Essay Eschar

Re-imagining the Enslaved Eighteenth-Century Freedom Seekers as Twenty-First Century Sitters

Charmaine A. Nelson

FIG 1 Fugitive notice for Thursday, placed by John Rock of Halifax, in the Nova Scotia Gazette and Weekly Chronicle, September 1, 1772.

Since at least the seventeenth century, Africans arrived in Canada in bondage. Their forcible relocation from Africa, or other parts of the Americas, was facilitated by their designation, first as cargo, and subsequently as chattel; a strategy that excluded them from the category of settler. That these histories—spanning over two hundred years and two empires (British and French)—are overwhelmingly disavowed is a result of Canada’s national myth of racial tolerance and, concomitantly, the profound failures of Canada’s education system. However, it does not take much digging to uncover the lie of our blinkered, heroic, national self-aggrandizement as the territory to which enslaved African Americans fled.¹

On Tuesday, September 1, 1772, John Rock of Halifax, Nova Scotia, placed a fugitive notice in the Nova-Scotia Gazette and the Weekly Chronicle for an enslaved Black girl known as Thursday (Figure 1). Rock’s notice for Thursday obscenely juxtaposed descriptions of her self-care and beautification practices (the red ribbon worn about her head) with what was almost assuredly evidence of her physical abuse (the lump above her right eye). The fugitive notices placed for Bell and Bett, both of whom briefly escaped captivity in Quebec, also convey something of the specific horrors of female enslavement (Figures 2–4). Bell’s two documented escapes, less than three months apart, attest to the urgency of her desire to flee.2 That she first ran away in August 1778, with “no shoes or stocking on,” and fled again in October 1778, when fall temperatures made escape even more perilous, speaks to her desperation. But the conditions of Bett’s escape were even more dramatic. When the approximately eighteen-year-old Bett escaped on the winter evening of March 7, 1787, the merchants Johnston and Purss described her as “big with child, and within a few days of her time”3 (Figure 4).

FIG 2 Fugitive notice for Bell, placed by Geo. Hipps in the Quebec Gazette, August 20, 1778.

FIG 3 Fugitive notice for Bell, placed by Geo. Hipps in the Quebec Gazette, November 3, 1778.

FIG 4 Fugitive notice for Bett, placed by Johnston and Purss in the Quebec Gazette, March 8, 1787.

Fast-forward to 2017, and Bell and Bett have been re-imagined: Bell as a stunning, caramel-coloured vision in a figure-flattering dress and stiletto heels, her gaze confidently confronting us for daring to interrupt her mid-phone call; and the exquisite seated Bett, eyes concealed behind fashionable dark sunglasses, showing off her beautiful, chocolate-coloured legs beneath her multi-coloured, ruffled skirt (Figures 5 and 6). But what does it mean to re-imagine these eighteenth-century enslaved freedom seekers as poised and beautiful, twenty-first century divas?4 The colonial archive of fugitive slave advertisements (including significant collections in Nova Scotia, Quebec, and Ontario) calls us to understand the retention of African self-care practices within the world of psychic, physical, and social abuse and material deprivation that was Transatlantic slavery. Through their innovative photographic reinterpretations of enslaved Africans in Canada, Camille Turner and Camal Pirbhai exploit this archive to provoke a conversation about Canada’s role in Transatlantic slavery, the stolen potential of our enslaved ancestors, and the resilience of Canada’s diverse African populations. The fugitive or runaway slave advertisement provides for us a window into the lives and worlds of the enslaved. Frequently printed in weekly newspapers alongside other news and advertisements of transatlantic significance, such notices routinely incentivized the public’s cooperation with the offer of rewards and the threat of judicial retribution. Ubiquitous across the Americas, each example was about the recapture of an individual, or individuals, who had fled, and as such, required that their owners share details that illuminated what made the runaways unique, both in manner and appearance.

Research on the enslaved poses several substantial problems for the researcher; not the least among them are the ways in which the colonial nature of the archive occludes the lives of people who were held in bondage. Since the enslaved were considered cargo, commodities, or chattel in economic and legal discourses, white slave owners and their surrogates strategically prohibited them from being recorded in registries, ledgers, and documents, which were used to individualize and humanize whites.

Such advertisements are what Graham White and Shane White have referred to as “the most detailed descriptions of the bodies of enslaved African Americans available.”5 I would argue that their contention also generally applies to the regions of the Americas that practiced the Transatlantic slave trade, particularly places where abolition predated the development of photography.6 Displaced from their homelands and forced to take up the role of un-free labour in the Americas, enslavement severely impeded the ability of Africans to remember their histories, maintain their ethnic specificity, practice their cultures, and care for their bodies. This was strategic on the part of white colonialists and the slave-owning classes, and evident in the immediate implementation of slave practices—like branding and renaming—that were meant to break the enslaved from their sense of individuality, family, and ancestry.7 Indeed, as Marcus Wood contends, “Slavery, as a legal and economic phenomenon, was premised upon the denial of personality, and of a personal history, to the slave.”8 Furthermore, ruling-class whites deliberately developed the colonial archive in ways that allowed Africans to enter almost always as the objects or “stock” owned by another, and therefore as partial and incomplete entries. This disturbing fact— that the most detailed representations of the enslaved were produced by their owners—provokes a confrontation with the archive, not as an objective or neutral container of facts and information, but as a site through which the elite secured their power by determining who could be represented and in what fashion.

Camal Pirbhai and Camille Turner, Bell (Wanted Series)

Camal Pirbhai and Camille Turner, Bett (Wanted Series)

Reading the Runaway

FOURTEEN DOLLARS Reward
RUN-AWAY, on Sunday Night last [28 Feb.] . . . a Negro-Man, named ISHMAEL, about 36 Years of Age, and nearly 5 Feet 6 Inches high . . . his Face much pitted with the small Pox. He wants some of his Upper-fore Teeth, as likewise the first Joint of the fourth Finger of his left Hand; and besides, on the middle of his Right-Leg, he has a fresh Eschar from a Horse Kick lately received and cured.9

FIG 7 Fugitive notice for Ishmael, placed by John Turner in the Quebec Gazette, March 11, 1784.

