Respiratory Flashcards
What is a common organism which causes pneumonia in bird owners?
chlamydia psittaci
cavitating pneumonia in the upper lobes, mainly in diabetics and alcoholics suggest what?
Klebsiella pneumoniae
Long term use of what can precipitate restrictive lung disease?
Nitrofurantoin
Which condition is immune deficiencies such as hypogammaglobulinemia associated with?
Bronchiectasis
What type of picture do you get on pulmonary function testing in asbestosis?
Restrictive - FEV1 goes down, FVC goes down A LOT therefore overall FEV1/FVC increases
What is the investigation of choice for occupational asthma?
Peak flows at work and home
What is the pathogen involved in Farmer’s lung?
Saccharopolyspora rectivirgula
Chlamydophila psittaci is associated with what?
Contact with birds
How should any critically ill patient be managed with oxygen?
15L high flow oxygen via non-rebreather as hypoxia kills before hypercapnia
What should you aim for in step down treatment of asthma?
reduction of 25-50% in the dose of inhaled corticosteroids
pulmonary fibrosis predominantly affecting the lower zones
Asbestosis
How would opiate overdose present on blood gas?
Respiratory acidosis
Redcurrant jelly sputum is found in what?
Klebsiella pneumonia
What is the COPD exacerbation treatment?
- Give O2 if <90%; Venturi 24% mask at 2-3l or nasal cannula flow rate 1-2l/min; Target oxygen sats 88-92%
- Nebulised bronochodilators: salbutamol (beta adrenergic agonist) or ipratropium (muscarinic antagonis)
- Steroid therapy: 30mg oral pred od for 5d or IV hydrocortisone
- Consider need for Abx: amoxicillin 500mg 3x d for 5d (or clarithromycin or doxy) or if at high risk of treatment failure then co-amoxiclav 500/125mg 3xd for 5d
- IV Theophylline if not responding to bronchodilators
- Non invasive ventilation e.g. BIPAP (if develop T2resp failure)
Why does hypotension occur in tension pneumothorax?
Cardiac outflow obstruction
Most common organism causing infective exacerbation of COPD?
H influenzae
30-40 year old with basal emphysema and abnormal LFTs
Alpha-1-antitrypsin deficiency
Fine end-inspiratory crepitations
pulmonary fibrosis
Investigation of choice for sleep apnoea?
Polysomnography
Coal workers’ pneumoconiosis causes what?
Upper zone fibrosis
What should be sent with diagnostic pleural taps?
- Biochemistry to determine protein
- Cytology
- Microbiology for gram staining and culture
What is important to remember about lung cancers?
Lesion can sometimes be too small to see on CXR
Paratracheal lymph nodes should raise alarm bells for?
Lung cancer
Sarcoidosis can cause what?
Hypercalcaemia
What is atelectasis?
A post op complication when the airways become blocked by bronchial secretions leading to respiratory collapse
- Managed with chest physio and positioning the patient upright
Normal/raised total gas transfer with raised transfer coefficient
Asthma
Lung collapse vs pleural effusion on CXR?
Lung collapse - trachea pulled towards the side of the white out
Pleural effusion - trachea pulled away from the side of the white out
Management of bronchiectasis?
Muscle training + postural drainage techniques
Patients who have frequent COPD exacerbations should have home supply of what?
Abx plus prednisolone
Investigation of choice for pulmonary fibrosis?
High res CT
Pack years formula
No of packs per day (1 pack is 20) x no of years smoking
Everyone over the age of 5 should have what to diagnose asthma?
Spirometry with bronchodilator reversibility testing
ENT, respiratory and kidney involvement
Think of Granulomatosis with polyangiitis
A negative result on spirometry does not what?
Exclude asthma -> FeNO testing needed
What pattern on lung function does bronchiectasis have?
Obstructive
When should Abx be given for COPD exacerbation?
- If purulent sputum or signs of pneumonia
Facial rash plus lymphadenopathy
Sarcoidosis
Cavitating lesions are associated with what?
Squamous cell carcinoma
increased FEV1/FVC ratio and reduced transfer factor
Pulmonary fibrosis
Which paraneoplastic syndrome is associated with squamous cell carcinoma?
Parathyroid hormone related protein secretion
Decrease in pO2/FiO2 in poorly patient with non-cardiorespiratory presentation
ARDS
Neuromuscular disorders present how on pulmonary function tests?
Restrictive pattern
How is asthma diagnosed on spirometry?
Improvement in FEV1 by > 15% following administration of bronchodilator
How does salbutamol work?
Stimulates ß2 receptors of respiratory tract, which increases sympathetic activity and relaxes bronchial smooth muscle.
What physiological measurement is used to determine the severity
of COPD?
FEV1
What must patients do to qualify for long term oxygen therapy?
Stop smoking
What are some examination signs of consolidation?
Reduced chest expansion, dull percussion note, increased tactile
vocal fremitus, increased vocal resonance, bronchial breathing.
Why should statins and macrolides not be given together?
Increased risk of myositis
What are some complications of pneumonia?
- Resp failure
- Sepsis
- Empyema
- Lung abscess
- Shock
How would pleural effusion present on examination?
- Reduced chest expansion
- Stony dull to percuss
- Reduced breath sounds
How would pneumothorax present on examination?
- Reduced chest expansion
- Hyper resonant on percussion
- Reduced breath sounds
What is an indication for surgery in bronchiectasis?
If the disease is localised to one lobe
Massive PE + hypotension
Thrombolysis
What is used to guide if patients need Abx with acute bronchitis?
CRP levels - if >100 -> offer Abx
multiple lip telangiectases
Think hereditary haemorrhagic telangiectasia -> strong association with epistaxis
Investigation of choice for suspected PE in someone with renal impairment?
V/Q scan
When should LTOT be started for COPD patients?
When 2 measurements of pO2 are < 7.3
pO2 of 7.3 - 8 AND polycythaemia/peripheral oedema/pulmonary HTN
Causes of upper zone fibrosis
C - coal workers pneumoconiosis
H - histiocytosis
A - ankylosing spondylitis
R - radiation
T - TB
S - Silicosis/Sarcoidosis
Causes of lower zone fibrosis
D - drugs
A - asbestosis
I - idiopathic
M - Most connective tissue disorders except AS
Non-obs based admission criteria for asthma?
- Previous near fatal attack
- Pregnancy
- Oral steroids not helping with symptoms
Bilateral parotid gland swelling can be indicative of what?
Sarcoidosis
What are some complications of bronchiectasis?
Pneumonia, sepsis, recurrent infections, resp failure
What is the mechanism of PE?
T1 Resp failure due to V/Q mismatch
Pemberton’s test
Test for SVC obstruction - raise arms above head and they go cyanosed
Non respiratory causes of pulmonary fibrosis
- Amiodarone, methotrexate
- RA
- SLE
- Sjogrens
- UC
ECG signs of cor pulmonale
- right axis deviation
- P pulmonale
Causes of bilateral hilar lymphadenopathy
Lymphoma, TB, Sarcoidosis, bronchial carcinoma
What are extra-pulmonary manifestations of sarcoidosis?
- Erythema nodosum
- Anterior uveitis
- Neuropathy
- Cardiomyopathy
- CN palsies
Where should pleural tap needle be inserted?
Above rib to avoid neurovascular bundle
What could an area of dull to percuss in someone with a pneumothorax suggest?
Haemothorax -> needs chest drain
Lung cancer can present as what?
SVC obstruction
What helps to reduce mortality in someone with ARDS?
Low tidal volume mechanical ventilation
Uncompensated type 2 resp failure with pH <7.35
Think about non invasive ventilation
Radiation exposure can cause what?
Lung cancer
What is the pathophysiology of ARDS?
Diffuse bilateral alveolar injury due to inflammation
Previous history of haemorrhagic stroke at any time is a C/I to what?
Thrombolysis
Excessive daytime sleepiness with visual hallucinations
Narcolepsy -> multiple sleep latency test needed
What is PERC criteria used for?
To rule out PE
What are indications for steroids in sarcoidosis?
PUNCH
Parencymal lung disease
Uveitis
Neuro involvement
Cardio involvement
Hypercalcaemia
Large round well circumscribed masses in the lungs?
Cannonball metastases -> renal cell carcinoma
Investigations for lung cancer?
- CXR
- CT with contrast
- Bronchoscopy
Raised platelets can be a sign of what?
Lung cancer
When are Abx used in acute bronchitis?
If there are existing co-morbidities
Preceding influenza predisposes you to what?
Staph aureus pneumonia
What is the treatment for latent TB?
3 months of isoniazid and rifampicin or 6 months of isoniazid
How should patients with acute asthma who do not respond to medical treatment and become acidotic be managed?
Intubation and Ventilation
Where should needle thoracostomy be placed?
cannula into the second intercostal space in the midclavicular line on the affected side
egg shell calcification of lymph nodes?
Silicosis
What are causes of resp alkalosis?
- Anxiety
- PE
- Stroke, sub arachnoid
- Altitude
What are causes of resp acidosis?
- COPD
- Neuromuscular disease
- Sedating drugs like benzos/opiates
Pneumothorax management
- Asymptomatic -> conservative care
- If symptoms and high risk -> chest drain
- If symptoms and not high risk -> can manage conservatively/needle aspiration
How should pneumothorax be followed up when managed conservatively?
- If primary -> review every 2-4 days as outpatient
- If secondary -> monitor as inpatient
- Everyone should be reviewed in outpatients in 2-4 weeks
CURB65 criteria
Confusion
Urea > 7
RR > 30
BP <90 systolic or <60 diastolic
Aged > 65
Community acquired pneumonia treatment
0 - treat at home - Amoxicillin/Clarithromycin
1-2 - consider hospital - Amoxicillin + Clarithromycin
3-4 - urgent hospital - Co-amoxiclav or
+ Clarithromycin
Hospital acquired pneumonia treatment
No severe signs: Co-amoxiclav
Sever signs: Piperacillin with Tazobactam
Exudate vs Transudate pleural effusion
Exudate - >30
Transudate - <30
What are exudative causes of pleural effusion?
- Pneumonia
- RA/SLE
- Neoplasia
What are transudative causes of pleural effusion?
- HF
- Liver disease
- Hypothyroidism
How to diagnose mesothelioma?
- CXR
- Pleural CT with biopsy
- Thoracoscopy can be used
Types of non small cell lung cancer?
- Large cell
- Squamous cell
- Adenocarcinoma
What paraneoplastic features do lung cancers have?
Small cell
- SIADH
- Cushings
- Lambert-Eaton
Squamous
- PTHrP
- Hypercalcaemia
- Hypertrophic pulmonary osteoarthropathy
Adenocarcinoma
- Gynaecomastia
How long should patients hold breath when taking inhaler?
10 seconds after pressing down on cannister
Wait 30 seconds before repeating next dose
What is Churg Strauss syndrome?
Eosinophilic granulomatosis with polyangiitis -> asthma features with pANCA positive
What is the triangle of safety?
- Located in the mid axillary line of the 5th intercostal space
- Bordered by anterior edge of latissimus dorsi, lateral border of pectoralis major, line superior to the horizontal level of the nipple
Where is aspiration pneumonia most common?
- Right middle and lower lobes
How is alpha 1 antitrypsin deficiency inherited?
Autosomal recessive
How can A1AD be managed?
- Obstructive picture on spirometry
- Supportive treatment with bronchodilators
- Lung volume reduction surgery can be done in severe cases
Moderate asthma features
PEFR 50-75% best or predicted
Speech normal
RR < 25
Pulse < 110
Acute severe asthma features
PEFR 33-50% best or predicted
Can’t complete sentences
RR > 25
Pulse > 110
Life threatening asthma features
PEFR < 33% best or predicted
Sats <92%
Normal PCO2
Silent chest, cyanosis or poor resp effort
Bradycardia/Hypotension
Exhaustion/Confusion/Coma
What are some blood tests for sarcoidosis?
- elevated ACE, ESR, calcium, immunoglobulins
- Deranged LFTs
ECG signs of PE
- Sinus tachycardia
- Right BBB
- S1 Q3 T3
Complications of recurrent or untreated PE?
- Pulmonary HTN
- Right sided heart failure
Surgical interventions for COPD?
- Bullectomy
- Lung reduction surgery
Extra-respiratory manifestations of cystic fibrosis
- Pancreatic insufficiency
- DM
- Cirrhosis
- Nasal polyps
- Sinusitis
- Male infertility
- Osteoporosis
Over rapid aspiration/drainage of pneumothorax can result in what?
Reexpansion pulmonary oedema
What test should be offered to all patients with TB?
HIV
What size of pneumothorax would be indicated to do a needle aspiration?
> 2cm
Bilateral, mid-to-lower zone patchy consolidation in an older patient
Legionella
Deranged LFTs, hyponatraemia, low lymphocytes?
Legionella
Mycoplasma pneumonia can cause what?
Immune mediated neurological diseases e.g Guillan Barre
Pneumonia + red cell agglutination?
Mycoplasma
Large bullae in COPD can mimic what?
Pneumothorax
Why should intranasal decongestants not be used for prolonged periods?
Risk of tachyphylaxis -> increasing doses are needed
What is the Abx of choice for acute bronchitis?
Doxycycline
When to use NIV vs IV?
NIV - 7.25 - 7.35
IV - <7.25
What is used to assess drug sensitivities in TB?
Sputum culture
Staph aureus pneumonia is associated with what?
Cavitating lesions
What is the gold standard test for TB?
Sputum culture
HIV decreases what?
Sensitivity to sputum smear for TB
Investigation to diagnose mesothelioma?
Thoracoscopy with histology
Pneumonia with cold sores?
Strep pneumoniae
Marked volume loss of the lung with thickening of the pleura?
Think mesothelioma
What is the management of empyema?
Chest drain insertion for drainage + IV Abx
What is the advice around air travel following pneumothorax?
No travel until full resolution on CXR
Acute asthma steps
- Oxygen
- Nebulised salbutamol
- Oral steroids
- Nebulised Ipratropium
- IV Mag Sulph
- IV Aminophylline -> discuss with seniors
- Intubation and Ventilation in HDU/ITU
What is criteria for discharge following asthma exacerbation?
- Stable on discharge meds for 12-24 hours
- Inhaler technique checked
- PEFR > 75%
Asthma stepwise management for adults
- SABA
- SABA + ICS
- SABA + ICS + LTRA
- SABA + ICS + LABA (+LTRA if helping)
- SABA + MART (ICS+LABA) (+LTRA if helping)
- SABA + medium dose MART (+LTRA if helping)
- Seek help from secondary care
Asthma stepwise management for children
- SABA
- SABA + ICS
- SABA + ICS + LTRA
- SABA + ICS + LABA
- SABA + MART
- SABA + medium dose MART
- Seek help from secondary care
COPD stepwise medical Mx
- SABA or SAMA
- SABA + LABA + LAMA if no asthma features OR SABA + LABA + ICS if asthma features
- SABA + LAMA + LABA + ICS (even if no asthma features)
- Seek help from secondary care
What would chronic bronchitis COPD show on V/Q?
Low V/Q due to decreased ventilation
What would emphysema COPD show on V/Q?
High V/Q due to loss of alveolar surface area causing more ventilation per available perfusion area
CXR signs for COPD
- Hyperinflated chest
- Bullae (if large may mimic pneumothorax)
- Decreased peripheral vascular markings
- Flattened diaphragm
Where will pancoast tumours be?
- Same side as the Horner’s signs
- At the lung apex
Heart sounds
1st - mitral/tricuspid
2nd - aortic/pulmonary
Split second heart sound with loud pulmonary component?
Cor pulmonale
TB Treatment
RIPE - 2 months
RI - 4 more months
Management of secondary pneumothorax which is not improving post chest-drain insertion?
Discuss with cardiothoracic
Diffuse alveolar damage with hyaline membrane formation
Acute respiratory distress syndrome
Pleural effusions due to rheumatoid arthritis have what?
Low glucose levels
massive haemoptysis
Think lung abscess
What does a pancoast tumour invade when it causes Horners?
Cervical sympathetic plexus
bilateral pulmonary infiltrates
Think ARDS
Patient with swallowing difficulties/previous stroke with resp pathology?
Think lung abscess
What is the initial management of hypercalcaemia?
IV Fluids
What pharmacological therapy can be used for idiopathic pulmonary fibrosis?
Pirfenidone / Nintedanib
What is a pneumothorax?
Air in the pleural cavity which is the potential space between the visceral and parietal pleura
Where do you measure for pneumothorax?
Chest wall to the outer edge of the lung at level of hilum
What are surgical options for recurrent pneumothorax?
Video assisted thorascopic surgery
Surgical pleurodesis
PE like symptoms following a percutaneous vertebroplasty?
Pulmonary cement embolism
diffuse bilateral opacities on x ray?
Think ARDS
Management of solitary pulmonary nodules?
CT guided needle aspiration biopsy if >8mm
Unilateral pleural effusion?
Rule out malignancy
Why can people with carbon monoxide poisoning have?
Normal O2 sats as monitors cannot differentiate between the 2
Investigation of choice for pnemocystitis jiroveci?
Bronchoalveolar lavage
Acute bronchitis?
LRTI which causes inflam in bronchial airways causing oedematous large airways and sputum production.
Normally resolves in 3w but 25% will have cough after
Mx for acute bronchitis?
- self-care: NSAIDs/paracetamol; honey; stop smoking; seek help if systemically unwell or don’t improve after 3-4w
- Abx if indicated but not routine (only shortens cough by half a day and S/Es & resistance)
When to offer Abx for acute bronchitis?
- Immediate= systemically unwell
- Consider= high risk of Cx eg. CF, immunosupression, comorbid condition; >65yrs with 2 or >80yrs with 1: DM, hospital admission <1yr, CHF, take corticosteroids
- Back-up prescription= if not needed but pick up if worse rapidly
- CRP levels
When to offer Abx for acute bronchitis based on CRP levels?
CRP <20= not routine
CRP 20-100= consider delayed
CRP >100= Abx
Abx for acute bronchitis if indicated?
Oral doxycycline 200mg 1st day then 100mg OD for 4d
pregnant or 12-17yrs = amoxi 500mg 3xd 5d
or clarithro
Cause of acute bronchitis?
uncertain but likely virus; 80% cases in autumn/winter
CP of acute bronchitis?
- cough: productive or not
- sore throat
- rhinorrhoea
- may have wheeze
- low grade fever
Differentiate acute bronchitis from pneumonia?
Hx= sputum, wheeze, breathlessness may be absent in AB but at least one present in P
Ex= no other focal chest signs (dullness to percussion, creps, bronchial breathing) in AB except wheeze. Systemic symptoms more likely in pneumonia (malaise, myalgia, fever)
Ix for acute bronchitis?
CLINICAL
- CRP can be used to guide if Abx therapy indicated
Who can not take doxycycline?
children or pregnant women, use amoxicillin instead
Allergic rhinitis?
inflam disorder of nose that occurs when nasal mucosa becomes exposed and sensitised to allergens, to produce typical symptoms of sneezing, nasal itching, rhinorrhoea and congestion
What type of inflam reaction is allergic rhinitis?
IgE mediated
Classification of allergic rhinitis?
Mild or moderate to severe or..
- seasonal eg. grass, pollen (hayfever), around same time every yr
- perennial (throughout yr) eg. dust mites, animals
- intermittent= <4d a w or <4 consecutive w
- persistent= >4d a w AND >4 consecutive w
- occupations (allergens in work environment)
When does allergic rhinitis usually begin?
childhood/adolescence
Cx of allergic rhinitis?
reduced QOL, impaired school/work performance, disturbed sleep, reduced conc, possible development of: asthma, sinusitis, nasal polyps
Features of allergic rhinitis?
- occurs after exposure to known causative allergen
- sneeze, nasal itch, rhinorrhoea, congestion, post-nasal drup
- associations: allergic conjunctivitis, asthma, eczema
Mx for allergic rhinitis?
- ?saline nasal irrigation
- allergen avoidance
- prn intranasal antihistamine or non-sedating oral
- regular intranasal corticosteroids during allergen exposure for moderate to severe or if inital Mx ineffective
- review 2-4w if persist
- refractory= intranasal antihis + corticosteroid spray
- ? add on eg. short course intranasal decongestant, intranasal anticholinergic or LTRA
- severe uncontrolled: short course oral corticosteroids
When to refer to allergy or ENT for allergic rhinitis?
- Red flags
- unresponsive to Mx
- allergy testing may be needed if think its house dust mite or animal
- uncertain
Why should nasal decongestants eg. oxymetazoline not be used for prolonged periods?
Increasing doses will be needed to achieve same effect (tachyphylaxis) and rebound hypertrophy of nasal mucosa (rhinitis medicamentosa) may occur upon withdrawl
Types of allergy tests?
- skin prick
- Radioallergosorbent test (RAST)
- skin patch
Skin prick allergy test?
- most common
- drops of diluted allergen placed on skin after which the skin in pierced with needle
- large no. allergens can be tested in 1 session
- Normally incl. histamine (+ve) and sterile water (-ve control)
- a wheal will typically develop if pt has allergy after 15minds
- good for food allergy and pollen
Radioallergosorbent test for allergy?
- determines amount of IgE that reacts with suspected or known allergens eg. IgE to egg protein
- results given in grades: 0 (-ve) to 6 (strongly +ve)
- good for food allergies, inhaled allergens (eg. pollen) and wasp/bee venom
- when skin prick not suitable eg. extensive eczema or pt taking antihistamines
Skin patch allergy testing?
- useful for contact dermatitis
- 30-40 allergens placed on back
- irritants may also be tested for
- patches are moved 48hrs later with results being read by derm after further 48hrs
Food allergy describes what?
adverse immune-mediated response which occurs when person is exposed to specific food allergen(s).
IgE mediated food allergy produces what?
immediate and consistently reproducible multi-organ symptoms
Common food allergies?
cow’s milk, eggs, peanuts and other legumes, tree nuts, shellfish, fish and wheat
RFs for development of food allergy?
pre-existing food allergy, atopic eczema, FHx food allergy and/or atopy
Possible Cx of food allergy?
- severe/life-threatening rections (incl. anaphylaxis)
- anxiety
- reduced QOL (restrictions, social interactions, peer pressure, stigma, embarrassment, social exclusion)
- restricted diet and malnutrition
When should diagnosis of IgE mediated food allergy be suspected?
classic symptoms develop within secs or mins to 1-2hrs after ingestion of trigger food:
- urticaria
- angioedema
- itching
- cough
- hoarseness
- wheeze
- SOB
- N & V
- diarrhoea
- abdo pain
consider if unexplained persistent symptoms of atopic eczema
Assessment of suspected IgE mediated food allergy?
