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Evaluation of the collapsed adult athlete

Evaluation of the collapsed adult athlete
Literature review current through: Jan 2024.
This topic last updated: Jul 06, 2022.

INTRODUCTION — On occasion, athletes collapse. This can occur in the midst of competition, during practice, or at the completion of long endurance races. Often the cause is benign and the athlete recovers quickly and completely. However, in a small number of cases, collapse is caused by a serious or life-threatening medical condition or by traumatic injury. Clinicians responsible for providing medical supervision at endurance races and other athletic events must be prepared to evaluate, triage, and provide emergency medical care for the collapsed athlete [1,2].

This topic discusses our approach to assessing, diagnosing, and stabilizing the collapsed athlete. Also provided are links to additional topics describing the management of specific conditions that may cause collapse. Medical planning for endurance sporting events is reviewed separately. (See "Preparation and management of mass-participation endurance sporting events".)

DEFINITION — Collapse can be defined as failure of a physiologic system (eg, cardiovascular, pulmonary, nervous, or musculoskeletal); in the sporting environment, collapse means the athlete is unable to continue participating and unable to remove themselves under their own power from the race course or field due to such a failure [3-5].

Collapse is not necessarily defined by an alteration in the athlete's level of consciousness. While a cardiovascular arrhythmia may cause a complete loss of consciousness and exertional heat stroke may cause acute delirium, a musculoskeletal injury or a compilation of sickle cell trait can cause collapse without an alteration in consciousness, yet the athlete remains unable to render themselves off the sporting field without assistance.

The National Center for Catastrophic Sport Injury Research (NCCSIR), which is dedicated to compiling data on catastrophic sports injuries among high school and collegiate athletes in the United States, categorizes significant injury mechanisms as either direct or indirect [6]. Direct injuries result from performing skills required of the sport (eg, neck injury sustained by a tackler in American football or rugby), while indirect injuries are caused by systemic failure as a result of exertion while participating in a sport (eg, cardiac arrest sustained by a marathoner) or by a complication that was secondary to a nonfatal injury (eg, acute kidney injury due to exertional heat stroke). Direct and indirect mechanisms generally mean traumatic and exertional, respectively, and these are the terms we use in this topic. The challenge for the clinician assessing a collapsed athlete is to distinguish serious from benign causes, and to provide appropriate care expeditiously.

EPIDEMIOLOGY — The epidemiology of collapsed athletes varies by sport, by whether collapse occurred during practice or competition, and by a range of potential risk factors, including characteristics of the individual participant (eg, comorbidities) and environmental conditions. Clinician understanding of the most likely potential diagnoses affects athlete morbidity and mortality, as it plays a fundamental role in preventive planning and acute management. The epidemiology literature, while limited, provides some guidance. Below we briefly review the epidemiology of the collapsed athlete by setting, including the important and common causes during endurance events and field sports, and by exertional and trauma-related causes of collapse.

Mass participation endurance sporting events — The epidemiology of collapse during mass participation endurance sporting events is well described and represents a subgroup of the total number of medical encounters. This epidemiology is discussed in greater detail separately; below we note some highlights of particular importance to clinicians assessing the collapsed athlete. (See "Preparation and management of mass-participation endurance sporting events", section on 'Epidemiology'.)

Medical conditions encountered at the finish areas of endurance races are relatively well defined. Exercise-associated postural hypotension (EAPH) accounts for nearly 60 percent of the medical encounters at the conclusion of marathons and ultramarathons [7]. In a study of 153,208 runners participating in 21.1- and 56-km races (Two Oceans Marathon) over an eight-year period, the overall incidence of exercise-associated collapse (EAC) was 1.5 (95% CI 1.31-1.71) [8]. Longer race distance (incidence ratio [IR] 2.1; 95% CI 1.6-2.7) and slower running speed (IR 1.3; 95% CI 1.1-1.5) were significant risk factors for EAC.

EAPH is a benign process that must be distinguished from the potentially life-threatening conditions that occur with far less frequency, including sudden cardiac arrest (SCA), exertional heat stroke (EHS), and exercise-associated hyponatremia (EAH). At triathlons, drowning may occur but is even less common. EAPH and the life-threatening conditions listed here occur more often at or near the finish line, but can present anywhere along the course of an endurance race. (See 'Initial management of the collapsed athlete without trauma' below.)

Environmental conditions affect both the incidence of medical encounters and the nature of the injuries sustained. Particularly in warm, humid conditions, EHS is significantly more common than the other life-threatening conditions mentioned above. Cold temperatures and high winds increase the risk for frostbite and hypothermia among participants in Nordic events (eg, cross-country skiing). (See "Exertional heat illness in adolescents and adults: Epidemiology, thermoregulation, risk factors, and diagnosis", section on 'Epidemiology' and "Preparation and management of mass-participation endurance sporting events", section on 'Epidemiology' and "Preparation and management of mass-participation endurance sporting events", section on 'Hazardous conditions and indications to cancel an event'.)

Field and court sports — The National Center for Catastrophic Sport Injury Research (NCCSIR) of the United States categorizes athletic injury as either direct (traumatic) or indirect (exertional). Exertional injuries are caused by systemic failure as a result of physical exertion while participating in a sport (eg, EHS) or by a complication of a nonfatal injury (eg, seizure due to EAH). Traumatic injuries are sustained during the performance of techniques or actions required of the sport (eg, tackling in American football resulting in a catastrophic neck injury). (See 'Definition' above.)

Exertional collapse — According to the NCCSIR annual report, a total of 112 catastrophic injuries or illnesses occurred during high school and college sports in 2016 [6]. The majority occurred among high school athletes (81 percent). Of the exertional catastrophic events, 47.5 percent were fatal; the majority occurred during training or practice (65 percent) rather than competition. The majority of the exertional catastrophes were cardiac-related (60 percent) or secondary to exertion in the heat (22.5 percent). American football (35 percent), basketball (15 percent), and football (ie, soccer, 12.5 percent) accounted for the majority of exertional events. (See "Athletes: Overview of sudden cardiac death risk and sport participation" and "Screening to prevent sudden cardiac death in competitive athletes".)

Exertional heat illness (EHI) is a potentially life-threatening cause of collapse among athletes playing during high heat and humidity. The epidemiology of EHI is discussed in detail separately. (See "Exertional heat illness in adolescents and adults: Epidemiology, thermoregulation, risk factors, and diagnosis", section on 'Epidemiology'.)

