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Occlusion of the hepatic artery
Manifestations of occlusion of the hepatic artery are determined by its level and the possibility of developing collateral circulation. With occlusion distal to the mouths of the gastric and gastroduodenal arteries, a lethal outcome is possible. Surviving patients develop collateral circulation. Slow development of thrombosis is more favorable than acute circulatory blockade. The combination of hepatic artery occlusion with portal vein occlusion almost always leads to the death of the patient.
Rice. 11-4. Celiacography in the same patient (see Fig. 11-3) immediately after arterial embolization. The obliteration of the aneurysm and the vessels leading to it is determined.
The size of the infarction is determined by the degree of development of collateral vessels and rarely exceeds 8 cm. The infarction is a focus with a pale central area and a congestive hemorrhagic corolla on the periphery. In the zone of infarction, randomly located non-nuclear hepatocytes with eosinophilic granular cytoplasm, devoid of glycogen inclusions or nucleoli, are determined. The subcapsular region remains intact due to the dual blood supply.
Liver infarction also occurs in the absence of hepatic artery occlusion in patients with shock, heart failure, diabetic ketoacidosis, systemic lupus erythematosus, and also with preeclampsia. When using imaging techniques, hepatic infarcts are often detected after percutaneous liver biopsy.
Etiology
Occlusion of the hepatic artery is extremely rare and until recently was thought to be fatal. However, the advent of hepatic arteriography has improved early diagnosis and prognosis in these patients. The causes of occlusion may be periarteritis nodosa, giant cell arteritis, or embolism in patients with acute bacterial endocarditis. Sometimes a branch of the hepatic artery is ligated during cholecystectomy. Such patients usually recover. Damage to the right hepatic or cystic artery may be one of the complications of laparoscopic cholecystectomy [I]. In case of trauma to the abdomen or catheterization of the hepatic artery, its stratification is possible. Embolization of the hepatic artery sometimes leads to the development of gangrenous cholecystitis.
Clinical manifestations
The diagnosis is rarely made during the life of the patient; there are few works describing the clinical picture. Clinical manifestations are associated with an underlying disease, such as bacterial endocarditis, periarteritis nodosa, or are determined by the severity of the surgery in the upper abdominal cavity. Pain in the epigastric region on the right comes on suddenly and is accompanied by shock and hypotension. Pain is noted on palpation of the right upper quadrant of the abdomen and the edge of the liver. Jaundice develops rapidly. Leukocytosis, fever are usually found, and in a biochemical blood test - signs of a cytolytic syndrome. Prothrombin time sharply increases, bleeding appears. With occlusion of large branches of the artery, a coma develops and the patient dies within 10 days.
It is necessary to carry out hepatic arteriography. It can be used to detect obstruction of the hepatic artery. In the portal and subcapsular regions, intrahepatic collaterals develop. Extrahepatic collaterals with neighboring organs are formed in the ligamentous apparatus of the liver [3].
Scanning. Heart attacks are usually round or oval, occasionally wedge-shaped, located in the center of the organ. In the early period, they are detected as hypoechoic foci on ultrasound (ultrasound) or indistinctly demarcated areas of reduced density on computed tomograms that do not change with the introduction of a contrast agent. Later, infarctions look like confluent foci with clear boundaries. Magnetic resonance imaging (MRI) can detect infarcts as areas of low signal intensity on T1-weighted images and high intensity on T2-weighted images. With a large infarction, the formation of "lakes" of bile, sometimes containing gas, is possible.
Treatment should be aimed at eliminating the cause of the damage. Antibiotics are used to prevent secondary infection in liver hypoxia. The main goal is the treatment of acute hepatocellular insufficiency. In case of arterial injury, percutaneous embolization is used.
Damage to the hepatic artery during liver transplantation
When the bile ducts are damaged due to ischemia, they speak of ischemic cholangitis . It develops in patients undergoing liver transplantation with thrombosis or stenosis of the hepatic artery or occlusion of the paraductal arteries |8[. Diagnosis is hampered by the fact that the picture in the study of biopsy specimens may indicate obstruction of the biliary tract without signs of ischemia.
After liver transplantation, hepatic artery thrombosis is detected using arteriography. Doppler study does not always allow to detect changes, moreover, the correct assessment of its results is difficult [b]. The high reliability of helical CT is shown.
