Fatal errors in the treatment of vascular compression syndromes
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All vascular compression syndromes can be traced back to an increased lordosis of the lumbar spine. It is therefore not uncommon for several vascular compression syndromes to occur simultaneously in one patient (usually women are affected).

In venous compression syndromes, the blood flow from the blocked vein is returned to the heart via a collateral circulation. But this venous collateral circulation can also be compressed as a result of the increased lordosis, so that the individual vascular compression syndromes may influence each other.

To explain the patient’s symptoms, but above all for his successful therapy, it is therefore essential to uncover all known vascular compression syndromes.

In a second step, the quantitative impact of each individual vascular compression syndrome on the prevailing symptoms must be determined. This does not only require measurements of the blood flow velocity at numerous points in the venous and arterial circulation, but also measurements of the diverted blood volumes. They are of crucial importance for the effect of the venous compression.

For this purpose we have developed the PixelFlux software, which makes such exact measurements possible for the first time.

Without mesuring the venous back pressure at different sites of the venous circulation and without measuring the collateralised blood volumes and without determining the reserve capacity of the collateral circulation a successful therapy is endangered or unlikely.

In my practice I often see patients who have been treated surgically or interventionally after the diagnosis of a vascular compression syndrome was made but whose symptoms persist because the above-mentioned circumstances have been ignored.

In the following,  some examples are meant to illustrate fatal misjudgements and mistreatments of various vascular compression syndromes to point out the risks of certain treatment methods.

Embolisation of ovarian veins and pelvic veins in patients with pelvic congestion syndrome

The pelvic congestion syndrome consists of a congestion of venous blood in the pelvic organs. The uterus and the left ovary are most frequently affected. But also other organs in the pelvis such as the vagina, in men the prostate, the urethra, rectum and urinary bladder can be congested to varying degrees. The consequence of this venous congestion is chronic pain, often particularly severe at the beginning of the menstruation, in the area of the aforementioned organs.

A common treatment in these patients is the obliteration of the left ovarian vein, sometimes also of the right ovarian vein and other pelvic veins. The starting point for these therapeutic considerations is usually the detection of congested pelvic veins on the left side of the pelvis in a phlebography or an MR angiography or a CT angiography. After the detection of such dilated veins these are then usually regarded the therapeutic target. The treating physician’s aim is to eliminate the pain by eliminating the painful organ, which  in this case is a dilated vein. For this purpose, these veins are often obliterated during a catheter examination by placing metal spirals in the veins (embolization), or they are ligated during a laparoscopic intervention.

According to my observations, these procedures, after a short interval of improvement, result in even greater pain in the pelvis, in the left flank and in the area of the left kidney.

The reason for such a treatment failure is an insufficient knowledge about the connections of pelvic congestion and their causes. In most cases, the underlying causes are not sought. Instead, a weakness of the wall of the left ovarian vein is assumed. It is not asked for why the left ovarian vein should have a weak wall if other veins are not dilated. This wall weakness, then is claimed, be the cause for the dilatation of the left ovarian vein. Sometimes it is also assumed that venous valves do not close properly and this being the cause of the varicose dilatation of the left ovarian vein.

In fact, however, an increase of the venous pressure in the ovarian vein is the cause of its dilatation. This pressurisation is triggered by a narrowing of the left renal vein, as soon as an increased lordosis pushes the lumbar spine towards the abdominal wall and thus compresses the left renal vein from behind. This happens since the left renal vein crosses the spinal column above the umbilicus from left to right. Since the left ovarian vein opens into the left renal vein in a rectangular fashion, the increased pressure from the left renal vein is transmitted to the left ovarian vein. After an initial widening of the ovarian vein the vein later becomes tortuous like a varicose vein on the leg. Such a varicose vein is the cause of cramping and dull pain in the leg as well as in the abdomen, the left flank and the left renal fossa.

If the pressure increases further and no counter-pressure from pelvic veins counteracts the drainage of blood from the left kidney, then the blood flow in the ovarian vein starts to flow backward into the pelvis.

