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ORIGINAL ARTICLE
Year : 2014  |  Volume : 2  |  Issue : 2  |  Page : 87-92

Clinico-biochemical correlation of ocular manifestations and visual prognosis in victims of hooch tragedy


Department of Ophthalmology, Government Medical College, Kozhikode, Kerala, India

Date of Submission18-Jul-2013
Date of Acceptance15-Feb-2014
Date of Web Publication11-Apr-2014

Correspondence Address:
Suma Unnikrishnan
Department of Ophthalmology, Government Medical College (P.O), Kozhikode - 673 008, Kerala
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2320-3897.130535

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  Abstract 

Background: Hooch tragedies are very common in India, especially in the low socioeconomic group resulting in varying mortality and morbidity. Various biochemical changes occur following methanol poisoning. An attempt is made to follow up such patients to correlate these biochemical changes and clinical presentations to the final visual outcome. Aim: To study the visual problems in the victims of acute methanol poisoning and its correlation with biochemical changes. We also studied the visual prognosis and sequel of acute methanol poisoning in correlation with the initial presentation, biochemical changes and treatment modalities. Study Design: Observational study. Materials and Methods: Twenty-nine patients attended in ophthalmology casualty of a tertiary center with history of blurring of vision after consuming illicit liquor were included in the study. Four patients presented with no perception of light, 15 patients were having poor vision (<6/18). On follow up, the two patients remained with no perception of light. Even though four patients showed initial improvement, they later deteriorated. Patients who permanently lost vision were having severe metabolic acidosis at presentation. Statistical Analysis: Was done by chi square test using SPSS 16 version software for studying the significance. Results and Conclusion: Acute methanol poisoning can badly affect the visual functions. Blood pH and serum bicarbonate level has got direct correlation with visual deficit. The presence of metabolic acidosis, if not corrected early will result in permanent visual impairment. Early intervention with hemodialysis and systemic steroids can improve the visual outcome.

Keywords: Blood pH, methanol, metabolic acidosis, optic neuropathy


How to cite this article:
Unnikrishnan S, Raju KV. Clinico-biochemical correlation of ocular manifestations and visual prognosis in victims of hooch tragedy. J Clin Ophthalmol Res 2014;2:87-92

How to cite this URL:
Unnikrishnan S, Raju KV. Clinico-biochemical correlation of ocular manifestations and visual prognosis in victims of hooch tragedy. J Clin Ophthalmol Res [serial online] 2014 [cited 2022 Jun 28];2:87-92. Available from: https://www.jcor.in/text.asp?2014/2/2/87/130535

Methyl alcohol is a highly toxic substance, which is commonly used to adulterate ethyl alcohol. [1] Once it is ingested, it is converted to formic acid in the liver by an enzyme called alcohol dehydrogenase. Formic acid inhibits oxidative phosphorylation in the mitochondria producing cellular hypoxia that results in edema of vital organs like brain, lungs, heart, optic nerve and retina. Severe metabolic acidosis produced by the formic acid if not corrected immediately will lead to death of the patient.

The symptoms of acute methanol poisoning start within 12-24 hours in the form of nausea, vomiting, epigastric pain, vertigo, blurring of vision, etc. The lowest lethal dose of methanol reported is 30 ml. [2] Formic acid accumulation in the optic nerve results in acute optic neuritis resulting in blurring of the disc margin, hyperemia, edema of the optic disc. There can be peripapillary edema and internal limiting membrane folds due to intra retinal edema. Optic nerve demyelination has also been reported due to destruction of myelin by formic acid. [3]

The frank blindness that develops often responds to immediate therapy; however, complete loss of vision is a common sequel due to primary optic atrophy. [4] Visual field defects can occur in the form of central scotoma or constriction of peripheral fields. Pathologically, there is a widespread degeneration of retinal ganglion cells probably caused by histotoxic anoxia

Since the systemic and ocular manifestations are correlated to the severity of metabolic acidosis, the specific treatment is directed toward rapid correction of acidosis by parenteral administration of sodium bicarbonate, enteral or parenteral ethyl alcohol and hemodialysis. Ethyl alcohol competes with methanol for alcohol dehydrogenase for its metabolism, thus inhibiting the formation of toxic formic acid. Experimental data suggests that administration of folic acid hastens the metabolism of formic acid to carbon dioxide. [5] Hemodialysis corrects metabolic acidosis and helps in eliminating methanol and formic acid. [6]

In this study, an attempt was made to study the visual problems and its sequel in the victims of acute methanol poisoning in correlation with biochemical changes and treatment modalities.


