Resp Flashcards
types of pneumothorax
primary spontaneous
- tall, thin males
- no history of lung disease
- family history, marfans, smoking
secondary spontaneous
- due to underlying lung disease
- most commonly COPD
- also
- > TB
- > pneumocystis jerovecii
- > cystic fibrosis
traumatic
- penetrating or blunt chest trauma
- iatrogenic
tension
-complication of any of above
tension pneumothorax
- occurs when pleural pressure exceeds atmospheric during inspiration and expiration
- forms one way valve
- > air can enter pleural space with inspiration
- > less can exit with expiration
- increasing pressure compresses veins
- > reduced venous return
- > decreased CO and hypotension
- compression of lung tissue
- > resp failure
hx and exam pneumothorax
hx
- dyspnoea
- pleuritic chest pain
- > usually ipsilateral
- spontaneous often occurs at rest
- > can recount it occuring
- risk factors
- tension
- > distressed
- > severe dyspnoea
exam
- typical
- > increased work of breathing
- > decreased chest expansion
- > ipsilateral hyperinflation with intercostal widening
- > tracheal deviation to contralateral
- > hyper-resonate to percussion
- > decreased breath sounds ipsilateral
- > subcut emphysema
- tension
- > cyanosis
- > decreased GSC
- > diaphoresis
- > hypotension
- > tachycardia
ddx pneumothorax
EMPTIED
- embolus
- musculoskeletal
- pericarditis
- tamponade (haemopericardium)
- infarct
- effusion (eg haemothorax)
- dissection
investigations pneumothorax
ABG
-resp alkalosis
ECG
FBC
trops
d-dimer
CXR
- visceral pleural line
- simple
- > no mediastinum shift
- tension
- > mediastinum and tracheal shift to contra
- > flaying of ribs
- > flattening diaphragm
consider
- ultrasound
- > in trauma
- > absence of lung sliding
- CT
- > in occult
- > more sensitive than CXR
PE investigations
ECG -non specific changes (RV strain) ABG -hypoxia -alkalosis, hypocapnea
D-dimer Troponin -can be elevated (RV strain) FBC -leukocytosis EUC -contrast ESR LFTs Coags -INR and aPTT (anti-coagulation) bHCG -pregnant female (thrombolysis)
CXR -hamptoms hump -westermarks sign CTPA V/Q scan Compression U/S leg (proximal/whole)
PE investigation pathway
Pretest probability
- Well’s PE
- Geneva
Score interpretation
- low=<2
- intermediate=2-6
- high=>6
PERC rule
-8 criteria to identify patients with low probability of PE where risk of testing outweighs risk of PE
Low
- fulfil 8 PERC criteria = no testing needed
- doesn’t fulfil all 8 = D-Dimer
- D-Dimer >500ng/mL = CTPA
- D-Dimer <500ng/mL = no further testing needed
Intermediate
- D-Dimer <500ng/mL = no testing (unless frail)
- D-Dimer >500ng/mL = CTPA
High
- negative D-dimer cannot rule out (5% risk)
- CTPA
indications for intubation
Airway patency?
- decreased level of conscious –> loss of protective resp reflexes
- PEF
Oxygenation/ventilation (respiratory failure)
- worsening hypoxia/hypercapnea
- RR>40
Clinical
- work of breathing
- exhaustion
- cyanosis
Expectation of need for intubation
- senior clinician expects deterioration
- need for transport out of ED
Non responsive to NIPPV
investigations acute asthma
Pulse oximetry ABG PEF -normal = >80% -severe = <60% ECG
FBC EUC LFTs Trops NT- BNP/BNP D-Dimer
CXR
Consider
- CT chest (foreign body if non-opaque)
- tryptase (anaphylasis)
- spirometry (once stable)
- > safety to discharge (%FEV1)
- > useful in follow up
ddx asthma
Immediately Page FACEM
- infection (pneumonia)
- pneumothorax
- foreign body
- Anaphylaxis
- COPD exacerbation
- Embolism
- MI (APO)
asthma pathophys
Most commonly IgE mediated hypersensitivity
Airway inflammation
- mast cell activation central
- > sensitisation to allergen
- > degranulation of pulmonary mast cells with further exposure
- early phase
- > release of preformed mediators (eg. histamine)
- > production of eicosanoids (eg. PGD2, cysteinyl LTs)
- > direct stimulation of airway smooth muscle
- > mucous production
- > stimulation of neural reflex pathways (release of ACh)
- late phase
- > influx of inflammatory cells (basophils, eosinophils neutrophils, T helper cells)
- > release of cytokines activates smooth muscle
- > bronchoconstriction
Airway obstruction
- can be regional or global
- large and small airways involved
- initially obstruction -> air trapping and hyperinflation
- > predominately due to bronchoconstriction
- > oedema and thickening of airway wall
- > airway plugging with mucous and cellular debris
Airway remodelling
- irreversible structural change superimposed on effects of inflammation and bronchoconstriction
- histopath
