Diabetes Leading to an Extension of the Inflammatory Stage of Repair Essay

Diabetes, which is an endocrine disorder, is caused when the cells of the pancreas are unable to produce insulin or there is a deficiency of insulin within the body (WHO 2006). A diabetic foot ulcer is a major complication of diabetes. According to Bowering (2001), foot ulcers in diabetic patients are common and frequently lead to lower limb amputation unless a prompt, rational, multidisciplinary approach to therapy is taken. Diabetic wounds have been described as “complex microcosms of multiple pathophysiologic processes” (Al-Watban et al., 2007, p72 ), and are predominantly characterized by polymicrobial infection, peripheral neuropathy, structural deformity, altered immune function or increased susceptibility to infection, decreased wound nitric oxide (NO) production, and often, hypoxia/ischaemia. Diabetes Leading to an Extension of the Inflammatory Stage of Repair Essay. Hence, it is important for podiatrists who are involved with wound care management to have a proper understanding of the functional relationships of the biological processes of normal compared to pathological and non-healing ulcers in order to be able to devise treatment strategies. They also need to be aware of all the factors that influence the process of wound healing, especially in diabetic ulcers. The degree of metabolic control, the presence of ischaemia or infection, and continuing trauma to feet from excessive plantar pressure are some of the factors that affect the development and healing of diabetic patients foot ulcers.
According to Grey et al. (2006), most wounds, regardless of aetiology, heal without difficulty. But, at times, certain local and systemic factors can impede the healing of the wound. For example, local factors such as inadequate blood supply, poor venous drainage, infection, foreign body reactions, wound dehiscence can delay wound healing. Some of the systemic factors that hinder wound healing are advancing age, systemic malignancy, chemo- and radiotherapy, impaired macrophage activity and malnutrition.

There has been a great deal of debate around diabetic foot ulcers (DFUs) and pressure ulcers (PUs) on the feet of patients with diabetes, in terms of how to define, detect, assess and treat them. The confusion and lack of evidence in differentiating between these two types of foot ulcers, particularly on the heel, can lead to misdiagnosis, which can increase both financial and patient-related costs.

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To address and tackle those inconsistencies, the Journal of Wound Care (JWC) has published its first international consensus document, Identifying and treating foot ulcers in patients with diabetes: saving feet, legs and lives. Diabetes Leading to an Extension of the Inflammatory Stage of Repair Essay.The main objectives of this project were to:

• Provide information on the differences between a DFU and a PU in patients with diabetes

• Help reduce misdiagnosis by providing and discussing assessment guidelines

• Make a difference in practice through improved patient outcomes.

With this in mind, an international panel of ten key opinion leaders from Australia, England, Republic of Ireland, Malaysia, Poland, Portugal, Spain, United Arab Emirates and US met on 1 and 2 March 2018 in London. They discussed the definitions of a DFU and a PU, and concluded that one way to distinguish between them is knowing whether the patient is mobile (usually associated with DFUs) or immobile (normally related to PUs), although this should be considered along with simple assessments for ischaemia and neuropathy. To this end, and given the importance of an early and correct assessment, the mnemonic ‘VIPS’ was suggested:

• V: vascular (ischaemia)

• I: infection (local signs, odour, exudate, slough, inflammation, etc.)

• P: pressure (causes mobility or immobility)

• S: sensation (neuropathy).

The panel also agreed that another key point was that, if the health professional treating the ulcer is unable to perform a full diabetic foot assessment, it is crucial that the patient be referred to a health professional/department who can. As many members of the professional team would usually come across an ulcer—job titles varying throughout the world—a referral pathway focusing on the referee’s skills rather than their specialties was suggested.

The importance of prevention and the need to follow clear management and treatment strategies, which will vary from centre to centre, were emphasised. The issues around education were also discussed, as well as future research needed. Finally, potential new technologies or alternative therapies that could help treat a DFU or a PU when standard care fails were summarised. Diabetes Leading to an Extension of the Inflammatory Stage of Repair Essay.

Given the international focus of this document, and the various levels of knowledge among the health professionals that come across a foot ulcer, it was highlighted that this document should be read and implemented in conjunction with the clinician’s local guidelines.

