A 30-year-old unconscious housewife was brought to the hospital with a history of domestic violence. On examination, she had constricted pupils, low blood pressure, high blood sugar, metabolic acidosis on ABG, bradycardia on ECG, and elevated serum amylase. The diagnosis was organophosphorus poisoning based on the clinical features and laboratory findings.

1. Clinical Vignette
You are posted as a CMO, casualty in the month of June.
A 30 year old housewife from a nearby village is
brought in the afternoon in an unconscious state.
There is h/o domestic violence. Patient’s clothes are
wet and are soiled with urine and feces.
O/E pupils are constricted with BP= 80/60mmHg. You
check patient’s blood sugar level which is 480 mg%.
You order an ABG which is s/o metabolic acidosis.
ECG is done and it shows bradycardia. Routine blood
workup reveals normal serum electrolytes with a
raised amylase level of 300.
Diagnosis ??? ??

2. Organophosphorus Poisoning
Presenters : Dr Lohit Chauhan
: Dr Dhananjay Gupta
Moderator : Dr. Gurmeet Kaur

3. INTRODUCTION
• OP are a group of insecticides or ‘nerve-
agents’ which act at acetyl-cholinesterase
• Have been used as insecticides, petroleum
additives and chemical warfare agents
• Carbamates are another group of insecticides
which act at the same site, with a slight
different MOA

4. WHO CLASSIFICATION (simplified)
HIGHLY TOXIC MODERATELY TOXIC
1. Phosphamidon (Dimecron) 1. Malathion
2. Ethyl parathion 2. Fenthion (Baytex)
3. Methyl parathion 3. Temephos (abate)
4. Chloro-thiophos 4. Fenitrothin (tik-20)
5. Carbo-phenothion 5. Diazinon (spectacide)
* Shivakumar S, Ishaq RM. Management of Organophosphorus compounds
(OPC) Poisoning : Current Status 2008. taken from drshivkumar.org

5. Epidemiology (WHO)
• Acute OP poisoning is one of the common and
serious medical emergencies
• Asia : 3 million cases/ year of acute
pesticide poisoning
• 3 lakh deaths per year (CFR =10-15 %)
• 99% cases are seen in developing world

6. Indian Data
• Poisoning is 4th MC cause of deaths annually
• OP poisoning is the MC poisoning
• Pattern of poisoning is region-dependant
• OP poisoning is more common in south India
• North India- aluminium phosphide > OP

7. RML Data

8. Why is OP poisoning common ??
• India is an agarian country
• routinely used in farming
CAUSES OF HIGH MORTALITY
1. High toxicity of available compounds
2. Time gap in transporting patients
3. Paucity of Health care personnel
4. Lack of training facilities
5. Lack of antidotes

9. Why is OP poisoning common ??
Limited resources and infrastructure for
health care delivery

10. 1. Mode of poisoning
85%
15%
SUICIDAL
ACCIDENTAL
* Banerjee I, Tripathi SK, Roy AS. Clinico-Epidemiological Characteristics of Patients
Presenting with Organophosphorus Poisoning. N Am J Med Sc. Vol 4(3), JMarch 2012

11. 2. Occupation
42%
34%
10%
9%
5%
HOUSE WIVES
FARMERS
SHOPKEEPERS
LABOURERS
STUDENTS
* Maharani B, Vijayakumari M. Profile of poisoning cases in a tertiary care hospital in
Tamil Nadu, India. J of App Pharma Sc. Vol 3(01), Jan 2013

12. 3. Seasonal distribution
21%
12%
32%
35%
SPRING
WINTER
RAINY
SUMMER
* Maharani B, Vijayakumari M. Profile of poisoning cases in a tertiary care hospital in
Tamil Nadu, India. J of App Pharma Sc. Vol 3(01), Jan 2013

13. 4. Type of Poison
36%
29%
19%
16%
Me Parathion
Diazinon
Chlorpyriphos
Dimecron
* Banerjee I, Tripathi SK, Roy AS. Clinico-Epidemiological Characteristics of Patients
Presenting with Organophosphorus Poisoning. N Am J Med Sc. Vol 4(3), JMarch 2012

