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Ascites Related
Complications
Chaired by : Dr. Ardaman Singh
Presented by: Dr. Amith Kumar S
Ascites
 derived from Greek term “askos”
Other Etiologies of Ascites (account for <2% of all cases)
Complications
 Ascitic Fluid Infections
 Hepatic Hydrothorax
 Refractory Ascites
 Hepatorenal Syndrome
 Miscellaneous
Ascitic Fluid Infections
When to suspect…
 Fever
 Abdominal pain
 Abdominal Tenderness
 Rebound tenderness
 Altered sensorium
 Leucocytosis
Why to suspect….
 Prevalence of SBP
 33% of patients with SBP land up in renal
impairment
 Untreated mortality is 90% which is reduced
to 20% with early diagnosis and prompt
treatment.
 No survivors have been reported when
the diagnosis of SBP has been made
after Serum Creatinine is more than 4
mg/dl or after shock had developed
Prevalence
Outpatients 1.5 –3.5%
In hospital >10%
Classification
 Culture Negative Neutrocytic Ascites
 Monomicrobial non-neutrocytic
bacterascites
 Polymicrobial Bacterascites
 Secondary Bacterial Peritonitis
 Spontaneous Bacterial Peritonitis
Diagnosis
 Abdominal Paracentesis & Ascitic
fluid analysis
 Ascitic fluid culture
 Complete Blood count
 Renal function tests
 Blood culture
 GI endoscopy
 X ray abdomen erect
Ascitic fluid culture
 Culture is positive in ~ 80% of cases
 Most common pathogens include Gram-
negative bacteria (GNB), usually
Escherichia coli and Gram-positive cocci
 Ascitic fluid culture methods:
◦ Conventional - chocolate agar and
thioglycolate broth
◦ Modified - inoculation of 10 ml of ascitic fluid
in a tryptic soy broth blood culture bottle at
the patient's bedside
Blood agar plate inoculated with the ascitic fluid
showing a growth of Klebsiella pneumonia
Bacteriology
Frequency (%)
Organism SBP MNNB Sec BP SBP with SID
E. Coli 37 27 20 0
Klebsiella
pneumonia
17 11 7 7
Strep Pneumonia 12 9 0 29
Strep viridans 9 2 0 0
Staph aureus 0 7 13 0
Misc gram neg 10 14 7 7
Misc gram
positive
14 30 0 50
Polymicrobial 1 0 53 7
Pathogenesis
Bowel Flora
Bacteria in mesentric LN,
abdominal lymphatics
and thoracic duct
Bactremia
Bacteria in Hepatic
Lymph
Bacterascites
SBP CNNA Sterile Non
neutrocytic ascites
Respiratory tract
infection
Complement deficiency
Urinary tract infection
RE system dysfunction
Poor opsonic activity Good opsonic activity
Modr opsonic activity
Culture Negative Neutrocytic
Ascites
1. Ascitic fluid culture grows no
bacteria
2. Ascitic fluid PMN count is > or = 250
cells/mm3
3. No antibiotics has been prescribed
4. No other explanation for an elevated
ascitic PMN count
Monobacterial Non-neutrocytic
Bacterascites
1. Positive ascitic fluid culture for a
single organism
2. Ascitic fluid PMN count lower than
250 cells/mm3
3. No evidence of an intra abdominal
surgically treatable source of
infection
Polymicrobial Bacterascites
1. Multiple organisms are seen on gram
stain or cultured from the ascitic fluid
2. Ascitic fluid PMN count is lower than
250 cells per mm3
Associated with traumatic paracentesis
Secondary Bacterial
Peritonitis
1. Ascitic fluid culture is positive for
multiple organisms
2. Ascitic fluid PMN count more than
250 cells per mm3
3. Intrabdominal surgically treatable
primary source of infection
Spontaneous Bacterial Peritonitis
1. Positive ascitic fluid culture for a
single organism
2. Elevated ascitic fluid PMN count of
more than 250 cells/mm3
3. No evidence of surgically treatable
source of infection
Risk Factors for SBP
 Cirrhosis
◦ Low ascitic fluid proteins
◦ Phagocytic dysfunction
 GI bleed
◦ 40 % cumulative probablity of infection
◦ Risk peaks 48 hrs after bleed
 Systemic infections
 Earlier episodes of SBP
SBP Vs Secondary Bacterial
Peritonitis
Ascitic Fluid PMN count > or =
250 cells/ mm3
Abdominal imaging
showing free air or
extravasations of
contrast media
Any two out of the following three
1. Ascitic Fluid protein > 1 g/dL
2. Ascitic fluid glucose < 50
