Acute Liver Failure - PBworks

advertisement
Acute Liver Failure
30 year old woman presents to hospital with a
two day history of nausea, vomiting, and right
upper quadrant pain.
She has been healthy and denies any
medication use.
She recently traveled to Vietnam where she
twisted her ankle while bungee jumping. The
pain has been well controlled with over the
counter and natural remedies.
On examination, she is slightly confused to
date and in moderate distress from the
pain.
Vital signs are: 123/41, heart rate 109,
respiratory rate 24, and saturations 95%
on room air.
She is has diffuse abdominal tenderness
and palpable liver edge with a scleral
icterus.
What is the most likely cause of this patient’s
presentation?
What are the common etiologies of acute liver
failure?
– Consider:
A – acetaminophen, hepatitis A, autoimmune
B – hepatitis B
C – cryptogenic, hepatitis C
D – hepatitis D
E – esoteric causes such as Wilson’s and Budd-Chiari
F – fatty infiltration such as fatty liver of pregnancy and Reye
Initial bloodwork comes back:
– ALT 3826, AST 4826, TBili 59, Alk Phos
283,INR 4.2, creatinine 436, pH 7.31
What in the history gives us clues to the
cause?
– Travel: hepatitis virus?
– Over the counter drugs: acetaminophen?
– Natural remedies: drug or toxin?
– Childbearing age: fatty liver of pregnancy?
Obtaining further history, her family tells
you that she has been vaccinated against
hepatitis B because she is a lab tech, she
is not pregnant but do not know what
medications and remedies she takes.
You take the history from the family
because the patient is rapidly becoming
unresponsive.
What is the definition of fulminant hepatic
failure?
– Severe acute liver injury with impaired synthetic
function and encephalopathy in a person with a
normal liver or well-compensated liver disease.
What are the grades of encephalopathy?
The patient has become completely
unresponsive with posturing to stimulation. You
rapidly intubate and resuscitate her and obtain
an urgent CT scan.
Head CT
What has happened?
How do you grade hepatic
encephalopathy?
Grade
Mental Status
Asterixis
EEG
I
Euphoria/depression
Mild confusion
Slurred speech
Disordered sleep
Yes/No
Usually
normal
II
Lethargy
Moderate confusion
Yes
Abnormal
III
Marked confusion
Incoherent
Sleeping but arousable
Yes
Abnormal
IV
Coma
No
Abnormal
How do you treat hepatic encephalopathy
with and without intracranial hypertension?
What is the role for intracranial monitoring
in this case?
After appropriate resuscitation and
treatment, the patient is more stable. The
family approaches you for more
information. They want to know whether
she is going to need liver transplant.
What do you tell them and how do you
know?
Acetaminophen-induced disease
Arterial pH <7.3 (irrespective of the grade of encephalopathy)
OR
Grade III or IV encephalopathy AND
Prothrombin time >100 seconds AND
Serum creatinine >3.4mg/dL (301 µmol/L)
All other causes of fulminant hepatic failure
Prothrombin time >100 seconds (irrespective of the grade of encephalopathy)
OR
Any three of the following variables (irrespective of the grade of
encephalopathy)
1. Age <10 years or >40 years
2. Etiology: non-A, non-B hepatitis, halothane hepatitis, idiosyncratic drug
reactions
3. Duration of jaundice before onset of encephalopathy >7 days
4. Prothrombin time >50 seconds
5. Serum bilirubin >18 mg/dL (308 µmol/L)
•By the way, what are
some of the drugs
that can cause
fulminant hepatic
failure?
Acetaminophen
Alcohol
Amiodarone
Carbon tetrachloride
Dideoxyinosine
Gold
Halothane
Isoniazid
Ketoconazole
MAO inhibitors
Methyldopa
NSAIDs
Phenytoin
Poison mushrooms (Amanita
phalloides)
Propylthiouracil
Rifampin
Sulfonamides
Tetracycline
Tricyclic antidepressants
Valproic acid
Next patient
68 year old man with known chronic liver
dysfunction from NASH.
He presents to his family doctor with increasing
confusion. He admits the patient to hospital and
consults you because of persisting fevers.
On assessment, he is febrile, slightly jaundiced
with signs of chronic liver disease and
abdominal tenderness.
Blood cultures come back positive for E. coli
What is the most likely problem?
How is the diagnosis of spontaneous
bacterial peritonitis made?
A paracentesis reveals a WBC count of
375 cells/mL with 95% PMNs.
What is the appropriate treatment of
spontaneous bacterial peritonitis?
The next day, the patient feels better but his
urine output has been poor.
His creatinine is 242, last level 6 months ago
was 109.
What are the possible causes of this problem?
– Consider:
Volume depletion from paracentesis
Abdominal compartment syndrome
ATN from nephrotoxins such as aminoglycosides
Interstitial nephritis from B-lactams
Hepatorenal syndrome
How would you investigate this?
There is no change in renal function after
fluid challenges and his urine sodium is <
10 mmol/L.
What is the criteria for hepatorenal
syndrome?
What is the pathophysiology behind
hepatorenal syndrome?
The diagnosis of HRS is confirmed. The
family asks you what this means. He has
refused transplant workup and long term
dialysis.
What do you tell the family?
What is the role of albumin in HRS?
What is the role of vasopressors such as
midodrine/octreotide or
levophed/vasopressin in HRS?
Questions??
Download
Related flashcards

Biomolecules

48 cards

Chemical weapons

46 cards

Metabolic disorders

39 cards

Lachrymatory agents

32 cards

Create Flashcards