Diabetic food ulcer full detailed history taking and physical examination

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Diabetic Foot Ulcer: Full History Taking and Physical Examination


OVERVIEW

A diabetic patient has a lifetime risk of ~15% for developing a diabetic foot ulcer (DFU), with an annual incidence of 2%. Approximately 15-20% of DFUs result in a lower extremity amputation, and ~85% of all amputations are preceded by a DFU. The triad driving DFU is neuropathy, ischemia, and infection.

PART 1 - HISTORY TAKING

A. Presenting Complaint

  • Nature of the wound: when first noticed, how it started (blister, callus, crack, trauma)
  • Duration of the ulcer
  • Rate of change: getting larger, smaller, or static
  • Pain or painlessness (painless = suggests neuropathy; painful = suggests ischemia or infection)
  • Any discharge: character (serous, purulent, bloody, foul-smelling)
Because of impaired sensation, patients may deny any history of trauma or pain before the development of a foot ulcer. - Campbell's Operative Orthopaedics 15e

B. Diabetes History

  • Type of diabetes (Type 1 or Type 2), duration of diagnosis
  • Current medications: insulin (type, dose, regimen), oral hypoglycaemics
  • Glycaemic control: last HbA1c, home blood glucose monitoring, pattern of readings
  • Frequency of hypoglycaemic episodes
  • Compliance with medications and diet
  • Monitoring: frequency of seeing diabetic nurse/dietitian/podiatrist

C. Foot-Specific History

  • Previous ulcers: number, sites, healing time, treatment required
  • Previous amputations: level, side, reason, year
  • History of Charcot neuroarthropathy (Charcot joint): sudden swelling, warmth, redness of foot or ankle in absence of infection
  • Footwear: type of shoes worn, whether custom therapeutic footwear has been prescribed, ability to feel foreign bodies or seams inside the shoe
  • Foot care routine: ability to inspect own feet daily, ability to reach feet (limited by obesity, visual impairment), hygiene habits
  • Prior foot surgeries or procedures

D. Neuropathy Symptoms

  • Sensory neuropathy: numbness, tingling, burning, "walking on cotton", loss of feeling in the feet
  • Motor neuropathy: weakness, difficulty walking, change in foot shape
  • Autonomic neuropathy: decreased sweating (anhidrosis), dry cracked skin, postural dizziness (orthostatic hypotension)
  • Pain characteristics: burning, stabbing, electric, or absence of pain (protective sensation loss)

E. Vascular / Ischemia History

  • Claudication: calf or thigh pain on walking (intermittent claudication) - note claudication distance
  • Rest pain: pain in toes/forefoot at rest, worse at night, relieved by hanging the leg over the bed edge
  • Critical limb ischemia: rest pain, non-healing wounds, or gangrene
  • Prior vascular interventions: angioplasty, bypass surgery, stenting
  • Smoking history (pack-years) - major risk factor for peripheral arterial disease (PAD)
  • History of stroke or myocardial infarction (markers of systemic atherosclerosis)

F. Infection History

  • Constitutional symptoms: fever, chills, rigors, malaise
  • Local symptoms: increasing redness, warmth, swelling around the wound
  • Discharge: purulent or foul-smelling
  • Crepitus felt around wound (gas-forming organisms)
  • Recent antibiotic treatment (type, duration, response)
  • Hospitalisation for foot infection in the past
  • Any probe-to-bone sensation during dressing changes

G. Systemic Diabetic Complications

  • Retinopathy: visual impairment or blindness - impacts ability to inspect own feet; increases falls risk
  • Nephropathy: CKD stage, dialysis, transplant history - impacts wound healing, drug dosing
  • Cardiovascular disease: IHD, heart failure, hypertension, dyslipidaemia
  • Cerebrovascular disease: stroke, TIA

H. Social and Functional History

  • Living situation: alone or with carers, home support
  • Mobility and weight-bearing status prior to ulceration
  • Occupation (if still working)
  • Smoking, alcohol use
  • Access to healthcare, follow-up, transport
  • Body weight and BMI

I. Drug and Allergy History

  • Full medication list including anticoagulants, immunosuppressants, steroids (all impair healing)
  • Allergy history (important before antibiotic prescribing)
  • Previous antibiotic sensitivities or resistance patterns

J. Family History

  • Family history of diabetes, PAD, or lower extremity amputation

PART 2 - PHYSICAL EXAMINATION

General Inspection

  • Overall appearance: unwell, febrile, confused (sepsis screening)
  • Body habitus: obesity
  • Mobility: weight-bearing or non-weight-bearing
  • Diabetic facial/body features

Vital Signs

  • Temperature (fever suggests infection)
  • Heart rate (tachycardia in sepsis)
  • Blood pressure (hypertension common)
  • Respiratory rate and oxygen saturation
  • Blood glucose (at time of presentation)

Shoe Inspection (Box 91.1 - Campbell's Orthopaedics)

"Inspect the patient's shoes." - Campbell's Operative Orthopaedics 15e
  • Undersized shoes increase pressure over bony prominences, leading to ulceration and infection
  • Toe box must be adequate to accommodate forefoot deformities
  • Abnormal wear pattern indicates structural or dynamic foot deformity
  • Presence of prominent seams or foreign bodies inside the shoe that the patient cannot feel = indicates neuropathy

Lower Limb Inspection

Both feet must always be examined and compared.
  • Deformities: claw toes, hammer toes, hallux valgus, flat foot (pes planus), pes cavus, Charcot foot (rocker-bottom deformity)
    • Weak intrinsic muscles overpowered by extrinsic muscles lead to claw/hammer toes and distal migration of the fat pad - Campbell's
  • Muscle wasting: atrophy of the extensor digitorum brevis = motor neuropathy
  • Calluses and corns: indicate sites of elevated pressure; precursors to ulceration
  • Arch and hindfoot alignment (with patient weight-bearing): abnormalities alter plantar pressure distribution

Skin Assessment

FeatureSignificance
Shiny, taut, hairless skinPeripheral arterial disease (PAD)
Dry, scaly, cracked, fissured skinAutonomic neuropathy (anhidrosis)
Erythema, warmth, swellingInfection or Charcot neuroarthropathy
Dependent rubor (red when limb hangs down)Severe ischemia
Pallor on elevationIschemia
Skin temperature difference between feetVascular asymmetry
  • Distinguish Charcot from infection: elevate the extremity - Charcot erythema/warmth usually subsides with elevation; infection does not.

Ulcer Assessment

A systematic description of the ulcer must be documented:
  1. Site: plantar surface (most common in neuropathic), toes (pressure/ischemia), heel (pressure), inter-digital (maceration/infection), malleolus
  2. Size: measure in two dimensions (longest x widest) to obtain cross-sectional area; depth should be recorded
    • Ulcers <1 cm² have 96% healing rate without amputation; ulcers >3 cm² have only 72% - Campbell's
  3. Shape and margins: punched-out (ischemic), irregular, undermined edges
  4. Depth: superficial (skin only), partial thickness, full thickness, exposed tendon/bone/joint
  5. Wound base: granulation tissue (healthy, pink/red), fibrinous slough (yellow), necrotic tissue (black/eschar)
  6. Surrounding tissue: callus, maceration, cellulitis, lymphangitis
  7. Discharge: serous, serosanguineous, purulent, foul-smelling
  8. Probe-to-bone test: use a sterile cotton swab to probe the wound depth and extent
    • Probing to bone has 57% positive predictive value for osteomyelitis and 96% negative predictive value - Campbell's Orthopaedics 15e

Vascular Assessment

"Physical examination of the foot for ischemia begins with the assessment of pulses. However, this can be exceedingly tricky in the diabetic patient population..." - Current Surgical Therapy 14e
Pulse examination (both limbs):
  • Femoral artery
  • Popliteal artery
  • Posterior tibial artery (behind medial malleolus)
  • Dorsalis pedis artery (dorsum of foot, lateral to extensor hallucis longus)
  • Grade: normal, diminished, absent
  • Note: diabetic medial calcinosis can cause falsely elevated or non-compressible vessels - absent pulses on palpation do not always mean absent flow
Ankle-Brachial Index (ABI):
  • Non-invasive screening tool using Doppler and blood pressure cuff
  • Normal: 1.0-1.3
  • Mild PAD: 0.7-0.9
  • Moderate PAD: 0.4-0.7
  • Severe/critical ischemia: <0.4
  • ABI >1.3 suggests medial calcinosis (non-compressible vessels) - measure toe-brachial index (TBI) instead
  • ABI is a useful noninvasive screening tool that predicts wound healing potential - Campbell's
Capillary refill time: prolonged (>2 seconds) in ischemia
Buerger's test: elevate limb at 45 degrees - pallor within 2 minutes = severe ischemia; dependent rubor on lowering = confirmed ischemia
Skin temperature: cool skin on palpation compared to contralateral limb

Neurological Assessment

Sensory testing (using validated tools):
  1. Semmes-Weinstein 10-g monofilament (most important):
    • Test 10 standard plantar sites (hallux, 1st/3rd/5th metatarsal heads, plantar arch, heel, dorsum)
    • Inability to feel 10 g of pressure = loss of protective sensation (LOPS)
    • "The threshold of importance is the inability to feel a Semmes-Weinstein 5.07 monofilament" - Campbell's
    • Inability to feel 10 g of pressure is one of the most predictive risk factors for foot morbidity
  2. Additional sensory modalities (at least one required alongside monofilament):
    • Pinprick sensation (pain)
    • Temperature discrimination (warm/cold test tubes)
    • Vibration sense: 128 Hz tuning fork at great toe and medial malleolus
    • Proprioception: joint position sense at hallux
  3. Ankle and knee reflexes: absent ankle jerk is characteristic of peripheral neuropathy
Motor testing:
  • Power of toe extension and flexion, ankle dorsiflexion and plantarflexion
  • Assessment for foot drop
Autonomic:
  • Sweating: dry feet, cracked heel skin
  • Postural blood pressure drop

Range of Motion Assessment

Silfverskiöld test (gastrocnemius contracture):
  • Record ankle dorsiflexion with knee flexed and extended
  • Gastrocnemius contracture: dorsiflexion less with knee extended than flexed (gastrocnemius origin is proximal to knee)
  • Achilles tendon contracture: equal decrease in both positions
  • Equinus deformity increases forefoot plantar pressure and contributes directly to plantar ulceration
Toe and MTP joint mobility:
  • Fixed hammer or claw toe deformities
  • Limited joint mobility (LJM) syndrome in diabetes: joint stiffness due to glycosylation of collagen

Systemic Examination

  • Cardiovascular: heart sounds, signs of cardiac failure (elevated JVP, ankle oedema), peripheral oedema
  • Respiratory: examine if suspecting systemic sepsis
  • Eyes: refer history of retinopathy - not always formally examined in clinic
  • Renal: oedema may reflect CKD-related fluid retention (impacts healing)
  • Lymph nodes: inguinal lymphadenopathy in lower limb infection

PART 3 - ULCER CLASSIFICATION SYSTEMS

Wagner-Meggitt Classification (most widely used)

