Journal of Emergencies, Trauma, and Shock

CASE REPORT
Year
: 2012  |  Volume : 5  |  Issue : 4  |  Page : 356--359

Rare combination of bilateral putaminal necrosis, optic neuritis, and polyneuropathy in a case of acute methanol intoxication among patients met with hooch tragedy in Gujarat, India


Bhavesh S Jarwani1, Puja Motiani2, Ruchir Divetia3, Gurudutta Thakkar4,  
1 Department of Emergency Medicine, VSGH, India
2 Consultant Pathologist, SCLGH Smt. NHL Municipal Medical College, Ahmedabad, Gujarat, India
3 Department of Neurology, LG, SCLGH, Smt. NHL Municipal Medical College, Ahmedabad, Gujarat, India
4 Department of Radio-diagnosis, SCLGH Smt. NHL Municipal Medical College, Ahmedabad, Gujarat, India

Correspondence Address:
Bhavesh S Jarwani
Department of Emergency Medicine, VSGH
India

Abstract

Methanol poisoning is a rare but extremely hazardous form of intoxication, generally occurring after suicidal or accidental events. Methanol is a cheap and potent adulterant of illicit liquors. In India, we have witnessed number of mass emergencies due to adulterated alcohol consumption. Although Gujarat State had banned alcohol consumption since 1961, worse hooch tragedies have often taken place. The most severe consequences of methanol intoxication are blindness, a profound metabolic acidosis and various forms of neurological impairment; which occur characteristically after a latent period of several hours or days after ingestion. We present a unique case of acute methanol intoxication presented with, apart from metabolic acidosis and optic neuritis, involvement of central nervous system and peripheral nervous system. He had bilateral optic neuritis, delayed onset polyneuropathy with axonopathy, and radiculopathy. Magnetic resonance imaging findings were consistent with bilateral putaminal necrosis.



How to cite this article:
Jarwani BS, Motiani P, Divetia R, Thakkar G. Rare combination of bilateral putaminal necrosis, optic neuritis, and polyneuropathy in a case of acute methanol intoxication among patients met with hooch tragedy in Gujarat, India.J Emerg Trauma Shock 2012;5:356-359


How to cite this URL:
Jarwani BS, Motiani P, Divetia R, Thakkar G. Rare combination of bilateral putaminal necrosis, optic neuritis, and polyneuropathy in a case of acute methanol intoxication among patients met with hooch tragedy in Gujarat, India. J Emerg Trauma Shock [serial online] 2012 [cited 2020 Jul 4 ];5:356-359
Available from: http://www.onlinejets.org/text.asp?2012/5/4/356/102413


Full Text

 Introduction



Methanol is a cheap and potent adulterant of illicit liquors. In India, we have witnessed number of mass emergencies due to adulterated alcohol consumption. [1] The most severe consequences of methanol intoxication are blindness, a profound metabolic acidosis and various forms of neurological impairment. [1],[2] We present a unique case of acute methanol intoxication presented with, apart from metabolic acidosis and optic neuritis, involvement of central nervous system and peripheral nervous system in form of bilateral optic neuritis, delayed onset polyneuropathy with axonopathy, and radiculopathy. Magnetic resonance imaging (MRI) findings were consistent with bilateral putaminal necrosis.

 Case Report



A 26-year-old non-diabetic, normotensive, previous healthy man brought in E/R with history of binge of country-made liquor (lately proved to be methyl alcohol adulterated with ethyl alcohol). He was one of hundreds of victims of hooch tragedy that broke out 2009 in Ahmedabad (Gujarat, India), and it is one of the largest outbreaks of methanol intoxication. [1],[2]

The patient had consumed about 300 ml of the adulterated alcohol 2 days back. He had episodes of vomiting and abdominal pain and blurred vision. He took some local treatment and was at home for last 2 days. Then he was brought to our in stupor state, GCS 8 and with acidotic breathing. The blood pressure was 120/80 mmHg, pulse rate 90/min, respiration rate 30/min with normal body temperature. Pupils were bilaterally mildly dilated and normally reacting to light. Initial laboratory studies revealed random blood sugar level, 114 mg/dL serum acetone, nil; an increased anion gap of 34 mEq/L (normal 20-22 mEq/L); acidosis (pH 6.8); HCO3 - , 4 mmol/L (22-30 mmol/L); serum creatinine, 1.9 mg/dL (0.8-1.3 mg/dL)); elevated WBC with shift to left.

He was intubated and put on ventilator support. Gastric lavage through large size Ryle's tube was performed (although it was late presentation), was given ethyl alcohol (500 ml of 10% IV and 50 ml of 95% through Ryle's tube), sodium bicarbonate (10 amp.(100 cc) IV stat followed by 10 amp in 500 ml NS IV slowly. He was treated with co-factor therapy folinic acid (leucovorin) 50 mg IV every 6 h to accelerate formate metabolism. We administered supplemental thiamine (100 mg IV) and pyridoxine (50 mg IV) and methylcobalamin. Fomepizole is not available in India.

