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Hospital Based Practice – Shortness of Breath.
Acute shortness of breath.
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
Other respiratory symptoms can suggest a diagnosis.
o Wheezing
Asthma
COPD
Heart failure
Anaphylaxis
o Stridor (upper airway obstruction)
Foreign body
Tumour
Acute epiglottitis
Anaphylaxis
Trauma eg. laryngeal fracture
o Crepitations
Heart failure
Pneumonia
Bronchiectasis
Fibrosis
o Clear chest
Pulmonary embolism
Hyperventilation
Metabolic acidosis.
Eg. Diabetic acidosis
Anaemia
Drugs.
Eg. salicylates
Shock.
May cause air hunger
Pneumocystis pneumonia
Central causes
o Others
Pneumothorax.
Pain
Increased resonance
Pleural effusion.
Stony dullness
History in the breathless patient.
Try to quantify the severity.
o Exercise tolerance.
o Impact on daily life.
Specific types of dyspnoea.
o Orthopnoea.
Dyspnoea on lying down.
Characteristic of heart failure.
Can occur with other things, eg. diaphragmatic paralysis.
o Paroxysmal nocturnal dyspnoea.
Breathlessness that wakes the patient from sleep.
Generally symptom of heart disease.
Onset.
o Duration of onset, and rate of decline, will give an indication of aetiology.
Acute onset.
Foreign body aspiration.
Pneumothorax.
PE
Asthma
Acut pulmonary oedema
Subacute onset.
Suggestive of parenchymal disease.
o Alveolitis
o Pleural effusion
o Pneumonia
o Carcinoma of the bronchus or trachea.
Chronic onset & decline
COPD
Cryptogenic fibrosing alveolitis
Occupational fibrotic lung disease
Non – respiratory causes.
o Heart failure
o Anaemia
o Hyperthryroidism.
o Other factors in the history.
Association with cough?
Smoking
Asthma
COPD
Drugs.
o ACE inhibitors
Occupational agents
Heart failure
Psychogenic factors
Duration?
Variations in intensity through the day?
Precipitating factors?
Sputum production
Moderate quantity of purulent sputum.
o Bronchitis
o Pneumonia
Large quantity of purulent sputum.
o Bronchiectesis
o Pneumonia
Pink & frothy.
o Pulmonary oedema
Blood stained.
o Causes of haemoptysis
Rust coloured.
o Pneumococcal lobar pneumonia
Haemoptysis.
Frank blood or blood tinged sputum?
Needs to be distinguished from nasopharyngeal bleeding and haemetemesis.
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.
Examination findings in breathless patients.
Condition Movement on side of lesion
Position of trachea
Percussion Tactile vocal fremitus
Breath sounds
Pleural effusion
Reduced Central, or deviated away if effusion is large.
Reduced
(“stony dull”)
Reduced Reduced.
Bronchial breathing at top of effusion
Pneumothorax Reduced Central or deviated away
Increased Reduced Reduced
Pneumonia Reduced Central, or deviated toward if collapsed
Reduced Increased Increased vocal resonance.
Bronchial breathing (absent if obstruction of bronchus)
Coarse crepetations.
Pulmonary fibrosis
Reduced Central, or deviated towards if upper lobe involved.
Reduced Increased Bronchial breathing.
Fine crepetations.
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.
Full blood count
o Anaemia
o Leucocytosis.
Penumonia
U&Es
o Renal failure secondary to
Dehydration
Sepsis
Acidosis
Blood sugar.
o Acute dyspnoea can be due to diabetic ketoacidosis.
Particularly in younger patients.
Chest X – ray.
Region Diagnosis X – ray findings
Pericardium Tuberculosis or constrictive pericarditis
Calcification
Myocardium Effusion Globular cardiomyopathy
Left ventricular dilatation Cariomegaly, with left ventricular diplaced inferolaterally.
Right ventricular dilatation Cardiomegaly
Left atrium Double right heart border
Splaying of carina
Left ventricular aneurysm Calcified mural thrombus
Endocardium Rheumatic heart disease Calcification
Valves Valve replacement Sternal wires
Metalic valves
Surgical clips
Mitral stenosis Widened carina
Calcified valve
Straight left heart border
Atheroma Calcification
Aorta Coarctation Rib notching
Dissection Widened mediastinum
Lungs Pulmonary oedema Upper lobe vein dilatation
Kerley B lines
Bat’s wing shadowing (perihilar oedema)
Fluid in horizontal fissure
Pleural effusion (usually bilateral but can be unilateral).
