COMPLICATIONS

 OF  CIRRHOSIS  
 
Fluid  Overload:    
Fluid   accumulates   within   the   abdomen   (ascites)   and   on   the   legs   (pedal   edema).  
This   is   due   to   both   increased   pressure   inside   the   liver   and   because   of   the   decreased  
production  of  proteins  (especially  albumin)  by  the  liver.  Treatment  is  usually  with  
medications   to   help   lose   the   retained   sodoum   and   water,   or   by   draining   the   fluid  
with   a   needle.     The   higher   the   dietary   salt   intake,   the   higher   the   likelihood   of  
developing   fluid   overload.   Thus,   patients   with   cirrhosis   and   fluid   overload   are   often  
restricted  to  2g/day  of  dietary  sodium.    
Part  of  the  pathophysiologic  mechanism  behind  fluid  accumulation  in  the  setting  
of   cirrhosis   is   due   to   an   alteration   in   the   renin-­‐angiotensin-­‐aldosterone   axis,   and  
therefore,   medical   treatment   is   targeted   towards   combatting   this.   Thus,   patients  
with  ascites  or  pedal  edema  are  often  started  on  spironolactone  in  combination  with  
furosemide.   The   spironolactone,   an   anti-­‐mineralocorticoid   agent,   works   well   in  
patients   with   cirrhosis,   but   is   required   to   be   used   in   higher   doses   than   in   patients  
with  heart  failure.  As  well,  the  combination  of  both  a  loop  diuretic  (furosemide)  and  
anti-­‐aldosterone   (spironolactone)   is   more   efficacious   than   either   diuretic   alone.  
Thus,   these   2   medications   are   used   together,   with   100mg   of   Spironolactone   being  
used  with  40  mg  of  Lasix.  The  two  drugs  are  then  titrated  up  together  to  maintain  
this  ratio,  barring  any  complications  or  electrolyte  abnormalities.  
 
Hepatic  encephalopathy:    
Normally,   the   liver   detoxifies   the   various   toxins   that   are   both   produced   by   the  
body   and   ingested   (usually   as   medications).   In   the   setting   of   liver   failure,   or  
cirrhosis,   the   liver   is   no   longer   able   to   do   this,   and   the   toxins   build   up   in   the  
bloodstream   and   cross   over   into   the   liver.   Patients   with   encephalopathy   can   have  
problems  with  decreased  concentration,  excessive  fatigue  (sleeping  a  lot),  confusion,  
or   even   coma.     One   of   these   toxins   is   ammonia.   Hepatic   encephalopathy   can   be  
precipated   by   medications   (any   sedating   medications,   such   as   narcotics,  
benzodiazepines,   or   neuroleptics),   infections   (especially   spontaneous   bacterial  
peritonitis,   UTI,   or   URTI),   constipation,   renal   failure,   or   electrolyte   abnormalities.  
Treatment   is   aimed   at   treating   the   precipitating   cause   and   simultaneous   removal   of  
the   ammonia.   Lactulose   serves   to   draw   ammonia   from   the   bloodstream   into   the  
colon,   and   then   stimulates   colonic   motility   to   expel   the   ammonia   from   the   body.  
Thus,  lactulose  acts  as  more  than  a  simple  laxative.    
 
Variceal  Bleeding:    
As  the  amount  of  scarring  in  the  liver  increases,  it  becomes  more  difficult  for  the  
blood   to   flow   through   the   liver,   and   it   starts   looking   for   other,   lower   resistance  
routes  through  which  to  flow.  This  leads  to  the  development  of  varices,  both  in  the  
esophagus  and  stomach,  as  well  as  elsewhere.  As  these  veins  get  bigger,  they  are  at  
risk  for  bursting  and  bleeding.  If  this  occurs,  it  can  be  catastrophic,  and  may  lead  to  
death.   In   order   to   prevent   this   from   occurring,   there   are   2   methods   of   treatment.  
The   first   is   to   decrease   the   pressure   in   the   portal   system,   which   can   be   achieved  
through   the   administration   of   non-­‐selective   beta-­‐blockers   such   as   Nadolol   or  
Carvedilol.  Another  method  of  variceal  treatment  is  through  endoscopic  ligation  or  
gluing  of  the  varices.    Which  of  these  methods  is  used  to  control  the  varices  is  based  
on  the  severity  of  the  patient’s  liver  disease,  the  size  of  the  esophageal  varices,  and  
whether   there   are   any   high   risk   features   seen   endoscopically   to   indicate   whether  
the   varices   are   at   higher   risk   for   rupture   and   bleeding.   Once   a   patient   has   been  
banded,  they  are  then  placed  into  a  banding  program,  where  they  are  brought  back  
to   the   endoscopy   suite   for   banding   every   4   weeks   until   the   varices   have   been  
completely  eradicated.  
 
Jaundice:    
As  the  liver  becomes  less  and  less  able  to  function,  patients  may  start  to  develop  
yellowing  of  either  the  skin  or  the  eyes,  which  is  due  to  the  build-­‐up  of  bilirubin  in  
the  blood  (bilirubin  is  normally  excreted  into  the  intestines  by  the  liver  via  the  bile  
ducts,  and  from  there,  into  the  stool).  Although  this  can  be  seen  in  acute  hepatitis,  in  
patients  with  pre-­‐existing  liver  disease,  the  development  of  jaundice  can  indicate  an  
acute  flare  of  their  underlying  disease,  or  worsening  liver  function.  
 
Liver  Cancer:    
Having   cirrhosis   is   a   risk   for   developing   liver   cancer   (hepatocellular  
carcinoma,   or   HCC).   If   this   develops,   there   are   a   number   of   different   options   for  
treatment   of   the   cancer,   based   on   how   well   your   liver   is   functioning,   and   its   size.  
Please  refer  to  the  “Liver  Tumour”  section  for  further  information.  All  patients  with  
cirrhosis  should  undergo  a  screening  program  with  an  abdominal  ultrasound  every  
6  months  as  part  of  HCC  surveillance.