(A) Causes of morbidity
In patients with primary liver cancer, upper gastrointestinal bleeding is one of the main causes of death. As patients with liver cancer are mostly combined with cirrhosis, the incidence of portal hypertension and esophagogastric fundic varices is higher; in addition, the inactivation ability of corticosteroids and hormones in the body is low, and peptic ulcers and gastric mucosal lesions are also more common.
1.Esophagogastric fundic varices
Esophageal and fundic varices are the most important causes of upper gastrointestinal bleeding in hepatocellular carcinoma. When the portal vein or hepatic vein is obstructed, it can aggravate the portal hypertension and lead to the rupture and bleeding of the varices of esophagus and fundus, causing upper gastrointestinal bleeding; liver cancer can aggravate the damage of liver function and aggravate the degree of cirrhosis, leading to the aggravation of high portal vein; when the lesion of liver cancer is located in the portal part of liver, it can compress the esophagus and fundus. When the liver cancer lesion is located in the portal part of liver, it can compress the main trunk of portal vein, which can also increase the portal vein pressure.
2.Disorder of blood coagulation mechanism
Due to the reduction of normal liver tissues, the coagulation factors synthesized by the liver are reduced, and the coagulation mechanism is impaired in liver cancer patients. Due to hypersplenism and increased platelet destruction, the coagulation mechanism will also be impaired. In addition, after the cancer embolus enters the blood, it can easily cause acute diffuse intravascular coagulation and cause gastrointestinal bleeding.
3.Gastrointestinal mucous membrane erosion
Due to portal hypertension, patients with hepatocellular carcinoma often suffer from gastrointestinal bruising, mucosal edema and erosion; the inactivation ability of corticosteroids and hormones in the body is low, and peptic ulcers and gastric mucosal lesions are also common, which easily cause bleeding.
4.Biliary tract bleeding
Biliary bleeding caused by hepatocellular carcinoma is uncommon, accounting for about 5%, mainly due to the following reasons.
(1) Infiltrative growth of tumor into the intrahepatic bile duct, bleeding when the mass breaks down, blood flows into the bile duct and biliary bleeding occurs.
(2) The tumor encroaches on the large intrahepatic blood vessels and intrahepatic bile ducts, forming a vascular-biliary fistula, leading to biliary hemorrhage.
(3) After necrosis of bile duct cell carcinoma originating from the biliary epithelium, the mass ruptures and bleeds into the lumen of the intrahepatic bile duct, resulting in biliary hemorrhage.
(ii) Clinical manifestations
The clinical manifestations of gastrointestinal bleeding depend on the nature and location of the bleeding lesion, the amount and speed of blood loss, and are also related to the patient’s age, liver and kidney function and other systemic conditions.
1, bleeding mode: acute massive bleeding mostly manifested as vomiting blood; chronic small amount of bleeding is manifested by positive fecal occult blood; if the speed of bleeding and the amount of bleeding is high, it is manifested as vomiting blood, and the color of vomitus is bright red.
2, hemorrhagic peripheral circulation failure: acute peripheral circulation failure caused by massive bleeding in the upper gastrointestinal tract. Blood loss up to a large amount, bleeding or untimely treatment can cause a decrease in tissue blood perfusion and cellular hypoxia in the organism. In turn, hypoxia, metabolic acidosis and accumulation of metabolites can cause peripheral vasodilatation and extensive capillary damage, resulting in a large amount of body fluid stagnation in the abdominal cavity bone organs and surrounding tissues, causing a sharp decrease in effective blood volume and seriously affecting the blood supply to the heart, brain and kidney, finally forming irreversible shock and leading to death. During the development of circulatory failure around the hemorrhage, clinical dizziness, palpitations, nausea, thirst, black haze or syncope may occur; the skin is gray and wet and cold due to vasoconstriction and insufficient blood perfusion; the nail bed appears pale after pressing and does not recover after a long time. Venous filling is poor, and body surface veins are often deflated. The patient feels tired and weak, and further may appear mental atrophy, irritability, and even unresponsiveness and blurred consciousness.
3, azotemia: It can be divided into 3 kinds of intestinal origin, renal and pre-renal azotemia. Enterogenic azotemia refers to the intestinal absorption of the breakdown products of blood proteins after massive upper gastrointestinal bleeding, resulting in elevated nitrogen in the blood. Prerenal azotemia is caused by a temporary decrease in renal blood flow due to hemorrhagic peripheral circulatory failure and a decrease in glomerular filtration rate and renal excretion function, resulting in nitrogen storage. After correction of hypotension and shock, blood urea nitrogen can be rapidly reduced to normal. Renal azotemia is due to tubular necrosis (acute renal failure) caused by severe and prolonged shock, or blood loss that exacerbates the renal damage of pre-existing nephropathy. Clinically, there may be oliguria or anuria. In the case of hemorrhage cessation, azotemia often persists for more than 4 days, and the blood urea nitrogen cannot be normalized after replenishment of blood volume and correction of shock.
4.Fever: After massive bleeding, most patients often develop hypothermia within 24 hours. The cause of fever may be due to the dysfunction of the thermoregulatory center caused by the reduction of blood volume, anemia, peripheral circulation failure, absorption of hemolytic proteins and other factors. When analyzing the cause of fever, attention should be paid to finding other factors, such as the presence of concurrent pneumonia.
5, compensatory function after bleeding: when the amount of gastrointestinal bleeding exceeds 1/4 of the blood volume, the cardiac output and diastolic blood pressure drop significantly. At this time, the body accordingly releases a large amount of catecholamines, which increase the peripheral circulatory resistance and heart pulse rate to maintain the amount of blood perfusion in each organ. In addition to the cardiovascular response, the hormonal secretion and hematopoietic system compensate accordingly. Aldosterone and posterior pituitary hormone secretion increases to minimize intertissue water loss to restore and maintain blood volume.
