Causes and Management of Ascites in Children

ASCITES in children
PRESENTER : Dr VIJITHA A S

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

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.

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.

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

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.

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.

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.

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.

• 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.

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.

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

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.

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

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.

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.

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.

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)

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.

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

• 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.

• 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.

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.

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.

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.

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.

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)

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

CELL COUNT:
• Normally total leukocyte count is less than 500 cells/cumm with less than 250
polymorphs/mm3
• 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.)

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.

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.

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.

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’.

TYPES OF ASCITES ACCORDING TO THE LEVEL OF SAAG

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

SPONTANEOUS BACTERIAL PERITONITIS
• It is an infection of ascitic fluid
• Its is defined by an ascitic fluid PMN count of more than 250
cells/𝑚𝑚3
• 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.

• 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.

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/𝑚𝑚3 Positive SBP
>250 cells/𝑚𝑚3 Negative False negative culture
Normal Positive Contamination of
culture/ early SBP

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

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.

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.

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.

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

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.

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.

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.

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.

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.

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.

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.

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.

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.

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

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.

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

Causes and Management of Ascites in Children

Recommended

Recommended

More Related Content

What's hot

What's hot (20)

Similar to Causes and Management of Ascites in Children

Similar to Causes and Management of Ascites in Children (20)

More from Vijitha A S

More from Vijitha A S (9)

Recently uploaded

Recently uploaded (20)

Causes and Management of Ascites in Children

Editor's Notes