OP poisoning treatment

1. ORGANOPHOSPHORUS
POISONING
BY DR.BRAMHA GHUGE
DATE-26/10/23

2. DIAGNOSIS
MANAGEMENT
COMPLICATIONS AND TREATMENT

3. DIAGNOSIS
 IT IS BASED ON H/O EXPOSURE TO OP COMPOUNDS
,CHARACTERISTICS MANIFESTATIONS OF TOXICITY AND
IMPROVEMENT OF SIGN AND SYMPTOMS AFTER ADMINISTRATION OF
ATROPINE .
 GARLIC-LIKE SMELL IS AN ADDED CLINICAL SIGN ESPECIALLY IS THE
PATIENT HAS INGESTED SULPHUR CONTAINING OP COMPOUND.
 THIS MAY BE AIDED BY INSISTING THE PATIENT ATTENDENT TO
SEARCH FOR A POSSIBLE POISON CONTAINER IN THE VICINITY OF
THE PATIENT .

4.  CHOLINESTERERASE (ChE)
1) PLASMACHOLINESTERASE
 GRADED AS
MILD -20-50 % ENZYME ACTIVITY .
MOD -10-20% ENZYME ACTIVITY .
SEVERE-<10% ENZYME ACTIVITY .
 ENZYME ACTIVITY DOSE NOT CORRELATE WELL WITH CLINICAL
SEVERIITY
 EASLY ASSAYED
2) RED CELL ACETYLCHOLINESTERASE
 DIFFICULT TO ASSAY
 CORERELATE WELL WITH CLINICAL SEVERITY AND INCREASE ACTIVITY
AFTER PRALIDOXIME THERAPY

5.  ANALYTICAL IDENTIFICATION OF OP COMPOUND IN GASTRIC ASPIRATE
OR IN BODY FLUIDS GIVES THE CLUE THAT PATIENT HAS BEEN EXPOSED
TO OP COMPOUND .
 IN DOUBTFUL CASES AND IF LAB FACILITY NOT AVAILABLE ,1MG
ATROPINE CAN BE GIVEN IV .IF THIS DOES NOT PRODUCE MARKED
ANTICHOLINERGIC MANIFESTATIONS ,ANTICHOLINESTERASE POISONING
SHOULD BE STRONGLY SUSPECTED .

6. MANAGEMENT
 DECONTAMINATION AND SUPPORTIVE THERAPY
 BLOCKADE OF MUSCARINIC ACTIVITY WITH ATROPINE .
 REVERSAL OF CHOLINESTERASE INHIBITION WITH OXIME
 CORRECTIONS OF METABOLIC ABNORMALITIES
 PREVENTION OF INFECTIONS

7. DECONTAMINATION AND SUPPORATIVE
THERAPY
 COMATOSE OR VOMITING PT SHOULD BE KEPT IN LEFT LATERAL ,PREFERABLY
DOWN POSITION WITH NECK EXTENSION TO REDUCE RISK OF ASPIRATION .
 PT AIRWAY SHOULD BE SECURED WITH PLACEMENT OF AIRWAY OR
ENDOTRACHEAL INTUBATION ESPECIALLY IF THE PT IS UNCONSCIOUS OR
HAVING SEIZURE .
 FREQUENT SUCTIONING IS ESSENTIAL AS EXCESSIVE OROPHYRANGEAL AND
RESPIRATORY SECERATIONS MAY OCCLUDE THE AIRWAY.
 NEED OF OXYGEN THERAPY.
 ALL CLOTHING ,HAIR ACCESSORIES ARE TO BE REMOVED AND PLACED IN
APPROPRIATE WAETW BAGS.THE PERSON IS TO WASHED WITH COPIOUS
AMOUNT OF WATRER AND SOAP .

8. GASTRIC LAVAGE
 SHOULD BE CONSIDERED IN PT PRESENTING WITHIN 1-2 HR OF INGESTION OF
POISONS .
 RISK OF GASTRIC LAVAGE INCLUDE ASPIRATION,HYPOXIA AND LARYNGEAL SPASM
 REDUCE WITH PROPER MANAGEMENT OF AIRWAY.
ACTIVATED CHARCOAL
 REDUCE THE POISON LOAD BY ABSORBING IT
 SINGLE AND MULTIPLE DOSE IS ROUTINELY USED IN CLINICAL PRACTICE (25GM
2 HOURLY)

