- The document describes a case of acute paraquat poisoning in a 45-year-old female patient who was admitted to the hospital with multiorgan failure. She had a history of accidental exposure to paraquat and developed vomiting, hematemesis, jaundice, and respiratory failure. She was managed supportively but ultimately left against medical advice due to poor prognosis. Paraquat poisoning causes oxidative damage leading to injury of lungs, kidneys, liver and other organs. Management involves decontamination, supportive care and dialysis or ventilation as needed, but outcomes are generally poor.

1. IM1-IM2-EMW COMBINED
ROUNDS
CASE OF ACUTE PARAQUAT
POISONING
IM-1
6/07/2021
JR - Dr. Aman Agrawal
SR – Dr. Sandeep

2. PATIENT DETAILS
• Name : Mrs. P
• CR No : 202102210901
• Age : 45 yrs / female
• Address : Kangra, Himachal Pradesh
• DOA : 24/06/2021
• DOD : 01/07/2021
• Duration of stay : 8 days
• Treating Unit : 24/6 – 26/6 EMOPD
• 27/6 – 1/07 IM1, FMW

3. CHIEF COMPLAINTS
Alleged history of accidental exposure ( ?while spraying pesticides on the field ) to
paraquat on 19/06/21 followed by c/o –
• Vomiting
• Hematemesis and Malena
• Yellowish discoloration of eyes and skin

4. HISTORY OF PRESENTING ILLNESS
• She was in usual state of health till afternoon of 19th June, when she she
had alleged ( ?while spraying pesticides on the field ) exposure to paraquat,
quantity not known, following which she developed vomiting from around
midnight –
• Non projectile
• Contain food particles
• Non bilious
• 10-12 episodes per day

5. After 2 days, she had history of blood in vomitus ~ 5-10 mL per episode –
• a/w Malena
• No h/o bleeding PR
• a/w abdominal discomfort in the epigastric region
She also developed yellowish discoloration of eyes and skin 2 days after
exposure –
• Insidious onset and progressive in nature
• No h/o itching
• No h/o high colored urine or clay colored stools

6. • No h/o abdominal distension/ constipation
• No h/o altered mental status/ seizures
• No h/o chest pain/ SOB/ DOE
• No h/o hematuria/ decreased urine output
For these complaints patient was initially evaluated in Govt. Hospital in Dharamshala,
where she was found to have deranged RFT and was referred to PGIMER Chandigarh.

7. PAST HISTORY
• No h/o TB/DM/HTN
• No h/o CKD/ CAD/
• No h/o prior blood transfusions.

8. PERSONAL HISTORY
• Mixed diet consumer
• No addictions
• Bowel and bladder normal
• Sleep and apetite normal
FAMILY HISTORY
• Not significant

9. GENERAL PHYSICAL EXAMINATION
• Conscious , oriented to Time , place and person
• Vitals
• BP= 130/80
• Pulse=68/min, Regular
• RR=24/min
• Temp = afebrile
• Spo2 = 91 % at room air
• Icterus +/ No Pallor/ Cyanosis/Clubbing/Lymphadenoapthy
• Mild B/L Pitting edema +

10. ORAL CAVITY EXAMINATION
• Multiple oral ulcers +
• Tongue ulcers +

11. SYSTEMIC EXAMINATION
• CVS
• S1 S2 +
• No murmurs
• Respiratory System
• B/L air entry equal, B/L NVBS
• No crepitations present

12. • P/A
-Scar of cholecystectomy present
-No dilated veins
-Soft non tender
-No free fluid
-Liver and spleen not palpable
• CNS : B/L pupils equal and reactive
-No Focal neurological deficit
-No meningeal signs

13. INVESTIGATIONS
Date 24/06/21 27/06/21 28/06/21 30/06/21
Hb 11.8 11.1 11.3 11.8
TLC 3100 4800 8700 18000
DLC 90/4/0/5/0 70/20/3/7/0
Platelets 113K 112K 140K 198K
MCV/MCH/MCHC 94.8/23.7/34.5 91/32/ 92/31.9/34.7
RDW 15.0 15.1 15.5

14. BIOCHEMISTRY
Date 24/06/21 27/06/21 28/06/21 30/06/21
Na/K 136/4.6 137.8/4.5 139/3.96 141/4.5
Urea/Creatinine 123/11.6 83/5.87 113.7/6.94 123/5.47
Bilirubin 9.7/6.2 9.39/8.27 12.41/11.27
Ca/P 9.18/4.85
AST/ALT/ALP 536/443 324/456/618 121/286/572
Protein/Albumin 6.2/3.4 5.44/3.07 6.22/2.62
CK NAC 42

