Cold Water Immersion: A review of the literature for winter swimming

Prepared by Dr Justen OConnor for the Mt Martha Ice Bergers Winter swimming (WS) episodes in cold water are considered severe ambient cold exposures, which are voluntarily practiced by humans in minimal clothing. Regular swimming in cold water during the winter season, albeit uncommon, is popular all over the world. Polar bear clubs are found from the Baltic Sea to the Aegean Sea, and from the icy shorelines of Moscow River to Lake Michigan. Members of these clubs claim that winter swimming gives them energy and health, while the majority would consider it as an extreme sport (Kolettis and Kolettis 2003). Swimming is an excellent physical activity that trains the cardiovascular system and contributes to health and wellbeing amongst participants. Swimming however in cold water during the winter season is also associated with significant additional physiologic alterations that could be detrimental in most individuals who have not adequately prepared or acclimatized to the activity. There is some evidence to suggest that, repeated exposure to cold stimuli results in an increased tolerance to cold, through a variety of adaptive mechanisms. In regular winter swimmers, physiological adaptation occurs that makes them more tolerant to cold water immersion. There is some evidence to suggest that the adaptations to cold swimming may also confer protection against several diseases (ie. Greater production of anti-oxidants). The degree of adaptation or habituation and the degree to which hypothermia or cold shock sets in varies from individual to individual and is mitigated by a range of factors including body fat (Kolettis and Kolettis 2003).

Death due to cold water immersion

Tipton, Mekjavic and Eglin (2000) noted that every year in the UK alone 400-1000 deaths occur in open water (note there are large numbers of participants so this is quite rare), most of these deaths occur within three mins of a safe haven and involve good swimmers. It is likely that individuals with circulatory or heart pathology may not be able to deal with the increased cold-induced vasoconstriction and increased cardiac workload (tachycardia) associated with cold shock. In 1981, Golden and Hervey reported on four stages in which death may occur during sudden, unexpected cold-water immersion. These were: stage 1, initial immersion, which kills within 23 min of immersion; stage 2, short-term immersion, which kills within 315 min of immersion; stage 3, long-term immersion, which kills after 30 min of immersion; and finally, stage 4, postimmersion, which kills during or shortly after rescue. In the survival textbooks and training courses, these stages have been called cold shock, swimming failure, hypothermia and post-rescue collapse. Immersion in water below 15 degrees C is considered dangerous and this should be emphasized for all participants in voluntary winter swimming programs. The temperature of Port Phillip Bay as of Tuesday 21 July, 2009 was 11.6 degrees, given immersion in water loses body heat at a rate 30 times greater than exposure to ambient air, swimming in this water will ultimately result in hypothermia (subtract up to 4 degrees C from ambient air temp for wind chill out of water less some more for being wet). The rate at which this happens is not determined by how macho you are or how strong you are, even how much training you have done, but rather a combination of factors including physiology, circulatory responses, cardiac responses and the amount of body fat the individual possesses.

Brooks, Howard and Neifer (2005) noted that the underlying causes of drowning amongst fishermen were reclassified from hypothermia and drowning to: cold shock (5.4%), swimming failure (5.4%), hypothermia (5.4%), post-rescue collapse (0.8%), cardiac event (0.8%) and drowning/other (10%). In the remaining 72.2% of deaths, there was insufficient information to determine an underlying cause. They concluded that contrary to much of the safety manual materials, cold shock and swimming failure played at least as important a part in the cause of drowning as hypothermia. If hormonal responses to cold water prove ineffective, shivering thermogenesis comes into play, producing thermal energy through muscle contractions. However, shivering decreases exercise (swimming) tolerance, due to a decrease in muscle coordination and, mainly, due to muscle fatigue. Persistent exposure (over 30 min) to low temperatures can lead to hypothermia, i.e., core temperature below 35 C, with detrimental cardiovascular and neurophysiological effects, which can lead to serious damage or death (Kolettis and Kolettis 2003).
Cold Shock and Swimming Failure

