ascites

1. Dr sumer yadav
DEPARTMENT OF SURGERYDEPARTMENT OF SURGERY

2. ASCITESASCITES
DEFINITION – FREE
FLUID IN THE
ABDOMINAL CAVITY

3. PATHOPHYSIOLOGY OF
ASCITES
• HYDROSTATIC PRESSURE
CIRRHOSIS
CHF
CONSTRICTIVE PERICARDITIS
• OSMOTIC PRESSURE
NEPHROTIC SYNDROME
MALNUTRITION
PROTEIN LOSING ENTEROPATHY

4. PATHOPHYSIOLOGY OF ASCITES
(Cont.)
• HEPATIC VEIN OUTFLOW
OBSTRUCTION
–EXTENSIVE OBLITERATIVE
FIBROSIS OF HEPATIC VEIN
• RENAL SODIUM RETENTION
• PERITONEAL ABSORPTION OF
ASCITES
• HYPOALBUMINEMIA

5. PATHOPHYSIOLOGY OF ASCITES
(Cont.)
• HORMONAL INFLUENCES
–ALDOSTERONE
–ANTIDIURETIC HORMONE
–ATRIAL NATRIURETIC PEPTIDE

6. PATHOPHYSIOLOGY OF ASCITES
(Cont.)
• FLUID PRODUCTION
EXCEEDING RESORPTIVE
CAPACITY
INFECTION – TB
MALIGNANCY

7. DIAGNOSIS

8. HISTORY (Cont.)
• H/O INCREASED
ABDOMINAL GIRTH
• H/O PEDAL EDEMA
• H/O WEIGHT GAIN
• H/O CHF
• H/O HEPATITIS

9. • Most Cases of Ascites Are Due to
Liver Disease. Patients often State
That Their Increasing Abdominal
Girth Has Been Noted For A Short
Period.
• Patients With Ascites Should Be
Asked About Risk Factors For Liver
Diseases. These Include The
Following:
HISTORY (Cont.)

10. • Alcohol Use and its Duration
• Jaundice
• Drug Abuse
• Sexual Promiscuity
• Sexual Orientation
• Transfusions: Hepatitis C Has Been
Linked To Transfusions Occurring Before
1980.
• Tattoos
• Habitation or Origination From An Area
Endemic For Hepatitis

11. PHYSICAL EXAMINATION
• Ascites May Be Semiquantified Using The
Following System:
– 0 : No Ascites
– 1+ : Just Detectable
– 2+ : Easily Detectable But Small
Volume
– 3+ : Obvious But Not Tense
– 4+ : Tense Ascites

12. SHIFTING DULLNESS
METHOD OF EXAMINATION
BEGIN BY PERCUSSING AT THE UMBILICUS AND MOVING TOWARD THE
FLANKS. THE TRANSITION FROM AIR TO FLUID CAN BE IDENTIFIED WHEN
THE PERCUSSION NOTE CHANGES FROM TYMPANIC TO DULL.
ROLL THE PATIENT ON THEIR SIDE AND PERCUSS AS BEFORE. THE AREA
OF TYMPANY WILL SHIFT TOWARDS THE TOP AND THE AREA OF
DULLNESS TOWARDS THE BOTTOM.
JAMA 1992;267:2645-2648

13. SHIFTING DULLNESS
METHOD OF EXAMINATION
HAVE THE PATIENT OR ASSISTANT PLACE
THEIR HANDS IN THE MIDLINE
TAP ONE FLANK SHARPLY AND USE THE
FINGERTIPS OF THE OPPOSITE HAND TO
FEEL FOR AN IMPULSE ON THE OPPOSITE
FLANK JAMA 1992;267:2645-2648
TAPFEEL
PATIENT OR
ASSISTANT

14. PUDDLE SIGN
METHOD OF EXAMINATION
PATIENT IS PRONE FOR 3-5 MINUTES AND THEN
RISES TO ALL FOURS
DIAPHRAGM OF THE STETHOSCOPE IS PLACED
OVER MOST DEPENDENT AREA OF THE
ABDOMEN
BEGIN BY FLICKING A FINGER OVER A LOCALIZED
FLANK AREA
MOVE THE STETHOSCOPE OVER THE OPPOSITE
FLANK
SUDDEN INCREASE IN INTENSITY IS A POSITIVE
SIGN (NO LONGER USED) JAMA 1992;267:2645-2648

15. BULGING FLANKS
JAMA 1992;267:2645-2648
ASCITES OR OBESITY?

16. • The Signs of Portal
Hypertension And Chronic
Liver Disease Like :
– Jaundice
– Palmar Erythema
– Spider Angiomas.
EXAMINATION (Cont.)

