ORGAN SYSTEM
DISORDERS
A. Respiratory System .......41
1. Upper Respiratory Tract Infections.......41
2. Exercise-Induced Asthma .......42
3. Spontaneous Pneumothorax .......44
B. Cardiovascular System .......46
SPORT
MEDICINE MANUAL
1. Sudden Death .......46
2. Mitral Valve Prolapse .......47
3. Hypertension .......50
4. Paroxysmal Supraventricular Tachycardia (PSVT) .......53
C. Hematological System .......55
1. Anemia .......55
2. Infectious Mononucleosis .......57
D. Genitourinary System .......59
1. Traumatic Haematuria .......59
2. Acute Renal Failure/Myoglobinuria .......62
3. Proteinuria .......65
4. Testicular Trauma .......67
3 - Organ System Disorders
3
E. Gastrointestinal System .......69
1. Diarrhea and Exercise .......69
2. Runner’s Stitch .......71
3. Reflux Esophagitis .......72
F. Metabolic and Endocrine System .......73
1. Overtraining .......73
G. Nervous System .......77
1. Headache in Athletes .......77
2. Epilepsy .......79
H. Ear, Nose and Throat Disorders .......81
1. Swimmers Ear (Otitis Externa) .......81
2. Cauliflower Ear (Haematoma Auris) .......82
3. Middle Ear Barotrauma .......83
4. Injuries to the Face and Neck .......84
I. Ocular System .......94
1. Visual Acuity and the Athlete .......94
2. Blowout Fracture .......94
3. Chemical Conjunctivitis .......95
4. Trauma to the Eye .......96
- 39 -
J. Dermatology.......97
1. Dermatological Conditions seen in Runners .......97
2. Other Foot Dermatoses .......100
3. Contagious Skin Infection .......103
4. Sunburn.......106
K. Prevention of Infectious Disease Associated with
International Travel.......108
1. Personal Prevention Strategies.......108
2. Disease Spread by Food and Water .......112
3. Disease Spread by Arthropod and Animal Vectors.......116
4. Disease Spread by Human Contact.......121
5. Fever in the Returning Traveller.......127
L. Rheumatological Conditions.......128
1. Single Swollen Joint.......128
2. Low Back Pain and Stiffness.......129
3. Multiple, Painful, Swollen Joints.......131
3 - Organ System Disorders
M. References.......133
- 40 IOC Sport Medicine Manual 2000
ORGAN SYSTEM DISORDERS
A. Respiratory System
3
1. Upper Respiratory Tract Infections
Case History - Upper Respiratory Tract Infections
An 18-year-old female track and field athlete came to you before training complaining of a
cold. In the past 24 hours, she has developed a sore throat, fever, cough with production of a
nonpurulent sputum and a runny nose. She sought your advice whether she should participate in
the workout scheduled that afternoon. There was no history of respiratory diseases or allergies.
She was a university student living in a dormitory where there has been an outbreak of upper
respiratory tract infections. She was not on any medication.
Physical examination revealed she was a healthy girl who was not distressed. Her temperature
was 39º C and her pulse 105 b/min. Her tonsils had mild erythema, no exudate, and were not
enlarged. She had mild erythema of her pharynx. The tympanic membranes were red, but there
was no fluid in the middle ear. There were a few, small, mobile, slightly tender anterior and posterior
cervical lymph nodes. Her nasal turbinates were not enlarged and there were no nasal polyps. She
had no skin rash.
Discussion
This athlete has the signs and symptoms of an upper respiratory tract infection due to a viral or bacterial
agent. The average adult has 3-5 acute episodes of this nature per year.
Investigation should include a throat swab, a full blood count including differential and a Monospot
test. The Monospot test checks for the antibody to the E-B virus and therefore may be normal during
the first 7-10 days of the infection. In the absence of any chest findings, a chest x-ray in a young
female is not warranted at this time.
The most likely diagnosis is a viral upper
respiratory tract infection transmitted by airborne means. Her throat swab grew no
significant pathogens. There was a mild
neutropenia and the Monospot test was
negative.
Treatment is symptomatic. She should be
advised not to participate in track training
for two days until she is seen in follow-up
with her laboratory results. If she has a fever
or has symptoms including profound
fatigue, myalgia, arthralgia, anorexia, then
- 41 IOC Sport Medicine Manual 2000
3 - Organ System Disorders
The differential diagnosis in this age group includes infectious mononucleosis. This infection is
common in the young adult population and can be devastating for an elite athlete. It is caused by the
Epstein-Barr (E-B) virus. Early recognition can limit its effect on longterm training. If an athlete
keeps training, then this may increase the severity of the attack and prolong recovery.
she should rest and avoid any forms of stress. If she does not have a fever and the symptoms are from
the neck up (ie. sore throat, nasal congestion, mild headache etc), then she can exercise but at a volume
and intensity that allows recovery. Acetaminophen, Acetylsalicylic Acid, and Ibuprofen may be given
to reduce her fever and sore throat. Mouthwashes and gargles can also be used. She should be encouraged
to drink additional fluids to prevent dehydration. Antibiotics are not indicated for this athlete. If the
illness is caused by Influenza A or B, then newer anti-influenza drugs (neuroaminadase inhibitors)
maybe helpful if initiated early.
It is important to limit physical activity until the fever subsides. The development of a viral myocarditis
following strenuous activity in athletes with febrile illnesses is a possibility that must be prevented by
judicious activity.
When the athlete returned two days later for follow-up, she was afebrile and the symptoms of the
upper respiratory tract infection were subsiding. She resumed her regular training program.
Every athlete should be offered the influenza vaccine to provide partial or full immunity to the most
prevalent strains of the virus which are causing the current epidemic.
2. Exercise-Induced Asthma
Case History - Exercise-Induced Asthma
3 - Organ System Disorders
A 22-year-old female middle distance runner presented with complaints of dyspnea, chest
tightness and poor performances. For the past six months, she has had episodes of breathlessness
while running that are out of proportion to the exercise stress; in one instance, it was necessary to
stop running altogether. She is an Olympic athlete, a non-smoker and has no history of cardiac
disease. She does, however, have a brother with asthma and she was treated as a child for episodes
of “wheezy bronchitis”. On physical examination her blood pressure was normal. There was a
sinus bradycardia, normal heart sounds without murmurs or clicks and her chest was clear to
auscultation with no signs of chronic lung disease. There was no chest wall tenderness.
Discussion
The symptoms of chest tightness, dyspnea and fatigue are nonspecific and in an individual with this
athletic profile, a number of possible diagnoses must be considered.
a. cardiac disease:
ischemic heart disease
mitral valve prolapse (MVP)
valvular lesion
myocarditis
cardiomyopathy
upper respiratory tract infection (URTI)
asthma
exercise-induced laryngomalacia
pulmonary embolism
c. chest wall problems:
costochondritis
stress fracture rib
d. nonspecific:
overtrained
iron deficiency anaemia
b. respiratory disease:
- 42 IOC Sport Medicine Manual 2000
The lack of physical findings eliminates most of the above. Ischemic heart disease is a possibility but
unlikely in a 22-year-old female athlete. There were no features upon clinical examination to suggest
mitral valve prolapse or other valvular heart lesions. The lack of fever, upper respiratory symptoms,
and sputum production argues against URTI. Similarly, the absence of localized chest pain on history
and examination excludes costochondritis and stress fracture of a rib. If she has a family history of
blood clots, is on an estrogen-containing oral contraceptive pill, and/or has leg swelling, then the
diagnosis of pulmonary embolism should be pursued with ventilation/perfusion nuclear scan, plasma
D-dimer test, venous ultrasonography of the lower extremities, spiral CT scan and/or pulmonary
angiogram. Myocarditis, cardiomyopathy, exercise-induced asthma (EIA), exercise-induced
laryngomalacia, the overtrained state and iron deficiency anemia remain reasonable diagnostic
possibilities. Minimal investigation for this athlete should include:
chest x-ray
spirometry
exercise challenge test: pre- and post-test spirometry and the response to an aerosol
bronchodilator and/or methacholine challenge test
electrocardiogram
complete blood count and serum ferritin
Exercise-induced laryngomalacia is an uncommon entity that can be misdiagnosed as exercise-induced
asthma. The pathology involves upper airway collapse during inspiration. The symptoms include
dyspnea and noisy respiration especially inspiration (inspiratory stridor). Antiasthma medications are
not helpful and the pulmonary function tests are negative for asthma. Diagnosis is confirmed by
laryngoscopy during exercise which reveals the laryngeal collapse.
If the routine pulmonary function tests at rest are normal, then further testing with an exercise challenge
test or methacholine (or histamine) challenge test can identify exercise-induced asthma. The exercise
challenge test can be done on a cycle ergometer, free range run or treadmill and lasts 6-8 min in
duration at an intensity of 85% of the maximal heart rate. Pre- and post-test spirometry every five
minutes for 15-20 min post-exercise may confirm the diagnosis. An aerosol bronchodilator may be
administered to reverse an exercise-induced fall in FEV 1, or alternatively, may be inhaled prior to a
subsequent exercise test to ascertain if the post-exercise lung volumes will be unchanged. For centres
with more sophisticated laboratory equipment, a methacholine or histamine challenge test will also
confirm the increased bronchial reactivity.
Several factors can influence the severity of the bronchoconstriction. The type of activity is important;
running outdoors is the most asthmogenic activity, followed by treadmill running, cycling, swimming,
and walking. Intermittent activities are also less asthmogenic in nature. The severity of the
bronchoconstriction is maximal when the intensity of the work is 65-75% of VO2 max; at intensities
above 85%, there is little or no change in bronchoconstriction.
Treatment can include non-pharmacological and pharmacological approaches. The nonpharmacological approaches include a 15 min warm-up at 60% VO2 max, avoidance of known
pollutants, allergens, and dry, cold air, which increase the degree of bronchoconstriction.
- 43 IOC Sport Medicine Manual 2000
3 - Organ System Disorders
A fall in forced expiratory volume over one sec (FEV 1) or peak expiratory flow rates (PEFR) of 15%
or greater is indicative of asthma. FEV 1 is a measure of large airway resistance, whereas changes in
the resistance of small airways are best seen in measurements of maximal mid-expiratory flow rate
(MMEFR = 25% – 75%FEV 1). The response of a patient to bronchodilation with a beta-agonist is an
essential diagnostic step, as asthma is a reversible airway disease.
Most patients will require pharmacological intervention and the selective beta 2 adrenergic agonists,
such as Salbutamol, Terbutaline and Salmeterol, are powerful bronchodilators and are the drugs of
choice. The aerosol route is preferred as it induces more bronchodilation than the clinically equivalent
oral dose and it has less side-effects. It takes effect immediately and therefore can be taken just prior
to or even during training sessions. Also the oral form of these drugs are on the IOC Banned Substance
List. Salbutamol, Terbutaline or Salmeterol taken as two puffs 5-10 min prior to exercise is the first
line of pharmaceutical prophylaxis for EIA. Other medications, such as Sodium Cromoglycate, can
be used in combination with the beta-agonists to provide additional protection for the patient with
EIA. Each of these medications, through aerosol administration, is permitted by the Medical
Commission of the IOC for use by athletes at international competition, as are Theophylline,
Ipratropium, Nedocromil, inhaled Corticosteroids and the recent Antileukatrines.
Our 22-year-old middle distance runner had a normal chest x-ray, full blood count and serum ferritin.
An eight minute run on a treadmill achieving a final heart rate of 170 b/min resulted in a 34% reduction
in her FEV 1, from the pre-exercise value. This was recorded 10 minutes post-exercise, thus confirming
the diagnosis of EIA. The obtained good control of her EIA with pre-exercise aerosol Salbutamol and
her Olympic performance was not hampered as she achieved a top 10 finish in the 1500 m event.
3. Spontaneous Pneumothorax
Case History - Spontaneous Pneumothorax
3 - Organ System Disorders
A 23-year-old male cyclist had been taken to the hospital complaining of a sudden onset of
severe chest pain accompanied by shortness of breath. The pain began during the training ride
and was not associated with any trauma. The patient has no history of respiratory disease and had
not been ill recently. He has no family history of any respiratory disorder.
Examination revealed the patient was distressed with tachypnea (respiratory rate 32/min) and
pain. Blood pressure was 145/90 with tachycardia of 110. He localized the pain to the left side of
the chest. Examination of the chest wall revealed uneven chest expansion with a decrease on the
left. Percussion elicited hyperresonance over the entire left lung field and on auscultation, decreased
air entry on the left. The air exchange was normal in the right chest. The athlete was afebrile.
There was no lymphadenopathy. The rest of the physical examination was normal.
Discussion
Symptoms of sudden onset of chest pains and shortness of breath in the absence of trauma suggests a
number of possible diagnoses:
a. acute myocardial infarction
b. pulmonary embolism
c. spontaneous pneumothorax
d. dissecting aortic aneurysm
e. pathological rib fracture
Myocardial infarction and pulmonary embolism in an elite athlete are rare possibilities. The appropriate
investigative procedures for an acute myocardial infarction includes electrocardiogram, serum cardiac
enzymes and possibly an echocardiogram and/or radionucleide imaging; for a pulmonary embolus,
ventilation/perfusion lung scan, plasma D-dimer test, electrocardiogram, venous ultrasonography of
the lower extremities, spiral CT scan and possibly a pulmonary angiogram.
In this case, the history and classical physical findings of sudden onset chest pain, tachypnea,
hyperresonance and reduced air entry are indicative of spontaneous pneumothorax.
- 44 IOC Sport Medicine Manual 2000
A dissecting aortic aneurysm is possible in this age group if one had a congenital disorder, such as
Marfan’s syndrome. However, the classical physical examination findings mentioned above would
not be present.
Rib fracture would be responsible for acute pain and shortness of breath and, in the absence of trauma
or overuse, the only possibility would be pathological fracture secondary to some other disease process.
In the case of rib fracture, the pain is localized to the area where the fracture occurs. There is an
increase in the intensity of the pain with deep inspiration and palpation of the area elicits exquisite
tenderness.
The initial laboratory investigation for this athlete is a chest x-ray (posterior/anterior view in full
inspiration and expiration and a lateral view). Further investigation of the differential diagnosis have
been discussed. X-rays, however, may not demonstrate the fracture and a radionuclide bone scan may
be necessary to identify any pathological process involving the ribs.
In this case, the chest x-ray demonstrated a large, left pneumothorax with approximately 75% collapse
of the left lung.
3 - Organ System Disorders
Figure 3.1 X-ray of the thoracic cavity of a patient with a fractured rib and pneumothorax of the left
lung.
If the collapse is less than 15%, then the treatment is supportive care awaiting resorption of the air. If
the collapse is greater than 15%, then the treatment involves the insertion of a chest tube into the left
pleural space. The tube must be attached to an underwater seal. This will allow the left lung to reinflate
and, following a period of 2-5 days, it will be possible to remove the chest tube. Once the x-ray has
demonstrated full inflation of the left lung, the athlete can be discharged from the hospital.
The athlete should not be allowed to train until he has returned two weeks later for a follow-up visit
and repeat x-rays. In this case, x-rays repeated two weeks following discharge from the hospital
demonstrated no recurrence and the athlete was allowed to begin a very light aerobic exercise program
on his bicycle, consisting of 20-30 minutes of low intensity cycling on alternate days. Two weeks
- 45 IOC Sport Medicine Manual 2000
later, as the discomfort associated with the chest tube placement site was resolving, the intensity was
gradually increased. He returned to full training in eight weeks time.
The risk of recurrent pneumothorax is approximately 30% in the healthy individual, rising to 50% for
patients with chronic lung disease. The risk of recurrence also increases with each subsequent
pneumothorax. Patients who present with severe chest pain and shortness of breath due to traumatically
induced fractures of the rib are treated in a different manner (see Unit 6 - Rib Fracture).
B. Cardiovascular System
1. Sudden Death
Despite the positive benefit of regular exercise, sudden death during or shortly after participation in
sport or exercise, does occur occasionally. The death of a young elite athlete while exercising usually
provokes media attention.
At least 70% of the cases of sudden death during and within an hour of exercise are a result of coronary
atherosclerosis. Although sudden death is the first manifestation in as many as 30% who succumb,
many older athletes (older than 30 years) have significant prodromal symptoms. In many instances,
these have been ignored by the victim, often believing that his or her exercise habits will be protective.
For the same reason, doctors may fail to pay sufficient attention to symptoms indicative of ischemic
heart disease occurring in an athlete.
3 - Organ System Disorders
It is important to remember that even people who have trained to run marathon distances and beyond
are not immune to coronary artery disease. Such persons should be investigated in the same manner as
a sedentary patient presenting with chest pains and other symptoms suggestive of ischemic heart
disease. This is especially important if coronary risk factors are evident.
The risk factors for the development of coronary artery disease are:
strong family history of coronary disease
hyperlipidemia
hypertension
cigarette smoking
diabetes
inactivity
gender - male
age - eg. postmenopausal female
Other coronary causes of sudden death include congenital coronary artery anomalies, exercise-induced
coronary spasm, and drug-induced coronary spasm (eg. cocaine). Fortunately, chest pain and palpitations
may occur during exercise leading the athlete to see their physician. Appropriate investigation, including
electrocardiogram, serum cardiac enzymes, echocardiography, stress tests including the use of thallium,
and coronary angiograms establish the diagnosis. When coronary artery disease is suspected in women,
an exercise echocardiography appears to be the preferred diagnostic test.
Non-coronary heart disease is a significant cause of sudden death in the young athlete. Below the age
of 21, some 50% of sudden death is a result of subaortic stenosis from congenital hypertrophic
cardiomyopathy. Studies indicate that a major proportion of these athletes had warning symptoms of
chest pain, syncope or shortness of breath on exertion. Hypertrophy of the left ventricle may be shown
on the ECG, but diagnosis is confirmed by an echocardiogram. The proven risk factors in this group
include episodes of ventricular tachycardia and a family history of sudden death.
- 46 IOC Sport Medicine Manual 2000
Other non-coronary causes of sudden cardiac death during exercise would include:
mitral valve prolapse
primary cardiomyopathies (congestive)
electrical disorders including Wolff-Parkinson-White syndrome
aortic dissection (especially in Marfan’s syndrome)
blunt cardiac trauma
post-viral myocarditis
A 1980’s tragedy occurred with the death of an international calibre volleyball player who died as a
result of a dissecting aneurysm associated with Marfan’s syndrome. Many basketball and volleyball
teams are now routinely screening their athletes for features of Marfan’s syndrome and having
echocardiograms done to detect evidence of aortic root dilation and dissection. Typical features of
Marfan’s would include:
arachnodactyly and loose jointedness
very tall and thin with excessively long lower segment
deformity of anterior chest wall
high arch palate
scoliosis
ectopia lentis in about 75% of cases
aortic root dilation, aortic regurgitation, and dissecting aneurysm
autosomal dominant inheritance
Noncardiac causes of sudden death in young athletes include arteriovenous cerebral malformations
and a ruptured cerebral (berry) aneurysm.
3 - Organ System Disorders
2. Mitral Valve Prolapse
Case History - Mitral Valve Prolapse
A 38-year-old male marathon runner presented with intermittent central chest pain during his
training. The pain was described as sharp and did not radiate into the left shoulder or into the
neck. There were no associated palpitations or shortness of breath. There was no history of upper
respiratory infection, cough, or indigestion. The pain occurred intermittently over two weeks and
he had no pain at rest. He was a fit, tall, lean endurance runner with a normal blood pressure and
a resting heart rate of 48 b/min. The lung fields were clear and, upon auscultation of the heart, a
click sound was heard at the apex during mid to late systole. There was also a late systolic ejection
murmur. Examination of the musculoskeletal system revealed no evidence of pectus excavatum or
thoracic scoliosis. There were no features to suggest Marfan’s syndrome.
Discussion
Differential diagnoses would include:
a. mitral valve prolapse
b. angina
c. myocardial infarction
d. chest wall pain
e. pleural pain
f. pericarditis
g. reflux esophagitis
Investigation included a chest x-ray which was normal and a resting electrocardiogram followed by
exercise stress test and echocardiogram. The resting electrocardiogram revealed a first degree heart
- 47 IOC Sport Medicine Manual 2000
block with an increased P-R interval and ventricular hypertrophy, features commonly found in
endurance athletes.
Figure 3.2 Two dimensional echocardiogram of normal heart. V = ventricle, A = atrium, R and L = left
and right.
3 - Organ System Disorders
The exercise stress test was normal with no evidence of any S-T segment depression or arrhythmias.
The blood pressure both at rest and during exercise was within normal limits. During exercise the
electrocardiogram showed evidence of ventricular hypertrophy with high T-waves and a high QRS
complex, normal for an endurance athlete. Following the stress test, a two-dimensional echocardiogram
was performed. The findings showed late systolic dipping of the leaflets.
Figure 3.3 Two dimensional echocardiogram of patient with late systolic prolapse of mitral valve. LV
= left ventricle, LA = left atrium.
- 48 IOC Sport Medicine Manual 2000
From these findings, mitral valve prolapse (MVP) was diagnosed. Mitral valve prolapse is a common
condition, usually presenting in a young individual with chest pain associated with anxiety and shortness
of breath. Mitral valve prolapse is seen more frequently in females than in males, being reported in
17% of 20-29-year-old females and 2-4% in all age groups of males. The individual usually presents
with a history of atypical chest pain: often sharp pain unrelated to exercise, unrelieved by nitroglycerine
and continuous for hours. Dyspnea, fatigue, dizziness, palpitations and anxieties are often associated
features. Some athletes are only symptomatic during the high emotion of competition.
The past history of the athlete usually reveals no history of respiratory tract infections or asthma.
There are often thoracoskeletal abnormalities such as pectus excavatum or thoracic scoliosis demanding
the consideration of the diagnosis of Marfan’s syndrome. Occasionally there is a history of transient
ischemic attacks and partial strokes in the older athlete. There may be episodes of unexplained loss of
consciousness with palpitations (arrhythmias).
On physical examination, the athlete is often tall, thin and may have features suggestive of Marfan’s
syndrome. The chest is clear and in many cases the physical examination can be completely normal.
The diagnostic hallmark on auscultation is the mid- or late non-ejection systolic click present with a
late systolic ejection murmur. Prolapse can often be induced with exercise (tachycardia), change of
posture from supine to standing, or the Valsalva manoeuvre.
The typical findings on the echocardiogram are pansystolic hammocking (the bulging back towards
the atrium of both leaflets) or late systolic dipping when one of the leaflets folds back on itself. The
athlete is usually referred to a cardiologist.
As patients with MVP and a regurgitant murmur are at risk of developing endocarditis, prophylactic
antibiotics are required for surgery and dental work. The silent MVP (ie. without the murmur) does
not require antibiotics. Penicillin-V 2 gm orally 30 minutes prior to dental work and 500 mg orally
every six hours for eight doses is recommended.
The long-term prognosis for MVP is generally excellent.
Rarely, a recognized group of complications are associated with MVP. These are:
infective endocarditis (1% of patients with MVP)
progression of mitral insufficiency
rupture of the chordae tendinae
transient ischemic attack and stroke (accounts for 40% of cases of MVP that have resulted in
death)
sudden death - the most common complication; it affects less than 1% of patients with MVP
per year and is the result of a fatal arrhythmia. Patients with MVP and murmurs are the
greatest risk group. Classic angina pectoris occurs in only 8-10% of patients with MVP and
30% experience arrhythmias
- 49 IOC Sport Medicine Manual 2000
3 - Organ System Disorders
Often, the only treatment that is required is to reassure the individual that the symptoms are not an
indication of cardiac dysfunction. Many of the symptoms are felt to be a manifestation of anxiety and
autonomic dysfunction, thus beta-blockers can be used for disabling anxiety and arrhythmias (use
small doses, ie. Propranolol 10 mg three times a day). Beta-blockers are banned drugs, and will also
reduce endurance capacity. Calcium channel blockers are an excellent alternative to avoid reducing
endurance performance.
The marathon runner of this case was reassured that the symptoms were not those of significant
cardiac dysfunction. The athlete was encouraged to continue his exercise program. He was instructed
to take penicillin for any dental or surgical work to avoid the possibility of bacterial endocarditis. He
was advised that if he experienced palpitations or increasing chest pain he could be placed on suitable
medication. The athlete was reviewed and subsequently participated in two marathons without
problems.
3. Hypertension
For an adult, hypertension is usually described as a systolic pressure greater than 140 mmHg and a
diastolic pressure over 90 mmHg. Hypertension is a very common health problem in the older athlete.
It is usually asymptomatic but easily detectable and in most cases readily treatable. Large population
studies indicate that in a Caucasian population, 20% would have blood pressures greater than 160/95
mmHg with 45% having blood pressures greater than 140/90 mmHg. Estimates are that 25% of
hypertensives are adolescents. Higher prevalence rates are seen in the nonwhite population. In sport,
high risk groups are weightlifters and throwers in track and field. It is important that the blood pressure
cuff size is large enough for the patient’s arm since a cuff that is too small may result in a falsely
elevated reading.
Hypertension is classified as essential (primary) hypertension with no definable cause or secondary
hypertension with a specific cause. Secondary hypertension accounts for only 5% of the total
hypertensive population.
The causes of secondary hypertension include coarctation of the aorta, renal disease (parenchymal
and renovascular) and endocrine disease (primary aldosteronism and pheochromocytoma).
Hypertension can also be seen with hypercalcemia and oral contraceptives.
3 - Organ System Disorders
Hypertension may be controlled by non-pharmacological means or, if this does not work, then a
pharmacological regime will be required. Complications of long-term hypertension include myocardial
infarction, congestive cardiac failure, cerebrovascular accident (stroke) and renal failure.
Laboratory investigation for causes of secondary hypertension should include:
i. urinalysis and possible 24 hour urine for catecholamines, metanephrine or vanellyl-mandelic
acid (VMA)
ii.
blood analysis for:
blood urea nitrogen (BUN) – creatinine, Na+, K+, Cl, CO2
calcium
uric acid
fasting blood sugar and two hour post-prandial sugar(check for concomitant diabetes)
fasting cholesterol and triglycerides
iii. chest x-ray
iv.
renal ultrasound with Doppler (in lieu of rapid sequence intravenous pyelogram)
v.
ECG and stress test
Other investigations that could be carried out are dependent on the clinical evaluation and include:
i. for Cushing’s syndrome:
morning plasma cortisol
Plasma ACTH
- 50 IOC Sport Medicine Manual 2000
ii.
24 hour urine free cortisol, urinary 17-OHS
dexamethasone suppression test
if renal ultrasound suggests renal artery stenosis:
captopril renogram
MRI angiography
iii. if primary aldosteronism is suggested by hypokalemia:
plasma aldosterone
plasma renin activity during sodium restriction
abdominal CT scan or MRI
Long-term studies indicate that treatment for hypertension should begin at a sustained diastolic pressure
greater than 90 mmHg on three separate readings. It is interesting that at most 50% of hypertensives
are being treated, and only 25% have their blood pressures under control (ie. less than 140/90).
a. Non-pharmacologic treatment of hypertension
Initial therapy should begin with a non-pharmacologic approach for mild hypertension. This
should include regular dynamic cardiovascular exercise (eg. running, cycling, swimming)
that is done 3-4 times per week at an intensity of 60-80% of maximal heart rate and for a
duration of 20-40 minutes, plus achievement of ideal weight. Isometric static exercise, such
as weightlifting, which result in marked increases in systolic and diastolic pressures, are
contraindicated.
b. Pharmacologic treatment of hypertension
If the hypertension does not respond to non-pharmacologic approaches, then appropriate drug
therapy must be established. An algorithm is portrayed in Figure 3-4. The usual first line of
defence includes diuretics and beta-blockers. For many Olympic athletes, however, these two
choices are not appropriate due to deleterious effects on performance and, in fact, are on the
banned list for doping control. Diuretics may lead to hypokalemia and volume depletion,
both disastrous for an endurance athlete. The beta-blockers can lead to poor performances
because of a suppression of heart rate and cardiac output, impaired carbohydrate metabolism
and chronic fatigue with lethargy. More suitable initial therapy might include the use of the
calcium channel blockers (Nifedipine, Verapamil), the peripheral vasodilator (Prazosin) or
the angiotensin-converting enzyme inhibitors (Captopril or Enalapril).
Evaluation of the hypertensive athlete should include a resting and stress ECG plus monitoring
of blood pressure during the progressive maximal exercise stress tests. These tests should
ensure good hypertensive control during exercise and rule out coronary insufficiency.
Significant elevations in diastolic pressure over 110 mmHg indicates a poor response of the
peripheral vascular system associated with chronic hypertension. Systolic pressures over 220
mmHg during maximal exercise testing should be the criteria for ending the test and also
indicate a need for an increase in the anti-hypertensive drug/pharmacological program.
- 51 IOC Sport Medicine Manual 2000
3 - Organ System Disorders
Weight control, restriction of alcohol to less than 30 gm daily (ie. 0.2 litres of wine, 0.5 litres
of beer or 30 ml of 100-proof whiskey), reduction of sodium to less than 2 gm daily, and
maintainence of dietary potassium (greater than 1000 mEq/day) and calcium (1000 mg/d for
adults less than age 65, 1500 mg/d if 65 and over) have all proven to be successful for the
non-pharmacologic management of hypertension.
Begin or continue lifestyle modifications
Patient not at goal blood pressure (<140/90 mm Hg)
Lower goals for patients with diabetes or renal disease
Uncomplicated Hypertension
Diuretics
Beta blockers
Specific Indications for the
Following Drugs
ACE inhibitors
Angiotensin II
receptor blockers
Alpha blockers
Alpha-beta blockers
Beta blockers
Calcium antagonists
Diuretics
Initial Drug Choices*
Compelling Indications
Insulin-dependent diabetes
mellitus with proteinuria
-ACE inhibitors
Heart Failure
-ACE inhibitors
-Diuretics
Isolated systolic hypertension
(older persons)
-Diuretics preferred
-Long-acting dihydropyridine
calcium antagonists
Myocardical Infarction
-Beta blockers (non-ISA)
-ACE inhibitors(with systolic
dysfunction)
3 - Organ System Disorders
-Start with a low dose of a long-acting once-daily drug and titrate dose
-Low-dose combinations may be appropriate
Patient not at goal blood pressure
No reponse or troublesome
side effects
Inadequate response but
well tolerated
Subsitute another drug from
a different class
Add a second agent from a
different class (diuretic, if
not aldready used)
Patient not at goal blood pressure
Continue adding agents from other classes
Consider referral to a hypertension specialist
* Unless contraindicated
Figure 3.4 Treatment algorithm: Primary Hypertension.
