Discussion
Retrobulbar hematoma following the repair of the orbital wall is a rare complication but requires considerable caution because it can cause visual impairment or blindness due to ischemic optic nerve injury or occlusion of the central retinal artery through increased intraocular pressure [
6,
7].
When retrobulbar hematoma occurs, patients present with a variety of signs and symptoms, including circumbulbar pain, reduced visual acuity, blindness, proptosis, pupillary abnormalities, reduced extraocular movements, and increased intraocular pressure. In addition, nausea, vomiting, and headache may also be present [
1‐
7]. Therefore, if such symptoms appear after surgery, it is important to confirm the presence of hematoma by CT scan, and the patient must be referred to an ophthalmologist to check their visual acuity and intraocular pressure.
If CT scans show hematoma and sudden visual impairment, active medical or surgical decompression should be considered to prevent the loss of vision and to recover any reductions in vision as soon as possible [
4‐
6].
In the first case, the central retinal artery was occluded due to postoperative retrobulbar hemorrhage, leading to blindness. The next morning after surgery, the patient developed severe pain, proptosis, and decreased visual acuity. It seems that the bleeding had already advanced and the retinal arteries had begun to compress. In the intraocular pressure test, the patient’s intraocular pressure was not high; thus, it was decided to observe his progress. However, the patient’s impaired vision did not recover, eventually leading to blindness. Therefore, the time of surgical treatment was missed, and as a result, the patient missed their chance for visual recovery.
A central retinal artery occlusion is a very rare complication after surgery of the orbital fracture and is thought to be due to elevated intraocular pressure, mechanical stress, or optic nerve injury [
7]. In this patient, reconstruction of a large orbital wall defect was performed through a transcaruncular approach with relatively poor visual access, and it is thought that there was a considerable pressure on the eyeball during this process. Postoperative bleeding developed into the retrobulbar hematoma, which led to elevated intraocular pressure and optic nerve atrophy. In addition, the effort to completely cover the fracture site may have impeded drainage of the hematoma into the sinus. Therefore, the intraorbital pressure could not be reduced, which is thought to have resulted in central retinal artery occlusion.
Irreversible ischemic damage often occurs within 60 min, and certainly within 2 h; thus, ischemia lasting for just 60–120 min can lead to permanent visual loss [
6,
8‐
11]. Therefore, it is thought that rapid diagnosis and surgical decompression should have been made within at least 2 h.
The second case exhibited severe pain, proptosis, decreased visual acuity, and increased intraocular pressure from the second day of surgery. After the intraocular pressure was checked, lateral canthotomy and cantholysis were performed immediately by the ophthalmologist, and the patient’s intraocular pressure began to drop immediately. Additionally, the access was reopened, and the hematoma was removed under general anesthesia. Compared with the first case, it was thought that aggressive treatment could minimize the sequelae.
Lateral canthotomy and cantholysis are regarded as the treatment of first choice, as an effective method of orbital decompression for sight-threatening acute retrobulbar hemorrhage. This procedure is relatively simple and can be carried out in an outpatient or emergency room setting, under local anesthesia by any member of the medical staff [
12,
13]. It is less clear whether more aggressive management of the source of the hemorrhage and hematoma is needed. Colletti et al. stated that if immediate symptom relief is not seen, one must proceed with open exploration of the orbit in search of the source of the bleed and remove the hematoma [
1].
The third case showed a significant amount of retrobulbar hematoma and exophthalmos on the day after surgery, but the pain was not severe, and the patient exhibited normal vision. Therefore, corticosteroid in a standard dosage was administered, and the patient’s progress was observed. No visual loss or other complications occurred.
There are several guidelines for the treatment of retrobulbar hematoma. Many investigators insist on surgical decompression of the intraorbital region within a short time, but some investigators have reported good results with medical therapy alone [
5,
14]. In addition, some authors have reported that medical therapy was not at all effective, while others have reported that the patients recovered by themselves without any treatment [
15,
16].
Christie et al. analyzed 16 articles and 93 cases of retrobulbar hematoma and reported that time to treatment had a robust correlation with outcomes, which were extremely time-sensitive. A shorter time to treatment was associated with a greater likelihood of full recovery and less likelihood of blindness. While the addition of steroids to surgery was not found to be statistically significant for improving visual outcomes, the overall intervention of steroids (with or without surgery) trended towards an improvement in visual outcomes [
5].
Finally, to prevent retrobulbar hematoma, care should be taken to control bleeding during surgery, and excessive retraction should be avoided. After surgery, an icepack should be applied to reduce swelling and bleeding. Procedures that can increase intraocular pressure should be avoided. For example, valsalva manipulation, which would apply excessive force during sneezing, coughing, nose blowing, waist bending, vomiting, or bowel movement, should be avoided.
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