Introduction

Ischemic changes in the abdominal organs develop slowly and are therefore often diagnosed at a late stage. These changes can cause dramatic illnesses. Mortality from diseases related to ischemic changes in the abdominal organs has not been significantly reduced over the course of the last decade. The cause of these high mortality rates is the insufficient integration of the overall clinical picture into the differential diagnostics. This means that an appropriate therapy or treatment option is often applied too late.

Acute mesenteric ischemia should be considered distinct from etiological, therapeutic, and prognostic chronic visceral ischemia. Acute intestinal ischemia is a vascular emergency with a mortality rate of 60–80%; this is due to the difficulty of diagnosis and the rapid nature of ischemic tissue deterioration.

The incidence of chronic visceral vascular disorders accounts for approximately 1–2% of all abdominal conditions. The difference with intestinal ischemia is the progressive nature of the condition and the increase of arteriosclerotic-related multimorbidity in an increasingly elderly population. Due to excellent collateralization, extensive chronic occlusion processes affecting the visceral arteries can be asymptomatically treated on a long-term basis.

The symptom-producing visceral artery, the superior mesenteric artery (SMA), is involved in 85% of all cases. Progressive malperfusion causes abdominal resting pain and tissue lesions to develop. All symptomatic stages of visceral ischemia provide indications for invasive treatment. The diagnostic tools of choice in this case are a CT angiography with an early arterial contrast agent bolus injection, followed by evaluation of the axial primary layers and multiplanar reconstruction of the imaging technique. Alternatively, prior to diagnostics, a color-coded duplex sonography is performed; in individual cases, a contrast agent-enhanced MR-angiography should be considered. The duplex sonography should be considered the primary diagnostic technique because it allows for the evaluation of the hemodynamic relevance of a stenosis. However, it should be noted that the assessment potential of this technique is limited if the patient is obese or has an excessive amount of air in the intestinal loops. Classic angiography is used only for interventional therapy planning and its effectiveness can be limited especially when the patient has extreme overlying intestinal gas (by previous endoscopy).

The visceral vascular system is characterized by excellent collateralization and compensation capacities. Embryonic development is characterized by the development of segment arteries. The three remaining segment arteries will later develop into the truncus coeliacus, the SMA, and the mesenteric inferior artery (IMA). Anomalies or system variants relate almost exclusively to the flow region of the truncus coeliacus and the SMA, which are abundant and extremely complex and can be traced back to a partial or atypical regression of the primitive intestinal arteries [1].

From an anatomic–topographic point of view, the median arcuate ligament and the muscular structure of the diaphragm are also of interest as they are adjacent to the truncus outflow and can cause compression resulting in the corresponding symptoms (Dunbar syndrome, Arcuate ligament syndrome). Variants often develop at the truncus, the most widely known of which is Haller’s tripod.

The most pronounced branch of the truncus coeliacus is the lienal artery, which almost always branches off from the truncus [2]. The course of the artery is variable. Along with the classic topography, courses running both dorsally and ventrally to the pancreas have been reported. In 50% of cases, the course of the lienal artery is gyrose (increasing with age); therefore, it can measure up to 50 cm in length. This can be useful when transpositioning the artery. The common hepatic artery has the most positional variations, 20–30% of all the branches of the truncus coeliacus. In 3–5% of cases, an arterial outflow from the SMA is identified. This is known as a hepatic mesenteric trunk. However, more often (12–18%), the arterial perfusion of the liver takes place through the SMA and the coeliacus circulation territory [3]. Buehler’s anastomosis, which creates an additional connection between the proximal MSA and the truncus circulation territory through persistence of the embryonic artery, is present in only 1–2% of cases.

The SMA is the most important visceral vessel. The artery begins just 0.5 to 2 cm distal to the truncus ventrally from the aorta. The SMA supplies the pancreatic head, duodenum, and the complete small intestine and colon extending to the left colic flexure (Griffith’s Point). It initially runs below the pancreas and then crosses the horizontal part of the duodenum and the uncinate process before flowing into mesenteric root where the majority of its branches terminate. Starting at the left colic flexure, it connects distally with the area supplied by the IMA, the weakest of the three main visceral arteries [4].

