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Amputations are common after severe frostbite injuries, often mediated by postinjury arterial thrombosis. Since 1994, the authors have performed angiography to identify perfusion deficits in severely frostbitten digits and treated these lesions with intraarterial infusion of thrombolytic agents, usually combined with papaverine to reduce vasospasm. A retrospective review was performed of patients admitted to the regional burn center with frostbite injury from 1994 to 2007. Patients with severe frostbite, without contraindications to thrombolytic therapy, underwent diagnostic angiography of the affected extremities. Limbs with perfusion defects received intraarterial thrombolytic therapy according to protocol and the response was documented. Delayed amputation was performed for mummified digits. Angiogram results and amputation rates were tabulated. In this 14-year review, 114 patients were admitted for frostbite injuries. There was a male predominance (84%) and the mean age was 40.4 years. Of this group, 69 patients with severe frostbite underwent angiography; 66 were treated with intraarterial thrombolytic therapy. Four treated were excluded due to incomplete data. In the remaining 62 patients, angiography identified 472 digits with frostbite injury and impaired arterial perfusion. At the termination of thrombolytic infusion, a completion angiogram was performed. Partial or complete amputations were performed on only four of 198 digits (2.0%) with distal vascular blush, and in 71 of 75 digits (94.7%) with no improvement. Amputations occurred in 73 of 199 digits (36.7%) with partially restored flow. Overall complete digit salvage rate was 68.6%. Angiography after severe frostbite is a sensitive method to detect impaired arterial blood flow and permits catheter-directed treatment with thrombolytic agents. Improved perfusion after such treatment decreases late amputations following frostbite injury.

In recent years, Burn Center has evolved to become a "wound intensive care unit" treating disease processes other than those due to thermal injury. Recent data have shown that more than 16% of admissions to Burn Centers are for nonburn injuries, particularly severe dermatologic diseases. The role of the Burn Center has been expanded to include treatment of patients with severe cutaneous manifestations of rheumatologic diseases. This approach has not been described before. All collagen vascular disease admissions to the Burn Center from 2005 to 2010 have been reviewed. There were 16 admissions where intensive wound management was a major component of the disease management. Disease processes included systemic lupus erythematosus, progressive systemic sclerosis, Raynaud's phenomenon, antiphospholipid syndrome, and dermatomyositis, among others. The authors describe five of these cases in detail. Comanagement of these patients by the Rheumatology and Burn services led to outstanding, successful outcomes. Collagen vascular diseases represent another area where the Burn Center may be the appropriate site for therapy.

The pathophysiology of true frostbite reveals that the direct injury produced during the initial freeze process has a minor contribution to the global tissue damage. However, rapid rewarming to reverse the tissue crystallization has essentially been the lone frostbite intervention for almost half a century. The major pathologic process is the progressive microvascular thrombosis following reperfusion of the ischemic limb, with the cold-damaged endothelial cells playing a central role in the outcome of these frozen tissues. Newer interventions offer the opportunity to combat this process, and this article offers a scientific approach to frostbite injuries of the upper extremities.

Hydrofluoric acid (HF) is highly corrosive substance often used in industrial processes. HF burns to the skin cause local tissue injury. Systemic hypocalcemia may ensue, with the potential to produce life-threatening arrhythmias. Medical treatment consists of local application of topical calcium gels, subcutaneous injection of calcium gluconate, and intravenous or intra-arterial infusion of calcium gluconate. Calcium gluconate infusions have been used for HF burns on distal extremities and digits. We report a case of HF burn to the face that was treated by the use of calcium gluconate infusion via the external carotid artery.

Toxic epidermal necrolysis (TEN) is a potentially fatal disorder that involves large areas of skin desquamation. Patients with TEN are often referred to burn centers for expert wound management and comprehensive care. The purpose of this study was to define the presenting characteristics and treatment of TEN before and after admission to regional burn centers and to evaluate the efficacy of burn center treatment for this disorder. A retrospective multicenter chart review was completed for patients admitted with TEN to 15 burn centers from 1995 to 2000. Charts were reviewed for patient characteristics, non-burn hospital and burn center treatment, and outcome. A total of 199 patients were admitted. Patients had a mean age of 47 years, mean 67.7% total body surface area skin slough, and mean Acute Physiology and Chronic Health Evaluation (APACHE II) score of 10. Sixty-four patients died, for a mortality rate of 32%. Mortality increased to 51% for patients transferred to a burn center more than one week after onset of disease. Burn centers and non-burn hospitals differed in their use of enteral nutrition (70 vs 12%, respectively, P < 0.05), prophylactic antibiotics (22 vs 37.9%, P < 0.05), corticosteroid use (22 vs 51%, P < 0.05), and wound management. Age, body surface area involvement, APACHE II score, complications, and parenteral nutrition before transfer correlated with increased mortality. The treatment of TEN differs markedly between burn centers and non-burn centers. Early transport to a burn unit is warranted to improve patient outcome.