17. • The Liver May Be Difficult To Palpate
If A Large Amount of Ascites Is
Present.
• The Puddle Sign Indicates That As
Little As 120 Ml of Fluid Is Present.
• When Peritoneal Fluid Exceeds 500
Ml, Ascites May Be Demonstrated By
The Presence of Shifting Dullness or
Bulging Flanks.
• A Fluid-wave Sign Is Notoriously
Inaccurate.
EXAMINATION (Cont.)

18. • Elevated Jugular Venous Pressure
May Suggest A Cardiac Origin of
Ascites.
• A Firm Nodule In The Umbilicus,
The So-called Sister Mary Joseph
Nodule, Is Not Common But
Suggests Peritoneal
Carcinomatosis Originating From
Gastric, Pancreatic, or Hepatic
Primary Malignancy.
EXAMINATION (Cont.)

19. • A Pathologic Left-sided
Supraclavicular Node (Virchow
Node) Suggests The Presence of
Upper Abdominal Malignancy.
• Patients With Cardiac Disease or
Nephrotic Syndrome May Have
Anasarca.
• Patients With Tuberculous
Peritonitis Have Abdominal
Tenderness and Guarding or
Rigidity
EXAMINATION (Cont.)

20. WORK-UP
• Routine Investigations :
– Blood Counts : Total and Differential
– Liver Function Test : Serum Proteins,
Total and Albumin
– Ascitic Fluid Analysis
– SAAG (Serum Ascites Albumin
Gradient)
– Diagnostic Laparoscopic Examination

21. Group
Designation
A B C
Bilirubin (mg/dl) <2.0 2.0-3.0 >3.0
Albumin (g/dl) >3.5 3.0-3.5 <3.0
Ascites None
Easily
Controlle
d
Poorly
Controlle
d
Neurological
Disorder
None Minimal Advanced
Nutrition Excellent Good Wasting
Child’s Classification of
Hepatocellualr Function in Cirrhosis

22. TESTS OF ASCITIC FLUID
Routine Tests Optional Test Unusual Tests
Cell Count Glucose
Tuberculosis
Smear and
Culture
Albumin
Lactate
Dehydrogenase
Cytrologic Exam
for Cancer
Bacterial Culture
(In Blood
Culture
Bottles)
Amylase
Gram’s Stain
Total Protein

23. CAUSES OF ASCITES BASED ON SAAG
AND ASCITIC FLUID TOTAL PROTEIN
CONCENTRATION
Portal
Hypertension
SAAG >1.1
Non-Portal
Hypertension
SAAG <1.1
Low Protein Normal Protein
Chronic Liver Disease
Massive Hepatic
Metastasis
Cardiac Disease
Budd-Chiari
Syndrome
Veno-Occlusive
Disease
Myxedema
Peritoneal Carcinomatosis,
Chronic Peritoneal
Infection (Ie,
Tuberculosis, Fungal,
Cytomegalovirus),
Nephrotic Syndrome,
Pancreatic Ascites,
Protein-Losing
Enteropathy

24. IMAGING
STUDIES

25. • Chest And Plain Abdominal Films
Elevation of The Diaphragm, With
or Without Sympathetic Pleural
Effusions (Hepatic Hydrothorax),
Is Visible In The Presence of
Massive Ascites.
• More Than 500 Ml of Fluid Is
Usually Required For Ascites to
Be Diagnosed Based On Findings
From Abdominal Films.

26. • Diffuse Abdominal Haziness.
• Bulging of The Flanks
• Indistinct Psoas Margins
• Erect Position Density Increase
• Separation of Small Bowel Loops
• Centralization of Floating Gas
Containing Small Bowel.

27. • ULTRASOUNDULTRASOUND
–Most Sensitive Technique For The
Detection of Ascitic Fluid.
–Volumes as Small As 5-10 Ml Can
Routinely be Visualized.
–The Smallest Amounts of Fluid
Tend to Collect in The Morison
Pouch And Around The Liver as a
Sonolucent Band.

28. • Most Patients (95%) With
Carcinomatous Peritonitis Have A
Gallbladder Wall That Is Less Than
3 Mm Thick.
• Mural Thickening of The
Gallbladder Is Associated With
Benign Ascites In 82% of Cases.
• The Thickening of The Gallbladder
Is Primarily A Reflection of Cirrhosis
And Portal Hypertension.

