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Endoscopic haemostasis can be effective in non-variceal upper gastrointestinal haemorrhage, and should be regarded as potential front-line treatment. Diverse methods are available, and although no single technique has become firmly established, current evidence favours thermal coagulation and injection therapy.
Krypton laser photocoagulation of the posterior fundus of the rat created white retinal lesions comparable with therapeutic burns in the human. Twenty-four hours after injury, the retinal pigment epithelium was destroyed and the majority of the endothelial cells survived. The choriocapillary lumen was occluded. Bruch's membrane was not fractured nor had it undergone thermal lysis in any area studied but choriocapillary endothelial cell buds invaded the choroidal side of Bruch's membrane. After seven days, cellular protrusions arising from retinal pigment epithelial cells traversed Bruch's membrane through full-thickness defects and entered the choroid. Although intense laser burns may destroy Bruch's membrane, we conclude from this data that many so-called "breaks" in Bruch's membrane following laser therapy are formed by cellular processes and are not caused primarily by laser coagulation.
Peptic ulcer disease remains the most common upper GI hemorrhagic diathesis, except, of course, for esophageal varices. But mucosal lesions such as vascular ectasias and superficial ulcers of Dieulafoy's disease are being increasingly recognized. Therapeutic endoscopic techniques, notably laser coagulation and injection sclerotherapy, may obviate surgery.
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The authors observed three cases (6 eyes) of vaso-occlusive retinopathy associated with the lupus anticoagulant and the related antiphospholipid antibody anticardiolipin. The disease occurred in patients who had no definable autoimmune disease such as systemic lupus erythematosus (SLE) and was characterized by severe bilateral retinal vascular occlusion. There was profound visual loss from intraretinal ischemia as well as vitreous hemorrhage from preretinal neovascularization. Results of laboratory testing showed a prolonged partial thromboplastin time (PTT) in two patients, and the presence of the lupus anticoagulant in all. Treatment with panretinal photocoagulation appeared to stabilize the neovascularization. The role of systemic anticoagulation and immunosuppressive therapy is uncertain.
The early and accelerated atherosclerosis associated with diabetes mellitus is probably multifactorial in origin. Hyperglycemia, in addition to its numerous pathologic effects on lipids, hormonal profiles, the vascular tree, and platelets, is also associated with effects on the fluid phase of coagulation. The most striking abnormality of coagulation described in diabetes mellitus is a decrement in fibrinogen survival that is rapidly reversible with correction of hyperglycemia or the administration of heparin but not with aspirin and dipyridamole administration, suggesting a hypercoagulable state. Abnormalities of clotting factor assays and circulating levels have been reported in patients with diabetes mellitus, but most of these studies are complicated by the controversy over the results being due to diabetes mellitus or due to the presence of vascular lesions concomitant with diabetes. Nevertheless, an increasing amount of evidence implicates the participation of the fluid phase of coagulation in both the initiation and propagation of diabetic vascular complications.
A technique for examining chorioretinal adhesion in vitro investigated the strength of the adhesion resulting from photocoagulation. The adhesion was reduced only within the first days following photocoagulation, returned to normal by the third day and became enhanced at the fourth day, much earlier than previously supposed. Optimal adhesion and enhanced adhesion resulted only when the coagulation intensities used were sufficient to produce clearly visible lesions that became pigmented subsequently; second, best adhesion was produced with spot-diameters of 200 microns and greater; third, even under optimal coagulation conditions, single barriers were not able to resist extensive forcing, even when the exposures were confluent; fourth, only double barriers, consisting of two rows of exposures, were consistently able to withstand prolonged forcing. The best treatment for retinal tears is a double barrier of large, high-intensity coagulation spots, which affords enhanced adhesion after four days.
At the present time, photocoagulation is the treatment of choice of diabetic retinopathy. It is founded on well-defined principles. The results are better than in the non-treated cases, on the condition that the indications are well established and the techniques appropriate. Fluorescein angiography remains indispensable. The objective of the photocoagulation is the destruction of ischaemic and avascular zones by large coagulations (avascular retinal photocoagulation). Depending on the severity and the rapidity of the evolution of the retinopathy, more extensive coagulations have to be performed in non-ischaemic zones (vascular retinal photocoagulation). The association of these two techniques is the so-called panretinal photocoagulation. This step need not be taken at once, but is indicated in some well-defined cases. The newly formed vessels are not coagulated, except when they are intraretinal.
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