Spirometry is the most widely used pulmonary function test (aka lung function test). It measures the volume and flow of air during inspiration and expiration; it is an assessment of how effectively the lungs can be emptied and filled. Spirometry uses various measures of inspired and expired air to give an indication of any underlying lung disease.

Modern spirometry is usually performed in the GP surgery or respiratory clinic.

It can be used to assist the diagnosis of:

• Asthma
• COPD
• Pulmonary fibrosis
• Cystic Fibrosis

Although, results need to be interpreted in clinical context and spirometry alone cannot always provide an exact diagnosis.

Sometimes, spirometry results are talked about as being:

• On obstructive pattern – e.g.
  • COPD
    • Including Alpha1-antitrypsin deficiency
  • Asthma
  • Cystic fibrosis
  • Bronchiectasis
• A restrictive pattern – e.g.
  • Pulmonary fibrosis
  • Neuromuscular conditions
  • Heart Failure
  • Sarcoidosis
  • Obesity

There is a separate article about differentiating obstructive vs restrictive lung disease.

Spirometry is also used to monitor the effectiveness of treatment in lung conditions.

Definitions

There are a lot of terms involved in measuring lung function! These include:

• FVC – Forced vital capacity
  • This is a measure of the maximum volume of air than can be exhaled
  • Normal values vary based on age, sex and height
• FEV1 – Forced expiratory volume in one second
  • The volume expired during the first second of maximum expiration
• FEV1/FVC – The FEV1 expressed as a percentage of the FVC
  • Normal value – 75-80%
• FEV6 – Forced expiratory volume in six seconds
  • Often considered synonymous with the FVC – FVC values which take longer than 6 seconds to perform are thought to less accurate. This also leads to calculations such as FEV1/FEV6
• PEF – Peak expiratory flow – the maximal expiratory flow rate – occurs early in the forced expiration phase
• FEF – Forced expiratory Flow
• FIF – Forced inspiratory Flow
• FEF25-75% – Forced expiratory flow in the middle half of expiration
  • A more sensitive measurement of airway narrowing than FEV1
  • However, very variable from individuals and easily inaccurate in when FVC is reduced
• Flow-Volume Loop – This shows maximum inspiratory and expiratory effort on the same graph
• Volume-time curve – shows how quickly air can be expelled from the lungs (FEV1), and the total volume expelled (FVC)

Understanding these concepts is a bit easier if we visualise the volumes graphically:

The Graphs

There are typically two types of graph produced by spirometry.

• Flow-Volume loop
• Volume-time curve

Understanding the patterns seen in both of these can help to diagnose the various lung conditions.

Volume-Time Curve

This involves a single breath, taken after full inspiration, after which the patient is asked to exhale as quickly and fully as possible. The rate at which the air is expelled gives an indication of the function of the lungs.

This curve is useful for measuring the FVC and FEV1, and subsequently the FEV1/FVC ratio.

Curve	Interpretation
	FEV1 is >80% of FEV FVC is completely relatively quickly Flat plateau once FVC has been expired
	FEV1/FVC ratio is reduced Takes much longer to achieve a full FVC – no flat plateau (or takes longer to achieve flat plateau) FVC is similar to a healthy adult (may even be slightly larger) Total lung capacity is larger than healthy adult
	FEV1/FVC ratio is usually normal FVC is reduced Total lung capacity is reduced

Flow-volume loop

During this part of the test, the patient takes multiple FVC breaths in and out through the spirometer. There is no indication of time included on this graph, just the volume (x-axis) plotted against the rate of flow on the y-axis.

During the “live” tests, multiple “loops’ are plotted on top of each other to see an “average” of the lung function. The graph is traced in real time in a clockwise direction.

What is important about the flow-volume loop is the pattern of the expiratory phase. FVC and FEV1 cannot be easily determined from these graphs. 

Loop	Interpretation
NORMAL FLOW VOLUME LOOP	Typical volume for a normal adult male is about 6L Note the initially fast increase in flow, and a more gradual decrease after peaking Inspiration happens more slow, even distribution
OBSTRUCTIVE DISEASE	Note that the total lung volume is often increased (although FVC remains the same – there is a bigger residual volume) Not the characteristic “kink” in the expiratory phase The dotted line indicates the normal flow-volume loop Note that some versions of the flow volume loop have the x-axis inverted – with “0” to the right – in these graphs, the “curve” will shift to the left compared to normal – in our example it shifts to the right
RESTRICTVIE DISEASE	“Tall and narrow” Note that the initial flow rate is similar normal But the total volume is much less (and the FVC is reduced) The dotted line indicates the normal flow-volume loop Note that some versions of the flow volume loop have the x-axis inverted – with “0” to the right – in these graphs, the “curve” will shift to the right compared to normal – in our example it shifts to the left

Interpreting the results

Typically the results can be divided into 4 categories

• Normal
• Obstructive
  • Which could be subdivided into reversible (asthma) and non-reversible (COPD)
• Restrictive
• Mixed

Obstructive disease

• A reduction in airflow
• FVC often normal
• FEV1 reduced <80% predicted
• FEV1/FVC ratio <70%
  • “Classical” definition
• FEV1/FVC < LLN
  • LLN – “Lower limit of normal”
  • A more modern definition
  • LLN defined by age, gender, weight

Bronchodilator reversibility

• Determines degree of responsiveness of always to bronchodilators
• Helps to confirm, the presence of obstructive disease if reversibility is present (particularly asthma)
• Reversibility is defined as:
  • >12% AND 200ml increase in FEV1 OR FVC
• Assessed by:
  • Giving short acting B-agonist (e.g. salbutamol 2-6 puffs via spacer)
  • Repeat spirometry 10 minutes later
• Failure to respond does not determine the need to prescribe bronchodilators
  • Many patients with COPD wills till benefit from bronchodilators even if they don’t meet the above criteria
• Also provides a good opportunity to check inhaler technique
  • If patient doesn’t respond – then ensure adequate inhaler technique

Restrictive disease

• A reduction in lung capacity
• FVC reduced
• FEV1 often normal
• FEV1/FVC ratio usually normal
• FVC < LLN

Performing The Test

Contraindications

Performing spirometry causes a significant increase in intra-thoracic pressure. As such, it should not be formed in the following patients:

• Pneumothorax within the last 6 weeks
• Acute coronary syndrome within the last 4 weeks
• Haemoptysis within last 48 hours
• Thoracic, abdominal or eye surgery (including cataracts) within last 6 weeks
• Known thoracic, abdominal or cerebral aneurysm
• Known TB or influenza, or other acute illness

The Test

Patients sit upright in a chair. They wear a nose clip, and then are asked to blow out forcibly into a tube, with the lips tightly sealed around the tube, from a position of maximum inspiration.

• Patients should refrain from using bronchodilators on the day of the test before the test is performed – its difficult to assess airway reversibility if they have already taken their medication!
• Not smoke on the day of the test
• Avoid strenuous exercise on the day of the test
• Avoid alcohol on the day of the test
• Avoid eating a large meal in the 4 hours before the test
• Avoid restrictive clothing

Indications

• Symptoms of respiratory disease
  • Chronic cough
  • SOB
  • Wheeze
  • Orthopnoea (SOB on lying flat
  • Sputum production
• Signs
  • Cyanosis
  • Wheeze
  • Unexplained crackles
  • Hypoxia
  • Abnormal CXR – e.g. hyperexpansion

Summary

• Spirometry is a way of diagnosing the type of lung disease present
• With the help of history and examination, it is possilbe in most cases to ermine the exact lung disease present
• There are two types of graph to be familiar with – flow-volume loops and volume-time curves
• Don’t forget that patients can present with a mixed obstructive and restrictive pattern
• If you are still confused, then this youtube video from Armando Hasudungan (no association with almostadoctor) is a great explanation – but be aware that the flow-volume curves he uses use a reversed axis compared to those discussed in this video (see tables of charts above)

References

• Spirometry – RACGP
• A Stepwise Approach to the Interpretation of Pulmonary Function Tests
• Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt
• Oxford Handbook of General Practice. 3rd Ed. (2010) Simon, C., Everitt, H., van Drop, F.
• Beers, MH., Porter RS., Jones, TV., Kaplan JL., Berkwits, M. The Merck Manual of Diagnosis and Therapy

Read more about our sources

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Smoking is the number one risk factor associated with preventable disease and premature death.

