key: cord-0977261-8qdrshz3
authors: Scully, Crispian
title: 15 Respiratory medicine
date: 2014-12-31
journal: Scully's Medical Problems in Dentistry
DOI: 10.1016/b978-0-7020-5401-3.00015-1
sha: 3974fa1e8081ccc1bc775386255a27e8e5e2046f
doc_id: 977261
cord_uid: 8qdrshz3

●. Upper respiratory infections are commonplace, especially in young people, and are often contagious; ●. Lower respiratory infections are often contagious and some are potentially fatal; ●. Asthma is common and may be life-threatening; ●. Chronic obstructive pulmonary disease is common and disabling; ●. Tuberculosis worldwide is an important infection, affecting people with HIV/AIDS or malnutrition particularly; ●. Lung cancer is common and usually has a poor prognosis.

• Upper respiratory infections are commonplace, especially in young people, and are often contagious The respiratory tract consists of the upper respiratory tract (URTnose, paranasal sinuses, pharynx and larynx; discussed in Ch. 14) and the lower respiratory tract (LRT): the respiratory airways (trachea, bronchi and bronchioles) and lungs (respiratory bronchioles, alveolar ducts, alveolar sacs and alveoli), discussed in this chapter.

Protective mechanisms in the respiratory tracts include a mucociliary lining. Particles or pathogens are trapped in the mucus and driven by ciliary action (the ciliary elevator) to the pharynx. Mucociliary trans port declines with age but any effect on clinical infection has not been proved. Lymphoid tissues of the Waldeyer ring (adenoids, palatine and lingual tonsils) are important in developing an immune response to pathogens. However, the best respiratory defence mechanism is the cough reflex, the components of which include cough receptors, affer ent nerves, the cough centre, and efferent nerves and effector muscles. Impairment of any of these -as may be seen in older patients or those with conditions associated with lowered consciousness (e.g. sedative use and neurological disease) -can weaken protection. Dysphagia or impaired oesophageal motility may exacerbate the tendency to aspi rate foreign material. The alveolar defence mechanisms include mac rophages, immunocytes, surfactant, phospholipids, immunoglobulin G (IgG), IgE, secretory IgA, complement components and factor B; many immune defects manifest with recurrent respiratory infections.

Lung function is vital to gas exchange -the blood absorbs oxygen and releases carbon dioxide. Normal gas exchange requires adequate alveolar ventilation, normal ventilation/blood flow relationships and adequate alveolar-capillary membrane surface area. Breathing (ven tilation) depends on respiratory drive, which reacts to the respiratory load. This process requires work and results in gas exchange.

Oxygen is transported in combination with haemoglobin in erythro cytes and a small amount dissolved in plasma. The oxyhaemoglobin dissociation curve is sigmoidal; once the oxygen saturation falls below 95%, the amount of O 2 transported to the tissues and brain falls rapidly. High temperatures, acidosis, raised CO 2 and raised 2,3 diphosphoglycerate (2,3DPG) levels encourage oxygen offloading, whereas fetal haemoglobin and carboxyhaemoglobin have the con trary effect. Chronic hypoxaemia (e.g. at high altitudes) stimulates release of erythropoietin from the kidneys, with a rise in red cell pro duction, and raised 2,3DPG. Athletes have abused erythropoietin to gain competitive advantage (Ch. 33).

The most common LRT disorders are asthma and chronic obstructive pulmonary disease (COPD).

Respiratory disorders are common, and are often caused or aggravated by tobacco smoking. They may significantly affect general anaesthesia (GA) and conscious sedation (CS), since they are often a contraindica tion to use of benzodiazepines, opioids, GA agents and other respira tory depressants.

Impaired gas exchange leads to laboured breathing and can cause significant incapacity. Features include cough, sputum production, wheeze, dyspnoea, chest pain, cyanosis, fingerclubbing ( Fig. 15.1) , use of accessory muscles of respiration with indrawing of the intercostal spaces (hyperinflation), and abnormalities in chest shape, movements, respiratory rate and breath sounds.

Cough may be a feature of any respiratory problem but, if chronic, may herald serious disease -for example, COPD, cancer or infec tion such as tuberculosis. Mucoid or mucopurulent sputum is often a feature ( Fig. 15 .2); purulent sputum indicates acute bronchitis, bronchiectasis or lung abscess. Blood (haemoptysis) or bloodstained sputum, though common in acute infections (especially in preexisting COPD), bronchiectasis and pulmonary embolism, may herald an even more serious condition -for example, possibly one due to carcinoma or tuberculosis. Wheezing is caused by airways obstruction and is a typical sign of asthma or COPD. Breathlessness (dyspnoea) is distress ing, and may be caused by respiratory or cardiovascular disease, or by anaemia, and is particularly ominous if it persists at rest. Excessive resistive load, such as in asthma, COPD and cystic fibro sis, impairs airflow. Elastic load increases because of, for example, interstitial fibrosis, muscle paralysis and obesity.

Diagnosis of respiratory disorders is from the clinical features sup ported by imaging (especially chest radiography). Spiral computed tomography (CT) can now scan the lungs in a quick 20-30second breathhold and therefore, instead of producing a stack of individual CT slices, which may be misaligned due to patient movement or breathing in between slices, provides highresolution three dimensional images.

Respiratory function tests can measure individual components of the respiratory process. Spirometry is the basic screening test for assess ing mechanical load problems, the quantification involving determi nation of the vital capacity (VC) -slow vital capacity (SVC) and/or forced vital capacity (FVC) -and the speed of maximal expiratory flow (MEF; Fig. 15 .3). In health, about 75% of a normalsized VC is expelled in 1 second (FEV 1 ). The peak flow meter, which measures the peak expiratory flow rate (PEFR; the earliest portion of forced expiration), is a simple measure of airflow obstruction, when the FEV 1 is a much smaller fraction of the VC. In lung restriction, the diminished VC can be mostly expelled in about 1 second. Serial meas urements (e.g. in asthma) provide valuable information about disease progress. The reversibility of airways obstruction is usually assessed by spirometry before and after use of a bronchodilator agent.

Arterial blood gas analysis yields considerable information about gas exchange efficiency. Arterial hypoxaemia in adults is defined as PaO 2 below 10.7 kPa breathing room air, although it is not usually treated as clinically important unless below 8 kPa, when oxygen saturation will be 90% or less (Table 15 .1).

Arterial carbon dioxide tension (PaCO 2 ) is used as an inversely pro portional index of 'effective' alveolar ventilation. Hence, a high PaCO 2 is taken to indicate poor alveolar ventilation. Alveolar hypoventila tion (raised PaCO 2 ) with a normal pH probably represents a primary ventilatory change present long enough for renal mechanisms to compensate, as in chronic ventilatory failure. Ventilation/blood flow relationships are most simply assessed by considering the size of the difference between the amounts of oxygen and carbon dioxide in the blood and in the air; the differences are small if the lungs are work ing efficiently. Disparity between ventilation/blood flow ratios results in abnormally wide differences -and then alveolar-arterial PO 2 and arterial-alveolar PCO 2 gradients will be abnormal.

Alveolar capillary surface area is assessed by measuring the uptake of carbon monoxide -usually abnormal in diffuse interstitial inflam matory and fibrotic processes and in emphysema.

Assessing bronchial reactivity and the exercise response can help evaluate breathlessness. Simple exercise testing provides information about overall fitness and the appropriateness of cardiorespiratory responses. Radionuclide lung scanning, blood gas analysis and sputum cytology or culture are sometimes needed in addition.

Management can include oxygen administration by mask or nasal cannula (Figs 15.4 and 15.5) .

LRT disorders can cause significant incapacity and are often a con traindication to GA, and even to CS.

Asthma is common, affecting 2-5% of the overall population; it is on the increase, particularly in childhood, with a frequency of up to 20% in some highincome countries. Asthma usually begins in childhood or early adult life; about half the patients with asthma develop it before age 10 years. Bronchial hyperreactivity causes reversible airway obstruction from smooth muscle constriction (bronchospasm), mucosal oedema and mucus hypersecretion. There are two main types, extrinsic (allergic) and intrinsic asthma (Table 15 .2).

Extrinsic (allergic) asthma, the main childhood type, may be pre cipitated by allergens in animal dander, feathers or hair, drugs (e.g. nonsteroidal antiinflammatory drugs [NSAIDs] and some antibiot ics), food (e.g. eggs, fish, fruit, milk, nuts), house dust (mite allergens) or moulds. Patients frequently have or develop other allergic diseases, such as eczema, hay fever and drug sensitivities. Extrinsic asthma is associated with IgE overproduction on allergen exposure, and release of mast cell mediators (histamine, leukotrienes, prostaglandins, bradykinin and platelet activating factor), which cause bronchospasm and oedema. About 75% of asthmatic children lose their asthma or improve by adulthood.

Intrinsic asthma is usually of adult onset and not aller gic, but appears rather to be related to mast cell instability and airway hyperresponsivity. Triggers include emotional stress, gastro oesophageal reflux or vagally mediated responses.

Either type of asthma can be triggered by: infections (especially viral, mycoplasmal or fungal); irritating fumes (e.g. traffic or cigarette smoke); exercise (possibly due to cold air); weather changes; emotional stress; foods (e.g. nuts, shellfish, strawberries or milk) or additives (such as tartrazine); and drugs (e.g. aspirin and other NSAIDs, beta blockers and angiotensinconverting enzyme inhibitors [ACEIs]).

In wellcontrolled patients with asthma, clinical features may be absent. During an asthmatic episode, symptoms may include dysp noea, cough and paroxysmal expiratory wheeziness with laboured expiration. The frequency and severity of attacks vary widely between individuals (Table 15 .3). Patients may become distressed, anxious and tachycardic, have reduced chest expansion and be using accessory respiratory muscles to increase their ventilatory effort. Nasal polyps are common, especially in aspirinsensitive asthmatics. Children with asthma initially suffer from repeated 'colds' with cough, malaise and fever, often at night.