Aneurysms of the hepatic artery
Hepatic artery aneurysms are rare and account for one fifth of all visceral aneurysms. They may be a complication of bacterial endocarditis, periarteritis nodosa, or arteriosclerosis. Among the causes, the role of mechanical injuries is increasing, for example, due to traffic accidents or medical interventions, such as operations on the biliary tract, liver biopsy and invasive x-ray studies. False aneurysms occur in patients with chronic pancreatitis and pseudocyst formation. Hemobilia is often associated with false aneurysms. Aneurysms are congenital, intra- and extrahepatic, ranging in size from a pinhead to a grapefruit. Aneurysms are found on angiography or found incidentally during surgery or at autopsy.
Clinical manifestations varied. Only a third of patients have the classic triad: jaundice |24|, abdominal pain and hemobilia. Abdominal pain is a common symptom; the period from their appearance to rupture of the aneurysm can reach 5 months.
In 60-80% of patients, the reason for the primary visit to the doctor is a rupture of the altered vessel with the outflow of blood into the abdominal cavity, biliary tract or gastrointestinal tract and the development of hemoperitoneum, hemobilia or hematemesis.
Ultrasound allows you to make a preliminary diagnosis; it is confirmed by hepatic arteriography and contrast-enhanced CT (see Figure 11-2). Pulse Doppler ultrasound can detect turbulence in the blood flow in the aneurysm.
Treatment. For intrahepatic aneurysms, angiographically guided vessel embolization is used (see Figures 11-3 and 11-4). In patients with aneurysms of the common hepatic artery, surgical intervention is necessary. In this case, the artery is ligated above and below the site of the aneurysm.
Hepatic arteriovenous fistulas
Common causes of arteriovenous fistulas are blunt abdominal trauma, liver biopsy, or tumors, usually primary liver cancer. Patients with hereditary hemorrhagic telangiectasia (Rendu-Weber-Osler disease) have multiple fistulas that can lead to congestive heart failure.
If the fistula is large, a murmur can be heard over the right upper quadrant of the abdomen. Hepatic arteriography can confirm the diagnosis. As a therapeutic measure, gelatin foam embolization is usually used.
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Dual blood supply (a. hepatica, v. porta) causes the rarity of heart attacks in the liver.
Violation of blood flow in the intrahepatic branches of one or both vessels can lead to liver infarction. Objectively, liver infarction is most often said due to a decrease in blood flow along a. hepatica, which provides 50-70% of the oxygen needed by the tissues. The portal vein is responsible for 65-75% of blood flow to the liver and 30-50% of tissue oxygenation. Arterial blood flow is closely related to venous blood flow, so that the total blood flow through the liver remains constant.
It is customary to talk about the equal participation of the artery and vein in the blood supply (oxygenation) of the liver, although under extreme conditions, “load redistribution” is possible. The mechanism of regulation of general blood flow is mediated only by the hepatic artery, the portal vein cannot regulate blood flow. Arterial blood flow is regulated by specific sites that release adenosine (a powerful vasodilator). When blood flow is high, adenosine is rapidly removed, resulting in arterial vasoconstriction. Conversely, when portal blood flow is low, an adenosine-mediated vasodilation effect in arterial vessels is required to increase total blood flow.
The reasons liver ischemia can be very diverse:
1. Systemic lowering of blood pressure:
— shock(in 50% of cases);
- syndrome of compression of the celiac trunk.
2. Hepatic artery. Local decrease in blood flow:
- thrombosis (any etiology);
- embolism (any etiology);
- torsion of the accessory lobe of the liver;
- tumor compression (extremely rare);
- manipulations (surgical and diagnostic) both endoarterial (for example, angiography), and actually on the liver tissues (for example, radioablation of a tumor); the second cause of liver ischemia after shock;
- injury to the artery (including rupture).
3. Hepatic portal vein:
- thrombosis and embolism (of any etiology);
external compression.
to iatrogenic injury. relate:
- arterial hypotension, causing insufficient perfusion of internal organs and a decrease in portal blood flow;
- action of anesthetics;
- right ventricular or left ventricular failure;
- severe hypoxemia;
- reperfusion injury of the liver.
- Patients with cirrhosis of the liver are especially sensitive to the damaging effects of intraoperative ischemia, since the liver tissue in this pathology is more dependent on the blood flow through the hepatic artery.
Acute obstruction of the hepatic artery may occur as a result of thrombosis in patients with systemic vasculitis (nodular periarteritis and others), myeloproliferative diseases (polycythemia, chronic myeloid leukemia). It occurs with a tumor (compression, germination, embolism), atherosclerosis, inflammatory processes in neighboring organs, after an injury, etc.