The IMA produces several inconsistently formed anastomoses; therefore, one cannot rely on collateral perfusion in individual cases in this area. The Riolan’s anastomosis is the most important of these connections. This is a preformed connection, close to the intestines and between the mesenteric arteries. In contrast, Drummond’s arcade is composed of the outer most arcade complex directly adjacent to the colon (marginal artery). Furthermore, there is the inconsistent anastomosis from Williams and Klop, which sprouts directly from the SMA and runs retroperitoneal into the mesenteric root leading to the IMA or colic artery (mesenteric arcade). The strongest functioning branch of the IMA is its most caudal branch: the superior rectal artery. This branch provides the most important supply of blood to the rectum. The superior rectal artery and the medial rectal artery, which branches from the internal iliac artery, join to create a net which supplies the rectal ampulla. The farthest extending branches of the internal iliac artery (IIA), the medial and inferior rectal artery, provide an important compensatory and collateral function in the case of intestinal occlusion processes.

Intestinal circulation is not evenly spread out among the individual intestinal segments. Instead, it undergoes functional fluctuations which are initiated by the digestion process. As a consequence, the coeliac circulation territory is insignificantly affected by flow fluctuations, whereas the area supplied by the SMA is intensely affected. The blood flow system within the intestines is based on an autonomous system. This means that despite considerable fluctuations, heart performance remains constant. Approximately one third of the complete heart minute volume flows through the splanchnic region, whereby physiological fluctuations can cause the amount to halve or double. Only after reducing blood flow in these areas do ischemic changes develop, beginning exclusively in the mucosa. The visceral main vessels are not significantly involved here.

Along with cardiovascular factors (cardiac output), the vegetative nervous system can, with vasocontrictoric sympathic and vasodilatatoric parasympathic stimulation and vasoactive substances (i.e., histamine, dopamine, serotonin, gastrin, prostaglandin, adrenaline, noradrenaline, etc.) affect intestinal blood circulation and thereby significantly affect reabsorption capacity. The vasopressin and angiotensin II hormones in particular can cause pathological non-occlusive disease (NOD) when released during mesenteric ischemia. This situation can be controlled and treated using metabolites of arachidonic acid (prostaglandin), calcium antagonists, and papaverine. These help treat the local vasoconstriction and guarantee sufficient perfusion [5].

Acute mesenteric ischemia

In most cases of acute mesenteric ischemia, an interruption of blood flow to vessels supplying the small or large intestine can be imaged. When imaging diagnostics confirm “acute mesenteric artery occlusion”, a time period of several hours has already passed, making the probability of a positive prognosis unlikely despite therapy being begun immediately [6]. Pathologically and histologically, acute mesenteric ischemia is divided into four primary clinical categories:

  1. 1.

    Acute mesenteric embolus

  2. 2.

    Acute mesenteric thrombus

  3. 3.

    Non-occlusive disease (NOD) and

  4. 4.

    Mesenteric vein thrombosis.

The symptoms of acute mesenteric ischemia are most commonly caused by hemodynamic relevant vascular changes in the circulation territory of the superior mesenteric artery and the mesenteric vein. However, it should be taken into consideration that collateral supply from the truncus coeliacus and the inferior mesenteric artery is possible as long as these vessels are permeable.

Embolus of the inferior mesenteric artery is rare due to the fact that the vessel has a far smaller diameter than that of the SMA and truncus coeliacus [1]. Nevertheless, embolic occlusions are the most common cause of an acute mesenteric ischemia (50%). Arterial thrombosis is the cause in 25% of cases, NOD in 20%, and mesenteric vein thrombosis in less than 10% [7]. In the event of an acute mesenteric ischemia, primary consideration should be given to a thrombus cardiac cause, which can, in turn, provide evidence of a different pathogenesis. An embolic occlusion can usually be localized 6–8 cm distally from the outflow of the superior mesenteric artery in the vicinity of the medial colic artery.

On the other hand, if a progressive thrombosis develops in the mesenteric vessels—which should be seen as a late complication of an existing visceral arteriosclerosis—the clinical symptoms develop after only two of the three arteries supplying the intestine are stenosed or completely blocked, in contrast to an acute embolism [8, 9].

Clinical diagnosis

The etiological and therapeutic points of view differentiate between acute and chronic intestinal ischemia. Acute intestinal ischemia (mesenteric infarction) is an urgent, life-threatening vascular condition with a mortality rate of approximately 70% [10–14].

