Journal of Pediatric Ophthalmology and Strabismus

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Short Subjects 

Carbon Monoxide Poisoning: A Patient With Bilateral Internuclear Ophthalmoplegia and Exotropia

Mohammad Etezad Razavi, MD; M. Khalife, MD

Abstract

Carbon monoxide poisoning, which occurs in poorly ventilated areas, is associated with different symptoms and signs. This report describes an 8-year-old girl with severe carbon monoxide intoxication, scattered retinal nerve fiber layer and subhyaloid hemorrhages, and exotropia with bilateral internuclear ophthalmoplegia.

Abstract

Carbon monoxide poisoning, which occurs in poorly ventilated areas, is associated with different symptoms and signs. This report describes an 8-year-old girl with severe carbon monoxide intoxication, scattered retinal nerve fiber layer and subhyaloid hemorrhages, and exotropia with bilateral internuclear ophthalmoplegia.

From the Mashad Eye Research Center, Medical University of Mashad, Mashad, Iran.

The authors have no financial or proprietary interest in the materials presented herein.

Address correspondence to Mohammad Etezad Razavi, MD, Khatam-Al-Anbia Eye Hospital, Vakil Abad Ave., No 47, Ghadir Street, Medical University of Mashad, Mashad, Iran.

Received: June 12, 2008
Accepted: September 24, 2008
Posted Online: May 21, 2010

Introduction

Carbon monoxide is an odorless, colorless, and tasteless product of incomplete fuel combustion. Because of its ubiquitous but silent presence, it is one of the leading causes of poisoning death.1 The systemic clinical symptoms of carbon monoxide poisoning are highly variable. The mild symptoms are often mistaken for other etiologies, such as viral illness, the flu, gastroenteritis, or food poisoning.2,3

Physical examination may show different signs affecting all organ systems. Neurologic or neuropsychiatric signs include memory disturbance (most common), including retrograde and anterograde amnesia with amnesic confabulatory states.2 Ophthalmologic signs reported include flame-shaped retinal hemorrhage, bright red retinal veins (a sensitive early sign), papilledema, and homonymous hemianopia.4,5

No report was found in the literature on specific ocular motility problems predictive of localized hypoxic insult of the internuclear pathways.

Case Report

An 8-year-old girl presented to the authors’ clinic with severe visual loss and outward ocular deviation in the left eye after severe carbon monoxide poisoning.

The current patient was admitted to the toxicology ward of Mashhad University of Medical Sciences, Mashhad, Iran, along with her 30-year-old father, 28-year-old pregnant mother, and 11-year-old brother. The patient and other family members had a history of 48 hours of inhaling carbon monoxide gas from a poorly ventilated gas stove in a closed room. Adequate life support procedures were performed during transport from home to the hospital. Unfortunately, the 11-year-old boy had cardiopulmonary arrest and died at the site of the accident.

The fetus was aborted as a result of fetal arrest. The father and the mother had no residual sequelae as a result of carbon monoxide toxicity. No history of medical problems was recorded for the family members.

At the time of admission, the current patient was unconscious, with bilateral dilated pupils, blood pressure of 100/70 mm Hg, pulse rate of 72 beats per minute, respiratory rate of 13 breaths per minute, and body temperature of 37.2°C. No other cardiopulmonary signs were noted.

The patient was properly treated with hyperbaric oxygen therapy. Twelve hours after admission, the patient became conscious. She was safely discharged after 1 week.

During hospitalization, the patient had blurred vision and outward deviation of the left eye. At the time of discharge, eye examination showed visual acuity of 20/20 in the right eye and 20/800 in the left eye. In addition, examination showed 35 prism diopters of exotropia in the left eye with −3 adduction limitation and abducting nystagmus of the right eye in right gaze. The right eye had −1 limitation of adduction (Fig. 1).

The Left Eye Shows 35 Prism Diopters of Exotropia with −3 Adduction Limitation. The Right Eye Has −1 Limitation of Adduction.

Figure 1. The Left Eye Shows 35 Prism Diopters of Exotropia with −3 Adduction Limitation. The Right Eye Has −1 Limitation of Adduction.