15. BLOOD GAS ANALYSIS
Date 24/04/21 26/06/21 28/06/21 01/07/21
pH 7.371 7.424 7.427 7.177
pCO2 27.3 23.9 27.6 55.5
pO2 41.8 55 39.4 55.9
HCO3 15.5 15.3 17.8 20.1
Lactate 1.17 0.68 1.05

16. COAGULOGRAM –
24/06/21 : PT= 14.5, PTI=90, INR=1.11, apTT=25.7
28/06/21: PT= 17.4, PTI=75, INR=1.32, apTT=30.4
URINE RME (24/06/21) – Protein 1+, Sugar nil
USG ABDOMEN (24/06/21)
Liver 11.5 cm, normal liver echotexture,
Post op GB
Spleen – 11 cm
Nil free fluid

17. HRCT CHEST (29/06/21)

18. COURSE AND MANAGEMENT
24/6/2021
• Patient presented with alleged history of paraquat poisoning with
multiorgan failure to EMOPD.
• Patient managed with IV Fluids (guided) and IV Dexamethasone
(8MG IV TDS) and antibiotics (Piptaz 4.5 g stat f/b 2.25g TDS)
• Inj. NAC Infusion was started i/v/o acute liver injury.
25/6/2021
• In view of hematemesis and dysphagia UGI endoscopy was done
which showed grade 2B esophageal injury and NJ was placed. The
patient was started on NJ Feed.
• i/v/o advanced Azotemia and decreased Urine Output hemodialysis
was started.
• 2 sessions of dialysis was given on 25th and 26th June.

19. 27/6/2021
• Patient became tachypneic with saturation dropping to 89%.
Patient was put on O2 Support. Patient was maintaining saturation
on NP @4L/min.
• CXR was done which showed B/L infiltrates predominantly in
Lower Lobes.
• HRCT chest was done, which showed B/L LL>UL GGOs and
peribranchial thickening.
28/06/21
• Patient's respiratory failure worsoned
•Inj Methylpred was started at 15mg/kg/day for 3 days.
•Inj Cyclophosphamide was started at 5mg/kg for 2 days.
•Elective intubation was done and patient was put on ventilatory
support.

20. 30/06/21
• Patient’s symptoms showed no improvement, with FiO2
requirement 100 %. ( PEEP – 10mm Hg, CMV mode, SpO2 92%)
01/07/21
• Due to exhaustion of resourceS and considering poor outcome,
patient took Leave Against Medical Advice.

21. FINAL DIAGNOSIS
• Paraquat Poisoning (accidental ?inhalational)
• Grade 2B Esophageal Injury
• Multiorgan dysfunction ( Liver Injury, Kidney injury, Hematological )
• Type 1 Respiratory Failure

22. DISCUSSION
1. Introduction
2. Mechanism of Action
3. Clinical features
4. Management
5. Outcomes
6. Take home message

23. INTRODUCTION
• Paraquat is a toxic chemical that is widely used as an herbicide (plant
killer), primarily for weed and grass control.
• Poisoning by paraquat herbicide is a major medical problem in parts of
Asia while sporadic cases occur elsewhere.
• The most likely route of exposure to paraquat that would lead to
poisoning is ingestion (swallowing). Other possible routes can be skin
exposure, inhalational (more likely to cause lung damage).
• The very high case fatality of paraquat is due to inherent toxicity and
lack of effective treatments.

25. MECHANISM OF ACTION
• Paraquat generates reactive oxygen species which cause cellular
damage via lipid peroxidation, activation of NF-κB, mitochondrial
damage and apoptosis in many organs.
• Paraquat toxicity is most severe in the lungs and leads to an acute
alveolitis. Further effects include diffuse alveolar collapse, vascular
congestion and adherence of activated platelets and
polymorphonuclear leucocytes to the vascular endothelium.
• Kidneys exposed to paraquat demonstrate development of large
vacuolation in proximal convoluted tubules which leads to necrosis.
• Congestion and hepatocellular injury associated with rough and
smooth endoplasmic reticulum degranulation and mitochondrial
damage occur in the liver.

27. CLINICAL FEATURES
• The clinical manifestations that follow paraquat ingestion depend upon
the quantity ingested.
• Ingestion of large amounts of liquid concentrate (>50–100 ml of 20%
ion w/v) results in fulminant organ failure: pulmonary oedema,
cardiac, renal and hepatic failure and convulsions due to CNS
involvement.
• These patients generally have hypoxia, shock and a metabolic acidosis
at presentation. Death results from multiple organ failure within
several hours to a few days.

28. • Ingestion of smaller quantities usually leads to toxicity in the two key
target organs (kidneys and lungs) developing over the next 2–6 days.
• Renal failure develops quite rapidly, and creatinine and/or cystatin-C
concentrations can be monitored over the first day to detect this group
and these also predict long-term outcome.
• However, the major effect of this quantity of paraquat follows its
accumulation in the lungs with lung cell damage producing decreased
gas exchange and respiratory impairment.

