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Heatstroke in the Super-sized Athlete
Ericka Fink, MD,* Barbara W. Brandom, MD,yand Klaus D. Torp, MDz
Abstract: We present a 16-year-old male athlete with hyperthermia,
altered mental status, and respiratory distress during summer football
practice. Multisystem organ failure ensued, which he survived.
Malignant hyperthermia was suspected in this patient who had a
history of rhabdomyolysis. Specific muscle contracture testing later
eliminated this diagnosis. This case discusses the importance of rapid
hydration with isonatremic fluid, aggressive cooling, and full support
measures, including plasmapheresis, further diagnostic efforts to
evaluate potential causes of rhabdomyolysis, and planning for physi-
cal and emotional rehabilitation.
Key Words: heatstroke, exertional heat injury, multiorgan system
injury, rhabdomyolysis, dantrolene
CASE
A 16-year old, 135-kg male athlete presented to a local
hospital unresponsive, hyperthermic, tachypneic, diaphoretic, and
cyanotic immediately after summer football team practice in humid,
26.78C (808F) weather. The patient was admitted overnight 7 days
before this presentation for treatment of exertional rhabdomyolysis.
At that time, he complained of generalized muscle cramps after
vigorous practice with peak creatinine 1.6 mg/dL, creatine kinase
(CK) 1384 IU, and normal electrolytes. After a few days of rest, he
resumed practice. He did not take any medications and had no
surgical history. He strongly denied exposure to any performance-
enhancing substances such as ephedra.
In the emergency department, his rectal temperature was
42.28C.An endotracheal tube was placed secondary to altered
mental status, and cooling measures, including nasogastric and
bladder ice washes, fans, and a cooling blanket, were applied by
emergency personnel while the patient was transported to the local
emergency department. Initial vital signs included heart rate
168/min, respiratory rate 57/min, and blood pressure 146/103 mm
Hg. His initial arterial blood pH was 7.33 with base deficit of 8.5
meq/L. Serum potassium was 5.9 meq/L, and CK was 785 IU. Two
liters of normal saline were infused, and 500 mL of urine was
collected in the first hour of treatment. Then the patient became
oliguric. The intensive care unit physician supervising transport of
this critically ill patient to the tertiary care facility requested
treatment with sodium bicarbonate, calcium gluconate, kayexalate
enema, administration of 4 more liters of normal saline, and
dantrolene. After 1 hour of cooling measures, his rectal temperature
was 38.08C, and blood pH and potassium were normal. Twenty-five
milligrams of dantrolene, all that was available, (which contains
300 mg of mannitol/20 mg dantrolene per vial) and an additional 25
g of mannitol were given before transport to maintain temperature
control and urine output.
The patient was admitted to the pediatric intensive care unit
with the diagnoses of heatstroke and exertional rhabdomyolysis.
Computerized tomography of his head was normal, and 18 hours
later, his mental status and pulmonary status had improved. The
endotracheal tube was removed. He received oxygen via facemask
without respiratory complication. To treat rhabdomyolysis and renal
failure (creatinine 2.3 mg/dL), bicarbonate was added to his
intravenous fluids to maintain urine pH above 7, and urine output
was maintained at greater than 2 mL/kg per hour using furosemide
and mannitol (3 g/h) infusions. On the second hospital day, fever
returned to 398C, prompting resumption of dantrolene (1 mg/kg)
every 6 hours intravenously. At this time, troponin I was found to be
9.2 ng/mL (normal < 0.08) with occasional inverted T waves on
electrocardiogram. An echocardiogram showed normal findings. On
the first hospital day, CK was 5947 IU. On the second day, it was
19,140 IU. On the third hospital day, CK peaked at 90,720 IU. Urine
myoglobin reached a peak of 66,700 mg/L on the fourth hospital day.
The patient met criteria for liver failure with a combination of
impaired coagulation (peak prothrombin time, international normal-
ized ratio, and partial thromboplastin time: 26.1, 2.3, and 33.7,
respectively) and elevated liver function tests (peak aspartate
transaminase 8682 U/L and alanine transaminase 7430 U/L). On
the third hospital day, peak total and direct bilirubin of 7.5 mg/dL and
5.7 mg/dL, respectively, peak ammonia of 53 mg/dL, and
thrombocytopenia (low 49,000/mL) on the fourth hospital day.