- examine nutritional status and signs of clinical reaction/comorbid conditons + Hx
- arrange skin prick testing and/or serum-specific IgE allergy testing
Referral for pt with food allergy?
- A&E= systemic symptoms or ?anaphylaxis
- allergy specialist= multiple; uncertain; signif atopic eczema; Hx of systemic symptoms or increased risk anaphylaxis; persistent food allergy
- Dietician= nutritional concerns or already on restricted diet
Mx of food allergy?
- individualised written allergy Mx plan
- advise on prompt recognition and Mx of acute symptoms= immediate oral antihistamines (cetirizine or chlorphenamine if <2yrs) for non-severe symptoms or adrenaline auto-injector for suspected anaphylaxis
- review annually
Systemic symptoms of food allergy that suggest anaphylaxis?
resp distress; wheeze; hypotension; tachy or bradycradia; drowsiness; confusion; collapse; loss of consciousness
Differential diagnosis for IgE-mediated food allergy?
- acute spontaneous urticaria and angioedema (no allergic trigger, often following viral infection)
- carcinoid syndrome
- food intolerance (non-immune, non-specific reactions, delay in CP and prolonged symptoms)
- food poisoning and toxic reactions
- food aversion or refusal
- IBS/IBD
- urticaria
- asthma exacerbation
- atopic dermatitis
- coeliac
- GORD
- gastroenteritis
Mx of IgE mediated allergy vs non-IgE mediated?
IgE= skin prick or bloods specific for IgE antibodies
Non-IgE= eliminate suspected allergen for 2-6w then introduce; consult dietician about nutritional adequancies, timing and follow up
IgE-mediated food allergy vs Non-IgE mediated presentation?
IgE:
- anaphylaxis
- skin= pruritus, erythema, urticaria, angioedema
- GI= N, V, D, colicky abdo pain
- Resp= URT symptoms (nasal itching, sneezing, rhinorrhoea, congestion); LRT symptoms (cough, wheeze, chest tightness, SOB)
Non-IgE:
- skin= pruritus, erythema, atopic eczema
- GI= GORD; loose/frequent stool; blood/mucus in stool; abdo pain; infantile colic; food refusal or aversion; contipation; perianal redness; pallor/tired; faltering growth + other symptoms above
Sensitivity to latex may cause what problems?
- type I hypersensitivity (anaphylaxis)
- type IV hypersensitivity (allergic contact dermatitis)
- irritant contact dermatitis
Latex allergy is more common in who?
children with myelomeningocele spina bifida
Latex-fruit syndrome?
people who are allergic to latex are also allergic to fruits, particularly: banana, avocado, pineapple, kiwi, chestnut, mango, passion fruit, strawberry
Oral allergy syndrome?
aka pollen-food allergy
IgE mediated hypersensitivity reaction to specific raw, plant-based foods incl. fruits, vegetables, nuts and certain spices.
How does oral allergy syndrome (pollen-food allergy) typically present?
mild tingling or pruritus of lips, tongue and mouth
How is the hypersensitivity reaction in oral allergy syndrome initiated?
by cross-reaction with non-food allergen, most commonly birch pollen whereby the protein in food is similar but not identical in structure to original allergen (explains why OAS strongly linked with pollen allergies & why cooking culprit food prevents symptoms-denatures the protiens)
What is oral allergy syndrome (OAS) strongly linked with?
pollen allergies and seasonal variation
What can you do to prevent symptoms occurring in oral allergy syndrome?
cooking culprit food- denatures the proteins
OAS vs food allergy?
- food allergy= direct sensitivity to a protein present in food. OAS= cross-sensitisation to a structurally similar allergen present in pollen
- food allergens can be caused by plant or non-plant foods but OAS is not caused by non-plant foods
- OAS normally limited to oropharynx but food allergies more likely to cause systemic symptoms (V&D)
Why do non-plant foods not cause OAS but food allergies can be caused by plant and non-plant foods?
OAS= no cross-reactive allergens in pollen which would be structurally similar to meat
Food allergy= allergens occur in response to substances that are more stable and able to survive stomach enzymes and acid processing and cooking
Why are food allergies more likely to cause systemic symptoms (eg. V&D) but OAS is limited to oropharynx?
Food allergy= allergens are not readily broken down
OAS= proteins that cause the symptoms are denatured by stomach enzymes
About 1/2 of pts with general pollen allergy and 3/4 pts with allergy to birch pollen (most common allergen in UK) report symptoms of what?
OAS
Associations with OAS?
- birch pollen allergy (most common)
- Rye grass pollen allergy
- Rubber latex allergy
Presentation of OAS?
- suspect in pts with Hx of seasonal allergy symptoms and present with symptoms mins after eating a specific raw food
- itching, tingling of lips, tongue and mouth
- mild swelling and redness of lips, tongue and throat may occur
- severe= N&V
- fully resolve within 1hr of contact
- anaphylaxis very rare
Ix for OAS?
- clinical but can use allergy testing to rule out food allergies if Hx unclear
Mx for OAS?
- avoid culprit foods
- can take oral antihistamine if get symptoms
- inform that once cooked it shouldn’t cause symptoms
Many pts who report an allergy to penicillin may be describing what?
intolerance/side efects eg. diarrhoea or a coinincidental rash eg. amoxicillin in pts with infectious mononucleosis
0.5-6.5% of pts who are allergic to penicillin are also allergic to what?
cephalosporins
Pts with Hx of immediate hypersensitivity to penicillin should not receive a what? What if it is essential because an alternative Abx is not available?
Cephalosporin.
If pt needs cephalosporin then can use: cefixime, cefotaxime, ceftazidime, ceftriaxone or cefuroxime with caution.
AVOID= cefaclor, cefadroxil, cefalexin, cefradine and ceftaroline fosamil
Types of penicillin? (to be aware of to avoid accidental prescription if pt has allergy)
- phenoxymethylpenicillin
- benzylpenicillin
- flucloxacillin
- amoxicillin
- ampicillin
- co-amoxiclave (Augmentin)
- co-fluampicil (Magnapen)
- piperacillin with tazobactam (Tazocin)
- ticarcillin with clavulanic acid (Timentin)
Allergic reactions to venom eg. after insect bite/sting may be considered as long or systemic, what does this mean?
- Local= redness, swelling, pain limited to skin and soft tissues directly related to the site of venom exposure but spreading >10cm from the site
- Systemic= cutaneous reactions that are relatively distant from the exposure site eg. widespread redness, itching, urticaria and/or angioedema (not affecting mouth or throat)
Anaphylaxis may occur with/without evidence of systemic cutaneous reaction & any reaction there is any airway compromise or signs of haemodynamic compromise should be managed as anaphylactic in nature
Mx of venom allergy eg. after insect bite or sting?
Supportive: remove stingers by scraping sideways with fingernail or card; cold compress; avoidance of scratching to prevent secondary infection.
Can use oral paracetamol/ibuprofen for pain, topical hydorcortisone and oral antihistamines eg. chlorphenamine to reduce itching.
When should referral to an allergy specialist be made for pt with venom allergy (insect bite or sting)?
if pt has had or suspected of having a systemic reaction
Testing for venom allergy is recommended in who?
pt with a history of systemic reaction causing airway compromise or haemodynamic instability
Mx for pt with history of previous reaction to insect bite/sting which presented with airway and/or haemodynamic compromise and raised levels of venom-specific IgE on skin prick or in vitro testing?
Venom immunotherapy (VIT)
Baseline tryptase level should be preformed to exclude indolent mastocytosis or monoclonal mast cell activation syndrome
What can asbestos cause in the lung?
- Pleural plaques
- Pleural thickening
- Asbestosis
- Mesothelioma
- Lung cancer
What are pleural plaques (can be caused by asbestos)?
benign and do NOT undergo malignant change
- don’t require follow uo
- most common form of asbestos related lung disease
- occur after a latent period of 20-40yrs
What is pleural thickening (can be caused by asbestos)?
asbestos exposure can cause diffuse pleural thickening in similar pattern seen following an empyema or haemothorax
What is asbestosis (can be caused by asbestos)?
- Typically causes lower love fibrosis
- severity linked to length of exposure (contrast to mesothelioma- limited exposure can cause disease)
- Patent period 15-30yrs
Features of asbestosis?
- SOB & reduced exercise tolerance
- clubbing
- bilateral end-inspiratory crackles
- restrictive pattern with reduced gas transfer on lung function tests
What do lung function tests show for asbestosis?
restrictive pattern with reduced gas transfer
Treatment for asbestosis?
conservative as no interventions offer signif benefit
What is mesothelioma?
Cancer of the mesothelial layer of the pleural cavity that is strongly associated with asbestos exposure (other m. layers may be affected eg. abdo in small no. of cases).
- Latent period= 30-40yrs
- Even very limited exposure to asbestos can cause it
Most dangerous form of mesothelioma?
Crocidolite (blue) asbestos
Possible features of mesothelioma?
- progressive SOB
- chest wall pain
- painless pleural effusion (30%)
- 20% have pre-existing asbestosis
- weight loss
- clubbing
- 85-90% have Hx of asbestos exposure
Mx for mesothelioma?
- palliative chemo, surgery if operable
- industrial compensation
- prognosis v. poor= median survival from diagnosis of 8-14m
Most common form of cancer associated with asbestos exposure?
LUNG cancer most common
Mesothelioma also associated but less common
What is important for pt to do if they smoke and have a history of asbestos exposure?
smoking cessation as the risk of lung ca in smokers who have history of asbestos exposure is very high
Overview of the malignancy in mesothelioma?
- malignancy of mesothelial cells of pleura
- mets to contralateral lung and peritoneum
- R lung affected more than L
Ix and diagnosis for mesothelioma?
- CXR shows pleural effusion or pleural thickening
- get pleural CT= if area of pleural nodularity seen then image-guided pleural biopsy
- pleural effusion present= send fluid for MC&S, biochemistry and cytology
- cytology -ve exudative effusion= local anaesthetic thoracoscopy
DIAGNOSIS= histology following thoracoscopy
Asthma?
chronic inflam condition of the airways: airways are hyper-responsive and constrict easily in response to wide range of stimuli. May result in coughing, wheezing, chest tifhtness and SOB.
Suspect asthma in who (CP)?
- wheeze, breathlessness, chest tightness, cough
- Diurnal= worse at night and early morning
- occur in response to exercise, allergen exposure, cold air; occur after taking NSAIDs, BB; occur in absence of URTI
- Hx of atopic disorder
- Widespread bilateral polyphonic expiratory wheeze
- may be triggered by emotion and laughing in children
Ix that help support asthma diagnosis (not one single diagnostic test)?
- Fractional exhaled nitric oxide (FeNO) testing (sometimes primary care but may require referal). (ALL)
- Spirometry (all symptomatic pts >5yrs) then do Spirometry with bronchodilator reseversibility (BDR). (ALL).
- Peak expiratory flow (can do in ALL or if uncertain)
- direct bronchial challenge testing with histamine or methocholine (specialist referal needed) (if uncertain/negative results)
FeNO test for asthma?
in steroid naive adults…
+ve if 40ppb or higher (adults) or 35 in children (only do in children in uncertain after spirometry)
Spirometry test for asthma?
all symptomatic pts >5yrs (FeV1/FVC <70% is +ve result and suggest airflow obstruction).
THEN DO:
- Spirometry with bronchodilator reversibility (BDR): adults= improvement of 12%+ with increased volume of 200mL+ in response to SABA or corticosteroids is positive for asthma. Improvement >400mL in FEV1 is strongly suggestive. Children= improvement of FEV1 of 12%+ is positive.
Peak expiratory flow test for asthma?
Value of >20% variability after monitoring at least twice daily for 2-4w if positive for asthma. PEF variability calculated: difference between highest and lowest readings expressed as a % of the average PEF. Upper limit of normal is approx 20% using at lest PEF reading per day but may be lower when using twice daily readings.
Direct bronchial challenge testing with histamine or methocholine (specialist referal needed) for asthma?
PC20 value of 8mg/ml or less is positive. Offer if normal spirometry and FeNO of 40 but no variability in PEF or FeNO <40 but with variablility in PEF
When to diagnose, suspect or consider alternative diagnosis/refer for specialist opinion in asthma?
- DIAGNOSE= FeNO level 40ppb+ with either +ve BDR, +ve PEFV or bronchial hyperactivity. OR + BDR AND +ve PEFV irrespective of FeNO level.
- SUSPECT= obstructive spirometry with: -ve BDR, FeNO level 40+ or FeNO level 25-39 but with +ve PEFV
- alternative diagnosis/specialisgt if normal spirometry, FeNO and PEFV
What if suspect asthma in pt <5yrs?
use CP to determine likelihood and when reach 5 carry out the objective tests
Asthma Mx in pts aged 5-11yrs?
1) twice daily paeds low dose ICS + SABA
if can manage MART then…
2) paeds low dose MART
3) paeds moderate dose MART
4) refer to specialist
if can’t manage MART regimen then…
2) paeds low dose ICS + SABA + LTRA
3) paeds low dose ICS/LABA combination + SABA (+/- LTRA)
4) paeds moderate dose ICS/LABA combination + SABA (+/- LTRA)
5) Refer to specialist
Asthma Mx in pts aged 12yrs and older?
1) low dose ICS/formoterol combination inhaler (as needed AIR therapy)
2) low dose MART (regular low dose ICS/formoterol combination inhaler) (straight to this if symptoms v severe when diagnosed)
3) moderate dose MART
4) - FeNO level or blood eosinophils raised= refer to specialist
- Neither raised= trial LTRA or LAMA + moderate dose MART
- Not improved= stop & trial alternative
5) Refer to resp specialist
Asthma Mx for children <5yrs?
1) 8-12w trial of twice daily paeds low dose ICS then stop and review after 3m
2) if symptoms recur= restart low dose ICS (can titrate up to moderate) + SABA
3) consider another trial without Tx
4) still uncontrolled= trial ICS + SABA + LTTRA for 8-12w, stop if side effects or ineffective
5) still uncontrolled= stop LTRA and refer to specialist
When to refer to resp for pt with asthma?
if symptoms not controlled after all Mx steps, lower threshold for children
Follow up for asthma?
annual
FeNO testing in asthma can be effected by what?
inhaled corticosteroids
approx 1 in 5 with -ve result will have asthma
approx 1 in 5 with +ve result won’t have asthma
Red flags that suggest an alternative diagnosis to asthma and prompt immediate resp referral?
Adults= systemic features (myalgia, fever, weight loss); non-variable SOB; unexpected clincial signs (crackles, clubbing, cyanosis, cardiac disease, monophonic wheeze, stridor); chronic sputum; CXR shadowing; unexplained restricted spirometry; blood eosinophilia
Children= FTT; focal signs, abdnorm voice/cry, dysphagia, inspiratory stridor; symptoms present from birth; XS vomiting/posseting; severe URTI; persistent wet productive cough; FHx unusual chest disease; nasal polyps
Obstructive vs restrictive spirometry?
Obstructive:
- eg. asthma, COPD, bronchitis
- FEV1 decreased
- FVC normal or decreased
- FEV1/FVC ratio= <70%
Restrictive:
- eg. sarcoidosis, pulmonary fibrosis, interstitial lung disease, (conditions affecting chest wall, muscles or pleura)
- FEV1 decreased
- FVC decreased
FEV1/FVC= >=70%
Spirometry: FEV1 vs FVC?
FEV1= forced expiratory volume in 1 sec
FVC= forced vital capacity
How is complete control of asthma defined?
- no daytime symptoms
- no night waking due to asthma
- no need for rescue meds (SABA)
- no asthma attacks
- no limitations on activity incl exercise
- normal lung function (PEF >80% predicted or best)
- minimal side effects from meds
Advice for pt with asthma?
- keep up to date with routine vaccinations incl. annual flu
- avoid triggers
- weight loss and smoking cessation
- assess for anxiety/depression
- ensure pt has own peak flow meter
- explain how to use inhaler incl if using a spacer (can use tidal breathing, washed and dry in air)
- SABA for reliever therapy and ICS for preventer
Asthma MX: lose dose ICS?
400ug (micrograms) budesonide
if =<16yrs= 200ug
Asthma Mx: moderate dose ICS?
400-800ug budesonide
=<16yrs= 200-400ug
Asthma Mx: high dose ICS?
> 800ug budesonide
=<16yrs= >400ug
Asthma Mx: MART?
Maintenance and reliever therapy.
Pt takes the ICS/formoterol combination inhaler for maintenance and reliever therapy (regularly and as required); NOT just as required
Asthma Mx: as needed AIR therapy?
a low-dose inhaled corticosteroid (ICS)/formoterol combination inhaler to be taken as needed for symptom relief
this is termed anti-inflammatory reliever (AIR) therapy
MART is when this inhaler is took as needed and regularly also
When could you consider decreasing maintenance therapy for pts asthma?
once it has been controlled with their current maintenance therapy for at least 3m.
decrease ICS dose slow: every 3m by 25-50%
Monitoring pts for asthma?
Annually
But review response to Mx after 4-8w
- spirometry or peak flow
- advice on inhaler technique
- no. of attacks, ICS use, time off school/work due to asthma; nocturnal symptoms; adherence; hospital admissions
- use of SABA (overuse= >12 per hr)
If on long term steroid (>3m) then monitor= BP; HbA1c; cholesterol; BMD; vision
3 questions to ask every pt with asthma?
Have you had difficulty sleeping because of your asthma symptoms (including cough)?
Have you had your usual asthma symptoms during the day (e.g. cough, wheeze, chest tightness, or breathlessness)?
Has your asthma interfered with your usual activities (e.g. housework, work, school)?
Asthma Mx: SABA?
Short-acting beta-2 agonists
eg. salbutmol
rapid onset (<5mins) and last up to 4hrs
up to 4x a day (not exceding 4hrly)
Asthma Mx: LABA?
Long-acting beta-2 agonists
eg. salmeterol
last 12hrs
What drugs should pts with asthma avoid?
NSAIDs
Beta-blockers
Adverse effects of beta-2 agonists (SABA & LABA)
- fine tremor: hands, worse in 1st few days of Mx
- palpitations
- headache
- seizure
- hypokalaemia
- anxiety
- cardiac arrhythmia and paradoxoical bronchospasm (rare)
- acute angle-closure glaucoma
Use beta-2 agonists eg. SABA & LABA with caution in who?
- hyperthyroidism (may stimulate T activity)
- DM (rare risk ketoacidosis)
- CVD & HTN
- QT-prolongation
- hypokalaemia
- convulsive disorders
Asthma Mx: LTRA?
leukotriene receptor antagonist
eg. montelukast 10mg OD in evening
5-16yrs= 5mg
<5yrs= 4mg
What pts need hospital admission for acute exacerbation of asthma?
- all life-threatening
- severe which persists after initial bronchodilator Mx
- moderate with worsening symptoms despite BD Mx and/or had previous near fatal attack in past. Or if: <18yrs; poor treatment adherence; live alone; recent hospital admission; previous severe attack
Mx for acute exacerbation of asthma whilst awaiting admission to hospital?
1) supp O2 if hypoxia to maintain sats 94-98%
AND
2) severe= NEBULISED SALBUTAMOL (5mg) oxygen driven (flow rate 6L/min) over 30-60mins.
2) moderate= pressurised metered-dose inhaler with large volume spacer; 4 piuffs then 2 puffs every 2mins up to 10 puffs; can repeat every 10-20mins. (children-puff every 30-60secs up to 10puffs)
AND if severe/poor response
3) NEBULISED IPRATROPIUM BROMIDE (500ug adults, 250ug children). Do not repeat within 4hrs.
AND
4) give 1st dose of PREDNISOLONE (40-50mg adults, 30-40mg >5yrs, 20mg <5) ; if can’t swallow then IV hydrocortisone 100mg
AND
5) monitor PEF and O2 sats to assess response to Mx
6) short course oral pred
Mx for acute exacerbation of asthma if pt does not need hospital admission?
1) SABA via large volume spacer
AND
2) Adults= short course oral prednisolone
Acute exacerbation of asthma follow up?
within 48hrs if not admitted to hospital; or within 48hrs of discharge
- PEF and review CP
- check inhaler technique
- consider stepping up Mx
- advice on recognising poor asthma control and early signs of exacerbation (sudden persistent worsening symptoms)
- give oral corticosteroids to take if have early signs of exacerbation
When to consider referral to resp for asthma after acute exacerbation?
2 asthma attacks within 12m
Summary of Mx for acute exacerbation of asthma if pt is admitted to hospital and attack is severe/life-threatening?
1) NEBULISED SALBUTAMOL (5mg) oxygen driven (flow rate 6L/min) over 30-60mins.
AND
2) NEBULISED IPRATROPIUM BROMIDE (500ug adults, 250ug children)
AND
3) 1st dose of PREDNISOLONE (40-50mg adults, 30-40mg >5yrs, 20mg <5) ; if can’t swallow then IV hydrocortisone 100mg
How long should pt take oral pred after acute exacerbation of asthma?
5d
Moderate attack of asthma in children 2-5yrs?
SpO2 > 92%
No clinical features of severe asthma
Severe attack of asthma in children 2-5yrs?
SpO2 < 92%
Too breathless to talk or feed
Heart rate > 140/min
Respiratory rate > 40/min
Use of accessory neck muscles
Life-threatening attack of asthma in children 2-5yrs?
SpO2 <92%
Silent chest
Poor respiratory effort
Agitation
Altered consciousness
Cyanosis
Moderate attack of asthma in children >5yrs?
SpO2 > 92%
PEF > 50% best or predicted
No clinical features of
severe asthma
Severe attack of asthma in children >5yrs?
SpO2 < 92%
PEF 33-50% best or predicted
Can’t complete sentences in one breath or too breathless to talk or feed
Heart rate > 125/min
Respiratory rate > 30/min
Use of accessory neck muscles
Life-threatening attack of asthma in children >5yrs?
SpO2 < 92%
PEF < 33% best or predicted
Silent chest
Poor respiratory effort
Altered consciousness
Cyanosis
Normal pCO2 in acute asthma attack?
indicates exhaustion and should be classified as life-threatening
Near-fatal asthma?
Raised pCO2 and/or requiring mechanical ventilation with raised inflation pressures
Mx for pts who fail to respond to any intervention for acute asthma attack?
admit ITU/HDU for intubation and ventilation
Criteria for discharge after acute asthma exacerbation?
