Does ethanol affect the reliability of pelvic bone examination in blunt trauma?

STUDY OBJECTIVE: We sought to determine whether the reliability of clinical evaluation for pelvic bone fracture after trauma is compromised by a serum ethanol level of 100 mg/dL or greater. METHODS: This is a retrospective case control study of trauma registry patients presenting from October 1, 1995, to March 31, 1997, to an urban level I trauma center. Inclusion criteria were as follows: blunt trauma, age 13 years or older, and Glasgow Coma Scale score of 13 or greater. Exclusion criteria were as follows: isolated penetrating injury and suspected spinal injury. Patients were separated into 2 groups: those with an ethanol level of 100 mg/dL or greater, and those with an ethanol level of less than 100 mg/dL. Physician performance in clinical identification of pelvic bone fracture by using a complaint of pain, pelvic tenderness, with or without deformity, was compared between the 2 groups. RESULTS: Seven hundred sixty-three patients met inclusion criteria. Fifty-five (7. 2%) patients had a pelvic fracture, 75% of which were isolated acetabulum or pubic ramus fractures. Two hundred six control patients without pelvic fractures were randomly selected. The sensitivity and specificity of the complaint of pain and tenderness, deformity, or both for identification of a pelvic fracture was not significantly different between the ethanol groups. Five (9%) of 55 patients with pelvic fractures had neither a complaint of pain nor bony tenderness or deformity on examination. This was not statistically associated with an ethanol level of 100 mg/dL or greater (P =1.000). CONCLUSION: In our study, clinical evaluation for pelvic fracture in trauma patients with a Glasgow Coma Scale score of 13 or greater was not compromised by an ethanol level of 100 mg/dL or greater. The most common reason for clinically missed pelvic fractures was the presence of additional painful distracting injuries.     

Can Bridge to Recovery Help to Reveal the Secrets of the Failing Heart?

Despite several decades of research and clinical experience, the basic mechanisms of the failing heart remain largely a secret. While pharmacological therapy can induce limited reverse remodeling, left ventricular assist device (LVAD) therapy offers the opportunity to induce significant improvements to the structure and function of the heart, with major clinical implications. LVAD therapy also provides significant insight into which changes have an impact on function and which do not, and could therefore reveal some of the secrets of the failing heart. In addition, LVAD-induced mechanical unloading may unlock further myocardial properties hitherto unknown such as the proliferation of the stem cell compartment. It may also serve as an important platform for emerging therapies such as gene and cell therapies. In this review, we highlight the most recent novel discoveries related to LVAD therapy and bridge to recovery (BTR). Discovering the integrated network of events that underlies BTR could unravel the secrets of the failing heart.     

Heart failure therapy at a crossroad: are there limits to the neurohormonal model?

The advent of neurohormonal blockade in heart failure (HF) has been an overwhelming success, but current evidence points to a ceiling effect as newer neurohormonal targets are exploited in an incremental manner. This has lead us to question whether the neurohormonal model of HF can be sustained by simply stacking multiple neurohormonal or cytokine blockers together as treatment. A unifying theme in some of these disparate trials relates to either a lack of efficacy or, more importantly, adversity resulting in regression of already achieved benefits. It is our contention that the available evidence has uncovered the remarkable complexity of interaction within the context of the neurohormonal construct. As we stand at a crossroad in HF and begin to fervently pursue non-neurohormonal therapeutic targets, we must also direct attention at navigating the multifaceted labyrinth of the neurohormonal model that has led to the current imbroglio.     

Does physical trauma lead to an increase in the risk of new onset widespread pain?

OBJECTIVE: To determine the rate of new onset of widespread pain after a traumatic event (motor vehicle crash). METHODS: A prospective cohort study of persons registered with an insurance company who had or had not experienced a motor vehicle crash. All participants were sent a questionnaire to assess pre-crash (or for the non-crash group, prior) psychosocial factors and widespread pain. Participants reporting pre-crash (prior) widespread pain were excluded. At six months, participants were sent a follow up questionnaire to ascertain new prevalent widespread pain. RESULTS: 597 (51%) of participants returned a baseline questionnaire (465 crash and 132 non-crash). Among the cohort who had experienced a crash, the new onset rate of widespread pain six months later was low (8%), though in comparison with the non-crash group there was an increased risk (RR = 1.9 (95% CI, 0.8 to 4.8, adjusted for age and sex)); this was attenuated after adjustment for pre-crash (prior) psychological distress and somatic symptoms (RR = 1.4 (95% CI, 0.5 to 3.2)). CONCLUSIONS: The findings suggest that a motor vehicle crash (as an example of a physically traumatic event) is unlikely to have a major impact on the new onset of widespread pain. Any observed relation may, in part, be explained by psychological distress.     

Does the response of bone mass to calcium supplements depend on calcium absorption efficiency?

OBJECTIVE: Calcium supplements can reduce bone resorption and slow bone loss after the menopause, but these effects may be limited by poor intestinal absorption. Since the increase in blood ionised calcium and decrease in serum parathyroid hormone after a calcium load are diminished in patients with poor calcium absorption, we aimed to see whether the response of bone mineral content (BMC) to calcium is related to initial calcium absorption. DESIGN: We retrospectively examined the changes in forearm BMC in 164 patients (139 women and 25 men) receiving calcium therapy alone for low bone density in a university hospital. METHODS: BMC was measured in a Molsgaard single energy absorptiometer and calcium absorption in a single blood sample 1 h after a dose of 5 microCi (45)Ca in 20 mg calcium carrier. Results were analysed by simple and multiple regression analysis. RESULTS: Mean forearm BMC did not change significantly over the mean 43 (S.D., 33) months of treatment (1.023 (0.247) to 1.017 (0.246) g/cm). The annual percentage of change was positively related to both body weight (r=0.180; P=0.020) and radiocalcium absorption (r=0.185; P=0.017). Multiple linear regression confirmed that both variables contributed to the change in BMC (P=0.023 and 0.019 respectively). The mean annual percentage of change in BMC on calcium therapy was not related to age, initial BMC, serum 1,25-dihydroxyvitamin D or fasting urinary calcium/creatinine ratio. CONCLUSIONS: These results support our earlier studies which suggest that poor calcium absorption limits the response of bone to calcium supplements.