Ishmael, twice represented by Turner and Pirbhai, ran away from the Quebec City merchant John Turner Sr. at least three times: in July 1779, March 1784, and June 1788 (Figure 7). Re-imagined as a dignified modern-day dandy (Figure 8) and a dignified cape-wearing gentleman (Figure 9), his scarred, marked, disabled, and no doubt abused body has been represented as that of self-assured, confident men. While John Turner described Ishmael as possessing a “black and copper coloured mixt Complexion,” the modern-day Ishmaels emerge in two decidedly distinct hues—a move that challenges the authority with which whites laid claim to a knowledge of black bodies.10 Gone is the “old Hat bedawbed with white Paint” (1779) and the pox-marked face.11 Instead, the twenty-first-century Ishmaels exude confidence as both composure and self-possession. While the most obvious glimpse of the original eighteenth-century Ishmael’s ability to take control of his appearance arguably resides in the change in John Turner’s description of his hairstyle—from “wears his own Hair which is black, long and curly” (1779),12 to “his Hair is short, strong black and curly” (1784),13 and finally to “black short curled hair” (1788)—the portraits of the re-imagined Ishmaels leave no doubt about who controls their likenesses.14 Although Turner and Pirbhai are staging our epic re-encounters with enslaved freedom fighters, their fashionable, confident namesakes appear to have more in common with models in contemporary fashion magazines than with the enslaved people who navigated what Trevor Burnard has called “radical uncertainty.”15 The power of this potential reincarnation is that it allows us to think not only about what John Turner stole from Ishmael (his labour, years of his life, his access to self-determination), and how John Turner imagined and wanted to see Ishmael, but also how Ishmael, liberated from bondage, may have imagined and represented himself.

Camille Turner and Camal Pirbhai, Ishmael1  (Wanted Series)

Camal Pirbhai and Camille Turner, Ishmael2  (Wanted Series)

Fugitive Slave Advertisements as Portraits

FIG 10 George Theodore Berthon, Portrait of William Henry Boulton, 1846. Oil on canvas, 240.5 x 147.5 cm. Collection of the Art Gallery of Ontario, The Goldwin Smith Collection, GS111.

What is called for is a rereading of fugitive slave advertisements not as mere texts but as portraits, however questionable, that function primarily through vision. However, the reconceptualization of fugitive slave advertisements as portraits of the enslaved is not a seamless fit for several reasons. First, while traditional “high” art portraiture—like that produced in marble or oil paint—was the end-product of a contract between a patron and an artist for a flattering likeness, the representations of enslaved fugitives generated by slave owners were designed to normalize slavery and to criminalize the enslaved for what Marcus Wood has termed “an act of theft, albeit a paradoxical self-theft”16 (Figure 10). Second, while in the traditional relationship the sitter and the patron were often one and the same, with fugitive notices the slave owner was the patron and creator of the notice, and the sitter was an unwilling participant in their representation. Third, while the artistic term for the represented subject in a portrait—the sitter—expresses the stillness required in the actual process of capturing a human likeness, a fugitive’s escape was characterized by their self-directed motion, something that was literally coded as illegal under colonial law. Therefore, the portrait of the enslaved person that a fugitive slave advertisement captured was not of a stationary person—a sitter—but instead, of a person in motion, a runner.

Finally, since a fugitive’s likeness was published against their will, these portraits were “stolen” and unauthorized. Yet they were also “fugitive” in the sense that they were elusive and often highly false images. They were false in the sense that slave owners deliberately vilified the character of the enslaved in the advertisements they placed, and could often not comprehend or accurately describe the African cultural practices of the enslaved. Furthermore, the commonality of fugitive tactics—like altering one’s appearance or changing clothing to “pass” as another social group (mainly free people) in an age when most poor people had only one set of clothing—meant that the enslaved often did not precisely match their descriptions. The medium of these printed portraits was text, as opposed to images, but the words were often strategically deployed with the goal of creating a mental image of the enslaved. Besides the height, weight, and clothing of the fugitive, such notices regularly recounted bodily marks. Ishmael is a case in point. The legalization of corporal punishment within colonial law meant that the bodies of the enslaved were commonly riddled with signs of violence. But the exposure of slave-owner violence in the description of the enslaved person’s injured and tortured body—seen as necessary to the economic ends of the advertisement—signalled the moment in which the fugitive notice became a weapon against the slave-owning classes. As Wood explains, “the runaway emerges as a metaphor for white moral failure.”18

Conclusion

Returning to my original question, what is the meaning of such a deliberate re-imagination? Decked out in the most fashionable clothing, beautiful, charismatic, and self-possessed, these re-imagined subjects are no longer oppressed, frightened, hunted, and terrorized. They exude confidence, delight in frivolity, and embrace luxury—things not afforded their namesakes. By insisting that Bell, Bett, and Ishmael were not slaves, but enslaved—not possessions, but humans—we can see in their desire for freedom, as documented in their eighteenth-century fugitive notices, their heroism. This heroism resides not only in their literal quests for freedom but in their insistence that their bodies were their own, to be dressed (Thursday’s red ribbon), styled, coiffed (Ishmael’s cropped hair), and beautified as they—and not the slave owners—saw fit. As Canadians reflect on the 150th anniversary of our nation, it behooves us to challenge the customary image of a homogeneously white Canada, one that strategically excludes the memory of Canadian participation in Transatlantic slavery and erases the centuries-long presence of people of African descent. Through the re-imagining of Bell, Bett, Ishmael, and other valiant freedom seekers, Camille Turner and Camal Pirbhai challenge us to think anew about the tremendous importance of integrating the memory and histories of Black Canada into our national narrative.

Dr. Charmaine A. Nelson holds a Ph.D. in Art History from the University of Manchester. A professor at McGill University, she lives in Montreal. Her book Slavery, Geography, and Empire in Nineteenth-Century Marine Landscapes of Montreal and Jamaica was published in 2016.

NOTES

Abstract

Burns are a prevalent and burdensome critical care problem. The priorities of specialized facilities focus on stabilizing the patient, preventing infection, and optimizing functional recovery. Research on burns has generated sustained interest over the past few decades, and several important advancements have resulted in more effective patient stabilization and decreased mortality, especially among young patients and those with burns of intermediate extent. However, for the intensivist, challenges often exist that complicate patient support and stabilization. Furthermore, burn wounds are complex and can present unique difficulties that require late intervention or life-long rehabilitation. In addition to improvements in patient stabilization and care, research in burn wound care has yielded advancements that will continue to improve functional recovery. This article reviews recent advancements in the care of burn patients with a focus on the pathophysiology and treatment of burn wounds.