GradeDescription
0No open lesion; preulcerative site, healed ulcer, bony deformity
1Superficial ulcer involving full skin thickness, no subcutaneous tissue
2Deep ulcer penetrating to tendon, capsule, or bone
3Deep ulcer with osteomyelitis, abscess, or joint sepsis
4Localised gangrene of forefoot or toe(s)
5Extensive gangrene of whole foot requiring major amputation

University of Texas (UT) Classification

Adds ischemia (A/B) and infection (C/D) to each Wagner-like depth grade:
  • A: clean wound
  • B: infected wound
  • C: ischemic wound
  • D: infected and ischemic wound
"Ulcers that are infected and ischemic are 90 times more likely to be treated with amputation than ulcers without infection or ischemia. The presence of an infected ulcer portends a 40% to 55% chance of some form of amputation." - Campbell's Operative Orthopaedics 15e

WIfI Classification (Society for Vascular Surgery)

  • Wound grade 0-3
  • Ischemia grade 0-3
  • foot Infection grade 0-3
  • 64 possible permutations; predicts amputation risk at 1 year and benefit of revascularisation - Current Surgical Therapy 14e

PART 4 - INVESTIGATIONS TO PLAN AFTER HISTORY AND EXAM

InvestigationPurpose
Blood glucose + HbA1cGlycaemic control assessment
FBC, ESR, CRPInfection baseline; inflammatory markers
Renal function (eGFR, creatinine)Nephropathy assessment, drug dosing
3-view foot X-rayOsteomyelitis, structural deformities, foreign bodies, gas
MRI footMost sensitive for bone involvement and deep soft tissue infection
Wound swab / deep tissue cultureIdentify organisms (note: superficial swabs are unreliable for deep infection)
Ankle-Brachial Index (ABI)Vascular sufficiency for wound healing
Doppler duplex USSVascular mapping if PAD suspected
Probe-to-bone testOsteomyelitis screening (bedside)

KEY CLINICAL PEARLS

  • Painlessness of an ulcer does not mean it is benign - it signals dangerous loss of protective sensation
  • Neuropathic ulcers are typically plantar, punched-out, surrounded by callus, with a warm foot and palpable pulses
  • Ischemic ulcers are typically at the toes or heel margins, painful, pale/cyanotic, with absent pulses and cool skin
  • Neuroischemic ulcers (most common in clinical practice) share both features
  • Charcot neuroarthropathy can mimic infection - the key distinguishing test is elevation of the limb
  • The probe-to-bone test is a critical bedside test - a negative result has a 96% negative predictive value for osteomyelitis
  • HbA1c >7% is an independent risk factor for DFU development and post-surgical complications

Sources:
  • Campbell's Operative Orthopaedics 15th Ed. 2026, Chapter 91 (Diabetic Foot - History and Physical Examination, Box 91.1)
  • Current Surgical Therapy 14e (Evaluation of the Diabetic Foot - Wound, Ischemia, Infection, WIfI Classification)
  • Bailey and Love's Short Practice of Surgery 28th Ed. (Diabetic Foot Infection, Chapter 43)
  • Rosen's Emergency Medicine (The Diabetic Foot, Chapter 15)

Also can you guide what all muscles and anything else and I need to know to remember in this

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Muscles, Anatomy & High-Yield Memory Guide for Diabetic Foot Ulcer


1. THE MUSCLE IMBALANCE CONCEPT (THE ROOT CAUSE of Deformity)

This is the single most important concept to understand for DFU:
Weak intrinsic muscles become overpowered by stronger extrinsic muscles → deformity → abnormal pressure → callus → ulcer
  • Campbell's Operative Orthopaedics 15e
Motor neuropathy in diabetes selectively damages the intrinsic muscles first (shorter nerve supply, smaller fibres), while the extrinsic muscles (long muscles from the leg) remain relatively strong. The result is unopposed extrinsic pull.

2. INTRINSIC MUSCLES OF THE FOOT (Weakened in DFU)

These are muscles that both originate and insert within the foot. Motor neuropathy causes them to waste and weaken.

Dorsal Surface

MuscleActionEffect when weak
Extensor digitorum brevis (EDB)Extends toes 2-4 at MTPAtrophied EDB = visible sign of motor neuropathy (look for it on exam!)
Extensor hallucis brevisExtends hallux at MTPContributes to hallux deformity

Plantar Surface (4 Layers - know these)

Layer 1 (most superficial):
MuscleAction
Abductor hallucisAbducts + flexes hallux at MTP
Flexor digitorum brevisFlexes toes 2-5 at PIP
Abductor digiti minimiAbducts little toe
Layer 2:
MuscleAction
Quadratus plantae (flexor accessorius)Corrects pull of FDL, assists toe flexion
Lumbricals (4)Flex MTP, extend IP joints (critical for toe posture)
Layer 3:
MuscleAction
Flexor hallucis brevisFlexes hallux at MTP
Adductor hallucis (oblique + transverse heads)Adducts hallux; stabilises transverse arch
Flexor digiti minimi brevisFlexes little toe
Layer 4 (deepest):
MuscleAction
Plantar interossei (3)Adduct toes 3-5, flex MTP
Dorsal interossei (4)Abduct toes 2-4, flex MTP

Why Lumbricals and Interossei Matter Most

  • Normally: lumbricals and interossei flex the MTP joint and extend the IP joints - keeping toes flat on the ground
  • When these weaken: the long flexors (FDL, FDB) and long extensors (EDL) dominate unopposed
  • Result: MTP hyperextension + IP flexion = claw toe or hammer toe
  • The fat pad (under the metatarsal heads) migrates distally with the toes, exposing the metatarsal heads to direct plantar pressure
  • This is why plantar metatarsal head ulcers are the most common site in neuropathic DFU

3. EXTRINSIC MUSCLES (Remain Strong - Cause the Deformity)

These originate in the leg and insert in the foot via long tendons.

Anterior Compartment (Dorsiflexors/Extensors)

MuscleNerveAction
Tibialis anteriorDeep peronealDorsiflexes + inverts foot
Extensor hallucis longus (EHL)Deep peronealExtends hallux, dorsiflexes
Extensor digitorum longus (EDL)Deep peronealExtends toes 2-5, dorsiflexes
Peroneus tertiusDeep peronealDorsiflexes + everts foot

Lateral Compartment (Everters)

MuscleNerveAction
Peroneus (Fibularis) longusSuperficial peronealEverts foot, plantarflexes, supports plantar arch
Peroneus brevisSuperficial peronealEverts foot

Posterior Compartment - Superficial (Plantarflexors)

MuscleNerveAction
GastrocnemiusTibialPlantarflexes foot, flexes knee
SoleusTibialPlantarflexes foot (key in weightbearing)
PlantarisTibialWeak plantarflexion
Gastrocnemius/soleus contracture (equinus deformity) is directly tested by the Silfverskiöld test and is a major contributor to forefoot plantar pressure and ulceration - Campbell's

Posterior Compartment - Deep (Toe Flexors/Invertors)

MuscleNerveAction
Flexor hallucis longus (FHL)TibialFlexes hallux at IP joint
Flexor digitorum longus (FDL)TibialFlexes toes 2-5 at DIP
Tibialis posteriorTibialInverts + plantarflexes; supports medial longitudinal arch
PopliteusTibialUnlocks the knee

4. THE DEFORMITY CHAIN - CONNECT THE DOTS

Motor neuropathy
        ↓
Intrinsic muscle wasting (especially lumbricals + interossei)
        ↓
Unopposed extrinsic muscle pull (EDL, FDL dominate)
        ↓
MTP hyperextension + IP flexion
        ↓
Claw toe / Hammer toe
        ↓
Distal migration of plantar fat pad
        ↓
Metatarsal heads exposed on plantar surface
        ↓
Repetitive pressure → Callus → Breakdown → Plantar ulcer
Gastrocnemius/soleus contracture (equinus)
        ↓
Increased forefoot plantar pressure
        ↓
Forefoot ulceration (especially metatarsal heads 1-5)
Autonomic neuropathy → loss of sweating (anhidrosis)
        ↓
Dry, cracked skin → portal of entry for bacteria
        ↓
Infection
Autonomic neuropathy → arteriovenous shunting in skin
        ↓
Decreased cutaneous perfusion + O₂ saturation
        ↓
Impaired wound healing + infection response

5. NERVES TO KNOW (Motor Supply to the Foot)

NerveCompartment SuppliedTest
Deep peroneal nerveAnterior compartment (dorsiflexors, EHL, EDL, EDB)Sensation: 1st web space
Superficial peroneal nerveLateral compartment (everters)Sensation: dorsum of foot
Tibial nervePosterior compartment + all plantar intrinsicsSensation: sole of foot
Sural nerveSensory: lateral footSensation: lateral border of foot
Saphenous nerveSensory: medial aspect of leg/footSensation: medial arch
In DFU, the tibial nerve supply to intrinsic plantar muscles is most clinically affected by the dying-back peripheral neuropathy of diabetes.

6. COMMON ULCER SITES - LINKED TO ANATOMY

Ulcer SiteCauseMuscle/Structure Involved
Plantar 1st metatarsal headHallux valgus + fat pad migrationEHL overpull, adductor hallucis weakness
Plantar lesser metatarsal heads (2nd-4th)Claw/hammer toes, fat pad shiftLumbrical/interossei weakness
Plantar 5th metatarsal baseLateral pressure from inverted footPeroneus longus/brevis dysfunction
Tip of toesClaw toe rubbing in shoeFDL overpull (IP flexion)
PIP joint dorsumHammer toe rubbing shoe toe boxFDL overpull at PIP
Heel/CalcaneumPressure (immobile patient) + ischemiaGastrocnemius-soleus pull (equinus)
MalleolusShoe pressure, footwear rubbing-
InterdigitalMaceration, fungal infection-

7. KEY REFLEXES AND TESTS - WHAT THEY TEST

TestWhat It TestsNormal vs. Abnormal
Semmes-Weinstein 10-g monofilamentPressure sensation (large fibre)Cannot feel = LOPS = major ulcer risk
128 Hz tuning fork (hallux/medial malleolus)Vibration sense (large fibre Aβ)Reduced/absent in neuropathy
Pinprick testPain sensation (small fibre Aδ)Reduced = small fibre neuropathy
Temperature (warm/cold tubes)Temperature sense (small fibre C)Reduced = small fibre neuropathy
Proprioception (hallux)Joint position sense (large fibre)Lost = balance problems, Charcot risk
Ankle jerk reflex (S1)Tibial nerve, S1 arcAbsent = peripheral neuropathy
Knee jerk reflex (L3/L4)Femoral nerveRelatively preserved unless severe
Silfverskiöld testGastrocnemius vs. Achilles contractureDorsiflexion worse with knee extended = gastrocnemius tight
ABI (Ankle-Brachial Index)Peripheral arterial disease<0.9 = PAD; >1.3 = calcified (non-compressible)
Probe-to-bone testOsteomyelitisPositive = 57% PPV; Negative = 96% NPV
Buerger's testSevere ischemiaPallor on elevation, dependent rubor = ischemia
Capillary refill timePerfusion>2 sec = impaired

