Tobacco-alcohol amblyopia: A rare complication of prolonged alcohol abuse.

Tobacco-alcohol amblyopia is rare, however, extremely disabling complication seen in patient with alcohol dependence syndrome, which if not addressed properly and at the right time may lead to persisting deficits. We here report a patient of alcohol-dependence syndrome who presented with significant diminution of vision bilaterally in the background of excess alcohol consumption.

Tobacco-alcohol amblyopia was often described prior to World War II in patients with heavy tobacco and ethanol consumption. Presently, tobacco-alcohol amblyopia is either far less common or is seldom checked for and reported.[12] Alcoholic amblyopia presents as a painless bilateral loss of vision in association with alcohol abuse. The majority of patients are also smokers.[3] The clinical pattern of this disorder is quite stereotyped. Almost all patients complain of a blurring or dimness of vision and of difficulty in reading small prints. Occasionally patients may complain of difficulty in differentiating red from green. The disease usually evolves over a period of several weeks to several months. Funduscopic examination may be normal or may demonstrate a mild to moderate degree of pallor of the optic nerve heads; most apparent in the temporal half of the discs. Besides signs referable to other coexisting diseases, such as polyneuropathy or the Wernicke–Korsakoff syndrome, no other neurologic abnormalities are found. Objective stigmata of under nutrition are commonly encountered. Improvement in the patient's visual acuity almost always follows the institution of adequate dietary and vitamin intake. Despite the element of toxicity implied in the term tobacco-alcohol amblyopia, the bulk of the evidence favors the interpretation that this disease is nutritional in origin. Most if not all of the patients have a poor dietary history and often exhibit frank stigmata of nutritional depletion. Diseases of recognized nutritional origin, such as alcoholic polyneuropathy, Wernicke's encephalopathy, or pellagra are not infrequently found in conjunction with the amblyopia. The specific dietary lack however is as yet uncertain. Thiamin and riboflavin have all been implicated by various authors, but no single report is conclusive.[4] Abnormal visual evoked responses (VERs) were found in 23% of patients without and 37% of patients with the Wernicke–Korsakoff syndrome. The main VER abnormalities of all the alcoholic groups were prolonged latency and reduced amplitude of the P100 component.[5] Optical coherence tomography has shown reduced retinal nerve fiber layer in temporal quadrants of these chronic alcoholics.[6] One of such case is being discussed here. The case has its salience in novelty.

CASE REPORT

This 33-year-old male carpenter by profession in an industry started consuming alcohol since year 1999. Initially, he used to drink with peers in moderation and on social occasions. Gradually he increased his consumption over next 6 years in frequency and quantity to around 180 mL rum four to five times a week with features of dependence in craving, loss of control, tolerance, daytime relief drinking, and withdrawal tremors and restlessness on abstinence. Year 2006 onwards he started consuming vodka as he found it to be odorless and thus could take to his place of work mixed in water without getting caught. Gradually, he increased it to 360–480 mL five to six times a week regardless of the advises by the relatives and family members to reduce his consumption. This pattern continued till Jan 2011 when he had to suddenly abstain from alcohol due to non availability of vodka in his village. He had strong craving and did not feel like eating during the next 7 days. After a week he finally was able to procure vodka from the city and consumed around 360 mL. Next day onwards he developed sudden onset blurring of vision and diminished perception of colors and depth. He consulted local practitioner who advised him to stop alcohol but he continued to consume owing to strong craving and its withdrawal effects. The visual disturbance worsened over next 3–4 weeks. At work he was unable to see clearly, which was noted by people necessitating referral to tertiary care centre. Further history at psychiatric centre revealed excess consumption of tobacco for last 5 years (ie, up 60 gm/week). Family history revealed regular consumption of alcohol in his father. Evaluation on admission revealed elevated systolic blood pressure, tachycardia, tremulousness of body, moist cold palm, perception of only hand movement both eye, subtle cerebellar sign in dysmetria, and dysdiadochokinesia (left side) and tingling and reduced fine touch sensation both lower limb below knee. Investigation revealed mean corpuscular volume 97 fl, gamma glutamyl transferase-97 IU/L, and Bilirubin 2.1 mg%, ultrasonography abdomen was normal. Evaluation by neurologist revealed no localizing pathology requiring specific neurological intervention. Ocular coherence tomography revealed normal fundus, reduced flash visual evoked potential (VEP) P100 latency in both eyes, and bilateral temporal thinning of retinal nerve fiber layer on temporal quadrant both eyes, possibly due to toxic etiology. Psychometric evaluation revealed high perseveration on Wisconsin card sorting test and mild impairment in visual retention and recognition on the post graduate institute memory scale. He was managed with forced abstinence, vitamin supplementation, and detoxification with tapering doses of chlordiazepoxide. Gradually his subtle neurological signs and symptoms improved over 1 week along with improvement in withdrawal symptoms. He was also managed by ophthalmologist for his visual symptoms. Visual acuity that was initially limited to hand movements improved to 6/12 to 6/18 both eyes. He was also noted to have constriction of field of vision and had his color vision was noted to be colour perception IV that continued throughout his period of admission. He was further given psychoeducation, counseling, group therapy all aimed at relapse prevention and anticraving treatment Tab Baclofen XL 30 mg hora somni that he tolerated well. Presently he is asymptomatic from psychiatric side and motivated for further abstinence. He slowly resumed his carpentry work but required brighter lighting in his place of work.

