Key words
abdomen - angiography - embolization - interventional procedures - hemorrhage
Introduction
Non-variceal gastrointestinal bleeding is often an urgent, potentially life-threatening
emergency [1]. In 75–85 % of cases they are located in the upper gastrointestinal tract [2]
[3]. Treatment generally requires a structured interdisciplinary approach with therapeutic
options ranging from conservative, surgical, endoscopic to endovascular procedures.
The indication for endovascular therapy is closely oriented to the recently published
S2k guideline of the German Society for Gastroenterology, Digestive and Metabolic
Diseases (DGVS) [4].
Classification, Epidemiology and Etiology
Classification, Epidemiology and Etiology
Upper gastrointestinal bleeding (UGIB) is bleeding above the ligament of Treitz. With
an incidence of 50 to 100 per 100 000 population, it is a common pathology with a
median disease age of 60–70 years [5]. In 70–75 % of cases an upper GI bleed ceases spontaneously. The mortality rate
is between 3 and 14 %, for intensive care patients between 42 and 64 % [1]. In approximately 50 % of cases, UGIB results from an ulcer disease such as a gastric
ulcer or duodenal ulcer. Other causes include esophageal or gastric tumor bleeding,
Mallory-White syndrome, erosive gastritis or duodenitis, reflux esophagitis, angiodysplasia
and iatrogenic or post-traumatic changes.
A special case of UGIB is acute hemorrhagia of the peripancreatic vessel branches
or collaterals, which etiologically often result from pancreatitis, tumors and trauma.
Hemorrhages after pancreatic surgery due to pancreatic jejunostomy or biliodigestive
anastomosis, with a mortality rate of 11–38 %, are among the most complex and difficult
to treat complications due to vascular congestion. In many cases, such postoperative
complications of endovascular therapy are easily accessible, which can significantly
reduce morbidity and mortality rates [6].
Lower gastrointestinal bleeding (LGIB) beyond the ligament of Treitz, with an incidence
of about 20 to 30 per 100 000 population and a median age of 65–80 years increases
dramatically with age [7]. In 80–85 % of cases LGIB ceases spontaneously. Recent studies indicate the mortality
between 2 and 5 % [1]. Etiologically, LGIB can be attributed to causes such as diverticulitis, angiodysplasia,
polyps, tumors, proctitis or chronic inflammatory bowel disease [8].
Anatomy
The upper gastrointestinal tract contains pronounced vascular anastomoses and physiological
collaterals, which on the one hand make the intestinal segments less susceptible to
post-embolic ischemia, but on the other hand can make bleeding control more difficult
due to the maintenance of bleeding via the “back door” and the necessity of occlusion
of the feeder vessel proximal and distal to the bleeding source or due to the occurrence
of recurrent bleeding. These vascular anastomoses consist of branches of the pancreaticoduodenal
arteries between the celiac trunk and the superior mesenteric artery. The arch of
Riolan and the Drummond anastomosis connect the superior and inferior mesenteric arteries.
Anastomoses exist between branches of the superior mesenteric artery and the internal
iliac artery via branches of the superior and medial rectal arteries. A large number
of anatomical variants, in particular the branches of the celiac trunk, require a
thorough evaluation of the vascular anatomy before planned embolization [9].
Symptomology
The clinical presentation of gastrointestinal bleeding varies as a function of the
severity and localization of bleeding. Occult bleeding can manifest itself as iron
deficiency anemia or lead to a positive hemoccult test if there are other symptoms.
In the case of heavy bleeding of the upper GI tract, clinical signs such as regurgitation
of blood or hematemesis are evident; melena may also occur. Hematochezia is indicative
of heavy bleeding of the upper or lower GI tract. In chronic forms, non-specific signs
such as fatigue, tiredness or shortness of breath may occur. Depending on its severity,
acute bleeding leads to symptoms of circulatory insufficiency or a hypovolemic shock
with tachycardia, hypotension and collapse.
