Noninvasive assessment of regional albumin extravasation in porcine septic shock

In order to study noninvasively the regional distribution of changes in microvascular albumin flux in septic shock, ¹³¹I human serum albumin and ^98mTc red blood cells were injected IV into anesthetized pigs randomized to receive saline (n = 4) or live E. coli bacteria 3 × 10⁸ × kg⁻¹ IV (n = 8). Images of thorax, abdomen, and left hindlimb were obtained using a gamma camera and a computer. Septic pigs developed pulmonary hypertension and low cardiac output circulatory shock. Hematocrit rose and plasma colloid osmotic pressure fell. Regions of interest were drawn in the ^99mTc images. For each region we calculated an albumin leak index. The albumin leak index over the lungs was higher in sepsis than in controls (1.62 ± 0.42 × 10⁻³ v 0.45 ± 0.05 × 10-3 × min⁻¹, P < .005), even when divided by the pulmonary intravascular filtration pressure, incorporating hydrostatic and colloid osmotic pressures (P < .01). The index was also higher in abdominal regions (for the peripheral abdomen, 6.07 ± 2.98 × 10⁻³ v 0.40 ± 0.72 × 10⁻³ × min⁻¹, P < .005), but not in the hindlimb. In sepsis, the albumin leak index increased more in the abdomen than in the lungs (P < .05). We conclude that in porcine septic shock pulmonary microvascular permeability is increased, but the microvascular albumin flux and thus plasma extravasation increased more in the abdomen than in the lungs.     

Central venous pressure, pulmonary artery occlusion pressure, intrathoracic blood volume, and right ventricular end-diastolic volume as indicators of cardiac preload

Central venous pressure (CVP), pulmonary artery occlusion pressure (PAOP) and right ventricular end-diastolic volume (RVEDV) are often regarded as indicators of both circulating blood volume and cardiac preload. To evaluate these relationships, the response of each variable to induced volume shifts was tested. The relationships between these variables and cardiac index (CI) and stroke volume index (SVI) was also recorded to assess the utility of each variable as an indicator of cardiac preload. The responses of the new variable intrathoracic blood volume (ITBV) to the same maneuvers was also tested. To examine the effects of changes in cardiac output alone on ITBV, the effects of infusing dobutamine were studied.

Ten anesthetized piglets were studied during conditions of normovolemia, hypovolemia, and hypervolemia. The effects of an infusion of dobutamine were examined under normovolemia and hypovolemia. Cardiac output was measured by thermodilution, and ITBV was measured by double-indicator dilution.

CI was correlated to CVP with r² = .42 (P ≤ .01), to PAOP with r² = .43 (P ≤ 5.01), to RVEDV index with r² = .21 (P ≤ .01), and to ITBV with r² = .78 (P ≤ .01) (pooled absolute values). Bias (mean difference of the percent changes with NORMOVOLEMIA = 100%) ± 1 SD; for SVI - ITBV index was 1 ± 22%, for SVI — CVP it was −128 ± 214%; for SVI — PAOP it was −36 ± 46%; and for SVI -RVEDV index it was 1 ± 29%. Dobutamine infusion increased heart rate (to about 190 × min⁻¹) and CI by 30% in normovolemia and hypovolemia, while ITBV remained basically unchanged.

Under the experimental conditions choosen neither CVP, PAOP, nor RVEDV reliably indicated changes in circulating blood volume, nor were they linearly and tightly correlated to the resulting changes in SVI. ITBV reflected both changes in volume status and the resulting alteration in cardiac output. The possibility that ITBV might be cardiac output-dependent was not supported. ITBV, therefore, shows potential as a clinically useful indicator of overall cardiac preload.     

Lazaroid pretreatment preserves gas exchange in endotoxin-treated dogs

: The lazaroids are a new class of potent free-radical scavengers. We tested whether U-74389G, a lazaroid, could attenuate some of the adverse cardiopulmonary effects of sepsis.

: Dogs were randomized to receive either 10 mg/kg U-74389G (n = 10), or a saline control (n = 11). After baseline measurements of hemodynamics and gas exchange, they were then randomized to receive either 0.2 mg/kg endotoxin or a saline infusion. Measurements of hemodynamics and gas exchange were repeated. The study was concluded 70 minutes after endotoxin infusion and the lungs were then removed for histologic evaluation.

