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Ocular Manifestations of Acute Pancreatitis
61
Ciortescu I, et al. Purtscher’s-like Retinopathy – A Rare Complication of
Acute Pancreatitis. J Gastrointestin Liver Dis 2011 Dec; 20 (4): 345.
37 year old male with medical history significant for chronic alcohol
consumption presented in Emergency department with acute upper abdominal
pain, nausea, vomiting, sweating, and loss of vision following alcohol abuse.
Visual acuity was .05 in right eye and left eye was 1/50. Ophthalmoscopy
showed cotton wool spots, polygon shaped retinal whitening and retinal
hemorrhages. Fluorescein angiography showed capillary leakage and non-
perfusion of the small arterioles. The patient showed limited improvement in
vision due to macular involvement.
Bonacin D, et al. Purtscher’s retinopathy associated with acute
pancreatitis. Intern Med J. 2012 Mar; 42 (3): 339.
27 year old woman with 6 day history of fever, abdomen pain, nausea and
vomiting reports bilateral loss of vision. Fundus examination revealed cotton
wool spots, flame and dot blot hemorrhages. Fluorescein angiography showed
multiple areas of ischemia in the choroidal and retinal microvasculature in
both eyes. Three weeks later, vision had completely recovered and retinopathy
had resolved.
Dholakia S, et al. Blind drunk. BMJ Case Rep 2013 March 6; 2013.
43 year old Caucasian man admitted to Emergency department with
history of progressive epigastric and abdominal pain. While in hospital, patient
complained about blurred vision in just his left eye. Assessment with
ophthalmology revealed “obvious and sudden reduction in visual acuity.”
Fundus exam showed cotton wool spots and evidence of retinal ischemia. The
patient’s acute pancreatitis resolved within 8 days following admission to
hospital and he was discharged. At his follow-up visit 6 weeks later,
spontaneous visual recovery was observed.
Hamp AM, et al. Purtscher’s Retinopathy Associated with Acute
Pancreatitis. Optom Vis Sci 2014 Feb; 91 (2): e43-51.
57 year old Caucasian presented with acute onset of “holes in my vision”
and decreased bilateral visual acuity 1 week after being admitted to hospital
for acute pancreatitis secondary to alcoholism. He reported classic symptoms
of acute pancreatitis, mainly, lower back and abdominal pain. He admitted to
drinking abusing alcohol for the past 40 years, typically drinking a “pint of
vodka and a couple beers a day,” including the day he was admitted to the
hospital. At the time of hospitalization, his blood alcohol level was 0.20%.
Edward Chu
62
Best corrected visual acuities were 20/100 right eye and 20/50 left eye without
improvement with refraction. Dilated fundus exam revealed deep intraretinal
whitening surrounding the disk and along the arcades. The retinal veins
appeared dilated OU and multiple intraretinal hemorrhages in the posterior
pole were visible. Despite the hemes and ischemic tissue surrounding the optic
nerves, disk margins were distinct and no pallor was visible OU. Patient was
educated on the link between his vision loss and the alcohol-induced
pancreatitis. Alcohol cessation was strongly encouraged and he was referred to
his hospital’s substance abuse rehabilitation program. At his 2 month follow-
up appointment, best corrected visual acuity was 20/30+ right eye and 20/30+
left eye and dilated exam revealed resolution of retinopathy.
PATHOPHYSIOLOGY
One distinct feature of Purtscher’s retinopathy is its predilection for the
posterior pole. This may be explained by the organization of the anatomic
blood supply of the peripapillary and macular areas. With regards 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. The capillary anatomy at the macula
region is distinct in that there are three capillary layers instead of two. Both of
these regions are more vulnerable to embolic occlusion: there are less
arteriolar anastomoses in the peripapillary region, and end vessels that supply
the macula are thought to be more susceptible to ischemia.
Another characteristic feature of Purtscher flecken is an area of normal or
clear retina between the retinal whitening and adjacent arterioles. This zone
represents a capillary-free area on either side of retinal arteries and
precapillary arterioles. This may account for the unique patchy areas of retinal
whitening that distinctly differ from the confluent whitening seen in retinal
artery occlusions and smaller cotton wool spots. The clear zones adjacent to
larger-diameter arterioles, suggests pathology within the precapillary
arterioles, an intermediate-caliber vessel linking larger branch arteries and
smaller capillaries in the nerve fiber layer.
Current evidence suggests that the activation of the complement cascade is
the common link between the wide variety of systemic causes of Purtscher’s
Ocular Manifestations of Acute Pancreatitis
63
retinopathy. One proposed pathophysiology of Purtscher’s retinopathy in acute
pancreatitis involves the release of activated proteases following 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. A single activated complement
component, C5a, can clump granulocytes into masses of ten or more cells in
vitro, which would create the necessary intermediate sized emboli needed to
cause Purtscher’s retinopathy. These emboli can travel to the retinal
circulation and potentially produce Purtscher flecken and other signs of
retinopathy. The size of these aggregates (~50 to 80 um) 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. For reference,
the size of the central retinal artery is 163+/- 17 um, which would easily allow
for the aggregates to pass through retinal circulation until they occlude the
aforementioned precapillary arterioles. Based on animal experiments, the
intermediate size of emboli appears to be critical to reproduce the Purtscher
flecken seen in Purtscher’s retinopathy. Alcohol abuse, a common cause of
acute pancreatitis, can also potentiate the complement activated
leukoembolization of retinal arterioles described above, providing further
support for this theory.
