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100 Cards in this Set

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Community aquired acute Typical:
Streptococcus Pneumoniae

Haemophilus influenza
Community aquired acute Atypical:
Legionelle pneumophila
Chlamydia pneumoniae
Mycoplasma pneumoniae
various viruses
Community aquired chronic:
Mycobacterium tuberculosis (everywhere)

Histoplasma capsulatum
Nursing home aquired:
Mixed aerobic and anaerobic oral flora

Staph aureus, Enteric bacilli Influenze, Mycobacterium tuberculosis
Immunocompromised pts could succumb to:
Pneumocystis carinni
CMV
Aspergillus species
Cryptococcus neoformans
Re-activation of tuberculosis or histoplasmosis
Nosocomial infections: Aspiration:
Mixed aerobic and anaerobic species
Enteric (Gram negetive usually)
S. aureus
Nosocomial VAPs
Pseudomonas aeruginosa
Acinetobacter species
Enterobacter species
Klebsiella
Spaph. aureus
Moraxella catarrhalis
Acute onset of fever suggests:
Bacterial involvement
Pleuritic chest pain with pneumonia suggests
Possible pleural friction rub
Exudate is typically ____
cloudy (due to protein) usually infection
Transudates _____
Clear fluid, caused by too much hydrostatic pressure. (CHF)
Streptococcal Pneumonia
Gram: +ve
bacterial spheres in singles or small chains
Transmission: Aerosol—cough---sneeze
Tx: Most strains are sensitive to penicillin, amoxicillin, erythromycin, cephalosporins, clindamycin, vancomycin
Comments: Accounts for over 80 % of bacterial pneumonias. They are enclosed in a sugar jacket (polysaccharide) which accounts for their virulence. Serotype 3 is the worst of over 80 strains.
Often follows a viral URT infection.
Staphylococcal Pneumonia
Gram: +ve
Transmission: Aerosol—cough etc. also on surfaces; floors bedding etc. (fomites) often after a viral infection.
Origin: Normal flora on/in humans
Tx: Cloxacillin, clindamycin, Gentamicin, more frequently seen nafcillin resistant varieties require vancomycin (Pulm. Fibrosis ), rifampin etc.
Comments: S. aureus is most virulent; S. epidermidis is normal flora of skin etc---often nosocomial---‘Super Infection’ after viral insult—empyema, cavitation, abscess.
Klebsiella; (Friedländer's)
bacterial rods singly or in chains
Transmission: Can be aerosol but more likely contact, surfaces, food, health workers hands.
Origin: Fecal/oral route. Normal flora of GI tract. Aerosol.
Tx: 3rd generation cephalosporins (ceftazidime), gentamicin, tobramycin, ticarcillin, clavulanate.
Comments: diabetics and alcoholics---sudden onset---hemoptysis---significant mortality---often nosocomial--- often leads to septicemia
Name: Pseudomonas aeruginosa
Gram: -ve
Type: bacterial rods in singles or chains
Type: bacterial rods in singles or chains
Type: bacterial rods in singles or chains
Type: bacterial rods in singles or chains
Transmission: aerosol or freshly contaminated surfaces.
Origin: normal GI flora
Tx: aminoglycosides (gent & tobra), broad spectrums like amoxicillin, 3rd generation cephalosporins (ceftazidime), imipenem, aztreonam, etc.
Comments: ICU, or other immuno-compromised Pt.---copious purulent, greenish, sweet smelling sputum, high fever, rigors, abscesses---36 to 80 % mortality rate---often nosocomial with respiratory equipment often cultured.---many aqueous soln’s will culture.
Name: Haemophilus Influenza
Gram: - ve
Type: very small bacilli, 6 types, “B” often pathogenic
Transmission: aerosol and recently contaminated surfaces
Origin: Aerosol, contaminated surfaces (very sensitive to cold) will not live long outside the body.
Tx: Ampicillin, clavulanate, 2nd & 3rd gen. cephalosporins, chloramphenicol, streptomycin, erythromycin, tetracycline
Comments: Often secondary to a viral infection. Commonly seen in small children where it causes acute epiglottitis. COPD pts, alcoholics; presents with low level cough, fever growing to dyspnea, purulent sputum and patchy infiltrates on X-ray. 30% mortality rate with severe infection.
Mycoplasmas
“A genus of highly pleomorphic, gram negative, aerobic to (non-obligatory) anaerobic microorganisms that lack true cell walls.”
Mycoplasma pneumoniae causes primary atypical pneumonia.