Asthma is typically diagnosed when the patient has more than one of the following -wheeze, cough, difficulty breathing and chest tightness -particularly if these are frequent and recurrent; are worse at night and in the early morning; occur in response to, or are worse after, exercise or other triggers, such as exposure to pets, cold or damp air, or with emotions or laughter; or occur without an association with colds. There is often: ■ a personal history of atopic disorder ■ a family history of atopic disorder and/or asthma ■ widespread wheeze, heard on chest auscultation ■ a history of improvement in symptoms or lung function in response to adequate therapy.

A prolonged asthmatic attack, which is refractory to treatment, may lead to lifethreatening status asthmaticus (persisting for more than 24 hours). Failure of the patient to complete a sentence, indrawing of the intercostal muscles, a rapid pulse, a silent chest and signs of exhaustion are suggestive of impending respiratory arrest.

Diagnosis of asthma is from the clinical history and presentation, based on recognizing a characteristic pattern of episodic symptoms in the absence of an alternative explanation. Investigations include a chest radiograph (to exclude other diagnoses, such as a pneumo thorax), spirometry (serial PEFR), skin tests and blood examination (usually eosinophilia, raised total IgE and specific IgE antibody concentrations, which may help identify allergens). Occasionally, a histamine or methacholine challenge is used if the diagnosis is unclear. In children with an intermediate probability of asthma, who can perform spirometry and have evidence of airways obstruction, assess the change in FEV 1 or PEFR in response to an inhaled bronchodilator (reversibility) and/or the response to a trial of treatment for a speci fied period; if there is significant reversibility, or if a treatment trial is beneficial, a diagnosis of asthma is probable.

Management includes patient education, smoking cessation advice, avoidance of identifiable irritants and allergens, and use of drugs. Home use of peak flow meters allows patients to monitor progress and detect any deterioration that may require urgent modification of treatment. Treatment should be based on the amount by which peak flow is reduced (a PEFR diary should be kept).

Drugs used for asthma management (Table 15 .4) include oxygen, shortacting β 2 agonists (SABAs; such as salbutamol), corticosteroids, leukotriene receptor antagonists and omalizumab (a recombinant humanized monoclonal antiIgE antibody that reduces the antigen specific IgE).

Inhaled longacting β 2 agonists (LABAs) may be needed ( Fig. 15.6 ). Deaths from asthma are usually a result of failure to recognize dete rioration or reluctance to use corticosteroids.

Other factors that have been studied include: ■ air pollution -There is an association between air pollution and aggravation of existing asthma ■ allergen avoidance -There is no consistent evidence of benefit ■ breast-feeding -There is evidence of a protective effect in relation to early asthma ■ electrolytes -There is no consistent evidence of benefit ■ fish oils and fatty acid -There is no consistent evidence of benefit ■ house dust mites -Measures to reduce the numbers of house dust mites do not affect asthma severity ■ immunotherapy -Allergenspecific immunotherapy is beneficial in allergic asthma ■ microbial exposure -There is insufficient evidence to indicate that the use of probiotics in pregnancy reduces the incidence of childhood asthma ■ modified milk formulae -There is no consistent evidence of benefit pets -There are no controlled trials on the benefits of removing pets from the home ■ tobacco -Exposure to cigarette smoke adversely affects quality of life, lung function, need for rescue medications and longterm control with inhaled steroids. There is an association between maternal smoking and an increased risk of infant wheeze ■ weight reduction -There is an association between increasing body mass index and symptoms of asthma.

Elective dental care should be deferred in severe asthmatics until they are in a better phase; this can be advised by the patient's general practitioner. Asthmatic patients should be asked to bring their usual medica tion with them when coming for dental treatment. Local anaesthe sia (LA) is best used; occasional patients may react to the sulphites present as preservatives in vasoconstrictorcontaining LA, so it may be better, where possible, to avoid solutions containing vasoconstric tor. Adrenaline (epinephrine) may theoretically enhance the risk of arrhythmias with betaagonists and is contraindicated in patients using theophylline, as it may precipitate arrhythmias.

Relative analgesia with nitrous oxide and oxygen is preferable to intravenous sedation and gives more immediate control. Sedatives in general are better avoided as, in an acute asthmatic attack, even ben zodiazepines can precipitate respiratory failure.

GA is best avoided, as it may be complicated by hypoxia and hyper capnia, which can cause pulmonary oedema even if cardiac function is normal, and cardiac failure if there is cardiac disease. The risk of post operative lung collapse or pneumothorax is also increased. Halothane or, better, enflurane, isoflurane, desflurane and sevoflurane are the preferred anaesthetics, but ketamine may be useful in children.

Allergy to penicillin may be more frequent in asthmatics. Drugs to be avoided, since they may precipitate an asthmatic attack (see later), include those listed in Box 15.1.

Acute asthmatic attacks may also occasionally be precipitated by anxiety; it is important to attempt to lessen fear of dental treatment by gentle handling and reassurance. Even routine dental treatment can trigger a clinically significant decline in lung function in approximately 15% of asthmatics. Acute asthmatic attacks are usually selflimiting or respond to the patient's usual medication, such as a betaagonist inhaler, but status asthmaticus is a potentially fatal emergency (Ch. 1). There may be complications caused by the antiasthmatic drugs (Table 15 .5).

Gastrooesophageal reflux is not uncommon, with occasional tooth erosion. Periodontal inflammation is greater in asthmatics than in those without respiratory disease. Persons using steroid inhalers may develop oropharyngeal candidosis or, occasionally, angina bullosa haemorrhagica.

Guidelines on the management of asthma may be found at: http://www.sign.ac.uk/guidelines/fulltext/101/index.html, http:// www.nice.org.uk/guidance/qualitystandards/indevelopment/Asthma. jsp and http://www.britthoracic.org.uk/Portals/0/Guidelines/ AsthmaGuidelines/qrg101%202011.pdf (all accessed 30 September 2013). 

Churg-Strauss syndrome (CSS) is a rare, potentially fatal, systemic vasculitis similar to polyarteritis nodosa (PAN), characterized by severe asthmalike attacks with peripheral eosinophilia, and intravas cular and extravascular granuloma formation with eosinophil infiltra tion and skin lesions in 70%. Cardiopulmonary involvement is the main cause of death.

CSS is diagnosed if at least 4 of the 6 criteria listed in Box 15.2 are positive.

The 5year survival of untreated CSS is 25%. Combination treatment with cyclophosphamide and prednisolone (prednisone) provides a 5year survival of 50%.

Management problems relating to patients with CSS may include res piratory impairment and corticosteroid treatment (Ch. 6).

Chronic obstructive pulmonary disease (COPD; chronic obstructive airways disease, COAD) is a common, chronic, slowly progressive, irre versible disease (most frequently a combination of chronic bronchitis and emphysema), characterized by breathlessness and wheeze (airways obstruction), cough and sputum. Chronic bronchitis is defined as the excessive production of mucus and persistent cough with sputum production, daily for more than 3 months in a year over more than 2 consecutive years. It leads to production of excessive, viscous mucus, which is ineffectively cleared from the airway, obstructs and stag nates, and becomes infected, usually with Streptococcus pneumoniae, Moraxella catarrhalis and Haemophilus influenzae. Patchy areas of alveolar collapse can result. Emphysema is dilatation of air spaces dis tal to the terminal bronchioles with destruction of alveoli, reducing the alveolar surface area available for respiratory exchange. COPD is now the preferred term for conditions with airflow obstruction because of a combination of airway and parenchymal damage; patients were previ ously diagnosed as having chronic bronchitis or emphysema.

COPD is characterized by airflow obstruction -defined as an FEV 1 / FVC ratio reduced to less than 0.7. If FEV 1 is 80% or more, a diagno sis of COPD should only be made if there are respiratory symptoms (e.g. dyspnoea or cough). The airflow obstruction is not fully revers ible, does not change significantly over months, and is usually progres sive in the long term.

The most important causes of COPD include cigarette smoking, environmental pollution, dusts, chemicals or occupational exposures to various substances. Exposure to smoke from home cooking or heating fuels may contribute. Deficiency of the antiproteolytic enzyme alpha1antitrypsin is a rare cause of emphysema.

There is often significant airflow obstruction before the person is aware of it and so COPD typically remains undiagnosed until patients are in their fifties. Differentiation from asthma is important (Table 15 .6).

A diagnosis of COPD should be considered in patients over the age of 35 who have a risk factor (e.g. smoking) and exertional breath lessness, chronic cough, regular sputum production, frequent winter 'bronchitis' or wheeze. Clinical judgment is based on history, physical examination, confirmation of airflow obstruction using spirometry (postbronchodilator spirometry) and assessment of the severity of dyspnoea (Tables 15.7 and 15.8).

COPD is characterized by breathlessness and wheeze (airways obstruction), cough and an early morning mucoid sputum production. To investigate symptoms that seem disproportionate to spirometric impairment Progressive dyspnoea, low oxygen saturation, carbon dioxide accumu lation (hypercapnia) and metabolic acidosis mean that patients may ultimately become dyspnoeic at rest ('respiratory cripples'), especially when recumbent (orthopnoea), and eventually develop respiratory failure, pulmonary hypertension, right ventricular hypertrophy and rightsided heart failure (cor pulmonale). Two clinical patterns of COPD are recognized: ■ 'Pink puffers' -patients with emphysema who manage to maintain normal blood gases by hyperventilation, and are always breathless but not cyanosed; rather they are pink from vasodilatation ■ 'Blue bloaters' -patients with chronic bronchitis who lose their CO 2 drive, fail to maintain adequate ventilation and become both hypercapnic and hypoxic with central cyanosis, cor pulmonale and oedema (for these patients, the respiratory drive is from the low PO 2 and thus oxygen administration is contraindicated) (Table 15 .9).

