Biomedical subjects
J V Boykin
Publications and source records attributed to J V Boykin.
Wound healing management: enhancing patient outcomes and reducing costs.
Biomedical technology as applied to wound healing management allows specific evaluations of the oxygen-related pathophysiology of non-healing wounds. In many of these cases the use of transcutaneous oxygen mapping of the skin and hyperbaric oxygen (HBO) therapy as an adjunctive treatment for non-healing wounds speeds the healing process. While HBO treatment has remained a covered service for hospital-based care, only recently have treatment algorithms for its application in an outpatient setting been available. This technological advancement has also been a factor in the development of cost effective wound healing centers (WHC) in community hospitals. Better outcomes for many chronic wounds are achieved by combining a multidisciplinary team approach using advanced technologies. In this article the case of a soft-tissue radiation necrosis ulceration of the leg successfully treated with adjunctive HBO is presented. In this example, a reduction in patient charges of greater than 30% was achieved as compared to costs associated with traditional surgical/hospital management of the condition.
Mechanisms of cimetidine protection following thermal injury.
Experimental studies have shown that treatment with cimetidine within 30 minutes of severe thermal injury decreases resuscitative fluid volume requirements by 70 percent. In treated animals, marked hemodynamic improvement was shown as compared with the untreated animals. Administration of the histamine (H2)-receptor antagonist ranitidine was not effective in reducing resuscitative fluid volume, leading to the hypothesis that cimetidine acts via predominantly non-H2-receptor antagonist mechanisms. Evidence is presented for a multifactorial mechanism by which cimetidine offers protection from burn shock. The mechanisms under investigation include inhibition of the hepatic cytochrome P-450 enzymes, cimetidine/copper scavenging of oxygen free radicals, inhibition of thromboxane synthesis, and imidazole buffering capacity. Acting via one or all of these mechanisms, cimetidine may protect against the vascular permeability changes and circulatory collapse that can follow severe thermal injury.
The acridine orange fluorochrome microassay: a new technique for quantitation of neutrophil function in burned patients.
A new assay for determination of neutrophil bacterial killing and phagocytosis is presented. The acridine orange (AO) fluorochrome microassay is a simple, reliable technique for assessing polymorphonuclear (PMN) function. It requires small amounts of blood and provides a rapid and reproducible quantitation of neutrophil activity. Using this technique, bacterial killing and phagocytosis were assessed in a group of five severely burned patients admitted to the Medical College of Virginia Burn Unit. All patients studied demonstrated a significant decrease in bacterial killing at some point during their clinical course. The AO assay was found to be a reliable and effective means of quantitating PMN bacterial phagocytosis and killing in this group of burned patients.
Cimetidine therapy for burn shock: a quantitative assessment.
Optimal cardiac output (CO) resuscitation for severely burned guinea pigs is obtained with intravenous volumes of lactated Ringer's (LR) calculated at 4 cc/kg/%burn/24 hr. When one half this volume of LR is given (2 cc/kg/%burn/24 hr) CO is significantly (p less than 0.05) reduced at 2, 4, and 8 hours after injury. When early postburn cimetidine therapy (0.5 hours after injury) is added to only 1 cc/kg/%burn/24 hr LR, CO is significantly elevated for the same time periods and is not significantly different from CO values of LR at 4 cc/kg/%burn/24 hr for the first 24 hours after injury. However, postburn cimetidine therapy delayed until 1 hour after burn injury did not improve CO compared to treatment with LR at 2 cc/kg/%burn/24 hr. These observations suggest that early postburn cimetidine therapy administered within 1/2-hour of severe scald injury will result in significant CO improvement while simultaneously reducing resuscitative fluid volume requirements by as much as 70% for the first 24 hours after injury.
Mechanisms of burn shock protection after severe scald injury by cold-water treatment.
