Acute liver failure is quite a rare occurrence whilst chronic liver disease is relatively more common.
The two conditions can sometimes be confused in the jaundiced patient and even missed entirely if a careful history and physical examination is not taken.
Patients with acute liver failure do not usually have a history of liver disease and in fact, they may have no unusual history at all.
Nevertheless, a careful history should be taken concerning the causes of liver failure e.g. viral hepatitis, drugs, alcohol etc...
So, how do you spot a patient with acute liver failure with no pathognomonic signs?
Well, conscious level is important.
Always score the Glasgow Coma Scale and aim to use a mini mental test scoring system of up to ten questions to see if the patient can remember immediate memory, short term memory and long term memories. These scores can be compared as the patient improves or worsens and can be used as a guide.
Always check for a Hepatic Flap (arms extended and hands extended at the wrists with all digits spread open)-- a typical intermittent flexion-extension motion can be seen.
Smell your patient's breath for Liver Breath (fetor hepaticus) and check the eyes for jaundice.
None of the above can delineate acute from chronic decompensated liver disease.
However, the absence of chronic signs e.g. spider naevae, gynaecomastia, palmar erythema, clubbing, Dupytreen's contracture, gross ascites and caput medussa are clues that the disorder may be acute.
Moreover, in acute liver failure, the liver can be enlarged and tender on palpation whereas chronic liver patients tend to have hard and non-tender livers which may be impalpable.
Both conditions have increased bleeding tendencies but acute failure is far more serious as worsening clotting is a sign of worsening acute liver dysfunction. Patients can develop profound metabolic acidaemia and hence, their symptoms may be confused as a respiratory condition through increased respiratory rate from a Kussmaul-type of reactive breathing.
Patients may also present with unconsciousness due to profound hypoglycaemia, something not so common in chronic failure, and this may be due to decreased storage capacity, reduced glycogenolysis and gluconeogenesis in the acutely failing liver. Simply treating with 50% dextrose is not enough as patients may soon become hypoglycaemic again, so an infusion is required.
Of course, liver results showing very high AST and ALT in the thousands is highly significant of an acute process rather than the smaller rise seen in cirrhotic livers.
I hope the above helps you to separate the two conditions, as treatment and prognosis are different especially as acute liver failure patients may require acute liver transplantation.
The two conditions can sometimes be confused in the jaundiced patient and even missed entirely if a careful history and physical examination is not taken.
Patients with acute liver failure do not usually have a history of liver disease and in fact, they may have no unusual history at all.
Nevertheless, a careful history should be taken concerning the causes of liver failure e.g. viral hepatitis, drugs, alcohol etc...
So, how do you spot a patient with acute liver failure with no pathognomonic signs?
Well, conscious level is important.
Always score the Glasgow Coma Scale and aim to use a mini mental test scoring system of up to ten questions to see if the patient can remember immediate memory, short term memory and long term memories. These scores can be compared as the patient improves or worsens and can be used as a guide.
Always check for a Hepatic Flap (arms extended and hands extended at the wrists with all digits spread open)-- a typical intermittent flexion-extension motion can be seen.
Smell your patient's breath for Liver Breath (fetor hepaticus) and check the eyes for jaundice.
None of the above can delineate acute from chronic decompensated liver disease.
However, the absence of chronic signs e.g. spider naevae, gynaecomastia, palmar erythema, clubbing, Dupytreen's contracture, gross ascites and caput medussa are clues that the disorder may be acute.
Moreover, in acute liver failure, the liver can be enlarged and tender on palpation whereas chronic liver patients tend to have hard and non-tender livers which may be impalpable.
Both conditions have increased bleeding tendencies but acute failure is far more serious as worsening clotting is a sign of worsening acute liver dysfunction. Patients can develop profound metabolic acidaemia and hence, their symptoms may be confused as a respiratory condition through increased respiratory rate from a Kussmaul-type of reactive breathing.
Patients may also present with unconsciousness due to profound hypoglycaemia, something not so common in chronic failure, and this may be due to decreased storage capacity, reduced glycogenolysis and gluconeogenesis in the acutely failing liver. Simply treating with 50% dextrose is not enough as patients may soon become hypoglycaemic again, so an infusion is required.
Of course, liver results showing very high AST and ALT in the thousands is highly significant of an acute process rather than the smaller rise seen in cirrhotic livers.
I hope the above helps you to separate the two conditions, as treatment and prognosis are different especially as acute liver failure patients may require acute liver transplantation.
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