  Materials and Methods Top


An observational study conducted among patients affected with acute methanol poisoning in a hooch tragedy. The study was conducted in the department of Ophthalmology of a tertiary center with the help of departments of internal medicine and nephrology. The patients who came to the casualty with the history of consuming adulterated alcohol (involved in the hooch tragedy in September 2010) were included in the study. Unconscious patients were excluded from the study since their history taking and detailed ocular examination was impossible. Patients with pre-existing diseases of the optic nerve were also excluded from the study.

At baseline, all patients were subjected to routine ocular examination. History was taken from conscious patients or from the bystander in the case of unreliable and disoriented patients. Ophthalmic examination included torch light examination in the darkroom to assess the pupillary reaction. Relative afferent pupillary defect (RAPD) if present was documented. Visual acuity was noted using Snellen's chart and color vision using Ishihara chart. Visual field charting was done using perimeter and tangent screen. In cooperative patients, field charting was done by a Humphrey field analyzer. Intraocular pressure was assessed by the indentation method. All patients were subjected to retinal examination after dilating the pupil with tropicamide eye drops. Special attention was given to the presence of hyperemia, blurring of disc margin, disc edema, peripappillary edema and macular edema. In macular edema optical coherence tomography (OCT) was done in cooperative patients. In the presence of severe metabolic acidosis with acidotic breathing and drowsiness or with severe visual blurring, serum bicarbonate level, arterial blood gas estimation with blood pH were done. Serum methanol estimation was not done due to nonavailability.

All the patients who had clinical and laboratory evidence of acidosis were treated with intravenous infusion of 7.5% of sodium bicarbonate 100 ml four hourly. [5] These patients were given ethyl alcohol 5% initially15 ml/kg bolus followed by 2-3 ml/kg/hr as maintenance infusion through Ryle's tube, the dose being guided by the clinical condition and the plasma bicarbonate level. Folinic acid 1 mg/kg (maximum 50 mg/dose) four hourly for six doses were given after monitoring and supporting the vitals. [5] Hemodialysis was done in patients with severe metabolic acidosis and optic nerve involvement who were not responding to initial therapy. [5]

After correcting metabolic acidosis with hemodialysis till the blood pH comes to the normal (7.35-7.45), intravenous pulse steroid in the form of 1 gram of methyl prednisolone for 3 days was also tried in patients with optic disc changes. [7] In Patients who presented with blurred vision without any optic disc findings injection dexamethasone 8 mg twice daily was tried for 3 days, then tapered dose of prednisolone over a period of 1 month. These patients underwent repeated assessment of the visual status at first week, first month, third month, sixth month and at 1 year interval.

At each follow-up pupillary reaction, visual acuity, color vision, visual field and detailed fundus evaluation were done in all patients. Optical coherence tomography was repeated in patients who had macular edema

The consent was taken for including in the study. There was no additional financial burden for the patient in participating in the study. There was no drug trial or other modalities of treatment imposed on to the patient other than described in the literature. This study was approved by the Ethics committee of the institution in accordance with ICMR on 23.11.2010. Written informed consent was taken from the patients included in the study.


  Results Top


Twenty-nine patients who got admitted with history of consuming adulterated ethyl alcohol in the Hooch tragedy were included in the study. All patients were male. The age group varied from 23 to 80 years. Fourteen patients (48.3%) were between 30 and 49 years. Eight patients (27.6%) were from the age group between 40 and 59 years and five (17.2%) each from the age of 20-29 years and 60-80 years.

Both eyes were affected in 24 patients (82.8%), only right eye in 3 patients (10.3%) and no involvement in 2 (6.9%). Out of the 29 patients, 19 presented with sudden loss of vision (65.5%) and 8 (27.6%) with gradual loss. Two (6.9%) patients didn't have any visual deficit. Head ache was seen in 12 patients (41.3%). Seventeen patients (58.2%) complained of ocular pain. Fifteen patients (51.7%) had conjunctival congestion; one was having subconjunctival hemorrhage (3.4%). None of them had uveal involvement. Intraocular pressure was normal in 27 patients (93.1%) and below normal in 2 patients (6 and 7 mm of Hg).

