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Paraquat is a rapidly acting, non selective
herbicide ; inexpensive
Dermal /spray exposure(inhalation)-limited
Ingestion-high case fatality rate
Diquat is a related herbicide-similar mechanism,
clinical features, treatment
Coformulated with an antiemetic/alginate to reduce
Pharmacology and cellullar
Chemically- bi pyridyl compounds
Absorption..concentrated inside cells..redox
cycling( repetitive enzyme mediated cycling
between paraquat and its radicals)
Byproduct- superoxide radical
Redox cycling –consumes NADPH(antioxidant)
Oxidative stress-cellullar damage
Secondary inflammatory response
Multiorgan failure-organs with high blood
flow,oxygen tension and energy requirements-
Highly polar and corrosive
Ingestion ..rapid absorption..rapid distribution
Max tissue levels..6hrs
Active uptake by cell membrane transporters(eg:
High conc: in liver, lungs, kidney,muscle
No significant phase 1/phase 2 biotransformation
Minor-most ingested will appear in urine by 24 hrs
Severe-kidney function impaired..elimination
delayed..elimination half life can exceed 100 hrs
Formulation , strength and dose are important-
>30ml of 20% paraquat can be lethal.
Kidney disease and age>50yrs- bad prognosis
Time of ingestion
Painful mouth, difficulty in swallowing, nausea,
vomiting , abdominal pain
Burning skin sensation
Respiratory complaints-systemic poisoning
Physical examination and basic
Mouth,pharynx- necrosis, inflammation, ulceration-
maybe delayed to upto 12 hours, peak severity in
some days later
Monitor respiratory rate, pulse oximetry- O2 only if
Heart rate, BP- progressive refractory hypotension
Chest-dyspnoeic, tachypnoeic, crackles
Abdominal pain, diffuse tenderness
Topical contact- corneal ulceration, non specific
Blood tests- on admission, every 6 to 12th hourly for
first 48 hours, then based on clinical severity-
vomiting, diarrhea, kidney injury.
If prognosis is poor - palliative measures
Serum electrolytes- may be altered due to
vomiting, diarrhea, acute kidney injury and multi
◦ AKI suggests significant poisoning-acute tubular
necrosis/volume depletion-increased mortality
◦ Serum creatinine-rate of increase correlates with survival -
<0.034mg% per hr over 5 hrs(survival); >0.049mg% per hr
◦ Serum cystatin C- >0.009mg/L per hr over 6 hrs (death)
◦ Alkalemia-vomiting, early in the course
◦ Acidemia- respiratory acidosis( alveolitis,
pneumonitis) and metabolic acidosis( diarrhea,
AKI, mitochondrial toxicity, hypotension)
Respiratory index >1.5(death)
Arterial Lactate- MODS, hypotension, ARDS.
Lactate concentration >40mg%-fatal outcome-
helps determine prognosis
Chest radiograph- for assessing acute lung injury(
hypoxia/hyperventilation/crackles)-direct effect of
paraquat(bilateral) / aspiration( focal-mostly right
early phase(1-2 weeks)-diffuse alveolar
late phase-reticulointerstitial infiltrates-
Toxicology screen- for patients in altered mental
status-usually not caused by paraquat- but by
acetaminophen exposure etc
Urine paraquat- inexpensive; based on color
change after addition of dithionite soln to urine-
positive within 6 hrs after large ingestion,remains
positive for several days.
Positive test-40% mortality. Negative- 100 %
Methods : 100mg sod.dithionite to 10ml of 2M
sodium hydroxide- 200ul of this to 2ml urine-
blue(paraquat), green(diquat)- darker the color,
more the concentration
Serum paraquat- nomograms –correlate serum
paraquat concentration with mortality risk
The proudfoot nomogram, best cut off for the
Severity in Paraquat Poisoning(Sipp)
Sipp score-paraquat concentration(mg/dl) x time
since poisoning(hrs)..score <10 survival is likely.
Challenges –imprecise time of exposure, paraquat
assay within a relevant time frame.
Qualitative serum paraquat- in patients with
positive urinary dithionite test
soln prepared as before.. But added to 2ml of
plasma instead of urine- equivocal color change-
50% mortality, definitive color change-100 %
Topical exposure-no need of investigations.
If in doubt- urinary dithionite at 6 and 12 hrs for
Physical examination-oropharyngeal burns etc
Subsequent development of: AKI, metabolic
acidosis, or ARDS
Lab confirmation-urine dithionite test
No other pesticide makes such severe oral burns
Most corrosives do not cause acute systemic
Previously was mistaken for HIV related infections-
oral candidiasis/Pneumocystis jiroveci pneumonia
Determined on an individual basis based on
amount ingested, time elapsed since exposure
None of the current treatments are effective in
Symptoms/signs manifest in 6 to 12 hrs- need
monitoring atleast for this duration.
Negative urinary dithionite test at 6 hrs- minimal
GI decontamination to limit systemic exposure
Hemoperfusion followed by
hemodiafiltration/repeated hemoperfusion may be
beneficial if commenced within 4 hrs of exposure
Antedotes- antiflammatory and antioxidant
therapies- limited data to support efficacy.
For severe poisoning- better approach may be
Follows standard guidelines??
O2 should not be administered unless SpO2 <90%.
Hydration -2 to 3 L of isotonic crystalloids or more
Continuous pulse oximetry
For severe systemic illness- active management
may be futile.but decision can be taken based on
history/prognostic tests/clinical signs
Gastro intestinal decontamination:
◦ If presented within 2 hrs of exposure: Activated
charcoal 1g/kg in water, max dose 50g ; per oral or via NG
◦ Gastric lavage and forced emesis are contraindicated- caustic
◦ NG tube aspiration prior to charcoal administration
◦ Wash with soap and water for 15 mins.
◦ Staff should use universal precautions
◦ Ocular exposure- standard treatment for corrosive exposure??-
rinsing for 30 mins then standard protocol??
Monitoring: pulse oximetry.
Specific treatments and
Indications for extracorporeal therapies:
◦ Hemoperfusion for 4 hrs if initiated within 4 hrs of ingestion.
◦ Haemodialysis/hemofiltration may be used –paraquat has
less protein binding.??; can also be used in AKI as renal
◦ Rebound in plasma paraquat following hemoperfusion can
be minimised with continuous extracorporeal technique.
Antinflammatory and immunosuppressive therapy:
Cyclophosphamide+glucocorticoid- not validated
Antioxidant therapy-acetylcysteine, sodium
salicylate, deferoxamine, vitamin C, vitamin E.
Avoid O2 unless hypoxic
Correct electrolyte abnormalities
Monitor blood lactate concentrations, renal function
Acute hepatic injury/pancreatitis- do not influence
The likely outcome is generally apparent within a
day or two:
◦ Either critically ill with severe poisoning
◦ Mild to moderate poisoning but adequately compensated
Renal failure resolves in weeks
Lung injury becomes progressively more severe for
◦ Lung transplant ineffective- paraquat injures the allograft
Diquat- may be associated with MODS and rapid
death similar to paraquat.
◦ But survivors are most likely to recover and not experience
delayed or progressive respiratory failure