Resultados - Compromiso de proceso - Análisis descriptivo de los compromisos de gestión escolar

Dimensión 2. Compromiso de proceso

III. Resultados

Alyn H. Morice

Cough is a vital protective mechanism defending the airways from inhalation and aspiration. Patients with a defective cough reflex, such as those with stroke or Parkinson’s disease, have an increase in mortality and morbidity caused by the increased propensity for aspiration.

However, in lung disease, cough is often not helpful. Thus, in the commonest form of cough, that due to upper respiratory tract infection, coughing serves no useful purpose from the sufferer’s point of view, but aids viral transmission. In chronic cough, the frequency and severity of coughing bouts may cause serious disruption to the patient’s life. Quality-of-life instruments have indicated that patients with chronic cough may have a similar decrement to that seen with conditions such as cancer and severe COPD. Cough may also have significant comorbidity. 50% of the females attending cough clinics are incontinent and cough syncope is thought to be responsible for a number of driving fatalities.

Acute cough

Acute cough due to one of the myriad upper respiratory tract viruses places an enormous demand on the healthcare community. It is the commonest new presentation to primary care, accounting for 50% of consultations.

In temperate regions there is a marked seasonal variation with autumn and winter epidemics. Viral transmission requires person-to-person contact, either through airborne droplet infection or the manual passage of secretions. Superimposed on this seasonal pattern are peaks caused by socialisation,e.g. return to school for the autumn term and Christmas family

gatherings. Apart from general health measures, such as hand washing and avoidance of contact, there is no specific treatment for upper respiratory tract infection-induced cough. The demonstrable effect of the many cough remedies is likely to be due to a physicochemical (demulcent) effect rather than through a specific pharmacological action of any particular agent.

Chronic cough

Chronic cough is one of the commonest presentations to the respiratory physician. A survey in Yorkshire, UK, indicated that 12%

of the normal population complain of a chronic cough and 7% of these thought it interfered with activities of daily living. Many reports from specialist cough clinics point to a particular syndrome in patients with chronic cough. The typical patient is middle-aged and female. The cough appears to have no pattern to it but a careful history will often reveal many common features of the presenting complaint. It has been traditional to divide these patients without

radiographic abnormalities and no obvious other lung disease into a triad of diagnoses,

Key points

N

Cough is characterised by irritant receptor hypersensitivity.

N

Nonacid reflux into the airways frequently precipitates cough.

N

Clinical history followed by

therapeutic trials is the management strategy of choice.

namely asthmatic cough, post-nasal drip syndrome (rhinitis) and reflux cough (table 1). These subdivisions have recently been called into question. For example, asthmatic cough is unlike classic atopic asthma in that it is usually of late onset without obvious precipitants and often without evidence of bronchoconstriction. In the form known as eosinophilic bronchitis there is even an absence of bronchial hyperreactivity. Similar caveats apply to post-nasal drip syndrome and reflux cough.

Thus, the latter frequently does not conform to the criteria for peptic gastro-oesophageal reflux disease. Because of the commonality of the clinical history in chronic cough (table 2), it has been suggested that there is a single unifying diagnosis of cough hypersensitivity syndrome, with the other diagnoses representing different phenotypes of the condition. The risk factors for chronic cough suggest that nonacid reflux may be an important precipitant (table 3).

Virtually all patients presenting with a chronic cough complain of increased

sensitivity to a wide range of environmental stimuli. This hypersensitivity can be objectively demonstrated in the laboratory using cough challenge. Thus, patients cough with ethanol inhalation, whereas normal subjects do not. There is a wide variation in cough reflex sensitivity in normal subjects, with females being more sensitive than males. Sensitivity is accentuated in cough patients. Inhalation of capsaicin, the pungent extract of peppers, is typically used to demonstrate cough reflex responsiveness (fig. 1). Capsaicin works by stimulating one of a family of nociceptors of the transient receptor potential (TRP) group (fig. 2). The capsaicin-sensitive ‘hot’ receptor (TRPV1) is upregulated in patients with cough. This is due to pro-inflammatory mediators increasing expression of TRPV1, either in neurones or in other airway tissues. Rather than directly causing a cough, angiotensin-converting enzyme inhibitors alter cough sensitivity by a TRPV1-dependent

mechanism, thus explaining the continued irritation long after drug withdrawal. Another TRP receptor, TRPA1, is highly reactive to a

