Hepatic Injury From Toxins

Published on 19/07/2015 by admin

Filed under Radiology

Last modified 22/04/2025

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Most other toxins result in ↓ density due to steatohepatitis ± hepatocellular necrosis

• May show other inflammatory changes, such as periportal or gallbladder wall edema

• Volume loss of liver and ascites are bad prognostic signs

TOP DIFFERENTIAL DIAGNOSES

• Hepatitis (alcoholic, viral, autoimmune)

Imaging cannot distinguish among causes of acute hepatitis

• Steatosis (fatty liver)

PATHOLOGY

• Acetaminophen (paracetamol or Tylenol)

Most common cause of severe toxic injury in USA and Europe (40-50% of cases)

CLINICAL ISSUES

• Acute abdominal pain, nausea, vomiting

• May quickly progress to complete hepatic failure

• Usually leads to complete recovery or liver failure within 72 hours

Acute liver failure must be treated with liver transplantation to avoid fatal outcome

DIAGNOSTIC CHECKLIST

• Global or focal liver volume loss ± ascites = bad prognosis

(Left) Axial NECT of a 41-year-old woman who developed acute liver failure after taking an excessive dose of acetaminophen shows diffuse low attenuation throughout the liver, which is due to acute massive hepatocellular necrosis rather than steatosis, although the imaging features are indistinguishable.

(Right) Axial CECT section of the same patient shows only diffuse hypoattenuation throughout the liver and ascites on lower sections. The patient developed hepatic failure within 24 hours of this scan.

(Left) The same patient required urgent liver transplantation. The explanted liver shows signs of massive hepatocellular necrosis and acute inflammation.

(Right) H&E of acute liver failure shows confluent necrosis with lymphoplasmacytic inflammation (left). Swelling and inflammation are seen in the remaining parenchyma (right). (Courtesy S. Kakar, MD.)

TERMINOLOGY

Definitions

• Injury to liver induced by exogenous toxins, either through direct hepatotoxicity or idiosyncratic reaction

IMAGING

General Features

• Best diagnostic clue

Imaging may be normal or show diffuse ↑ or ↓ density

– May show other inflammatory changes, such as periportal or gallbladder wall edema

– Amiodarone results in increased density; most other toxins result in ↓ density due to steatohepatitis ± hepatocellular necrosis

CT Findings

• Hepatomegaly

• Diffuse or multifocal hypodensity in liver

May represent steatosis, steatohepatitis, &/or hepatocellular necrosis

• Volume loss of liver (global or lobar)

Bad prognostic sign

Often indicates massive hepatocellular necrosis

• Ascites (bad prognostic sign)

MR Findings

• Steatosis in some cases

Signal loss on opposed-phase T1W GRE MR

Ultrasonographic Findings

• Hepatomegaly

• ↑ or ↓ echogenicity of liver

Steatosis vs. hepatic “edema” from acute injury

• Periportal edema ± gallbladder wall edema

Imaging Recommendations

• Best imaging tool

CT to detect signs of severe injury

– Hepatic volume loss and ascites

DIFFERENTIAL DIAGNOSIS

Hepatitis (Alcoholic, Viral, Autoimmune)

• Imaging cannot distinguish among causes of acute hepatitis

Steatosis (Fatty Liver)

• Steatosis or steatohepatitis may result from other etiologies besides toxic injury

PATHOLOGY

Staging, Grading, & Classification

• Intrinsic hepatotoxins

Direct and predictable injury to liver

– Dose dependent

Common agents

– Acetaminophen (paracetamol or Tylenol)

As part of deliberate suicide attempt or unintentional consumption of excessive amounts

Most common cause of severe toxic injury in USA and Europe

Accounts for 40-50% of cases of acute toxic injury with acute liver failure

Threshold for injury is lowered by coexisting alcoholic or nonalcoholic steatohepatitis

Liver failure or recovery within 72-96 hours after ingestion

– Toxic mushrooms, poisons, carbon tetrachloride

– Other medications

Amiodarone (dense liver on NECT)

Calcium channel blockers, steroids, anti-HIV drugs

• Idiosyncratic hepatotoxins

Produce injury only in small proportion of individuals who are susceptible

– e.g., isoniazid, halothane anesthesia, chlorpromazine, phenytoin

Microscopic Features

• Cytotoxic or cholestatic injury

• Amiodarone and other drugs cause phospholipidosis

Granular, foamy appearance of hepatocytes

Amiodarone gets trapped within lysozymes

Hepatocyte swelling

• Steatohepatitis

• Fibrosis or cirrhosis with progressive disease

• Massive necrosis due to intrinsic or idiosyncratic hepatotoxins

CLINICAL ISSUES

Presentation

• Most common signs/symptoms

Acetaminophen or other direct toxins

– Acute abdominal pain, nausea, vomiting

– May quickly progress to complete hepatic failure

– Usually leads to complete recovery or liver failure within 72 hours

– Acute liver failure must be treated with liver transplantation to avoid fatal outcome

