Cold urticaria is a disorder characterized by the rapid onset of itching, redness, and swelling of the skin within minutes after exposure to a cold stimulus. It is probably the most common form of urticaria (hives). In extreme cases, anaphylactic shock may occur. This condition can begin at any age, affects both men and women, and is most prevalent in young adults (18-25 yr old). There are two forms of the disorder: essential (acquired) cold urticaria, and familial (hereditary) cold urticaria. The symptoms of the acquired form become obvious in two to five minutes after exposure to the triggering substance or situation, while it takes 24 to 48 h for symptoms of familial cold urticaria to appear. Also, symptoms tend to last longer with the familial form, typically about 24 h although they may remain for as long as 48 h. With the acquired form, symptoms tend to last for one to two hours. Diagnosis of cold urticaria is made by placing an ice cube or ice water on the skin. Management of cold urticaria occurs through patient education, avoiding cold exposure, and giving patients epinephrine pens.
Exercise-induced bronchoconstriction (EIB) is defined as a transient narrowing of the airways that is caused by exercise[46,187] and clinically is demonstrated by a > 10% decrease in the forced expiratory volume in 1 s (FEV1). EIB has an incidence rate of ~ 4-20% in the general population and 11-50% in elite athletes.[46,154] In people with asthma, exercise causes EIB in ~ 80% of these individuals. Cold exposure has been implicated as a trigger for bronchoconstriction and asthma-like symptoms. Cold-weather athletes have an increased prevalence of EIB (23% of Olympic winter athletes) with cross-country skiers reportedly having an incidence rate of 33-50%.[107,191] Additionally, women are reported to have higher rates of EIB than men.[187,191] Two mechanisms have been postulated for EIB. One theory (the osmotic theory) suggests that airway drying caused by hyperventilation causes surface airway cells to become hyperosmotic and thus draw fluid from adjoining cells. This leads to a cascade of vasoconstrictor mediators to be secreted.[3,46] The second theory suggests that cooling of airways (exacerbated by cold air and higher ventilations) and subsequent rewarming causes high blood flow, engorgement of blood vessels, and edema formation in the airway vasculature leading to airway obstruction.[46,156] Evans et al. tested this hypothesis and found that cold air per se did not lead to EIB, but that dry air associated with cold exposure is the likely cause of EIB, suggesting hyperosmolality as a trigger for airway narrowing. Thus the use of bottled dry air during eucapnic voluntary hyperventilation is the recommended test for identifying EIB in athletes. Other studies also report that facial or torso cooling alone can cause FEV1 to be lower in people with asthma and normal controls (126,197). Thus EIB caused by cold exposure is likely caused by a combination of breathing dry air along with a reflex response due to skin or facial cooling, leading to high amounts of inflammation, especially in athletes who have high ventilation rates.[95,169] Persons who experience EIB when breathing cold air during heavy exercise exhibit a reduced FEV1[79,156] which can limit maximal ventilation, thus maximal performance. Lastly, even healthy persons can experience an increase in respiratory passage secretions and decreased mucociliary clearance when breathing very cold air during exercise, and any associated airway congestion may impair pulmonary mechanics and ventilation during exercise, also impacting on performance. One possible countermeasure for decreasing the occurrence of EIB in cold-weather is to use a mouth-borne heat and moisture exchanger[41,59] or even a scarf, although the increased resistance when ventilation rates are high may preclude the use of a moisture exchanger for most competitive athletes.
EIB is more prevalent in indoor ice rink athletes compared to warm-weather athletes.[119,154,155,191] Data from several investigators implicate air quality in the rink to the higher incidence.[113,152] Ice rink resurfacing machines produce high levels of carbon monoxide, nitrogen dioxide, and ultrafine and fine particulate matter with observed levels as much as 20-times higher than the outside air. Particulate matter increases allergic sensitization and airway hyperresponsiveness and exercise increases deposition of ultrafine particulate matter, which is related to the resting FEV1. Thus indoor ice rink athletes (figure skaters, ice-hockey players, speedskaters) and their health-care providers need to be aware that exercise in this environment may be a causative factor for EIB. Evidence Statement. Winter athletes, especially those exercising at high intensities and ventilation rates and in indoor ice rinks, have a higher incidence of EIB than the general population. Breathing dry air and skin/facial cooling act in synergy to trigger exercise-induced bronchospasm during winter activities. Indoor pollutants are also a trigger for EIB. Category C
Mortality/Morbidity in Winter
Mortality rates are higher in winter[45,98] compared to summer months; however hypothermia only accounts for a very minor percentage of these excess deaths. Instead, there are significant increases in death due to ischemic heart disease, stroke, and respiratory disease.[45,84] Mortality increases to a greater extent in regions with relatively warm winters that have cold snaps and in people who are less active outdoors.
Exercise-cold stress, compared to exercise in warm environments, increases sympathetic nervous activity, total peripheral resistance, mean arterial pressure, cardiac work, and myocardial oxygen requirements during rest or exercise.[36,43,85] For example, mean arterial pressure increases by ~ 17 mm Hg (18%) and rate pressure product (systolic pressure × heart rate) increases by 10%. Facial cooling by wind, alone, lowers the heart rate by ~ 10 bpm during low intensity exercise (< 35%V·O2max) but also causes mean arterial blood pressure and rate pressure product to rise, secondary to an increase in peripheral vasoconstriction and systemic vascular resistance. Therefore whole-body and facial cooling can theoretically lower the threshold for the onset of angina during aerobic exercise and many studies support this view.[15,43,51,131,151]
The type and intensity of exercise-cold stress also modifies the risk for the cardiac patient. Activities that involve the upper body or increase metabolism potentially increase risk. Snow shoveling has an isometric component which raises systolic blood pressures above that observed with arm ergometry alone and shoveling has been shown to raise the heart rate to 97% of maximal heart rate and systolic blood pressure to increase to 200 mm Hg. The data are limited on how cold exposure affects these responses. Dougherty et al. found that mean arterial pressure was higher during static-dynamic shoveling in the cold (-8°C vs. 27°C), but there were no adverse changes to the electrocardiogram. Other studies suggest that patients with coronary artery disease (CAD) self-select exercise intensities below their angina threshold during snow shoveling. Walking in snow (either packed or soft) significantly increases energy requirements and increases myocardial oxygen demands, so patients with CAD may have to slow their walking pace. Swimming in water below 25°C (77°F) can be a threat to patients with CAD because they may not be able to recognize angina symptoms and therefore may place themselves at greater risk. Twenty five percent of patients reported angina while swimming in 25°C water and 13% while swimming in 18°C water, but ST-segment depression was observed in 75% of the patients tested. Evidence Statement. Patients with CAD must use caution when exercising/working in the cold and should be knowledgeable of angina symptoms. Swimming in cold water may not be a good choice because it can potentially mask symptoms of angina. Category C
Cite this: Prevention of Cold Injuries during Exercise - Medscape - Nov 01, 2006.