• The WHO estimates that 5.4 million people die prematurely each year as a result of tobacco related illness.
• In smokers, stopping smoking is “the best” thing they can do to improve their health
• Half of smokers will be killed by smoking
  • The average life expectancy of a smoker is 8-12 years less than for a smoker
  • There is also a large chronic disease burden – the quality of life in later years of life is reduced – not just the duration of life
  • Those who stop by age 35 avoid almost all of the excess risk
• Redcuing parental smoking is the most effective way of reducing youth uptake of smoking

The chemicals in cigarette smoke:

• 4,000 chemicals
• 60 of them are known to cause cancer

Rates of smoking have been falling in the developed world since the 1960s. Different countries have taken different approaches to reducing smoking. Australia is leading the way in the developed world. In many developing countries, the incidence of smoking is still on the rise.

In Australia in 2018, 13.8% of the general population were current smokers.

• In indigenous populations the prevalence is about double

In the UK, figures are similar, with 14.7% of the population smoking in 2018.

The approaches to smoking cessation in the UK and Australia are similar but not identical. In particular, there is more of an emphasis on the use of vaping devices in UK policy, compared to Australia.

On average, it takes 7-9 quit attempts to become a successful long term non-smoker.

• The average 40-year old will have made 20 quit attempts – most of them unsupported
• Quit attempts are more successful if supported – by healthcare professional, medication and support groups – about 25-30% successful

There are three medical therapies available:

• Nicotine replacement therapies (NRT)
• Bupropion
• Varenicline (Champix(R))

NRT may be used in combination with either of the other two. A recent Cochrane review concluded that NRT (particularly patch combined with fast-acting oral form) and varenicline are more effective than bupropion, and equally effective as each other.

Diseases associated with smoking

• Lung cancer
  • 80% of cases are directly related to smoking
• Cardiovascular disease and peripheral vascular disease
  • 15% of cases directly related to smoking
• COPD
  • 80% of cases directly caused by smoking
• Respiratory tract infections
• Sexual dysfunction – particularly in men
• Asthma
• Peptic ulcer disease / GORD
  • More likely in smokers
• Osteoporosis
• In pregnancy
  • Miscarriage
  • Low birth weight
  • Prematurity
• Other cancers
  • Oral, throat
  • Cervical
  • Pancreatic
  • Gastric
  • Bladder
  • Breast
• Macular degeneration
• Cataracts
• Hair loss
• Premature ageing of the skin
• Thought to be the cause of 1% of all sick days from work!

Nicotine

• Highly addictive
• Absorbed into the blood through both the lungs and the mouth
• Reaches the brain in 7-10 seconds
• Nicotine receptors when activated, promote the release of dopamine
• Nicotine withdrawal symptoms
  • Sleep disturbance
  • Tiredness
  • Headache
  • Difficulty concentrating
  • Increases appetite
  • Anxiety
  • Cravings!
  • Depressed mood
  • Irritability
  • All of these symptoms can be relieved by the administration of nicotine
• Nicotine receptors are stimulated to proliferate by smoking – it is particularly the pulsatile nature of smoking – short, sharps “hits” that causes massive proliferation

Factors that encourage young people to smoke

• Most people will try smoking in their teenage years (or younger) but <20% go on to become regular smokers
• Factors that make someone more likely to smoke include:
  • Parental smoking
  • Best friend smoking
  • Beleif it relieves stress
  • Belief it prevents weight gain
  • Belief that the negative consequences wont affect them
  • Challenge to authority

Effects of smoking cessation

• 20 minutes
  • BP and pulse return to normal
• 8 hours
  • Nicotine and CO levels halved
  • O2 returns to normal
• 24 hours
  • CO eliminated
  • Lungs start to clear excess mucus
• 48 hours
  • Nicotine eliminated
  • Sense of smell and taste improve
• 72 hours
  • Bronchiole dilatation, resulting in sensation of easier breathing
• 2-12 weeks
  • Circulation improves
• 3-9 months
  • Lung function increases by up to 10%
  • Cough and wheezing decreased
• 5 years
  • Risk of MI halved
• 10 years
  • Risk of lung cancer halved
  • Risk of MI equal to having never smoked

Frameworks

The 5A’s

The 5A’s framework is used in several lifestyle related illnesses, including smoking and obesity.

• Ask – Firstly – if they smoke! Then about their concerns their smoking. Ask if they have tried to stop previously
• Assess – The stage of change (see stages of change below)
• Advise – of the benefits of smoking – “It is the best thing you can do for your health”
• Assist / Agree – attempt motivational interviewing – “What are the things you don’t like about smoking”. Explore doubts. Explore barriers to quitting. Offer written information, refer to Quitline. Discuss relapse prevention. Advise about medication options that may assist (see below).
• Arrange – Follow-up. Encourage continuation of pharmacological methods. Discuss relapse prevention. Congratulate patient if smoking has ceased!

Stages of change

The stages of change model refers to the mental thought processes involved with smoking cessation. Traditionally it has been used as a framework to understand the process of quitting, although there is not much evidence behind it.

It involves 6 stages, and often patients cycle through the process several times

• Not interested in quitting
  • “Precontemplation”
• Thinking about change
  • “I know I should…”
  • “I don’t think I’ve got the willpower”
  • “I don’t know where to start”
• Preparing
  • “This is my last pack / day / week”
  • Have prepared some coping strategies – e.g. nicotine replacement, signed up to a quit smoking group, agreed with a friend or partner to stop at a given date / time
• Making a quit attempt
• Maintaining the quit attempt
  • Patients can leave the cycle with a continued prolonged effective quit attempt!
• Relapsing

Smoking Cessation Methods

A practical approach

• Use nicotine and medication options (e.g. champix) in combination
  • Don’t under-dose the nicotine replacement!
  • Use patches, plus a short acting oral replacement – such as gum, tabs or oral spray to assist with cravings
• The use of a quitting service – such as QuitLine, in-person support groups, or apps, increases the chances of a successful quit attempt
• About half of those attempting to quit do so with medical support – usually in the form of medication

Addressing barriers to quitting

• Weight gain
  • On average, smokers gain 4-5kgs within 12 months of smoking cessation
  • The health effects of quitting typically dramatically outweigh the health effects of the additional weight
  • 20% of quitters do not gain weight
  • Advise to focus on the quitting now, and address any weight gain later
• Stress
  • Smoking generally increases stress, but temporarily relief is felt with each cigarette – this is actually the effect of the nicotine combatting nicotine withdrawal that has built up between cigarettes
  • With smoking cessation, long-term stress levels typically fall
  • Warn about the short term symptoms of nicotine withdrawal
• Managing withdrawal
  • Reassure that craving typically only last 2-3 minutes
  • Get less frequent and less severe with time – but may last years
  • Severe symptoms worst int he first week and typically last 2-4 weeks
  • Usually can be controlled with nicotine therapy and other medications
• Fear of failure
  • Reassure that the average is about 7 attempts before a successful quit
  • Reframe failures as learning experiences that are likely to increase effectiveness of the next attempt
  • Advise that with professional support, quitting is more likely to succeed
• Peer pressure
  • Discuss methods of avoiding peer pressure situations
  • Advise friends they are quitting
  • May be best to avoid certain friends and social situations temporarily in the first few weeks

Nicotine replacement therapy

• A typical “20-a-day” smoker has an average nicotine level of 40ng/mL
  • Nicotine replacement therapies are commonly under-dosed
  • The strongest patches deliver nicotine levels of 10ng/mL, and gum 15ng/mL and thus x2 patches or combinations of agents are often required
• Dosage needs to be sufficient to relieve withdrawal symptoms!
• Often preferred by patients because they don’t require a prescription
• Can be used in pregnancy
  • Safety not formally established, but widely believed to be safer than smoking in pregnancy
• Patients typically should use at least 8 weeks of therapy
  • Analogy – a plaster cast for a fracture. The cast needs to be in place for 8 weeks to allow healing to occur

Options for nicotine replacement include:

• Patches
  • Be wary of night-time patch use as it can affect sleep
  • Patient may prefer to remove the patch overnight
  • If using multiple patches, could try one patch on at night, and a second added in the morning
• Inhalator
• Nasal spray
• Lozenges
• Gum
  • Useful to manage cravings
  • Don’t be afraid to recommend using gum in addition to patches to manage the short-term cravings
  • Nicotine from the gum is absorbed by the oral mucosa
  • More effective if made into a disc shape and placed against the mucosa
  • Chewing it a lot just results in lots of nicotine being swallowed – and in the stomach it is not effective!
• Micro-tabs