The cause of the delay in making the final diagnosis is the rapid progression of the condition with irreversible consequences stemming from the intestinal wall necrosis [15–18]. Therefore, the slightest suspicion of mesenteric ischemia should be ruled out through imaging diagnostics. In patients with advanced ischemia with evidence of diffuse peritonitis, shock and severe metabolic crisis, the mortality rate is 90%. In patients over 70 years of age, it is assumed that abdominal symptoms are caused by hypoventilation in 10% of cases. However, the rate of acute and chronic intestinal circulatory disorders is presumably higher.

While the circulation territory of the celiac trunk and the IMA are phylogenetically relatively well protected by proximal occlusions in the event of a collapse, the SMA and its main outflow territory should be functionally deemed a highly sensitive circulation territory, since only in the central part do collateralization possibilities exist. An acute proximal occlusion of this artery therefore almost always lead to a mesenteric infarction.

Special pathologies, which can be found in 2% of cases, are created by dissection of the SMA, vasculitis (lupus erythematosus, thromboangiitis obliterans, Takayasu arteritis), embolizing aneurysms, strangulation of the foregut, volvulus or invagination, advanced small and/or large intestinal ileus as well as external compressions (aneurysms, tumors).

Pathogenetically, the local occlusion process is followed by an excessive vasoconstrictoric reaction, which causes a large, transmural intestinal infarction to develop, so that the mucosal inner layer necrosis becomes more affected. Evidence of this is the resistant exterior positioned tunica serosa. The clinical presentation is initially uncharacteristic and characterized by the symptoms listed in Table 1.

Table 1 Frequency of the symptoms during acute mesenteric ischemia [taken from: 11, 19]
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Also, often, comorbidities have to be considered when compiling the medical history (Table 2).

Table 2 Frequency of comorbidities during acute mesenteric ischemia [taken from: 4, 19]
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Typically, the course of an ischemic condition is a triphasic one. In the initial stage (0–6 h), there is intense, acute abdominal pain which is often accompanied by shock and diarrhea. This is normally followed by a phase with little evidence of symptoms known as a silent phase (7–12 h), which is characterized by dull abdominal pain, intestinal paralysis, and a rapid deterioration of the general condition. In the final phase (12–24 h), a manifest ileus and bacterial peritonitis with sepsis are evident, and multi-organ failure has begun. Satisfactory treatment results are only possible in the early stages (0–12 h). Therefore, diagnostics and treatment must be carried out on an emergency basis. Due to the fact that the symptoms in this phase are usually uncharacteristic, it is essential that the first attending physician considers the full clinical picture when deciding on diagnostics. Anamestic data should be evaluated to assess eventual cardiovascular risk factors. In the event of long-term inpatient treatment (intensive care), the possible presence of NOD should be considered. NOD, in combination with old age, cardiovascular comorbidity, complex surgical procedures, and reintubation means that dialysis with large fluid volume is a possibility.

The moment when acute mesenteric ischemia is first suspected is the decisive point and determines the prognosis for further development of the condition. No laboratory-chemical parameters currently exist which are specifically honed to determine intestinal necrosis. Characteristically, however, the necrosis is usually accompanied by a lactate increase in the serum (>4 mmol/l), a CRP increase (>10 mg/l), and a leukocytosis (>15,000/ml). The blood gas analysis will point to an ischemic necrosis showing acidosis with a ph of <7.2 and a base excess of minus 7–8 mmol/l. Because of the fact that these parameters are only relevant in combination with anamnesis, clinical symptoms, and imaging diagnostics, there is only a narrow window of time in which treatment has a chance of success. If acute mesenteric ischemia is even suspected, this is reason enough to commence treatment (see below) (Fig. 1).

Fig. 1
figure 1

Diagnostic algorithm of intestinal ischemia (according to [5])

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Diagnostic imaging of acute mesenteric ischemia

In 20–60% of cases of suspected acute mesenteric ischemia, the abdominal X-ray will not show any specific findings. However, the imaging procedure is justified (left-side and dorsal position) in order to rule out an intestinal perforation and excess peritoneal air.

