Brief Communications A rare case of toxic optic neuropathy secondary to consumption of neem oil Suresha AR, Rajesh. P, Anil Raj KS, Radhika Torgal A 35-year-old female was referred to our hospital with bilateral loss of vision of two days duration. She gave history of consumption of about 150 ml of neem oil five days back. Examination revealed no perception of light in both eyes. Both pupils were dilated and sluggishly reacting to light. Her fundus examination showed bilateral hyperemic, edematous discs and also edema extending along the superior and inferior temporal vascular arcade. Magnetic resonance imaging (MRI) scan showed bilateral putaminal regions with altered signal, hypointensities in T1-weighted images, hyperintensities on T2-weighted, images and hyperintense on Fluid Attenuation Inversion Recovery (FLAIR) images suggestive of cytotoxic edema due to tissue hypoxia. Her vision improved to 20/200 in both eyes with treatment after two months. This is the first case report of such nature in the literature to the best of our knowledge. Key words: Disc edema, neem oil, putamen, toxin-induced encephalopathy, Toxic Optic Neuropathy Secondary to Consumption of Neem Oil
Neem oil (also known as Margosa oil) is a deep yellow oil with an unpleasant taste and smell. It is an extract of the seed of the Neem tree (Azadirachta indica A. Juss ) a native tree of India but now widely distributed throughout Indo-Malaysia.[1] Consumption is usually accidental, rarely suicidal or may be due to nasal instillation for common cold in children as practiced in southern parts of India. Even small doses of neem oil are known to cause severe metabolic acidosis along with seizures which can be refractory with known late neurological sequelae.[2] The diagnosis is based on patient history and neuroophthalmological findings.[3] We report a rare case of toxic optic neuropathy secondary to neem oil consumption associated with neurological manifestations. Access this article online Quick Response Code:
Website: www.ijo.in
Case Report A 35-year-old female patient presented with bilateral visual loss of two days duration (on 16.12.2009) with history of consumption of about 150 ml neem oil five days back (12.12.2009) in an attempted suicide, for which she was taken to the nearby government hospital. She was admitted and treated with induced vomiting after about 2-3 hours of consumption. Patient was asymptomatic for about 48 h in the hospital. Later patient noticed sudden bilateral visual loss and was referred to us for further ophthalmic evaluation. Ophthalmic examination revealed no perception of light in both eyes. Anterior segment examination revealed bilateral 6-mm, dilated and sluggishly reactive pupils. Rest of her anterior segment examination was normal. Her fundus examination showed bilateral, hyperemic and edematous discs with extension of edema along the superior and inferior temporal arcuate fibers for about 2-3 disc diopters from the disc margins. The veins around the disc were mildly dilated and tortuous [Fig. 1 and 2]. The rest of the vitreous, fundus examination revealed no abnormal findings. Neurological examination showed exaggerated deep tendon reflexes and an extensor bilateral plantar reflex. Complete hemogram was within normal limits, Venereal Disease Research Laboratory (VDRL ), HIV1 and 2 were nonreactive. A magnetic resonance imaging (MRI) scan showed bilateral putaminal regions with altered signal, hypointensities in T1-weighted images, hyperintensities on T2-weighted images and hyperintense on Fluid Attenuation Inversion Recovery (FLAIR) images suggestive of cytotoxic edema due to tissue hypoxia [Fig. 3 and 4]. Medical therapy was initiated which included methyl prednisolone 1 g intravenously (IV) for three days followed by oral prednisolone 50 mg /day for 11 days along with 1000 µg vitamin B12 (injection methyl cobalamin – 1000 µg intramuscularly) every five days for eight weeks. Patient did not show any visual improvement after one week of treatment but pupillary reactions improved. During her subsequent follow-up after about 15 days her vision in both eyes improved to counting fingers 1/2 meters and at one month follow-up vision was 20/200 in both eyes and pupillary reactions were normal in both eyes. Her fundus examination showed reduced disc edema [Fig. 5 and 6]
DOI: 10.4103/0301-4738.121129
At two months follow-up her vision remained 20/200 in both eyes and injection methyl cobalamin 1000 µg intramuscular was continued.
