The pathophysiology of burn injury is well described [1] and is based on the depth of thermal injury and classically deemed as first, second, or third degree. Current nomenclature allows for a more detailed description of burn depth by stating how much of the dermis is injured. Previously classified second-degree burns are now categorized as superficial partial-thickness, mid-partial-thickness, and deep partial-thickness burns. Full-thickness injuries are analogous to previous described third-degree burns. Further classification of thermal injury now included fourth degree which involves the tendon, bone, or muscle. It is important to note that even a partial-thickness burn may require surgical intervention, can get infected, and/or cause a compartment syndrome if it is circumferential. The later of these presentations are the most worrisome due to the potential for conversion to a deeper tissue injury without the appropriate care.

Vascular bed responses to thermal injury have been examined and characterized in animal and human models. To date, these studies have been in prototypes with no known vascular disease or with unknown vascular perfusion. Many studies have well established that total circulating volume increases in a proportional response to percent body surface thermally injured [2, 3]. Elevated skin arterial flow has been described in the setting of thermal injury with concomitant increase in temperature [4]. This blood flow relationship is curvilinear in nature and is focused in the isolated burnt lower extremity with unchanged hemodynamics in the uninjured limb in the same patient [5]. Deep third-degree burn wounds, or full-thickness burns, have been found to be associated with a superficial vascular thrombosis [6] resulting in delayed increased blood flow to the skin which peaks at 1 week [3]. In contrast, superficial partial-thickness wound injuries do not impair the superficial vascular network, resulting in an immediate increase in superficial blood flow once circulatory blood volume is restored [3]. Muscle blood flow in the affected burnt limb has also been discovered to have unchanged skin perfusion [7]. Again, the limitation of this conceptual understanding of arterial and venous responses to thermal injury is that there is minimal to no existing underlying vascular disease.

The incidence of diabetes mellitus (DM) in the United States is expected to increase to a projected 15 cases per 1000 by 2050 [8]. One of the leading associated pathology states of diabetes is its known relation to arterial insufficiency in particular of the lower extremity small vessels. Additionally, peripheral neuropathy is a known complication. This latter manifestation is estimated to affect just over a quarter of all patients who suffer from diabetes [9]. As described by Kimball et al., the presence of lower extremity burns is expected to almost double in the next 50 years [10]. Reduced sensation to the foot is a large factor in foot burns as described in several case studies by Balakrishnan et al. in 1995 [11]. The University of Davis detailed their 10-year experience of 68 admissions of diabetic patients with foot burns half of which had neuropathy on admission [12]. Of these patients, roughly 16 % required either minor or major amputation secondary to their burn wound.

We reviewed 27 patients with diabetes and foot burns in our institute on an IRB-approved protocol to examine outcomes of patients admitted to our burn center from January 2008 to August 2011. These patients were compared to a control group matched by age, total body surface area of burn, complication, and length of hospitalization. Patients with underlying diabetes and thermal injury were found to have a higher rate of nosocomial infections as well as readmissions. These patients also tended to have longer hospital stays and presented at a later stage of their thermal injury. We also discovered that diabetic patients with foot burns respond appropriately to surgical intervention although they need more interventions comparatively [13].

It is well known that successful management of the underlying diabetes disease state is essential for wound healing and can be followed with serial hemoglobin A1C measurements. Elevated hemoglobin A1C has a known association with wound healing failure rates in diabetic patients. Diabetes not only makes one more susceptible to the burn injury but also worsens the extent of the injury by compromising the underlying arterial perfusion. The initial measure of this factor at admission can give the provider an idea of the patient’s underlying diabetic state and forecast the potential future healing of the thermally injured extremity as well as serve as a surrogate marker for distal limb arterial insufficiency.

Any patient who presents with thermal injury must be evaluated for concomitant trauma. One must not overlook life-threatening traumatic injuries in the setting of the obvious superficial or deep burn. That being said, the burn examination begins with assessment of the size of the burn. This involves all areas that are at least second degree or partial thickness in depth. First-degree burns are excluded in the determination of the patient’s total body surface area affected because of known false elevation of calculated fluid requirements. As stated by the Baux formula [14], mortality is directly related to the patient’s age and the total body surface area of thermal injury. This formula was recently updated based on the burn trauma database, which shows a less than one to one relationship to the Baux formula and mortality than 50 years ago [15]. There are multiple ways to determine total body surface area (TBSA) including: the rule of palms, the Lund-Browder chart, the rule of nines, as well as more modern flash-based or IOs-based apps.

