Biomedical subjects
Publications and source records attributed to L D Solem.
It is often difficult to determine the true extent of a burn, but most small thermal burns can be easily evaluated and managed by primary care physicians. In this article, the authors review the characteristics of different types of burns, describe those that require treatment in a burn center, and discuss appropriate measures to hasten healing and promote a satisfactory cosmetic outcome.
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.
The disposition of piperacillin was prospectively evaluated in nine severely burned patients who had normal renal and hepatic function. Wide interpatient variations were demonstrated in the drug's distribution volume, half-life, and clearance, with mean (+/- SD) values of 55.0 (+/- 44.2) liters, 3.6 (+/- 5.2) hours, and 14.9 (+/- 6.3) liters/hour, respectively. Piperacillin clearance was best explained by patient factors other than age, renal function, and the percentage of body surface area burns. Piperacillin disposition was related to the patients' serum albumin, total bilirubin, blood urea nitrogen, and the amount of urea nitrogen excreted daily in urine. Altered piperacillin disposition thus appeared to occur secondary to changes in the patients' physiologic and metabolic state caused by injury-related stress and fluid therapy. The patient's physiologic and metabolic response to injury, along with age and renal function, should be considered when instituting treatment with piperacillin or other agents cleared from the body in a similar manner.
The disposition of piperacillin was prospectively evaluated in 11 critically ill surgical patients who had no evidence of pre-existing renal and hepatic disease. Interpatient variations were demonstrated in the drug's half-life, distribution volume, and clearance, with values of 1.50 +/- 2.05 (SD) h, 25.0 +/- 17.2 L, and 23.8 +/- 17.2 L/h, respectively. Variations in piperacillin disposition were best explained by serum concentrations of albumin, total protein, and bilirubin, and the amount of urea nitrogen excreted daily in urine. Age and renal function were moderately associated with piperacillin elimination rate and clearance. Altered piperacillin disposition thus appeared to occur as secondary to changes in the patients' physiologic and metabolic state caused by injury-related stress and fluid/colloid therapy. These alterations may necessitate dosage modifications to achieve optimal patient response when treating patients with piperacillin as well as with other similar drugs eliminated via renal and nonrenal routes.
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.
The common acute lymphoblastic leukaemia antigen (CALLA/CD10) is a normal component of the circulating neutrophil cell surface membrane. In order to examine the potential functional significance of CALLA/CD10 we analysed the expression of this molecule on neutrophils isolated from thermal injury patients, since these patients have a well-documented constellation of neutrophil defects affecting their microbicidal functions. Expression of neutrophil CALLA/CD10 was monitored by indirect immunofluorescence and flow cytometry. We observed that CALLA/CD10 expression was quantitatively reduced on burn patient neutrophils, compared to healthy donors (P less than 0.001). In contrast, burn patient neutrophils expressed normal levels of class I HLA molecules and the C3bi receptor. Reduced expression of CALLA/CD10 was not associated with neutrophil activation or exposure to plasma 'factor(s)' in vivo. Analysis of normal bone marrow neutrophils by cell sorting indicated that expression of CALLA/CD10 occurs late in neutrophil maturation, since 25% of polymorphonucleated bone marrow neutrophils did not express cell surface CALLA/CD10. Attempts to examine the chemotactic responses of CALLA/CD10 positive and negative neutrophils from burn patients were hampered by previous exposure of these cells to chemoattractants in vivo. Collectively, our findings suggest that burn patient peripheral blood neutrophils may be deficient in CALLA/CD10 due to insufficient maturation time in the bone marrow following thermal injury.
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.
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.
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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.
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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.
We undertook a retrospective study of 36 victims of high-voltage electrical contact injuries to determine the incidence and possible source of elevated creatine kinase (CK)-MB enzyme in their serum. Only two sustained myocardial infarctions (one late) according to history, electrocardiographic findings, and clinical course. Serum lactate dehydrogenase isoenzyme levels were abnormal but revealed no myocardial infarction patterns. Creatine kinase total activity, however, reached 1.5 to 1,140 times normal in 92% and the CK-MB level was abnormal in 50% despite the low incidence of myocardial damage. Skeletal muscle CK and CK-MB levels in four nonelectrically injured patients were comparable to those in normal muscle while CK and CK-MB activity was elevated in six such electrical injuries. There was a gradient in CK-MB activity with greatest CK-MB activity in "normal" muscle near the injury site, lesser amounts in border tissue, and least in the worst-injured site. We conclude that myocardial injury is uncommon in high-voltage electrical injury and skeletal muscle injured by high electrical voltage is stimulated to produce, as well as release, CK-MB.
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.
Conflicting reports regarding copper status in thermal injury patients have been published. We determined serial serum-copper and serum-ceruloplasmin levels and 24-h urinary excretion of copper in 23 patients with second- and third-degree thermal burns. Throughout hospitalization, mean serum-copper concentration was significantly depressed; lowest levels were found in patients with greater than 40% total body surface area burns. Serum ceruloplasmin was also depressed, an unexpected finding because this protein is a positive acute-phase reactant poststress. Mean urinary excretion of copper was elevated, reaching 2.5 times the upper limit of normal 2 wk postburn. Depressed serum-copper levels paralleled the serum-ceruloplasmin levels rather than the increased urinary-copper losses. Further studies are required to determine the mechanism(s) of this altered copper metabolism and whether physiological or biochemical evidence of copper deficiency accompanies the observed hypocupremia.