3. Patient came in casualty on 9th March at 5:20 pm with
complains of;
-Vomiting since 3 days
-Fever since 3 days
-Pain in abdomen since 3 days
-Yellowish discolouration of eyes and tongue since 2 days
-Chest pain since 1day
4. On general examination her findings were as follows:
Patient was conscious and oriented
Temperature: Febrile (100 F)
Pulse:125/min
B.P: 110/80mm hg
RR: 32/ min
Spo2 : Off O2- 88%
On O2- 98% @ 5lit/ min on o2 by mask
Weight: 35 kgs
Icterus: Present
Local Examination: Yellowish discoluration of tongue.
5. On systemic examination her air entry was decreased in lower
lobes, bilateral crepitations were present and she was tachypnic.
She was conscious and oriented, S1 S2 heart sound present, no
murmur.
Her per abdomen was soft and non tender.
Then from casualty she was referred to Paediatrics department.
The following routine investigation were sent CBC, LFT, RFT, CXR,
ABG, Weil Felix, USG abdomen pelvis, Urine R/M, H3 and HRCT
She was started with injectable Piptaz 2.25gm tds, Pan 40 OD,
Ondem TDS, Pidimol SOS, Deriphylline150 BD, Hydrocort100 mg
BD, nebulisation TDS and tablet Udigold BD
7. CXR shows infiltration in left upper
zone.
There are diffuse patchy non
homogenous infiltrates in both lower
zone.
There is prominent radio lucent
shadow seen around aortic knob and
upper half of left heart border. This
radiolucent shadow doesn’t show any
broncho vascular marking, suggestive
of
pneumomediastinum.
8. In ABG
pH is 7.40 which is in the normal range
But pCO2 has decreased
And HCO3 is on lower side too
Which is suggestive of Metabolic Acidosis
mixed with Respiratory Alkalosis.
9. As she had fever, breathlessness, abnormal chest x-ray she was
transferred to Medicine department on the same day at 11pm to rule
out Covid-19 .
Then on Day 0
In TICU
Her vitals was as follows
Pulse: 90/min
BP: 110/70 mm of Hg
Spo2: off O2-85%
On O2-98% @5 lit/min on nasal prongs
RR-27/min
Hoarseness of voice and dysphagia was present.
On local examination she had yellowish ulcers on tongue and oral cavity,
erosions over tongue and pain was present.
10. On palpating both side of neck crepitus was felt which is suggestive of
subcutaneous emphysema.
We suspected she might have oesophageal perforation so Ryle's Tube
was not inserted due to risk of profuse bleeding.
Then to the ongoing treatment we added Inj. Meropenem 1gm BD,
Tb.Ketorite BD, Tb. Auxisoda BD, Tb. Liv 52 BD
Then on Day 1,
HRCT report showed
Surgical emphysema,
Extensive pneumomediastinum,
Bilateral mild pneumothorax
Bilateral lung shows extensive patchy ground glass opacity
Above mentioned findings were suggestive of lower oesophageal tear
(Boerhave Syndrome) was needed to be ruled out
11. Vitals on Day 1 at 9 am were as follows
Pulse: 82/min
BP: 110/70 mmHg
Spo2: O2 requirement further increased to 10 lit/min to
maintain saturation to 98% on nasal prongs
RR-25/min
She was complaining of Vomiting and pain in abdomen.
12. Then in the morning ICU rounds of our consultant Dr. Shaikh Sir;
assessed the patient in detail.
By looking at her oral ulcers, glossitis, bilateral crepitations on
auscultation, her suddenly going in acute renal failure, severely
deranged LFT, HRCT findings; Shaikh sir had a very strong suspicion of
paraquat poisoning.
We then kept the patient NBM. Added Inj. Methyl prednisolone120
mg BD, IV fluids ,inj. Auximin 10% OD
Then sir asked the patient for history of any poisoning, but she
refused. Then while counselling with her relatives they refused of any
poisoning too. But sir was very confident about his diagnosis and
ordered the resident to take detail history from mother. The resident
then took the mother in confidence and then she revealed that the
patient first poisoned a cat and after
13. confirming the cat’s death she consumed that unknown poison
because of some familial issues.
Shaikh Sir then asked the mother to bring a photo of that poison
and as expected it turned out to be Paraquat Dichloride 24% SL
MLC was done
These confession was a great breakthrough in changing the line of
management of this patient. All the unnecessary medication like
Inj. Deriphylline were stop Inj. Hydrocortisone was changed to Inj.
Methyl Prednisolone 40mg OD.
Antioxidant Inj. N acetylcysteine 1gm BD and Injectable Vit. C
500mg BD, Tb. Vit. E 400mg TDS was added . Though she
presented 4 days late after ingestion and knowing the bad
prognosis of paraquat poisoning both parents and Shaikh sir
decided to treat the patient aggressively.
