Medical Problems Of Athletes

Chapte r4Medical  problems  of athletes    

 

Part One:  The environment and sport  •

Introduction

•

Heat

•

WBGT

•

Heat problems

•

•

○

Mild

○

Moderate

○

Severe

○

Classical heat stroke

○

Hyponatraemia

Cold problems ○

Frostbite

○

Cold urticaria

○

Prevention of cold problems

Altitude problems ○

Acute Mountain Sickness

○

High Altitude Pulmonary Oedema

○

High Altitude Cerebral Oedema

○

Retinal pathology

○

Chronic Mountain Sickness

Introduction Athletes do battle with themselves, their competitors and the environment. The result maybe glory,  

injury or illness. In this chapter we describe the medical and environmental problems facing athletes. Many are potentially serious but often maybe prevented by proper preparation and education.

 

Heat It is important to understand thermoregulatory factors. Thermoregulation results from reflex responses from the various temperature receptors in the skin, central vessels, viscera, and (preoptic area) anterior hypothalamus, signalling sympathetic shunting of blood and sweat gland stimulation when temp>37°C (Benzinger reflex). It is well depicted in Fig 1. The body maintains core temperature between the normal range of 36.1 to 37.8°C by balancing heat production/gain and heat loss. Heat is produced by metabolic functions (65 to 85 kcal/hour at rest) and work done by muscles (both smooth and skeletal; muscular contraction produces 300to 700 kcal/hour). Heat is gained by radiant energy from the sun(100 to 200 kcal/hour).Fever can add at a rate of 15% rise per degree F of fever. Heat is lost to the environment in the following ways: •

Radiation (65% heat loss, only works when body temp>ambient temp)

•

Evaporation (sweating, air-skin interface, the latent heat of evaporation is the amount of heat passed to the environment by vaporization (0.6 kcal of heat/ml sweat), it is the major physiological defense against over heating as the ambient temperature rises, reduced by high humidity as the ambient vapour pressure approximates moist skin).

•

Convection (needs air movement,12 to 15%)

•

Conduction (direct contact)

•

Reflected Radiation (from nearby surfaces)

WBGT (Fig 2) It is important to evaluate all aspects of the exercise environment viz. temperature, humidity, air movement (if outdoors) and solar radiation. This is done by the Wet Bulb Globe Temperature (WBGT) which is a single temperature, which is dependent upon air temperature, solar & ground radiation, humidity and wind velocity. It thus represents a sum of the impact of the environment upon the athlete. It can be measured with cheap simple instrumentation or calculated with data from the weather bureau (either degrees F or C).The WBGT calculation uses three measurements-natural wet-bulb temp(place a wetted wick over the thermometer bulb), air temp, and globe temp (temp. inside a copper globe painted flat black). It is calculated thus: •

Indoor WBGT = (0.7 x natural wet-bulb temp) + (0.3 x globe temp)

•

Outdoor WBGT=(0.7 x natural wet-bulb temp) + (0.2 x globe temp) + ( 0.1 x air temp)

Whether to or how to exercise in hot environments can be decided by considering the two criteria-RAL (Recommended Alert Limit - above which action should be taken to reduce heat stress) and – C (Ceiling Limit, above which exercise should not be undertaken without somehow changing the environment). This is illustrated in Fig 2.. This graph presents limits based on exercise intensity (energy expenditure per hour) and WBGT.

When the temperature is between C and RAL exercise is OK but with risk; therefore suggest this: •

Change the environment (fans or air conditioning) or move to area where WBGT is within acceptable limits

•

For the exercise session, decrease the intensity of the exercise (slow the pace and/or add rest periods).Useful guide is the TARGET HEART RATE (unchanged from cool conditions) .Exercise HR is increased one beat/min for every degree Centigrade above 25°C and two beats/min for every mmHG above 20mmHg water vapour pressure. Stick to a determined HR.

1.

MD Bracker 1992 Environmental and thermal injury Clin Sports Med 11(2) p 419-436

2.

M J Leski 1994 Thermoregulation and safe exercise in the heat. Chap 18 in Sports Medicine Secrets Ed M B Mellion Hanley and Belfus Phila p77-82

3.

W Larry Kennedy et al 1995Eds ACSMs Guidelines for Exercise Testing and Prescription 5th Ed Williams and Williams Phila p288-293

4.

National Institute for Occupational Safety and Health :Criteria for a recommended standard…occupational exposure to hot environments.DHHS NIOSH Publ No 86-113 US Dept Health and Human Services Wash DC 1986

5.

JT Marron JB Tucker 1994 Environmental Factors Chap 10 in Sports Medicine for the Primary Care Physician RB Birrer Ed CRC Florida p83

6.

WL Kenney E Kamon 1984 Comparative physiological responses of normotensive and essentially hypertensive men to exercise in the heat Eur J Appl Physiol 52 196-201

7.

JR Sutton Physiological and clinical consequences of exercise in heat an humidity Chap 2.4 in Oxford

8.

D Richards R Richards et al 1979 Management of heat exhaustion in Sydney’s The Sun City-to-City fun runner.Med J Aust 2 457-461

9.

W Larry Kennedy et al 1995Eds ACSMs Guidelines for Exercise Testing and Prescription 5th Ed Williams and Williams Phila p294

10. E Sherry D Richards 1986 Hypothermia amongst resort skiers Nineteen cases from the Snowy Mountains Med J Aust 144(9) 457-461 11.

