REVIEW ARTICLE Annals of Gastroenterology (2019) 32, 1-9

Pathophysiology of internal hemorrhoids

Nikolaos Margetis
University of Athens; Athens Euroclinic, Athens, Greece

Abstract Hemorrhoidal disease is a fairly common and debilitating clinical entity. Despite centuries’ of
attempts to shed light on its pathophysiology, to cure those affected and to improve sufferers’
quality of life, many aspects of the disease remain elusive. Individual beliefs and historical legends,
accompanied by undocumented theories, have established and perpetuated the confusion
regarding the mechanisms leading to the development of the disease and the rules governing its
treatment. Hemorrhoids are classified as internal or external and are viewed as a disease when
they become symptomatic. Returning to basic medical sciences, this mini-review focuses on
internal hemorrhoids and aims to define the histology and anatomy of the normal and abnormal
internal hemorrhoidal plexus and to encourage clinicians to comprehend the pathophysiology of
the disease. If doctors can understand the pathophysiology of hemorrhoidal disease, they will be
able to clarify the nature of the associated symptoms and complications and to make the correct
therapeutic decision.
Keywords Internal hemorrhoids, anal cushions, anal nodules, prolapse, sliding anal canal
Ann Gastroenterol 2019; 32 (2): 1-9

Introduction venous system returns conflicting information [7,10,12,13].

Additionally, real life has proven that significant parts of the
Hemorrhoidal disease has been recorded through accepted wisdom regarding hemorrhoids are in fact clinical
centuries of history. Primitive references are found in the Old misunderstandings and personal beliefs passed on from one
Testament and in Egyptian, Babylonian and Greek written unsuspecting generation to the next. The purpose of this
sources  [1-3]. Hippocrates approached the pathophysiology manuscript is to dispel these legends and to provide a well-
and the treatment of the disease in his treatise “On documented account of the etiopathogenesis of internal
Hemorrhoids” [3]. Many physicians have tried to detect and hemorrhoidal disease.
describe the precise pathophysiological events of symptomatic
disease [2-4]. Many surgeons have tried to derive conclusions
based on operative findings [2,3,5-7]. Despite numerous
efforts, the true etiopathogenesis of hemorrhoidal disease still Normal anatomy and histology of hemorrhoids
remains elusive [8-9].
Pathophysiology is not the sole aspect of hemorrhoids to lack Hemorrhoids are normal structures of the human
full elucidation. Many other factors need more investigation: body [9-11]. Internal hemorrhoids arise from the internal
for instance, the epidemiology of the disease [10], the optimal hemorrhoidal plexus, while external hemorrhoids arise from
therapy for every single stage of hemorrhoids [8], and an the external plexus. The anatomical boundary that divides
explanation for the transition of asymptomatic hemorrhoids to the internal from the external hemorrhoidal plexus is the
symptomatic [11]. Moreover, a detailed search in the literature dentate line [8-10]. The normal internal hemorrhoidal plexus
regarding the anatomy and histology of hemorrhoidal tissue consists of 3 soft engorgements, referred to as anal cushions
and the relationship between hemorrhoids and the portal or “hemorrhoids” [14,15]. Consequently, the term “internal
hemorrhoids” does not signify a state of disease if viewed in its
strict literal definition. However, in clinical practice the term
Endoscopy Unit, Athens Euroclinic, Greece
“internal hemorrhoids” is used to describe solely the disease
Conflict of Interest: None resulting from the abnormal enlargement of anal cushions,
i.e.,  their transformation to anal nodules [10,14,15]. More
Correspondence to: Nikolaos Margetis, 46 Gennimata Street, 15238
Halandri, Athens, Greece, e-mail: nmargetis@yahoo.gr precisely, this definition is limited to symptomatic hemorrhoidal
disease: i.e.,  anal cushions are named “hemorrhoids” when
Received 2 October 2018; accepted 11 December 2018; they bleed and/or prolapse [16].
published online 23 January 2019
The internal hemorrhoidal plexus is placed submucosally
DOI: https://doi.org/10.20524/aog.2019.0355 above the dentate line and below the anorectal ring [17].

