Resp Ix Mx Flashcards
Acute bronchitis
Patients typically present with an acute onset of:
cough: may or may not be productive
sore throat
rhinorrhoea
wheeze
Differentiating acute bronchitis from pneumonia;
History: Sputum, wheeze, breathlessness may be absent in acute bronchitis whereas at least one tends to be present in pneumonia
Examination: No other focal chest signs (dullness to percussion, crepitations, bronchial breathing) in acute bronchitis other than wheeze. Moreover, systemic features (malaise, myalgia, and fever) may be absent in acute bronchitis, whereas they tend to be present in pneumonia!
Ix = Clinical diagnosis
However, if CRP testing is available this may be used to guide whether antibiotic therapy is indicated
Mx:
analgesia
good fluid intake
Consider antibiotic therapy(Doxy*) if patients:
are systemically very unwell
have pre-existing co-morbidities
have a CRP of 20-100mg/L (offer delayed prescription) or a CRP >100mg/L (offer antibiotics immediately)
*Doxycycline cannot be used in children or pregnant women
alternatives include amoxicillin
Asbestos-related lung disease (incl. asbestosis and mesothelioma)
Asbestos can cause a variety of lung diseases from benign pleural plaques to mesothelioma.
- Pleural plaques = benign and do not undergo malignant change. They, therefore don’t require any follow-up
- They are the most common form of asbestos-related lung disease and generally occur after a latent period of 20-40 years.
- Asbestosis = The latent period is typically 15-30 years
The severity of asbestosis is related to the length of exposure. This is in contrast to mesothelioma where even very limited exposure can cause disease.
Features
dyspnoea and reduced exercise tolerance
clubbing
bilateral end-inspiratory crackles
lung function tests show a restrictive pattern with reduced gas transfer
Mx = conservative
*Lung cancer
Whilst mesothelioma is in some ways synonymous with asbestos, lung cancer is actually the most common form of cancer associated with asbestos exposure.
It also has a synergistic effect with cigarette smoke in terms of the increased risk. Therefore, smoking cessation is very important as the risk of lung cancer in smokers who have a history of asbestos exposure is very high.
*Mesothelioma
Mesothelioma is a malignant disease of the pleura. Crocidolite (blue) asbestos is the most dangerous form.
Possible features
progressive shortness-of-breath
chest pain
pleural effusion
Ix: Chest X-Ray -> CT -> pleural biopsy/fluid MC&S
cytology -ve -> local anaesthetic thoracoscopy
X-ray shows pleural effusion/thickening
If an area of pleural nodularity is seen on CT then an image-guided pleural biopsy may be used!
Mx:
Symptomatic
Industrial compensation
Chemotherapy, Surgery if operable
Prognosis poor, median survival 12 months
Aspergillus lung disease
In the exam questions often give a history of bronchiectasis and eosinophilia. Raised IgE and ‘waxing and waning consolidation’
Ix:
eosinophilia
flitting CXR changes
positive RAST test to Aspergillus
positive IgG precipitins (not as positive as in aspergilloma)
raised IgE!
Mx:
1st = oral glucocorticoids
2nd = itraconazole
RAST = radioallergosorbent
Asthma
Ix = spirometry + BDR + FeNO
Pt should be asked if their symptoms are better on days away from work/during holidays. If so, patients should be referred to a specialist as possible occupational asthma
FeNO
>= 40 parts per billion (ppb) = positive
in children its >=35
Spirometry
FEV1/FVC < 70% = obstructive
Reversibility testing
An improvement in FEV1 of >12% + increase in volume of >200 ml = Positive
In children, its just an improvement in FEV1 of 12% or more
A chest x-ray is not routinely recommended, unless:
life-threatening asthma
suspected pneumothorax
failure to respond to treatment
Mx:
1 = SABA
2 = SABA + low-dose ICS*
3 = SABA + low-dose ICS + LTRA
4 = SABA + low-dose ICS + LABA
SILT - S(aba) I(CS) LT(RA), then LABA
Continue LTRA depending on patient’s response to LTRA
Can enter in at 2 if:
Newly-diagnosed asthma with symptoms >= 3 / week or night-time waking
*If candidiasis develops because of steroid useage - switch to a large volume spacer!