Others include M. mycoides, M. hominis may cause pleuro-pneumonia, common in cattle.
Tx include; clarithromycin, tetracycline
Viruses
Viruses have protein spikes on their surface which can match receptor sites on specific cells. These spikes can facilitate penetration of the usually intact cell membranes and allow the virus to either inject RNA or the entire viral packet into the cell.

Once inside the cell the viral RNA will force copies of itself to be made. Viruses will often kill the host cell by using up all the cells’ nutrients and proteins and initiating over production of RNA packets, eventually bursting the cell membranes.
Name: Influenza Pneumonia
Viral
Type: A & B cause most of cases of viral pneumonia
Transmission: aerosol droplets
Origin: Human carriers, horses, swine, birds
Tx: Supportive measures only, time limited (3-5 days)
Comments: All are mutable (especially A), therefore will return to the pop. with slightly different configuration and start a new epidemic.
Complications include con-commitant bacterial infection.
Criteria for Severe Designation Pneumonia
Any one of the following may indicate severe;
RR over 30 at rest (adult)
PaO2 less than 60 on 30% or more oxygen.
Multiple lobe involvement.
Shocky; Low BP, systolic--under 90, dia--under 60.
Low urine output---less than 20 ml / hr.
Dry Drownling
Dry- Drowning is where the URT and glottis spasms enough to prevent significant water from entering the lungs. (10 to 15%)
Wet Drowning
Wet- Drowning is when large amounts of water enter the lungs. (85 to 90%) Could be sea water (hyper-tonic) or fresh water.
Near drowning prognosis via Orlowski Scale
Unfavorable Prognosis Factors:
Age  3 years.
Submersion of greater than 5 minutes.
No resuscitation on scene.
Patient comatose on arrival to ER.
ABGs---pH  7.10
2 or less, 90 % chance of positive outcome.
3 or more, 95 % chance of a negative outcome, (death or survival with permanent neurological deficit).
what is Gastric Aspiration?
One of many types of chemical pneumonitis; caused by aspiration of gastric contents into lung parenchyma.
Gastric contents typically have a very low pH. (2.5) Food stuffs will have fatty acids and oils that can foster bacterial growth. (multiple GI pathogens)
Often a delayed onset (12 hours or more), of symptoms as inflammatory process continues.
Risk for Gastric Aspiration
More often seen in patients with diminished gag reflex due to ETOH abuse, drug overdose, sedatives, stroke, neuro-muscular disease or any other condition that causes poor airway guarding.
Conditions that cause high intra-gastric pressures will also increase risk. Eg. double pregnancy, morbidly obese pt., supine position.
Substance abuse
Sedation or anesthesia
Seizure disorders
CVAs, MI
Myasthenia Gravis, Guillain Barré, ALS
T-E fistula, pregnancy
Trauma, near drowning
Gastric Aspiration Pathology?
Original insult,
Inflammation of receiving tissue (deposition dynamics),
Laryngospasm, bronchospasm, ciliary function,
Increased A/C membrane permeability,
Hemorrhagic exudate in alveolar fields,
 surfactant efficacy,  compliance,
More edema, more atelectasis, more hypoxic metabolism,
Progression to ARDS.
Gastric Aspiration Severity?
R lower lobe is most likely.
The severity of the insult depends on the pH, the size and quantity of particles, the presence of bacteria and the general lung health of the individual.
Gastric contents are often oils and carbohydrates that foster micro-organism growth.
If left untreated, may very well lead to ARDS.
inhalation of this toxic gas kills quickly. Stops 02 from entering cells.
Hydrogen Cyanide—polyurethanes
Inhalation of toxic gas Clinical Manifestations
Entirely dependant on agent and level of exposure.
Irritation of the eyes, nose, throat, URT and lung fields--- “Burning” sensation often reported.
Cough, hemoptysis, wheezing, dyspnea.
Hypoxemia.
Inhalation of toxic gas Laboratory Findings
PFTs; If severe enough can reduce DLco
ABGs;
Early: pH, PaCo2, PaO2, HCO3
Late: pH, PaCO2, PaO2, HCO3
Chest X-ray;
AP view will be normal at first, if severe enough
the picture will change to edema, infiltrates,
opacities, ARDS.
02 toxicity Etiology:
Requires prolonged exposure to FiO2’s of over 0.6, although some injury can result from lower concentrations.
This is much easier to achieve in intubated patients.
Pre-mature neonates have a further risk of Retrolental fibroplasia, “Retinopathy of Prematurity”.
