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Unusual Complication of OPC Poisoning
 

Unusual Complication of OPC Poisoning

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    Unusual Complication of OPC Poisoning Unusual Complication of OPC Poisoning Presentation Transcript

    • DR. PRIYA KUBENDIRAN PROF. DR. MAGESH KUMAR M 1 UNIT
    • The Case…
      • 18 Yrs old female was admitted on 23 rd April
      • Alleged h/o consumption of organo phosphorus pesticide (chlorpyrifos)
      • Qty unknown; h/o vomiting present
      • O/E Pt Conscious, oriented, afebrile,
      • excesive salivation
      • Pupils miotic, 0.5mm
      • PR: 70/min
      • BP: 100/70mm Hg
      • RR: 15/min
      • Spo2: 90%
      • CVS: S1S2 heard
      • RS: NVBS heard, B/L crepitations
      • P/A soft
      • CNS: NFND
      • INVESTIGATIONS
      • Sr cholinesterase: 190 IU/L
      • CBC:
      • Hb: 10g%
      • TC: 8000/cu mm
      • DC: P60/L38/E2
      • ESR: 4/10
      • RFT:
      • Sugar: 90mg%
      • Urea: 20mg%
      • Creatinine: 0.5mg%
      • CXR: WNL
      • ECG: NSR
      • Treatment Given:
      • Supportive
      • Atropine
      • Pralidoxime
      • DAY 4
      • Patient was shifted to ward
      • DAY 5
      • H/O altered sensorium since morning
      • H/O breathlessness
      • H/O increased Salivation
      • O/E : Pt conscious, drowsy, afebrile
      • Puplils miotic 0.5mm
      • CVS:S1S2 heard
      • RS:NVBS heard,B/L Crackles heard
      • P/A:soft
      • CNS: Pupils miotic
      • Plantar B/L flexor
      • Diagnosis - INTERMEDIATE SYNDROME
      • Was shifted back to IMCU
      • Serum cholinesterase levels :
      • 28/04:221 IU/L
      • 29/04:310IU/L
      • 30/04:331 IU/L
      • 01/05:500 IU/L
      • DAY 10
      • Pt transferred to ward
      • DAY 12
      • Pt experienced difficulty in walking
      • H/O dragging of feet while walking
      • Had difficulty in holding slippers
      • H/O difficulty in standing from squatting posture
      • No H/O upper limb involvement
      • No H/O muscle twitching
      • NO H/O cramps
      • NO H/O cranial nerve involvement
      • NO H/O unsteadiness in dark,swaying, involuntary movements
      • H/O tingling sensation in the legs
      • NO H/O alteration in bladder/bowel habits
      • NO H/O fever ,head injury
      • O/E : Pt conscious ,oriented,
      • Hr functions normal
      • Cranial nerves clinically normal
      • EOM full range, pupils B/L 4mm ERLA
      • Tone UL N N
      • LL
      • Power UL 5 5
      • LL hip 3 3
      • knee 3 3
      • ankle 3 3
      • Reflexes UL + +
      • knee - -
      • ankle - -
      • plantar no response
      • Gait - couldn’t be tested
      • No sensory deficit
      • no cerebellar signs
      • Provisional diagnosis -
      • ? Toxin induced demyelination
      • NEURO LOGIST’S OPINION:
      • ?post toxic demyelination
      • Suggested inj methyl prednisolone
      • NCS of all 4 limbs, EEG, MRI brain
      • INVESTIGATIONS :
      • EEG : normal
      • MRI BRAIN: normal
      • LP : acellular,
      • sugar - 50 mg/dl
      • protein - 76 mg/dl
      • NCS : s/o demyelination
      • TREATMENT & COURSE
      • Inj methylprednisolone 1g iv od - 5 days
      • Inj B complex im od
      • Her power gradually improved to grade 4
      • She was advised :
      • T.Prednisolone 60 mg od - tapering dose
      • T. Ranitidine 150 mg bd
      • BCT bd
    • FINAL DIAGNOSIS
      • ORGANOPHOSPHORUS POSONING /
      • INTERMEDIATE SYNDROME /
      • OPC INDUCED DELAYED NEUROPATHY (OPIDN)
    • OPC POISONING
      • Very Common Poisoning In Tamilnadu
      • 3 Million Cases, 20,000 Deaths /YR World Wide.
      • 1930, Schrader, German, Studied Mech of Toxicity
      • Weapon of Chemical Warfare.
    • Mechanism of OP’s
    • ANS Preganglionic Parasympathetic Sympathetic Somatic Nerves Ach Ach Ach Ach Ach Ganglion Epi Skeletal Muscle Ach Ach Norepi Via Bld Effector Organs + Pupil -Heartrate +Exocrine Glands +GIT Smooth Muscle +Lung Smooth Muscle +Sweatgld -Bloodvessel [Some ] - Pupil +Heart Rate -Gastrointestinal SM -Lung SM +Blood Vessels [Most] Often The Parasympathetic Features Predominates Post Ganglionic
    • Clinical Syndrome
      • Acute Cholinergic:
        • Central
        • Peripheral Muscarinic
        • Peripheral Nicotinic
      • Intermediate Syndrome
      • OPIDN: Delayed peripheral neuropathy
      • Neurocognitive dysfunction
      + Death Respiratory failure }
    • Muscarinic Effects (Wadia Type 1 syndrome
      • D iarrhoea
      • U rination
      • M iosis
      • B radycardia, Bronchorrhoea, Bronchospasm
      • E mesis
      • L acrimation
      • S alivation
    • NICOTINIC FEATURES: CENTRAL : LESS WITH CARBAMATES
      • Muscle Fasciculations
      • [Striated]
      • Paralysis
      • Muscle Weakness
      • Hypertension
      • Tachycardia
      • Mydriasis [Rare]
      • Unconsciousness
      • Confusion, Fatigue
      • Toxic Psychosis, Seizures
      • Resp. Depression
      • Ataxia, Dysarthria
      • Extra Pyramidal Features.
    • DELAYED COMPLICATIONS
      • Occurs 24-96hrs,
