It is well established that lower limb complications in diabetes are the result of peripheral arterial disease (PAD; reduced blood flow to the limbs), neuropathy (loss of sensation), infection, or any combination of the three (Jeffcoate and Harding, 2003; Hinchcliffe et al, 2019; Lipsky et al, 2019). The sequence of foot ulceration tends to occur with underlying neuropathy and/or PAD as a precursor, followed by trauma that leads to tissue breakdown/ulceration (Jeffcoate and Harding, 2003; Clayton and Elsay, 2009). The ulcerative foot in diabetes can then deteriorate further due to PAD/ischaemia and/or infection, which leads to amputation. Infection of foot ulceration in diabetes increases amputation risk by 150 times compared to non-infected ulcers (Prompers et al, 2007; Figure 1).
Hardest to heal
Figure 1. Hard-to-heal diabetic foot ulcer.
 

Peripheral Arterial Disease

Peripheral arterial disease relates to a partial or complete obstruction of the blood vessels to the head, organs, or limbs (National Heart, Lung and Blood Institute, 2019). PAD, as a term, is used interchangeably in the text with a variety of other similar terms (e.g. peripheral arterial occlusive disease, peripheral vascular disease, ischaemia). This article will focus on PAD to the lower limbs only. PAD is an umbrella term used to describe all forms of disease, whether symptomatic or not and irrespective of disease severity.
 

Ischaemia

The term ischaemia is more often used to describe the severe end of PAD, where tissues do not receive enough oxygen and lead to cell death (Teo, 2019). Ischaemia is usually seen with clinical signs and symptoms such as intermittent claudication, ischaemic rest pain, ulceration, necrosis and/or gangrene (whereas PAD may be asymptomatic).

There are two main types of ischaemia:
  • Acute limb ischaemia
  • Chronic limb-threatening ischaemia (CLTI).
Acute limb ischaemia is a clinical emergency characterised by pain, pallor, perishing cold, paraesthesia, paralysis and pulselessness — this is not being discussed in this article. Chronic limb-threatening ischaemia (CLTI) encompasses the term critical limb ischaemia, but critical limb ischaemia implies threshold values of impaired tissue perfusion, rather than a continuum. CLTI is a clinical syndrome defined by the presence of PAD in combination with rest pain, gangrene, or lower limb ulceration greater than two weeks’ duration and can be graded in severity (Conte et al, 2019a).
 

Diagnosing PAD

Approximately half of all patients with a diabetic foot ulcer (DFU) have PAD (Brownrigg et al, 2015). The absence of foot pulses at initial presentation of a DFU has been shown by the National Diabetes Footcare Audit (NDFA) to have a strong association with one-year mortality (NDFA, 2019). Indeed, one in four people die at 12 months if absent foot pulses are seen in combination with two or more of the following characteristics:
  • Neuropathy
  • Ulcer located on the hind-foot
  • Bacterial infection at presentation
  • Greater than 1cm area ulceration
  • The ulcer probes to bone (NDFA, 2019).
Therefore, diagnosis of PAD is important in the diabetic foot, given its association with failure to heal ulceration, amputation, cardiovascular events and increased risk of premature mortality (Brownrigg et al, 2015). Infection, oedema and neuropathy often present with ulceration and may adversely affect the performance of PAD diagnostic tests that are otherwise reliable in patients without diabetes. 
Early recognition and expert assessment of PAD allows measures to be taken to reduce the risk of amputation and cardiovascular events, while determining the need for revascularisation to promote ulcer healing (Brownrigg et al, 2015).

Diagnosis of PAD is based on symptoms, such as:
  • Intermittent claudication, which can be described and experienced as muscle pain on mild exertion — ache, foot pain/great toe pain, numbness or sense of fatigue classically in the calf muscle, which occurs during exercise, such as walking, and is relieved by short rest (British Lymphology Society [BLS], 2018)
  • Chronic ischaemic rest pain, usually described as night cramps in the foot and lower limb, with the inability to lie in bed and need to hang leg out/sleeping in a chair (BLS, 2018; National Institute for Health and Care Excellence [NICE], 2018).
However, symptoms of PAD, such as intermittent claudication, are less likely to present in diabetes due to the high incidence of neuropathy co-existing with arterial disease (Abouhamda et al, 2019).
 
