FIRST IMPRESSIONS

The examination commences as the patient walks into the consulting room or as you sit down at the bedside to take a history. At this first encounter, even before you initiate the history, decide whether the patient looks well or not and whether there is any striking physical abnormality. You will also gain an immediate impression of dress, grooming and personal hygiene.

As the patient approaches you in the consulting or examination room, observe the posture, gait and character of the stride. Diseases of nerves, muscles, bones and joints are associated with abnormal gaits and postures. You should quickly recognise the slow shuffling gait and ‘pill rolling’ tremor of Parkinson’s disease or the unsteady broad-based gait of the ataxic patient. Patients with proximal muscle weakness may have difficulty rising from the waiting room chair and their gait may have a waddling appearance. Patients with osteoporosis lose height as the vertebrae progressively collapse: you may be struck by the typically stooped (kyphotic) appearance and ‘round shoulders’ of these patients. Take note if the patient walks with a stick or some form of additional physical support. A white stick indicates partial or complete blindness. The gait also conveys body language: the patient may have a spring in the step, make rapid eye contact and immediately offer a firm handshake. This contrasts with the patient with drooping shoulders and a slow (but otherwise normal) step who avoids eye contact.

When making your initial acquaintance with the patient, a warm handshake serves a number of functions (Fig. 2.1). The touching of hands may reassure the patient and serve as a gentle and symbolic introduction to the more intimate physical contact of the examination that follows the history. Before shaking hands, glance momentarily at the hand to ensure that you will not be grabbing a prosthesis or deformed hand. A well-made prosthesis may cause considerable embarrassment as you suddenly realise that the hand you are shaking is hard and lifeless. You may also note other abnormalities such as a potentially painful rheumatoid hand or missing fingers. The grip of the handshake usually provides some useful information. A normal grip conveys different information from a weak, lethargic handshake, which may imply distal muscle weakness, general ill-health or depression. The handshake is a useful physical sign in patients with myotonia dystrophica, a rare autosomal dominant inherited disease of muscle. A feature of this disease is the abnormally slow relaxation of the grip on completion of the handshake. The syndrome is also characterised by premature frontal balding, testicular atrophy and cataracts.

Fig. 2.1 The handshake serves as a gentle introduction to the physical contact that will occur during the formal physical examination.

On first contact with the patient, you may be struck by an unusual physical stature. Unusually short stature may reflect constitutional shortness, a distinct genetic syndrome or the consequence of intrauterine, childhood or adolescent growth retardation. Unusually tall stature is most often constitutional, although hypothalamic tumours in childhood or adolescence may cause excessive growth hormone release, resulting in abnormally rapid linear growth and gigantism. If excess growth hormone release occurs after the bony epiphyses have fused, body shape changes (acromegaly). Severe malnutrition and obesity are readily recognised on the first encounter with a patient.

In hospitalised patients, posture may provide helpful information. Patients with acute pancreatitis find some relief lying with knees drawn towards the chest. Patients with peritonitis lie motionless, as any abdominal wall movement causes intense pain. The pain of acute pyelonephritis or perinephric abscess might be partly relieved by lateral flexion to the side of the pathology. In acute pericarditis, the patient finds modest relief by sitting forward; and in left ventricular failure, patients breath more easily when lying propped up on three or four pillows (this is termed orthopnoea).

SETTING

A separate examination room or adequate screening should be provided to ensure privacy while the patient is undressing and being examined. The room should be comfortably warm. Ensure that there are fresh sheets (either linen or disposable) and a clean blanket for cover. The examination couch should be positioned to allow you to examine from the patient’s right side and there must be good general illumination. You should be fully equipped to undertake the examination without disruption. Ensure you have a working penlight torch and stethoscope. Close at hand there must be a sphygmomanometer, ophthalmoscope, otoscope, tongue depressors and disposable gloves (for genital and rectal examination). Basic equipment for the neurological examination should be available. This includes a patellar hammer, tuning fork, cotton wool buds, an appropriate object for testing pin-prick responses, test tubes to fill with hot and cold water for temperature testing, and hat pins with red and white tops to assess visual fields. A cupful of drinking water should also be available, as you may ask the patient to swallow a mouthful to check for a thyroid goitre or other neck swelling.

