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Experienced clinicians appear to generate hypotheses more readily than less expert clinicians, and they also appear to be better able to identify sources of data needed for hypothesis testing. 10 We believe many new therapists, like many new physicians, often conduct a plethora of tests because: (1) they have been taught methods of patient management that require suspension of hypothesis generation until all the data are collected, or (2) they do not have enough experience to generate a tentative idea (hypothesis) on which to base a focused examination strategy. We recognize that, for some patients, therapists may be unable to generate examination strategies, and the algorithm calls for consultation when this occurs and provides a mechanism for documenting and justifying the use of a consultant.

When using the HOAC II as a guide to documentation, therapists must describe their examination strategies, including how they arrived at these strategies (based on available data) and why they believe the chosen examination techniques will lead to information that can be used to confirm or deny hypotheses. This may appear to require a lot of information. Notes in the patient's medical record, however, may be as simple as “the patient's inability to walk down stairs may be due to balance problems. Testing of balance appears to be most important, and tests of muscle force and range of motion will be conducted to rule out less likely causes of the functional limitation.” In this example, the balance testing directly addresses the hypothesis, whereas muscle force measurements and range-of-motion measurements could lead to rejection of the hypothesis. The important element is that a link exists between the logic that guides the examination strategy, the information available, and the therapists' hypothesis. This does not require elaborate documentation on the part of the therapist.

Examination procedures for a given type of patient may be governed by departmental policies, critical paths, or a variety of other influences. Ideally, approaches should be data driven (evidence based) and based on research suggesting best methods of examination and data analysis. 11 The HOAC II does not specify how or what to examine, but, for the process to be useful, the examination must follow logically from the examination strategy and not include extraneous procedures if they are not part of the examination strategy. That is, examination procedures should be related to the tentative hypotheses, either to confirm or to reject those hypotheses. The measurements obtained during this phase should be of the type and quality specified by the APTA's Standards for Tests and Measurements in Physical Therapy Practice . 12

For documentation, all descriptions and analysis of the data obtained during the examination should be clear. Reasons why hypotheses were supported or rejected need to be specified, and, when findings call for additional examination procedures, this should also be described.

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Table 4 lists the major categories of immunodeficiency and gives some examples of disorders within each category that can present with severe, recurrent, persistent or unusual chest infections. As the nature of the immune defect determines the susceptibility to particular micro-organisms, identifying the pathogen is not only important in deciding what treatment is appropriate, but it may also indicate which part of the immune system is defective. For example, identification of Pneumocystis carinii and cytomegalus virus (CMV) in bronchial lavage fluid from a child with interstitial pneumonia would suggest a defect of T-cell function, whilst recurrent cavitating staphylococcal pneumonia, which is refractory to appropriate antibiotics suggests a neutrophil defect, such as chronic granulomatous disease.

Table 4.

Classification of primary immunodeficiencies

This is not an exhaustive or complete classification. The investigations are for disorders of that component of the immune system and not the specific disorders.

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Table 4.

Classification of primary immunodeficiencies

This is not an exhaustive or complete classification. The investigations are for disorders of that component of the immune system and not the specific disorders.

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Antibody deficiencies are the commonest of immunodeficiencies 33 . There are many different types of antibody deficiency, ranging from severe deficiencies of all immunoglobulins (X-linked agammaglobulinaemia, Bruton's disease) to milder deficiencies of specific antibodies in children with normal immunoglobulin levels. They may occur as an isolated defect or as part of a wider immunodeficiency. It is not possible to give a comprehensive review of all of these defects and only some of the commonest types which present with chest problems in children are described here.

The normal term infant has undetectable serum levels of IgM and IgA at birth and these rise progressively in the first 2–3 years of life 32 ,33 . The maternal IgG which crosses the placenta into the fetus disappears within 5–7 months. The infant's own IgG appears at significant levels at 4–8 months and rises for 2–3 years. Anti-protein antibodies are produced in the first few months of life, but the ability to produce IgG antibodies against polysaccharide antigens, such as the capsules of certain bacteria, matures much more slowly and is only effective after 2 years. IgG has four sub-classes (1–4) which differ in concentration, structure and function. Antibodies against protein are mainly of the IgG1 and IgG3 subclasses and those against polysaccharides are predominantly of the IgG2 subclass.

It is now recognised that many children with recurrent chest infections have abnormalities in their ability to produce specific antibodies to common respiratory pathogens such as the Strep. pneumoniae or H. influenzae which is commonly isolated from their sputum. Many of these children are diagnosed as suffering from asthma and are receiving high doses of inhaled steroids and other asthma therapies. Important clues to the diagnosis include the lack of response to high doses of asthma treatment, the presence of a productive cough and coloured sputum, and improvement with courses of antibiotics. There may be a history of recurrent upper respiratory infections, such as otitis media or tonsillitis. If an antibody deficiency is suspected, total serum levels of IgG, IgM, IgA and IgE should be measured. As the normal ranges of these proteins change during childhood, the measured values must be compared to the age-appropriate normal values, ideally from the same laboratory. There is controversy about the value of also measuring IgG sub-class levels as not all children with ‘deficient’ sub-classes have evidence of an increased susceptibility to infection 34 . Nevertheless, IgG subclass deficiency, and particularly IgG2 deficiency, can be associated with severe bronchiectasis and many clinicians still measure IgG subclasses.

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