: In endotoxin-treated control animals, P0₂ decreased (278 ± 123 mm Hg to 67 ± 13 mm Hg, P < .05) and intrapulmonary shunt increased (12.9% ± 1.1% to 28.2% ± 11.4%, P < .05) after endotoxin. Pretreatment with U-74389G attenuated the decrease in PO₂ (476 ± 61 mm Hg to 226 ± 143) and the increase in intrapulmonary shunt (12.6% ± 6.1% to 14.3% ± 6.8%) observed after endotoxin. The extent of lung injury and systemic hemodynamics were similar between control or U-74389G-treated dogs.

: A free-radical-scavenger can attenuate the gas exchange defect commonly associated with endotoxin but it does not improve the derangement of systemic hemodynamics.     

Circuit factors in the high cardiac output of sepsis

The increase of cardiac output (CO) in sepsis must be matched by an increase in venous return. Our goal was to determine which of the determinants of venous return are responsible in volume-loaded and nonvolume-loaded pigs with endotoxemia. The determinants include stressed volume, venous compliance (C_v), venous resistance (RVR) and right atrial pressure (Pra). We also tested the effect of the nitric oxide (NO) synthase inhibitor, N^ω-nitro- -arginine-methyl ester (L-NAME) after the hemodynamics with endotoxin stabilized.

Pigs were anesthetized and mechanically ventilated. We measured CO by thermodilution, mean circulatory filling pressure (MCFP) by inflating a balloon in the right atrium, blood volume by dye dilution, and C_v by rapid blood infusions. RVR was calculated from MCFP - Pra/CO). After baseline measurements, we infused 10 μg/(kg x h⁻¹) of Escherichia coli endotoxin. Eight animals also received 30 mL × kg⁻¹ of dextran over the 2 hours (volume treated), and seven did not (no volume). After 2 hours we injected 25 mg × kg⁻¹ of the NO synthase inhibitor, L-NAME, and repeated the measurements.

In volume-treated animals, CO increased from 3.9 ± 0.7 to 5.4 ± 0.8 L x min⁻¹ (P < .05), and blood pressure (BP) fell from 118 ± 9 to 76 ± 12 mmHg. MCFP rose, and there was no change in RVR or C_v, whereas capacitance increased (ie, right shift of pressure-volume curve). Cardiac function (ie, Starling curve) did not change. In no-volume animals, CO fell from 4.47 ± 0.64 to 2.50 ± 0.86 L × min⁻¹, BP from 114 ± 10 to 9 13 mmHg and MCFP fell. Systemic vascular resistance did not change. Cardiac function was markedly depressed, and the heart rate increased from 143 ± 13 to 203 ± 30 beats x min⁻¹. L-NAME restored BP in both groups but also increased RVR and depressed cardiac function.

Changes in vascular tone during endotoxemia are dependent on volume status. The increased cardiac output in volume-treated septic animals occurred because of an increase in stressed volume due to the volume given in combination with a dilated vasculature. L-NAME restored arterial tone but decreased CO because of a rise in RVR and decrease in cardiac function.     

老年髋部骨折术后发生急性肾损伤的临床特点及危险因素分析

目的 探讨老年髋部骨折术后发生急性肾损伤(AKI)的临床特点及危险因素分析.方法 髋部骨折手术患者470例,根据AKI的诊断标准将患者分为非AKI组(276例)和AKI组(194例).检测两组白细胞(WBC)、红细胞(RBC)、血肌酐(SCr)、血尿素氮(BUN)、白蛋白(ALB)、肾小球滤过率(eGFR)、血红蛋白(...     

Treatment with N-acetylcysteine during acute respiratory distress syndrome: A randomized, double-blind, placebo-controlled clinical study

Intravenous N-acetylcysteine (NAC) has been reported to improve systemic oxygenation and reduce the need for ventilatory support in patients with an acute lung injury. In the more serious form, namely established adult respiratory distress syndrome (ARDS) (Pao₂/Fio₂ ≤ 200 mm Hg), we tested the hypothesis that treatment with intravenous NAC may be beneficial.

Respiratory dysfunction was graded daily according to the need for mechanical ventilation and Fio₂ and to the evolution of the lung injury score (LIS) and the Pao₂/Fi0₂ ratio in 42 patients with established ARDS receiving either NAC 190 mg/kg/day or placebo as a continuous intravenous infusion over the first 3 days of their clinical course.