Clinical Evaluation and Diagnosis
Clinical Evaluation and Diagnosis
Initial and pre-interventional management includes the anamnesis of clinical manifestation
and bleeding duration as well as the assessment of accompanying symptoms, medication,
concomitant and pre-existing conditions and interventions such as polypectomy or surgery.
Further procedure depends on the hemodynamic status of the patient and the suspected
location of bleeding. The hemoglobin value and the (modified) Glasgow-Blatchford score,
in which vital parameters, laboratory values and pre-existing conditions are taken
into account for risk stratification (open recommendation, strong consensus), can
be used for the initial assessment of the severity of bleeding and for clinical decision
making [4]
[10]
[11]
[12].
According to the guideline, hemodynamically unstable patients with non-variceal UGIB
should receive intensive medical care, after stabilization, should be examined promptly
(< 12 h) using EGD (strong recommendation, strong consensus) [4]
[12]. In hemodynamically stable patients, endoscopy should be performed within the first
72 hours after continuous monitoring of the vital parameters (open recommendation,
strong consensus) [4]
[13]. Since severe consequences of LGIB are less frequent and mortality and bleeding-related
mortality are lower, outpatient treatment is often possible [14]. Severe hemorrhages of the lower GI tract with hemodynamic compromise should be
promptly colonoscopied after drug stabilization (recommendation, strong consensus).
Detection of the source of bleeding in these situations is only possible in about
42 % of cases due to inadequate intestinal preparation in emergency management and
the limited visibility of the colon and proximal ileum [15].
Depending on the bleeding type and genesis, endoscopic hemostasis can be achieved
by various mechanical methods (rubber band ligation, hemoclips) and thermal procedures
(electrocoagulation), injection therapy (e. g. with adrenalin) and the use of Hemospray
(open recommendation, strong consensus) [4]. If an endoscopic hemostasis attempt remains unsuccessful, endoscopy can nevertheless
contribute to precise endovascular intervention planning and facilitate superselective
catheterization of the corresponding bleeding vessel branch by means of clip marking
of the detected bleeding source, especially if no active contrast extravasation can
be detected angiographically [16].
In the case of frustrated identification of the bleeding source during endoscopy,
further diagnostic procedures are available, depending on the bleeding dynamics and
availability of other diagnostic procedures, provided that the affected patients concerned
are hemodynamically stable or stabilized. Detection using contrast-enhanced multi-line
computed tomography can be performed at bleeding rates of 0.5 ml/minute and above
[17]. In multi-phase technology, CT as non-invasive imaging allows rapid diagnosis with
good sensitivity and specificity and can contribute to the planning of further therapy
regimes in addition to localization of bleeding [18]. According to current data, due to its high spatial resolution, digital subtraction
angiography (DSA) allows the identification of a bleeding source at bleeding rates
between 0.5 and 1 ml/minute [21]. There is high variability in the literature with respect to regard to sensitivity
and specificity of catheter angiography [22]. The invasive character of DSA, which can be considered disadvantageous, is countered
by the possibility of simultaneous treatment of GI bleeding. In a direct comparison
with CTA, several studies showed its superiority with regard to the sensitivity of
the detection of the bleeding source and the cause of bleeding [22]
[23]. In summary, it can be recommended that patients, after a frustrated endoscopic
search for the source of hemorrhage, should first be referred to multi-phase CT diagnostics
in the case of hemodynamic stability, since important information can be obtained
regarding the cause of the bleeding, possible vascular anomalies and variants. This
can contribute to an exact planning of the subsequent (endovascular) therapy and a
consecutive shortening of the intervention time [19]
[22]. In addition, this approach is in line with the recommendations of the current S2k
guideline [4]. A blood cell scintiscan using 99 mTc-marked red blood cells with a sensitivity of 93 % and specificity of 95 % enables
the localization of intermittent GI bleeding from low bleeding rates of 0.2 ml/minute
[20].
Pre-interventional Preparation
Pre-interventional Preparation
In the case of hemodynamic instability, hypovolemia should be balanced with erythrocyte
concentrates, crystalloids or colloids and catecholamine or vasoconstrictor therapy
prior to intervention [12]
[24]
[25].
