Respiratory Conditions Flashcards
What is acute bronchitis, what is the cause and risk factors
Lower respiratory tract infection characterised by inflammation of the bronchi
Result of inflammation of the trachea and major bronchi and is therefore associated with oedematous large airways and the production of sputum. Usually happens after an upper respiratory tract infection
Chest infection which is usually self-limiting in nature, the disease usually resolves within 30 days
Most commonly viral infection from
- Influenza A
- Influenza B
- Parainfluenza
- RSV
- Coronavirus
- Adenovirus
Risk Factors
- Smoking
- Exposure to infection
CLINICAL FEATURES
- cough that lasts less than 30 days (4 weeks)
- may be a productive cough→ white/clear sputum
- Fever
- Preceding URTI symptoms
- Runny nose
- Sore throat
- Headache
- Wheeze
- No history of chronic resp illness
INVESTIGATIONS
Usually clinical diagnosis
Other investigations:
- Pulmonary function test: will improve over time which rules out asthma bcs asthma wont improve
- Chest Xray: rule out pneumonia as cause
- CRP: see if ABx are needed
MANAGEMENT
Analgesia and good fluid intake. Just observe until reaches 4 weeks then think of whether it might be another pathology
If CRP is 20-100 offer delayed prescription
If CRP over 100/has a comorbidity or systemically unwell: oral doxycycline, can use amoxicillin if pregnant or child
COMP: chronic cough and pneumonia
PROG: self limiting but poorer prog in those with preexisting lung conditions, elderly or immunocompromised
How is acute bronchitis differentiated from pneumonia
- Sputum, wheeze, breathlessness may be absent in acute bronchitis
- At least one tends to be present in pneumonia
- No other focal chest signs (dullness to percussion, crepitations, bronchial breathing) in acute bronchitis other than wheeze (no radiological changes either)
- Systemic features (malaise, myalgia, and fever) may be absent in acute bronchitis whereas they tend to be present in pneumonia
What is bronchiectasis, the types, the causes
Permanent dilation of the airways secondary to chronic infection or inflammation due to destruction of elastic and muscular components of bronchial wall
Classified into:
- CF bronchiectasis
- Non-CF bronchiectasis
Causes:
- Post-infective/recurrent pulmonary infections
- Measles
- Pertussis
- Pneumonia
-Cystic Fibrosis
- TB
- COPD
- Aspiration
- Chronic Inflammatory diseases- coeliac, RA
- Allergic bronchopulmonary aspergillosis (ABPA)
- Primary ciliary dyskinesia (Kartagener’s syndrome)
- Bronchial obstruction (lung cancer or foreign body)
- Immune deficiency (selective IgA (lack of IgA) and hypogammaglobulinaemia)
Obstructive diseases cause bronchiectasis because the mucus plugs form in airways and obstruct
Organisms that most commonly cause:
- Haemophilus influenzae - most common
- Pseudomonas aeruginosa
- Klebsiella spp.
- Streptococcus pneumoniae
CLINICAL FEATURES
- Chronic cough associated with large (copious) amounts of purulent sputum (green/rusty colour). May be worsened by lying flat or on one side
- Haemoptysis
- Recurrent chest infections
- Inspiratory coarse crackles on auscultation
- Clubbing
- SOB (especially on exertion)
- Fever
- Acute exacerbation often presents with fatigue, weight loss and wheezing
INVESTIGATIONS
1st- Chest X-ray : will show obscured hemidiaphragm, thin-walled ring shadows woth/without fluid levels, tubular or ovoid opacities, tram lines (parallel line shadows)
Gold standard is : HRCT : would show thickened dilated airways (widened black dots with thick white walls around), varicose constrictions along airways, cysts and/or in bud tree pattern, signet ring, tram-track sign
Spirometry: Obstructive pattern (<0.7)
Sputum MCS: look for underlying cause like haemophilus influenzae (most common) or psudomonas aeruginosa (common in CF)
CYstic fibrosis sweat test- high chloride
MANAGEMENT
- Exercise and improved nutrition
- Airway clearance therapy (chest physiotherapy)
Postural drainage
Percussion
Vibration
Use of oscillatory devices
Maintenance of oral hydration
- Inhaled bronchodilator (salbutamol)- dilate so help clear mucus
- Mucoactive agent e.g. nebulised hypertonic saline
- Abx → amoxicillin, vancomycin
- Immunisations
Lobectomy in uncontrolled haemoptysis or localised disease
COMP
- Massive haemoptysis
- Respiratory failure
- Cor pulmonale
- Ischaemic stroke
PROG: irreversible has periods of good control and period of exacerbation
What is Cystic Fibrosis, clinical findings, investigations and management
Autosomal recessive disorder causing increased viscosity of secretions due to defect in cystic fibrosis transmembrane regulator (CFTR)
Clinical features
- Recurrent chest infections
- Failure to thrive (delayed puberty)
- Malabsorption (steatorrhoea)
- Short stature
- Male infertility
Investigations: Via sweat test (will have abnormally high sweat chloride)
Screened at birth via heel prick
Management: Chest physiotherapy
What is Allergic bronchopulmonary aspergillosis (ABPA),clinical features, investigations and management
Bronchiectasis + bronchoconstriction caused by hypersensitivity response to aspergillus fungus (mould)
Clinical features?