Lifestyle factors affecting the efficacy of quitting

• Trying to change smoking patterns – help patients identify their triggers to smoke and minimise them
• Avoiding usual areas or venues where they smoke
• Involving their family and friendship group – avoiding friends trying to sabotage quit attempts!
• Focus on positives – e.g. money saved and what they can do with this money

Medication

Bupropion – Zyban(R)

• Bupropion hydrochloride is a dopamine and noradrenaline re-uptake inhibitor
• Also used in obesity to treat food cravings
• Advise patients to start taking in 1-2 weeks before smoking cessation
• Continue for 7-12 weeks
• Side effects:
  • Nausea
  • Vomiting
  • Headaches
  • Dizziness
  • Dry mouth
  • Seizure (1 in 1000)
• Contraindications
  • History of seizures
  • Patient is on MOAI
  • Caution when used with other drugs that lower the seizure threshold

Varenicline – Champix (R)

• Nicotine receptor partial agonist
• Gradually increasing dose for the first week, then 1mg twice daily for 12 weeks
  • A further course of 12 weeks can be given
• Relieves cravings
• Appears to make smoking less pleasurable
• Patients typically find that they feel the need to smoke less after several days of the medication
• 2 weeks after starting medication, 25% of patients are no longer smoking. Most of the rest will have reduced their smoking
  • In those still smoking – ensure adequate nicotine replacement
  • Complete non-responders probably have a genetic pre-disposition, and champix should be ceased
• The most effective agent when used alone (compared to bupropion and NRT)
• Side effects
  • Depression of mood – be wary in people with a history of mental health disorder (consider alternatives)
  • Sleep disturbance – unusual or memorable dreams, not usually scary or nightmares
  • Nausea – 30% of patients. Tends to settle with ongoing use. Reduced if the medication is taken with food
• Contraindications
  • Pregnancy
  • Age <18

Interventions that have been proven to be ineffective

• Hyponotherapy
• Acupuncture
• Trying to “wean” down
• Motivational interviewing
• Explaining the stages of change model to patients

Smoking cessation and drug metabolism

Smoking has effects on several classes of drugs, and increases their metabolism. As such, when a patient stops smoking, if they are on any of the following, then doses may need to be reduced:

• Antipsychotics
• Antidepressants – including SSRIs and tricyclics
• Benzodiazepines
• Warfarin
• Clopidogrel
• Beta-blockers – particularly propranolol
• Calcium channel blockers – particularly verapamil
• Insulin
• Metformin
• Theophylline
• Triptans

Flashcard

References

• Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt
• Oxford Handbook of General Practice. 3rd Ed. (2010) Simon, C., Everitt, H., van Drop, F.
• Beers, MH., Porter RS., Jones, TV., Kaplan JL., Berkwits, M. The Merck Manual of Diagnosis and Therapy
• Supporting smoking cessation – RACGP
• Helping Smokers Quit – RACGP

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Psittacosis (aka Ornithosis) is an infectious disease, sometimes associated with an atypical pneumonia, caused by the gram-negative bacterium Chalmydia psittaci. It is usually transmitted to humans from birds.

It is contracted through inhalation of bacteria – usually from bird droppings and feather dust from infected birds. Infection may also be passed when handling birds, or in the case of a well-loved pet, mouth-to-beak contact. Humans can catch the illness from many types of bird, but pet birds are most commonly implicated. This means that those at risk include pet owners, vets, and those working with birds in other contexts. About 70% of cases are thought to from pets to their owners.

• There are cases of humans contracting the disease as a result of inhaling dust from bird faeces that has been stirred by by a lawn mower

Person-to-person spread is possible but is rare.

Birds themselves may be asymptomatic, or can be very sick. Birds may show symptoms such as diarrhoea, ruffled feather, poor feeding and runny eyes / nose.

It is a rare disease – there are about 50 confirmed cases in the UK each year – although this is likely an underestimation.

It is not related to bird fancier’s lung (aka pigeon fanciers lung) which instead refers to a chronic pneumonitis caused by exposure to bird faeces, and is non-infectious in origin.

Presentation

Incubation period varies from 4 days to about 4 weeks, usually within 14 days following exposure. It typically produces a flu-like illness.

• Headache
• Fever
• Cough
• Myalgia
• Sore throat
• Malaise
• Dry cough
• SOB
• Chest pain

Severe cases can cause sepsis and require ICU care. Most cases are mild.

• Mortality is <1% in treated cases, around 15% if untreated

Investigations

• CXR
  • Signs of pneumonia
  • Often the CXR findings are no concordant with the clinical findings on examination
  • There are no specific sings that identify psittacosis as the cause
• Sputum culture
  • Often not much sputum is produced and thus no often reliable
• Serological testing. Severe methods are available:
  • Compliment fixing
  • Micoimmunofluorescent antibody test
  • May cause fate positive due to cross-activity with other chlamyida species
  • Often two samples are required to show an increasing number of antibodies between the times the samples were taken
• PCR testing
  • Quick
  • Sensitive and specific
  • Requires specialist reagents and equipment. Often needs to be sent away to specialist laboratory

Differentials

• Bird Fancier’s Lung
• Pneumonia
• Q fever
• TB
• Avian influenza

Management

Sensitive to:

• Tetracyclines – e.g. doxycycline, tetracycline
  • Often not suitable for children
  • 2-3 weeks required
• Macrolides
  • Azithromycin
  • Clarithromycin
  • Erythromycin
    • This is the usual second-line agent

You may need to seek advice from the local infectious diseases specialist / microbiologist.

Pet bird owners should be advised of ways of treating their bird, and reducing the risk of transmission. Remember that infected birds may not show any symptoms.

• Wash hands after handling birds
• Don’t let faeces build up in the bottom of cages
• Wear a respirator and gloves when cleaning cages
  • Wash hands after cleaning cages
• Avoid mouth-to-beak contact
• Good ventilation of bird cages
• Avoid overcrowding of birds

References

• Psittacosis – patient.info
• Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt
• Psittacosis – NSW Health
• Psittacosis – CDC
• Oxford Handbook of General Practice. 3rd Ed. (2010) Simon, C., Everitt, H., van Drop, F.

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Pneumoconiosis is a term used to describes a range of interstitial lung diseases caused by inhalation of mineral dusts, resulting in interstitial fibrosis.

They are usually occupational diseases (but not always).

Pneumoconiosis can vary greatly in severity, from diseases that cause death, to those that never cause any significant symptoms.

Common types include asbestosis, silicosis and coal worker’s pneumoconiosis. 

In the UK and to some extent in Australia, financial compensation is available to patients of they can prove their lung disease is the result of industrial exposure.

Most exposure to the causative agents occurred int he 1950s and 1960s in the developed world and thus these diseases are on the decline in these societies. In the developing world, or in mining communities, incidence is higher.

Epidemiology

• Asbestosis causes about 5,000 deaths per year in the UK
  • It is the most common work-related cause of death in the UK
  • Asbestos related lung cancer (rather than pneumoconiosis) is under-diagnosed, as it is indistinguishable from that caused by smoking
• There are about 250 cases of coal workers pneumoconiosis and about 40 cases of silicosis in the UK every year
• It is thought that about 15% of cases of COPD are a result of industrial disease – usually coal mining

The three most common causes of pneumoconiosis are:

Asbestos

• Asbestos was widely used as an insulating and fireproofing material in the middle of the 20th century, before its disease-causing effects were known
• It was available in various forms, including sheets (which were often sawn to size), as a paste-like substance which was applied around pipes, and even as a powder that was mixed to make a paste to insulate other objects.
• Particular occupations with exposure include:
  • Plumbers
  • Roofers
  • Mechanics
  • Shipyard workers
• Asbestosis is correlated to the level of exposure, but the disease can take 10-60 years to develop from the time of exposure
• Asbestos has been banned fro many decades, but lots of asbestos remains in the environment in older buildings.
• Asbestos is also an important cause of lung cancers, both the asbestos specific mesothelioma and other types of lung cancer.