The cause of blockage of the arteries can be an embolism in infective endocarditis and other heart diseases (especially accompanied by atrial fibrillation), with aortic atheromatosis. Possible accidental ligation or trauma to the hepatic artery during surgery.
Pathogenesis
The arterial blood supply to the liver is variable: the branches of the hepatic artery themselves and numerous anastomoses vary. Therefore, the consequences of occlusion of the hepatic artery depend on its location, collateral circulation and the state of portal blood flow. Occlusion of the main trunk is very dangerous, as well as situations with simultaneous violation of blood circulation in the portal vein system.
Infarcts with occlusion of the terminal branches and insufficient collateral blood flow are segmental in nature, they rarely reach a diameter of 8 cm, although cases have been described when an entire lobe and even the gallbladder are necrotized.
Morphological picture. Liver infarction is always ischemic with surrounding congestive hemorrhagic streak. Subcapsular fields are not affected due to additional blood supply. On the periphery of the infarction, the portal fields are preserved.
Portal vein thrombosis(pylethrombosis) is a rare disease, the idiopathic variant occurs in 13-61% of all portal vein thromboses.
Etiology:
- taking contraceptives;
- compression of the portal vein from the outside by tumors, cysts;
- inflammatory changes in the wall of the portal vein (with peptic ulcer, appendicitis, injuries of the abdominal wall, abdomen);
- with cirrhosis of the liver;
- with intra-abdominal sepsis;
- with compression of a vein by a tumor;
- with pancreatitis and other inflammatory processes in the abdominal cavity;
- as a postoperative complication;
- with injuries;
- with dehydration;
- in violation of coagulation.
Pathogenesis
Portal vein thrombosis is a common thrombosis that leads to varicose veins in areas located in front of the site of the clot. Possible fusion of the thrombus with the wall, its organization and recanalization.
In chronic impairment of portal blood flow, shunts open and anastomoses are formed between the splenic and superior mesenteric veins on the one hand, and the liver on the other.
If portal vein thrombosis is not formed against the background of cirrhosis (acute thrombosis), then there may be no changes in the liver. Possible thromboembolism of the veins of the liver, as well as the spread of thrombosis to the branches of the portal vein with the development of hemorrhagic infarcts of the spleen, intestines.
Source: diseases.medelement.com
When the body's strength is running out, various diseases occur, including liver infarction. This is the sudden death of a part of an organ, which is provoked by focal ischemia of any etiology. How dangerous this condition is, what are its main symptoms, how to recognize it and how to treat it, we will find out further.
What it is?
Liver infarction (ischemic hepatitis, shock liver) is a lesion of liver tissues and cells that die due to malnutrition as a result of blockage of the liver artery. It develops against the background of surgery, pathologies of other organs and complications of diseases of the gastrointestinal tract.
According to statistics, liver infarction occurs in men almost 20% more often than in women. As a rule, men suffer from it after the age of 60, and women - after 55 years.
Liver infarction refers to diseases of the digestive system. Class - XI. The entire block has codes from K70 to K77. Liver infarction code - K76.3.
Causes and risk factors
When the blood supply to the liver is disturbed, a heart attack often occurs. The main reason for this is thrombosis of one of the vessels in the liver. It is very important that when arterial and venous blood are supplied to this organ, the load is the same. If the vessels function smoothly, then everything is in order. But sometimes, with individual violations, the load is redistributed. The main work is performed by the artery, and the portal vein cannot cope with the regulation of the blood flow. There is an adjustment of the arterial blood flow in certain areas due to the release of the nucleotide - adenosine, which reduces the tone of the venous wall of the vessel. This causes thrombosis and, as a result, a heart attack.
Other reasons include:
- a sharp decrease in blood pressure;
- twisting of the accessory hepatic lobe;
- squeezing of the vessel by the formed tumor;
- artery rupture;
- atherosclerosis;
- the occurrence of an embolism that blocks a blood vessel;
- cirrhosis of the liver;
- heart failure;
- postoperative complications.
Risk factors for liver ischemia can be:
- heart disease;
- malnutrition;
- obesity;
- taking hormonal contraceptives;
- stress;
- high cholesterol;
- bad habits;
- tumors;
- diabetes;
- age over 55-60 years.
The most common cause of liver infarction is cardiovascular disease, which accounts for about 70% of cases. This is followed by factors such as respiratory failure and sepsis. They account for up to 15% of cases.
