1. ASCITES & PERITONITIS

2. Diagnosis of Ascites Physical exam: Shifting dullness Fluid wave
Organ ballotment
For cirrhosis related ascites: stigmata of cirrhosis
Jaundice
Spider angioma
Muscle wasting
Abdominal wall collaterals

3. Physical Exam for Ascites
Sensitivity and specificity related to volume and body habitus
50-90% sensitive
30-80% specific
Absence of any flank dullness is best indicator of no/minimal ascites (under 1500 cc)

4. Causes of Ascites History should make diagnosis
Cirrhosis/Acute hepatic injury (~80%) ( 5% have multifactorial cause)
Malignancy ( ~ 10%)
Right sided heart failure (3%)
Renal disease (1%)
Pancreatic (1%)
TB (2%)
Other ( SLE, myxedema, surgical complication: chylous: 2%)
HIV ( 75% cirrhosis and 25 % HIV related: TB, fungal, lymphoma)
History should make diagnosis

5. Causes Cirrhosis causes 80-85% of ascites
Underfill vs Overlow theories
Recent Peripheral Arterial Vasodilation theory: incorporates both
Fundamental abnormality is Portal HTN
PHT--> nitric oxide--> vasodilation--> renal Na retention--> overfill of intravasc vol--> ascites formation--> neurohumoral activation
figure 78.1

7. Pathogenesis

8. Physical Exam Related to Pathophysiology of Hepatic Ascites
Portal hypertension
Ascites
Varices/ collaterals
Palmer erythema and gonadal atrophy
estrogen metabolic impairment
Arterial vascular “under filling”
Flat neck veins
System relative hypotension
Tachycardia

10. Evaluation Radiology: US supplanted by CT Signs of cirrhosis
Malignancy
Portal vein thrombosis
Hepatic vein thrombosis
Caveat is risk of IV contrast with the common underlying renal insufficiency/volume depletion of associated conditions

11. Clinical deterioration of any kind
Paracentesis
Ascites fluid analysis in all patients with
New onset ascites
Abdominal pain and known ascites
Fever and ascites
Clinical deterioration of any kind

13. Pathogenesis: Non-Liver disease
Depends on site of abnormality
Malignancies
peritoneal carcinomatosis- exudation of proteinaceous fluid from tumor cells lining peri
Massive liver mets- portal HTN
Hepatocellular CA- underlying cirrhosis, PVT
Lymphoma- chylous ascites, obstruction of LN
Cardiac- hear failure, PHT

14. Clinical Features
Pts with stable cirrhosis and “sudden”ascites, suspect hepatocellular CA
Should suspect malignant ascites in pts with malignancy however need to rule out cirrhosis
Breast, lung, colon and pancreatic are often complicated by ascites
Malignant ascites is usually painful

15. Diagnosis: Paracentesis
Complications of Paracentesis:
Rare and related to inexperience
Perforation
Past surgery and adhesions to peritoneum
Absence of ascites
Bleeding
Coagulapathy (clotting factors and thrombocytopenia)
Abdominal wall collaterals
Studies have excluded those with INR over 1.6 /PT over 21 seconds and Plt under 50,000 or clinically evident DIC
Leak
Large bore catheter
Tense ascites

16. Paracentesis: technique
Avoid surgical scar- risk of adhesions
Supine or lateral decubitus
Tap out area of shifting dullness
Head of bed slightly elevated
Avoid collaterals and inferior hypogastric artery
Left or Right lateral versus midline
Main issue is to examine for contraindications to use of site and optimal area of shifting dullness
Scant ascites, scars and or obesity w/o shifting dullness
Prone near midline: “puddle”
US guided if not emergently needed in this setting

17. Paracentesis: technique
Needle
Bruce Runyon: Up to Date and Slesinger and Fortran
1.5” 22 gauge diagnostic and 16 gauge for large volume
3.5” spinal for obese abdominal wall
Steel needle or blunt tipped cannula with sharp stylet that can be removed
Goldkind: Boston University/Boston City Hospital
Angiocath : do not reinsert metal stylet after insertion in to abdominal wall to prevent sheering off of plastic
Angiocath may be less likely to perforate bowel or nick vessel after metal stylet removed
Kinking is an issue

