Surgical scars are associated with tethering of the bowel to the abdominal wall, increasing the risk of bowel perforation. Bowel perforation by the paracentesis needle occurs in approximately 6/1000 taps. Fortunately, it is generally well tolerated .
Hepatic hydrothorax is defined as a pleural effusion, usually greater than 500 mL, in patients with cirrhosis and without primary cardiac, pulmonary, or pleural disea
Definition of ascites
Causes of ascites
Diagnosis of ascites:
History, physical examination, investigations, and procedures
Management of ascites
A 42 years gentleman k/c/o:
HTN since 3 years on medication
Liver cirrhosis secondary to chronic HBV infection
Oesophageal varices treated with sclerotherapy and
Presented to the A&E complaining of
headache since one day
and abdominal distension since four days.
The headache is in the frontal area, dull in nature, scored
by 8, not radiating. It is associated with drowsiness and
He denied any Hx of nausea/ vomniting, weakness, fever, or trauma to
head. He complain of tremor of both hands to the extend that he can't
hold any thing. He gave Hx of two days constipation.
Fursmide 40 mg OD
Spironolacton 100 mg OD
Propranolo 100 mg TID
Entacavir 0.5 mg OD
He is not smoker or alcohol consumer.
Rest of Hx: unremarkable.
Young gentleman alert oriented not in pain or
distress GCS 15/15, MMSE 27
Vitals: BP 161/102 mmHg; PR 75 bpm; RR 18;
temp 36.7; saturation 99%
General assessment: jaundice, pallor, pitting
edema in both legs up to the knee,
dehydrated, JVP 5cm rised, no cynosis or LN
enlargement. Have mild flapping tremor. No
other sings of chronic liver disease.
Distended, everted umbilicus , no dilated viens
Tens, non tender, no organomegaly.
Massive ascites +4
I couldn’t appreciate bowel sounds
DRE: pt refused
Chest bilateral inspiratory basal crepitation
CBC: Hb9.7; hemtocrits n; plt 99; WBC 6.6
Coagulation: all are abnormal; INR 2.11
NH3: 386 on admission; on discharge 87
LFT: AST 220; ALT 81; ALP normal; albumin39 low; total bilirobin 122 high
Lipid profile : normal
U&E: AG16; urea 8.7; rest WNL
CT chest and abdomen: Liver cirrhosis with mass in segment 3 suggstive of
HCC; gross ascites; chest normal
CT brain: no lesion
Lactulose enema 50 ml
Continue oral lactulose
Follow up in gastro OPD after 1 month
Ascites is defined as the accumulation of free
fluid in the peritoneal cavity.
It is a common clinical finding with a variety of
both extraperitoneal and peritoneal etiologies.
It is most often caused by:
-liver cirrhosis 75% of patients
heart failure (3%)
Approximately 85% of patients with ascites
have cirrhosis, Past history of cancer, heart
failure, or TB.
painless or associated with abdominal discomfort
course of days (eg, bloody ascites due to trauma) or months
(eg, malignant ascites)
Weight gain, shortness of breath, early
satiety, and dyspnea due to fluid
accumulation and increased abdominal pressure.
Spontaneous bacterial peritonitis fever,
abdominal tenderness, and altered mental status.
Cirrhosis: confusion and GI bleeding
Malignant ascites: weight loss
Heart failure: dyspnea, orthopnea, and peripheral
Chylous ascites: diarrhea and steatorrhea,
malnutrition, edema, nausea, enlarged lymph
nodes, early satiety, fevers, and night sweats
Approximately 1.5 L must be present before
flank dullness is detected.
If no flank dullness is present, the patient has
less than 10% chance of having ascites.
Shifting dullness & fluid thrill mean that more
fluid is present.
Abdominal ultrasound to determine with
certainty if fluid is present and in obese.
flank dullness; shifting dullness; fluid wave;
evidence of pleural effusion
PE findings related to the underlying
cause of the ascites, such as:
Stigmata of cirrhosis.
Two grading systems for ascites have been
used in the literature.
An old system which grades ascites from 1+
to 4+, depending on the detectability of fluid
on physical examination.
More recently, the International Ascites Club
has proposed a system of grading from 1 to
The older system
1+ is minimal and barely detectable.
2+ is moderate.
3+ is massive but not tense.
4+ is massive and tense.
The International Ascites Club grading
Grade 1: mild ascites detectable only by US.
Grade 2: moderate ascites manifested by moderate
symmetrical abdominal distension.
Grade 3: large or gross ascites with marked abdominal
Patients suspected of having ascites based on history
and physical examination should undergo radiographic
Ultrasound is probably the most cost-effective
In cirrhotic pt, US, CT, or MRI may reveal evidence of a
US findings in patients with portal HTN may
Dilation of the portal vein to ≥13 mm
Dilation of the splenic and superior mesenteric veins to ≥11
Abdominal paracentesis is mainly to identify the
cause of ascites.