mg/dL
3. LDH > ULN
Spontaneous Bacteria
Peritonitis
Perforation
peritonitis
Non perforating
secondary
peritonitis
Ye
s
No
Yes No
Indications for Empirical Antibiotic
Therapy of Suspected
Spontaneous Ascitic Fluid
Infection
•Ascitic fluid neutrophil count ≥
250/mm3 or positive “dipstick” test
•Convincing symptoms or signs of
infection
Inj. Cefotaxim 2 gm i/v q8h
Diagnosis Treatment
Monobacterial
Nonneutrocytic
bacterascites
Five days of intravenous antibiotic to
which the organism is highly susceptible
Culture negative
neutrocytic ascites
Five days of intravenous third
generation cephalosporin
Secondary bacterial
Peritonitis
Surgical intervention plus approx 2
weeks of intravenous cephalosporin
plus anti anaerobic drug (metronidazole)
Polymicrobial
Bacterascites
intravenous third generation
cephalosporin plus anti anaerobic drug
(metronidazole)
Spontaneous
Bacterial Peritonitis
Five days of intravenous antibiotic to
which the organism is highly susceptible
 If preliminary cultures are negative,
paracentesis can be repeated after 48
hrs of therapy to assess the response of
PMN count to antibiotics
 Patients with cirrhosis and ascites with
convincing features of infections should
be put on antibiotics even if ascitic fluid
PMN count is less than 250 cells/mm3
Treatment contd…
 Injectable amoxicillin clavulanic
acid, oral ofloxacin, ciprofloxacin
may be used instead of cephalosporin
 Intravenous albumin – 1.5 gm/kg on
the day of diagnosis, with a second
dose of 1.0 gm/kg on the day three.
Prognosis
 SBP is an indication of End Stage
Liver Disease
 33% of patients with SBP land up in
renal impairment
 No survivors have been reported
when the diagnosis of SBP has been
made after Serum Creatinine is more
than 4 mg/dl or after shock had
developed
Prevention
 Indications for preventive measures
◦ Ascitic fluid protein < 1.0 g/dl
◦ Variceal hemorhage
◦ Previous episode of SBP
 Prior SBP
 Cirrhosis with gastrointestinal
hemorrhage
 Norfloxacin 400 mg orally once daily
until death or liver transplantation
 66% Reduction in recurrence
Intervention
•Norfloxacin 400 mg orally twice daily x 7 days
•Ceftriaxone 1 g intravenously/day x 7 days
Outcome
•73% Reduction in infection
•67% Reduction in infection compared with
norfloxacin
 Cirrhosis with ascitic fluid
◦ Total protein <1.5 g/dL and either
◦ Child-Turcotte-Pugh score ≥9 and total bilirubin
≥3 mg/dL, or
◦ Creatinine ≥1.2 mg/dL, or
◦ Blood urea nitrogen ≥25 mg/dL, or serum sodium
≤130 mEq/L
Intervention
• Norfloxacin 400 mg/day orally x1 year
Outcome
•89% Reduction in SBP
•32% Reduction in hepatorenal syndrome
•52% Increase in 3-month survival
•25% Increase in 1-year survival
 Cirrhosis with ascitic fluid total
protein <1.5 g/dL
Intervention :
Ciprofloxacin 500 mg orally daily x1 year
Outcome
•31% Reduction in infection
•30% Improvement in survival
Hepatic Hydrothorax
 Hepatic hydrothorax develops in
approximately 5%–10% of patients with
cirrhosis,
 Mechanism
◦ Hypoalbuminemia
◦ Azygous vein hypertension
◦ Leakage of ascitic fluid through
diaphragmatic defect
◦ Trans diaphragmatic migration of fluid via
lymphatics
 Pleural effusion is right-sided in 85%,
left-sided in 13%, and bilateral in 2% of
Refractory Ascites
 Refractory ascites is defined as fluid
overload that is
I. Unresponsive to sodium-restricted diet
and high-dose diuretic treatment (400
mg/day spironolactone and 160 mg/day
furosemide) or
II. Recurs rapidly after therapeutic
paracentesis
 Diuretic-resistant ascites
 ascites that cannot be mobilized or the early
recurrence of which cannot be prevented
because of lack of response to dietary
sodium restriction and maximal doses of
diuretics
 Diuretic-intractable ascites
 ascites that cannot be mobilized or the early
recurrence of which cannot be prevented
because of the development of diuretic-
induced complications that preclude the use
of effective diuretic dosages.