Underlying vascular disease can usually be ascertained based on a careful history prior to the thermal injury. For example, if a patient has more proximal arterial insufficiency (i.e., aortoiliac stenosis or obstruction), symptom complex usually focuses around pain with exertion in dedicated muscle groups (known as vascular claudication or simply claudication) involving the buttock, hip, or thigh. The majority of arterial insufficiency focuses in the lower extremity usually sparing the upper extremity. The reason for this incongruity disease distribution is currently unknown and has been the subject of only minimal research efforts [16]. For the simplicity of this chapter, we will focus on the lower extremity as a focal point of our comments.

Arterial insufficiency can be described on the spectrum of symptoms from claudication to rest pain. Intermittent claudication is classically described as calf symptoms ranging from fatigue to aching with exertion. Ischemic neuropathy involving the small unmyelinated A delta and C sensory fibers as well as intramuscular acidosis is thought to contribute to the etiology of this pain [17]. Once the activity has abated, pain subsides.

On the other extreme of the arterial insufficiency spectrum are patients with ischemic rest pain or critical limb ischemia. This is commonly described as pain that can awaken the patient from sleep and necessitates hanging their foot off the bed or walking to alleviate pain (usually centered in the foot). These patients have high risk of foot amputation and/or limb loss, while patients with claudication rarely progress to amputation [17]. These patients may also present with an element of tissue loss indicating a significant risk to progression to amputation if not addressed.

Part of the patient’s history at initial presentation should be an assessment of associated vascular disease and predisposing risk factors . Patients with known claudication may also have a history of coronary artery disease and/or stroke. Well-described predisposing risk factors for arterial disease include but are not limited to hyperlipidemia, hypertension, chronic renal insufficiency, diabetes, and history of smoking.

In terms of underlying venous disease , there are known associations with obesity, immobility, diagnosed and undiagnosed carcinoma states, trauma, inherited hypercoagulability, and a history of deep venous thrombosis. It should be mentioned that many patients suffer from mild forms of chronic venous disorders including simple telangiectasia (spider veins) and reticular veins, varicose veins, and leg edema. Severe forms of this chronic venous disease stem from venous hypertension as related to venous valve incompetence (venous insufficiency) and to a lesser extent abnormal calf muscle pump function. This extreme aspect of the spectrum manifests hyperpigmented skin changes, dermal sclerosis, and potential skin ulceration. Venous insufficiency commonly leads to chronic wound states and only rarely leads to limb loss.

A history of venous insufficiency is usually that of heaviness or fullness in the lower limb with or without pain that is usually increased as the duration of the day wears on. Additionally, patients with venous insufficiency could have history of deep venous thrombosis or recurrent ulceration on the medial aspects of the lower limb (gaiter region). Recurrent ulceration is an advanced presentation of venous insufficiency.

Patients with burns serve as a unique diagnostic problem due to routine swelling (making palpation of a pulse difficult), erythema (making skin assessment difficult), tenderness (making examination of the limb difficult for physical exam and duplex imaging), as well as acute presentation (making history taking challenging to ascertain underlying vascular disease).

The one aspect of examination that might be preserved in this type of patient is the contralateral limb. The majority of time patients will present with similar levels of arterial and/or venous insufficiency in their lower extremity limbs bilaterally. Closely examining and/or testing the unaffected or unburned limb might lead practitioners to an idea of the underlying vascular disease in the thermally injured lower extremity. Such assessment would lead to earlier vascular specialist consultation and potential intervention that might help with future burn wound healing.

As in all aspects of disease, the cornerstone of vascular assessment of any given patient is the physical exam . In the setting of an acute thermal injury, the utility of the physical exam maybe limited secondary to the acute wound created by a thermal injury.

First assessment of any patient with presumed vascular disease is direct palpation of the femoral, popliteal, posterior tibial, and dorsalis pedis artery. When palpation a concurrent palpation of the radial artery to confirm in the mind of the practitioners that what they believe they are palpating is truly a pulse in the lower extremity. In the setting of a thermal injury, with ongoing resuscitation, pulses might be diminished based on low total body volume secondary to ongoing losses due to thermal injuries. It is important to assess the pulse exam of the contralateral possibly unaffected limb to provide an assessment of what the patient’s arterial insufficiency was prior to the thermal injury with the assumption that vascular disease occurs with some regularity in a symmetrical fashion.

A secondary assessment is the use of a handheld Doppler for audible cataloging of perfusion. Doppler signal assessments range from triphasic waveforms (normal arterial flow; three distinct tones) to biphasic waveforms (moderate arterial insufficiency; two distinct tones) to monophasic waveforms (severe arterial insufficiency; single tone).