(iii) Diagnosis of upper gastrointestinal bleeding
The diagnosis of upper gastrointestinal bleeding can be made on the basis of clinical manifestations of vomiting, black feces and hemorrhagic peripheral circulatory failure, a strong positive occult blood test in vomitus or black feces, and laboratory evidence of decreased hemoglobin concentration, red blood cell count and red blood cell pressure volume, but attention must be paid to the estimation of the severity of bleeding and the determination of the status of peripheral circulation. According to studies, adults with daily gastrointestinal bleeding >5-10 ml show positive fecal occult blood test, and black feces may appear with daily bleeding of 50-100 ml. Systemic symptoms, such as dizziness, panic and weakness, may appear when the bleeding volume exceeds 400-500 ml. If the bleeding volume exceeds 1000ml in a short period of time, peripheral circulatory failure may appear.
The most valuable criterion for estimating the severity of acute hemorrhage is the clinical manifestation of peripheral circulatory failure caused by blood volume reduction, which is the direct cause of death due to acute hemorrhage. Therefore, in patients with acute gastrointestinal hemorrhage, the examination of the status of peripheral circulation should be given priority, and the corresponding emergency treatment should be made accordingly. Blood pressure and heart rate are the key indicators, which need to be observed dynamically and judged by integrating other relevant indicators. If the patient’s blood pressure decreases (by more than 15-20mmHg) and heart rate increases (by more than l0 times/minute) when changing from lying to sitting position, it indicates that the blood volume is obviously insufficient and is an indication for emergency blood transfusion. If the systolic blood pressure is lower than 90 mmHg, heart rate is greater than 120 times/minute, accompanied by pale face, cold extremities, irritability or confusion, the patient has entered into shock, which is a serious massive bleeding and needs to be actively resuscitated.
It should be noted that although the frequency and amount of vomiting blood and black feces are helpful in estimating the amount of bleeding, it is not possible to make an accurate estimation of the amount of bleeding because most of the bleeding accumulates in the gastrointestinal tract and the vomiting blood and black feces are mixed with stomach contents and feces, respectively. In addition, routine blood tests including hemoglobin concentration, red blood cell count, and red blood cell pressure can estimate the extent of blood loss, but they do not reflect acute blood loss immediately and are influenced by the presence or absence of anemia prior to bleeding, so they can only be used as a reference for estimating the amount of bleeding. Since it takes several days (usually about 3 days) for the accumulated blood in the intestine to be drained, black stools cannot be used as an indicator of continued bleeding.
Continued bleeding or rebleeding should be considered in the following clinical situations.
(1) Recurrent vomiting of blood, or an increased number of black stools and thin stools with hyperactive bowel sounds.
(2) Manifestations of peripheral circulatory collapse that have not improved significantly with adequate rehydration and transfusion, or that have worsened despite temporary improvement.
(3) Continued decline in hemoglobin concentration, red blood cell count and red blood cell pressure volume, and persistent increase in reticulocyte count.
The diagnosis of the etiology of hemorrhage in the past history, symptoms and signs can provide important clues to the etiology of hemorrhage, but the diagnosis of the cause and site of hemorrhage needs to be confirmed by instrumental examination.
1. Clinical and laboratory tests provide clues
A past history of viral hepatitis, schistosomiasis or alcoholism with clinical manifestations of liver disease and portal hypertension may be a ruptured esophagogastric variceal bleeding. Abnormal liver function test results, routine blood leukocytes and thrombocytopenia can help to diagnose liver cirrhosis.
2.Gastroscopy is currently the preferred examination method to diagnose the cause of upper gastrointestinal bleeding.
Gastroscopy sequentially observes the esophagus, stomach, duodenum bulb up to the descending section under direct vision, so as to determine the site, cause and bleeding of the bleeding lesion. It is mostly advocated that the examination be performed within 24 to 48 h after bleeding, called emergency gastroscopy. It is generally believed that this can improve the accuracy of the diagnosis of the cause of bleeding. Emergency gastroscopy can also determine whether bleeding continues or estimate the risk of rebleeding based on the characteristics of the lesion, and endoscopic hemostasis can be performed at the same time. Before emergency gastroscopy, it is necessary to replenish blood volume, correct shock and improve anemia, and try to perform it in the interval of bleeding.
3.Barium X-ray examination
Barium X-ray examination has been replaced by gastroscopy, so it is mainly applied to those who have contraindications to gastroscopy or are unwilling to undergo gastroscopy. The examination is usually carried out several days after the bleeding has stopped.
4.Other tests
Selective arteriography, radionuclide 99mTc-labeled red blood cell scan and small intestinal microscopy are mainly applied to unexplained gastrointestinal bleeding. Since gastroscopy has been able to thoroughly search for gastrointestinal lesions above the descending duodenum, the above tests are rarely used for the diagnosis of upper gastrointestinal bleeding.
According to clinical data, about 80%-85% of patients with acute massive upper gastrointestinal bleeding can stop bleeding spontaneously within a short period of time without special treatment except for supportive therapy. Only l5-z20 % of patients have persistent or recurrent bleeding, and it is mainly this group of patients who die due to bleeding complications. Early identification of patients with high risk of rebleeding and death, intensive monitoring and active treatment become the focus of the management of acute massive upper gastrointestinal bleeding. In addition, biliary bleeding caused by hepatocellular carcinoma is extremely rare, so it is easy to be ignored or misdiagnosed. Ultrasound and CT examination can be performed to further clarify the diagnosis. Generally, ultrasound examination can clarify the diagnosis; if ultrasound cannot clarify, CT examination can be performed.