© 2019 Hellenic Society of Gastroenterology www.annalsgastro.gr

2  N. Margetis

It extends from the upper border of the anatomical anal and MRA, oxygenates the non-vascular part of the cushion,
canal to the upper border of the surgical anal canal. It is and ultimately emits venous blood to the tiny root venules
located, therefore, outside the anatomical anal canal. It is of the SRV and MRV. In this way, blood from the arterial,
covered by transitional columnar epithelium and originates systemic venous and portal venous circulations is mixed inside
embryologically by the cloacal part of the anal canal, which the sinusoids (Fig. 1).
contains both ectodermal and endodermal elements [14]. This Why is the hemorrhoidal vasculature concentrated into 3
epithelium is approximately 1 cm long [14] and, as anatomically distinct anal cushions? Several theories have been developed,
authentic rectal epithelium, it secretes mucus [10] and is not none of which fully explains their formation [13-17]. The
innervated by visceral pain fibers [16]. preferential arterial supply into specific locations of the upper
anus favors the development of sinusoidal plexus in these
locations almost exclusively. Indeed, the position of the anal
cushions corresponds directly to the location of the terminal
The vascular part of the anal cushion principal arterial branches in the submucosal tissue: left lateral
(3 o’clock), right anterior (11 o’clock) and right posterior
The hemorrhoidal tissue located between the mucosa of the (7 o’clock) [14,18]. An alternative explanation is that normal
surgical anal canal and the internal sphincter is not uniform anal cushions are not real protrusions; they rather represent
in its appearance. The hemorrhoidal vasculature is normally the unavoidable creases appearing during the closure of the
condensed in the form of anal cushions; these cushions anal canal and disappearing when the anal canal widens during
represent well-shaped, deep-purple, hemispherical masses, defecation. The aim of these folds is to seal the anal canal in the
which protrude towards the lumen of the upper surgical anal resting state [17].
canal [14,15]. Three main anal cushions are easily recognized
in the usual surgical anal canal [15,18]. Despite being tissues
that are predominantly vascular in origin, anal cushions
also contain a significant non-vascular portion. The internal The crucial role of the non-vascular part of the anal
hemorrhoidal plexus consists of arterioles, venules and direct cushion
communications between them (arteriolar-venular functional
anastomoses). The presence of vessels inside cushions The non-vascular part of the cushion consists of the
contributes to the scarlet color of the surgical anal canal [14]. transitional epithelium, connective tissue, elastic and
The internal hemorrhoidal plexus receives blood from collagenous, and the muscle of Treitz [8,16]. Treitz’s muscle
the superior (SRA) and the middle (MRA) rectal arteries. tightly maintains the cushions in their normal position;
In the majority of cases these arteries form a plexus just its deterioration is considered one of the most important
behind the rectum. This plexus, absolutely distinct from the pathogenetic factors in the formation of hemorrhoids. Treitz’s
internal hemorrhoidal plexus, commonly provides 3 principal muscle consists of 2 distinct parts: the anal submucosal muscle,
terminal branches, which penetrate the rectal wall, ultimately whose fibers subside submucosally between the sinusoids,
terminating submucosally in the anus above the dentate line fixes the cushions to the “floor” of the hemorrhoids (i.e., to the
in 3 positions: the left lateral, the right anterior and the right internal anal sphincter), while the mucosal suspensory ligament
posterior position. (Park’s ligament) penetrates the internal sphincter and fixes the
Despite the conflicting reports in reference textbooks sinusoids to the conjoined longitudinal muscle [17].
regarding veins emerging from anal cushions [5,7,10,12,14,18], Although the conjoined longitudinal muscle is not an
venous drainage from the internal hemorrhoidal plexus anatomical part of the anal cushion, it is just as important as
is currently widely accepted to be directed to all 3 rectal Treitz’s muscle for the prevention of hemorrhoidal disease.
veins [14], which communicate with each other [5,7,10]. The It appears to function like a backbone, which supports the
superior (SRV) and middle (MRV) rectal veins are commonly internal and the external sphincter and fixes the anorectum to
the predominant venous branches of the internal hemorrhoid the pelvis. It is located just beneath the internal sphincter and
cushions [7,10]. The SRV drains blood to the inferior mesenteric serves as the constant platform where the hemorrhoidal tissue
vein, which belongs to the portal venous circulation, while the is fixed via Park’s ligament [17]. Moreover, its fibers form a loop
MRV and the inferior rectal veins are tributaries of the systemic at the distal end of the internal sphincter. This is the reason why
circulation. Consequently, blood from anal cushions is drained some investigators claim that conjoined longitudinal muscle
through both circulations, systemic and portal. continues above the internal anal sphincter to form the anal
Inside cushions, blood moves directly from arterioles to submucosal muscle [19] (Fig. 1).
venules, via a plethora of arteriolar-venular anastomoses. The firm fixation of normal anal cushions above the dentate
Most arteriolar-venular anastomoses lack muscular wall; line, the maintenance of their usual size and the prevention of
therefore, they are considered as sinusoids [15,16]. The cluster their prolapse is ensured by 4 anatomical safety features: first,
of sinusoids forms a spongy capillary network that resembles the integrity of the accompanying connective tissue found
penile erectile tissue, since sinusoids consist of numerous, between the sinusoids, which supports sinusoids and fixes them
dilated, uneven vascular spaces covered by endothelium  [7]. to the internal sphincter [20]; second, the anatomical entirety of
Sinusoidal hemorrhoidal tissue is an imaginary 3-way Treitz’s muscle and of the conjoined longitudinal muscle [15,17];
crossroad, which initially receives arterial blood from the SRA third, the sphincter-like structure present in the terminal