As you approach the patient, re-establish both verbal and eye contact. You may ask the patient whether they feel comfortable and are prepared for the examination. Start the examination with the patient supine and the head and shoulders raised to approximately 45° above the horizontal. Most modern examination couches and hospital beds are designed to allow easy adjustment of the upper body. Most of the examination takes place with the patient comfortably resting in this position (Fig. 2.2). Three further adjustments will be made in the course of the examination. When auscultating the mitral area of the heart it is helpful to roll the patient towards the left lateral position as this brings the apex closer to the stethoscope. To examine the neck, posterior chest, back and spine you will ask the patient to sit forward. For assessing the abdomen, reposition the patient to lie flat, as this provides optimal access for the abdominal examination. Plan the examination to ensure the most economical movements for both you and the patient.

Fig. 2.2 The position of the patient at the start of the examination.

Following the history, reflect on which physical signs may help you confirm or refine your initial assessment. Anticipation of physical signs will help you to direct and focus the examination. For example, if a patient complains of breathlessness, you may anticipate anaemia or respiratory or cardiac disease, therefore, you should gear the examination towards determining which of these possibilities is responsible for the symptoms.

Begin with an inspection of overall appearance.

THE EYE

The history might be helpful in distinguishing possible causes of the red eye. Ask about duration, previous attacks, pain (and its character), photophobia and possible direct causes of traumatic damage. It is useful to distinguish the sensation of a foreign body from less specific symptoms such as ‘grittiness’ and ‘itching’. A foreign body sensation feels as if there is something in the eye and is associated with some difficulty opening the eye. This symptom is characteristic of an active corneal process causing the red eye.

Begin the examination by inspecting the eyes. In lid and conjunctival disorders, there is no foreign body sensation or photophobia and the patient sits in a brightly lit room without discomfort. In bacterial conjunctivitis the patient complains of pussy discharge (especially in the morning on waking) and this might be seen on inspection. A foreign body sensation (rather than gritty or itchy sensation) is typical of active corneal disease. In infectious keratitis the patient has difficulty keeping the affected eye open, and a similar sign occurs with contact lens abrasion. Patients with iritis may present with difficulty keeping the eye open and some photophobia but without the complaint of a foreign body sensation. In acute angle closure glaucoma the patient often clutches the affected eye and complains of associated headache and malaise. Visual acuity may be affected in red eye and should be assessed. The pinhole test helps distinguish refractive errors from other causes of visual loss. In refractive visual disturbances (e.g. myopia), vision is improved when peering through a small hole. In nonrefractive disorders, improvement does not occur.

Next, use a penlight to inspect the pupils and anterior segment. In angle closure glaucoma the pupil may be fixed in mid-dilation and may not respond to light. In corneal abrasion, acute keratitis and iritis, the pupil might be pinpoint. A purulent discharge suggests bacterial conjunctivitis or keratitis. The pattern of redness might be helpful. Diffuse injection of both the palpebral and bulbar conjunctivae suggests primary conjunctival disorders (bacterial, viral, allergic, toxic or associated with dry eyes). In contrast, more serious disorders such as keratitis, iritis and angle closure glaucoma present with a ‘ciliary flush’ with injection most marked at the limbus (the sclerocorneal junction). A white spot or opacity on the cornea indicates keratitis and further slit-lamp examination with fluorescein is required to delineate the lesion. Hypopyon is seen as a layer of pus in the anterior chamber and is associated with infectious keratitis, acute iritis and endophthalmitis and is an ophthalmic emergency. Hyphaema refers to the presence of a layer of blood in the anterior compartment and is usually caused by injury. Subconjunctival haemorrhage is painless and characterised by demarcated areas of extravasated blood which resolves in 1–2 weeks.

FACIES AND SYNDROMES

Certain diseases are readily identified by a distinctive combination of physical characteristics. There are a large number of recognisable congenital syndromes that were probably diagnosed during childhood and should not present as an undiagnosed problem to physicians caring for teenagers or adults. In addition, only a proportion survives into adulthood. There are several recognisable genetic or chromosomal syndromes that may present to clinicians caring for adults; examples include Down’s syndrome (trisomy 21; Fig. 2.3), Turner’s syndrome (Fig. 2.4), Marfan’s syndrome (Fig. 2.5), tuberous sclerosis (Figs 2.6, 2.7), albinism (Fig. 2.8), the fragile X chromosome (a common genetic cause of mental subnormality in which affected males have unusually large testes), Peutz–Jeghers syndrome (Figs 2.9–2.11), Waardenburg’s syndrome (Fig. 2.12), familial hypercholesterolaemia (Figs 2.13–2.17) and neurofibromatosis. Other readily recognisable syndromes include the endocrine disorders and major organ failure (liver, heart, lungs and kidneys).

