Biomedical subjects

D G Greenhalgh

Publications and source records attributed to D G Greenhalgh.

At least 19 recordsLinked to original sources

PubMed1999

Expression of HSP70 in healing wounds of diabetic and nondiabetic mice.

BACKGROUND: Heat shock proteins (HSPs) stabilize intracellular processes of cells under stress. Little is known about the role of HSPs in wound healing, or whether their expression is altered by systemic disease. The focus of this study was to examine the local heat shock response to wounding in diabetic mice. METHODS: Congenitally diabetic and phenotypically normal mice underwent standardized full-thickness cutaneous wounding. Mice were sacrificed at sequential time points and the wound beds excised. Tissues underwent immunohistochemical (IHC) and RT-PCR analyses for inducible HSP70. RESULTS: HSP70 protein expression in the wound bed by IHC peaked at 24 h in the nondiabetic mice. Expression of HSP70 was delayed in the diabetic mice until Day 3, which correlates with the clinical delay in healing seen in this model. The protein was especially prominent in the epithelium and in inflammatory cells migrating into the granulation tissue matrix. RT-PCR demonstrated upregulation of HSP70 mRNA within 12 h after wounding, lasting until Day 3, and decreasing thereafter in both the nondiabetic and the diabetic animals. CONCLUSION: Cutaneous wounding produces a HSP response in inflammatory cells, and expression of inducible HSP70 is delayed in diabetic mice. This delay may be related to the impaired inflammatory response of diabetics, and may contribute to impaired wound healing. The wound may be a continuing source of the heat shock response in inflammatory cells after injury.

Animals↗

PubMed1999

The Nf1 tumor suppressor regulates mouse skin wound healing, fibroblast proliferation, and collagen deposited by fibroblasts.

Neurofibromatosis type 1 patients develop peripheral nerve tumors (neurofibromas) composed mainly of Schwann cells and fibroblasts, in an abundant collagen matrix produced by fibroblasts. Trauma has been proposed to trigger neurofibroma formation. To test if loss of the neurofibromatosis type 1 gene (Nf1) compromises fibroblast function in vivo following trauma, skin wounding was performed in Nf1 knockout mice. The pattern and amount of collagen-rich granulation bed tissue, manufactured by fibroblasts, was grossly abnormal in 60% of Nf1+/- wounds. Nf1 mutant fibroblasts showed cell autonomous abnormalities in collagen deposition in vitro that were not mimicked by Ras activation in fibroblasts, even though some Nf1 effects are mediated through Ras. Nf1+/- skin wound fibroblasts also proliferated past the normal wound maturation phase; this in vivo effect was potentiated by muscle injury. In vitro, Nf1+/- fibroblasts showed higher proliferation in 10% serum than Nf1+/+ fibroblasts. Macrophage-conditioned media or epidermal growth factor potentiated Nf1+/- fibroblast proliferation in vitro, demonstrating abnormal response of mutant fibroblasts to wound cytokines. Thus Nf1 is a key regulator of fibroblast responses to injury, and Nf1 mutation in mouse fibroblasts causes abnormalities characteristic of human neurofibromas.

Animals↗

PubMed1999

Multicenter trial to evaluate the safety and potential efficacy of pooled human fibrin sealant for the treatment of burn wounds.

OBJECTIVE: The primary purpose of this multicenter study was to evaluate the safety and potential efficacy of a solvent/detergent-treated commercial fibrin sealant (human) for topical hemostasis in skin grafting. METHODS: The study involved a prospective evaluation of changes in viral titers in patients with burns less than 15% after treatment with fibrin sealant (human). Each patient served as his/her own control for an unblinded, randomized comparison of donor site hemostasis and healing. Preoperative serum was obtained to screen for viral titers. At autografting, the recipient site and one of two randomly chosen donor sites were treated with fibrin sealant (human). The use of other hemostatic agents, including epinephrine was prohibited. Each donor site was covered with gauze to collect blood for estimation of the relative amount of bleeding. The healing of the graft and donor sites was observed. Viral titers and wounds were checked monthly for 6 months, and at 9 and 12 months postoperatively. RESULTS: Viral titers for human immunodeficiency virus; hepatitis A, B, and C; Epstein-Barr virus; and cytomegalovirus were obtained before and after treatment. Of 47 patients, 34 completed the full year of observation. After treatment, there were no seroconversions to any of the aforementioned viruses. Bleeding at the recipient site appeared well controlled with fibrin sealant (human). Although investigators felt that fibrin sealant (human) improved donor site hemostasis, differences in hemoglobin measurements of blood-soaked dressings failed to reach significance. No differences were noted with regard to acceleration of donor site healing, graft take, or scar maturation at the two groups of donor sites. Anecdotally, the maturation of the recipient site appeared to be accelerated. CONCLUSION: Fibrin sealant (human) is safe for use during excision and grafting, and its topical hemostatic potential needs to be examined in patients with larger burns. Its role in scar maturation also needs to be investigated.

