Prevention of venous thromboembolism in long term care: results of a multicenter educational intervention using clinical practice guidelines: part 2 of 2 (an AMDA Foundation project).

INTRODUCTION: Implementation of prophylaxis for venous thomboembolism (VTE) through risk assessment based on clinical practice guidelines (CPGs) is variably adopted in long term care facilities (LTCF). Current guidelines recommend venous thromboembolism prophylaxis (VTE-P) following risk assessment, individualized to patient status. In LTCF, differing comorbidity, life-expectancy, ethical, and quality-of-life issues may warrant a unique approach. This article examines VTE-P practices in LTCF before and after educational intervention to bring practice patterns consistent with CPGs. METHODS: Phase 1 (preceding article in this issue) identified current practice to assess risk and implement VTE-P (17 geographically diverse LTCFs, 3260 total beds). Phase 2 (educational intervention using CPGs) and Phase 3 (outcomes) reexamined VTE-P at the same 17 centers. RESULTS: The frequency of indications for VTE-P and contraindications to anticoagulation were similar during Phases 1 and 3 (all P > .05). In Phase 3, use of aspirin alone decreased more than 50% (P < .0005), whereas use of compression devices increased (P < .0005). Regression models predicted no relationship between any indication or contraindication and VTE-P in Phase 1 (all P > .05) but identified significant relationships between indication and contraindications and VTE-P in Phase 3 (P = .022 to P < .0005), suggesting adequate understanding of current CPGs following education as the basis for improved VTE-P. CONCLUSIONS: The study confirms the presence of significant comorbidity in LTC residents, many with indications for VTE-P, some with contraindications for anticoagulation. Following educational intervention, more residents received VTE-P, influenced by risk-benefit ratio favoring treatment. These findings suggest that even a modest educational intervention significantly improves provider knowledge pertinent to risk assessment consistent with CPG and more appropriate VTE-P.

Prevention of venous thromboembolism: practice patterns in 17 geographically diverse long term care facilities in the United States: part 1 of 2 (an AMDA Foundation project).

INTRODUCTION: Current guidelines recommend antithrombotic prophylaxis for venous thromboembolism (VTE) using risk assessment, factoring contraindications. This report represents a summary of current practice patterns to prevent VTE in long term care as Phase 1 of a 3-phase educational intervention study. PHASE 1 PARTICIPANTS: Participants were 376 new admissions/readmissions (77 ± 12 [SD] years; 67% female) from 17 geographically diverse long term care facilities (3260 total beds). MEASUREMENTS: The process describes current VTE prophylaxis (VTE-P) practices; a companion article describes the educational intervention (Phase 2) and outcome (Phase 3). Phase 1 data were collected on use of nonpharmacological measures and antithrombotic drugs for VTE-P between July and September 2009. RESULTS: Indications for VTE-P were evident in 85% of new admissions, of which two-thirds received VTE-P. Contraindications for anticoagulation were observed in 54.8% of admissions, including quality of life or patient/caregiver wishes. Logistic regression analysis predicted no relationship between any indication for or any contraindication to VTE-P and use of VTE-P, suggesting an inadequate understanding of current clinical practice guidelines. CONCLUSIONS: Residents of long term care have significant comorbidity that poses risk for VTE; although many received VTE-P, contraindications were common, warranting individualized considerations. The likelihood of VTE-P was greatest following orthopedic surgery, severe trauma, and medical illness.

Pressure ulcers: prevention, evaluation, and management.

A pressure ulcer is a localized injury to the skin or underlying tissue, usually over a bony prominence, as a result of unrelieved pressure. Predisposing factors are classified as intrinsic (e.g., limited mobility, poor nutrition, comorbidities, aging skin) or extrinsic (e.g., pressure, friction, shear, moisture). Prevention includes identifying at-risk persons and implementing specific prevention measures, such as following a patient repositioning schedule; keeping the head of the bed at the lowest safe elevation to prevent shear; using pressure-reducing surfaces; and assessing nutrition and providing supplementation, if needed. When an ulcer occurs, documentation of each ulcer (i.e., size, location, eschar and granulation tissue, exudate, odor, sinus tracts, undermining, and infection) and appropriate staging (I through IV) are essential to the wound assessment. Treatment involves management of local and distant infections, removal of necrotic tissue, maintenance of a moist environment for wound healing, and possibly surgery. Debridement is indicated when necrotic tissue is present. Urgent sharp debridement should be performed if advancing cellulitis or sepsis occurs. Mechanical, enzymatic, and autolytic debridement methods are nonurgent treatments. Wound cleansing, preferably with normal saline and appropriate dressings, is a mainstay of treatment for clean ulcers and after debridement. Bacterial load can be managed with cleansing. Topical antibiotics should be considered if there is no improvement in healing after 14 days. Systemic antibiotics are used in patients with advancing cellulitis, osteomyelitis, or systemic infection.

Multimodality of Ca2+ signaling in rat atrial myocytes.

It has been suggested that the multiplicity of Ca(2+) signaling pathways in atrial myocytes may contribute to the variability of its function. This article reports on a novel Ca(2+) signaling cascade initiated by mechanical forces induced by "puffing" of solution onto the myocytes. Ca(i) transients were measured in fura-2 acetoxymethyl (AM) loaded cells using alternating 340- and 410-nm excitation waves at 1.2 kHz. Pressurized puffs of bathing solutions, applied by an electronically controlled micro-barrel system, activated slowly (approximately 300 ms) developing Ca(i) transients that lasted 1,693 +/- 68 ms at room temperature. Subsequent second and third puffs, applied at approximately 20 s intervals activated significantly smaller or no Ca(i) transients. Puff-triggered Ca(i) transients could be reactivated once again following caffeine (10 mM)-induced release of Ca(2+) from sarcoplasmic reticulum (SR). Puff-triggered Ca(i) transients were independent of [Ca(2+)](o), and activation of voltage-gated Ca(2+) or cationic stretch channels or influx of Ca(2+) on Na(+)/Ca(2+)exchanger, because puffing solution containing no Ca(2+), 10 microM diltiazem, 1 mM Cd(2+), 5 mM Ni(2+), or 100 microM Gd(3+) failed to suppress them. Puff-triggered Ca(i) transients were enhanced in paced compared to quiescent myocytes. Electrically activated Ca(i) transients triggered during the time course of puff-induced transients were unaltered, suggesting functionally separate Ca(2+) pools. Contribution of inositol 1,4,5-triphosphate (IP(3))-gated or mitochondrial Ca(2+) pools or modulation of SR stores by nitric oxide/nitric oxide synthase (NO/NOS) signaling were evaluated using 0.5 to 500 microM 2-aminoethoxydiphenyl borate (2-APB) and 0.1 to 1 microM carbonylcyanide-p-trifluoromethoxyphenylhydrazone (FCCP), and 1 mM Nomega-Nitro-L-arginine methyl ester (L-NAME) and 7-nitroindizole, respectively. Only FCCP appeared to significantly suppress the puff-triggered Ca(i) transients. It was concluded that neither Ca(2+) influx nor depolarization was required for activation of this signaling pathway. These studies suggest that pressurized puffs of solutions activate a mechanically sensitive receptor, which signals in turn the release of Ca(2+) from a limited Ca(2+) store of mitochondria. How mechanical forces are sensed and transmitted to mitochondria to induce Ca(2+) release and what role such a Ca(2+) signaling pathway plays in the physiology or pathophysiology of the heart remain to be worked out.