 Treatment duration
 Patients must be on intensive diuretic therapy
(spironolactone 400 mg/d and
furosemide160mg/d) for at least 1 wk and on a
saltrestricted diet of less than 90 mmol/d
 Lack of response
 Mean weight loss of < 0.8 kg over 4 days and
urinary sodium output less than the sodium intake.
 Early Ascites Recurrence
◦ There is an reappearance of grade 2 or 3 ascites
(clinically detectable) within 4 wk of initial
mobilization.
Management
a) Serial large volume therapeutic
paracentesis,
b) Liver transplantation,
c) Transjugular intrahepatic
portasystemic stent-shunt (TIPSS)
d) Peritoneovenous shunt
e) Experimental medical therapy
Hepatorenal Syndrome
 Potentially reversible functional renal
failure in the setting of liver
dysfunction (cirrhosis with ascites,
acute liver failure and severe alcoholic
hepatitis), in the absence of intrinsic
renal disease.
International Ascites Club
Consensus Criteria
 Cirrhosis with ascites
 Serum Creatinine level > or = to 1.5 mg/dl
(133 micromol/L) or creatinine clearance
of < 40 ml/min
 No or insufficient improvement in serum
creatinine level, 48 hours after diuretic
withdrawal and adequate volume
expansion with intravenous albumin
 Absence of shock
 No evidence of recent use of nephrotoxic
agents
 Absence of intrinsic renal disease
Classification
 Type 1 Hepatorenal Syndrome
 Serum creatinine doubles to a value
higher than, 2.5mg/dl, in a period of
two week or less
 Type 2 Hepatorenal Syndrome
 Observed in patients with diuretic
resistant ascites
 Serum creatinine less than 2.5 mg/dl
Drugs Dosage Endpoint Duration
Terlipressin Started at a dose of 1 mg/4–6
h and increased to a maximum
of 2 mg/4–6 h if there is no
reduction in serum creatinine
of at least 25% compared to
the baseline value at day 3 of
therapy
Slowly progressive
reduction in serum
creatinine (to below
1.5 mg/dl, and an
increase in arterial
pressure, urine
volume, and serum
sodium concentration.
Maximum of 14 days/
Sr. Creatinine < 1.5 /
Liver Transplant
Midodrine Initiate at a dose of 2.5 – 5.0
mg orally three times daily and
may be increased to a max
dose of 15 mg three times
daily.
An increase in mean
arterial pressure of
atleast 15 mm Hg
Sr. Creatinine < 1.5 /
Liver Transplant
And
Octreotide 100 microgm s/c three times
daily and increase to a max of
200 microgm s/c thrice daily
An increase in mean
arterial pressure of
atleast 15 mm Hg
Sr. Creatinine < 1.5 /
Liver Transplant
25 microgm i/v bolus and a
continuous infusion at a rate of
Drugs Dosage Endpoint Duration
Noradrenaline 0.1 – 0.7 microgm
/kg/min as i/v infusion,
with an increase the
dose by 0.05
microgm/kg/min every
4 hours
Titrate to an increase in
MAP of 10 mm Hg or an
increase in 4 hour urine
output to more than 200
ml
Sr. Creatinine <
1.5 / Liver
Transplant
Intravenous
albumin
Bolus of 1gm/kg at
presentation (max of
100 gm). Continue at a
dose of 20 – 60 gm
daily as needed to
maintain central
venous pressure
between 10 and 15 cm
of H20
Continue at a dose of 20 –
60 gm daily as needed to
maintain central venous
pressure between 10 and
15 cm of H20. To be
discontinued if serum
albumin concentration
exceeds 4.5g/dl or in case
of pulmonary edema
Sr. Creatinine <
1.5 / Liver
Transplant
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Ascites related complications final

  • 1. Ascites Related Complications Chaired by : Dr. Ardaman Singh Presented by: Dr. Amith Kumar S
  • 2. Ascites  derived from Greek term “askos”
  • 3. Other Etiologies of Ascites (account for <2% of all cases)
