You are on duty on a hot, humid Sunday afternoon in late June when you are called to a park for a report of a "female unconscious."
You are directed to a small crowd in the middle of the park, where a local running club has been holding a marathon-preparation run. The crowd has surrounded a 30-year-old female, who is lying supine on the gravel. She is being given water by a gentleman who identifies himself as the trainer.
You start to assess the patient and find that she is alert and complains of becoming dizzy while running the event. She also complains of a headache, which she rates as a 5 out of 10, and abdominal cramps. Her running shorts and shirt are soaking wet, and she says she is extremely thirsty. Vital signs are: B/P: 122/70; Pulse: 100; Respirations: 22.
Physical examination findings include: lung sounds clear bilaterally, pupils equal and reacting bilaterally, skin is cool and moist, negative JVD, negative pedal edema, extremities exhibit normal strength. She denies neck stiffness and says she did not lose consciousness, but fell to her knees onto the grass from dizziness. She denies hitting her head, and there is no visible trauma. Her medical history is unremarkable, except for "pulling" her shoulder earlier in the week lifting weights, for which she has been taking ibuprofen. She denies any history of diabetes, cardiac problems, hypertension, palpitations or shortness of breath. The patient says she has run similar races before without any problems. She also says she had been running for about five hours without any problems, but started getting a headache that she attributed to dehydration. She says she has been keeping up with her fluid replacement, having a cup of water at every mile along the route. Although she has cramps, she denies nausea, so you continue to encourage her to replace her water loss. Paramedics responding to the "unconscious" arrive and, after getting her history, start an IV with D5W (5% dextrose in water) for more fluid and prepare to transport.
An EKG is obtained, which is read as sinus tachycardia with no signs of cardiac ischemia or pulmonary embolism. The patient complains of increasing headache and nausea. As you get ready to transport, she becomes lethargic and vomits water. Repeated vital signs are BP: 100 palp; pulse: 100; resps: 22. En route to the hospital, the patient suffers a tonic-clonic (grand mal) seizure and becomes unresponsive. She is intubated and ventilated, and thiamine, D50 (concentrated dextrose) and naloxone are administered. There is no change in her mental status. A glucometer reading of 145 mg/dl is obtained. At the ED, a stat electrolyte panel is done. Diagnosis: Exercise-associated hyponatremia.
Dehydration, or more likely the idea of dehydration, is supposed common knowledge. We have been told to drink water from our earliest gym classes through all levels of athletics and into everyday activities. The concept of overhydration is barely mentioned, if at all, in most protocols. Only recently has the life-threatening danger of overhydration come to the forefront, in part because of the tragic death of a runner at the 2002 Boston Marathon. While you may never see a case of hyponatremia in an entire EMS career, it is because of the potentially lethal effect of treating it as dehydration that you should be aware of the common situations where it occurs (marathons, endurance activities) and keep it in mind before improperly (and lethally) treating it as dehydration. This should not be taken as new medical advice not to drink during athletic activities. Athletes and those undertaking athletic activities should consult knowledgeable medical professionals about their hydration and liquid intake.
Hyponatremia is a condition of low concentration of sodium in the blood. It is also called "water intoxication." Exercise-associated hyponatremia may occur during prolonged sports activity, such as marathons, triathlons, long hikes or bicycling, when fluid intake exceeds fluid loss. When water dilutes the body's salts, the blood has too much water and too little sodium, which causes brain cells to absorb too much water and swell (cerebral edema). As brain tissue swells inside the closed box of the skull, it compresses the brain structures and causes neurological signs and symptoms.
Although hyponatremia and dehydration are physiologically opposed, the symptoms of both conditions are similar, further complicating the assessment. Both conditions commonly present with apathy, confusion, nausea and fatigue, although some individuals show no symptoms at all. In hyponatremia, swelling of the hands and feet may be noted.
Exercise-associated hyponatremia is a life-threatening condition that has been described in endurance athletes, Grand Canyon hikers and military personnel over the past 15 years.1 To date, at least seven fatalities and more than 250 cases of this condition have been described in the medical literature.2 In actuality, while there is not a single case report or clinical trial that unambiguously links exercise-induced dehydration with specific life-threatening, exercise-related disorders, there is absolute evidence of the deadly consequences of fluid overload by healthcare providers.3
The patient in the case scenario was differentiated from "heat exhaustion," heatstroke and hypoglycemia more by history than clinical symptomatology. This patient drank too much fluid. When exercise in the heat is prolonged, hyponatremia is suggested either by altered mental status or seizures, in the absence of hyperthermia or hypoglycemia.
