RETINAL FAT EMBOLI AS A SEQUELA TO ACUTE PANCREATITIS DAVID M. INKELES, M.D., AND JOSEPH B. WALSH, M.D. Bronx, New York F a t embolism is not uncommon in many organs in cases of acute pancreatitis. H o w ever, the ocular manifestations of acute pancreatitis have not been previously recog nized. T h r e e patients with acute pancreatitis developed a fundus picture compatible with Purtscher's retinopathy. F a t emboli in the retina present as multiple cotton-wool spots around the optic nerve head, often confluent and usually not ex tending past the macula. These are usually accompanied by varying numbers of super ficial hemorrhages. Most cases present bi laterally, but uniocular cases have been re ported. Initially, there are field defects and a decline in visual acuity; the course is, how ever, variable. T h e condition is generally as sociated with trauma, and is thought by many to be the same as Purtscher's 1 angiopathic retinopathy. F a t emboli are found in many other or gans besides the eye, including the brain, lungs, heart, and kidneys. 2 While the most common source is intramedullary fat in long bone fractures, 3 ' 4 emboli also occur after surgical trauma to fatty areas 4 ' 5 and after injections of oily materials and paraffins. 6 T h e y also appear in acute pancreatitis, pre sumably due to enzymatic destruction of omental adipose tissue. 7 ' 8
dilated and responded sluggishly to light. The ocular fundi were unremarkable. Laboratory studies disclosed the following values: serum amylase, 860 dye units/100 ml (nor mal, 45-200) ; and urinary amylase, 1,876 mg/1000 ml. On awakening, he complained of decreased vision. On the sixth hospital day, visual acuity was finger counting at 3 feet in each eye. Pupils were round, 5 mm in diameter, and reacted sluggishly to light. The anterior segments were normal. Ophthalmoscopic examination revealed a large confluence of cotton-wool spots surrounding each disk and extend ing temporally, giving the appearance of a cherryred spot in each macula (Fig. 1). The white mounds were superficial and, in places, obscured the larger retinal vessels. There were superficial flame-shaped hemorrhages in each fundus. On Sept. 8, fluorescein angiography in the left eye revealed nonfilling of several macular arterioles O.S disk diameter off the disk at 3 o'clock, and 1 disk diameter from the disk at 1:30 o'clock (Fig. 2). Capillary perfusion was absent between the disk and the macula. In a 2-disk diameter area, peripapillary superficial hemorrhages were demon strated as several small areas of blocked fluores cence. No leakage was observed in the late phases. A similar picture was present in the right eye. The area of arteriolar nonfilling and capillary nonperfusion, however, was less extensive.
C A S E REPORTS
Case 1—A 40-year-old man was admitfed Aug. 28, 1974, with a three-day .history of epigastric pain, vomiting, and diarrhea. Past medical history included excessive drinking for many years. Physical examination revealed an agitated man in delirium tremens. The pupils were moderately From the Albert Einstein College of Medicine, Montefiore Hospital and Medical Center, Morrisania Hospital, Bronx, New York. This study was sup ported in part by grant EY-00613 of the National Eye Institute, National Institutes of Health. Reprint requests to David M. Inkeles, M.D., Montefiore Hospital and Medical Center, 111 E. 210th St., Bronx, NY 10467.
Fig. 1 (Inkeles and Walsh). Case 1. Right eye. The inner portion of the sensory retina surrounding the optic nerve is partially opacified by confluent whitish areas. Superficial retinal hemorrhages are present.