Presenting visual acuity was normal in nine patients (34.5%). Twenty patients had visual deficit [Figure 1]. Those patients with initial normal vision did not have any deterioration at final visit. Among the patients with initial vision in the range of hand movement (HM) to 6/60, 66.7% had poor vision even at the last follow up. All patients who had no perception of light initially remained with same at final follow up. Pupillary abnormality was noted in 15 patients (51.7%).This included Grade 1 RAPD (n = 6, 20.7%) and Grade 4 RAPD (n = 5, 17.2%). Anisocorea (n = 1, 3.4%) Hippus (n = 2, 6.8%) [Figure 2]. All patients with grade 3 and 4 RAPD continued to have poor visual acuity even at final follow up. Among the patients with grade1 RAPD, 66.7% were having abnormal visual acuity at last follow up. Color vision was normal in 21 patients (72.4), impaired in three (10.3%) and absent in 3 (10.3%). It could not be tested in two patients (6.9 %) due to poor vision.
Figure 1: Initial visual acuity

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Figure 2: Color vision defects

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Visual field defects in the form of constricted peripheral field were present in two patients (6.9%) [Figure 3]. Optic disc involvement was noted in 21 patients. This included hyperemia (n = 18, 62%), disc edema (n = 1, 3.4%) and both hyperemia and disc edema (n = 1, 3.4%). Out of the 18 patients with hyperemic disc, one had severe arterial narrowing. Nine patients (31%) did not have any optic disc involvement [Figure 4].
Figure 3: Field defects

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Figure 4: Initial optic disc appearance

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Internal limiting membrane folds (ILM) were seen in five patients (17.2%). No evidence of retinal elevation or detachment is seen in any of the patients. There was macular edema in five (17.2%) patients. OCT was done in them. Out of this a 24 year old who had optic disc edema, peripapillary edema and internal limiting membrane folds in both eyes showed nerve fiber layer loss with dip into the red zone in both the eyes on the fourth day of methanol intake [Figure 5], [Figure 6], [Figure 7].
Figure 5: Fundus showing hyperemic disc, peripapillary edema, ILM folds and macular edema

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Figure 6: OCT showing nerve fiber layer loss with dip into the red zone in right eye

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Figure 7: OCT showing nerve fiber layer loss with dip into the red zone in left eye

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Systemic complaints were present in nine (31%) patients in the form of convulsions, loss of consciousness, vomiting, vertigo in two each and abdominal pain in one patient. Arterial blood gas (ABG) analysis was done in 19 patients. Out of this 10 patients (53%) had blood pH of <7.35 indicating metabolic acidosis. The blood pH of rest nine patients (47%) were between 7.35 and 7.45 which lies within the normal range. The normal level of serum bicarbonate (HCO 3 ) varies from 22 to 26 mille equivalents/liter. Among the 19 patients who were suspected to have metabolic acidosis, HCO 3 was analyzed. It was normal in 4 (21%), <22 meq/l in 14 (74%) patients. One had >26 meq/l. (5%). Typical features of metabolic acidosis were present in 13 patients. Those patients with metabolic acidosis or severe visual loss not responding to initial conventional treatment were undergone hemodialysis. Hemodialysis was done for 15 (52%) patients. Out of this 2 patients received hemodialysis twice and 1 patient received three times, and 13 patients got single sitting. Among the 17 patients (59%) treated with systemic steroids, 9 patients were given injection dexamethasone and 8 patients were treated with injection methyl prednisolone [Figure 8].
Figure 8: Treatment with systemic steroids

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These patients were reviewed after 1 week. Out of the 23 patients who turned up, 4 patients had no perception of light (10.3%). Two patients were having HM vision (6.9%), two had <6/18 (6.9%) and three had >6/18 (10.3%). Eleven patients were normal. After 1 month second follow-up was done. Out of the 15 who came, 2 patients (6.9%) had no perception of light (PL) and 2 (6.9%) had poor vision (<6/18). Two patients were having >6/18 (6.9%). Nine patients (31%) were normal. After 6 months third follow-up was done. Out of the 17 who turned up, 10 (34%) were normal. Two patients remained with no PL (6.9%) [Figure 9]. Final follow-up was done after 1 year. Eleven patients came. Seven patients were normal (24.1%). Two remained with no PL (6.9%). One each had HM vision and <6/18 vision.
Figure 9: Final visual Acuity

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Optic disc changes were noted at the end of 6 months. Seven had features of either temporal pallor or primary optic atrophy. Two patients who didn't have any fundus changes at presentation developed temporal pallor at the end of 1 year. Four patients who presented with very poor vision and grade 4 RAPD with hyperemic disc initially, on follow-up developed early optic atrophy as early as 3 weeks. Out of the seven patients whose fundus changes disappeared on follow up, five were initially treated with hemodialysis and dexamethasone, one with intravenous methyl prednisolone and one with only hemodialysis.


