Respiratory Flashcards
Venous thromboembolism (VTE)
an umbrella term used to describe deep vein thrombosis (DVT) with or without pulmonary embolism (PE)
Risk factors for Venous thromboembolism (VTE)
↑ age obesity FH of VTE pregnancy immobility hospitalisation anaesthesia surgery acute medical illness prolonged travel smoking dehydration
Underlying conditions predisposing to Venous thromboembolism (VTE)
malignancy thrombophilia HF antiphospholipid syndrome Behcets polycythaemia sickle cell nephrotic syndrome Homocystinuria
Drugs predisposing to Venous thromboembolism (VTE)
COCP
HRT (risk higher in oestrogen + progesterone vs only oestrogen)
tamoxifen/raloxifene
antipsychotics e.g. olanzapine
Prophylaxis for Venous thromboembolism (VTE)
mechanical:
- compression stocking
- intermittent pneumatic compression devices
medication:
-LMWH/UFH/fondaparinux (use UFH if CKD/↓ renal function)
presurgical intervention
-stop COPC/HRT 4 weeks before surgery
postsurgical interventions
- early mobilisation
- sufficent hydration
Deep vein thrombosis (DVT)
the development of a blood clot in the major vein in the leg/thigh/pelvis/abdomen
Pathological conditions leading to DVT
Virchows triad
- vascular endothelial damage
- venous stasis
- hypercoaguability
Presentation of Deep vein thrombosis (DVT)
may be asymptomatic or present with PE
symptoms usually unilateral
-limb pain & tenderness, swelling of calf/thigh, pitting oedema, distension of superficial veins, ↑skin temp, erythema, heard/thickened palpable vein, discolouration (red/purple)
NB severe signs of DCT can mimic cellulitis
Wells score for Deep vein thrombosis (DVT)
Clinical feature:
-Active cancer (treatment ongoing,
within 6 months, or palliative) 1
-Paralysis, paresis or recent
plaster immobilisation of the lower extremities 1
-Recently bedridden for 3 days or more or
major surgery within 12 weeks requiring
general or regional anaesthesia 1
-Localised tenderness along the distribution
of the deep venous system 1
-Entire leg swollen 1
-Calf swelling at least 3 cm larger than
asymptomatic side 1
-Pitting oedema confined to the symptomatic leg 1
-Collateral superficial veins (non-varicose) 1
-Previously documented DVT 1
-An alternative diagnosis is at least as likely as DVT -2
Actions for wells score for Deep vein thrombosis (DVT)
IF wells score ≥2 points (DVT is likely)
- proximal leg USS within 4h
- if +ve = treat DVT
- if -ve do a d-dimer
- if USS can’t be done within 4h
- do d-dimer +interim therapeutic anticoagulation until USS (should be within 24h)
NB if D-dimer is +ve but scan is negative then the USS should be repeated after 6-8 days
IF wells score <1 point (DVT unlikely)
- d-dimer within 4h
- if -ve = DVT unlikely
- if +ve = arrange USS within 4h (if not possible then as above)
Investigations for Deep vein thrombosis (DVT)
D-dimer (↑)
Doppler USS
Wells score for DVT
≥2 points DVT is likely
<1 point DVT is unlikely
Pulmonary embolism (PE)
caused by obstruction of the pulmonary arterial tree by an embolus (usually thrombus)
Presentation of Pulmonary embolism (PE)
sudden onset, may have precipitating event that sets them off
dyspnoea, pleuritic*/retrosternal chest pain, haemoptysis, tachycardia, tachypnoea, low grade fever
dizziness, syncope, ↑JVP
obstructive shock (if massive PE)
signs of DVT (unilateral, swollen, erythematous leg/calf)
Wells score for Pulmonary embolism (PE)
Similar to DVT score
≤4 points = PE unlikely
>4 points = PE likley
NB you can also use the PE rule out criteria (PERC)
a negative PERC reduces likelihood of PE to <2%
Actions based on Wells score for Pulmonary embolism (PE)
Wells score >4 (PE likely)
- immediate CTPA
- if delay in CTPA = give interim anticoagulation
- if CTPA -ve consider USS doppler of leg if DVT symptoms
Wells score ≤4 (PE unlikely)
- arrange D-dimer
- if +ve = immediate CTPA / if delayed give interim anticoagulation
- if -ve = PE unlikely so consider alternative diagnosis
Investigations for Pulmonary embolism (PE)
CTPA
-preferred for definitive diagnosis of PE
ECG
- sinus tachycardia
- S1Q3T3 (large S wave in lead I, large Q wave & inverted T wave in lead III)
D-Dimer (↑)
-very non specific but very sensitive
Investigations for Pulmonary embolism (PE)
CTPA
-preferred for definitive diagnosis of PE
ECG
- sinus tachycardia
- S1Q3T3 (large S wave in lead I, large Q wave & inverted T wave in lead III)
D-Dimer (↑)
-very non specific but very sensitive
CXR
- usually normal
- recommended for all pts prior to CTPA*
V/Q scan
-preferred over CTPA in pts with renal impairment
Leg USS, ABG
Management of Pulmonary embolism (PE)
If haemodynamically unstable = thrombolysis
If in cardiac arrest with suspected PE give thrombolysis and continue CPR for 60-90 min