935
936
AMERICAN JOURNAL OF OPHTHALMOLOGY
Fig. 2 (Inkeles and Walsh). Case 1. Left eye in the venous phase. Nonfilling of several arteries is noted (arrows). Large areas of capillary nonperfusion are present, most marked between the disk and the macula. On Sept. 17, there was slight clearing of the exudates. Visual acuity was finger counting at 3 feet in both eyes. By Nov. 21, all of the cotton-wool spots had disappeared but visual acuity had only improved to R.E.: 20/200, and L.E.: 6/200. Case 2—A 26-year-old woman presented on Sept. 24, 1973, with a complaint of blurred vision in both eyes for one week. Previous ocular history was un remarkable. Eleven days previously she had been
Fig. 3 (Inkeles and Walsh). Case 2. Right eye. Superficial white fluffy patches are scattered throughout the posterior pole. Superficial retinal hemorrhages are present.
NOVEMBER, 1975
hospitalized for five days with acute pancreatitis occurring after alcoholic abuse. Visual acuity was R.E.: 20/25, and L.E.: 20/30. At the posterior pole in each eye, a normal optic disk was surrounded by multiple cotton-wool spots and a few flame hemorrhages, extending to 2 disk diameters. These changes were most marked in the area between the disk and macula (Fig. 3). A fluorescein angiogram demonstrated multiple small areas of capillary nonperfusion, temporal to both disks and extending somewhat beyond the maculae. A few small areas of blocked fluorescence were present, representing superficial hemorrhages. In the late phases, mild intraretinal leakage oc curred (Fig. 4). The patient was lost to follow-up. Case 3—A 34-year-old man presented on Sept. 21, 1961, with a history of painless blurred vision in both eyes for several weeks. He was a heavy drinker who had recently been discharged from another hospital with the diagnosis of acute pan creatitis and delirium tremens. Corrected visual acuity was 20/50 in both eyes. Findings were confined to the posterior pole. The disks appeared hyperemic but flat. The arteries were burnished with some slight nicking at the arteriovenous crossings. Multiple cotton-wool spots were present throughout the posterior poles, extending to just beyond the maculae. Some superficial flame hemorrhages were also noted in the same distribu tion (Fig. 5). The peripheral retinas were unre markable. Fluorescein angiograms were unavailable. The patient was lost to follow-up. DISCUSSION
In 1910, Purtscher 1 described posttraumatic retinal changes consisting of multiple
Fig. 4 (Inkeles and Walsh). Case 2. Right eye in the late phase. Scattered areas of intraretinal leakage of fluorescein are present in the posterior pole.
VOL. 80, NO. S
RETINAL FAT EMBOLI
937
white spots with scattered hemorrhages. He ascribed the changes to a sudden increase of cerebrospinal fluid pressure. Stahli9 and Best10 felt the condition was similar to Berlin's edema and due to a sudden increase in venous pressure. However, Urbanek, 11 in 1934, provided the first clinicopathologic correlation of traumatic retinopathy and fat emboli by demonstrating fat in both retinal and choroidal vessels. He proposed that this was the cause of Purtscher's retinopathy. Additional clinicopathologic studies12"14 of Purtscher's retinopathy have been published, demonstrating fat emboli in retinal and uveal vessels. These reports seem to establish fat emboli as the most probable explanation of Purt Fig. 5 (Inkeles and Walsh). Case 3. Left eye. scher's retinopathy. In 1964, Ash ton and Superficial white areas are present throughout the Henkind" produced cotton-wool spots and posterior pole and several superficial hemorrhages superficial hemorrhages experimentally, us are present. The dark spots just inferior to the disk are artifacts from the old carbon-arc fundus ing glass emboli of various diameters. Yet, camera. despite both pathologic and experimental evidence for emboli as the cause of Purt cases of acute pancreatitis and demonstrated scher's retinopathy, the