- been stable on their discharge medication (i.e. no nebulisers or oxygen) for 12-24 hours
- inhaler technique checked and recorded
- PEF >75% of best or predicted
When diagnosing asthma, what tests should all pts have?
Adults:
- spirometry with BDR
- FeNO test
5-16yrs:
- spirometry with BDR
- FeNO if normal S or obstructive S with -ve BDR
<5yrs:
- clinical
Asthma-COPD overlap syndrome (ACOS)?
pts with airway disease who have features of both asthma and COPD
10-30% of asthma and COPD pts
Criteria for asthma-COPD overlap syndrome?
- > 40yrs
- resp symptoms (eg. exertional dyspnoea) persistent but variability in symptoms may be prominent
- persistent airflow obstruction
- Hx of asthma or evidence of partial BDR
- exposure to a RF eg. >=10 pack yr tabacco smoking or equivalent indoor/outdoor air pollution
Pathophysiology of asthma-COPD overlap syndrome?
- Asthma= eosinophilic inflam, reversible airway obstruction and airway hyperresponsiveness
- COPD= neutrophilic inflam, irreversible airway obstruction and progressive airflow limitation due to alveolar destruction (emphysema) and chronic bronchitis
- ACOS= combination of both so more complex disease process
Mx for ACOS?
- smoking cessation, immunisation, inhaler technique
- SABA for symptomatic control
+ ICS (low or moderate) - can + LABA or LAMA
need specialist input as more exacerbations, lower QOL and decline in lung function and mortality worse in ACOS than just asthma or COPD
Bronchiectasis?
Persistent or progressive chronic debilitating disease characterised by permanent dilation of the bronchi due to irreversible damage to elastic and muscular components of the bronchial wall
What is bronchiectasis caused by?
inflam damage to airways:
irreversible damage to elastic and muscular components of bronchial wall causing permanent dilation of the bronchi
Clinical features of bronchiectasis?
- daily expectoration of large volumes of purulent sputum
- cough
- SOB
- haemoptysis
- non-pleuritic chest pain between exacerbations
- coarse crackles during early inspiration
- wheeze
- high pitched inspir squeaks
- large airway rhonchi (low pitched sore like sound)
- palpable chest secretions on coughing
Suspect bronchiectasis in adults with what?
- cough >8w with sputum production or Hx of trigger
- RA + chronic productive cough or recurrent chest infections
- COPD with 2+ exacerbations annually and/or +ve sputum culture for Pseudomonas aeruginosa whilst stable
- IBD + chronic productive cough
Suspect bronchiectasis in children with what?
- chronic productive cough unresponsive to 4w Abx, between viral colds or with +ve sputum culture for = s. aureus, H. influenza, P.aeruginosa, non-TB mycobacteria or Burkholderia capacia complex
- wet wough >6w
- asthma unresponsive to Mx
- severe pneumonia where symptoms, signs or radiological changes don’t complete resolve
- recurrent pneumonia
- localised chronic bronchial obstruction
- exertional SOB
- unexplained haemoptysis
- persistent & unexplained signs or CXR abnormalities
Ix for bronchiectasis?
- sputum culture
- CXR
- spirometry
- O2 sats
- and FBC incl WCC
- refer to resp to confirm diagnosis
Mx for infective exacerbation of bronchiectasis? (most in primary care but sometimes hospital admission may be needed)
- previous microbio cultures should guide Abx therapy
- if not available then local protocols, if not available then amoxicillin or clarithromycin/erythromycin
Signs on examination in bronchiectasis?
- Coarse crackles, especially in the lower lung zones.
- Wheeze.
- High-pitched inspiratory squeaks.
- Large airway rhonchi (low pitched snore-like sounds).
- Palpable chest secretions on coughing or forced expiratory manoeuvre, persisting over time.
- Finger clubbing (uncommon).
Clinical symptoms of bronchiectasis?
- Daily expectoration of large volumes of purulent sputum
- Dyspnoea
- Fever
- Fatigue, reduced exercise tolerance.
- Haemoptysis that can be frank (up to 10 mL) or massive (more than 235 mL) (26–51.2%).
- Rhinosinusitis.
- Weight loss.
- Chest pain that is present between exacerbations and is usually non-pleuritic
- Sputum colonization with P. aeruginosa.
- Young age at presentation.
- History of symptoms over many years.
- Absence of smoking history.
Differential diagnosis of bronchiectasis?
- asthma
- COPD
- chronic sinusitis
- pneumonia
- lung ca
- interstitial lung disease (asbestosis, hypersensitivity pneumonitis, pulmonary fibrosis, sarcoidosis)
- TB
When to suspect an infective exacerbation in pt with bronchiectasis?
- change in 1+ symptoms: increased sputum vol or purulence, worse SOB, increased cough or fatigue/malaise
- new symptoms eg. fever, pleuritic pain or haemoptysis
Ix in secondary care for bronchiectasis?
- high-resolution computed tomography (HRCT)= most frequently used to diagnose
- test for CF
- screen for gross antibody def eg. IgG, IgA, IgM= for all pts with confirmed diagnosis
- serum total IgE and specific IgE/skin prick test to Aspergillus (exclude allergic bronchopulmonary aspergillosis)
- specific antibody levels against strep pneumonia
could do= RF, anti-CCP, ANA and ANCA; HIV serology; A1AT def
What pts with bronchiectasis to be followed up in secondary care?
all to diagnose then
either follow up in primary care or
follow up in secondary care if:
- 3+ exacerbations in 1 yr
- chronic p.aeruginosa, MRSA or non-TB mycobacteria colonisation
- deteriorating or advanced disease
- allergic pulmonary aspergillosis
- long term Abx therapy
- associated RA, immune def, IBD, or primary ciliary dyskinesia
- considering lung transplant
Follow up for bronchiectasis?
- Baseline severity score= Bronchiectasis Severity Index
- Offer pulmonary rehab
- BMI
- check exacerbation Hx (refer for ?long-term prophy Abx if 3+ in 1yrs)
- sputum sample and culture (refer if chronic colonisation for p.a, mycobacteria or MRSA)
- MEDICAL RESEARCH COUNCIL DYSPNOEA SCALE
- spirometry
- O2 sats
- sputum clearance exercises compliance (refer to physio if havent been taught)
- Immunisation against influenza and strep pneumonia
- tell pt how to recognise exacerbations and what to do if get one
Arrange hospital admission for pt with bronchiectasis and?
- so unwell that need IV Abx (eg. cardioresp failure or sepsis)= cyanosis, confusion, marked SOB, rapid resps or laboured, peripheral oedema, 38C+
Mx for infective exacerbation of bronchiectasis if don’t need hospital admission?
- sputum for C&S before starting Abx but don’t wait for results
- Empirical Abx 7-14d (if already taking then stop and prescribe from different class)
- airway clearance technique
- Review Abx response once C&S available
- Offer a LABA but NOT ICS
- consider prophylactic Abx
Empirical Abx for acute exacerbation of bronchiectasis?
- amoxicillin 500mg 3td for 7-14d
or clarithromycin 500mg 2tds 7-14d
Prophylactic Abx for bronchiectasis if needed?
1st= azithromycin 500mg 3 times a week
min 6m but can use up to 1yr
If current P.aeruginosa= inhaled colistin
What should be done before starting pt on oral macrolides eg. azithromycin prophylaxis for bronchiectasis exacerbation?
- ECG: assess QT interval
- baseline LFTs
- baseline exacerbation rate
- microbio testing of sputum before starting
What should you do after starting pt on oral macrolides?
- LFTs 1m and then every 6m after starting
- ECG 1m after starting: if new QT prolongation then stop
What can cause bronchiectasis?
- Post-infective= TB, measles, pertussis, pneumonia
- CF
- bronchial obstruction eg. lung ca, forign body
- immune def: selective IgA, hypogammaglobulinaemia
- allergic bronchopulmonary aspergillosis (ABPA)
- ciliary dyskinetic syndromes: Kartagener’s, Young’s
- yellow nail syndrome
Summary of 3 features and 3 signs of bronchiectasis?
Features:
- persistent productive cough, large vol of sputum may be expectorated
- dyspnoea
- haemoptysis
Signs:
- abnormal chest auscultation= coarse crackles; wheeze
- clubbing may be present
Most common organisms isolated from pts with bronchiectasis?
- Haemophilus influenzae (most common)
- Pseudomonas aeruginosa
- Klebsiella spp.
- Streptococcus pneumoniae
Bronchiolitis?
Acute bronchiolar inflammation. Most common cause of serious lower resp tract infection in <1yr olds (90% are 3-6m).
Pathogen that causes bronchiolitis in 75-80% of cases?
Respiratory syncytial virus (RSV)
What provides protection to newborns against RSV (causing bronchiolitis)?
maternal IgG
Higher incidence of bronchiolitis when?
winter
Causes of bronchiolitis?
- RSV (most)
- mycoplasa, adenoviruses
- may be secondary bacterial infection
What can cause bronchiolitis to be more severe?
if bronchopulmonary dysplasia (eg. premature), congenital heart disease or CF
Features of bronchiolitis?
- coryzal symptoms (eg. mild fever) precede:
- dry cough
- increasing SOB
- wheezing, fine inspiratory crackles (not always)
- feeding difficulties
Most often reason for hospital admission due to bronchiolitis?
feeding difficulties associated with increased dyspnoea
Immediate hospital admission (999 ambulance) in pts with bronchiolitis when?
any of…
- apnoea
- looks seriously unwell
- severe resp distress= GRUNTING, marked chest recession, resp rate >70
- central cyanosis
- peristent O2 sats <92% on air
Consider hospital admission in pt with bronchiolitis when?
any of…
- resp rate >60
- difficulty feeding or inadequate oral fluid intake (50-75% of usual volume)
- clinical dehydration
Ix for bronchiolitis?
immunofluorescence of nasopharyngeal secretions may show RSV
Mx for bronchiolitis?
Whilst awaiting hospital admission= supp O2 to all pts with O2 sats <92%
- Largely supportive
- humidified O2 via head box if O2 sats persistently <92%
- NG feeding if can’t take enough fluid/feed my mouth
- suction sometimes used for XS upper airway secretions
How to determine the severity of a child’s condition with bronchiolitis?
- degree of agitation and consciousness (can be sign of hypoxia)
- signs of exhaustion, cyanosis and invl. of accessory muscles of respiration at rest
- examine chest, RR, pulse and BP
- O2 sats on air (pulse oximetry)
- hydration status= cap refill time, skin tugor and dryness of mucous membranes, urine output
Impending resp failure in pt with bronchiolitis may be indicated by what?
listlessness or decreased resp effort, recurrent apnoea, and/or failure to maintain O2 sats despite O2 supp
Low threshold for hospital admission in pt with bronchiolitis?
- <3m
- chronic lung disease
- haemodynamically signif congenital heart disease
- immunodef
- born premature (esp. <32w)
- long distance to healthcare in case of deterioration
What type of illness is bronchiolitis and when do symptoms tend to peak?
self-limiting
peak between 3-5d of onset
Mx advice is pt with bronchiolitis does not need hospital admission?
- paracetamol/ibuprofen for fever and then for as long as child appears distressed
- do not undress to try and reduce fever
- regular fluids
- check child regularly, incl. through the night
- seek medical advice is child deteriorates
Sign of deterioration in child with broncholitis?
- RR increaases
- episodes of apnoea, cyanosis, increased effort of breathing (grunting, nasal flaring, marked chest recession)
- fluid intake reduced to 50-75% of normal or signs of dehyration eg. dry mouth or no wet nappy for 12hrs
- less responsive
- worsening of fever
COPD stands for what?
chronic obstructive pulmonary disease
COPD?
Common treatable (but not curable) and largely preventable lung condition.
Persistent resp symptoms and airflow obstruction which is usually progressive and not fully reversible.
Major RF for development of COPD?
tobacco smoking
Cx of COPD?
reduced QOL and increased morbidity & mortality
Diagnosis/Ix for COPD?
- Clinical +
- Spirometry with BDR +
- CXR (exclude other causes) +
- FBC (identify anaemia or polycythaemia)
Spirometry findings in COPD?
A post bronchodilator FEV1/FVC of <0.7 (70%) confirms persistent airflow obstruction.
Mx for COPD?
- info
- smoking cessation
- pnumococcal and influenza vaccine
- pulmonary rehab
- self-management plan
- medical therapy
What is the use of ICSs in COPD associated with?
increased risk of pneumonia
When to refer to resp specialist in COPD?
- lung ca, cor pulmonale or bronchiectasis suspected
- very severe/worsening
- <40yrs and/or FHx of A1AT def
- uncertain
- O2 therapy, long-term non-invasive ventilation therapy, long-tern oral corticosteroids or lung surgery being considered
Referral for pulmonary rehab in COPD is indicated when?
- is functionally disabled by COPD
- has had recent hospitalisation for acute exacerbation
Emergency admission for pt with acute exacerbation of COPD if?
- severe SOB
- inability to cope at home/living alone
- poor or deteriorating condition
- acute confusion/impaired consciousness
- cyanosis or reduced O2 sats
- worsening peripheral oedema
- new arrhythmia
Mx of acute exacerbation of COPD not requiring admission?
- increased dose of SABA
- consider oral corticosteroids and an Abx
- seek medical help if worsen rapidly or signif
All pts with COPD should be what?
- followed up, frequency depending on their severity
- end-of-life issues should be discussed and advance care planning offered when appropriate
Signs and symptoms of COPD?
- SOB (persistent, progressive over time, worse on exertion)
- chronic/recurrent cough
- regular sputum production
- frequent LRTI
- wheeze
- waking up at night with SOB
- reduced exercise tolerance
- cyanosis
- raised JVP, peripheral oedema (may indicate cor pulmonale)
- cachexia
- hyperinflation of the chest
- use of accessory muscles and/or pursed lip breathing
- wheeze and/or crackles on auscultation
COPD auscultation?
wheeze and/or crackles
What may indicate cor pulmonale in COPD?
- ankle swelling (peripheral oedema)
- raised JVP
- systolic parasternal heave
- loud pulmonary second heart sound (over 2nd L ICS)
- hepatomegaly
What symptoms are uncommon in COPD?
chest pain and haemoptysis uncommon- consider other causes
Cor pulmonale?
RHF secondary to lung disease. Caused by pulmonary HTN as a consequence of hypoxia.
Stages of severity of airflow obstruction (COPD) according to reduction in FEV1?
Post-BD FEV1/FVC= <0.7 (70%)
AND
Stage 1= mild- FEV1 80% of predicted or higher
2= moderate- 50-79%
3= severe- 30-49%
4= very severe- <30% or <50% with resp failure
Medical Research Council (MRC) dyspnoea scale?
Grade 1= not troubled by SOB except during strenuous exercise
2= SOB when hurrying or walking up slight hill
3= walks slower than others on the level because of SOB or has to stop for breath when walking at own pace
4= stops for breath after walking about 100m or after few mins on the level
5= too SOB to leave the house, or breathless when dressing/undressing
Differential diagnosis for COPD?
- Asthma (nocturnal/variable symptoms, Hx atopic disease, non-smoker, <35yrs)
- Bronchiectasis (copious sputum, freq chest infect, Hx of childhood pneumonia, coarse lung crepitations)
- HF (SOB when lying flat, Hx of IHD, fine lung crepitations)
- Lung ca (persistent cough, haemoptysis, weight loss or persistent hoarse voice)
- Interstitial lung disease (dry cough, fine lung crepitations)
- Anaemia (fatigue, SOB, palpitations)
- TB (persistent productive cough, SOB, haemoptysis)
- CF
- Upper airway obstruction eg. tracheal tumour
Coarse crackles (crepitations)?
- louder, low pitch, long lasting
- like bubbling or crackling
- during inspiration and expiration
- typically in conditions where secretions or fluid present in larger airways:
- pnuemonia
- chronic bronchitis
- late-stage pulmonary oedema
- bronchiectasis
- COPD exacerbation
Fine crackles (crepitations)?
- soft, high pitched, brief
- like velcro being pulled apart or hair rubbing near the ear)
- mostly during inspiration
- often in conditions affecting alveoli or small airways:
- pulmonary fibrosis (common)
- interstitial lung disease
- early HF (pulmonary oedema)
Lung sounds associated with COPD?
- wheezing (due to airway narrowing)
- rhonchi (low pitch related to mucus in larger airways
- diminished breath sounds in later stages (air trapping and hyperinflation)
- coarse crackles during exacerbation
Crackles (crep) in pulmonary oedema?
fine crackles that may progress to coarse as fluid accumulates
- often associated with HF
Crackles (crep) in pulmonary fibrosis?
fine, late inspiratory crackles
“velcro crackles”
Crackles (crep) in bronchiectasis?
coarse crackles due to mucus build up in dilated airways
Crackles (crep) in pneumonia?
coarse crackles usually localised to area of lung infection
Early inspiratory crackles?
heard early during inspiration
often associated with chronic bronchitis or emphysema
Late inspiratory crackles?
heard later in inspiration
common in pulmonary fibrosis, HF and atelectasis
Examples of interstitial lung diseases?
asbestosis, pneumoconiosis, fibrosing alveolitis, sarcoidosis
Acute exacerbation of COPD definition?
sustained worsening of a pts symptoms from their usual stable state (beyond normal day to day variations)
Triggers of acute exacerbation of COPD?
- resp tract infections eg. rhinovirus, h.influenzae, s.pneumoniae, moraxella catarrhalis
- smoking
- envrionmental pollutants
Common trigger of COPD exacerbation?
H.influenzae (most common)
rhinovirus
many exacerbations won’t respond to Abx as not caused by bacterial infections
CP of COPD exacerbation?
increased…
- SOB
- cough
- sputum production & change in sputum colour
- wheeze and chest tightness
- URTI symptoms eg. cold, sore throat
- reduced exercise tolerange
- ankle swelling
- increased fatigue
- acute confusion
Differential diagnosis of COPD exacerbation?
- pneumonia
- PE
- pneumothorax
- acute HF
- cardiac ischaemia or arrhythmia
- lung ca
- upper airway obstruction
You should you not refer for pulmonary rehab if they have COPD?
- unable to walk
- unstable angina/recent MI
Oxygen is the treatment for what?
hypoxaemia not SOB
Inappropriate O2 therapy in pts with COPD may cause what?
resp depression
When to offer LTOT (long term O2 therapy) to pt with COPD?
Only after specialist assessment. Can improve survival in stable COPD and chronic hypoxia.
Refer for LTOT if…
- O2 sats 92% or less
- very severe or severe airflow obstruction
- cyanosis
- polycythaemia
- peripheral oedema
- raised JVP
Prophylactic Abx for COPD (initiated in secondary care)?
if have had 3+ exacerbating needing steroid therapy and at least 1 requiring hospital admission in previous yr= consider referral for Abx prophy
Azithromycin 500mg 3x per week for min 6-12m; assess benefit after 6m and 12m
Adverse effects of macrolides?
GI upset, hearing and balance disturbance, cardiac effects (prolongation of QTi) and microbio resistance
Follow up for COPD?
At least once per yr.
Very severe airway obstruction= twice per yr.
- MRC D scale to assess severity
- exacerbation freq and severity
- meds incl. inhaler technqiue
- smoking status and BMI
- annual flu vaccine and once-only pneumococcal
- Cx or cormorbities
- Spiraometry
- very severe= + pulse oximetry
What indicates rapidly progressing disease in COPD?
loss of 500ml or more over 5yr on spirometry
Target O2 sats for pt with COPD?
88-92% as risk of hypercapnia; adjust to 94-98% if pCO2 normal
SAMA?
short-acting muscarinic antagonist
eg. Ipratropium
slow onset: 30-60min and lasts 3-6hrs
LAMA?
long-acting muscarinic antagonists
eg. tiotropium
have prolonged binding to muscarinic receptors which lengthens duration of bronchodilator effect
SAMA for COPD?
ipratropium aerosol inhalation 1-2puffs (20-40ug) 3-4x daily
LAMA for COPD?
tiotropium (for maintenance)
Spiriva Respimat® 5 micrograms once daily by inhalation of aerosol (2 puffs is equivalent to 5 micrograms of tiotropium)
Causes of COPD?
- smoking!
- A1AT def
- cadmium (used in smelting)
- coal
- cotton
- cement
- grain
Why is the use of peak flow limited in COPD?
can underestimate the degree of airflow obstruction
Offer LTOT to who in COPD?
pO2 of <7.3kPa or those with pO2 of 7.2-8kpa and one of:
- secondary polycythaemia
- peripheral oedema
- pulmonary HTN
assessment done by ABG on 2 occasions at least 3w apart in pts with COPD stable
When to not offer LTOT to pt with COPD?
if continue to smoke despite being offered smoking cessation advice
Risk assessment for LTOT?
- smoking status
- risks of falls from tripping over equipment
- risk of burns and fires and increased risk of those who live in homes where someone smokes (incl. e-cigs)
Pts on LTOT for COPD should breathe the supp O2 for how long?
at least 15hrs a day
Things to do before starting azithromycin prophylaxis in pts with COPD who are indicated to have it?
- LFTS and ECG to exclude QT prolongation
- CT thorax to exclude bronchiectasis
- Sputum culture to exclude atypical infections and TB
What can reduce risk of COPD exacerbations in pts with severe COPD and Hx of freq exacerbations?
Phosophodiesterase-4 (PDE-4) inhibitors eg. roflumilast
If pt has COPD and is said to have ‘asthma features’ (which affects COPD mx) what are these?
- diagnosis of asthma or atopy
- raised esosinophil count
- substantial variation in FEV1 over time (at least 400ml)
- substantial dinural variation in PEFlow (at least 20%)
Cystic fibrosis?
autosomal recessive disorder causing increased viscosity of secretions (eg. lungs and pancreas).
What causes CF?
defect in the cystic fibrosis transmembrane conductance regulator gene (CFTR) which codes a cAMP-regulated chloride channel
What does CFTR gene code for?
a cAMP-regulated chloride channel
Most cases of CF are due to what?
delta F508 on long arm of chromosome 7 causing defect in CFTR gene
CF affects how many births?
1 per 2500
Carrier rate or CF?
1 in 25
Organisms which may colonise CF pts?
- Staph. aureus
- P. aeruginosa
- Aspergillus
- Burkholderia cepacia (p. cepacia)
Diagnosis of CF?
- +ve test result on infant screening (blood spot immunoreactive trypsin test) followed by sweat and gene tests to confirm
or
- CP + sweat test (children & young adults) or gene test (adults)
Assess for CF (sweat test or gene test) in people with what?