1st line:
- DOACs e.g. apixaban/riveroxaban
- in renal impairment use UFH/LMWH
- in antiphospholipid syndrome use LMWH
Duration:
- 3 months minimum if provoked
- 6 months minimum if unprovoked
- 3-6 months if caused by cancer
NB for unprovoked PE consider investigating the patient for underlying cancer or follow up closely
Asthma
a chronic inflammatory disease of the respiratory system characterised by bronchial hyperresponsiveness,
Asthma
a chronic inflammatory disease of the respiratory system characterised by bronchial hyperresponsiveness, episodic acute exacerbation and reversible airway obstruction (i.e. intermittent bronchospasm)
affects ~10% of children & 5-10% of adults
Risk factors for asthma
personal history of atopy (hay fever/eczema) Family history of asthma/atopy inner city environment socio-economic deprivation obesity prematurity maternal smoking low birth weight
Presentation of asthma
wheeze, chest tightness, SOB, cough
- worse at night / early morning cough
- presents on exercise, exposure to cold, other triggers or irritants
expiratory wheeze on auscultation
Investigations of asthma
FEV1/FVC ratio
- <80% of predicted
- FEV1 ↓ & FVC normal
- obstructive picture
PEFR ± reversibility testing with salbutamol
-PEFR ↓ but reversible with SABA
fractional exhaled nitrous oxide (FeNO) (↑)
CXR
-for smokers & older people
Management of asthma
All pts should have a personalised asthma action plan
All pts should have a SABA e.g. salbutamol for symptomatic relief
between each step ensure adequate inhaler technique and compliance
consider stepping down treatment every 3 months or so if asthma is well controlled
1: SABA + low dose ICS
2: SABA + low dose ICS + trial of LTRA
3: SABA + low dose ICS + LABA ± LTRA
4: SABA + MART (ICS + LABA) ± LTRA
5: SABA + medium dose ICS in MART ± LTRA
6: expert help
Step 1 for asthma management
SABA + low dose ICS
consider SABA only therapy if infrequent short lived wheeze & normal lung function after SABA
Step 3 for asthma management
SABA + low dose ICS + long acting beta agonist (LABA) ± leukotriene receptor antagonist (LTRA)
LTRA only used if pt shows response to it
examples of LABA include salmetarol
Step 4 for asthma management
SABA
Low dose ICS + LABA in a MART regime ± leukotriene receptor antagonist (LTRA)
MART = maintenance & deliver therapy i.e. 1 inhaler as preventer and reliever
Step 5 for asthma management
SABA + moderate dose ICS in MART ± leukotriene receptor antagonist (LTRA)
can also consider separate ICS & LABA inhalers
Step 6 for asthma management
Options include
- seek expert help
- try high dose ICS as a separate inhaler
- trial of long acting muscarinic receptor antagonist (LAMA)
- trial of theophylline
Acute asthma exacerbation
an acute/subacute episode of progressive worsening of symptoms of asthma
generally a clinical diagnosis
Risk factors for severe exacerbation of asthma
previous near fatal asthma previous admission for asthma need ≥3 medication for control non compliance/denial of illness obesity smoking/second hand smoke ≥1 severe exacerbations in last 12 months
Presentation of Acute exacerbation of asthma
dyspnoea/wheeze/cough -worsening -no response to salbutamol tachycardia, tachypnoea accessory muscle use hypoxia, altered mental status silent chest paradoxical breathing exhaustion
Moderate acute asthma exacerbation
PEFR 50-75% sats ≥92% normal speech RR <25 HR <110
severe acute asthma exacerbation
PEFR 33-50% sats ≥92% can't complete sentences RR ≥25 HR ≥110
life threatening acute asthma exacerbation
PEFR <33% sats <92% silent chest/cyanosis/poor respiratory effort bradycardia/dysrhythmia/hypotension altered consciousness
near fatal acute asthma exacerbation
indicated by a ↑ PCO2 / normal PCO2 or need for mechanical ventilation
indicates exhaustion
Severity of acute asthma exacerbation
may be moderate, severe, life threatening or near fatal
depends on PEFR, RR, sats, HR, ability to complete sentences and PCO2
Management of acute asthma exacerbation
ABCDE assessment, ABG
O2 via non rebreather mask (target sats 94-98%)
SABA e.g. salbutamol
- via spacer or O2 driven nebuliser
- 5mg
- 4 puffs + 2 puffs every 2 min for up to 10 puffs
- nebs can be back to back, but monitor K+
Ipratropium bromide
- 500 micrograms via nebuliser
- can be given with salbutamol but not back to back
Steroids
- 100mg hydrocortisone IV
- 40-50mg prednisolone PO for minimum 5 days
IV Magnesium sulphate
IV amiophylline
ITU support for airway management
-make sure you call for help early
Discharge criteria post acute asthma exacerbation
stabile on discharge medications for 12-24h
no use of nebulisers for >24h
inhaler technique checked & recorded
PEFR >75% of best/predicted