Introduction

Acute thermal injuries requiring medical treatment affect nearly half a million Americans each year, with approximately 40,000 hospitalizations and 3,400 deaths annually [1]. The survival rate for admitted burn patients has improved consistently over the past four decades [2] and is currently a favorable 97 % for patients admitted to burn centers [3]. This can be largely attributed to national decreases in burn size, improvements in burn critical care, and advancements in burn wound care and treatment that have been driven by research, as reflected in the dramatic increase in burn publications over the last several decades [4, 5]. Since the first International Congress on Research in Burns over 50 years ago, progress has been made in a host of areas, and vital improvements in early resuscitation, infection management, wound excision and coverage, and fluid management have helped in the fight against burn mortality [6, 7]. This review presents an update on the care of burn patients, with special emphasis on the mechanisms underlying burn wound healing and recent advancements in burn wound care.

Pathophysiology of burn wounds

Thermal burns from dry sources (fire or flame) and wet sources (scalds) account for approximately 80 % of all reported burns [8] and can be classified based on the depth of burn [9, 10]. In addition to local injury at the site of burn, severe thermal injury over a large area of the skin, roughly 20 % total body surface area (TBSA) or greater, results in acute systemic responses collectively known as burn shock [11]. Burn shock is characterized by increased capillary permeability, increased hydrostatic pressure across the microvasculature, protein and fluid movement from the intravascular space into the interstitial space, increased systemic vascular resistance, reduced cardiac output, and hypovolemia requiring fluid resuscitation [12]. The edema that forms in the interstitial space forms rapidly in the first 8 h following burn injury, and continues to form more slowly for at least 18 h [13]. Volume requirements for resuscitation can be estimated by the total burn size and the patient’s weight (or body surface area). Additional factors influencing these needs include the presence or absence of inhalation injury, the extent of full-thickness burns, and the time since injury [12]. The actual fluid infusion rate is then titrated hourly, based on the adequacy of physiological responses, such as the urine output [14].

Following successful resuscitation, patients with larger burns then enter a more prolonged period of hypermetabolism, chronic inflammation, and lean body mass wasting, all of which may impair wound healing [15]. Additionally, an increased susceptibility to infection due to altered immune status may lead to sepsis, further exacerbating systemic inflammation [16]. Sustained hypermetabolism and inflammation impair wound healing through delayed re-epithelialization [17, 18]. The extent of inflammation and hypermetabolism is related to the extent [19] and depth of burn, as deeper burns show higher levels of circulating cytokines [20] and a greater hypermetabolic response [21]. Similarly, the extent of burn is an efficient predictor of hospital length of stay [19, 22] and mortality [19, 23].

According to one model, the burn wound can be divided into three zones based on the severity of tissue destruction and alterations in blood flow [10, 24–26]. The central part of the wound, known as the zone of coagulation, is exposed to the greatest amount of heat and suffers the most damage. Proteins denature above 41 °C (106 °F), so excessive heat at the site of injury results in extensive protein denaturation, degradation, and coagulation, leading to tissue necrosis. Around the central zone of coagulation is the zone of stasis, or zone of ischemia, which is characterized by decreased perfusion and potentially salvageable tissue [10]. In this zone, hypoxia and ischemia can lead to tissue necrosis within 48 h of injury in the absence of intervention [27]. The mechanisms underlying apoptosis and necrosis in the ischemic zone remain poorly understood, but appear to involve immediate autophagy within the first 24 h following injury and delayed-onset apoptosis around 24 to 48 h postburn [27]. Other studies have shown apoptosis to be active as early as 30 min postburn [28] depending on the intensity of the burn injury [29]. Oxidative stress may play a role in the development of necrosis, as preclinical studies have demonstrated promising reductions in necrosis with systemic antioxidant administration [30]. At the outermost regions of the burn wound is the zone of hyperemia that receives increased blood flow via inflammatory vasodilation and will likely recover, barring infection or other injury [25].

Although burns are different from other wounds in some respects, such as the degree of systemic inflammation [31], healing of all wounds is a dynamic process with overlapping phases [32] (Table ​1). The initial inflammatory phase brings neutrophils and monocytes to the site of injury via localized vasodilation and fluid extravasation, thereby initiating an immune response that is later sustained by the recruitment of macrophages by chemokines [31]. The inflammatory phase serves not only to prevent infection during healing, but also to degrade necrotic tissue and activate signals required for wound repair [33]. Following, and overlapping with the inflammatory response, the proliferative phase is characterized by keratinocyte and fibroblast activation by cytokines and growth factors [34]. In this phase, keratinocytes migrate over the wound to assist in closure and restoration of a vascular network, which is a vital step in the wound healing process [35]. This network of communication between stromal, endothelial, and immune cells determines the course of healing, including closure and revascularization.

Overlapping with the proliferative phase, the final phase of healing involves remodeling the wound [36]. During the remodeling phase, the wound scar matures [31] as collagen and elastin are deposited and continuously reformed as fibroblasts become myofibroblasts [37]. Myofibroblasts adopt a contractile phenotype, and thus are involved in wound contracture [38]. The conversion from fibroblasts to myofibroblasts controls a delicate balance between contraction and re-epithelialization that, in part, determines the pliability of the repaired wound [39]. In addition to fibroblast conversion, apoptosis of keratinocytes and inflammatory cells are key steps in the termination of wound healing and the overall final appearance of the wound [40].

Optimization of burn wound healing

Inflammation

Inflammation is vital to successful burn wound healing, and inflammatory mediators (cytokines, kinins, lipids, and so forth) provide immune signals to recruit leukocytes and macrophages that initiate the proliferative phase [37]. Wound re-epithelialization, or closure, in the proliferative phase via keratinocyte and fibroblast activation, or migration from dedifferentiated hair follicles and other epidermal analogs [41, 42], is mediated by cytokines recruited in the inflammatory phase. While this indicates that inflammation is essential for wound healing, aberrant inflammatory pathways have also been linked to hypertrophic scarring, and anti-inflammatory treatments could potentially aggravate symptoms and delay wound healing [40, 43, 44].

