fluctuating urine flow
Introduction
Introduction Abdominal aortic aneurysm, which is an arterial dilatation disease, is the most common type of aneurysm. In recent years, the incidence of abdominal aortic aneurysms in China has shown an upward trend. Statistics show that among elderly people over the age of 65, the incidence of abdominal aortic aneurysm is about 8.8%. Moreover, many patients have sudden aneurysm rupture without any symptoms, and the mortality rate of patients with such tumor rupture can reach more than 90%. Therefore, the medical community also refers to the abdominal aortic aneurysm as a "time bomb" in the human body. Most patients with abdominal aortic aneurysm have no symptoms and are often referred to as a quiet abdominal aortic aneurysm when performing routine physical examination. With the development of regular physical examinations, it has been found that this type of aneurysm is also gradually increasing in symptomatic patients. The common symptoms are abdominal pulsating masses, followed by dull pain in the umbilical or upper abdomen or only abdominal discomfort. When the aneurysm invades the lumbar vertebrae, there may be pain in the lumbosacral region. Sometimes the aneurysm may enlarge or even penetrate into the duodenum or jejunum, thereby producing gastrointestinal bleeding. In addition, the enlargement of the tumor may produce some compression symptoms such as compression of the gallbladder. The general canal has jaundice; oppression of the duodenum causes intestinal obstruction; compression of the ureter causes renal colic or hematuria; when the bladder is compressed, there may be frequent urination and fluctuations in urine flow. The pattern of urination should be normal in the shape of a bell, smoothing up to the maximum urinary flow rate, and smoothing out. When urinating is difficult, it sometimes breaks, and the graph will appear fluctuating. Some people will use the abdomen to force, and the shape will also see jagged shape, which can provide doctors' diagnosis.
Cause
Cause
(1) Causes of the disease
Atherosclerosis is considered to be the most basic cause of abdominal aortic aneurysms. The abdominal aorta below the renal artery opening is the most common site of atherosclerosis, and is the most easily formed part of the aneurysm, and often extends to the aortic bifurcation. Only 2% to 5% of abdominal aortic aneurysms occur. Above the renal artery opening, the latter is mostly caused by the extension of the thoracic aortic aneurysm to the abdominal aorta.
Hereditary factors play a role in the development of abdominal aortic aneurysms. It is reported that about 28% of patients have hereditary diseases among first-degree relatives. Further studies have also shown that the defects of cell tissue are also the pathogenesis of abdominal aortic aneurysm, which can show the middle layer of elastic fiber rupture and inflammatory reaction in the aorta, and there are a large number of infiltration of macrophages and cell active substances.
(two) pathogenesis
To understand the formation of abdominal aortic aneurysms, we should first understand the structure of the normal arterial wall. Elastin and collagen are the most important structural components of the aortic wall, and together with smooth muscle cells constitute the medial membrane of the aorta. Under normal circumstances, elastin is a folded sieve-like structure. When external force is applied, it can stretch 70% than its natural length, providing longitudinal retraction traction for the artery and traction to maintain the normal cross-sectional area of the artery in the circumferential direction. It is the first-order force of the arterial wall to withstand the pressure load. Degradation is a key initial step in the formation of tumor-like expansion of the arteries. The main forms of collagen in the arterial wall are collagen types I and III. The collagen fiber is composed of three spiral-wrapped polypeptide chains. Although the stretchability is small, the tensile strength is 20 times larger than that of the elastic fiber, and its function is to maintain the tensile strength of the arterial wall. In the normal structure, the collagen of the aorta is enclosed in the form of an elastin load, making the aorta an elastic duct that is easy to stretch. When the load increases and the blood vessels continue to stretch, the collagen fibers expand spirally and act as a load-bearing component, supplementing the action of elastin to reduce the expansion of blood vessels. Elastin is the main bearer of the load, and collagen acts as a reserve, acting as a secure network with little and no expansion. The matrix layer formed by the two has a clear boundary for the pressure load. Abnormalities in genetics, degradation of elastin and collagen, destruction of matrix junctions by arteriosclerosis, and increasing pulse pressure are concentrated in this layer, exceeding a certain limit, leading to the formation of abdominal aortic aneurysms.
1. The role of arteriosclerosis Because abdominal aortic aneurysm and arteriosclerosis mainly occur in the elderly population, the two often coexist, so people have always believed that abdominal aortic aneurysm is the result of the evolution of arteriosclerosis, and often describes it as "arteriosclerosis Sexual abdominal aortic aneurysm." Studies have shown that atherosclerosis is associated with the formation and expansion of aneurysms. Its possible mechanisms mainly have the following three aspects. First of all, due to the lack of nourishing blood vessels, the nutritional supply of the abdominal aorta wall is mainly derived from the diffusion of blood in the lumen, and the formation of arteriosclerotic plaque and its attached thrombus is bound to cause obstacles in the dispersion of nutrients, leading to the intima of the artery. Necrosis of the membrane makes the wall weak and easy to form an aneurysm. Secondly, after the atherosclerotic plaque is detached, the naked smooth muscle cells will activate collagenase, which will degrade a large amount of collagen, which is one of the factors leading to weak membrane formation in the aortic wall. In addition, in areas of low shear stress (such as above the bifurcation of the aorta), the blood flow is distorted, the hardening factor in the blood is prolonged in contact with the wall, and the hardened plaque and its attached thrombus cause two fistulas at the bifurcation. The total arterial diameter is narrower, so that the aortic wall is subjected to greater reflex pressure, and it is also easy to induce aneurysm formation.