Signs/symptoms of PAD include:
  • Active foot ulcer
  • Presence of intermittent claudication
  • Rest pain
  • Diminished or absent foot pulses
  • Monophasic Doppler signals
  • Ankle brachial pressure index (ABPI) less than 0.9, or absolute ankle pressure less than 70mmHg
  • Toe brachial index (TBI) less than 0.7, or absolute toe pressure (TP) less than 60mmHg
  • Positive Buerger’s sign, leg elevation above the level of heart causes the presence of pallor, followed by rubor on being dependent (referred to as the sunset foot) (Lundin et al, 1999; Dolan et al, 2002; Scissons, 2008; Brownrigg et al, 2015; NICE, 2018; Conte et al, 2019).
Assessment and diagnosis of PAD is therefore based on:
  • Clinical indicators (presence of lower limb ulceration, necrosis, gangrene)
  • Symptom analysis of claudication (with validated tools such as the Edinburgh claudication questionnaire [Lend and Fowkes, 1992])
  • Subjective assessment of the Buerger’s test (see Box)
  • Pulse palpation
  • Doppler insonation. Normal peripheral arterial waveforms at rest have three phases (triphasic), with forward flow during systole, a back flow in early diastole, and a smaller forward flow component in late diastole. The loss of the second forward flow (leaving two phases — ‘biphasic’) is a normal part of the aging process of the artery. The complete loss of diastolic flow reversal (one phase or ‘monophasic’) is a widely accepted characteristic for differentiating normal from diseased peripheral arteries (Scissons, 2012)
  • ABPI measurement
  • Toe pressure assessment.
Buerger’s test This involves observing for colour changes of the foot during elevating and lowering the leg. A positive result suggests a major artery occlusion and is indicated by pallor on elevation, best seen on the sole, with a reactionary hyperaemic (sunset red) flush over the dorsum of the foot on lowering. There is no such colour change in a healthy limb (Buerger, 1924).
However, the questioning for intermittent claudication, although highly specific (likely to identify disease), is the low sensitivity (high number of false positives picked up) (Brownrigg et al, 2015). The Buerger’s test is non-quantifiable and has a questionable reliability. The reliability of pulse palpation can be influenced by the ambient temperature, and experience levels of the examiner may lead to a high degree of misdiagnosis (McGee and Boyko, 1998; Lundin et al, 1999; Brownrigg et al, 2015). Doppler is useful at excluding significant PAD, but signal interpretation is subjective in nature and use in non-expert hands is unproven (Scissons, 2008; Alavi et al, 2015). ABPI is advocated as the first-line non-invasive test for PAD in symptomatic or signs suggestive of PAD, but caution must be used as false elevated readings can occur in diabetes due to calcification (Society for Vascular Surgery Lower Extremity Guidelines Writing Group et al, 2015; NICE, 2018). Toe pressures and toe pressure indices are indicated in all patients suspected of CLTI and who have tissue loss, but are not currently used widely (Conte et al, 2019).

In essence, there is no single assessment to diagnose PAD and the full clinical picture should be considered. The hierarchy of assessment should start with symptom analysis, clinical indicators and considering subjective tests, including pulse palpation. If uncertainty exists at this point, further assessment with Doppler for monophasic signals, alongside an ABPI and ideally a toe pressure measurement should be considered. Referral to specialist vascular services (or to multidisciplinary footcare services [MDFS], where vascular are involved) is therefore indicated by intermittent claudication, diminished or absent foot pulses, monophasic Doppler signals, ABPI less than 0.9, TP less than 60mmHg or TBI less than 0.7, plus the presence of active lower limb ulceration greater than two weeks’ duration, rest pain or gangrene (Brownrigg et al, 2015; Conte et al, 2019).

