The general principles of physical examination

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Chapter 3 The general principles of physical examination

Students beginning their training in physical examination will be surprised at the formal way this examination is taught and performed.1,2 There are, however, a number of reasons for this formal approach. The first is that it ensures the examination is thorough and that important signs are not overlooked because of a haphazard method.3 The second is that the most convenient methods of examining patients in bed, and for particular conditions in various other postures, have evolved with time. By convention, patients are usually examined from the right side of the bed, even though this may be more convenient only for right-handed people. When students learn this, they often feel safer standing on the left side of the bed with their colleagues in tutorial groups, but many tutors are aware of this device, particularly when they notice all students standing as far away from the right side of the bed as possible.

It should be pointed out here that there is only limited evidence-based information concerning the validity of clinical signs. Many parts of the physical examination are performed as a matter of tradition. As students develop their examination skills, experience and new evidence-based data will help them refine their use of examination techniques. We have included information about the established usefulness of signs where it is available, but have also included signs that students will be expected to know about despite their unproven value.

For clinical viva voce (with live voice) examinations and objective structured clinical examinations (OSCEs), the examiners expect all candidates to have a polished and thorough examination method.

This formal approach to the physical examination leads to the examination of the parts of the body by body system. For example, examination of the cardiovascular system, which includes the heart and all the major accessible blood vessels, begins with positioning the patient correctly. This is followed by a quick general inspection and then, rather surprisingly for the uninitiated, seemingly prolonged study of the patient’s fingernails. From there, a set series of manoeuvres brings the doctor to the heart. This type of approach applies to all major systems, and is designed to discover peripheral signs of disease in the system under scrutiny. The attention of the examining doctor is directed particularly towards those systems identified in the history as possibly being diseased, but of course proper physical examination requires that all the systems be examined.

The danger of a systematic approach is that time is not taken to stand back and look at the patient’s general appearance, which may give many clues to the diagnosis. Doctors must be observant, like a detective (Conan Doyle based his character Sherlock Holmes on an outstanding Scottish surgeon).4 Taking the time to make an appraisal of the patient’s general appearance, including the face, hands and body, conveys the impression to the patient (and to the examiners) that the doctor or student is interested in the person as much as the disease. This general appraisal usually occurs at the bedside when patients are in hospital, but for patients seen in the consulting room it should begin as the patient walks into the room and during the history taking, and continue at the start of the physical examination.

Diagnosis has been defined as ‘the crucial process that labels patients and classifies their illnesses, that identifies (and sometimes seals) their likely fates or prognoses and that propels us towards specific treatments in the confidence (often unfounded) that they will do more good than harm’.5

In normal clinical practice, the detail of the physical examination performed will be ‘targeted’ and will depend on clues from the history and whether the consultation is a follow-up or new consultation. Students however must know how to perform a complete examination of the body systems even though they will not often perform this in practice (except perhaps during examinations).

Facies

A specific diagnosis can sometimes be made by inspecting the face, its appearance giving a clue to the likely diagnosis. Other physical signs must usually be sought to confirm the diagnosis. Some facial characteristics are so typical of certain diseases that they immediately suggest the diagnosis, and are called the diagnostic facies (Table 3.1 and Figure 3.2). Apart from these, there are several other important abnormalities that must be looked for in the face.

TABLE 3.1 Some important diagnostic facies

Amiodarone (anti-arrhythmic drug)—deep blue discoloration around malar area and nose
Acromegalic (page 307)
Cushingoid (page 309)
Down syndrome (page 314)
Hippocratic (advanced peritonitis)—eyes are sunken, temples collapsed, nose is pinched with crusts on the lips and the forehead is clammy (page 27)
Marfanoid (page 50)
Mitral (page 57)
Myopathic (page 391)
Myotonic (page 392)
Myxoedematous (prolonged hypothyroidism) (page 305)
Pagetic (page 320)
Parkinsonian (page 396)
Ricketic (page 314)
Thyrotoxic (page 302)
Turner’s syndrome (page 314)
Uraemic (page 207)
Virile facies (page 315)
image

Figure 3.2 Some important diagnostic facies: (a) myopathic; (b) myotonic

From Mir MA, Atlas of Clinical Diagnosis, 2nd edn. Edinburgh: Saunders, 2003, with permission.

