A Scoping Review of Strategies for the Prevention of Hip Fracture in Elderly Nursing Home Residents

Background

Elderly nursing home residents are at increased risk of hip fracture; however, the efficacy of fracture prevention strategies in this population is unclear.

Objective

We performed a scoping review of randomized controlled trials of interventions tested in the long-term care (LTC) setting, examining hip fracture outcomes.

Methods

We searched for citations in 6 respective electronic searches, supplemented by hand searches. Two reviewers independently reviewed all citations and full-text papers; consensus was achieved on final inclusion. Data was abstracted in duplicate.

Findings

We reviewed 22,349 abstracts or citations and 949 full-text papers. Data from 20 trials were included: 7 - vitamin D (n = 12,875 participants), 2 - sunlight exposure (n = 522), 1 - alendronate (n = 327), 1 - fluoride (n = 460), 4 – exercise or multimodal interventions (n = 8,165), and 5 - hip protectors (n = 2,594). Vitamin D, particularly vitamin D₃ ≥800 IU orally daily, reduced hip fracture risk. Hip protectors reduced hip fractures in included studies, although a recent large study not meeting inclusion criteria was negative. Fluoride and sunlight exposure did not significantly reduce hip fractures. Falls were reduced in three studies of exercise or multimodal interventions, with one study suggesting reduced hip fractures in a secondary analysis. A staff education and risk assessment strategy did not significantly reduce falls or hip fractures. In a study underpowered for fracture outcomes, alendronate did not significantly reduce hip fractures in LTC.

Conclusions

The intervention with the strongest evidence for reduction of hip fractures in LTC is Vitamin D supplementation; more research on other interventions is needed.     

Hypohydration and prior heat stress exacerbates decreases in cerebral blood flow velocity during standing.

Hypohydration is associated with orthostatic intolerance; however, little is known about cerebrovascular mechanisms responsible. This study examined whether hypohydration reduces cerebral blood flow velocity (CBFV) in response to an orthostatic challenge. Eight subjects completed four orthostatic challenges (temperate conditions) twice before (Pre-EU and Pre-Hyp) and following recovery from passive heat stress ( approximately 3 h at 45 degrees C, 50% relative humidity, 1 m/s air speed) with (Post-EU) or without (Post-Hyp) fluid replacement of sweat losses (-3% body mass loss). Measurements included CBFV, mean arterial pressure (MAP), heart rate (HR), end-tidal CO(2), and core and skin temperatures. Test sessions included being seated (20 min) followed by standing (60 s) then resitting (60 s) with metronomic breathing (15 breaths/min). CBFV and MAP responses to standing were similar during Pre-EU and Pre-Hyp. Standing Post-Hyp exacerbated the magnitude (-28.0 +/- 1.4% of baseline) and duration (9.0 +/- 1.6 s) of CBFV reductions and increased cerebrovascular resistance (CVR) compared with Post-EU (-20.0 +/- 2.1% and 6.6 +/- 0.9 s). Standing Post-EU also resulted in a reduction in CBFV, and a smaller decrease in CVR compared with Pre-EU. MAP decreases were similar for Post-EU (-18 +/- 4 mmHg) and Post-Hyp (-21 +/- 5 mmHg) from seated to standing. These data demonstrate that despite similar MAP decreases, hypohydration, and prior heat stress (despite apparent recovery) produce greater CBFV reduction when standing. These observations suggest that hypohydration and prior heat stress are associated with greater reductions in CBFV with greater CVR, which likely contribute to orthostatic intolerance.     

Role of core temperature as a stimulus for cold acclimation during repeated immersion in 20 degrees C water.

The relative importance of skin vs. core temperature for stimulating cold acclimation (CA) was examined by 5 wk of daily 1-h water immersions (20 degrees C) in resting (RG) and exercising (EG) subjects. Rectal temperature fell (0.8 degrees C; P < 0.05) during immersion only in RG. Skin temperature fell (P < 0.05) similarly in both groups. Physiological responses during cold-air exposure (90 min, 5 degrees C) were assessed before and after CA. Body temperatures and metabolic heat production were similar in both groups with no change due to CA. Cardiac output was lower (P < 0.05) in both groups post-CA (10.4 +/- 1.2 l/min) than pre-CA (12.2 +/- 1. 0 l/min), but mean arterial pressure was unchanged (pre-CA 107 +/- 2 mmHg, post-CA 101 +/- 2 mmHg). The increase in norepinephrine was greater (P < 0.05) post-CA (954 +/- 358 pg/ml) compared with pre-CA (1,577 +/- 716 pg/ml) for RG, but CA had no effect on the increase in norepinephrine for EG (pre-CA 1,288 +/- 438 pg/ml, post-CA 1,074 +/- 279 pg/ml). Skin temperature reduction alone may be a sufficient stimulus during CA for increased vasoconstrictor response, but core temperature reduction appears necessary to enhance sympathetic activation during cold exposure.     