14. 5. Relative human Toxicity
Eddleston M et al. Differences between organophosphorus insecticides in human self-
poisoning: a prospective cohort study. Lancet. 2005 Oct 22-28;366(9495):1452-9

15. Mechanism Of Action

16. Clinical Features
1. Acute O-P poisoning
- Muscarinic features Resp distress
- Nicotinic features Death
- CNS features
2. Intermediate Syndrome
3. Delayed neuropathy (OPIDP)
4. Neuro-psychiatric disorder (COPIND)

17. 1. Acute O-P poisoning
MUSCARININC FEATURES NICOTINIC FEATURES CNS FEATURES
D iarrhoea Muscle weakness Fatigue
U rination Muscle fasiculations Confusion
M iosis Muscle paralysis Unconsciousness
B ronchorrhea
B ronchospasm Seizues
E mesis Hypertension Ataxia
L acrimation Tachycardia Resp. depression
S alivation
S weating

18. 2. Muscarinic / Wadia type 1 syndrome
1. Excessive Sweating
2. Miosis
3. Bronchorrhoea / spasm
4. Bradycardia
5. Hypotension

19. 3. Bronchorrhoea
• Early cause of morbidity and mortality
• Excess fluid is from airway secretions
• Obstruction of upper and lower airways
• Pulmonary edema - - hypoxia - - death

20. The Grading of Clinical severity
Severity AChE
(RBC)
Muscarinic Nicotinic CNS
Mild > 40% nausea, vomiting,
diarrhoea, salivation,
bronchorrhoea and
-constriction,
bradycardia
headache,
dizziness
Moderate 20 - 40% as above, + miosis,
incontinence
fasciculations
(fine muscles)
as above, +
dysarthria, ataxia
Severe < 20% as above, +
fasciculations
(diaphragm, resp.
muscles)
as above, +
coma,
convulsions

21. 4. Intermediate syndrome
• Described in 1987 (Karalliedde and Senanayake)
• Occurs 24-96 hours after resolution of acute
cholinergic crisis
• Most imp. factor responsible is
quantum of exposure of OPC
• May occur from inadequate oxime therapy

22. IMS - pathophysiology
• Incidence = 10-50 %
• Prolonged effects on Nicotinic receptors
• Primary motor end plate degeneration
• Leads to muscle weakness

23. IMS- muscle weakness of
• Muscles innervated by cranial nerves : III-VII and X
• Neck flexors
- a constant feature
- one of the earliest signs
- inability of patients to raise heads off pillow
• Proximal limb muscle weakness
- typically involve shoulder abductors, hip flexors
• Respiratory muscles - death

24. IMS – other features
• Deep tendon Reflexes :
Usually absent / decreased
• Sensory system usually intact
• Muscarinic symptoms :
absent
rarely short relapses may occur

25. IMS- complications
• Weakness -- Frank paralysis
• Respiratory distress -- Death
• Main cause of morbidity and mortality
in Indian patients.

26. 5. OPIDP
• OP induced Delayed Polyneuropathy
• Delayed, rare, neurotoxic effect
• 1-5 weeks after severe acute poisoning, due to
slow release of OP from body fat
• symmetrical sensory-motor axonal degeneration
of the peripheral nerves and SC

27. 5. OPIDP - C/f
Motor
1. Sharp cramp like pain in calf
2. High stepping gait (initially)
3. Shuffling gate in severe cases
4. Quadriplegia / paraplegia
5. Wrist and foot drop
6. Mild pyramidal signs
Sensory
1. Glove-stocking anesthesia
2. Cerebellar signs +/-

28. 6. COPIND
• Chronic OP induced Neuro-psychiatric disorder
• Chronic low-dose exposure to OP compounds
• 40 hours/week, 9 months/ year
• No cholinergic symptoms
• Non responsive to levodopa
• Plasma cholinesterase levels are normal