Adolescent↗

PubMed1998

The role of apoptosis in wound healing.

Wound healing involves a series of rapid increases in specific cell populations that prepare the wound for repair, deposit new matrices and finally, mature the wound. Upon completing their tasks, these specific cell types must be eliminated from the wound prior to the progression to the next phase of healing. The most logical method of cellular down-regulation is through apoptosis. Apoptosis allows for the eliminations of entire populations without tissue damage or an inflammatory response. This review discusses which cells dominate the various phases of tissue repair and how the cellular pattern may vary after differing types of injury. The potential mechanisms involved in the down-regulation of inflammation and fibrosis are also covered. The studies that support the hypothesis that apoptosis is involved in the regulation of wound healing are discussed. The evidence supporting potential cell signals involved in the induction of apoptosis in tissue repair are examined. Finally, the review ends with a presentation of how dysregulation of apoptosis can lead to pathologic forms of healing such as excessive scarring and fibrosis. By understanding the mechanisms controlling apoptosis and tissue repair, one may eventually develop therapeutic modalities to minimize scarring, a final pathway for many disease processes.

Animals↗

PubMed1997

Apoptosis down-regulates inflammation under the advancing epithelial wound edge: delayed patterns in diabetes and improvement with topical growth factors.

BACKGROUND: Wound healing is involved in many aspects of care, ranging from anastomoses and skin incisions to foot ulcers and decubitus. Clinical healing failures are a major challenge to the physician and cause significant morbidity and mortality in select patient populations. As we are starting to understand more fully the mechanisms of impaired wound healing, the diabetic mouse (C57BL/KsJ-db/db) has been a good model for research. The diabetic wound exhibits significant delays in healing, previously identified as impaired cellular infiltration and granulation tissue formation. Apoptosis, or programmed cell death, is intimately involved in the regulation of inflammation and ultimately should play a role in the inflammatory phase of wound healing. METHODS: To examine its role in wound healing, patterns of apoptosis in large, full-thickness cutaneous wounds were compared between groups of diabetic and nondiabetic mice. RESULTS: Initially apoptosis was mainly limited to the wound edge and followed the advancing epithelial edge toward the center of the wound as healing progressed. Significant delays in the appearance of the apoptotic pattern were noted in the diabetic mice. Wounds in diabetic mice were then treated with topical application of growth factors. The delay in apoptotic pattern was reversed after treatment with the combination of insulin-like growth factor-II and platelet-derived growth factor, approaching levels in nondiabetic animals. CONCLUSIONS: Apoptosis appears concurrently with reepithelialization of the wound and may signal the end of the inflammatory phase of healing at that site in the wound. One can speculate that a signal for apoptosis and down-regulation of inflammation in the wound is derived from the epithelium.

Animals↗

PubMed1997

Differential expression and localization of insulin-like growth factors I and II in cutaneous wounds of diabetic and nondiabetic mice.

