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• SOB is the subjective feeling of breathlessness that is excessive for the level of activity.
• It may be due to several causes.
o Pulmonary disease.
Airway disease
Diseases of the lung parenchyma
Disease of the pleura
Respiratory muscle disease
Chest wall disease
o Cardiac disease.
Eg. Rise in left atrial pressure associated with cardiac dysfunctioncausing
pulmonary oedema.
o Metabolic disease.
Eg. thyrotoxicosis
ketoacidosis
o Anaemia
o Psychogenic causes.
Anxiety
Hyperventilation
• Acute infections.
o Eg. exacerbation of COPD.
• Bronchiectesis.
o Can cause massive haemoptysis.
• Bronchial CA.
o Secondary deposits and benign deposits can also cause
haemoptysis.
o This is less common.
• Pulmonary TB.
o Common cause worldwide.
• PE with infarction.
• Left ventricular failure.
o Can cause pink, frothy sputum.
• Vasculitis.
o Goodpasteur’s syndrome.
o Wegener’s granulomatosis.
• Other infections.
o Lobar pneumonias.
“rusty sputum”
o Lung abscess.
Less common.
• Trauma.
o Chest contusions.
o Inhalation of foreign bodies
o After intubation.
• Rarer causes include:
o Bleeding disorders.
o Interstitial lung disease.
o Mitral stenosis
o Idiopathic pulmonary haemosiderosis
o Arteriovenous malformations
Osler – Weber – Rendu disease.
• Hereditary haemorrhagic telangiectasia
• Favourite in exams, but rare in practice.
o Eisenmenger’s syndrome
o Sarcoidosis
o Amyloidosis
o Primary pulmonary hypertension
o Cystic fibrosis
• 15% of cases have no apparent cause.
Stridor?
• Inspiratory stridor.
o Extrathoracic obstruction
• Expiratory stridor.
o Intrathoracic obstruction
• Stridor on both inspiration and expiration.
o Fixed obstruction
Wheeze.
• Commonest cause is asthma.
Occupational history.
• Exposure to asbestos and dust.
• Working environment may affect symptoms and recovery.
• Patient also may be due financial compensation.
• Improvement at weekends suggests a occupational cause.
History of lung disease.
• Asthma
• TB
• Atopy
Pet ownership.
• Allergies
• Extrinsic allergic alveolitis in pigeon fancier’s lung.
Drug history
• Non – cardioselective beta – blockers can aggrevate wheeze.
• Concerns over cardioselectivity are probably exaggerated.
• Past history of amiodarone use can cause pulmonary fibrosis
General health.
• Weight loss
• Appetite
• Looking for non – respiratory causes for dyspnoa, such as tumours.
Full smoking history.
• Inspection.
o Central cyanosis commonly associated with:
Lung disease
Cardiac disease.
Unreliable marker of hypoxaemia.
o Peripheral cyanosis due to poor peripheral circulation
Cardiac failure
Peripheral vascular disease
Arterial obstruction
Cold
o Carefully watch for:
Anaemia
Tar staining of fingers
Clubbing.
• Carcinoma of the bronchus
• Pus in the respiratory tract
o Empyema
o Lung abscess
o Bronchiectesis
o Cystic fibrosis
• Fibrosisn alveolitis
• Chronic supperative pulmonary TB
• Mesothelioma.
Chest movements on inspiration.
• Pathology normally found on the side with reduced movement.
Barrel shaped chest.
• Emphysema
Kyphoscoliosis.
• Can decrease chest size and expansion.
Ankylosing spondylitis.
• Can “fix” the chest.
Use of accessory muscles of respiration.
Paradoxical abdominal movments.
• Diaphragmatic weakness
Rhythm of respiration.
• Cheyne – Stokes respiration.
o Periods of fast and deep breathing, followed by periods of
apnoea.
o Due to depression of central respiratory centre in the
medulla.
o Seen in:
Neurological disease.
Severe left ventricular failure.
High altitude.
• Palpation.
o Lymphadenopathy.
Malignancy
Infection
o Tracheal displacement.
Chest disease
Cardiac disease
• Percussion.
o Decreased resonance indicates solid matter beneath.
Infection
Effusion
o Increased resonance indicates air beneath.
Pneumothorax
Emphysema
• Auscultation.
o Expiration.
May be prolonged in COPD
o Bronchial breathing.
Consolidation
Caviation
Top of effusion
o Breath sounds are decreased over
Effusion.
Pneumothorax
Obesity
o Rhonchi/ wheeze
Due to partially obstructed bronchi.
Found in:
• Asthma
• Bronchitis
• Left ventricular failure.
o Rare
Polyphonic wheeze
• Suggests multiple small airway obstructions
Monophasic wheeze
• Suggests single lesion, eg. central malignant lesion.
o Crepetations/ crackles.
Due to sudden opening of small airways.
Caused by:
• Pulmonary congestion
o Fine crepetations in early inspiration
• Fibrosing alveolitis.
o Fine crepetations in late inspiration
• Bronchial secretions.
o Coarse crepetations.
o Friction rub
Pleural disease.
Investigating breathlessness.
• ECG
o Pulmonary embolism
Deep S wave in Lead I
Q wave in Lead III
T wave inversion in Lead III
o COPD with cor pulmonale
Tall P waves in Lead II
o Cardiac conditions leading to breathlessness.
Eg. MI with secondary pulmonary oedema
• Arterial Saturation.
o Easy to perform.
o May avoid need for ABGs.
• ABGs.
o Should be first taken with patient on room air if possible.
o Arterial pH
o Partial pressures of oxygen and carbon dioxide.
o Hydrogen ion concentraion
• Spirometry.
o Distinguishes restrictive from obstructive pathologies
o Tests reversibility of conditions with therapy.
o Best done in a well patient.
• Peak expiratory flow.
o Good for measuring acute decline.
o Particularly good in asthmatics, who often know their best results.
• VQ scans.
o Suspected PE.
• Bronchoscopy.
o With or without
Washing.
Brushing
Biopsy
• CT scanning.
o Acute.
Eg. Diagnosis of PE.
o Chronic
Eg. Diagnosis and quantify pulmonary fibrosis and bronchiectesis
Acute Asthma
• Presentation.
o Classic triad is:
Wheeze
Dyspnoea
Cough
o Pleuritic pain may be present due to:
Diaphragmatic stretch.
Pneumothorax
Acute infection
o May build up over minutes – days.
