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In: Acute Pancreatitis ISBN: 978-1-63485-229-6
Editor: Shane Copeland © 2016 Nova Science Publishers, Inc.
Chapter 3
OCULAR MANIFESTATIONS OF
ACUTE PANCREATITIS:
PURTSCHER’S RETINOPATHY
Edward Chu
*
, OD, FAAO
Long Beach VA Medical Center, Long Beach, CA, US
Adjunct Faculty Marshall B. Ketchum University, Fullerton, CA, US
Adjunct Faculty Western University of Health Sciences, Pomona, CA, US
ABSTRACT
Purtscher’s retinopathy is a posterior segment condition which is
most often a consequence of head, neck or thoracic injury.
It is a rare
disease that can also be seen in patients who suffer from systemic
disorders such as acute pancreatitis, which commonly occurs when there
is blocked outflow of pancreatic secretions alcohol poisoning. The
complement system, activated during episodes of acute pancreatitis, 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
polygonal patches of retinal whitening are often associated with
significant retinal hemorrhaging. Hemorrhages predominantly are flame-
shaped, dot, or blot, but can also be pre-retinal as well. Other possible
clinical findings include venous dilation, arteriole attenuation, and optic
disk swelling. The retinopathy typically resolves within 1-3 months
*
Eddiechu@gmail.com.
Edward Chu
56
regardless of etiology and treatment. Possible persistent ocular sequelae
include optic disk pallor, retinal pigment epithelium changes, and/or
attenuation of arteries. Decreased bilateral visual acuity, ranging from
mild loss to hand movement, can be accompanied by central, paracentral,
or arcuate pattern visual field loss.
Keywords: Purtscher’s retinopathy, purtscher flecken, pancreatitis,
complement cascade, alcoholism
INTRODUCTION
Pancreatitis complicated by Purtscher’s retinopathy is usually alcohol
related, with few reported exceptions. It has been reported that the
development of Purtscher’s retinopathy is unrelated to the severity of the
pancreatitis and can occur even in mild cases. The outcome and resolution of
ocular complications depends on resolution of the underlying pancreatic
disease. The presence of Purtscher’s retinopathy secondary to acute
pancreatitis has been shown to have negative implications for the patient. In
patients with acute necrotizing pancreatitis, Purtscher’s retinopathy was
associated with multiple organ failure and poor prognosis for the patient.
BACKGROUND
Purtscher’s retinopathy was first described by Otmar Purtscher in 1910.
He fell from a tree and suffered head trauma and loss of consciousness. After
noticing vision changes, there were areas of retinal whitening and hemorrhage
in both eyes. Despite initial vision loss, he made a full recovery without any
treatment. Besides trauma to the head, chest, as well as long bone fracture,
multiple systemic causes for Purtscher’s retinopathy have been reported that
include acute pancreatitis, pancreatic adenocarcinoma, autoimmune disease,
fat embolism syndrome, renal failure, and amniotic fluid embolization. Rare
causes such as thrombotic thrombocytopenic purpura, hemolytic uremic
syndrome, and cryoglobulinemia have been associated with Purtscher’s
retinopathy as well. The overall frequency of Purtscher’s retinopathy is
approximately 0.24 patients/million.
Ocular Manifestations of Acute Pancreatitis
57
OCULAR FEATURES
Purtscher’s Retinopathy usually presents bilaterally with vision loss
ranging from minimal changes to hand movement visual acuity. In most cases,
the vision loss is delayed by 24-48 hours from onset of the underlying
systemic illness. Visual field loss varies patient to patient and can be central,
paracentral, or arcuate in nature. Asymmetric cases can present with an
afferent pupillary defect.
Acute fundus findings include Purtscher flecken, cotton-wool spots,
retinal hemorrhage, and optic nerve swelling. The classic finding of Purtscher
flecken consists of multiple well-defined areas of retinal ischemia in the
superficial layers of the retina, between the arterioles and venules. These
polygon shaped areas range from ¼ to several disk diameters in size. In many
cases, a clear zone between the area of ischemia and adjacent arteriole
corresponds to a capillary free area, approximately 50u on either side of the
retinal arteries and precapillary arterioles. Fundus abnormalities are confined
to the posterior pole and primarily affect the macula and the peripapillary
region, nasal more than temporal. When retinal whitening surrounds the fovea,
a pseudo cherry red spot may develop mimicking ones seen in central retinal
artery occlusions. Due to the ischemic and nerve fiber layer thinning, on
Stratus OCT (Carl Zeiss Meditec, Inc., Dublin, CA) macula scans, patients
have been found to have retinal and macular thickening.
