Cirrhosis of Liver

Download as pdf or txt
Download as pdf or txt
You are on page 1of 6

Original Article

Cirrhosis of liver: Etiological factors, complications


and prognosis
Suhail Ahmed Almani, A. Sattar Memon, Amir Iqbal Memon, M. Iqbal Shah,
M. Qasim Rahpoto, Rahim Solangi

ABSTRACT
OBJECTIVE: To determine the etiological factors, complication(s) and prognosis of patients suf-
fering from liver cirrhosis in our setup.
DESIGN: Cross-sectional study.
SETTING: Medical and surgical departments of Liaquat University Hospital Hyderabad/
Jamshoro, Sindh – Pakistan, from April 2005 to April 2007.
METHODS: Patients having an evidence of cirrhosis of liver on ultrasound examination of abdo-
men were enrolled. All those patients who were not confirmed to be cirrhotic, excluded from
this study. All cases were studied to determine the etiological factors, complications and prog-
nosis of disease. All data were recorded on a proforma. Patients with acute variceal hemorrhage
were referred to surgical department for endoscopic sclerotherapy or variceal band ligation.
RESULTS: Total 100 patients were studied, 67(67%) males and 33(33%) females. Their mean age
was 53.09 with SD= 8.85814 years. Majority of patients, 52(52%) had HCV infection, 16(16%) had
HBV infection, 16(16%) had HBV and HCV co-infection, 08(08%) had alcohol abuse, 01(01%) had
primary biliary cirrhosis, 02(02%) had Wilson’s disease and no etiological factors were recorded
in 05(05%) patients. Ascites was present in 59(59%) cases, portal hypertension in 42(42%), eso-
phageal varices in 29(29%), spontaneous bacterial peritonitis in 29(29%), acute variceal hemor-
rhage in 27(27%), hepatic encephalopathy in different grades in 24((24%), hepatorenal syndrome
in 09(09%) and hepatocellular carcinoma in 07(07%) patients. All patients with acute variceal
episode(s) were adequately and timely treated in surgical department. When cirrhotic patients
were grouped into child-Pugh’s classification, 37(37%) were in class ‘A’ category, 37(37%) in
class ‘B’ category, and 26(26%) in class ‘C’ category.
CONCLUSION: HCV infection is the major risk factor for cirrhosis in our setup. Ascites was the
commonest complication. Patients with child-Pugh’s class ‘A’ cirrhosis had significantly longer
survival than patients with child-Pugh’s class ‘B’ and ‘C’. A multidisciplinary approach for pre-
vention and control of ever increasing HCV infection must be adopted and to make the public
awareness through the mass media about its drastic complications, and possible modes of its
transmission.
KEY WORDS: Liver. Cirrhosis. Viral hepatitis. HCV infection. Ascites.

INTRODUCTION recorded in 74% of patients.8,9 HCV is now more com-


mon as compared to HBV in our country, and a high
Cirrhosis is a serious and irreversible disease. It is a
frequency of HCV seropositive individuals of both
consequence of chronic liver disease characterized by
sexes among patients referred for chronic liver dis-
replacement of liver tissue by fibrotic scar tissue as
ease.9,10 Portal hypertension, ascites and variceal
well as regenerative nodules, leading to progressive
hemorrhage are common in cirrhotic patients.
loss of liver function.1,2 It is a major cause of mortality
Esophagogastric varices have the greatest clinical
and morbidity worldwide.3 It is also a common cause
impact, with a risk of mortality of 17–42% per bleeding
of mortality amongst Pakistani population4 and fre-
episode.5 Ascites, important complication of advanced
quent cause of admission in our hospitals.5 Cirrhosis
cirrhosis and severe portal hypertension, is sometimes
develops in about 10-20% within 5-30 years. The most
refractory to treatment and is complicated by sponta-
common cause being viral hepatitis as compared to
neous bacterial peritonitis and hepatorenal syn-
West where alcohol is more common.6,7 Majority of
drome.11,12 Hepatic encephalopathy is another compli-
patients (90%) with chronic liver disease had evidence
cation, with a mortality of about 30%.13 About 15% of
of HBV, HCV or co-infection. Disease is reported more
patients with cirrhosis will finally develop hepatocellu-
severe in patients with co-infection and cirrhosis is
lar carcinoma.6 The prognosis of the disease was as-
JLUMHS MAY - AUGUST 2008 61
Cirrhosis of liver

