Article, Sports Medicine

Medical problems of marathon runners

Review

Medical problems of marathon runners

Leon D. Sanchez MD, MPHa,*, Brian Corwell MDb, David Berkoff MDc

aDepartment of Emergency Medicine, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA bDepartment of Emergency Medicine, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA cDepartment of Emergency Medicine, Coordinator Physiologic Testing, Mike Krzyzewski Human Performance Lab/Duke University, Duke University, Durham, NC, USA

Received 14 January 2006; accepted 22 January 2006

Abstract Several organ systems can be affected by marathon running. Acute musculoskeletal injuries are common, but running does not result in increased rates of musculoskeletal disability. gastrointestinal complaints are also common among runners; some of these complaints are explained by the decreased mesenteric blood flow during exercise. Although cardiac events are rare, they can be devastating. Symptomatic hyponatremia is another serious but mostly preventable problem.

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Introduction

In the United States, there are now approximately 375 marathons and in 2002 approximately 450000 partic- ipants completed one. The largest US marathons now have more than 30000 participants, with women constituting 40% of the field and runners older than 40 years (masters), 43%. The median finishing time is now 4 hours and 20 minutes for men and 4 hours 56 minutes for women [1]. Of marathon participants, 2% to 8% will seek medical attention during or immediately after completing the race [2,3].

In cities that host one of the large marathons, marathon day can seem a preplanned mass casualty incident for the event medical tents and nearby EDs. The rigors of training and the stress of the race itself place great demands on the marathoner and frequent runner. We will discuss problems that can affect marathoners during and immediately after the race.

This article has not been published previously and is not being submitted elsewhere. The manuscript is the original work of the authors and there are no conflicts of interest to disclose.

* Corresponding author.

E-mail address: [email protected] (L.D. Sanchez).

Problems of marathoners

Musculoskeletal

While running, the repetitive impact of each foot strike transmits forces to the body estimated to be 2 to 3 times the body weight of the runner [4]. During a 12-year period at the Twin Cities marathon, Musculoskeletal problems accounted for 17% of visits [3], most commonly, muscle cramps, blisters, and acute ankle and knee injuries [5]. Most of these complaints are addressed at the race medical tents. Knee injuries are more common in road racing, and ankle injuries predominate in track races [6]. An inverse relation- ship was noted between the number of miles trained per week and the number of injuries seen on the day of the marathon [5].

When downhill running, the quadriceps muscles must brake the falling body subjecting the muscle to stresses that exceed level or uphill running, leading to more muscle damage. Greater creatine kinase (CK) and myosin heavy chain blood levels are observed with downhill running [7]. Rhabdomyolysis should be considered in competitors pre- senting post race with Muscle pain, low-grade fever, and dark

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urine. The classic triad of muscle swelling, tenderness, and weakness is rarely found, especially in the setting of concomitant dehydration. The most sensitive indicator of muscle injury is the serum CK, and a level greater than 5 times normal is diagnostic in the general population. Elevations are seen 2 to 12 hours after injury and peak in 1 to 3 days. Four hours post marathon, the average rise in CK is 540% [8]. Most marathon runners clear their excess CK with oral hydration. Close monitoring for renal, cardiac, and metabolic complications coupled with early and aggressive hydration are indicated in those competitors whose renal function is thought to be compromised.

Although marathoners are 2 to 3 times as likely to report musculoskeletal problems after a race when compared with runners of shorter races, there is no clear evidence that frequent running leads to long-term musculoskeletal dis- ability [9]. Long-term weekly distance was found to be the strongest predictor of future injury, but on race day, increased training volume is associated with a decreased incidence of injury [9]. The more the athlete runs during training, the lesser the risk of injury on race day.

Gastrointestinal

Of runners, 30% to 81% report gastrointestinal (GI) complaints during long runs and races.

Runners can suffer from bloating, cramps, nausea, vomiing, diarrhea, and fecal incontinence while runn- ing [10,11].

With exercise, blood flow is preferentially redirected to working muscles, and flow to the gut can be reduced by as much as 80% [12]. This low flow state can compromise gut function to varying degrees from the mild, manifested by commonly experienced GI symptoms such as cramping, to the severe cases of ischemic colitis. The pattern of ischemia has been compared with a shock state [13,14]. With training, this decrease in blood flow becomes less pronounced, although this does not reliably predict which patients will become symptomatic. There is no clear evidence that less fit individuals are more prone to symptomatic ischemia.

