Glyphosate Poisoning
PRESENTER : PRABU
MEDICAL OFFICER : DR. NG KL
SPECIALIST : DR KAUTHMAN
Patients Details
Madam SP
54 years old, Indian lady
Premorbid
1. Depression since 3months ago
-T. Respiridone 1mg OD
-T. Sertraline 50mg OD
-T. Alprazolam 0.5mg ON
2. hypertension since 2 years ago
- follow up under KK Sg Baru
- T. Amlodipine 10mg OD
Case
Allerged ingestion of round up(herbicide)
glyphosate + isoproplyamortum 41%
First suicidal attempt, never attempted before.
Unsure reason
Amount around 100cc
Post ingestion
1. Vomiting x10
2. Epigastrial pain-burning in sensation
3. Burning sensation over mouth and throat
4. Hyper salivation
5. Diarhea x8
.Estimated drug ingestion was between 8am - 9am
Further Hx
Married, blessed with 2 children( 1 son 1
daughter)
Husband work as a farmer
She currently live with her husband at masjid
tanah
Previously, working in a factory.
Had to quit the job after she reached 45years old
currently helping her husband in farm
Non smoker, non alcohol drinker
Cont ..
Her husband claimed patient looks depressed
since both son and daughter leave them last three
months
Loss of appetite
Always in a sad mood and crying
Rarely talk to anybody, social withdrawal
Noted recently patient being sad and talking
about their end
On arrival..
O/E: GCS E4V5M6,pink
No respiratory effort
Vital signs:
BP: 99/55 mm/Hg
PR: 108
T : 37.0 degree celcius
Spo2 : 99 % under room air
GM ; 14.0 mmol/l
Lungs bibasal crepts. A/E equal bilaterally.
CVS DRNM
Abdomen soft, not distended, liver and spleen not
palpable, bowel sound active, No pedal edema
Investigation
FBC 13.3 / 15.8/ 265 / 36.2
Buse cr 3.7 / 136 / 4.0 / 108 / 67
ALT/ALP 71 / 66
AST/CK 111 / 267
Mg/Ca/Po - 0.80 / 1.90 / 1.45
PT/APTT/INR 10.9 / 0.93 / 1.07
CRP 4.5
ECG - Sinus rythm, no ischemic changes
ABG
pH
7.34
PCO2
32.8
PO2
100
HCO3
18.2
BE
- 7.8
Impression
Alleged gliphosate ingestion
With u/l psychiatry disorder
History to suggest glyposate
poisoning
Management
[Link]
[Link] @ ED d/t poor GCS
[Link] atropine 6mg/hr was given initially. Atropine
score 8. Reduce IVI atropine to 3mg/hr.
[Link] pralidoxime 2g in 100cc NS over 1 hour
[Link] score chart
[Link] for ICU care
In ICU ..
1. Mainstay of treatment
2. IVI atropine. Atropine score still 8. Reduce to
1mg/hr.
3. Titration of atropine according to atropine score
4. IVI pralidoxime started in view of poor respiratory
effort
5. Management mainly by GA and toxicology team
Progression
Patient was in ICU for 22 days
Trial of extubation x 2 but failed due to
desaturation
-pH
extubated to Bipap7.15
but desaturated SpO2 80%
PCO2 unresponsive 90
and
PO2
90
HCO3
25.6
BE
4.3
GCS E1V1M1
Decided to re intubation
14/10/2014
patient was extubated to Bipap (but patient not
cooperative)
GCS E4V3-4M6
15/10/2014
changed to FM 5L/min, SpO2 94%
Oxygen was tapered down gradually
Serum Cholinesterase level
Males : 3100 - 6500 U/L
Females :
18-491800 - 6600 U/L
50 and above 2550-6800
9 / 10 / 2014
1015
14 / 10 / 2014
3991
21 / 10 / 2014
6816
30 / 10 / 2014
6976
CT brain
9 October 2014
Imp : B/L maxillary and sphenoid sinusitis
No ICB
17 October 2014
Imp : No significant intracranial abnormality
B/L maxillary and sphenoid sinusitis
PSY review 15/10/14
Imp : Schizophrenia in relapse due to poor
compliances
Plan : T. Olanzapine 5mg ON
Refered ENT for tracheostomy in view of failed extubation
x2
Tracheostomy done on the 20/10/14 (D19)
Tracheostomy off on 10/11/14 D40
Pralidoxime off on D33 in view of increase serum
cholinesterase
Discharged home with
T. Olanzapine 10mg ON
T. Fluoxetine 20 mg ON
TCA PSY x 1/12
Discussion
Glyphosate
Organophosphorous insecticides include
malathion, parathion, dichlorvos and diazinon.
Acts through phosphorylation of the
acetylcholinesterase enzyme at nerve endings
It irreversibly inhibit acetylcholinesterase and
nicotinic synapses.
The result is a loss of available AChE so that the
effector organ becomes overstimulated by the
excess acetylcholine (ACh, the impulsetransmitting substance) in the nerve ending.
Absorbed by inhalation, ingestion, and skin
penetration
What are the signs and
symptoms of glyphosate
poisoning?