Trauma-related collapse — According to the NCCSIR 2016 annual report, over 60 percent of catastrophic events were the result of direct traumatic injury, occurring principally during competition (59.4 percent) [6]. American football competitions accounted for most such injuries (83.6 percent), followed by basketball. Thus, the estimated 1.1 million high school and 75,000 college athletes who participate in tackle football annually in the United States represent a relatively high-risk group for catastrophic injury.

Nearly 15 percent of trauma-related catastrophes were fatal, with most occurring during competition (80.4 percent). The majority of deaths were due to injuries of the cervical spine (50.8 percent), followed by the head or brain (31.1 percent), and heart (ie, commotio cordis, 4.9 percent). (See "Cervical spinal column injuries in adults: Evaluation and initial management" and "Acute traumatic spinal cord injury" and "Management of acute moderate and severe traumatic brain injury" and "Acute mild traumatic brain injury (concussion) in adults" and "Commotio cordis".)

According to a report from the US Centers for Disease Control, from 2005 to 2014 a total of 28 deaths (2.8 deaths per year) occurred from traumatic brain and spinal cord injuries among high school (24 deaths) and college (4 deaths) American football players [9]. Most deaths occurred during competitions and resulted from tackling or being tackled. All 4 of the college deaths and 14 (58 percent) of the 24 high school deaths occurred from 2010 to 2014.

Other sports with relatively high rates of catastrophic injury from trauma (although still rare overall) include ice hockey, lacrosse, gymnastics, track and field (eg, pole vault), and cheerleading [10-15]. Participants sustaining such devastating injuries often present with post-traumatic collapse.

CAUSES OF COLLAPSE DURING EXERCISE OR SPORT — Athletes may collapse during activity from many possible causes. The first task of the clinician providing the initial care for a collapsed athlete is to distinguish life-threatening from benign conditions. Below are listed the important and common causes of collapse; our approach to the assessment and management of the collapsed athlete is found further below. (See 'Initial management of the collapsed athlete without trauma' below and 'Differences in assessment and initial management by setting' below.)

Life-threatening causes of collapse — The serious medical conditions most likely to be encountered during an endurance event or athletic competition are listed immediately below (table 1), along with links to the UpToDate topics that discuss the acute management of these conditions in detail:

Sudden cardiac arrest (SCA) (see "Advanced cardiac life support (ACLS) in adults" and "Adult basic life support (BLS) for health care providers")

Exertional heat stroke (EHS) (see "Exertional heat illness in adolescents and adults: Management and prevention", section on 'Management of exertional heat stroke')

Exercise-associated hyponatremia (EAH) (see "Exercise-associated hyponatremia", section on 'Treatment')

Anaphylaxis (see "Anaphylaxis: Emergency treatment" and "Anaphylaxis: Acute diagnosis")

Insulin shock (acute hypoglycemia) (see "Hypoglycemia in adults with diabetes mellitus")

Acute severe asthma exacerbation (see "Acute exacerbations of asthma in adults: Home and office management")

Major trauma (see "Initial management of trauma in adults")

Brain injury (see "Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis" and "Management of acute moderate and severe traumatic brain injury" and "Acute mild traumatic brain injury (concussion) in adults" and "Sideline evaluation of concussion")

Cervical spine injury (see "Cervical spinal column injuries in adults: Evaluation and initial management" and "Acute traumatic spinal cord injury")

Cardiac injury (see "Commotio cordis" and "Initial evaluation and management of blunt cardiac injury")

Blunt torso trauma (see "Initial evaluation and management of blunt abdominal trauma in adults" and "Initial evaluation and management of blunt thoracic trauma in adults" and "Initial evaluation and management of chest wall trauma in adults")

Exercise-associated postural hypotension (EAPH) — EAPH (our preferred term), a subcategory of exercise-associated collapse (EAC), involves collapse after completion of an exertional event (eg, endurance race) in a conscious athlete who is unable to stand or walk unaided as a result of lightheadedness, faintness, or dizziness [4]. Runners with a normal or only mildly elevated core body temperature who collapse, and in whom major medical causes have been ruled out, typically have EAPH. Such patients are often described as "weak, wobbly, and dizzy."

EAPH appears to be the most common condition confronted by medical providers attending to collapsed athletes at mass participation sporting events; however, clinicians must maintain vigilance for potentially life-threatening causes of EAC, such as cardiac arrest, exertional heat illness (EHI), and EAH. (See 'Epidemiology' above and 'Causes of collapse during exercise or sport' above.)  

EAPH is a physiologic consequence of the specific training adaptations that occur in endurance athletes (eg, runners, triathletes, cyclists). Endurance training is associated with an increased cardiac output and volume load for the left and right ventricles. Repeated exposure to these conditions during endurance training causes the heart to compensate by developing eccentric hypertrophy, which manifests as a dilatation of the left ventricle and mild-to-moderate increases in left ventricular wall thickness. The increase in cardiac output causes trained athletes to develop a lower resting heart rate compared with nontrained individuals. (See "Hypertrophic cardiomyopathy: Clinical manifestations, diagnosis, and evaluation", section on 'Athlete's heart'.)

In addition, during exercise, the muscles of the lower extremities require increased blood flow and peripheral vascular resistance decreases to accommodate this need. To generate the large cardiac output, and counter the decrease in resting heart rate, athletes must increase their stroke volume. Maximum heart rate does not change with exercise training.

Changes in skeletal muscle activity contribute to EAPH. During exercise, the repeated contractions of skeletal muscle increase venous return to the heart from the dilated lower extremity vasculature. When activity ceases, so too do these contractions, leading to diminished venous return. Large volumes of blood may pool in the lower extremities, thereby contributing to EAPH. In other words, the very adaptations that contribute to successful completion of endurance activities play a major role in the postural hypotension experienced by endurance athletes once exercise stops.

Noakes was among the first to describe EAPH based on his work with long-distance runners in South Africa [7]. He hypothesized that: "the most likely mechanism for exercise-associated collapse is a syncopal episode resulting from postural hypotension caused by a sudden cessation of exercise and loss of the skeletal muscle pump in the lower extremities." According to Noakes, additional factors that might contribute included mild dehydration, excessive effort during the race, and a reduction in the vasoconstrictor response to hypotensive stress brought on by long-term endurance training. Noakes' insights inform our approach to the management of EAPH, which is discussed below. (See 'Management of exercise-associated postural hypotension' below.)