Significant edema that is initiated by several factors including vasodilation, extravascular osmotic activity, and increased microvascular permeability often accompanies inflammation [45]. Excessive or prolonged edema and inflammation exacerbate pain and impair wound healing [17, 18]. Interestingly, studies suggest that in the absence of infection, inflammation might not be required for tissue repair [46]. Since inflammation can have both beneficial and detrimental effects on burn wound healing, the clinical challenge becomes management, applying therapeutic intervention only when inflammation and edema become excessive.

Treatment of inflammation in large burns is difficult, as recently discussed in detail elsewhere [16]. Traditional anti-inflammatory treatments that focus on the inhibition of prostaglandin synthesis, such as nonsteroidal anti-inflammatory drugs or glucocorticoids, impair wound healing [47]. However, steroid administration has been shown to reduce inflammation, pain, and length of hospital stay in burn patients in several small studies [48, 49]. Early excision and grafting has become the gold standard for treatment of full and deep partial thickness burns [50, 51], in part because early excision helps reduce the risk of infection and scarring [52–54]. The timing of debridement coincides with the inflammatory phase of healing, as the burn eschar removed during excision is an inflammatory nidus and a rich pabulum for bacterial proliferation.

Nontraditional anti-inflammatory treatments, such as opioids, have gained considerable attention but have yet to translate promising preclinical results into clinical practice for wound healing. While the majority of animal studies have demonstrated consistent anti-inflammatory effects of opioids on peripheral neurons [55], clinical studies have shown little to no effect on inflammation [56]. Furthermore, topical morphine delayed the early inflammatory phase and accelerated the later proliferative phase [57, 58], which is supported by in vitro studies showing opioid stimulation of keratinocyte migration [59]. Large-scale clinical trials evaluating opioid efficacy on wound healing have not yet been conducted [60].

Infection

The skin functions as a barrier to the external environment to maintain fluid homeostasis and body temperature, while providing sensory information along with metabolic and immunological support. Damage to this barrier following a burn disrupts the innate immune system and increases susceptibility to bacterial infection [61]. Burn wound infection was defined in a rat model with Pseudomonas aeruginosa [62, 63], in which the following progression was observed: burn wound colonization; invasion into subjacent tissue within 5 days; destruction of granulation tissue; visceral hematogenous lesions; and leukopenia, hypothermia, and death. Burn patients are at high risk for infection [64], especially drug-resistant infection [65], which often results in significantly longer hospital stays, delayed wound healing, higher costs, and higher mortality [66]. Infection can lead to the development of a pronounced immune response, accompanied by sepsis or septic shock, which results in hypotension and impaired perfusion of end organs, including the skin – all processes that delay wound healing. Furthermore, the leading causes of death following a severe burn are sepsis and multiorgan failure [67–69], so prevention and management of infection is a primary concern in the treatment of burn patients. Early and accurate diagnosis of infection is difficult: C-reactive protein and the white blood cell count are most often used, since the diagnostic power of procalcitonin is questionable in burns [70]. Consensus definitions of sepsis and infection have recently been proposed that are more relevant to the burn population and are often used clinically but still require validation [71].

The management of burn wound infections has been extensively reviewed elsewhere [61, 64–66, 72–77]. Since the adoption of topical antibiotics, such as mafenide in the 1960s and silver sulfadiazine in the 1970s, and of early excision and grafting in the 1970s and thereafter, systemic infections and mortality have consistently decreased [68, 72, 78]. However, Gram-positive and Gram-negative bacterial infections still remain one of the most common causes of mortality following burn injury [73]. Bacterial cultures can aid in the selection of an appropriate antibiotic, especially in cases of bacterial drug resistance, but altered pharmacokinetic parameters in burn patients must be considered and dosing should be adjusted accordingly to maximize antibiotic efficacy [79]. Importantly, effective topical antimicrobials do not exist for invasive fungal infections, and fungal wound infections are associated with greater mortality rates in large burns (>30 % TBSA) [80]. Owing to high lethality, suspicion of an invasive burn wound infection mandates rapid diagnosis, often by histopathology, and excision or re-excision of the wound.

Nutrition

Sustained hypermetabolism, hormone elevations, and muscle wasting following severe burn injury all contribute to the clinical outcome, with magnitude and duration that are unique to burns [81, 82]. Accordingly, reducing the impact of a hypermetabolic state and providing adequate nutrition are key factors that affect burn wound healing and recovery [83], as has been reviewed elsewhere [84]. There is a difficult balance between the additional caloric needs to meet the demand from hypermetabolism and the consequences of nutrient overconsumption. Nutritional support following a burn injury is a complex issue. For example, early excision and aggressive feeding in children does not diminish energy expenditure but is associated with decreased muscle protein catabolism, a decreased rate of burn sepsis, and significantly lower bacterial counts from excised tissue [85]. In adults, early nutritional support is correlated with shorter stays, accelerated wound healing, and decreased risk of infection [86].

Several nutritional factors must be considered. For example, excess carbohydrate consumption may lead to hyperglycemia [87] that can exacerbate systemic inflammation and muscle degradation [88, 89]. Furthermore, excess fat consumption may exaggerate the immunosuppressed state [90]; and since major burn injuries may also result in immunosuppression [91], this exaggeration may increase the risk for infection and sepsis. Carbohydrate and fat intake must therefore be closely monitored in burn patients. Guidelines for nutritional support of burn patients vary, but consensus recommendations have been given by the American Burn Association and the American Society for Parenteral and Enteral Nutrition for carbohydrates, proteins, and fats [84].

