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Case Report Retinal Vein Occlusion in High Altitude Atul Gupta, 1 Surinderpal Singh, 2 Tejinder Singh Ahluwalia, 3 and Anurag Khanna 1 Abstract Gupta, Atul, Surinderpal Singh, Tejinder Singh Ahluwalia, and Anurag Khanna. Retinal vein occlusion in high altitude. High Alt. Med. Biol. 12:393–397.—Staying at high altitude has been reported to be associated with thrombosis in lowlanders. We report 3 cases of retinal vein occlusion in high altitude. Two were males 31 and 37 years of age, who developed nonischemic central retinal vein occlusion while staying at high altitude. The former developed central retinal vein occlusion after 90 days at 6309 m, while the latter was affected at an altitude of 3353 m where he had been for the past 1 year and had recurrence of central retinal vein occlusion in the other eye on re-entry to the same altitude. The third case is that of a 40-year-old female who developed inferotemporal branch retinal vein occlusion on the second day after entry into high altitude (3353 m) by air, while ascending further in a vehicle at an altitude of approximately 4572 m. All three did not have any systemic disease and showed complete recovery on descent to a lower altitude. Key Words: Retinal vein occlusion; high altitude; hypoxia Introduction A scent to high altitude (HA), defined typically as el- evations above 9000 ft (2700 m), exposes individuals to hypobaric hypoxia, cold, and low ambient humidity. Accli- matization to hypobaric hypoxia begins immediately on exposure and continues over days, weeks, and indeed months of stay at HA, thereby reducing the risk of high al- titude illness, and also allowing improved performance at HA. However, some changes that occur in the process of acclimatization itself are implicated in the pathophysiology of HA ailments (e.g., increased hematocrit may lead to chronic mountain sickness). The development of a pro- thrombotic milieu at HA is debatable but well-known effects of HA such as increased hematocrit (Douglas et al, 1913), enforced inactivity, dehydration, and tight clothing may all predispose individuals to thrombosis. An increased risk of spontaneous vascular thrombosis has been reported with prolonged stay at high altitude (Anand et al, 2001). Case reports of thrombosis in people predisposed due to throm- bophilias, but asymptomatic at near sea level suggest that hypoxia may potentiate the effects of such a predisposition. Here, we report three cases of retinal vein occlusion in healthy young individuals with no known predisposing conditions. All three cases were initially managed at a hos- pital at an altitude of 3353 m. Case Histories Case 1 A 31-year-old man, who had been at 6309 m (approx 20,700 ft) for 90 days, developed complaint of sudden onset, painless, and diminution of vision in his right eye accompanied with floaters. He descended over 14 days to a hospital at 3353 m, experiencing some improvement in his vision. Descent had caused his vision to improve from perception of hand movement close to the face to counting fingers at 3 m distance. There was no improvement of vision with pinhole in the right eye. Distance visual acuity in the left eye was 6/6. Case 2 A 37-year-old male sojourner, who had been at an altitude of 11,000 feet (3353 m) for 1 year, developed sudden onset, painless, diminution of vision in the right eye. Visual acuity was reduced to 6/60 in the affected eye, while the left eye had normal vision. Case 3 A 40-year-old female presented with complaint of sudden onset sectorial loss of vision in her right eye involving the superior half of the field of vision. She had arrived a day 1 General Hospital, Ladakh, India. 2 High Altitude Medical Research Centre, Ladakh, India. 3 Command Hospital (NC), Udhampur, India. HIGH ALTITUDE MEDICINE & BIOLOGY Volume 12, Number 4, 2011 ª Mary Ann Liebert, Inc. DOI: 10.1089/ham.2010.1093 393

