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B-mode image of the longitudinal section of the abdominal aorta showing clearly the compression of the celiac trunk TC by the inferior portion of the diaphragm — the arcuate ligament arrow. We report here our experience with sonographic diagnosis in more than cases with actually 53 operated on. It was in Trondheim that some Norwegian colleagues expressed their interest in my talk dealing with abdominal vascular compression syndromes and now inspired this contribution to this journal.

Espen Skjønberg - Wikipedia

It was barely inconceivable to give back something someday. Now we have got so many friends and colleagues just in Norway — in part due to many German doctors living here in part due to the openness of mind in many Norwegian colleagues with whom I had the privilege to make friends with. This still moves me and the whole story reminds me to another deep experience related not only to Doppler and blood flow: B-mode image of the longitudinal section of the abdominal aorta during inspiration demonstrating the release of the celiac trunk right arrow by the retracting diaphragm left arrow.

In 3 of them, an epigastric bruit was audible prompting the suspicion of an arterial stenosis which was confirmed by preoperative angiography. The other 10 patients underwent surgery for a variety of other reasons, and in all cases, celiac artery compression was found.

The constituents of this triad but changed: Color Doppler sonograms of the celiac trunk in different diaphragmatic positions during breathing. See the dilation behind the compression site and the filling of collaterals blue during deep expiration. Diverging pathophysiological concepts and therapeutic conclusions Not rarely the terms compression and stenosis were used interchangeably or even in a joint manner [11, 12] what may have further contributed to blur the apprehension of the exact nature of this syndrome [7, 13, 14].

The origin of pain was suspected in diminished blood flow thus causing ischemia downstream the stenosis i. Some questioned this causal connection and favored the neuropathic origin from the compressed neural tissue of the celiac ganglion [1, 2, 15, 16].

The longstanding uncertainties of the true origin of the prevailing pain [17, 18] has much contributed to the diversification of operation techniques [], recommendations [25] and mixed results [13, 26, 27]. This is the main reason for disbelief of the very existence of the syndrome at all [28] and the decades of debate to find the best operation technique with the longest lasting results [29].

The main objection against the ischemia theory came from the frequent observation, that in severe cases of compression collaterals arising from the superior mesenteric artery bridged the narrowing [30]. For some authors it seemed thus highly unlikely for ischemia to play a major role in the disease [31] or they even declined the entire concept [32, 33]. Others stressed that patency of the celiac artery CA in postoperative follow up was linked to persistence of pain relief [29].

Rarely attempts were made to stent the compression site aiming at restoring the original lumen in order to ease the blood flow. The many recommendations often simply ignored the fundamental difference between an arterial stenosis and arterial compression from outside [34].

Often the argument was raised, that the many severe stenoses of the celiac trunk found at autopsies [35] which were completely asymptomatic during lifetime and thus ruled out a causal link of celiac compression and complaints[36]. The results were mixed and so the debate persists to date [37, 38]. Deep expiration in CGCS: Only the superior mesentric artery is still visible. The course of the aorta points to the strong diaphragmatic compression of the celiac trunk bending the underlying vessels i.

No flow in the celiac trunk arrow. The coloration of the ventral part of the aorta white arrows makes evident that here the superior mesentric artery is pressed into the aortic surface.

No flow in the celiac trunk blue arrow , Slower flow in the aorta itself green arrow. The main and fundamental difference is the cause of lumen reduction of the celiac artery. In celiac ganglion compression syndrome synonyms are Dunbar-syndrome, celiac artery compression syndrome, celiac trunk compression syndrome, median arcuate ligament syndrome [MALS] the celiac artery and the straddling celiac ganglion are both compressed by the arching arcuate ligament.

So, the compression is one sided, guillotine-like and often results in a sharp incision of the celiac artery from above, which is easily visible in color Doppler and very often, but substantially less clear in B-mode images of the longitudinal section of the abdominal aorta figure 1. The celiac ganglion is not visible with the conventional imaging techniques. Thus it evades the direct examination and its irritation can only be concluded from the compression of the underlying celiac artery.

This is the reason why the author proposes a new name for this condition: Change of the diameter of the compresssed celiac trunk from expiration to inspiration. B-mode sonography in many cases can clearly delineate all relevant structures figure 1 but is of limited value in adipose patients and in cases with a slightly laterally directed CA. Color Doppler, often at a first glance, can show if there are turbulences and depicts the course of the CA quite clearly.

Also aneurysms with a typically whirling flow patterns and post-compression dilation are easily recognized. Moreover, collateral arteries from the superior mesenteric artery to distal portions of the CA can be shown — nearly impossible with B-mode ultrasound. The compression is clearly visible in a midposition of the diaphragm figure 3 and diminished in inspiration.

Expiration leads to the strongest compression figure 4. But a clear change of diameter and flow velocities can always be demonstrated with deep inspiration figure 5. This maneuver is more easily accomplished by many children —compared to expiration. Another confusing fact is that in many cases a complete compression of the artery occurs with deep expiration figure 4.

