All pedicle screws at the caudal end of the construct should be protected by a supplemental laminar hook.
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Biomedical subjects
Publications and source records attributed to C E Johnston.
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BACKGROUND: Both ethanol ingestion and hyperthermia contribute to orthostatic intolerance (OI). HYPOTHESIS: Since ethanol has been cited as a major risk factor for hyperthermia-related deaths, we hypothesized that ethanol exacerbates OI induced by hyperthermia. METHODS: There were seven subjects (four males, three females) rendered hyperthermic (esophageal temperature = 39 degrees C) in a 40 degrees C water bath on two separate days: Condition 1) Control (juice ingestion); and Condition 2) Ethanol [ethanol (1 ml x kg(-1) body mass) and juice ingestion]. To test for OI, 5-min supine periods were followed by 5-min 63 degrees head-up tilts prior to and following immersion. BPs, heart rate and esophageal temperatures were monitored throughout the experiments. RESULTS: For first and second post-immersion tilts, mean arterial BP (MAP) during tilting increased by 5.9 +/- 3.6 (SE) and 9.8 +/- 2.6 mm Hg in the control condition, while it decreased by 7.9 +/- 5.8 and 0.6 +/- 4.3 mm Hg in the ethanol condition. This gave significantly lower MAP (ethanol vs. control) of 63.6 +/- 3.1 vs. 71.8 +/- 4.5 mm Hg (p < 0.05) for the first and 79.6 +/- 2.3 vs. 86.7 +/- 4.4 mm Hg (p < 0.05) for the second post-immersion tilts. These values were all significantly less (p < 0.05) than normothermic tilted values of 94.7 +/- 4.7 mm Hg in the ethanol and 93.6 +/- 2.9 mm Hg in the control condition. Prior to warm water immersion, subjects tolerated all head-up tilts. In the control condition, only one subject experienced orthostatic intolerance following the first post-heating tilt and no intolerance was experienced following 30 min post-heating. However, during the ethanol condition, 4 subjects experienced orthostatic intolerance following the first tilt with episodes of intolerance lasting as long as 80 min (8 supine/tilt cycles). CONCLUSION: Ethanol ingestion prolonged and increased the magnitude of OI in hyperthermic subjects. This may at least partly explain why ethanol is a major risk factor in hyperthermia-related deaths.
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PURPOSE: This study was conducted to test the hypothesis that clonidine produces a dose-dependent increase in the sweating threshold and dose-dependent decreases in vasoconstriction and shivering thresholds. METHODS: Six healthy subjects (two female) were studied on four days after taking clonidine in oral doses of either 0 (control), 3, 6 or 9 micrograms.kg-1. The order followed a balanced design in a double-blind fashion. Oesophageal temperature and mean skin temperature (from 12 sites) were measured. Subjects were seated in 37 degrees C water which was gradually warmed until sweating occurred (sweat rate increased above 50 g.m-2.h-1). The water was then cooled gradually until thresholds for vasoconstriction (onset of sustained decrease in fingertip blood flow) and shivering (sustained elevation in metabolism) were determined. Thresholds were then referred to as the core temperature, adjusted to a designated mean skin temperature of 33 degrees C. RESULTS: High dose clonidine similarly decreased the adjusted core temperature thresholds for vasoconstriction by 1.16 +/- 0.30 degrees C and for shivering by 1.63 +/- 0.23 degrees C (P < 0.01). The dose response effects were linear for both cold responses with vasoconstriction and shivering thresholds decreasing by 0.13 +/- 0.05 and 0.19 +/- 0.09 degree C.microgram-1 respectively (P < 0.0001). The sweating threshold was unaffected by clonidine, however the interthreshold range between sweating and vasoconstriction thresholds increased from control (0.19 +/- 0.48 degree C) to high dose clonidine (1.31 +/- 0.54 degrees C). CONCLUSION: The decreases in core temperature thresholds for cold responses and increased interthreshold range are consistent with the effects of several anaesthetic agents and opioids and is indicative of central thermoregulatory inhibition.