- 52 IOC Sport Medicine Manual 2000
4. Paroxysmal Supraventricular Tachycardia (PSVT)
Case History - Paroxysmal Supraventricular Tachycardia (PSVT)
A 27-year-old male school teacher and competitive triathlete presented with frequent episodes
of palpitation, dizziness and dyspnea over the past six months. He was accompanied by his wife
who describes these brief but very frightening attacks. He reported the associated presence of left
chest pain and no syncope. There was no history of rheumatic fever. There was no family history of
coronary artery disease. The attacks occurred primarily at rest, although he had two brief episodes
of palpitations during a competitive 10 km run, associated with shortness of breath and extreme
fatigue, causing him to stop running. He recalled two similar occurrences at rest three years
previously. He had found that a Valsalva procedure could abort the shorter attacks. Stimulants
such as coffee, tea and coca-cola did not appear to increase the frequency or severity of the attacks.
He had not attempted vagotonic stimulation, such as carotid massage or ocular pressure.
Examination was normal; he was a tall, lean, athletic appearing individual. Specific examination
of the cardio-respiratory system was normal, blood pressure being 120/80 mmHg, heart rate being
48 b/min with a normal sinus rhythm. There was no stigmata of Marfan’s syndrome. The heart
sounds were normal.
Discussion
In the athlete presenting with a suspected tachyarrhythmia, we must include in the differential diagnosis:
a. atrial flutter, atrial fibrillation or atrial premature beats
b. paroxysmal supraventricular tachycardia
c. pre-excitation - the Wolff-Parkinson-White syndrome
d. non-paroxysmal junctional tachycardia
e. ventricular arrhythmias (premature beats, ventricular tachycardia, ventricular fibrillation)
The mechanism responsible for his tachycardia was identified utilizing the ECG. He had an
atrioventricular (AV) nodal re-entrant form of tachycardia (with its microreentry within the AV node).
Atrial activation usually occurs simultaneously with ventricular activation, and hence, no P-waves
were visible. Treadmill stress testing was performed, and was normal. This is often the case since
most episodes of PSVT are not provoked by exercise.
There is a great variability of presentation in individuals with PSVT in regards to the frequency,
severity and duration of attacks. The severity of symptoms relate to the ventricular rate, the duration
of the attack and the presence or absence of organic heart disease. As with this case study, the typical
symptoms include palpitations, dizziness, dyspnea and, occasionally, angina and syncope.
- 53 IOC Sport Medicine Manual 2000
3 - Organ System Disorders
A presumptive diagnosis of paroxysmal supraventricular tachycardia (PSVT) was made and a chest
x-ray and electrocardiogram (ECG) were ordered. The chest x-ray was normal, as was the resting
ECG. At that point, Holter electrocardiogram monitoring for 24 hours was obtained. During a period
of rest an the Holter monitoring, the classic electrocardiographic diagnosis of PSVT was established.
That is:
the tachycardia is paroxysmal in onset and termination
the rhythm is precisely regular and remains so for the duration of the paroxysm
the atrial rate ranges between 120-140 b/min (in our case, the atrial rate was 132)
the ventricular rate equals the atrial rate
the QRS complexes are narrow (less than or equal to 0.10 seconds)
Attacks usually occur at rest and not during exercise. The attacks themselves are usually benign in
terms of cardiovascular damage, but are certainly frightening to the patient.
Sixty to 70% of patients with PSVT have been identified by electrophysiological studies as having a
re-entrance involving the AV node. This re-entrance, or circus movement, describes the situation
where an impulse is continually propagated in a circuit of excitable tissue. The tachyarrhythmia occurs
from the wave front radiating from this circus movement. These circuits have been identified with
abnormal anatomical structures, such as by-pass tracts, or as a result of functional abnormalities of
diseased cardiac tissue and can be either microscopic or macroscopic in size. In 20% of individuals
with PSVT, the etiology is the circus movement involving a concealed Kent bundle. The Kent bundle
is an anomalous pathway which connects the atrium directly with the ventricle and which conducts
only in a retrograde direction. This condition is in contrast to the situation in pre-excitation or the
Wolff-Parkinson-White syndrome (WPW), which also involves a Kent bundle. However, unlike WPW,
in this second most common variant of PSVT, the concealed Kent bundle is undetectable during sinus
rhythm, as it does not conduct an impulse in an antegrade direction. The presence of the concealed
pathway is demonstrated by means of ventricular pacing during electrophysiological studies.
In approximately 50% of the patients with the AV nodal re-entrance variety, organic heart disease has
been identified. Usually, the organic heart disease is of a minor degree. The concealed anomalous
pathways or Kent bundles are congenital abnormalities without demonstrable organic heart disease.
The sinoatrial re-entrant tachycardia variant is often associated with the Sick Sinus syndrome.
3 - Organ System Disorders
Diagnosis of the specific tachycardia is made by electrocardiographic investigation and the diagnosis
also must involve investigation of any underlying heart disease. The investigation will usually involve
24 hour ambulatory monitoring. However, this may or may not be useful because frequently the
arrhythmia is sporadic and may not occur in any given 24 hour period. If electrocardiographic
transmitting systems which allow patients to transmit the arrhythmias over the telephone when they
develop palpitations are available, then these have been found to be very useful. In addition,
electrophysiological studies should be performed, which involve studying the effects of atrial and
ventricular extra stimuli as well as incremental pacing of the atria and ventricles. These studies usually
allow replication of PSVT, and also delineate its mechanism and distinguish between PSVT and
ventricular tachycardia. The electrophysiological investigation can also determine the effectiveness
of specific drugs in the prevention of the arrhythmia induced in the laboratory setting. Treadmill
stress testing is important to rule out organic heart disease. However it is not particularly helpful in
the investigation of individuals with PSVT because, as mentioned, these episodes are not usually
provoked by exercise itself.
The treatment of PSVT has two ultimate goals. First, the conversion of the acute attack, and second,
the prevention of recurrent attacks. The AV nodal re-entrant or AV re-entrant tachycardia can often be
converted by simple vagotonic stimulation which increases refractoriness within the AV node. These
measures include carotid massage, ocular pressure (this can increase the risk of retinal detachment
and is not usually recommended), performing of Valsalva manoeuvre or evoking a diving reflex by
emersion of the face in cold water.
If the PSVT persists, then the next step is pharmacological treatment. Verapamil 5-10 mg is the usual
drug of choice. Prophylactic therapy is usually not necessary, however in individuals with frequent
and disabling attacks, digitalis, beta-blockers or Verapamil may depress conduction. Drug testing
with programmed electrical stimulation, as described above, is now recommended as a means for the
establishment of effective prophylactic therapy and should certainly be carried out in patients who
- 54 IOC Sport Medicine Manual 2000
have serious disabling forms of paroxysmal tachycardia. A danger of continuing to compete with
PSVT is the development of an ischemic coronary event.
Treatment for the patient in this case study consisted of reassurance that he had no organic heart
disease, use of intravenous Verapamil for the prolonged episodes, and vagal stimulation in the form of
carotid massage for brief paroxysms. After 6 months, the episodes have been brief and widely separated,
being easily controlled with vagal stimulation.
C. Hematological System
1. Anemia
Athletes may develop anemia from a number of causes, totally unrelated to sport. The causes may be
categorized into these groups:
inadequate production of red blood cells
increased destruction of red blood cells-hemolytic anemias
blood loss
Inadequate Production of Red Blood Cells
i. Nutritional
The most common dietary deficiencies leading to inadequate production of red blood cells
are iron, vitamin B12 and folic acid. Iron deficiency is the most prevalent problem and is
discussed in Unit 13 - Nutrition.
Folic acid deficiency on a dietary basis is common in the general population. Folic acid is
present in green vegetables (peas and beans), liver, yeast and nuts. Folic acid deficiency can
occur within two months of a folate poor diet. Antibiotics and oral contraceptives decrease
the absorption of folic acid. Nutritional changes usually correct this problem.
Occasionally, an athlete with a totally adequate diet may have nutritional deficiencies resulting
in anemia. A variety of gastrointestinal disorders may cause a malabsorptive syndrome. Gluten
sensitive enteropathy can recognized by increased frequency and volume of stool. Avoidance
of wheat, barley and oats leads to improvement. Also, inflammatory bowel disease and
gastrointestinal surgery can result in nutritional deficiencies in the face of an adequate diet.
ii. Reduced Production in Bone Marrow
Anemia can also be caused by decreased red blood cell production by the bone marrow. This
may occur from a variety of causes:
drug side-effect
malignant cell invasion
renal failure
hypothyroidism
chronic disease-neoplastic, infectious, inflammatory plus liver diseases, congestive heart
failure, diabetes mellitus
- 55 IOC Sport Medicine Manual 2000
3 - Organ System Disorders
Vitamin B12 deficiency is a rare cause of anemia in athletes. Deficiency caused by inadequate
diet will occur only in an athlete with a poor vegetarian diet and would take many years to
develop. A more common B12 deficiency, pernicious anemia, results from a person’s inability
to produce intrinsic factor by the parietal cells of the stomach. Intrinsic factor binds with
nutritional vitamin B12 and facilitates absorption in the small intestine. This disease would be
unlikely in the young athletic population. The use of vitamin B12 injections to improve athletic
performance in individuals who do not have pernicious anemia has no known physiological
basis. Any improvement that occurs must be attributed to the placebo effect.
These would be uncommon factors in elite athletes but should always be considered and
assessed for. Treating the underlying disease plus the use of erythropoietin is helpful in
improving the anemia.
Increased Destruction of Red Blood Cells-Hemolytic Anemias
i. Sickle Cell Disease
Sickle cell disease is an example of a hemolytic disorder associated with a structural defect in
the haemoglobin molecule. A single amino acid substitution produces haemoglobin S. The
abnormal molecule aggregates in states of reduced oxygen tension and produces deformity in
the red blood cell. The usual biconcave disc shaped cell is transformed into a rigid spindle
shaped cell, which causes the cell to obstruct the normal flow of blood through capillaries and
sharp bends in blood vessels.
The defective gene is inherited as an autosomal recessive gene. When both parents have the
sickle cell gene, the child will have sickle cell disease. This is a serious disorder and is likely
to exclude elite athletic performance. Patients with sickle cell disease have a chronic, severe
hemolytic anemia, cardiovascular decompensation and painful organ infarctions.
When only one parent has a sickle cell gene, the offspring has sickle cell trait, that is, less than
50% of the haemoglobin in the red cell is haemoglobin S and there is no anemia. This is a
relatively benign condition and does not shorten life but does create some risks with extreme
exercise or altitude exposure. The defective gene is common in malaria endemic areas such
as Africa, the Mediterranean, India and the Arabian peninsula where it may confer a natural
selection advantage against malaria which is/was endemic. Almost 10% of American blacks
have sickle cell trait. Studies of this population indicated an increased risk for haematuria and
pulmonary embolism. Splenic infarction caused by sickling of red blood cells upon exposure
to altitude appears to be a real, but small, risk.
3 - Organ System Disorders
Exertional rhabdomyolysis with renal failure and death may be a possible risk for the athlete
with sickle cell trait. Current information suggests that sickle cell trait is not a barrier to
outstanding athletic performance, but the athlete should take sensible precautions:
initiate exercise gradually
avoid dehydration and heat exposure
avoid exercise if a viral infection is present
There is the suggestion that sickle cell trait is disadvantageous for endurance events, but may
be of benefit when power is required such as sprints and field events by an unknown
mechanism.
ii. Thalassemia
Thalassemia refers to a heterogenous group of genetic disorders characterized by a decreased
rate of synthesis of one or more of the hemoglobin polypeptide chains. Mediterranean anemia
is the most common type of this heterozygote form in which there is a decreased production
of normal hemoglobin by one of the beta chains, producing an altered shape of the red cells.
The individual with beta thalassemia trait will have a normal red blood cell count but will
have a hypochromic anemia with a hemoglobin at 10-12 g/dl. It can be easily confused with
iron deficiency anemia and would not respond to oral iron therapy.
Blood Loss
An anemia in a young female who is menstruating can be attributed to the blood loss of menses,
although this requires laboratory confirmation. An anemia in a child, a male, or a postmenopausal
female requires investigation to discern the cause.
- 56 IOC Sport Medicine Manual 2000
The most common sites of loss are the gastrointestinal and genitourinary systems. Causes include:
gastrointestinal bleeding
- ulcers (duodenal and gastric)
- gastritis
- diseases of the colon
- hemorrhoids
genitourinary
- haematuria
menstrual losses (menorrhagia)
Use of aspirin and oral anti-inflammatories may cause acute ulceration in the stomach and trigger
occult blood loss. Endurance running can result in an increase in fecal iron excretion. If no cause can
be found for the anemia, then running itself may be the culprit, possibly due to mild ischemic colitis.
A stool test will be positive for occult blood. Blood tests will show a microcytic hypochromic anemia
and iron storage parameters will be reduced. Treatment is directed at the specific causes and may
include increased dietary iron and iron supplementation.
The presence of anemia in an athlete demands proper diagnosis. The differential diagnosis of anemia
focuses on morphological classification (eg. hypochromia and/or microcytosis, etc) or on kinetic
analysis (production defects, increased destruction-hemolysis or blood loss). Laboratory tests such as
stool or occult blood, reticulocyte counts, and serum haptoglobin are used in kinetic analysis.
2. Infectious Mononucleosis
Case History - Infectious Mononucleosis
A 26-year-old male field hockey player returned from a pre-Olympic tournament with fatigue.
Four days before the end of the tournament he had a sore throat and a low-grade fever. At that
time, the diagnosis was a viral upper respiratory infection. He was treated with acetaminophen
and throat lozenges. He had a poor performance in the last two games but still felt only mildly ill.
When he returned home, his sore throat became worse. Fever, chills and skin rash developed,
associated with profound fatigue.
On physical examination, his tonsils were enlarged and covered with an exudate. There was
generalized lymphadenopathy in the cervical, axillary and inguinal areas. A pale red macular
rash was diffusely present, and the spleen edge was felt in the left upper quadrant of the abdomen.
Discussion
The athlete with fever, rash and fatigue could have a wide variety of infectious conditions. Differential
diagnoses would have to include:
a. infectious mononucleosis (IM)
b. streptococcal tonsillitis
c. measles
d. diphtheria
e. acute leukemia
f. cytomegaloviral infections
g. HIV
- 57 IOC Sport Medicine Manual 2000
3 - Organ System Disorders
Cell morphology is essential in establishing the initial differential diagnosis. Chronic blood loss usually
results in iron deficiency and therefore has a low hemoglobin with hypochromic microcytic morphology
and low serum ferritin. Production deficiencies will show a low reticulocyte count and bone marrow
examination usually defines a specific diagnosis. Hemolytic anemias can be determined by morphology,
elevated reticulocyte count and specialized tests like the Coombs’ test.
Laboratory tests showed an increased leukocyte count with many atypical lymphocytes. Throat cultures
for bacteria were negative. A monospot test was positive and a heterophile screening test showed the
presence of IgM antibodies specific to infectious mononucleosis (IM). Thus the diagnosis of infectious
mononucleosis was confirmed.
Infectious mononucleosis is almost always a benign, self-limited disease but can account for
considerable symptomatic illness in athletes. It is commonly known as the “kissing disease” or glandular
fever. The causative organism in IM is the Epstein-Barr virus (EBV). This virus is a member of the
herpes group and is found in all human societies.
Acute infectious Mononucleosis
The course of the disease may begin with an acute phase of 1-2 weeks. Features include high fever,
sore throat, profound malaise and fatigue. Palatine petechiae, nausea or vomiting may indicate a
prolonged period of symptomatic illness. In the acute case, exercise in the early phase may increase
the severity of the infection. Fatalities are rare (less than one death per 3,000 cases) and usually follow
complications such as meningoencephalitis and the Guillain-Barre syndrome. A rash may develop
with the use of Amoxicillin and Ampicillin. More common complications include:
upper airway obstruction
bacterial superinfection
splenic rupture
pneumonia
3 - Organ System Disorders
The monospot test will help distinguish IM from cytomegalovirus (CMV) infections. Treatment usually
includes one week reduced or no sport activity, high fluid intake, and Acetaminophen for fever and
headache. Splenic enlargement should be monitored by physical examination and/or scan. No collision
or contact sport should be allowed until spleen size has returned to normal because of the risk of
splenic rupture. This usually takes 6-12 weeks to occur. Ultrasound assessment is helpful in the
determination of splenic size.
After 3 weeks of limited physical activity, the Olympic field hockey player gradually returned to
training with no residual complaints.
- 58 IOC Sport Medicine Manual 2000
D. Genitourinary System
1. Traumatic Haematuria
Case History - Traumatic Haematuria
A hockey player collided with the boards and fell motionless to the ice. The trainer, who arrived
at the scene first, informed you that the player was checked heavily from behind, knocking his
head into the glass and he suffered a momentary loss of consciousness. The athlete was lying
supine with his eyes open and answering questions appropriately. The initial assessment of vital
signs was normal except that the player could not remember the immediate events that occurred 5
minutes surrounding the collision. After ruling out significant spinal injury, the player was helped
to his feet and escorted to the dressing room. There, the player complained of back pain localized
to the right costovertebral angle. Although he had moderate tenderness to percussion in the right
costovertebral angle, there was no associated bruising, swelling, or abrasion. The player did not
remember being struck in this area. The remainder of the back examination was completely normal
and, in particular, there was no evidence of rib fracture or spinal injury. The diagnosis of Grade 2
concussion was made based on the history and normal neurologic findings.
Discussion
Traumatic haematuria is a common occurrence in collision sports. Although the kidney is well protected
by overlying musculature, ribs, and viscera, blunt trauma can distribute forces sufficient to produce
microscopic and macroscopic tears in the renal parenchyma or collecting systems. The kidney is
somewhat mobile but fixed ligamentous attachments function as anchor points where parenchymal
tears may occur. These injuries are of immediate concern because of their propensity for haemorrhage,
extravasation of urine, renal parenchymal damage and infection. Late sequelae of renal trauma can
include hypertension and renal dysfunction but the vast majority of these injuries heal spontaneously
without sequelae with conservative treatment.
The initial consideration must be to assess the overall clinical status of the athlete to determine the
extent of the haemorrhage. In addition, consideration should be given to other coexisting injuries
which may represent a management priority (see Unit 6 - Trauma). Once these two issues are dealt
with, the physician can focus on determining the location and extent of the renal injury.
Physical examination should assess for the presence of swelling, bruising or abrasions over the
costovertebral angle as these may indicate the extent of the force delivered. In addition, fractured ribs
over the kidney area increase the likelihood of significant trauma. Haematuria can arise from any site
in the genitourinary tract - kidneys, ureters, bladder, urethra - and blood in the urine is a finding that
- 59 IOC Sport Medicine Manual 2000
3 - Organ System Disorders
Plans were made to assist the player in showering and changing and frequent neurologic followup over the next 24 hours was arranged. Thirty minutes later, the athlete noted frank blood in his
urine. He voided once, approximately 400 cc, and reported the urine as bright red with no clots.
He had no previous history of any kidney abnormality. In addition, there was no family history of
renal abnormalities. The athlete had previous dental surgery without any coagulation problems
and had had no upper respiratory or other infections in the preceding month. The athlete was
involved in hockey only and did not participate in endurance running. He stated that he was well
hydrated prior to the game. Additional history obtained from other players indicated that the
patient may have received a blow to the right costovertebral angle area by the knee of an opposing
player. The re-examination revealed nothing new. A second diagnosis of blunt renal trauma was
made and the athlete was advised that this required further investigation.
correlates poorly with the degree of genitourinary injury. Transient small amounts of blood in the
urine probably arise from small vessel disruption in the kidney or bladder wall and no evidence exists
that these minimal injuries have any short- or long-term consequence.
When assessing a patient with post-traumatic haematuria, the intravenous pyelogram (IVP) is used to
demonstrate the bilateral presence of normal kidneys as well as details of renal parenchymal
morphology, contusions or fractures, or extravasation of contrast in the kidney, calyx or ureter. If the
IVP is preceded by cystography to rule out bladder damage, or when significant urethral injury has
been excluded by the performance of urethrography, then few genitourinary tract injuries are missed.
If the IVP demonstrates non-visualization of the kidney or complete renal fracture, then further tests
are required. These further tests could include ultrasonography, renal arteriography, computerized
tomography, MRI, and/or radionuclide scanning. All these investigations are performed to assess if
therapeutic intervention such as drainage or removal of a badly lacerated kidney is indicated.
Nevertheless, there is little data that early operative intervention is more effective that conservative
treatment in preventing longterm renal dysfunction following renal contusions and lacerations. IVPs
should be reserved for injured athletes in which a large amount of frank blood is present in the urine
(defined as at least 4+ on labstick testing) or in those athletes where the risk of renal injury is high
(flank pain or haematoma, low rib fractures). However, microscopic haematuria following trauma is
itself a poor indicator of genitourinary damage and can be followed with serial urinalysis without
obtaining an IVP.
3 - Organ System Disorders
The best criteria for minor injury are a strong history of blunt trauma to the renal area and rapid
resolution of the haematuria. The physician should bear in mind the non-traumatic differential diagnosis
of haematuria which includes:
a. haematologic causes
b. renal (non-glomerular) etiology
c. renal (glomerular) etiology
d. post-renal etiology
e. false haematuria
The following algorithm depicts the investigation for microscopic haematuria (Figure 3.5).
- 60 IOC Sport Medicine Manual 2000
HEMATURIA
Proteinuria (>500 mg/24 h),
Dysmorphic RBCs or RBC casts
+
Pyuria, WBC casts
+
Urine culture
Urine eosinophils
Hemoglobin electrophoresis
Urine cytology
UA of family members
24 h urinary calcium/uric acid
Serolgoic and
hematologic
evaluation: blood
cultures, anti-GBM
antibody, ANCA,
complement levels,
cryoglobulins,
hepatitis B and C
serologies, VDRL,
HIV, ASLO
IVP +/- renal
ultrasound
+
+
Cystoscopy
As indicated:
retrograde
pyelography or
arteriogram, or cyst
aspiration
Renal biopsy
Biopsy and
evaluation
+
Open renal biopsy
Follow periodic
urinalysis
Figure 3.5 Investigation for microscopic haematuria.
If an athlete has a positive urinalysis for blood, then the physician must be assured that the episode of
traumatic haematuria does not represent the unmasking of an underlying renal disease and that the
haematuria has resolved.
Following the renal injury, the urinalysis should be checked daily as long as the hematuria is gross
(4+) and bi-weekly or weekly thereafter. Recommendations regarding return to collision or contact
sports are arbitrary but the current suggestion is to avoid collision sports for one month following
return of the urinalysis results to normal. Follow-up examinations at monthly intervals should include
urinalysis, blood pressure determination, and tests of renal function, such as blood urea nitrogen
(BUN), creatinine, and electrolytes. Use of ultrasound may be helpful.
Consideration should be given to prevention of recurrence of this problem through the use of protective
equipment (eg. padding the flank area) and by advising the athlete to avoid where possible situations
which cause further injury.
- 61 IOC Sport Medicine Manual 2000
3 - Organ System Disorders
Renal CT scan
Since there is no evidence that a single injury produces long term sequelae, the athlete with trauma to
the genitourinary tract in which the IVP is normal can be advised that the injury will resolve completely.
There is some evidence to indicate that repeated trauma may produce scarring in the kidney and the
physician must bear this in mind at the yearly pre-participation physical examination. Kidney function
should be reviewed occasionally.
Our ice hockey player had a normal IVP, and his hemoglobin, haematocrit, blood pressure, BUN and
creatinine, as well as electrolytes, were also normal. After several hours, the patient was allowed to
return home and advised to avoid any exertion until his urinalysis results had returned to normal. He
was monitored at home by relatives and his macroscopic hematuria resolved quickly over the next
three days.
Microscopic hematuria persisted for 10 days. At this point, he was advised to resume his dryland
training and skating but to avoid physical contact for one month. In actual fact, he resumed playing
hockey in two weeks with a specially fitted pad to protect the flank area. At follow-up during the next
six months, his urinalysis, blood pressure, and kidney function were normal. The hockey player switched
to a protective girdle type of padding with an additional flank protection pad.
2. Acute Renal Failure/Myoglobinuria
Case History - Acute Renal Failure/Myoglobinuria
3 - Organ System Disorders
A previously healthy 24-year-old 400 m runner awoke the day of a race feeling unwell after
having been at a party the night before at which he consumed a moderate amount of alcohol. He
did not ingest his normal pre-race diet and fluids and the races were delayed. The ambient
temperature was 29º C and the relative humidity 96%. He eventually ran the 400 m at 14:00 hours
and the 800 m at 17:00 hours. After the 800 m race, he vomited and experienced nausea and thirst,
but despite the intake of fluids his thirst was not satisfied. One hour later he developed restlessness
and low back pain of increasing severity.
The following day the symptoms continued and severe myalgias appeared. He was diagnosed
as having influenza but his symptoms worsened dramatically. Eventually, he was taken to the
emergency room where examination revealed a blood pressure of 170/105 mmHg. Laboratory
examination revealed a high serum potassium (5.5 mmol/I), BUN 28 mmol/1, creatinine 1227umol/
l, creatinine phosphokinase (CPK) 1680umol/I. The urinalysis revealed a specific gravity of 1.010,
the presence of protein (2+) myoglobin.
Discussion
Rhabdomyolysis is a fairly common occurrence even in non-contact sports, as evident by elevated
CPK levels post-participation. However, acute tubular necrosis or renal failure after severe exertion is
very uncommon and may or may not be related to the rhabdomyolysis. Prolonged, strenuous exercise,
particularly in a hot, humid environment produces profound decrements in renal blood flow and urine
production. For this reason, renal failure is most common during the summer months or after extreme
exertion in which fluid replacement prior to and during the competition has been inadequate. In addition,
it occurs more commonly in individuals who are not acclimated to hot environments. Acute renal
failure in these instances results from a combination of profound renal ischemia and nephrotoxicity
from the myoglobin released from the muscle during the heat injury.
The magnitude and duration of dehydration during exercise may convert the normal physiologic
stress of reduced renal blood flow into that of a more significant injury. In the above case, the failure
- 62 IOC Sport Medicine Manual 2000
to increase fluid intake to compensate for the alcohol ingested the night before and the severe
environmental conditions on the day of the race were precipitating factors.
Sustained decreases in renal blood flow perfusion pressure may limit the autoregulatory ability of the
renal artery to maintain flow above a critical threshold, therefore, resulting in a reduced glomerular
filtration rate. Ischemic injury, if sufficient, may result in acute tubular necrosis.
The blood-coloured urine in the above case was not hematuria. The urine dipstick tests the peroxidaselike activity of hemoglobin by catalyzing the oxidation of orthotolidine to a blue colour and myoglobin
may also give a positive result. Myoglobin is a haeme protein like hemoglobin and is present in large
quantities in the skeletal muscle, giving it both its red appearance and functioning to bind oxygen
intracellularly with greater affinity than hemoglobin. Strenuous exercise is often associated with an
increased urinary myoglobin for several reasons. Local muscle hypoxia as a result of strenuous exercise
and the redistribution of blood flow away from substrate depleted muscle may disrupt the sarcolemma
and release myoglobin into the plasma (rhabdomyolysis). Hyperpyrexia from exercise in hot, humid
environments causes further substrate depletion and shunting of blood from the core to the skin for
temperature regulation. If myoglobin is released along with muscle enzymes, it may serve to increase
the hypoxic insult to the renal tubular cells. This is shown in Figure 3.6.
Rhabdomyolysis
Muscle Cell Damage
3 - Organ System Disorders
Increased Blood Flow
to Muscle and Skin
Exercise
Decreased Renal
Blood Flow
Heat,
Humidity
Myoglobinuria
Hyperuricema
Increased
Sweat
Losses
Renal
Ischemia
Decreased
Extracellular
Volume
Acute
Renal
Failure
Increased
Angiotensin,
Catecholamines
Figure 3.6 Possible mechanisms in acute renal failure. (From Goldszer, RC, Siegel, AJ, Renal
Abnormalities During Exercise, Sports Medicine, Ed. Strauss, WB Saunders, Toronto, 1984, P.137).
- 63 IOC Sport Medicine Manual 2000
The major differential diagnosis with red urine, in addition to myoglobinuria, is hematuria as a result
of trauma or as a spontaneous occurrence in an athlete. Microscopic hematuria is defined as greater
than five red blood cells per high power field (rbc/hpf) or greater than 8,000 red blood cells per ml of
urine and macroscopic hematuria as greater than 35 rbc/hpf or greater than one million red blood cells
per ml of urine.
Hematuria has been found in as many as 11% of athletes in a variety of sports, the incidence varying
with the intensity and duration of exercise. Many healthy people have a red cell count as high as 8,000
per ml of urine. Using phase contrast microscopy it is possible, with great accuracy, to separate red
cells which have their origin in the glomerulus versus non-glomerular blood cells.
The erythrocytes from glomeruli are dysmorphic, showing great variation in size, shape and hemoglobin
content whereas red cells from non-glomerular sites such as infection, tumour, stones or trauma are
uniform and non-dysmorphic unless the urine is highly acidic. Alteration in the shape of red cells of a
glomerular origin is caused by osmotic hemolysis and partial phagocytosis by renal tubular epithelium.
In addition to microscopic hematuria, the urine sediment in many athletes contains urinary casts of
red cells, white cells, or epithelium and protein. These findings, together with evidence that increased
post-exercise urinary protein originates from circulating plasma albumin, leads to speculation that
intense physical activity without trauma may be accompanied by abnormalities in urine sediment
without abnormalities in renal function. Another source for red cells in the urine may be bladder
contusions occurring in long distance runners.
