Cushing’s Syndrome Examination – OSCE Guide

This guide discusses how to approach performing a focused examination of a patient with Cushing’s syndrome in an OSCE setting.
Download the Cushing’s syndrome examination PDF OSCE checklist, or use our interactive OSCE checklist. You may also be interested in our guide to Cushing’s syndrome.
In OSCE scenarios, you may be asked to perform a focused examination to determine the presence (or absence) of a certain condition. It is important to be able to confidently elicit the main diagnostic signs of the condition.

Background
Cushing’s syndrome is a hormonal disorder that results from prolonged exposure to high levels of glucocorticoids.
The most common cause of Cushing’s syndrome is exogenous glucocorticoid use (e.g. prednisolone).
Endogenous Cushing’s syndrome can be classified into adrenocorticotropic hormone (ACTH) dependent or ACTH-independent causes.
ACTH-dependent
In ACTH-dependent Cushing’s syndrome, high ACTH levels stimulate the adrenal glands to produce glucocorticoids.
80% of ACTH-dependent Cushing’s syndrome is due to pituitary adenomas (also known as Cushing’s disease).
Less commonly, it is caused by ectopic ACTH production from bronchogenic (small cell lung cancer) or neuroendocrine tumours.1
ACTH-independent
In ACTH-independent Cushing’s syndrome, excess glucocorticoid secretion from the adrenal glands occurs despite low ACTH levels.
This is often due to adrenal adenomas and, less commonly, bilateral adrenal hyperplasia or adrenal carcinoma.1
Clinical features of Cushing’s syndrome
Clinical features of Cushing’s syndrome include:

Truncal obesity
Buffalo hump
Supraclavicular fat pads
Moon facies
Proximal muscle wasting
Bruising
Peripheral oedema
Acne
Headaches, visual field defects and galactorrhoea (in Cushing’s disease due to a pituitary adenoma)

Cushing’s syndrome can cause various complications, including hypertension, osteoporosis, diabetes mellitus, cataracts and myopathy.
Specific clinical features of excess ACTH (such as in Cushing’s disease) include:

Hyperpigmentation (skin and oral mucosa)

In exogenous Cushing’s syndrome (due to treatment with glucocorticoids), there may be clinical features of the underlying disease process being treated (e.g. COPD, rheumatoid arthritis, organ transplantation). 
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Introduction
Wash your hands and don PPE if appropriate.
Introduce yourself to the patient including your name and role.
Confirm the patient’s name and date of birth.
Briefly explain what the examination will involve using patient-friendly language.
Gain consent to proceed with the examination.
Adjust the head of the bed to a 45° angle.
Adequately expose the patient’s chest for the examination (offer a blanket to allow exposure only when required and if appropriate, inform patients they do not need to remove their bra). Exposure of the patient’s lower legs is also helpful to assess for oedema and skin thinning. 
Ask the patient if they have any pain before proceeding with the clinical examination.

General inspection
Significant information can be obtained from inspection in patients with Cushing’s syndrome, so a general inspection is a vital part of the assessment.
Clinical signs
Perform a brief general inspection of the patient, looking for clinical signs suggestive of Cushing’s syndrome:

Facial plethora: facial fullness (moon facies) and rounding of the face
Dorsocervical fat pad (‘buffalo hump’)
Thinning of the skin and easy bruising
Weight gain and central obesity

Objects and equipment
Look for objects or equipment on or around the patient that may provide useful insights into their medical history and current clinical status:

Medical equipment: note any oxygen delivery devices and ECG leads.
Mobility aids: items such as walking aids give an indication of the patient’s current mobility status.
Vital signs: charts on which vital signs are recorded will give an indication of the patient’s current clinical status and how their physiological parameters have changed over time.
Prescriptions: prescribing charts or personal prescriptions can provide useful information about the patient’s recent medications.

Hands
Inspection
The following signs may be seen on close inspection of the hands:

Finger pricks: finger prick marks on the tips of the fingers may indicate diabetes
Reduced skin fold thickness: due to skin thinning
Pigmentation (excess ACTH / Cushing’s disease)
Signs of arthritis (e.g. joint swelling or deformities): a potential reason for long-term exogenous glucocorticoid use

Arms
Inspect the arms
Bruising
Cushing’s syndrome causes skin thinning and makes patients more susceptible to bruising.
Pulses and blood pressure
Radial pulse
Palpate the patient’s radial pulse, located at the radial side of the wrist, with the tips of your index and middle fingers aligned longitudinally over the course of the artery.
Once you have located the radial pulse, assess the rate and rhythm.
Blood pressure
Offer to measure the patient’s blood pressure (see our blood pressure guide for more details). Cushing’s syndrome commonly causes hypertension. 
A comprehensive blood pressure assessment should also include lying and standing blood pressure.
In an OSCE station, you are unlikely to have to carry out a thorough blood pressure assessment due to time restraints, however, you should demonstrate that you have an awareness of what this would involve.

