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Objectives. To determine the incidence as well as contributing factors to fatal hypothermia.

Study design. Retrospective, registry-based analysis.

Methods. Cases of fatal hypothermia were identified in the database of the National Board of Forensic Medicine for the 4 northernmost counties of Sweden and for the study period 1992-2008. Police reports, medical records and autopsy protocols were studied.

Results. A total of 207 cases of fatal hypothermia were noted during the study period, giving an annual incidence of 1.35 per 100,000 inhabitants. Seventy-two percent occurred in rural areas, and 93% outdoors. Many (40%) were found within approximately 100 meters of a building. The majority (75%) occurred during the colder season (October to March). Some degree of paradoxical undressing was documented in 30%. Ethanol was detected in femoral vein blood in 43% of the victims. Contributing co-morbidity was common and included heart disease, earlier stroke, dementia, psychiatric disease, alcoholism, and recent trauma.

Conclusions. With the identification of groups at high risk for fatal hypothermia, it should be possible to reduce risk through thoughtful interventions, particularly related to the highest risk subjects (rural, living alone, alcohol-imbibing, and psychiatric diagnosis-carrying) citizens.

INTRODUCTION: The ability of fingers to rapidly rewarm following cold exposure is a possible indicator of cold injury protection. We categorized the post-cooling hand-rewarming responses of men before and after participation in 15 mo of military training in a cold environment in northern Sweden to determine: 1) if the initial rewarming category was related to the occurrence of local cold injury during training; and 2) if cold training affected subsequent hand-rewarming responses. METHODS: Immersion of the dominant hand in 10 degrees C water for 10 min was performed pre-training on 77 men. Of those, 45 were available for successful post-training retests. Infrared thermography monitored the dorsal hand during 30 min of recovery. Rewarming was categorized as normal, moderate, or slow based on mean fingertip temperature at the end of 30 min of recovery (TFinger,30) and the percentage of time that fingertips were vasodilated (%VD). RESULTS: Cold injury occurrence during training was disproportionately higher in the slow rewarmers (four of the five injuries). Post-training, baseline fingertip temperatures and cold recovery variables increased significantly in moderate and slow rewarmers: TFinger30 increased from 21.9 +/- 4 to 30.4 +/- 6 degrees C (Moderate), and from 17.4 +/- 0 to 22.3 +/- 7 degrees C (Slow); %VD increased from 27.5 +/- 16 to 65.9 +/- 34% (Moderate), and from 0.7 +/- 2 to 31.7 +/- 44% (Slow). CONCLUSIONS: Results of the cold recovery test were related to the occurrence of local cold injury during long-term cold-weather training. Cold training itself improved baseline and cold recovery in moderate and slow rewarmers.

PURPOSE: Differences among individuals concerning susceptibility to local cold injury following acute cold exposure may be related to function of the autonomic nervous system. We hypothesized that there are differences in heart rate variability (HRV) between individuals with normal or more pronounced vasoconstriction following cold exposure and that there is an adaptation related to prolonged cold exposure in autonomic nervous system response to cold stimuli.

METHODS: Seventy-seven young men performed a cold provocation test, where HRV was recorded during cold hand immersion and recovery. Forty-three subjects were re-examined 15 months later, with many months of cold weather training between the tests. Subjects were analyzed as 'slow' and 'normal' rewarmers according to their thermographic rewarming pattern.

RESULTS: For the 'pre-training' test, before cold climate exposure, normal rewarmers had higher power for low-frequency (P(LF)) and high-frequency (P(HF)) HRV components during the cold provocation test (ANOVA for groups: p = 0.04 and p = 0.005, respectively). There was an approximately 25 % higher P(HF) at the start in normal rewarmers, in the logarithmic scale. Low frequency-to-high frequency ratio (P(LF)/P(HF)) showed lower levels for normal rewarmers (ANOVA for groups: p = 0.04). During the 'post-training' cold provocation test, both groups lacked the marked increase in heart rate that occurred during cold exposure at the 'pre-training' setting. After cold acclimatization (post-training), normal rewarmers showed lower resting power values for the low-frequency and high-frequency HRV components. After winter training, the slow rewarmers showed reduced low-frequency power for some of the cold provocation measurements but not all (average total P(LF), ANOVA p = 0.05), which was not present before winter training.

CONCLUSIONS: These HRV results support the conclusion that cold adaptation occurred in both groups. We conclude that further prospective study is needed to determine whether cold adaptation provides protection to subjects at higher risk for cold injury, that is, slow rewarmers.