2.  Defenetion  Pathogenesis  Causes  Clinical features  Complications  Investigations  Management

3. ASCITES  it’s the accumulation of fluid in the peritoneal cavity.  It Could Be Either: Transudate Or Exudate.  it’s a common complication of liver cirrhosis.

6. pathogenesis  The factors that involved in its pathogenesis include: 1-sodium and water retention. 2-portal hypertension. 3-low serum albumin as a consequence of poor synthetic liver function, this lead to reduction in plasma oncotic pressure.

7. Causes

8. Malignant disease : 1.It can cause lymphatic obstruction 2. Affect the permeability of the cells Cirrhosis : 1.Decrease the production of albumin this will decrease the oncotic pressure. 2. Portal hypertension. 3.Sodium and water retention. –decrease ALDOSTERONE metabolism 4.lymphatic obstruction.

9. Right sided heart failure : cause ascites by cause portal hypertension. pancreatitis : cause ascites when there is destruction of pancreatic duct and fluid leak to peritoneal cavity. Infection like TB : cause ascites by exudation of proteinaceous fluid from the tubercles.

10.  Ascites Is One Of The Causes Of Abdominal Distension.  Other causes ( 5F ) : Fat----obesity. Flatus----pseudo-obstruction, obstruction Faeces----sub acute obstruction, constipation Fetus. Functional– bloating as in irritable bowel disease.

11. Clinical feature  Small amounts of ascites are asymptomatic.  but with larger accomulation of fluid (>1L) : abdominal distension Fullness of the flanks Shifting dullness on percussion

12.  In sever ascites : fluid thrill Eversion of the umbilicus Herniae Abdominal stria Divarication of the recti Scrotal oedema

13.  There is Other sign of ascites may be present due to its underlying cause : ** dilated superficial abdominal vein,leg swelling, bruising, gynecomastia, hematemesis in Portal hypertension **mental change in Encephalopathy **chronic fatigue or weight loss in Cancer **shortness of breath, wheezing and exercise intolerance in Heart failur

15. complication 1)Renal failure can occure in patient with ascites. It can be pre-renal due to : Vasodilatation from sepsis Diuretic therapy Or due to hepatorenal syndrom

16. 2) Hepatorenal syndrom : ** occure in 10% of patient with advanced cirrhosis complicated by ascites. **there are 2 clinical type Both are mediated by : renal vasoconstriction due to underfilling of the arterial circulation

17. Type 1 : *Progressive oliguria. * Rapid raise of serum creatinine. * Urine sodium excretion 1.5 * No proteinuria. * Very poor prognosis ( without treatment median survival is less than 1 month ) * Other non functional causes of renal failure must be excluded befor the diagnosis is made *Treatment : consist of albumin infusion in combination with terlipressin and is effective in about 2 third of patient

18. * Patient who survive should be considered for liver transplantation type 2 *occure in the patient with refractory ascites * characterised by moderate and stable increase in serum creatinin * has abetter prognosis

19. 3) Spontaneous bacterial peritonitis  may present with : Abdominal pain, rebound tenderness, absent bowel sound and fever. In patient with obvious feature of cirrhosis and ascites * Abdominal sign are mild or absent in about one third of patient, and in these patient hepatic encepalopathy and fever are the mean feature  diagnostic paracentesis may show : Cloudy fluid and acites neutrophil count >250*10^6

20. ** The Source of infection : cant usually be determined but most organism isolated are of enteric origin and escherichia coli is frequantly found. ** in ascites blood culture afinding of multiple organism should arouse suspecion of perforated viscus ** Treatment : should be started immediately with broad spectrum antibiotics (such as cefotaxime or piperacillin/tazobactam ). ** Recurrence of SBP is common but may be reduced with prophylactic quinolone such as nor-floxacin or ciprofloxacin

21. Examination Inspection for : jaundice,everted umpilicus, spider naevi Palpate for : splenomegaly, hepatomegaly Percuss for : shifting dullness, fluid thrill Auscultate for : Hepatic bruit, Bowel sound,Renal bruit.

24. Palpation of the liver

25. Palpation of the spleen

26. Fluid thrill test

27. Shifting dullness

28. Investigations Ultrasonography : the best way to detect ascites particularly in obese and those with small volumes of fluid, the sonographer can estimate the amount of fluid we have elevation of the diaphram and poor defenition of intra abdominal organs. CT scan more accurate but not common. Doppler studies may show the direction of flow in the portal vein as well as detecting portal vein thrombosis

29. Plueral effusion found in 10% of patients usually on the right side (hepatic hydrothorax) most are small and only identified on chest x-ray, occasionally massive hydrothorax occurs. Effusions on the left side shouldn’t be assumed to be due to the ascites Paracentesis : drainage of ascitic fluid recommended if ascites is new, can be used to confirm prescence of ascites or as therapeutic way but is most useful to obtain fluid for analysis. ( can be done under guidance of ultrasound)

30. Ascites in patient with abdominal cancer seen on ultra sound

31. paracentesis

32. Gross appearance of the ascitic fluid may point to the underlying cause causeGross appearance cirrhosisStraw-coloured or light green Infection (Peritonitis, Primary bacterial infection,Perforated bowel, appendicitis,pancreatitis) Strangulated or infarcted bowel Cloudy / turbid High protein content or high cell count due to infection Lymphatic obstruction (usually) TB Parasitic infection Milky-white (chylous) Due to high lipid content Benign or malignant tumor Hemorrhagic pancreatitis perforated ulcer Trauma ( blood will clot) Bloody Requires 10,000 RBC/microlitre to appear pink And 20,000 to have bloody appearance

33. In the past ascitic fluid has been classified as : Transudate : total protein concentration less than 25 g/L, it indicates systemic disease. Like : liver cirrohsis, renal failure, hypoalbuminamea(nephrosis), cardiac (RHF, pericarditis, valve disease ) Exudate : total protein concentratioin more than 25 g/L, it indicates local disease. Like : malignancy, pancreatitis, infection(TB) lymphatic obstruction, venous obstruction.