Insulin-like growth factor (IGF)-I has profound effects on tissue repair. IGF-II is felt to exert its influence predominately during fetal development. The purpose of this study was to localize and quantify the expression of IGF-I and IGF-II mRNA and protein during early wound healing in diabetic and nondiabetic mice. The hypothesis is that IGF-I and IGF-II are up-regulated in the healing wound, but their expression is inhibited in diabetics. Full-thickness cutaneous wounds were made on genetically diabetic (C57BL/ KsJ-db/db) mice and their nondiabetic littermates. At various times after wounding, one-half of each wound was fixed and paraffin embedded for immunohistochemistry and in situ hybridization. The other half was flash-frozen for quantification of IGF mRNA by competitive reverse transcriptase polymerase chain reaction and protein by radioimmunoassay. IGF-I mRNA rose sharply in nondiabetics at day 3. Expression in diabetic wounds was significantly delayed until 14 days after wounding. Even then, diabetic IGF-I mRNA levels were 50% less than those in the nondiabetics at their peak. Although not usually considered active in adult life, IGF-II mRNA expression was augmented after wounding, peaking at 3 days in nondiabetics. As with IGF-I, diabetic wounds exhibited a delay in IGF-II mRNA expression, with maximal levels at 10 days after wounding. Interestingly, peak concentrations of IGF-II mRNA were four times greater in diabetics versus nondiabetics. Trends in IGF-I protein expression followed the patterns of mRNA expression. IGF-I levels in nondiabetics were initially double those in diabetics and peaked at 5 days. Diabetic wound concentrations of IGF-I did not peak until 21 days after wounding, at which time they rose to nondiabetic levels. IGF-I and IGF-II proteins were localized to the advancing epithelial edge, to the epithelial cells of adjacent hair follicles, and to the granulation tissue of the wounds. IGF-I and IGF-II mRNA expression was noted in the epithelial edge and in the hair follicles adjacent to the wound, paralleling protein expression. Both IGF-I and IGF-II are up-regulated in the healing wound. A delay in IGF-I and -II presence is noted in the diabetic wound. The impairment in tissue repair in diabetic animals is at least partially due to a deficiency in the production of the IGFs.

Animals↗

PubMed1996

Expression of interleukin-1alpha, interleukin-6, and basic fibroblast growth factor by cultured skin substitutes before and after grafting to full-thickness wounds in athymic mice.

OBJECTIVES: Cultured skin substitutes (CSSs), consisting of human keratinocytes and human fibroblasts attached to collagen-glycosaminoglycan substrates, have been demonstrated to cover wounds, and may release detectable quantities of growth factors that promote wound healing. MATERIALS AND METHODS: Basic fibroblast growth factor (bFGF), interleukin-1alpha (IL-1alpha), and interleukin-6 (IL-6) were assayed by enzyme linked immunosorbent assay and immunohistochemistry in CSSs in vitro and at days 1, 3, 7, 14, and 21 after grafting to full-thickness wounds in athymic mice. MEASUREMENTS AND MAIN RESULTS: When isolated cells were tested, IL-1alpha was found to come primarily from the keratinocytes, whereas bFGF was from the fibroblasts. Combinations of both cell types in the CSSs resulted in a synergistic enhancement of IL-6 expression. Quantities of all three cytokines from CSSs were greater in vitro compared with in vivo levels at all time points after grafting. bFGF increased from day 1 to day 7, and then remained relatively constant until day 21. At day 3 maximal levels of IL-1alpha were observed. By day 7, IL-1alpha decreased to approximately 40% of maximal levels, and subsequently increased until day 21. IL-6 levels were highest at day 7 after grafting. All cytokines had reached elevated levels during the time of wound revascularization (days 3-7). CONCLUSIONS: The sequence of cytokine synthesis in the wounds (i.e., rapid IL-1alpha increase followed by IL-6 expression) parallels serum levels reported after a septic challenge. These findings support the hypothesis that the wound is a source of systemic cytokines.

Animals↗

PubMed1996

The role of growth factors in wound healing.

Growth factors have many activities that make them attractive agents for stimulating tissue repair. Growth factors attract cells into the wound, stimulate their proliferation, and have profound influence on extracellular matrix deposition. Since developing the ability to mass-produce these cytokines by recombinant techniques, hundreds of studies have demonstrated that growth factors can augment all aspects of tissue repair in normal and impaired healing models. After demonstrating that growth factors augment healing, investigators have started to detect and measure growth factors in wounds and have found that wounding initiates the expression of various growth factors. Impaired healing has also been linked to altered growth factor production. These findings have prompted great interest in the use of growth factors to augment clinical healing. Preliminary clinical trials have not produced the results expected. Growth factor treatment has occasionally led to statistically significant improvements in tissue repair, but whether the results are clinically significant can be debated. It appears that to be cost effective, clinical trials must focus on targeting growth factors for specific types of impaired healing. Although growth factors have not been the panacea that was originally expected, they have the potential for making significant clinical improvements when targeted for specific problem wounds.

Animals↗

PubMed1996

The healing of burn wounds.

Burn injuries can be the most devastating wounds of all. Knowledge of burn wound healing can be valuable not only for the care of small, minor burns but improved wound coverage of major burns can also lead to improved survival. Differentiating between types of burns and how these wounds heal will be discussed. Strategies for treating patients with extensive burns will also be presented. Finally, an evaluation of the newer technologies that are available for these injuries will be covered. Understanding the processes of burn wound healing will help optimize care of these often overwhelming injuries.