if life threatening then GP follow up organised within 2 days of discharge
Chronic obstructive pulmonary disease (COPD)
a lung disease characterised by airway obstruction that is not fully reversible leading to persistent respiratory symptoms
the airflow limitation is usually progressive & is associated with an abnormal inflammatory response in the lungs
usually diagnosed in people in the 50s
Aetiology of Chronic obstructive pulmonary disease (COPD)
smoking*** (~90% of cases)
alpha-1 anitrypsin deficiency
air pollution
fine dust
Presentation of Chronic obstructive pulmonary disease (COPD)
chronic productive cough dyspnoea (especially exertional) wheeze barrel chest nail clubbing peripheral oedema hyperresonant lung
Investigations of Chronic obstructive pulmonary disease (COPD)
FEV1/FVC
- <70%
- no reversibility
CXR
- hyperinflation & bullae
- flat hemidiaphragm
- also to exclude lung cancer
FEV1 (↓)
FBC (
Investigations of Chronic obstructive pulmonary disease (COPD)
FEV1/FVC
- <70%
- no reversibility
CXR
- hyperinflation & bullae
- flat hemidiaphragm
- also to exclude lung cancer
FEV1 (↓)
FBC (↑ haematocrit, anaemia)
Severity of Chronic obstructive pulmonary disease (COPD)
Mild (Stage I)
- FEV1/FVC <70%
- FEV1 >80%
- symptoms must be present for diagnosis
Moderate (Stage II)
- FEV1/FVC <70%
- FEV1 50-79%
severe (Stage III)
- FEV1/FVC <70%
- FEV1 30-49%
very severe (Stage IV)
- FEV1/FVC <70%
- FEV1 <30%
Management of Chronic obstructive pulmonary disease (COPD)
Smoking cessation***
pulmonary rehabilitation
Step 1
- asthmatic features present = LABA + ICS + SABA
- no asthmatic features = LABA (e.g. salmeterol) + LAMA (e.g. tiotropium) + SABA
Step 2
- SABA (PRN)
- LABA + LAMA + ICS for everyone
Step 3:
-trial of theophylline
Oral prophylactic Abx
- azithromycin (1st line)
- do ECG to exclude QT prolongation & LFTs
- give to pts who don’t smoke, have optimised treatment but have frequent exacerbations
Long term O2 therpay
-if pt fits criteria
Features suggesting steroid responsiveness in Chronic obstructive pulmonary disease (COPD)
I.e. asthmatic features
- previous history of asthma / atopy
- ↑ eosinophils
- substantial variation in FEV1 (≥400ml)
- substantial diurnal variation in PEFR (≥20%)
Most important intervention in Chronic obstructive pulmonary disease (COPD) management
smoking cessation
vital in any pt that still smokes
Acute exacerbation of Chronic obstructive pulmonary disease (COPD)
defined as an acute worsening of respiratory symptoms that results in addition therapy needs
one of the most common reasons for pts to present to the hospital
Aetiology of Acute exacerbation of Chronic obstructive pulmonary disease (COPD)
Most commonly viral
haemophilus influenzae (most common) strep pneumonia (most common bacterial cause) Others: mortadella catarrhalis, staph aureus
Presentation of Acute exacerbation of Chronic obstructive pulmonary disease (COPD)
↑ dyspnoea ↑ cough ↑ wheeze ↑ volume/purulence of sputum fevers, chills, sore throat ↓ exercise tolerance respiratory distress (dyspnoea, tachypnoea, confusion, cyanosis, peripheral oedema) respiratory failure
Investigations for Acute exacerbation of Chronic obstructive pulmonary disease (COPD)
ABG
-↓PaO2, ↑PaCO2, pH <7.35
CXR
- hyperinflation, flattened diaphragm
- possible consolidation if infection
sats (↓)
sputum/blood cultures
ECG, FBC, U&Es
Management of Acute exacerbation of Chronic obstructive pulmonary disease (COPD)
↑ dose & frequency of SABA via inhalers with spacers
oral steroids:
- 30mg prednisolone for 7-14 days
- consider osteoporosis prophylaxis if requiring frequent courses
Abx (PO)
- if sputum purulent / clinical signs of pneumonia
- amoxicillin / clarithromycin / doxycycline (all 1st line on BNF)
O2 if below target sats
consider NIV
-for persistent hypercapnia respiratory failure
consider IV theophylline
-if poor response to bronchodilators
Small cell lung cancer (SCLC)
also known as oat cell carcinoma, is a malignant epithelial tumour arising from the cells lining the lower respiratory tract
~15% of all lung cancer
rapidly growing & highly malignant, spreading early (almost always inoperable at presentation)
seen generally in older adult smokers (both active & passive smoking is a risk factor)
Presentation of Small cell lung cancer (SCLC)
dyspnoea, cough, haemoptysis, chest pain weight loss, fatigue dysphagia, hoarseness, wheezing/stridor recurrent pneumonias superior vena cava syndrome
Investigations for Small cell lung cancer (SCLC)
CXR
- central mass
- hilar lymphadenopathy
- pleural effusion
CT chest/abdo/pelvis
-investigation of choice
bronchoscopy ± biopsy
PET scan
Management of Small cell lung cancer (SCLC)
consider pts in early stages for surgery