These data prompted institution of plasma exchange and vitamin K
treatment of disseminated intravascular coagulation (DIC) and
multiple organ failure for 2 consecutive days. After consultation
with the liver transplantation service, the patient received continuous
fresh frozen plasma, alprostadil to dilate the hepatic vasculature, and
lactulose until liver function approached normal. Results of plasma
exchange were remarkable for resolution of coagulopathy, decrease
in CK by 67%, aspartate transaminase and alanine transaminase by
88%, and gradual increase in platelet count by more than 100,000/
mL. Methylprednisolone was added on the fourth hospital day for a
7-day course based on preliminary animal studies showing increased
survival benefits in heatstroke. Toxicology reports were positive for
caffeine and negative for amphetamine, including ephedrine.
Ampicillin-sulbactam, later changed to ceftazidime, was started
on the third hospital day to treat a nosocomial urinary tract infection
with Escherichia coli and Klebsiella pneumoniae.No fevers occurred
after the third hospital day. Myoglobinuria was present until the tenth
hospital day.
Dantrolene was discontinued on the eighth hospital day and
mannitol on the tenth hospital day without rebound of symptoms or
worsening of laboratory studies. No adverse events were observed
during the course of these medications.
510 Pediatric Emergency Care Volume 22, Number 7, July 2006
Illustrative Case
From the *Children’s Hospital of Pittsburgh, Pittsburgh, PA; yDepartment of
Anesthesiology, University of Pittsburgh Medical Center, Pittsburgh,
PA; and zMayo College of Medicine, Mayo Clinic, Jacksonville, FL.
Supported by internal funding of the Department of Anesthesiology, UPMC.
Address correspondence and reprint requests to Barbara W. Brandom, MD,
North American Malignant Hyperthermia Registry, Department of
Anesthesiology, Children’s Hospital of Pittsburgh, 3705 Fifth Avenue,
DeSoto St, Room 7446, Pittsburgh, PA 15213. E-mail: bwb@pitt.edu.
Copyright n2006 by Lippincott Williams & Wilkins
ISSN: 0749-5161/06/2207-0510
Copyr ight © Lippincott Williams & Wilkins. Unauthor ized reproduction of this article is prohibited.
The patient was discharged on the fourteenth hospital day. His
electrocardiogram was normal, and a liver ultrasound with Doppler
was normal. His only medication was nystatin for oral thrush. Upon
follow-up 1 month after discharge, he complained of weakness and
muscle pain when he walked further than 1 block. His CK was more
than 1000 IU for several weeks after hospital discharge. Because he
still wanted to play team sports, he underwent muscle biopsy and
contracture testing to evaluate his risk for malignant hyperthermia
(MH), which has been previously associated with exertional
rhabdomyolysis and heatstroke. The result of his contracture test
was normal. His muscle was not subject to other histological or
histochemical tests. He did not have any history of adverse events
with anesthesia nor did he have family history suggestive of MH, and
therefore, his exertional heatstroke occurred independently of the
MH Syndrome.
DISCUSSION
Heatstroke is a life-threatening acute illness. By defi-
nition, heatstroke is the presence of a core temperature more
than 408C accompanied by altered mental status manifested as
delirium, coma, or seizure. Heatstroke may occur because of
environmental exposure or exertion. Classic heatstroke is the
term applied to an individual who develops heatstroke while
exposed to a hot ambient temperature. Typically, classic heat-
stroke occurs in the elderly with chronic medical conditions or
in the very young confined with inadequate ventilation and
cooling during summer heat waves. Anhydrosis, as well as
pyrexia, and altered level of consciousness are typical of
classic heatstroke. The cytokine profile of patients with clas-
sic heatstroke resembles that of sepsis: increased levels of
endotoxin, tumor necrosis factor alpha (TNF-a), interleukin
(IL) 1B, IL-6, and IL-2. These inflammatory cytokines may be
released during cerebral ischemia and help explain the clinical
effects of heatstroke.