Sudden immersion in cold water initiates an inspiratory gasp response followed by uncontrollable hyperventilation and tachycardia. The body responds to the cold by increasing heart rate (tachycardia) and increasing vasoconstriction (constriction of blood vessles in periphery can increase BP). It is known that this response, termed the "cold shock" response, can be attenuated following repeated immersion. In an investigation examined how long this habituation lasts. Repeated immersions in cold water result in a long-lasting (7-14 months) reduction in the magnitude of the cold shock response (Tipton, Mekjavic et al. 2000). Michael Tipton and colleagues report that immersion deaths in cold water are associated with deterioraton in swimming performance leading to drowning rather than severe hypothermia (Tipton, Eglin et al. 1999). Although hypothermia is an important cause of swimming failure, the investigators clearly indicate that therapeutic strategies should focus on near-drowning symptoms rather than hypothermia-related symptoms. Cold exposure elicits substantial alterations both in metabolic and physiological aspects. Free radical formation is increased during cold stress. Further, cold stress elicits shivering and muscle movement to maintain body temperature, and this action increases production of reactive oxygen species. Lower body temperature during cold water immersion may inhibit enzyme activity. Thus, metabolism of glutathione, which is important in protecting various cells against oxidative stress and plays a part in cellular protein and immune function, may be impaired during cold water immersion (Teramoto and Ouchi 1999). Tipton and colleagues conducted a study in Stockholm that involved 10 healthy participants, wearing swim-wear, who completed self-paced breaststroke swims in water at 25C, 18C, and 10C. Results revealed all swimmers swam for 90 min in water at 25C. In 18C water, eight of ten swimmers swam for 90 min. One of the remaining two swimmers was withdrawn at 27 min with a rectal temperature of 350C (hypothermia), the other was withdrawn at 60 min with cold-induced shoulder pain. In 10C water, five swimmers completed 90 min swims. Four swimmers were withdrawn after swim times between 22 min and 50 min, when they were close to swim failure, with a mean rectal temperature of 350C; one swimmer was withdrawn at 61 min because of swim failure, at which point rectal temperature was 353C. This study shows that even after 27 mins in 18 degree water one participant experienced dangerously low core temperature. Many of the remaining swimmers at 10 degrees demonstrated swimming failure related to cold exposure and leading into hypothermia. The decrease in swimming efficiency seen in the 10C water was accompanied by a change in characteristics of swim stroke in which the volunteers swam with shorter, more rapid strokes in a more upright position. These changes lead to further decreases in swim speed and efficacy and the 2

increase in swimming angle increases drag and sinking force. Since stroke length and rate and swim angle are more easily observed than swimming efficiency, they may also help to identify individuals who are about to reach swim failure. Carrying extra subcutaneous body fat provides a substantial buffer against heat loss in cold-water. The correlation between thickness of fat over the arms and swimming efficiency in cold water supports previous findings, which suggest that the arms are especially susceptible to cooling when exercised in cold water. Thus, arm cooling and consequent muscle fatigue, rather than general hypothermia, may be the primary mechanism that led to the decline in swimming ability seen in this study (if cold, do not move arms around in water, use your legs). So although hypothermia has been reported to be an important cause of swimming failure, Tipton and colleagues found swim failure in cold water to be a progressive decrease in swimming efficiency in the absence of general hypothermia. Therefore, even if an individual survives the initial responses to cold-water immersion, drowning remains the major threat, since local muscle cooling impairs swimming performance and, consequently, the ability to keep the airway clear of the water. The implication for rescuers is that, with the exception of children rescued after long submersion in icy water, the major challenge for treatment is likely to be symptoms resulting from near-drowning rather than from severe hypothermia. Regular winter swimmers appear to have improved anti-oxidant functioning due to habituation to the conditions although this was not found for all individuals (Tipton, Mekjavic et al. 2000). According to Tipton et al. (2000) studies that demonstrate peripheral acclimatization support a hypothesis that cold-induced alterations in function may last a considerable time. Indeed Eskimos demonstrated greater finger blood flow then did mountain climbers on exposure to cold and this effect was noted for some time following exposure to a temperate environment. Regardless of any potential habituation effects from repeated cold exposures, habituation will not prevent hypothermia or swim failure and may not manifest in all individuals.
Hypothermia