generally chemo + radiotherapy = management of choice
if extensive disease = palliative chemo
Complications of Small cell lung cancer (SCLC)
Lambert-Eaton syndrome:
- myasthenia like syndrome
- antibody against presynaptic voltage-gated calcium channel
SIADH
-leading to hyponatraemia
ACTH secretion
-leads to bushings syndrome & adrenal hyperplasia
Superior vena cava syndrome
-dyspnoea, face & arm swelling, periorbital & conjunctival oedema, pulseless JVP distension
Referral criteria for suspected lung cancer
referral to specialist on 2 week wait
- if CXR findings are suggestive of cancer
- if ≥40 y/o + unexplained haemoptysis
Urgent CXR (within 2 weeks)
- if age ≥40yrs + ≥2 of the following unexplained symptoms
- if age ≥40yrs + ≥1 symptom if they ever smoked
- cough
- fatigue
- SOB
- chest pain
- weight loss
- loss of appetite
Non-Small cell lung cancer (NSCLC)
a group of malignant epithelia tumours representing ~85% of all lung cancers
most common risk factor is active & passive smoking
Types of Non-Small cell lung cancer (NSCLC)
Squamous (42& of NSCLC)
- often central presenting as obstructive lesion of bronchus leading to infection
- local spread common but metastasis occur relatively late
adenocarcinoma (39% of NSCLC)
- typically peripheral
- most common type of cancer in non-smokers
large cell lung carcinoma (8% of NSCLC)
- anaplastic, poorly differentiated tumours that metastasis early
- poor prognosis
carcinoid tumours (7% of NSCLC)
Bronchoalveolar tumour (4% of NSCLC) -associated with ++ sputum
Presentation of Non-Small cell lung cancer (NSCLC)
persistent cough haemoptysis dyspnoea chest pain weight loss fatigue anorexia hoarseness recurrent pneumonias superior vena cava syndrome
Investigations for Non-Small cell lung cancer (NSCLC)
CT chest/abdo/pelvis
-investigation of choice
CXR
- usually preliminary
- may show mass
bronchoscopy + biopsy
pet scanning
Management of Non-Small cell lung cancer (NSCLC)
surgery (indicated in ~20% of pts)
- lobar resection
- lobectomy
curative or palliative radio therpay
generally poor responsiveness to chemo
Respiratory failure
the acute or chronic inability of the reparatory system to maintain adequate gas exchange leading to hypoxia ± hypercapnia
Types of respiratory failure
Type I respiratory failure:
- hypoxic respiratory failure
- PaO2 <8kPa
- PaCO2 normal
Type II respiratory failure:
- hypercapnic respiratory failure
- PaO2 <8kPa
- PaCO2 >6kPa
Aetiology of type I respiratory failure
COPD pneumonia pulmonary oedema pulmonary fibrosis asthma PE cyanotic congenital heart disease ARDS bronchiectasis obesity kyphoscoliosis
Aetiology of type II respiratory failure
COPD severe asthma (when pt is exhausted) drug overdose/poisoning muscular disorders severe ARDS
Presentation of respiratory failure
tachypnoea dyspnoea cyanosis tachycardia confusion ↓GCS arrhythmias hypercapnia (hypoventilation, headache, coma, asterix)
NB clinical features of the underlying cause will be present
Investigations for respiratory failure
ABG***
CXR, FBC, TFTs, U&Es, LFTs, CK, troponin, ECG, CT-CTPA
Management of respiratory failure
resuscitation & ABCDE assessment
treat underlying cause
Hypoxia
- O2
- CPAP (↑ O2)
- mechanical ventilation
Hypercapnia
- NIV/BIPAP (↑O2, ↓CO2)
- mechnaical ventilation
BIPAP (NIV) vs CPAP
CPAP helps ↑ O2 but doesn’t affect CO2
NIV/BIPAP helps ↑O2 & ↓CO2
Tuberculosis (TB)
an infectious disease caused by mycobacterium tuberculosis typically affecting the lungs
NB notifiable disease in the UK
spreads via inhalation of infected droplets
Types of Tuberculosis (TB)
Primary TB
latent TB/inactivated TB
secondary TB
-e.g. from reactivation of latent disease
miliary TB
-disseminated TB usually seen in immunocompromised pts
Risk factors for Tuberculosis (TB)
homelessness institutionalisation e.g. prisons alcohol/drug misuse HIV +ve immunocompromised crowded lying ethnic minority background travel to/heritage from high prevalence areas
presentation of Tuberculosis (TB)
cough fever haemoptysis night sweats malaise chest pain dyspnoea erythema nodosum
Investigations for Tuberculosis (TB)
CXR
- upper lobe opacities ± consolidation
- bilateral hilar lymphadenopathy
Sputum smear
- 3 samples needed
- uses Ziehl-Nielsen staining
Sputum culture
- gold standard
- helps asses drug sensitivity
- take a long time to get back
NAAT
-can help with rapid diagnosis
mantoux test
- to screen for latent TB
- alternative is inferno-gamma test (if mantoux test is inconclusive)
Management of Tuberculosis (TB)
Active TB:
- 2 months of rifampicin + isoniazid + pyrazinamide + ethambutol
- then 4 months of rifampicin + isoniazid
Latent TB:
- 3 months of rifampicin + isoniazid
- alternatively 6 months of isoniazid
