Use of Intervention Mapping to Adapt a Psychologically Informed Physical Therapy Telerehabilitation Intervention for Latino Persons with Chronic Spine Pain.

The need for culturally tailored pain care is well recognized yet few studies report how existing interventions can be adapted to the needs of culturally and linguistically diverse (CALD) populations. This report describes a formative mixed methods approach using Intervention Mapping-Adapt (IM-Adapt) and the expanded Framework for Reporting Adaptations and Modifications to Evidence based interventions (FRAME) to adapt and report modifications of an existing physical therapy intervention for Latino persons with chronic spine pain in Federally Qualified Health clinics in the southwestern United States (US). Mixed methods included literature reviews, patient surveys, an Adaptation Advisory Panel, and sequential case series with semi-structured interviews. Six steps of IM-Adapt guided the adaptation process and adaptations were prospectively documented with FRAME. A needs assessment revealed an absence of culturally tailored physical therapy interventions for Latino persons with chronic spine pain in the US. An intervention logic model and review of the sociocultural context guided selection of essential interventions, determinants of behavior change, and outcomes. An existing Cognitive Behavioral based Physical Therapy (CBPT) telerehabilitation intervention was selected for adaptation based on accessibility and strong congruency with the logic model. An Adaptation Advisory Panel planned and evaluated iterative adaptations of the CBPT intervention content, activities, delivery, materials, and design. The adapted Goal Oriented Activity for Latino persons with Spine pain (GOALS/Metas) intervention aimed to reduce pain intensity and disability through patient-centered goal setting in physical and cognitive treatment domains. Sequential case series supported feasibility and acceptability of the adapted intervention in the target population. PERSPECTIVE: We describe the systematic adaptation and reporting of an evidence-based physical therapy intervention for culturally and linguistically diverse populations. Greater rigor and transparency in adapting evidence-based interventions using tools such as IM-Adapt and FRAME in future studies will accelerate efforts to reduce ethnic and racial disparities in pain rehabilitation.

Feasibility and acceptability of self-collection of Human Papillomavirus samples for primary cervical cancer screening on the Caribbean Coast of Nicaragua: A mixed-methods study.

Background: Cervical cancer is the primary cause of cancer death for women in Nicaragua, despite being highly preventable through vaccination against high-risk genotypes of the Human Papillomavirus (hrHPV), screening for hrHPV, and early detection of lesions. Despite technological advances designed to increase access to screening in low resource settings, barriers to increasing population-level screening coverage persist. On the Caribbean Coast of Nicaragua, only 59% of women have received one lifetime screen, compared to 78.6% of eligible women living on the Pacific and in the Interior. In concordance with the WHO's call for best practices to eliminate cervical cancer, we explored the feasibility and acceptability of self-collection of samples for hrHPV testing on the Caribbean Coast of Nicaragua through a multi-year, bi-national, community-based mixed methods study. Methods: Between 2016 and 2019, focus groups (n=25), key informant interviews (n=12) [phase I] and an environmental scan [phase II] were conducted on the Caribbean Coast of Nicaragua in partnership and collaboration with long-term research partners at the University of Virginia and community-based organizations. In spring 2020, underscreened women on the Caribbean Coast of Nicaragua were recruited and screened for hrHPV, with the choice of clinician collection or self-collection of samples. Results: Over the course of the study, providers and potential patients expressed significant acceptability of self-collection of samples as a strategy to reduce barriers currently contributing to the low rates of screening (phases I and II). Ultimately 99.16% (n=1,767) of women chose to self-collect samples, demonstrating a high level of acceptability of self-collection in this pilot sample (phase III). Similarly, focus groups, key informant interviews, and the environmental scan (phases I and II) of resources indicated critical considerations for feasibility of implementation of both HPV primary screening and subsequently, self-collection of samples. Through phase III, we piloted hrHPV screening (n=1,782), with a 19.25% hrHPV positivity rate. Conclusion: Self-collection of samples for hrHPV testing demonstrated high acceptability and feasibility. Through concerted effort at the local, regional, and national levels, this project supported capacity building in reporting, monitoring, and surveilling cervical cancer screening across the continuum of cervical cancer control.