The diagnosis of COPD is based upon clinical history and presen tation. Investigations include a chest radiograph (which may show hyperinflated lung fields with loss of vascular markings); arterial blood gases (which should be measured if pulse oximetry shows oxygen satu ration less than 92%); spirometry; and lung function tests. FEV1 is reduced in all cases (FEV 1 of less than 40% signifies severe COPD) and the flow-volume curve shows a typical pattern, with reduced flow rates at mid and lowerlung volumes. A ratio of FEV 1 :FVC of less than 70% confirms airways obstruction.

Patients with COPD and their family should be educated about the disease, and about required lifestyle changes and medication.

Nondrug therapy includes: stopping smoking (nicotine replacement therapy or bupropion may help); exercise by pulmonary rehabilitationof proven benefit; weight loss (improves exercise tolerance); and vaccination (pneumococcal and influenza vaccines). Drug therapy includes shortacting bronchodilators (anticholinergic drugs [ipra tropium bromide]) and β 2 agonists (salbutamol) to treat the reversible component of airway disease; corticosteroids (inhaled or systemic); and antibiotics (amoxicillin, trimethoprim or tetracycline). Mucolytics, such as carbocisteine, reduce acute exacerbations by almost onethird. Longterm oxygen therapy (LTOT) reduces mortality.

People with stable COPD who remain breathless or have exacerba tions, despite using shortacting bronchodilators, should be offered the following as maintenance therapy: ■ If FEV 1 is 50% of predicted or more: use either a longacting β 2 agonist (LABA) or longacting muscarinic antagonist (LAMA). ■ If FEV 1 is less than 50% predicted: either a LABA with an inhaled corticosteroid (ICS) in a combination inhaler, or a LAMA.

Offer a LAMA in addition to a LABA plus ICS to people with COPD who remain breathless or have exacerbations, despite taking LABA plus ICS, irrespective of their FEV 1 .

Provide pulmonary rehabilitation for all who need it; noninvasive ventilation (NIV) is the treatment of choice for persistent hyper capnic ventilatory failure during exacerbations not responding to medical therapy. The frequency of exacerbations should be reduced by appropriate use of inhaled corticosteroids and bronchodilators, and vaccinations.

Bronchodilators (shortacting β 2 agonists [SABA] and shortacting muscarinic antagonists [SAMA]) should be the initial empirical treat ment for the relief of breathlessness and exercise limitation. ICS have potential adverse effects (including nonfatal pneumonia) in people with COPD. Offer a oncedaily LAMA in preference to fourtimes daily SAMA to people with stable COPD who remain breathless or have exacerbations, despite using shortacting bronchodilators as required, and in whom a decision has been made to commence regular maintenance bronchodilator therapy with a muscarinic antagonist (see above).

Most patients -whatever their age -are able to acquire and main tain an adequate inhaler technique. Bronchodilators are usually best administered using a handheld inhaler device (including a spacer device if appropriate).

Patients with distressing or disabling dyspnoea, despite maximal therapy using inhalers, should be considered for nebulizer therapy. They should be offered a choice between a face mask and a mouth piece to administer their nebulized therapy, unless the drug specifically requires a mouthpiece (for example, anticholinergic drugs).

Some patients with advanced COPD may require maintenance oral corticosteroids when these cannot be withdrawn following an exacer bation. These individuals should be monitored for the development of osteoporosis and given appropriate prophylaxis.

Theophylline should only be used after a trial of SABA and LABA, and only to those who are unable to use inhaled therapy, as there is a need to monitor plasma levels and interactions. The dose of theo phylline prescribed should be reduced at the time of an exacerbation if macrolide or fluoroquinolone antibiotics (or other drugs known to interact) are given. There is insufficient evidence to recommend prophylactic antibiotic therapy in the management of stable COPD. Mucolytic drug therapy should be considered in patients with a chronic cough productive of sputum.

If patients remain symptomatic on monotherapy, their treatment should be intensified by combining therapies from different drug classes, such as: ■ β 2 agonist and theophylline ■ anticholinergic and theophylline.

Inappropriate oxygen therapy in people with COPD may depress respiration. LTOT is indicated in patients with COPD who have a PaO 2 of less than 7.3 kPa when sta ble, or a PaO 2 greater than 7.3 kPa and less than 8 kPa when stable, and one of: secondary polycythaemia, nocturnal hypoxaemia (oxygen saturation of arterial blood [SaO 2 ] of less than 90% for more than 30% of the time), peripheral oedema or pulmonary hypertension.

To reap the benefits of LTOT, patients should breathe supplemental oxygen for at least 15 hours per day. To ensure that all those eligible for LTOT are identified, pulse oximetry should be available in all health care settings. The assessment of patients for LTOT should comprise the measurement of arterial blood gases on two occasions at least 3 weeks apart in patients who have a confident diagnosis of COPD, who are receiving optimum medical management and whose COPD is stable.

Patients should be warned about the risks of fire and explosion and told not to smoke when using oxygen.

Ambulatory oxygen therapy should be considered in patients on LTOT who wish to continue oxygen therapy outside the home, and who have exercise desaturation, are shown to have an improvement in exercise capacity and/or dyspnoea with oxy gen, and are motivated to use oxygen.

Adequately treated patients with chronic hypercapnic respiratory failure who have required assisted ventilation during an exacerbation, or who are hypercapnic or acidotic on LTOT, should be referred to a specialist centre for consideration of longterm NIV. Advanced emphysema is occasionally treated with sur gery -excision of large acquired bullae or, rarely, lung transplantation.

Patients with COPD who need dental care can be classified as follows: ■ Patients at low risk -experience dyspnoea on effort but have normal blood gas levels. These patients can receive all dental treatment with minor modifications. ■ Patients at moderate risk -experience dyspnoea on effort, are chronically treated with bronchodilators or recently with corticosteroids, and PaO 2 lowered. A medical consultation is advised to determine the level of control of the disease before any dental treatment. ■ Patients at high risk -have symptomatic COPD that may be end stage and poorly responsive to treatment. With these patients, a medical consultation is essential before any dental treatment is carried out.

Patients with COPD are best treated in an upright position at midmorning or early afternoon, since they may become increasingly dyspnoeic if laid supine. It may be difficult to use a rubber dam, as some patients are mouthbreathers and not able to tolerate the additional obstruction. LA is preferred for dental treatment, but bilateral mandibular or palatal injections should be avoided. Patients with COPD should be given relative analgesia only if absolutely necessary, and only in hospital after full preoperative assessment. CS with diazepam and midazolam should not be used, as benzodiazepines are respiratory depressants. Patients should be given GA only if absolutely necessary, and intravenous barbiturates are contraindicated. Secretions reduce airway patency and, if lightly anaesthetized, the patient may cough and contaminate other areas of the lung.

Postoperative respiratory complications are more prevalent in patients with preexisting lung diseases, especially after prolonged operations and if there has been no preoperative preparation. The most important single factor in preoperative care is cessation of smok ing for at least 1 week preoperatively. Respiratory infections must also be eradicated; sputum should first be sent for culture and sensitivity, but antimicrobials such as amoxicillin should be started without await ing results.

The medical management of COPD should be optimized prior to surgery. The ultimate clinical decision about whether or not to proceed with surgery should rest with a consultant anaesthetist and consultant surgeon, taking account of comorbidities, functional status of the patient and necessity for the surgery.

Composite assessment tools, such as the American Society of Anesthesiologists (ASA) scoring system, and not just lung function, are the best criteria for the assessment of patients with COPD before surgery. Those taking corticosteroids should be treated with appropri ate precautions (Ch. 6). Interactions of theophylline with other drugs, such as adrenaline (epinephrine), erythromycin, clindamycin, azithro mycin, clarithromycin or ciprofloxacin, may result in dangerously high levels of theophylline. Ipratropium can cause dry mouth.

Guidelines for the management of COPD may be found at: http:// publications.nice.org.uk/chronicobstructivepulmonarydisease cg101 (accessed 30 September 2013).

Respiratory viruses usually spread by touch or airborne transmission and the very small particles (2-0.2 micrometres) can avoid the upper respiratory tract defences and the mucociliary elevator to reach the lung alveoli. A range of viruses can cause lower respiratory tract infections (LRTIs ; Table 15 .10). Some viruses (e.g. influenza and respiratory syncytial) can spread from the upper to the lower respira tory tract via infection of the respiratory epithelium and can lead to bacterial superinfection and pneumonitis (pneumonia). Mycoplasmal (atypical) pneumonia and tuberculosis (TB) may be direct infections. Epidemics of a potentially fatal severe acute respiratory syndrome (SARS) have been caused by a coronavirus that originated in China and spread worldwide; H5N1 bird influenza also arose as an epidemic; and a similar epidemic, but of swine influenza (H1N1), emanated from Mexico (see later).

Bacterial infections, such as pneumonia or lung abscess, can also result from material aspirated into the lungs, and are usually unilat eral. Those who aspirate more than others have, as a result, more frequent LRTI and this is seen in alcohol and other drug abusers, as well as comatose patients. Exogenous penetration and contamination of the lung can result from trauma (e.g. a stab wound or road traffic accident) or surgery. Entamoeba histolytica can occasionally cause pneumonia -by direct extension from an amoebic liver abscess (Table  15 .11). Patients with endocarditis, or septic pelvic or jugular thrombo phlebitis, may experience LRTI acquired haematogenously and then it is often bilateral.

Immunocompromised persons (e.g. those with human immunode ficiency virus/acquired immune deficiency syndrome [HIV/AIDS] and transplant recipients) and people with bronchiectasis or cystic fibrosis are also susceptible to respiratory infections by a range of opportun istic microbes. Pneumocystis jiroveci (P. carinii), for example, is a com mon cause of potentially fatal pneumonia in immunocompromised patients -especially those with HIV/AIDS (Chs 20 and 21).