NB isoniazid is always given with pyridoxine to prevent peripheral neuropathy
Side effects of Tuberculosis (TB) drugs
Rifampicin:
- enzyme inducer
- orange secretions
- hepatitis
Isoniazid:
- enzyme inhibitor
- agranulocytosis
- hepatitis
Pyrazinamide:
- hyperuraemia (gout)
- arthralgia
- hepatitis
Ethambutol:
- optic neuritis
- monitor visual acuity
Pneumonia
inflammation of the lungs with consolidation & interstitial infiltration most commonly caused by bacteria
Types of pneumonia
Community acquired pneumonia (CAP):
-pneumonia acquired outside hospital/healthcare facilities
Hospital acquired pneumonia (HAP):
-pneumonia acquired >48h after admission to hospital
Atypical pneumonia
-caused buy atypical organisms e.g. legionella
Causes of pneumonia
CAP:
- strep pneumoniae (most common)
- H. Influenzae, staph aureus, mycoplasma pneumoniae
HAP:
- <5 days = strep pneumoniae
- > 5 days = H.influenzae ± staph aureus (also pseudomonas or MRSA)
In alcoholics the usually cause is klebsiella pneumoniae
NB pneumonia post H.influenzae is often caused by staph aureus
Risk factors for pneumonia
infants/young children elderly smoking alcohol misuse asthma COPD malignancy immunosuppression IVDU hospitalisation
Presentation of pneumonia
cough with purulent sputum fever malaise dyspnoea chest pain (pleuritic) tachycardia hypoxia bronchial breathing & crackles on auscultation dullness on percussion
Investigations for pneumonia
CXR
-new consolidation
FBC (↑ WCC)
CRP (↑)
U&Es
Blood cultures
Scoring system for pneumonia
CURB65 score -C = Confusion -U = Urea >7.0 mmol/L -R = RR ≥30 -B = BP ≤90/60 =65 = age ≥65yrs
Score 0-1 = home based care
Score ≥2 = consider hospital care
Score ≥3 = intensive care assessment
NB in primary care the CRB65 score can be used, i.e. leaving out the urea
Management of Community acquired pneumonia (CAP)
low severity:
- 5 days of amoxicillin
- 5 days of clarithromycin/erythromycin if penicillin allergy)
moderate severity:
-7 days of amoxicillin + macrolide e.g. erythromycin
high severity:
-co-amoxiclav, ceftriaxone, tazocin
NB clarithromycin is contraindicated in pregnancy so if pregnant & allergic to penicillin then use erythromycin, otherwise clarithromycin tends to be favoured
Management of Hospital acquired pneumonia (HAP)
Consider broad spectrum IV Abx
then tailor treatment when sensitivities available
generally based on local guidelines & sensitivities
Aspiration pneumonia
results from the inhalation of oropharyngeal secretions or stomach contents into the lower airways leading to chemical pneumonitis, lung injury and resultant bacterial infection
most commonly seen in hospitals & care homes
Risk factors for Aspiration pneumonia
impaired consciousness poor mobility NBM advanced age swallowing disorders (e.g. oesophageal strictures, dysphagia) neurological disorders (e.g. strokes, MS, Parkinsons) poly pharmacy poor dental hygiene
Aetiology of Aspiration pneumonia
Similar to normal pneumonia
strep pneumoniae, staph aureus, H. influenzae, pseudomonas aeruginosa
IN alcoholics its frequently Klebsiella pneumoniae
Presentation of Aspiration pneumonia
fever, headache, N&V, anorexia, myalgia cough dyspnoea pleuritic chest pain purulent sputum tachycardia ↓ breath sounds on auscultation crackles on auscultation dullness on percussion
Investigations for Aspiration pneumonia
CXR
- new consolidation
- or atelectasis
FBC (↑WCC, neutrophilia)
sputum & blood cultures
Management of Aspiration pneumonia
- tracheal suction if aspiration is noticed early
- mechanical removal of object via bronchoscopy (e.g. in children)
- Abx treatment as per pneumonia
- NB if severe then IV/PO co-amoxiclav
NB remember to be mindful of pts swallow with PO meds even Abx
Sarcoidosis
a chronic granulomatous disorder of unknown aetiology characterised by non-caseating granulomas commonly affecting the lungs, skin and eyes, its a diagnosis of exclusion
NB lungs are affected in 90% of pts
Epidemiology of sarcoidosis
most commonly seen in young adults (20-40y/o)
more common in people of african or northern european/scandinavian origin
Presentation of sarcoidosis
- erythema nodosum
- swinging fever
- polyarthralgia (common in acute attacks)
- dyspnoea, non productive cough
- weight loss, night sweats, fatigue
- lupus pernio (violaceous soft infiltration of skin of nose/cheeks)
- anterior & posterior uveitis
- lymphadenopathy
NB acute attacks are more common in white populations remitting after 2yrs
Investigations for Sarcoidosis
CXR
- bi-hilar lymphadenopathy
- bilateral infiltrations
FBC
- anaemia
- leukopenia
mantoux test
- negative
- to exclude TB
spirometry:
-restrictive pattern
Ca2+ (↑), ACE levels (↑)
U&Es, phosphate, LFTs
Pleural effusion