Patients may deteriorate very rapidly and present with respiratory or cardio
–respiratory arrest.
o Factors increasing risk of severe, life threatening asthma include:
Previous artificial ventilation
Hospital admission for asthma in the past year.
Heavy rescue medicine use
> 3 classes of asthma medication used
Repeated A&E attendance for asthma
Brittle asthma
• Precipitants.
o No clear precipitant in 30% of patients.
o Exposure to allergen or irritants.
Smoke
Pollen
Animals
Dust
o Upper respiratory tract infection.
Normally viral
o Chest infection.
Viral
Bacterial
o Poor compliance with regular inhaled or oral steroids.
o Emotional stress.
o Cold air
o Exercise
Markers of severity.
• Asthma attacks can be catagorised for ease of description
• Near fatal.
o Raised PaCO2 or immediate need for ventilation.
o Raised inflation pressures.
• Life – threatening asthma
o Severe airway obstruction
PEF < 33% best or predicted.
Soft breath sounds or “silent chest”.
Feeble respiratory effort.
o Increased work of breathing and haemodynamic stress.
Exhaustion
Hypotension
• Systolic BP < 100 mmHg
Bradycardia, or arrythmias
o Ventilation – perfusion mismatch.
Cyanosis
Hypoxia.
• SpO2 <92%
• Admission is required if ANY of the markers are present of asthma that is:
o Near fatal
o Life threatening
o Severe
Investigations
• ABGs.
o Hypoxaemia on room air is almost inevitable.
o In order to maintain alveolar ventilation, the patient will hyperventilation
Hypocapnoea
Respiratory alkalosis
o As patient become fatigued by hyperventilating, PaCO2 will gradually rise.
High PaCO2 is a sign of approaching respiratory failure.
Contact ITU immediately.
o Poorly controlled asthma over several days may give a mild “non ion gap” acidosis.
Serum Bicarbonate = 20 – 24 mmol/L.
o Lactic acidosis seen in severe asthma.
• Pulse oximetry.
o Continuous monitoring is essential.
o Aim for SaO2 > 92%
• Chest X – ray.
o Exclude pneumothorax.
o Diagnose any parenchymal infection.
• ECG.
o Usually normal
o Severe asthma may cause right heart strain.
• Blood tests.
o FBC
o U&Es
o CRP
o Assess for signs of infection.
o Potassium may be lowered by high doses of β – agonists.
Immediate therapy
• Priorities.
Treat hypoxia
Treat bronchospasm and inflammation
Assess need for ITU
o Ensure patients is on at least 1mg inhaled steroid per day (eg. beclamethasone).
o Advise patient to:
Get early GP follow up
Monitor PEF
Return to hospital early if asthma deteriorates.
• Moderate attack.
o No acute severe features.
Inhaled β – agonist.
Consider referral to chest clinic.
o Advise patient.
See GP within 48 hours.
Return to A&E if symptoms worsen
CO2 retention
• Causes.
o Infective exacerbation
No new CXR changes.
Viral
H. influenzae
S. pneumoniae
Moraxella catarrhalis
o Community acquired pneumonia.
Changes on CXR.
See later for full details.
o Exposure to known allergen.
COPD may co – exist with allergic asthma
o Pneumothorax.
Ensure it is not a large bullae before aspirating.
See later for full details.
o Expansion of large bullae.
o Sputum retention.
Atelectasis.
• Lobar or segmental collapse.
Pneumonia
Excessive sedation or opiod analgesia.
• Trauma
• Post – surgery.
Impaired conciousness
o Confounding or contributing factors.
Myocardial ischemia
Pulmonary oedema
Cor – pulmonale
Pulmonary embolism.
• Investigations.
o All patients should have.
U&E.
• Dehydration
• Renal failure
• Altered potassium
FBC.
• Leucocytosis
• Anaemia
• Polycythaemia due to chroninc respiratory failure.
Pulse oximetry & ABGs.
• Assess degree of respiratory failure.
• Assess pH
• Guide appropriate oxygen treatment.
Septic screen.
• Sputum should be sent for culture.
• Blood cultures if febrile or CXR suggests pneumonia.
Peak flow.
• Assess against what is normal for the patient.
CXR
• Focal changes suggest pneumonia
ECG.
• MI
• Arrythmias.
• Assess severity.
o History.
Assess severity of COPD when stable, and compare with current state.
• Symptoms.
• Functional capacity.
o Distance walked on flat.
o Ability to climb stairs.
o Frequency of exacerbations
o Previous admissions
o Previous need for ventilation.
• Level of usual treatment.
o Regular nebulized bronchodilators.
o Oral steroids
o Home oxygen
• Concurrent illness.
o IHD
o Renal impairment
• Previous documentation.
o PFTs
o ABGs
o Examination.
Assess severity of respiratory distress
• RR > 25 bom
• Use of accessory muscles
• Paradoxical chest movements
Hypoxia
• Cyanosis
Hypercapnoea.
Management
• First priority is to treat hypoxia and respiratory failure.
o Distinction between pink puffer and blue bloater is unhelpful.
Most patients have signs of both.
Give them all oxygen until proven otherwise.
o Uncontrolled oxygen therapy will worsen CO2 retention in patients with hypoxic –
drive.
Debate between me and the book.
Book says give 24 – 28% oxygen via venture mask until ABGs available,
then adjust.
• Nasal cannulae give unreliable inspired oxygen concentration.
If patient not retaining CO2 (PaCO2 < 6 kPa) and is hypoxic (PaO2 < 10
kPa).
• Give oxygen 28 – 40%.
• Repeat ABGs after 30 minutes, or sooner if drop in GCS.
o Worsening hypoxia
o Rising CO2
• Aim to maintain SaO2 > 92%
Mechanical ventilation.
• COPD per say is not a contraindication to mechanical ventilation.
• Should be considered when.
o PaO2 < 7.3 kPa, regardless of CO2 levels
o Poor response to NIV
o Very unwell and unlikely to response to less invasive methods.
• Before intubating, discuss with senior colleagues and ITU seniors.
Type II failure patients may need PaCO2 = 6 – 7.5 kPa, with or without mild
hypoxia to successful wean.
Respiratory stimulants.
• Generally been superseded by NIV.
• Trial of doxapram may be worthwhile if:
o NIV not available.
o NIV not successful
o Mechanical ventilation not appropriate.
• Not beneficial in type II respiratory failure due to poor respiratory effort.
