By:

Dr Jami Swathi

Prof Dr A.Gowrishankar’s unit

A RARE COMPLICATION OF A COMMON POISONING

Mrs Jasmine, 22yr old,

Admitted in IMCU on 3/3/11 at 12.05am with history of consumption of unnamed agricultural poison, on 2/3/11 at 8pm

she was brought in, in an unconscious state with h/o excesssive salivation & frothing from the mouth

O/E:

unconscious

not responding to oral commands

moving limbs to deep pain

afebrile

No pallor, icterus, cyanosis, lymphadenopathy, edema

Vitals: pulse: 92/min

BP: 90/60 mm Hg

SpO2: 90%

CVS: S1 S2 heard, no murmurs

RS: NVBS heard, Min wheeze + B/L

P/ A : soft

CNS: unconscious

not responding to oral commands

moves all the limbs to pain

pupil- pin point B/L

She was immediately treated along the lines of OPC posioning with stomach wash; Atropine- 2mg stat initially then titrated according to the responsePralidoxime: 1500 mg infusion over 30mins followed by 500mg/ hr

After about 16 cc of atropine, pts BP picked up to 110/70 mm Hg,

SpO2: 99%

RS: clear

GCS: 9/15

Patient was then treated with atropine 2mg every 30mins- 1hr and

Pralidoxime ( P2AM) infusion- 500mg/hr

InvestigationsCBC: Hb 11 gm%

TC DC

12000 cells/ cu mm P68 L32

ESR 6/ 15

Platelets 1,80,000

RBS 82 mg %

RFT: UREA: 28 mg/dl

CREATININE: 0.8 mg/dl

LFT WNL

Serum cholinesterase 1,500 (normal: 3000- 11,000)

3/3/11:At 9 pm, pt was intubated in view of excessive secretions, poor GCS (9/15) & falling SpO2 (79%) and connected to the ventilator

Pralidoxime & atropine (sos) was continued but pts general condition didnt improveInj Taxim and Metrogyl added

Serum cholinesterase- 1500

5/3/11:8am:

Proptosis of both the eyes & chemosis of

B/L conjunctiva noticed. Secretions+, no

pus, swab taken & sent for C/S. Antibiotic

eye drops added

8/3/11: Pts GCS improved and was weaned off the ventilator & put on T ‘piece’ Serum cholinesterase: 1368 Pralidoxime infusion continued Conjunctival chemosis persisted

13/3: day 10 of admission: Pt extubated Serum cholinesterase: 5480 Pralidoxime infusion as well as atropine

stopped

14/3: EOM: restriction in all the directions noticed ophthal opinion obtained, & as pts vitals were

stable she was then shifted to medical ward on

15th

15/3: conjunctiva & cornea clear EOM: B/L restriction in all the directions swab C/S - negative

Right Left

Visual acuity Perception of light + Perception of light +

Cornea& conjunctiva Clear Clear

EOM Restricted in all the directions Restricted

Pupil Dilated & not reacting to light Dilated & not reacting to light

• Over the next few days, patient recovered from the opthalmoplegia but visual acuity improved only slightly.

• Pt can now appreciate finger movements

What are the possibilities??...

Cavernous sinus thrombosis???..

Demyelination as a complication of OPC???!!!!...

CT

ORBIT

NORMAL

MRI BRAIN

Ophthal opinion: on 5/3/11

imp: B/L acute proptosis ? Caverous sinus thrombosis

Right LeftEdema of lids Present Present

Conjunctival chemosis

Present Present

Proptosis Present Present

Pupil Mid dilated Mid dilated

EOM Could not be assessed

Ophthal review: 17/3/11:

Right LeftVisual acuity Perception of light + Perception of light +

Cornea& conjunctiva Clear Clear

EOM Restricted in all the directions

Restricted

Pupil Dilated Dilated

Fundus examination Retina pale,Arteriolar narrowing + Disc appears paleMacular hyperpigmentation seen? Cherry red spot

Retina pale,Arteriolar narrowing + Disc appears paleMacular hyperpigmentation seen? Cherry red spot

Ophthal chief’s opinion: 19/3/11

Retina mottled,

Pigment mottling in macula

Imp: Retinal pigment degeneration

Suggested ERG:

ERG

Retinal pigment degeneration secondary to OPC poisoning

WHAT MAKES RETINA VULNERABLE TO TOXIN INDUCED DAMAGE??..

