ExerciseAssociated

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Exercise-Associated Hyponatremia Consensus
Statement of the 2nd International
Exercise-associated Hyponatremia Consensus
Development Conference, New Zealand, 2007
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Five otherwise healthy marathon runners have
died during or after running a marathon since
1993 Big Sur 1993 (female) Chicago 1998 (female)
Boston 2002 (female) Washington DC 2002
(female) London 2007 (male)
3
If 500,000 Runners participate in 375 Marathons
annually in the USA and the incidence of EAH is
13, 50,000-60,000 runners are at risk of
developing EAH in marathons alone.
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The 2007 EAH Consensus Conference
Independent panel of 18 international experts
NIH Consensus Development Conference protocol
Primary Goal Review existing data and update
2005 Consensus Statement
The 2007 Consensus Statement represents a concise
summary of the data synthesized by the 2007 EAH
Consensus Panel and represents an evolution of
the most current knowledge on EAH. This Statement
serves to replace the 2005 Consensus Document.
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The 2007 EAH Consensus Panel
Delegates represented 7 countries and 8 medical
and scientific sub-specialties pertaining to
exercise physiology, sports medicine, water
metabolism and body fluid homeostasis.
Tamara Hew-Butler DPM, PhD J. Carlos Ayus MD
Courtney Kipps BMBS, MSc Ronald Maughan
PhD Samuel Mettler MSc Willem Meeuwisse MD,
PhD Anthony Page MD Stephen Reid MBBS,
PhD Nancy Rehrer PhD William Roberts MD, MSc
Ian Roger MBBS Mitchell Rosner MD Arthur Siegel
MD Dale Speedy MBChB, MD Kristin Stuempfle PhD
Joseph Verbalis MD Louise Weschler MAT, PT
Paul Wharam MMedSc
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Definition and Classification
Etiology and Pathophysiology
Risk factors
Prevention
Treatment
Dissemination of Advice
Future Research
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DEFINITION
EAH is the occurrence of hyponatremia during or
up to 24 hours after prolonged physical activity
and is defined by a serum or plasma sodium
concentration below the normal reference range
of the laboratory performing the test. For most
laboratories, this is a Na lt 135 mmol/L.
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CLASSIFICATION
EAH should be classified using the same
clinical criteria as any rapid onset hyponatremia.
The most important factor is the presence or
absence of clinical signs and symptoms,
specifically neurological manifestations.
Individual variability is great and the
numerical value of Na is NOT a reliable
predictive index of the clinical severity of EAH.
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CLASSIFICATION
Signs and symptoms may occur when Na falls
below 135 mmol/L however a Na between
130-134 mmol/L is generally asymptomatic.
Early signs and symptoms include
bloating, puffiness, headache, nausea and
vomiting.
As EAH progresses, more serious indicators
include altered mental status, seizures,
respiratory distress, obtundation, coma and death.

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CLASSIFICATION
The presence of any of these signs and
symptoms represents an absolute indication to
measure Na.

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Definition and Classification
Etiology and Pathophysiology
Risk factors
Prevention
Treatment
Dissemination of Advice
Future Research
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EAH is primarily a dilutional hyponatremia caused
by an increase in total body water relative to
the amount of total exchangeable Na
13
The primary etiological factor in most cases
appears to be the consumption of fluids in excess
of body fluid losses.
14
In most reported cases of symptomatic EAH there
is bodyweight gain suggestive of an absolute
increase in total body water.
Body weight loss is expected during prolonged
endurance exercise due to substrate oxidation
without a net loss of total body water.
A dilutional hyponatremia may therefore
occur despite unchanged or decreased body weight.
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Although some cases of EAH may be due to pure
water intoxication from the overconsumption of
fluids, recent data indicate that non-osmotic
AVP secretion is an exacerbating factor in most
cases.
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Non-osmotic AVP secretion

• During exercise, AVP is not maximally suppressed
• AVP reduces maximal kidney excretory capacity
• AVP secretion causes increased urine osmolality
  and decreased urine excretion
• The higher the AVP in plasma, the more reduced
  will be the maximum urine excretory capacity
• This effect can potentially account for the
  marked inter-individual variability in the
  development of EAH, as well as individual
  variability in outcome across different events
  despite similar fluid intakes.

