mangement of kerosene poisoning in children

1. Evidence based management
-kerosene poisoning
DR.KANIMOZHI
JUNIOR RESIDENT
DEPT OF PEDIATRICS
JIPMER

2. Introduction
Aliphatic hydrocarbon
Most common ingested poison in indian children esp
under 5 yrs
Easy accessibility and inappropriate storage
Pulmonary toxicity- fatal

3. Pathophysiology
Low viscosity (<60 SSU) and high volatality - high
aspiration potential
low viscosity- deep penetration into
tracheobronchial tree
Low surface tension- enhance spreading on lung
tissue
High volatality- displaces the alveolar gas and
interfere with ventilation and CNS depression

4. Pulmonary toxicity
d/to aspiration
Poor GI absorption
Even <1ml – significant injury
Fatal chemical pneumonitis
Loss of surfactant- poor oxygen exchange, atelectasis
and pneumonitis

5. Pneumatocoele necrosis of pulmonary
tissue
local obstruction-over distention and alveolar rupture
Usually during recovery period

6. CNS toxicity
Direct toxicity- highly lipid soluble
- neurons have high lipid
content
Secondary to hypoxia- most common

7. Cardiac toxicity
Dysarrythmias
Hypoxia
Direct myocardial injury
Myocardial sensitization to catecholamines

8. Other effects
Bone marrow toxicity and hemolysis
GI irritation- nausea, vomiting, abdominal pain
Local irritation and chemical burns

9. Clinical manifestations
Mostly aymptomatic with h/o exposure
Symptoms soon after ingestion- typically progress to
respiratory failure
Local effects- burning sensation, abdominal pain,
vomiting or loose stools
Characteristic odour

10. Vitals
 fever ( 30-60% - 100.4- 104 F )
persistance beyond 48 hrs s/o bacterial
superinfection
 pulsoximetry- decreased SpO2

11. Respiratory
Within 30 min; peak -12 to 24 hrs
Usually lasts 2-8 days
If no sympt ms after 6 hrs usually remain
asymptomatic
cough, choking,gagging, vomiting
Tachypnea, cyanosis, grunting, wheezing,
diminished resonance on percussion

12. Major complications-necrotising
chemical pneumonitis, lipoid
pneumonia, hemorrhagic pulmonary edema,
pneumothorax, pleural effusion ,empyema,
barotrauma, ARDS

13. CNS
Headache, ataxia, somnolence, blurred vision,
weakness, fatigue, lethargy, stupor, seizures and
coma
Pupils initially constricted and dilated later
as coma supervenes

14. Scoring system- gupta et al
Parameter Absent Present Others
FEVER 0 1 -
SEVERE
MALNUTRITION
0 1 -
RESPIRATORY
DISTRESS
0 2 4
(cyanosis)
NEUROLOGICAL
SYMPTOMS
0 2 4
(convulsion
s)

15. Imaging
CXR in all symptomatic pts
Significant 2-8 hrs after ingestion
Mc- multiple patchy densities with ill defined
margins
emphysema, pneumothorax, pneumatocoeles
Resolution usually lags behind clinical
improvement

16. ABG- hyoxemia and hpocarbia
-later, hpoxemia and hypercarbia
ECG

17. Admission criteria
significant respiratory symptoms- immediate
admission
Normal or mildly abnormal CXR who become
symptomatic in observation period
Mild symptoms and normal CXR who fail to
improve during observation period
CNS depression,severe GI symptoms, ingested
significant amount

18. Indications for discharge after
6 hrs of observation
Asymptomatic with normal CXR obtained 4 or more
hrs after exposure
Asymptomatic with mild abnormal CXR who does
not develop symptoms in observation period and
who can recieve timely follow up next day

19. Management
STABLISATION:
Endotracheal intubation and conventional
mechanical ventilation if severe respiratory distress
or decreased level of consciousness*
*zucker et al. Crit care Med 1986

20. Mild to moderate symptoms
 keep NPO
Supplemental oxygen
Get CXR
Aymptomatic
Keep NPO
CXR at 4-6 hrs or sooner if become symptomatic

21. Decontamination
EXTERNAL DECONTAMINATION
Health care team should don personal protective
equipment
 remove contaminated clothing
 irrigate affected skin,eyes and hair*
*Arena JM. Ped Ann 2014

22. GI DECONTAMINATION:
Ipecac induced emesis and gastric lavage- NOT
RECOMENDED*
Risk of aspiration outweigh benefit*
*Vale et al. J Clin Toxicol,2004
*shannon et al. N Eng J Med.2000

23. ACTIVATED CHARCOAL:
Increases risk of spontaneous vomiting and
additional aspiration
Does not bind well to hydrocarbons
NOT RECOMMENDED

24. Pulmonary management
Mainly supportive
Supplemental oxygen and close monitoring
Selective Beta 2 agonist for bronchospasm
Epinephrine avoided- can cause fatal arrythmias in
hydrocarbon sensitised myocardium

25. Role of ECMO & HFV
Hydrocarbon pneumonitis and respiratory
failure unresponsive to conventional mechanical
ventilation
- hydrocarbon induced lung injury reversible
- children have ability to regenerate new lung
tissue

26. ECMO
In a case series that evaluated survival
after ECMO, 13 out of 19 with hydrocarbon
pneumonitis versus 459 out of 883 with other
respiratory disease*
*chyka PA et al. J Toxicol Clin Toxicol 1996

27. High frequency ventilation
case reports indicate that HFV (HFJV,
HFOV,HFPV) may be life saving *
*Bysani et al. Chest 1994
*Mabe TG et al. Pediatr Crit Care Med.2007

28. Role of steroids
No beneficial effects even when used early and
in large doses*
*wolfsdorf J et al.AAP. July 1974

29. Indications for antibiotics
Recurrence of fever after first 48 hrs
Leukocytosis after first 48 hrs
Increasing infiltrate in CXR
Sputum or tracheal aspirate positive for bacteria

30. Role of surfactant
one animal study in sheep showed
significantly increased rate of change of arterial
oxygen saturation, mixed venous oxygen saturation,
and PO2
Widner LR et al.Crit Care Med. 1996

31. Treatment for pneumatocoele?
resolve spontaneously and do not
require specific treatment*
*Thalhammer et al.Wein Klin Wochenschr. 2005
*Bergeson et al. Am J Dis Child.1975

32. Summary
Mainstay of treatment is SUPPORTIVE
NO induced emesis, gastric lavage or activated
charcoal
NO role for steroids
Use antibiotics only when indicated
Rescue therapy- HFV, ECMO, surfactant
Most patients usually recover fully with supportive
care

33. Thank you