Autonomic Dysreflexia and Boosting: Non-pharmacological doping in disability sport

Sport and Exercise Medicine: The UK trainee perspective – a BJSM blog series

By Dr Robin Chatterjee @sportsdocrob and Dr Sonia Bains @DrSoniaBains

Participation and interest in disability sport is at an all-time high. This was demonstrated by record audiences, TV viewership and levels of income generated by the 2012 London Paralympics and 2017 IAAF World Para-Athletic Championships. The increased recognition of disability sport has resulted in athletes becoming more competitive than ever before. Most physicians are familiar with the dangers of pharmacological doping in sport, however there is less awareness about ‘boosting’. Boosting is defined as the intentional induction of autonomic dysreflexia (AD) by athletes with a spinal cord injury (SCI) at or above the level of T6 for the purpose of improving sports performance1, 2. AD is an acute syndrome that occurs in those with an SCI due to excessive sympathetic output3. Para-athletes may ‘boost’ because the dysreflexic state reduces the rate of perceived exertion and increases top wheelchair speed4. A recent study showed that competing in a dysreflexic state caused a 9.7% average improvement in race time5. Boosting is dangerous because AD is a medical emergency that can have catastrophic health consequences including seizure, myocardial infarction, cerebral haemorrhage and death1. Although not specifically listed as a prohibited method on the World Anti-Doping Agency (WADA) Prohibited list, the International Paralympic Committee (IPC) forbids athletes to compete in a hazardous dysreflexic state, due to the health threat6.

Epidemiology & Associations

Although anecdotal and clinical evidence suggest that the intentional induction of AD occurs, its true prevalence remains uncertain1. Although 27.1% of athletes believe that boosting is common in their sport, no athlete has ever tested positive for boosting at an event sanctioned by the IPC7. A recent study found that only 56% of the surveyed athletes reported having knowledge of the practice of boosting3. 16.7% of the respondents (all male) reported having used AD to improve performance at some point in the past. In the non-athletic population it is probable that between 50% and 70% of patients with lesions at or above T6 experience symptoms of AD8, 9. AD can occur in both complete and incomplete lesions though symptoms are less common and less severe in the latter group9. Though AD mainly occurs in cases of SCI at T6 or above, it has less commonly been reported in non-traumatic causes such as spinal cord tumour, post neurosurgery at T6 or above and also in medical conditions such as multiple sclerosis9.

Pathophysiology

An athlete with a high level SCI has reduced physiological resources for improving cardiac output and obtaining maximal oxygen uptake, and thus for maintaining endurance when competing10. The loss of sympathetic cardiac innervations often results in a maximum heart rate of 110-130 bpm as determined by sinoatrial activity11. This is known as ‘cardiovascular blunting’ and can inhibit sporting performance12. In addition to the restricted heart rate reserve and reduced stroke volume, athletic capability is further impeded by a decreased catecholamine response to exercise and an absent venous pump response in the legs13. Therefore due to these limitations to athletic ability some competitors with high level SCI try to induce a dysreflexic state. A noxious stimulus is deliberately applied by the athlete below the level of the lesion (boosting), stimulating a systemic efferent sympathetic response (AD). This causes vasoconstriction beneath the level of the SCI, which results in increased blood pressure and blood flow to the working muscles, thus improving sporting performance. However due to the presence of the SCI, no central inhibitory control is provided by the brain to control the sympathetic response below the level of the injury thus risking the individual to potential catastrophic effects.

Clinical signs & symptoms

An episode of AD characteristically presents with an acute uncontrolled rise in blood pressure, a vagally mediated bradycardia (tachycardia has also been documented) and vasodilation above the level of the SCI, resulting in severe bilateral headache. The signs and symptoms of AD above the level of SCI typically reflect a parasympathetic response, including flushing, sweating, blurred vision and nasal congestion. Sympathetic responses occur below the SCI level consisting of pale cool skin, cutis anserina and piloerection14.

The increase in blood pressure varies in presentation, from normal or slight elevation, to a systolic blood pressure (SBP) up to as high as 300mmHg and diastolic to rise to 150mmHg15. This is significant elevation as the resting blood pressure is reduced after a SCI, usually to a range of 90/60 mmHg. The IPC states that a dysreflexic state is likely to be present when the SBP rises above 160mmHg6.

Investigations

The primary test required in the detection of AD is sphygmomanometry (see clinical signs and symptoms). Once hypertension has been established, the noxious stimulus that has caused the AD must be identified. Purposeful distension of the urinary bladder by catheter locking or infrequent intermittent catheterisation to allow overfilling is one of the most common ways of causing AD16, 17. Other forms of self-harm that may provide the noxious stimulus include winding leg straps too tightly, delivering electric shocks to the lower leg muscles, constricting the feet, legs, scrotum or testicles or by deliberate fracture of the lower limb bones16.

The current approach of the IPC to detect boosting is to test an athlete’s blood pressure before competition. If the SBP is found to be above the 160mmHg threshold then the individual is re-examined 10 minutes later. If the SBP still is above 160mmHg then the athlete is withdrawn from competition18.

