Approach to ascites

Approach to a pediatric patient with ascites made simplified with referrence from all standard textbooks

1. Dr Pravakar Sethi Diagnostic approach to ascites

2. ASCITES Askites  a Greek word which means ‘bag’ or ‘sac’ . definition ASITES IS AN ACCUMULATION OF FREE FLUID WITHIN THE PERITONIAL CAVITY. In CHILDREN, hepatic,renal,and cardiac disease are the most common causes .

3. CAUSES OF ASITES HEPATIC Cirrhosis Cong.hepatic fibrosis Fulminant hepatic failure Budd- chiari syndrome Lysomal storage ds . RENAL Nephrotic synd. Obst.uropathy Perforation of urinary tract Peritoneal cyst

4. Cont. CARDIAC Heart failure Constrictive pericarditis Inferior venacaval web INFECTION Tuberculosis Abscess chlamydia schistosomiasis

5. Cont. GASTROINTESTINAL Infected bowel Perforation NEOPLASM Lymphoma Neuroblastoma GYNAECOLOGIC Ovarian tumor ovarian torsion,rupture PANCREATIC Pancreatitis rupture pancreatic duct.

6. Cont. MISCELLANIOUS SLE Ventriculo peritoneal shunt Eosinophillic ascites Chyllous ascitis Hypothyroidism

7. Pathophysiology of Ascites From: Robbins Basic Pathology

8. pathogenesis According to starling’s hypothesis the exchange of fluids between the blood and tissue spaces is controlled by the balance between two factors; Capillary blood pressure Osmotic pressure of plasma proteins (plasma colloid osmotic pressure) capillary blood pressure / Plasma colloid osmotic pressure  Ascites

9. Mechanisms Underfill theory Overfill theory Vasodilatation theory

10. UNDERFILL THEORY HYPOVOLAEMIA Kidney feels  Body is under filled & require more salt and water Stimulates JG cell to release RENIN angiotensinogen  anginsioten -I in lungs by ACE Angiotensin II Releases aldosterone from the zona glomerulosa Increase the reabsorption of sodium and water & excretion of potassium from the DCT ASCITES

11. Overfill theory The combination of portal hypertension and circulating hypervolaemia results in ‘over flow’ from the congested portal system to the peritoneal cavity, to produce ascites Decrease in vasodilatory prostaglandins like PGE2 & PGE1 deteriorates the renal fuctionASCITES

12. NITRIC OXIDE THEORY(PERIPHERAL ARTERIAL VASODILATATION THEORY) Most recent theory When a portal pressure increases above a critical threshold, nitric oxide levels increase leading to vasodilatation As the state of vasodilatation worsens  plasma levels of vasoconstrictor, sodium retentive hormones increase and renal function deteriorates ASCITES

13. EVALUATION …

14. Evaluation of ascites patient history Age child : Tuberculous ascites and nephrosis Middle age : cirrhosis of liver Old age : malignance Sex Female : meigs synd., pelvic tumours and infection and ovarian tumours Order of Development of Ascites cardiac causes : Leg oedema precedes ascites . Kidney causes : Puffiness of face precedes ascites . Cirrhosis of liver : Ascites is the first feature . Ascites is the part of generalised anasarca caused by nephrosis , anaemia , hypoproteinaemia etc.

15. General examinations Enlarged lymph nodes : Suggestive of TB , leukaemia , malignancy , and lymphomas . Associated jaundice : Cirrhosis of liver . Dyspnoea , PND , orthopnoea , and oedema : congestive cardiac failure . Periorbital oedema , puffiness of face and oedema associated with ascites : acute nephritis , nephrotic synd. Severe anaemia : Ascites of haematologic origin . Other signs of malnutrition with ascites : Kwashiorkor .

16. Systematic examination Abdominal Examination Inspection Abdomen is distended . Umbilicus is everted and slit transversely( laughing umbilicus ) The distance between umbilicus and xiphisternum is more than the distance between umbilicus and pubic symphysis . Flanks are full. Nearly 1500 mL of fluid is required to make the flanks full . Veins are dilated over the abdomen . Scrotal oedema indicates nephrotic synd.