In addition, the relevant coagulation parameters (INR, PTT) should be determined and,
if necessary, optimized, since mechanical embolic agents in particular often only
cause sufficient vessel occlusion if the coagulation cascade is intact [21]. Administration of glucagon or buscopan may be considered to reduce intestinal peristalsis.
Peri-interventional observation should be performed with continuous monitoring of
blood pressure, electrocardiographic parameters, arterial oxygen saturation and, if
necessary, respiration rate. Depending on the patient’s hemodynamic status, the presence
of an anesthesiological team may be necessary for monitoring. The condition of the
patient ultimately also determines whether the intervention takes place under local
anesthesia and analgosedation or under general anesthesia.
Indications
Based on existing clinical data, there is a strong consensus and an open recommendation
for the treatment of GI bleeding. This means that open surgical or radiological endovascular
intervention may be performed after a) technical failure of endoscopic hemostasis
including reserve procedures; b) relapse bleeding after second endoscopic intervention;
and in the case of c) endoscopically non-localizable source of bleeding [4]. This also includes bleeding which is not endoscopically accessible due to special
circumstances (e. g. after Billroth II or Whipple surgery). Peripancreatic bleeding,
resulting from acute and chronic pancreatitis or after pancreatic surgery, is a critical
scenario with high mortality rates. The underlying release of proteolytic pancreatic
enzymes leads to damage of vessels with consecutive formation of pseudoaneurysms and
vascular ruptures [26]
[27]. Surgical treatment in this context is difficult due to the often retropancreatic
localization of bleeding and inflammatory environmental reaction. High mortality rates
and frequently the necessity of a radical surgical procedure, e. g. (hemi) pancreatectomy
and splenectomy, are the result [28]. In such situations, endovascular therapy represents an effective alternative with
good success rates, the primary use of which should be considered in relevant centers
[28]
[29]
[30].
Obscure bleeding includes GI bleeding that intermittently leads to symptoms perceptible
to the patient, such as hematemesis, hematochezia or melena, but is not detected by
endoscopic diagnostics. Occult bleeding is only noticeable due to the presence of
iron deficiency anemia or the positive result of a hemoccult test. Obscure and occult
bleeding can occur in any section of the GI tract and represent a diagnostic and therapeutic
challenge. Further diagnostic procedure depends crucially on the clinical symptoms,
which in turn can lead to repeated endoscopic evaluation including special techniques
such as deep enteroscopy and capsule endoscopy. In the case of a non-detectable source
of bleeding and persistent symptoms, an angiography with the willingness to intervene
may be considered since there is at least a low probability of identifying it compared
to occult hemorrhages [31]. Since the angiographic depiction of bleeding requires a bleeding intensity of at
least 0.5 ml/min, angiography plays a subordinate role in the diagnosis and treatment
of occult GI bleeding.
Contraindications
Contraindications for endovascular therapy – such as contrast agent allergy, hyperthyroidism,
pregnancy, sepsis, acute kidney failure and consumption coagulopathy – are to be regarded
as relative, especially in acute threatening situations. Depending on the intensity
of the bleeding, the possible superiority of surgical therapy must be considered.
