Macular holes are classified by cause into idiopathic and secondary types. Among secondary types, those caused by trauma are called traumatic macular holes. The mechanism involves compression and rebound stretching of the posterior pole retina at the time of trauma, along with traction on the fovea by the attached vitreous, leading to a foveal tear.
Traumatic macular holes account for approximately 5–10% of all macular holes. While idiopathic macular holes are more common in middle-aged and older women, traumatic macular holes are epidemiologically characterized by a higher incidence in young men.
Idiopathic macular hole
Predominant age/sex: More common in middle-aged and older women (50s–80s)
Mechanism: Mainly due to traction on the anterior fovea caused by age-related changes in the vitreous
Spontaneous closure: Rare; surgery is the basic treatment strategy
Associated findings: No traumatic changes such as commotio retinae or choroidal rupture
Traumatic Macular Hole
Commonly affected population: Young males (sports, assault, accidents)
Mechanism: Retinal stretching and vitreous traction due to eyeball deformation, or tissue destruction by laser
Spontaneous closure: Cases of spontaneous closure within a few months have been reported
Associated findings: Often accompanied by surrounding hemorrhage, retinal contusion necrosis, choroidal rupture, and vitreous hemorrhage
Traumatic macular holes are classified into full-thickness holes and partial-thickness (lamellar) holes based on OCT findings. Full-thickness holes are defects extending from the internal limiting membrane to the retinal pigment epithelium (RPE), while partial-thickness holes involve only a portion of the retinal layers. OCT examination is essential for differentiating between the two.
Traumatic holes are more common in young males and are often accompanied by traumatic changes such as retinal commotion, hemorrhage, and choroidal rupture around the hole. Additionally, the possibility of spontaneous closure is a major difference from idiopathic holes. In addition to a history of trauma, anterior segment findings such as angle recession can be clues for differentiation.
When only a macular hole is present, the main symptoms are decreased visual acuity and distortion (metamorphopsia). When there are associated injuries, symptoms can be diverse.
In traumatic macular holes, unlike idiopathic cases, extensive damage to the surrounding retina and choroid is often present.
Choroidal rupture, vitreous hemorrhage, and subretinal hemorrhage are factors that prevent visual improvement even after hole closure. The presence and extent of these complications greatly influence the final visual prognosis.
The causes of traumatic macular holes are broadly divided into blunt trauma and laser trauma.
Blunt ocular trauma (most common cause):
Laser injury:
Being a young male (higher incidence of sports and trauma) is the greatest risk factor. Participation in sports without protective eyewear and improper handling of high-power laser devices are triggers.
When directly viewing a high-energy laser such as a pulsed YAG laser, the macular tissue can be thermally and photochemically destroyed, leading to a macular hole. Damage from laser pointers has also been reported, especially high-power ones (equivalent to Class 3B or Class 4). Laser-induced macular holes primarily involve damage to the photoreceptor cells themselves, unlike blunt trauma.
If there is a clear history of trauma, differentiation from idiopathic macular hole and pseudohole is easy. If the trauma history is unclear or the time of injury cannot be determined, the following findings can aid in differentiation.
OCT examination is essential for differentiation from pseudo macular hole (lamellar hole, foveal schisis).
| Examination | Purpose |
|---|---|
| OCT (Optical Coherence Tomography) | Presence of hole, full-thickness/partial-thickness differentiation, postoperative follow-up |
| Fluorescein angiography | Detection of RPE damage, choroidal rupture, choroidal neovascularization (CNV) |
| Visual field test | Confirmation of traumatic visual field defects other than macular hole |
| Gonioscopy with compression | Confirmation of traumatic changes such as angle recession |
OCT is a core examination for diagnosis and follow-up of traumatic macular hole. It objectively enables differentiation between full-thickness and partial-thickness holes, measurement of hole diameter, evaluation of surrounding retinal layer structure, and assessment of vitreoretinal relationship (presence of posterior vitreous detachment). It is also indispensable for determining postoperative hole closure.
Fluorescein angiography is performed to evaluate the extent of choroidal rupture and retinal pigment epithelium (RPE) damage, and to confirm the presence and location of choroidal neovascularization (CNV). Note that traumatic cases often involve RPE and choroidal damage, unlike idiopathic cases.
Visual field testing is performed to evaluate the central scotoma due to the macular hole, as well as visual field defects caused by commotio retinae or choroidal rupture.
Gonioscopy is performed to confirm traumatic angle changes including angle recession, providing objective evidence of traumatic etiology.