Positive changes in the abdominal image point to advanced stage acute mesenteric ischemia but could also be unspecific (ileus, small intestinal obstruction, edematosis, thickening of the intestinal wall, major gas accumulation in the intestine). Intestinal pneumatosis is a specific indicator. Gas accumulation within the intestinal wall showing an advanced stage intestinal wall ischemia should be considered a signum mali ominis. Air accumulation in the portal vein is also a sign of an advanced stage of disease. The procedure of choice here is the CT angiography, which offers a sensitivity of 96% and specificity of 94% [20]. When one differentiates between the individual pathomorphological findings, then clinical pictures of intestinal pneumatosis, venous gas, occlusions of the three upper abdominal arteries caused by thrombosis or embolus, demonstrate specificity and sensitivity of 50% and 94%, respectively [21]. Multidetector CT technology provides an ever higher level of accuracy [22–24]. The intra-arterial angiography using digital subtraction angiography (DSA) is hardly relevant today, especially as mesenteric vein thrombosis, combined with the often poor examination situation, can be overlooked in the affected patient group. In comparison, the CT enables an intestinal pneumatosis as well as air accumulation in the portal vein wall edema in the affected intestinal segment, abnormal gas distribution, and organ infarction to be evaluated definitively [25]. However, the DSA offers diagnosis confirmation and a possible therapy combination (i.e., intra-arterial prostaglandin infusion) when the patient is suffering from non-occlusive disease (NOD). In this case, a spasmus of the mesenteric arcades and a belated filling of the intramural flow vessel of the intestine are characteristic. Catheter-guided loco-regional prostaglandin infusion can lead to restitution. Duplex sonography also provides high-level specificity of 92–100% when detecting acute mesenteric ischemia. However, the sensitivity level only reaches 70–89%, which is less than angiography and computer tomography [26]. The disadvantage of this procedure is that it is sufficient only when assessing the proximal vascular segments/main vascular stems and is not suitable for diagnosis of a NOD. Therefore, an ultrasound is considered the second procedure of choice when diagnosing mesenteric ischemia. This method, however, has well-documented limitations when evaluating dilated, fluid, and gas-filled intestinal loops.

MRT and MR angiography possess neither sensitivity nor specificity when assessing mesenteric ischemia. Therefore, these procedures (currently) play no role in the emergency diagnostics. The rapid emergency restoration of the visceral circulation is of utmost priority. In individual cases, suspicion can be an indication enough to justify an explorative laparoscopy. Along with diagnostic evaluation of acute mesenteric ischemia, basic therapeutic applications should be begun immediately. Also, due to the fibrinolytic effect of heparin, anticoagulation therapy using 5,000 IU of heparin as a bolus should be administered followed by a perfusor controlled heparinization (15,000–20,000 IU/25 h). Maintaining fluid balance and volume control through a central-venous indwelling catheter is also of great importance. Due to expected bacterial translocation, a calculated, antibiotic therapy to treat both Gram-negative and Gram-positive pathogens should be commenced. Sufficient analgesic therapy for the patient is one of the most important primary basic applications and should be administered before further applications are begun. Due to the known acuteness and dynamics of the condition, therapy should be administered under intensive care conditions [20].

Endovascular therapy techniques

Acute mesenteric ischemia has a surgical clinical picture and the management of the condition is handled by surgeons (general and/or vascular surgeons). In the beginning, the possibility of endovascular reconstruction of the visceral arteries should be assessed, as surgical access trauma is immensely stressful on the organism. This is especially true for patients who had already undergone abdominal operations in the past, have high comorbidity (ASA > 3), the NOD and peripheral and segmental occlusion processes. The indications of catheter-controlled medication perfusion are given in the event of NOD (prostaglandin) and segmental peripheral types of occlusion without peritonitis (lysis therapy). This can also be used supportively among pre-, intra-, and postoperatively as it promotes spontaneous lytic thrombotic formation and allows organs and intestinal segments affected by the ischemia tolerance to regenerate [27–29]. An intra-arterial papaverine infusion measuring 30 to 60 mg should be administered for at least 24 h and for a maximum of 5 days. It should be noted that significant hypotonic symptoms can develop if the catheter becomes dislocated from the aorta [30]. There is also a heparin incompatibility (crystallization). Along with a local thrombolytic therapy [31], angioplasty or direct stent implantation in the stenosized/occluded intestinal segment is also an option [32–34]. Even when the PTA successfully leads to complete recanalization, the clinical picture must undergo regular evaluation by a surgeon because a laparoscopic abdominal exploration with possible removal of irreversibly damaged intestinal segments may be necessary at a later date. Indications for an aspiration embolectomy must be discussed at an interdisciplinary conference with the attending physicians present, as only they have accompanied the patient from the first diagnosis and can therefore better assess the acuteness of the patient’s condition.

