Occupational Lung Dz And Toxic Lung Injury Flashcards
What are the three effects of smoke inhalation
1) Impaired tissue oxygenation
2) Thermal injury to upper airway
3) Chemical injury to the lower airways and lung parenchyma
Describe Impaired tissue oxygenation 2/2 smoke inhalation injury
Carbon monoxide avidly binds with hemoglobin!
—Greater affinity than oxygen
S/S: severe headache or acutely altered mental status, seizures, coma, cherry red skin (rarely seen)
Tx: high flow O2 followed if needed by hyperbaric oxygen and supportive care
—100% NRB Mask:
—Despite the Pulse Ox reading 100%
What is the resting level of Carbon o oxide in smokers and non smokers
Nonsmokers may have up to 3 percent carboxyhemoglobin at baseline
smokers may have levels of 10 to 15 percent.
What effect does cyanide have in smoke inhalation injuries
Causes impaired Tissue Oxygentaion
Cyanide disrupts cell function and prevents tissue from taking up oxygen leading to lactic acidosis
S/s: Dyspnea, confusion, hypotension, headache, dizziness, syncope
Seizures, coma, cardiovascular collapse, death
Tx: cyanide antidote kit (Cyanokit®) and supportive care
What is the cyanide kit
Contains hydroxocobalamin
precursor to vitamin B-12
Binds to cyanide and neutralizes it
Eliminated harmlessly from the body through urination
ADE of RX: temporary discoloration of the skin and urine
Describe thermal injury with smoke inhalation
inhalation of hot gases injures mucosal surfaces
—Complications become evident w/in 18-24 hours
S/S: Mucosal edema, Upper airway obstruction ,increased secretions,
inspiratory stridor
—Respiratory failure possible
Tx: Humidifed O2, with suction PRN,
Elevated HOB 30*
Racemic Epi to reduce edema,
Order ABGS and monitor pulse ox
Intubation as necessary
Or Trach if unable to intubate
Describe chemical injury in smoke inhalation injury
from toxic gases & products of combustion
Early S/S: Bronchorrhea, bronchospasm with dyspnea, tachypnea & tachycardia
Late S/s: Labored breathing & cyanosis
+diffuse wheezing/rhonchi
Bronchial edema & sloughing leading to obstruction, atelectasis, and increasing hypoxemia
—ARDS possible in 1-2 days
—Pneumonia common 5-7 days after exposure
Tx: humidified O2, Bronchdilators, with suction of secretions,
Intubation as necessary with PEEP
Chest physical therapy
IVF and Fluid MGMT
Daily Sputum Gram Stains
Are Routine corticosteroids & antibiotics recommended for the tx of smoke inhalation chemical injury
Routine corticosteroids & antibiotics are ineffective & not recommended
Define bronchiolitis obliterans
A ground glass hazy opacities on CXR 2/2 to damage to the bronchioles
In a pt post fire with a markedly elevated lactate think
Cyanide
DO pts with burns typically have long term pulm problems ?
Patients who survive burns and recover generally do not have long-term pulm problems
May get impaired PFTs
—Reactive airway dysfunction syndrome
What is the Tx for Vaping Lung Injury
E-VALI
—E-cigarette or vaping associated lung disease
S/s:
Cough, fever, bilateral infiltrates
Vitamin E acetate – now removed
Reduced incidence of E-VALI
Treatment: supportive
These are a group of chronic fibrotic dz caused by inhalation of INORGANIC dusts
Usually asymptomatic with diffuse nodular opacites on CXR
Think
Coal works lung
Silicosis
Asbestosis
Pneumoconioses from inhalation of coal dust that leads to coal macules from alveolar macrophage ingestion
Leads to severer lung impairment and premature death
Think? CXR? tx?
Coal workers lung
CXR: diffuse 2-5mm opacities on CXR, prominent in upper lung fields
Tx: Supportive
Pneumoconioses from prolonged inhalation of free silica particle that leads to small rounded nodules in the lungs
2/2 Quartz, granite, sandstone
Quarries, mines, etc
Think? CXR? Tx?
Silicosis
CXR: Small rounded opacities throughout the lung
—Calcification of hilar lymph nodes (“eggshell” calcification)
-strongly suggests silicosis
Simple silicosis usually asymptomatic & normal PFTs
Complicated silicosis – conglomerates of irregular masses >1cm leading to large upper lung densities, dyspnea, obstructive & restrictive PFTs
Tx: supportive
Pts with silicosis are at an increased risk of what infection
TB!
Silica is cytotoxic to alveolar macrophages; pts with silicosis are at greatest risk of acquiring lung infections that involve macrophages as a primary defense
(TB, Atypical mycobacteria and fungi)
All silicosis pts should have tuberculin skin test & current CXR
This pneumoconioses presents with nodular interstitium fibrosis
Common to Shipyard & construction workers, pipe fitters, insulators
—10-20 years of exposure
S/s : progressive dyspnea, inspiratory crackles; sometimes clubbing, cyanosis
THink? CXR? Tx?