See US Air Force Survival Manual 64-3

12. Aceazolamide is banned from Olympic competition 13. R B Schoene 1994Mountaineering and climbing Chap 96 in Sports Medicine Secrets Ed MB Mellion Hanlet and Belfus PA p430-434 with permission

14. PP Bartsch M Maggiorini C Ritter et al 1991 Prevention of high altitude pulmonary edema by nifedipine N Eng J Med 325 1284-1289

Marron and Tucker have provided a useful guide for exercise in the heat: Table 1

Table 1 Exercise in the Heat Football practice WBGT reading (°F)

Recommendations

60

Go ahead

61­66

Watch for >3% water loss

67­72

Take water onto field

73­77

Change schedule(30 min work/rest periods

78

Call off

Running

 

WBGT >82

Call off

73­82 red flag

High risk, put off until after 4pm or before  9am,not for those at risk

65­73 amber flag

Moderate risk

50­65 green flag

Minimal risk

<50 white flag

Risk of hypothermia esp slow runners in the cold  over long race

From Table 10-2 JT Marron JB Tucker 1994 Environmental factors In Sports Medicine for the Primary Care physician RB Birrer Ed CRC Florida p83 It is important to acclimatize to exercise in a hot environment.25% of the thought-to-be healthy population maybe heat intolerant if unacclimatized (but will decrease to 2% with proper preparation with aerobic exercise starting with a 10-15 min and over a 10-14 day period). Especially for those > 60 years (as thirst becomes less useful guide to hydration). The following conditions predispose to heat stress:  

•

HBP (alters control of skin blood flow)

•

diabetes (because of neuropathy)

•

drugs (diuretics, *-blockers, *-agonists, vasodilators, opiates, salicylates, thyroxine, CNS stimulants,

parasympatholytic or anticholinergics) •

alcohol

•

obesity

•

prior heat tolerance problems

The American College of Sports Medicine in 1984 recommended that endurance events were unsafe to be held if the WBGT >28 degrees.  

Heat problems These are a group of clinical presentations due to increased core temperatures which are generally classified into mild, moderate or severe. There is an increased risk in children, female athletes (where

prolonged exercise in the luteal phase) and older athletes. •

Mild

Presents as heat fatigue, (heat) cramps or syncope. Symptoms include weakness, fatigue and muscle cramps which occur during exercise, whereas fainting or dizziness usually occurs at the end of exercise (when venous blood pools). Usually of short duration but maybe excruciating. Signs are muscle tightness or cramps. Also see postural hypotension and tachycardia (heat syncope). Treatment is rest, ice and message cramps. Oral fluids. Lie in cool area and elevate legs if syncope. Remove excess clothing. Note other terms used: Heat oedema (self-limited swelling of hands/feet, resolves with acclimatization); heat tetany-carpopedal spasm; Miliaria rubra-maculopapular rash from keratin plugs over clothed areas, need better hygiene. •

Moderate

Also known as heat exhaustion. There is headache, weakness, exhaustion, nausea, vomiting, ataxia and mild confusion. Examination reveals increased sweating, hypotension (especially postural) and tachycardia. Raised core temperature is present but its significance is doubtful since well marathon runners can have temperatures up to 41 degrees Celsius. Rectal temperature should be measured to monitor athlete’s true temperature status and to exclude heat stroke. Treatment: Measures as for mild, as well as ice packs to groin and axillae and possibly intravenous fluids. •

Severe (Heat Stroke)

Core temp > 41°C. There is collapse with impaired consciousness from exercise. Note: Clinical picture may be masked by presence of hot, dry skin or cold and sweaty (therefore always take rectal temperature). •

Classical heat stroke

Occurs in those at risk (old, homeless, poor, ill, fat, drunk, drugged); whilst exertional heat stroke occurs in summer in those exercising. Treatment - Initiate ABC of resuscitation. Start rapid cooling (cool packs over neck/groin/axilla; atomized spray of warm air with fanning with warm air-The Mecca Cooling Unit) and intravenous fluids (one to two litres of dextrose-saline solution). Transfer to nearest hospital as this is a medical emergency with potentially life threatening multi-organ failure with DIC (with similarities to septic shock).

•

Pathophysiology and complications

In severe heat illness, this chain of events is seen: Heat injury * gut ischaemia * endotoxins enter portal circulation * hepatic clearance overwhelmed * cytokine release Dehydration and cytokines both contribute to hypotension and other complications. Complications of severe head illness include:

Cardiac

Postural hypotension, conduction disturbances,  myocardial infarct, and cardiac failure.

Neurological

Convulsions, cerebro­vascular events and coma.

Abdominal

Gastrointestinal bleeding, liver damage and renal  failure.

Other

Rhabdomyolysis or breakdown of skeletal  muscle membrane. This results in toxic 

 

metabolites such as myoglobin which may lead  to renal failure. Present with myoglobinuria  (brown urine) and raised serum phosphokinase  and potassium. An associated disseminated  intravascular coagulation may also develop.    Prevention (Guidleines established from the City to Surf Race in Sydney dating from 1971)

•

Wear appropriate cool, light coloured clothing

•

Stay well hydrated before, during and after exercise ( 2 cups cold water 15-20 mins prior exercise, one cup every 15 mins of exercise, and more than thirst demands afterwards).