Technique
As a rule, endovascular treatment of upper GI or lower GI bleeding is performed under
local anesthesia via a transfemoral access pathway, although transbrachial access
can also be considered, especially in the case of an unfavorable angle of descent
of the visceral vessels. Depending on the vascular anatomy, insertion of a long reinforced
guide sheath for catheter stabilization may be useful. Especially in the absence of
pre-interventional imaging, mechanical preparation of a survey angiography via a multi-hole
pigtail catheter allows evaluation of the vascular anatomy for subsequent targeted
vascular exploration. The most suspicious or identified visceral vessel is probed
using a preferred selective catheter, and a selective angiography is performed. For
UGIB, the celiac trunk and then the superior mesenteric artery are probed; in the
case of LGIB the superior and inferior mesenteric arteries are examined. The use of
approximately 50 ml 1:1 diluted contrast agent at a flow rate of 15 ml/s is recommended
for a proper aortography; for selective angiography of the celiac trunk, the superior
and inferior mesenteric arteries, 30–50 ml 1:1 diluted contrast agent at flow rates
of approximately 6–7 ml/s is recommended [32]. In case of rectal bleeding and inconclusive presentation of the inferior mesenteric
artery, angiography of the internal iliac artery including the middle and inferior
rectal arteries should be performed [33]. In this case, care must be taken to ensure sufficient exposure time to distinguish
between contrast agent extravasation and venous washout. Angiographic evidence of
GI bleeding in the active bleeding interval presents as contrast extravasation in
the arterial phase with pooling in the venous phase. However, indirect signs such
as evidence of pseudoaneurysms, vascular spasms or – in the case of inflammatory changes
– blushing and focal hyperemia can also be interpreted as angiographic evidence of
(intermittent) GI bleeding [34]. Early venous discharge may indicate angiodysplasia.
Superselective vascular probing and thus the use of coaxial or triaxial microcatheter
technique is often necessary to identify an upper or lower GI bleed. The coaxial technique
involves the use of a microcatheter within a selective catheter; the triaxial technique
involves the use of a microcatheter and a selective catheter within a reinforced guide
sheath or guide catheter.
The frequently intermittent character of gastrointestinal bleeding may lead to a negative
angiographic result despite recent relevant bleeding. In these cases, repeated angiography
at a later stage or bleeding provocation by selective intra-arterial application of
nitroglycerin, heparin or tPA may be considered [35].
In the absence of evidence of active contrast extravasation, blind or empirical embolization
based on an endoscopic finding may be possible, although prior endoscopic clip marking
may be helpful [16]
[36].
The patient should promptly undergo surgery in the event of technically frustrated
intervention due to feeder vessels that cannot be probed, or even in the case of diffuse
bleeding. Until the patient is transferred to the OR, balloon occlusion can be used
to achieve preoperative hemodynamic stabilization. Additional options for facilitating,
identifying and accelerating surgical therapy include catheter-assisted staining of
the bleeding intestinal segment with methylene blue.
Once angiographically identified, the location of the upper or lower GI bleeding (distal
vs. proximal) determines the endovascular procedure to be used.
Embolization
In more distal hemorrhages, embolization is performed by coaxial or triaxial microcatheterization
([Fig. 1], [2], [3], [4]). The choice of the appropriate embolic material to stop the respective hemorrhage
is at the discretion of the interventionist and is influenced by practical experience,
local availability of material, the cause of bleeding, coagulation situation and extent
of the angiographic findings. The use of a temporary embolic agent such as a gelatin
sponge as the sole embolization material has been associated with an increased rate
of secondary bleeding and should therefore be avoided [34]. Microspirals are the most commonly used mechanical embolization material in the
treatment of GI bleeding. With technical success rates between 80–90 % for upper gastrointestinal
bleeding and 40–88 % for the lower gastrointestinal bleeding, microspirals support
practicable placement with good radiopacity and, precisely because of their good visualization
properties, reliable embolization [37]. However, the use of microspirals alone has been associated with a significantly
increased rate of recurrent bleeding compared to a combination with cyanoacrylates
or particles [34]. Cyanoacrylates as the sole liquid embolic material or in combination with other
agents have been shown to be particularly effective in patients with impaired coagulation
[34]
[38]
[39]. Especially in the case of hemodynamic instability, they offer the advantage of
a significantly shorter procedure time [40] The likelihood of reflux, misembolization or adherence of the catheter tip to the
polymerized adhesive or vessel wall is considered a relative risk. Ethylene-vinyl
alcohol copolymer can be used as an alternative liquid embolization material [41]
[42]. Particulate embolic agents such as polyvinyl alcohol particles or microspheres
have a particle diameter of less than 250 µm and therefore carry the risk of intestinal
ischemia due to reaching the intramural vascular bed [7]. Nevertheless, particles have been shown to be effective in controlling bleeding
due to malignant tumors without increasing the incidence of post-embolic-ischemic
complications [43]. The low radiopacity – despite combination with contrast medium – thus providing
only indirect visualizability requires a limited control of embolization and necessitates
a certain amount of experience for this embolic agent as well.