Acute overventilation does not cause lung damage in moderately hemorrhaged swine.

Airway management is important in trauma and critically ill patients. Prolonged mechanical ventilation results in overventilation-induced lung barotrauma, but few studies have examined the consequence of acute (1 h or less) overventilation. We hypothesized that acute hyperventilation, as might inadvertently be performed in prehospital settings, would elevate systemic inflammation and cause lung damage. Female Yorkshire pigs (40-50 kg, n = 10/group) were anesthetized, instrumented for hemodynamic measurements and blood sampling, and underwent a 25% controlled hemorrhage followed by 1 h of 1) spontaneous breathing, 2) "normal" bag ventilation (4.8 L·min volume, ∼400 mL tidal volume, 12 breaths/minute), 3) bag hyperventilation (9 L·min volume, ∼750 mL tidal volume, 12 breaths/minute), 4) maximum hyperventilation (15 L·min volume, ∼750 mL tidal volume, 20 breaths/minute), or 5) mechanical ventilation. Pigs then regained consciousness and recovered for 24 h, followed by euthanasia and collection of blood and tissue samples. No level of manual ventilation had any significant impact on hemodynamic variables. Blood markers of tissue damage and plasma cytokines were not statistically different between groups with the exception of a transient increase in IL-1ß; all values returned to baseline by 24 h. On pathological review, severity and distribution of lung edema or other gross pathologies were not significantly different between groups. These data indicate hyperventilation causes no adverse effects, to include inflammation and tissue damage, and that acute overventilation, as could be seen in the prehospital phase of trauma care, does not produce evidence of adverse effects on the lungs following moderate hemorrhage.NEW & NOTEWORTHY Appropriate airway management is essential in trauma and critically ill patients. Prolonged mechanical ventilation can result in overventilation-induced lung barotrauma, but few studies have examined the consequence of acute overventilation. We investigated the outcome of hemorrhage followed by 1 h of overventilation in swine. We found that acute overventilation, as could be seen in the prehospital phase of trauma care, does not produce evidence of adverse effects on otherwise healthy lungs following moderate hemorrhage.

Efficacy of resuscitation with fibrinogen concentrate and platelets in traumatic hemorrhage swine model.

BACKGROUND: This study compared the resuscitation effects of platelets and fibrinogen concentrate (FC) on coagulation and hemodynamics in pigs with traumatic hemorrhage and reduced platelet counts. METHODS: Thirty pigs (40 ± 3 kg) were anesthetized and catheterized with an apheresis catheter to remove platelets using the Haemonetics 9000 (Haemonetics, Braintree, MA). Afterward, a femur fracture was induced, followed by hemorrhage of 35% the estimated blood volume. Pigs were then randomized to be resuscitated with 5% human albumin (12.5 mL/kg), FC (250 mg/kg, 12.5 mL/kg), or platelets collected from apheresis (11.0 ± 0.5 mL/kg). Animals were monitored for 2 hours or until death. Blood samples were collected before (baseline [BL]) and after apheresis, after hemorrhage, and after resuscitation to assess changes in hemodynamics and coagulation using Rotem. RESULTS: No change in mean arterial pressure (MAP) or heart rate (HR) was observed by platelet apheresis. Hemorrhage reduced MAP to 57% ± 5% and elevated HR to 212% ± 20% of BL (both p < 0.05). Resuscitation with albumin, FC, or platelets did not revert MAP or HR to BL. Platelet counts were reduced by apheresis from BL 383 ± 20 × 10/µL to 141 ± 14 × 10/µL and were reduced further after resuscitation with albumin (88 ± 18 × 10/µL) or FC (97 ± 13 × 10/µL, all p < 0.05), but improved with platelet resuscitation (307 ± 24 × 10/µL). Fibrinogen concentration was reduced by apheresis from BL 225 ± 9 mg/dL to 194 ± 8 mg/dL, fell after albumin infusion (134 ± 11 mg/dL), increased to 269 ± 10 mg/dL after FC resuscitation (all p < 0.05), and was not affected by platelet resuscitation. Rotem α-angle decreased from 79 ± 2 degrees to 69 ± 1 degrees by apheresis and hemorrhage (p < 0.05), and recovered similarly by resuscitation with FC (87 ± 1 degrees) or platelets (78 ± 2 degrees), but not by albumin (63 ± 3 degrees). Similar responses were observed in Rotem maximum clot firmness. CONCLUSION: In this traumatic hemorrhage swine model, low-volume resuscitation with FC or platelets was similarly effective in restoring coagulation.