sessed by using modified Child-Pugh’s classification prognosis of the disease was assessed by using
for grading prognosis in cirrhotic patients. It was de- modified Child-Pugh’s classification for grading prog-
vised in 1964 by Child and Turcotte and modified in nosis in cirrhotic patients. Child-Pugh’s classification
1973 by Pugh, et al.14 We undertook this study to de- has scores for five parameters i.e. serum bilirubin,
termine the etiological factors, complications and serum albumin, prothrombin time, ascites and hepatic
prognosis of patients suffering from liver cirrhosis. encephalopathy. It grades cirrhosis in three grades;
Child-Pugh’s 'A' grade (score less than 7), Child-
PATIENTS AND METHODS
Pugh’s 'B' grade (score 7-9) and Child-Pugh’s 'C'
This study was conducted in the medical and surgical grade (score more than 9).14 Patients were followed
departments of Liaquat University Hospital Hydera- during their stay in the hospital and subsequent follow
bad/ Jamshoro from April 2005 to April 2007. Patients up visit(s) at hospital and whether they survived or
having an evidence of cirrhosis of liver on ultrasound expired. Statistical analysis was performed by using
examination of abdomen were included in study. All SPSS 13.0.
those patients who were not confirmed to be cirrhotic,
RESULTS
excluded from this study. These patients were care-
fully examined to determine the etiology of the dis- During the study period, 100 patients with a diagnosis
ease, complication(s) at the time of presentation and of cirrhosis of liver were studied. Majority 67(67%)
prognosis of the disease. Data were recorded on a were males and 33(33%) were females. Their mean
proforma specially designed for this purpose. For each age was 53.09 with SD=8.85814 years. Various etio-
patient full blood count, liver function tests, serology logical factors of cirrhosis of the liver are given in Ta-
for hepatitis, renal function tests, blood sugar, serum ble I. Table II shows distribution of complications
electrolytes, serum albumin and coagulation profile among patients. Using modified Child-Pugh’s classifi-
were carried out. Blood was also collected for antimi- cation for grading prognosis in cirrhotic patients is
tochondrial antibodies, serum copper and serum shown in Table III. In the analysis of laboratory find-
caeruloplasmin. An abdominal ultrasound for liver ings, high bilirubin was found in 58%, hyponatremia,
and splenic size, parenchymal echogenicity, portal and low hemoglobin were found in 68% and 59% pa-
vein diameter, and ascites was also carried out. In tients respectively. In 42% patients, there was high
case of ascites, an ascitic tap was done to look for blood urea while creatinine was above normal limits in
spontaneous bacterial peritonitis. Any evidence of the 18% patients. Hypoalbuminemia (serum albumin
presence of other co-existent complications of cirrho- <3.3g/dl) was found in 40% patients. Leukocytosis
sis of liver was also recorded. CT scan of the abdo- (total leukocyte count >11000/ml) was a feature in the
men was also carried out in suspected eight cases of laboratory data of 47% patients. The rest of patients
liver cell mass. Patients with acute variceal hemor- had either normal or low TLC. Coagulation profile was
rhage were referred to surgical department for endo- abnormal in a fraction of patients with 54% patients
scopic sclerotherapy or variceal band ligation. The having prothrombin time > 5 seconds. However,

TABLE I:
ETIOLOGICAL FACTORS

Factors Male Female Positive proportion


No. % No. % No. %
HCV Infection 34 65.4 18 34.6 52 52
HBV Infection 11 68.7 5 31.3 16 16
HBV and HCV co-infection 10 62.5 6 37.5 16 16
Alcohol 8 100 0 0 8 8
Primary biliary cirrhosis 0 0 1 100 1 1
Wilson’s disease 1 50 1 50 2 2
Unknown 3 60 2 40 5 5
Total 67 67 33 33

