Spontaneous recanalization after acute common carotid artery occlusion: a case report

Abstract

Introduction and importance:

Albeit rare, spontaneous recanalization after common carotid artery (CCA) occlusion is an important medical phenomenon, as it can lead to increased blood flow to the brain tissue, thereby improving cerebral perfusion. However, it also increases the risk of reperfusion injury and distal cerebral embolism.

Case presentation:

The patient was a 54-year-old man who presented with sudden right-sided limb weakness and speech impairment. Emergency computed tomography angiography (CTA) showed complete occlusion of the left CCA and internal carotid artery. CTA on day 1 indicated moderate-to-severe stenosis of the left CCA. Extensive low-density areas and hemorrhagic transformations were observed in the territory supplied by the left middle cerebral artery. Follow-up cranial CT on day 15 showed obvious hemorrhagic transformation following infarction. High-resolution magnetic resonance imaging of the carotid arteries on day 25 revealed no significant stenosis. The patient was given medications to improve circulation and antiplatelet aggregation, as well as lipid-lowering therapy. Follow-up cranial CT on day 37 showed significant absorption of the cerebral hemorrhage.

Clinical discussion:

This case report presents a rare spontaneous recanalization of acute CCA occlusion without thrombolysis or thrombectomy. Neurological deficits resolved completely following the delayed recanalization, challenging conventional understanding of intervention timelines. The case highlights potential thrombolytic-independent recanalization mechanisms.

Conclusion:

These findings raise questions about the optimal management approach in select common carotid artery occlusion cases and emphasize the importance of individualized treatment decisions based on real-time vascular imaging assessment. Early and rapid spontaneous recanalization can lead to a reperfusion injury; close monitoring and follow-up assessments are essential.

Introduction

Common carotid artery occlusion (CCAO) can lead to extensive cerebral infarction with a high risk of hemorrhagic transformation and malignant brain edema, posing great risks to patient outcomes. Spontaneous recanalization, which is the natural restoration of blood flow in an occluded artery, without surgical or thrombolytic intervention, is rarely reported in CCAO cases, although it is an important medical phenomenon. Spontaneous recanalization after CCAO can lead to increased blood flow to the brain tissue, thereby improving cerebral perfusion. However, it also increases the risk of reperfusion injury and distal cerebral embolism due to dislodgment of the emboli[1]. Our understanding of the natural history, incidence, and clinical characteristics of spontaneous recanalization after CCAO remains insufficient. Here, we report a case of spontaneous recanalization with hemorrhagic transformation in a patient with acute CCAO and analyze the clinical features and mechanisms underlying spontaneous recanalization.

HIGHLIGHTS

• This case report details rare spontaneous recanalization of acute common carotid artery occlusion.

• It shows complete neurological recovery after delayed recanalization.

• Findings stress the necessity of individualized treatment based on real-time imaging.

• It highlights vigilance against reperfusion injury after spontaneous recanalization.

Case presentation

Chief complaints

The patient was a 54-year-old man who presented to a local hospital after experiencing right-sided limb weakness and speech impairment.

History of present illness

On day 1 (day of admission), at approximately 6 AM, the patient suddenly experienced weakness in his right limbs and was unable to lift them, which was accompanied by speech difficulties. He was transferred to our emergency department at approximately 9 PM on day 1.

History of past illness

The patient had no history of hypertension, diabetes, coronary heart disease, or atrial fibrillation.

Personal and family history

He had a smoking history of more than 20 pack-years and occasional alcohol use.

Physical examination upon admission

Upon admission, physical examination revealed drowsiness, mixed aphasia, a shallow right nasolabial fold, muscle strength of 2/5 in the right upper limb, muscle strength of 3/5 in the right lower limb, muscle strength of 4/5 in the left limb, and a positive Babinski sign on the right side; no other neurological abnormalities were observed. The National Institutes of Health Stroke Scale score was 11.