- FHx
- congenital intestinal atresia
- meconium ileus
- distal intestinal obstruction syndrome
- faltering growth
- undernutrition
- recurrent and chronic pulmonary disease
- chronic sinus disease
- obstructive azzoospermia
- acute/chronic pancreatitis
- malabsorption
- rectal prolapse in children
- pseudo-Barreter syndrome
Sweat test for CF?
- abnormally high sweat chloride if have CF
CF= >60mEq/l
normal= <40mEq/l
Causes of false positive sweat test (when testing for CF)?
- malnutrition
- adrenal insufficiency
- glycogen storage diseases
- nephrogenic diabetes insipidus
- hypothyroidism, hypoparathyroidism
- G6PD
- ectodermal dysplasia
Common reasons for false negative sweat test (when testing for CF)?
skin oedema, often due to hypoalbuminaemia/hypoproteinaemia secondary to pancreatic exocrine insuff
Features of CF?
- neonatal (20%)= meconium ileus, less common: prolonged jaundice
- recurrent chest infections (40%)
- malabsorption (30%)= steatorrhoea, failure to thrive
- other features (10%)= liver disease
- short stature
- DM
- delayed puberty
- rectal prolapse (due to bulky stools)
- nasal polyps
- male infertitlity, female subfertility
When are pts diagnosed with CF?
most on newborn screening or early childhood; 5% >18yrs
Meconium ileus in neonatal period can be sign of what?
CF
Recurrent chest infections, steatorrhoea, short stature, delayed puberty and male infertility?
CF
Symptoms/signs of malabsoption?
steatorrhoea, failure to thrive
Mx for CF? (7)
MDT approach
1) regular (2+ per d) chest physio and postural drainage (pts taught to do this); also deep breathing exercises
2) high calorie, high fat diet
3) minimal contact with other CF pts
4) vitamin supplements
5) pancreatic enzyme supplements taken with meals (Creon)
6) lung transplant
7) Lumacaftor/Ivacaftor (Orkambi)
Why should CF pts try to minimise contact with eachother?
to prevent cross infection with Burkholderia cepacia complex and Pseudomonas aeruginosa
What is an important CF specific contraindication to lung transplantation?
chronic infection with Burkholderia cepacia
Lumacaftor/Ivacaftor (Orkambi) for CF Mx?
used for CF pts who are homozygous for the delta F508 mutation
How does lumacaftor help pts with CF?
increased number of CFTR proteins that are transported to cell surface
How does ivacftor help pts with CF?
a potentiator of CFTR that is already at the cell surface, increasing the probability that the defective channel will be open and allow chloride ions to pass through the channel pore
Type of diet recommended for pts with CF?
high calorie and high fat
Why do pts with CF get thick secretions?
Due to defect in CFTR gene that encodes for a protien (cAMP-regulated chloride channel) that functions as a chloride channel, which helps regulate movement of chloride and sodium across epithelial cells that line organs eg. lungs, pancreas and intestines.
- Movement of chloride secretion is reduced and there is increased sodium absorption causing less water to be drawn into the mucus
- Thicker sticky mucus in lungs= harder to clear and trap bacteria so chronic infections and inflam
- Pancreas= thick secretions can block pancreatic ducts, preventing digestive enzymes reaching bowel so impairs digestion and absorption
- Sinuses and reproductive system= mucus can causes blockages and Cx eg. sinus infections or infertility
Drugs causing lung fibrosis?
- amiodarone
- cytotoxic agents: busulphan, bleomycin
- anti-rheumatoid drugs: methotrexate, sulfasalazine
nitrofurantoin - ergot-derived dopamine receptor agonists (bromocriptine, cabergoline, pergolide)
Idiopathic pulmonary fibrosis (IPF) (previously called crytpogenic fibrosing alveolitis)?
chronic lung condition characterised by progressive fibrosis of interstitium of the lungs
Causes of lung fibrosis?
medications, asbestos, connective tissue disease
Cause of IPF?
no underlying cause
IPF is typically seen in who?
men (2x as common); 50-70yrs
Features of IPF?
- progressive exertional dyspnoea
- bibasal fine end-inspiratory crackles on auscultation
- dry cough
- clubbing
Crackles in IPF?
bibasal fine end-inspiratory crackles on auscultation
progressive exertional dyspnoea, bibasal fine end-inspiratory crackles on auscultation, dry cough, clubbing
IPF
Diagnosis of IPF?
- Spirometry
- Impaired gas exchange- reduced transfer factor (TLCO)
- Findings may be seen on CXR but high-resolution CT is GOLD for diagnosis
- ANA +ve (30%); RF +ve (10%)
Spirometry results for IPF?
restrictive picture (FEV1 normal/decreased, FVC decreased, FEV1/FVC increased)
What may be seen on CXR for IPF (CT is gold for diagnosis)?
bilateral interstitial shadowing
(typically small, irregular, peripheral opacities - ‘ground-glass’ - later progressing to ‘honeycombing’)
Mx for IPF?
- pulmonary rehab
- very few meds useful but pirfenidone (antifibrotic agent) may help in selected pts
- many will need supp O2 and lung transplant eventually
Prognosis of IPF?
poor
average life expectancy 3-4yrs
bilateral interstitial shadowing (typically small, irregular, peripheral opacities - ‘ground-glass’ - later progressing to ‘honeycombing’) on CXR?
IPF
Lung fibrosis in upper zones vs lower?
difficult to differentiate
most common causes (IPF and drugs) tend to affect lower zones
Causes of lung fibrosis predominantly affecting the upper zones?
CHARTS
C - Coal worker’s pneumoconiosis
H - Histiocytosis/ hypersensitivity pneumonitis
A - Ankylosing spondylitis
R - Radiation
T - Tuberculosis
S - Silicosis/sarcoidosis
Causes of lung fibrosis predominantly affecting the lower zones?
- IPF
- most connective tissue disorders (except ankylosing spondylitis) e.g. SLE
- drug-induced: amiodarone, bleomycin, methotrexate
- asbestosis
Honeycombing on CXR/CT?
pulmonary fibrosis
When might you suspect occupational asthma?
- pts concerened that chemicals at work are worsening their asthma
- Hx that symptoms are better at weekends/away from work
Exposure to what chemicals is associated with occupational asthma?
- isocyanates - most common cause; eg. spray painting and foam moulding using adhesives
- platinum salts
- soldering flux resin
- glutaraldehyde
- flour
- epoxy resins
- proteolytic enzymes
What is recommended for pts with suspected occupational asthma?
serial measurements of peak expiratory flow at work and away from work
Mx for suspected occupational asthma?
referral to resp
Coal worker’s pneumoconiosis (or black lung disease)?
occupational lung disease caused by long term exposure to coal dust particles
Pneumoconiosis?
accumulation of dust in the lungs and the response of the bodily tissue to its presence, most commonly used in relation to coal worker’s pneumoconiosis.
Who most commonly experiences coal worker’s pneumoconiosis?
those who have been invl in coal mining industry or in populations with higher levels of exposure (areas with large coal mining industries); severity linked to extent of exposure; long lead time between first exposure and development of disease (around 15-20yrs after initial exposure).
Pathophysiology of coal workers’ pneumoconiosis?
coal dust (2-5um in size) is inhaled and enters lungs -> reaches terminal bronchioles and engulfed by alveolar and interstitial macrophages -> dust particles then moved by macrophages via mucociliary elevator and removed from the body as mucus
In coal miners who are exposed over many yrs, the system is overwhelmed and the macrophages begin to accumulate in alveoli, starts an immune response causing damage to lung tissue
Exposure to coal dust can lead to what presentations?
1) simple pneumonconiosis (most common; asymtomatic, increases risk of lung disease eg. COPD; may lead to PMF)
or
2) Progressive Massive Fibrosis (PMF)- 30% of those with stage 3 grading
Staging of coal workers’ pneumoconiosis: simple pneumoconiosis?
graded by appearance on CXR
Category 1= some opacities but normal lung markings visible
Cat 2= large no. of opacities but normal lung markings visible
Cat 3= large no. of opacities with normal lung not visible
Coal worker’s pneumoconiosis: Progressive Massive Fibrosis/complicated CWP?
- duct exposure causes pt to develop round fibrotic masses which can be several cm in diameter
- most common in upper lobes
- often symptomatic= COB on exertion and cough, BLACK sputum (may have)
- lung function testing= mixed obstructive/restrictive picture
Ix for coal workers’ pneumoconiosis?
- CXR= upper zone fibrosis
- Spirometry= restrictive lung function tests: a normal or slightly reduced FEV1 and a reduced FVC
Mx of coal workers’ pneumoconiosis?
- avoid exposure to coal dust and other resp irritants eg. smoking
- Mx symptoms of chronic bronchitis
- Pts may be eligible for compensation via Industrial Injuries Act
Silicosis?
fibrosing lung disease caused by inhalation of fine particles of crystalline silicon dioxide (silica)
Silicosis is a risk factor for developing what?
TB (silica is toxic to marcophages)
Occupations at risk of silicosis?
- mining
- slate works
- foundries
- potteries
Features of silicosis?
upper zone fibrosing lung disease
‘egg-shell’ calcification of the hilar lymph nodes
‘egg-shell’ calcification of the hilar lymph nodes
silicosis
Legionnaire’s disease is caused by what?
intracellular bacterium Legionella pneumophilia
(legionella pneumonia)
Where does Legionella pneumophilia colonise?
water tanks so may get from aircon or forgein holidays
Transmission of Legionella pneumonia?
air-con or foreign holidays as it colonises in water tanks
person-person transmission NOT seen
Features of Legionella pneumonia?
- flue-like symptoms icl. fever
- dry cough
- relative brady
- confusion
- lymphopaenia
- hyponataemia
- deranged LFTs
- pleural effusion (in 30%)
Ix for Legionella?
- Diagnostic= urinary antigen
- CXR non-specific= mid-to-lower predominance of patchy consolidation; pleural effusion in 30%
non-specific CXR signs incl. mid-to-lower zone predominance of patchy consolidation
Legionella pneumonia
Mx of Legionella pneumonia?
erythromycin/clarithromycin
Legionella pneumonia vs Mycoplasma pneumonia?
L= lymphopenia, hyponatraemia, diagnosis: urinary antigen
M= haemolytic anaemia/ITP, erythema multiforme, encephalitis/GBS, per/myocarditis, diagnosis: serology
Both= atypical pneumonia; flu like symptoms; dry cough; deranged LFTs; treat with macrolide eg. erythromycin
Mycoplasma penumoniae is a cause of what?
atypical pneumonia often affecting younger pts
Main Cx associated with mycoplasma pneumoniae?
erythema multiforme and autoimmune haemolytic anaemia
Epidemics of Mycoplasma pneumoniae classically occur how often?
every 4yrs
Why is it important to recognise atypical pneumonia?
may not respond to penicillins or cephalosporins due to it lacking a peptidoglycan cell wall
Examples of atypical pneumonia?
- mycoplasma
- legionella
Features of mycoplasma pneumoniae?
- prolonged and gradual onset
- flu-like symptoms precede a dry cough
- bilateral consolidations on CXR
- Cx may occur
Cx associated with Mycoplasma pneumoniae?
- cold agglutins (IgM): may cause an haemolytic anaemia, thrombocytopenia
- erythema multiforme, erythema nodosum
- meningoencephalitis, Guillain-Barre syndrome and other immune mediated neuro disease
- bullous myringitis
- pericarditis/myocarditis
- GI: hepatitis, pancreatitis
- renal: acute glomerulonephritis
Bullous myringitis? (eg. Cx of Mycoplasma pneumoniae)
painful vesicles on tympanic membrane
Ix for Mycoplasma pneumoniae?
- Diagnosis= Mycoplasma serology
- +ve cold agglutination test= peripheral blood smear may show RBC agglutination
Mx of Mycoplasma pneumoniae?
doxycycline or a macrolide (eg. erythro/clarithromycin)
Pneumonia?
infection of lung tissue in which the alveoli become filled with microorganisms, fluid, inflammatory cells which affect function of lungs
majority pts this is 2 to bacterial infection
Most common type of pneumonia?
bacterial
viral and fungal less common
Causes of pneumonia?
- Strep. pneumoniae (pneumococcus)
- H.influenzae
- Staph.aureus
- Mycoplasma pneumoniae
- Legionella pneumonophilia
- Klebsiella pneumoniae
- Pneumocystis jiroveci
Most common cause of pneumonia?
Strep.pneumoniae (pneumococcus) (80%)
- high fever, rapid onset, herpes labialis (cold sores)
- vaccine to pneumococcus is available
Causes of CAP?
- Strep.pneumoniae= most common
- H.influenzae= pts with COPD
- Moraxella= immunocompromised
Causes of Atypical pneumonia?
- Legionella= aircon eg. on holiday; rusty sputum
- Chlamydiophilae psittacci= birds
- Mycoplasma pneumoniae
- Chlamydiophilae pneumoniae
Causes of HAP?
- psuedomonas aeruginose= most common
- E.coli; Kelbsiella; s.aureus (MRSA)
Staph.aureus pneumonia often occurs following what?
influenza infection
Klebsiella pneumoniae classically seen in who?
alcoholics
Pneumocystis jiroveci (fungal) is typically seen in who?
Pts with HIV
- dry cough, exerise-induced desaturations and absence of chest signs
Idiopathic interstitial pneumonia?
group of non-infective causes of pneumonia eg. cryptogenic organising pneumonia (form of bronchiolitis that may develop as a Cx of RA or amiodarone therapy)
Majority of pts develop pneumonia where?
community-aquired pneumonia (CAP
When is someone classed as having HAP?
pts who develop pneumonia within hospitals, occuring 48hrs or more after admission
Signs and symptoms of pneumonia?
Symptoms= cough, sputum, dyspnoea, chest pain (may be pleuritic), fever
Signs= signs of systemic inflam response (fever, tachy); reduced O2 sats; auscultation= reduced breath sounds and bronchial breathing
Classical CXR finding in pneumonia
consolidation
Ix for pneumonia?
- CXR= consolidation
- FBC= neutrophilia if bacterial
- U&Es= dehydration (U for urea in CURB65), other changes seen with some atypicals
- CRP raised
- sputum sample to diagnose causative organism
- ABG if O2 low or pt has pre-existing resp disease eg. COPD
- Legionella antibodies in intermediate or high risk pts
Mx of pneumonia?
- Abx
- Supportive= O2 therapy if hypoxaemic; IV fluids if hypotensive or signs of dehydration
Mx of pts with CAP is usually determined according to a risk score called what?
CURB-65 (CRB-65 if primary care as can’t get serum urea)
CURB-65 score stands for what?
C= confusion (abbreviated metal test score <=8/10
U= urea/BUN >19mg/dL (>7mmol/L urea)
R= resp rate >=30
B= systolic BP <90mmHg or diastolic BP <=60
Age >=65
CRB-65 score in primary care is used for what?
to decide whether pt with CAP requires hospital admission:
3+= urgent admission
1 or 2= consider
0= Mx at home considered
Abx for CAP?
amoxicillin 500mg 3xd 5d
if atypical suspected or allergy= doxycycline 200mg 1st day then 100mg od 4d OR clarithromycin 500mg 2xd 5d OR erythromycin (pregnancy) 500mg 4xd 5d
Expected speed of improvement of pnuemonia symptoms once started Abx?
1w= fever resolved
4w= chest pain & sputum production reduced
6w= cough and SOB reduced
3m= mostly resolved but fatigue may still be present
6m= fully resolve
Arrange a CXR 6w after Mx for pneumonia in who?
- S&S persist despite Mx
- higher risk of malignancy eg. smokers and >50yrs
Prognosis of pneumonia?
CURB-65 score also correlates with an increased risk of mortality at 30 days with patients with a CURB-65 score of 4 approaching a 30% mortality rate at 30 days.
Mx of low-severity CAP?
amoxicillin 1st line 5d
allergic= macrolide or tetracycline
Mx of moderate and severe CAP?
dual Abx therapy= amoxicillin + macrolide 7-10d
if high severity use co-amoxiclav +macrolide
( beta-lactamase stable penicillin)
When to not discharge pt with pneumonia?
DO NOT if have 2+ of:
- T >37.5
- RR 24+
- HR >100bpm
- SBP 90 or less
- O2 sats <90% on air
- abnormal mental status
- inability to eat without assistance
Why is CRP measured in pts with pneumonia?
monitored in admitted pts to help determine response to Mx and also can be used to determine Abx is needed
CRP <20mg/L= do not routinely offer Abx
20-100= consider delayed prescription
>100= Abx
What does consolidation look like on CXR?
opacity in the area of infection
Pneumothorax definition?
accumulation of air in the pleural space, resulting in partial or complete collapse of affected lung
Types of pneumothoraxes?
- Spontaneous P
- Traumatic P
- Tension P
- Iatrogenic P
- Catamenial P
Types of spontaneous pnuemothorax?
- primary spontaneous P (PSP)
- secondary spontanous P (SSP)
Primary spontaneous pneumothorax?
- no underlying disease
- tall, thin, young individuals most commonly affected; smokers
- Caused by/associated with rupture of subpleural blebs or bullae
Secondary spontaneous pneumothorax?
- in pre-existing lung disease eg. COPD, asthma, CF, lung ca, pneumocystis pneumonia
- connective tissue diseases eg. Marfan’s also a RF
Traumatic pneumothorax?
results from penetrating or blunt chest trauma, leading to lung injury and pleural air accumulation
Tension pneumothorax?
severe, results in displacement of mediastinal structures that may result in severe resp distress and haemodynamic collapse
Iatrogenic pneumothorax?
occurs as Cx of medical procedures eg. thoracentesis, central venous catheter placement, ventilation, non-invasive ventilation, lung biopsy
Catamenial pneumothorax?
cause of 3-6% of spontaneous Ps occurring in menstruating women; thought to be caused by endometriosis within the thorax
Symptoms and signs of pneumothorax?
Symptoms= sudden; dyspnoea, pleuritic chest pain
Signs= hyper-resonant lung percussion; reduced breath sounds; reduced lung expansion; tachypnoea; tachycardia
3 signs of tension pneumothorax?
- resp distress
- tracheal deviation away from side of pneumothorax
- hypotension and tachy if severe so shocked
Resp distress, tracheal deviation away from area an d hypotension?
tension pneumothorax
Mx of pneumothorax?
1) is pt symptomatic?
- No or minimal= conservative regardless of size
- Yes= next step
2) Are there high risk characteristics?
3) Is it safe to intervene?
4) Safe and no high risk= choice of conservative, ambulatory device or needle aspiration (depending on pt preference and local availability)
4) Safe but high risk= chest drain
High risk characteristics of pneumothorax?
- haemodynamic compromise (tension pneumothorax)
- signif hypoxia
- bilateral pneumothorax
- underlying lung disease
- > =50yrs with signif smoking Hx
- haemothorax
How is it determined if it is safe to intervene in pneumothorax Mx? (before needle aspiration or chest drain insertion)
usually:
2cm laterally or apically on CXR OR any size on CT scan which can be safely accessed with radiological support
Conservative care for pneumothorax?
- PSP managed conservatively should be reviewed every 2-4d as outpt
- SSP managed conservatively should be monitored as inpatient
- stable= follow up in outpts in 2-4w
Ambulatory care for pneumothorax?
- eg. Rocketµ Pleural Vent: FG catheter mounted on an 18G needle and a pigtail catheter to minimize the risk of occlusion
- have one way valve and vent to prevent air and fluid return to pleural space while allowing for controlled escape of air and drainage of fluid
- many also have indication diaphragm that signals the catheter tip enters the pleural space and continues to fluctuate with respiration, aiding assessment of P resolution
Needle aspiration for pneumothorax?
- chest drain inserted if needle aspiration unsuccessful
- if resolved, discharge and follow up in outpt in 2-4w
Chest drain review for pneumothorax?
- daily review as inpt
- remove drain when resolved
- discharge and follow up in outpt in 2-4w
Where is a chest drain inserted for pneumothorax?
in triangle of safety= 5th ICS, midaxillary line and anterior axillary line
just above rib to avoid neurovascular bundle
CXR after to check position
Cx of chest drain?
- air leaks around drain site= persistent bubbling of fluid
- surgical emphysema= air collects in subcut tissue
Ix for pneumothorax?
1st= Erect CXR: measure horizontally from lung edge to inside of the chest wall at the level of the hilum
1st= clinical
- If P too small= CT thorax
Mx for persistent or recurrent pneumothorax (persistent air leak or insuff lung reexpansion despite chest drain insertion, or recurrent P)?
Video-assisted thoracoscopic surgery (VATS) to allow for mechanical/chemical pleurodesis +/- bullectomy
Discharge advise following pneumothorax?
- avoid smoking
- contraindication to fly= must wait to 1w post check CXR or after 2w after successful drainage and no residual air
- Scuba diving should be permanently avoided unless pt has undergone bilateral surgical pleurectomy and has normal lung function and chest CT scan postop
What does tension pneumothorax result in?
life-threatening; accumulation of air in pleural space under +ve pressure, leading to collapse of lung on affected side and shift of the mediastinum towards the contralateral side; results in impaired venous return to heart and so reduction in cardiac output posing signif risk of cardiovascular collapse
Causes of tension pneumothorax?
- trauma: penetrating or blunt chest trauma
- iatrogenic: thoracentesis; central venous catheter placement; positive pressure mechanical ventilation
- spontaneuous: particularly if underlying lung disease eg. COPD or CF; lung blebs (small blisters on lung surface) can rupture spontaneously causing air to leak into pleural space
Pathophysiology of tension pneumothorax?
air enters pleural space and is unable to escape -> creates one way valve effect (due to flap of tissue acting as a valve or similar mechanism in traumatic/iatrogenic wound) -> continuous accumulation of air leads to increased intrapleural pressure which exceeds atmospheric pressure throughout the resp cycle -> as intrapleural pressure rises, it exerts several deleterious effects
Effects of tension pneumothorax?
- lung collapse
- mediastinal shift
- impaired venous return
- reduced cardiac filling
Tension pneumothorax: lung collapse?
affected lung compressed -> decrease in functional residual capacity and impaired gas exchange
Tension pneumothorax: mediastinal shift?
increased pressure pushed mediastinum towards the contralateral side; shift can compress the opposite lung further impairing lung function.
Tracheal deviation (late sign) is key diagnostic indicator.
Tension pneumothorax: impaired venous return?
Mediastinal shift and raised intrathoracic pressure compress the great veins reducing venous return to the heart. This diminishes cardiac output and can lead to obstructive shock: hypotension and tachycardia/
Tension pneumothorax: reduced heart filling?
Direct pressure on the heart, coupled with reduced venous return, impairs both RV & LV filling; can lower cardiac output and SBP.