Hypothermia can cause death and is a potentially avoidable condition, making education and preparation the cornerstones of prevention. Hypothermia continues to kill people involved in recreational sports throughout the world. According to McCullough and Arora (2004), the clinical presentation of hypothermia includes a spectrum of symptoms and is grouped into the following three categories: mild, moderate, and severe. Body heat is lost to the environment via five mechanisms: radiation, conduction, convection, evaporation, and respiration. Radiative heat loss is secondary to infrared heat emission, occurs primarily from the head and non-insulated areas of the body, is the most rapid, and accounts for more than 50 percent of heat loss. Conduction, which is the transfer of heat via direct contact, is an important mechanism in immersion incidents, because the thermal conductivity of water is approximately 30 times that of air. Factors influencing hypothermia include the environment (water temp, wind, air temp); length of exposure; amount of insulation (body fat lean people cool much faster, clothing); Age (children cool faster than adults); Activity (note less than 24 deg, exercise can exacerbate heat loss pre swim running to warm the body may not actually work; fatigue; exhaustion; low glucose levels). To maintain temperature homeostasis, the hypothalamus orchestrates a counter-attack against heat loss via heat conservation and heat production. Heat conservation is achieved by peripheral vasoconstriction reducing heat conduction to the skin, and behavioral responses, such as the layering of warm clothing, to increase insulation. Heat production is accomplished by shivering, which can increase the normal basal metabolic rate by two to five times, and through nonshivering thermogenesis via increased levels of thyroxine and epinephrine. In a cold environment, 3

homeostasis can be overwhelmed, heat production can cease, and the core body temperature can drop rapidly in cold water. Signs and symptoms Signs and symptoms include: Lethargy / apathy (I dont care, I dont want to swim anymore); pale to blue cold skin; confusion disorientation, memory loss, slurred speech (note same for hypoglycaemia); drowsiness; slow pulse may be irregular; slow shallow breathing; loss of muscle control, breakdown in swimming technique, slowing down the speed of swim; muscle rigidity; uncontrollable shivering that will stop as the condition worsens; loss of consciousness; irrational behaviour.

It is worth noting that standard clinical thermometers, which measure only as low as 34.4C (94F). Clinical measurement of hypothermia relies on special low-reading rectal thermometers or rectal thermistor probes, when available (do you want to buy one of these for the Ice Bergers?). The body will also have temperature gradients which provide different readings so as many measures as possible are advocated. This is another reason why you should call an ambulance. Hypothermia masks the clinical signs of hypoglycaemia and in clinical settings a glucose trial is advocated. Caution is needed in providing fluids/foods orally to patients in first aid settings. Additionally pulses may be difficult to appreciate in hypothermic patients. A myriad of electrocardiographic changes may be seen in patients with hypothermia, ranging from tachycardia to bradycardia to atrial fibrillation with slow ventricular response to ventricular fibrillation and asystole. This is another reason why you should call an ambulance.
TABLE 2

Stages of Hypothermia and Clinical Features

Hypothermia zone Mild

Body temperature 32.2 to 35 (90 to C C F 95 F)

Clinical features Initial excitation phase to combat cold: Hypertension Shivering Tachycardia Tachypnea Vasoconstriction With time and onset of fatigue: Apathy Ataxia Cold diuresis-kidneys lose concentrating ability Hypovolemia Impaired judgment Atrial dysrhythmias Decreased heart rate Decreased level of consciousness Decreased respiratory rate Dilated pupils Diminished gag reflex Extinction on shivering Hyporeflexia Hypotension J wave (see Figure 1) Apnea Coma Decreased or no activity on electroencephalography