In addition to support with amino acids and vitamins [84], administration of insulin has been shown to decrease healing time by reducing protein catabolism and increasing skeletal muscle protein synthesis [92–96]. More research is needed to optimize insulin delivery, as many recombinant growth factors, such as epidermal growth factor and transforming growth factor, are often cost prohibitive [93]. Other anabolic agents, such as oxandrolone, have been shown to increase lean body mass recovery, decrease length of stay, and improve overall outcomes, including wound healing [97–100]. Additionally, while conventional theory suggests that hemoglobin levels must be maintained above 10 g/dl to promote wound healing [101], preliminary evidence suggests that mild to moderate anemia has no effect on graft success if perfusion is maintained with proper circulatory volume [102]. The results of a multicenter, randomized, controlled trial (ClinicalTrials.gov NCT01079247) comparing blood transfusion with lower volumes (target hemoglobin of 7 to 8 g/dl) and conventional volumes (target hemoglobin >10 g/dl) for a large cohort of patients are expected soon and will allow for more definitive clinical guidelines on blood transfusion volumes.

Resuscitation

Severe thermal injuries over a large area of the skin (>20 % TBSA) require fluid resuscitation for stabilization. Although volume guidelines and fluid compositions vary widely between centers, the goal of fluid resuscitation is to maintain organ perfusion with the least amount of fluid necessary [12]. Common traditional resuscitation formulas, such as the modified Brooke, and Parkland formulas, employ crystalloids such as lactated Ringer’s that contain sodium, chloride, calcium, potassium, and lactate. During large-volume resuscitations, the addition of colloids (for example, albumin, fresh frozen plasma) as adjuncts has been successful in reducing the total volume [12]. Despite extensive research into resuscitation fluid compositions and volumes, little is known about the effect of resuscitation on wound healing. A recent meta-analysis showed a positive association between the number of grafting procedures and hypernatremia, suggesting that high serum sodium levels may inhibit graft take [103]. Additionally, we have recently shown that the rate of wound closure (healing rate) is significantly faster in patients who received lower 24-h fluid resuscitation volumes [104]. More work is needed to evaluate the effect of resuscitation on wound healing trajectories before clinical recommendations for preferred fluid compositions and volumes can be made.

Wound coverage and grafting

Early excision and grafting has been the standard of care for decades. Most studies have shown that excision within 24 to 48 h after injury is associated with decreased blood loss, infection, length of hospital stay and mortality, and increased graft take [105–108], although mortality reductions may only occur in patients without inhalation injury [109]. Since one of the main challenges in treating acute thermal injuries is preventing infection, excising the eschar and covering the wound as early as possible are critical. The standard for rapid and permanent closure of full-thickness burns is a split-thickness skin graft from an uninjured donor site on the same patient (autograft). Such grafting provides sufficient coverage without risk of rejection, although meta-analyses have yet to determine the failure rate of split-thickness skin grafts in burn patients. Split-thickness skin grafts can be meshed with variable expansion ratios to increase the coverage area, but concerns remain over the effect that meshing has on range of motion [110] and the graft site healing rate. On the other hand, donor sites are painful and impose their own wound-healing burden on the patient [111]. Various dressings have been used to cover donor sites during healing, with variable results [112].

Patients with more extensive burns often require temporary coverage with an allograft, xenograft, skin substitute, or dermal analog due to insufficient or unavailable donor sites. Allografts, or tissue taken from a living or deceased human donor, and xenografts, taken from a different species, promote re-epithelialization and prepare the wound bed for autograft, increasing the healing rate when compared with traditional dressings [113]. A recent meta-analysis suggested that since allografts and xenografts appear to be equally effective, xenografts may be a superior choice for their increased safety and reduced price [114]. However, caution should be exercised in drawing broad conclusions from this meta-analysis because the cited studies lack standardization and critical details such as depth and size of burn, and many studies cited were merely anecdotal. A cadaver allograft is thus widely considered the best material for temporary closure of excised wounds in patients with extensive, life-threatening burns and inadequate donor sites. The cadaver allograft is also the preferred material for protection of widely meshed autografts (3:1 or higher meshing ratios) during healing. In the latter setting, the allograft is applied over the meshed autograft in the manner of a sandwich.

A variety of different skin substitutes and dermal analogs exist [115–119] (Table ​2) that can be broadly divided into those which replace the epidermis or replace the dermis [120, 121]. Epidermal substitutes are normally only a few cell layers thick and lack normal dermal components [122, 123]. Commercially available dermal substitutes include acellular matrices, commonly from human – for example, Alloderm (LifeCell, Bridgewater, NJ, USA) or GraftJacket (KCI, San Antonio, TX, USA) – or other sources (for example, Integra; Integra LifeSciences, Plainsboro, NJ, USA). Biobrane (Smith & Nephew, London, UK) is a semisynthetic, bilaminar material consisting of a nylon-mesh dermal analog (bonded with porcine collagen) and a silicone epidermal analog. Biobrane is used for temporary closure of superficial burns and donor sites [124, 125]. Products currently under development integrate the concept of dermal scaffolds that actively promote revascularization by incorporating stem cells and growth factors to recreate a favorable cellular microenvironment [126, 127].

Table 2

Skin substitutes and coverage options

Numerous options exist for dressings [128, 129]. The selection of an appropriate dressing depends on several factors, including depth of burn, condition of the wound bed, wound location, desired moisture retention and drainage, required frequency of dressing changes, and cost. While many factors must be considered in dressing selection, the goals in selecting the most appropriate dressing should include providing protection from contamination (bacterial or otherwise) and from physical damage, allowing gas exchange and moisture retention, and providing comfort to enhance functional recovery. The traditional approach to burn wound care developed at the US Army Burn Center includes alternation of mafenide acetate cream in the morning and silver sulfadiazine cream in the evening, with gauze dressings used over the creams. More recently, silver-impregnated and other dressings have been introduced. Major classes of dressings include: alginate, for example Aquacel (ConvaTec, Bridgewater, NJ, USA), Comfeel (Coloplast, Minneapolis, MN, USA), or Sorbsan (Mylan, Morgantown, WV, USA); antimicrobial, for example Acticoat (Smith & Nephew, London, UK) or Silverlon (Argentum, Geneva, IL, USA); collagen, for example Fibracol (Johnson & Johnson, New Brunswick, NJ) or Puracol (Medline, Mundelein, IL, USA); hydrocolloid, for example Duoderm (ConvaTec, Bridgewater, NJ, USA), Granuflex (ConvaTec, Bridgewater, NJ, USA), or Tegaderm (3M, Maplewood, MN, USA); hydrogel, for example Dermagel (Maximilian Zenho & Co, Brussels, Belgium), SilvaSorb (Medline, Mundelein, IL, USA), or Skintegrity (Medline, Mundelein, IL, USA); and polyurethane foam, for example Allevyn (Smith & Nephew, London, UK) or Lyofoa (Molnycke, Gothenburg, Sweden). Notably, many of these dressings exhibit antimicrobial properties through silver impregnation, but recent studies suggest silver may delay wound healing and should not be routinely used on uninfected donor skin [130, 131] even though silver dressings may reduce wound pain [132]. In patients with extensive or deep burns, antimicrobial efficacy should be the first priority in burn wound care.