Following these assessments, to inform the vascular surgery opinion, Duplex ultrasound scanning is usually the first-line, non-invasive assessment to help establish the anatomical distribution of the disease. Vascular services may well then look at a variety of more invasive tests before intervention, such as digital subtraction angiography (DSA), magnetic resonance (MR) or computer tomographic (CT) angiography (Brownrigg et al, 2015; Conte et al, 2019).

Overall, assessment of PAD in the diabetic foot is complicated and the recommendation is that in the presence of DFU, referral is made to MDFS and that these patients have tissue perfusion assessed and, where indicated, the anatomical location of the disease. Treatment plans should then be discussed with the patient by the MDFS (Hingorani et al, 2016).
 

Infection

Infection is a continuum that can progress rapidly in the diabetic foot from a suspected colonised wound/ulcer to severe infection (Figure 2). It is the clinician’s responsibility to recognise covert signs (as listed below) of infection that may occur before the overt signs of infection characterised in Table 1. Prior to the presence of overt infection, there is believed to be a tipping point from wound contamination and colonisation leading to local infection. This perceived tipping point was historically called ‘critical colonisation’. However, this term is no longer advocated due to the lack of clarity in its definition and is now referred to as covert infection (International Wound Infection Institute  [IWII], 2016).
Figure 2. Continuum of infection.
Figure 2. Continuum of infection.

Infection in the diabetic foot is not fully understood and is potentially over diagnosed and/or treated. Guest et al (2018) recognised that 14% of DFUs were documented as infected at initial presentation, with a further 31% documented as being treated with an antimicrobial. Therefore, up to 45% of DFUs may be infected at initial presentation. This is less than previously reported by Prompers et al (2007), who estimated the number of infected DFUs at initial presentation to be 58%, but similar to the figures reported by NDFA, which showed 43.6% of ulcers at presentation to MDFS having clinical signs of infection
(NDFA, 2019).

Where people are admitted to hospital because of DFUs, the number of people with infection increases to 82% (Prompers et al, 2007). Therefore, at initial presentation, the number of DFUs with infection is between 14% and 58%, rising to 82% if the first presentation is via admission. This is a significant spread and possibly implies the difficulty in diagnosing effectively, or else the overuse of antimicrobial agents in the treatment of DFUs.

 
Table 1

Antimicrobial agents

The use of antibiotics is not advocated in the absence of clinical signs of infection (Table 1), but the characteristics of other diabetic foot problems, such as Charcot neuro-osteoarthropathy (discussed below), the ischaemic foot, or a wound with chronic inflammation, may present similar to infection (Department of Health [DH], 2019). The high use of antimicrobials arises as they are advocated in the ‘pre-infection’ (covert infection) stage within the infection continuum (IWII, 2016), but, in the author’s clinical opinion, what this stage looks like is difficult to ascertain. There is a consensus of opinion that suggests biofilms play a significant role at this stage through to overt clinical infection (IWII, 2016). The clinical signs of biofilms and therefore covert infection are:
  • Excessive moisture/exudate
  • Poor-quality granulation tissue (e.g. friable, hypergranulation)
  • Localised infection
  • Antibiotic failure or recurring infection
  • Negative wound culture
  • Non-healing in spite of optimal wound management
  • Infection more than 30 days
  • Responding to corticosteroids and anti-tumor necrosis factor (TNF) medication
  • Gelatinous material easily removed from wound surface (Keast et al, 2014).
The decision to start topical antimicrobials in DFUs may be guided by the clinical signs and symptoms of covert infection, or when local infection is recognised alongside the prescribing of systemic antibiotics. As said, infection in DFUs can increase the risk of amputation by 150 times (Prompers, 2007) — therefore, recognising and starting appropriate antibiotic therapy is imperative. The antibiotic decision should be done in line with local guidance and national guidelines (NICE, 2019), and with the support of the MDFS where possible. Principles to consider when prescribing antibiotics are:
  • Do not start antibiotics in the absence of clinical evidence of bacterial infection
  • If there is evidence/suspicion of bacterial infection, use local guidelines to initiate prompt effective empirical antibiotic treatment
  • Document clinical indication, duration or review date, route and dose
  • Obtain cultures before commencing antibiotics, or as soon as possible after starting.
Once infection is diagnosed and antibiotics started, the next steps to consider are:
  • Review the clinical diagnosis and the continuing need for antibiotics by 48 hours and make a clear plan of action — the ‘antimicrobial prescribing decision’
  • The five antimicrobial prescribing decision options are: stop, switch intravenous (IV) to oral, change, continue and outpatient parenteral antibiotic therapy (OPAT) (DH, 2019).

