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A 56-year-old man with alcoholic cirrhosis (Child-Pugh C), known ascites and oesophageal varices is admitted with a 3-day history of increasing abdominal distension, drowsiness and reduced urine output. He has been taking spironolactone 400 mg daily and furosemide 80 mg daily for refractory ascites, and has taken ibuprofen 400 mg three times daily for the last week for back pain. On examination he is icteric, flapping tremor is present, temperature 37.9 degrees C, BP 92/58 mmHg (MAP 69), pulse 96, abdominal tenderness with shifting dullness. Bloods: creatinine has risen from a baseline of 1.0 to 2.4 mg/dL over 4 days; sodium 126 mmol/L; potassium 5.2 mmol/L; bilirubin 6.2 mg/dL; INR 2.1; albumin 2.4 g/dL. Urine dipstick: trace protein, no blood; microscopy: bland, no casts; urine sodium 7 mEq/L; urine output 25 mL/h (under 0.5 mL/kg/h). Ascitic tap: 380 polymorph neutrophils/mm3, total protein 0.9 g/dL.[1][4]
Questions
a) What are the two acute diagnoses, and which ICA criterion for hepatorenal syndrome is challenged by the presence of shock-like physiology? (2 marks)
Two acute diagnoses: spontaneous bacterial peritonitis (the typical bacterial trigger of HRS-AKI) and acute kidney injury in cirrhosis (creatinine rise from 1.0 to 2.4 mg/dL meeting ICA AKI criteria: rise of at least 0.3 mg/dL within 48 hours or at least 50 percent from baseline within 7 days — urine output and FeNa have significant limitations and do not make the diagnosis). The exclusion that is challenged is shock / ischaemia — MAP 69 mmHg plus a septic picture raises septic-shock AKI rather than HRS, so treat SBP with antibiotic plus albumin and complete volume expansion before writing HRS.[1][4]
b) Reproduce the diagnostic criteria for hepatorenal syndrome (ICA AKI definition plus the exclusion/albumin-challenge steps). (3 marks)
- Cirrhosis with ascites.[1][3]
- AKI by the ICA definition — creatinine rise of at least 0.3 mg/dL within 48 hours, or at least 50 percent above baseline within 7 days. (Do not treat urine output or FeNa as diagnostic: both have significant limitations in advanced cirrhosis.)
- No recovery after diuretic withdrawal and albumin 1 g/kg (maximum 100 g) for two consecutive days.
- Other causes of AKI excluded — hypovolaemia, shock or prolonged ischaemia, nephrotoxic drugs, postrenal obstruction.
- No structural kidney injury — no significant proteinuria; kidney histology structurally normal.
c) Outline the immediate management. (3 marks)
Immediate: stop the ibuprofen (NSAIDs inhibit protective renal prostaglandins), withdraw diuretics, give albumin 1 g/kg (maximum 100 g) for two consecutive days; treat SBP with an antibiotic PLUS albumin 1.5 g/kg on day 1 and 1 g/kg on day 3 (Sort: renal impairment 10 vs 33 percent, in-hospital mortality 10 vs 29 percent). Treat hyperkalaemia and encephalopathy in parallel. If shock is excluded and creatinine does not recover after the two-day albumin challenge, proceed to vasoconstrictor plus albumin.[4][18]
d) Outline the definitive pharmacotherapy and the definitive cure. (2 marks)
Definitive pharmacotherapy is terlipressin plus albumin: bolus 0.5 to 1 mg every 4 to 6 hours, increased to a maximum of 2 mg every 4 hours if no response, or continuous infusion 2 to 12 mg/day, plus albumin 1 g/kg on day 1 then 20 to 40 g/day, for up to 14 days. Target verified reversal (two creatinine values of 1.5 mg/dL or less at least 2 hours apart, survival free of RRT for at least 10 days). Contraindicated in hypoxaemia and ongoing coronary, peripheral or mesenteric ischaemia; CONFIRM showed verified reversal 32 vs 17 percent but 90-day death 51 vs 45 percent and respiratory-disorder deaths 11 vs 2 percent. The only cure is liver transplantation. Noradrenaline 0.5 to 3.0 mg/h plus albumin is a cheaper ICU alternative (50 percent reversal in a 40-patient pilot); midodrine plus octreotide recovered renal function in only 28.6 vs 70.4 percent versus terlipressin.[5][3][6]
References19ShowHide
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