We are pleased that our Leader has engendered interest, thank Prof
Lippi and his colleagues for their letter, and are grateful to the Journal
for the opportunity to reply. We fully agree with their ideas: using
normative data from non-athletic population may well result in over-
investigation and unnecessary worries for athletes. This is why we believe
that serum concentrations of the enzymes in quest...
We are pleased that our Leader has engendered interest, thank Prof
Lippi and his colleagues for their letter, and are grateful to the Journal
for the opportunity to reply. We fully agree with their ideas: using
normative data from non-athletic population may well result in over-
investigation and unnecessary worries for athletes. This is why we believe
that serum concentrations of the enzymes in question should be only part
of the picture, and accurate clinical history and examination should still
rule: a purely mechanistic approach would not serve our patients well.
Also, data should be generated for oher sports: for example, athletes
involved in contact sports and high level martial arts seem to have higher
levels of CK than endurance athletes[1], as have athletes on anabolic
steroids, as pointed out in our Leader. In the absence of a clinical picture of frank pathololgy, we would not
subject these athletes to tests. Furthermore, to further diminish
unnecessary invasive investigations, if CK and LDH levels are elevated, we
suggest a rest from athletic activities for two weeks before testing again
CK and LDH levels[2]. If still elevated, then further, more invasive,
investigations may be necessary
Paola Brancaccio, Francesco Mario Limongelli, Nicola Maffulli
Seconda Università di Napoli
Department of Experimental Medicine
Centre of Excellence of Cardiovascular Disease
Napoli, Italy (PB, FML)
Department of Trauma and Orthopaedic Surgery
Keele University School of
Medicine
Thornburrow Drive
Hartshill, Stoke on Trent
ST4 7QB Staffs
ENGLAND (NM)
I read with interest the article written by Dr. G.J. Buse entitled,
No holds barred sport fighting: a 10 year review of mixed martial arts
competition published in the 6 February 2006 edition of your journal. As
a researcher focused on injury prevention, I have recently been part of a
research group reviewing data from both mixed martial arts competitions
and professional boxing and enjoyed reading...
I read with interest the article written by Dr. G.J. Buse entitled,
No holds barred sport fighting: a 10 year review of mixed martial arts
competition published in the 6 February 2006 edition of your journal. As
a researcher focused on injury prevention, I have recently been part of a
research group reviewing data from both mixed martial arts competitions
and professional boxing and enjoyed reading the information presented by
Dr. Buse.
In an article published in October 2005 in the Southern Medical
Journal, our research group attempted to define the overall injury rate of
athletes participating in professional boxing.[1] We reviewed data from
the fight cards published by the Nevada State Athletic Commission and
noted any injury comments recorded by the ringside physicians. Our
research demonstrated an overall injury rate of 17.[1] injuries per 100
boxer-matches with 11.3% of those matches ending in knockout.
In an attempt to compare boxing injuries to mixed martial arts (MMA)
injuries, we did a review of the fight cards for MMA matches using the
same protocol as for the professional boxing matches. Our data—to be
published soon by The Journal of Sports Science and Medicine—indicate that
the overall injury rate for MMA matches is similar to professional boxing
and the knockout rate is almost half that of professional boxing.[2]
In reviewing Dr. Buse’s data, I would have liked to have seen a
comparison of injury rates before and after the sanctioning of the sport
in September 2001. Though MMA began in the United States in 1993, these
first fights only superficially resemble MMA matches today and were really
very different competitions. Sanctioning brought about many rule changes
that mandated weight classes, time limits for rounds and matches, and
eliminated many of the most dangerous techniques including stomps, head
butts, and groin attacks. Combining MMA matches prior to sanctioning with
the sanctioned matches of today is confusing and is not helpful in
attempting to determine the true injury risk for participants in these
competitions.