In contrast, exertional heatstroke (EHS) describes the
individual who collapses with signs of heatstroke during or
shortly after strenuous exercise. Exertional heatstroke may
occur in any ambient temperature, although it is more common
during hot and humid weather. Exertional dehydration, muscle
cramps, heat exhaustion, and rhabdomyolysis may precede
EHS. Exertional heatstroke results from both an elevation
of body core temperature and the circulatory responses to
exercise and thermoregulation. During exercise, there is pro-
fuse sweating, peripheral vasodilation and increases in heart
rate and cardiac index to promote heat loss through evapo-
ration and radiation. Sweat rates in excess of 2 L/h can be
observed. Thus, dehydration leads to abnormal heat dissipa-
tion. Increased heat production may continue during exertion,
leading to abnormal central regulation of temperature and the
development of EHS. In severe EHS, splanchnic ischemia
produced either primarily by shock or heat can elicit the
systemic inflammatory response. Elevated concentrations of
cytokines have been measured 2 hours after onset of exertional
heat illness, but these may not always correlate well with rectal
temperatures. When core temperature is elevated long enough,
multiorgan dysfunction syndrome (MODS) will occur.
1
This patient met the diagnostic criteria for heatstroke:
core temperature more than 408C and central nervous system
abnormality.
1
This patient also developed MODS with renal
failure, respiratory failure, liver failure, coagulopathy, and
myocardial injury. Lastly, rhabdomyolysis was demonstrated
by myoglobinuria and elevated CK.
The primary treatment of heatstroke is cooling, and
more rapid cooling has been shown to improve survival.
2
Modalities of cooling include water immersion, evaporative
cooling using sprayed water and fans, ice pack or blanket
application, invasive cooling such as through a nasogastric
tube or peritoneal lavage, and intravenous dantrolene.
3
A
literature review demonstrated that the choice of cooling
modality is dependent on the patient’s age, clinical back-
ground, and location. For example, a player on the field can
be splashed with cool water and fanned until reaching a
hospital where nasogastric cold-water flush can be instituted.
Time is of the essence. A study by Chou et al
4
showed that
neuronal damage increased with increasing lag time to in-
stitution of hypothermia in their model using a cooling
blanket applied to rats with heatstroke.
There is no literature stating how much fluid
resuscitation should be undertaken in heatstroke. However,
our patient had good outcome and increasing urine output
using aggressive intravenous hydration with approximately
45 mL/kg of normal saline.
Hypertonic saline has been advocated by Kuo et al
5
,
who found that intravenous treatment with 3% saline before
or immediately after onset of heatstroke significantly reduced
hypotension, and improved cerebral perfusion, cerebral is-
chemic damage, and survival times in a rat model. Possible
explanations for the beneficial effect of 3% saline include
reduction in intracranial pressure postischemia, attenuation of
cytokine production, and maintenance of mean arterial
pressure. One can argue about the fluid of choice, but aggres-
sive hydration to restore intravascular volume and urine out-
put should be a goal of initial therapy, which in this case was
accomplished with normal saline.
Mannitol may also be useful in the treatment of EHS.
Mannitol attenuated cerebral ischemia and neuronal damage
in a rat model of heatstroke. Niu et al
6
proposed the
mechanism to be mannitol’s ability to reduce intracranial
pressure after ischemia-induced cerebral edema and its
antioxidant properties. Mannitol also produces alkaline
urine, which will decrease the toxic effect of myoglobin on
renal tubules. Mannitol was used concomitantly with 1
1
/
2
to
2 times maintenance fluid in our patient primarily to promote
excellent urine output and was decreased as the patient’s
renal function improved.
The use of dantrolene for the treatment of heatstroke is
controversial. Although one study supports
7
its use, a ran-
domized, placebo-controlled study showed that 2 mg/kg
dantrolene ‘‘did not prove beneficial’’ to patients with
environmental heatstroke. In particular, dantrolene did not
alter cooling times, complications, and length of hospital
stay.
8
But these patients reported by Bouchama et al
8
were not
typical EHS. Their characteristics were predominantly those
of environmental heat illness. Dantrolene decreased intracel-
lular calcium elevation in muscle fibers from patients with
exertional rhabdomyolysis by 83%, associated with an
n2006 Lippincott Williams & Wilkins 511
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Copyr ight © Lippincott Williams & Wilkins. Unauthor iz ed reproduction of this article is prohibited.
improvement in clinical symptoms and laboratory values.
