Confusion and worsening renal function in a patient with cirrhosis and ascites
A 61-year-old man with alcohol-related cirrhosis and ascites is admitted with three days of worsening confusion and vague abdominal discomfort. He takes spironolactone 100 mg daily and furosemide 40 mg daily. He has drunk no alcohol for eight months. Observations: temperature 38.0°C, heart rate 102/min, blood pressure 96/60 mmHg. He is disorientated to time and place, with asterixis. There is tense ascites but no abdominal rigidity. Bloods: sodium 128 mmol/L, creatinine 168 micromol/L (baseline 88), bilirubin 54 micromol/L, albumin 26 g/L, INR 1.8, platelets 88 ×10⁹/L. Diagnostic paracentesis: neutrophil count 380 cells/mm³, protein 12 g/L, glucose 2.1 mmol/L, lactate dehydrogenase above the serum level.
1. What is the principal diagnosis, and how do the ascitic fluid results support it?
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Principal diagnosis: spontaneous bacterial peritonitis (SBP) precipitating hepatic encephalopathy.
The ascitic fluid is diagnostic:
- Absolute neutrophil count 380/mm³ - the diagnostic threshold is ≥250/mm³. This alone is sufficient to start treatment; culture results are not required and should not delay antibiotics.
- Protein 12 g/L - low ascitic protein (<15 g/L) indicates poor opsonic activity and identifies him as at high risk of SBP.
- Glucose 2.1 mmol/L and LDH above serum - these suggest either a secondary peritonitis or a severe/established infection. The classical threshold for secondary peritonitis is a Runyon criterion set (glucose <2.8 mmol/L, LDH above serum, protein >10 g/L, with at least two of three). Here glucose and LDH are both abnormal, so a surgical cause (perforation, ischaemic bowel) must be actively excluded, particularly if there is free air or a deteriorating course.
Important distinction: the confusion is not simply hepatic encephalopathy to be treated with lactulose alone. The infection is the precipitant and the cause of the acute kidney injury; failure to treat the infection will allow the encephalopathy and renal failure to progress.
2. Outline your immediate management, including the reasoning behind each component.
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- Start intravenous antibiotics immediately - a third-generation cephalosporin (e.g. cefotaxime 2 g 8-hourly) is standard first-line. Do not wait for culture. If there has been prior quinolone prophylaxis or recent hospitalisation, use a broader agent covering resistant organisms per local policy.
- Intravenous albumin - 1.5 g/kg on day 1 and 1 g/kg on day 3. This reduces the incidence of type 1 hepatorenal syndrome and mortality; it is a specific adjunct in SBP, not a general supportive measure.
- Hold diuretics - spironolactone and furosemide should be stopped while he is hypotensive and in acute kidney injury; continuing them worsens the renal injury and the hyponatraemia.
- Avoid nephrotoxins - no NSAIDs, aminoglycosides or contrast unless essential.
- Treat the encephalopathy - lactulose titrated to two or three soft stools per day, and address precipitants (infection, constipation, GI bleeding, electrolyte disturbance, drugs).
- Assess for secondary peritonitis - surgical review, imaging if there is any suspicion of perforation or ischaemia, and repeat paracentesis if he fails to improve within 48 hours.
- Supportive care - cautious fluid resuscitation with crystalloid for the hypotension, close monitoring of urine output and creatinine, and nutritional support.
The judgement tested is recognising that the renal injury and encephalopathy are consequences of the infection, so antibiotics and albumin take priority over symptomatic treatment of the confusion.
3. What prophylaxis would you plan after recovery, and how long should it continue?
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Secondary prophylaxis is indicated after an episode of SBP.
- The recurrence rate within one year without prophylaxis is high (roughly 40–70%), so prophylaxis is standard.
- Norfloxacin 400 mg once daily is the classical choice; ciprofloxacin or trimethoprim–sulfamethoxazole are alternatives depending on availability and local resistance patterns.
- Continue until liver transplantation, death, or until the ascitic protein rises/clinical circumstances change - i.e. lifelong in practice for a transplant-ineligible patient.
Other things to address at the same visit:
- Primary prophylaxis would have been indicated if his ascitic protein were <15 g/L with advanced disease - he now qualifies for secondary prophylaxis regardless.
- Assess for transplantation, since SBP is a marker of decompensation and a trigger for referral.
- Alcohol abstinence - already eight months, which favours a good hepatic recovery trajectory; continue support.
- Reassess diuretic dose and consider whether he needs long-term albumin or TIPS assessment if refractory ascites develops.