8. THREE NEUROPATHIES - HIGH-YIELD SUMMARY

TypeNerves AffectedClinical Signs in DFU
Sensory neuropathyLarge fibres (Aβ): vibration, pressure, proprioception; Small fibres (Aδ, C): pain, temperatureLoss of protective sensation (LOPS); painless ulcer; ataxia
Motor neuropathyMotor fibres to intrinsic foot musclesEDB atrophy; claw/hammer toes; fat pad migration; high plantar pressure; Charcot joint
Autonomic neuropathyAutonomic fibres to sweat glands, skin vessels, AV shuntsDry cracked skin; warm foot with distended veins; AV shunting; Charcot joint; impaired healing

9. NEUROPATHIC vs. ISCHEMIC ULCER - MASTER COMPARISON TABLE

FeatureNeuropathic UlcerIschemic Ulcer
SitePlantar (pressure points, MTH)Toes, heel margins, between toes
PainPainless (LOPS)Painful (rest pain, worse at night)
MarginsPunched-out, surrounded by callusIrregular, sloping, no callus
BasePink granulation tissuePale, grey, necrotic/sloughy
Surrounding skinWarm, normal colourCold, pale, cyanotic or dependent rubor
PulsesPresent and boundingAbsent or weak
ABINormal or raised (calcification)<0.9 (often <0.5)
Foot temperatureWarmCool or cold
Foot appearanceClaw/hammer toes, callus, dry skinShiny, hairless, atrophic skin
OedemaMay be presentUsually absent
VeinsDistended (AV shunting)Collapsed (guttered)

10. CHARCOT NEUROARTHROPATHY - DO NOT MISS

Charcot foot (neuropathic arthropathy) is a limb-threatening diagnosis that is frequently mistaken for cellulitis/infection.
Mechanism: Autonomic neuropathy + sensory neuropathy → repeated unrecognised trauma → inflammatory cascade → bone resorption → fracture + dislocation → collapse of arch → rocker-bottom deformity
Classic presentation:
  • Warm, red, swollen foot/ankle in a diabetic with peripheral neuropathy
  • History of minor trauma (often forgotten)
  • Relatively painless
  • Blood glucose often normal, inflammatory markers normal or mildly raised
Key distinguishing feature from infection:
Elevate the limb - Charcot erythema and warmth subsides with elevation; infection does not - Campbell's Orthopaedics
Midfoot collapse → rocker-bottom foot → plantar bony prominences → midfoot ulceration (characteristic site)

11. MEMORY MNEMONICS

"SINK" - Risk factors for DFU

  • S - Sensory neuropathy (LOPS)
  • I - Ischemia (PAD)
  • N - Neuropathy (motor + autonomic)
  • K - Know your footwear (ill-fitting shoes)

"VINE" - Differences in Neuropathy types

  • Vibration + proprioception = large fibre
  • Ill-fitting shoe goes unnoticed = sensory
  • No sweating = autonomic
  • Extensor digiti brevis atrophy = motor

Wagner grades - "Superficial, Deep, Bone, Gangrene x2"

  • 0 = Pre-ulcer / healed
  • 1 = Superficial ulcer
  • 2 = Deep (tendon/capsule)
  • 3 = Bone (osteomyelitis/abscess)
  • 4 = Gangrene - local (toe/forefoot)
  • 5 = Ganglrene - global (whole foot)

"PAD LOPS = BAD PROGNOSIS"

  • PAD (peripheral arterial disease) + LOPS (loss of protective sensation) = 90x higher amputation risk when infection added

Probe-to-bone rule of 57/96

  • 57% PPV for osteomyelitis if positive
  • 96% NPV if negative (very useful to rule out)

Silfverskiöld test memory

  • "Knee bends, gastrocnemius relents"
  • When you bend the knee, gastrocnemius tension is relieved (it crosses the knee)
  • If dorsiflexion improves with knee flexed = gastrocnemius tight (not Achilles)
  • If dorsiflexion equally limited with knee bent and straight = Achilles contracture

12. THE ESSENTIAL EXAMINATION SEQUENCE (Memory Framework)

S - Shoes (inspect first)
I - Inspect both feet (deformity, callus, ulcer)
N - Neurological (monofilament, vibration, pinprick, reflexes)
V - Vascular (pulses, ABI, temperature, Buerger's)
U - Ulcer assessment (size, depth, probe-to-bone)
L - Locomotion/ROM (Silfverskiöld test, toe joints)
A - Additional (skin, sweat, EDB atrophy)
R - Record and classify (Wagner/WIfI)

Sources:
  • Campbell's Operative Orthopaedics 15e (Diabetic Foot, Basic Science + Physical Examination Box 91.1)
  • Dermatology 2-Volume Set 5e (Pathogenesis of Diabetic Ulcers)
  • Current Surgical Therapy 14e (Evaluation of the Diabetic Foot)

Now can you create a whole length case scenario long case including history taking right from pt name chief complaint Hopi systemic review past medical surgical history diet history allergic history medication history family history social history then physical examination thorough then findings then ix mx

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LONG CASE: DIABETIC FOOT ULCER

A Complete Clinical Case for Medical Students and Postgraduates


PATIENT IDENTIFICATION

NameMr. Muhammad Rafiq
Age58 years
SexMale
OccupationRetired government officer
AddressUrban residential area
Date of Admission03 June 2026
WardGeneral Surgery / Vascular Ward
Referred byGeneral Practitioner
InformantPatient himself (reliable historian)

CHIEF COMPLAINT

"I have a wound on the bottom of my right foot that is not healing for the past 3 months."

HISTORY OF PRESENTING ILLNESS (HOPI)

Mr. Muhammad Rafiq, a 58-year-old retired male with a 14-year history of Type 2 Diabetes Mellitus, presents with a non-healing ulcer on the plantar aspect of his right foot of 3 months duration.
Onset and development: The patient first noticed a small blister under the ball of his right foot approximately 3 months ago. He does not recall any specific injury. He reports that he was wearing a new pair of shoes the week before. Because of numbness in his feet, he did not experience pain and did not seek medical attention at that time. Over the following 2 weeks, the blister burst on its own, leaving a small open wound. He applied antiseptic cream (povidone-iodine) at home and covered it with gauze. The wound did not heal and gradually increased in size over 6 weeks.
Progression: Approximately 6 weeks ago, the surrounding skin became red and slightly swollen. He noticed a foul-smelling yellowish discharge from the wound. He visited his GP at that point and was started on oral co-amoxiclav 625 mg three times daily for 7 days. There was partial improvement in the surrounding redness, but the wound itself did not close. Over the past 2 weeks, he noticed the wound had become deeper and he could probe it himself with a matchstick, feeling something hard at the base.
Current state:
  • Wound size has increased to approximately 3 cm × 2 cm
  • Discharge is now thick, purulent, and foul-smelling
  • Surrounding skin is red, warm, and swollen
  • He denies feeling pain in the ulcer itself (due to neuropathy)
  • He reports a dull aching in the right foot that is worse at night - he hangs the leg over the bedside for some relief (suggesting ischemic component)
  • He has been limping but continues to bear weight on the affected foot
  • No crepitus noticed
Associated symptoms:
  • Fever for the past 5 days: documented temperature of 38.4°C at home
  • Chills and rigors: present, mild
  • Reduced appetite over the past 2 weeks
  • Increased thirst and urination over the past 3 weeks
  • No vomiting
  • No symptoms of upper respiratory tract infection

SYSTEMIC REVIEW

Cardiovascular:
  • Exertional chest pain: none
  • Palpitations: occasional, non-specific
  • Leg pain on walking (claudication): YES - right calf pain after walking approximately 200 metres on flat ground, relieved by rest (intermittent claudication)
  • Orthopnoea or PND: absent
  • Ankle swelling: mild bilateral ankle oedema
Respiratory:
  • No cough, shortness of breath, or haemoptysis
Gastrointestinal:
  • Nausea: mild, present
  • Appetite reduced over past 2 weeks
  • No diarrhoea or constipation
  • Diabetic gastroparesis: uncertain (occasional bloating and fullness after meals)
  • Bowel habit otherwise normal
Genitourinary:
  • Polyuria: yes, for the past 3 weeks (waking 3 times at night)
  • Polydipsia: yes
  • No dysuria, haematuria, or frothy urine (no known proteinuria but not recently checked)
  • Erectile dysfunction: present, for approximately 3 years (autonomic neuropathy feature)
Neurological:
  • Bilateral foot numbness and tingling: present for approximately 5 years, worse at night
  • "Walking on cotton wool" sensation: present
  • No burning pain in feet (he had this 3 years ago but it has now gone - suggests progression to complete LOPS)
  • No visual disturbance currently (but was told he has "background retinopathy" 2 years ago)
  • Dizziness on standing up quickly (postural hypotension - autonomic neuropathy)
  • No seizures, weakness of upper limbs, or speech difficulty
Musculoskeletal:
  • Reduced mobility over past 3 months due to foot wound
  • No joint pain in upper limbs
  • Right foot deformity noted by patient
Skin:
  • Dry cracked skin on both heels (chronic)
  • No other skin rashes

PAST MEDICAL HISTORY

ConditionDurationControlled?
Type 2 Diabetes Mellitus14 yearsPoorly controlled (last HbA1c 10.2%)
Hypertension10 yearsOn medications
Dyslipidaemia8 yearsOn statin
Peripheral Arterial DiseaseDiagnosed 2 years ago on DopplerOn antiplatelet
Diabetic Retinopathy (background)2 years agoUnder ophthalmology review
Chronic Kidney Disease Stage 318 months ago (eGFR 42 ml/min)Under nephrology
Previous right 5th toe amputation4 years ago (for infected gangrenous toe)Healed

PAST SURGICAL HISTORY

ProcedureYearIndication
Right 5th toe amputation2022Gangrenous toe - diabetic foot
Appendicectomy1998Acute appendicitis
Coronary angiography2023Chest pain workup (normal coronaries)

DIET HISTORY

  • Diet: mixed non-vegetarian diet
  • Carbohydrate intake: HIGH - patient admits to eating white rice at least twice daily, bread, sugary tea (3-4 cups per day with 2 teaspoons of sugar each)
  • Fruit and vegetable intake: low
  • Compliant with diabetic diet: NO - not following dietitian advice
  • Alcohol: denies current use (stopped 10 years ago, previously social drinker)
  • Fluid intake: adequate
  • Weight: 92 kg (obese)
  • BMI: approximately 31 kg/m²

ALLERGIC HISTORY

  • Penicillin allergy: Yes - developed a maculopapular rash when given ampicillin 6 years ago
  • No allergy to latex, iodine, or other medications
  • No food allergies

MEDICATION HISTORY

DrugDoseFrequencyDuration
Metformin 500 mg500 mgBD with food12 years
Glibenclamide 5 mg5 mgOD morning8 years
Insulin Glargine (Lantus)24 units SCOD at night3 years
Enalapril 10 mg10 mgOD10 years (ACE inhibitor for BP + renal protection)
Atorvastatin 40 mg40 mgOD at night8 years
Aspirin 75 mg75 mgOD5 years
Clopidogrel 75 mg75 mgOD2 years (dual antiplatelet for PAD)
Co-amoxiclav 625 mg625 mgTDSStarted 6 weeks ago (last prescribed by GP)
Compliance: Admits to missing insulin injections on weekends. Takes oral tablets irregularly when he "feels well."