Fig. 2.3 Down’s syndrome: epicanthic folds, Brushfield’s spots and hypertelorism (increased interorbital distance).

Fig. 2.4 Turner’s syndrome: typical facial appearance, webbed neck and widely spaced nipples.

Fig. 2.5 Marfan’s syndrome.

Fig. 2.6 Tuberous sclerosis: flecks of white hair.

Fig. 2.7 Tuberous sclerosis: shagreen patch.

Fig. 2.8 Albinism: typical translucent iris.

Fig. 2.9 Peutz–Jeghers syndrome: freckles on lips.

Fig. 2.10 Peutz–Jeghers syndrome: pigmentation of the buccal mucosa.

Fig. 2.11 Peutz–Jeghers syndrome: pigmentation of the big toe.

Fig. 2.12 Waardenberg’s syndrome: typical white forelock.

Fig. 2.13 Familial hypercholesterolaemia: corneal arcus senilis.

Fig. 2.14 Familial hypercholesterolaemia: tendon xanthomas.

Fig. 2.15 Familial hypercholesterolaemia: tendon xanthomas.

Fig. 2.16 Familial hypercholesterolaemia: skin xanthomas.

Fig. 2.17 Familial hypercholesterolaemia: xanthelasmata around the eyelids.

Structure and function

The thyroid gland develops from a ventral pouch of the fetal pharynx. This pouch evolves into the thyroid gland by migrating caudally to a resting place in front of the trachea. The migration may leave thyroid remnants along the embryonic tract which extends from the back of the tongue (where a residual lingual thyroid ‘rest’ may occur). A midline thyroglossal cyst may develop if the migration tract fails to obliterate.

The thyroid gland consists of two lateral lobes joined by an isthmus. The gland lies in front of the larynx and trachea with the isthmus overlying the second to fourth tracheal rings (Fig. 2.19). The lateral lobes extend from the side of the thyroid cartilage to the sixth tracheal ring. Two nerves lie in close proximity to the thyroid gland: the recurrent laryngeal nerve runs in the groove between the trachea and the thyroid; and the external branch of the superior laryngeal nerve lies deep to the upper poles. In thyroid cancer, these nerves may be invaded and damage may occur in the course of thyroid surgery.

Fig. 2.19 Anatomy of the thyroid gland and surrounding structures.

THYROXINE SYNTHESIS AND SECRETION

The anterior pituitary hormone, thyroid stimulating hormone (TSH), stimulates the synthesis of thyroxine (T₄) (Fig. 2.20). The functioning unit of the thyroid is the follicle, which consists of epithelial cells lining a central colloid space. The epithelial cells concentrate iodide, which is oxidised to iodine and incorporated with tyrosine to form mono-iodotyrosine and di-iodotyrosine. These two iodinated tyrosines are combined in the colloid to form either tri-iodothyronine (T₃) or tetra-iodothyronine (T₄). The two active hormones, T₃ and T₄, are stored in the colloid and bound to a specific binding protein (thyroglobulin). The protein-bound hormones are taken back up into the follicle epithelium by endocytosis. In the cells, the colloid droplets are disrupted by proteolytic enzymes, allowing the release of T₃ and T₄ into the circulation where most circulate bound to thyroid binding globulin (TBG). Free hormone levels dictate the metabolic effects of T₄. T₄ is synthesised only in the thyroid but T₃ can also be produced from conversion of circulating T₄ in the liver, the kidney and other tissues. The hepatic conversion of T₄ results in two species of T₃: an active T₃ and an inactive reverse T₃.

Fig. 2.20 The hypothalamus secretes thyroid releasing hormone (TRH) which stimulates the anterior pituitary to produce thyroid stimulating hormone (TSH). This stimulates the synthesis of thyroxine (T₄) in the follicles. Iodide taken up into the follicular cell is oxidised to iodine and then incorporated into tyrosine to form mono-iodotyrosine (MIT) and di-iodotyrosine (DIT), which binds with thyroglobulin and is secreted into the colloid where T₃ and T₄ are synthesised. These are taken back into the follicular cells taken up by endocytosis where the T₃ and T₄ are split from thyroglobulin and released into the circulation, where they are bound to T₄ binding globulin (TBG).

