Diabetic Foot OSCE Examination
During any examination in an OSCE it is important to understand the pathology and reasoning behind each of the signs and symptoms elicited, even if the patient being examined is ‘normal’. This article explains how to perform a diabetic foot examination and the key findings you should look for, showing you what each sign means and what conditions it may indicate.
The diabetic foot examination is fundamentally an assessment of two pathological processes that frequently coexist in diabetes: peripheral neuropathy (nerve damage) and peripheral arterial disease (impaired blood supply). Together these are responsible for the development of diabetic foot ulcers, infection, and ultimately amputation. The purpose of the examination is to identify the ‘at-risk’ foot before tissue breakdown occurs, so the structure of the examination follows these two themes: looking for the consequences of disease (inspection), assessing the blood supply (vascular assessment), and assessing nerve function (neurological assessment).
Introduction
Wash your hands thoroughly and don personal protective equipment if appropriate.
Introduce yourself to the patient and ensure to mention your grade e.g. 3rd year medical student/junior doctor/consultant.
Confirm the patient’s details taking 3 points of identification usually; full name, date of birth and NHS/hospital number.
Obtain consent for the examination, ensuring to explain what the examination will entail. A useful explanation is that you would like to look at their feet, feel the pulses, and test the feeling in their feet to make sure their diabetes is not affecting them.
Ensure the patient is positioned comfortably on the bed or couch, and adequately expose both lower limbs to the knee, removing both shoes and socks. It is important to examine both feet so the two sides can be compared.
Ask the patient if they have any pain anywhere before you begin, and watch their face for signs of discomfort throughout. Remember that in advanced neuropathy the foot may be painless even in the presence of significant pathology, so the absence of pain is itself a relevant finding.
General Inspection
Begin with a general inspection of the patient from the end of the bed. Look for clues that the patient has diabetes and that it may be poorly controlled, such as the patient appearing unwell, signs of weight loss, or evidence of complications elsewhere. Note any obvious limb amputations on the contralateral side, as a previous amputation is one of the strongest risk factors for further ulceration and amputation.
Inspect the area around the bedside for objects and equipment that give clues about the patient’s condition and management. Useful findings include blood glucose monitoring equipment, an insulin pen or pump, mobility aids such as a walking frame or wheelchair, specialist footwear or orthotics, and dressings or wound care supplies which suggest existing ulceration.
Be alert to signs of sepsis in a patient with an infected diabetic foot, as this should prompt urgent escalation.
Closer Inspection of the Feet
Inspect both feet carefully and systematically, comparing one side with the other. Make sure to examine the dorsum, the sole, the heel, the sides of the feet, and crucially the skin between every toe, as ulcers and fungal infection are easily missed in these hidden areas.
Look at the skin for the following:
- Ulcers – the most important finding. Note the site, size and appearance. Neuropathic ulcers are typically painless, have punched-out edges with surrounding callus, and occur over pressure points such as the metatarsal heads and heel. This is because loss of protective sensation allows repetitive trauma to go unnoticed. Ischaemic ulcers tend to be painful and occur at the tips of the toes or other peripheral ‘watershed’ areas where perfusion is poorest.
- Callus formation – thickened skin over pressure areas indicates abnormal load distribution, often as a consequence of neuropathy and deformity. Callus can act as a foreign body, raising the pressure on underlying tissue and predisposing to ulceration.
- Colour changes – a pale or white foot suggests poor arterial supply, whilst a dusky, red or black area may indicate critical ischaemia, infection or gangrene. Redness that does not blanch may represent cellulitis.
- Signs of infection – erythema, swelling, discharge or an offensive smell. Spreading erythema suggests cellulitis, and a deep, malodorous ulcer raises concern for underlying osteomyelitis.
- Dry, cracked skin and loss of hair – autonomic neuropathy reduces sweating, leaving the skin dry and prone to fissuring, which provides a portal of entry for bacteria. Hair loss over the toes and dorsum of the foot is a sign of chronic arterial insufficiency.
- Nail changes – thickened, discoloured nails may indicate fungal infection (onychomycosis), and poorly trimmed or ingrowing nails can be a source of trauma and infection.

Image - A neuropathic ulcer on the heel of a diabetic foot. Note the punched-out appearance over a pressure point, which develops because loss of protective sensation allows repetitive trauma to go unnoticed
Creative commons source by Jonathan Moore [CC BY 3.0 (https://creativecommons.org/licenses/by/3.0)]
Next, look at the overall shape and structure of the foot for deformity, which alters the way pressure is distributed across the sole and creates new high-pressure points at risk of ulceration:
- Clawing or hammer toes – motor neuropathy weakens the small intrinsic muscles of the foot, leaving the long flexors and extensors unopposed. This pulls the toes into a clawed position and pushes the metatarsal heads downwards, exposing them to high pressure.