Neuropathy

In a simplified description, diabetes neuropathy is caused by an imbalance between nerve fibre damage and its repair (Charnogursky et al, 2014). The damage within diabetes predominantly affects autonomic and distal sensory nerves leading to a progressive loss of sensation. In diabetes, this is caused by consistently high blood sugars causing a glycoslisation of the nerves (a covalent [chemical bond] attachment of sugar to a protein or lipid), as well as microvascular ischaemic factors and inflammation leading to permanent and irreversible nerve damage (Charnogursky et al, 2014).

Peripheral neuropathy often masks damage to the diabetic foot and therefore allows the development of tissue and bone damage without the patient being aware. This can lead to problems such as tissue damage and ulceration, but in some instances it can cause an unknown foot fracture that triggers a sequence of events and inflammation cascade leading to Charcot neuropathic osteo-arthropathy (or Charcot foot; Figure 3) (Rogers et al, 2011).

 


Figure 3. Charcot neuro-osteoarthropathy.
Figure 3. Charcot neuro-osteoarthropathy.

Charcot foot

Charcot foot is a serious and potentially limb-threatening syndrome that affects the bones, joints and soft tissues of the foot and ankle. It is characterised by inflammation, varying degrees of bone and joint disorganisation secondary to underlying neuropathy, trauma, and disturbances in the bone metabolism (Rogers et al, 2011). Clinically, Charcot foot presents as:
  • Red (due to localised inflammation)
  • Hot (greater than 2 degrees Celsius)
  • Swollen foot (subtle or gross deformity)
  • With or without pain
  • History of trauma (may or may not be recalled, can be single or repetitive trauma)(Rogers et al, 2011).
There is no definitive criteria or set of tests to confirm Charcot foot and diagnostic assessment should include neurological, vascular, musculoskeletal, and radiographic abnormalities. There are no reported cases of Charcot foot occurring in the absence of neuropathy (Rogers et al, 2011). Neurologically, the 10g monofilament is a highly sensitive predictor of neuropathy and is a quick, relatively easy and cheap assessment modality (Pham et al, 2000). The vascular picture and the presenting patient usually have a well preserved or even exaggerated arterial blood flow in the foot, with pedal pulses characteristically bounding (unless obscured by concurrent oedema) (Rogers et al, 2011). Musculoskeletal deformity is often subtle in the early stages and is accompanied by heat and swelling, with minimal radiological changes. As a result, in the earlier stages, it is often misdiagnosed as gout, deep vein thrombosis (DVT), cellulitis, or an acute fracture by those with little experience of the foot in diabetes (Rogers et al, 2011; Concannon and Sharpe, 2012). The potential impact of Charcot foot is significant — long-term foot shape change that often leads to long-term ulceration and increased risk of amputation.

If Charcot foot is suspected, it should be referred to the MDFS and treated as Charcot foot until proven otherwise, even in the presence of normal radiographic images. Diagnosis is based on clinical picture, history-taking, presence of neuropathy, radiographic imaging followed by magnetic resonance imaging (MRI) if necessary, and presence of deformity. Sequential X-rays are often used to observe for radiographic changes over time. The treatment for Charcot foot is complete offloading of the affected limb with a total contact cast or removable walker until the inflammation and remodelling of the foot have settled, which may take up to or over 12 months (Rogers et al, 2011).