Annals of Gastroenterology 32
 Pathophysiology of internal hemorrhoids  3

7
1

13
15 6

8
16
14 5
17

20 18 18 12

19

10 9 11

Figure 1 A proposed schematic representation of the anatomy of the anal cushion. Anal cushion consists of a non-vascular part (the transitional
epithelium – 1, the submucosal connective tissue – 2 and the muscle of Treitz, which has 2 elements, the anal submucosal muscle – 3 and the
mucosal suspensory ligament or Park’s ligament - 4) and a vascular part (the small arterioles - 5, the tiny arterioles – 6, the tiny venules – 7 and the
direct arteriolar-venular anastomoses between arterioles and venules, that form a subcutaneous spongy network of capillaries, the sinusoids – 8).
Arterial blood from the retrorectal plexus - 9 (formed by the SRA -10 and MRA -11) supplies the sinusoidal plexus via 3 terminal arterial branches
(here one of them is shown - 12). Before turning into sinusoids - 8, the terminal branch subdivides into small - 5 and tiny - 6 arterioles in the lamina
propria. These small and tiny arterioles are the source of bleeding, when the anal cushion is transformed to an anal nodule. Sinusoid drainage
is accomplished via tiny venules - 7, which direct venous blood both to the portal circulation – 13 (through the SRV -15) and to the systemic
circulation – 14 (mainly through the MRV-16 and to a lesser extent through the IRV -17). The cluster of sinusoids is tightly fixed to the inner anal
sphincter -18 by the anal submucosal muscle -3 and by the submucosal connective tissue - 2 (which extends between the sinusoidal anastomoses)
and to the conjoined longitudinal muscle -19 by the mucosal suspensory ligament -4. According to several researchers, anal submucosal muscle -3
is thought to represent the continuity of the conjoined longitudinal muscle -19; the latter is believed to form a loop -20 at the lower end of the
internal anal sphincter (based on references 5,7,8,10,12-20)
IRV, inferior rectal vein; MRA, middle rectal artery; MRV, middle rectal vein; SRA, superior rectal artery; SRV, superior rectal vein

arterioles; and fourth, the fairly small caliber of the terminal leaves a gap of 7-8  mm, closed as long as the anal cushions
branches of the supplying arteries [13,20]. The last 2 anatomical demonstrate anatomical and functional integrity  [15].
features also prevent the hyperperfusion of sinusoids [13]. If Therefore, the 15-20% contribution of hemorrhoids to anal
the aforementioned structures fail anatomically or functionally, continence is crucial [21]. During the resting state, the
hemorrhoidal disease emerges [8,10,13,15,17,20]. increased pressure of the internal anal sphincter impedes the
These anatomical relationships bear physiological venous drainage of anal cushions, enhancing their congestion
importance and contribute to the uneventful function of the and contributing to their notable size. This volume-occupying
anal region. Anal continence is ensured by the interaction effect seals the anal canal and continence is achieved [10,15].
between the hemorrhoidal tissue and the internal anal Just before defecation, hemorrhoidal tissue contributes to the
sphincter. The internal anal sphincter is responsible for 60-80% sensing of a sample of intrarectal contents (liquid, gas, stool),
of normal anal pressure. Nevertheless, the internal sphincter as it has sensory innervations [22].