Both pupils measured 3 mm, with fair pupillary response. Findings on slit-lamp examination were normal. Fundus examination showed several patchy subhyaloid retinal hemorrhages, which were more prominent in the left eye (Fig. 2).

(A and B) Fundus Photographs of (A) the Right Eye and (B) The Left Eye Show Several Patchy Subhyaloid Retinal Hemorrhages that Are More Prominent in the Left Eye.

Figure 2. (A and B) Fundus Photographs of (A) the Right Eye and (B) The Left Eye Show Several Patchy Subhyaloid Retinal Hemorrhages that Are More Prominent in the Left Eye.

The patient was evaluated for visual and motility outcomes, and no therapy was required. Results of eye examination 1 month after the first visit included visual acuity of 20/20 in the right eye and 20/400 in the left eye. Exotropia was reduced to 25 prism diopters in the left eye, and −2 limitation of adduction remained. There was full motility of the right eye, with a lesser amount of abduction nystagmus. Funduscopic examination showed partial absorption of subhyaloid hemorrhages.

At the last follow-up 1 year after CO poisoning, visual acuity in both eyes was normal (20/20), with normal contrast vision (functional acuity contrast test) and high-grade stereopsis (60 seconds of arc; Titmus test).

There was no deviation of the left eye, and normal ocular motility was evident (Fig. 3). Fundus examination showed that the subhyaloid retinal hemorrhages were completely resolved without any sequelae.

One Year After Carbon Monoxide Poisoning, Ocular Motility Is Normal.

Figure 3. One Year After Carbon Monoxide Poisoning, Ocular Motility Is Normal.

Discussion

Carbon monoxide is a colorless, odorless gas produced by the combustion of organic (carbon-containing) materials. The most common causes of carbon monoxide poisoning are indoor fires, gas stoves, furnaces, and automobiles, usually in poorly ventilated areas.

Carbon monoxide binds to hemoglobin with an affinity 210 to 280 times greater than that of oxygen. It also causes hemoglobin to hold on to oxygen, preventing release to tissues. The result is tissue hypoxia. The areas most affected are those that have high oxygen demands, especially the brain and heart. Hemoglobin carbon monoxide levels often do not reflect the clinical picture, although symptoms typically begin with headaches at levels of approximately 10%. Levels of 50% to 70% may result in seizure, coma, and even death. Other signs include stupor, coma, gait disturbance, movement disorders, and rigidity. Patients display brisk reflexes, apraxia, agnosia, tic disorders, hearing and vestibular dysfunction, central blindness, and psychosis.2

Accidental carbon monoxide poisoning at home typically occurs during severe winter weather because of the use of defective or improperly installed household appliances that operate on combustible fuel (gas, oil, coal, wood, and kerosene).6 A second factor is poor ventilation as a result of blocked chimneys, improper venting of appliances, and overzealous home insulation, as occurred in the current case.

The symptoms and signs of carbon monoxide poisoning vary. Because of the insidious and often nonspecific manifestations of carbon monoxide toxicity, a high level of suspicion is needed, particularly when individuals or groups living or working together present with an afebrile influenza-like illness or are found with unconsciousness of uncertain etiology.2,3,7

Qyrdedi et al.8 concluded that visual outcome seems to be favorable even if hyperbaric oxygen treatment is started as late as 6 to 8 days after exposure to carbon monoxide. The current patient was treated with hyperbaric oxygen after 48 hours of exposure to carbon monoxide gas. She had two significant ocular problems. At first, there was scattered retinal nerve fiber layer and subhyaloid hemorrhages in both eyes, but more severe in the left eye, which caused significant visual loss (Fig. 2). Macular involvement of the left eye caused severe visual impairment, which was completely resolved after 1 year. In one case series, retinal hemorrhages were found in all patients with carbon monoxide exposure for longer than 12 hours (including approximately 50% of the patients in the series).9 Case studies and series suggested that retinal hemorrhages may occur superficially or deeper in the nerve fiber layer (flame hemorrhages), with a tendency to be peripapillary. In general, these changes reflect the extent of the hypoxic insult to the retina.4

Carbon monoxide poisoning may result in focal and diffuse neuropathologic changes, especially basal ganglia lesions.10 Damage to the basal ganglia may cause ocular dipping distinguished by slow downward eye movement with rapid upward movement.11

Another specific sign in the current case is the adduction limitation of both eyes, especially on the left side, without any other duction limitations. This bilateral adduction limitation was accompanied by nystagmus in the abducting eyes. These features indicate bilateral internuclear ophthalmoplegia.