presence of this pic fat emboli in the heart, lung, and brain. In ture after traumatic incidences that did not another patient who died after a period of involve fractures led some to question recovery, the kidneys were fibrotic and 8 whether a concurrent or separate physio Lynch speculated that the original insult logic process might be involved. Marr and had probably been fat emboli. Marr, 16 Spaeth,17 Madsen,18 and Duane19 There have not been any reported fluoresproposed causes based on vessel damage cein angiograms in patients who were later secondary to suddenly increased intraocular proven to have fat emboli in the eye at venous pressure. While plausible, this has autopsy. There have been several studies yet to be demonstrated clinicopathologically. of patients with the clinical picture of The presence of fat emboli in a patient Purtscher's disease after trauma. Amalric 20 who died of acute pancreatitis was first re and Bonnin cited a case that showed small 21 7 ported by Edmondson and Fields in 1942. areas of arteriolar occlusion. Kelly dem The patient was a 48-year-old man who died onstrated areas of leakage without areas of 22 reported a case in nine hours after admission to the hospital nonperfusion. Gass with the clinical diagnosis of acute pan which white material lay between and also creatitis. The peripancreatic tissue had se anterior to the retinal vessels. There were vere necrosis with both calcium soaps and superficial hemorrhages, areas of capillary free fat present. The omental venules and nonperfusion, and other areas in which the lymphatics had free fat within their lumina. capillary bed was obscured by the white The lungs had many vessels with fat drop lesion. There was late leakage in the retina. lets, ranging from the size of a platelet to Gass felt the confluent appearance and super those so large as to occlude the capillary ficial location of the exudate made it dif completely. The heart was similarly involved. ferent from the typical cotton-wool patches caused by embolic infarction. He concluded The eyes were not mentioned. that they were the result of exudates forcibly 8 In 1954, Lynch stained for fat in two
938
AMERICAN JOURNAL OF OPHTHALMOLOGY
extruded from the retinal vessels. He also felt that much of the loss of transparency was due to edema of the perivascular retinal cells. Both of our patients who had fluorescein angiography showed areas of retinal arteriolar and capillary nonperfusion and obscura tion of the background fluorescence as de scribed by Gass.22 We propose that embolic phenomena explain this angiographic find ing. Ashton and Henkind 15 showed that emboii could produce cotton-wool type le sions in the nerve fiber layer at the posterior pole. The occlusion of many small posterior polar arterioles could account for the areas of nonperfusion as well as the massive con fluence of cotton-wool spots that could ob scure retinal vessels. Ashton and Henkind15 also noted that retinal edema accompanied the emboii. Initially it was a slight haze but later in the first week it became dense white and well delineated from the unaffected sur rounding tissue. Both the confluent cotton wool spots and this dense white edema are present in our patients. In our three patients, the ophthalmoscopic appearance of large areas of confluent cot ton-wool spots and superficial hemorrhages is best explained by occlusion of small arterioles and capillaries. This theory was proposed in 1961 by G. N. Wise (unpub lished data). The fluorescein angiograms lend support to this conclusion in the two cases in which this diagnostic test was per formed. The experimental work of Ashton and Henkind,15 occluding arterioles with glass beads, produced a clinical result essen tially identical to our cases. Their subsequent pathologic studies showed the obstruction was at the arteriolar level with loss of capil lary bed in the area originally supplied by the obstructed vessel. SUMMARY
