A flat abdominal cavity predisposes to vascular compression – the interplay of increased lordosis and a flat rib cage

Vascular compression syndromes are triggered primarily by increased lordosis of the lumbar spine, which pushes the vessels and sections of the gastrointestinal tract forward and compresses them from behind. If the abdominal cavity is particularly flat, the low-lying abdominal wall constricts the abdominal cavity even further. This can be especially significant when intestinal loops or the stomach enlarge after eating and additionally press against veins, compressing them further.
A flat rib cage in which the lower opening of the rib cage (lower thoracic aperture) is relatively wide but relatively flat can further reduce the space in the abdominal cavity. The sternum is then only slightly spaced from the upper lumbar spine. Since the abdominal wall extends from the sternum and ribs to the pubic bone and iliac crest , the height of the rib cage and the iliac crest is significant in this context.
A flat chest also leads to less efficient thoracic breathing. When breathing in, the ribs are lifted. If the ribs have a relatively pronounced curvature, this results in a flat chest. Patients with weak connective tissue often develop a flat chest during childhood. It is possible that the soft rib bone gives in to gravity more easily in the supine position. I do not know whether the external pressure of the amniotic fluid and the uterus itself in utero may already impede the depth expansion of the rib cage in foetuses with a connective tissue weakness.
Ribs that extend further lead to a wider chest. When breathing in, the ribs are lifted. If the ribs are particularly curved, the chest widens relatively little when breathing in. If the ribs describe a large arc, breathing in results in a greater widening of the chest. In this case, more negative pressure is generated in the chest, allowing a larger volume to be inhaled.
The height of the iliac wings also plays an important role. If the iliac wings protrude far forward , they raise the abdominal wall, widening the abdominal cavity. If, on the other hand, the pelvis is wide and flat, spatial conflict between intestinal loops and veins occurs more quickly, especially after eating.
It is not uncommon for the minimal distance between the front edge of the spine and the abdominal wall in these patients to be less than 1 cm at the apex of the lordosis of the lumbar spine! The bowel can move to the right and left of the spine where the abdominal cavity is deeper. However, because of the continuity of the bowel, the spine must also be crossed by individual bowel loops. Then, due to the low height of the abdominal cavity in front of the spine, the blood flow from the pelvis may still function satisfactorily when the bowel is empty. However, if the bowel fills up and normally develops a diameter of at least 2 cm, the very flat abdominal cavity can lead to both an obstruction of the food transport in the bowel over the spine and to additional compression of veins in front of the spine. These patients then characteristically report pain in the middle and lower abdomen about 30 minutes after eating. This is the time it takes for the food to be transported from the start of the meal to the small intestine in the middle and lower abdomen.
In patients with a particularly flat abdominal cavity, the organs in the upper abdomen also suffer from a lack of space.
In addition to the
1. compression of the left renal vein (so-called nutcracker syndrome),
2. compression of the splenic vein when crossing the superior mesenteric artery,
3. compression of the superior mesenteric vein or the root of the portal vein at the hepatic artery,
4. compression of the gastric outlet (antrum pylori) between the aorta and abdominal wall,
5. compression of the duodenum between the aorta and the superior mesenteric artery (Wilkie’s syndrome)
6. compression of the inferior vena cava against the right renal artery,
7. compression of the left renal vein by the stomach,
8. compression of the duodenum by the stomach,

9.compression of the right renal vein by the duodenum and
10. compression of the vena cava at the diaphragm, as well as
11th compression of the celiac trunk by the arcate ligament. Further compressions are possible in rare cases, such as
12th compression of the renal arteries by the diaphragm or the
13th compression of the superior mesenteric artery by the arcuate ligament, if, in the case of severe lordosis, the aorta is diverted to the left of the spine, turns axially to the left and thus the right diaphragmatic crus crosses the aorta at an angle, exposing the superior mesenteric artery.

The arcuate ligament is usually unable to reach this artery because the celiac trunk emerges from the aorta just cranial to the superior mesenteric artery in a short distance and is first contacted by the arcuate ligament. In particularly pronounced cases, the superior mesenteric artery and celiac trunk can be jointly compressed  by the arcuate ligament.

The consequences of a flat abdominal cavity are therefore complex and must be examined individually.

Compression often also occurs due to the simultaneously increased lordosis of the cervical spine. These are
1. compression of the jugular veins by the processus styloideus (Eagle’s syndrome)
2. compression of the jugular vein between the bulb of the internal carotid artery and in the sternocleidomastoid muscle
3. compression of the jugular vein in the upper thoracic aperture
4. compression of the subclavian vein between the first rib and clavicle (thoracic inlet syndrome)
5. compression of the brachial plexus or brachial artery (thoracic outlet syndrome)

The following case of a 19-year-old female patient with a flat thorax and increased lordosis shows a whole spectrum of such compressions.
The patient was no longer able to take in food orally and had to be fed via a percutaneous jejunostomy in the left mid-abdomen. She also suffered from severe postprandial abdominal pain, pain in the genital area (dyspareunia, menstrual pain), flank and back pain on the left, severe circulatory dysregulation (effect of compression of the vena cava and May-Thurner syndrome), especially after eating. These effects were still pronounced even with nutrition via the jejunal tube. The patient had lost 25 kg of weight due to nausea, early satiety and frequent vomiting and now weighs 45 kg with a height of 173 cm (BMI= 15.2). She also suffers from bitemporal headaches, weakness in both legs and paraesthesia in the legs, as well as numerous autonomic symptoms such as sudden discolouration of the skin (red or blue), dizziness, breathing difficulties, especially when inhaling, with a feeling of shortness of breath. The patient often has to pass small amounts of urine.
Her symptoms started gradually but became very distressing in the summer of 2021 and continued to worsen.