We hope you enjoy this document and that it helps make a difference in practice.

In developed countries, it has been estimated that the overall incidence of non-healing wounds is approximately 1–2%.¹ Pressure ulcers (PUs) and diabetic foot ulcers (DFUs) are among the most prevalent chronic wounds in many countries.^2,3 They are a major global clinical and health economic challenge, which is expected to escalate as the population increases, poor lifestyle leads to increased diabetes and obesity and the population ages.^4, 5, 6

International expert consensus guidelines recommend, in general terms, similar pathways for the prevention and management of PUs and DFUs.⁷Nevertheless, critical differences in the precise delivery of effective care lie within the guidelines, which, if not administered appropriately to the diagnosis, are likely to lead, at best, to slow healing. PUs and DFUs, despite describing clinically different indications, share commonalities in definition, for example, shear and friction, pressure and ischaemia.⁸ However, they require quite different approaches to management. These differences can lead to patients being managed on the wrong pathway.

This consensus paper addresses these similarities and differences with two key objectives: first, to differentiate between PUs and DFUs with regard to their definition, causes, assessment, diagnosis, management and treatment, and second, to address confusion and lack of evidence when differentiating PUs and DFUs.Diabetes Leading to an Extension of the Inflammatory Stage of Repair Essay.

Prevalence

Approximately 451 million adults worldwide have diabetes, a figure projected to increase to 693 million by 2045 globally.⁴ The prevalence of DFUs will also increase in line with this. The lifetime incidence of DFUs is reported to be 25%⁹and the global prevalence of DFUs in patients with diabetes is 6.3%,¹⁰ with wide variation by country.^{11, 12, 13, 14, 15} When PUs occur on the foot, those on the heel are the most common;^16,17 the overall PU prevalence in five European countries in 2008 was 18.3%,¹⁶ while more than 2.5 million people in the US develop a PU annually,¹⁸ where the prevalence across all settings is 12.3%.¹⁶More recent figures suggest the prevalence of PUs in Canada is 26%^19,20 and in Western Australia between 6.3% and 9.5%.²¹

Issues around misdiagnosis

Differentiating between a heel wound that is a PU rather than a DFU presents a diagnostic challenge for clinicians. Furthermore, the prognosis, complications and treatment pathways/responsibility of care for PUs and DFUs are different. Risk factors for PUs include diabetes and perfusion,^22, 23, 24 which should be considered in the formation of PU guidelines.^{7,25, 26, 27} Pressure is a common factor in the formation of both a PU on the foot and DFU, and both are managed in fundamentally the same way by reducing or redistributing the pressure.Diabetes Leading to an Extension of the Inflammatory Stage of Repair Essay. ^7,28 However, care pathways for PUs and DFUs are different, reflecting the specific characteristics of the wounds and skill sets required. It is critical to understand the patient clearly, to make an accurate diagnosis and to implement the management strategy appropriate to the wound, particularly where overlap in definitions exists.⁸ Among nurses caring for DFUs, around 35% may have only minimal knowledge of the diabetic foot.²⁹ Furthermore, PUs and DFUs on the heel may be diagnosed differently, depending on the specialism of the health professional, leading to inappropriate care, particularly in the community setting.^8,30 In countries such as the US, where payment for care depends on the identity assigned to the wound, the correct diagnosis may make the difference between receiving, or not, certain types of management and products.^31,32 For example, Apligraf for PU treatment is not even mentioned for reimbursement in the US.³³

Cost of misdiagnosis

Incorrect diagnosis leading to an inappropriate care pathway will to lead to financial and patient-related cost. Management of PUs in all health-care systems is costly,^{34, 35, 36, 37, 38} and associated with higher mortality.^39, 40Complications in the diabetic foot are among the most serious and costly in patients with diabetes. A third of the total cost of managing diabetes is attributable to DFUs, and these are significantly higher after ulceration compared with patients with diabetes and no foot ulcers.⁴¹ If not successfully treated, DFUs often lead to amputations, which involve lengthy stays in hospital.⁴² In fact, amputation in the diabetic foot is preceded by a DFU in approximately 80% of cases.⁴³ The cost of a DFU is high in all health-care systems^34,44,45 and increases with severity. DFUs are widely recognised to have a major impact on patients’ quality of life (QoL)^46,47 and impact on the wider family and friends. QoL is also adversely affected by PUs and any misdiagnosis is likely to exacerbate this.Diabetes Leading to an Extension of the Inflammatory Stage of Repair Essay.