a collection of fluid between the pleural & visceral pleural surfaces in the thorax i.e. the pleural cavity
Aetiology of pleural effusion
Transudates (<30g/L of protein)
- HF (most common cause of transudates)
- cirrhosis, hypoalbuminaemia, hypothyroidism, nephrotic syndrome, meigs syndrome (bening ovarian tumour causing ascites + pleural effusion)
Exudates (>30g/L of protein)
- pneumonia (most common)
- malignancy (often cause large unilateral effusion)
- especially breast & lung cancer
- RA, SLE, PE, TB, pancreatitis, Dresslers syndorme
Haemothorax
- pleural effusion due to blood
- usually secondary to trauma
Presentation of Pleural effusion
small effusions <300ml are usually asymptomatic
dyspnoea, pleurite chest pain, dry non productive cough dullness on percussion ↓ breath sounds ↓ chest expansion ↓ tactiel vocal remits
signs & symptoms of underlying cause will be present
Investigations for Pleural effusion
CXR
- blunting of costophrenic angles
- opacification of lung fields with fluid level
Pleural fluid analysis
- from USS guided aspiration
- pH, protein, LDH, cytology, microbiology
USS + aspiration
CT/MRI (helps find underlying cause)
NB use lights criteria if protein levels between 25-35g/L i.e. borderline of transudate & exudate
Management of Pleural effusion
treat underlying cause
therapeutic thoracentesis (avoid taking >1.5L as it can cause fluid shift leading to pulmonary oedema)
pleurodesis
chest drain / long term indwelling pleural drainage
Criteria for pleural effusion
Lights criteria
-used if protein level 25-35g/L in pleural fluid to differentiate transudate & exudate
Criteria for pleural effusion
Lights criteria:
used if protein level 25-35g/L in pleural fluid to differentiate transudate & exudate
Exudate is likely if one of the following
- pleural fluid protein divided by serum protein >0.5
- pleural fluid LDH divided by serum LDH >0.6
- pleural fluid LDH >2/3 of upper limit of serum LDH
Pneumothorax
a collection of air in the pleural cavity leading to partial or complete collapse of the lung
Types of Pneumothorax
Primary spontaneous Pneumothorax (PSP)
-usually seen in health young people
Secondary spontaneous Pneumothorax (SSP)
- in pts with pre-exisitng lung disease
- e.g. rupture of bullae in COPD
Traumatic pneumothorax
-traumatic cause
Tension pneumothorax
- life threatening emergency
- usually post trauma
Presentation of Pneumothorax
dyspnoea pleuritic chest pain with sudden onset ipsilateral reduced breath sounts ipsilateral hyper resonance on percussion tachypnoea hypoxia tachycardia
Investigations for Pneumothorax
CXR
- visible rim on air between lung margin & chest wall
- absence of lung markings
consider CT or USS
-usually for complex cases
Management of Primary spontaneous Pneumothorax (PSP)
<2cm rim of air + pt not SOB
- consider discharge
- repeat CXR to check resolution
> 2cm or symptomatic pt
-attempt simple aspiration
If aspiration failed i.e. >2cm rim of air or still SOB
-chest drain
Management of Secondary spontaneous Pneumothorax (SSP)
pt >50y/o / rim >2.0cm / pt SOB
-chest drain
Rim of air = 1-2cm
- trial of aspiration
- if it fails = chest drain
Rim of air <1cm
-admit for 24h of observation ± O2
Tension Pneumothorax
life threatening emergency usually seen post trauma
presents with respiratory distress (hypoxia, cyanosis, diaphoresis, dyspnoea, tachypnoea), haemodynamic instability (hypotension, tachycardia), trachea is deviated away from affected side
this is a clinical diagnosis and should be treated immediately (do not wait for imaging)
treatment includes emergency needle decompression & chest drain insertion
Obstructive sleep apnoea (OSA)
a clinical condition in which there is intermittent & repeated upper airway obstruction during sleep leading to poor sleep quality & frequent arousals
- apnoeas (≥10sec pauses in breathing) - hypopnoea (≥10sec periods with breathing ↓50%)
pone of the most common causes of secondary hypertension
Risk factors for Obstructive sleep apnoea (OSA)
obesity*** male gender smoking excess alcohol consumption macroglossia acromegaly hypothyroidism
adenotonsilar hyperplasia especially in children
Presentation of Obstructive sleep apnoea (OSA)
sleep partner complains of excessive snoring or describes apnoeas
daytime somnolence snoring waking headaches unrefreshing sleep sleep fragmentation irritability
Investigations for Obstructive sleep apnoea (OSA)
Epworth sleepiness scale (asses for daytime sleepiness)
- score >10 suggests need for investigation
- score >18 / Road traffic accident or near miss = urgent referral
Polysomnography
-≥5 respiratory events e.g. apnoea/hypopnoea/arosals per hour associated with OSA symptoms
Management of Obstructive sleep apnoea (OSA)
weight loss