Acidosis did not improve 2 hours after these initial treatment; his ABG analysis showed pH 6.9 and HCO3 level, 10 mEq/L. His methanol level, 147.3 mg/dl (FSL, i.e., forensic Science Laboratory analysis report) was available by now. His ethanol level was 115.4 mg/dl. His sensorium was not good (GCS 6), immediately he was transferred to dialysis unit for hemodialysis; he had to undergo dialysis three time at an interval of 12 hours.

On the next day, he was transferred back to medical ward as his acidosis had improved (pH, 7.34; normal anion gap, i.e., 21; HCO3 - , 24 mEq/dL), his sensorium was improving (GCS 10). He was conscious, oriented, and was extubated now. His fasting and post-prandial sugar levels, thyroid profile, and Vitamin B12 levels were within normal limits.

However, his voice had changed, he had nasal regurgitation of fluids and difficulty in swallowing, developed limb weakness. His neurological examination revealed bilateral lower motor neuron type 9 th and 10 th cranial nerve paresis (weak gag reflex, nasal regurgitation, and typical nasal twang). However, facial and vestibule-cochlear nerves were clinically normal bilaterally. All sensations (pain, temperature, and vibration) were diminished in both upper and lower limbs. He had weakness and power of 4/5 at major joint in all possible movements in both upper and lower limbs. Reflexes were sluggish to absent. Planter was equivocal. Fundus examination revealed disc pallor.

T2W images [Figure 1] in MRI revealed bilateral symmetrical hyper intense areas in region of bilateral putamen and in bilateral striatronigral area, which were hypo intense on T1W images [Figure 2], and on contrast showed enhancement. These MR findings are suggestive of acute necrosis in bilateral putamen and bilateral striatronigral areas in this setting.{Figure 1}{Figure 2}

Limb weakness was worsening and now his power in upper limbs was 4/5, while in lower limbs 3/5. He was unable to walk, had difficulty in eating, combing and buttoning-unbuttoning.

Electro diagnostic studies (EMG-NCV) showed sensory-motor polyneuropathy involving mainly lower limbs with secondary axonopathy and early polyradiculopathy. Cerebrospinal FluidCSF revealed proteins 112 mg/dL and cells 5/cumm, all neutrophil (suggestive of cyto-protein dissociation).

He was on supportive therapy and folic acid. Intra-vitreous steroid were tried for his optic neuritis. On discharge, after 20 days of stay in our hospital, he had no significant improvement in sensory and motor functions. He was discharged with Ryle's Tube in situ. His vision had slight improvement clinically. However, long term follow-up is awaited.

 Discussion



Methanol (wood spirit or methyl alcohol), a highly toxic substance, is used as industrial solvent in automobiles, in windshield wiper fluid, gasoline antifreeze, paint remover, de-icing solutions, varnish, photocopying fluid, and in some eau de cologne [1] .

Acute methanol poisoning is a rare accidental or suicidal intoxication. It has also been described as a result of fraudulent adulteration of alcoholic drinks. Many mass casualties are reported world-over due to adulterated alcohol consumption with high morbidity and mortality. [1],[ 2]

Methanol poisoning is fairly common in India [1],[2] Being cheap and potent, it is the first adulterant of illicit liquors. It goes by the names of khopadi, ladda, dalda, bewada, french polish, etc. Methanol poisoning, whether sporadic or mass poisoning is an acute medical emergency. If not recognized in time and treated on sound basis of pharmacology and toxicology of this alcohol, it can lead to considerable magnitude of morbidity as well as mortality . [3],[ 4]

We treated more than 180 patients of fraudulent adulteration of alcoholic drink in two of those tragic days. We present this case because, apart from classic metabolic acidosis and bilateral optic neuritis, this patient developed delayed onset, bilateral sensory-motor polyneuropathy with radiculopathy. MRI scan showed classical bilateral putaminal necrosis consistent with acute methanol intoxication. To the best of our knowledge, central and peripheral nervous system involvement in the same patient has not been reported previously in literature.

Methyl alcohol is quite toxic to humans. After ingestion, it is metabolized into formaldehyde and finally into formic acid. These metabolic products have toxic effects on the body. [5]

The MR picture in this patient is consistent with the findings described in literature. [6],[7] The most characteristic MR findings in methanol toxicity are bilateral putaminal necroses, degrees of hemorrhage. Putaminal necrosis and hemorrhage probably result from the direct toxic effects of methanol metabolites and metabolic acidosis in the basal ganglia. [7] In methanol intoxication, putaminal necrosis is usually permanent; however, in some series, significant regression of the neurological findings and disappearance of extrapyramidal symptoms are reported. [7]