  • 4. Complications  Ascitic Fluid Infections  Hepatic Hydrothorax  Refractory Ascites  Hepatorenal Syndrome  Miscellaneous
  • 6. When to suspect…  Fever  Abdominal pain  Abdominal Tenderness  Rebound tenderness  Altered sensorium  Leucocytosis
  • 7. Why to suspect….  Prevalence of SBP  33% of patients with SBP land up in renal impairment  Untreated mortality is 90% which is reduced to 20% with early diagnosis and prompt treatment.  No survivors have been reported when the diagnosis of SBP has been made after Serum Creatinine is more than 4 mg/dl or after shock had developed Prevalence Outpatients 1.5 –3.5% In hospital >10%
  • 8. Classification  Culture Negative Neutrocytic Ascites  Monomicrobial non-neutrocytic bacterascites  Polymicrobial Bacterascites  Secondary Bacterial Peritonitis  Spontaneous Bacterial Peritonitis
  • 9. Diagnosis  Abdominal Paracentesis & Ascitic fluid analysis  Ascitic fluid culture  Complete Blood count  Renal function tests  Blood culture  GI endoscopy  X ray abdomen erect
  • 10. Ascitic fluid culture  Culture is positive in ~ 80% of cases  Most common pathogens include Gram- negative bacteria (GNB), usually Escherichia coli and Gram-positive cocci  Ascitic fluid culture methods: ◦ Conventional - chocolate agar and thioglycolate broth ◦ Modified - inoculation of 10 ml of ascitic fluid in a tryptic soy broth blood culture bottle at the patient's bedside
  • 11. Blood agar plate inoculated with the ascitic fluid showing a growth of Klebsiella pneumonia
  • 12. Bacteriology Frequency (%) Organism SBP MNNB Sec BP SBP with SID E. Coli 37 27 20 0 Klebsiella pneumonia 17 11 7 7 Strep Pneumonia 12 9 0 29 Strep viridans 9 2 0 0 Staph aureus 0 7 13 0 Misc gram neg 10 14 7 7 Misc gram positive 14 30 0 50 Polymicrobial 1 0 53 7
  • 13. Pathogenesis Bowel Flora Bacteria in mesentric LN, abdominal lymphatics and thoracic duct Bactremia Bacteria in Hepatic Lymph Bacterascites SBP CNNA Sterile Non neutrocytic ascites Respiratory tract infection Complement deficiency Urinary tract infection RE system dysfunction Poor opsonic activity Good opsonic activity Modr opsonic activity
  • 14. Culture Negative Neutrocytic Ascites 1. Ascitic fluid culture grows no bacteria 2. Ascitic fluid PMN count is > or = 250 cells/mm3 3. No antibiotics has been prescribed 4. No other explanation for an elevated ascitic PMN count
  • 15. Monobacterial Non-neutrocytic Bacterascites 1. Positive ascitic fluid culture for a single organism 2. Ascitic fluid PMN count lower than 250 cells/mm3 3. No evidence of an intra abdominal surgically treatable source of infection
  • 16. Polymicrobial Bacterascites 1. Multiple organisms are seen on gram stain or cultured from the ascitic fluid 2. Ascitic fluid PMN count is lower than 250 cells per mm3 Associated with traumatic paracentesis
  • 17. Secondary Bacterial Peritonitis 1. Ascitic fluid culture is positive for multiple organisms 2. Ascitic fluid PMN count more than 250 cells per mm3 3. Intrabdominal surgically treatable primary source of infection
  • 18. Spontaneous Bacterial Peritonitis 1. Positive ascitic fluid culture for a single organism 2. Elevated ascitic fluid PMN count of more than 250 cells/mm3 3. No evidence of surgically treatable source of infection
  • 19. Risk Factors for SBP  Cirrhosis ◦ Low ascitic fluid proteins ◦ Phagocytic dysfunction  GI bleed ◦ 40 % cumulative probablity of infection ◦ Risk peaks 48 hrs after bleed  Systemic infections  Earlier episodes of SBP
  • 20.