3 - Organ System Disorders
There have been no reports to indicate that exercise hematuria may produce cumulative renal damage.
The physician is relatively safe in making this diagnosis provided the history and physical examination
are normal, a definite temporal relationship between the exercise and hematuria exists, the red cells
are dysmorphic by phase contrast microscopy, the patient is young and healthy, and the hematuria
resolves completely in 48-72 hours post-exercise. If these criteria cannot be met or if the hematuria is
recurrent, then additional investigations are indicated.
In addition to myoglobinuria, urinary tract trauma, and true exercise-induced hematuria, the physician
must keep in mind the possibility of underlying disease states uncovered by exercise. True exerciseinduced hematuria is considered a benign entity in the opinion of most investigators.
Shortly after admission to the hospital, our athlete required haemodialysis to treat his renal failure.
The differential diagnosis of acute renal failure was investigated and it was concluded that this athlete
suffered from non-traumatic rhabdomyolysis as a cause of his acute tubular necrosis. In addition to
preventive measures, prompt fluid replacement sufficient to restore urine flow is the specific treatment
for this problem. Intravenous fluids should be used for athletes with dehydration and with a heat
stress syndrome.
- 64 IOC Sport Medicine Manual 2000
3. Proteinuria
Case History - Proteinuria
A 21-year-old female field hockey player underwent a routine pre-participation examination
and 2+ protein was found in the urine. She was asymptomatic and her past history was
unremarkable. She was not menstruating, was not taking medication and had no allergies. Her
family history was negative. Although she has had occasional low back pain and cyclical edema
related to her periods, she had no history of bladder infections and no recent kidney infections.
She had no history of trauma to the genitourinary system.
The physical examination was within normal limits. Laboratory examination revealed a normal
complete blood count (CBC), blood urea nitrogen (BUN) 6 mmol/l, and creatinine 90 umol/l.
Urinalysis of an early morning, mid-stream specimen again showed 2+ protein and microscopic
examination of the urine sediment showed eight white cells per high power field, no red cells,
occasional hyaline casts, and a few course granular casts. Culture and sensitivity showed no
growth.
At the time of the examination, the athlete was participating in a rigorous training program for
field hockey which included running 8 km/day and performing 10 sets of anaerobic sprints, in
addition to her regular skill practices. After three days of complete rest, her urinary findings
reverted to normal only to recur with the resumption of vigorous exercise.
Discussion
A diagnosis of athletic pseudonephritis was made and no further investigations were carried out.
Proteins found in the urine after exercise are of plasma origin. A slight decrease in the reabsorption of
proteins may exist but the major component is albumin from plasma. Renal haemodynamic alterations
associated with exercise are the accepted source of the proteins.
The most commonly observed pattern of renal function with exercise is an acute decrease in renal
blood flow with maintenance of the glomerular filtration rate (GFR) because of autoregulation of
blood flow within the kidney. This results in a net rise in the filtration fraction (filtration fraction =
glomerular filtration rate/renal blood flow). In warm weather with dehydration, there is a sustained
reduction in renal blood flow during prolonged exercise and a maintained glomerular filtration rate.
As a result of this increased filtration fraction, the concentration of plasma proteins is increased along
the glomerular membrane permitting increased passage of proteins into Bowman’s space by diffusion.
- 65 IOC Sport Medicine Manual 2000
3 - Organ System Disorders
Proteinuria, like hematuria, has been shown to occur following many forms of strenuous exercise.
The frequency of exercise proteinuria is greater with strenuous and prolonged exertion. Exertional
proteinuria is usually 2+ to 3+ by dipstick determination and is always transient if due to exercise
alone. A quantitative measurement of protein in the urine over 24 hours would be in the 100-300 mg
range.
Proteinuria
NL
Repeat Urinalysis (24-48 hours)
ABNL
No Further Studies
NL
Upright and Supine Collections
(+) Tubule Protein
Supine (+)
24 Hour Collection: Creatinine,
Protein, Urine Protein
Electrophoresis, Serum Creatinine,
Bun, IVP
Serum Cholesterol,
Albumin, Serology
Glucose
1-2 g/day
Proteinuria
Follow Patient Closely
Evaluation for Tubular
Interstitial Disease
3 - Organ System Disorders
> 3 g / d a y Proteinuria
Consider Kidney Biopsy
Figure 3.7 Evaluation of the patient with proteinuria. NL = Normal, ABNL = Abnormal. (From Acute
Renal Failure, Sports Medicine, Ed. Strauss, WB Saunders, Philadelphia, 1984, p.135).
The usual time course for the duration of exercise proteinuria is similar to that of hematuria and
resolution is expected within 24-48 hours. When the proteinuria is due to exercise alone, it carries a
benign prognosis. The same phenomenon has been observed in children.
Proteinuria detected initially after exertion may be independent of exercise and may be secondary to
underlying renal disease. If the urine of an athlete is not clear within 48 hours, then further investigation
is indicated as suggested in Figure 3.7. A personal family history of renal disease or other signs of
illness such as hypertension, edema or anemia would suggest a further need for testing. If proteinuria
persists in a resting urine specimen, then evaluation begins with an overnight collection or supine and
upright urine samples to exclude benign orthostatic proteinuria. If proteinuria persists while in the
supine position, then serum tests for renal function and a 24 hour urine collection for creatinine and
total protein are obtained.
In difficult cases, urinary protein electrophoresis may be helpful by measuring beta-2 microglobulin,
a protein of low molecular weight that is normally reabsorbed in the renal tubules. Glomerular injury
results in proteinuria with low levels of this protein whereas tubular pathology may produce elevations
of beta-2 microglobulin. Assessment of renal size and number is important and may be accomplished
by ultrasound or intravenous pyelography if renal function is normal. Patients showing greater than
one gram of albumin in a 24 hour collection may require referral to a nephrologist.
- 66 IOC Sport Medicine Manual 2000
There is no risk for increased renal disease with exercise-induced proteinuria and no reason to limit
physical activity. These individuals should have a medical check-up and urinalysis on a yearly basis.
In the above case, the field hockey player continued active participation and follow-up urine checks
showed no change in the pattern of proteinuria.
4. Testicular Trauma
Case History - Testicular Trauma
A 23-year-old soccer player was accidentally kicked by an opponent in the groin. He immediately
experienced severe testicular pain and was unable to continue play.
Physical examination shortly after the injury showed an extremely tender right testicle with
minimal swelling and the player was advised to rest while cold packs were applied He was reexamined an hour later and the right testicle was found to be swollen, tense, and very tender to
palpation. The scrotum did not trans-illuminate.
The soccer player was referred to a urologist for consideration of the drainage of an haematocele.
Discussion
Of greater concern is a more significant injury in which the testicle may undergo complete rupture
with bleeding into the tunica vaginalis. This injury, a haematocele, is associated with marked swelling
and a risk of compromising the blood supply to the testis which would result in atrophy and sterility
of that testis. The most important physical finding of rupture into the tunica vaginalis is the inability
to trans-illuminate the scrotum. If testicular swelling and injury are minimal, a tense hematocele may
be treated with bed rest, scrotal elevation and an ice pack. However, if the testicle itself is grossly
swollen or tender and a rupture is suspected, then surgical intervention should be considered. Scrotal
ultrasound can be useful in making the diagnosis and planning treatment. If surgery is required, the
tunica vaginalis would be opened, the haematoma drained and the tunica repaired.
Lacerations and avulsion of the scrotal skin are quite uncommon. Scrotal skin should not be debrided
since it usually regenerates quite rapidly. However, the testicle needs to be protected during this period
and consultation with a surgeon should be advised. A rupture of the tunica albuginea requires the
testis be trapped against either the symphysis pubis or the thigh. Rupture of the tunica albuginea is a
more serious injury and requires prompt surgical treatment to ensure viability of the testis. However
the diagnosis can be difficult.
A severe blow to the scrotum can result in testicular dislocation and often this can be dealt with
through closed reduction. Perineal trauma may cause a forceful cremasteric contraction, drawing the
testes into the inguinal canal.
- 67 IOC Sport Medicine Manual 2000
3 - Organ System Disorders
Trauma to the testicle is relatively common but, fortunately, usually minor. The testes are anatomically
unprotected from an anterior or oblique blow, making them subject to injury. However, their mobility,
location between the thighs, and the instinctive protective recoil in most athletes, together with the
use of an athletic supporter, minimizes the frequency and severity of these injuries. Testicular contusion
itself is relatively common but generally results in no sequelae. There may be a minimal amount of
swelling and tenderness of the testicle with minimal scrotal bruising. The immediate pain may be
excruciating and disabling but usually resolves over several days. With more extensive bruising or
swelling, ice packs should be applied for up to 24 hours.
Trauma may result in testicular torsion. One should not be lulled into a false sense of security with the
athlete who presents with a history of testicular trauma if there are other historical factors or findings
that raise the suspicion of testicular torsion. Urgent referral to a urologist is essential, otherwise necrosis
of the testis may result.
With contusion or hematocele of the testis, one should wait for complete resolution of symptoms and
physical findings before advising full return to physical activity. The absence of one testicle may be
considered a contraindication to involvement in collision sports. Protective equipment is mandatory
in those individuals who are returning to activity following a testicular injury.
3 - Organ System Disorders
In the above case, a hematocele was diagnosed and the soccer player was treated with bed rest, elevation
of the scrotum and ice packs. He made a gradual recovery over the next 3- 4 days with no long-term
sequelae.
- 68 IOC Sport Medicine Manual 2000
E. Gastrointestinal System
1. Diarrhea and Exercise
Case History - Diarrhea and Exercise
A 23-year-old long distance runner training for a competition had recently increased his weekly
mileage from 40 to 80 km. In the past two weeks, he had experienced diarrhea with loose bowel
movements following his daily run or after approximately one hour of hard, fast running. He had
several bouts of explosive diarrhea. In the last week, he developed peri-umbilical abdominal
cramping, bloating and frequent watery stools. On one occasion he noticed melena.
This athlete was previously healthy and had no other medical problems. There was no family
history of bowel disease and he had never had a bowel problem like this. There was no recent
travel. The physical examination was within normal limits.
Discussion
Diarrhea and abdominal cramps are very common symptoms in athletes. Differential diagnoses include:
a. infectious gastroenteritis
b. irritable colon syndrome
c. gluten sensitivity and primary lactase deficiency
d. emotional stress
e. ischemic colitis
f. “runner’s trots”
Infectious gastroenteritis is also common, particularly in the athlete who travels.
Symptoms can include nausea, vomiting, diarrhea and systemic symptoms of fever,
malaise, weakness and anorexia.
Viral gastroenteritis usually has an acute onset. The cornerstone of treatment in this condition is clear
liquids which contain a small amount of carbohydrate and electrolyte fluid since hydration is the
single most important treatment. The state of hydration can be assessed by body weight, urine output
or skin turgor. It is advisable to have the athlete within 2% of his previous normal weight before
practice or competition can be resumed. Fluids should be encouraged and ingested in small amounts
but caffeine containing fluids, alcohol and Acetylsalicylic Acid should be avoided. As the illness
subsides, more complex carbohydrates, proteins and fats are added to the diet. High fibre foods are
not added until complete resolution and milk products are withheld for 7-10 days.
Bacterial gastroenteritis may also have an acute onset but its diagnosis is confirmed by stool cultures.
If an outbreak of bacterial gastroenteritis occurs in more than one athlete, then food and/or water are
frequently the source. Athletes in close contact with each other should be reminded to follow good
hygiene to prevent spread of this disease. Antibiotics are indicated in certain types of bacterial
gastroenteritis with Ciprofloxacin or Norfloxacin being the drug of choice for shigella, cholera and
travellers’s diarrhea. The use of these antibiotics in salmonella enteritis may prolong the carrier state
- 69 IOC Sport Medicine Manual 2000
3 - Organ System Disorders
Because of his persistent symptoms, it was decided to investigate his complaints.
Complete blood count (CBC) and urinalysis were normal. Electrolytes and liver
and kidney function tests were also normal. Three stool specimens for culture and
sensitivity and parasites were negative. An upper gastrointestinal series and barium
enema were also within normal limits, as was sigmoidoscopy.
and thus this practice is resisted unless the patient is febrile, acutely unwell, or immunocompromised.
Anti-motility agents such as Loperamide can provide some relief in cramping and in the severity of
diarrhea, but they may also prolong the bacterial carrier state. Therefore, they should be used sparingly,
if at all, in any illness which is self-limited and controlled by diet. At times, frequent diarrhea
necessitates their use.
Giardia lamblia is an occasional cause of intestinal disease for those athletes who are exposed to
contaminated water supplies. This is caused by a protozoan parasite and the diagnosis can be made by
examination of stool. Treatment is with Tinidazole or Metronidazole.
The irritable colon syndrome includes symptoms of lower abdominal pain, constipation alternating
with diarrhea and the passage of small-calibre stools during the symptomatic period. This is also
termed spastic colitis. Although the cause of this condition is not well known, there appears to be a
strong association between this condition and an exaggerated intestinal response to psychological
stress. Since athletic competitions are stressful, these events may evoke the symptoms in an individual
who has had previous episodes of this problem.
3 - Organ System Disorders
Primary lactase deficiency is a deficiency of the enzyme lactase, essential for the hydrolysis of lactate.
This problem leads to abdominal cramps, bloating, distension and diarrhea after the ingestion of even
small quantities of milk or milk products. These symptoms occur because lactose, when not hydrolyzed
to glucose and galactose, cannot be absorbed by the intestinal mucosa. Osmotic fluid shifts into the
lumen of the intestine cause osmotic diarrhea. The condition is hereditary and occurs much more
frequently in blacks and Orientals than in whites. The symptoms may not be manifest until the infected
individual is in the adolescent years. Chronic abdominal complaints should always suggest lactase
deficiency which can be confirmed by a trial of a milk-free diet.
Emotional stress may also be a cause of diarrhea. Emotions can cause hyperfunction (spasm or hyperperistalsis), hypofunction (stasis), hypomotility and combinations of each of these manifestations of
impaired function. It has been estimated that 60-70% of gastrointestinal complaints are ultimately
found to arise from psychological factors.
Ischemic colitis is considered in the presence of crampy abdomenal pain and bloody diarrhea. Due to
the high sympathetic tone of exercise, the mesenteric blood flow can decrease by 80% at peak exercise.
Although this entity usually resolves with supportive measures, some athletes have required a subtotal
colectomy.
“Runner’s trots” are most likely to occur after an episode of unusually severe exertion, during a
period of rapidly increased distance running or training, or after running sessions of greater than one
hour. The mechanism is not well understood and melena may occur and necessitate further
investigations. Postulated mechanisms include increased parasympathetic tone, but relative intestinal
ischemia is also a possibility. Runner’s trots can be as exasperating to the clinician as it is to the
athlete. Most cases will subside with rest. The prevention of recurrence is best managed by a gradual
increase in intensity and duration of running sessions.
In the above case, a diagnosis of “runner’s trots” was made. After a one week period without running,
the athlete was advised to return to running to a maximum duration of 30 minutes on alternate days,
three days per week. He experienced some diarrhea episodically but gradually improved. The runner
slowly increased the duration of his run by 10% per week, initially at a slow pace. This, together with
adequate hydration, was successful in restoring his gastrointestinal function to normal.
- 70 IOC Sport Medicine Manual 2000
2. Runner’s Stitch
Case History - Runner’s Stitch
A 44-year-old distance runner restarted running one year after fracturing his left tibia in a
motor vehicle accident. During his initial low mileage training, he experienced no difficulties.
However, as his pace picked up, he began to notice a sharp pain in the right upper quadrant at
about the 3 km mark. This progressively worsened over the next km and he had to stop running.
The pain was localized to the right upper quadrant and was sharp and severe. Although the pain
lessened considerably with walking, it did not completely abate until approximately 20 min after
his run. He had been experiencing this problem for two weeks without resolution.
He was healthy with no gastrointestinal symptoms or any history of gastrointestinal problems.
He made a point of being well hydrated. The physical examination was within normal limits. The
resting electrocardiogram, complete blood count, chest x-ray and urinalysis were normal.
Discussion
Many athletes complain of sharp, colicky pain during exercise, most commonly in the right upper
quadrant. Differential diagnoses include:
a. abdominal stitch
b. ischemic heart disease
c. gastrointestinal reflux
d. gall bladder disease (cholecystitis)
If the physician has assured himself that ischemic heart disease has been ruled out, the treatment of
abdominal stitch is symptomatic. The symptoms of sharp or crampy abdominal pain often disappear
spontaneously with a modification in the training schedule to lessen the pace.
A runner may be able to “run through” the pain by exhaling through pursed lips, breathing deeply or
manually massaging the area of pain.
If the pain persists, then the runner can usually obtain relief by stretching the torso or flexing the chest
to the knees. As fitness improves, the frequency and severity of the stitch declines. If the pain still
persists, then a period off from exercise may be indicated. Adequate hydration and the avoidance of
food prior to participation are important reminders. Persistent pain at rest requires further medical
evaluation.
In this case, a tentative diagnosis of abdominal stitch was made and the runner was advised to alter his
training schedule so that his pace was reduced. Gradually, over the next six weeks, his complaints
resolved. Thereafter he was able to increase the volume and intensity of his running.
- 71 IOC Sport Medicine Manual 2000
3 - Organ System Disorders
The cause of an abdominal stitch is not well understood and one explanation suggests the possibility
of trapped intestinal gas at the hepatic or splenic flexure of the colon. Since physical activity has been
shown to increase propulsive movements in the colon, if intestinal gas moves to the hepatic or splenic
flexure and is trapped, then the increase in intraluminal pressure could produce pain. Another theory
for the onset of an abdominal stitch is related to intestinal ischemia brought on by a shift of blood
from the abdominal cavity to the large muscles during strenuous activity. This is particularly common
in athletes who have ingested food or water prior to participating in exercise. A third possibility is
local muscle ischemia in the diaphragm or intercostal muscles which may occur at the high rates of
pulmonary ventilation required for strenuous exercise.
3. Reflux Esophagitis
Case History - Reflux Esophagitis
A 42-year-old previous long distance runner restarted an exercise program which included
running after a period of inactivity of approximately 12 years. Her health had been good. She
began jogging 3 km, 3 times a week, at approximately a 7 min/km pace. During the second week of
her program, she began to experience a burning pain in the lower sternal region of her chest. This
usually occurred towards the end of her run and she usually ran in the evening after her meal. The
pain was unaccompanied by shortness of breath, diaphoresis, palpitations, syncope, or nausea.
Her family history was negative for coronary heart disease or gastrointestinal disease. Physical
examination was normal.
Discussion
The major differential diagnoses are:
a. gastroesophageal reflux
b. coronary artery disease
c. peptic ulcer
Because of her symptoms, she received a resting electrocardiogram, a stress
electrocardiogram, and a nuclear cardiac scan (MIBI). These were normal.
A series of upper gastrointestinal x-rays following barium swallow revealed
gastroesophageal reflux.
3 - Organ System Disorders
Gastroesophageal reflux is a relatively common occurrence at all ages.
The symptomatology can include a burning epigastric or retrosternal pain
which may radiate toward the neck or the back. It may also produce pain
which radiates to the arms or neck.
The age of this runner could suggest the possibility of underlying ischemic heart disease since this
should be considered in any participant over 30 years. If the initial cardiac tests had been abnormal,
then the individual would have required further evaluation with stress echocardiogram and/or coronary
angiography.
Gastroesophageal reflux can generally be managed effectively by recommending exercise on an empty
stomach and by drinking a small amount of water or liquid antacid which serves to dilute and neutralize
the hydrochloric stomach acid. In this instance, the individual was running shortly after a meal when
the stomach was full.
If symptoms are persistent, then esophagoscopy or endoscopy can document the extent of the reflux
esophagitis. A H2-receptor antagonist, a prokinetic agent (eg. Cisapride) or a protein pump inhibitor
is required if erosions have occurred.
In the above case, the runner was advised to avoid the intake of food at least four hours prior to
exercise and to treat her symptoms with frequent ingestions of small amounts of water and liquid
antacid. Using this regimen, her symptoms resolved and she was able to increase her mileage and
pace.
- 72 IOC Sport Medicine Manual 2000
F. Metabolic and Endocrine System
1. Overtraining
Case History - Overtraining
A 26-year-old marathon runner complained of a four week history of progressive fatigue and
poor performance during workouts. He had been previously healthy with no recent illnesses. His
subjective complaints included fatigue, insomnia, mood changes, irritability, loss of motivation,
lack of a desire to train and compete, gastrointestinal upset, weight loss and poor performances
during training runs. He was training upwards of 175 km per week; only six weeks ago his coach
increased his training intensity as well as mileage. During this period, he raced twice, once at 20
km and another at 32 km. In both, his performance did not reflect the increased training that he
had been doing and he was discouraged. On physical examination, his resting heart rate was 42 b/
min, which was similar to his normal early morning heart rate. Blood pressure was normal. There
were one or two cervical nodes on palpation of the neck but these were not tender.
The remainder of the examination was completely normal. The laboratory investigations of
complete blood counts, liver function tests, ferritin, urinalysis and electrocardiographic evaluation,
all returned normal values. In particular, there was no sign of anemia or low iron stores, nor were
there any changes in the white cell count or differential that would indicate a chronic infection.
Discussion
The initial evaluation should include a complete history as well as physical examination. Blood and
urine tests for organic causes to explain the symptoms should be done. This would include a complete
blood count, including hemoglobin, white count, differential, ESR, Monospot, HIV serology, PPD for
tuberculosis, serum ferritin, electrolytes, glucose, AST, ALT, BUN, Cr, T4, TSH, and urinalysis. Once
you are more comfortable that the athlete does not suffer from a specific organic disease identifiable
on laboratory testing, the diagnostic possibilities are more limited.
The diagnosis of chronic fatigue syndrome requires meeting specific criteria including unexplained
persistent or relapsing fatigue that is not relieved by rest and reduces daily activity by at least 50%
plus eight or more minor symptoms and signs. There is no clear diagnostic test(s), etiology or definitive
therapy. Treatment approaches have been devised with variable success.
Depression is a very common reason for fatigue accounting for over 15% of the cases in some studies.
The presence of sleep disorder, poor appetite, decreased concentration, sadness, irritability, being
teary, labile mood, general apathy, feelings of guilt or worthlessness, suicidal ideation, and flat affect
form the diagnostic criteria.
- 73 IOC Sport Medicine Manual 2000
3 - Organ System Disorders
Fatigue in an athlete is a particularly difficult medical problem to deal with as it encompasses not only
the medical field but also the physiological and psychological aspects of elite performance. As a
physician, your primary responsibility is to ensure that the symptoms are not a result of organic
disease. A partial differential diagnosis would include:
a. chronic infection
b. connective tissue disorders
c. anemia (see section C of this unit)
d. endocrinological cause-hypothyroidism, diabetes mellitus, adrenal insufficiency
e. chronic fatigue syndrome
f. depression
g. overtraining/overstress syndrome (OTOSS)
Overtraining/overstress syndrome (OTOSS) (also called underperformance), which is the diagnosis
of our marathoner, is a vague term that is not well understood in the medical or sport science literature.
Recent research would suggest that there is a central OTOS phenomenon; that is, OTOSS may reflect
the suppression of the hypothalamic-pituitary axis. Studies have investigated this possibility by creating
an insulin-induced hypoglycemic challenge and measuring the response to this and the level of change
in some of the stress hormones. Individuals that have the classical symptoms and signs of OTOSS
have a blunted response to such a hypoglycemic stress. Other studies have indicated that there is a
decrease in the free testosterone/cortisol ratio in athletes that are undergoing OTOS phenomena.
The complaints of lethargy, fatigue, irritability, anorexia, marked bradycardia, and weight gain may
indicate hypothyroidism secondary to hypothalamic dysfunction. These symptoms are likely to be
experienced in an athlete recently undertaking very large training loads. Thyroid tests reveal depressed
levels of thyroxin (T4) and thyroid stimulating hormone (TSH).
Thyroid regulating hormone (TRH) produced in the hypothalamus and transported to the pituitary
regulates the production of TSH. OTOSS can produce this reduced hypothalamic function. Treatment
is aimed at the OTOSS and therefore involves marked reduction in training - both in volume and
intensity. Thyroid supplements should not be prescribed as this will result in further reduction of the
level of endogenous thyroxine by suppression of TSH production.
Regretfully, there is no simple urine or blood test to determine OTOSS and the tests that have just
been mentioned are difficult and expensive to do. In addition, the blood often takes several days to be
analysed and thus these results lose their applicability to the athlete who is concerned about imminent
competitions.
3 - Organ System Disorders
A more practical approach would be to look at this in a preventive manner. All the stresses that prey
upon the elite athlete should be identified. These could include psychological stressors such as financial
status, interaction with school or work, social/personal relationships, medical stressors such as the
presence or absence of disease, systemic infections, injuries, etc, as well as physiological stress such
as the volume, intensity and duration of the training schedule. Other stressors such as the environment,
travel, and diet should also be evaluated. It is possible to put these stresses into a simple one or two
page questionnaire that the athlete could fill out on a regular basis to allow the coach and sports
science team some regular, easy access measurement of the stressors involved with these particular
individuals.
The morning heart rate has been used to diagnose OTOSS. If the resting morning heart rate is increased
more than 5 b/min above the usual morning heart rate, then it should alert the coach and the physician
that the athlete may have OTOSS.
No blood measure currently done on a routine basis in a laboratory can be used as a reliable indicator
of OTOSS; that is, hemoglobin, white cell count or ferritin levels simply are not reliable indicators.
Once OTOSS occurs, it is not a simple matter of resting the athlete for one or two days and then
returning the athlete to the previous program. OTOSS may reflect hypothalamic-pituitary suppression.
Clinical practise and research suggest that the recovery from this state may take one, or perhaps even
several months. There is no effective treatment for OTOSS except rest, which should place the emphasis
on prevention. Other interventions include optimal hydration, diet, general recovery and addressing
the stressors as best as possible.
- 74 IOC Sport Medicine Manual 2000
Our marathon runner required a one month period of very light aerobic activity before the symptoms
of OTOSS resolved. Upon resumption of training, he closely monitored his morning heart rate and
other indices of OTOSS in his daily log book. His performances in workouts improved dramatically
and after only three weeks of moderately stressful training, he recorded a personal best in a 20 km
road race.
2. Unexplained Underperformance
Case History - Unexplained Underperformance
Two members of a national endurance running squad presented complaining of
underperformance. One (A) had suffered from 3 upper respiratory tract infections in the last 6
weeks, the other (B) an unexpected sense of effort and heavy muscles for the last 4 weeks. Both
complained of fatigue headache and poor sleep. Both had also attended a hard and intensive 4
weeks training programme 1 month before with the rest of the international squad whose
performance had improved, unlike that of athletes A and B. Resting pulse rates had been raised 4
weeks before at the end of the training camp, but on presentation were normal.
Athlete A also described intermittent sore throat, swollen tender cervical glands (lymph nodes),
a dry irritant cough and coryza. Athlete B had a depressed mood, irritability, loss of motivation,
appetite and weight loss. Both were desperately trying to get back into contention for a national
squad place.
Discussion
This is a difficult problem to deal with. Coaches and athletes are often frustrated and angry. The
doctor’s first duty is to exclude organic disease such as true anaemia, thyroid disease, glycogen depletion
(often in the form of an eating disorder), or even atopy and asthma. Thus evaluation includes a careful
history and examination and special tests as indicated by these. A reasonable screen is a full blood
count and differential, ESR, a biochemistry profile, TSH and CK. The diagnosis of unexplained
underperformance syndrome (UPS) is by exclusion. Labelling the problem as overtraining syndrome
may blame and so alienate the coach. If training is felt to be the main cause, then “under-recovery
syndrome” is a better description.
Unexplained underperformance syndrome (previously called overtraining syndrome) maybe arbitrarily
divided into 3 main presentations:
1. mood disturbance (depression, irritability, anxiety), poor sleep and loss of motivation
2. fatigue, heavy muscles, unexpected sense of effort
3. frequent minor infections
Some athletes may suffer from a combination of symptoms from all 3 groups.
In these cases, athlete A’s symptoms were primarily of apparent immunosuppression, athlete B’s a
mixture of mood changes and physiological fatigue.
- 75 IOC Sport Medicine Manual 2000
3 - Organ System Disorders
On examination, both athletes looked well. Athlete A had a few tender cervical lymph nodes
but nothing else to find, a clear chest and normal lung function. Laboratory tests in athlete A
showed an apparent anaemia and neutropenia. Tests on athlete B were normal except for a raised
creatine kinase (CK). Ferritin levels were normal in both. Their coach, attending with the 2 athletes
felt that they could not be overtrained as the rest of the squad had improved on the same programme.
The underlying pathophysiology of UPS is complex and varied. Current research suggests a number
of factors such as low glutamine levels, low immunoglobulin A in saliva, a drop in T helper/suppressor
cell ratio and loss of NK cell activity all contribute to immunosuppression. There are probably many
other unknown factors. A change in 5HT (Seretonin) receptor sensitivity may cause central fatigue,
and neuroendocrine factors (noradrenaline, adrenaline, hypothalamic pituitary axis changes) may cause
fatigue and under-recovery. One consequence of hypothalamic pituitary axis dysfunction may be
apparent hypothyroidism, so thyroid function must be checked after recovery before committing to
treatment. Tests based on the above pathophysiology are not diagnostic and are expensive. However,
in the future, a battery of tests, psychological/stress and physiological data analysed on a frequent and
individualised basis (eg. with every taper) may form the best method of intervention and optimisation
of training and recovery for each athlete, leading to their best possible health and performance.
Assessment should be multi-disciplinary if at all possible with consideration of physiological,
nutritional, psychological and medical factors together.
In the case of athlete B, the neutropenia was of ethnic origin and the low haemoglobin (12.5 G/dl) due
to physiological dilution as seen normally in endurance athletes, accompanied by a low haematocrit
(37%) and high MCV (98) and normal ferritin (iron stores). Serum glutamine levels were measured in
the whole squad and the 2 athletes were in the lower end of this group.
There was concern that athlete B might be suffering from an undiagnosed eating disorder, but upon
questionning, this proved negative. Evaluation by a clinical psychologist provided further reassurance.