Respiratory Failure
• Occurs when gas exchange becomes significantly impaired.
• Physical examination.
o Listen to breathing.
Stidor
Wheeze
• Localised.
o Local obstruction
• Generalised
o Asthma
o COPD
o Pulmonary oedema
Coarse crackles.
• Infection
• Pulmonary oedema
• Pulmonary fibrosis
Bronchial breathing.
• Consolidation
• Collapse
• Pulmonary fibrosis
• Overlying pulmonary oedema
Signs of pneumothorax.
• Hyper – resonance
• Absent breath sounds
Pleural effusion.
• Stony dullness
• Decreased breath sounds
o Palpate upper chest and neck for crepitations.
Pneumothorax
Pneumomediastinum
o Look for signs of DVT.
Swollen hot leg
Pain.
• Common causes
o Acute asthma
o Exacerbation of COPD
o Pneumonia
o Pulmonary oedema
o Pulmonary embolism
o Infection complicating kyphoscoliosis or other chronic lung disease.
o Pleural effusion
o Pneumothorax
o ARDS/ALI
o Respiratory depression
o Drugs, eg. opiates.
• Rarer causes.
o Lung collapse/ atelectasis.
Tumour
Foreign body
Sputum plug
Infection
o Acute respiratory muscle weakness
Guillain – Barre syndrome
Myasthenia gravis
Poliomyelitis
o Upper airway obstruction.
Foreign body
Tumour
Epiglottitis
o Chest trauma
o Anaphylaxis.
Urgent investigations
• ABGs.
o On air immediately, if possible.
o If not possible on air, on oxygen, but not FiO2
• CXR.
o As for pneumonia
• ECG.
o Pulmonary Embolus.
Tachycardia
Right bundle branch block
Anterior T – wave changes
RAD
S1Q3T3
• Rare
o Tacchyarrythmias
o Myocardial ischemia
• Blood tests.
o FBC.
Leucocytosis
Anaemia
o U&Es
o Glucose
• Inspect sputum.
• CXR assessment.
o Consolidation/ alveolar shadowing:
May be lobar or patchy.
Presence of air bronchogram suggests pneumonia.
o Cardiogenic pulmonary oedema
Due to left ventricular failure.
Typically perihilar (‘bat – wing’)
Upper lobe venous congestion.
Kerley B lines in peripheral lung fields.
Sometimes.
• Pleural effusions
• Cardiomegaly.
o Non – cardiogenic pulmonary oedema.
Normally due to ARDS/ALI.
Typically peripheral alveolar shadowing ± air bronchogram.
In non – cardiogenic pulmonary oedema, there is no:
• Upper lobe venous congestion.
• Kerley B lines
• Pleural effusions
• Cardiomegaly.
o Pleural effusions
o Masses suggesting bronchogenic carcinoma
o Pulmonary embolism.
Wedge – shaped peripheral opacities.
Small pleural effusions
Localised areas of oligaemia
Enlarge pulmonary artery.
o Pneumothorax.
Distinguish from large bullae.
o Trauma/ rib fractures.
o Diffuse lung disease.
Eg. fibrosing alveolitis.
Small lung fields
Interstitial reticulo – nodular shadowing.
• “ground glass” appearance.
Management
• Severity of respiratory failure depends on response to oxygen.
o Failure of hypoxia to correct on 40 – 60% oxygen or progressive hypercapnia implies
need to consider non – invasive or mechanical ventilation.
• General resuscitation.
o Ensure airway is patent and mouth is clear.
If stridor present, call for anaesthetic and/or ENT or assistance.
o Sit patient upright and give 60% oxygen.
Leave patient lying down if hypotensive
If history of COPD, give 24 – 28% oxygen.
o Ensure respiratory effort is effective and adequate.
Measure respiratory rate.
Assess depth of respiration
Measure oxygen saturation with a pulse oximeter.
o If the patient is exhausted, with failing respiratory drive, refer to ITU.
o If patient is comatose, with poor respiratory drive, consider drug overdose.
If pin – point pupils, consider opiates.
If normal pupils, consider benzodiazepines.
Give IV nalaxone
• 2 – 4 μg/kg bolus, followed by infusion based on response.
• Oedema
Pulmonary embolism
• Raised JVP
• Tachycardia
• Hypotension
• Normal breath sounds
• With or without pleural rub.
Acute Pneumonia.
• Classic presentation.
o Cough.
Productive or non – productive.
o Fever
o Pleuritic chest pain
o Consolidation on CXR.
o Prodrome consisting of.
Cough
Coryza
Headache
Muscle ache
Immediate management.
• Assess ABC
• Arrange for urgent CXR
• Secure venous access.
o Take bloods for:
FBC
U&E
LFT
CRP
Culture
o If dehydrated, give IV crystalloid.
Examine regularly for signs of overload.
• Take ABGs.
• Hospital acquired pneumonia, and pneumonia in the immunocompromised, can involve any
pathogen from the above list.
• Investigations.
o All patients should have.
ABGs.
• On air and oxygen if possible
Bloods.
• FBC
• U&Es
• LFTs
• ESR
• CRP
• Blood cultures
• Pneumococcal antigen
ECG
Sputum.
• Gram stain
• ZN stain
o If suspicious of TB
• Cytology
• Pneumococcal antigen
• Legionella culture.
Pleural fluid aspiration.
• Microscopy
• Culture & sensitivity
• Protein
• pH
Serology
• Acute & convelescnet
Cold agglutinins
• Day 7 – 14 in Mycoplasma infection
Urine
• Pneumococcal antigen
• Legionella antigen.
Chest X – ray.
Caviation
Diffuse infiltration • Fungi
Acute.
• Anaerobes
• PCP
• Staph. Aureus
• Viral (eg. CMV)
• TB
• Drug reactions.
• Gram –ve bacteria
o Cyclophosphamide
• Malignancy
o Bleomycin
o Busufan Focal infiltrates.
Acute
• Alveolar haemorrahage
• Pneumococcus
Chronic • Staphylococci
• Fungi • Klebsiella
Pleural effusion
Reactive (sterile) • Gram negatives
• Lymphagitis
TB • Mycoplasma
• Carcinomatosa
Empyema
• Drugs (eg. Amiodarone) • Pulmonary embolus
Chronic
• TB
Management.
• Blind treatment should be started as soon cultures have been sent.
o Modify treatment based on subsequent investigations and culture results.
