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LibraryMBBS

MBBS SAQ

Ascites and Spontaneous Bacterial Peritonitis — SAQ

15 marks12 minSource-verified ·

Exam tags

NEET-PGINICETUSMLEPLAB
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Exam tags

NEET-PGINICETUSMLEPLAB

Write your answer

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Stem

A candidate is asked to manage a classic presentation of Ascites and Spontaneous Bacterial Peritonitis in an exam setting. Use precise definitions, scores, doses, and decision thresholds.[1]

Core knowledge (model answer backbone)

Ascites is the pathological accumulation of fluid in the peritoneal cavity. Cirrhosis causes over 80 percent of cases through portal hypertension, hypoalbuminaemia, splanchnic vasodilation (nitric oxide) and renal sodium and water retention (RAAS and sympathetic activation). The serum-ascites albumin gradient (SAAG) of 1.1 g/dL or more separates portal-hypertensive from non-portal causes. Spontaneous bacterial peritonitis (SBP) is a monomicrobial infection of ascitic fluid without an obvious intra-abdominal source, defined by an ascitic polymorphonuclear neutrophil count of 250 cells/mm3 or more, treated with a third-generation cephalosporin (cefotaxime 2 g IV every 8 hours; ceftriaxone is the accepted alternative per guideline convention) plus intravenous albumin (1.5 g/kg on day 1 and 1 g/kg on day 3).[3] The immediate risk in a deteriorating cirrhotic with ascites is untreated SBP with renal impairment. Refractory ascites — recurring rapidly despite sodium restriction and diuretics — carries about 50 percent mortality at 6 months and mandates TIPS and transplant assessment.. Ascites management is built on sodium restriction, spironolactone with furosemide in a 100:40 ratio, large-volume paracentesis with albumin, TIPS for refractory ascites, and liver transplantation as definitive therapy.

Red flags

  • Cirrhotic with ascites and fever, abdominal pain, new or worsening encephalopathy, renal dysfunction or unexplained deterioration - spontaneous bacterial peritonitis until proven otherwise; do diagnostic paracentesis immediately, treat if PMN 250 cells/mm3 or more
  • Tense ascites with respiratory compromise or renal impairment - large-volume paracentesis with albumin replacement; do not over-diurese
  • Rising creatinine in a decompensated cirrhotic after fluid challenge - hepatorenal syndrome; stop diuretics and nephrotoxins, give albumin and consider terlipressin
  • Refractory ascites recurring rapidly after paracentesis despite maximum diuretics - 50 percent mortality at 6 months without transplant; refer for TIPS and transplant assessment

High-yield structure examiners expect

Cover: Overview & Definition, Classification, Epidemiology & Risk Factors, Pathophysiology, Clinical Presentation, Differential Diagnosis.

Key doses / thresholds (from topic teaching)

  • SAAG 1.1 g/dL or more = portal hypertension (96.7 percent accurate versus 55.6 percent for the exudate-transudate concept).[1]
  • SBP: ascitic PMN 250 cells/mm3 or more, irrespective of the culture result.[2]
  • Cefotaxime 2 g IV every 8 hours for 5 days (2 g every 12 hours equally effective).[4]
  • Plus albumin 1.5 g/kg on day 1 and 1 g/kg on day 3 (renal impairment 33 to 10 percent; in-hospital mortality 29 to 10 percent).[3]
  • Norfloxacin 400 mg daily for secondary prophylaxis (1-year recurrence 68 to 20 percent).[5]
  • Diagnostic tap: all cirrhotics with ascites on admission; coagulopathy is not a contraindication (AASLD convention).
  • Ascites regimen: sodium 2 g/day plus spironolactone 100 mg with furosemide 40 mg titrated together (AASLD convention); when 5 L or more is drained give albumin 6 to 8 g per litre removed.[5]

Questions

a) Define the condition and give the most important classification or severity framework used in exams. (3 marks)

  • Clear one-line definition matching standard teaching.
  • Named classification / stages / types with discriminating features.
  • One sentence on why classification changes management (SAAG directs the cause-directed workup).[1]

b) Outline pathophysiology in a mechanism chain that explains the main clinical features. (3 marks)

  • Initiating insult → intermediate pathway → end-organ effect.
  • Link at least two symptoms/signs to mechanism.
  • Mention one complication pathway (e.g. SBP-driven hepatorenal syndrome, umbilical hernia rupture).[3]

c) List discriminating clinical features and bedside assessment. (3 marks)

  • Classic presentation plus one atypical group (elderly, pregnancy, child, immunocompromised).
  • Named signs/manoeuvres if relevant.[1]
  • What must never be missed on exam/bedside (the diagnostic tap in any deteriorating cirrhotic with ascites).[2]

d) Investigations with thresholds and one named score if applicable. (3 marks)

  • First-line tests and what positive findings mean.
  • Gold-standard or definitive investigation when needed.[2]
  • Score components reproduced exactly if a named score is standard for this topic.

e) Immediate resuscitation and definitive management with doses where standard. (3 marks)

  • ABC / time-critical steps first.
  • First-line drug(s) with agent + dose + route (or procedure steps).
  • Escalation triggers (theatre, ICU, TIPS, transplant referral, antidote, etc.).[3]
  • Disposition and safety-netting.[4]

Marking tips

Full marks require specificity (numbers, names, doses) not generic "give antibiotics/fluids." Regional practice (ICMR / NICE / AHA) may be cited as alternative where relevant.[5]

References5ShowHide
  1. [1]Runyon BA, Montano AA, Akriviadis EA, et al. The serum-ascites albumin gradient is superior to the exudate-transudate concept in the differential diagnosis of ascites Ann Intern Med, 1992.PMID 1616215
  2. [2]Koulaouzidis A Diagnosis of spontaneous bacterial peritonitis: an update on leucocyte esterase reagent strips World J Gastroenterol, 2011.PMID 21448413
  3. [3]Sort P, Navasa M, Arroyo V, et al. Effect of intravenous albumin on renal impairment and mortality in patients with cirrhosis and spontaneous bacterial peritonitis N Engl J Med, 1999.PMID 10432325
  4. [4]Runyon BA, McHutchison JG, Antillon MR, et al. Short-course versus long-course antibiotic treatment of spontaneous bacterial peritonitis Gastroenterology, 1991.PMID 2019378
  5. [5]Ginés P, Rimola A, Planas R, et al. Norfloxacin prevents spontaneous bacterial peritonitis recurrence in cirrhosis Hepatology, 1990.PMID 2210673