Diabetes Mellitus — Clinical Case

DCE Long Case

Patient brief (provided to trainee)

Patient: Mr David Chen, 58 years old. [1]

Presenting complaint: Referred by his GP for suboptimal diabetes control and progressive numbness in both feet. He has noticed a sore on the sole of his right foot for 3 weeks that is not healing. [1]

Past history:

• Type 2 diabetes, diagnosed at age 42 (16 years duration)
• Hypertension, 15 years
• Dyslipidaemia
• Ischaemic heart disease — STEMI 4 years ago, primary PCI with DES to LAD
• Diabetic retinopathy — had panretinal photocoagulation 2 years ago for proliferative changes
• Gout
• Ex-smoker, stopped after his STEMI (30 pack-year history) [1]

Current medications:

• Metformin 1g BD
• Gliclazide MR 120mg daily
• Perindopril 5mg daily
• Amlodipine 10mg daily
• Atorvastatin 80mg nocte
• Aspirin 100mg daily
• Allopurinol 300mg daily [1]

Examination findings (trainee elicits):

• BMI 32, BP 146/88, HR 78 regular
• Cardiovascular: no murmurs, no signs of heart failure, normal S1 S2, carotids no bruits
• Feet: 1.5 cm plantar ulcer under right first metatarsal head with surrounding callus, no surrounding erythema, dorsalis pedis and posterior tibial pulses palpable bilaterally but reduced volume, 10g monofilament not felt at 7 of 10 sites on the right and 5 of 10 on the left, vibration sense reduced at both great toes, ankle reflexes absent bilaterally, skin dry and fissured
• Eyes: previous laser scars visible on fundoscopy
• Hands: no clues, no limited joint mobility [1]

Investigations:

• HbA1c 76 mmol/mol (9.1%)
• eGFR 41, urine ACR 28 mg/mmol
• Total cholesterol 3.8, LDL 1.9, HDL 0.9, triglycerides 2.2
• Na 139, K 4.8, creatinine 145
• FBE: Hb 128, MCV 86 [1]

Candidate's structured presentation (model)

Opening statement (SASPOP): [1]

"Mr Chen is a 58-year-old ex-smoker with a 16-year history of type 2 diabetes who presents with suboptimal glycaemic control, progressive peripheral neuropathy, and a non-healing plantar foot ulcer. He has established macrovascular disease (STEMI 4 years ago, DES to LAD) and microvascular complications (proliferative retinopathy requiring laser, diabetic nephropathy with albuminuria). [1]

His main problems are:

1. Type 2 diabetes with poor glycaemic control (HbA1c 76 mmol/mol) on metformin and sulphonylurea — needs escalation to organ-protective agents
2. Diabetic nephropathy — CKD stage 3B (eGFR 41) with macroalbuminuria (ACR 28) — needs SGLT2i and optimised RAAS blockade
3. Established ischaemic heart disease (post-STEMI) — needs cardiovascular risk reduction with evidence-based agents
4. Diabetic peripheral neuropathy with loss of protective sensation
5. Neuropathic diabetic foot ulcer — right plantar, needs offloading and multidisciplinary care
6. Proliferative diabetic retinopathy (post-laser) — needs ongoing ophthalmology surveillance
7. Hypertension above target (146/88) — target below 130/80 for a proteinuric diabetic patient
8. Obesity (BMI 32) contributing to insulin resistance
9. Gout and polypharmacy" [1]

Investigation summary: [1]

"His HbA1c of 76 mmol/mol confirms poor glycaemic control on two oral agents. His eGFR of 41 with macroalbuminuria (ACR 28) indicates stage 3B diabetic nephropathy — this is progressive and a major predictor of cardiovascular and renal events. His blood pressure is above target. His lipid profile is acceptable on atorvastatin 80mg (LDL 1.9). His potassium is normal. The normocytic anaemia (Hb 128) may reflect early chronic kidney disease or anaemia of chronic disease — I would check iron studies." [1]

Management plan: [1]