14. Nephrology call was given and then Nephrologist advised urgent
Haemodialysis.
Double lumen HD catheter was inserted in the right femoral vein by
residents at 5:30 pm
Dialysis was initiated at 6pm for 6 hours
Her vitals on day 1 at 8 pm were as follows
Pulse: 82/min
BP: 106/80 mmHg
Spo2: O2 requirement further increased to 15 lit/min to maintain
saturation to 98% on nasal prongs
RR-30/min
Surgery call was given for surgical emphysema. They advised SOS
ICD insertion if spo2 falls below 90%
15. Day 2
After 1st dialysis dyspnoea improved a bit; oxygen
requirement came down from 15 lit./min to 10 lit/min.
Her vitals on day 2 at 9am were as follows
Pulse: 70/min
BP: 110/70 mmHg
Spo2: 98% @ 10lit/min on nasal prongs
RR-27/min
Complain of vomiting persisted but abdominal pain was
resolved
In round repeat LFT and RFT were advised.
Psychiatry call for depression and ENT call for dysphagia
and oral ulceration was advised.
16. RFT improved
• S. Creat: 11.7 to 8.6 mg/dl
but
LFT further deteriorated
• Total Bilirubin: 5.2 to 6.9 mg/dl
• Direct Bilirubin: 3.3 to 4.7 mg/dl
• Indirect Bilirubin: 1.9 to 2.2 mg/dl
• SGOT:146 to 161 IU/L
• SGPT: 118 to 141 IU/L
• ALP: 183 to 280 IU/L
Nephrologist again advised haemodialysis for 4 hours. So
2nd session of dialysis was performed at 6pm again on day 2.
17. Her vitals on day 2 at 8 pm were as follows
Pulse: 66/min
BP: 110/70 mmHg
Spo2: 98%@ 10lit/min on nasal prongs
RR-27/min
18. After 2nd haemodialysis dyspnoea significantly improved.
Oxygen requirement came down from 10 lit./min to 5 lit/min.
On auscultation her chest was clear
Clinically also she improved a lot.
After refraining multiple times for not going to latrine in
washroom she went because she felt a lot of improvement in
her condition.
On day 3 her vitals at 9 am were as follows
Pulse: 86/min
BP: 110/80 mmHg
Spo2: 98%@ 5lit/min on nasal prongs
RR-27/min
RS: AEBE and clear
Episodes of vomiting were reduced.
19. USG abdomen and pelvis was suggestive of acute renal
parenchymal disease
In consultants round on Day 3
Total Parenteral Nutrition (TPN) and zytee ointment for local
application on oral ulcers were advised
A repeat Chest X-ray was ordered and the rest line of
management was kept same
Psychiatrist added tab. Sizodon 0.5mg
ENT resident could not examine as the patient was not able to
open the mouth. So no active intervention from ENT
Department.
20. Right lower lobe haziness.
Pneumomediastinum noted.
Cardiomegaly is seen can be due to
supine position.
21. On day 3 her vitals at 8 pm were as follows
Pulse: 86/min
BP: 130/80 mmHg
Spo2: 98%@ 10lit/min on nasal prongs
RR-28/min
On day 4 at 1 AM
She looked tachypneic with RR of 34
So she was shifted on Dual O2. Her vitals were
Pulse: 115/min
BP: 110/70 mmHg
Spo2: 95%@ 10lit/min on nasal prongs and 10lit/min on
oxygen mask.
22. On day 4 at 9 am her vitals were as follows
Pulse: 96/min
BP: 110/70 mmHg
Spo2: 97%@ 10lit/min on nasal prongs and 10lit/min on
oxygen mask.
RR: 32
On consultant round at 10:40 am
Though her O2 requirement was increased she seemed to be
good. Repeat LFT, RFT, ABG was ordered to assess the
condition.
23. Tests Day 0 Day2 Day 4
Total Bilirubin 5.2 6.9 9.5
Direct Bilirubin 3.3 4.7 6.4
Indirect Bilirubin 1.9 2.2 3.1
SGOT 146 161 271
SGPT 118 141 201
ALP 183 280 320
Sr. Urea 129 144 221
Sr. Creatinine 11.7 8.6 6.5
The above chart shows consistently deteriorating LFT in
spite of continuous liver supportive and improving
creatinine after haemodialysis.
24. ABG on day 4 at 11:55 AM showed
Severe metabolic Acidosis with hypoxia
settling in.
25. All of a sudden she went in gasping at 2:05pm and
then emergency intubation was performed.
On ventilator volume control mode with ARDS type of
settings that is low tidal volume and high PEEP was
followed.
In spite of all the resuscitation measure she was
declared dead at 3:01PM.
Cause of Death: As per MLC PM
27. Paraquat is bipyridyl herbicide , quaternary ammonium compound.
Bipyridyl herbicides are rapidly acting and non selective, being toxic to wide range
of grasses and broad leafed weeds when applied topically in presence of sunlight.