Asbestosis
CXR: Linear streaking at lower lung fields
Opacities of various shapes/sizes
—Honeycomb changes – advanced disease
—Pleural calcifications may be best diagnostic clue
DX: High rest CT
—Parenchymal fibrosis & coexisting pleural plaques
Tx: supportive
O2 for SOB
Resp. physiotherapy to remove secretions
What pattern of pct will pts with asbestosis Present with
Restrictive dysfunction
Reduced FVC & FEV1
Normal or elevated FEV1/FVC ratio
Reduced DLCO
(Diffusing capacity for carbon monoxide)
This is an inflammatory D/o of the lung involving the alveolar walls and terminal airways
Induced by exposure to ORGANIC agents that leads to an acute illness
(Avian droppings, microorganisms, avian proteins, fungi, mold)
S/s acute: Sudden malaise, chills, fever, cough, dyspnea, nausea, onset after leaving work/ at night .
Subacute: Insidious onset (weeks to months) of chronic cough, slowly progressive dyspnea, anorexia, wt loss
Chronic: progressive respiratory insufficiency & fibrosis
THink? CXR? Tx?
Hypersensitivity Pneumonitis
CXR acute: small nodular densities, sparing apices & bases
Chronic: pulmonary fibrosis and honeycombing
Dx: increased WBCs with neutrophilia, elevated ESR, CRP
PFTs: restrictive dysfunction & reduced DLCO
Lung Bx may be necessary for chronic
Tx: Identification of offending agent & avoidance of further exposure
Severe/protracted cases: oral corticosteroids in long (4-6 week) followed by long taper (3 months)
This D/o presents like asthma but recovers when away from work
Think? Dx? Tx?
Occupational Asthma
Can develop weeks to years after exposure
Dx: Spirometry before & after exposure
Peak flow measurements in the workplace
Tx: bronchodilator’s and Pulm consult
Chronic bronchitis is commonly seen in what professions
Coal miners
Exposures to Cotton, flax & hemp dust
Which is worse occupational or non occcupations COPD
Occupational
This is an asthma like d/o in textile workers from inhalation of cotton dust
S/s Chest tightness, cough, dyspnea characteristically worse on Monday (or the first day back to work)
Think?
Byssinosis
This is an acute toxic pulmonary edema caused by inhalation of nitrogen dioxide from recently filled silos
Think? Tx? And progression?
Silo filers Disease
Tx: early cortiosteroids
Progresssion to bronchilitis obliterans and death
This is from chronic inhalation of diacetyl that leads to bronchilitis obliterans
popcorn lung
Describe what happens if you acutely aspirate gastic contents
Pure gastric acid (pH<2.5) leads to extensive desquamation of bronchial epithelium, bronchiolitis, hemorrhage, pulmonary edema
This is one of the most common causes of ARDS
S/s Cough, wheeze, fever even in the absence of infection, tachypnea, crackles at the bases
With early hypoxemia and leukocytosis
CXR: patchy alveolar opacities in dependent lung fields
What is the Tx for Acute aspiration of gastric contents
O2
Airway MGMT
Possible intubation and mech vent
MGMT with IVF
No need to prophylaxis with ABX
What are the complications of chronic aspiration of gastric contents
Achalasia
Esophageal stricture
Systemic sclerosis (scleroderma)
Esophageal carcinoma
Esophagitis
Gastroesophageal reflux Dz (GERD)
Relaxation of LES (lower esophageal sphincter) – esp at night
What effect does Cigarette smoking, etoh, caffeine, theophylline have on the lower esophageal sphincter?
Relaxes it leading to chronic aspiration of gastric content
What is the tx for Hydrocarbon pneumonitis–caused by aspiration of ingested petroleum distillates
Tx: supportive, protect lungs from repeated aspiration
Cuffed endotracheal tube if necessary
What is the onset, S/s, PFT, CXR and Tx for Radiation pneumonitis
Onset is 2-3 months after rads exposure
PFT: reduced lung volume/lung compliance, diffusing capacity
S/S: Insidious onset of dyspnea, intractable dry cough, chest fullness/pain, weakness, fever
CXR: alveolar or nodular opacities limited to irradiated area
Tx: prednisone
This fibrosis is common in pts after a full treatment for lung or breast cancer
Presents with slow progressive dyspnea
Think?
CXR?
Tx?
Pulm Radiation Fibrosis
CXR: tented diaphragms, obliteration of normal lung markings, reduced lung volumes, reticular and dense opacities
TX; corticosteroids x2-3wk with taper
What is the onset of O2 Toxicity
It appears to occur with exposure to Fio2of 50 to 60% after exposures as short as 6 hours in duration
A pt is receiving blood products and within minutes goes into respiratory distress with a PaO2 less than 60 and a PaCO greater than 45 with tachypnea and tachycardia
What happened? What should we do ? What would you see on CXR ?
TRALI
This is indistinguishable from ARDS
Ts: STOP THE TRANSFUSION
Supportive care and O2 with IVF and pressure support ventilations
(Recovery in 2-5 days)
A climber gets a headache and malaise at 7,000 feet
What is this called
Acute mountain sickness
A native of the mountains gets headache, fatigue, dyspnea, and indigestion at 10,000 feet
What is this called
Chronic mountain sickness
At 950o feet a climber gets dyspnea, cough and tachycardia
What is this called
High altitude pulm edema
A climber at 15000 feet gets vision changes
What is this callled
High alt retinal hemorrhage
At 15,000 feet a pt gets confusion ataxia, hallucinations, and a coma
This is called
HACE
What is the prevention and treatment for High Altidue injuries
Prevention: gradual ascent, acclimatization, meds (acetazolamide)
TX: immediate descent, O2/hyperbaric chamber,
—If mild: sildenafil, acetazolamide, theophylline SR, NSAIDS, Tylenol, aspirin