This catheter-guided reconstruction technique can be used to treat central occlusion processes in patients who are considered operatively high-risk. In the event that a peripheral embolism develops a surgical embolectomy and if possible, a low-risk resection of the affected intestinal segment should be undertaken.

Vascular operations

To assess the circulation flow in the intestines and the necessary extent of the resection, the vascular reconstruction should be carried out before the resection. Before dissection of the SMA, a careful partial mobilization of the pancreas is necessary, as the pancreas can react to inadequate preparation trauma with severe pancreatitis. Dissection of the truncus coeliacus also requires great care. Multiple side branches initially hemorrhage very little, but after the revascularization, severe hemorrhaging can develop. With a healthy vascular wall, it is possible to perform the thrombectomy using a transverse arteriotomy followed by direct closure. Degenerative changes require a longitudinal section followed by an augmentation patch plasty. After a local thromboarterectomy, often a local endarterectomy of hyperplastic intima distally to the occlusion process is required as the distal stenosized plaques rarely level off. In these cases, a distal suture of the intima is recommended. Alloplastic material should be avoided due to the high risk of infection. After recanalization, a decision must be taken with regard to the avital, not revitalizable intestinal segments. Signs of revitalization are red coloring of the intestinal serosa, re-starting of the intestinal peristaltic, and evidence of pulsatility in the mesenteric arcades.

Other instrumental-technical measurement methods (Laser flowmetry, P02 measurement, Doppler sonography, fluorescein dyeing, etc.) have not yet been proven to be effective; thus, the assessment and experience of the surgeon remains the most effective predictor of outcome. The uncertainties relating to enteral vitality manifest themselves during an atrial continuity operation as an anastomosis insufficiency with up to 60% fatal deterioration of the prognosis quo ad vitam [13].

The reason for this is that the mucosal inner layer necrosis extends far further than the tunica muscularis and serosa, both of which appear at first glance to have good blood circulation. Therefore, the resection margins should not be in the apparent necrobiotic margin area but 5–20 cm into the area which show good blood circulation. Even when an acute situation requires bringing the life-threatening condition under control and the patient’s survival is the priority, it should be taken into account that a remaining small intestinal segment of less that 70–100 cm is associated with both metabolic and nutritive dysfunctions corresponding to a small intestine syndrome.

An alternative to primary continuity resection for the primary intervention is a discontinuity resection with insertion of (several) terminal enterostomies. The advantage of this method is the simple, and where necessary, endoscopic, evaluation of the intestinal mucosa. The question over whether the remaining intestinal segments will regain functionality after the first operation and whether further ischemic regions will develop always causes uncertainty for the surgeon. Therefore, indications for a Second Look Operation within 24 h of the primary intervention should be considered liberal [13] (Fig. 2).

Fig. 2
figure 2

Treatment algorithm in intestinal ischemia (according to [5])

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Imaging diagnostics are not particularly helpful when assessing the indications. Therefore, justifiable indications are based on the initial intraoperative findings and clinical progress [35, 36]. After successful revascularization of the mesenteric arteries, there are no digestive problems due to the high compensation capacity of the liver and the rapid regeneration of the enteric structures. Six percent of patients can expect to fully recover within 4–6 weeks. Until the patient is completely recovered, obstipation and diarrhea are common symptoms, caused not only by inappropriate nutrition but dysfunctional regulation of the vegetative nervous system. In 18% of cases, chronic mesenteric ischemia develops. Stenosises and occlusions can develop and manifest themselves as abdominal angina, particularly when arterial thrombosis is evident.

Chronic intestinal ischemia

With an increase in age and the related cardiovascular morbidity, the intestinal arteries become part of the chronic occlusion process [37, 38]. The diagnosis usually takes place after the completion of the differential diagnostic evaluation, which means long-term discomfort for the patient. Abdominal angina should be included at the beginning of the abdominal pain differential diagnostic. Abdominal angina is both a pathognomonic and warning symptom.