•

Adequate physical fitness preparation for sport/event/conditions is essential. This may include heat acclimatization. The physiological adjustments in increased blood volume, venous tone and especially sweating, seen during acclimatization usually requires two weeks to take effect

 

(although this is variable). •

Avoid exercise in extreme heat (and humidity). At risk events and sports should have guidelines with medical advice.

•

Do not exercise with intercurrent illness(such as fever, URTI or gastroenteritis).

•

Proper planning with fluids, sunscreen and medical /or first aid cover.

•

Education of the early signs of heat illnesses.

•

Run within one’s capabilities

NOTE:ONE VICTIM OF HEAT STRESS MEANS OTHERS ARE AT RISK IN THE GROUP.   •

Hyponatraemia

This can cause collapse associated with exercise, in heat and is commonly mistaken for heat stroke.

Though only seen in ultra-endurance events (>34 hours),under extreme conditions, where profuse sweating, not acclimatized, thought to be caused by fluid overload from hypotonic drinks.  

Cold problems Though less of an immediate worry than heat stress, need to consider frostbite, exposure (hypothermia) and masking of angina (cold air and/or cold peripheries may mask the onset of angina, lower the threshold or cause angina at rest). Those involved in snow, water and mountaineering sports are at risk as well as endurance events in cold temperatures. The wind chill factor accelerates temp loss through convection and radiation. Hypothermia(defined as physiological state where core temp falls below 35oC) can be mild, moderate or severe and clinical features vary accordingly-

•

Mild: Core temp (34-36ºC). Athlete usually displays cold extremities, shivering, tachycardia, tachypnoea, urinary urgency, and slight incoordination. Patient is aware of this temperature loss.

•

Moderate: Core temp (32-34ºC). Blood sugars begin to fall and cerebral function begins to fail at 35ºC, with unsteadiness, muscle weakness, cramps and increased coordination. If warmth, shelter and food are found at this stage, recovery is rapid. If exposure to the cold continues, A FAILURE OF SHIVERING (the critical difference between mild and moderate as when shivering stops patient can no longer rewarm spontaneously and external heat is necessary) and a loss of vasoconstrictor tone results in an accelerating loss of temperature control. Speech becomes slurred, fatigue, dehydration, amnesia, poor judgement, drowsiness, anxiety and irritability takes place.

•

Severe: Core temp (<32ºC).Significant mortality with total loss of shivering, inappropriate behaviour, impaired or loss of consciousness(coma), muscle rigidity, hypotension, pulmonary oedema, extreme bradycardia, and cardiac arrhythmias ( especially ventricular fibrillation-VF).

Treatment: Measure the rectal temperature to assess the severity of hypothermia and to monitor treatment(the diagnostic dilemma of unexpected confusion and agitation in the snow is solved by measuring the rectal temp). Principles of treatment include basic life support measures (such as fluids, nutrition, and cardiac support), minimizing further heat loss, re-warming in a controlled manner, treatment of other injuries and transportation. It is a fallacy that voluntary activity increases body heat (in fact, movement increases peripheral blood flow and so increases body surface area exposure to the surrounding elements, resulting in increased heat loss and body heat requirements) Use full cardiac and oximetric monitoring, establish an IV, start CPR,(if necessary. REMEMBER THAT A COLD PATIENT IS NOT PRONOUNCEABLE AS DEAD UNTIL THEY ARE ‘WARM AND PINK’.CPR may need to be continued for well over an hour until you are convinced there are no sustainable signs of life in the rewarmed patient. This can be a difficult call-if possible talk to a more senior colleague). In a severely hypothermic and pulseless patient(suspended animation) CPR, at half standard rates, should only be started if full warming can be done. Establish airway(may need to intubate).Then institute re-warming manoeuvres. Re-warming maybe:

•

passive - insulation from wet, wind and cold. Removal of wet clothing and drying the body (even in dry snow!). Allowing the body to gradually re-warm by its own metabolic heat.

•

external active - hot packs and baths, heated aerosols, electric blankets, another body(such measures are adequate for mild or moderate hypothermia). Caution should be exercised in severe cases where shift of already reduced fluid volume to a warmed periphery may cause hypotension and a cardiac event.

•

internal active - warm drinks or food are reasonably simple measures. Most effective is venous to venous haemodialysis (raise temp 1-2°F/hour).Otherwise use nasogastric tube, urinary catheter, peritoneal catheter and enema tube with warm fluids. The rough handling of the patient can precipitate irreversible ventricular fibrillation.

Frostbite  

Frostbite is a local destruction of superficial tissues caused by cold exposure (commonly toes, fingers, ears), subdivided into: Frost nip

 

 Incipient frostbite with sudden blanching of skin  and is painless

Superficial

Skin place, waxy and firm but not frozen 

Deep frostbite 

Cold, pale, solid, fragile tissue

   Treatment is local re-warming, analgesia, protection (with blanket cotton wool) and gentle handling. Avoid rubbing area or applying snow and watch for secondary vascular occlusion by oedema, gangrene and infection. Possible use of calcium channel blockers (peripheral vasodilatation) and NSAIDs (protect against prostaglandin effects).