Annals of Gastroenterology 32
4  N. Margetis

During defecation, the hemorrhoids and internal anal civilization has adopted the sitting position during defecation,
sphincter aid one another: the lowered pressure of the relaxed which does not permit the straightening of the anorectal angle
internal anal sphincter permits blood to drain from the anal (in contrast, this angle is eliminated if defecation is performed
cushions to the SRV and MRV, helping to reduce them in in the primitive squatting position), necessitating even greater
size. Two more mechanisms contribute to the decrease in effort and exaggerated intraabdominal pressure to overcome
anal cushion size: the direct dilation of the anal canal by the the relative obstacle met by the descending stool [8,27].
descending stool and the contraction of the anal cushions Nevertheless, these factors have not been studied in detail [8].
by the submucosal ligament of Treitz’s muscle. At the same Pregnancy, for instance, was not associated with hemorrhoids
time, the anal cushions slide down, forming anal lips [15], in 2 recent studies [26,28], whereas an increased body mass
which protect the underlying internal anal sphincter [23]. As index had only an ambiguous relationship with hemorrhoid
the anal cushions return upwards to their usual position after development [26,28].
defecation, they rapidly fill with blood until they reach their Although constipation (due to the absence of dietetic
usual size. In this way, fecal soiling is prevented [14,15,17]. fibers, among other factors), has traditionally been considered
an important risk factor for hemorrhoid development [10],
recent studies doubt on this relationship [29,30]. Nonetheless,
constipation increases intraabdominal pressure and directly
The pathologic basis of hemorrhoidal disease impedes venous return, via the effect of hard stool in the rectal
veins [30], while hard stool applies strong intra-anal forces to
The pathophysiology of internal hemorrhoids is still not the anal cushions during defecation [13]. Moreover, prolonged
fully understood. Many functional, histopathological and defecation attempts in the constipated patient may lead to
anatomical findings have been accumulated during the last repeated and ineffective evacuation, which impedes the venous
decades, but the relation between them remains obscure. In the return to hemorrhoids even more.
majority of cases, we do not know whether they are primary Anal submucosal muscle firmly connects anal cushions
or secondary. Despite the plethora of candidates for the initial to the internal sphincter. Park’s ligament firmly connects anal
steps, we are not aware which is the most prevalent. Every single cushions to conjoined longitudinal muscle. Since the anal
hemorrhoid patient demonstrates a different combination cushions and internal sphincter move in opposite directions
of starting points and distinct pathophysiological events, (the former slips down, the latter relaxes), both parts of Treitz’s
connected in a personalized order. As the proposed algorithm muscle are elongated and stretched during defecation. Repeated
in Fig.  2 illustrates, the pathophysiology is complicated and and successive cycles of elongation and shortening of Treitz’s
comprises many vicious cycles. muscle following chronic strained defecations result initially
Four theories have been developed regarding the in its relaxation and ultimately in its disintegration [15,31].
pathophysiology of hemorrhoids. First, the varicose vein Treitz’s muscle fibers may also disintegrate as a result of pelvic
theory has been shown to be faulty [15], as it is now globally floor disorders [15] and with increasing age [25,32]. The final
accepted that hemorrhoids are not varicosities [24]. Theories result is the persistence of the prolapsed anal cushions outside
involving vascular hyperplasia (the theory that hemorrhoids the anus after defecation. In the initial grades of hemorrhoidal
resemble penile erectile tissue) and internal anal sphincter disease (1st and 2nd degree), anal cushions reverse back into the
hypertonia hold part of the truth, but they cannot be totally anus without any effort from the patient. In advanced grades, the
accepted [10,13,15,17]. The globally accepted theory is that of additional disintegration of conjoined longitudinal muscle results
the sliding anal canal, or cushion theory, which postulates the in their remaining permanently outside the anus, either manually
abnormal slippage of cushions through the anal canal as the reversible (3rd degree) or nonreversible (4th degree) [15,17].
major pathophysiological event [15]. Furthermore, relaxation of the supportive connective tissue
A look at Fig. 2 makes it clear that many events are believed enhances the permanent prolapse of anal cushions. First,
to initiate the disease. Regardless of the initiation points, 4 core functional or anatomical deterioration of Treitz’s muscle per se
pathophysiological events are universally recognized: first, the disrupts the integrity of the connective tissue [15,20]. Second,
sliding process of anal cushions; second, the deterioration of the abnormalities in the quality of collagen (loose collagen tissue
connective tissue of the cushion; third, the reduction of venous is commonly found in Ehlers-Danlos syndrome [33] and in
return from sinusoids to the SRV and MRV during defecation; aging individuals [25]) lead to deterioration of the connective
and fourth, the stagnation of blood inside the dilated plexus. tissue. Indeed, an increase in matrix metalloproteinases
These crucial events are highlighted in red in Fig. 2. (MMP)-2 and MMP-9 activity, known to degrade elastic fibers
A chronic rise in intraabdominal pressure, in combination and to enhance tissue remodeling, is detected in patients with
with the absence of valves within rectal veins, can limit venous hemorrhoids  [5,34]. Third, redundant connective tissue is
drainage from sinusoids during defecation, resulting in generated as the overlying mucosa is stretched; fibrous tissue
abnormal dilatation of the arteriolar-venular anastomoses of the hypertrophy results in the loss of its elasticity and hence its
internal hemorrhoidal plexus [10,25]. Human erect position, ability to shorten after defecation [10,15]. Fourth, heredity
pregnancy, obesity, ascites [25], straining with defecation confers a part in the disintegration of both Treitz’s muscle and
[16,22], excessive time spent on the toilet [22], strenuous lifting the supportive connective tissue; their deterioration with age
[16] and strenuous exercise [24] may all cause an excessive may be familial [25]. Last, relaxation of the connective tissue
increase in intraabdominal pressure. Furthermore, human is provoked by chronic or intermittent diarrhea; moreover,

