1, the concept of hemorrhoids in the 20th century, especially after the 1970s, with the progress of science and technology, people have a leap of understanding of hemorrhoids, has formed a new concept, that is: hemorrhoids are lip-like flab or analcushions at the lower end of the rectum (analcushions), is the normal structure of each person; anal cushions are arranged in the right front, right back and left side of the three lobes, and the rectum on the arterial branches have nothing to do. They are like the tricuspid valves of the heart, assisting the sphincter to maintain normal closure of the anal canal; pathological hypertrophy of the anal cushions is known as hemorrhoid disease. The principle of treatment of hemorrhoids is based mainly on symptoms; for asymptomatic hemorrhoids even if they are very large next door is not necessarily an indication for treatment; conversely, hemorrhoids must be treated if they are small but at risk of serious complications. The above concept was first proposed by Thomson in 1975 and supported by some famous scholars such as Melzier (1984), etc. It was unanimously confirmed at the 9th International Hemorrhoid Symposium held in Kölnberg, Germany in 1983. The new definition of hemorrhoids has been widely adopted in the newly published monographs on anorectology abroad. The embryology of hemorrhoids The anal cushion is also called the haemorrhoidalzone or zonacolumaris, and embryologists call this zone the cloacogeniczone or the transitionalzone, the invaginationalzone ). Since this zone is located at the union of anal canal and rectum, the embryonic progenitors of epithelium, glands, blood vessels and muscles are intertwined here, thus it has its morphological characteristics and is an important critical zone. 2.1 Rectal descent and anorectal lasso Early in the embryo, the end of the primitive rectum (of the hindgut) is located in the abdominal cavity and descends below the pelvic diaphragm in the third month of fetal life to come into contact with the original anal recess; then the original anal recess is lassoed upward into the lower end of the hindgut. At the sleeve, the hindgut mucosa is folded into a double layer, the inner side of which is the epithelium of the anal canal, and the three gradually fuse and thicken to form a ring-like spongy tissue band, i.e., the anal pad. Due to the contraction of the internal sphincter, the anal cushion is divided into the right anterior, right posterior and left side by the Y-shaped sulcus, which is usually called the “mother hemorrhoid” and its “favored site”. As early as 1954, Last found that the internal sphincter, which is the marker of the hindgut, and the external sphincter of the proximal anal cavity, were aligned up and down during fetal life, and became aligned inside and outside as the human embryo developed; therefore, early scholars used to call the former the upper sphincter and the latter the lower sphincter. The squamous epithelium of the proximal anus. The above findings can be used as a corroboration of anorectal condyloma. 2.2 Anal membrane rupture and ATZ epithelial formation Data suggest that the hemorrhoidal epithelium is the ATZ epithelium, and the occurrence of ATZ is related to the location of anal membrane rupture. The anal membrane is the septum between the primitive rectum and the protoanus, with the endoderm above the anal membrane and the ectoderm below. Previously, from an embryological point of view, it has been considered that the anal membrane ruptures at 8 weeks of gestation and the ectodermal squamous epithelium crawls upward to form the migrating epithelial zone, known as the ATZ. However, there are conflicting opinions regarding the location of anal membrane rupture, as Nobles (1984) observed; the morphology provided by the anal membrane to adults in early embryonic life is only approximate, because as the sphincter emerges and migrates, i.e., the ectodermal sphincter grows upward and the endodermal sphincter moves downward, the anal membrane attachment changes accordingly. Rupture of the anal membrane precedes the appearance of the anal flap (or dentary line). The earliest appearance of the anal flap is at approximately 30 mm of the human embryo. At the 35 mm stage of the human embryo, an overlapping zone of squamous and columnar epithelium appears at the upper border of the pectineal membrane to its union with the rectal mucosa, and this zone gradually expands to about 15 mm wide in adults. Therefore, there is not a clear demarcation line at the combination of anal canal and rectum, but an irregular area of interlacing squamous and columnar