29. • CT SCAN
– 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. A Number
of CT Features Suggest Neoplasia.
– 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 Tend to
Have Proportional Fluid Collections in The Greater
and Lesser Sacs; Whereas, in Patients With Benign
Ascites, The Fluid is Observed Primarily in The
Greater Sac and Not in The Lesser Omental Bursae.

30. COMPLICATION OF ASCITES
• SPONTANEOUS BACTERIAL
PERITONITIS
• ABDOMINAL WALL HERNIAS
• PLEURAL EFFUSION
• BLOODY ASCITES

31. TREATMENT
• ASCITES TREATED BY: -
– MEDICAL
– SURGICAL

32. MEDICAL CARE
• Sodium Restriction (20-30 Meq/D)
And Diuretic Therapy Constitute
The Standard Medical Management
For Ascites And Are Effective In
Approximately 95% Of Patients.
• Water Restriction Is Used Only If
Persistent Hyponatremia Is Present.

33. MEDICAL CARE (Cont.)
• Therapeutic Paracentesis Should Be
Reserved For Patients Who Need Rapid
Symptomatic Relief Of Tense Ascites.
• Tips Is An Interventional Radiologic
Technique That Reduces Portal Pressure
And May Be The Most Efficacious For
Treatment Of Patients With Diuretic-resistant
Ascites. This Procedure Consists Of
Inserting A Long Metal Needle From The
Right Jugular Vein Into The Hepatic Vein.
This Is Slowly Becoming The Standard Of
Care In Patients With Diuretic-refractory
Ascites.

34. SURGICAL TREATMENT
Surgical Treatment Depends
upon Etiology Like: -
– Portal Hypertension and
Malignancy
•Internal Drainage
•Peritoneovenous Shunt
– Side-to-side Portacaval Shunt
– End-to-side Portacaval Shunt

35. SURGICAL TREATMENT
• The Peritoneovenous Shunt Is An
Alternative For Patients With
Medically Intractable Ascites.
• This Is A Megalymphatic Shunt
That Returns The Ascitic Fluid To
The Central Venous System.

36. SURGICAL TREATMENT
• Beneficial Effects Of These Shunts
Include Increased Cardiac Output,
Renal Blood Flow, Glomerular
Filtration Rate, Urinary Volume, And
Sodium Excretion And Decreased
Plasma Renin Activity And Plasma
Aldosterone Concentration.

37. PERITONEOVENOUS SHUNT
• In This Pressure Activated One-way
Wall That Shunted Ascetic Fluid From
High Pressure Peritoneal Cavity To The
Low-pressure Superior Vena Cava.
• One Limb of The Shunt Lies Free In
The Peritoneal Cavity And Other One
Limb Is Inserted Through The Internal
Jugular Vein Into The Superior Vena
Cava.

38. PERITONEOVENOUS SHUNT
• Flow In The Shunt Is Maintained In
Between The 30 To 50 Mm Saline
Pressure Gradient The Valve Closes
When The Gradient Falls Below 30
MM, Preventing Blood From Flowing
Back Into The Tubing

40. COMPLICATIONS OF
PERITONEOVENOUS SHUNT
EARLY
• Shunt Occlusion or Malfunction
• DIC
• Sepsis and Bacterial Peritonitis
• CHF and Pulmonary Edema Due to Fluid
Overload
• Bleeding Varices
• Air Embolism
• Allergic Fever
• Ascites Leakage

41. COMPLICATIONS OF
PERITONEOVENOUS SHUNT
LATER
•Shunt Occlusion or Malfunction
•Sepsis and Bacterial Peritonitis
•Abdominal Abscess
•Central Venous Thrombosis
•Pulmonary Emboli
•Abdominal Wall Infection
•Bleed Varices
•Adhesive Intestinal Obstruction

42. OTHER
• Consultations: Consultation With A
Gastrointestinal Specialist and/or
Hepatologist Should be Considered
For All Patients With Ascites,
Particularly If The Ascites Is
Refractory To Medical Treatment.

43. OTHER
• Diet: Sodium Restriction Of 500
Mg/D (22 Mmol/D) Is Feasible In A
Hospital Setting; However, It Is
Unrealistic In Most Outpatient
Settings. A More Appropriate
Sodium Restriction Is 2000 Mg/D
(88 Mmol). Indiscriminate Fluid
Restriction Is Inappropriate. Fluids
Need Not Be Restricted Unless
The Serum Sodium Level Drops
Below 120 Mmol/L.