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Biomedical subjects

Richard L Gamelli

Publications and source records attributed to Richard L Gamelli.

At least 55 records · Page 3Linked to original sources
PubMed2003

The use of free tissue transfers in acute thermal and electrical extremity injuries.

BACKGROUND: This article presents a retrospective analysis of a case series of patients requiring free tissue transfers for acute thermal and electrical injuries in a single burn center. METHODS: Eight patients, in the period between 1997 and 2001, were referred for evaluation of extensive thermal injury to one or more extremities, which required free tissue transfer to achieve coverage. A total of 12 flaps were performed on eight patients. Data including flap type, flap viability, complications, hospital stays, length of rehabilitation, and time until return to work were collected. RESULTS: Twelve flaps were performed on eight patients. One patient died. We report a flap failure rate of 9% (1 of 12) and two postoperative infections. Follow-up ranged from 3 months to 4 years. Flap types included lateral arm, radial forearm, rectus abdominis, posterior lateral thigh, and omentum and temporoparietal fascia. Mean hospital stay was 22 days, with a mean rehabilitation time of 9.7 months. Sixty-two percent of patients returned to work. CONCLUSION: Free tissue transfer is a safe and efficacious method of early surgical management of thermal and electrical burns. Electrical burns account for a disproportionate number of injuries requiring free tissue transfers. These injuries frequently necessitate the use of multiple free flaps. Postoperative complications and length of stay can be minimized by the use of split donor flaps during one operative session.

Acute Disease↗
PubMed2003

Differential angiogenic and proliferative activity of surgical and burn wound fluids.

BACKGROUND: Invasive surgical wounds exhibit the rapid production of a robustly proangiogenic environment. To compare the immediate angiogenic environment of wounds of different types, the angiogenic activity of fluid derived from burn injuries and wounds confined to the dermis was examined and compared with that of deeper surgical wounds. METHODS: The angiogenic activity of surgical wound fluid (SWF) (n = 7), skin graft wound fluid (SGF) (n = 3), and burn wound fluid (BWF) (n = 4) was assessed by measuring endothelial cell (EC) proliferative activity, EC chemotactic activity, and angiogenic activity in the rat corneal assay. The fibroblast growth factor-2 (FGF-2) level of each wound fluid was determined by enzyme-linked immunosorbent assay. RESULTS: SWF exhibited significant EC proliferative activity, SGF exhibited intermediate activity, and BWF displayed no EC proliferative activity. Seventy-one percent of SWF samples, 33% of SGF, and 0% of BWF contained significant EC chemotactic activity. Each wound fluid sample that demonstrated significant chemotactic activity also evoked a positive corneal angiogenic response. SWF contained 914 +/- 170 pg/mL of FGF-2, whereas SGF and BWF contained just 164 +/- 54 pg/mL and 37 +/- 7 pg/mL of FGF-2, respectively. CONCLUSION: The results suggest that injuries confined to the dermis, whether thermal or excisional, elicit a less robust initial angiogenic stimulus than deep surgical wounds.

Adolescent↗
PubMed2003

Reducing trauma payment denials with computerized collaborative billing.

BACKGROUND: Trauma care demands constant physician availability, resulting in rotational coverage systems. Third-party payors consider separate trauma surgeon bills as originating from the same individual. Trauma surgeons may be unaware of their colleagues' billing history on jointly managed patients. Not all postoperative procedures and evaluation and management services are denied by global surgical package rules. We investigated whether a networked billing program designed to crosscheck for global package coding concerns would reduce payment denials. METHODS: A networked relational database was created for trauma surgeons to enter billable encounters, displaying global periods and operative diagnoses while prompting for postoperative modifiers. Denials were compared for equivalent time periods before and after program initiation. RESULTS: Payment denials fell from 361 to 16 for "bundled" evaluation and management services and from 55 to 13 for bundled postoperative procedures. Time spent on billing decreased and legibility improved. Overall savings totaled $183,404. CONCLUSION: Collaborative billing can improve payments for professional trauma care.

Forms and Records Control↗
PubMed2003

A role for CD1d-restricted NKT cells in injury-associated T cell suppression.

