Internal carotid artery agenesis: A narrative review.

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Learn more: PMC Disclaimer | PMC Copyright Notice Surg Neurol Int . 2026 May 22;17:297. doi: 10.25259/SNI_272_2026 Internal carotid artery agenesis: A narrative review Khalid Talal Alghamdi 1, # , Badr E Hafiz 2, # , Zubaidah Alahmari 3 , Thamer H Alsharif 4 , Homoud Aldahash 1 , Saleh S Baeesa 2, * Author information Article notes Copyright and License information 1 Department of Neurosurgery, King Faisal Specialist Hospital and Research Centre, Riyadh, Saudi Arabia 2 Department of Neurosciences, King Faisal Specialist Hospital and Research Centre, Jeddah, Saudi Arabia 3 Department of Neurosurgery, Imam Abdulrahman Bin Faisal University, King Fahad Hospital of the University, Khobar, Saudi Arabia 4 Department of Neurosurgery, King Abdulaziz Specialist Hospital, Taif, Saudi Arabia * Corresponding author: Saleh S. Baeesa, Department of Neurosciences, King Faisal Specialist Hospital and Research Centre, Jeddah, Saudi Arabia. sbaeesa@kfshrc.edu.sa #: These authors have equally contributed as a first author Received 2026 Mar 2; Accepted 2026 Apr 10; Collection date 2026. Copyright: © 2026 Surgical Neurology International This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-Share Alike 4.0 License, which allows others to remix, transform, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms. PMC Copyright notice PMCID: PMC13224272  PMID: 42232383 Abstract Background: Congenital anomalies of the internal carotid artery (ICA), including hypoplasia, aplasia, and agenesis, are rare vascular conditions with a prevalence below 0.01%. Most patients remain asymptomatic because of collateral cerebral circulation, yet these anomalies may cause cerebrovascular complications, particularly ischemic events and intracranial aneurysm formation. Methods: A narrative literature review was performed to synthesize available data on demographics, embryology, pathophysiology, clinical presentation, imaging evaluation, classification systems, management, and outcomes of congenital ICA anomalies. Results: ICA agenesis is commonly detected incidentally, especially in unilateral cases with adequate collateral pathways. Symptomatic cases, more frequent in bilateral involvement, may present with headache, transient ischemic attack, stroke, or impaired consciousness. Risk factors include bilateral absence, incomplete collateral circulation, and classification patterns such as Lie types C and D and Jamous type 1b, associated with increased hemodynamic stress and aneurysm formation. Computed tomography (CT) angiography, magnetic resonance angiography, and digital subtraction angiography are central to diagnosis, whereas skull base CT distinguishes agenesis from hypoplasia. Management is usually conservative in asymptomatic patients, whereas surgical or endovascular treatment is reserved for aneurysms or hemodynamic compromise. Conclusion: ICA agenesis is a rare but clinically important anomaly. Recognition of variants, imaging features, and complications is essential for diagnosis and procedural planning. Surveillance imaging and individualized management help reduce cerebrovascular morbidity. Keywords: Internal carotid artery agenesis, Internal carotid artery aplasia, Internal carotid artery hypoplasia, Internal carotid artery anomalies INTRODUCTION Cerebrovascular insufficiency is a clinical condition that may be either acquired or congenital. Acquired causes, such as atherosclerosis, are far more common than congenital anomalies. Congenital anomalies of the internal carotid artery (ICA) are rare and include hypoplasia, aplasia, and agenesis.[ 13 , 28 ] The reported incidence of these anomalies is <0.01% in the general population.[ 3 , 4 , 23 , 38 , 36 ] Although most affected individuals are asymptomatic, incidental imaging performed for other purposes may reveal these anomalies. However, some patients may present with headaches, seizures, or cerebrovascular events, including transient ischemic attacks (TIAs) and ischemic or hemorrhagic strokes. The etiology of these anomalies remains unclear but is thought to result from developmental failure of the aortic arch during the intrauterine period.[ 13 , 23 ] Various terminologies have been used in the literature; nevertheless, the Lie classification remains the most consistent and widely accepted framework. Agenesis is defined as the complete absence of arterial development, aplasia refers to developmental failure with the presence of precursor structures, and hypoplasia denotes incomplete arterial development. Computed tomography (CT) of the skull base can aid in distinguishing agenesis from hypoplasia by demonstrating the complete or partial absence of the bony carotid canal, respectively.