Overall, the diabetic foot can present with a variety of complicated limb- and life-threatening/shortening conditions. Often, these conditions can be
fairly similar in their initial presentation. Considering the text above, arterial disease, infection and Charcot foot all have characteristics of painful, red, swollen feet and can present in combination with each other, or a number of other differential diagnoses not discussed here. The following case report was a patient who presented to an outpatient clinic with a red, swollen, painful foot.
 
This 64-year-old male patient, with type 2 diabetes (20-year history), a body mass index (BMI) of 20, and known peripheral neuropathy presented to an outpatient clinic with a red, swollen, painful foot (Figure 4). His current medications were vitamin B compound, trazodone 50mg, thiamine 200mg, spironolactone 100mg, omeprazole 80mg, nirtazapine 45mg, metformin 1.5g, and folic acid 5mg.
 

Figure 4. Foot at initial presentation. Photographs reproduced
courtesy of Salford Royal NHS Foundation Trust.

He regularly attended ongoing treatment for active foot ulceration to the left foot and a recently healed ulcer to the right foot, with underlying osteomyelitis. On a particular occasion, he attended his weekly clinical review and mentioned that he had injured his right foot during the week. He recalled kicking a radiator, which caused a traumatic injury to his right foot. There was a 1x1.5cm (length x width) active ulcer to the dorsum of his right foot with redness, heat and swelling extending from the ulceration in the foot. At initial presentation, there was evidence of suspected clinical infection. The patient was suspected of having Charcot neuro-osteoarthropathy (Charcot foot) and possible undiagnosed underlying osteomyelitis. He was referred for X-ray and was currently on clindamycin 1.8g (450mg QDS) and ciprofloxacin 1g (500mg BD) for osteomyelitis in his right third and fifth toes.
At initial X-ray there was no bony destruction noted (radiology reported that bones were osteopenic, no osteolysis or bony destruction to suggest frank osteomyelitis) and the patient was given a removable walker device, i.e. knee-to-toe offloading that offers similar offloading to a total contact cast but could be removed at night.

The patient had a history of ABPI assessments which showed incompressible arteries due to calcification. Toe pressures were done following traumatic injury, with an absolute toe pressure of 35mmHg, indicative of severe PAD. It was therefore decided that total contact casting was contraindicated due to severe PAD, and that the removable walker would be continued (Figure 5). Six days later, the foot’s architecture had severely collapsed with multiple fractures and dislocations, and so Charcot foot was confirmed. Unfortunately, due to the severity of the destruction, the associated PAD and ongoing ulceration and infection risk, the decision to perform below-knee amputation was taken. Management of the patient was through the MDFS clinic.
 
Figure 5. Foot five days later. Photographs reproduced courtesy of Salford Royal NHS Foundation Trust.
Figure 5. Foot five days later. Photographs reproduced courtesy of Salford Royal NHS Foundation Trust.
Figure 5. Foot five days later. Photographs reproduced courtesy of
Salford Royal NHS Foundation Trust.
 

Discussion of case study

The clinical picture of active Charcot was complicated by the concurrent presentation of infection and PAD. It is not a common occurrence, as discussed, for Charcot to occur in the presence of PAD, which made the diagnosis more difficult. The MDFS took the view to manage as Charcot until proven otherwise, but as total contact casting was contraindicated the removable walker boot was used instead. As this can be removed, there have been known instances in the past where patients do not use them at all times and weight bear. Also, the re-applying of the device becomes the responsibility of a patient or their carer, and this may have an impact if not fitted correctly.
 

Conclusion

 Active diabetic foot disease is a complicated and multifaceted problem, which requires expertise from a multiple number of professions (multiprofessional approach). Early recognition and prevention lies at the heart of best outcomes. To inform the referral and ensure a person is seen in a timely manner, an assessing healthcare practitioner can significantly improve the referral through steps such as pulse palpation, neurological assessment, comparison of limb temperatures and presence
of deformity.

