2025 Volume 12 Pages 499-503
Mycotic cerebral aneurysms secondary to infective endocarditis carry a high risk of fatal rupture. Early identification and appropriate intervention are critical. We present a case in which a punctate hyperdense lesion on noncontrast-enhanced computed tomography appeared several days before aneurysm formation and rupture. A 43-year-old man with infective endocarditis presented with a ruptured mycotic aneurysm in the peripheral left middle cerebral artery. The patient underwent emergency craniotomy. During the postoperative follow-up, 2 new punctate hyperdense lesions were detected on noncontrast-enhanced computed tomography. A total of 3 days later, one of these lesions progressed to aneurysm formation and hemorrhage, requiring repeat surgery. The outcome was favorable, with a modified Rankin scale score of 2. This case highlights that punctate hyperdense lesions on noncontrast-enhanced computed tomography may serve as an early radiological marker of impending mycotic aneurysm formation and suggests the importance of close imaging surveillance to prevent catastrophic rupture.
Mycotic cerebral aneurysms are rare complications of infective endocarditis, occurring in 4%-15% of cases; however, they carry a high mortality rate when ruptured.1) The presumed pathophysiology involves septic embolization from valvular vegetations, followed by vascular occlusion, wall degeneration, and aneurysmal dilation.2)
Early-stage diagnosis is challenging because of the absence of definitive imaging findings before aneurysm formation. We report a case in which a punctate hyperdense lesion on noncontrast-enhanced computed tomography (CT) preceded the angiographic appearance and rupture of a mycotic aneurysm, offering potential insight into early radiological markers.
A 43-year-old male construction worker presented with fever, chills, and headache for several weeks. The patient's medical history included childhood inguinal hernia and gout. On admission, no focal neurological deficits were noted.
Blood cultures were positive for Streptococcus species, and transthoracic echocardiography revealed mitral valve vegetation with severe regurgitation. A diagnosis of infective endocarditis was made, and intravenous ampicillin therapy was initiated.
On hospital day 3, noncontrast-enhanced CT was performed to evaluate the patient's persistent headache and revealed left hemispheric intracerebral hemorrhage (Fig. 1A). CT angiography (CTA) revealed contrast pooling within the hematoma, suggesting aneurysmal rupture (Fig. 1B and C). Subsequent digital subtraction angiography (DSA) confirmed a ruptured peripheral aneurysm in the left middle cerebral artery (MCA) (Fig. 1D). The patient underwent emergency craniotomy and aneurysm resection on hospital day 4 (Fig. 1E).
Pre- and postoperative imaging of the initial hemorrhage and aneurysm.
(A) Noncontrast-enhanced CT showing intracerebral hemorrhage in the left cerebral hemisphere (arrowhead).
(B, C) CTA demonstrating contrast enhancement within the hematoma, indicating a ruptured aneurysm (arrowhead).
(D) Digital subtraction angiography: left, anteroposterior view; right, lateral view. Arrowheads indicate pooling of the contrast agent, which is consistent with a ruptured aneurysm.
(E) Postoperative CT after the initial craniotomy. The arrowhead marks the surgical resection cavity.
CT: computed tomography; CTA: computed tomography angiography
On hospital day 15, a routine follow-up noncontrast-enhanced CT revealed 2 new punctate hyperdense lesions in the left cerebral hemisphere: one located within the Sylvian fissure (lesion A) and the other on the cortical surface of the occipital lobe (lesion B) (Fig. 2, top row). Lesion A is also clearly visualized in the axial CT slice, as shown in Fig. 3A. To further evaluate these lesions, magnetic resonance imaging (MRI), including MR angiography (MRA), was performed on the same day. The patient remained asymptomatic. MRA revealed no definite evidence of aneurysm formation at either lesion, and other MRI sequences showed no obvious abnormalities on diffusion-weighted imaging or fluid-attenuated inversion recovery (Figs. 3B, 3C). Susceptibility-weighted imaging revealed subtle hypointensity at both sites, although differentiation from normal arteries was difficult (Fig. 3D). Although MRA demonstrated subtle arterial narrowing at the site of lesion A (Fig. 2, bottom row), its clinical significance was not fully appreciated at that time. Therefore, based on these findings, a strategy of close imaging surveillance was chosen over preemptive invasive treatment. For context, no vascular abnormalities had been observed at these sites on the initial preoperative DSA performed on hospital day 3.
