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SBP and hepatic encephalopathy
- 1. Spontaneous Bacterial Peritonitis(SBP) & Hepatic Encephalopathy Kimberly Treier PharmD Candidate 2016 2 May 2016
- 2. SBP- Definition Asciticfluid infection without evident intra-abdominal surgicically treatable source Usually occurs in patients with cirrhosis and ascites
- 3. SBP - Pathogenesis Overgrowth of intestinal flora (usually E. coli) and spread outside into mesentery and lymph nodes (translocation) Cirrhosis decreases intestinal motility Increased permeability OR from other infections (e.g. UTI, cellulitis) Lymphatic rupture of contaminated lymph d/t portal hypertension (bacteriascites) Microbes overwhelm host defenses Cirrhosis = acquired immune deficiency (decreased compliment capability)
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- 6. SBP – RiskFactors Advanced cirrhosis Ascitic fluid total protein <1g/dL Prior SBP Serum total bilirubin >2.5 mg/dL Variceal hemorrhage Malnutrition PPI use Ascitic fluid total protein <1.5 g/dL + Child-Pugh score ≥9 points + serum bilirubin ≥3 gm/dL OR Plasma creatinine ≥1.2 mg/dL, BUN ≥25 mg/dL or plasma Na ≤130 mEq/L
- 7. SBP – Signsand Symptoms Fever (most common) Abdominal pain/tenderness Altered mental status Diarrhea Paralytic ileus* Hypotension* Hypothermia* Abnormal laboratory values (e.g. leukocytosis, metabolic acidosis, azotemia) *Advanced infection
- 8. SBP - Diagnosis Clinical presentation Ascitic fluid positive for bacteria Ascitic fluid absolute polymorphonuclear leukocyte (PMN) count ≥250 cells/mm3 Exclusion of secondary causes
- 9. SBP - Treatment AsciticPMN <250 cells/mm3 + Signs/symptoms of infection: Empiric antibiotic therapy, e.g. ceftotaxime 2 g IV q8h, while awaiting cultures American Association for the Study of Liver Disease (2012)
- 10. SBP - Treatment AsciticPMN ≥250 cells/mm3 + Community-acquired setting + absence of β-lactam antibiotic exposure: Empiric antibiotic therapy, e.g. IV third generation cephalosporin, preferably cefotaxime 2 g IV q8h Nosocomial setting ± in the presence of recent β-lactam antibiotic exposure: Empiric antibiotic therapy based on local susceptibility testing of bacteria in patients with cirrhosis Can substitute with ofloxacin 400 mg PO BID in inpatients without prior exposure to quinolones, vomiting, shock, grade ≥II hepatic encephalopathy, or SCr >3 mg/dL American Association for the Study of Liver Disease (2012)
- 11. SBP - Treatment AsciticPMN ≥250 cells/mm3 + High suspicion of secondary peritonitis Test for protein, LDH, glucose, gram stain, carcinoembryonic antigen and alkaline phosphatase (distinguish between SBP and secondary peritonitis) Computed tomographic scanning Nosocomial setting ± recent β-lactam antibiotic exposure ± atypical organism or atypical clinical response to treatment Follow-up paracentesis after 48 hours of treatment Clinical suspicion of SBP, SCr >1 mg/dL, BUN >30 mg/dL or tBili >4 mg/dL Albumin 1.5 g/kg within 6 hours and 1 g/kg on day 3 American Association for the Study of Liver Disease (2012)
- 12. SBP - Prophylaxis Cirrhosis and GI bleeding IV ceftriaxone or norfloxacin BID x 7 days Survived an episode of SBP Long-term norfloxacin 400 mg QD (or SMX/TMP) Cirrhosis and ascites but no GI bleeding + ascitic fluid protein <1.5 g/dL + renal insufficiency (SCr ≥1.2 mg/dL, BUN ≥25 mg/dL or serum Na+ ≤130 mE/L) or hepatic failure (Child-Pugh ≥9 points + bilirubin ≥3 mg/dL) Long-term norfloxacin (or SMX/TMP) Daily (vs. intermittent) antibiotic dosing recommended American Association for the Study of Liver Disease (2012)
- 13. Hepatic Encephalopathy -definition
- 14. Hepatic Encephalopathy -pathogenesis Drugs Benzodiazepines Narcotics Alcohol Increased ammonia production, absorption or Brain entry Excess dietary protein intake GI bleeding Infection Electrolyte disturbances Constipation Metabolic alkalosis
- 15. Hepatic Encephalopathy -pathogenesis Dehydration Vomiting/diarrhea Hemorrhage Diuretics Large volume paracentesis Portosystemic shunting Radiographic or surgically placed shunts Spontaneous shunts Vascular occlusion Hepatic vein thrombosis Portal vein thrombosis Primary hepatocellular carcinoma