3 - Organ System Disorders
The management of both underperforming athletes was similar with expectancy of recovery. Both
were counselled on the importance of regeneration strategies including careful attention to diet and
fluids, time for relaxation with the help of a psychologist and masseur, and normalisation of sleep.
Supplements were not prescribed in these cases and are not normally needed, but consideration can be
given to a carbohydrate supplement, mulivitamin and glutamine supplements under the guidance of a
sports nutritionist or sports medicine doctor.
Both athletes were told they could not recover from or benefit from training but could use very gentle
exercise to speed their recovery. They were given a 6 week recovery programme starting with 10
minutes of light exercise not involving running (mostly cycling and swimming) building up to 1 hour
over the next 5 weeks. They also included 2 short sprint sessions with 10 seconds of maximal activity
with at least 3 minutes of rest in between each sprint. They used a visual analogue scale (1 to 10) to
monitor their symptoms. In athlete A, these scales were used for glands, sore throat and fatigue. In
athlete B, 5 scales were used for heavy muscles, fatigue, sleep, motivation and appetite.
Both built up their exercise successfully over 6 weeks and returned to full training with 1 rest day a
week and alternate light and heavy days of training after 6 weeks. Athlete A suffered no further
respiratory infections and the symptoms score (on the visual analogue scale) reduced to zero.
Both athletes and coach realised the importance of recovery and regeneration in order to give the
coach’s training programme a chance to work. They were selected for the national squad and competed
successfully through the summer season.
- 76 IOC Sport Medicine Manual 2000
G. Nervous System
1. Headache in Athletes
Case History - Headache
A 19-year-old male gymnast had a three month history of headaches brought on by exertion.
These headaches would commence during and persist up to 12 hours to resolve after training. The
pain was described as severe, throbbing and located bilaterally in the temporal regions. The
headache was accompanied by nausea, vomiting, and photophobia. The athlete had no history of
previous head injury and no history of headaches. Physical examination was completely normal.
Cervical spine x-rays, skull x-rays, and computerized tomography (CT) scan of the brain were
normal.
Discussion
Differential diagnoses would include:
a. benign exertional headache
b. space-occupying lesions
c. effort migraine
d. post-concussional headache
e. pheochromocytoma
The sports physician must be aware that headaches associated with exertion may occasionally be a
sign of underlying organic disease. In a study by Rooke, of 103 cases of exertional headaches, only 10
individuals had an underlying identifiable lesion. Looking at this problem from the opposite standpoint,
that being the relationship of headaches to known organic disease within the brain, Rooke documented
the infrequency of exertional headaches in 221 patients with known brain tumours and in 22 cases of
subdural haematoma, reporting that only five experienced exertional headaches in the tumour group
and only two in the latter. (Rooke, ED, Benign Exertional Headaches, Med. Clin. of Nor. Amer, 52,
1968, p. 801-808.)
Headaches associated with brain tumours in Rooke’s study have no particular distinguishing features
other than the onset is usually abrupt with intense unilateral or bilateral pain. Vascular malformations
may also present with exertional headaches and make differentiation from benign exertional headaches
difficult. A typical unilateral headache without features of a migraine may suggest this diagnosis.
Effort migraine can occur with any type of all-out muscular effort. This syndrome is characterized by
the sudden onset of a scintillating scotoma followed by nausea and a unilateral throbbing headache
which is often retro-orbital, usually lasting 15-60 minutes. The symptoms closely resemble those of
- 77 IOC Sport Medicine Manual 2000
3 - Organ System Disorders
Headaches are relatively common in a variety of
sporting activities and are usually benign,
collectively being referred to as benign exertional
headaches. The benign exertional headache described
by Rooke occurs not only with sporting activity but
also with coughing, sneezing, bending and straining. It also occurs with running and heavy lifting. No
clear-cut clinical pattern of pain has emerged from studies of patients with this problem and the pain
can occur in almost any part of the head and extend or radiate in any direction. The lack of specific
features of these headaches makes them difficult to understand pathophysiologically and difficult to
characterize clinically.
classical migraine and the etiology has been postulated to be similar. It is thought that the initial
vasoconstriction is probably related to hyperventilation and a reduction of carbon dioxide tension in
the blood.
Another type of vascular headache encountered in athletes is far less dramatic in onset and more of a
generalized throbbing bitemporal headache. There is no scotoma, nausea is less intense, and it is not
unusual for the headache to begin after the activity is over. This is particularly common in humid
conditions and in untrained athletes.
In certain individuals, a minor head injury associated with collision sport may be followed by a severe
headache. Initial contact is usually around the head or face but typically not severe enough to produce
loss of consciousness. This is followed by a symptom free period of several minutes and then an aura
and finally blurred vision, visual field defects, paresthesia of the arm and face and nausea and vomiting.
The headache that follows is usually bilateral and throbbing and recovery may not take place for 24
hours. Headaches of this type often occur in the individual exposed to similar precipitating
circumstances.
One of the most important underlying causes to recognize in association with exertional headaches is
pheochromocytoma. The characteristic headache is rapid in onset and usually throbbing, occurring
bilaterally without a consistent location. It is often associated with nausea and vomiting and is usually
of short duration (minutes to an hour).
3 - Organ System Disorders
The other symptoms which are classic with this syndrome may be obscured by physical activity
including palpitations, sweating, tremor, pallor, flushing and anxiety. Hypertension, particularly in a
well-trained athlete in whom blood pressure is often below normal, should alert one to the possibility
of this syndrome.
The decision as to how far to pursue with investigations in an attempt to differentiate a benign exertional
headache from one with an underlying organic lesion is case dependent. If there is an abnormal
neurological examination or persistent symptoms, it is appropriate that skull films and a computerized
tomography/MRI scan is performed. The skull film is valuable in cases of pituitary adenoma, platybasia,
and basilar impression. To document pheochromocytoma, blood pressure, as well as a 24 hour urine
collection for catecholamines is indicated. Exertional headaches are well-described in a variety of
sporting activities and although organic causes are rarely identified, repeated episodes require evaluation
and further investigation.
The treatment of any headaches associated with effort may be difficult. In the highly competitive
athlete, medication may interfere with performance. Certain medications, such as Ergotamine, may
be used but the risk/benefit ratio requires careful consideration. Newer medications such as Naratriptan,
Sumatriptan, Fluarizine, and Zolmitriptan can also be useful. After ruling out underlying disease,
initial treatment attempts should be focused at preventing precipitating events and controlling pain
with simple analgesics.
A diagnosis of benign exertional headache was made but attempts to treat the condition with
Acetylsalicylic Acid and codeine were ineffective. Ergotamine Tartrate was prescribed prior to running
and was successful in preventing the headaches from occurring. After several months, this patient was
able to taper the dose of Ergotamine Tartrate and eventually to discontinue it due to resolution of the
headaches.
- 78 IOC Sport Medicine Manual 2000
2. Epilepsy
Case History - Epilepsy
A 16-year-old competitive diver came to your office for advice following a suggestion by his
family doctor that he discontinue diving because of his epilepsy. He was an otherwise healthy
male who had a diagnosis of grand mal epilepsy since a febrile convulsion at the age of four. His
brain scan was normal but his electroencephalogram had consistently shown a Type I abnormality
with a focal spike in the temporal region. Although his seizures had been well controlled with oral
Phenobarbitone at a younger age and more recently with oral Sodium Phenytoin, he had experienced
two seizures in the past 12 months. His serum phenytoin level was well within the therapeutic
range and he was not able to tolerate the side effects of several other oral anti-convulsants. Both
seizures occurred at rest and were not precipitated by any particular event. The seizures were
typical grand mal seizures, lasting approximately 30 sec with a 10-15 min post-ictal state.
He did not want to discontinue his one metre, three metre or platform diving. His doctor’s
concern was that he might suffer an injury if the seizure were to occur while on the platform or
upon entry into the water. His coach was in the waiting room eagerly awaiting your opinion, since
his family physician would not sign his pre-participation medical certificate.
Discussion
The traditional view of limiting activity in individuals with epilepsy is no longer valid. For example,
several studies have failed to show a greater drowning rate amongst epileptic ocean and lake swimmers
compared with normals and some evidence even indicates that the seizure threshold is raised during
physical activity. In addition, hyperventilation at rest, a known precipitating cause of grand mal seizures
in epileptics, is not a concern during exercise. The greatest concern lies in the injury risk during
activities which involve elevation (eg. diving tower, ski jump ramp), equipment (eg. weightlifting,
javelin throw), or altered environment (eg. distance swimming) since these sports pose injury risk to
the athlete and surrounding persons.
In making a decision, the physician must consider the following factors:
Diagnosis should be accurately documented, although idiopathic epilepsy is the most common
diagnosis, the physician should be sure that no other disease processes are contributing to the
seizures.
An accurate seizure record should be reviewed - one that is compiled in conjunction with the
athlete, family, and medical records. The past frequency of seizures will help to predict the
frequency of future events and is a very important determinant in the decision regarding
competition.
The level of maturity and responsibility of athlete/parent including compliance with medication
requirements and restrictions should be noted.
- 79 IOC Sport Medicine Manual 2000
3 - Organ System Disorders
Petit mal, grand mal, and focal motor seizures all pose risks to individuals who have these disorders
and participate in sport activities. For example, a seizure while climbing a ladder to a diving tower
may produce a serious injury if a fall results. An additional consideration is the risk posed to others
who may be injured as a result of the athlete’s seizure, an example being the accidental discharge of a
gun during a shooting event. Thus it is important that the sport physician be knowledgeable regarding
seizures during physical activity, and that he communicate this knowledge to the athlete, parents, and
coaches.
Serum anti-convulsant levels should be checked to ensure compliance and to measure the
level of anti-convulsant. Consideration should be given to additional or alternate medication
if greater control is required.
A frank discussion should occur in which the athlete, family, and coaches are made aware of
the risks and particular dangers involved in the sport.
The liability for injury to the athlete and others should be known before a specific
recommendation is given.
Safety should be ensured, eg. spotters in gymnastics and swimming.
The vast majority of athletes with epilepsy can continue to participate in their sport. However, selected
cases should be advised to modify their sport until the risk of seizure is lower, in the same way that
individuals with single organs (eg. single organs in contact sports) are similarly advised. Although the
risk of seizure cannot be accurately predicted, the antecedent history will provide the major determinant
of the likelihood of an event.
3 - Organ System Disorders
In the present case, the athlete was advised to continue one metre and three metre events, but to
discontinue the platform event until seizure-free for one year. His serum phenytoin level was in the
therapeutic range and a second medication (Valproic Acid) was added to achieve greater control.
- 80 IOC Sport Medicine Manual 2000
H. Ear, Nose and Throat Disorders
1. Swimmers Ear (Otitis Externa)
Case History - Otitis Externa
A 10-year-old male competitive swimmer had an acute onset of extreme ear pain, itchiness and
inflammation 12 hours after a training session. The swimmer also noted a fluid discharge from the
ear and complained of ear ache and diminished hearing. There had been no previous history of
otitis externa and no history of cotton-tipped applicator cleaning of the ear canal. The swimmer
had no recent episode of upper respiratory infection or ear pain. On examination, the athlete was
found to have severe pain when traction was applied to the tragus or external ear. Otoscopic
examination revealed a swollen external auditory meatus and adjoining area of the ear, with a
normal tympanic membrane.
Discussion
Differential diagnoses include:
a. otitis externa
b. perforation of the tympanic membrane
c. impacted external canal with cerumen
The diagnosis in this case is diffuse otitis externa. Otitis externa is a world-wide problem seen
particularly with competitive swimmers. It is more commonly found in hot, humid areas and often
follows cotton-tipped applicator cleaning of the ear.
On physical examination, especially if it is of a severe nature, a swollen external auditory meatus and
base of the ear is usually found. The periauricular skin may be red and swollen. Tenderness is elicited
when traction is applied to the tragus. Otoscopic examination of the external auditory canal shows
erythema, swelling and yellowish debris. The tympanic membrane will be intact and will have a
normal appearance. Occasionally the yellowish debris may be seen migrating to the intact tympanic
membrane.
The investigation includes otoscopic examination and possible culture of the debris. The bacteria
cultured is usually pseudomonas aeruginosa, staphylococcus or streptococcus with a fungal infection
(aspergillus niger) occasionally found.
The treatment of otitis externa can be initiated with a thorough cleansing of the external canal by
suctioning material from the ear or in the early milder stages by syringing with clean water. This can
be followed with rinsing the ear with Burow’s solution. A very useful drying and antibacterial agent is
VoSol (2% acetic acid, 3% propylene glycol diacetate and 0.02% benzonium chloride) solution. This
treatment is then followed with a combination antibacterial/anti-inflammatory steroid drop placed
directly in the ear canal with the use of a dropper. One of these solutions is applied 4 times daily for 710 days. To prevent recurrent episodes of otitis externa, an acetic acid/alcohol drop solution can be
utilized before and after swim workouts as a drying agent. This could be the “VoSol”, as mentioned
- 81 IOC Sport Medicine Manual 2000
3 - Organ System Disorders
The chief complaint of the athlete is usually one of ear pain, itchiness and discharge and occasional
partial hearing loss. The history of the chief complaint is usually that of a slow onset of increasing ear
pain following swimming. It can be associated with progressive itchiness and pain when sleeping on
the affected ear. There is often a past history of otitis externa and/or of excessive cerumen build-up in
the ear due to a sharply angled canal.
above, or a simple solution consisting of 10 ml of rubbing alcohol and 10 drops of vinegar (3% acetic
acid). One to two drops of either of these solutions is then applied prior to and especially after swimming.
Additional ear drying with a clean towel and hair dryer can be utilized. For recurrent episodes,
individually moulded earplugs and the wearing of a bathing cap is useful.
The basic pathophysiology of otitis externa is that of maceration of the external canal due to the
consistent presence of water and loss of cerumen. When an ear canal lacks cerumen and is exposed to
dampness and heat, a bacterial or fungal overgrowth may occur. The normal acidic pH of the cerumen
usually inhibits the growth of bacteria and fungus. Constant cotton-tipped applicator cleansing, retained
pool water and soapy water remove the protective cerumen. Treatment and prevention are aimed at
drying the retained water, reducing the inflammation and regaining the antibacterial environment of
the external canal.
For the swimmer in this case study, treatment consisted of a thorough ear cleansing by suctioning
material from the ear, later followed by syringing with clean, warm water. Topical anti-inflammatory/
anti-bacterial steroid drops and a prophylactic acetic acid propylene glycol solution were used following
each swimming workout. Since the swimmer was returning to training the following day, individually
sized and fitted earplugs were suggested accompanied by a bathing cap. At a follow-up examination
two weeks after the initial exam, the ear canal pain and swelling had disappeared as well as the
otorrhea (discharge).
2. Cauliflower Ear (Haematoma Auris)
3 - Organ System Disorders
Blunt trauma to the pinna, as seen in boxing, wrestling or in the members of a rugby scrum, results in
a subperichondrial haematoma. As bleeding occurs between the cartilage and the pericondrium, the
pinna becomes a reddish-purplish, shapeless mass. The perichondrium carries the blood supply to the
cartilage and the possible consequence of this situation is an avascular necrosis of the cartilage. As a
result, over time the pinna becomes shrivelled and, in addition, the haematoma may become organized
and calcify, producing the classic cauliflower ear seen in wrestlers or boxers. The external ear in this
condition is white, nodular, firm and deformed. The immediate first-aid measures for auricular
haematoma should be ice application and compression to reduce bleeding and swelling. A good
suggestion following ice application is to use a half squash ball (soft) held firmly over the ear with an
elasticized bandage to provide compression to the contours of the ear.
Medical treatment consists of aspiration of the haematoma and packing of the skin and pericondrium
tightly over the cartilage by means of a moulded splint of cotton soaked in benzoine and a pressure
dressing. Aspiration of the clot can usually be achieved with the use of a 25 gauge needle attached to
a 5 ml syringe. If the clot has been persistent for some time, then one may need a large-gauge needle.
If blood reaccumulates, then reaspiration may be necessary. If insufficient aspiration is achieved, then
a dependent site incision will be required to permit blood drainage. Protective headgear is essential
for these athletes on return to sport, otherwise the injury may reoccur.
Lacerations of the pinna extending through the skin and cartilage require repair by suturing of the skin
margins of the wound, and external splinting of the cartilage and pinna with moulded cotton impregnated
with benzoine and protective dressing. Sutures are not placed in the cartilage itself. Collodion solution
has been utilized successfully rather than benzoine in many situations. Collodion painted over the
outer ear can provide intimate elastic compression.
- 82 IOC Sport Medicine Manual 2000
3. Middle Ear Barotrauma
Case History - Middle Ear Barotrauma
A 22-year-old female elite tower diver complained of a sudden onset of severe left ear pain
upon entry during a training session. She reported transient nausea, dizziness and a loss of hearing.
She had no previous history of ear pain, but she has had a recent upper respiratory tract infection
free of ear pain. She did have difficulty in “clearing her ears” after diving. On otoscopic
examination, a haemorrhage in the middle ear with a 30% perforation of the tympanic membrane
was observed. An ear swab was taken for culture but was reported as “normal flora”.
Discussion
The differential diagnosis, in this case, would include:
a. otitis media
b. perforation of the tympanic membrane secondary to trauma from
a poor dive
c. bacterial or viral infection
d. external, middle and inner ear barotrauma
The diagnosis in this athlete was middle ear barotrauma or aerotitis media,
a condition which occurs when the tympanic membrane is exposed to
sudden changes in barometric pressure such as in diving. The condition
occurs especially when the eustachian tube is blocked and negative pressure
develops in the middle ear.
ii.
Middle ear barotrauma is the most common form of barotrauma. This occurs when the
eustachian tube is blocked and the tympanic membrane is pulled inwards and ruptures as the
pressure inside the middle ear attempts to equalize with that of the external canal. The
developing negative pressure within the middle ear also extracts serous fluid from the capillary
vessels within the middle ear. An ear drum can rupture in as little as one metre of water if the
eustachian tube is blocked. As cold water enters the middle ear, nausea and vertigo occur as a
result of caloric stimulation.
iii. Inner ear barotrauma is a result of forced auto-inflation (Valsalva) which ruptures the round
or oval window. Marked vestibular disturbances (vertigo and nausea) occur as the increased
pressure alters the function of the labyrinth and cochlea.
Middle ear barotrauma occurs as a result of descent while diving or travelling in an aeroplane when a
sudden change in external pressure on the ear from a low pressure to a high pressure environment
occurs. When the eustachian tube does not allow air into the middle ear, the raised pressure in the
external environment pushes the tympanic membrane inwards with a dampening down of the movement
of the membrane. If significant pressure changes occur or if there is any previous weakness in the
tympanic membrane, then rupture may result.
As with this case study, the chief complaint is usually severe ear pain and hearing loss associated
initially with a pressure sensation following tower diving, scuba diving or descent in an aeroplane. If
- 83 IOC Sport Medicine Manual 2000
3 - Organ System Disorders
Barotrauma affects three areas of the ear - external, middle and inner ear.
i. External ear barotrauma, or “reverse ear”, occurs when the eustachian tube is open but the
external auditory canal is blocked by such things as swimming or diving caps, earplugs,
cerumen or severe otitis externa. A negative pressure in the external auditory canal on descent
produces tissue damage and haemorrhagic blisters in the canal and on the tympanic membrane.
the tympanic membrane ruptures, then transient nausea and dizziness may occur. Often an associated
upper respiratory infection or allergies can result in poor eustachian tube functioning. There may be a
history of allergic rhinitis or hay fever and difficulty clearing ears during diving or descent in an
aeroplane.
On physical examination, the otoscopic findings are of free haemorrhage in the middle ear with a
perforation of the tympanic membrane together with a conductive hearing loss. Investigation includes
culture of the otorrhea and follow-up hearing tests.
The treatment consists of:
nasal decongestants (5 days maximum) and systemic non-sedating antihistamine (Note: Oral
decongestants are on the lOC banned list, eg. Ephedrine, Pseudoephedrine,
Phenylpropanolamine, but the imidiazole group of topical decongestants, eg. Naphazoline,
Oxymetazoline, Tetrametazoline and Xylometazoline, is permitted). A positive drug test from
an oral decongestant is a common drug infraction
systemic antibiotics for 10 days if the perforation occurred by a contaminated object or
environment (ie. swimming pool)
To permit re-entry to water, one needs to prevent water entry into the middle ear by using:
vaseline impregnated ribbon gauze placed in external auditory canal
mastisol, a plastic wrap-like material, to be wrapped around the auricle and taped in place
with transpore tape
3 - Organ System Disorders
To prevent barotrauma, it is essential to ensure that the eustachian tube is patent prior to diving and
flying. Regular and early auto-inflation (ear clearing) is important. In addition, if the individual has an
upper respiratory tract infection, then he/she can use a topical nasal decongestant and/or oral
antihistamine, but must be able to clear his/her ears.
The treatment of the tower diver was conservative and consisted of ear cleaning, local decongestants
and oral antibiotics. This athlete had a major international competition in five days and to allow her to
return to diving, a specialized ear covering was made. To prevent water entry into the middle ear, the
covering consisted of a vaseline impregnated ribbon gauze placed in the external auditory canal. Then
mastisol, a plastic wrap-like material, was used to wrap around the auricle and taped in place with
transpore tape. When seen in follow-up 18 days later, the tympanic membrane was healing satisfactorily
and there was no residual hearing loss. Follow-up hearing tests were performed which indicated full
auditory function. In the usual situation, the athlete would not be back in the water until full healing
had occurred. An obvious modification was made here due to the proximity of an international event.
This case report emphasizes the dangers of diving with an upper respiratory infection and the resultant
middle ear barotrauma. Individualization of treatment by adequately covering the ear to prevent water
entry allowed this individual to return to diving five days post-injury and to make a full recovery.
4. Injuries to the Face and Neck
a. Dental Injuries and Disease
Prevention of dental injuries must be high on the priority list for a team physician in contact sports
and sports with sticks and high velocity balls and pucks. This can be accomplished with custom fitted
mouth guards and, in sports such as hockey, lacrosse and cricket, by helmets and face masks or cages.
Immediate assessment of dental injuries is essential to the health of the tooth. The physician must
apply prompt care for the unstable tooth. A tooth that is avulsed must be prevented from drying out
- 84 IOC Sport Medicine Manual 2000
and ideally replanted and splinted within an hour to ensure the best chance of survival. The avulsed
tooth must be cleaned with sterile saline to remove any debris before replanting. If the tooth cannot be
replanted immediately, then it should be stored in either moist sterile gauze or, ideally, in cold milk.
An excellent storage site is in the vestibule of the athlete’s mouth.
To test the stability of a tooth after an injury, apply finger pressure forward and backward to assess the
degree of movement and pain on movement as compared to adjacent non-injured teeth. A loose tooth
may either be separated from its alveolar margin or fractured at the crown or root, both of which can
compromise the vascular supply to the tooth. For the athlete with a suspected fractured tooth, dental
assessment and x-rays are required. Small, pain-free corner dental fractures that are stable and not
sensitive to pressure or cold air can safely be treated by the dentist within 24 hours and the athlete can
continue to play. However, if the tooth is sensitive to air, then dentin is usually exposed and this tooth
requires emergency dental treatment (within 2-3 hours), especially if the pulp is exposed.
Case History – Dental Fracture
A 25-year-old male defenceman for an ice hockey team attempts to block a shot from an opposing
player. The puck, travelling at high velocity, glances off his own stick and makes contact with the
athlete in the mouth. The athlete does not lose consciousness.
In addition to soft tissue damage, examination indicates two teeth that have been fractured to
different extents.
Discussion
The severity of a dental fracture, and urgency of treatment, is to a great extent based on the layer or
structure that has been damaged. A small fracture, just involving the enamel layer, will result in minimal
sensitivity and should not prevent an athlete from returning to competition almost immediately. Care
must be taken, however, to ensure that there are no sharp or jagged edges of the tooth that could result
in lip lacerations.
If the dentin layer is damaged, the athlete may experience significant sensitivity to both temperature
and air. In most cases, the athlete can return to competition, especially if a desensitizing agent - such
as dental cement or fluoride varnish - can be placed over the exposed dentin by the team dentist or
medical staff.
The greatest concern arises when the dental pulp has been exposed. Not only will the athlete suffer
considerable discomfort, but the tooth is at risk of infection and pulpal necrosis if the nerve is exposed
for any significant time period. With a pulp exposure, the athlete should be removed from competition
and arrangements made for appropriate treatment.
In all cases of dental fractures, any fragments that can be located should be retained in a tooth
preservation solution or other appropriate storage medium (see next case history on dental avulsions).
- 85 IOC Sport Medicine Manual 2000
3 - Organ System Disorders
Teeth are composed of three layers. In the centre, the dental pulp
contains both the neural and vascular components that make the
tooth a living structure. Surrounding the pulp is the dentin layer,
which, while itself a hard structure, contains multiple microscopic
tubules that allow the transfer of sensation to the centre of the tooth.
The outer layer, or enamel, is the hardest structure in the human
body and allows the tooth to function effectively in chewing.
In many cases, these fragments can be reattached using a tooth bonding system. Treatment in all cases
of dental fracture must begin with appropriate periapical radiographs, ideally from two different angles,
to help in identifying the presence of any root fractures which may not be clinically visible. As well,
the extent of the fracture, along with any mobility, must be documented.
Follow-up treatment should include reassessment of the health of the nerve and tooth, including vitality
tests and radiographs where indicated, at regular periods over the next 12 months. Without appropriate
follow-up, conditions such as external resorption of the root structure can develop and progress.
Many dental fractures can be prevented with the use of appropriate mouth protection. While there are
many different types of mouthguards available, the most effective of these are custom-made by a
dentist. Athletes often complain of xerostomia, breathing difficulties, nausea and poor speech with
many of the stock or “boil-and-bite” varieties of mouthguards. However, the current technology of
“pressure lamination”, where thin layers of protective material are sequentially bonded to a model of
the athlete’s teeth, provides a mouthguard with an excellent combination of comfort, fit and protection.
Custom-made guards can be designed to accommodate the specific requirements of the sport. For
example, in a sport such as field hockey, where an anterior blow to the face with a ball or stick is likely
to cause the most damage, additional protection can be built into this area of the guard. However in
boxing, where the guard is designed to cushion the impact of an upward blow to the jaw, the mouthguard
may be fabricated with a thicker biting surface.
Among Olympic sports, mouthguards would be recommended for basketball, field and ice hockey,
waterpolo, soccer, team handball, wrestling, taekwondo, judo, volleyball, and mountain biking.
3 - Organ System Disorders
b. Avulsion Injury
Case History - Avulsion Injury
During the course of an international basketball match, a 26-year-old female player suffers a
collision. Her facial area makes contact with the head of an opposing player, and one of her front
teeth is completely avulsed. Two adjacent teeth are also loosened and in a slightly posterior position.
Discussion
The anatomy of the dental socket allows this type of avulsion
injury to occur in sports. The tooth is attached to the dental
socket by means of a periodontal ligament. With a blow to
the tooth, the ligament can be torn and the tooth lost. It is also
possible to partially loosen the tooth laterally (lateral luxation)
or to knock the tooth inward (intrusion).
In most cases, the immediate goal of treatment is the
repositioning of the tooth to its original position or, in the case of an avulsion, to reimplant the tooth.
In luxation injuries, the athlete will usually be able to advise if the tooth “feels” as if it is out of
position according to the bite of the opposing jaw. If malpositioned, and a root fracture has been
eliminated by examination or a radiograph, the tooth can usually be digitally repositioned with relative
ease. In most cases, there will be a period of transient dysesthesia which will allow this repositioning
with minimal discomfort.
- 86 IOC Sport Medicine Manual 2000
In the case of an avulsion, it is imperative to first locate the tooth. If the tooth cannot be found, and
there has been any period of altered consciousness as a result of the blow, the possibility that the tooth
has been aspirated must be eliminated by means of appropriate chest radiographs.
If the tooth has been found, it should be handled with care to avoid damage to the ligament fragments
that may remain on the root surface. It can be gently rinsed if any debris is present, but should not be
scrubbed.
If reimplantation is not immediately possible, the tooth should be stored in an appropriate storage
medium. There are commercially available storage kits, or one can use cold milk or sterile saline. One
of the best storage sites is in the labial vestibule of the patient if they are conscious and alert.
The success of the reimplantation will depend on many factors, but the one that the physician or
therapist should be most conscious of is time. Relative to other issues such as storage and socket
damage, it is generally felt that teeth which are reimplanted within 30 minutes have the greatest
likelihood of long-term retention, while those which have been out for more than 3 hours begin to
have a much poorer statistical prognosis. That is not to say that teeth avulsed for more than 3 hours
cannot be reimplanted, but only that success is time dependent.
In both reimplantation and luxation cases, there will need to be some form of splinting of the affected
teeth to retain them in their ideal position. As well, analgesics, antibiotics and anti-inflammatory
medications may all play a post-operative role, as may consideration of tetanus prophylaxis if the
tooth was not clean after the avulsion.
c. Temporomandibular Joint Injury
Case History - Temporomandibular Joint Injury
While both in the air during a match, two opposing soccer players make contact, with the
shoulder of one player hitting the jaw of a 23-year-old male athlete. The athlete does not lose
consciousness, but immediately complains of muscle tenderness and pain in the right
temporomandibular joint area. As well, he is unable to bring his teeth together in their usual
manner.
Discussion
The temporomandibular joint (TMJ) is a unique joint in that it allows both rotational (opening and
closing) and lateral movements. This is accomplished by means of a meniscus that moves forward on
opening towards an anterior articular eminence in the joint itself.
With certain blows, especially those resulting in lateral contact to the body of the mandible, the head
of the condyle of the mandible can be knocked anteriorly towards and over the articular eminence,
with the meniscus trapped in behind.
A review of the anatomy of the TMJ shows the result of this type of trauma, and also indicates that
repositioning must first involve a downward movement of the mandible to allow it to pass under the
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3 - Organ System Disorders
As well, appropriate radiographic and clinical follow-up will need to take place, with the possibility
of endodontic or nerve treatment being a likely result. A custom-fit mouthguard must be made available
before any return-to-play can be considered.
articular eminence and allow the condylar head to slip back
into the condylar fossa.