Annals of Gastroenterology 32
 Pathophysiology of internal hemorrhoids  5

INCREASED ABDOMINAL PRESSURE

Constipation Pregnancy, erect position, obesity,
ascites, strenuous exercise,
strain ondefecation,
excessive time on the commode

Strong pressures Sitting on

in rectal veins and defecation
in anal cushions

Prolonged attempt to evacuate ARTERIAL HYPERPERFUSION

OF SINUSOID
Reduction in venousreturn to
Impaired sphincteraction
repeat

SRV-MRV during defecation

Increased caliber of arterioles
Increased
Intraanal
Pressure
Congestion of Decreased
Diarrhea Blood stagnation vascular
sinusoids
Relaxation of Treitz’s muscle and tone of
of conjoined longitudinal muscle sinusoids
Newly
formed
Aging vessels
Relaxation of the
connective tissue Dilated Dilated
of anal cushion small tiny
Impaired quality of collagen
arterioles arterioles
Fibrous
in LP in LP
tissue
hypertrophy
Disintegration of Treitz’s
muscle Anal cushion slides Erosion of LP
and of conjoined longitudinal
Inflammation, arterioles during
muscle
friability, injury passage of hard
of the nodule or diarrheal stool
Mild Anal cushion enlarges
Soiling and transforms to
incontinence
anal nodule Thrombosis

Spurting
Prolapse of the nodule Pain Necrosis
Itching Impaired
closure of
anal canal
Incarceration and strangulation of the nodule
Oozing

Increased
Increased mucus
mucus in the Increased
transfer mucus
perianal skin
production