Clinical examination of the thyroid gland and function

Although considered part of the general examination, the thyroid gland is usually examined when examining the head and neck (see Ch. 4).

Like any other organ, the thyroid examination relies on inspection, palpation, percussion and auscultation. Examine the thyroid gland with the patient sitting forward in bed or seated in a chair.

Ensure complete exposure of the neck and upper chest. Inspect the thyroid from the front of the neck. The normal thyroid gland is neither visible nor palpable. An enlarged thyroid, or goitre, is seen as a fullness on either side of the trachea below the cricoid cartilage, or as a distinct, enlarged, nodular organ with one or both lobes easily visible (Figs. 2.21–2.23). If the lobes are visible, determine whether they look symmetrical or irregular. Ask the patient to sip a little water and hold it in the mouth. When you give the instruction to swallow, watch for the characteristic upward movement of the goitre as the pharyngeal muscles contract. This test helps distinguish a thyroid mass from other neck masses (e.g. enlarged lymph nodes, which hardly move with swallowing). The midline remnant of the thyroid (thyroglossal cysts or thyroid remnants) also moves with swallowing.

Fig. 2.21 Smooth goitre appearing as fullness in the anterior neck.

Fig. 2.22 Readily visible multinodular thyroid goitre.

Fig. 2.23 Asymmetrical multinodular goitre.

Next, explain to the patient that you wish to feel the front of the neck for the thyroid gland. Position yourself to the right and slightly behind the patient. Feel for the left and right lobes with the finger pulps of both hands (Fig. 2.24). Ensure a gentle examination, as your hands are positioned in a throttling posture; reassure the patient by standing to the side rather than at the rear so that you remain in the patient’s peripheral field of vision. Assess the texture (hard or soft, single or multiple nodules), symmetry and extent of the goitre. A soft, smooth goitre may be more easily seen than felt. It is unusual for the goitre to be tender unless the enlargement is caused by acute inflammatory thyroiditis. In the course of thyroid palpation, again ask the patient to take a sip of water and to swallow when you indicate. As the patient gulps, you should feel the goitre move beneath your fingers. Complete the palpation by feeling for the carotids, which may be encased by a malignant thyroid gland. Thyroid carcinoma may spread to local neck lymph nodes, so it is important to conclude the palpation by checking for palpable regional lymph nodes.

Fig. 2.24 Position for palpation of the lateral lobes of the isthmus of the thyroid.

The thyroid gland may also enlarge in a downward direction behind the manubrium sterni. This retrosternal goitre may extend deeply into the superior mediastinum and may even cause compression symptoms (i.e. breathlessness and dysphagia). Retrosternal extension can be assessed by percussing over the manubrium and upper sternum (Fig. 2.25). Normally, this area resonates, yet when there is retrosternal enlargement the percussion note is dull. Auscultate the gland for bruits by applying the diaphragm of the stethoscope to each lobe in turn (Fig. 2.26). Ask the patient to stop breathing for a moment while you listen on either side for a bruit. A soft bruit is characteristic of the smooth symmetrical hyperthyroid goitre of Graves’ disease.

Fig. 2.25 A retrosternal goitre is suggested by dullness to percussion over the manubrium sterni.

Fig. 2.26 Auscultation of the thyroid gland.

Clinical assessment of thyroid function

T₄ has a number of important metabolic effects and over- or underactivity results in characteristic clinical syndromes that may readily be recognised. Diagnosis of hyperthyroidism is confirmed by measuring the serum levels of T₄ and T₃, whereas in hypothyroidism the serum TSH level is elevated and T₄ is subnormal.