We demonstrated previously that esophageal temperature (T(es)) remains elevated by approximately 0.5 degrees C for at least 65 min after intense exercise. Following exercise, average skin temperature (T(avg)) and skin blood flow returned rapidly to pre-exercise values even though T(es) remained elevated, indicating that the T(es) threshold for vasodilation is elevated during this period. The present study evaluates the hypothesis that the threshold for sweating is also increased following intense exercise. Four males and three females were immersed in water (water temperature, T(w) = 42 degrees C) until onset of sweating (Immersion 1), followed by recovery in air (air temperature, T(a) = 24 degrees C). At a T(a) of 24 degrees C, 15 min of cycle ergometry (70% VO2max) (Exercise) was then followed by 30 min of recovery. Subjects were then immersed again (T(w) = 42 degrees C) until onset of sweating (Immersion 2). Baseline T(es) and T(skavg) were 37.0 (0.1) degrees C and 32.3 (0.3) degrees C, respectively. Because the T(skavg) at the onset of sweating was different during Exercise [30.9 (0.3) degrees C] than during Immersion 1 and Immersion 2 [36.8 (0.2) degrees C and 36.4 (0.2) degrees C, respectively] a corrected core temperature, T((es) (calculated)), was calculated at a single designated skin temperature, T((sk)(designated)), as follows: T((es)(calculated)) = T(es) + [beta/(1-beta)][T(skavg)-T((sk)(designated))]. The T((sk)(designated)) was set at 36.5 degrees C (mean of Immersion 1 and Immersion 2 conditions) and beta represents the fractional contribution of T(skavg) to the sweating response (beta for sweating = 0.1). While T((es)(calculated)) at the onset of sweating was significantly lower during exercise [36.7 (0.2) degrees C] than during Immersion 1 [37.1 (0.1) degrees C], the threshold of sweating during Immersion 2 [37.3 (0.1) degrees C] was greater than during both Exercise and Immersion 1 (P < 0.05). We conclude that intense exercise decreases the sweating threshold during exercise itself, but elicits a subsequent short-term increase in the resting sweating threshold.
During severe hypothermia, shivering is absent. To simulate severe hypothermia, shivering in eight mildly hypothermic subjects was inhibited with meperidine (1.5 mg/kg). Subjects were cooled twice (meperidine and control trials) in 8 degrees C water to a core temperature of 35.9 +/- 0.5 (SD) degrees C, dried, and then placed in sleeping bags. Meperidine caused a 3.2-fold increase in core temperature afterdrop (1.1 +/- 0.6 vs. 0.4 +/- 0.2 degree C), a 4.3-fold increase in afterdrop duration (89.4 +/- 31.4 vs. 20.9 +/- 5.7 min), and a 37% decrease in rewarming rate (1.2 +/- 0.5 vs. 1.9 +/- 0.9 degrees C/h). Meperidine inhibited overt shivering. Oxygen consumption, minute ventilation, and heart rate decreased after meperidine injection but subsequently returned toward preinjection values after 45 min postimmersion. This was likely due to the increased thermoregulatory drive with the greater afterdrop and the short half-life of meperidine. These results demonstrate the effectiveness of shivering heat production in attenuating the postcooling afterdrop of core temperature and potentiating core rewarming. The meperidine protocol may be valuable for comparing the efficacy of various hypothermia rewarming methods in the absence of shivering.
We recently developed a nonshivering human model for severe hypothermia by using meperidine to inhibit shivering in mildly hypothermic subjects. This thermal model was used to evaluate warming techniques. On three occasions, eight subjects were immersed for approximately 25 min in 9 degrees C water. Meperidine (1.5 mg/kg) was injected before the subjects exited the water. Subjects were then removed, insulated, and rewarmed in an ambient temperature of -20 degrees C with either 1) spontaneous rewarming (control), 2) inhalation rewarming with saturated air at approximately 43 degrees C, or 3) forced-air warming. Additional meperidine (to a maximum cumulative dose of 2.5 mg/kg) was given to maintain shivering inhibition. The core temperature afterdrop was 30-40% less during forced-air warming (0.9 degree C) than during control (1.4 degrees C) and inhalation rewarming (1.2 degrees C) (P < 0.05). Rewarming rate was 6- to 10-fold greater during forced-air warming (2.40 degrees C/h) than during control (0.41 degree C/h) and inhalation rewarming (0.23 degree C/h) (P < 0.05). In nonshivering hypothermic subjects, forced-air warming provided a rewarming advantage, but inhalation rewarming did not.