29. 6. COPIND – c/f
Neurological Symptoms Psychiatric Symptoms
1. Impairment in memory 1. Anxiety
2. Impairment in concentration 2. Dysthymia
3. Impairment in leaning 3. Depression
4. Chronic fatigue
5. EPS : dystonia
6. Resting tremor, bradykinesia
7. Rigidity of face Parkinson-like
8. Postural instability
Non responsive to levodopa

30. Diagnosis and Management

31. Diagnosis of OP poisoning
Diagnosis is mainly clinical, Based on :
1. H/o Ingestion of poison
2. Characteristic clinical features
3. Clinical improvement after atropine/ oxime
4. Inhibition of cholinesterase activity

32. 1. Inhibition of cholinesterase
• Demonstrating a decrease in cholinesterase
• Definitive or gold standard method
• Theoretically RBC/ true cholinesterase is more
accurate than plasma/ pseudo
• But plasma / pseudo-cholinesterase is more easily
available test

33. Diagnosis :
Plasma / SChE :
- easy to measure
- easily available
- more useful in acute exposure
1. 50 % reduction in normal values : diagnostic
(baseline values usually NA)
2. Progressive increase in SChE with treatment

34. 2. Cholinesterase levels
Useful in monitoring clinical course of illness
persistent Low levels are a predictor of IMS
(Intermediate syndrome)
SChE activity is < 20 % during onset of IMS
* Tajune J, Robert J. Organophosphoric poisoning. Ann Emerg Med 1987 ; 16:193.

35. 3. Electro-neuro-myogram (ENMG)
• 30 Hz rapid nerve stimulation - decremental
responses correlate best with clinical weakness
• Most useful diagnostic test of IMS *
* Senanayake N et al. Neurotoxic effects of OP insecticides : an intermediate
syndrome. NEJM. 1987 ; 316 :761-63.

36. 4. Other tests of prognostic value
a. Hyperglycemia
b. Neutrophilic leucocytosis
c. Proteinuria / glycosuria
d. ECG changes (QTc prolongation)
e. Blood pH (acidosis)
f. Hyper amylasemia
g. Serum CPK levels

37. 5. Hyperglycemia in OP-poison
a. Oxidative stress
b. Renal tubular damage
c. Stimulation of adrenals
d. Release of catecholamines
Transient hyperglycemia and glycosuria are
often seen in acute OP-poisoning
* Namba T, Nolte CT, Jackrel J, Grob D. Poisoning due to organophosphate
insecticides: Acute and chronic manifestations. Am J Med. 1971;50:475–92.

38. 6. Blood pH
• Metabolic Acidosis develops in patients of OP
poisoning, more common with hypotension*1.
• Unknown mechanism.
• If pH < 7.20, treatment with sodium
bicarbonate beneficial*2.
1. *Prakash O.et al. Low ph predicts mortality in OPP and carbamates poisoning, JAPI
2002; 50:857.
2. *Roberts DM, Buckley NA. Alkalinisation for treating organophosphorus pesticide
poisoning. Cochrane Database of Systematic Reviews 2005;1:CD004897.pub2.

39. 7. QTc prolongation
• Indicates poor prognosis in OP- poisoning
1. Cholinergic stimulation of heart : M2
a. negative ionotropy
b. negative chronotropy
2. Oxidative stress causes conduction problems
* Shadnia S, Okazi A, et al. Prognostic value of long QTc interval in acute
and severe OP poisoning. J of Med Toxico 2009 ; 5(4).

40. 8. Hyper- amylasemia
• Cholinergic stimulation of salivary glands
• Cholinergic stimulation of pancreas
• Acute pancreatitis (rare)
Raised amylase levels correlate with severity
and presence of shock in acute OP poisoning *
* Lin CL, Yang CT, Pan KY, Huang CC. Most common intoxication in nephrology
ward organophosphate poisoning. Ren Fail 2004 ;26:349-54. .

41. 9. Acute Pancreatitis
• d/t Excessive cholinergic stimulation and
ductular hypertension
• Painless Ac. Pancreatitis has been reported
• Amylase (>300) : low Sn, low Sp
• Lipase (>300) : useful for diagnosis
* Hsiao CT, Yang CC, Deng JF, Bullard MJ, Liaw SJ. Acute Pancreatitis following
Organohosphate Intoxication. J Toxicol Clin Toxicol. 1996 ;34(3):343-7.

