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עמוד בית
Tue, 28.05.24

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November 1999
Gideon Paret MD, Tamar Ziv MD, Arie Augarten MD, Asher Barzilai MD, Ron Ben-Abraham MD, Amir Vardi MD, Yossi Manisterski MD and Zohar Barzilay MD, FCCM

Background: Acute respiratory distress syndrome is a well-recognized condition resulting in high permeability pulmonary edema associated with a high morbidity.

Objectives: To examine a 10 year experience of predisposing factors, describe the clinical course, and assess predictors of mortality in children with this syndrome.

Methods: The medical records of all admissions to the pediatric intensive care unit over a 10 year period were evaluated to identify children with ARDS1. Patients were considered to have ARDS if they met all of the following criteria: acute onset of diffuse bilateral pulmonary infiltrates of non-cardiac origin and severe hypoxemia defined by <200 partial pressure of oxygen during ³6 cm H2O positive end-expiratory pressure for a minimum of 24 hours. The medical records were reviewed for demographic, clinical, and physiologic information including PaO22 /forced expiratory O2, alveolar–arterial O2 difference, and ventilation index.

Results: We identified 39 children with the adult respiratory distress syndrome. Mean age was 7.4 years (range 50 days to 16 years) and the male:female ratio was 24:15. Predisposing insults included sepsis, pneumonias, malignancy, major trauma, shock, aspiration, near drowning, burns, and envenomation. The mortality rate was 61.5%. Predictors of death included the PaO2/FIO2, ventilation index and A-aDO23 on the second day after diagnosis. Non-survivors had significantly lower PaO2/FIO2 (116±12 vs. 175±8.3, P<0.001), and higher A-aDO2 (368±28.9 vs. 228.0±15.5, P<0.001) and ventilation index (43.3±2.9 vs. 53.1±18.0, P<0.001) than survivors.

Conclusions: Local mortality outcome for ARDS is comparable to those in tertiary referral institutions in the United States and Western Europe. The PaO2/FIO2, A-aDO2 and ventilation index are valuable for predicting outcome in ARDS by the second day of conventional therapy. The development of a local risk profile may allow early application of innovative therapies in this population. 


1ARDS = acute respiratory distress syndrome

2 PaO2 = partial pressure of oxygen

3A-aDO2 = alveolar–arterial O2 difference

Ilan Cohen MD, Avraham Nyska PhD, Uri Givon MD, Aharon Chechick MD, Valentin Rzetelny MD and Eitan Bogin PhD

Background: The growth plate increases its activity in response to exercise. Likewise, decreased physical activity exerts a negative effect on bone growth and development, leading to rarefaction of the subepiphyseal bone. Limb immobilization inhibits the growth plate’s activity, indirectly shown by a recorded arrest in longitudinal growth of the long bones. However, there is no direct evidence concerning the growth plate itself.

Objective: To determine whether the growth plate exhibits measurable microstructural changes in response to decreased levels of physical activity.

Methods: Histomorphometric analysis was used to qualitatively and quantitatively assess the changes in the epiphyseal plate in response to single hind limb immobilization in the rat. In 16 of 25 Sprague-Dawley male rats the left hind limb was immobilized for 3 weeks; the remaining 9 rats served as controls. The left proximal tibia of each animal was examined by computerized image analysis.

Results: There was a decrease in epiphyseal height, cell column density and subepiphyseal trabecular area - all indices of growth plate activity. Metaphyseal cortical thickness was also depressed, thereby confirming the efficacy of the immobilization method applied.

Conclusions: Limb immobilization in the rat induces inhibitory histological changes in the epiphyseal growth plate, which are in contrast to the excitatory microscopic changes seen with exercise. These changes can be assessed quantitatively. Their potential for reversibility remains to be determined by future experiments.

Mordechai R Kramer MD, Victor Krivoruk MD PhD, Joseph Lebzelter PhD, Mili Liani BSc and Gershon Fink MD
Background: Hypoxemia is a common complication of chronic obstructive pulmonary disease and a major factor in patients’ prognosis and quality of life. The response to exercise has been evaluated by various means but no standardization has been accepted.

Objectives: To suggest a simple outpatient technique for evaluating the response of arterial oxygen saturation to exercise for use as a marker of disease severity.

Patients and methods: Ninety-six patients with various degrees of COPD1 were divided into three groups: mild (forced expiratory volume in 1 sec >65%), moderate (FEV12 between 50 and 65%), and severe (FEV1 <50%). Using continuous oximeter recording we measured oxygen saturation during 15 steps of climbing, and quantified  oxygen desaturation by measuring the “desaturation area”, defined as the area under the curve of oxygen saturation from the beginning of exercise through the lowest desaturarion point and until after recovery to the baseline level of oxygen percent saturation. Desaturation was correlated to spirometry, lung gas volumes, blood gas analysis, and 6 min walking distance.

Results A good correlation was found between severity of COPD and baseline SaO23, lowest SaO2, recovery time, and desaturation area.  A negative correlation was found between desaturation area and FEV1 (r=-0.65), FEV1/forced vital capacity (r=-0.58), residual volume to total lung capacity (r=0.52), and diffusing lung capacity for carbon monoxide (r=-0.52). In stepwise multiple regression analysis only FEV1 correlated significantly to desaturation area.  A good correlation was noted between 6 min walking distance and desaturation area with the 15 steps technique (r=0.56).

Conclusions: In patients with severe COPD, arterial hypoxemia during exercise can be assessed by simple 15 steps oximetry. This method can serve both as a marker for disease severity and to determine the need for oxygen supplementation.


COPD = chronic obstructive pulmonary disease

FEV1 = forced expiratory volume in 1 sec

SaO2 = arterial oxygen saturation

September 1999
Derek Le-Roith, MD, Michael Karas, MD, Shoshana Yakar, MD, Bao-He Qu, MD, Yiping Wu, MD, and Vicky A. Blakesley, MD.
Pnina Langevitz, MD, Avi Livneh, MD, Shai Padeh, MD, Nurit Zaks, MD, Yael Shinar, MD, Deborah Zemer, MD, Elon Pras, MD, and Mordechai Pras, MD.
Ittai Shavit, MD, Naim Shehadeh, MD, Osnat Zmora, MD, Israela Avidor, MD, and Amos Etzioni, MD.
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