PMID: ***
Discussion
Department of Ophthalmology, J. J. M. Medical College, Davangere, Karnataka. Correspondence to: Dr. Suresha Rajappa, Pavan Sadan, No. 2603/12, 2nd Cross, MCC A Block Davangere, Karnataka – 577 004, India E-mail: [email protected] Manuscript received: 25.02.10; Revision accepted: 17.05.10
Neem oil, also known as Margosa oil is obtained from the neem plant (Azadirachta indica A. Juss). Neem oil is extracted from oil seed kernels. It contains neutral oils such as palmitic and stearic acids. The active ingredients are terpenoids such as azadirachtin, nimbin, picrin and sialin. It also contains aflatoxin, but in very low concentrations. Azadirachtin is attributed with the pesticide action of neem oil. It is used as an insecticide for arthropod pests.[1]
338
Indian Journal of Ophthalmology
Vol. 62 No. 3
Figure 1: Right Eye Fundus picture showing disc edema, venous tortuosity with extension of edema along the superior and inferior arcades for about 2-3 disc diopters from the disc margins
Figure 2: Left Eye Fundus picture showing disc edema, venous tortuosity with extension of edema along the superior and inferior temporal arcades for about 2-3 disc diopters from the disc margins
Figure 3: Bilateral putaminal regions showed altered signal hypointensities in T1W images
Figure 4: Hyperintensities on T2W images
Figure 5: Right Eye Fundus picture showing reduced disc edema
Figure 6: Left Eye Fundus picture showing reduced disc edema
Neem oil is used as a traditional medicine in India for various diseases like headache, gastrointestinal disorders, as a male contraceptive, menstrual disorders, asthma etc.
Neem oil poisoning causes vomiting which occurs within minutes to hours following ingestion of the oil. Drowsiness and tachypnea with acidotic respiration followed by recurrent
March 2014
Brief communications
generalized seizures are the other clinical features. The seizures are usually associated with loss of consciousness and coma.[4] In our case, patient had bilateral toxic optic neuropathy. Patient had consumed 150 ml of neem oil which had the following contents: Neem oil kernel extract in solvent methanol containing 0.15%, Azadirachtin – 60%, Emulsifier-5%, treated Neem oil – 35%. No specific antidote is available. Gastric lavage is not recommended. Treatment is primarily symptomatic. [5] She had bilateral toxic optic neuropathy with exaggerated deep tendon reflexes and extensor plantar reflex. MRI scan findings were suggestive of acute toxic encephalopathy and it can be considered as a possible etiology for bilateral toxic optic neuropathy.[6] We treated her with injection IV methyl prednisolone 1 g per kg body weight for three days based on case reports on methanol poisoning.[7]
References 1. Rahaman A, Talukder FA. Bio efficacy of some plant derivatives that protect grain against the pulse beetle. Callosobruchus maculates.
339
J Chem Ecol 1993;19:246-7. 2. Dhongade RK, Kavade SG, Damle RS. Neem Oil Poisoning. Indian Pediatr 2008;45:55-7. 3. Halavaara J, Valanne L, Setala K. Neuroimaging supports the clinical diagnosis of methanol poisoning. Neuroradiology 2002;44:924-8. 4. Sinniah D, Baskaran G. Margosa oil poisoning as a cause of Reye’s Syndrome. Lancet 1981;1:487-9. 5. Lai SIM, Lim KW, Ching HK. Margosa Oil Poisoning as a cause of toxic encephalopathy. Singapore Med J 1990;31:463-5. 6. Dietemann JL, Botelho C, Nogueira T, Vargas MI, Audibert C, Abu Eid M, et al. Imaging in acute toxic encephalopathy. J Neuro radiol 2004;31:313-26. 7. Sodhi PK, Goyal JL, Mehta DK. Methanol-induced optic neuropathy: Treatment with intravenous high dose steroids. Int J clin pract 2001;55:599-602. Cite this article as: Suresha AR, Rajesh P, Anil Raj KS, Torgal R. A rare case of toxic optic neuropathy secondary to consumption of neem oil. Indian J Ophthalmol 2014;62:337-9. Source of Support: Nil. Conflict of Interest: None declared.
Limbal dermoid in Nager acrofacial dysostosis: A rare case report
with Nager syndrome. We did not find such an association of “Limbal dermoid in Nager acrofacial dysostosis syndrome” on PubMed using Nager acrofacial dysostosis, limbal dermoid and ocular manifestations as the keywords.