34. Evidence for these ascites:serum ratios is controversial – Ascitic fluid protein/Serum Protein >0.5 – Ascitic Fluid LDH/Serum LDH >0.6 – Ascitic Fluid LDH >400 Presence of any 2 of these three findings is usually associated with TB, Malignancy or Pancreatitis Absence of all three usually indicates hepatic cause 30% of systemic diseases patients have total protein concentration more than 30g/L. So we calculate the SAAG

35. Serum-ascites albumin gradient (SAAG): SAAG = serum albumin – ascites albumin If its more than 1.1 mg/dl its due to portal hypertension (implies exudate). Less than 1.1 mg/dl non-portal hypertensive etiology (implies transudate). It’s the most useful measure for fluid protien.

36. SAAG < 1.1 gm/dlSAAG > 1.1 gm/dl Peritoneal Carcinomatosis Tuberculous Peritonitis Pancreatic Ascites Bowel Obstruction Biliary Ascites Nephrotic Syndrome Posteroperative Lymphatic Leak Serositis in Connective Tissue Disease Cirrhosis Alcoholic Hepatitis Cardiac Ascites Massive Liver Metastasis Fulminant Hepatic Failure Portal Vein Thrombosis Veno-Occlusive Disease Myxedema Fatty Liver of Pregnancy

37. Cell count : RBC : - normally none - >100/microlitre indicates malignancy or TB - >100,000/microlitre indicates trauma WBC: - normally < 300/microlitre - > 300/microlitre abnormal Spontaneous Bacterial Peritonitis (90%), cirrhosis (50%) >25% neutrophils TB, chylous ascites>25% lymphocytes TB peritonitisMesothelial cells

38. Biochemistry : - low ascites glucose (less than 6) suggest malignancy or tuberculosis - ascitic amylase activity above 1000 U/L identifies pancreatic ascites - cytological examination may reveal malignant cells (1/3 of cirrhotic patients with a bloody tap have hepatoma) - polymorph nuclear leukocyte count above 250x10^6/L strongly suggest infections.(SBP)

39. Other important tests : - liver enzymes - coagulation - basic metabolic profile. Additioinal tests if indicated : - microbiological culture - gram stain gram + cocci >> primary peritonitis gram - >> secondary

40. Management Sodium and water restriction. Diuretics. Paracentesis. Peritoneo-venous shunt. Transjugular intrahepatic portosystemic stent shunt (TIPSS)

41.  Exudative ascites due to malignancy is treated by paracetesis.  Transudative ascites is treated by : Sodium and water intake restriction and Increase urinary output with diuretics and If necessary, removing ascites directly by paracentesis.

42. Sodium and Water intake restriction  It aims to redistribute fluid from intraperitoneal cavity to intravascular space.  Sodium intake restriction is essential to achieve negative sodium balance.  Decrease intake to 100mmol/day is usually adequate.

43.  Some drugs contain significant amounts of sodium( as phenytoin and antacids) and others cause sodium retention( such as NSAIDs and corticosteroids) should be avoided.

45. Water intake restriction to 1-1.5L/day is indicated Only if plasma sodium is below 125mmol/L.

46. Diuretics  Diuretics should be tittered to remove no more than 1 liter per day so body weight should not falls more than 1 kg/day.

47.  The first line diuretic is Spironolactone because its an aldosterone antagonist. We start by 100mg daily and increase it up to 400mg daily according to response of the pt.  It causes painful gynaecomastia and hyperkalemia in which case ameloride (5- 10mg/day) can be substituted.

48.  If response to spironolactone is poor we can add loop diuretic such as furosemide (20- 40mg/day) but these can cause hyponatremia, hypokalemia and fluid depletion.

49. Paracentesis  It’s the fist-line treatment of refractory ascites.  It can be used as an initial therapy or when other treatments fail.  It is Also used as a means of rapid therapy in patients with ascites and peripheral oedema, thus avoiding prolonged hospital stay.

50.  The main complication is hypovolaemia and renal dysfunction (post-paracentesis circulatory dysfunction) as the ascites reaccumulates at the expense of the circulating volume.  This is more likely with > 5 litres removal and worse liver function.  So its safe provided the circulation is supported with an IV colloid such as human albumin(6-8 g per liter of ascites removed).

51. Paracentesis

52. Transjugular intrahepatic portosystemic stent shunt (TIPSS)  TIPSS can relieve resistant ascites and it maybe an option where the only alternative is frequent, large- volume paracentesis.  It can be used in pt.s waiting for liver transplantation or in those with resonable liver function but can aggravate hepatic encephalopathy in those with poor function.

53. TIPSS

54. Peritoneo-venous shunt  It is a long tube with a non-return valve running subcutaneously from the peritoneum to the internal jugular vein in the neck which allows the ascitic fluid to pass directly into the systemic circulation.  It may lead to infection, DIC, SVC thrombosis, pulmonary oedema and bleeding from esophageal varices, so its rarely used now.

55. References: Davidson’s principles & practice of medicine 21 st edition. Kumar Lifeinthefastlane.com Kaplan Master the boards internal medicine second edition