9. BLOCKADE OF MUSCARINIC ACTIVITY
WITH ATROPINE
 NO EFFECT ON NICOTINIC SYMPTOMS .
 RECOMMENDED DOSE –
INITIAL IV BOLUS 1.8 -3 MG WITH SUBSEQUENT DOSES DOUBLED EVERY 5 MIN IF
THERE IS NO RESPONSE OR REPEAT SAME DOSE UNTIL ATROPINISATION IS ACHIEVED
 MAINTEINANCE DOSE
20% OF INITIAL ATROPINIZING DOSE PER HR FOR FIRST 48 HR AND GRADUALLY
TAPER OVER 5-10 DAYS ,CONTINUOUSLY MONITORING THE ADEQUACY OF THERAPY
 TARGET END POINTS FOR ATROPINE THERAPY
HR>80/MIN,DILATED PUPPILS,DRY AXILLAE ,SYSTOLIC BP >80 ,CLEAR CHEST ON
AUSCULTATION WITH RESOLUTION OF BRONCHORRHEA (ABSENSE OF WHEEZE AND
CREPTS)

10.  LOOK FOR ATROPINE TOXICITY
 AGITATION,CONFUSION,HYPERTHERMIA,URINARY RETENTION ,SEVERE
TACHYCARDIA
 CAN PRECIPITATE ISCHEMIC EVENTS IN PT WITH UNDERLYING CAD.
 GLYCOPYRROLATE
 ANTICOLINERGIC AGENT GLYCOPYRROLATE ALONG WITH ATROPINE CAN BE
USED IN ORDER TO LIMIT THE CENTRAL STIMULATION PRODUCED BY ATROPINE .
 GLYCOPYROLATE 7.5 MG IN 200ML OF SALINE IS STARTED AS INFUSION AND
TITRATED AS PER DESIRED EFFECT IF ATROPINE NOT AVAILABLE AND COPIOUS
SECREATIONS .

11. REVERSAL OF CHOLINESTERASE
INHIBITION BY OXIMES
 OXIMES WORK BY REACTIVATING ACETYLCHOLINESTERASE THAT HAS BEEN BOUND
TO THE OP MOLECULE
 PRALIDOXIME
 MOST FREQUENTLY USED OXIMES WORLDWIDE.(OTHER MEMBERS LIKE OBIDOXIME
,TRIMEDOXIME ETC.)
 THE THEREPEUTIC WINDOW FOR OXIMES IS LIMITED BY THE TIME TAKEN FOR
“AGEING” OF THE ENZYME OP COMPLEX ,BECAUSE AGED ENZYME CAN NO LONGER
BE REACTIVATED BY OXIMES .
 MECHANISM OF ACTION
 OXIME GET ATTACHED TO THE FREE ANIONIC SITE OF ENZYME ChE.THE OXIME END
THEN REACTS WITH THE PHOSPHORUS ATOM OF OP ATTACHED AT THE
ESTERATIC SITE OF THE ENZYME .THIS OXIME PHOSPHATE SO FORMED DIFFUSES
AWAY LEAVING THE ENZYME INTACT (REACTIVATED ChE)

12.  DOSE
 WHO RECOMMENDS PRALIDOXIME DOSE OF 30MG/KG BOLUS IV OVER 20-30
MIN F/B CONTINUOUS INFUSIONS OF 8MG/KG/HR INFUSION CONTINUED TILL
RECOVERY :12HRS AFTER ATROPINE HAS BEEN STOPPED AND BChE NOTED TO
INCREASE .
 SIDE EFFECTS
 DIZZINESS ,HEADACHE,BLURRED VISION AND DIPLOPIA ,RAPID ADMINISTRATION
MAY LEAD TO TACHYCARDIA ,LARYNGOSPASM ,MUSCLE SPASM AND TRANSIENT
NEUROMUSCULAR BLOCKADE.

13. SUPPORATIVE TREATMENT
 ANTIBIOTIC PROPHYLAXIS
USE BROAD SPECTRUM ANTIBIOTICS
 FUROSEMIDE –IT IS RECOMMENDED IF PULMONARY OEDEMA PERSISTS,EVEN
AFTER FULL ATROPINISATION.
 MAGNESIUM SULPHATE
 BLOCKS LIGAND –GATED CALCIUM CHANNELS,RESULTING IN REDUCED
ACETYKCHOLINE RELEASE FROM PRE-SYNAPTIC TERMINALS,THUS IMPROVING
FUNCTION AT NMJ AND REDUCED CNS OVERSTIMULATION MEDIATED VIA NMDA
RECEPTOR ACTIVATION.
 IV MGSO4 (4GM) ON FIRST DAY SHOWN TO DECREASE HOSPITALIZATION PERIOD
AND IMPROVE OUTCOME .

