By Dr. Marcus Judge

OSCE

During any examination in an OSCE it is important to understand the pathology and reasoning behind each of the signs and symptoms elicited. This applies even if the patient being examined is ‘normal’. This article explains how to perform a Cushing’s syndrome examination and the key findings you should look for, showing you what each sign means and what conditions it may indicate.

Cushing’s syndrome is the clinical state that results from prolonged exposure to excess glucocorticoid (cortisol). The commonest cause overall is exogenous (from outside the body): long-term treatment with corticosteroid medication. Endogenous causes (the body makes too much cortisol itself) are divided into two groups. ACTH-dependent disease involves too much adrenocorticotropic hormone (ACTH), the pituitary hormone that drives the adrenal glands to make cortisol. It is most often caused by a pituitary adenoma (a benign gland tumour) secreting ACTH, termed Cushing’s disease, or by ectopic ACTH (made by a tumour outside the pituitary gland, such as a small-cell lung cancer). ACTH-independent disease is caused by a cortisol-secreting adrenal adenoma or carcinoma. Because cortisol acts on almost every tissue, the signs are widespread, which is why a structured head-to-toe approach is so useful.

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° and expose appropriately. You will need to see the face, neck, arms, trunk and lower legs. To do this, 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 (overall body build and shape) 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 (a rounded, plethoric facial appearance, meaning red and flushed) 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). Iatrogenic steroid use (caused by medical treatment) 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. 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 (weakness of the muscles nearest the trunk, such as the shoulders and hips) or a fragility fracture (a bone broken by a minor fall or knock) 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. Psychiatric features such as depression, emotional lability (rapid, exaggerated mood swings) and even psychosis (loss of contact with reality, such as hallucinations or delusions) are well recognised. A flat affect (little visible emotional expression) at the bedside is a genuine clue rather than incidental.

Cushing's Syndrome Body Habitus SimpleMed

Image - Truncal changes in a patient with iatrogenic Cushing’s syndrome, demonstrating hirsutism (excess coarse hair) and purplish abdominal striae (stretch marks) 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. These suggest the patient is monitoring capillary blood glucose, which 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 (the deeper layer of the skin) becomes atrophic (thinned). 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 (darker skin than normal), 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 (the skin cells that make pigment). 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 these, 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. Weakness of the shoulder girdle is therefore 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 because cortisol makes the blood vessels tighten more strongly in response to adrenaline and similar hormones (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 (male-type sex hormone) production. Prominent virilisation (development of male features in a woman, such as a deep voice) should raise concern about an adrenal carcinoma, which can co-secrete androgens.

Briefly examine the eyes and mouth. Chronic glucocorticoid exposure is associated with cataracts (clouding of the lens of the eye) and a raised intraocular pressure (the pressure inside the eye), which can progress to glaucoma (damage to the optic nerve). Steroids also predispose to oral candidiasis (oral thrush) because of relative immunosuppression (weakened immune defences). 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 (comparing the patient’s field of vision with your own while facing them), screening each eye for a bitemporal hemianopia (loss of the outer half of vision in both eyes). This is relevant because the commonest endogenous cause, Cushing’s disease, is a pituitary adenoma (a benign tumour of the gland). Most of these tumours are small (under 10 mm) and do not press on the optic chiasm, so a normal result is usual. If a larger 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. A larger tumour may also cause persistent headache, so it is worth asking about this when the bedside findings point towards Cushing’s disease.

Inhaled or topical steroids and injected steroids, not only systemic tablets, can cause the same facial features, particularly at higher doses and with longer use. The dose, route and duration of any steroid therapy are therefore 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 (fat moving towards the centre of the body) 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. 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. 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, ask about reduced libido, because cortisol excess often lowers testosterone (a state called hypogonadism). Gynaecomastia (enlargement of the breast tissue) is not a typical feature of Cushing’s syndrome. If you find it, think of another cause, for example a very rare oestrogen-secreting adrenal carcinoma. Ask too about galactorrhoea (inappropriate milky nipple discharge). It is not a typical feature of Cushing’s syndrome either. It points to a raised level of prolactin (the pituitary hormone that stimulates milk production), for example from a prolactin-secreting pituitary tumour (a prolactinoma). It therefore needs separate assessment and is not a pointer towards a pituitary rather than an adrenal cause of Cushing’s syndrome.

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. Consider scars over the flanks (which might follow adrenal surgery) or a trans-sphenoidal approach (surgery through the nose to reach the pituitary gland) for pituitary disease. 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 you exposed 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 (low blood potassium with blood that is too alkaline).

Finally, look at the lower legs and feet for evidence of poor healing, such as chronic ulcers or longstanding bruises. Also look 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.

Pitting Oedema SimpleMed

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 with the patient seated, as hypertension is common (add lying and standing readings if the patient has dizziness or falls on standing).
  • Check a capillary blood glucose and send HbA1c (glycated haemoglobin, a measure of average blood glucose over the past two to three months), 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 (to look for glucose, which suggests diabetes if present in the urine) and request relevant bedside observations, such as pulse, temperature and weight.
  • Take a focused history, paying particular attention to corticosteroid use, weight gain, low mood, reduced libido and menstrual changes.

First-line investigations confirm cortisol excess before you look for its cause. Exogenous glucocorticoid use is excluded first. The options are an overnight dexamethasone suppression test (a dose of dexamethasone is taken at night, and in healthy people cortisol falls by the next morning), late-night salivary cortisol (cortisol measured in a saliva sample taken late at night, when levels are normally low) or a 24-hour urinary free cortisol collection (all the urine passed in a day is collected and its cortisol measured). Each of these tests can give false-positive and false-negative results, so a positive result is repeated or confirmed with a second test, and specialist (endocrinology) advice is sought. Measuring plasma ACTH then separates ACTH-dependent from ACTH-independent disease, and imaging is used to localise the cause.

Quiz

Preview the Cushing's Syndrome OSCE Examination quiz

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