SAVED
File name .JPG
File alt. text
Image should be px wide x px tall.
Select Image
home - Liver - Ascites - Pathogenesis of spontaneous bacterial peritonitis Written by Dr Sebastian Zeki
Knowledge


Defines the causes (both hepatic and non hepatic) of ascites and
has a clear understanding of their pathogenesis

Recognises how to define resistant and refractory ascites
Understands the management of patients with ascites (including fluid
restriction use of colloids diuretics) as well as the indications for and
the role of interventional procedures such as paracentesis TIPS

Knows the value of laboratory investigation of acites including
diagnosis of spontaneous bacterial peritonitis its prognosis and
treatment

Appreciates the evidence for the prophylactic use of albumin
infusions to reduce risk of hepatorenal syndrome

Understands the indications for alternative interventions (e g TIPS
surgical shunt peritoneal–venous shunt and transplantation) and the
criteria for appropriate referral

Skills
Can perform safely both diagnostic and large volume paracentesis
Behaviours
Can refer patients in a timely manner to specialist liver services
Understand the implications on quality of life as well as the nutritional
impact of resistant ascites

Shows ability to develop and sustain supportive relationships with
patients and their families

Pathogenesis of spontaneous bacterial peritonitis

C o m p l e m e Clinical Presentation Midodrine and octreotide —Midodrine (selective alpha-1 adrenergic agonist) and octreotide (a somatostatin analog) may prevent renal failure Intravenous albumin —Give iv albumin as possible survival advantage Microbiology and choice of antibiotic If no norfloxacin prophylaxis give cefotaxime 2 g iv tds - gives a resolution rate of 80%.If norfloxacin prophlaxis consider further gram +ve cover eg oral ofloxacin in asymptomatic Malignant and cardiac ascites v v rare to get infected Possibly malnutrition PPI use Prior episode of SBP Usually have cirrhosis: PPI Variceal hemor-rhage Ascitic fluid total protein concentra-tion less than 1 g/dL (<10 g/L) Serum total [bilirubin]>2.5 mg/dL Treatment of SBP Repeat paracentesis if anything atypical or no dramatic responseIf no resolution consider secondary peritonitis with further evaluation/surgical intervention5 days is sufficient unless it is an unusual organism.When PMN count is <250 cells/mm3,stop tx.WhenPMN count is > pretreatment value, consider surgical source.If PMN count is elevated but < pretreatment value, continue antibiotics for 48h then retap.Consider liver tranplant if the patient survives SBP. Paralytic ileus, hypotension, hypothermia —These more severe signs are indicative of advanced infection and a poor likelihood of survival.If this stage is reached, survival is unlikely.Laboratory abnormalities —Leukocytosis, metabolic acidosis, and azotemia. Diarrhea —May develop diarrhoea as gut flora can change (usually get more E. coli) Altered mental status —Occurs in 54% Fever —most common mani-festation of SBP Abdominal pain —Diffuse continuous abdo painDifferent from stretching pain due to tense ascites Safety of ParacentesisTransfusion for paracentesis-related hemorrhage <1 %.There’s no need to reverse anticoagulation or to give platelets. Bowel perforation usually occurs with inexperienced operator/ needle too close to surgical scar/ ileus present Usually the first line of defense, but if inadequate, then neutrophils and complement activated The function of both motile (eg, PMNs) and stationary phagocytes (eg, Kupffer cells) is reduced in patients with advanced liver diseas Serum complement deficiency is quite common in patients with liver disease that is advanced enough to produce ascites Macrophages Neutrophils Defense mechanisms Risk factors for SBP — Pathogenesis of spontaneous bacterial peritonitis Clinical setting —Usually occurs in advanced cirrhosis.Usually in clinically obvious ascitesOnly occurs in established ascites Usually E. coli and KlebsiellaLess frequently staphs and streps 4. Entry from external instrumenta-tion Routes of entry Change in gut floraIncreased bacterial translocation esp in cirrhotics 2. Organism moves from the mesenteric LN to the systemic circulation and then percolate through the liver and weep across Glisson's capsule to enter the ascitic fluid 3. Can occur if the lymphatic carrying the contaminated lymph ruptures because of the high flow and high pressure associated with portal hypertension 1. Luminal bacteria within colonize mesenteric LN’s Duration of therapy — Written by Dr Sebastian Zeki

Related Stories

•Clinical factors to predict changes of esophagogastric varices after sustained viral response with direct-acting antiviral therapy

•Twenty-five percent human albumin solution in clinical practice: indications, risks and monitoring protocols

•Tuberculous Pericarditis in an Immunocompromised Patient: A Case Report

•An Acute Hepatic Hydrothorax Causing Tension

•Comparative efficacy of endoscopic variceal ligation versus non-selective beta-blockers in primary prevention of gastroesophageal varix type 2: an IPTW-adjusted study