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CC BY-NC-ND 4.0 · Asian J Neurosurg
DOI: 10.1055/s-0045-1811244
Case Report

Anterior Cerebral Artery Dissection Leading to Severe Subarachnoid Hemorrhage in a Post-Pandemic COVID-19 Patient: A Case Report and a Call for Continued Vigilance

Sho Hanai 
1   Department of Neurosurgery, Tsukuba Memorial Hospital, Tsukuba, Ibaraki, Japan
,
Kiyoyuki Yanaka
1   Department of Neurosurgery, Tsukuba Memorial Hospital, Tsukuba, Ibaraki, Japan
,
Minami Saura
1   Department of Neurosurgery, Tsukuba Memorial Hospital, Tsukuba, Ibaraki, Japan
,
Toshihide Takahashi 
1   Department of Neurosurgery, Tsukuba Memorial Hospital, Tsukuba, Ibaraki, Japan
,
Hitoshi Aiyama
1   Department of Neurosurgery, Tsukuba Memorial Hospital, Tsukuba, Ibaraki, Japan
,
Aiki Marushima
2   Department of Neurosurgery, Institute of Medicine, University of Tsukuba, Tsukuba, Ibaraki, Japan
,
Eiichi Ishikawa
2   Department of Neurosurgery, Institute of Medicine, University of Tsukuba, Tsukuba, Ibaraki, Japan
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Funding None.
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Abstract

Coronavirus disease 2019 (COVID-19) can lead to systemic vascular complications, such as endothelial damage and hypercoagulability. Although COVID-19-associated nonaneurysmal subarachnoid hemorrhage (SAH) has been reported, cases involving anterior cerebral artery (ACA) dissection, particularly in the A1 segment, are extremely rare. A 57-year-old man with a recent COVID-19 infection was brought to the emergency department in an unconscious state. Imaging revealed diffuse SAH, and computed tomography angiography identified dissection of the right ACA A1 segment. Urgent surgical intervention with clipping of the dissected segment was performed. Although the patient initially stabilized postoperatively, he subsequently developed severe cerebral infarction, leading to progressive neurological decline. Despite intensive care, the patient succumbed to these complications 10 days after the initial presentation. Although the overall threat of COVID-19 has diminished, vigilance is still required because its vascular complications remain potentially fatal. COVID-19-associated SAH may have a higher mortality rate due to mechanisms distinct from saccular aneurysm rupture, such as arterial dissection and systemic effects. Dissecting an aneurysm of the A1 segment of the ACA is an extremely rare but serious complication, and its management remains challenging. Further studies are required to understand and mitigate COVID-19-related vascular pathologies.


 

Keywords

COVID-19 - subarachnoid hemorrhage - dissection - anterior cerebral artery - clipping

Introduction

Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), primarily affects the respiratory system and induces systemic complications, including vascular endothelial damage, hypercoagulability, and inflammatory cytokine storms.[1] [2] These mechanisms can predispose individuals to various vascular pathologies, such as arterial dissection, thrombosis, and hemorrhagic events.[2] [3] One of the serious neurological complications of COVID-19 is subarachnoid hemorrhage (SAH). However, SAH remains relatively rare, occurring in approximately 0.1% of patients with COVID-19.[4] Although cases of SAH without saccular aneurysm rupture have been reported in association with COVID-19,[5] instances involving cerebral artery dissection (CAD), particularly in the anterior cerebral artery (ACA), are exceptionally rare.[6] [7] [8]

The pathophysiology of SARS-CoV-2 infection suggests that it triggers systemic endothelialitis through angiotensin-converting enzyme 2 (ACE2) receptor-mediated mechanisms, contributing to hypercoagulability, vascular inflammation, and potential vessel wall injury.[2] [3] Collectively, these factors increase the susceptibility to arterial dissections. Spontaneous dissections of the ACA, particularly in the A1 segment, are exceedingly rare but carry a catastrophic prognosis because of the risk of rebleeding and ischemic complications.