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plasma osmolality (mOsm/kg H2O)
plasma AVP (pg/ml)
296 294 292 290 288 286 284 282 280 278
276
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8
urine osmolality (mOsm/kg H2O)
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maximal urine excretion rate (ml/h)
thirst osmotic threshold
6
5
4
250
3
500
1000
2
1
300
AVP osmotic threshold
0
100
(Verbalis JG, Best Practice and Research Clin
Endocrinology and Metabolism 2003 )
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Potential Non-osmotic Stimuli of AVP during
Exercise includes
Nausea/vomiting Hypovolemia Hypoglycemia Hypotensi
on Stress cytokines
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Sodium Loss and EAH
Excessive sodium loss has not yet been
demonstrated to be a causative factor in the
pathogenesis of EAH.
Sodium loss has been shown to be no greater in
individuals who develop EAH than in individuals
who do not, but data are limited.
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There are 2 potential mechanisms whereby sodium
losses may play a role in the pathogenesis of EAH

• Hypovolemia produced by sodium losses can act as
  a stimulus to AVP, producing a secondary
  retention of water as is seen medically in some
  cases of diuretic-induced hyponatremia

2. Sodium losses themselves can worsen the degree
of hyponatremia, although in most cases not
nearly as much as water retention when summed up
over time.
21
Further (direct measurement) studies are
necessary to investigate the possible role of
sodium losses on this small cohort of athletes
who develop EAH in warmer climates in events
lasting over 12 hours.
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Definition and Classification
Etiology and Pathophysiology
Risk factors
Prevention
Treatment
Dissemination of Advice
Future Research
23
The presence of a risk factor implies
a correlation with higher rates of EAH, but not
necessarily causation.
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Athlete Related
Excessive drinking Weight gain Low body
weight Female sex Slow running Event
inexperience NSAIDs
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Event Related
High fluid availability gt 4 hours
exercise Unusually hot conditions Extreme cold
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Definition and Classification
Etiology and Pathophysiology
Risk factors
Prevention
Treatment
Dissemination of Advice
Future Research
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Avoid over consumption of fluids before,
during and after exercise.
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Never gain weight. Expect to lose up to 2 of
body weight during prolonged endurance exercise.
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Two Methods to Prevent EAH
1. Drink to thirst
2. Monitor body weight
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Athletes should be encouraged to weigh themselves
pre- and post- training in a variety of
conditions to estimate fluid requirements during
competition. HOWEVER, athletes should recognize
the potential limitations of this method. In
situations where AVP is not appropriately
suppressed, a drinking schedule that worked well
in identical training conditions and at the same
pace may lead to weight gain and EAH in
competition.
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Ingestion of electrolyte-containing sports
drinks cannot prevent the development of EAH
in athletes who drink to excess.

• All such drinks have a sodium content lt 135
  mmol/L and will therefore cause a dilution of
  blood sodium concentration.
• The ingestion of sodium will be excreted in the
  urine rather than retained the body if
  non-osmotic AVP secretion (SIADH) is a mitigating
  factor in the development of EAH.

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There is conflicting evidence as to the effect
of sodium supplementation, either by tablet or
drink on the incidence of EAH and rate of change
of Na during exercise.

