Fig. 4.1
Anatomic description of the anorectal junction. The rectum specimen is cut longitudinally
Several anatomic investigations have demonstrated the existence of arteriovenous communications between the terminal branches of the superior rectal artery (SRA) and the CCR [13, 19]. This subepithelial vascular plexus is known to be a complex system of thin-walled tortuous venous structures supported by smooth muscle and fibroelastic tissue scaffolding [9]. These vascular structures, surrounded by fibromuscular tissue, have been described as so-called anal glomerula, corresponding to the anal cushions [18]. Anatomic investigations suggest the existence of a specialized functional vascular network at the anorectal region, similar to that of the penile corpora cavernosum. Others hypothesized the presence of some kind of regulating veins in the CCR [2]. Anatomic studies provide clear morphological and functional evidence for distinct vascular glomerula equipped with sphincter-like constrictions; these are most likely responsible for regulating the filling and drainage of the CCR [2, 18]. Data suggest that the CCR possesses an intrinsic active contractile mechanism that is able to ensure effective blood transport through the CCR [2]. Disruption of this intrinsic blood flow regulation and concomitant replacement of smooth muscle tissue with connective tissue seem to be key factors in the pathogenesis of hemorrhoidal disease.
4.3 Symptoms
The most common complaints of patients with hemorrhodial disease are bleeding upon defecation, pruritus, anal seepage or soiling, anal pain, and mucoanal prolapse. For symptomatic assessment, the individual burden of suffering is essential, since asymptomatic piles or skin tags are not an indication for treatment of hemorrhoids.
4.4 Etiology
The pathogenesis of hemorrhoidal disease is multifactorial and controversial [19]:
- 1.
The hyperplasia theory describes disturbance of the drainage of the CCR as a result of increased sphincter resting tone, on the one hand, and prolapse of the ATZ into the anal canal, on the other.
- 2.
The varicose vein theory has been abandoned because patients with portal hypertension do not show an increased incidence of hemorrhoidal disease.
- 3.
The anal sliding lining theory is associated with the first theory: increased intraabdominal pressure (during pregnancy or upon straining during dfaecation, especially by constipated patients) results in distension and rupture of submucosal smooth muscle fibers and subsequent prolapse of the ATZ.
4.5 Classification
The traditional Goligher classification is applied for grading hemorrhoidal disease:
Grade 1 hemorrhoids do not prolapse at examination and are only visible through a proctoscope.
Grade 2 hemorrhoids prolapse during defecation but reduce spontaneously.
Grade 3 hemorrhoids prolapse and need manual repositioning.
Grade 4 hemorrhoids prolapse but cannot be reduced digitally into the anal canal by the patient.
From a clinical point of view, the Goligher classification is rather rigid, since other symptoms such as mucosal prolapse, fecal incontinence, and segmental or circular prolapse of the hemorrhoidal tissue (Fig. 4.2a, b) are not included. The classification according to Müeller-Lobeck [10] also differentiates between acute thrombosed (grade 4a) and chronic fibrosing (grade 4b) hemorrhoids.
Fig. 4.2
Segmental (a) and circular (b) hemorrhoidal prolapse of patients with grade 3 hemorrhoidal disease
4.6 Diagnosis
History taking is the most important step toward a diagnosis of hemorrhoidal disease and should include a question about pretreatment for hemorrhoidal complaints. Individual complaints and burden of disease should be taken into account. Questions about pain and discomfort upon defaecation, pruritus, bleeding, soiling, mucosal discharge, and any kind of preexisting fecal incontinence, as well as the extent of prolapsing tissue, are mandatory.
The position of the patient during examination and surgical intervention depends on the investigator’s preference and does not matter from a clinical point of view (either the left lateral, lithotomy, or jacknife position). Inspection of the perianal region should determine the presence of anal fissures, fistula openings, and erythema. A digital rectal examination using the examinor’s index finger should exclude tumor masses, polypoid structures, rectoceles, and internal fistula openings and should assess the anal resting and squeeze pressures. The Valsalva maneuver can induce any kind of prolapse and facilitates the differentiation bewteen hemorrhoidal and rectal prolapse.
Rigid proctoscopy and rectosocopy visualizing at least 15 cm of the rectum is a standard requirement before treatment. Colonoscopy is recommended whenever the history suggests anything more than hemorrhoidal symptoms (e.g., colorectal cancer).