Moderate

28 (82.4 to 32.2 C F) C

Severe

< 28 C

Nonreactive pupils Oliguria Pulmonary edema Ventricular dysrhythmias/asystole

Recovery from cold water immersion / hypothermia

Based upon the findings Tipton and others, treatment should consider drowning symptoms and not merely the symptoms of hypothermia. Management of hypothermia depends on the degree of hypothermia present. According to McCullough (2004), treatment modalities range from noninvasive, passive external warming techniques for mild hypothermia (e.g., removal of cold, wet clothing; movement to a warm environment) to active external rewarming (e.g., hot water bottles, warm bath) to active core rewarming (e.g., warmed intravenous fluid infusions, heated humidified oxygen, body cavity lavage, and extracorporeal blood warming). Mild to moderate hypothermia is treated easily with supportive care in most clinical settings and has good patient outcomes. The treatment of severe hypothermia is more complex, and outcomes depend heavily on clinical resources (McCullough 2004). Recovery from cold water immersion is not a simple matter of returning the person to normal ambient air temperatures or indeed wrapping them in a blanket. Decrease of deep body temperature in humans due to exposure to cold water continues after the exposure ends and carries major danger for human health and life. A moderate to severely hypothermic patient will likely require ACTIVE REWARMING as they may be incapable of generating their own heat. If the person has slowed or stopped shivering this is a sign that they are in chronic. Active external rewarming is adequate for acute and mild hypothermia, whereas active core rewarming may be necessary for chronic and severe hypothermia this requires emergency treatment and is difficult to diagnose. A Russian study by Losik and Afanas'eva (2004) explored the warming of people following cold water swimming. Participants who rejected a cold (10 +/- 1 degree C) water environment possessed more severely decreased "core" and "capsule" temperature vs that in air environment. Studies of heat state in 38 volunteers practicing winter swimming demonstrated comparative evaluation of various heating methods among which the most effective are immersion into warm (38 degrees C) water with simultaneous hydromassage and being in sauna at air temperature of 65 +/- 5 degrees C. Note however hot baths, activity, massage and reheating the periphery can result in after-drop where cold acidic blood quickly returns to the core and can cause arythmia. McCullough (2004) provided the following information on re-warming hypothermic patients in clinical settings. In patients with hypothermia, the decision to use passive or active rewarming techniques should be based on several clinical parameters and the degree of hypothermia. Passive rewarming can be used as the sole treatment modality of patients with mild hypothermia and involves moving the patient to a warm, dry environment and providing adequate insulation. For passive rewarming to be successful, the patient must have intact thermoregulatory mechanisms, normal endocrine function, and adequate energy stores to create endogenous heat. A disadvantage of passive rewarming is that the body's core temperature rises very slowly. Active external rewarming is simply the application of heat directly to the skin, and is only effective in the presence of intact circulation that can return peripherally rewarmed blood to the core. It will not work if the circulatory system has shut down. Hot water bottles and heating pads (applied to truncal areas only) may cause burns to cold and vasoconstricted skin. Forced-air warming systems are an efficient way to initiate heat transfer via convection during active external rewarming.

A major complication of active external rewarming is "core temperature afterdrop," which results when cold peripheral blood rapidly returns to the heart. Historically, this has led to many unwarranted deaths because patients were thought to be getting worse and rewarming was aborted. This complication can be minimized by always using minimally invasive core rewarming before active external rewarming. In addition, "rewarming acidosis" may occur as pooled lactic acid from the periphery joins the central circulation. Peripheral vasodilation in response to active external rewarming may cause venous pooling and "rewarming shock." The most effective method of active core rewarming is extracorporeal blood warming, accomplished by cardiopulmonary bypass, arteriovenous rewarming, venovenous rewarming, or hemodialysis. These techniques are highly effective and increase core temperature by 1C to 2C (3.6F) every three to five minutes. Active core rewarming also can be accomplished by warm lavage of several body cavities. First Aid Treatment: Call an ambulance do not try and re-warm a moderate to severe hypothermic patient on your own without calling an ambulance, this is an emergency situation. Prevent further heat loss by placing in a warm environment. Remove wet clothing once sheltered. Provide active heat if available but avoid heating the periphery (this will send cold blood to the core leading to after-drop). Instead wrap in space blankets 1st layer with additional layers over top; try warmed up water bottles (not hot) and ensure they cant burn cold skin (ie, outside of space blanket, close to core); someone elses body heat; warm sweet drinks if fully conscious. Avoid overly hot things (fire, hot bath), activity, massage and heating the periphery.

Asthma
Highly trained athletes are repeatedly and strongly exposed to cold air during winter training. As discontinuing high-level exercise has proved effective in reducing eosinophilic airway inflammation, exercise or training should be restricted in athletes having troublesome symptoms and sputum eosinophilia. Standard inhalers appear to make little difference. Switching training to less irritating environments should be considered whenever possible. It appears to be difficult to change the 'natural course' of asthma in athletes by anti-inflammatory treatment.

