Cushing's Syndrome OSCE Examination

Contents

1. Introduction
2. General Inspection
3. Hands and Arms
4. Face
5. Neck and Upper Back
6. Chest and Trunk
7. Proximal Myopathy
8. Legs and Oedema
9. Completing the Examination
10. Quiz

Introduction

Wash your hands and don personal protective equipment if appropriate.

Introduce yourself to the patient, giving your name and grade e.g. 3rd year medical student/junior doctor/consultant.

Confirm the patient’s details, taking 3 points of identification; full name, date of birth and NHS/hospital number.

Briefly explain the examination in patient-friendly language and obtain consent to proceed.

Ask whether the patient has any pain anywhere before you begin.

Position the patient on the bed at 45^o and expose appropriately. You will need to see the face, neck, arms, trunk and lower legs, so expose the chest and abdomen and roll up the trouser legs while maintaining the patient’s dignity throughout.

General Inspection

A great deal can be gathered from the end of the bed before you lay a hand on the patient. Look for the characteristic body habitus of cortisol excess: central (truncal) obesity with relatively thin limbs. This pattern occurs because glucocorticoids redistribute fat centrally while promoting proximal muscle breakdown (a catabolic effect), giving the classic ‘lemon on matchsticks’ appearance.

Note any obvious moon face (rounded, plethoric facial appearance) and a buffalo hump (a fat pad over the upper back and lower neck). Look around the bedside for clues to the underlying cause, particularly corticosteroid medication (for example inhalers, eye drops or tablets such as prednisolone), as iatrogenic steroid use is the single most common cause of the syndrome.

Glance for objects that point to the metabolic complications of cortisol excess, such as a capillary blood glucose monitor, insulin pen or sugary drinks, since glucocorticoids drive insulin resistance and frequently unmask diabetes mellitus. A walking stick or frame at the bedside is also worth noting, as it may reflect the proximal myopathy or a fragility fracture from steroid-induced osteoporosis.

Assess whether the patient appears comfortable and well, or is in distress. Also take a moment to note mobility aids or signs of difficulty moving, which may hint at the proximal myopathy assessed later. Patients with chronic cortisol excess may also appear low in mood or anxious, as psychiatric features such as depression, emotional lability and even psychosis are well recognised; a flat affect at the bedside is a genuine clue rather than incidental.

Image - Truncal changes in a patient with iatrogenic Cushing’s syndrome, demonstrating hirsutism and purplish abdominal striae caused by glucocorticoid excess

Creative commons source by Celik O, Niyazoglu M, Soylu H, Kadioglu P [CC BY 2.5 (https://creativecommons.org/licenses/by/2.5)]

Hands and Arms

Begin the close examination at the hands. Look first for finger-prick marks on the fingertips, which suggest the patient is monitoring capillary blood glucose and points towards the diabetes mellitus that cortisol-driven insulin resistance commonly produces. The skin may appear thin and fragile; cortisol inhibits fibroblasts and reduces collagen synthesis, so the dermis becomes atrophic. As a direct consequence, the skin bruises easily, and you may see spontaneous bruising on the forearms with little or no history of trauma. This combination of thin skin and easy bruising is one of the most discriminating signs of Cushing’s syndrome.

Look for hyperpigmentation, particularly in the skin creases of the palms and over any scars. Pigmentation suggests very high circulating ACTH, because ACTH is derived from the same precursor molecule (proopiomelanocortin) as melanocyte-stimulating hormone, so when ACTH is grossly elevated it also stimulates melanocytes. Marked pigmentation therefore points towards an ACTH-dependent cause, especially ectopic ACTH secretion (where ACTH levels are often highest), rather than an adrenal tumour or exogenous steroids, in both of which ACTH is typically suppressed and pigmentation is absent.

