Snowboarding – soft landings

When I bought my first snowboard 10 years ago, the sales assistant told me, “snowboarding is 25% about your skills on a board and 75% about looking cool”. The snow-sports fashion industry has infiltrated every snowboard movie since the sports inception, and its baggy legacy hangs beautifully from Seasonnaires all over the world.

Yet the oversized T-shirts and low-hanging pants of today’s teenage ‘park rats’ often hide a deadly secret: In the world of snow sports, fashion can be dangerous.

In 2013, World-class freestyle snowboarder Kevin Pearce starred in “The Crash Reel”; an autobiographical documentary film detailing his partial recovery from a severe brain injury. Following his life-changing injury in 2009, Kevin may never snowboard at the top level again. Happily however, he survived his accident at Park City in Utah, a fact he attributes to wearing a helmet.

Two years on from Kevin’s tragic injury, the biggest-budget snowboard film of all time dominated iPads and laptops around the world. “The Art of Flight” (2011) featured Travis Rice, a would-be role model for impressionable young riders, throwing down huge back-country cliff drops in Alaska and hitting kickers the size of small mountains, much of the time without wearing a helmet.

Head injuries are the leading cause of severe injury and death among snowboarders. Happily, helmet usage among snowboarders is increasing. While only 25% of riders in 2002/2003 wore helmets, 57% wore them in 2009 /2010. This figure rose to 67% in 2011/12, and this trend has continued following Michael Schumacher’s high profile injury in December 2013. According to the Journal of Trauma and Acute Surgery Care, wearing a helmet clearly reduces the risk of head injury during skiing and snowboarding and does not increase the risk of neck injury or ‘risk compensation behavior’.

Severe head injuries can be horrific, but fortunately they are fairly uncommon. Most snowboard injuries affect the upper limb, with 20% involving the wrist. In fact, wrist injuries are 10 times more common in snowboarders than skiers. Two thirds of these injuries are fractures. Many experienced snowboarders believe that wrist fractures only affect novices. While they are indeed more common among those new to the sport, advanced riders are relatively more likely to sustain ‘intra-articular’ or ‘communicated’ fractures. These are complex injuries which require surgery and frequently result in a permanent reduction in wrist motion, with subsequent osteoarthritis and long-term pain.

There is a popular myth in snowboarding that wrist guards increase the risk of a serious fracture by “breaking the bones further up the arm”. I have heard this repeatedly over the last 10 years while hanging around resorts, guiding holiday guests and treating injured snowboarders both in the Alps and in the UK. In fact, while I was donning my wrist guards for a park night at the Snow Centre in Hemel Hempstead last week, a member of staff helpfully informed me that I was going to “break my arm”.

The evidence is clear: This is simply not true. Wrist guards are beneficial in preventing serious wrist injuries, yet fewer than 10% of riders wear them. There is a nearly three-fold increase in wrist injuries among riders who do not use wrist protection. Children and inexperienced snowboarders are most likely to benefit.

Most concerns about wrist guards seem to relate to the idea they will simply transfer injury to other forearm locations. It is true that wrist guards should possess a degree of flexibility to avoid generating localised forces above or the below the device, but studies have failed to demonstrate increased rates of injuries to other parts of the arm. On a personal level, I have only ever seen one wrist fracture in a rider wearing wrist guards. The patient was an experienced park rider and the fracture occurred at his wrist joint, rather than further up the arm.

As a sports physiotherapist, I am passionate about minimising the risk to young people involved in extreme sports, but I am myself not immune to peer-pressure. In 2012, I fell off a rail in Montgenevre and dislocated my right acromioclavicular joint (where the collar bone meets the shoulder blade). I was pleased that the local doctor checked if I was wearing a helmet and wrist guards, but she did not enquire whether I was using any shoulder protection. My injury is common among snowboarders and might have been avoided had I been wearing the back and shoulder protection that I now use.

But where does it all stop? Should we go snowboarding wrapped up in cotton wool? Well, British doctors seem have an infuriating habit are telling patients that “common things occur commonly”. There is certainly some sense in this. My view is that we should promote devices that reduce the risk of common injuries, especially where they do not restrict snowboarders while on the mountain. For me, my essential gear includes helmet, wrist guards and shoulder/back protection. I use impact shorts when hitting rails (usually with my backside), and never go off-piste without local knowledge along with my transceiver, shovel and probe.

It is in the spirit of snowboarding not to conform to stereotypes, so I encourage young riders not to be labelled as ‘dumb snowboarder’. Ignore urban myths and don’t bow down to fashion. Instead, use common sense and follow the science. Wear protective gear and have fun. Body armour may not be fashionable, but neither is a devatating head injury, returning from a ski season in January or having osteoarthritis in your 30’s.

We look to the people at the top of any sport to promote the safety of youngsters taking it up. “The Fourth Phase”, the major new snowboard film from Red Bull Media House, promises to be their biggest production to date. Why then, are trailers for this film already available online showing the stars launching mind-blowing jumps without helmets? With a release planned for 2016, these riders should be wearing helmets, even if it means they can’t model their sponsors’ latest beanies.