- > loss of normal pseudostratified epithelium
- > increase in goblet cells
- > fibrosis and thickening of reticular layer of basement membrane
- > increased myofibroblasts
- > increased vascularity
- > increased smooth muscle mass and ECM
Bronchial hyper-responsiveness
- decrease in FEV1 20% with challenge (eg. histamine)
- alteration in smooth muscle function/mass
- enhanced sensitivity of neural pathways
- remodelling and structural abnormalities (eg. loss of airway parenchymal interdependence)
- > tethering forces maintaining patency
Additional histo
- Curschmann spirals
- > spiral of mucous plugs from subepithelial glands
- Charcot leyden crystals
- > eosinophilic binding protein in sputum
Pathophys pneumonia
Gain access to lower respiratory tract
- aspiration from oropharynx most common
- > microaspiration normal, particularly in elderly
- > increased risk with decreased LOC
- > intubation
- > dysphagia/motility disorders
- haematogenous spread
- > eg. tricuspid IE
- local spread
- > pleural or mediastinum
Overcome mechanical factors
- gag and cough reflex
- > bypassed with intubation
- > decreased LOC
- > neuromusculuar dysfunction (eg. stroke)
- hairs and turbinates of nares
- > sufficiently small particles
- mucociliary elevator
- > impaired in chronic lung disease (eg. COPD/CF)
- > mucous thinned by influenza
- > chlamydia pneumoniae produce ciliostatic factor
- > mycoplasma pneumoniae shears off cilia
- normal flora crowds out potential pathogens
- > overwhelming inoculum
- > overgrowth of commensals
Evade innate immune system
-alveolar macrophage phagocytosis, destruction, mucociliary elevator or lympthatics
->overwhelming inoculum
->virulence factors (eg. mycobacterium resistant to phagocytes)
-IgA opsonisation
->Strep pneumoniae produce protease that splits IgA
Neutrophil response
-immunocompromise
->diabetes, HIV
-drugs
->anti TNF alpha
path pneumonia
Pathology
Increased alveolar capillary permeability
-initially oedema (proteinaceous exudate)
->red hepatization (extravasation of RBCs and neutrophils)
->grey hepatization (neutrophils and fibrin deposition with bacterial clearance)
-resolution
->clearance of cell debris and fibrin by macrophage
ddx pneumonia
BE ACCTIVE
- Bronchiectasis exacerbation
- Exacerbation COPD/Asthma
- Aspiration/foreign body
- Cancer/mets
- CCF
- TB
- ILD
- Viral (bronchitis/influenza)
- Empyaema (eg. IE)
CXR pneumonia types
Lobar
- > most common strep pneumoniae
- > consolidation of alveolar spaces
- > homogenous opacification of lobe
- > sparing of bronchi -> air bronchogram
Bronchopneumonia (lobular)
- > associated with staph aureus
- > direct inhalation and colonisation of bronchi
- > patchy nodular or reticularnodular
- > asymetrical and bilateral
- > often lung bases
- > does not cross fissures
Atypical
- atypical bacteria, viruses and fungi
- inflammation confined to interstitium and interlobular septa
- patchy reticular pattern
- often involves hilum
- lack of consolidation
Round
- seen only in paediatric
- > lack of pores of Kohn
- rounded opacities
Cavitating
- complication of pneumonia
- radiolucency superimposed on consolidation
Hemorrhagic
ddx PE
EMPPATHIIC
- exacerbation of COPD/asthma
- musculoskeletal
- pneumothorax
- pericarditis
- aortic dissection
- tamponade
- HTN (pulmonary - chronic emboli)
- infarct (MI)
- infection (pneumonia/bronchitis)
- CCF
DDx for DVT (BITCH Leg)
- bakers cyst (ruptured)
- injury (eg. tear)
- tumour (leading to venous congestion)
- cellulitis
- haematoma
- lymphagitis
investigations pneumonia
ABG
FBC EUC -risk score LFT -liver failure = poor prognosis ESR -monitor treatment -non specific but high levels supports infection Procalcitonin -non specific -higher levels correlate with bacterial infection
Microbiology: -treatment is usually successful with empiric -diagnosis of causative agent rare -indicated here due to severity/treatment resistance Blood cultures -positive for causative oragnism Sputum culture and gram stain -prior to antibiotics PCR ->faster than bacterial culture ->improves sensitivity/specificity ->can provide information on resistance ->predominately for rapid identification of viral infection
CXR
-PA and lateral
Consider
-bronchoscopy
->bronchoalverolar lavage = 10^4 CFU/mL
->protected specimen brushing = 10^3CFU/mL
-urinary antigen
->once diagnosis has been made, if it can change therapy
->legionella
->strep pneumoniae
Serology for atypicals
->IgM for mycoplasma
->acute and convalescent phase (change in IgG status) for mycoplasma, chlamydophila, coxiella