Silica

• The main component of sand and rock
• Types of workers who might be exposed to silica include:
  • Miners
  • Sandblasters
  • Stonemasons
• Pneumoconiosis risk correlates to the length of exposure
• Chronic simple silicosis
  • Caused by long periods of low level exposure
  • Multiple nodules throughout the lungs
  • Mild symptoms (sometimes none)
• Progressive massive fibrosis (PMF)
  • Develops from chronic simple silicosis
  • The nodules enlarge and coalesce into large masses
  • Severe respiratory symptoms
• Acute silicosis
  • Large exposure over a short period of time
  • Rapidly advancing silicosis – often results death

Coal

• Often co-exists with silicosis
• Takes on average about 10 years from exposure to the development of pneumoconiosis
• Causes coal-workers pneuomoconiosis
• Similar disease pattern to silicosis – most cases are chronic simple pneumoconiosis
• Generally cases are mild, but just like silicosis – in some cases it can progress to progressive massive fibrosis

Pathology

The most important factor of the inhaled dust particles is their size. Particles in the 1-5um range are most dangerous as these get stuck at the bifurcations of the airway

• Smaller particles pass right into and out of the alveoli
• Larger particles get stuck higher up the airway
• Most dust particles are cleared by the normal mucocilliary clearance of the lungs
• Those that remain – particularly those that are stuck at the bifrucations, become encased in macrophages and set off localised inflammatory responses
  • This leads to an inflammatory cascade that ultimately leads to fibroblast proliferation and collagen deposition
• The level of immune response always depends on the chemical make-up of the dust
  • Coal is not very reactive and large amounts of coal dust are required to cause pneuomoconiosis
  • Asbestos, silica and beryllium are much more reactive
• Where the process of pneumoconiosis occurs alongside rheumatoid arthritis, it is called Caplan’s syndrome. 

Presentation

• Shortness of breath – particularly on exertion
• Cough – with or without sputum production

Differentials

• COPD
• Heart Failure
• Cardiomyopathy

Diagnosis

• CXR – may demonstrate evidence of fibrotic nodule in simple pneumocosis, or larger masses in PMF
  • High resolution CT is then often used to further quantify the extent of the disease
• Spirometry

Treatment

• There is no specific treatment and no cure
• Most interventions are aimed at reducing the risk of further lung damage
• Other treatments are often similar to those used in COPD
  • Pulmonary rehabilitation
  • Inhaled corticosteroids
  • Inhaled bronchodilators
  • O2 if sats / symptoms indicate it is required
  • Smoking cessation
• Lung transplant may be considered in more severe cases (but finding a suitable donor is difficult and in reality only a small number of patients undergo transplant)

References

• Pneumoconiosis – Chest Foundation
• Industrial Dust Diseases – patient.info
• Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt
• Oxford Handbook of General Practice. 3rd Ed. (2010) Simon, C., Everitt, H., van Drop, F.

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Sleep apnoea (aka Obstructive Sleep Apnoea or OSA, or OSAS – obstructive sleep apnoea syndrome) describes a condition in which there are multiple (often frequent) pauses in respiration (“apnoeas”) during sleep, as a result of upper airway collapse, usually at the level of the oropharynx.

The apnoeas in sleep apnoea can range from a few seconds, up to 90 seconds, and cause hyperaemia, hypercapnia and even respiratory acidosis. These resulting clinical effects stimulate the patient to awaken (often unnoticed or not remember by the patient), which re-establishes the airway.

• A complete apnoea is defined as a period of >10 seconds without respiration
• A partial apnoea (aka hypoapnoea) is a period of >10 seconds where respiration is reduced by >50%

This pattern of frequent apnoeas, following by frequent, brief periods of awakening result in extremely poor quality of sleep, often causing symptoms of tiredness, and in severe cases, the patient falling asleep during the day (e.g. whilst driving).

Typically a result of obesity, mainly in middle age and older patients (although can be seen at any age), it is also seen in children with large tonsils and adenoids, and is a common indication in children for tonsillectomy and / or adenoidectomy.

Sleep apnoea is associated with an increased risk of cardiovascular disease, atrial fibrillation, hypertension and death.

Diagnosis is usually by polysomnography (“sleep study”) in which the respiratory rate and pattern, as well as oxygen saturations are measured whilst the patient is asleep. True polysomnography often also includes EEG monitoring (for phases of sleep), airflow monitoring at the nose and mouth, and electro-occulography to assess for rapid eye movement (REM) sleep. However, in reality, many sleep studies are conducted using home-kits and measure only respiratory rate and heart rate with a chest strap, as well as O2 saturation.

Management involves weight loss and / or use of CPAP (positive airways pressure) at night to keep the airway open. In severe cases associated with significant obesity, weight loss surgery may be indicated. In children, sleep apnoea is an indication for tonsillectomy.

It is thought that the majority of cases are undiagnosed.

Epidemiology & Aetiology

• Prevalence about 4% (in men) and 2% (in women) in developed nations
  • Some speculate it may be as high as 9%
• Incidence is increasing in line with the incidence of obesity
• Strongly associated with diabetes
• Risk factors:
  • Obesity – 7x as common in patients with BMI >30
    • Obesity is thought to account for about 60% of cases
  • Fat deposition around the neck
    • >48cm neck circumference is high risk
    • <37cm is low risk
  • Male
  • Smoking
  • Alcohol
  • Sedative drugs
  • Family history – possibly genetic factors related to shape of jaw
• Nasal obstruction accounts for about 10% of cases
  • Assess for nasal deformity, polyps, nasal septal deviation

Presentation

• Excessive daytime sleepiness
  • Consider assessing this using a scale – such as the Epworth Sleepiness Scale (ESS) or STOP-BANG
  • Consider investigations with a score >10 (ESS)
  • Urgent referral to sleep specialist (usually respiratory physicians) if score >18 or any recent road traffic accident or near miss
  • May be implications for driving – especially if patient drives commercially
• Sleep symptoms
  • Snoring
    • Present in 85% of cases of OSA
    • Most people who snore do not have sleep apnoea
  • “Thrashing”
  • Feeling of choking during sleep
  • Most patients are not aware of their sleep symptoms – these symptoms are usually reported by a partner. Partners may report noticing long periods without a breath being taken
• Waking with a headache
• Irritability / personality change
• Decreased libido
• Difficulty concentrating
• Partner or other relative may witness apnoeas

Differentials

• Insufficient sleep (!)
  • Including shift work
• Hypothyroidism
• Narcolepsy
• Depression
• Drugs
• Excess alcohol

Diagnosis

Diagnosis of OSA requires a sleep study. The definition of sleep apnoea requires at least five apnoeas per hour recorded on a sleep study, plus symptoms of OSA. A true apnoea is usually defined as >10 seconds without breathing. The level of OSA can be graded with a scale such as the Apnoea-hypopnoea Index (AHI) – although this scale is not fully standardised, and several alternatives exist.

The AHI measures the number of apnoeas or hypopnoeic events per hour – usually defined as an event where the patient does not breath for >10 seconds (or has disordered breathing for >10 seconds) with a drop on O2 saturations (definitions vary).

• Mild OSA – 1-14 apnoeas per hour
• Moderate OSA – 15-30 apnoeas per hour
• Severe OSA – >30 apnoeas per hour

The gold stand test is polysomnography. This involves an EEG, electro-oculogram (to measure eye movements / REM sleep), and and electromyogram to monitor muscle movement. However, this is expensive and not always available. An appropriate alternative more frequently used is a respiratory monitor and pulse oximetry. It is likely that home testing kits which measure these two metrics only will become more widely used in future.

Associated Diseases

OSA is important because it is associated with a wide range of serious diseases:

• Hypertension
• Cardiovascular disease
• Obesity
• Metabolic syndrome
• Diabetes
• Asthma

Sleep apnoea is thought to increase the risk of CVD by about 30%, the risk of heart failure by 140%, and the risk of arrhythmia by 200-400%.

Complications

• Accidents at home, at work and whilst driving due to sleepiness
• Increased cardiovascular disease risk, and cardiovascular complications such as HTN, coronary artery disease and CCF
• Irritability, depression and other mood disturbance
• Increased risk of T2DM

Management

The goal of treatment is to reduce day-time sleepiness and improve day time functioning.

Note that symptom reduction has no correlation with reduction in risk for cardiovascular disease, but that CPAP (and weight loss) has been proven to reduce cardiovascular disease risk.