The results of Allardice et al. showed that the incidence of abdominal aortic aneurysm was significantly increased in patients with sclerotic performance in the leg and neck arteries, and Gaspar found that in the study of patients undergoing abdominal aortic aneurysm surgery, 44% of patients have atherosclerotic disease at the same time.
Although recent studies suggest that arteriosclerosis is likely to be a disease that coexists with abdominal aortic aneurysms, it plays a role in its formation and development. However, most studies and clinical data show that arteriosclerosis is still the most common and most important cause of abdominal aortic aneurysm.
2. The structural defects of the abdominal aorta and the structural components of the aortic wall are the weakening of the wall of the abdominal aorta, which is an indispensable local factor for the formation of abdominal aortic aneurysm. First, compared with the aorta, the abdominal aorta wall is weak, and the number of elastin layers is significantly reduced, often below 40 layers. Experiments have shown that when the aortic layer of the aorta is destroyed to below 40 layers, it is easy to form an aneurysm. The half-life of elastin is 70 years, which is consistent with the peak incidence of clinical aneurysms. Secondly, the abdominal aorta has fewer nourishing blood vessels, and the nutrient supply of the membrane and the intima is mainly derived from the diffusion of blood in the lumen. When there is atherosclerotic plaque formation, it can lead to dysfunction of nutrient dispersal, so that the intima and medial membrane are necrotic and the wall becomes weak. Again, the repair capacity of the abdominal aortic wall is weak. Smooth muscle cells play an important role in the repair of damaged blood vessel walls. The cell needs to synthesize collagen and elastin under the stimulation of pulse pressure. Due to the greater stiffness of the abdominal aorta, the shock pressure of the pulsed pressure on smooth muscle cells is reduced, and the synthetic motility is decreased. In addition, after the angioblastic neoplastic expansion, many smooth muscle cells are replaced by fibrotic connective tissue. The synthesis of collagen and elastin is reduced. Quantitative analysis showed that elastic fibers accounted for 35% of the dry weight tissue in the middle layer of normal aorta, but only 8% in patients with aneurysms. Existing animal models have demonstrated that intra-arterial infusion of elastase or laparotomy exposure of a portion of the abdominal aorta with elastase and destruction of elastin can lead to the formation of abdominal aortic aneurysms. Loosemore et al. also provided changes in collagen protein and amount in 1988, which may be evidence of the basis of aneurysm formation. In this way, the matrix of the arterial wall is continuously inactivated and degraded, and at the same time, effective nutrition and timely supplementation and repair are not obtained, so that the arterial wall is continuously thinned and the strength is lowered, eventually leading to the appearance of an aneurysm.
The local load of the abdominal aorta increases, and it plays an important role in the formation of an aneurysm. In the aortic system, from the proximal end to the distal end, the compliance gradually decreases, and its congenital upper and lower narrow vertebrae structure, the pressure on the aortic wall gradually increases from top to bottom. In addition, blood pressure pulses to the peripheral vascular arteries are reflected and amplified in the abdominal aorta. The size depends on the ratio of the aorta and the diameter of the vessel after the bifurcation. This reflection is minimal when the sum of the diameters of the two common iliac arteries is 1.1 to 1.2 times the diameter of the abdominal aorta. As the age increases, the proportion gradually declines, and has dropped to 0.75 at the age of 50. Clinically, the incidence of abdominal aortic aneurysm below the renal artery is the highest, because in elderly patients often accompanied by arteriosclerotic disease, arteriosclerotic plaque and its wall thrombus, the two common iliac arteries at the bifurcation The caliber is narrower, so that the abdominal aorta segment below the level of the renal artery is subjected to greater reflex pressure, and the retention time of the local sclerosis factor is longer, so that the incidence of the aneurysm is significantly increased.
3. The role of genetic factors has shown that abdominal aortic aneurysms have a family-genetic tendency. Johnson and Koepsell compared the family history of 250 patients with abdominal aortic aneurysm and controls, and found that 19.2% of patients had a first-degree blood relationship with known aneurysms, compared with only 2.4% of controls. The risk of illness has increased by 11.6%, especially for siblings. Abdominal aortic aneurysm is mainly characterized by the sexual inheritance of the X chromosome and autosomal dominant inheritance. The genetic defects of elastin and collagen directly cause the weakening of the aortic wall, and the genetic changes of various enzymes increase the inactivation and degradation of the matrix structure protein of the arterial wall, and the integration of the integration is destroyed. A weakened arterial wall, such as a thoracic and abdominal aortic aneurysm that occurs in Marfan syndrome.