Since spontaneous closure of traumatic macular holes has been reported in some cases, observation is initially recommended if no complications are present. Follow-up with OCT over several months is performed; if no closure tendency is observed, vitrectomy is considered.
| Condition | Recommended Management |
|---|---|
| With submacular hemorrhage | Urgent vitrectomy |
| Closure tendency present (confirmed by OCT) | Continue observation |
| No closure tendency (after several months) | Consider vitrectomy |
| Complicated by choroidal neovascularization (CNV) | Consider anti-VEGF therapy |
If subretinal hemorrhage occurs, urgent surgery is necessary. The longer subretinal hemorrhage persists, the more toxic it becomes to photoreceptors, worsening visual prognosis 1).
Similar to idiopathic macular hole, surgery is performed using the following steps 2):
Postoperatively, maintaining a face-down position allows the gas to tamponade the macula and promote hole closure. Activities are restricted while gas remains, and air travel is prohibited.
Spontaneous closure within a few months has been reported. Therefore, if there is no complication such as subretinal hemorrhage, observation with OCT is often performed first, and vitrectomy is considered if no closure tendency is seen. Spontaneous closure rates vary among reports, and smaller holes are more likely to close spontaneously 1).
The macular hole closure rate after vitrectomy is reported to be over 90%. However, visual improvement depends not only on hole closure but also on the extent of choroidal rupture, hemorrhage, and photoreceptor damage. If the associated injuries are severe, improvement may be difficult. Adequate preoperative explanation and sharing of realistic expectations are important 3).
When a blunt external force is applied to the eye, the eyeball undergoes a temporary rapid deformation (shortening of the anteroposterior diameter and expansion of the equatorial diameter). This sudden deformation places the following complex mechanical stresses on the posterior pole retina.
These mechanisms act in combination, and when tissue tolerance is exceeded, a crack (macular hole) forms at the fovea. One reason traumatic macular holes are more common in young people is that posterior vitreous detachment has not occurred, making vitreous traction more likely.
When high-energy laser light is directed at the macula, thermal and photochemical tissue destruction occurs due to absorption of light energy by the retinal pigment epithelium (RPE), photoreceptors, and retinal pigment. With pulsed YAG lasers, high-density energy is concentrated in a short time, causing explosive destruction of the retinal tissue at the irradiation site, leading to perforation. In laser-induced cases, the photoreceptors themselves are damaged, so the visual prognosis tends to be poorer compared to blunt trauma.
Choroidal rupture results from a tear in Bruch’s membrane, leading to bleeding from the choriocapillaris (subretinal and choroidal hemorrhage) and impaired blood flow to the photoreceptors. Choroidal neovascularization (CNV) may later develop at the site of choroidal rupture. CNV is an important late complication that causes significant vision loss when it occurs in the macula.
Commotio retinae is an opacification and degeneration of the photoreceptor outer segments that occurs early after trauma, reflecting the acute phase of photoreceptor damage. In severe cases, photoreceptors undergo irreversible degeneration, resulting in permanent visual dysfunction.
Research is progressing on the spontaneous closure rate of traumatic macular holes and its predictive factors. Miller et al. (2015) reported a spontaneous closure rate of approximately 30%, and factors such as small hole size in the early post-injury period, presence of posterior vitreous detachment, and OCT morphological findings are being investigated as predictors of spontaneous closure 1).
Yamashita et al. (2002) examined the optimal timing of vitrectomy for traumatic macular holes and suggested that relatively early intervention may be superior in terms of closure rate and visual prognosis 2). However, policies regarding the waiting period considering the possibility of spontaneous closure vary among institutions, and a unified protocol has not been established.
Internal limiting membrane (ILM) peeling is standard for idiopathic macular holes, but for traumatic macular holes, spontaneous closure is possible. It is important to determine the timing of surgery and follow-up based on OCT findings, and the indication for peeling should be considered on a case-by-case basis 4).
The therapeutic efficacy of anti-vascular endothelial growth factor (anti-VEGF) drugs for CNV arising at the site of choroidal rupture has been reported. Intravitreal injections of ranibizumab, aflibercept, and bevacizumab are expected to improve visual acuity and suppress exudation, but large-scale RCTs specifically for traumatic CNV are currently lacking 5).
Pharmacologic vitreolysis with ocriplasmin (recombinant microplasmin) was developed for non-invasive release of vitreoretinal traction. It has shown some efficacy for idiopathic small macular holes, but its application to traumatic macular holes is still at the research stage 6).