A retrospective study of 2442 patients who had idiopathic scoliosis was performed to determine the prevalence of back pain and its association with an underlying pathological condition. Five hundred and sixty (23 per cent) of the 2442 patients had back pain at the time of presentation, and an additional 210 (9 per cent) had back pain during the period of observation. There was a significant association between back pain and an age of more than fifteen years, skeletal maturity (a Risser sign of 2 or more), postmenarchal status, and a history of injury. There was no association with gender, family history of scoliosis, limb-length discrepancy, magnitude or type of curve, or spinal alignment. At the latest follow-up evaluation, 324 (58 per cent) of the 560 patients who had had back pain at presentation had no additional symptoms. Forty-eight (9 per cent) of the 560 patients who had back pain had an underlying pathological condition: twenty-nine patients had spondylolysis or spondylolisthesis, nine had Scheurmann kyphosis, five had a syrinx, two had a herniated disc, one had hydromyelia, one had a tethered cord, and one had an intraspinal tumor. A painful left thoracic curve or an abnormal neurological finding was most predictive of an underlying pathological condition, although only eight of the thirty-three patients who had such findings were found to have such a condition. When a patient with scoliosis has back pain, a careful history should be recorded, a thorough physical examination should be performed, and good-quality plain radiographs should be made. If this initial evaluation reveals normal findings, a diagnosis of idiopathic scoliosis can be made, the scoliosis can be treated appropriately, and non-operative treatment can be initiated for the back pain. It is not necessary to perform extensive diagnostic studies to evaluate every patient who has scoliosis and back pain.
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Elevated blood alcohol levels are often seen in hypothermia and hyperthermia related deaths, leading to the belief that alcohol renders humans poikilothermic. We examined the core temperature (Tco) thresholds for sweating, vasoconstriction and shivering as well as core cooling rates of seven subjects immersed in 28 degrees C water. On two separate days, subjects exercised on an underwater cycle ergometer to elevate Tco above the sweating threshold. They then rested and cooled until they shivered vigorously. Subjects drank orange juice (7 ml.kg-1) prior to immersion during the control trial and 1 ml.kg-1 absolute ethanol, added to orange juice in a 1:6 ratio, during the alcohol trial. Mean blood alcohol concentration (breath analysis) was 0.097 +/- 0.010 g% at the start of cooling and 0.077 +/- 0.008 g% at the end of the cooling period. Alcohol lowered the vasoconstriction threshold by 0.32 +/- 0.2 degrees C and elevated finger tip blood flow, but had no effect on thresholds for sweating and shivering or core cooling rate. Considering these minor effects it is unlikely that moderate alcohol consumption predisposes individuals to hypothermia or hyperthermia via impaired thermoregulation, but rather likely due to behavioral factors.
An underwater cycle ergometer was designed consisting of an aluminum cycle frame in water connected with a 1:1 gear ratio to a mechanically braked standard cycle ergometer supported above the water. Three progressive maximal exercise tests were performed (n = 10): (a) the underwater ergometer in water (UEW), (b) underwater ergometer in air (UEA), and (c) a standard cycle ergometer in air (SEA). At submaximal power outputs, oxygen consumption (VO2) and heart rate (HR) were generally lower in the SEA condition (p < .05), indicating that exercise in the upright position was more efficient. Exercise in water (UEW) resulted in lower total exercise duration, maximal HR, and maximal Tes than in air conditions. The upright position (SEA) resulted in greater total exercise duration and maximal power output than the semirecumbent positions. Because of positional differences between the standard and underwater ergometers, air-water comparisons should be made by using the underwater ergometer in water and on land.