Management options include:

• Weight loss – aim for 10-15% of body weight. Can result in complete resolution of OSA. Weight loss is the most effective treatment. It is difficult to achieve.
• Regular exercise – advise 150 minutes per week of moderate intensity (equivalent to a brisk walk) exercise, including 60 minutes of strengthening exercise
• Avoidance of triggers
  • Cease any drugs suspected of having an effect
  • Advise alcohol within safe drinking limits and no alcohol in the three hours before bed
  • Smoking cessation
• Sleep advice
  • Practice good sleep hygiene – e.g. similar, regular bed time each night, no food or drink in the last 2 hours before bed, no caffeine after 2pm, avoid looking at screens in the 1 hour before bed
  • Avoid lying on back (supine) – encourage lying on the side
• CPAP – Continuous positive airways pressure

• • A machine at the bedside which pumps air through a face mask covering the nose, mouth or the entire face. Can be noisy and uncomfortable.
  • CPAP is the mainstay of treatment for most patients – however, many cannot tolerate the mask
  • Can be nasal mask or full face mask
  • Positive pressure keeps the airway open
  • Needs to be worn for 8 hours each night
  • Side effects include:
    • Claustrophpbia
    • Rhinitis
    • Nasal Irritation
  • Symptoms usually recur within a few days of cessation of use of the face mask
  • Successful treatment can reduce blood pressure and greatly reduce the risk of cardiovascular disease
  • Proven to reduce all cause mortality in patients with OSA and hypertension
  • Compliance is poor

• Surgery
  • Most commonly in children – for removal of tonsils
  • Occasionally in adults for the same
  • Sometimes used to correct nasal structural defects or other anatomical defects and should be considered first line treatment if an anatomical abnormality is identified
  • Other surgical options include:
    • Uvulopalatopharyngoplasty (UPPP)
    • Radiofrequency ablation of the tongue base
    • Suspension of hyoid bone
    • Advanced of mandible with Maxillofacial surgery (rare)
    • Weight loss surgeries
• Medication
  • Not usually recommended
  • Steroid nasal sprays may be useful for rhinitis, and oral sprays for large tonsils
  • Amitriptyline may help to increase REM sleep in patients with OSA who cannot tolerate a CPAP mask
• Oral appliances
  • Commonly used and appear to be safe
  • Common example is a mandibular advancement splint – attach to upper and lower teeth and pull the mandible forwards
  • Can cause arthralgia, tooth pain, excessive salivation and dry mouth
  • Are becoming more widely accepted
  • Evidence is not conclusive, but probably as effective as CPAP in mild to moderate cases
  • Less effective in severe cases

Driving

• Patients with day-time sleepiness may need to cease driving (depending on the severity)
• Include a thorough assessment of sleepiness in any driving assessment
• In Australia, patients with diagnosed OSA on CPAP who are commercial drivers require regular assessment via their specialist to ensure compliance and control of symptoms

References

• Sleep Apnea – Merck Manual
• Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt
• Oxford Handbook of General Practice. 3rd Ed. (2010) Simon, C., Everitt, H., van Drop, F.
• Obstructive sleep apnoea syndrome – patient.info

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General Instructions

• Always examine the patient from their right.
• Make sure you get consent at the start of the examination, but then you don’t need to keep asking the patient again as you do the rest of the examination! You should still explain what you are going to do, but don’t keep asking them if its ok.
• Remember you are always comparing the two lungs. Practice lots so you know what normal is.
• You may also be asked to palpate the apex beat to see if it has been displaced.
• Always ask the patient to strip to the waist, even women! Check they feel comfortable, women may want to keep a bra on, and always explain what you are doing, so that they don’t think you are just having a grope!
• The middle lobe of the lung can only be auscultated from the axilla and back of the patient.
• About 90% of diagnostic information will be gained from patient history – therefore examination should only ever be used as a subsidiary! Never just dive in and examine someone without knowing the proper history first.
• Always look for a sputum pot!
  • Yellow/green sputum – sign of infection
  • Massive amounts of sputum – most likely bronchiectasis
  • Look for signs of blood – could be infection, could be malignancy
  • You may get very suspicious if they also have a hoarse voice and/or weight loss

Chest Examination

General observation of the patient

Inspection

• check the colour of the patient (e.g. are they cyanosed)
• patient should be sat at 45’ for this examination. If the patient is very breathless in this position, then allow them to sit up straight. Patient comfort is the most important factor.
• see if there are any obvious signs of weight loss
• see if there is any ‘’breathlessness’’ – see if they are already propped up on many cushions (heart failure)
• see if there is any wasting of the accessory muscle of breathing. This may be present if the patient suffers from COPD)
• see if the patient is pursing their lips on breathing.
• look at the patient’s expiratory time. Normally expiratory time is shorter than inspiratory time, however, in lung diseases, often there is very short inspiration followed by prolonged expiration.
• listen if there are any audible breathing sounds (normally there aren’t.)
• check the surroundings, e.g. is there oxygen, inhalers or a nebulizer etc. as these are clues to possible respiratory disorders. Also look for a drip, any medications, sputum pots, nasal specs or masks.

Patient’s Hands

1. Loss of the angle of the nail bed
2. Drumstick-like appearance
3. Boggy nailbed (increased fluctuance)
4. Increased curvature of the nail

• Respiratory causes of clubbing include: Empyema, Bronchiectesis, Non-small cell carcinoma, Lung fibrosis, CF, Abscesses, suppurative diseases – diseases that produce a lots of pus!

• Check for signs of cyanosis
• check for tar staining
• Duypetren’s contracture
• check for asterixis. Ask the patient to hold out their arms and bend their wrists so that their palms are vertical pointing away from them. Wait up to 30 seconds. If there is a flapping tremor (a ‘coarse flap’) this suggests a retention of carbon dioxide.
• Other signs that show CO2 retention include warm sweaty palms (due to vasodilation), and a bounding pulse – always check the pulse!
• Koilonychia – iron deficiency anaemia.
• Leukonychia – white nailsa as a result of hypoalbuminaemia – liver disease
• Beau’s lines – sign of serious illness in the past 3 months (nails take 3 months to grow fully). They are horizontal ridges in the nail – a bit like rings in a tree trunk.
• Splinter haemorrhages (endocarditis) – although they are very commonly caused by trauma (manual labour).
• Fine tremor – there is a fine tremor often present in respiratory patients that is caused by β₂– agonists – i.e. salbutamol.
• Check the BP – or at least say you would check it

Check the pulse!

• Rate – tachy >100 / norm / brady <60
• Rhythm – regular / irregular / regularly irregular / irregularlyirregular
• Character
  • Bounding pulse – anything with hyperdynamic circulation – fluid overload e.g. aortic regurg, thyrotoxicosis
  • Slow rising pulse – put four fingers on the pulse (radial or carotid) and you can feel the pulse hit each of your fingers in turn caused by aortic stenosis. in the normal individual it should hit all fingers at once.

Patients head / neck

• check for cyanosis on the underside of the patient’s tongue.
• check for lesions
• check the eyes – e.g. for anaemia, jaundice, xanthelasma and Horner’s sign – consists of: constricted pupils, a droopy eyelid and reduced sweating – all on the same side of the face – e.g. no sweating on the affected side of the face. This is a common symptom of an upper lung tumour.
  • Sympathetic nerves cause dilation of the pupil
  • Parasympathetic cause constriction. Thus in this case, there is no sympathetic, so the pupil is always constricted – however – as the parasympathetic is still active, you may be able to constrict the pupil even further by shining a light into it – this does not mean that Horner’s is not present!
  • The arrangement of sympathetic nerves in this area – the sympathetic chain! – 1^st order neurons travel from the brain, to the spinal chord between levels C8 and T2. From here, second order neurons pass out of the spinal chord, out over the apex of the lung, and then up alongside the carotid artery, to the superior cervical ganglion. There are then two sets of nerves originating from here. One lot of these 3^rd order neurons goes over the cavernous sinus and to the eye, the other goes along the external carotid and then goes to the sweat glands of the face.
  • A lung tumour can damage the second order neurons over the apex of the lung, resulting in Horner’s Sign
• Arcus – caused very commonly by age, and the least common cause is Wilson’s disease.
• check for angular stomatitis – sign of iron deficiency anaemia and pernicious anaemia
• Check for glossitis – can be a sign of iron deficiency anaemia or pernicious anaemia (b12 deficiency)
• Check under the toungue for central cyanosis
• Smell the breath – check for ketones – smell like pear drops
• Check dental state
• Look for thrush and leukoplakia – signs of immunosupression – thus can be linked with chest infections
• HHT – hereditary haemorrhagic telangactasia
• Purtz-Jager-syndrome (PJS) – freckles on the lips.
• Buccal pigmentation – caused y Addisson’s disease – a brown discolouration.
• Ocronosis – grey pigmentation of the skin around the oropharynx – and theu urine will also turn dark on standing.

• Check for general signs of swelling – this can be caused by SVC obstruction as a result of lung cancer. The cancer can either cause this directly, or can cause a thrombus in this region. The SVC collects blood from the head, neck and arms. When this is blocked there is swelling in the head and neck and engorged veins. There is a loss of the normal JVP pulsations – because the JVP becomes raised and non-pulsatile. The head and neck becomes swollen, but there is enough collateral circulation to spare the arms. There may be visible distended veins on the chest wall.

