ASCITIS IN CHILDREN BY DR VIJITHA

ASCITIS IN CHILDREN BY DR VIJITHA

1. ASCITES in children PRESENTER : Dr VIJITHA A S

2. CONTENTS INTRODUCTION PATHOPHYSIOLOGY ETIOLOGY CLINICAL FEATURES STAGING INVESTIGATION MANAGEMENT COMPLICATIONS DIFFERENTIAL DIAGNOSIS NEWER TREATMENT MODALITIES PROGNOSIS CONCLUSION

3. INTRODUCTION Ascites is of greek derivation (“ askhos ”) means “bag or sack “. Defined as the pathologic accumulation of fluid in the peritoneal cavity . In children, hepatic and renal disease are the most common causes, but ascites can also be caused by cardiac disease, trauma, infection, or neoplasia.

4. BACKGROUND Inside the abdomen there is a membrane called peritoneum which has 2 layers. One layer lines the abdominal wall and other layer covers the organs inside abdominal cavity. The peritoneum produces a fluid which helps the abdominal organs to slide smoothly over one another. Excess of this fluid builds up between these layers and termed as ascites .

5. ETIOPATHOGENESIS Ascites can be broadly classified into Cirrhotic ascites non cirrhotic ascites.

6. CIRRHOTIC ASCITES: PATHOGENESIS UNDERFILLING THEORY Portal hypertension leads to decreased blood volume leading to decreased renal perfusion. This activates RAAS and sympathetic nervous system resulting in sodium and water retention and leads to ascites. OVER FLOW THEORY Hepatorenal reflex causes inappropriate sodium and water retention followed by increased blood volume, which together with PHT leads to ascites.

7. PERIPHERAL ARTERIAL VASODILATATION THEORY Vasodilatation of peripheral vessels leads to systemic hypotension and decrease in cardiac output, followed by retention of sodium and water and ascites .

8. NON CIRRHOTIC ASCITES : PATHOGENESIS Hepatic causes- Acute viral hepatitis- transient PHT due to sinusoidal collapse, SBP and hypoalbuminemia are possible explanation. Post sinusoidal PHT – when hydrostatic and osmotic pressures within hepatic capillaries produce a shift of fluid from blood to the lymphatics at a rate, which exceeds its drainage capacity. Pancreatic ascites- Fluid Initially due to leakage of pancreatic juice from a disrupted pancreatic duct or a pseudocyst. Further occurs secondary to chemical reaction of peritoneum .

9. Biliary ascites- Bile leak in to peritoneum due to spontaneous or iatrogenic perforation of bile duct. Malignant ascites- Malignant cell produce fluid rich in protein which drags fluid into peritoneal cavity.

10. Chylous ascites Rupture of obstruction or distorted abdominal lymphatics as occurs in cong. Lymphangiectasia or other acquired conditions. Tuberculous ascites Peritoneal tubercles secrete proteinaceous material causing an osmotic drag of fluid and present as either diffuse or loculated ascites. Eosinophilic ascites In eosinophilic gastroenteritis, eosinophils infiltrate the peyer’s patches and if the serosa is infiltrated, it results in eosinophilic ascites. Infections Transient ascites may occur. Third spacing of fluid in dengue shock may cause ascites In leptospirosis, scrub typhus and typhoid fever, ascites is due to serositis.

11. CAUSES OF ASCITES IN CHILDREN

12. CLINICAL PRESENTATION The child may be asymptomatic The clinical hallmark of ascites is abdominal distention. If minimal fluid, mild abdominal discomfort Early satiety and dyspnea can occur with a moderate amount of ascites. Increase in abdominal girth and weight gain are early symptoms Anorexia, nausea, and growth failure are indicators of increasing ascites. Pain is usually not there unless infected Depending upon the etiology there will be other features like jaundice, gastrointestinal bleed, altered sensorium etc.

