JD is a previously healthy 33-year-old white man, married and father of 2 children, who, while working as an agronomist, was inadvertently exposed to anhydrous ammonia. His only recollection of the event was a "puff of smoke” and the smell of ammonia. He lost consciousness almost immediately and awoke several days later in the intensive care unit. He was blind. Over the days that followed, he regained central vision; however, the loss of peripheral vision in all fields persisted. He said that upon first waking in the morning, he could "only see shadows.” For the rest of the day, he had “tunnel vision.” Ophthalmology and neurology evaluations uncovered no obvious reasons for the persistent vision loss.
The patient also complained of mild headache and discomfort behind his eyes for which he was taking aspirin. The discomfort behind his left eye was worse than on the right. He remained on disability following his work injury, and began to feel increasingly distressed and hopeless. His wife noted he was uncharacteristically irritable with her and the children, and that he had vivid nightmares and said he could smell ammonia. He also had trouble keeping up his yard because of the agitation and anxiety he experienced in approaching his workshed and equipment on the property.
A month later, an ophthalmologist reexamined JD and, again, found no cause for the ocular abnormality and suggested artificial tears for dry eyes. Two months later, he saw an optometrist, who documented constricted visual fields and referred JD to a second ophthalmologist. This consultant suggested possible brain injury and doubted it was psychosomatic in nature. He referred the patient to a neurologist. The neurologist found no organic explanation for his vision loss. He suspected a somatoform disorder and told JD his vision should recover. JD and his wife initially declined the neurologist’s idea of a neuroophthalmology consultation, but eventually agreed. The neuro-ophthalmologist also suspected a functional disturbance as the cause for visual impairment; and he required the patient to stop driving a motor vehicle until his vision improved.
The patient was subsequently referred for psychological evaluation. When initially seen by a psychologist and a family medicine resident, JD was working as a farmhand to make ends meet.
Effects of ammonia exposure
Ammonia is a water-soluble, colorless gas—an alkaloid with a unique odor. In the past, most exposures were related to its use as a fertilizer, as was the case with JD. In recent years, it has also been used to illegally manufacture methamphetamine, which has led to ammonia accidents and increased exposures.1-3
Systems commonly injured are the respiratory tract, ocular system, skin, and gastrointestinal tract (only if ingested).2
Ammonia destroys the mucosal barrier of the respiratory tract, causing loss of cilia, edema, and smooth muscle contraction.3,4 Long-term effects include chronic cough or hoarseness, obstructive or restrictive airway disease, reactive airway disease, or bronchiectasis.1,3
The extent of ocular injury is related to the degree of ammonia exposure. In mild cases, there is eye irritation, increased tear production, a sensation of stinging or burning, and perhaps conjunctivitis or spasmodic winking. The patient may also experience photophobia.1,3,4 In more severe cases, there may be corneal ulcerations, iritis, anterior or posterior synechia, opacification of the cornea, cataracts, glaucoma, atrophy of the retina, or severe pain.1,3 Blindness may occur, temporarily or permanently.4 This complete or partial vision loss is secondary to physical damage that can be seen during an ophthalmologic examination.1,4
Skin injuries can range from a mild erythematous rash to a full thickness burn with bullae and even denudation.1 Long-term effects include scarring or dermatitis.3
Our patient had respiratory and skin symptoms that fit with classic ammonia exposure (respiratory distress requiring intubation, rash). His initial blindness was consistent with ammonia exposure; however, his subsequent peripheral loss was inconsistent with known reaction to ammonia.
Causes of acute visual loss
Vision loss can be caused by injury to the media of the eye (cornea, lens, etc), the retina, or the neural visual pathways. It may also have a psychogenic component.5 Media-related causes of acute vision loss include keratitis or uveitis, edema of the cornea, blood in the anterior chamber (hyphema), disturbance of the lens, or hemorrhage into the vitreous.5,6 Retinal causes include occlusion of the central retinal artery or vein, detachment of the retina, or acute maculopathy.5-8 Neurologic causes include injury to the optic nerve itself (normally monocular) or defects in the chiasmal or retrochiasmal regions (causing partial loss in both eyes).5,9 If all of the above possibilities have been ruled out, consider psychogenic contribution to visual loss.5 Often this diagnosis is called “functional vision loss,” which can include feigning visual loss for secondary gain or subjective blindness as is seen with a somatoform disorder (eg, conversion disorder).