17. Quantifications of ascites 1+ : Detectable only by careful examinations 2+ : Easily detectable but of relatively small volume 3+ :obvious ascites but not tense 4+ :Tense ascites

18. Palpation of abdomen Features Significance Tenderness and local rise of temperature Peritonitis Rebound tenderness or Blumberg sign Peritonitis Doughy or rubbery feel Tuberculous peritonitis Presence of splenomegaly , ascites , and caput medusase Cirrhosis of liver Enlarged tender liver and ascites Congestive cardiac failure Palpation of intra-abdominal masses TB Palpation of lumps and enlarged glands TB, malignancy , leukaemia , and Hodgkin’s lymphoma

19. Examination of veins over the abdomen Vein obstructed Site of engorged veins Direction of flow of blood 1. Portal vein obstruction Veins around the umbilicus and upper abdominal wall Veins above umbilicus : bellow upwards . Veins bellow umbilicus : from above down words . Veins around umbilicus is called caput medusae 2.Hepatic vein obstruction Lower thorax and upper abdomen From above downwards 3.Inferior vena cava obstruction Lower third of abdominal wall and flanks From bellow upwards

20. percussion Shifting dullness is an important sign of free fluid in the peritoneal cavity . It requires nearly 500 mL of fluid to elicit this sign . Fluid thrill is present in tense ascites . If the fluid is small in amount nearly 120 mL , it will be demonstrated by puddle sign ( lawson’s sign ) . Ausculation It is not of much use in ascites .

21. Onset of ascites SUDDEN INSIDIOUS Acute Budd- Chiari synd. Acute right heart failure Sudden decompensation of previously compensated cirrhosis Pancreatic ascites Decompensated cirrhosis Chro.Budd-Chiari synd. TB ascites Nephrotic synd. Hypothyroidism Constr. pericarditis

22. Demonstration of ascites FIVE CLASSICAL PHYSICAL SIGN Bulging flanks  belly of a frog Flank dullness or horse-shoe dullness Shifting dullness  high sensitivity (85%) & low specificity (50%) Fluid wave / thrill PUDDLE SIGN(Lawson’s sign)- decreased auscultation of high freqency vibrations in the central abd.when flicking the side of the abd.with the patient of hands knees .

23. GRADING OF ASCITES GRADE SEVERITY SIGNS 1 Mild Puddle signs + USG abdomen+ 2 Moderate Shifting dullness+ No fluid thrill 3 Severe Fluid thrill+ Resp. embarrassment+

24. Minimum amount of fluid required Test Minimum fluid in ml. Diagnostic tap Puddle sign Shifting dullness Fluid thrill Ultrasound scan CT scan 10-20 120 500 1000-1500 100 100

25. dignosis of ascites

26. After the diagnosis of ascites is made, its cause should be determined by laboratory analysis. ascitic fluid study (diagnostic paracentesis )

27. DIAGNOSTIC PARACENTESIS 10 to 20 mL The bladder should be emptied prior to the procedure Most common Site left lower quadrant Other site In the midline between the pubic- symphysis & umbilicus, Right iliac fossa , lateral to the inf. epigastric artery or a few cm above the inguinal lig . Z-technique

28. DIAGNOSTIC PARACENTESIS

29. CONTRAINDICATIONS Severe Coagulopathy Abdominal wall hematoma Local infecction Relative Repeated surgeries

30. complications Infection & peritonitis Bladder or bowel perforation Hypovolaemia & shock (>1 lit. remove rapidly), especially if the patient does not have oedema Blockage of needle

31. Tests on Ascitic Fluid Routine Optional Unusual Cell count and differential Glucose concentration Tuberculosis smear and culture, adenosine deaminase Albumin concentration LDH concentration Cytology Total protein concentration Gram stain Triglyceride concentration Culture in blood culture bottles Amylase concentration Bilirubin concentration

32. Colour / appearance of ascitic fluid Straw coloured / Transparent Bloody fluid Opaque / milky Dark -brown Black / tea colour normal Cirrhosis TB Malignancies Trauma TB peritonitis Pancreatitis Perforated viscus Traumatic tap Chylous ascites Billiary ascites Deep jaundice Pancreatic ascites (pigment ascites ) Malignant melanoma