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%
PaO2 < 8kPa
o Ventilatory failure
Rising PaO2
Confusion or coma
Acute severe asthma.
o PEF = 30 – 50% best or predicted
o Respiratory rate > 25 bpm
o Tachycardia < 100 bpm
o Inability to complete sentences in one breath.
Brittle asthma.
o Type I.
Wide PEF variation, in spite of intensive and regular therapy.
o Type II.
Sudden severe asthma attacks, on the background of apparently well controlled asthma.
Admission is required if ANY of the markers are present of asthma that is:
o Near fatal
o Life threatening
o Severe
The severity of an attack is easily underestimated. Remember to consider:
o Degree of airway obstruction
o Effect of increased work of breathing on the patient.
o Extent of ventilation – perfusion mismatch.
o Evidence of ventilatory failure.
Patients with marked “morning dips” in PEF are at high risk of sudden severe asthma attacks.
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
Hypoxia PaO2 < 8 kPa/ 60 mmHg, in spite of FiO2 = 60%
Rising PaCO2 or PaCO2 > 6 kPa (45 mmHg)
Exhaustion, drowsiness or coma
Respiratory arrest
Failure to improve, in spite of appropriate therapy.
4. Treat underlying conditions
Patients may deteriorate rapidly.
o Should not be left unattended.
Remain calm.
o Reassurance is important in reducing patients anxiety.
o Reduced anxiety means less hyperventilation.
Severe or life – threatening asthma.
o Initial treatment.
Sit the patient upright in bed.
Give high flow oxygen.
Maintain SaO2 > 92%
Nebulized bronchodilators.
Salbutamol 5 mg or terbutaline 10 mg.
Repeat every 15 – 30 minutes if required.
Consider continuous nebulizatio of salbutamol at 5 – 10 mg/hour if response is poor to intermittent salbutamol.
Add ipratropium bromide 0.5 mg ever 4 – 6 hours if initial response to β – agonists is poor.
Obtain IV access.
Start steroids.
200 mg IV hydrocortisone.
o Use even in pregnant women due to high risk of foetal anoxia due to asthma attack.
Continue with IV hydrocortisone 100 mg QDS, or oral prednisolone 30 – 50 mg once daily.
Antibiotics if evidence of infection.
Abnormal CXR
Raise WCC
Fever
Purulent sputum.
Adequate hydration.
Essential part of management
Prevents mucus drying out and plugging airways.
Ensure intake of 2 -3 ml.kg/day
o Be careful not to fluid overload.
o Replace potassiumas required.
o Monitoring progress.
Check peak flow pre – and post – nebulizers
Repeat ABGs every 2 – 3 hours, or according to response.
Especially if SaO2 < 93%
o If response to above treatment is not brisk, or patient is deteriorating.
Continue oxygen.
Give β – agonists every 25 minutes.
Give single dose of IV magnesium sulphate.
1.2 – 2 g infused over 20 minutes.
Only give single dose as multiple doses associated with hypermagnesaemia.
o Muscle waekenss.
o Respiratory failure.
Consider aminophylline infusion.
Loading dose.
o 4 – 5 mg/kg IV over 20 minutes.
Maintainance dose
o 0.5 – 0.7 mg/kg/h
o 250 mg in 1 L of saline at 2 – 4 mg/h
If patient on oral theophylline, check level before giving loading dose.
Halve dose in patients with.
o Cirrhosis
o CCF
o Treatment with:
Erythromycin
Cimetidine
Ciprofloxacin
Monitor levels every 24 hours.
o Aim for level of 10 – 20 mg/L
Consider salbutamol infusion.
Loading dose.
o 100 – 300μg over 10 minutes
Maintainance dose.
o 5 – 20 μg/min
o 5 mg in 500ml saline at 1 – 3 ml/min.