Chronological imaging of punctate hyperdensity appearance, aneurysm formation (lesion A), and disappearance of the hyperdensity (lesion B).
Top row (CT): Noncontrast-enhanced CT series from hospital day 5 to 45. Arrowheads indicate a punctate hyperdense lesion located within the Sylvian fissure (lesion A), which later corresponds to hemorrhage and surgical management by trapping. Arrows show another hyperdense lesion on the occipital cortical surface (lesion B) that gradually resolved over time.
Middle row (CTA): CTA series showing normal vasculature evolving into aneurysm formation and eventual aneurysm trapping at the site of lesion A (arrowhead).
Bottom row (MRA): MRA series demonstrating initial arterial narrowing, subsequent aneurysm formation, and final artifact from the trapping clip at the location of lesion A (arrowhead). The rightmost image is obscured by the clip artifact.
CT: computed tomography; CTA: computed tomography angiography; MRA: magnetic resonance angiography
Multimodal imaging of lesion A at the time of punctate hyperdensity appearance.
(A) Magnified view of a noncontrast-enhanced CT on hospital day 15, showing the punctate hyperdense lesion in the Sylvian fissure (lesion A, arrowhead).
(B-D) Corresponding magnetic resonance images performed on the same day. (B) Diffusion-weighted imaging, (C) fluid-attenuated inversion recovery, and (D) susceptibility-weighted imaging. No clear aneurysm formation or distinct signal changes corresponding to lesion A were observed.
CT: computed tomography
On hospital day 18, the patient suddenly developed aphasia and right hemiparesis. Noncontrast-enhanced CT revealed a new intracerebral hemorrhage, and CTA revealed a newly formed aneurysm and associated bleeding at the site of lesion A (Fig. 2, middle row). Emergent hematoma evacuation and decompressive craniectomy were performed. The aneurysm was treated by trapping; the proximal parent artery was occluded with a surgical clip, and the distal parent artery was coagulated and transected. Postoperative transthoracic echocardiography revealed that the filamentous echogenic structure previously observed on the mitral valve had disappeared.
The patient was extubated on hospital day 22, and the patient's condition gradually improved with rehabilitation. Oral intake was resumed on hospital day 28. Follow-up CTA on hospital day 45 revealed no new aneurysms. Notably, lesion B observed on hospital day 15 remained asymptomatic and gradually resolved on subsequent imaging (Fig. 2, top row). The patient's infective endocarditis, including severe mitral regurgitation, was managed by the cardiology team. Although valve surgery was considered for the future, no signs of heart failure were observed, and rehabilitation was prioritized. Streptococcal bacteremia was treated with a 4-week course of intravenous ampicillin, after which the patient remained afebrile and exhibited no elevation in inflammatory markers, indicating successful infection control. On hospital day 46, the patient was transferred to a rehabilitation hospital, with a modified Rankin scale (mRS) score of 3. The patient regained independent ambulation using a short-leg brace, and the patient's mRS score improved to 2 at the 3-month follow-up.
This case presents a rare but clinically important phenomenon: the appearance of punctate hyperdense lesions on noncontrast-enhanced CT before angiographic visualization and rupture of a mycotic aneurysm. These lesions most likely represented early septic embolic occlusion of the distal cerebral arteries, followed by vessel wall weakening and subsequent aneurysmal dilation.2,3) Postrupture echocardiography revealed the disappearance of the filamentous echogenic structure previously observed on the mitral valve, supporting the hypothesis that the punctate hyperdense lesions originated from septic emboli derived from valvular vegetations.