Patient diagnosed with CMI are usually over 60 years old. Whereas autopsy data discovered relevant stenosises of the intestinal arteries in approximately 80% of persons over 60 years of age, the clinical symptomatic had no higher correlation to these findings. The discrepancy can be explained by the fact that first the high-grade vascular stenosis (>70%) and then the affection of several intestinal arteries leads to hypoperfusion of the organ. Furthermore, the complex visceral circulation network causes early hemodynamic decompensation, meaning that two major intestinal arteries usually need be affected in order for the patient to experience problems. However, over 90% demonstrate evidence of an occlusion process affecting the SMA. The intestinal collateral circulation system does not always sufficiently protect against abdominal angina in the event of SMA occlusions, so the assumption that an individual SMA occlusion is without symptoms in each case is not justified [14]. The problem with chronic mesenteric ischemia is its progressiveness, which ultimately causes the failure of collateral circulation and the fatal mesenteric infarct with high mortality rates. For this reason, the evaluation of the intestinal vascular morphology should belong to the repertoire during diagnostics of unclear abdominal situations [14, 39].

Etiology

The large majority of those affected (98%) suffer from general progressive arteriosclerosis and the corresponding complications (plaque embolism, arterial thrombosis, dissection). Ostial calcification where an aorta-near sclerotic block causes flow problems in the otherwise healthy circulation territory is also typical. Exceptional cases are the coral-reef sclerosis affecting the visceral aorta and juvenile arteriosclerosis. It is not rare to find the intestinal outflows included in the aneurysmic aortic deformations.

Longitudinal occlusion processes of this that take place far from the ostium are rare and point to other metabolic conditions (diabetes mellitus, chronic kidney insufficiency, amyloidosis). These are more dangerous as their development limits or hinders the mesenteric collateral circulation which can cause clinical symptomatic to develop earlier. Intermediate forms are aortal and local wall dissections (arterial hypertension, fibromuscular dysplasia) as these can lead to a sudden circulation reduction in the intestinal arteries. Anomalies, dysfunctions, infections, and external vascular compressions occur in only 2% of chronic mesenteric ischemia cases.

Collateral circulation

The visceral vascular system is the most extensive regional vascular system in the body and is characterized by its excellent collateralization and compensation capacity. The development of preformed connections to major collateral circulation areas depends on the intensity of the existing chronic occlusion processes and completion requires several months. Therefore, an acute mesenteric ischemia cannot be compensated for. Length and lumen increases in the secondary branches leads to the development of bizarre intestinal vascular convolutions. However, hemodynamic and capacity limitations do exist, thus the normal blood flow cannot be completely compensated for [39]. This explains the common asymptomatic status on the one hand and the development of chronic infectious changes in the upper abdominal organs and the gastrointestinal systems on the other. Because mesenteric ischemia is progressive, it has been categorized into four distinct stages as defined by Fontaine:

  1. Stage I

    Symptom-free, but with evidence of pathology

  2. Stage II

    Intermittent abdominal pain (abdominal claudication, abdominal angina)

  3. Stage III

    Abdominal pain when resting abdominal resting pain

  4. Stage IV

    Ischemic necrosis (mesenteric infarction)

Apparative diagnostics

Currently, there are no specific enteral function laboratory parameter tests with which it is possible to either confirm or rule out the existence of mesenteric ischemia. Chronic mesenteric ischemia is diagnosed through the use of suitable imaging diagnostics, often coupled with functional examinations. The plain abdominal X-ray, which is usually the first imaging technique employed in suspected cases of chronic mesenteric ischemia, usually does not present any abnormalities. However, as with acute mesenteric ischemia, it is able to rule out other conditions and diseases (ileus, peritoneal air). Also, evaluations of the intestines (gastrointestinal passage, Sellink examination, Peritrast enema) enhanced by contrast agents are not able to identify intestinal vascular disorders. The delayed passage of the contrast agent can be indirect evidence of slow transit constipation.

Sonography and computer tomography are not only useful alternative diagnostic techniques, but duplex sonography can also confirm an existing vascular occlusion process in the visceral arteries. Patients are easier to examine due to their chronically poor nutritional status. Flow speeds of more than 200 cm/s in the poststenotic intestinal arteries are considered pathognomonic for a high-grade stenosis. This procedure has an 81% sensitivity and 96% specificity rate. Obscured position of the visceral arteries, especially in overweight patients and in those whose stomachs are not empty at the time of the evaluation can limit the accuracy of the procedure [40, 41]. Therefore, a diagnosis cannot be made based solely on the duplex sonography findings. Computer tomography without the application of a contrast agent can, however, indicate the presence of an existing chronic mesenteric vascular disorder by confirming the existence of aortal and aorta-adjacent calcifications.