Bilateral putaminal lesions are found on MR in a variety of conditions including Wilson's disease, hypoxic-ischaemic insults, encephalitis, Leigh's syndrome, Kearns-Sayre syndrome, striatal degeneration associated with Leber's optic atrophy and certain types of metabolic disorders. In addition, carbon monoxide inhalation and hypoxic - anoxic injuries such as near-drowning should be considered in the differential diagnosis. However, in carbon monoxide poisoning specific focus of toxicity is the globus pallidus while hypoxic - anoxic injuries additionally involve the caudate nucleus and other central gray nuclei. The combination of optic atrophy and bilateral putaminal haemorrhagic infarctions is unique to methanol intoxication. [6]

Multiple bilateral cranial nerve impairment and polyneuropathy are delayed sequel of ethylene glycol intoxication and usually develops 5 to 20 days after ingestion. [8] It is often associated with limb weakness, areflexia, and CSF albuminocytologic dissociation, mimicking Guillain-Barré syndrome (GBS) [8],[9] like in this patient.

The pathogenesis of this severe polyradiculopathy is not known. Ethylene glycol is metabolized in the liver, generating toxic products, including oxalate. Deposition of calcium oxalate in the leptomeninges or its blood vessels and subarachnoid space of cranial nerves has been reported at postmortem examinations. [8]

This patient had optic disc pallor and that is the frequent and common affection in acute methanol intoxication. Optic nerve demyelination secondary to myelinoclastic effect of formic acid has been suggested as responsible for optic nerve damage with or without axonal loss. [6] Outcome in blurred vision remains good, while outcome in blindness cannot be predicted. [3]

Treatment in acute intoxication is by drug elimination (e.g., hemodialysis) and inhibition of the metabolism of methanol to toxic formic acid by competitive inhibition of the enzyme alcohol dehydrogenase (ADH). Ethanol has 10 to 20 time's greater affinity for alcohol dehydrogenase (ADH). Fomepizole has approximately 500 to 1000 times greater affinity for ADH than ethanol and can completely inhibit ADH at a much lower serum concentration. [5] However, fomepizole is not available in India.

HD provides a clearance of 200 mL/min for methanol and 223 mL/min for formate at blood flows of 100-400 mL/ min [5] . HD significantly reduced formate elimination half-life compared with endogenous elimination and questionable role of folate. Peritoneal dialysis and other forms of continuous renal replacement therapy are inefficient at clearing toxic alcohols and their metabolites, and are not recommended. [5]

Hyperglycemia is considered bad prognostic marker in methanol intoxication, however, this patient had normal blood glucose level. [4]

Acute methanol poisoning should be suspected in all patients with metabolic acidosis with an elevated anion gap, neurological deterioration, or vision disturbances.

 Conclusion



Combination of bilateral putaminal necrosis and delayed polyneuropathy can be sequelae in acute methanol intoxication and should be suspected in such settings.

 Acknowledgements



We would like to thank Dr. Sanaei-Zadeh of the Department of Forensic Medicine and Toxicology, Tehran University of Medical Sciences, Hazrat Rasoul Akram Hospital, Tehran, Iran for his useful comments during the revision of the article.This work should be attributed to the VSGH and attached hospitals, along with Smt. NHL Municipal Medical College, Ahmedabad, Gujarat, India.

References

1Kumar SS, Boopathy SK, Bhaskar ME. Methanol poisoning-a Chennai experience. J Assoc Physicians India 2003;51:425-6.
2Ravichandran RR, Dudani RA, Almeida AF, Chawla KP, Acharya VN. Methyl alcohol poisoning. (Experience of an outbreak in Bombay). J Postgrad Med 1984;30:69-74.
3Sanaei-Zadeh H, Zamani N, Shadnia S. Outcomes of visual disturbances after methanol poisoning. Clin Toxicol (Phila) 201149:102-7.
4Sanaei-Zadeh H, Esfeh SK, Zamani N, Jamshidi F, Shadnia S. Hyperglycemia is a strong prognostic factor of lethality in methanol poisoning. J Med Toxicol 20117:189-94.
5Kute VB, Godara SM, Shah PR, Gumber MR, Goplani KR, Vanikar AV,et al. Hemodialysis for methyl alcohol poisoning: A single-center experience. Saudi J Kidney Dis Transpl 2012; 23:37-43.
6Kuteifan K, Oesterle H, Tajahmady T, Gutbub AM, Laplatte G. Necrosis and haemorrhage of the putamen in methanol poisoning shown on MRI. Neuroradiology 1998;40:158-60.
7Berger JR, Ayyar DR. Neurological complications of ethylene glycol intoxication. Report of a case. Arch Neurol 1981;38:724-6.
8Zhou L, Zabad R, Lewis RA. Ethylene glycol intoxication: Electrophysiological studies suggest polyradiculopathy. Neurology 2002;59:1809-10.
9Lewis LD, Smith BW, Mamourian AC. Delayed sequelae after acute overdoses or poisonings: Cranial neuropathy related to ethylene glycol ingestion. Clin Pharmacol Ther 1997;61:692-9.