- Wheeze
- Cough
- Dyspnoea
Bloods show
- Eosinophilia
- Raised IgE
Management
Oral prednisolone
What are the clinical features of primary ciliary dyskinesia (Kartagener’s syndrome
Bronchiectasis + dextrocardia (or complete sinus inversu-heart on wrong sides) + recurrent sinusitis
Male infertility
What is COVID-19, its transmission route and incubation period
Potentially severe acute respiratory infection caused by the novel coronavirus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)
Transmitted via respiratory droplets
Incubation period is 5 days
CLINICAL FEATURES
- Fever
- Cough
- Dyspnoea
- Altered sense of smell/taste
- Headache
- Sore throat
- Nasal congestion
INVESTIGATIONS
Real-Time Reverse Transcription Polymerase Reaction (RT-PCR) from a nasopharyngeal swab
Pulse oximetry
Chest X-ray if pneumonia is suspected
MANAGEMENT
mild/moderat
isolation + supportive measures + antipyretic/analgesic
severe
hospital admission, VTE prophylactic, oxygen therapy, mechanical ventilation
COMPLICATION
- Thrombosis
- AKI
- Long covid
- Cardiac arrest
- Sepsis
- DIC (disseminated intravascular coagulation)
Prognosis: most die if respiratory failure from ARDS
What diseases come under the term lower respiratory tract infection, how does it compare to URTI and does influenza cause upper or lower
- Pneumonia
- Lung abscess
- Acute bronchitis
LTRI is more serious
Influenza causes upper + lower
CLINICAL FEATURES
-Sneezing
- Sore throat
- Nasal congestion & discharge
- Malaise
- Muscle fatigue
- Pain
What is an upper respiratory tract infection, where in the body does it affect and what are some examples
Consists of
- Nose
- Sinuses
- Pharynx
- Larynx
- Trachea
- Mainly viral
- Bacterial in some instances
- Tonsillitis
- Laryngitis
- Sinusitis
- Otitis media
- Rhinitis
- Common cold
CLINICAL PRESENTATION
- Cough
- Sore throat
- Runny nose & sneezing
- Nasal congestion
- Headache
- Fever
- Facial pressure
MANAGEMENT
Symptomatic support
- Analgesia
- Decongestants
- Cough medicine
If see unilateral polyps then urgent referral to ENT as its a red flag
What is Tuberculosis,the types and risk factors
An infectious, chronic granulomatous disease caused by Mycobacterium tuberculosis
Affects the lungs, especially upper lobes but can spread through blood to cause extrapulmonary TB
- M tuberculosis is dormant in many patients, if host becomes immunocompromised the initial infection may become reactivated into secondary TB
- Primary TB is asymptomatic and happens in immunocompetent individuals who become exposed to M tuberculosis- this usually heals in them
Risk factors:
- Exposure to infection
- Immunosuppression:
- Diabetes
- Cushings
- Steroid use
- Silicosis (form of lung fibrosis)
- HIV
- Malignancy
- Birth in an endemic country
- India
- Bangladesh
- Sub Saharan Africa
- Overcrowded areas
CLINICAL FEATURES
- Cough → productive (may have haemoptysis), doesn’t respond to conventional antibiotic therapy
- Fever
- Weight loss
- Night sweats
- SOB
- Anorexia
- Malaise
- Pleuritic chest pain
- Cervical lymphadenopathy + hilar lymphadenopathy
- Pott’s Disease → spread to bones
similar presentation to cancer so look at age and presence of fever
MANAGEMENT
1st line : Chest X-ray
- Consolidation
- Bilateral hilar lymphadenopathy
- Cavitating lesion in upper lobe (Caseating granulomas)
Gold standard diagnostic test: Sputum culture- most sensitive and specific test
Sputum acid-fast bacilli smear uses a ziehl-neelson stain or auramine stain: If have TB show acid fast bacillus positive
Offer: HIV test
For contacts of infected patients do : Mantoux test to screen for latent TB but immunosuppression can cause a false-negative e.g. in
- sarcoidosis
- steroid use
- lymphoma
- AIDS
MANAGEMENT
Latent TB:
Rifampicin + Isoniazid
Active TB:
Rifampicin + Isoniazid + Pyrazinamide + Ethambutol
- Rifampicin and Isoniazid for 6 months
- Pyrazinamide and ethambutol for 2 months
Pyridoxine supplementation
Before commencing treatment ⇒ U&E’s, LFTs, Vision Testing, FBC
Prevention: tuberculin skin test
COMP
transmission of TB
ARDS
Pneumothorax
Haemoptysis
Bronchiectasis
PROG: without treatment mortality rate over 50%. if treated do well
What are the side effects of the medication used to treat TB
Rifampicin
- Red/orange secretions
- Hepatitis as P450 induces which increases metabolism of warfarin and decreases INR
Isoniazid
- Drug induced lupus
- Peripheral neuropathy: give pyridoxine VitB6
- Hepatitis
Pyrazinamid
- Can cause gout due to hyperuricaemia
- Hepatitis
Ethambutol
May cause optic neuritis
Avoid in CKD
What is influenza, when do most infections occur, how is type A and B spread, what classifications of type A are there, what can prevent the spread and how is influenza categorised
Highly contagious disease caused by influenza viruses A, B, and C
RF: winter, healthcare worker, have diabetes or cardio/resp issue, immunocomprimised, over 65 yrs or 6months to 5 years old
A+B (RNA viruses) spread via person-to-person transmission directly through respiratory droplets and indirectly through contact with contaminated surfaces
A is classified into groups based on glycoproteins of viral envelope
- Haemagglutinin (H)
- Neuraminidase (N)
Hygiene products and vaccination can protect
CLINICAL FEATRES
Characterised by upper + lower respiratory tract symptoms
- Fever
- Acute bronchitis- cough
- Headache
- Arthralgia
- Myalgia
- Fatigue and malaise
INVESTIGATIONS
Clinical Diagnosis
Can do:
Reverse Transcriptase-Polymerase Chain Reaction (RT-PCR)
Viral culture
MANAGEMENT
At risk individuals: antiviral prophylaxis
Antivirals → neuraminidase inhibitors- inhibit release of virus from host cells
- Oseltamivir (’tamiflu’)
- Zanamivir
Influenza vaccination in winter between september and early november for at risk groups such as:
- >65 years
- Chronic respiratory, heart, kidney, liver, neurological disease
- Diabetes mellitus
- Immunosuppressed
- Splenic dysfunction
- Pregnant women
- BMI ≥ 40 kg/m^2
- NHS staff
(Shouldn’t be given to acutely unwell patients, must wait until they have recovered)
Vaccines given routinely to children are live, to the elderly they are inactivated- important because different contraindications
Adults
1st line = paracetomol
If at risk/present within 48 hours: antivirals
If develop bacterial pneumonia: ceftriaxone, cefotaxime, cefuroxime