Natural killer T (NKT) cells are known to modulate T cell responses during autoimmunity, tolerance, and antitumor immunity; however, their potential role in regulating the immune response to injury has not been reported. Using a murine model of burn injury, we investigated whether CD1d-restricted NKT cells played a role in the T cell suppression that occurs early after injury. A functional role for CD1d stimulation of NKT cells in the injury-related immune suppression was demonstrated by experiments in which the suppression of antigen (Ag)-specific delayed-type hypersensitivity and in vitro T cell-proliferative responses were prevented if mice were given anti-CD1d monoclonal antibody (mAb) systemically just before injury. The CD1d-NKT cell-dependent suppression of the T cell response after injury occurred in the absence of quantitative changes in NKT cells themselves or CD1d(+) Ag-presenting cells. We observed that elevated production of the immunosuppressive cytokine interleukin (IL)-4 correlated with burn-induced immune dysfunction, and we found that NKT cells but not conventional T cells were the source of IL-4 early after injury. Lastly, we observed that the injury-induced production of NKT cell-derived IL-4 could be blocked by systemic treatment of burn-injured mice with anti-CD1d mAb. Together, our results reveal a novel mechanism involving CD1d stimulation of NKT cells in the onset of T cell suppression that occurs subsequent to injury.

Animals↗
PubMed2002

The effect of sepsis on wound healing.

BACKGROUND: Normal wound healing is a regulated sequence of events that successfully restore tissue integrity. Previous studies have suggested that wound healing is impaired in a septic host. The current study examines the effect of sepsis on the inflammatory and proliferative phases of wound healing at a remote site of secondary injury. METHODS: Polyvinyl alcohol sponges, either inoculated with a standard dose of Pseudomonas aeruginosa (experimental) or soaked in normal saline (control), were placed subcutaneously in the anterior abdominal region of male B6D2F1 mice. Immediately following sponge placement, full thickness excisional dermal wounds were created on the dorsum. Wound healing was examined at days 3, 5, and 7 postinjury. The infiltration of neutrophils and macrophages into wounds was quantified, and the reepithelialization rate and collagen content were measured. RESULTS: Peripheral neutrophil counts were significantly elevated in infected mice, yet neutrophil content of the remote wound of infected animals was significantly reduced (5% of control, P < 0.05). Wounds of infected mice also showed a 30% reduction in the macrophage content. Wounds of infected animals exhibited delayed reepithelialization (76 +/- 3 vs 97 +/- 3% at day 5, P < 0.05) and collagen synthesis (55.3 +/- 9.5 vs 105 +/- 13.0 microg/wound, P < 0.05). CONCLUSION: Systemic infection alters both the inflammatory and the proliferative processes at remote sites of injury. Multiple factors seem likely to contribute to the increased incidence of wound complications in septic patients.

Animals↗
PubMed2002

Endotoxin potentiates hepatocyte apoptosis in cholestasis.

BACKGROUND: Cholestasis is a component of liver disease of almost any etiology, including septic liver injury. The cellular mechanisms of liver injury in cholestasis and sepsis remain unresolved. We evaluated apoptosis, a well-orchestrated and potentially reversible mechanism of cell death, in bile duct-ligated and endotoxin-injected rats. STUDY DESIGN: Male Sprague-Dawley rats were randomly assigned to six groups (n = 6-9): bile duct-ligated+endotoxin (B+E), sham+endotoxin (S+E), bile duct-ligated (B), sham (S), endotoxin (E), and normal (N). On day 1, the bile ducts of B+E and B rats were ligated and severed. S+E and S animals underwent biliary manipulation only. On day 3, B+E, S+E, and E groups received 3 mg/kg endotoxin i.v.. On day 4, livers from all rats were excised, fixed, and stained (hematoxylin and eosin and terminal deoxynucleotidyl transferase dUTP nick-end labeling [TUNEL]). Portions were frozen for DNA fragmentation analysis. Caspase 3 activity was determined using isolated hepatocytes. RESULTS: Livers from all groups (B+E, S+E, E, and B) except normal and sham displayed apoptosis by hematoxylin and eosin staining, TUNEL staining, and DNA fragmentation. Histologic evaluation revealed 10% to 20% necrosis in endotoxin-treated animals (B+E, S+E, and E). Caspase 3 activity was significantly higher in endotoxin-treated animals versus animals without endotoxin (treated 0.450 +/- 0.08 versus nontreated 0.135 +/- 0.05, p < 0.0001) (mean +/- SD). CONCLUSIONS: Cholestatic livers had apoptosis without progression to necrosis. When exposed to the second insult of endotoxin, cholestatic livers received an acute on chronic apoptotic trigger, and proceeded to necrosis. Endotoxin was a potent hepatotoxic insult because all treated rat livers displayed both apoptosis and necrosis.

