Validation of Histologic Bone Analysis Following Microfil Vessel Perfusion.

The ability to examine bone vascularity using Micro-Computed Tomography (µCT) following vessel perfusion with Microfil® and to subsequently perform histologic bone analysis in the same specimen would provide an efficient method by which the vascular and cellular environment of bone can be examined simultaneously. The purpose of this report is to determine if the administration of Microfil® precludes accurate histologic assessment of bone quality via osteocyte count and empty lacunae count. Sprague-Dawley rats (n=6) underwent perfusion with Microfil®. Left hemi-mandibles were harvested, decalcified and underwent vascular analysis via µCT prior to sectioning and staining with Gomori's Trichrome. Quantitative Histomorphometric evaluation was performed. Ninety-five percent confidence intervals were used to determine statistical differences from an established set of controls (n=12). Histologic analyses were successfully performed on specimens that had undergone previous perfusion. Quantitative measures of bone cellularity of perfused versus control specimens revealed no statistical difference in osteocyte count per high-power field (95.33 versus 94.66; 95 percent CI,-7.64 to 6.30) or empty lacunae per high-power field (2.73 versus 1.89, 95 percent CI, -1.81 to 0.13). Here we report a statistical validation allowing for histological analysis of cell counts in specimens in which Microfil® perfusion has previously been performed.

[Acute respiratory failure in obesity]. / Les décompensations respiratoires aiguës de l'obèse.

Obstructive sleep apnea, obesity-related hypoventilation - a hypoventilation which is independent of apneas and increased by sleep -, and hypoxemia related to local ventilation-perfusion disorders are the main mechanisms of respiratory failure occurring during acute respiratory decompensation following an often minimal triggering event. Non-invasive ventilation has been found to be an effective treatment, particularly with a ventilator capable of maintaining positive expiratory and pressure. The level of the expiratory positive airway pressure must be adapted to cure episodes of obstructive apnea or hypopnea. The level of the inspiratory positive airway pressure (pressure support ventilator), or the tidal volume (volume-controlled ventilator) must be adapted to correct the residual hypoventilation. These adaptations can be made by proper assessment of nocturnal SaO(2) recordings. In particularly severe cases, use of endotracheal ventilation may be necessary to control a state of shock or consciousness disorders incompatible with the patient cooperation necessary for non-invasive ventilation.

[Fat embolism with lung hemorrhage]. / Embolie graisseuse à forme hémorragique pulmonaire.

Post-traumatic fat embolism was disclosed by a picture of alveolar hemorrhage. Acute hypoxemia associated with dense bilateral pulmonary infiltrates was observed in a 21 year-old woman, 4 days after an accident with closed tibial fracture. Cruoric pulmonary thromboembolism was ruled out, as was an acute pulmonary edema. Neither infectious nor immunologic etiology was found. The diagnosis of alveolar hemorrhage was based on bronchoalveolar lavage. Lipid droplets in macrophages stained by "Oil Red O" established the relationship with fat embolism. The outcome was favorable. The association of fat embolism and alveolar hemorrhage has already been reported, but remains rare.

[Management of obesity and respiratory insufficiency. The value of dual-level pressure nasal ventilation]. / Prise en charge de l'obèse en décompensation respiratoire. Intérêt de la ventilation nasale à double niveau de pression.

Obstructive Sleep Apnea (OSA), Obesity-Linked Hypoventilation (OLH)--a hypoventilation which is independent of apneas and increased by sleep--, and COPD are mechanisms for respiratory failure in obese patients. We thought nasal bi-level positive airway pressure to be a suitable treatment: EPAP is useful to maintain upper airway patency and IPAP-EPAP difference to correct OLH and COPD hypoventilation. Our purpose is to report the results of such a therapeutic approach. We included 41 patients that we first treated by nasal bi-level positive airway pressure for a respiratory failure with an uncompensated respiratory acidosis. The initial setting was about 4 cm H2O for EPAP and 16 for IPAP. Under supervision of a real-time printed oximetry tracing, we furthermore increased EPAP until disappearance of repetitive dips in oxygen saturation (that we assimilated to obstructive events) and IPAP until obtaining an acceptable level of steady saturation (we assimilated a low level to a steady hypoventilation). Age (mean +/- SD) was 63 +/- 11 years, BMI 42 +/- 9 kg/m2, pH 7.32 +/- 0.04, PaCO2 71 +/- 13 mmHg, PaO2 45 +/- 7 mmHg. Thirty-nine out of 41 patients returned home without need for tracheal intubation. At 7 days of treatment, PaCO2 was 50 +/- 6 mmHg. Thus, nasal bi-level position airway pressure appears to be an efficient treatment in these patients.

Relative survival analysis of 252 patients with COPD receiving long-term oxygen therapy.