  • 21. SBP Vs Secondary Bacterial Peritonitis Ascitic Fluid PMN count > or = 250 cells/ mm3 Abdominal imaging showing free air or extravasations of contrast media Any two out of the following three 1. Ascitic Fluid protein > 1 g/dL 2. Ascitic fluid glucose < 50 mg/dL 3. LDH > ULN Spontaneous Bacteria Peritonitis Perforation peritonitis Non perforating secondary peritonitis Ye s No Yes No
  • 22. Indications for Empirical Antibiotic Therapy of Suspected Spontaneous Ascitic Fluid Infection •Ascitic fluid neutrophil count ≥ 250/mm3 or positive “dipstick” test •Convincing symptoms or signs of infection Inj. Cefotaxim 2 gm i/v q8h
  • 23. Diagnosis Treatment Monobacterial Nonneutrocytic bacterascites Five days of intravenous antibiotic to which the organism is highly susceptible Culture negative neutrocytic ascites Five days of intravenous third generation cephalosporin Secondary bacterial Peritonitis Surgical intervention plus approx 2 weeks of intravenous cephalosporin plus anti anaerobic drug (metronidazole) Polymicrobial Bacterascites intravenous third generation cephalosporin plus anti anaerobic drug (metronidazole) Spontaneous Bacterial Peritonitis Five days of intravenous antibiotic to which the organism is highly susceptible
  • 24.  If preliminary cultures are negative, paracentesis can be repeated after 48 hrs of therapy to assess the response of PMN count to antibiotics  Patients with cirrhosis and ascites with convincing features of infections should be put on antibiotics even if ascitic fluid PMN count is less than 250 cells/mm3
  • 25. Treatment contd…  Injectable amoxicillin clavulanic acid, oral ofloxacin, ciprofloxacin may be used instead of cephalosporin  Intravenous albumin – 1.5 gm/kg on the day of diagnosis, with a second dose of 1.0 gm/kg on the day three.
  • 26. Prognosis  SBP is an indication of End Stage Liver Disease  33% of patients with SBP land up in renal impairment  No survivors have been reported when the diagnosis of SBP has been made after Serum Creatinine is more than 4 mg/dl or after shock had developed
  • 27. Prevention  Indications for preventive measures ◦ Ascitic fluid protein < 1.0 g/dl ◦ Variceal hemorhage ◦ Previous episode of SBP
  • 28.  Prior SBP  Cirrhosis with gastrointestinal hemorrhage  Norfloxacin 400 mg orally once daily until death or liver transplantation  66% Reduction in recurrence Intervention •Norfloxacin 400 mg orally twice daily x 7 days •Ceftriaxone 1 g intravenously/day x 7 days Outcome •73% Reduction in infection •67% Reduction in infection compared with norfloxacin
  • 29.  Cirrhosis with ascitic fluid ◦ Total protein <1.5 g/dL and either ◦ Child-Turcotte-Pugh score ≥9 and total bilirubin ≥3 mg/dL, or ◦ Creatinine ≥1.2 mg/dL, or ◦ Blood urea nitrogen ≥25 mg/dL, or serum sodium ≤130 mEq/L Intervention • Norfloxacin 400 mg/day orally x1 year Outcome •89% Reduction in SBP •32% Reduction in hepatorenal syndrome •52% Increase in 3-month survival •25% Increase in 1-year survival
  • 30.  Cirrhosis with ascitic fluid total protein <1.5 g/dL Intervention : Ciprofloxacin 500 mg orally daily x1 year Outcome •31% Reduction in infection •30% Improvement in survival
  • 31. Hepatic Hydrothorax  Hepatic hydrothorax develops in approximately 5%–10% of patients with cirrhosis,  Mechanism ◦ Hypoalbuminemia ◦ Azygous vein hypertension ◦ Leakage of ascitic fluid through diaphragmatic defect ◦ Trans diaphragmatic migration of fluid via lymphatics  Pleural effusion is right-sided in 85%, left-sided in 13%, and bilateral in 2% of
  • 32.