It is clear that the costs of both PUs and DFUs are high and escalate with severity. Ensuring that the correct diagnosis is made and a care pathway, designed by appropriately-qualified and experienced health professionals, is followed, will help control patient-related and health-care-related costs of PUs and DFUs, and provide the greatest probability of success in healing the ulcer and avoiding complications.

This is a working document that addresses general principles and provides guidance designed to minimise the likelihood of misdiagnosis and inappropriate management of PUs and DFUs. It should be read and implemented in conjunction with local guidelines. It brings theory and practice together, and offers areas of reflection that allow the reader to review the information and then decide where and how to use it to underpin their own clinical area. The consensus will inform and enable opportunities for practice change.

Differentiation between DFUs and PUs

Diabetic foot ulcers (DFUs) and pressure ulcers (PUs) have been defined in detail by a number of expert panels, consensus documents and publications.^7,8,48,49 According to the International Working Group on the Diabetic Foot,⁴⁹ a DFU is defined as:

The key elements are the location of the wound and the diagnosis of diabetes. The breadth of this definition means that a PU on the foot in a patient with diabetes is a DFU, as would be any foot wound in a patient with diabetes.⁸ A DFU can occur on any part of the foot, including the plantar and dorsal surfaces. A DFU may be neuropathic, ischaemic or a combination of these two factors (known as neuroischaemic), but the three types of DFUs have overlapping pathophysiology.⁴⁸

A PU is defined by the European Pressure Ulcer Advisory Panel (EPUAP), National Pressure Ulcer Advisory Panel (NPUAP), and Pan Pacific Pressure Injury Alliance (PPPIA) as (Box 1):⁷

This implies that merely diagnosing a wound as a PU does not necessarily fully describe the ulcer and therefore the care that it should receive. Diabetes Leading to an Extension of the Inflammatory Stage of Repair Essay. The definition of PU also encompasses those that occur at the end of life, related to Skin Changes at Life’s End or Kennedy Terminal Ulcers,^49,50 and PUs that are caused by medical devices such as respirator masks, intubation, catheters, splints, casts, and compression bandaging.^8,51

Where heel PUs and DFUs are concerned, there is clear room for overlap in their definitions, if not their precise underlying causes. The consensus panel recognises, in addition to other diagnostic features, that the degree of patient mobility could be a defining characteristic. PUs tend to be associated with immobility; DFUs tend to be associated with mobility. This is not an absolute differentiator. Where a heel PU is related to friction and shear, the patient may have been able to move, resulting in friction. This may be deliberate movement, where the patient tries to reposition themselves, pushing with their heels. However, movement may be passive, where the patient is moved manually by health professionals as part of care. For example, passive friction and shear may be caused by articulating bed frames, used widely in EU hospitals to assist in patient handling, while reducing risk of injury to staff. Involuntary sliding movement of the heel up to 15 or 20cm, which is recognised as a risk for heel injury, occurs when these bed frames are articulated.⁵² On the other hand, mobility/weight bearing is more prominent in the development of a DFU, where repeated friction and pressure on the foot, as the result of patient walking (ambulating), can cause the trauma component of ulceration.

From the viewpoint of management of the wound, and the patient on the appropriate pathway, the critical factor is accurate assessment and diagnosis, rather than the precise terminology used. Guidelines followed to achieve accurate assessment may be expert consensus guidelines, but they should be used in conjunction with local or national guidelines. Diabetes Leading to an Extension of the Inflammatory Stage of Repair Essay. The name ascribed to the ulcer is a start point; the factors that underlie the ulcer are the targets for management and must be clearly identified to develop an effective care plan.