Increased susceptibility: Advanced age, catecholamines, Bleomycin, steroids, hyperthermia, hyperthyroidism, premature birth, vitamin E or protein deficiency.
Decreased susceptibility : Youth, adrenalectomy, hypothermia, prior lung damage, anti-oxidants (glutathione, Vitamin C, E).
Etiology cont’
Exposure to 100% O2 can cause changes in a relatively short time.
0-12 hrs.---Tracheo-bronchitis, sub-sternal pain.
12-24 hrs.--- Vital Capacity.
24-30 hrs.--- lung compliance, A-a d O2,  exercise tolerance.
30-72 hrs.---Further decreased DLco
Changes can happen much more rapidly under hyper-baric conditions. (CNS injury)
02 toxicity Clinical Manifestations:
Resembles broncho-pneumonia picture.
Early: Retro-sternal chest pain, restlessness, cough, fatigue, dyspnea, emesis.
Late: Cyanosis, frothy sputum, WOB, respiratory failure.
Oxygen induced hypo-ventilation—hypoxic drive.
Depression of cilia may lead to mucous plugging.
Absorption atelectasis; areas of hypo-resonance (or dullness) can be found on careful percussive examination and auscultation.
Hyperbaric O2 can be neurotoxic: Diaphoresis, pallor, convulsions, coma…etc.
Pulmonary contusion and edema Pathophysiology
Pulmonary contusion and edema:
Blunt trauma—hemorrhage and edema under the site of impact, edema and bleeding cause the age old picture of inflammation, consolidation, atelectasis, decreased lung compliance, WOB etc.
This condition can be worsened by over zealous fluid resuscitation.
Pulmonary Hemorrhage:
Piercing chest wound has a slightly different picture than blunt chest trauma.
Sharp object wound will tear apart parenchyma and vasculature, leading to severe bleeding into lung fields.
Asphyxiation and death can occur quickly.
“ Death by drowning”
Pulmonary contusion Laboratory Findings
PFTs’---restrictive picture
ABGs’ Mild: pH, PaCO2, PaO2, HCO3 Severe:  pH, PaCO2, PaO2, HCO3
Blood Sampling--- RBCs’, Hgb, HCT
X-ray:
Contusion--- local infiltrates, atelectasis.
Hemorrhage---Blunting of costo-phrenic angle, depressed diaphragm(s), mediastinal shift, large fluid spaces, pneumo-thorax, atelectasis.
ARDS AKA
Also called:
Shock Lung White Lung
Acute Alveolar Failure Wet Lung
Da Nang Lung---Capillary Leak Syndrome
Adult Hyaline Membrane Disease
ARDS Prognosis
However caused, it can quickly lead to multi-system organ failure; respiratory—cardiac—renal—hepatic—G.I.—CNS.
Mortality is very high, ranging from 50 to 70% of patients diagnosed.
Recent study of 361 ICU’s---50%
High in at risk groups like COPD.
ARDS Etiology
O2 Toxicity ^ICP
Prolonged bypass surgery CHF
DIC Drug Overdose
Emboli Fluid overload
Toxic gas / irritant Infection/ inflammation
Blood Transfusions Trauma
Shock (hypo-volemia) Pulmonary Ischemia
Radiation injury Sepsis
Burns Uremia
Pneumonia Aspiration
3 Phases of ARDS
Exudative Phase 1: Days 1 – 3 to 7 or more

Proliferative Phase 2: Days 3 to 7+

Fibrotic Phase 3: 7 to 14+ days
ARDS Exudative Phase
Capillary endothelial cell swelling, widening of the intracellular junctions, Type II cell damage, surfactant dysfunction. Compliance, WOB.
Pulm. vascular engorgement, capillary permeability, ensuing alveolar edema allows proteins and debris to enter alveoli.
Interstitial edema, hemorrhage, consolidation. A/C width. Pulmonary emboli (PAP).
Potential hyaline membrane formation:
Fibrin, cellular debris, eosinophils.
On autopsy: lungs are red, heavy with fluid, blood.
ARDS Proliferative Phase
Regeneration of type II alveolar cells.
Macrophages ‘eat’ exudate and debris.
Fibrin deposition begins.
Still very stiff lung, compliance, WOB, PAP.
On autopsy, lungs are pale and gray at this point. Large quantities of leukocytes, neutrophils, macrophages etc.
ARDS Fibrotic Phase
Fibrin deposition continues.
Fibroblasts lay down collagenous tissue, alveolar septa thicken.