• Other signs/symptoms

Acute, subacute, or chronic cholestatic injury

– Pruritus, jaundice

Natural History & Prognosis

• For direct toxins

Withdrawal of toxic agent

Rapid recovery or death within 48 hours without transplantation

Treatment

• Liver transplantation

DIAGNOSTIC CHECKLIST

Image Interpretation Pearls

• Global or focal liver volume loss ± ascites = bad prognosis

(Left) Axial arterial phase CECT in a 29-year-old man with acute severe hepatic dysfunction shows an enlarged heterogeneous liver.

(Right) Another arterial phase CT image in the same patient shows more of the heterogeneous enlarged liver, along with periportal edema . This was attributed to the combined toxic effects of alcohol abuse and acetaminophen used to treat a hangover.

(Right) Another arterial phase CT image in the same patient shows more of the heterogeneous enlarged liver, along with periportal edema . This was attributed to the combined toxic effects of alcohol abuse and acetaminophen used to treat a hangover.

(Left) This portal venous phase image in the same patient shows the hepatomegaly and periportal edema, but the heterogeneity of the liver is less apparent. The liver injury represents a combination of steatosis and hepatocellular necrosis.

(Right) CT in the same patient with acute hepatic injury from alcohol and acetaminophen shows nonspecific gallbladder wall edema .

(Right) CT in the same patient with acute hepatic injury from alcohol and acetaminophen shows nonspecific gallbladder wall edema .

(Left) Axial CT section through the pelvis in the same patient shows ascites , a bad prognostic sign in the setting of acute toxic hepatic injury.

(Left) Axial CT section through the pelvis in the same patient shows ascites , a bad prognostic sign in the setting of acute toxic hepatic injury.

(Right) Multiacinar hemorrhagic necrosis , congestion , and lack of inflammation with sparing of periportal hepatocytes are typical of acetaminophen toxicity but can also be seen in acute ischemia and acute Budd-Chiari syndrome. (Courtesy S. Kakar, MD.)

(Right) Multiacinar hemorrhagic necrosis , congestion , and lack of inflammation with sparing of periportal hepatocytes are typical of acetaminophen toxicity but can also be seen in acute ischemia and acute Budd-Chiari syndrome. (Courtesy S. Kakar, MD.)

(Left) Axial CT in a 24-year-old man with acute hepatic failure probably due to alcohol and drug abuse shows a heterogeneous liver with evidence of volume loss (capsular retraction) . A large amount of ascites and pleural effusions are also noted. These are ominous findings, usually associated with death or requiring urgent transplantation.

(Left) Axial CT in a 24-year-old man with acute hepatic failure probably due to alcohol and drug abuse shows a heterogeneous liver with evidence of volume loss (capsular retraction) . A large amount of ascites and pleural effusions are also noted. These are ominous findings, usually associated with death or requiring urgent transplantation.

(Right) Lower CT section in the same patient shows more of the damaged liver with volume loss and ascites. The patient died of acute hepatic failure.

(Right) Lower CT section in the same patient shows more of the damaged liver with volume loss and ascites. The patient died of acute hepatic failure.

(Left) Frontal digital radiograph in a 41-year-old woman with intractable arrhythmias and abnormal liver function shows an implantable cardioverter defibrillator (AICD) with numerous wire leads to the heart.

(Right) Axial NECT in the same patient shows some of the cardiac leads from the AICD .

(Right) Axial NECT in the same patient shows some of the cardiac leads from the AICD .

(Left) Another NECT section in the same patient shows diffuse increased density within the liver due to amiodarone deposition. Amiodarone is an iodine-containing antiarrhythmic that may cause hepatic (and pulmonary) toxicity.

(Right) Ballooned hepatocytes containing abundant Mallory hyaline bodies are surrounded by neutrophils, known as satellitosis . This is a frequent feature of amiodarone toxicity. Steatosis may or may not be present. (Courtesy L. Lamps, MD.)

(Right) Ballooned hepatocytes containing abundant Mallory hyaline bodies are surrounded by neutrophils, known as satellitosis . This is a frequent feature of amiodarone toxicity. Steatosis may or may not be present. (Courtesy L. Lamps, MD.)

Diagnostic Imaging_ Gastrointes - Michael P Federle