Clinical features of LRTI vary according to the part of the respiratory tract mainly affected: ■ Bronchiolitis causes rapid respiration, wheezing, fever and dyspnoea -but is restricted mainly to infants. ■ Bronchitis causes cough, wheezing and sometimes dyspnoea. ■ Pneumonia causes cough, fever, rapid respiration, breathlessness, chest pain, dyspnoea and shivering.

Antimicrobial therapy is indicated, particularly for pneumonia. Antivirals have not been highly effective. Oxygen may be needed. Pneumococcal vaccine is indicated for older people.

The majority of LRTIs are severe illnesses, and are contraindications to all but emergency dental treatment. GA is hazardous and absolutely contraindicated. Dental treatment should be deferred until recovery, or be limited to pain relief.

Influenza is mainly a communitybased infection transmitted in house holds and communities. Healthcareassociated influenza infections can arise in any healthcare setting, most commonly when influenza is also circulating in the community.

Influenza is a contagious disease caused by influenza virus types A, B or C. Type A has two main subtypes (H1N1 and H3N2); it causes most of the widespread influenza epidemics and can occasionally be fatal. Type B viruses generally cause regional outbreaks of moderate severity, and type C viruses are of minor significance.

A person can spread influenza starting 1 day before they feel sick and for another 3-7 days after symptoms start. Influenza can be pre vented or ameliorated by vaccination each autumn; this is especially indicated for older people and those with cardiorespiratory disease.

Influenza attacks virtually the whole respiratory tract; symptoms appear suddenly after 1-4 days and include fever, sore throat, nasal congestion, headache, tiredness, dry cough and muscle pains (myalgia). Most people recover in 1-2 weeks but infection can be lifethreatening, mainly because primary influenzal viral pneumonia can lead to sec ondary bacterial pneumonia or can exacerbate underlying conditions (e.g. pulmonary or cardiac disease). The old and very young, and those with chronic disorders, are more likely to suffer complications, such as pneumonia, bronchitis, sinusitis or otitis media. Influenza has also been followed by depression, encephalopathy, myocarditis, myositis, pericarditis, Reye syndrome and transverse myelitis.

Rest, maintenance of fluid intake, analgesics, antipyretics, and avoid ance of alcohol and tobacco help relieve symptoms. Aspirin must never be given to children under the age of 16 years who have 'flulike symptoms, and particularly fever, as this can cause Reye syndrome. Zanamivir (an antiviral that works against influenza types A and B) can shorten the symptoms by approximately 1 day, if treatment is started during the first 2 days of illness. Other antiviral drugs include amantadine, oseltamivir and rimantadine; they may be helpful but their use is restricted mainly to immunocompromised persons, since they can cause adverse effects.

Influenza can be a severe contagious illness so all but emergency den tal treatment should be deferred until recovery. GA is hazardous and absolutely contraindicated.

Influenza type A subtype H5N1 can cause an illness known as 'avian influenza' or 'bird 'flu' in birds, humans and many other animal spe cies. HPAI A(H5N1) -'highly pathogenic avian influenza virus of type A of subtype H5N1' -is the causative agent and is enzootic in many bird populations, especially in SouthEast Asia. It has spread globally and resulted in the deaths of over 100 people and the slaughter of mil lions of chickens. A vaccine that could provide protection (Prepandrix) has been cleared for use in the European Union. H5N7 is a more recent emergent infection, similar in many respects.

Swine influenza is common in pigs in the midwestern United States, Mexico, Canada, South America, Europe (including the UK, Sweden and Italy), Kenya, China, Taiwan, Japan and other parts of eastern Asia. Transmission of swine influenza virus from pigs to humans is not com mon, but can produce symptoms similar to those of influenza. A 2009 outbreak in humans ('swine 'flu') was due to an apparently new strain of H1N1 arising from a reassortment produced from strains of human, avian and swine viruses. It can pass from human to human. Antiviral agents such as oseltamivir may help. Vaccines are now available.

An outbreak of a lifethreatening febrile respiratory infection appeared in 2003, originating from Guangdong, China, and was named severe acute respiratory syndrome (SARS). Caused by a newly recognized coronavirus (SARSassociated coronavirus, SARSCoV), SARS spread via close contact to many countries across the world. According to the World Health Organization, 8437 people worldwide became sick with SARS during the course of the first recognized outbreak and 813 died.

The incubation period of 2-7 days is followed by a high fever (above 38.0°C), malaise, headache and myalgia. Some people also experience mild upper respiratory symptoms and, after 2-7 days, lower respiratory signs -a dry cough and dyspnoea, potentially progressing to hypox aemia. SARS can cause a pneumonia with a mortality approaching 10%, particularly in older or immunocompromised people.

Artificial ventilation has been needed in 10-20% of cases. Antiviral agents, such as oseltamivir or ribavirin, may help. Inactivated vaccines, virally and bacterially vectored vaccines, recombinant protein and DNA vaccines, as well as attenuated vaccines, are under development.

SARS is a severe illness, and all but emergency dental treatment should be deferred until recovery. GA is hazardous and absolutely contraindicated. For all contact with suspect SARS patients, careful hand hygiene is important, including handwashing with soap and water; if hands are not visibly soiled, alcoholbased handrubs may be used as an alternative to handwashing. If a suspected SARS patient is admitted to hospital, infection control personnel should be notified immediately. Infection control measures (www.cdc.gov/ncidod/hip/iso lat/isolat.htm; accessed 30 September 2013) should include standard precautions (e.g. hand hygiene): healthcare personnel should wear eye protection for all patient contact; contact precautions (e.g. gown and gloves for contact with the patient or their environment); and airborne precautions (e.g. an isolation room with negative pressure relative to the surrounding area and use of an N95 filtering disposable respirator for persons entering the room).

Pneumonia is classed as 'primary' if it occurs in a previously healthy individual, and is usually lobar; it is called 'secondary' if it follows some other disorder, such as previous viral respiratory infections, aspir ation of foreign material, lung disease (bronchiectasis or carcinoma), depressed immunity (e.g. alcoholism or immunosuppression), or aspir ation of oral bacteria ( 

Pneumonia causes cough, fever, rapid respiration, breathlessness, chest pain, dyspnoea and shivering. Complications can include lung abscess or empyema (pus in pleural cavity).

It is important to avoid alcohol and tobacco, but use analgesics and antipyretics to relieve the symptoms. Broadspectrum antimicrobi als given promptly and empirically usually include a macrolide (azithromycin, clarithromycin or erythromycin), quinolone (moxiflox acin, gatifloxacin or levofloxacin), or doxycycline for outpatients. For in patients, cefuroxime or ceftriaxone plus a macrolide is used.

Prophylaxis includes immunization against influenza and pneumococci.

Pneumonia is a severe illness and all but emergency dental treatment should be deferred until recovery. GA is hazardous and absolutely contraindicated.

Ventilatorassociated pneumonia (VAP) is discussed later.

Legionellosis is a bacterial respiratory infection caused by one of the family Legionellaceae, Gramnegative aerobic bacilli, ubiquitous in water and soil but particularly preferring warm aquatic environments. The term Legionnaire's disease was coined as a result of an outbreak of the previously unrecognized respiratory disease in an American Legion meeting in Philadelphia in 1976, but it is now recognized worldwide, many infections being contracted during travel abroad, particularly to Spain, Turkey and some other Mediterranean areas.

Legionella bacteria can be found in natural freshwater environments, usually in insufficient numbers to cause disease. Legionella grow best in warm water, as in hot tubs, cooling towers, hot water tanks, large plumbing systems, or the airconditioning systems of large buildings. Though there are over 30 Legionellaceae, most infections are caused by Legionella pneumophila. Disease is contracted by inhalation of contaminated mist or vapour, mainly (approximately 46%) through aerosolization of infected water in airconditioning systems, hotwater systems, humidifiers, nebulizers, showers and spa pools. Outbreaks have mostly been linked to aerosol sources in the community, cruise ships and hotels, with the most likely sources being whirlpool spas, air conditioning units in large buildings, potable (drinking) water systems, and water used for bathing. Risk factors include: ■ exposure to: recent travel with an overnight stay outside of the home (outbreaks of travelassociated legionellosis are infrequently identified but more than 20% of cases are thought to be associated with recent travel) whirlpool spas recent repairs or maintenance work on domestic plumbing ■ systemic illhealth: alcohol use chronic kidney disease diabetes immune defects liver disease malignancy smoking.

Illness mainly affects males over 45, smokers, heavy drinkers, older people and the immunocompromised. Also vulnerable are travellers, especially middleaged and older tourists, and conference or business groups, possibly because of tiredness or age. Many young people have been exposed to infection and become seropositive, but remained healthy.

There is no evidence of persontoperson transmission of legionellosis.

Legionellosis manifests as one of two clinical syndromes (Table 15 .14). Legionnaire's disease is typically a lobular type of pneumonia, which can be fatal but is fortunately rare; infection can range from discrete patches of inflammation and consolidation to involvement of whole lobes. Pontiac fever is milder and usually subsides rapidly, often with out treatment. People who should be tested for Legionnaire's disease include those with pneumonia in the following groups: Because Legionella is commonly found in the environment, clinical isolates are necessary to interpret the findings of an environmental investigation. Diagnosis can be by rapid urine molecular testing for L. pneumophila antigen, and culture of respiratory secretions on selective media. Sensitivity and specificity of the diagnostic tests are shown in Table 15 .15.

Pontiac fever is a selflimited illness; most cases recover within 1 week and few benefit from antibiotic treatment. Overall mortality in Legionnaire's disease may be as high as 10%, and over 25% in older people and up to 80% in the immunocompromised. Erythromycin is standard treatment; cephalosporin is an alternative.