Table 1. Early reports from cough clinics illustrating the variety of cough diagnosis dependent on criteria used Mean age

years

Patients (females) n

Diagnosis % total

Asthma syndrome

GOR Rhinitis

Irwin et al. (1981) 50.3 49 (27) 25 10 29

Poe et al. (1982) 109 (68) 36 0 8

Poe et al. (1989) 44.8 139 (84) 35 5 26

Irwin et al. (1990) 51 102 (59) 24 21 41

Hoffstein et al. (1994) 47 228 (139) 25 24 26

O’Connell et al. (1994) 49 87 (63) 6 10 13

Smyrnios et al. (1995) 58 71 (32) 24 15 40

Mello et al. (1996) 53.1 88 (64) 14 40 38

Marchesani et al. (1998) 51 92 (72) 14 5 56

McGarvey et al. (1998) 47.5 43 (29) 23 19 21

Palombini et al. (1999) 57 78 (51) 59 41 58

Brightling et al. (1999) 91 (0) 31 8 24

The typical patient is a middle-aged female. These diagnoses are now thought to represent phenotypes of the cough hypersensitivity syndrome. GOR: gastro-oesophageal reflux. Studies can be found in Moriceet al.

(2004).

Table 2. Areas of enquiry in chronic cough Hoarseness or a problem with your voice Clearing your throat

The feeling of something dripping down the back of your nose or throat Retching or vomiting when you cough

Cough on first lying down or bending over Chest tightness or wheeze when coughing

Heartburn, indigestion or stomach acid coming up, or do you take medications for this?

A tickle or a lump in your throat

Cough with eating (during or soon after meals) Cough with certain foods

Cough when you get out of bed in the morning

Cough brought on by singing or speaking (e.g. on the telephone) Coughing more when awake than asleep

A strange taste in your mouth

Responses may either lead to further questioning or be scored 0–5 and used as a diagnostic tool to demonstrate the presence of cough hypersensitivity syndrome. A questionnaire version in various languages is available at www.issc.info

Table 3. Risk factors for chronic cough

Variable With cough

n/N (%)

Unadjusted OR (95% CI)

p-value

Sex

Male 78/1704 (4.6) 1.0

Female 135/2179 (6.2) 1.38 (1.03–1.86) 0.028

Heartburn

No 148/2990 (4.9) 1.0

Yes 65/889 (7.3) 1.51 (1.10–2.06) 0.009

Regurgitation

No 158/3314 (4.8) 1.0

Yes 54/568 (9.5) 2.10 (1.49–2.92) ,0.0001

IBS

No 111/2914 (3.8) 1.0 ,0.0001

Yes 98/909 (10.8) 3.05 (2.27–4.09)

BMI category

Normal 74/1547 (4.8) 1.0

Overweight 72/1448 (5.0) 1.04 (0.74–1.47) 0.86

Obese 60/776 (7.7) 1.67 (1.15–2.41) 0.006

Nonacid reflux symptoms in the form of regurgitation are more closely associated with cough than acid reflux.

IBS: irritable bowel syndrome.

wide range of environmental irritants and causes cough in humans. Upregulation of this receptor provides a mechanism for the exquisite hypersensitivity complained of by patients to agonists such as acrolein, the pro-tussive ingredient in smoke.

Management of chronic cough

All patients presenting with chronic cough should have a chest radiograph. The clinical history should indicate the most likely treatment options. The European Respiratory Society guidelines recommend therapeutic trials based on clinical judgement. Thus, in patients with episodes of wheezing and evidence of eosinophilic inflammation, a trial of asthmatic medication may well be beneficial (fig. 3). Where available, exhaled nitric oxide fraction may be a useful screening tool. Bronchoconstriction may not be a major component of this phenotype of cough hypersensitivity syndrome and, consequently, long-acting b-agonists may be less effective than anti-eosinophilic medication such as leukotriene antagonists. Reflux disease may be very problematical, as much airway reflux is nonacidic and, therefore, not amenable to blockade by proton pump inhibitors. Pro-motility agents, such as metoclopramide and domperidone, may be used. Other motility agents, such as erythromycin, azithromycin and magnesium, have also been advocated.

Operative treatmentvia Nissen

fundoplication can be effective in intractable coughing. An alternative strategy is to treat the hypersensitivity component with agents

such as gabapentin. Finally, the use of central cough suppression in the form of antitussive agents, such as low-dose morphine, can ameliorate cough in a third of patients with otherwise intractable symptoms.

Sputum

In subjects with chronic cough, production of moderate amounts of sputum does not alter the diagnostic profile. The separation from individuals with excessive sputum production is arbitrary, but is generally regarded as a cup of sputum per day. Above this limit, a diagnosis of bronchiectasis becomes increasingly likely. The presence of sputum purulence indicates a greater likelihood but does not seem to predict the degree of anatomical damage to the airway.

Indeed, the diagnosis of bronchiectasis, relying as it does on the dilation and destruction of the airways, will not include many patients with functional abnormalities of the bronchi.

In conditions characterised by sputum hypersecretion, there is usually a change in the composition of the mucus. Several mechanisms are responsible for this change.