Hypoxia lowers the basic thermoregulatory responses of animals and humans. In cold-exposed animals, hypoxia increases core temperature (Tco) cooling rate and suppresses shivering thermogenesis. In humans, the experimental effects of hypoxia on thermoregulation are equivocal. Also, the effect of hypoxia has not been separated from that of hypocapnia consequent to hypoxic hyperventilation. To determine the isolated effects of hypoxia on warm and cold thermoregulatory responses and core cooling during mild cold stress, we examined the Tco thresholds for sweating, vasoconstriction, and shivering as well as the core cooling rates of eight subjects immersed in 28 degrees C water under eucapnic conditions. On 2 separate days, subjects exercised on an underwater cycle ergometer to elevate Tco above the sweating threshold. They then rested and cooled until they shivered vigorously. Subjects inspired humidified room air during the control trial. For the eucapnic hypoxia trial, they inspired 12% O2-balance N2 with CO2 added to maintain eucapnia. Eucapnic hypoxia lowered the Tco thresholds for vasoconstriction and shivering by 0.14 and 0.19 degrees C, respectively, and increased core cooling rate by 33% (1.83 vs. 1.38 degrees C/h). These results demonstrate that eucapnic hypoxia enhances the core cooling rate in humans during mild cold stress. This may be attributed in part to a delay in the onset of vasoconstriction and shivering as well as increased respiratory heat loss during hypoxic hyperventilation.
Four patients who had Larsen syndrome and cervical kyphosis were managed operatively and followed for an average of seventy months (range, forty to ninety-two months). The preoperative cervical kyphosis ranged from 35 to 65 degrees. The patients had had a posterior cervical arthrodesis alone when they were infants, at an average age fo fourteen months (range, ten to sixteen months). In three infants, the kyphosis either stabilized (one patient) or reversed into lordosis (two patients). Thus, the kyphosis corrected gradually by continued anterior growth in the presence of a solid posterior fusion. In the fourth infant, the kyphosis progressed to 110 degrees because of pseudarthrosis. This child had anterior decompression and arthrodesis for an acute neurological deficit. We believe that cervical kyphosis is sometimes present but not diagnosed in patients who have Larsen syndrome. Early diagnosis followed by operative stabilization should help such patients avoid neurological deficits. Posterior cervical arthrodesis alone, performed in infancy, provided stability and the opportunity for the gradual correction of the deformity by continued anterior growth in three of our four patients.
BACKGROUND: Hypercapnia, which may be encountered during diving operations or by patients under general anesthesia with spontaneous respiration, alters the basic thermoregulatory responses of animals and humans. In cold-exposed animals, 3-10% inspired CO2 impairs thermal homeostasis by attenuating shivering and promoting heat loss through peripheral vasodilation. Experimental results with humans are equivocal. PURPOSE: To determine the effects of hypercapnia on warm and cold thermoregulatory responses and core cooling rates during mild cold stress, we examined the core temperature (TCO) thresholds for sweating, vasoconstriction and shivering, as well as core cooling rates of eight subjects immersed in 28 degrees C water under hypercapnic conditions. METHODS: On two separate days, subjects exercised on an underwater cycle ergometer to elevate TCO above the sweating threshold. They then rested and cooled until they shivered vigorously. Subjects inspired humidified room air during the control trial and 4% CO2/20.9% O2/balance N2 during the hypercapnia trial. RESULTS: Hypercapnia lowered the threshold for shivering by 0.13 degrees C and increased the core cooling rate by 0.35 degrees C.h-1 (25%). Minute ventilation was approximately 12.0 L.min-1 throughout cooling during control and increased from 25.3 to 28.7 L.min-1 during hypercapnia. CONCLUSIONS: Therefore, hypercapnia enhances the core cooling rate during mild cold stress. This may be attributed in part to a delay in shivering onset, as well as increased respiratory heat loss during hypercapnic hyperventilation.