29. PULMONARY INVOLVEMENT
• The pulmonary lesion has two phases: an acute alveolitis
over 1–3 days followed by a secondary fibrosis.
• The patient typically develops increasing signs of respiratory
involvement over 3–7 days and ultimately dies of severe
anoxia due to rapidly progressive fibrosis up to 5 weeks later.

30. Chest X-ray
showing consolidation with
reticular and nodular interstitial
patterns of opacities
diffusely involving bilateral lung fields
suggestive
of chemical pneumonitis.
HRCT of
chest showing reticulation with
nodules diffusely
involving bilateral lung field along with
interlobular and
intralobular septal thickening and few
consolidations
predominantly at the peripheral lung
field.

31. CT scans in the survivor group. (a) A female (22 years) admitted 6 h after acute paraquat
poisoning; baseline CT scan 3 days after admission showing scattered effusion in the
lungs and (b) CT scan taken 3 days after baseline showing significant progression of
lesions (arrow), as well as significant consolidation and fibrosis. (c) A partially resolved
lesion in the lungs (arrow). (d) CT scan showing that the lesion had significantly resolved
in the lungs (arrow). The patient was discharged when all lesions were stabilised.
Zhang H, Liu P, Qiao P, et al. CT imaging as a prognostic indicator for patients with pulmonary injury from acute
paraquat poisoning. Br J Radiol. 2013;86(1026):20130035. doi:10.1259/bjr.20130035
A retrospective review
of 78 patients with
acute PQ poisoning

32. CT scans in the non-survivor group. (a) A female (16 years) admitted 10 h after acute
paraquat poisoning; baseline CT scan 1 day after admission showing no clear abnormal
signs and (b) scattered effusion and fibrosis (arrow) after 3 days. (c) Lesions
progressed and consolidation rapidly appeared (arrow). (d) Further lesion progression
was observed, showing consolidation in most of the lungs (arrow) and elevated
bronchial gas volumes. The patient died from respiratory failure 15 days after
admission.

33. ORAL AND GI INVOLVEMENT
• Gastrointestinal toxicity is universal in those ingesting paraquat
concentrate. Mucosal lesions of the mouth and the tongue (‘paraquat
tongue’) begin to appear within the first few days and may become
ulcerated with bleeding.
• Mucosal lesions in the pharynx, oesophagus and stomach are also very
common and much more sinister.
• These may result in perforation, mediastinitis and/or
pneumomediastinum.

35. RENAL INVOLVEMENT
• As mentioned earlier, renal toxicity of paraquat poisoning is because
it is largely excreated unexchanged in Urine.
• Rapid and large increases in Cr are a common clinical presentation of
severe paraquat poisoning and greatly exceed the value that predicted
by a large decreases in glomerular filtration rate.
• The rapid rise in serum creatinine most probably represents increased
production of creatine and creatinine to meet the energy demand
following severe oxidative stress.

36. ACUTE LIVER FAILURE
• the liver is one of the major organs to accumulate the paraquat toxin
• Paraquat injury to the liver is biphasic: initially hepatocellular, but
later becoming cholangiocellular after 2 days.
• Although liver failure is commonly observed in acute paraquat
poisoning, cause of death is mostly the respiratory failure.
Yang CJ, Lin JL, Lin-Tan DT, Weng CH, Hsu CW, Lee SY, Lee SH, Chang CM, Lin WR, Yen TH. Spectrum of toxic hepatitis following
intentional paraquat ingestion: analysis of 187 cases. Liver Int. 2012 Oct;32(9):1400-6. doi: 10.1111/j.1478-3231.2012.02829.x. Epub
2012 Jun 5. PMID: 22672665.

37. MANAGEMENT AND TREATMENT
OPTIONS

38. RESUSCITATION
• The standard principles of resuscitation (assessment and management
of airway, breathing and circulation) should generally be followed as
per routine guidelines.
• The airway may be compromised due to mucosal toxicity or the
presence of vomitus.
• Tachypnoea and/or hypoxia may be due to metabolic acidosis,
aspiration and/or acute alveolitis and a blood gas and chest radiograph
may help make the correct diagnosis.
• However, mild to moderate hypoxia should not be routinely treated
with oxygen as it will worsen oxidative stress

39. • Initially, hypotension is generally due to hypovolaemia and should be
treated with boluses of fluids (15–20 ml kg−1 over 15–30 min)
repeated as necessary.
• A high urine output is desirable as renal failure commonly develops
over the first 24 h.
• Patients generally maintain a normal level of consciousness. Altered
consciousness generally results from hypoxia, hypotension and severe
acidosis. Intubation and mechanical ventilation becomes necessary in
such cases.

40. GASTROINTESTINAL DECONTAMINATION
• Gastric lavage followed by a dose of activated charcoal has been
recommended for patients who present within 1 h of ingestion of
paraquat.
• Since paraquat is a life threatening poison with no known antidote, GI
decontamination should be tried in every patient who present early.

