Ischemic hepatitis, hepatic infarction, and ischemic ...
Ischemic hepatitis
INTRODUCTION
• The liver's complex vascular supply and high metabolic activity make it particularly vulnerable to circulatory disturbances.
• The severity and characteristics of hepatic injury depend upon the blood vessels that are involved and the degree to which injury is related to passive congestion or diminished perfusion.
• There are several well-recognized forms of vascular injury to the liver including:
o Budd-Chiari syndrome.
o Hepatic veno-occlusive disease.
o Passive congestion due to heart failure.
o Hepatic infarction.
o Ischemic hepatitis.
ISCHEMIC HEPATITIS (SHOCK LIVER, HYPOXIC HEPATITIS)
• Definition: refers to diffuse hepatic injury resulting from acute hypoperfusion.
• The syndrome is characterized by three criteria:
o Clinical setting of circulatory failure.
o Sharp but transient increase in either ALT or AST to levels greater than 20x upper limit of normal.
o Exclusion of all other causes of acute hepatitis especially drug and viral induced causes.
Etiology
• Ischaemic hepatitis is a consequence of reduced blood flow into the liver due to acute hypotension caused by low cardiac output or shock of various aetiology.
|Congestive, backward heart failure |
|Forward heart failure (myocardial infarction, arrhythmia) |
|Shock of diverse etiology |
|Chronic respiratory insufficiency |
|Thromboembolism |
|Hematological diseases (Sickle cell syndrome) |
|Dissecting aortic aneurysm |
|Postoperative conditions in thoracic and abdominal surgery |
|Occlusion of hepatic artery |
PATHOGENESIS:
• Hepatic ischemia develops when there is an imbalance between hepatic oxygen supply and demand.
Regulation of blood flow
• Hepatic oxygen delivery is related to:
o Oxygen content of blood perfusing the liver.
o Total hepatic blood flow.
• Once oxygen delivery is decreased( compensatory mechanisms ( increased oxygen extraction by hepatocytes.
• Autoregulation of blood flow
• Blood flow is regulated primarily by the activity of smooth muscle cells that surround hepatic arterioles ( constant total hepatic blood flow.
• When portal flow declines( smooth muscle cells around hepatic arterioles relax ( increased arteriolar flow.
Blood flow under systemic stress
• Under situations of systemic stress ( redistribution of blood flow to more vital organs( compensatory decrease in peripheral and splanchnic blood flow.
• The resulting decrease in hepatic blood flow ( exceeds capacity of the liver to increase oxygen extraction ( hepatocellular hypoxia.
Reperfusion injury
• Mediated by generation of reactive oxygen species once ischemic hepatocytes are reexposed to oxygen ( cell injury via lipid peroxidation.
• Kupffer cells react to ischemia by producing cytokines, including TNF-alpha ( triggers the recruitment and activation of PNLs.
Cellular mechanisms of ischemic injury
• Disruption of mitochondrial respiration (
o Depletion of adenosine triphosphate.
o Rise in cytosolic calcium (and possibly sodium) levels.
o Activation of cellular proteases.
Clinical settings that increase the risk of ischemic injury
• Patients who have preexisting liver disease and portal hypertension
o Total hepatic blood flow may already be reduced due to blood shunting through collateral circulation.
• Patients who have preexisting passive congestion of the liver
o Elevated central venous pressure ( leads to atrophy of hepatocytes ( fibrosis( impairs diffusion of nutrients to hepatocytes.
• Sickle cell anemia
o Focal interruption of the hepatic blood supply in occlusive crisis.
• Preexisting portal vein thrombosis
Clinical manifestations:
Type of patient
• Shocked or hemodynamically unstable admitted to the ICU with:
o Myocardial infarction.
o Heart failure.
o Accident.
o Acute respiratory failure.
o Sepsis.
o Severe bleeding.
o Postoperative complication.
History
• The patient may have history of coronary heart disease, valvular disease, sickle cell anemia, liver cirrhosis or portal hypertension, chronic obstructive pulmonary disease.