Obliteration of micro-vasculature and increased arteriolar musculature may cause permanent pulmonary hypertension.
The degree of fibrosis is highly variable.
ARDS xray stages:
Stage 1: Can be normal to pneumonia like

Stage 2: Bi-lateral, fluffy interstitial and alveolar infiltrates, “WHITE-OUT”, indicative of ARDS. Heart size is normal--- differentiates ARDS from cardiogenic pulmonary edema

Stage 3: Alveolar clearing happens first, then interstitial. Emphysema may occur.
Neoplasm Etiology
Smoking, Asbestos, chromium, nickel, uranium, vinyl chloride, bis(chloromethyl)ether, decay products of radon gas, ionizing radiation, certain fibers and chemical fumes increase risk.
Exposure to more than one agent will stack the risk level: Eg. Chronic asbestos inhalation and smoking yields a 92 fold increase in risk of lung cancer
Types of Bronchogenic carcinoma:
Squamous Cell Carcinoma
Small (Oat) Cell Carcinoma
Adeno-Carcinoma
Large Cell Carcinoma
Squamous Cell Carcinoma
Most common –30-50%.
Basal epithelial cells grow through the airway walls and invade other tissue.
Easily metastasizes, and can double in size in 100 days.
X-ray or bronchoscopy reveals hilar mass, some nodes in periphery of lung.
Cavitation in 20-30% of cases
Small Cell or Oat Cell Carcinoma
20-30% of cases.
Arises from ‘K’ cells in bronchial epithelium.
Tumor cells are oval (oat) shaped and can double in 30 days.
Metastasizes quickly, frequently, fatally.
Adenocarcinoma
15-35% of cases
Originates from (often peripheral) mucous cells.
Doubles in 180 days.
Cavitation is common.
Large Cell Carcinoma
10-35% of cases
Can begin in central or peripheral areas.
Spreads rapidly, grows quickly.
Can double in 100 days.
Cavitation is common.
Carcinoma table
Fungal infections, Histoplasmosis
Latent asymptomatic---lesions heal on their own, may leave some scar tissue.
Self-limiting primary histoplasmosis---pneumonia like, muscle and joint pain, hives and subQ nodules may appear, single or multiple lesions appear on chest x-ray.
Chronic Histoplasmosis---marked by cavitations usually in the upper lobes of smokers, often progressive, resembles TB.
Disseminated histoplasmosis---Pts are the very young or old, and immuno-compromised. Hepatomegaly, anemia, thrombocytopenia, leukopenia, ulcerations, abdominal pain-----meningitis.
Fungal infections, Coccidioidomycosis
Coccidioidomycosis immitis: 80% of the POP in hot dry areas of the US southwest may test positive.
Wind borne spores are ubiquitous in these regions.
Most pts are asymptomatic---some cases will progress to an acute self-limiting pulmonary infection---fewer still may become disseminated to other organ systems.
Meningitis cases are rare but potentially fatal.
Fungal infections, Blastomycosis
Blastomycosis dermatitidis: Western hemisphere, Africa & the Middle East.
Inhaled spores may cause fever, cough, myalgia, pleuritic pain.
Abscesses may form in the lung, sputum is copious and purulent.
ILD Simplified Classification System --- ILDs
ILD: Hyper-sensitivity Pneumonitis
Allergic response to some inhaled particulate.
“Extrinsic allergic alveolitis”.
Dusts, pollens, particulate matter, animal dander, spores, chemicals etc. Generally organic material.
Diagnosis is via open lung biopsy, skin testing and history.
Air Conditioners’ Lung---fungi from A/C units
Aspergillosis---from indigenous soil fungi
Bagassosis—from moldy sugar cane waste
Bird Breeders’ Lung—protein from bird guano
Farmers’ Lung---moldy hay (Thermoactinomyces vulgaris)
Mushroom Workers’---T. vulgaris
ETC.
ILD: Inorganic Dusts (Usually occupational)
Silica (Silicosis)
Sand like tiny particles from sand blasting, grinding, tunneling, foundries.
Increased risk of cancer and active TB
Coal dust, etc. (Coalminers Pneumoconiosis)
Similar picture to Silicosis
Once a major problem in England, now perhaps increasing in China etc.
Asbestos (picture next slide)
Calcified pleural plaques, restrictive picture.
Malignant Mesothelioma; cancer of pleural surfaces.
ILD: Drugs as Triggers
Many chemo-therapy drugs cause ILD, many patients will eventually die from the ILD vs the CA itself.