Retinal Vein Occlusion in High Altitude

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Case Report

Retinal Vein Occlusion in High Altitude

Atul Gupta,1 Surinderpal Singh,2 Tejinder Singh Ahluwalia,3 and Anurag Khanna1

Abstract

Gupta, Atul, Surinderpal Singh, Tejinder Singh Ahluwalia, and Anurag Khanna. Retinal vein occlusion in highaltitude. High Alt. Med. Biol. 12:393–397.—Staying at high altitude has been reported to be associated withthrombosis in lowlanders. We report 3 cases of retinal vein occlusion in high altitude. Two were males 31 and 37years of age, who developed nonischemic central retinal vein occlusion while staying at high altitude. Theformer developed central retinal vein occlusion after 90 days at 6309 m, while the latter was affected at analtitude of 3353 m where he had been for the past 1 year and had recurrence of central retinal vein occlusion inthe other eye on re-entry to the same altitude. The third case is that of a 40-year-old female who developedinferotemporal branch retinal vein occlusion on the second day after entry into high altitude (3353 m) by air,while ascending further in a vehicle at an altitude of approximately 4572 m. All three did not have any systemicdisease and showed complete recovery on descent to a lower altitude.

Key Words: Retinal vein occlusion; high altitude; hypoxia

Introduction

Ascent to high altitude (HA), defined typically as el-evations above 9000 ft (2700 m), exposes individuals to

hypobaric hypoxia, cold, and low ambient humidity. Accli-matization to hypobaric hypoxia begins immediately onexposure and continues over days, weeks, and indeedmonths of stay at HA, thereby reducing the risk of high al-titude illness, and also allowing improved performance atHA. However, some changes that occur in the process ofacclimatization itself are implicated in the pathophysiologyof HA ailments (e.g., increased hematocrit may lead tochronic mountain sickness). The development of a pro-thrombotic milieu at HA is debatable but well-known effectsof HA such as increased hematocrit (Douglas et al, 1913),enforced inactivity, dehydration, and tight clothing may allpredispose individuals to thrombosis. An increased risk ofspontaneous vascular thrombosis has been reported withprolonged stay at high altitude (Anand et al, 2001). Casereports of thrombosis in people predisposed due to throm-bophilias, but asymptomatic at near sea level suggest thathypoxia may potentiate the effects of such a predisposition.Here, we report three cases of retinal vein occlusion inhealthy young individuals with no known predisposingconditions. All three cases were initially managed at a hos-pital at an altitude of 3353 m.

Case Histories

Case 1

A 31-year-old man, who had been at 6309 m (approx 20,700ft) for 90 days, developed complaint of sudden onset, painless,and diminution of vision in his right eye accompanied withfloaters. He descended over 14 days to a hospital at 3353 m,experiencing some improvement in his vision. Descent hadcaused his vision to improve from perception of handmovement close to the face to counting fingers at 3 m distance.There was no improvement of vision with pinhole in the righteye. Distance visual acuity in the left eye was 6/6.

Case 2

A 37-year-old male sojourner, who had been at an altitudeof 11,000 feet (3353 m) for 1 year, developed sudden onset,painless, diminution of vision in the right eye. Visual acuitywas reduced to 6/60 in the affected eye, while the left eye hadnormal vision.

Case 3

A 40-year-old female presented with complaint of suddenonset sectorial loss of vision in her right eye involving thesuperior half of the field of vision. She had arrived a day

1General Hospital, Ladakh, India.2High Altitude Medical Research Centre, Ladakh, India.3Command Hospital (NC), Udhampur, India.

HIGH ALTITUDE MEDICINE & BIOLOGYVolume 12, Number 4, 2011ª Mary Ann Liebert, Inc.DOI: 10.1089/ham.2010.1093

393

before at 3353 m on a 70-min flight from near sea level. On thesecond day at HA, she was ascending further in a vehiclewhen symptoms of visual disturbance occurred at an altitudeof about 15,000 ft (4572 m). Immediate descent was associatedwith partial resolution of symptoms in the 2 hours it took toreach 3353 m. On examination, visual acuity in the right eyewas 6/12 and 6/6 in the left eye.

Diminution in vision was not accompanied by symptomsof redness of the eye, colored halos, headache, metamor-phopsia, flashes, photophobia, or altered sensorium in anypatient. They did not smoke, had not exerted unusually, norsuffered any illness that could lead to dehydration before theonset of symptoms. On the contrary, they had been consum-ing large amounts of fluids as advised by their physicians onascent to high altitude. The patients did not suffer from hy-pertension, diabetes mellitus, or chronic obstructive pulmo-nary disease (COPD), and did not have features suggestive ofhyperthyroidism. The third patient was not on oral contra-ceptives. All patients were found to be healthy on general andsystemic examination.