epithelium. Recent light and electron microscopic observations have shown that the ultrastructure of the ATZ epithelium is similar to that of the cloacal epithelium, thus confirming that the ATZ above the plane of the anal flap (or dentine) (anal cushion) represents the boundary between the endo- and ectodermal layers, i.e., the attachment of the anal membrane and the interface between the anal canal and the rectum. The rectal columnar epithelium stained blue, whereas the squamous epithelium of the anal canal did not contain mucin and did not stain. The migrating epithelium of the anal cushion contains less mucin and therefore stains light blue, which can be distinguished from the above two types of epithelium. In summary, from the point of view of occurrence, hemorrhoids are anorectal overlap development, is the normal structure of human anatomy. 3, hemorrhoidal epithelium The mucous membrane of the anal cushion is purplish red and turns pink at the borders with the rectum upwards. Histologically, the epithelium of the anal cushion is the migrating epithelium between the single layer of columnar epithelium and the double layer of squamous epithelium, the cells are columnar, cuboidal or hypocuboidal, in which there is still a single layer of columnar or double layer of squamous cells constituting the islets. Histochemical methods demonstrated a small amount of mucus on the surface of the columnar cells or within the more typical cup-shaped cells. The majority of squamous epithelium is undifferentiated, and in approximately 31.9% of the population, differentiated types, i.e. normal squamous epithelium, are seen, with a distribution area of at least 2 mm. In 1982, Fenger et al. found that the anal pad epithelium was lined with secretory silverophilic cells, i.e. EC cells, which appeared to be associated with its mucosal plexus, cutting off the pubic nerve, and that the silverophilic cells contained significantly less ribonucleic acid, suggesting that silverophilic cells have the potential to initiate afferent excitation regarding anal six atresia. In 1985, Toshoguchi et al. performed IgA tissue staining of anal pad resection specimens by the enzyme antibody method (PAP method) and found that within the epithelium of the anal pad, there were cells with moderate to highly scattered deep spindle staining. However, few deeply stained cells were seen in the rectal tissue above the anal pad. This suggests that IgA secretion in the epithelium of the anal cushion is hyperactive in the presence of inflammation in the anal canal area, and even after internal hemorrhoidectomy, IgA secretion is thought to be partly related to the prevention of infection. The Krause terminal bulb, Glogi-Mazzoni bodies, and Pacinian vesicles are abundant; the former is responsible for temperature sensation, the latter for tension and pressure changes, and the Meissner vesicles are relatively sparse in number and are responsible for mild tactile sensation. In addition, there are somatotopic sensory nerves that extend across the dentate line to the lower edge of the anal pad. The distribution of nerves in the anal pad differs from that of the skin and bears a distinct resemblance to the innervation of the mouth and lips. These nerves are important receptors in anal reflexes and have a fine discrimination of the nature of rectal contents, which may be a function of the internal rectal pressure. The sensory epithelium is able to discriminate the nature of the pressure and trigger the try reflex. Therefore, although the receptors of the anal pad area are small, they have a protective function because they can alert the anal canal when stool is approaching. It is worth noting that the ATZ epithelium is a highly specialized sensory nerve terminal zone, which is very sensitive and is the center of evoked defecation sensation, also known as the triggerzone. When the stool reaches the anal canal from the rectum, the ATZ is stimulated to reach the brain through the sensory nerves, and the sense of defecation can be produced. If this zone is completely destroyed, the sense of defecation disappears and the feces in the rectum becomes stagnant. Based on the above physiological properties of the ATZ, it can clinically explain the occurrence of certain abnormal bowel sensations. For example, in prolapsed anal disorders (rectal prolapse, polyps, etc.), the prolapsed material is embedded in the anus or prolapsed outside the anus during defecation; after the feces is expelled, the prolapsed material remains in its original state, stimulating the epithelium of the ATZ of the anal cushion and producing the sense of defecation, at which time the patient mistakes this abnormal sense of defecation for residual feces and strains to blame, and the prolapsed material prolapses even more, causing a vicious circle. This is the reason why patients with rectal cancer in the lower rectum often have abnormal defecation sensation. In summary, the epithelium of the anal cushion has certain immune and endocrine functions, a fine sense of discrimination, and a variety of chemical and mechanical receptors that can trigger protective anal reflexes. It is extremely important to maintain normal defecation activity. 