Nitrofurantoin, Bleomycin and other antibiotics are known causes.
Anti-arthritis drugs like Aspirin, Gold and penicillamine have been proven to cause ILD.
Amiodarone, a long acting, potent anti-dysrhythmic drug given for serious dysrhymias that don’t respond to other drugs has shown up to 18% involvement.
Illicit drugs like heroin & methadone may cause ILD and are often ‘cut’ with talc which may contribute as well.
ILD: Oxygen
Oxygen toxicity and the resultant ILD may take days to present with high FiO2s, much shorter in HBOT situations.
After 48 hours in 100% O2, pulmonary edema develops and an ARDS like picture will develop.
Review PiO2, A-a dO2 calculations
Pt. on a 70% Cold Neb in the Rockyview Hospital.
PaO2 measured at 112 mmHg, PaCO2 = 66 mmHg
PiO2 = ?
A-a dO2 = ?
ILD: Radiation
Treatment for thoracic or abdominal CA often includes weeks of radiation therapy.
“… doses in excess of 6000 rads over 6 weeks almost always cause ILD in and near the radiated site.” des Jardin 5th, pg 385
Acute pneumonitis, non-acute, or latent deposition of significant fibrosis.
Often associated with pleural effusions.
ILD: Sarcoidosis (Sarcoid = Flesh-like)
Idiopathic, progressive, multi-system.
The most common ILD in America.
Usually effects lung or lymph tissue.
Produces granulomas often in hilar regions.
Seen on CXR as increased density nodules.
ILD: Collagen / Vascular Diseases
Connective tissue disorders generally are multisystem inflammatory diseases where fibrosis deposition occurs in various tissue, including the lungs.
Rheumatoid Arthritis
Pleurisy, IIP, Destruction of lung tissue, Caplan’s Syndrome, Pulm hypertension etc.
Polymyositis Dermatomyosis
Dysfunction of striated muscles of the neck, pharynx, diaphragm, leads to multiple aspiration Pneumonias.
Sjogren’s Syndrome
Primarily secretatory glands of the mouth and eyes, pleurisy (perhaps w/effusions), ILD
Systemic Lupus Erythematosus ---cont’
Progressive Systemic Sclerosis ---cont’
ILD Lupis
Immunologically mediated, multi-system, collagen disorder (with lung involvement), idiopathic.
Presents on skin, joints, liver, kidney, heart, respiratory and nervous system.
Extreme fatigue, butterfly rash on face, pleurisy often with effusions, photosensitivity, oral ulcers, arthritis, pericarditis, renal & neural dysfunction.
Anti-nuclear antibody (ANA) test positive in 95% of cases, LE cell prep test; 70–80% pts are positive.
ILD Progressive Systemic Sclerosis
Also known as Scleroderma.
Usually effects skin and small blood vessels but can also involve GI tract, lungs, kidneys and heart.
Esophagus is often hard hit.
Main lung findings are interstitial fibrosis, vascular degrading, pleural disease and possible aspiration due to esophageal incompetence.
The most pulmonary damaging collagen disease causing scarring and hypo-plasticity. (compliance)
Typical pt is female, 30 to 50 years old with familial history of auto-immune disorder.
Scleroderma
ILD: Idiopathic Pulmonary Fibrosis
Varies greatly depending on level of exposure to known causative agents and state of progression.
Exertional dyspnea is the usual first complaint of any patient.
Nagging non-productive cough.
Anorexia, weight loss, fatigue.
Vague chest pains often on inhalation.
In later stages, patient will complain of SOB even at rest
ILD: Acute Alveolar Proteinosis
Significant amorphous lipo-protein, not unlike surfactant, fills alveoli.
Similar picture to pulmonary edema but without cardiomegally.
Air bronchograms and dysfunctional macrophages.
Most pts are men 20 to 50 years old.
ILD: Miscellaneous
BOOP: Bronchiolitis Obliterans with Organizing Pneumonia.
Connective tissue plugs in small airways, surrounding tissue shows pneumonic process.
Goodpastures Syndrome:
Involves the deposition of anti-bodies in the basement membrane of the nephron and recurrent hemorrhage in pulmonary vessels.
Usually affects young adults. Many die ≈15 weeks after Dx from either pulmonary hemorrhage or renal failure.
ILD: Pathophysiology
Acute Stage;
Generalized edema with WBCs in alveoli and interstitial spaces.
Bronchial inflammation, smooth muscle and connective tissue constriction.