42. Management

43. What to do ??
1. Call AIIMS poison cell : (NPIC)
- National Poisons Information Cell
- Toll free no. 1800 116 117
- Other : 011 - 26589391
- Open 24 X 7 , 365 days a year

44. The Paradox of Poisoning….
“The only thing I know is
that I don’t know anything”
- Socrates

45. 1. Identification of poison
• History by patient/ attendant
• Clinical presentation.
• By showing photographs.
• WHO colour code on container.

46. Poison :Identification
WHO colour code on container.
Red label Extremely toxic Monocrotophos, zinc phosphide, ethyl mercury acetate,
and others.
Yellow
label
Highly toxic Endosulfan, carbaryl, quinalphos, and others.
Blue label Moderately toxic Malathion, thiram, glyphosate, and others.
Green label Slightly toxic Mancozeb, oxyfluorfen, mosquito repellant oils and
liquids, and most other household insecticides.

47. Identification of poison
• Signs of cholinergic excess or developing
intermediate syndrome
• Disparity between history and clinical presentation,
follow, clinical judgment.
• After identification classify as Organophosphorus
and non-Organophosphorus.
Organophosphosphate

48. Management :Immediate, Protocol
Assess and record 15-point Glasgow Coma Scale.
Pulse rate, BP and auscultate
Patient : left lateral position- head lower than the feet.
Oxygen, Intubate if respiratory distress.
Start atropine : reduce bronchorrhoea.
0.9% normal saline, Aim SBP > 80 mm Hg & urine output >30 ml/h

49. When not sure about the poison..??
• ‘Atropine test‘ : Inject 0.6- 1 mg IV
atropine.
• If pulse rate goes up by 25 per minute or
skin flushing develops patient has mild or
no toxicity for OP’s.

50. Management : Specific
General Principles of Therapy :
• Decontamination, Resuscitation, Stablization.
• Muscarinic antagonists
• Fluids.
• Acetylcholinesterase reactivators.
• Gastric Decontamination.
• Miscellaneous.

51. Decontamination
• Healthcare workers and OP Poisoning.
• Few western hospitals, reported such poisoning.
• None shows inhibition of Acetyl/Butyryl
cholinesterases.
• Cases from Asia : Health-care workers take no
special precautions , No cases of secondary
poisoning reported.

52. Decontamination
• Guidelines : Universal Precautions, Maximum
Ventilation, Frequent rotation of staff to keep exposure
minimum.
• PPE should not consist Latex / Vinyl.
• Patient : All clothing to be removed, discard in
ventilated area.
• Thorough irrigation with water.
• Wash with soap and water.
• Soaps containing 30% ethanol advocated.
• Ocular decontamination : water only.

53. Initial Stabilisation
• Patent Airway, adequate Breathing and Circulation.
• Oxygen at first opportunity.
• Little evidence, Atropine not to be given until oxygen
availability*1.
• However, in hospitals where oxygen not available, Atropine to
be started early*2.
• Patient Position : Left Lateral, Neck Extended.
 Reduce aspiration risk.
 Keeps airway patent.
 Decrease pyloric emptying and absorption of poison.
*1 Erdman AR. Insecticides. In: Dart RC, Caravati EM, McGuigan MA, et al, eds. Medical toxicology, 3rd edn. Philadelphia:
Lippincott Williams & Wilkins, 2004: 1475–96.
*2 Aaron CK. Organophosphates and carbamates. In: Shannon MS,Borron SW, Burns M, eds. Clinical management of
poisoning and drug overdose, 4th edn. New York, Elsevier Science, 2006.

