DR.KANIMOZHI
JUNIOR RESIDENT
DEPT OF PEDIATRICS
JIPMER
Evidence based management -kerosene poisoning
Introduction
Aliphatic hydrocarbonMost common ingested poison in indian children esp
under 5 yrsEasy accessibility and inappropriate storagePulmonary toxicity- fatal
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
Pulmonary toxicity
d/to aspirationPoor GI absorptionEven <1ml – significant injuryFatal chemical pneumonitisLoss of surfactant- poor oxygen exchange, atelectasis
and pneumonitis
Pneumatocoele necrosis of pulmonary
tissue
local obstruction-over distention and alveolar rupture Usually during recovery period
CNS toxicity
Direct toxicity- highly lipid soluble
- neurons have high lipid
content Secondary to hypoxia- most common
Cardiac toxicity
DysarrythmiasHypoxiaDirect myocardial injuryMyocardial sensitization to catecholamines
Other effects
Bone marrow toxicity and hemolysisGI irritation- nausea, vomiting, abdominal painLocal irritation and chemical burns
Clinical manifestations
Mostly aymptomatic with h/o exposureSymptoms soon after ingestion- typically progress to
respiratory failureLocal effects- burning sensation, abdominal pain,
vomiting or loose stoolsCharacteristic odour
Vitals
fever ( 30-60% - 100.4- 104 F )persistance beyond 48 hrs s/o bacterial
superinfection pulsoximetry- decreased SpO2
Respiratory
Within 30 min; peak -12 to 24 hrsUsually lasts 2-8 daysIf no sympt ms after 6 hrs usually remain
asymptomaticcough, choking,gagging, vomitingTachypnea, cyanosis, grunting, wheezing,
diminished resonance on percussion
Major complications-
necrotising chemical pneumonitis, lipoid pneumonia, hemorrhagic pulmonary edema, pneumothorax, pleural effusion ,empyema, barotrauma, ARDS
CNS
Headache, ataxia, somnolence, blurred vision, weakness, fatigue, lethargy, stupor, seizures and coma
Pupils initially constricted and dilated later
as coma supervenes
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 (convulsions)
Imaging
CXR in all symptomatic ptsSignificant 2-8 hrs after ingestion Mc- multiple patchy densities with ill defined
marginsemphysema, pneumothorax, pneumatocoelesResolution usually lags behind clinical
improvement
ABG- hyoxemia and hpocarbia
-later, hpoxemia and hypercarbia
ECG
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
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
Management
STABLISATION:
Endotracheal intubation and conventional mechanical ventilation if severe respiratory distress or decreased level of consciousness*
*zucker et al. Crit care Med 1986
Mild to moderate symptoms keep NPOSupplemental oxygenGet CXR
Aymptomatic Keep NPOCXR at 4-6 hrs or sooner if become symptomatic
Decontamination
EXTERNAL DECONTAMINATIONHealth care team should don personal protective
equipment remove contaminated clothing irrigate affected skin,eyes and hair*
*Arena JM. Ped Ann 2014
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
ACTIVATED CHARCOAL:Increases risk of spontaneous vomiting and
additional aspirationDoes not bind well to hydrocarbons
NOT RECOMMENDED
Pulmonary management
Mainly supportiveSupplemental oxygen and close monitoringSelective Beta 2 agonist for bronchospasmEpinephrine avoided- can cause fatal arrythmias in
hydrocarbon sensitised myocardium
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
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
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
Role of steroids
No beneficial effects even when used early and in large doses*
*wolfsdorf J et al.AAP. July 1974
Indications for antibiotics
Recurrence of fever after first 48 hrsLeukocytosis after first 48 hrsIncreasing infiltrate in CXRSputum or tracheal aspirate positive for bacteria
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
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
Summary
Mainstay of treatment is SUPPORTIVE NO induced emesis, gastric lavage or activated
charcoalNO role for steroidsUse antibiotics only when indicatedRescue therapy- HFV, ECMO, surfactant
Most patients usually recover fully with supportive care
Thank you