Exercise collapse associated with sickle cell trait (ECAST) — Sickle cell trait (SCT) is a carrier condition, usually with none of the symptoms of sickle cell anemia or other sickle cell diseases. However, SCT is associated with an increased relative risk of exercise-related sudden death in athletes. SCT is discussed in detail separately; some aspects of the relationship between SCT and exercise-related collapse are discussed below. (See "Sickle cell trait".)

In studies of military personnel, the risk of exercise-related death in warfighters with SCT is reported to be approximately 40 times higher than those without SCT, although the absolute risk of death remains small (approximately 1:3000 African American warfighters who are SCT positive). While the mechanism of ECAST is unknown, it is speculated that intravascular sickling is induced by relative hypoxia, acidosis, and hyperthermia in strenuously exercising muscles [16]. Intravascular sickling, in turn, is hypothesized to trigger a fulminant exertional rhabdomyolysis. Many patients can develop sustained acute exertional compartment syndromes, often involving multiple compartments. Most studies identify potential risk factors as excessive heat, poor hydration status, and lack of exercise acclimatization. ECAST may manifest as or comorbidly present with EHI. (See "Chronic exertional compartment syndrome" and "Exertional heat illness in adolescents and adults: Epidemiology, thermoregulation, risk factors, and diagnosis" and "Exertional heat illness in adolescents and adults: Management and prevention".)

Most cases of ECAST occur during physical training or physical fitness testing [17]. The initial presentation of ECAST is often confused with heat cramping, heat exhaustion, or EHS. Unlike EHS, ECAST often occurs early in a workout, before an athlete’s core temperature has had time to rise. Furthermore, ECAST is often a "conscious collapse," which may help differentiate it from an acute cardiac event or EHS. The most telling symptom of ECAST is increasing pain and weakness in the working muscles, especially the legs, buttocks, and low back [18].

INITIAL MANAGEMENT OF THE COLLAPSED ATHLETE WITHOUT TRAUMA — The key factor in the proper management of postexercise collapse is to make the correct decisions during the initial evaluation and triage. Important elements of the initial evaluation and our management approach are described here. Our suggested approach is outlined in the following table (table 2); a summary of the key findings associated with important causes of collapse is found in the following table (table 1).

Distinguishing dangerous and benign conditions — The first task of the clinician providing the initial care for a collapsed athlete without trauma is to distinguish life-threatening from benign conditions. This is accomplished by rapidly performing a focused history and physical examination. This is true regardless of whether the athlete has collapsed on a race course, track, or a playing field or court. (See 'Life-threatening causes of collapse' above.)

A life-threatening injury or condition should be assumed for any athlete who collapses after direct trauma to the head, neck, or trunk. Such conditions as traumatic brain injury, intracranial hemorrhage, cervical spine injury, and commotio cordis must be quickly recognized and managed [10]. The approach and initial management of the athlete who has collapsed following significant trauma is reviewed separately. (See 'Trauma-related collapse' below and "Initial management of trauma in adults".)

Field-side observation — Team clinicians present at field-side may directly observe the collapse of the athlete, which may help them to distinguish dangerous from benign events. However, such distinctions can be difficult even when the collapse is witnessed.

Several studies have included assessments of video footage of fatal collapses. In one such study of six fatalities among soccer players, no athlete showed any sign of distress prior to collapse [19]. Four became unstable while standing and unexpectedly collapsed onto their backs, while two suddenly fell face down. All six had a fixed gaze and pupils when initially examined. In a second study, 13 deaths were analyzed (11 soccer, 2 martial arts) [20]. In 10 of 12 cases of cardiac–related collapse, the initial posture involved bowing and/or kneeling, followed by further collapse, often to a decubitus position. The authors concluded that in the absence of head injury, athletes who bow or kneel and then immediately collapse are likely to have sustained a life-threatening cardiac event.

History — The history surrounding the collapse is critical. Important questions to consider include the following:

Did collapse occur during, immediately after, or several minutes or more after cessation of exercise? (table 3)

Did the athlete experience any symptoms prior to the collapse, such as chest pressure or pain, palpitations, wheezing, pruritus, lightheadedness, or nausea?

If witnessed, did the athlete exhibit any seizure activity before the collapse? Was there any loss of bowel or bladder function?

Does the athlete have comorbidities that may have caused or contributed to collapse (eg, diabetes mellitus, asthma, ischemic heart disease, sickle cell trait, hypertrophic cardiomyopathy)? Is there a medical alert bracelet?

Acute collapse without trauma during exercise frequently stems from a cardiac emergency, such as myocardial infarction, a complication of hypertrophic cardiomyopathy, or an arrhythmia [21]. Clinicians should assume that any athlete who collapses abruptly on the court or field during play, or on the course during an endurance event, is experiencing a cardiac emergency. (See "Hypertrophic cardiomyopathy: Clinical manifestations, diagnosis, and evaluation".)

Although a serious condition is possible, an athlete who collapses after the conclusion of an athletic event (during "cool-down period" or later) typically suffers from exercise-associated postural hypotension (EAPH), a benign condition that rapidly improves with supportive care [21]. However, such athletes should be triaged expeditiously, including vital signs, and blood work if indicated, to confirm the benign nature of the collapse. (See 'Exercise-associated postural hypotension (EAPH)' above and 'Management of exercise-associated postural hypotension' below.)

Focused physical examination — Vital signs and a focused physical examination help to distinguish serious from benign causes of collapse. Low blood pressure (<90/60 mmHg), high blood pressure (>180/110 mmHg), persistent relative tachycardia not improving with standard care (eg, patient supine with legs elevated above heart level), symptomatic bradycardia, hypothermia, and symptomatic hyperthermia (typically a rectal temperature >40°C) are all signs of potentially life-threatening conditions.

Clinicians must look closely for signs of significant head injury, including depressed mental status, vision loss or decline, rhinorrhea or otorrhea, and diffuse facial swelling or obvious deformity. Midline cervical spine tenderness or deformity (eg, bony step-off) and any evidence of motor or sensory deficits suggest cervical spinal cord injury. Particularly in athletes who sustained chest trauma, such findings as a new, prominent heart murmur, muffled heart sounds or a rub, distant or asymmetric breath sounds, or poor air movement are concerning findings suggesting a life-threatening condition. Any sign suggesting significant injury mandates evaluation in the emergency department. (See "Initial management of trauma in adults" and "Initial evaluation and management of facial trauma in adults" and "Skull fractures in adults" and "Cervical spinal column injuries in adults: Evaluation and initial management" and "Initial evaluation and management of blunt thoracic trauma in adults".)