54. Initial Stabilisation

55. Gastrointestinal decontamination
• Often first intervention
• To be considered only
after stabilization,
oxygen, atropine and
oximes.
• Lavage only if patient
arrives within 1 hour.
• Only consider if patient
intubated or conscious
and willing to
cooperate. * The Hazards of Gastric Lavage for Intentional Self Poisoning
in a Resource Poor Location Clin Tox 2007;45(2):136-43
Not beneficial, rather increases chances of
Aspiration Pneumonia & Deaths*

56. Gastrointestinal decontamination
• Induced emesis : Ipecacuanha induced ,
Contraindicated.
• Activated charcoal : Studies failed to
find any benefit ( Why..??)
 It binds in vitro, but not in gut due to
rapid absorption.
 Ingested dose too large for the
amount of charcoal.
NO evidence suggests that patients
with pesticide poisoning benefit with
activated charcoal.*
* Eddleston M, Juszczak E, Buckley NA, et al. Randomised controlled trial of routine single or
multiple dose superactivated charcoal for self-poisoning in a region with high mortality. Clin
Toxicol 2005; 43: 442–43.

57. Muscarinic antagonist
Atropine
Muscarinic Antagonist
Good CNS penetration, cause Anticholinergic delirium, agitation and
psychoses.
Glycopyrrolate
Less CNS penetration, Less CNS side effects.
Lesser respiratory complications
Ineffective in countering Coma and reduced respiration.
Hyoscine methobromide and Hyoscine
Hyoscine has the best CNS penetration
Methbomide form not permeable to BBB.

58. Muscarinic antagonist
• A small RCT found no difference in mortality or
ventilator rates, comparing Atropine and
Glycopyrrolate.
• Hyoscine : best for severe Extra-pyramidal features
with few peripheral signs
• In animal studies, found more effective than Atropine
for control of seizures induced by inhaled nerve gas
agents.
• However, Atropine remains mainstay of therapy.
 Easy and wide availability.
 Affordability .
 Moderate ability to penetrate CNS.

59. Muscarinic antagonist
AIM OF THERAPY : ATROPINE
• To reverse cholinergic features.
• To improve Cardiac and Respiratory functions.
• Target Endpoints of Atropinization.
1. Drying of Pulmonary secretions, ie. Clear lung fields on
auscultation. (Most reliable)
2. Heart rate > 80 beats / min.
3. SBP > 80 mmHg.
4. Pupils : No longer pinpoint.
5. Dry Axillae.
6. Bowel sounds : just present.

60. End points of atropinisation
1. Lung secretions
2. Hypotension
3. Bradycardia
4. Sweating
5. Miosis
6. Bowels : Hyperactive
A
T
R
O
P
I
N
E
1. Clear Chest
2. SBP > 80mmHg
3. HR > 80/min
4. Dry Axillae
5. Pupils no longer pinpoint.
6. Bowel sounds : Just present

61. Atropine Dosing
Incremental Dosing
1.8 to 3 mg Atropine (i/v)
Repeat every 5 minutes with doubling the dose
each time.
Endpoint : Atropinization.
Followed by : 10 to 20 % of total dose required
for atropinization every hour via i/v infusion
To be held once anticholinergic effects
occur.(Absent bowel sounds, urinary retention,
agitation).
Bolus DosingV/S
2-5 mg Atropine every 10 to 15 min.
Endpoint : Atropinization.
Followed by maintenance using reduced doses
or increasing time duration in b/w doses.
Various studies clearely found
Incremental Dosing far superior
to bolus dose administration

62. Atropine Monitoring
• Patient to be assessed every 15 min to check adequacy of
dosages.
• If clinical features recur, further increment in boluses and
doubling.
• Once parameters reached, Monitoring hourly for atleast 6
hours to check effectiveness of infusion.
Time heart rate Clear lung Pupil Dry
axilla
SBP
> 80
mm
Hg
Bowel
sounds
mental
state
Fever
>37.5c
SPO2
Atropine
infusion
dose
OP / Carbamate Observation Sheet

63. Atropine : When to stop..??
Bronchorrhoea : most important, for titrating dose.
• Atropine toxicity = absent bowel sounds + fever +
confusion.
• Stop infusion for 60 min, if toxicity.
• Re-start infusion at 80% of initial rate, once the temp.
comes down and patient calms.
• Most do not need >3-5 mg (5-9 ml) / hour of atropine
infusion.
• Reduce rate by 20% every 4 hourly once patient is
stable. STOP.

