Cerebral abscess is a rare but severe disease and can result in severe disability or even death, especially if misdiagnosed or improperly managed. In most cases a brain abscess is preceded by a phase of cerebritis with headache followed by symptoms of increased intracranial pressure (nausea, vomiting, somnolence) and only about 30% of patients present initial focal neurological deficits [1]. Most often brain abscesses arise from direct penetration after brain injury, operation, sinusitis or otitis. About 20-30% are caused by metastatic spread which most frequently originates from infectious endocarditis (2.8% of these patients [2,3]) or from paradoxical embolism in patients with a right-to-left shunt [1]. The rare metastatic spread from a pulmonary abscess has however been described in the literature [4]. Embolisation of septic material e.g. in infective endocarditis is a known reason for strokes but only in very rare cases is the condition complicated by formation of a secondary brain abscess [5,6].

We report the case of a 35-year-old man with a 21-year history of intravenous heroin abuse who developed moderate global aphasia on the day of admission. Cerebral magnetic resonance imaging (MRI) was in line with an acute ischemic infarction in the left supplementary motor cortex (Figure ​(Figure1a-c).1a-c). 4.5 h after symptom onset, systemic thrombolysis was no longer a therapeutic option. Laboratory parameters on admission were consistent with an acute bacterial infection with a C-reactive protein level of 23.0 mg/dl and leukocytosis of 21.3x10³/μl. Detailed clinical examination revealed a Janeway lesion on the fingertip of his left hand (Figure ​(Figure1d),1d), which was highly indicative of a septic-embolic focus as the cause also of the ischemic stroke. Transthoracic as well as transesophageal echocardiography provided no evidence for an endocarditis or cardiac right-to-left shunt and repeated aerobic and anaerobic blood cultures came out negative. Magnetic resonance angiography and doppler/duplex-sonography revealed no relevant stenoses of the cervical or cerebral arteries. Chest X-ray, however, showed a large fluid and air containing lesion in the right lower lobe (Figure ​(Figure1e)1e) which was confirmed as a lung abscess by computed tomography (CT, Figure ​Figure1f).1f). There were no further lesions suspicious of septic emboli in the high-resolution CT-scan or other chest X-rays. Antibiotic treatment with piperacillin/tazobactam 3x4.5g/d was immediately initiated. Bronchoscopy confirmed a pulmonary abscess; culture of the aspired purulent liquid revealed no bacterial growth. Tuberculosis was considered unlikely due to the negative interferon-gamma release assay, negative Ziehl Neelsen stain and cultures of sputum, urine, and gastric juice. HIV serology was also negative. As a right-to-left shunt was excluded and echography gave no evidence of a tricuspid endocarditis, we considered the pulmonary abscess to be a consequence of the intravenous heroin abuse.

This case illustrates that septic embolism should be considered as a cause of ischemic stroke in patients with pulmonary abscess. Even though paradox embolism due to cardiac or pulmonary right-to-left-shunting is a common reason of stroke in patients with i.v. drug abuse we do not believe this was the case in our patient as one would expect a shunt to persist and be detectable by the transoesophagic echocardiography or the contrast transcranial Doppler shunt-detection exam which togeather have a very high sensitivity (reviewed in [11]). We therefore believe that an erosion of a pulmonary vein by the pulmonary abscess and consecutive transcardiac embolisation of septic material was the most probable cause of the ischemic stroke and the Janeway lesion of our patient.

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