Delayed Cerebral Abscess Formation After Posterior Cerebral Artery Stroke in a Patient With Opioid Use Disorder.
Delayed Cerebral Abscess Formation After Posterior Cerebral Artery Stroke in a Patient With Opioid Use Disorder.
复制标题
阿片类药物使用障碍患者后脑动脉中风后脑脓肿延迟。
DOI:
10.1161/strokeaha.120.031081
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发表时间:
2021-03
期刊:
影响因子:
8.3
通讯作者:
Fehnel CR
中科院分区:
文献类型:
--
作者:
Zuflacht JP;Fehnel CR
A 33-year-old right-handed man with opioid use disorder presented with right arm weakness and confusion. He was febrile, tachycardic, and somnolent but able to open his eyes to repeated verbal stimulation. There was minimal spontaneous speech output. Inattention limited full mental status testing. Other pertinent features of the examination included a right homonymous hemianopia, left gaze preference, right nasolabial fold flattening, and right hemiparesis. National Institutes of Health stroke scale score was 15. Head computed tomography (CT) demonstrated a hypodensity in the left temporal and occipital lobes. CT angiography revealed an abrupt cutoff of the left posterior cerebral artery (PCA) at the bifurcation of the parieto-occipital and calcarine arteries, consistent with a distal occlusion of the PCA. Given these imaging findings (completed infarction on CT, distal occlusion on CT angiography), and unknown last known well, he was not a candidate for reperfusion therapy. He was started on empirical, broad-spectrum antibiotics out of concern for infective endocarditis (IE). Transthoracic echocardiogram revealed a moderately sized mobile mass attached to the aortic valve suspicious for a vegetation, supporting the diagnosis of IE based on the Duke criteria. 1 Serial blood cultures were positive for methicillin-susceptible Staphylococcus aureus. A large mediastinal abscess required multiple debridements. The patient was transitioned to nafcillin given multiple positive cultures with the same organism from both the blood and manubrium.The patient underwent magnetic resonance imaging (MRI) of the brain 2 days later (Figure 1), confirming a large left PCA territory infarct. Given the extent of the infarct—involving both the thalamus and medial temporal lobes—it was hypothesized that a septic thrombus had initially occluded the proximal PCA (causing the large left PCA infarct) and subsequently embolized distally (as seen on vessel imaging).