1. Glycaemic and pharmacological — the paradigm shift (organ-protective agents):

   • Add dapagliflozin 10mg daily — SGLT2 inhibitor. This patient has three indications: established ASCVD, CKD with albuminuria, and heart failure risk. The DAPA-CKD trial showed a 39% reduction in the renal composite. EMPA-REG OUTCOME showed a 38% reduction in cardiovascular death with empagliflozin.
   • Add a GLP-1 receptor agonist (liraglutide or semaglutide) — for ASCVD reduction (LEADER showed 22% CV death reduction) and weight loss (BMI 32).
   • Reduce metformin to 500mg BD — halve the dose given eGFR 41 (between 30 and 45). Continue as it has a mortality benefit (UKPDS) and is weight-neutral.
   • Stop gliclazide — now third-line, causes weight gain and hypoglycaemia, no organ-protection evidence.
   • Target HbA1c 53 to 58 mmol/mol — moderate target given established ASCVD and CKD (ACCORD caution). [1]

2. Nephropathy:

   • Optimise RAAS blockade — perindopril is appropriate; consider uptitrating to the maximally tolerated dose. Monitor creatinine and potassium at 1 to 2 weeks (accept rise up to 30%).
   • Dapagliflozin for renoprotection.
   • Blood pressure target below 130/80. May need to add a thiazide-like diuretic if BP remains above target after optimising ACEi. [1]

3. Cardiovascular risk reduction:

   • Confirmed on aspirin, atorvastatin 80mg (high-intensity statin for secondary prevention).
   • BP control, SGLT2i, GLP-1 RA.
   • Smoking cessation already achieved. [1]

4. Diabetic foot ulcer:

   • Refer to multidisciplinary diabetic foot clinic urgently.
   • Total contact cast for offloading (gold standard for plantar neuropathic ulcers).
   • Sharp debridement of callus by podiatrist.
   • Probe-to-bone test and MRI if osteomyelitis suspected.
   • Assess vascular status properly — reduced pulse volume warrants ABI and toe pressures (ABI may be falsely elevated in diabetes due to medial calcinosis).
   • Monitor for infection; no antibiotics currently (no clinical infection). [1]

5. Retinopathy:

   • Ophthalmology review — he has had laser for proliferative disease, needs ongoing surveillance.
   • Note: rapid glycaemic improvement can worsen retinopathy early — coordinate with ophthalmology during therapy escalation. [1]

6. Lifestyle and education:

   • Structured diabetes education, dietitian referral.
   • Weight loss target (GLP-1 RA will assist).
   • Foot care education — daily inspection, appropriate footwear, never walk barefoot. [1]

7. Annual review checklist:

   • HbA1c every 3 months, eGFR/ACR every 3 to 6 months, annual retinal screening, annual foot exam (more frequent given active ulcer), lipid panel, BP, weight, vaccinations. [1]

Examiner discussion questions

Q: "Why would you not start insulin in this patient?" [1]

"Insulin is not the first escalation step for this patient, despite his poor glycaemic control. The reason is that he has specific indications for organ-protective agents — established ASCVD and CKD with albuminuria — which SGLT2i and GLP-1 RA address and insulin does not. Insulin causes weight gain (he is already BMI 32), has a significant hypoglycaemia risk, and has neutral cardiovascular outcomes. The paradigm shift in diabetes management is that we treat the cardiorenal risk first. If his HbA1c remains above target after optimising SGLT2i, GLP-1 RA, and metformin, then I would add basal insulin — starting at 0.2 units/kg/day, titrating by fasting glucose. But insulin is not the first escalation here." [1]

Q: "He has gout. Does that influence your choice of diuretic?" [1]

"Yes. Thiazide diuretics raise serum uric acid and can precipitate gout. If I need a third antihypertensive agent, I would prefer a calcium channel blocker (he is already on amlodipine — consider switching to lercanidipine or adding a non-dihydropyridine if appropriate) or a loop diuretic (less hyperuricaemic than thiazide, but less effective as an antihypertensive). Indapamide is a thiazide-like diuretic with a lower gout risk than hydrochlorothiazide. I would continue his allopurinol and aim for a serum uric acid below 360." [1]

