A STUDY OF 50 CASES OF

HEPATORENAL
SYNDROME AND ITS OUTCOME

DR.
DR.
DR.
DR.

RISHABH GUPTA (R2),

JAYDEEP PATEL (R3),
PRASHANT DUDHAGARA (R1),
JANAK CHOKSI (A.P.),

DR. B.B. SOLANKI (PROF. & H.O.U.),

B.J MEDICAL
COLLEGE,AHMEDABAD

AIMS AND OBJECTIVES

To study the clinical and biochemical profile of

patients who present with hepatorenal syndrome.
To study the underlying etiology in cases of
hepatorenal syndrome.
To study the various precipitating factors of
hepatorenal syndrome.
To study the relationship of the type and severity of
hepatorenal syndrome with the outcome.
To study the response of hepatorenal syndrome to
the available drugs

MATERIALS & METHODOLOGY

STUDY DESIGN

This prospective and observational study contains data of

cluster of 50 patients admitted from september 2014 to
october 2015 presenting with signs & symptoms of
Hepatorenal syndrome.

INCLUSION CRITERIA:

Patients with age 12 years.

Patients with clinical symptoms and signs of hepatorenal syndrome.
Patients with pre-existing liver disease developing hepatorenal syndrome.
EXCLUSION CRITERIA:

Patients with age <12 years.

Patients with intracranial lesions such as subdural hematoma, cerebral infarction,
meningitis, encephalitis, brain abscess were excluded from the study as these
conditions might have signs overlapping with hepatic encepalopathy

Patients with pre-existing Renal disease were excluded as per the definition and
criteria of HRS by International Ascites Club 2007.

Patients with Heart failure, Respiratory failure, Coronary artery disease, Peripheral
artery disease should be excluded as the most important drug in the study Terlipressin
is contraindicated in patients having these conditions.

METHODS

For data collection a detailed clinical history of each patient was taken regarding the
present and past illnesses.
Details of symptoms like fever, gastro-intestinal bleeding (hematemesis and/or
melena),constipation, diarrhea, vomiting, any trauma or surgery were noted. Drug history
regarding use of diuretics, sedatives/tranquilizers, NSAIDs was also noted.
All patients were carefully examined for vital signs, fever, jaundice, dehydration, anemia,
pedal edema, asterixis, splenomegaly, hepatomegaly and ascites.
Child Turcotte Pugh Score(CPS) and Model for End Stage Liver Disease(MELD) Score
and clinical grade of hepatic encephalopathy on admission were noted.

OBSERVATION

Total 50 adult patients fulfilling our inclusion criteria and who presented at the hospital from September 2014 to

October 2015 were studied.

Among them 40(80%) were male and 10(20%) were female. Mean age of our study group was 48.7 9
Most common age group affected in males was 51-60 years while in case of females it was 41- 50 years.
Mean age of males was 50 9 and that of females was 46 10 years.
In our study we did not get any patients in the adolescent age group, in which cirrhosis from causes such

as Wilsons disease, Secondary Hemochromatosis, Post necrotic cirrhosis can be there.

The

most common symptoms

of HRS present similarly in
both males and females are
Jaundice.

Abdominal distension and

Decreased urine output,
present in almost 100%
patients, which are s/o
ongoing liver cell failure
along with renal
involvement.
The most common sign
in our study are Icterus and
Ascites
(mild/moderate/severe),
which shows liver cell
failure and portal
hypertension, present in
almost 100% patients.
Severe ascites which is
refractory to treatment is
found in patients with
HRS2.

In our study most no. of patients were of HRS 1 with 38(76%) pts. and HRS 2 with 12(24%)pts.
Males were predominant in number in both types of HRS.
There are two types of HRS as defined below, the definition being clinical.
1. In type 1 HRS the serum creatinine level doubles to greater than 2.5 mg/dL within 2 weeks. The key features of type 1 HRS are its
rapid progression and high mortality, with a median survival of only 1 to 2 weeks
In type 2 HRS, the serum creatinine increases slowly and gradually during several weeks or months with a reciprocal gradual
reduction in glomerular infiltration rate (GFR). This generally occurs without a precipitating factor. The median survival of type 2 HRS
is about 6 months, significantly longer than for type 1.
So, HRS 1 is a condition developing with acute deterioration and HRS 2 is a chronically developing
condition. As a result patients come to hospital for treatment when there is rapidly progressive jaundice,
low urine output, hematemesis, altered behaviour and they are defined under HRS1. This seems to be a
significant reason for increased number of In hospital patients with HRS 1.

The predominant etiology in our study is Alcoholic Cirrhosis(70%) followed by Postnecrotic Cirrhosis following Hepatitis B and C.