It should also be noted that although there were five deaths in the
boxing ring in the United States during 2005, there has never been an MMA
death in the United States. The death cited by Dr. Buse occurred in an
unregulated event during 1998 in the Ukraine.[3] MMA fighters in the
United States now must pass all the prefight screening tests of
professional boxers and are supervised by referees and ringside
physicians. It is important not to lump MMA competitions with the
infamous “Toughman” competitions—a “sport” that matches amateur
participants against trained fighters using “one size fits all” protective
gear and often supervised by chiropractors and other untrained medical
staff—when comparing MMA to other combat sports. While MMA has never had
a casualty in the United States, at least 12 deaths have resulted from
Toughman competitions.[4]
MMA also has some rules that seem to be an improvement over
professional boxing. The fact that MMA has no “standing eight count”
enabling a concussed participant time to recover and continue fighting is
a tremendous step toward diminishing traumatic brain injury. Furthermore,
by allowing leg and arm attacks opponents have a more diverse target area
and do not focus solely on attacking the head, and if in trouble, a
participant can “tap out” to signify his desire to end the match. In our
study, the “tap out” was the second most common means of ending a bout and
ended approximately 30% of matches.2 Last, most MMA matches are far
shorter than boxing matches. Sanctioned MMA events usually consist of
three 5 minute rounds as compared to the usual ten to twelve rounds of
boxing.
In sum, mixed martial arts competitions are a controversial subject
in today’s sporting world and while no one would argue that these events
are safe, it is important that we in the medical and research communities
stay disciplined in our response to these subjects. I am thankful that
your journal has taken an active role in seeking to determine the inherent
risks of MMA competitions, and I hope that it will continue giving
balanced and constructive suggestions regarding MMA and other such
controversial subjects.
Sincerely,
Gregory H. Bledsoe MD, MPH
Assistant Professor
Department of Emergency Medicine
The Johns Hopkins University School of Medicine
Baltimore, Maryland
References
1. Bledsoe GH, Li G, Levy, F. Injury risk in professional boxing.
Southern Med J 2005; 98:994-998.
2. Bledsoe GH, Hsu EB, Grabowski JG, Brill JD, Li G. Incidence of
injury in professional mixed martial arts competitions. The Journal of
Sports Science and Medicine (in press).
3. Porter K. Chipley man dies from injuries suffered in “ultimate
fighting” match [news article online]. Panama City, FL: The News Herald,
1998, http://ap.emeraldcoast.com/nharchive/index.php (accessed 6 Feb
2006).
4. Branch, G. Toughman Competition Faces Its Own Battle. USA Today,
3C, 20 May 2003.
We were very interested by the article of Brancaccio and Collegues
(1), which concluded that biochemical monitoring of athletes, including
measurement of serum creatine kinase (CK) and lactate dehydrogenase (LDH)
activities, might be helpful to reveal the state of the muscle and its
biochemical adaptation to the physical workload. This is a valuable
consideration, and both CK and LDH monitoring in...
We were very interested by the article of Brancaccio and Collegues
(1), which concluded that biochemical monitoring of athletes, including
measurement of serum creatine kinase (CK) and lactate dehydrogenase (LDH)
activities, might be helpful to reveal the state of the muscle and its
biochemical adaptation to the physical workload. This is a valuable
consideration, and both CK and LDH monitoring in elite athletes might turn
out to be reliable markers for athletes’ guidance towards the most suited
individual degree of physical training or recovery and to prevent muscle
damage and decay of the athletic performance. However, a further issue
should be addressed in this perspective. Which are the reference limits
for these markers in elite and professional athletes? This is a crucial
point, to establish whether an athlete is really undergoing unsafe and
disadvantageous training regimens. We have previously demonstrated that
reference intervals calculated from a healthy reference population might
not be widely applicable to subjects undergoing a regular and demanding
physical training (2). This applies also to widely utilized markers of
skeletal muscle and heart injury, such as LDH, total CK and CK isoenzyme
MB, which might be markedly elevated in athletes at resting,
irrespectively of the relative physical workload (3,4). In a further
analysis of these data, we have now estimated the reference ranges for CK
and LDH in 50 male elite endurance athletes, 24 to 48 after exercise and
in 35 matched male sedentary controls. Although values were distributed
over a wide range and seldom overlapping, the upper limits of the relative
reference intervals calculated at the 95th percentile were yet
substantially higher in elite athletes when compared to sedentary
controls, for both CK (395 vs 262 IU/L) and LDH (397 vs 302 IU/L).
Therefore, increased markers of muscle damage might reflect adaptation to
a demanding aerobic physical activity rather than an underlying muscle
sufferance. In this respect, we believe that identification and
implementation of reliable and specific reference limits for laboratory
parameters in elite athletes are necessary prerequisites to avoid
equivocal interpretation of results and to prevent further unnecessary
examinations.
References
1. Brancaccio P, Limongelli FM, Maffulli N. Monitoring of serum
enzymes in sport. Br J Sports Med 2006;40:96-7.