Legionella species are present in roughly twothirds of potable water samples collected from domestic and institutional taps and drinking fountains, and from a similar percentage of dental units, but water from these dental units often has higher bacterial concentrations (Ch. 31). There are reports of Legionella infections in dental unit water lines, and antibodies and occasionally frank infection demonstrated in dental staff; at least one patient appears to have contracted and died from infection emanating from a dental practice.

Prevention is crucial, involving (Ch. 

General aspects Tuberculosis (TB) , an infection caused by mycobacteria, affects approxi mately onethird of the world's population (1.5 billion people); it is a major global health problem, some 2 million people dying from it annu ally. TB disproportionately affects the poorest persons in both high income and developing countries. In highincome countries, most human TB arises from Mycobacterium tuberculosis, transmitted from person to person through the air. TB usually affects the lungs initially (pulmonary TB) but can also involve brain, kidneys, spine and other parts. From Victorian times to about the Second World War, Mycobacterium bovis infection from infected cows' milk (bovine or bTB) was a major cause of morbidity and mortality; it was clinically and pathologically indistin guishable from infection caused by M. tuberculosis. Cattletesting and a slaughter programme became compulsory in 1950 and, by the 1980s, the incidence of TB in cattle had been substantially reduced. Tuberculosis from M. bovis in cows' milk was virtually eliminated in highincome countries by the tuberculin testing of cattle and pasteurization of milk. In the developing world, many cattle still have TB, and bTB is still seen. bTB has also increased in highincome countries over the last two dec ades and an infection rate of up to 38% in badgers -and transmission to cattle -may explain this.

TB is not spread by touch or by drinking glasses, dishes, sheets or clothing. It is usually transmitted by infected sputum, typically from close contacts such as family members, but is unlikely to be transmit ted between normal social contacts. TB can present an occupational risk to healthcare professionals, including dental staff. One outbreak of drugresistant TB in New York involved at least 357 patients, most of whom contracted TB in one of 11 hospitals; nearly 90% of the patients were also HIVpositive, and most were young males of Hispanic or African heritage. TB has been transmitted between pas sengers during longhaul airline flights. The risk of transmitting TB though air circulation is now low because the highefficiency particu late air (HEPA) filters on newer commercial aircraft are of the same type as those used in hospital respiratory isolation rooms; indeed, the number of times air is cleaned each hour exceeds the recommendation for hospital isolation rooms.

SubSaharan Africa has the highest rates of active TB per capita, driven primarily by the HIV epidemic. The absolute number of cases is highest in Asia, with India and China having the great est burden of disease globally. In the USA and most Western European countries, the majority of cases occur in foreignborn residents and recent immigrants from countries in which tubercu losis is endemic. Immunocompromised people -such as diabetics and severely immuno deficient patients, like those with HIV/AIDS (about 30% of South Africans with HIV/AIDS also have TB) -and patients in prisons or institutions are at risk. TB also mainly affects medically neglected persons, such as vagrants, alcoholics, intravenous drug abusers or older homeless people. The main groups at increased risk for infection therefore include people who are resourcepoor or immunoincompetent, especially: TB in developing countries is particularly widespread and is increasing, the highest rises in incidence being in SouthEast Asia, subSaharan Africa and Eastern Europe. In highincome countries, the incidence is also rising, probably because of worsening social deprivation, homelessness, immigration, HIV infection and intra venous drug abuse. It is now as common in London as in the devel oping world, and is seen especially in immigrants, such as those from the Indian subcontinent, Africa and South Asia. This increase appears to be a result of the development of TB disease in individu als who may have been infected for some time and of new infections acquired in the UK, or as a result of travel to other countries where TB is common. London accounted for the highest proportion of cases in the UK in 2011 (39%), followed by the West Midlands region (11%); 74% of these were born outside the UK and mainly originated from South Asia and subSaharan Africa. In 2011, there was a rise in the number of TB cases compared to 2010, as well as an increase in drug resistance. More information on TB, including statistics, can be found at: http:// www.hpa.org.uk/Publications/InfectiousDiseases/Tuberculosis/ and http://www.tbfacts.org/tbstatistics.html (both accessed 30 September 2013).

Initial infection with TB is usually subclinical. About 10% of those infected develop overt disease; of these, half will manifest within 5 years (primary TB), while the remainder will develop postprimary disease. Inhaled mycobacteria may cause subpleural lesions (primary lesion) and lesions in the regional lymph nodes (primary complex). Body defences usually localize the mycobacteria, though these remain viable; infected persons are not obviously ill and are unlikely to know they are infected (latent ; Table 15 .16). Latent TB infection (LTBI) usu ally becomes active only after many years, if body defences become weakened (Box 15.3). However, active TB can develop shortly after mycobacteria enter the body, if body defences are impaired such as in ageing, drug or alcohol abuse, or HIV/AIDS. Also, in massive infec tions, acute active TB can result, typically causing a chronic productive cough, haemoptysis, weight loss, night sweats and fever. Erythema nodosum may be associated. Extrapulmonary TB is less common; it may appear as glandular involvement in the neck or elsewhere, and is less infectious than pulmonary TB. Lymph node TB may lead to lymphadenopathy, caseation of the nodes and pressure symptoms -for example, on the bronchi.

Postprimary TB follows reactivation of an old primary pulmonary lesion and results in features ranging from a chronic fibrotic lesion to fulminating tuberculous pneumonia. The pulmonary lesions may extend and lead to a pleural effusion. Reactivation or progression of primary TB may also result in widespread haematogenous dissemina tion of mycobacteria -'miliary TB'. Multiple lesions may involve the central nervous system, bones, joints, and cardiovascular, gastrointes tinal and genitourinary systems.

Clinical presentation in TB is thus variable, depending on the extent of spread and the organs involved. As it frequently passes unrecog nized for so long, the mortality is high.

Similar illnesses to TB may also be caused by atypical (nontuber culous) mycobacteria, such as M. avium complex (MAC; see below).

The diagnosis of TB is suggested by the history and confirmed by physical examination, a massively raised erythrocyte sedimentation rate (ESR), positive tuberculin skin tests (TSTs; Mantoux or Heaf test for a delayed hypersensitivity reaction to protein from M. tuberculosis [purified protein derivative; PPD]) and chest imaging. Hypersensitivity develops with 2-8 weeks of infection and can be detected by conversion of the TST from negative to positive, but TSTs are neither 100% sensi tive nor specific. A positive Mantoux reaction indicates previous immu nization (BCG; bacille Calmette-Guérin -live attenuated M. bovis) or current infection -not necessarily disease. Chest radiography may show scarring and hilar lymphadenopathy. Computed tomography (CT) may show areas of calcification or highlight a tuberculous abscess. Smears and culture of sputum, blood, laryngeal swabs, bronchoalveolar lavage, gastric aspirates or pleural fluid may be tested for mycobacteria.

Polymerase chain reaction (PCR) techniques have greatly acceler ated the diagnosis and speciation, though Ziehl-Neelsen, auramine or rhodamine microbial stains are still used. The mycobacteria growth indicator tube (MGIT) system gives results as early as 3-14 days. Blood assay for M. tuberculosis (BAMT) may be positive by interferongamma release assay (IGRA). Some 15% of people over 65 years have a positive IGRA. The IGRA can be used in place of (but not in addition to) TST. IGRAs measure the immune reactivity to M. tuberculosis. White blood cells from most persons that have been infected with M. tuberculosis will release interferongamma (IFNγ) when mixed with M. tuberculosis antigens. A positive test result sug gests that M. tuberculosis infection is likely; a negative result suggests that infection is unlikely.

Latent infection (LTBI) can be diagnosed with either a tuberculin skin test or an IGRA (more specific). IGRA gives a result within 24 hours and should be used biological therapy is given, such as for rheumatoid arthritis or inflammatory bowel disease. Prior BCG vacci nation does not cause a falsepositive IGRA test result. More informa tion on the IGRA is available at: http://www.cdc.gov/tb/publications/ factsheets/testing/igra.htm (accessed 30 September 2013).

Active TB is diagnosed by sputum microscopy and culture in liquid medium with subsequent drugsusceptibility testing. Nucleic acid People who should be tested for TB include those who have symp toms, those who have had close daytoday contact with active TB disease (family member, friend or coworker), those who have HIV infection or AIDs, those with lowered immunity, those who are required to for employment or school, and those about to be treated with biological agents.

The top priority of TB control programmes is to identify and give complete treatment to all patients with active disease. TB is a notifi able disease and contact tracing is an important aspect of limiting spread. Treatment with antibiotics is indicated for people who are sick with TB, those infected but not sick, and those who are close contacts of infectious TB cases. Treatment for 'symptomatic sputumpositive' patients, which should be instituted as soon as possible, is combination chemotherapy, usually isoniazid plus rifampicin plus pyrazinamide or ethambutol for 2 months, with continuation of daily isoniazid and rifampicin for a further 4 months. Treatment for 'asymptomatic' patients who are believed to have been infected by contacts, but are not unwell, includes isoniazid for 6 months or isoniazid and rifampicin for 3 months. Rifapentine is a longacting rifampicin used once weekly. Fluoroquinolones (moxifloxacin) may also act against TB. There may be resistance to one or more than one antibiotic.

Currently, given the potential risk of drugresistant TB being present, treatment is usually started with isoniazid, rifampicin, pyrazinamide and ethambutol (or a quinolone such as gatifloxacin or moxifloxacin) for 2 months, then isoniazid and rifampicin for 4 months.

All antituberculous drugs (Table 15 .17) have potentially serious adverse effects and require careful monitoring. If patient compliance is considered to be poor, directly observed therapy (DOT), where drugs are dispensed by and taken in the presence of a healthcare profes sional, may be indicated. New drugs are on the horizon. Immunization using BCG is advocated for schoolchildren, highrisk individuals and healthcare professionals -although its efficacy has been questioned. New vaccines are in development.

Chemoprophylaxis with isoniazid and rifampicin is indicated in a number of situations (Box 15.4) .