Physiological Impact of Platelet Apheresis in Pigs: Oxygen Metabolism and Coagulation.

INTRODUCTION: Platelet apheresis is a routine clinical practice, but the physiological impact on the donors has been incompletely characterized. This study measured the effects of platelet apheresis on hemodynamics, oxygen metabolism, and coagulation in pigs to assess its impact before employing the animals in experimental studies. METHODS: Forty pigs (39.8 ± 0.6 kg) were anesthetized and catheterized with an apheresis catheter in the femoral vein. During the platelet apheresis process, blood was withdrawn from the pig to separate platelets, and the remaining red blood cells and plasma returned back to the pigs, using the Haemonetics MCS+9000 system. A total of 12 cycles of blood withdrawn and return were performed during the entire apheresis procedure to reduce platelet counts to a target of 50% of baseline. During the process, hemodynamics was recorded in each cycle. Blood samples were collected before and after apheresis to assess changes in oxygen metabolism and coagulation by prothrombin time, activated partial thromboplastin time (STA-R Evolution Stago), and using Rotem thrombelastometry, and platelet aggregation using a Chrono-Log 700 aggregometer. RESULTS: During each cycle of the apheresis, mean arterial pressure (MAP) was decreased and heart rate was increased by blood withdrawal, but both recovered after blood return. On the completion of the apheresis, platelet count decreased from baseline 345 ± 15 109/L to 141 ± 14 109/L and fibrinogen levels were reduced from 124 ± 5 to 99 ± 4 mg/dL (both p < 0.05). Although oxygen delivery remained unchanged, oxygen consumption was decreased from 4.0 ± 0.2 to 3.2 ± 0.0 mL O2/kg/min (p < 0.05). Rotem alpha (clotting speed) decreased from 79 ± 0 to 69 ± 1° and maximum clot firmness (MCF or clot strength) decreased from 71 ± 1 to 57 ± 1 mm (both p < 0.05). No changes were observed in prothrombin time or activated partial thromboplastin time. Platelet aggregation induced by arachidonic acid or collagen was decreased to 28 ± 6% or 71 ± 3% of baseline values (p < 0.05), respectively. CONCLUSION: Platelet apheresis caused significant fluctuations in hemodynamics, reduced oxygen consumption, in addition to the compromised platelet aggregation and clotting function expected. The observations warrant consideration in humans undergoing apheresis over extended periods.

Dose Responses of Ibuprofen In Vitro on Platelet Aggregation and Coagulation in Human and Pig Blood Samples.

INTRODUCTION: Ibuprofen is commonly used by warfighters in the deployed environment. This study investigated its dose effects on in vitro coagulation in human and pig blood. METHODS: Blood samples were collected from 6 normal volunteers and 6 healthy pigs and processed to make platelet-adjusted samples (100 × 10(3)/µL, common transfusion trigger in trauma). Ibuprofen was added to the samples at concentrations of 0 µg/mL (control), the concentration from the highest recommended oral dose (163 µg/mL, 1×), and 2×, 4×, 8×, 10×, 12×, 16×, and 20×. Platelet aggregation by Chrono-Log aggregometer and coagulation by rotational thrombelastogram (Rotem) were assessed at 15 minutes after the addition of ibuprofen. RESULTS: A robust inhibition of ibuprofen on arachidonic acid-induced platelet aggregation was observed at all doses tested in human or pig blood. Collagen-stimulated platelet aggregation was inhibited starting at 1× in human blood and 4× in pig blood. Rotem measurements were similarly compromised in pig and human blood starting at 16×, except clot formation time was prolonged at 1× in human blood (all p < 0.05). CONCLUSION: Ibuprofen inhibited platelet aggregation at recommended doses, and compromised coagulation at higher doses. Human blood was more sensitive to ibuprofen inhibition. Further effort is needed to investigate ibuprofen dose responses on coagulation in vivo.

