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CRAO a Continuing Look at HBOT as a Treatment for this Vascular Event




Reproduced with permission from Wound Care & Hyperbaric Medicine, Vol.1 Issue 3, July-September 2010


A study in retrospect, although now continuing, to determine vision improvement (number of treatments v. time between insult and pressurization) using a standardized protocol v. a randomly picked group not treated with HBOT.



Patients in the region presented signs and symptoms such as deterioration in vision, acute loss of vision, and/or sharp pain in the eye along with vision change associated with ischemic tissue damage. After the etiology was determined to be a vascular event, either HBOT or other recognized modalities were selected. If a hyperbaric oxygen therapy consult was ordered, the patients were treated on the Long Beach Memorial protocol (Hart and Colleagues, JoHM, Vol. 7, No. 1, 1992, page 33-42). Time from event to pressurization ranges from greater than 28 hours to less than four hours. Patients with vascular events not treated with HBOT were treated with other measures such as paracentesis or eye massage. The non-HBOT group had times ranging from greater than 120 hours to less than 12 hours from insult to definitive care. Vision status was monitored using the standard eye chart.



Eight patients treated on the standard protocol had an improvement rate, on average, of 9.125 visual acuity gradations with an average of 14 hours between insult and pressurization. Seven out of eight patients treated with HBOT experienced improvement. Two of the patients had insult greater than 24 hours; one improved remarkably; the other did so minutely. Eight non-HBOT patients had an improvement rate, on average, of 2.13 visual acuity gradations with an average of 36.5 hours between insult and traditional treatments. Only 38 percent of non-HBOT patients had any improvement.



HBOT is a logical treatment for central retinal artery occlusion. This continuing study corroborates improvement of vision using HBOT when the occlusion is under 24 hours, and further study will be needed to determine effectiveness of treatment after a 24-hour period has elapsed.


Addresses Abstract In Circumstance >>>>

A retrospective study of central retinal artery occlusion treated with hyperbaric oxygen therapy in 1994 compared with a randomly picked group of patients not receiving hyperbaric oxygen therapy.

Eight patients with central retinal artery occlusion treated with an intense hyperbaric oxygen therapy regime in 1994.  They improved an average of seven (6.83) visual acuity gradations.  75% had significant (<two gradations) improvement.  The average time between insult and treatment was fourteen hours.  We discouraged treatment if the occlusion was over 24 hours, although one late patient improved remarkably.  Eight patients, picked at random, were used in comparison.  Their improvement averaged two (1.86) visual acuity gradations.  Only 25% improved significantly.  Our report supports the use of hyperbaric oxygen therapy in the treatment of central retinal artery occlusion when begun early.


The objective of hyperbaric oxygen therapy in the treatment of central retinal artery occlusion [CRAO] is to oxygenate and maintain viability of the retina until adequate perfusion has been established. Results were dismal in previous attempts to preserve sight with pressurization three times a day. The intensive treatment protocol in the Journal of Undersea and Hyperbaric Medicine in 1992 (Hart, and colleagues, JoHM, Vol. 7, No. 1, 1992, page 33-42), on the treatment of central retinal artery occlusion with hyperbaric oxygen [HBOT] showed a method much more successful. We adopted their protocol. Dr. Logan Brooks, a retinal specialist, had a regional referral network. He informed his sources of the adoption of the protocol and the patients were mostly funneled through his office. The visual acuity was checked before and after therapeutic efforts by the ophthalmologist. The diagnosis of central retinal artery occlusion was made by an ophthalmologist, frequently with photographs and Fluorescein angiography. The patients were then evaluated for HBOT by the hyperbaric physician. A standard visual chart was used by the HBOT personnel to evaluate vision before and after each treatment. The on-site evaluations helped in modifying the protocol to the response to HBOT.


