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Causes and Diagnosis of Ascites
1. Diseases of the Peritoneum and
ascites
Dr. Tumaini, BB MD
Resident in Internal Medicine
For MD students year 3
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From: peri “around” - tonos “to stretch”
5. Introduction
• Peritoneum is a continuous transparent serous
membrane which lines the abdominal cavity and covers
the viscera
• Peritoneal cavity is lined by visceral and parietal layers.
• Visceral-poorly innervated; vague pain.
• Parietal: richly innervated; very painful; pain precisely
localized.
• In visceral perforation contents flow inferiorly directed by
anatomical landmarks; e.g., into the pelvis via paracolic
gutters.
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6. Functions of the peritoneum
• Pain perception
• Visceral lubrication:
• Fluid and particulate absorption
• Inflammatory and immune response
• Fibrinolytic activity
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7. Peritoneal inflammation: Causes
• Bacterial infection eg. Appendicitis; TB
• Chemical injury eg bile peritonitis
• Ischaemic injury eg strangulated bowel
• Direct trauma eg surgery
• Allergic reaction eg starch peritonitis.
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8. Acute peritonitis
• Due to invasion of peritoneal cavity by
bacteria
• Polymicrobial: aerobic, anaerobic (exception:
Primary peritonitis due to streptococcal,
pneumococcal or H. Influenza spp.)
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9. Bacteriology:
• Bacteria from GI tract
– E. coli,
– Aerobic and anaerobic streptococci
– Bacteroides
• Non-GI causes:
– PID
– Chlamydia, gonococcus,
– Mycobacteria e.g., Mycobacterium bovis
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11. Clinical features
• Localized peritonitis
– Symptoms and signs are those of the causative
disease
– Abdominal pain
– Guarding and rigidity of the abdominal wall
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12. Clinical features
• Generalized peritonitis
– Abdominal pain
– Vomiting
– Abdominal rigidity with guarding and rebound
tenderness
– Absence of bowel sounds
– Fast pulse and high temperature
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13. Diagnosis
Mainly clinical
• CBC
• X-rays-chest, erect
-abdominal plain
• Serum amylase and lipase, creatinine,
electrolytes
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14. Management
• General
– Correction of fluid and electrolyte imbalance +
fluid balance charts
– Gastrointestinal decompression: NGT
– Antibiotic therapy: IV
– Analgesia
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15. Management
• Specific
– Surgery e.g., perforated DU, appendicitis
gangrenous cholecystitis
– Peritoneal lavage
– Non-surgical: pancreatitis, salpingitis
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16. Complications: systemic
• Bacteremia/endotoxic shock
• Bronchopneumonia/respiratory failure
• Renal failure
• Bone marrow suppression
• Multisystem failure
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17. Complications-abdominal
• Small bowel obstruction
• Paralytic ileus
• Residual/recurrent abscess
• Portal pyaemia
• Liver abscess
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19. Tuberculous peritonitis
• Acute
– Resembles acute pyogenic peritonitis
– Straw coloured fluid escapes at laparotomy
– Tubercles are seen over peritoneum and greater
omentum
– Take specimen for macroscopic (caseous necrosis)
and histological examination
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20. Tuberculous peritonitis-chronic
• Origin
– Tb of mesenteric lymph nodes
– Ileocaecal TB
– TB pyosalphinx
– Blood borne TB usually milliary TB
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21. TB peritonitis-chronic
• Types:
• Ascitic form
– Peritoneum seeded with TB tubercles
– Ascites is preset
– No pain
– Diagnosis:
• Exclude other causes of ascites
• Ascitic fluid – exudate (protein content > 30gm/L)
• Histology from other lesions e.g., tubercles
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22. TB peritonitis chronic
• Encysted form
– Similar to ascitic type but localizedto one part of
abdominal cavity.