If develop otitis media: amoxicillin
Children : same, different if develop bacterial pneumonia
but only ceftrixone in bacterial
if staph aureus : oxacillin, naficillin, vancomycin, linezolid
COMPLICATIONS
- Bacterial pneumonia
- Otitis media
- Encephalitis
(influezae infection predisposes to streptococcus pneumoniae infection)
What is pneumonia, what are the types, the different causes and the risk factors
Respiratory infection characterized by inflammation of the alveolar space
Causes
- Bacterial pneumonia- most common- Streptococcus pneumoniae most common pathogen
- Viral
- Fungal (e.g. Pneumocystis jiroveci)
RF
- Old age
- Chronic diseases:
- COPD
- HF
- Bronchiectasis
- Immunosuppression e.g. HIV
- Crowded living conditions
Types: CAP (typical and atypical), HAP, idiopathic interstitial pneumonia and aspiration pneumonia
1) CAP
2 types= typical and atypical
TYPICAL
1) Streptococcus pneumoniae- clinical features
- Gram +ve encapsulated lancet shaped coccobacilli
- Rusty sputum
- Can reactivate HSV and cause cold sores
2) Staphylococcus aureus
- Gram +ve cocci found in clusters
- Common in IVDU
- Also occurs after influenza
- Causes cavitating lesions (gas filled lesions) on CXR
-
3) Haemophilus influenzae
- Gram -ve coccobacilli
- Especially in COPD patients
4) Klebsiella pneumoniae
Gram -ve non motile encapsulated bacillus
- Alcoholics and diabetics
- Causes cavitating lesion (gas filled lesions) on CXR, typically upper lobe
- Blood stained sputum (red-currant jelly)
- Commonly due to aspiration
- Causes lung abscess formation and empyema (pus collection in lungs)
Lung Abscesses: - chest pain
- Subacute productive cough
- Foul smelling sputum
- Night sweats
- Fever
IV ABX, dont usually need to drain
TYPICAL CAP TREATED WITH:
Amoxicillin or Co-Amoxiclav
ATYPICAL
1) Mycoplasma pneumoniae
- Associated with erythema multiforme (ring-shaped rash)
- Autoimmune haemolytic anaemia (cold agglutins, IgM) → RBC agglutination on blood smear
Diagnosed with serology and positive cold agglutination test
2) Legionella pneumophilia
- from faulty air conditioning, recently returned from holiday
Legionella = Low sodium, Liver derangement, Leukopenia
- hyponatraemia
- abnormal LFTs
- leukopenia
Daignosed with urinary antigen
3) Chlamydia psittaci
Associated with pet birds
4) Pneumocystis jirovecii
Affects HIV (any immunosuppressed individual)
causes desaturation on exercise
treated with co-trimoxazole (trimethoprim and sulfamethoxazole)
ATYPICAL CAP TREATED WITH Clarithromycin
2) HAP
- Staphylococcus aureus
Cavitating lesions on CXR
MRSA treated with vancomycin
NMRSA flucloxacillin/rifampcin
- Psudomonas aeruginosa
causes: CF and bronciectasis
treated with tazocin
3) Idiopathic Interstitial Pneumonia
Group of non-infective causes of pneumonia e.g Cryptogenic organising pneumonia → a form of bronchiolitis that may develop as a complication of RA or amiodarone therapy
4) Aspiration Pneumonia
Seen in patients with dysfunctional/unsafe swallow : stroke, MA, bulbar palsy, alcoholics. Aspiration of stomach contents is a cause in patients who have neurological injury or who have been intubated
Right lung usually affected since right bronchus is wider and more vertical. Would see consolidation at right lung base
Treat with amoxicillin and metronidazole
CLINICAL PRESENTATION
TYPICAL PNEUMONIA
- Productive cough with purulent sputum (yellow-greenish)
- High fever and chills
- Pleuritic chest pain
- Malaise
- SOB
- Tachypnoea
- O&E
- Crackles on auscultation (bronchial breathing)
- Decreased breath sounds
- Dullness on percussion
- Increased tactile fremitus
ATYPICAL PNEUMONIA
- More slow onset
- Non productive cough
- SOB
- Fever
- Headache
- Myalgia
- Diarrhoea
INVESTIGATIONS
Chest X-ray
- Alveolar opacification
- Air bronchograms
- Consolidation
patients with pneumonia have to redo X-ray at 6 weeks after clinical resolution to rule out any underlying malignancies that were hidden by penumonia consolidation
Bloods
- FBC- neutrophilia in bacterial infections
- CRP- raised in response to infection
- Urea and electrolytes- Dehydration (high urea)
- Procalcitonin- Increased in lower respiratory tract infections
ABG
- Indicates if the oxygen saturations are low
- If patient has any pre-existing respiratory disease e.g. COPD
Urinary Antigen test
Rapid bedside test for diagnosis of
- Legionella (atypical)
- Streptococcus pneumoniae
Sputum MCS
MANAGEMENT
CAP
1) Amoxicillin- typical cover
2) Clarithromycin- Atypical : give if allergic penicillin, avoid in patients with long QT, give pregnant women erythromycin
3) Doxycycline: if allergic to penicillin
HAP
Co-amoxiclav within 5 days of admission as can cause cholestasis (high ALP, high bilirubin)
If after 5 days Tazocin
Supportive ALL PNEUMONIA
- Oxygen- If hypoxaemic
- IV fluids- If hypotensive or signs of dehydration
If patient also has COPD then give Prednisolone, even if there’s no sign of exacerbation of the COPD
COMP
- Pleural effusions
- ARDS
- Respiratory failure
- Sepsis
PROG
- Mortality increases with age and increasing CURB-65 score
- HAP has higher mortality than CAP
What is the scoring system used for pneumonia
CURB-65
Scoring system used for risk stratification for the management of patients with community acquired pneumonia
- Confusion
- Abbreviated mental test score ≤ 8/10
- Urea > 7 mmol/L
- Respiratory rate ≥ 30/min
- Systolic ≤ 90mmHg or diastolic ≤ 60 mmHg
- Age ≥ 65 years
0-1= Outpatient- treat with amoxicillin
2= Hospitalisation- treat with amoxicillin and clarithromycin
3 or more= ICU level of care- treat with IV co-amoxiclav and clarithromycin
In primary care CRB-65 as cant get serum urea result
0= treatment at home- oral amoxicillin
1 or more= hospitalise
What is allergic disorder, the pathophysiology, causes
Conditions caused by hypersensitivity of the immune system to typically harmless substances
IgE binds to receptor on mast cell or basophil, triggering release of histamine
Causes
- Dust
- Foods
- Latex
- Medications
- Insect stings
- Genetics
- Stress
CLINICAL FEATURES
- Runny nose & sneezing
- Redness & itching of eyes
- Coughing & wheezing
- Rashes & hives (urticaria)
INVESTIGATIONS
Skin prick testing: for type 1 hypersensitivity reactions that caused a systemic reaction
Scratch testing: For contact dermatitis, usually type 4 hypersensitivity