STUDY DESIGN: Three segment (L3-L5) pedicle screw constructs were implanted in caprine spines, and the resulting ankylosis evaluated mechanically and compared 12 weeks after surgery. OBJECTIVES: To determine if a construct of maximal stiffness could impair the biologic process of spinal arthrodesis by "stress-shielding." SUMMARY OF BACKGROUND DATA: Fusion mass stiffness is believed to be enhanced by increasing construct stiffness, although previous studies have used semirigid, nonconstrained constructs, which lose stiffness through cyclical loading. Device-related osteoporosis, reported to occur with stiff, constrained implants, may be more related to the presence of fusion induced by the implants rather than the implants themselves. METHODS: In 15 goats, L3-L5 segments were instrumented with pedicle screws, and four different diameters of rods (3.2 cm, 4.8 cm, 6.4 mm, and no rods) were implanted as longitudinal connections to vary the stiffness of the constructs. After 12 weeks, animals were killed and the segments were tested to determine their stiffness. RESULTS: In lateral bending, spines "fused" with rods (any size) were significantly stiffer (P = 0.03) than nonrodded spines. There was a trend toward stiffer segments with larger rods (4.8 cm or 6.4 mm) compared with 3.2 mm or no rods. There was a highly significant (P < 0.0001) increase in stiffness of all operated (rodded or nonrodded) segments compared with unoperated controls. CONCLUSIONS: The enhancement of segmental stiffness by stiffer constructs was confirmed, suggesting a beneficial effect on spinal arthrodesis by increasing stiffness. Stress shielding could not be shown.
The bony pathoanatomy of clubfoot has been assessed by a three dimensional reconstruction of transverse CT images obtained from 27 feet in children aged 3-10 years. Principal axes of the bones were determined to quantitate interosseous deformity, while visual inspection of the reconstructed images demonstrated intraosseous deformity. "Medial spin" and midfoot adduction were analyzed on the AP view of the foot ("top" view), while hindfoot pronosupination was analyzed on the AP view of the ankle (posterior view). This technique allows visualization of deformities which normally cannot be analyzed on plain radiographs, and also shows that a variety of interosseous relationships make up the clinical entity known as clubfoot. Abnormal talar pronation ("intorsion") was an unexpected finding of this three dimensional analysis.
BACKGROUND: Whole body cooling impairs manual arm performance. The independent contributions of local (peripheral) and/or whole body (central) cooling are not known. Therefore, a protocol was developed in which the arm and the rest of the body could be independently cooled. METHODS: Biceps temperature (Tmus), at a depth of 20 mm, and esophageal temperature (Tes) were measured. Six subjects were immersed to the clavicles in a tank (body tank) of water under 3 conditions: 1) cold body-cold arm (CB-CA); 2) warm body-cold arm (WB-CA); and 3) cold body-warm arm (CB-WA). In the latter two conditions, subjects placed their dominant arm in a separate (arm) tank. Water temperature (Tw) in each tank was independently controlled. In conditions requiring cold body and/or cold arm, Tw in the appropriate tanks was 8 degrees C. In conditions requiring warm body and/or warm arm, Tw in the appropriate tanks was adjusted between 29 and 38 degrees C to maintain body/arm temperature at baseline values. A battery of 6 tests, requiring fine or gross motor movements, were performed immediately before immersion and after 15, 45, and 70 minutes of immersion. RESULTS: In CB-CA, Tes decreased from an average of 37.2 to 35.6 degrees C and Tmus decreased from 34.6 to 22.0 degrees C. In WB-CA, Tmus decreased to 18.1 degrees C (Tes = 37.1 degrees C), and in CB-WA, Tes decreased to 35.8 degrees C (Tmus = 34.5 degrees C). By the end of immersion, there were significant decrements (43-85%) in the performance of all tests in CB-CA and WB-CA (p < 0.0002); scores for each test were similar in these two conditions. There was no significant change in scores throughout the CB-WA condition. In both conditions with arm cooling (i.e., WB-CA and CB-CA), Tmus accounted for 85-98% of the variance in all tests. When the core was cooled in the CB-WA condition, Tes was significantly correlated to scores in only two tests (accounted for 90 and 93% of the variance) although the actual effect was small. In the CB-CA condition, partial correlations indicated that Tes accounted for 4-10% of the variance in scores of 4 tests. CONCLUSIONS: We conclude that cooling of the body and/or the arm elicits large decrements in finger, hand and arm performance. The decrements are due almost entirely to the local effects of arm tissue cooling.