Bronchiectasis
Bronchiectasis describes a permanent dilatation of the airways secondary to chronic infection or inflammation. There are a wide variety of causes are listed below:
Features
persistent productive cough. Large volumes of sputum may be expectorated
dyspnoea
haemoptysis
Signs
abnormal chest auscultation
coarse crackles
wheeze
clubbing may be present
Most common organisms isolated from patients with bronchiectasis:
Haemophilus influenzae (most common)
Pseudomonas aeruginosa
Klebsiella spp.
Streptococcus pneumoniae
Mx:
physical training (e.g. inspiratory muscle training) - has a good evidence base for patients with non-cystic fibrosis bronchiectasis
postural drainage
antibiotics for exacerbations + long-term rotating antibiotics in severe cases
bronchodilators in selected cases
immunisations
surgery in selected cases (e.g. Localised disease)
Chronic obstructive pulmonary disease (COPD)
a1AT can cause COPD in young non-smokers
Emphysema is most prominent in the lower lobes in A1AT deficiency and the upper lobes in COPD
Ix: FEV1/FVC
Mx:
Ongoing;
- SABA/SAMA
- no asthma = LABA+LAMA
- asthma* = LABA+ICS
- LAMA+LABA+ICS*
- azithromycin
The non-asthmatic lamb!
4 = Only if they have 1 severe/2moderate exacerbations per year or day-today sx adversely affect quality of Life
5 = 3+ exacerbations (with 1 hospital stay) = Azithromycin prophylaxis
Acute exasterbation;
Oral prednisolone is recommended for 5 days
NICE only recommend giving oral antibiotics in an acute exacerbation of COPD in the presence of purulent sputum or clinical signs of pneumonia
Most common cause if H. influenza
Home supply of oral pred+antibiotic is recommended after a severe exacerbation!
*This includes ‘asthma features - ie. high eosinophils,
steroid-responsive features,
previous diagnosis of asthma/atopy,
substantial variation in FEV1 over time (at least 400 ml)
substantial diurnal variation in peak expiratory flow (at least 20%)
Extrinsic allergic alveolitis
acute (occurs 4-8 hrs after exposure)
dyspnoea
dry cough
fever
chronic (occurs weeks-months after exposure)
lethargy
dyspnoea
productive cough
anorexia and weight loss
Ix: CT + bronchoalveolar lavage
imaging: upper/mid-zone fibrosis
bronchoalveolar lavage: lymphocytosis
serologic assays for specific IgG antibodies
blood: NO eosinophilia
Mx = avoid precipitating factors + oral glucocorticoids
Idiopathic pulmonary fibrosis
Can be caused by amiodarone therapy (presents with no clubbing!)
Ix: spirometry + TLCO + high-res CT
Mx = pulmonary rehabilitation
Many patients will require supplementary oxygen and eventually a lung transplant
Spirometry: classically a restrictive picture (FEV1 normal/decreased, FVC decreased, FEV1/FVC increased)
impaired gas exchange: reduced transfer factor (TLCO)
imaging: bilateral interstitial shadowing (typically small, irregular, peripheral opacities - ‘ground-glass’ - later progressing to ‘honeycombing’) may be seen on a chest x-ray but high-resolution CT scanning is the investigation of choice and required to make a diagnosis of IPF
ANA positive in 30%, rheumatoid factor positive in 10% but this does not necessarily mean that the fibrosis is secondary to a connective tissue disease. Titres are usually low
Very few medications have been shown to give any benefit in IPF
Obstructive sleep apnoea
Ix: sleep study + polysomnography
Sleep studies (polysomnography) - ranging from monitoring of pulse oximetry at night to full
Polysomnography where a wide variety of physiological factors are measured including EEG, respiratory airflow, thoraco-abdominal movement, snoring and pulse oximetry
Mx
mild = weight loss
mod/severe: 1st = CPAP !
