Subhyaloid premacular hemorrhage usually leads to an acute and pronounced decrease in vision. Different mechanisms including vasoproliferative diseases (e.g., ischemic retinal venous thromboses or diabetic retinopathy), vascular anomalies (e.g., retinal macroaneurysms), or rare pathologies such as leukemia or Terson syndrome may cause these hemorrhages [
1‐
4]. A Valsalva maneuver may also be a typical trigger, because an increase in intraabdominal/intrathoracic pressure may result in an increase in cranial pressure and consequently, an increase in intraocular venous pressure [
5]. The absence of venous valves in the head/neck area favors this occurrence. Each mechanism could lead to a bleeding into the vitreoretinal interface. Due to a still attached posterior hyaloid membrane, a premacular hemorrhagic bubble will be formed leading to a decreased vision and/or a central scotoma. The visual acuity may decrease to the level of light perception [
4]. Spontaneous reabsorption is possible. However, the time course is unclear. Preretinal bleeding can lead to the formation of epiretinal membranes [
2], and there may also be changes in the retinal pigment epithelium or damage to the photoreceptors from the iron ions [
3,
6]. For this reason, prompt removal of the hemorrhage is important [
7]. Various therapeutic approaches may be used, such as the intravitreal administration of SF
6 gas or a pars plana vitrectomy [
8‐
10]. Opening the posterior hyaloid membrane by laser (referred to as membranotomy) presents a minimally invasive option that had been previously described in the 1970s [
11].