- Loss of the foot arches and abnormal pressure loading.
- Charcot foot (Charcot neuroarthropathy) – in a patient with dense neuropathy, repeated unperceived microtrauma and an exaggerated inflammatory response cause progressive destruction of the bones and joints of the midfoot. The arch collapses, producing the characteristic ‘rocker-bottom’ deformity. In its acute phase the foot is typically warm, red and swollen, and is frequently mistaken for infection or gout – recognising it is important because the foot must be offloaded urgently to prevent permanent deformity.

Image - A Charcot foot with collapse of the midfoot producing the characteristic rocker-bottom deformity, with overlying skin changes at the new pressure point
Creative commons source by Medicalpal [CC BY-SA 4.0 (https://creativecommons.org/licenses/by-sa/4.0)]
Finally, look for any scars from previous surgery or amputations (including amputation of individual toes), as these confirm previous foot disease and place the patient in a high-risk category.
Palpation and Temperature
Before palpating, check again that the patient is not in any pain. Using the dorsal (back) surface of your hand, assess and compare the temperature of both feet, working from the toes upwards. The back of the hand is used because the skin here is thin and more sensitive to temperature differences.
A cold foot suggests poor arterial supply and peripheral arterial disease. A generally warm foot is reassuring for perfusion, but a localised area of warmth is significant: it may indicate infection or an acute Charcot foot. Comparing the two feet is essential, as a unilateral difference is far more informative than absolute temperature.
Gently palpate any areas of callus or suspected ulceration. A useful clinical sign is to feel for fluctuance or crepitus, which may suggest a deep abscess or gas-forming infection respectively. Be gentle and stop if the patient is uncomfortable.
Vascular Assessment
The vascular assessment evaluates the arterial supply to the foot. Diabetes accelerates atherosclerosis, and impaired perfusion is a major contributor to ulceration that fails to heal and to gangrene.
Assess the capillary refill time by pressing on the pulp of a toe (or the nail bed) for five seconds and releasing. Colour should return within two seconds; a prolonged refill time suggests impaired peripheral perfusion.
Palpate the two foot (pedal) pulses in both feet, comparing the two sides:
- Dorsalis pedis pulse – felt on the dorsum of the foot, just lateral to the tendon of extensor hallucis longus. This artery is the continuation of the anterior tibial artery.
- Posterior tibial pulse – felt behind and slightly below the medial malleolus, where the artery passes into the foot.

Image - Location of the dorsalis pedis pulse on the dorsum of the foot, found just lateral to the tendon of extensor hallucis longus
SimpleMed original image, credit ‘SimpleMed original’

Image - Location of the posterior tibial pulse, palpated just behind and below the medial malleolus
SimpleMed original image, credit ‘SimpleMed original’
An absent or weak pedal pulse is suggestive of peripheral arterial disease. It is worth remembering that the dorsalis pedis pulse is congenitally absent in a small proportion of healthy people, which is another reason both feet are compared and the posterior tibial pulse is also assessed.
If the pulses are difficult to feel or you suspect arterial disease, Buerger’s test can be used to assess the adequacy of the arterial supply. With the patient lying flat, lift both legs to roughly 45 degrees and hold them there for a minute or two, watching the feet. In a healthy limb the foot stays pink; in a poorly perfused limb the sole becomes pale as gravity overcomes the arterial pressure. The angle at which pallor appears is the Buerger’s angle, and the lower it is the worse the disease – an angle below about 20 degrees indicates severe ischaemia. Then sit the patient up and hang the legs over the edge of the bed: an ischaemic foot turns a dusky red (reactive hyperaemia) as blood floods back into the dilated, oxygen-starved capillary bed. Note that vascular calcification in diabetes can make this test less reliable.
To complete a fuller picture of the lower limb circulation, you would also palpate the popliteal and femoral pulses, and in clinical practice an ankle-brachial pressure index (ABPI) would be measured using a hand-held Doppler. A normal ABPI is approximately 0.9–1.2. A value below 0.9 indicates arterial disease. Importantly, an abnormally high value (above 1.3) can occur in diabetes because medial arterial calcification makes the vessels incompressible, so a falsely normal or high ABPI does not exclude significant arterial disease in a diabetic patient.
