ABDOMINAL SWELLING

Introduction
• Common complaint
– Bloating or abdominal fullness
– Increased in clothing or belt size
• (+) pain frequently result of
– Intraabdominal infection
– Peritonitis
– Pancreatitis
 Causes (six F’s)

Flatus

Fat

Fluid

Fetus

Feces

“Fatal Growth”
 Flatus
• May be result of increased intestinal gas
• Normal small intestine: 200 mL of gas (
– N2, O2,  swallowed,
– CO2, H2, and methane  produced intraluminally
by bacterial fermentation
 Flatus
• Conditions:
– Aerophagia (swallowing of air)
– Consequence of bacterial metabolism of excess
fermentable substances such as lactose and other
oligosaccharides  lead to production of hydrogen,
carbon dioxide, or methane
– IBS and bloating  impaired intestinal transit of gas
rather than increased gas volume
– Result of lack coordination between diaphragmatic
contraction and anterior abdominal wall relaxation 
increase intraabdominal volume loads
 Fat
• Weight gain  increase in abdominal fat
• Caused by imbalance between caloric intake
and energy expenditure (poor diet and
sedentary lifestyle)
 Fluid
• Accumulation of fluid within abdominal cavity
(ascites)  abdominal distention
 Fetus
• Pregnancy  increased abdominal girth
• First noted at 12-14 weeks if gestation when
uterus moves from pelvis into the abdomen
• Result of fluid retention and relaxation of the
abdominal muscles
 Feces
• Severe costipation or intestinal obstruction 
increased stool in the colon  increased
abdominal girth
• Usually accompanied with abdominal
discomfort or pain, nausea, and vomiting
• Diagnosed by imaging studies
 Fatal Growth
• Abdominal mass
• Enlargement of intraabdominal organs,
specificially liver (hepatomegaly), or spleen
(splenomegaly) or abdominal aortic aneurysm,
bladder distention
• Malignancies, abscesses or cysts  grow 
increased abdominal girth
 Approach to Patient
• Symptoms suggestive of malignancy  weight loss, night
sweats, and anorexia
• Inability to pass stool or flatus together with nausea and
with nausea or vomiting suggests bowel obstruction, severe
constipation, or an ileus (lack of peristalsis).
• Increased eructation and flatus may point toward
aerophagia or increased intestinal production of gas.
• Risk factor
– Chronic liver disease  excessive alcohol use and jaundice
which suggest KBS
– Heart failure and TB  ascites
 Physical Examination
• Assessment for signs of systemic disease.
• Presence of lymphadenopathy, especially supraclavicular lymphadenopathy (Virchow’s node), suggests
metastatic abdominal malignancy.
• Care should be taken during the cardiac examination to evaluate for elevation of jugular venous pressure
(JVP); Kussmaul’s sign (elevation of the JVP during inspiration); a pericardial knock, which may be seen in heart
failure or constrictive pericarditis; or a murmur of tricuspid regurgitation. Spider angiomas, palmar erythema,
dilated superficial veins around the umbilicus (caput medusae), and gynecomastia suggest chronic liver
disease.
• The abdominal examination should begin with inspection for the presence of uneven distention or an obvious
mass. Auscultation should follow. The absence of bowel sounds or the presence of highpitched localized bowel
sounds points toward an ileus or intestinal obstruction.
• An umbilical venous hum may suggest the presence of portal hypertension, and a harsh bruit over the liver is
heard rarely in patients with hepatocellular carcinoma or alcoholic hepatitis.
• Abdominal swelling caused by intestinal gas can be differentiated from swelling caused by fluid or a solid mass
by percussion; an abdomen filled with gas is tympanic, whereas an abdomen containing a mass or fluid is dull
to percussion.
• Finally, the abdomen should be palpated to assess for tenderness, a mass, enlargement of the spleen or liver,
or presence of a nodular liver suggesting cirrhosis or tumor. Light palpation of the liver may detect pulsations
suggesting retrograde vascular flow from the heart in patients with right-sided heart failure, particularly
tricuspid regurgitation
Imaging and Laboratory Evaluation
• Abdominal x-rays can be used to detect dilated
loops of bowel suggesting intestinal obstruction
or ileus. Abdominal ultrasonography can detect
as little as 100 mL of ascitic fluid,
hepatosplenomegaly, a nodular liver, or a mass.
• Ultrasonography is often inadequate to detect
retroperitoneal lymphadenopathy or a pancreatic
lesion because of overlying bowel gas. If
malignancy or pancreatic disease is suspected, CT
can be performed.
Imaging and Laboratory Evaluation
• Laboratory evaluation should include liver biochemical
testing, serum albumin level measurement, and
prothrombin time determination (international