64. Oximes
• Reactivate Acetyl cholinesterase, remove phosphoryl group.
• Discovered in 1950’s by Wilson et al.
• Among various oximes (obidoxime and trimedoxime)
Pralidoxime (PAM) remains, most widely used.
• Prevent continued toxicity by Scavenging and detoxifying
enzyme.
• Also endogenous anticholinergic effects.
• Available in four Salts : chloride, iodide, metilsulfate, and
mesilate.
• Chloride and iodide most widely used in developing countries.
• Chloride salt better than iodide.
 More active compound per gram of salt.
 No risk of thyroid toxicity.

65. Oximes
Therapeutic effectiveness depends on
1. Concentration of poison consumed (Poison load).
2. Time lapse between poisoning and administration
3. Type of OPC. (More effective on diethyl than dimethyl).
Dimethyl compound reactivate and “age” at slower rate.
4. Lipid solubility of OPC.
5. Concentration of Oxime in blood.

66. Oximes
The Controversies
• Two RCT’s in Vellore, India in early 1990’s noted,
Harm from low dose PAM infusion.
• A Cochrane review ( included two RCT’s , 2005) &
two other meta-analysis reported no clear benefit or
harm.
• An RCT in Baramati, India studying very high dose of
PAM in 200 patients with moderate OP poisoning
showed reduced Case fatility. (1% vs 8%).

67. Oximes
The consensus
• Oximes will not be effective in very severe (large
dose) poisoning.
• Treatment with oximes should be started as early as
possible, no role if started after 48 hours.
• Less effective in severe complications such as
aspiration pneumonia or hypoxic brain injury before
treatment.
• Less or no effectiveness with dimethyl compounds
and atypical organophosphates.
• Not effective in carbamates but are not
contraindicated either.

68. Oximes
Dosing
• PAM : 1-3 gm/day, no role after 48 hrs.
• Serum levels of > 4 mg/lit is necessary for effective
treatment.
• To achieve this, administered as bolus 20-40mg/kg
followed by continuous infusion at 500mg/hr.
• WHO recommendations : Loading dose 30mg/kg,
followed by infusion of 8mg/kg/hr.

69. Oximes
Therapeutic end point
• Resolution of muscle fasciculation and weakness,
Reactivation and Increment in SChE levels.
• Use longer than 24 hours indicated if unaged OP’s
release from fat tissue.
• Infusion continued until patient remains symptom
free for atleast 12 hours without additional atropine.
• Or until extubated.

70. Role of Benzodiazepines
• Control agitation.
• Sedation in ventilated patients.
• Many opioids, metabolized via SChE, so use for
sedation in pulmonary edema can worsen CNS
manifestation.
• Control of seizures : First line therapy in OP
poisoning, phenytoin not recommended d/t
membrane stabilizing effects.
• Seizures uncommon in oxygenated patients, more
common in nerve gas agents (soman and tabum).
• Diazepam reduce neural damage and prevent
respiratory failure (animal studies).

71. Role of Magnesium Sulphate
• MgSO4 (4g) i/v in first day after admission,
decrease hospitalization period and mortality.
• It blocks Calcium channels and reduce
acetylecholine release from presynaptic
terminals.
• Also reduces CNS overstimulation from
NMDA receptor activation.

72. Role of Clonidine
• Centrally acting α2-adrenergic receptor
agonists.
• Reduces acetylcholine synthesis and release
from presynaptic terminals
• Animal studies, shown benefit in combination
with atropine. Effect in humans unknown.

73. Advanced Neuroprotective Drugs
1. Ketamine : Noncompetitive NMDAR
antagonist, within 1 hour of nerve gas agent
induced seizures along with
Midazolam/diazepam.
2. Tezampanel : Glutamate receptor antagonist
specific for kainate subtype Rc, useful in
soman(nerve gas) induced seizures and
neuropathy.
3. Gacyclidine : Another antiglutamatergic
compound found beneficial in conjunction to
standard therapy in nerve gas poisoning .