Paraquat is a bipyridyl compound widely used as a contact herbicide. Since its introduction in 1962, hundreds of deaths have occurred, usually after suicidal or accidental ingestion. Death after dermal absorption of paraquat is uncommon, but has occurred after either contact with undiluted paraquat, disruption of skin integrity, or prolonged exposure. It is the purpose of this case report to describe a patient who had fatal dermal paraquat absorption after a crop-dusting accident in which he sustained 37% TBSA burns. After 9.5 hours of cutaneous exposure, a paraquat level of 0.169 mg/ml was obtained at 20 hours, the standard lethal dose at 16 hours being 0.16 mg/ml. In light of the apparently irreversible pathophysiology of paraquat poisoning with plasma levels as low as 3 mg/L, prevention and early intervention are the best treatments. Our patient may have survived an otherwise routine thermal injury had his wounds been aggressively irrigated in the field.

The evaluation and treatment of head and neck burns remains a challenge to the burn surgeon, because of the long-term emotional and psychologic effects of even the most minor change in facial appearance. Fortunately, the results currently achieved are orders of magnitude better than previously available, but they still remain far below the perfect outcome desired by both the physician and the burn victim.

The agent(s) and mechanism(s) responsible for suppression of neutrophil chemotaxis in association with major thermal injury have not been identified. We have proposed that the reduced random motility characterizing patients' cells may contribute to their generalized chemotactic dysfunction. Here we report that actin polymerization may be responsible for the loss of neutrophil motility associated with major thermal injury. Using a fluorescent ligand specific for polymerized or filamentous actin (NBD-phallacidin) in conjunction with flow cytometry, we have discovered that peripheral blood and exudate neutrophils from patients with major thermal injury contain increased levels of actin in a stably polymerized form. Because cyclic polymerization and depolymerization of actin is essential to cell motility, we suggest that actin polymerization may contribute in a major way to the attenuation of neutrophil random and chemotactic functions induced by major thermal injury.

Urinary zinc excretion normally plays a minor role in zinc homeostasis; however, urinary zinc excretion is markedly elevated after trauma or surgery, and mechanism(s) for this zinc loss are poorly defined. In this study we evaluated multiple potential mechanisms for increased urinary zinc excretion in patients with thermal injury. We documented that patients with severe thermal injury had markedly elevated urinary zinc excretion. Above 20% total body surface area burn, however, the severity of thermal injury did not correlate with urinary zinc excretion. Serum zinc concentrations were depressed on initial evaluation and gradually increased during the hospital course, whereas peak urinary zinc excretion occurred 2 to 5 weeks after injury. Thus the depression in serum zinc concentration did not temporally relate to the observed pattern of hyperzincuria. Increased urinary zinc excretion also did not temporally relate to urinary excretion of the amino acids cysteine and histidine (both of which tightly bind zinc) nor to urinary 3-methylhistidine excretion, a marker of muscle breakdown. Urinary amylase excretion, a marker of renal tubular dysfunction, did follow the pattern of urinary zinc loss to some extent, although this correlation was not perfect. Increased oral intake of zinc via zinc supplements resulted in significantly increased urinary zinc excretion. Patients receiving total parenteral nutrition (TPN) did not have significantly increased urinary zinc excretion when compared with people receiving their total nutrient intake by mouth.(ABSTRACT TRUNCATED AT 250 WORDS)

