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Purtscher’s Retinopathy Associated with Acute Pancreatitis

Hamp, Ania M.*; Chu, Edward*; Slagle, William S.*; Hamp, Robert C.*; Joy, Jeffrey T.*; Morris, Robert W.*

doi: 10.1097/OPX.0000000000000132

Purpose Purtscher’s retinopathy is a rare condition that is associated with complement-activating systemic diseases such as acute pancreatitis. After pancreatic injury or inflammation, proteases such as trypsin activate the complement system and can potentially cause coagulation and leukoembolization of retinal precapillary arterioles. Specifically, intermediate-sized emboli are sufficiently small enough to pass through larger arteries yet large enough to remain lodged in precapillary arterioles and cause the clinical appearance of Purtscher’s retinopathy. This pathology may present with optic nerve edema, impaired visual acuity, visual field loss, as well as retinal findings such as cotton-wool spots, retinal hemorrhage, artery attenuation, venous dilation, and Purtscher flecken.

Case Report A 57-year-old white man presented with an acute onset of visual field scotomas and decreased visual acuity 1 week after being hospitalized for acute pancreatitis. The retinal examination revealed multiple regions of discrete retinal whitening surrounding the disk, extending through the macula bilaterally, as well as bilateral optic nerve hemorrhages. The patient identified paracentral bilateral visual field defects on Amsler Grid testing, which was confirmed with subsequent Humphrey visual field analysis. Although the patient presented with an atypical underlying etiology, he exhibited classic retinal findings for Purtscher’s retinopathy. After 2 months, best corrected visual acuity improved and the retinal whitening was nearly resolved; however, bilateral paracentral visual field defects remained.

Conclusions Purtscher’s retinopathy has a distinctive clinical presentation and is typically associated with thoracic trauma but may be a sequela of nontraumatic systemic disease such as acute pancreatitis. Patients diagnosed with acute pancreatitis should have an eye examination to rule out Purtscher’s retinopathy. Although visual improvement is possible, patients should be educated that there may be permanent ocular sequelae.


W.G. Hefner Veterans Affairs Medical Center, Salisbury, North Carolina (AMH, EC, JTJ, RWM); Salem Veterans Affairs Medical Center, Salem, Virginia (WSS); and University Eye Associates, Charlotte, North Carolina (RCH).

Ania M. Hamp, 8601 University East Drive Charlotte, NC 28213 e-mail:

Purtscher’s retinopathy is a condition manifested in the retina that is most often a consequence of head, neck, or thoracic injury.1,2 It is a rare condition that can also be seen in patients who have systemic disorders such as acute pancreatitis. Acute pancreatitis often occurs when there is blocked outflow of pancreatic secretions because of gallstones (∼45% cases) or because of metabolic poisoning primarily from alcohol.3 The complement system, activated during episodes of acute pancreatitis,4 may lead to embolization of clumped granulocytes, which can travel to the retinal circulation and potentially produce the Purtscher flecken classically seen with Purtscher’s retinopathy. These typically bilateral and distinctive polygonal patches of retinal whitening (Purtscher flecken) are often associated with significant retinal hemorrhaging, both confined to the posterior pole. Hemorrhages predominantly are flame-shaped, dot, or blot but can also be preretinal in the subhyaloid space. Other possible clinical findings include venous dilation,5 arteriole attenuation,6 and optic disk swelling.6,7 Irrespective of treatment and etiology, the retinopathy typically resolves within 1 to 3 months, with possible persistent ocular sequelae such as disk pallor, retinal pigment epithelium changes, and/or attenuation of arteries. Decreased bilateral visual acuity, ranging from mild loss to no light perception, can be accompanied by central, paracentral, or arcuate pattern visual field loss.6 Besides trauma, multiple systemic causes for Purtscher’s retinopathy have been reported that include autoimmune disease,8 acute pancreatitis,5,7,9–14 fat embolism syndrome,15 pancreatic adenocarcinoma,16 renal failure,17,18 and amniotic fluid embolization.19 Rare causes such as thrombotic thrombocytopenic purpura,20,21 hemolytic uremic syndrome,22 and cryoglobulinemia23 have been associated with Purtscher’s retinopathy as well.

