ABDOMINAL
DISTENSION
ANEESA REMY ZAMANI & Olagunju Abisola Ashiat
DR SSEBULIBA MOSES
ABDOMINAL
DISTENSION
ETIOLOGY
• 6 F’s: flatus, fat, fluid, fetus, feces, or a “fatal growth” (commonly a neoplasm)
Flatus Fat Fetus Feces & fatal growth
• Normal small intestine • ↑ Abd fat in: • First noted at 12-14ks • Feces: IO, severe
contains ≈ 200mL gas • Wt gain; imbalance gestation constipation +/- N+V
• Swallowed:N2 O2 btwn caloric intake & • Prior to this; due to • Fatal growth: organ
• Produced intra- energey expenditure fluid retention & enlargement, aortic
luminally: H2, CO2CH4 • Manifestation of relaxation of aneurysm, bladder
• Impaired transit/ ↑gas disease e.g. Cushing’s abdominal muscles distension,
malignancies,
vol abscesses, or cysts
• ↑Vol: Aerophagia,
bacterial met. of
excess fermentable
substances,
• Impaired transit; IBS
HISTORY
General Night sweats Wt loss Anorexia
Constipation/
GIT N+V
obstipation
Alcohol use Ascites
PMHx HF, TB
HISTORY
• Any symptoms suggestive of malignancy? eg weight loss, night sweats, and
anorexia.
• Inability to pass stool or flatus together with N+V? Think IO, severe constipation,
or an ileus (lack of peristalsis).
• ↑ Eructation & flatus? Aerophagia/ ↑ intestinal production of gas.
• Risk factors for or symptoms of chronic liver disease? Eg excessive alcohol use and
jaundice (ascites)
• Other symptoms of medical conditions? e.g HF, TB which may cause ascites
PHYSICAL EXAM
General Chronic liver dse:
Abd
Percussion: flatus =
Spider angiomas, resonant, fluid = dull
palmar erythema,
caput medusae & Distended bladder:
gynecomastia can’t go below it
Virchow’s node: Aortic aneurysm:
Metastatic abd Expansile. Masses
malignancy can also be pelvic
ASCITES
ANEESA REMY ZAMANI
DR SSEBULIBA MOSES
L/O
• Definition • Etiology
• Epidemiology • Approach to patient
• Pathophysiology
EPIDEMIOLOGY (BSG, 2020)
DEFINITION
Etiology
“Accumulation of fluid with in the
peritoneal cavity” 3% 1%
≈20% Pts with cirrhosis have ascites at 11%
their 1st presentation, and 20% of
those presenting with ascites die in the Cirrhosis
1st yr of dx (BSG,2020) Cancer
Cardiac ascites
5% of patients with ascites have 2 or Other
more causes of ascites formation, i.e.,
“mixed” ascites (AGS, 2015)
85%
PATHOPHYSIOLOGY – with cirrhosis
↑Hepatic ↑VEGF + TNF
Pooling of blood +
resistance occurs causing
↓effective
via several splanchnic
circulating vol
mechanisms vasodilatation
i) Devt of hepatic ↑Systemic Kidney perceives
fibrosis circulating NO it as hypovolemia
ii) Activation of
iii) ↓Endothelial SNS + RAAS
hepatic stellate
eNOs activation
cells
PATHOPHYSIOLOGY – no cirrhosis
Peritoneal Tumor cells lining
peritoneum produce
Extracellular fluid
drawn into
carinomatosis protein-rich fluid peritoneum
Tubercles deposited
Tuberculous on peritoneum
exude a
peritonitis proteinaceous fluid
Pancreatic Leakage of
pancreatic enzymes
ascites into peritoneum
ETIOLOGY
Grading of ascites (SRB, 2010) :
Grade 1–Detectable only by imaging;
Grade 2–Easily detectable small volume;
Grade 3–Obvious ascites but not tense; Classification of
ascites (BSG,2020)
Grade 4 –Tense ascites.
Uncomplicated Refractory
Moderate – mod
Mild -US Large – marked Diuretic Diuretic
symmetrical
detectable only abd distension resistant intractable
distension
HISTORY
• Progressive abd distension +/- pain
• Risk factors? e.g.TB exposure, prior malignancies, sexual partners, transfusion
history, metabolic syndrome, increased risk of nonalcoholic steatohepatitis
progressing to cirrhosis
• Weight gain, dyspnea/orthopnea, edema, early satiety, nausea
• Fever, abdominal tenderness, and altered mentation; SBP
• Weight loss? underlying malignancy
PHYSICAL EXAMINATION
• Abdominal distention: Shifting dullness [most sensitive (83%) & specific (56%)];
requires >1,500 mL of fluid to detect
• Edema: penile/scrotal/pedal, pleural effusion, rales
• Stigmata of cirrhosis: palmar erythema, spider angiomata, dilated abd wall
collateral veins
• Other signs of advanced liver disease: jaundice, muscle wasting, gynecomastia,
leukonychia
• Signs of underlying malignancy: cachexia; Virchow’s node suggests upper abd
malignancy, Sister Mary Joseph’s node
MANAGEMENT
Investigations
Treatment
Imaging
• CXR: Pleural effusions found in about 10% of pts, usually on the right side (hepatic
hydrothorax); most are small and only identified on CXR, but occasionally a
massive hydrothorax occurs.