  Discussion Top


Methanol being cheap and potent, is used commonly as an adulterant of illicit liquors. [1] Because acute methanol poisoning is a medical emergency if not recognized early and treated promptly on the sound basis of toxicology, it may land up with considerable amount of mortality and morbidity. Little attention has been given to the sequel and persistent visual problems in the survivors of acute methanol poisoning. In some patients blindness improves but in others it deteriorates after initial improvement. In various studies conducted on methanol poisoning, arterial pH and serum bicarbonate level correlated significantly with the serum methanol level stressing the point that these could be taken as the indicators of severe methanol poisoning in cases of non-availability of serum methanol estimation. [8]

All the 29 patients in this study were males. [9] Age group varied from 23 to 80 years with 48% in the age group 30-50. The mean age was 47 years. Bilateral eye involvement was seen in 82.8%. No involvement documented in 6.9%. Most common symptoms were sudden blurring of vision (65.5%), ocular pain (58.2%), redness (51.7%) and head ache (41.3%). Most common signs were pupillary abnormality (51.7%), reduced visual acuity (70%), color vision defect (20.6%), visual field defect (6.9%), optic disc involvement (68.8%), ILM folds (17.2%) and macular edema (17.2%). Systemic complaints were seen in 31% of patients which included convulsions, vomiting, vertigo and abdominal pain. Arterial blood gas analysis was done. Fifty three percent of patients had blood pH <7.35 indicating acidosis. Serum bicarbonate values were <22 meq/l in 74% of patients. Hemodialysis was done in 52% of patients. Systemic steroids were given for 59%, of which 41% got intravenous methyl prednisolone as described earlier. In addition, folinic acid and thiamine were also given.

In this study, an attempt was made to correlate each presenting symptoms, signs, biochemical changes and treatment modalities with final visual outcome statistically by the chi-square test. SPSS 16 version software was used for studying the significance. No statistical or clinical significance was observed on the onset of visual drop whether sudden loss of vision or gradual loss (P value = 0.556) when correlated with final visual acuity. No correlation was detected with the eye affected and final visual acuity (P value = 0.452).

Regarding head ache, 57% with head ache had abnormal visual acuity and 42.9% had normal visual acuity. So even though the presence of head ache is a poor prognostic factor clinically, it is not statistically significant (P value = 0.263). The presence of ocular pain was associated with abnormal visual acuity in 41.2% of patients which was not clinically and statistically significant (P value = 0.949). No correlation was noted between the initial conjunctival congestion and abnormal visual acuity on follow up (P value = 0.129). Pupil involvement at presentation is significantly correlated with abnormal visual acuity both clinically and statistically (P value = 0.007). Presenting visual acuity is clinically correlated significantly with final visual acuity (P value = 0.048). Color vision defect at presentation is a bad prognostic sign for final visual acuity (P value = 0.042). Visual field defect at presentation is statistically correlated with final visual acuity (P value = 0.006). No correlation was noted with intraocular pressure and final visual acuity. The presence ILM folds were seen in 66.7% of patients with abnormal VA, though clinically significant, it is not statistically significant (P value = 0.323). No correlation was observed between macular edema and final visual acuity.

Optic disc involvement at presentation is not correlated statistically with final visual acuity (P value = 0.125), though clinically significant. Out of this one patient developed convulsion in the first week and on investigation MRI brain showed infarct in the parieto-occipital region. [10] Of the seven patients who developed temporal pallor two patients had received hemodialysis for metabolic acidosis initially. For them, fundus returned to normal after the initial management, but on follow up they developed temporal pallor. This suggests that disappearance of hyperemia with visual recovery does not exclude the possibility of further deterioration on follow up stressing the need to follow up these patients frequently. One patient who presented with no perception of light, disc edema, and ILM folds improved initially to HM in the right and 6/18 in the left eye with inferior field defect. But after 6 months his vision deteriorated to counting finger close to face. His optic disc showed cupping and pallor [11],[12] [Figure 10].
Figure 10: Pallor and cupping of optic disc

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The presence of metabolic acidosis is correlated both clinically and statistically with final visual acuity (P value = 0.057). Patients who were treated sufficiently early with hemodialysis for metabolic acidosis recovered fast and regained good vision unlike the observation from other study. [13]

Treatment with systemic steroids either injection dexamethasone or intravenous methyl prednisolone has got significant correlation with good visual outcome both clinically and statistically (P value = 0.002) suggesting a positive role of systemic steroids in the management of acute methanol poisoning in addition to hemodialysis. Rationale behind the use of steroids is based on the postulation that blurring of vision in methanol poisoning could be following acute optic neuritis [14] due to retro laminar demyelination. [15] Another observation was two young patients with good body mass index (BMI) didn't develop any visual deficit or fundus changes, even with the presence severe metabolic acidosis, may be related to the nutritional status.