Particularly with systemic causes, other authors and researchers have used specific clinical characteristics relative to retinal vascular anatomy to support an embolic pathogenesis. Notably, the predilection for posterior pole involvement may be related to the anatomic blood supply of the peripapillary and macular areas.24 With regard to retinal vasculature, most of the retina consists of two intraretinal capillary layers with interrelated anastomoses. However, there are two distinct regions of the retina that are the exception to this capillary arrangement: the peripapillary and macular regions. Around the optic disk, there are four layers of capillaries, which account for greater density and thickness of the nerve fiber layer in the arcuate and papillomacular bundles.25 Because of less arteriolar anastomosis in this region, peripapillary capillaries tend to be more vulnerable to embolic occlusion.25 In addition, the capillary anatomy at the macula region is distinct in that there are three capillary layers that exist instead of two. This central retinal area is supplied by end vessels that are thought to be more susceptible to ischemia compared with the anastomosing plexus of capillaries found in the peripheral retina.9 Another characteristic feature of Purtscher flecken is an area of normal or clear retina between the retinal whitening and adjacent arterioles.25 This zone represents a capillary-free area on either side of retinal arteries and precapillary arterioles.25 This may account for the unique patchy areas of retinal whitening that distinctly differ from the confluent whitening seen in branch retinal artery occlusions and smaller cotton wool spots. The appearance of Purtscher flecken, restricted to the posterior pole with clear zones adjacent to larger-diameter arterioles, suggests pathology within the precapillary arteriole(s), an intermediate-caliber vessel linking larger branch arteries and smaller capillaries in the nerve fiber layer.6 Experiments on cats have found that intermediate-sized emboli did in fact produce lesions resembling the retinal whitening seen in Purtscher’s retinopathy, providing further support for this theory.26,27

Intermediate-sized emboli from a variety of sources are capable of inducing retinal changes consistent with the findings in Purtscher’s retinopathy. Purtscher’s retinopathy has been proposed to result from embolic occlusions of the retinal microcirculation secondary to air,2 fat,15 leukocyte aggregates,28 platelets,27 fibrin,27 or amniotic fluid.19 Unilateral Purtscher’s retinopathy in patients with chest compression syndrome is thought to be the result of air emboli.2 Other unilateral cases have also been described after retrobulbar anesthesia and thought to be the result of orbital injection of steroid particles.29–32 Emboli from amniotic fluid have been noted to also cause Purtscher’s retinopathy after childbirth.19 Fat emboli are commonly released into systemic circulation after long-bone fracture, surgery, and acute pancreatitis and therefore thought to be the causative factor under these circumstances.33,34 There have however been questions raised regarding whether fat emboli (5 to 10 μm) are large enough to occlude the 45-μm diameter precapillary arterioles.25 Complement activation also occurs during acute pancreatitis,5,7,9–14 pancreatic adenocarcinoma,16 renal failure,17,18 amniotic fluid embolization,19 thrombotic thrombocytopenic purpura,20,21 hemolytic uremic syndrome,22 and cryoglobulinemia,23 which are all conditions associated with Purtscher’s retinopathy. Complement activation may lead to the aggregation of leukocytes and/or platelets system wide. In the eye, when aggregates are large enough, they may cause vascular occlusion. The size of these aggregates (∼50 to 80 μm) is of sufficient size to pass through larger branch arteries but not small enough to pass through the precapillary beds, therefore, causing occlusion of those vessels.28 For reference, the size of the central retinal artery is 163 ± 17 μm,35 which would easily allow for the aggregates to pass until they occlude the aforementioned precapillary arterioles.

Multiple systemic conditions, which have in common the activation of the complement cascade, can lead to Purtscher’s retinopathy. Acute pancreatitis, precipitated by alcohol poisoning or gallstones, activates the complement cascade and leads to embolization of clumped granulocytes. These intermediate-sized emboli can travel to the retinal circulation and produce the ocular signs and symptoms associated with Purtscher’s retinopathy.