2. Lippi G, Brocco G, Franchini M, Schena F, Guidi G. Comparison of
serum creatinine, uric acid, albumin and glucose in male professional
endurance athletes compared with healthy controls. Clin Chem Lab Med
2004;42:644-7.
3. Lippi G, Brocco G, Salvagno GL, Montagnana M, Dima F, Guidi GC.
High-workload endurance training may increase serum ischemia-modified
albumin concentrations. Clin Chem Lab Med 2005;43:741-4.
4. Lippi G, Salvagno GL, Montagnana M, Schena F, Ballestrieri F,
Guidi GC. Influence of physical exercise and relationship with biochemical
variables of NT-pro-brain natriuretic peptide and ischemia modified
albumin. Clin Chim Acta 2005 Dec 30; [Epub ahead of print].
The influence of a regular physical exercise on health and fitness is
well-established, as physically active subjects are characterized by a
consistently decreased risk of cardiovascular disease, diabetes, cancer,
osteoporosis, obesity, fractures and mental health problems. Accordingly,
the current guidelines recommend 30 minutes or more of moderate-intensity
activity on most days of the week, and tha...
The influence of a regular physical exercise on health and fitness is
well-established, as physically active subjects are characterized by a
consistently decreased risk of cardiovascular disease, diabetes, cancer,
osteoporosis, obesity, fractures and mental health problems. Accordingly,
the current guidelines recommend 30 minutes or more of moderate-intensity
activity on most days of the week, and that people already achieving this
would benefit further from participation in more vigorous activity.[1]
However, there is still an open debate regarding the intensity and the
type of physical activity required to achieve most favourable health
changes in the general population without overwhelming the relative
benefits or eliciting osteoarthritis and cardiovascular abnormalities not
present at rest.[2] It was recently observed that the volume of lifestyle
activities of moderate intensity in leisure time was inversely associated
with all cause mortality in women but not in men and. Therefore, with
regard to the health enhancing physical activity recommendation as a
threshold, there were favourable findings only in women.[3]
In recent
investigations on male professional athletes, we demonstrated that a
vigorous and regular endurance aerobic training regimen does not influence
markers of hemostatic or endothelial activation,[4] does not induce any
persistent phlogistic reaction,[5] nor it is associated with biochemical
signs of significant and irreversible chronic cardiac involvement, as
reflected by normal concentrations of the NT-pro-brain natriuretic peptide.[6]
Therefore, as a substantial intensification in leisure-time physical
activity within the population does not apparently produces any acute
increase of the risk of adverse cardiovascular events[4-6] and it is
likely to be more effective for eliciting supplemental gains in health,[2] we suggest that higher intensities and amounts of aerobic training
may be safely implemented in free-living sedentary individuals as a
preventive or therapeutic measure to increase the health benefits,
especially in individuals who are most at risk of developing health
problems.
References
1. Willett W. Harvesting the fruits of research: new guidelines on
nutrition and physical activity. Cancer J Clin 2002; 52: 66-67.
2. Lee, IM, Sesso, HD, Oguma, Y, Paffenbarger, RS Jr Relative
intensity of physical activity and risk of coronary heart disease.
Circulation 2003; 107: 1110-1116.
3. Bucksch J. Physical activity of moderate intensity in leisure time
and the risk of all cause mortality. Br J Sports Med 2005;39:632-8.
4. Lippi, G, Salvagno, GL, Montagna, M, Guidi, GC Chronic influence
of vigorous aerobic training on hemostasis. Blood Coagul Fibrinolysis
2005; 16: 533-534.
5. Lippi, G, Salvagno, GL, Guidi, GC Other advantages to aerobic
exercise. CMAJ 2005;173:1066.
6. Lippi, G, Salvagno, GL, Montagnana, M, Schena, F, Balestrieri, F,
Guidi, GC Influence of physical exercise and relationship with biochemical
variables of NT-pro-brain natriuretic peptide and ischemia modified
albumin. Clin Chim Acta (in press).
This study emphasizes use of personal experience rather than the
scientific evidence in medical treatment of patellofemoral pain sydrome
(PFMS) and Achilles tendinopathy (AT). Being a physiatrist working in
this field, I feel that we need to look at observations of these
practitioners more carefully. The authors suggested the following four
factors not using scientific evidence for the management of P...