NAC and placebo groups (22 and 20 patients, respectively) were comparable for demographic characteristics, ARDS categories, severity of illness (simplified acute physiology score [SAPS II]) LIS and Pao₂/Fio₂ ratio. Mortality rate was 32% for the NAC and 25% for the placebo group (difference not significant). At admission (day 1), 91% of patients in the NAC and 95% in the placebo group required ventilatory support; at days 2, 3, 5, and 7 after admission, the percentage of patients receiving ventilatory support was not significantly reduced for both groups in comparison with day 1. Moreover, there were no differences between the two groups at the same observation days. In both groups, the Fio₂ was significantly lower and the Pao₂/Fio₂ ratio was significantly higher than the initial values during the evolution (Fio₂ at day 3, P < .01 for NAC and P < .05 for placebo; Pao₂/Fio₂ at day 3: P < .01 for NAC and P < .02 for placebo), but this improvement was similar for both groups and, moreover, the between-group comparison was never significantly different at the various collection days. The LIS decreased significantly in NAC group between days 1 and 3 (2.23 ± 0.62 v 1.76 ± 0.17; P < .05), whereas no changes were observed in the placebo group; at day 5, there was a significant difference between the two groups (1.53 ± 0.21 for the NAC v 2.15 ± 0.19 for the placebo group; P < .05). In the prevalent sepsis category (10 patients in the NAC and 9 in the placebo group), the mortality rate, the need of ventilatory support, the intensive care unit stay, and the Pao₂/Fio₂ evolution did not differ significantly in both subgroups.

In this relatively small group of patients presenting with an established ARDS subsequent to a variety of underlying diseases, intravenous NAC treatment during 72 hours neither improved systemic oxygenation nor reduced the need for ventilatory support oxygenation nor reduced the need for ventilatory support.     

Nitric oxide metabolism in canine sepsis: relation to regional blood flow

To investigate the role of nitric oxide (NO) in early endotoxemia on the systemic and regional blood flow by measuring the plasma nitrite/nitrate (NOx) and blood nitrosyl-hemoglobin (NO-Hb) levels.

This was a prospective, controlled, experimental study conducted in an animal research laboratory on 15 male mongrel dogs. Escherichia coli endotoxin (1 mg/kg) was injected intravenously.

Hepatic, renal, and iliac blood flow and cardiac output (CO) were measured before and 15, 30, 45, 90 and 180 minutes after injection of Escherichia coli endotoxin (1 mg/kg) (n = 6). NOx efflux from the organs was calculated by measuring plasma NOx levels. The arterial blood levels of NO-Hb were also measured (n = 4). As control studies, blood samples from dogs (n = 5) without exposure to endotoxin were assayed at 180 minutes for NOx and NO-Hb. Following endotoxin injection, mean arterial pressure decreased and reached its lowest value at 90 minutes (baseline vs. 90 minutes: 119.1 ± 5.8 vs. 82.5 ± 16.7 mm Hg, P < .0001). Hepatic artery bloodflow increased significantly (baseline vs. 180 minutes: 23.6 ± 12.0 vs. 170.0 ± 68.4 mL/min, P < .0001). There were no significant changes in plasma levels of NOx, uptake or release of NOx across the measured vascular beds, NO-Hb levels at anytime point. In the portal system, the portal vein flow correlated with NOx release (R = 0.69, P < .0001).

In the early phase of endotoxemia in the dog, the significant reduction in systemic vascular resistance and hepatic arterial resistance are not associated with any measurable NOx release in the systemic circulation or the liver.     

冠状动脉钙化积分与冠状动脉疾病及全因性死亡相关性的Meta分析

目的系统评价冠状动脉钙化积分(CACS)与冠状动脉疾病(CAD)及全因死亡事件相关性。方法计算机检索Pubmed、The Cochrane Library、EMbase、CKNI、WanFang Data数据库,搜集CACS与CAD及全因性死亡(All-cause mortality)相关性的队列研究,检索时限从建库至2020年6月。由2名资料员提取文献并进行评价纳入研究的偏倚风险后,采用Stata 14.0软件进行Meta分析。结果纳入11个队列研究,包括59143例被研究者。Meta结果显示:与CACS<10相比,CACS≤100组[HR=2.46,95%CI(1.77,3.41),P=0.000,I^(2)=55.5%]、100     

Heat shock protein (HSP70) expression in septic patients

: This study investigates heat shock protein 70 (HSP₇₀) expression by peripheral blood mononuclear cells (PBMCs) of septic patients admitted to an intensive care unit and examines the possibility of a correlation between HSP₇₀ levels and plasma tumor necrosis factor alpha (TNF-) concentrations. Additionally, we evaluated whether the HSP₇₀ production could be regarded as a prognostic factor for the development of septic shock as well as for patient survival.