(1) Genetic variation associated with elastin degradation: The genetic variation of elastin has not been confirmed in aneurysm patients. What is clear now is the variation of the haptoglobin gene on the long arm of the 16th autosome and the cholesterol ester transfer protein gene adjacent thereto. In patients with abdominal aortic aneurysm, the frequency of expression of the globin 1 allele is significantly increased, resulting in increased synthesis of haptoglobin, which promotes the degradation of elastin by elastase, thereby affecting the integrity of the connective tissue of the arterial wall. Sex, leading to the occurrence of an aneurysm. The variation of the cholesterol ester transfer protein gene can affect lipid metabolism, lowering the concentration of high-density lipoprotein (HDL) in the blood of patients, and increasing the concentration of triglyceride and low-density lipoprotein (LDL), leading to arteriosclerosis. The emergence of indirect promotion of aneurysm formation and development.
Corresponding to this is the loss of 1-AT (1 antitrypsinogen) gene expression. 1-AT is the main inhibitor of elastase. About 35% of the gene phenotype responsible for 1-AT is a monozygous gene, and this gene phenotype is not expressed in about 90% of patients with abdominal aortic aneurysm, resulting in a significant decrease in the inhibition level of 1-AT. The activity of elastase is significantly increased, a large amount of elastin is degraded, the aortic wall becomes weak, and the occurrence and development of aneurysm is easy.
(2) Gene mutations related to collagen and its metabolism: One or a single base of the type III collagen gene is mutated, and the glycine at position 619 is replaced by arginine, which can cause abnormal expression of type III collagen. Experiments have shown that this is associated with the formation of abdominal aortic aneurysms. However, since the mutation of the gene appears to be personalized, it has not been confirmed in the majority of patients. A recent study on genetic variation in 54 patients with abdominal aortic aneurysm suggests that the gene mutation of type III procollagen is only present in a small number of patients, but the replacement of a single amino acid residue can also cause profound geological changes in collagen. This gene mutation plays an important role in the pathogenesis of abdominal aortic aneurysm.
The gene for the collagenase inhibitor associated with collagen metabolism is located on the X chromosome. In patients with abdominal aortic aneurysm, the gene is deleted, the synthesis of collagen inhibitor is reduced, the level of collagenase inhibition is reduced, and finally the degradation of collagen is significantly increased, the arterial wall is weak, and aneurysm is formed.
In short, the inheritance of abdominal aortic aneurysm is a very complex multi-factor mechanism involving several different genes. It is precisely because of the synergistic effect of these genes that the occurrence and development of aneurysms.
4. The role of enzyme chemistry
(1) The role of elastase: The results showed that the content and activity of elastase in the wall of patients with abdominal aortic aneurysm were higher than those in patients with aortic occlusion. In addition, after arteriosclerosis occurs, smooth muscle cells of the arterial wall are stimulated to produce and secrete SME in large amounts. The large increase of these two types of elastase causes the degradation rate of elastin to be abnormally increased, and the normal folded sieve-like structure is destroyed, and sufficient elastic traction force is not provided in the longitudinal direction and the circumferential direction, thereby causing distortion of the artery. Further expansion into tumor. The lysis of the elastic connecting tissue in the entire aortic wall lays the foundation for the formation of aneurysm. In addition to being affected by genetic factors, the increase in elastase activity is also affected by many environmental factors. Studies have shown that smoking, trauma, high blood pressure, etc. can promote the activity of elastase by a factor of two.
(2) The role of collagenase: Studies have shown that the concentration and activity of collagenase in the aortic wall of patients with abdominal aortic aneurysm increase. Its possible mechanism is the loss of collagenase inhibitor gene expression. In addition, when the elastin is degraded, the balloon-like tumor formed by the artery can also activate collagenase. Under the action of collagenase with increased concentration and activity, the normal structure of collagen is destroyed, the degradation is significantly increased, and the tensile strength of the arterial wall is significantly reduced. When the collagen is depleted, it cannot be transferred due to the inactivation of elastin. The aneurysm ruptures under pressure loading.
(3) The role of metalloenzymes: In 1984, Tilson et al. found in the animal model of abdominal aortic aneurysm that the lack of copper metabolism in mice caused a decrease in the activity of a copper-containing metalloenzyme, dissolved oxidase. This enzyme plays an important role in the integrated connection of collagen and elastin. It is suggested that the lack of this enzyme will lead to weak aortic wall and easy aneurysm. In patients with Menkes syndrome, the reduction of elastic tissue of the arterial wall and the abnormality of copper metabolism were also found, indicating that the abnormality of metalloenzyme plays a certain role in the pathogenesis of abdominal aortic aneurysm. In 1994, Karen et al. found that zinc-related matrix metalloproteinases MMP-3 and MMP-9 were active in patients with abdominal aortic aneurysms, which are responsible for the degradation of matrix components in the vessel wall, while the arteries Destruction of the normal matrix component of the wall will result in a weakened arterial wall and an aneurysm in severe cases.