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A 57-year-old white man presented to the eye clinic complaining of severely decreased vision bilaterally. He reported that this occurred 1 week ago while he was hospitalized for acute pancreatitis secondary to alcoholism. He reported that the blur was sudden, and he noted an appearance of “holes in my vision,” which had persisted since the second day of his hospitalization. He denied concomitant photopsia, floaters, or visual dimming before the loss of vision. In addition, there were no previous episodes of any vision loss. He did not report any ocular pain, although he did report “classic” pancreatitis pain, which consisted mainly of lower back and abdominal pain. He subjectively rated the pain at an intensity of 7 on a 10-point scale. His medical history was significant for hyperlipidemia, hypertension, depression, hiatal hernia, and the aforementioned pancreatitis related to alcoholism. No history of autoimmune disease was present nor did he have any skin rashes or joint pain. There was no history of radiation exposure or diabetes. Although his social history was significant for drug and alcohol abuse, he stated that, presently, he was only drinking alcohol and not using any illicit drugs. He admitted to abusing alcohol for the past 40 years, typically drinking a “pint of vodka and a couple of beers a day,” including on the day he was admitted to the hospital. At the time of hospital admittance for acute pancreatitis, his blood alcohol level was 0.20%. Drug screening was negative for benzodiazepines, opiates, amphetamines, cocaine, and cannabinoids. Medications included the following: fluoxetine, gabapentin, ranitidine, naltrexone, thiamine, folic acid, quetiapine, and atenolol. The patient was given supportive treatment for his pain while hospitalized and released after 3 days at which point he came to the Veterans hospital to have an eye examination. His blood pressure measured in the eye clinic was 177/105 mm Hg right arm sitting at 3:00 PM, and the pulse measured 79 beats per minute. The patient reported that he did not take atenolol on the morning of his eye clinic appointment; the last dose was reportedly taken more than 24 hours before his appointment. In addition, he was still in a great deal of pain and experiencing anxiety over his visual loss, which may have contributed to the elevated reading. Review of blood pressure values during the last few years indicated that it predominantly stayed under 140/90 mm Hg. Review of laboratory tests ran at our hospital revealed that he was human immunodeficiency virus (HIV) negative (undetectable HIV antibody by enzyme-linked immunosorbent assay just 3 months before the eye clinic appointment) and had a negative hepatitis C antibody 5 months before the eye clinic appointment. Nonreactive rapid plasma regain (RPR) was noted just 2 months before the eye clinic appointment. Recent complete blood count (CBC) had been evaluated and provided no contributory findings. Lipase and amylase were both elevated, which was expected given the diagnosis of pancreatitis. Because he was seen at an outside civilian hospital, the lipase and amylase values were not accessible; however, they were noted to be elevated by his primary care doctor. Best corrected visual acuities were 20/100 OD and 20/50 OS, without improvement using a pinhole. The refraction was OD: −0.75–1.00 × 080, OS: plano-1.00 × 100. There was an afferent pupillary defect detected in his left eye. The intraocular pressures measured with Goldmann tonometry were 20 mm Hg bilaterally. Anterior segment examination was unremarkable, with trace nuclear sclerosis of the lenses OU. Dilated fundus examination revealed deep intraretinal whitening surrounding the disk and extending along the arcades to the macula OU. The retinal veins appeared dilated OU, the arteries appeared unremarkable OU. There were multiple intraretinal hemorrhages in the posterior pole OU, particularly superior to the nerve OS. Despite the hemorrhages and edematous tissue surrounding the optic nerves, there did not appear to be any blurring of the disc margins or pallor OU (Fig. 1). The left macula was significant for an area of retinal pigment epithelial mottling. The Stratus OCT (Carl Zeiss Meditec, Inc., Dublin, CA) fast macula scan revealed a central subfield thickness of 275 μm, with thickening superior and inferiorly OS as well as significant thickening inferiorly OD, with a central subfield thickness of 353 μm (Fig. 2). Central foveal thickness for healthy eyes measured on the Stratus is 182 ± 23 μm.36





A Humphrey 30-2 visual field OD showed paracentral defects that were denser superiorly. Although the OS field lacked reliability, because of elevated false-negatives, it did show even more extensive central defects that involved all four quadrants and extended all the way to the nasal edge of the 30-2 field (Fig. 3). Via history and review of laboratory test results, other causes for the retinopathy (radiation, HIV, malignant hypertension, hepatitis with interferon treatment, autoimmune disease, diabetes, vascular occlusions, blood disorders, and syphilis) were ruled out, and the patient was diagnosed with Purtscher’s retinopathy OU secondary to acute pancreatitis. The patient was educated on the link between his vision loss and alcohol-induced pancreatitis. Alcohol cessation was strongly encouraged, and referral for substance abuse rehabilitation was offered. To rule out possible undiagnosed and underlying diabetes and to evaluate the level of inflammation, the following laboratory tests were also ordered: CBC, erythrocyte sedimentation rate, C-reactive protein, blood sugar, and hemoglobin A1c. He was educated that the potential for complete resolution of his visual symptoms was unknown. He was scheduled for a fluorescein angiogram and follow-up in 1 week. In addition, subsequent to the eye clinic visit, the patient was sent to the evaluation department of the hospital per policy based on his measured blood pressure and reported pain level, both of which required addressing. The hemoglobin A1c and blood sugar came back unremarkable (4.4% and 137 mg/dL, respectively), and the CBC was again noncontributory. As expected, given the inflammation associated with the pancreatitis, the C-reactive protein came back positive at 1:32, whereas the erythrocyte sedimentation rate was only mildly elevated at 31 mm/h. In the evaluation department, serum amylase and lipase were ordered and found to be elevated: amylase 597 IU/L (reference, 25 to 125 IU/L) and lipase 973 U/L (reference, 22 to 51 U/L), indicating that he continued to have active pancreatitis. He was subsequently cautioned about drinking, his ranitidine was increased, and he was placed on tramadol and discharged from the hospital.