Rohit Malik, Sumit Goel1, Saurabh Aggarwal2
Key words: Absent thumb, craniofacial defects, limbal dermoid, Nager syndrome
Nager syndrome, also called preaxial acrofacial dysostosis, comprises two groups of defects involving the limbs and craniofacial region, respectively. This syndrome is rare and only 70 cases have been reported in the literature. The exact cause of this syndrome is unknown, but there is indication that it is genetically based. Ocular manifestations of this syndrome include widely separated downward slanting eyes, absence of eyelashes, ptosis of upper eyelids and colobomas on the inner aspect of lower eyelids. We report limbal dermoid in a patient
Access this article online Quick Response Code:
Website: www.ijo.in DOI: 10.4103/0301-4738.111194 PMID: ***
Department of Oral Medicine and Radiology, Institute of Dental Studies and Technologies, Modinagar, 1Department of Oral Medicine and Radiology, Subharti Dental College and Hospital, Meerut, Uttar Pradesh, 2Department of Ophthalmology, Moolchand Hospital, Meerut, Uttar Pradesh, India Correspondence to: Dr. Sumit Goel, B 202 Nandan Apartment, 31 A Saket, Meerut, Uttar Pradesh, India. E‑mail: [email protected] Manuscript received: 11.08.10; Revision accepted: 09.07.12
Nager syndrome, also called preaxial acrofacial dysostosis, was first described by Nager and Reynier in 1948.[1,2] It consists of a defect in the development of the first and second branchial arches and in the formation of cartilage.[1,2] Typically, Nager acrofacial dysostosis (NAFD) comprises two groups of defects involving the limbs and craniofacial region, respectively.[1,3] The former are mainly deficiencies mostly affecting the upper limbs. The latter form a complex indistinguishable from mandibulofacial dysostosis (MFD).[2] The prevalence is unknown; about 70 cases of Nager syndrome have been published. The MFD complex is unmistakable and comprises hypoplasia of the malar eminences and zygomata, hypoplasia of maxilla with cleft of secondary palate or highly‑arched palate, absence of velum (rarely with choanal atresia), and extension of a “tongue” of temporal hair down the sides of the cheeks. The ocular features are important and include downward slant of palpebral fissures, ptosis of upper lids, coloboma of lower lids, and deficiency of eyelashes of the medial one‑third to two‑thirds of the lower eyelids. Hypoplasia or absence of thumbs is the most characteristic feature almost invariably associated with radio‑ulnar synostosis. Triphalangeal thumbs and index finger are equally characteristic. Most NAFD individuals have normal intelligence, and after infancy most are healthy and are presumed to have a normal lifespan. All acrofacial dysostosis must be considered as genetic disorders until proven otherwise, and parents deserve careful scrutiny for mild manifestations.[1‑3]
Copyright of Indian Journal of Ophthalmology is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
Neem oil (also known as Margosa oil) is a deep yellow oil with an unpleasant taste and smell. It is an extract of the seed of the Neem tree (Azadirachta indica A. Juss ) a native tree of India but now widely distributed throughout Indo-Malaysia.[1] Consumption is usually accidental, rarely suicidal or may be due to nasal instillation for common cold in children as practiced in southern parts of India. Even small doses of neem oil are known to cause severe metabolic acidosis along with seizures which can be refractory with known late neurological sequelae.[2] The diagnosis is based on patient history and neuroophthalmological findings.[3] We report a rare case of toxic optic neuropathy secondary to neem oil consumption associated with neurological manifestations. Access this article online Quick Response Code:
Website: www.ijo.in
Case Report A 35-year-old female patient presented with bilateral visual loss of two days duration (on 16.12.2009) with history of consumption of about 150 ml neem oil five days back (12.12.2009) in an attempted suicide, for which she was taken to the nearby government hospital. She was admitted and treated with induced vomiting after about 2-3 hours of consumption. Patient was asymptomatic for about 48 h in the hospital. Later patient noticed sudden bilateral visual loss and was referred to us for further ophthalmic evaluation. Ophthalmic examination revealed no perception of light in both eyes. Anterior segment examination revealed bilateral 6-mm, dilated and sluggishly reactive pupils. Rest of her anterior segment examination was normal. Her fundus examination showed