19. Culture SBP most common bacterial infection usually monomicrobial
low bacteria count
Conventional plating not sensitive (50%)
Bedside inoculation of blood culture bottles 80% sensitive

20. Appropriate Tests Cell count single most helpful test
EDTA purple top tube
WBC in cirrhotics usually < 500cells/m3
PMN > 250cells/m3 ABNORMAL
SBP most common cause of increased WBC
Traumatic tap accounts for most bloody ascites (subtract 1 PMN for each 250 RBCs)

21. Diagnosing TB AFB from ascites almost always negative
centrifuged pellet only 50% sensitive
Best method- peritoneal biopsy and culture combined for close to 100% sensitivity

22. Cytology
Should be expected in malignancies with cells lining the peritoneum
Essentially 100% of pts with peritoneal carcinomatosis have positive cytology
Other malignancies (mets, hepatocellular CA) may cause ascites but may have negative cytology

23. Serum-Ascites Albumin Gradient
Before the 1980s we used transudate vs. exudate, never fully validated
SAAG has been shown superior to exudate-transudate categories and total protein values in several studies
SAAG= serum albumin - ascites albumin (same day specimens)
Correlates with portal pressure
Discard Transudate and Exudate terminology

24. Serum-Ascites Albumin Gradient
SAAG > 1.1 g/dL (11 g/L),
pt has portal HTN (97% accuracy)
SAAG < 1.1 g/dL, no portal HTN
Does not give pathogenesis or dx cirrhosis
Not affected by:
infection, diuresis, etiology of liver disease
Not a test for peritonitis
cell count and culture used for this question

25. SAAG: high gradient >1.1g/dL
Cirrhosis
Alcoholic Hepatitis
Cardiac ascites
“Mixed” ascites
Hepatic failure
Budd-Chiari syndrome
Portal vein thrombosis
Veno-occlusive dis.
Myxedema
Fatty liver of pregnancy

26. SAAG: low gradient < 1.1g/dL
Peritoneal Carcinomatosis
Tuberculous peritonitis
Pancreatic ascites
Bowel obstruction or infarction
Biliary ascites
Nephrotic Syndrome
Post-op lymphatic leak
Serositis in CTD

29. Complications of Ascites
Infection
SBP
Tense Ascites
Respiratory compromise ( restriction)
Pain
Pleural Effusions (hepatic hydrothorax)
Abdominal Wall Hernias

30. Spontaneous bacterial peritonitis
Correia and Conn coined term in 1975
Goal to distinguish SBP from surgical peritonitis
Diagnosis
positive ascitic fluid culture
elevated ascitic PMN count > 250cells/mm3
and
no intra-abdominal surgically treatable source

31. Spontaneous bacterial peritonitis
Spontaneous bacterial peritonitis (variants)
Monomicrobial non-neutracytic:
(culture + without 250 polys)
Culture negative Neutrocytic
high poly count but culture negative: simply presumed false neg culture
SBP and variants
only occur in severe liver disease
In the presence of pre-existing ascites
Almost always in patients with elevated bili and INR

32. Begin here to finish presentation

34. SBP: Pathogenesis MNB: CNNA: more common than SBP
probably early stage of SBP
good opsonic activity results in sterile ascites
poor opsonic activity results in SBP
CNNA:
probably poor culture technique
resolving SBP after killing of bacteria but before normalization of PMN count

35. SBP: presentation

36. SBP: Prevalence
Overall 10% of pts. with ascites are infected on admission
27% of cirrhotic ascites are infected
Secondary bacterial peritonitis occurs in <2% of pts.

37. SBP: organisms E. coli most common 37% Klebsiella 17% Pneumococcus 12%
Strep. viridans 9%
Miscellaneous
gram positive 14%
gram negative 10%

38. SBP: Diagnosis High index of suspicion: Ascitic fluid PMN>250
Signs and symptoms of infection
Rule out secondary peritonitis- imaging, surgical consult
Repeat tap after 48 hours of treatment
antibiotics can’t control secondary peritonitis but rapidly cure SBP

39. SBP: Treatment Empiric antibiotics for all suspected SBP
5 days of IV antibiotics
cefotaxime 2 gm q8 better than amp and tobra
cefotaxime covered 98% of the flora
no renal toxicity
sterile culture after 1 dose in 86% of pts
change spectrum according to sensitivities
repeat tap in 48 hours to assess for change in PMN count (decline often >80%)