Usually, this repositioning will occur from behind, with
thumbs on the eminence of the mandible lateral to the lower
molars. The fingers should NOT be placed on the biting
surfaces of the teeth while repositioning a jaw, as the trismus
resulting from the dislocation may cause the jaw to snap
shut violently.
Before attempting to reduce a TMJ dislocation, the
possibility of a ramus, body or condylar fracture must be
eliminated. One method is to use a tuning fork (or tongue
blade tightly held between the teeth and vibrated) to help
identify a fracture.
The other is to closely examine the malocclusion, or bite,
that has resulted from the injury. In the case of a dislocation of the TMJ, the condyle of the damaged
side is effectively longer, resulting in an inability of the teeth on the ipsilateral side to come together.
This resulting ipsilateral open bite is characteristic of TMJ dislocation. With a fractured condyle, the
resulting shortening usually leads to a contralateral open bite.
3 - Organ System Disorders
Anti-inflammatory medications, along with a soft diet and minimized opening, are recommended
after this type of injury. A panographic or TMJ radiograph should be taken to eliminate the likelihood
of a fracture. Harmful activities such as chewing gum should be avoided for an appropriate period of
time. A custom-fit mouthguard will also protect the TMJ by opening up a protective space in the joint.
There is some thought that properly fitting mouthguards may help in reducing the incidence or severity
of brain concussions in one of two ways. As described above, the joint space which is opened upon
placement of a mouthguard mat help to reduce the impact between the jaw joint and temporal fossa.
Or, biting down hard on the guard at the point of collision may activate additional head and neck
muscles to provide resistance to the rotational forces to the head that can lead to concussion.
d. Gum Disease
Case History - Gum Disease
During routine physical examination prior to the Olympic Games, a dental assessment is
performed on a 19-year-old baseball player. A white lesion is noted in the area of his lower incisors,
and two partially impacted wisdom teeth are recorded. The athlete admits to a two-year history of
smokeless tobacco usage, and as well notes that he has had occasional pain, swelling and drainage
from the wisdom teeth areas.
Discussion
Many athletes in the 17-24 age group have problems with their third molars or wisdom teeth. In most
cases, there is inadequate room for these teeth to erupt into the mouth, and as a result they remain
either completely or partially impacted under either the bone or gums.
Problems arise when the teeth are partially impacted. In this case, the teeth have a small communication
with the oral cavity, but are partially covered with a flap of tissue which can collect both food and
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bacteria, leading to a pericoronitis. If this pocket is
not cleaned or eliminated by removing the tooth, the
result can be pain, swelling, drainage and
lymphadenopathy.
Another concern with impacted wisdom teeth relates
to the strength of the mandible. The presence of
impacted wisdom teeth leads to a weakening of the
jaw bone in that area, and one study has shown that
athletes with impacted wisdom teeth are four times
more likely to suffer a fractured jaw.
Immediate treatment of pericoronitis is irrigation of
the area under the flap, along with systemic antibiotics
if indicated. Once the acute situation has resolved, plans can be made for the extraction of these teeth,
but this should be done during a relative period of inactivity for the athlete, as there may be significant
post-operative recovery required.
The use of smokeless tobacco is gaining increasing prominence in young athletes. In most cases, the
tobacco is held in a consistent location, and the result is often a significant soft-tissue lesion in the
area. This lesion may exhibit a whitish hyperkeratosis, a reddish inflammation or many other
manifestations. The gingiva around the adjacent teeth may suffer from recession or other trauma.
e. Epistaxis
Epistaxis may be the result of either localized or systemic disease, however the most common cause
is nasal trauma. Other common local factors include:
mucosal disruption and inflammation (allergic congestion or infection)
anatomical deformities (septal deviation or perforation)
foreign bodies
Systemic causes of recurrent epistaxis include:
vascular disorders (hereditary haemorrhagic telangiectasia)
clotting disorders (platelet dysfunction, coagulation deficiencies)
hypertension and arteriosclerosis
tumours (benign, juvenile angiofibroma, or malignant)
Over 90% of epistaxis are anterior and arise from Little’s area at the anterior inferior septal region.
The posterior epistaxes are from the nasal branches of the internal maxillary artery or the ethmoid
arteries. Both anterior and posterior epistaxes can occur from nasal fractures. Once the nasal fracture
is reduced, most of these settle with pressure.
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3 - Organ System Disorders
While there is some concern over the use of smokeless tobacco in that it can and has been aspirated by
athletes during competition, the main concern is that the tobacco is carcinogenic and has led to many
cases of oral cancer. Athletes should be regularly screened for this habit, and should be counselled to
assist with the elimination of it from their system. There are non-nicotine mint-based chews that may
provide a similar satisfaction to the athlete without the tissue damage.
The immediate management of an anterior epistaxis is nasal compression. The head should be slightly
forward and pressure should be applied firmly over the ala for five minutes. It may be helpful to place
a small cotton ball soaked with topical decongestant from a spray placed anteriorly in the nose for
vasoconstriction. If after three attempts of nasal compression bleeding continues, then the athlete
should be managed in the emergency ward.
For minor anterior bleeds, suction out clots and then apply a cotton pad soaked with a topical anesthetic
and vasoconstrictor (ie. 4% phenylephrine and topical lignocaine spray) which is left in place for five
minutes. As the bleeding stops, cauterizing can be performed with a silver nitrate stick placed gently
but firmly over the bleeding source. Following this, a topical antibiotic is applied three times daily.
No nose blowing is allowed for 24 hours.
For a major anterior bleed where you cannot identify a bleeding point, an anterior nasal pack is indicated.
Local anesthesia and vasoconstriction is obtained by applying cotton swabs, soaked as before, along
the nasal floor, inferior turbinates and into the nasal roof. Follow this with nasal packing using 1 cm
vaseline or iodoform gauze coated with a topical antibiotic. After removing the cotton swabs, the
flattened gauze is applied in layers, as far posterior as possible, compressing each layer with forceps
and continuing until the root is packed. The nostrils are then taped together. This nasal pack is left in
place for three days with no exercise, hot showers, whirlpools or hot drinks allowed during this period.
Prophylactic antibiotics are appropriate. Removal of the pack is painful and must be done gently.
Follow-up antibiotic ointment for a further 3-4 days is required. Anterior gauze will collect any
serosanguineous drainage that often occurs.
3 - Organ System Disorders
Posterior epistaxis is rare in the athlete and treatment is usually not within the province of the primary
care sports physician. Emergency consultation with an ear, nose and throat (ENT) specialist is required
for the regional anesthesia, posterior nasal pressure with a balloon or Foley catheter, possible
angiography, and follow-up care.
f. Nasal Fractures
Nasal fractures are the most common fracture of the facial bones. Fractures of the nasal bones may
involve the ascending processes of the maxilla and the nasal processes of the frontal bones, as well as
the nasal bones. A fracture of the nose is often an open fracture. The skin of the dorsum of the nose
may be lacerated and the mucous membrane of the nasal cavity is often torn. A very common deformity
is a deviation of the nasal bone to the right with depression of the nasal bones on the left, as seen with
a right hook in boxing. Fractures of the nose may be associated with septal fractures and septal
haematomas. Nasal fractures should be suspected when accompanied by profuse epistaxis. Soft tissue
swelling is usually very prominent and may obscure the underlying bony deformity associated with
the nasal fracture. In addition, one may see ecchymosis that may spread into the upper and lower
eyelids.
Upon examination, the obvious deformity can often be seen. On palpation, instability and crepitus
can often be demonstrated, as well as point tenderness. Since nasal fractures are often associated with
fractures of other facial bones, routine x-rays of the paranasal sinuses and facial bones is advised. in
addition, extensive facial fractures and trauma to facial bones can be associated with cerebrospinal
fluid rhinorrhea. Any watery discharge from the nose should be examined for glucose content to
differentiate cerebrospinal fluid (CSF) from nasal mucous.
Cerebrospinal fluid rhinorrhea requires prophylactic antibiotic therapy to prevent meningitis, and
consultation with a neurosurgeon.
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Often, on the side line before swelling occurs, the nasal
fracture can be rapidly reduced by the team physician after
an ice pack has been applied. Reduction of the nasal fracture
requires good local anesthesia and a cooperative patient,
and in children, usually requires general anesthesia.
Following local anesthesia in an adult, the nasal fracture is
reduced by internal traction on the fracture fragment with a
blunt periosteal elevator in association with external traction
with the fingers. The need for internal splinting/packing and
external protection depends on the post-reduction stability
of the fracture. With anterior packing and external protection
applied for 10-14 days, the security of this reduction can be maintained. Minor nasal fractures may be
left unreduced until swelling has resolved and the cosmetic effect determined. These minor nasal
fractures can often be left until the end of the season unless nasal obstruction is present. They should
be protected by a face mask for many sports, however, these may not be allowed for some sports.
Fractures of the nasal septum and septal haematomas usually require referral to a plastic or an ENT
surgeon. Septal haematomas frequently become infected resulting in avascular necrosis of the septal
cartilage, which may result in a saddle deformity of the nose.
g. Facial Fractures
Most fractures to the jaw and face are due to trauma associated with falls, fights, motorcycle/cycling
accidents or high, illegal tackles. These fractures usually occur in well-defined patterns located at
weak points in the bones, particularly in the mid-face. Mandibular fractures are often accompanied by
severe displacement as a result of the strong pull from the powerful muscles of mastication.
A diagnosis of fractures of the mandible are usually made by physical examination. Crepitus and
movement at the point of maximal tenderness may identify the fracture site. The patient will usually
complain of an abnormal position of the teeth on bite. Numbness of the lower lip may occur if the
inferior alveolar nerve has been traumatized. Fractures of the body of the mandible are often
compounded into the oral cavity itself, and should be referred to a plastic, ENT, or oral surgeon.
In condylar fractures, the external auditory canal should be examined to exclude a fracture. In addition,
dislocations of the temporomandibular joint may be associated with fracture of the condylar head.
Dislocation of the temporomandibular joint without fracture results in considerable pain due to muscle
spasm, as the jaw is locked in the opened bite position.
This can be treated with local injection of Lidocaine and downward traction on the molar teeth to
secure full reduction. Occasionally, general anesthetic is required to relieve the muscle spasm in order
to reduce the dislocation.
i. Mid-face Fractures
Mid-face fractures usually involve the two maxillae and the paired palatine bones. The athlete with a
mid-face fracture will usually complain of malocclusion and an open bite deformity. On examination,
mobility of the upper jaw and hard palate can be identified when the upper teeth are grasped between
the examiner’s thumb and index finger. Diagnosis is confirmed by x-ray; the Waters view provides an
excellent x-ray view to visualize mid-face fractures. It is with these fractures that a watery cerebrospinal
fluid leak can occur from the nose, particularly if the cribriform plate has been fractured. Plastic
surgery or ENT referral is required, as these fractures are treated by direct surgical exposure and
wiring.
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3 - Organ System Disorders
h. Mandibular Fractures
j. Zygoma Fractures
The zygomatic arch is often fractured with injuries to the upper jaw. These fractures may be associated
with displacement of the upper teeth or maxilla.
Diagnosis is made on clinical examination and x-ray. The cheekbone is often flattened, local tenderness
and irregularity of the bone may be felt, and swelling may be present. There may be a loss of sensation
over the infraorbital foramen. In addition, there may be crepitus over the fracture that involves the
maxillary sinus, producing surgical emphysema. The injured athlete may complain of numbness of
one-half of the upper lip. The athlete must be warned not to blow his nose. If the floor of the orbit has
been displaced, the individual may complain of diplopia and will have also traumatized the infraorbital
nerve (see the next section I, of this unit, for a discussion of orbital fractures).
Treatment of the zygomatic fracture usually involves closed or open reduction and fixation with the
appropriate transosseous wiring. It should be noted that in athletes suffering major fractures of the
upper and lower jaws, approximately 7% of all these patients will have associated injuries to the
cervical vertebrae. Hence, in these patients, careful examination, C-spine protection, and x-rays of the
neck are mandatory.
k. Facial Lacerations
3 - Organ System Disorders
Facial lacerations tend to bleed profusely, hence prompt administration of basic first-aid is important.
The physician must be aware of the likelihood of associated injuries to an underlying muscle and/or
gland, especially the salivary gland, salivary duct, and/or a nerve injury. The physician should also
check for imbedded foreign bodies, for example, in dealing with a cyclist who has had a road crash.
Initial management of a facial laceration involves direct application of digital pressure with a sterile
gauze pad. This is often sufficient to control haemorrhage. In addition, cold application with a clean
cloth filled with crushed or flaked ice further helps to reduce haemorrhage and bruising.
Many small superficial lacerations about the face and eyes can be adequately treated with 1.6 mm, 3
mm or even as large as 6 mm surgical tape closures. These can yield excellent results. If, due to
perspiration, it is difficult to get the surgical tape to stick, a small amount of tape adherent (eg. benzoin
or collodion) painted along the wound margins with a cotton tip applicator will usually allow adhesion.
More extensive facial lacerations will require local anesthesia and suturing with 6-0 material on a
small needle. These sutures should be removed at five days. After the wound has been closed, the
athlete should be encouraged to apply cold to reduce swelling and to keep the facial area elevated,
particularly during sleep over the next 48 hours.
l. Laryngeal Trauma
Laryngeal trauma is usually the result of a stick, ball, puck, forearm or elbow to the throat. The athlete
will be hoarse and may have pain on swallowing or breathing. If significant trauma has occurred, then
the athlete will have haemoptysis. The diagnosis is made by indirect or direct laryngoscopy. The
majority of cases involve edema with small petechial haemorrhages.
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Figure 3.8 Laryngeal trauma - blunt trauma causing fracture of the thyroid cartilage.
Laryngeal fracture, associated with a fall against bicycle handlebars or riding a horse or bike into a
taut line, requires ENT referral. These fractures can involve the thyroid or cricoid cartilage; however,
a blow to the neck can often spare the larynx and transect the trachea. Subcutaneous emphysema is
usually present in fractures of the larynx or trachea. Due to the soft tissue swelling, neither the laryngeal
cartilages nor the trachea can be palpated. On indirect laryngoscopy, exposed cartilage or lacerated
mucosa may be seen along with a reduced laryngeal lumen. Vocal cord paralysis may be identified. Xrays of the lateral neck may indicate the degree of trauma and associated cervical vertebral fracture or
dislocations.
Surgical repair of laryngeal fractures is mandatory. Failure to reduce a dislocated or fractured laryngeal
cartilage will lead to laryngeal stenosis.
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3 - Organ System Disorders
Treatment involves close observation, topical ice packs to the anterior neck and non-steroidal antiinflammatory medication. If dysphagia and further dyspnea develop with progressive laryngeal
obstruction from significant edema, haemorrhage or fracture, then emergency laryngoscopic
examination and early intubation or tracheostomy are performed. Cricothyroidotomy is indicated in
the emergency situations where a formal tracheostomy cannot be performed. (See Unit 5 - Emergency
Treatment.)
I. Ocular System
1. Visual Acuity and the Athlete
Visual acuity of the athlete has important implications for sport performance. It is important for athletes
to have binocular, stereoscopic vision. Athletes who suffer an injury to an eye resulting in loss of
vision or who have an eye patch as treatment for an eye disorder have difficulty judging distance and
fast-moving objects. They are at a greater risk for injury, and a decision regarding their participation
in sports must be made.
Examination of the ocular system is an important part of the overall medical evaluation of the athlete,
and the appropriate steps must be taken to correct any deficits in visual acuity. Glasses or contact
lenses can be used to correct for simple errors in refraction. Consideration must be given to the
possibility of these devices causing injury and it is important, for safety reasons, to follow the
manufacturers’ instructions with regard to their use. Safety considerations should guide the choice of
the materials composing both glasses and contact lenses. It is also important to consider the use of
protective devices, such as masks, shields or goggles, that can be used to minimize the risk of injury
to the eye.
2. Blowout Fracture
Case History - Blowout Fracture
3 - Organ System Disorders
A 21-year-old basketball player was struck in the right eye by an opponent’s elbow during a
game. There was no loss of consciousness but the player was stunned for a short period of time
and left the court. There was no obvious trauma to the eye itself. Ice was used around the orbit to
minimize swelling. Following the game, there was considerable pain about the right eye and the
player sought advice regarding further treatment.
Examination revealed extensive swelling and bruising of the right orbit. The pupils were equal
and reacted to light. The fundus appeared normal and visual acuity was normal. There was no
evidence of injury to the cornea or conjunctiva. However, testing the extra-ocular movements
revealed that the right eye did not deviate upwards following the examiner’s finger. The left eye,
however, was capable of moving in all planes. The right eye did not have any other obvious
pathology. The other extra-ocular movements were full and painless.
Discussion
This patient has had direct trauma to the orbit and this has resulted in an apparent loss of function of
one of the extra-ocular muscles. There has been damage to the inferior portion of the orbit and the
inferior oblique muscle has been trapped at the fracture site. When the patient is asked to look upwards,
the superior rectus muscle attempts to pull the eye in this manner yet the trapping of the inferior rectus
prevents the eye from moving upwards. Movement medially and laterally is, of course, possible.
Other investigations would include routine x-rays of the orbit, and tomography and/or computerized
tomography (CT scanning) to confirm the initial diagnosis of a blowout fracture.
It is possible to note a fracture which extends into the infra-orbital sinus and this will give symptoms
of sinus irritation and pain below the orbital rim. It is also possible that the infraorbital nerve may
become trapped at the fracture site and this will create numbness to the skin immediately below the
orbit.
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Treatment for this condition is usually surgical. Some opthalmologists will observe the patient for up
to 10 days to allow the condition to settle without surgical intervention. If, however, surgery is required,
this involves the release of the inferior oblique muscle and exploration of the inferior orbital rim. In
some cases, reconstruction of the orbital floor by an ophthalmologist or plastic surgeon is necessary.
In the case of the basketball player, the diagnosis of blowout fracture was made on clinical grounds.
This was confirmed by CT scanning and the player underwent surgical reconstruction of the orbit.
This treatment returned full, normal function to the eye.
Figure 3.9 Blowout fracture of the orbital floor of the eye caused by direct impact.
3 - Organ System Disorders
3. Chemical Conjunctivitis
Case History - Chemical Conjunctivitis
An 18-year-old soccer player participating in a game collided with another player near the
sidelines. There appeared to be no obvious injury to the head and yet the player left the field
immediately and reported intense pain in the left eye. There was excessive lacrimation of this eye
yet no obvious injury was seen or determined on examination. There was intense redness and
lacrimation of the globe but no obvious trauma to the eye or the globe itself.
The field markings had been recently limed.
Discussion
This patient suffers from chemical conjunctivitis and must be treated on an urgent basis. Occasionally,
it is possible to identify the source of the irritant; in this case, there was some lime in and about the
eye and this would appear to be the causative agent.
The treatment is directed at removing the source of the irritation. Eyes exposed to acid or alkali must
be irrigated immediately with copious amounts of normal saline or water. The lids should be everted
and the cul-de-sacs cleaned with a cotton swab to remove any residual particle matter. Fluorescein
staining of the cornea is essential to evaluate the integrity of the cornea. Should there be damage to
the cornea, further evaluation by an opthalmologist is necessary. There should be no attempt made to
neutralize the chemical since heat of neutralization may cause additional damage to the globe.
Subsequent treatment following vigorous irrigation will depend on the nature of the injury to the
orbital structures.
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In this case, the soccer player was treated on the sidelines with a thorough washing and irrigation of
the eye. The pain resolved and the player was able to return to the game shortly thereafter. When seen
in follow-up after the game, there was no sign of chemical irritation to conjunctiva.
4. Trauma to the Eye
Case History - Trauma to the Eye
A 26-year-old male squash player was participating in a major competition. During the course
of the game, he was struck in the right orbit by the squash ball on recoil from the front wall. There
was immediate pain and tearing in the eye and vision was severely impaired. Swelling around the
orbit commenced immediately and rapidly caused the lids to be swollen shut. The player was
compelled to forfeit the match and seek urgent medical attention.
Discussion
In this case, it was impossible to evaluate thoroughly the status of the ocular injury at the competition
site. Once it was determined that the athlete could be transported safely to a hospital. The athlete was
referred for definitive care to an ophthalmologist.
Lacerations to the globe are often obvious but they can be missed if the lids are swollen shut, as in this
case, or if care is not taken in exploring the lid and brow lacerations if these exist. It is possible that a
seemingly small laceration of the eyebrow may penetrate the globe.
3 - Organ System Disorders
In this case, fundiscopic examination of the eye revealed blood in the anterior chamber; this is a
hyphema and is frequently seen as a result of sporting participation. It is important to evaluate the eye
further, as other injuries such as retinal, scleral and/or choroidal tears may be associated with the
hyphema. As there is an increased risk of further bleeding (15-20%) in the anterior chamber, the
athlete is confined to bed-rest and mandatory follow-up is necessary.
Corneal abrasion might occur as the result of trauma. In this case, the surface epithelium of the cornea
was scratched, resulting in exquisite pain and excessive tearing. The diagnosis is made by using a
fluorescein stain.
The eye should be carefully examined for the presence of a corneal foreign body. Should this occur,
they usually can be removed after application of a topical anesthetic. During this type of treatment,
magnification with a slit lamp generally is preferred and should this prove to be a difficult task,
referral to an ophthalmologist is in order.
The highly myopic athlete is at increased risk of developing retinal detachment following eye trauma
in sports. This must be kept in mind and careful fundiscopic examination should be performed. Longterm sequellae to blunt trauma are glaucoma and cataract formation.
Once the eye has been evaluated for corneal abrasion and a foreign body is not seen, the eye should
then be treated with a topical antibiotic ointment and an immediate-acting dilating drop such as 5%
homatropine solution to relieve ciliary spasm. The eye is then covered with a patch and re-checked by
a family physician in 48 hours. It is a mistake to offer the patient topical anesthetics for pain relief to
be used at home. These agents delay corneal healing and, patients with significant pain should be
reviewed frequently in order to offer other alternatives to pain management. This injury can be prevented
by the mandatory use of protective glasses in squash and racquetball.
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This injured squash player was confined to bed for one week and when seen in follow-up, the hyphema
was resolving. Two weeks later there was no abnormality on clinical examination and six weeks from
the date of injury, with suitable protective glasses which meet industry standards, the player returned
to play squash.
J. Dermatology
1. Dermatological Conditions seen in Runners
Case History - Foot Dermatitis
A 22-year-old female middle distance runner presented to your office during a spell of hot
weather with a two week history of an itchy burning eruption on the soles of both feet. She was
concerned because the Olympic Trials were only two weeks away. A month ago, she purchased a
new pair of running shoes. The symptoms increased after her runs, and the eruption had become
progressively worse.
Examination revealed that the soles of both feet were affected with a moderately well demarcated
red, swollen, vesicular and scaly eruption over the weight-bearing surfaces, sparing the instep,
and web spaces. Microscopy failed to reveal any fungal hyphae.
Discussion
There are three conditions that are most likely to cause this runner’s foot dermatitis:
a. tinea pedis
b. endogenous dermatitis (pompholyx, dyshidrotic dermatitis)
c. contact dermatitis (exogenous)
Tinea pedis is a dermatophyte fungal infection which commonly affects the sole of the foot. There are
three basic patterns of infection:
interdigital toe web involvement which may spread to contiguous skin
vesicular or blistering tinea which is frequently unilateral and involves the instep
a red scaly “moccasin” frequently involving the soles of both feet, as well as the interdigital
spaces
This latter form is seen in patients with low resistance to the fungus, usually Trichophyton rubrum.
Tinea infection of the toenails (tinea unguium, onychomycosis) is frequently associated with tinea
pedis, particularly of the moccasin pattern.
Unusual patterns of tinea may occur on the feet when strong topical steroids have been erroneously
used in therapy (tinea incognito).
Fungal infection can occur in other areas in association with tinea pedis particularly in the genitocrural region (tinea cruris), especially in males.
Clues to clinical diagnosis other than the patterns listed above, include asymmetrical involvement of
the feet and an arcuate border, frequently with fine vesicles or pustuIes.
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3 - Organ System Disorders
a. Tinea Pedis
Figure 3.10 Interdigital Tinea Pedis.
3 - Organ System Disorders
Laboratory confirmation of tinea infection can be achieved by scraping the border of an affected area,
applying the scales to a glass slide, adding a drop of 20% potassium hydroxide (KOH) and a cover
slip followed by microscopic viewing under low power. In vesicular tinea pedis, the best sample is
taken by shaving off the roof of a blister for microscopic examination. In positive samples, branching
fungal hyphae are visualized coursing over epidermal squamous cells. Similar samples can be sent for
fungus culture. These should be folded up in black paper and allowed to dry out to prevent overgrowth
of bacteria and yeast. Culture of dermatophytes may take 2-4 weeks.
Figure 3.11 Blistering Tinea Pedis.
Treatment of tinea pedis includes:
general measures to reduce heat and humidity of the foot. It is important to avoid prolonged
contact with rubber, plastic, or other nonabsorbent footwear.
topical antifungals such as terbinafine or clotrimazole cream used twice daily. This should be
placed on the involved area of the foot and 1 cm beyond, and continued for 2-4 weeks, even in
the face of apparent clearing of the infection.
systemic treatment is best reserved for those with symptomatic toenail involvement or extensive
or resistant involvement of the skin. Terbinafine (Lamisil) 250 mg. once daily is the drug of
choice. This should be used for 4 weeks for skin only infection, 6 weeks for fingernails and 12
weeks for toenail infection. Side-effects include G.I. upset (5%), skin rash (2%) and much
less commonly leukopenia and hepatic inflammation. Itraconazole (Sporonox) and griseofulvin
are alternatives.
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b. Endogenous Dermatitis (pompholyx, dyshidrotic dermatitis)
Endogenous dermatitis is usually seen in an individual with a history of prior dermatitis, who may
also have allergies, hay fever, or asthma. There may be a family history of similar conditions.
The eruption is usually symmetrical, involving the soles and/or palms more than the dorsum of the
feet or hands. The borders are usually ill-defined. In the acute phase, there are usually multiple small
deep papules and vesicles with oozing, crusting erythema, and swelling. In the chronic phase, one
sees erythema, scaling, and fissuring.
Potassium hydroxide examination of the scales in endogenous dermatitis will be negative. Patch testing
for allergic contactants would similarly be negative.
Treatment involves general measures, including similar footwear modifications as listed under tinea
pedis. In the acute vesicular phase, the lesions should be compressed with Burow’s solution for 10
minutes daily. If there appears to be significant secondary bacterial infection, then appropriate oral
anti-staphylococcal antibiotics should be administered. A strong topical steroid such as clobetasol
cream should be applied twice daily. Occasionally oral steroids are necessary for severe vesiculobullous flares. Rest or modified rest may be required.
c. Contact Dermatitis
Contact dermatitis is due to either irritant compounds or topical allergens which come in contact with
the affected skin.
Irritant contact dermatitis may be due to a chronic low-grade repetitive irritation with wetting and
drying of the skin, or to a short-term exposure to more caustic compounds.
3 - Organ System Disorders
Figure 3.12 Contact dermatitis.
Allergic contact dermatitis is due to a cell-mediated immune response to specific compounds. Allergic
shoe dermatitis is usually due to rubber and associated chemicals, adhesives, or leather tanning
compounds. Topical medication, particularly those containing neomycin, topical antihistamines, or
benzocaine, may also be offending agents. Clinically, shoe contact dermatitis tends to be symmetrical
and spares the flexural creases of the toes. In severe acute cases, the eruption may be vesiculo-bullous
with considerable swelling and erosion. In the more chronic low-grade reaction erythema, scaling and
fissuring predominate. Secondary bacterial infection is common. Prolonged shoe contact, hyperhidrosis,
and wet footwear increase the rate of allergic contact reactions.
- 99 IOC Sport Medicine Manual 2000
Specific types of contact dermatitis that are seen in sport include:
running shoes, from the rubber, adhesives or dyes
swim goggles, from the neoprene, producing a peri-orbital dermatitis
topical antibiotics, antihistamines or anesthetics that are used to treat common skin problems
adhesive tapes
lotions used in massage
Treatment of acute contact dermatitis includes cold compresses and attention to secondary bacterial
infection. If the reaction is severe, a three week tapering course of oral corticosteroids may be indicated.
For less severe reactions, strong topical corticosteroids will suffice. Further avoidance of contact with
the offending footwear is of paramount importance. If this is impossible, then new insoles, maintenance
of dry shoes, and clean, dry, cotton socks may reduce the problem.
Patch testing with specific compounds will help to identify the cause, however, false negative reactions
are common. It may be necessary to test the patient with water soaked shavings from the shoe to
further elucidate the cause of the dermatitis.
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A further condition of the sole that requires mention is juvenile plantar dermatosis. This is seen in
children and adolescents up to mid-puberty. It involves the weight-bearing aspects of the sole, especially
the forefoot as well as the toes. It is aggravated by recurrent wetting and drying of the foot and presents
as marked erythema and fissuring with a glazed appearance. Patch testing and fungal studies are
negative. Management includes reducing the wet/dry cycle by use of dry absorbent footwear, regular
lubricants such as petroleum jelly, and occasionally strong topical steroids.
The clinical diagnosis of our middle distance runner was an allergic contact dermatitis to the adhesive
used in the fabrication of the running shoe. She was advised to return to her prior shoes, to wear new
cotton socks, and to utilize an absorbent insole. Since the eruption was acute, the feet were soaked in
Burow’s solution followed by regular application of clobetasol cream. Arrangements were made for
patch testing after the Olympic trials.
2. Other Foot Dermatoses
a. Plantar Warts
Plantar warts are due to cutaneous infection with human papilloma virus (HPV). Such infection usually
resolves spontaneously without scarring. Plantar warts are caused by specific types of HPV which
infect the sole of the foot and are hallmarked by:
a break in the epidermal ridge pattern
tenderness on lateral rather than direct pressure
presence of thrombosed capillaries seen as small reddish brown spots
sharp demarcation from the surrounding skin
These features can best be appreciated after scalpel paring of the lesion.