Abdominal paracentesis is indicated for all
patients with new onset ascites
- New onset ascites
- Hospitalization of a patient with ascites
- Clinical deterioration of an inpatient or outpatient
- Abdominal pain
- Abdominal tenderness
- Hepatic encephalopathy
- Peripheral leukocytosis
- Deterioration in renal function
Patients with disseminated intravascular
Patients with a massive ileus with bowel distension.
The location of the paracentesis should be modified
in patients with surgical scars so that the needle is
inserted several centimeters away from the scar.
Distended urinary bladder
Abdominal wall cellulitis
Initial tests that should be performed on the ascitic fluid:
Serum-to-ascites albumin gradient determination (SAAG)
Cell count and differential; culture
Total protein concentration
Additional tests that may be performed to aid in confirming a
Culture with bedside inoculation of aerobic and anaerobic blood culture bottles
Glucose concentration (malignancy, infection, bowel perforation)
Lactate dehydrogenase concentration (malignancy, infection, or bowel perforation)
Gram stain (suspected bowel perforation)
Amylase concentration (pancreatic ascites or bowel perforation)
Tuberculosis smear, culture, and adenosine deaminase activity (tuberculous
Cytology and possibly carcinoembryonic antigen level (malignancy)
Triglyceride concentration (chylous ascites)
Bilirubin concentration (bowel or biliary perforation)
Ascitic Fluid Testing
Cell count &
TB smear and
Translucent or yellow
GB or biliary perforation
Cloudy or turbid
Pink or blood tinged
traumatic tap; Malignancy
Thoracic duct injury
Smear & culture for mycobacteria.
Cytology : in
peritoneal carcinomatosis (sensitivity
increased by centrifuging large volume).
Elevated bilirubin level suggest
biliary or gut perforation.
LDH >225mU/L, glucose <50mg/dL, total protein >1g/dL and
multiple organisms on gram stain suggest secondary bacterial
High level of TG's confirms
Elevated amylase level suggest
pancreatitis or gut
The Serum-ascites albumin gradient (SAAG) is probably
a better discriminant than older measures (transudate
versus exudate) for the causes of ascites.
A high gradient (> 1.1 g/dL) >>>portal hypertension.
A low gradient (< 1.1 g/dL) >>>non-portal hypertensive
Bed rest : No clinical trials
Upright posture activates sodium retaining
mechanisms , impairs renal perfusion and
Sodium restriction :
Aim for 2000mg (88 mmol) per day
Studies show severe restriction (22mmol/day)
compared with less restricted is associated
with longer duration of evolution of ascites,
but higher incidence of diuretic induced renal
impairment and hyponatraemia
One controlled study, showed slightly
reduced salt diet (120mmol/day) was equally
effective when compared to a low salt diet (
No significant survival difference, although
low salt diet (50mmol/day ) improved survival
in those with previous GI bleed
Central hypovolaemia stimulates ADH
receptors decreases free water clearance
Therefore, treat by water restriction –
no trials to assess effect of water restriction in patients
with cirrhosis and dilutional hyponatraemia.
Restriction may worsen central hypovolaemia.
Antimineralocorticoids – Secondary
hyperaldosteronism promotes sodium retention in
distal tubules and collecting ducts
• Controlled and uncontrolled trials Spironolactone
• S.E gynaecomastia, renal impairment, hyperkalaemia
• Other K sparing diuretics: amiloride, triamterene
• Loop Diuretics : Frusemide
• S.E : hyponatraemia, hypokalaemia, hypovolemia, renal
impairment of prerenal origin
Diuretics are administered intially fluid loss from the Intravascular
space decrease hydrostatic pressure fluid move from interstitial
space to intravascular space
In patients with generalized edema due to heart failure, the nephrotic
syndrome, or primary sodium retention, the edema fluid can be
mobilized rapidly, since most capillary beds are involved.
In patients with cirrhosis and ascites but no peripheral edema
300 to 500 mL/day is the maximum amount that can be mobilized
In patients with anasarca, removal of 2 to 3 liters of edema fluid or
more in 24 hours can usually be accomplished without a clinically
significant reduction in plasma volume
Weight loss of 0.5kg/day in absence of oedema
and 1kg/day when oedema present
Use Spironolactone & Frusemide 100mg/40mg
Medical treatment based on sodium restricted
diet, diuretics – response in 90 % without renal
Ascites that does not recede or that recurs shortly after therapeutic
paracentesis, despite sodium restriction and diuretic treatment.
To date, there is no approved medical therapy specifically for refractory
Management of these patients is based upon procedures such as large-
volume paracentesis and transjugular intrahepatic portosystemic
shunts (TIPS), which temporarily alleviate symptoms but are not
These patients have a poor prognosis and are at risk for a series of
pontaneous bacterial peritonitis, hepatic hydrothorax, spontaneous
bacterial empyema, and umbilical hernia.
The predicted survival rate is as low as 50% at 1 year, and prognosis
worsens as patients present with comorbidities such as hepatorenal
syndrome, renal failure, and hepatocellular carcinoma.
The only curative treatment is liver transplantation, though current
studies have shown that TIPS also increases survival.
o Oxford handbook of clinical medicine.
o Macleod’s clinical examination,12th edition