Blood testing- measure concentration of specific IgE antibodies in blood and serum tryptase which is a specific marker of mast cell activation
MANAGEMENT
- Antihistamines e.g. Cetirizine
- Glucocorticoids: nasal beclometosone, nasal budenoside, mometasone nasal or triamcinolone nasal
- Emergency → Adrenaline auto-injectors for self-treatment
- Allergen Immunotherapy
Describe type 1-4 hypersensitivity reactions
Type 1 Anaphylactic/Immediate: Allergens (or antigens) are presented to T-cells by Antigen-presenting cells (APCs) during the sensitization phase of Type I hypersensitivity. T-cells then signal for stimulation of B-cells to produce IgE antibodies, which bind to the FcER1 receptors on mast cells and basophils. Subsequently, the free antigen induces the crosslinking of these mast cell and basophil bound IgE antibodies. This results in the degranulation of the cells and the release of histamine, proteolytic enzymes, and other mediators. Causes :
Anaphylaxis
Atopy (e.g. asthma, eczema, hayfever-allergcic rhinitis)
Type 2 Cell Bound: IgG or IgM binds to antigen on cell surface and destroys. Causes
- Autoimmune haemolytic anaemia
-Haemolytic disease of newborns
- Acute haemolytic transfusion reactions
- ITP
- Goodpasture’s sydrome
- Pernicious anaemia
- Rheumatic fever
- Pemphigus vulgaris/bullous pemphigoid
Type 3 Immune Complex: Free antigen and antibody (IgG, IgA) combine should be cleared by immune system, if not then antibodies start to react and deposited in blood vessel walls causing inflammation, rashes, fever . Causes:
- Serum sickness
- Systemic lupus erythematosus
- Post-streptococcal glomerulonephritis
- Extrinsic allergic alveolitis (especially acute phase)
Type 4 Delayed Hypersensitivity: T cell mediated. Antigen presented to naive T cell. When T cell meets then starts to promote inflammation, is slow so takes 2-3 days
Causes:
- TB
- GvH disease (Graft verses host)
- Allergic contact dermatitis
- Scabies
- Extrinsic allergic alveolitis
- MS
- Guillain-Barre syndrome
What is asbestos-related lung disease, difference between ARLD and asbestoisis, risk factors and the most dangerous form of asbestos
Restrictive interstitial lung disease with symptoms caused by fibrotic changes in the lungs
Asbestoisis is a type of pneumoconiosis caused by inhalation of asbestos fibres. Happens 5-10 years after exposure. Asbestos-related lung disease is classified as asbestoisis when it leads to interstitial lung disease - if its just plaque then not called asbestoisis
Risk factors
- Occupations involving manufacture
- Demolition of ships
- Plumbing
- Roofing
- Insulation
- Smoking
Crocidolite (blue) is the most dangerous
Causes lung changes
- Pleural plaques
- Pleural thickening
- Asbestoisis- causes lower lobe fibrosis so get SOB and reduced exercise tolerance (treat conservatively)
- Mesothelioma- malignant diseases of pleura get progressive SOB, chest pain and pleural effusion (Offered palliative chemotherapy but usual survival 8-14 months)
- Lung cancer
lower lobe and pleura usually the point thats most commonly affected
CLINICAL FEATURES
- Long latent period- most patients asymptomatic 15-20 years after exposure
- Progressive dyspnoea- typically exertional
- Dry cough- productive if develop COPD
- Digital clubbing
- Can see FLAWS and haemoptysis if malignant
INVESTIGATIONS
Chest X ray: see diffuse bilateral infiltrates/fibrosis in lower lobes, pleural thickening
Lung function tests- Restrictive or Obstructive pattern- Reduced DLCO in both.
Restrictive: reduced forced vital capacity (FVC), normal FEV1/FVC ratio, reduced slow vital capacity (SVC), reduced total lung capacity (TLC), reduced lung diffusion capacity testing (DLCO).
Obstructive changes: reduced FEV1, reduced FEV1/FVC ratio, increased residual volume (RV)/TLC ratio, reduced DLCO
High resolution CT- pleural thickening and pleural plaques
Bronchial Lavage: unusual but may find
Lung biopsy if malignancy
ABG (if acute)- Type 1 respiratory failure- Low oxygen with normal CO2
MANAGEMENT
No curative treatment, stop smoking
Oxygen therapy+ pulmonary rehabilitation
If obstructive airways then bronchodilators
Immunisation against influenza and pneumococcal pneumonia
Pleural plaques are benign and dont require therapy
Lung transplant if Pao2 under 60
COMPLICATIONS
- Mesothelioma (malignant tumour of mesothelial cells of the pleura)
- Occurs 20-40 years after exposure
What is mesothelioma, the clinical features, the investigations and what would a CXR show
- Mesothelioma (malignant tumour of mesothelial cells of the pleura)
- Occurs 20-40 years after exposure (asbestos)
- Dry chronic cough
- SOB
- Chest pain
- Weight loss
- Chest X-ray and CT scan
- Pleural tap
- Thoracoscopy- preferred over bronchoscopy as peripherally located
- Histology for diagnosis
- If pleural effusion, should send it for MC&S, biochemistry and cytology
- Pleural effusion
- Pleural thickening
- Mass along the pleura
Surgery+ chemo before or after if operable
chemo and immuno if inoperable
What is occupational lung disease and the main types- including what it is, what occupations its prevalent in and what tests would show
Long term exposure to irritants being breathed into the lungs
1) Coal worker’s penumoconiosis
coal miners 15-20 years after exposure to coal dust
-Simple pneumoconiosis : asymptomatic, increased COPD risk, may lead to massive fibrosis
-Progressive massive fibrosis: exertional SOB, cough +/- black sputum. Affects the upper lobes the most
OE- upper zone fibrosis and spirometry shows restrictive pattern
2)Silicosis
Fibrotic lung disease caused by inhalation of silica
Puts at risk of TB
Occupation: Stonemason, Pottery, Ceramics
on Chest X-ray see ‘Egg shell’ calcification of hilar lymph nodes
3)Asbestos exposure
-Asbestosis
-Mesothelioma: malignant disease of the pleura presents with : progressive SOB, chest pain, pleural effusion
4) Occupational asthma
isocyanates- in paints
CLINICAL FEATURES
- Insidious onset SOB
- Dry cough
- Black sputum- coal worker pneumoconiosis
- Pleuritic chest pain- due to acute asbestos pleurisy
INVESTIGATIONS
Chest X-ray
CT scan
Pulmonary function tests- spirometry shows restrictive pattern
MANAGEMENT
acute silicosis: lung lavage
coal workers pneumonoisis : smoking cessation and remove exposure to irritant.
