Ayako Ro

Intracranial vertebral artery dissection resulting in fatal subarachnoid hemorrhage: clinical and histopathological investigations from a medicolegal perspective

OBJECT Subarachnoid hemorrhage (SAH) due to a ruptured intracranial vertebral artery (VA) dissection sometimes results in a sudden fatal outcome. The authors analyzed the relationship between clinical features and histopathological characteristics among fatal cases to establish valuable information for clinical diagnostics and prophylaxis. METHODS This study included 58 medicolegal autopsy cases of ruptured intracranial VA dissection among 553 fatal nontraumatic cases of SAH that occurred between January 2000 and December 2007. Their clinical features were obtained from autopsy records. Histopathological investigations were performed on cross-sections obtained from all 4-mm segments of whole bilateral intracranial VAs and prepared with H & E and elastica van Gieson staining. RESULTS The autopsy cases included 47 males and 11 females, showing a marked predilection for males. The mean age was 46.8 +/- 7.7 years, with 78% of the patients in their 40s or 50s. Hypertension was the most frequently encountered history; it was found in 36% of cases from clinical history and in 55% of cases based on autopsy findings. Prodromal symptoms related to intracranial VA dissections were detected in 43% of patients. Headache or neck pain lasting hours to weeks was a frequent complaint. Of patients with prodromal symptoms, 44% had consulted doctors; however, in none of these was SAH or intracranial VA dissection diagnosed at a preventable stage. Autopsy revealed fusiform aneurysms with medial dissecting hematomas. Apart from ruptured intracranial VA dissection, previous intracranial VA dissection was detected in 25 cases (43%); among them, 10 showed previous dissection of the bilateral intracranial VAs. The incidence of prodromal symptoms (60%) among the patients with previous intracranial VA dissection was significantly higher than that (30%) among cases without previous dissection (chi-square test; p = 0.023). Most previous intracranial VA dissections formed a single lumen resembling nonspecific atherosclerotic lesions, with the exception of 3 cases (12%) with a double lumen. CONCLUSIONS Intracranial VA dissection resulting in fatal SAH frequently affects middle-aged men with untreated hypertension. Related to the high frequency of prodromal symptoms, latent previous intracranial VA dissection was histopathologically detected. Furthermore, intracranial VA dissection tends to induce multiple lesions affecting both intracranial VAs recurrently. This suggests the importance of an awareness of sustained whole intracranial VA vulnerability for the prevention of recurrence. The incidence of prodromal symptoms was significantly higher among patients with previous intracranial VA dissections. Thus, earlier diagnosis of intracranial VA dissections at the unruptured stage is desirable for prophylaxis against fatal SAH.

Significance of the Soleal Vein and its Drainage Veins in Cases of Massive Pulmonary Thromboembolism

In this report, we review the anatomical features of the crural veins and the importance of the soleal vein and its drainage veins for thrombi formation and propagation. The result of our investigation of 120 legs of 60 autopsy cases with fatal pulmonary thromboembolism showed that the soleal vein was the most frequent site of deep vein thrombosis, both for fresh and for organized thrombi. Furthermore, the detection rate of thrombi, both fresh and organized, showed that the most common site was in the soleal vein and then decreased progressively according to the drainage route of the soleal vein. Anatomical characteristics and physiological mechanisms play a major role in the occurrence and propagation of venous thrombi. Thus, an understanding of these features is essential for effective prophylaxis of venous thromboembolism.

Pathomorphometry of ruptured intracranial vertebral arterial dissection: adventitial rupture, dilated lesion, intimal tear, and medial defect.

OBJECT Subarachnoid hemorrhage (SAH) due to ruptured intracranial vertebral artery (VA) dissection is a life-threatening disease. Angiographic and symptomatic prognostic factors for rupture and rerupture have been investigated, but the pathological characteristics have not been fully investigated. The authors aimed to investigate these features by performing a pathomorphometic study of ruptured intracranial VA dissections. METHODS This study included 50 administrative autopsy cases of fatal SAH due to ruptured intracranial VA dissection among 517 fatal nontraumatic cases of SAH occurring between March 2003 and May 2011. Pathomorphometry was performed using serial 5-μm histological cross-sections with elastica van Gieson staining from each 0.2-mm segment around the ruptured intracranial VA. The longitudinal lengths of 4 types of vascular lesions-adventitial ruptures, dilated lesions where the internal elastic lamina (IEL) was ruptured with adventitial extension, intimal tears where the IEL was ruptured, and medial defects-were calculated based on the numbers of the slides in which these lesions were continuously detected (minimum 2 adjoining slides). The distance from the vertebrobasilar junction to the center of adventitial rupture was also calculated in 37 cases. RESULTS All cases showed one adventitial rupture with a mean length of about 1.9±1.1 mm. The center of the adventitial rupture was located 5.0-26.8 mm (mean 14.6±5.5 mm) from the intracranial VA bifurcation. Adventitial ruptures existed in the centers of dilated lesions, where the adventitia was highly extended. Other vascular lesions were serially observed surrounding the adventitial rupture. The mean lengths of dilated lesions, intimal tears, and medial defects were 9.4±4.8 mm, 13.2±6.3 mm, and 15.6±7.2 mm, respectively. The lengths between proximal lesions and distal lesions from the center of the adventitial rupture for both medial defects and intimal tears were significantly longer at proximal lesions than at distal ones (chi-square test, p<0.01). CONCLUSIONS Every ruptured intracranial VA dissection has a single point of adventitial rupture where the adventitia was maximally extended, so dilation appears to be a valuable predictive factor for hemorrhagic intracranial VA dissections. The adventitial ruptures were as small as 2 mm in length, and clinically detectable dilated lesions were about 9 mm in length. However, vascular vulnerability caused by IEL ruptures and medial defects existed more widely across a length of VA of 1.3-1.5 cm. Comparatively broader protection of the intracranial VA than the clinically detected area of dissection might be desirable to prevent rebleeding. Broader protection of proximal lesions than distal lesions might be effective from the viewpoint of site distribution of vascular lesions and blood flow alteration to the pseudolumen caused by the dissecting hematoma. Medial defects are the most widely seen lesions among the 4 types of vascular lesions studied. Medial degenerative disease, known as segmental arterial mediolysis, is suspected in the pathogenesis of intracranial VA dissections.