An altered mental state that does not quickly improve with rest, legs elevated, and observation is concerning and inconsistent with a diagnosis of EAPH. Such patients require immediate reevaluation.

Diagnostic testing — If available, point-of-care laboratory work, specifically serum or finger stick glucose, serum sodium, and hemoglobin, should be measured to help differentiate serious from benign causes of collapse. An electrocardiogram (ECG), or a cardiac monitor rhythm strip at a minimum, should be obtained if there is concern for arrhythmia or possible cardiac ischemia or infarction. We obtain an ECG in the following circumstances:

Chest pain or pressure

Pulse below 50 beats per minute associated with cardiopulmonary symptoms or altered mental status

Pulse above 120 beats per minute associated with cardiopulmonary symptoms or altered mental status

Symptomatic hypotension not improving with elevated legs and fluid resuscitation

Respiratory distress

Approach to the collapsed athlete without trauma — Rapid initial assessment of the collapsed athlete is based on a focused history, vital sign measurements, a focused physical examination with an emphasis on cognitive status, and targeted diagnostic testing. Our suggested approach is outlined in the following table (table 2); a summary of the key findings associated with important causes of collapse is found in the following table (table 1). (See 'History' above and 'Focused physical examination' above and 'Diagnostic testing' above.)

Clinicians should approach the differential diagnosis of the collapsed athlete in the following order:

Sudden cardiac arrest (SCA) – SCA is ruled out by the presence of normal respirations and strong regular pulses. (See "Advanced cardiac life support (ACLS) in adults" and "Adult basic life support (BLS) for health care providers".)

Exertional heat stroke (EHS) – EHS is ruled out by measuring a rectal temperature less than 40°C (or 104°F) and determining the athlete has a clear or clearing sensorium. (See "Exertional heat illness in adolescents and adults: Management and prevention", section on 'Management of exertional heat stroke'.)

Exercise-associated hyponatremia (EAH) – EAH is ruled out by measuring a normal blood sodium concentration with a point-of-care testing device. (See "Exercise-associated hyponatremia", section on 'Treatment'.)

Anaphylaxis (exercise-related or allergic) – Anaphylaxis is ruled out clinically. Common symptoms and signs include skin and mucosal findings (eg, hives, flushing, swollen lips or tongue), respiratory findings (eg, stridor, wheezing, sensation of throat closure or choking), and possibly gastrointestinal findings (eg, vomiting, diarrhea, abdominal cramping) and cardiovascular findings (hypotension, syncope). A medical alert bracelet may be helpful. Particularly with atypical cases, it is important to keep this diagnosis in mind as the presenting signs can vary. (See "Anaphylaxis: Emergency treatment" and "Anaphylaxis: Acute diagnosis".)

Insulin shock (hypoglycemia) – Hypoglycemia is ruled out by measuring a normal fingerstick glucose concentration with a point-of-care testing device. (See "Hypoglycemia in adults with diabetes mellitus".)

Asthma Asthma is ruled out by the absence of expiratory wheezing or other signs of respiratory difficulty (eg, retractions), and by the presence of normal air movement, as determined clinically or measured by peak flow meter. The athlete often has a known history of asthma. (See "Acute exacerbations of asthma in adults: Home and office management".)

Exercise collapse associated with sickle cell trait (ECAST) – Collapse in an athlete with known sickle cell trait. Athletes often remain conscious while slumping to the ground, complaining more of weakness than pain. (See "Sickle cell trait".)

Once these conditions are ruled out, the diagnosis of EAPH may be entertained. Of note, the clinical scenario may initially appear benign but may in fact be caused by a serious condition that is early in its evolution. Therefore, all athletes who collapse and receive medical care should be reassessed, including their response to any treatment.

If EAPH is suspected, the athlete is placed in a Trendelenburg or "feet up" position (picture 1) at the start of the evaluation. This helps to redistribute blood to the brain and torso and speeds recovery. The treatment of EAPH is discussed in greater detail below. (See 'Management of exercise-associated postural hypotension' below.)

EAPH is marked by facial flushing combined with a subtle or pronounced perioral vasoconstriction (diamond of vasoconstriction) (picture 2) that resolves as the condition clears. By contrast, EHS and EAH present with facial pallor that is distinctly different, with no perioral vasoconstriction.

Endurance athletes can appear "near death" upon crossing the finish line, only to walk out of the medical area 15 minutes later healthy and unharmed. However, distinguishing between EAPH and a life-threatening medical condition such as exertional heat illness (EHI) can be difficult even for seasoned sports medicine physicians, and clinicians must remain vigilant and assess each patient carefully.

Contrary to common belief, dehydration is not a common cause of EAPH in most athletic settings. Intravenous (IV) fluids are rarely required for runners who have completed a marathon or shorter-distance races. Participants in extreme endurance activities may require IV fluids, once it is determined that acute hyponatremia is not present. (See 'Determining whether IV fluid is necessary' below.)

DIFFERENCES IN ASSESSMENT AND INITIAL MANAGEMENT BY SETTING — Regardless of setting, it is critical to perform a focused, rapid assessment of the collapsed athlete to identify and treat any life-threatening conditions. Nevertheless, the setting and nature of the collapse alter the list of the more likely life-threatening causes, thereby altering the immediate concerns and approach of the clinician. One critical piece of history is the location of the collapsed endurance athlete: collapse on the course is ominous; collapse after completion of the event is more likely from a benign condition (table 3). These concerns and differences are discussed here.

Endurance race collapse

Preparation and risk factors — Careful preparation that anticipates the common medical conditions (including collapse) that a clinician may encounter at an endurance sporting event is imperative. Preparation for such events is discussed in detail separately. (See "Preparation and management of mass-participation endurance sporting events", section on 'Medical planning' and "Preparation and management of mass-participation endurance sporting events", section on 'Equipment, supplies, and communications'.)

Part of the medical preparation for every mass participation endurance sporting event should include the development of an emergency action plan (EAP) (table 4). During the pre-race medical meeting, all key medical personnel should review the EAP together. If time allows, an EAP rehearsal helps to alleviate confusion and clarify defined roles in the event of an emergency.

Important elements to consider when trying to determine the cause of an athlete's collapse during an endurance event include the following:

Known comorbidities, particularly cardiovascular disease, asthma, anaphylaxis, diabetes, or sickle cell trait (SCT)

Event distance

Wet bulb globe temperature (WBGT) before and during the race

How long the athlete spent on the course before collapsing (ie, how long were they running?)