FAMILY HISTORY

RelativeConditionAge of Onset / Remarks
FatherType 2 DM, hypertensionDied aged 70, complications of DM
MotherHypertension, strokeAlive, aged 82
Elder brotherType 2 DMDiagnosed at 52
Son (32 years)No known illnessHealthy

SOCIAL HISTORY

  • Occupation: Retired government officer (sedentary lifestyle for 15 years)
  • Living situation: Lives with wife and adult son; has family support at home
  • Smoking: Ex-smoker - smoked 20 cigarettes/day for 25 years; stopped 8 years ago (50 pack-years)
  • Alcohol: Ex-drinker, stopped 10 years ago
  • Exercise: Minimal - walks short distances only; no regular exercise
  • Footwear: Wears ordinary closed leather shoes purchased from a regular shop; not custom-made or therapeutic
  • Foot care: Does not inspect feet daily (cannot see them due to obesity and mild visual blurring); wife assists occasionally
  • Mobility: Ambulatory with limp; uses a walking cane for the past 4 weeks
  • Financial status: Middle income; has health insurance coverage
  • Vaccination: No recent tetanus booster recalled

PHYSICAL EXAMINATION

General Physical Examination

General appearance:
  • Obese, middle-aged male
  • Alert and oriented to time, place, and person
  • In mild distress; right foot elevated on a pillow
  • Appears unwell but not critically ill
Vital Signs:
ParameterFinding
Temperature38.5°C (febrile)
Heart Rate96 bpm, regular
Blood Pressure148/90 mmHg (right arm, sitting)
Respiratory Rate18 breaths/min
SpO₂98% on room air
Blood Glucose (RBS)18.4 mmol/L (331 mg/dL)
Weight92 kg
Height172 cm
BMI31.1 kg/m² (obese)
Postural BP check:
  • Sitting: 148/90 mmHg
  • Standing: 132/78 mmHg
  • Drop of 16 mmHg systolic = orthostatic hypotension (autonomic neuropathy)

Head and Neck

  • Anicteric sclerae
  • No pallor (conjunctival)
  • Dry mucous membranes (hyperglycaemia)
  • No cervical lymphadenopathy
  • Fundoscopy not performed at bedside (ophthalmology to review)

Cardiovascular Examination

  • Pulse: 96 bpm, regular, good volume bilaterally in upper limbs
  • JVP: not elevated
  • Apex beat: 5th intercostal space, mid-clavicular line (not displaced)
  • Heart sounds: S1 and S2 present, no murmurs
  • No pericardial rub
Lower limb pulses:
PulseRightLeft
FemoralPalpable, normalPalpable, normal
PoplitealPalpable, reducedPalpable, normal
Posterior tibialAbsentPalpable, reduced
Dorsalis pedisAbsentPalpable, reduced

Respiratory Examination

  • Chest expansion: equal bilaterally
  • Percussion: resonant throughout
  • Auscultation: vesicular breath sounds, no added sounds
  • No features of pulmonary oedema

Abdominal Examination

  • Abdomen: soft, obese, non-tender
  • No hepatomegaly or splenomegaly
  • Appendicectomy scar: present, well-healed, right iliac fossa
  • No renal angle tenderness
  • Bowel sounds: present and normal

Lymph Node Examination

  • Right inguinal lymph nodes: palpable, enlarged, tender (reactive to right foot infection)
  • Left inguinal: not enlarged
  • No axillary or cervical lymphadenopathy

LOWER LIMB EXAMINATION (Detailed - Right vs. Left)

SHOE INSPECTION

  • Ordinary closed leather shoes, right shoe worn more medially
  • No custom insoles or therapeutic footwear
  • Seam visible on the inner right shoe lateral side where the 5th toe used to be
  • Abnormal wear pattern on the right sole: increased under the 1st metatarsal head area

GENERAL INSPECTION OF BOTH FEET

FeatureRight FootLeft Foot
DeformityClaw toes (2nd-4th), hallux valgus, old 5th toe amputation stumpClaw toes (2nd-3rd), hammer toe (4th)
Skin colourErythema around ulcer; dependent rubor (foot dependent)Pale, dull
Skin textureDry, fissured heel; skin around ulcer maceratedDry, cracked heel; shiny, hairless dorsum
HairAbsent on dorsum of right footAbsent on dorsum of left foot
Venous gutteringPresent bilaterally when elevatedPresent
TemperatureWarm around wound, cool toesCool throughout
SweatingAbsent (anhidrosis) both feetAbsent
OedemaMild pitting oedema right ankleMild bilateral ankle oedema
Muscle wastingExtensor digitorum brevis (EDB) atrophy visible on dorsumEDB atrophy present

ULCER ASSESSMENT (RIGHT FOOT)

Site: Plantar surface of the right foot, directly over the 1st metatarsal head (most common neuropathic site)
Size: 3.2 cm × 2.1 cm (cross-sectional area approximately 6.7 cm²)
Shape: Round, punched-out appearance
Margins: Well-defined, callus surrounding the ulcer on all sides; undermined edge at 9 o'clock position
Depth: Deep - probing with a sterile cotton swab reaches a hard surface (bone) at the base
Wound base: Mixed - 40% pale yellow fibrinous slough, 30% necrotic black tissue at the edges, 30% pink granulation tissue
Surrounding tissue:
  • Erythema extending 2.5 cm beyond the wound margin (cellulitis)
  • Warmth and induration
  • No crepitus on palpation (no gas-forming organisms)
  • Callus thickened, moist, and malodorous
Discharge: Thick, purulent, foul-smelling, yellow-green
Probe-to-bone test: POSITIVE - rigid resistance felt at wound base (57% PPV for osteomyelitis; strongly suspicious)
Lymphangitic streaking: faint red line tracking up medial side of right leg (early lymphangitis)

VASCULAR ASSESSMENT

Skin temperature: Right foot cool from mid-foot distally; left foot cool at toes
Capillary refill time:
  • Right hallux: >4 seconds (markedly prolonged - ischemia)
  • Left hallux: 3 seconds (prolonged)
Buerger's Test (Right Foot):
  • Elevation to 45° for 2 minutes: pallor appears within 90 seconds
  • Lowering to dependent position: sluggish dependent rubor after 3 minutes
  • Buerger's angle: approximately 30° (positive; significant ischemia)
Ankle-Brachial Index (ABI - measured with handheld Doppler):
RightLeft
Brachial systolic BP148 mmHg146 mmHg
Ankle systolic BP (posterior tibial)62 mmHg94 mmHg
ABI0.420.64
  • Right ABI 0.42 = severe peripheral arterial disease (critical ischemia threshold)
  • Left ABI 0.64 = moderate PAD

NEUROLOGICAL ASSESSMENT

Semmes-Weinstein 10-g Monofilament (10 sites each foot):
SiteRightLeft
Hallux pulpUnable to feelUnable to feel
1st metatarsal headUnable to feelUnable to feel
3rd metatarsal headUnable to feelUnable to feel
5th metatarsal headAbsent (5th toe amputated)Unable to feel
Plantar archUnable to feelAble to feel (barely)
HeelUnable to feelUnable to feel
Dorsal 1st web spaceUnable to feelUnable to feel
ResultComplete LOPSLOPS (partial)
Vibration sense (128 Hz tuning fork):
  • Right hallux: absent
  • Right medial malleolus: absent
  • Left hallux: reduced (feels vibration for 4 seconds vs. 18 seconds on examiner's finger)
Pinprick sensation:
  • Right foot: absent below ankle
  • Left foot: reduced below ankle
Temperature discrimination:
  • Right foot: unable to distinguish warm from cold
  • Left foot: reduced
Proprioception:
  • Right hallux: absent (cannot detect up/down movement)
  • Left hallux: reduced
Ankle jerk reflex (S1):
  • Right: absent
  • Left: absent
Knee jerk reflex (L3/L4):
  • Bilateral: present but reduced

RANGE OF MOTION - SILFVERSKIÖLD TEST (Right)

  • Ankle dorsiflexion with knee extended: -5° (5° plantarflexion - cannot get to neutral)
  • Ankle dorsiflexion with knee flexed 90°: +8° (improves significantly)
  • Interpretation: Gastrocnemius contracture (equinus) on the right - contributing to increased forefoot plantar pressure and 1st metatarsal head ulceration

MOTOR EXAMINATION

  • Tibialis anterior (L4): 4/5 bilaterally
  • Extensor hallucis longus (L5): 4/5 right, 4/5 left
  • Peronei (L5/S1): 4/5 bilaterally
  • Gastrocnemius/soleus (S1/S2): 4+/5 bilaterally
  • Toe flexion and extension: reduced (3/5) all toes, right foot
  • EDB atrophy: visible and confirmed by palpation bilaterally (sign of motor neuropathy)

Charcot Assessment

  • No acute Charcot changes currently present
  • No acute bony swelling or marked warmth of ankle/midfoot
  • Old 5th toe amputation stump well-healed

SUMMARY OF FINDINGS

Mr. Muhammad Rafiq is a 58-year-old obese male with 14-year poorly-controlled Type 2 DM, hypertension, dyslipidaemia, CKD stage 3, background diabetic retinopathy, and known PAD, presenting with a 3-month history of a non-healing plantar ulcer over the right 1st metatarsal head.
Key positive findings:
  1. Plantar ulcer right 1st MTH: 3.2 × 2.1 cm, punched-out, callus-surrounded, purulent discharge, probe-to-bone positive
  2. Surrounding cellulitis 2.5 cm, early lymphangitis
  3. Systemic infection: fever 38.5°C, tachycardia 96 bpm, hyperglycaemia 18.4 mmol/L
  4. Complete loss of protective sensation both feet (10-g monofilament)
  5. Severe PAD right foot: absent posterior tibial and dorsalis pedis pulses, ABI 0.42, positive Buerger's test
  6. Gastrocnemius contracture: Silfverskiöld positive right foot
  7. Motor neuropathy: EDB atrophy, claw toes 2nd-4th right, hammer toe 4th left
  8. Autonomic neuropathy: anhidrosis, orthostatic hypotension, erectile dysfunction
Classification:
  • Wagner Grade 3 (deep ulcer with suspected osteomyelitis)
  • University of Texas: Grade 3D (deep ulcer + infection + ischemia)
  • WIfI Stage: W2, I3, fI2 (wound grade 2, severe ischemia, moderate foot infection) → High amputation risk; revascularisation likely to benefit

INVESTIGATIONS

Bedside

InvestigationResult
RBS18.4 mmol/L
Urine dipstickGlucose 3+, Protein 1+, Ketones trace
Wound swab (for culture and sensitivity)Sent - pending

Haematology

InvestigationResultReference
Haemoglobin10.8 g/dLLow (anaemia of chronic disease)
WBC16.4 × 10⁹/LHIGH (infection)
Neutrophils13.2 × 10⁹/LHIGH (neutrophilia)
Platelets425 × 10⁹/LMildly elevated (reactive)
ESR88 mm/hourHIGH (normal <20)
CRP112 mg/LHIGH (normal <5)

