An Autopsy case of Rupture of an Aneurysm of the Splenic Artery
We present here a case of sudden death resulting from the rupture of an aneurysm of the splenic artery. From the histopathological findings, we concluded that the formation of the splenic aneurysm was associated with the fibromuscular dysplasia.
A splenic artery aneurysm (SAA)
is a one of the most common aneurysms in the visceral artery,
although its incidence is still rare (10). Here we report a case of
sudden death due to a rupture of a splenic artery aneurysm.
A 32 year old male with no
remarkable past medical history was found dead in his room. An
autopsy was performed to clarify the cause of death.
The deceased was a slender
Japanese male, 176 cm in height and 56 kg in weight. At autopsy, no
external injury was observed. The abdominal cavity was filled with
approximately 2000 ml of blood with coagula. There was an aneurysm in
a distal portion of the splenic artery, approximately 4cm in
diameter, the lower portion of which was ruptured (Figure 1). The
heart, weighing 275g contained 30ml of blood without coagula and the
brain weighed 1350g, neither having any abnormal findings. No
morphological abnormality of the liver (organ weight 1230g), or
spleen (organ weight 125g) was observed. No aneurysm was observed in
the other arteries. There were no notable changes in the other
The rupture site of the aneurysm
showed bleeding to the surrounding tissues (Figure 2 (a)). The normal
structure of the arterial wall was destroyed with a withdrawal of the
internal elastic lamina (Figure 2 (b)). Hyperplasia of the intima,
muscular hypertrophy and fibrosis of media were observed. No lesions
such as atheromatous plaque, calcification, periarterial
inflammation, fibrinoid necrosis, mucoid medial degeneration,
dissection and vacuolar degeneration of the medial smooth muscle
cells were observed. Histopathological findings of the aneurysm
revealed fibromuscular hyperplasia, corresponding to medial
fibromuscular dysplasia. No inflammatory changes were present. No
fibrosis or inflammatory change was observed in the liver, and there
were no inflammatory changes or calcification in the pancreas.
screening using a TriageTMDrugs
of Abuse panel plus Tricyclic Antidepressants (Biosite Diagnostic
Inc., San Diego) was negative. No ethanol was detected from the
SAA is the third most common
intra-abdominal aneurysms, following aneurysms of the infrarenal
aorta and iliac arteries (8, 11). The incidence of SAA varies from
0.01-0.2% in autopsy studies (1, 7, 8, 10, 11), to 0.78% in a study
of angiography (9). Most SAA are solitary, and approximately 80% are
located in the distal portion of the splenic artery (10,11). It is
usually asymptomatic, and found incidentally (3, 10). Spontaneous
rupture is one of the complications of SAA. Although the true
incidence of rupture is difficult to ascertain, it is said to be from
3–10% in some studies, to 28% for giant aneurysm (2, 5, 9, 10).
Although the pathogenesis of SAA
is poorly understand, it has been reported that various contributing
factors are associated with SAA formation, including arterial
fibrodysplasia, portal hypertension with splenomegaly,
arteriosclerosis, inflammatory process, multiple pregnancies, blunt
trauma, connective tissue disease and mycotic aneurysm (3, 6, 8–11).
In the present case, portal hypertension, arteriosclerosis and
pancreatitis were excluded, based on macroscopic and
histopathological findings of the liver, pancreas, spleen and splenic
artery. Histological changes involving arteriosclerosis are observed
in up to 99% of SAA, but are most likely secondary events (5, 9).
Traumatic SAA was also excluded, since the victim had no history of
trauma and there were no external injuries.
Histological SAA findings
revealed fibromuscular dysplasia, which is associated with the
formation of SAA (12). Fibromuscular dysplasia is a
non-arteriosclerotic, non-inflammatory vascular disease, involving
medium or small arteries such as the renal, carotid and vertebral
arteries (4). Fibromuscular lesion of the splenic artery is
relatively rare (4). It is characterized by focal abnormalities in
the structure of the arterial wall, and classified by the dominant
site of dysplasia in the arterial wall. Although, the pathogenesis of
fibromuscular dysplasia is not well understood, humoral, mechanical
and genetic factors as well as mural ischemia may play a role (4).
From the macroscopic and
histological findings, we concluded that the cause of death was
hemorrhage in the abdominal cavity due to rupture of the SAA,
associated with fibromuscular dysplasia.
correspondence concerning this paper should be addressed to:
of Legal Medicine, Hyogo College of Medicine,
Mukogawa-cho, Nishinomiya, Hyogo, 663-8501, Japan
+81-798-45-6578, FAX: +81-798-49-3279
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