13. PHYSICAL FINDINGS Protuberant abdomen Tense and shiny skin Fullness of flanks Smiling/inverted umbilicus Distended anterior abdominal veins Organomegaly - Dipping method is used to palpate abdominal organs in tense ascites Formation of hernias – umbilical hernia

14. OTHER SIGNS- Check for jugular venous distention in constrictive pericarditis. Heart: Check for tricuspid murmur or signs of heart disease. Lungs: Examine for signs of Pleural effusion. Skin: May show cutaneous spider angiomas , palmar erythema, Dupuytren’s contracture, or large veins on the abdomen, asterixis may be present. Ascites may be part of generalized oedema in patients with cardiac disease or nephrotic syndrome. Lymph nodes enlargement - A pathologic left-sided supraclavicular node (Virchow's node) suggests the presence of upper abdominal malignancy.

15. STAGING OF ASCITES STAGE SIGNS 1+ Detectable only after careful examination 2+ Easily detectable but of small volume 3+ Obvious ascites but not tense ascites 4+ Tense ascites

16. Demonstration of ascitic fluid PUDDLE/LAWSON’S SIGN This test detects a small amount of ascitic fluid in children(120 ml) Method – make the patient lie down in prone position for 3-5 minutes then rise to knee elbow position. Percussion over umbilicus gives dull note. Perculto auscultatory method – change in note heard at the edge of fluid accumulation if the diaphragm of the stethoscope is moved laterally from the umbilicus while the flank is percussed lightly.. Sudden tympanic sound is the edge of ascites.

17. SHIFTING DULLNESS This finding is based on alteration of percussion note in flank when the position is changed and the air filled loops are displaced by fluid. In children greater than 500 ml is necessary for demonstration. Method – Percuss from umbilicus and move towards the flanks until dullness is reached. Mark this point and ask the patient to roll towards you. Wait for 30sec. then repeat percuss again. The area of tympanic will shift towards the top and the area of dullness towards the bottom. If the dull area become resonant indicates ascites.

18. FLUID THRILL Demonstration of a fluid wave indicates large amount greater than 1000 ml in peritoneal cavity. Method – Place one hand flat over the lumbar region of one side. Ask the patient/assistant to place the ulnar surface of their hand firmly in the midline of the abdomen. Flick/tap the other side of the abdominal wall and feel the thrill on the other hand placed on the opposite abdominal wall.

19. Minimum amount of fluid

20. INVESTIGATIONS Complete blood count Urine examination Liver function test Renal function test Clotting screen, especially for invasive investigations X ray abdomen USG abdomen CT and MRI abdomen Diagnostic abdominal paracentesis (ascitic fluid analysis)

21. IMAGING STUDIES X ray Chest and plain abdominal films More than 500 ml of fluid is required for ascites to be diagnosed on x ray. Elevation of the diaphragm, with or without sympathetic pleural effusions (hepatic hydrothorax), is visible in massive ascites.

22. The direct signs are more reliable and specific. In 80% cases, the lateral liver edge is medially displaced from the thoracoabdominal wall ( Hellmer sign).

23. In the pelvis, fluid accumulates in the rectovesical pouch and then spills into the paravesical fossa. The fluid produces symmetric densities on both sides of the bladder, which is termed a “dog’s ear” or “Mickey Mouse” appearance.

24. Medial displacement of the cecum and ascending colon and lateral displacement of the properitoneal fat line present in more than 90% of patients with significant ascites.

25. USG abdomen It can detect as little as 100 ml of fluid in peritoneal cavity. Uncomplicated ascites - appears as homogenous, freely mobile, anechoic collection in peritoneal cavity. The smallest amounts of fluid first tend to collect in the Morison pouch and around the liver as a sonolucent band. With massive ascites, the small bowel loops have a characteristic polycyclic, “lollipop,” or arcuate appearance because they are arrayed on either side of the vertically floating mesentery.

26. CT & MRI abdomen Ascites is demonstrated well on CT scan images. Small amounts of ascitic fluid localize in the right perihepatic space, the posterior subhepatic space (Morison pouch), and the Douglas pouch. Hepatic, adrenal, splenic, or lymph node lesions associated with masses arising from the gut, ovary, or pancreas are suggestive of malignant ascites. Patients with malignant ascites - proportional fluid collections in the greater and lesser sacs benign ascites- fluid is observed primarily in the greater sac and not in the lesser omental bursae.