Thus, in CF, the increase in sodium reabsorption leads to a reduction in the sol phase of the airway surface liquid. Airway inflammation, particularly that caused by release of enzymes such as myeloperoxidase (which produces the characteristic green colour) and neutral endopeptidase, and by polymorphs, causes alteration of mucin (MUC) gene expression through proteinase-activated receptors. The death of

inflammatory cells and bacteria lead to a soup of DNA that cross-links with filamentous actin, producing gelatinous plugs that increase ventilation/perfusion ratio mismatch with resulting systemic hypoxia.

The treatment of mucus hypersecretion may be challenging. In the presence of purulent sputum, every effort should be made to identify the causative organism. Eradication with appropriate high-dose antibiotic therapy may lead to sustained remission. More frequently, there is rapid relapse, indicating the need for maintenance antibiotics either orally orvia the nebulised route.

■

Capsaicin µmoL·L^-¹

10 20

Coughs per min

■

●

Placebo Captopril

Figure 1. Capsaicin cough challenge in normal subjects, the effect of captopril enhancing cough reflex sensitivity.

The advantage of this latter strategy is that side-effects may be minimised by using agents with high local potency but poor oral bioavailability, such as colomycin or tobramycin. Antioxidant mucolytics are widely prescribed but evidence of efficacy is limited. The largest study ofN-acetylcysteine over 3 years showed no effect on decline in lung function or exacerbation rate. In COPD, two agents, azithromycin and roflumilast, have been shown to be efficacious in those with exacerbations of chronic bronchitis.

Perhaps because of the paucity of specific agents for mucus hypersecretion,

nonpharmacological therapy in the form of airway clearance techniques is frequently advocated. However, a recent Cochrane

review found the quality of randomised studies to be poor and concluded that any benefits achieved may be small (Osadnik et al., 2012).

Haemoptysis

Haemoptysis presents in two clinical scenarios. First, the patient may present withde novo haemoptysis without pre-existing lung disease. Any mucosal lesion may cause haemoptysis of small amounts of blood mixed with sputum. Since this is a common presentation of lung cancer, chest radiography is obligatory in patients when presenting with haemoptysis and, in heavy smokers, CT or bronchoscopy is also required. Aspergilloma and TB may similarly cause blood-stained bronchitis. More peripheral lung pathology, such as lobar pneumonia, gives rise to sputum that is frequently described as ‘rusty’. Haemoptysis of frank blood is a common sign of pulmonary embolism or infarction.

Obviously, recurrent haemoptysis initially presents with acute haemoptysis. Typically, bronchiectasis leads to recurrent, sometimes massive and occasionally fatal haemoptysis.

The bronchial blood supply arises from the aorta and, in contrast to the pulmonary circulation, is at systemic pressure. In bronchiectasis, there is hypertrophy of the bronchial arteries as a consequence of recurrent infection. When the patient presents with life-threatening haemoptysis,

Hot

55°C 43°C 33°C 30°C 25°C 17°C

TRPA1

Thymol Osmotic Cold/

menthol Isothiocyanates Acreolin Cinnamaldehyde

etc.

Cold

Figure 2. The thermosensitive transient receptor potential (TRP) channels that are important in cough reflex sensitivity. Typical ‘natural’ agonists are listed below each channel. THC: tetrahydrocannabinol.

■

Citric acid nM 3

Figure 3. Cough challenge with citric acid in eosinophilic bronchitis and the response to inhaled steroids. Number of coughs off and on budesonide is shown.

radiographic percutaneous bronchial artery embolisation is the treatment of choice.

Vasculitis is a common and frequently missed cause of recurrent haemoptysis and diffuse alveolar haemorrhage. While the systemic connective tissue diseases, such as systemic lupus erythematosus, may produce small-vessel haemoptysis, the commonest cause is microscopic polyangiitis. The perinuclear anti-neutrophil cytoplasmic antibody (MPO ANCA) is positive in ,70% of cases. Finally, haemoptysis may be the result of alveolar haemorrhage. Disease of the vascular or alveolar wall, such as Goodpasture’s syndrome or alveolar haemosiderosis, may present with recurrent haemoptysis. Clearly, disorders of coagulation, both congenital and acquired, and including warfarin therapy or thrombocytopenia, will predispose to haemoptysis.

Dyspnoea

Pierantonio Laveneziana and Giorgio Scano Dyspnoea is the major reason for referral for pharmacological treatment and respiratory rehabilitation programmes in patients with COPD. Dyspnoea is a subjective experience of breathing difficulty that consists of qualitatively distinct sensations that vary in intensity. This definition underlines the

importance of the different qualities (cluster descriptors) covered by the term dyspnoea, the involvement of integration of multiple sources of neural information about breathing and the physiological

consequences. More specifically, it has been postulated that dyspnoea arises when there is a conscious awareness of a mismatch between what the brain expects and what it receives in terms of afferent information from the lungs, airways and receptors in the tendons and muscles of the chest wall (fig. 1 and table 1).

