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CR - COPD + A1AT deficiency (i) (Signs (hands (warm, sweaty, dilated veins…
CR - COPD + A1AT deficiency (i)
intro
preventable, txable, usually progressive, but not fully reversible (unlike asthma) airflow limitation
significant extra-pul effects that may contribute to severity
abnormal inflamm response to noxious particles/gases
lots of people affected - 4th leading cause of death worldwide (predicted to move to 3rd)
prevalence varies in different countries (4-20%) due to PFTs not being available everywhere
younger when began smoking -> more damage
more women are smoking
never too late to quit smoking to prevent COPD (different for cancer, risk never fully returns to normal, but close 10 yrs later)
Classic subtypes
chronic bronchitis
productive cough most days for @ least 3 months of 2 consecutive yrs
no other attributable cardiac/resp cause
emphysema
pathological/radiological Dx of abnormal/permanent enlargement of airways distal to terminal bronchiole
Causes/risk factors
smoking (95%)
incl cigs, pipes, cigars, marijuana, passive
15-20% of heavy smokers get COPD
biomass fuel burning (esp in developing world)
cessation of risk factors decreases resp symptoms + slows rate of lung function decline (i.e. FEV1)
sulphur dioxide (smog)
occupational dusts
coal
silica
quartz
welding fumes
cadmium (emphysema)
chest infections in 1st yr of life (also increased risk of bronchiectasis)
adenovirus + HIV
Baseline symptoms
chronic cough
initially intermittent, becomes persistent
productive (unlike asthma)
usually grey/white (unite CF/bronchiectasis which is purulent)
only purulent in infective exacerbations
increase in natural Hx of COPD
dyspnoea (initially on exertion, progresses to @ rest)
ask can they walk + talk @ same time
wheeze/chest tightness
initially intermittent, becomes persistent
Acute exacerbations
increased duration + severity of SOB + wheeze
purulent sputum
pleuritic chest pain (dDx = pneumonia, PE, pneumothorax)
ankle oedema
orthopnoea, PND
haemoptysis (must rule out cancer)
compare infective Hx to baseline Hx
ask about smoking (pack-yrs), exercise tolerance, meds, GP/ED/hosp/ICU admissions
Signs
only when advanced
tripod postion
central cyanosis
use of accessory resp muscles
Hoover's sign
indwelling intercostals
inward movement of lower rib cage on inspiration
flaring nose
pursed lip breathing (attempting to keep airways from collapsing)
hyperinflation (barrel-chested)
decreased chest expansion
decreased breath sounds
rhonchi (continuous low-pitched rattling, resembles snoring)
wheeze
prolonged expiratory time
increased RR
decreased SaO2
hands
warm
sweaty
dilated veins
resting tremor - B-agonist SE
asterixis (flapping tremor due to CO2 retention)
possibly RHF features
dDx
CHF
MI
tachyarrhythmia
PE
pneumonia
asthma
atelectasis secondary to mucus plugging
exclude using CXR, SCG, ABG, D-dimers, peak expiratory flow rate, PFTs, CT-thorax, bronchoscopy
aims of acute management
adequate oxygenation (SaO2 > 90%)
pH homeostasis (>7.3)
bronchospasm relief
tx concurrent infection
Acute management
oxygenation
nasal prongs not great
dilution as mouth is still breathing room air (21% O2)
face mask better
start low (28-40%) to prevent hyperoxygenation
low O2 + low pH physiologically cause tachypnoea to compensate
if patient retain bicarb to physiologically correct acidosis then only relying on hypoxia to breath
if O2 suddenly increased then patient will stop breathing
acidosis Tx
NIPPV with BiPAP if pH < 7.35
sometimes invasive ventilation needed (endotracheal tube)
VAP
hard to take patient off it
barotrauma (damage due to excessive pressure changes)
CPAP contraindicated in severe air trapping diseases with hypercarbia - asthma or COPD
bronchodilators
nebulised
repeat until symptomatic relief, then repeat every 4-6 hrs for maintenance
salbutamol, atrovent (ipratropium bromide)
steroids
IV hydrocortisone every 6 hrs
2/3 days later switch to PO prednisolone
taper off on discharge