Q: "His ABI is 1.3. How do you interpret this?" [1]

"An ABI of 1.3 is abnormally high — it suggests medial arterial calcinosis, which is common in diabetes and makes the ankle arteries non-compressible. This falsely elevates the ABI and masks peripheral arterial disease. The correct interpretation is that an ABI above 1.4 is uninterpretable, and I would measure toe pressures and the toe-brachial index instead. A toe-brachial index below 0.7 indicates peripheral arterial disease. I would also consider an arterial Doppler ultrasound or CT angiogram if clinical suspicion of ischaemia is high." [1]

Q: "What is the prognosis for this patient?" [1]

"His prognosis is guarded but improvable. He has multi-system diabetic disease — 16 years of type 2 diabetes with microvascular (nephropathy, retinopathy, neuropathy) and macrovascular (prior STEMI) complications, CKD stage 3B, and an active foot ulcer. His 10-year cardiovascular risk is high. However, the Steno-2 trial showed that multifactorial intervention — addressing glucose, blood pressure, lipids, and aspirin — reduces all-cause mortality by 46% and cardiovascular events by 59% in high-risk diabetic patients. So with optimised therapy (SGLT2i, GLP-1 RA, ACEi, statin, BP control), his outlook is substantially better than without. The foot ulcer has a good prognosis if offloaded and managed by a multidisciplinary team, but he is at high risk of recurrence and future amputation — long-term foot care is critical." [1]

DCE Short Case — Diabetic Foot Examination

Instruction

"Examine this patient's feet. You have 7 minutes for examination and 8 minutes for discussion." [1]

Systematic examination routine

Step 1 — Inspect (with shoes and socks off, both feet exposed):

• General: deformity (claw toes, Charcot foot, prominent metatarsal heads, hallux valgus), muscle wasting (intrinsic muscle atrophy suggests chronic neuropathy).
• Skin: colour, dryness (autonomic neuropathy), fissuring (especially heel), callus (pressure points), ulceration (plantar surface, between toes, heel, tips of toes), necrosis, gangrene.
• Nails: onychomycosis, ingrown toenails, subungual ulceration.
• Between the toes: maceration, fungal infection (tinea pedis), ulceration (often missed).
• Shoes: examine the footwear — are they appropriate? Is there abnormal wear pattern? Do they accommodate deformity? [1]

Step 2 — Palpate:

• Temperature: compare both feet. A warm foot with palpable pulses suggests adequate perfusion; a cold pulseless foot suggests ischaemia. A warm foot with absent pulses may indicate autonomic neuropathy (vasodilation).
• Pulses: femoral, popliteal, dorsalis pedis, posterior tibial. Document presence, volume, character. Absent pulses suggest PAD.
• Capillary refill (should be less than 2 seconds). [1]

Step 3 — Test neuropathy:

• 10g monofilament (Semmes-Weinstein): apply to 10 sites on each foot (the 1st, 3rd, and 5th metatarsal heads, the plantar hallux, and the heel, plus the lateral border). Inability to feel the monofilament at 4 or more sites indicates loss of protective sensation — the single best predictor of foot ulceration.
• 128 Hz tuning fork (vibration sense): apply to the bony prominence of the hallux interphalangeal joint and the medial malleolus. Reduced vibration sense is an early sign of neuropathy.
• Pinprick: test in a distal-to-proximal pattern to map the sensory level.
• Ankle reflexes: absent in advanced neuropathy. Use the Jendrassik manoeuvre if difficult to elicit.
• Proprioception: move the hallux up and down — impaired in advanced neuropathy. [1]

Step 4 — Examine the ulcer (if present):

• Site, size, depth.
• Base: granulating, sloughy, necrotic, exposed tendon or bone.
• Surrounding skin: callus, erythema, warmth (infection).
• Probe-to-bone test: gently probe the ulcer base with a sterile blunt probe. If bone is reached, osteomyelitis is likely. [1]