Protocol >>>>

The protocol of Hart et. al. (Hart, and colleagues, Journal of Hyperbaric Medicine, Vol. 7, No. 1, 1992, page 33-42) was modified slightly to fit this facility's multiplace chamber. The initial treatment consists of 120 minutes at 2.4 atmospheres absolute [ATA]. Oxygen intervals are 20 minutes in length with five minute air breaks. The patient is out of the chamber for 60 minutes. He or she is then treated for 180 minutes at 1.8 ATA. Oxygen breathing intervals are 30 minutes in length with five minute air breaks. At this time a decision is made whether or not to proceed with HBOT. If there has been significant improvement, treatment is continued after a surface interval of 60 minutes. Treatment number three is 120 minutes at 1.8 ATA with 30 minutes on oxygen alternating with five minute air breaks. This regimen is continued for the rest of the first 24-hour period with two hour surface intervals for every 120 minute treatment. For the second 24 hours, the patient has four hour surface intervals for every 120 minute treatment. The third 24 hours consists of six hour surface intervals for every 120 minute treatment. All subsequent treatments are at 2.4 ATA for 90 minutes b.i.d. or t.i.d. The treatments are stopped when vision is stable.


The Patients >>>>

Patients with CRAO that received hyperbaric oxygen therapy from June, 1994, through December, 1994:


*Mr. HUR was exempted from the study after he was found to have arteritis.

Ms. MIT, 83-years-old, was seen on June 10, 1994. She was almost blind in the left eye when the dressing was removed the morning following an extracapsular cataract extraction. The patient had a history of treated hypertension and occasional irregular heart rhythm. The visual acuity in her left eye [OD] was counting fingers [CF]. Central retinal artery occlusion with cherry red spot was diagnosed in her left eye. After five days of hyperbaric oxygen therapy, visual acuity had improved to 20/200. The artery showed good perfusion and a significant disease in the edematous tissue. Although she is legally blind, she has functional vision, if not reading and driving vision.

Mr. AND, a 79-year-old male, awakened June 22, 1994, with light perception [LP] only in the right eye [OS] at 5:30 a.m. The patient had a history of atherosclerotic cardiovascular disease. After five days of HBOT, his visual acuity [VA] was hand motion [HM] only. His VA had improved to 20/200 and then regressed over a five day period. Exam showed the retinal arterial blood flow had been re-established, but there was still opacification of the inner retina. Patient died six months post CRAO.

Mr. BR, a 78-year-old male with a history of hypertension, had a VA of 20/200 in the 00. He had transient loss of vision the previous day. The patient had a superior branch artery occlusion with edema into the macula. HBOT was initiated the same day of presentation. He responded promptly, and two months post hyperbaric oxygen therapy, his VA was 20/40.

Mr. HUB, 77-years-old, with a history of stable atherosclerotic cardiovascular disease, presented on July 21, 1994, for a decrease in vision for a 24-hour period. VA was CF, with fluctuation to 20/400. The patient had a superior branch artery occlusion due to fibrin plugs. With four days of HBOT, the VA was 20/30, with a decrease in retinal edema. VA on August 11, 1994, had stabilized at 20/30.

Mr. BAR, 49-year-old male with significant atherosclerotic cardiovascular disease and diabetes, was seen on July 3, 1994, less than five hours after CRAO. Patient's VA was HM. After two HBOT sessions, his VA was 20/70. The patient developed a pneumo-mediastinum and therapy was discontinued. Patient's VA rapidly deteriorated after treatment ended, and VA was only LP in October, 1994. *Mr. BAR was exempted from the study due to the condition.

Mr. WAL, 70-year-old male with a history of atherosclerotic cardiovascular disease, was seen on September 2, 1994, with CRAO. VA was LP. He received HBOT within four hours of vision loss with gratifying results. VA on November 4, 1994, was 20/40 in OD. Mr. STE, 64-year-old male with no significant past history, presented with acute loss of vision in OD on October 19, 1994. The patient received HBOT within 12 hours of vision loss. Patient had combined CRAO and central retinal vein occlusion. VA was CF, and six days post treatment, VA was 20/25. The fovea reflex, as well as the macular edema, had improved. Three weeks post therapy, VA again deteriorated to CF. Laser ablation of the peripheral retina for cystoid macular edema resulted in 20/25 VA. We believe the HBOT reversed the acute ischemia and the combination relieved the venous stasis sufficiently to preserve VA after laser surgery.