Estimates of the incidence of occult blood after a race range from 8% to 85% [15-17]. The range is wide because different studies have used varying race distances. With longer distances, the incidence increases. As many as 16% of runners in one study report having bloody diarrhea on at least one occasion after a race or hard run [11]. The mechanical trauma suffered by the gut from the repetitive impact of running, as well as Mesenteric ischemia, has been proposed as reasons for GI bleeding [11,18]. Presence of bloody bowel movements after an endurance event should raise the possibility of ischemic colitis and hemorrhagic gastritis.

The origin of occult blood can be from both upper and lower GI sources. Endoscopy of subjects after a race found that all 16 subjects had some degree of gastritis with 4 having heme-positive stools, 2 of which were of a lower GI source [19]. The use of cimetidine before and during a race can

reduce the incidence of heme-positive stools afterward, although this finding has not been consistent [20,21].

Nonsteroidal anti-inflammatory drug (NSAID) use has not been prospectively shown to be associated with GI bleeding in runners in one study, although both aspirin and NSAIDs have been shown to increase intestinal permeabil- ity in separate studies and may increase the incidence of GI complaints [14,22,23]. The use of NSAIDs in the peri-race period should be discouraged.

When evaluating a postmarathon patient for Abdominal complaints, relevant history questions particular to the race should include prior episodes of GI complaints with racing, as well as the timing of symptoms. Finish time, especially when compared with finish time in prior marathons, will give an idea of the level of exertion during the race. Environmental factors on race day, as well as the amount of fluid ingested, should be taken into consideration because hypovolemia from dehydration exacerbates the low-flow state and increase GI complaints [24].

Cardiac

Exercise training may reveal underlying congenital or acquired heart disease. In a 21-year prospective study of sudden death in adolescents and young adults (12-35 years old) in competitive athletes vs the general population, being an athlete carried a Relative risk of sudden death between 1.95 to 2.0. This risk was largely related to underlying heart disease such as congenital coronary artery anomaly (RR, 79), arrhythmogenic right ventricular cardio- myopathy (RR, 5.4) and premature coronary artery disease (RR, 2.6). [25]. A study examining sudden death in a younger population (median age, 17 years) of competitive athletes found that the most common identified disease entity (48 [36%] of 158 deaths) was hypertrophic cardio- myopathy. In 21.5% of cases, the event was due to coronary artery abnormalities, most common of which were malfor- mations involving an anomalous coronary artery origin (13% athletes) [26].

Another prospective study investigated 273 consecutive cases of clinically silent sudden cardiac death. Of these cases, 72% had structural heart disease apparent on macroscopic examination of the heart such as cardiomyop- athy (21%), obstructive (20%) and nonobstructive (10%) coronary artery disease, valve disease (12%), and aortic rupture (5%). Of the remaining 28% with normal macro- scopic hearts, histologic examination found abnormalities in almost 80% including focal myocarditis, right ven- tricular regional cardiomyopathy localizing to the Right ventricular outflow tract, and Conduction system abnormal- ities [27].

A 1986 review of all published cases of myocardial infarction or sudden death in marathon runners (n = 36) found that 75% had coronary artery disease and 71% had premonitory symptoms such as exertional angina. The next most common diagnosis was Hypertrophic cardiomyopathy

Laboratory parameter

Premarathon

Postmarathon

Postmarathon

4 h (% [absolute change])

24 h (% [absolute change])

WBC (th/mm3)a

5.5 F 0.2

216% (17.4 F 1.5)*

71% (9.4 F 1.2)*

% Neurophilsb

57 F 10.6

49% (85 F 10.9)*

11% (63 F 14.9)*

% Lymphocytesb

30 F 6.6

77% (7 F 2.4)*

30% (21 F 5.4)*

HCT (mL/mm3)a

44.8 F 0.4

No change

3% (43.6 F 0.4)**

PLT (th/mm3)a

226 F 25

12% (253 F 27)**

No change

Na (mmol/L)b

142.4 F 1.58

No change (141.5 F 4.04)

2% (139.0 F 3.21)*

K (mmol/L)b

4.5 F 0.41

No change (4.5 F 0.52)

4% (4.3 F 0.24)**

BUN (mg/dL)b

16 F 5.52

22% (19.5 F4.35)*

29% (20.7 F 7.5)*

Cr (mg/dL)b

1.0 F 0.16

30% (1.3 F0.32)*

20% (1.2 F0.24)*

Calcium (mg/dL)b

9.2 F 0.34

2% (9.4 F 0.51)**

2% (9.4 F 0.35)