High rate of oxidative mitochondrial metabolism Highly fenestrated choriocapillaries high turn over of rods & cone outer segments high susceptibility of rods & cones to degeneration due to

inherited retinal dystrophies very high choroidal blood flow additive/ synergestic action of certain chemicals with light

• Nippon Ganka Gakkai Zasshi. 1973 Oct;77(10):1835-86.

• [Chronic optico-neuropathy due to environmental exposure of organophosphate pesticides (Saku disease) --clinical and experimental study (author's transl)].

• J Appl Toxicol. 1994 Mar-Apr;14(2):119-29.

• Ocular effects of organophosphates: a historical perspective of Saku disease.• Dementi B.

• Source• US Environmental Protection Agency, Washington, DC 20460.

• Abstract• Many publications, primarily of work performed in Japan, report findings in human populations of an

increased incidence of myopia and of a more advanced visual disease syndrome) (Saku disease), which reportedly correlated with increasing use of organophosphate pesticides in agriculture. Follow-up studies in animals performed in Japan using such agents as ethylthiometon, fenthion and fenitrothion demonstrate adverse effects of organophosphates on the visual system. The several ocular effects in question are dose dependent, ranging in severity from lenticular and electro-retinographic changes to the seemingly more serious histophysiological changes in such tissues as the ciliary body and retina. An important question arising from this work is that of the role of cholinesterase inhibition in the etiology of the effects. Studies currently in progress on particular organophosphates being conducted at EPA's research facility and by certain registrants of pesticides, which are in various stages of completion, appear to be substantiating much that has been reported in Japan. While animal studies clearly show that some organophosphates elicit ocular toxicity, there are many knowledge gaps with regard to effects in humans and the ocular toxicity in general, e.g. time and dose dependency, cholinesterase inhibition vs ocular effects and effects of routes of exposure.

• Environ Health Prev Med. 2006 May;11(3):102-7.

• Ocular toxicity from pesticide exposure: A recent review.• Jaga K, Dharmani C.

• Source• Department of Psychiatry, Mount Sinai School of Medicine, 51 Eiler Lane, 10533, Irvington, New York,

USA, Kushik.laga@med.va.gov.

• Abstract• Toxic effects on eyes result from exposure to pesticides via inhalation, ingestion, dermal contact and

ocular exposure. Exposure of unprotected eyes to pesticides results in the absorption in ocular tissue and potential ocular toxicity. Recent literature on the risks of ocular toxicity from pesticide exposure is limited.Ocular toxicity from pesticide exposure, including the dose-response relationship, has been studied in different animal species. Cholinesterase enzymes have been detected in animal ocular tissue, with evidence of organophosphate-induced inhibition. Pathological effects of pesticides have been observed in conjunctiva, cornea, lens, retina and the optic nerve. Pesticide exposure has been associated with retinopathy in agricultural workers and wives of farmers who used pesticides. Saku disease, an optico-autonomic peripheral neuropathy, has been described in Japan in people living in an area where organophosphates were used. Pesticide exposure is also associated with abnormal ocular movements.Progressive toxic ocular effects leading to defective vision are a serious health concern. Agricultural workers are at high risk of exposure to pesticides and associated ocular toxicity.

Retinal Degeneration and Other Eye Disorders in Wives of Farmer PesticideApplicators Enrolled in the Agricultural Health Study

Ellen F. Kirrane1, Jane A. Hoppin2, Freya Kamel2, David M. Umbach2, William K. Boyes3,

Anneclaire J. DeRoos4,5, Michael Alavanja6, and Dale P. Sandler2

Internuclear Ophthalmoplegia after Insecticide Exposure Katherine A. KovacsAnn Intern Med December 5, 2000 133:926

Thank you