27. ABDOMINAL PARACENTESIS It is the most rapid cost effective method for diagnosing cause of ascites. Therapeutic paracentesis can be performed for refractory or tense ascites. Position Large volume ascites: supine with head slightly elevated Low volume ascites: lateral decubitus position Small volume ascites: knee elbow position Site Midline site : below the umbilicus - avascular area. When midline is inappropriate then, a site two finger breadth medial to anterior superior iliac spine. Ultrasonic guidance is needed only in specific situations.

28. Procedure It is performed under local anaesthesia in aseptic precautions. Needle is inserted using a Z tract to prevent leakage of fluid. Retract the skin approximately 2 cm caudal in relation to the deep abdominal wall and then slowly inserting the needle. The skin is not released until the needle has penetrated or fluid flows. When the needle is finally removed at the end of the procedure, the skin resumes its original position and seals the needle pathway. Complications of paracentesis Infection Electrolyte imbalance Bleeding Bowel perforation Large volume paracentesis - large intravascular fluid shifts, avoided by administering albumin replacement, if more than 5 litres is removed.

29. ASCITIC FLUID ANALYSIS Gross appearance Total protein, Albumin and glucose Gram’s stain, AFB smear and culture Cell count cytology Triglycerides, Amylase and Lactate dehydrogenase(LDH)

30. GROSS APPEARANCE OF ASCITES COLOR ASSOCIATION Translucent/yellow Normal/sterile Brown Hyperbilirubinemia(most common) Gall bladder or biliary perfusion Cloudy or turbid Infection Pink or blood tinged Mild trauma at the site Grossly bloody Malignancy Abdominal trauma Milky( chylous ) Cirrhosis Thoracic duct injury Lymphoma

31. CELL COUNT: Normally total leukocyte count is less than 500 cells/ cumm with less than 250 polymorphs/mm 3 Polymorphonuclear count greater than 250 cells is suggestive of bacterial peritonitis. Predominance of lymphocytes - tuberculous peritonitis and peritoneal carcinomatosis. Red cell count: when greater than 50,000/microliter - haemorrhagic ascites, (malignancy , tuberculosis or trauma .)

32. GRAM STAIN AND AFB: Gram stain is only 10% sensitive for helping visualize bacteria. Approximately 10,000/ml bacteria are required for detection by gram’s stain. AFB staining for TB rarely gives positive results . CULTURE: The common bacterial infection of ascitic fluid are monomicrobial(as seen in SBP) with a very low bacterial concentration. The sensitivity with bedside inoculation of blood culture bottles with ascites results in 92% detection of bacterial growth in neutrocytic ascites. Secondary bacterial peritonitis – usually polymicrobial infection occur due to underlying pathological/procedural cause.

33. TOTAL PROTEIN: Exudate if ascitic fluid protein is>2.5 gm/Dl Transduate if ascitic fluid protein is<2.5 gm/dl CYTOLOGY They are reported to be 58-75% sensitive for detecting malignant ascites. Sensitivity increased by centrifuging large volume .

34. BIOCHEMISTRY: LDH (Lactate dehydrogenase) Useful in differentiating spontaneous bacterial peritonitis from perforation. LDH>225 U/L , Glucose <50 mg/dl, total protein>1gm/dl and multiple organisms suggest secondary bacterial peritonitis (ruptured viscus or loculated abscess). Triglycerides : A high level of triglycerides confirms chylous ascites. Amylase: In pancreatitis or gut perforation it is markedly elevated, usually greater than 2000 IU. Bilirubin : An elevated bilirubin level suggest biliary or gut perforation.

35. SERUM ASCITIC ALBUMIN GRADIENT SAAG is the simple best test to classify ascites into portal hypertensive (SAAG >1.1 gm/dl) and non portal hypertensive (SAAG<1.1 gm/dl)causes. It is calculated by subtracting SAAG = serum albumin - ascitic fluid albumin specimen obtained on the same day. The accuracy of the SAAG results is approximately 97% in classifying ascites. High albumin gradient and low albumin gradient should replace the ‘term transudate and exudate’.