[ 8 , 15 , 31 , 32 ] Because of the rarity of these anomalies, current knowledge regarding ICA pathophysiology, clinical presentation, and management remains limited. This study seeks to comprehensively review the existing literature on patients with ICA anomalies, with the objective of enhancing the characterization of their demographics, clinical manifestations, pathophysiology, risk factors for complications, and management strategies. METHODS This narrative review was conducted to synthesize existing knowledge on congenital anomalies of the ICA. A literature search was performed using PubMed, Web of Science, and Embase to identify relevant peer-reviewed articles. Search terms included combinations of “internal carotid artery,” “ICA,” “congenital hypoplasia,” “congenital aplasia,” “congenital agenesis,” “congenital absence,” “congenital dysgenesis,” and “congenital anomalies.” Articles were selected based on relevance to congenital ICA anomalies, including case reports, case series, observational studies, and review articles. Studies focusing on acquired ICA occlusion, animal studies, non-English publications, conference abstracts, and reports lacking sufficient clinical or imaging data were excluded. The identified literature was reviewed and synthesized to summarize patient demographics, clinical presentation, imaging findings, classification type, associated syndromes, management, and outcomes to identify predictors of cerebrovascular complications. Definitions and types ICA anomalies can be classified as either congenital (dysgenesis) or acquired. Congenital ICA anomalies are rare and are further classified according to the Lie classification into hypoplasia, aplasia, and agenesis.[ 26 ] ICA dysgeneses encompass hypoplasia, aplasia, and agenesis. ICA hypoplasia is characterized by a patent artery with a reduced luminal diameter. ICA aplasia, which is sometimes used interchangeably with agenesis, refers to the absence of the ICA or its presence in a rudimentary form, accompanied by the presence of a carotid canal. Finally, ICA agenesis is defined by the complete absence of the ICA and the bony carotid canal at the skull base, as well as the absence of external carotid artery branches. The key distinguishing feature between agenesis and the other form of dysgenesis is the absence of the bony carotid canal, underscoring the importance of CT imaging for accurate differentiation.[ 11 , 28 ] [ Figure 1 ]. Figure 1: Open in a new tab Graph showing the types of internal carotid artery dysgenesis. Congenital anomalies of the internal carotid artery (ICA). In contrast, acquired ICA abnormalities, such as stenosis, may result from arteriosclerosis, arteritis, fibromuscular dysplasia, intimal dissection, or Moyamoya disease.[ 41 ] Epidemiology The reported prevalence of ICA anomalies in the literature is <0.01%.[ 4 - 7 ] However, several studies have suggested a higher incidence. Akdemir et al .[ 1 ] identified three patients (0.16%) among 1847 individuals who underwent CT angiography (CTA). Similarly, studies by Ito et al .[ 17 ] and Taşar et al .[ 41 ] reported 3 cases (0.24%) among 1275 patients and 7 cases (0.13%) among 5100 patients undergoing CTA, respectively, based on angiographic evaluations. ICA anomalies may be unilateral or bilateral, with unilateral involvement reported most frequently.[ 11 ] Our literature review indicates that bilateral ICA anomalies account for <10% of cases in most studies.[ 11 , 34 ] In contrast, a cohort study by Fitzgerald and Zuccoli[ 10 ] reported bilateral involvement in two of nine patients. Regarding laterality, the left ICA is more commonly affected than the right, with an approximate ratio of 3:2. This finding aligns with prior reports, although slight variations have been noted; Akdemir et al .[ 1 ] and Lee et al .[ 24 ] reported left-to-right ratios of 3:1 and 5:3, respectively. Furthermore, ICA anomalies appear to be more prevalent in females, with a male-to-female ratio of approximately 1:1.6.[ 11 , 24 ] Embryology To elucidate ICA development, Lasjaunias and Berenstein[ 21 ] divided the ICA into seven segments based on its embryological branches.[ 23 ] During the earliest stages of development, three aortic arches connect the ventral and dorsal aortae. The ventral aorta subsequently regresses, whereas the dorsal components of the aortic arch persist as embryonic arteries. These arteries form the basis for the division of the ICA into seven embryological segments, as described by Lasjaunias and Santoyo-Vazquez.