Alanine Transaminase↗
PubMed2002

Enterococcus faecalis exacerbates burn injury-induced host responses in rats.

Pathophysiology of burn injury with complications of gram-positive infections is not well characterized. We have developed an in vivo rat model to study the effects of burn injury along with intra-abdominal inoculation of Enterococcus faecalis. We hypothesized that although burn injury or E. faecalis inoculation by itself may not induce significant pathophysiological responses, the combination of the two can lead to adverse pathophysiological consequences. Sprague-Dawley rats were divided into 4 groups: group 1(C), controls; group 2(B), burn injury on 30% total body surface area; group 3(EF), intra-abdominal implantation of bacterial pellet impregnated with E. faecalis; group 4(B+EF), burn injury plus bacterial pellet implantation. The mortality was 25% and 60% on day 1 and 2 in Group 4(B+EF), respectively; no significant mortality was observed in other groups. In group 4(B+EF), metabolic acidosis, respiratory alkalosis, and a hyperdynamic state developed on day 1, and metabolic and respiratory acidosis and a hypodynamic state on day 2. There were no significant alterations in metabolic or hemodynamic measurements in other groups. Intestinal microvascular permeability to albumin on day 1 and 2 was increased in group 4(B+EF). In group 2(B), microvascular permeability was not increased significantly. Although the permeability was increased on day 1 in group 3(EF), it declined on day 2. The metabolic and hemodynamic alterations were correlated with increased intestinal microvascular permeability to albumin. E. faecalis appeared to be involved in initiating a vicious cycle of burn injury-mediated disruption of intestinal integrity along with metabolic and hemodynamic derangements.

Albumins↗
PubMed2002

Gut-associated lymphoid T cell suppression enhances bacterial translocation in alcohol and burn injury.

The mechanism of alcohol-mediated increased infection in burn patients remains unknown. With the use of a rat model of acute alcohol and burn injury, the present study ascertained whether acute alcohol exposure before thermal injury enhances gut bacterial translocation. On day 2 postinjury, we found a severalfold increase in gut bacterial translocation in rats receiving both alcohol and burn injury compared with the animals receiving either injury alone. Whereas there were no demonstrable changes in intestinal morphology in any group of animals, a significant increase in intestinal permeability was observed in ethanol- and burn-injured rats compared with the rats receiving either injury alone. We further examined the role of intestinal immune defense by determining the gut-associated lymphoid (Peyer's patches and mesenteric lymph nodes) T cell effector responses 2 days after alcohol and burn injury. Although there was a decrease in the proliferation and interferon-gamma by gut lymphoid T cells after burn injury alone; the suppression was maximum in the group of rats receiving both alcohol and burn injuries. Furthermore, the depletion of CD3(+) cells in healthy rats resulted in bacterial accumulation in mesenteric lymph nodes; such CD3(+) cell depletion in alcohol- and burn-injured rats furthered the spread of bacteria to spleen and circulation. In conclusion, our data suggest that the increased intestinal permeability and a suppression of intestinal immune defense in rats receiving alcohol and burn injury may cause an increase in bacterial translocation and their spread to extraintestinal sites.

Alcohol Drinking↗
PubMedDate not supplied

Mast cells modulate the inflammatory but not the proliferative response in healing wounds.