Biochemistry

InvestigationResultReference
Fasting glucose14.2 mmol/LHigh
HbA1c10.2%Very poorly controlled
Urea11.8 mmol/LHigh (CKD + dehydration)
Creatinine162 µmol/LHigh (CKD stage 3)
eGFR38 ml/minReduced
Sodium136 mmol/LNormal
Potassium4.4 mmol/LNormal
LFTsAll normalNormal
Albumin28 g/LLOW (poor nutritional state - impairs healing)
Total cholesterol5.8 mmol/LElevated
LDL3.6 mmol/LHigh
Triglycerides2.4 mmol/LHigh

Microbiology

InvestigationExpected findings
Deep wound swab culturePolymicrobial: likely S. aureus (dominant), Pseudomonas aeruginosa, anaerobes
Blood cultures (×2 peripheral sets)Sent - if bacteraemia
Bone biopsy culture (if surgery performed)Gold standard for osteomyelitis organism ID

Radiology

InvestigationFindings
Plain X-ray right foot (3 views: AP, lateral, oblique)Cortical erosion and irregularity of the 1st metatarsal head; soft tissue swelling; no gas in soft tissues; old 5th toe amputation changes
MRI right foot (with gadolinium)Most sensitive for osteomyelitis - expected: bone marrow oedema 1st metatarsal head, deep soft tissue collection, sinus tract
Doppler duplex ultrasound of right lower limbConfirms PAD: significant flow reduction right popliteal to pedal vessels
CT angiography right lower limbPlanned: to map arterial anatomy for revascularisation planning (tibial/peroneal disease pattern)
EchocardiogramTo assess cardiac function before any vascular surgery

MANAGEMENT

Immediate (Acute Admission - First 24-48 hours)

1. Strict non-weight-bearing - right foot
  • Bed rest, right foot elevated
  • Patient must NOT bear weight on affected foot
2. IV access and fluid resuscitation
  • Two large-bore IV cannulae
  • IV normal saline (adjust for CKD - careful fluid balance)
3. Glycaemic control
  • Stop oral hypoglycaemics (CKD - metformin contraindicated at eGFR <30; risk worsens)
  • IV insulin sliding scale protocol to achieve BG 7-10 mmol/L
  • Endocrinology referral for long-term insulin optimisation
  • Target HbA1c <8% (more liberal given co-morbidities per current evidence)
4. Empirical antibiotic therapy
  • Note: patient has penicillin allergy (maculopapular rash to ampicillin)
  • Avoid beta-lactams/penicillins
  • Empirical regimen (severe infected DFU with suspected osteomyelitis):
    • IV Vancomycin 15 mg/kg q12h (gram-positive cover including MRSA) - dose-adjust for CKD (renal function guided dosing)
    • IV Metronidazole 500 mg q8h (anaerobic cover)
    • IV Ciprofloxacin 400 mg q12h (gram-negative including Pseudomonas cover) - dose-adjust for CKD
  • Switch to culture-guided therapy once results available (5-7 days)
  • Duration: if bone resected with clear margins: 2-3 weeks; if bone infected and not fully resected: 4-6 weeks IV then oral
5. Wound management
  • Bedside debridement of callus and necrotic tissue (surgical team)
  • Normal saline wound irrigation
  • Moist wound dressing: non-adherent dressing with antimicrobial cover
  • Daily wound review with wound size documentation
  • Mark cellulitis margins with a skin marker pen to monitor spread
6. Analgesia
  • Paracetamol 1g QDS regular (safe in CKD)
  • Avoid NSAIDs (CKD, cardiovascular disease)
  • If neuropathic pain present: consider Pregabalin (dose-reduce in CKD) or Amitriptyline low dose

Surgical Management

Urgent surgical referral:
  1. Surgical debridement: formal theatre debridement of necrotic tissue, infected bone, and collection under anaesthesia
  2. Bone biopsy at time of debridement: send for histology and culture (gold standard osteomyelitis diagnosis)
  3. Vascular surgery review: CTA findings to guide revascularisation
    • Right ABI 0.42: severe ischemia - wound will not heal without revascularisation
    • Options: percutaneous transluminal angioplasty (PTA) of tibial vessels (first choice, less invasive) or bypass surgery (if anatomy suitable)
    • Revascularisation should precede or accompany definitive wound surgery where possible
  4. Possible ray amputation (resection of 1st metatarsal + toe) if bone and soft tissue non-salvageable
  5. Silfverskiöld test positive → Consider surgical gastrocnemius lengthening or percutaneous Achilles tendon lengthening at a later stage to reduce forefoot plantar pressure

Medical Management (Ongoing)

IssueManagement
HypertensionContinue Enalapril; adjust dose for CKD; target BP <130/80 mmHg in DM
DyslipidaemiaContinue atorvastatin 40 mg; consider increasing to 80 mg (high-intensity)
CKD Stage 3Nephrology review; hold metformin; careful drug dosing; monitor renal function
Antiplatelet therapyContinue aspirin 75 mg; continue clopidogrel (PAD/anticoagulation review pre-surgery)
Nutritional supportDietitian referral: high-protein diet (albumin 28 g/L); targeted nutritional supplementation; reduce refined carbohydrates; calorific goal 30-35 kcal/kg/day
AnaemiaCheck iron studies, B12, folate; treat underlying cause; ensure adequate nutrition

Multidisciplinary Team (MDT) Referrals

SpecialtyReason
Vascular SurgeryRevascularisation - ABI 0.42, absent pedal pulses
Orthopaedic SurgeryOsteomyelitis management, bone debridement, deformity correction
Endocrinology / DiabetologistGlycaemic optimisation
NephrologyCKD management, drug dosing
OphthalmologyBackground retinopathy follow-up
PodiatryWound care, offloading, custom footwear planning post-healing
DietitianNutritional rehabilitation
PhysiotherapyMobility, non-weight-bearing gait training, post-surgical rehabilitation
Wound Care NurseDaily wound dressing, assessment, documentation
Pain TeamNeuropathic pain management

Long-Term Prevention and Foot Care Education

  • Custom therapeutic footwear with extra-depth toe box and moulded insoles (once healed)
  • Daily foot inspection: patient + wife (given visual blurring); use of a foot mirror
  • No barefoot walking at any time (indoors or outdoors)
  • Annual comprehensive foot examination
  • Monofilament testing at every diabetic review appointment
  • Regular podiatry: nail care, callus debridement (every 6-8 weeks minimum)
  • Smoking cessation: already achieved (8 years) - reinforce and document
  • Glycaemic education: structured diabetes education programme
  • Stocking/footwear advice: no tight elastic socks, no synthetic non-breathable materials

PROGNOSIS

  • Wagner Grade 3 + University of Texas Grade 3D (infection + ischemia): carries a 40-55% risk of amputation without optimal management
  • ABI 0.42: wound healing unlikely without revascularisation
  • Positive probe-to-bone: confirmed osteomyelitis likely; will require surgical bone debridement
  • With optimal multidisciplinary management (revascularisation + debridement + glycaemic control + offloading): amputation-free survival achievable in approximately 65-70% of cases

Sources: Campbell's Operative Orthopaedics 15e; Harrison's Principles of Internal Medicine 22e; Current Surgical Therapy 14e; Bailey & Love's Short Practice of Surgery 28e; Rosen's Emergency Medicine 10e; Dermatology 2-Volume Set 5e

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DIABETIC FOOT ULCER

Complete History Taking + Expanded Physical Examination + Investigations + Management


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PART 1: HISTORY TAKING

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1. PATIENT IDENTIFICATION

Always establish these before anything else:
  • Full name
  • Age / Date of birth
  • Sex
  • Occupation (current and past - standing/walking occupations increase DFU risk)
  • Address (urban vs. rural = access to care)
  • Referred by (GP, A&E, community nurse)
  • Informant and reliability

2. CHIEF COMPLAINT

State exactly in the patient's own words, with duration:
"I have a wound on the bottom of my foot that is not getting better, for 3 months."
The four key words to establish immediately: where, what, when, and what happened.

3. HISTORY OF PRESENTING ILLNESS (HOPI)

Structure using SOCRATES for the wound, then expand into the diabetic context.
S - Site
  • Exact location of the wound: plantar (sole), dorsum, toes, heel, interdigital, malleolus
  • Which foot: right, left, or bilateral?
  • Which specific anatomical area: metatarsal head, toe tip, heel, arch
O - Onset
  • How did it start? (blister, callus that broke down, cut, burn, pressure sore, spontaneous)
  • Was there any preceding trauma? (patient may deny injury - ask specifically about new shoes, foreign body, stepping on something)
  • Was it noticed by the patient or by someone else? (if found by another person = complete LOPS - clinically significant)
C - Character
  • Nature of the wound: open, closed blister, crack
  • Painless or painful?
    • Painless ulcer = sensory neuropathy (commonest)
    • Painful ulcer = ischemia, infection, or intact sensation
    • Night pain worse at rest, relieved by hanging leg = ischemic rest pain
R - Radiation / Spread
  • Has the wound increased in size?
  • Is surrounding redness spreading (cellulitis)?
  • Any red lines tracking up the leg (lymphangitis)?
A - Associated symptoms
  • Discharge: yes/no, colour (clear, yellow, green, brown), consistency (watery, thick purulent), smell (foul = infection/anaerobes)
  • Swelling: local or spreading
  • Warmth
  • Fever, chills, rigors (systemic sepsis)
  • New confusion or deterioration in elderly diabetics = sepsis until proven otherwise
T - Time course
  • Duration of ulcer
  • Speed of progression: slow (weeks/months - neuropathic) vs. rapid (days - infected/ischemic)
  • Any prior healing and re-breakdown at same site?
E - Exacerbating / Relieving factors
  • Weight bearing makes it worse (pressure)
  • Elevation relieves ischemic pain
  • Rest relieves claudication
  • Tight footwear exacerbates
S - Severity
  • Impact on mobility: walking with limp? Completely non-weight-bearing?
  • Impact on daily activities, sleep
  • Prior visits to GP/hospital for this wound - treatments tried (antibiotics, dressings, debridement)

4. DIABETES HISTORY (Dedicated Section)

  • Type of DM: Type 1 or Type 2
  • Duration of diagnosis
  • How was it diagnosed? (symptoms, routine screening, incidental finding)
  • Current medications: insulin (type, dose, timing), oral agents
  • Glycaemic control:
    • Most recent HbA1c and date
    • Home blood glucose monitoring frequency and values
    • Frequency of hypoglycaemic episodes
  • Compliance: missing doses? Dose adjustment by patient?
  • Dietary adherence: following diabetic diet?
  • Regular monitoring appointments (diabetic clinic, GP)

5. FOOT-SPECIFIC HISTORY

  • Previous ulcers: number of episodes, sites, how they healed, time to heal
  • Previous foot infections requiring hospitalisation
  • Previous amputations: level (toe, ray, transmetatarsal, below-knee, above-knee), side, year, reason
  • History of Charcot neuroarthropathy: sudden hot swollen foot/ankle in the past
  • Footwear: type normally worn (open sandals, closed shoes, slippers), custom therapeutic footwear, fitting
  • Daily foot care routine: does the patient inspect their own feet daily? Can they reach their feet? Do they use a mirror?
  • Nail care: who cuts nails, how (clippers or scissors - important to ask)
  • Previous callus removal or podiatry visits
  • Any history of foreign body in the shoe unnoticed (classic neuropathy story)