On intravenous fluorescein angiography (IVFA), the retinal swelling from
ischemia may block choroidal fluorescence and areas of non-perfusion can be
observed. Early dye leakage and occlusion of the small terminal peripapillary
arterioles can also be observed. Indocyanine green angiography has also
shown choroidal hypofluorescence, suggesting involvement of the choroidal
circulation in Purtscher’s retinopathy.
As Purtscher’s retinopathy resolves, significant reduction in retinal
thickening relative to the initial visit can be observed and macula OCT scans.
In addition, retinal whitening may be replaced by retinal pigment epithelium
(RPE) mottling, another finding that suggests possible choroidal vasculature
involvement in the acute phase. Optic nerve pallor and vessel attenuation may
also be observed. In one case series, all acute retinal signs resolved in 26% of
eyes within 1 month and all eyes within 6 months.
The diagnosis of Purtscher’s retinopathy is made based on retina
appearance and confirmation of associated systemic disease. With regards to
acute pancreatitis, diagnosis is based on a history of alcohol abuse, epigastric
tenderness, high serum and urinary amylase and lipase, and abdominal
Edward Chu
58
ultrasound or computed tomography scan. Other potential causes of retinal
ischemia include central retinal artery occlusion and branch retinal artery
occlusion. Commotio retinae also needs to be considered with a recent history
of trauma leading to vision changes. However, Purtscher’s retinopathy is
unique in that the symptoms and signs are usually delayed 24-48 hours relative
to the systemic event or trauma, there are no visible emboli, and there is a
clear zone adjacent to the retinal arterioles.
CASE REPORTS AND SERIES IN LITERATURE
Toshniwal PK, et al. Purtscher’s Retinopathy Secondary to Pancreatitis.
Aspects of the topography of retinal abnormalities. Journal of Clinical Neuro-
Ophthalmology 1986; 6 (3): 160-165.
22 year old African American male with history of alcohol abuse was
hospitalized after experiencing severe epigastric pain for 3 days coupled with
recurrent vomiting. On the 2
nd
day of hospitalization, the patient reported
bilateral acute blurring of vision. His vision was measured on the 4
th
day as
counting fingers at 2 feet in right eye and left eye. The fundus exam was
significant for large, dense, confluent, areas of whitening around and between
the disks and maculae. Both maculae had cherry red spot appearance and there
was mild blurring of the optic disk margins in both eyes. At 16 weeks, there
was optic nerve pallor, vascular sheathing, and resolution of all retinopathy;
however, the patient’s vision did not improve and still measured as counting
fingers at 2 feet in both right and left eye.
Campo SM, et al. Acute pancreatitis with Purtscher’s retinopathy: case
report and review of the literature. Dig Liver Dis. 2000 Nov; 32 (8): 729-732.
32 year old man suffering from alcoholism reported to emergency
department with vomiting, fever (39.5 degrees Celsius), and sharp epigastric
pain. Diagnosis of acute pancreatitis was made based on high amylase, high
lipase levels, and computed tomography scans typical for the disease. On day
3 after admission, patient reported bilateral decreased vision measuring 1/10
right eye and 2/50 left eye. Fundus examination revealed retinopathy
characteristic for Purtscher’s retinopathy including pale and swollen optic
nerves, multiple cotton wool spots, and flame shaped and dot blot
hemorrhages. Fluorescein angiography showed multiple areas of ischemia in
both eyes in choroidal and retinal microcirculation. After 4 weeks, vision had
improved and measured 8/10 right eye and 7/10 left eye. The retinopathy had
Ocular Manifestations of Acute Pancreatitis
59
completely resolved with residual pigmented epithelial hypoplasia in the
macular area and pale optic nerves.
Umlas et al. Purtscher’s Retinopathy in a patient with acute pancreatitis.
Ophthalmic Surgery and Lasers: May/Jun 2001; 32, 2: 263-264.