Receptors known as DREG adhesion molecules on human neutrophils and monocytes provide for homing of these phagocytic leukocytes to sites of inflammation. They mediate the initial adhesive interaction of the leukocytes to vascular endothelial cells and are then shed from the cell surface in response to chemotactic factors and inflammatory mediators. Systemic accumulation of these agents following major injury or sepsis may therefore promote shedding of DREG receptors from circulating leukocytes and impair their recruitment to sites of inflammation. To test this hypothesis, we have analyzed the expression of DREG receptors on neutrophils and monocytes from 25 patients admitted to the Surgical Intensive Care Unit. Receptor expression was measured by flow cytometry of cells stained with murine monoclonal DREG-56 anti-DREG antibody. For 14 nonseptic patients, mean monocyte positivity for DREG was reduced from 64% to 40%. For 11 septic patients, mean neutrophil and monocyte positivity for DREG was reduced from 94% to 82% and 64% to 34%, respectively. These results suggest that monocytes are more affected than neutrophils in vivo by conditions expected to stimulate shedding of DREG and that sepsis promotes shedding of these adherence receptors. Accumulation of DREG-negative monocytes in association with sepsis may be sufficient to impair their recruitment to inflammatory sites and limit their contribution to host defense against infection and tissue repair.

Penetrating wounds in burn tissue may become infected, therefore primary closure of such wounds has only been recommended for lacerations of the face. To determine if wounds in burned areas can be closed primarily if seen early, we created partial- or full-thickness thermal burns in guinea pigs (n = 54) and made incisions through the burned tissue. One side was closed primarily at variable time intervals postburn. Infectious complications were determined by observation and the quantitative bacterial smear technique. All wounds closed primarily at 24 hours or longer postburn became infected. Wounds closed primarily at 4 hours postburn had fewer infectious complications than wounds left open (p less than 0.05). We also reviewed our experience with 23 multiply injured burn patients over an 11-year period who had peritoneal lavage or exploratory laparotomy. There were no wound infections in 12 patients with incisions closed primarily in unburned areas or in 11 patients with wounds through burned tissue. We conclude that lacerations or surgical incisions in burned tissues seen early (less than 12 hrs) postburn should be treated as wounds in unburned patients. Wounds in burned tissue seen late (greater than 24 hrs) postburn should be considered contaminated.

Zinc is an essential trace element required for RNA and DNA synthesis and the function of over 200 zinc metalloenzymes. After surgery or trauma, the serum zinc concentration usually decreases. The magnitude and duration of this hypozincemia after thermal injury are unclear, as are mechanisms for this hypozincemia. In this study we evaluated, over the duration of their hospital course, serum zinc concentrations in 23 thermal injury patients. The initial mean serum zinc concentration was significantly depressed (42 +/- micrograms/dl; normal 66-110 micrograms/dl). By the second week of hospitalization, serum zinc concentrations gradually increased into the normal range in the majority of patients. Mechanisms for this hypozincemia were evaluated. Decreases in the serum zinc concentration did not correlate with increased urinary zinc excretion; thus increased urinary zinc excretion was an unlikely mechanism for the observed hypozincemia. Values for albumin, the major zinc binding protein in serum, generally were inversely correlated with the serum zinc concentration. Thus, hypoalbuminemia could not explain the decreased serum zinc concentration. Certain cytokines such as interleukin-1 are known to cause a decrease in the serum zinc concentration as part of the acute phase response. Therefore, we measured serum C reactive protein concentrations as an indicator of the acute phase response. Thermally injured patients initially had markedly elevated C-reactive protein levels which gradually decreased during hospitalization. We suggest that the initial hypozincemia observed in thermally injured patients may be a reflection of interleukin-1 mediated acute phase response. Whether one should vigorously attempt to correct this initial marked hypozincemia requires further investigation.

Although silver sulfadiazine has been used extensively as an effective topical antimicrobial agent in thermal injury patients, little is known about the cutaneous absorption of the silver moiety in these patients. Therefore, we longitudinally evaluated both serum silver concentration and 24-hour urinary excretion of silver in 23 patients with second- and third-degree thermal burns. Mean serum silver concentrations were modestly elevated throughout the patients' hospital course. Urinary excretion of silver was markedly elevated, especially in those patients with more severe burns. Indeed, in patients who had burns covering more than 60% of the total body surface area mean peak silver excretion was 1100 micrograms/24 hr (normal, less than 1 micrograms/24 hr). Thus, silver ion is absorbed across the burn wound in thermal injury patients treated with silver sulfadiazine. The 24-hour urinary excretion of silver appears to be a very sensitive indicator of cutaneous absorption in these patients. Possible implications of this cutaneous silver absorption warrant further evaluation.

