done by Al Yaqdhan Al Atbi Senior clerkship medical student SQUH - Oman

2.  Case scenario
 Definition of ascites
 Causes of ascites
 Diagnosis of ascites:
 History, physical examination, investigations, and procedures
 Management of ascites

3.  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
banding
 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
slurred speech.

4.  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.
 Medication:
 Fursmide 40 mg OD
 Spironolacton 100 mg OD
 Propranolo 100 mg TID
 Omeprazol
 Lactelose
 Entacavir 0.5 mg OD
 He is not smoker or alcohol consumer.
 Rest of Hx: unremarkable.

5.  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.

6.  Abdominal examination:
 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

7. Investigations:
 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
 AFP: 5509
 CT chest and abdomen: Liver cirrhosis with mass in segment 3 suggstive of
HCC; gross ascites; chest normal
 CT brain: no lesion

8.  Lactulose enema 50 ml
 Continue oral lactulose
 Start ciftrixione
 Follow up in gastro OPD after 1 month

9.  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
-malignancy (10%)
heart failure (3%)
pancreatitis (1%)
TB (2%)

10. Non-peritoneal causes
Examples
Intrahepatic portal
hypertension
Cirrhosis
Fulminant hepatic failure
Veno-occlusive disease
Extrahepatic portal
hypertension
Hepatic vein obstruction
(ie, Budd-Chiari syndrome)
Congestive heart failure
Hypoalbuminemia
Nephrotic syndrome
Protein-losing enteropathy
Malnutrition
Miscellaneous disorders
Myxedema
Ovarian tumors
Pancreatic & Biliary ascites
Chylous
Secondary to malignancy, trauma

11. Peritoneal Causes
Examples
Malignant ascites
Primary peritoneal mesothelioma
Secondary peritoneal
carcinomatosis
Granulomatous peritonitis
Tuberculous peritonitis
Fungal and parasitic infections
Sarcoidosis
Foreign bodies (cotton ,starch,
barium)
Vasculitis
Systemic lupus erythematosus
Henoch-Schönlein purpura
Miscellaneous disorders
Eosinophilic gastroenteritis
Whipple disease
Endometriosis

13.  Approximately 85% of patients with ascites
have cirrhosis, Past history of cancer, heart
failure, or TB.
 Symptoms:
 abdominal distension:
 painless or associated with abdominal discomfort
 course of days (eg, bloody ascites due to trauma) or months
(eg, malignant ascites)

14.  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.

15.  Cirrhosis: confusion and GI bleeding
 Malignant ascites: weight loss
 Heart failure: dyspnea, orthopnea, and peripheral
edema
 Chylous ascites: diarrhea and steatorrhea,
malnutrition, edema, nausea, enlarged lymph
nodes, early satiety, fevers, and night sweats

16.  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.

17.  Signs:
 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.
 HF
 Other causes

21.  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
3.

22.  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
(2003)
 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
distension.

23.  Patients suspected of having ascites based on history
and physical examination should undergo radiographic
imaging.
 Ultrasound is probably the most cost-effective
modality.
 In cirrhotic pt, US, CT, or MRI may reveal evidence of a
nodular liver.
 US findings in patients with portal HTN may
include:
 Dilation of the portal vein to ≥13 mm
 Dilation of the splenic and superior mesenteric veins to ≥11
mm

24.  Abdominal paracentesis is mainly to identify the
cause of ascites.
 Abdominal paracentesis is indicated for all
patients with new onset ascites

25. - New onset ascites
- Hospitalization of a patient with ascites
- Clinical deterioration of an inpatient or outpatient
with ascites
- Fever
- Abdominal pain
- Abdominal tenderness
- Hepatic encephalopathy
- Peripheral leukocytosis
- Deterioration in renal function
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26.  Patients with disseminated intravascular
coagulation.
 Primary fibrinolysis.
 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.
 Relative contraindications:
 Pregnancy
 Distended urinary bladder
 Abdominal wall cellulitis
 Distended bowel
 Intra-abdominal adhesions
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27.  Initial tests that should be performed on the ascitic fluid:
 Appearance assessment
 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
diagnosis include:
 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
peritonitis)
 Cytology and possibly carcinoembryonic antigen level (malignancy)
 Triglyceride concentration (chylous ascites)
 Bilirubin concentration (bowel or biliary perforation)

28. Ascitic Fluid Testing
Routine
Sometimes useful
Rarely helpful
Cell count &
differential
Total protein
pH
Albumin
Culture
LDH
Glucose
Lactate
Gram stain
Amylase
Triglycerides
Bilirubin
Cytology
TB smear and
culture

29. Color
Appearance
Translucent or yellow
Normal/sterile
Brown
Hyperbilirubinemia
GB or biliary perforation
Cloudy or turbid
Infection
Pink or blood tinged
Mild Trauma
Grossly bloody
traumatic tap; Malignancy
Abdominal trauma
Cirrhosis
Thoracic duct injury
Lymphoma
Milky ("chylous")

30.  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
peritonitis.
 High level of TG's confirms
chylous ascites.
 Elevated amylase level suggest
perforation.
pancreatitis or gut

31.  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
etiology.

34.  Ascitic fluid leak
 Bleeding
 Infection
 Mortality
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36.  Bed rest
 Diet
 Diuretics
 Fluid Restriction
 Paracentesis
 TIPSS
 Shunts
 Transplant

37.  Bed rest : No clinical trials
 Upright posture activates sodium retaining
mechanisms , impairs renal perfusion and
sodium excretion.

38.  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

39.  One controlled study, showed slightly
reduced salt diet (120mmol/day) was equally
effective when compared to a low salt diet (
50mmol/day).
 No significant survival difference, although
low salt diet (50mmol/day ) improved survival
in those with previous GI bleed

40.  Central hypovolaemia stimulates ADH
receptors decreases free water clearance 
dilutional hyponatraemia.
 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.

41.  Antimineralocorticoids – Secondary
hyperaldosteronism promotes sodium retention in
distal tubules and collecting ducts
• Controlled and uncontrolled trials Spironolactone
effective antimineralocorticoid
• 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

42.  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

43.  Weight loss of 0.5kg/day in absence of oedema
and 1kg/day when oedema present
 Use Spironolactone & Frusemide 100mg/40mg
ratio
 Medical treatment based on sodium restricted
diet, diuretics – response in 90 % without renal
failure.

44.  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
ascites.
 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
curative.

46.  These patients have a poor prognosis and are at risk for a series of
complications:
 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.

47.  http://ezproxy.squ.edu.om:2265/contents/evaluation-of-adults-with-
ascites?detectedLanguage=en&source=search_result&search=ascites&
selectedTitle=1~150&provider=noProvider#H56451750
 http://ezproxy.squ.edu.om:2265/contents/ascites-in-adults-with-cirrhosis-
initialtherapy?detectedLanguage=en&source=search_result&search=ascites
&selectedTitle=2~150&provider=noProvider
 http://emedicine.medscape.com/article/170907-treatment
 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2886420/
o Davidson
o Oxford handbook of clinical medicine.
o Macleod’s clinical examination,12th edition