Upon stimulation, mast cells release a heterogeneous group of factors that promote inflammation and influence cell proliferation. Mast cells accumulate at sites of injury, further suggesting a critical role in wound healing. To assess the importance of mast cells in tissue repair, we compared wound healing in mast cell-deficient WBB6F1/J-KitW/KitW-v (KitW/KitW-v) and wild type WBB6F1/++ (WT) mice. During the inflammatory phase, neutrophil infiltration into wounds of the KitW/KitW-v mice was significantly less than that of WT mice (84.6 +/- 10.3 vs. 218 +/- 26.0 cells/10 high-power fields at day 3, p < 0.001), while wound macrophage and T cell infiltration were similar in both strains. The decrease in neutrophils could not be explained by changes in tumor necrosis factor-alpha or macrophage inflammatory protein-2 levels, because the amounts of these two neutrophil chemoattractants were similar in both KitW/KitW-v and WT mice. Surprisingly, the absence of mast cells had no effect on the proliferative aspects of wound healing, including reepithelialization, collagen synthesis, and angiogenesis. Although mast cells are known to release proangiogenic mediators, vascular endothelial growth factor levels were similar in WT and KitW/KitW-v mice. Moreover, levels of fibroblast growth factor-2 were increased in KitW/KitW-v mice (4206 +/- 107 vs. 1865 +/- 249 pg/ml, p < 0.01). These results suggest that mast cells modulate the recruitment of neutrophils into sites of injury, yet indicate that mast cells are unlikely to exert a major influence on the proliferative response within healing wounds.

Animals↗
PubMedDate not supplied

Toxic epidermal necrolysis: does immunoglobulin make a difference?

Experimental evidence implicates Fas ligand-mediated keratinocyte apoptosis as an underlying mechanism of toxic epidermal necrolysis syndrome (TEN). In vitro studies indicate a potential role for immunoglobulin (Ig) therapy in blocking Fas ligand signaling, thus reducing the severity of TEN. Anecdotal reports have described successful treatment of TEN patients with Ig; however, no study to date has analyzed outcome data in a large series of patients treated with Ig using institutional controls. The SCORTEN severity-of-illness score ranks severity and predicts prognosis in TEN patients using age, heart rate, TBSA slough, history of malignancy, and admission blood urea nitrogen, serum bicarbonate, and glucose levels. A retrospective chart review was performed that included all patients treated for TEN at our burn center since 1997. Ig therapy was instituted for all patients with biopsy-proven TEN beginning in January 2000. Twenty-one TEN patients were treated before Ig (no-Ig group), and 24 patients have been treated with Ig. SCORTEN data were collected, as well as length of stay (LOS) and status upon discharge. Each patient was given a SCORTEN of 0 to 6, with 1 point each for age greater than 40, TBSA slough greater than 10%, history of malignancy, admission BUN greater than 28 mg/dl, HCO3 less than 20 mg/dl, and glucose greater then 252 mg/dl. Outcome was compared between patients treated with Ig and without Ig. Overall mortality for patients treated before Ig was 28.6% (6/21), and with Ig, mortality was 41.7%% (10/24). There was no significant difference in age or TBSA slough. The average SCORTEN between the groups was equivalent (2.2 in no-Ig group vs 2.7 in Ig group, P = 0.3), and no group of patients with any SCORTEN score showed a significant benefit from Ig therapy. Overall LOS as well as LOS for survivors was longer in the Ig group. This series represents the largest single-institution analysis of TEN patient outcome after institution of Ig therapy. Our data do not show a significant improvement in mortality for TEN patients treated with Ig at any level of severity and may indicate a potential detriment in using Ig. Ig should not be given to TEN patients outside of a clinical trial. A multicenter, prospective, double-blinded randomized trial is necessary and urgently indicated to determine whether Ig therapy is beneficial or harmful in the care of TEN patients.

Adult↗
PubMedDate not supplied

A survey of airway and ventilator management strategies in North American pediatric burn units.