The eyes were examined by direct as well indirect oph-thalmoscopy, and findings in all patients are summarized inTable 1. The unaffected eye was normal on examination in allcases. Blood hematocrit, coagulation profile, qualitative D-dimer assay (Tulip Diagnostics, India), and routine bio-chemical profile was investigated in all patients and found tobe within normal limits.

Carotid Doppler was performed to rule out atheroma andECG recorded to investigate cardiac pathology. Investigationfindings are presented in Table 2.

Case 1 was diagnosed to have central retinal vein occlusion(CRVO) of the right eye, was hospitalized, and observed forabout 1 week, with no specific treatment. On subsequenttransfer to a hospital near sea level, he was observed forneovascularization of the retina and iris. However, all signsand symptoms resolved spontaneously within 6 weeks. Thesecond case also recovered completely over 8 weeks of stay atnear sea level. On recovery, he returned to high altitude(3353 m). Six months later, he again developed features sug-gestive of CRVO; this time in the left eye. The clinical andocular examination picture resembled that seen earlier in theother eye. Hematological, coagulation, biochemical, and ca-rotid Doppler findings were all within normal limits. He was

then sent to a hospital near sea level with advice not to visithigh altitude areas again. He recovered completely over thenext 6 weeks.

The third case was diagnosed to have inferotemporalbranch retinal vein occlusion of the right eye. She descendedto sea level by air after 48 h. All signs resolved over 4 weeksand she regained full visual acuity of 6/6 in her right eye.

Discussion

Central retinal vein occlusion (CRVO) occurs as a result ofthrombosis at or just behind the lamina cribrosa. At this place,the central retinal vein is bound in a tight adventitial sheathwith the central retinal artery. Also, since the retinal venouscirculation is a relatively high resistance, low flow system, it issensitive to hematological factors. (Morley and Heier, 2004)The mechanisms by which the clinical picture of CRVO occursmay be divided into conditions that produce a physical blockat the lamina cribrosa, and those in which hemodynamicfactors result in obstructed blood flow. These mechanismsprobably coexist in many patients with CRVO. The flow ofblood through the central retinal vein becomes increasinglyturbulent as the vein progressively narrows at the laminacribrosa, where it may be further impinged upon by arterio-sclerosis of the adjacent central retinal artery. The turbulencedamages the endothelium in the retrolaminar vein, whichexposes collagen and initiates platelet aggregation andthrombosis. Thus, as flow velocities increase, the chances ofthrombosis also increase.

The known risk factors for CRVO are systemic hyperten-sion, diabetes mellitus, increased erythrocyte sedimentationrate (ESR), and glaucoma (The Eye Disease Case-ControlStudy Group, 1996). The risk factors for developing branchretinal vein occlusion (BRVO) are similar. In case of BRVO, theblock occurs at arteriovenous crossings where the vessels arebound in a tight adventitial sheath. CRVO and BRVO com-monly affect individuals between 50 and 70 years of age(Hayreh et al, 1994). When these occur below the age of 50years, thrombophilic screening is suggested to exclude acti-vated protein C resistance, lupus anticoagulant, antic-ardiolipin antibodies, elevated factor V Leiden, deficiency ofprotein C or protein S, and antithrombin III levels. (Morleyand Heier, 2004).

Table 1. Summary of Ocular Findings

RAPD Media Optic discRetinalartery Retinal vein Hemorrhage Cotton wool spots Macula

IOT(mmhg)

CASE 1 No Clear Edematous,hyperemic,cup filled

Normal Dilated,tortuousin all quadrants

Superficial anddeep allquadrants

Few allquadrants

Edema,hemorrhage,dull fovealreflex

14

CASE 2 No Clear Edematous,hyperemic,cup filled

Normal Dilated,tortuousin all quadrants

Superficial anddeep allquadrants

Few allquadrants

Edema,hemorrhage,dull fovealreflex

13

CASE 3 No Clear Normal Normal Dilated,tortuousinferotemporalquadrant

Superficialand deepinferotemporalquadrant

Fewinferotemporalquadrant

Edema,hemorrhagein inferiorpart, dullfoveal reflex

10

IOT, intraocular tension; RAPD, relative afferent papillary defect.