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One-Week Follow-up

The patient returned for 1-week follow-up and reported no noticeable changes to his vision. Best corrected visual acuity was 20/80 OD and 20/50 OS, with a similar refraction compared with that of the initial visit and no improvement on pinhole testing. Dilated retinal examination revealed improvement of clinical appearance of the posterior pole OU, with a marked decrease in the retinal whitening compared with the initial visit (Fig. 1). Stratus OCT fast macula scanning confirmed the marked decrease in thickening, with an 87-μm decrease in central subfield thickness in the right eye and a 71-μm decrease in the left eye (Fig. 2). As expected, the fluorescein angiogram (Fig. 4) did not demonstrate any leakage in the macular region. In the right eye, there was an enlarged area of decreased perfusion at the macula. The macular thickening associated with areas of superficial retinal whitening and swelling therefore looked to be a result of poor perfusion rather than fluid leakage. There were also blocking defects (hypofluorescence) associated with the retinal hemorrhages and areas of pigment clumping OS. Hyperflourescence was noted and associated with retinal pigment epithelium atrophy. The patient tolerated the procedure well and was scheduled for his next follow-up and educated to return to the clinic sooner with any worsening of vision.



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Two-Month Follow-up from Original Visit

The patient returned feeling more optimistic, reporting that his vision, “seemed to be getting better,” although it still looked washed out or faded in certain areas centrally OU. This was a noticeable improvement from his initial examination when he stated that there were areas in his vision that were “gone.” Best corrected visual acuity was 20/30+3 OD and 20/30+1 OS, with no improvement with pinhole testing. The refraction was only mildly changed from initial examination (OD: −1.00–1.25 × 080, and OS: −0.25–1.00 × 115). On dilated examination, the retinal whitening and thickening seen 2 months previously was nearly resolved (Fig. 1). This was confirmed by OCT macula fast scan (Fig. 2), with a 147-μm reduction in central subfield thickness OD and 131 μm decrease OS compared with the initial visit. The OCT also showed loss of the central foveal depression. To further evaluate his central vision, a 10-2 Humphrey visual field was completed. The test revealed paracentral visual field defects indicating that his Purtscher’s retinopathy may have persistent visual ocular sequelae. Findings were discussed with the patient, new spectacle lenses were ordered to improve visual acuity, and a follow-up appointment was scheduled.

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The pancreas is a dual-function gland organ with both endocrine and exocrine functions. The endocrine function involves production of glucagon and insulin, which are important hormones in glucose control. The exocrine system of the pancreas produces digestive enzymes that are secreted into the small intestines and aid in the breakdown of carbohydrates, protein, and fat. Several mechanisms exist that enable the pancreas to avoid digesting itself. These include translating proteins into inactive forms while within the pancreas as well as segregating them into subcellular compartments. Under certain conditions, these protective mechanisms are disrupted and can result in intracellular enzyme activation, pancreatic self-digestion, and acute pancreatitis.37