4, hemorrhoidal vessels 4.1 The branching pattern of the superior hemorrhoidal artery is not related to the site of origin of the parent hemorrhoid In 1919 Miles proposed that the superior hemorrhoidal artery is divided into 2 branches, left and right, and the right branch is divided into 2 anterior and posterior branches and distributed in the hemorrhoidal area together with the left lateral branch, and emphasized that the branching pattern is related to the genesis of the 3 parent hemorrhoids. Foster (1984) and Morikeyan (1984) pointed out that the left and right branches of the superior hemorrhoidal artery can each divide into anterior and posterior branches or most secondary branches without a fixed pattern. The author (1986) observed 76 cadavers by autopsy and found that only 5 cases (6.6%) of the right anterior, right posterior and left lateral 3-branch type as described by Miles were seen. Therefore, Miles used the branching pattern of the superior rectal artery to explain the preferred site of internal hemorrhoids, which lacks anatomical support. Moreover, the vasculature is variable, and the right anterior, right posterior and left side of the anal cushion are fixed and variable, and there is no logical connection between the two. It has been confirmed that the arteries of the anal pad are mainly from the inferior rectal artery (middle hemorrhoidal artery) and the anal artery (inferior hemorrhoidal artery), while the superior rectal artery generally does not participate. The trilobar arrangement of the anal pad is independent of the branching pattern of the superior rectal artery. The traditional concept also suggests that the density of microvessels in the hemorrhoidal area varies, with the parent hemorrhoid often occurring there because of the particularly dense distribution of vessels to the right anterior, right posterior, and left sides. For this reason, Hajio Miyazaki (1976) and the author (1986) observed the density of microvessels in the anal cushion area by arteriography and found that the microvessels of the middle hemorrhoidal artery and the anal artery converged in this area from six directions with equal distribution throughout the circumference without bias, and did not find that the microvessels in the right anterior, right posterior, and left side were particularly dense compared with other areas. If hemorrhoid formation is related to microvasculature, it is unlikely that hemorrhoids would be limited to specific 3 locations. Thus, the pattern of distribution of arterial microvessels within the anal cushion is not related to the site of hemorrhoid predilection. 4.2 Non-pathological dilatation of hemorrhoidal veins As early as the 18th century Sappey, Dyret, Waldeyer and until 1975 Thomson et al. demonstrated that the venous dilatation of the hemorrhoidal plexus is constant from newborn infants to healthy adults and that, unlike the saphenous vein or esophageal varices, there is no pathological damage to the venous wall and it is a normal physiological dilatation. In 1982, the French scholar Saint-Pierre discovered that the female internal hemorrhoidal plexus has estrogen receptors, and when the level of estrogen stimulates these chemical receptors during pregnancy and menstrual cycle, it can reflexively cause venous dilatation, which is also a physiological phenomenon. The submucosal veins of the anal pad from (internal hemorrhoid plexus) are the normal pattern of veins of the pelvic organs, as are the adjacent pubic plexus, bladder plexus, and uterovaginal plexus. Under normal conditions, the internal hemorrhoidal plexus has extensive communication with the portal veins of the rectum and the veins of the body circulation, and blood from the portal veins can be shunted to the body circulation (internal iliac veins) via the interhemorrhoidal communication veins and the hemorrhoidal genital veins, and this shunt is more pronounced during rectal contraction during defecation. In 1985 Shafik found that the genital veins of hemorrhoids have a venous