33. CELL NORMAL UNCOMPLICATED CIRRHOTIC ASCITES SBP IN CIRRHOTIC ASCITES TB ASCITES WBC count  Cell RBC < 250 / cc Lymphocytic < 500 / cc ANC < 250 cells > 500 / cc PMN > 250 High Lymphocytic predominance > 50,000 cells Also in trauma , malignancy

34. cytology At least 50 ml of fluid 50 – 80% accurate –diagnosis of malignant ascites Differentiate malignant cells from atypical mesothelial cells

35. GRAM STAINING/CULTURE Gram stain – 10 % sensitive --approximately 10,000 bacteria / ml are required Culture in blood culture bottle 92 % yield

36. TOTAL PROTEIN Low sensitivity in differentiating exudate from transudate . Elevated TP ( ≥2.5 g ) + high SAAG hepatic congestion Elevated TP + low SAAG malignancy

37. Differences bet. exudative & transudative ascites Features Exudative ascites Transudative ascites Protein in g% Sp gravity LDH Fibronectin Cholesterol Hyaluronic acid ADA >3 g% >1015 High 75 mg%--(malignant ascites ) >48 mg%--(malignant ascites ) >0.25 mg% ( mesothelioma ) High in TB ascites <3 g% <1015 Low Low Low Low Normal

38. SERUM-ASCITES ALBUMIN GRADIENT (SAAG) SAAG= serum albumin – ascitic fluid albumin The gradient correlates directly with portal pressure. A gradient > 1.1 g/ dL , ascitic is due to portal hypertension (high gradient or transudative ascites or portal hyper tensive ) A gradient < 1.1g/ dL (low gradient / exudative or non potal hyper tensive ) suggests that the ascites is not due to portal hypertension . The specificity & sensitivity of SAAG around 97% SAAG-Is far superior to the old exudate-transudate concept . SAAG does not explain the pathogenesis of PTN

39. ERRORS IN SAAG Timing of collection Arterial hypotension Chylous ascites Serum hyperglobulinemia

40. Classification of ascites based on SAAG

41. Classification of ascites based on SAAG High-gradient ascites (SAAG>1.1 gm/dl) Low gradient ascites (SAAG<1.1 gm/dl) Cirrhosis Veno -occlusive disease Budd- chiari syndrome Fulminant hepatic failure Cardiac ascites Mixed ascites Massive liver metastasis Tuberculous ascites Nephrotic synd. Pancreatic ascites Chylous ascites Biliary ascites Serositis in collagen disease Peritoneal carcinomatosis Postoperative lymphatic leak Bowel obstr ./infarction

42. imaging

43. X RAY Non specific Direct signs Elevation of diaphragm Diffuse abdominal haziness Bulging of flanks Indistinct psoas margins Separation of small bowel loops Centralization of floating bowel Hellmer’s sign ‘ Dog’s ear’ or ‘Mickey Mouse’ Medical displacement of cecum and ascending colon Lateral displacement of properitoneal fat line

44. USG Extreamly sensitive, can detect as little as 100 mL , “ lollipop”/ arcuate appearance of small bowel loops Coarse internal echoes blood Fine internal echoes chyle Multiple septa TB , pseudomyxoma peritonei Matting or clumping of bowel loops, thickning of fluid- wall interface Tethering of bowel along post . abd . wall with loculated fluid in between malignancy Gall bladder thickening cirrhosis

45. CT Can differentiate malignant from benign Lymph nodes Focal liver , spleenic lesions Pancreatic and colonic masses Malignant ascites fills greater & lesser sac More useful than USG in detecting hepatic lesions , primary or secondary Detect up to 100 ml of fluid

46. Complications of ascites Spontaneous bacterial peritonitis ( SBP) Hydrothorax Gastro- oesophageal reflux Respiratory distress and atelectasis due to elevation of diaphragm Inguinal / umbilical / femoral hernia Scrotal oedema Collection of fluid in the pleural sac Mesenteric venous thrombosis Functional renal failure.