Acute pancreatitis often occurs because of blocked outflow of pancreatic secretions caused by gallstones or alcohol poisoning.3 There have also been reports of acute pancreatitis occurring as a side effect of HIV medications, which eventually led to Purtscher’s retinopathy.10 The overall mortality rate of patients with acute pancreatitis is 10 to 15% but can be as high as 30% in severe cases that affect respiratory and renal function. Patients often present with epigastric pain that radiates through the back and also report nausea and/or vomiting.5,9,11,12 Diagnosis is based on a history of alcohol abuse, epigastric tenderness, high serum and urinary amylase and lipase, and abdominal ultrasound or computed tomography scan.3 Amylase and lipase are used to diagnose and monitor the treatment of acute pancreatitis. Both are normally produced by the pancreas as well as other glands in the body and are present in higher concentrations in blood and urine with inflammation. Serum amylase and lipase levels can be elevated upward of three times the normal level in patients with pancreatitis.3 Testing should be performed during the acute episode because serum amylase levels can normalize within 3 days.5 Lipase also appears in the blood after pancreatic damage and is useful in late diagnosis of pancreatitis when amylase levels may have returned to normal. Serum lipase elevation is also more specific for acute pancreatitis compared with serum amylase, which can be elevated with other causes of abdominal pain.3

A proposed pathophysiology of Purtscher’s retinopathy involves the release of activated proteases after pancreatic injury or inflammation. Proteases such as trypsin can activate the complement system, specifically, complement C5a, which can cause coagulation and leukoembolization of retinal arterioles.5,11,13,38 Alcohol abuse has been associated with approximately 35% of acute pancreatitis cases.3 Patients usually have a long history of alcohol intake (100 to 150 g ethanol per day), and it has been hypothesized that alcohol can potentiate the complement-activated leukoembolization of retinal arterioles previously described.11 Of note, Purtscher’s retinopathy is not believed to be correlated to the severity of pancreatitis.5,12 There has even been one case reported of an individual presenting with Purtscher’s retinopathy 6 months before experiencing acute pancreatitis.13 Individuals with Purtscher’s retinopathy and a history of alcohol abuse, but without acute pancreatitis, should be evaluated for chronic pancreatitis and monitored closely to minimize the risk of an acute attack in the future.13

Current evidence suggests that the activation of the complement cascade is the common link between the wide variety of systemic causes of Purtscher’s retinopathy. The complement system, activated during episodes of acute pancreatitis,4 may lead to embolization of clumped granulocytes, which can travel to the retinal circulation and potentially produce the Purtscher flecken and other signs of retinopathy. Based on animal experiments on cats and monkeys, the size of the emboli seems to be critical to reproduce the hemorrhages and Purtscher flecken seen in Purtscher’s retinopathy. Animal studies conducted by Ashton and Henkind, found that intermediate-sized glass emboli, 15 to 75 μm in size, are needed to produce Purtscher’s retinopathy.26 It is believed that emboli of this size are sufficiently small enough to pass through larger arteries, yet large enough to remain lodged in precapillary arterioles rather than pass through the capillary beds.28 A single activated complement component, C5a, can clump granulocytes into masses of 10 or more cells in vitro, which would create the necessary intermediate-sized emboli needed to cause Purtscher’s retinopathy.38

In additionally, to further support the role of inflammation in leukoaggregation, it has been noted that both leukoaggregation and free radical–mediated endothelial injury can be inhibited by large doses of steroid. Several reports have noted improvement in vision after high-dosage intravenous steroids.39,40 However, in another case series, patients who were monitored without treatment experienced greater visual recovery than those who were given steroids.41 The role of systemic steroids in the management of Purtscher’s retinopathy is uncertain; however, the clinician should consider the ratio of risks to potential benefits of steroid treatment while taking into account the reports that more than half of individuals have spontaneous visual recovery without intervention.

Overall, visual outcome of Purtscher’s retinopathy secondary to acute pancreatitis seem to be variable and unpredictable. In one report involving 15 cases of Purtscher’s retinopathy, three cases were deemed secondary to acute pancreatitis.41 These were bilateral cases. During an average of 4.5 months, half of all the eyes in the study experienced visual improvement while the other eye had persistent vision loss. The three patients with Purtscher’s retinopathy secondary to acute pancreatitis each had at least one eye, which was count fingers at the final acuity measurement.41 In other case reports of Purtscher’s retinopathy secondary to acute pancreatitis, presenting visual acuity measured between 20/50 and hand motion in the affected eyes, with six of eight eyes experiencing some improvement in vision at the final visual acuity measurement (Table 1).5,7,9,14 Fortunately, our patient experienced bilateral improvement in vision with final best corrected visual acuity of at least 20/30 in each eye, significantly better than that of most published cases.