Signs and symptoms of tension pneumothorax?
- acute onset dyspnoea
- pleuritic chest pain
- tachypnoea
- hyperresonance on percussion, diminished breath sounds on affecterd side
- tracheal deviation away from affected side
- severe= shock: hypotension and tachycardia
Ix for tension pneumothorax?
CLINICAL, do not await imaging before Mx
Aim of Mx of tension pneumothorax?
decompression of pleural space
Mx of tension pneumothroax?
Needle thoracostomy= insert a large bore cannula into the 2nd ICS in midclavicular line on affected side
Then follow this by placement of chest drain (tube thoracostomy) in the safe triangle of chest to allow continuous drainage of air for definitive Mx
Pulmonary arterial hypertension (PAH) defined as what?
resting mean pulmonary artery pressure of >=20mmHg
What is thought to play a key role in pathogenesis of PAH?
endothelin
Pulmonary arterial HTN is more common in who?
females
30-50yrs
What increases risk of pulmonary arterial HTN?
HIV, cocaine, anorexigens (eg. fenfluramine), inherited (autosomal dominant)
What may pulmonary arterial HTN develop secondary to what?
chronic lung diseases eg. COPD
Features of pulmonary arterial HTN?
- progressive exertional dyspnoea
- exertional syncope
- exertional chest pain
- peripheral oedema
- cyanosis
What are the examination findings of pulmonary arterial HTN?
R ventricular heave, loud P2, raised JVP with prominent ‘a’ wave, tricuspid regurg
Mx of pulmonary arterial HTN?
- TUC eg. anticoag, oxygen
+ve response to acute vasodilator testing (minority)= oral CCB
-ve response (majority)= prostacyclin analogues (treprostinil, iloprost); endothelin receptor antagonists (non-selective: bosentan; selective a of endothelin receptor A: ambrisentan); phosphodiesterase inhibitors= sildenafil
Progressive symptoms= consider heart-lung transplant
Ix to decide on Mx for pulmonary arterial HTN?
Acute vasodilator testing
Acute vasodilator testing to decide on Mx for pulmonary arterial HTN?
aims to decide which pts show signif fall in pulmonary arterial pressure following the administration of vasodilators eg. IV epoprostenol or inhaled nitric oxide
Pulmonary HTN defined as?
sustained elevation in mean pulmonary arterial pressure >20 at rest
How many groups of pulmonary HTN?
5
Pulmonary HTN: group 1?
PAH:
- idiopathic
- familial
- associated conditions: collagen vascular disease; congen heart disease with systemic to pulmonary shunts; HIV; drugs and toxins; sickle cell
- persistent pulmonary HTN of the newborn
Pulmonary HTN: group 2?
Pulmonary HTN with left heart disease:
- leftsided A, V or valvular disease eg. LV systolic and diastolic dysfunction; mitral stenosis and mitral regurg
Pulmonary HTN: group 3?
Pulmonary HTN secondary to lung disease/hypoxia:
- COPD
- interstitial lung disease
- sleep apnoea
- high altitude
Pulmonary HTN: group 4?
Pulmonary HTN due to thromboembolic disease
Pulmonary HTN: group 5?
Pulmonary HTN due to miscellaneous conditions:
- lymphangimatosis eg. secondary to carcinomatosis or sarcoidosis
5 causes of pulmonary HTN?
1) Pulmonary arterial HTN (PAH)
2) PHTN with left heart disease
3) PHTN secondary to lung disease/hypoxia
4) PHTN due to thromboembolic disease
5) PHTN due to miscellaneous conditions
Pulmonary embolism?
Life-threatening condition which one or more emboli, usually arising from a blood clot formed in the veins, are lodged in and obstruct the pulmonary arterial system, causing severe resp dysfunction
Major source of a PE?
deep vein thrombosis (DVT) in lower limb
RFs for PE?
- DVT
- recent surgery
- signif immboility eg. wheelchair
- previous DVT or PE
- active ca
- long-duration travel
- COCP/HRT
- antiphospholipid syndrome
- lower limb trauma
- recent MI
- increasing age
- FHx DVT
- pregnancy, esp. 6w postpartum
- ciagrette smoking
- obesity
Cx of PE?
chronic thromboembolic pulmonary hypertension
untreated= high risk of death
Suspect PE in who? (CP)
1 or more of:
dyspnoea, haemoptysis, chest pain, syncope/pre-syncope, tachypnoea, features of DVT
When to arrange immediate admission to hospital in pt with suspected PE?
- has signs of haemodynamic instability
- is pregnant or has given birth within 6w
What should be used to estimate the clinical probability of PE (except if haemodynamically unstable, pregnant or given birth <6w)?
two-level PE Wells score
2-level PE Wells score of >4
PE likely
What does CTPA stand for?
computed tomography pulmonary angiogram
2-level PE Wells score of 4 points or less?
PE unlikely
What to do if pt has 2-level PE Wells score of >4 and so a PE is likely?
- hospital admission for immediate CTPA
- if can’t be done
immediately then interim therapeutic anticoag + hospital admission
What to do if pt has 2-level PE Wells score of 4 or less and so a PE is unlikely?
- D-dimer test with results available within 4hrs
- if >4hrs then interim therapeutic anticoag whilst waiting results
- if D-dimer +ve= immediate CTPA (same as if PE likely on Wells)
- D-dimer -ve= stop anticoag and consider alternative diagnosis
Mx of confirmed PE?
anticoag in secondary care
Follow up in primary care following PE?
- monitor treatment
- anticoag info book and anticoag alert card
What to offer during follow up of an unprovoked PE?
Ix to assess possibility of undiagnosed cancer, hereditary thrombophilia testing or antiphospholipid antibodies.
Must stop anticoag before.
Signs of PE?
may have…
- elevated JVP
- fever
- gallop rhythm, wide split-2nd HS, tricuspid regurg
- hypotension and cardiogenic shock (haemodyn instab rare and indicates central/extensive PE with severely reduced haemodyn reserve)
- hypoxia
-pleural rub
- tachycardia
Symptoms of PE?
- dyspnoea
- haemoptysis
- pleuritic or one sided chest pain
- syncope/pre-syncope
- tachypnoea
- features of DVT
may have…
- retrosternal chest pain (due to RV ischaemia)
- cough
ECG signs that may be present in pt with PE?
sinus tachycardia may be seen
large S wave in lead I, large Q in lead III and inverted T in lead III (S1Q3T3) but only in 20% pts
RBBB and right axis deviation also associated
PE differential diagnosis?
- acute bronchitis
- exacerbation of asthma
- exacerbation of COPD
- pneumonia
- pneumothorax
- ACS
- acute CHF
- aortic dissection
- cardiac tamponade
- MI
- pericarditis
- unstable angina
- MSK chest pain (can be present with PE)
- GORD
- panic disorder
- causes for collapse= arrythmias, stroke/TIA, orthostatic hypotension, seizures, vasovagal syncope
- non-thrombotic sources of emboli= air; amnitoic fluid; fat (pelvic/long bone fracture); forgein material; sepsis; tumours (prostate, GI, liver, kidney, breast)
Signs of haemodynamic instability?
- cardiac arrest
- obstructive shock: SBP <90
- persistent hypotension
How is persistent hypotension defined?
SBP less than 90 mmHg or a drop in SBP of 40 mmHg or more, lasting longer than 15 minutes and not caused by new-onset arrhythmia, hypovolaemia, or sepsis.
How is obstructive shock defined?
SBP of less than 90 mmHg or vasoactive drugs required to achieve a BP of 90 mmHg or more despite adequate filling status, plus end-organ hypoperfusion (altered mental status, cold, clammy skin, oliguria/anuria, increased serum lactate).
2-level PE Wells score features?
Clinical features of deep vein thrombosis (DVT; minimum of leg swelling and pain with palpation of the deep veins) = 3
An alternative diagnosis is less likely than PE= 3
Heart rate greater than 100 beats per minute= 1.5
Immobilization for more than 3 days or surgery in the previous 4 weeks= 1.5
Previous DVT or PE= 1.5
Haemoptysis= 1
Cancer (receiving treatment, treated in the last 6 months, or palliative)= 1
Interim therapeutic anticoag for PE if required?
apixaban or rivaroxaban
What to do for people starting interim anticoag therapy?
Baseline bloods= FBC, renal and hepatic function, PT, APTT
don’t wait on results before starting Tx
Secondary care Mx for PE?
1st= DOAC (apixaban or ribaroxaban)
- If not suitable= LMWH for 5d then dabigatran or edoxaban OR LMWH + VKA (vit K antagonist) 5d or until INR is 2+ in 2 consec readings, then VKA on own
Haemodynamically unstable= Thrombolytic therapy
Repeat embolisms despite anticoag=Inferior vena cava (IVC) filters
Inferior vena cava (IVC) filters for PE?
trap fragmented thromboemboli from the deep leg veins en route to the pulmonary circulation (whilst preserving blood flow in the IVC filter)
if anticoagulation is contraindicated or PE has occurred during anticoagulation treatment.
Thrombolytic therapy for PE?
- thrombolytic agent can either be given into a peripheral vein (systemic thrombolysis) or directly into the pulmonary arteries via a catheter (catheter-directed thrombolysis).
- Open pulmonary embolectomy (surgical removal of clots in the pulmonary arteries) is an alternative used less commonly in modern practice.
Triad for PE (rare it actually fits this in real world)?
pleuritic chest pain, haemoptysis and dyspnoea
What Ix for PE is prefered if there is renal impairment?
V/Q scan as doesn’t require contract like in CTPA
Why is CTPA used and is better than V/Q scanning for PE?
speed, easier to perform out-of-hours, a reduced need for further imaging and the possibility of providing an alternative diagnosis if PE is excluded
D-dimer for PE?
- sensitivity = 95-98%, but poor specificity
- age-adjusted D-dimer levels should be considered for patients > 50 years
CXR in PE?
normal but can have wedged-shaped opacification
can used to exclude other pathology
Causes of V/Q mismatch?
old PE, AV malformations, vasculitis, previous radiotherapy
What may be missed in CTPA for PE?
peripheral emboli affecting subsegmental arteires
Anticoag Tx for how long if have PE?
3m if provoked
3-6m if active ca
6m if unprovoked
First line anticaog for PE?
DOACs= apixaban or ribaroxaban for 3m
- If renal impairment severe (<15) then LMWH
- If antiphospholipid syndrome= LMWH + VKA
Assess bleeding risk?
ORBIT score
Dose of apixaban for PE? Rivaroxaban?
A= 10mg 2xd for 7d then maintenance 5mg 2xd
R= 15mg 2xd 21d, to be taken with food, then maintenance 20mg od
Key indications for non-invasive ventilation (NIV)?
- COPD with resp acidosis pH 7.25-7.35
- T2RF secondary to chest wall deformity, neuromuscular disease or obstructive sleep apnoea
- cardiogenic pulmonary oedema unresponsive to CPAP
- weaning from tracheal intubation
Recommended initial settings for bi-level pressure support in COPD?
- expiratory +ve airway pressure (EPAP)= 4-5cm H2O
- inspiratory +ve airway pressure (IPAP)= 12-15cm H2O
- back up rate= 15 breaths/min
- back up inspiration:expiration ratio= 1:3
What is respiratory failure?
inability of the resp system to maintain adequate gas exchange
Type 1 resp failure?
↓ pO2 with a
normal or ↓ pCO2
Type 2 resp failure?
↑ pCO2 with a normal or ↓ pO2
What do you get in T1RF?
hypercapnia → ↓ pH → respiratory acidosis
Causes of T1RF?
- pneumonia
- PE
- asthma
- pulmonary oedema
- acute resp distress syndrome
Causes of T2RF?
- COPD
- decompensation in other resp conditions eg. life threatening asthma/pulmonary oedema
- neuromuscular disease
- obesity hypoventilation syndrome
- sedative drugs: benzos, opiate overdose
What drugs can cause T1RF?
sedatives eg. benzodiazepines; opiate overdose
Sarcoidosis?
Multisystem disease of unknown aetiology.
Characterised by the presence of non-caseating granulomas (non-necrotising nodules of inflammation and scarring)
What condition is characterised by the presence of non-caseating granulomas (non-necrotising nodules of inflam and scarring)?
Sarcoidosis
Most commonly affected organs affected in sarcoidosis?
1) lungs (90% pts)
2) skin (30%)
3) eyes (30%), brain, NS, liver, heart
Cause of sarcoidosis?
Unknown; may be due to inflam response to environmental agent or infection in genetically predisposed individuals
Prognosis/disease course of sarcoidosis?
2/3 remission within 2-5yrs with majority requiring no Tx.
25% develop residual fibrosis in lungs or elsewhere
10-30% pts: disease will become chronic and require prolonged Tx
CP of sarcoidosis?
- can be asymptomatic: detected incidental on CXR
- dyspnoea
- persistent cough
- wheezing
- non-cardiac chest pain
- skin changes: hyper/hypopigmentation; keloid reaction; erythema nodosum
- eye invl: uveitis
- Fatigue and mood disturbance
- peripheral lymphadenopathy: C submand nodes (non-tender)
- Hepatic: megaly (non-tender), RUQ pain
- Neuro: VII nerve palsy, headaches, seizures
- MSK: acute arthritis of lower legs, ankles, knees, fingers
- Renal: kidney stones (due to abnorm Ca metabolism)
Ix for sarcoidosis?
1) CXR
2) Chest CT if CXR suggests sarcoidosis
3) Bloods:
LFTs (ALP elevated);
U&Es (hypercalcaemia); FBC (lymphopenia, leukopenia and/or anaemia)
4) ECG: ?cardiac invl and/or pulmonary HTN
5) Spirometry= may show restrictive
4) then refer to secondary care to confirm
eg. tissue biopsy= non-caseating granulomas
Mx for sarcoidosis?
If Tx required:
1st= corticosteroids (topical/oral)- sufficient with only skin/eye invl only
2nd line= immunosupressants eg. methotrexate
3rd= biologics eg. anti-TNF drugs such as infliximab
Monitoring for sarcoidosis?
1) stage 1 pulmonary S= monitoring for up to 2yrs to assess remission or progression
2) Stage II-IV P S= likely to need longer term monitoring
3) signif extrapulmonary invl= long term monitoring every 6m
4) withdrawing from corticosteroids= ongoing monitoring
Skin invl. in sarcoidosis?
espec face, hands, legs
- hyper/hypopigmentation
- erythema nodosum
- Lupus pernio
- prutitus, purple-red or borwn thickened circular plaques and sarcoidosis of scars and tattoos
Lupus pernio?
specific to sarcoidosis and is suggested by large bluish-red and dusky purple infiltrated nodules and plaque-like lesions on the nose, cheeks, ears, fingers and toes
What would CXR in sarcoidosis show?
- isolated bilateral hilar lymphadenopathy
- diffuse infiltrates and disseminated nodules
- fibrosis in upper lobes
What would chest CT show in sarcoidosis?
granulomatous inflam along lymphatic tracts
Bloods in sarcoidosis?
- LFTs= elevated ALP
- U&Es= hypercalcaemia
- FBC= lymphopenia, modest leukopenia and/or anaemia
- Renal= urea and serum creatinine elevated if renal involvement
Elevated ALP, lymphopenia and hypercalcaemia on bloods + isolated bilateral hilar lymphadenopathy on CXR + granulomatous inflam along lymphatic tracts?
sarcoidosis
Staging of sarcoidosis?
CXR findings:
0= normal
I= enlarged nodes only (BHL)
II= enlarged nodes + parenchymal changes (BHL + intersitial infiltrates)
III= parenchymal changes without enlarged nodes or fibrosis (diffuse intersitial infiltrates only)
IV= fibrosis
Who to refer pt with sarcoidosis to if more than one affected organ system?
MDT
Ix in secondary care for sarcoidosis to confirm diagnosis, determine severity and identify extra-pulmonary invl.?
bronchoscopy; tissue biopsy; CT; PET and MRI can be useful.
echo if ?cardiac invl.
When in Mx for sarcoidosis indicated?
dangerous disease and/or unacceptable loss of QOL
eg. stage 2/3 symptomatic; hypercalcaemia or eye, heart or neuro invl.
When may palliative care arrangements be needed for pt with sarcoidosis?
progressive fibrotic pulmonary sarcoidosis with resp failure
Differential diagnosis for sarcoidosis?
- TB
- non-small-cell lung ca
- lymphoma
- CHF
- idiopathic pulmonary fibrosis
- drug induced fibrosis
- pulmonary fibrosis caused by connective tissue diseases
- Berylliosis (Hx of employment in nuclear and aerospace industries)
- Silicosis (Hx in mining, quarrying or stonemasonry)
- Hypersensitivity pneumonitis
- Histoplasmosis (Hx of living in endemic area eg. South America, continental Africa, Madagascar)
Who is sarcoidosis more common in?
young adults & people of African descent
Acute and insidious features of sarcoidosis?
Acute= erythema nodosum; bilateral hilar lymphadenopathy; swinging fever; polyarthralgia
Insidious= dyspnoea, non-productive cough, malaise, weight loss
Why can you get hypercalcaemia in sarcoidosis?
macrophages inside granulomas cause increased conversion of Vit D to its active form (1,25-dihydroxycholecalciferol)
Syndromes associated with sarcoidosis?
- Lofgren’s syndrome
- Heerfordt’s syndrome (uveoparotid fever)
- Mikulicz syndrome (unhelpful as overlap with Sjogren’s)
Lofgren’s syndrome?
acute form of sarcoidosis characterised by bilateral hilar lymphadenopathy (BHL), erythema nodosum, fever and polyarthralgia.
excellent prognosis
Heerfordt’s syndrome (uveoparotid fever)?
associated with sarcoidosis
parotid enlargement, fever and uveitis secondary to sarcoidosis
Mikulicz syndrome?
outdated and unhelpful as overlap with Sjogren’s
enlargement of parotid and lacrimal glands due to sarcoidosis, TB or lymphoma
What would tissue biopsy for sarcoidosis show?
non-caseating granulomas
Factors in sarcoidosis associated with poor prognosis?
- insidious onset, symptoms > 6 months
- absence of erythema nodosum
- extrapulmonary manifestations: e.g. lupus pernio, splenomegaly
- CXR: stage III-IV features
- black African or African-Caribbean ethnicity
What is tuberculosis caused by?
bacteria- members of the Mycobacterium tuberculosis complex
How is TB spread?
inhaling via resp droplets released when a person with pulmonary or laryngeal TB coughs
2 types of TB
active disease and latent
Active TB?
symptomatic or progressive disease of the lung (most common) and/or other organs (extrapulmonary TB)
Latent TB?
no clinically active TB (asymptomatic and not infectious)
RFs for TB?
born in high prevalence area, children, adult males, people with previously untreated infection, close contact with active TB, immunosuppressive conditions or drugs, under-served groups
Suspect TB in who?
weight loss, fever, night sweats, anorexia, malaise, RFs for TB
pulmonary invl= persistent productive cough, haemoptysis, dyspnoea
extrapulmonary= organ-specific S&S
Ix for TB
?active pulmonary= CXR + 3 spontaneously produced sputum samples
?active extrapul= same as above + Ix depending on likely site of disease
- can do sputum smear= stained for acid-fast bacilli (Ziehl-Neelsen stain), but all mycobacteria will stain +ve (even nonTB)
Asymptomatic people who are at risk of TB should be screened through the local multidisciplinary TB team, including who?
- people in contact with pt with active pulmonary or laryngeal TB (contact tracing needed)
- immunocompromised at high risk for latent TB
- new entrants to UK from high TB prevalence country, who present to healthcare services and not had pre-entry screening
- new NHS employees who will be working with pts or clinical specimens
- evidence of TB scarring or untreated fibrotic changes on CXR
What if pt has known active or latent TB but not completed treatment as planned?
re-referral to local multidisciplinary TB team
Primary care Mx of pt with confirmed active TB?
- encourage adherence to specialist Tx
- smoking cessation & lifestyle
- pulmonary or larygneal TB can be transmitted to close contacts and screening via contact tracing will be arranged by local specialist team
- symptoms suggesting relapse after finishing Tx need to inform primary care/local specialist team immediately
Why may active TB be difficult to detect so may be diagnositic delays or misdiagnosis?
onset can be insidious and early stages may be difficult to detect
Is dyspnoea and haemptysis an early or late feature of TB?
late
examples of possible extra-pulmonary invl. in TB?
- Lymphadenopathy (painless, Cervical or supraclav)= lymphatic TB
- bone/joint pain, back pain, joint swelling= joint or skeletal TB
- abdo or pelvic pain, constip, bowel obstruct= GI TB
- urinary symptoms (dysuria, haematuria, frequency)= GU TB
- sterile pyuria= renal TB
- headache, V, irritability, confusion, cranial nerve abnorm= TB meningitis
- skin lesions= cutaneous TB
-SOB, chest pain, ankle swelling= TB pericarditis
- occular inflam or visual disturbance= ocular TB (rare)
Examples of skin lesions in cutaneous TB?
erythema nodosum (hypersensitivity reaction triggered by TB)
lupus vulgaris (painful nodular lesions affecting face)
How may children present with TB?
non-specific
poor weight gain, faltering growth, fatigue, persistent fever
CXR finding for active pulmonary TB?
- bilateral hilar lymphadenopathy
- upper lobe cavitation is classic of reactivated TB
NICE= cavitation; pleural effusion; mediastinal or hilar lymphadenopathy or parenchymal infiltrates mainly in the upper lobes
Sputum samples for TB?
3, esp if CXR suggest TB
3 spontaneously produced, deep cough sputum samples; one early morning.
- for microscopy for acid-fasr bacilli(Ziehl-Neelsen stain), mycobacteria culture and specialist molecular test/drug sensitivity testing
What Ix could you do if pt has suspected active extrapulmonary TB?
CXR + 3 sputum samples + either….
joint or spinal plain X-ray; abdo, renal tract or lymph node USS; early morning urine sample for dip, microscopy (sterile pyuria) and Mycobacteria culture; ECHO (pericarditis); CT chest, CNS or bone/joints, LP (CNS TB)
False negative results for TB are more common in who?
children and the immunocompromised eg. HIV
Screening for TB helps identify what?
latent TB
The results of specialist screening tests to identify latent TB should be interpreted taking into account what?
immune status; Hx of exposure to TB and the BCG vaccine; other RFs
Types of screening test for TB (latent)?
1) Mantoux test
2) Interferon-gamma release assay (IGRA) test
Mantoux test used to screen for latent TB?
