Neodymium: YAG laser transscleral cyclophotocoagulation for glaucoma after penetrating keratoplasty.

Nd:YAG laser cyclophotocoagulation (CPC) of the ciliary body is a promising cyclodestructive treatment for the management of refractory glaucoma following penetrating keratoplasty. Twenty-eight eyes (27 patients) were treated between August 1985 and September 1987 and followed 6 to 24 months (median, 18 months). The mean intraocular pressure (IOP) was initially 39 mm Hg (range, 30 to 70 mm Hg) on maximally tolerated medications. The Lasag Microrupter 2 was used in the free-running thermal mode with a mean pulse energy of 4.13 J. The laser was retrofocused 3.6 mm from the conjunctival surface and 30 to 50 applications per treatment (mean, 37.5) were given 2 to 3 mm from the limbus for 360 degrees (71%) or 180 degrees (29%). Multiple treatments were necessary in 13 eyes (46%). After CPC, IOP fell to 22 mm Hg or below in 18 eyes (64%) at 3 months, in 20 of 27 eyes (74%) at 6 months, and in 16 to 24 eyes (67%) at 1 year. Inadequate IOP control in four of 28 eyes necessitated cyclocryotherapy in three patients and a Schocket procedure in one other. Of the 14 clear pre-CPC grafts six (43%) became edematous during follow-up. All of the failed grafts had undergone multiple CPCs.

Dysrhythmias caused by histamine release in guinea pig and human hearts.

Histamine is released into the systemic circulation during anaphylaxis, by drugs and by surgical procedures. Studies in animal models have conclusively demonstrated that released cardiac histamine is a major mediator of arrhythmias that occur during anaphylaxis and following the administration of histamine-releasing drugs. Several lines of evidence suggest a similar arrhythmogenic role for cardiac histamine in humans: (1) The human heart is rich in histamine; (2) cardiac histamine can be readily released from human heart in vitro by therapeutic concentrations of drugs; (3) histamine has potent arrhythmogenic effects on the human heart in vitro. Arrhythmogenic effects of histamine include enhancement of normal automaticity, induction of abnormal automaticity, induction of triggered tachyarrhythmias, depression of atrioventricular conduction, and increase in the vulnerability of the ventricles to fibrillation. A combination of H1 and H2 antihistamines is needed to block the arrhythmogenic effects of histamine. Certain arrhythmogenic effects of histamine (e.g. induction of slow responses and delayed afterdepolarizations) can also be blocked by drugs which inhibit the influx of cations through slow channels. In contrast, the commonly-used drug digitalis potentiates the arrhythmogenic effects of histamine. We propose that histamine release produced by drugs and surgical procedures may be an overlooked factor in fatal cardiac arrhythmias. Experimental studies suggest that selective pharmacological methods can be developed to block the arrhythmogenic effects of histamine.