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Subarachnoid hemorrhage due to nonbranching aneurysm of the middle cerebral artery in a young adult with a history of Kawasaki disease.

Ishida A, Matsuo S, Kawamura S, Nishikawa T - Surg Neurol Int (2014)

Bottom Line: The incidence of subarachnoid hemorrhage (SAH) in young adults is relatively rare.Two weeks later, the patient was discharged without any apparent neurological deficit.We also performed a circumstantial pathological study on specimens obtained from the aneurysm wall.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurosurgery, Moriyama Memorial Hospital, Tokyo, Japan.

ABSTRACT

Background: The incidence of subarachnoid hemorrhage (SAH) in young adults is relatively rare. Kawasaki disease is a systemic vasculopathy that is known to cause coronary artery aneurysms; however, its effect on cerebral arteries remains largely unclear.

Case description: We report the case of a 20-year-old male with a history of Kawasaki disease who presented with SAH caused by the rupture of a nonbranching middle cerebral artery aneurysm. This is the third report of SAH associated with Kawasaki disease. Preoperative echocardiography of the patient rejected the presence of bacterial endocarditis and other heart abnormalities. An emergency craniotomy and clip occlusion of the aneurysm was successfully performed without obstructing the parent artery. Two weeks later, the patient was discharged without any apparent neurological deficit. We also performed a circumstantial pathological study on specimens obtained from the aneurysm wall. Our histological findings suggest that the elastic lamina and tunica intima were completely destroyed during the acute vasculitis phase of Kawasaki disease, which possibly led to the aneurysmal formation.

Conclusions: Lack of active inflammatory changes and atherosclerotic lesions may explain the chronic feature of Kawasaki disease, not a typical aneurysmal formation.

No MeSH data available.


Related in: MedlinePlus

Histopathological studies of the surgical specimen. (a) Hematoxylin and eosin (H and E) staining. The upper side is the vascular lumen. Atherosclerotic change was not observed. (b) Elastica van Gieson (EVG) staining shows thickened intima and mild invasion of inflammatory cells. (c) Masson's trichrome staining. (d) SMA (smooth muscle actin) immunohistochemistry. Staining reveals lack of smooth muscle cells in the tunica media. Scale bar: 600 μm
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Figure 3: Histopathological studies of the surgical specimen. (a) Hematoxylin and eosin (H and E) staining. The upper side is the vascular lumen. Atherosclerotic change was not observed. (b) Elastica van Gieson (EVG) staining shows thickened intima and mild invasion of inflammatory cells. (c) Masson's trichrome staining. (d) SMA (smooth muscle actin) immunohistochemistry. Staining reveals lack of smooth muscle cells in the tunica media. Scale bar: 600 μm

Mentions: Histopathological examination revealed that the aneurysm wall primarily consisted of thinkened tunica intima. Granulation tissue presented with edematous chronic inflammatory cell invasion and intermediate invasion of macrophages, fibroblasts, myofibroblasts, and vascular endothelial cells. There was mild invasion of lymphocytes and plasmacytes, but no neutrophils [Figure 3]. Lack of black Elastica van Gieson (EVG) staining demonstrated complete absence of elastic lamina. EVG staining, Masson's trichrome staining, and smooth muscle actin (SMA) immunohistochemistry also demonstrated the lack of smooth muscle cells in the tunica media. There was no atherosclerotic change in the tunica intima, which is usually observed in cerebral aneurysms [Figure 3].


Subarachnoid hemorrhage due to nonbranching aneurysm of the middle cerebral artery in a young adult with a history of Kawasaki disease.

Ishida A, Matsuo S, Kawamura S, Nishikawa T - Surg Neurol Int (2014)

Histopathological studies of the surgical specimen. (a) Hematoxylin and eosin (H and E) staining. The upper side is the vascular lumen. Atherosclerotic change was not observed. (b) Elastica van Gieson (EVG) staining shows thickened intima and mild invasion of inflammatory cells. (c) Masson's trichrome staining. (d) SMA (smooth muscle actin) immunohistochemistry. Staining reveals lack of smooth muscle cells in the tunica media. Scale bar: 600 μm
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3927094&req=5

Figure 3: Histopathological studies of the surgical specimen. (a) Hematoxylin and eosin (H and E) staining. The upper side is the vascular lumen. Atherosclerotic change was not observed. (b) Elastica van Gieson (EVG) staining shows thickened intima and mild invasion of inflammatory cells. (c) Masson's trichrome staining. (d) SMA (smooth muscle actin) immunohistochemistry. Staining reveals lack of smooth muscle cells in the tunica media. Scale bar: 600 μm
Mentions: Histopathological examination revealed that the aneurysm wall primarily consisted of thinkened tunica intima. Granulation tissue presented with edematous chronic inflammatory cell invasion and intermediate invasion of macrophages, fibroblasts, myofibroblasts, and vascular endothelial cells. There was mild invasion of lymphocytes and plasmacytes, but no neutrophils [Figure 3]. Lack of black Elastica van Gieson (EVG) staining demonstrated complete absence of elastic lamina. EVG staining, Masson's trichrome staining, and smooth muscle actin (SMA) immunohistochemistry also demonstrated the lack of smooth muscle cells in the tunica media. There was no atherosclerotic change in the tunica intima, which is usually observed in cerebral aneurysms [Figure 3].

Bottom Line: The incidence of subarachnoid hemorrhage (SAH) in young adults is relatively rare.Two weeks later, the patient was discharged without any apparent neurological deficit.We also performed a circumstantial pathological study on specimens obtained from the aneurysm wall.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurosurgery, Moriyama Memorial Hospital, Tokyo, Japan.

ABSTRACT

Background: The incidence of subarachnoid hemorrhage (SAH) in young adults is relatively rare. Kawasaki disease is a systemic vasculopathy that is known to cause coronary artery aneurysms; however, its effect on cerebral arteries remains largely unclear.

Case description: We report the case of a 20-year-old male with a history of Kawasaki disease who presented with SAH caused by the rupture of a nonbranching middle cerebral artery aneurysm. This is the third report of SAH associated with Kawasaki disease. Preoperative echocardiography of the patient rejected the presence of bacterial endocarditis and other heart abnormalities. An emergency craniotomy and clip occlusion of the aneurysm was successfully performed without obstructing the parent artery. Two weeks later, the patient was discharged without any apparent neurological deficit. We also performed a circumstantial pathological study on specimens obtained from the aneurysm wall. Our histological findings suggest that the elastic lamina and tunica intima were completely destroyed during the acute vasculitis phase of Kawasaki disease, which possibly led to the aneurysmal formation.

Conclusions: Lack of active inflammatory changes and atherosclerotic lesions may explain the chronic feature of Kawasaki disease, not a typical aneurysmal formation.

No MeSH data available.


Related in: MedlinePlus