if hypoxia- supplementary oxygen
if COPD- bonchodilators and COPD treatment
if exertional dyspnoea- pulmonary rehabilitation
occupational asthma- stay away from irritant, quit
What is sarcoidosis, who is affected and what is the diagnosis criteria
Multisystem disorder, characterised by non-caseating granulomatous (no central necrosis) inflammation which deposit around the body
Lungs, skin and eyes most affected
Diagnosed by excluding granulomatous lung diseases
Female, African-americans, bimodal 25-35 and 50-65
Unknown aetiology
CLINICAL FEATURES
- Chronic dry cough
- Dyspnoea
- Wheezing
- facial nerve palsy
- Chronic fatigue
- Arthralgia- pain in knees, ankles and wrists
- Erythema nodosum- rash on shin
- Lupus pernio- rash on face, nose, ears
- Lymphadenopathy of cervical and submandibular nodes
- Anterior uveitis- symptoms include:
- Photophobia
- Red painful eye
- Blurred vision
INVESTIGATIONS
1st- Chest X ray- will show bilateral hilar lymphadenopathy
If cxr is suspicious do high resolution CT
Gold standard for diagnosis = Bronchoscopy with lung biopsy (should show non-caseating granulomas)
Other:
Spirometry- restrictive pattern (over/ normal ratio 0.7 (low FEV1 more than FVC, but thats still low))
U&E= hypercalcaemia, high urea and creatinine if kidneys involved
FBC- anaemia, leukopenia
Raised serum ACE in sarcoidosis
MANAGEMENT
1st line : Corticosteroids (prednisolone)
given if CXR stage 2/3 who are symptomatic, if have high calcium, if have eye, heart or neuro involvement. Would not give if only bilateral hilar lymphadenopathy without symptoms (have to be stage 2 bilateral hilar with infiltrate or stage 3 just infiltrate)
Also give:
- immunosuppressive therapy: methotrexate + azathioprine (before giving azathioprine check for TMPT (thiopurine methytransferase deficiency)
- Antimalarial drugs: choroquine and hydroxychloroquine
For symptoms: NSAIDs
Final resort: lung transplant
COMP
- increased risk of malignancy
- bronchiectasis
- lung fibrosis
- chronic renal failure
- corticosteroid-related conditions (hyperglycaemia, osteoporosis, infection)
Prog: Increased calcium is associated with a poorer prognosis- Indicated renal failure
What is interstitial lung disease and the most common type
Intersitital lung disease = Group of disorders characterised by inflammation and progressive scarring (fibrosis) of the lungs
Idiopathic pulmonary fibrosis most common : diagnosed when no identifiable cause, men 50-70 years old
Upper Lobe vs Lower Lobe Fibrosis has different causes
Upper Zone (CHARTS)
- Coal workers pneumoconiosis
- Histiocytosis/Hypersensitivity pneumonitis (extrinsic allergic alveolitis - exposure to bird poop, type 3 hypersensitivity)
- Ankylosing spondylitis
- Radiation
- TB
- Sarcoidosis/silicosis
Lower Zone (DIAL)
- Drugs/ Substance-induced
- Abx esp nitrofurantoin
- Amiodarone
- Chemo
- Methotrexate
- Idiopathic
- Asbestosis (pneumoconoises)
- Lupus
CLINICAL FEATURES
- Progressive dyspnoea → initially exertional dyspnoea, that progresses to dyspnoea at rest
- Chronic dry cough
- Bibasal fine end-inspiratory crackles on auscultation
- Digital clubbing
- Fatigue
INVESTIGATIONS
Spirometry
- Restrictive lung disease pattern (reduced FEV1, significantly reduced FVC, increased FEV1/FVC ratio >0.7)
- Reduced TLCO (diffusing capacity of the lung for CO)
hrCT scan
Honeycombing
- Multiple cystic lesions within the lung parenchyma due to fibrosis, ‘ground glass’ appearance
- Investigation of choice to make diagnosis of idiopathic pulmonary fibrosis
Chest X-Ray
Bilateral lower zone reticulo-nodular shadowing
RF, anti-cyclic citrullinated perptide, anti-nuclear antibdodies
MANAGEMENT
Treat cause
Supportive:
- Oxygen therapy
- Pulmonary rehabilitation
- Vaccinations
- Influenza
- Pneumococcal
Drug to slow disease progression in Interstitial pulmonary fibrosis
Pirfenidone (or nitendanib)- antifibrotic agent
Stop smoking, pulm rehab + oxygen
If acute (worsening dyspnoea and HRCT shows new opacities of consolidation) then high dose CC = prednisolone
Only definitive treatment is lung transplantation (given in end stage)
COMPLICATIONS
- Pulmonary hypertension
- Cor pulmonale (right heart failure due to pulmonary hypertension)
- Respiratory failure
Prog- poor, 3-4 years
Who is lung cancer most common in, what are the causes, what are the types
Leading cause of cancer death worldwide
M>F, 65-75 years old
Causes:
Tobacco smoking
Exposure to carcinogens e.g radon, asbestos
Family history
TYPES
1) Small Cell Lung cancer:
Central, strong association with smoking, associated wih paraneoplastic syndromes (SIADH, cushings, LEMS-Lambert-Eaton myasthenic syndrome), causes superior vena cava obstruction- present with dyspnoea, swelling of face/neck/arms, headache worse in morning, visual disturbances, raised JVP
2) Non-small cell lung cancer
a) Adenocarcinoma : peripheral, non-smokers (TF-1, napsin A)
b) squamous cell carcinoma: central, associated with smoking, PTHrP causes hypercalcaemia, finger clubbing, associated with cavitating lesions (eosinophilic/pink cytoplasm, p63,p40 markers
c)large cell carcinoma- diagnosis of exclusion, large nuclei and moderate cytoplasm
SSS= squamous and small are sentrally located
Paraneoplastic syndromes in each type of cancer
1) ADENOCARCINOMA
gynaecomastia
2) SMALL CELL
SIADH: low sodium, high urine osmolality, high urine sodium (concentrated urine)
Cushings (ACTH)
Lambert-Eaton-Syndrome : difficulty walking (waddling giat), muscle tenderness, hyporeflexia, muscle weakness thats better with exercise, antibodies against pre-synaptic voltage gated calcium channels at neuromuscular junction
3) SQUAMOUS CELL
1) PTHrP (parathyroid hormone related protein):
- hypercalcaemia
- Constipation
- Myopathy
- Polydipsia
- Polyuria
- Low mood
- Bone pain
- clubbing
- cavitating lesions
- hyperthyroidism
2) Hypertrophic pulmonary osteoarthropathy = clubbing and periostitis of small hand joints
Apical Lung cancer
Pancoast tumour : almost always NSCLC and more than 50% are squamous cell. Can cause horner syndrome:
- Ipsilateral miosis
- Ptosis
- Anhidrosis
- Laryngeal nerve damage (in some cases) → hoarseness
