|DIAGNOSTIC AND THERAPEUTIC CHALLENGES
|Year : 2016 | Volume
| Issue : 1 | Page : 56-60
Is it blunt trauma?
Department of Ophthalmology, Little Flower Hospital, Angamaly, Kerala, India
|Date of Web Publication||11-Nov-2016|
Flat No 101, Sidhi Vinayaka Apartments, Temple Road, Thottakattukara, Aluva/Kochi - 683 108, Kerala
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Nataraj A. Is it blunt trauma?. Kerala J Ophthalmol 2016;28:56-60
A 63-year-old gentleman came to our outpatient department (OPD) with complaints of decreased central field of vision of 1 day duration in the left eye associated with seeing floaters. He provided a history of blunt trauma in the left eye with associated bleeding through the nose 1 week back. No history of loss of consciousness or vomiting following the episode.
Past medical history – He was a known hypertensive on regular medications. His blood pressure recorded at the time of presentation at our centre was 180/110 mm Hg.
Best corrected visual acuity in the right eye was 6/6 and the left eye counting fingers was 2 m. Anterior segment examination showed bilateral immature senile cataract in both the eyes. Indirect ophthalmoscopy showed right eye disc and macula to be normal, CDR 0.3, arteriovenous (AV) nipping along the majorarcades, and periphery were normal.
[Figure 1] shows the fundus right eye and [Figure 2] shows the fundus left eye.
Left eye showed a normal disc, CDR 0.4, subretinal fluid over the macular area with whitening of the posterior pole; blood vessels showed arteriorlar attenuation with AV nipping along the arcades; periphery was normal. Fundus fluorescein angiography (FFA) of the right eye was normal, however, the left eye showed multiple leaks at the macula and inferiorly [Figure 3],[Figure 4],[Figure 5],[Figure 6],[Figure 7],[Figure 8].
Optical coherence tomography (OCT) of the right eye was within normal limits [Figure 9]; left eye OCT showed foveal detachment with turbid fluid [Figure 10]. [Figure 11] shows the OCT of the left eye 2 weeks after the presentation. [Figure 12] and [Figure 13] shows FFA of the left eye 2 weeks after the presentation.
| What Is the Possible Diagnosis and How Would You Manage This Case?|| |
Dr. Mahesh Gopalakrishnan
Senior Retina Consultant, Giridhar Eye Institute, Kochi, Kerala
The positive clues are: (1) History of trauma even though there is a delay in presentation. (2) OCT shows inner retinal whitening. (3) Serous macular detachment is very little. (4) FFA shows diffuse leak. (5) Foveal and retinal atrophy in follow up. (6) No delay in vascular filling in FFA.
My first diagnosis is in favor of trauma-related concussion injury to the posterior pole. Points against are defective vision of 1 day duration when the trauma was 1 week prior to the loss of vision. Probably the vision problem was detected late due to other manifestations such as epistaxis. Moreover, there is no other retinal or subretinal hemorrhage usually seen in trauma. This type of diffuse leak in posterior pole and atrophy of macula can be seen in closed globe injury.
Vascular events such as retinal artery occlusion or combined occlusion can be another diagnosis. Lack of delay in filling in FFA rules out venous occlusion. Further, there are no hemorrhages or tortuous dilated veins. Isolated arterial occlusion is possible, however, there is no cherry red spot or features of central retinal artery occlusion.
Inflammatory pathology such as Harada can be considered, however, OCT shows very little fluid and there is no disc leakage, literally ruling out inflammation.
Putting all together, this looks like a posttraumatic maculopathy with posterior pole whitening leading to macula atrophy.
Dr. Biju Raju
Senior Retina Consultant, Dr NSD Raju's Eye Institute, Kochi, Kerala.
The sudden loss of vision in an uncontrolled hypertensive, more often than not, is secondary to a retinal vascular occlusion. Hypertensive crisis, at times, can lead to fibrinoid necrosis of the choroidal vasculature, and thus result in hypertensive choroidopathy. The near normal appearance of the retinal vasculature, both clinically and angiographically, in the presence of a large area of pale outer retina in the left eye, as seen in this patient, suggests a disturbance in the choroidal circulation. The absence of cherry red spot and a normal retinal arterial filling in fluorescein angiography (FA), rules out central retinal artery occlusion and other vascular retinopathies.
In the early phase of the FA, if one looks at the negative image [Figure 14], the area of hypoperfusion at the outer retina is clearly visible. Going through the phases of the FA, it is evident that there are multiple areas of punctate hyperfluorescence that eventually coalesce to form larger areas of staining with faint leaks at the level of the outer retina, more so within the area of choroidal hypoperfusion. Such changes at the outer retina occur secondary to ischemic damage to the retinal pigment epithelium. This can also manifest clinically as serous detachment, which, in this patient's left eye, has been well-documented on OCT. OCT of the left eye also shows hyper-reflectivity of the inner layers of the retina, a finding for which I have no valid explanation. It is probably due to some hypoperfusion in the central retinal artery, which, in FA probably would have resulted in a delayed arm-to-retina time.