Radiologically, although the location and morphology differ, this finding bears resemblance to the well-known "hyperdense MCA sign" typically associated with acute ischemic stroke.4-6) In this context, the hyperdensity reflects thrombotic material occluding the MCA trunk, which is composed primarily of fibrin and platelets.6) In contrast, the hyperdense lesions in our case were presumed to represent septic emboli consisting of bacterial vegetation and inflammatory debris originating from infective endocarditis.2) Thus, although both findings indicate intravascular obstruction, the underlying pathophysiology differs: thromboembolism in stroke versus septic embolism in mycotic aneurysms.2,7)
This distinction is clinically relevant. Thrombotic occlusions in ischemic stroke primarily result in hypoperfusion and tissue infarction, whereas septic emboli not only occlude vessels but also incite local infection and inflammation, predisposing them to vessel wall necrosis and aneurysm formation.2)
It is important to consider the differential diagnosis for such punctate hyperdense lesions, which could include microhemorrhages, calcified emboli, or small thrombotic emboli. In our patient, however, the rapid evolution of one lesion into a mycotic aneurysm, combined with the context of active infective endocarditis and the subsequent disappearance of valvular vegetation on postrupture echocardiography, strongly supports a septic embolic origin. The absence of distinct signal changes on MRI, particularly, susceptibility-weighted imaging, which is sensitive to hemorrhage and calcium, makes these alternatives less likely, although they cannot be definitively excluded without histopathological confirmation. The definitive nature of these lesions is a subject for future pathological studies.
Histopathological studies have shown that septic emboli initiate intense inflammation extending into the muscularis media and adventitia, leading to the destruction of the internal elastic lamina and rapid aneurysmal dilatation. Molinari et al.2) observed aneurysm formation as early as 24 hrs after embolism formation in a canine model using virulent Staphylococcus strains without antibiotic therapy, mirroring the rapid clinical course observed in our patient.
In our case, 2 punctate hyperdense lesions were observed on noncontrast-enhanced CT; however, only one (lesion A) progressed to aneurysm formation and rupture. The other (lesion B) resolved spontaneously, with no clinical symptoms. This suggests that not all hyperdense lesions carry an equal risk, and the natural history of septic emboli may vary depending on the embolus size, bacterial virulence, host immune response, and integrity of the affected vessel wall.2,8)
Another important consideration is that these punctate hyperdense lesions were detectable on noncontrast-enhanced CT, which is a widely available and noninvasive imaging modality. Some patients with infective endocarditis may have impaired renal function, which can limit the feasibility of repeated contrast-enhanced imaging.9) If such early changes can be identified on routine CT, this approach provides a practical and low-risk method for early screening and longitudinal monitoring of potentially unstable vascular lesions in high-risk populations.
To the best of our knowledge, this is the first case report to describe such CT findings before aneurysm development and rupture in a patient with infective endocarditis. Most previously published reports on mycotic aneurysms have focused on diagnosis and treatment only after rupture or the appearance of clear angiographic findings.1-3,8,10) This reflects the typical clinical course, in which diagnosis is often made retrospectively after hemorrhage or based on vascular imaging prompted by acute neurological deterioration.1,10) Recognizing earlier radiological changes-before aneurysm formation becomes angiographically visible-could expand the diagnostic window and allow preventive monitoring or timely intervention.
However, this report is based on the findings of a single case, and it remains uncertain whether this punctate hyperdensity is a universal early marker for mycotic aneurysm formation. The sensitivity and specificity of this finding are unknown. Therefore, our observation should be considered a hypothesis at this stage. Further multi-center case series or prospective cohort studies are necessary to validate its clinical utility and establish a definitive link.
With these limitations in mind, recognition of punctate hyperdense lesions on noncontrast-enhanced CT as a potential early marker of mycotic aneurysm formation may hold substantial clinical value. In patients with infective endocarditis, regardless of the presence or absence of neurological symptoms, the appearance of such lesions could be a crucial alert, warranting close serial imaging and careful consideration of preemptive intervention to prevent devastating hemorrhagic complications.
All authors have no conflicts of interest.
We obtained informed consent for publication from the patient.