Plantar wart infection may follow three patterns - solitary, multiple, or mosaic. This latter pattern is
due to the clustering of many small warts and indicates low patient resistance to the virus.
- 100 IOC Sport Medicine Manual 2000
Figure 3.13 Plantar Warts.
Treatment is aimed at maintaining pedal function, avoiding patient discomfort and scarring, and can
be achieved by:
application daily or every second day of 40-70% Salicylic Acid plasters with regular paring
and reapplication. Collodion based solutions may be more convenient.
occasionally, surgical removal can be undertaken but this should be reserved for a highly
selected minority of patients. The ideal surgical case is the patient with one or two warts
which are spontaneously painful or very tender and not in a major weight-bearing surface. If
a surgical approach is indicated, careful curettage should be employed. Haemostasis should
be achieved by chemical coagulants and pressure, rather than by electrodesiccation.
Excessive liquid nitrogen, electrodesiccation, excisional surgery, and certainly radiotherapy must be
avoided. In general, one is better to err on the side of conservative therapy in plantar warts.
b. Calluses
A callus is a thickened area of skin over pressure points usually on the sole or lateral foot. Most are
due to shearing or rotational forces. The skin is, in essence, the “innocent bystander” being pinched
between bone and shoe. Like other tissues, the skin hypertrophies under stress. A thin, tough, flexible
callus is a functional adaptation whereas a thicker, tender, fissured callus is dysfunctional. A callus
should be differentiated from a plantar wart. A callus has the following features:
continuation and accentuation of epidermal ridge pattern
direct pressure more tender than lateral pressure
absence of thrombosed capillaries (see Figure 3.14)
Treatment of a callus depends on the cause and usually involves improved foot-wear to spread out and
decrease the causative forces. Appropriate padding, customized insoles, or orthotics may be helpful.
- 101 IOC Sport Medicine Manual 2000
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liquid nitrogen is of limited benefit on the sole of many active athletes because of discomfort
associated with weight-bearing, but may be of use for selected warts in low pressure areas or
in the “off-season”.
Careful scalpel paring or pumice stone abrasion will help to decrease an excessively thick callus but
this represents treatment of the effect rather than the cause.
Figure 3.14 Callus.
A clavus is a specific type of callus seen under points of excess focal pressure such as the sole under
the second metatarsal head in a Morton’s foot. This presents as a conical core of keratin. Treatment is
as for a callus.
c. Black Heel (Talon Noir, Calcaneal Petechiae)
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Black heel is a painless and harmless condition due to microhaemorrhage in the upper dermis and
epidermis caused by shearing trauma in deceleration/acceleration activities such as court and racquet
sports. This can be differentiated from other pigmented lesions, including melanoma and plantar
wart, by paring. Superficial paring removes the pigment of black heel almost entirely, whereas this
would not be the case in a wart or melanoma.
Figure 3.15 Black heel.
d. Friction Blisters
Painful vesicles and bullae can be caused by an acute increase in intra-epidermal shearing forces.
Blister formation is promoted by heat and moisture, new or ill-fitting footwear or an abrupt increase
in activity.
Treatment of friction blisters includes:
draining the lesion with a sterile needle up to three times over the first 24 hours then applying
a compressive dressing
maintaining the roof of the blister as a natural protective cover if it is intact
using a sterile occlusive dressing if the roof is torn off
- 102 IOC Sport Medicine Manual 2000
observing closely for signs of infection and treating as necessary with soaks and antibiotics
changing activity or modifying rest to allow healing of the blister with maintenance of
conditioning is possible in most sports
Figure 3.16 Friction blisters.
Prevention of friction blisters includes:
slow break-in of new shoes
gradual increase of activity
using a thin inner and a thicker outer pair of socks
protecting incipient blisters or “hot spots” by appropriate padding when they start to develop
3 - Organ System Disorders
3. Contagious Skin Infection
Case History - Contagious Skin Infection
Seven to 10 days after a game, three rugby players from an Australian team presented with
painful skin eruptions on the head and neck. Recently they had noted fatigue and mild fever. Other
than acne there was no past history of skin problems.
On examination, the skin lesions were a scattering of vesicles on an erythematous base on the
head and neck with regional lymphadenopathy.
Discussion
There are a number of contagious skin infections that pose significant health concerns in contact
sports, such as rugby and wrestling, where the risk of transmission is high. This is such a problem that
the participants are regularly screened before competition and are excluded from participation if a
skin infection is found. These infections include:
a. herpes simplex (herpes gladiatorum, scrum pox)
b. staphylococcal impetigo
c. streptococcal impetigo
a. Herpes Simplex
Primary infection with herpes simplex virus (HSV) occurs when the human host has had no previous
immunological exposure to this virus. Primary cutaneous infection presents as scattered papules,
vesicles, and pustules in the area of contact. The patient is frequently ill with regional lymphadenopathy
- 103 IOC Sport Medicine Manual 2000
and intra-oral lesions may be present. The lesions may take three weeks or longer to heal. It is at this
time that the cornea is at particular risk of infection and auto-inoculation may occur. It is also during
this period that the virus travels up sensory nerve dendrites to take permanent residence in the nerve
cell ganglia. It is here that HSV infection remains in a latent phase.
Figure 3.17 Herpes simplex.
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Secondary infection, the common cold sore or fever blister, represents re-activation of the latent virus
rather than re-infection from external sources. The lesions present as clustered vesicles and pustules
on a red base and tend to be more localized. The patient usually has no malaise and limited adenopathy.
Intra-oral lesions are distinctly unusual and auto-inoculation is unlikely. The cornea is at markedly
less risk than with primary infection. Both primary and secondary lesions represent sources of infection
for other players who have not previously been infected with HSV.
Management of suspected herpes lesions includes:
light microscopic examination of a Giemsa or other blood stain from scrapings of the blister
base to look for multinucleated herpes infected giant cells
electron microscopy, if available, to visualize herpes virus
herpes virus cultures (herpes simplex should grow in about 48 hours in tissue culture)
oral acyclovir or famciclovir should be instituted as soon as possible in all primary cases and
in severe recurrences
topical treatment including topical acyclovir is of very limited value
bacterial culture may be of use for lesions which appear to be secondarily infected and, if in
doubt, appropriate antibiotics may be prescribed
b. Staphylococcal Impetigo
The primary lesion is usually a large bulla which develops into an erosion with a thin yellow-brown
crust and a collarette of scale. Pustules may be present in the surrounding skin or at distant sites.
Infection is spread by player to player contact or by fomites such as mats in wrestling. Superficial
abrasions may become impetigenized. The diagnosis can be confirmed by a Gram stain and bacterial
culture.
c. Streptococcal Impetigo
The primary lesion is a microvesicle that quickly evolves into a thick, yellow “honey-coloured” crust
on an erythematous base. There may be surrounding cellulitis, regional lymphadenopathy, malaise
and fever. Some strains of strep are nephritogenic and can result in post-streptococcal
glomerulonephritis. Therefore, systemic therapy and close follow-up with urinalysis is warranted.
- 104 IOC Sport Medicine Manual 2000
Again, the diagnosis can be confirmed by Gram stain and bacterial culture. Staph. aureus may coinfect streptococcal impetigo.
Treatment of impetigo includes:
systemicantibiotics (cloxacillin, erythromycin or cephalexin)
topical antibiotics (mupirocin, fusidic acid) may be useful in limited forms of staphylococcal
impetigo
antibacterial cleansers containing hexachlorophene or chlorhexidine
Figure 3.18 Streptococcal impetigo.
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An expanded list of skin problems that should result in disqualification from competition include:
herpes simplex
chicken pox (varicella) or herpes zoster
staphylococcal impetigo
streptococcal impetigo
secondary syphilis
Infestations that may result in disqualification include:
scabies
lice
Skin infections require accurate diagnosis. The athlete and coach should then be informed that it is in
the best interest of the teammates and opponents for a player to not act as a vector of infection. For an
athlete who is otherwise feeling quite well, withdrawing from competition takes maturity.
The three rugby players were diagnosed as having primary herpes simplex (herpes gladiatorum or
scrum pox). This was confirmed by a Giemsa strain and viral culture. They were advised to keep the
area clean and dry and were treated with oral acyclovir. Opthalmological consultation was sought to
rule out and prevent corneal infection. Players were not allowed to participate in any rugby matches or
practices until all crusting had cleared. Thereafter, they were able to rejoin the team.
- 105 IOC Sport Medicine Manual 2000
4. Sunburn
Case History - Sunburn
An 18-year-old novice rower enters her first regatta in late spring. This event will run all day
for 3 days. Your athlete is freckled with red hair.
Discussion
1.
2.
3.
4.
5.
What are the short and long term consequences of acute sunburn?
Who is at greatest risk of sunburn, and when is it most likely to occur?
How can sunburn be prevented?
What common drugs are photosensitizers?
How do you treat established sunburn?
Sunburn is caused by ultraviolet (UV) radiation, particularly UVB with a wavelength of 290-320nm.
It begins to appear 4-6 hours after exposure and maximizes at 24-48 hours. Your athlete could receive
considerable solar excess in the first day of the regatta without realizing the problem. Acutely, sunburn
causes redness, swelling and pain. More exposure leads to blistering, fluid imbalance and temperature
dysregulation. This would clearly affect her comfort, health and short term performance. Sunburns
acquired at a younger age are a significant risk factor for skin cancer, particularly malignant melanoma,
in later years.
3 - Organ System Disorders
The individual at greatest risk for sun damage has fair skin that readily freckles, always burns and
never tans. Red and blonde haired people with blue-green eyes and clear white skin are most susceptible.
The darker the innate skin colour, the lower the risk. The times of greatest sunburn risk are in late
spring and early summer and around mid-day when large quantities of UVB readily penetrate the
atmosphere. Remember that with daylight savings time solar noon is at 1 pm. Reflection off snow and
water can also be a significant factor.
Prevention is the best treatment for sunburn and involves 3 simple steps.
1. avoid direct solar radiation by seeking shade
2. cover exposed skin with appropriate clothing and hats
3. apply topical sunscreening agents
Our rower has no shade on the water, but much time at a regatta is spent off the water where shade is
available and should be utilized.
When exposed to sunlight, particularly between 10am and 4pm, the athlete should wear clothing to
cover as much skin as possible, and a hat with a minimum 3 inch (8 cm) all-around brim. The clothing
should be made of tightly woven opaque fabric. Dark colours will usually block more UV light, but
will also absorb more infra-red radiation causing heat build-up.
Sunscreening agents are effective at preventing sunburn if used properly. Sunscreens with a Sun
Protective Factor (SPF) of 15 or greater and preferably covering a the whole UV spectrum (UVB plus
UVA) are recommended. Some agents contain physical blockers such as zinc oxide and titanium
dioxide that reflect UV as well as chemical agents that absorb UV before it enters the living layers of
the skin. In athletes it is usually advisable to use a hat or other head gear to protect the scalp and
forehead, otherwise perspiration will cause sunscreen to run into and irritate the eyes.
- 106 IOC Sport Medicine Manual 2000
Some common drugs are photosensitizers, ie. they will augment sunburn. The list includes some
tetracyclines, thiazide diuretics, chlorpromazine and amiodarone.
The treatment of established sunburn is less than ideal and depends upon the degree of damage to the
skin. The first principle is to avoid further sun exposure. Aspirin and other NSAID’s will reduce
redness and pain in the first 24 hours only. Topical steroids will be of some value in mild sunburns.
Blistering and more severe sunburns should be treated as thermal burns utilizing cool compresses,
correcting fluid balance, attending to temperature regulation, observing for secondary infection, and
relieving pain with analgesics and a bed cradle to keep sheets off the skin. Systemic steroids may help
to reduce the inflammatory reaction, but only if started in the first day or two of the burn. Topical antihistamines and benzocaine-type anaesthetics should be avoided because of allergic sensitization. Shake
lotions such as calamine may soothe when applied but tend to “cake” on the skin and become
uncomfortable.
Our 18-year-old fair skinned rower would be advised to take the following measures to prevent sunburn:
stay in the shade between events
wear a brimmed hat and long-sleeved shirt and pants while warming-up on the water
wear a T-shirt rather than a singlet while racing
apply sunscreen to skin not shaded by hat and clothing, 1/2 hour before exposure
re-apply sunscreen before further races, as even waterproof sunscreen will be diluted by heavy
sweating
application to the hands may cause slipperiness when gripping her oar
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- 107 IOC Sport Medicine Manual 2000
K. Prevention of Infectious Disease Associated with International
Travel
Introduction
The current ease, breadth and speed of international travel effectively enlarges the global infectious
disease reservoir by allowing for rapid transport of infectious disease to regions remote from the
source of infection. The impact of travel-associated infectious disease may range from minor
inconvenience to life threatening illness, and is almost always problematic for the competing athlete.
Hence, it is incumbent on any physician caring for a travelling athlete to be aware of the risk for
travel-associated disease, to counsel prevention, and upon return from travel, to maintain a high index
of suspicion for acquired infection. In this section, personal prevention strategies are outlined, followed
by a brief overview of common infectious diseases associated with international travel, and concluding
with an approach to the returning traveller. More in depth discussion of tropical and infectious diseases
can be found in several excellent print and Internet resources listed at the end of the section.
1. Personal Prevention Strategies
Effective immunization and chemoprophylaxis does not exist for all travel-associated diseases. Personal
prevention strategies against food and water contamination, insect bites, and sexually transmitted
infections offer greater protection and should be emphasized.
Food Precautions
3 - Organ System Disorders
The majority of cases of traveller’s diarrhea are attributable to bacterial contamination of food.
Escherichia coli, Campylobacter, Shigella and Salmonella species are the primary causative
microorganisms. The global distribution of disease is inconsistent and a number of factors, including
climactic, geographic, agricultural, eating and sanitary practices, influence which diarrhea-causing
bacteria are more prevalent. Hence, general precautionary measures are most appropriate and can be
summarized in the statement “boil it, cook it, peel it, or forget it”.
Precautions against food contamination:
wash your hands with soap and water before eating
ensure meat and fish have recently been thoroughly cooked
eat only washed, self-peeled fruits and cooked fruits and vegetables
avoid raw/undercooked meats, fish, shellfish, vegetables and eggs
drink pasteurized or canned milk
avoid buffet food, food that has been rewarmed, or food that has been left out in the sun
eat street vendor food only if it is cooked in front of you and is served fresh and hot
Safe Drinking Water
Potable tap or ground water is unavailable in many parts of the world. Contamination with enteric
bacteria, viruses and protozoa, chemical and nuclear wastes, may not be immediately recognizable.
Therefore, it is prudent for any outdoor traveller or travellers to a developing country to take measures
to disinfect their drinking water. Appropriately filtered and chlorinated water is available in many
cities and resorts and is safe to drink, but this should not be assumed. The main mechanisms to
remove microorganisms from water include heat, chemical disinfection, filtration or some combination
thereof. Alternately, commercially bottled water, canned or hot beverages should be used.
- 108 IOC Sport Medicine Manual 2000
Precautions against water contamination:
boil drinking water (brought to boiling point and allowed to cool)
hot drinks (tea, coffee) are generally safe
commercially bottled or canned drinks, fruit juices, beer and wine are safe
filtered water using a pore size no greater than 4.0 microns will remove common parasites,
while a pore size of 0.2 microns is required to reliably filter bacteria. No field filtration device
is sufficient to remove viruses. Additional chemical treatment is needed
chemical treatments with iodine or chlorine are excellent disinfectants against bacteria and
viruses, but are less effective against parasites. At least 30 minutes should follow treatment
before drinking
beware of locally bottled or uncapped water bottles
avoid untreated tap water in mixed drinks, ice cubes, and when brushing your teeth
swim in pools with disinfected water or in salt water bodies away from sewage outlets or
river mouths
do not swim in fresh water rivers or lakes
avoid walking barefoot on beaches or soil
Insect And Mosquito Protection
Precautions against insect bites:
stay within well screened areas between dusk and dawn
sleep under a permethrin treated mosquito net if the room is unscreened
wear long trousers and long sleeved shirts when outdoors
apply mosquito repellants to exposed skin and clothing (permethrin)
Chemoprophylaxis
i. Traveller’s Diarrhea
Meticulous adherence to food and beverage precautions, as outlined above, decreases the likelihood
of developing TD. Prophylactic bismuth subsalicylate (Pepto-Bismol 2 oz. 4 times a day or two tablets
4 times a day) can decrease the incidence of diarrhea up to 60%, but is not recommended for prophylaxis
of TD for more than 3 weeks.
Prophylactic use of doxycycline, trimethoprim/sulfamethoxazole, trimethoprim alone, ciprofloxacin
and norfloxacin, is partially effective in preventing traveller’s diarrhea, but their effectiveness depends
on antibiotic resistance patterns. Fluoroquinolone resistance is least common, but is likely to increase
as these agents become more widely used. Furthermore, viral and parasitic diseases are unaffected by
antibiotics and travellers may develop a false sense of security. Known risks of antibiotic use include
- 109 IOC Sport Medicine Manual 2000
3 - Organ System Disorders
Mosquitoes, insects, ticks and biting flies are near ubiquitous. All may transmit disease. Mosquitoes
are either day or nighttime feeders. Those that transmit malaria and Japanese encephalitis (Anopheles
and Culex mosquitoes, respectively) feed primarily at dusk, whereas those that transmit dengue and
yellow fever (Aedes mosquitoes) feed during the day. Protective measures against insect bites are
underutilized, but offer the best protection against the most common mosquito-transmitted diseases,
malaria and dengue, and particularly since effective immunization for either does not exist. Personal
protection measures against mosquitoes will also protect against biting flies and ticks that may transmit
diseases such as Lyme disease, tick-borne encephalitis, typhus, leishmaniasis, trypanosomiasis and
others. A multifaceted approach, incorporating insect repellants, protective clothing and personal
behaviour is most effective.
allergic, skin, mucous membrane, blood and bowel adverse effects. Therefore, in light of the risk/
benefit ratio, prophylactic antibiotics are not recommended for traveller’s diarrhea. Current data instead
support the recommendation that travellers utilize prophylactic dietary measures and early treatment
(see section K 2).
ii. Malaria
Antimalarial medications for malarial chemoprophylaxis do not prevent infection, but rather prevent
parasite multiplication during the erythrocyte phase. In doing so, they are able to inhibit the clinical
illness. Therefore, effective measures against insect bites are to be strongly encouraged as the first
line of defence against malaria. Antimalarial medications for chemoprophylaxis are selected based on
the geographic distribution of chloroquine-resistant Plasmodium falciparum (CRPF). Detailed
information on malarial risk can be obtained from the Centre for Disease Control (CDC) (http://
www.cdc.gov/travel/regionalmalaria/index.htm) or the World Health Organization (http://www.who.int/
ith/english/map3.htm).
3 - Organ System Disorders
In brief, antimalarial regimens begin one week before travel or, if using proguanil or doxycycline, the
day before travel. Chemoprophylaxis is then taken for the duration of stay in the region of malaria risk
and continued for 4 weeks upon return. Adverse reactions are minor and should be weighed against
the risk of malaria. Presently, in areas of chloroquine sensitivity, including malaria risk areas in
temperate South America, central America (except in the region east of the canal in Panama), the
Caribbean, eastern Europe, north Africa, the Phillipines, Iraq, Syria, Saudi Arabia and Turkey,
chloroquine 5 mg base/kg by mouth per week is recommended. In areas of CRPF, including malaria
risk areas of tropical South America, the region east of the canal in Panama, central, east, west and
southern Africa, the Middle East, the Indian subcontinent, east and southeast Asia, Australia and the
south Pacific, mefloquine 5 mg/kg by mouth per week is recommended. The region along the ThailandCambodian border demonstrates both chloroquine and mefloquine-resistance and doxycycline 1.5
mg salt/kg by mouth once daily is currently recommended.
Immunization
Immunizations required for international travel are destination and traveller specific and vary according
to the traveller’s age, state of health, current immune status, coexisting medical conditions, the
destination, the nature and duration of travel, the time available prior to departure and legal requirements.
Hence, an up-to-date, in depth discussion of immunizations for travel is beyond the scope of this
section. The reader is referred to the CDC travel health website (http://www.cdc.gov/travel/), the
travel health recommendations of Health Canada’s Committee to Advise on Tropical Medicine and
Travel (http://www.hc-sc.gc.ca/hpb/lcdc/osh/tmp_e.html) the World Health Organization’s International
Travel and Vaccination Requirements (http://www.who.int/ith/english/index.htm). The WHO
recommendations are also available in a booklet format entitled International Travel and Healthvaccination requirements and health advice, from the WHO and most travel agents.
Completing an immunization schedule prior to departure is an essential step to prevent travel-associated
infectious disease. Ideally, travellers should inquire up to 8 weeks before departure to allow for multiple
doses of one or more vaccines. However, it is possible to give most vaccines at separate injection sites
during a single session if travel must be undertaken on short notice and the traveller is prepared to
tolerate the potential side effects. Those travellers with drug allergies, underlying chronic medical
conditions or altered immunocompetence may need to begin 3 months in advance.
- 110 IOC Sport Medicine Manual 2000
Currently Recommended Immunizations for Immune Competent Adults
Primary immunizations should be up-to-date, including:
Measles, Mumps and Rubella
Diphtheria, Tetanus and Pertussis
Polio
Hepatitis B
Varicella (for those without a history of chickenpox)
Additional or booster doses of Tetanus-diphtheria, polio and measles may be required. Influenza and
pneumococcal vaccines are recommended for adults aged 65 or older and other high-risk individuals
(eg. asplenic).
Additional recommendations vary according to the destination:
Yellow fever vaccine is recommended for travel to parts of Africa and South America
Hepatitis A vaccine is recommended for all travellers except those travelling to Australia,
New Zealand, Northern and Western Europe, Japan, and North America (excluding Mexico)
Typhoid vaccination is recommended for travellers spending time in regions where food and
water precautions are required
Meningococcal vaccine is recommended for travellers to sub-Saharan Africa during the dry
season (December through June)
Japanese encephalitis and/or tick-borne encephalitis vaccines should be considered for longterm travellers to areas of risk
Cholera vaccine is of questionable benefit since the risk of contracting cholera is low in
healthy travellers
Safer Sex
Travellers who have sex outside of a monogamous relationship, and particularly those who engage in
sex with overseas commercial sex workers in developing countries where sexually transmitted
infections (STIs) are hyperendemic, are at higher risk for a range of STIs, including hepatitis B,
hepatitis C and HIV. Isolation, anonymity and experience seeking may reduce social and sexual
inhibitions and precipitate higher risk behaviour. Although condoms offer protection against STIs
they are not 100% protective. Celibacy or monogamy carries a lower risk than the safest of “safer
sex”. Hepatitis B immunization and the consistent and proper use of latex condoms are strongly
recommended where sexual activity with a new partner may occur.
- 111 IOC Sport Medicine Manual 2000
3 - Organ System Disorders
Hepatitis B vaccine is recommended for travellers spending greater than 6 months in endemic
areas (Southeast Asia, Africa, Middle East, Amazon region of South America, and islands of
the South Pacific) or who will have frequent close contact with the local population
Precautions for safer sex:
plan ahead
get immunized against hepatitis B
talk about safer sex with your partner(s)
know your limits with alcohol and drugs
use a new latex condom every time you have sex
store condoms away from exposure to light or temperature extremes
nonoxynol-9 spermicidal may offer extra protection during vaginal intercourse against
gonorrhea and herpes
put the condom on before any genital contact
2. Disease Spread by Food and Water
a. Traveller’’s Diarrhea
Traveller’s diarrhea is the most common travel-associated infectious disease. As previously mentioned,
(see section K1 above), the majority of cases result from food and water contamination with enteric
bacteria and comprise an acute self-limiting illness of 4 to 6 days duration with symptoms of watery
diarrhea, low-grade fever, malaise, abdominal cramping, nausea and headache.
Most cases are caused by noninvasive pathogens, of which enterotoxigenic strains of E. coli (ETEC)
are the most commonly identifiable. Others causative agents include Norwalk virus, rotavirus, Giardia
lamblia and Vibrio cholerae. High fever with blood and pus in the stool suggests an invasive organism
such as Campylobacter, E. coli O157:H7, Salmonella, Shigella, or Entamoeba histolytica. Other, less
common causes of travel-associated diarrhea include Yersinia enterocolitica, Cryptosporidium,
Clostridium, anogenital gonorrhea, Hepatitis A or E, and shellfish and seafood toxidromes.
3 - Organ System Disorders
The severity of illness dictates the clinical approach and diagnostic work-up. Mild illness is effectively
self-managed and rarely presents for medical attention. For the traveller with fewer than 5 days of
diarrhea, and no dehydration, fever, abdominal pain, or blood or pus in their stools, the illness is
usually self-limited and further investigation is not required. More prolonged symptoms, or greater
illness severity, prompt assessment for evidence of dehydration, postural hypotension and systemic
toxicity. Oral rehydration is often successful and should be attempted, but intravenous hydration and
hospitalization may be needed. Laboratory investigations, including serum electrolytes, liver function
studies, blood cultures, a stool Methylene blue or Gram stain looking for leukocytes, and stool cultures
for bacteria and parasites should be considered in patients with invasive disease (dysentery) who are
systemically ill or severely dehydrated. Serologic tests for Entamoeba histolytica, rotavirus, Norwalk
virus and hepatitis A may be considered based on clinical features and community disease patterns.
Patients with gross blood or large numbers of stool leukocytes and severe illness should undergo
sigmoidoscopy to examine the bowel mucosa.
Bismuth subsalicylate (1 oz. of liquid or two tablets every 30 minutes for 8 doses) and antimotility
agents (eg. loperamide) provide prompt but temporary symptomatic relief of uncomplicated TD.
However, they should not be used in patients with high fever or bloody stools, and should be
discontinued if symptoms last greater than 48 hours.
Travellers with greater than three loose stools in an 8-hour period, particularly if accompanied by
fever, nausea, vomiting, abdominal cramps, or bloody stools, may benefit from antibiotic treatment.
The average 3- to 5-day illness can be reduced by over half with effective antimicrobial agents. Two
common and effective antibiotic regimes are TMP/SMX (160 mg TMP and 800 mg SMX) or
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ciprofloxacin (500 mg) taken twice a day for 3 days. Medical attention should be sought if the diarrhea
is severe, or fails to resolve within several days, if blood and/or pus is seen in the stool, if fever occurs
with shaking chills, or if there is dehydration with persistent diarrhea.
Most cases of diarrhea only require simple replacement of fluids and electrolytes and this is best
achieved with an oral rehydration solution such as the World Health Organization (WHO) Oral
Rehydration Salts (ORS) solution. ORS is prepared by adding one packet to boiled or treated water as
per instructions, and should be consumed or discarded within 12 hours if held at room temperature or
24 hours if kept refrigerated.
Table 3.1 WHO ORS for Diarrheal Illness.
Ingredient
Amount (grams/litre)
Sodium chloride
Potassium chloride
Glucose
Trisodium citrate
3.5
1.5
20.0
2.9
Iced drinks and noncarbonated bottled fluids made from water of uncertain quality should be avoided.
Dairy products and drinks with a high carbohydrate load can aggravate diarrhea in some people and
should be avoided.
b. Hepatitis A
In common with all forms of viral hepatitis, acute hepatitis A can be divided into prodromal, icteric
and convalescent phases. The incubation period for hepatitis A ranges between 2 to 6 weeks, followed
by rapid onset of clinical disease. Most cases are subclinical, but typical prodromal features include
non-specific symptoms of fatigue, malaise, anorexia, low grade fever, nausea and occasionally diarrhea.
Right upper quadrant tenderness and liver enlargement is commonly found. Darkening of the urine,
followed by scleral or palatine icterus and frank jaundice heralds progression to the icteric phase.
Pruritis is usually prominent. Symptom resolution occurs over a period of several weeks and, for the
majority of patients, liver function abnormalities return to normal within 3 months. Patients with
hepatitis A are infectious during the period of viral shedding, which begins approximately 2 weeks
before the onset of clinical disease and ends 1 to 2 weeks after.
Diagnosis of hepatitis A is formed on evidence of hepatic dysfunction and presence of antibodies to
hepatitis A virus (anti-HAV). Liver transaminases, alanine aminotransferase (ALT) and aspartate
aminotransferase (AST), are elevated and mark hepatocellular injury. Serum bilirubin levels generally
correspond to the degree of enzyme elevation, with the exception of widespread hepatocellular failure.
In this scenario, the functional capacity of the residual liver parenchyma may be so impaired that the
transaminase levels appear normal, but bilirubin levels remain high. Fulminant hepatitis is uncommon
with hepatitis A infection (0.5%). Almost all cases of acute hepatitis A resolve without sequelae and
no carrier state develops.
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3 - Organ System Disorders
Hepatitis A virus (HAV) is an RNA virus transmitted almost exclusively via fecal-oral contact. Poor
sanitation and personal hygiene of food handlers is the primary risk factor. Hence, although found
worldwide, it is predominantly seen in developing countries.
Hepatitis A can be prevented by administration of immune globulin (IG) or inactivated hepatitis A
vaccination. IG may be an alternative to vaccination when only short-term protection is needed. If
travelling for less than 3 months, travellers can be protected by a single intramuscular dose of 0.02 ml
per kg. However, hepatitis A vaccine, although initially more expensive, is more cost-effective and
longer lasting for the longer term or frequent traveller. Several hepatitis A vaccines are currently
available, have a seroconversion rate of greater than 95%, confer immunity against HAV within 4
weeks of immunization, and last for up to 10 years.
c. Enteric Fever
Typhoid and paratyphoid fever is caused by contact with food or drink that is contaminated with
Salmonella typhi or S. paratyphi. Both are characterized by sudden onset of sustained fever, severe
headache, nausea and anorexia. Paratyphoid fever generally runs a milder course. A hoarse cough,
constipation or diarrhea may also be present. Relative bradycardia is neither a sensitive nor a specific
sign and occurs in less than 50% of patients. Approximately a third of patients will have a faint
salmon coloured maculopapular truncal rash, and half will demonstrate hepatosplenomegaly.