: Blood samples of 29 patients were taken 24 hours after the diagnosis of sepsis. HSP₇₀ expression and TNF- level were measured using indirect immunofluorescent analysis and a commercially available enzyme-linked immunosorbent assay method, respectively.

: PBMCs expressed significantly high levels of HSP₇₀ (11.9 ± 5.6 [sd]) compared with those of the healthy control group (3.2 ± 2.1 % positive cells). Such enhanced levels were correlated to plasma TNF- concentrations (r = .99, P < .01). This study failed to demonstrate a relationship between HSP₇₀ production and clinical outcome.

: These findings give further evidence that also in humans, heat shock response is activated during sepsis. The correlation observed between HSP₇₀ overproduction and TNF- plasma concentrations suggests that HSP₇₀ exerts a possible protective effect against TNF- cytotoxicity. Such hypothesis has not been confirmed by our clinical data.     

Ischemia/reperfusion injury to the ileum does not account for the ileal Vo2-Do2 alterations induced by endotoxin

Endotoxin (lipopolysaccharide [LPS])-induced systemic organ injury leads to disruption of normal systemic organ metabolic processes, which are manifest clinically by signs of accelerated anaerobic metabolism (eg, tissue acidosis and hyperlactatemia) and altered Vo₂-Do₂ relationships. The association of increased anaerobic metabolism with Vo₂-Do₂ alterations has led to the notion that ischemia/reperfusion (I/R) injury may be a prerequisite for the development of Vo₂-Do₂ alterations during endotoxemia. However, in contrast to sepsis, in which oxygen consumption is often increased, oxygen consumption is severely decreased after I/R injury. Based on these observations, we hypothesized that I/R injury would result in systemic organ Vo₂-Do₂ alterations, which are distinct from those that occur in sepsis.

We used the in situ autoperfused feline ileal preparation to simultaneously examine microvascular permeability, reflected as the ileal lymph to plasma protein concentration ratio (C_L/C _P), and ileal Vo₂-Do₂ relationships after either intravenous LPS (2.0 mg/kg; N = 5) or I/R injury (n = 5), and in matching controls (n = 5).

As expected, all LPS-treated and I/R-injured animals were found to have extensive ileal histological damage and marked increases in the C_L/C_P compared with controls (0.315 ± 0.009 and 0.329 ± 0.034, respectively, v 0.097 ± 0.009; P < .001, both comparisons). In addition, the critical Do₂ (Do₂c) was elevated, and the critical oxygen extraction was decreased in both the I/R and LPS groups relative to controls. However, as initially hypothesized, the Vo₂ at the critical Do₂ was markedly decreased in the I/R group compared with that of the LPS group.

These data indicate that I/R injury is insufficient to account for the systemic organ Vo₂-Do₂ alterations that occur with LPS injury.     

Increased cardiac output increases lung water in canine permeability pulmonary edema

We investigated the effects of increased cardiac output (CO) on oleic acid pulmonary edema in 14 open-chest, anesthetized, mechanically ventilated dogs. Pulmonary artery wedge pressure (Pawp) was adjusted to approximately 9 mm Hg via a left atrial balloon and CO to 1.7 L · m⁻¹ via systemic arteriovenous fistulas (AVF); five minutes after oleic acid (0.08 mL · kg⁻¹), dogs were randomly divided into two groups, high CO and low CO. In the high CO group, CO was increased by opening the AVFs. Pawp was maintained at 9 mm Hg for four hours in all dogs. The average CO time in the high CO group was 3.9 L · min⁻¹ and 1.3 L · min⁻¹ in the low CO group (P < .01). Lung water accumulation was significantly increased in the high CO group with a wet weight/ body weight ratio of 29 g ò kg⁻¹v 21 g · kg ⁻¹ in the low CO group (P < .004). With time, mean pulmonary artery pressure increased significantly (P < .05) in both groups, but was not different between groups at any time. While pulmonary vascular resistance remained constant in the high CO group, it increased markedly (P < .05) in the low CO group, possibly due to a decrease in pulmonary vascular surface area. The increase in lung water accumulation in the high CO group is probably due to prevention of pulmonary vascular derecruitment and therefore a greater perfused pulmonary vascular surface area.     