Neurological Assessment
The neurological assessment screens for peripheral sensory neuropathy, the loss of which removes the foot’s natural protection against trauma. Diabetic neuropathy classically affects the longest nerves first, producing a ‘glove and stocking’ distribution of sensory loss that begins at the toes and progresses proximally.
Throughout, first demonstrate each test on a site where sensation is intact (such as the sternum or forearm) so the patient knows what to expect, then ask them to close their eyes during testing so the responses are genuine.
Light touch sensation – Ipswich touch test: Where a monofilament is not to hand, the Ipswich touch test is a validated bedside screen for loss of protective sensation. With the patient’s eyes closed, lightly rest the tip of your index finger for a second or two on the tips of the first, third and fifth toes of each foot in turn, asking the patient to say when they feel a touch. Insensitivity at two or more of these sites suggests significant neuropathy. It is quick, needs no equipment and performs comparably to the monofilament, making it a useful screen on the ward.
Light touch and pressure sensation – 10g monofilament: The 10g monofilament is the key screening tool for the loss of protective sensation. Press the monofilament perpendicularly against the skin until it buckles, which applies a reproducible 10g of force, hold it for about one second and ask the patient to say ‘yes’ when they feel it. Test several sites on the plantar surface, classically the pulp of the great toe and the heads of the first, third and fifth metatarsals. Avoid testing directly over callus or ulcers, as sensation will be falsely absent there. Inability to feel the monofilament at one or more sites indicates loss of protective sensation and identifies a foot at high risk of ulceration.
Vibration sensation – 128Hz tuning fork: Vibration sense, carried by the large myelinated fibres of the dorsal columns, is often one of the earliest modalities lost in diabetic neuropathy. Strike a 128Hz tuning fork and place its base on a bony prominence, starting at the distal interphalangeal joint of the great toe (or the tip of the toe). Ask the patient to tell you when they feel the vibration and when it stops. If vibration is not felt distally, move proximally to the next bony landmark (the medial malleolus, then the tibial tuberosity) to map the level at which sensation returns.
Proprioception (joint position sense): Hold the sides of the patient’s great toe and demonstrate ‘up’ and ‘down’ movements with their eyes open. Then, with their eyes closed, move the toe up or down a few degrees and ask them to identify the direction. Like vibration, joint position sense is carried in the dorsal columns, and its loss reflects large-fibre neuropathy. Impaired proprioception also contributes to the unsteady gait seen in advanced disease.
Pinprick (pain) sensation: Using a disposable neurological pin (Neurotip), gently test pain sensation, comparing the toes with a more proximal site and comparing both feet. This assesses the small-fibre component of the sensory system. Discard the pin safely after use.
Ankle (Achilles) reflex: Test the ankle-jerk reflex by gently dorsiflexing the foot to put the Achilles tendon under slight tension and striking the tendon with a tendon hammer, watching and feeling for plantarflexion of the foot. A diminished or absent ankle reflex is a common and relatively early sign of peripheral neuropathy. If the reflex appears absent, use a reinforcement manoeuvre (asking the patient to clench their teeth or interlock their fingers and pull) before concluding it is truly absent.
Footwear and Gait
Always inspect the patient’s footwear, both inside and out. Ill-fitting shoes are a common and preventable cause of ulceration in the insensate foot. Look for abnormal or asymmetrical wear patterns on the soles, which reveal abnormal pressure loading and gait, and run your hand inside the shoe to feel for foreign objects, prominent seams or worn linings that a patient with neuropathy would not be able to feel. Note whether the patient is wearing appropriate protective or bespoke diabetic footwear.
If it is safe and appropriate to do so, ask the patient to walk a short distance, turn, and walk back while you observe their gait. An abnormal or antalgic gait may reflect deformity, ulceration, amputation or loss of proprioception, and an unsteady, broad-based gait can be a feature of sensory ataxia from severe neuropathy.
Completing the Examination
Explain to the patient that the examination is finished and help them to redress if required.
Thank the patient and wash your hands.
Summarise your findings and state whether, on the basis of your examination, the foot is at low, moderate or high risk of ulceration.
To complete the examination, state that you would:
- Measure a bedside capillary blood glucose and send blood for HbA1c to assess glycaemic control.
- Perform a full lower limb neurological examination and peripheral arterial examination, including measurement of the ankle-brachial pressure index with a hand-held Doppler.
- Carry out a formal diabetic foot risk assessment and document it clearly.
- If an ulcer or infection is present, take wound swabs, request imaging (such as a foot X-ray to look for osteomyelitis or Charcot changes), and consider blood tests including inflammatory markers.
- Provide foot-care education and refer to the multidisciplinary diabetic foot team (podiatry, vascular and diabetes specialists) as indicated.
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