9
In
addition, dantrolene has been reported to decrease Ca
+2
elevation in macrophages in response to lipopolysaccharide.
10
Dantrolene could affect the inflammatory response that is a
result of heatstroke. Dantrolene was given to this patient at a
dose of 1 mg/kg IV every 6 hours while myoglobinuria per-
sisted. This is similar to the maintenance dose of dantrolene
recommended for the treatment of MH.
Steroids have been shown to improve survival and
neurological morbidity when given before onset of heat-
stroke in an animal model.
11
This is thought to be secondary
to an inhibitory effect on proinflammatory cytokines, par-
ticularly TNF-aand IL-1. Lu et al
12
demonstrated that in
exertional heatstroke, IL-1B, TNF-a, IL-6, interferon gamma,
IL-2R, IL-4, and IL-10, and plasma chemokines IL-8, mono-
cyte chemoattractant protein 1, and RANTES were signifi-
cantly higher than in exertional control subjects. An IL-1
receptor antagonist, given before onset of heatstroke in
rats, decreased cerebral ischemia and improved neuronal
survival.
13
Lui et al
14
found that pretreatment and posttreat-
ment with dexamethasone attenuated arterial hypotension,
cerebral ischemia, neuronal damage, and IL-1B levels and
increased time to death in induced heatstroke in rats. Human
studies of the effects of steroids in heatstroke are limited
to case reports. Controlled studies are needed. In this case, a
7-day course of methylprednisolone was given.
Disseminated intravascular coagulation is often a
feature of heatstroke, possibly as a secondary effect after
cerebral ischemia and its release of inflammatory cytokines.
Bleeding complications are the most common manifestations
in heatstroke with the occurrence of microthrombi affecting
the perfusion of multiple organs. Bouchama et al
15
found
that levels of thrombin-antithrombin III, fibrin monomers,
plasmin-alpha 2-antiplasmin, and dimerized plasmin frag-
ment D were elevated in heatstroke patients versus normal
controls and correlated with the degree of hyperthermia. In a
study of 52 consecutive patients with heatstroke, thirteen
developed DIC.
16
Liver damage and, rarely, liver failure
17
can
accompany heatstroke and may be due to direct thermal injury
and hypoxia secondary to splanchnic ischemia. Thus, both
consumption of clotting factors and inadequate production
may produce bleeding in EHS. Plasma exchange is one treat-
ment option that has been shown to be successful in a small
case series in patients with DIC and multiorgan failure.
18
It may also be useful in removing inflammatory cytokines.
19
In our patient, administration of fresh frozen plasma did not
lead to amelioration of coagulopathy. Coagulopathy resolved
after plasma exchange for 2 days.
This patient had an episode of exertional rhabdomyol-
ysis 1 week before his life-threatening episode of EHS. What
risk factors did he have that could have contributed to this
repeated injury? If the individual is not accustomed to the
environment in which exercise occurs and if the intensity of
exercise is much greater than accustomed, the risk of EHS is
greater. This episode of EHS occurred early in the training
season when there was much motivation to exercise as hard as
possible. Performance-enhancing drugs, such as ephedra and
diuretics, may be used in such circumstances and will increase
the risk of dehydration and muscle injury. The National
Football League, National Collegiate Athletic Association,
International Olympic Committee, and minor league baseball
banned the use of ephedra, whether synthetic or derived from
the herb Ma-huang. Our patient denied the use of these drugs
and herbs, but caffeine was identified in his urine. Thus,
toxicological urine screening did not change the course of this
patient’s management, but we suggest that such measure-
ments should be performed.
His massive bulk certainly made it more difficult for
him to loose heat. Could there have been anything else about
his muscle that would increase his risk of EHS? Controlled
studies of high-force eccentric exercise found that approxi-
mately 3% of patients experience rhabdomyolysis of the
exercised muscle.
20
It is not known if these 3% have an in-
herent difference in muscle that makes them more susceptible
to injury induced by exercise. Exercise-induced rhabdomyol-
ysis came to the attention of the medical community from
reports of military training units. For example, a 25-year-old
man with exertional rhabdomyolysis had muscle pain and
acute renal failure, with no other findings.