Introduction to haemostasis – a life-preserving process

Human blood: Red, white cells and platelets
Plasma (55%), contains clotting factors
Cellular component, 45%
Haemostasis – restore vascular integrity, limit infection.

Four key components to clotting:
Primary (the platelet plug), secondary haemostasis and fibrinolysis (the body’s hoovering process!)

Response to incision:
Vascular spasm – vasoconstriction, endothelium initiates
Fibrin mesh – strengthens clot, comes out of solution
Platelet adhesion and aggregation
Coagulation – stabilisation of clot
Fibrinolysis

Platelet life cycle: 7-10 days – fragments off megakaryocyte
Eventually removed by reticuloendothelial system
Platelets activated – increases surface area and becomes like putty.
Platelets recognise sub-endothelial tissue via Von Willebrand factor. v sticky (collagen,basement membrane etc). Platelets degranulate.
Von Willebrand factor – circulates and located in endothelial tissue. VW disease – clotting disorder, excessive bleeding
Tissue factor – thrombin. initiates development of fibrin. Stabilises platelets
Platelet science – v complicated. Lots of molecules they can release. Can remodel and change shape
Platelets adhere, activate and aggregate. Fibrin mesh stabilises.
Platelet acts as template to promote coagulation pathway, reactions leading to fibrin can take place on surface.

Exposure to sub endothelial tissue is required for platelet activation (extrinsic pathway).
Coagulation cascade tightly regulated. Factors turn system.
Fibrinolysis balances system.
13 clotting factors, mostly produced in liver. Named and numbered. Cascade of enzyme managed reactions

Tissue factor: Promotes clotting, by binding factor 7a recognising fibrin development
Tissue damage – thrombin (enzyme) and cascade of clotting: fibrinogen to insoluble fibrin

Extrinsic pathway – tissue factor outside of circulation
Intrinsic pathway – inherent coagulability of blood. Eg cut finger on bench. Blood on bench coagulates as a result of non-physiological contact. Contact coagulation
Coagulation pathway actually more complicated than just having these two arms.
Thrombin burst – tissue factor and 7a complex initiates thrombin enzyme and conversion of fibrinogen to fibrin.
Fibrinolysis: clot limiting, repair and healing mechanism (clot dissolution)
Plasminogen – enzyme, activated by another enzyme (tPA) to Plasmin. Eats clot.
The leftover part is D-Dimer, which can be measured clinically (eg in DVT).
tPA can be mimicked in clot busting medication

The body has natural anticoagulants eg.
Anti-thrombin inhibits thrombin.
Normal Clotting requires equilibrium of all of the above constituents
Can be disregulated by disease – eg infection, bone marrow insufficiency – thrombocytopenia – no platelets formed (results in non blanching rash)
Almost every inpatient takes some form of anticoagulant to prevent DVT

Thrombocytopenia – 450 hypercoagulability.
Bleeding disorders can be inherited (eg. Haemophilia) or acquired (liver disease)
Avoid intramuscular injections in these patients
Haemophilia – haemarthrosis v common. Patients become disabled with arthritis
Lab evaluations: FBC and film, coagulation tests, platelet function (inc VWF)
Blood incubated with reagents (eg calcium collater) until tests applied.
Clotting dependent upon calcium (as a co-factor), hence removal block coagulation
Calcium returned before test. Tissue factor can also be added to measure coagulation.
Prothrombin time (PT): measures extrinsic pathway. add tissue factor (also phospholipid and calcium), should take 11-13 seconds until fibrin forms. If around 20seconds, a clotting factor is lacking.
Activated partial thromboplastin time (APTT) – measures intrinsic clotting pathway. Normal time is 28-44 seconds
These tests don’t show which clotting factor is lacking
Thrombin time (TT): add thrombin. Tests final stage in clotting cascade.

In summary, haemostasis is tightly regulated and involves endothelium, platelets, clotting factors and fibrinolysis. Disregulation results in disease.

Introduction to pharmacology

Introduction to Pharmacology 

Pharmacology is the study of drugs on living systems

Why Pharmacology?

  • Diagnostic skills useless without properly prescribed medication
  • Fractured lower limb > 10 drugs used during process
  • Most errors are due to prescribing errors
  • Patients are better informed – doctors need to be too
  • Drugs are chemicals producing a biological effect
  • Drugs can be endogenous substances, given artificially

Fundamentals of pharmacology:

  • Pharmacodynamics – what drug does to body
  • Pharmacokinetics: what body does to drug: route into body, metabolised where
  • Mechanism
  • Indications: hence Clinical uses
  • Adverse effects
  • Contraindications
  • Eg. Aspirin – NSAID. Anti platelet aggregation properties.
  • The process is the most important thing – the mechanism
  • Aspirin inhibits COX enzymes, which catalyzes the breakdown of arachdonic acid to prostaglandins (PGs)
  • By knowing action of PGs, possible to learn pharmacology and physiology
  • By blocking PGs, GI healing is impaired. Can cause Reye’s syndrome in children and bronchial constriction in asthmatics
  • Long term use: adverse effects influence treatment

