Assessment of elevated compartment pressures by pressure-related ultrasound: a cadaveric model.

PURPOSE: There is a risk of misinterpreting the clinical signs of acute compartment syndrome of the lower limb resulting in delayed fasciotomy. Up to date, the diagnosis of compartment syndrome is based on clinical assessment and of invasive needle pressure measurement in uncertain cases. Close monitoring is necessary for early recognition of raising compartment pressures. Clinical assessment of muscle firmness by the physician's palpation alone is unreliable. Thus, a device objectifying this assessment would be beneficial. The purpose of this study was to determine the feasibility of muscle compartment elasticity measurements by a novel and non-invasive device using pressure-related ultrasound. METHODS: In a cadaveric model, the anterior tibial compartment was prepared to simulate raising intra-compartmental pressures (0-80 mmHg) by saline infusion. Standard invasive pressure monitoring was compared with a novel method to determine tissue elasticity. Changing cross-sectional view in B-mode ultrasound was exerted to measure the compartment depth before and after physician's probe compression of 100 mmHg. Compartment displacement (∆d) was measured and related to the corresponding compartmental pressure (Spearman correlation coefficient). Delta (mm) of the control group at 10 mmHg compartment pressure was compared with measured data at rising compartmental pressures of 30, 50, and 70 mmHg using the Wilcoxon rank-sum test. The intra-observer reliability (κ) was additionally calculated. RESULTS: Fresh and never frozen lower human limbs (n = 6) were used. The average displacement measured in the anterior tibial compartment was 2.7 mm (0.3-6.7 mm). A concordant consistent correlation between the compartmental displacement and the intra-compartmental pressure occurred. The Spearman coefficient (r s = 0.979) showed a significant correlation between the rising pressure and the decreasing tissue displacement visualized by ultrasound. The intra-observer value kappa showed reliable values (κ 10 = 0.73, κ 30 = 0.80, and κ 70 = 0.79). CONCLUSIONS: We introduce a new method of ultrasound imaging enhanced with probe pressure measurement to determine changes of the visco-elastic behavior of isolated muscle compartments. Pressure-related ultrasound could be a reliable tool to determine the correlation between the measured compartmental displacement and the increasing intra-compartmental pressure. Its accuracy revealed promising results. This technique may help the physician to objectify the clinical assessment of compartment elasticity, mainly indicated in cases of unconscious patients and imminent pathology. Further clinical studies and improvements of this technique are required to prove its accuracy and reliability in cases of compartment syndrome.

Home parenteral nutrition: clinical and laboratory analysis of initial experience (1994-1997). Implications for patient management.

UNLABELLED: BACKGROUND/AIM AND METHOD: Severe malabsorption often necessitates prolonged parenteral nutrition. Home parenteral nutrition (HPN) offers the opportunity for treatment at home. We report clinical and laboratory data of initial 27 HPN patients of one center since its opening in 1994. RESULTS: Clinical and biological markers of nutritional status were normalized and well maintained in most patients. Except for vitamin E and selenium (lower in HPN patients), the other vitamin and micronutrient levels were normal. There was no obvious essential fatty acid deficiency. Cholestasis was usual, but only 1 patient had a severe hepatic disease. Catheter infection occurred 18 times in 13 patients, but the frequency decreased with time (from 4.2 to 1.7 infections/1,000 days on HPN). No patient died from HPN complications. Social rehabilitation and, in some patients, full professional rehabilitation were constant. CONCLUSIONS: These data confirm that HPN performed in centers with expertise allowed patients to overcome gut failure and to recover subnormal or normal nutritional status. Satisfactory social rehabilitation was obtained in all patients. HPN complications were rarely life-threatening, and their frequency decreased with experience.

Detection of induced mitotic chromosome loss in Saccharomyces cerevisiae--an interlaboratory assessment of 12 chemicals.

Induced mitotic chromosome loss was assayed using diploid yeast strain S. cerevisiae D61.M. The test relies upon the uncovering and expression of multiple recessive markers reflecting the presumptive loss of the chromosome VII homologue carrying the corresponding wild-type alleles. An interlaboratory study was performed in which 12 chemicals were tested under code in 2 laboratories. The results generated by the Berkeley and the Darmstadt laboratories were in close agreement. The solvents benzonitrile and methyl ethyl ketone induced significantly elevated chromosome loss levels. However, a treatment regime that included overnight storage at 0 degree C was required to optimize chromosome loss induction. Hence, these agents are postulated to induce chromosome loss via perturbation of microtubular assembly. Fumaronitrile yielded inconsistent results: induction of chromosome loss and respiratory deficiency was observed in both laboratories, but the response was much more pronounced in the Darmstadt trial than that observed in Berkeley. The mammalian carcinogens, benzene, acrylonitrile, trichloroethylene, 1,1,1-trichloroethane and 1,1,1,2-tetrachloroethane failed to induce chromosome loss but elicited high levels of respiratory deficiency, reflecting anti-mitochondrial activity. Trifluralin, cyclophosphamide monohydrate, diazepam and diethylstilbestrol dipropionate failed to induce any detectable genetic effects. These data suggest that the D61.M system is a reproducible method for detecting induced chromosome loss in yeast.

The detection of chemically induced aneuploidy in Saccharomyces cerevisiae: an assessment of mitotic and meiotic systems.

Several systems have been evaluated for their ability to detect aneuploidy. Chromosome gain can be detected in mitotic haploid cells as well as meiotically derived haploid spores. Both chromosome gain and loss are detectable in mitotic diploid cells. Several chemicals have been identified that clearly induce aneuploidy in at least one or more of the systems.