Magnesium (mEq/L)b

1.7 F 0.13

12% (1.5 F 0.16)*

No change (1.7 F 0.12)

Phosphorus (mg/dL)b

2.8 F 0.44

14% (3.2 F 0.80)*

7% (3.0 F 0.45)

AST (U/L)b

29.3 F12.76

76% (51.6 F17.98)*

265% (106.9 F55.65)*

ALT (U/L)b

21.8 F14.4

14% (24.8 F 11.49)**

37% (29.8 F 13.45)**

Bilirubin (mg/dL)b

Direct

0.2 F 0.1

50% (0.3 F 0.16)*

100% (0.4 F 0.20)**

Total

0.5 F 0.27

60% (0.8 F 0.44)*

60% (0.8 F 0.59)

CRP (ng/mL)a

343 F 611

122% (762 F 973)*

NA

vWF (ng/mL)a

109 F 47

114% (233 F 65)*

74% (190 F 74)*

D-dimer (ng/mL)a

177 F 137

199% (529 F 279)*

112% (376 F 269)*

Total cholesterol (mg/dL)b

194.9 F 29

No change (196.5 F 29)

13% (169.1 F 32.6)*

HDL (mg/dL)a

50 F 3

NA

No change

Triglycerides (mg/dL)b

114.2 F 58.13

4% (109.5 F 60.43)

36% (73.1 F 56.07)

Brain natriuretic peptide (pg/mL)c

16.7 F 4.5

10% (18.4 F 4.4)

191% (48.6 F 10.2)*

Myoglobin (lg/L)c CK (U/L)b

95 F 11

131.9 F 57.8

N425% (N500)*

540% (843.8 F 782.3)*

299% (379 F 43)*

1773% (2470.0 F 1950)*

CK-MB (ng/mL)b

2.3 F 1.61

935% (23.8 F 25.17)*

2343% (56.2 F 46.54)*

Troponin I (ng/mL)b

0 (0)

0.02 F 0.04*

0 (0)

in 9%. Coronary risk factors present in this population included smoking (9%), family history of heart disease (64%), hypertension (32%), and elevated serum cholesterol or low high-density lipoprotein/total cholesterol ratios (77%). Of the 26 cardiac events, 50% occurred during or within 24 hours of the race, and 85% occurred within 1 month of the race [28]. Two other studies investigating death during jogging found coronary artery disease to be the cause of death in 72.2% and 91.6%, respectively [29,30].

Table 1 Laboratory abnormalities after running a marathon

WBC indicates white blood cell; HCT, hematocrit; PLT, platelet; CRP, C-reactive protein; HDL, high-density lipoprotein; AST, aspartate aminotransferase;

ALT, alanine aminotransferase.

a Ref. [36].

b Ref. [8].

c Ref. [37].

* P b .005.

** P b .05.

The estimated risk of sudden death from jogging is 1 death per 396000 man-hours of jogging and 1 death per

215000 man-hours of running a marathon [30,31]. Overall, the additional risk of cardiac arrest with exercise may be greater than 56 to 100-fold during or after strenuous exertion [32,33]. This risk was further stratified by the amount of time spent exercising. Individuals who exercise on a regular basis (habitual runners) had a 5-fold increased risk of death during activity, as compared with less active

individuals (sporadic runners), who carried a 56-fold increase risk of sudden death [33]. This risk is counter- balanced by the benefits of Regular exercise, which, in the long term, exceed the acute risk of exertion [34,35].

In addition to the electrocardiogram, cardiac markers are routinely used to evaluate cardiac injury in the acute setting. A prospective study looked at these inflammatory cardiac markers in 82 middle-aged participants over the course of 3 annual marathons. Blood samples were drawn before the race, 4 and 24 hours after the race (Table 1). Significant increases were found in myoglobin (38.4-fold at 4 hours post race), creatine kinase-MB (CK-MB) (4.9-fold and 13.5-fold at 4 and 24 hours post race), and Cardiac troponin I (6.5-fold at both 4 and 24 hours post race) [38]. Repeating this study using a rapid quantitative fluorescence immunoassay, the elevations in myoglobin and CK-MB were confirmed (significantly elevated at 4 and 24 hours post race). In contrast, however, there were no significant

increases in cTnI or Cardiac troponin T at either time point. Brain natriuretic peptide, used as a marker of transient left ventricular dysfunction, was significantly elevated at 24 hours but not at 4 hours post race [37]. None of these individuals had an increased incidence of acute cardiac events over the 5-year observation period [37]. These results were largely replicated in an older population of mara- thoners (N60 years old). Mean CK-MB levels were significantly increased at 0 and 24 hours post race, whereas CK-MB, percentage of total CK index, and cTnI levels were not significantly increased post race [39].