Visualization of the azygos arch valves on multidetector-row computed tomography

To evaluate the frequency and appearance of the azygos arch valves on chest examinations using multidetector-row computed tomography (MDCT), we retrospectively reviewed findings from 194 contrast-enhanced MDCT examinations of the chest. Rate of injection of 300 mgI/ml contrast materials was low (2.0 ml/s) and high (3.0 ml/s). Scanning delay was 80 s on examination on low-rate injection of contrast material and 20 s on high-rate injection of contrast material. The presence of residual contrast material in the azygos arch valves and reflux of contrast material into the azygos arch were recorded. The Cochran-Armitage trend test was used to compare the frequency of residual contrast material in the azygos arch valves and reflux of contrast material into the azygos arch in both groups. Of 92 examinations of high-rate injection of contrast material, 63 (68.5%) demonstrated residual contrast material in the azygos arch valves and 71 (77.2%) demonstrated reflux of contrast material into the azygos arch. A significantly higher frequency of reflux of contrast material into the azygos arch and residual contrast material in the azygos arch valves was seen in the high-rate injection group than in the low-rate injection group (P < 0.05). Residual contrast material in the azygos arch valves was demonstrated more frequently when contrast material was administered in the right side of the arm than in the left side of the arm (P < 0.05). Reflux of contrast material into the azygos arch was common in the high-injection-rate group and residual contrast material in the azygos arch valves was far more frequently seen in the high-injection-rate group than in the low-injection-rate group on MDCT.

Histopathological study of pulmonary arteries in 14 autopsy cases with massive pulmonary thromboembolism

As the pathological features of acute massive pulmonary thromboembolism (PTE) remain unclear, early diagnosis is difficult. We examined 14 autopsy cases of sudden death by massive PTE. Eight cases were male and six female, with a mean age of 57+/-18 years. While none of the cases were diagnosed with PTE during their lifetime, 12 cases had predicting factors for thrombosis. Deep vein thrombosis was found at autopsy in 11 cases. Cross sections of each segmental pulmonary artery were dissected for histological examination. The distribution of fresh thrombi and organized thrombi in the pulmonary arteries was investigated. Results revealed that 13 cases contained both fresh and organized thrombi. More detailed examination indicated that as the organized thrombi were spread in all lobes, the distribution of thrombi extended from the proximal to peripheral arteries. Our findings indicated that most cases of fatal PTE had a subclinical recurrent history. Thus, proper diagnosis and treatment of prior emboli may be vital for the prophylaxis of sudden death by PTE.

Clinical Significance of the Soleal Vein and Related Drainage Veins, in Calf Vein Thrombosis in Autopsy Cases with Massive Pulmonary Thromboembolism.

OBJECTIVE To clarify the histopathological characteristics of deep vein thrombosis (DVT) resulting in lethal pulmonary thromboembolism (PE). SUBJECTS AND METHODS We investigated 100 autopsy cases of PE from limb DVT. The distribution and chronology of DVT in each deep venous segment were examined. Venous segments were classified into three groups: iliofemoral vein, popliteal vein and calf vein (CV). The CV was subdivided into two subgroups, drainage veins of the soleal vein (SV) and non drainage veins of SV. RESULTS Eighty-nine patients had bilateral limb DVTs. CV was involved in all limbs with DVT with isolated calf DVTs were seen in 47% of patients. Fresh and organized thrombi were detected in 84% of patients. SV showed the highest incidence of DVTs in eight venous segments. The incidence of DVT gradually decreased according to the drainage route of the central SV. Proximal tips of fresh thrombi were mainly located in the popliteal vein and tibioperoneal trunk, occurring in these locations in 63% of limbs. CONCLUSIONS SV is considered to be the primary site of DVT; the DVT then propagated to proximal veins through the drainage veins. Lethal thromboemboli would occur at proximal veins as a result of proximal propagation from calf DVTs.

Acute coronary syndrome as a cause of sudden death in patients with old myocardial infarction: a pathological analysis

Old myocardial infarction (OMI) is one of the most important pathological manifestations in sudden cardiac death. Fatal arrhythmia arising from a fibrotic scar has been determined as the cause of death in most cases with old myocardial infarction. However, the significance of acute plaque disruption/thrombosis of the coronary arteries in those patients has not been investigated. We examined a series of 33 hearts from individuals with OMI who died suddenly during the period from 1998 to 2001. Detailed coronary pathological findings on these hearts indicated fresh or recent rupture of the coronary plaque with thrombosis in 18 cases (55%). As a result of comprehensive analysis, the sudden deaths were explained by acute coronary syndrome in 18 cases (55%), fatal arrhythmia in eight (24%), cardiac pump failure in five (14%), and other causes in two (6%) cases. Our findings revealed that a new coronary plaque rupture independent of the old infarct was a major cause of sudden cardiac death with OMI.