Glaucoma in the immediate postoperative period after penetrating keratoplasty.

In a prospective study 155 consecutive patients undergoing penetrating keratoplasty were examined for postoperative increase in intraocular pressure to determine the frequency and duration of intraocular pressure spikes, risk factors, and response to treatment. Patients were maintained on preoperative glaucoma medications except miotics. Additional medications to lower intraocular pressure perioperatively were not given. Intraocular pressure was measured two to five hours, one day, and one week postoperatively. An intraocular pressure of 30 mm Hg or greater was considered an increase in pressure and was treated according to a standardized protocol. The results were analyzed by procedure as well as by variables commonly perceived to be associated with intraocular pressure increase (history of glaucoma, use of hyaluronate, lysis of the synechiae, or vitrectomy at the time of the operation). Overall, intraocular pressure increases in the early postoperative period occurred in 18 of 155 patients (12%). Pressure increases occurred in ten of 48 patients (21%) with a history of glaucoma; five of 24 patients (21%) undergoing combined penetrating keratoplasty, extracapsular cataract extraction, and posterior chamber intraocular lens implantation; and ten of 43 patients (23%) undergoing vitrectomy at the time of penetrating keratoplasty.

Propionibacterium acnes endophthalmitis after intracapsular cataract extraction.

The authors report a case of Propionibacterium acnes endophthalmitis after intracapsular cataract extraction with implantation of an anterior chamber intraocular lens. The patient's chronic inflammation persisted for 5 years after cataract surgery despite treatment with pars plana vitrectomy, intraocular lens removal, topical and oral steroids, and topical fortified antibiotics. Fluctuations in the inflammation were paralleled by changes in the size and appearance of a white plaque on the posterior corneal surface. Anterior chamber tap cultures were positive for P. acnes after 8 days of incubation under anaerobic conditions. The inflammation was not controlled until the posterior corneal plaque, which was the presumed nidus of the chronic infection, was removed and the patient was treated with intravitreal and oral antibiotics.

Acute angle-closure glaucoma from spontaneous massive hemorrhagic retinal or choroidal detachment. An updated diagnostic and therapeutic approach.

Acute angle-closure glaucoma from a spontaneous massive hemorrhagic retinal or choroidal detachment occurred in five eyes. The source of the hemorrhagic detachment was a disciform macular lesion in all instances. The mechanism for the angle closure is the abrupt forward displacement of the lens-iris diaphragm resulting from the massively detached choroid and retina. Four of the five patients had either systemic hypertension or a primary or anticoagulant-induced clotting disorder. All patients underwent ultrasonographic studies, and one patient had magnetic resonance imaging (MRI) to rule out melanoma. Only one eye required enucleation for pain relief. Glaucoma medication, cyclophotocoagulation, or retrobulbar alcohol controlled the other four eyes. The clinical, ultrasonographic, MRI, and histopathologic features of this rare condition are described, and an updated therapeutic approach is discussed.

Direct observation of the "oxygen paradox" in single rat ventricular myocytes.

By phase contrast microscopy with video length tracking, we followed the sequence of morphological changes in individual isolated rat ventricular myocytes during anoxia followed by reoxygenation. Cells appeared normal during early anoxia. After a duration of anoxia T1, which varied from 17-47 minutes in different cells, each cell abruptly contracted an average of 33% in length to an inert rectangular form presumed to be a rigor state. Cells which were reoxygenated before the onset of rigor showed normal morphology and an unchanged extent of shortening on field stimulation, compared to control. Cells that were reoxygenated after a time in the rigor state, T2, either partially recovered to a shortened rectangular form capable of stimulated twitches or rounded up rapidly to a disordered hypercontracture form. The distribution of T1 was the same for cells which recovered and which hypercontracted. In contrast, the outcome of reoxygenation depended markedly on T2: all cells that were reoxygenated after less than 10 minutes of rigor recovered function, whereas all cells that spent more than 20 minutes in rigor hypercontracted when reoxygenated. The hypercontracture appears to be the cellular analog of the "oxygen paradox" in whole hearts. Its occurrence is reliably related to duration of rigor state but not to duration of hypoxia, because of marked cellular variability in the time of onset of rigor.