Internuclear ophthalmoplegia results from a lesion of the medial longitudinal fasciculus, the pathway that connects the sixth and third cranial nerve nuclei to coordinate conjugate horizontal eye movements. Features of internuclear ophthalmoplegia include slow ipsilateral adduction (the hallmark sign), abducting nystagmus, and possibly skew deviation. Common causes of internuclear ophthalmoplegia are demyelinating disease in younger patients (especially when bilateral) and vascular insufficiency in older patients.12

There is no previous report of such specific hypoxic brain stem damage with typical features of bilateral internuclear ophthalmoplegia with exotropia after carbon monoxide intoxication.

In addition, left exotropia accompanied by bilateral internuclear ophthalmoplegia resembles “wall-eyed” bilateral internuclear ophthalmoplegia syndrome, which is a large-angle exodeviation that may occur when bilateral internuclear ophthalmoplegia is caused by a lesion near the third cranial nerve nuclei.

Hypoxic and ischemic insult may cause damage to the brain stem at the level of the medial longitudinal fasciculus and third nerve nucleus. In the current patient, the damage fortunately resolved with hyperbaric oxygen therapy and the passage of time.

References

  1. Fisher J. Carbon monoxide poisoning: a disease of a thousand faces. Chest. 1999;115:322–323. doi:10.1378/chest.115.2.322 [CrossRef]
  2. Heckerling PS, Leikin JB, Maturen A, et al. Predictors of occult carbon monoxide poisoning in patients with headache and dizziness. Ann Intern Med. 1987;107:174–176.
  3. Fisher J, Rubin KP. Occult carbon monoxide poisoning. Arch Intern Med. 1982;142:1270–1271. doi:10.1001/archinte.142.7.1270 [CrossRef]
  4. Ferguson LS, Burke MJ, Choromokos EA. Carbon monoxide retinopathy. Arch Ophthalmol. 1985;103:66–67.
  5. Simmons IG, Good PA. Carbon monoxide poisoning causes optic neuropathy. Eye. 1998;12:809–814.
  6. Howell J, Keiffer MP, Berger LR. Carbon monoxide hazards in rural Alaskan homes. Alaska Med. 1997;39:8–11.
  7. Kasanof D. Could it be carbon monoxide poisoning?Patient Care. November15, 1983;154–177.
  8. Qyrdedi T, Ay H, Togrol E, Yildiz S, Ersanli D. Visual loss as a late complication of carbon monoxide poisoning and its successful treatment with hyperbaric oxygen therapy. Swiss Med Wkly. 2004;134:650–655.
  9. Kelley JS, Sophocleus GJ. Retinal haemorrhages in subacute carbon monoxide poisoning: exposures in homes with blocked furnace flues. JAMA. 1978;239:1515–1517. doi:10.1001/jama.239.15.1515 [CrossRef]
  10. Foley JF, Weaver LK, Fearing MA, Hopkins RO. Basal ganglia lesions following carbon monoxide poisoning. Brain Inj. 2006;20:273–281. doi:10.1080/02699050500488181 [CrossRef]
  11. Ropper AH. Ocular dipping in anoxic coma. Arch Neurol. 1981;38:297–299.
  12. American Academy of Ophthalmology. Basic and Clinical Science Course, Section 5. San Francisco: Author; 2004–2005:231–232.
Authors

From the Mashad Eye Research Center, Medical University of Mashad, Mashad, Iran.

The authors have no financial or proprietary interest in the materials presented herein.

Address correspondence to Mohammad Etezad Razavi, MD, Khatam-Al-Anbia Eye Hospital, Vakil Abad Ave., No 47, Ghadir Street, Medical University of Mashad, Mashad, Iran.

Received: June 12, 2008
Accepted: September 24, 2008
Posted Online: May 21, 2010

10.3928/01913913-20090616-12

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