Liver failure Flashcards
56 year old man has been referred to the Ambulatory Care Unit by his GP with worsening jaundice.
It has been present and getting worse for the last year and a half, and he only recently saw his GP about it.
On examination the patient is icteric, with cachexia and abdominal distention.
You have been asked to assess him by the consultant running the clinic and to arrange some suitable investigations.
what information would you like to know from the history
IS this acute chronic
-when did he notice the jaundice and abdominal distention
any association with right upper quandrant tenderness , nausea , vomiting , pruritus
any fever or diarrhoea
has the weightless been intentional
any night sweats
what colour are his stools - pale , any blood , do they smell offensive and do they float
=====
past medical history
any history of gallstones
history of liver disease - such as fatty liver , or primary sclerosis cholangitis , hepatitis, alpha 1 antitripsin deficiency
ulcerative colitis
diabetes
recent blood transfusion
=========
use or overdose of regular medication - such as paracetamol
or antibiotic use - such as erythromycin
=====
does he have any family history of liver or pancreas and gastrointestinal diseases
such as haemochromatosis , wilson disease , gilberts , sickle cell
=====
social history
does he drink alcohol - how many units a week
any intravenous drug
recent foreign travel
=====
vaccination history status - including hepatitis b
signs of chronic liver disease
rise in JVP
hepatomegaly
sider nevi
gynecomastia
ecchymosis / increased bleeding
testicular atrophy
jaundice
ascites
causes of liver cirrhosis ?
infection :
hepatitis b and C
autoimmune causes:
autoimmune hepatis
primary billary cirrhosis
primary sclerosis cholangitis
metabolic
non alcoholic fatty liver disease
genetic disease - hemochrombtosis , wilson disease , alpha 1 antitrypsin deficiency (AR) , cystic fibrosis
alcohol
drugs :
methotrexate
amiodarone
isoniazid
investigation to arrange ?
FBC
ue
LFT
crp
amylase
CLOTTING PROFILE
IF evidence of ascites - i would arrange for ascitic tap - sent for culture , microscopy and white cell count
US abdomen - look for any pancreatic or biliary tree pathology. It will also pick up any evidence of liver cirrhosis or liver malignancy
If underlying liver pathology is suspected a liver biopsy
if suspecting :
haemochromatosis dx
- transferrin saturation
and ferritin
wilson disease ddx
slit lamp examination for Kayser-Fleischer rings
reduced serum caeruloplasmin
reduced total serum copper (counter-intuitive, but 95% of plasma copper is carried by ceruloplasmin)
free (non-ceruloplasmin-bound) serum copper is increased
increased 24hr urinary copper excretion
autoimmune hepatitis ddx
Anti-nuclear antibodies (ANA) and/or anti-smooth muscle antibodies (SMA)
Anti-liver/kidney microsomal type 1 antibodies (LKM1)
raised IgG levels
hepatitis serology
vaccinated : anti-HBs positive
past infection : anti HBs positive , anti HBc positive
acute infection : HBsAg positive , IgM anti HBc positive
chronic : HBsAg positive , IgG anti HBc positive
hep c serology
no vaccine for hepatitis C
HCV RNA
anti HCV antibodies
hepatitis A serology
Primary sclerosing cholangitis ddx
p-ANCA may be positive
endoscopic retrograde cholangiopancreatography (ERCP) or magnetic resonance cholangiopancreatography (MRCP) are the standard diagnostic investigations, showing multiple biliary strictures giving a ‘beaded’ appearance
primary billary cirrhosis
nti-mitochondrial antibodies (AMA) M2 subtype are
raised serum IgM
The patient presents to hospital three weeks later and is seen in A+E. He is now confused and disorientated and was bought in after his family became concerned that he was becoming more drowsy. He is tachycardic and hypotensive.
What could be the cause of this?
CHRONIC LIVER DISEASE WITH HEPATIC ENCEPHALOPATHY
some of the acute decompensation of chronic liver disease ?
vatical bleeding
there could be hepatic renal syndrome - splanchnic vasodilation which in turn reduces the systemic vascular resistance. This results in ‘underfilling’ of the kidneys.
Name some causes of acute decompensation of chronic liver disease
Intercurrent infection
Spontaneous bacterial peritonitis
Pneumonia
Additional hepatotoxic insult:
Alcoholic binge
Acute viral hepatitis
Hepatotoxic drugs
Metabolic derangement
Hypoglycaemia
Electrolyte disturbance
gastrointestinal bleeding
what is hepatic encephalopathy
not fully understood but is thought to include excess absorption of ammonia and glutamine from bacterial breakdown of proteins in the gut.
Features
confusion, altered GCS (see below)
asterix: ‘liver flap’, arrhythmic negative myoclonus with a frequency of 3-5 Hz
constructional apraxia: inability to draw a 5-pointed star
triphasic slow waves on EEG
raised ammonia level (not commonly measured anymore)
precipitants of hepatic encephalopathy ?
Precipitating factors
infection e.g. spontaneous bacterial peritonitis
GI bleed
post transjugular intrahepatic portosystemic shunt
constipation
drugs: sedatives, diuretics
hypokalaemia
renal failure
increased dietary protein (uncommon)