Side effects.
o Tremor
o Tachycardia
o Hypokalaemia
o Hyperglycaemia
o Lactic acidosis is a rarer side effect.
Responds within hours to a reduction in salbutamol infusion rate.
Summon anaesthetic help
Mild to moderate asthma attacks.
Mild attack.
o No severe features.
PEF > 75% of predicted, or of best when well.
o Administer patient’s usual bronchodilators.
o Observe for 60 minutes.
If PEF remains > 75%predicted or best, discharge.
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.
PEF = 51 – 75% predicted, or best when well.
o Give nebulized β – agonists
Salbutamol 5mg
Terbutaline 10mg
o Give oral prednisoolone 30 – 60 mg.
o Reassess after 30 minutes.
If PEF < 50% or symptoms worsening
Admit and treat for severeasthma.
If PEF = 51 – 75%
Repeat nebulizers
Observe for further 60 minutes.
o Patient may be discharged from A&E if both:
PEF >75%
Patient stable after 1 – 2 nebulizers.
o If, after second nebulizer and 60 minutes of observation, patient is improving and PEF > 50%, discharge may be considered on:
Oral prednisolone 30 – 40 mg daily for 7 days.
Inhaled corticosteroid 1mg daily
Inhaled β – agonist.
Consider referral to chest clinic.
o Advise patient.
See GP within 48 hours.
Return to A&E if symptoms worsen
Sending patients home from A&E.
o Mild to moderate exacerbations may be discharged when well.
o If there are any features of severe asthma, admission is vital.
PEF = 30 – 50%
Respiratory rate > 25 bpm
Heart rate > 100 bpm
Inability to complete sentences in one breath.
o History of brittle asthma, or previous ventilation require admission.
Acute exacerbation of COPD.
Presentation
o Deterioration of pre – existing symptoms of exertional breathlessness.
Cough.
Sometimes productive.
Wheeze
o Respiratory failure.
See later.
o Wheeze unrelieved by normal inhalers.
o Increased production of prurulent sputum.
Eg. infection as a precipitant.
o Positive smoking hisotyr.
If not, late onset asthma is more likely
o Confusion/ impaired consciousness.
Exhaustion
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.
CO2 retention flap
Confusion
Cor pulmonale
Peripheral oedema
o Need for admission.
Marked increase in symptoms.
Baseline of severe COPD
New physical signs.
Eg. cyanosis, peripheral oedema
Failure to respond to initial management at home
Significant co – morbidities
Diagnostic uncertainty
Age > 70 years
Insufficient home support.
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%
If patient is retaining CO2 and is hypoxic.
Give oxygen 24 – 28%.
Repeat ABGs after 15 – 30 minutes.
Aim to keep:
o PaO2 >7.3 kPa
o PaCO2 <7.5 kPa
o These limits may not be achievable.
Hypoxia can kill, but it is important to balance it against.
o Consciousness level
o pH
o Respiratory drive.
Consider:
o Non – invasive ventilation
o Mechanical ventilation
o Doxapram.
Non – invasive ventilation.
First line treatment of choice for exacerbation of COPD with Type II respiratory failure, who fail to respond to initial therapy.
Allows administration of higher levels of O2 without loss of respiratory drive.
Non – invasive ventilation reduces:
o Need for intubation
o Mortality
o Length of hospital stay.
Should be considered in all patients who have failed to respond to initial bronchodilator therapy and have:
o PaCO2 > 6.0 kPa
o ph < 7.35
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.
Features suggesting good prognosis on ventilation.
o Acute respiratory failure.
Short history
No metabolic compensation
o Realtively young patient.
o Reversible cause for failure.
Eg. pneumonia
o Recent good exercise tolerance and functional ability
o No history of CO2 retention
Features suggesting poor prognosis on ventilation.
o Relatively old.
o Other co – morbidities.
Eg. IHD, renal failure.
o Chronic progression with poor exercise tolerance and function.
o Previous difficulty on weaning from ventilation.
o On maximal therapy at home.
Nebulized bronchodilators.
Home oxygen
Management of gas exchange on ventilation.
o Patients who are chronically hypoxic, or CO2 retainers tolerate poor blood gases better than patients with other causes of failure.
o May not be appropriate to try and achieve “normal” blood gases on ventilation.
