Question 8

A 62-year-old man presents to ICU with progressive oliguria and shortness of breath. He had been admitted to the ward a week before because of jaundice. His previous medical history is unremarkable, except for heavy alcohol consumption. There is no history of gastrointestinal bleeding or ingestion of nephrotoxic drugs. There is no past history of renal dysfunction. Clinical 
examination reveals a blood pressure of 124/60 mm Hg, jaundice, oedema and a distended non-tender abdomen. Cardiovascular examination is normal.

Investigations reveal: 
Ultrasound abdomen: Nodular cirrhosis of liver, ascites and normal sized, regular shaped kidneys.


No proteinuria, White cell count <10 X 1~6/L (Normal< 10) 

Ascitic tap

White cell count <10 X 10 6 /L (Normal< 10) 
Red cell count <10 X 10 6 /L (Normal< 10), 
No organisms on Gram stain.

On admission to hospital

On admission to
ICU (7 days later)

Na   (135-145 mmol/L)



K     (3.5-5.0 mmol/L)



Creatinine (0.06-0.14



Urea       (4-6 mmol/L)



Bilirubin (0-20 J!mol/L )



ALT  (<40  U/L)



AST(<50 U/L)



Hb  (120-1500/L)



wcc (4-11 x 1011/L)



a)  What is the most likely cause of the renal deterioration? Give reasons.

List 4 important management measures specifically for the treatment of this patient's renal dysfunction.

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College Answer

a)  What is the most likely cause of the renal deterioration? Give reasons.

Hepatorenal syndrome .
Reasons: Fulfils criteria for Type 1 HRS -(Acute deterioration, absent renal parenchymal disease, absent proteinuria, no shock and no history of nephrotoxic drugs)

List 4 important management measures specifically for the treatment of this patient's renal dysfunction.
Management of complications of renal dysfunction- hyperbilirubinaemia
Albumin administration
Terlipressin Midodrine/ Octreotide
Consideration for liver transplantation


Hepatorenal syndrome is discussed in greater detail in the answer to Question 13 from the first paper of 2001, and in a chapter or rambling digressions.

This case fits the criteria for diagnosis, which are as follows:

  • Cirrhosis
  • Ascites
  • Creatinine level over 150mmol/L
    • failure of this to improve after 2 days of fluid replacement
  • Absence of other causes of renal failure, such as nephrotoxic drugs or some sort of serious parenchymal renal disease (eg. glomerulonephritis)

i.e. it is renal failure in a patient with coexisting liver failure and no other good reason to have renal failure. "Absence of proteinuria" promotes a view that this is a purely pre-renal disease, with no glomerular damage.

Type 1 hepatorenal syndrome is an acute episode, whereas Type 2 is gradual in onset.

As for "4 important management measures"...

  • Albumin and fluid resuscitation:
    • On its own, the effect from this is minimal; mortality is ~ 70%
  • Terlipressin
    • Improves mortality to from 70% to 50%
    • Thought to improve renal perfusion by decreasing the tension within the ascites compartment.
  • Noradrenaline
    • The idea is to increase renal perfusion by increasing the MAP by about 10mmHg
  • Octreotide
    • potent agent of splanchnic vasoconstriction
    • Mortality perhaps 60% 

If all else fails, TIPS procedure may be appropriate. As this disorder has an abysmal survival rate, those who qualify for transplant should be worked up for one.

The college examiners prescriptively asked for "management measures specifically for the treatment of this patient's renal dysfunction", but in their answer gave a generic support strategy ("Management of complications of renal dysfunction- hyperbilirubinaemia"). This answer is puzzling on several levels, and probably had no value in terms of marks for the actual trainees, revealing more information about the CICM quality control process than about hepatorenal syndrome.


UpToDate has an excellent synopsis of hepatorenal syndrome.


Salerno, Francesco, et al. "Diagnosis, prevention and treatment of hepatorenal syndrome in cirrhosis." Postgraduate medical journal 84.998 (2008): 662-670.


Solà, Elsa, Mónica Guevara, and Pere Ginès. "Current treatment strategies for hepatorenal syndrome." Clinical Liver Disease 2.3 (2013): 136-139.


Arroyo, Vicente, et al. "Definition and diagnostic criteria of refractory ascites and hepatorenal syndrome in cirrhosis." Hepatology 23.1 (1996): 164-176.


Velez, Juan Carlos Q., and Paul J. Nietert. "Therapeutic response to vasoconstrictors in hepatorenal syndrome parallels increase in mean arterial pressure: a pooled analysis of clinical trials." American Journal of Kidney Diseases 58.6 (2011): 928-938.


Gluud, L. L., M. S. Kjaer, and E. Christensen. "Terlipressin for hepatorenal syndrome." Cochrane Database Syst Rev 4 (2006).


Kalambokis, Georgios, et al. "The effects of chronic treatment with octreotide versus octreotide plus midodrine on systemic hemodynamics and renal hemodynamics and function in nonazotemic cirrhotic patients with ascites."The American journal of gastroenterology 100.4 (2005): 879-885.


Rössle, Martin, and Alexander L. Gerbes. "TIPS for the treatment of refractory ascites, hepatorenal syndrome and hepatic hydrothorax: a critical update." Gut59.7 (2010): 988-1000.


Malinchoc, Michael, et al. "A model to predict poor survival in patients undergoing transjugular intrahepatic portosystemic shunts." Hepatology 31.4 (2000): 864-871.