Subarachnoidal hemorrhage from berry aneurysms as a cause of natural death

Abstract

Subarachnoidal hemorrhage (SAH) is the fourth most common intracranial cause of death. Approximately 50 to 85 percent of non-traumatic SAH is caused by rupture of congenital berry aneurysm. Symptoms of rupture are typically sudden and without any heralds. In most SAH cases, the vasospasm following the rupture is the most probable cause of death. In forensic pathology, an isolated SAH episode after minor head trauma should be considered dubious, and as mode of death. The objective of this paper was to establish the frequency of sudden natural death caused by SAH originating from ruptured berry aneurysm and to establish the epidemiologic characteristics of the deceased, as well as pathoanatomic characteristics of ruptured aneurysms. A retrospective autopsy study of the material of the Institute of Forensic Medicine in Belgrade was performed over a period of eighteen years. Some risk factors were estimated: smoking habits, hypertension, alcoholism, and stress 24 hours preceding the rupture. The following pathoanatomic features of berry aneurysms were determined: localization, size, number, spread to surrounding structures and any association with atherosclerosis of brain blood vessels. The analyzed sample consisted of 63 examined individuals: 33 male and 30 female. Their age ranged from 9 to 89 years, with mean age of 46.2 +/- 14.5 years. In our sample, there were 47 smokers (25 male and 22 female), 41 individuals who suffered from hypertension (22 male and 19 female), and 15 alcoholics (14 male and one female). In our sample, physical or mental stress preceded the berry aneurysm's rupture in 26 cases. Most of fatal berry aneurysms were localized in the anterior part of the circle of Willis (41 of them): 20 of them were localized in bifurcations. In 46 cases, the berry aneurysms were less than 5 mm in diameter, in 10 cases with a diameter measuring 5 to 10 mm and in 7 cases the aneurysms were larger than 10 mm in diameter. The association with macroscopically visible atherosclerotic lesions of the arteries of the circle of Willis was evident in 34 cases. Nine people had multilocular berry aneurysms. Polycystic kidney disease associated with berry aneurysms was evident in nine cases. The difference between the number of males and females in our sample was not statistically significant (c2=0.014; p>0.10). The age of the deceased mostly ranged from 30 to 60 years. There was no significant difference between the mean age of the males and females in our sample (t=1.65; p>0.05). In our sample, statistically significant localization of fatal berry aneurysm was the anterior part of the circle of Willis (c2=5.74; p<0.05). The frequency of the berry aneurysms larger than 10 mm in diameter was less significant than those with smaller diameters (c2=31.10; p<0.001). The individuals in our sample with aneurysms smaller than 5 mm in diameter were not significantly younger than individuals with larger ones (t=0.98; p>0.05). The number of individuals in our sample with berry aneurysms associated with atherosclerotic lesions was not statistically significant (c2=0.32; p>0.1). Sometimes, it is not possible to detect the exact localization of the ruptured berry aneurysm: the rupture may destroy the aneurysm completely. In such case, an autopsy should rule out other possible sources of intracranial bleeding, such as vascular malformations, intraventricular spreading of intracerebral hematomas, neoplasia, hematological disorders, etc.