Bronchial asthma [antikvár]

I. Definition - functional pathology 'Asthmatic dyspnoea', definable as a reversible obstructive ventilatory disturbance, is the only, and the essential, central symptom of the clinical entity called bronchial, or to be more precise, bronchiolar asthma (Hansen, 1957). All the other symptoms of asthma may or may not be present and relate to the type and length of the disease course, its severity and the liability to paroxysmal attacks, combination with equivalents, etc. No less diverse than the multiplicity of its symptomatological variants is the pathogenesis of bronchial asthma. It is by no means restricted to an allergic mode of origin, even though this is the most common, particularly at an early age. There are a number of other asthmogenic stimuli impinging upon the airways and capable of provoking an 'asthmatic dyspnoea'. Circulatory disorders of haemodynamic origin, particularly left-sided heart failure, may alsó lead to a reversible bronchiolar obstruction, as may bacteriogenic inflammation in the lower reaches of the bronchi, etc. Another factor, to which Rackemann constantly drew attention as long ago as 1931 in the light of his longitudinal studies and observations of the course of the disease, is that, as the disease proceeds, the primary form of pathogenesis may be joined by a second or even a third form, and these compete with each other in such a way that, for instance, a primary extrinsic asthma modulates into an intrinstic asthma, or, to take another example, a psychogenic component assumes an independent role and dominates the disease process to such an extent that the primary mode of origin becomes irrelevant to the further course of the disease. The multiplicity of aetiologic factors and the vagaries, indeed the 'fickleness' (Bray, 1937), of the individual course run by the disease - the inconstancy which allows an initially paroxysmal dyspnoea to change into a chronic asthma, an episodic form into one free of asthma attacks, or a 'catarrhe sec' into a hypersecretory spastic bronchitis - have, together with the changing meaning and plurivalence of the pathogenesis, resulted in a persistent failure to provide an unequivocal definition. From the clinical point of view we (Gronemeyer and Fuchs, 1967), together with Werner (1965), believe that it is useful to distinguish materially and conceptually between bronchial asthma as an 'actual disease' and "bronchial asthma as a syndrome' in order to ensure that, in daily practice, diagnostic errors are recognized and therapeutic omissions made good before it is too late. Asthma as a syndrome occurs only as a phenomenon accompanying a different kind of underlying disease of the bronchi, the lung or the heart - so-called symptomatic asthma, exemplified (to name but a few instances) by left-sided heart failure, bronchial carcinoma, sarcoidosis or pulmonary tuberculosis - and exhibiting, in addition to the symptoms of the causal disease, varying degrees of asthmatic dyspnoea which do not sui generis exclusively characterize the complex clinical picture as its cardinal symptom. By contrast asthma as an independent disease is characterized by a reversible impairment of ventilation preponderantly of functional origin in the small bronchi and bronchioli, which are incompletely supported by cartilage. The localization of the obstructions is fundamental to asthma as a disease. 'Asthmatic dyspnoea' is the clinical symptom which is never absent from the complex pattern of findings when examination of respiratory function is determined. The 'asthmatic dyspnoea' characteristic of bronchial asthma is a functional abnormality; again in the definition recently given by Scadding (1977), the functional aspect of this disease is central: "Asthma is a disease characterized by wide variations over short periods of time in resistance to flow in intrapulmonary airways". The morphological changes in the lung revealed by pathological anatomy are the results of the morbid changes of function. From the clinical point of view Hansen (1957) summarized the totál complex of tissue involved in the pathologically disturbed function in the term 'asthma apparatus'. His pathological substrate is the lung 'histion', the acinus, representing the basic functional unit of the lung and corresponding to the vascular territory of the bronchiolus terminális (Letterer, 1957, 1974). Because of the functional synergism of the structural elements united in the tissue of the acinus, the triggering of asthmatic dyspnoea can, provided the effect of the stimulus is adequate, proceed from any of the individual tissues of the basic lung unit - irrespective of whether it is mesenchymal, vascular, or epithelial - or even via the neural control to which the individual tissues are subject. Consequently bronchial asthma can be elicited by a multiplicity of very different causes - allergic and