Causes of PUs and DFUs

The pathophysiology of a DFU is complex and multifactorial (Fig 1). A patient with type 1 or type 2 diabetes may develop a number of underlying comorbidities that lead to an at-risk foot. At this stage, the foot does not have an active DFU, but is at high risk of forming one. Key factors in the risk of development of DFUs include:^43,53

• Peripheral neuropathy, which reduces the ability to sense touch and pain and causes loss of protective sensation

• Foot deformity as a result of damage to the distal nervous system, which leads to small muscle wasting and muscle atrophy. The deformed foot (sometimes referred to as a Charcot deformity) is subject to increased pressure where bony prominences become more pronounced and the protective fat pads under the heels and metatarsal heads shift, exacerbating the harmful effects of pressure

• Autonomic neuropathy, causing loss of sweating that leads to dry skin and callus formation increases pressure locally, and the likelihood of the skin cracking. Autonomic neuropathy also causes increased peripheral blood flow and distended foot veins and a warm, dry foot.Diabetes Leading to an Extension of the Inflammatory Stage of Repair Essay.  This can appear to be a healthy foot when, in fact, it is at risk

• Peripheral arterial disease (PAD) is present in nearly half of patients with diabetes,⁵⁴ leading to reduced blood supply and tissue ischaemia. PAD is more common in type 2 diabetics than in type 1⁵⁵

• A history of previous DFU or amputation.

Older patients who have had diabetes for longer and male patients are at higher risk of DFU formation. When one or more of these underlying causes are overlaid with pressure and trauma from footwear or other sources, skin damage can lead to ulceration.⁵⁶ Infection is not regarded as a cause of DFUs, but a consequence of it.⁴³ Once an at-risk foot has skin damage, without the correct care, the wound can deteriorate rapidly as the tissue becomes hyperinflammatory, leading to the overexpression of powerful tissue-destructive proteinases and reactive oxygen species (ROS).^57, 58, 59 Amputation in the diabetic foot is preceded by a DFU in approximately 80% of cases.⁴³

The pathway to PU formation comprises three well-documented key factors: pressure, friction and shear (Fig 1). A period of immobility is a fourth component. Patients may be bed-bound with comorbidities, elderly with end-stage conditions, immobile from spinal cord injury or during surgery. Moisture alone will not lead to PU formation,⁷ but in combination with pressure, and/or friction and shear, it is associated with ulcer formation. Shear is recognised by the NPUAP as a primary cause of PUs.⁶⁰ Moisture increases friction between the skin and a surface, such as a bed sheet,⁶¹ which causes tissue deformation when the different layers of skin move tangentially relative to each other as the patient moves. These forces may damage tissue directly⁶² or cause injury to superficial skin structures when a patient moves on a bed surface.⁶³ Friction and shear predict the development of PUs in adult critical care patients.⁶⁴Tissue shear forces may cause cell damage and death more rapidly, over a period of minutes, than pressure alone.⁶⁵ Pressure over bony prominences in an immobile patient directly damages deep tissue by compression and restriction of blood flow, leading to tissue death and ulceration. In contrast to shear forces, pressure acts over longer time periods, measured in hours.⁶⁶Pressure over bony prominences may be three to five times higher than other tissues, and this is doubled by shear forces.^67,68 Pressure over bony prominences does not occur in isolation from shear forces and as tissue is deformed by compression, shear forces also form around the deformation.  As with DFUs, the physicDiabetes Leading to an Extension of the Inflammatory Stage of Repair Essay.al aetiology of PUs leads to uncontrolled expression of tissue-destructive hyperinflammation that breaks tissue down, resulting in ulceration.^57, 58, 59

Risk factors for the development of heel PUs⁶⁹ include: a previous or current heel PU, indicative of reduced tissue tolerance; diabetes and peripheral neuropathy; stroke or cerebrovascular accident (CVA), restricting the patient’s ability to move; paralysis; hip fracture and dragging injuries resulting from knee replacements; dementia and cognitive impairment; PAD reducing tolerance to mechanical forces; leg spasms, Parkinson’s disease or tremors causing heel rubbing; agitated heels; leg oedema, which may compromise capillary flow and reduce tissue tolerance; and frequent sliding on the bed or chair. Also at risk of developing a PU are patients with diabetes, those undergoing surgical procedures longer than two hours,²⁴ those admitted to a nursing home after transfer from hospital compared with transfer from the community,²³ patients at the end of life²² and those using a medical device.^70,71, 72

Summary

There are similarities as well as important differences between a PU on the heel and a DFU.⁸ The risk and causative factors coincide in several areas, including pressure, shear forces, and peripheral blood supply. Furthermore, heel PUs and DFUs may appear similar on clinical examination and assessment. A difference in causation is immobility/mobility. A patient with diabetes and a heel ulcer may not be recognised as having a DFU; clinically, the ulcer may be confused with a non-diabetic heel PU if the correct assessment is not conducted.Diabetes Leading to an Extension of the Inflammatory Stage of Repair Essay.

