Ischemic hepatitis: Difference between revisions
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==Overview== | |||
'''Ischemic hepatitis''' (also known as '''shock liver''') is a condition of decreased blood supply to the [[liver]] resulting in injury to liver cells ([[hepatocyte]]s), which occurs in a diffuse fashion. | |||
The decreased blood flow ([[perfusion]]) to the liver is usually due to [[shock]] or [[hypotension|low blood pressure]]. However, local causes involving the [[hepatic artery]] that supplies oxygen to the liver, such as [[sickle cell anemia|sickle cell crisis]] and [[thrombosis]] of the [[hepatic artery]], can also cause ischemic hepatitis. Patients with ischemic hepatitis are usually very ill. | |||
Blood testing usually shows high levels of the [[liver function tests|liver transaminase]] enzymes, [[AST]] and [[ALT]], which may exceed 1000 U/L. People who develop ischemic hepatitis may have [[abdominal pain|pain]] in the right upper part of the [[abdomen]], but they usually feel more unwell because of the serious reason that they developed the [[ischemia]], than due to the ischemic hepatitis itself. [[Jaundice]] can occur, but is rare and transient, as is actual loss of function of the liver. | |||
Ischemic hepatitis is related to another condition called [[nutmeg liver|congestive hepatopathy]] or [[nutmeg liver]], which is a backflow condition due to poor drainage of the liver, usually due to [[heart failure]]. As a result, the two entities can co-exist. | |||
==Historical Perspective== | |||
The most frequent cause of severe acute liver damage in the US is ischemic hepatitis, which affects around 2% of patients hospitalized to the intensive care unit. | |||
About 80% of patients had an underlying cardiac condition. | |||
== | ==Pathophysiology== | ||
The pathophysiology of hypoxia and necrosis in hepatic tissue: | |||
1-Congestion in the liver brought on by an underlying illness (heart failure, for example) can lead to anatomical alterations in the liver (hepatocyte atrophy, sinusoidal centrilobular dilatation, etc.) and altered hepatic blood flow. | |||
2-Hepatic blood flow is affected by reduced cardiac output, hypovolemic shock, or cardiac arrest. | |||
3-Septic shock is caused by the following factors: circulating endotoxins, inflammatory cytokines, hepatic metabolic demands, hepatocytes' capability to collect and use oxygen, and hepatic blood flow. | |||
==clinical features== | |||
Symptomless | |||
Weakness, exhaustion, and changed mental state | |||
hypertension and bradycardia | |||
Hepatomegaly, right upper quadrant pain, nausea, vomiting, and anorexia | |||
==Diagnosis== | |||
clinical history and physical examination - | |||
cardiopulmonary disease, hypotension | |||
-lab investigations | |||
AST levels that are extremely high (> 1000 U/L) | |||
Levels of serum peak 1-3 days | |||
Values stabilize about 7–10 days after the restoration of hepatic perfusion. | |||
elevated levels of bilirubin | |||
increased LDH concentrations | |||
ALT:LDH ratio less than 1.5 | |||
elevated BUN and creatinine levels in the blood | |||
Normal levels of alkaline phosphatase | |||
Studies on coagulation: prothrombin time may be extended | |||
Imaging: to detect portal vein thrombosis or hepatic artery blockage (e.g., using Doppler ultrasonography, MRI, or arteriography) | |||
Other: to rule out other potential causes of acute liver damage, such as acute viral hepatitis or acetaminophen overdose. | |||
==Differential Diagnosis== | |||
1.Drug induced acute liver failure | |||
2.Acute viral hepatitis | |||
3.Hepatic infarction | |||
==Treatment== | |||
===Medical Therapy=== | |||
Ischemic hepatitis does not have a particular therapy. | |||
Address the root cause. | |||
Hemodynamic assistance (vasopressor, inotropes, volume resuscitation) and restoration of cardiac output are required. | |||
===Prognosis=== | |||
Depends on the underlying condition, duration, and extent of the hemodynamic compromise | |||
Higher death rates are linked to the following factors: | |||
patient on Vasopressor therapy | |||
high INR | |||
septic shock | |||
failure of the kidneys | |||
==References== | |||
{{reflist|2}} | |||
[[Category:Hepatology]] | [[Category:Hepatology]] | ||
Latest revision as of 11:15, 7 July 2024
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: ; Rithish Nimmagadda,MBBS.[2]
Overview
Ischemic hepatitis (also known as shock liver) is a condition of decreased blood supply to the liver resulting in injury to liver cells (hepatocytes), which occurs in a diffuse fashion.
The decreased blood flow (perfusion) to the liver is usually due to shock or low blood pressure. However, local causes involving the hepatic artery that supplies oxygen to the liver, such as sickle cell crisis and thrombosis of the hepatic artery, can also cause ischemic hepatitis. Patients with ischemic hepatitis are usually very ill.
Blood testing usually shows high levels of the liver transaminase enzymes, AST and ALT, which may exceed 1000 U/L. People who develop ischemic hepatitis may have pain in the right upper part of the abdomen, but they usually feel more unwell because of the serious reason that they developed the ischemia, than due to the ischemic hepatitis itself. Jaundice can occur, but is rare and transient, as is actual loss of function of the liver.
Ischemic hepatitis is related to another condition called congestive hepatopathy or nutmeg liver, which is a backflow condition due to poor drainage of the liver, usually due to heart failure. As a result, the two entities can co-exist.
Historical Perspective
The most frequent cause of severe acute liver damage in the US is ischemic hepatitis, which affects around 2% of patients hospitalized to the intensive care unit. About 80% of patients had an underlying cardiac condition.
Pathophysiology
The pathophysiology of hypoxia and necrosis in hepatic tissue:
1-Congestion in the liver brought on by an underlying illness (heart failure, for example) can lead to anatomical alterations in the liver (hepatocyte atrophy, sinusoidal centrilobular dilatation, etc.) and altered hepatic blood flow.
2-Hepatic blood flow is affected by reduced cardiac output, hypovolemic shock, or cardiac arrest.
3-Septic shock is caused by the following factors: circulating endotoxins, inflammatory cytokines, hepatic metabolic demands, hepatocytes' capability to collect and use oxygen, and hepatic blood flow.
clinical features
Symptomless Weakness, exhaustion, and changed mental state hypertension and bradycardia Hepatomegaly, right upper quadrant pain, nausea, vomiting, and anorexia
Diagnosis
clinical history and physical examination - cardiopulmonary disease, hypotension
-lab investigations
AST levels that are extremely high (> 1000 U/L) Levels of serum peak 1-3 days Values stabilize about 7–10 days after the restoration of hepatic perfusion. elevated levels of bilirubin increased LDH concentrations ALT:LDH ratio less than 1.5 elevated BUN and creatinine levels in the blood Normal levels of alkaline phosphatase
Studies on coagulation: prothrombin time may be extended
Imaging: to detect portal vein thrombosis or hepatic artery blockage (e.g., using Doppler ultrasonography, MRI, or arteriography) Other: to rule out other potential causes of acute liver damage, such as acute viral hepatitis or acetaminophen overdose.
Differential Diagnosis
1.Drug induced acute liver failure 2.Acute viral hepatitis 3.Hepatic infarction
Treatment
Medical Therapy
Ischemic hepatitis does not have a particular therapy. Address the root cause. Hemodynamic assistance (vasopressor, inotropes, volume resuscitation) and restoration of cardiac output are required.
Prognosis
Depends on the underlying condition, duration, and extent of the hemodynamic compromise
Higher death rates are linked to the following factors: patient on Vasopressor therapy high INR septic shock failure of the kidneys