Journal of Neuroinfectious Diseases
Open Access

Acute ischemic stroke; Endovascular thrombectomy; Hyperperfusion; Prognosis; neuroimaging; Clinical outcomes

Introduction

Acute ischemic stroke represents a major healthcare challenge globally, with significant morbidity and mortality rates. The advent of endovascular thrombectomy has revolutionized acute stroke management, offering a promising therapeutic option for eligible patients [1]. However, despite its efficacy in achieving vessel recanalization and improving perfusion, endovascular thrombectomy may inadvertently lead to global hyperperfusion, a phenomenon associated with adverse clinical outcomes. This article aims to explore the relationship between global hyperperfusion following endovascular thrombectomy and prognosis in acute ischemic stroke [2]. Global hyperperfusion refers to a state of increased cerebral blood flow exceeding metabolic demands, leading to cerebral edema, hemorrhage, and ultimately, neuronal injury. Following successful recanalization of the occluded vessel, reperfusion injury may occur due to the restoration of blood flow to previously ischemic tissue [3]. The abrupt increase in perfusion pressure can overwhelm the compromised blood-brain barrier, resulting in extravasation of fluid and blood constituents into the brain parenchyma. Additionally, dysregulation of cerebral auto regulation mechanisms may contribute to hyperperfusion, exacerbating tissue damage.

Discussion

Recent studies have demonstrated a significant association between global hyperperfusion and adverse clinical outcomes in patients undergoing endovascular thrombectomy for acute ischemic stroke. Neuroimaging modalities, including perfusion-weighted imaging and CT perfusion, have been instrumental in identifying hyperperfusion patterns post-thrombectomy [4]. These imaging findings correlate with poor prognosis markers such as hemorrhagic transformation, cerebral edema, and neurological deterioration. Furthermore, hyperperfusion syndrome, characterized by headache, seizures, and focal neurological deficits, may manifest in susceptible individuals, further complicating post-thrombectomy management. The presence of global hyperperfusion following endovascular thrombectomy portends a poorer prognosis for acute ischemic stroke patients. Increased risk of hemorrhagic transformation, malignant cerebral edema, and long-term disability has been observed in individuals experiencing hyperperfusion post-thrombectomy [5]. The severity and duration of hyperperfusion, as well as underlying comorbidities such as hypertension and diabetes, influence the prognostic trajectory. Timely recognition of hyperperfusion-related complications is crucial for risk stratification and targeted intervention to optimize outcomes [6]. Management of global hyperperfusion following endovascular thrombectomy necessitates a multifaceted approach aimed at mitigating cerebral edema and reducing the risk of hemorrhagic transformation. Tight blood pressure control, avoidance of hyperglycemia, and judicious fluid management are cornerstone strategies in the acute phase. Additionally, neuroprotective agents such as osmotic diuretics and corticosteroids may be considered in selected cases to alleviate cerebral edema and minimize secondary brain injury [7]. Close monitoring of neurological status and serial neuroimaging facilitate early detection of hyperperfusion-related complications, guiding therapeutic interventions. Future research endeavors should focus on elucidating the underlying mechanisms driving global hyperperfusion and its impact on long-term functional outcomes in acute ischemic stroke patients [8]. Advanced neuroimaging techniques, including functional MRI and diffusion tensor imaging, may provide valuable insights into the dynamics of cerebral perfusion and tissue viability post-thrombectomy. Furthermore, prospective multicenter studies are warranted to develop standardized protocols for the management of hyperperfusion-related complications and optimize post-thrombectomy care algorithms [9].

Conclusion

Global hyperperfusion following endovascular thrombectomy represents a double-edged sword in the management of acute ischemic stroke. While successful recanalization restores cerebral perfusion and salvages ischemic tissue, the ensuing hyperperfusion may precipitate neurovascular complications and worsen clinical outcomes. Recognizing the clinical implications of hyperperfusion syndrome and its prognostic significance is paramount for clinicians involved in acute stroke care. By implementing tailored management strategies and advancing our understanding of hyperperfusion pathophysiology, we can strive to improve outcomes and enhance the quality of life for acute ischemic stroke survivors.

Acknowledgement

None

Conflict of Interest

None

References

1. Rao NP, Shailaja U, Mallika KJ, Desai SS, Debnath P (2012)Traditional Use Of Swarnamrita Prashana As A Preventive Measure: Evidence Based Observational Study In Children.IJRiAP 3: 1-5.

Indexed at, Google Scholar, Crossref

2. Aniket P, Pallavi D, Aziz A, Avinash K, Vikas S (2017)Clinical effect of suvarna bindu prashan.JAIMS 2: 11-18.

Indexed at, Google Scholar

3. Gaikwad A (2011)A Comparative pharmaco-clinical study of Madhu-Ghrita and SwarnaVacha Madhu-Ghrita on neonates. Ayurved MD Research thesis.Jam 12: 2-7.

Indexed at, Google Scholar, Crossref

4. Singh (2016)A Randomized Controlled Clinical Trial on Swarna Prashana and its Immunomodulatory Activity in Neonates. Jam 24: 4-9.

Indexed at, Google Scholar, Crossref

5. Rathi R, Rathi B (2017)Efficacy of Suvarnaprashan in Preterm infants-A Comparative Pilot studyJ Ind Sys Med 5: 91.

Google Scholar, Crossref

6. Ismaili K, Hall M, Donner C, Thomas D, Vermeylen D, et al. (2003)Results of systematic screening for minor degrees of fetal renal pelvis dilatation in an unselected population.Am J Obstet Gynecol 188: 242-246.

Google Scholar, Crossref

7. Coplen DE, Austin PF, Yan Y, Blanco VM, Dicke JM (2006)The magnitude of fetal renal pelvic dilatation can identify obstructive postnatal hydronephrosis, and direct postnatal evaluation and management.J Urol 176: 724-727.

Google Scholar, Crossref

8. Grignon A, Filion R, Filiatrault D, Robitaille P, Homsy Y, et al. (1986)Urinary tract dilatation in utero: classification and clinical applications.Radio 160: 645-647.

Google Scholar, Crossref

9. Ocheke IE, Antwi S, Gajjar P, McCulloch MI, Nourse P (2014)Pelvi-ureteric junction obstruction at Red Cross Children’s Hospital, Cape Town:a six year review.Arab J Nephro Tran 7: 33-36.

Indexed at, Google Scholar

10. Capello SA, Kogan BA, Giorgi LJ (2005)Kaufman RP. Prenatal ultrasound has led to earlier detection and repair of ureteropelvic junction obstruction.J Urol 174: 1425-1428.

Google Scholar, Crossref