An occlusive vasculopathy, generally on an atherosclerotic basis, affecting two
of the three major splacnic vessels may be associated with intermittent,
unintended intermittent or cramp-like abdominal pain, called "abdominal angina".
The pain begins when oxygen demands increase, as happens after the meal,
generally from 15 to 30 minutes later and the pain lasts at least 2-3 hours
because the food goes into the small intestine and the process of digestion
continues, being an adequate blood perfusion by the vascular system is required
to allow an adequate intestinal blood flow and a considerable oxygen consumption.
However, for partial or total occlusion of the superior mesenteric artery and
for the presence of other vessels that are able to provide effective collateral
circulation, relative ischemia is determined and the patient is subjected to
pain, which can be considered analogous to that of angina pectoris.
Patients with this syndrome typically belong to the more advanced age group. They soon realize the relationship between food intake and the appearance or aggravation of pain. Therefore they start to fear food intake and tend to reduce both the amount of individual meals ("small meal syndrome") and overall food intake. As a consequence, the marked loss of weight is the rule, probably exacerbated to a certain extent by mild-moderate steatorrhea. There may be other, less constant symptoms, such as diarrhea, constipation, nausea, vomiting, and abdominal swelling. The duration of the symptomatology from the appearance to the recognition can vary considerably depending on the severity of the pathological picture and the diagnostic sensitivity of the clinician.
In retrospect, however, it is clear that many patients with an established
intestinal infarction have previously complained of abdominal angina symptoms
for weeks and months. Consequently, this syndrome assumes considerable clinical
importance not only for the ailments and disability it entails, but also as a
potential warning of an imminent catastrophe. The physical examination next to a
marked weight loss in general detects signs of atherosclerotic disease in
advanced stages. An abdominal murmur may be felt, whose presence or absence,
however, has no significant diagnostic value, being deficient in many patients
with advanced mesenteric vasculopathy and, on the other hand, completely
innocent breaths are described in normal individuals. The interesting
possibility that the phonoangiographic documentation of a diastolic phase can
discriminate significant breath deserves further evaluation. Laboratory results
are generally not specific. However, in a number of patients the steatorrhea has
been well documented.
It is generally mild to moderate up to about 20 g of faecal fat per day; in atherosclerotic mesenteric insufficiency it is almost always associated with pain. Although the steatorrhea may contribute to the state of malnutrition, generally the main factor is reduced food intake, while malabsorption is not an important clinical problem. The cause of malabsorption is not well understood, but it probably reflects the mesenteric blood hypo-flow; specific morphological changes in the mucosa have been reported in patients. However, it is interesting how the steatorrhea may persist after the restoration of the vascularization, even if the intestinal morphology is normal. Perhaps the ischemic damage of the autonomic nervous system or the formation of stenosis can alter intestinal motility and lead to the development of bacteria.
It makes use of the following instrumental investigations:
• Eco-color-doppler
• Angio-CT
• Angio-RM
• Arteriography of the celiac tripod
The presence of intense recurrent abdominal pain with progressive weight loss in
an elderly subject may suggest the diagnosis of endoabdominal malignant lesion.
However, with careful questioning it is generally possible to clarify how
reduced food intake depends more on fear of consequences than lack of appetite.
Signs of advanced atherosclerotic vasculopathy are often present. An abdominal
systolic murmur may be detectable, but, as noted, this clinical sign (or its
absence) is generally of little use. The barite investigations do not usually
detect alterations that justify the clinical picture. In the suspected diagnosis
of angina abdominis, and, if the patient's condition allows for a possible
corrective surgery, a splanchnic angiographic examination is indicated. A
positive finding shows significant stenosis (> 50 percent) in at least two of
the three main arteries and often a collateral circulation. Unfortunately, the
available techniques generally allow an accurate assessment of the vessel
diameter and not of the blood flow. Adequate tissue oxygenation depends on blood
flow more than on vessel size and therefore the lack of clinical signs of
vascular insufficiency in many patients apparently affected by severe mesenteric
vasculopathy defined by angiography is understandable. For this reason it is not
possible to consider angiography as a diagnostic method of angina abdominis.
Instead, a diagnosis of presumption must be placed; the angiogram can be
interpreted to be compatible with this diagnosis or can exclude it by
demonstrating normal splanchnic vessels. In strong suspicion that the anamnesis
and clinical data refer to angina abdominis, angiography, if negative, will be
particularly valid to exclude this diagnosis. The diagnostic accuracy of
angiography may eventually improve if associated with other techniques that more
directly reflect blood flow, such as radio-active xenon wash-out. The decision
to resort to angina abdominis to reconstructive vasal surgery should be taken
only after excluding other significant and potentially causal pathological forms
and after angiographic demonstration of important inxtaorrhoidal stenosis (surgical
accessibility area) generally of at least two main arteries.
By-pass techniques, reimplantation and endarterectomy
cfr indice di gastroenterologia