The incubation period of S. typhi ranges from 5 to 21 days, followed by onset of diarrhea that may last
several days, and usually resolves prior to the onset of fever. The disease is communicable as long as
the bacteria remain present in affected individuals.
3 - Organ System Disorders
Enteric fever is uncommon in developed countries and the majority of cases are imported (Ryan et al.
1989). Students are a higher risk group. Typhoid vaccination is recommended for people travelling to
endemic regions of Africa, Asia, and Central and South America. The oral attenuated live vaccine is
better tolerated and appears as effective as the parenteral one. It is given in four doses on alternate
days. Typhoid vaccine is only about 70 percent effective in preventing infection with Salmonella
typhi and travellers must maintain vigilance with regard to food and water.
The annual occurrence of typhoid fever is estimated at 17 million cases, with approximately 600,000
deaths, despite availability of appropriate antibiotic therapy that can reduce case-fatality rates of 10%
to less than 1%. If untreated, 10% of patients will discharge bacteria for up to three months and 2 to
5% of patients will become permanent carriers.
Definitive diagnosis of enteric fever requires isolation of S. typhi or S. paratyphi from blood, bone
marrow, stool, or duodenal string cultures. Serologic tests, including the Widal test, have been developed
to detect S. typhi antigen or antibody, but none is sufficiently sensitive, specific, or rapid enough for
clinical use.
Treatment with chloramphenicol (500 mg orally four times daily) reduces typhoid fever mortality and
morbidity, but has been associated with a high relapse rate (10 to 25%), the emergence of resistance,
a high rate of chronic carriage, and bone marrow toxicity. Chloramphenicol is bacteriostatic against in
vitro S. typhi, whereas ceftriaxone, ampicillin, and the quinolones are bactericidal. Emergence of
chloramphenicol-resistant strains has prompted use of amoxicillin (1 g orally every 6 hours) and
trimethoprim-sulfamethoxazole (one double-strength tablet twice daily) as alternatives for treatment
of typhoid fever. In areas with a high prevalence of multidrug-resistant Salmonella infection (eg.
Indian subcontinent, Southeast Asia, and Africa), patients suspected of having typhoid fever should
be treated with a quinolone or third-generation cephalosporin until the results of culture sensitivity
studies become available. Ceftriaxone (1 to 2 g daily) administered either intravenously or
intramuscularly for 10 to 14 days is equivalent to oral or intravenous chloramphenicol administered
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for the treatment of susceptible S. typhi strains. After initial control of typhoid fever symptoms with a
parenteral third-generation cephalosporin, an oral agent may be used to complete 10 to 14 days of
therapy.
d. Worms
Case History - Worms
A 16-year old Kenyan male swimmer presents with a one-week history of intermittent fever,
malaise and muscle pains. He recalled patchy red, itchy skin approximately five weeks earlier
after swimming in a fresh water lake but this had resolved spontaneously. Physical examination is
unremarkable.
Discussion
i. Schistosomiasis
Schistosomiasis, second only to malaria in terms of socio-economic and public health importance in
tropical and subtropical areas, infects more than 200 million people world wide. Schistosome dermatitis
(swimmer’s itch) is seen when avian cercariae penetrate the skin of previously sensitized persons and
are destroyed. A pruritic papular rash begins within 24 hours after cercariae penetration and reaches
maximal intensity in 2 or 3 days.
Eggs deposited in tissue induce a granulomatous reaction, which, in the case of S. haemobium infections,
leads to lesions along the urinary tract. Left untreated, renal failure and bladder cancer may result.
Hepatosplenic involvement, including hepatic fibrosis and portal hypertension, is the most important
cause of morbidity in S. mansoni and S. japonicum infections.
Urinary schistosomiasis can be diagnosed by simple sedimentation and microscopic or macroscopic
hematuria is common. The eggs of intestinal schistosomiasis can be detected in fecal specimens by
sedimentation or between glass slides.
Praziquantel is effective against all forms of schistosomiasis and has few side effects. Metrifonate is
also safe and effective for treatment of urinary schistosomiasis, while Oxamniquine is used exclusively
in South America and Africa to treat intestinal schistosomiasis. Standard recommended treatment
consists of a single dose of praziquantel 40 mg/kg for S. mansoni, S. hematobium, and S. intercalatum
infection. In S. japonicum infection, a total dose of 60 mg/kg is recommended, given in two or three
doses over 24 hours. S. mekongi may require two treatments at 60 mg/kg.
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3 - Organ System Disorders
The major forms of human schistosomiasis are caused by five species of water-borne flatworms, or
blood flukes, called schistosomes, which vary biologically and geographically. Schistosomes enter
the body through contact with infested surface water and colonize the bladder (S. haemobium) or
intestines (S. mansoni and S. japonicum). The pathology of schistosomiasis varies according to the
invading species and the host immune response. Acute schistosomiasis (Katayama fever) may represent
an immune-complex disease, although immediate hypersensitivity and the inflammatory response
are also contributory. Acute schistosomiasis occurs 20 to 50 days after primary exposure and coincides
with egg deposition. The disease is marked by fever and chills, hepato-splenomegaly, lymphadenopathy,
weight loss, headache, and cough. An elevated white blood cell count with eosinophilia is typically
seen.
ii. Intestinal Worms
Intestinal roundworms, tapeworms and flukes are acquired by ingestion of contaminated food. Infected
patients are generally asymptomatic but may complain of vague abdominal discomfort. Clinical
symptoms are related to the worm burden, and in severe cases can produce intestinal obstruction,
perforated viscus, biliary tract obstruction and pancreatitis (Ascaris), or systemic dissemination
(Strongyloides). Prevention is achieved by personal strategies against contaminated food. Diagnosis
is variably made by stool examination and culture, serology and/or the duodenal string test
(Strongyloides) the Scotch tape test (Enterobius).
Pyrantel pamoate (11 mg/kg to a maximum of 1 gram in a single oral dose) and mebendazole (100 mg
by mouth twice daily x 3 days, or 100 mg by mouth in a single dose and repeated in 2 weeks for
Enterobius infection) are effective against Ascaris, Enterobius and hookworm. Thiabendazole (25
mg/kg by mouth twice daily, to a maximum of 3 grams per day, x 2 days, or 5 days for disseminated
Strongyloides) and albendazole (400 mg by mouth in a single dose) are additionally effective against
Strongyloides. Albendazole is also effective against Taenia. Praziquantel (75 mg/kg by mouth divided
in three doses over 24 hours) is recommended for treatment of intestinal flukes.
3 - Organ System Disorders
iii. Extraintestinal Worms
Extraintestinal tapeworms and flukes are also acquired by ingestion of contaminated food. Clinical
symptoms present after invasion of extraintestinal organs and vary according to the organ affected.
Hydatid disease results from deposition of larval cysts of Echinococcus species in liver (60%), lung
(25%), bone or brain. Surgical excision is preferred, but if not feasible, treatment with high dose
mebendazole or albendazole may be useful. Praziquantel is the treatment of choice for liver and lung
flukes.
3. Disease Spread by Arthropod and Animal Vectors
a. Malaria
Malaria is second only to tuberculosis as the most common cause of death due to communicable
disease. By far the most important tropical parasitic disease, it constitutes a major public health problem
for 40% of the world’s population. More than 90% of all cases of malaria occur in sub-Sahara Africa
where the majority of deaths occur among young children with poor health care access. Non-immune
expatriate travellers going to malaria endemic areas are also at high-risk and preventive measures are
strongly advised. Chemoprophylaxis (see section K1 above) is not effective against infection and
precautionary measures against insect bites remain the most important intervention.
Malaria is caused by species of Plasmodium – P. falciparum, P.vivax, P. ovale and P. malariae – a
single cell protozoal parasite transmitted from person to person by female Anopheline mosquitoes. Of
these, P. falciparum infection is the both the most common and the most lethal, accounting for 4060% of malarial cases worldwide and 95% of all malarial deaths. Transmission is influenced by
geography and climate, and is often associated with the tropical rainy season.
The natural life cycle of Plasmodium species involves a mosquito phase (sporogony) and a human
phase (schizogony). During sporogony, sexual forms (gametocytes) of the parasite unite to form
sporozoites. These, in turn, form a cyst within the stomach lining of the mosquito, which, following an
interval of 7-20 days, ruptures, allowing sporozoites to migrate to the salivary glands ready for
inoculation.
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Following human inoculation, sporozoites invade and replicate in the liver parenchyma (preerythrocytic schizogony or PE phase). This asymptomatic phase of incubation usually lasts 1 to 3
weeks, but can last up to a year with P. vivax infection. Mature forms (merozoites) rupture in the liver
and are released into the blood stream where they invade red blood cells and begin an asexual phase of
their life cycle (erythrocytic shizogony or E phase). A ball of merozoites, or schizont, forms within the
erythrocyte and eventually breaks to release more merozoites into the blood, which, in turn, invade
other red blood cells to amplify the infection. The erythrocytic phase is associated with the clinical
hallmark of a cyclical spiking fever, accompanied by chills and headache, which recurs every 48 to 72
hours depending on the species of Plasmodium. Malarial relapses may occur months later with P.
vivax and P. ovale infections secondary to latent liver parasites (hyponozoites) in exo-erythrocytic
schizogony or EE phase. P. malariae infections can persist at low levels for more than 30 years, but do
not induce malarial relapse from hyponozoites.
Table 3.2 from the Travel and Tropical Medicine Manual, 2nd Edition, Jong EC, McMullen R, Eds.
WB Saunders, 1995, p53.
Vector
Yellow fever
Dengue
Bancroftian filariasis
Typhus
Plague
African trypanosomiasis (sleeping sickness)
S. American trypanosomiasis (Chagas Disease)
Onchocerciasis (river blindness)
Loa loa (eye worm)
Visceral/cutaneous leishmaniasis
Sand fly fever (Papataci)
mosquito (Aedes aegypti)
mosquito (Aedes)
mosquito (Culex)
louse (Pediculus)
flea (Pulex)
tse-tse fly (Glossina)
kissing bugs (Reduviid)
black fly (Simulium domnosum)
horse fly (Chrysops)
sand fly (Phlebatomus)
sand fly (Phlebatomus)
P. falciparum malaria is more aggressive and potentially lethal than other species of Plasmodium
because it is able to invade all ages of red blood cells and produces overwhelming parasitemia, is
more often drug-resistant, and is the only human malaria parasite that produces microvascular disease.
Enhanced capillary and postcapillary venule endothelial cytoadherence and peripheral sequestration
of parasitized red blood cells, producing microvascular flow obstruction, organ hypoxia, hypoglycemia,
and lactic acidemia, is the most probable underlying pathology of the cerebral, renal and pulmonary
complications that accompany severe malaria.
Central nervous system dysfunction in cerebral malaria ranges from confusion and obtundation to
seizures and coma. Other causes of fever and CNS dysfunction, including meningitis, encephalitis
and hypoglycemia, should be considered and ruled out.
Acute renal failure is frequent in nonimmune persons with severe malaria. Some will require dialysis.
It generally presents as acute tubular necrosis and oliguria (blackwater fever). Hemolysis and
haemoglobinuric renal failure may also occur with use of quinine or primaquine in patients with
glucose-6-phosphate dehydrogenase (G6PD) deficiency.
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3 - Organ System Disorders
Disease
Light microscopy of thick and thin Giemsa-(preferred) or Wright-stained peripheral blood smears is
required to diagnose malaria and to identify the infecting species. Practically, it is less important to
identify the particular species of Plasmodium than to distinguish P. falciparum from the rest. Obtaining
blood smears for interpretation by an experienced observer should be considered part of the diagnostic
workup for any patient living in or returning from a malaria endemic area who presents with a fever.
Treatment of patients with malaria includes antimalarial drugs, supportive management of
hypoglycemia, lactic acidosis, seizures, renal failure and pulmonary edema, and consideration of
exchange transfusion for parasitemia greater than 15% in nonimmune persons (Miller et al, 1989).
Infections susceptible to chloroquine may be treated with 25 mg chloroquine/kg over 3 days given
orally if tolerated, or parenterally if unable to take oral medication.
Chloroquine-resistant P. falciparum may be treated with quinine (650 mg orally every 8 hours for 3
days) and pyrimethamine-sulfadoxine (3 tablets orally of1500 mg sulfadoxine/75 mg pyrimethamine
as a single dose), mefloquine (750 mg orally followed by 500 mg in 6-8 hours) or halofaltrine (500
mg orally every 6 hours x 3 doses and repeated in 1 week), but a drug other than the agent used for
chemoprophylaxis should be used. Parasites resistant to mefloquine are also generally resistant to
halofaltrine. Halofaltrine is contraindicated in pregnant and lactating women and has been associated
with QT prolongation, cardiac dysrrhythmias and death in susceptible persons with QT prolongation,
thiamine deficiency, or recent or concurrent use of mefloquine. Alternative medications should be
used when possible.
3 - Organ System Disorders
Chloroquine-resistant P. vivax is effectively treated with mefloquine (15 mg/kg orally as a single
dose) or halofaltrine (500 mg orally every 8 hours x 3 doses). Eradication of persistant P. vivax or P.
ovale hypozoites is usually achieved with primaquine(15 mg (26.3 mg primaquine phosphate) orally
once daily x 14 days).
b. Other Mosquito-Borne Disease
i. Dengue
Dengue is a mosquito-borne infection that has recently become a major international public health
concern. Dengue is found in tropical and sub-tropical regions around the world, and Dengue
haemorrhagic fever (DHF) is a leading cause of childhood mortality in several Asian countries. Dengue
viruses are transmitted to humans by female Aedes mosquitoes, and the spread of dengue is attributed
to expanding geographic distribution of the four dengue viruses and their mosquito vectors. The most
important mosquito vector, Aedes aegypti, is predominantly an urban species. The rapid rise in
urbanization exposes greater numbers of people to Aedes aegypti, and particularly in areas favourable
for mosquito breeding. Personal strategies against insect bites, in combination with insect control, are
currently the best prevention against dengue fever.
Dengue fever is a severe, flu-like illness that rarely causes death. The clinical features vary according
to the age of the patient. Infants and young children typically have a non-specific febrile illness with
rash, whereas older children and adults have either a mild febrile syndrome or an incapacitating
symptom complex with abrupt onset of high fever, severe headache, pain behind the eyes, muscle and
joint pains, and rash. The onset of illness is marked by a sudden rise in temperature in company with
facial flushing and non-specific constitutional symptoms. The fever usually persists for 2-7 days and
is often as high as 40-41° C. In moderate cases of DHF, signs and symptoms abate after the fever
subsides. Severe DHF, on the other hand, is a potentially lethal complication characterized by high
fever, haemorrhagic complications, and circulatory failure. Clinical management is focused on intensive
supportive therapy and maintenance of circulating fluid volume.
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ii. Yellow Fever
Yellow fever virus is a flavivirus that has been responsible for large epidemics in Africa and the
Americas. It is transmitted to humans and monkeys by Aedes and Haemogogus (S. America only)
mosquitoes in one of three transmission cycles: sylvatic (jungle), intermediate, or urban. Yellow fever
causes a wide spectrum of disease from mild symptoms to severe illness and death. Following a silent
incubation period of 3 to 6 days, the disease can progress through two phases. The acute phase is
characterized by fever and chills, backache, headache, anorexia, nausea and/or vomiting, and
paradoxical bradycardia. Resolution occurs over three to four days. However, 15% enter a toxic phase
in the subsequent 24 hours. The fever returns accompanied by jaundice, abdominal pain, vomiting,
and bleeding from the mouth, nose, eyes and/or stomach. Renal function deteriorates and can progress
to anuric renal failure. Mortality in the toxic phase approaches 50% while the remainder will usually
recover without significant organ damage. Diagnosis of yellow fever is made on the evidence of
blood serology. Treatment is supportive.
Vaccination is the single most important measure for preventing yellow fever. A vaccination certificate
is required for entry to many countries, and particularly for travellers arriving in Asia from Africa or
South America. Yellow fever vaccine is safe and highly effective, and offers protective immunity
within one week in 95% of people vaccinated. A single dose provides protection for 10 years and
probably for life. Mosquito control measures and personal strategies against insect bites are additionally
protective.
iv. Filariasis
Filarial worms are parasites transmitted by biting arthropods that carry the infective larval stage.
Depending on the species, macrofilariae, the adult worm stage, variably reside primarily in the
lymphatics (Brugia malayi, Brugia timori, Wuchereria bancrofti), skin (onchocerciasis, streptoserciasis,
and loiasis), or body cavities (Mansonella perstans) of humans. Lymphatic filariasis, the most common
type, presents as one of asymptomatic microfilaremia (detected incidentally on blood examination),
filarial fever with lymphangitis/lymphadenitis, and lymphatic obstruction. The diagnosis of filariasis
is often made on clinical suspicion, unless detection of microfilaremia is possible. Treatment is limited.
Diethylcarbamazine, 6 mg/kg per day in single or divided doses x 14 to 21 days, is effective against
microfilaremia, but not macrofilaria. Ivermectin, 150 mg/kg by mouth in a single dose, is the drug of
choice for onchocerciasis.
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3 - Organ System Disorders
iii. Haemorrhagic Fevers
In addition to Flaviviridae haemorrhagic syndromes (yellow fever and dengue), viruses of the
Bunyaviridae, Filoviridae and Arenaviridae families, such as Rift Valley Fever and Crimean-Congo
Haemorrhagic fever viruses, hantavirus, Ebola virus, Lassa fever virus, and viruses causing the various
South American haemorrhagic fever syndromes, induce an acute non-specific febrile illness, with
headache, myalgias and malaise, which is associated with vascular permeability haemorrhagic
complications and a high rate of mortality. Arthropod and rodent vectors carry the viruses and personal
avoidance strategies offer the best protection. Diagnosis is made by ELISA, reverse transcriptase
polymerase chain reaction, or cell culture in a BL-4 laboratory with maximal containment (eg. CDC).
Treatment is supportive. Ribavirin (loading dose of 33 mg/kg, 16 mg/kg every 6 h for 4 days, and 8
mg/kg every 8 h for 3 days) can be dramatically effective when given early.
c. Ticks
i. Lyme Disease
Lyme disease is caused by infection with the Borrelia burgdoeferi spirochete, which in turn is
transmitted by the bite of an Ioxdes tick. It is endemic in the northeastern United States and poses a
risk to people who travel in wooded or grassy areas. Tick nymphs are the most active feeders and are
seen primarily in the spring and early summer.
After an infected tick bite, the disease progresses through three stages. The initial stage is marked by
a spreading rash (erythema migrans) and may be associated with lymph node swelling and fatigue.
However, the rash is absent in 15% to 40% of infected people, which makes diagnosis difficult. If the
first stage is missed, the spirochetes are able to replicate and spread. A flu-like illness, with fever,
headache, fatigue, malaise, nausea, joint and muscle aching, and anorexia is typical. More severe
symptoms, including meningitis, encephalitis, cardiac conduction abnormalities, myopericarditis, and
cardiomyopathy may complicate the early phase of disseminated infection. The final stage is marked
by chronic changes including arthritis, chronic fatigue, polyneuritis, and encephalopathy.
All ticks should promptly be removed by grasping the tick as close to the skin as possible using a pair
of narrow-tipped forceps and slowing pulling upward until the tick releases its bite. Attempts to remove
a tick with caustics or heat should be avoided. If the patient presents within 48 hours, the prevalence
of Lyme disease is known to be low, or the patient is asymptomatic, then prophylactic antibiotics are
not required. An exception is made if the person is pregnant in light of the increased risk of spontaneous
abortion, premature labour and intrauterine growth retardation. Penicillin G or amoxicillin (500 mg
by mouth three times daily for 3 weeks) is recommended.
3 - Organ System Disorders
The diagnosis of Lyme disease is made on historical evidence of a tick bite or travel to a risk area, and
a symptom complex of erythema migrans (if present) and flu-like illness. Laboratory confirmation
using an ELISA should be performed, but should not delay antibiotic treatment. Doxycycline, 100 mg
by mouth twice daily for 14 to 21 days, is currently the intervention of choice. Severe disease may
require treatment with intravenous ceftriaxone (2 grams per day x 14 to 28 days).
ii. Rickettsiae
Louse-borne typhus, caused by Rickettsia prowazekii transmission by the human body louse, Pediculus
humanus corporis, can cause explosive epidemics in humans. It should be suspected when people in
crowded, louse-infected conditions experience sudden onset of high fever, chills, headaches, generalized
pain, and lassitude alternating with agitation, followed on the fifth or sixth day by a macular eruption.
Clinical diagnosis is confirmed by serology. A single 200 mg oral dose of doxycycline, irrespective of
the patient’s age, is curative.
Treating clothing with insecticide is simple and inexpensive, and affords protection for at least six
weeks, even with repeated washings. The pyrethroid insecticide, permethrin, is recommended.
d. Rabies
Rabies is a major public health problem in the developing world; an estimated 35,000 people die from
rabies worldwide each year. Dogs are the most commonly infected animal and are the primary source
of transmission to humans. In Canada, Europe, the Arctic and sub-Arctic regions, the principle carrier
is the fox. In Africa, jackals are the main wildlife reservoir.
Rabies is caused by a neurotropic rhabdovirus of the genus Lyssavirus. An infected animal may display
aggressive behaviour, ataxia, irritability, anorexia, lethargy, or excessive salivation. What may be
most apparent is a change in instinctive behaviour.
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Almost all cases of rabies have been transmitted by a bite. The virus replicates in muscle cells around
the site of the bite, then ascends via peripheral nerves to the central nervous system. The incubation
period ranges from 30 to 90 days, but bites on the head and neck have a shorter incubation period (as
short as 15 days) than bites on the trunk or lower extremity. The prodrome in humans is nonspecific.
Patients may present with headache, fever, runny nose, sore throat, myalgias, backache and
gastrointestinal symptoms. Paresthesias or pain at the bite site may be the first neurologic symptom
and progress to what appears to be a polyradiculitis until the encephalitis occurs.
Full-blown rabies occurs in two forms. The encephalitic form is marked by agitation, hydrophobia,
and extreme irritability. The less common paralytic form of resembles Guillain-Barre syndrome. Coma
and death are the final outcomes. Rabies is usually fatal within 3 to 10 days. Survival times are
improved with intensive care support but the outcome remains poor. No effective rabies treatment
currently exists. Pooled human rabies immune globulin, ribavirin and interferon administered after
onset of symptoms is ineffective.
The decision about postexposure prophylaxis after a bite depends on the type of exposure, the location
of the incident, and the biting animal. Bites are considered significant exposures. High-risk animals
are raccoons, skunks, foxes, and bats. Dogs in developing countries are also high risk. Bites of highrisk animals in areas where rabies is endemic require prophylaxis.
Prophylaxis consists of wound care, passive immunization, and active immunization. Treatment should
begin within 24 hours and discontinued if, after testing or consultation with public health officials,
prophylaxis is deemed unnecessary. Rabies is easily killed by sunlight, soap, or drying, and wound
care is an essential component of postexposure rabies prevention. Current recommendations are simply
immediate and thorough washing of all bite wounds with soap and water.
For individuals commonly exposed to rabies, pre-exposure prophylaxis is indicated. These include
veterinarians, animal handlers, and persons spending long periods in countries where rabies is endemic.
After a rabid exposure, patients who have had pre-exposure prophylaxis do not require HRIG and
HDVC given on days 0 and 3 only.
4. Disease Spread by Human Contact
a. Tuberculosis
Tuberculosis (TB) kills 2 to 3 million people each year and is the most common cause of death due to
infectious disease. In view of the spread of HIV/AIDS and the emergence of multidrug-resistant TB,
the World Health Organization has declared tuberculosis a global emergency. HIV and TB form a
lethal combination; TB is the leading cause of death among people who are HIV-positive. It accounts
for almost one-third of AIDS deaths worldwide, 40 percent of AIDS deaths in Africa, and 40 percent
of AIDS deaths in Asia. The traveller heading to regions where TB is endemic for any extended length
of time should consider pre- and post-travel skin testing.
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3 - Organ System Disorders
Immunoprophylaxis against rabies includes passive and active immunization. Human rabies immune
globulin (HRIG) 20 IU/kg is given at the time of the bite, one half as a local infiltrate into the wound,
the other half IM. Human diploid cell rabies vaccine (HDCV) is also given on the first day and four
subsequent injections are required. HRIG and HDCV should not be mixed in the same syringe.
Antimalarials, corticosteroids and other immunosuppressives interfere with development of active
immunity and should be withheld when possible.
Tuberculosis is caused by Mycobacterium tuberculosis, an aerobic, non-spore-forming bacillus. It is
characterized by a latency period between initial infection and clinical disease, a predilection for
tissue with a high regional oxygen tension (lungs) a granulomatous response.
Infection is spread almost exclusively by aerosolization of contaminated respiratory secretions.
Following inoculation, the inflammatory illness and tissue destruction are mediated by the host’s
response to the infection. Delayed type hypersensitivity is associated clinically with the development
of the tuberculin reaction. Skin test reactivity typically develops 4 to 6 weeks after infection, although
intervals up to 20 weeks have been noted.
Tuberculosis is generally classified in these internationally recognized stages:
TB 0: no exposure, no infection
TB I: exposure, no infection, and insignificant reaction to purified protein derivative (PPD) test
TB II: infection, no disease (positive PPD reaction), greater than 10 mm of induration
TB III: active disease
TB IV: inactive disease, history of previous tuberculosis; residuum of granulomatous disease visible
on radiograph
TB V: abnormal chest radiograph but unclear whether disease is active, pending sputum cultures;
can keep this classification only for 3 months
3 - Organ System Disorders
In general, hosts with more competent immunity tend to have disease limited to their lungs or other
single sites, whereas those with weakened defences experience disseminated disease. Overall, about
85% of adults present with pulmonary parenchymal disease, 15% with disease at extrapulmonary
disease, and approximately 4% with simultaneous intrathoracic and extrathoracic disease. Cough is
nearly universal. It progresses with increasing volumes of purulent secretions and the variable
appearance of blood streaking or gross haemoptysis. Fever is common and drenching night sweats are
typical. Malaise, fatigue, weight loss, non-pleuritic chest pain, and dyspnea are also common.
Localized crackles on lung auscultation are early findings, but signs of lung consolidation are rarely
heard. The chest radiograph is central to the diagnosis. Fibronodular shadowing involving one or both
apices is seen in the majority of cases. Sputum smears and cultures are more specific. Given the rising
prevalence of resistance to standard drugs, susceptibility testing on all initial M. tuberculosis isolates
is recommended.
Treatment for most patients is initiated before diagnosis is confirmed on culture, but care should be
taken to obtain optimal diagnostic specimens before commencing medication. Patients with active
tuberculosis should receive multiple agents both to prevent the emergence of drug-resistant mutants
and to accelerate the bacterial clearance. Recent CDC recommendations advocate a four-drug regimen
for most cases of known or suspected tuberculosis that incorporates isoniazid, rifampin, pyrazinamide
and ethambutol.
b. Hepatitis B and C
Case History - Hepatitis B and C
A 33-year-old male national team exercise physiologist presents with a two-day history of
malaise, headache, anorexia, generalized muscle and joint aching, and non-focal abdominal
discomfort. On examination, he is febrile (39° C), mildly jaundiced, and has palpable tenderness
in his right upper quadrant.
- 122 IOC Sport Medicine Manual 2000
Discussion
The differential diagnosis of fever and jaundice is extensive. In the context of recent travel, Table 3.3
provides a list of possibilities:
Table 3.3 Intrahepatic and extrahepatic differential diagnoses.
Intrahepatic:
Extrahepatic:
Viral Disease
Non-viral Infectious Disease
Toxic
Acute hepatitis
(A, B, C, D, E)
Herpes viruses
-Epstein-Barr
virus
-cytomegalovirus
-herpes simplex
Coxsachie virus
Yellow fever
virus
Sepsis
Malaria
Tuberculosis
Typhoid fever
Liver Abscess
Q fever
Drug
Lymphoma
hypersensitivity
Chemical
Secondary
syphilis
Leptospirosis
Toxoplasmosis
Schistosomiasis
Liver flukes
Ascariasis
Neoplasm
Cholecholithiasis
Cholangitis
Hepatitis B virus (HBV) is a DNA virus transmitted by contact with infected body fluids, including
saliva, blood and semen, that can cause acute hepatitis, chronic hepatitis and hepatocellular carcinoma
(HCC). It is 50 to 100 times more infectious than HIV and is now one of the major vaccine-preventable
diseases of humankind.
The incubation period for hepatitis B averages 12 weeks, with a range of 4 weeks to 6 months. Two to
4 weeks before onset of symptoms, hepatitis B surface antigen (HBsAg) appears in the serum, followed
by a rise in liver transaminase levels. HBsAg is usually cleared by 4 to 6 months and persistence
beyond 6 months suggests chronic infection.
Symptoms of acute hepatitis B typically last 4 to 6 weeks, ranging from subclinical disease to fulminant
hepatocellular failure and death. The fatality rate for acute hepatitis B is about 0.1 percent. Age,
immunocompetence, undefined host factors, and virulence are among the determinants of disease
severity.
Hepatitis B vaccine is recommended for universal vaccination in childhood and in high-risk groups.
Three deltoid injections are recommended: the first two given 1 month apart and the third given at 6
months. The duration of protection after hepatitis B vaccine is not definitively known but appears to
be at least 5 to 7 years. A combination of HBIG and hepatitis B vaccine is recommended for post
exposure prophylaxis. Early prophylaxis is paramount after an HBsAg needlestick; HBIG should be
administered immediately and without delay.
- 123 IOC Sport Medicine Manual 2000
3 - Organ System Disorders
Laboratory screening for hepatic dysfunction and acute hepatitis demonstrated elevated liver
transaminases and the presence of HBsAg thereby confirming the diagnosis of acute hepatitis B.
Unfortunately, despite hepatitis B being a recognized health hazard among health care personnel
exposed to body fluids, the physiologist had not been immunized. His symptoms of lassitude and
malaise lasted 5 weeks and he gradually recovered. By 4 months his liver transaminases had returned
to normal levels and HBsAg was no longer detectable.
