Ghost cell glaucoma (GCG) is a type of secondary glaucoma occurs due to long standing vitreous hemorrhage. The  rigid and less pliable degenerated red blood cells (ghost cells) block the trabecular meshwork and increase the pressure inside eyes. Pathophysiology
The ghost cells develop within the vitreous cavity, 1–3 weeks after vitreous hemorrhage. They obstruct the trabecular meshwork and eventually the pressure inside eye (intraocular pressure) increases and leads to glaucoma. A variety of ocular conditions may cause GCG. Main causes include ocular trauma, diabetes, sickle cell disease, uveitis, UGH syndrome, many eye surgeries etc. Signs and symptoms
Myriad small cells may be seen in the aqueous humor during slit lamp examination. Intraocular pressure rises up to 30 to 70 mm Hg. The increased intraocular pressure may cause blurring of vision, headache, brow ache, nausea and/or vomiting. The angle of anterior chamber is seen open with gonioscopy. Complications
If the increased intraocular pressure is uncontrolled, it may lead to optic nerve damage and irreversible visual impairment. Treatment
The condition usually resolves once the vitreous hemorrhage has cleared. But, depending on the seriousness of the increased intraocular pressure, medical or surgical treatment may be advised. If IOP is not so high, medical therapy with aqueous suppressants is preferred. Surgery is advised if the intraocular pressure remains in 40- to 50-mm Hg range even after medical therapy. Anterior chamber can be cleaned by making a small paracentesis in the cornea and irrigating the anterior chamber with a saline solution.
There can be vestibular dysfunction, such as some minor hearing loss after using the medication for 2 to 4 months. A certain block effect of neuromuscular. Can cause allergic reactions: rash, drug fever, facial flushing or pale, asthma, palpitations, sense of suppression in the chest, abdominal pain, anaphylactic shock. Interactions
Combined with an aminoglycoside, it can increase the possibility of ototoxicity, nephrotoxicity and neuromuscular blockage, result in some hearing loss or can continue to deafness. It could be a temporary symptom, but often be permanent. Neuromuscular blockade can lead to skeletal muscle weakness and respiratory depression or paralysis (apnea). Using anti-cholinesterase or calcium salts may release this block. Combined with amphotericin B, vancomycin, bacitracin, paromomycin, cyclosporine, kanamycin, cisplatin, bumetanide, etoric acid, furosemide: Would Increase the possibility of ototoxicity and nephrotoxicity. Combined with antihistamines, buclizine, cyclizine, meclizine, phenothiazines, thioketones, trimethamine, and capreomycin: can ameliorate the symptoms of tinnitus, dizziness or vertigo and other ototoxic symptoms. Combined with anti-neuromuscular block drugs: can antagonize the effect of the anti-neuromuscular block drugs on the skeletal muscle (so need to adjust the dose of the drugs for anti-muscle weakness. Combined with ethyl sulfide isoniazid: may increase the side effects. Combined with methoxyflurane or polymyxin injection: may increase renal toxicity or neuromuscular blockade effect. Combined with opioid: The effect of central respiratory inhibition may increase, lead to prolonged respiratory inhibition or respiratory paralysis (apnea). History
Capreomycin, an antiphlogistic antibiotic which was produced in the United States in 1960, and be applied in clinic in 1968.