Early hyponatremia symptoms are nonspecific and are similar to the spectrum seen in exertional heat illness (heat exhaustion). For this reason, early consideration of hyponatremia, and excluding it when appropriate, is critical for prompt diagnosis and appropriate treatment in an exercising individual who consumes fluids.
EMS textbooks typically refer to a continuum of heat injury and dehydration, starting with heat cramps, then heat exhaustion, then heatstroke.5 Of these, only heatstroke, which occurs infrequently, is definitely a heat illness. It is caused by an increased rate of heat production unmatched by adequate heat loss, causing progressive heat retention and the body temperature rising to dangerously high levels.6 Heat exhaustion is classically considered a condition of hyperthermia caused by dehydration, although neither of these components has ever been proven.6 It is taught that heat exhaustion may progress to heatstroke as the body's thermoregulatory abilities fail to compensate.5 The terms "heat cramps" and "heat exhaustion" are misleading, as neither is caused by an elevated body temperature, nor is there evidence that either is caused by specific fluid or electrolyte abnormalities.6 Cramps occur during or after exercise regardless of whether the exercise is performed in the heat or cold, or in water. Current evidence suggests cramping is unrelated to biochemical changes in either blood or the affected skeletal muscles. No modern studies have shown that exercise-related heat exhaustion is necessarily caused by specific fluid deficit or electrolyte abnormalities. Similarly, there is no published evidence that fluid loss is a critical determinant of heatstroke.6
Heat Exhaustion (Exercise-Associated Collapse)
The most commonly encountered medical condition at endurance-athletic events is collapse after the event. Athletes who finish the race and then collapse are usually fully conscious and are simply suffering from postural hypotension, caused by peripheral blood-pooling not being pushed back up to the heart and brain by muscle activity.7 If you think about it, if patients are so severely dehydrated that they are going to collapse, wouldn't it stand to reason that they would do this when they are in a state of great cardiovascular demand and not during the cooling-off period? As stated above, the term heat exhaustion has been classically considered a condition of hyperthermia caused by dehydration, although neither of these components has ever been proven. For this reason, IV lines have been started on untold scores of athletes to replace their "fluid loss." The thought that "fluid can't hurt" has been disproved with current literature and science in much the same way the belief that hyperventilating the head-injured patient without evidence of hypoxia has been disproved.
Heatstroke is defined by end-organ damage, and clinically is manifested and diagnosed by the presence of CNS dysfunction, altered mental status, confusion, seizure activity and coma in the presence of hyperthermia. As with all cases of potential altered mental status, interviewing friends and family of the patient is appropriate to determine if the patient's current mental status is his/her normal behavior.
Clinically, two forms of heatstroke are differentiated. Classic heatstroke, which occurs during environmental heat waves, is more common in very young persons and in the elderly population and should be suspected in children, elderly persons and chronically ill individuals who present with altered mental status. Classic heatstroke occurs because of failure of the body's heat-dissipating mechanisms. Exertional heatstroke commonly is observed in young, healthy individuals (e.g., athletes, firefighters, military personnel) who, while engaging in strenuous physical activity, overwhelm their thermoregulatory systems and become hyperthermic.8
Heatstroke is potentially lethal hyperthermia. As the body loses its ability to cool itself and core temperature rises, cerebral edema and cerebrovascular congestion arise, which culminates in increased intracranial pressure (ICP). This increased ICP, combined with a decreased mean arterial pressure (MAP is the average value for arterial pressure and is the systolic pressure+diastolic pressure/2) causes cerebral blood flow to decrease. This is manifested clinically as CNS dysfunction (altered mental status, confusion, seizures).