394 GUPTA ET AL.

Thrombophilias such as deficient APC (Kappert et al, 2008),Protein S (Nair et al, 2008) and Factor V Leiden mutation havealso been implicated in venous thrombosis, stroke, andmyocardial infarction at high altitude in otherwise healthyindividuals. However, factors other than thrombophilia maycontribute to a greater risk of thrombosis at high altitude.These include hemoconcentration, raised hematocrit, forcedinactivity, constrictive clothing, and extreme cold. The sum ofthese physical and patho-physiological factors appears tomanifest as a greater propensity to thrombosis in acclimatizedlowlanders at HA. Based on the Indian army experience,Anand et al. reported a thirty times greater risk of spontane-ous vascular thrombosis at HA (Anand AC et al, 2001). Anincreased risk of venous thrombosis after long haul flights isalso known and has been suggested to be due to factors otherthan prolonged immobilization (Schreijer et al, 2006). Alteredrheology of blood has been reported at HA (Palareti et al,1984) and platelet numbers, activation, and aggregation havebeen variably reported to be increased, decreased, and unal-tered at high altitude (Chatterji et al, 1982; Hudson et al, 1999;Lehmann et al, 2006; Sharma, 1980). The coagulation cascadeand fibrinolysis have also been studied with inconclusiveevidence for a role in thrombosis at HA. (Bartsch et al, 1989a;1982b; 1989c; Grover and Bartsch, 2001). Increased homo-cysteine levels at HA have been suggested to predispose tothrombosis at HA (Kotwal et al, 2007) and patients with highaltitude pulmonary edema were shown to have systemic en-dothelial dysfunction that may activate coagulation (Bergeret al, 2005). It is, therefore, likely that high altitude exposuremay contribute to venous thrombo-embolism, especially inpeople predisposed by thrombophilias. However, an in-creased predisposition has been difficult to prove because ofthe multifactorial nature of the disease and in the absence ofwell controlled epidemiological studies (Van Veen andMakris, 2008).

As regards hemodynamic factors, retinal circulatory flowand flow velocity have been shown to increase with altitudesup to 5500 m and with duration of stay (Bosch et al, 2009;Frayser et al, 1971; 1974). Accelerated blood flow velocity mayactivate platelets by shear stress or by exposure to the capil-lary basement membrane due to damage caused by high

transmural pressures (Lehmann et al, 2006). The increasedvelocities of flow, as suggested earlier, may lead to increasedturbulence, especially at points of venous narrowing such asthe A-V crossings and behind the lamina cribrosa. This maycause endothelial damage and accentuate platelet activationand aggregation induced by hypobaric hypoxia, therebyprecipitating thrombosis of the retinal vein. This phenomenonmight be accentuated in those predisposed by thrombophiliasor oral contraceptive intake.

The cases reported here did not have any of the known riskfactors. Neither was evidence of increased fibrin formationpresent as seen by the negative D-dimer test. The first twocases did not have history suggesting dehydration, coldexposure, use of tight constrictive clothing, or enforced inac-tivity. The third, who had entered HA a day before devel-oping complaints, had been traveling for 2 h in a vehicle whenshe suffered partial loss of vision. Inactivity could possiblyhave contributed in this case. Hemoglobin values were wellwithin normal limits in all three patients.