Compensated hypoxics and CO2 retainers unlikely to successfully wean with normal levels of CO2 or O2.
Should run the ventilator at “normal for that patient”
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.
After treating hypoxia, next priority is treatment of bronchospasm and obstruction.
o Nebulized β2 – agonists QDS and PRN
Salbutamol 5 mg
Tebutaline 10 mg
Give with oxygen for most paitnets.
Give with air if CO2 retaining.
If patient is very hypoxic, give oxygen 2 L/min via nasal cannula during nebulizer.
o Patients with COPD may normally have relatively fixed bronchospasm.
If patient unwell, may be worth trying IV aminophylline and/or β – agonists as for severe asthma.
Amiophylline.
o Loading dose: 4 – 5 μg/kg over 20 minutes.
o Maintainance dose: 0.5 -0.7 μg/kg/h
250 μg in 1 litre saline at 2 – 4 ml/kg/h
o If on theophylline, check levels before giving loading dose
o Halve dose in patients with:
Liver cirrhosis
CCF
Treatment with:
Erytthromycin
Ciprofloxacin
Cimetidine
o Check levels every 24 hours.
Aim for concentration of 10 – 20 μg/L
Salbutamol
o Loading dose: 100 – 300 μg over 10 minutes.
o Maintainance dose: 5 – 20 μg/min
5 mg in 500 ml saline at 1 – 3 ml/min
o Side effects include.
Tremor
Tacchycardia
Hypokalaemia
Hyperglycaemia
Lactic acidosis.
Rare, and resolves within hours of stopping salbutamol therapy.
o Give iprotropium bromide.
500 μg every 6 hours.
o Give steroids, either:
Oral prednisolone 30 – 40 mg.
IV hydrocortisone 200 mg
o Urgent physiotherapy may help clear bronchial secretions.
Treat causes of exacerbation.
o Infective exacerbation.
Suggested by increased or purulent sputum.
For lobar or bronchial pneumonia.
Treat as for normal pneumonia.
Otherwise treat with oral or IV amoxicillin 500 mg – 1 g TDS
If unwell, or no response, give IV cefuroxime 750 mg TDS.
Particularly for resistant Haemophilus species.
Beyond this, follow local protocols.
o Pneumothorax.
Unless very small, consider aspiration ± drain.
o Pulmonary oedema.
See later
o Pulmonary embolism.
See later.
Respiratory Failure
Occurs when gas exchange becomes significantly impaired.
Clinically it isn’t possible to predict PaCO2 or PaO2.
o Diagnosis is on ABG analysis.
Type I: PaO2 < 8 kPa with normal or low PaCO2.
Generally a ventilation – perfusion mismatch.
Type II: PaO2 < 8 kPa with PaCO2 > 6 kPa
Predominantly alveolar hypoventilation.
In practice, both types may co – exist.
Presentation.
Commonest symptom is shortness of breath.
o Ask about speed of onset, as sudden onset may suggest.
Pneumothorax.
Cardiac failure
Pulmonary embolus.
o Respiratory failure may present without dyspnoea, particularly in:
Exacerbation of COPD.
Neuromuscular disease.
Eg. Guillain - Barre
Drug overdose
In the elderly, confusion may be the only symptom.
History may point to cause of failure.
o Smoking.
Asthma
Chronic bronchitis.
o Chronic lung disease.
Fibrosing alveolitis
Sarcoidosis.
o Sputum production & Fever.
Pneumonia
o Swollen legs.
Chronic lung disease.
Mechanism is cor pulmonale or renal fluid retention due to hypoxia/ hypercapnia.
o Haemoptysis
PE
Pneumonia
o Cardiac – type history.
Palpatations
Chest pain
o Drug reaction/overdose.
o Neurological symptoms.
Painful legs
Parasthesia
o Allergies.
o Try to assess functional capacity when well.
Distance able to walk on the flat.
Climbing stairs without stopping
Frequency of attack.
Previous attacks
Ever ventilated.
Concurrent disease.
Heart disease
Renal impairment
Liver impairment
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.