The following sonographic images and videos illustrate the complex anatomical and clinical situation.

The inability to ingest food orally is essentially due to tight compression of the duodenum by the superior mesenteric artery and one of its branches ventral to the duodenum and the aorta dorsal to the duodenum.

The duodenum struggles with increased peristalsis against the constriction by the superior mesenteric artery and aorta without being able to transport food via the vascular clamp – a fully developed Wilkie syndrome.

Even when the stomach is empty, the high-resolution transducer reveals the insurmountable incarceration of the duodenum. The duodenum expands (left in the image), but cannot open the compressed pars horizontalis duodeni (right in the image)

Colour Doppler sonography clearly shows that 2 arterial vessels ventrally contribute to the compression – the superior mesenteric artery and one of its main branches

Several reasons were found for the patient’s postprandial accentuated upper abdominal pain. The Wilkie syndrome described above, but also a ligamentum arcuatum syndrome and further compressions which are described below.

Compression of the coeliac trunk by the arcuate ligament-yellow-green turbulence as a sign of strong flow acceleration at the point of contact with the diaphragm-flat dark structure ventral to the aorta.

Flow acceleration in the coeliac trunk with arcuate ligament syndrome – shown here in inspiration after retraction of the diaphragm (note the marked thickening of the now contracted diaphragm). The systolic flow velocity exceeds 3 m/s!

Even the aorta is slightly compressed by the tightly attached median arcuate ligament. The exit of the coeliac trunk is still cranial to the aortic hiatus.

With subtle power Doppler, the actual origin of the coeliac trunk 14 mm cranial to the aortic hiatus can be clearly visualised as a light-coloured vessel (accelerated blood flow due to compression) in comparison to the darker aorta (comparatively slow blood flow).

The permanent maximum compression of the left renal vein also inevitably led to pain, particularly in the left upper abdomen, when the stomach enlarged after eating.

The patient suffers from a maximum form of the so-called nutcracker syndrome with complete interruption of the blood flow in the completely ventrally compressed left renal vein of the aorta. The renal vein blood is drained via a strong paravertebral collateral (Tronc réno-rachidièn).

The blood flow in the left renal vein (strong red vessel at the bottom right) ceases between the aorta and the superior mesenteric artery (transverse, round vessels in the center of the image)

The left renal vein (red blood flow to the ventral side) does not continue to the right but describes a complete arc (blue réno-rachidièn tronc because the blood flow is reversed in the direction of the spine)

Another cause of upper abdominal pain is compression of the splenic vein.

Compression of the splenic vein (top right of image) when crossing the superior mesenteric artery. At the bottom of the image, compression of the left renal vein between the aorta and the superior mesenteric artery.

The pronounced compression of the inferior vena cava, especially after eating due to the distended duodenum, but already on an empty stomach due to a dilated transverse colon with impaired peristalsis from the ventral side and due to the elevation of the right renal artery, which is pushed against the vena cava from the dorsal side by the lordosis, causes not only pain in the right upper abdomen but also circulatory disorders when the blood from the lower half of the body no longer reaches the heart in sufficient quantities. The so-called vena cava syndrome is often accompanied by an accelerated heartbeat (missing in this case) and reduced blood flow to the brain. The patient reported feeling light-headed.

Compression of the vena cava when crossing the right renal artery (oblique oval structure dorsal to the vena cava)

Wide vena cava in the lower abdomen-3.27 cm²

Longitudinal section of the vena cava with compression from the dorsal side through the spinal column and from the ventral side through intestinal loops.

Compression of the inferior vena cava by the contracting transverse colon from the ventral side and by the lordotic curvature of the spine from the dorsal side.

Cross-section of the vena cava to illustrate its compression by the duodenum

Headaches are essentially triggered and maintained by the collateralisation of renal venous blood via the réno-rachidièn tronc into the spinal canal. The additional blood volume increases the pressure not only in the spinal canal but also in the skull.

The patient’s circulatory problems can be explained by the reduction in the ejection capacity of the heart with a reduction in blood flow volume to the brain as soon as the patient stands up. Gravity then pulls the blood more strongly into the lower half of the body. Due to the simultaneous compression of the left common iliac vein (May-Thurner syndrome) and the compression of the vena cava – particularly pronounced after eating – the blood cannot be transported back to the heart sufficiently. In addition, blood from the congested left renal vein is fed into the pelvic circulation via the left ovarian vein, further increasing venous pooling in the pelvis. The extent of venous pooling can best be determined by measuring the volume perfusion of the aorta.

When lying down, the patient has a significantly higher aortic flow volume (2483 ml/min) than when standing.

When standing, the circulatory volume drops to 1879 ml/min in the abdominal aorta.

Although the patient showed no signs of connective tissue weakness on physical examination, the right kidney descended to a large extent into the pelvis due to the sinking of the liver.

The pelvic congestion, a consequence of May Thurner syndrome and compression of the vena cava, exacerbated by the collateralisation of blood from the congested left renal vein via the left ovarian vein into the pelvis, led to such an increase in pressure in the left common iliac vein that the left internal iliac vein was unable to supply blood from the pelvic organs. The blood from this vein was diverted to the right side of the pelvis via the midline organs (uterus, vagina, urinary bladder – hence the pollakisuria, and urethra).

The patient’s severe clinical picture can only be adequately diagnosed if the changes in the blood vessels and intestines are examined functionally and quantitatively.

This means that all patients with vascular compression must be fully examined while lying down and in an upright position, before, during and after eating. A time of 2, sometimes up to 4 hours must be planned for this. The flow phenomena must then be quantified using the PixelFlux technique. This involves analysing hundreds of images from video sequences.