Unveiling the Complexity: A Rare Case of Subarachnoid Hemorrhage Caused by a Ruptured Distal Anterior Communicating Artery Aneurysm and Its Surgical and Anesthetic Management

ABSTRACT

Distal anterior communicating artery aneurysms require complex surgical exposure, often necessitating extensive dissection or frontal lobe manipulation, increasing neurological risks. When endovascular therapy is unfeasible, ruptured distal anterior communicating artery aneurysms require meticulous microsurgical clipping and coordinated anesthetic care to optimize outcomes.

1. Introduction

Intracranial aneurysms, though relatively rare, affect approximately 3% of the general population [1]. Many of these aneurysms are found at the junction of the anterior cerebral artery (ACA) and the anterior communicating artery (AComA) [2]. However, aneurysms located in the distal AComA are exceptionally uncommon [3]. Ruptured aneurysms lead to subarachnoid hemorrhage, which in turn increases the morbidity and mortality of the patient [4]. Their challenging and complex location makes them particularly difficult to manage, with the potential for significant risks, including catastrophic bleeding and the need for extensive brain tissue removal. These factors necessitate a high level of coordination between the neurosurgeon and anesthesiologist throughout the management process. This case report explores the intricate aspects of treating a patient with a ruptured distal AComA aneurysm and subsequent subarachnoid hemorrhage, with a focus on the role of cerebral autoregulation and careful perioperative management. The report underscores the need for meticulous attention to maintaining cerebral perfusion, the delicate balance of hemodynamics, and the critical collaboration between the surgical and anesthesiology teams to ensure optimal patient outcomes in these high‐risk cases.

2. Case Presentation

A 46‐year‐old woman with a 5‐year history of hypertension (on amlodipine 5 mg/day) presented to the emergency department with a 3‐day history of severe fronto‐parietal headache, dizziness, and progressive blurring of vision. The headache was refractory to oral analgesics. She denied loss of consciousness, vomiting, fever, or trauma. On examination, her blood pressure was elevated (170/95 mmHg), but other vitals were stable.

Neurological assessment revealed:

• –Cranial nerves: Bilateral pupillary symmetry with normal light reflexes; no optic atrophy, but mild bitemporal hemianopia suggestive of chiasmatic compression. Apart from that, all other cranial nerve examination tests were within normal limits.
• –Motor/sensory systems: No focal weakness, but subtle left‐sided pronator drift on motor examination.
• –Cognitive screening: Mild executive dysfunction (difficulty with serial‐7 subtractions) and short‐term memory deficits, raising concern for anterior cerebral artery (ACA) territory involvement.

3. Methods (Differential Diagnosis, Investigations, and Treatment)

NCCT (Non‐Contrast Computed Tomography) head confirmed subarachnoid hemorrhage (Fisher grade 4), and cerebral angiography identified a ruptured 4 × 8 mm saccular aneurysm at the distal AComA (World Federation of Neurosurgical Societies‐WFNS grade 2) (Figure 1). Other collateral circulation in the brain appeared to be grossly within normal limits. Given the aneurysm's location and potential mass effect on adjacent structures (optic chiasma, ACA branches), microsurgical clipping was preferred over endovascular coiling due to anatomical constraints. The patient was optimized in the ICU and scheduled for urgent surgical intervention.

FIGURE 1.

CT Angiogram showing Distal Anterior Communicating Artery Aneurysm.

This detailed neurological evaluation underscores the distal AComA aneurysm's potential to cause subtle yet significant deficits, guiding perioperative management and prognostication. Her routine laboratory investigations were within normal limits. Written informed consent was taken, and an adequate quantity of packed red blood cells was kept ready. The patient party was counseled regarding the condition of the patient. The possible risk of major bleeding and frontal lobectomy, which may lead to postoperative neurological deficits that included seizures, behavioral changes, and executive disturbances, was well explained to the patient. With all necessary preoperative preparations, the patient was shifted inside the operating room (OR) for aneurysmal clipping. Inside the OR, American Society of Anesthesiologists (ASA) II monitoring, which included electrocardiography, non‐invasive blood pressure, pulse oximetry, temperature, and urine output monitoring, was attached. Two 16‐gauge intravenous (IV) cannulae were attached to the right upper limb and left lower limb. A 16 French central venous catheter with 3 ports was inserted into the right subclavian vein via the Seldinger technique with the aid of ultrasound. A 20‐gauge IV cannula was also inserted into the left radial artery, and invasive blood pressure monitoring was done. Surgery was planned to be performed in a supine position. With standard induction and intubation technique, the airway was secured with a 7.5 mm endotracheal tube. Normal saline was attached as an IV drip. Maintenance of anesthesia with Total Intravenous Anesthesia (TIVA) technique using propofol infusion was adopted in order to maintain cerebral autoregulation.