OBJECTIVES: A survival analysis was conducted on patients with COPD receiving long-term oxygen therapy (LTOT) to compare two different statistical methods. METHODS: We used a multivariate crude (observed) survival model (Cox) and a multivariate relative survival model (Hakulinen). Only the latter is able to correct the survival by adjusting it to the normal life expectancy of the studied patients. PATIENTS: Two hundred fifty-two hypoxemic COPD patients (207 male) requiring LTOT were included. Mean PaO2 was <50 mm Hg before oxygen therapy. Mean age was >69 years (SE: 9.9). They had severe bronchial obstruction: mean FEV1 was <33% (10.6) of predicted values, with some CO2 retention: mean PaCO2 was 45.6 (7.1) mm Hg. By December 31, 1995, 189 patients had died (75%) and 13 (5%) were unavailable for follow-up. RESULTS: The overall crude survival was poor: 80.9% after 1 year, 67.1% after 2 years, 34.7% after 5 years, and 7.1% after 10 years. In the crude multivariate analysis (Cox), the negative prognostic factors were age and hypercapnia. The overall relative survival (Hakulinen), corrected for life expectancy, was 82.8% after 1 year, 70.8% after 2 years, 41.5% after 5 years, and 10.25% after 10 years. In the final multivariate relative model, age was no longer significant and the only bad prognostic factor was hypercapnia with a relative risk of 1.97 (1.16 to 3.34). CONCLUSION: This work shows the inadequacy of the Cox observed survival model when it comes to appreciating the real prognostic impact of age, because of the confusing factor associated with a normal life expectancy.

Central sleep apnoea in Arnold-Chiari malformation: evidence of pathophysiological heterogeneity.

We report on the case of two young patients with type I Arnold-Chiari malformation (ACM), as revealed by a central sleep apnoea (CSA) syndrome without any other neurological defect. Case 1 was a 14-yr-old male patient, who developed severe alveolar hypoventilation and needed long-term mechanical ventilation via a tracheostomy. Case 2 was a 39-yr-old male patient, who developed features suggestive of sleep apnoea and responded to nasal continuous positive airway pressure ventilation despite the central type of apnoeas. These two cases illustrate the different pathophysiological mechanisms involved in CSA, namely a blunted chemical drive (in hypercapnic patients) and an increased chemical drive, which destabilizes the breathing pattern during sleep (in normo/hypocapnic patients). Central sleep apnoea can be the initial manifestation of Arnold-Chiari malformation and can lead to a life-threatening condition.

Fatal ball-valve airway obstruction by an extensive blood clot during mechanical ventilation.

A ball-valve airway obstruction by a blood clot cast of almost the whole bronchial tree occurred in a small-cell lung cancer patient, who had been on mechanical ventilation for 9 days. Chest radiographs revealed overinflated lungs. Attempts to remove the cast via fibreoptic bronchoscopy were unsuccessful and the patient died. A postmortem extraction of the clot was performed with a rigid tube. This case is rare because of absence of severe haemoptysis and lung volume reduction.

Diurnal blood pressure variability in essential hypertension and vascular reactivity to isometric stress.

The present study was designed to assess the hemodynamic conditions, by means of impedance cardiography methods, and the relation existing between vascular reactivity to isometric stress (isometric handgrip test) and the day/night blood pressure variations, estimated by ABPM. Fifty unselected untreated non-obese EEH adult subjects (WHO class I) with a duration of disease not exceeding 3 years were classified as dippers or non-dippers according to commonly accepted criteria. Twenty three normotensive volunteers acted as controls. SBP, DBP, HR, CI and SVRI were assessed at rest and after IHG test. At rest dippers, non-dippers and controls showed comparable CI. SVRI were more enhanced in EEH than in controls and, although not significantly, in non-dippers than in dippers. During IHG all subjects showed a significant rise of SBP, DBP and HR; CI variations were of comparable size in all groups while SVRI increases were not. Non-dippers showed a significant SVRI rise after IHG in comparison with resting values. In dippers and in controls SVRI increment was insignificantly different in comparison with resting values. Non-dippers showed a closest correlation between BP and SVRI rise during IHG while dippers showed a less consistent association. In conclusion, our data suggest that in adults with short duration EEH the existence of non-dipper condition may be unrelated to myocardial hypertrophy. Blunted nocturnal BP fall is associated with vascular hyper-reactivity revealed by a bigger elevation of SVRI during IHG.(ABSTRACT TRUNCATED AT 250 WORDS)

Defective fibrinolytic response in atherosclerotic patients--effect of iloprost and its possible mechanism of action.

Plasma fibrinolytic activity and tissue-type plasminogen activator (t-PA) were defective in response to venous stasis in five out of ten patients with peripheral occlusive artery disease. Discontinuous infusions of iloprost, a stable synthetic analogue of prostacyclin, restored a normal fibrinolytic response in all five patients but did not induce a parallel increase of plasma t-PA. These findings suggest that in addition to the possible benefits due to its vasodilatory and antiplatelet activity, iloprost may improve the fibrinolytic activity in patients with atherosclerotic disease, providing them with further antithrombotic protection. The profibrinolytic effect of iloprost seems not to depend on its ability to induce vascular t-PA release. Rather, it might be related to its inhibitory effect on PAI release from platelets, endothelial cells and/or hepatocytes. Venous occlusion test represents an easy diagnostic approach to fibrinolytic defects, even if related to arterial disease, and may help select patients who need therapeutic intervention.