TB can become resistant to the drugs used to treat it particularly when the drugs are misused or mismanaged. This may occur, for example, when: 

In some developing countries, approximately 10% of cases are multi ple antibioticresistant; this is termed multidrugresistant tuberculosis (MDRTB); in the UK, only a small minority currently fall into this category but the number of cases is increasing. MDRTB is defined as resistance to rifampicin and isoniazid; it may be atypical in presenta tion and the infection disseminates. More than 4% of people with TB worldwide have MDRTB, and Eastern Europe has a high prevalence. MDRTB is seen mainly in people with HIV/AIDS and in HIV/AIDS and in Africans. Bedaquiline, is a new antitubercular agent the first active agent against tuberculosis to be registered since 1963.

Extensively drugresistant tuberculosis (XDRTB) is a rare type of MDRTB, not only resistant to isoniazid and rifampin, but also to any fluoroquinolone and at least one of three injectable secondline drugs (i.e. amikacin, kanamycin, or capreomycin). XDRTB is of special concern for immunocompromised people (e.g. with HIV/AIDS), who are more likely to develop TB, and have a higher risk of death if they do develop it. XDRTB is most often encountered in people from Eastern Europe, Russia and Africa. It has been transmitted in healthcare facilities and is now seen worldwide. It is essentially untreatable, though capreomycin has been used effectively to treat MDRTB in HIVpositive individuals.

Totally drugresistant TB was reported initially in 2007-2009 in India, Iran and Italy; it is spreading, despite denials, and is most disquieting. 

Chronic ulcers, usually on the tongue dorsum, are the main oral manifestation of TB. They result from coughing of infected sputum from pulmonary TB, including in HIVinfected persons with TB, but are rare and such cases (usually middleaged males) may result from neglect of symptoms or default from treatment. Occasionally, the diagnosis is made from biopsy of an ulcer after granulomas are seen microscopically. Acidfast bacilli are rarely seen in oral biopsies, even with the help of special stains, so unfixed material should also be sent for culture if possible. Tuberculous cervical lymphadenopathy is the next most common form of the infection and is particularly com mon among those from South Asia. Most TB lymphadenitis is pain less, with several enlarged, matted nodes, but systemic symptoms are present only in a minority and only about 15% have pulmonary mani festations on radiography (Fig. 15.7) . Diagnosis relies on tuberculin testing, which can be positive in both tuberculous and non tuberculous mycobacterial cervical lymphadenitis. Any person with lymphadenop athy and recent conversion from a negative to positive tuberculin test should be suspected of having mycobacterial infection, and this should prompt biopsy (e.g. fineneedle aspiration biopsy) for culture or histo logical confirmation. PCR will improve diagnosis, as culture must wait 4-8 weeks for a result. Oral complications of antitubercular therapy are rare, but rifabutin and rifampicin can cause red saliva. Pulmonary TB is of high infectivity, as shown by cases of tuber culous infection of extraction sockets and cervical lymphadenitis in 15 patients treated by an infected member of staff at a dental clinic. Dental staff who themselves were HIVpositive, working in a dental clinic for HIVinfected persons in New York, have died from TB con tracted occupationally. Transmission of MDRTB between two dental workers may have occurred in an HIV dental clinic. Infection control is thus important, so staff with TB are usually precluded from their occupation until treated.

Management of a patient with TB depends upon the level of poten tial infectivity (Table 15.18) . Patients with open pulmonary TB are con tagious, and dental treatment is thus best deferred until the infection has been treated. Treatment with appropriate drugs for 2 weeks drasti cally reduces the infectivity of patients with pulmonary TB. If patients with open pulmonary TB must be given dental treatment, special pre cautions should be used to prevent the release of mycobacteria into the air, to remove any that are present and to stop their inhalation by other persons. Reduction of splatter and aerosols, by minimizing cough ing and avoiding ultrasonic instruments, and use of a rubber dam, are important. Improved ventilation, ultraviolet germicidal light, new masks and personal respirators, and other personal protective devices, such as HEPA filters, are indicated ( Fig. 15.8) . Mycobacteria are very resistant to disinfectants, so that heat sterilization must be used.

LA is safe and satisfactory. Relative analgesia is contraindicated because of the risk of contamination of the apparatus. GA is also contraindicated for dental treatment because of the risk of contamina tion of the anaesthetic apparatus and because of impaired pulmonary function. Aminoglycosides, such as streptomycin, enhance the activity of some neuromuscular blocking drugs and in large doses may alone cause a myasthenic syndrome. Possible drug interactions are shown in Table 15 .19.

Other factors, such as alcoholism or intravenous drug use (Ch. 34), hepatitis (Ch. 9) or HIV disease (Ch. 20), may also influence dental management.

Mycobacteria other than tuberculosis (MOTT) are widely distributed in water, soil, animals and humans, and rarely cause disease. Severe MOTT infections have been seen, however, in individuals predisposed because of defects in the interleukin12 (IL12) and interferongamma (IFNgamma) pathways.

Mycobacterium abscessus, a bacterium found in water, soil and dust, has been known to contaminate medications and products, including medical devices. Healthcareassociated M. abscessus can cause a vari ety of infections, usually of the skin, but it can also cause lung infec tions in persons with various chronic lung diseases and is increasingly recognized as an opportunistic pathogen in cystic fibrosis (CF) patients Persontoperson transmission of atypical mycobacteria is not important in acquisition of infection, except for skin infections. On rare occasions, MOTT skin infections have followed tattooing with contaminated tattoo inks. Many people become infected with and har bour MOTT in their respiratory secretions without any symptoms or evidence of disease. Individuals with respiratory disease from MOTT do not readily infect others and, therefore, do not need to be isolated. MOTT are generally not infectious to others.

Infection with M. abscessus is usually caused by injections of con taminated substances or by invasive medical procedures employing contaminated equipment or material. Infection can also occur after accidental injury where the wound is contaminated by soil. There is very little risk of transmission from person to person. MAC complex, M. scrofulaceum and M. kansasii are possible causes of tuberculous cervical lymphadenitis. MAC may also infect the lungs (similar to TB), skin or lymph nodes. Lung disease is also caused occasionally by M. kansasii, mainly in middleaged and older persons with underlying chronic lung conditions. M. fortuitum and M. chelonae may cause skin and wound infections and abscesses, frequently associated with trauma or surgery. M. marinum may cause 'swimming pool granuloma', a nodular lesion that may ulcerate, usually on an extremity. M. ulcerans may produce chronic ulcerative skin lesions, usually of an extremity. M. abscessus skin infections present with swollen and/ or painful areas that are usually red, warm and tender to the touch, and which can also develop into boils or pustules. Other features of M. abscessus infection are fever, chills, muscle aches and malaise.

Cervical lymphadenitis due to MAC, M. scrofulaceum and M. kansasii may affect otherwise healthy young children, most commonly pre school females who have unilateral cervical lymphadenopathy, typically in the submandibular or jugulodigastric nodes, and they may form a 'cold abscess'. MOTT is the usual cause in children under 12 years but TB is more common in older patients. Absence of fever or tuber culosis, a positive tuberculin test and failed response to conventional antimicrobials are highly suggestive of MOTT, but definitive diagnosis is by smear, culture or PCR of biopsy material obtained by fineneedle aspiration or removal of nodes.

Treatment is based on results of laboratory testing, which should identify the appropriate antibiotic. Preventive treatment of close contacts of persons with disease caused by MOTT is not needed. Most MOTT are resistant to standard antitubercular medication and, though it is possible that clarithromycin or clofazimine may have some effect, excision of affected nodes is the usual recommended therapy.

Water from dental units may contain MOTT species; mycobacterial proliferation in biofilms may explain the extent of this contamination (Ch. 31).

Aspiration syndromes are conditions in which foreign substances are inhaled into the lungs and which can have consequences ranging from asphyxia to infection and lung abscess. Dental restorations or frag ments of teeth, plaque, gastric contents and other materials may be aspirated, especially if material enters the pharynx, and particularly if the cough reflex is impaired for any reason.

Most commonly, aspiration syndromes involve oral or gastric contents associated with gastrooesophageal reflux disease (GORD), swallowing dysfunction (Ch. 7), neurological disorders and structural abnormalities, such as a pharyngeal pouch. Cricopharyngeal dys function involves cricopharyngeal muscle spasm or achalasia of the superior oesophageal sphincter, and can be seen in infants who have a normal sucking reflex but have incoordination during swallowing, pos sibly secondary to delayed development or cerebral palsy. Anatomical disorders, such as cleft palate, pharyngeal pouch, oesophageal atresia, tracheooesophageal fistula, duodenal obstruction or malrotation, and motility disorders, such as achalasia, may have an aspiration risk. Infirm older patients are also at risk of aspiration, especially if they are bedbound or have neurological disorders. Isolated superior laryngeal nerve damage, vocal cord paralysis, cerebral palsy, muscular dystrophy and Riley-Day syndrome (familial dysautonomia) are all associated with increased risk of aspiration.

Ventilatorassociated pneumonia (VAP), as defined by the Centers for Disease Control and Prevention (CDC), is present when the chest radiograph shows new or progressive infiltrate, consolidation, cavitation or pleural effusion in conjunction with either new onset of purulent sputum or change in character of sputum, and an organism isolated from blood, or the isolation of an aetiological agent from a specimen obtained via suction aspiration through an endotracheal or tracheostomy tube. The major route for acquiring endemic VAP is oropharyngeal colo nization by endogenous flora or by exogenously acquired pathogens from intensive care units. VAP is the most commonly reported health careacquired infection in patients receiving mechanical ventilation, with prevalence rates consistently in the 10-20% range. Mortality rates in VAP are at least double those in patients without VAP, ranging from 24% to 85% when the infection is caused by a multidrugresistant Gramnegative pathogen.