Figure  2 A suggested integrated algorithm summarizing contemporary thinking regarding the pathophysiology of internal hemorrhoids.
Hemorrhoidal disease can arise from separate origins or from various combinations of them: these are the eight starting points, shown in the
orange boxes (increased intraabdominal pressure, sitting on defecation, constipation, diarrhea, arterial hyperperfusion of the hemorrhoidal plexus,
decreased vascular tone of sinusoids, impaired quality of collagen and relaxation of the supporting muscles of the internal hemorrhoidal plexus).
These initiation points force the physiological and histological status of the internal hemorrhoidal plexus towards distinct, divergent, abnormal
directions. Nonetheless, they finally converge on 4 central pathophysiological events that are almost invariably encountered in internal hemorrhoids.
These events (sliding of the anal cushion, relaxation of the connective tissue of the cushion, reduction of venous return from sinusoids to SRV and
MRV during defecation and stagnation of blood inside the dilated plexus) are illustrated in the red boxes. The bond between the starting points and
the core pathophysiological events is strong and consists of a plethora of consecutive pathophysiological stages, indicated by the gray boxes, which
are interconnected, interdependent and inter-fortified. The conceptual network of events leading to hemorrhoidal disease is complicated and has
not been fully elucidated in every detail; nevertheless it is established and perpetuated with the assistance of many vicious cycles, either direct—for
example between the increased intra-anal pressure and the reduction of venous return during defecation—or multi-step, as between the congestion
of sinusoids and incarceration. It is noteworthy that this multimodal and multidirectional network is continuously auto-reinforced, as is implied by
the universally green color of the arrows. This means that, according to this model, internal hemorrhoids offer only one option: to become worse
over time. Ultimately, symptoms (shown in blue) occur. This happens when the order of events meets critical pathophysiological steps (shown in
purple); the erosion of arterioles of the lamina propria of the anal nodule during passage of hard or diarrheal stool is typically responsible for the
various forms of hemorrhoidal bleeding. Last, pain, a non-typical symptom of internal hemorrhoids, appears when complications (brown boxes)
such as inflammation, incarceration, thrombosis and necrosis arise (based on references 4,7-11,13,15-17,19,2131,34,38,39)
LP, lamina propria; MRV, middle rectal vein; SRV, superior rectal vein

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6  N. Margetis

chronic diarrhea exerts pressure on the draining venous system The combination of sinusoidal congestion, strangulation [10]
of sinusoids [29]. Indeed, diarrhea is currently believed to and chronic inflammatory process inside the nodule [40] results
represent a stronger risk factor for hemorrhoids compared to ultimately in blood stagnation inside sinusoids. Stagnation
constipation [35]. causes locally restrained hypercoagulability, which enhances
One central hallmark of hemorrhoidal disease is the clot formation and finally results in thrombosis. Thrombosis
congestion of sinusoids. This is primarily due to increased may eventually lead to ischemia, ulceration and necrosis of the
abdominal pressure and to the reduced venous return during surface of the nodule [13].
defecation [15-18]. Moreover, arterial hyperperfusion of sinusoids
(as a result of an impaired arteriolar sphincteric mechanism [36])
and the decreased vascular tone (because of the dominance of the
endothelium-derived relaxing nitric oxide over the endothelium- Symptomatic hemorrhoidal disease
derived vasoconstricting reactive oxygen radicals [37]) enhance
the congestion of sinusoids. Additionally, the relaxed and Approximately 4 of 10  patients with hemorrhoids are
hypertrophied connective tissue loses its capacity to support symptomatic [28]. It is uncertain why hemorrhoids become
the vascular network; thus, sinusoids congest passively. Finally, symptomatic. They are believed to start producing symptoms
increased internal anal sphincter activity [17,38], either primary when anal cushions start their sliding down process [5-7].
or secondary [23], impedes venous return, worsening congestion. Bleeding is the commonest symptom of internal
Apart from the above, cushion enlargement is amplified hemorrhoids [41]. In the vast majority of cases bleeding is
by fibrous tissue hypertrophy and by neovascularization. painless, because of the absence of pain fibers [16]. Hemorrhage