A survey was used to gather information regarding airway management patterns in thermally injured children. North American pediatric burn centers listed by the American Burn Association were sent a survey designed to examine patterns of pediatric airway management in children with acute respiratory failure. The sample population means for the number of patients ventilated more than 48 hours and the number of patients ventilated more than 48 hours with inhalation injury were used to separate centers into large and small pediatric burn centers. Small pediatric burn centers had less than 50 patients who were intubated during a 5-year period. A five-point nominal scale was used to facilitate statistical analysis. Twenty-five pediatric burn centers included in the analysis estimated that 11,494 children were admitted during the 5-year period. There was no statistically dominant ventilator mode being used in the setting of acute respiratory failure identified by this survey. Large pediatric burn centers reported more frequent use of cuffed endotracheal tubes and more frequent change from an uncuffed to a cuffed endotracheal tube in patients who were difficult to ventilate because of an excess leak. Large pediatric burn centers reported a higher prevalence of tracheomalacia then small pediatric burn centers. Steroids were used by most centers before extubation in patients with persistent airway edema. No centers reported complications from steroid use. There is lack of clear consensus regarding the application of various ventilator modes in the setting of acute respiratory failure irrespective of center volume. There were divergent of practice patterns between large and small pediatric burn centers regarding the use of cuffed endotracheal tubes and the timing of tracheostomy. There was agreement between large and small pediatric burn centers in tracheostomy use in children older the age of 7 and the use of steroids as an adjunct to extubation in patients with lingering airway edema. Pediatric burn patients may benefit from clinical trials that clarify the advantages and disadvantages of various ventilator modes, the use of cuffed tubes, and the timing of tracheostomy.

Adolescent↗
PubMedDate not supplied

Editorial.

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Burns↗
PubMedDate not supplied

Role of the gastrointestinal tract in burn sepsis.

During the last 50 years, our understanding of the role of the gastrointestinal tract as a first-line defense against the development of postburn sepsis has increased dramatically. Starting with the concept of that gut-derived bacteria cause distant injury, investigators have delineated a complex series of physical changes in the barrier of the gastrointestinal tract. Along with an understanding of these physical changes has come an appreciation of the role of the immune system in modulating postburn organ failure. Importantly, recent investigations into the role of mesenteric lymph have fundamentally changed the paradigm of organ failure and have implicated the gut as a cytokine-secreting organ. This article traces the development of key concepts in the study of burn sepsis and their clinical implications.

Bacterial Translocation↗
PubMedDate not supplied

A primer in cytokines.

The host response to injury or infection is a complex interplay of endocrine, metabolic, and immunological alterations designed to promote wound healing and restore the system to a state of homeostasis. Cytokines are the primary mediators of the inflammatory response to injury. This article serves as an introduction to this important class of inflammatory mediators. The major pro- and anti-inflammatory cytokines as well as the chemokines are discussed. Results from laboratory and clinical attempts at manipulation of these mediators are discussed and recommendations for future research in anticytokine therapy are made.

Burns↗
PubMedDate not supplied

Who will follow?

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Burn Units↗
PubMedDate not supplied

Burn injury exacerbates hemodynamic and metabolic responses in rats with polymicrobial sepsis.

The most common and life-threatening complication of severe burn injury is infection, which often results in multiple organ failure (MOF). However, the mechanism of development of MOF after burn injury associated with infection is not fully understood. Our previous studies showed that when polymorphonuclear neutrophils (PMNs) are depleted, burn injury-induced increase in microvascular permeability to albumin is markedly attenuated. Thus, we hypothesized that the combination of burn injury and polymicrobial infection exacerbates PMN activation, increases intestinal microvascular permeability to albumin, and alters hemodynamics and metabolism more than burn injury or infection alone. Sprague-Dawley rats (250-275 g) were divided into four groups. In the burn group, rats were subjected to a 30% TBSA burn injury. In the cecal-ligation puncture (CLP) group, CLP was performed using a 22-gauge needle with one puncture. In burn+CLP group, rats were subjected to CLP immediately after burn procedure. In sham group, rats were subjected to sham procedures. Transient polymicrobial bacteremia and persistent polymicrobial bacteremia were induced in the CLP group and burn+CLP group, respectively. Microvascular permeability, myeloperoxidase, and PMN production of elastase and reactive oxygen species increased in the burn group and CLP group and further increased in the burn+CLP group. Hemodunamic and metabolic alterations on day 1 and 3 after injury correlated with those alterations. Although there was only a low mortality in the burn group and CLP group, there was a high mortality in burn+CLP group (79%). The mechanism of MOF that leads to high mortality in burn injury complicated by infection may involve uncontrolled microvascular damage mediated by PMN activation.

Animals↗