The Healthcare Infection Control Practices Advisory Committee of the CDC has developed guidelines for the prevention of VAP. These include strategies aimed at preventing aspiration of contaminated oral or gastric material (e.g. raising the head of the bed and draining subglottic secretions), and interventions to alter bacterial coloniza tion of stomach (e.g. stress ulcer prophylaxis and selective digestive decontamination) and mouth. Oral hygiene, suctioning and the provi sion of moisture to lips and oral mucosa, plus toothbrushing, may be important in prevention of VAP. There are also strategies for manag ing ventilator circuits (e.g. replacement of ventilator circuits, use of closed rather than open suction, and use of heat moisture exchange as opposed to heated circuit technology).

Lung abscess is a localized infection leading to cavitation and necro sis. While some cases result from aspiration of foreign material, most develop from pneumonia caused by infection with Staph. aureus or Klebsiella pneumoniae. Bronchial obstruction by carcinoma is another important cause.

Symptoms resemble those of suppurative pneumonia. There is a risk of infection spreading locally or leading, via septicaemia, to a brain abscess.

Diagnosis rests mainly on the chest radiograph, which may sometimes show cavitation or a fluid level. Antimicrobial chemotherapy, postural drainage and relief by bronchoscopy of any obstruction are indicated.

A wellrecognized cause of lung abscess is inhalation of a tooth or fragment, a restoration or rarely, an endodontic instrument. When undertaking endodontics or cementing restorations, such as inlays or crowns, a rubber dam or other protective device should always be used to avoid the danger of inhalation.

Lung abscesses may also result from aspiration of oral bacteria, particularly anaerobes, especially in infirm older patients or those who are intubated.

The other main dangers in dentistry are with GA, particularly if an inadequate throat pack has been used. Patients who inhale tooth frag ments or dental instruments must have chest radiographs (lateral and posteroanterior) and, if necessary, bronchoscopy.

Loeffler syndrome appears to be an allergic reaction, usually to the parasitic worm Ascaris lumbricoides, or drugs such as sulphonamides. It manifests with pulmonary infiltrates (and abnormal chest radio graph) and eosinophilia (eosinophilic pneumonia). The disease usually clears spontaneously.

Sarcoidosis, so named because skin lesions resembled a sarcoma, is a multisystem granulomatous disorder, seen most commonly in young adult females in northern Europe, especially in people of African heritage. The aetiology is unclear but Propionibacterium acnes and P. granulosum have been implicated and associations have been reported with exposure to inorganic particles, insecticides, moulds and occupations such as firefighting and metalworking. Serum sam ples contain antibodies directed against Mycobacterium tuberculosis antigens. Sarcoidosis is associated with HLADRB1 and DQB1, and a butyrophilinlike 2 (BTNL2) gene on chromosome 6. Thelper 1 (Th1) cells release IL2 and IFNγ, and augment macrophage tumour necrosis factor alpha (TNFα) release. CD25 regulatory T cells cause a limited impairment of cellmediated immune responses (partial anergy) but no obvious special susceptibility to infection.

Sarcoidosis affects the thorax in 90%, but has protean manifestations and can involve virtually any tissue (Table 15 .20). Sarcoid most typi cally causes Löfgren syndrome (fever, bilateral hilar lymphadenopathy, arthralgia and erythema nodosum, especially around the ankles; Figs 15.9 and 15.10).

Other common presentations may include pulmonary infiltration and impaired respiratory efficiency, with cough and dyspnoea in severe cases, or acute uveitis, which can progress to blindness. Susceptibility to lymphomas has been suggested but not confirmed.

Because of its vague and protean manifestations, sarcoidosis is under diagnosed. In the presence of suggestive clinical features, helpful investigations include: chest radiography (enlarged hilar lymph nodes); raised serum angiotensinconverting enzyme (SACE ; Table 15 .21) in acute disease (this is insensitive, nonspecific and a poor guide to therapy); positive gallium67 citrate or gadolinium or positron emis sion tomography (PET) scans; labial salivary gland or transbronchial biopsy (for histological evidence of noncaseating epithelioid cell granulomas) -except in Löfgren syndrome, which is a classical clini cal diagnosis. 18 Fdeoxyglucose PET is helpful in identifying sites for biopsy. Nonspecific findings may include mild anaemia, leukopenia, eosinophilia, hypergammaglobulinaemia, raised ESR and low serum albumin. Hypercalcaemia is common because of extrarenal produc tion of active vitamin D and can result in renal damage. Alkaline phosphatase, 5'nucleotidase, lysozyme and adenosine deaminase levels are raised in hepatic sarcoidosis. Evidence of impaired delayed hypersensitivity reactions to some antigens may be useful. Kveim skin tests are not now used.

Half the patients with sarcoidosis remit within 3 years and about 66% remit by 10 years. Patients with only minor symptoms usually need no treatment but corticosteroids, sometimes with azathioprine, methotrexate, tetracyclines, hydroxychloroquine, infliximab or etaner cept, are given if there is active organ disease (ocular disease, progres sive lung disease, hypercalcaemia or cerebral involvement).

Biopsy of the minor salivary glands frequently shows noncaseating granulomas and association with other features of sarcoidosis, par ticularly hilar lymphadenopathy. This is an important diagnostic find ing that may obviate more invasive procedures. Sarcoidosis can involve any of the oral tissues but has a predilection for salivary glands. Asymptomatic swelling of the parotid glands or cervical nodes, and less frequently the lips, may accompany systemic disease. Superficial or deepseated red submucosal nodules may develop intraorally and on the lips. Nontender, wellcircumscribed, brownishred or violaceous nodules with superficial ulceration have also been reported. The oral and lip lesions may occasionally precede systemic involvement.

There is enlargement of the major salivary glands in about 6% of cases; some have xerostomia, and the association of salivary and lacri mal gland enlargement with fever and uveitis is known as uveoparotid fever (Heerfordt syndrome). Salivary swelling may also be seen with out other features of Heerfordt syndrome. The salivary gland swellings usually resolve on treatment of sarcoidosis but this may take up to 3 years.

Facial palsy and other cranial neuropathies may be seen. There is also an association with Sjögren syndrome, when SSA and SSB serum autoantibodies are found. Rarely there is an association of thyroiditis with Addison disease, Sjögren syndrome and sarcoidosis (TASS syndrome). There is a group of patients who have histologi cal features of sarcoid in one or more sites in the mouth, such as the gingivae, but no systemic manifestations. A few of these patients may ultimately develop other more or less systematized disease but the majority probably have isolated lesions. Such cases, where no exog enous cause for the granulomatous reaction can be found, are regarded as having 'sarcoidlike' reactions (orofacial granulomatosis) and treat ment is unnecessary. However, patients should be kept under observa tion for as long as possible.

Management of patients with systemic sarcoidosis may include con sideration of respiratory impairment, uveitis and visual impairment, renal disease, jaundice or corticosteroid treatment.

LA is safe and satisfactory. CS is contraindicated if there is any res piratory impairment. GA should only be given in hospital. 

Lung cancer is the most common cancer in highincome countries in males and most frequently affects adult urban cigarettesmokers. Bronchogenic carcinoma accounts for 95% of all primary lung cancer and has also become increasingly common in women (because of increased tobacco use), to the extent that the mortality rate for the two sexes has become almost equal. Metastases from cancers elsewhere are also frequently found in the lungs.

Recurrent cough, haemoptysis, dyspnoea, chest pain and recurrent chest infections are the predominant features. Local infiltration may cause pleural effusion, lesions of the cervical sympathetic chain (Horner syndrome), brachial neuritis, recurrent laryngeal nerve palsy or obstruction of the superior vena cava with facial cyanosis and oedema (superior vena cava syndrome).

There are many nonmetastatic extrapulmonary effects of bron chogenic (or other) carcinomas -for example, weight loss, anorexia, fingerclubbing, neuromyopathies, thromboses (thrombophlebitis migrans), muscle weakness, various skin manifestations and ectopic hormone production (of antidiuretic hormone, adrenocorticotropic hormone, parathyroid hormone and thyroidstimulating hormone).

Metastases from bronchogenic cancer are common and typically form in the brain (which may manifest with headache, epilepsy, hemi plegia or visual disturbances), liver (hepatomegaly, jaundice or ascites) or bone (pain, swelling or pathological fracture).

The diagnosis is based on history and physical examination, supported by radiography, CT and magnetic resonance imaging (MRI), sputum cytology, bronchoscopy and biopsy. Spiral CT appears to detect tumours at an early stage.

The overall 5year survival rate is only 8%. Radiotherapy is the most common treatment. Only some 25% of patients are suitable for surgery but, even then, the 5year survival is only about 25%. Chemotherapy has been disappointing, except in smallcell carcinomas.

Dental treatment under LA should be uncomplicated. CS should preferably be avoided. GA is a matter for specialist management in hospital, as patients often have impaired respiratory function, espe cially after lobectomy or pneumonectomy. This, along with any muscle weakness (myasthenic syndrome, Eaton-Lambert syndrome) that can make the patient unduly sensitive to the action of muscle relaxants, makes GA hazardous.

Oral cancer may be associated with lung cancer, and vice versa, or develop at a later stage (Ch. 22). Such synchronous or metachronous primary tumours must always be ruled out.

Metastases can occasionally affect the orofacial region and cause enlargement of the lower cervical lymph nodes, epulislike softtissue swellings or labial hypoaesthesia or paraesthesia in the jaw. Soft palate pigmentation is a rare early oral manifestation.

Lung cancer is a fairly common cause of death in dental techni cians, but it is unknown whether this is due to smoking alone or to dust inhalation.

Cystic fibrosis (CF) is one of the most common fatal hereditary dis orders. Inherited as an autosomal recessive trait, with an incidence of about 1 in 2000 births, it is the most common inherited error of metabolism and is seen mainly in people of European descent. The gene responsible is on chromosome 7q. CF is caused by defects in the cystic fibrosis transmembrane conductance regulator (CFTR), a protein that appears to be part of a cyclic adenosine monophosphate (cAMP)regulated chloride channel, regulating Cl − and Na + transport across epithelial membranes, and ion channels and intracellular fluid flow in sweat, digestive and mucus glands.