Differential Diagnoses

If no obvious noxious stimulus is found then non-noxious causes of AD need to be considered such as bowel distension from faecal impaction due to haemorrhoids or another obstruction. If no stimulus can be determined at all then alternate syndromes need to be considered. These include essential hypertension, migraine, cluster headaches, posterior fossa tumours and phaemochromocytoma.

Management

In both primary or secondary care settings, the first intervention is to sit the patient upright, instigating an orthostatic decrease in blood pressure. It is imperative that the precipitant of the AD is identified and removed as soon as possible. If bladder distension is the precipitant, any obstruction of the indwelling urinary catheter must be removed. Should the bladder still not be draining well, the catheter must be irrigated or changed aseptically. Alternatively, if no indwelling catheter is found, an intermittent catheterisation should be performed. Importantly. Tight or restrictive clothing should also be removed to decrease any added noxious stimuli.

Clinicians working in a sporting setting should ensure immediate transfer to an emergency department (ED). Verbal and written handover between the sports physician and ED is extremely important as boosting and AD are uncommon incidents in most EDs and delay in management may potentially be fatal.

In a hospital setting, if symptoms are still present and if the SBP >150mmHg then pharmacological treatment is indicated to reduce the blood pressure. Medication is given to alleviate symptoms and avoid the serious complications associated with uncontrolled hypertension, rather than its effects on the end organs associated with most hypertensive crises. The antihypertensive medication of choice is one with a rapid onset and short duration of action. Commonly used medications are nifedipine (immediate release form and bite and swallow rather than sublingually, which may lead to erratic absorption) or glyceral trinitrate spray sublingually19. If symptoms persist, the dose can be repeated after 20 minutes. However, should the blood pressure remain elevated an intravenous hypotensive may be required such as hydralazine.

Should symptomatic hypotension develop from pharmacological therapy then laying the patient down and elevating the legs is usually sufficient to manage the symptoms.

Discussion

All physicians working in a sporting setting need to be aware of the rare but potentially life threatening condition of AD and the practice of boosting.

AD is an acute presentation of uncontrolled sympathetic drive and can have potentially serious consequences including cerebral haemorrhage, subarachnoid haemorrhage, seizures, retinal haemorrhage, coma and death. Early recognition is essential to enable prompt therapeutic intervention, decreasing the risk of adverse significant complications.

Because of the life-threatening complications and performance enhancing benefits, the IPC forbids the practice of boosting6. Those who do practice boosting are disqualified from competition. If an athlete attempts to trigger AD prior to competition they may also be disqualified from an event, even if their systolic blood pressure is below 160mmHg6.

The desire to win may mean that disabled athletes, like their able bodied counterparts, have the potential to use any advantage that is available to them, regardless of the threat to their health. This is why the sports physician needs to be vigilant for the signs and symptoms of AD in this particular cohort.

Those physicians who work regularly with disabled athletes should ensure education about the deleterious effects of AD and effective deterrence is instilled in their patients.

Take Home Messages

  • Boosting is the intentional induction of AD by athletes with a SCI at or above the level of T6 for the purpose of improving sports performance
  • AD presents with an acute uncontrolled rise in blood pressure, bradycardia and severe bilateral headache. The signs and symptoms of AD above the level of SCI including flushing, sweating, blurred vision and nasal congestion. Symptoms below the SCI level consist of pale cool skin, cutis anserina and piloerection
  • AD can have catastrophic health consequences including seizure, myocardial infarction, cerebral haemorrhage and death
  • Initial management consists of sitting the patient up and early detection and removal ofthe noxious stimulus that caused the AD
  • Disabled athletes should be transferred as soon as possible from a sporting setting to the nearest emergency department for further management
  • Education and deterrence is key to prevention of AD
Image retrieved from here.

 

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Dr Sonia Bains is a ST4 Specialist Registrar in Sport and Exercise Medicine (SEM) in the London Deanery. She works as the match day doctor for AFC Wimbledon andis the trainee representative for the SEM specialty training committee. Her sporting interests include football, karate and tennis.  Twitter: @DrSoniaBains

Dr Chatterjee is a Specialist Registrar in Sports & Exercise Medicine (SEM) and also a GP with a Special Interest in SEM. He first became interested in SEM when he gained experience in hyperbaric medicine, cardiopulmonary exercise testing and chronic musculoskeletal pain management whilst working as an anaesthetist in Australia. He currently works as a medical officer at Homerton NHS University Hospital, London Broncos Rugby League, the Royal Ballet School and Musculoskeletal Interface Clinical Assessment Service (MICAS) at Battersea Health Centre. He is on the research committee for the European College for Sports & Exercise Physicians (ECOSEP) and is also a lecturer on the MSc SEM course at Queen Mary University of London. Research interests include low vitamin D and low back pain. Outside of work he is a sleep-deprived father to a 2 year old, PADI certified diver and a long-suffering Liverpool FC fan.Twitter: @sportsdocrob

Dr Craig Sheridanco-ordinates the BJSM Trainee Perspective Blog. To contribute to this series, please email Craig: craigsheridan@gmail.com

References

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