Nichols: PE, Acute Lung Injury, ILD, Cryptogenic organizing pneumonia, Pneumothorax Flashcards
What are the common sources of PE?
DVT and thrombi around long term catheters
What are risk factors from developing a PE?
smoking immobilization malignancy surgery central venous instrumentation thrombophilia, obesity oral contraceptives pregnancy
Virchow’s triangle
endothelial injury
abnormal blood flow
hypercoagulable
Do small emboli cause infarction in the lung? Why or why not?
no bc the lung has dual blood supply
Saddle embolus
large PE that obstructs the pulm trunk
consequences of a saddle embolus
acute cor pulmonale or sudden death
What happens to the small emboli that make it to the lung but are not big enough to cause an infarction?
become organized into vessel wall (may leave a fibrous band)
describe the gross appearance of a pulmonary infarct
subpleural, wedge-shaped and hemorrhagic
CXR finding of peripheral wedge-shaped opacity that is suggestive o PE
hampton hump
focal oligemia that is suggestive of PE
Westermark sign
most common symptom of PE
dyspnea
PE Tx
anti-coagulation
most specific and sensitive Dx test for PE
spiral CT with IV contrast
hypoxemia, neurological impairment and petechial rash 1-3 days after trauma
fat embolism
**petechia in <50%
3 etiologies of a fat embolism
long bone fractures
orthopedic surgery
sickle cell disease
(also liposuction, burns, pancreatitis, osteomyelitis – in his word doc)
describe the clinal syndrome assc with a fat embolus
acute onset of dyspnea, confusion, tachypnea, tachycardia, irritability, restlelssness, anemia and thrombocytopenia
How long after trauma will a fat embolus present? Why?
1-3 days
*due to metabolism of fat creating toxic intermediates –> inflammation –> CRP agglutinates lipids
Where do the petechia form that may present with a fat embolus (pulm)
head, neck, and anterior chest
How is a fat embolus differentiated from air bubbles microscopically?
oil-red-O stain of fresh tissue or freshly frozen tissue
or
electron microscopy with osmium tetroxide of fixed tissue
Tx for fat embolus
supportive care
What is the pathogenesis of an air embolus?
hole in blood vessel open to air at higher pressure than the blood (or formation of gas within the blood)
What are the 4 etiologies of air embolus?
- vascular catheterization: breakage of vascular catheter connections, failure to occule catheter during insertion or removal
- sugery: brain in sitting postion, back in prone)
- chest wall injury
- barotrauma: MV at high press with blood vessel rupture in lungs, rapis ascent during underwater trauma)
signs of air embolism
dyspnea, gasp, cough, millwheel heart murmur, tachypena, rales, shock
Generally, more than ____ ml needed to have a clinical effect, but ____ ml introduced at a rate of _____ ml/second is fatal
100 ml = clinical effect
300-500 ml at a rate of 100ml/s = fatal
How is air embolus Dx?
Dx of exclusion
Tx of air embolus
left lateral decubitus positioning (Durant’s maneuver)
non-cardiogenic pulmonary damage manifested by edema with an inflammatory and fibrosing response
acute lung injury
ALI starts with edema. Where in the lung does this edema start?
interstitial –> alveolar and sometimes with hemorrhaging
What causes ALI to be hemorrhagic?
when the injury kills capillary endothelial cells and pneumocytes
What are the stages of ALI?
Exudative –> transition –> proliferative –> fibrotic
Describe the pathogenesis of ALI.
binding of microbial products or cell injury activates innate immune response –>
dysregulated inflammation (macrophage production of IL1, 8, TNF) –>
inc permeability of endothelium and epithelium (disruption of cadherins and adherens) –>
edema –>
TGF-B and PDGF released –> fibrosis
How does the gross appearance of ALI change as the disease progresses?
red, edematous –> white and fibrous
Describe the microscopic changes assc with ALI
exudative phase: hyaline membranes, congestion, lymphocytes, macrophages
proliferative: less hyaline, intersitial infitration by lymphocytes, macrophages, and proliferating fibroblasts
* *type 2 pneumoplasia and fibroplasia
fibrosis: interstitial and progressive
lipid laiden macrophages
amiodarone toxicity
How does ALI commonly present?
rapidly progressive dyspnea and bilateral pulmonary infiltrates superimposed on the manifestations of the cause of injury
=ARDS
Tx of ALI
MV but with low TV to protect lungs from further injury/inflammation, conservative fluid resuscitation
How long after radiation exposure will radiation pneumonitis present? How does it present?
1 -2 mos after exposure
with dyspnea, cough, pleuritic chest pain, fever, CXR infilrates
What are the microscopic findings specific to radiation pneumonitis?
atypical type 2 pneumocyte hyperplasia and blood vessel injury
LATE: hemosiderin and interstitial fibrosis
IPF/UIP is (acute or chronic) fibrosis of what part of the lung?
chronic, septa btwn airspaces
How does a pt with IPF/UIP present
In a late-middle aged (male) smoker with…
insidious onset of dyspna and dry cough
inspiratory velcro crackles
CXR: asymmetric subpleural peripheral reticular opacities in the lower lobes
What it is the radiologic finding with advanced IPF/UIP?
honeycombing
What is the hallmark microscopic finding of UIP/IPF
fibroblast foci of immature fibroblasts bulging into the alveoli from the interstitium
Tc for IPF/UIP
transplantation
Corticosteriods + immunosuppressive drugs + INF-gamma
necrotizing infection –> organizing pneumonia is known as
cryptogenic organizing pneumonia
How doe COP preset
in late middle age non-smoker with…
dyspnea and cough with ground glass opacities that are less dense than acute bacterial pneumonia
It is different to distinguish COP from IPF/UIP. WHy?
COP responds to corticosteriod treatment while UIP usually does not
Masson bodies
seen in COP = fibrosing granulation tissue in the alveoli
All of Nichols pneumothorax stuff was covered in that other lecture
so check that out