Properties of Drugs

  • Tissue selective
  • Chemical selectivity
  • Amplification of action – small dose producing profound effects
  • Drugs act at RECEPTIVE sites – expressed in selective tissues
  • Most drugs act at specific receptors including 4 main types: receptors, enzymes, carrier molecules, ions channels
  • eg B adrenoceptor in heart. The drugs changes action of protein channel, amplifying effect.
  • There are hundreds of thousands of receptors – new receptor = new drug
  • Receptor – target site, which produces cellular response/biological effect
  • Agonist – produces biological effect
  • Antagonist – blocks receptor
  • Occupancy =Affinity – ability to bind (therefore antagonist has affinity, not efficacy)
  • Efficacy – response from drug

Binding – different types:

  • Mostly reversible, weak (hydrogen bonds, van der vaals)
  • Or permanent (aspirin) by covalent bonding
  • Affinity- Reversible binding governed by law of mass action
  • Drug dose based on equilibrium constant (50% of receptors are free, 50% bound to agonist). Level of drug required to reach equilibrium constant describes affinity
  • Each drug has KA (affinity value)
  • Higher affinity means lower dose can be used
  • Affinity give sigmoid curve, as there is finite number of receptors available
  • EC50 – effective concentration giving 50% biological response. (Depends on affinity and efficacy). EC50 is used to compare drug potency
  • Pharmacokinetic properties (how well absorbed) will also affect drug potency
  • This is a basic explanation; because pharmacogenetics will also have an effect (receptor density varies)
  • Remember: receptors amplify signals. You don’t need full occupancy to provide an EC50.

Partial and Inverse Agonist

  • Full agonist – full efficacy
  • Partial agonist used in opioid addict
  • Antagonist – no efficacy
  • Inverse angonist – reduces basal receptor activity (has an action so is not an antagonist). Effect could be to reduce heart rate, for example. Could prevent action of another route

Competitive antagonism

  • Eg. Beta blocker
  • Agonist and Antagonist compete for binding site. Both bind reversibility.
  • Surmountable antagonism – To overcome antagonist, increase concentration of agonist
  • Sigmoid curve shifts to right
  • Non-surmountable antagonism consists of:
  • Non-competitive antagonism – agonist binds to different site to antagonist
  • Irreversible antagonism
  • Competitive antagonism is surmountable

Introduction to Imaging

Introduction to Imaging

  • X-Ray – first image of bones of hand. Silhouette of anatomy.
  • Silhouette sign – bony material silhouetted against air. Lost on chest X-ray with pathology
  • Age of patient important in radiology. Multiple lesions on chest X-ray – most likely secondary.
  • Only 25% of world has access to X-ray
  • First scanner developed in Wimbledon by Godfrey Hansfield – a SGUL graduate. First scan in 1976
  • CT chest = 400 chest X-rays. Particularly important to consider in children. And brain/eyes are particularly radiosensitive. Repetitive exposure give cumulative risk. Risk of cancer with CT chest 1 in 1000 (smoking doubles your risk).
  • Childrens’ doses kept low with ultrasound where possible.
  • CT scanning has evolved due to computer progress.
  • EMI record label funded 1st CT, so The Beatles indirectly helped fund CT scanning
  • Functional CT due to labelled glucose – tumours can be imaged due to glucose uptake
  • PET (functional) and CT (anatomy) scans fused together allows tumour to be staged -PETCT
  • All imaging carries risk, due to energy being imputed to patient (ultrasound and MRI heat, X-ray ionising).
  • 1/3 of admissions are for chest pain. Half don’t have heart. Computed coronary angiography is 99% effective for screening. Very high negative predictive value.
  • In fluoroscopy, user gets dose (cardiologists, interventional radiologists and some surgeons are high risk users)
  • Ultrasound – Ian Donald. Uses sonar (WWII technology) used first in 1950s, published in Lancet. High frequency bell which rings
  • Risk is tissue cavitation
  • Black on image is fluid (transmits), white (reflects), grey (partially reflects).
  • Seeing the anatomy can sometimes give you the diagnosis.
  • Doppler effect can assess patency of blood vessels
  • Moore’s law. Every 10 years, size halves. Ultrasound is now ‘point of care’, can be size of smartphone.
  • Ultrasound can image stomach – eg. Pyloric stenosis in child
  • Ultrasound – high negative predictive value, good for excluding pathology inc fractures in remote locations, due to portability
  • Ultrasound prices £40-£120,000
  • MRI – invented by Peter Mansfield in Nottingham
  • 20% of patients cannot tolerate
  • Protons align due to magnetic field, water has most protons,
  • Magnetic field strength is icreasingtarted with 1tesla, now 3tesla which improves signal to noise ratio
  • Radio frequency added (this causes the noise during the scan), which knocks protons off axis. During time they are knocked off, they emit signal, which can be measured
  • Exquisite resolution. Can see bone bruises, MS plaques, tumour inc blood vessels
  • Cannot perform with pacemaker, metal artefacts, certain heart valves
  • Can image mother in first trimester
  • Shall we image early? – eg locked knee before pt sees surgeon
  • Cost of MRI is coming down, more private providers, hence availability is going up