This study emphasizes use of personal experience rather than the
scientific evidence in medical treatment of patellofemoral pain sydrome
(PFMS) and Achilles tendinopathy (AT). Being a physiatrist working in
this field, I feel that we need to look at observations of these
practitioners more carefully. The authors suggested the following four
factors not using scientific evidence for the management of PFPS and AT:
1. The literature base in sports medicine is smaller than other clinical
fields.
2. Practitioners were unaware of supporting literature.
3. Management plans can not be adapted by busy clinical personnel to improve
scientific experience in medical treatment.
4. Patients preferred not to
use some of the scientific applications in the management plan. Moreover,
we also frequently seen clinicians attempting to practice evidence based
medicine who become frustrated with the process when they are unable to
find any useful practical information to answer their clinical questions.
In some cases, information may become available, but the evidence might be
inconclusive or contradicting. These observations clearly shows us the
need for a close cooperation between practitioners and clinical medical
personnel for a medical treatment in sports and exercise medicine.
Research programs structured using this cooperation will certainly create
conclusive and practically applicable medical treatments in this area. It
is important for clinicians to keep in mind that clinical decisions are
not made by evidence alone; as such, research evidence should never be
accepted blindly. Research study results must include not only knowledge
and experiences of clinician and practitioner but also scientific evidence
and most importantly appreciation of the patient.
It was a pleasure to read Paul McRory championing the cause of comparative animal and human physiology, and of his equine example.(1) To the latter he might have added that, because the horse is entirely a nasal breather, attempts were made, from 1800 BC in Egypt to 17th century Europe, to increase its ventilation by slitting the nostrils, paralleling the (equally futile) attempts of modern runners with nas...
It was a pleasure to read Paul McRory championing the cause of comparative animal and human physiology, and of his equine example.(1) To the latter he might have added that, because the horse is entirely a nasal breather, attempts were made, from 1800 BC in Egypt to 17th century Europe, to increase its ventilation by slitting the nostrils, paralleling the (equally futile) attempts of modern runners with nasal strip dilators.
More seriously, alongside its ventilatory-locomotor coupling due to the threefold effects of the visceral piston, the cervical pendulum and scapular-thoracic-compression which he mentioned, is the fact that the horse effectively blood dopes during its race warm-up. Autonomic splenic contraction releases enough erythrocytes to increase the haematocrit from a resting mean of around 40% to an extraordinary racing level of 60% or higher. The horse also undergoes a longer term training hypervolaemia comparable to human endurance athletes. All this gives it a VO2max of the order of 180? 200ml.kg.min, and a mile time of 1min 35s, so perhaps the horse is not particularly 'physiologically limited'? Mind you, this hardly compares with the VO2max of ~300ml.kg.min, and 58mph top speed, of the North American Pronghorn Antelope. However, the horse's particular pulmonary hypertension and highly elevated left atrial pressure are believed to cause stress failure of pulmonary capillaries, giving the syndrome of equine exercise-induced pulmonary haemorrhage,(2) although the exact pathogenesis has not been elucidated. Finally, regarding the horse and its rider, in some equine events, the rider may be nearer the human maxima for heart rate and blood lactate than the horse is to its maxima, i.e. the rider may be working harder than the horse.
Competing interests
None declared
References
1 McCrory P. Horses for courses. Br J Sports Med 2005; 39:581.
2 West JB, Matthieu-Costello O. Stress failure of pulmonary capillaries
as a mechanism for exercise-induced pulmonary hypertension in the horse.
Equine Vet J 1994; 26: 441-7.
We thank Mitchell and Hayen for their criticisms of our consensus
definition of cricket injuries. We agree that our “injury” definition is
based on maintenance of high level function (i.e., ability to continue
playing at elite level) rather than physical tissue damage. We accept that
this introduces a certain bias into the definition, namely that some
players may be able to continue to play with a cert...
We thank Mitchell and Hayen for their criticisms of our consensus
definition of cricket injuries. We agree that our “injury” definition is
based on maintenance of high level function (i.e., ability to continue
playing at elite level) rather than physical tissue damage. We accept that
this introduces a certain bias into the definition, namely that some
players may be able to continue to play with a certain level of physical
injury whereas others may need to stop playing with apparently the same
physical damage.
An alternate definition based on “physical tissue damage” rather than
function would introduce a more problematic bias. The incidence of
physical tissue damage in elite cricketers is extremely high.[1] Of
course, not every physical symptom is investigated, nor is it even
necessarily reported to the team injury surveillance recorder. The
variation in what might be reported as a cricket injury with a “tissue
damage” definition would be enormous and we believe would be far greater
than the variations in ability to function under our proposed definition.