14.  CLONIDINE
 ALPHA 2 ADRENERGIC RECEPTOR AGONIST
 REDUCE ACETYLCHOLINE SYNTHESIS AND RELEASE FROM PRESYNAPTIC
TERMINALS.
 ANIMAL STUDIES SHOWS BENEFITS BUT EFFECT IN HUMAN BEINGS ARE
UNKNOWN .
 DOSE-0.15-0.3 MG IV BOLUS F/B 0.5 MG OVER 24 HR
 SODIUM BICARBONATE
 INCREASED IN BLOOD PH ( 7.45 UPTO 7.55 )HAVE BEEN REPORTED TO IMPROVE
OUTCOME IN ANIMALS THROUGH AN UNKNOWN MECHANISM
 USEFUL IN NERV GAS POISONING
 DOSE-5MEQ/KG OVER 1 HR F/B 5-6 MEQ/KG/DAY.

15. COMPLICATIONS AND TREATMENT
 CVS-
 MUSCARINIC RECEPTOR STIMULATION-BRADYCARDIA,HYPOTENSION USUALLY
RESPOND TO ATROPINE ,SEVERE HYPOTENSION MAY NEED VASSOPRESSORS .
 NICOTINIC RECEPTOR STIMULATION-SINUS TACHYCARDIA AND HYPERTENSION
 ECG CHANGES-PROLONG QTC INTERVAL AND PROLONG PR INTERVAL,ST
SEGMENT ELEVATIONS
 CNS –
 FREQUENTLY DEVELOP AGITED DELERIUM
 SEIZURES –DIAZEPAM AS FIRST LINE
 THREE DIFFERENT TYPE OF PARALYSIS ARE RECOGNIZED BASED LARGELY ON
THE TIME OF OCCURANCE AND THEIR DIFFERENT PATHOPHYSIOLOGY

16.  TYPE I PARALYSIS OR ACUTE PARALYSIS
 IS SEEN DURING INITIAL CHOLINERGIC PHASE LEADING TO PERSISTENT
DEPOLARISATION AT NMJ
 CF-FASICULATIONS,CRAMPS,TWITCHINGS AND WEAKNESS
 AT THIS STAGE PT MAY REQUIRED VENTILATORY SUPPORT DUE TO WEAKNESS OF
RESPIRATORY MUSCLES LEADING TO RESPIRATORY DEPRESSION AND ARREST.
 TYPE 2 PARALYSIS /INTERMEDIATE SYNDROME
 IT OCCURS TO 24 TO 96 HRS AFTER THE INGESTION OF AN OP COMPOUND .
 APPROX 10 -40 % OF PT TREATED FOR ACUTE POISONING DEVELOP THESE ILLNESS.
 ONSET OF IMS OFTEN RAPID WITH PROGRESSION OF MUSCLE WEAKNESS LIKE
OCULAR MUSCLES,NECK MUSCLES,PROXIMAL LIMBS ,RS MUSCLES
 TREATMENT OF IMS-MAINLY SUPPORATIVE

17.  TYPE 3 PARALYSIS OR ORGANOPHOSPHATE –INDUCWD DELAYED
POLYNEUROPATHY (OPIDP)
 IS A SENSORY-MOTOR DISTAL AXONOPATHY THAT USUALLY OCCURS AFTER
INGESTION OF LARGE DOSES OF AN OP COMPOUND.
 THE NEUROPATHY PRESENTS AS WEAKNESS AND ATAXIA FOLLOWING A LATENT
PERIOD OF 2-4 WEEKS .
 CF-INITIAL STIMULATION CAUSES EXCITATORY FASICULATION THEN PROGRESS TO
INHIBITORY PARALYSIS.
 CARDINAL SYMPTOMS –DISTAL WEAKNESS OF HAND AND FEET PRECEDED TO CALF
PAIN AND PARASTHESIA WITH DELAYED CNS SIGNS INCLUDES TREMERS ,ANXITY AND
COMA .
 RECOVERY FROM OPIDN IS INCOMPLETE AND MAY BE LIMITED TO HANDS AND
FEETS ,ALTHOUGH SUBSTANTIAL FUNCTIONAL RECOVERY AFTER 1-2 YR MAY OCCURE
IN YOUNGER PATIENT .

19. THANK YOU