Purtscher-like retinopathy following mechanical thrombectomy: A case report

Introduction

In addition to high incidence, disability, and mortality rates, stroke is also the leading cause of death across the Chinese population, the most common type being ischemic stroke, constituting 80% of all stroke events. ¹ In the initial stages of acute cerebral infarction, recanalization of occluded blood vessels is a crucial treatment, protecting ischemic penumbra nerve function and limiting expansion of the core infarct area. Mechanical thrombectomy (MT), as an effective means of vascular recanalization, has gained clinical value through a series of high-quality studies. In 2014, the MR CLEAN study first confirmed the therapeutic benefits of endovascular stent thrombectomy for patients with anterior circulation large vessel occlusion, while in 2015, randomized controlled trials, such as ESCAPE and AddenD-IA, further validated the superiority of MT over drug therapy alone.^2–6 However, the MT technique carries risks of certain complications, mainly hemorrhagic transformation (symptomatic or asymptomatic bleeding), new distal artery embolism, reocclusion, restenosis, intraoperative vascular dissection, perforation, spasm, and hyperperfusion syndrome. ⁷ An additional—though rare—complication is Purtscher-like retinopathy, a rare retinal disease often caused by embolism due to mechanical or non-mechanical factors. Clinically, it manifests as vision loss, and its characteristic fundoscopic findings include Purtscher spots.

The inner layer of the retina is supplied with blood by the central retinal artery and its terminal branches, which lack collateral supply. Consequently, microembolic occlusion can induce ischemic necrosis of the photoreceptor–bipolar–ganglion cell neuronal pathway within minutes, typically manifesting as acute and irreversible visual impairment. ⁸ The optic nerve gathers ~1.2 million ganglion cell axons to transmit visual information to the central nervous system; Its blood supply also depends on the branches of the ophthalmic artery, so it is highly vulnerable to ischemia. ⁹ Although theoretically retinal artery embolism can be caused by the source of any tiny thrombus, it is extremely rare for it to occur due to thrombus fragmentation or microemboli escape after MT surgery.

This study reports in detail a case of retinal artery embolism secondary to MT surgery in a patient with M1 segment occlusion of the middle cerebral artery. Combined with fundus fluorescein angiography (FFA) and follow-up data, we analyze the structural alterations, visual acuity progression, and pathogenesis of retinal and optic nerve pathology. We aim to improve clinical awareness of this rare complication and to inform strategies for optimizing surgical strategies.

Case report

The patient, a 66-year-old male, complained of dizziness for 3 h and right-hand weakness for 2 h. In addition to experiencing unexplained dizziness without vertigo, nausea, or vomiting for 3 h before admission. Two hours after it began, the dizziness improved, but weakness in the right hand continued. One hour thereafter, the dizziness improved further, but there was weakness during grasping in the right hand and difficulty with flexible walking. During his outpatient visit to our hospital, the patient’s right-hand weakness was relieved, but he was admitted to the neurology ward with a diagnosis of stroke. Upon admission, a head computed tomography (CT) scan showed no significant abnormalities (Figure 1), and a physical examination on admission produced the following results: T: 37.0°C; P: 92 beats/min; R: 18 breaths/min; BP: 130/70 mmHg. He was conscious and had fluent speech, and both pupils were normal in size and shape, at 3.0 mm in diameter, with a sensitive light reflex. Eye movement in all directions was normal, with no nystagmus or diplopia, and the nasolabial folds on both sides were symmetrical, and the tongue was positioned at the midline. Pharyngeal reflex was positive, the neck was soft, and there were low breath sounds in both lungs, with no rales. The heart rate was 75 beats/min, considered regular, and the abdomen was soft with no tenderness. The liver and spleen were not palpable, and there was no edema in the lower limbs. Muscle strength in all limbs was grade V, with normal muscle tone, and tendon reflexes on both sides were normal. The Babinski sign was negative bilaterally, and pain and temperature sensations were normal on both sides, with no meningeal irritation. The patient presented with an NIHSS score of 0 and a modified Rankin Scale (mRS) score of 0, initially suggesting a preliminary diagnosis of cerebral infarction. Due to mild symptoms, the patient was treated with aspirin, clopidogrel, atorvastatin, and so on (Supplementary Figure 1).