A further benefit of our injury definition is that an “injury” can be
more easily verified by an independent surveillance coordinator: that is,
for each match in question, was the player physically able to play or not?
(And, therefore, if he was physically unable to play, we have defined him
as being injured). If physical tissue damage was present at the time of a
match but it was forgotten or ignored, then it would be much more
difficult to recover this information at a later date.
We also accept that there is an argument that perhaps we should not
have included “injuries” or “illnesses” that clearly occurred outside
cricket. However, there are quite a few injuries or medical conditions
that may fall into a grey area in terms of mechanism. Was the pain
associated with a lumbar disc degeneration caused by bowling or lifting
objects around the house? Was a player’s dehydration due to a gastric
virus or heat stress on the field? By including all injuries or medical
conditions which incapacitate a player (irrespective of cause) we again
use function as the yardstick and avoid any confusion over causation. The
majority of conditions which prevent the playing of cricket will still
appear to have been caused by cricket.[2]
Our published article is the first international consensus definition
of injury in a particular sport. We therefore did not have any previously
successful models in sport on which to base our statement. The success of
our definitions can be judged by whether or not future published studies
comply with our proposed definitions and whether or not the results of
studies from different authors appear to be directly comparable, which is
the ultimate goal. Future consensus definitions (for different sports or
cricket at amateur levels) may be similar to ours or alternatively based
on either “physical tissue damage” or on presentation to medical staff. It
will be interesting to see which of these definitional approaches is best
able to achieve compatibility between different studies.
References
(1) Ranson CA, Kerslake RW, Burnett AF et al. Magnetic resonance
imaging of the lumbar spine in asymptomatic professional fast bowlers in
cricket. J Bone Joint Surg Br; 2005;87(8):1111-6.
(2) Orchard J, James T, Alcott E et al. Injuries in Australian
cricket at first class level 1995/1996 to 2000/2001. Br J Sports Med;
2002;36(4):270-4.
While Orchard and colleagues[1,2] should be congratulated for their
attempt at developing an international consensus on the definition of a
cricket-related injury, a broader look at the literature on definitions of
injury might have provided a more robust definition of a cricket injury.
Orchard et al.[1, 2] define a cricket injury (or significant injury)
as “any injury or other medical conditio...
While Orchard and colleagues[1,2] should be congratulated for their
attempt at developing an international consensus on the definition of a
cricket-related injury, a broader look at the literature on definitions of
injury might have provided a more robust definition of a cricket injury.
Orchard et al.[1, 2] define a cricket injury (or significant injury)
as “any injury or other medical condition that either (a) prevents a
player from being fully available for selection for a major match or (b)
during a major match, causes a player to be unable to bat, bowl, or keep
wicket when required by either the rules or the team’s captain.” While
the definition proposed seems easy to implement in practice, it does not
actually define what would be considered to be a cricket-related injury in
terms of physical tissue damage, which is the basis of generally accepted
definitions of injury, nor does it define what is a medical condition.
The confusion may stem from the theoretical versus the operational
definitions of an injury. For example, one of the most common theoretical
injury definitions defines an injury as being “...caused by acute exposure
to physical agents such as mechanical energy, heat, electricity,
chemicals, and ionizing radiation interacting with the body in amounts or
at rates that exceed the threshold of human tolerance. In some cases (for
example, drowning and frostbite), injuries result from the sudden lack of
essential agents such as oxygen or heat”.[3] However, to operationalise
this definition of an injury, many injury professionals rely on the
International Classification of Disease, 10th revision (ICD-10) injury and
poisoning chapter XIX (S00-T98)[4] or the earlier ICD-9 external cause
codes (800-999)[5] to define what constitutes an injury.
What is lacking for the Orchard et al injury definition for
cricketers is how an injury would be specifically defined theoretically
(i.e. in terms of physical tissue damage), and then how such a definition
would be operationalised (i.e. how will physical tissue damage be
consistently identified and recorded). Although latent effects of
physical tissue damage, such as musculoskeletal injuries, are excluded
from the general theoretical injury definition above, as these conditions
do not immediately exceed the threshold of human tissue tolerance (but
rather often result from low energy exposures that can accumulate over
time until tolerance is exceeded)[6], it is likely that Orchard et al
would wish to include these injuries in an operational definition of a
cricket-related injury as musculoskeletal injuries represent a large
proportion of reported cricket-related injuries.[7,8] In addition, using
Orchard et al’s injury definition, other medical conditions (for example,
an illness such as influenza) would also be included, even those these are
not injuries. Indeed, it is unclear whether something like stress would
be included under their definition. Finally, it is also unclear whether
an injury sustained outside the sporting arena, for example from a motor
vehicle crash, that prevented the player from being ‘fully available for
selection’ would be included in the Orchard et al definition of injury.