Hepatitis C virus (HCV) is an enveloped RNA virus in the flaviviridae family now recognized as the
most common cause of post-transfusion hepatitis worldwide. Transmission primarily occurs via
unscreened blood, inadequately sterilized surgical equipment, or needle sharing among injection drug
users (IDU). Sexual and vertical perinatal transmission may also occur, and social, cultural and
behavioural practices using percutaneous procedures (ie. ear and body piercing, circumcision, tattooing)
may also be important.
HCV has a very high propensity (80%) of inducing chronic infection, of which an estimated 20% of
patients develop cirrhosis, and 1% to 5% of cirrhotic patients develop liver cancer within 10 years.
The clinically silent incubation period of HCV ranges from 15 to 150 days, followed by fatigue and
jaundice in approximately 10% of patients. The majority of cases are asymptomatic.
HCV is diagnosed serologically with an enzyme immunosorbent assay (EIA). False positives are
common and supplementary tests such as the recombinant immunoblot assay (RIBA) should be carried
out.
Treatment with interferon is effective in about 20% of patients. Ribavirin shows some promise against
HCV when used in combination with interferon, but does not appear to be effective when used alone.
Studies on combination therapy are under way.
In the absence of a vaccine, all precautions to prevent infection by other means, ie. blood screening,
rigorous sterilization, and personal risk-reduction strategies, must be taken.
c. HIV/AIDS
3 - Organ System Disorders
Human immunodeficiency virus (HIV) is a cytopathic retrovirus with a predilection for CD4 T
lymphocytes. As a result of infection, immunologic impairment eventually occurs, marked by severe
defects in cellular immunity and the development of opportunistic infections and neoplasms. AIDS is
diagnosed by laboratory evidence of antibodies to HIV and the presence of one or more indicator
conditions (Table 3.4)
Table 3.4 Indicator conditions for AIDS.
Indicator Conditions for the Diagnosis of AIDS
Esophageal candidiasis
Herpes simplex virus
CMV retinitis
Cryptococcosis
Cryptosporidosis
Mycobacterium avium complex
Pneumocystis carinii pneumonia
Pulmonary tuberculosis
Recurrent bacterial pneumonia
Brain toxoplamosis
Isosporiasis
Disseminated histoplasmosis
Disseminated TB
Recurrent Salmonella septicemia
Progressive multifocal leukoencephalopathy
Kaposi's sarcoma
Brain lymphoma
Invasive cervical cancer
HIV encephalopathy
HIV wasting syndrome
CD 4 cell count <200 cells/µL
- 124 IOC Sport Medicine Manual 2000
Worldwide, an estimated 30.6 million people are living with HIV or AIDS, and since the first reported
cases in 1981, an estimated 11.7 million people have died from HIV-related illnesses. The risk factors
for HIV infection are the same as for hepatitis B infection. Those at risk include neonates, haemophiliacs,
recipients of blood products prior to 1985, heterosexual partners of HIV infected persons, men who
have sex with men, and injection drug users.
Transmission is best reduced through personal risk reduction behaviour. Barrier methods such as
condoms are essential. HIV is a labile virus and is not transmitted through casual contact. It is easily
neutralized by heat or disinfectants such as a 1:10 solution of household bleach, 0.3% hydrogen
peroxide, 35% isopropyl alcohol, or 50% ethanol.
Acute HIV infection presents with a flu-like illness 2 to 4 weeks after exposure. Fever, sore throat,
fatigue, myalgias, and weight loss may persist for up to 2 weeks. Quantitative analysis of plasma HIV
RNA will allow a diagnosis of HIV infection to be made at this point. Seroconversion, denoting a
detectable antibody response to HIV, occurs 3 to 12 weeks after infection, but delays of up to 11
months have been reported. This is generally followed by a long asymptomatic incubation period that
averages 8.23 years for adults and 1.97 years for children under 5 years of age. CD4 count and viral
load is most reflective of disease stage. As CD4 cell counts fall below 500 cells/mL early symptoms
appear. Opportunistic infections and neoplasms manifest as CD4 counts fall below 200 cells/mL.
Antiretroviral therapy is directed to reducing levels of HIV RNA by interfering with activity of HIV
protease (protease inhibitors) and reverse transcriptase (nucleoside and nonnucleoside reverse
transcriptase inhibitors). Generally, antiretroviral therapy is started when the CD4 cell count falls
below 500 cells/mL, but drug side effects, drug interactions, preservation of immune function, and
the patient’s preferences must be taken into consideration.
d. Sexually Transmitted Infections
Sexually transmitted infections (STIs) are among the most common causes of illness. An estimated
333 million new STIs occur worldwide every year, and at least a third occur in people under 25 years
of age. Far-reaching health, social and economic consequences, including infertility and spread of
HIV, are often their unfortunate legacy.
STIs are often asymptomatic and are passed from partner to partner unknowingly. Risk factors for
STIs are similar to those for HIV and hepatitis B. Unprotected sex with a person who may have an
infection, including new partners, partners who have sex with others, and partners with a history of
injection drug use, body part piercing or tattoos, is the primary risk behaviour.
Travellers are at increased risk for STIs. Gonorrhea, chlamydia, genital herpes simplex, and human
papilloma virus (HPV) infections are most common, but unprotected sex in developing countries, and
in particular with commercial sex workers in regions of south and south-east Asia and sub-Saharan
Africa, will also expose travellers to HIV, hepatitis B, syphilis, lymphogranuloma venereum, chancroid,
and granuloma inguinale. Personal risk modification, emphasizing safer sex, condom use and
immunization against hepatitis B, is the best form of prevention. Treatment guidelines change frequently
and the reader is referred again to the websites of the CDC (http://www.cdc.gov/travel) or Health
Canada (http://www.hc-sc.gc.ca).
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3 - Organ System Disorders
The spectrum of clinical disease induced by HIV infection is greatly varied. Common community
infections and uncommon opportunistic infections are both seen. Prophylactic antibiotic therapy against
recurrent Pneumocystis carinii pneumonia and toxoplasmosis is an important preventive measure.
Oral trimethoprim-sulfamethoxazole (TMP-SMX) one double strength tablet once daily is preferred.
Gonorrhea is a common, but underreported disease. Up to 80% of infected women and 10% of infected
men are asymptomatic, do not seek treatment, and risk transmitting the disease to their sexual partners.
Disseminated gonorrhea occurs in up to 2% of untreated cases, and can lead to blindness and infertility.
Diagnosis is suspected on history of urethritis, cervical discharge, dypareunia and abdominal pain
and confirmed on Gram stain (Gram-negative intracellular diplococci) and culture. Urethral or cervical
swabs are routine and pharyngeal and/or rectal swabs should be considered if suggested by history.
Uncomplicated gonorrhea is effectively treated with a single dose of cefixime (400 mg by mouth),
cefuroxime axetil (1 gram by mouth), ceftriaxone (125 to 250 mg IM or IV), or one of several
fluoroquinolones. Chlamydial coverage should be instituted at the same time with one of doxycycline
(100 mg by mouth twice daily x 7 days), erythromycin (500 mg by mouth four times a day x 7 days),
or azithromycin (1 gram by mouth in a single dose). The single dosing regimes are useful for poorly
compliant patients.
Chlamydia, like gonorrhea, is a common disease, which has similar asymptomatic rates in women,
but higher asymptomatic rates in men. Since many infections are neither detected nor treated, prevalence
rates are high. Chlamydia infection is also a significant cause of pelvic inflammatory disease, infertility
and ectopic pregnancy.
Chlamydia trachomatis is the major cause of nongonoccocal urethritis and cervicitis. A clear urethral
or cervical discharge is more suggestive of chlamydia. Diagnosis is confirmed either by a urine
polymerase chain reaction test in men, or a cervical swab for culture. Treatment with a weeklong
course of a macrolide antibiotic (doxycycline, erythromycin) or a single dose of azithromycin is
recommended. Abstinence or barrier protection should be strongly encouraged for a week following
treatment.
3 - Organ System Disorders
Trichomonas vaginalis is a protozoa that causes symptoms in approximately 50% of infected women,
and may be associated with HIV seroconversion. It generally presents as vaginosis with discharge.
Wet preparations of cervical swabs or spun urine samples reveal the motile parasites. Treatment with
a single dose of metronidazole (2 grams by mouth) is effective.
Genital ulcer disease (GUD) is more common in tropical regions than in North America and Europe.
Herpes simplex accounts for the majority of GUD in North America and Europe, but falls well behind
chancroid, syphilis and lymphogranuloma venereum in tropical regions.
The genital ulcers produced by chancroid are a major risk factor for HIV transmission. The incidence
of chancroid varies greatly between countries and regions. In western Algeria, for example, chancroid
is the most common STI observed and the primary cause of genital ulcer disease. Culture of Hemophilus
ducreyi from the base of the pustular genital ulcer is diagnostic. Treatment is effected with singledose therapy with ceftriaxone (250 mg IM) or azithromycin (1 gram by mouth), or week long therapy
with erythromycin (500 mg by mouth four times daily) or amoxicillin/clavulanic acid (500 mg/125
mg by mouth three times daily).
Syphilis is a controllable and treatable disease; untreated, syphilis can lead to nerve and blood vessel
injury, mental disorientation, and eventually to death. Syphilis results from Treponema pallidum
infection and its clinical manifestations are protean. First-stage symptoms are small, painless ulcers
that appear three weeks after the primary infection and then resolve spontaneously. Second-stage
symptoms appear 1 to 6 months following the infection and include oral ulcers, a rash on the hands
and feet, lymphadenopathy and patchy alopecia. Finally, third-stage symptoms appear 2 to 40 months
after infection and include blindness, paralysis, deafness, brain and heart complications.
- 126 IOC Sport Medicine Manual 2000
Darkfield microscopic identification of spirochetes from lesions of primary or secondary syphilis is
the diagnostic gold standard. Nontreponemal serologic tests (VDRL and RPR) are useful for screening,
and treponemal serologic tests (FTA-ABS and MHA-TP) are useful for confirmation. False-positive
results occur with both types, but simultaneous false-positives are unusual. Lumbar puncture should
be performed in early syphilis with neurological symptoms and signs, or latent syphilis of greater
than 1-year duration.
Penicillin remains the treatment of choice. In primary, secondary and early latent syphilis, benzathine
penicillin G 2.4 million U IM is given. Alternatives include longer treatment regimes with ceftriaxone,
doxycycline or erythromycin. Syphilis infection in HIV-infected patients may benefit from benzathine
penicillin G 2.4 million U IM weekly for 3 weeks.
5. Fever in the Returning Traveller
Case History - Fever in the Returning Traveller
A 23-year-old wrestler from Hong Kong competed in a tournament in Pailin Kampuchea near
the Thai border a week ago. He presented 2 days ago with severe headaches, muscle, joint and
lower back pains, and is now complaining of abrupt onset of shaking chills, fever, and flushed dry
skin.
Two weeks following a tournament in the Dominican Republic, three members of the women’s
national volleyball team report complaining of a 3-4 day history of non-specific headache, anorexia,
malaise, and muscle and joint aching. On examination, all are moderately pyretic (37.8-39.4° C)
with a relative bradycardia. Two of the players are constipated and one has a non-productive
cough. The remainder of the physical examination is within normal limits.
Both of these cases demonstrate the non-specific presentation of fever in the returning traveller. Posttravel fever is an important symptom that should not be overlooked and can often present a diagnostic
challenge. Most are a result of self-limited illness, but others are due to highly infectious or potentially
lethal infectious diseases. Historical details, including pretravel immunizations, chemoprophylaxis,
destination, duration and nature of travel, is helpful in narrowing the potential causes. Estimated
incubation periods, fever patterns and symptom complexes may also be of assistance.
The primary diseases to consider are malaria, typhoid fever, arboviral infections (dengue, yellow
fever, and viral haemorrhagic syndromes), acute hepatitis, Rickettsial infections (Q fever, typhus,
tick-borne disease), bacterial enteritis/enterocolitis, and schistosomiasis. Noninfectious causes of fever
should also be considered.
Laboratory investigations to consider include thick and thin blood smears for malaria, complete blood
count and white cell differential, eosinophil count, liver function studies, hepatitis serology, blood,
urine and stool cultures, Dengue serology, chest radiographs, and TB skin test. Saving an acute serum
sample for future serology is prudent.
Patients should be hospitalized if severe malaria, typhoid fever, or viral haemorrhagic fever is suspected.
All cases of suspected viral haemorrhagic fever should be reported to local public health officials and
to the CDC.
- 127 IOC Sport Medicine Manual 2000
3 - Organ System Disorders
Discussion
Patients with less severe illness, and whose preliminary investigations are unremarkable, should keep
a temperature record over 48 to 72 hours and then return if unresolved, or earlier if worse.
Post-travel workup of the wrestler revealed positive blood smears for malaria, while blood cultures in
the volleyball players detected Salmonella typhi. All were treated successfully and eventually were
able to return to training and competition.
Summary
Travel-associated infectious diseases are common, may range from minor inconvenience to life
threatening illness, and are almost always problematic for the competing athlete. Pre-travel planning,
immunization and chemoprophylaxis, in combination with personal prevention strategies against food
and water contamination, insect bites, and sexually transmitted infections, offer protection and should
be emphasized. Post-travel fever is a potential harbinger of serious illness and must be treated with a
high index of suspicion, vigilance, and a comprehensive diagnostic workup.
L. Rheumatological Conditions
1. Single Swollen Joint
Case History - Single Swollen Joint
3 - Organ System Disorders
A 33-year-old triathlete presented with a 4 month history of a swollen right knee. He did not
recall injuring the knee. The knee pain and swelling was associated with prominent morning stiffness
for 2 hours and this was often worse after activity the day before. He gave a past history of patellar
tendinopathy, plantar fasciitis and psoriasis affecting the skin of his elbows and buttocks and
finger nails. His father also had psoriasis and arthritis affecting his hands and feet.
Examination revealed a warm, swollen right knee with quadriceps wasting. There were extensive
plaques of psoriasis over the buttocks and psoriatic nail dystrophy of the fingers and toes. There
was no restriction of spinal movement and no tenderness of the sacro-iliac joints.
Discussion
In the athlete with a single swollen joint without a history of trauma, a possible inflammatory cause
should be considered (see Table 3.5).
Common Conditions
Less Common Conditions
Gout/Pseudogout
Septic arthritis
Psoriatic arthritis (PsA)
Reactive arthritis (ReA)
Peripheral ankylosing
spondylitis (AS)
Peripheral enteropathic
arthritis (EnA)
Osteoarthritis (OA)
Pigmented villo-nodular
synovitis (PVNS)
Juxtaarticular bone tumors
Synovial sarcoma
Monoarticular rheumatiod
arthritis (RA)
Acute sarcoidosis
Table 3.5 Differential diagnoses of a single swollen joint.
- 128 IOC Sport Medicine Manual 2000
The key to the accurate diagnosis of alternative non-mechanical causes of a swollen joint is through
careful history, physical examination and an appropriate index of suspicion. Inflammatory joint
problems are characterized by pain, swelling, warmth, redness, night pain and prominent morning
stiffness. In all athletes, and especially in youngsters, inflammatory, infective or neoplastic conditions
should be considered in the light of these symptoms.
Many of these diseases are associated with extra-articular features which may provide additional
clues. Psoriatic arthritis may be associated with rash, nail dystrophy, enthesopathy or low back pain.
A history of inflammatory bowel disease (ulcerative colitis, Crohn’s disease or Celiac disease), urethral
discharge or eye inflammation may also provide clues in diagnosing enteropathic or reactive arthritis,
respectively. Rheumatoid arthritis is characteristically a small joint (hands, wrists and feet), symmetrical,
polyarthritis but can present as a single swollen joint in 15% of cases. Hypothyroidism,
hyperparathyroidism and haemochromatosis maybe associated with calcium pyrophosphate dihydrate
deposition in articular tissues (pseudogout or CPPD) and previous renal disease or diuretic use, may
give clues to diagnosing gout. It is important to remember that these associations should be actively
sought as they are unlikely to be proffered by the athlete. Septic arthritis is uncommon in the normal
joint but the possibility should be considered in arthritic or recently arthrocentesed joints and in diabetic
or immunocompromised patients. In many patients there may be a strong family history of inflammatory
arthritis.
Once sepsis has been excluded, treatment options include rest, NSAIDs, joint aspiration with intraarticular injection with corticosteroid and local anesthetic. This may need to be repeated. Troublesome
synovitis can be treated with arthroscopic synovectomy.
2. Low Back Pain and Stiffness
Case History - Low Back Pain and Stiffness
A 28-year-old male cyclist presented with a six year history of progressive low back pain and
stiffness. He did not recall an injury to his back. He experienced pain at night and was woken on
several occasions. His stiffness was worse in the morning, lasted for several hours, though was
eased with NSAIDs and gentle cycling. On direct questioning, he had an episode of iritis 4 years
earlier requiring topical corticosteroids. He has a brother diagnosed with ankylosing spondylitis.
Examination revealed limitation of lumbar spine range of motion, especially in lateral flexion.
He was tender to palpate and spring the sacroiliac joints, bilaterally. There was no peripheral
joint involvement or entheseal tenderness. Eyes and skin were also unremarkable.
- 129 IOC Sport Medicine Manual 2000
3 - Organ System Disorders
As well as examination of the affected joint, detailed physical examination should be performed
looking specifically for additional musculoskeltal involvement and for extra-articular manifestations
associated with a single swollen joint. This helps to accurately identify possible inflammatory causes.
Laboratory tests and imaging should be guided by the clinical findings to help confirm of refute a
suspected diagnosis. The clinician should avoid blanket screening. Infectious or inflammatory
conditions maybe associated with non-specific elevation of acute phase reactants (ESR, CRP). Synovial
fluid aspiration should be considered mandatory in cases of acute monoarthritis. If septic arthritis is
suspected, arthrocentesis must be performed before antibiotics are given. The choice of antibiotic can
be adjusted depending on the results of synovial fluid gram stain, culture and blood culture. Uric acid
(gout) or calcium pyrophosphate dihydrate (pseudogout) crystals maybe detected under polarized
light microscopy. It is important to remember that acute crystal arthropathy can be associated with
fever, leucocytosis and may mimic septic arthritis. Furthermore, these conditions may co-exist.
Discussion
Up to 10% of low back pain is associated with systemic illness. The challenge for the physician is to
be able to identify, diagnose and treat those patients with a non-mechanical cause for their low back
pain. The differential diagnosis includes inflammatory arthritis of the spine and sacroiliac joints
(spondyloarthropathy [SpA]). SpA is a generic term applied to the clinical, radiological and
immunogenetic features shared by a group of diseases that include ankylosing spondylitis (AS), reactive
arthritis (ReA) following genito-urinary or gut infection, psoriatic arthritis (PsA) and enteropathic
arthritis (Crohn’s disease, ulcerative colitis or coeliac disease) (EnA). These conditions are variably
associated with HLA B27. Individuals with these conditions frequently exhibit overlapping clinical
and radiological features.
SpA is more common in young men with near full disease expression by age 35 years and so commonly
presents to the sports medicine clinic. Pain is often worse at night, with prominent morning stiffness
(of 2 hours or more) though eased with gentle exercise and NSAIDs. Pain is often referred to the
buttocks or posterior thigh. With this pattern of back pain the physician should search for other relevant
features in the history. These include a past history of psoriasis or nail dystrophy (PsA), inflammatory
bowel disease (EnA), recent genito-urinary of gut infection (ReA). SpA is characterized by inflammation
of the entheses, commonly patellar tendon, achilles tendon and the plantar fascia. There may be
peripheral joint involvement. Asymmetric, lower limb, large joint inflammation is characteristic of
SpA. The shoulder or hip is involved in 30% of AS patients. A history of extra-articular involvement
may provide clues to the specific cause of the back pain syndrome. These include anterior uveitis
(iritis), the rash of keratoderma blenorrhagica or circinate balanitis (ReA), It is important that the
clinician actively seeks these associations, as the athlete may not link these features together.
3 - Organ System Disorders
Positive findings on physical examination include tenderness over the sacroiliac joints with perhaps
pain on sacroiliac springing. Restriction of lumbosacral spine movement occurs earliest in lateral
flexion. Examination must not be restricted to the spine and careful locomotor examination may
reveal evidence of enthesopathy or peripheral joint involvement. Thorough inspection of the skin
may detect previously unrecognized plaques of psoriasis. The umbilicus, natal cleft and scalp are
common sites and these changes may be subtle.
The diagnosis of SpA is essentially clinical. Investigations may help confirm or refute a suspected
diagnosis and should not be used as a blanket-screening tool. There may be a non-specific elevation
of acute phase reactants (ESR, CRP), particularly with peripheral joint involvement, but only 1/3 to 2/
3 of patients with active AS mount an acute phase response. HLA B27 is associated with AS in up to
95% cases and approximately 70% of patients with ReA are HLA B27 positive. The association is
weaker in EnA and PsA with only about 50% of spondylitics being HLA B27 positive. As 7% of the
general population are positive for HLA B27 there is no place for using HLA B27 as a screening tool
for back pain.
The detection of sacroiliitis on plain x-ray is required for the diagnosis of AS. Early changes include
erosion and sclerosis of the sacroiliac joint progressing to ankylosis. Concurrently, there may be
erosion at the edges of, and squaring of the vertebral bodies in the thoracolumbar spine progressing to
syndesmophyte formation and bony bridging (“bamboo spine”). These changes may take many (up to
10) years to develop. Plain radiography is therefore insensitive in identifying inflammatory spine and
sacroiliac lesions in athletes with a short history of symptoms. MRI, however, may detect up to 75%
of cases of x-ray negative early sacroiliitis, and this may be considered in such cases.
- 130 IOC Sport Medicine Manual 2000
The goals of treatment are to reduce pain and stiffness and to maintain posture and function. Exercise
therapy to maintain spine mobility and NSAIDs are the cornerstones of treatment. When peripheral
joints are involved (knees, shoulders) intra-articular corticosteroid injections may help.
3. Multiple, Painful, Swollen Joints
Case History - Multiple, Painful, Swollen Joints
A 35-year-old female recreational runner presented with a 2 month history of pain in both feet.
She had a sensation of walking on pebbles first thing in the morning lasting for a couple of hours
and also when running. In the last 2 weeks she had also noticed pain and swelling in both hands
and knees also worse in the morning. She experiences some benefit with NSAIDs. She had no
significant past medical history but had an aunt with rheumatoid arthritis.
Examination revealed tenderness, warmth and swelling of both wrists, metacarpo-palangeal
and proximal inter-palangeal joints of both hands. There were small effusions in both knees and
tenderness to squeeze the metatarso-phalangeal joints of both feet. There was no skin rash, alopecia,
mouth ulceration or cutaneous vasculitis. The remainder of the physical examination was
unremarkable.
Discussion
Occasionally patients may attend the sports medicine clinic with multiple joint problems. When faced
with the athlete with widespread joint pain and synovitis (polyarthritis), a methodical approach is
central to making an accurate diagnosis. In this section, we will discuss the differential diagnosis of
polyarthritis, the cardinal features on history and examination and the investigations of choice (see
Table 3.6).
Less Common Conditions
Rheumatoid arthritis
Viral Arthritis
- Parvovirus B19
- Epstein-Barr virus
Polyarticular psoriatic arthritis
Polyarticular gout/pseudogout
Polyarticular reactive arthritis
Inflammatory osteoarthritis
Systemic lupus erythmatosus
Lyme disease
Viral arthritis
- Hepatitis B, C
- Rubella
Rheumatic fever
Enteropathic polyarthritis
Overlap syndrome (with inflammatory
myositis, scleroderma)
3 - Organ System Disorders
Common Conditions
Table 3.6 Differential diagnoses of the patient presenting with a polyarthritis.
Polyarthritis with joint pain, stiffness and swelling should be distinguished from multiple joint pain
alone (polyarthralgia). Joint inflammation is characterized by night pain, prominent morning stiffness,
of at least 60 minutes, but often for hours, swelling, warmth redness and loss of function. In many of
these conditions the diagnosis is clinical. Attention must be paid to the onset and pattern of joint
involvement. Rheumatoid arthritis (RA) symmetrically affects the small joints of the hands, wrists
and feet (PIPs, MCPs, MTPs) with onset for 2/3 patients over weeks or months. Reactive arthritis
(following genito-urinary or gastrointestinal infection), on the other hand, is often more rapid in onset
- 131 IOC Sport Medicine Manual 2000
and has a propensity to asymmetric involvement of the large joints of the lower limb, together with
enthesitis or dactylitis. The duration of symptoms should be recorded. Parvovirus B19 polyarthritis
frequently affects young women looking after small children (mothers or school teachers) who develop
Parvovirus B19 infection (Fifth disease or “Slapped cheek” syndrome). It may be clinically
indistinguishable from early RA. Symptoms and signs usually settle within 6 weeks whereas RA
often follows a chronic and progressive course. The presence or absence or extraarticular manifestations
of rheumatological conditions may also aid accurate diagnosis. The pattern of joint involvement in
polyarticular pseudogout or psoriatic arthritis may resemble RA but without nodulosis, vasculitis or
other systemic features seen in RA.
Clinical examination should therefore not only involve the locomotor system, but a thorough evaluation
of all systems. The polyarthritis of systemic lupus erythematosus (SLE) maybe associated with alopecia,
mouth ulceration, cutaneous vasculitis or livido reticularis in the young female athlete. The characteristic
photosensitive facial rash in SLE is often follicular or sometimes urticarial in nature. The overlap
connective tissue disorders may be associated with Raynaud’s phenomenon, dyspepsia due to
oesophageal dysmotility, scleroderma of the hands and face and soft tissue calcification.
3 - Organ System Disorders
Investigations should only be requested to help confirm or refute a suspected diagnosis and must be
guided by the clinical findings There is no place for blanket screening tests as this is likely to lead to
a high number of false positive results. There may be a non-specific elevation of acute phase reactants
(ESR, CRP). Aggressive RA is associated with a highly elevated ESR in the early stages of disease.
Rheumatoid factor (RhF) and anti-nuclear antibodies (ANA) are frequently requested for the diagnosis
of RA and SLE respectively. RhF is positive in 75-85% of patients with RA, but may also be associated
with conditions other than RA including, Sjogrens syndrome, SLE and lung disease such as TB. Five
percent of the general population may be RhF positive. Anti-nuclear antibodies are found in nearly
100% of patients with SLE but ANA may also be found in individuals with other conditions such as
scleroderma, RA and chronic liver or lung disease. Up to 15% of healthy older persons may be ANA
positive. Rising IgM antibody titers to Borrelia burgdorferi may aid in the diagnosis of Lyme disease
when suspected. Likewise, antibody screening may help with the diagnosis viral arthropathies
(parvovirus B19, EBV and hepatitis). Where crystal arthropathy is suspected, arthrocentesis and crystal
microscopy should be performed. Radiographs of the hands and feet may detect early erosive change
in RA or psoriatic arthritis (not seen in SLE).
The treatment of polyarthritis will depend on the cause so accurate diagnosis is imperative. The clinician
may then consider referral to a rheumatologist. Treatment for RA often requires disease modifying
immuno-suppressive drugs such as methotrexate, sulphasalazine, hydroxychloroquine and
corticosteroids as well as NSAIDs. Flares in particular joints may respond to intra-articular
corticosteroid injections. A gradual return to sport may be considered once inflammation is better
controlled.
- 132 IOC Sport Medicine Manual 2000
M. References
Budgett, R. (1998). Fatigue and underperformance in athletes: the overtraining syndrome.
British Journal of Sports Medicine, 32, 107-110.
2.
CDC Travel Health Information
1-770-232-3228
3.
CDC Malaria Hotline for Physicians
1-770-488-7788
4.
Cook, GC. (Ed.). (1996). Manson’s Tropical Diseases, 20th Edition. WB Saunders.
5.
Hoffman, SL, Punjabi, NH, Kumala, S, Moechtar, MA, Pulungsih, SP, Rivai, AR, Rockhill,
RC, Woodward, TE, & Loedin, AA. (1984). Reduction of mortality in chloramphenicoltreated severe typhoid fever by high-dose dexamethasone. N Engl J Med, 310: 82-88.
6.
Hooper, SL & Mackinnon, LT. (1995). Monitoring overtraining in athletes. Sports Medicine.
Vol 20 pp 321-327.
7.
Huggins, JW, Hsiang, CM, Cosgriff, TM, Guang, MY, Smith, JI, Wu, ZO, LeDuc, JW, Zheng,
ZM, Meegan, JM, Wang. QN, et al. (1991). Prospective, double-blind, concurrent, placebocontrolled clinical trial of intravenous ribavirin therapy of hemorrhagic fever with renal
syndrome. J Infect Dis, 164: 1119-1127.
8.
Jong, EC, McMullen, R, ( Eds). (1995). The Travel and Tropical Medicine Manual, 2nd Edition,
WB Saunders.
9.
Mandell, GL, Bennett, JE, Dolin, R. (2000). Principles and Practice of Infectious Disease, 5th
Edition. Churchill Livingstone. (available on MD Consult at http://www.mdconsult.com).
10. Miller, KD, Greenberg, AE, Campbell, CC. (1989). Treatment of severe malaria in the United
States with a continuous infusion of quinidine gluconate and exchange transfusion. N Engl J
Med, 321: 65-70.
11. Ryan, CA, Hargrett-Bean, NT, Blake, PA. (1989). Salmonella typhi infections in the United
States, 1975-1984: Increasing role of foreign travel. Rev Infect Dis,11: 1-8.
For further information, refer to the following web sites:
http://www.cdc.gov/travel/
http://www.fims.org/state.html
http://www.hc-sc.gc.ca/hpb/lcdc/osh/tmp_e.html
http://www.hc-sc.gc.ca/hpb/lcdc/osh/reccom_e.html#catmat
http://www.istm.org/index.html
http://www.ncbi.nlm.nih.gov/PubMed/
http://www.netdoctor.co.uk/
http://www.sportsa.co.za/dsrindex/symposium.html
http://www.who.int/home/map_ht.html
http://www.who.ch/emc/outbreak_news
- 133 IOC Sport Medicine Manual 2000
3 - Organ System Disorders
1.
3 - Organ System Disorders
- 134 IOC Sport Medicine Manual 2000