Amount and type of fluid ingested

Food and medications taken before or during the event

The longer the athlete is on a course, the higher the chance of developing exercise-associated hyponatremia (EAH) [22]. EAH typically occurs among slower, less experienced "charity" runners who tend to drink water at every break station during a marathon. (See "Exercise-associated hyponatremia".)

Hypothermia and hyperthermia must be considered when an athlete is on the course for many hours during cooler or warmer temperatures, respectively. Dehydration is always a consideration for athletes competing in long endurance events. (See "Accidental hypothermia in adults" and "Exertional heat illness in adolescents and adults: Epidemiology, thermoregulation, risk factors, and diagnosis" and "Exertional heat illness in adolescents and adults: Management and prevention".)

Management of mid-course collapse — An endurance athlete who collapses on the course, before finishing a race, must be evaluated promptly with a high suspicion for a cardiac event (table 2). Exertional heat stroke (EHS), EAH, hypoglycemia, and anaphylaxis must also be considered (table 3).

Key initial management steps include:

Assess circulation, airway, and breathing (CAB); secure the airway as necessary (algorithm 1 and algorithm 2). (See "Adult basic life support (BLS) for health care providers" and "Basic airway management in adults".)

Call for emergency medical services (EMS) assistance. Start cardiopulmonary resuscitation (CPR) if pulseless. Attach an automated external defibrillator (AED); perform defibrillation as indicated. (See "Advanced cardiac life support (ACLS) in adults" and "Automated external defibrillators".)

Vital signs and patient position – Elevate the patient's feet above the level of their heart (picture 1) and obtain vital signs. If the athlete is unconscious or with an altered sensorium, obtain a rectal temperature.

Treatment of exertional heat illness – Begin rapid cooling immediately if the athlete has a rectal temperature >40°C and an altered sensorium (table 5). (See "Exertional heat illness in adolescents and adults: Management and prevention", section on 'Management of exertional heat stroke'.)

IV access – If intravenous (IV) access is obtained at the site of collapse, obtain a blood sample prior to initiating fluids. Start isotonic fluid at a "keep vein open" (KVO) rate. Treat dehydration, if present, with rapid IV boluses (eg, 500 mL per bolus) of isotonic fluid (eg, isotonic saline).

Treatment of exercise-associated hyponatremia – Administer 100 mL of 3 percent hypertonic saline over 10 minutes (slow IV push). (See "Exercise-associated hyponatremia", section on 'Treatment'.)

Ensure smooth transfer of care to EMS upon their arrival.

Management of collapse after finish line — The athlete who collapses after crossing the finish line of an endurance event is more likely to have done so from exercise-associated postural hypotension (EAPH), and less likely to have a cardiac emergency (table 3). Nevertheless, the patient's circulation, airway, and breathing should be quickly assessed. In most such cases, more time is available to assess and observe the patient's response to treatment. The management of EAPH is described below. (See 'Management of exercise-associated postural hypotension' below.)

Field or court sport collapse — Sudden cardiac arrest (SCA) is likely the most catastrophic event that can cause the collapse of an athlete during a court or field sport. Therefore, an AED must be available at court- or field-side, and deployed whenever a cardiac event is suspected. An interval of less than five minutes from collapse to administration of the first AED shock maximizes the likelihood of survival [1]. (See "Automated external defibrillators".)

Initial evaluation and management of the collapsed field or court athlete is slightly different than the endurance athlete. Nevertheless, the same basic principles of evaluation and management that inform our approach to collapsed athlete described above apply here. In the absence of observed or reported trauma, the clinician's major concerns include:

Cardiovascular emergencies; SCA must be assessed immediately (algorithm 1 and algorithm 2) (see "Adult basic life support (BLS) for health care providers" and "Basic airway management in adults" and "Advanced cardiac life support (ACLS) in adults")

Exertional hyperthermia; rapid cooling – a critical intervention – is described in the following table (table 5) (see "Exertional heat illness in adolescents and adults: Management and prevention", section on 'Management of exertional heat stroke')

Anaphylaxis; emergency management of anaphylaxis is summarized in the following table (table 6) (see "Anaphylaxis: Emergency treatment" and "Anaphylaxis: Acute diagnosis")

Exercise collapse associated with sickle cell trait (ECAST) - There are no evidence-based guidelines to aid the management of ECAST. Consensus recommendations include early provision of oxygen and immediate transfer to the emergency department while being prepared to manage fulminant rhabdomyolysis and metabolic storm [23]. (See "Sickle cell trait".)

Metabolic abnormalities (eg, hypoglycemia, acute hyponatremia) (see "Hypoglycemia in adults with diabetes mellitus" and "Exercise-associated hyponatremia", section on 'Treatment')

EAPH and EAH are unlikely etiologies of collapse in field or court athletes.

At a field or court event, the clinician may not have point-of-care laboratory testing available. The ability to obtain IV access, too, may be limited. If a metabolic abnormality, such as hypoglycemia, is suspected and the medical resources needed to care for the patient are unavailable, the athlete should be transported immediately to a higher level of care for testing and management. Basic interventions, such as giving oral glucose to the athlete with suspected hypoglycemia, may be performed at field-side.

At field and court venues used regularly for sport, an emergency action plan (EAP) should be in place that accounts for the limitations of the venue, including immediately available medical support and equipment, and coordination with local ambulance services and emergency departments (EDs). The EAP should be reviewed regularly. The key elements of an EAP are found in the table (table 4).

Trauma-related collapse — The assessment and management of patients following acute trauma is reviewed in detail separately. Athletes who may have sustained major injury are stabilized and transferred immediately to the closest ED. (See "Initial management of trauma in adults".)