TREATMENT AND MANAGEMENT
Overall, visual outcome of Purtscher’s retinopathy secondary to acute
pancreatitis appears to be variable and unpredictable in the published
literature. In 13 published case reports of Purtscher’s retinopathy specifically
related to acute pancreatitis, initial vision ranged from 20/40 to hand motion
vision. All 13 cases reported retinopathy in both the right and left eye
indicating a predilection for bilateral involvement when the underlying cause
is acute pancreatitis. The length of time for visual recovery ranged from 1
month to 6 months with full visual recovery reported in 10 of 26 eyes (~38%)
and no visual recovery reported in 8 of 26 eyes (~31%). The other eyes
experienced incomplete recovery of their vision by the end of follow-up. In a
recent case report from Hamp and associates, the patient experienced bilateral
improvement in vision with final best corrected visual acuity of at least 20/30
in each eye, significantly better than most published cases. It was unclear from
the case reports why some eyes experienced visual recovery while others did
not.
Edward Chu
64
With regards to treatment of Purtscher’s retinopathy, the role of steroids
may 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. There are a few case reports in the
literature that have shown success with intravenous high-dose steroid:
Wang et al. reported a case involving Purtscher’s retinopathy
secondary to trauma. The patient experienced an improvement in
vision from counting fingers to 6/12 after initial treatment with 1 g of
intravenous methylprednisolone for 3 days and then oral steroids for 3
weeks
Atabay et al. reported successful late recovery of vision after
intravenous methylprednisolone started 3 weeks after initial trauma.
The 25 year old patient was started on 60 mg of oral prednisolone
shortly after injury and diagnosis. After 3 weeks, patient presented
with 20/800 vision and was then treated with intravenous
methylprednisolone at 1 g/day for 3 days. The vision improved to
20/70.
Possible theories to explain the treatment success with high-dose steroids
included stabilization of damaged neuronal membrane and microvascular
channels, which enabled partial recovery of nerve fibers. Another theory stated
that high-dose steroids may inhibit granulocyte aggregation secondary to
activated complement cascade. An experiment on rats showed that
methylprednisolone prevented the granulocyte aggregation that complement
5a usually induces. However, in another case series, patients who were
monitored without treatment experienced greater visual recovery than those
who were given steroids.
Although there have been reports in the literature of success with various
treatments, there is not enough evidence to show an advantage over
observation in Purtscher’s retinopathy. The original case of Purtscher’s
retinopathy reported by Dr. Otmar Purtscher himself resolved without any
treatment. 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 over half of individuals have spontaneous visual recovery without
intervention. The mainstay of therapy remains to treat the underlying systemic
condition.
Ocular Manifestations of Acute Pancreatitis
65
CONCLUSION
Purtscher’s retinopathy is a rare condition most commonly seen in patients
with a history of trauma. Nevertheless, Purtscher’s retinopathy has also been
seen and described in association with various systemic conditions in patients
without 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 the
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. 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 and prepared for the possibility of permanent vision loss.
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BIOGRAPHICAL SKETCH
Name: Dr. Edward Chu, OD, FAAO
Affiliation: Long Beach VA Medical Center
Education:
B.A: Molecular Cell Biology, Minor Business Admin (University of
California, Berkeley)
O.D. Optometry (Berkeley Optometry)
Residency: Ocular Disease, San Francisco VA Medical Center
Address: 5901 E. 7
th
Street, Long Beach, CA 90822
Research and Professional Experience:
Staff Optometrist: Salisbury VA Medical Center, Salisbury, NC (2009-
2014)
Staff Optometrist: Long Beach VA Medical Center, Long Beach, CA
(2014 to present)
Professional Appointments:
Residency Coordinator for Long Beach VA Optometry Program
Adjunct Faculty Ketchum B Marshall University
Adjunct Faculty Western University of Health Sciences
Accreditation Council on Optometric Education – Consultant
Veterans Affairs Field Advisory Committee Recruitment and Retention
American Academy of Optometry Communications Committee
American Academy of Optometry Education Quality Assurance
Committee
Honors:
Fellow in the American Academy of Optometry
Lecturer at annual American Academy of Optometry meeting past 6 years
Publications Last 3 Years:
Chu E. Stroke Awareness: The Role of the Optometrist. California Optometry.
Sept/Oct 2013: 32-34.
Chu E. Vitreous Wick Syndrome and Cystoid Macular Edema: Advanced
Ocular Care. July/August 2013: 63-66.
Chu E. Eye on Stroke Prevention. Review of Optometry. June 2013. 40, 43-44,
46, 48-49.
Chu E. The Topless Optic Disk Syndrome. Advanced Ocular Care. March/
April 2013: 57-58.
Edward Chu
70
Chu E, Hamp A. Branded vs Generic Medications. Review of Optometry.
February 2012. 68-75.
Hamp A, Chu E, Slagle S, Hamp R, Joy J, Morris R. Purtscher’s Retinopathy
Secondary to Acute Pancreatitis. Optometry and Vision Science. 2014
Feb; 91(2): e43-51.