5. Risk factors Many factors above are the basic conditions for the formation of abdominal aortic aneurysm, and various risk factors play a role in the development of aneurysms.
(1) Smoking: It is clear that smoking is closely related to abdominal aortic aneurysm more than 20 years ago. The incidence of abdominal aortic aneurysm increases with the increase of cigarette consumption. In addition to being associated with various toxic components in cigarette tar, the gaseous substances produced by the burning of tobacco can be oxidized to methionine sulfoxide after being absorbed into the blood, thereby inactivating 1-AT and increasing the activity of proteolytic enzymes. Aggravation of the degradation of aortic wall elastin causes a weakening of the aortic wall strength, leading to the occurrence and development of aneurysms. Statistics show that smokers die from aneurysm rupture four times more than non-smokers, and smoking sputum sputum is up to 14 times more than the latter. (2) Inflammatory reaction: In 4% to 10% of patients with abdominal aortic aneurysm, it is found that it has a thick white tumor wall and is closely adhered to the surrounding. This is called "inflammatory abdominal aortic aneurysm". It is characterized by a large amount of inflammatory cell infiltration, often spreading to the surrounding tissue outside the aortic wall. It is currently believed that this aneurysm change is an autoimmune reaction of the components of the arterial wall, and the lipid oxidation product, waxy, is exuded from adjacent tissues.
Histological examination of the aortic wall of any aneurysm can be seen with varying degrees of inflammatory infiltration, and the extent of inflammatory infiltration of lymphocytes and histiocytes in the adventitia and media is the same as the tenderness and enlargement of the palpation Arterial diameter related. Recent studies have shown that macrophages and activated T and B lymphocytes are involved in chronic inflammatory responses. TL-1B and TNF- secreted by macrophages play an important role in the process of inflammation. They can stimulate the production of metalloproteinases, promote the degradation of connective tissue, thereby weakening and destroying the middle layer of the aorta, and inflammation may be one of the causes of abdominal aortic aneurysm.
(3) Impact of trauma: It was reported in the literature that 10 patients had rupture of abdominal aortic aneurysm within 36 hours after exploratory laparotomy. It is likely that the exploratory laparotomy disrupts the dynamic balance between stromal and connective tissue anabolism and catabolism, and is a risk factor for rupture of aneurysms. Studies have shown that surgical trauma such as intestinal resection, exploratory laparotomy, etc. can cause a significant increase in aortic elastase activity.
(4) The role of hypertension: Hypertension is also a risk factor for abdominal aortic aneurysm, which is associated with increased morbidity and increased risk of rupture. Recent studies on a mouse model of abdominal aortic aneurysm have shown that the presence of hypertension is a basic condition for aneurysm formation, especially systolic hypertension plays an important role in the formation of aortic aneurysm. However, whether hypertension is involved in the formation of an aneurysm or only the expansion of the aortic wall that has been weakened has not yet reached a definitive conclusion.
(5) Effects of advanced age: Abdominal aortic aneurysm is an senile disease, which is rare in people under 50 years old. Under normal circumstances, changes in the structure of the arterial wall are accompanied by age. As the age increases, the elastin fibers of the arterial wall degrade, break and calcify. The aging aortic wall is unable to resist the effects of aortic aneurysm expansion, and thus causes an aortic aneurysm in the elderly.
In summary, the occurrence and development of abdominal aortic aneurysm is an inevitable result of many long-term interactions between factors that cause weak aortic wall and increase its load. Degradation and inactivation of elastin will lead to the formation of abdominal aortic aneurysms, which is a key factor in tumor formation. The depletion of collagen stores can cause irreversible, continuous aneurysm expansion, and even the final rupture. Risk factors such as smoking, inflammation, trauma, advanced age, and hypertension have a positive effect on the occurrence and development of abdominal aortic aneurysm.
The diagnosis of abdominal aortic aneurysm depends mainly on clinical symptoms and in combination with invasive or noninvasive examinations in order to make a correct diagnosis. Abdominal aortic aneurysms are also increasing with age and arteriosclerosis. How to screen out such patients in clinical practice, early diagnosis and early treatment are still urgent problems to be solved. In the diagnosis, the medical history, physical examination and organic imaging examination are still emphasized to make a correct diagnosis. Otherwise, simply emphasizing clinical manifestations or imaging examinations is not conducive to diagnosis and treatment.