      • Weakness of Ocular, Bulbar, Proximal Limb Muscles, And Respiratory Failure.
      • Common With Dimethoate, Parathion, Malathion & Methly Parathion
      • ChE Activity 20% or Less During Onset
      • Causative Factor – Inadequate Oxime Therapy / Premature DIS.
      • Recovery in 4 – 18 Days.
      • Electrophysiological study shows significant decremental response at low frequency stimulation
      INTERMEDIATE SYNDROME : [FIRST DESCRIBED IN 1987] [WADIA TY-II]
    • OPIDN ( Organophosphorus induced delayed neurotoxicity)
      • The underlying pathology in OPIDN involves
      • bilaterally symmetrical degeneration of sensory and motor axons in distal regions of peripheral nerves and spinal cord tracts.
      • The distal part of longest, largest diameter fibers tend to be preferentially affected.
      • Lesions are characterized by the degeneration of axons with subsequent secondary degeneration of myelin
    • Pathogenesis
      • Due to inhibition of a protein called Neuropathy target esterase (NTE) by phosphorylation
      • NTE is an integral membrane protein present in all neurons and in some non-neural-cell types of vertebrates.
      • Recent data indicate that NTE is involved in a cell-signalling pathway controlling interactions between neurons and accessory glial cells in the developing nervous system
      • Organophosphates + NTE
      • initiate unknown events
      • toxin covalently attached to active-site of NTE
      • Toxic gain of function of NTE
      • (delay of 1±3 weeks),
      • neuropathy with degeneration of long axons
    • Neurological dysfunction of OPIDN
      • Latent period: Days to weeks
      • Progressive phase: Symmetric cramping,
      • numbness and tingling in feet and legs, bilateral dragging of toes (foot-drop), flaccid paralysis.
      • 3. Stationary Phase
      • 4. Improvement Phase: Results from regeneration of PNS; CNS damage becomes unmasked as spasticity and exaggerated knee jerk.
      • 5. Prognosis: Depends on severity of initial symptoms
    • Factors involved in the Development of OPIDN
      • Chemical Structure
      • Animal Species: Humans are most sensitive
      • Individual differences
      • Dose or Concentration at Neurotoxicity Site:
      • a. Exposure dose
      • b. Frequency of exposure
      • c. Duration of exposure
      • d. Route of Exposure
      • e. Other chemical exposure
      • f. Stress
    • Chlorpyrifos-induced delayed polyneuropathy
      • Chlorpyrifos [0,0-diethyl 0-(3,5,6-trichloro-pyridyl) phosphorothioate] caused delayed polyneuropathy in man. Chlorpyrifos was slowly absorbed after single oral doses and the threshold of inhibition (>70%) of neuropathy target esterase (NTE) , the putative target for delayed neuropathy, was reached within 5–6 days
      Eugenio Capodicasa et al, Archives of Toxicology Volume 65, Number 2 ,
    • CASE REPORT -Toxin induced neuropathy presenting as acute inflammatory demyelinating polyneuropathy
      • Calicut Medical Journal 2010 (Manthappa M et al)
      • An adult male patient presented to us with with
      • bilateral symmetric polyneuropathy resembling
      • acute inflammatory demyelinating neuropathy
      • (AIDP). On further questioning, patient gave
      • history of exposure to organophosphate
      • insecticides. Sural nerve biopsy revealed
      • features consistent with toxin induced
      • neuropathy.
    • CASE REPORT - Guillain-Barre Syndrome Due to Organophosphate Compound Poison
      • D Rajasekaran et al, JAPI October 2009
      • Clinical features and investigations of our patient strongly indicated that GBS that he had manifested as a sequelae of OPC poisoning which is possibly toxin induced delayed demyelination
    • Methylprednisolone treatment of an organophosphorus-induced delayed neuropathy
      • A high-dose regimen of methylprednisolone started 30 to 40 min after DFP exposure and lasting for 20 days prevented the development of OPIDN.
      Thomas Baker and Anna Stanec Toxicology and Applied Pharmacology Volume 79, Issue 2 , 30 June 1985,
    • Effects of Prednisolone and complex of vitamin B1,B2,B6 & B12 on organophosphorus compound induced delayed neurotoxicity Fengyuan Piao et al, J Occup Health 2004
      • It was observed that delayed neuropathy induced by OPs could not be resisted completely by the treatment with prednisolone or vitamin b complex, but clinical signs of OPIDN and pathological changes in hens that received these 2 protective agents after OPs were less severe than those in hens that received only OPs
    • Chronic organophosphate induced neuro psychiatric disorder (COPIND)
      • Is a neurodegenerative disorder that results from large toxic or small subclinical doses of OPCs.
      • Clinical signs, which continue for weeks to years, consist of neurological abnormalities
      • drowsiness,
      • confusion, lethargy, anxiety, emotional lability,
      • depression, fatigue ,irritability, memory disturbances
      • Neuronal cell death is seen in various brain areas including cerebral cortex, hippocampal formation and cerebellum.
      • Cell death results from early necrosis or delayed apoptosis.
    •