DISCUSSION

Our patient reported here with subacute bilateral painless diminution of vision in the background of prolonged abuse of alcohol, excessive smoking and poor nutritional intake before the onset of ocular symptom. He had subtle cerebellar signs and peripheral neuropathy. Relevant investigations that reflected the chronicity of alcohol consumption were also higher. These findings are characteristic of tobacco-alcohol amblyopia and have been brought out by researchers in the past.[3] Evaluation revealed features of alcohol dependence syndrome that developed over a decade, amblyopia that developed suddenly and progressed over next few weeks due to sudden withdrawal of alcohol consumption and subtle features of cerebellar insult and polyneuropathy, the same evolved over 12 years of drinking. The clinical picture was akin to what have been found by researchers in the past in cases of tobacco-alcohol amblyopia.[4] Ophthalmological evaluation revealed normal fundus, reduced flash VEP P100 latency in both eyes and bilateral temporal thinning of the retinal nerve fiber layer on temporal quadrant both eyes. Similar characteristic of salience has been brought out earlier by the researches.[4] Prolonged latency and reduced amplitude of the P100 component has been common in this not so common entity.[5] Optical coherence tomography found similar reduced retinal nerve fiber layer in temporal quadrants in chronic alcoholics as discussed in the literature[6] His cerebellar signs and polyneuropathy reversed significantly with forced abstinence, vitamin supplements, and adequate dietary intake. The nutritional deficiency has been the hallmark of this entity.[4] These neurological problems abated adequately with timely dietary supplementation. Though his visual problems improved with time and intervention, he persisted with residual deficits. This might be due to a certain level of irreversibility of damage over time/severity of affection or mechanism other than pure nutritional deficiency being responsibility for these dysfunctions. The final word in this direction is yet a matter of research. He was given adequate psychotherapy aimed at abstinence and relapse prevention and subsequently anticraving agents were instituted to reduce the possibility of relapse in future. He expressed adequate motivation for future abstinence. Presently individual is gainfully employed at work but needs supervision. He has been given sheltered appointment to avoid work which requires skillful visual function. But for his residual limitation in vision, he is gainfully employed. An ophthalmic complication of such nature though rare can be extremely disabling in a patient with the alcohol-dependence syndrome. An adequate knowledge of this rare but serious complication of substance abuse, strong clinical suspicion of such complication in this setting, a keen eye on the part of clinician and prompt therapeutic effort with efficient multidisciplinary collaboration will not only yield better clinical satisfaction, but also help patient ward off such eminent loss of vision. Psycho education on this line will prevent such occurrences in an industry that might deprive an individual from his gainful employment.