Thermoregulatory responses to upper body exercise

The purpose of this study was to compare thermoregulatory responses between upper body and lower body exercise. Nine male subjects performed 60 min of arm crank (AC) and cycle (CY) exercise at the same absolute intensity (oxygen uptake = 1.61 X min-1) and at the same relative intensity (60% of ergometer specific peak oxygen uptake) in a temperate (24 degrees C, 20% rh) environment. During the absolute intensity experiments, rectal temperature and sweating rate responses were essentially the same for both modes of exercise. In addition, no differences were found for chest, back, arm, or thigh skin temperatures, but calf skin temperature was significantly (P less than 0.05) lower during arm crank than cycle exercise. During the relative intensity experiments, thermoregulatory responses were lower during arm crank than cycle exercise. In addition, we found no difference between esophageal and rectal temperature values elicited by arm crank exercise. These results indicate that the examined thermoregulatory responses are independent of the skeletal muscle mass employed and dependent upon the absolute metabolic intensity.     

Homologies of the adductor mandibulae muscles in Tetraodontiformes as indicated by nerve branching patterns

Homologies of the adductor mandibulae muscles in eight families of Tetraodontiformes were hypothesized from the branching patterns of ramus mandibularis trigeminus. Insertions of the muscles to the upper or lower jaw were weak indicators of homology, migrations of the sites occurring frequently in A1, A2, A2, and A3. In monacanthids, tetraodontids, and diodontids, A1 tended to be split into numerous subsections, whereas in aracanids and ostraciids, A3 was highly developed, comprising three or four subsections. In tetraodontids, A2 was found to be a composite of A1 subsection and A2. The methods of and limits to applying nerve branching patterns to muscle homology are discussed. A new naming system that reflects both muscle homologies and insertions is proposed.     

Thermoregulation during cold exposure: effects of prior exercise.

This study examined whether acute exercise would impair the body's capability to maintain thermal balance during a subsequent cold exposure. Ten men rested for 2 h during a standardized cold-air test (4.6 degrees C) after two treatments: 1) 60 min of cycle exercise (Ex) at 55% peak O(2) uptake and 2) passive heating (Heat). Ex was performed during a 35 degrees C water immersion (WI), and Heat was conducted during a 38.2 degrees C WI. The duration of Heat was individually adjusted (mean = 53 min) so that rectal temperature was similar at the end of WI in both Ex (38.2 degrees C) and Heat (38.1 degrees C). During the cold-air test after Ex, relative to Heat 1) rectal temperature was lower (P < 0.05) from minutes 40-120, 2) mean weighted heat flow was higher (P < 0.05), 3) insulation was lower (P < 0.05), and 4) metabolic heat production was not different. These results suggest that prior physical exercise may predispose a person to greater heat loss and to experience a larger decline in core temperature when subsequently exposed to cold air. The combination of exercise intensity and duration studied in these experiments did not fatigue the shivering response to cold exposure.     

Exertional fatigue, sleep loss, and negative energy balance increase susceptibility to hypothermia

The purpose ofthis study was to determine how chronic exertional fatigue and sleepdeprivation coupled with negative energy balance affectthermoregulation during cold exposure. Eight men wearing only shortsand socks sat quietly during 4-h cold air exposure (10°C)immediately after (<2 h, A) they completed 61 days of strenuousmilitary training (energy expenditure ~4,150 kcal/day, energy intake~3,300 kcal/day, sleep ~4 h/day) and again after short (48 h, SR)and long (109 days, LR) recovery. Body weight decreased 7.4 kg frombefore training to A, then increased 6.4 kg by SR, with an additional6.4 kg increase by LR. Body fat averaged 12% during A and SR andincreased to 21% during LR. Rectal temperature(T_re) was lower before andduring cold air exposure for A than for SR and LR.T_re declined during cold exposurein A and SR but not LR. Mean weighted skin temperature(_sk)during cold exposure was higher in A and SR than in LR. Metabolic rate increased during all cold exposures, but it was lower during A and LRthan SR. The mean body temperature (0.67 T_re + 0.33 _sk) threshold for increasing metabolism was lower during A than SR and LR.Thus chronic exertional fatigue and sleep loss, combined withunderfeeding, reduced tissue insulation and blunted metabolic heatproduction, which compromised maintenance of body temperature. A shortperiod of rest, sleep, and refeeding restored the thermogenic responseto cold, but thermal balance in the cold remained compromised untilafter several weeks of recovery when tissue insulation had beenrestored.