Elevated serum levels of CK-MB are thought to originate from skeletal muscle through exertional rhabdomyolysis and not from a cardiac source demonstrated through numerous series including one involving post marathon needle muscle biopsy [40]. A few series have demonstrated post marathon elevations in cardiac troponin T and cTnI, but these were largely done with first generation assays and/or involved an isolated patient. Nonetheless, no subsequent cardiac events were found on follow-up [38,41]. If evaluation for cardiac injury is necessary, use of troponin assays rather than CK-MB is indicated.

Hyponatremia

Hyponatremia is a potentially serious, electrolyte-related consequence of marathon racing [42]. The symptoms of hyponatremia can range from cramping, dizziness and weakness to seizures, altered mental status, cerebral and pulmonary edema, coma, and death.

During exercise, as much as 75% of the energy generated from metabolism must be dissipated from the body as heat. Evaporative cooling through sweating is one primary mode of heat dissipation [43]. The fluid lost when sweating is a mixture of water and electrolytes, including sodium and smaller amounts of potassium, calcium, and iron. Individual sweat rates vary depending on body size, individual physiological differences, exercise intensity, ambient temperature, humidity, and acclimation and can exceed 1800 mL/h [43]. To compensate for the fluid lost in sweat, athletes drink a variety of liquids repleting both the water and electrolyte losses to varying degrees.

There are 3 mechanisms that may play a role in exercise- induced hyponatremia (EIH). The first is that athletes lose water and electrolytes in their sweat as they run. Drinking restores their water losses but does not replace enough sodium and other electrolytes. A second mechanism is that EIH is a result of fluid overload. Although, running participants end up consuming more fluids than they lose. Over the course of a marathon, it is expected that an athlete will lose 1 to 2 kg of body weight in metabolic losses, in addition to that of fluid loss. When measuring post-race weights, those athletes who are at or over their pre-race weight are likely overhydrated. These athletes have, in effect, diluted the concentration of electrolytes in their blood [44,45]. Lastly, a mechanism for EIH is related to

inappropriate fluid retention. This can be a result of either abnormal aldosterone or vasopressin levels or some other mechanism of inappropriate fluid retention without elevated antidiuretic hormone (ADH) and arginine vasopressin levels [46]. A study done at the San Diego Marathon found that EIH may have a component related to inappropriate fluid retention with an increased extracellular volume without evidence of a large sodium loss and with no associated elevations in arginine vasopressin concentrations [45].

Factors contributing to EIH include race temperature, fluid availability, weight gain during the race, consumption of fluids every mile, consumption of greater than 3 L of fluid during the race, a body mass index of less than 20, female sex, increased frequency of voiding during race, and slower finishing times [47,48]. At one Ironman triathlon, a pre-race education program regarding EIH, fluid ingestion, and race temperatures decreased the number of athletes suffering EIH from 25 of 114 the previous year to 4 of 117 [49]. A prospective study of 488 marathoners found that immediately after race completion, 13% of the 488 runners demonstrated hyponatremia (Na =135 mmol/L) with 0.6% (3 runners) showing critical hyponatremia (Na =120 mmol/L) [48].

The American College of Sports Medicine and American Diabetic Association now make recommendations regarding Fluid replacement during races suggesting both repletion amounts and type of fluid ingested. In addition, athletes have begun using oral salt supplements to attempt to correct for these losses. Studies have not shown any significant alterations in serum sodium in athletes who use oral supplements or sports drinks [48,50]. Recently published was the Consensus statement of the 1st International exercise-associated hyponatremia Consensus Develop- ment Conference, Cape Town, South Africa 2005 [51]. This consensus statement was the first of its kind relating to EIH, identification, and management. They now recom- mend that all medical practitioners who cover ultraendur- ance events have a means to check serum sodium onsite. If an athlete is found to be either euvolemic or hypervolemic, then the recommendations are for 3% saline in small volume boluses. The practice challenge that faces the practitioner is determining dehydration or heat exhaustion from symptom- atic hyponatremia because the treatments have now been clearly defined and are different. Normal saline is the fluid of choice when volume repletion is also required. Hypotonic fluids should be avoided.