- SVC obstruction: Positive pembertons test - raise arms get red face - give oral dexamethosone
Lung cancers most likely to metastasise to :
Brain, bone, liver, adrenals
- Headaches
- Seizures
- Bone pain
- Jaundice
- Hepatomegaly
CLINICAL FEATURES
- persistent cough
- haemoptysis
- Progressive dyspnoea
- Constitutional symptoms- weight loss, fever, weakness
- chest pain
- hoarseness- seen with Pancoast tumours pressing on the recurrent laryngeal nerve
- Clubbing
- Supraclavicular or persistent cervical lymphadenopathy
-SVC obstruction
INVESTIGATIONS
1st - Chest X-ray
then CT with contrast to look at chest, liver and adrenals
other;
PET-CT : look for mets and lymph node
Bronchoscopy : biopsy and TNM staging
CT-guided lung biopsy: if peripheral lung adenocarcinoma
Bloods look for :
- Thrombocytosis- raised platelets
- Hyponatraemia- small cell lung cancer
- Hypercalcaemia- Bone mets or PTHrP (squamous cell)
- ALP- Bone mets
- LFTs- Liver mets
MANAGEMENT
1st for NSCLC lobectomy
surgery contraindicated if :
- SVCO
- Malignant pleural effusion
- Vocal cord paralysis
- FEV <1.5
- Curative radiotherapy offered if stage 1,2,3
- Chemotherapy to stage 3,4 to control disease and improve QoL
- If advanced non small cell lung cancer then targeted therapy e.g:
EGFR inhibitors
ALK tyrosine kinase inhibitors
FOR SCLC
palliative chemotherapy + correct SIADH slowly by
- fluid restriction
- demeclocycline: reduces the responsiveness of the collecting tubule cells to ADH
- ADH (vasopressin) receptor antagonists have been developed= tolvaptan and conivaptan
If have a pleural effusion then put in a chest drain but check INR for bleeding risk first
COMPLICATIONS
Comp- lobar collapse
Prog: NSCLC better than SCLC
What is asthma, who most commonly has it, risk factors and pathophysiology
Chronic inflammatory disease of the respiratory system characterised by:
- Bronchial hyper-responsiveness
- Episodic acute asthma exacerbations
- Reversible airflow obstruction
Allergic asthma- most common type, symptoms begin in childhood and are more common in males if under 18 years. Is associated with atopy e.g eczema and allergic rhinitis
RF:
Fhx asthma
exposure to allergens- dust mites or pets
History of atopic diseases e.g eczema and allergic rhinitis
low socioeconomic status
- IgE-mediated type 1 hypersensitivity leading to mast cell degranulation and release of histamine
- 3 main pathological processes include:
- Bronchial hyper-responsiveness
- Bronchial inflammation
- Endobronchial obstruction
CLINICAL FEATURES
Persistant dry cough
- Worse at night
- Worse with exercise
- Worse with exposure to irritants
End-expiratory wheeze
Dyspnoea/SOB
Chest tightness
Symptoms worse after NSAID use
On examination: prolonged expiratory phase on auscultation and hyper resonance to lung percussion
These symptoms will come and go in response to triggers
INVESTIGATIONS
History:
-recurrent episodes of symptoms
-Wheeze heard by clinician
Spirometry= variable airflow obstruction: FEV1/FVC ratio less than 0.7 and FEV1 is significantly reduced (FVC normal as no restriction).
- Once given salbutomol FEV1 improves by at least 12% (bronchodilator reversibility).
-Normal/raised total gas transfer
-Raised transfer coefficient KCO
-History of atopy
In patients who have a high likelihood of asthma: 6 week trial of ICS- if there’s good response to it then can be diagnosed as asthma
Other investigations
1) FeNO:
- Exhaled FeNO of 40 parts per billion or more
- Can show degree of eosinophilic inflammation
- Can be used to follow patients over time
- Monitor adherence
2) Peak Expiratory Flow Rate
- Help monitor patients progression and characterise severity
3) Chest X-ray
Hyper-inflated lungs
4) FBC
eosinophilia
Occupational asthma: Serial peak flow measurements at home and work
Acute asthma attack:
ABG showing type 2 respiratory failure (hypoxia and hypercapnia)
MANAGEMENT
-Assess treatment adherence
-Assess inhaler-technique
-Manage co-morbidities
-Manage environmental factors
-Explain the importance of peak expiratory flow monitoring
1st SABA salbutomol (blue inhaler, tremor side effect)
2nd SABA + low dose ICS beclomethasone budesonide (add if waking up at night or having symptoms more than 3 times per week) (brown inhaler, oral candidiasis risk and taken twice per day regardless of symptoms)
3 SABA + ICS + LABA salmetorol (can have MART which is ICS+LABA combined if have history of attacks) If when add LABA there no improvement can take out, if some improvement but suboptimal go to step 4 and continue with LABA.
4 SABA + higher ICS +LABA + (consider LTRA (montelukast)
5 SABA + high ICS + LABA + LTRA or if LTRA was tried in last step then do a specialist referral and theyll add a specialist therapy like theophylline or tiotropium (adult)
6 daily steroid tablet + high dose ICS + refer to specialist care
If need to step-down treatment: reduce 25-50% of ICS
COMPLICATIONS
- Growth retardation
- Chest wall deformity
- Recurrent infections
- Pneumothorax
- Respiratory failure
- Exacerbations
Prognosis- children usually improve as get older. Adult onset is usually chronic
What are the different levels of severity for asthma attacks, what differntiates them and how are they managed
asthma attack severity:
Moderate acute asthma
Increasing symptoms;
Peak flow > 50-75% best or predicted;
- Normal speech
- RR <25
- Pulse <110
No features of acute severe asthma.
Severe acute asthma
Any one of the following:
Peak flow 33-50% best or predicted;
Respiratory rate ≥ 25/min;
Heart rate ≥ 110/min;
Inability to complete sentences in one breath.
Life-threatening acute asthma
Any one of the following in a patient with severe asthma:
Peak flow < 33% best or predicted;
Arterial oxygen saturation (SpO2) < 92%;
Partial arterial pressure of oxygen (PaO2) < 8 kPa;
!!!Normal!!! partial arterial pressure of carbon dioxide (PaCO2) (4.6–6.0 kPa);
Silent chest;
Cyanosis;
Poor respiratory effort;
Arrhythmia;
Exhaustion;
Altered conscious level;
Hypotension.
Confusion + bradycardia
Near-fatal acute asthma
Raised PaCO2 and/or the need for mechanical ventilation with raised inflation pressures.