This is the first case report of the clinical use of intraoperative streptokinase to promote free flap salvage. A latissimus dorsi free flap was mobilized to cover a scalping type injury. After 4 1/2 hours of ischemia and recurrent thrombosis, streptokinase was perfused into the thoracodorsal artery (7,500 units of streptokinase in 30 cc of normal saline). The free flap was exposed to this concentration of streptokinase for 10 minutes followed by drainage of the venous effluent in order to avoid possible deleterious systemic effects of the streptokinase. Good flow throughout the free flap resulted, and the flap remained viable, providing good coverage for the patient's skull. Controversies regarding the no-reflow phenomena and the use of various thrombolytic agents are discussed.

Information concerning selenium status in thermal injury patients is limited. Therefore, both serum selenium concentration and 24 h urinary excretion of selenium were evaluated throughout the hospital course for 23 patients with partial and full skin thickness thermal burns. Serum selenium levels were depressed throughout the hospital course in the majority of patients, and only two patients' serum selenium levels had reached the normal range by discharge. Urinary selenium losses were essentially within normal range throughout the same period and thus were not responsible for the observed depression in serum selenium levels. A possible antagonistic relationship between selenium and silver is discussed.

Serial serum creatine kinase (CK) and creatine kinase myocardial band isoenzyme (CK-MB) levels were obtained from 116 of 125 electrical burn patients admitted from 1976 through 1986. We divided patients into three groups (peak CK within 2 days after admission) as follows: group 1, CK less than 400 U/L; group 2, CK = 400 to 2500 U/L; group 3, CK greater than 2500 U/L. Clinical myocardial infarction (MI) was determined by ischemic ECG changes, LDH isoenzyme patterns, and clinical course. Skin grafts occurred in 2 of 24 patients from group 1, in 15 of 31 from group 2, and in 37 of 61 from group 3. Hospital stay (mean +/- SEM) was 4.6 +/- 1.3 days for group 1, 20.2 +/- 5.4 for group 2, and 37.7 +/- 3.6 for group 3. Group 1 patients required no amputations; group 2 had 1 limb and 5 digit amputations; group 3 had 22 limb and 16 digit amputations. Only three clinical MIs were found (all in group 3), although 1 of 31 patients from group 2 and 32 of 61 from group 3 had CK-MB greater than 4%. Highly elevated CK and CK-MB are associated with longer hospitalization, and a greater risk of skin grafting or amputation, than with levels less than 400 U/L. Clinical MI is rare and cannot be diagnosed by elevated CK-MB alone.

The increased susceptibility to infection of patients with thermal injury is related to loss of host defense, which is reflected, in part, by the temporal loss of chemotactic function of leukocytic phagocytes. Our studies of patient neutrophils to define the mechanism of this phenomenon involved evaluation of both random and chemotactic migratory functions of patient neutrophils, measurement of receptors for chemotactic ligands, and measurement of receptors mediating substrate adherence of the cells. Measurements of migratory functions were made using the under-agarose technique and measurements of receptor expression were accomplished by flow cytometry using fluorescein-labeled ligand or receptor-specific antibody. We conclude that loss of chemotaxis in response to C5a/C5adesArg is the results of down-regulation of receptors for C5a and of reduced motility, and that loss of chemotaxis in response to the tripeptide FMLP is the result of reduced motility alone. Measurements of changes in the expression of "adherence" (iC3b) receptors revealed that up-regulation occurs early and can be sustained for weeks after injury. These results are taken to suggest that either hyper- or hypo-adherence could explain the loss of random migratory function observed for patient cells. Evidence of auto-oxidative alteration of cytoskeletal elements, to produce loss of random migratory function, also is reviewed. Considering the evidence for activation of the complement cascade after thermal injury C5a and C5adesArg are likely primary factors in effecting the down-regulation of C5a receptors, stimulation of secretion to mobilize iC3b receptors, and stimulation of respiration to auto-oxidize cell components. Such evidence of injury-mediated complement activation included data derived from application of a novel immunoassay for iC3b.