Cold urticaria Where patients exposed to cold similarly develop urticarial eruptions which may evolve into angiooedema. In severe cases may go to hypotension and syncope. A mast cell mediated, IgE dependent disorder, although cryoglobulins and cold agglutinins may be recognized in the blood. The urticaria may affect only the exposed limb. Previous asymptomatic exposure to cold stimuli does not exclude cold urticaria. Treatment is by re-warming, antihistamines and sympatheticomimetic agents if severe . Prevention of cold problems

•

Adequate preparation(clothing, communication, equipment, weather forecasts).

•

Stay well hydrated and nourished(chocolate bar in pack).Caution with alcohol.

•

Do not exercise to exhaustion.

•

Adequate fitness level for required activity including cold and altitude acclimatization if indicated. (NB. Cold acclimatization is less effective than heat acclimatization).

Note: Death in snow avalanche is from suffocation, injury, hypothermia(in that order).  

Altitude problems Distinct medical problems are encountered in sport at high attitudes and are made worse with rapid ascent. Performances at high altitudes are helped by reduced wind resistance and gravity, and worsened by the reduced oxygen pressure (FiO2 remains constant but *barometric pressure and so *PiO2 and possibly *PaO2 and *SaO2) and by the dropping temperatures (temperatures reduce by about 2C for every additional 300m above sea level). Changes with physical activity (acclimatization) at high altitude include: •

*pulmonary ventilation (with breathlessness), variable, may not become apparent for several days, leads to mild respiratory alkalosis(to counter the *PaO2)

•

*HR in order to *CO and offset the *SaO2(to maintain oxygenation),this*HR is transient(returns to N after 2-3 days however HRmax may remain below sea level value).Note target HR guidelines developed at lower altitudes are still useful guide in presence of high heat and humidity

•

*Vo2 max(by 5% at 4,000 feet)with *physical work capacity(and greater above 4,000feet)

•

*RBC(to*oxygen-carrying capacity blood)with shift of O2-haemoglobin curve over days to weeks

•

* capillary and *mitochondrial density over weeks

NOTE-Myocardial ischaemia may occur where CAD (because of relative hypoxia) A resolution was made at the 20th World Congress of Sports Medicine (Melbourne 1974) urging extreme caution at altitudes of more than 2290m (8700ft) and an absolute prohibition of contests above 3050m (10000ft). Various adaptations occur over varying time frames at altitude, including a reduction in bicarbonate, an increase in haemoglobin levels, a restoration of blood volume and an increase in various tissue enzymes. Problems encountered at altitudes include the following: Acute Mountain Sickness (over 8,000 feet), AMS With non-specific symptoms such as headache, dizziness, nausea, vomiting, irritability and insomnia from hyperventilation and associated acid-base disturbances. It is usually a temporary condition affecting the first 2 or 3 days of a rapid ascent over 2000m. There is mild tachycardia and peripheral oedema. Symptomatic treatment is usually adequate (rest, hydration, analgesics), in severe cases return to lower altitudes is advisable and the use of acetazolamide (125 mg bid) may help (beware diuretic effect on plasma volume).

High Altitude Pulmonary Oedema (over 10,000 feet), HAPE A life threatening (non-cardiac)condition occurring in the first few days of an ascent and manifests with symptoms dyspnoea, blood-stained(pink) frothy sputum, coughing, and chest discomfort/pain. Signs of tachycardia and tachypnoea, low grade fever and cyanosis.. It is more common in the presence of intercurrent cardio-respiratory conditions.O2 desaturation (moderate to severe)with relative

hypoventilation. Treatment is immediate descent, oxygen, nifedipine (20mg slow rel q8)and dexamethasone (4mg q6h). Note both these drugs thought to be useful but not proven. Hyperbaric therapy(if descent not possible). High Altitude Cerebral Oedema (above 12,000 feet), HACE A rare condition with severe headache, confusion, hallucination, impaired consciousness or coma. Signs of ataxia, focal neurological/visual signs, retinal haemorrhage. Usually associated with rapid ascents above 4000m. Moderate oxygen desaturation. Treatment is URGENT return to low altitude, oxygen and intravenous corticosteroids (dexamethasone 8mg bolus then 4mg q6h), hyperbaric oxygen bag (if descent not possible). LT to check Retinal pathology These small retinal haemorrhages are mainly benign and occur above altitudes of 4000m. Visual impairment can occur with central scotomata and impaired colour vision. Chronic Mountain Sickness (above 10,000 feet),CMS Takes months/years to develop. There is lethargy and reduced exercise capacity. Signs of plethora, peripheral oedema and conjunctival injection. Polycythaemia, hypercapnia (relative) and oxygen desaturation. Treatment is descent,O2 and respiratory stimulants (acetazolamide, progesterone, phlebotomy). Prevention is possible and essential. •

Avoid rapid ascents

•

Altitude acclimatization. Approximately 3 weeks at a moderate altitude (2500 - 3000m).

•

Appropriate medical screening(patients with pulmonary hypertension, uncompensated CHF, unstable angina, recent MI or severe anaemia are at greater risk when travelling to higher altitudes)

•

Education of participants about early symptoms, signs and management of altitude illnesses.