bilateral, hyperemic and edematous discs with extension of edema along the superior and inferior temporal arcuate fibers for about 2-3 disc diopters from the disc margins. The veins around the disc were mildly dilated and tortuous [Fig. 1 and 2]. The rest of the vitreous, fundus examination revealed no abnormal findings. Neurological examination showed exaggerated deep tendon reflexes and an extensor bilateral plantar reflex. Complete hemogram was within normal limits, Venereal Disease Research Laboratory (VDRL ), HIV1 and 2 were nonreactive. A magnetic resonance imaging (MRI) scan showed bilateral putaminal regions with altered signal, hypointensities in T1-weighted images, hyperintensities on T2-weighted images and hyperintense on Fluid Attenuation Inversion Recovery (FLAIR) images suggestive of cytotoxic edema due to tissue hypoxia [Fig. 3 and 4]. Medical therapy was initiated which included methyl prednisolone 1 g intravenously (IV) for three days followed by oral prednisolone 50 mg /day for 11 days along with 1000 µg vitamin B12 (injection methyl cobalamin – 1000 µg intramuscularly) every five days for eight weeks. Patient did not show any visual improvement after one week of treatment but pupillary reactions improved. During her subsequent follow-up after about 15 days her vision in both eyes improved to counting fingers 1/2 meters and at one month follow-up vision was 20/200 in both eyes and pupillary reactions were normal in both eyes. Her fundus examination showed reduced disc edema [Fig. 5 and 6]
DOI: 10.4103/0301-4738.121129
At two months follow-up her vision remained 20/200 in both eyes and injection methyl cobalamin 1000 µg intramuscular was continued.
PMID: ***
Discussion
Department of Ophthalmology, J. J. M. Medical College, Davangere, Karnataka. Correspondence to: Dr. Suresha Rajappa, Pavan Sadan, No. 2603/12, 2nd Cross, MCC A Block Davangere, Karnataka – 577 004, India E-mail: [email protected] Manuscript received: 25.02.10; Revision accepted: 17.05.10
Neem oil, also known as Margosa oil is obtained from the neem plant (Azadirachta indica A. Juss). Neem oil is extracted from oil seed kernels. It contains neutral oils such as palmitic and stearic acids. The active ingredients are terpenoids such as azadirachtin, nimbin, picrin and sialin. It also contains aflatoxin, but in very low concentrations. Azadirachtin is attributed with the pesticide action of neem oil. It is used as an insecticide for arthropod pests.[1]
338
Indian Journal of Ophthalmology
Vol. 62 No. 3
Figure 1: Right Eye Fundus picture showing disc edema, venous tortuosity with extension of edema along the superior and inferior arcades for about 2-3 disc diopters from the disc margins
Figure 2: Left Eye Fundus picture showing disc edema, venous tortuosity with extension of edema along the superior and inferior temporal arcades for about 2-3 disc diopters from the disc margins
Figure 3: Bilateral putaminal regions showed altered signal hypointensities in T1W images
Figure 4: Hyperintensities on T2W images
Figure 5: Right Eye Fundus picture showing reduced disc edema
Figure 6: Left Eye Fundus picture showing reduced disc edema
Neem oil is used as a traditional medicine in India for various diseases like headache, gastrointestinal disorders, as a male contraceptive, menstrual disorders, asthma etc.
Neem oil poisoning causes vomiting which occurs within minutes to hours following ingestion of the oil. Drowsiness and tachypnea with acidotic respiration followed by recurrent
March 2014
Brief communications
generalized seizures are the other clinical features. The seizures are usually associated with loss of consciousness and coma.[4] In our case, patient had bilateral toxic optic neuropathy. Patient had consumed 150 ml of neem oil which had the following contents: Neem oil kernel extract in solvent methanol containing 0.15%, Azadirachtin – 60%, Emulsifier-5%, treated Neem oil – 35%. No specific antidote is available. Gastric lavage is not recommended. Treatment is primarily symptomatic. [5] She had bilateral toxic optic neuropathy with exaggerated deep tendon reflexes and extensor plantar reflex. MRI scan findings were suggestive of acute toxic encephalopathy and it can be considered as a possible etiology for bilateral toxic optic neuropathy.[6] We treated her with injection IV methyl prednisolone 1 g per kg body weight for three days based on case reports on methanol poisoning.[7]
References 1. Rahaman A, Talukder FA. Bio efficacy of some plant derivatives that protect grain against the pulse beetle. Callosobruchus maculates.
