Within the EMTP curriculum, specific longitudinal educational trainings on the diagnosis and treatments of MSI and fractures were provided through lectures and workshops. Research studies regarding the epidemiology of injuries and the impact of emergency training on patient outcomes have been conducted, although specific epidemiology regarding fractures and the impact of training on patient outcomes is lacking.The purpose of our research was twofold: 1) to understand the epidemiology of MSI fractures in Rwanda; and 2) to evaluate the progress of the country’s first EM residency program in treating MSI-related injuries by assessing ED mortality rates, length of stay, and complication rates.This was a pre-post study examining the characteristics and outcomes of MSIs before and after implementation of an EMTP at the University Teaching Hospital of Kigali in Kigali, Rwanda. UTH-K is an urban referral and tertiary-care teaching hospital with approximately 560 inpatient beds and 40 ED beds. UTH-K contains a 24-hour Accident and Emergency Department that serves adult patients with acute complaints, as well as pediatric and obstetric trauma patients. Resources at UTH-K include 24-hour surgical coverage, 24-hour access to radiologic services including radiograph, ultrasound, and computed tomography, as well as continuous access to general surgery, orthopedic and neurological specialists.The A&E department is covered by general practice physicians and EM residents. An EM post-graduate diploma program was initiated on November 1, 2013, and most physicians enrolled subsequently participated in the official EM residency,hydroponic drain table which began in September 2015. Both programs are herein formally referred to as the EMTP.
Prior to initiation of these training programs, care was provided exclusively by GPs. Since initiation of EMTP, ED care has been provided jointly by GPs and EM resident-trainees who have oversight by board-certified emergency physicians. All patients who presented at UTH-K during the two data collection periods, from November 2012- October 2013 and August 2015-July 2016, were eligible for inclusion. These preand post-time periods for data collection were chosen to correspond with the absence of an EMTP and implementation of an EMTP, respectively. We identified cases and queried data from institutional records via protocolled methods, as previously described in prior studies.7,18,19,20 Briefly, using a multi-point composite index generated from an electronic hospital database, we identified all cases during each month of the accruement periods. Subsequently, all cases were coded with a unique identification number and were sampled at random until a sufficient number of records meeting inclusion criteria were identified . We then narrowed the dataset to those with MSI, either with open, closed, or mixed fractures. Next, we applied the following exclusion criteria: incomplete or erroneous evaluation documentation dates from the ED, comprising patients without admission dates, or patients with admission dates that preceded discharge dates. Measured variables included age, sex, mechanism of injury, injury type, hospital vital signs, hospital admissions, surgical interventions, medical treatments, discharge date, and disposition. If more than one anatomical region was indicated as injured, each region was recorded.We did not collect post-discharge outcomes, such as subsequent emergency visits, hospitalizations, or post-discharge death,. Long-term cognitive impairment , defined as new or worsening deficit in cognition that persists following acute illness, is a well described phenomenon occurring in an estimated 16% of older adults who are acutely ill.This often leads to increased disability, loss of independence, and decreased quality of life.
Currently no effective therapies, especially those that can be administered early in the acute illness course, exist to prevent or treat LTCI following acute illness. While the mechanism of LTCI has not been fully elucidated, it is hypothesized that systemic proinflammatory cytokines, in response to an acute medical illness such as sepsis,lead to increased central nervous system inflammation, microglial activation, and neuronal injury and death.Vitamin D is a pleotropic hormone that modulates systemic and CNS inflammatory responses.Therefore, patients with Vitamin D deficiency may be particularly vulnerable to LTCI following an acute illness. Several observational studies have suggested that Vitamin D deficiency is associated with poorer long-term cognition among community-dwelling adults.4 However, the relationship between Vitamin D deficiency in the setting of acute illness and subsequent development of LTCI remains unknown in acutely ill patients, especially in the emergency department setting. Therefore, we sought to determine whether serum Vitamin D at ED presentation was associated with poorer six-month cognition in acutely ill older adults. This study was an observational secondary analysis within the DELINEATE prospective cohort study, which enrolled ED patients age 65 years and older who were subsequently admitted the hospital for an acute illness at a large, academic, tertiary care hospital.This study enrolled patients from March 2012 – November 2014. The local institutional review board reviewed and approved this study. Details and rationale of the selection of participants have been described previously.Briefly, we included patients if they were 65 years or older and in the ED for less than four hours at the time of enrollment. Patients were excluded if they were non-English speaking; previously enrolled; deaf, comatose, non-verbal or unable to follow simple commands prior to their current illness; were considered unsuitable for enrollment by the treating physician or nurse; were unavailable for enrollment within the four-hour time limit secondary to clinical care ; or were discharged home from the ED. Patients were included for this analysis if they had blood specimen available for Vitamin D measurement and had a surrogate available to complete a short form Informant Questionnaire on Cognitive Decline in the Elderly obtained at enrollment to establish pre-illness cognition.