Fig. 1 Lower GI bleeding with unidentified genesis in a 55-year-old male. a An axial CTA in the arterial contrast phase shows an intraluminal contrast extravasation
within a jejunal loop in the left lower abdomen. b Superselective DSA using coaxial microcatheter technique allows the identification
of the related feeder vessel. c Superselective DSA using coaxial microcatheter technique allows the identification
of the related feeder vessel. d Selective DSA after microspiral embolization, in which active bleeding can no longer
be detected.
Fig. 2 Iatrogenic upper GI bleeding after PEG placement in a 55-year-old female. a Overview of the non-selective DSA shows a pronounced contrast extravasation from
the left gastric artery. b In superselective DSA, a microcatheter is used to identify the true extent of active
bleeding from the left gastric artery. c Superselective DSA after microspiral embolization shows the successful elimination
of active bleeding. d Selective final DSA again documents cessation of the iatrogenic upper GI bleeding
from the left gastric artery.
Fig. 3 Lower GI bleeding as a consequence of ulceration in a 57-year-old male under intensive
care. a Coronal CTA shows active contrast extravasation in the arterial contrast phase at
the level of the cecum. Evidence of abundant fresh blood within the ascending colon.
b Selective DSA impressively shows active bleeding in the final flow area of the ileocolic
artery. c Superselective DSA via a microcatheter after spiral embolization identifies a further,
circumscribed active bleeding from another vasum rectum of the ileocolic artery. d Selective control DSA demonstrates successful hemostasis in the final flow area of
the ileocolic artery.
Fig. 4 Upper GI bleeding in a 73-year-old male with bleeding duodenal ulcer and unsuccessful
endoscopic hemostasis. a, b Selective DSA shows extensive active contrast extravasation from the gastroduodenal
artery. c Superselective DSA with positioning of a microcatheter beyond the bleeding source.
d Selective control DSA shows successful elimination of the bleeding source after microspiral
embolization within the gastroduodenal artery using front door-back door technique.
Due to pronounced vascular anastomoses, especially of the upper GI tract, the front
door-back door technique with occlusion of the feeder vessel proximal and distal to
the bleeding source is often necessary for sufficient embolization. Alternatively,
embolization of two supplying vessels (initially branches of the celiac trunk, then
the superior mesenteric artery or vice versa) may be necessary.
The level of embolization plays a significant role here. Since the risk of territorial
ischemia increases with too proximal vascular occlusion, distal, super-selective probing
of the vessel supporting the bleeding should be sought. This applies in particular
to endovascular treatment of lower gastrointestinal bleeding and especially to bleeding
of the colon, as this has a much lower collateralization compared to the upper GI
tract [44].
Vasoconstriction
Selective intra-arterial infusion of vasopressin for vasoconstriction thus providing
temporary hemostasis has been used since the 1970s; but due to its significantly increased
rate of recurrent bleeding and potential side effects, it has fallen into general
disuse [27]
[28]. However, this technique may be considered in situations where superselective vascular
probing and embolization is not possible [29].
Covered stents
Covered stents can be a suitable alternative in the treatment of GI bleeding, especially
for vascular injuries to larger proximal main or secondary branches ([Fig. 5]). With suitable anatomy and bleeding localization, their use supports lumen-preserving
prevention of bleeding. Selection of an appropriate stent size is of particular importance,
as too small a diameter can result in stent migration and formation of endoleaks;
too large a diameter can lead to vessel rupture. The presence of vascular spasms as
well as reduced vascular diameter in the case of circulatory instability and centralization
complicate this selection. In general covered stents are available as over-the-wire
or rapid exchange systems. The use of reinforced guide catheters or sheaths is recommended
for the proper and smooth placement of covered stent systems.