•

Susceptible patients(often young and healthy) need a slow gradual ascent with prophylactic use of nifedipine

•

Consider carrying a portable hyperbaric bag (In the USA, the Gamow Bag is available from Chinook Medical Products in Boulder, CO)

Chapte r4Medical  problems  of athletes  

Eugene Sherry, Sameer Viswanathan, Amitabha Das, and Lawrence Trieu  

 

Part One:  The environment and sport  •

Introduction

•

Heat

•

WBGT

•

Heat problems

•

•

○

Mild

○

Moderate

○

Severe

○

Classical heat stroke

○

Hyponatraemia

Cold problems ○

Frostbite

○

Cold urticaria

○

Prevention of cold problems

Altitude problems ○

Acute Mountain Sickness

○

High Altitude Pulmonary Oedema

○

High Altitude Cerebral Oedema

○

Retinal pathology

○

Chronic Mountain Sickness

Introduction Athletes do battle with themselves, their competitors and the environment. The result maybe glory,  

injury or illness. In this chapter we describe the medical and environmental problems facing athletes. Many are potentially serious but often maybe prevented by proper preparation and education.

Heat It is important to understand thermoregulatory factors. Thermoregulation results from reflex responses  

from the various temperature receptors in the skin, central vessels, viscera, and (preoptic area) anterior hypothalamus, signalling sympathetic shunting of blood and sweat gland stimulation when temp>37°C (Benzinger reflex). It is well depicted in Fig 1. The body maintains core temperature between the normal range of 36.1 to 37.8°C by balancing heat

production/gain and heat loss. Heat is produced by metabolic functions (65 to 85 kcal/hour at rest) and work done by muscles (both smooth and skeletal; muscular contraction produces 300to 700 kcal/hour). Heat is gained by radiant energy from the sun(100 to 200 kcal/hour).Fever can add at a rate of 15% rise per degree F of fever. Heat is lost to the environment in the following ways: •

Radiation (65% heat loss, only works when body temp>ambient temp)

•

Evaporation (sweating, air-skin interface, the latent heat of evaporation is the amount of heat passed to the environment by vaporization (0.6 kcal of heat/ml sweat), it is the major physiological defense against over heating as the ambient temperature rises, reduced by high humidity as the ambient vapour pressure approximates moist skin).

•

Convection (needs air movement,12 to 15%)

•

Conduction (direct contact)

•

Reflected Radiation (from nearby surfaces)

WBGT (Fig 2) It is important to evaluate all aspects of the exercise environment viz. temperature, humidity, air movement (if outdoors) and solar radiation. This is done by the Wet Bulb Globe Temperature (WBGT) which is a single temperature, which is dependent upon air temperature, solar & ground radiation, humidity and wind velocity. It thus represents a sum of the impact of the environment upon the athlete. It can be measured with cheap simple instrumentation or calculated with data from the weather bureau (either degrees F or C).The WBGT calculation uses three measurements-natural wet-bulb temp(place a wetted wick over the thermometer bulb), air temp, and globe temp (temp. inside a copper globe painted flat black). It is calculated thus: •

Indoor WBGT = (0.7 x natural wet-bulb temp) + (0.3 x globe temp)

•

Outdoor WBGT=(0.7 x natural wet-bulb temp) + (0.2 x globe temp) + ( 0.1 x air temp)

Whether to or how to exercise in hot environments can be decided by considering the two criteria-RAL (Recommended Alert Limit - above which action should be taken to reduce heat stress) and – C (Ceiling Limit, above which exercise should not be undertaken without somehow changing the environment). This is illustrated in Fig 2.. This graph presents limits based on exercise intensity (energy expenditure per hour) and WBGT. When the temperature is between C and RAL exercise is OK but with risk; therefore suggest this: •

Change the environment (fans or air conditioning) or move to area where WBGT is within acceptable limits

•

For the exercise session, decrease the intensity of the exercise (slow the pace and/or add rest periods).Useful guide is the TARGET HEART RATE (unchanged from cool conditions) .Exercise HR is increased one beat/min for every degree Centigrade above 25°C and two

beats/min for every mmHG above 20mmHg water vapour pressure. Stick to a determined HR.

1.

MD Bracker 1992 Environmental and thermal injury Clin Sports Med 11(2) p 419-436

2.

M J Leski 1994 Thermoregulation and safe exercise in the heat. Chap 18 in Sports Medicine Secrets Ed M B Mellion Hanley and Belfus Phila p77-82

3.

W Larry Kennedy et al 1995Eds ACSMs Guidelines for Exercise Testing and Prescription 5th Ed Williams and Williams Phila p288-293

4.

National Institute for Occupational Safety and Health :Criteria for a recommended standard…occupational exposure to hot environments.DHHS NIOSH Publ No 86-113 US Dept Health and Human Services Wash DC 1986

5.

JT Marron JB Tucker 1994 Environmental Factors Chap 10 in Sports Medicine for the Primary Care Physician RB Birrer Ed CRC Florida p83

6.

WL Kenney E Kamon 1984 Comparative physiological responses of normotensive and essentially hypertensive men to exercise in the heat Eur J Appl Physiol 52 196-201

7.

JR Sutton Physiological and clinical consequences of exercise in heat an humidity Chap 2.4 in Oxford

8.

D Richards R Richards et al 1979 Management of heat exhaustion in Sydney’s The Sun City-to-City fun runner.Med J Aust 2 457-461

9.