Neck

JVP

Trachea

Lymph nodes

• lung cancer can spread to the lymph nodes of the neck
• when it does, it usually produces very hard nodes, that form a mass, which is fixed to underlying structures
• nodes associated with lung cancer are most commonly found in the supraclavicular area, particularly between the clavicular heads of SCM.
• Other causes of lymph nodes enlargement tend to cause rubbery (not hard) nodes, and these are not usually tethered to underlying structures.

Causes of enlarged lymph nodes

CHEST

Inspection

Palpation

First of all, you should asses the upper part of the chest. Ask the patient to take a deep breath out, then, lay your hands on flat on the upper part of the chest, and ask them to take deep breaths. Yu should feel both sides of the chest moving in and out equally. Remember the ribs of the chest move like bucket handles.
For the lower part of the chest you should use fingertips and the lateral aspect of the chest, and put your thumbs next to eachother in the middle of the chest. Really ‘scoop’ up the chest in your hands. It is easier to feel expansion here than in the upper part and you should see your thumbs move away from eachother as the patient breathes in. You should check that both hands deviate equally.
check both the front and back! – i.e. check for expansion twice; once on the front and once on the back.
when checking on the patient’s front, your hands should go under the patient’s breasts
You should also feel for vocal fremitus. Here you ask the patient to say ‘99’ and feel their chest for resonance. You should use the side of your hand (i.e. down the edge of your little finger) and make ‘v’ shapes on the patient’s chest with your palms facing upwards as you feel both sides of the chest at the same time. It is actually much easier to hear* differences in fremitus that is to feel them. If you ask the patient to whisper ‘one, one, one, one’ and use your stethoscope then you can hear fremitus. If there is consolidation then on the side that there is consolidation you will here ‘one’ very clearly through your stethoscope.
In consolidation, there is a loud-speaker effect of fremitus! – i.e. fremitis is better on the side of consolidation!
Make sure you feel on both the front and the back, and at all the places

• Front – apices, upper lobs, laterally
• Back – upper lobes, lower lobes

When you hear it, it is called whispering pectoriliquae. it is easiest to hear when they whisper (rather than talking).
You can listen for it while they are talking, in which case it is called vocal resonance. You just get them to say ‘99’ in the same way you would when feeling for it. Make sure you listen over:

• The apices
• Upper lobes
• Lateral aspects (under axilla)
• Upper and lower lobes on the back
• These are all basically the same places you would listen for the breath sounds!

Increased vocal fremitus – consolidation
Decreased vocal fremitus – empyema, pneumothorax,pleural effusion
Sound waves travel more freely through solid (i.e. consolidation) than through air. Liquid, or air, or anything that increases the distance between the lung and the chest wall will cause decreased fremitus.
Assessing vocal fremitus is most useful when combined with percussion:

The book also suggests you may want to palpate the precordium and axillary lymph nodes
Precordium
Not always that useful in respiratory exam, but you may be able to palpate:
Rib fractures – this may be highlighted by a very tender area on the chest, and a grinding/crunching sensation called crepitus. Often due to trauma, and may co-exists with pneumothorax / haemothorax. Very rarely you may find a pathological fracture from cancer.
Subcutaneous emphysema – this can cause general swelling of the head and neck, and when palpated, will produce a crackling sensation under the hand.
Apex beat – right lower lobe / right lung collapse can shift the apex beat to the right. Left lower lobe / left lung collapse can displace the beat to the left.
A tension pneumothorax or a large pleural effusion can push the beat away from the side of the pathology.
Axillary lymph nodes – these drain the breasts and the pleurae. The lungs are primarily drained through the lymph nodes of the neck. It is often possible to palpate axillary lymph nodes, although they are unlikely to be pathological if less than 0.5cm. if they are greater in size than 1cm in diameter then they are always pathological.

• If the lump is hard, then this is suspiscious of breast cancer or rarely, mesothelioma.
• if the lump is firm as opposed to hard, then many generalised lymph node pathologies could apply

How to examine

Ask if there are any painful or tender areas. If there are, ask if you can palpate them, and do this gently. Can you elicit tenderness? Does it feel like rib injury?
Palpate any swollen areas that are suggestive of subcutaneous emphysema. Feel for the distinctive crackling
Palpate the apex beat
Examine the axillary lymph nodes. Take the weight of the patients arm on your own shoulder. Make sure you palpate the medial, anterior, lateral and posterior aspects of the axilla. If you feel any lumps, make sure you get a clear feel of size and consistency.

• Do the same at both sides!
• Press on reasonably hard – don’t just wiggle your fingers around, because you will just tickle them!

Percussion

Auscultation

• Wheeze – whistley, noisy breathing
• Crackles – e.g. like a rustling crisp packet
• Rubs – squelching squeaky sound, like walking in fresh snow
• Crepitations – shorter that cracks.

The quality of breath sounds

Vesicular – these are normal breath sounds. They are soft sounding – they sound like rustling leaves. They are caused mainly by the sound of air in the alveoli. This means the intensity of the sound gradually increases as inspiration continues, as more and more air reaches the alveoli. During expiration, vesicular breath sounds fade away, as the alveoli empty, and air is only travelling through the bronchi (which are further away from the stethoscope, and thus harder to hear).
Bronchial breath sounds – these are abnormal breath sounds.

• An example of this is bronchial breathing. Consolidation, fibrosis or collapse can alter the structure of the alveoli. In these instances, the breath sounds are no longer soft and rustling. Instead they become harsh. They can also be heard at different times of the respiratory cycle. They change so that they can be heard throughout inspiration, just stopping near the end (when air is only rushing through the alveoli). There is then a short gap, before air can once again be heard rushing through the bronchi. The sound is harsh, and generally louder than that of vesicular breathing.
• Expiratory sounds tend to be louder and longer than inspiratory sounds – this is the opposite to vesicular breath sounds.
• Detecting areas of bronchial breathing is very difficult
• In COPD and asthma there may be quieter normal breath sounds.
• Mild damage to the alveoli (as in mild fibrosis, consolidation or collapse) can also cause quieter breath sounds
• Pneumothorax and pleural effusion can also cause quiet breath sounds, because they push the lungs further away from the chest wall.
• Occasionally in very thin patients, the vesicular breath sounds are louder than in normal patients
• Over the upper chest it can be particularly difficult to distinguish vesicular from bronchial breath sounds. In fact, in these areas, normal breath sounds that you can hear may infact be bronchial. In these instances, the normal breath sounds are referred to as bronchovesicular.
• Rhonchi – these are long continuous sounds, that sound a bit like snoring. They are caused by obstruction to the airway; often by excess secretion of mucus, mucosal swelling or tumour tissue in the airway. They can be diffuse or localised. They are a common expiratory diffuse finding in COPD, and also found during inspiration in asthma.

• They are nearly always inspiratory
• They may also occur in COPD, bronchiectasis and resolving pneumonia
• Crackles can be described as fine, medium or coarse. Fine crackles are high pitched and squeaky, course are low pitched, and medium are somewhere inbetween.

Wheeze – this is sometimes called ronchi. It is a continuous whistling sound caused by the narrowing of airways. They are usually due to small airways obstruction, such as in COPD and asthma. Wheeze is only usually heard on expiration. This may mean it is heard on inspiration and expiration, but if it is heard only on inspiration, then it is called stridor – and stridor is a very bad prognostic sign (cancer), as is monophonic wheeze (as this is caused by a single blockage to a single airway).

• The pitch and duration of the wheeze is related to the severity of the pathology. The loudness of the wheeze is not related to the severity of the underlying pathology.
• Rarely, heart failure can cause bronchospasm which results in a wheeze.

Friction rub – this is the sound of the two layers of pleura rubbing together as the lungs expand and contract. The main causes are pneumonia, pulmonary infarct and malignancy. Usually these causes lead to inflammation, and it is the inflammation that causes the actual rub.

• Rub is often very localised
• Often the patient complains of pain in the region of the sound – in which case the patient has pleurisy.
• In contrast to crackles, rub only tends to be heard in expiration.