A clinical picture of Purtscher's retinop athy was observed in three patients with acute pancreatitis. In two patients, fluores cein angiography revealed arteriolar obstruc tion. Since fat emboii occur in pancreatitis,
NOVEMBER, 1975
and since fat emboii may produce the picture of Purtscher's retinopathy, we proposed that fat emboii caused the retinal findings in these patients. REFERENCES
1. Purtscher, O.: Noch unbekannte befunde nach schadeltrauma. Ber. Otsch. Ophthalmol. Ges. 36: 294, 1910. 2. Scuderi, C. S.: Fat embolism. Surg. Gynecol. Obstet. 72:732, 1941. 3. Lehman, E. P., and Moore, R. M.: Fat em bolism. Arch. Surg. 14:621, 1927. 4. Gauss, H.: Studies in cerebral fat embolism. Arch. Intern. Med. 18:76, 1916. 5. Morgan, 0. G.: Some cases of fat embolism of the retina. Trans. Ophthalmol. Soc. U. K. 69: 441, 1949. 6. Shiba, S.: Experimented untersuchungen uber die embolie der netzhaut und aderhaut. Al brecht von Graefe's Arch. Ophthalmol. 63:393, 1906. 7. Edmondson, H. A., and Fields, I. A.: Rela tion of calcium and lipids to acute pancreatic ne crosis. Arch. Intern. Med. 69:177, 1942. 8. Lynch, M. J.: Nephrosis and fat embolism in acute hemorrhagic pancreatitis. Arch. Intern. Med. 94:709, 19S4. 9. Stahli, J.: Zur kenntnis der angiopathia retinae traumatica. Klin. Monatsbl. Augenheilkd. 55:300, 1915. 10. Best, F.: Commotio retinae als fernwirkung. Klin. Monatsbl. Augenheilkd. 63:578, 1919. 11. Urbanek, J.: Uber fettembolie des auges. Albrecht von Graefe's Arch. Ophthalmol. 131:147, 1934. 12. Fritz, M. H., and Hogan, M. J.: Fat embolization involving the human eye. Am. J. Oph thalmol. 31:527, 1948. 13. DeVoe, A. G.: Ocular fat embolism. Arch. Ophthalmol. 43:857, 1950. 14. Kearns, T. P.: Fat embolism of the retina. Am. J. Ophthalmol. 41:1, 1956. 15. Ashton, N., and Henkind, P.: Experimental occlusion of retinal arterioles. Br. J. Ophthalmol. 49:225, 1965. 16. Marr, W. G., and Marr, E. G.: Some obser vations on Purtscher's disease. Am. J. Ophthalmol. 54:693, 1962. 17. Spaeth, E. B.: Traumatic liporrhagia retinalis (Verhoeff). Arch. Ophthalmol. 31:191, 1944. 18. Madsen, P. H.: Traumatic retinal angiop athy. Acta Ophthalmol. 43:776, 1965. 19. Duane, T. D.: Valsalva hemorrhagic reti nopathy. Am. J. Ophthalmol. 75:637, 1973. 20. Amalric, P., and Bonnin, P.: L'angiographic fluoresceine. Bull. Soc. Ophtalmol. Fr. Suppl. 141, 1969. 21. Kelly, J. S.: Purtscher's retinopathy related to chest compression by safety belts. Am. J. Oph thalmol. 74:278, 1972. 22. Gass, J. D. M.: Stereoscopic Atlas of Macular Diseases. St. Louis, C. V. Mosby, 1970, pp. 185-188.
dilated and responded sluggishly to light. The ocular fundi were unremarkable. Laboratory studies disclosed the following values: serum amylase, 860 dye units/100 ml (nor mal, 45-200) ; and urinary amylase, 1,876 mg/1000 ml. On awakening, he complained of decreased vision. On the sixth hospital day, visual acuity was finger counting at 3 feet in each eye. Pupils were round, 5 mm in diameter, and reacted sluggishly to light. The anterior segments were normal. Ophthalmoscopic examination revealed a large confluence of cotton-wool spots surrounding each disk and extend ing temporally, giving the appearance of a cherryred spot in each macula (Fig. 1). The white mounds were superficial and, in places, obscured the larger retinal vessels. There were superficial flame-shaped hemorrhages in each fundus. On Sept. 8, fluorescein angiography in the left eye revealed nonfilling of several macular arterioles O.S disk diameter off the disk at 3 o'clock, and 1 disk diameter from the disk at 1:30 o'clock (Fig. 2). Capillary perfusion was absent between the disk and the macula. In a 2-disk diameter area, peripapillary superficial hemorrhages were demon strated as several small areas of blocked fluores cence. No leakage was observed in the late phases. A similar picture was present in the right eye. The area of arteriolar nonfilling and capillary nonperfusion, however, was less extensive.
