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IMMERSION INTO COLD WATER
By: Dr. Alan Steinman Website: www.expertwitness.com/steinman
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Immersion in cold water is a hazard for anyone who participates in recreational, commercial or military activities in the oceans, lakes, and streams of all but the tropical regions of the world. Recreational aquatic activities include swimming, fishing, sailing, power-boating, ocean kayaking, white-water rafting, canoeing, ocean-surfing, wind-surfing, water-skiing, diving, hunting and the use of personal water craft. In addition, use of a snowmobile, although not technically a water sport can involve cold-water exposure due to accidental entry into lakes and streams. Commercial activities involving water include fishing, shipping, offshore oil drilling, and diving. Military operations over cold water include Coast Guard, Navy and Marine Corps missions; Army, Air Force and Marine Corps forces, as well, may encounter cold-water exposure during winter operations on land.
The definition of cold water is variable. The temperature of thermally neutral water, in which heat loss balances heat production for a nude subject at rest (i.e., not shivering), is approximately 33-35° C. Hypothermia eventually results from immersion in water below this temperature. For practical purposes, significant risk of immersion hypothermia usually begins in water colder than 25° C. Using 25° C as the definition of cold water, the risk of immersion hypothermia in North America is nearly universal during most of the year.
Cold water immersion is associated with two significant medical emergencies: near drowning and hypothermia.
Physiological Responses to Cold-Water Immersion
The primary pathophysiologic effects of hypothermia are a decrease in tissue metabolism and a gradual inhibition of neural transmission and control. However, in the initial stages of cooling of an intact, conscious victim, secondary responses to skin temperature cooling predominate. Sudden immersion in cold water results in an immediate decline in skin temperature which, in turn, initiates shivering thermogenesis with increases in metabolism (VO2), ventilation (VE), heart rate (HR), cardiac output (CO), and mean arterial pressure (MAP). As body temperature declines and shivering ceases, VO2, HR, MAP and CO decrease proportionally with the fall in core temperature, while hematocrit and total peripheral resistance increase. Renal diuresis and extravascular fluid shifts can lead to a considerable loss of intravascular volume, thus decreasing systemic perfusion.
The body's responses to cold-water immersion can be divided into three phases: 1) initial immersion and the cold-shock response; 2) short-term immersion and loss of performance; and 3) long-term immersion and the onset of hypothermia. Each phase is accompanied by specific survival hazards for the immersion victim from a variety of pathophysiologic mechanisms. Deaths have occurred in all three phases of the immersion response.
Phase 1: Initial Immersion and the Cold Shock Response:
The cold shock response occurs within the first 1-4 minutes of cold water immersion and is dependent on the extent and rate of skin cooling. The responses are generally those affecting the respiratory system and those affecting the heart and the body's metabolism. Rapid skin cooling initiates an immediate gasp response, the inability to breath-hold, and hyperventilation. The gasp response may cause drowning if the head is submersed during the initial entry into cold water. Subsequent inability to breath-hold may further potentiate drowning in high seas. Finally, hyperventilation causes arterial hypocapnia, which leads to decreased brain blood flow and oxygen supply. This may lead to disorientation, loss of consciousness and drowning.
Skin cooling also initiates peripheral vasoconstriction as well as increased cardiac output, heart rate and arterial blood pressure. The increased workload on the heart may lead to myocardial ischemia and arrhythmias, including ventricular fibrillation. Thus, sudden death can occur either immediately or within a matter of minutes after immersion (i.e., due to syncope or convulsions leading to drowning, vagal arrest of the heart, and ventricular fibrillation) in susceptible individuals.
Phase 2: Short-Term Immersion and Loss of Performance:
For those surviving the cold shock response, significant cooling of peripheral tissues, especially in the extremities, continues with most of the effect occurring over the first 30 minutes of immersion. This cooling has a direct deleterious effect on neuromuscular activity. This effect is especially significant in the hands, where blood circulation is negligible, leading to finger stiffness, poor coordination of gross and fine motor activity, and loss of power. It has been shown that this effect is primarily due to peripheral and not central cooling. The loss of motor control makes it difficult, if not impossible, to execute survival procedures such as grasping a rescue line or hoist, etc. Thus the ultimate cause of death is drowning, either through a failure to initiate or maintain survival performance (i.e., keeping afloat, swimming, grasping onto a liferaft, etc.) or excessive inhalation of water under turbulent conditions.
These phenomena have obvious survival implications. It is, of course, advisable to avoid cold water exposure completely. If cold-water immersion does occur however, it is best to quickly determine and execute a plan of action: 1) try to enter the water without submersing the head; 2) escape (i.e., pull oneself out of the water, inflate and board a liferaft); 3) minimize exposure (i.e., get as much of one's body as possible out of the water and onto a floating object); 4) ensure flotation if one must remain in the water (i.e., don or inflate a personal flotation device); and 5) call for assistance (i.e. activate signaling devices). It may be difficult to execute these actions while the cold shock responses predominate. However, once the respiratory effects are under control, immediate action should be taken. If self-rescue is not possible, actions to minimize heat loss should be initiated by remaining as still as possible in the Heat Escape Lessening Position (HELP), where arms are pressed against the chest and legs are pressed together, or huddling with other survivors. Drawstrings should be tightened in clothing to decrease the flow of cold water within clothing layers.