Alternatively, cell-based techniques for more permanent coverage have made progress. Research on cultured epithelial cells has made advancements, especially with respect to culture time. Culture-based options, such as Epicel (Genzyme, Cambridge, MA, USA), use a small biopsy of the patient’s skin to provide keratinocytes, which are expanded over 2 to 3 weeks (for Epicel, in the presence of proliferation-arrested murine fibroblasts) into a confluent epidermal autograft. Other options, such as ReCell (Avita, Northridge, CA, USA), take a small biopsy of the patient’s skin and prepare a mixture of keratinocytes, melanocytes, and stem cells in a liquid formulation for spraying onto the excised burn wound during the same operation [133–135]. These techniques may reduce the amount of donor skin needed for treatment of large burns, significantly reducing the healing time of both the donor and the burn sites, and increasing overall graft success and scar quality [136]. More work is needed on cell-based coverage options before widespread implementation can be recommended.

Keratinocytes and stem cells

As mentioned previously, keratinocytes play a vital role in wound closure. Cytokine activation causes keratinocyte migration in the proliferative phase, leading to closure and restoration of a vascular network [35]. Keratinocytes can also be activated by mu opioid receptor agonists [59] but the role of these agonists on inflammation and wound closure remains unclear [57, 58]. Despite positive studies with EpiDex (Modex, Lausanne, Switzerland) – an engineered, fully differentiated autologous skin substitute derived from keratinocytes showing efficacy comparable with split-thickness skin grafts in wound closure and healing [137] – results have yet to translate into clinically viable options. Studies evaluating expansion of keratinocytes on human fibroblasts following trypsin extraction [138], and using engineered skin with keratinocytes on a fibrin matrix [139], have demonstrated improvements in wound healing. Retrospective analyses on autologous keratinocytes showed that cultured allogeneic or autologous keratinocytes may accelerate wound healing [140, 141]. Taken together, the future impact of keratinocyte-mediated cell coverage options is promising, but more research is needed [134]. Additionally, keratinocyte-based treatments should be pursued carefully, as overactivation of keratinocytes can contribute to the development of hypertrophic scarring [43, 142].

The use of adult stem cells, including bone marrow stem cells, hair follicle stem cells, and adipose stem cells, in acute burn care is an exciting topic [143]. Addition of bone marrow stem cells to nonhealing chronic wounds leads to engraftment of cells and enhanced wound healing [144, 145]. Moreover, studies have reported that bone marrow stem cells can transdifferentiate towards multiple skin cell types [146]. Mechanisms of action of bone marrow stem cells in burns are not fully elucidated, but modulation of inflammation has occurred after radiation burns in humans [147]. Similarly, adipose stem cells accelerate re-epithelialization by paracrine activation of host cells via growth factor secretion [148, 149]. Also, hair follicle stem cells are capable of generating a stratified epidermis on human burn wounds [150]. Additionally, the possibility of generating a cellular skin equivalent is being explored. Hair follicle stem cells have been incorporated into products, such as Integra, to investigate wound healing [151]. A cultured skin substitute using adipose stem cells and keratinocytes has been developed that produces epidermal, dermal, and hypodermal stratification [152]. Moreover, human adipose stem cells that would normally be discarded have recently been isolated from debrided burn eschar tissue [153] and used to generate a tri-layered, vascularized construct [154]. Promising data with nonembryonic stems cells such as these have stimulated interest into future applications and development, and undoubtedly further investigations will produce exciting results.

Other considerations and future directions

Monitoring and predicting wound healing

No new skin-based technology can substitute for careful attention by the burn team to the progress (or lack thereof) of wound healing. The WoundFlow computer software program was developed as an enhancement over the traditional paper Lund–Browder diagram to more accurately quantify and track burn injuries over time [104, 155]. WoundFlow is an electronic mapping program that calculates burn size and tracks wound healing [104, 155]. The ability to accurately track burn wound healing over time will support both clinical care and future studies that compare healing rates and outcomes following different treatments. Notably, this study demonstrated that delayed wound healing was associated with a significantly higher risk of mortality [104, 155].

The ability to predict whether a burn wound will spontaneously heal or not would greatly improve patient care. Furthermore, the ability to uniquely tailor treatment to each individual patient would improve patient outcomes and decrease the time to functional recovery, reducing the overall cost of care. Biomarkers may provide a means to allow for tailored treatments and to give insight into wound healing mechanisms [156–161]. Significant efforts in the search for predictive biomarkers for wound failure have determined that serum cytokines, such as interleukin-3 and 12p70, and serum procalcitonin are independently associated with wound failure [161]. Additional candidates have been identified [158–160] but further work is needed to model complex, temporal serum cytokine profiles into an effective predictor for wound healing. In addition to evaluating serum cytokine profiles, candidate biomarkers have been identified in wound effluent [161], which may be a better medium for predicting local wound healing than cytokines in the circulation [162]. Wound exudate has been shown to contain elevated levels of immunosuppressive and proinflammatory cytokines, such as interleukin-1β, interleukin-2, interleukin-6, and tumor necrosis factor alpha [163]. In fact, dipeptidyl peptidase IV and aminopeptidase have been identified in burn wound exudate with a significantly different ratio from that found in plasma [164]. Other work on local wound biomarkers using biopsies has shown that a host of proteins are upregulated during wound healing [165]. More work is needed to establish a biomarker profile that can accurately predict wound healing and to identify potential novel areas for therapeutic intervention.

