A call from the Hepatology FY1: She has been asked to ring due to concerns on the morning ward round about worsening renal function – specifically do we think this is hepato-renal syndrome?
56yo with history of alcohol excess, chronic obstructive airways disease and known cirrhosis with and previous oesophageal varices (in banding program). Admitted 5 days previously with worsening jaundice and mild confusion. An ascitic tap was performed on day 1 and a Bonano catheter inserted through which 4 litres of ascitic fluid was drained over the following 24 hours, with concurrent administration of 2x bottles of 20% human albumin solution. Gram stain of the ascitic fluid demonstrated numerous neutrophil polymorphs, and the patient was therefore commenced on piperacillin/tazobactam at a dose of 4.5g tid i.v pending culture results.
Usual Medications: Levofloxacin (stopped on commencing i.v. antibiotics), Spironolactone (started in clinic, now withheld), Vitamin B co-strong, Seretide inhaler, Bisoprolol (now withheld), Citalopram.
Serial Blood tests Urea Creatinine
Clinic 2 months ago 1.7 53umol/L
Admission 5.5 76umol/L
Day 6.7 89umol/L
Day 2 7.1 103umol/L
Day 3 9.9 131umol/L
What further information would you seek before giving your opinion?
See more of the history or other available results?
Other blood tests:, Bilirubin 121, Hb 121, WCC 13.2 (Neuts 11.1) Platelets 53, Prothrombin time 21 seconds
Abdominal USS : shrunken nodular liver consistent with cirrhosis. 15cm Splenomegaly. 11cm kidneys bilaterally, no evidence of obstruction.
Blood pressure has been between 70 and 90mmHg systolic throughout the admission. There has been a borderline temperature (max 37.8degrees). Urine output has not been completely documented due to poor patient compliance, however a urinary catheter has just been inserted. Post catheter dipstick shows + haematuria, no proteinuria.
Now consider what advice you would give.
Write your advice
Now read what the expert wrote
His hepatic impairment is a sensitizing factor for subsequent acute kidney injury. The precise aetiology for the current dysfunction cannot be stated with certainty, but potentially includes components of
i) Sepsis induced renal dysfunction (from presumed bacterial peritonitis)
ii) Hypoperfusion from low BP (liver disease+ (i))
iii) Over-diuresis & intra-vascular depletion from Spironolactone
iv) Haemodynamic upset from large volume paracentesis (although replacement regime used was appropriate)
All the above lead to a state of pre-renal failure or established acute tubular injury. An important differential would be the onset of the hepato-renal syndrome, characterised by oliguria in the face of volume repletion, extreme salt retention, progressive renal impairment, and a very poor prognosis (>90% mortality) in those not suitable for liver transplantation.
The common immediate management pathway for all of the above should be active volume resuscitation aiming to leave the patient intra-vascularly replete (this may be aided by the insertion of a central venous pressure line). Investigation and treatment of sepsis should be undertaken, and consideration given to the use of laxatives to prevent constipation worsening encephalopathy. Once the patient is volume replete (and assuming no diuretics are prescribed) then a spot urinary sodium can be measured, with a result <20umol/L consistent with HRS. The hepatologists may wish to consider the use of alpha-agonists such as midodrine as a means to support BP in the event of ongoing hypotension. At this stage renal replacement is not required, however the renal team should stay involved with the patients care, as RRT could be required in the event of ongoing deterioration. If this is occurring in the context of established HRS then careful discussion with the senior hepatologists would required as to the appropriateness of ongoing invasive and potentially injurious therapies in the setting of a very poor prognosis.