Classically, EMT and first aid courses have differentiated between heat exhaustion and heatstroke by the presence of sweat. Generations of EMTs have been instructed that a hot, sweaty patient has heat exhaustion, while a hot, dry patient has heatstroke. This is not an accurate guideline, although anhydrosis (absence of sweating) may be a classic feature of heatstroke. More than half of presenting patients are sweating, especially in cases of exertional heatstroke. Because their ability to sweat remains intact, patients with exertional heatstroke are able to cool down after cessation of physical activity and may present for medical attention with temperatures lower than they had been. Anhydrosis usually is a late finding.9 Some authors have written that the diagnosis of heat exhaustion or heatstroke can only be made after recovery when organ damage can be assessed.10
Take-Home Point: CNS dysfunction in a hyperthermic patient is heatstroke until proven otherwise!
Patients, especially those participating in an athletic event, may present with simple dehydration. These patients should be able to walk over to the medical tent or ambulance to receive oral fluid replacements and have no acute complaints. Patients presenting with an altered mental status or other symptoms must be fully assessed and interviewed for other, more serious pathologies.
For the athlete who collapses to the ground, but does not lose consciousness immediately after finishing an event (exercise-associated collapse), an appropriate treatment option (after assessing ABCs and excluding life-threatening conditions) is simply to lay the patient in a head-down (Trendelenburg) position. This facilitates vascular perfusion, and the symptoms should resolve quickly. Again, it must be repeated that the exercise-associated collapse patient does not have an altered mental state, nor is he presenting with other symptoms of a more serious event. No study has demonstrated that treating collapsed athletes with IV fluids helps them to recover more quickly than nursing them in the head-down position.11 In the first two years of the South African Ironman Triathlon, it was not necessary to give IV fluids to a single collapsed athlete. All of them recovered rapidly with placement in the head-down position only.12
Patients who are displaying signs of CNS dysfunction in the presence of hyperthermia and are so presumed to be suffering a heatstroke need urgent care. As with all conditions, ABCs must be evaluated and serially reassessed. One of the dangers in heatstroke is the patients' loss of ability to maintain their own airway, as well as seizure activity. The tonic-clonic activity in seizures produces even more heat, of which the body cannot rid itself. This is a true heat emergency; rapid cooling is the rule. Evaporative cooling via spraying water on the patient's skin and having it fanned off, in addition to placing cold packs in the patient's groin, axilla and on both sides of the neck, has been shown to be a very effective method in the prehospital setting. Airway control measures and oxygen administration as dictated by protocol are indicated, but vigilance is important and constant reassessment is essential, as the heatstroke patient's condition can deteriorate in a matter of seconds. As there is no evidence that heatstroke is caused by dehydration, minimal (TKO/KVO) intravenous fluids should be administered, unless otherwise dictated by other processes, protocol or medical control.
Exertional hyponatremia should be considered in the patient who:
presents with CNS dysfunction
has been participating in strenuous or endurance activities
is not hyperthermic
has no evidence of trauma
has no evidence of hypoglycemia.
In addition to monitoring ABCs, prehospital treatment consists of intravenous normal saline (0.9%) administration. You should now be able to go back and see why IV D5W actually worsened the patient's condition. The patient's sodium level decreased as a result of her overhydration by drinking too much water. Administration of a solution like D5W, which is mostly free water, exacerbates the patient's fluid overload and even further dilutes the sodium level in the blood. Some authorities advocate using intravenous hypertonic (3%) saline for the severe hyponatremia patient, but this consideration is being excluded because most prehospital agencies do not readily stock hypertonic intravenous fluids. Intravenous furosemide is also indicated to ensure excess water is rapidly excreted. In-hospital treatment consists of a full assessment of the patient's sodium and fluid status and proper replenishment in a controlled setting with serial reassessment.
While a thorough medical history is always important, it is vital to ask athletic competitors about their intake of medications, both prescription and nonprescription. Pay particular attention and document the use of diuretics, muscle-builders, fat-burners, appetite-suppressants, creatine, etc., as they may have affected the patient's metabolic status.
The purpose of this article is to remind field providers that not all calls on hot days are simple heat exhaustion or dehydration, as well as to advise providers that there is active debate and research into exercise-related and heat-related illnesses. Emergency medical services, like all areas of medicine, are constantly being researched, challenged and evaluated. All providers are reminded that they must follow the protocols established by their EMS agency.