In addition to examining burn wounds directly, and the wound exudate, another potential method for examining the ability of burn wounds to heal is non-invasive imaging [166]. To this end, a number of non-invasive imaging techniques have been investigated for their use in determining burn depth. Such techniques include terahertz imaging, spatial-frequency-domain imaging, near-infrared spectroscopic imaging, and reflectance-mode confocal microscopy, among others [167–172]. While many of these techniques have not yet been refined sufficiently for clinical application, the most successful research efforts into imaging techniques for burn wounds examine blood flow, such as laser Doppler imaging and indocyanine green angiography [173]. Laser Doppler imaging provides the most evidence for accurately assessing burn severity [174], but it has been shown that laser Doppler imaging is only superior to visual assessment 48 h after thermal injury [175]. Additional studies are needed to fully explore the potential for incorporation of non-invasive imaging modalities into the routine treatment of burn wounds.

Obese patients

As the obese population continues to grow [176], new treatment approaches will be required. Obese burn patients present with a variety of unique characteristics that include: increased rates of diabetes, hypertension, cardiac disease, and pulmonary disease; altered pharmacokinetics and pharmacodynamics; and altered immune responses [177]. Even the commonly used Lund–Browder chart for estimation of TBSA is problematic for obese patients because it fails to account for altered body-mass distribution in these patients [178]. Hence, analysis of group differences and controlled clinical studies in unique patient populations are needed [179].

Older patients

Census predictions suggest that the older population will double in the next 20 years. Since older people are at increased risk for burn injury, an increasing number of burn injuries among the older population should be expected. A recent review delineated the unique burn pathophysiology, comorbidities, and treatment strategies for the older population [180]. Detailing all of the unique considerations for the older burn population is outside the scope of this review, but several key points are noteworthy. Most burns among older people occur at home, especially in the kitchen and bathroom, due to diminished alertness, slower reaction time, and reduced mobility [181]. Reductions in metabolic rate and skin thickness with age result in more severe burns, and more extensive full-thickness burns are associated with increased mortality [182]. Comorbidities such as diabetes and cardiovascular disease complicate treatment, and may exacerbate the postburn hypermetabolic response [183]. Several formulas for predicting the survival of older patients, such as the Baux score [184], have received wide acceptance and can help guide clinicians in patient treatment. Unique treatment considerations for older patients should include attentive resuscitation to reduce the risk of volume overload, judicious ventilator support, careful analgesic administration, prudently timed excision and grafting, and extended rehabilitation for functional recovery [180]. The older population presents a unique challenge to the burn clinician, and the treatment of patients must be carefully considered on a case-by-case basis.

Future directions

Adult burn patients with increased markers of inflammatory stress exhibit reduced serum levels of vitamin A despite normal markers of oxidative stress [185–187]. Additionally, limited preclinical studies show that polyprenoic acid and retinol can facilitate wound healing [188], and that retinoids are efficacious on a variety of other skin conditions [189]. Moreover, early clinical studies have shown that retinoid treatment effectively increases scar elasticity [190, 191]. Taken together, these data highlight the need for studies evaluating retinoids on burn wound healing outcomes.

Pirfenidone was originally developed as an antihelminthic and antipyretic agent, but recent work has demonstrated that it also has anti-inflammatory, antioxidative, and antiproliferative effects [192]. In particular, the antifibrotic properties of pirfenidone attenuate fibroblast proliferation and collagen deposition in vitro and in preclinical models [192]. Pirfenidone is approved for the treatment of idiopathic pulmonary fibrosis in Europe, Japan, and the USA. The antifibrotic actions of pirfenidone and other data suggest that pirfenidone could modulate the tissue response to injury at multiple stages of wound repair to improve scarring and function as an adjuvant for abnormal wound healing processes. Preclinical investigations are currently underway in rabbits [193, 194] and rats [195], but controlled clinical studies are needed to evaluate the safety and efficacy of pirfenidone on abnormal wound healing.

The treatment of burn wounds with hyperbaric oxygen was first investigated in the mid-1960s and garnered some attention in the decades following, but controversy remains over potential risks and costs [196, 197]. Recent work in rat models has shown that hyperbaric oxygen reduces healing time and improves scar appearance of burn injuries [198]. Advancements in hyperbaric chambers have reduced the overall cost associated with treatment, and controlled clinical trials in humans are beginning to produce data supporting the conclusion that hyperbaric oxygen is safe and effective for improving burn wound healing [199–201]. However, more data are needed before broad conclusions can be made about the overall utility of hyperbaric oxygen for treating burns.

Future research on burn patient care will focus on a variety of areas [202]. Considering a current survival rate of over 97 % for burn patients [3], major advancements from the past several decades have improved patient care such that significant future improvements in patient survival rate will be more difficult. However, improvements are still needed in individualized care, namely prediction of patient outcomes and the ability to tailor treatment to optimize functional recovery. Improvements are also needed to accelerate wound closure and healing and to improve psychological care to promote successful reintegration. Research in inflammation, infection, stem cells, grafting, biomarkers, inflammation control, and rehabilitation will continue to improve individualized care and create new treatment options.

Conclusion

The various clinical challenges in treating acute thermal injuries include balancing the many factors that affect wound healing to reduce the length of stay (and associated cost of treatment), the risk of infection, the time to wound closure, and the overall time to functional recovery. The treatment of burn wounds has evolved over several decades through clinical and preclinical research. Significant advancements have been made in patient care, including tracking wound healing, developing novel graft and coverage options, controlling inflammation, optimizing dietary needs, and testing unique pharmacological interventions. As a result of these efforts, patient survival has improved along with a concomitant decrease in the length of stay, which in turn results in a decreased cost to the patient and the medical providers. A summary of selected clinical recommendations is provided (Table ​3) to aid the intensivist, but it is important to remember that burn patients present unique challenges based on multiple variables (for example, age, TBSA, comorbidities) and treatment decisions must be tailored to each patient’s needs. Current and future research will continue to identify novel targets and treatment paradigms to further improve burn wound care.

Table 3

Recommendations for the intensivist

Acknowledgements

The authors would like to thank the staff of the Clinical Trials task area at the US Army Institute of Surgical Research for administrative support. The authors would also like to thank Dr Harold Klemcke for critical review of this manuscript. This work was supported in part by an appointment (MPR) to the Postgraduate Research Participation Program and an appointment (LCC) to the Knowledge Preservation Program at the US Army Institute of Surgical Research administered by the Oak Ridge Institute for Science and Education through an interagency agreement between the US Department of Energy and US Army Medical Research and Materiel Command.