Intra-oral devices (e.g. mandibular advancement) may be used if CPAP is not tolerated or for patients with mild OSAHS where there is no daytime sleepiness
the DVLA should be informed if OSAHS is causing excessive daytime sleepiness
limited evidence to support use of pharmacological agents
Pneumoconiosis
Ix: X-Ray + spirometry
Chest x-ray: upper zone fibrosis
Spirometry: restrictive lung function tests - a normal or slightly reduced FEV1 and a reduced FVC
Mx = Avoid exposure to coal dust and other respiratory irritants (e.g. Smoking)
Manage symptoms of chronic bronchitis
Pneumonia
Ix:
Mild risk = Chest x-ray
mod/high risk = X-ray + blood/sputum cultures + pneumococcal and legionella urinary antigen tests
Treatment monitoring = CRP levels
Patients diagnosed with pneumonia who have COPD should be given corticosteroids even if no evidence of the COPD being exacerbated!
Mx low-severity CAP:
1st = amox (5days)
Pen allergic = macrolide (-mycins) or tetracycline
Mx moderate and high-severity CAP;
Dual ab’s: amoxicillin + macrolide (7-10 days)
High severity = (co-amoxiclav/ceftriaxone/pip&taz) + macrolide
If on aspiration an empyema (collection of pus) has formed, then it should be drained
Discharge criteria and advice post-discharge
No discharge if in the past 24 hours they have had 2+ of the following findings:
>37.5°C
RR>24/min
HR>100bpm
SBP<90 mmHg
SpO2< 90% on room air
abnormal mental status
inability to eat without assistance
Pneumothorax
With an increase of air in the pleural space, there is impairment of venous return which results in reduced cardiac output;
This eventually leads to pulseless electrical activity as the heart is no longer able to pump properly, but the conducting system of the heart is intact.
Mx:
Primary;
SOB+rim>2cm->aspirate->chest drain
Secondary;
SOB+rim of air>2cm = chest drain
rim is 1-2cm = aspirate -> admit to monitor or if aspiration doesn’t work -> chest drain
<1cm = oxygen + admit for 24hrs
Sarcoidosis
Facial rash plus lymphadenopathy or shin rash + cough?
think sarcoidosis
Ix: hypercalcaemia + raised ESR
A chest x-ray may show the following changes:
stage 0 = normal
stage 1 = bilateral hilar lymphadenopathy (BHL)
stage 2 = BHL + interstitial infiltrates
stage 3 = diffuse interstitial infiltrates only
stage 4 = diffuse fibrosis
Other investigations
spirometry: may show a restrictive defect
tissue biopsy: non-caseating granulomas
gallium-67 scan - not used routinely
the Kveim test (where part of the spleen from a patient with known sarcoidosis is injected under the skin) is no longer performed due to concerns about cross-infection
Mx: Steroids
Indications for steroids
patients with chest x-ray stage 2 or 3 disease who are symptomatic. Patients with asymptomatic and stable stage 2 or 3 disease who have only mildly abnormal lung function do not require treatment
hypercalcaemia
eye, heart or neuro involvement
How to tell the difference between trans/exudative pleural effusions?
What are some examples of each?
What happens if its drained too quickly?
Lights criteria for exudate?
Pleural effusions can be categorised into transudates and exudates
according to their protein content. Transudates (protein content <30 g/L)
Occur as a result of:
- Increased venous pressure (cardiac failure, restrictive
pericarditis, fluid overload), - Hypoproteinaemia (cirrhosis, nephrotic syndrome, malabsorption)
Hypothyroidism and Meig’s syndrome
(right pleural effusion coupled with ovarian fibroma)
Exudates occur as a
result of: (infection, inflammation malignancy)
- Increased capillary permeability secondary to infection (pneumonia,
tuberculosis), - Inflammation (pulmonary infarction, rheumatoid arthritis,
SLE) - Malignancy (bronhogenic carcinoma, secondary metastases,
lymphoma, mesothelioma, lymphangitis carcinomatosis).
If a pleural effusion is aspirated* too quickly, a rare but important complication that can develop is re-expansion pulmonary oedema
mx = aspirate, not drain
Lights criteria = Effusion LDH level greater than 2/3rds the upper limit of serum LDH points to exudate
Key things that differentiate granulomatosis with polyangitis (Wegeners) from eosinophilic granulomatosis with polyangitis (churg-strauss)
Wegeners = epistaxis, saddle shaped nose, haemoptysis, eye involvement, c-ANCA
Management
steroids
cyclophosphamide (90% response)
plasma exchange
median survival = 8-9 years
CS = eosinophilia, asthma, nasal polyps, p-ANCA