JLUMHS MAY - AUGUST 2008 62


Suhail Ahmed Almani, A. Sattar Memon, Amir Iqbal Memon, et al.

thrombocytopenia (platelate count <150,000/ml) was a complications. In advanced stages of cirrhosis the
consistent finding in 72% patients. Antimitochondrial only option is a liver transplant.15 Nadeem, et al has
antibodies were found positive in one patient, whereas reported that cirrhosis of liver is a frequent cause of
serum copper and serum caeruloplasmin were posi- admission in hospitals and HCV was the most com-
tive in two patients. An abdominal ultrasound con- mon cause. At least 50% of infected patients, develop
firmed features of liver cirrhosis in 100% and ascites
TABLE II:
DISTRIBUTION OF COMPLICATIONS
Male Female
Complication Total
No. % No. %
None 28 68.2 13 31.7 41
Ascites Slight 27 65.8 14 34.2 41
Mod- Severe 12 66.6 6 33.4 18
Portal hypertension 31 73.8 11 26.2 42
Esophageal varices 22 75.8 7 24.2 29
SBP 20 68.9 9 31.1 29
None 53 69.7 23 30.3 76
Encephalopathy Slight- moderate 12 63.2 7 36.8 19
Mod- severe 2 40 3 60 5
Hepatorenal syndrome 6 66.7 3 33.3 9
Heptocellular carcinoma 4 57.2 3 42.8 7
Hematamesis 21 77.8 6 22.2 27

TABLE III: chronic liver disease and cirrhosis develops in about


10-20% patients within 5-30 years.5 This study
CHILD PUGH SCORE
showed that HCV infection was the major etiological
Child Turcutte Pugh Male Female Total factor and was responsible for 52% of the total cases
Score presented with cirrhosis, as observed by Shah, et al
A (5-6) 26 11 37 that most of their patients with HCV infection, pre-
sented with established cirrhosis.16 We observed 16%
B (7-9) 26 11 37 of cirrhotic patients with HBsAg infection, similarly
C (10-15) 15 11 26 Bukhtiari, et al has reported that cirrhosis was present
in 74% cases, chronic hepatitis in 18.6% and among
Total 67 33 100 the patients with cirrhosis, 28% were HBsAg positive,
in 59% of patients. Ascitic fluid DR and culture and 55% anti-HBc positive.8 We observed co-infection of
sensitivity showed spontaneous bacterial peritonitis in HBV and HCV in 16% of cirrhotics, while Bukhtiari, et
29% of patients with cirrhotic ascites. CT scan of the al has reported 07% co-infection of anti-HCV and
abdomen confirmed hepatocellular carcinoma in 07% HBsAg as well as 35% of anti-HCV and anti-HBC
of patients. Out of 100 patients, 26% expired including positive.8 Farooqui, et al has also reported that anti-
15 males and 11 females during study period, who HCV was positive in 59% and HBsAg was positive in
were found in class ‘C’ of Child-Pugh’s classification. 32% patients. Both were positive in 03% patients.9 In
DISCUSSION contrast, previous studies also included patients with
non-viral forms of cirrhosis, mainly alcohol related,
Cirrhosis of liver is generally irreversible disease, and
where the pathogenesis and pathophysiology of liver
treatment focusses on preventing progression and
damage are quite different.17-19 Similarly, we observed