Pre-emptive analgesia using intravenous fentanyl plus low-dose ketamine for radical prostatectomy under general anesthesia does not produce short-term or long-term reductions in pain or analgesic use

The aim of the study was to evaluate post-operative pain and analgesic use after pre-operative or post-incisional i.v. fentanyl plus low dose i.v. ketamine vs. a standard treatment receiving i.v. fentanyl but not ketamine. Men undergoing radical prostatectomy under general anesthesia were randomly assigned in a double-blinded manner to one of three groups. Patients received i.v. fentanyl before incision followed by an i.v. bolus dose (0.2 ml kg⁻¹) and an i.v. infusion (0.0025 ml kg⁻¹ min⁻¹) of 1 mg ml⁻¹ ketamine (group 1) or normal saline (groups 2 and 3). Seventy minutes after incision, patients received i.v. fentanyl followed by an i.v. bolus dose (0.2 ml kg⁻¹) and an i.v. infusion (0.0025 ml kg⁻¹ min⁻¹) of saline (groups 1 and 3) or ketamine (group 2). Pain, von Frey pain thresholds, and cumulative morphine consumption using patient-controlled analgesia (PCA) were assessed up to 72 h after surgery. 143 patients completed the study (group 1, n=47; group 2, n=50; group 3, n=46). Cumulative PCA morphine (mean±SD) did not differ significantly among groups (group 1, 92.3±45.9 mg; group 2, 107.2±58.4 mg; group 3, 103.6±50.4 mg; P=0.08 for groups 1 vs. 2, and groups 1 vs. 3). On day 3, the hourly rate (mean±SEM) of morphine consumption was significantly lower (P<0.0009) in group 1 (0.61±0.013 mg h⁻¹) than group 2 (0.86±0.011 mg h⁻¹) and group 3 (0.89±0.008 mg h⁻¹). Pain scores and von Frey pain thresholds did not differ significantly among groups. Two-week and 6-month follow-ups did not reveal significant group differences in pain incidence, intensity, disability or mental health. Pre-operative, low-dose administration of i.v. ketamine did not result in a clinically meaningful reduction in pain or morphine consumption when compared with post-incisional administration of ketamine or a saline control condition.     

Measurement of gastric mucosal carbon dioxide tension by saline and air tonometry

This study compares the balloon air tonometry method of measuring gastric mucosal CO₂ to standard saline tonometry. Also, this study investigates the effect of histamine-2 receptor blockade on the precision of tonometric measures of gastric mucosal Pco₂ (P_tco₂).

We obtained hourly measurements of P_tco₂ from two gastric tonometers inserted orally in 19 healthy volunteers. One tonometer measured P_tco₂ by the intermittent saline method, whereas the other measured P_tco₂ using a newer continuous air method. Subjects received intravenous 5% dextrose during the first 6 hours of the experiment followed by a continuous infusion of a solution of ranitidine in 5% dextrose for another 6 hours. The ranitidine infusion was titrated to maintain gastric fluid pH ≥ 4.

Comparison of air to saline tonometry yielded a bias of −1.3 mm Hg with a limit of agreement of 6.6 mm Hg under optimal conditions of optimal gastric fluid pH (gastric fluid pH ≥ 5.0). Measures of P_tco₂ were lower with ranitidine for either group, 45.3 ± 1.3 mm Hg versus 39.7 ± 0.5 mm Hg for saline (P < .01) and 45.9 ± 1.0 versus 41.3 ± 0.5 for air (P < .01). The mean Pco₂ gap (P_tco₂ - P_arterialco₂) at gastric fluid pH ≥ 5.0 was 1.4 mm Hg, with a standard deviation of 2.7 mm Hg. A span of three standard deviations yields a normal limit for Pco₂ gap of 9.5 mm Hg.

Measures of P_tco₂ with the air tonometer method are similar to those obtained with saline tonometry. The reliability of P_tco₂ measurements with either method improved with the use of ranitidine to maintain gastric fluid pH ≥5.     

Anti-CD18 antibodies improve cardiac function following cardiopulmonary bypass in dogs

Cardiopulmonary bypass is associated with activation of neutrophils, which may adhere to vascular endothelium causing lung, heart, and brain injury. We tested whether blocking neutrophil adherence would improve organ function following cardiopulmonary bypass in dogs.