36. TYPES OF ASCITES ACCORDING TO THE LEVEL OF SAAG

37. COMPLICATIONS MECHANICAL COMPLICATIONS Respiratory distress Compression of great vessels Abdominal wall hernias(umbilical, inguinal, or femoral) Gastroesophageal reflux disease, delayed gastric emptying Obstructive sleep apnoea syndrome Pleural effusion or hepatic hydrothorax(common in cirrhosis) OTHER COMPLICATIONS Dyselectrolytemia Hepatorenal syndrome Infection - Spontaneous bacterial peritonitis

38. SPONTANEOUS BACTERIAL PERITONITIS It is an infection of ascitic fluid Its is defined by an ascitic fluid PMN count of more than 250 cells/ Pathogenesis - due to delayed intestinal transit and increased permeability of intestinal wall. M/C organism gram negative bacilli – E-coli, klebsiella species. C/F – fever, abdominal pain, chills, malaise, loss of appetite, nausea vomiting.  

39. Diagnosis – Diagnostic paracentesis – done to all patients with cirrhosis and ascites with GI bleeding, shock, fever, other signs of systemic inflammation worsening of RFT/LFT and hepatic encephalopathy. Ascitic fluid culture – helps for antibiotic therapy. Blood culture – should be done before starting antibiotics. Reagent strips – detects leucocyte esterase – corresponds to WBC presence, it’s a rapid and cost effective test.

40. INTERPRETATION- Treatment - Empirically a broad spectrum antibiotic is administered intravenously, e.g. cefotaxime (third-generation cephalosporin). Others alternative – amoxicillin/clavulanic acid and quinolones such as ciprofloxacin or ofloxacin. Co-treatment with intravenous albumin, 1.5 g/kg at the time of diagnosis and 1 g/kg on day 3, reduces the incidence of renal impairment and improves survival. PMN COUNT ASCITIC FLUID CULTURE INTERPRETATION > 250 cells/ Positive SBP > 250 cells/ Negative False negative culture Normal Positive Contamination of culture/ early SBP PMN COUNT ASCITIC FLUID CULTURE INTERPRETATION Positive SBP Negative False negative culture Normal Positive Contamination of culture/ early SBP

41. MANAGEMENT of ascites Principles of management Initial evaluation Identify and treat the underlying cause Diagnostic ascitic fluid tap Ascitic fluid analysis Treatment of diuretic sensitive ascites Indications to stop diuretics Spontaneous bacterial peritonitis

42. NON DRUG MANAGEMENT Bed rest: upright position increases renin aldosterone activity, increased retention of sodium or water. bed rest reduces this activity. Diet: Sodium restriction - (1-2mEq/kg/day for infant and children and 1-2g/day{44-88mEq} adolescent) Fluid restriction – It is only indicated when there is persistent hyponatremia, serum sodium<120 mEq /l Measurement of 24 hour urinary sodium excretion A major goal is to increase urinary sodium excretion to >78mmol/day .

43. DRUGS : DIURETICS Spironolactone (aldosterone antagonist) : 2-3mg/kg/day single dose in the morning, max:100mg. If necessary, increased by 2mg/kg once in 5-7days till max dose of 4-6mg/kg (400mg/day) is reached. Furosemide 1-2 mg/kg/dose, not exceed 6mg/kg/dose added to spironolactone as dual therapy. Metalazone 5-20 mg/kg/dose q 24 h SUPPLEMENTAL ALBUMIN may be advisable to replace low serum albumin.

44. Large volume paracentesis(LVP) first line treatment for tense ascites with respiratory compromise and second line treatment for refractory ascites. Should be done under cover of 0.5-1g/kg albumin or 8g/L of AF drained.

45. DURATION OF DIURETIC THERAPY To treat: diuretic therapy is continued till ascites regresses To prevent: in certain conditions like cirrhosis effective doses of diuretic have to be continued for months to years, to prevent accumulation of fluid INDICATIONS TO STOP DIURETICS Encephalopathy Serum sodium <120 mmol/L despite fluid restriction Serum creatinine >2 mg/dl Clinically significant complications of diuretics Hyperkalemia and metabolic acidosis Muscle cramps

46. Management of low albumin Gradient ascites These patients usually do not have portal hypertension and do not respond to salt restriction and diuretics. Tuberculous peritonitis - antitubercular therapy. Pancreatic ascites - resolve spontaneously, require endoscopic stenting or operative intervention or need ‘somatostatin’ therapy. Lymph leak - resolves spontaneously or may require surgical intervention or peritoneovenous shunting. Chlamydial peritonitis - tetracycline therapy. Nephrotic and lupus ascites may require steroids. Malignant requires surgical debulking and chemotherapy.