Mr. MCR, 79-year-old male with history of hypertension and atherosclerotic disease, seen on December 27, 1994, for acute vision loss of OS. Patient's VA was HM only. Patient received HBOT within four hours of vision loss for CRAO. Cherry red spot noted, as well as pale optic nerve disc. Patient's VA on February 1, 1995, was 20/50 with no apparent papillary defect.


The Non HBOT Patient >>>>

Patients treated with traditional methods for CRAO. Date of occurrence ranges from April, 1990, to July, 1994.


76-year-old male with decrease in vision to LP in OS for over 36 hours. Patient had a history of hypertension and atherosclerotic cardiovascular disease. Numerous cotton wool spots and a cherry red spot were observed. Paracentisis was performed that day. Three months later, patient's VA was CF.

81-year-old male with decrease in vision to CF for 48 hours. Patient had a history of hypertension. Retinal hemorrhage in papillomacular bundle with macular edema and rosy color was observed. Intravenous fluoroscien angiography [IVFA] was done. Timoptic and Visine were given. One month later, VA was CF, unchanged.

80-year-old male arrived eight hours after loss of vision to CF only. He had no significant history, although a carotid bruit was noted to exist on the left side. An unsuccessful attempt was made with paracentesis and palpation to move the plaque. Diamox and Timoptic were given as well. Three months later, VA was fluctuating and spotty at 20/70.

81-year-old male with loss of vision to CF for 48 hours. He had history of atherosclerotic cardiovascular disease and lung cancer. IVFA revealed a large embolus. One month later, VA was CF.

65-year-old male with loss of vision to CF in OD for greater than 48 hours. He had a history of hypertension. The patient was started on prednisone. Slow flow observed in left central retinal artery, and superior macular occlusion seen with mild staining of artery wall. VA after one year was an astonishing 20/20.

66-year-old male with decrease in vision to CF for less than eight hours. Patient had a history of COPD and melanoma. IVFA was done. Timoptic and Diamox were given. A cherry red spot was observed. After three months, VA was CF.

68-year-old male with decrease in vision to CF for greater than 48 hours. Patient had a history of hypertension, atherosclerotic cardiovascular disease, and chronic renal failure. IVFA and fundus photos [FP] done. After one month, VA was CF.

78-year-old male with decrease in vision to CF for greater than 48 hours. Patient had a history of hypertension, diabetes, and congestive heart failure. IVFA and FP done. Optic nerve pallor, flame shaped hemorrhages, and slightly narrowed arterioles were observed. After one month, VA was CF.


The degree of vascular occlusion and the time between the insult and the treatment seem to have the greatest effect on the outcome. Only two of our HBOT patients failed to get a good result. One patient, Mr. BAR, responded, but developed a pneumo-mediastinum and HBOT had to be discontinued. The improvement from count fingers to 20/70 was lost.

Patients receiving HBOT had times ranging from less than four hours to greater than 24 hours. It was often difficult to establish the time of the occlusion, because several patients awoke to their blindness. Time of onset for the CRAO was measured the moment vision was lost. We tried not to treat patients who were blind for greater than 24 hours, but in extenuating circumstances, such as the only eye, intermittent symptoms, and/or if the ophthalmologist insisted, we would give HBOT two or three times as a trial.

We have not actively attempted to dissolve the obstructing material, but we are considering the use of thrombolytic agents. If the diffusion of oxygen with HBOT from the choroid plexus to the retina maintained viability of the retina while the clots were being dissolved in the immediate post infarct period, our results might be improved.



We believe our experience with HBOT for CRAO justifies continuing its use as the treatment of choice. It is hoped that our experience will encourage more referrals in the favorable first eight hours. The intensive treatment regimen was satisfying to us, and we hope others find it equally effective in preserving vision.





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