Inspect the arms for wasting of the muscle bulk and for striae – broad, purple/violaceous stretch marks. Striae form when the weakened, thinned skin is stretched over enlarging fat deposits and tears, exposing the vascular dermis beneath; the breadth (often more than 1 cm) and dark colour help distinguish them from the pale, narrow striae of ordinary weight gain or pregnancy. You may also notice thin, papery skin on the back of the hands and forearms with prominent superficial veins, again reflecting dermal atrophy.

Assess for a proximal myopathy by testing power at the shoulders, asking the patient to hold their arms out and resist as you push down. Glucocorticoids are catabolic and preferentially break down the type II (fast-twitch) fibres of the proximal muscles, so weakness of the shoulder girdle is characteristic while distal grip strength is usually preserved.

Palpate the radial pulse to assess the rate and rhythm. At this point it is good practice to offer to measure the blood pressure, as hypertension is one of the most consistent features of Cushing’s syndrome: it arises both from the mineralocorticoid effect of excess cortisol (sodium and water retention) and from cortisol’s potentiation of the vasoconstrictor response to catecholamines.

Face

Inspect the face for the classic moon facies – a rounded, full face produced by fat deposition in the cheeks and temporal regions. The cheeks often have a plethoric (reddened) appearance, called facial rubor, owing to thinning of the overlying skin and an increased red cell mass.

Look for acne and, in women, hirsutism (excess coarse hair in a male pattern, for example on the upper lip and chin). These features reflect the fact that adrenal pathology, and ACTH stimulation of the adrenal cortex, can also drive androgen production. Prominent virilisation should raise concern about an adrenal carcinoma, which can co-secrete androgens.

Briefly examine the eyes and mouth. Cushing’s syndrome is associated with cataracts and a raised intraocular pressure (glaucoma), both recognised consequences of chronic glucocorticoid exposure, and steroids also predispose to oral candidiasis (oral thrush) because of relative immunosuppression, so inspect the tongue and palate for the white plaques of thrush, and check the gums and dentition. While inspecting the mouth, look also for hyperpigmentation of the buccal mucosa, which, as in the palms, points to markedly raised ACTH.

Test the visual fields by confrontation, screening each eye for a bitemporal hemianopia. This is relevant because the commonest endogenous cause, Cushing’s disease, is a pituitary adenoma; if the tumour enlarges upwards it compresses the optic chiasm, where the nasal retinal fibres (carrying the temporal visual fields) cross, producing loss of the outer halves of vision in both eyes. For the same reason, a patient with a pituitary cause may volunteer a history of persistent headache, so it is worth asking about this when the bedside findings point towards Cushing’s disease.

If the patient is being treated for an endocrine condition, it is worth remembering that the same facial features can also be seen with inhaled or topical steroids, not only systemic tablets, so the dose and route of any steroid therapy is highly relevant when interpreting these signs.

Neck and Upper Back

Examine the lower neck and shoulders for the interscapular fat pad, commonly known as the buffalo hump, and for supraclavicular fat pads that fill in the normal hollows above the collarbones. These represent the centripetal fat redistribution typical of glucocorticoid excess and, like the moon face, are among the most recognisable features of the syndrome.

Inspect the upper spine from the side for a thoracic kyphosis (an exaggerated forward curve of the upper back). Glucocorticoids cause osteoporosis, and the resulting vertebral wedge fractures collapse the front of the vertebral bodies, tipping the spine forward; a new kyphosis or loss of height is therefore an important clue to the bony effects of cortisol excess.

The fat pads are the key findings here, but while at the neck it is reasonable to glance at the jugular venous pressure and the thyroid as part of a complete endocrine assessment.

Chest and Trunk

Inspect the chest and abdomen. The truncal obesity seen from the end of the bed becomes more obvious here, and the abdomen is frequently the best site to appreciate striae. On the trunk these stretch marks are typically wide and purple, running across the abdomen and flanks, again reflecting the combination of thin skin and central fat accumulation.

