Etiology and diagnosis of hepatic hemangioma

  Hepatic cavernous hemangioma pinyamycin combined with endovascular sclerosis with iodinated oil
  Hepatic cavernous hemangioma, also known as hepatic hemangioma, is actually not a true tumor but an intrahepatic venous malformation. Most patients have no autonomic symptoms, but giant hepatic hemangioma may produce symptoms due to its occupancy and compression of the surrounding tissues and its impact on liver function. With the popularization and improvement of various imaging methods, more and more hepatic hemangiomas are detected and new treatment methods are emerging.
  1.Etiology
  The cause of hemangioma is unknown, but some believe it is due to abnormal development of intrahepatic vascular structures, while others believe it is related to estrogen levels. The incidence of hemangioma is more than 10%, in other words, there is one out of 10 people on the street, and it usually does not affect the life expectancy and health of patients, therefore, most hepatic hemangiomas do not need treatment. The incidence of this disease is more common in middle-aged women and is six times higher in women than in men. It is thought that it may be related to long-term use of birth control pills.
  2. Diagnosis.
  (1) Swelling and pain in the liver area, large liver or palpable mass.
  (2) Color ultrasound shows hepatic hemangioma-like changes.
  (3) CT examination: there is a hypodense area with uniform density in the liver, and a “C”-shaped enhancement zone may appear in the marginal area of the tumor after enhancement.
  (4) Hepatic arteriogram: A “vascular lake” image appears around the lesion site, with a long retention time of contrast medium.
  (5) MR examination shows “light bulb sign”.
  3. Blood supply of hepatic hemangioma There are many controversies!
  Most scholars prefer the hepatic artery as the blood supply artery. The reasons for this are.
  (1) Proximal ligation or embolization of the hepatic artery for hepatic hemangioma often does not result in significant postoperative lesion reduction.
  (2) Methacrylate methadone is perfused into the portal and hepatic veins of resected specimens, while the hepatic artery is not perfused, and corroded specimens are seen with complete detachment of the tumor.
  (3) CT or MRI enhancement scans and hepatic arteriography can visualize the lesion at an early stage.
  (4) Transhepatic artery embolization or sclerosis can result in significant reduction or even disappearance of the hepatic hemangioma.
  However, it has also been suggested that the portal vein is involved in the blood supply for the following reasons.
  (1) In some cases, indirect portal venography and trans-splenial puncture portal venography can show blood sinuses.
  (2) A small percentage of hepatic hemangiomas do not show the lesion clearly on CT or MRI enhancement scans and hepatic arteriograms.
  Prof. Lawrence Ouyang’s explanation is more reasonable: hepatic hemangioma is an abnormal malformation of the development of the blood sinusoids connecting the hepatic artery, portal vein and hepatic vein. So the communication of the blood sinusoid with both hepatic artery and portal vein actually exists, only because the hepatic artery-anomalous blood sinusoid-portal vein (or hepatic vein) pressure step change is clinically manifested as hepatic artery blood supply. Once the hepatic artery blood supply is interrupted, as after ligation, it is not surprising that the portal vein supplies blood to the blood sinusoids.
  So the principle of treatment is to fibroticize the abnormal blood sinusoid itself. He went on to classify hepatic hemangiomas into four types: rapidly intensifying, moderately intensifying, slowly intensifying, and atypical, according to the speed of intensification on CT-enhanced scans. He also pointed out that for the fast intensifying type, if there is an arteriovenous shunt, sclerotic embolization of the anomalous sinus should be performed along with embolization of the blood supply artery, and if there is a significant shunt in a small lesion, it indicates that the blood supply is rich and may increase, and embolization is also needed.
  Treatment
  1.Hepatic arteriosclerosis
  Treatment mechanism: Pingyangmycin is a mild vascular sclerosing agent, which can destroy the abnormal vascular endothelial cells of CHL by inhibiting the synthesis of DNA and removing the DNA strands, causing the collapse and fibrosis of the blood vessels to achieve the treatment purpose. The addition of pinyamycin to iodine oil not only increases its vascular expectorant effect, but also iodine oil acts as an X-ray impermeable carrier to facilitate the release of embolic agents under imaging surveillance. Blocking its blood supply artery with gelatin sponge particles further improves the interventional efficacy.
  Indications.
  (1) Tumor compressing adjacent tissues and organs, causing obvious symptoms;
  (2) Large tumor, >5cm, with a tendency to continue to grow;
  (3) Close to the surface, theoretically at risk of rupture, tumor rupture and bleeding or at risk of rupture and bleeding under the liver peritoneum (Note: the chance of rupture is very small);
  (4) Patients with serious psychological disorders (can be done or not).
  Complications and side effects
  (1) PLE is a slow process of sinusoidal destruction of CHL, and the post-bolus syndrome is relatively mild and can be relieved by symptomatic treatment for about a week. Normal hepatocytes flush and eliminate iodine oil emulsion faster, and a small amount of PLE accidentally embolized liver tissue usually does not cause serious consequences, but there are reported cases of anhydrous alcohol treatment of CHL and accidental embolization of gallbladder artery leading to gallbladder necrosis, so it is advocated to super-select the catheter to close to the tumor to prevent accidental embolization of non-target organs.
  (2) The cannulation action should be gentle to prevent vasospasm and arterial entrapment and thrombosis leading to interventional failure.
  (3) Larger arteriovenous fistula openings are difficult to seal, and pulmonary embolism and pulmonary fibrosis can occur during intervention, so embolization therapy should be cautious when CHL is combined with arteriovenous fistula. Zeng Qingle et al. concluded that even without arteriovenous fistula, pulmonary fibrosis occurred in 30% of patients when the clinical dosage of Pingyangmycin accumulated to 450-500 mg.
  (4) Tumor >15cm, multi-branch blood supply, abnormal liver function, age >60 years old can first embolize its main blood supply artery and branch embolization therapy for several times to reduce side effects.
  2.Surgical resection
  Surgical resection of hepatic cavernous hemangioma is difficult and bleeding is frequent. Simple hepatic artery ligation and embolization treatment can not achieve the purpose of radical cure because of the establishment of collateral circulation in a short time.
  Although the interventional treatment of hepatic hemangioma is simple, it cannot be done indiscriminately and there are certain rules. I’ve heard of people dying from hepatic hemangioma interventions, but most of them are related to the beginners’ poor grasp of indications and operating techniques. The liver hemangioma must be super-selected for intubation, and then embolized after reaching the nearest blood supply artery of the tumor. It is very easy to have problems without super-selective intubation!
  Pingyangmycin combined with iodinated oil embolization sclerosis CHL is progressive, less traumatic, faster, less side effects, can be the preferred method for the treatment of hepatic hemangioma.