Fig. 5 Upper GI bleeding in a 70-year-old female after pylorus-preserving Whipple surgery.
a Selective DSA shows active bleeding in the flow area of the proper hepatic artery.
b A slightly more selective DSA via a reinforced guide sluice confirms the active contrast
extravasation in the flow area of the proper hepatic artery. c Radiography represents the sluice-supported placement of a balloon-expandable covered
stent. d The final angiography documents the sealing of the arroded vascular segment.
Post-interventional Procedure
Post-interventional Procedure
The focus here is on the patient's hemodynamic status to determine the extent of the
effectiveness of the endovascular measure. In addition, regular monitoring of lactate
levels should be carried out, the increase of which, in combination with abdominal
symptoms, may be indicative of intestinal ischemia. If necessary, a control endoscopy
can be useful. The utility of antibiotic treatment with first generation cephalosporins
depends on the respective clinical conditions and should therefore be decided on a
case-by-case basis.
Results
The body of data regarding endovascular treatment of upper and lower GI bleeding,
in particular embolization using coaxial or triaxial microcatheter technology, is
constantly increasing, but must be viewed cautiously due to the inhomogeneity of the
underlying pathologies. In this context, the data published so far are often based
on retrospective results, often small to medium case series and with at most short
to medium-term follow-up periods. It is relevant for the interpretation of the clinical
results that corresponding published studies are partly based on differing reporting
standards.
According to current clinical literature, bleeding of the upper gastrointestinal tract
can be treated with technical success using endovascular procedures in 69–100 % of
cases [34]
[45]
[46]
[47]
[48]
[49]. In contrast, clinical success rates are between 58 and 91 % [34]
[49]
[50]. Compared to surgical procedures, interventional radiological strategies in the
treatment of upper GI bleeding show similar efficacy in terms of technical success
and rate of recurrent bleeding, but with lower mortality [51]
[52]
[53]. In the respective cohorts, however, patients treated with interventional therapy
had a higher rate of comorbidity as well as higher age, which could explain the relatively
high mortality rate of up to 33 % [34]. Recurrent bleeding, which occurred in about one-third of cases, was accessible
for a new intervention in 50 % of the cases; in 20 % of the patients surgical measures
were necessary for definitive bleeding control [34]. Apparently selective, empirical arterial embolization without angiographically-detectable
contrast extravasation may also be effective. Thus, in different study cohorts, no
difference was found with regard to the outcome among patients in whom blind embolization
was performed based on endoscopic or surgical findings and those in whom embolization
relied on an angiographic image of the bleeding [24]
[26]
[47]. In contrast, if one considers the publication by Schenker et al. [48], who blindly embolized 103 of 163 patients (63 %) within their patient cohort due
to different bleeding etiologies, the question arises to what extent this therapeutic
approach might have contributed to the high recurring bleeding rate of 42 % (68 out
of 163 patients) and mortality rate of 33 % (54 out of 163 patients).
These results are based on only sparse data if one considers the endovascular results
of acute bleeding of the peripancreatic vessels, which is difficult to treat and is
often based on erosion due to released proteolytic enzymes in the course of acute
pancreatitis or surgical intervention. Nevertheless, technical success rates of up
to 93 % have been described in this respect, while clinical success rates of up to
91 % have been described, with mortality rates being reduced by up to 60 % compared
with surgical procedures [54]
[55]
[56]
[57].
There is agreement that the survival of patients after endovascular upper GI bleeding
therapy is highly influenced by the general condition of the patient at the time of
intervention [48]
[58]. Thus, patients with multi-organ failure exhibit significantly higher mortality
rates. In this context, mortality is highly dependent on the primary technical success
of endovascular treatment with mortality rates of up to 96 % in the event of treatment
failure [48].