47. Spontaneous bacterial peritonitis Characterized by the spontaneous infection of ascitic fluid in the absence of an intra-abdominal source of infection Prevalence  10-30 % Sex  M = F Age  Before 6 year age – most common Most cases occure in children with ascites nephrotic synd. cirrhosis infection. WBC >250 cells / mm3 (>50 % PMN)

48. Cont… Organisim - Pneumococci (most common) Gr. A strept . , Enterococci , Staph. Gr. – ve enterobiacteria  E. coli, Klebsella pneu . Involves the translocation of bacteria from the intestinal lumen to the lymph nodes, with subsequent bacteremia and infection of ascitic fluid . Third – generation cephalosporins ( cefotaxime ) + Aminoglycoside . Duration  10-14 days Amoxicicillin + clavulanic acid  also effective Vancomycin  resistant pneumococci

49. Sbp recurrence 70 % probability of recurrence at one year Long – term antibiotic prophylaxis with quinolones reduces the rate of recurrence Cotrimoxazole may be an alternative to quinolones .

50. Complication of sbp The most severe is the hepato -renal syndrome, which occurs in up to 30 % of patients and carries a high mortality rate Intravenous albumin (1.5 gm /kg at diagnosis and 1gm/kg 48 hours later ) helps to prevent the hepato -renal syndrome and improves the probability of survival

51. CHYLOUS ASCITES Turbid, milky, or creamy peritoneal fluid due to the presence of thoracic or intestinal lymph. Shows staining fat globules with sudan black Oil red Opaque milky fluid usually has a triglyceride concentration of >1000 mg/ dL .

52. Cont.. Is most often the result of lymphatic obstruction from Trauma/ surgeries Tumor Tuberculosis Filariasis Congenital abnormalities Nephrotic syndrome

53. PSEUDOCHYLOUS A turbid fluid due to leukocytes or tumor cells may be confused with chylous fluid. TESTS CHYLOUS ASCITES PSEUDOCHYLOUS ASCITES Fat globules by Sudan red stain present absent Ether test Top thick layer becomes clear, as fat dissolves in ether Remains turbid Alkali test No change in colour Becomes clear , as alkali dissolves cellular proteins

54. MUCINOUS ASCITIC FLUID Pseudomyxoma peritonei Colloid carcinoma of the stomach or colon with peritoneal implants.

55. Ascitic fluid study CIRRHOSIS TB PYOGENIC PERITONITIS CCF NEPH. SYND. PANCRE. ASCITES NEOPLASMS COLOR STRAW / BILE STAINED Clear, turbid, hmgic or chylous Turbid or purulent Straw Straw / chylous Turbid , hmgic or chylous Straw, Hmgic,chylous,mucinous PROTEIN < 2.5 g/dl >2.5 g/dl < 2.5 g/dl Variable <2.5 g/ dl Variable / >2.5 g /dl >2.5 g /dl Very high SAAG >1.1 g/dl <1.1 g/dl < 1.1 g/dl >1.1 g /dl <1.1 g /dl <1.1 g /dl <1.1 g/ dl RBC ( / µl) >10,000 - 1% >10,000 - 7% >10,000 Unusual >10,000 >10,000 unusual >10,000 Blood stain >10,000 - 20% WBC ( / µl) < 250 >1000 lymph 70 % Definit Δ  peritonial biopsy Predom . Polymorphs Gram stain + ve <1000 Usually mesothelial mononuclear < 250 mesothelial or mononuclear Variable Increase am ylase (>2000 u/ l ) >1000

56. TREATMENT

57. Management of ascites GOAL-To achieve ascites -free status -To maintain it thereafter INDICATION FOR HOSPITALIZATION If there is no response to outpatient management for 4-6 weeks. Tense (grade III) ascites with respiratory embarrassment Spontaneous bacterial peritonitis Diuretic – induced complications like ; Hyponatraemia , Na < 125 mEq /L Hypokalaemia , K < 3 mEq /L Hyperkalaemia , K > 6 mEq /L Hepatorenal synd. Hepatic encephalopathy Refractory ascites

58. TREATMENT OF HIGH SAAG ASCITES Bed rest Salt restriction Fluid restriction Diuretics Therapeutic paracentesis Albumin Peritoneovenous shunt TIPS transplantation 1000 ml / day Goal  wt loss to prevent renal failure of prerenal origin is 300-500 g per day in patients without peripheral edema and 800 - 1000 g per day in those with peripheral edema 1 gm / D in smallar children,2 - 3 gm / D in adolescents.