Newly formed vessels emerge when inflammation develops is due to congestion of the sinusoids, transferred backwards
as hemorrhoids worsen [10,13,40]. Metalloproteinase to the presinusoidal arterioles. Bleeding from hemorrhoids
overactivity leads to a breakdown of the capillary bed and is therefore arterial in origin, hence bright red [7,10]. Since
permits the action of transforming growth factor beta (exhibits dilated arterioles are located in the lamina propria, just below
an angioproliferative effect) and of vascular endothelial growth the inflamed, injured and friable epithelium of the descending
factor (leads to sinusoidal hypertrophy) [13]. nodule, they are easily eroded during defecation by hard [25],
To make things more complex, 2 more vicious cycle are dehydrated [22] or diarrheal [29,35] stool. As presinusoidal
established, the first between sinusoidal congestion and the arterioles are usually tiny, oozing is the commonest type of
already loose and hypertrophied connective tissue of anal bleeding; blood is present in the toilet paper exclusively and
cushions [4,10,11], and the second between the congestion is typically associated with bowel movements [16,23]. When
of sinusoids and increased anal pressure due to a hypertonic small arterioles are corroded, bright red blood will spurt [7]; in
internal anal sphincter [23]. this case bright red blood drips into the toilet bowl during or
Consequently, anal cushions become increasingly congested, immediately after evacuation [11,16]. Blood may rarely emerge
enlarged and engorged and are transformed into abnormal anal from the newly-formed, hypertrophied arterioles, leading to
cushions, anal nodules or “hemorrhoids”. As they have also lost serious bleeding, manifesting as blood spray around the toilet
their muscular and fibrous fixation, they prolapse through the bowl [16]. In rare cases, blood from internal hemorrhoids may
anal canal. The sliding down process of anal cushions is the follow a cranial direction towards the rectum, and then return
most crucial pathophysiologic feature of the disease [15]. In this caudally to the anus, presenting as hematochezia. Bleeding is
gradually worsening chronic process, the prolapsed nodules usually the first complaint to appear, before the hemorrhoids
are trapped in the narrow anal canal where they are gradually start to prolapse (first degree) [11,42]. In this initial stage, the
strangulated and incarcerated, increasing anal pressure and dilatation of sinusoids is still in evolution, rendering them
venous obstruction and aggravating congestion. The hyper- prone to bleeding, while the deterioration of the fibromuscular
congested nodules then further exacerbate the incarceration supporting tissue has just begun. Therefore, although
and strangulation (vicious cycle) [11,39]. hemorrhoidal cushions may be prominent on endoscopic
Prolapse of the cushions can occur acutely as well. In evaluation, their prolapse is not obvious on strenuous clinical
acute prolapse, hemorrhoidal tissue is trapped abruptly by the examination [11,25].
sphincter mechanism outside the anus; this can ultimately lead The mucosa of the prolapsing nodule is rectal and mucus-
to complete obstruction of venous return and strangulation [39]. producing [14]. The prolapsed mucosa, therefore, permits
As anal nodules prolapse through the anatomical anal canal, the passive transfer of a greater amount of mucus outside
the tissue of the nodule becomes injured, inflamed and the anus. Moreover, the inflamed mucosa of the prolapsing
friable  [10]. Indeed, a chronic serious inflammatory reaction nodule produces even more mucus [10]. The net result is the
involving both the vascular part (sinusoidal wall) and non- presence of increased mucus in the perianal skin, which causes
vascular part (supportive tissue) has been demonstrated in perineal irritation, itching and soiling. Besides this, patients
hemorrhoids  [13,40]. The inflammatory process renders the with prolapsed hemorrhoids lack the capability to sense the
arterioles of the lamina propria of the nodule vulnerable to composition of rectal sample [22] and to seal the anus after
erosion during defecation with resultant hemorrhage. This defecation [10,15,17]. Consequently, they complain of mild
bleeding presents as oozing when tiny arterioles of the lamina fecal incontinence and of finding unknown material in their
propria are eroded, and as spurting when small arterioles are underclothes [10,16]. Prolapsed internal hemorrhoids are also
corroded [40]. manifested by rectal fullness and/or a feeling of incomplete