Poorly defined operational definitions of injury are not new to the
sports area.[9] We would encourage Orchard and colleagues to consider the
development and publication of a more specific theoretical definition
together with an operational definition of cricket-related injury in order
to ensure standardisation of a case definition and to contribute towards
obtaining high sensitivity and specificity for identification of injuries
to cricketers. Otherwise the incidence of cricket-related injury is sure
to vary due to different interpretations of what is an injury, making
international comparisons difficult.
Furthermore, the currently proposed cricket injury definition appears
to be intended for elite cricketers and whether or not this definition
could be consistently applied to other levels of the competition (eg.
community level) would be of interest.
References
1. Orchard, J., Newman, D., Stretch, R., Frost, W., Mansingh, A., and
Leipus, A., Methods for injury surveillance in international cricket.
British Journal of Sports Medicine, 2005. 39(4): p. e22-e29.
2. Orchard, J., Newman, D., Stretch, R., Frost, W., Mansingh, A., and
Leipus, A., Methods for injury surveillance in international cricket.
Journal of Science & Medicine in Sport, 2005. 8(1): p. 1-14.
3. Baker, S., O'Neil, B., Ginsburg, M., and Guohua, L., The Injury
Fact Book. 1992, New York: Oxford University Press.
4. World Health Organisation, ICD-10 International Classification of
Diseases, 10th revision. 1992, Geneva: WHO.
5. World Health Organisation, ICD-9 International Classification of
Diseases, 9th revision. 1977, Geneva: WHO.
6. Kumar, S., Theories of musculoskeletal injury causation.
Ergonomics, 2001. 44(1): p. 17-47.
7. Leary, T. and White, J., Acute injury incidence in professional
country club cricket players (1985-1995). British Journal of Sports
Medicine, 2000. 34: p. 145-147.
8. Orchard, J., James, T., Alcott, E., Carter, S., and Farhart, P.,
Injuries in Australian cricket at first class level 1995/1996 to
2000/2001. British Journal of Sports Medicine, 2002(270-275).
9. Finch, C.F., An overview of some definitional issues for sports
injury surveillance. Sports Medicine, 1997. 24(3): p. 157-63.
Much of the controversy about the cooling methods
used in hyperthermia arises because of a failure to
consider the underlying physiology. There are two
distinct mechanisms for the development of
hyperthermia, SLOW and FAST, and each requires a
different method of cooling.
The SLOW hyperthermia involves exposure to heat with
only mild physical activity. In this situation the
hyperthermia develo...
Much of the controversy about the cooling methods
used in hyperthermia arises because of a failure to
consider the underlying physiology. There are two
distinct mechanisms for the development of
hyperthermia, SLOW and FAST, and each requires a
different method of cooling.
The SLOW hyperthermia involves exposure to heat with
only mild physical activity. In this situation the
hyperthermia develops purely because of an
inadequacy of the heat loss mechanisms. The body is
then in a situation where skin vasodilatation is maximal
and there is very little heat being generated by the body.
In this case cold on the skin will cause a reduction in
the vasodilatation, a reduction in heat loss with a
possible stimulus to increased heat production and the
core temperature will continue to rise and cause
disaster. This mechanism is found in the elderly, those
with heart disease, and, classically, among the
pilgrims to Mecca. The safest cooling method for this
group is bathing with warm/tepid water and fanning.
The FAST hyperthermia involves vigorous exercise in
hot conditions with the complication that in some cases
the conditions may not be excessively hot but the
casualty has been wearing too much body insulation.
This is the type found in sport and also, classically, in
situations such as military personnel running across
mudflats wearing wetsuits. In this mechanism the
main problem is the excess generation of heat from the
skeletal muscles, and survival will depend mainly on
curbing this excess heat production. These muscles
are subcutaneous and any vasoconstrictor stimulus
from cold on the skin will be overridden by the
excessive subcutaneous heat generation. For FAST
hyperthermia therefore ice or very cold water will not be
harmful but will be beneficial because it will penetrate
to the muscles and will reduce their heat generation by
direct cooling. Failure to stop the continuing heat
generation will be disastrous.