[ 23 ] The first segment is the cervical segment, which arises from the remnant of the third aortic arch. The second segment, the ascending intrapetrous segment, develops from the dorsal aorta between the second and third aortic arches. The junction between the second and third segments corresponds to the origin of the hyoid artery, a dorsal remnant of the second aortic arch. The third segment is the horizontal intrapetrous segment, derived from the dorsal aorta between the first and second aortic arches, and gives rise to the mandibular artery. The fourth segment, the ascending intracavernous segment, originates from the dorsal arch between the first aortic arch and the primitive maxillary artery. The fifth segment is the horizontal intracavernous segment, formed from the dorsal aorta between the primitive maxillary artery and the primitive dorsal ophthalmic artery. The junction between the fourth and fifth segments marks the origin of the trigeminal artery, which provides a primitive connection between the cavernous ICA and the basilar artery. The sixth segment, the clinoidal segment, corresponds to the dorsal aorta between the primitive dorsal ophthalmic artery and the primitive ventral ophthalmic artery. Finally, the seventh segment, or terminal segment, represents the distal ICA between the primitive ventral ophthalmic artery and the primitive bifurcation of the ICA into the future anterior cerebral artery (ACA) and posterior communicating artery (PComA).[ 4 , 21 , 23 ] Lasjaunias and Berenstein[ 21 , 23 ] proposed that the agenesis of one of the seven ICA segments would lead to the absence of all proximal segments. However, this hypothesis has been debated because the development of proximal ICA segments appears to depend mainly on the presence of an alternative embryonic artery at the time of agenesis that can preserve blood flow to the proximal ICA.[ 4 ] Pathophysiology and risk factors The pathophysiology of ICA anomalies is not yet fully understood. Some studies have suggested that ICA agenesis results from abnormal regression of the first and third aortic arches.[ 22 ] An alternative theory proposed by Lasjaunias and Santoyo-Vazquez[ 23 ] postulates that the ICA system is composed of seven embryological segments, and that defective development or the absence of one or more of these segments can lead to the development of ICA anomalies. Several genetic disorders have been identified as potential risk factors for ICA anomalies, including Alagille syndrome and posterior fossa malformation, hemangiomas, arterial anomalies, coarctation of the aorta/cardiac defects, and eye abnormalities (PHACE) syndrome. Alagille syndrome is an autosomal dominant condition caused by mutations in the Jagged1 ( JAG1 ) gene, leading to disruption of the Notch signaling pathway, which plays a critical role in the development of major arteries.[ 19 , 22 ] This syndrome has been reported in association with ICA agenesis.[ 22 ] PHACE syndrome is a neurocutaneous syndrome characterized by structural abnormalities of the brain, cerebral vasculature, eyes, aorta, and heart and has been linked to ICA agenesis. In a study by Heyer et al .,[ 16 ] ICA aplasia was identified in 11 of 126 patients diagnosed with PHACE syndrome. Clinical presentation and diagnosis The clinical presentation of patients with ICA defects largely depends on whether the anomaly is congenital or acquired. Congenital ICA anomalies are typically asymptomatic and are often discovered incidentally, particularly in cases of unilateral involvement, owing to well-developed collateral circulation. Our literature review indicates that most patients with ICA anomalies are asymptomatic and are diagnosed incidentally. Although patients with bilateral ICA anomalies are more likely to develop symptoms, incidental findings have also been reported in individuals with bilateral ICA agenesis.[ 12 , 34 , 37 ] When symptomatic, patients may present with a wide range of manifestations, including weakness, TIA, tinnitus, headache, vomiting, dizziness, impaired consciousness, numbness, visual disturbances, aphasia, and sensorineural hearing loss. In our review, headache was the most frequently reported symptom. The spectrum of clinical presentations associated with ICA agenesis is summarized in Table 1 . Table 1: Spectrum of clinical presentations in patients with congenital internal carotid artery agenesis. Open in a new tab These clinical features may result from reduced cerebral perfusion and insufficient collateral circulation. Alternatively, symptoms may be attributable to associated conditions, such as intracranial aneurysms and subarachnoid hemorrhage (SAH), which are believed to arise from increased hemodynamic stress within collateral vessels.[ 6 , 21 ] Furthermore, several anomalies associated with ICA agenesis may contribute to symptom development, including atresia of the upper basilar artery, anomalous origin of the middle cerebral artery (MCA), agenesis of other supra-aortic vessels, transsphenoidal encephaloceles, and olivopontocerebellar atrophy.[ 3 , 5 , 24 , 27 ] In contrast, patients with acquired ICA stenosis or occlusion often experience acute or subacute reductions in cerebral perfusion, which may result in ischemic stroke.