The diabetic foot can present with a variety of complicated limb and life-threatening/shortening conditions. Often these conditions can be similar in their initial presentation. Arterial disease, infection and Charcot foot all have characteristics of pain, redness and swelling in the feet at different stages and can present on their own, in combination with each other, or in a non-characteristic/ ‘textbook’ way, as discussed in the case report. There are also a number of other significant differential diagnoses that are not discussed here which may also mirror these symptoms, for example, gout
or DVT.

Therefore, the red, swollen foot with or without pain should be considered a clinical emergency and referred urgently to the MDFS.

This article originally appeared in the Journal of Community Nursing and can be found here.
 

References

Abouhamda A, Alturkstani M, Jan Y (2019) Lower sensitivity of ankle-brachial index measurements among people suffering with diabetes-associated vascular disorders: A systematic review. SAGE open medicine 7, 2050312119835038

Alavi A, Sibbald RG, Nabavizadeh R, Valaei F, Coutts P, Mayer D (2015) Audible handheld Doppler ultrasound determines reliable and inexpensive exclusion of significant peripheral arterial disease. Vascular 23(6): 622–9

British Lymphology Society (2018) Position Paper for Ankle Brachial Pressure Index (ABPI). Informing decision making prior to the application of compression therapy. Available online: www.thebls.com

Brownrigg JRW, Schaper NC, Hinchcliffe RJ (2015) Diagnosis and assessment of peripheral arterial disease in the diabetic foot. Diabetic Med 32(6): 738–47
Buerger L (1924) Circulatory disturbances of the extremities. WB Saunders, Philadelphia: 162–8

Charnogursky G, Lee H, Lopez N (2014) Diabetic neuropathy. In: Handbook of Clinical Neurology. Vol 120. Elsevier: 773–85

Clayton W, Elsay TA (2009) A review of the pathophysiology, classification, and treatment of foot ulcers in diabetic patients. Clin Diabetes 27(2): 52–8

Concannon MJ, Sharpe A (2012) The importance of screening for Charcot neuroarthropathy. Practice Nurs 23(8), published online 29 Sept 2013

Conte MS, Bradbury AW, Kolh P, White JV, Dick F, Fitridge R, et al (2019) Global vascular guidelines on the management of chronic limb-threatening ischemia. J Vasc Surg 69(6S): 3S–125S

Department of Health (2019) The 9th annual report from the Advisory Committee on Antimicrobial Prescribing, Resistance and Healthcare Associated Infection (APRHAI). APRHAI annual report, 2017 to 2018. Available online: www.gov.uk/government/publications/aprhai-annual-report-2017-to-2018 (accessed 19 January, 2020)

Dolan NC, Liu K, Criqui MH, Greenland P, Guralnik JM, Chan C, et al (2002) Peripheral artery disease, diabetes, and reduced lower extremity functioning. Diabetes Care 25(1): 113–20

Guest JF, Fuller GW, Vowden P (2018) Diabetic foot ulcer management in clinical practice in the UK: costs and outcomes. Int Wound J 15(1): 43–52

Hinchliffe RJ, Forsythe RO, Apelqvist J, Boyko EJ, Fitridge R, Pio Hong J, et al on behalf of the International Working Group on the Diabetic Foot (2019) IWGDF Guideline on diagnosis, prognosis and management of peripheral artery disease in patients with a foot ulcer and diabetes. Available online: www.iwgdfguidelines.org

Hingorani A, LaMuraglia GM, Henke P, Meissner MH, Loretz L, Zinszer KM, et al (2016) The management of diabetic foot: A clinical practice guideline by the Society for Vascular Surgery in collaboration with the American Podiatric Medical Association and the Society for Vascular Medicine. J Vasc Surg 63(2 Suppl): 3S–21S