Key signs the patient demonstrates

• Plantar ulcer under the first metatarsal head with surrounding callus (neuropathic pressure ulcer)
• Loss of protective sensation (10g monofilament not felt at multiple sites)
• Reduced vibration sense at great toes
• Absent ankle reflexes
• Dry, fissured skin (autonomic neuropathy — anhidrosis)
• Clawed toes (motor neuropathy — intrinsic muscle imbalance)
• Palpable pulses (neuropathic rather than ischaemic ulcer, but assess properly given medial calcinosis risk) [1]

Presentation template

"I examined Mr Chen's feet. On inspection, there is a 1.5 cm plantar ulcer under the right first metatarsal head with surrounding callus. The ulcer base is clean and granulating with no exposed tendon or bone. There is no surrounding erythema or warmth. The skin on both feet is dry with heel fissures, and the toes are clawed bilaterally with prominent metatarsal heads. [1]

On palpation, the feet are warm and well-perfused. The dorsalis pedis pulses are palpable but reduced in volume bilaterally. The posterior tibial pulses are palpable. Capillary refill is 2 seconds. [1]

On neurological testing, the 10g monofilament is not felt at 7 of 10 sites on the right foot and 5 of 10 on the left, indicating loss of protective sensation. Vibration sense using a 128 Hz tuning fork is reduced at both great toes. Pinprick sensation is reduced in a stocking distribution to mid-shin. Ankle reflexes are absent bilaterally. [1]

In summary, these findings are consistent with a neuropathic diabetic foot ulcer with loss of protective sensation, autonomic neuropathy (dry fissured skin), and motor neuropathy (clawed toes). The reduced pulse volume warrants further vascular assessment with ankle-brachial index and toe pressures, noting that ABI may be falsely elevated in diabetes due to medial arterial calcinosis." [1]

Discussion questions

Q: "What is the mechanism of foot ulceration in diabetes?" [1]

"Diabetic foot ulcers result from the interaction of three pathological processes: neuropathy, ischaemia, and infection. Neuropathy causes loss of protective sensation — the patient does not feel repetitive minor trauma (a tight shoe, a stone, a fissure). Motor neuropathy causes foot deformity (clawed toes, prominent metatarsal heads), creating abnormal pressure points. Autonomic neuropathy causes anhidrosis, dry fissured skin that is prone to cracking and bacterial entry. Ischaemia from peripheral arterial disease impairs wound healing and increases the risk of gangrene. Infection, often polymicrobial, can extend deep to bone (osteomyelitis). The classic pathway is: neuropathy allows unrecognised trauma, the wound does not heal due to ischaemia and hyperglycaemia, and infection complicates and deepens the ulcer." [1]

Q: "What is the probe-to-bone test and what does a positive result mean?" [1]

"The probe-to-bone test involves gently probing the ulcer base with a sterile blunt metal probe. If bone is encountered at the base of the ulcer, the test is positive. A positive probe-to-bone test has a sensitivity of approximately 66% and specificity of 85% for osteomyelitis. It is a bedside screening test — a positive result should prompt further investigation with MRI (the imaging gold standard for osteomyelitis) and consideration of bone biopsy (the diagnostic gold standard) for culture and histology. A negative result does not exclude osteomyelitis." [1]

Q: "What is the most effective offloading method and why?" [1]

"The total contact cast (TCC) is the gold standard for offloading plantar neuropathic ulcers. It is a well-moulded, minimally padded cast that applies total contact to the plantar surface of the foot and leg, distributing pressure evenly and reducing peak pressure at the ulcer site by up to 80%. The TCC works by converting the foot into a non-weightbearing rigid structure and redistributing weight to the leg. It also prevents the patient from removing it (non-removable), ensuring compliance. Contraindications include active infection, severe ischaemia, and deep ulcers with exposed bone. A removable cast walker is an alternative but is less effective because patients remove it — converting it to an instant total contact cast (irremovable) improves compliance and outcomes." [1]