[ 17 ] Noncardiac anomalies have also been reported in pediatric patients with ICA agenesis, including musculoskeletal malformations, cleft palate, laryngomalacia, tracheoesophageal fistula, aberrant subclavian artery, left inferior vena cava, anorectal malformations, vertebral segmentation defects, and tethered cord with lumbar syringohydromyelia. ICA anomalies are most often diagnosed incidentally using CT, magnetic resonance imaging, color Doppler carotid ultrasonography, or angiography performed for unrelated indications. Based on our literature review, angiography was the initial diagnostic modality in most reported cases.[ 32 , 41 ] CT imaging of the head is particularly valuable for differentiating ICA anomaly subtypes because its superior bone resolution allows for assessment of the presence or absence of the bony carotid canal.[ 8 , 15 - 32 ] Classifications Several classification systems for ICA anomalies have been proposed, including those of Lie,[ 26 ] Tsuruta and Miyazaki,[ 42 ] Jamous et al .,[ 18 ] and Bonasia et al .[ 4 ] Lie and Hage’s classification The Lie and Huge classification, proposed in 1968, categorizes collateral circulation patterns associated with ICA anomalies into six types. Type A involves unilateral absence of the ICA, with collateral supply to the ACA through the anterior communicating artery (ACOM) and to the MCA from the PComA. Type B describes unilateral absence of the ICA, with collateral supply to both the ACA and MCA through the ACOM. Type C refers to bilateral absence of the ICAs, with collateral supply to the ACA and MCA provided by carotid-vertebrobasilar anastomoses. Type D involves unilateral absence of the cervical portion of the ICA, with collateral flow through intercavernous communication from the contralateral cavernous ICA. Type E is characterized by bilateral ICA hypoplasia, with enlarged PComA supplying both the ACAs and MCAs. Type F describes unilateral absence of the ICA, with collateral supply arising from anastomoses between the internal maxillary branches of the external carotid artery (ECA). Furthermore, a variant has been described in which unilateral absence of the ICA is compensated by a persistent trigeminal artery[ 26 ] [ Figure 2 ]. Figure 2: Open in a new tab Scheme of the Lie and Hage classification of the internal carotid artery anomaly showing the collateral supply. Tsuruta and Miyazaki classification The Tsuruta and Miyazaki classification, proposed in 1977, divides ICA anomalies into three types. Type 1 consists of unilateral ICA agenesis with the absence of the A1 segment of the ACA. In this pattern, the ACA is supplied by the contralateral ICA through the ACOM, whereas the MCA is supplied by the ipsilateral PComA. This configuration corresponds to Type A in the Lie and Huge classification. Type 2 includes unilateral ICA agenesis in which both the ACA and MCA are supplied by the ipsilateral PComA. Type 3 includes unilateral ICA agenesis with both the ACA and MCA supplied through the ipsilateral ACOM, corresponding to Type B in the Lie and Huge classification[ 42 ] [ Figure 3 ]. Figure 3: Open in a new tab Scheme of the Tsuruta and Miyazaki classification of the internal carotid artery anomalies. Jamous’s classification The Jamous classification, proposed in 2007, is based on the timing of ICA agenesis and includes three main types with several subtypes. Type 1 involves ICA agenesis with collateral supply from primitive vessels. It is further divided into three subtypes: Type 1a: Collateral supply from the ECA through rete mirabile; Type 1b: collateral supply to the MCA and ACA through a persistent trigeminal artery; and Type 1c: collateral supply to the ACA through the ACOM and to the MCA through an intercavernous anastomosis. Type 2 features collateral supply from ICA branches and also has three subtypes: Type 2a: MCA supplied by the PComA and ACA supplied by the ACOM; Type 2b: Both the MCA and ACA supplied by the ACOM; and Type 2c: Both the MCA and ACA supplied by the PComA. Type 3 resembles Type 1a, with collateral supply originating from the ECA but without the presence of rete mirabile[ 18 ] [ Figure 4 ]. Figure 4: Open in a new tab Scheme of the Jamous classification of the internal carotid artery anomalies. Bonasia’s classification The Bonasia classification emphasizes the embryological segment affected by the vascular insult and the timing of this event during development. It categorizes ICA anomalies into four types based on the source of collateral circulation: collateral supply through the circle of Willis, persistent embryonic arteries, arterio-arterial anastomoses, and rete mirabile[ 4 ] [ Figure 5 ]. Figure 5: Open in a new tab Scheme of the Bonasia classification of the internal carotid artery anomalies. Predictors of complications Cerebrovascular complications of congenital ICA anomalies, such as ischemic events and intracranial aneurysms, are influenced by anatomical, demographic, and syndromic factors. Classification and collateral circulation Bilateral ICA agenesis (Lie type C) and anomalies relying on a persistent trigeminal artery (Jamous type 1b) increase hemodynamic stress, raising the risk of aneurysms and ischemia. In contrast, unilateral anomalies with robust circle of Willis collateralization (Lie type B or Tsuruta type 1) are typically well tolerated.