FEV1 & FVC
o If suspected muscle weakness
Septic screen
o If febrile, or CXR suggests infection
o Sputum culture
o Blood cultures
Where indicated, also consider checking.
o Aspirin & paracetamol.
o Plasma and urine for toxicology
o Urinalysis for glucose and ketones
o Examine the CXR systemically for any abnormalities.
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.
Poor prognostic signs on presentation include.
o Inability to speak due to dyspnoea.
o Respiratory rate > 40 bpm
o Peak flow < 33% of predicted in acute asthma
o Tachycardia > 100 bpm
o Bradycardia < 60 bpm
o Exhaustion or coma.
Ventilatory support is urgently required.
o Stridor.
Indicates upper airway obstruction
o Pulse oximetry saturation of < 90%
o Shock.
Tachycardia and hypotension.
May indicate:
Tension pneumothorax.
Severe LVF
Severe pneumonia
Large PE
o Hypercapnoea is the end result of many causes of respiratory failure.
Asthma
Pneumonia
COPD.
o It indicates a tiring patient.
o Even if relatively elderly.
Patient may respond well to ventilation with satisfactory final outcome.
Depends on disease and premorbid condition.
Indications for intensive care
o Progressive exhaustion or impaired consciousness level
o Shock that doesn’t respond rapidly to initial resuscitation.
o Respiratory failure not responding rapidly to initial therapy.
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.
Alternatively, give IV flumazenil
200 μg bolus over 15 seconds.
100 μg every minute.
Max total dose on ward is 1 mg
Max total dose on ITU is 2 mg
o Secure IV access.
o Measure BP and heart rate.
o Look for signs of specific conditions.
Cardiac failure.
Raised JVP
Inspiratory crackles
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
Aeitiological agent can not be reliably predicted from clinical symptoms.
Immunocompromised patients may present with.
o Agitation
o Fever
o Tachyopnoea
o Decreased saturation or pulse oximetry
o Subtle CXR changes
Patients with right sided endocarditis (eg. IV drug users) may present with.
o Haemoptysis
o Fever
o Consolidation
o With or without caviation
Poor prognostic features in pneumonia.
o Pre – existing.
Aged > 50 years
Co – morbidities (eg. IHD, cancer etc.)
o Clinical features.
Confusion
Urea > 7 mmol/L
Respiratory rate > 30 bpm
SBP < 90 mmHg and/or DBP < 60 mmHg
If 2 or more of these features are present
o High mortality rate.
o Consider admission to ITU
o Other features.
Hypoxia, regardless of inspired oxygen concentration.
PaO2 < 8 kPa
SaO2 < 92%
WCC < 4, or > 20 x 109.
Bilateral or multilobar involvement on CXR.
Admit to ITU, if appropriate, if there are:
o 2 or more “core clinical features”
o Signs of hypoperfusion that are resistant to therapy.
SBP < 90 mmHg
Oliguria
Confusion
o Respiratory failure
PaO2 < 8 kPa
o Significant acidosis.
pH < 7.25
Base excess < -8
o Progressive exhaustion.
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.
Correct hypoxia until PaO2 > 10 kPa
Start at 35% oxygen and work up.
Patient likely to require ventilation if:
Hypoxia resistant to high flow oxygen.
PaCO2 > 6 kPa
Culture sputum.
o Gram stained microscopy can b e helpful, but not definitive.
Give pain relief.
o Paracetamol or NSAIDs normally suffice.
Morphine can be given as respiratory depression unlikely to be a problem if PaCO2 is low
If patient does need reversing, naloxone can easily be given.
Who can be discharged from A&E?
o Have a low threshold for admission
o The following patient can be discharged:
Young
No adverse prognostic factors
Single lobe involvement on CXR
No complications.
Eg. caviation
Effusions
o Arrange for outpatient review in 2 – 3 days.
Causes and incidence of pneumonia.
Community acquired Atypicals
Organism Incidence Organism Incidence
S. pneumoniae 40% Chlamydia pneumoniae 13%
Unknown organism 30% Mycoplasma spp. 11%
Mixed culture 14% Legionella pneumophilia
4%
Influenza A&B 11% Other Chlamydia spp 4%
H. influenzae 5%
S. aureus 2%
Moraxhella catarrhalis 2%
Other viruses 2%
Gram –ve bacteria/ anaerobes
1%
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.