6. NEUROPATHY SYMPTOMS

Sensory neuropathy:
  • Numbness: feet, ankles, legs - how far up does it go?
  • Tingling / "pins and needles"
  • Burning, shooting, electric pains (small fibre neuropathy - these are early symptoms)
  • Loss of burning sensation in feet (absent pain when stepping on hot surface = LOPS)
  • "Walking on cotton wool" or "walking on pebbles" sensation
  • Unsteadiness in the dark (proprioceptive loss)
  • Duration of symptoms
Motor neuropathy:
  • Has foot shape changed?
  • Difficulty walking, tripping, foot drop
  • Weakness in ankles or toes
Autonomic neuropathy:
  • Dry feet (no sweating): a direct question since patients rarely volunteer this
  • Dizziness on standing (postural hypotension)
  • Bloating, nausea, fullness after small meals (gastroparesis)
  • Diarrhoea alternating with constipation (autonomic gut)
  • Erectile dysfunction (men) / female sexual dysfunction
  • Urinary retention or incontinence (neurogenic bladder)
  • Palpitations (cardiac autonomic neuropathy)

7. VASCULAR / ISCHEMIA HISTORY

  • Leg pain on walking: which muscles? (calf = SFA disease; thigh/buttock = aortoiliac disease)
  • Claudication distance: how far can the patient walk before pain starts?
  • Does pain resolve within 2-3 minutes of rest? (claudication) vs. persists longer?
  • Rest pain: pain in toes/forefoot at rest, worse at night, relieved by hanging leg out of bed (critical ischemia)
  • Previous vascular surgery: angioplasty, stenting, bypass
  • Cold feet: persistent, one side worse than other?
  • Colour changes: pallor, blueness of toes
  • Smoking history: current/ex, how many cigarettes per day, for how many years (pack-years = packs/day × years)
  • Previous MI, stroke, TIA, or angina (systemic atherosclerosis)

8. SYSTEMIC REVIEW

Cardiovascular:
  • Chest pain, shortness of breath on exertion, orthopnoea, PND
  • Palpitations
  • Ankle swelling
Respiratory:
  • Cough, shortness of breath
  • Important if patient will need surgery/anaesthesia
Gastrointestinal:
  • Nausea, vomiting, reduced appetite (infection, uraemia)
  • Bowel habit change
  • Weight loss (malnutrition = impaired wound healing)
Genitourinary:
  • Polyuria, polydipsia (hyperglycaemia)
  • Frothy urine (proteinuria = nephropathy)
  • Reduced urine output (AKI on CKD in sepsis)
Eyes:
  • Visual changes, blurring (retinopathy)
  • Inability to inspect feet due to poor vision - a safety concern
Systemic infection symptoms:
  • Fever, chills, rigors
  • Confusion in elderly (septic encephalopathy)

9. PAST MEDICAL HISTORY (PMH)

Ask specifically about each complication of diabetes:
ConditionAsk directly
Type 2 DMDuration, control
HypertensionDuration, medications
DyslipidaemiaOn statin?
Peripheral Arterial DiseaseDiagnosed? Treated?
Ischaemic Heart DiseaseAngina, MI, stents
Cerebrovascular DiseaseStroke, TIA
Diabetic RetinopathyGrade, last eye review
Diabetic Nephropathy/CKDeGFR, dialysis, transplant
Previous DFU / AmputationSite, level, year
Charcot neuroarthropathyHistory of hot swollen foot
OsteomyelitisPrevious episodes, treatment
ObesityBMI

10. PAST SURGICAL HISTORY (PSH)

  • Previous amputations (level, side, year)
  • Vascular procedures (angioplasty, bypass)
  • Any foot/ankle surgeries
  • Any other surgeries and complications

11. DRUG AND ALLERGY HISTORY

Medications - ask systematically:
  • Antidiabetic agents: metformin, sulfonylureas, SGLT2 inhibitors, GLP-1 agonists, insulin (type + dose + timing)
  • Antihypertensives: ACE inhibitors, ARBs, calcium channel blockers, beta-blockers
  • Antiplatelet agents: aspirin, clopidogrel
  • Statins
  • Anticoagulants (warfarin, DOAC): important for surgical planning
  • Steroids or immunosuppressants: impair healing and mask infection signs
  • Any recent antibiotics: which ones, duration, response - critical for culture interpretation
Allergy history:
  • Drug allergies: specify drug name AND type of reaction (rash, anaphylaxis, GI upset)
  • Penicillin allergy: very common, affects antibiotic choice
  • Latex allergy (relevant for theatre)
  • Iodine/antiseptic allergy
Compliance:
  • Are medications taken regularly?
  • Any recent changes in dosing?

12. DIET AND NUTRITIONAL HISTORY

  • Type of diet: vegetarian, non-vegetarian, mixed
  • Carbohydrate intake: rice, bread, sugary drinks, sweets
  • Protein intake: meat, fish, eggs, dairy (albumin <30 = poor healing prognosis)
  • Fruit and vegetable intake
  • Fluid intake
  • Alcohol: type, frequency, quantity (units/week)
  • Following diabetic diet advice: yes/no
  • Seen a dietitian? How long ago?
  • Appetite: reduced recently? (chronic illness, infection, depression)
  • Recent unintentional weight loss?

13. FAMILY HISTORY

  • Diabetes mellitus in parents, siblings, children
  • Peripheral vascular disease, cardiovascular disease
  • Lower limb amputations in family members
  • Hypertension, stroke, renal disease

14. SOCIAL HISTORY

  • Occupation: seated desk job vs. standing/walking job
  • Retired or working?
  • Living alone or with family - crucial for wound care compliance and follow-up
  • Home support: is anyone able to assist with foot inspection, dressing changes?
  • Ability to attend clinic: transport, mobility
  • Smoking: current, ex, never; pack-years
  • Alcohol: units/week
  • Exercise level: minimal, moderate, active
  • Ability to inspect own feet: limited by obesity? Reduced vision?
  • Financial status and insurance: impacts access to custom footwear, podiatry, specialist care
  • Tetanus vaccination status

════════════════════════════════

PART 2: PHYSICAL EXAMINATION (FULLY EXPANDED)

════════════════════════════════


STEP 1: GENERAL INSPECTION (Before touching the patient)

Stand back and observe for 30 seconds.
What to look for:
  • Level of consciousness and orientation
  • Facial appearance: flushed (fever), pale (anaemia), grimacing (pain vs. expressionless in neuropathy)
  • Body habitus: obesity (BMI estimate)
  • Obvious distress: patient holding or elevating affected foot
  • Sitting position: is the affected leg elevated or dependent?
  • Prosthetics visible on the bed
  • Wound dressing or bandaging already in place
  • Walking aids present: crutches, wheelchair, walking frame, cane
  • Smell: foul odour from wound (anaerobic or polymicrobial infection)

STEP 2: VITAL SIGNS

ParameterWhat to look for in DFU
TemperatureFever >38°C = systemic infection; Hypothermia in elderly sepsis
Heart rateTachycardia >90 = stress response, sepsis, dehydration
Blood pressureHypertension (common in DM); Postural drop (autonomic neuropathy)
Respiratory rateTachypnoea in sepsis; Kussmaul breathing if DKA
SpO₂Baseline assessment; low = sepsis complication
Blood glucose (RBS)Usually elevated; very high >20 mmol/L = poor control + stress response
Weight + Height + BMIObesity drives poor control, poor healing, pressure
Postural blood pressure: Measure lying/sitting and standing.
  • Drop of >20 mmHg systolic or >10 mmHg diastolic = orthostatic hypotension = autonomic neuropathy

STEP 3: SHOE AND FOOTWEAR INSPECTION (Before removing shoes)

This is done before removing the shoes - a step many students forget.
What to examine:
  • Type of shoe: open sandal, closed shoe, trainer, slipper, therapeutic shoe
  • Size: is it the correct size? Too small = pressure over bony prominences
  • Toe box depth and width: must accommodate toe deformities
  • Seams or ridges on the inner surface that the patient cannot feel (a foreign body inside a shoe that causes an ulcer = hallmark of LOPS)
  • Sole wear pattern:
    • Uniform wear = normal
    • Excessive wear under 1st MTH = hallux valgus, equinus
    • Lateral sole wear = supination/cavus foot
    • Medial sole wear = pronation/flatfoot
  • Any blood staining or discharge on the inner lining
  • Insoles: present? Custom-moulded?

STEP 4: LOWER LIMB INSPECTION (Both feet - shoes and socks removed)

Examine both feet simultaneously and compare.

A. Overall Lower Limb Look

  • Compare both limbs side by side
  • Look from the front, side, and then sole (use a foot mirror or ask patient to lift foot)
  • Note the general colour, size difference, swelling

B. Deformities

DeformityWhat it means clinically
Claw toeMTP hyperextension + PIP + DIP flexion = intrinsic minus; increases pressure at toe tip and MTH
Hammer toeMTP neutral + PIP flexion (flexible or fixed) = FDL/FDB imbalance; rubbing on shoe = dorsal PIP ulcer
Mallet toeDIP flexion only; tip-of-toe pressure ulcer
Hallux valgus1st toe deviated laterally; prominence over 1st MTH; pressure + 2nd toe deformity
Pes cavus (high arch)Increased forefoot and heel loading; callus at 1st and 5th MTH and heel
Pes planus (flat foot)Medial arch collapse; midfoot pressure; Charcot flat foot = rocker-bottom
Rocker-bottom footMidfoot bony collapse; characteristic of Charcot neuroarthropathy; midfoot ulceration
Equinus (foot dropped down)Gastrocnemius contracture; forefoot plantar pressure; 1st MTH ulcer
Foot dropCannot dorsiflex against gravity; high steppage gait; dragging of foot

C. Muscle Wasting (Visible)

  • Extensor digitorum brevis (EDB): small mound on the dorsolateral aspect of the foot. Atrophy = visible hollowing in this area = motor neuropathy sign. This is the most visible intrinsic muscle of the foot.
  • Interossei wasting: deep grooves between the metatarsals on the dorsum of the foot (interosseous guttering)
  • Calf muscle wasting: compared bilaterally (measure calf circumference at the same level if asymmetric)
  • Intrinsic wasting = "intrinsic minus" foot = the mechanism of claw toes

D. Skin and Nail Changes

FeatureSignificance
Dry, cracked, fissured skin (especially heels)Autonomic neuropathy - loss of sweating (anhidrosis)
Shiny, thin, atrophic skinPeripheral arterial disease (PAD)
Absent hair on dorsum of foot/toesPAD (loss of hair growth = chronic ischemia)
Callus (thick, yellowish, hyperkeratotic skin)Chronic pressure; precursor to ulcer; always over bony prominences
Maceration (pale, waterlogged, soft skin)Excessive moisture, infection, poor drainage
Erythema (redness)Infection, Charcot neuroarthropathy
Cyanosis / Blue-purple toesSevere ischemia, emboli
Gangrene (black/brown, dry or wet)Severe ischemia ± infection
Interdigital maceration/scalingTinea pedis (fungal); portal for bacterial entry
Thickened, dystrophic, discoloured nailsOnychomycosis (fungal nail infection) = chronic infection reservoir
Ingrown toenailPortal of entry for cellulitis in neuropathic foot
Prominent veins (distended) on dorsumArteriovenous shunting in neuropathic foot = warm foot with good-looking veins but poor microcirculation
Guttered/collapsed veinsIschemia - no blood to fill veins