0.1ml of 1:1000 purified protein derivative Tuberculin is injected intradermally. Skin inspected for signs of local reaction (induration) after 2-3d.
+ve= induration of 5mm or more, regardless of previous BCG vaccine Hx.
Offered to children/young people 2-17yrs who gace been in close contact with pt with TB & new entrants to UK from high TB prevalence country.
<2yrs who are close contacts should be referred to specialist.
Interferon-gamma release assay (IGRA) test for screening for latent TB?
Blood test= detects response of WBC to TB antigens.
Less likely to give false positive and gives rapid result.
<65yrs from under-served groups (eg. IVDU or homelessness) may be offered IGRA test.
Who may be offered both Mantoux test and IGRA test to screen for latent TB?
severely immunocompromised at risk of TB
What if latent TB screening test is +ve?
assessed for active TB
if no signs of active infective on basis of symptoms and CXR then treat for latent TB by local MD TB team to prevent progression to active disease
Mx for latent TB?
3m of isoniazid (with pyridoxine) + rifampicin= <35yrs at low risk of hepatotoxicity
or
6m of isoniazid (with pyridoxine)= if rifamycin interactions may be concern (eg. pts with HIV or transplants)
Is TB a notifiable disease?
yes, notify within 3 working days
notify a new culture confirmed case of TB or where TB is suspected and decision made to Tx pt
Specialist assessment for TB?
Rapid diagnostic nucleic acid amplification tests (NAATs) for the Mycobacterium tuberculosis complex may be used on primary specimens if there is:
-clinical suspicion & HIV, or
- a rapid diagnosis needed or
- contact tracing of large numbers of people may be needed.
- May need sputum induction, bronchoscopy and lavage, gastric aspiration; organ-specific aspiration or biopsy; or CT/MRI
Mx for active TB?
6m isoniazid (with pyridoxine) + rifampicim AND in the 1st 2m: pyrazinamide + ethambutol
How is TB Tx success defined?
by completion of therapy with negative follow-up sputum samples
Pts with active TB of CNS require what?
prolonged Tx regimen
May also receive corticosteroids (dexa or pred) for 4-8w
For TB, altered Tx regimens may be required in who?
pts with renal impairment (particularly ethambutol and pyrazinamide which are renally excreted)
Mx for multidrug-resistant (MDR) TB?
prolonged Tx (18-24m) with at least 6 drugs to which Mycobacterium is likely sensitive
often less efficaious and more poorly tolerated due to increased adverse effects
Who may be a candidate for surgical Mx of MDR TB?
pts with potentially resectable unilateral disease (or apical bilateral disease in selected cases) with adequate lung function who have not responded to medical Tx
Differential diagnosis for active pulmonary TB?
- viral URTI
- asthma
- chest infection
- COPD
- lung fibrosis
- lung ca
- pulmonary sarcoidosis (more of dry cough)
Differential diagnosis for active extrapulmonary TB?
- lymphoma
- malignant pleural effusion
- IBD
Common side effects of TB Abx?
R.ifampicin= red urine, hepatitis
I.soniazid= peripheral neuropathy, hepatitis
P.yranzinamide= gout, rash, hepatitis
E.thambutol= optic neuritis
Why do you give pyridoxine (vit B6) with isoniazid for TB?
S/E of isoniazid is peripheral neuropathy and so give it to prevent this
What should you do before and during taking ethambutol for TB?
check visual acuity before and during Tx
Are pts with latent TB infectious?
NO so no restrictions in terms of employment ect. unless becomes active
RFs for developing active TB eg. if have latent?
silicosis
chronic renal failure
HIV positive
solid organ transplantation with immunosuppression
intravenous drug use
haematological malignancy
anti-TNF treatment
previous gastrectomy
How are pts typically diagnosed with latent TB?
+ve tuberculin skin test (Mantoux test) or Interferon-Gamma Release Assay (IGRA) combined with a normal chest x-ray (which excludes active TB)
Directly observed therapy 3x a week dosing regimen may be used in what groups of pts with TB?
- homeless pts with active TB
- pts who are likely to have poor concordance
- all prisoners with active or latent TB
Overall possible Cx of TB treatment?
Immune reconstitution disease= typically 3-6 after starting; presents with enlarging lymph nodes
TB pathophysiology?
macrophages migrate to regional lymph nodes -> affected lymph codes + lung lesion= Ghon complex -> leads to formation of granuloma which is a collection of epithelioid histiocytes; presence of caseous necrosis in the centre
inflam response is mediated by type 4 hypersensitivity reaction
What is Ghon complex in TB?
lung lesion + affected lymph nodes
What is a granuloma in TB?
collection of epithelioid histiocytes
TB in healthy individuals vs immunocompromised individuals?
healthy= TB may be contained
immunocompromised= disseminated (miliary TB) may occur
What countries may be RFs for TB?
Asia, Latin America, Eastern Europe, Africa
Examples of immunocompromised individuals that may have increased risk of TB?
diabetics, pts on immunosuppressive theraoy, malnourished or those with haematological malignancies
Primary TB?
non-immune host exposed to M.TB may develop primary infection of lungs
Small lung lesion (Ghon focus) develops- composed of tubercle-laden macrophages.
Ghon focus + hilar lymph nodes= Ghon complex
Immunocompetent pts= inital lesion usually heals by fibrosis.
Immunocompromised- may develop disseminated disease (miliary TB)
Secondary (post-primary) TB?
if host becomes immunocompromised the initial infection may become reactivated.
reactivation generally occurs in apex of lungs and may spread locally or to more distant sites
causes of immunocompromised= HIV, drugs eg. steroids, malnutrition
Most common site for secondary TB?
lungs
Extra-pulmonary infection in secondary TB examples?
- CNS= TB meningitis (SERIOUS)
- vertebral bodies (Pott’s disease)
- Cervical lymph nodes= scrofuloderma
- renal
- GI
Pott’s disease?
TB that has moved from lungs (pulmonary TB) to vertebral bodies in the spine (extra-pulmonary TB)
CP of common cold?
mild, self-limiting, viral, URTI
nasal congestion, irritation, rhinorrhoea, sneezing, sore throat, cough after nasal symptoms clear; hoarse voice (associated largyngitis); malaise, headache
no known Tx improves time course of infection
Most common cause of common cold?
Rhinovirus
How long are people with common cold infectious?
several weeks
Average number of common colds people get?
Adults= 2-3 per yr
Children= 5-8 (primary school or preschool)
Cx of common cold?
sinusitis, LRTI, acute otitis media
secondary bacterial infection eg. pnuemonia
COPD or asthma exacerbations
young children/infants= viral wheeze, bronchiolitis, croup
How long does common cold last?
acute
peak at 2-3d then decrease
around 1 week, cough can be up to 3w
younger children= lasts 10-14d
Nasal discharge in common cold?
often profuse and clear at first then becomes thicker and darker as infection progresses
Uncommon features of common cold?
fever, headache, myalgia, loss of taste & smell, eye irritability, feeling of pressure in ears or sinuses
CP of common cold in young child?
Restlessness or irritability.
Nasal congestion, nasal discharge (rhinorrhoea), and sneezing. Severe nasal congestion may interfere with feeding, breathing, and sleep.
Cough. Occasionally, vomiting may follow a bout of coughing.
Fever.
Mx for common cold?
- adequate rest; normal activity won’t prolong illness
- paracetamol or ibuprofen (if <5yrs only if has fever & distressed)
What do URTIs involve?
mucosa of nasal cavity, sinuses, nasopharynx, oropharynx, larynx
Causes of URTI?
Rhinovirus (most common)
Corona virus
Adenovirus
Influenza
Parainfluenza
RSV
Enterovirus
Another name for URTI?
‘cold’
Coryzal symptoms
Sings of UTRI?
- erythema or injection at back of throat
- nasal discharge
- tender cervical lymphadenopathy
- mild fever
Criteria for assessment of URTI (common cold)?
- <5yrs= NICE fever traffic light system
- FeverPAIN score= likelihood of strep infection in adults with sore throat and guide decision making re Abx
Boehaaves syndrome?
spontaneous rupture of oesophagus following repeated episodes of vomiting
distally sited and on L side
Hx of sudden onset severe chest pain that may complicate severe vomiting
severe sepsis occurs secondary to mediastinitis
Diagnosis of Boerhaaves syndrome?
CT contrast swallow
Tx for Boerhaaves syndrome?
thoracotomy and lavage
if <12hrs after onset= primary repair
> 12hrs= insertion of T tube to create controlled fistula between oesophagus and skin
> 24hrs= high mortality rate
Angio-oedema?
swelling of deep dermis, subcut or submucosal tissue , often affecting face (lips, tongue and eyelids), genitalia, hands or feet.
Less common= submucosal swelling affecting bowel and airway
Types of angio-oedema?
- allergic
- non-allergic drug reaction
- hereditary angio-odema
- acquired
- idiopathic
What usually causes acquired angio-oedema?
secondary to lymphoma or connective tissue disorder
What usually causes non-allergic drug reaction angio-oedema?
ACE inhibitors
Anaphylaxis?
severe, life-threatening, generalised or systemic hypersensitivity reaction characterised by rapidly developing airway and/or breathing and/or circulation problems usually associated with skin and mucosal changes
Pathophysiology of anaphylaxis and angio-oedema?
both invl. histamine and/or bradykinin
but in anaphylaxis the reaction is more marked, resulting in an increase in vascular permeability and subsequent circulatory collapse
Diagnosis of angio-oedema?
clinical
Ix may be used to identify associated condition, tirgger or exclude differential
Approach to recognise and manage amnaphylaxis?
ABCDE
Mx for pt with rapidly developing angio-oedema without anaphlaxis?
Slow IV or IM chlorphenamine and hydrocortisone + emergency admission
Mx for pt with stable angio-oedema without anaphylaxis?
- identify and remove underlying cause
- non-sedating antihistamine (cetirizine up to 6w)
- severe= + oral corticosteroid (pred 40mg od up to 7d)
- refer to immuno or derm if cause is not identifiable or avoidable
Mx for anaphylaxis?
1) unresponsive and not breathing= CPR
2) IM adrenaline 1:1000
3) assess response after 5mins
4) repeat adrenaline dose if no improvement
5) no improvement after 2 doses= IM adrenaline every 5mins until adequate response
Also give high flow O2, IV fluid challenge (if hypotension, shock or no initial response) and monitor pulse, O2 sats, BP and ECG.
- Consider inhaled salbutamol or ipratropium if wheezy
Position to put pt in anaphylaxis?
pt with airway and breathing problems may prefer to sit up
low BP= lie flat with or without leg elevation helpful
breathing and unconscious= recovery position
pregnant= lie on left side to prevent caval compression (inferior vena cava)
Mx following emergency treatment for anaphylaxis?
- refer to specialist allergy service
- give 2 adrenaline auto-injectors as interim measures before their allergy appointment (instruct how and when to use)
General clinical features of angio-oedema?
- surface of skin may be normal or may be weals or other rashes
- skin swelling less defined than in urticaria and can affect eyes, lips, genitalia, hands and/or feet
- swelling often more painful than itchy and can take up to 72hrs to resolve
- may be resp symptoms (stridor, wheeze or SOB) or gins of circulatory collapse= if present then consider anaphylaxis
When to suspect idiopathic angio-oedema?
recurrent episodes of angio-oedema & urticaria and allergic cause can’t be identified
more common in autoimmune disorders eg. SLE and autoimmune thyroiditits
consider CRP, ESR, autoantibody screen and thyroid autoantibodies
refer to immuno or derm if suspected
Angio-odema without urticaria?
non-allergic cause likely eg. non-allergic drug reaction; hereditary angio-odema (HAE) or acquired angio-oedema (AA)
When to suspect hereditary angio-oedema (HAE)?
Hx of parent affected
presents after puberty
recurrent oedema of limbs, trunk, face, genitals
swelling (non-itchy, non-pitting, painless) take 24hrs to peak usually and resolve over 48-72hrs+
GI symptoms common (can mimic acute abdo); upper airway swelling less common
if suspect refer to immuno or derm
How is diagnosis of HAE confirmed?
low serum levels of complement C1 inhibitor in pt with FHx of angio-oedema
How is diagnosis of acquired angio-oedema confirmed?
low serum levels of complement C1 inhibitor in pt with known cause for the condition (eg. lymphoma= splenic villous lymphoma; or connective tissue disorder eg. SLE)
Anaphylaxis is likely when what 3 criteria are met?
1) Sudden onset and rapid progression of symptoms
2) Life-threatening Airway and/or Breathing and/or Circulation problems
3) Skin and mucosal changes
Onset of anaphylaxis?
several mins (acute)
feel and look unwell
anxious and can experience ‘sense of impending doom’
IV fasted trigger then stings then oral ingested trigger
Airway problems in anaphylaxis?
- airway swelling (throat and tongue swelling= pharyngeal/laryngeal oedema)
- difficulty breathing and swallowing= feeling throat closing up
- hoarse voice
- stridor
Stridor?
high-pitch inspiratory noise caused by upper airway obstruction
Breathing problems in anaphylaxis?
- SOB= increased RR
- wheeze
- tiredness
- confusion= due to hypoxia
- cyanosis (appear blue= late sign)
- peripheral cap O2 sat <92%
- resp arrest
Respiratory arrest?
med emergency when stop breathing -> lack of O2 supply; needs immediate intervention to prevent brain damage or death
Features of respiratory arrest?
- cessation of breathing
- hypoxia
- no chest movement
- loss of consciousness
Causes of respiratory arrest?
1) Airway obstruction (e.g., choking, swelling, foreign objects).
2) Severe asthma or COPD exacerbation.
3) Drug overdose eg. opioids or sedatives.
4) Severe respiratory infections (e.g., pneumonia, COVID-19).
5) Head or neck injury that affects the brain’s control of breathing.
6) Neuromuscular disorders affecting respiratory muscles (e.g., Guillain-Barré syndrome, myasthenia gravis).
7) Severe allergic reactions (anaphylaxis).
Mx of respiratory arrest?
- Basic life support= open airway, rescue breaths and CPR is needed
- Advanced life support= airway Mx (eg. intubation), mechanical ventilation and TUC (eg. reverse opioid overdose with naloxone)
Circulatory problems in anaphylaxis?
- signs of shock (pale, clammy)
- tachycardia
- low BP (faint, dizzy, collapse)
- decreased level/loss of consciousness
- cardiac arrest
- can cause MI and ECG changes
D part of A to E in anaphylaxis?
Disability
A, B & C can alter neuro status (D) due to decreased brain perfusion, confusion and agitation
Skin and/or mucosal changes in anaphylaxis?
Exposure in A to E
Often first features, in over 80% of reactions and can be subtle or dramatic
May be erythema (patchy or generalised red rash), urticaria or angio-oedema
Skin changes without life-threatening airway, brathing or circulation problems?
DO NOT signify anaphylactic reaction.
Skin and mucosal changes can be subtle or absent in what percent of anaphylactic reactions?
20% (so be aware when looking at anaphylaxis criteria)
Some people with anaphylaxis may only present with what?
decrease in BP (circulatory problem)
What other symptoms apart from A,B & C and skin/mucosal changes may be present in anaphylaxis?
GI symptoms eg. vomiting, abdo pain and incontinence
Biphasic anaphylactic reaction?
Occasionally can occur.
Life-threatening recurrence of symptoms of anaphylaxis after initial presentation; without re-exposure to trigger.
Infrequent so difficult to predict.
What may increase or decrease risk of bisphasic reactions following anaphylaxis?
Less likely= food induced anaphylaxis
Increased risk= present with hypotension or idiopathic anaphylaxis
When would a biphasic reaction following anaphylaxis occur?
hrs to days after initial; typically 1-72hrs following
Why may a biphasic reaction occur following anaphylaxis?
1) ongoing release of inflam mediators eg. histamine, leukotrienes and prostaglandins and so can cause a delayed resurgence of symptoms
2) incomplete clearance of inflam mediators
3) insuff Tx: may have controlled symptoms but not have stopped immune response so reaction may flare up again once Tx worn off
4) severity and prolonged initial reaction
5) duration of allergen exposure before Tx (eg. ongoing ingestion of allergenic food) may cause prolonged immune response increasing risk of biphasic reaction
Differential diagnosis of angio-oedema?
- acute contact dermatitis
- cellulitis
- connective tissue disorders eg. SLE
- erysipelas
- idiopathic scrotal oedema in children
- lymphoedema
- Rosenthal-Melkersson syndrome
- surgical abdomen
Differential diagnosis of anaphylaxis?
- angio-oedema
- asthma
- acute anxiety
- breath-holding episode in a child
- foreign body aspiration
- hypoglycaemia
- PE
- urticaria
- vasovagal episode
- mastocytosis
- carcinoid syndrome
- scombroid poisoning (from contaminated fish)
- seizure
- septic shock
What if it is likely for stable angio-oedema without anaphylaxis to be persistent or recurrent?
daily antihistamine 3-6m then review
If long Hx of urticaria & A-O then 6-12m
Where to infection IM adrenaline for anaphylaxis?
anterolateral aspect of the middle third of thigh (ideally) or arm depending on access
How to assess response to adrenaline during anaphylaxis?
RR, O2 sats, HR, BP, level of consciousness and auscultate for wheeze
If possible, how to give O2 for anaphylaxis and what are the target sats?
highest conc possible asap using mask with oxygen reservoir
94-98% target sats (or 88-92% in pt at risk of hypercapnic resp failure)
During Mx for anaphylaxis, what do you do in the presence of hypotension/shock or poor response to initial dose of adrenaline?
obtain IV access and give rapid IV bolus (Hartmann’s or normal saline) using 500-1000mL in adult or 10mL/kg in child.
more fluids can be given if needed
What should you consider giving in the Mx of anaphylaxis if pt is wheezy (esp in pt with known asthma)?
inhaled salbutamol or ipratropium bromide
Follow up for pt with anaphylaxis once discharged?
- refer to specialist allergy service
- provide 2 adrenaline auto-injectors before allergy appointment (carry at all times, check expiry dates)
Advice to give pt if they have another anaphylactic reaction?
- use one adrenaline auto-injector and call 999 even if symptoms improving
- lie flat with legs raised to maintain blood flow; if breathing diff then sit up
- use 2nd auto-injector if don’t feel better after 15mins after first
A dose of adrenaline IM for anaphylaxis if >12yrs?
adrenaline (IM) 1:1000
500 micrograms (0.5mL)
A dose of adrenaline IM for anaphylaxis if 6-12yrs?
adrenaline (IM) 1:1000
300 micrograms (0.3mL)
A dose of adrenaline IM for anaphylaxis if 6m-6yrs?
adrenaline (IM) 1:1000
150 micrograms (0.15mL)
A dose of adrenaline IM for anaphylaxis if younger than 6m?
adrenaline (IM) 1:1000
100-150 micrograms (0.1-0.15mL)
Dose of chlorphenamine for anaphylaxis and angio-oedema?
slow IM or IV
> 12yrs= 10mg
6-12yrs= 5mg
6m-6yrs= 2.5mg
<6m= 250 ug/kg
Dose of hydrocortisone for anaphylaxis and angio-oedema?
slow IM or IV
> 12yrs= 200mg
6-12yrs= 100mg
6m-6yrs= 50mg
<6m= 25mg
Dose of nebulised salbutamol for anaphylaxis and angio-oedema?
> 12yrs= 5mg
6-12yrs= 5mg
6m-6yrs= 2.5mg
<6m= 2.5mg
How to inject adrenaline for anaphylaxis?
25mm needle IM at 90 degrees to skin, skin stretched not bunched
Example of adrenaline auto-injector given to pt for self-administration at first signs of anaphylaxis?
EpiPen Autoinjector 0.3mg
- 300 micrograms (1 pen) inject then another 300 microgram pen after 5 mins
What dose adrenaline 1:1000 500micrograms (0.5mg) mean?
0.5ml 1 in 1000 adrenalinew
Discharge guidance following anaphylaxis?
1) Fast-track (2hrs after symptom resolution)
2) Minimum of 6hrs after resolution
3) Minimum of 12hrs after resolution
When can pt be discharged 2hrs after symptoms resolve following anaphylaxis?
- good response to single dose adrenaline
- complete resolution of symptoms
- been given auto-injector and trained how to use
- adequate supervision following discharge
When must pt be discharged min 6hrs after symptoms resolve following anaphylaxis?
2 doses of IM adrenaline needed or previous biphasic reaction
When must pt be discharged min 12hrs after symptoms resolve following anaphylaxis?
- severe reaction needing >2 doses adrenaline
- severe asthma
- possibility of ongoing reaction eg. slow release meds
- presents late at night
- pt in areas where access to emergency care may be difficult
- observation for 12hrs
What can be used to determine whether a resp disease is obstructive or restrictive?
pulmonary function tests
Signs of obstructive lung disease on pulmonary function tests?
FEV1= significantly reduced
FVC= reduced or normal
FEV1/FVC (FEV1%)= reduced
Examples of obstructive lung disease?
asthma
COPD
bronchiectasis
bronchiolitis obliterans
Signs of restrictive lung disease on pulmonary function tests?
FEV1= reduced
FVC= significantly reduced
FEV1/FVC (FEV1%)= normal or increased
Examples of restrictive lung disease?
Pulmonary fibrosis
Asbestosis
Sarcoidosis
Acute respiratory distress syndrome
Infant respiratory distress syndrome
Kyphoscoliosis e.g. ankylosing spondylitis
Neuromuscular disorders
Severe obesity
Causes of haemoptysis?
- lung ca
- pulmonary oedema
- TB
- PE
- LRTI
- bronchiectasis
- mitral stenosis
- aspergilloma
- Granulomatosis with polyangiitis
- Goodpasture’s
Short summary of pulmonary oedema signs/symptoms?
Dyspnoea
Bibasal crackles and S3 are the most reliable signs
Haemoptysis
Short summary of TB signs/symptoms?
Fever, night sweats, anorexia, weight loss, haemoptysis
Short summary of PE signs/symptoms?
Pleuritic chest pain
Tachycardia, tachypnoea, haemoptysis
Short summary of LRTI signs/symptoms?
Usually acute history of purulent cough
Short summary of bronchiectasis signs/symptoms?
Usually long history of cough and daily purulent sputum production
Short summary of mitral stenosis signs/symptoms?
Dyspnoea
Atrial fibrillation
Malar flush on cheeks
Mid-diastolic murmur
Haemoptysis
Short summary of Aspergilloma signs/symptoms?
Often past history of tuberculosis.
Haemoptysis may be severe
Chest x-ray shows rounded opacity
Short summary of Granulomatosis with polyangiitis signs/symptoms?