The literature suggests that females are affected by hyponatremia more than males, and that the less-competitive athlete (toward the back of the race) is affected more than the competitive athlete. A study by Runner's World indicated that 74% of runners take analgesics and more than 88% report using NSAIDs (non-steroidal anti-inflammatory drugs), including naproxen sodium (Naprosyn) and ibuprofen (Advil).4 NSAIDs seem to increase the risk, probably because the drugs impair the body's ability to excrete water. The seven runners who died from hyponatremia all had a history of NSAID use. In fact, Tylenol is a sponsor of the ING NYC Marathon and is the only approved anti-inflammatory agent for distribution by the marathon medical staff because it does not pose this risk. It should be noted that some physicians may not be aware of NSAIDs' effect on the kidneys, especially if they are not sports-oriented physicians, and may be misadvising athletes to take NSAIDs prior to endurance activities.
According to the National Oceanic and Atmospheric Administration (NOAA), approximately 175¡V200 persons die from heat-related disorders during an average year in the United States. This statistic rises to more than 1,500 persons during heat waves. The exact number of persons seeking treatment for heat-related disorders is not recorded but reaches the thousands. Estimates of fatalities caused by heat-related illness in the United States range from 300 to several thousand per year. The mortality rate in patients with heatstroke has been reported to be 10%¡V70%, with the highest number of deaths occurring when treatment is delayed for more than two hours.
Heat waves increase the mortality rate. The heat wave in July 1995 caused 91 deaths in Milwaukee and 465 deaths in Chicago.
Publication in 1969 of an article by Wyndham and Strydom, incorrectly titled "The Danger of an Inadequate Water Intake During Marathon Running," paved the way for numerous studies, many funded by the sports drinks industry, culminating in guidelines for ingestion of fluids during exercise. That the article never identified any dangers apparently never bothered anyone. Rather, it showed that the most dehydrated athletes usually won the 32-km races they were evaluating.
1. Flinn SD, Sherer RJ. Seizure after exercise in the heat recognizing life-threatening hyponatremia. The Physician and Sportsmedicine 28(9):61–67, Sept. 2000. 2. Noakes TD. Overconsumption of fluids by athletes. Br Med J, July 19, 2003. 3. Noakes TD. Hyponatremia in distance athletes. The Physician and Sportsmedicine 28(9):71–76, Sept. 2000. 4. Cimons M. Hyponatremia. Water hazard. Runner’s World, p. 46, October 2000. 5. Browner BD, Lenworth MJ, Pollak AN. Environmental Emergencies, Chapter 20, pp. 472–475. Emergency Care and Transportation of the Sick and Injured, 7th Edition. AAOS, 1999. 6. Noakes TD. Fluid and electrolyte disturbances in heat illness. International Journal of Sports Medicine, Suppl 2:S146–149, June 19, 1998. 7. Noakes TD. Pulling the IV on the “dehydration myth.” The Physician and Sportsmedicine 28(9):71–76, September 2000. 8. Helman RS, Habal R. Heatstroke. Available from www.emedicine.com/med/topic956.htm. Accessed on 4/4/04. 9. Kunihiro A, Foster J. Heat exhaustion and heatstroke. Available from www.emedicine.com/emerg/topic236.htm. Accessed on 3/16/04. 10. Department of the Army, U.S. Army Research Institute of Environmental Medicine. Available at http://www.usariem.army.mil/heatill/htstroke.htm. Accessed on 3/18/04. 11. Mayers LB, Noakes TD. A guide to treating Ironman triathletes at the finish line. The Physician and Sportsmedicine 28(8):35–50, 2000. 12.Speedy D, Noakes TD. Exercise-associated collapse: Postural hypotension or somethingdeadlier? The Physician and Sportsmedicine 31(3):23¡V29, March 2003.
The author thanks Timothy Noakes, MD, Discovery Health Chair of Exercise and Sports Science at the University of Cape Town for his time in answering my questions, and for his remarkable contributions to this area of medicine. Thanks, also, to Stephen Perle, DC, associate professor of clinical sciences at the University of Bridgeport College of Chiropractic for his assistance.
Rob Curran has been an EMT in New York City for over 15 years. He instructs undergraduate and graduate pathophysiology at SUNY-Downstate and Human Anatomy and Physiology at CUNY-Brooklyn College.