6. Pathology
Abdominal aortic aneurysm walls are generally single spherical or prismatic, and there are many. Histological examination showed that the aneurysm wall was broken by elastic fibers and the content of elastin was reduced; the chronic inflammation of the media and the outer membrane, and the infiltration of B lymphocytes and plasma cells. It also contains a large amount of immunoglobulin, suggesting an autoimmune response. Regardless of the aneurysm wall, the intima disappears and the elastic layer breaks. When the intra-arterial pressure exceeds the expansion limit of the arterial wall, the aneurysm will rupture. Almost all abdominal aortic aneurysm has blood clots, blood clots can be mechanized and infected, and blood clots can cause distal arterial embolization. B-mode ultrasound scan was used to follow up the abdominal aortic aneurysm, and the diameter of the tumor was found to increase by an average of 3.8 mm per year. Traumatic aneurysms, infectious aneurysms, and anastomotic pseudoaneurysms are arterial pulsating hematomas formed after rupture of the arterial wall, all of which are pseudoaneurysms.
Pathological type:
(1) Classification: According to the structure of the aneurysm wall, it can be divided into three categories:
1 true aneurysm: the structure of each layer of the tumor wall is complete, and the cause is mostly arteriosclerosis.
2 pseudoaneurysm: formed after arterial rupture, no complete arterial wall structure, the tumor wall is composed of part of arterial intima and fibrous tissue, blood flow in the tumor cavity through the arterial rupture and the real lumen of the arteries, clinically more common in Traumatic aneurysm.
3 dissection aneurysm: After the rupture of the intima of the artery, the arterial blood flows through the intima of the artery and the middle membrane, so that the arterial wall separates and bulges, and the endometrium of the distal artery of the tumor can be broken, and the true cavity of the artery Interconnected, sandwiched double cavity. Affinity can form a wall thrombus in the aneurysm, which can be secondary to infection. The weak wall of the tumor can be ruptured, causing serious bleeding and life-threatening.
(2) Classification: According to the different parts of the tumor invasion, abdominal aortic aneurysm can be divided into 2 types:
1 High abdominal aortic aneurysm above the level of renal artery opening, also known as thoracic and abdominal aortic aneurysm and suprarenal abdominal aortic aneurysm.
2 Aneurysm is located below the level of renal artery opening, called abdominal aortic aneurysm or sub-renal abdominal aortic aneurysm. Clinically, it is more common in the abdominal aortic aneurysm below the level of the renal artery and above the radial artery. This type of aneurysm has a normal arterial wall near the distal end, which provides favorable conditions for surgical treatment.
Examine
an examination
Related inspection
Urine routine
1. Pain: Pain is a common clinical symptom of abdominal aortic aneurysm, and about one-third of patients show pain. Most of its location is located in the umbilical circumference of the abdomen, two ribs or the waist. The nature of the pain may be dull pain, pain, tingling or knife-like pain. It is generally believed that pain is an increase in the tension of the tumor wall, causing traction of the adventitia and posterior peritoneum, and compression of adjacent somatic nerves. A huge abdominal aortic aneurysm can also cause radiculopathy when the tumor erodes the spine. It is worth noting that sudden severe abdominal pain is often a characteristic manifestation of ruptured abdominal aortic aneurysm or acute. The characteristics of pain caused by acute dilatation of abdominal aortic aneurysm are very similar to their rupture and are difficult to distinguish. The pain is persistent, painful for severe knife cuts, and not relieved by changes in body position. Only the pain that occurs when the abdominal aortic aneurysm is acutely dilated is often associated with hypotension or shock. Because the performance of pain is so important, sudden abdominal pain in the abdominal aortic aneurysm is considered the most dangerous signal. Pain is closely linked to surgical indications and is associated with mortality from surgery. In general, patients with pain-free non-ruptured abdominal aortic aneurysm have a mortality rate of 4.9% in elective surgery, and in patients with pain and non-rupture, the mortality rate is as high as 26.5%, especially in patients with pain and tenderness. More than twice as many patients with abdominal pain.
Because abdominal aortic aneurysm has a variety of pain manifestations and is not specific, it often leads to misdiagnosis and rapid deterioration of the condition. In a few cases, a patient with a controlled rupture of the abdominal aortic aneurysm (hematoma obstruction rupture, etc.), due to a small amount of blood loss and reflex tachycardia, may be associated with angina symptoms, which must be well differentiated to prevent misdiagnosis.
2. Compression symptoms: With the continuous expansion of abdominal aortic aneurysm, it is possible to oppress adjacent organs and cause corresponding symptoms, which is more common in clinical practice.
(1) Intestinal compression symptoms: This is the most commonly compressed organ of abdominal aortic aneurysm. Due to the small activity of the duodenum, symptoms can be early due to oppression. Can show abdominal discomfort, fullness, loss of appetite, severe cases of nausea, vomiting, cessation of exhaustion and other symptoms such as incomplete or complete intestinal obstruction. Mostly misdiagnosed as other diseases of the gastrointestinal tract, delaying the early diagnosis of abdominal aortic aneurysm.
(2) urinary system compression symptoms: due to abdominal aortic aneurysm compression or inflammatory abdominal aortic aneurysm invading into the ureter, ureteral obstruction, renal pelvic effusion, and the incidence of urinary stones will also increase, may appear The pain in the lower back and even the severe abdominal pain that is released into the groin area. And may be accompanied by hematuria. Due to the anatomical relationship, the left ureter is most susceptible.
