Liver normal parenchyma

The total dose to be delivered depends not on the tumor burden but on the total volume of the liver (normal parenchyma plus tumor) to be embolized. A CT or MRI should be obtained, based on which the liver volume to be embolized is calculated. The same MRI (which should include contrast-enhanced and diffusion/perfusion sequences) can be used as baseline to quantify the response to treatment. Studies have shown that a total dose of 120-150 Gy yields better results than lower doses [1,4,8]. The total activity to be injected is calculated by ... 

Liver collapse fibrosis must be differentiated from proper liver fibrosis, which displays increased deposition of a qualitatively altered extracellular matrix. It results from a collapse of the reticular fibres following liver cell necrosis. A primary collapse arises subsequent to confluent cell-group necrosis in a previously normal parenchyma. A secondary collapse develops as a result of extensive necrosis in previously damaged parenchyma (e.g. cirrhosis). 

Chong, V.F., Fan, Y.F. Ultrasonographic hepatic pseudolesions normal parenchyma mimicking mass lesions in fatty liver. Clin. Radiol. 1994 49 326-329... 

Background. Radiation induced hepatitis was first described in the 1960s [8] and results in various degrees of hepatic decompensation. It is a well recognized complication of external beam radiation that encompasses the liver [9] since it involves the irradiation of normal parenchyma beyond that which can be tolerated (35 Gy when exposed to uniform radiation fields). However, it is a rare complication after microsphere treatment since this technique allows the safe delivery of radioactive particles to liver tumors with healthy liver tissue sparing [10]. Doses greater than 70 Gy to liver tumors can be delivered without involving the normal liver tissue [11]. 

Pancreas. Typically, the pancreas is surrounded by various organs like the stomach, liver, transverse colon, kidney, or major vessels. In particular, needle biopsy of small suspect masses in the pancreatic head is therefore usually regarded as technically sophisticated, and CT guidance preferred instead of ultrasound (Fig. 37.5). For differentiation of the tumor from surrounding normal parenchyma or inflammation, a contrast-enhanced CT scan obtained in an arterial phase should generally be performed prior to the intervention. The most common access route is from an anterior approach and often... 

Another cause of abnormal liver enhancement can be seen in the arterial phase around highly vascularized liver neoplasms. In the dynamic study, the liver around a hypervascular neoplasm can be significantly hypodense compared to the remainder of the normal parenchyma since the iodinated arterial blood flow is strongly diverted to feed the hypervascular liver lesion. This phenomenon maybe seen around benign or malignant liver tumors, which are essentially dependent on the amount of arterial vascularization of the hepatic neoplasm (Fig. 11.18). The phenomenon is transitory and in the portal venous phase of liver enhancement it returns to iso density. 

Focal fatty change and focal fatty sparing show the same contrast behaviour as normal liver parenchyma in all phases, since they contain no abnormal vessels and essentially consist of normal parenchyma. Again, these lesions usually disappear after contrast injection (Fig. 18.11). 

The first extensively tested RES-specific contrast agent on the basis of iodinated lipids was EOE-13 with its precursors, AG 52-315 and AG 60-99. EOE-13 is an aqueous emulsion of the iodinated ester of poppy seed oil and is able to selectively enhance the normal liver and spleen parenchyma [10-12]. However, severe adverse events such as headache, fever and chills prevented further use of these contrast agents [13-15], although their extent could be decreased by hydrocortisone given prior to contrast injection. 

Fig. 12.3. Time course of sonographic enhancement by LCM of Novikoff hepatoma in anesthetized rats using an immobilized transducer. These representative rat liver scans were obtained before injection, and 2, 30, and 60 minutes after i.v. injection, respectively. Arrows indicate the relatively bright, contrast-enhanced tumor area in the liver (within the image plane) at 2 minutes after injection. Contrariwise, the same area before injection (first panel) is only slightly hyperechoic compared with the surrounding normal liver parenchyma. (Taken from ref. 528.)...

Fig. 12.4. Demonstration of tumor targeting ability of LCM after i.v. injection into a rat bearing Novikoff hepatoma. All histologic sections were stained with Oil Red-O and counterstained with hematoxylin. (Top panel) A low-power view of the hepatoma and surrounding normal liver tissue. (Bottom panels) High-power insets of the neighboring normal liver parenchyma (bottom left) and the Novikoff hepatoma itself (bottom right). The lipid-coated microbubbles can be appreciated as solid black discs ranging in size from submicron up to 4 or 5 pm. (Taken from ref. 528.)...

Other than in sensitive individuals, the aromatic nitro compounds are only moderately irritating to the skin, but very toxic to the liver, kidneys and nervous system. The basic mechanism of toxicity is stimulation of oxidative metabolism in cell mitochondria through interference with the normal coupling of carbohydrate oxidation to phosphorylation (ADP to AT ). The increased oxidative metabolism leads to pyrexia, tachycardia, dehydration and the ultimate depletion of fat stores. The most severe toxicity occurs when workers are concurrently exposed to hot, humid environments. Pyrexia and direct action on the brain cause cerebral edema, clinically evidenced by toxic psychosis and, at times, convulsions. Degenerative changes occur in the liver parenchyma, and renal tubules, and clinical signs of renal injury appear (albuminuria, hematuria, pyuria, increased BUN). 

In delayed-phase imaging, the signal increase in the liver parenchyma does not necessarily increase the conspicuity or detection of lesions because residual hepatocytes of a tumor of hepatocytic origin, such as hepatocellular carcinoma (HCC) and focal nodular hyperplasia, may influence the contrast enhancement. Gd-BOPTA is effective for use with delayed-phase MRI to detect metastases [130]. In cirrhosis, liver functioning is impaired and the number of normal hepatocytes is reduced. The entry of Gd-BOPTA into cirrhotic hepatocytes decreases, but the accumulation in the liver increases due to reduced biliary excretion [131]. As a consequence, contrast enhancement is reduced and the window of acquisition is widened. The contrast enhancement of a cirrhotic liver is therefore different from that observed in normal liver parenchyma. 

False-normal GPT values are often found - despite the presence of liver damage - in (7.) haemochroma-tosis, (2.) ileo-jejunal bypass, (2.) marked (e. g. alcohol-induced) deficiency of pyridoxal phosphate (Bg), 4.) severe loss of liver parenchyma, and (5.) during the terminal stages of liver disease with exhaustion and/or blockage of hepatocellular enzyme synthesis caused by toxins. (31) In healthy persons, slightly elevated GPT values were detected in 0.5% of cases. 

Fig. 8.4 Segmental fatty degeneration of the liver (2 = 37.3 HU) following application of CM compared with liver parenchyma of normal density (1 = 68.5 HU), and the spleen (3)...

Most malignant liver tumours are hypodense the difference in value to normal liver parenchyma is usually 15-25 HU. Evidence of hepatic malignancy is obtained by CT, especially by CTAP, in approx. 85% of cases with tumours of >0.5 to 1 cm in diameter. (50, 53)... 

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