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Figure 1.

Cranial CT scan results of the patient.

At 90 min post-admission, he suddenly developed aphasia and right-sided limb paralysis, and a physical examination revealed consciousness, motor aphasia, right-sided central facial, and tongue palsy, grade 0 muscle strength in the right limbs, and a positive right Babinski sign. At this moment, the patient presented with an NIHSS score of 15 and an mRS score of 4. Emergency brain MRI, including diffusion-weighted imaging (DWI), apparent diffusion coefficient, T1-weighted imaging (T1WI), T2WI, and magnetic resonance angiography (MRA), was completed within 12 min. DWI revealed multiple scattered acute infarcts in the left subcortical region (Figure 2(a1) and (a2)), while MRA demonstrated occlusion of the left middle cerebral artery (Figure 3). With symptom onset exceeding 4.5 h, intravenous thrombolysis was precluded by the 2013 AHA/ASA Guidelines for the Early Management of Acute Ischemic Stroke. ¹⁰ After informed consent was obtained from the family, MT was performed. Digital subtraction angiography performed emergently confirmed left middle cerebral artery occlusion (Figure 4(a) and (b)). The patient was treated with a Solitaire 4 × 20 stent-based thrombectomy, and follow-up angiography showed restored blood flow in the left MCA, indicating successful revascularization (Figure 4(c) and (d)), with a thrombolysis in cerebral infarction grade of 3. After surgery, tirofiban was continuously pumped for 48 h, and the day after the thrombectomy, he had fluent speech and strong limb movements, with an NIHSS score of 0 and an mRS score of 0. On the fourth day post-surgery, the patient developed decreased vision in the left eye and patchy vision, accompanied by a headache. During hospitalization, an ophthalmologist was consulted to assist with diagnosis and treatment, and comprehensive evaluations, including visual acuity assessment, fundus photography, optical coherence tomography (OCT), and FFA, were performed. The intraocular pressure was measured at 14 mmHg in the right eye and 13 mmHg in the left eye. Slit-lamp examination revealed no significant abnormalities in the cornea, anterior chamber, iris, or ciliary body of either eye. Lens opacity was observed in the right eye. Visual acuity assessment showed counting fingers at 1 m in the left eye and 20/50 in the right eye. After refractive correction, visual acuity remained unchanged in the left eye, while the right eye improved to 20/32. Fundus photography demonstrated cotton wool spots (CWSs) in the left eye, whereas the right eye appeared normal (Figure 5(a) and (b)). OCT examination showed loss of the foveal contour, thickening of the neurosensory retina, and inner retinal hyperreflectivity in the left eye (Figure 5(c)). FFA indicated delayed filling of some branches of the left branch retinal artery, with the absence of filling at the distal ends (Figure 6(a)–(c)), while the right eye was normal (Figure 6(d)). The ophthalmologist diagnosed retinal edema and occlusion of the branch retinal artery in the left eye, and cataract in the right eye, so the patient was treated with pregabalin and hyperbaric oxygen. The headache improved, but vision in the left eye remained poor. Follow-up at 1, 6 months, and 1 year showed no significant changes in vision, and no further fundus examination was performed.

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Figure 2.

Cranial MRI scan results of the patient. (a1, a2) Cranial MRI DWI sequence images. Red arrows indicate scattered punctate hyperintensities. (b1, b2) Cranial MRI ADC sequence images. Red arrows indicate scattered punctate hypointensities. (c1, c2) Cranial TIW1 sequence images. (d1, d2) Cranial T2WI sequence images.