Laboratory examinations

Laboratory test results showed elevated levels of C-reactive protein (24.4 mg/L; reference range, 0–5 mg/L) and B-type natriuretic peptide (227.0 pg/mL; reference range, 0–125 pg/mL). No abnormalities in the levels of protein S, protein C, electrolytes, cholesterol, alpha-fetoprotein, carcinoembryonic antigen, or carbohydrate antigen 19-9 were noted. Antithrombin III activity, coagulation function test results, liver and kidney function test findings, and urinalysis values were all normal.

Imaging examinations

Cranial computed tomography, which was performed at approximately 7 AM on day 1, revealed a large area of cerebral infarction in the left frontal, parietal, and temporal lobes, with an increased density in the left middle cerebral artery. Computed tomography angiography (CTA) of the head and neck (Fig. 1A) revealed complete occlusion of the left common carotid artery (CCA) and internal carotid artery (ICA). Electrocardiography showed no abnormalities. CTA on day 1 indicated moderate-to-severe stenosis of the left CCA and varying degrees of stenosis of the left ICA from segments C1 to C7 (Fig. 1B and C). Extensive low-density areas and hemorrhagic transformations were observed in the territory supplied by the left middle cerebral artery (Fig. 1D). Cranial CT revealed low perfusion in the region supplied by the left ICA (Fig. 1E).

Figure 1.

CTA, CT, and Doppler imaging findings. CTA of the head and neck, revealing complete occlusion of the left CCA (arrow) (A) and ICA. On day 1, CTA shows occlusion of the left middle cerebral artery, moderate-to-severe stenosis of the left CCA, occlusion of the left external carotid artery, and varying degrees of stenosis of the left ICA from segments C1 to C7: (B) volume reconstruction; (C) maximal intensity projection (arrows). (D) Extensive low-density areas and hemorrhagic transformations are observed in the territory supplied by the left middle cerebral artery (arrow). (E) Cranial CT showing low perfusion in the region supplied by the left ICA (arrow). (F) Enhanced transcranial Doppler imaging showing an inherently large right-to-left shunt. (G) On day 12, CTA reveals spontaneous recanalization of the ICA occlusion with a suspected carotid web or dissection (arrow). (H) Cranial CT on day 15 showing obvious hemorrhagic transformation following infarction (arrow). (I) Follow-up cranial CT on day 37 showing significant absorption of the cerebral hemorrhage (arrow). CCA, common carotid artery; CT, computed tomography; CTA, computed tomography angiography; ICA, internal carotid artery.

Final diagnosis

Spontaneous recanalization after CCA occlusion

Treatment

The patient was given medications to improve circulation and antiplatelet aggregation, as well as lipid-lowering therapy. As the patient had already exceeded the time window for emergency thrombectomy, he was given oral aspirin and atorvastatin calcium, and continuous mannitol drip, butylphthalide, edaravone, and sodium citicoline were administered intravenously. On day 11, enhanced transcranial Doppler ultrasound revealed an inherently large right-to-left shunt (Fig. 1F). On day 12, CTA revealed spontaneous recanalization of the ICA occlusion (ICAO) with a suspected carotid web or dissection (Fig. 1G).

Outcome and follow-up

On day 15, the patient was transferred to the rehabilitation department. Follow-up cranial CT on day 15 showed obvious hemorrhagic transformation following infarction (Fig. 1H). High-resolution magnetic resonance imaging of the carotid arteries on day 25 revealed no significant stenosis, ruling out a carotid web. Follow-up cranial CT on day 37 showed significant absorption of the cerebral hemorrhage (Fig. 1I). The patient is satisfied with the treatment outcomes.

Discussion

In this case, the thrombus underwent gradual dissolution within 12 days of onset, resulting in spontaneous recanalization, with a relatively early recanalization time. To the best of our knowledge, this is the first report on complete spontaneous recanalization after CCAO. As such, the incidence and timing of recanalization are unclear; however, data on ICAO can serve as a reference, with spontaneous recanalization occurring in 2.3%–10.3% of patients with ICAO[2]. The incidence of spontaneous recanalization within 7 days after ICAO has been reported to be 33%[3]. In our case, spontaneous recanalization of the CCAO occurred on the day of onset (Fig. 1B) and later progressed to ICAO recanalization.