33 year old alcohol man was admitted to hospital with acute pancreatitis.
During hospital stay, the patient noted bilateral blurred vision, best corrected
20/40 right and left upon eye examination. Fundus exam revealed multiple
areas of superficial ischemic retinal whitening and hemorrhages. Eight weeks
after initial presentation patient had complete resolution of retinopathy and
vision was 20/20 right and left eye.
Tai YJ, et al. Sudden Blindness following acute pancreatitis. Intern Med J.
2004 Aug; 34 (8): 518-519.
31 year old male with history of alcohol abuse with upwards of 25 drinks
per day presented to clinic with severe bilateral vision loss. Vision was
reduced to hand movements in both eyes following a week long alcoholic
binge and reported abdominal pain 4 days prior. Retinal exam revealed
multiple cotton wool spots and deep retinal whitening at the macular with
cherry red spots. Patient was referred for alcohol detoxification. On follow-up
eye exam 4 weeks later, clinical appearance had improved, but vision was
measured at less than 6/60 in the right and left eye.
Sharma AG et al. Purtscher’s Retinopathy that occurred 6 months before
acute pancreatitis. Am J Ophthalmology. 2006 Jan; 141 (1): 205-7.
45 year old man with 20 year history of alcohol abuse and chronic
pancreatitis reported a 3 day history of bilateral decreased vision. Visual acuity
was measured at counting fingers right and left eye. Diffuse retinal whitening
and intraretinal hemorrhages were found on dilated fundus examination.
Fluorescein angiography showed macular ischemia in both eyes. Serum
amylase and lipase levels were normal. After 6 months of intermittent
epigastric pain, patient experienced severe and intractable abdominal pain and
was admitted to the hospital for acute pancreatitis. At this visit, repeat blood
work showed markedly elevated serum amylase and lipase levels. Visual
acuity was measured at 20/200 right eye and counting fingers left eye. Fundus
examination revealed near complete resolution of previous retinopathy noted 6
months ago. Authors recommended evaluation for chronic pancreatitis in
patients with history of alcohol abuse and Purtscher’s retinopathy. These
Edward Chu
60
individuals may be at risk for episode of acute pancreatitis in future without
appropriate treatment.
Devonport et al. Purtscher’s Like Retinopathy as presenting feature of
Acute Alcoholic Pancreatitis. Eye (2006) 20, 254-255.
31 year old man reports bilateral vision loss following 24 hours of
abdominal pain and vomiting after binge drinking. He presented to clinic 4
days later with count fingers vision right eye and 6/24 left eye and an afferent
pupillary defect right eye. Fundus examination revealed bilateral cotton wool
spots and retinal and pre-retinal hemorrhages right eye. Pancreatitis was
suspected based on eye exam findings and supported by systemic symptoms,
raised C-reactive protein, and low platelets. After 7 weeks, the visual acuity
was 6/9 right eye and 6/6 left eye with resolution of retinopathy.
Agrawal et al. Purtscher’s Retinopathy: Epidemiology, Clinical Features,
and Outcome. Br J Ophthalmology 2007; 91: 1456-1459.
15 cases were followed over a 12 month period. Acute pancreatitis was the
underlying cause in 3 patients. There was bilateral involvement in all 3 cases
with all 6 eyes presenting with Purtscher flecken and 5 of 6 eyes presenting
with retinal hemorrhages.
Case 1: 36 year old female. Initial acuity was counting fingers right eye
and counting fingers left eye. Final acuity did not improve after resolution of
retinopathy.
Case 2: 38 year old female. Initial acuity was counting fingers right eye
and counting fingers left eye. Final acuity was 6/60 right eye and counting
fingers left eye.
Case 3: 31 year old male. Initial acuity was 6/18 right eye and hand
motion left eye. Final acuity was 6/6 right eye and counting fingers left eye.
Compared to other precipitating factors such as chest compression, and
traffic accidents with or without long bone fracture, the individuals who
suffered from Purtscher’s retinopathy secondary to acute pancreatitis had
worse visual outcomes. Four out of 6 eyes involved had counting fingers
vision at final acuity reading. In addition, 100% of the individuals in the acute
pancreatitis group suffered bilateral involvement compared to 67% and 33% of
the cases precipitated by chest compression and motor vehicle accidents.