Dr sumer yadav

DEPARTMENT OF SURGERYDEPARTMENT OF SURGERY

ASCITESASCITES

DEFINITION – FREE FLUID IN THE

ABDOMINAL CAVITY

PATHOPHYSIOLOGY OF ASCITES

• HYDROSTATIC PRESSURE

CIRRHOSISCHFCONSTRICTIVE PERICARDITIS

• OSMOTIC PRESSURE

NEPHROTIC SYNDROMEMALNUTRITIONPROTEIN LOSING ENTEROPATHY

PATHOPHYSIOLOGY OF ASCITES (Cont.)

• HEPATIC VEIN OUTFLOW OBSTRUCTION –EXTENSIVE OBLITERATIVE FIBROSIS

OF HEPATIC VEIN

• RENAL SODIUM RETENTION

• PERITONEAL ABSORPTION OF ASCITES

• HYPOALBUMINEMIA

PATHOPHYSIOLOGY OF ASCITES (Cont.)

• HORMONAL INFLUENCES–ALDOSTERONE

–ANTIDIURETIC HORMONE

–ATRIAL NATRIURETIC PEPTIDE

PATHOPHYSIOLOGY OF ASCITES (Cont.)

• FLUID PRODUCTION EXCEEDING RESORPTIVE CAPACITY

INFECTION – TB

MALIGNANCY

DIAGNOSIS

HISTORY (Cont.)

• H/O INCREASED ABDOMINAL GIRTH

• H/O PEDAL EDEMA

• H/O WEIGHT GAIN

• H/O CHF

• H/O HEPATITIS

• 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.)

• 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

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

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

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

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

BULGING FLANKS

JAMA 1992;267:2645-2648

ASCITES OR OBESITY?

• The Signs of Portal Hypertension And Chronic Liver Disease Like : – Jaundice

– Palmar Erythema

– Spider Angiomas.

EXAMINATION (Cont.)

• 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.)

• 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.)

• 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.)

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

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 NoneEasily Controlle

d

Poorly Controlle

d

Neurological Disorder

None Minimal Advanced

Nutrition Excellent Good Wasting

Child’s Classification of Hepatocellualr Function in Cirrhosis

TESTS OF ASCITIC FLUIDRoutine Tests Optional Test Unusual Tests

Cell Count GlucoseTuberculosis

Smear and Culture

AlbuminLactate

DehydrogenaseCytrologic Exam

for Cancer

Bacterial Culture (In Blood Culture Bottles)

Amylase Gram’s Stain

Total Protein

CAUSES OF ASCITES BASED ON SAAG AND ASCITIC FLUID TOTAL PROTEIN

CONCENTRATION Portal

HypertensionSAAG >1.1

Non-PortalHypertension

SAAG <1.1

Low Protein Normal Protein

Chronic Liver DiseaseMassive Hepatic

Metastasis

Cardiac DiseaseBudd-Chiari

SyndromeVeno-Occlusive

DiseaseMyxedema

Peritoneal Carcinomatosis, Chronic Peritoneal

Infection (Ie, Tuberculosis, Fungal,

Cytomegalovirus), Nephrotic Syndrome, Pancreatic Ascites,

Protein-Losing Enteropathy

IMAGING STUDIES

• 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.

• 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.

• 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.

• 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.

• 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.

COMPLICATION OF ASCITES

• SPONTANEOUS BACTERIAL PERITONITIS

• ABDOMINAL WALL HERNIAS

• PLEURAL EFFUSION

• BLOODY ASCITES

TREATMENT

• ASCITES TREATED BY: -– MEDICAL

– SURGICAL

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.

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.

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

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.

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.

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.

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

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

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

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.

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.