INVESTIGATION
S

OUTCOME OF TREATMENT

MARKERS OF RESPONSE TO TREATMENT

mg/dl

ml

SURVIVAL AND IN-HOSPITAL MORTALITY

Out of the 38 patients of HRS 1, even after treatment the In-hospital mortality was 53% which
was far more than HRS 2 of just 9%.
This shows that HRS 1 is a highly moribund condition with the only option of reversal is
treatment with Terlipressin with Albumin which can be used for reversal and patients are
having bad prognosis with high CP Score and MELD.
Compared to HRS 1, HRS 2 has a better prognosis as it is slowly progressive.
The mortality in HRS is also increased in patients having associated Hepatic encephalopathy,
Hemetemesis and Altered Coagulopathy.

SUMMARY

Total 50 adult patients fulfilling our inclusion criteria and who presented at the hospital from september 2014 to october

2015 were studied. Among them 40(80%) were male and 10(20%) were female.Most common age group affected in
males was 51-60 years while in case of females it was 41- 50 years.
The most common symptoms of HRS present similarly in both males and females are Jaundice, Abdominal distension
and Decreased urine output, present in almost 100% patients.
The most common sign in our study is Icterus and Ascites, which can be mild/moderate/severe, present in almost 100%
patients. Severe ascites which is refractory to treatment is found in patients with HRS 2.
In our study most no. of patients were of HRS 1 with 38(76%) pts. and HRS 2 were 12(24%)pts. Males were
predominant in number in both types of HRS.
The predominant etiology in our study and other studies is Alcoholic Cirrhosis(70%), followed by Postnecrotic cirrhosis
following Hepatitis B and C.
The major precipitating factors is Electrolyte imbalance in form of Hyponatremia and Hypokalemia. Others being
Infection, Spontaneous bacterial peritonitis and Hemetemesis.The cause for the electrolyte imbalance is in major case
diuretics which the patients are taking due to predominant refractory ascites, which also is a risk factor for developing
HRS.
In our study the most common associated finding of Liver Cell Failure was Hypoalbuminemia, a component of CPS,
followed by Coagulopathy and Hepatic Encephalopathy.
In haematological examination findings were; >60% patients were moderate-severe anemic(Hb<9gm/dl), presence of
infection in 44% pts. and presence of thrombocytopenic (Platelet count <1 lac) in approximately every patient.

In biochemical examinations mean s.creatinine is 2.9 mg/dl and s.billirubin is 9.5 mg/dl, with presence of
hypoalbuminemia and hyponatremia and higher PT INR.
The most common finding in Ultrasound abdomen was Liver Parenchymal Disease with portal hypertension with
ascites.
The mean CP Score in our study is 11.45 which is having a bad prognosis in Group C with one year survival of
45% and two year survival 35%. The CPS in HRS 1 and HRS 2 is 11.78 and 10.25 respectively.
The mean MELD score, which is also a prognostic factor was 35.44 in our study with HRS 1 and HRS 2 having
mean MELD 37.47 and 29 respectively.
As seen the best drugs useful for HRS in our study was combination of Terlipressin and Albumin with a response
rate of 77%.Next was the Octreotide and Albumin with a response of 29%. Majority of patients were given
Albumin and Supportive treatment in form of Inj. Fresh Frozen Plasma which had a response of just 16%.
Out of the 38 patients of HRS 1, even after treatment the In-hospital mortality was 53% which
was far more than HRS 2 of just 9%.Mortality was higher in males.

CONCLUSION

Hepatorenal Syndrome (HRS) is defined as the occurrence of renal failure in a patient with advanced liver disease
in the absence of an identifiable cause of renal failure.
HRS is defined according to the INTERNATIONAL ASCITES CLUB 2007 criteria after ruling out pre renal and
intrinsic renal failure in a patient with cirrhosis. There are 2 types - HRS 1and 2. Both types have a poor
prognosis with median survival 1-2 weeks and 6 months in HRS 1 and 2 respectively. CPS and MELD Score are
predictors of prognosis. The only effective treatment option available is Terlipresin.
In the present study of HEPATORENAL SYNDROME, HRS type 1 was associated with higher mortality.
Spontaneous bacterial peritonitis and Hepatic Encephalopathy were associated with a higher mortality. A higher
creatinine level and a higher bilirubin value was associated with a rapid progression and higher grade of hepatic
encephalopathy and thus a higher mortality.
MELD score levels were found to be a strong predictor for mortality in hepatorenal syndrome. There was a higher
mortality rate in males as compared to females. Mortality in cirrhotics was seen only in those belonging to Child
Pugh Stage C. Thus hepatorenal syndrome poses a huge drain on financial and human resources combined with a
rather unsatisfactory outcome profile with the only effective drug is Terlipressin. Therefore early detection,
prompt management and preventive measures should form the mainstay of approach.