• Start on IV therapy fro atleat 48 hours..
o Adjust according to clinical condition and response.
• In patients with asthma or COPD, consider adding nebulized salbuatmol.
o 2.5 – 5 mg nebulized, 4 – 6 hourly.
o Relieves bronchospasm
o Loosens secretions.
o Improve mucocilliary action.
• Continue IV fluids as necessary to maintain hydration.
• Monitor response to therapy with:
o FBC
o CRP
o ABGs/ Pulse oximetry
o CXR at day 3 – 5.
Sooner if deteriorating.
• Total duration of therapy normally about 10 days.
• Follow up at 4 – 6 weeks after discharge with a CXR.
o Excludes underlying endobronchial pathology.
Likely pathogens
COPD Alcoholism Recent ‘flu Risk of aspiration
S. pneumoniae S. pneumoniae S. pneumoniae Anaerobes
H. influenzae H. influenzae H. influenzae Gram –ve bacteria
M. catarrhalis S. aureua S. aureau
Klebsiella
TB
Anaerobes
Gram –ve bacteria
Specific pneumonias.
• Community acquired.
o Dose every 6 – 8 hours with either:
1g Amoxycillin
750 mg – 1.5 g cefuroxime
o Cover atypicals with 500 mg – 1 g erythromycin QDS
o Cover S. aureus with 1 – 2 g flucloxacillin QDS
o If penicillin resistant.
If only a rash, cephalosporins are generally safe.
If full blown anaphylaxis, consider 500 mg clarithromycin BD as solo
therapy.
• Aspiration.
o Risk factors.
Seizures
Reduced consciousness
Stridor
Dysphagia
Periodontal disease
General aneasthesia
o Always admit
o Clinical features.
Wheeze
Frothy, non – purulent sputum.
• As quickly as 2 – 4 hours post aspiration.
Tachypnoea.
Cyanosis
Respiratory distress
o Gastric acid destroys alveoli, resulting in:
Increase capillary permeability
Pulmonary oedema
Heamorrhage is common.
Severe necrotizing pneumonia may result.
o Treatment.
750 mg – 1.5 g cefuroxime + 500 mg metronidazole TDS
Amoxycillin + metronidazole + gentamicin.
• Hospital – acquired.
o Most common pathogens are
Enteric gram –ve
Anaerobes.
o Treatment.
Broad spectrum cephalosporins.
• Eg,. 2g cefotaxime TDS
500 mg Metronidazole TDS
o If intubated for > 24 hours use anti – pseudomonal cover.
2 g ceftazidime TDS.
• Reduce dose in renal failure.
o Organ transplant patients have depressed cell mediated immunity, causing additional
susceptibility to:
PCP.
Viruses.
• CMV
• RSV
• Influenza
• Parainfluenza
• Adenovirus
Fungi.
• Aspergillus spp
• Candida spp
o CXR abnormalities tend to be non – specific.
Treatment should cover all possible pathogens.
o Early bronchoscopy and lavage is indicated for diagnosis.
Managemnt should be discussed early with respiratory, microbiology and
infectious disease teams.
• Complications.
o Unresponsive community acquired pneumonia
Review diagnosis, other possibilities include.
• PE
• Pulmonary oedema
• Pulmonary vasculitis
• Alveolar haemorrhage
• Caviation
• Organising pneumonia
• Eosinophilia pneumonia
• Bronchiecteis
Repeat CXR and arrange for CT chest.
• To look for caviation.
Repeat culture of relevant specimens
Consider resistant organisms, or underlying disease.
• Eg. bronchial carcinoma
Consider broncoscopy to exclude.
• TB
• PCP
• Obstructing lesion
Review antibiotic doses and intensify.
• Eg. inadequate oral erythromycin for Mycoplasma pneumonia.
o Caviation or abscess.
Any severe pneumonia may caviate.
• Particulalry:
o Staph. aureus
o TB
o Aspiration
o Klebsiella spp
o Bronchial obstruction
Foreign body
Tumour
o PE.
Thrombus
Septic emboli
Due to:
• DVT with super – added infection
• Tricuspid endocarditis.
• Treatment.
o Seek advice from chest team.
o Most respond to appropriate antibiotics.
May require prolonged course.
o Surgical drainage or CT – guided percutaneous drainage
may be required.
o Blind treamtment is with 4 or 5 drug therapy.
1.5 g cefuroxime TDS IV/ 2 g cefotaxime TDS
IV.
1 – 2 g flucloxacillin QDS IV
Gentamicin
• Loading dose: 100 – 120 mg IV
• Maintainance: 6 – 7 mg/kg OD IV
• Dose depends on renal function and
levels.
With or without 500 mg metronidazole TDS IV.
o Likely that 4 – 6 weeks of antibiotic therapy will be
required.
o Other complications.
Respiratory failure.
Rhabdomyolysis
DIC.
• Especially in Legionella.
Pneumothorax.
• Presentation.
o Normally no underlying lung disease.
o Commonest symptoms are:
Breathlessness.
• Abrupt in onset
• Young fit patients may have no breathlessness
• Patients with Asthma or COPD may deteriorate rapidly.
Chest pain.
• Dull
• Chentral
• Heavy
• May be pleuritic
o In inpatients, exclude pneumothorax in any patient who is:
Breathless after nivasive chest.procedure
• Eg. sub – clavian vein cannulation.
Increasingly hypoxic or rising inflation pressures on mechanical ventilation.
• Causes.
o Primary spontaneous.
Healthy patients.
No underlying lung disease
More common in:
• 20 – 40 year olds
• Tall
• Smoking
• Men
Probably due to spontaneous rupture of apical subpleural blebs/ bullae.
o Secondary spontaneous
Pleural rupture due to underlying lung disease, eg.
• Emphysema
• Fibrosing alveolitis
• Cystic fibrosis
• Sarcoidosis
o Infection.
Caviating pneumonia, due to:
• Staphylococci
• Lung abscess
• TB
• PCP
o Traumatic/ Iatrogenic.
Particularly following chest injuries in RTA
Pleural biopsy or aspiration.
Transbronchial biopsy
Percutaneous biopsy
Subclavian vein cannulation
Mechanical ventilation with high airway pressures.
• CXR
o Classical signs may not always be present.
o It may be difficult to see pneumothorax in the CXR of a patient who is lying down.
Look for
Hyperlucency of one lung field.
Clear right heart border
Horizontal line, showing right middle lobe retraction.
o If patient has COPD with bullae, make sure what you are diagnosisng as a
pneumothorax is not a thin walled bullus.