Given the distal AComA aneurysm's deep and complex location, a right frontal craniotomy with partial frontal lobectomy (2.5 × 1.5 cm) was performed to optimize exposure while minimizing excessive retraction (Figure 2).

FIGURE 2.

Arrow showing cut section of portion of Frontal lobe.

Circle of Willis was properly visualized (Figure 3). A pterional approach was considered but deemed insufficient due to the aneurysm's superior and posterior projection. Dural opening was tailored to facilitate interhemispheric dissection, and CSF drainage via lumbar puncture was utilized.

FIGURE 3.

Brain Dissection involving Circle of Willis to locate the site of aneurysm.

The aneurysm was carefully dissected from surrounding perforators under high magnification. Given its broad neck, a fenestrated clip (Sugita type) was selected to preserve flow in the A2 segments while ensuring complete occlusion. Indocyanine green angiography confirmed exclusion of the aneurysm without compromise to adjacent vessels. No temporary clipping was required due to excellent visualization after meticulous arachnoid dissection. Hemostasis was achieved with fibrin‐thrombin sealant, and dural closure was reinforced to prevent CSF leakage.

Vitals were meticulously monitored throughout the surgery with special focus on blood pressure (BP), as cerebral perfusion and transmural pressure gradient of the aneurysm are dependent on mean arterial pressure. BP was kept in the range of 160–180 mmHg systolic and diastolic of 90–95 mmHg at the time of clipping. Temporary clipping before permanent clipping of the aneurysm was not done in this case, as the aneurysmal site was clearly visible after tissue dissection. Higher blood pressure was maintained with the administration of noradrenaline infusion via central line at the rate of 0.05–0.15 microgram/kg/min. There was no major bleeding throughout the surgery. Blood loss of around 500 mL was noted. Urine output was also adequate. The patient was shifted to the intensive care unit with noradrenaline infusion to keep BP above 170/90 mm of hg.

Postoperatively, the patient remained sedated and ventilated overnight, with serial transcranial Doppler (TCD) monitoring. There was no evidence of vasospasm (no significant velocity elevations detected) in TCD. Nimodipine (60 mg q4h) was continued prophylactically. Upon extubation, formal neuropsychological testing revealed mild executive dysfunction (deficits in verbal fluency and delayed recall), consistent with frontal lobe manipulation, which resolved.

4. Conclusion and Results (Outcome and Follow‐Up)

The patient was discharged without focal deficits. Three‐month NCCT and angiography confirmed no residual aneurysm or ischemia (Figure 4). Cognitive function normalized, and she resumed independent daily activities. This case highlights the importance of tailored surgical access, intraoperative adjuncts, and rigorous postoperative cognitive monitoring in distal AComA aneurysms.

FIGURE 4.

Normal CT Angiogram after 3 months follow‐up. It reveals no evidence of rebleeding, edema or infarction.

5. Discussion

Intracranial aneurysms, although relatively uncommon, are a significant cause of morbidity and mortality due to the potential for rupture and the resulting subarachnoid hemorrhage (SAH) [1]. The AComA is a common site for these aneurysms, and the majority of them are located at the junction of the ACA and the AComA [2]. However, aneurysms located at the distal end of the AComA are exceedingly rare and present unique challenges due to their complex location, small size, and difficult access, especially when rupture leads to SAH. While proximal AComA aneurysms are well documented, distal variants pose unique challenges due to their deep location and proximity to critical perforators supplying the hypothalamus and optic apparatus.

5.1. Clinical Implications of Distal AComA Aneurysms

The clinical manifestations of a ruptured distal AComA aneurysm typically include severe headache, dizziness, visual disturbances, and subtle executive dysfunction as seen in the presented case. The non‐specific nature of the symptoms can delay diagnosis, making it crucial to maintain a high index of suspicion, particularly in patients with risk factors such as systemic hypertension [5]. The presentation of a headache, especially in the context of a patient with uncontrolled hypertension, should prompt consideration of an intracranial aneurysm, particularly in cases where traditional pain relief methods fail to manage the headache. Notably, the absence of classic third nerve palsy (more typical of posterior communicating artery aneurysms) underscores the need for heightened suspicion when evaluating atypical headache syndromes.

In our case, the patient's elevated blood pressure of 170/95 mmHg was consistent with her long‐standing history of systemic hypertension. Hypertension has been identified as a risk factor for the development and rupture of intracranial aneurysms, and this risk is further compounded when aneurysms are located in more challenging anatomical locations like the distal AComA [6].