40. SBP: Prognosis Old studies 48-95% of pts died despite tx
Now <5% die of infection if timely and appropriate antibiotics are used
earlier detection, treatment
avoidance of nephrotoxic agents
Maximize survival:
tap all pts admitted to hospital
repeat if deterioration, change in sx
tap all outpatients with NEW ascites

41. SBP: Prevention Risk factors
previous SBP
low ascitic protein
variceal hemorrhage
Norfloxin 400 mg QD prevents SBP in low protein and previous SBP and 400mg BID for pts with variceal hemorrhage
Oral antibiotics do not prolong survival

42. Treatment: depends on etiology
Low SAAG:
Peritoneal Carcinomatosis- most common
outpt therapeutic paracentesis
Tuberculous ascites
cured by anti-TB therapy
Pancreatic ascites
may resolve spontaneously

43. Treatment: depends on etiology
High SAAG:
hospitalization (large volume)
diet education (low sodium)
urine sodium excretion
fluid restriction (hyponatremia)
DIURETICS
no bed rest, sodium bicarb, foleys

44. Treatment Hospitalization for diagnosis, large volume paracentesis
Diet education with salt restriction key to management (2gm Na/day)
Check urinary Na excretion to ensure compliance
Fluid restriction not needed unless Na < 120 or pt symptomatic

45. Treatment Diuretics: Spironolactone Furosemide Amiloride
is mainstay of tx, better than furosemide
long half life=slow onset (2 weeks to full effect), gynecomastia, hyperkalemia
Furosemide
faster onset, hypokalemia
Amiloride
more rapid onset, more expensive
less gynecomastia

46. Treatment Combination diuretics most effective Single day dosing
Spironolactone 100mg
Furosemide 40mg
Single day dosing
Double dose when ineffective
Start simultaneously
IV not needed

47. Treatment No limit to weight loss in pts with massive edema
Then 0.5 Kg/day
Stop diuretics for
encephalopathy
creatinine > 2 mg/dL
sodium < 120 mmol/L

48. Treatment: outpt management
Re-evaluate in 1-2 weeks
Goal of diuretics is weight loss (negative sodium balance)
Check urine sodium
if excretion of Na> than 88mmol/day and pt is on 88mmol Na diet, they should lose weight

49. Refractory Ascites
Defined as fluid overload unresposive to salt restriction and high-dose diuretics
< 10% of pts with cirrhotic ascites are refractory
Viable options include peritoneovenous shunt, LVP and transplant

50. Refractory Ascites Peritoneovenous shunts:
complications include shunt failure, fatal complications of insertion
no survival advantage in RCT
relegation to 3rd line therapy of cirrhotic ascites

51. Refractory Ascites
Therapeutic abdominal paracentesis- one of the oldest medical procedures
first line therapy in pts with TENSE ascites and second line therapy for refractory ascites
large taps tolerated

52. Colloid Replacement Albumin Expensive: $2-$25/g or $100-$1250 per tap
markedly increase albumin degradation
58% of infused albumin was accounted for by increased degradation
15% increase in serum albumin led to 39% increase in degradation
Barcelona study used pts with tense ascites, not refractory ascites (31% not on diuretics)

53. Colloid Replacement Albumin
Tense ascites paracentesis > 10L with or without albumin
No albumin developed statistically sig. Changes in electrolytes, plasma renin and creatinine
All changes were asymptomatic
No increased morbidity or mortality in pts who did not receive albumin
pilot study by Runyon showed no difference in morbidity, hepatorenal or mortality p1330

54. TIPS Side-side portocaval shunt placed by IR Local anaesthesia
Originally used for variceal bleeding

55. TIPS Rossle used a RCT to compare TIPS vs LVP (NEJM 2000)
60 pts with good hepatic and renal function, refractory or recurrent ascites
survival 1 and 2 year was 69 and 58% vs 52 and 32% respectively
40% required stent opening
cost $25,000 to $50,000
trial of LVP and if unsuccessful in “select” pts refer for TIPS

56. Liver Transplant
12-month survival for refractory pts ranges from 25-50%
Early referral after decompensation:
refractory ascites
encephalopathy
gi hemorrhage
Transplant has a 12-month survival close to 75%

57. Summary