E. Colour Changes on Elevation and Dependency

  • Elevation test: raise the leg to 45° for 60 seconds
    • Normal: slight pallor
    • Ischemic: rapid pallor within 30-60 seconds (Buerger's positive)
  • Dependency test: sit the patient upright and let leg hang
    • Normal: returns to normal colour in <10 seconds
    • Ischemia: slow return + dependent rubor (reactive hyperaemia) = confirms ischemia
    • Buerger's angle: the angle at which pallor appears on elevation (normal = 90°; <30° = critical ischemia)

STEP 5: PALPATION OF THE FOOT

A. Skin Temperature

  • Use the back of your hand
  • Start proximally and work distally
  • Compare corresponding levels bilaterally
  • Neuropathic foot: warm throughout (AV shunting)
  • Ischemic foot: cool, especially distally
  • Infected area: localised warmth
  • Charcot foot: warm, diffuse, bounding warmth
  • Document: warm/cool/cold; any asymmetry

B. Pulse Palpation (Four Pulses in Both Legs)

Use two or three fingertips, press gently:
PulseLocationHow to feel
FemoralMidpoint of inguinal ligament (midway between ASIS and pubic symphysis)Press firmly, lies medial to femoral nerve, lateral to femoral vein (VAN from medial to lateral)
PoplitealPosterior knee (popliteal fossa) - MOST DIFFICULTPatient prone OR supine with knee slightly flexed 30-40°; grip the knee from both sides and press your thumbs into the popliteal fossa; deep pulse, firm pressure needed
Posterior tibialBehind the medial malleolusBetween medial malleolus and Achilles tendon; press against the posterior border of the tibia
Dorsalis pedisDorsum of footLateral to extensor hallucis longus tendon, between 1st and 2nd metatarsals
Grade each pulse:
  • 0 = absent
  • 1+ = weak/diminished
  • 2+ = normal
  • 3+ = bounding
Note: In diabetics with medial calcinosis, vessels may feel like a hard lead pipe but still carry blood - absence of palpable pulse does NOT always mean absent flow; Doppler is essential.

STEP 6: VASCULAR ASSESSMENT (In Detail)

A. Capillary Refill Time (CRT)

  • Press the pulp of the hallux firmly for 5 seconds until white
  • Release and count seconds until colour returns
  • Normal: ≤2 seconds
  • Prolonged >2 seconds = impaired perfusion
  • 4 seconds = significant ischemia
  • Assess at toes, dorsum of foot, and shin

B. Buerger's Test (Fully Described)

Step 1: Lay the patient flat. Raise both legs to 45°. Hold for 60 seconds. Observe colour of the feet.
  • Normal: slight pallor only
  • Ischemia: pallor appears within 1-2 minutes (note which angle this occurs at = Buerger's angle)
  • Buerger's angle <30° = critical ischemia
Step 2: Sit the patient up and let legs hang dependently. Observe:
  • Normal: pink colour returns within 5-10 seconds
  • Ischemia: dusky pallor first, then slow spread of dependent rubor (brick-red/dark red) over 1-3 minutes
  • This rubor = reactive hyperaemia from maximal vasodilation in ischemic tissue
  • A positive Buerger's test = pallor on elevation + dependent rubor on lowering = confirms significant ischemia

C. Ankle-Brachial Index (ABI) - Step by Step

Equipment needed: Handheld 8-MHz Doppler probe + sphygmomanometer cuff
Method:
  1. Patient lies supine for 10 minutes
  2. Place cuff around right upper arm; apply Doppler gel over brachial artery
  3. Inflate cuff above systolic; slowly deflate; record pressure at which Doppler signal returns = right brachial systolic BP
  4. Repeat on left arm; use the higher of the two brachial readings
  5. Place cuff just above the right ankle; apply Doppler gel
  6. Identify posterior tibial artery signal; inflate cuff and deflate; record pressure = right ankle (PT) systolic
  7. Repeat for dorsalis pedis
  8. Use the higher of PT or DP as the ankle pressure
Calculation: ABI = Ankle systolic BP ÷ Higher brachial systolic BP
Interpretation:
ABI ValueInterpretation
>1.3Medial calcinosis - non-compressible vessels (false high); perform toe-brachial index (TBI) instead
1.0 - 1.3Normal
0.9 - 1.0Borderline
0.7 - 0.9Mild PAD
0.4 - 0.7Moderate PAD
<0.4Severe / critical ischemia
<0.25Limb-threatening ischemia
Note on TBI (Toe-Brachial Index):
  • Used when ABI >1.3 (calcified vessels)
  • TBI <0.7 = PAD
  • TBI <0.15 = critical ischemia
  • More reliable in diabetics

STEP 7: ULCER ASSESSMENT (Systematic 10-Point Evaluation)

Examine the ulcer in a systematic order every time:
1. Site
  • Exactly where: plantar 1st MTH, tip of hallux, dorsal PIP, heel, malleolus, interdigital
  • Neuropathic: plantar pressure points (MTHs, heel)
  • Ischemic: distal (toe tips, margins, heel)
  • Venous (not DFU but must exclude): gaiter zone (medial lower leg)
2. Number
  • Single or multiple ulcers?
  • Multiple ulcers at different pressure points = motor neuropathy + high plantar pressure
3. Size
  • Measure longest dimension × widest perpendicular dimension
  • Document in cm²
  • Repeat at every visit to track healing progress
  • 50% reduction in size at 4 weeks = good prognostic indicator for healing
4. Shape and Outline
  • Round, oval, irregular
  • Punched-out = neuropathic
  • Irregular / serpiginous edges = ischemic or infected
5. Margins
  • Callus surrounding = neuropathic (chronic pressure)
  • Undermined edges = deep tracking infection or Buruli ulcer
  • Raised, rolled edges = may indicate malignancy (Marjolin's ulcer in chronic wounds)
  • Sloping edges = healing margin
  • Punched-out vertical edges = ischemic
6. Depth
  • Superficial (skin only - Wagner 1)
  • Deep (subcutaneous tissue - Wagner 1-2)
  • Tendon/capsule visible (Wagner 2)
  • Bone visible or palpable (Wagner 3)
7. Probe-to-Bone Test
  • Use a sterile blunt metal probe or a sterile cotton swab
  • Gently probe the wound base and walls
  • Feel for firm, gritty resistance = bone contact
  • Positive probe-to-bone = 57% positive predictive value for osteomyelitis
  • Negative probe-to-bone = 96% negative predictive value (rules out osteomyelitis)
  • Also probe for sinuses, tracts, undermining
8. Wound Base (Bed) Description
Use the TIME framework:
LetterStands forDescription
TTissueGranulation (pink/red, good), Slough (yellow/grey, fibrinous), Necrosis (black/brown eschar), Bone
IInfection/InflammationSigns of local infection: pus, biofilm (shiny, grey film), smell
MMoistureDry (ischemic), Moist (ideal for healing), Macerated (excess moisture - too wet)
EEdgeAs described above: callus, undermined, sloping
Document as percentage: e.g., "50% granulation, 30% slough, 20% necrosis"
9. Surrounding Tissue
  • Erythema: measure and mark extent with a skin marker pen (to track cellulitis spread)
  • Induration: hard, woody consistency = deep infection, necrotising fasciitis risk
  • Warmth: localised (infection) vs. diffuse (Charcot)
  • Oedema: pitting or non-pitting
  • Maceration: excessive moisture
  • Crepitus on palpation: CRITICAL SIGN - gas in tissue = gas-forming organisms (Clostridia, E. coli, Klebsiella) = surgical emergency
  • Lymphangitic streaking: red lines tracking proximally = lymphangitis
10. Discharge
  • Amount: scanty, moderate, copious
  • Colour: clear/serous, straw-coloured, yellow, green (Pseudomonas), brown, bloody
  • Consistency: watery, purulent, thick
  • Smell: odourless, mild, foul (anaerobes), sweetish (Pseudomonas = grape-like smell)

STEP 8: NEUROLOGICAL EXAMINATION (Four Modalities)

Examine sensation in all four modalities. Compare both feet. Document as reduced, absent, or intact.

A. Large Fibre Sensory (Aβ fibres)

1. Semmes-Weinstein 10-g Monofilament (Most Important)
Technique:
  • Calibrated filament that buckles at exactly 10 g of pressure
  • Patient closes eyes or looks away
  • Apply perpendicular to skin until filament bends (takes about 1-2 seconds)
  • Do NOT apply over callus, ulcer, or scarred skin (test nearby normal skin)
  • Do NOT test in a rhythmic predictable pattern (patient will anticipate)
  • Ask: "Do you feel this? If so, where?" (yes/no response)
10 standard test sites (plantar surface):
  1. Plantar surface of hallux
  2. Plantar surface of 3rd toe
  3. Plantar surface of 5th toe
  4. Plantar 1st metatarsal head
  5. Plantar 3rd metatarsal head
  6. Plantar 5th metatarsal head
  7. Plantar midfoot (medial)
  8. Plantar midfoot (lateral)
  9. Plantar heel (medial)
  10. Dorsal 1st web space
Score: number of sites felt out of 10.
  • 10/10 = normal
  • <8/10 = loss of protective sensation (LOPS) = at risk
  • Complete failure to feel any site = severe LOPS = very high ulcer risk
2. Vibration Sense (128 Hz tuning fork)
Technique:
  • Strike the 128 Hz tuning fork against the heel of your hand
  • Apply the base to the bony prominence of the great toe (IP joint) first
  • Ask: "Do you feel a buzzing/vibrating sensation? Tell me when it stops."
  • Note the duration the patient feels vibration vs. how long you feel it on your own finger = comparison
  • If absent at hallux, move to medial malleolus, then tibial tuberosity, then iliac crest (ascending)
  • Vibration loss is one of the earliest signs of large fibre neuropathy
3. Proprioception (Joint Position Sense)
Technique:
  • Hold the sides of the hallux between your thumb and index finger (not the top and bottom - that gives pressure cues)
  • Move the toe up or down in small increments (start with a large movement, reduce to small)
  • Patient closes eyes: ask "Is the toe pointing up or down?"
  • Normal: detects movement of 1-2 mm
  • Impaired proprioception = risk of falls, Charcot neuroarthropathy

B. Small Fibre Sensory (Aδ and C fibres)

4. Pain (Pinprick sensation)
Technique:
  • Use a Neurotip or clean safety pin
  • Apply gently to the dorsum of the foot (proximal to distal)
  • Ask: "Is this sharp or dull?"
  • Compare corresponding areas bilaterally
  • Glove-and-stocking distribution loss = typical peripheral neuropathy
5. Temperature
Technique:
  • Use a Tip-Therm device or two test tubes (one filled with warm water ~40°C, one cold/ice water)
  • Apply alternately to the dorsum of foot and sole
  • Ask: "Is this warm or cold?"
  • Reduced temperature discrimination = small fibre neuropathy
  • Often lost before vibration in early DM neuropathy