International Wound Infection Institute (2016) Wound Infection in Clinical Practice. International Consensus. Wounds International, London. Available online: https://bit.ly/2iWLDAc (accessed 9 January, 2020)

Jeffcoate WJ, Harding KG (2003) Diabetic foot ulcers. Lancet 361(9368): 1545–51
Keast D, Swanson T, Carville K, Fletcher J, Schultz G, Black J (2014) Ten Top Tips... understanding and managing wound biofilm. Wounds Int 5(2): 20–4

Lend GC, Fowkes FGR (1992) The Edinburgh Claudication Questionnaire: An improved version of the WHO/Rose questionnaire for use in epidemiological surveys. J Clin Epidemiol 45(10): 1101–09

Lipsky BA, Berendt AR, Cornia PB, Pile JC, Peters EJG, Armstrong DG, et al (2012) 2012 Infection Diseases Society of America Clinical Practice Guidelines for the Diagnosis and Treatment of Diabetic Foot Infections. Clin Infect Dis 54(12): e132–2173

Lipsky BA, Senneville E, Abbas ZG, Aragón-Sánchez J, Diggle M, Embiln J, et al  on behalf of the International Working Group on the Diabetic Foot (2019) IWGDF Guideline on the diagnosis and treatment of foot infection in persons with diabetes. Available online: www.iwgdfguidelines.org

Lundin M, Wiksten JP, Peräkylä T, Lindfors O, Savolainen H, Skyttä J, et al (1999) Distal pulse palpation: is it reliable? World J Surg 23(3): 252–5

McGee SR, Boyko EJ (1998) Physical examination and chronic lower-extremity ischemia: a critical review. Arch Intern Med 158(12): 1357–64

National Diabetes Footcare Audit (2019) National Diabetes Footcare Audit, 2014–2018. Available online: https://digital.nhs.uk/data-and-information/publications/statistical/national-diabetes-footcare-audit/2014-2018. Accessed 19/01/2020

National Heart, Lung and Blood Institute (2019) Peripheral Arterial Disease. Available online: www.nhlbi.nih.gov/health-topics/peripheral-artery-disease (accessed 9 January, 2020)

National Institute for Health and Care Excellence (2018) Peripheral arterial disease: diagnosis and management. Clinical guideline [CG147]. NICE, London. Available online: www.nice.org.uk/guidance/cg147

National Institute for Health and Care Excellence (2019) Diabetic foot problems: prevention and management. NG19. NICE, London. Available online: www.nice.org.uk/guidance/ng19 (accessed 19 January, 2020)

Pham H, Armstrong DG, Harvey C, et al (2000) Screening techniques to identify people at high risk for diabetic foot ulceration: a prospective multicentre trial. Diabetes Care 23: 606–11

Prompers L, Huijberts M, Apelqvist J, Jude E, Piaggesi A, Bakker K, et al (2007) High prevalence of ischaemia, infection and serious comorbidity in patients with diabetic foot disease in Europe. Baseline results from the Eurodiale study. Diabetlogia 50(1): 18–25

Rogers LC, Frykberg RG, Armstrong DG, Boulton AJM, Edmonds M, Ha Van G, et al (2011) The Charcot foot in diabetes. Diabetes Care 34(9): 2123–29

Scissons R (2008) Characterizing triphasic, biphasic, and monophasic Doppler waveforms: should a simple task be so difficult? J Diagnostic Med Sonography 24(5): 269–76

Society for Vascular Surgery Lower Extremity Guidelines Writing Group, Conte MS, Pomposelli FB, et al (2015) Society for Vascular Surgery practice guidelines for atherosclerotic occlusive disease of the lower extremities: management of asymptomatic disease and claudication. J Vasc Surg 61(3 suppl): 2S–41S

Teo KK (2019) Occlusive Peripheral Arterial Disease. MSD Manual. Available online: www.msdmanuals.com/en-gb/home/heart-and-blood-vessel-disorders/peripheral-arterial-disease/occlusive-peripheral-arterial-disease (accessed 9 January, 2020)

Back to journal