valve that allows blood from the hemorrhoidal plexus to flow only to the prostatic plexus or the vaginal plexus (body circulation), while blood from the body circulation cannot flow to the portal vein system. Thus, there is no direct connection between portal hypertension and hemorrhoids. According to statistics, the incidence of hemorrhoids in patients with portal hypertension is not high; Jacobs et al. (1980) investigated 188 patients with portal hypertension and 52 patients (28%) had hemorrhoids. In contrast, the incidence of hemorrhoids in the general population is as high as 50% to 80%. Other scholars such as Hunt, Orloff, etc. have reported the same, thus the above assertion has been clinically confirmed. The traditional concept of stasis and varicosity of the hemorrhoidal plexus as hemorrhoids has been discarded. Since the internal hemorrhoidal plexus is part of the rectal static plexus, if the plexus is stagnant, the latter has the effect of absorbing the hyperemia without causing varices; if varices occur, they will also involve the entire rectal plexus and will not be limited to the internal hemorrhoidal plexus. Therefore, although the venous plexus of the anal cushion is closely related to hemorrhoids, it is not the main aspect that causes the disease. 4. anastomosisarteriovenosa is a regulator of blood volume in the anal cushion. 1962 Stelzner et al. found an arteriovenous anastomosis in the submucosa of the anal cushion in serial tissue sections. 1963 Staubesand et al. used X-ray imaging and 1975 Thomson used latex injection, both successively confirming the presence of this special vessel. Thomson called these vessels “sinus veins”. The arteriovenous anastomosis in the form of a filamentous spheroid structure is a unique vascular pattern in the anal cushion. An arteriovenous anastomosis is a direct anastomotic tube between a small artery and a small vein. Blood may not flow from the artery to the vein via capillaries. These vessels may be straight or globular or tortuous. Under normal circumstances, the opening or closing of the arteriovenous anastomosis in the anal cushion is alternating, with about 8 to 12 openings per minute, and also with several days of opening or closing. Since the anastomosis can open freely, it plays a major role in the regulation of temperature and blood volume in the anal cushion area. The presence of such anastomotic ducts in the anal cushion is strongly confirmed by the experimental studies of blood gas analysis and temperature conductivity (thermoconeuctibility) of hemorrhoidal blood by Thulesins et al. and provides a reasonable explanation for the bright red color of hemorrhoidal blood (arterial blood). The answer is reasonable. The arteriovenous anastomosis is a good regulator of blood volume to the anal cushion. The amount of blood supply to the anal pad is closely related to its functional status and the stimulation of the internal and external environment. Under normal conditions, the blood flow in the anastomotic duct of the anal pad accounts for 20% or even up to 50% of the total rectal blood volume. In children, the anastomotic duct is poorly developed due to low sex hormone levels, and does not develop completely until puberty, so the anal cushion is rarely enlarged in children. During pregnancy, the level of estrogen increases, the anastomotic ducts become thicker, and the blood flow increases, so the incidence of hemorrhoid disease in pregnant women is high. The contraction and diastole of the smooth muscle of the arteriovenous anastomoses is innervated by sympathetic nerve fibers and regulated by vasoactive substances in the blood. The active substances can be divided into two main groups, namely hemoconstrictors (norepinephrine, epinephrine, 5-hydroxytryptamine, angiotensin, etc.) and vasodilators (histamine, vasomotor bradykinin, pancreatic vasodilator, nucleotides and lactic acid, etc.). The former is systemic and its concentration varies very little, while the latter is produced by local tissues. When the anal cushion is stimulated by some undesirable factors, the sympathetic nerves are stimulated and initially the secretion of amines increases, causing spasm of the anastomotic duct and tissue ischemia and hypoxia; then the cushion tissue is stimulated by hypoxia, releasing histamine and producing local histamine effects, dilatation of the anastomotic duct, blood stagnation, tissue edema and blood clot formation, which can develop into localized necrosis and vesicular bleeding in severe cases. Therefore, the arteriovenous anastomosis occurs with dysregulation (dysregulation), which may be one