Introduction
Colonic angioectasia are the most common vascular lesions in the gastrointestinal
tract and are among the most common causes for chronic or recurrent lower gastrointestinal
bleeding [1]
[2]. Angioectasia are an acquired vascular malformation associated with advanced age.
Pathogenesis of colonic angioectasia formation is multifactorial and commonly attributed
to mild chronic venous obstruction and to chronic mucosal hypoxemia resulting in increased
vascular endothelial growth factor (VEGF) expression [3]. Low-grade, intermittent, obstruction of venous drainage, hypothesized to be related
to colonic luminal dilation, results in dilatation of submucosal veins. This in turn
leads to mucosal venule and capillary dilatation and when the pre-capillary sphincter
loses competency, arteriovenous fistula form, resulting in formation of the characteristic
mucosal lesion [4].
Colonic angioectasia are most commonly found in the right colon (54 % – 89 % located
in cecum and ascending colon). Prevalence of colonic angioectasia is estimated to
be 0.8 % – 6.2 % [2] and is higher in patients with comorbidities such as aortic stenosis, Von Willebrand
Disease (vWD) and chronic kidney disease (CKD). Colonic angioectasia more often presents
as multiple lesions rather than a single lesion (40 % – 60 %) [5].
Most colonic angioectasia are found incidentally, are asymptomatic and do not require
treatment [2]. However, they have been implicated as the source of bleeding in 3 % to 15 % of
lower gastrointestinal bleeding [6] and up to 30 % in cases of severe hematochezia [7].
Multiple endoscopic modalities have been reported for treatment of colonic angioectasia.
The most commonly used endoscopic treatment is argon plasma coagulation (APC) but
other modalities have also been described, including bipolar or heater probe coagulation,
endoscopic clips, and injection sclerotherapy [3]. APC is simple to use and widely accepted but it is not complication-free with a
perforation rate of 1 % [8]. Post-treatment rebleeding rates of up to 34 % have been described [9] and many patients will need ongoing iron supplementation on long-term follow-up.
Most patients need more than one course of endoscopic treatment [10].
All existing endoscopic therapies target the mucosal expression of the underlying
vascular lesion. We propose a technique that targets the submucosal “feeding” vessel
to definitively treat colonic angioectasia.
Methods
Elevate, snare resect, coagulate (ESC) method
The mucosal lesion is resected by endoscopic mucosal resection (EMR). Submucosal injection
is
made with normal saline or succinylated gelatin (“Gelofusine”; B. Braun, Crissier,
Switzerland)
[11] and adrenaline at a final concentration of 1:100 000. Inert dye
(methylene blue or indigo carmine) can be added to the solution to enhance delineation
of the
colonic angioectasia margin. The mucosal part of the colonic angioectasia is resected
en bloc
with fractionated electrocautery set to EndoCut Q, effect 3 (ERBE, Tübingen, Germany).
The
underlying feeding vessel is then identified and cauterized with coagulation forceps
using soft
coagulation, effect 4, 80 watts (ERBE, Tübingen, Germany). The defect is then closed
with
endoscopic clips ([Fig. 1], [Fig. 2],
[Video 1]). Specimens were retrieved for histopathological examination ([Fig. 3]). Snare tip soft coagulation with the same energy settings can be used for small
flat vessels within the defect that are difficult to grasp.
Fig. 1 a Cecal angioectasia. Elevation with saline without dye. b, arrow Feeding vessel clearly seen after mucosal resection.
Fig. 2 a Elevate, snare resection, coagulate (ESC) of a proximal ascending colon angioectasia.
b Elevation with chromogelofusion solution is followed by c snare resection. d The submucosal feeding vessel is identified (yellow arrow) and e treated by soft coagulation. f The defect is then closed by clips.
Fig. 3 Histopathology from resected colonic angioectasia. Hematoxylin & eosin stain × 40.
Dilated, clustered vessels in mucosa and submucosa, with tortuous feeding vessel at
the resection base (marked with black arrows).
Video 1 Elevate, snare resection, coagulate (ESC) of a proximal ascending colon angioectasia.
Elevation with chromogelofusion solution is followed by snare resection. Bleeding
is encountered from the submucosal feeding vessel and is treated immediately by snare
tip soft coagulation followed by coagulation forceps soft coagulation. The defect
is then closed by clips.
Results
Between May 2016 and Nov 2018, six patients with a total of 14 colonic angioectasia
were treated with ESC ([Table 1]). The most common indication was iron deficiency anemia. Other indications were
recurrent lower gastrointestinal bleeding. Mean size of the treated lesions was 6 mm
(3 mm to 10 mm). All lesions were in the right colon with the majority in the cecum.