Pneumothorax will have a pleual line that is convex to the lateral chest wall.
Bullae will have a pleural line that is concave to the lateral chest wall.
If in doubts, CT chest will definitively distinguish the two.
• Secondary pneumothorax
Y Y
N
Intercostal drain. Admit to hospital for 24
Successful? hours observation
N Y
Tension pneumothorax.
• Usually seen in patients who are:
o On mechanical ventilation
o Post – CPR
• Patient is usually.
o Distressed
o Tachypnoeic
o Cyanosies
o Sweating profusely
o Tachycardia
o Hypotension
o Tracheal deviation.
Away from pneumothorax.
o Reduced breath sounds over pneumothorax.
• An emergency.requiring immediate attention.
• Management.
o Don’t leave patient alone.
o Give high flow oxygen.
o Insert large cannula (minimum 18 gauge) perpendicular to chest wall.
Mid – clavicular line.
Bottom of intercostal space (neurovascular bundle runs along bottom of rib,
so top of rib space)
o Relief should be immediate, with air rushing out.
If this doesn’t happen, tension pneumothorax was not the diagnosis
Remove the cannula.
o Improvise a seal.
Fluid filled IV line connected to cannula.
Other end of line in a bowl of water
o Insert a chest drain ASAP.
Investigations
• Real time B – mode venous compression ultrasonography is now first line investigation.
o Replaced venogram.
o Quick
o Non – invasive.
o Sensitivity and specificity both > 90%
o No risk of phlebitis or allergy to contrast medium.
o Can simultaneously assess progression of thrombus, particularly into pelvic vessels.
• D – dimmers have a high negative predictive value for DVT.
o Low clinical suspicion of DVT, and negative D – Dimers, doesn’t need any more
investigation.
o Positive D – Dimers are followed up with ultrasonography.
• Venography.
o Use if results are uncertain and clinical suspicion is high.
• Consider baseline investigations for all patients.
o FBC
o U&E
o ECG
o CXR
o Urinalysis
o Pulse oximetry ± ABGs
• If appropriate look for underlying cause.
o Coagulation screen.
o Pro – coagulant screen.
Refer to local screening .
Get haematology advice.
CRP
ESR
Protein C and S
Antithrombin III
Factor V Leiden mutation
Auto – Ab screen
• Management.
o If there is a high clinical suspicion of DVT, start empirical LMWH therapy.
This can be stopped if subsequent investigations are negative.
o If DVT is below knee there is a lower risk of embolisation, so can be treated with.
TED stockings.
SC LMWH until able to mobilise.
Systemic LMWH may reduce pain from below knee DVT.
o If DVT is above kinee, there is a greater risk of embolisation.
Full anticoagulation with LMWH/UFH
Follow up with warfarin.
o Anticoagulation.
Heparin.
• LMWH has now replaced UFH as treatment for DVT and PE.
o Do not require daily monitoring.
o Can be given on outpatient basis.
• Must overlap heparin and warfarin therapies until INR is in a
thereputic range and stable.
• LMWH is normally given as a daily SC injection.
o Dose is dependant on patient’s weight.
Warfarin.
• Always anti – coagulate with LMWH before conversion to solo
therapy with warfarin.
o Protien C (a vitamin K depedent anticoagulant) has a
shorter half life than most coagulation factors.
o Starting warfarin with normal coagulation factors will
reduce vitamin K levels, so reduce action of Protein C, so
lead to a pro – coaguable state.
• If DVT is confirmed:
o Commence warfarin.
o Maintain LMWH treatment until INR > 2.
• Anticoagulate (INR = 2 – 2.5) for 3 months.
• Consider lifelong anti – coagulation if:
o Recurrent DVTs
o High risk of recurrent DVTs.
o Thrombolysis.
Consider for recurrent, extensive proximal venous thrombosus (eg. femoral,
iliac) as, compared to anti – coagulation alone, it is:
• More effective at clot dilution.
• Produces better clinical outcomes.
Catheter – directed thrombolysis (rt – PA or SK) is better than systemic
thrombolysis..
One approach is to give Streptokinase
• 250 000 U over 30 minutes
• 100 000 U every hour, for 24 – 72 hours.
Contraindications:
• Complications.
o Bleeding in 10% of patients.
Normally minor bleeding at venopuncture site.
• Treated with local compression.
Occasionally transfusion is needed.
If needed, streptokinase can be reversed with
tranexamic acid 10 mg/kg by slow IV.
o Hypotensio during infusion.
Lay patient supine.
Stop/slow infusion until BP rises.
Treatment with cautious boluses (100 – 500 ml)
may be required.
Not an allergic reaction, as doesn’t require
treating as such.
o Allergic reactions to streptokinase are common.
Low grade fever
Nausea
Flushing
Headache.
Give hydrocortisone 100 mg IV with
chlorpheniramine 10 mg IV
o Intercranial bleeds seen in:
0.3% of patients treated with streptokinase.
0.6% of patients treated with rt – PA.
• Relative contraindications.
o Trauma and/or surgery within 2 weeks.
o BP > 180/110 mmHg
o Non – haemorrhagic stroke > 1 year ago.
o Known bleeding disorder.
o Current anticoagulant therapy with INR > 2.
o Significant liver or renal dysfunction.
o Streptokinase within past 6 – 9 months.
o Pregnancy or post – partum.
o Lumbar puncture/ Spinal anaesthesia within 1 month.
o Menstrual bleeding or lactation.
o History of chroninc severe hypertension.
o Non – compressible venous puncture sites.
Eg. Sub – clavian central venous lines.
• Absolute contraindications.
o Active internal bleeding.
o Suspected aortic dissection
o Recent head trauma and/or intercranial neoplasm.
o Previous haemorrhagic stroke
o Previous ischemic stroke within 1 year.
o Previous allergic reaction to fibrinolytic agents.
o Trauma and/or surgery within past 2 weeks at risk of
bleeding.
o Further management.
Women taking the COCP should be advised to stop this.
If there are contraindications to anti – coagulation/ thrombolysis, consider
fitting a caval filter to prevent PE.
All patients should be given thigh high TED stockings.
• Reduces venous dilatation when mobilising.
Pulmonary embolism.
• Symptoms.
o Classically presents with:
Sudden onset
Pleuritic chest pain
Dyspnoea
Haemoptysis
Posutral dizziness or syncopy.
o Massive PE may present with:
Cardiac arrest.
