Instrumento para la monitorización de la evolución de una úlcera por presión / Pressure ulcers evolution assessment tools

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An instrument to measure healing in pressure ulcers: development and validation of the pressure ulcer scale for healing (PUSH).

BACKGROUND: Currently, there is no instrument that provides an accurate and simple method of monitoring pressure ulcer healing in clinical practice. This article reports the two studies that were conducted to assess the validity of the Pressure Ulcer Scale for Healing (PUSH) as a tool to monitor healing of stage II-IV pressure ulcers. METHODS: Subjects in both studies (N = 103 and N = 269) were elderly (mean Study 1, 75 years, mean Study 2, 80 years), and the majority were women (Study 1, 51%, Study 2, 70%). Study data were extracted from patients' permanent records. RESULTS: Principal components analysis confirmed that the PUSH tool accounted for 58% to 74% of the wound healing variance over a 10-week period in Study 1 and 40% to 57% of the wound healing variance over a 12-week period in Study 2. In addition, multiple regression analysis, used to measure the sensitivity of the model to total healing, showed PUSH accounted for 39% of the variance in 6 weeks and 31% of the variance over 12 weeks (p <.001; Studies 1 and 2, respectively). CONCLUSIONS: Data from these two studies confirmed that the PUSH tool, with the components of length times width, exudate amount, and tissue type, is a valid and sensitive measure of pressure ulcer healing. It is a practical approach that provides clinically valid data regarding pressure ulcer healing. Further testing is needed to confirm these findings.

Local control of oligodendrocyte development in isolated dorsal mouse spinal cord.

The earliest oligodendrocyte precursors have been proposed to arise in the ventral ventricular zone of the embryonic thoraco-lumbar spinal cord and subsequently migrate to populate dorsal spinal cord. Using the expression of O4 immunoreactivity to define cells of the oligodendrocyte lineage, the development of oligodendrocytes in different regions of the mouse spinal cord was assayed. Consistent with earlier studies in other species, isolated explants of E11 ventral but not dorsal mouse spinal cord developed oligodendrocytes after 7 days in vitro. In contrast, in cultures derived from E13 embryos O4(+) oligodendrocytes developed in both ventral and dorsal cultures after 5 days in vitro. These data are consistent with a ventral to dorsal migration of committed oligodendrocyte progenitors occurring between E11 and E13. Although isolated early embryonic dorsal spinal cord does not give rise to oligodendrocytes in short term cultures, in long term cultures O4(+) cells develop in a subset of dorsal explants. After 10 days in vitro approximately 25% of both cervical and thoraco-lumbar E11 derived dorsal explants contained significant numbers of O4(+) cells. The molecular requirements for the dorsally-derived oligodendrocytes was similar to that in ventral cord. The appearance of O4(+) cells was dependent on sonic hedgehog and enhanced by neuregulin. These data suggest that early embryonic dorsal mouse spinal cord has an independent potential to generate oligodendrocytes under appropriate conditions. Whether this potential is realized during normal spinal cord development is currently unknown.

Protein kinase C regulation of p-glycoprotein-mediated xenobiotic secretion in renal proximal tubule.

Fluorescence microscopy, fluorescent substrates [daunomycin and a fluorescent cyclosporin A (CSA) derivative] and digital image analysis were used to examine the role of protein kinase C (PKC) in the control of p-glycoprotein in killifish renal proximal tubules. PKC activators, phorbol ester (phorbol 12-myristate 13-acetate, PMA) and dioctylglycerol, reduced luminal drug accumulation, and protein kinase inhibitors, staurosporine and 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H-7), increased luminal accumulation; a PMA analog that does not activate PKC was without effect. PMA effects were blocked by staurosporine. The increase in luminal fluorescence caused by staurosporine was blocked by the p-glycoprotein substrate, CSA, indicating that this component of transport was indeed mediated by p-glycoprotein. Neither PMA, dioctylglycerol, nor protein kinase inhibitors altered cellular drug accumulation. Finally, in primary cultures of flounder proximal tubule cells, PMA decreased transepithelial [3H]daunomycin secretion. This pharmacological approach demonstrates that in teleost renal proximal tubule, p-glycoprotein-mediated xenobiotic secretion is negatively correlated with changes in PKC activity, a finding that conflicts with results from studies using mammalian tumor cells that express p-glycoprotein.

Draft definition of stage I pressure ulcers: inclusion of persons with darkly pigmented skin. NPUAP Task Force on Stage I Definition and Darkly Pigmented Skin.

The National Pressure Ulcer Advisory Panel appointed a task force to review the definition of Stage I pressure ulcers, specifically to assess its adequacy in people with darkly pigmented skin. The process used by the task force to draft a new definition is described in this preliminary report of their work. The proposed definition and initial critique of it are given.

Presenting a draft pressure ulcer scale to monitor healing.

The PUSH Tool, a scientifically derived and validated tool for measuring and monitoring pressure ulcer healing, has been introduced. Input has been received from a multidisciplinary audience of participants in a collegial atmosphere conducive to the exchange of ideas. The audience represented many different care settings and included clinicians, educators, researchers, and policy makers. Steps have begun to refine the characteristics and utility of the PUSH Tool. The PUSH Task Force will continue a validation and development process that will include participation from the wound care community.

Pressure ulcer scale for healing: derivation and validation of the PUSH tool. The PUSH Task Force.