As in any medical situation deciding treatment on a
single measurement diagnosis (in this case
temperature) can be disastrous cf anaemia or
hypothermia, and a history should be taken before
treatment is decided. Safety is more important than
rate of cooling.
It is with interest we read the comments by Rompe, regarding our
systematic review and we take this opportunity to respond.
1. Rompe found it ‘annoying’ that our systematic review showed no
benefit in the use of extracorporeal shock wave therapy (ESWT) for lateral
epicondylalgia (LE) and did not include recent evidence. The census date
of our comprehensive database searches was clearly stated...
It is with interest we read the comments by Rompe, regarding our
systematic review and we take this opportunity to respond.
1. Rompe found it ‘annoying’ that our systematic review showed no
benefit in the use of extracorporeal shock wave therapy (ESWT) for lateral
epicondylalgia (LE) and did not include recent evidence. The census date
of our comprehensive database searches was clearly stated in our review[1] (p412, ‘Selection’ column 1, paragraph 1), which was prior to the
studies Rompe mentions.
2. Rompe questions the methodology we used in performing a meta-
analysis on LE. We followed the methodology recommended by the Cochrane
Collaboration[3] and believe this to be appropriate.
3. Rompe considers inter-study heterogeneity to bias the assessment
of ESWT. Heterogeneity is a serious issue when considering the
implications of RCTs. The influence of heterogeneity on outcomes of RCTs
has been studied in LE. Smidt et al.[4] assessed heterogeneity between
three studies on LE and found this did not significantly affect the
outcomes of the studies, nor the conclusions drawn. In our review, the
two studies on ESWT[2,5] found similar results, despite the inter-study
heterogeneity. There is no clear evidence that implicates population
heterogeneity as a significant determinant of outcomes for RCTs in LE.
4. Rompe justifies his standing on heterogeneity based on
recommendations of the Cochrane Back Review Group. This is not a credible
basis. Treatment and patient selection for back studies cannot be
compared to those for LE studies. It is well accepted that the cause of
most low back pain cannot be diagnosed and 80% of presentations are
therefore classified as ‘non-specific’. There is substantial
heterogeneity within the back pain patient population.[8,9] This same
patient heterogeneity does not exist in patients with LE. LE is easily
recognisable through clinical examination, there are well documented
inclusion / exclusion criteria that are consistent across most studies and
apart from length of duration and previous treatments, there is little
difference between patient populations of LE. Moreover, the two pooled
papers that looked at ESWT in our review[2,5] showed no significant
difference on statistical tests for heterogeneity. The combined results
supported the conclusions of the individual studies. Therefore we were
justified in stating that, at the time our systematic review was
completed, the heterogeneity between these two studies did not
significantly influence their outcome or our conclusions.
5. Rompe performs a selective qualitative review on ESWT. His search
was limited to English-only papers within MEDLINE and the FDA Databases.
The Cochrane Reviewer’s Handbook[3] clearly states that a search strategy
restricted by language leads to bias, as English language papers are more
likely to report results in favour of the intervention, which may result
in an overestimate of effectiveness.[10-13]
It is noteworthy that Rompe did not include Speed et al.[2] in his
review because it failed to meet his rating criteria. We found the paper
by Speed rated sufficiently well (73%) to be included in our review. The
PEDro database (http://www.pedro.fhs.usyd.edu.au/index.html) has rated the
Speed et al paper at 80%, which supports the inclusion of this paper in
our systematic review.
6. Rompe alleges serious debate amongst participating centres in the
Haake et al.[5] RCT. We are not aware of this debate, as it was not
reported within the paper.
7. Since our published review, we have conducted an updated
systematic review on ESWT using the same methodology. We identified three
papers[6,7,14] that met our inclusion criteria and rated them using the
same criteria in our original systematic review. The results were: (i)
Chung B and Wiley J[14] which rated 11/15 (73%); (ii) Rompe J et al.[6]
which rated 13/15 (87%) and (iii) Pettrone F and McCall B[7] which rated
13/15 (87%).