C A S E REPORTS
Case 1—A 40-year-old man was admitfed Aug. 28, 1974, with a three-day .history of epigastric pain, vomiting, and diarrhea. Past medical history included excessive drinking for many years. Physical examination revealed an agitated man in delirium tremens. The pupils were moderately From the Albert Einstein College of Medicine, Montefiore Hospital and Medical Center, Morrisania Hospital, Bronx, New York. This study was sup ported in part by grant EY-00613 of the National Eye Institute, National Institutes of Health. Reprint requests to David M. Inkeles, M.D., Montefiore Hospital and Medical Center, 111 E. 210th St., Bronx, NY 10467.
Fig. 1 (Inkeles and Walsh). Case 1. Right eye. The inner portion of the sensory retina surrounding the optic nerve is partially opacified by confluent whitish areas. Superficial retinal hemorrhages are present.
935
936
AMERICAN JOURNAL OF OPHTHALMOLOGY
Fig. 2 (Inkeles and Walsh). Case 1. Left eye in the venous phase. Nonfilling of several arteries is noted (arrows). Large areas of capillary nonperfusion are present, most marked between the disk and the macula. On Sept. 17, there was slight clearing of the exudates. Visual acuity was finger counting at 3 feet in both eyes. By Nov. 21, all of the cotton-wool spots had disappeared but visual acuity had only improved to R.E.: 20/200, and L.E.: 6/200. Case 2—A 26-year-old woman presented on Sept. 24, 1973, with a complaint of blurred vision in both eyes for one week. Previous ocular history was un remarkable. Eleven days previously she had been
Fig. 3 (Inkeles and Walsh). Case 2. Right eye. Superficial white fluffy patches are scattered throughout the posterior pole. Superficial retinal hemorrhages are present.
NOVEMBER, 1975
hospitalized for five days with acute pancreatitis occurring after alcoholic abuse. Visual acuity was R.E.: 20/25, and L.E.: 20/30. At the posterior pole in each eye, a normal optic disk was surrounded by multiple cotton-wool spots and a few flame hemorrhages, extending to 2 disk diameters. These changes were most marked in the area between the disk and macula (Fig. 3). A fluorescein angiogram demonstrated multiple small areas of capillary nonperfusion, temporal to both disks and extending somewhat beyond the maculae. A few small areas of blocked fluorescence were present, representing superficial hemorrhages. In the late phases, mild intraretinal leakage oc curred (Fig. 4). The patient was lost to follow-up. Case 3—A 34-year-old man presented on Sept. 21, 1961, with a history of painless blurred vision in both eyes for several weeks. He was a heavy drinker who had recently been discharged from another hospital with the diagnosis of acute pan creatitis and delirium tremens. Corrected visual acuity was 20/50 in both eyes. Findings were confined to the posterior pole. The disks appeared hyperemic but flat. The arteries were burnished with some slight nicking at the arteriovenous crossings. Multiple cotton-wool spots were present throughout the posterior poles, extending to just beyond the maculae. Some superficial flame hemorrhages were also noted in the same distribu tion (Fig. 5). The peripheral retinas were unre markable. Fluorescein angiograms were unavailable. The patient was lost to follow-up. DISCUSSION
In 1910, Purtscher 1 described posttraumatic retinal changes consisting of multiple
Fig. 4 (Inkeles and Walsh). Case 2. Right eye in the late phase. Scattered areas of intraretinal leakage of fluorescein are present in the posterior pole.