     

Determination of maximal aerobic power during upper-body exercise

The purpose of this investigation was to evaluate four protocols for their effectiveness in eliciting maximal aerobic power (peak VO2) during arm-crank exercise. Comparisons were made 1) between a continuous (CON) and an intermittent (INT) protocol (both employed a crank rate of 50 rpm) and 2) among the CON protocols employing crank rates of 30, 50, or 70 rpm. For the first group of experiments no significant (P greater than 0.05) differences were found between the CON and INT protocols for peak VO2, maximal pulmonary ventilation (VEmax), maximal heart rate (HRmax), or maximal blood lactate (LAmax) responses. For the second group of experiments, the CON-50 was compared with the CON-30 and CON-70 protocols. In comparison to the CON-50, significantly higher peak VO2 (+10%) and VEmax (+14%) responses were elicited by the CON-70 protocol, whereas significantly lower peak VO2 (-11%), VEmax (-23%), HRmax (-8%), and LAmax (-29%) responses were elicited by the CON-30 protocol. Of the arm-crank protocols examined the combination of a continuous design and a crank rate of 70 rpm provided the most effective protocol to elicit peak VO2 values.     

Effects of pyridostigmine bromide on human thermoregulation during cold water immersion

This study examined the effects of an oral 30-mg dose of pyridostigmine bromide (PYR) on thermoregulatory and physiological responses of men undergoing cold stress. Six men were immersed in cold water (20 degrees C) for up to 180 min on two occasions, once each 2 h after ingestion of PYR and 2 h after ingestion of a placebo. With PRY, erythrocyte cholinesterase inhibition was 33 +/- 12% (SD) 110 min postingestion (10 min preimmersion) and 30 +/- 7% at termination of exposure (mean 117 min). Percent cholinesterase inhibition was significantly related to lean body mass (r = -0.91, P less than 0.01). Abdominal discomfort caused termination in three of six PYR experiments but in none of the control experiments (mean exposure time 142 min). During immersion, metabolic rate, ventilatory volume, and respiratory rate increased significantly (P less than 0.05) over preimmersion levels and metabolic rate increased with duration of immersion (P less than 0.01) in both treatment but did not differ between conditions. PYR had no significant effect on rectal temperature, mean body temperature, thermal sensations, heart rate, plasma cortisol, or change in plasma volume. It was concluded that a 30-mg dose of PYR does not increase an individual's susceptibility to hypothermia during cold water immersion; however, in combination with cold stress, PYR may result in marked abdominal cramping and limit cold tolerance.     

Postsynaptic density antigens: preparation and characterization of an antiserum against postsynaptic densities

Long-term immunization of rabbits with postsynaptic densities (PSD) from bovine brain produced an antiserum specific for PSD as judged by binding to subcellular fractions and immunohistochemical location at the light and electron microscope levels. (a) The major antigens of bovine PSD preparations were three polypeptides of molecular weight 95,000 (PSD-95), 82,000 (PSD-82), and 72,000 (PSD-72), respectively. Antigen PSD-95, also present in mouse and rat PSDs was virtually absent from cytoplasm, myelin, mitochondria, and microsomes from rodent or bovine brain. Antigens PSD-82 and PSD-72 were present in all subcellular fractions from bovine brain, especially in mitochondria, but were almost absent from rodent brain. The antiserum also contained low-affinity antibodies against tubulin. (b)Immunohistochemical studies were performed in mouse and rat brain, where antigen PSD-95 accounted for 90 percent of the antiserum binding after adsorption with purified brain tubulin. At the light microscope level, antibody binding was observed only in those regions of the brain where synapses are known to be present. No reaction was observed in myelinated tracts, in the neuronal cytoplasm, or in nonneuronal cells. Strong reactivity was observed in the molecular layer of the dentate gyrus, stratum oriens and stratum radiatum of the hippocampus, and the molecular layer of the cerebellum. Experimental lesions, such as ablation of the rat entorhinal cortex or intraventricular injection of kainic acid, which led to a major loss of PSD in well- defined areas of the hippocampal formation, caused a correlative decrease in immunoreactivity in these areas. Abnormal patterns of immunohistochemical staining correlated with abnormal synaptic patterns in the cerebella of reeler and staggerer mouse mutants. (c) At the electron microscopic level, immunoreactivity was detectable only in PSD. The antibody did not bind to myelin, mitochondria or plasma membranes. (d) The results indicate that antigen PSD-95 is located predominantly or exclusively in PSD and can be used as a marker during subcellular fractionation. Other potential uses include the study of synaptogenesis, and the detection of changes in synapse number after experimental perturbations of the nervous system.