• Particulary with electromechanical disassociation)
Shock.
o Presentation may be atypical.
Unexplained breathlessness
Unexplained hypotension
Unexplained syncopy.
o PE should be suspected in all patients who have:
Breathlessness with risk factors for DVT.
Breathlessness with proven DVT.
o Recurrent PE may present with .
Chronic pulmonary hypertension
Progressvie right heart failure.
• Signs.
o Signs can consist of only tachycardia and tachyopnoea.
o Check for postural hypotension in raised JVP.
o Check for signs of raised right heart pressure and cor pulmonarle.
Raised JVP with prominent “a – wave”
Tricuspid regurgitation
Parasternal heave
Right ventricular S3
Loud pulmonary closure sound, with wide splitting of S2
Pulmonary regurgitation.
o Cyanosis suggests a large pulmonary embolism.
o Examine for pleural rub (can be transient) or effusion.
o Examine lower limbs for obvious thrombophlebitis.
o Mild fever (> 37.5) may be present.
o May be signs of co – existing COPD.
• Causes.
o Most frequently, secondary to DVT
o Other causes include
Secondary to right ventricular thrombus.
• Eg. post – MI
• Rare.
Septic emboli.
• Eg. Tricuspid endocarditis.
Fat emboli.
• Post fracture.
Amniotic fluid emboli
Parasites
Neoplastic cells
Foreign materials.
• Eg. venous catheters.
o Prognostic features.
Varies depending on underlying condition
Generally poor prognosis is associated with:
• Large emboli
• Hypotension
• Hypoxia
• ECG changes.
o Other than non – specific T wave changes.
• General investigations.
o ABGs.
Normal ABGs do not exclude and PE
• S1Q3T3
• Right axis deviation
• RBBB
Less commonly findings include AF.
o CXR.
May be normal.
• Normal CXR in the context of severe respiratory compromise is PE
until proven otherwise.
Less common findings are:
• Focal pulmonary oligaemia
o Westermark’s sign
• Raised hemidiaphragm
• Small pleural effusion
• Wedge shaped shadows based on the pleura
• Sub – segmental atelectasis
• Dilated proximal pulmonary arteries.
o Blood tests.
There is no specific blood test for PE, but other tests can hint at the
diagnosis.
FBC
• Raised neutrophils
• Raised WCC
• Raised CK
Troponin levels
LFTs
• Raised bilirubin
o Echo/ TOE.
Insensitive for diagnosis, but can exclude other causes of hypotension and
raised right – sided pressure.
• Tamponade
• RV infarction
In PE it will show:
• RV dilatation
• Global hypokinesia with sparing of the apex
o McConnell’s sign
• Pulmonary artery dilatation
Doppler may show tricuspid/pulmonary regurgitation.
• Allows estimation of RV systolic pressure
Rarely, the thrombus will be visible on Doppler.
• Specific investigations.
o D – Dimer.
Hihgly sensitive, but non – specific tests.
Useful in ruling out PE in patients with low or intermediate probability.
Results can be affected by:
• Advancing age.
• Pregnancy
• Trauma
• Surgery
• Malignancy
• Other inflammatory states.
o V/Q scanning.
Perfusion scan should be performed in all cases of suspected PE.
• Uses IV Technetium – 99 labelled albumin.
Ventilation scan in conjunction improves specificity by assessing whether
defects in ventilation and perfusion match or mis – match.
• Uses inhaled Xenon – 133
Pre – existing lung disease makes interpretation difficult.
o CTPA.
Recommended initial modality for patients with non – massive PE.
Allows direct visualisation of.
• Emboli.
• Other parenchymal disease which may be an alternative
explanation of symptoms.
Sensitivity and Specificity are very good (>90%) for lobar pulmonary
arteries.
• Not as good for segmental and sub – segmental arteries.
A patient with a positive CTPA doesn’t require any further investigations to
confirm PE.
A patient with a negative CTPA, but high clinical suspicion of PE requires
more investigation.
o Evaluation of leg veins with US.
Not very reliable.
• Only about 50% sensitive
Useful in combination with CTPA or V/Q scan.
Studies show that it is safe to not coagulate patients who have:
• Negative leg ultrasound
• Negative CTPA
• Low/ intermediate probability clinically.
o Pulmonary angiogram.
Gold standard investigation.
Invasive and associated with 0.5% mortality.
Indicated in patients where possibility of PE can not be ruled out by non –
invasive means.
A PE will be demonstrated by:
• Sharp cut off of vessels.
• Obvious filling defects
If PE demonstrated, clot can be broken up with catheter or guide wire
After angiography, the catheter can be used to deliver thrombolysis directly
into the affected pulmonary artery.
Side effects:
• Systemic vasodilation
• Haemodynamic collapse in previously hypotensive patients.
o MR pulmonary angiogram.
Results comparable to pulmonary angiography in preliminary studies.
Can simultaneously assess ventricular function.
Monitor area
O2, IV fluids, analgesia,
ABGs, ECG, CXR, bloods
High risk of PE
Low risk of PE
Treat as inpatient
or in A&E Admit
Give LMWH
US Lower limb
D - Dimers
Negative Positive
V/Q or CTPA
Discharge
Negative for PE
Positive for PE
V/Q or CTPA
Whichever one not performed Anti – coagulate Discharge
Pulmonary angiogram with warfarin.
Management
• Stabilise patient.
o Treat for PE unless another diagnosis is made.
o Set up 15 minute observations, monitoring.
ECG
Pulse
BP
Respiratory rate
o Constantly monitor pulse oximetry.
o Ensure resuscitation facilities are available ant to hadn.
o Gain IV access and give fluids.
Crystaloid or colloid.
o Give high flow oxygen via a facemask to correct hypoxia.
Mechanical ventilation may be needed.
Beware cardiovascular collapse when sedating for endotracheal intubation.
o Give UFH or LMWH to all patients with intermediate or high risk of PE.
Multiple Meta – analyses has shown LMWH to be superior to UFH
• Reduced mortality
• Reduced bleeding complications.
For dose, consult BNF.
o If there is evidence of haemodynamic instability or cardiac arrest, consider
thrombolysis.
`Systemic hypotension.
Signs of right heart failure.
Absent pulse
Dose of thrombolysis.
• Rt – PA.
o 0.6 mg/kg over 15 minutes.
o Maximum dose of 50 mg
o Follow up with heparin.
