Liver failure Flashcards
A 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 gentleman’s history
Specific about jaundice:
* When first notice, how long
* Any associated symptoms? - RUQ discomfort, nausea, vomiting, pruritus (these are all features of hepatitis of any cause)
* Fever? Diarrhoea?
* Steatorrhoea, dark urine, pruritus - seen in obstruction of biliary flow
* Weight loss, fever, night sweats (malignancy)
* Bronzed skin & signs of DM - suggestive of haemochromatosis
PMHx
- Gallstones
- Hx of liver disease: fatty liver disease, Hepatitis B/C, alpha-1 antitripsin deficiency, Primary biliary cholangitis & Primary sclerosing
DHx
- Any allergies
- Drug history, recent changes
- Regular analgesia - paracetamol
- ABx use can lead to cholestasis (co-amoxiclav, macrolides)
FHx - any FHx of liver problems / jaundice
- Gilbert’s syndrome
- Haemochromatosis
- Wilson’s disease
- Sickle cell disease
- Hereditary spherocytosis
SHx
- Excessive alcohol consumption - quantify the number of units
- IV drug use
- Unprotected sex / multiple partners
- Recent foreign travel - exposure to malaria, Hep A, Hep E
- Tattoos
- Vaccination Hx (including against Hep B)
Wilson’s - rare AR disease, impaired copper metabolism
Gilbert’s syndrome - benign hereditary condition characterized by intermittent jaundice caused by mild unconjugated hyperbilirubinemia.
Haemochromatosis - genetic disorder characterized by excessive absorption and storage of iron, leading to iron overload in various organs, including the liver, pancreas, heart, joints, and skin
What signs of chronic liver disease might you find on examination?
ABCDE-LIVER
A
* Asterixis
* Ascites
* Ankle oedema
* Atrophy of testicles
B - Bruising (ecchymosis)
C
* Caput Meduase
* Clubbing + leukonychia
D - Dupuytren’s contracture
E
* Encephalopathy
* palmar Erythema
* o(E)dema - hypoalbuminaemia & portal HTN
F - Foetor hepaticus
G- Gynaecomastia
H - Hepatomegaly
I - Icterus/jaundice
What causes of liver cirrhosis do you know?
Alcohol
Viral
* Hep B
* Hep C
* A
Autoimmune
* Non-alcoholic steatohepatitis
* Haemochromatosis
* Alpha-1 antitrypsin deficiency
* Wilson’s disease
* Cystic fibrosis
Drugs
* Methotrexate
* Isoniazid
* Amiodarone
What investigations will you arrange?
Bloods
- FBC, U&E, LFTs
- Amylase (if pancreas involvement suspected)
- Coagulation screen
- Blood film - useful for further analysis - e.g. thrombocytopaenia
- Viral blood screen will be important if pt’s LFTs are raised
- This would include serology for Hep B/C and Hep A if indicated (also for CMV and EBV)
Autoimmune screen:
- ANA/ASMA (for autoimmune hepatitis)
- AMA (PBC)
- Ferritin, serum copper and caeruloplasmin (Haemochromatosis and Wilson’s disease)
Further
- If evidence of ascites > arrange ascitic tap for MC&S
Imaging
- Ultrasound of the abdomen
- To look for pancreatic / biliary tree pathology)
- To look for any evidence of liver cirrhosis / liver malignancy
If underlying liver pathology suspected»_space; liver biopsy may be necessary
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?
Based on the initial presentation and the current deterioration, this likely represents a decompensation of chronic liver failure and hepatic encephalopathy
Name some causes of acute decompensation of chronic liver disease
Intercurrent infection
- Spontaneous bacterial peritonitis
- Pneumonia
Acute GI Haemorrhage
Additional hepatotoxic insult
- Alcoholic binge
- Acute viral h epatitis
- Hepatotoxic drugs
Drugs
- Diuretics
- Sedatives/narcotis
Metabolic derangement
- Hypoglycaemia
- Electrolyte disturbance
What is hepatic encephalopathy?
A neuropsychiatric disturbance of cognitive function in a patient with acute on chronic liver disease.
Clinically there is altered conscious level, asterixis, abnormal EEG, impaired psychometric tests, and an elevated arterial ammonia concentration.
How is hepatic encephalopathy graded?
Grade 1 – Insomnia/reversal of day/night sleep pattern
Grade 2 – Lethargy/disorientation
Grade 3 – Confusion
Grade 4 - Coma
Asterixis may be present at any stage
How would you manage hepatic encephalopathy?
The aim of treatment is to improve morbidity
- Exclude other causes of confusion
- Identify and correct the precipitating cause
- Give lactulose. This alters faecal pH and nitrogen utilisation by bowel flora.
- Phosphate enemas help to purge the large bowel.
How would you manage this patient’s liver cirrhosis in the long term?
Treatment based on the underlying disease:
* Abstinence in alcohol liver disease
* Antiviral therapy in viral hepatitis
* Immunosuppression in autoimmune hepatitis
* All improve liver fibrosis
To screen for complications:
* 6 monthly abdominal ultrasound & alpha-fetoprotein
When would a patient be recommended for liver transplantation?
A transplant centre should make this decision.
Based on the severity of the underlying liver disease against the presence of any comorbidities
Some conditions should be considered for transplant irrespective of disease severity (PBC and recurrent cholangitis in PSC)
You now have one minute to handover the patient in this scenario to your registrar/consultant as if you were at the Acute Medical Handover.
S – I am handing over a 56 year old man with decompensated chronic liver disease and grade two hepatic encephalopathy.
B – He has previously presented with jaundice and signs consistent with chronic liver disease. The cause of this decompensation is not currently known.
A – I have sent blood tests to rule out infection and acute viral hepatitis, electrolyte imbalance and hypoglycaemia. I have initiated treatment with lactulose and prescribed phosphate enemas to help the patient open their bowels.
R – I would recommend that this patient is admitted and urgently discussed with the gastroenterology team as hepatic encephalopathy carries a high risk of mortality. Treatment with rifaximin may be indicated if there is no response to initial treatment, but this should be discussed with the gastroenterology team.