smoking cessation avoid alcohol/sedative
CPAP (gold standard)
- 1st line in moderate/severe OSA
- acts as pneumatic splint maintaining airway patency
- min 4h per night
BiPAP
-considered if hypoventilation or COPD
Mandibular advancement splints
-alternative to CPAP if mild/moderate OSA or intolerant to CPAP
Driving and Obstructive sleep apnoea (OSA)
must inform DVLA & stop driving until adequate control is achieve i.e. ↓daytime sleepiness
Pulmonary hypertension
a rise in mean pulmonary arterial pressure (mPAP) which can be due to a variety of use
defined as ↑ mean PAP ≥25 mmHg at rest
Idiopathic Pulmonary hypertension (PAH)
a rare disorder defined by ↑ pulmonary arterial pressure & ↑ pulmonary vascular resistance with normal pulmonary artery wedge pressure in the absence of a known cause
often severe and rapidly progressing
treated with high dose calcium channel blockers
Aetiology of Pulmonary hypertension
Group 1:
-idiopathic
Group 2:
-secondary to left heart disease, Valvular heart disease or restrictive cardiomyopathy
Group 3;
-secondary to chronic lung disease or environmental hypoxaemia
Group 4:
-due to chronic thrombotic disorders, embolic disease or both
Group 5:
-metabolic disorders, haematological disease & systemic illness
NB generally the most common causes are severe respiratory or cardiac disease
Presentation of Pulmonary hypertension
progressive dyspnoea weakness fatigue exertional dizziness/syncope loud S2 (often split) ↑ JVP symptoms of right HF
Investigations for Pulmonary hypertension
Right heart catheterisation
-↑ PAP ≥25 mmHg at rest
CXR
-prominent R heart border
ECG, Echo, CT/MRI thorax
Management of Pulmonary hypertension
treat underlying cause
pulmonary vasodilators if acute deterioratio
if idiopathic PH (PAH) give high dose calcium channel blockers
Cor Pulmonale (Pulmonary heart disease)
altered structure (hypertrophy/dilation) or impaired function of the right ventricle due to pulmonary hypertension
diagnosed via echo
prominent signs of right sided HF will be present
Cystic fibrosis (CF)
autosomal recessive disorder causing ↑ viscosity of secretion due to defect in the cystic fibrosis transmembrane conductance regulatory gene (CFTR) which codes cAMP-regulated chloride channels
80% of cases in UK are due to delta F508 (DF508)
most common inherited condition in white populations
Presentation of Cystic fibrosis (CF)
- meconium ileus in neonates (very indicative fo CF)
- failure to thrive
- recurrent chest infections (causes include staph aureus, pseudomonas, Burkholida cepacia, aspergillus)
- malabsorption, steatorrhoea, pancreatitis
- CF related diabetes
- nasal polyps
- clubbing
- cholestasis, cholecystolithiasis
- subfertility/infertility
Investigations for Cystic fibrosis (CF)
Newborn screening
- +ve on newborn blood spot test
- day 5-7 post birth
Sweat test
- +ve
- > 60mmol/L of sweat chloride
genetic testing
-for CFTR gene
lung function tests
sinus X-ray/CT
Genetics of Cystic Fibrosis (CF)
autosomal recessive disorder of cystic fibrosis transmembrane conductance regulatory gene (CFTR)
80% of cases in UK are due to delta F508 (DF508) gene
Management of Cystic fibrosis (CF)
regular chest physio & postural drainage
- twice a day minimum
- should be taught from young age
high calorie diet
-with high fat intake
minimise contact with other CF pts
-to prevent spread of burkholdia cepacia
Vitamin supplementation & pancreatic enzyme supplementation
if DF508 +ve
-trial lumacaftor or Ivacaftor
Bronchiectasis
an abnormal, irreversible dilation in the bronchial tree caused by cycles of bronchial inflammation leading to mucous plugging & progressive airway destruction
~70% of cases are in older women
Aetiology of Bronchiectasis
post-infective (most common cause)
-TB, measles, pertussis, pneumonia
cystic fibrosis, primary ciliary dyskinesia/Kartengers syndrome, immunodeficiency & HIV, bronchial obstruction e.g. malignancy, allergic brochopulmonary aspergillosis, COPD
Presentation of Bronchiectasis
chronic productive cough with copious mucopurulent sputum (may be blood stained)
dyspnoea
chest pain
clubbing
On auscultation
- coarse early inspiratory crackles
- rhonchi (low pitch snore like noises)
- wheeze
Investigations for Bronchiectasis
CXR
- baseline CXR for all pts
- ~90% of pts have abnormal CXR
- tram lines, fluid levels, ring shadows
high resolution CT chest (HRCT)
- gold standard
- bronchial wall dilation
- bronchial wall thickening
Sputum MC&S
-H.influenzae is the most commonly isolated
routine bloods, serum immunoglobulins, serum electrophoresis, antibody screening, ciliary function tests, lung function tests
Management of Bronchiectasis
Influenza & pneumococcal vaccines
chest physio & postural drainage