The causes of CCAO may be related to carotid atherosclerosis, cardioembolic events, or carotid artery dissection. In this patient, high-resolution magnetic resonance imaging of the carotid artery ruled out carotid bulb formation or dissection. Enhanced transcranial Doppler imaging revealed a significant right-to-left shunt, leading us to speculate that the CCAO may be related to an embolism associated with a patent foramen ovale. The mechanisms underlying the spontaneous recanalization of CCAO may include the following: dissolving of the thrombus under the influence of the fibrinolytic system[4]; the use of antiplatelet or anticoagulant medications preventing new thrombus formation or promoting the dissolution of existing thrombi; changes in atherosclerotic plaques within the occluded vessel (e.g. loss of the lipid core) leading to lumen recanalization[4]; and hemodynamic changes (e.g. alterations in shear stress) following carotid occlusion facilitating vascular recanalization[5].

We used CTA to assess recanalization of the carotid artery occlusion and achieved satisfactory results. CTA is a rapid, safe, minimally invasive, and highly accurate method for detecting CCAO^[4]. Carotid ultrasound is an effective noninvasive examination technique that can serve as an initial diagnostic tool or for follow-up assessment. Although digital subtraction angiography is considered the gold standard for diagnosing arterial occlusions, it is relatively expensive and invasive and was not performed in the present case. High-resolution magnetic resonance imaging of the vascular wall is valuable for differentiating vascular wall lesions.

The risk of spontaneous recanalization in CCAO is closely related to the timing and extent of recanalization. Early and rapid spontaneous recanalization can lead to a reperfusion injury, whereas late and gradual recanalization tends to be relatively safe. In patients with late spontaneous recanalization of the ICAO, functional capacity appears to be preserved, resulting in favorable clinical outcomes[6]. Although spontaneous recanalization may have a positive impact on improving patient prognosis, close monitoring and follow-up assessments are essential, as well as proactive interventions if necessary. Additionally, post-stroke disruption of the blood-brain barrier and reperfusion injury may negatively affect patient outcomes.

Conclusion

Early spontaneous recanalization in CCAO is a rare but important medical phenomenon. It is important to note that recanalization does not equate to successful reperfusion of ischemic tissue, as it can cause acute reperfusion injuries. Hence, careful monitoring of hemorrhagic transformation, particularly with the mass effect, is crucial, along with prompt adjustments to treatment to optimize patient outcomes.

Ethical approval

This study was approved by the ethics review board of the First Affiliated Hospital of Shenzhen University (no. 20230413011) and adhered to the ethical standards of the 1964 Declaration of Helsinki and its subsequent amendments.

Consent

Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal on request.

Sources of funding

This study was funded by Noncommunicable Chronic Diseases-National Science and Technology Major Project (NO: 2023ZD0504800, 2023ZD0504802), Shenzhen High-level Hospital Construction Fund, Open Project of Shenzhen Clinical Medical Research Center for Nervous System Diseases (NO. SCRCND202503), and Elite Talent Cultivation Project of the Health Commission of Shenzhen (NO.2024XKG089).

Author contributions

X.H. and L.C. conceptualized the study and collected the resources. G.Z., R.Z., Y.F., and L.C. prepared and wrote the original draft. X.H. and L.C. reviewed and edited the manuscript. All authors read and approved the final manuscript.

Conflicts of interest disclosure

The authors declare no conflict of interest.

Research registration unique identifying number (UIN)

No. 20230413011.

Guarantor

Liming Cao.

Provenance and peer review

Not commissioned, externally peer-reviewed.

Data availability statement

Data sharing is not applicable to this article, as no datasets were generated or analyzed during the current study.