47. SURGICAL management Trans jugular intrahepatic portal systemic shunt (TIPSS) Treatment for patients with refractory ascites and main indication for TIPSS remains variceal bleeding refractory to endoscopic therapy TIPSS is associated with suppression of antinatriuretic systems, and an improvement in renal function and renal response to diuretics. Also reduces the activity of the RAAS and increases natriuresis and GFR. Shunt dysfunction remain the major concerns in this patient group.

48. Peritoneovenous shunt (e.g . LeVeen or Denver shunts) A channel is created within the peritoneum for the fluid to drain into SVC via internal jugular vein. Have been shown to have poor long-term patency. complications including peritoneal fibrosis, and confer no survival advantage relative to standard therapy. It should be reserved for diuretic-resistant patients who are candidates for neither liver transplantation nor serial large-volume paracentesis.

49. Surgical Portosystemic shunting Portocaval shunt operation involves the anastomosis of the portal vein and the inferior vena cava, consequently reducing the portal pressure. The shunt also produces a marked diuresis and natriuresis . This shunts are rarely used in advanced cirrhotic ascites, - high incidence of post-shunt encephalopathy.

50. Liver transplantation The ultimate treatment modality available for refractory ascites in end stage liver disease. By replacing the cirrhotic liver, portal hypertension and its underlying mechanisms of ascites are corrected. A patient with cirrhosis, the development of ascites refractory to standard medical therapy is associated - 50% 6-month survival, and an approximately 25% 12-month survival.

51. NEWER MODALITIES- vaptans , ( arginine vasopressin(AVP) receptor antagonists) Used in management of hyponatremia seen in refractory ascites Act by directly inhibiting the effect of increased AVP resulting in excretion of electrolyte-free water. Terlipressin infusion, partial splenic artery embolization and peritoneal urinary drainage - tried to manage resistant ascites and where liver transplant is not feasible.

52. REFRACTORY ASCITES It is defined as ascites that cannot be mobilized or prevented from recurring by medical therapy It is divided into diuretic resistant – ascites not mobilised despite maximum diuretic dosage diuretic intractable ascites – development of diuretic induced complications that preclude use of an effective diuretic dosage .

53. CRITERIA Lack of response to maximal doses of diuretic for at least 1 week. Diuretic induced complications in absence of other precipitating factors. Early recurrence of ascites within 4 weeks of fluid mobilization. Persistent ascites despite sodium restriction. Mean weight loss less than 0.8 kg over 4 days. Urinary sodium excretion less than sodium intake. MANAGEMENT Serial large volume paracentesis (6-10 L) are safe and effective in controlling refractory ascites. Surgical management – peritoneovenous shunt and Liver transplantation.

54. FOLLOW UP OF ASCITES FURTHER IP CARE Patients can actually be maintained free of ascites if sodium intake is limited to 10 mmol/dL. 24hour urinary sodium - portal hypertension in order to assess the degree of sodium avidity, monitor the response to diuretics, and assess compliance with diet. For grade 3 or 4 ascites, therapeutic paracentesis necessary intermittently. Monitor body weight and the intake and output of fluids. A reasonable goal for a patient without peripheral edema is a negative sodium balance with a weight loss of 0.5 kg per day. S.electrolytes , Creat , urea and LFT are monitored every 4 weeks .

55. DIFFERENTIAL DIAGNOSIS FOR ASCITES Mesenteric cyst Ovarian cyst Distension of bladder Simple obesity Gastric dilation Abdominal organomegaly or tumours

56. PROGNOSIS Prognosis depends upon the underlying etiology . Refractory ascites and SBP are poor markers of prognosis. Persisting ascites with cirrhosis is a marker of decompensation .

57. REFERENCES OP GHAI 9 TH EDITION IAP TEXTBOOK OF PEDIATRICS 7 TH EDITION PG TEXTBOOK OF PEDIATRICS 2 ND EDITION NELSON TEXTBOOK OF PEDIATRICS 21 TH EDITION WALKER’S PEDIATRIC GASTROINTESTINAL DISEASE VOLUME 2

58. THANK YOU