The human body has thus created a (primary) collateral circulation which enables the transport of accumulated blood from the left kidney back to the heart. This collateral pathway begins at the mouth of the left ovarian vein, taking up blood from the left renal vein and guiding it downwards to the left ovarian vein. From here, across the left fallopian tube, the blood runs to the uterus, then passes through the muscle layers of the uterus to accumulate in veins on the right fallopian tube and at the right side of the uterus. From there, the blood runs via the often significantly enlarged and then usually painful right deep pelvic vein into the superficial right pelvic vein, from where it is transported directly into the lower vena cava and this way back to the heart.

The functioning of this collateral pathway depends basically on the pressure conditions within those vessels and organs, which must be passed by the diverted blood volume. Originally the width of  all vessels is adjusted to the blood requirements of the organs which are fed or drained. This means that the ovarian vein does lack the sufficient capacity for such large amounts of blood which have to be bypassed through the collateral circulation.

The kidney is the organ with the strongest blood supply in the entire abdominal cavity, since its blood supply must not only cover the kidney’s own metabolic requirements but the kidney merely functions as a filter for the entire circulating blood and therefore receives many times more blood than it would be expected from the size of the organ. If the drainage from the kidney is congested by compression of the left renal vein, high pressure quickly develops due to the high blood volume that is accumulating in the collateral circulation. This pressure causes to the aforementioned dilatation of the bypassing veins and all of them become pressurized over time. The high intravascular blood pressure damages the venous walls and fuels their inflammation, the source of the devastating pain.

The sudden interruption of this delicate collateral circulation by surgical or interventional measures inadvertently leads to a further increase of pressure in the left renal vein.

Initially the patients feel an improvement of their pain because the former dilated and painful veins collapse. The reduction of the wall tension after the collapse reduces the pain in the former collateral pathways.

Now, there even higher pressurised blood in the left renal vein is pressed into other, smaller collateral veins. These veins then form a secondary collateral pathway with the same aim: to find a way back to the heart. These secondary collateral veins have an even smaller diameter than those veins which have been obliterated. Because of the above-mentioned pathophysiological mechanisms and even stronger inflammation is provoked in their wall. After a few days or weeks the patients develop even stronger pain than before the embolization.


That is why it is not advisable to interrupt or occlude dilated veins if the very origin of the dilatation is not found and an increased pressure within these veins is not ruled out. This requires a thorough functional colour Doppler sonographic examination with blood flow velocity and blood flow volume measurements as described at the beginning of this article.

The same considerations apply of course, to the removal of organs which are part of the collateral circulation. The same detrimental consequences can therefore be expected when the left ovary or the uterus is removed.

Unfortunately, the patients are then often no longer treated by the physicians who carried out the embolisation or organ removal, because from their point of view the procedure was technically successful and because of the lack of the understanding of the overarching concept of lordogenetic vascular compression syndromes the reason for the persisting pain is not recognized.

The patients are then often sent to a psychologist or psychiatrist with such diagnoses as “pain amplification syndrome”, a “too strong pain memory” or a mental illness.


Renal autotransplantation into the left iliac fossa in patients with May-Thurner-syndrome

In patients with compression of the left renal vein sometimes the autotransplantation of the left kidney is recommended in order to get rid of the left renal vein compression. In these cases it is important to rule out that pre-existing compressions of the left or right common iliac vein or the vena cava inferior hamper to venous return from the transplanted kidney.

Unfortunately, it is not well known that abdominal compression syndromes in most patients occur as a sequence. This means that the detection of one compression syndrome requires a complete workup to find coexisting vascular compressions.

I give here a report of a young girl where one compression syndrome was detected and operated after another and finally ended up with unbearable pain in her renal transplant due to a ptotic hyperperfusion of the transplant due to orthostatic strangulation of the right renal blood flow and a subsequent flooding of the transplanted kidney.

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