HYPERTHYROIDISM

Hyperthyroidism occurs most commonly in young women presenting with smooth diffuse goitres (Graves’ disease). However, in elderly people, hyperthyroidism may be caused by an autonomous ‘toxic’ adenoma and, rarely, a functioning carcinoma. Rarely factitious hyperthyroidism caused by excessive T₄ intake masquerades as classical hypothyroidism. In both young and older thyrotoxic patients, you may be alerted to the diagnosis by a history of weight loss, recent intolerance to hot weather, sweating, palpitations, abnormal irritability and nervousness and increased bowel frequency. Most hyperthyroid patients feel warm and sweaty, have a tachycardia, staring eyes (caused by lid retraction) and abnormally brisk tendon reflexes. A fine peripheral tremor is common in thyrotoxicosis. This can be demonstrated by placing a sheet of paper on the back of the outstretched hand and watching the tremor, which is amplified by the sheet of paper ‘trembling’ (Fig. 2.27). Although similar signs of hyperthyroidism may occur in the young and old, Graves’ disease is more readily recognisable from the characteristic facial appearance and associated physical signs.

Fig. 2.27 Place a sheet of paper on the outstretched fingers to demonstrate the fine tremor of hyperthyroidism.

GRAVES’ DISEASE

The facies in Graves’ disease is dominated by a staring appearance caused by retraction of the upper eyelid. Normally, during a relaxed forward gaze, the upper lid protects the eye by lying in a horizontal position which crosses the eye in a plane just above the upper pole of the pupil. In Graves’ disease, autonomic overactivity causes increased tone and spasm of levator palpebrae superioris. This causes retraction of the upper lid, which exposes most, if not all, of the iris, exposing sclera above the iris and creating the typical staring appearance (Fig. 2.28). Spasm of the muscles supplying the upper lid also results in an abnormal following reflex. Normally, if you ask a patient to follow the movement of an object (e.g. your fingertip) (Fig. 2.29) from a point above eye level to a vertical point below eye level, you will note that as the eye moves, the upper lid follows the upper margin of the pupil in a fully synchronised downward movement. In hyperthyroidism, this coordination is lost and the movement of the upper lid lags well behind the pupil (this is termed ‘lid lag’) (Fig. 2.30).

Fig. 2.28 Bilateral lid retraction in a patient with Graves’ disease. Note that the upper lid is positioned well above the pupil and the palpebral fissure is widened.

Fig. 2.29 Lid lag. With the patient sitting, position yourself on the patient’s right side. Watch how the lid moves with the downward movement of the eye as the patient follows your finger moving from a point approximately 45° above the horizontal to a point below this plane. Normally there is perfect coordination as the lid follows the downward movement of the eye.

Fig. 2.30 In hyperthyroidism the downward movement of the lid lags behind the movement of the bulb as it follows your finger through an arc.

In progressive Graves’ disease, abnormal connective tissue (especially hyaluronic acid) is deposited in the orbit and external ocular muscles. The globes are pushed forward, resulting first in proptosis and in the more severe form, exophthalmos (defined as >18  mm protrusion). To examine for exophthalmos, seat the patient in a chair and inspect the globes from above by looking over the forehead or from the side of the profile (Fig. 2.31). A Hertel exophthalmometer can be used to make an accurate baseline measurement of the degree of exophthalmos and this measurement is used to monitor progression and regression. Other eye signs of Graves’ disease include ophthalmoplegia caused by weakness and infiltration of the external ophthalmic muscles. These patients complain of double vision (diplopia) and on examination there is a loss of gaze symmetry. Conjunctival oedema (chemosis) may also occur. The eye signs can be either bilateral or unilateral (Fig. 2.32), although, in the latter, always consider a space-occupying lesion of the orbit. Other features of Graves’ disease include finger clubbing, onycholysis (separation of the nail from its bed), pretibial myxoedema (brawny swelling of lower legs), and periostitis (inflammation of the periosteum).

Fig. 2.31 Graves’ disease: proptosis of the eye.

Fig. 2.32 Graves’ disease: unilateral eye condition.

A rare complication of hyperthyroidism is thyroid storm. This is an exaggerated manifestation of hyperthyroidism and is life threatening. While thyroid storm can develop in patients with longstanding untreated hyperthyroidism, it is more often precipitated by an acute event such as thyroid or nonthyroid surgery, trauma, infection or an acute iodine load.

Symptoms and signs

Graves’ disease (autoimmune hyperthyroidism)

• Diffuse goitre with audible bruit

Only gold members can continue reading. Log In or Register to continue

Share this:

• Click to share on Twitter (Opens in new window)
• Click to share on Facebook (Opens in new window)

Like this:

Like Loading...

Related

Related posts:

1. medical history and record taking
2. male genitalia
3. abdomen
4. joints and muscle

Stay updated, free articles. Join our Telegram channel

Join