Measuring progress toward healing is fundamental to the management of pressure ulcers. A method to assess progress of an individual ulcer over time is lacking. Given the limitations of currently available instruments and the need for a precise and practical method of monitoring healing in clinical practice, the National Pressure Ulcer Advisory Panel initiated the development of a new tool for measuring pressure ulcer healing. The key elements in developing an instrument include simplicity of use in clinical settings, validity for measuring whether ulcers are improving or worsening, and sensitivity to changes in the ulcer between observations. A new tool incorporating surface area, exudate amount, and surface appearance is proposed. Content validity, correlation validity, prospective validity, and sensitivity to change can be met by the proposed Pressure Ulcer Scale for Healing instrument.

Heat shock-induced protection and enhancement of Na+-glucose cotransport by LLC-PK1 monolayers.

Monolayers of the porcine-derived renal epithelial cell line, LLC-PK1, were used to characterize the effects of heat stress on Na+-glucose cotransport. Transepithelial current dependent on 5 mM glucose (I(Glc)), phloridzin-sensitive current (I(phz)), and total transepithelial current (I(total)) were measured as indicators of Na+-glucose cotransport. Severe heat shock (SHS; 45 degrees C for 1 h, then 37 degrees C for measurements) decreased transepithelial electrical resistance (TER), I(Glc), I(phz), and I(total) 50-70%. Mild heat shock (MHS; 42 degrees C for 3 h, then 37 degrees C for 12 h) induced accumulation of 72-kDa heat shock protein (HSP-72), decreased damage to TER from SHS, and prevented damage to I(Glc), I(phz), and I(total). Kinetic analysis showed that SHS damaged and MHS protected total Na+-glucose transport capacity (Vmax of I(Glc)). MHS alone increased TER (50%), I(Glc) (20%), I(total) (20%), and Vmax of I(Glc) (25%). On enhancement of the Na+ gradient by depletion of intracellular Na+, MHS increased I(Glc) 50% and had no effect on transepithelial Na+-dependent sulfate reabsorptive flux measured concurrently or in Na+-replete tissues. These effects of MHS were not reflected in effects on cell survival or luminal membrane surface area as indicated by lactate dehydrogenase or alkaline phosphatase release. In conclusion, HSP-72-inducing heat treatment both protected and enhanced Na+-glucose cotransport independently of the luminal membrane Na+ gradient and selectively with respect to effects on TER, reabsorptive sulfate transport, cell survival, and luminal membrane surface area.

Increased pro-opiomelanocortin-derived peptide release in myotonic dystrophy.

The response of plasma immunoreactive (IR)-ACTH, IR-beta-endorphin (beta-END) and IR-cortisol to insulin-induced hypoglycaemia, an acute stimulus to the pituitary corticotrophs through the central nervous system, and to synthetic ovine corticotrophin-releasing hormone (CRH), a direct corticotroph stimulator, were studied in normal males and males with myotonic dystrophy. Myotonics had an increased IR-ACTH and IR-beta-END response to hypoglycaemia and an increased IR-ACTH response to CRH compared with normals. Plasma IR-cortisol response were not different in either group of subjects to both stimuli. This neuroendocrine abnormality in myotonic dystrophy may represent a manifestation of the purported specific cell membrane defect underlying the disease. This is the first report of an abnormality in proopiomelanocortin peptide release in myotonic dystrophy.

Clinical characteristics of hospitalized diabetic patients.

In an inpatient diabetes control unit established to fulfill the special needs of hospitalized diabetic patients, 29% of the admissions were for control of diabetes. In 71% the metabolic abnormalities of diabetes were incidental to the cause of admission. Of the first 232 patients, 162 had type II diabetes. The degree of hyperglycemia in the type II patients was virtually identical to that in the type I patients, as measured by hemoglobin A1C levels at admission and by mean blood glucose values in the hospital. The mean hemoglobin A1C level at admission was 9.1% in both groups (normal 3.2 to 6.1). During hospitalization the patients admitted for medical and surgical problems achieved average blood glucose levels similar to levels in those who were admitted strictly for diabetes control. Regardless of the reason for admission, hospitalization of a diabetic patient is an opportunity for improvement in metabolic control and for patient education.

Pediatric resuscitation without an intravenous line.

The case of a 3-month-old male infant who was found unresponsive and cyanotic in a crib at home is presented. On arrival in the emergency department the child was receiving basic cardiopulmonary resuscitation (CPR) by a rescue squad and was without vital signs in asystole. The patient achieved a stable rhythm and blood pressure before intravenous access was obtained. Epinephrine and atropine were given via the endotracheal route and sodium bicarbonate through intraosseous infusion.

Renin exists in human adrenal tissue.

Readily detectable levels of renin activity were demonstrated in human adrenal tissues. This activity was inhibited by specific antibody raised against pure renin, indicating that it was not due to the nonspecific action of proteases. The renin activity was predominantly in the cortex rather than in the medulla of the adrenal. An adrenal gland that was surgically removed from a patient with Cushing's disease and had high renin activity was used for further characterization of the enzyme. It shared many biochemical features with kidney renin, such as molecular weight, isoelectric point, glycoprotein nature, optimum pH of enzyme activity, affinity to pepstatin, and the presence of trypsin-activatable inactive renin. The lack of correlation between PRA and the adrenal renin, and the particulate localization of the subcellular distribution of adrenal renin suggested its local origin rather than contamination or contribution of the plasma enzyme.