Pre-illness and six-month cognition were measured using the short form IQCODE in patients who had a surrogate in the ED who knew the patient for greater than 10 years. It ranges from 1 to 5 . This surrogate-based cognitive screen was used because patient-based measurements in the ED may not accurately reflect true baseline cognition especially in the setting of delirium.6 The IQCODE is also a validated measure of cognition, which has been previously used to assess cognitive decline.At time of study enrollment, informants were asked to assess the patients’ pre-illness cognition at two weeks prior to ED presentation,rolling benches hydroponics and followup assessment at six months over telephone with all attempts made to have the same person complete the IQCODE questionnaire as the individual who completed the pre-illness questionnaire. The primary independent variable was serum Vitamin D measured at ED enrollment. We used Vitamin D level at ED presentation to identify patients with pre-existing Vitamin D deficiency prior to hospitalization for an acute illness. Vitamin D deficiency was defined as a serum Vitamin D concentration <20 milligrams per deciliter.We collected blood in citrate anti-coagulated collection tubes immediately upon study enrollment. Tubes were placed on ice and centrifuged at 3000 g-force within one hour to isolate plasma. Samples were stored at -80C until batched Vitamin D measurements were performed using the Abbott Architect i2000 . We used the Charlson comorbidity index to quantify patient comorbid burden.8 The Acute Physiology Score of the Acute Physiology and Chronic Health Evaluation II score, including age, was used to quantify severity of illness.The presence of a CNS diagnosis was determined by two physician reviewers via medical record review. Any disagreement was adjudicated by a third physician reviewer. To determine whether Vitamin D was associated with poorer six-month cognition, we performed multiple linear regression with Vitamin D deficiency as a binary variable adjusting for covariates, IQCODE, the Charlson comorbidity index, APS, and presence of a CNS diagnosis, which were all defined a priori. Because we previously observed that pre-existing cognition may modify any associations and long-term cognition,10 we incorporated a cross product of Vitamin D and pre-illness IQCODE in the linear regression model. If the interaction p-value was < 0.25, then it was retained in the multiple regression model. Because the IQCODE is a continuous variable, vitamin D’s b-coefficients are reported at the 25th and 75th percentile values of the pre-illness IQCODE to represent those who were cognitively intact and cognitively impaired at baseline, respectively. Another multi-variable model was run where serum Vitamin D deficiency was the independent variable. We used SAS version 9.4 for statistical analysis. Our findings suggest that Vitamin D deficiency is common among older patients presenting to the ED with an acute medical illness, and Vitamin D deficiency is associated with increased risk for LTCI among older adults who are cognitively intact prior to an acute illness. Unfortunately, no intervention exists to preserve long-term cognition after an acute illness. The first step toward discovering an intervention is to identify modifiable risk factors early on in the course of an acute illness, and this is the impetus for our study. Future studies should determine if early Vitamin D repletion in the ED improves cognitive outcomes in acutely ill older patients. We also observed that the association between serum Vitamin D concentrations and six-month cognition was more prominent in patients with intact cognition at baseline. It is possible that Vitamin D deficiency in the setting of acute illness may more profoundly affect those with intact cognition.
It is also possible that patients with intact cognition at baseline are more at risk for cognitive decline following acute illness that is detectable with the measures currently available to assess cognition. Future studies should confirm this finding using more robust neuropsychiatric evaluations to quantify long-term cognition. Our study builds upon the work conducted in the outpatient settings, which also reported that low- serum Vitamin D level is associated with the development of Alzheimer’s disease.Because systemic and CNS inflammation are the underpinning of LTCI pathophysiology, we hypothesize that Vitamin D treatment could potentially improve long-term cognition by attenuating systemic and CNS inflammatory responses. Vitamin D is a pleiotropic secosteroid hormone that modulates systemic and CNS inflammatory responses.12 Inflammation in response to an acute illness plays a prominent role in LTCI pathogenesis.Vitamin D down regulates systemic inflammation by inhibiting the release of peripheral pro-inflammatory cytokines such as tumor necrosis factor-α , IL-6 and IL-12.Additionally, Vitamin D also inhibits CNS inflammation by attenuating systemic inflammation and more directly by specifically targeting the brain. Based upon in-vitro models, Vitamin D further attenuates CNS inflammation by inhibiting microglial production of pro-inflammatory cytokines such as IL-6 and TNF-α.Emergency department overutilization costs the U.S. healthcare system nearly $38 billion annually.ED recidivism by older adult patients is a substantial contributing factor to ED overutilization with estimated rates varying between nearly 20% to over 40%, depending on time elapsed since the index ED visit, 30 days to six months, respectively.Older adults have more comorbid conditions and complex medical histories as compared to younger adults, often necessitating more expensive and lengthy ED diagnostic testing.2, 8, 9 Their utilization of the ED despite having health insurance and a primary care physician, suggests other contributors, such as poor health literacy, cognitive impairment, and lack of social support.Understanding the factors leading to ED recidivism in older adults is necessary to build prevention strategies to decrease unnecessary testing, overutilization of healthcare resources, and hospital admissions. High rates of recidivism coupled with the projected rise in the older adult population makes it critical that effective prevention strategies targeting older adults are developed.This narrative review will discuss risk factors for ED recidivism in older adults.Several diagnoses in older adults are associated with ED returns . Diagnoses most commonly reported as predictive of recidivism include those related to the respiratory system, traumatic injuries, and pain.It is possible that the association of respiratory diagnoses with ED recidivism may reflect the season in which the studies were conducted. Information regarding the time of year the studies were conducted or whether a large percentage of the study population were enrolled in the fall and winter months is not available. Another possibility is that patients with respiratory diagnoses may have underlying chronic respiratory conditions such as emphysema or asthma and that these patients represent a sicker population. Common ED complaints in older adults include abdominal and chest pain. According to the National Health Statistics Reports of 2007, abdominal pain was the third most common reason for ED visits among all adults aged 65 years or older.Many patients presenting to the ED with abdominal pain or chest pain often do not receive a definitive diagnosis for the cause of their complaint despite extensive diagnostic testing.