Renal

While exercising, blood is redirected to the working muscles decreasing renal perfusion. Dehydration can exac- erbate the problem [52]. Exercise-induced renal dysfunction ranges from asymptomatic changes in renal function to acute renal failure. When exercise intensity exceeds 50% V? o2 max, renal blood flow, glomerular filtration rate (GFR),

sodium excretion and urine flow rate all decrease [53].

There is a reduced excretion of sodium and increased water absorption at the renal tubules, together with a transient impairment in renal concentrating activity [52]. These changes can persist for 2 to 3 days post race.

Sodium and water balance are regulated by aldosterone and ADH. Running can lead to elevated levels of ADH, renin, and aldosterone, which may contribute to postrace fluid retention owing to increased sodium retention. ADH is released in response to decreased plasma volume increasing distal tubule permeability and increasing water absorption. Aldosterone acts to increase sodium reabsorption in the distal tubules of the kidney. These elevated levels may contribute to EIH. Acute renal failure (ARF) has been reported in a small number of athletes completing marathons and, in nearly every instance, is associated with rhabdo- myolysis [54].

Hematuria is a common problem that runners encounter and can be of either renal or lower tract origin. There have been cases of ARF because of hematuria of glomerular origin caused by prolonged intense activity. Kallmeyer and Miller [55] looked at 45 athletes completing the Comrade’s Marathon (89-km race) and found that 24.4% of the athletes had red blood cells in the urine. Urinary mean corpuscular volume and cell morphology suggest that the hematuria is primarily of lower tract origin [56].

The effect of NSAIDs on renal function in marathon runners is unclear. Nonsteroidal anti-inflammatory drugs inhibit cyclooxygenase, which prevents the breakdown of arachidonic acid to prostaglandins (PGs). PGE2 and PGI2 contribute to vasodilation in the kidney [57]. Without these PGs, there is reduced renal perfusion leading to impaired GFR ranging from mild elevations in renal function laboratory parameters to ARF. In healthy people, renal vasoconstrictor tone is low, and the vasodilation produced by prostaglandins is not necessary for normal kidney function [58]. Studies have examined NSAID use and renal function in exercising individuals and found no significant changes; however, the subjects were never stressed to the degree that a marathon does. One study by Farquhar et al

[53] attempted to add renal stressors (salt restriction, dehydration, and exercise in the heat) examining if, in this state, ibuprofen would cause transient reductions in GFR. The ibuprofen-related reductions in GFR were mild, but increased exercise intensity and dehydration could lead to more significant changes. Although there is no clear evidence that NSAID use is deleterious to endurance athletes, its use during a race should be discouraged.

Pulmonary

pulmonary complications related to marathon running range from exercise-induced bronchospasm (EIB) to non- cardiogenic pulmonary edema. Exercise-induced broncho- spasm is a transient obstruction of airflow that usually occurs 5 to 15 minutes after onset of exercise, peaking approximately 10 minutes after exercise and lasting 30 to

60 minutes. After a relatively quiescent refractory period lasting some 30 to 90 minutes, late-acting mediators may create rebound symptoms some 3 to 12 hours after the primary flare. Exercise-induced bronchospasm likely occurs secondary to both airway cooling and drying from exercise- induced hyperventilation. Exercise-induced bronchospasm can be present in healthy individuals with symptoms only occurring in the setting of exercise in the absence of any underlying allergic or asthmatic disorder. In the general population, EIB has an incidence of approximately 10% to 15% and, in elite athlete studies, have estimated an incidence ranging from 10% to 50% [59]. Continuous high-intensity exercise is more likely to cause EIB [60]. Early studies post marathon found that runners have a decrease in vital capacity postrace of up to 17% [61]. It was hypothesized that the decrease in vital capacity was equal to the increase in residual volume [62]. In 1983, Miles et al studied these parameters finding that there was a decrease in pulmonary diffusing capacity and a decrease in lung recoil, suggesting a minimal amount of pulmonary edema. The reduction in pulmonary diffusing capacity was found to be up to 15% 2 hours after Strenuous exercise and presumed to be related to an adult respiratory distress syndrome such as injury to the lungs [63]. Also found in that study was that the endotoxins commonly associated with adult respiratory distress syndrome are not present in exercise-related changes in pulmonary diffusing capacity.