Ankle brachial index (ABI) is an easily preformed bedside measurement to assess arterial perfusion. ABI is calculated by measuring the higher brachial pressure with a blood pressure cuff and handheld Doppler and dividing that pressure by the higher ankle pressure (posterior tibial artery, anterior tibial artery, or dorsalis pedis artery). To measure brachial and ankle pressures, a Doppler probe is placed beyond an inflated pressure cuff in line with an axial artery to assess when arterial perfusion is extinguished. The pressure cuff is released slowly, and when return of arterial signal is heard, then the pressure measurement is measured. This procedure is depicted in Fig. 31.1. It should be noted that posterior tibial, anterior tibial, and dorsalis pedis artery pressures can be obtained. Calcified atherosclerotic vessels may be noncompressible and thereby falsely elevate ABI. ABI values greater than or equal to 1.3 are considered unreliable, and additional imaging should be sought to assess the patient’s perfusion. ABI values ranging from 0.90 to 1.3 indicate normal arterial perfusion.

As arterial insufficiency increases in the lower extremity, ABI decreases. A single level of arterial stenosis or occlusion is usually associated with ABI between 0.5 and 1.0 with multilevel disease less than 0.5. The utility of ABI measurement for initial triage of vascular patients is well known. In his ground breaking study, Yao [18] observed patients with intermittent claudication usually demonstrate an ABI between 0.5 and 0.9, but it may be as high as 1.0 or as low as 0.2. Patients presenting with pain at rest were found to have ABIs below 0.4 and those with impending gangrene generally a measure less than 0.3.

Despite its common use, ABI has well-known limitations among patients with medial arterial calcifications, a common finding in diabetic and renal failure patients. Such arterial wall changes often falsely elevate ankle pressure measurements, and subsequent ABI measurements may be rendered as falsely negative. Based on the works of others [19, 20], our practice has been to use with increasing frequency arterial duplex examination of the tibial vessels to classify patients into various levels of arterial insufficiency. We have adopted an arterial assessment of peak ankle velocity (PAV) . PAV is defined as the highest arterial perfusion velocity at any tibial vessel in the limb of interest [21]. We have found in investigation of nondiabetic patients that a PAV ≤ 40 cm/s detects severe to critical arterial insufficiency. We have begun implementing this measure to assess our diabetic patient population that has known limitations of ABI measurements. Arterial duplex examination of this sort is an easier assessment in a thermally injured lower extremity when application of blood pressure cuffs for ABI assessment might be problematic due to wound and/or patient tolerance.

Venous insufficiency can be measured with duplex interrogation and associated limb maneuvers to assess for physiological function of the venous system as well as occurrence of thrombus in the vein. Venous insufficiency leads to increased venous pressures in limbs (venous hypertension). Venous duplex with direct compression and flow assessments can be used to diagnose deep vein thrombosis. Venous valvular competency is essential to prevent regurgitation during relaxation of the lower limb muscles, protecting the superficial veins and capillaries from elevations in venous pressure [22]. Valvular incompetency causes an increase in superficial venous pressure (venous hypertension), resulting in the development of tissue trauma and eventual ulceration. This chronic ulcerative state usually does not result in limb loss; however, in the setting of thermal injury, such claims might not hold true and have yet to be studied.

Other modalities have been used in the measure of arterial insufficiency in the lower limb. These range from further noninvasive test such at segmental pressures, direct arterial duplex examination, and pulse volume recordings. Additionally, magnetic resonance imaging (MRI) and computer tomography angiography (CTA) technologies have utilized in the characterization arterial and venous insufficiency. The current gold standard for imaging of the arterial vasculature remains direct arterial puncture with subsequent angiogram. This later approach allows not only diagnosing arterial insufficiency but allows for possible endovascular intervention. This ability to intervene with minimal morbidly has resulted in a substantial increase in this treatment modality not only for severe presentation of arterial insufficiency but for venous disease as well. Endovascular interventions range in nature from balloon angioplasty to intra-arterial stent placement to percutaneous atherectomy, all of which has been addressed elsewhere in this volume.

Once the need for vascular intervention is established, close collaboration with the burn surgery team should be maintained to optimize initial assessment, predict future treatment , and if need be intervene to aid in wound healing in the setting of thermal injury. Even patients with mild arterial insufficiency can potentially pose a challenge to the vascular specialist in that lower extremity wounds require increased perfusion for adequate healing [23]. Thus, the vascular consultant involvement early in the process is reasonable. Once level and severity of arterial disease has been confirmed, the vascular specialist will determine the risk-benefit ratio of an intervention versus conservative management for underlying arterial disease. This decision, in large part, should be based on the stability of the patient as well as the extent of the thermal injury. If initial injury to the extremity exists, intervention might not be warranted if wound burden of the thermal injury far exceeds the any functional outcome and amputation is contemplated. Again early consultation and active communication among all practitioners involved in the patient’s care is needed to formulate a treatment plan that is tailored to the individual case.