STEP 9: REFLEXES

ReflexRootMethod
Ankle jerk (S1)S1, via tibial nervePatient kneels on chair or foot hangs off bed; tap Achilles tendon; normal = plantarflexion jerk
Knee jerk (L3/L4)L3/L4, via femoral nerveTap patellar tendon with knee supported at 90°; normal = knee extension
In DFU:
  • Ankle jerk absent bilaterally = peripheral neuropathy (highly sensitive)
  • Knee jerk reduced = more severe or proximal neuropathy
  • If reflexes absent, consider reinforcement (Jendrassik manoeuvre) before recording as absent

STEP 10: RANGE OF MOTION - SILFVERSKIÖLD TEST

Purpose: Differentiate gastrocnemius contracture (tight gastrocnemius only) from Achilles tendon contracture (both gastrocnemius and soleus tight).
Why it matters: Equinus deformity = foot plantarflexed at rest. During walking, because the ankle cannot dorsiflex adequately, all of the weight is forced onto the forefoot, dramatically increasing plantar pressure under the metatarsal heads - causing or perpetuating plantar MTH ulcers.
Technique:
  1. Lay the patient supine
  2. Support the subtalar joint in neutral (slight eversion)
  3. Measure passive ankle dorsiflexion with the knee fully extended (gastrocnemius is stretched - it crosses both knee and ankle)
  4. Measure again with the knee flexed to 90° (gastrocnemius is relaxed, only Achilles remains tensioned)
Interpretation:
FindingMeaning
Dorsiflexion improves with knee flexedGastrocnemius contracture (isolated)
Dorsiflexion equally limited with knee bent and straightAchilles (combined gastroc-soleus) contracture
Normal: >10° dorsiflexion in both positionsNo contracture
Memory cue: "Knee bends → gastrocnemius relents" - because the gastrocnemius crosses the knee. If bending the knee gives you more dorsiflexion, the gastrocnemius is the culprit.

STEP 11: SYSTEMIC EXAMINATION

Lymph Nodes

  • Inguinal lymph nodes (bilateral): palpate for size, tenderness, consistency
  • Tender, enlarged inguinal nodes = reactive to lower limb infection
  • Document size in cm

Cardiovascular

  • Auscultate heart sounds: S1, S2, murmurs
  • Check JVP
  • Assess for heart failure (bilateral ankle oedema, crackles at lung bases, raised JVP)

Abdominal

  • Aortic aneurysm: palpate for expansile pulsatile mass midline (associated with PAD)
  • Renal size: enlarged = polycystic kidney disease (can be associated with DM)
  • Scars from previous surgery

Eyes (if possible)

  • Note: formal fundoscopy is done by ophthalmology; however, document any obvious visual impairment as it directly impacts ability to inspect feet

════════════════════════════════

PART 3: INVESTIGATIONS

════════════════════════════════

Bedside

TestWhy
RBS (random blood glucose)Immediate glycaemic status
Urine dipstickGlucose, protein (nephropathy), ketones, leucocytes
Skin marker pen + rulerMark cellulitis margin, measure ulcer
Probe-to-bone testOsteomyelitis screen
ABI with DopplerVascular sufficiency

Haematology

TestWhat to expect
FBCWBC elevated (neutrophilia) in infection; Hb low in anaemia of chronic disease
ESRElevated in infection and osteomyelitis (>70 = suspicious)
CRPMore sensitive and faster than ESR; >10 = infection; >100 = severe
Coagulation (INR/APTT)Pre-surgical; if on warfarin

Biochemistry

TestWhat to expect
HbA1cMost important: reflects 3-month average; >7% = suboptimal; >10% = very poor
Fasting glucoseBaseline
Renal function (U&E, creatinine, eGFR)CKD affects drug dosing (metformin, vancomycin, aminoglycosides)
LFTsBaseline before antibiotics
Albumin<30 g/L = poor nutritional state = poor wound healing
Lipid profileCardiovascular risk
Blood cultures × 2If febrile >38°C or sepsis suspected
Calcium, phosphateIf CKD (renal osteodystrophy affects bone health)

Microbiology

TestNotes
Deep tissue swab cultureFrom wound base after debridement; NOT surface swab (surface swabs = unreliable)
Bone biopsy cultureGold standard for osteomyelitis organism identification - done in theatre
Sensitivity and susceptibilityGuides antibiotic switch from empirical to targeted

Radiology

TestIndicationFindings in DFU
X-ray foot (3 views: AP, lateral, oblique)First-line alwaysCortical erosion, periosteal reaction, osteolysis = osteomyelitis; soft tissue gas = necrotising; structural deformity
MRI foot with contrastGold standard for osteomyelitis; soft tissue infectionBone marrow oedema, abscess, sinus tract, deep space infection; sensitivity 90%, specificity 83%
Doppler duplex ultrasoundNon-invasive vascular mappingLevel and degree of arterial stenosis/occlusion
CT angiography (CTA) lower limbPre-revascularisation planningFull arterial anatomy, calcification pattern, suitable vessels for bypass/angioplasty
MR angiographyAlternative if CTA contraindicated (CKD - contrast concern)Arterial anatomy without radiation
Nuclear bone scan (Tc-99m)When MRI contraindicatedSensitive for osteomyelitis but low specificity; cannot distinguish infection from Charcot
Transcutaneous oxygen (TcPO₂)Predicts healing potentialTcPO₂ >40 mmHg = likely to heal; <20 mmHg = unlikely without revascularisation

════════════════════════════════

PART 4: MANAGEMENT

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The Five Pillars of DFU Management

"DANCE": Debridement + Antibiotics + Neuropathy management + Circulation (revascularisation) + Education/offloading

Pillar 1: Glycaemic Control

  • Admit if RBS >15 mmol/L with active infection
  • Withhold metformin if eGFR <30 or contrast needed
  • IV insulin sliding scale protocol (target BG 7-10 mmol/L inpatient)
  • Endocrinology referral for optimisation
  • Discharge with clear insulin instructions and HbA1c target <7-8%

Pillar 2: Offloading Pressure

MethodComments
Total Contact Cast (TCC)Gold standard for plantar neuropathic ulcer offloading; reduces plantar pressure by distributing load over entire limb; shown to heal 80-90% of neuropathic DFUs
Removable Cast Walker (RCW)Less effective than TCC (patient removes it); can be made irremovable by wrapping with cast material
Forefoot offloading shoeOffloads forefoot; suitable for Wagner 1-2 wounds
Strict bed restIf acute infection/cellulitis
Crutches / wheelchairFor ambulatory patients who must be non-weight-bearing

Pillar 3: Wound Care and Debridement

  • Sharp surgical debridement: remove all callus, necrotic tissue, fibrinous slough, and infected material; creates a clean wound base to stimulate healing
  • Wound irrigation: normal saline
  • Dressings: match dressing to wound moisture level:
    • Dry/necrotic wound: hydrogel dressings (donate moisture)
    • Moderate exudate: foam dressings
    • Infected: silver-impregnated, iodine, or honey-based antimicrobial dressings
    • Heavily exuding: alginate dressings
  • Biofilm management: biofilm (organised bacterial colonies) must be disrupted by debridement; no antibiotic penetrates intact biofilm
  • Negative pressure wound therapy (NPWT/VAC): for large wounds post-debridement; promotes granulation tissue formation
  • Biological agents: Becaplermin (PDGF) gel for chronic non-healing neuropathic ulcers

Pillar 4: Infection and Antibiotic Management

IDSA/IWGDF Classification of Infection severity:
GradeDescriptionManagement
1 (uninfected)No infection signsNo antibiotics; wound care + offloading
2 (mild)Local infection, cellulitis <2 cm, superficialOral antibiotics; outpatient
3 (moderate)Cellulitis >2 cm, deep tissue/bone/joint, limb-threateningIV antibiotics; hospital admission
4 (severe)Systemic toxicity (SIRS/sepsis)IV antibiotics + urgent surgical review; ICU if needed
Empirical antibiotic principles:
  • No recent antibiotics: cover gram-positive cocci (Strep, MSSA) - flucloxacillin OR clindamycin
  • Recent antibiotics: expand to cover gram-negatives - add fluoroquinolone or co-amoxiclav
  • Severe/limb-threatening: broad-spectrum including MRSA and Pseudomonas cover:
    • Vancomycin (MRSA) + piperacillin-tazobactam (gram-negatives + Pseudomonas) + metronidazole (anaerobes)
    • If penicillin allergic: vancomycin + ciprofloxacin + metronidazole
  • Switch to culture-directed therapy at 48-72 hours
  • Duration: mild = 7-14 days oral; moderate = 2-3 weeks; osteomyelitis = 4-6 weeks (IV then oral)

Pillar 5: Revascularisation (if ABI <0.7 or absent pulses)

  • Vascular surgery referral is mandatory if pulses absent or ABI <0.7
  • Pre-operative imaging: CTA or MRA for arterial mapping
  • Options:
    • Endovascular (angioplasty ± stenting): minimally invasive; first-line for tibial/peroneal disease in DFU
    • Surgical bypass: femoral-popliteal, femoral-tibial, femoral-peroneal; for long segment occlusions
  • Target: restoration of pulsatile flow to the foot to enable wound healing
  • Without revascularisation: ABI <0.4 = wound will not heal regardless of antibiotics or dressings

Surgical Options for Osteomyelitis

OptionIndication
Surgical debridement + bone curettageAccessible bone, early osteomyelitis
Ray amputation (toe + metatarsal)Irreversibly infected digit and metatarsal
Transmetatarsal amputationMultiple ray involvement; forefoot salvage
Below-knee amputation (BKA)Failed local surgery, spreading infection, severe ischemia
Above-knee amputation (AKA)Failed BKA healing or advanced proximal disease

MDT Referrals Summary

SpecialistRole
Vascular surgeryRevascularisation
Orthopaedic surgeryBone debridement, deformity correction, amputation
EndocrinologyGlycaemic optimisation
NephrologyCKD management
PodiatryWound care, callus debridement, custom footwear
DietitianNutritional rehabilitation (albumin correction)
PhysiotherapyPost-surgery rehabilitation, gait training
Wound care nurseDaily dressing, wound documentation
OphthalmologyRetinopathy review
OrthoticsCustom therapeutic footwear once healed

Long-Term Prevention

  • Custom therapeutic footwear: extra-depth, wide toe box, moulded insoles permanently after a healed ulcer
  • Annual comprehensive foot review (monofilament, ABI, structural exam)
  • Daily foot self-inspection (patient + carer if vision impaired)
  • Regular podiatry every 6-8 weeks minimum
  • HbA1c optimisation
  • Smoking cessation
  • Structured diabetic education programme

Sources: Campbell's Operative Orthopaedics 15e; Sabiston Textbook of Surgery; Harrison's Principles of Internal Medicine 22e; Current Surgical Therapy 14e; Bailey & Love's 28e; Rosen's Emergency Medicine
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