JLUMHS MAY - AUGUST 2008 63


Cirrhosis of liver

ascites and liver related problems among 08% of pa- rhosis with the hepatorenal syndrome as reported in
tients with previous alcohol abuse. In this study, one other studies that hepatorenal syndrome is a progres-
cirrhotic patient had primary biliary cirrhosis, which is sive disorder associated with advanced cirrhosis and
not an uncommon finding as reported in other stud- portal hypertension.37,38 In this study, we evaluated the
ies,20-23 whereas 02% of patients had Wilson’s dis- prognostic staging of patients with cirrhosis on the
ease, as reported in other studies.21-23 Surprisingly, in basis of Child-Pugh’s classification and observed 37%
our study the etiological factor was not recognized in had Child-Pugh’s 'A' grade of prognosis, 26% had
05% of patients and known as cryptogenic cirrhosis as Child-Pugh’s 'B' grade of prognosis and 26% had
reported by Nadeem, et al.5 Early studies conducted Child-Pugh’s 'C' grade of prognosis. Yan, et al has
in which patients recruited at different stages of cirrho- reported that 22% of the patients had cirrhosis of
sis usually identified portal hypertension and its main Child-Pugh grade A, 41% of grade B and 36% of
clinical consequences (that is, ascites and oesophag- grade C.14 Liver function tests showed a steady de-
eal bleeding) as the most frequent causes of transition crease from Child-Pugh’s grade A to grade B and to
from compensated to decompensated cirrhosis and of grade C. During our study period, 26% of total patients
liver related probelms. Furthermore such events were with class ‘C’ of Child-Pugh’s classification, expired as
reported to have profound effects on survival rates.24- reported in other studies that differences between the
26
In this study, ascites was recorded as commonest three Child-Pugh’s grades were significant.14,39
complication of cirrhosis and was present in 59% of
CONCLUSION
patients and to mark decompensation of liver disease
as reported in other studies.24,27 The incidence of SBP We conclude that chronic HCV infection is the major
in patients with cirrhosis and ascites varies from 7- risk factor for cirrhosis in our patients. Ascites is the
23% in the West.28,29 It is around 33% in Pakistan30,31 commonest complication. Patients with Child-Pugh’s
and we observed that spontaneous bacterial peritoni- class ‘A’ cirrhosis had significantly longer survival than
tis developed in up to 29% of patients with cirrhosis patients with Child-Pugh’s class ‘B’ and ‘C’. A multidis-
and ascites. In this study, 27% of patients presented ciplinary approach for prevention and control of ever
with acute variceal hemorrhage, who were referred to increasing HCV infection must be adopted to make
surgical department for endoscopic sclerotherapy or the public awareness through the mass media about
variceal band ligation, were adequately treated. The its drastic complications, and possible modes of its
most frequent complication of cirrhosis and portal hy- transmission.
pertension with a mortality of 17–42% per bleeding
REFERENCES
episode is ducumented in other studies.24-26 Prevent-
ing death from variceal bleeding requires adequate 1. Gildea TR, Cook WC, Nelson DR, Aggarwal A,
and timely resuscitative measures, specific treatments Carey W, Younossi ZM. Predictors of long-term
aimed at arresting the bleeding quickly, and skilled mortality in patients with cirrhosis of the liver ad-
management of the liver disease and secondary com- mitted to a medical ICU. Am Coll Chest Physi-
plications.32,33 We observed hepatic encephalopathy in cians. 2004;126:1598-603.
different grades in 24((24%) patients, as reported in 2. Runyon BA, Testa M. Hepatitis B and C. Am J
other studies that hepatic encephalopathy is a com- Gastroenterol. 1999; 16: 835-40.
plex neuro-psychiatric syndrome, which may compli- 3. Maddrey WC. Update in hepatology. Ann Intern
cate acute or chronic liver failure.34 The results of this Med. 2001;13(4):216–23.
study show that HCC is indeed a major (07%) and 4. Khan AA. Endemic transmission of hepatitis C. J
early complication of compensated cirrhosis of viral Coll Physicians Surg Pak. 1995; 5(1):11–3.
etiology, being the most frequent first complication 5. Nadeem MA, Waseem T, Sheikh AM, Grumman
and cause of death in HCV positive patients, as re- N, Irfan K, Hasnain SS. Hepatitis C virus: An
ported in other studies, conducted in more homogene- alarmingly increasing cause of liver cirrhosis in
ous cohorts of cirrhotic patients with initially well com- Pakistan. Pak J Gastroenterol. 2002; 16(1):3-8.
pensated "early" cirrhosis of viral etiology have clearly 6. Naheed T. Antigenemia in chronic liver disease.
shown that HCC is another important complication that Specialist (Pak J Med Sci) 1998; 14(4): 303-8.
patients may frequently develop in the compensated 7. Hussain I, Nasrullah M, Shah AA. Prevalence of
phase of disease.35,36 We recorded 09% cases of cir- hepatitis B and C viral infections in liver cirrhosis