Jaundice

When the serum bilirubin level rises to about twice the upper limit of normal, bilirubin is deposited in the tissues of the body. It then causes yellow discoloration of the skin (jaundice) and, more dramatically, the apparent discoloration of the sclerae. The usual term scleral icterus is misleading, since the bilirubin is actually deposited in the vascular conjunctiva rather than the avascular sclerae. The sclerae (conjunctivae) are rarely affected by other pigment changes. In fact, jaundice is the only condition causing yellow sclerae. Other causes of yellow discoloration of the skin, but where the sclerae remain normal, are carotenaemia (usually due to excess consumption of carotene, often from intemperate eating of carrots or mangoes), acriflavine, fluorescein and picric acid ingestion.

Jaundice may be the result of excess production of bilirubin, usually from excessive destruction of red blood cells (termed haemolytic anaemia), when it can produce a pale lemon-yellow scleral discoloration. Alternatively, jaundice may be due to obstruction to bile flow from the liver, which, if severe, produces a dark yellow or orange tint. Scratch marks may be prominent due to associated itching (pruritus). The other main cause of jaundice is hepatocellular failure. Gilbert’s disease is also a common cause of jaundice. It causes a mild elevation of unconjugated bilirubin and is due to an inherited enzyme deficiency that limits bilirubin conjugation; it has a benign prognosis.

Jaundice is discussed in detail in Chapter 6.

Cyanosis

This refers to a blue discoloration of the skin and mucous membranes; it is due to the presence of deoxygenated haemoglobin in superficial blood vessels. The haemoglobin molecule changes colour from blue to red when oxygen is added to it in the lungs. If more than about 50 g/L of deoxygenated haemoglobin is present in the capillary blood, the skin will have a bluish tinge.7 Cyanosis does not occur in anaemic hypoxia because the total haemoglobin content is low. Cyanosis is more easily detected in fluorescent light than in daylight.

Central cyanosis means that there is an abnormal amount of deoxygenated haemoglobin in the arteries and that a blue discoloration is present in parts of the body with a good circulation, such as the tongue. This must be distinguished from peripheral cyanosis, which occurs when the blood supply to a certain part of the body is reduced and the tissues extract more oxygen than normal from the circulating blood: for example, the lips in cold weather are often blue, but the tongue is spared. The presence of central cyanosis should lead one to a careful examination of the cardiovascular (Chapter 4) and respiratory (Chapter 5) systems (see also Table 3.2).

TABLE 3.2 Causes of cyanosis

Central cyanosis

Peripheral cyanosis

Pallor

A deficiency of haemoglobin (anaemia) can produce pallor of the skin and should be noticeable, especially in the mucous membranes of the sclerae if the anaemia is severe (less than 70 g/L of haemoglobin). Pull the lower eyelid down and compare the colour of the anterior part of the palpebral conjunctiva (attached to the inner surface of the eyelid) with the posterior part where it reflects off the sclera. There is usually a marked difference between the red anterior and creamy posterior parts (see Figure 13.3a, page 425). This difference is absent when significant anaemia is present. Although this is at best a crude way of screening for anaemia, it can be specific (though not sensitive) when anaemia is suspected for other reasons as well (Good signs guide 3.1). It should be emphasised that pallor is a sign, while anaemia is a diagnosis based on laboratory results.

image

Figure 3.3 Fagan’s nomogram for interpreting a diagnostic test result

Adapted from Sackett DL, Richardson WS, Rosenberg W, Haynes RB. Evidence-based medicine: how to practice and teach EBM. Churchill-Livingstone: London, 1997.

Good signs guide 3.1 Anaemia

Sign Positive LR* Negative LR
Pallor at multiple sites 4.5 0.7
Facial pallor 3.8 0.6
Palm crease pallor 7.9 NS
Conjunctival pallor 16.7

NS = not significant.

* Positive likelihood ratio: when the finding is present, describes the probability change. The higher the LR is above 1, the more likely there is disease.

Negative likelihood ratio: when the finding is absent, describes the probability change. The closer the LR is to 0, the more likely there is not disease.

From McGee S, Evidence-based physical diagnosis, 2nd edn. St Louis: Saunders, 2007.

Facial pallor may also be found in shock, which is usually defined as a reduction of cardiac output such that the oxygen demands of the tissues are not being met (Table 3.3). These patients usually appear clammy and cold and are significantly hypotensive (have low blood pressure) (page 27). Pallor may also be a normal variant due to a deep-lying venous system and opaque skin.

TABLE 3.3 Causes of shock

3 Massive pulmonary embolus 4 Sepsis, e.g. gram-negative bacteria (endotoxin) 5 Anaphylaxis 6 Endocrine failure, e.g. adrenal failure, hypothyroidism 7 Neuropathic—from drugs (e.g. antihypertensives, anaesthesia), spinal cord injury of autonomic neuropathy

Hair

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