Important injuries to consider in the athlete who has collapsed as a direct result of impact include:

Head and neck injuries:

Intracranial hemorrhage (see "Spontaneous intracerebral hemorrhage: Pathogenesis, clinical features, and diagnosis")

Traumatic brain injury (see "Management of acute moderate and severe traumatic brain injury" and "Acute mild traumatic brain injury (concussion) in adults")

Cervical spine injury (see "Cervical spinal column injuries in adults: Evaluation and initial management")

Concussion is a diagnosis of exclusion (see "Sideline evaluation of concussion")

Chest injury: Commotio cordis, arrhythmia (see "Commotio cordis" and "Advanced cardiac life support (ACLS) in adults")

In sports that involve regular contact or collision between athletes, it may be obvious when an athlete has collapsed due to the effect of direct impact. If the traumatic incident was witnessed or seen on video replay, this may help determine the severity and nature of the injury. In some circumstances, however, it may be difficult to ascertain whether collapse occurred because of direct trauma. This may be due to a substantial delay between the impact and manifestations of injury (eg, small pneumothorax leading to tension physiology, splenic laceration with slow hemorrhage) or due to some other underlying cause of the collapse (eg, arrhythmia) unrelated or indirectly related to the impact [10]. Clinicians should assume the worst in cases of trauma-related collapse and assess the patient according to standard trauma protocols. (See "Initial management of trauma in adults", section on 'Primary evaluation and management'.)

When providing medical support for sports that involve regular contact or collision, it is critical to be prepared to manage SCA, head and neck injuries, airway injuries and respiratory distress, and chest injuries. An EAP for such scenarios should be in place, skilled medical personnel needed to implement such a plan should be at field-side, and all necessary equipment available. This includes an AED, and equipment for airway management and cervical spine stabilization [24]. (See "Preparation and management of mass-participation endurance sporting events", section on 'Medical planning' and "Preparation and management of mass-participation endurance sporting events", section on 'Equipment, supplies, and communications'.)

Head and neck injuries caused by direct trauma are the leading cause of catastrophic injuries among athletes, often presenting immediately, but sometimes hours later (eg, subdural hemorrhage), with sudden collapse [10]. Any collapsed athlete who clearly sustained direct trauma to the head and neck, or may have sustained such trauma, must be assumed to have a cervical spine and traumatic brain injury until proven otherwise. The airway and cervical spine must be protected as indicated.

Although rare in sport, disruption of cardiac or major vascular structures (eg, aortic rupture) causes immediate collapse, and outcomes are usually dismal [10]. Among athletes who collapse immediately after sustaining a direct blow to the chest, commotio cordis is of greatest concern. This can occur with or without a protective chest pad in place [10]. Therefore, when approaching the unconscious athlete who collapsed immediately after direct trauma to the chest, be prepared to begin CPR and apply an AED to correct any lethal arrhythmia. (See "Commotio cordis".)

The athlete who sustains direct trauma to the chest and develops a pneumothorax, hemothorax, pulmonary contusion, cardiac contusion, or other intrathoracic or chest wall injury rarely collapses immediately after sustaining that injury. Typically, some delay is needed for the effects of the injury to manifest. Any severe or increasing respiratory difficulty or pain or weakness warrants close evaluation of the athlete. (See "Initial evaluation and management of blunt thoracic trauma in adults" and "Initial evaluation and management of chest wall trauma in adults" and "Initial evaluation and management of blunt cardiac injury".)

Abdominal trauma resulting in immediate collapse is rare in sport. Pain may cause the athlete to "buckle over" and possibly experience a pain-induced vasovagal event. Splenic laceration or rupture is the injury that most often leads to a delayed syncopal presentation, although this is uncommon [25]. The clinician should perform a careful initial abdominal examination, followed by serial examinations if the pain is not resolving. The athlete must be evaluated at a higher level of care with imaging if there is any suspicion for splenic or other intraabdominal injury. (See "Initial evaluation and management of blunt abdominal trauma in adults".)

MANAGEMENT OF EXERCISE-ASSOCIATED POSTURAL HYPOTENSION

General management — Exercise-associated postural hypotension (EAPH) is likely the most common form of exercise-associated collapse (EAC), particularly among racers who collapse after crossing the finish line at mass participation sporting events (eg, road races, triathlons). Nevertheless, EAPH remains a diagnosis of exclusion, and the clinician must first rule out life-threatening causes of collapse. To help prevent EAPH, we encourage athletes, and medical personnel assisting athletes, to keep walking upon completion of an event. This helps to prevent venous pooling in the extremities and promotes active recovery.

Our recommended approach to assessment and initial management of the collapsed athlete is provided in the following table (table 2); management of athletes more likely to have life-threatening causes of collapse are discussed above. (See 'Initial management of the collapsed athlete without trauma' above and 'Differences in assessment and initial management by setting' above.)

If the initial assessment does not identify life-threatening conditions, the collapsed athlete presumed to have EAPH is managed as follows [3,4,21,26]:

Elevate the patient's feet above the level of their heart (picture 1) and obtain vital signs.

Placing the heart at a level below the limbs and pelvis helps to redistribute blood to the brain and torso. This redistribution leads to increases in right atrial filling pressure, ultimately reversing the state of low peripheral resistance and postural hypotension.

If the athlete is unconscious or has an altered sensorium, obtain a rectal temperature. Drapes and appropriate equipment should be available to maintain patient privacy.

Treat with rapid cooling if the rectal temperature is >40°C with altered sensorium. Patients with exertional heat stroke (EHS) are at risk for sudden death if not rapidly cooled. (See "Exertional heat illness in adolescents and adults: Management and prevention", section on 'Management of exertional heat stroke'.)

Monitor the patient closely; reexamine them. Patients with EAPH typically show some signs of recovery within 10 to 15 minutes. We reassess the patient and remeasure vital signs every 10 to 15 minutes until the patient appears clinically improved and vital signs have stabilized.

In addition to collapse, EAPH is marked by facial flushing combined with a subtle or pronounced perioral vasoconstriction (diamond of vasoconstriction) (picture 2) that resolves as the condition clears. By contrast, EHS and exercise-associated hyponatremia (EAH) present with facial pallor that is distinctly different, with no perioral vasoconstriction. (See 'Approach to the collapsed athlete without trauma' above and 'Life-threatening causes of collapse' above.)

Offer oral fluids to the athlete not at risk for aspiration (clear sensorium) and able to tolerate them (not vomiting).

Contrary to common belief, dehydration is not a common reason for EAPH in most settings, and treatment with intravenous (IV) fluids is rarely required for runners who have completed a marathon or shorter-distance races. Moreover, such treatment may be life-threatening if collapse is due to EAH from excessive intake of free water over the course of the race. Collapsed participants in longer-duration activities (eg, Iron Man races) may require IV fluids. (See 'Determining whether IV fluid is necessary' below.)

If after 15 minutes of treatment, the athlete's sensorium or vital signs are not improving, obtain a blood sample for point-of-care testing of sodium and glucose. Start IV fluids with isotonic ("normal") saline at a "keep vein open" (KVO, ie, very slow) rate until laboratory results are available. Treat EAH or hypoglycemia as indicated.