VOL. 80, NO. S
RETINAL FAT EMBOLI
937
white spots with scattered hemorrhages. He ascribed the changes to a sudden increase of cerebrospinal fluid pressure. Stahli9 and Best10 felt the condition was similar to Berlin's edema and due to a sudden increase in venous pressure. However, Urbanek, 11 in 1934, provided the first clinicopathologic correlation of traumatic retinopathy and fat emboli by demonstrating fat in both retinal and choroidal vessels. He proposed that this was the cause of Purtscher's retinopathy. Additional clinicopathologic studies12"14 of Purtscher's retinopathy have been published, demonstrating fat emboli in retinal and uveal vessels. These reports seem to establish fat emboli as the most probable explanation of Purt Fig. 5 (Inkeles and Walsh). Case 3. Left eye. scher's retinopathy. In 1964, Ash ton and Superficial white areas are present throughout the Henkind" produced cotton-wool spots and posterior pole and several superficial hemorrhages superficial hemorrhages experimentally, us are present. The dark spots just inferior to the disk are artifacts from the old carbon-arc fundus ing glass emboli of various diameters. Yet, camera. despite both pathologic and experimental evidence for emboli as the cause of Purt cases of acute pancreatitis and demonstrated scher's retinopathy, the presence of this pic fat emboli in the heart, lung, and brain. In ture after traumatic incidences that did not another patient who died after a period of involve fractures led some to question recovery, the kidneys were fibrotic and 8 whether a concurrent or separate physio Lynch speculated that the original insult logic process might be involved. Marr and had probably been fat emboli. Marr, 16 Spaeth,17 Madsen,18 and Duane19 There have not been any reported fluoresproposed causes based on vessel damage cein angiograms in patients who were later secondary to suddenly increased intraocular proven to have fat emboli in the eye at venous pressure. While plausible, this has autopsy. There have been several studies yet to be demonstrated clinicopathologically. of patients with the clinical picture of The presence of fat emboli in a patient Purtscher's disease after trauma. Amalric 20 who died of acute pancreatitis was first re and Bonnin cited a case that showed small 21 7 ported by Edmondson and Fields in 1942. areas of arteriolar occlusion. Kelly dem The patient was a 48-year-old man who died onstrated areas of leakage without areas of 22 reported a case in nine hours after admission to the hospital nonperfusion. Gass with the clinical diagnosis of acute pan which white material lay between and also creatitis. The peripancreatic tissue had se anterior to the retinal vessels. There were vere necrosis with both calcium soaps and superficial hemorrhages, areas of capillary free fat present. The omental venules and nonperfusion, and other areas in which the lymphatics had free fat within their lumina. capillary bed was obscured by the white The lungs had many vessels with fat drop lesion. There was late leakage in the retina. lets, ranging from the size of a platelet to Gass felt the confluent appearance and super those so large as to occlude the capillary ficial location of the exudate made it dif completely. The heart was similarly involved. ferent from the typical cotton-wool patches caused by embolic infarction. He concluded The eyes were not mentioned. that they were the result of exudates forcibly 8 In 1954, Lynch stained for fat in two
938
AMERICAN JOURNAL OF OPHTHALMOLOGY