Upper respiratory tract: epistaxis, sinusitis, nasal crusting
Lower respiratory tract: dyspnoea, haemoptysis
Glomerulonephritis
Saddle-shape nose deformity
Short summary of Goodpasture’s signs/symptoms?
Haemoptysis
Systemically unwell: fever, nausea
Glomerulonephritis
How can pleural effusions be classified?
transudate or exudate according to the protein concentration
Transudate vs exudate pleural effusion?
Transudate= <30g/L protein
Exudate= >30g/L protein
Causes of transudate pleural effusion?
- Heart failure (most common)
- Hypoalbuminaemia= liver disease, nephrotic syndrome, malabsorption
- hypothyroidism
- Meig’s syndrome
Causes of exudate pleural effusion?
- infection= pneumonia (most common); TB; subphrenic abscess
- connective tissue disease= RA; SLE
- neoplasia= lung ca; mesothelioma; metastases
- pancreatitis
- PE
- Dressler’s
- yellow nail syndrome
CP of pleural effusion?
- dyspnoea, non-productive cough, chest pain
- dullness to percussion, reduced breath sounds and reduced chest expansion
Transudate fluid eg. in pleural effusion?
Clear
Low protein (<30g/L)
Results from systemic factors that alter the balance of fluid movement across capillary membranes such as increased hydrostatic pressure or decreased oncotic pressure.
Causes of transudate= CHF, cirrhosis and nephrotic syndrome
Exudate fluid eg. in pleural effusion?
Cloudy or turbid and high protein content (>30g/L)
Occurs due to local factors that increase permability of capillary membranes, often related to imflam, infection or malignancy.
Causes= infection (pneumonia), malignancy, inflam condicitons eg. rheumatoid arthritis
Why is there a high protein content in exudate?
Exudate high= due to inflam, infection or injury to tissues -> causes blood vessels (capillary membranes) to become more permeable (leaky) -> increased permability means that fluid, protein and cells can pass through vessel wall into surrounding tissue/cavity (large molecules can escape)
Why is there a low protein content in transudate?
Forms due to systemic imbalance in fluid dynamics rather than local inflam. These imbalances can be caused by:
- increased hydrostatic pressure (eg. in CHF)
or
- decreased oncotic pressure (eg. in hypoalbuminaemia)
Fluid is pushed out of blood vessels (capillary membrane) due to pressure changes but the vessel walls remain intact so only water and small solutes (like electrolytes) can escape; but proteins and larger molecules remain in bloodstream.
Ix for pleural effusion?
- posterioranterior (PA) CXR in all pts
- Pleural aspiration using USS
- can use contrast CT to Ix underlying cause, esp. for exudative effusions
Pleural aspiration for pleural effusion?
21G needle and 50ml syringe
with USS
- send fluid for pH, protein, lactate dehydrogenase (LDH), cytology and microbio
Criteria to distinguish between transudate and exudate in pleural effusion? (esp. in borderline cases)
Light’s criteria
Light’s criteria to distinguish between transudate and exudate in pleural effusion? (esp. in borderline cases)
If protein level 25-35g/L, use Light’s criteria. Exudate likely if at least 1 of the following is met:
- pleural fluid protein divided by serum protein >0.5
- pleural fluid LDH divided by serum LDH >0.6
- pleural fluid LDH more than 2/3rds the upper limits of normal serum LDH
What may low glucose from fluid aspiration in pleural effusion suggest?
RA, TB
What may raised amylase from fluid aspiration in pleural effusion suggest?
pancreatitis; oesophageal perforation
What may heavy blood staining from fluid aspiration in pleural effusion suggest?
mesothelioma; PE; TB
Pt with pleural effusion in association with sepsis or pneumonic illness require what?
diagnostic pleural fluid sampling
Pt with pleural effusion + sepsis or pneumonic illness require diagnostic pleural fluid sampling. How does the result of this determine Mx?
- fluid is purulent or turbid/cloudy= chest tube to allow drainage
- fluid is clear but pH is <7.2 in pts with suspected pleural infection= chest tube
Mx for recurrent pleural effusion?
- recurrent aspiration
- pleurodesis
- indwelling pleural catheter
- medical= eg. opioids to relieve dyspnoea
infection= ?chest drain is required following pleural fluid sampling
Predisposing factors for obstructive sleep apnoea/hypopnoea syndrome?
- obesity
- macroglossia= acromegaly, hypothyroidism, amloidosis
- large tonsils
- Marfan’s
CP of obstructive sleep apnoea/hypopnoea syndrome?
partner complains of XS snoring and may report periods of apnoea
Consequence of obstructive sleep apnoea/hypopnoea syndrome?
- daytime somnolence
- compensated resp acidosis
- HTN
Assess sleepiness in obstructive sleep apnoea/hypopnoea syndrome?
- Epworth Sleepiness Scale= questionnaire completed by pt +/- partner
- Multiple Sleep Latency Test (MSLT)= measure time to fall asleep in dark room (using EEG criteria)
Ix for obstructive sleep apnoea/hypopnoea syndrome?
- Assess sleepiness
- refer for diagnostic test= Sleep studies (polysomnography)
Sleep studies (polysomnography) to diagnose obstructive sleep apnoea/hypopnoea syndrome?
monitor pulse oximetry at night or can do full polysomnography= EEG, resp airflow, pulse oximetry, thoraco-abdo movement and snoring
Mx for obstructive sleep apnoea/hypopnoea syndrome?
- weight loss
1st= CPAP for moderate/severe OSAHS
- not tolerated= intra-oral devices (eg. mandibular advancement)
inform DVLA is causing XS daytime sleepiness
OSAHS? OSAS?
obstructive sleep apnoea/hypopnoea syndrome
OSAS= obstructive sleep apnoea syndrome
Obstructive sleep apnoea/hypopnoea syndrome?
sleep-related breathing disorder characterized by recurrent episodes of complete or partial obstruction of the upper airway during sleep, causing apnoea (complete airflow obstruction with temporary absence or cessation of breathing) or hypopnoea (decreased airflow), respectively.
Why does OSAHS occur?
due to XS collapsing forces around pharynx that exceed the decreased muscle tone during sleep
RFs for OSAS?
age, male sex, obesity, family history of OSAS, nasopharyngeal obstruction (for example adenotonsillar hypertrophy), craniofacial abnormalities, neuromuscular disorders, and lifestyle factors (such as smoking, alcohol, and sleeping supine).
Child with OSAS?
- refer ENT if there is nasopharyngeal obstruction and snoring at night.
- paediatrician if there is a congenital or developmental disorder, associated condition, or obesity contributing to symptoms.
A1AT stands for?
alpha-1 antitrypsin def
Alpha-1 antitrypsin def (A1AT)?
common inherited condition caused by lack of protease inhibitor (Pi) normally produced by liver
classically causes emphysema (i.e COPD) in pts who are young and non-smokers
COPD in young pt who are non-smokers (may have liver cirrhosis/ hepatocellular carcinoma in adults of cholestasis in children)?
think A1AT def
Role of A1AT?
protect cells from enzymes such as neutrophil elastase
A1AT def genetic inheritance?
A1AT located on chromosome 14
autosomal recessive/co-dominant
A1AT def alleles?
alleles classified by electrophoretic mobility= M is normal, S for slow, Z for very slow
Normal= PiMM
Heterozygous= PiMZ
Homozygous PiSS= 50% normal A1AT levels
Homozygous PiZZ= 10% normal A1AT levels
Features of A1AT def?
- pt who manifest disease usually PiZZ genotype
- lungs= panacinar emphysema, most marked in lower lobes
- liver= cirrhosis and hepatocellular carcinoma in adults, cholestasis in children
Ix for A1AT def?
- A1AT conc
- spirometry- obstructive
Mx for A1AT def?
- no smoking
- supportive= bronchodilators, physiotheraoy
- IV AT1T protein concentrates
- surgery= lung volume reduction surgery, lung transplant
Allergic bronchopulmonary asperigillosis?
results from allergy to Aspergillus spores
Hx of bronchiectasis and eosinophilia?
allergic bronchopulmonary aspergillosis
Features of allergic bronchopulmonary aspergillosis?
bronchoconstriction= wheeze, cough, dyspnoea; may have previous label of asthma
bronchiectasis (proximal)
Ix for allergic bronchopulmonary aspergillosis?
- eosinophilia
- flitting CXR changes
- positive radioallergosorbent (RAST) test to Aspergillus
- positive IgG precipitins (not as positive as in aspergilloma)
- raised IgE
Mx of allergic bronchopulmonary aspergillosis?
Oral glucocorticoids
2nd line= itraconazole
3 types of altitude related disorders?
1) acute mountain sickness (AMS)
may progress to…
2) high altitude pulmonary oedema (HAPE) or
3) high altitude cerebral oedema (HACE)
What are AMS, HAPE and HACE (altitude related disorders) all due do?
chronic hypobaric hypoxia which develops at high altitudes
Acute mountain sickness features?
- self-limiting
- headache
- nausea
- fatigue
When do features of AMS start to occur and how long do they last?
above 2500-3000m
develop gradually over 6-12hrs and can last a number of days
Prevention of AMS?
- risk may be correlated to physical fitness
- gain altitude of no more than 500m a day
- acetazolamide
What is acetazolamide?
a carbonic anhydrase inhibitor used to prevent AMS
causes primary metabolic acidosis and compensatory resp alkalosis which increases RR and improves oxygenation
Treatment of AMS?
descent
Pt with AMS may develop HAPE or HACE (potentially fatal) when?
if go above 4000m (minority of people will go on to develop this)
Presentation of HAPE (high altitude pulmonary oedema)?
classic pulmonary oedema features
Mechanism of HAPE (high altitude pulmonary oedema)?
hypobaric hypoxia → uneven hypoxic pulmonary vasoconstriction → uneven blood flow in the lungs → areas of the lung receiving more blood experience an increase in capillary pressure → more fluid leakage. Hypoxia may also directly increase capillary permeability, exacerbating fluid leakage into the alveolar space.
Features of HACE (high altitude cerebral oedema)?
headache, ataxia, papilloedema
Mechanism of HACE (high altitude cerebral oedema)?
in contrast to HAPE, cerebral vasodilation is the problem. Hypoxia → cerebral vasodilation → elevated cerebral blood volume
also, hypoxia → increase in the permeability of the blood-brain barrier → capillaries in the brain more leaky → leading to fluid accumulation in the extracellular spaces
both these factors → cerebral oedema
Mx of HACE (high altitude cerebral oedema)?
descent and dexamethasone
Mx of HAPE (high altitude pulmonary oedema)?
descent; O2 if available and medication= nifedipine, dexa, acetazolamide, or phosphodiesterase type V inhibitors (all reduce systolic pulmon artery pressure)
5 steps for ABG interpretation?
1) How is the pt?
2) Is the pt hypoxaemic? (<10kPa)
3) Is the pt acidaemic (pH <7.35) or alkalaemic (pH >7.45)?
4) Respiratory component= what has happened to PaCO2? (resp acidosis/alkalosis or resp compensation)
5) Metabolic component= what is the bicarb level/base excess? (metabolic acidosis/alkalosis or renal compensation)
ABG: step 2- how to know if pt is hypoxaemic?
the PaO2 on air should be >10kPa if normal
ABG: step 3- how to know if pt is acidaemic or alkalaemic?
Acidaemic= pH <7.35
Alkalaemic= pH >7.45
ABG: step 4- how to work out the respiratory component?
What has happened to PaCO2.
- PaCO2 >6.0kPa= resp acidosis (or resp compensation for metabolic alkalosis)
- PaCO2 <4.7kPa= resp alkalosis (or resp compensation for metabolic acidosis)
ABG: step5- how to work out the respiratory component?
What is the bicarb/base excess.
- Bicarb <22mmol/l (or base excess < -2mmol/l)= metabolic acidosis (or renal compensation for resp alkalosis)
- Bicarb >26 (or base excess > +2)= metabolic alkalosis (or renal compensation for resp acidosis)
ABG: PaCO2 > 6.0 kPa?
respiratory acidosis (or respiratory compensation for a metabolic alkalosis)
ABG: PaCO2 < 4.7 kPa?
respiratory alkalosis (or respiratory compensation for a metabolic acidosis)
ABG: bicarbonate < 22 mmol/l (or a base excess < - 2mmol/l)?
metabolic acidosis (or renal compensation for a respiratory alkalosis)
ABG: bicarbonate > 26 mmol/l (or a base excess > + 2mmol/l)?
metabolic alkalosis (or renal compensation for a respiratory acidosis)
ABG: low pH and high PaCO2?
resp acidosis
ABG: high pH and low PaCO2?
resp alkalosis
ABG: low pH and low bicarb?
metabolic acidosis
ABG: high pH and high bicarb?
metabolic alkalosis
ABG: way to remember resp/met acidosis/alkalosis results?
ROME
Respiratory = Opposite
low pH + high PaCO2 i.e. acidosis, or
high pH + low PaCO2 i.e. alkalosis
Metabolic = Equal
low pH + low bicarbonate i.e. acidosis, or
high pH + high bicarbonate i.e. akalosis
ABG: resp acidosis vs alkalosis reading?
Acidosis= PaCO2 > 6.0 kPa (HIGH) and pH <7.35 (LOW)
Alkalosis= PaCO2 < 4.7 kPa (LOW) and pH >7.45 (HIGH)
ABG: metabolic acidosis vs alkalosis reading?
Acidosis= bicarb <22 (or base excess <-2) (LOW) and pH <7.35 (LOW)
Alkalosis= bicarb >26 (or base excess >+2) (HIGH) and pH >7.45 (HIGH)
ABG: what could resp acidosis or alkalosis also mean?
Resp acidosis or could be resp compensation for a metabolic alkalosis.
Resp alkalosis or could be resp compensation for metabolic acidosis.
ABG: what could metabolic acidosis or alkalosis also mean?
Met acidosis or could be renal compensation for resp alkalosis.
Met alkalosis or could be renal compensation for resp acidosis.
ABG: how to determine if there if compensation?
1) identify if primary issue is acidosis or alkalosis
2) check if HCO3- is moving in same direction as pH to indicate compensation
3) if pH is normal then there is complete compensation
What does compensation mean in ABG?
body’s attempt to restore normal pH through changes in resp or metabolic function
ABG: respiratory compensation explained?
Changes in PaCO2 levels through changes in ventilation. Fast.
eg. Metabolic acidosis low pH, low bicarb) then with compensation there is increase in ventilation to get rid of CO2 to raise pH (so low PaCO2)
Example of ABG result showing metabolic acidosis with resp compensation?
pH LOW
bicarb LOW
PaCO2 LOW (due to hyperventilation)
ABG: metabolic compensation explained?
Changes in bicarb through renal function. Longer-hrs to days.
eg. Resp acidosis (low pH, high PaCO2) then with compensation the kidneys retain bicarb to increase levels to increase pH (so high bicarb)
Example of ABG result showing resp acidosis with metabolic compensation?
pH LOW
PaCO2 HIGH (hypoventilation)
Bicarb HIGH
ABG results that mean if there is compensation?
In resp acidosis: compensation if high bicarb to increase pH.
Resp alkalosis: compensation if low bicarb to decrease pH.
Met acidosis: compensation if PaCO2 low to increase pH (due to hyperventilation)
Met alkalosis: compensation if PaCO2 high to increase pH (due to decrease pH)
Aspiration pneumonia?
pnuemonia that develops as a result of forgein materials gaining entry to bronchial tree; eg. food or saliva
What can develop as a result of aspiration pneumonia?
chemical pneumonitis depending on acidity of the aspirate; bacterial pathogens can add to the inflam
Causes of aspiration pneumonia?
incompetent swallowing mechanism eg. due to neuro diease/injury= stroke, MS, intoxication.
Iatrogenic= intubation
RFs for aspiration pneumonia?
- poor dental hygiene
- swallowing difficulties
- prolonged hospitalisation or surgical procedures
- impaired consciousness
- impaired mucociliary clearance
Most common site affected in aspiration pneumonia and why?
Right middle and lower lung lobes due to larger calibre and more vertical orientation of R main bronchus
Examples of aerobic bacteria implicated in aspiration pneumonia?
- strep pneumoniae
- staph aureus
- H.influenzae
- p. aeruginosa
- Klebsiella
Aerobic bacteria often seen in aspiration lobar pneumonia in alcoholics?
Klebsiella
Anaerobic bacteria implicated in aspiration pneumonia?
- bacterioides
- prevotella
- fusobacterium
- peptosteptococcus
Common postop Cx where basal alveolar collapse and lead to resp difficulty?
atelectasis
What causes atelectasis?
when airways become obstructed by bronchial secretions
Features of atelectasis?
suspected in presentation of dyspnoea and hypoxaemia around 72hrs post op
Suspect what if pt has dyspnoea and hypoxaemia around 72hrs post op?
atelectasis
Mx of atelectasis?
- position pt upright
- chest physio: breathing exercises
Causes of bilateral hilar lymphadenopathy?
Most common= TB and sarcodiosis
- lymphoma/malignancy
- pneumoconiosis eg. berylliosis
- fungi eg. histoplasmosis, coccidiodomycosis
What is bilateral hilar lymphadenopathy?
bilateral enlargement of the lymph nodes of pulmonary hila
What is a chest drain?
tube inserted into pleural cavity which creates a one-way valve, allowing movement of air or liquid out the cavity
Indications of chest drain?
- pleural effusion
- pneumothorax (not for conservative Mx or aspiration)
- empyema
- haemothorax
- haemopnuemothorax
- chylothorax
- sometimes in penetrating chest wall injury in ventilated pts
Contraindications for chest drain (except resp compromise in emergency then assess on individual case basis)?
- INR >1.3
- platelet count <75
- pulmonary bullae
- pleural adhesions
Steps to insert chest drain?
1) consent and imaging
2) supine position or at 45º angle
3) forearm behind head for easy access to axilla
4) 5th ICS mid axillary line; use USS in all cases of fluid within pleura
5) lidocaine (up to 3mg/kg) injection
6) insert tube using seldinger technique
7) secure with straight stitch or adhesive dressing
How to confirm position of chest drain?
aspiration of fluid from drainage tubing, by ‘swinging’ of the fluid within the drain tubing when pt inspires and on CXR
Cx of chest drain?
- failure of insertion
- bleeding (around site of drain or into pleural space)
- infection
- penetration of lung
- re-expansion pulmonary oedema
What if there is failure of insertion of chest drain?
drain may be abutting the apical pleura, in which case it should be pulled back, or may be subcutaneous or in rare cases could enter the abdominal cavity. In both latter cases, the drain should be removed and re-sited.
Cx of chest drain: re-expansion pulmonary oedema?
onset of cough and/or SOB
if suspect, clamp chest drain and emergency CXR
to avoid= clamp the drain tubing regularly in the event of rapid fluid output ie. drain output should not exceed 1L of fluid over <6hrs
Removal of chest drain depends upon initial indication, eg?
- fluid drainage from pleural cavity= remove when no output for >24hrs and imaging shows resolution
- pneumothorax= remove when no longer bubbling spontaneously or when pt coughs and ideally when imaging shows resolution
- penetrating injury= review by specialist
Anatomy of insertion for chest drain?
‘safe triangle’
mid axillary line of 5th ICS; bordered by: Anterior edge latissimus dorsi, the lateral border of pectoralis major, a line superior to the horizontal level of the nipple, and the apex below the axilla.
Another anatomical site for insertion of chest drain?
triangle of auscultation
behind the scapula. It is bounded above by the trapezius, below by the latissimus dorsi, and laterally by the vertebral border of the scapula; the floor is partly formed by the rhomboid major. If the scapula is drawn forward by folding the arms across the chest, and the trunk bent forward, parts of the sixth and seventh ribs and the interspace between them become subcutaneous and available for auscultation
Causes of clubbing can be grouped into what?
cardiac, resp and other
Cardiac causes of clubbing?
cyanotic congenital heart disease (Fallot’s, TGA)
bacterial endocarditis
atrial myxoma
Resp causes of clubbing?
- lung ca
- pyogenic conditions: CF, bronchiectasis, abscess, empyema
- TB
- asbestosis, mesothelioma
- fibrosing alveolitis
Other causes of clubbing?
- Crohn’s, to lesser extent UC
- cirrhosis, primary biliary cirrhosis
- Graves (thyroid acropachy)
- rare: Whipple’s disease
Another name for eosinophilic granulmatosis with polyangiitis (EGPA)?
Churg-Strauss syndrome
What is eosinophilic granulmatosis with polyangiitis (EGPA)?
an ANCA associated small-medium vessel vasculitis?
Features of eosinophilic granulmatosis with polyangiitis (EGPA)?
- asthma
- blood eosinophilia (eg >10%)
- paranasal sinusitis
- mononeuritis multiplex
- pANCA positive in 60%
Granulomatosis with polyangiitis (Wegener’s granulomatosis) vs Churg-Strauss syndrome (eosinophilic granulmatosis with polyangiitis)?
Wegener’s= renal failure; epistaxis/haemoptysis; cANCA
Churg= asthma; pANCA; eosinophilia
Both= vasculitis; sinusitis; dyspnoea
What may precipitate eosinophilic granulmatosis with polyangiitis (EGPA)?
leukotriene receptor antagonists (LTRA)
Another name for extrinsic allergic alveolitis? (EAA)
hypersensitivity pneumonitis
What is extrinsic allergic alveolitis (hypersensitivity pneumonitis)?
condition caused by hypersensitivity induced lung damage due to variety of inhaled organic particles
What is though to cause extrinsic allergic alveolitis (hypersensitivity pneumonitis)?
immune-complex mediated tissue damage (type III hypersensitivity) although delayed hypersensitivity (type IV) thought to play a role, esp in chronic phase
Examples of extrinsic allergic alveolitis (hypersensitivity pneumonitis)?
- bird fancier’s lung
- farmers lung
- malt workers lung
- mushroom worker’s lung
Example of extrinsic allergic alveolitis (hypersensitivity pneumonitis): what causes bird fancier’s lung?
avian proteins from bird droppings
Example of extrinsic allergic alveolitis (hypersensitivity pneumonitis): what causes farmers lung?
spores of Saccharopolyspora rectivirgula from wet hay (formerly Micropolyspora faeni)
Example of extrinsic allergic alveolitis (hypersensitivity pneumonitis): what causes malt worker’s lung?