Pulmonary Oedema
Pulmonary oedema induced by swimming in cold water has previously been described in fit young men. Three cases were described in young men undergoing US Navy SEAL underwater demolition training. An Israeli study found that 60% of athletic swimmers had symptoms of pulmonary oedema. Another Israeli study found similar features in young men undergoing military fitness training (Biswas, Shibu et al. 2004). The following factors are thought to contribute to the temporary increase in capillary venous pressure. Exercise causes increased cardiac output. Excessive drinking of water before swimming, to counteract dehydration, causes increase in preload and pulmonary venous pressure. 6

Swimming in cold water (even wearing a wet suit) can cause a decrease in core temperature resulting in redistribution of blood from peripheral to thoracic vessels resulting in a further increase in preload. Cold temperatures can also increase preload and after load as well as pulmonary vascular resistance.

It has been reported that most patients do not have recurrence of symptoms. Owing to gravity dependent increases in pulmonary capillary pressure, signs are usually present on the right side.

Prevention is the only treatment

The Ice Berger principles are based upon a shared social experience designed to enhance health and wellbeing. Its intentions are good but on occasion may be misplaced. The challenge associated with pushing the body to its limits brings with it inherent and real risks, including the very real possibility of death. Some people are capable of handling cold water conditions for extended periods. Habituation is likely with repeated exposure. However certain people will suffer heat loss and at a far greater rate than others and in a water environment can quickly translate to swimming failure leading to drowning, or hypothermia leading to cardiac arrest or drowning. This has nothing to do with ability, inner strength, fitness, endurance, technique or how someone else might be able to deal with the cold. Premature death due to subjecting the body to extreme environments is not something that is healthy, socially enhancing or smart. The pressure to conform to the Ice Bergers formal rules (no wetsuit) and its unwritten informal pressures presented by its social norms is high (internal and passive external competition, pressure to conform, pressure to be seen as worthy/capable). Everyone involved in presenting these social norms are responsible for how far an individual will push themselves and therefore everyone associated, will be in some way complicit in any trauma or death that results. That is to say that in this context, an individual decision is often influenced by subtle or subliminal messages received from the group; the individual will push themselves beyond safe limits to remain included. It is up to the group and the individual to make the distinction about what is the healthy pursuit of activity and what is an unacceptable risk. Any incident of moderate or severe hypothermia must involve an ambulance and this decision should not be made by the participant. It is likely that any incident where the patient loses swimming efficiency should also be classed as a near drowning event. NOTE: this situation is completely preventable and the MMLS club should not be putting themselves in a position where an emergency situation arises consistently. Essentially, the club should not knowingly allow people to put themselves at risk. Prevention includes limiting exposure, the wearing of protective clothing, providing protection for the arms in particular, understanding the signs and symptoms and not pushing through them. The group needs to understand the social pressure it places on people to conform in doing so facilitates a risk taking behaviour. It is the recommendation of this paper, that the MMLSC Ice Bergers consider developing a code of conduct and procedures around issues associated with its rules, social norms as well as its approach to prevention and treatment. This code of conduct should accommodate without prejudice the priority of safety over bravado, machismo or competition. The activity itself should be viewed as healthy if the participants are capable of staying within their limitations. The risks are very real and unfortunately death is a consequence that can arise from this healthy pursuit.

Note: This is not an official paper and was not referenced according to APA standard referencing techniques.

Biswas, R., P. K. Shibu, et al. (2004). "Pulmonary oedema precipitated by cold water swimming." Br J Sports Med 38(6): e36-. Kolettis, T. M. and M. T. Kolettis (2003). "Winter swimming: healthy or hazardous?: Evidence and hypotheses." Medical Hypotheses 61(5-6): 654-656. McCullough, L. (2004). "Diagnosis and treatment of hypothermia." American Family Physician 70(12): 2325. Teramoto, S. and Y. Ouchi (1999). "Swimming in cold water." The Lancet 354(9191): 1733-1733. Tipton, M., C. Eglin, et al. (1999). "Immersion deaths and deterioration in swimming performance in cold water." Lancet 354: 626-629. Tipton, M., I. Mekjavic, et al. (2000). "Permenance of the habituation of the initial responses to cold-water immersions in humans." European Journal of Applied Physiology 83: 17-21.