– May be difficult to differentiate from a mesenteric
cyst
– Laparotomy needed for diagnosis
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23. TB peritonitis chronic
• Fibrous (dry, plastic) form
– There is no ascites
– There are a lot of adhesions
– Bowel walls are matted together
– Present as bowel obstruction
• Treatment
– Surgery – adhesiolysis; excision of stenosed bowel
– Anti-TB medications
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24. Ascites
• The accumulation of fluid in the peritoneal
cavity
• Has many extraperitoneal and peritoneal
causes
• Commonest cause: cirrhosis
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25. Peritoneal fluid
• It is a normal, lubricating fluid found in the
peritoneal cavity
• Peritoneum secretes about 50 ml of fluid per
day
• The fluid is mostly water with electrolytes,
antibodies, WBCs, albumin, glucose and other
biochemicals.
• Reduces the friction between the abdominal
organs as they move around during digestion.
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27. Etiology of ascites: commonest causes
• Portal HTN secondary to chronic liver
diseases (cirrhosis)
• Congestive Heart Failure
• Mycobacterium tuberculosis
• Intra-abdominal malignancy
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28. Portal Hypertension
• It is a high blood pressure in the portal vein
and its tributaries(portal venous system).
• It is defined as a portal pressure gradient (the
difference in pressure between the portal vein
and the hepatic veins) of 5 mm Hg or greater.
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29. Causes of portal hypertension
• Intrahepatic causes: liver cirrhosis and hepatic
fibrosis (e.g. due to Wilson's disease,
hemochromatosis, or congenital fibrosis).
• Prehepatic causes : portal vein thrombosis or
congenital atresia.
• Posthepatic obstruction occur at any level between
liver and right heart, including hepatic vein
thrombosis, IVC thrombosis, IVC congenital
malformation, and constrictive pericarditis.
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30. Cirrhosis
Commonest causes of cirrhosis:
• Alcoholic liver disease or alcoholic hepatitis
• viral hepatitis (B or C)
• fatty liver disease
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36. Pathophysiology
2. Decreased colloid osmotic pressure
• End-stage liver disease with poor protein
synthesis
• Nephrotic syndrome
• Malnutrition
• Protein-losing enteropathy
3. Increased permeability of peritoneal
capillaries
• Tuberculous peritonitis
• Bacterial peritonitis
• Malignant disease of the peritoneum
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37. Pathophysiology
4. Leakage of fluid into the peritoneal cavity
• Bile ascites
• Pancreatic ascites
• Chylous ascites
• Urine ascites
5. Miscellaneous causes
• Myxedema
• Ovarian disease (Meigs syndrome)
• Chronic hemodialysis
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38. Morbidity and Mortality
• Ambulatory patients with an episode of
cirrhotic ascites have a 3-year mortality rate of
50%. The development of refractory ascites
carries a poor prognosis, with a 1-year survival
rate of less than 50%.
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39. Diagnosis: history
Pts should be questioned about:
• Liver diseases
• Risk factors for viral hepatitis: IDU, needle
sharing, blood transfusion, etc
• Pts with obesity, diabetes, hyperlipidemia -
Nonalcoholic steatohepatitis (NASH)
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40. • Pts with ascites who lack risk factors for
cirrhosis should be questioned about to rule
out cancer, heart failure, TB, dialysis, and
pancreatitis
• Operative injury to the ureter or bladder can
lead to leakage of urine into peritoneal
cavity.
• HIV pts may have infections leading to
ascites
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41. Diagnosis
2-clinical Features
A - Asymptomatic (fluid <100 - 400ml):
Mild ascites
B - symptomatic (fluid >400ml):
Increased abdominal girth, presence of
abdominal pain or discomfort, early satiety,
pedal edema, weight gain and respiratory
distress depending on the amount of fluid
accumulated in the abdomen.
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42. Physical examination findings:
• Umbilicus Eversion (often with umbilical
herniation)
• Tympany at the top of the abdomen
• Fluid wave
• Peripheral edema
• Shifting dullness (> 500ml fluid)
• Bulging flanks (>500ml fluid)
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43. Bulging Flanks and Umbilical Hernia
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44. Diagnosis 3 - paracentesis
• It is a diagnostic procedure to establish the
etiology of new-onset ascites or to rule out
spontaneous bacterial peritonitis in patients
with preexisting ascites. Large volume
paracentesis is performed in hemodynamically
stable patients with tense or refractory ascites
to alleviate discomfort or respiratory
compromise.
