1 inhalational injury: pathophysiology, diagnosis, treatmentoer.unimed.edu.ng/lecture...
TRANSCRIPT
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At the end of this lecture you should be able to:
• Describe the physiology of the respiration ofthe patient with inhalation injury.
• Describe how to perform a respiratoryassessment on the patient with inhalationinjury.
• Appreciate the importance of airwaymanagement in the patients with InhalationInjury.
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Causes of inhalation injury:• Noxious asphyxiant gases released during thermal
decomposition include carbon monoxide (CO) andhydrogen cyanide.
• Other byproducts produced by combustion of furnitureand cotton (aldehydes) or rubber and plastics (chlorinegas, ammonia, hydrocarbons, various acids, ketones)produce injury.
• Heat generated during combustion can cause significantthermal injury to the upper airway.
• Particulate matter produced during combustion (soot)can mechanically clog and irritate the airways, causingreflex bronchoconstriction.
• Exposure to metal fumes and fluorocarbons, systemictoxins typically released during industrial fires
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Pathophysiology
• Cell injury and pulmonary parenchymaldamage by irritants
• Hypoxemia by interruption of oxygendelivery by asphyxiants
• End organ damage by absorption ofsystemic toxins through the respiratorytract.
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Type Inhalant Source Injury/Mechanism
Irritantgases
AmmoniaFertilizer, refrigerant,manufacturing of dyes,plastics, nylon
Upper airwayepithelial damage
ChlorineBleaching agent, sewageand water disinfectant,cleansing products
Lower airwayepithelial damage
Sulfur dioxide Combustion of coal, oil,cooking fuel, smelting
Upper airwayepithelial damage
Nitrogendioxide
Combustion of diesel,welding, manufacturing ofdyes, lacquers, wall paper
Terminal airwayepithelial damage
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Asphyxiants
Carbonmonoxide*
Combustion ofweeds, coal, gas,heaters
Competes for oxygen siteson hemoglobin, myoglobin,heme-containingintracellular proteins
Hydrogencyanide†
Burning ofpolyurethane,nitrocellulose (silk,nylon, wool)
Tissue asphyxiation byinhibiting intracellularcytochrome oxidase activity,inhibits ATP production,leads to cellular anoxia
Hydrogensulfide‡
Sewage treatmentfacility, volcanicgases, coal mines,natural hot springs
Similar to cyanide, tissueasphyxiant by inhibition ofcytochrome oxidase, leadsto disruption of electrontransport chain, results inanaerobic metabolism
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Systemictoxins
Hydrocarbons
Inhalant abuse(toluene, benzene,Freon); aerosols;glue; gasoline; nailpolish remover;typewriter correctionfluid; ingestion ofpetroleum solvents,kerosene, liquidpolishes
CNS narcosis,anesthetic states, diffuseGI symptoms, peripheralneuropathy withweakness, coma,sudden death, chemicalpneumonitis, CNSabnormalities, GIirritation,cardiomyopathy, renaltoxicity
OrganoPhosphates
Insecticides, nervegases
Blocksacetylcholinesterase,cholinergic crisis withincreased acetylcholine
Metal fumesMetal oxides of zinc,copper, magnesium,jewelry making
Flulike symptoms, fever,myalgia, weakness
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Pathophysiology
• Cell injury and pulmonary parenchymaldamage by irritants
• Hypoxemia by interruption of oxygendelivery by asphyxiants
• End organ damage by absorption ofsystemic toxins through the respiratorytract.
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Cell injury and pulmonary parenchymaldamage
• Thermal or chemical damage to the epithelialsurfaces of the intrathoracic and extrathoracicairways lead to respiratory embarrassment .
• Secondary insult with bacterial pneumonia mayoccur days after inhalation, causing furthercytotoxic damage. Ciliary function is impaired,leading to accumulation of airway debris. Theinflammatory cascade initiates neutrophilinfiltration.
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Hypoxemia :
• a decrease in inspired oxygenconcentration at the scene of injury,
• a mechanical inability to exchange gasbecause of airway obstruction orparenchymal pulmonary disease,
• inhibition of oxygen delivery and tissueuse by toxins.
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Symptoms
• Inhalation injury does not always cause noticeable symptomsinitially.
• All burn victims must be watched carefully for inhalationinjuries.
• Inhalation injury should be suspected in anyone trapped in abuilding fire or who has lost consciousness during a fire orwhen there is heavy smoke.
• Victims may have a cough, hoarse voice, or sore throat.
• If the injury involves the lower part of the respiratory tract, thenthey may have chest discomfort or pain or difficulty breathing.
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• Between 0 and 10% is not dangerous.• Heavy smokers commonly have levels
approaching 10%.• Between 10 and 20% a person may
experience nausea and a poundingheadache.
• Drowsiness and an overall feeling ofweakness occur at levels between 20 and30%.
• Above 30%, confusion and agitation arecommon.
• Over 40% causes coma and death occursat levels above 50%.
Symptoms (in relation to CO level)
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Signs
• Dyspnoea• Facial or neck burns• Singed hair of the eyebrows or in the
nose• Oral mucosal hyperaemia and ulceration• Wheezing• Sputum that is black or sooty.
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Clinical indications for intubation
absolute: relative:
• Burn of the palate,tongue and pharynx
• Oedema of theposterior pharynx andupper glottis
• Burn of vocal cords
• Hoarseness• Facial burn• Sooty sputum
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Diagnosis
• Clinical• Bronchoscopic• Blood gas assessment.• Xenon 133 lung scan• Pulmonary function studies
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pH 7.25–7.45
PaO2 55–80 mmHg or SaO2 of 88–95%
PaCO2 35–55 mmHg(permissive hypercapnia can be used if pH 7.25)
Targeted arterial blood gas goals
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Management
• Airway issues and early intubation• Bronchial hygiene therapy• Chest physiotherapy• Early ambulation• Airway suctioning• Pharmacological adjuncts
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•Titrate humidified oxygen to maintain SaO2s’ > 90%
•Cough, deep breath exercises every 2 h
•Turn patient side to side every 2 h
•Chest physiotherapy every 4 h
•Aerosolize 3 cc’s of 20% N-acetylcysteine every 4 h with abronchodilator
•Alternate aerosolizing 5000 units of Heparin with 3 cc’s ofnormal saline every 4 h
•Nasotracheal suctioning as needed
•Early ambulation Sputum cultures for intubated patients
A management protocol