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Purtscher’s retinopathy is a rare condition most commonly seen in patients with a history of trauma.2 Nevertheless, Purtscher’s retinopathy has also been seen and described in association with various systemic conditions in patients, absent any history of trauma. Polygon-shaped patches of retinal whitening and intraretinal hemorrhages are pathognomonic for Purtscher’s retinopathy and should elicit a thorough history regarding the events leading up to visual changes. Systemic conditions that activate the complement cascade, such as acute pancreatitis, can presumably lead to occlusion of precapillary arterioles and cause bilateral visual acuity and visual field loss. It is important to recognize the potential underlying causes of Purtscher’s retinopathy so they can be appropriately diagnosed and managed to minimize morbidity and mortality.

Ania M. Hamp

8601 University East Drive

Charlotte, NC 28213


Received May 2, 2013; accepted September 18, 2013.

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1. Purtscher O. Noch unbekannte befunde nach schadeltrauma. Ber Tsch Ophthalmol Ges 1910; 36: 294–301.
2. Burton TC. Unilateral Purtscher’s retinopathy. Ophthalmology 1980; 87: 1096–105.
3. Aronson BS. Update on acute pancreatitis. Medsurg Nurs 1999; 8: 9–16.
4. Goldstein IM, Cala D, Radin A, Kaplan HB, Horn J, Ranson J. Evidence of complement catabolism in acute pancreatitis. Am J Med Sci 1978; 275: 257–64.
5. Devonport H, Oworu O, Mohla A, Kolli S, James T. Purtscher’s like retinopathy as the presenting feature of acute alcoholic pancreatitis. Eye (Lond) 2006; 20: 255–7.
6. Agrawal A, McKibbin MA. Purtscher’s and Purtscher-like retinopathies: a review. Surv Ophthalmol 2006; 51: 129–36.
7. Campo SM, Gasparri V, Catarinelli G, Sepe M. Acute pancreatitis with Purtscher’s retinopathy: case report and review of the literature. Dig Liver Dis 2000; 32: 729–32.
8. Sellami D, Ben Zina Z, Jelliti B, Abid D, Feki J, Chaabouni M. [Purtscher-like retinopathy in systemic lupus erythematosus. Two cases]. J Fr Ophtalmol 2002; 25: 52–5.
9. Toshniwal PK, Berman AA, Axelrod AJ. Purtscher’s retinopathy secondary to pancreatitis. Aspects of the topography of retinal abnormalities. J Clin Neuroophthalmol 1986; 6: 160–5.
10. Bui SK, O’Brien JM, Cunningham ET Jr. Purtscher retinopathy following drug-induced pancreatitis in an HIV-positive patient. Retina 2001; 21: 542–5.
11. Jacob HS, Goldstein IM, Shapiro I, Craddock PR, Hammerschmidt DE, Weissmann G. Sudden blindness in acute pancreatitis. Possible role of complement-induced retinal leukoembolization. Arch Intern Med 1981; 141: 134–6.
12. Soledad Donoso Flores M, Narvaez Rodriguez I, Lopez Bernal I, del Mar Alcalde Rubio M, Galvan Ledesma A, Pascasio Acevedo JM, Soria Monge A. Retinopathy as a systemic complication of acute pancreatitis. Am J Gastroenterol 1995; 90: 321–4.
13. Sharma AG, Kazim NA, Eliott D, Houghton O, Abrams GW. Purtscher’s retinopathy that occurred 6 months before acute pancreatitis. Am J Ophthalmol 2006; 141: 205–7.
14. Tai YJ, Testro AG, Hoffman PM. Sudden blindness following acute pancreatitis. Intern Med J 2004; 34: 518–9.
15. Roden D, Fitzpatrick G, O’Donoghue H, Phelan D. Purtscher’s retinopathy and fat embolism. Br J Ophthalmol 1989; 73: 677–9.
16. Tabandeh H, Rosenfeld PJ, Alexandrakis G, Kronish JP, Chaudhry NA. Purtscher-like retinopathy associated with pancreatic adenocarcinoma. Am J Ophthalmol 1999; 128: 650–2.
17. Zwolinska D, Medynska A, Galar A, Turno A. Purtscher-like retinopathy in nephrotic syndrome associated with mild chronic renal failure. Pediatr Nephrol 2000; 15: 82–4.