Ulbar|Materials and Methods: All dogs received a standard anesthetic, and then one group (n = 6) received 2 hours of cardiopulmonary bypass followed by 4 hours of observation. A second group (n = 6) received a monoclonal antibody (6 mg/kg) to CD18, a neutrophil adherence factor, immediately before cardiopulmonary bypass. A third group (n = 6) did not receive cardiopulmonary bypass or antibody.

Using flow cytometry we found that the antibody bound essentially all neutrophil CD18 sites. All three groups had similar gas exchange and hemodynamics. Lung and heart histology results were similar between groups. By echocardiography, five animals receiving cardiopulmonary bypass alone showed regional wall abnormalities, whereas only one receiving antibody showed wall motion abnormality (P < .05). Following cardiopulmonary bypass, intracellular myocardial pH was higher (P < .05) in the antibody-treated group compared with the group that had cardiopulmonary bypass alone (7.23 ± 0.05 v 7.07 ± 0.07 respectively).

Monoclonal antibodies to CD18 can prevent the deterioration in cardiac function routinely observed following cardiopulmonary bypass.     

Parameters of thick and thin nerve-fiber functions as predictors of pain in carpal tunnel syndrome

Pain intensity in carpal tunnel syndrome (CTS) was correlated with neuro- and psychophysiological parameters related to the function of different nerve fiber classes within the median nerve in 23 patients. Control data were obtained from 16 normal subjects.

Mean intensity of all pain attacks which occurred 14 days before surgical treatment was assessed on visual analogue scales (average CTS pain). Functions of thick myelinated nerve fibers were determined by motor and sensory nerve conduction studies. Functions of thin myelinated and unmyelinated nerve fibers were evaluated by measuring thresholds of warmth, cold and heat pain on the index and little finger. Pain intensity and neurogenic vasodilation following noxious mechano-stimulation on the interdigital web between index and middle finger provided additional information on the functioning of nociceptive nerve fibers. Sympathetic reflexes induced by these painful stimuli were assessed by means of infrared thermography and photoplethysmography.

Mean intensity of pain attacks (40 ± 19% VAS) correlated significantly with latency (r = 0.58, P < 0.01) and amplitude (r = −0.50, P < 0.01) of the compound action potential from abductor pollicis brevis muscle following distal median nerve stimulation. Thresholds of warmth, cold and heat pain on index finger were significantly increased during CTS when compared to the control subjects. The magnitude of neurogenic vasodilation and sympathetic vasoconstrictor reflexes were not significantly different. Average CTS pain correlated inversely to the threshold of heat pain on index (r = −0.46, P < 0.05), but also on the little finger (r = −0.41, P < 0.05), which is not innervated by the median nerve. Pain intensity due to noxious mechano-stimulation was significantly higher in patients than with control persons. In a multiple regression model, with distal motor latency of the median nerve and heat pain threshold on the index finger as independent variables, ongoing pain due to CTS was predicted with R = 0.72 (P < 0.001).

The conclusion is that intensity of pain due to CTS depends on alterations of peripheral and central nervous functions.     

Flow triggering added to pressure support ventilation improves comfort and reduces work of breathing in mechanically ventilated patients

The purpose of this study was to measure the effect of flow triggering (FT), added to pressure support ventilation (PSV), during spontaneous breathing in intubated patients.

A prospective observational study was conducted at a Comprehensive Cancer Center, University Hospital. Fourteen consecutive critically ill, mechanically ventilated patients on PSV with positive end-expiratory pressure were studied. Flow triggering was added to PSV in spontaneously breathing ventilated patients.

Respiratory rate (f), minute ventilation (V), patient work of breathing (WOB_p), respiratory drive (P_0.1), rapid shallow breathing index (f/V_t), tidal volume (V_t) and a visual analog scale of breathing effort and comfort all improved. There was a large decrease in WOB_p, and P_0.1, when flow triggering was added to PSV (P < .001). There was a moderate decrease in f/V_t during the same procedure (P < .01). Twelve patients felt subjectively better with the intervention.

Flow triggering offers an excellent complement to PSV because it improves patient comfort and reduces the magnitude of the inspiratory effort as well as the delay time between inspiratory muscle contraction and gas flow. It augments gas exchange at no metabolic cost to the patient while reducing the work of breathing.     

Influence of preoperative mechanical bone quality and bone mineral density on aseptic loosening of total hip arthroplasty after seven years

Objective. To test mechanical bone quality and bone mineral density of the femoral head at the day of implantation as indicators for femoral prosthesis loosening.