Today, the most commonly employed imaging technique is the 3D reconstructed CT angiography. The treatment and therapy options are then implemented based on the findings of the 3D reconstructed CT angiography. Both frontal and lateral multiplanar reconstruction of the abdominal aorta and its branches and selective imaging of the individual main arteries require careful reconstruction and planning. Vascular variants as well as the entire collateral circulation area can be imaged. The vascular diameter can be determined through imaging so that the planned stent implantation can be performed. The stent is inserted entering either transbrachial on the left-side or inguinal. The contrast agent-enhanced MR angiography imaging of the abdominal-pelvis-leg circulation on patients with a peripheral occlusion condition often detects stenosises in the visceral arteries. Although MRT is an effective procedure, it is not the procedure of choice in this case.

Indications and treatment

In the asymptomatic stage (stage I), no therapy is indicated. This does not apply, however, when intervention has already been planned because of an aortic aneurysm or aortoiliac occlusive disease. Intervention can provide an opportunity to perform simultaneous reconstructions of the visceral arteries. In any case, asymptomatic patients with a confirmed pathology should undergo to regular testing. The available options are aortic corrective surgery, operations on the renal arteries (cave sinking of the compensatory hypertension), major visceral surgical interventions affecting the intestinal main and collateral arteries, and rapidly progressing double or triple occlusion processes. The only exceptions from the regime of regular testing are symptom-free mesenteric or aortal dissection involving the superior mesenteric artery. In Stages II and III, treatment is definitely indicated.

Endovascular therapy

Due to the severity of the surgical access trauma and the associated morbidity rates, endovascular methods are becoming ever more common, particularly in inoperable patients with serious mesenteric ischemia and in post surgical reconstruction and corrections [41–43]. Cumulative primary patency was 65% while secondary primary patency was 99%. Although studies on stent-supported PTA produced the best patency rates, there is no significant statistical difference [44]. For stent-supported PTA, morbidity is less that 30%, severe complications are reported at 8.8% and mortality at 7.7% [38, 44–46].

In the long-term, 25.3% stenosis revision was reported. Thus, there was no apparent or clear difference between PTA and stent-supported PTA [38, 44, 47]. The preferred treatment method for ostial lesions is direct stent implantation [33, 34, 48]. Due to the rapid in-stent stenosing and symptomatic relapse, every fourth patient requires careful monitoring in order to minimize the risk of infarct-causing stent occlusion.

Comparative studies between stent-supported and open surgical reconstruction show, interestingly, no difference in the peri-interventional complication rate [49–53]. The mortality rate is also comparable at 11% vs. 8%. In the long-term, however, operative reconstruction proves to be more advantageous: after 3 years, 13% of patients developed a relapse stenosis compared with 34% in the stent group. The majority of the relapse stenosises developed in the first year post-intervention, whereas the sub-group analysis found no difference between the one vessel and multivessel conditions [54]. Another study which consecutively compared 80 patients with one another (31 PTA/Stent, 49 open surgery) found the radiologically checked patency rate to be at 58% after 1 year compared with 90% operative therapy [55].

A current study, with an admittedly small study size (n = 17) reported, after two secondary interventions, a strikingly high patency rate of 98% 24 months after stent supported PTA [27, 56].

Overall, minimally invasive procedures should always be considered for patients with multimorbidity. Arcuate ligament syndrome (Dunbar syndrome) is a special condition, where the chosen method is operative intervention (preferably minimally invasive) to decompress the celiac trunk [57–60].

