Patterns of death among avalanche fatalities: a 21-year review.

BACKGROUND: Avalanches are a significant cause of winter recreational fatalities in mountain regions. The purpose of this study was to determine the relative contributions of trauma and asphyxia to avalanche deaths. METHODS: We reviewed all avalanche fatalities between 1984 and 2005 that had been investigated by the offices of the British Columbia Coroners Service and the Chief Medical Examiner of Alberta. In addition, we searched the database of the Canadian Avalanche Centre for fatal avalanche details. We calculated injury severity scores for all victims who underwent autopsy. RESULTS: There were 204 avalanche fatalities with mortality information over the 21-year study period. Of these, 117 victims underwent autopsy, and 87 underwent forensic external examination. Asphyxia caused 154 (75%) deaths. Trauma caused 48 (24%) deaths, with the rate of death from trauma ranging from 9% (4/44) for snowmobilers to 42% (5/12) for ice climbers. In addition, 13% (12/92) of the asphyxia victims who underwent autopsy had major trauma, defined as an injury severity score of greater than 15. Only 48% (23/48) of victims for whom trauma was the primary cause of death had been completely buried. INTERPRETATION: Asphyxia and severe trauma caused most avalanche fatalities in western Canada. The relative rates differed between snowmobilers and those engaged in other mountain activities. Our findings should guide recommendations for safety devices, safety measures and resuscitation.

Myofibroblasts are increased in the lung parenchyma in asthma.

BACKGROUND: Increased airway smooth muscle is observed in large and small airways in asthma. Semi-quantitative estimates suggest that cells containing alpha smooth muscle actin (α-SMA) are also increased in the lung parenchyma. This study quantified and characterized α-SMA positive cells (α-SMA+) in the lung parenchyma of non-asthmatic and asthmatic individuals. METHODS: Post-mortem sections of peripheral lung from cases of fatal asthma (FA), persons with asthma dying of non-respiratory causes (NFA) and non-asthma control subjects (NAC) were stained for α-SMA, quantified using point-counting and normalised to alveolar basement membrane length and interstitial area. RESULTS: α-SMA+ fractional area was increased in alveolar parenchyma in both FA (14.7 ± 2.8% of tissue area) and NFA (13.0 ± 1.2%), compared with NAC (7.4 ± 2.4%), p < 0.05 The difference was greater in upper lobes compared with lower lobes (p < 0.01) in both asthma groups. Similar changes were observed in alveolar ducts and alveolar walls. The electron microscopic features of the α-SMA+ cells were characteristic of myofibroblasts. CONCLUSIONS: We conclude that in asthma there is a marked increase in α-SMA+ myofibroblasts in the lung parenchyma. The physiologic consequences of this increase are unknown.

Abnormalities of the bronchial arteries in asthma.

STUDY OBJECTIVES: The bronchial arteries supply systemic blood to the airways, tracheobronchial lymph nodes, and nerves. Their structure has not been studied in patients with asthma. DESIGN: Case-control study of pathologic changes of bronchial arteries in asthma. PARTICIPANTS AND METHODS: Postmortem lungs were examined from three case groups: (1) fatal asthma (n = 12), death due to asthma; (2) nonfatal asthma (n = 12), asthmatic and death due to nonrespiratory causes; and (3) nonasthmatic control subjects (n = 12), no history of asthma and death due to nonrespiratory causes. In bronchial arteries with outer diameters of 0.1 to 1.0 mm, the areas of lumen, intima, and media were measured and compared between case groups. RESULTS: There were no significant differences in artery size (outer diameter) or in medial area between the three groups. In the two asthma groups, the intimal area was increased (p < 0.05), with a corresponding decrease in luminal area compared with the control group. There was a significant effect of gender, age, and smoking on intimal area. In the asthma cases, the area of bronchial artery intima was related to duration of asthma (p < 0.05), and this increase was associated with smooth muscle proliferation, reduplication, and calcification of the elastica, but not with inflammatory cell infiltration. CONCLUSIONS: While the pathophysiologic significance of these changes is uncertain, the relation to duration of asthma, age, and smoking suggests a secondary response to chronic airway disease.