• Streptokinase.
o 250 000 Units over 30 minutes.
o 100 000 Units/h for the next 24 hours.
• Analgesia.
o Patient may respond to NSAIDs.
o Opiate analgesia should be used carefully.
Vasodilation caused by the opiates, may worsen hypotension.
Give small doses slowly.
• 1 – 2 mg diamorphine IV
Hypotension should respond to IV colloids.
Avoid IM injections
• Anticoagulation.
o Patients with a positive diagnosis should be anti – coagulated with warfarin.
o Should be an overlap with LMWH until INR = 2 – 3
o Standard length of therapy is:
4 – 6 weeks for temporary risk factors.
3 months for first idiopathic cause.
At least 6 months for other causes
With recurrent events and underlying predisposition to clotting, lifelong
anti - coagulation may be needed lifelong.
• With and INR > 3.
• Cardiac arrest.
o Massive PE may present as cardiac arrest due to electromechanical disassociation.
Exclude other causes of EMD before PE is diagnosed as the cause.
o Chest compressions may help break up the thrombus and allow it to progress distally
Allow some cardiac output to return.
o If clinical suspicion of PE is high, thrombolysis with rT – PA may be commenced.
o If sufficient cardiac output returns, consider mechanically disrupting the clot with.
Pulmonary catheter.
Pulmonary angiography.
• Hypotension.
o Acute increase in pulmonary vascular resistance results in right ventricular dilatation
and pressure overload.
Impairs left ventricular filling and function.
o Patients require higher than normal right filling pressures, but are at risk from
overload.
o Insert internal jugular sheat prior to anti – coagulation.
This can be used for ongoing access if needed.
o If hypotensive, give 500 ml colloid
o If hypotension continues,
Start invasive monitoring.
Consider inotropic support
• Adrenaline is inotrope of choice.
o JVP is a poor measure of left sided filling in cases like this.
o Femoral – femoral cardiopulmonary bypass may be used to support circulation until
thrombolysis or surgical embolectomy can be performed.
o Pulmonary angiography in a hypotensive patient is dangerous.
Contrast will cause vasodilatation
Vasodilatation when already hypotensive may cause cardiovascular collapse.
• Pulmonary embolectomy.
o If thrombolysis is contraindicated for a shocked patient, there may be a role for
embolectomy.
o Can be performed
Percutaneously in catheterization lab, using a number of devices.
• May be combined with peripheral or central thrombolysis.
Surgically on cardiopulmonary bypass.
• Radiological confirmation of extent and site of embolus is
preferable before thoracotomy.
o Seek specialist advice early.
Best results are achieved before onset of cardiogenic shock.
o Mortality from PE and embolectomy is 25 – 30%.
• IVC filter.
o Infrequently used as little evidence to show improved short– or long – term mortality.
o Filters are positioned percutaneously.
o If possible, patients should remain on anti – coagulants to prevent new thrombus
formation.
o Most are positioned infra – renally (bird’s nest filter), but some are fitted
supra – renally (Greenfield filter).
o Indications for IVC filter.
Anti – coagulation contraindicated.
• Active bleeding
• Heparin – induced thrombocytopaenia
• Planned intensive chemotherapy.
Anti – coagulation failure, in spite of maximum therapy.
Prophylaxis in high risk patients.
• Progressive venous thrombosis
• Severe pulmonary hypertension.
• Fat embolism.
o Commonly seen in patients with major fractures.
o There is embolisation of fat and micro – aggregation of:
Platelets
RBC
Fibrin
o These emboli will spread through the systemic and pulmonary circulations.
o Pulmonary damage may be:
Directly due to emboli (infarcts)
Chemical pneumonitis.
ARDS
o Clinical presentation.
History of fractures.
24 – 48 hours later.
• Breathlessness
• Cough
• Haemoptysis
• Confusion
• Rash
o Signs
Fever
Widespread petechial rash.
• 25 – 50%
Cyanosis
Tachypnoea
Scattered crepetations in all lung fields
Reduced consciousness
• Confusion
• Drowsiness
• Seizures
• Coma
.Check eyes for:
• Conjunctival and retinal haemorrhages.
• Fat globules in retinal vessels.
o Severe fat embolism may present with shock.
• Investigations.
o ABGs.
Hypoxia
Respiratory alkalosis
o FBC.
Thrombocytopaenia
Acute intravascular haemolysis
o Coagulation.
Disseminated Intravascular coagulation
o U&Es.
Renal failure.
Hypoglycaemia
Calcium may be low
o ECG.
Non – specific changes.
Often sinus tachycardia
Sometimes signs of right heart strain.
o CXR.
Usually lags behind the clinical course.
There may be patchy, bilateral air space opacifications.
Effusions are rare.
o CT head.
Consider if there is a possibility of head injury with expanding subdural or
epidural bleed.
• Differential diagnosis.
o Pulmonary thromboembolism.
o Other causes of ARDS.
Direct lung injury.
• Aspiration.
o Gastric contents
o Near drowning
• Inhalation injury
o Noxious gases
o Smoke
• Pneumonia.
• Pulmonary vasculitides
• Pulmonary contusion
• Drug toxicity/ overdose.
o Oxygen
o Opiates
o Bleomycin
o Salicylates
Indirect lung injury.
• Septicaemia
• Shock
• Amniotic fluid emboli
• Acute pancreatitis
• Massive haemorrhage
• Multiple transfusions
• DIC
• Massive burns
• Major trauma
• Head injury.
o Raised ICP
o Intercranial bleed
• Cardiopulmonary bypass
• Acute liver failure.
o Septic shock
o Hypovolaemia
o Cardiac or pulmonary contusion
o Head injury
o Aspiration pneumonia
o Transfusion reaction
• Management.
o Treat respiratory failure.
o Give high flow oxygen
Using NIV or mechanical ventilation if needed.
o Ensure adequate circulating volume and cardiac output.
CVP is a poor estimator of left – sided filling pressure.
PA catheter (Swan – Ganz) should be used to guide fluid replacement.
Try to keep PCWP at 12 – 15 mmHg.
Give diuretics if needed.
Use inotropes to support circulation if required.
o In acute stage, there is some benefit in giving:
Heparin
Aspirin
Dextran 40.
• 500 ml over 4 – 6 hours.
May exacerbate bleeding at site of trauma.
o High – dose steroids improve hypoxaemia.
3 doses of methyprednisolone 30 mg/kg TDS.