The recommended strategy of classification is as follows:
Minor to moderate
Symptoms are localised to oral mucous or the gastrointestinal symptoms is less than 24 hours,
with inflammation of the oesophagus, oral ulceration, increase in urine output, liver or renal
damage and acid base disturbance.
Severe
Respiratory failure, renal failure, reduction of blood pressure, cardiac arrest, coma and seizures
could occur.
Dermal exposures
When an exposure to glyphosate occurs locally, the clinical effects seen are usually classified
as mild to moderate effects. These local effects include erythema, piloerection and contact
dermatitis. It is expected that the severity of a skin exposure will be significantly decreased
with a less concentrated product. As the contact time with the product and the skin is
decreased, the severity of a reaction will also be decreased.
Eye exposure
Corrosive effects would not be expected from the formulated consumer products, especially
after dilution. Among the most common effect seen from eye contact with the herbicide is mild
conjunctivitis which normally clears in one to two days. It is expected that the consequences of
an eye exposure will be less severe with a less concentrated product. Rapid removal of the
herbicide from the eye by irrigation reduces the likelihood of serious effects..
Muscarinic effect
SLUDGE
salivation,
lacrimation,
urination,
diarrhea,
GI upset,
emesis) and
DUMBELS
diaphoresis and diarrhea; urination; miosis;
bradycardia, bronchospasm, bronchorrhea;
emesis; excess lacrimation; and salivation).
Muscarinic effects by organ system include the
following:
Cardiovascular - Bradycardia, hypotension
Respiratory - Rhinorrhea, bronchorrhea,
bronchospasm, cough, severe respiratory distress
Gastrointestinal - Hypersalivation, nausea and
vomiting, abdominalpain, diarrhea, fecal
incontinence
Genitourinary - Incontinence
Ocular - Blurred vision, Miosis is often a helpful
diagnostic sign
Glands - Increased lacrimation, diaphoresis
Nicotinic effect
Twitching
Fasciculation
Weakness
Cramps
Hypoventilation with diaphragmatic failure
CNS
Anxiety
Restlessness
Tremors
Convulsion
Confusion
Weakness
Coma
Investigation
Cholinesterase activity in plasma and RBC is
reduced to less than 50% normal
Based on the serum PCE levels, the severity of
poisoning was defined as per Kumaret al.
Latent: PCE level >50% of normal or >3,500 IU/L
Mild poisoning: PCE level 20-50% of normal or
>1,401-3,500 IU/L
Moderate poisoning: PCE level 10-20% of normal or
701-1,400 IU/L
Severe poisoning: PCE level is <10% of normal or
<700 IU/L.
Identified in urine toxicology screen
Management
Decontamination
Gastric lavage if presentation is within 1 hour,
followed by activated charcoal, continue lavage
until returning fluid is free from odour of poison.
Airway protection and adequate oxygenation
Hydration NS or D5%
Drugs Atropine, Pralidoxime, Diazepam
Atropine
Muscarinic receptor antagonist
Initial dose 0.5 2mg IV every 5-10min until
atropinization is adequate or continuos infusion
(mix 8mg of atropine in 100ml of NS) at rate of
0.02-0.08mg/kg/hr with additional 1-5mg boluses
as needed to dry the secretion
Pt may require 40-1500mg/day
Titrated according to Atropine score
Adequate Atropinization-drying tracheobronchial
secretion, dry mouth, flushing, heart rate >120,
dialted pupil)
Watch out for over atropinization - very dry mouth
and skin, PR >160
Should not be stopped prematurely
As toxic wear off, the effect of atropinization
become greater
Down titration and weaning off atropine is the
preferred way and would prevent rebound
pulmonary edema
Pralidoxime
Oxime
Reactivates phosphorylated cholinesterase
It counteract weakness, fasciculation and
respiratory depression
To be administered within 48 hours of OP
poisoning
1-2g IV in 100ml NS over 30mins (not exceeding
200mg/min rate)
Repeat in 1 hr if muscle weakness not been
relieved
Severe cases, IV infusion up to 500mg/hr
Maximum 12g in 24 hrs
Contraindicated for carbamate poisoning and
organophophorous compounds without anticholinesterase activity
Diazepam
IV diazepam may be used to treat seizure and
reduce twitching of muscles
Long term side effect of OP
poisoning
early childhood : associated with behaviour and
learning deficits later in life
cognitive and behavioural impairments
in utero : reduced birth weight, head
circumference, and gestational length in infants
Motor Inhibition and Learning Impairments in School-Aged Children Following Exposure
to Organophosphate Pesticides in Infancy, Pediatric Res. 2006 Jul;60(1):88-92.
Take Home Message
Organophosphate poisoning is a
clinical diagnosis.
More based on history and clinical
presentation.
Supported by lab investigations.
Atropine and pralidoxime : mainstay
of treatment
Clinical Neurotoxicology: Syndromes,
Substances, EnvironmentsBy Michael R.
Dobbs
[Link]
C3877488/
[Link]
e/handbook/[Link]
THANK YOU
