrictor • Potent stimulant for ADH • Potent activator of adrenergic system Underfilling theory Cirrhosis RAAS Hypovolemia Aldosterone Albumin ADH Oncotic pressure Fluid →outside capillaries Sodium & water retention Hypovolemia Ascites Overfilling theory Hepatorenal reflex Aldosterone Least accepted Cirrhotic liver Unable to metabolize aldosterone Aldosterone Salt – water retention Ascites Diagnosis Diagnostic paracentesis 1. SAAG 2. Total ascetic fluid protein concentration If > 1.5 gm/dL → ↑ risk of SBP 3. Screened for spontaneous bacterial ascites Usually 1000 cells/mm3 4. Concentration of RBCs in cirrhotic ascites Hepatocellular carcinoma 5. Ascetic fluid cytology (Pathology) 50.000 cells/mm3 Bloody ascetic fluid Malignant ascetic Chylous ascites Filariasis DUE TO lymphatic obstruction → Lymph leakage How to diagnose Bedside test High fat content Triglyceride Infectious causes of ascites ❑ TB ❑ Filariasis Malignant ascites ❑ Peritoneal carcinomatosis (primary) ❑ Metastasis from distant organs (secondary) Milky white color Criteria ❑ ❑ ❑ ❑ ❑ Low SAAG ratio Exudate Rapidly accumulating ± Hemorrhage ± malignant cells Hemorrhagic ascites Traumatic tapping Ascetic fluid + Blood During sampling How to differentiate BY frequent sampling 3 samples by the same syringe Persistence of blood Causes all through 3 samples ❑ Malignant ascites ❖ ❖ ❑ ❑ ❑ Peritoneal carcinomatosis Rupture of HCC Rupture of internal organs. Tuberculous ascites Parietal hematoma Red color fades in the second and third samples Treatment Bed rest Salt restriction Diuretics TIPS Trans jugular intrahepatic portosystemic shunt Liver transplantation Spironolactone K. Sparing diuretics Aldosterone antagonist Natriuresis DOSE Initial daily dose = 100 mg Up to 400 mg TO achieve adequate natriuresis Beginning of Onset of 3-5 days treatment natriuretic effect Side effects Antiandrogenic activity In men ❑ Decrease libido ❑ Impotency ❑ gynecomastia In women ❑ Menstrual irregularity furosemide Cause marked natriuresis and diuresis in normal subjects DOSE Initial daily dose = 40 mg Every 4-7 days Up to 160 mg/ day Side effects ❑ Severe electrolyte disturbance ❑ Metabolic alkalosis DO NOT EXCEED Therapeutic paracentesis Large Large volume paracentesis Ascites Colloid replacement Refractory 8 gm albumin/ liter Complications Abdominal bleeding Infection Leakage If Prevention ❑ Proper sterile technique ❑ Autoclaved instruments Hematoma Abdominal P. Coughing Defecation Prevention Suturing Post-Paracentesis circulatory disturbance Rapid shift in Rapid I.V volume removal Drop in B.P Prevention Complication s Pleural effusion Pressure symptoms Dyspepsia – Constipation – dyspnea – Proteinuria Abdominal wall hernias Complications of paracentesis Spontaneous bacterial peritonitis SBP Infection of ascetic fluid in the absence of any source of infection: ❑ Intra-abdominal Diagnosis Paracentesis ❑ Surgical treatable Empiric antibiotic treatment Treatment Etiology E. Coli Klebsiella Third generation cephalosporines Pathology Bacterial translocation *Cefotaxime* Sympathetic overactivity SBP variants bacterascites PMN < Culture: multiple organisms Polymicrobial ❑ Inadvertent puncture of the intestine during paracentesis ❑ Multiple scars ❑ Post-operative adhesion ❑ Presence of ileus Refractory ascites Ascites can not be mobilized Or early recurrence of which cannot be satisfactorily prevented by medical therapy Diuretic intractable ascites Diuretic resistant ascites Refractory to: ❑ Dietary sodium restriction (4.6-6.3g of salt/ day) ❑ Intensive diuretic treatment *FOR at least 1 week* o Spironolactone 400mg/day o Frusemide 160 mg/day Refractory to therapy DUE TO: ❑ Development of diuretic induced complications → preclude use of effective diuretic dosage Treatment ➢ Repeated large volume paracentesis ➢ Shunt operation (peritoneovenous) TIPS ➢ Liver transplantation Hepatorenal syndrome Rapid deterioration of kidney function DUE TO cirrhosis – fulminant liver failure Usually fatal UNLESS a liver transplant is performed Dialysis can prevent advancement of the condition Major criteria ❑ Low GFR *Indicated by serum creatinine >1.5 mg/dl* ❑ Exclusion of: ❖ Shock ❖ Ongoing bacterial infection ❖ Volume depletion ❖ Use of nephrotoxic drugs ❑ Stopping diuretics – volume repletion with 1.5L of saline → NO improvement in renal function ❑ NO proteinuria ❑ NO ultrasonographic evidence of: Obstructive uropathy Or parenchymal renal disease Minor criteria ❑ Urine volume < 500ml/day ❑ Urine sodium < 10 mEq/L ❑ Urine osmolality > plasma osmolality ❑ Urine RBCs < 50/high power field ❑ Serum sodium conc. < 130 mEq/L Clinical tests for ascites Tense ascites moderate ascites Mild ascites Minimal ascites Transmitted thrill test Tense ascites Tense ascites → False Negative transmitted thrill Loculated ascites Shifting dullness moderate ascites Modified shifting dullness Mild ascites Knee chest position Minimal ascites