Key points

• The degree of patient mobility status could be a characteristic that helps differentiate between a DFU and a PU. DFUs tend to be associated with mobility and PUs with immobility

• Neuropathy and peripheral arterial disease (PAD) are the key risk factors for developing a DFU

• The factors that underlie the ulcer are the targets for management and they must be clearly identified to develop an effective care plan

• A critical factor when managing a wound is accurate assessment and diagnosis.

Assessment, referral and the multidisciplinary team

Correct assessment of the patient to identify the ulcer aetiology, independent of the terminology used to describe it, is critical to allocating the correct care pathway. An ulcer on the heel may be described as a PU, but if the patient has diabetes, it must be assessed as a DFU. This ensures that not only is the wound itself treated effectively, but also the underlying causes are clearly identified and managed and the correct guidance is given to the patient and their carer(s)/family. For example, a heel ulcer in a patient with diabetes, if managed as a PU, is highly unlikely to receive the required multidisciplinary team (MDT) approach which is recommenced for a DFU and will be at risk of complications, deterioration and amputation, all of which could have been avoided if the correct care pathway was followed.

Having identified the condition, the next step is referral to the health professional and/or team that is best qualified to manage the patient. The assessment should identify the key clinical and patient characteristics to be managed and indicates the skill sets required to address them. In the case of a DFU, referral to an MDT is the optimal pathway.

When a patient presents with a heel ulcer, the first step should be to exclude the possibility of diabetes and that it is therefore a DFU.⁸ If necessary, this step can be taken in the absence of the patient’s notes.Diabetes Leading to an Extension of the Inflammatory Stage of Repair Essay. Where no diagnosis of diabetes has been made, two clinical signs that differentiate between a PU and a DFU should be evaluated:

• Presence of diabetic peripheral neuropathy (DPN), leading to loss of protective sensation

• Reduced arterial blood supply (ischaemia).

Furthermore, mobility/immobility can help differentiate between a DFU and PU. If any of these signs (DPN, ischaemia, mobility) are present, then the patient should be directed to the DFU care pathway for further assessment. If these signs do not suggest that the patient has a DFU, the patient may follow the PU pathway. The following section provides guidance on simple tests for identifying the presence or absence of DPN and reduced blood supply in the patient’s feet, and to assess mobility.

Before the ulcer is assessed, the patient history should be taken according to local practice.

Assessment of diabetic peripheral neuropathy

Several tests are available for assessing the presence and severity of DPN. Diagnosis of DPN is made by determining presence or absence of sensation in the foot. The equipment required to conduct the tests varies between the simple and the highly complex, where access to power supplies is required.

Toe Touch Test: The simplest test, which requires no specialist equipment, is the Toe Touch Test or the Ipswich Touch Test (IpTT).^73,74 The sensitivity (78.3%) and specificity (93.9%) are high. The test is always at hand, simple to conduct, safe to do, quick and easy to perform, and easily learned. It can be administered effectively by family and non-specialist carers after training.

The test is conducted by lightly touching the tips of the first, third and fifth toes and the dorsum of the hallux of both feet with the index finger, and noting whether or not the patient can feel or sense the touch.Diabetes Leading to an Extension of the Inflammatory Stage of Repair Essay.  It is important that the index finger touch is light, without pushing, prodding, tapping or poking, to avoid the patient feeling the test by sensing movement or force. To ensure the patient is unaware of the point of touch, he or she should be blindfolded or shielded from viewing the test. If the patient cannot feel the touch on two or more sites out of eight, a diagnosis of reduced sensation is made. If the test indicates potential DPN, the patient should be referred for monofilament testing, where available.