JLUMHS MAY - AUGUST 2008 64


Suhail Ahmed Almani, A. Sattar Memon, Amir Iqbal Memon, et al.

in Pakistan. Pak J Gastroenterol 1998;12(1-2):7- tology 1990;11:458-64.


11. 22. Myszor M, James OF. The epidemiology of pri-
8. Bukhtiari N, Hussain T, Iqbal M, Malik AM, Qurai- mary biliary cirrhosis in north-east England: an
shi AH, Hussain A. Hepatitis B and C single and increasingly common disease? Q J Med.
co-infection in chronic liver disease and their ef- 1990;75:377-85.
fect on the disease pattern. J Pak Med Assoc. 23. Metcalf JV, Bhopal RS, Scott LMD, Gray J, Howel
2003; 53: 136-40. D, James OFW. Temporal and geographical
9. Farooqi JA, Khan PM. Viral aetiology of liver cir- variations in the prevalence of primary biliary cir-
rhosis patients in Swat. Pak J Gastroenterol. rhosis (PBC) in a stable population. Hepatol-
2002;16(2):39-42. ogy.1995;22:384A.
10. Khan TS, Rizvi F, Rashid A. Hepatitis C seroposi- 24. Brewer GJ, Yuzbasiyan-Gurkan V. Wilson dis-
tivity among chronic liver disease patients in ease. Medicine 71:139–64, 1992.
Hazara, Pakistan. J Ayub Med Coll Abbottabad. 25. Scheinberg IH, Sternlieb I. Wilson's disease. In:
2003;15: 53-5. Smith LH Jr., Ed. Major problems in internal medi-
11. Dib N, Oberti F, Cales P. Current management of cine. Philadelphia: WB Saunders Company, Vol
the complications of portal hypertension: variceal 23, 1984.
bleeding and ascites. CMAJ. 2006; 174: 1433-43. 26. Schilsky ML. Wilson disease: genetic basis of
12. Gines P, Cardenas A, Arroyo V. Management of copper toxicity and natural history. Sem Liver Dis.
cirrhosis and ascites. N Engl J Med. 2004: 350- 1996; 16: 83–95.
61. 27. Hui AY, Chan HL, Leung NW. Survival and prog-
13. Maqsood S, Saleem A, Iqbal A. Precipitating fac- nostic indicators in patients with hepatitis B virus-
tors of hepatic encephalopathy. J Ayub Med Coll related cirrhosis after onset of hepatic decompen-
Abbottabad. 2006; 18. sation. J Clin Gastroenterol. 2002; 34: 569–72.
14. Yan GZ, Duan YY, Ruan LT, Cao TS, Yuan LJ, 28. Ascites. In: Sherlock S, Dooley J eds. Diseases of
Yang YL. Non-invasive quantitative testing of liver the liver and biliary system.11 ed. Oxford, Black-
function using ultrasonography in patients with well Science, 2002; 127 – 46.
cirrhosis. Hepatogastroentrology. 2006;53:15-20. 29. Fernandez J, Navasa M, Gomez J. Bacterial In-
15. Anslo P, Brinton LA, Nyren O. Viral hepatitis and fections in cirrhosis: epidemiological changes with
cirrhosis. N Engl J Med. 1996;13:203-6. invasive procedures and norfloxacin prophylaxis.
16. Shah HA, Jafri W, Malik I, Prescott L, Simmonds Hepatology. 2002; 35:140–48.
P. Hepatitis C virus (HCV) genotypes and chronic 30. Iqbal M, Jamal S, Rathore OI, Qureshi MA. SBP
liver disease in Pakistan. J Gastroenterol Hepatol. in hospitalized chronic liver disease patients.
1997; 12:758-61. JMMC.1997; 1:2–5.
17. D’Amico G, Morabito A, Pagliaro L. Survival and 31. Jaffary W, Shah, Hamid S. Spontaneous bacterial
prognostic indicators in compensated and decom- peritonitis. Specialist. 1992; 8: 33–8.
pensated cirrhosis. Dig Dis Sci. 1986; 31:468–75. 32. Graham D, Smith JL. The course of patients after
18. Gines P, Quintero E, Arroyo V. Compensated cirr- variceal hemorrhage. Gastroenterology. 1981; 80:
hosis: natural history and prognostic factors. 800–9.
Hepatology.1987;7:122–8. 33. Jenkins SA, Shields R, Davies M, et al. A multi-
19. Pagliaro L, D’Amico G, Pasta L. Portal hyperten- centre randomised trial comparing octreotide and
sion in cirrhosis: natural history. In: Bosch J, injection sclerotherapy in the management and
Groszmann R, eds. Portal hypertension: patho- outcome of acute variceal haemorrhage. Gut.
physiology and treatment. Cambridge, MA: Black- 1997; 41: 526–33.
well Scientific, 1994:72–92. 34. Ferenci P. Hepatic encephalopathy. In: Haubrich
20. Sherlock S. Primary biliary cirrhosis (chronic intra- WS , Schaffner F, Berk JE, editors. Gastroenterol-
hepatic obstructive jaundice). Gastroenterology. ogy, 5th edition. Philadelphia: WB Saunders.1995;
1959; 37:574-86. 1988-2003.
21. Danielsson A, Boqvist L, Uddenfeldt P. Epidemiol- 35. Collier J, Sherman M. Screening for hepatocellu-
ogy of primary biliary cirrhosis in a defined rural lar carcinoma. Hepatology. 1998; 27: 273–8.
population in the northern part of Sweden. Hepa- 36. Tanaka R, Itoshima T, Nagashima H. Follow-up