Fibrin has classically been considered a defense mechanism of the peritoneal cavity. We have studied the role of purified fibrin in the pathogenesis of intraperitoneal infection. Implantation of 0.5% bovine fibrin clots containing 2 X 10(8) E. coli into the rat peritoneal cavity reduces the 24-hour mortality rate from 100% to 0% compared to bacteria in a similar volume of saline solution. However, the 10-day mortality rate with fibrin is 90%; 100% develop intraperitoneal abscesses. Animals receiving sterile clots lyse than over 1 to 2 weeks without abscess formation. As few as 10(2) E. coli per fibrin clot produce abscesses, but 10(7) or more are required to produce death; without fibrin less than 10(7) E. coli neither kill nor produce intraperitoneal infections. Both late death and abscess size with 2 X 10(8) E. coli are directly proportional to the fibrin clot size but not the concentration of fibrin in the clot. Operative debridement of the fibrin at 4 or 24 hours completely eliminates abscess formation in surviving animals. In vitro growth of E. coli is neither stimulated nor inhibited by fibrin or fibrinogen. Fibrin delays systemic sepsis, but the entrapped bacteria cannot be easily eliminated by normal intraperitoneal bactericidal mechanisms and abscess formation occurs. Thus radical peritoneal debridement or anticoagulation may reduce the septic complications of peritonitis.

We report the results of a new test, indium oxine in 111 scanning, in the diagnosis of postoperative infection. Indium 111 was used to label autologous polymorphonuclear leukocytes, which when reinjected migrate to sites of infection, inflammation, or both. Standard scintigraphy localizes the labeled inflammatory cells at these sites. Sixty-six scans were performed in 43 surgical patients. Thirty-seven scans were categorized as true-positive; 19 scans were categorized as true-negative. Therefore, the accuracy rate was 85%. Two scans (3%) in one patient represented false-positive results. Two scans (3%) were positive for inflammation but there was no infection present; this group was denoted as equivocal. Six scans (9%) were false-negative; false-negative scans are more likely in old lesions with poor blood supply and in areas that overlap regions of normal uptake. The noninvasive nature of the test, high accuracy rate, and ease of administration make it a potentially useful tool in the diagnosis of postoperative infection.

At laparotomy, many surgeons routinely instill crystalloid solutions into the peritoneal cavity, presumably to dilute out necrotic debris, bacteria, and adjuvant substances which foster bacterial growth. We examined the effect on mortality, bacterial growth, clearance, and phagocytosis of various volumes of saline instilled into the peritoneal cavity of rats during Escherichia coli peritonitis. Minimal intraperitoneal bacterial growth was seen after the introduction of a nonlethal inoculum of viable E. coli in 1 ml of saline, while administration of an identical inoculum in 30 ml of saline intraperitoneally (i.p.) led to increased 48-hour mortality (p less than 0.01), and associated rapid bacterial proliferation (p less than 0.01). Clearance of nonviable radiolabelled E. coli from the peritoneal cavity was delayed, bacterial association with host peritoneal leukocytes was decreased, and blood uptake of radiolabelled bacteria was diminished in animals receiving 30 ml of saline i.p., compared to controls which received the identical inoculum in 1 ml of saline i.p. The clinical relevance of these studies is manifold: (1) they provide a possible explanation why patients with ascites due to cirrhosis or the nephrotic syndrome, or those patients undergoing peritoneal dialysis are more susceptible to primary and secondary bacterial peritonitis, possibly on the basis of impaired peritoneal clearance or diminished phagocytosis and, (2) although irrigation of the peritoneal cavity with crystalloid solution would seem prudent during laparotomy, these solutions must be removed prior to closure to prevent interference with normal peritoneal host defense mechanisms.

Extensive scalping injuries offer a unique challenge for tissue coverage because of the wide expanse of bone and lack of deep soft tissue or significant perforating vessels. For smaller injuries, pedicle flaps offer ideal coverage. Larger defects can be covered by omental flaps. Coverage with a free muscle flap followed by split-thickness skin grafting offers optimal long-term coverage. Two new techniques are introduced. The wire-button technique offers stabilization, and the halo frame provides good support and protection for a new free-flap graft and may increase the success rate of flaps in patients with scalping injuries.

Between January 1, 1968 and March 1977, 100 of 131 patients who lost their first transplant at the University of Minnesota received a second renal allograft. Overall patient survival in the retransplanted group was 10% less than that in the dialysis group. The best results (graft function and patient survival were seen in young patients, nondiabetics, patients who received two sequential living related groups, and in those whose first graft was lost secondary to chronic rejection. The poorest results were seen in older patients (greater than 40 years), diabetics, and patients with acute rejection during the initial graft. Shared donor antigens do not affect graft outcome. These findings, although not the product of a randomized prospective study, may be useful in advising patients of the relative risks of retransplantation or hemodialysis.