Paraquat is available for agricultural use as a soluble liquid concentrate(SL),
emulsifiable concentrate (EC) & soluble granule (SG) formulatios.
SL &EC contain 20-24%w/w paraquat.
SG contain 5% or more paraquat ion.
Liquid formulations enter the small intestine rapidly, particularly if stomach is
empty.
When absorbed ,paraquat distributed to most of the organ but highest
concentration found initially in the lung.
Several organs including the lungs and skeletal muscle provide Reservoir for
paraquat which then slowly redistribute into bloodstream .
28. Paraquat has been detected in the urine up to three months after ingestion
possibly from a deep body compartment reservoir.
Lung is the primary target organ of paraquat toxicity in humans and several
animal species because selective uptake and accumulation of paraquat by
Type 1 and type 2 alveolar epithelial cells and Clara cells.
Paraquat causes renal tubular necrosis, renal failure which is the result of
direct tubular toxicity.
Paraquat uptake into the lung occurs by a slow energy dependent active
transport process reaching concentration that maybe 50 times greater than
those in plasma.
29. TOXICITY
1) SKIN- Dermal erythema ,blistering ,ulceration and dermatitis .nail damage
occurs after contact with concentrated paraquat .
2) MUCOSA -Corrosive damage to the oral mucosa leading to burning in the
mouth and painful haemorrhagic ulceration of the oropharynx and
oesophagus is a common early feature following ingestion of concentrated
paraquat solution.
3) INHALATION- Aerosolized droplets have diameter exceeding 5 micrometer
and therefore do not reach the alveolar membrane to cause either direct or
systemic toxicity via inhalation .
However excessive inhalation of the spray during formulation, mixing or
application can cause epistaxis, stomatitis, headache and sore throat.
30. SYSTEMIC TOXICITY –
1)Gastrointestinal Tract :-
• Patient develop nausea, vomiting ,abdominal pain and diarrhoea soon
after ingestion as a result of local irritant action on the gut .
• In moderate to severe poisoning a burning sensation, soreness and pain in
mouth, throat ,retrosternal area and abdomen are common.
• Severe and extensive inflammation and ulceration occurs in the mouth,
oesophagus ,stomach and small intestine with sloughing of the
oropharyngeal mucosa, an inability to swallow senile dysphagia and
aphonia.
• Perforation of the oesophagus may result in mediastinitis, surgical
emphysema and Pneumothorax or plural effusion in association with
pleuritis.
31. 2) LIVER
- Jaundice, hepatomegaly and Central abdominal pain due to pancreatitis
are frequent complication.
Raised serum transaminase and pancreatic enzyme activity is correlated
with poor outcome.
3) RENAL
Oliguric or non oliguric renal failure may occur usually due to acute
tubular necrosis becoming evident after about 24 hours.
Renal dysfunction commonly result in proteinuria, microscopic
haematuria, glycosuria ,aminoacidic urea and phosphaturia and excessive
leaking of sodium and urate.
4)PULMONARY
Many patient develop a cough which may be productive and blood
stained.
32. Dyspnoea is prominent feature due to development of adult respiratory
distress syndrome and bronchopneumonia. plural effusion and iatrogenic
pulmonary oedema may precipitate dyspnoea.
Radiological changes do not always parallel the severity of clinical symptoms.
chest X-ray may be normal particularly in patient dying early from multiple
organ failure.
In patient less severely poisoned with paraquat the onset of dyspnoea may
occur later and because of pulmonary Fibrosis. Patchy infiltration occurs on x-
ray which may progress to an opacification of one or both lung fields. survivor
of paraquat poisoning may recover normal pulmonary function or be left with
a restrictive type pulmonary dysfunction.
5) CARDIOVASCULAR
Ventricular tachycardia, intraventricular conduction disturbance and
nonspecific T wave changes on ECG occur in terminal phase.
33. CXR shows massive cardiomegaly.
DIAGNOSIS
The diagnosis can usually be made based on the history, the local mucosal
damage seen in the mouth after ingestion and ensuing characteristic organ
damage.
The diagnosis of paraquat should be confirmed with laboratory analysis of urine or serum.
A qualitative urine test should be performed with alkaline sodium dithionite.
The presence of paraquat turns the mixture blue.
The test has some prognostic value in urine taken within 24 hours of poisoning,
concentration less than 1 mg/L generally predict survival while those more than 1 mg/L
generally predict a poor outcome.
34. A negative test doesn't exclude the possibility of bipyridyl ingestion,
repeated urine test are suggested over the next 6 hours.
Plasma can also be tested for paraquat using sodium dithionite .
Quantitative methods of analysis in biologic flows include
spectrophotometry,
Ion exchange chromatography ,gas chromatography and radioimmune
assay.