W Larry Kennedy et al 1995Eds ACSMs Guidelines for Exercise Testing and Prescription 5th Ed Williams and Williams Phila p294

10. E Sherry D Richards 1986 Hypothermia amongst resort skiers Nineteen cases from the Snowy Mountains Med J Aust 144(9) 457-461 11.

See US Air Force Survival Manual 64-3

12. Aceazolamide is banned from Olympic competition 13. R B Schoene 1994Mountaineering and climbing Chap 96 in Sports Medicine Secrets Ed MB Mellion Hanlet and Belfus PA p430-434 with permission

14. PP Bartsch M Maggiorini C Ritter et al 1991 Prevention of high altitude pulmonary edema by nifedipine N Eng J Med 325 1284-1289

Marron and Tucker have provided a useful guide for exercise in the heat: Table 1 Table 1 Exercise in the Heat Football practice WBGT reading (°F)

Recommendations

60

Go ahead

61­66

Watch for >3% water loss

67­72

Take water onto field

73­77

Change schedule(30 min work/rest periods

78

Call off

Running

 

WBGT >82

Call off

73­82 red flag

High risk, put off until after 4pm or before  9am,not for those at risk

65­73 amber flag

Moderate risk

50­65 green flag

Minimal risk

<50 white flag

Risk of hypothermia esp slow runners in the cold  over long race

From Table 10-2 JT Marron JB Tucker 1994 Environmental factors In Sports Medicine for the Primary Care physician RB Birrer Ed CRC Florida p83 It is important to acclimatize to exercise in a hot environment.25% of the thought-to-be healthy population maybe heat intolerant if unacclimatized (but will decrease to 2% with proper preparation with aerobic exercise starting with a 10-15 min and over a 10-14 day period). Especially for those > 60 years (as thirst becomes less useful guide to hydration). The following conditions predispose to heat stress:  

•

HBP (alters control of skin blood flow)

•

diabetes (because of neuropathy)

•

drugs (diuretics, *-blockers, *-agonists, vasodilators, opiates, salicylates, thyroxine, CNS stimulants,

parasympatholytic or anticholinergics) •

alcohol

•

obesity

•

prior heat tolerance problems

The American College of Sports Medicine in 1984 recommended that endurance events were unsafe to be held if the WBGT >28 degrees.  

Heat problems These are a group of clinical presentations due to increased core temperatures which are generally classified into mild, moderate or severe. There is an increased risk in children, female athletes (where prolonged exercise in the luteal phase) and older athletes. •

Mild

Presents as heat fatigue, (heat) cramps or syncope. Symptoms include weakness, fatigue and muscle cramps which occur during exercise, whereas fainting or dizziness usually occurs at the end of exercise (when venous blood pools). Usually of short duration but maybe excruciating. Signs are muscle tightness or cramps. Also see postural hypotension and tachycardia (heat syncope).

Treatment is rest, ice and message cramps. Oral fluids. Lie in cool area and elevate legs if syncope. Remove excess clothing. Note other terms used: Heat oedema (self-limited swelling of hands/feet, resolves with acclimatization); heat tetany-carpopedal spasm; Miliaria rubra-maculopapular rash from keratin plugs over clothed areas, need better hygiene. •

Moderate

Also known as heat exhaustion. There is headache, weakness, exhaustion, nausea, vomiting, ataxia and mild confusion. Examination reveals increased sweating, hypotension (especially postural) and tachycardia. Raised core temperature is present but its significance is doubtful since well marathon runners can have temperatures up to 41 degrees Celsius. Rectal temperature should be measured to monitor athlete’s true temperature status and to exclude heat stroke. Treatment: Measures as for mild, as well as ice packs to groin and axillae and possibly intravenous fluids. •

Severe (Heat Stroke)

Core temp > 41°C. There is collapse with impaired consciousness from exercise. Note: Clinical picture may be masked by presence of hot, dry skin or cold and sweaty (therefore always take rectal temperature). •

Classical heat stroke

Occurs in those at risk (old, homeless, poor, ill, fat, drunk, drugged); whilst exertional heat stroke occurs in summer in those exercising. Treatment - Initiate ABC of resuscitation. Start rapid cooling (cool packs over neck/groin/axilla; atomized spray of warm air with fanning with warm air-The Mecca Cooling Unit) and intravenous fluids (one to two litres of dextrose-saline solution). Transfer to nearest hospital as this is a medical emergency with potentially life threatening multi-organ failure with DIC (with similarities to septic shock).

•

Pathophysiology and complications

In severe heat illness, this chain of events is seen: Heat injury * gut ischaemia * endotoxins enter portal circulation * hepatic clearance overwhelmed * cytokine release Dehydration and cytokines both contribute to hypotension and other complications. Complications of  

severe head illness include: Cardiac

Postural hypotension, conduction disturbances,  myocardial infarct, and cardiac failure.

Neurological

Convulsions, cerebro­vascular events and coma.

Abdominal

Gastrointestinal bleeding, liver damage and renal  failure.

Other

Rhabdomyolysis or breakdown of skeletal 

muscle membrane. This results in toxic  metabolites such as myoglobin which may lead  to renal failure. Present with myoglobinuria  (brown urine) and raised serum phosphokinase  and potassium. An associated disseminated  intravascular coagulation may also develop.    Prevention (Guidleines established from the City to Surf Race in Sydney dating from 1971)

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Wear appropriate cool, light coloured clothing

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Stay well hydrated before, during and after exercise ( 2 cups cold water 15-20 mins prior exercise, one cup every 15 mins of exercise, and more than thirst demands afterwards).