normalized ratio) to assess hepatic function as well
as a complete blood count to evaluate for the presence
of cytopenias that may result from portal hypertension
or of leukocytosis, anemia, and thrombocytosis that
may result from systemic infection.
Imaging and Laboratory Evaluation
• Serum amylase and lipase levels should be checked to
evaluate the patient for acute pancreatitis. Urinary
protein quantitation is indicated when nephrotic
syndrome, which may cause ascites, is suspected.
• In selected cases, the hepatic venous pressure gradient
(pressure across the liver between the portal and
hepatic veins) can be measured via cannulation of the
hepatic vein to confirm that ascites is caused by
cirrhosis. In some cases, a liver biopsy may be
necessary to confirm cirrhosis.
Ascites
 Cirrhosis +
• Result of portal hypertension, renal salt +
water retention
• ↑ hepatic resistance:
– Hepatic fibrosis → disrupt hepatic sinusoid,
impede normal blood flow
– Activation hepatic stellate cell → fibrogenesis →
smooth muscle contraction, fibrosis
- Intrahepatic:↓ endothelial nitric oxide synthetase
(eNOS) → NO ↓, ↑ vasoconstriction
- Systemic: ↑ NO, ↑ vascular endothelial GF, ↑ TNF
→ splanchnic arterial vasodilatation → pooling blood
→ ↓ volume effective circulation → kidney:
hipovolemia? → release ADH → compensatory
vasoconstriction → SNS + RAAS active → retention:
water + salt
 Cirrhosis -
• Result from:
– Peritoneal carcinomatosis: primary peritoneal
malignancy (mesothelioma/sarcoma), abdominal
malignancy (gastric/colonic adenocarcinoma),
metastatic (breast/lung/melanoma)
• Tumor cell → produce protein-rich fluid →
draw fluid from extracellular space → ascites ↑
– Infection (tuberculous peritaonitis)
• Tubercles @ peritoneum → proteinaceous fluid
– Pancreatic disease (leakage enzyme to
peritoneum)
 Etiology
• 84% cirrhosis
• Less common: massive hepatic metastasis,
infection (TB, Chlamydia), pancreatitis, renal
disease (nephrotic syndrome),
hypothyroidism, familial Mediterranean fever
Evaluation
• Paracentesis
– Insert transcutaneously needle/small cath
– LLQ: greater depth ascites, abdominal wall thinner
– Safe even coagulopathy.
– Complication <<: hematoma, hypotension,
infection, hepatorenal syndrome
 ①. Inspection
• Turbid: infection or tumor cells
• White milky → TG> 200 mg/dL: chylous
ascites → trauma, cirhosis, tumor, TB
• Dark brown: bilirubin >> → perforation biliary
tract
• Black: pancreatic necrosis or metastatic
melanoma
 ②. Measurement
• Albumin → calculate serum-ascites albumin
gradient (SAAG)
– SAAG ≥ 1.1 g/dL: + portal HT → due to ↑ pressure @
hepatic sinusoid
– Total protein level
• Protein > 2.5 g/dL: hepatic sinusoid normal → protein pass
to ascites
• Protein < 2.5 g/dL: hepatic sinusoid damage & scarred →
protein no longer pass
– SAAG ≤ 1.1 g/dL: - portal HT
• Cell and diff count
• Infection +: Gram’s stain and Culture
• Other: Pro-brain-type natriuretic peptide (BNP):
↑ in heart failure
• Pancreatic ascites:
– Amilase ascitic > 1000 mg/dL
• Peritoneal carcinomatosis:
– Cytology: obtain 50 ml fluid
• TB:
– Ascitic fluid lymphocytosis, smear acid-fast bacilli (0-
3%), culture (35-50%), elevated adenosine deaminase
> 30-45 U/L (>90%)
• Ascitic glucose and LDH: suspect perforation
hollow viscus → secondary peritonitis:
– Ascitic glucose < 50 mg/dL, LDH ascitic > serum,
multiple pathogens + on culture
• Uncertain: laparotomy or laparoscopy +
peritoneal biopsi: histology and culture (gold
standart)
 Treatment
• Initial: restriction sodium (2 g/day)
• Oral diuretics (Spironolactone (max 400mg) +
furosemide (max 160 mg))
• If refractor cirrhotic ascites: + midodrine or
clonidine → vasoconstrictor + repeated large-
volume paracentesis (LVP) → + albumin 6-8 g/L
fluid remove
• Malignant ascites: not respont to diuretics and
sodium restriction → LVP serial, transcutaneus
drainage cath placement, peritoneovenous shunt
• Tb peritonitis: antituberculosis
 Complications
• Spontaneous bacterial peritonitis
– Common, potential lethal
– Abdominal girth ↑, tenderness (40%), rebound
tenderness <<, fever, nausea, vomit, hepatic
encephalopathy
– (!) PMN 250/L @ ascitic fluid, 1 bacterial pathogen
• Most common: rod gram negative (E.coli, Klebsiella,
Streptococci, Enterococci)
– VS Multiple pathogen + PMN ↑: secondary
peritonitis from ruptur viscus or abscess
– VS Multiple pathogen – PMN ↑: bowel
perforation from neddle paracentesis
 - Th/: IV cefotaxime for 5 days
- AB prophylactic if: cirrhotic with history SBP,
protein total ascitis < 1g/dL, active GIT bleeding
• Hepatic hydrothorax: ascites migrates via
diaphragm fenestrae to pleural space
– Shortness breath, hypoxia, infection
– Th/ sodium restriction, diuretic, thoracentesis.