The basic defect in CF is abnormal chloride ion transport across the cell membrane of nearly all exocrine glands. The blockage of salt and water movement into and out of cells results in the cells that line the lungs, pancreas and other organs producing abnormally thick, sticky mucus that can obstruct the airways and various glands, especially in the respiratory tract and pancreas. Involved glands (lungs, pancreas, intestinal glands, intrahepatic bile ducts, gallbladder, submaxillary and sweat glands) may become obstructed by this viscid or solid eosino philic material.

Recurrent respiratory infections result in a persistent productive cough and bronchiectasis, with the lungs becoming infected with a variety of organisms including Staph. aureus, Haemophilus influenzae, Pseudomonas aeruginosa, Strep. pneumoniae, Burkholderia cepacia, and sometimes mycoses or mycobacteria. Mycobacterium abscessus is a nontuberculous mycobacterium increasingly recognized as an opportunistic pathogen in CF patients. Viral infections, such as mea sles, can have severe sequelae.

Pancreatic duct obstruction leads to pancreatic insufficiency, with malabsorption and bulky, frequent, foulsmelling, fatty stools. Gallstones, diabetes, cirrhosis and pancreatitis may result. Sinusitis is very common.

Growth is frequently stunted. The mutations can also cause con genital bilateral absence of the vas deferens, so fertility is impaired in most males with CF. In women, fertility may be impaired by viscid cervical secretions, but many women have carried pregnancies to term.

Most patients have a high concentration of sodium in their sweat (also reflected in the saliva); a sweat test showing sodium and chloride values of more than 60 mmol/L is considered positive, between 40 and 60 mmol/L equivocal, and less than 40 mmol/L negative.

Physiotherapy and postural drainage are crucially important. Clearance of sputum is helped by water aerosols and bronchodila tors (terbutaline or salbutamol), but mucolytics such as carbocisteine, methyl cysteine and dornase alfa are of questionable effectiveness. Treatment with ivacaftor, a CFTR potentiator, improves chloride transport through the ion channel.

Amoxicillin and flucloxacillin are effective prophylactic antimicrobi als and may be given by aerosol. Vaccination against measles, whoop ing cough and influenza is important. A low fat intake, adequate vitamins and oral pancreatic enzyme replacement (pancreatin) are also necessary.

Doublelung or heart-lung transplantation may eventually become necessary.

Sinusitis is very common; most CF patients have recurrent sinusitis and nasal polyps. The major salivary glands may enlarge and hyposali vation sometimes occurs. The lowfat, highcarbohydrate diet and dry mouth may predispose to caries. Enamel hypoplasia and black stain may be seen, and both dental development and eruption are delayed. Tetracycline staining of the teeth was common but should rarely be seen now. Pancreatin may cause oral ulceration if held in the mouth.

LA is satisfactory but CS is usually contraindicated because of poor respiratory function. GA is contraindicated if respiratory function is poor. Lung disease, such as bronchiectasis, liver disease and diabetes, may complicate treatment.

Bronchiectasis is dilatation and distortion of the bronchi. Causes include:

■ Congenital defects, which should be considered in all patients include cystic fibrosis, Kartagener syndrome, alpha1antitrypsin deficiency, collagen defects (e.g. Marfan syndrome) 

There is no identifiable underlying cause in about 50% of adults and 25% of children.

The damaged and dilated bronchi lose their ciliated epithelium and therefore mucus tends to pool, causing recurrent LRTIs, typically with Strep. pneumoniae, Haemophilus influenzae or Pseudomonas aeruginosa.

Overproduction of sputum, which is purulent during exacerbations, a cough (especially during exercise or when lying down) and finger clubbing are typical features, with recurrent episodes of bronchitis, pneumonia and pleurisy. Haemoptysis is not uncommon. In advanced bronchiectasis, chest pain, dyspnoea, cyanosis and respiratory failure may develop. Complications may include cerebral abscess and amyloid disease.

Chest radiography and pulmonary function tests are required. High resolution CT (HRCT) is useful. Postural drainage is important. Antimicrobials, such as amoxicillin, cephalosporins or ciprofloxacin, are given for acute exacerbations and for longterm maintenance treatment.

GA should be avoided where possible and is contraindicated in acute phases.

Workers exposed to airborne particles may develop pulmonary disease (pneumoconiosis), which ranges from benign (e.g. siderosis) to malig nant, as in mesothelioma from asbestosis (see Appendix 15.1), but any pneumoconiosis can cause significant incapacity.

GA may be contraindicated; the physician should be contacted before treatment.

Berylliosis may be a hazard in some dental technical laboratories, when lung cancer is more frequent.

Respiratory complications following surgical operations under GA include segmental or lobar pulmonary collapse and infection. They are more common after abdominal surgery or if there is preexistent respiratory disease or smoking (see also Ch. 3), and can be signifi cantly reduced by smoking cessation, preoperative physiotherapy and bronchodilators, such as salbutamol.

If postoperative pulmonary infection develops, sputum should be sent for culture, and physiotherapy and antibiotics should be given. The common microbial causes are Strep. pneumoniae and Haemophilus influenza; in this case, suitable antibiotics include amoxicillin and erythromycin. Hospital infections may include other microorganisms, such as MRSA, Klebsiella, Pseudomonas and other Gramnegative bacteria.

Inhalation (aspiration) of gastric contents can cause pulmonary oedema and may be fatal (Mendelson syndrome); it is most likely if a GA is given to a patient who has a stomach that is not empty, has a hiatus hernia or is in the last trimester of pregnancy. Prevention is by ensuring the stomach is empty preoperatively; if it is not, an anaes thetist should pass an endotracheal tube. Antacids or an H2receptor blocker, such as cimetidine or ranitidine, may be given by mouth pre operatively to lower gastric acidity.

If gastric contents are aspirated, the pharynx and larynx must be carefully sucked out. Systemic corticosteroids have been recommended but probably do not reduce the mortality.

Respiratory distress in premature infants may be caused by immaturity of surfactantproducing cells, when the alveoli fail to expand fully; this necessitates endotracheal intubation for many weeks. It may, in turn, result in midface hypoplasia, palatal grooving or clefting, or defects in the primary dentition. The same oral effects may be seen with prolonged use of orogastric feeding tubes. The degree to which subsequent growth corrects these deformations is currently unknown, though the palatal grooves typically regress by the age of 2 years. Using soft endotracheal tubes does not obviate this problem and, at present, the best means of avoiding palatal grooving appears to be the use of an intraoral acrylic plate to stabilize the tube and protect the palate.

Acute respiratory distress syndrome (ARDS) is a sequel to several types of pulmonary injury and some infections, including those with oral viridans streptococci.

Patients with endstage pulmonary disease are considered for potential transplantation, usually using a lung from a braindead organ donor. A combination of ciclosporin, azathioprine and glucocorticoids is usu ally given for lifelong immunosuppression to prevent a Tcell, alloim mune rejection response.

Inhaled nitric oxide modulates pulmonary vascular tone via smooth muscle relaxation and can improve ventilation/perfusion matching and oxygenation in diseased lungs. Early graft failure following lung transplantation has been described by various investi gators as reimplantation oedema, reperfusion oedema, primary graft failure or allograft dysfunction. Pathologically, this entity is diffuse alveolar damage.

See also Chapter 35.

A meticulous presurgery oral assessment is required and dental treatment must be undertaken with particular attention to establishing optimal oral hygiene and eradicating sources of potential infection. Dental treatment should be completed before surgery. For 6 months after surgery, elective dental care is best deferred. If surgical treat ment is needed during that period, antibiotic prophylaxis is probably warranted.

Cardiopulmonary transplantation (heart and lung transplantation) is the simultaneous surgical replacement of the heart and lungs in patients with endstage cardiac and pulmonary disease, with organs from a cadaveric donor.

All transplant recipients require lifelong immunosuppression to pre vent a Tcell, alloimmune rejection response.

See also Chapter 35.

A meticulous presurgery oral assessment is required and dental treatment must be undertaken with particular attention to establishing optimal oral hygiene and eradicating sources of potential infection. Dental treatment should be completed before surgery. For 6 months after surgery, elective dental care is best deferred. If surgical treat ment is needed during that period, antibiotic prophylaxis is probably warranted. 

National Institutes of Health: National Institute of Allergy and Infectious Diseases

Healthcare Infection Control Practices Advisory Committee Guideline for the prevention of healthcare associated pneumonia

Nosocomial pneumonia: state of the science

Extensively drugresistant tuberculosis as a cause of death in patients coinfected with tuberculosis and HIV in a rural area of South Africa

A review of the possible role of oral and dental colonization on the occurrence of health careassociated pneumonia: underappreciated risk and a call for interventions

Reducing ventilatorassociated pneumonia through advanced oraldental care: a 48month study

APIC infection control and applied epidemiology: principles and practice

Sepp. Ventilatorassociated pneumonia and oral care: a successful quality improvement project

Guidelines for preventing the transmission of Mycobacterium tuberculosis in healthcare settings

A randomized trial of dental brushing for preventing ventilatorassociated pneumonia

Pneumonia associated with a dental unit waterline

The pathogenesis of ventilatorassociated pneumonia: its relevance to developing effective strategies for prevention

Aspects of human disease 32

Chronic obstructive pulmonary disease (COPD)

Aspects of human disease 31

In vitro antibacterial activities of oral care products against ventilatorassociated pneumonia pathogens

The impact of a simple, lowcost oral care protocol on ventilatorassociated pneumonia rates in a surgical intensive care unit

Intermittent suction of oral secretions before each positional change may reduce ventilatorassociated pneumonia: a pilot study

Current trends and newer concepts on diagnosis, management and prevention of respiratory tract infections