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An educational program combined with limiting
fluid availability have resulted in a decreased
incidence of EAH. Fluid stations should be
placed every 20 km in cycle portion of an
ironman triathlon and every 3-5 km in a standard
marathon
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Definition and Classification
Etiology and Pathophysiology
Risk factors
Prevention
Treatment
Dissemination of Advice
Future Research
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Medical facilities at endurance events should
include onsite analysis of Na. Any
athlete exhibiting signs or symptoms of acute
hyponatremia should have blood drawn
immediately for electrolyte determination.
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Common Causes of Collapse In Endurance Athletes
CRITICAL (Hospitalization) Myocardial
infarction Heatstroke Hyponatremic
encephalopathy Acute renal failure Myocarditis Hyp
erkalemia
NON-CRITICAL (treat and observe) Postural
hypotension Hypernatremia Hypoglycemia Hypokalemia

Immediate measurement of vital signs, rectal
temperature, blood electrolyte and glucose
determination should be performed on all
collapsed athletes.
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(biochemical diagnosis) Restrict fluid intake
until onset urination Seek medical attention if
symptoms develop IV isotonic or hypotonic fluid
administration is contraindicated
Asymptomatic EAH
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Symptomatic EAH Onsite
The definitive emergency treatment of EAH
encephalopathy is immediate onsite
administration of IV hypertonic saline because
of the known rapid progression of
life-threatening encephalopathy and its
complications.
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Symptomatic EAH Onsite
Administer a bolus infusion of 100 ml 3
NaCl. Up to 2 additional 100 ml bolus infusions
of 3 NaCl may be given at 10 minute intervals if
no clinical improvement. This regime should not
pose any substantial danger to the patient.
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Symptomatic EAH Onsite
STABILIZE TRANSPORT IMMEDIATELY COMMUNICATE
with ER
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Symptomatic EAH Onsite
Avoid the administration of isotonic or hypotonic
fluids to prevent worsening the degree of
hyponatremia and fluid overload.
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Symptomatic EAH In Hospital
Do not delay treatment to await the results of
diagnostic tests Re-evaluate Na Specialist
consult
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pulmonary edema
HYPONATREMIA
NORMONATREMIA
encephalopathy
normal
Ayus JC et al. Ann Intern Med 2000
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Definition and Classification
Etiology and Pathophysiology
Risk factors
Prevention
Treatment
Dissemination of Advice
Future Research
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ATHLETES and COACHES Promote rational fluid
replacement guidelines to avoid
overdrinking. Recognize signs and symptoms of
EAH. Identify athletes with risk
factors. Special attention should be paid
to susceptible athletes with any of the risk
factors outlined.
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MEDICAL and RACE DIRECTORS
Medical directors should be involved in All
decisions regarding strategies for optimal
hydration including Number and placement of aid
stations Drinking advice disseminated to
athletes Drinking advice distributed to
participants by sponsors should be reviewed by
and not conflict with information approved by the
race medical director.
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MEDICAL and RACE DIRECTORS
Pre-race (training weight) should be recorded
(by bib number) so that it is available for
comparison by the medical team. Medical
directors should ensure availability of onsite
Na analysis hypertonic saline A record of
EAH cases should be kept, including follow-up and
outcome.
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MEDICAL STAFF Educate staff on signs and
symptoms of EAH Weigh athletes at entrance to
medical area (if possible) Set up relationship
with local response teams and emergency room
doctors

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Definition and Classification
Etiology and Pathophysiology
Risk factors
Prevention
Treatment
Dissemination of Advice
Future Research
50
Future Research

• Investigate alternative therapies
• Investigate maintenance of normonatremia despite
  overhydration and weight gain
• Determine if cases occur with sodium depletion
  and weight loss
• Investigate different forms of sodium
  supplementation in the modification of EAH
• Investigate the etiology of non-suppressed AVP
  during endurance exercise
• Investigate the role of endogenous water
  production in the pathogenesis of EAH.

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All cases of EAH should be recorded and monitored
on the International EAH Registry
at www.overhydration.info Anyone interested in
discussing EAH is invited to join the EAH
Discussion Group List at https//lists.uct.ac.za/
mailman/listinfo/eah-discuss-l