Continue to treat and reassess. Athletes with EAPH tend to improve within 10 to 30 minutes of conservative treatment. Those that do not clinically improve should be transferred to a higher level of care.

Patients may be discharged once they meet all criteria. Full recovery generally takes no longer than 30 minutes. (See 'Disposition and discharge criteria for EAPH' below.)

Determining whether IV fluid is necessary — IV fluids are rarely needed to manage EAPH. Indications for administering IV fluids are summarized in the following table (table 7).

Over 12 years of finish-line care at the Twin Cities Marathon, only 106 IV catheters were placed out of 81,300 finishers [27]. The main reasons to start an IV in an athlete with EAPH include fluid replacement for those with persistent emesis or diarrhea, and administration of medications.

The number of IVs started at an endurance race medical facility appears to vary according to the training and experience of the clinicians involved and their comfort managing collapsed athletes. Clinicians with less experience start more IVs, so close supervision by experienced staff reduces unneeded interventions. Aggressive IV hydration is rarely needed in post-race field management, and doing so runs the risk of exacerbating undetected acute hyponatremia (ie, EAH), which can be life threatening. Many race medical teams check a blood sodium concentration prior to administering IV fluids using a point-of-care device. (See "Exercise-associated hyponatremia".)

Current insights into the appropriate use of IV hydration in collapsed endurance athletes is due in large part to the research of Noakes and his colleagues, who found that EAPH is rarely due to dehydration. Noakes argued that the infusion of large volumes of IV fluid, a common practice previously, would be ineffective, as such fluids do not reverse the state of low peripheral vascular resistance causing the condition. Moreover, in cases where collapse is caused by acute hyponatremia due to excessive intake of free water, such treatment could be potentially life-threatening [28]. (See 'Exercise-associated postural hypotension (EAPH)' above and "Exercise-associated hyponatremia".)

Disposition and discharge criteria for EAPH — The medical team should determine the disposition and discharge criteria for patients managed in the major on-site medical care area in advance of the event. At the Marine Corps Marathon and Twin Cities in Motion events, we discharge runners when they meet the following criteria:

Hemodynamically and clinically stable (no recurrent episodes of hypotension or lightheadedness)

Normothermic

Ambulatory without assistance and without symptoms

Tolerating oral liquids

When assessing participants recovered from self-limited EAPH, we follow the approach described in the following reference to determine when they may be discharged [27]:

Sit test ‒ The first stage of assessment is the "sit test," which involves moving the patient to the sitting position to check for an orthostatic reaction (eg, lightheadedness).

Stand test ‒ If sitting upright is tolerated for a few minutes, the patient may stand with a clinician or helper beside them.

Walk test ‒ If standing is well tolerated, the patient is permitted to walk, again with someone beside them.

Once the patient is walking without any problem and meets all other criteria noted above, they may be discharged. Typically, recovery occurs within approximately 30 minutes, although it can take longer in some cases. The athlete should be given written discharge instructions that discuss continued fluid and energy replacement, criteria for reevaluation, and follow-up recommendations.

Ideally, the athlete is handed off personally to family or friends as part of the transition out of the medical area. For athletes with more severe problems, transfer is made to an emergency department. For athletes thought to have EAPH but who are not responding to standard treatment, transfer to the hospital is appropriate. Admission or continued observation may be needed for such patients if they are unable to tolerate oral fluids or have persistent diarrhea.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Exertional heat illness".)

SUMMARY AND RECOMMENDATIONS

Emergency evaluation and rapid guides – Rapid initial assessment of the collapsed athlete is based on a focused history, vital sign measurements, a focused physical examination with an emphasis on cognitive status, and targeted diagnostic testing. Our suggested approach is outlined in the following table (table 2); a summary of the key findings associated with important causes of collapse is found in the following table (table 1). (See 'Approach to the collapsed athlete without trauma' above.)

Definitions and causes of athlete collapse – Adult athletes collapse when the cardiovascular, pulmonary, nervous, or musculoskeletal system fails, making the athlete unable to continue participating and unable to remove themselves from the race course or field under their own power. Exercise-associated postural hypotension (EAPH) is the most common cause of collapse at the conclusion of endurance races, but it must be distinguished from the potentially life-threatening conditions that occur with far less frequency, including sudden cardiac arrest (SCA), exertional heat stroke (EHS), and exercise-associated hyponatremia (EAH). Collapse during field or court sports may be related to exertion or trauma. Other potential life-threatening causes of collapse during sport include anaphylaxis, insulin shock, and asthma exacerbation. (See 'Definition' above and 'Epidemiology' above and 'Causes of collapse during exercise or sport' above.)

Exercise-associated postural hypotension – EAPH involves collapse after completion of an exertional event (eg, endurance race) in a conscious athlete who is unable to stand or walk unaided due to lightheadedness, faintness, or dizziness. EAPH develops from a precipitous decline in venous return immediately following cessation of activity. EAPH is a benign condition that rapidly improves with supportive care. (See 'Exercise-associated postural hypotension (EAPH)' above and 'Management of exercise-associated postural hypotension' above.)

Timing of collapse – Clinicians should assume that any athlete who collapses abruptly on the court or field during play, or on the course during an endurance event, is experiencing a cardiac emergency. Although a serious condition is still possible, an athlete who collapses after the conclusion of an athletic event (during "cool-down period" or later) typically suffers from EAPH. (See 'Distinguishing dangerous and benign conditions' above.)

Key questions for history – The first task is to distinguish life-threatening from benign conditions. This is accomplished by rapidly performing a focused history and physical examination. Important questions for the history include the following:

Did collapse occur during, immediately after, or several minutes or more after cessation of exercise?

Did the athlete experience any symptoms prior to the collapse, such as chest pressure or pain, palpitations, wheezing, pruritus, lightheadedness, or nausea?

If witnessed, did the athlete exhibit any seizure activity before the collapse? Was there any loss of bowel or bladder function?

Does the athlete have comorbidities that may have caused or contributed to collapse (eg, diabetes mellitus, asthma, ischemic heart disease, sickle cell trait, hypertrophic cardiomyopathy)? Is there a medical alert bracelet? (See 'History' above.)

