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          Patterns, pearls and practical medicine

Diabetic foot complications

Foot complications include

  • Ulceration – chronic or acute
  • Abscess or collection
  • Osteomyelitis
  • Gangrene
  • Critical limb ischaemia / peripheral arterial disease – bear in mind that a patient is unlikely to have vascular disease of one vascular bed, these patients often have coronary or cerebral disease too
  • Acute Charcot’s neuroarthropathy
  • Puncture wounds

Statistics

  • After amputation, survival is around 50% at 2 years – most die of CV disease which can worsen after amputation
  • Foot complications confer significantly higher mortality in patients with DM (end stage DM) – it’s a marker for multi-organ damage
  • Major amputation rates are falling
  • 5-year mortality in those with a diabetic foot crisis is comparable to cancer

The impact of foot disease on patients

  • Frequent healthcare attendance – podiatry, admissions, OPAT, scans
  • Restrictions – foot washing, mobility, activities, footwear
  • Insecurity – employment, finances, housing
  • Psychological – pain, insomnia, anxiety especially about amputations

A few tips for managing inpatients

  • Refer all admitted patients with diabetic foot conditions to the multidisciplinary foot team which may consist of diabetology, podiatry, vascular surgery, microbiology, tissue viability, surgical appliance team
  • Minor seeming problems can turn into major ones
  • Patients can be quite stigmatised and blamed for their condition – avoid doing so
  • Ask about symptoms that suggest vascular disease – eg intermittent claudication, rest pain, pain that’s better when sitting than lying (ie gravity needed to help blood perfuse feet), medical history (antiplatelet use, previous MI, CVA)

Assessment in clinic

  • Assess risk
      • Low risk – callus
      • Moderate risk – deformity, neuropathy or PAD
      • High risk
          • Previous ulcers, or amputation
          • Or on RRT
          • Or two of: neuropathy, peripheral arterial disease (PAD), deformity
      • Active foot disease – ulcer, infection, ischaemia, gangrene, Charcot’s
  • General advice / prevention
      • Regular self-check of feet/between toes (useful diabetes UK video on YouTube)
      • Footwear advice, insoles etc
      • Nail cutting
      • Treating fungal infections
      • Changing socks
      • Daily emollient
      • Safety net – see podiatrist if any cuts, sores, ulcers, blisters. Can give written advice leaflet (available on diabetes UK)
      • Glycaemic control

Foot assessment in the acute setting

  • Examine the whole foot including the back of the heel and between toes
  • Check for infection
      • Suggested by heat, pus, swelling, pain (especially if foot normally insensate), malodour – but may not be present if co-existent PAD or neuropathy
      • Check the skin integrity and thickness
      • Assess the wound bed – suspect infection if grey granulation, hypergranulation, friable granulation tissue, exudate, slough, necrosis
      • Assess for sepsis
      • Suspect deep-seated soft tissue or bone infection in a grossly swollen foot with shiny skin
      • If you can probe to bone (can try to do this) – around 90% chance of osteomyelitis
  • Check sensation in feet – the monofilament test
      • Apply monofilament to the foot at 90 degrees for 2 seconds
      • Test beneath big toe, 4th toe and on distal medial sole (just before big toe)
      • Protective sensation intact if monofilament detected at all sites at least once out of two times
  • Vascular exam
      • Check pulses – Dorsalis Pedis, Posterior tibialis +/- popliteal and femoral
      • Capillary refill is not a good marker
      • Assess temperature
      • Look for trophic changes (absent hair, thin skin, thickened nails)
      • Assess for colour changes (compare feet) – pale or red, difference is key. Can be difficult in darker skin, but look for difference.
      • Venous guttering
      • ‘Sunset foot’ or ischaemic rubor is often mistaken for cellulitis
      • A blue foot – usually due to peripheral venous disease and usually not serious, however if cyanosis is non-blanching this could indicate pre-gangrene or end artery embolism – refer to vascular
      • Very severe pain points to ischaemia
      • The 6 P’s are not always present, but assess for pallor, pulselessness, pain, poikilothermia (cold limb), parathaesia, paralysis
      • Buerger’s test – with patient supine, elevate both legs to 45 degrees and hold for 1-2 mins. Observe colour in feet – pallor indicates ischaemia. Then sit patient on the edge of the bed, colour should return to the ischaemic leg
  • The PEDIS Score for diabetic foot ulcers – grades severity, and predicts 6-month risk of amputation and mortality in diabetic foot ulcers.
      • Based upon
          • Perfusion
          • Extent
          • Depth
          • Infection
          • Sensation
      • PEDIS 2 generally has <2cm of surrounding cellulitis
      • PEDIS 3 is systemically well but with deeper or wider infection
      • PEDIS 4 is unwell
  • SINBAD score also used – Site, ischaemia, neuropathy, bacterial infection, area, depth