No immediate or delayed complications occurred. Mean follow up is 10 months (range
3 – 18). None of the treated patients have required blood or iron products nor required
repeat endoscopies for ongoing blood loss.
Table 1
Patients characteristics.
|
Patient
|
Age
|
Sex
|
Indication
|
Previous treatment
|
No. of lesions
|
Location
|
|
1
|
79
|
Male
|
IDA, LGIB
|
APC
|
3
|
Cecum, ascending
|
|
2
|
81
|
Male
|
IDA
|
APC
|
1
|
Cecum
|
|
3
|
84
|
Female
|
IDA
|
None
|
1
|
Cecum
|
|
4
|
58
|
Female
|
IDA
|
None
|
2
|
Cecum
|
|
5
|
66
|
Male
|
IDA
|
None
|
4
|
Cecum, ascending
|
|
6
|
66
|
Male
|
IDA
|
None
|
3
|
Cecum
|
IDA, iron-deficiency anemia; LGIB, lower gastrointestinal bleeding; APC, argon plasma
coagulation.
Discussion
Colonic angioectasia are an important etiology of chronic, recurrent and acute gastrointestinal
bleeding. While the majority of these lesions are asymptomatic, treatment is usually
warranted for overt bleeding and occult bleeding leading to iron deficiency anaemia.
In 2019 the majority of colonic angioectasia are treated with APC. This targets mucosal
expression of the primary pathology located in the deeper submucosal layer. Scientific
and clinical data attest to APC’s lack of precision. Accurate lesion targeting is
suboptimal, even when en-face, and depth of tissue destruction is not standardized
or predictable and subject to the angle of influence of the argon beam to the mucosal
surface. An en-face position delivers deeper, possibly dangerous tissue destruction,
whilst a tangential approach is less injurious and possibly suboptimal. Moreover,
immediate APC-induced bleeding is common and formation of a carbonized coagulum of
blood over the lesion limits energy penetration and the ability to achieve complete
mucosal layer destruction, as manifested by APCʼs failure to prevent recurrent adenoma
[12]. These aspects may explain the high rebleeding rate and need for multiple procedures
[9]. The majority of colonic angioectasia are located in the right colon where risk
of perforation with thermal ablative therapies is highest.
Targeting submucosal vessels for treatment of vascular pathologies elsewhere in the
gastrointestinal tract has been described, primarily with polidocanol submucosal injection.
This sclerosing agent, historically used for variceal [13] and ulcer treatment [14], has also been used for angioectasia treatment in the small bowel [15]. However, it has been associated with delayed perforations in the esophagus and
stomach as the sclerosing tissue effect can be unpredictable [16].
These issues challenge endoscopists to develop a standardized, predictable, and reproducible
method to treat the primary pathology of colonic angioectasia.
ESC targets the primary pathology of colonic angioectasia, the submucosal feeding
vessel or vessels by a modification of standard EMR. Basic EMR forms part of the core
endoscopic training and, even in the right colon, is proven to be safe with a reported
perforation rate of 0.05 % to 0.07 % [17]. In addition, EMR for these small vascular lesions, < 10 mm, is inherently safe
due to the small lesion size, however, it easily exposes the primary submucosal pathology
to facilitate precisely targeted therapy. Snare tip soft coagulation has also proven
to be a safe and effective method of securing hemostasis for bleeding during colonic
EMR and polypectomy and can be used safely in this submucosal context as previously
shown [18]. Clip closure of small mucosal defects is well established and adds an additional
safety measure against delayed perforation or bleeding [19]. Defect closure may not be necessary, but additional study is required and there
seems little down side when it is easily achieved with few clips.
Because our study describes a novel technique and introduces the concept of endoscopic
targeting of the colonic angioectasia’s feeding vessel, we did not compare outcomes
to current treatment options, such as APC. This limitation will need to be addressed
in future research.
Conclusion
In conclusion, ESC appears to be safe and effective for treatment of colonic angioectasia.
It specifically targets the primary pathological feeding vessel(s) underlying the
mucosal lesion allowing for definitive destruction of the colonic angioectasia. This
treatment skillset is within that of most endoscopists who remove polyps and thus
it is readily available. Large prospective randomized trials are required to establish
the role of ESC in treatment of colonic angioectasia. These may prove to be logistically
challenging to conduct; however, ESC has the potential to replace APC as the standard
of care for symptomatic colonic angioectasia.