Effect of Ibuprofen dose on platelet aggregation and coagulation in blood samples from pigs.

INTRODUCTION: Ibuprofen is commonly used by Soldiers in the deployed environment. This study investigated its dose-effects on in vitro coagulation. METHODS: Blood samples were collected from 4 normal healthy pigs and were processed to make platelet-adjusted (100×10(3)/µL) blood samples. Ibuprofen was added to the samples at doses of 0 µg/mL (control), recommended oral dose (163 µg/mL, 1×), 2×, 4×, 8×, 10×, 12×, 16×, and 20×. Arachidonic acid or collagen-stimulated platelet aggregation was assessed at 15 minutes after the addition of ibuprofen. Coagulation was assessed with measurements of prothrombin time (PT) and activated partial thromboplastin time (aPTT), and thrombelastography by Rotem. RESULTS: A robust inhibition of ibuprofen on arachidonic acid-induced platelet aggregation was observed at all doses tested. Collagen-stimulated platelet aggregation was inhibited to 71%±5% and 10%±5% of the control values at ibuprofen doses of 4× and 20×, respectively (both p<0.05). No changes were observed in PT at any dose, but aPTT was prolonged at dose of 16× and 20×. Rotem measurements of coagulation time, clot formation time, maximum clot firmness, and A10 were compromised at dose 16× and 20× (all p<0.05). CONCLUSION: Ibuprofen inhibited platelet aggregation at recommended doses, but did not compromise aPTT or coagulation profile until at 16 times the recommended doses and higher. Further effort is needed to clarify whether there are different dose-responses between human and pig blood samples in trauma situations.

Acetaminophen and meloxicam inhibit platelet aggregation and coagulation in blood samples from humans.

Acetaminophen (Ace) and meloxicam (Mel) are the two types of analgesic and antipyretic medications. This study investigated the dose responses of acetaminophen and meloxicam on platelet aggregation and coagulation function in human blood samples. Blood samples were collected from six healthy humans and processed to make platelet-adjusted (100 × 10 cells/µl) blood samples. Acetaminophen (Tylenol, Q-PAP, 100 mg/ml) was added at the doses of 0 µg/ml (control), 214 µg/ml (the standard dose, 1 ×), 4 ×, 8 ×, 10 ×, 12 ×, 16 ×, and 20 ×. Similarly, meloxicam (Metacam, 5 mg/ml) was added at doses of 0 µg/ml (control), 2.85 µg/ml (the standard dose, 1 ×), 4 ×, 8 ×, 10 ×, 12 ×, 16 ×, and 20 ×. Fifteen minutes after the addition of acetaminophen and/or meloxicam, platelet aggregation was stimulated with collagen (2 µg/ml) or arachidonic acid (0.5 mmol/l) and assessed using a Chrono-Log 700 aggregometer. Coagulation function was assessed by prothrombin time (PT), activated partial thromboplastin time (aPTT), and using Rotem thrombelastogram. A robust inhibition by acetaminophen and/or meloxicam was observed in arachidonic acid-stimulated platelet aggregation starting at 1 × dose. Collagen-stimulated platelet aggregation was inhibited by ACE starting at 1 × (78 ± 10% of control), and by meloxicam starting at 4 × (72 ± 5% of control, both P < 0.05). The inhibitions by acetaminophen and meloxicam combined were similar to those by acetaminophen or meloxicam. aPTT was prolonged by meloxicam starting at 4 ×. No changes were observed in PT or any of Rotem measurements by acetaminophen and/or meloxicam. Acetaminophen and meloxicam compromised platelet aggregation and aPTT. Further effort is warranted to characterize the effects of acetaminophen and meloxicam on bleeding in vivo.