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Paraquat Poisoning
Introduction
 Paraquat is a rapidly acting, non selective
herbicide ; inexpensive
 Dermal /spray exposure(inhalation)-li...
Pharmacology and cellullar
toxocology
 Chemically- bi pyridyl compounds
 Absorption..concentrated inside cells..redox
cy...
Kinetics
 Highly polar and corrosive
 Ingestion ..rapid absorption..rapid distribution
 Max tissue levels..6hrs
 Activ...
Clinical features:
History
 Formulation , strength and dose are important-
>30ml of 20% paraquat can be lethal.
 Kidney ...
Physical examination and basic
monitoring
 Mouth,pharynx- necrosis, inflammation, ulceration-
maybe delayed to upto 12 ho...
Lab evaluation
 General testing:
 Blood tests- on admission, every 6 to 12th hourly for
first 48 hours, then based on cl...
 Serum electrolytes- may be altered due to
vomiting, diarrhea, acute kidney injury and multi
organ dysfunction.
 Renal f...
 Blood gas-
◦ Alkalemia-vomiting, early in the course
◦ Acidemia- respiratory acidosis( alveolitis,
pneumonitis) and meta...
 Chest radiograph- for assessing acute lung injury(
hypoxia/hyperventilation/crackles)-direct effect of
paraquat(bilatera...
 Specific testing:
 Urine paraquat- inexpensive; based on color
change after addition of dithionite soln to urine-
posit...
 Serum paraquat- nomograms –correlate serum
paraquat concentration with mortality risk
 The proudfoot nomogram, best cut...
 Qualitative serum paraquat- in patients with
positive urinary dithionite test
 soln prepared as before.. But added to 2...
Diagnosis
 h/o ingestion/exposure
 Physical examination-oropharyngeal burns etc
 Subsequent development of: AKI, metabo...
Differential diagnosis
 No other pesticide makes such severe oral burns
 Most corrosives do not cause acute systemic
tox...
Management -overview
 Determined on an individual basis based on
amount ingested, time elapsed since exposure
 None of t...
 GI decontamination to limit systemic exposure
 Hemoperfusion followed by
hemodiafiltration/repeated hemoperfusion may b...
Initial resuscitation
 Follows standard guidelines??
 O2 should not be administered unless SpO2 <90%.
 Hydration -2 to ...
 Gastro intestinal decontamination:
◦ If presented within 2 hrs of exposure: Activated
charcoal 1g/kg in water, max dose ...
Specific treatments and
antidotal therapy:
 Indications for extracorporeal therapies:
◦ Hemoperfusion for 4 hrs if initia...
 Antinflammatory and immunosuppressive therapy:
 Cyclophosphamide+glucocorticoid- not validated
by studies
 Antioxidant...
Ongoing management
 Avoid O2 unless hypoxic
 Correct electrolyte abnormalities
 Monitor blood lactate concentrations, r...
 Renal failure resolves in weeks
 Lung injury becomes progressively more severe for
several weeks.
◦ Lung transplant ine...
 Thankyou
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Paraquat poisoning