5.2. Challenges in Surgical and Anesthetic Management

Surgical management of distal AComA aneurysms is technically challenging, especially when the aneurysm is ruptured. The decision to pursue microsurgical clipping via frontal lobectomy was guided by the aneurysm's superior projection and adherence to the A2 segments, which limited endovascular options. Furthermore, the decision for surgical clipping was also supported by the evidence shown by the systematic review and meta‐analysis done by Jiang et al. [7] Surgical clipping, which involves placing a clip across the neck of the aneurysm to prevent further bleeding, is the preferred treatment option for ruptured aneurysms in many cases [8]. However, in cases of distal AComA aneurysms, these procedures may require complex retraction, brain tissue removal, and meticulous dissection, which increase the risk of perioperative complications, including major bleeding, neurological deficits, and even brain herniation.

In our case, the use of frontal lobectomy to access the aneurysm highlights one of the potential complications of surgery at such a location [9]. While lobectomy allows access, it carries the risk of postoperative neurological deficits, including memory loss, seizures, and motor deficits, especially if significant brain tissue is removed. Furthermore, a study by Molyneux et al. [10] emphasized that even in cases where surgical clipping is successful, the risk of neurological impairment is considerable, especially when dealing with complex aneurysms.

The perioperative management of cerebral autoregulation is crucial to prevent cerebral ischemia or further hemorrhage [11]. In our case, anesthesia was maintained with total intravenous anesthesia (TIVA) using propofol, which helps preserve cerebral autoregulation. Propofol has neuroprotective properties and is preferred in neurosurgical patients due to its ability to maintain stable hemodynamics and reduce cerebral metabolic demand [12]. Maintaining a higher blood pressure intraoperatively (160–180 mmHg systolic) is essential in ensuring adequate cerebral perfusion pressure, which is critical in the context of a ruptured aneurysm.

Moreover, noradrenaline infusion was used to support mean arterial pressure (MAP), ensuring that the aneurysm site remained well perfused. This is particularly important because the transmural pressure gradient across the aneurysm wall is closely linked to the MAP. Suboptimal blood pressure could lead to ischemic damage, while excessive blood pressure could increase the risk of re‐rupture.

5.3. Postoperative Considerations and Outcomes

The postoperative course (TCD) in these cases is often unpredictable, and careful monitoring with tools like Transcranial Doppler is essential to prevent complications such as vasospasm, rebleeding, or delayed neurological deficits. Vasospasm, which occurs due to the breakdown of blood in the subarachnoid space, is a significant risk after SAH, particularly in the first 7–14 days post‐rupture [13]. Nimodipine, a calcium channel blocker, is commonly used in the postoperative period to reduce the risk of vasospasm, as was done in our case.

The patient's hemodynamic stability postoperatively, along with the absence of significant complications such as rebleeding or ischemia, was a positive outcome. There were no postoperative neurological deficits, including memory loss, seizures, and motor deficits. Neuropsychological assessment revealed no abnormality in executive function, memory, etc. after 6 weeks of surgery. CT Angiogram done after 3 months of surgery did not reveal any evidence of rebleeding, edema, or infarction. Additionally, early extubation and smooth transition to the high‐dependency unit suggest that the surgical and anesthetic management strategies were successful. However, ongoing surveillance for delayed neurological deficits and vasospasm remains essential during the recovery period.

6. Conclusions

The key finding in the management of a ruptured distal anterior communicating artery aneurysm is that it requires a highly coordinated, multidisciplinary approach to address the complex challenges posed by its location and associated risks, such as major bleeding, frontal lobectomy, and neurological impairment. This case underscores that distal AComA aneurysms demand tailored management. Surgical clipping, despite its challenges, remains definitive when anatomy precludes endovascular therapy. Future innovations in endovascular devices and hybrid techniques may expand options, but meticulous microsurgery and hemodynamic optimization are currently pivotal for success.

Author Contributions

Rahul Kumar Chaudhary: conceptualization, writing – original draft, writing – review and editing. Deepak Poudel: conceptualization. Lalit Kumar Rajbanshi: data curation. Sajjad Ahmed Khan: conceptualization. Sunil Munakomi: data curation.

Consent

Written informed consent was obtained from the patient to publish this report in accordance with the journal's patient consent policy.

Conflicts of Interest

The authors declare no conflicts of interest.

Chaudhary R. K., Poudel D., Rajbanshi L. K., Khan S. A., and Munakomi S., “Unveiling the Complexity: A Rare Case of Subarachnoid Hemorrhage Caused by a Ruptured Distal Anterior Communicating Artery Aneurysm and Its Surgical and Anesthetic Management,” Clinical Case Reports 13, no. 10 (2025): e70953, 10.1002/ccr3.70953.

Data Availability Statement

Data will be provided by the corresponding author upon reasonable request. Images are uploaded in the separate files.