(3) Symptoms of bile duct compression: It is relatively rare in clinical practice, and patients often show discomfort in the liver area and tired of greasy food. In severe cases, yellow staining of the skin and sclera of the whole body may occur, and the urine may be reddish and the stool is terracotta. Biochemical examination showed a change in obstructive jaundice.
3. Embolism symptoms: The thrombus of abdominal aortic aneurysm becomes an embolus once it has fallen off, embolizing the blood supply organs or limbs and causing acute ischemic symptoms corresponding to it. If the embolization site is mesenteric blood vessels, it shows intestinal ischemia, and severe cases can cause intestinal necrosis. The patient developed severe abdominal pain and bloody stools, which in turn showed hypotension and shock, as well as abdominal peritoneal irritation. Embolization into the renal artery can cause infarction in the corresponding part of the kidney, and the patient presents with severe low back pain and hematuria. When embolized to the main artery of the lower extremity, the pain of the corresponding limb occurs, the pulse is weakened and disappeared, the limb is paralyzed, the color is pale, and the sensory abnormality is observed.
4. Abdominal pulsatile mass: This is the most common and most important sign of abdominal aortic aneurysm. Most patients feel pulsating around the heart or around the umbilicus. About one in six patients report that the heart falls to the abdominal cavity. This pulsation is particularly prominent in the supine position and at night. The mass is mostly located in the left abdomen, with a continuous and pulsating and expanding sensation in multiple directions. The upper boundary between the mass and the rib arch can accommodate two horizontal fingers, often indicating that the lesion is below the renal artery. If there is no gap, it indicates that the aneurysm is mostly located above the renal artery. At the same time, palpation of the abdomen is the simplest and most effective method for diagnosing abdominal aortic aneurysm. The accuracy rate is between 30% and 90%. Although the abdominal aortic aneurysm can be diagnosed by touching the abdominal pulsatile mass, the size and extent of the tumor still need to be confirmed by other auxiliary examinations. The surface of the mass can be tender, and systolic murmurs and/or convulsions and tremors can be heard. Partial obesity, ascites, and uncooperative patients may lead to failure of palpation of abdominal aortic aneurysms. Of course, clinically, it is necessary to distinguish from pancreatic masses, cystic lesions of the posterior abdominal wall or aortic distorted.
5. Rupture symptoms: Abruption of abdominal aortic aneurysm is an extremely dangerous surgical emergency. The mortality rate is as high as 50% to 80%. The diameter of an aneurysm is the most important factor in determining rupture. According to Laplace's law, the load pressure of the tube wall is proportional to the radius of the tumor. The larger the diameter of the tumor, the greater the risk of rupture. The data showed that the rupture rate of abdominal aortic aneurysm within 5 years was 10% to 15% of the diameter of the tumor within 4 cm, 20% within 5 cm, 33% of 6 cm, and 75% to 95% of 7 cm or more. According to the relationship between the rupture rate of abdominal aortic aneurysm and the diameter of the tumor, a person with a diameter of 6 cm or more is called a dangerous aneurysm. However, a large number of recent imaging observations have shown that when the diameter of the abdominal aortic aneurysm reaches 5 cm, the risk of rupture is significantly increased. This view has been agreed by the vascular surgery community.
A study by Gronenwet et al found that the risk of ruptured abdominal aortic aneurysm was significantly increased in patients with chronic obstructive pulmonary disease and systolic hypertension. Although the rate of expansion of small aneurysms is not well predicted, the results of vascular ultrasound and CT have shown that the rate of expansion of aneurysms is also significantly increased in patients with increased pulse pressure differences. The annual average expansion rate is 0.4 cm in anteroposterior diameter and 0.5 cm in transverse diameter. In the average patient, the anteroposterior diameter is only 0.19 cm and the transverse diameter is only 0.22 cm. Usually, the aneurysm expands in the lateral direction more than the anterior-posterior direction, so the cross-section of the aneurysm is mostly elliptical, which coincides with the fact that the lateral aortic aneurysm ruptures.
The clinical symptoms and duration of rupture of the abdominal aortic aneurysm are determined by the specific circumstances of the rupture. In general, a typical abdominal aortic aneurysm rupture has the following triads: sudden mid-abdominal or diffuse abdominal pain, hypotension, and even mild to severe hemorrhagic shock and pulsatile abdominal mass. There are five ways of rupture in abdominal aortic aneurysm. Clinical manifestations vary according to their specific methods.