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Figure 3.

Cranial MRI and MRA results of the patient. (a) 3D TOF MRA. (b) 3D TOF-MRA MIP. Red arrows indicate occlusion of the M1 segment of the left middle cerebral artery.

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Figure 4.

Cerebral angiography results of the patient. (a, b) Angiography results before MT. Red arrows indicate occlusion of the left middle cerebral artery. (c, d) Angiography results after MT. Red arrows indicate complete recanalization of the left middle cerebral artery.

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Figure 5.

Fundus photography and OCT results of the patient. (a) Fundus photograph of the patient’s right eye. (b) Fundus photograph of the patient’s left eye. Red arrows indicate cotton wool spots in the fundus. (c, d) OCT results. (c) Multiple clustered hyperreflective lesions within the thickened and elevated nerve fiber layer of the patient’s left eye, obscuring the underlying structures. (d) No obvious abnormalities in the OCT examination of the patient’s right eye.

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Figure 6.

FFA results of the patient. (a–c) FFA results of the patient’s left eye. Red arrows indicate delayed filling of some branches of the left retinal terminal artery, with no filling observed at the distal end. (d) FFA results of the patient’s right eye.

Discussion

On the fourth day post-MT for left middle cerebral artery occlusion, the patient had a decline in left eye vision, with patchy vision. Fundus examination revealed CWSs, ¹¹ which are characteristic lesions of retinal nerve fiber layer ischemic infarction, caused by axoplasmic transport disorders in the unmyelinated axons of retinal ganglion cells. These disorders lead to the accumulation of axonal components and local enlargement of nerve fibers, presenting as white, cotton-like, cloudy lesions under fundus microscopy. The primary cause of CWS formation is pre-capillary microvasculature occlusion in the retina. Theoretically, such factors as ischemia, hypoxia, infection, inflammation, and poisoning mostly cause local retinal ischemia and hypoxia, leading to axial flow obstruction in retinal nerve fibers and the formation of CWSs.

CWSs are most typically associated with Purtscher-like retinopathy caused by trauma ¹² and their pathogenesis involves traumatic asphyxia, with fundus manifestations demonstrating both venous dilation and retinal hemorrhages due to elevated venous pressure, as well as ischemic changes resulting from occlusion of arterioles and capillaries. Purtscher-like retinal lesions are caused by non-traumatic factors, such as systemic connective tissue disease, acute pancreatitis, thrombotic thrombocytopenic purpura, intracranial arterial embolization, and fat embolism. Unlike the acute elevation of venous and capillary pressure in traumatic cases, its pathogenesis primarily stems from extensive microthrombosis formation within retinal vessels or widespread emboli occlusion. ¹³

In this case, the patient developed a diminished vision in the left eye on the fourth day post-MT; thus, it is hypothesized that during thrombectomy, microemboli dislodged and migrated, obstructing the prearterioles of the retinal capillaries, and leading to retinal ischemia and subsequent vision loss. The potential mechanism involves the withdrawal of the thrombectomy device from the middle cerebral artery, a relatively narrow vessel, into the internal carotid artery, a wider vessel. Due to the thrombus’ inherent tension, the external pressure drops suddenly, creating an imbalance. This may cause the thrombus to expand and fracture, ¹⁴ and the resulting microthrombi then travel along the internal carotid artery’s branch—the ophthalmic artery—to the retinal capillary arterioles’ terminus, inducing ischemia–hypoxia and the formation of CWSs. The patient experienced visual impairment only 4 days post-surgery due to the formation of CWSs, which generally involves three stages. First, local blood circulation stops due to blood loss, followed by ischemia, hypoxia, and swelling of cell tissues, which lasts 24–72 h. Finally, the accumulation of organelles in the axial plasma block leads to the formation of CWSs, resulting in decreased vision. ¹¹ However, the retinal artery embolism rare but serious complication following MT. A nationwide study analyzing over 5000 patients with central retinal artery occlusion (CRAO) reported that only 0.38% of CRAO patients underwent MT. ¹⁵ In addition, the overall incidence of retinal artery occlusion in the general population is low, with a reported rate of 7.38/100,000 person-years. ¹⁶ The current evidence is limited to isolated case reports due to the absence of large-scale prospective screening. In 2018, Neurology published a case report about a 46-year-old woman who developed blurred vision and visual loss with CWSs on fundoscopy after thrombectomy for acute middle cerebral artery occlusion, attributed to retinal ischemia. ¹⁷