TREATMENT
– Oxygen (target sats 94-98%)
- Salbutamol nebulisers
- Ipratropium Bromide nebulisers
- Oral prednisolone - if pt cant swallow then IV hydrocortisone. To reduce inflammation
- IV magnesium sulfate (dont use for COPD). To aid in relaxation of the ronchi
If not responding to this treatment aka low O2 still, high CO2 and respiratory acidosis then intubation and ventilation
If normal PaCO2 then escalate to intensive care team as its a sign of exhaustion and is life threatening
What s asthma-COPD overlap syndrome
- Condition in which you have symptoms of both asthma and COPD
- ‘Persistent airflow obstruction with features of asthma’
CLINICAL PRESENTATION
- Wheeze
- Cough → With or without mucus
- Tightness in chest
- SOB
Also has asthmatic symptoms:
- Response to bronchodilators
- Reversibility of airflow
- Eosinophilic inflammation
INVESTIGATIONS
Spirometry
MANAGEMENT
- Low dose ICS → Reduces inflammation in airways
- Long-acting bronchodilator (LABA) → Can help keep airways open
- Long-acting muscarinic agonist (LAMA) e.g. tiotropium
- Vaccinations
have SABA or SAMA as required.
If asthmatic features such as previous diagnosis of atopy or asthma, raised blood eosinophil count OR features suggestive of steroid responsiveness such as substantial variation of FEV1 overtime (400ml) or substantial (20%) diurnal variation in peak expiratory flow :
No asthamtic symptoms or steroid responsiveness= SABA as required with LABA+LAMA regulary
yes= SABA or SAMA as required with LABA +ICS
if these dont work then combine to
SABA as required with LABA + LAMA+ ICS
What is Chronic Obstructive Pulmonary Disorder, what two conditions does this disease include, who is most affected and what are the causes
progressive disorder characterised by airflow obstruction with little or no reversibility
COPD includes:
- chronic bronchitis
- emphysema
Men over 65
CAUSE:
smoking
exposure to air pollution
Alpha-1-antitrysin deficiency (COPD in younger patients)
If young usually means they have alpha-1-antitrypsin deficiency so are at risk of Hepatocellular carcinoma.
Late stage A1AT should have lung volume reduction surgery.
CLINICAL FEATURES
- Chronic cough
- Usually productive (clear/white sputum)
- May become green/yellow with exacerbations or infections
- Dyspnoea and tachypnoea
- Wheeze
- Pursed lip breathing
- Barrel chest (hyperinflation)
- O&E
- Hyper-resonance on percussion
- End-expiratory wheeze on auscultation
- Coarse crackles
- Reduced breath sounds
INVESTIGATIONS
Post-bronchodilator spirometry: FEV1/FVS ration less than 0.7 but no bronchodilator reversibility. Reduced FEV1, slightly reduced COPD
COPD severity
Based on FEV1 and all must have FEV1/FVC less than 0.7
Stage 1 (mild): FEV1 80% or over MUST HAVE SYMPTOMS, 1 flare up in a year max, never hospitalised
Stage 2 (moderate): FEV1 of 50%-79%,
Stage 3 (severe): FEV1 of 30%-49%,
Stage 4 (v severe): FEV1 less than 30%, admitted to hospital at least once
GOLD stages (in addition to COPD severity)
A: 1 flare up in a year max, never hospitalised. stage 0-1 on MRC breathlessness scale
B: 1 major flare up in a year max, not hospitalised in the last year, 2 or over on MRC
E: hospitalised
Chest X-ray:
- Hyperinflation (>6 anterior ribs seen above diaphragm)
- Bullae- If large may mimic a pneumothorax
- Hyperlucent lung fields
- Flat hemidiaphragm
Alpha-1antitrypsin levels if a patient who has never smoked (young)
- on CT for A1AT deficiency will see emphysema in lower lobes, COPD has emphysema in upper lobes (emphsema shows as dark black patches : the X-rays arent taken up well as no active tissue)
FBC: exclude secondary polycythamia
ABG: if acute exacerbation to check oxygen and carbon dioxide levels: COPD causes CO2 retention- type 2 resp failure
MANAGEMENT
1st step of management : Smoking cessation offer
-Nicotine replacement therapy (esp to preg women as the other two options cant be used)
- Varenicline
- Bupropion: NOT IN EPILEPSY
also offer:
- Annual influenxa vaccine
- one time pneumococcal vaccine
- pulmonary rehabilitation for those who find COPD to be disabling
1st treatment:
Bronchodilators SABA(salbutomol) or SAMA (ipratropium bromide)
2nd: if have no asthmatic features and no steroid responsiveness= add LABA (salmetorol) + LAMA (tiotropium). If on SAMA change to SABA
if have asthmatic features/steroid responsiveness= add LABA + ICD, have SABA, SAMA as required
Asthmatic features= history of asthma or atopy, eosinophilia, FEV1 variability 400ml+, diurnal variation in peak flow 20%+
3rd still no response then combine everything but only one muscarinic at a time so if taking SAMA+ SABA switch to SAMA then add LABA + LAMA + ICS
If frequent exacerbations : CC Prednisolone
diff starting points
Group a: SABA or LABA a just gets bronchodilator
Group B: LABA/LAMA + SABA b gets broncho and muscarinic
Group E: LABA + LAMA + (ICS if eosinophils over 300) e gets all long acting +ICS
COMPLICATIONS
Acute exarcerbations due to infection- haemophilus influenzae usually
Cor pulmonale (right sided HF)
Lung cancer
Recurrent pneumonia
Pneumothorax
Resp failure
PROG: higher the FEV1 the less likely exacerbation is
What is chronic bronchitis
Chronic narrowing of the airways defined clinically as a productive cough on most days for at least 3 months per year for 2 consecutive years
What is emphysema
Permanent destructive enlargement of air spaces distal to the terminal bronchioles
How is an acute exacerbation of COPD managed and what is the most common cause
Haemophilus influenzae most common cause
24% oxygen (blue venturi mask): target for 88-92% if have risk factors for hypercapnia, if pCO2 normal then 94-98%
Nebulised bronchodilators (contain SAMA salbutomol and SAMA ipratropium bromide)
Corticosteroids (oral prednisolone for 5 days of IV hydrocortisone if clinically unstable
IV theophylline ?