Pleural effusionReactive (sterile)
TB
Empyema
Diffuse infiltrationAcute.
PCP
Viral (eg. CMV)
Drug reactions.
o Cyclophosphamide
o Bleomycin
o Busufan
Alveolar haemorrahage
Chronic
TB or atypical mycobacteria
Fungi
Lymphagitis
Carcinomatosa
Drugs (eg. Amiodarone)
Focal infiltrates.Acute
Pneumococcus
Staphylococci
Legionella
Klebsiella
Gram negatives
Mycoplasma
Pulmonary embolus
Chronic
TB
Fungi
Malignancy
Organising pneumonia
Eosinophilic pneumonia
Caviation Fungi
Anaerobes
Staph. Aureus
TB
Gram –ve bacteria
Malignancy
Other investigations
Where appropriate, consider:
o Bronchoscopy. ± Lavage
Immunocompromised
Failure to respond to 1st line antibiotics, and no organism identified.
o Echo.
Right heart endocarditis.
o VQ scan.
Excluse infective pulmonary infarction.
o Lung biopsy.
Trans – bronchial
Open lung
o Aspiration of pleural fluid.
For MC&S
o Viral titres.
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.
Blind antibiotic treatment.
Most patients do well on oral antibiotics.
Consider IV antibiotics if adverse prognostic features are present.
o Age > 50 years
o Co – morbid disease.
IHD, cancer etc.
o Confusion
o Urea > 7 mmol/L
o Respiratory rate > 30 bpm
o SBP < 90 mmHg and/ or DBP < 60 mmHg
o Pa O2 < 8 kPa/ Pa O2 < 92%
o WCC < 4 x 109/ > 20 x 109
o Bilateral or multi – lobar involvement.
Type of pneumonia Antibiotic recommended for blind therapy
Community acquired pneumonia ± atypical features
Amoxycillin ± Erythromycin
Post influenza pneumonia
(Staph. Aureus possible)
Cefuroxime OR
Amoxycillin + Erythromycin + Flucloxacillin
Hospital – acquired pneumonia Cefotaxime/ Caftazidime ± Metronidazole
Suspected/ Known MRSA isolated Amoxycillin + Erythromycin + Vancomycin
Aspiration pneumonia Cefuroxime + Metronidazole OR
Benzyl penicillin + Gentamicin + Metronidazole
Patient with risk factors for HIV and suspicion of PCP
Amoxycillin ± Erythromycin + High dose
co - trimoxazole
Likely pathogens
COPD Alcoholism Recent ‘flu Risk of aspiration
S. pneumoniae
H. influenzae
S. pneumoniae
H. influenzae
S. pneumoniae
H. influenzae
Anaerobes
Gram –ve bacteria
M. catarrhalis S. aureua
Klebsiella
TB
Anaerobes
Gram –ve bacteria
S. aureau
Contact with birds Haemoptysis Diarrhoea/ abdominal pain
C. psittaci Streptococci
S. aureus
Lung abscess
Necrotizing Gram –ve bacteria
Invasive aspergillosis
Legionella
Pharyngitis/ Otits media Risk factors for HIV Hospital acquired
Mycoplasma
Anaemia/cold agglutination
S. pneumoniae
H. influenzae
CMV
PCP
Cryptococcus
Gram –ve bacteria
S. aureus
Neutropenia Drug addicts Nursing home patients
P. aeruginosa
Gram – ve bacteria
Aspergillus
S. aureus
Candida
Aspiration pneumonia – type bacteria
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.
Pneumonia in the immunocompromised.
o All routine pathogens are possible,
Other pathogens depend on nature of immunocompromise
o TB and mycobacteria are more common.
o Since development of combination anti – retrovirals, complications of HIV are less common.
Pulmonary Kaposi’s sarcoma and lymphoma are rarely seen.
o Pulmonary opportunistic infection can be the first presenting symptoms before diagnosis.
Most common pathogen is pneumocystis cariniii
Desaturation on exercise in the presence of:
o Normal CXR
o Diffuse shadowing on CXR.
Fungal and viral (CMV) pneumonias may also occur.
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 Parapneumonic pleural effusions of empyema.