Methods. Mechanical bone quality of a femoral head slice was assessed by destructive compression testing combined with bone mineral density measurements using peripheral quantitative computed tomography. Fourteen patients with walking pains were attainable for a radiographical follow-up mean 7.1 years after implantation.

Results. Radiolucent lines along the stem were evident in 11 of 14 femurs, most of them seen in Gruen zones 7, 6, 1, 3, 14, and showed strong correlations to preoperative bone strength (r=−0.80; P<0.001) and axial stiffness (r=−0.75; P=0.002), yet not to bone mineral density (r=−0.67; P=0.009). Slight varus deviations <3° were noted in six femurs. Preoperative strength was reduced in this femurs to 54% (P=0.006), and stiffness to 61% (P=0.038), while bone mineral density did not differ significantly.

Conclusions. Femoral prosthesis loosening after seven years can be predicted by mechanical bone quality of the femoral head at the time of implantation. Bone mineral density measurements may also indicate future stem loosening but have to interpreted carefully, keeping in mind a poorer predictive value.

Relevance Indications and choice of type of hip arthroplasty should be balanced in osteoporotic bones in particular. While preoperative bone mineral density measurement allows the prediction of mechanical bone quality, its relevance in predicting failure in arthroplasty treatment remains unclear.     

Blood interleukin 10 levels parallel the severity of septic shock

The aim of this study was to investigate the relation between interleukin (IL) 10, tumor necrosis factor alpha (TNF), IL-1, and IL-6 levels in patients with septic shock and relate these cytokine levels to the development of organ failure.

In 11 patients with septic shock of recent onset, blood was sampled for determinations of TNF, IL-1, IL-6, and IL-10. The degree of organ failure was scored for four organ systems (respiratory, hepatic, renal, hematologic) in the first 48 hours of the study.

The APACHE II score was 21 ± 4. Three patients died. IL-10 levels were directly correlated with TNF levels (r = 0.73, P < .05) and IL-6 levels (r = 0.67, P < .05); and inversely correlated with total C3 (r = −0.73, P < .05) and CH50 (r = −0.68, P < .05). Both IL-10 and TNF levels were correlated to the organ failure score (r = 0.75 and r = 0.68, both P < .01). Six patients with high IL-10 levels (>60 pg/mL) had lower C3 (37 ± 11 v 62 ± 10 mg/dL) and CH50 (32 ± 7 v 68 ± 19%), and higher organ failure scores (5.7 ± 0.8 v 3.8 ± 1.3) than those with low IL-10 levels (all P < .05).

Although IL-10 has an inhibitory effect on the production of cytokines, it is released together with TNF and IL-6 in patients with septic shock. IL-10 blood levels are directly related to the severity of inflammation and the development of organ failure in septic shock.     

The effect of three levels of foot orthotic wedging on the surface electromyographic activity of selected lower limb muscles during gait

Background. Some types of foot orthoses have been researched for their effect on lower limb electromyographic muscle activity during walking. However, foot orthoses with high levels of medial rearfoot wedging (‘inverted’ foot orthoses) have not been investigated.

Methods. In a cross-sectional study, asymptomatic participants with a pronated foot type (n = 15) were each issued with a pair of 0°, 15° and 30° inverted custom-made foot orthoses. After four weeks of habituation to the orthoses, surface electromyography was used to measure the onset and maximum EMG amplitude of tibialis anterior, peroneus longus, medial gastrocnemius and soleus muscles using five conditions [barefoot, shoe-only, 0°, 15° and 30° inverted foot orthoses conditions].

Findings. A statistically significant increase in tibialis anterior maximum EMG amplitude occurred using the shoe only (30% increase), 0° (33% increase), 15° (38% increase) and 30° (30% increase) inverted orthoses conditions compared to walking barefoot (P < 0.01). Peroneus longus maximum EMG amplitude increased significantly using the 15° inverted orthosis condition compared to walking barefoot (21% increase, P = 0.04).

Interpretation. Footwear and orthoses can significantly alter the maximum EMG amplitude of leg muscles during walking. Foot orthoses appear to increase peroneus longus EMG amplitude compared to footwear alone. However, the level of medial rearfoot posting within an orthosis does not appear to significantly alter maximum EMG amplitude. The individual responses to foot orthoses are highly variable. The changes in EMG amplitude with the use of foot orthoses and shoes may have clinical implications.