This is somewhat surprising in the patient who had spent90 days at extreme high altitude. This however may be amanifestation of nutritional deficiencies reported in up to24.3% of adult Indian men aged 15–49 years (Nair and Iyen-gar, 2009). Bosch et al. have reported stable retinal oxygendelivery throughout a 20-day high altitude expedition con-sequent to increased retinal vessel diameter and greater bloodflow velocity with increasing altitude to 5500 m. Subsequentdecrease in blood flow velocity with altitude has been at-tributed to increase in hematocrit with time spent at altitude(Bosch et al, 2009). Our patient from an extreme altitude lo-cation did not show a commensurate increase in hematocrit.Retinal blood flow velocities are likely to have been high inthis individual leading to venous endothelial damage. Thesecond patient who developed CRVO twice probably sufferedfrom a thrombophilia resulting in a predisposition to venousthrombosis, although this could not be confirmed. The thirdcase might have developed BRVO mainly as a result of in-creased retinal blood flow combined with endothelial dys-function and platelet activation as a result of exposure to acutehypoxia. An element of hemoconcentration known to occurdue to fluid loss early in the process of acclimatization as well

Table 2. Summary of Investigations

Hb PCVBlood sugar

(mg/dl)Serum lipid profile

(mg/dl)PT

(sec)PTTK(sec) INR D-Dimer VDRL ECG

CarotidDoppler

CASE 1 14 gm/dl 42% F-70 TC-187 C-14 C-32 1.2 Negative Nonreactor NAD NormalPP-110 TG-162 P-16 P-34

HDL-40LDL-115VLDL-32

CASE 2 16 gm/dl 45% F-80 TC-190 C-14 C-30 1.2 Negative Nonreactor NAD NormalPP- 120 TG-160 P-16 P-32

HDL-42LDL-113VLDL-35

CASE 3 11 gm/dl 40% F-90 TC-192 C-12 C-30 1.2 Negative Nonreactor NAD NormalPP-130 TG-162 P-14 P-32

HDL-42LDL-110VLDL-40

C, control; F, fasting; P, patient; PP, postprandial; TC, total cholesterol; TG, triglyceride.

RETINAL VEIN OCCLUSION 395

as inactivity (she was traveling in the vehicle for almost 2 hbefore the onset of the symptoms) may also have contributed.

All the possible etiologies are postulations. Thrombophilicscreening in these cases could have helped in further under-standing the mechanism of venous occlusion in high altitude.However, thrombophilias could not be ruled out, owing tolaboratory investigations for these being not available in thehospitals where they were admitted either on presentation athigh altitude or for convalescence near sea level.

We are aware of one earlier report of CRVO and one re-ported case of retinal arterial thrombosis at HA (Butler et al,1992; Anand et al, 2001a). Here we have presented three casesof retinal vein occlusion, all occurring at HA but at differentdurations of stay and at different altitudes. All three occurredin individuals who had no known predisposing conditionsand were in a younger age group than is typical of retinal veinocclusion. One suffered from CRVO twice at a moderate highaltitude. While likely etiologies may differ in all three it is verytempting to see hypobaric hypoxia at HA as the unifyingfactor in causation of retinal vein occlusion in these cases. Inthe face of such likelihood, the role of adequate hydration,regular activity, well fitting and adequate clothing is espe-cially important for prevention of venous thrombosis duringsojourns at HA. This advice may also be relevant for patientssuffering chronic hypoxia at near sea level due to diseasesuch as COPD; especially if they concomitantly have athrombophilia. It may also be relevant to screen patients ofCOPD for thrombophilias, since chronic hypoxia might bethe factor responsible for the higher risk of retinal vein oc-clusion in patients suffering from COPD. The role of hyper-homocysteinemia in venous thrombosis at HA deservesfurther study, especially since the reduced availability of freshvegetables in HA areas might cause elevation of homocysteinethat may be rather easily avoided by supplementation withfolate and vitamins B6 and B12. Dietary supplementationwith folate has been shown to reduce the risk of primarystroke by 18% (Wang et. al, 2007).

Whether patients with thrombophilias should be advisedagainst sojourns at HA may be established only with longi-tudinal cohort studies of such populations ascending to HA.The role of anti-thrombotic prophylaxis in these individuals,allowing successful sojourns at high altitude also needs to beexplored.

Author Disclosure Statement

No competing financial interests exist.

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396 GUPTA ET AL.

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Address correspondence to:Dr Atul Gupta

HNO783Sector16

Panchkula-134109India

E-mail: [email protected]

Received December 13, 2010;accepted in final form July 26, 2011.

RETINAL VEIN OCCLUSION 397