of the factors in the pathogenesis of hemorrhoids. The former refers to the intrinsic component of the submucosa, while the latter refers to the fibers of the joint longitudinal muscle through the internal sphincter into the anal cushion, forming a layer of fibromuscular tissue with collagen fibers, elastic fibers and smooth muscle fibers mixed with the inner side of the internal sphincter. Fine-Lswes (1940) called it the submucosal muscle. Jit (1974) demonstrated that the anus is a mixed muscle, and the fibers that penetrate the anal cushion are not transverse muscle but smooth muscle, and are networked around the hemorrhoidal venous plexus; when it contracts, the muscle network tightens, restraining the hemorrhoidal vein, and the anal cushion shrinks; when it relaxes, the venous plexus passively expands, and the anal cushion then expands, maintaining anal self-control. Maintain anal self-control. The ratio of the thickness of the Treitz muscle to the thickness of the internal sphincter is 1:4 in newborns, 1:2 in adults, and 1:1.5 in the elderly, and the Treitz muscle fibers in young people are finely arranged, parallel to each other, with a fine structure and more elastic fibers. Thomson’s (1975) observation confirmed that the distribution of this fibromuscular tissue in the anal cushion is mainly in the form of a network structure wrapped around the hemorrhoidal plexus, forming a supportive framework that holds the anal cushion above the internal sphincter, and its function is to prevent the cushion from slipping out. Therefore, Kohlvansch (1854) called the Treitz muscle a mucosal support (suspensory) apparatus (sustentatortuniaemucosae). In young people the supporter that wraps around the hemorrhoidal vessels is stronger and in old age degeneration occurs, the supporter loosens and the anal cushion has a tendency to protrude into the anal canal lumen. As mentioned above, the Treitz muscle is the network and supporting structure of the anal cushion. It has the effect of allowing the anal cushion to retract upward at the end of defecation. If the Treitz muscle is broken and the supporting tissues are loosened, the anal cushion can become impaired in its retraction and move downward from its original position fixed to the internal sphincter. In addition to genetic factors such as congenital Treitz muscle dysplasia, constipation, anger, prolonged diarrhea and dysentery, poor defecation habits and abnormal sphincter dynamics can increase the vertical pressure on the anal cushion and cause the Treitz muscle to overstretch and rupture, leading to the downward shift of the anal cushion. For example, if the arteriovenous anastomosis in the anal cushion becomes impaired and blood perfusion is greatly increased, the anal cushion will become congested and hypertrophied. The normal Treitz muscle network has a restraining effect on the volume of the anal cushion, and when congestion increases, the volume of the anal cushion will also increase, resulting in elongation, hypertrophy and rupture of the Treitz muscle. Once the anal cushion loses its muscular support, intermittent prolapse can occur over time and then develop into persistent prolapse. In 1984, Hass et al. showed that the degeneration of the Treitz muscle begins around the age of 18 to 20 years and increases with age, becoming twisted and flaccid. The incidence of hemorrhoids is greatly increased because of the natural fracture and downward shift of the anal cushion. 6, hemorrhoids in the maintenance of anal self-control Marti (1989) pointed out that the normal anal cushion is like the tricuspid valve of the heart, its main function is to assist the sphincter muscle to ensure the normal closure of the anus, to maintain fecal self-control. The cushion-like structure is a common feature of various mucosa-lined orifices in the body and assists in the closure of the orifice. For example, the mucosal rose knot at the mouth of the gastric cardia, similar in structure to the anal pad structure, which is involved in the one-way valve role of the cardia, preventing the reflux of gastric juice into the esophagus. Other pyloric flaps, ileocecal flaps, and appendicular flaps have similar functions to the anal cushion. alexander-Williams believes that the anal cushion is very similar to the mouth and lips; the mouth and lips have different shapes, such as thin, convex, wet, and congested, while the anal cushion can also have different shapes and should not be referred to as a disease. The trilobular arrangement of the anal cushion is the most ideal living flap device to adapt to changes in the enlargement or reduction