Purtscher's traumatic retinal angiopathy Pathogenesis and sequelae.
- Author:
Sang Ha KIM
1
;
Jung Youn KWON
;
Hui Deok KIM
Author Information
1. Maryknoll Hospital, Busan, Korea.
- Publication Type:Case Report
- MeSH:
Adult;
Atrophy;
Cyanosis;
Exudates and Transudates;
Hemorrhage;
Humans;
Hydrostatic Pressure;
Macular Degeneration;
Male;
Motor Vehicles;
Ophthalmology;
Optic Nerve;
Orbit;
Papilledema;
Prognosis;
Retina;
Retinal Degeneration;
Retinaldehyde*;
Ribs;
Thorax;
Unconsciousness;
Vision Disorders
- From:Journal of the Korean Ophthalmological Society
1972;13(3):177-183
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
In 1910 Purtscher first presented his original report of "angiopathia retinae traumatica" before the German Congress of Ophthalmology in Heidelberg. Since then many varying fundus pictures have been described as "Purtscher's Disease" and many theories have been advanced as to the cause. In 1962 Marr and Marr provided an extensive review of the literature on traumatie retniopathy and pointed out that the cause of Purtscher's retinopathy was an abrupt rise of intravascular pressure in the vessel entering and leaving the orbit, and in most cases the mechanism of the injury was a sudden and violent compression of the chest. Recently we have experienced a case of bilateral Purtscher's traumatic retinal angiopathy leading to optic nerve atrophy and macular degeneraion. Our patient is a 36-year-old previously healthy Korean male. who had his left chest compressed by a truck when he was working in the country farm. Just after the accident he fall into an unconscious state for a short time. Two days after admission he was referred to our ophthalmologic department because of visual impairment. Funduscopic examination revealed Purtscher's retinopathy in both eyes. His chest X-ray examination showed several fractured ribs anterolaterally. Within several days after the accident the whitish retinal exudates and hemorrhages gradually disappeared in the left ocular fundus, but in the right fundus the retinal edema, situated at posterior pole, persisted for about 7 months duration. During this period optic nerve atrophy developed ill the right fundus. As soon as the retinal edema subsided, retinal degeneration of the macular area appeared in the right fundus. Five months after the accident temporal optic nerve atrophy appeared and the patient complained of marked visual impairment in the left eye. We could not find any similar cases in the literature, that is, after the retinopathy and impaired vision recovered, later, the vision was markedly impaired again due to secondary optic nerve atrophy and development of macular Degeneration. In a survey of literature we want to say that the pathogenesis of Purtscher's traumatic retinal angiopathy is due mainly to the result of a sudden and severe increased intravascular pressure. particularly in the upper portion of body. Following points influenced our thought. 1. The ocular fundus changes similar with Purtscher's retinopathy could be seen in hydrostatic pressure syndrome and compression cyanosis syndrome. 2. Purtscher's retinopathy could developed in minor chest compression which is not strong enough to fracture ribs or other banes. 3. Usually Purtscher's retinopathy is developed in both eyes. If unilateral development occurs, it is almost on the right eye. If bilaterally the right eye is more severe than the left. This is postulated due to the shorter venous path to the rijsht eye. In addition, the prognosis of Purtscher's retinopathy seems to be good but poor result such as in our case and other previously reported cases are also possible.