Reconstructive operations

The surgical treatment of chronic occlusive processes affecting the intestinal arteries should have a mortality rate under 3% [37, 61]. Supra- and/or infracolic dissection is the most effective way to achieve a comprehensive overview of the aortal segment. All main and secondary intestinal arteries can then undergo longitudinal reconstruction. In special cases, (transaortic TEA) using a left- or right-side modified abdominal Crawford technique is the most suitable [5, 20, 36]. Since the clinic is usually faced with a double vascular occlusion affecting the truncus coeliacus and the superior mesenteric artery, both arteries should be reconstructed. This provides more assurance for a good short- and long-term prognosis (late recurring abdominal angina 11%). Taking into account technical difficulties, the sub-diaphragmal aortic-coeliacal reconstruction and the aorto-mesenteric pantaloon bypass are the preferred reconstruction methods. This is performed orthotopically, dorsal to the pancreas. Although mobilization of the pancreas is necessary, iatrogenic pancreatitis is rare. However, this dissection should be performed with the utmost care. In the event of potential danger of infection (bacterial translocation), an autologous reconstructive procedure is favored. Care should be taken to ensure that the interponate and the bypasses are created tension-free and kink-resistant. During longer periods of clamping, arterial perfusion of the peripheral vascular segments such as a thrombosis prophylaxis and lengthening of the tissue ischemic tolerance are recommended (see acute mesenteric ischemia).

The preferred procedure to treat short, ostium-near stenosises is the thromboendarterectomy and can be carried out during tangential transaortic clamping of the aorta or retrograde half-closure. Thoracic-abdominal entry is only unnecessary for reconstruction of the truncus coeliacus: here, a transhiatal procedure with incision in the crus of the diaphragm is recommended. A transabdominal entry with medial visceral rotation can also be used to reconstruct the central superior mesenteric artery. As an alternative to the local TEA with patch plasty is either caudal transposition or the construction of a short vein bypass. As there is usually significant calcification of the aortic wall, sufficient dissection is recommended to allow circular clamping for the aortic TEA. However, longitudinal occlusion requires alternative methods. Coeliacal interposition with a 2–4 cm long vein segment is recommended for longitudinal reconstruction of the celiac trunk or alternatively, interponation of a short PTFE or Dacron segment (recommended diameter 8 mm).

If a separate reconstruction of a longitudinal SMA stenosis is necessary, extra-anatomical bypass methods are applied. The course and the proximal connection can be determined individually and depend on the local anatomical situation (severity of aortic wall calcification, previous operations, etc.). Valid data stemming from medical literature evaluating long-term bypass function does not exist. Therefore, various procedures (French bypass, lieno-mesenteric interposition or transposition, iliac-mesenteric bypass, hepatico-mesenteric bypass, etc.) have been established. Basically, treatment should focus on the short and stretched bypass measurement in order to avoid kinking.

Complications

The main risk in all intestinal artery reconstruction procedures is enteral ischemia. However, peripheral embolisms, vascular dissection with arterial thrombosis, and bacterial translocation after reperfusion can lead to life-threatening multi-organ failure. This is why laboratory-chemical and image diagnostic evaluation on a regular basis is so important. Other complications are caused by infections and secondary hemorrhaging. In approximately 10% of late-term recurring cases, treatment is only necessary in the symptomatic stage. A procedure change using open surgical-endovascular method has proven itself to be effective [62]. Postoperative coagulation should be performed using thrombocyte aggregation inhibitors.

An annual duplex sonographic evaluation of the reconstructed intestinal arteries is recommended. Late-developing complications can normally be traced back to the progression of most of the underlying arteriosclerosis-related conditions.

Chronic colorectal ischemia

Only about 12% of visceral ischemic cases affect the colon, especially the colorectal segment. Tenesmus and pain in the left side are early symptoms, but the correlation often is not made. Late-stage symptoms include peritonitis, tachycardia, hypovolemia, and flatulence with traces of blood. Also notable is the extended recovery time with intensive care and recurring pneumonia coupled with unclear abdominal and kidney failure.

Depending of the severity of the colon ischemia, MARSTON has defined three differing levels of severity (Table 3).

Table 3 Severity and corresponding pathology of colorectal ischemia
Full size table

A suspected case of colorectal ischemia justifies a rectocoloscopy (sensitivity 100%, specificity 85%). Also, an abdominal CT should be carried out to rule out any additional pathologies. The colon contrast enema, which uses a water-dissolvable contrast agent, can confirm the typical changes: haustration reversal and longitudinal scarred stenoses in the ischemic colon segment. Laboratory tests show typical signs of infection (leukocytes, C-reactive protein). A lactate level increase is evident only in the first few hours and is usually missed. The causality of the colorectal ischemia must be evaluated together with the underlying condition. If a colon ischemia is confirmed, a resection of the ischemic colonic segment with a continuity resection is necessary. In emergency cases (ileus, perforation), a discontinuity resection (Hartmann’s procedure) cannot be avoided.