The Swedish fracture register: 103,000 fractures registered.

BACKGROUND: Although fractures consume large social and financial resources, little is known about their actual numbers, treatment methods or outcomes. The scarcity of data calls for a high-quality, population-based register. No previous registers have prospectively collected data and patient-reported outcome measures (PROMs) on fractures of all types. The Swedish Fracture Register was recently created to fill this gap in knowledge. Its purpose is to provide information on fractures of all types, whether treated by surgery or otherwise. The aim of this article is to describe how the register was developed and its current use. DESCRIPTION: The Swedish Fracture Register was developed during a 4-year period, 2007-2010. Data collection started in 2011. The register currently collects data on all extremity, pelvic and spine fractures in adults who have been diagnosed or treated at the affiliated departments. Data entry is fully web based, including date, cause of injury, classification and treatment. It is performed by the attending physician. Patients fill out PROMs - EQ-5D-3L and the Short Musculoskeletal Function Assessment (SMFA) - relating to health status and level of functioning before the fracture and one year later. Surgeon-reported outcome measures are registered as reoperation rates. The Swedish Fracture Register is now functioning effectively and is used in clinical routine. From January 2011 to September 2015, more than 103,000 fractures have been entered at 26 Swedish orthopedic departments. CONCLUSIONS: The Swedish Fracture Register is already a well-functioning, population-based fracture register that covers fractures of all types, regardless of treatment, and collects both surgeon- and patient-reported outcome measures. In the future the Swedish Fracture Register will be able to present both results of fracture treatment and valuable epidemiological data.

Oxygen-induced impairment in arterial function is corrected by slow breathing in patients with type 1 diabetes.

Hyperoxia and slow breathing acutely improve autonomic function in type-1 diabetes. However, their effects on arterial function may reveal different mechanisms, perhaps potentially useful. To test the effects of oxygen and slow breathing we measured arterial function (augmentation index, pulse wave velocity), baroreflex sensitivity (BRS) and oxygen saturation (SAT), during spontaneous and slow breathing (6 breaths/min), in normoxia and hyperoxia (5 L/min oxygen) in 91 type-1 diabetic and 40 age-matched control participants. During normoxic spontaneous breathing diabetic subjects had lower BRS and SAT, and worse arterial function. Hyperoxia and slow breathing increased BRS and SAT. Hyperoxia increased blood pressure and worsened arterial function. Slow breathing improved arterial function and diastolic blood pressure. Combined administration prevented the hyperoxia-induced arterial pressure and function worsening. Control subjects showed a similar pattern, but with lesser or no statistical significance. Oxygen-driven autonomic improvement could depend on transient arterial stiffening and hypertension (well-known irritative effect of free-radicals on endothelium), inducing reflex increase in BRS. Slow breathing-induced improvement in BRS may result from improved SAT, reduced sympathetic activity and improved vascular function, and/or parasympathetic-driven antioxidant effect. Lower oxidative stress could explain blunted effects in controls. Slow breathing could be a simple beneficial intervention in diabetes.

Oxygen deteriorates arterial function in type 1 diabetes.

AIMS: Although oxygen is commonly used to treat various medical conditions, it has recently been shown to worsen vascular function (arterial stiffness) in healthy volunteers and even more in patients in whom vascular function might already be impaired. The effects of oxygen on arterial function in patients with type 1 diabetes (T1D) are unknown, although such patients display disturbed vascular function already at rest. Therefore, we tested whether short-term oxygen administration may alter the arterial function in patients with T1D. METHODS: We estimated arterial stiffness by augmentation index (AIx) and the pulse wave velocity equivalent (SI-DVP) in 98 patients with T1D and 49 age- and sex-matched controls at baseline and during hyperoxia by obtaining continuous noninvasive finger pressure waveforms using a recently validated method. RESULTS: AIx and SI-DVP increased in patients (P < 0.05) but not in controls in response to hyperoxia. The increase in AIx (P = 0.05), systolic (P < 0.05), and diastolic (P < 0.05) blood pressure was higher in the patients than in the controls. CONCLUSIONS: Short-term oxygen administration deteriorates arterial function in patients with T1D compared to non-diabetic control subjects. Since disturbed arterial function plays a major role in the development of diabetic complications, these findings may be of clinical relevance.

Effects of a single bout of interval hypoxia on cardiorespiratory control in patients with type 1 diabetes.

Hypoxemia is common in diabetes, and reflex responses to hypoxia are blunted. These abnormalities could lead to cardiovascular/renal complications. Interval hypoxia (IH) (5-6 short periods of hypoxia each day over 1-3 weeks) was successfully used to improve the adaptation to hypoxia in patients with chronic obstructive pulmonary disease. We tested whether IH over 1 day could initiate a long-lasting response potentially leading to better adaptation to hypoxia. In 15 patients with type 1 diabetes, we measured hypoxic and hypercapnic ventilatory responses (HCVRs), ventilatory recruitment threshold (VRT-CO2), baroreflex sensitivity (BRS), blood pressure, and blood lactate before and after 0, 3, and 6 h of a 1-h single bout of IH. All measurements were repeated on a placebo day (single-blind protocol, randomized sequence). After IH (immediately and after 3 h), hypoxic and HCVR increased, whereas the VRT-CO2 dropped. No such changes were observed on the placebo day. Systolic and diastolic blood pressure increased, whereas blood lactate decreased after IH. Despite exposure to hypoxia, BRS remained unchanged. Repeated exposures to hypoxia over 1 day induced an initial adaptation to hypoxia, with improvement in respiratory reflexes. Prolonging the exposure to IH (>2 weeks) in type 1 diabetic patients will be a matter for further studies.

Baroreflex sensitivity and its response to deep breathing predict increase in blood pressure in type 1 diabetes in a 5-year follow-up.

OBJECTIVE: We have recently demonstrated that early autonomic dysfunction, defined as low baroreflex sensitivity (BRS), could be functional and reversible. However, potential temporal changes in BRS have not yet been addressed by longitudinal studies in type 1 diabetes. Moreover, it is not known whether low BRS predisposes to hypertension or other nonfatal diabetes complications. RESEARCH DESIGN AND METHODS: We conducted a 5-year prospective study including 80 patients with type 1 diabetes. We measured ambulatory blood pressure and autonomic function tests. BRS was assessed by six different methods during spontaneous, controlled, and slow deep breathing at baseline and follow-up. RESULTS: Spontaneous BRS declined over time (BRS(average) 16.2 ± 0.8 vs. 13.2 ± 0.8 ms/mmHg; P < 0.01), but the change was not significant when adjusted for time of follow-up. Low BRS at baseline did not progress to cardiac autonomic neuropathy but predicted an increase in the nighttime systolic blood pressure (BRS(average) r = -0.37; P < 0.05). Additionally, BRS response to deep breathing at baseline predicted an increase in 24-h ambulatory blood pressure (BRS-αLF r = 0.323-0.346; P < 0.05). CONCLUSIONS: The decline in spontaneous BRS over time in patients with type 1 diabetes seems to be due to normal aging, which supports a functional etiology behind early autonomic derangements. Decreased resting BRS and the magnitude of improvement by deep breathing may be due to sympathovagal imbalance, a well-known mechanism in the development of hypertension. Early interventions aiming to reduce sympathetic overactivity in patients with low BRS might delay the development of hypertension.