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Carbon Monoxide Poisoning in Children

This document discusses carbon monoxide poisoning in children. It outlines that CO is a colorless, odorless gas produced by incomplete combustion that binds to hemoglobin over 200 times more than oxygen, disrupting oxygen delivery and causing tissue hypoxia. Children are particularly susceptible due to higher metabolic rates. Sources include wood-burning stoves, heaters, and vehicles. Clinical presentation ranges from mild symptoms like headaches to severe symptoms like seizures or death. Diagnosis involves a compatible history, physical exam, and elevated carboxyhemoglobin levels in blood gas samples. Treatment focuses on high-flow oxygen and potentially hyperbaric oxygen therapy. Prevention emphasizes source identification and elimination, home CO detectors, and public education.

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Subash Paudeal
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128 views10 pages

Carbon Monoxide Poisoning in Children

This document discusses carbon monoxide poisoning in children. It outlines that CO is a colorless, odorless gas produced by incomplete combustion that binds to hemoglobin over 200 times more than oxygen, disrupting oxygen delivery and causing tissue hypoxia. Children are particularly susceptible due to higher metabolic rates. Sources include wood-burning stoves, heaters, and vehicles. Clinical presentation ranges from mild symptoms like headaches to severe symptoms like seizures or death. Diagnosis involves a compatible history, physical exam, and elevated carboxyhemoglobin levels in blood gas samples. Treatment focuses on high-flow oxygen and potentially hyperbaric oxygen therapy. Prevention emphasizes source identification and elimination, home CO detectors, and public education.

Uploaded by

Subash Paudeal
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PPTX, PDF, TXT or read online on Scribd
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Carbon Monoxide

Poisoning in Children
Overview:
• Introduction
• Pathophysiology
• Clinical presentation
• Diagnosis
• Treatment
• Prevention
Introduction:
• Carbon monoxide (CO) is a colorless, odorless, tasteless, and
highly poisonous gas produced during incomplete combustion
of any carbon-containing fuel.
• Although CO poisoning can be fatal to anyone, infants and
children have an increased susceptibility to its toxicity because
of their higher metabolic rates, higher oxygen utilization and
higher minute ventilation.
• Wood-burning stoves, kerosene heaters, old furnaces, hot-water
heaters, closed-space fires, and automobiles are the potential
sources of pediatric CO poisoning.
• CO is the most common gas involved in pediatric toxic
exposures.
Pathophysiology:
• CO binds to Hb with an affinity >200 times that of O2, forming
HbCO which displaces O2 that impairs its delivery and utilization
leading to tissue hypoxia.
• Beside that it binds to cytochrome oxidase disrupting cellular
respiration.
• In addition, it displaces NO from proteins allowing it to bind free
radicals and form toxic metabolite leading to lipid peroxidation
and cellular damage.
•  The average half-life of HbCO while a patient is breathing room
air is approximately 4 to 6 hours, while breathing high-flow
oxygen via a nonrebreathing face mask is about 90 minutes and
with 100 percent hyperbaric oxygen is approximately 30 minutes.
Clinical presentation:
• Mild intoxication – constitutional symptoms like headache,
malaise, nausea, vomiting and dizziness, and may be
misdiagnosed with acute viral syndromes or food poisoning.
• Moderate intoxication – change in mental status, confusion,
ataxia, syncope, tachycardia and tachypnea.
Clinical presentation:
• Severe intoxication – neurologic symptoms such as seizures or
coma; and cardiovascular and metabolic manifestations such
as myocardial ischemia, ventricular arrhythmias, MI,
pulmonary edema, profound lactic acidosis, cardiovascular
collapse, and potentially death.
• Delayed neuropsychiatric syndrome (DNS) – variable degrees
of cognitive deficits, personality changes, movement
disorders, and focal neurologic deficits; generally occur within
20 days of CO poisoning, and may persist for a year or longer.
Diagnosis:
• A compatible history and physical
examination
• An elevated HbCO level measured by CO-
oximetry of an arterial blood gas sample.
– Expected HbCO levels: non-smokers upto 5%,
smokers upto 10%.
• ECG, cardiac biomarker
• CT, MRI, and PET in the setting of DNS
Treatment:
• Prompt removal from the source of CO
• Maintaining Airway, Breathing and Circulation
• Institution of high-flow oxygen by face mask
• Hyperbaric oxygen therapy is recommended in following
circumstances:
– HbCO level >25 percent
– HbCO level >20 percent in pregnant patient
– Loss of consciousness
– Severe metabolic acidosis (pH <7.1)
– Evidence of end-organ ischemia (eg, ECG changes, chest pain, or
altered mental status)
Prevention:
• Source identification
and elimination
• Regular servicing of
heating systems
• Home CO detectors
• Public educational
initiatives
Thank you!

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