• US: Ultrasonography is the best means of detecting ascites, esp in obese & those
with small vol. of fluid.
Lab Investigations
Diagnostic paracentesis for fluid
analysis can differentiate between
ascites caused by portal HTN from
nonportal hypertensive ascites
High portal pressure: SAAG > 1.1
Normal portal pressure: SAAG < 1.1
SAAG: serum-ascites albumin gradient
• Cell count and differential:
• PMN leukocytes ≥250 cells/mm3
suggest infxn
Ascitic fluid • Albumin to calculate SAAG:
The initial lab Ix of ascitic fluid should
• <1.1 g indicates a low portal pressure
include; exudative process
An ascitic fluid cell count
Ascitic fluid total protein • ≥1.1 g indicates portal
SAAG.
hypertensive/transudative process
If ascitic fluid infxn suspected, fluid should be
cultured at the bedside in aerobic and anaerobic • Total protein (low in cirrhosis, nephrotic
blood culture bottles prior to initiation of antibiotics
disease and high in cardiac ascites)
• – Other tests (based on clinical
scenario)
ASCITIC FLUID FINDINGS
Test & finding Finding
Ascitic conc <1.5g/dL is a risk factor for SBP
Ascitis conc <2.5g/dL suggests damage of hepatic sinusoids e.g. massive liver mets
>2.5 g/dL within ascites & serum BNP >364 ng/L suggests underlying/ additional CVS dse e.g.
Total protein HF
Serum proteins <182 ng/L r/o cardiac disease
Site of tumour matters. Cytology & tumour markers must be combined.
Carcinoembryonic antigen (CEA), epithelial cell adhesion molecule (EpCAM), CA 15-3 and CA
Cytology (malignancy 19-9.20
context)
Min 50ml collected Serum/ ascitic CA 125 has no role as a discriminator; will commonly be ↑by ascites of any cause
Peritonitis Sec: Ascitic glucose <50mg/dL &/ or ascitic LDH > serum LDH &/ or polymicrobial culture
SBP: Monomicrobial culture, ascitic neutrophil >250 cells/mm3
Pancreatic ascites Ascitic amylase >1,000mg/dL
Tuberculous Ascitic fluid lymphocytsis
For all Pts
• Daily weight
• Restrict dietary sodium to ≤2 g/day if the cause is due to portal HTN (high SAAG)
• Water restriction (1 to 1.5 L/day) only necessary if serum sodium <120 to 125mEq/L
• If creatinine >2.0 mg/dL, decrease diuretic doses.
• Avoid alcohol and ensure adequate nutrition if liver disease
• Baclofen may be used to reduce alcohol craving/consumption
MGT Summary
• All pts with new-onset ascites
SBP • Dietary salt restriction
• initial fluid analysis: [total • Diuretics
protein] + calculation of SAAG • SEE SLIDE ON • LVP
• cytology, amylase, BNP + RECOMMENDATIONS • Albumin
adenosine deaminase should
be considered
Dx
paracentesis Definitive
Management
Dietary salt
Diuretics LVP Albumin
restriction
• No more than 5- • Moderate: • Consent • 20% or 25%
6.5g daily Spironolactone • US guided if infused after
• Nutritional monotherapy available paracentesis >5L
counselling 100mg starting @ a dose of 8g
• Recurrent severe/ HAS/L
IPD: Dual therapy • 20% or 25%
As above + infused after <5L
Furesemide 40mg paracentesis in
starting pts at high risk of
post-paracentesis
AKI 8g/L
COMPLICATIONS
• SBP - also complicates ascites caused by NS, HF, acute hepatitis, and acute liver
failure but is rare in malignant ascites.
[Cirrhotic patients with a history of SBP, an ascitic fluid [total protein] <1 g/dL, or
active GIT bleeding should receive prophylactic antibiotics to prevent SBP; oral daily
norfloxacin is commonly used.]
• Hepatic hydrothorax - occurs when ascites, often caused by cirrhosis, migrates
via fenestrae in the diaphragm into the pleural space.
Pts with refractory ascites not on liver
transplant list should be offered a
palliative care referral. Besides
repeated LVP, alternative palliative
interventions for refractory ascites
should also be considered.
HRS
• Pts with cirrhosis + ascites can develop a specific form of renal dysfct; hepatorenal syndrome
(HRS).
• Due to altered haemodynamics with hyperdynamic circulation + overactive endogenous
vasoactive system which results in renal hypoperfusion.
• Systemic inflammation also plays an important role in the pathophysiology of HRS.
• HRS-1, which reflects a rapid reduction in renal function, has been proposed to be changed to
HRS-acute kidney injury (HRSAKI).
• Definition of HRS-AKI; “↑Scr of ≥0.3 mg/dL (27 µmol/L) within 48 hours or ≥50% from baseline”
[final cut-off value of 1.5 mg/dL (133 µmol/L) unecessary].
• The mainstay of treatment of HRS-AKI involves HAS and vasoconstrictors, esp terlipressin
• HRS-2, which represents renal dysfunction that does not progress rapidly, has been proposed to
be changed to HRS-NAKI (non-AKI)..
THANK YOU
Any Questions?