74. Advanced Neuroprotective Drugs
4. For OPIDN : standard therapy plus
corticosteroids.
5. Protease inhibitors : target esterase and
prevent delayed neuropathy.
6. Intermediate syndrome resistant to standard
treatment, artificial respiration.
7. Antioxidants : lipid peroxidation and
thiobarbituric formed in OP poisoning,
Antioxidant beneficial.
Vitamin E reported to have therapeutic effect

75. Intermediate syndrome : Management
• Usually presents 12 to 96 hours after exposure.
• Early signs : action tremors and pharyngeal
weakness (difficult deglutition , pooling of
secretions).
• Later : inability to flex neck, DTR’s lost, cranial
neuropathies, proximal muscle weakness and
respiratory muscle paralysis.
• Not all require intubation and ventilation, but
patients with tremors and pharyngeal weakness, at
increased risk.
• Treatment : totally symptomatic. Ventilator support if
respiratory muscle paralysis.

76. Ventilatory Support
Indicated in stupor / coma, Hypoxemia (PaO2 <60
mmHg) and profound muscle weakness.
Predictors for need of mechanical ventilation.
1. Delay in the initiation of specific treatment.
2. Low level of sensorium at admission
3. Pinpoint pupils and generalized fasciculations.
4. Presence of convulsions
5. Presence of respiratory failure at admission.
6. High initial atropine requirement for atropinization.

77. Weaning off Ventilator
• Asses respiratory muscle performance before
weaning off patient.
• Reduce slowly and gradually pressure support level
in CPAP with PSV mode.
• Extubate if :
 spontaneous breathing with no distress.
 generates VT >5 mL/kg at Pressure of 3-5 cm of H2O.
Parameter Weaning threshold
PaCO2 <50 mmHg
Minute ventilation (spontaneous) <10-15 L/min
Tidal volumes >5 mL/kg
Maximum voluntary ventilation >20 L/min
Respiratory frequency <35 breaths/min or >6 breaths/min

78. Role of Alkalinization
• IV infusion of Soda. Bicarbonate produce moderate
alkalinization (pH : 7.45 to 7.55) in OP poisoning.
• Infusion of higher dosages (5mEq/Kg) in 60
minutes followed by 5-6 mEq/kg/day was shown
useful.(In dogs)
• More beneficial in Nerve agent poisoning.
• Cochrane review : Insufficient evidence to establish
use of NaHCO in human OP Poisoning.

79. Role of Early Enteral Feeding.
• Early enteral feeds associated with improved
outcomes in critically ill because it prevents
enterohepatic circulation.
• Early nutritional supplementation in OP poisoning
assumes importance as these patients may require
prolonged ventilatory support.

80. Role of Fresh Frozen Plasma.
• FFP contains important components like clotting
factors, proteins, enzymes, etc.
• It is hypothesized that butyrylcholinesterase present
in FFP sequester free poison in blood and remove it
from circulation.
• Two trials, both unfavourable to FFP intervention.
Current evidence not strong enough to
make clear conclusion regarding
bioscavenger role of FFP

81. For the future…..
• Removal of OP’s from blood : Hemodialysis,
Hemoperfusion or hemofiltration.
• Hemofiltration after dichlorovos poisoning revealed
beneficial therapeutic effects.
• Military research aims at : Injecting
Butyrylcholinesterase after cloning into soldiers
before exposure to nerve gases.
 Not practical for prophylaxis in self-poisoning as one cannot
predict when a person is going to ingest pesticide.
• Use of recombinant bacterial phosphotriesterases, or
hydrolases to break down OP’s enzymatically.

82. Take home message
1. Early stabilization and resuscitation.
2. Incremental dose Atropine.
3. Early institution of Oximes.
4. External decontamination, MgSO4, Clonidine, Use
of benzodiazepines and NMDA receptor antagonists,
Alklinization, Early Enteral feeding were found to
be beneficial.
5. FFP, forced emesis were found harmful.
6. Activated charcoal, Gastric lavage were found to
have no benefit or harm.
7. Gastric lavage : easily performed, cheap could be
used as an adjunct if performed within one hour.

83. Thank You