In fact, not rarely, a total compression can also be seen already in mid-breathing. If the lumen is near total obstruction the velocities decline instead to rise further. In most cases the lumen changes are perfectly mirrored by appropriate changes of peak systolic velocity figure 6. In inspiration, the velocity drops significantly and rises to maximum values in deep expiration, if the vessel is not pinched to an extent, where flow volume is severely reduced or nearly peters out at all.

Then a reduction of flow velocity and a total obstruction with blocked flow an be found. Here a twofold increase of peak flow velocity is often requested to make the diagnosis. Most important in elderly patients is the need to demonstrate the change of flow velocities with breathing.

In summary, three sonographic constituents must be sought to make the diagnosis of the celiac ganglion compression syndrome: The decrease of compression with inspiration accompanied by the drop of the increased flow velocity.

In expiration contradictory changes occur compa red to those from midposition to inspiration.

Camilla Stoltenberg

Comparison of angle-corrected flow velocities in the celiac trunk in CGCS. Typically flow velocities decrese from expiration via midposition to inspiration.

MRI Imaging MR-Angiography is helpful to provide a preoperative overview and to reassure the surgeon about the diagnosis and its severity. Images in in- and expiration are necessary to demonstrate the characteristic change of compression degree, most pronounced in expiration figure 7. In very severe compression the CA is sometimes pressed into the aortic lumen for the first centimeter of its course. Need to correlate and subordinate ultrasound findings under clinical aspects The diagnosis but cannot be made on sonographic grounds alone.

Always a characteristic pattern of clinical symptoms needs to be present. They are mandatory, and emerge from the altered celiac ganglion, which is touched and compressed too. The invisibility of the ganglion has for long times veiled its pathophysiologic contribution to the fancy clinical spectrum of the disease. Many symptoms can only be explained by referring to its irritation. Pain is the most impressive and outstanding feature but by far not the most frequent one.

Puzzling diversity of mainly vegetative symptoms may mock not only the unaware Many patients complain of a variety of vegetative symptoms that emanate from the ganglion.

These are dizziness, vertigo, anorexia, near -fainting, diarrheal bouts, gastric fullness soon after starting to eat, nausea, shortness of breath [32]. In animal experiments even eclamptic seizures could be produced by irritating the CG [41].

Difficulties in breathing are often confused with exertional asthma, since many patients complain about shortness of breath in sport activities.

The correct diagnosis can be suspected if the patient is asked to describe clearly if the problem consists of blocked deep inspiration which is provoked by physical activity — thus pointing to CGCS or if the expiration is not fully possible bronchial asthma.

My hypothesis is that wide amplitudes of diaphragmatic movements are suppressed by reflexes to diminish the unpleasant sensations caused by the celiac ganglion compression which are substantially aggravated by deep breathing and expiration. The typical patient is a young girl or woman with slender constitution and deep hollow back. Many afflicted patients have no contact to the bed with their central parts of the lumbar spine while lying supine.

Clearly visible increase of celiac trunk compression arrows from inspiration left to expiration right. Often they suffer more from vegetative symptoms than from the pain.

Pain is not regularly aggravated by eating as often claimed or sought for. It has its focus in the epigastric angle but sometimes radiates to the left thorax or the sternum.

Often another pain component is clearly discernible by its typical location from the celiac pain. This a dull but also activity-dependent pain whose maximum lies about 5 cm more caudally and merely radiates to the left flank, down towards the left paramedian region. Here it has a typical second maximum which often can be clearly demonstrated by one-finger palpation of the region of the left ovary.

This is caused, according to my experience, in many cases by the congestion of the left renal vein. The compression of the left renal vein, the so called nutcracker phenomenon, causes large amounts of left renal blood volumes to circumvent the compression site, the aortic-mesenteric arterial pinch, via retroperitoneal collaterals.

As a consequence pelvic congestion occurs, easily detected by left ovarian figure 8 and uterus varices in color Doppler sonography figure 9. Collateralization of the left renal vein: Meandering course with inversed flow towards the left ovary. I can offer the following explanation: With puberty the female pelvis extends more laterally than in boys. The widening of the pelvis [42, 43] pushes both femurs away from each other. Both psoas muscles form a triangle whose basis is the virtual line between both trochantera minora and whose peak is the insertion of both psoas muscles at the lumbar spine.

If the basis of this triangle widens and its sides do not elongate to the same extent then only one postural response is possible — the peak is forced to come down. Because the spine is not compressible, only one way out remains — it has to bow in order to reduce the vertical distance to the base of this triangle.

This — from my point of view — is the reason for the obvious female body shaping in puberty.

Nordmørs-slekter: Kristian Halse:

A wide pelvis combined with a strong lordosis compared to males [] is the dominant female feature. In fact, gender is the only variable that determines the extent of lordosis [], albeit Korean authors could not find gender differences of lumbar lordosis in their local study group [49].

Pregnancies, and height were significantly and positively correlated and weight significantly and negatively correlated to the lordosis degree [50]. If changing lifestyle and body shape is to be blamed for stronger lumbar lordosis in young people due to weaker back muscles and taller statures and thus might increase the susceptibility to CA compression remains an open question due to conflicting reports [50, 51].

If the girl is tall, the flexion of the lumbar spine will be stronger as well as if the connective tissue is less firm.