18. Stoumbos VD, Klein ML, Goodman S. Purtscher’s-like retinopathy in chronic renal failure. Ophthalmology 1992; 99: 1833–9.
19. Blodi BA, Johnson MW, Gass JD, Fine SL, Joffe LM. Purtschers’-like retinopathy after childbirth. Ophthalmology 1990; 97: 1654–9.
20. Patel MR, Bains AK, O’Hara JP, Kallab AM, Marcus DM. Purtscher retinopathy as the initial sign of thrombotic thrombocytopenic purpura/hemolytic uremic syndrome. Arch Ophthalmol 2001; 119: 1388–9.
21. Ong T, Nolan W, Jagger J. Purtscher-like retinopathy as an initial presentation of thrombotic thrombocytopenic purpura: a case report. Eye (Lond) 2005; 19: 359–61.
22. Lauer AK, Klein ML, Kovarik WD, Palmer EA. Hemolytic uremic syndrome associated with Purtscher-like retinopathy. Arch Ophthalmol 1998; 116: 1119–20.
23. Myers JP, Di Bisceglie AM, Mann ES. Cryoglobulinemia associated with Purtscher-like retinopathy. Am J Ophthalmol 2001; 131: 802–4.
24. Dollery CT, Henkind P, Paterson JW, Ramalho PS, Hill DW. I. Ophthalmoscopic and circulatory changes in focal retinal ischaemia. Br J Ophthalmol 1966; 50: 285–324.
25. Michaelson IC, Campbell AC. The anatomy of the finer retinal vessels. Trans Ophthalmol Soc U K 1940; 60: 71–111.
26. Ashton N, Henkind P. Experimental occlusion of retinal arterioles: ssing graded glass ballotini. Br J Ophthalmol 1965; 49: 225–34.
27. Lai JC, Johnson MW, Martonyi CL, Till GO. Complement-induced retinal arteriolar occlusions in the cat. Retina 1997; 17: 239–46.
28. Shapiro I, Jacob HS. Leukoembolization in ocular vascular occlusion. Ann Ophthalmol 1982; 14: 60–2.
29. Blodi BA, Williams CA. Purtscher-like retinopathy after uncomplicated administration of retrobulbar anesthesia. Am J Ophthalmol 1997; 124: 702–3.
30. Lemagne JM, Michiels X, Van Causenbroeck S, Snyers B. Purtscher-like retinopathy after retrobulbar anesthesia. Ophthalmology 1990; 97: 859–61.
31. Wilkinson WS, Morgan CM, Baruh E, Gitter KA. Retinal and choroidal vascular occlusion secondary to corticosteroid embolisation. Br J Ophthalmol 1989; 73: 32–4.
32. Lim BA, Ang CL. Purtscher-like retinopathy after retrobulbar injection. Ophthalmic Surg Lasers 2001; 32: 477–8.
33. Nayak H, Harun S, Palimar P. Purtscher’s retinopathy after fracture dislocation of shoulder joint. Emerg Med J 2005; 22: 831–2.
34. Chuang EL, Miller FS 3rd, Kalina RE. Retinal lesions following long bone fractures. Ophthalmology 1985; 92: 370–4.
35. Dorner GT, Polska E, Garhofer G, Zawinka C, Frank B, Schmetterer L. Calculation of the diameter of the central retinal artery from noninvasive measurements in humans. Curr Eye Res 2002; 25: 341–5.
36. Chan A, Duker JS, Ko TH, Fujimoto JG, Schuman JS. Normal macular thickness measurements in healthy eyes using Stratus optical coherence tomography. Arch Ophthalmol 2006; 124: 193–8.
37. Marieb EN, Wilhelm PB, Mallett J. Human Anatomy, 6th ed. San Francisco, CA: Pearson Benjamin Cummings; 2010.
38. Craddock PR, Hammerschmidt D, White JG, Dalmosso AP, Jacob HS. Complement (C5-a)-induced granulocyte aggregation in vitro. A possible mechanism of complement-mediated leukostasis and leukopenia. J Clin Invest 1977; 60: 260–4.
39. Atabay C, Kansu T, Nurlu G. Late visual recovery after intravenous methylprednisolone treatment of Purtscher’s retinopathy. Ann Ophthalmol 1993; 25: 330–3.
40. Wang AG, Yen MY, Liu JH. Pathogenesis and neuroprotective treatment in Purtscher’s retinopathy. Jpn J Ophthalmol 1998; 42: 318–22.
41. Agrawal A, McKibbin M. Purtscher’s retinopathy: epidemiology, clinical features and outcome. Br J Ophthalmol 2007; 91: 1456–9.

Purtscher’s retinopathy; purtscher flecken; pancreatitis; complement cascade; alcoholism

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