Steroids are probably most effective if given prophylactically.
Pleural effusion.
• Presentation.
o Dyspnoea
o Chest discomfort/ sensation of heaviness
Unilateral reduced chest movement indicates that pathology is on side with
decreased movement.
o Symptoms of malignancy
Weight loss
Poor appetite
Lack of energy
o Symptoms of infection.
Fever
Cough
Sputum produced
Night sweats.
• Causes.
o Transudate (Protien < 30 g/l)
Raisde venous pressure.
• Cardiac failure
• Constrictive pericarditis
• Fluid overload.
Hypoprotienaemia
Nephrotic syndrome
Cirrhosis with ascites
Protien – losing enteropathy
Miscellaneous.
• Hypothyroidism
• Meig’s syndrome
• Yellow nail syndrome
o Exudate ( Protien > 30 g/L)
Pancreatitis
Infection.
• Pneumonia
• Empyema
o Bacterial
o TB
• Subphrenic abscess.
Neoplasia
• Primary bronchial
• Mesothelioma
• Lung metasteses
• Lymphoma
• Lymphangitis carcinomatosa
Trauma
• Haemothorax
• Chylothorax.
o Thoracic duct trauma.
SLE & other autoimmune disease.
• SLE
• RA
• Dressler’s
Management.
• If acute.
o Stabilize patient
o Insert chest drain
• If chronic.
o Determine cause.
o Treat accordingly.
• Investigations.
o Diagnostic aspiration .
Ideally chest should be scanned and marked by ultrasound prior to drainage.
Underlying collapse can cause significant elevation of the hemidiaphragm.
o Sample of about 50 ml should be taken and split into three for sending to.
Biochemistry.
• Transudate or exudates.
• LDH for Light’s criteria.
o Further assessment of presence of an exudates.
o Pleural fluid protein divided by serum protein > 0.5
o Pleural fluid LDH divided by serum LDH > 0.6
o Pleural fluid LDH > Two times upper limit olf normal
serum LDH
• pH < 7.2 suggests empyema
• Glucose < 3.3 mol/l suggests:
o Empyema
o TB
o Auto – immune disease
• Amylase if acute pancreatitis is suspected.
Microscopy/ microbiology.
• Turbid fluid with neutrophils suggests infection.
• Bloody fluid suggests.
o Malignancy.
o Haemothorax.
In haemothorax, fluid haematocrit will be > half
blood haematocrit.
o ZN staining for acid – fast bacilli.
+ve in about 20% of pleural TB
o Routine cultures and sensitivities.
o Culture for TB.
Cytology.
• For primary and secondary tumours
• Sensitivity of about 60%, so negative doesn’t exclude malignancy.
o Take pleural biopsy if suspected:
TB
Malignancy
o Chest CT with contrast may help distinguish.
Malignancy
Pleural thickening
Mesothelioma
Intrapulmonary disease
• Management.
o Fluid drained by either:
Repeated aspiration of 1 L per day until dry.
Insertion of small bore intercostal drain.
• Clamp and release to drain 1.5 L per day.
• This is the only time you should ever clamp a chest drain.
• Drainage of 1.5 L per day may cause reperfusion pulmonary
oedema
o If malignant effusion recollects quickly, consider chemical or surgical pleurodesis
Empyema.
• Serious complication of bacterial chest infection.
• All effusions associated with pneumonia (parapneumonic) should be tapped.
• To avoid long term scarring and loculated infection, the effusion should be:
o Urgently drained under ultrasound.
o Chest drain considered.
• Frequent drainage may fail, due to adhesions causing loculated infections.
o Can be assessed by US.
o May require surgical drainage.
• All cases of suspected empyema should be discussed with respiratory physicians and/ or
cardiothoracic surgeons.
Acute upper airway obstruction.
Presentation
• Stridor.
o Inspiratory noise
o Caused by collapse of extra – thoracic airway on inspiration.
• Breathlessness
• Dysphagia
• Inability to swallow secretions.
o Hunnched forward
o Drooling
• Cyanosis
• Collapse
• If airway obstruction suspected, ask somebody else to fast bleep the senior anaesthetist and
ENT surgeon whilst you continue your assessment.
Causes
• Infective.
o Acute epiglottitis
o Diptheria
o Tonsillitus
o Adenoiditis
• Inhalation of foreign body
• Tumour of trachea or larynx
• Trauma
• Post – operatively.
o Thyroid surgery.
• History.
o Sudden onset
o Something in mouth/ child playing with small object.
o Fever.
Epiglottis
Diptheria
Tonsillitis
o Hoarse voice.
Epiglottitis
o Sore throat.
Infective causes.
o Travel.
• Management.
o If severe, liaise immediately with ITU and ENT or general sugery.
Potential for urgent tracheostomy.
o Priorities are:
Stabilize the patient.
• Ensure adequate airway.
• Take ABGs
• Give high flow oxygen
• If cause of obstruction is obvious, take appropriate measures to secure an
airway.
• Foreign body.
o If loss of airway is total, perform Heimlich manoeuvure.
o Otherwise:
CXR
Liaise with respiratory/ENT/cardiothoracic
surgeons about retrieval under direct vision.
• Epiglottitis.
o Usually.
H. influenzae
Group B Streptococci
Strep. pneumoniae.
o Give 3rd generation cephalosporin.
Eg. cefotaxime 2g tds
o Children more likely to require intubation.
If any concerns over airway, whether adult or
child, refer for monitoring on ITU after
anaesthetic assessment.
• Diptheria.
o Rare in the UK
o Occasionally seen in patients returning from abroad.
o Toxin – mediated problems include:
Myocarditis
Neuritis
o Treat with:
Diptheria anti – toxin.
Antibiotic erradiaction of organism.
• Consult with microbiologist.
• Tumour obstruction.
o Unlikely to cause life – threatening obstruction without
warning symptoms over more than a few days.
o If significant stridor present, give:
Initially, 200 mg hydrocortisone
Follow up with 40 mg prednisolone OD PO
o If laryngeal origin, liaise with ENT regarding
tracheostomy.
o Urgent radiotherapy/ laser or cyrotherapy via
bronchoscopy for:
Lung cancer in trachea
Extrinsic cancer eroding into the trachea.
• If patient is becoming increasingly fatigued, or is going into acute
ventilatory failure:
• Summon colleagues
• Be prepared to perform intubation or tracheostomy.
Identify cause of obstruction
Specific treatment measures.