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ABSTRACT: You have been caring for a 32-year-old woman for the past several years. She presented to your office 2 years ago because she noticed a new breast nodule. You examined her and noted marked breast density at her area of concern without an obvious mass. To be thorough, you referred her for mammography; the report stated that the breasts were asymmetrically dense without a distinct mass. You reassured her that her evaluation was negative. Two years later, the patient returned with an obvious mass at the same site. Biopsy revealed an infiltrating ductal carcinoma. Over the next 6 months, she is treated with lumpectomy, axillary node dissection, chemotherapy, and radiation. Shortly thereafter, you receive a letter from her attorney asking for your records. The patient claims that your care resulted in a delay in diagnosis of her breast cancer.
The Nurse Practitioner 11/2007; 32(10):22-32; quiz 32-3.
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Rhonda S Fishel
Critical Care Medicine 11/2007; 35(10):2431-2. · 6.33 Impact Factor
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ABSTRACT: To understand the mechanism of pathologic capillary leak in the critically ill patient.
Review of normal and altered physiology of the microvasculature. Review of recent literature describing pathogenesis, mediators, and interventions influencing capillary leak and microvascular repair.
In vitro and in vivo studies, the latter including animal and human subjects.
Capillary leak with resultant edema develops in the critical care setting on the basis of perturbations in Starling's equation, primarily as a result of increased capillary permeability to larger molecules. This process is most likely fueled by inflammatory mediators or mechanical stress. Attempts to prevent or treat this process remain largely unsuccessful; resuscitation is more often symptomatic than therapeutic. Models of microvascular repair focus on discrete injury and may not be applicable to the recovery of capillary damage secondary to a systemic leak
Our understanding of capillary leak syndrome remains fragmented and weighted toward specific mediators contributing to the leak. The implications of extensive edema and the mechanism by which it resolves continue to be the subject of speculation rather than study.
Critical Care Medicine 09/2003; 31(8 Suppl):S502-11. · 6.33 Impact Factor
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ABSTRACT: Supplemental arginine has been shown to enhance wound healing, in particular collagen synthesis. Ornithine is the main metabolite of arginine in the urea cycle and shares many of the biopharmacologic effects of arginine. The present study examines the effect of ornithine supplementation on wound healing and attempts to describe its possible mechanism.
Wild type (WT) and iNOS knockout (KO) mice were randomized to receive either normal chow and tap water or chow and water each supplemented with 0.5% ornithine (w/w). All animals underwent a midline dorsal skin incision with implantation of polyvinyl alcohol sponges into subcutaneous pockets. On postoperative day 14 the animals were sacrificed. The dorsal wound was harvested for breaking strength determination while the wound sponges were assayed for hydroxyproline content, total wound fluid amino acid, and nitrite/nitrate (NOx) concentration.
Dietary ornithine supplementation enhanced wound breaking strength and collagen deposition in both WT and KO mice. This was accompanied by increased wound fluid proline and ornithine levels but not arginine, citrulline, or NOx levels.
The results from this study demonstrate that ornithine supplementation enhances wound healing in both WT and KO mice. This suggests that ornithine's effect on wound healing is independent of the iNOS pathway.
Journal of Surgical Research 09/2002; 106(2):299-302. · 2.25 Impact Factor