  • 33. Refractory Ascites  Refractory ascites is defined as fluid overload that is I. Unresponsive to sodium-restricted diet and high-dose diuretic treatment (400 mg/day spironolactone and 160 mg/day furosemide) or II. Recurs rapidly after therapeutic paracentesis
  • 34.  Diuretic-resistant ascites  ascites that cannot be mobilized or the early recurrence of which cannot be prevented because of lack of response to dietary sodium restriction and maximal doses of diuretics  Diuretic-intractable ascites  ascites that cannot be mobilized or the early recurrence of which cannot be prevented because of the development of diuretic- induced complications that preclude the use of effective diuretic dosages.
  • 35.  Treatment duration  Patients must be on intensive diuretic therapy (spironolactone 400 mg/d and furosemide160mg/d) for at least 1 wk and on a saltrestricted diet of less than 90 mmol/d  Lack of response  Mean weight loss of < 0.8 kg over 4 days and urinary sodium output less than the sodium intake.  Early Ascites Recurrence ◦ There is an reappearance of grade 2 or 3 ascites (clinically detectable) within 4 wk of initial mobilization.
  • 36. Management a) Serial large volume therapeutic paracentesis, b) Liver transplantation, c) Transjugular intrahepatic portasystemic stent-shunt (TIPSS) d) Peritoneovenous shunt e) Experimental medical therapy
  • 37. Hepatorenal Syndrome  Potentially reversible functional renal failure in the setting of liver dysfunction (cirrhosis with ascites, acute liver failure and severe alcoholic hepatitis), in the absence of intrinsic renal disease.
  • 38. International Ascites Club Consensus Criteria  Cirrhosis with ascites  Serum Creatinine level > or = to 1.5 mg/dl (133 micromol/L) or creatinine clearance of < 40 ml/min  No or insufficient improvement in serum creatinine level, 48 hours after diuretic withdrawal and adequate volume expansion with intravenous albumin  Absence of shock  No evidence of recent use of nephrotoxic agents  Absence of intrinsic renal disease
  • 39. Classification  Type 1 Hepatorenal Syndrome  Serum creatinine doubles to a value higher than, 2.5mg/dl, in a period of two week or less  Type 2 Hepatorenal Syndrome  Observed in patients with diuretic resistant ascites  Serum creatinine less than 2.5 mg/dl
  • 40. Drugs Dosage Endpoint Duration Terlipressin Started at a dose of 1 mg/4–6 h and increased to a maximum of 2 mg/4–6 h if there is no reduction in serum creatinine of at least 25% compared to the baseline value at day 3 of therapy Slowly progressive reduction in serum creatinine (to below 1.5 mg/dl, and an increase in arterial pressure, urine volume, and serum sodium concentration. Maximum of 14 days/ Sr. Creatinine < 1.5 / Liver Transplant Midodrine Initiate at a dose of 2.5 – 5.0 mg orally three times daily and may be increased to a max dose of 15 mg three times daily. An increase in mean arterial pressure of atleast 15 mm Hg Sr. Creatinine < 1.5 / Liver Transplant And Octreotide 100 microgm s/c three times daily and increase to a max of 200 microgm s/c thrice daily An increase in mean arterial pressure of atleast 15 mm Hg Sr. Creatinine < 1.5 / Liver Transplant 25 microgm i/v bolus and a continuous infusion at a rate of
  • 41. Drugs Dosage Endpoint Duration Noradrenaline 0.1 – 0.7 microgm /kg/min as i/v infusion, with an increase the dose by 0.05 microgm/kg/min every 4 hours Titrate to an increase in MAP of 10 mm Hg or an increase in 4 hour urine output to more than 200 ml Sr. Creatinine < 1.5 / Liver Transplant Intravenous albumin Bolus of 1gm/kg at presentation (max of 100 gm). Continue at a dose of 20 – 60 gm daily as needed to maintain central venous pressure between 10 and 15 cm of H20 Continue at a dose of 20 – 60 gm daily as needed to maintain central venous pressure between 10 and 15 cm of H20. To be discontinued if serum albumin concentration exceeds 4.5g/dl or in case of pulmonary edema Sr. Creatinine < 1.5 / Liver Transplant
  • 42. Heal The World Make It A Better Place For You And For Me And The Entire Human Race There Are People Dying If You Care Enough For The Living Make A Better Place For You And For Me…

Editor's Notes

  1. Sympathetic system antagonistsV2 receptor antagonistsVasoconstrictors