Phase 3: Long-term immersion and the onset of hypothermia:
Most cold-water deaths likely result from drowning during the first two phases of cold-water immersion, as discussed above. In general, true hypothermia usually only becomes a significant contributor to death if immersion lasts more than 30 minutes. The individual who survives the immediate and short-term phases of cold-water immersion faces the possible onset of hypothermia as continuous heat loss from the body eventually decreases core temperature (Tco). Many predictive models to determine the core temperature response to cooling are based on the relationships between body composition, thermoregulatory response (i.e., shivering thermogenesis), clothing/insulation, water temperature and sea conditions. These variables and their impact on survival time are discussed in more detail in the Cold Water Survival section of this chapter.
Normal body Tco fluctuates around 37° C. The clinical definition of hypothermia is a Tco of 35° C or lower; however, any exposure to cold that lowers the temperature below normal levels results in the body becoming hypothermic. Although various temperatures and terms have been used to classify different levels of hypothermia, the following classifications will be used here. In mild hypothermia (Tco = 32-35° C) thermoregulatory mechanisms continue to operate fully, but ataxia, dysarthria, apathy and even amnesia are likely. In moderate hypothermia (Tco = 28-32° C) the effectiveness of the thermoregulatory system (i.e., shivering thermogenesis) diminishes until it fails; there is a continued decrease in level of consciousness; and cardiac dysrhythmias may also occur. In severe hypothermia (Tco ‹ 28° C) consciousness is lost, shivering is absent, acid-base disturbances develop, and the heart is susceptible to ventricular fibrillation or asystole. Death from hypothermia is generally from cardiorespiratory failure.
The rate of body core cooling during cold-water immersion depends on the following variables:
Cold Water Survival
Cold water survival depends on avoidance of drowning and hypothermia and on the many factors related to these risks.
Drowning is the most immediate survival problem following water entry. To maintain airway freeboard and to avoid drowning, a survivor must possess the physical skills and psychological aptitude to combat the effects of wave action. Although a PFD assists in maintenance of airway freeboard, waves can still submerge a survivor's head, even in moderately calm seas. To reduce the risk of drowning in rough seas, a survivor can increase effective airway freeboard by partially exiting the water (for example, clinging to an overturned vessel or other debris floating in the water) or by climbing totally out of the water into a life raft or onto a capsized vessel. In both these environments the survivor may still have to cope with the effects of cold wind, spray, and waves.
Prehospital management of hypothermia patients, both in the field and during transportation to a site of definitive medical care, varies with the patient's level of hypothermia, with the rescuer's level of training, with the resuscitative equipment available, with the type of transportation, and with the time required for delivery to definitive care. Medical personnel must exercise good clinical judgment in balancing all these factors to select appropriate therapeutic modalities.
Rescue and Management
The primary goals in prehospital management of victims of accidental immersion hypothermia are prevention of cardiopulmonary arrest, prevention of continued core temperature decline, moderate core rewarming if practicable, and transportation to a site of definitive medical care. Aggressive rewarming in the field is usually contraindicated, since the means to either diagnose or manage the many potential complications of severe hypothermia are unavailable in this setting. In unusual circumstances, when transportation to a site of definitive care is impossible, definitive rewarming in the field, using the principles and techniques of management described in the following paragraphs, may be appropriate.
Retrieval of a victim from cold water immersion must be performed with caution. Sudden reduction of the "hydrostatic squeeze" applied to tissues below the water's surface may potentiate hypotension, especially orthostatic hypotension. Since a hypothermic patient's normal cardiovascular defenses are impaired, the cold myocardium may be incapable of increasing cardiac output in response to a hypotensive stimulus. A victim's vertical posture may also potentiate hypotension. Hypovolemia, secondary to combined cold- and immersion-induced diuresis, and increased blood viscosity potentiate these effects. Peripheral vascular resistance may also be incapable of increasing, since vasoconstriction is already maximal because of cold stress. The net result of sudden removal of a hypothermic patient from the water is similar to sudden deflation of antishock trousers on a patient in hypovolemic shock: abrupt hypotension. This has been demonstrated experimentally in mildly hypothermic human volunteers, and it has been suspected as a cause of post-rescue death in many immersion hypothermia victims. Accordingly, rescuers should attempt to maintain hypothermic patients in a horizontal position during retrieval from the water and aboard the rescue vehicle. If rescuers cannot recover the patient horizontally, they should place the victim in a supine posture as quickly as possible after removal from cold water.
The patient's core temperature may continue to decline (depending on the quality of insulation provided, the patient's endogenous heat production, active or passive manipulation of extremities, and the site of core temperature measurement) even after he or she has been rescued, because of the physiologic processes described earlier for "afterdrop." To diminish this effect, the patient's physical activity must be minimized. Conscious patients should not be required to assist in their own rescue (for example, by climbing up a scramble net or ship's ladder) or to ambulate once out of the water (as by walking to a waiting ambulance or helicopter). Physical activity increases afterdrop, presumably by increasing perfusion of cold muscle tissue with relatively warm blood. As this blood is cooled, venous return (the circulatory component to afterdrop) contributes to a decline in myocardial temperature, increasing the risk of ventricular fibrillation. Experiments on moderately hypothermic volunteers (esophageal temperature 33° C) demonstrated a threefold greater afterdrop during treadmill walking than while lying still. Such an exercise-induced enhancement of afterdrop could precipitate post-rescue collapse. Throughout the rescue procedures and during subsequent management, hypothermic patients must be handled gently. Excessive mechanical stimulation of the cold myocardium is another suspected cause of deaths after rescue.
Dr. Alan Steinman is an expert in Maritime Medicine with particular emphasis on Sea-Survival, Drowning and Hypothermia. He has served as Surgeon General and Director of Health and Safety for the U.S. Coast Guard, as medical advisor to the Coast Guard's Chief of Operations, and as rescue physician on numerous Coast Guard search and rescue missions. He has an international reputation in hypothermia and cold-water survival.
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