Bandages↗

PubMed1995

Regulation of vascular endothelial growth factor expression in cultured keratinocytes. Implications for normal and impaired wound healing.

Recent in situ hybridization studies had demonstrated a strong increase in vascular endothelial growth factor (VEGF) mRNA expression in the hyperproliferative epithelium during wound healing. To determine potential mediators of VEGF induction during this process, we analyzed the regulation of VEGF expression in cultured human keratinocytes. We found a large induction of VEGF expression upon treatment of quiescent cells with serum, epidermal growth factor, transforming growth factor-beta 1, keratinocyte growth factor, or the proinflammatory cytokine tumor necrosis factor alpha, respectively. Since all these factors are present at the wound site during the early phase of wound healing, they might also be responsible for VEGF induction after cutaneous injury. To determine the importance of increased VEGF production for wound repair, we compared the time course of VEGF mRNA expression during wound healing of healthy control mice with the kinetics of VEGF expression during skin repair of genetically diabetic db/db mice which are characterized by impaired wound healing. In normal mice we found elevated VEGF mRNA levels during the period when granulation tissue formation occurs. In contrast, VEGF mRNA levels even declined during this period in db/db mice, suggesting that a defect in VEGF regulation might be associated with wound healing disorders.

Animals↗

PubMed1995

Pigmentation and microanatomy of skin regenerated from composite grafts of cultured cells and biopolymers applied to full-thickness burn wounds.

Rapid coverage and epithelial closure of extensive burns remains a major requirement for patient recovery. Although many skin substitutes have been described, permanent regeneration of both epithelial and connective tissues after a single surgical application of a skin substitute has not become routine. To replace both dermal and epidermal skin, cultured skin substitutes (CSS) were prepared from autologous keratinocytes and fibroblasts seeded onto collagen-glycosaminoglycan (C-GAG) substrates. CSS were applied to excised, full-thickness burns on 5 patients. Histologic analysis showed a fully stratified, hyperkeratotic epidermis within 12 days of grafting with little to no evidence of an inflammatory reaction. Epidermal and connective tissues are interdigitated in analogy to rete pegs and dermal papillae, and the neovascular plexus approximates the dermal-epidermal junction. Transmission electron microscopy identified a continuous basement membrane with hemidesmosomes and anchoring fibrils that connected the epidermis with the underlying connective tissue. Within 14-28 days, the C-GAG had been degraded and replaced by newly synthesized collagen in regenerated connective tissue. Spontaneous repigmentation of healing CSS from passenger melanocytes in keratinocytes culture was observed within 2 months after grafting. Electron microscopy revealed the presence of numerous melanosomes within the keratinocytes, illustrating pigment transfer between melanocytes and keratinocytes after wound closure. These results demonstrate that the CSS develop into functional permanent skin tissue capable of spontaneous repigmentation after grafting onto burn wounds.

Adolescent↗

PubMed1995

The use of extracorporeal life support in pediatric burn patients with respiratory failure.

Respiratory failure is the most common cause of death after thermal injury and may be caused by inhalation injury, acute respiratory distress syndrome (ARDS) or pneumonia. ARDS is usually associated with sepsis; however, it may also occur during burn shock, especially in patients that have a delayed or inadequate fluid resuscitation. During the past 24 months, five pediatric burn patients underwent extracorporeal life support (ECLS) for respiratory failure unresponsive to optimal medical management. The mean age of the patients was 26 months (range, 8.5 to 48 months), with a mean burn size of 46% TBSA (> 95% third degree). The etiology of the respiratory failure included severe bronchospasm in a 22-month-old former premature infant with bronchopulmonary dysplasia; three patients with ARDS; and one patient with a severe inhalation injury. All five patients required greater than 56 cm H2O peak pressures and 100% FIO2 at the time of beginning ECLS. The oxygenation index (OI) ranged from 45 to 180. Three (60%) of the patients survived. In the three patients who ultimately survived, significant improvements in pulmonary and hemodynamic parameters occurred within 96 hours of ECLS. The two patients who died showed no improvement and were removed from ECLS at 10 and 11 days; both expired within hours. The patients who expired developed significant hemodynamic instability, coagulopathy, and hemorrhage from their burn wounds. The extent and degree of burn injury did not seem to alter the outcome. Indications for considering ECLS in the pediatric burn patient are unmanageable, life threatening pulmonary insufficiency in patients that undergo a relative short course of pre-ECLS ventilator support.(ABSTRACT TRUNCATED AT 250 WORDS)

Burns↗

PubMed1995

Comparative assessment of cultured skin substitutes and native skin autograft for treatment of full-thickness burns.