Definitions

Nebulizer

Clubbing

Causes of clubbing

Chest deformities

• Pectus excavatum – funnel chest – a depress sternum – often congenital, but can also be linked to congential diseases, such as marfan’s syndrome. It is generally just cosmetic, but can have a minor effect on lung function. very rarely it can cause breathlessness.
• Pectus carinatum – pigeon chest – a prominent sternum – often develops during childhood in patients with Rickets or severe chest disease. It is thought that it may be due to strong contractions of the diaphragm while the ribcage is still pliable. Just cosmetic, very little effect on lung function (although there may be underlying disease remember)
• Kyphscoliosis – this is spinal deformity, resulting in increased A-P and lateral curvature of the spine. It affects 1 in 1000, and 1 in 10 000 severely. The patient will look like they have abnormal posture.It is mostly idiopathic, and first noticed in childhood. It can be quite severe (as well as being cosmetic) and often causes breathlessness in middle age.
• Thoracoplasty – This was a surgical treatment used in the past to treat TB. It involved removal of several ribs, and thus the affected side can appear very deformed. It reduced lung capacity, which can cause breathlessness in old age (particularly in smokers).

References

• Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt
• Oxford Handbook of General Practice. 3rd Ed. (2010) Simon, C., Everitt, H., van Drop, F.
• Beers, MH., Porter RS., Jones, TV., Kaplan JL., Berkwits, M. The Merck Manual of Diagnosis and Therapy

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• Wash hands
• Check patient name/DOB/hospital number
• Introduce- “My name is…”
• Consent
• “Is it ok if I have a look and feel of your head, neck, chest and hands?”
• Chaperone
• Confidentiality
• Position – 45
• Exposure – Chest

• General: Comfortable at rest? Look around bedside for Oxygen, Nebulisers, Medication
• Hands: Clubbing, Tar staining, Peripheral cyanosis, Flapping tremor, Pulse- character &rate
• Mouth: Central cyanosis
• Neck: JVP, Lymph Nodes
• Chest: Scars, Deformities, Use of accessory muscles, Resp rate

• Tracheal Deviation
  • Warn the patient this may be uncomfortable.
  • Best Technique:Single finger in sternal notch
• Chest Expansion 
• Vocal Fremitus is rarely helpful

• Chest: Start at the apices above the clavicle, include the 3 lung zones (Upper/ Mid/ Lower) and the axilla
• Compare right to left

• Upper/ Mid/ Lower Zones
• Normal sounds should be vesicular
• Listen for added sounds eg. Wheezes, crackles, rubs.
• Assess Vocal Resonance

• Repeat Inspection/ Palpation/ Percussion / Auscultation on the patients back

• At the end check the patients leg and sacrum for peripheral oedema

• “To complete my examination I would like to request further investigations including full bloods/CXR/PEFR/Spirometry/Lung function tests” Adapt this appropriately to the patient you are examining.
• Thank patient
• Cover up and check comfortable

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Introduce yourself, check the right patient, explain confidentiality.

• I am going to explain to you a little bit about how to use a nebulizer, how to clean it, and how to use it safely. If you have any questions feel free to interrupt at any time.

• Compressor – this is the noisy little box that compresses air and pumps it through the nebulizer.
• Oxygen – an oxygen canister

Keeping it clean

Oxygen safety

References

• Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt
• Oxford Handbook of General Practice. 3rd Ed. (2010) Simon, C., Everitt, H., van Drop, F.
• Beers, MH., Porter RS., Jones, TV., Kaplan JL., Berkwits, M. The Merck Manual of Diagnosis and Therapy

Read more about our sources

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• Congestive heart failure
• Malignancy – lung cancer and breast cancer are the most common causes, but many cancers can cause pleural effusion. About 15% of cancer patients will get a pleural effusion – this is a bad prognostic sign
• Pneumonia
• Pulmonary embolism

Pleural Fluid Samples

Clinical features

• Reduced chest expansion on the affected side
• Mediastinal displacement away from the affected side
• Stony dull to percussion
• Reduced or absent breath sounds
• Reduced or absent vocal resonance
• There will be no additional unusual sounds
• These will generally only be present when the effusion is greater than 500ml!

X-ray

• An effusion of less than 500ml is unlikely to cause anything other than blunting of the costophrenic recess. >500ml will cause a clear fluid level
• An effusion of less than 300ml may not be seen on x-ray
• Remember to look for the meniscus – it is likely to be a very long curve, perhaps rising all the way to the axilla.
  •  If the fluid level appear perfectly horizontal, it is likely to due co-existing pneumothorax
• If the effusion is large enough, the whole of one lung field may appear opaque, and the mediastinum may be shifted to the opposite side
• Fluid below the lung can simulate a raised hemidiaphragm.

Further diagnostics

• Diagnostic aspiration
  • Percuss the upper border of the effusion, then go 1-2 intercostal spaces below (any lower and you might end up in the abdomen!)
  • Use 5-10ml of lignocaine and inject down to the pleura
  • Insert a 21G needle with syringe just above the ribs upper boarder (to avoid the neurovascular bundle)
  • Take 10-30ml of fluid
  • Send sample for:
    • Clinical biochem – glucose, protein, pH, amylase, LDH
    • Bacteria culture
    • Cytology
    • Immunology (if indicated by clinical signs)
• If diagnosis is not possible from fluid sampling, it may be possible with a pleural biopsy, which may be CT guided for the best results.
• You should also take bloods for protein (to check for hypoalbuminaemia), glucose (to compare to the pleural fluid sample – see below)and LFTs, U+E’s (to check for renal failure)

Diagnosis – Transudates and Exudates

• are fluids that have left the circulatory system and have entered lesions or areas of inflammation.
• The composition of an exudate varies, but it can include pretty much anything that is in blood.
• It will nearly always have water and dissolved solutes, and may also have white and red blood cells, as well as platelets. Exudates have a high protiein content
• Definition – Protein content >35g/L (or more correctly, see Light’s criteria below) 
• are fluids that have left the circulatory system and gone into lesions or areas of inflammation.

• are caused by disturbances in oncotic pressure (i.e. increases in venous pressure), and not by inflammation.
• They have a lower protein content, and will contain fewer cells.
• The fluid typically only contains mononuclear cells (such as macrophages and lymphocytes).
• Definition – Protein content <25g/L (or more correctly, see Light’s criteria below)

• [Plerual Protein : serumprotein] ratio >0.5
• [Pleural LDH : serum LDH] ratio >0.6
• Pleural LDH > 200

Other Tests

• Glucose  – a low glucose content (in relation to the patient’s current blood glucose) indicates the presence of cells (possibly native or foreign) in the fluid – thus can indicate the presence of infection.
• pH – pH of <7.2 suggests empyema (exudate)
• Amylase – raised amylase may indicate carcinoma, pancreatic disease or an oesophageal rupture.

Management

• If there is clear evidence of a transudative cause (e.g. LVF, renal failure, hypoalbuminaemia), then BTS guidelines suggest to treat the cause with no nee dto drain the effusion.
• If unsure of a cause, then perform a Pleural Tap (thoracocentesis). This is not the same as a chest drain – which often remains in place for several days. Instead, a pleural tap just aspirates a sample of fluid. Send the fluid for cytology (cancer), LDH, protein, pH, Gram stain, AFB testing (Acid Fast Bacilli – TB). Also send bloods (ESR, CRP, albumin, amylase, LDH, glucose

• Treat the underlying disorder!
• DRAIN THE EFFUSION AS NECESSARY! – even if this means draining many times.
  • Fluid should be removed slowly – 2L every 24hr max. Large, fast fluid cahnges can cause pulmonary oedema.
  • Can be removed by needle aspiration (same method as diagnosis), or chest drain. If aspirating, don’t drain more than 1L at a time. Typically used for emypema and haemothorax.
• In Malignancy – most cases will reccurr within a month, and so pleurodesis or long-term in-dwelling chest drains may be considered. Pleurectomy may be used in certain instances.
• Pleurodesis – this is where the pleural space is effectively removed, and the two layers of the pleura are stuck together, either chemically or surgically, to prevent the accumulation of fluid. In cases of recurrent pleural effusion, chemical pluerodesis (e.g. with tetracycline, talc or bleomycin) may be useful.
  • Pleurodesis talc is most useful for effusions caused by malignancy
• Intrapleural streptokinase was used in the past, but is of no benefit

References

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Introduction

• Pneumonia is the most fatal hospital acquired infection
• As well as bacteria, other causes include viruses, fungus and parasites.