extruded from the retinal vessels. He also felt that much of the loss of transparency was due to edema of the perivascular retinal cells. Both of our patients who had fluorescein angiography showed areas of retinal arteriolar and capillary nonperfusion and obscura tion of the background fluorescence as de scribed by Gass.22 We propose that embolic phenomena explain this angiographic find ing. Ashton and Henkind 15 showed that emboii could produce cotton-wool type le sions in the nerve fiber layer at the posterior pole. The occlusion of many small posterior polar arterioles could account for the areas of nonperfusion as well as the massive con fluence of cotton-wool spots that could ob scure retinal vessels. Ashton and Henkind15 also noted that retinal edema accompanied the emboii. Initially it was a slight haze but later in the first week it became dense white and well delineated from the unaffected sur rounding tissue. Both the confluent cotton wool spots and this dense white edema are present in our patients. In our three patients, the ophthalmoscopic appearance of large areas of confluent cot ton-wool spots and superficial hemorrhages is best explained by occlusion of small arterioles and capillaries. This theory was proposed in 1961 by G. N. Wise (unpub lished data). The fluorescein angiograms lend support to this conclusion in the two cases in which this diagnostic test was per formed. The experimental work of Ashton and Henkind,15 occluding arterioles with glass beads, produced a clinical result essen tially identical to our cases. Their subsequent pathologic studies showed the obstruction was at the arteriolar level with loss of capil lary bed in the area originally supplied by the obstructed vessel. SUMMARY
A clinical picture of Purtscher's retinop athy was observed in three patients with acute pancreatitis. In two patients, fluores cein angiography revealed arteriolar obstruc tion. Since fat emboii occur in pancreatitis,
NOVEMBER, 1975
and since fat emboii may produce the picture of Purtscher's retinopathy, we proposed that fat emboii caused the retinal findings in these patients. REFERENCES
1. Purtscher, O.: Noch unbekannte befunde nach schadeltrauma. Ber. Otsch. Ophthalmol. Ges. 36: 294, 1910. 2. Scuderi, C. S.: Fat embolism. Surg. Gynecol. Obstet. 72:732, 1941. 3. Lehman, E. P., and Moore, R. M.: Fat em bolism. Arch. Surg. 14:621, 1927. 4. Gauss, H.: Studies in cerebral fat embolism. Arch. Intern. Med. 18:76, 1916. 5. Morgan, 0. G.: Some cases of fat embolism of the retina. Trans. Ophthalmol. Soc. U. K. 69: 441, 1949. 6. Shiba, S.: Experimented untersuchungen uber die embolie der netzhaut und aderhaut. Al brecht von Graefe's Arch. Ophthalmol. 63:393, 1906. 7. Edmondson, H. A., and Fields, I. A.: Rela tion of calcium and lipids to acute pancreatic ne crosis. Arch. Intern. Med. 69:177, 1942. 8. Lynch, M. J.: Nephrosis and fat embolism in acute hemorrhagic pancreatitis. Arch. Intern. Med. 94:709, 19S4. 9. Stahli, J.: Zur kenntnis der angiopathia retinae traumatica. Klin. Monatsbl. Augenheilkd. 55:300, 1915. 10. Best, F.: Commotio retinae als fernwirkung. Klin. Monatsbl. Augenheilkd. 63:578, 1919. 11. Urbanek, J.: Uber fettembolie des auges. Albrecht von Graefe's Arch. Ophthalmol. 131:147, 1934. 12. Fritz, M. H., and Hogan, M. J.: Fat embolization involving the human eye. Am. J. Oph thalmol. 31:527, 1948. 13. DeVoe, A. G.: Ocular fat embolism. Arch. Ophthalmol. 43:857, 1950. 14. Kearns, T. P.: Fat embolism of the retina. Am. J. Ophthalmol. 41:1, 1956. 15. Ashton, N., and Henkind, P.: Experimental occlusion of retinal arterioles. Br. J. Ophthalmol. 49:225, 1965. 16. Marr, W. G., and Marr, E. G.: Some obser vations on Purtscher's disease. Am. J. Ophthalmol. 54:693, 1962. 17. Spaeth, E. B.: Traumatic liporrhagia retinalis (Verhoeff). Arch. Ophthalmol. 31:191, 1944. 18. Madsen, P. H.: Traumatic retinal angiop athy. Acta Ophthalmol. 43:776, 1965. 19. Duane, T. D.: Valsalva hemorrhagic reti nopathy. Am. J. Ophthalmol. 75:637, 1973. 20. Amalric, P., and Bonnin, P.: L'angiographic fluoresceine. Bull. Soc. Ophtalmol. Fr. Suppl. 141, 1969. 21. Kelly, J. S.: Purtscher's retinopathy related to chest compression by safety belts. Am. J. Oph thalmol. 74:278, 1972. 22. Gass, J. D. M.: Stereoscopic Atlas of Macular Diseases. St. Louis, C. V. Mosby, 1970, pp. 185-188.