Nylon monofilament test: the next simplest test uses a monofilament nylon fibre, the Semmes-Weinstein monofilament, which bends or buckles when subjected to a force of 10g when pressed against a surface.⁷⁵ Different versions of the equipment used to conduct this test are available. The simplest is a short moulded plastic handle with the monofilament attached perpendicularly at one end. Other versions comprise a reusable handle with replaceable monofilaments.

The patient is introduced to the sensation by touching an area such as the hand or inside of the wrist. The monofilament is then applied to the tips and metatarsal heads of the first, third, and fifth toes⁷⁵ or the tips of the toes and the halluces (Fig 2).⁷⁶ The test should be conducted in such a way that the patient cannot see when the monofilament is applied to the skin to ensure fidelity. The monofilament is applied to the skin in a non-rhythmic pattern to rule out the possibility of the patient predicting when the test is being done. The patient should indicate if they can sense the monofilament. If the monofilament cannot be felt on any one site abnormal sensation in the foot has been detected. However, sensitivity increases when up to four plantar sites are tested. ⁷⁵ Each monofilament must be rested for 24 hours after 10 applications^75,77 and replaced when bent or depending on the manufacturer, after 70–90 applications to ensure that the filament has not weakened.⁷⁸ It should be noted that different monofilaments perform differently.⁷⁷ Those that meet the requirement for buckling at 10g force should be used. In busy clinics, it may be necessary to have more than one monofilament available to account for the need to rest the device. A further test based on the principle of the Semmes-Weinstein hair is the von Frey’s hairs test, which enables the practitioner to determine the threshold of touch sensation by using hairs that buckle at different forces.Diabetes Leading to an Extension of the Inflammatory Stage of Repair Essay.

Vibration perception threshold (VPT): the simplest-to-use vibration-related device for assessing loss of sensation is a tuning fork with a specific frequency of vibration, 128 Hz. In one version of the test,⁷⁹ the tuning fork is set vibrating by striking it on the palm of the hand for 40 seconds. As with the monofilament test, it is then applied to the hand or wrist. The test on the foot is conducted on the dorsal surface of the great toe on the bony prominence just proximal to the nail bed. The patient indicates whether the vibration is sensed and when the vibration has subsided and stopped. The test is repeated on the same foot and then the other foot in a non-predictable sequence.

An alternative to the tuning fork method is a small, battery-powered, hand-held device, the VibraTip.⁸⁰ This device has been reviewed by the UK National Health Service body that develops guidance on new medical device technologies, the Medical Technologies Advisory Committee (MTAC), and is recommended for identifying peripheral neuropathy in the diabetic foot.⁸¹ It is used in the same way as the tuning fork.

Other methods to determine diabetic peripheral neuropathy: simple manual and complex electromechanical devices are available to identify DPN.⁸² Manual devices include the tactile circumferential discriminator, which detects the ability of the patient to discriminate two points applied close together on the skin, and a test that uses ball bearings of increasing diameters to identify which is the smallest that the patient can feel.Diabetes Leading to an Extension of the Inflammatory Stage of Repair Essay.  A number of electromechanical devices are available to measure VPT. Examples are Biothesiometer, Neurothesiometer, Maxivibrometer, Vibrameter, Vibratron and the CASE IV system.⁸² These require access to power and may be unsuitable for use in many locations.

Ankle reflexes: absence of ankle reflexes is associated with an increased risk of foot ulcer formation in patients with diabetes. ⁸³ The test requires a tendon hammer, which is used to strike the Achilles tendon. The health professional performing the test dorsiflexes the foot to put the tendon on stretch before striking with a hammer. Absence of a reflex is abnormal and indicates the need for further assessment.