inspiratory muscle training
Abx for acute exacerbation
-1st line : amoxicillin/clarithromycin/doxycyline
Long term Abx
-if ≥3 expectations per year requiring Abx or exacerbations causing significant morbidity
Bronchodilators
-after assessing reversibility of airflow obstructions
surgery
-if localised disease
Asbestosis
a type of pneumoconiosis
Asbestosis
a type of pneumoconiosis caused by inhalation of asbestos fibres occurring primarily as a result of occupational exposure
severity is related to length of exposure, with a 20-30 year latent period
presents with gradual onset dyspnoea/SOB, ↓ exercise tolerance ± wheezing/productive cough, with fine bilateral inspiratory crackles, clubbing, cor pulmonale
Investigated with CXR (lower zone linear interstitial fibrosis & pleural thickening), pulmonary function tests (restrictive patterns), HRCT
no specific management available
Causes of upper zone lung fibrosis
Acronym for causes of upper zone fibrosis:
CHARTS C - Coal worker's pneumoconiosis H - Histiocytosis/ hypersensitivity pneumonitis A - Ankylosing spondylitis R - Radiation T - Tuberculosis S - Silicosis/sarcoidosis
Mesothelioma
an aggressive neoplasm arising from mesothelial cells lining the pleural cavity associated with asbestos exposure, more commonly seen in men aged >75yrs
often locally advanced but rarely metastasises
presents with dyspnoea, chest wall pain, weight loss, clubbing, painless pleural effusion
investigated with CXR (unilateral pleural effusion, irregular pleural thickening), CT, thoracoscopy
management includes radiotherapy, chemo and surgery
prognosis is poor, with median survival <12 months
Occupational asthma
pts with asthma may preset with concerns that chemical at their work are worsening their symptoms
OR
on history taking symptoms appear better at weekends / on holidays /away from work
Occupational asthma
pts with asthma may preset with concerns that chemical at their work are worsening their symptoms
OR
on history taking symptoms appear better at weekends / on holidays /away from work
most commonly associated with isocyanates
investigated with serial PEFR at work & away from work
treated by respiratory specialist
Silicosis
common occupational lung disease caused by inhalation of crystalline silica dusts commonly seen in mining, slate works, foundries and potteries
presents with chronic cough, sputum, exertional dyspnoea, fatigue, weight loss
investigated with CXR (egg-shell calcification of hilar lymph nodes, bilateral diffuse ground glass opacities), spirometry (restrictive pattern)
no definitive treatment
NB
Caplan syndrome - pneumoconiosis + RA
Coal workers pneumoconiosis (Black lung disease)
occupational lung disease caused by long term exposure to coal dust particles, severity linked to extent of exposure
may present with simple pneumoconiosis (often asymptomatic, often incidentally found)
may progress to progressive massive fibrosis (PMF) which presents as SOB on exertion & cough + black sputum
Investigated with CXR (upper zone fibrosis), spirometry (mixed obstructive / restrictive picture)
managed with irritant avoidance & supportive care
Interstitial lung disease (ILD)
a heterogenous group of disorders characterised by inflammation & progressive scarring (fibrosis) of the lung
Aetiology of Interstitial lung disease (ILD)
Idiopathic pulmonary fibrosis (IPF)
hypersensitivity pneumonitis (extrinsic allergic alveolitis) -Pigeon breeders lung, farmers lung, bird fanciers lung
pneumoconiosis
-asbestosis, coal workers lung, silicosis
radiation pneumonitis
Medication
- amiodarone, bleomycin, methotrexate
- nitrofurantoin, sulfalazine, cabergoline
cocaine sarcoidosis vasculitis sarcoidosis TB
Medications causing Interstitial lung disease (ILD)
- amiodarone
- bleomycin
- methotrexate
- nitrofurantoin
- sulfalazine
- cabergoline
- bromocriptine
Presentation of Interstitial lung disease (ILD)
progressive dyspnoea -exertional dyspnoea → dyspnoea at rest persistent non productive cough fatigue clubbing bibasal inspiratory crackles/rales cyanosis
Investigations for Interstitial lung disease (ILD)
CXR
- reticular opacities
- ground glass opacities
CT/HRCT
- honey combing
- traction bronchiectasis
Spirometry
- Restrictive pattern i.e. ↓FEV1 & ↓FVC
- normal/↑ FEV1/FVC
bronchoalveolar lavage & biopsy
Management of Interstitial lung disease (ILD)
smoking cessation
supportive therapy
- O2
- pulmonary rehab
- vaccination e.g. influenza/pneumococcal
lung transplant
-end stage ILD
For Idiopathic pulmonary fibrosis (IPF)
-antifibrotic agents e.g. pirfenidone
Idiopathic pulmonary fibrosis (IPF)
no underlying cause found
usually seen in men aged 50-75yrs
consider treating with antifibrotic agents e.g. pirfenidone