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PARAQUAT POISONING

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Paraquat poisoning

  1. 1. Paraquat Poisoning
  2. 2. Introduction  Paraquat is a rapidly acting, non selective herbicide ; inexpensive  Dermal /spray exposure(inhalation)-limited localised injury  Ingestion-high case fatality rate  Diquat is a related herbicide-similar mechanism, clinical features, treatment  Coformulated with an antiemetic/alginate to reduce absorption
  3. 3. Pharmacology and cellullar toxocology  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- lungs/heart/kidneys/liver
  4. 4. Kinetics  Highly polar and corrosive  Ingestion ..rapid absorption..rapid distribution  Max tissue levels..6hrs  Active uptake by cell membrane transporters(eg: spermidine/putrescine)  High conc: in liver, lungs, kidney,muscle  No significant phase 1/phase 2 biotransformation  Elimination –kidneys  Minor-most ingested will appear in urine by 24 hrs  Severe-kidney function impaired..elimination delayed..elimination half life can exceed 100 hrs
  5. 5. Clinical features: History  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
  6. 6. Physical examination and basic monitoring  Mouth,pharynx- necrosis, inflammation, ulceration- maybe delayed to upto 12 hours, peak severity in some days later  Dehydration(vomiting)  Monitor respiratory rate, pulse oximetry- O2 only if SpO2<90%  Heart rate, BP- progressive refractory hypotension  Chest-dyspnoeic, tachypnoeic, crackles (alveolitis).subcutaneous emphysema- mediastinitis  Abdominal pain, diffuse tenderness  Topical contact- corneal ulceration, non specific dermatitis
  7. 7. Lab evaluation  General testing:  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
  8. 8.  Serum electrolytes- may be altered due to vomiting, diarrhea, acute kidney injury and multi organ dysfunction.  Renal function- ◦ 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 over 6hrs(death) ◦ Serum cystatin C- >0.009mg/L per hr over 6 hrs (death)
  9. 9.  Blood gas- ◦ 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
  10. 10.  Chest radiograph- for assessing acute lung injury( hypoxia/hyperventilation/crackles)-direct effect of paraquat(bilateral) / aspiration( focal-mostly right lung).  early phase(1-2 weeks)-diffuse alveolar infiltrates-ARDS  late phase-reticulointerstitial infiltrates- progressive fibrosis  Toxicology screen- for patients in altered mental status-usually not caused by paraquat- but by acetaminophen exposure etc
  11. 11.  Specific testing:  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 % survival  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
  12. 12.  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.
  13. 13.  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 % mortality  Topical exposure-no need of investigations.  If in doubt- urinary dithionite at 6 and 12 hrs for reassurance.
  14. 14. Diagnosis  h/o ingestion/exposure  Physical examination-oropharyngeal burns etc  Subsequent development of: AKI, metabolic acidosis, or ARDS  Lab confirmation-urine dithionite test
  15. 15. Differential diagnosis  No other pesticide makes such severe oral burns  Most corrosives do not cause acute systemic toxicity  Previously was mistaken for HIV related infections- oral candidiasis/Pneumocystis jiroveci pneumonia
  16. 16. Management -overview  Determined on an individual basis based on amount ingested, time elapsed since exposure  None of the current treatments are effective in severe poisoning  Symptoms/signs manifest in 6 to 12 hrs- need monitoring atleast for this duration.  Negative urinary dithionite test at 6 hrs- minimal exposure.
  17. 17.  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 palliative care.  Titrated fentanyl/morphine.
  18. 18. Initial resuscitation  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
  19. 19.  Gastro intestinal decontamination: ◦ If presented within 2 hrs of exposure: Activated charcoal 1g/kg in water, max dose 50g ; per oral or via NG tube ◦ Gastric lavage and forced emesis are contraindicated- caustic injury ◦ NG tube aspiration prior to charcoal administration  Topical/inhalational exposure: ◦ 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.
  20. 20. Specific treatments and antidotal therapy:  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 replacement therapy. ◦ Rebound in plasma paraquat following hemoperfusion can be minimised with continuous extracorporeal technique.
  21. 21.  Antinflammatory and immunosuppressive therapy:  Cyclophosphamide+glucocorticoid- not validated by studies  Antioxidant therapy-acetylcysteine, sodium salicylate, deferoxamine, vitamin C, vitamin E.
  22. 22. Ongoing management  Avoid O2 unless hypoxic  Correct electrolyte abnormalities  Monitor blood lactate concentrations, renal function  Acute hepatic injury/pancreatitis- do not influence prognosis  The likely outcome is generally apparent within a day or two: ◦ Either critically ill with severe poisoning ◦ Mild to moderate poisoning but adequately compensated without intervention ◦ Asymptomatic
  23. 23.  Renal failure resolves in weeks  Lung injury becomes progressively more severe for several weeks. ◦ 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
  24. 24.  Thankyou

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