Referrals

  • Patients can sometimes self-refer to foot health team if being discharged
  • PEDIS score 1 or 2 – refer to foot protection service within 24 hours (may need admission or SDEC review if delays)
  • PEDIS 3 or above – ask patient to attend ED, admit
  • Orthopaedic review is advised for Charcot’s, abscesses, osteomyelitis
  • Diabetes team to see in all cases of cellulitis
  • Vascular review if no pulses / cold foot / bad infection – patient may need to be transferred to another hospital
  • Podiatry
      • Generally speaking podiatry will see foot wounds, any foot problem in diabetes / immunosuppression / peripheral arterial disease, ingrown toenails, sometimes musculoskeletal issues in diabetics
      • Technically the foot is below the malleolus!
      • They will not see verrucae, corns if patient healthy even if symptomatic, fungal skin / nail infections if otherwise well, leg ulcers

Ulceration / infection / foot crisis

  • May occur due to a combination of neuropathy, poor circulation (micro and macro-vascular disease), foot deformities, hyperglycaemia and impaired immune response
  • Risk factors include
      • Poor diabetic control
      • Trauma
      • Peripheral arterial disease (PAD)
      • Foot deformities
      • Previous ulcers
      • Neuropathy – diabetic, or due to another cause (autonomic neuropathy can leave people with dry skin due to lack of sweating)
  • Investigations
      • Xrays
      • MRI if suspected osteomyelitis but x-ray ok (but not if you see bone, then you assume OM is present)
      • Take wound swabs / tissue sample – these should be deep (clean superficial exudates). Can get from debrided ulcer base before antibiotics
      • Blood cultures
      • Check HBA1C
      • CRP (supportive but not diagnostic of diabetic foot infection)
      • Consider checking ABPI
      • Regular clinical review (and more frequently if higher risk)
  • Ischaemia and infection
      • Foot ulcers need 2-5 x more blood flow to heal when compared to intact skin, and infected ulcers 5-10x.
      • So if a chronic ulcer becomes infected this can cause critical ischaemia, which causes new ischaemic pain, rest pain, necrosis, wet gangrene
      • If a patient with known arterial disease gets new pain – suspect infection (unlikely they’ve had an acute thrombosis)
  • Management
      • Photos of the feet
      • Consider debridement
      • Foot team review. Podiatry input improves mortality and morbidity
      • Wound care / dressing – any diabetic wound should be dressed immediately with non-occlusive dressing and kept dry
      • Analgesia
      • Antibiotics – see below
      • Surgery – see below
  • Osteomyelitis
      • Attempt to probe to bone
      • Check x-ray (though can be a delay until changes are noted)
      • Consider MRI
      • Sausage toe – seen in some diabetics, may indicate underlying bone infection, especially if no hx of trauma, and always warrants further investigation. There may not be an obvious portal of infection
      • Forefoot OM without arterial disease is usually managed with 6 weeks of targeted antibiotics
      • Mid foot and hindfoot OM with arterial disease – much harder to treat
      • Heavily demineralised bone can return with treatment, it’s not gone
      • It is ‘resolved’, not ‘cured’ – can recur months/years later
      • Some patients get episodic antibiotics for relapsing-remitting disease