Following a 3-second subxiphoid immersion of shaved, unresuscitated guinea pigs in 100 degrees C water, cardiac output (CO), mean systemic blood pressure (BP), total peripheral resistance (TPR), hematocrit (HCT), serum histamine (SH), and serum lactate (SL) were measured in untreated and cold-water treated animals up to 24 hours after injury. Animals receiving cold-water treatment (CWT) were immersed in 15 degrees C water for 15 minutes immediately after scald injury. CWT significantly (p less than 0.05) reduced SH and SL for up to 8 and 24 hours, respectively, after injury compared to untreated injured animals. HCT of CWT animals remained significantly lower than that of untreated animals for the first 8 hours after injury. However, CWT-animal HCT was not significantly different from control-animal HCT for this same period. CWT-animal BP was significantly greater than untreated-animal BP for the first 8 hours after injury. CWT- and untreated-animal TPR progressively rose after injury; however, at 24 hours after injury CWT-animal TPR was significantly reduced to 87% +/- 18.0 of preinjury values while untreated-animal TPR was maximally elevated to 170% +/- 10.0 of preinjury values. At 4 hours after injury CO of both untreated and SWT animals was significantly depressed at 56% +/- 3.0 and 50% +/- 10.0 of preinjury values, respectively. However, by 24 hours after injury untreated-animal CO remained depressed at 52% +/- 3.0 while CWT-animal CO was significantly improved at 92% +/- 19.0 of preinjury values. These studies document a beneficial hemodynamic response of severely burned animals after CWT and further verify the phenomenon of cold inhibition of burn wound tissue histamine release after severe scald injury. A correlation between decreased serum histamine and lactate levels and improved cardiovascular function following severe scald injury and CWT is also suggested.
Cold-water treatment of scald injury and inhibition of histamine-mediated burn edema.
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Histamine-mediated delayed permeability response after scald burn inhibited by cimetidine or cold-water treatment.
Scald injury to one ear of the hairless mouse induced significant (P < .05) delayed edema formation in remote, uninjured skin. This remote edema formation was completely inhibited by immediate cold-water treatment of the scalded ear. Cold-water treatment significantly reduced histamine loss from the scalded ear, and the edema-inhibiting effect of the treatment could be mimicked by treating the animal prior to injury with the H2-histamine receptor antagonist cimetidine or a drug that causes histamine depletion. These observations suggest (i) that a histamine-mediated, delayed permeability response occurs after thermal injury that causes remote edema formation and (ii) that one mechanism of remote edema inhibition by cold-water treatment is the prevention of histamine release from thermally injured tissues.
Method for in vivo microscopy of the cutaneous microcirculation of the hairless mouse ear.
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In vivo microcirculation of a scald burn and the progression of postburn dermal ischemia.
The homozygous hairless mouse ear provides a reproducible model for the study of the microcirculatory changes of the burn wound during and following a scald burn injury. This model has allowed us to correlate the dynamic changes of the microcirculation to progressive zones of injury, which show an approximate tenfold increase in the area of complete capillary occlusion during the first 48 hours after injury. Platelet thromboembolism appears to be the major factor causing this progression of postburn dermal ischemia. Edema (increased skin water content) was greatest in the burned ear at 6 hours after the burn (20 percent greater than control values); edema of the unburned, contralateral ear was significant at 2 hours after the burn (9 percent greater than control values).
The angiographic evaluation of human renal allotransplants. Functional graft deterioration and hypertension.
The renal arteriogram is a highly reliable test in the differential diagnosis of early transplant anuria, graft rejection, and hypertension. The reliability of the renal arteriogram was 97.8% in either substantiating or disproving the presence of a suspected episode of graft rejection or renal artery stenosis. The earliest signs of acute humoral and acute rejection were a prolongation of arterial clearance time, diffuse edema with enlargement of the kidney, and progressive deterioration of the nephrogram. Renal artery stenosis may be a sharply localized septum or an elongated narrowing at or distal to the actual site of anastomosis. This was seen primarily in patients' arteriograms more than 60 days after transplantation, and it is important because it is a surgically correctable cause of hypertension.
Re: Oxygen in wound healing: more than a nutrient.
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5 questions--and answers--about hyperbaric oxygen therapy.
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The nitric oxide connection: hyperbaric oxygen therapy, becaplermin, and diabetic ulcer management.
Clinical experience with adjunctive hyperbaric oxygen therapy in the treatment of diabetic ulcers has shown that wound hyperoxia increases wound granulation tissue formation and accelerates wound contraction and secondary closure. In addition to wound hyperoxia, increased wound nitric oxide production caused by hyperbaric oxygen therapy also appears to be important for successful diabetic wound repair. The results of a preliminary retrospective study suggest that nitric oxide production is reduced in the nonhealing diabetic wound, and that topical becaplermin therapy is effective only when wound nitric oxide production deficiency is corrected. In addition, the data suggest that below a critical level of endogenous nitric oxide production, diabetic ulcer repair may not be achieved. Under this hypothesis, diabetic patients with chronic, nonhealing ulcers that respond to becaplermin should have substantially increased endogenous nitric oxide production compared with those ulcers that do not respond to becaplermin. The results of a preliminary clinical study support the use of combined therapy using topical becaplermin and hyperbaric oxygen therapy as a means of successfully treating the chronic diabetic ulcer patient with deficient nitric oxide production and local wound hypoxia.
Inhibition of increased serum histamine and lactate after severe scald injury and cold-water treatment.
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