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Adequate physical fitness preparation for sport/event/conditions is essential. This may include heat acclimatization. The physiological adjustments in increased blood volume, venous tone and especially sweating, seen during acclimatization usually requires two weeks to take effect

 

(although this is variable). •

Avoid exercise in extreme heat (and humidity). At risk events and sports should have guidelines with medical advice.

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Do not exercise with intercurrent illness(such as fever, URTI or gastroenteritis).

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Proper planning with fluids, sunscreen and medical /or first aid cover.

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Education of the early signs of heat illnesses.

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Run within one’s capabilities

NOTE:ONE VICTIM OF HEAT STRESS MEANS OTHERS ARE AT RISK IN THE GROUP.

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Hyponatraemia

This can cause collapse associated with exercise, in heat and is commonly mistaken for heat stroke. Though only seen in ultra-endurance events (>34 hours),under extreme conditions, where profuse sweating, not acclimatized, thought to be caused by fluid overload from hypotonic drinks.

 

Cold problems Though less of an immediate worry than heat stress, need to consider frostbite, exposure (hypothermia) and masking of angina (cold air and/or cold peripheries may mask the onset of angina, lower the threshold or cause angina at rest). Those involved in snow, water and mountaineering sports are at risk as well as endurance events in cold temperatures. The wind chill factor accelerates temp loss through convection and radiation. Hypothermia(defined as physiological state where core temp falls below

35oC) can be mild, moderate or severe and clinical features vary accordingly-

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Mild: Core temp (34-36ºC). Athlete usually displays cold extremities, shivering, tachycardia, tachypnoea, urinary urgency, and slight incoordination. Patient is aware of this temperature loss.

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Moderate: Core temp (32-34ºC). Blood sugars begin to fall and cerebral function begins to fail at 35ºC, with unsteadiness, muscle weakness, cramps and increased coordination. If warmth, shelter and food are found at this stage, recovery is rapid. If exposure to the cold continues, A FAILURE OF SHIVERING (the critical difference between mild and moderate as when shivering stops patient can no longer rewarm spontaneously and external heat is necessary) and a loss of vasoconstrictor tone results in an accelerating loss of temperature control. Speech becomes slurred, fatigue, dehydration, amnesia, poor judgement, drowsiness, anxiety and irritability takes place.

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Severe: Core temp (<32ºC).Significant mortality with total loss of shivering, inappropriate behaviour, impaired or loss of consciousness(coma), muscle rigidity, hypotension, pulmonary oedema, extreme bradycardia, and cardiac arrhythmias ( especially ventricular fibrillation-VF).

Treatment: Measure the rectal temperature to assess the severity of hypothermia and to monitor treatment(the diagnostic dilemma of unexpected confusion and agitation in the snow is solved by measuring the rectal temp). Principles of treatment include basic life support measures (such as fluids, nutrition, and cardiac support), minimizing further heat loss, re-warming in a controlled manner, treatment of other injuries and transportation. It is a fallacy that voluntary activity increases body heat (in fact, movement increases peripheral blood flow and so increases body surface area exposure to the surrounding elements, resulting in increased heat loss and body heat requirements) Use full cardiac and oximetric monitoring, establish an IV, start CPR,(if necessary. REMEMBER THAT A COLD PATIENT IS NOT PRONOUNCEABLE AS DEAD UNTIL THEY ARE ‘WARM AND PINK’.CPR may need to be continued for well over an hour until you are convinced there are no sustainable signs of life in the rewarmed patient. This can be a difficult call-if possible talk to a more senior colleague). In a severely hypothermic and pulseless patient(suspended animation) CPR, at half standard rates, should only be started if full warming can be done. Establish airway(may need to intubate).Then institute re-warming manoeuvres. Re-warming maybe:

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passive - insulation from wet, wind and cold. Removal of wet clothing and drying the body (even in dry snow!). Allowing the body to gradually re-warm by its own metabolic heat.

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external active - hot packs and baths, heated aerosols, electric blankets, another body(such measures are adequate for mild or moderate hypothermia). Caution should be exercised in severe cases where shift of already reduced fluid volume to a warmed periphery may cause hypotension and a cardiac event.

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internal active - warm drinks or food are reasonably simple measures. Most effective is venous to venous haemodialysis (raise temp 1-2°F/hour).Otherwise use nasogastric tube, urinary

catheter, peritoneal catheter and enema tube with warm fluids. The rough handling of the patient can precipitate irreversible ventricular fibrillation.

Frostbite  

Frostbite is a local destruction of superficial tissues caused by cold exposure (commonly toes, fingers, ears), subdivided into: Frost nip

 

 Incipient frostbite with sudden blanching of skin  and is painless

Superficial

Skin place, waxy and firm but not frozen 

Deep frostbite 

Cold, pale, solid, fragile tissue

Treatment is local re-warming, analgesia, protection (with blanket cotton wool) and gentle handling. Avoid rubbing area or applying snow and watch for secondary vascular occlusion by oedema, gangrene and infection. Possible use of calcium channel blockers (peripheral vasodilatation) and NSAIDs (protect against prostaglandin effects).