Although the global rate of COVID-19 infections is reportedly declining,[9] [10] severe vascular complications can still occur, necessitating continuous clinical vigilance. This case describes an instance of SAH resulting from A1 segment dissection in a patient with COVID-19, emphasizing the lingering risks the infection. Highlighting such rare and severe outcomes is essential for improving our understanding of postinfectious vascular complications and refining management strategies for high-risk patients.


 

Case Description

A 57-year-old hypertensive man, recovering from COVID-19 at home for 5 days, was found unconscious and transported to our hospital. The patient's Glasgow Coma Scale score was 4, with near-apneic respiration. The initial blood tests revealed leukocytosis (23,490/μL), elevated fibrinogen degradation products (49.2 μg/mL), and mild C-reactive protein elevation (0.07 mg/dL). Computed tomography (CT) revealed diffuse SAH with intraventricular hemorrhage and acute hydrocephalus ([Fig. 1A] and [B]). Ventricular drainage was promptly performed after the initiation of intubation and mechanical ventilation. On the next day, the hydrocephalus improved, and a new low-density area was observed in the right frontal lobe ([Fig. 1C] and [D]). Hemorrhage and infarction coincided, suggesting that the source of the hemorrhage was a dissecting lesion rather than a ruptured saccular aneurysm. Subsequent three-dimensional CT angiography revealed a slight bulging in the right ACA A1 segment ([Fig. 2A]). Digital subtraction angiography revealed a “string sign” in the same segment ([Fig. 2B]), suggesting ACA dissection as the source of the hemorrhage. Direct surgical intervention via right frontotemporal craniotomy was performed. The dissected vessel wall was thin with adherent hematoma, suggesting a pseudoaneurysm. The vascular wall on the opposite side of the lesion appeared normal. The A1 segment was carefully dissected distally; however, premature rupture occurred, confirming this area as the source of the hemorrhage ([Fig. 3]). Initially, we planned to perform wrapping to control the bleeding site while maintaining blood flow; however, we switched to clipping because the hematoma was firmly attached to the vessel wall, and wrapping could have narrowed the lumen. Although the vessel wall was thin, we were able to obliterate the lesion with a clip while maintaining the blood flow, which was confirmed by a Doppler flowmeter.

Zoom
Fig. 1 Computed tomogram on admission (A) Showing diffuse subarachnoid hemorrhage and no low-density area in the frontal lobe and (B) hydrocephalus. Computed tomogram on the next day (C) showing a new low-density area in the right frontal lobe (arrow) and (D) improved hydrocephalus.
Zoom
Fig. 2 Three-dimensional computed tomographic angiogram (A) showing a small bulge in the right A1 segment (arrow). Digital subtraction angiogram (B) showing vascular wall irregularities in the right A1 segment (arrowhead).
Zoom
Fig. 3 Intraoperative photograph after temporary clip placement for hemostasis immediately after premature rupture. Pseudoaneurysm is observed in the distal part of the clip (arrow).

On postoperative day 4, the patient developed signs of diabetes insipidus, for which vasopressin was administered. A CT scan showed a new infarct in the right frontal lobe, likely related to delayed cerebral ischemia (DCI), with worsening cerebral edema ([Fig. 4A]). Despite intensified osmotherapy, there was no significant improvement. Respiratory status also deteriorated progressively. The patient remained comatose, and on the eighth day after symptom onset, signs of cerebral deterioration were observed. On postoperative day 10, the patient died. An autopsy was not performed due to the family's wishes; however, postmortem CT imaging revealed no additional intracranial hemorrhage but demonstrated extensive cerebral edema and a large pleural effusion in the left lung ([Fig. 4B]).

Zoom
Fig. 4 Computed tomogram performed on day 4 (A) showing the appearance of a new low-density area in the right frontal lobe and significant brain swelling. Postmortem computed tomogram on day 10 (B) showing no new rebleeding, and indicating continued significant brain swelling.

 

Discussion

This case highlights the potential for ACA dissection and subsequent SAH in patients with COVID-19. Although CAD is inherently rare, particularly in the A1 segment, systemic endothelial dysfunction induced by SARS-CoV-2 can increase the vulnerability of cerebral arteries. The virus binds to ACE2 receptors expressed on endothelial cells, resulting in endothelial dysfunction, apoptosis of vascular smooth muscle cells, and weakening of arterial structural integrity.[2] [3] [11] [12] These pathological changes create a favorable environment for arterial dissection, particularly under conditions of hemodynamic stress and inflammatory insult.