Control of hypertension remains the most important aspect of management. A gradual lowering of blood pressure is recommended in such a situation to prevent other ischemic episodes such as an ischemic optic neuropathy in the better eye, which may result from a deranged autoregulation of blood pressure and flow. However, there is another school of thought that recommends rapid control of hypertension with intravenous antihypertensive management, which will protect the compromised retinal pigment epithelium (RPE) from further irreversible damage and necrosis. This decision is best left to the experts managing hypertension.
An interesting aspect in this patient is the history of trauma 1 week prior to the loss of vision. Blunt trauma can cause Berlin's edema, however, vision loss occurs immediately and then recovers gradually depending upon the severity of the injury. Moreover, the history of uncontrolled hypertension and epistaxis, clearly rules in favor of an acute hypertensive choroidopathy.
Once the hypertension is controlled, the RPE, if ischemic damage was minimal, will recover functionally and a gradual improvement in visual acuity is a possibility. If the ischemic insult on the RPE is severe, these cells would become necrotic, and over a period of time, there could be a loss of photoreceptors and foveal atrophy. Going through the follow-up image of the OCT done in the left eye after adequate control of hypertension, there is resolution of serous fluid along with foveal atrophy, suggesting a severe ischemic damage to the RPE and subsequent retinal atrophy.
Dr. Gopal. S. Pillai
Professor of Ophthalmology, Amritha Institute of Medical Sciences, Kochi, Kerala.
First, this elderly gentleman had a blunt trauma 1 week back and had loss of vision 1 day back. Hence, we can possibly think that the decrease of vision is not due to the blunt trauma. The only other positive history mentioned is regarding hypertension, which is quite significant. From history, I would consider one of the complications of hypertension such as a vascular block, anterior ischemic optic neuropathy or exudative macular detachment secondary to the hypertension as my initial differentials. The only other possibility is that he failed to recognize the decrease of vision in his left eye after trauma, and 1 day back, he noticed the drop in vision.
Examination shows sensorineural detachment in the macular region in the left eye associated with whitening of the posterior pole and hypertensive retinopathy. It may look like a central serous retinopathy (CSR) due to all the tension that he had following his blunt trauma. However, that does not completely explain the 2/60 vision that he exhibited. That can also be explained by a Berlins edema and traumatic optic neuropathy associated with trauma. He may not have noticed the decrease of vision initially. However, that is highly unlikely, as following trauma, one generally tends to notice any change in vision. Usually, Berlin's edema produces more diffuse whitening and a shiny retina, which is absent in this case.
Fundus fluorescein angiography features
Suggestive of initial hypo in the choroidal phase and later leakage and pooling into the sensorineural space. This is not a feature of traumatic Berlin's edema, CSR, or vascular block, which were earlier differentials, but that of a hypertensive choroidopathy. The patient may have had an acute rise in blood pressure, which may have resulted in a choroidal infarct near the posterior pole and caused the sensorineural detachment. The second subsequent FFA shows that the leakage is significantly reduced fast, which may occur in hypertensive choroidopathy.
Optical coherence tomography features
Predominantly, the affection is in the outer retina, fitting closely with our diagnosis. The follow-up OCT shows significant thinning of the fovea rapidly along with scarring, suggesting an acute event.
Even though the blunt trauma predated the decrease of vision by 1 week, posttraumatic Berlins edema is still a differential diagnosis. The other differential is hypertensive choroidopathy.
| Concluding Remarks|| |
Dr. Ashok Nataraj
Senior Retina Consultant, Little Flower Hospital, Angamaly, Kerala.
This elderly gentleman who presented with loss of vision in the left eye with a history of blunt trauma was a diagnostic dilemma. Initial examination of the retina showed features of blunt trauma but findings on further evaluation was not really adding up. FFA showed deeper diffuse leaks at the macula and follow-up angiogram pictures showed choroidal hypoperfusion, which could explain the poor visual outcome. The history of uncontrolled hypertension and high blood pressure on presentation despite being on antihypertensive medication pointed toward a vascular cause such as hypertensive choroidopathy for these peculiar findings. Other findings such as arteriolar attenuation and AV crossing changes also pointed toward hypertensive retinopathy.
OCT of the macula in Berlin's edema usually shows hyper-reflectivity of the photoreceptor layer  corresponding to photoreceptor damage that occurs following blunt trauma. Here, OCT showed turbid SRF at the macula corresponding to RPE damage and ischemia rather than trauma. Moreover, choroidal hypoperfusion is not a very common sequelae of blunt trauma.
To sum up, even though blunt trauma can explain many of the findings in this particular case, a careful examination and a detailed diagnostic evaluation can always shed light on additional factors such as hypertension which can explain this atypical course of events.
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Conflicts of interest
There are no conflicts of interest.
| References|| |
El Matri L, Chebil A, Kort F, Bouraoui R, Largueche L, Mghaieth F. Optical Coherence Tomographic Findings in Berlin's Edema. J Ophthalmic Vis Res 2010;5:127-9.
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10], [Figure 11], [Figure 12], [Figure 13], [Figure 14]