(1) Open rupture into the abdominal cavity: mostly the rupture of the anterior wall of the tumor. The clinical manifestations are mainly severe hemorrhagic shock, which is difficult to treat, and the patient died more quickly than in the short term. Most patients die before arriving at the hospital. Therefore, the actual incidence rate is higher than the clinical statistics. (2) retroperitoneal rupture: mostly the rupture of the posterior wall of the aneurysm, into the retroperitoneal space, forming a retroperitoneal hematoma. The patient presented with pain in the mid-abdominal knife, and about a quarter of the patients were mainly painful in the waist and ribs, and were released to the groin area and thigh roots, accompanied by cold sweat, pale complexion, pulse breakdown and other blood loss. The performance of sexual shock. It is easy to be confused with diseases such as acute pancreatitis, mesenteric vascular embolism, peptic ulcer perforation and dissecting aneurysm, so it should be well identified.
(3) Restrictive rupture: that is, the ruptured hole is blocked by hematoma, and its clinical manifestation is similar to that of retroperitoneal rupture. The duration is short for about ten minutes and the length can be longer than 24 hours. Chronic restrictive rupture can sometimes be misdiagnosed as inguinal hernia, femoral neuropathy, and the like. It will eventually develop into an open rupture, so early diagnosis and surgical treatment should be made.
(4) rupture into the intestinal lumen: the formation of the primary abdominal aorta. Clinical manifestations include gastrointestinal bleeding, abdominal pain, and infection. The patient had a few days or weeks of intermittent gastrointestinal tract bleeding, which eventually led to major bleeding and shock. Especially in male patients, hemorrhagic anemia is its main feature, and the symptoms of abdominal pain are relatively mild. The fever is often relaxation heat, and the blood culture bacteria are consistent with the normal intestinal flora. In a few cases, intestinal bacteria spread down the blood and can form septic arthritis or a localized infection of the lower extremities.
(5) rupture of the inferior vena cava or iliac vein: formation of aortic-inferior vena cava or aortic-iliac vein fistula. Its clinical incidence is less than 1%. Most occur in large abdominal aortic aneurysms. Patients may have congestive heart failure, varicose veins of the lower extremities, and some patients have large sputum and produce myocardial insufficiency, and clinical manifestations of left heart failure. Individual patients have oliguric renal failure. Abdominal examination, tremor can be touched at the proximal end of the pulsatile mass, auscultation can be heard and continuous murmur, but usually systolic murmur.
According to the slow onset of the disease, the periumpanal or mid-abdominal hernia and the swelling pulsation can be accompanied by acute or chronic ischemic symptoms of the lower extremity; the abdominal percussive tumor has mild tenderness, and some cases are Abdominal aortic aneurysms can be suspected by hearing vascular murmurs and tremors. Further color ultrasonography, CT examination or magnetic resonance examination showed the diameter of the abdominal aortic aneurysm, the relationship with adjacent tissues, and abdominal aorta angiography if necessary to further confirm the diagnosis.
Diagnosis
Differential diagnosis
The diagnosis should be differentiated from the following symptoms:
1. The urine flow becomes thin or interrupted: acute prostatitis urinary tract symptoms: burning pain during urination, urgency, frequent urination, urine drip and purulent urethral secretions. Bladder neck edema can cause poor urination, fine or interrupted urinary flow, and severe urinary retention.
2. Interrupted urinary flow: interruption of urinary flow means sudden interruption of urinary flow during urination, sometimes accompanied by severe pain in the head of the penis. The most common cause is that patients with benign prostatic hyperplasia must increase their abdominal muscles to drain their urine. In the late stage of the disease, the urine can not be drained at one time, and it takes a breath to continue to urinate, which is manifested as interruption of the urine flow. Patients with bladder stones, bladder tumors, bladder foreign bodies, ureteral cysts and other diseases during the urination process, stones, tumors or ureteral cysts, foreign bodies, etc. can continue to urinate after moving with the urine flow.
During the urination of patients with giant bladder diverticulum, vesicoureteral reflux, and ureteral effusion, although most of the urine has been excreted, a significant portion of the urine is still in the diverticulum or ureter. After the end of urination, this part of the urine quickly enters the bladder again, and produces urine, and urinates again. This condition is called two-stage urination, not interruption of urine flow.
3. Slow urine flow: The reason why women are susceptible to urinary tract infection is mainly because of the particularity of female reproductive system structure, female vaginal secretion is also a better medium, the use of bacteria is easier to breed, the urine flow is slow to form light Degree of fluid accumulation and other aspects.
Urinary tract infection, also known as urinary tract infection, refers to the urinary tract inflammation caused by pathogens growing in the urinary tract of the body and invading the mucosa or tissues of the urinary tract. Bacteria are the most common pathogens, and fungi, viruses, parasites, etc. can also cause infection.