Epidemiology

• Pneumonia is a dangerous condition, and is responsible for many deaths of patients over the age of 80
• Deaths amongst younger populations have dramatically decreased with the advent of antibiotics.
• Incidence is 1-3 per 1000 (i.e.. 0.1-03% of people have pneumonia at any one time)
• The incidence of bacterial pneumonia amongst those with HIV is higher than in the general population, particularly in IV drug users with HIV. However, the causatory organisms are the same.
• Most cases caused by bacteria, about 15% are viral

Classification

Precipitating factors

• Strep pneumoniae infection often follows viral infection with influenza or parainfluenza.
• Hospitalisation! – hospital acquired infection is often with Gram-negative organisms
• Cigarette smoking – this is the most important risk factor for pneumococcal disease
• Alcohol excess
• Bronchiectesis (e.g. in CF)
• Bronchial obstruction (e.g. carcinoma)
• Immunosupression
• IV drug use
• Dysphagia (both oesophageal and co-ordination disorders – leading to aspiration)

Symptoms

• Typically the same for hospital acquired / non-hopsital acquired cases
• Shortness of breath
• Cough
  • May be productive in adolescents and adults –  Purulent sputum possible
  • Often dry in infants and the elderly
• Fever
• Rigors
• Vomiting
• Headache
• Loss of appetite
• Very occasionally – haemoptysis
• Pleuritic chest pain – which may on occasion radiate to the shoulder (if diaphragm is involved) or the anterior abdominal wall
  • Pleuritic chest pain – a sharp shooting or stabbing pain, usually in the side, that is most painful on inspiration, but can also be felt on expiration, or even whilst talking.
• Upper abdominal tenderness in some patients with lower lobe pneumonia
• Signs of consolidation – both on examination and CXR
• Dyspnoea
• Tachypnoea
• Tachycardia
• Increased secretions – noticeable in ventilated patient in hospital acquired cases

Signs

• Vary with the type of pneumonia present
• In strep pneumoniae
  • Rapid shallow breathing
  • Pleural rub
• Confusion – may be the only sign in elderly patients

Diagnosis

Oxygen saturation – <92% is worrying
Usually an x-ray is performed after clinical suspicion to confirm the diagnosis. The x-ray may show:

• Evidence of infiltrate in the form of consolidation on the x-ray – can also show the spread of any infection by distribution of the infiltrate
• Changes may not appear on x-ray for up to 48 hours after symptoms, however, after effective treatmnet, consolidation may still be seen on x-ray for up to 6 weeks
  • Persistent x-ray changes may suggest underlying carcinoma with secondary pneumonia
  • X-ray should be repeated at least weekly as an inpatient, and then at 6 weeks follow-up. Any signs still present indicate the need for a further x-ray.

Blood cultures may be taken to asses for bacteraemia.
It is not routine practice to attempt to identify the causatory organism in community acquired infection.
FBC

• ↑WCC
• ↑ESR (>100mm/h) and ↑CRP
• Possible anaemia (sign of abscess)
• Blood cultures – in ill patients to check for septicaemia

Urine – in severe cases of pneumonia, where legionella is suspected, urine testing for legionella antigen may be indicated
Pleural fluid aspiration – to asses for organisms. Transthoracic aspiration may be performed (often with CT guidance) to identify lesions (e.g. empyema, abscess) and to gain samples.
The CURB-65 score – is a scale used to assess the severity of community-acquired pneumonia. It predicts the risk of mortality (CURB score 0 = <1% risk, CURB score 5= 60% risk). Each factor of the score is worth 1 point.

• C – Confusion – use the abbreviated mental test (score ≤8)
• U – Urea – >7mmol/L
• Respiratory rate – ≥30/min
• Blood Pressure <90 systolic, or <60 diastolic
• 65 – age >65 years
  • A score ≥3 is severe pneumonia. ≥2 requires hospitalisation.

Differentials

• Pulmonary embolism (PE) – patient is not usually systemically unwell. Shortness of breath is more likely to be sudden onset.
• Pulmonary / pleural TB
• Pulmonary oedema

Treatment

• If not vomiting, and CURB65 score ≤2, oral antibiotics. If severe and/or vomiting, IV antibiotics required, as per sensitivities.
• Keep Oxygen saturation >92%, using oxygen therapy as required
• IV fluids, to prevent dehydration and shock
• Monitor progress – don’t be afraid to repeat CXRs as necessary
• All patients should receive 6 week follow-up including repeat CXR

Complications

Respiratory failure – PaO₂ <8kPa. The most common complication. Relatively easy to treat, with 60% oxygen (high flow).

• If the PaCO₂ rises to >6kPa, or the hypoxia does not resolve with oxygen therapy, transfer to ITU.
• Be careful using O₂ in COPD patients – can reduce the drive to breathe.
• Aim to keep sats at 90-94%
• Do regular ABG testing, and consider intubation if situation not improving

Hypotension – another relatively common feature, thought to be the result of dehydration, and vasodilation due to sepsis. This should be treated if systolic BP drops below 90mmHg, with 250ml of crystalline infusion over 15mins. If systolic BP does not improve, consider transfer to ITU.
Atrial fibrillation – is a common complication in the elderly. It usually resolves with treatment of the pneumonia, but digoxin may be given to reduce the heart rate as short-term therapy.

Pleural effusion – the pleura may become inflamed, which can result in excess fluid production, causing a pleural effusion. In many cases, this will not require treatment, but in some individuals, it may require drainage. Clinical signs (see below) are not usually present until the volume of fluid is >500ml. Rarely, the fluid may become infected, resulting in empyema.
Empyema – typically presents in a patient who has partially recovered, but then develops a spike in temperature. Signs of pleural effusion may be present (decreased chest expansion, dullness, reduced breath sounds, pleural rub – all on affected side. The lung above the effusion can becomes compressed.)

• Fluid aspiration – the fluid is usually yellow, with a pH <7.2, and low levels of glucose. Samples can be obtained via aspiration, bronchoscopy, or sometimes via transthoracic aspiration using ultrasound/CT guidance. About 70% of cases of empyema consist purely of anaerobes, and in the other 30% both aerobic and anaerobic bacteria are present.
• Chest drainage – treatment is with the insertion of a chest drain – usually with radiological guidance. Reducing the risk of adhesions – it was thought that using streptokinase in a wash reduced the risk of adhesions, but there is not much evidence for this, and its use is not routinely recommended.
• Antibiotic therapy – should also be given, usually for 4-6 weeks. This should be something that is effective against both aerobic and anaerobic bacteria, and a typical regimen might include iv doses of cefuroxime and co-amoxiclav for 5 days, followed by 3-5 weeks of metronidazole alone. The treatment of empyema and abscess is typically very similar, however, rarely, abscess might require surgery, whilst empyema does not.

Lobar collapse – most commonly the result of sputum retention
Thromboembolsim
Pneumothorax – particularly with Staph Aureus

Lung abscess

• Is a serious complication.
• A lung abscess is a cavitating lesion containing pus, within the lung.
• Commonly results from aspiration (e.g. alcoholism, inhaled foreign body, oesophageal blockage, bulbar palsy) and also occurs in other instances of bronchial obstruction, e.g. – bronchial carcinoma. Most likely to occur if the pneumonia was not adequately treated.
• Pathology – certain causatory organisms are more likely to cause abscess than others, particularly staph aeurus  and klebsiella pneumoniae.
• In some instances, septic emboli, particularly in the case of staphylococci, can result in multiple lung abscesses.
• More rarely, pulmonary infarction can cavitate, and may become infected, resulting in abscess formation.
• Presentation – this would usually be a pneumonia that worsens despite treatment, with the production of purulent sputum, as a result of the growth of smelly anaerobic organisms. There is likely to be fever, malaise, anaemia and weight loss. Clubbing can occur if the abscess has been present for long enough.
• Investigations
  • X-ray – a walled cavity is visible, usually with a fluid level.
  • Bloods – FBC for anaemia and neutrophilia
  • ESR + CRP – will be raised
  • Sputum sample – microscopy to identify organism
  • Bronchoscopy – sometimes performed to get samples
• Treatment
  • Treat the infection as per antibiotic sensitivities for 4-6 weeks
  • Consider postural drainage to remove excess sputum
  • In serious cases, antibiotic instillation / aspiration, and sometimes even surgical excision may be required

Septicaemia

• Can occur if the bacteria enter the blood stream. May result in infective endocarditis and meningitis, and requires urgent treatment
• Patient will be very systemically unwell
• Take blood cultures to identify the causatory organism, and treat with IV antibiotics

ARDS / renal failure / multi-organ failure
Ectopic abscess – particularly with Staph aureus
Hepatitis, Pericarditis, Myocarditis and meningitis are seen most commonly in mycoplasma pneumoniae infection, which is most prevalent in young adults.

Types of infection in further detail

References

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