Approach to Ascites & SBP

Etiology & DDx

-Portal HTN: Increase in Hydrostatic Pressure

·       Cardiac & Hepatic

o   Pre-sinusoidal: portal or splenic vein thrombosis, schistosomiasis

o   Sinusoidal: cirrhosis, active hepatitis, extensive malignancy (HCC or mets)

o   Post-sinusoidal: Budd-Chiari syndrome, veno-occlusive disease, Right sided CHF, TR, constrictive pericarditis

-Non-Portal HTN

·       Decrease in Oncotic Pressure

o   Malnutrition, protein losing enteropathy, nephrotic syndrome, liver disease

·       Increased Capillary Permeability and/or change in Lymphatics (i.e. obstruction)

o   Infection: i.e. spontaneous bacterial peritonitis (SBP)

o   Malignancy: ovarian, peritoneal metastases

o   Pancreatitis

Others: hypothyroidism, sarcoidosis

Key Questions to ask on History- JAMA: DOES THIS PATIENT HAVE ASCITES?

·       Increased abdominal girth: SN 87%, SP 77%, +LR 4.16

·       Recent weight gain: SN 67%, SP 79%, +LR 3.2

·       Ankle swelling: SN 93%, SP 68%, +LR 2.8

Physical Exam- JAMA PHYSICAL EXAM PEARLS

·       Bulging Flanks: SN 81%, SP 59%, +LR 2

·       Flank Dullness: SN 84%, SP 59%, +LR 2

·       Shifting Dullness: SN 77%, SP 72%, +LR 2.7

·       Fluid Wave: SN 62%, SP 90%, +LR 6

·       Peripheral edema!

Paracentesis: Answers two important questions:

1)     Is the fluid infected?

2)     Is portal HTN present?

Serum-to-ascites albumin gradient (SAAG): helps identify the presence of portal HTN

·       Serum albumin – ascites albumin

·       SAAG ≥11 g/L predicts that the patient has portal HTN (97% accuracy)

o   i.e. cirrhosis, CHF, Hepatocellular Carcinoma, Alcoholic Hepatitis, Massive liver metastases

·       SAAG <11 g/L indicates that the patient does not have portal HTN

o   i.e. pancreatitis, peritoneal carcinomatosis, TB peritonitis, nephrotic syndrome

NOTE: patients with ascites due to heart failure, can narrow their gradient during diuresis, whereas the SAAG in cirrhosis remains stable unless BP or portal pressure decreases significantly

NOTE #2: Runyon et al., demonstrated that the accuracy of the SAAG was 97% in predicting portal HTN

Long Term Management of Ascites

1)     Identify the underlying cause and treat appropriately

2)     Sodium Restrict: <2 g/day

3)     Fluid Restrict: <1.5 L/day

4)     Diuretics: Lasix (40-160 mg PO daily) and Spironolactone 100-400 mg)

5)     Paracentesis: therapeutic, diagnostic

6)     Albumin: if you remove >5 L, replace with albumin (i.e. 100 mL of 25% for every 3L of ascites removed over 5L)

7)     EtOH Abstinence

8)     Drugs to Avoid: NSAID (reduce renal excretion of Na, can cause azotemia); ACEi (SBP falls with cirrhosisà reduced renal perfusion and GFR, which increases activity of RASà inc VCà support BP by compensating for the VD effects of NO; BP directly related to survival, thus, AVOID ACE/ARB)

9)     Trans-jugular intra-hepatic portosystemic shunts (TIPS)

10)   Followed closely by GI/hepatology

11)   Transplant discussions

Spontaneous Bacterial Peritonitis (SBP): an ascitic fluid infection without an evident intra-abdominal surgically treatable source; primarily in patients with advanced cirrhosis. Due to overgrowth of bacteria in the bowel (usually E.coli)à transverse bowel wallà infect ascites…the symptoms may be subtle as the visceral peritoneum is separated from the parietal peritoneum

Diagnosis: positive ascitic fluid bacterial culture, an elevated ascitic fluid absolute polymorphonuclear leukocyte (PMN) count (≥250 cells/mm³), and exclusion of secondary causes of bacterial peritonitis.

·       An elevated ascitic fluid absolute PMN count (≥250 cells/mm³) is a presumptive diagnosis of SBPà thus, start empiric therapy.

Importance of Recognition: early intervention leads to improved outcome; reduced risk of shock, MSOF

Clinical Setting: Patients with SBP usually have cirrhosis, advanced MELD score, large volume ascites

Clinical Manifestations: patients with cirrhosis who develop fever, abdominal pain/tenderness (diffuse, contiuous), AMS; other S&S include diarrhea, paralytic ileus, hypotension, hypothermia, lab abnormalities (peripheral leukocytosis, azotemia, metabolic acidosis)

NOTE: patients with advanced cirrhosis are usually mildly hypothermia, THUS, a T of 37.8C or greater should be taken seriously!

Indications for Treatment include ≥1 of:

·       T>37.8 C (patients w/ cirrhosis are more often hypothermic at BL)

·       Abdominal pain/tenderness

·       Alteration in mental status

·       Ascitic fluid PMN ≥250 cells/mm3

Antibiotics for SBP: most cases are d/t gut bacteria (i.e. E. coli, Klebsiella), infrequently streptococcal and staphylococcal

Cefotaxime 2g IV q8h, Ceftriaxone 2g IV daily (poorer penetration than Cefotaxime, d/t lower protein ascitic fluid)

·       Duration: 5-10 days

Renal dysfunction — develops in 30-40% of patients with SBP and is a major cause of death. The risk may be decreased with an infusion of IV albumin (1.5 g/kg body weight within six hours of diagnosis and 1.0 g/kg body weight on day 3).

·       Some evidence to suggest a reduction in mortality

SBP Prophylaxis: for those with RFs for SBP (prior episode, ascitic fluid protein <10 g/L, variceal hemorrhage);

·       Cipro 750 mg PO weekly, or Septra DS 1 tab PO daily