Presentation
• The patient is shocked with hypotension, pallor, tachycardia and arrhythmia.
• The patient may have cyanosis, tachypnea, acidosis.
• Fever, sweating, bleeding from body orifices or wound sepsis.
• Right upper quadrant tenderness.
• Physical examination may provide clues toward underlying liver disease.
• Rare patients have symptoms suggesting acute hepatitis, including nausea, vomiting, anorexia, malaise, and right upper quadrant pain.
• Occasional patients develop changes in mental status, which generally reflect impaired cerebral perfusion rather than hepatic encephalopathy.
• Hepatopulmonary syndrome develops in nearly one-half of patients but appears to be reversible following normalization of hepatic function.
Investigations:
• Picture of the cause
|Elevated cardiac enzymes |Leukocytosis |Disturbed blood gases |
|Anemia |Elevated serum urea & creatinine |DIC |
|Elevated ESR |Hypoglycemia |Electrolyte disturbances |
• Ischemic hepatitis is usually first detected because of elevations in liver biochemical tests following a hypotensive episode.
• The typical pattern of liver biochemical tests consists of:
o A rapid rise in serum aminotransferase levels.
o Peak 25 to 250x upper limit of normal reached within 1- 3 days.
o Decline steadily returning to normal within 7 to 10 days with stabilization.
o Early massive rise in LDH levels.
o Serum bilirubin level 4x upper limit of normal, usually beginning its rise after aminotransferase levels have begun to decline.
o Serum ALP levels are rarely higher than twice the upper limit of normal.
o Hepatic synthetic function usually remains normal or is only mildly impaired.
• Reasonable evaluation might include:
o Serologic testing for acute viral hepatitis.
o Blood acetaminophen level.
o Right upper quadrant ultrasound with Doppler studies of the portal and hepatic veins and hepatic artery.
o Evaluation for suspected underlying causes of ischemic injury such as cardiac or respiratory failure.
Differential diagnosis
• Ischemia should always be considered in the differential diagnosis of
|Acute viral hepatitis |Spontaneous reactivation of |Superimposition of HDV in a |Drugs & toxins (acetaminophen or herbal |
| |chronic HBV. |chronic carrier of HBV |medications) |
|Acute fatty liver of pregnancy |Metabolic disorders |Hepatic veno-occlusive disease |HELLP syndrome |
|Acute Budd-Chiari syndrome (especially those with concomitant |Acute exacerbation of autoimmune |Hepatic infarction |
|portal vein thrombosis). |hepatitis | |
• Features that suggest an ischemic rather than other causes:
o Early rapid rise in the serum LDH level is unusual in viral hepatitis.
o Ratio of serum ALT to LDH of less than 1.5 early in the course of acute hepatitis may be more likely to suggest ischemic hepatitis.
o Rapid fall in serum aminotransferase levels after the initial rise is characteristic of ischemic liver injury and atypical for other causes of hepatitis.
o End-organ hypoperfusion, especially acute tubular necrosis of the kidney.
o Concomitant, early rise in the serum creatinine.
Pathology:
• The histologic hallmark ( necrosis of hepatocytes in zone 3 of the hepatic acinus with few inflammatory cells.
• In patients with chronic or recurrent heart failure ( sinusoidal engorgement and collagen accumulates in zone 3.
• Hepatic architecture may return to normal after recovery from the ischemic event.
Management: (3As)
• There is no specific therapy for ischemic hepatitis.
• Aim: Restoring cardiac output and reversing the underlying cause of hemodynamic instability.
• Avoid aggressive diuresis since it may worsen hepatic perfusion.
• Augmentation of cardiac output enhances hepatic perfusion by Dopamine, at either "renal" or "cardiac" doses.
• Supportive ventilation may be needed.
• Correction of anemia, electrolyte and acid-base abnormalities.
• IV broad spectrum antibiotics to correct infection.