• For diagnostic purposes, a small amount
(20cc) may be enough for adequate testing.
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45. Ascitic fluid analysis
Cell count:
• A white blood cell count is the most
important.
• A neutrophil > 250 cells/mL spontaneous
bacterial peritonitis
• An elevated lymphocyte tuberculosis or
peritoneal carcinomatosis
• Gram stain and culture:
for bacteria and acid fast bacilli
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46. • RBCs
Seen in hemorrhagic ascites, which usually is
due to malignancy, tuberculosis or trauma.
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47. Serum-Ascites Albumin Gradient [SAAG]
• Best single test for classifying ascites into
portal hypertensive and non-portal
hypertensive causes.
• Calculated by:
Serum albumin – Ascites albumin= SAAG
SAAG >1.1 g/dL= Portal HTN
SAAG < 1.1 g/dL= Non-Portal hypertensive cause
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49. • Total protein:
Helpful in diagnosing spontaneous bacterial
peritonitis
Pts with a value<1 g/dl protein and glucose of
<50mg/dl
have high risk of SBP
• Cytology:
for malignant cells
• Amylase:
to exclude pancreatic ascites
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50. Imaging Studies
Ultrasound
• Easiest and most sensitive technique for
detection of ascitic fluid.
• Volume as small as 5-10ml can be seen.
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54. Imaging Studies
CT scan
• Well visualized
• Fluid may be visualized in the:
• Right perihepatic space
• Posterior subhepatic space (Morison
pouch)
• Pouch of Douglas
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56. Management of Ascites
The goal is to prevent Na loading and increase
renal excretion of Na and H2O and produce a net
re-absorption of fluid from the ascites back into the
circulating volume.
• Dietary Na restriction
Diet of 2g sodium per day
• Fluid Restriction:
Only done when serum Na is <128mmol/L
• Check Labs
Ck serum electrolytes and creatinine every other
day.
Weigh the patient and measure urinary output
daily.
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57. Management of ascites
• Management of underlying disease
• Dietary sodium restriction
• Fluid restriction
• Diuretic therapy
• Large-volume paracentesis
• Liver transplantation and shunts
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58. Management of Ascites
Diuretic therapy
• Spironolactone: diuretic of choice
• Others: furosemide etc
Paracentesis
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59. Paracentesis Contraindications:
• Acute abdomen (absolute)
• Severe bowel distention
• Previous abdominal surgery (if necessary perform open
procedure)
• Pregnancy (if necessary perform after first trimester using
an open technique above the umbilicus)
• Distended bladder that cannot be relieved by foley catheder
• Infection at site of insertion (cellulitis or abscess)
• Thrombocytopenia (relative)
• Coagulopathy (relative)
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60. Paracentesis Complications:
• Bladder perforation
• Small or large bowel perforation
• Stomach perforation
• Laceration of major vessels ( mesenteric, iliac, aorta)
• Laceration of catheter or guide wire and loss in
peritoneal cavity (requires laparotomy)
• Abdominal wall hematoma
• Incisional hernia
• Wound infection
• Wound dehiscence
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61. Management of Ascites
Transjugular Intrahepatic Portasystemic Shunt:
The TIPS procedure is an interventional
radiologic technique that reduces portal
pressure and may be the most effective
treatment for diuretic resistant ascites.
Risks:
• Hepatic Encephalopathy (30% of pts)
• Thrombosis and shunt stenosis.
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62. Management of Ascites
liver transplantation:
• Tx of choice
• Corrects portal hypertension
• Changes the natural course of progressive liver
failure due to cirrhosis
• Not all pts are candidates for transplant, and
those who are may wait for years for a donor
• Many die from complications of ascites while
waiting for transplant donor
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63. Complications from Ascites
Refractory Ascites
• Fluid overload that is unresponsive to Na-
restricted diet and high dose anti-diuretic
treatment.
• Usually in the setting of chronic or acute
liver diseases with associated portal
hypertension.
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64. Treatment of Refractory Ascites:
Liver transplantation is treatment of choice.
If unsuitable, treatment with:
• Serial paracentesis
• TIPS
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65. Complications of Ascites
• Hepatorenal syndrome
• Spontaneous bacterial peritonitis
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