Parapneumonic effusion develops in 50% of admitted bacterial pneumonias.
Diagnostic tap should be performed on all parapenumonic effusions to exclude empyema.
Send effusion fluid for urgent:
o Gram stain
o MC&S
o pH analysis
Empyema (cloudy fluid, pus or organisms on gram stain) or complicated effusions (clear fluid, pH < 7.2) should be drained from pleural space.
Discuss with cherst physicians.
Ultrasound may help:
Look at level of effusion.
Demonstrate any loculation with empyema.
If empyema fails to resolve with pleural drain.
Arrange chest CT
Discuss with cardiothoracic surgeons.
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.
o Signs of a significant pneumothorax.
Tension pneumothorax.
Midline shift away from the pneumothorax.
Engorged neck veins and raised JVP
Hypotension
Tachycardia
Shock
Size of pneumothorax.
Percentage of lung field affected is difficult to see.
Classify according to size of visible rim between chest wall and lung margin.
o Small pneumothorax: < 2 cm
o Large pneumothorax: > 2 cm
A large pneumothorax represents a loss of about 50% of lung volume.
Hypoxia
PaO2 < 10 kPa on air
May simply represent underlying lung disease.
Severe dyspnoea.
Management.
Primary pneumothorax.
o If patient not breathless, or has only a small pneumothorax, consider discharge.
o If patient doesn’t fit in to this category, protocol is:
Attempt aspiration up to twice.
Attempt intercostal drain.
Refer to chest physician within 48 hours, and to thoracic surgeon within 5 days.
o If the aspirations or drain are successful and patent is not breathless, patient can be discharged from A&E
Follow up in chest clinic in 10 – 14 days.
Advise patient to return if breathless or increasing chest pain.
Secondary pneumothorax
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.
Y
N
N
N
Y
N
Y
Breathless withAge > 50CXR rim > 2 cms
Intercostal drain.Successful?
Chest doc within 48 hours.Consider suction.
Successful?
Chest surgeon within 3 days
AspirationSucessful?
Admit to hospital for 24 hours observation
Remove drain after 24 hours of full expansion of chest/ leak stopped
Consider discharge
Y
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.
Pulmonary embolism & DVT
DVT Presentation.
o Most commonly asymptomatic.
o Most common clinical features include:
Mild leg discomfort.
Isolated swelling of the leg.
Can be confirmed by measuring calf circumference.
Measure 15 cm and 10 cm above tibial tuberosity
Swollen leg will be > 2 cm larger.
In all cases of leg swelling, exclude abdominal cause with:
o Abdominal exam
o Rectal exam
o Vaginal exam
Erythema of the leg.
Dilated superficial veins
Calf pain on dorsiflexion.
Homan’s sign
Thrombus may be palpable as fibrotic cord in popliteal fossa.
Risk factors of DVT.
Pro – coagulant states.
o Congenital
Factor V Leiden
Antithrombin III deficiency
Protein C deficiency
Protein S deficiency
o Acquired.
Malignant disease
Antiphospholipid syndrome
Meloproliferative disorders
COCP use.
Paticularly if co – existent Factor V Leiden deficiency.
Nephrotic syndrome.
Via renal AT II losses
Homocystinuria.
Paroxysmal nocturnal haematuria
Venous states.
o Immobility.
o Recent surgery
o Pelvic mass
o Pregnancy or recent childbirth.
o Severe obesity
Miscellaneous.
o Hyperviscosity syndromes.
Increased cellularity.
Polycythemia
o Haematocrit = 50 – 60%
Leucocytosis.
o Normally due to acute leukaemia.
o WCC > 50 – 100 x109/L
Raised plasma proteins.
o Waldenstrom’s macroglobulinaemia.
IgM paraprotein > 30 g/L
Paraprotein > 80 g/L
o Previous history of DVT/PE
o Family history of DVT/PE
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
Immunoglobulins and immunoelectrophoretic strip
Anticardiolipin antibody
Ham test.
Positive in paroxysmal nocturnal haematuria.
o Screen for malignancy.
Ultrasound ± CT pelvis and abdomen.
CXR
LFTs
PSA
CEA
CA – 125
CA – 19.9
β – HCG
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
Low PaO2 is inevitable with large PE.