59. TREATMENT OF LOW SAAG ASCITES Peritoneal carcinomatosis therapeutic Paracentesis Ovarian tumours  surgery + chemo Tb ATT Pancreatic ascites  endoscopic stenting , surgery, or respond to somatostatin , octrotide therapy. Lymphatic leak after surgery  peritoneovenous shunting Chlamydia peritonitis tetracycline,doxycycline . Lupus steroid Dialysis related ascites  aggressive dialysis Nephrotic syndrome steroid Malignant ascitesChemotherapy

60. diuretics Are the mainstay of treatment and should be used liberally but carefully All diuretics are best given in a single dose in the morning- maximizes the compliance Potassium-sparing diuretics Aldosterone antagonists Spironolactone - DOC in cirrhotic ascites , 1- 6 mg/kg/D Carninone , Potassium canrenoate Amiloride (10 mg /kg) or triamterene can be used if spironolactone is not effective B. Loop diuretics (high- cilling diuretics) Furosemide , Torsemide , azosemide , tripamide , bumetanide , piretanide , Muzolimine , Ethacrynic acid C. Thiazides – hydroclorothiazide,dose 2- 3 mg / kg/D

61. Response to diuretic theraphy Relief of abdominal distension Relief of respiratory distress Decrease in abdominal girth Achieving a negative sodium balance (when sodium excretion is more than intake) indicates a good diuretic response Monitoring during diuretic therapy Patient should be assessed 1 week after starting therapy & than every 2 week Weight & abdominal girth should be measured, Look for oedma , grade of ascites and subtle sign of SBP

62. Therapeutic paracentesis Indications Tense ascites that causes respiratory embarrassment Intractable ascites not responding to the usual treatment To release intra abdominal pressure in moderate to severe ascites Large volume paracentesis , up to 200- 400 ml/ kg/D can be removed slowly over 4 – 6 hours if the patient has peripheral oedema Large volume tap(>5 l) ,I.V. colloid replacement with albumin 6-8 gm /L Dextran 70 is less effective than albumin

63. Criteria for discharge of the ascitic child Adequate weight loss and natriuresis Absence of of infection/peritonitis Absence of diuretic- induced complications

64. REFRACTORY ASCITES 5 to 10 % Defined as a lack of response to high doses of diuretics (400 mg of spironolactone per day + 160 mg of furosemide per day). Patients in whom there are recurrent side effect ( e.g , hepatic encephalopathy , hyponatremia , hyperkalemia , or azotemia ) when lower doses are given are also considered to have refractory ascites .

65. Theraputic options in refractory ascites Chronic outpatient paracentesis Ascites ultra filtration and re-infusion Le Veen shunt TIPS-( Transjugular Intrahepatic Peritonial Shunt ) Liver transplantation

66. TIPS(TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMIC SHUNT) TIPS consists of an intrahepatic stent inserted between one hepatic vein and the portal vein by a transjugular approach Effective in preventing recurrence in patients with refractory ascites Decreases the activity of sodium – retaining mechanisms and improves the renal response to diuretics.

67. Transjugular intrahepatic portosystemic shunt (TIPS)

68. disadvantage High rate of shunt stenosis (up to 75 % after 6 to 12 months ) Lead to recurrence of ascites ;hepatic encephalopathy High cost Lack of availability in some centers .

69. Current therapeutic strategies include repeated large –volume paracentesis with the use of plasma expanders and transjugular intrahepatic portosystemic shunts

70. Peritoneovenous Shunt Ascitic fluid is shunted from the high pressure peritoneal cavity to the low pressure superior vena cava by 1 . Le Veen shunt 2 .Denver shunt 3 . Minnesota shunt Denver Shunt (Similar to LaVeen Shunt) Contraindications Protein > 4.5 g/l (occlusion) Loculated ascites Coagulopathy Advanced renal/cardiac disease GI malignancy Complications Infection DIC Pulmonary edema Pulmonary emboli Shunt occlusion Malfunction Air embolism Congestive cardiac failure Variceal haemorrhage

71. Prognosis of ascites Despite the recent advances in the treatment of ascites , the prognosis is always grave after ascites develops in a cirrhotic patient . Only a change of 40 % being alive 2years later . The presence of hepatocellular failure, evidenced by jaundice and encephalopathy is a very bad prognostic factor . The prognosis may be better if ascites develops rapidly , especially if there is a well defined precipitating factor such as GI bleed .

72. Thank u. . .