Two of these studies[6,7] reported results in favour of the ESWT
intervention and one[14] found no significant effect over that of a
placebo. We were able to pool data from 4 studies[2,5-7] for Pain
Visual Analogue Scale under strain at three months and calculated a pooled
standardised mean difference of 0.29 and 95%CI: -0.03 to 0.62. For this
outcome measure, there is still no significant effect of ESWT as a
treatment for LE. We were unable to include Chung and Wiley in this
pooled analysis because of differences in timing of outcome measure and
differences in presentation of data within the paper. Since Chung and
Wiley reported non-significant results, the pooled representation of pain
severity as reported herein is likely to be an overestimate of the effect
of ESWT on the measure of pain.
We also identified a paper by Stasinopoulos and Johnson[15] which
was a systematic review on the effects of ESWT on LE. This review
concluded that further research was required due to conflicting results
across current RCTs. Differences in outcome measures between studies
continues to be a major barrier to the pooling of data and potentially
limits conclusions that can be drawn by a systematic review.
It appears that Rompe continues to ignore the evidence that
highlights the lack of benefit of ESWT for Lateral Epicondylalgia. Rompe
would have the reader embrace ESWT as a treatment of choice for LE, but
the conflicting evidence of high quality clinical trials suggests that no
conclusions can currently be drawn as to its efficacy. Furthermore, an
expert opinion, as expressed in the Rompe letter, represents the lowest
level on the hierarchy of evidence and as such, should be interpreted with
caution.
References
1. Bisset L, Paungmali A, Vicenzino B, Beller E. A systematic review
and meta-analysis of clinical trials on physical interventions for lateral
epicondylalgia. Br J Sports Med 2005; 39: 411-22.
2. Speed C, Nichols D, Richards C, Humphreys H, Wies J, Burnet S, et
al. Extracorporeal shock wave therapy for lateral epicondylitis - A double
blind randomised controlled trial. J Orthop Res 2002; 20: 895-898.
3. Clarke M, Oxman A, editors. Cochrane Reviewers’ Handbook 4.2.0
[updated March
2003]. Update Software. Updated quarterly. ed. In: The Cochrane Library.
Issue 2. Oxford; 2003.
4. Smidt N, Lewis M, Hay E, van der Windt D, Bouter L, Croft P. A
comparison of two primary care trials on tennis elbow: issues of external
validity. Ann. Rheum Dis published online 30 Mar 2005
doi:10.1136/ard.2004.029363 2005.
5. Haake M, Konig I, Decker T, Riedel C, Buch M, Muller H.
Extracorporeal shock wave therapy in the treatment of lateral
epicondylitis: A randomized multicenter trial. J Bone Joint Surg-Am Vol
2002; 84(A): 1982-1991.
6. Rompe J, Decking J, Schoellner C, Theis C. Repetitive low-energy
shock wave treatment for chronic lateral epicondylitis in tennis players.
Am J Sports Med 2004; 32: 734-43.
7. Pettrone F, McCall B. Extracorporeal shock wave therapy without
local anesthesia for chronic lateral epicondylitis. J Bone Joint Surg-Am
Vol 2005; 87: 1297-1304.
8. Kent P, Keating J. Classification in nonspecific low back pain:
What methods do primary care clinicians currently use? Spine 2005; 30:
1433-1440.
9. Kent P, Keating J. Do primary-care clinicians think that non-
specific low back pain is one condition? Spine 2004; 29: 1002-31.
10. Moher D, Fortin P, Jadad A, Juni P, Klassen T, Le Lorier J, et
al. Completeness of reporting of trials published in languages other than
English: implications for conduct and reporting of systematic reviews.
Lancet 1996; 347: 363-6.
11. Gregoire G, Derderian F, LeLorier J. Selecting the language of
the publications included in a meta-analysis: is there a tower of Babel
bias? J Clin Epidemiol 1995; 48: 159-63.
12. Egger M, Zellweger-Zahner T, Schneider M, Junker C, Lengeler C,
Antes G. Language bias in randomised controlled trials published in
English and German. Lancet 1997; 350: 326-9.
13. Juni P, Holenstein F, Sterne J, Bartlett C, Egger M. Direction
and impact of language bias in meta-analyses of controlled trials:
empirical study. Int J Epidemiol 2002; 31: 115-23.
14. Chung B,Wiley JP. Effectiveness of extracorporeal shock wave
therapy in the treatment of previously untreated lateral epicondylitis: a
randomized controlled trial. Am J Sports Med 2004; 32: 1660-7.
15. Stasinopoulos D, Johnson M. Effectiveness of extracorporeal shock
wave therapy for tennis elbow (lateral epicondylitis). Br J Sports Med
2005; 39: 132-136.
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