21
He collapsed after
30 minutes of jogging, and mixed upper and lower body
exercises were performed in a tropical climate. There was no
history of muscle disease in the patient or the family. The
findings from the histological examination of his muscle
tissue were normal. He had a positive result on the diagnostic
test of MH susceptibility, the caffeine halothane contracture
test.
22
Malignant hyperthermia is a generally asymptomatic
condition, due in most cases to excess calcium release from
the sarcoplasmic reticulum through the ryanodine receptor.
Mostly in the presence of inhaled anesthetics and succinyl-
choline does the MH-susceptible person experience extreme
rhabdomyolysis. But there have been documented cases of
EHS in MH-susceptible individuals.
For example, there was a male adolescent who experi-
enced heatstroke with muscle rigidity after vigorous participa-
tion in a game. This athlete had experienced anesthesia-induced
hypermetabolism and rhabdomyolysis, the syndrome known
as MH, 8 months before his collapse after the game. Post-
mortem, he was found to have a mutation in the skeletal
muscle ryanodine receptor 1 (RYR1) that is known to be
causative of MH.
23,24
Exercise-induced rhabdomyolysis has
been found in other patients known to be MH susceptible and
to have mutations in the RYR1 gene.
25– 27
In more than 350
exertional heatstroke cases, there were metabolic abnormal-
ities in muscle found in 78% and MH susceptibility diagnosed
by contracture testing in 18% to 26%.
28
Because there may be a subset of patients who present
with heatstroke that are also susceptible to MH, it was
recommended that our patient undergo testing for MH sus-
ceptibility by muscle biopsy and contracture testing at one of
the specialized MH diagnostic centers.
29
The addresses of
these centers can be found at www.mhaus.org. The outcome of
a contracture test will influence the future anesthetic manage-
ment of the patient. It could also influence professional athletic
or military training. The result of the contracture test of this
EHS patient was negative. After months of rehabilitation, he
returned to the active practice of his sport. In the following
512 n2006 Lippincott Williams & Wilkins
Fink et al Pediatric Emergency Care Volume 22, Number 7, July 2006
Copyr ight © Lippincott Williams & Wilkins. Unauthor iz ed reproduction of this article is prohibited.
competitive season, his performance was excellent. A sports
scholarship a year later allowed him to continue his education.
However, he could not complete his first semester because of
posttraumatic stress disorder. He was unable to dress for the
sport without debilitating recall of the EHS episode.
Increased metabolism and muscle breakdown can
have many causes unrelated to genetic abnormalities in the
excitation-contraction coupling mechanism such as the RYR1
mutations associated with MH. Rhabdomyolysis may be
caused by an enzyme deficiency in muscle,
30
although this
seems an unlikely diagnosis in this athlete. Ingestion of
performance-enhancing drugs, even caffeine, can place ge-
netically healthy muscle at increased risk of exertional injury.
It may be that a previous episode of heat-related illness, such
as was experienced by this patient a week before the episode
of heatstroke, produced greater risk of a second episode. The
duration of such increased risk is not known.
Other than the factors related to the individual as dis-
cussed above, environmental conditions are important risk
factors for EHS. The wet-bulb globe temperature combines
temperature, radiant heat, and humidity to provide a stratified
risk category for that particular area and time.
31
The hot and
humid climate increased our patient’s risk of EHS. In the
presence of adverse environmental conditions, behavior modi-
fication is necessary. Prevention of exertional heat injury and
EHS is possible through the education of athletes and their
families, trainers, and coaches. The American College of
Sports Medicine has published recommendations for reducing
the risk of heatstroke in athletes, including discussions
regarding which conditions present the highest risk for heat-
stroke, and fluid management during sports.
32
CONCLUSIONS
We report the successful management of a case of EHS
in an athlete, discuss several treatment modalities, and suggest
a diagnostic pathway that may be pursued to support optimal
care of the athlete after recovery from the acute episode.
Heatstroke and exertional rhabdomyolysis are not common
diseases in North America. Few of the patients with EHS may
have abnormalities in ryanodine receptor function. This
patient had a good physical outcome because of rapid
institution of conventional and additional life-saving meas-
ures. Greater awareness in communities of the early warning
signs of exertional heat illness, and in some cases, medications
and supplements that athletes are consuming could help to
decrease both its occurrence and its progression to MODS.
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