Other changes include
Mild respiratory alkalosis, secondary to low PaCO2 due to hyperventilation.
Metabolic acidosis, secondary to shock.
o ECG.
Commonly shows sinus tachycardia.
Sometimes there are non – specific ST and T – wave changes in the anterior leads.
The classical picture only occurs with massive 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.
Normal perfusion scan rules out significant – sized PE.
Abnormal scans are reported as low, medium or high probability.
High probability scan strongly associated with PE, but includes a significant number of false positives.
Low probability result, with low clinical suspicion, should provoke searching for an alternative diagnosis.
If scan result is low or medium, and clinical suspicion is high, other investigations should be considered.
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.
o Summary of pathway for investigating a possible PE.
o Investigations for underlying cause of PE.
US of deep leg veins.
US of abdomen and legs.
Occult malignancy
Pelvic mass
CT abdomen/ pelvis
Screen for inherited pro – coagulant tendencies.
Protien C
US lower limb ) _ Treat if D – Dimer ) +ve
V/Q or CTPAWhichever one not performedPulmonary angiogram
Suspected PE
Monitor areaO2, IV fluids, analgesia, ABGs, ECG, CXR, bloods
High risk of PELow risk of PE
US Lower limbD - Dimers
Treat as inpatient or in A&E
PositiveNegative
DischargeV/Q or CTPA
Results confirm clinical suspicion
Negative for PEPositive for PE
DischargeAnti – coagulate with warfarin.
Results don’t confirm clinical suspicion
AdmitGive LMWH
Protien S
Factor V Leiden
Antithrombin III
Autoantibody screen.
Anticardiolipid
Anti – nuclear
Biopsy of suspicious lymph nodes/ masses
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.
Severity depends on:
o Speed of onset.
Traumatoc
Post - procedural
o Haemodynamic compromise.
Hypotension
Tachycardia
o Hpoxia or respiratory failure
o Presence of underlying disease.
Heart failure
COPD
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.
Acute massive effusion
Give oxygen.
Gain IV access.
o Peripheral or internal jugular central line.
o If central access is difficult, only attempt if peripheral access clearly inadequate.
o Only insert CVL on normal side.
Bilateral lung problem would be disasterous.
Take bloods for:
o FBC
o Clotting
o Urgent cross match.
6 units.
Correct coagulopathies.
Restore circulating volume.
o If BP low, or tachycardia, give 500 ml IV colloid.
Volume depends on size of effusion drained and response to fluid challenge.
Insert chest drain.
o Leave unclamped.
o Allow to drain freely.
o Monitor volume drained.
Indications for specialist referral.
o Refer traumatic haemothorax to cardiothoracic surgeons.
o Haemothorax secondary to procedures should be referred if:
Shock
Ongoing blood loss requiring transfusion of > 1 unit every 4 hours.
o When in doubt, discuss case with surgeons.
Massive chronic effusion.
Usually will have accumulated over weeks – months.
Commonest causes are:
o Malignancy
o Empyema
o TB
o Autoimmune disease.
Eg. rheumatoid
o Cirrhotic ascites with transdiaphragmatic movement.
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.
Eastern Europe is risk for diptheria
o Cancer risks.
Smoker
Longer history
Systemic symptoms
o Trauma
Examination.
o If infective cause is suspected, examine patient’s oropharynx in area where
Rapid intubation can be commenced.
Anaesthetis is standing by.
o Fever
o Drooling
o Stridor
o Bull neck
o Lymphadenopathy
o Pseudomembrane over oropharynx.
Diptheria
o Swollen throat and epiglottis on direct/ indirect laryngoscopy.
Epiglottitis.
Investigations.
o Don’t delay treatment if patient is in distress.
o If the patient is relatively stable.
CXR
Foreign body
Lateral next X – ray.
Swollen epiglottis
FBC
U&Es
Blood gases
Indications for ITU/surgical referral.
o Prior to examination of oropharynx if infective cause suspected.
o Failure to maintain adequate airway or oxygenation
o Inability to swallow secretions
o Ventilatory failure.
PaO2 < 10 kPa
PaCO2 > 6 kPa
o Collapse
o Severe dyspnoea
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.
