Abstract
Chronic liver failure (CLF) is the result of persistent liver damage. Given the multifaceted abilities of the organ, CLF is a multisystem progressive disease that evolves from an asymptomatic (compensated) to a clinically manifested phase (decompensated) driven by hemodynamic disturbances and systemic inflammation. Among the whole spectrum, several stages with prognostic relevance have been described. Clinical management of CLF aims to treat primary liver disease, screening, prevent and controlling the complications, and consider liver transplantation (LT) in advanced stages and life-threatening complications. Improvement and reversibility of liver damage and clinical consequences have been described with etiological cure.
Acute-on-chronic liver failure (ACLF) is an acute decompensation characterized by high short-term mortality related to the development of organ failure. Systemic inflammatory response seems to play a key role. Despite its high risk of short-term mortality, it is a very dynamic syndrome and potentially reversible. Management includes early treatment of potential triggers, prevention of progression and support of failed organs and consider for LT. Since there is very limited data on the impact of ACLF on LT outcomes, its clinical applicability remains controversial.
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Abbreviations
- ACLF:
-
Acute-on-chronic liver failure
- AKI:
-
Acute kidney injury
- BCLC:
-
Barcelona clinic liver cancer
- BT:
-
Bacterial translocation
- cACLD:
-
Compensated advanced chronic liver disease
- CLF:
-
Chronic liver failure
- CRP:
-
C-reactive protein
- Crs:
-
Serum creatinine
- DAMP:
-
Damage-associated molecular pattern
- DM:
-
Diabetes mellitus
- GA:
-
Glutaminase
- GS:
-
Glutamine synthetase
- HCC:
-
Hepatocellular carcinoma
- HE:
-
Hepatic encephalopathy
- HPS:
-
Hepatopulmonary syndrome
- HRS:
-
Hepatorenal syndrome
- LT:
-
Liver transplantation
- LVP:
-
Large volume paracentesis
- MELD:
-
Model for end-stage liver disease
- NAFLD:
-
Non-alcoholic fatty liver disease
- NSAIDs:
-
Nonsteroidal anti-inflammatory drugs
- NSBB:
-
Non-selective beta blockers
- PAMP:
-
Pathogen-associated molecular pattern
- PH:
-
Portal hypertension
- PPHT:
-
Portopulmonary hypertension
- PSS:
-
Portosystemic shunts
- SBP:
-
Spontaneous bacterial peritonitis
- TIPS:
-
Transjugular intrahepatic portosystemic shunt
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Self Study
Self Study
1.1 Questions
-
1.
Regarding AKI in Cirrhosis Which Is FALSE
-
(a)
Clinical manifestations are prominent and drive the diagnosis.
-
(b)
Once diagnosis is made, risk factors should be sought and corrected
-
(c)
Diagnostic criteria for AKI and HRS-AKI has been updated leading to the elimination of the Crs cut-off point of 2.5 mg/dL
-
(d)
The subtype HRS-AKI requires close monitoring and specific treatment based on vasoconstrictors and albumin infusion
-
(a)
-
2.
With Regard to the Physiopathology of HE Which Is TRUE
-
(a)
Ammonia is the only element involved and its serum level is diagnostic.
-
(b)
The amount of ammonia that enters portal vein is the result of catabolism of proteins by gut bacteria and deamination of glutamine in the gut.
-
(c)
Systemic inflammation is not important in the pathogenesis of HE.
-
(d)
Kidney eliminates ammonia in urea form and is not implicated in the ammoniagenesis.
-
(a)
1.2 Answers
-
1.
Regarding AKI in Cirrhosis Which Is FALSE
-
Right answer: a.
-
AKI doesn’t have prominent manifestations, it has to be suspected in patients with oliguria and unspecific symptoms. All the others are correct.
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2.
With Regard to the Physiopathology of HE Which Is TRUE
-
Right answer: b.
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Ammonia is an important factor in the physiopathology of HE together with others. Inflammation is also important, especially in clinical situations where the inflammatory response is marked as ACLF. The determination of plasma ammonia levels may suggest HE but there are no cut-off points to confirm or exclude HE. Ammonia that enters portal vein from the gastrointestinal tract derives from colonic bacteria and the deamidation of glutamine in the small bowel Muscle and kidney are important organs in ammonia homeostasis. Kidney can either eliminate or generate ammonia (through glutamine metabolism).
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Garcia-Martinez, R., Diaz-Ruiz, R., Millan, J., Bañares, R. (2020). Chronic Liver Failure and Acute-on-Chronic Liver Failure. In: Radu-Ionita, F., Pyrsopoulos, N., Jinga, M., Tintoiu, I., Sun, Z., Bontas, E. (eds) Liver Diseases. Springer, Cham. https://doi.org/10.1007/978-3-030-24432-3_33
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