of the anal canal lumen. Because of the rich arteriovenous anastomosis and Treitz muscle within the anal pad, the structure is like that of the corpus cavernosum of the penis, so Stelzner called the anal pad the corpuscavernosumrecti (rectal spongy body). The corpus cavernosum can contain a large amount of blood, so that the blood supply of the anal pad greatly exceeds the metabolic needs of the chemical itself, thus it can prove that the anal pad has the characteristics of erectile tissue, which is necessary to participate in anal self-control. The size of the anal cushion is related to the opening or closing of the arteriovenous anastomoses and the amount of blood supply in the anal cushion. Labor, defecation and position changes can affect the increase or decrease of the anal cushion, such as from lying to upright position, the intravascular pressure of the anal cushion can rise rapidly from 22.5 to 24.5kpa (230-250mmH2O) to 58.8 to 73.5kPa (600-750mmH2O). It can be said that the size of the anal cushion changes daily or hourly. The pad may prolapse or become engorged after defecation, but after a period of rest, it is not large enough to be seen on rectal microscopy. Patients often complain of “hemorrhoids” that are sometimes large and sometimes not; sometimes “hemorrhoid flare-ups” last for days or weeks. Therefore, the traditional classification of internal hemorrhoids as stage I, II, III or IV has little clinical and scientific significance. Under normal conditions, the resting pressure of the anal canal is the sum of the vascular pressure of the anal cushion and the tension of the sphincter, and the two are complementary: when the sphincter pressure is reduced, the anal cushion is distended; when the sphincter pressure is increased, the anal cushion is compressed. When the sphincter is relaxed, blood enters the venous space of the anal cushion, which expands and assists the resting pressure of the anal canal to maintain anal closure; Raz (1972) et al. did a good test of blocking blood to the submucosal spongy erectile tissue of the female urethra (clamping of the internal iliac artery) and found a rapid 35% decrease in intraurethral pressure, thus indirectly demonstrating the importance of the vascular component of the anal cushion in assisting the sphincter to maintain the importance of anal self-control. According to the literature, patients with hemorrhoidal prolapse or hemorrhoidectomy have varying degrees of impairment of anal self-control, Goligher (1962) reported 10% air leakage, 3% fecal leakage, and 2% foul stool. Bennett (1963) and others reported 26% mild incontinence, 9% air leakage, and 6% foul stool. Leakage of stool was 6% and soiled stool was 17%. The above clinical statistics also confirm the importance of the presence of anal pads for anal self-control. Therefore, some people call the anal pad “physiologicanalsphincter” (physiologicanalsphincter), so in the design of surgery for incontinent patients, should consider the reconstruction of the anal pad, that is, the choice of compressible material made of artificial anal pad, implanted in the anal canal, in order to enhance the mechanical effectiveness of the weak sphincter, when the sphincter is relaxed When the sphincter is relaxed, the anal canal can be kept closed and solid stool can be allowed to pass during defecation. Most patients with hemorrhoids show increased pressure in the anal canal, and some people suggest that the high pressure in the anal canal can affect the venous blood flow back to hemorrhoids during defecation, but this argument lacks anatomical and physiological basis. It is not possible to stasis the blood. Moreover, the vascularity of the anorectal area is very complex, and Steltzner (1963) has pointed out that the spongy venous gap in the upper part of the anal canal (hemorrhoidal area) is a normal structure, and the blood in the gap comes from small arteries, whose blood flow control factors are not yet known. Therefore, the exact mechanism by which high anal pressure affects hemorrhoids has not yet been satisfactorily answered. In conclusion, the anal cushion is a special mucosal epithelium rich in arteriovenous anastomoses and a large number of Treitz muscle fibers, a normal anatomical entity of the body, whose main function is to assist the sphincter in closing the anus. The recent concept of hemorrhoids suggests that altered pelvic floor dynamics, degenerative degeneration of the Treitz muscle and impaired regulation of the arteriovenous anastomosis within the anal cushion can lead to hypertrophy or prolapse of the anal cushion known as hemorrhoids.