The microbiology and antibiotics

  • Cultures are often polymicrobial
  • 5-10% are gram negatives
  • Milder infections tend to be caused by gram positive organisms
  • Staph aureus is the most common primary pathogen (65%), of which 18% is MRSA
  • Coagulase negative staph is common – staph lugdenensis is as serious as staph aureus. Staph caprae is a bit less virulent. Staph epidermis and simulans are rarely pathogens
  • Pseudomonas occurs in 3% – can be associated with metastatic infection eg spinal abscesses. Can be secondary pathogen or collateral and doesn’t always need treatment
  • Others include
      • E coli
      • Klebsiella
      • Enterobacter faecalis and Enterobacter hormaechai (formally cloacae)
      • Stenotrophomonas maltophilia – often treated with co-trimoxazole
  • If no active soft tissue infection – sometimes appropriate to hold antibiotics and culture tissue with close monitoring/safety netting (soft tissue infection kills people, not osteomyelitis)
  • Mistakes in antibiotic treatment
      • Patient treated too late
      • Antibiotics under-dosed (may need higher than usual dosing)
      • No extended cover
      • Use of the trust cellulitis guideline (use the diabetic foot infection guideline instead)
  • Choice of antibiotic
      • Beta lactams first choice usually, but check allergies and MRSA history
      • Empirical regimes must cover Staph Aureus, and streptococcus if cellulitis
      • Flucloxacillin IV – if given orally, bioavailability not great. Usually 1g QDS for 7-14 days
      • Doxycycline – good bioavailability, and only once daily, but strep resistance common
      • Clindamycin – good bone penetration but some strep resistance. QDS dosing.
      • Consider triple antibiotics if ischaemia/necrosis
  • Beta-lactam resistance
      • Can be due to Serratia, Enterobacter hormaechai and Citrobacter freundii
      • These might be susceptible on testing in the lab, but they have inducible resistance and become resistant after a bit of treatment
      • Always discuss these with micro
  • Failure of treatment may be due to
      • Pathogen not targeted
      • Retained bony sequestrate or foreign bodies
      • Arterial disease
      • Excess pressure

Surgical management of diabetic foot infections

  • Incision and drainage
  • Amputations
      • Often required due to healthcare workers not recognising the seriousness of diabetic foot complications and giving patients false reassurance (patients are often not listened to)
      • If BMI very high, may not be a candidate for amputation, and rehab is very difficult
      • Below knee amputations are done if you think patient can rehab and walk with a prothesis (otherwise they will get a contracture at the knee, which is a new pressure area). Surgery is also longer for a below knee than an above knee
      • Above knee if patient unlikely to rehab

Puncture wounds

  • Easy to underestimate extent of deep gangrene
  • Be extra cautious – can seem benign
  • Always x-ray even if no signs of infection (look carefully for foreign bodies)
  • They need antibiotic cover for staph but also for anaerobes – discuss with microbiology
  • Always refer to the foot health team

Charcot’s foot

  • Occurs in long standing diabetes with neuropathy. Can also occur in other causes of peripheral neuropathy without diabetes but less commonly
  • Due to bone and joint disorganization secondary to inflammation, underlying neuropathy, trauma, and perturbations of bone metabolism
  • Examination findings
      • Foot is swollen (localised and unilateral, usually)
      • Warm (obvious temperature difference between feet)
      • Erythematous
      • Mild/moderate pain (in 50%). Pain in the active stage is less than you’d expect
      • Bounding pedal pulses (though can occasionally be complicated by ischaemia)
      • Midfoot collapse with ‘rocker-bottom’ deformity is a late sign
      • There is neuropathy on exam
  • Can be misdiagnosed as cellulitis, gout or DVT
  • Do a foot x-ray – can show fractures and dislocations which can be subtle
  • MRI is highly sensitive /specific – do one if you suspect the diagnosis but x-ray normal
  • Management
      • Put foot in a cast and do not weight bear. Swelling will gradually subside
      • Little evidence for bisphosphonates
      • Surgery occasionally indicated

Arterial disease

  • Can get an angiogram (+/- proceed with angioplasty)
  • Ask about rest pain
  • Arterial duplex can miss stenoses, especially below the knee
  • If previous angioplasty (especially in the last 6 months)
      • Patients at risk of thrombosis, which is a vascular emergency
      • Can present with acute ischaemia/deteriorating foot
      • The revascularisation can destroy the collateral circulation, so you can get rapid tissue death in this scenario (with native vessels and collaterals, you are much less likely to go from poor blood supply to no blood supply)
  • See peripheral arterial disease

 

 

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