Vascular status assessment

Several tests are available for assessing the presence and severity of reduced blood supply, which is indicative of possible ischaemia. Initial assessment may be done using simple tests that require no or minimal equipment, or by equipment of increasing complexity and greater discriminatory potential. In order to ensure that the patient is directed to the optimal care pathway, it is necessary to conduct only simple tests. Where vascular issues and reduced blood supply are suspected, the patient should be referred for specialist vascular assessment. Simple tests that require no or minimal equipment include:

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Pulse palpation:^84, 85, 86 Where other methods of identifying vascular issues and ischaemia are not available, palpation of dorsal pedal pulses allows initial screening and requires no equipment. In this test, the health professional assesses the pulse in the posterior and anterior tibial arteries by palpation. The posterior tibial pulse is palpated just behind the medial malleolus. The anterior tibial pulse should be palpated at the ankle, at the midpoint between the two malleoli, not more distally in the foot, where it lies deeper. The dorsal most prominence of the navicular bone is marked. Pulse palpation is evaluated by using two fingers, the index and middle fingers of the dominant hand. The posterior tibial is felt posterior to the medial malleolus of the tibia. For the dorsalis pedis, feel on the dorsum of the foot, lateral to the extensor tendon of the great toe.

Note: a diabetic foot with neuropathy and no ischaemia may present with a warm limb and bounding pulses.⁸³ In this case, do not rely only on pulse palpation for differentiating between a PU and a DFU, but use all assessment outcomes as a set to inform the decision. Furthermore, PAD can still be present, despite the presence of a palpable pulse. Diabetes Leading to an Extension of the Inflammatory Stage of Repair Essay.

Ankle-brachial pressure index (ABPI): ABPI involves the ratio of systolic pressures in the brachial artery at each elbow and systolic pressures in the posterior tibial and dorsalis pedis arteries at each ankle. ABPI is calculated for each leg separately. ABPI is conducted with the patient in the supine position (lying down). Evidence states 10 minutes of supine rest as a minimum before pressure measurement is recommended, to allow equaling of the vascular beds which determine arterial pressure.^87,88 The sphygmomanometer cuff is placed around the ankle above the malleolus. The location may vary slightly from anywhere from just above the malleolus to 2.5cm above the malleolus, depending on which guidelines are followed. Where the ABPI is recorded ≤0.9,⁸⁹ the patient should be referred for further specialist vascular assessment, using more sensitive methods.

Patients with diabetes may have hardening of the arteries and medial arterial calcification (MAC) in the lower leg and foot, which reduces the compressibility of the arteries. The presence of MAC is known to reduce the compressibility of the vessel and can lead to false elevation of the ABPI. This makes ABPI interpretation in diabetes populations difficult. Health professionals should be aware that the ABPI should not be used as a stand-alone screening tool in diabetic populations, but in conjunction with other testing methods. Health professionals should consider using other non-invasive, vascular tools, such as hand-held Doppler auscultation alongside ABPI to aid accurate identification of PAD. Where the ABPI is measured as ≥1.3, further tests, such as a toe-brachial index (TBI), should be performed and if this is not possible, the patient should be referred for vascular assessment.

Note: diabetes involves the medium lumen and therefore the ABPI might not be accurate and a TBI is better.

Toe-brachial Index (TBI): TBI represents an alternative diagnostic tool in patients with diabetes and PAD. Digital arteries are usually less affected by calcifications, which provides insight into the microvascularity of the smaller vessels of the foot. TBI is obtained by dividing the toe systolic pressure by brachial systolic pressure. Since toe pressures are generally about 60% that of brachial pressures, prognosis is relatively good when toe systolic pressure is >50mmHg.⁹⁰ TBI>0.7 is considered within normal limits, TBI≤0.7 is an indication of PAD and TBI≥1 was an indictaion of distal arteries calcification.

Doppler ultrasound: assessing the sound waves from a hand-held Doppler can provide information about the condition of the arteries and blood flow. The Doppler machine provides an audible sound or visual tracing, which is created from the movement of blood in the vessel. PAD can change the sound and shape of the waveforms. A triphasic sound/waveform indicates healthy arterial flow. The third sound within the triphasic wave form comes from the dichrotic notch, which is formed from the elastic recoil within the artery. As the elasticity within the artery reduces, this can affect the production of this sound/wave; this represents a biphasic tone, which is an indication of arterial hardening, but not occlusive PAD. A monophasic wave form formed though a signal sound/wave is indicative of the presence of PAD.

The first test should be pulse palpation. Furthermore, ABPI could be false in patients with arterial calcification. If the patient does not have a pulse and has ulceration, refer, where possible, to a vascular specialist (or relevant health professional) for a full assessment. Diabetes Leading to an Extension of the Inflammatory Stage of Repair Essay.