The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the Department of the Army or the Department of Defense.

Abbreviation

TBSATotal body surface area

Footnotes

Competing interests

The authors declare that they have no competing interests.

Authors’ contributions

MPR and KKC outlined the paper. MPR wrote all drafts of the manuscript, with primary editing and revision support from LCC. All authors contributed information for the manuscript, participated in its revision, and approved the final version for publication.

References

1. Gibran NS, Wiechman S, Meyer W, Edelman L, Fauerbach J, Gibbons L, et al. American Burn Association consensus statements. J Burn Care Res. 2013;34:361–5. doi: 10.1097/BCR.0b013e31828cb249.[PubMed][Cross Ref]

2. Mann R, Heimbach D. Prognosis and treatment of burns. West J Med. 1996;165:215–20.[PMC free article][PubMed]

3. American Burn Association. Burn incidence and treatment in the United States: 2013 fact sheet. 2013. http://www.ameriburn.org/resources_factsheet.php. Accessed 12 May 2015.

4. Sen S, Palmieri T, Greenhalgh D. Review of burn research for the year 2013. J Burn Care Res. 2014;35:362–8. doi: 10.1097/BCR.0000000000000163.[PubMed][Cross Ref]

5. Wolf SE, Arnoldo BD. The year in burns 2011. Burns. 2012;38:1096–108. doi: 10.1016/j.burns.2012.10.002.[PubMed][Cross Ref]

6. Burd A. Research in burns – present and future. Indian J Plast Surg. 2010;43:S11–4. doi: 10.4103/0970-0358.70717.[PMC free article][PubMed][Cross Ref]

7. Thomas SJ, Kramer GC, Herndon DN. Burns: military options and tactical solutions. J Trauma. 2003;54:S207–18.[PubMed]

8. American Burn Association. National Burn Repository 2014. 2014. http://www.ameriburn.org/2014NBRAnnualReport.pdf. Accessed 12 May 2015.

9. Kagan RJ, Peck MD, Ahrenholz DH, Hickerson WL, Holmes J, Korentager R, et al. Surgical management of the burn wound and use of skin substitutes: an expert panel white paper. J Burn Care Res. 2013;34:e60–79. doi: 10.1097/BCR.0b013e31827039a6.[PubMed][Cross Ref]

10. Nisanci M, Eski M, Sahin I, Ilgan S, Isik S. Saving the zone of stasis in burns with activated protein C: an experimental study in rats. Burns. 2010;36:397–402. doi: 10.1016/j.burns.2009.06.208.[PubMed][Cross Ref]

11. Robins EV. Burn shock. Crit Care Nurs Clin North Am. 1990;2:299–307.[PubMed]

12. Pham TN, Cancio LC, Gibran NS, American Burn Association American Burn Association practice guidelines burn shock resuscitation. J Burn Care Res. 2008;29:257–66. doi: 10.1097/BCR.0b013e31818ba14d.[PubMed][Cross Ref]

13. Shirani KZ, Vaughan GM, Mason AD, Jr, Pruitt BA., Jr Update on current therapeutic approaches in burns. Shock. 1996;5:4–16. doi: 10.1097/00024382-199601000-00004.[PubMed][Cross Ref]

14. Dries DJ. Management of burn injuries – recent developments in resuscitation, infection control and outcomes research. Scand J Trauma Resusc Emerg Med. 2009;17:14. doi: 10.1186/1757-7241-17-14.[PMC free article][PubMed][Cross Ref]

15. Porter C, Hurren NM, Herndon DN, Borsheim E. Whole body and skeletal muscle protein turnover in recovery from burns. Int J Burns Trauma. 2013;3:9–17.[PMC free article][PubMed]

16. Farina JA, Jr, Rosique MJ, Rosique RG. Curbing inflammation in burn patients. Int J Inflamm. 2013;2013:715645. doi: 10.1155/2013/715645.[PMC free article][PubMed][Cross Ref]

17. Edgar DW, Fish JS, Gomez M, Wood FM. Local and systemic treatments for acute edema after burn injury: a systematic review of the literature. J Burn Care Res. 2011;32:334–47. doi: 10.1097/BCR.0b013e31820ab019.[PubMed][Cross Ref]

18. Sommer K, Sander AL, Albig M, Weber R, Henrich D, Frank J, et al. Delayed wound repair in sepsis is associated with reduced local pro-inflammatory cytokine expression. PLoS One. 2013;8 doi: 10.1371/journal.pone.0073992.[PMC free article][PubMed][Cross Ref]

19. Wilmore DW, Long JM, Mason AD, Jr, Skreen RW, Pruitt BA., Jr Catecholamines: mediator of the hypermetabolic response to thermal injury. Ann Surg. 1974;180:653–69. doi: 10.1097/00000658-197410000-00031.[PMC free article][PubMed][Cross Ref]

20. Sakallioglu AE, Basaran O, Karakayali H, Ozdemir BH, Yucel M, Arat Z, et al. Interactions of systemic immune response and local wound healing in different burn depths: an experimental study on rats. J Burn Care Res. 2006;27:357–66. doi: 10.1097/01.BCR.0000216330.93056.06.[PubMed][Cross Ref]

21. Pereira CT, Herndon DN. The pharmacologic modulation of the hypermetabolic response to burns. Adv Surg. 2005;39:245–61. doi: 10.1016/j.yasu.2005.05.005.[PubMed][Cross Ref]

22. Hussain A, Dunn KW. Predicting length of stay in thermal burns: a systematic review of prognostic factors. Burns. 2013;39:1331–40. doi: 10.1016/j.burns.2013.04.026.[PubMed][Cross Ref]

23. Colohan SM. Predicting prognosis in thermal burns with associated inhalational injury: a systematic review of prognostic factors in adult burn victims. J Burn Care Res. 2010;31:529–39. doi: 10.1097/BCR.0b013e3181e4d680.[PubMed][Cross Ref]

24. Jackson DM. The diagnosis of the depth of burning. Br J Surg. 1953;40:588–96. doi: 10.1002/bjs.18004016413.

0 thoughts on “Essay Eschar

Leave a Reply

Your email address will not be published. Required fields are marked *