Endovascular treatment of LGIB is possible with technical success between 89 and 100 %
and clinical success rates between 81 and 90 %, especially after failure of an endoscopic
attempt to stanch bleeding [7]
[21]
[29]
[44]. The improvement of the superselective embolization technique through the development
of microcatheter systems with an external diameter down to 1.8 French plays a major
role in this context, as this enables the precise probing of the smallest feeder arteries
(vasa recta). This minimizes the rate of misembolization, especially as the treatment
is mainly performed in the terminal branches. In this context, it appears to be highly
significant that recurrent bleeding in the sense of clinical failure is often located
in intestinal segments other than the actual area of embolization [59]
[60]. This may be primarily due to the relevant bleeding etiology. Diverticular bleeding
responds better to embolization than those of the lower gastrointestinal tract with
other etiologies such as tumors or bleeding resulting from angiodysplasia [60]. In this context, the distinction between early recurrent bleeding within 30 days
and late recurrent bleeding > 30 days after embolization may be useful, as suggested
by d'Othee et al. [59].
Various studies have identified technical and clinical predictors for a negative outcome
with respect to technical failure and recurrent bleeding in the endovascular treatment
of upper and lower GI bleeding. Previously untreated coagulopathy showed a strong
influence on the treatment outcome, underlining the importance of adequate peri-interventional
treatment of coagulation disorders [48]
[61]. Other risk factors for interventional treatment failure include multimorbidity,
low hemoglobin levels, hemorrhagic shock, corticosteroid treatment, prolonged duration
of intervention and increased need for transfusion of blood products [46]
[47].
Complications
Potential complications include general risks of endovascular therapy such as hematomas
in the access area, vascular dissections or contrast-associated complications (allergy,
nephropathy) [34]. In addition, fever, leukocytosis, sepsis and abdominal pain may occur as part of
post-embolization syndrome. The risk of related intestinal ischemia after embolization
shows a clear dependence on the localization and embolization agent used, and lies
between 0 and 20 % for UGIB and between 0 and 22 % for LGIB [29]
[33]
[34]
[44]
[59]
[62].
Due to distinct alternative circulatory routes, arterial embolization of the upper
gastrointestinal tract can be described as very safe and rarely leads to ischemic
complications. Agents reaching the distal vascular bed, such as liquid embolic agents
or small particles, are associated with an increased risk of significant ischemia
with gastroparesis, intestinal gangrene and necrotizing pancreatitis [63]. In addition, prior surgical procedures at the embolization site have been associated
with increased rates of severe ischemic complications following embolization of upper
GI bleeding [46]. In addition, symptomatic duodenal stenosis could be observed as a long-term complication
after embolization of terminal branches of the upper gastrointestinal tract [45].
The lower GI tract is significantly more sensitive to postprocedural intestinal ischemia
due to less pronounced collateralization, which depending on the extent of the embolization
area, may manifest as minor ischemia (mucosal ischemia) with transient abdominal discomfort
and increase in lactate levels, or in approximately 1–5 % of cases as major ischemia
(transmural infarction) with the need for surgical resection [29]
[64]
[65]. Nevertheless, the development and improvement of microcatheter technology and embolization
has led to a minimization of the rates of post-embolic minor and major ischemia [44]
[66]. Distal embolization at the level of the vasa recta or marginal arteries contributes
to a significant reduction of the risk of critical ischemic complications [41]
[42]
[43]. Major ischemic complications requiring surgery occur here only in isolated cases
and are mostly due to necessary superselective probing of the feeder branch in question,
especially in the context of generalized atherosclerosis [67]. In exceptional cases, however, the clinical relevance of intestinal ischemia should
be put into perspective, i. e. when hemostasis is used for preoperative bridging.
Within such a scenario, endovascular intervention with hemodynamic stabilization can
be followed by medical optimization of the patient's general condition and risk stratification.
Summary
Endovascular therapy of upper and lower GI bleeding is a minimally invasive measure
that should be carried out according to guidelines and with close interdisciplinary
cooperation. The underlying etiology of bleeding, the localization and dynamics of
bleeding, as well as the structural, staff and equipment conditions of the respective
site, are all factors that influence the choice of diagnostic and therapeutic measures.
Previous data indicate that endovascular strategies may be beneficial for morbidity
and mortality in patients with high surgical risk.