Face
General appearance
Inspect the general appearance face for features associated with Cushing’s syndrome:

Facial plethora: facial fullness and rounding of the face (moon facies) (Figure 1)
Facial acne
Hirsutism (Figure 2)
Butterfly rash: seen in systemic lupus erythematosus (a possible reason for long-term exogenous glucocorticoid use)

Figure 1. Moon facies

Figure 2. Hirsutism and abdominal striae

Mouth
Inspect the inside of the mouth for the following:

Oral thrush (candidiasis)
Buccal pigmentation (excess ACTH / Cushing’s disease)

Visual fields
Assess for bitemporal hemianopia (found in Cushing’s disease due to compression of the optic chiasm by a pituitary adenoma).
This method of visual field assessment relies on comparing the patient’s visual field with your own. Therefore, for it to work:

You need to position yourself, the patient, and the target correctly (see details below)
You need to have normal visual fields and a normal-sized blindspot

Visual field assessment
1. Sit directly opposite the patient, at a distance of around 1 metre.
2. Ask the patient to cover one eye with their hand.
3. If the patient covers their right eye, you should cover your left eye (mirroring the patient).
4. Ask the patient to focus on part of your face (e.g. nose) and not move their head or eyes during the assessment. You should do the same and focus your gaze on the patient’s face.
5. As a screen for central visual field loss or distortion, ask the patient if any part of your face is missing or distorted. A formal assessment can be completed with an Amsler chart.
6. Position the hatpin (or another visual target) at an equal distance between you and the patient (this is essential for the assessment to work).
7. Assess the patient’s peripheral visual field by comparing it to your own and using the visual target. Start from the periphery and slowly move the target towards the centre, asking the patient to report when they first see it. If you are able to see the target but the patient cannot, this would suggest the patient has a reduced visual field.
8. Repeat this process for each visual field quadrant, then repeat the entire process for the other eye.
9. Document your findings.

Chest and back
Inspection
The following signs may be noted on close inspection of the chest and back:

Dorsocervical fat pad: increased subcutaneous fat on the back of the neck
Supraclavicular fat pads (supraclavicular fullness): increased subcutaneous fat in the supraclavicular fossa
Kyphosis: resulting from vertebral wedge fractures due to osteoporosis
Gynecomastia in males
Acne on the chest or the back

Abdomen
Inspection
The following signs may be seen on close inspection of the abdomen:

Central obesity
Prominent purple striae (Figure 2)
Lipodystrophy from insulin injections (diabetes mellitus)
Organ transplantation scars (a possible reason for long-term exogenous glucocorticoid use)

Legs
Inspection
Bruising
Cushing’s syndrome causes skin thinning and makes patients more susceptible to bruising.
Peripheral oedema
Cushing’s syndrome can cause peripheral oedema. 
Proximal myopathy
Cushing’s syndrome can cause proximal muscle weakness. 
To screen for proximal myopathy, ask the patient to stand from a sitting position with their arms crossed (to minimise their ability to mask proximal muscle weakness). Make sure to stand close to the patient to prevent them from falling. An inability to stand up suggests proximal muscle weakness.

To complete the examination…
Explain to the patient that the examination is now finished.
Thank the patient for their time.
Dispose of PPE appropriately and wash your hands.
Summarise your findings.

Example summary
“Today I performed a focused Cushing’s syndrome examination on a 76-year-old woman. On general inspection, the patient had facial plethora.”
“The hands and arms demonstrated thinning of the skin, and bruises were visible on the forearms. There was no hyperpigmentation of the skin.”
“On inspection of the face, there was facial plethora and rounding of the face.”
“Assessment of the visual fields by confrontation was normal.”
“On inspection of the chest and back, a dorsocervical fat pad was visible.”
“On inspection of the abdomen, there was central obesity and prominent abdominal striae.”
“There was no evidence of peripheral oedema.”
“There was no proximal myopathy evident.”
“In summary, these findings are consistent with a diagnosis of Cushing’s syndrome.”
“For completeness, I would like to perform the following further assessments and investigations.”

Further assessments and investigations

Perform a full cardiovascular examination including measurement of blood pressure: to identify cardiovascular involvement, including hypertension.
Bedside capillary blood glucose and serum HbA1c: to test for diabetes.
Urea and electrolytes: Cushing’s syndrome can cause hypokalemia.
Late-night salivary cortisol, 24-hour urinary free cortisol, or low-dose dexamethasone suppression test: to confirm the diagnosis of Cushing’s syndrome.
Plasma ACTH: to help distinguish between ACTH-dependent and ACTH-independent Cushing’s syndrome.
High-dose dexamethasone suppression test: to distinguish between pituitary and ectopic ACTH production.
Imaging: pituitary MRI (if suspected Cushing’s disease), CT/MRI of adrenals (if suspected adrenal source), CT thorax/abdomen/pelvis (if ectopic ACTH production is suspected).3

Reviewer
Dr Marissa O’Callaghan
Special Lecturer in Medicine & Medical Registrar
St Vincent’s University Hospital

References

Sharma ST, Nieman LK, Feelders RA. Cushing’s syndrome: epidemiology and developments in disease management. Clin Epidemiol. 2015 Apr 17;7:281-93.
Nieman LK, Biller BM, Findling JW, et al. The diagnosis of Cushing’s syndrome: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2008 May;93(5):1526-40.
Ishikura K, Takamura T, Takeshita Y, Nakagawa A, Imaizumi N, Misu H, Taji K, Kasahara K, Oshinoya Y, Suzuki S, Ooi A, Kaneko S. Cushing’s syndrome and big IGF-II associated hypoglycemia in a patient with adrenocortical carcinoma. BMJ Case Rep. 2010. Epub 2010 Mar 30.

Image references

Figure 1. Ozlem Celik, Mutlu Niyazoglu, Hikmet Soylu and Pinar Kadioglu. Moon Facies. License: [CC BY 2.5]
Figure 2. Ozlem Celik, Mutlu Niyazoglu, Hikmet Soylu and Pinar Kadioglu. Hirsutism and abdominal striae. License: [CC BY 2.5]