41. INVESTIGATIONS
• Biochemistry (electrolytes and renal and liver function tests), and
hematology (full blood count) should be done at least daily.
• Blood- Gas analysis should be done daily to look for acidosis ( metabolic or
respiratory) and the need for HD.
• Measurement of plasma paraquat levels can be done but as yet they do not
have any role in guiding interventions and thus they are not urgent or
essential.
• A chest radiograph should be performed to look for pneumomediastinum,
pneumothorax or lung fibrosis.
• A CT scan of the chest may be useful in detecting early lung fibrosis or
assessing long-term damage in survivors

42. CLINICAL MONITORING
• Patients should be monitored for the development of:
1.Acute renal failure. Daily fluid balance should be maintained with the
aim of ensuring a good urine output without overloading the patient.
2.Liver toxicity. Clinical examination will usually detect jaundice and
right hypochondrial pain.
3.Respiratory failure: respiratory rate, auscultation of the lungs (for
crepitations) and measurement of peripheral oxygen saturation should
be performed on at least a twice-daily basis

43. • Mucosal injury: patients develop severe oral ulcers within a few days
after ingestion of paraquat. This generally prevents patients from
taking adequate food or oral fluids for up to 10 days. Early insertion of
a nasogastric/ naso-jejunal feeding tube will ensure adequate nutrition.
• In addition, pain relief with opiates is often required and these can
then be given.

44. HEMODIALYSIS
• Hemodialysis is a part of standard treatment in most centres. But the
benefits are very limited as shown in studies.
• In a dog model it was shown that HD removes paraquat from the
plasma compartment but only reduces paraquat taken up by the
lungs by negligible amounts and hence is unlikely to change overall
outcome.
• Haemodialysis could be considered in patients who have developed
symptomatic acute renal failure. However, such patients have a very
poor prognosis in terms of their lung injury, so this is unlikely to
change outcome

45. ANTIOXIDANTS
• Several antioxidants have been tested as potential antidotes for
paraquat poisoning –
• NAC (n- acetylcysteine)
• Deferoxamine (DFO)
• Salicylic acid (SA)
• Vit E and Vit C

46. IMMUNOSUPRESSION
• ‘Immunosuppression’ is widely practised as a treatment of paraquat
self-poisoning. The theory is that as paraquat leads to an acute
inflammatory response, interference with this may inhibit the
processes that follow that then lead to lung fibrosis and death.
• The most widely studied regimen uses cyclophosphamide,
methylprednisolone and dexamethasone.

47. Lin, JL., Lin-Tan, DT., Chen, KH. et al. Improved survival in severe paraquat poisoning with
repeated pulse therapy of cyclophosphamide and steroids. Intensive Care Med 37, 1006–
1013 (2011).

49. MANAGEMENT CONCLUSIONS
• There are two competing philosophies that drive management
decisions.
• The first recognizes that the outcome is dire and that no treatments are
likely to be effective and aims to do minimal low-risk interventions
(charcoal, i.v. fluids and maybe an anti-oxidant) and keep patients
comfortable.
• The second recognizes that the outcome is dire and that no treatments
are likely to be worse than the disease. This group does HP/HD,
immunosuppression and often adds to this a cocktail of other
treatments.

50. SUMMARY OF TRIALS
Gawarammana IB, Buckley NA. Medical management of paraquat ingestion. Br J Clin Pharmacol. 2011;72(5):745-757.
doi:10.1111/j.1365-2125.2011.04026.x

51. OUTCOMES
• Overall outcome after paraquat exposure depends on the amount of
exposure.
• Ingestion of large amounts of liquid concentrate (>50–100 ml of
20% ion w/v) results in fulminant organ failure and leads to
multiorgan failure and death in period of hours.
• Ingestion of smaller quantities usually has a longer survival period.
But organ failure ensues over period ultimately leading to mortality.
• Overall mortality is >90% despite the intensive care and all the
treatment options.

52. PGIMER DATA (RICU)
Agarwal R, Srinivas R, Aggarwal AN, Gupta D. Experience with paraquat poisoning in a respiratory
intensive care unit in North India. Singapore Med J. 2006 Dec;47(12):1033-7. PMID: 17139398.

53. TAKE HOME MESSAGE
• Paraquat (widely used herbicide) is a lethal poison having high
incidence of exposure in this part of the world, with no specific
antidote.
• It leads to Multiple Organ Failure by increasing the oxidative stress to
the body.
• Various treatment options in the form of antioxidants and
immunosuppressants (Cyclophosphamide, Pulse Methylpred ) are still
undergoing studies.
• However Multicentric RCTs are required to prove their efficacy and
formulate a widely accepted treatment guideline.

54. THANK YOU