Aspergillus clavatus
Example of extrinsic allergic alveolitis (hypersensitivity pneumonitis): what causes mushroom worker’s lung?
thermophulic actinomycetes
Presentation of extrinsic allergic alveolitis (hypersensitivity pneumonitis)?
acute (4-8hrs after exposure):
- dyspnoea
- dry cough
- fever
chronic (occurs w-m after exposure):
- lethargy
- dyspnoea
- productive cough
- anorexia and weight loss
Ix for extrinsic allergic alveolitis (hypersensitivity pneumonitis)?
- imaging= upper/mid-zone fibrosis
- bronchoalveolar lavage= lymphocytosis
- serologic assays for specific IgG antibodies
- blood= NO eosinophilia
Mx for extrinsic allergic alveolitis (hypersensitivity pneumonitis)?
- avoid precipitating factors
- oral glucocorticoids
Another name for granulomatosis with polyangiitis?
Wegener’s granulomatosis
Granulomatosis with polyangiitis?
autoimmune condition associated with necrotising granulomatous vasculitis affecting both upper and lower resp tract and the kidneys
Features of granulmatosis with polyangiitis?
- URT= epistaxis, sinusitis, nasal crusting
- LRT= dyspnoea, haemoptysis
- rapidly progressive glomerulonephritis (‘pauci-immune’, 80%)
- saddle-shaped nose deformity
- vasculitic rash, eye invl. (eg. proptosis), cranial nerve lesions
Ix for granulomatosis with polyangiitis?
- cANCA +ve in >905, pANCA +ve in 25%
- CXR= wide variety of presentations, incl. cavitating lesions
- renal biopsy= epithelial crescents in Bowman’s capsule
Mx of granulomatosis with polyangiitis?
- steroids
- cyclophosphamide (90% response)
- plasma exchange
- median survival= 8-9yrs
Inhaler technique?
1) remove cap & shake
2) breathe out gently
3) put mouthpiece in mouth & as you begin to breathe in deep and slow, press the canister down and continue to inhale steadily and deeply
4) hold breath for 10secs or as long as comfortable
5) for a second dose wait for approx 30secs before repeating
only use device for number of doses on label then start new inhaler
Kartagener’s syndrome (primary ciliary dyskinesia)?
rare autosomal recessive genetic ciliary disorder
triad= situs inversus, chronic sinusitis and bronchiectasis
most frequently occus in examinations due to its association with dextrocardia (eg. quiet heart sounds, small volume complexes in lateral leads)
Kartagner’s syndrome (primary ciliary dyskinesia) pathogenesis?
dynein arm defect results in immotile cilia
Features of kartagener’s syndrome (primary ciliary dyskinesia)?
- dextrocardia or complete situs inversus
- bronchiectasis
- recurrent sinusitis
- subfertility (secondary to diminished sperm motility and defective ciliary action in the fallopian tubes)
What is Klebsiella pneumoniae?
gram-negative rod part of the normal gut flora
What can Klebsiella pneumoniae cause?
pneumonia (typically following aspiration) and UTI
‘red-current jelly’ sputum?
Klebsiella pneumonia
Features of Klebsiella pneumonia?
- more common in alcoholics and diabetics
- may occur following aspiration
- red-current jelly sputum
- often affects upper lobes
Prognosis of Klebsiella pneumoniae?
- commonly causes lung abscess formation and empyema
- mortality 30-50%
Lung abscess?
well-circumscribed infection within lung parenchyma
Lung abscess most commonly forms secondary to what?
aspiration pneumonia (RFs: poor dental hygiene, previous stroke, reduced consciousness)
Causes of lung abscess?
- secondary to aspiration pneumonia
- haematogenous spread (eg. secondary to infective endocarditis)
- direct extension (eg. from an empyema)
- bronchial obstruction (eg. secondary from a lung tumour)
Lung abscess’s are typically polymicrobial. What are some monomicrobial causes?
- staph. aureus
- Klebsiella pneumoniae
- Pseudomonas aeruginosa
Features of lung abscess?
- similar to pneumonia but more subacute presentation: may develop over weeks
- may see systemic features eg. night sweats and weight loss
- fever
- productive cough= foul-smelling sputum, haemoptysis in minority
- chest pain
- dyspnoea
Signs of lung abscess?
- dull percussion and bronchial breathing
- may see clubbing
Ix for lung abscess?
- CXR= fluid filled space within area of consolidation; an air-fluid level is typically seen
- sputum and blood cultures also
Lung abscess Mx?
- IV Abx
- not resolving then percutaneous drainage may be needed or in v. rare cases surgical resection
Mediastinum?
region between the pulmonary cavities
What is the mediastinum covered by?
mediastinal pleura
Where is the mediastinum?
between the pulmonary cavities and extends from the thoracic inlet superiorly to the diaphragm inferiorly
Mediastinal regions?
Superior mediastinum (between manubriosternal angle and T4/5)
Middle mediastinum
Posterior mediastinum
Anterior mediastinum
Contents of the superior mediastinum?
Superior vena cava
Brachiocephalic veins
Arch of aorta
Thoracic duct
Trachea
Oesophagus
Thymus
Vagus nerve
Left recurrent laryngeal nerve
Phrenic nerve
Contents of the anterior mediastinum?
Thymic remnants
Lymph nodes
Fat
Contents of the middle mediastinum?
Pericardium
Heart
Aortic root
Arch of azygos vein
Main bronchi
Contents of the posterior mediastinum?
Oesophagus
Thoracic aorta
Azygos vein
Thoracic duct
Vagus nerve
Sympathetic nerve trunks
Splanchnic nerves
Microscopic polyangiitis?
small vessel ANCA vasculitis
Features of microscopic polyangiitis?
- renal impairment= raised creatinine, haematuria, proteinuria
- fever
- lethargy, myalgia, weight loss
- palpable purpura rash
- cough, dyspnoea, haemoptysis
- mononeuritis multiplex
Ix for microscopic polyangiitis?
- pANCA (against MPO)= +ve in 50-75%
- cANCA (against PR3)= +ve in 40%
Polyangiitis?
inflam of multiple types of vessels such as small arteries and veins
Indications for non-invasive ventilation? (NIV)
- COPD with resp acidosis pH 7.25-7.35
- T2RF secondary to chest wall deformity, neuromuscular disease or obstructive sleep apnoea
- cardiogenic pulmonary oedema unresponsive to CPAP
- weaning from tracheal intubation
Can NIV be used in COPD with resp acidosis in pts who are more acidotic eg. pH <7.25?
yes but need greater degree of monitoring eg. HDU and a lower threshold for intubation and ventilation should be used
Recommended initial settings for bi-level pressure (BiPAP) support in COPD?
- Expiratory Positive Airway Pressure (EPAP)= 4-5cm H2O
- Inspiratory Positive Airway Pressure (IPAP): 12-15cm H2O
- back up rate= 15 breaths/min
- back up inspiration:expiration ratio= 1:3
2 common types of non-invasive ventilation?
BiPAP (Bilevel Positive Airway Pressure) and CPAP (Continuous Positive Airway Pressure)
BiPAP vs CPAP (NIV)?
BiPAP= provides 2 levels of pressure (IPAP and EPAP); more comfortable as easier to exhale due to lower EPAP setting; more expensive as more complex (2 pressure settings); more flexible as can adjust pressures for both inhalation and exhalation; more severe conditions or if don’t respond to CPAP
CPAP= continuous constant pressure throughout entire breathing process; pressure is set at fixed level to prevent airway collapse; 1st line for OSA when it is mild-moderate; exhaling against constant pressure uncomfortable so long-term use difficult; cheaper
Why is the pressure in CPAP set at a fixed level?
to prevent airway collapse
When to use CPAP vs BiPAP?
BiPAP= higher pressure needs; central sleep apnea; chronic resp conditions eg. COPD (due to additional support); restrictive lung disease/hypoventilation syndrome; acute resp distress or resp failure; CHF (more complex breathing patterns)
CPAP= OSA; milder breathing issues and lower pressure needs (don’t need more complex airway support); post-surgery or during recovery to maintain airway stability
What does the oxygen dissociation curve describe?
relationship between % of sat Hb and partial pressure of O2 in blood; NOT affected by Hb conc
Why does O2 dissociation curve shift to the left?
Lower oxygen delivery
eg. due to
HbF, methaemoglobin, carboxyhaemoglobin
Low [H+] (alkali)
Low pCO2
Low 2,3-DPG
Low temperature
Why does O2 dissociation curve shift to the right?
Raised O2 delivery
eg. due to
Raised [H+] (acidic)
Raised pCO2
Raised 2,3-DPG
Raised temperature
What is the L rule for the O2 dissociation curve?
Shifts to L → Lower oxygen delivery, caused by
Low [H+] (alkali)
Low pCO2
Low 2,3-DPG
Low temperature
Another mnemonic is ‘CADET, face Right!’ for CO2, Acid, 2,3-DPG, Exercise and Temperature
What normally influences O2 affinity?
haemoglobin’s structural conformation, which is dependent on the heme component and globin chains. Normal adult haemoglobin (HbA) comprises two alpha and two beta chains.
Structural alteration in Hb that may alter O2 affinity/variant Hb?
- point mutations eg. HbS
- changes in Heme affinity (Hb Kempsey (β99 Asp→Asn) showcases increased oxygen affinity, leading to impaired oxygen release in tissues.)
- altered quaternary structure
- changes in allosteric regulators (eg. 2,3-BPG, pH and CO2 levels) for example: Hb Rainier (β145 Tyr→His) shows reduced affinity for 2,3-BPG, leading to higher oxygen affinity and less efficient oxygen delivery to tissues.
- Polymerisation eg. HbS polymerise under low O2 conditions, distorting RBCs and impairing O2 delivery
- Aggregation of abnormal Hb can lead to haemolysis
3 examples of clinical implications of variant Hb?
1) Polycythaemia= high O2-affinity variants may lead to tissue hypoxia and compensatory polycythaemia (can increase thrombotic risk so can Mx with low dose aspirin/ venesection)
2) cyanosis= Hb with reduced O2 affinity can cause cyanosis due to increased levels of deoxygenated Hb
3) Haemolytic anaemia= eg. sickle cell lead to chronic haemolytic anaemia
Immediate Mx for pts who are critically ill (anaphylaxis, shock etc) as hypoxia kills?
Oxygen via non-rebreather (reservoir mask) at 15L/min
exclude certain conditions where pt is acutely unwell eg. MI but stable
Oxygen sat targets?
- acutely ill= 94-98%
- risk of hypercapnia (eg. COPD pts)= 88-92%
O2 should be reduced in stable pts with satisfactory O2 sats
O2 management in COPD pts?
- prior to blood gas availability= 28% Venturi mask at 4L/min and aim for sats 88-92% (for pt with RF for hypercapnia but no prior history of resp acidosis)
- adjust target range to 94-98% IF pCO2 NORMAL
Situations where O2 therapy should not be routinely used if there is no evidence of hypoxia?
- MI and ACS
- stroke
- obstetric emergnencies
- anixety-related hyperventilation
Psittacosis?
infection caused by Chlamydia psittaci; most common presentation is a cause of atypical pneumonia. Rare.
When to suspect psittacosis?
- typical fever + history of bird contact (84%)
- or pneumonia with severe headache or organomegaly and failure to respond to penicillin Abx
- more common in young adults
What causes psiittacosis?
Chlamydia psittaci (obligate intracellular bacterium)
Transmission of psittacosis?
typically from birds or bird secretions eg. urine and faeces, typically after cleaning bird cages
pet birds and wild birds
transmission from other animals or humans possible but very rare
Presentation of psittacosis?
subacute onset of:
- flu-like symptoms (90%)= fever, headache, myalgia
- resp symptoms (82%)= dyspnoea, dry cough, chest pain
Signs of psittacosis?
- chest= unilateral crepitations and vesicular breathing (common), evidence of pleural effusion (uncommon)
- abdo= hepatomegaly and splenomegaly (rare)
Ix for psittacosis?
- raised inflam markers
- CXR= consolidation
- confirmation with serology (usually part of atypical pneumonia screening)
Mx of psittacosis?
1st line= tetracyclines e.g. doxycycline
2nd line= macrolides e.g. erythromycin
Causes of resp acidosis?
COPD
decompensation in other respiratory conditions e.g. life-threatening asthma / pulmonary oedema
neuromuscular disease
obesity hypoventilation syndrome
sedative drugs: benzodiazepines, opiate overdose
Causes of resp alkalosis?
anxiety leading to hyperventilation
pulmonary embolism
salicylate poisoning
CNS disorders: stroke, subarachnoid haemorrhage, encephalitis
altitude
pregnancy
Salicylate overdose- does it lead to resp/met acidosis or alkalosis?
a mixed respiratory alkalosis and metabolic acidosis. Early stimulation of the respiratory centre leads to a respiratory alkalosis whilst later the direct acid effects of salicylates (combined with acute renal failure) may lead to an acidosis
Tidal volume (TV?
volume inspired or expired with each breath at rest
500ml in males, 350ml in females
Inspiratory reserve volume (IRV)?
2-3 L
maximum volume of air that can be inspired at the end of a normal tidal inspiration
inspiratory capacity = TV + IRV
Expiratory reserve volume (ERV)?
750ml
maximum volume of air that can be expired at the end of a normal tidal expiration
significantly reduced in obesity (increased abdominal fat mass pushes up against the diaphragm, reducing the volume of air that can be expelled)
Residual volume (RV)?
1.2L
volume of air remaining after maximal expiration
increases with age
RV = FRC - ERV
Functional residual capacity (FRC)?
the volume in the lungs at the end-expiratory position
FRC = ERV + RV
Vital capacity (VC)?
5L
maximum volume of air that can be expired after a maximal inspiration
4,500ml in males, 3,500 mls in females
decreases with age
VC = inspiratory capacity + ERV
Total lung capacity (TLC)?
around 6L (4-6L)
sum of the vital capacity + residual volume
maximal volume of gas in the lungs after a maximal inspiration
Physiological dead space (VD) (lung volumes)?
VD = tidal volume * (PaCO2 - PeCO2) / PaCO2
where PeCO2 = expired air CO2
No Abx prescribing or delayed Abx prescribing is generally recommended for pts with what?
acute otitis media, acute sore throat/acute pharyngitis/acute tonsillitis, common cold, acute rhinosinusitis or acute cough/acute bronchitis
Immediate Abx prescribing approach may be considered for pts with what?
children younger than 2 years with bilateral acute otitis media
children with otorrhoea who have acute otitis media
patients with acute sore throat/acute pharyngitis/acute tonsillitis when 3 or more Centor criteria are present
Centor criteria for sore throat?
presence of tonsillar exudate
tender anterior cervical lymphadenopathy or lymphadenitis
history of fever
absence of cough
If 3+ of the centor criteria are present what does this mean?
there is 40-60% chance the sore throat is caused by Group A beta-haemolytic Streptococcus so give Abx
If pt is at risk of developing Cx, an immediate Abx prescribing policy is recommended. Examples?
- systemically very unwell
- S&S suggestive of serious illness and/or complications (particularly pneumonia, mastoiditis, peritonsillar abscess, peritonsillar cellulitis, intraorbital or intracranial complications)
- pre-existing comorbidity. eg. patients with significant heart, lung, renal, liver or neuromuscular disease, immunosuppression, cystic fibrosis, and young children who were born prematurely
- > 65 yrs with acute cough and two or more of the following, or older than 80 years with acute cough and one or more of the following:
hospitalisation in previous year; type 1 or type 2 diabetes; history of congestive heart failure; current use of oral glucocorticoids;
Examples of how long resp tract infections may last?
acute otitis media: 4 days
acute sore throat/acute pharyngitis/acute tonsillitis: 1 week
common cold: 1 1/2 weeks
acute rhinosinusitis: 2 1/2 weeks
acute cough/acute bronchitis: 3 weeks
Differential diagnosis for chronic SOB?
heart failure
asthma
aortic stenosis
recurrent PE
lung ca
pulmonary fibrosis
bronchiectasis
anaemia
obesity
Aortic stenosis main features?
Chest pain, SOB and syncope seen in symptomatic patients
An ejection systolic murmur radiating to the neck and narrow pulse pressure are found on examination
If pt smokes, find out about what?
- smoking behaviour
- level of nicotine dependence
- previous quitting attempts
Mx if pt wishes to quit smoking?
- refer to NHS Stop Smoking Services
- drug Tx to reduce withdrawl= NRT, varenicline or bupropion
(most effective= vareniciline or combination NRT- patch + short acting preparation)
Review once seen pt wishing to stop smoking?
review 2w after stopping smoking (for NRT or 3-4w after with V or B), then CO level measured at 4w
then professional judgement
if taking V then can reduce dose to 500ug 2xd
stop V or B if develop agitation, depressed mood
What to do if pt wants to stop smoking and use e-cigarettes?
use stop smoking medicine instead; if still want to then give info and support and referral
What could you offer pts who don’t want to or not ready to stop smoking?
harm reduction approach eg:
- stop smoking but continue to use NRT
- cut down before stopping, with or without NRT
- temporary abstinence, with or without NRT
- can use NRT as long as needed to prevent relapse
What type of pts should be strongly encouraged to take up referral to stop smoking services?
- aged 12-17yrs
- pregnancy women (incl who have stopped in past 2w or CO reading 4ppm+)
- mothers of young children, esp breastfeeding
if unwilling then risk and benefits of NRT and offer practical advice. Use clinical judgement whether to prescribe NRT to pregnant or young people
Can pregnant/breastfeeding/young pts be prescribed varenicline or bupropion to help stop smoking?
NO
How to ask about pts dependence on smoking and nicotine dependence?
- how many cigarretes per day
- how soon after waking do they smoke their 1st
What level of CO reading in expired air is classed as a non-smoker?
10ppm or less
Practical advise to help pt stop smoking?
- set quit date and commit
- 1st few days hardest and may get withdrawl symptoms but start to improve after 3rd or 4th day
- craving set off by: stress, seeing others smoke, being intoxicated
- manage cravings= short bouts of exercise eg. brisk walk; talking to friend; keep busy eg. game on phone or drink glass of water; change environment eg. another room/outside
- abrupt quitting eg. not a puff rule is most successful
Medical Mx for stopping smoking?
NRT, varenicline or bupropion.
Only one not any together
Combination NRT OR varenicline most effective
combination NRT= patch + short acting preparation
depends of pts preference and contraindications
Prescribe 2w of NRT or 3-4w of varenicline or bupropion then only give further prescriptions to pts who have demonstrated their attempt to quitting is continuing
Withdrawl symptoms of smoking cessation?
irritability, frustration, anger, anxiety, difficulty concentrating, increased appetitie, restlessness, depressed, insomnia
weight gain eg. 5-9kg but less likely with drug Tx
NRT for smoking cessation?
NRT= patch for 16hrs or 24hrs for background cravings and faster acting eg. lozenge or mouth spray for breakthrough urges. Don’t have acidic drinks (coffee/fruit juice) in 15mins before oral NRT. Start NRT on quit date
Varenicline for smoking cessation?
- start 7-14 days before quit date. (unavailable until further notice)
- recommended course is 12w (monitor regular and only continue if not smoking)
Bupropion for smoking cessation?
start 7-14d before quit date. 150mg prolonged release tablets.
If pt is unsuccessful using NRT, varenicline or bupropion, what should you do?
not offer a repeat prescription within 6m unless special circumstances have intervened
Can you combine NRT, varenicline or bupropion?
no
When should you offer a combination of NRT for smoking cessation?
NRT patches and another form of NRT (gum, inhalator, lozenge or nasal spray) to pts who show high level of dependence on nicotine or have found single forms of NRT inadequate in past
Varenicline (for smoking cessation) MOA?
nicotininic receptor partial agonist
Adverse effects of NRT?
nausea and vomiting, headaches and flu-like symptoms
Adverse effects of varenicline?
nausea (common), headache, insomnia, abnormal dreams
Use varenicline (smoking cessation) in caution in who? Contraindications?
- caution= Hx of depression or self-harm
- contraindicated= pregnancy and breast feeding
Bupropion (smoking cessation) MOA?
norepinephrine and dopamine reuptake inhibitor, and nicotinic antagonist
Bupropion has a small risk of what? Contraindicated in?
- small risk of seizures (1 in 1000)
- contraindication= epilepsy, pregnancy and breast feeding. Having eating disorder is relative contraindication.
NICE recommended in 2010 that all pregnant women should be tested for smoking using what?
CO detectors, partly as some women find difficult to say they smoke due to pressures not to during pregnancy
What pregnant women should be referred to NHS Stop Smoking Services?
all that smoke; stopped smoking within last 2w; CO reading of 7ppm or +
Interventions for pregnant women that smoke?
1st= CBT, motivational interviewing or structured self-help and support from NHS Stop Smoking Services
- NRT if above measures fail, remove before bed, no evidence affects childs birthweight
- varenicline and bupropion contraindicated
Very brief advice for any pt that says they smoke?
- ask current and past smoking behaviour
- verbal and written info on risks of smoking and benefits of stopping
- options for quitting= behavioural support, meds, e-cigs
- refer to stop smoking service if want to
Advice to pt who doesn’t want to stop smoking?
- advise to think about and encourage to return if decide to
- ask to adopt harm reduction approach
- record their smoking status & every opportunity ask again in sensitive way
What is transfer factor?
describes the rate at whichc a gas will diffuse from alveoli into blood
What is used to test transfer factor (the rate at which a gas will diffuse from alveoli into blood)?
carbon monoxide: results may be given as the total gas transfer (TLCO) or that corrected for lung volume (transfer coefficient, KCO)
Causes of a raised TLCO? (transfer factor)
- asthma
- pulmonary haemorrhage (e.g. granulomatosis with polyangiitis, Goodpasture’s)
- left-to-right cardiac shunts
- polycythaemia
- hyperkinetic states
- male gender, exercise
Causes of lower TLCO? (transfer factor)
pulmonary fibrosis
pneumonia
pulmonary emboli
pulmonary oedema
emphysema
anaemia
low cardiac output
What conditions may cause an increased KCO with a normal or reduced TLCO?
- KCO tends to increase with age
-pneumonectomy/lobectomy
-scoliosis/kyphosis
- neuromuscular weakness
- ankylosis of costovertebral joints e.g. ankylosing spondylitis
Summarise pneumothorax Mx?
1) Is the patient symptomatic (chest pain, breathless)?
- If no = conservative tx
- If yes = ?High risk characteristics (underlying lung disease - e.g. COPD in this pt/ haemodynamic instability/ hypoxia/ bilateral pneumothorax/ smoking >50years old/ haemothorax)
- If no high risk characteristics = conservative mx/ needle aspiration/ ambulatory device
- If yes has high risk characteristics = CHEST DRAIN if it is safe
