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home - Liver - Ascites - Pathogenesis of spontaneous bacterial treatment Written by Dr Sebastian Zeki

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

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

Can perform safely both diagnostic and large volume paracentesis
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 treatment

Cell Count: 1 mL into EDTA tube for cell count Ascitic Fluid Analysis Cell count —SBP=>250 PMN’s/mm3- counted manually)Subtract 1 PMN for every 250 red cells/mm3- PMN’s lyse faster than RBC’s so can get a -ve PMN count Gram Stain A separate syringe or tube of fluid should be sent for Gram stain Chemistries should include albumin, so that the serum-ascites albumin gradient can be determined, total protein concentration, glucose, lactate dehydrogenase, and amylase Blood culture bottle- at least 10 mL of fluid- the higher volume increases sensitivty to 93 % (53% for 1ml) Serum-ascites albumin gradient SAAG >1.1 g/dL = portal hypertension (97 % accuracy) Most SBP have PHTN secondary to cirrhosisSAAG < 1.1 g/dL =portal hypertension is not present- rarely develop SBP unless nephroticAscitic fluid [glucose] Low glucose with high PMN’sAscitic fluid LDH—Released from lysed PMNsAscitic fluid amylase —Increased in pancreatitis and gut perforation- only gallbladder perfs dont leak amylaseAscitic fluid [bilirubin] —If > serum and > 6 mg/dL and normal ascitic amylase can assume that the gallbladder has perforated into the peritoneum (choleperitoneum) Culture Negative Neutrocytic Ascites (neuts but no bugs) Definition = PMN count (>250 cells/mm3) with -ve ascitic fluid culture (in absence of antibiotics or pancreatitis) and not secondaryCourse —50% will resolve spontaneously, 50% will go on to develop culture positive SBPTreatment-Empirical as per SBPDue to1. Unrecognized previous treatment.2. Culture technique inadequate- inadequate fluid vol. in inoculum3. One of the other causes of culture-neg neutrocytic ascites took place, eg, hemorrhage into the fluid, tuberc-lous peritonitis, pancreatitis, and malignancy Monomicrobial non-neutrocytic bacteriascites (bugs but no neuts)Usually represents the colonization phase of ascitic fluid infectionUsually get fever if will develop SBP, otherwise asympto-matic Progression to SBP can occur very rapidly (ie witihn the hour) Polymicrobial bacteriascitesUsually due to traumatic paracentesis in which the bowel is entered by the paracentesis needle and bacteria leak, usually transiently, from the gut into the fluid Detected when stain or grow on culture of non-neutrocytic ascites (ie, PMN count <250 cells/mm3)Occurs 1/1000Only rarely needs surgery Distinguishing secondary from sponta-neous bacterial peritonitis—The mortality of secondary bacterial peritonitis is 100 % if antibiotics with no surgery.The mortality is approximately 80 % if a patient with SBP receives an unnecessary exploratory laparotomy .There are no peritonitis as acsites seperates visceral from parietal peritomeum.The [Protein] is >1 g/dL (10 g/L).The [Glucose] is <50 mg/dL (2.8 mmol/L). The LDH is > ULN for serum.If there is no free air/ extravasation of contrast, emer-gency laparotomy cannot be justified.Repeat the ascitic tap- if sterile after antibiotics, this confirms SBP.If rising PMN’s and polymicrobial culture (esp. with enterococcus /fungi ), then probable nonperforation secondary peritonitis due to abscesses. Spontaneous bacterial peritonitis variants For Cirrhosis and Transudative Ascites As An Inpatient (Discontinue on Discharge):Dose: 750 mg ciprofloxacin o.w as outpatientResults: If cirrhosis and transudative ascites: decrease incidence of SBP with ciprofloxacin (3.6 versus 22 %) without resistanceDose: 1 double-strength tablet of trimethoprim-sulfamethoxazole as outpatient (TMP-SMX) 5d/wk Results: Decreased incidence SBP (3 versus 27 % TMP-SMX vs placebo respec.)For History of SBP As An OupatientDose: NorfloxacinPatients also had to fulfil following criteriaChild-Pugh >9 points + bilirubin >3 mg/dL;Serum creat >1.2 mg/dL or BUN >20 mg/dL or serum Na<130 meq/L Results: Fewer episodes of SBP (7 v 61 %), Lower rate of hepato-renal syndrome (28 v 41 %)+ improved survival at 3 months (94 v 62 %) and 12 months (60 v 48%)Cost effectiveness —Only if had SBP historyIn the setting of bleeding —Give antibiotic prophylaxis- eg ix ceftriaxone initially, then complete 7 days on norfloxacin once eating Spontaneous Bacterial Peritonitis Clinical signs and symptoms Ascitic fluid analysis Response to treatment SBP Prophylaxis Written by Dr Sebastian Zeki

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