Annals of Gastroenterology 32
 Pathophysiology of internal hemorrhoids  7

evacuation, because of their space-occupying effect. contributes to pain and irritation of perianal skin [10,11,40].
Internal hemorrhoids are not typically palpated on digital rectal Nonetheless, solid evidence to justify their efficacy in
examination, unless they are large enough or prolapsed [9,13]. hemorrhoids is lacking [8-11].
Pain is not the typical symptom, as already noted. Pain 5. Preparation-H, which contains 0.25% phenylephrine,
may be due to complicated internal hemorrhoids (thrombosis, petrolatum, light mineral oil and shark liver oil, relieves acute
ischemia, incarceration, strangulation) [11,16]. Nevertheless, pain and bleeding on defecation by restoring the imbalance
thrombosis is a rare complication [10]. Consequently, between vasoconstrictive and vasodilating agents inside
when pain is the patient’s prominent symptom and possible sinusoids. Its vasopressor effect is attributed principally to
complications of internal hemorrhoids are not detected on phenylephrine, which acts mainly on the arterial branch
clinical or endoscopic examination, the physician should search of the hemorrhoidal plexus [53]. The clinical efficacy of
for an alternative diagnosis: for example, coexisting external this formulation in relieving hemorrhoidal symptoms has
hemorrhoids, perirectal abscess or anal fissure [9,11,16]. been proven in a recent prospective randomized open-label
Internal hemorrhoids may be found, clinically or study [54].
endoscopically, in 3 distinct anatomical locations: first, above
the dentate line, since they emerge and protrude from the
mucosa of the upper anal canal [7-9]; second, below the dentate
line, but remaining inside the anatomical anal canal; and third, Surgically valuable correlations
outside the anal verge, in advanced cases.
1. The principle of the “rubber-band ligation” technique
is to band the mucosa and the submucosa of the anal
cushion. Banding generates inflammation, with ultimate
Medically valuable correlations ischemia and necrosis of the banded part. Apart from
removing the nodule, the final sequela of the procedure is
1. One major goal of the conservative treatment of the fibrosis generated: it fixes the remaining tissue in the
hemorrhoids is to normalize stool consistency; both underlying tissue of the surgical anal canal and corrects
diarrhea and constipation are clinically potent causes and the prolapse [16,21,41,55]. It is considered the mainstay
triggering factors of symptoms in hemorrhoidal disease of therapy for hemorrhoids grade  I and II [10,22] and of
and their management is as invaluable as the treatment of selected patients with grade  III [10,56]. Several trials have
hemorrhoids per se. The remaining elements of conservative proven that this minimally invasive therapeutic procedure is
therapy (e.g., avoiding of straining on defecation) have been efficient, reliable and safe for hemorrhoidal patients [56,57].
proved to limit the prolapse of hemorrhoids [43,44]. 2. The modified (Ferguson) excision hemorrhoidectomy is
2. Increased anal pressure is very important in the currently the commonest type of hemorrhoidectomy. In
pathophysiology of hemorrhoids and is a frequent clinical this operation, both the prolapsed sinusoidal tissue and the
sign, manifested as anal spasm on rectal examination. hypertrophied connective tissue are removed, whereas the
Increased anal pressure is the rationale for using topical anoderm is preserved, the internal sphincter is protected
nitroglycerine 0.4% ointment in the treatment of pain due and the sliding process, the fundamental pathophysiologic
to internal hemorrhoids [45,46]. Intra-anal pressure returns feature of hemorrhoids, is totally inverted [58-63].
to normal after hemorrhoidectomy [22]. 3. The rationale of stapled hemorrhoidopexy is the fact that
3. The principle mode of action of flavonoids (especially the both the loose mucosa and the enlarged hemorrhoidal
micronized ones, which are easily absorbed and act very nodules above the dentate line contribute to the prolapse
shortly) is by increasing the impaired vascular tone [47]. of internal hemorrhoids [9,64]. This operation is not a
Moreover, they are supposed to relieve congestion inside hemorrhoidectomy. Instead, a circular device excises a ring
sinusoids (they reduce venous capacity and decrease capillary of redundant mucosa and fixes the hemorrhoidal plexus
permeability [48]) to facilitate lymphatic drainage [49] and above the dentate line. During this operation, 3 critical
to exert anti-inflammatory effects [50]. Recent clinical trials nodes in the pathogenesis of hemorrhoids are targeted: first,
have proven the effectiveness of treatment with flavonoids, prolapse is restored; second, the volume of the hemorrhoidal
both in chronic and in acute hemorrhoidal disease. In nodules is significantly reduced; and third, the vessels
chronic disease, conservative  therapy  with micronized supplying the internal hemorrhoidal plexus are ligated,
purified flavonoid fraction was found to be beneficial both limiting the blood supply to the nodules [65].
in relieving hemorrhoidal symptoms and in preventing 4. Doppler-guided hemorrhoidal artery ligation offers
disease relapse in the majority of patients [51]. In acute a tailored, individualized therapy, since it locates the
hemorrhoidal disease, a mixture of flavonoids (diosmin, feeding terminal branch of the SRA that supplies each
troxerutin and hesperidin) was shown to control symptoms hemorrhoidal nodule [21], ultimately performing targeted
efficiently and to manage both congestion and thrombosis suture ligation [13,66]. Consequently, the increased blood
of anal cushions [52]. supply to the anal cushion is diminished, its engorgement
4. Anti-inflammatory suppositories are used to improve the is prevented, its size is decreased and it is ultimately firmly
symptoms of hemorrhoids; the rationale of using them is fixed to the floor of the upper surgical anal canal [67]. This
that inflammation is the triggering factor of bleeding and alternative operational technique has been proven to relieve

Annals of Gastroenterology 32
8  N. Margetis

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Annals of Gastroenterology 32