[ 15 , 18 , 26 , 42 ] Table 2 summarizes ischemic and hemorrhagic stroke mechanisms reported in association with ICA agenesis. Table 2: Stroke Presentation in patients with internal carotid artery agenesis: Hemorrhagic versus ischemic mechanisms. Open in a new tab Laterality Bilateral anomalies (<10% of cases) carry a higher ischemic risk than unilateral cases. Left-sided involvement is slightly more common, but its impact on complications is unclear.[ 11 , 24 , 34 ] Collateral perfusion Adequate collateral flow through anterior/posterior communicating arteries or intercavernous anastomoses often prevents symptoms, whereas insufficient perfusion can lead to strokes or TIAs.[ 3 , 4 , 6 ] Syndromic associations PHACE syndrome and Alagille syndrome (JAG1 mutations) are linked to ICA anomalies and higher cerebrovascular risk due to abnormal arterial development.[ 16 , 19 , 22 ] Demographics Female predominance is reported (male-to-female ~1:1.6), but the effect of sex and age on complication risk is not well defined.[ 11 , 24 ] The main predictors associated with symptomatic presentation and cerebrovascular complications in ICA agenesis are summarized in Table 3 . Table 3: Factors associated with symptomatic internal carotid artery agenesis. Open in a new tab MANAGEMENT Considering the typically asymptomatic and congenital nature of carotid agenesis, there is currently no treatment available to restore the absent ICA. However, due to the high prevalence of associated cerebral aneurysms, management focuses on aneurysm treatment similar to that in the general population because no specific guidelines for ICA anomalies exist to date. Treatment options included conservative management with regular imaging follow-up, endovascular interventions, and open surgical procedures.[ 25 ] Aneurysm formation is often attributed to hemodynamic overload within compensatory collateral circulation. This varied collateral network must be carefully considered when planning endovascular or microsurgical interventions.[ 23 ] Conservative management In asymptomatic patients or those without hemodynamic compromise or aneurysmal disease, conservative management remains the cornerstone of care.[ 25 ] This approach includes clinical observation, control of vascular risk factors, and lifestyle modifications to reduce cerebrovascular risk.[ 23 , 25 ] Periodic neuroimaging – preferably magnetic resonance angiography (MRA) or CTA – is recommended to monitor collateral pathways and detect the development of aneurysms or other vascular abnormalities.[ 35 ] Antiplatelet therapy may be considered in select cases to reduce thromboembolic risk, particularly in patients with a history of TIA or minor strokes.[ 23 ] Endovascular intervention Endovascular therapy primarily targets associated intracranial aneurysms rather than the agenesis itself.[ 2 , 35 ] Techniques such as coiling or stent-assisted coiling are chosen based on aneurysm morphology, location, and neck width.[ 35 ] Altered hemodynamics due to ICA agenesis can complicate endovascular navigation, necessitating experienced interventionalists and thorough preprocedural planning.[ 2 , 35 ] Flow-diverting stents may be employed for select wide-necked aneurysms, particularly within the anterior circulation.[ 35 ] Y-shaped stenting is an option for aneurysms at bifurcations or in cases with multiple aneurysms; this involves deploying one stent in the parent artery and threading a second stent through its struts into a branching vessel.[ 14 ] However, concerns remain regarding their use in aneurysms with complex morphological features and the requirement for antiplatelet therapy, limiting their application in ruptured aneurysms. Furthermore, endovascular treatment availability is limited, particularly in developing regions.[ 2 , 25 ] Surgical intervention Surgical management is uncommon and generally reserved for symptomatic patients with inadequate collateral circulation or aneurysms unsuitable for endovascular treatment.[ 2 ] In cases of ischemic symptoms due to hemodynamic insufficiency, extracranial-to-intracranial (EC-IC) bypass surgery has been reported as an effective method to improve cerebral perfusion.[ 39 ] Microsurgical clipping remains a valid alternative for aneurysms located in surgically accessible sites or when endovascular access is not feasible.[ 2 , 35 ] However, altered anatomy from ICA agenesis can complicate surgical orientation, highlighting the importance of meticulous preoperative imaging and planning.