Cold urticaria Where patients exposed to cold similarly develop urticarial eruptions which may evolve into angiooedema. In severe cases may go to hypotension and syncope. A mast cell mediated, IgE dependent   

disorder, although cryoglobulins and cold agglutinins may be recognized in the blood. The urticaria may affect only the exposed limb. Previous asymptomatic exposure to cold stimuli does not exclude cold urticaria. Treatment is by re-warming, antihistamines and sympatheticomimetic agents if severe . Prevention of cold problems

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Adequate preparation(clothing, communication, equipment, weather forecasts).

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Stay well hydrated and nourished(chocolate bar in pack).Caution with alcohol.

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Do not exercise to exhaustion.

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Adequate fitness level for required activity including cold and altitude acclimatization if indicated. (NB. Cold acclimatization is less effective than heat acclimatization).

Note: Death in snow avalanche is from suffocation, injury, hypothermia(in that order).  

Altitude problems Distinct medical problems are encountered in sport at high attitudes and are made worse with rapid ascent. Performances at high altitudes are helped by reduced wind resistance and gravity, and worsened by the reduced oxygen pressure (FiO2 remains constant but *barometric pressure and so *PiO2 and possibly *PaO2 and *SaO2) and by the dropping temperatures (temperatures reduce by about 2C for every additional 300m above sea level). Changes with physical activity (acclimatization) at high altitude include:

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*pulmonary ventilation (with breathlessness), variable, may not become apparent for several days, leads to mild respiratory alkalosis(to counter the *PaO2)

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*HR in order to *CO and offset the *SaO2(to maintain oxygenation),this*HR is transient(returns to N after 2-3 days however HRmax may remain below sea level value).Note target HR guidelines developed at lower altitudes are still useful guide in presence of high heat and humidity

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*Vo2 max(by 5% at 4,000 feet)with *physical work capacity(and greater above 4,000feet)

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*RBC(to*oxygen-carrying capacity blood)with shift of O2-haemoglobin curve over days to weeks

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* capillary and *mitochondrial density over weeks

NOTE-Myocardial ischaemia may occur where CAD (because of relative hypoxia) A resolution was made at the 20th World Congress of Sports Medicine (Melbourne 1974) urging extreme caution at altitudes of more than 2290m (8700ft) and an absolute prohibition of contests above 3050m (10000ft). Various adaptations occur over varying time frames at altitude, including a reduction in bicarbonate, an increase in haemoglobin levels, a restoration of blood volume and an increase in various tissue enzymes. Problems encountered at altitudes include the following: Acute Mountain Sickness (over 8,000 feet), AMS With non-specific symptoms such as headache, dizziness, nausea, vomiting, irritability and insomnia from hyperventilation and associated acid-base disturbances. It is usually a temporary condition affecting the first 2 or 3 days of a rapid ascent over 2000m. There is mild tachycardia and peripheral oedema. Symptomatic treatment is usually adequate (rest, hydration, analgesics), in severe cases return to lower altitudes is advisable and the use of acetazolamide (125 mg bid) may help (beware diuretic effect on plasma volume).

High Altitude Pulmonary Oedema (over 10,000 feet), HAPE A life threatening (non-cardiac)condition occurring in the first few days of an ascent and manifests with symptoms dyspnoea, blood-stained(pink) frothy sputum, coughing, and chest discomfort/pain. Signs of tachycardia and tachypnoea, low grade fever and cyanosis.. It is more common in the presence of intercurrent cardio-respiratory conditions.O2 desaturation (moderate to severe)with relative hypoventilation. Treatment is immediate descent, oxygen, nifedipine (20mg slow rel q8)and dexamethasone (4mg q6h). Note both these drugs thought to be useful but not proven. Hyperbaric therapy(if descent not possible). High Altitude Cerebral Oedema (above 12,000 feet), HACE A rare condition with severe headache, confusion, hallucination, impaired consciousness or coma. Signs of ataxia, focal neurological/visual signs, retinal haemorrhage. Usually associated with rapid ascents above 4000m. Moderate oxygen desaturation. Treatment is URGENT return to low altitude,

oxygen and intravenous corticosteroids (dexamethasone 8mg bolus then 4mg q6h), hyperbaric oxygen bag (if descent not possible). LT to check Retinal pathology These small retinal haemorrhages are mainly benign and occur above altitudes of 4000m. Visual impairment can occur with central scotomata and impaired colour vision. Chronic Mountain Sickness (above 10,000 feet),CMS Takes months/years to develop. There is lethargy and reduced exercise capacity. Signs of plethora, peripheral oedema and conjunctival injection. Polycythaemia, hypercapnia (relative) and oxygen desaturation. Treatment is descent,O2 and respiratory stimulants (acetazolamide, progesterone, phlebotomy). Prevention is possible and essential. •

Avoid rapid ascents

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Altitude acclimatization. Approximately 3 weeks at a moderate altitude (2500 - 3000m).

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Appropriate medical screening(patients with pulmonary hypertension, uncompensated CHF, unstable angina, recent MI or severe anaemia are at greater risk when travelling to higher altitudes)

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Education of participants about early symptoms, signs and management of altitude illnesses.

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Susceptible patients(often young and healthy) need a slow gradual ascent with prophylactic use of nifedipine

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Consider carrying a portable hyperbaric bag (In the USA, the Gamow Bag is available from Chinook Medical Products in Boulder, CO)