• Patients should be monitored closely for evidence of end-organ hypoperfusion, particularly decreased renal function and altered mental status.
Prognosis
• The severity of the liver injury correlates with the duration and extent of the hemodynamic compromise.
• A continually rising bilirubin and progressive prolongation of the prothrombin time are poor prognostic signs.
• Rare patients develop fulminant hepatic failure.
• Mortality rates may reach 60 to 100 %.
HEPATIC INFARCTION
• Definition: focal ischemic injury of the liver.
• It is rare because the liver has a dual blood supply.
• Causes of hepatic infarction:
|Liver transplantation |Tumor embolism |Thrombosis of the h. a. due to atherosclerosis |
|Hypercoagulable state |Infective endocarditis |therapeutic embolization or chemoembolization |
|Iatrogenic ligation of the hepatic artery after laparoscopic cholecystectomy |
|Toxemia of pregnancy |Sickle cell anemia |Following radiofrequency ablation of HCC |
|Polyarteritis nodosa |cocaine intoxication |Hepatic artery aneurysms |
Clinical manifestations:
• Precipitating cause is evident before hepatic infarction develops.
• Asymptomatic hepatic infarction detected only on an imaging study.
• Fever, epigastric or right upper quadrant pain, back or right shoulder pain, jaundice, nausea, and vomiting.
• The aminotransferases rise transiently, sometimes to massive levels.
Diagnosis:
• Suggested radiographically in patients with a compatible clinical history.
• Abdominal CT scan with IV contrast( focal, wedge-shaped lesion of low attenuation, which may extend to the capsular surface of the liver.
o Gas in the lesion is highly suggestive of infection.
o Splenic and renal infarcts suggest an embolic source of the liver findings.
o No displacement hepatic blood vessels.
• Ultrasound or CT-guided needle aspiration establishes a definitive diagnosis.
• Magnetic resonance angiography or celiac arteriography in HA occlusion.
• Doppler ultrasound should be performed to assess the patency of the hepatic artery.
Pathology:
• Complete coagulative necrosis involving all three zones of the hepatic acinus.
Management:
• No specific therapy.
• Identify and treat the cause (e.g. emboli, infective endocarditis).
• In the absence of such a source, hypercoagulable states, including proteins C and S or antithrombin III deficiency, factor V Leiden mutation, lupus anticoagulant, paroxysmal nocturnal hemoglobinuria, polycythemia Vera, and possibly oral contraceptive use should be considered.
• Serial CT scans may show resolution of the infarct over weeks, residual scarring, or atrophy of the involved lobe of liver.
• In some patients, anticoagulation is indicated to prevent further systemic emboli or thrombosis.
• Patients who develop hepatic infarction after liver transplantation often require urgent retransplantation.
ISCHEMIC CHOLANGIOPATHY
• Involves principally the large intra- and extrahepatic bile ducts.
|Following liver transplantation |Vascular injury during biliary tract surgery |
|Hypercoagulable states |Arterial infusion of the chemotherapeutic agent |
|Chemoembolization and radiation therapy |
Clinical manifestations:
• Biliary obstruction, such as pruritus, dark urine, clay-colored stools, and jaundice.
• Elevations of serum bilirubin and alkaline phosphatase and variable elevations in serum aminotransferase levels.
• Ascending cholangitis or cholangitic liver abscesses, with associated fever.
Diagnosis
• ERCP or PTC or MRCP although it does not permit therapeutic intervention or biopsies.
• Cholangiographic findings consist of multiple intra- and extrahepatic strictures with diffuse irregularity or beading of the ducts, (usually affecting the large perihilar bile ducts).
• In liver transplantation ( Doppler ultrasound +/- arteriography to rule out HA thrombosis
Pathology: Liver biopsy is rarely useful and misleading ( biliary obstruction.
Management:
• ERCP with dilation and stenting is effective for treatment of biliary strictures.
• Ischemic cholangiopathy occurring within the first month after liver transplantation frequently requires urgent retransplantation.
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