kerosene poisoning -evidence based management

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