[ 35 ] For high-risk patients, endovascular coiling may be preferred over microsurgery due to its lower overall risk and avoidance of temporary arterial clipping.[ 35 ] Management strategy Management of congenital ICA anomalies is largely guided by symptoms, collateral circulation, and associated aneurysms. Asymptomatic patients are usually managed conservatively with regular imaging, risk factor control, and clinical monitoring. Endovascular interventions target associated aneurysms and are preferred when anatomy allows, whereas surgical options, such as EC-IC bypass or microsurgical clipping, are reserved for symptomatic patients with inadequate collateral flow or aneurysms unsuitable for endovascular treatment. Long-term follow-up and patient education are essential due to the increased risk of aneurysm formation and cerebrovascular events. Follow-up and prognosis The prognosis of ICA anomalies varies, largely depending on the anomaly type and associated conditions. Most patients remain asymptomatic due to sufficient collateral circulation compensation.[ 25 ] Routine vascular screening with noninvasive imaging modalities such as carotid Doppler ultrasound, CTA, or MRA is valuable for detecting progressive vascular changes or complications.[ 9 , 30 , 33 ] One significant complication is cerebral aneurysm formation, reported in approximately 27.8% of patients with ICA anomalies – markedly higher than the 2–4% prevalence in the general population.[ 43 ] Effective control of comorbidities, including hypertension and smoking cessation, is essential because these factors, combined with altered hemodynamics, contribute to vascular remodeling and aneurysm development. Screening for associated genetic syndromes, such as DiGeorge syndrome and neurofibromatosis, should also be incorporated into the management plan.[ 29 ] Patient education is critical, emphasizing awareness of warning signs such as sudden severe headache or visual disturbances. Early recognition of these symptoms is vital for prompt medical attention and timely management of potentially life-threatening events such as SAH, TIA, or intracerebral hemorrhage.[ 40 ] CONCLUSION Congenital anomalies of the ICA are extremely rare and are most often discovered incidentally during cerebrovascular imaging. Maintaining a high index of suspicion is important to facilitate early detection. Recognizing these anomalies is crucial for assessing the risk of ischemic stroke and associated aneurysms. While most reported cases are incidental, symptomatic ICA agenesis represents a higher-risk subgroup, with symptoms resulting from either cerebral hypoperfusion leading to TIA or ischemic stroke, or aneurysm-related hemorrhage. Such patients warrant thorough vascular assessment and individualized imaging surveillance. Acknowledgments: Original schematic illustrations created by Khalid Alghamdi for this manuscript; not adapted from previously published sources. We would like to thank Dr. Mouaz Bamsallm, Dr. Samir, and Dr. Sarah Bin Abdulaqdir for their contribution to data collection. Footnotes How to cite this article: Alghamdi KT, Hafiz BE, Alahmari Z, Alsharif TH, Aldahash H, Baeesa SS. Internal carotid artery agenesis: A narrative review. Surg Neurol Int. 2026;17:297. doi: 10.25259/SNI_272_2026 Contributor Information Khalid Talal Alghamdi, Email: kh-t@hotmail.com. Badr E. Hafiz, Email: neurosurg.badr@gmail.com. Zubaidah Alahmari, Email: zubaidah.sa8@gmail.com. Thamer H. Alsharif, Email: thameralsharif@outlook.com. Homoud Aldahash, Email: dr_homoud@hotmail.com. Saleh S. Baeesa, Email: sbaeesa@kfshrc.edu.sa. Availability of data and materials: All data generated or analyzed during this study are included in this article. Further enquiries can be directed to the corresponding author. Ethical approval: Institutional review board approval is not required. Declaration of patient consent: Patient’s consent is not required as there are no patients in this study. Financial support and sponsorship: Nil. Conflicts of interest: There are no conflicts of interest. Use of artificial intelligence (AI)-assisted technology for manuscript preparation: The authors confirm that there was no use of artificial intelligence (AI)-assisted technology for assisting in the writing or editing of the manuscript, and no images were manipulated using AI. Disclaimer The views and opinions expressed in this article are those of the authors and do not necessarily reflect the official policy or position of the Journal or its management. The information contained in this article should not be considered to be medical advice; patients should consult their own physicians for advice as to their specific medical needs. REFERENCES 1. Akdemir Aktaş H, Farımaz M, Fırat A, Göçmen R. 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