Symptoms
It is difficult to single out clear signs of the disease, since they coincide with the symptoms of other diseases. As a rule, liver ischemia is accompanied by such manifestations as:
- pain in the liver, upper abdomen;
- discomfort in the area of the shoulder blades, subclavian fossa, deltoid region;
- nausea and vomiting;
- increased body temperature;
- fever, if there are large lesions;
- jaundice.
What are the complications?
If you do not take action and do not consult a doctor for treatment, then every day the disease only worsens. Complications against the background of a liver infarction can be completely different and they manifest themselves differently in each person. Among the most common are:
- cirrhosis of the liver;
- various bleeding;
- blockage in the intestines;
- insufficient functioning of the kidneys;
- rupture of the spleen.
How is the diagnosis carried out?
Very often, thrombosis of certain sections of the arteries located in the liver disappears without specific manifestations, so it is impossible to identify them and it is difficult to diagnose liver infarction, especially if it occurs along with other diseases. So, for a correct diagnosis, it is necessary to conduct a comprehensive diagnosis.
Laboratory research
To recognize the disease, ultrasound or ultrasound is performed. The specialist checks the echogenicity, since it is low with liver ischemia. The focus acquires a triangular type, limited from healthy tissue.
Patients are also assigned to computed tomography. The subject of the study is the abdominal cavity. If a heart attack occurs, then a wedge-shaped focus is detected.
It is necessary to find out what is the patency of the artery in the liver, since during interventions in the liver area, accidental ligation of the largest branch of the liver artery may occur.
In addition to these studies, a biopsy can be performed, but it is not the main diagnostic method, but only an additional one. Does not give accurate results at an early stage of the lesion.
Differential Diagnosis
Liver infarction should be distinguished from viral or drug-induced hepatitis. The main difference is the activity of enzymes (aminotransferases). In hepatitis, the increase and decrease in activity does not occur as rapidly as in the case of ischemic liver damage. In addition, in the postoperative period, they occur at a later date.
Types of therapy
There is no universal treatment for the disease for all patients, since it is individual for each. The following factors are taken into account:
- the degree of the disease;
- the duration of the course of the disease;
- individual characteristics of the body.
At the initial stage, work is underway to stop the bleeding that has occurred, and all measures are being taken to eliminate hypoxemia, since it is necessary to provide the blood with oxygen, which is not enough. This condition leads to diseases of the heart, liver, kidneys, blood poisoning. If blood clots are found in the liver, angiography is recommended.
Next, antibiotics are prescribed to eliminate the secondary infection. Sometimes a surgical operation is performed to remove an embolism in the vessels leading to a blockage. In some cases, small vessels are stenised.
Forecast
In the vast majority of cases, liver infarction has a favorable outcome. In the most severe patients, pathology is one of the signs of multiple organ failure and indicates a poor prognosis.
In rare cases, the lesion can lead to fulminant renal failure. As a rule, this occurs in the presence of chronic congestive heart failure or cirrhosis. Such patients often fall into a coma. Death occurs within the first 10 days.
Secondary infection can join liver ischemia. It is also impossible to exclude the formation of a sequester from dead tissues of the organ and the development of secondary bleeding.
So, liver infarction is a disease that occurs more often in old age. It is not easy to diagnose, but it is one of the serious pathological conditions of the liver. It is important to consult a doctor in a timely manner, diagnose and recognize the disease, only after that begin the correct treatment.
Description:
Liver infarction - sudden death of part of the liver due to the cessation of its blood supply. Liver infarction rarely develops due to the presence of its dual blood supply (hepatic artery + portal vein). Clinically manifested by acute pain in the right hypochondrium.
Causes of liver infarction:
Liver infarction, as a rule, is caused by portal vein thrombosis, which occurs in chronic decompensated, pile-phlebitis, oncological diseases, cirrhosis of the liver, pancreatic necrosis, etc.
Symptoms of liver infarction:
Depends on the location and length of the portal vein, the speed of its development and the nature of the predisposing. It is manifested by bleeding from varicose veins of the esophagus, which is relatively well tolerated, since in many patients the functions of hepatocytes are preserved. Enlargement of the spleen is characteristic, especially in children. Violations of blood flow through the mesenteric veins cause paralytic ileus (abdominal pain, bloating, lack of peristalsis). The result of mesenteric thrombosis can be intestinal infarction and subsequent purulent. With purulent pylephlebitis, there are signs of liver abscesses (repeated stunning chills, pain on palpation of an enlarged liver, on the surface of which knots, abscesses are probed).