OBJECTIVE: Comparison of cultured skin substitutes (CSSs) and split-thickness autograft (STAG) was performed to assess whether the requirement for autologous skin grafts may be reduced in the treatment of massive burns. SUMMARY BACKGROUND DATA: Cultured skin substitutes consisting of collagen-glycosaminoglycan substrates populated with autologous fibroblasts and keratinocytes have been demonstrated to close full-thickness skin wounds in athymic mice and to express normal skin antigens after closure of excised wounds in burn patients. METHODS: Data were collected from 17 patients between days 2 and 14 to determine incidence of exudate, incidence of regrafting, coloration, keratinization, and percentage of site covered by graft (n = 17). Outcome was evaluated on an ordinal scale (0 = worst; 10 = best) beginning at day 14, with primary analyses at 28 days (n = 10) and 1 year (n = 4) for erythema, pigmentation, epithelial blistering, surface roughness, skin suppleness, and raised scar. RESULTS: Sites treated with CSSs had increased incidence of exudate (p = 0.06) and decreased percentage of engraftment (p < 0.05) compared with STAG. Outcome parameters during the first year showed no differences in erythema, blistering, or suppleness. Pigmentation was greater, scar was less raised, but regrafting was more frequent in CSS sites than STAG. No differences in qualitative outcomes were found after 1 year, and antibodies to bovine collagen were not detected in patient sera. CONCLUSIONS: These results suggest that outcome of engrafted CSSs is not different from STAG and that increased incidence of regrafting is related to decreased percentage of initial engraftment. Increased rates of engraftment of CSSs may lead to improved outcome for closure of burn wounds, allow greater availability of materials for grafting, and reduce requirements for donor skin autograft.

Animals↗

PubMed1995

Maintenance of serum albumin levels in pediatric burn patients: a prospective, randomized trial.

A prospective, randomized trial was performed to determine whether maintaining serum albumin levels in burned pediatric patients had any effect on morbidity and mortality. Patients < 19 years of age with burns > 20% total body surface area were randomized to receive supplemental albumin to maintain levels 2.5 to 3.5 g/dL ("High Albumin") or were given albumin only if levels dropped < 1.5 g/dL ("Low Albumin") after completing burn shock resuscitation. The 36 patients in the Low Albumin group were well matched for age, burn size, depth of injury, and inhalation injury when compared with the High Albumin group (34 patients). As expected, serum albumin levels were significantly lower in the Low Albumin group when compared with the High Albumin group. No differences between groups were noted for resuscitation needs, maintenance fluid requirements, urine output, tube feedings received, days of antibiotic treatment, or ventilatory requirements. No differences in hematology, electrolytes, or nutritional laboratories were found. Finally, length of stay, complication rate, and mortality were not affected by albumin treatment. Albumin supplementation to maintain normal serum levels does not seem to be warranted in previously healthy children who suffer severe burns and who receive adequate nutrition.

Adolescent↗

PubMed1995

Topical nutrients promote engraftment and inhibit wound contraction of cultured skin substitutes in athymic mice.

Routine treatment of burns with cultured skin substitutes (CSS) has been limited by poor engraftment and by scarring. Hypothetically, topical application of essential nutrients and/or growth factors may support epithelial survival temporarily during graft vascularization. CSS, composed of human epidermal keratinocytes and dermal fibroblasts attached to collagen-glycosaminoglycan substrates, were incubated for 19 d in media optimized for keratinocytes. CSS, human xenografts, murine autografts, or no grafts were applied orthotopically to full-thickness skin wounds (2 x 2 cm) in athymic mice. Wounds were irrigated for 14 d with 1 ml/d modified cell culture medium or with saline containing epidermal growth factor, or were treated with dry dressings. After 6 weeks, treated sites were scored for percentage original wound area (mean +/- SEM) and percentage HLA-ABC-positive healed wounds [(number positive/n) x 100], and tested for significance (analysis of variance, p < 0.0001; Tukey test, p < 0.05). The data showed that CSS irrigated with nutrient medium were not statistically different in wound area (67.8 +/- 5.1%) from murine autografts (63.3 +/- 2.9%) but were statistically larger than human xenograft, no graft, or CSS treated with saline irrigation or dry dressings. HLA-ABC expression was 100% in CSS with nutrient irrigation, 86% in CSS with saline irrigation, 83% in CSS without irrigation, and 75% in xenografts with nutrient irrigation. These findings suggest that availability of essential nutrients supports keratinocyte viability during graft vascularization of CSS.