So the risk factor of visual sequel in acute methanol poisoning includes low BMI and poor nutritional status.

Final visual acuity at the third follow up was taken for statistical analysis. Normal vision was documented in 34.5%. In 10.3% patients, fairly good vision (>6/18) were recorded. But 14% were having poor vision. The rest 41.4% were absent on follow up. So considering the valid percentage 58% had normal vision and 41.2% had abnormal vision.

Finally coming to the factor analysis, final visual acuity was poor in patients presented with initial poor vision, color vision impairment, visual field defects and pupillary abnormality. These signs and symptoms were associated with metabolic acidosis and abnormal ABG values. Visual prognosis was good in patients treated early with hemodialysis and systemic steroids. Elderly patients with poor nutritional status and low BMI had poor visual outcome.

Limitation of this study was that 41.4% of patients didn't turn up for follow-up as they were not compliant due to alcoholic behavior.


  Conclusion Top


Acute methanol poisoning is a serious threat to both life and vision. A majority of patients had visual loss due to optic nerve involvement in the form of disc edema, peripapillary edema, and macular edema. Pupillary abnormality was detected in these patients. There is a significant correlation with metabolic acidosis and serum bicarbonate level with presenting visual acuity. Poor visual acuity, impaired color vision, visual field defect and pupillary defects at initial presentation were statistically correlated with poor visual outcome on follow up. Early intervention with hemodialysis and systemic steroids can improve the visual outcome.

 
  References Top

1.Ravichandran R, Dudani RA, Almeida AF, Chawla KP, Acharya VN. Methyl alcohol poisoning (Experience of an outbreak in Bombay). J Postgrad Med 1984;30:69-74.  Back to cited text no. 1
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2.Gonda A, Gault A, Churchill D, Hollomby D. Hemodialysis for methanol intoxication. Am J Med 1978;64:749-58.  Back to cited text no. 2
    
3.Baumbach GL, Cancilla PA, Martin-Amat G, Tephly TR, McMartin KE, Makar AB, et al. Methyl Alcohol Poisoning Alterations of morphological findings of the Retina Optic Nerve. Arch Ophthal 1977;95:1859-65.  Back to cited text no. 3
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4.Parson's Diseases of the eye, 19 th ed. 2002 p. 384-385.  Back to cited text no. 4
    
5.Kumar SS, Seerala Boopathy K, Bhaskaran ME. Methanol poisoning - A Chennai experience. J Assoc Physicians India 2003;51:425-6.  Back to cited text no. 5
    
6.Kruse JA. Methanol Poisoning. Intensive Care Med 1992;18:391-7.  Back to cited text no. 6
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7.Sodhi PK, Goyal JL, Mehtha DK. Methanol-induced optic neuropathy: Treatment with intravenous high dose steroids. Int J Clin Pract 2001;55:599-602.  Back to cited text no. 7
    
8.Teo SK, Lo KL, Tey BH. Mass methanol poisoning: A clinico-biochemical analysis of 10 cases. Singapore Med J 1996;37:485-7.  Back to cited text no. 8
    
9.Bennett IL Jr, Cary FH, Mitchell GL Jr, Cooper MN. Acute methyl alcohol poisoning: Review based on experiences in an outbreak of 323 cases. Medicine (Baltimore) 1953;32:431-63.  Back to cited text no. 9
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10.Mc Lean DR, Jacobs H, Mielke BW. Methanol poisoning: A clinical and pathological study. Ann Neurol 1980;8:161-7.  Back to cited text no. 10
    
11.Sharma M, Volpe NJ, Dreyer EB. Methanol-induced optic nerve cupping. Arch Ophthalmol 1999;117:286.  Back to cited text no. 11
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12.Shin YW, Uhm KB. A case of optic nerve atrophy with severe disc cupping after methanol poisoning. Korean J Ophthalmol 2011;25:146-50.  Back to cited text no. 12
    
13.Desai T, Sudhalkar A, Vyas U, Khamar B. Methanol poisoning: Predictors of visual outcome. JAMA Ophthalmol 2013;131:358-64.  Back to cited text no. 13
    
14.Albert and Jacobie pages 2244 (Vol. 3) & 4173 (Vol. 5) (2nd editions).  Back to cited text no. 14
    
15.Sharpe JA, Hostovsky M, Bilbao JM, Rewcastle NB. Methanol optic neuropathy: A histopathological study. Neurology 1982;32:1093-100.  Back to cited text no. 15
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    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10]


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