While the paper did not elaborate on the pathogenesis, it provided preliminary insights for clinicians. This case raises an important question: should clinical surgeons consider administering low-dose thrombolytic drugs routinely during surgery to decrease distal capillary microembolic blockages? Balodis et al. ¹⁸ found that, compared with endovascular thrombectomy (EVT) alone, the bridging therapy group did not demonstrate significantly better neurological outcomes or notable effects on procedural parameters. Meanwhile, A meta-analysis study, ¹⁹ which included six randomized controlled trials (DIRECT-MT, DEVT, SKIP, MR CLEAN-NO IV, DIRECT-SAFE, and SWIFT-DIRECT), failed to confirm the non-inferiority of thrombectomy alone compared to alteplase-bridged thrombectomy, nor did it confirm the superiority of alteplase-bridged thrombectomy over thrombectomy alone. However, in May 2025, the BRIDGE-TNK study ²⁰ was published in the New England Journal of Medicine, demonstrating that for patients with large vessel occlusion stroke within 4.5 h, intravenous tenecteplase combined with EVT significantly improved functional independence at 90 days compared to thrombectomy alone (52.9% vs 44.1%, p = 0.04), with a favorable safety profile. Of note, the 2013 AHA/ASA guidelines then in force restricted intravenous thrombolysis to within 4.5 h of symptom onset. ²¹ Current ESO (2021) and AHA/ASA (2022) updates allow IV thrombolysis beyond this window when advanced imaging—CT perfusion, DWI-FLAIR mismatch, or perfusion-diffusion mismatch—confirms a favorable ischemic core/penumbra profile in patients selected for reperfusion therapy. ²² Therefore, with continuous advancements in technology, treatment strategies for acute cerebral infarction are constantly evolving. In recent years, new thrombectomy techniques, including SWIM, SAVE, double-stent thrombectomy, BADDASS, and ADAPT, have significantly improved revascularization rates and clinical outcomes in acute stroke while reducing procedural complications. ²³ Therefore, it is crucial to explore new thrombectomy devices and more advanced technologies to reduce or avoid the occurrence and complications of microthrombus fragmentation.

Conclusion

This case report describes the clinical course of a patient with acute middle cerebral artery occlusion who underwent MT and successfully achieved vascular recanalization. Following treatment, the patient’s neurological symptoms were completely alleviated. However, during postoperative follow-up, a rare and severe complication—Purtscher-like retinopathy—was unexpectedly observed, likely caused by microemboli fragmentation, escape, and blockage of the branch retinal artery during thrombectomy. This case highlights the importance of closely monitoring ocular symptoms and signs in similar cases and conducting timely fundus examinations to facilitate the early detection and treatment of retinal artery embolism. Furthermore, it indicates that minimizing microemboli production and detachment during MT are critical to reducing the risk of complications such as retinal artery embolism. These findings emphasize the urgent need for the continuous exploration and development of new thrombectomy devices and optimized treatment strategies in clinical practice. For instance, the use of intermediate catheters—such as the Penumbra ACE series or Navien catheters—in combination with stent retrievers can enhance thrombus engagement and retrieval efficiency. This approach not only reduces the risk of distal embolization and procedure-related complications but also contributes to improved vascular recanalization rates, patient prognosis, and overall treatment safety and efficacy.

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