ABx : if have green sputum, signs of pneumonia or infection then : amoxicillin, doxycycline or clarithromycin
prophylactic ABx= azithromycin if meet requirement
NIV BIPAP: if respiratory acidosis with high CO2 despite treatment (pH 7.25-7.35)
Long Term Oxygen Therapy if meet requirement
What patients should not have clarithromycin
Patients who have congenital long QT syndrome
When is azithromycin given
meets criteria of:
does not smoke
have optimised standard treatments
still having exacerbations
need to also have
- CT thorax to exclude bronchiectasis
- sputum culture to exclude infections like TB
- ECG as can cause QT interval prolongation
What is given to critically ill + CO2 retaining patients
High flow oxygen- reservoir mask at 15l/min
WHat patients need long term oxygen therapy
Assess ABG on 2 occassions 3 weeks apart and if shows
- pO2 <7.3kPa
OR - 7.3-8.0kPa + secondary polycythaemia(high Hbor Hcrt/peripheral oedema/pulmonary hypertension
Why can supplemental oxygen be harmful to COPD patients
- Reduces respiratory drive, causing hypoventilation, leading to more CO2 retention
- Patient will often already have chronic respiratory acidosis indicated by raised bicarbonate so more CO2 retention increases
When a COPD patient has trialled many SABA and LABA or cannot used inhaled therapies what is given to them, what needs to be checked before and when is the dose reduced
Oral theophylline
Check U+E and LFT before
reduce dose if macrolide (Azithromycin, clarithromycin, and erythromycin) or fluroquinolone antibiotics are co-prescribed
When are mucolytics considered in COPD
In patients with a chronic productive cough and continued if symptoms improve
How is cor pulmonale managed and what shouldnt be given
Loop diuretic for oedema
Consider Long term oxygen therapy
DONT GIVE
ACEI
CCB
Alpha blockers
What is a pneumothorax, the different types and the risk factors
Collection of air within the pleural space between the lung (visceral pleura) & chest wall (parietal pleura)
1) Primary Spontaneous : pts with no underlying lung disease (more common in males 16-25 year olds)
2) Secondary spontaneous: complication of underlying lung disease like COPD
3) Traumatic: from trauma (stab wound, gunshot)
4) Tension: Life threatening complication of the other types. Creates a one way valve, air can enter the pleural space but not leave so it shifts the trachea and can press on the heart. Signs are trachea deviation away from pneumothorax and sudden hypoxia and increased ventilation. Causes hypotension due to cardiac outflow obstruction due to mediastinal shift. If hypotension is severe can cause death. Suspect a tension penumothorax if there is sudden deterioration following intubation.
- Smoking
- Tall & slender body
- <40 years
- Recent invasive medical procedure (Chest drain)
- Chest trauma
- COPD
- Marfan’s disease
- CF
What are the clinical features of pneumothorax
- Sudden, severe pleuritic (on inspiration) chest pain
- Dyspnoea
- Reduced breath sounds
- Hyperresonant percussion
- Decreased fremitus on ipsilateral side
- Decreased chest expansion
- Haemodynamic instability (tension)
- Tachypnoea
- Tachycardia
- Hypotension
What investigations are needed if pneumothorax is suspected
basically whether patient can stand to do an erect chest X-ray or if not then US
IF stable pt and can sit upright then : Chest X-Ray: an erect PA x-ray in inspiration. will see:
- visible rim between lung margin and chest wall
- absence of lung marking between the lung margin and chest wall
IF immobilised following trauma: Chest US (need specialist)
Can do:
FBC and clotting screen- all should be fine
What is the management of pneumothorax
Primary pneumothorax, no SOB, less than 2cm = discharge and review in 2-4 weeks as outpatient
Primary pneumothorax, with SOB or over 2cm = aspiration, if unsuccessful then chest drain
Secondary pneumothoax, no SOB, less than 1cm = admit for 24h, give oxygen
Secondary pneumothoax, no SOB, 1-2 cm= aspiration
Secondary pneumothorax, with SOB and over 2cm = Chest drain in safety triangle:
- 4/5th intercostal space
- Lat dorsi
- Pec major
- Base of axilla
What complication can occur after chest drain: Re-expansion pulmonary oedema
Tension pneumothorax:
Insert large bore cannula (14G-16G) in 2nd ICS, MCL (needle decompression on ipsilateral side)
If tension pneumothorax suspected, no need for X ray to confirm- just cannula it
Discharge advice: stop smoking and never go scuba diving
What are the complications and prognosis of pneumothorax
- Respiratory failure
- Cardiac failure
Prog- 30-50% recurrance, lower rate if primary, higher rate of 50% if secondary cause
What is respiratory failure, the causes and the types
Acute or chronic inability of the respiratory system to maintain gas exchange- this can lead to:
- Failure to oxygenate the body
- Failure to eliminate carbon dioxide
1) Pulmonary causes:
- Acute exacerbation of asthma
- PE
- ARDS
- Pneumonia
- Pulmonary trauma
- Airway obstruction
- Pneumothorax
- CLD
2) Extrapulmonary causes:
- CNS depression (narcotic overdose or brain trauma)
- Respiratory muscle weakness (myasthenia gravis, motor neurone disease)
- Decreased chest wall compliance
- Increased oxygen consumption or CO2 production (sepsis, cardiogenic shock)
- Hypovolaemia
- Shock
Type 1 respiratory failure (only 1 thing is wrong in type 1) :
- Hypoxaemic
- Low oxygen PaO2 <8kPa
- Normal CO2
Type 2 respiratory failure :
- Low oxygen
- High CO2 (PaCO2 >6kPa from : Examples : respiratory muscle weakness due to neurological conditions or COPD exacerbation)
What are the clinical features of the different types of respiratory failure
Features for hypoxaemic respiratory failure (aka type 1&2):
- Tachypnoea
- Dyspnoea
- Cyanosis
- Pleuritic chest pain
Features for hypercapnic respiratory failure (type 2):
- Hypoventilation (cause) or hyperventilation to breathe CO2 out
- Headache
- Anxiety
- Papilloedema
- Asterixis
What are the investigationd for respiratory failure
ABG
What is the management of respiratory failure
1st check for obstruction and clear: relieve through head tilt, chin lift, jaw thrust
Non-mechanical ventilation/oxygen support to correct hypoxaemia
- Nasal cannula
- Face mask
Mechanical ventilation
-Invasive (endotracheal intubation) : given if patient is unconscious and supplemental O2 is not working
- Non-invasive (CPAP or BiPAP): given to patients in type 2 respiratory failure secondary to chest wall deformity, neuromuscular disease or obstructive sleep apnoea. Given in acute exacerbation of COPD who are in resp acidosis (pH 7.25-35). Patient sneed to be awake and conscious.
Type 1 failure get CPAP (useful if have pulmonary oedema due to HF)
Type 2 get BiPAP
What are the complications and prognosis of respiratory failure
- Pneumothorax
- Endotracheal tube misplacement
- Nosocomial infection
- Nasal mucosa damage
Prog- mortality based on persons overall health and potential of organ dysfunction