- 16. Hepatic Encephalopathy –Classification Underlying Disease Hepatic encephalopathy occurring in the setting of… Type A Acute liver failure Type B Portal-systemic bypass with no intrinsic hepatocellular disease Type C Cirrhosis with portal hypertension or systemic shunting Severity of Manifestations Minimal Abnormal results on psychometric or neurophysiologic testing without clinical manifestations Grade I Changes in behavior, mild confusion, slurred speech, disordered sleep Grade III Marked confusion (stupor), incoherent speech, sleeping but arousable Grade IV Coma, unresponsive to pain
- 19. Hepatic Encephalopathy -Diagnosis History and physical exam Cognitive and neuromuscular impairments Laboratory tests Ammonia, glucose, urea, electrolytes Psychometric tests Changes in mental function Number connection test (NCT; Reitan Test), Psychometric Hepatic Encephalopathy Score (PHES) Electrophysiology tests E.g. electroencephalogram (EEG) Imaging MRI, CT
- 20. Hepatic Encephalopathy –Differential Diagnosis Reye syndrome GI bleeding Renal disease UTI with urease-producing microbe (e.g. P. mirabilis) Shock Severe muscle exertion Metabolic abnormalities Salicylate intoxication
- 21. Hepatic Encephalopathy -Treatment
- 22. Hepatic Encephalopathy -Treatment
- 23. Hepatic Encephalopathy -Treatment
- 24. References Runyon BA.Pathogenesis of spontaneous bacterial peritonitis. In: UpToDate, Post TW (Ed), UpToDate, Waltham, MA. Accessed 27 April 2016. Runyon BA. Spontaneous bacterial peritonitis in adults: Clinical manifestations. In: UpToDate, Post TW (Ed), UpToDate, Waltham, MA. Accessed 27 April 2016. Runyon BA. Spontaneous bacterial peritonitis in adults: Diagnosis. In: UpToDate, Post TW (Ed), UpToDate, Waltham, MA. Accessed 27 April 2016. Runyon BA. Spontaneous bacterial peritonitis in adults: Treatment and prophylaxis. In: UpToDate, Post TW (Ed), UpToDate, Waltham, MA. Accessed 27 April 2016. Runyon BA. Practice Guideline: Management of Adult Patients with Ascites Due to Cirrhosis: Update 2012. American Association for the Study of Liver Diseases. (2012). p. 1-96. Ferenci P. Hepatic encephalopathy: Pathogenesis. In: UpToDate, Post TW (Ed), UpToDate, Waltham, MA. Accessed 27 April 2016. Ferenci P. Hepatic encephalopathy in adults: Clinical manifestations and diagnosis. In: UpToDate, Post TW (Ed), UpToDate, Waltham, MA. Accessed 28 April 2016. Leise MD, Poterucha JJ, Kamath PS, et al. Management of Hepatic Encephalopathy in the Hospital. Mayo Clin Proc. 2014; 89(2): 241-253. PMC4128786
Editor's Notes
- #3 SBP bacteria require phagocytosis via opsonization (complement) and/or Ig Ascitic fluid 10-fold more dilute than serum (less compliment factors) Serum complement deficient common in liver disease patients advanced enough to produce ascites
- #4 SBP bacteria require phagocytosis via opsonization (complement) and/or Ig Ascitic fluid 10-fold more dilute than serum (less compliment factors) Serum complement deficient common in liver disease patients advanced enough to produce ascites
- #7 SBP bacteria require phagocytosis via opsonization (complement) and/or Ig Ascitic fluid 10-fold more dilute than serum (less compliment factors) Serum complement deficient common in liver disease patients advanced enough to produce ascites
- #8 SBP bacteria require phagocytosis via opsonization (complement) and/or Ig Ascitic fluid 10-fold more dilute than serum (less compliment factors) Serum complement deficient common in liver disease patients advanced enough to produce ascites
- #9 SBP bacteria require phagocytosis via opsonization (complement) and/or Ig Ascitic fluid 10-fold more dilute than serum (less compliment factors) Serum complement deficient common in liver disease patients advanced enough to produce ascites
- #11 “Widespread use of quinolones to prevent SBP in high-risk subgroups of patients as well as frequent hospitalizaions and exposure to broad-spectrum antbiotics have led to a change in flora with more gram-positives and extended spectrum B-lactamase producing Enterobacteriaceae in recent years. Risk factors for multireisstant infections include: nosocomial origin of infection, long-term norfloxacin prophylaxis, recent infection with multiresistant bacteria, and recent use of B-lactam antibiotics.”
- #23 LOLA = L-ornithine L-aspartate BCCA = branch chain amino acids MARS = Molecular Adsorbent Recirculating System
- #24 LOLA = L-ornithine L-aspartate BCCA = branch chain amino acids MARS = Molecular Adsorbent Recirculating System