Examination findings suggesting life-threatening conditions – Low blood pressure (<90/60 mmHg), high blood pressure (>180/110 mmHg), persistent relative tachycardia not improving with standard care (eg, patient supine with legs elevated above heart level), symptomatic bradycardia, hypothermia, and symptomatic hyperthermia (typically a rectal temperature >40°C) are all signs of potentially life-threatening conditions. (See 'Focused physical examination' above.)

Diagnostic testing – If available, serum or finger stick glucose, serum sodium, and hemoglobin should be measured to help differentiate serious from benign causes of collapse. An electrocardiogram (ECG), or a cardiac monitor rhythm strip at a minimum, should be obtained if there is concern for arrhythmia or possible cardiac ischemia or infarction. (See 'Diagnostic testing' above.)

Trauma-related collapse – Life-threatening traumatic injuries that can cause athletes to collapse suddenly during sport include:

Intracranial hemorrhage

Traumatic brain injury

Cervical spine injury

Commotio cordis

Arrhythmia

Any sign suggesting significant injury mandates evaluation in the emergency department. Clinicians must look closely for signs of head injury, including depressed mental status, vision loss or decline, rhinorrhea or otorrhea, and diffuse facial swelling or obvious deformity. Midline cervical spine tenderness or deformity and any evidence of motor or sensory deficits suggest cervical spinal cord injury.

Particularly in athletes who sustained chest trauma, such findings as a new, prominent heart murmur, muffled heart sounds or a rub, distant or asymmetric breath sounds, or poor air movement are concerning and suggest a life-threatening condition. (See 'Trauma-related collapse' above.)

  1. Courson R. Preventing sudden death on the athletic field: the emergency action plan. Curr Sports Med Rep 2007; 6:93.
  2. Toresdahl B, Courson R, Börjesson M, et al. Emergency cardiac care in the athletic setting: from schools to the Olympics. Br J Sports Med 2012; 46 Suppl 1:i85.
  3. Roberts WO. Exercise-Associated Collapse in Endurance Events: A Classification System. Phys Sportsmed 1989; 17:49.
  4. Asplund CA, O'Connor FG, Noakes TD. Exercise-associated collapse: an evidence-based review and primer for clinicians. Br J Sports Med 2011; 45:1157.
  5. Roberts WO. Exercise-associated collapse care matrix in the marathon. Sports Med 2007; 37:431.
  6. https://nccsir.unc.edu/files/2013/10/NCCSIR-34th-Annual-All-Sport-Report-1982_2016_FINAL.pdf (Accessed on February 23, 2018).
  7. Holtzhausen LM, Noakes TD. The prevalence and significance of post-exercise (postural) hypotension in ultramarathon runners. Med Sci Sports Exerc 1995; 27:1595.
  8. Naidoo D, Sewry N, Schwellnus MP, et al. Longer distance races and slower running pace are associated with Exercise associated collapse: SAFER XXV study in 153,208 distance runners. J Sports Med Phys Fitness 2022; 62:1519.
  9. Kucera KL, Yau RK, Register-Mihalik J, et al. Traumatic Brain and Spinal Cord Fatalities Among High School and College Football Players - United States, 2005-2014. MMWR Morb Mortal Wkly Rep 2017; 65:1465.
  10. Gammons M. Evaluation and treatment of trauma related collapse in athletes. Curr Rev Musculoskelet Med 2014; 7:342.
  11. Hardy I, McFaull S, Saint-Vil D. Neck and spine injuries in Canadian cheerleaders: An increasing trend. J Pediatr Surg 2015; 50:790.
  12. LaBella CR, Mjaanes J, Council on Sports Medicine and Fitness. Cheerleading injuries: epidemiology and recommendations for prevention. Pediatrics 2012; 130:966.
  13. Wennberg RA, Cohen HB, Walker SR. Neurologic injuries in hockey. Phys Med Rehabil Clin N Am 2009; 20:215.
  14. Maron BJ, Doerer JJ, Haas TS, et al. Commotio cordis and the epidemiology of sudden death in competitive lacrosse. Pediatrics 2009; 124:966.
  15. Boden BP. Direct catastrophic injury in sports. J Am Acad Orthop Surg 2005; 13:445.
  16. Quattrone RD, Eichner ER, Beutler A, et al. Exercise collapse associated with sickle cell trait (ECAST): case report and literature review. Curr Sports Med Rep 2015; 14:110.
  17. O'Connor FG, Bergeron MF, Cantrell J, et al. ACSM and CHAMP summit on sickle cell trait: mitigating risks for warfighters and athletes. Med Sci Sports Exerc 2012; 44:2045.
  18. O'Connor FG, Franzos MA, Nye NS, et al. Summit on Exercise Collapse Associated with Sickle Cell Trait: Finding the "Way Ahead". Curr Sports Med Rep 2021; 20:47.
  19. Panhuyzen-Goedkoop NM, Wellens HJ, Piek JJ. Early recognition of sudden cardiac arrest in athletes during sports activity. Neth Heart J 2018; 26:21.
  20. Baltsezak S. Bowing, kneeling and 'prostration': athlete's collapse patterns during sudden cardiac arrhythmia/arrest on the field of play. Emerg Med J 2014; 31:939.
  21. O'Connor FG, Levine BD, Childress MA, et al. Practical management: a systematic approach to the evaluation of exercise-related syncope in athletes. Clin J Sport Med 2009; 19:429.
  22. Almond CS, Shin AY, Fortescue EB, et al. Hyponatremia among runners in the Boston Marathon. N Engl J Med 2005; 352:1550.
  23. Cools KS, Crowder MD, Kucera KL, et al. Sudden Death in High School Athletes: A Case Series Examining the Influence of Sickle Cell Trait. Pediatr Emerg Care 2022; 38:e497.
  24. Waninger KN, Swartz EE. Cervical spine injury management in the helmeted athlete. Curr Sports Med Rep 2011; 10:45.
  25. Gannon EH, Howard T. Splenic injuries in athletes: a review. Curr Sports Med Rep 2010; 9:111.
  26. Holtzhausen LM, Noakes TD. Collapsed ultraendurance athlete: proposed mechanisms and an approach to management. Clin J Sport Med 1997; 7:292.
  27. Roberts WO. A 12-yr profile of medical injury and illness for the Twin Cities Marathon. Med Sci Sports Exerc 2000; 32:1549.
  28. Holtzhausen LM, Noakes TD, Kroning B, et al. Clinical and biochemical characteristics of collapsed ultra-marathon runners. Med Sci Sports Exerc 1994; 26:1095.
Topic 114092 Version 11.0

References

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