JLUMHS MAY - AUGUST 2008 65


Cirrhosis of liver

study of 582 liver cirrhosis patients for 26 years in of refractory ascites and hepatorenal syndrome in
Japan. Liver. 1987; 7: 316–24. cirrhosis. Hepatology. 1996; 23:164 -76.
37. Gines A, Escorsell A, Gines P. Incidence, predic- 39. Daniel B, Fundakowski CE, Lisker-Melman M,
tive factors, and prognosis of the hepatorenal syn- Crippin JS, Pilgram TK, Chapman W, et al. Com-
drome in cirrhosis with ascites. Gastroenterology. parison of MELD and Child-Pugh scores to predict
1993; 105: 229–36. survival after chemoembolization for hepatocellu-
38. Arroyo V, Ginès P, Gerbes A, Dudley FJ, Gentilini lar carcinoma. J Vascular Interventional Radiol.
P, Laffi G, et al. Definition and diagnostic criteria 2004; 15:1209-18.

AUTHOR AFFILIATION:
Dr. Suhail Ahmed Almani (Corresponding Author)
Associate Professor, Department of Medicine
Liaquat University of Medical & Health Sciences
(LUMHS) Jamshoro, Sindh - Pakistan
Email: saalmani 123@ yahoo.com

Prof. A. Sattar Memon


Department of Surgery
LUMHS Jamshoro, Sindh - Pakistan

Dr. Amir Iqbal Memon


Department of Surgery
LUMHS Jamshoro, Sindh - Pakistan

Dr. M. Iqbal Shah


Department of Medicine
LUMHS Jamshoro, Sindh - Pakistan

Dr. M. Qasim Rahopoto


Department of Medicine
LUMHS Jamshoro, Sindh - Pakistan

Dr. Rahim Solangi


Department of Medicine
LUMHS Jamshoro, Sindh - Pakistan

JLUMHS MAY - AUGUST 2008 66

You might also like