Terson syndrome following traumatic brain injury

Dear Sir,

Terson syndrome (TS) is known as a distinctive ophthalmic complication associated with subarachnoid hemorrhage from rupture of an intracranial aneurysm (aneurysmal subarachnoid hemorrhage [aSAH]). As for other etiologies, intracerebral hemorrhage and traumatic brain injury (TBI) have also been reported to cause TS.^[1] The authors present details of a patient with TS development following TBI who underwent an early vitrectomy.

A 49-year-old woman presented with a consciousness disturbance after falling on the stairs. Upon arrival, the patient’s consciousness level was E2V2M5 on the Glasgow Coma Scale. Head computed tomography findings demonstrated a cerebellar hemorrhage and an acute epidural hematoma overlying the transverse sinus on the right side [Figure 1a and b]. Bifrontal contusions were also noted, along with a small amount of traumatic subarachnoid hemorrhage. Brain stem compression with effacement of the basal cistern was evident.

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Figure 1: (a and b) Head computed tomography images showing supra- and infratentorial epidural hematoma (red arrows). (a) A right intracerebellar hemorrhage (blue arrow) and (b) Cerebral contusions in the bifrontal base (yellow arrows) can be seen. Effacement of cerebral cisterns, parenchymal edema, and traumatic subarachnoid hemorrhage are also noted.

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An emergency operation was performed through supratentorial and suboccipital craniotomies with a bone strip left over the transverse sinus to evacuate the cerebellar hemorrhage and acute epidural hematoma. During the recovery period, consciousness disturbance began to improve, though cognitive deficits remained. The patient had severe visual impairment while writing or eating, though she did not report such symptoms. An ophthalmologic examination conducted 21 days after the injury revealed visual acuity for counting fingers at 10 cm, corresponding to <20/2000. Fundoscopic examinations revealed severe vitreous hemorrhages in both eyes [Figure 2a]. A diagnosis of TS was determined. The patient underwent pars plana vitrectomy 27 days after the injury. At 5 months following the injury, visual acuity was 20/25 in the right and 20/20 in the left. A fundoscopic examination indicated significant clearing of the vitreous hemorrhages [Figure 2b]. The patient was able to independently perform activities of daily life.

TS is defined as intraocular hemorrhage, including vitreous, intraretinal, and subhyaloid hemorrhages. It is classically described as a vitreous hemorrhage following aSAH, with development especially noted in poor-grade cases. However, in a setting of clinical practice for treating patients with consciousness disturbance and cognitive impairment, TS can be underestimated or overlooked. Transmission of sudden increased intracranial pressure can cause retrobulbar optic nerve dilatation, which compresses the central retinal veins. Subsequent retinal venous hypertension and congestion and rupture are regarded as the main pathogenesis of intraocular hemorrhage, though several other theories have been proposed.^[2] Because of the self-limiting nature of TS, a conservative strategy is generally selected for patients with mild symptoms, while a vitrectomy is the treatment of choice for those with severe visual impairment. A previous study found vitrectomy to be effective for 28 eyes in 20 TBI patients with TS.^[3] The report also noted that a typical clinical symptom was the sudden onset of visual loss without pain.

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Figure 2: (a) Fundoscopic images 21 days after the injury, revealing dense bilateral vitreous hemorrhages. (b) Fundoscopic images from 5 months after the injury showing that the vitreous hemorrhages had mostly cleared, with minor retinal hemorrhage remaining.

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Rapid improvement was obtained regardless of pre-operative visual acuity or whether surgery was early or delayed (within three or more than 3 months, respectively), with initial retinal detachment found to be a poor prognostic factor. Citirik et al. reported three cases with TS following TBI, in which delayed surgery (6 months later) for a young patient resulted in worse clinical outcome.^[4] Persistent visual impairment can be a negative factor affecting neurological recovery, while a relatively longer period of time, several months to years, is required for spontaneous absorption of vitreous hemorrhage.^[5]

Early recognition of TS is essential for performing a timely vitrectomy to prevent delayed ophthalmic complications and provide effective rehabilitation for the patient.