Evaluation of dyspnoea during physical tasks

Exertional dyspnoea can be easily defined as

‘the perception of respiratory discomfort that occurs for an activity level that does not normally lead to breathing difficulty’ (Killian et al., 1995). It follows that the intensity of dyspnoea can be determined by assessing the activity level required to produce dyspnoea (i.e. dyspnoea at rest is more severe than dyspnoea only when climbing stairs). The Medical Research Council (MRC) dyspnoea scale can be used for this purpose (table 2), as well as other scales such as the Baseline Dyspnoea Index.

Dyspnoea can also be evaluated during a physical task, such as cardiopulmonary exercise testing (CPET). For this purpose, the 10-point Borg scale can be used (table 2). In the Borg scale, the end-points are anchored such that zero represents ‘no breathlessness at all’ and 10 is ‘the most severe breathlessness that one had ever experienced or could imagine experiencing’.

Using the Borg scale, subjects rate the magnitude of their perceived breathing discomfort during exercise. Though Key points

N

Dyspnoea is a subjective experience of breathing discomfort that consists of qualitatively distinct sensations that vary in intensity.

N

The mechanisms of dyspnoea are complex and multifactorial: there is no unique central or peripheral source of this symptom.

N

The sense of heightened inspiratory effort is an integral component of exertional dyspnoea and is pervasive across health and disease.

N

The NVD theory of dyspnoea states that the symptom arises when there is a disparity between the central reflex drive (efferent discharge) and the simultaneous afferent feedback from a multitude of peripheral sensory receptors throughout the respiratory system. The feedback system provides information about the extent and appropriateness of the mechanical response to central drive.

N

Despite the diversity of causes, the similarity of described experiences of dyspnoea suggests common underlying mechanisms.

somewhat less popular, the visual analogue scale (VAS) is another dyspnoea measuring instrument with proven construct validity during CPET. Both the VAS and Borg scale have been shown to provide similar scores during CPET, and to be reliable and reproducible over time in healthy subjects, and in patients with asthma and COPD undergoing CPET.

Physiology

The recent American Thoracic Society statement has emphasised the

multidimensional nature of dyspnoea in the sensory–perceptual (intensity and quality), affective distress and impact domains. To gain more insight into our understanding of dyspnoea, a case can be made for answering the following questions.

1) What is the role of mechanical factors and ventilatory constraints in dyspnoea?

2) What are the neurophysiological underpinnings of the most selected cluster descriptors that define the qualitative dimension of dyspnoea in patients?

3) Do obstructive and restrictive lung diseases share some common underlying mechanisms?

Dyspnoea is perceived as a sense of effort During voluntary increase in ventilation, the motor cortex increases the outgoing motor signal to respiratory muscles and conveys a copy (central corollary discharge) through cortical interneurones to the sensory/

association cortex, which is informed of the voluntary effort to increase ventilation. It is also likely that the sense of the respiratory effort arises from the simultaneous activation of the sensory cortex and muscle contraction: a variety of muscle receptors provides feedback to the central nervous

Joint receptors (muscle displacement) Stretch receptors

(volume)

Spindles (muscle displacement)

Airway receptors

(flow)

Instantaneous feedback Forebrain sensory

areas

Motor cortex

Golgi (muscle tension)

Figure 1. Schematic representation of the neurophysiological underpinnings of perceived dyspnoea during exercise in healthy humans. During a voluntary increase in ventilation, the motor cortex increases the outgoing motor signal to the respiratory muscles and conveys a copy (central corollary discharge) through cortical interneurons to the sensory/association cortex, which is informed of the increased motor drive to increase ventilation. Volitional respiratory effort in healthy subjects is harmoniously matched with the appropriate increase in flow or volume displacement via concurrent afferent proprioceptive information transmitted via vagal, glossopharyngeal, spinal and phrenic nerves. This information is conveyed to the medulla and central cortex, where it is integrated. The result is a harmonious neuromechanical coupling with avoidance of respiratory discomfort or distress. Reproduced and modified from Scano et al. (2010) with permission from the publisher.

system about force and tension, and information from these receptors may conceivably underlie the sense of effort. For clinical purposes, the perceived magnitude of respiratory effort is expressed by the ratio of the tidal oesophageal pressure (Poes) to the maximal pressure generation capacity of the respiratory muscles (PImax). In healthy subjects, volitional respiratory effort is matched by lung/chest wall displacement (i.e. change in tidal volume (VT) as percentage of vital capacity (VC))via concurrent afferent proprioceptive information, transmittedvia vagal, glossopharyngeal, spinal and phrenic

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