Administration, Oral↗

PubMed1994

PDGF and TGF-alpha act synergistically to improve wound healing in the genetically diabetic mouse.

Impaired wound healing results in significant morbidity for the surgical patient. The genetically diabetic (C57BL/KsJ-db/db) mouse is obese, hyperglycemic, insulin-resistant, and exhibits markedly impaired wound healing. Previous studies have demonstrated that the fibroblast mitogens, BB homodimer of platelet-derived growth factor (PDGF-BB) or basic fibroblast growth factor, plus insulin-like growth factor, act synergistically to enhance wound closure in the genetically diabetic mouse. The purpose of this study was to determine whether the keratinocyte mitogens, epidermal growth factor (EGF) or transforming growth factor-alpha (TGF-alpha), in combination with the fibroblast mitogen, PDGF-BB, would produce a similar synergistic enhancement in tissue repair. Full-thickness skin wounds created on the backs of diabetic mice received topical applications of vehicle (5% polyethylene glycol), PDGF-BB (10 micrograms), EGF (1 microgram), TGF-alpha (1 microgram), or the combination of PDGF (10 micrograms) and EGF (1 microgram) or TGF-alpha (1 microgram) for 5 consecutive days starting at wounding. Application of PDGF-BB or TGF-alpha alone to wounds in diabetic animals improved wound closure when compared to vehicle treatment. EGF did not affect healing and did not have any additive effects when combined with PDGF-BB. Significant improvements in wound closure were observed with the combination of PDGF-BB and TGF-alpha when compared to treatment with the individual growth factors. The PDGF-BB/TGF-alpha combination accelerated healing in the diabetic animals to a rate that was closer to that seen in nondiabetic mice.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

The importance of intra-abdominal pressure measurements in burned children.

Four burned children suffering complications from elevated intra-abdominal pressures prompted initiation of a prospective study to determine the value of intra-abdominal pressure measurements in 30 children with large burns. Intra-abdominal pressures were measured every 4 hours during burn shock or sepsis, or daily during periods of stability. Patients were arbitrarily divided into those having one or more measurements > or = 30 mm Hg or all values < 30 mm Hg. Patients in the > or = 30 mm Hg group had significantly larger burns, higher mortality, and increased instances of sepsis. Five patients had elevated intra-abdominal pressures during burn shock, with two requiring abdominal escharotomies. Seven were at > 30 mm Hg during sepsis, with three requiring paralysis, and one each requiring placement of a peritoneal catheter or laparotomy. Significant intra-abdominal pressure elevations may occur in patients with extensive burns and are associated with a poorer prognosis. Elevation of intra-abdominal pressure should be considered in severely burned patients with oliguria, hypoventilation, or hypotension.

Abdomen↗

PubMed1994

The adequacy of limb escharotomies-fasciotomies after referral to a major burn center.

To determine the frequency of inadequate decompression and its complications, the medical records of 108 pediatric burn patients requiring escharotomies or fasciotomies were reviewed. Of 108 patients, 100 (93%) had escharotomies or fasciotomies performed at an outlying facility before transfer. Of these 100 patients, 44 (117 limbs) were inadequately decompressed and required further decompression after admission to our facility. Initial mean compartment pressures were 50.3 +/- 1.3 mm Hg, which were reduced to 16.3 +/- 0.5 mm Hg after decompression. Pulses were present in 74% of limbs requiring decompression. Twenty limbs required decompression despite noncircumferential burns. Complications of inadequate or delayed decompression included foot drop in 20 patients (35 limbs) and muscle necrosis in 13 patients (23 limbs). Four patients (seven limbs) required amputations because of progressive muscle necrosis and infection. Complications of the procedure itself were limited to bleeding in three patients. In conclusion, compartment pressures should be followed in patients with significant burns since pressures may increase over time and pulses are not predictive of ischemia. Failure to decompress extremities with elevated pressures leads to significant but preventable complications.

Burns↗