339
J Chem Ecol 1993;19:246-7. 2. Dhongade RK, Kavade SG, Damle RS. Neem Oil Poisoning. Indian Pediatr 2008;45:55-7. 3. Halavaara J, Valanne L, Setala K. Neuroimaging supports the clinical diagnosis of methanol poisoning. Neuroradiology 2002;44:924-8. 4. Sinniah D, Baskaran G. Margosa oil poisoning as a cause of Reye’s Syndrome. Lancet 1981;1:487-9. 5. Lai SIM, Lim KW, Ching HK. Margosa Oil Poisoning as a cause of toxic encephalopathy. Singapore Med J 1990;31:463-5. 6. Dietemann JL, Botelho C, Nogueira T, Vargas MI, Audibert C, Abu Eid M, et al. Imaging in acute toxic encephalopathy. J Neuro radiol 2004;31:313-26. 7. Sodhi PK, Goyal JL, Mehta DK. Methanol-induced optic neuropathy: Treatment with intravenous high dose steroids. Int J clin pract 2001;55:599-602. Cite this article as: Suresha AR, Rajesh P, Anil Raj KS, Torgal R. A rare case of toxic optic neuropathy secondary to consumption of neem oil. Indian J Ophthalmol 2014;62:337-9. Source of Support: Nil. Conflict of Interest: None declared.
Limbal dermoid in Nager acrofacial dysostosis: A rare case report
with Nager syndrome. We did not find such an association of “Limbal dermoid in Nager acrofacial dysostosis syndrome” on PubMed using Nager acrofacial dysostosis, limbal dermoid and ocular manifestations as the keywords.
Rohit Malik, Sumit Goel1, Saurabh Aggarwal2
Key words: Absent thumb, craniofacial defects, limbal dermoid, Nager syndrome
Nager syndrome, also called preaxial acrofacial dysostosis, comprises two groups of defects involving the limbs and craniofacial region, respectively. This syndrome is rare and only 70 cases have been reported in the literature. The exact cause of this syndrome is unknown, but there is indication that it is genetically based. Ocular manifestations of this syndrome include widely separated downward slanting eyes, absence of eyelashes, ptosis of upper eyelids and colobomas on the inner aspect of lower eyelids. We report limbal dermoid in a patient
Access this article online Quick Response Code:
Website: www.ijo.in DOI: 10.4103/0301-4738.111194 PMID: ***
Department of Oral Medicine and Radiology, Institute of Dental Studies and Technologies, Modinagar, 1Department of Oral Medicine and Radiology, Subharti Dental College and Hospital, Meerut, Uttar Pradesh, 2Department of Ophthalmology, Moolchand Hospital, Meerut, Uttar Pradesh, India Correspondence to: Dr. Sumit Goel, B 202 Nandan Apartment, 31 A Saket, Meerut, Uttar Pradesh, India. E‑mail: [email protected] Manuscript received: 11.08.10; Revision accepted: 09.07.12
Nager syndrome, also called preaxial acrofacial dysostosis, was first described by Nager and Reynier in 1948.[1,2] It consists of a defect in the development of the first and second branchial arches and in the formation of cartilage.[1,2] Typically, Nager acrofacial dysostosis (NAFD) comprises two groups of defects involving the limbs and craniofacial region, respectively.[1,3] The former are mainly deficiencies mostly affecting the upper limbs. The latter form a complex indistinguishable from mandibulofacial dysostosis (MFD).[2] The prevalence is unknown; about 70 cases of Nager syndrome have been published. The MFD complex is unmistakable and comprises hypoplasia of the malar eminences and zygomata, hypoplasia of maxilla with cleft of secondary palate or highly‑arched palate, absence of velum (rarely with choanal atresia), and extension of a “tongue” of temporal hair down the sides of the cheeks. The ocular features are important and include downward slant of palpebral fissures, ptosis of upper lids, coloboma of lower lids, and deficiency of eyelashes of the medial one‑third to two‑thirds of the lower eyelids. Hypoplasia or absence of thumbs is the most characteristic feature almost invariably associated with radio‑ulnar synostosis. Triphalangeal thumbs and index finger are equally characteristic. Most NAFD individuals have normal intelligence, and after infancy most are healthy and are presumed to have a normal lifespan. All acrofacial dysostosis must be considered as genetic disorders until proven otherwise, and parents deserve careful scrutiny for mild manifestations.[1‑3]
Copyright of Indian Journal of Ophthalmology is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
