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Irritants and Noncardiogenic Pulmonary Edema

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Genna Carlin

on 19 June 2014

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Transcript of Irritants and Noncardiogenic Pulmonary Edema

Irritants and Noncardiogenic Pulmonary Edema
Pulmonary Irritants and Insults
Interstitial Lung disease
Chronic Fibrotic changes
Caused by inhalation and deposition of inorganic particles and subsequent reaction of the lungs
Coal Workers Pneumoconiosis
Noncardiogenic Pulmonary Edema
AKA: Acute Respitory Distress Syndrome and Acute Lung Injury

Cardiogenic vs

Clinically-presence of radiographic evidence of alveolar fluid accumulation without evidence to suggest cardiogenic etiology

ARDS-Diffuse lung injury that is a secondary complication of another primary disease
Mainly Supportive - goal is to ensure adequate ventilation and oxygenation
ALI-may respond to non-invasive ventilation techniques
ARDS-intubation and ventilation often needed.
Alveoli fluid filled/collapsed
Lung compliance decreased
Decrease tidal volume
PEEP to maximize oxygenation without causing barotrauma

Usually asymptomatic
Can have:
Cough, Dyspnea, hypoxia/cyanosis
Imbalance in Starling Forces
Diffuse alveolar damage with marked increased permebilityof alveolar -capillary membrane and accumulation of protein rich fluids in the alveoli
Direct Injury

Diffuse Pulmonary Infection
Inhalation injuries
Pulmonary contusion

Indirect Injury
Sepsis and Septic Shock
Multisystem trauma
Transfusion Reactoin
Drug Overdose
Neurogenic Insults
Cardiopulmonary Bypass
Fat Emboli

Drug Overdose
Inhaled Toxins
Nitrous Oxide
ED Presentation
Shortness of Breath
Respiratory distress - Respiratory Failure
Tachypnea and dyspnea
Often within a few hours from inciting event-May be days
Decreased oxygen saturation on pulse ox/ABG
Unresponsive to oxygen
PaO2 <50 with FiO2 >50%
Decreased Lung Compliance
Lack of evidence for cardiogenic source
Etiologies-direct and indirect damage
Drugs and inhaled Toxins
These patient's are hypoxic, they're sick....
Remember this is usually secondary to another process. and labs/test will be related to suspected cause
ie cbc, BMP, blood cultures...
Pulmonary capillary wedge pressure-normal
Need to distinguish from cardiogenic pulmonary edema-EKG, Troponin, BNP
Tintinalli's Emergency Medicine
Rosen's Emergency Medicin
Harwood and Nuss
Hippo EM
"Noncardiogenci pulmonary edema" Emergency Medicine Clinics of North America
Up to Date
5 Minute Emergency Medicine

Toxic Gases, Fumes and Vapors-Respiratory Toxins
Simple Asphyxiants
Irritant gases that Interrupt Pulmonary Diffusion
Summary Tables
Create an oxygen poor environment

Examples: CO2, H, N, Methane, butane, propane
Gases build up in an enclosed space-decrease FiO2 (not good)
FiO2 <16 %- air hunger, tachypnea, dec level of consciousness
FiO2 <10%-LOC, Seizures, Vomiting.
Remove agent-correction of event that led to exposure
Restore higher FiO2 with supplemental oxygen.

These interfere with 1 (or more) of the four phases of oxygen delivery
1. Asphyxiants -displace oxygen
2. Interruption of pulmonary Diffusion -(vapors)
3. Agents that interrupt oxygen transport
4. Agents that interfere with Cellular oxygen utilization
Respiratory Toxins
gases, aerosoles, fumes or dusts that are inhaled
How toxic??
duration of exposure
enclosed space??
Pt factors
Metabolic rate
underlying reactive air way disease
Hx of smoking
Highly water Soluble - Ammonia
React with water in the upper respiratory tract-immediate irritation and discomfort
Ammonia-very common
Colorless, alkaline, corrosive gas with a pungent odor
gas reacts with water to form ammonium hydroxide
Immediate sxs-mucous membrane, eye and throat irritation
Lower airway-bronchospasm, pulmonary edema, and residual reactive airway disease.
Intermediate water solubility-Chlorine
Extremely common
Dense-yellow-green gas with acrid,pungent odor
When recombines with moisture forms Hydrochloric and hydrochlorous acids
Immediate ocular and upper airway irritation-with nausea and vomiting
Significant exposures-coughing, hoarseness and pulmonary edema. (ARDS)
Low solubility-Phosgene and Nitrogen Oxides
Minimal irritation to upper airways
Instead particles settle in lower airways and cause delayed injury to alveoli
Phosgene-hydrolyzes to CO2 and hydrochloric acid
Nitrogen oxides-triphasic illness
initial dyspnea and flulike illness
transient improvement
then worsening dyspnea-heralds pulmonary edema
Evaluation and Treatment
Removal agent
Humidified oxygen and inhaled bronchodilators for bronchospasms
Inspect the upper airway
evaluate for respiratory distress (stridor, hoarseness, dysphagia, cough, tachypnea, retractions, accessory muscle use, wheezing, cyanosis)
Potiential for rapid deteropration-low threshold for intubation
Mainly supportive care
Toxic effects of gases, fumes and vapors
Caused by inhalation and deposition of coal dust
Induce formation of coal macules in the alveoli
Characteristic findings-pigment and reticulin fibers accumulate in peribronchiolar location-large amorphous black masses +/- liquative centers
CXR-small opacities in upper lung fields
Most common pxeumoconiosis in US-occupations at risk-mining, quarrying, drilling, and sandblasting
Inhalation of crystalline silica-quartz, granite or sandstone
Must be less that 5 micrometers to reach alveoli
phagocytized by macrophages that then decay
Extrusion of lysosomal enzymes perpetuates the damage of free silica particles
Visible lung dx may continue to worsen even after cessation of exposure.

numerous sharply marginated small round opacities
CT-bilateral, symmetric, centrilobular and perilymphatic nodules with sharp margins
confluence of nodules-large opacities >1mm
Hilar Lymph node enlargement and calcification can occur
Higher risk for TB
CXR: Small round opacities throughout the lung: Calcified hilar nodules
Naturally occuring fibrous magnesium sillicate-formally uses in a variety of building materials.
Occupational and non-occupational exposure
Two types of fibers
Variety of pleural dxs-Pleural plaques, diffuse pleural thickening, benign asbestos pleural effusions and malignant mesothelioma
CXR-Thickened Pleura, interstitial fibrosis, calcified plaques on lateral chest wall/diaphragm
Diagnosis/ Treatment
Positive exposure history and suggestive CXR
Treatment -Supportive
Oxygen, vaccination
Smoking cessation
+/- Steroids
Indirect mechanisms
1. Initiation phase-precipitating event causing a variety of mediators and cytokines
2. Amplification phase-Neutrophils activated and sequestered in the lung
3. Injury phase-sequestered cells release reactive oxygen metabolites causing damage
Core Content-Genna L. Carlin, MD
Owen Lander, MD
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