Our patient, who was polymerase chain reaction-positive for SARS-CoV-2 and in the recovery phase at home, experienced a catastrophic hemorrhagic event without preceding trauma or known vascular anomalies. Although histopathological confirmation of viral involvement was not possible due to the family's refusal of autopsy, the temporal proximity of infection and the absence of alternative clear etiologies raise the possibility of an indirect relationship. Postmortem CT (“autopsy imaging”) demonstrated no evidence of rebleeding, but revealed diffuse cerebral edema and a large left-sided pleural effusion, the latter potentially indicating a systemic inflammatory response, cardiac dysfunction, or altered capillary permeability in the context of severe neurological and respiratory deterioration, despite pleural effusion being uncommon in typical COVID-19 pneumonia. Importantly, the patient had preexisting hypertension and was 57 years old—both recognized risk factors for arterial dissection and vessel wall fragility. These factors likely acted synergistically with the proinflammatory and prothrombotic state associated with COVID-19, potentially predisposing the patient to ACA dissection.

Following surgical intervention via craniotomy and clipping, the clinical course was marked by rapid deterioration. On postoperative day 4, the patient developed diabetes insipidus and a new infarct in the right frontal lobe, likely due to DCI. Despite vasopressin therapy and intensified osmotherapy, cerebral edema progressed, and the patient ultimately died on day 10. This sequence of events illustrates the difficulty of managing COVID-19 patients with SAH and the complex interplay between systemic complications and cerebrovascular injury.

Our case of ACA A1 segment dissection is a rare presentation within the spectrum of COVID-19-related CADs. Most reported cases predominantly involve the internal carotid artery and vertebral artery.[13] [14] While the anatomical location in our patient is unusual, the clinical presentation and proposed underlying mechanisms share commonalities with the existing literature.

Patients with COVID-19-related dissections exhibit diverse clinical presentations, from headache to severe neurological deficits, including SAH, aligning with our patient's critical presentation. Furthermore, the hypothesized pathophysiology, involving endothelial dysfunction, hypercoagulability, and inflammatory vasculopathy driven by SARS-CoV-2 infection, is consistent across reported cases and our own. The temporal association, with dissections often occurring days to weeks postinfection, was also observed in our patient.

This case, despite its rare anatomical site, underscores the broad impact of COVID-19 on the cerebrovasculature. It reinforces the need for continued vigilance among clinicians, recognizing that any cerebral artery may be vulnerable to dissection in patients presenting with acute neurological symptoms following COVID-19 infection.

Although ruptured saccular aneurysms account for most SAH cases,[15] SAH in patients with COVID-19 has been noted to have a higher mortality rate because of the complexity of surgical interventions and systemic complications.[5] Dissecting aneurysms, particularly those characterized by a single pseudolumen entrance, are associated with a greater risk of rebleeding than those with multiple points of entry and exit.[16] Conservative management may be appropriate in select cases; however, high-risk scenarios, such as pseudoaneurysms with imminent rupture potential, necessitate prompt surgical intervention.[17] Management strategies should involve thorough diagnostic imaging using CT angiography and digital subtraction angiography to confirm the presence of dissection and to evaluate the extent of vascular damage. Endovascular approaches, including stent-assisted coiling and flow diversion, are preferred in patients with favorable vascular anatomy, whereas direct surgical clipping may be necessary when endovascular access is limited or ineffective. In this case, we opted for craniotomy over endovascular treatment for the following reasons: First, the suspected bleeding site was located in an atypical region, and the findings from imaging studies were subtle. This finding raises the possibility of misidentifying the true source of the hemorrhage. Therefore, direct visualization during surgery is crucial for accurately pinpointing the bleeding origin and ensuring appropriate intervention. Second, COVID-19 infection can induce a hypercoagulable state, and antithrombotic therapy is vital for preventing DCI after SAH. In this context, the precise identification of the bleeding source is essential for subsequent antithrombotic management. Consequently, craniotomy was performed to achieve definitive hemostasis and optimize postoperative care.

