Vitreous hemorrhage is a relatively common complication of conventional cataract surgeries, such as ECCE and intracapsular cataract extraction ; however, bleeding from the central artery is rare in these conventional surgeries. Furthermore, bleeding is a rare complication of newer cataract surgeries, such as small-incision phacoemulsification [1, 2, 4]. The causes of vitreous hemorrhage after cataract surgeries have been reported to be wound bleeding [5, 6], iris bleeding after an iris resection, and vascular rupture of the ciliary body and peripheral retina caused by zonular traction .
Herein, we report a case of a massive intraocular hemorrhage after cataract surgery, in which hemostasis was notoriously difficult to achieve. The bleeding site was identified on the nasal side of the optic disc in the second vitreous surgery under general anesthesia, and hemostasis was achieved thereafter. The most common cause of bleeding from the vicinity of the optic disc is bleeding from neovascularization of the disc (NVD). However, in the present case, there were several findings that indicated that the bleeding originated from the central retinal artery and not from NVD. First, the bleeding site did not appear to arise from the optic disc and did not exhibit the characteristics of NVD (which grows with the posterior vitreous face as the scaffold). Hence, direct diathermy to the bleeding sites over the optic disc could not be avoided for obtaining hemostasis. However, there was a limitation in that the intraoperative video was not centered in the area of active bleeding. Second, during the first vitrectomy, bleeding continued even though the IOP increased transiently and the blood was aspirated; thus, it was impossible to identify the hemostatic point. In case of bleeding from NVD, we could have reduced the amount of bleeding by temporarily increasing the IOP, identified the bleeding point, and obtained hemostasis by diathermy coagulation. The present case involved massive intraocular bleeding (which we had never encountered before), and it was extremely difficult to identify the bleeding point and achieve hemostasis. Third, no fundus lesions that could cause NVD, such as those indicative of DR or ischemic ocular diseases, were observed in the affected or fellow eyes before the cataract surgeries by the previous physician. Fourth, no significant carotid artery occlusion, which could cause the ocular ischemic syndrome and lead to NVD, was identified in the bilateral carotid arteries after performing a carotid Doppler test. Lastly, no iris rubeosis or increased ocular pressure suggestive of the ocular ischemic syndrome were observed. Based on these findings, the possibility of bleeding from NVD was low in this case, and we concluded that the bleeding originated from the central retinal artery on the optic disc. Paleness of the retina and the optic disc, which may be observed in the ocular ischemic syndrome, were observed during the vitrectomies in the present case. However, this paleness may have been caused by retinal ischemia, which was attributed to an impaired retinal circulation secondary to bleeding from the central retinal artery. Although the possibility of bleeding from NVD cannot be ruled out completely, we believe that bleeding from the central retinal artery was more likely in the present case.
However, in this case, the perception of light was lost after the second vitrectomy. This could be attributed to the fact that ocular ischemia was associated with bleeding from the central retinal artery; intraoperative findings may reveal paleness of the optic disc and retina, which are attributed to secondary ocular ischemia following bleeding from the central retinal artery. The other possible cause was the direct damage to the optic nerve due to diathermy coagulation. Due to bleeding from the central retinal artery on the optic disc, direct diathermy at the bleeding sites over the optic disc could not be avoided to achieve hemostasis; this procedure can cause a loss of light perception. In contrast, in cases of bleeding from NVD, diathermy away from the optic disc can prevent a loss of light perception.
In this case, the central retinal artery (and not the peripheral retinal blood vessels as previously reported ) was presumed to be damaged. To the best of our knowledge, there are no reports of bleeding from the central retinal artery as the cause of intraocular hemorrhage after cataract surgery. It remains unclear why the damage to the central retinal artery occurred, as this cataract surgery was performed by another physician. As the IOL had dislocated near the bleeding site, it was possible that the use of a larger IOL (7.0 mm) with rigid haptics made of polyvinylidene difluoride may have been associated with the central retinal artery damage, indicating the possibility of mechanical damage by the IOL to the optic disc vasculature.
Suprachoroidal and expulsive hemorrhage are other severe hemorrhagic complications of cataract and intraocular surgeries [3, 7]. The contents of the eye are expelled, especially in case of expulsive hemorrhage, thereby leading to blindness. Moreover, it is important to consider suprachoroidal and expulsive hemorrhage as possible causes of severe hemorrhagic complications; however, in the present case, no choroidal ridge characteristics of suprachoroidal and expulsive hemorrhage were observed before or during surgery.
Perioperative hypertension may increase the risk of blood loss, myocardial ischemia, and cerebrovascular events . Although the BP during the initial surgery under local anesthesia was high at 175/86 mmHg (SBP/DBP), the BP during the second surgery under general anesthesia was low at 125/61 mmHg. Consequently, the second surgery had significantly reduced bleeding  and an improved intraoperative visibility; thus, hemostasis was achieved by intraocular diathermy coagulation of the bleeding site. It is important to maintain a low perioperative BP to reduce bleeding . Therefore, surgery under general anesthesia by an anesthesiologist, and not under local anesthesia by an ophthalmologist, should be recommended in cases of severe arterial bleeding, as in the present case.
In conclusion, we encountered a rare massive intraocular hemorrhage, which probably originated from the central retinal artery after cataract surgery. For massive intraocular hemorrhage after an intraocular surgery, considering the potential for arterial bleeding, local anesthesia by an ophthalmologist may be insufficient to control the BP and stop the hemorrhage; in such cases, surgery with general anesthesia, wherein the BP is controlled by an anesthesiologist, should be considered.