Chronic Stage;
Inflammation progresses, A/C thickening, destruction of tissue, fibrosis, granulomas, cavitation. Pleural effusions.
Histology identifies two types of IPF.
Desquamative interstitial pneumonia --- hyperplasia and sloughing of type II alveolar cells.
Ordinary interstitial pneumonia --- consolidated alveoli with A/C thickening and destructive honey combing.
ILD: Clinical Manifestations
Exertional dyspnea is the usual first complaint of any patient.
Nagging non-productive cough.
Anorexia, weight loss, fatigue.
Vague chest pains often on inhalation.
In later stages, patient will complain of SOB even at rest.
ILD: Lab Findings
The fibrosis will lead to a restrictive picture while presence of small airway disease will look like obstruction. Pts will may have a combined defect. decreased Dlco
ILD: Lab Findings X-ray
Bilateral infiltrates, nodular densities, cavitations, honey combing.
Air bronchograms.
Pleural thickening and effusions
ILD: Differential Diagnosis
Chronic Obstructive Lung Disease
Acute pulmonary disease.
Pneumonia, asthma etc
Cancer
Tuberculosis reemergence
ILD: Management, Prognosis, Prevention
Therapy is largely supportive in nature.
Avoidance of exposure, filter masks in high dust areas.
Most therapy is geared at the inflammatory process.
Cortico-steroids, broncho-dilators.
Oxygen and ventilation according to ABGs.
There are no cures for this list of interstitial lung diseases.
ARDS AKA
shock lung, white lung, acute alveolar failure, wet lung, da-nang lung, capillary leak syndrom, Adult HMD
Mortality of ARDS
50-70% of pts diagnosed
ARDS etiology
Aspiration, fluid overload, trauma, o2 toxicity, DIC, embili, Shock, burns, pneumonia, sepsis, CHP
ARDS mediators
Leukotrienes, protaglandins, Thromboxane, Interleukin 1, tissue necrosis factor,
ARDS phase 1
Exudative. Days 1-3-7
less compliance, more WOB,
ARDS phase 2
Proliferative days 3-7+
Regeneration of type II cells
fibrin deposition begins
Macrophages in lung
ARDS phase 3
Fibrotic phase 7-14+ days
++Fibrin
Alveolar sepa thicken
ARDS xray
stage 1
stage 2
stage 3
1) pneumonia like
2) white out
3) alveolar clearing then interstitial clearing... Maybe emphysema
VAPS
Make Ps
M oraxella catarrhalis
A cinobacter
K lebsielle
E nterobacter
P seudomonas
S taphlococcus
Pneumo SEVER disignation
RR > 30
Pa02 < 60 on > 30% 02
Multiple lobe involvement
Shocky, Systolic <90
Diastolic < 60
Urine output < 20ml/hr
Used to treat cyanide poisoning
Amyl Nitrite since it forms methemoglobin
increased 02 tox susceptability
old, on catecholamines, bleomycin, steroids, hyperthermia, hyperthyroidism, preemies, vitamin E deficiency
decreased 02 tox susceptability
young, adrenalectomy, hypothermia, prior lung damage, anti oxidants (Glutothione, vitamin c,e)
O2 tox etiology
0-12 hrs
12-24
24-30
30-72
0-12 Sub sternal pain
less VC
less compliance, SOBOE
DLCO
02 tox free radicals
OH, H202, lipid peroxidase
Tumor not linking to smoking, or dudes
Adenocarcinoma
double in 180 days
Tumor. Most common.
Squamous
Double in 100 days
tumor arises from K cells
Small oat cell
double in 30 days,
metastasizes
Tumor begin in central or peripheral aread, rarest
Large cell carcinoma
double in 100 days.
Burns early stage
0-48 hours
inflammation
retention of secretions
bronchospasm
pulm edema
Burns intermediate
2-5 days
Mucus plugging, atelectasis
Lower airways injury peak
Risk for pneumonia
Burns late
5-7 days
Sepsis and MOSF
Pneumonia
Pulmonary emboli
Airway remodelling
Edema confined to burn area
<20% BSA
Edema not confined to burn area, whole body
> 20% BSA
1 degree burn
first 2-5 layers of epidermis. Heals 5-10 days. Red
2 degree burn.
All epidermis, some of dermis. Thick skin, maybe blister, maybe yellow if infected
3 degree burn
All epidermis, all dermis, some fat underneath. Loos white, black, brown. Leathery or charred. No cap refill, no pinprick response, no spontaneous healing.