Postoperative care should emphasize DCI prevention, which is often achieved through calcium antagonist administration and meticulous fluid management. However, hyperdynamic therapy although effective in non-COVID-19 cases, may intensify respiratory complications in infected patients. Therefore, balancing DCI prevention with the management of systemic COVID-19 complications is essential. Furthermore, monitoring for thrombocytopenia and cytokine storm manifestations should be an integral part of the treatment strategy, including the use of steroids.[13]

Although the global pandemic is waning due to vaccination and herd immunity, this case serves as a stark reminder of the severe and often unpredictable complications COVID-19 can present. In this case, a direct histopathological confirmation of viral involvement in the vessel wall was not possible, as an autopsy could not be performed due to the family's wishes. While this limitation prevents definitive evidence of causality, the absence of other underlying causes—such as trauma, preexisting vascular malformation, or uncontrolled chronic hypertension—combined with the timing of the COVID-19 infection, supports a potential association between the systemic effects of SARS-CoV-2 and the development of arterial dissection.

Similar cerebrovascular complications have been increasingly reported in association with COVID-19, and our case adds to this emerging body of literature. Furthermore, dissection of the A1 segment of the ACA remains an extremely rare event regardless of COVID-19 status, and its presentation with massive SAH poses significant diagnostic and therapeutic challenges.

The documentation of such cases remains important to raise clinical awareness, particularly in the current phase of declining pandemic activity, where postinfectious vascular complications may still pose significant risks.


 

Conclusion

This case serves as a critical reminder that even as the pandemic appears to wane, the potential for severe and unexpected complications from COVID-19 remains a serious concern. This case highlights that significant cerebrovascular events, such as ACA dissection leading to SAH, can still occur in the aftermath of COVID-19. Therefore, clinicians should maintain high levels of vigilance for postinfectious vascular sequelae. Continued research and clinical awareness are essential for improving the identification, management, and ultimately outcomes of these rare but devastating complications.


 

 

Conflict of Interest

None declared.

Acknowledgment

The authors would like to thank Enago for the English review and editing.

Authors' Contributions

S.H. drafted this case report. K.Y. made the design of this case report and revised the report. M.S., T.T., and H.A. treated this patient and checked this report. A.M. and E.I. revised the report and advised the manuscript. All authors reviewed the final version of the case report.


Ethical Approval

This case report complies with the Declaration of Helsinki.



Address for correspondence

Eiichi Ishikawa, MD, PhD
Department of Neurosurgery, Institute of Medicine, University of Tsukuba
1-1-1 Tennodai, Tsukuba, Ibaraki 305-8575
Japan   

Publikationsverlauf

Artikel online veröffentlicht:
08. September 2025

© 2025. Asian Congress of Neurological Surgeons. This is an open access article published by Thieme under the terms of the Creative Commons Attribution-NonDerivative-NonCommercial License, permitting copying and reproduction so long as the original work is given appropriate credit. Contents may not be used for commercial purposes, or adapted, remixed, transformed or built upon. (https://creativecommons.org/licenses/by-nc-nd/4.0/)

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Zoom
Fig. 1 Computed tomogram on admission (A) Showing diffuse subarachnoid hemorrhage and no low-density area in the frontal lobe and (B) hydrocephalus. Computed tomogram on the next day (C) showing a new low-density area in the right frontal lobe (arrow) and (D) improved hydrocephalus.
Zoom
Fig. 2 Three-dimensional computed tomographic angiogram (A) showing a small bulge in the right A1 segment (arrow). Digital subtraction angiogram (B) showing vascular wall irregularities in the right A1 segment (arrowhead).
Zoom
Fig. 3 Intraoperative photograph after temporary clip placement for hemostasis immediately after premature rupture. Pseudoaneurysm is observed in the distal part of the clip (arrow).
Zoom
Fig. 4 Computed tomogram performed on day 4 (A) showing the appearance of a new low-density area in the right frontal lobe and significant brain swelling. Postmortem computed tomogram on day 10 (B) showing no new rebleeding, and indicating continued significant brain swelling.