Respiratory Medicine. Stephen J. Bourke. Читать онлайн. Newlib. NEWLIB.NET

Автор: Stephen J. Bourke
Издательство: John Wiley & Sons Limited
Серия:
Жанр произведения: Медицина
Год издания: 0
isbn: 9781119774235
Скачать книгу
extremely useful but much neglected sign in respiratory examination. It is probably wise to start with it, lest it be missed. The clues it provides to later examination findings are so useful it can almost feel like cheating.

      If airway obstruction is present, the cough will have a wheezy quality (listen out for it). As described already, the expiratory flow rate during a cough is greater than that generated in a normal forced expiration. Therefore, if airway obstruction is mild, it may be that wheeze is only heard during a cough.

      When reporting a cough, a patient is usually asked if they produce sputum. The answer ‘no’ normally results in the doctor documenting that the cough is ‘dry’. Beware: an inability to ‘bring up’ sputum doesn’t imply it isn’t there. Consciously listening to the quality of a cough will avoid such a mistake.

      Knowing whether a cough is wet or dry can be invaluable when it comes to determining the nature of the crackles heard later in the examination. Whilst in theory the ‘coarse’ crackles of bronchiectasis are different from the ‘fine’ crackles of fibrosis, in practice – on sound quality alone – it can be a difficult call. If you’ve already listened to the quality of the cough by the time of auscultation, your ability to distinguish fine from coarse will be uncannily good.

      A loud, booming cough heard from one end of the ward to the other is unlikely to be as serious as it sounds.

      Next, start with the hands and look for signs en route to the chest.

      Hands

      Look for clubbing, tar staining or features of rheumatoid arthritis. Signs of CO2 retention include peripheral vasodilation and asterixis: a flapping tremor detected by asking the patient to spread their fingers, cock their wrists back and close their eyes. CO2 retention dulls proprioception and the hands tend to drift forward, particularly when the eyes are closed. Eventually, an awareness that the hands are no longer in position leads to a sudden corrective movement. In understanding the underlying mechanism of this sign, it should be clear why a doctor holding the patient’s hands in place (as many do to ‘feel’ for asterixis) will always miss it. Count the pulse rate and note any abnormalities in rhythm (e.g. atrial fibrillation) or character (e.g. a bounding pulse of carbon dioxide retention).

      Count the respiratory rate over a period of at least 30 seconds. The respiratory rate is best counted surreptitiously, perhaps whilst feeling the pulse, as patients tend to breathe faster if they are aware that a doctor is focusing on their breathing. The respiratory rate is an incredibly easy observation to make and is a highly sensitive index of physiological derangement (as such, it is an integral part of all early‐warning systems in hospital), yet it is all too frequently missed. Do it. Do it properly.

       Clubbing

      Next examine the head and neck. Check for elevation of jugular venous pressure or lymph node enlargement. In the face, seek signs of cyanosis and anaemia (pallor of conjunctiva). Be alert for uncommon signs such as Horner syndrome (ptosis, meiosis, enophthalmos, anhydrosis), which indicates damage to the sympathetic nerves by a tumour situated at the lung apex (see Chapter 4).

      Jugular veins

      The jugular veins are examined with the patient in a semi‐reclining position, with the trunk at an angle of about 45° from the horizontal. The head is turned slightly to the opposite side and fully supported so that the sternocleidomastoid muscles are relaxed. The jugular venous pulse is seen as a diffuse superficial pulsation of multiple waveform that is distinct from the carotid arterial pulse. The height of the pulse wave is measured as the vertical height of the top of the oscillating column of blood above the sternal angle. The jugular venous pressure normally falls during inspiration. It is elevated in right heart failure, which may occur as a result of pulmonary embolism or cor pulmonale in COPD, for example. Other signs of right heart failure, such as hepatomegaly and peripheral oedema, may also be present.

Schematic illustration of clubbing.

      Cyanosis

      This is a bluish discolouration of the skin and mucous membranes that results from an excessive amount of reduced (deoxygenated) haemoglobin (usually >5 g/dL in patients of European descent; the sign may be harder to detect in darker skin). As it relates to the quantity of deoxygenated blood rather than the proportion, it follows that it will be more readily observed in those with polycythaemia than anaemia. Central cyanosis is best seen on the tip of the tongue and is the cardinal sign of hypoxaemia, although it is not a sensitive sign because it is not usually detectable until the oxygen saturation has fallen to well below 85%, corresponding to a PO2 of <8 kPa (60 mmHg). Because of the poor sensitivity of cyanosis, it is essential to measure oxygenation by oximetry or arterial blood gas sampling in patients at risk for hypoxaemia. Peripheral cyanosis will be present if there is central cyanosis, but it may also be caused by local circulatory slowing in the peripheries, resulting in more complete extraction of oxygen from the blood (e.g. blue hands and ears in cold weather).

      Chest

      Ask the patient to undress to the waist and examine the chest in a methodical way: inspection, palpation, percussion and auscultation.

      Tip: in isolation, a particular finding (e.g. percussion note or breath sound) is often difficult to call as normal or abnormal. Difference is much easier to detect. Remember: the only reason we have two lungs is to allow doctors to compare one side with the other. Make full use of that fact on examination of the chest.

       Inspection

      When airway obstruction is present, tidal breathing occurs at a higher lung volume; in part, this is an unconscious attempt to hold the airways open. This hyperinflation can be even more pronounced if the obstruction is due to emphysema, when the loss of lung elastic recoil allows the chest wall to find its neutral