1. Pain: Pain is a common clinical symptom of abdominal aortic aneurysm, and about one-third of patients show pain. Most of its location is located in the umbilical circumference of the abdomen, two ribs or the waist. The nature of the pain may be dull pain, pain, tingling or knife-like pain. It is generally believed that pain is an increase in the tension of the tumor wall, causing traction of the adventitia and posterior peritoneum, and compression of adjacent somatic nerves. A huge abdominal aortic aneurysm can also cause radiculopathy when the tumor erodes the spine. It is worth noting that sudden severe abdominal pain is often a characteristic manifestation of ruptured abdominal aortic aneurysm or acute. The characteristics of pain caused by acute dilatation of abdominal aortic aneurysm are very similar to their rupture and are difficult to distinguish. The pain is persistent, painful for severe knife cuts, and not relieved by changes in body position. Only the pain that occurs when the abdominal aortic aneurysm is acutely dilated is often associated with hypotension or shock. Because the performance of pain is so important, sudden abdominal pain in the abdominal aortic aneurysm is considered the most dangerous signal. Pain is closely linked to surgical indications and is associated with mortality from surgery. In general, patients with pain-free non-ruptured abdominal aortic aneurysm have a mortality rate of 4.9% in elective surgery, and in patients with pain and non-rupture, the mortality rate is as high as 26.5%, especially in patients with pain and tenderness. More than twice as many patients with abdominal pain.
Because abdominal aortic aneurysm has a variety of pain manifestations and is not specific, it often leads to misdiagnosis and rapid deterioration of the condition. In a few cases, a patient with a controlled rupture of the abdominal aortic aneurysm (hematoma obstruction rupture, etc.), due to a small amount of blood loss and reflex tachycardia, may be associated with angina symptoms, which must be well differentiated to prevent misdiagnosis.
2. Compression symptoms: With the continuous expansion of abdominal aortic aneurysm, it is possible to oppress adjacent organs and cause corresponding symptoms, which is more common in clinical practice.
(1) Intestinal compression symptoms: This is the most commonly compressed organ of abdominal aortic aneurysm. Due to the small activity of the duodenum, symptoms can be early due to oppression. Can show abdominal discomfort, fullness, loss of appetite, severe cases of nausea, vomiting, cessation of exhaustion and other symptoms such as incomplete or complete intestinal obstruction. Mostly misdiagnosed as other diseases of the gastrointestinal tract, delaying the early diagnosis of abdominal aortic aneurysm.
(2) urinary system compression symptoms: due to abdominal aortic aneurysm compression or inflammatory abdominal aortic aneurysm invading into the ureter, ureteral obstruction, renal pelvic effusion, and the incidence of urinary stones will also increase, may appear The pain in the lower back and even the severe abdominal pain that is released into the groin area. And may be accompanied by hematuria. Due to the anatomical relationship, the left ureter is most susceptible.
(3) Symptoms of bile duct compression: It is relatively rare in clinical practice, and patients often show discomfort in the liver area and tired of greasy food. In severe cases, yellow staining of the skin and sclera of the whole body may occur, and the urine may be reddish and the stool is terracotta. Biochemical examination showed a change in obstructive jaundice.
3. Embolism symptoms: The thrombus of abdominal aortic aneurysm becomes an embolus once it has fallen off, embolizing the blood supply organs or limbs and causing acute ischemic symptoms corresponding to it. If the embolization site is mesenteric blood vessels, it shows intestinal ischemia, and severe cases can cause intestinal necrosis. The patient developed severe abdominal pain and bloody stools, which in turn showed hypotension and shock, as well as abdominal peritoneal irritation. Embolization into the renal artery can cause infarction in the corresponding part of the kidney, and the patient presents with severe low back pain and hematuria. When embolized to the main artery of the lower extremity, the pain of the corresponding limb occurs, the pulse is weakened and disappeared, the limb is paralyzed, the color is pale, and the sensory abnormality is observed.
4. Abdominal pulsatile mass: This is the most common and most important sign of abdominal aortic aneurysm. Most patients feel pulsating around the heart or around the umbilicus. About one in six patients report that the heart falls to the abdominal cavity. This pulsation is particularly prominent in the supine position and at night. The mass is mostly located in the left abdomen, with a continuous and pulsating and expanding sensation in multiple directions. The upper boundary between the mass and the rib arch can accommodate two horizontal fingers, often indicating that the lesion is below the renal artery. If there is no gap, it indicates that the aneurysm is mostly located above the renal artery. At the same time, palpation of the abdomen is the simplest and most effective method for diagnosing abdominal aortic aneurysm. The accuracy rate is between 30% and 90%. Although the abdominal aortic aneurysm can be diagnosed by touching the abdominal pulsatile mass, the size and extent of the tumor still need to be confirmed by other auxiliary examinations. The surface of the mass can be tender, and systolic murmurs and/or convulsions and tremors can be heard. Partial obesity, ascites, and uncooperative patients may lead to failure of palpation of abdominal aortic aneurysms. Of course, clinically, it is necessary to distinguish from pancreatic masses, cystic lesions of the posterior abdominal wall or aortic distorted.
5.50%80%Laplace54cm10%15%5cm20%6cm33%7cm75%95%6cm5cm
GronenwetCT0.4cm0.5cm0.19cm0.22cm
5
(1)
(2)1/4
(3)24h
(4)
(5)--1%
;CT