Diagnostics:
Ultrasound registers signs that are combined with a normal biopsy, an increase in fibrinogen and PTI, a decrease in VSC, angiography of the liver vessels, CT and ultrasound of the liver.
On ultrasound with liver infarction, there is a focus of low echogenicity, which, as a rule, is of a triangular type, located on the periphery of the organ, well demarcated from normal tissue.
The liver is an unpaired organ of the abdominal cavity, the largest gland in the human body, performing a variety of functions. In the liver, the toxic substances that enter it with blood from the gastrointestinal tract are neutralized.
In the liver, the most important protein substances of the blood are synthesized, glycogen and bile are formed; The liver is involved in lymph formation, plays an essential role in metabolism.
The liver has the property of enhancing body functions. It occupies a leading place in ensuring metabolism, being the "biochemical laboratory" of the body. Proper metabolism promotes growth, constant self-renewal of the body. The liver is a blood depot, performing the function of storing, regulating the amount of blood. Regulates blood composition, blood coagulation system, produces biologically active substances. The emotion of intense anger hurts the liver. At the same time, adrenaline is intensively released into the blood, which is accompanied by the release of blood from the blood depot.
With liver disease, a state of angry irritability is characteristic. A number of brain syndromes are associated with liver disease. Due to an increase in the amount of nitrogenous metabolic products that are not detoxified in the liver and enter the blood in large quantities, as well as disturbances in the metabolism of trace elements in the body, liver intoxication leads to irritability, insomnia, delirium, etc.
The most common liver disease is stone formation. This happens mainly from malnutrition, but the influence of stress factors is also possible. Stones are hardened bile. They are formed both in the liver and in the gallbladder. According to the content they are divided into cholesterol, salt, pigment. Sizes of stones from grains to a walnut.
The only place where such a quantity of proteins can accumulate is the vascular system itself. Most of the excess proteins are absorbed into the capillary walls and converted into collagen fibers, which have a 100% protein structure and are stored in the membranes of the vessel walls. The membrane has the ability to thicken tenfold, accumulating proteins. But this means that the cells of the body do not receive the proper amount of oxygen and nutrients. The cells of the heart muscles are also starved, as a result they are weakened, the work of the heart worsens, and all sorts of diseases develop, including cancer.
When excess protein can no longer fit in the walls of the capillaries, the membranes of the arteries take over its absorption. The beneficial consequence of this is that the blood remains fluid enough to ward off the threat of a heart attack, at least temporarily. But over time, this saving tactic leads to damage to the walls of blood vessels. (Only the body's most basic survival mechanisms avoid serious side effects.) The inner surface of artery walls becomes rough and thick, like a water pipe rusting from the inside. Here and there cracks, wounds, adhesions appear.
Platelets (platelets) deal with minor vascular injuries. They secrete the hormone serotonin, which helps narrow the vessel and stop bleeding. But to cope with larger wounds, as they usually are in diseased coronary arteries, platelets on their own cannot. This requires a complex process of blood clotting and clot formation. However, if a blood clot breaks off, it can travel to the heart and cause a myocardial infarction, colloquially referred to as a heart attack. (If a blood clot enters the brain, the result is a stroke. And a clot that blocks the entrance to the pulmonary artery, which carries “used” blood to the lungs, can be fatal.)
To prevent danger, the body uses a whole arsenal of first aid, including the release of lipoprotein-5 into the blood. Due to its viscous nature, this substance acts as a "band-aid", sealing wounds more tightly to prevent blood clots from breaking off. The second, no less important life-saving measure is the "smearing" of wounds with a special kind of cholesterol. It turns out a kind of "gypsum bandage". But since cholesterol itself does not yet provide sufficient protection, connective tissue and smooth muscle cells begin to grow inside the blood vessel. These deposits, called atherosclerotic plaques, can eventually completely block an artery, obstructing blood flow and contributing to the formation of life-threatening blood clots. When blood flow to the heart is severely reduced, the activity of the heart muscle decreases and a heart attack occurs. Although the gradual blockage of blood vessels, the so-called atherosclerosis, initially protects a person's life from a heart attack caused by a detached blood clot, over time it leads to the same result.
The role of liver dysfunction in the development of atherosclerosis and, as a result, myocardial infarction is obvious. Our task is to restore the functioning of the liver and eliminate the causes leading to the formation of atherosclerotic plaques.
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