4.7 Treatment
4.7.1 Conservative Treatment
Preventive treatment for hemorrhoidal disease should be considered as concomitant therapy (e.g., stool softeners, a fiber-rich diet, sufficient fluid intake, and avoiding excessive straining during defecation), independent of the hemorrhoidal grade. Drugs (e.g., suppositories, ointments, creams, flavonoids) can reduce hemorrhoidal symptoms. The effect is characterized by the anti-inflammatory, analgesic, and local anaesthetic properties of the drugs. Topical steroids should be applied only for short periods to avoid atrophy of the perianal skin and anoderm. A series of prospective randomized trials highlighted the healing effect of diosmin (flavonoid) regarding the end points of pain, bleeding, and pruritus in terms of hemorrhodial disease [6].
4.7.2 Surgical Treatment
The leading indication for invasive techniques is the individual burden of hemorrhoidal disease, rather than grade of hemorrhoidal prolapse, since it is assumed that the associated symptoms are partly independent of the anatomic derangement (Table 4.1). Nonresecting minimally invasive techniques can be performed on an outpatient basis, with low morbidity. The major target is an induced inflammatory stimulus (e.g., sclerosing injection or rubber band ligation), resulting in “controlled” scarring and thereby fixation of the ATZ and the prolapsed mucosa to the rectal wall.
Table 4.1
Surgical treatment of hemorrhoidal disease
Nonresection techniques |
Sclerosing injection |
Rubber band ligation |
Infrared coagulation |
Laser hemorrhoidoplasty |
Ligation-based techniques |
Hemorrhoidal artery ligation without mucopexy |
Resection techniques |
Stapled hemorrhoidopexy |
Conventional hemorrhoidectomy |
Milligan-Morgan |
Parks |
Ferguson |
Fansler-Arnold |
4.7.3 Sclerosing Injection
Slerotherapy is widely used for grade 1 and 2 hemorrhoids and consists of submucosal injection of a tissue-irritating agent (ethoxysclerol or 5 % phenol in almond oil), which causes fibrosis and fixation of the hemorrhoidal zone to the rectal wall [8].
4.7.3.1 Technique
The needle is inserted into the rectal submucosa above the hemorrhoidal pedicle, and 2–3 mL are injected at each site, depending on the agent and its concentration. It is important not to inject directly into the CCR, the muscularis recti, or the internal sphincter muscle. Depending on the agent and its concentration, up to three injection sites are possible during one session. The injection procedure can be repeated at monthly intervals until symptoms (e.g., bleeding) have ceased. The complication rate is rather low (0.7–6.5 %) [10]; however, recurrence is common in the long term (up to 70 %).
4.7.4 Rubber Band Ligation
This method is the most commonly applied treatment for grade 1 and 2 hemorrhoids [3]. Rubber band ligation of the rectal mucosa above the hemorrhoidal pedicle causes ulceration and scarring of the respective area, resulting in fixation of the ATZ.
4.7.4.1 Technique
Rubber bands are applied through a proctoscope (several modifications of the applicator are available), with or without simultaneous injection of sclerosing agents both to avoid early rejection of the rubber band by the contraction of the smooth muscularis mucosae and to provide an additional sclerosing effect to the banded rectal mucosa. Up to three applications can be made during one session, which can be repeated at monthly intervals on an outpatient basis. The most common pitfall is setting the ligation too close to or below the dentate line, which causes immediate pain and subsequent perianal thrombosis caused by painful hypercontraction of the sphincter muscles. Bleeding—especially after rejection of the rubber band and necrotic rectal mucosa on postintervention days 5–7—might be the cause for readmission, and a 25 % recurrence rate of haemorrhoidal complaints within 5 years of follow-up are common.
4.7.5 Infrared Coagulation
Application of infrared energy causes localized submucosal coagulation and necrosis with consecutive inflammation and, again, fixation of the ATZ. Recurrence rates are similar to those for rubber band ligation; however, the lack of pain during this procedure favors infrared coagulation. This technique may cause local necrosis, and its use has been widely abandoned in Europe [3].
4.7.6 Laser Hemorrhoidoplasty
Laser hemorrhoidoplasty uses an 980-nm laser diode to deliver energy to the submucosal branches of the SRA that supply blood to the hemorrhoids. The laser energy is applied in a pulsed fashion, resulting in photocoagulation of the arterial branches and fixation of the rectal mucosa and submucosa to the muscular layer. Authors have demonstrated that this is a safe, effective, and painless technique for the treatment of symptomatic grade 2–3 hemorrhoids with minimal or moderate mucosal prolapse, and it is suitable as ambulatory treatment [4]. These early results are positive, but more confirming studies are mandatory.
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