In men, look for gynaecomastia (enlargement of the breast tissue). This can arise when the cortisol pathway is grossly overactive: in some tumours the excess steroid drive disturbs the normal balance between androgens and oestrogens, tipping it towards oestrogen effect on the breast. Ask too about galactorrhoea (inappropriate milky nipple discharge), which can accompany Cushing’s disease: a pituitary tumour, or its pressure on the stalk, may also disturb prolactin regulation, so this symptom is another pointer towards a pituitary rather than an adrenal cause.

Look for any signs of infection or poorly healing wounds. Cortisol suppresses the immune response and impairs wound healing, so patients may have frequent or persistent skin infections and fungal infections in the skin folds. This relative immunosuppression is clinically important because it can mask the signs of serious infection, so a high index of suspicion is needed in unwell patients.

Where there are previous surgical scars, note any that are slow to heal or pigmented, and consider scars over the flanks (which might follow adrenal surgery) or a trans-sphenoidal approach for pituitary disease, as these give clues to a known underlying cause and its treatment.

Proximal Myopathy

A focused test for proximal muscle weakness is a high-yield part of this examination. Ask the patient to stand up from a sitting position with their arms folded across their chest. Folding the arms prevents them from pushing up on the chair or their thighs to compensate, so the manoeuvre genuinely tests the hip and thigh muscles.

Difficulty rising, or needing several attempts, indicates a proximal myopathy. This occurs because glucocorticoids are catabolic to skeletal muscle, preferentially wasting the large proximal muscle groups of the limb girdles. The same process can be demonstrated at the shoulders, and patients often report difficulty climbing stairs, rising from a low chair or brushing their hair.

It is also worth remembering that cortisol excess drives osteoporosis, so these patients are at increased risk of fragility fractures – another reason their functional mobility matters.

Legs and Oedema

Examine the lower legs, which is why exposure of the legs was arranged at the start. As in the arms, look for thin skin, bruising and striae, and assess the bulk and power of the proximal leg muscles at the hips, where wasting is often most pronounced.

Press firmly over the shins or ankles for a few seconds to check for pitting oedema. Cortisol has weak mineralocorticoid activity, and when present in large amounts it overwhelms the enzyme that normally protects the mineralocorticoid receptor, acting on the kidney to promote sodium and water retention. This contributes both to oedema and to the hypertension seen in this syndrome. In severe or ectopic ACTH-driven disease, the same mineralocorticoid effect drives potassium loss and can cause a hypokalaemic metabolic alkalosis.

Finally, look at the lower legs and feet for evidence of poor healing, such as chronic ulcers or longstanding bruises, and for skin that is so thin it has torn over the shin. These findings reinforce the impression of glucocorticoid excess and are a reminder that these patients heal slowly and are prone to infection.

Image - Pitting oedema, demonstrated by an indentation that remains after firm pressure. The mineralocorticoid action of excess cortisol promotes sodium and water retention, contributing to oedema in Cushing’s syndrome

SimpleMed original image, credit 'SimpleMed original'

Completing the Examination

Thank the patient and allow them to dress, then wash your hands.

Summarise your findings and offer a differential, distinguishing where possible between an exogenous (iatrogenic) cause, an ACTH-dependent cause (pituitary or ectopic) and an ACTH-independent adrenal cause.

To complete the examination, state that you would:

• Perform a full cardiovascular examination and measure the blood pressure (lying and standing), as hypertension is common.
• Check a capillary blood glucose and send HbA1c, since glucocorticoids promote insulin resistance and may cause diabetes mellitus.
• Send urea and electrolytes, looking in particular for a hypokalaemia driven by the mineralocorticoid effect of excess cortisol.
• Perform a urine dipstick (for glucose) and request relevant bedside observations.
• Take a focused history, paying particular attention to corticosteroid use, weight gain, low mood, reduced libido and menstrual changes.

Appropriate first-line investigations to confirm cortisol excess include an overnight dexamethasone suppression test, late-night salivary cortisol, or a 24-hour urinary free cortisol collection, followed by measurement of plasma ACTH and further imaging to localise the cause.

Quiz

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