Another proposed etiology of exercise-induced non- cardiogenic pulmonary edema is hyponatremia. Most of the reported cases of severe pulmonary edema after a marathon have been in patients with severe concomitant hyponatremia. For all of these patients, the pulmonary edema resolved as the Electrolyte disorder was corrected.

Although likely unrelated, a rare but extreme form of EIB is exercise-induced anaphylaxis. Symptoms may begin with itchiness and fatigue, followed by urticarial rash and GI symptoms, headache, and wheezing. This may progress to early onset of worsening urticaria, angioedema, and anaphylaxis. Aerobic activities such as jogging or brisk walking have been cited as the most frequent triggers among others such as certain foods (wheat and nuts), medications (aspirin and NSAIDs) and exercise temperatures [64]. Antihistamines may be helpful prophylactically and for treatment in combination with the use of a self-injectable epinephrine kit.

Exercise-associated collapse

Exercise-associated collapse (EAC) is the most common reason for treatment at the medical tents and accounted for 59% of all medical tent visits in a 12-year study [3]. The sudden cessation of exertion combined with the long duration of the event is thought to be a major con- tributing factor to EAC. Postural hypotension is a consistent finding but is not clearly related to dehydration, hypother- mia, or hyperthermia [3,65]. Most runners will recover

with 30 minutes of rest and oral hydration, whereas approximately15% of runners with EAC will require intravenous hydration [3]. Most of these runners are discharged from the medical tent without further treatment. Runners who collapse before the finish line are more likely to have an identifiable medical condition to account for the collapse [66]. Exercise-associated collapse is probably a combination of runners who are simply exhausted from their exertion, together with a smaller subset with more serious problems, chief among them, hyponatremia and Heat stroke/ exhaustion. The term EAC is properly reserved for those runners with no other identifiable cause for their collapse, who recover in a short time. Oral hydration is preferred to intravenous hydration unless the patient is hypotensive in the supine position or can not tolerate oral hydration. If intravenous fluid is necessary before obtaining a serum sodium level, an isotonic fluid is preferable because it will not exacerbate pre-existing hyponatremia.

Heat exhaustion is a clinical syndrome resulting from heat exposure with a constellation of signs and symptoms including headache, extreme fatigue, nausea, vomiting, dizziness, myalgias, tachycardia, and profuse sweating. Body temperature will be normal or slightly elevated. Heat stroke, in contrast, involves an alteration of mental status and an elevated body temperature (N40.58C). neurologic findings such as ataxia, agitation, seizures, and coma may be present. Although in heat exhaustion treatment involves bed rest in a cool environment and rapid IVF volume and Electrolyte replacement, the treatment of heat stroke has a different focus. Because morbidity is directly related to the severity and duration of hyperthermia, the immediate institution of rapid cooling to a temperature of 398C is indicated. Fans together with atomized water optimize evaporative cooling. ice packs to the groin and axillae are commonly used as adjuncts. Ice water baths have been used but they tend to present technical difficulties in the hospital setting. Benzodiazepines can be used to control agitation and reduce shivering. Additional treatment should include moderate IVF and electrolyte replacement and monitoring serial core temperature via rectal probe, urine output, finger stick glucose, electrolytes, coagulations profile, and liver function tests. Finger stick glucose evaluation should be done early in the management because these patients are often hypoglycemic.

Conclusions

Most of the abnormalities present in the immediate postmarathon period are related to the event itself and resolve after a few days of rest. Testing asymptomatic patients during this period with several screening examina- tions may precipitate unnecessary workups for laboratory abnormalities such as for GI bleeding or hematuria. Testing in the immediate postrace period should be done with a specific question in mind and the understanding of how the

endurance event can affect laboratory parameters. The alteration of laboratory parameters and the presence of occult blood in stool or microscopic hematuria can extend to individuals who have completed endurance events of a distance shorter than a marathon or who have completed training runs of considerable distance.

Environmental factors will play a role in how many patients will be in need of medical attention. A spring marathon, for which training is done in the winter, will probably generate more patients if run in an unseasonably hot day than a comparable fall marathon where the bulk of the training is done in the heat and the competitor has had a greater opportunity to adapt to it. Most runners seeking medical attention are treated and released at the event medical tents. Life threats to consider when evaluating a postmarathon patient include Severe dehydration, hypona- tremia, heat stroke, renal failure, acute coronary syndrome, and ischemic colitis. Complaints of a cardiac nature in endurance athletes should not be ignored. Most patients seen in the postmarathon period do not have any major problems and improve with time and rest.

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