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A young man collapse in Ruby competition

HKCEM College Tutorial. A young man collapse in Ruby competition. Author Dr. Tang ka yuen July 2013. A 14-year-old boy collapsed during a rugby competition…. If you are the on-site medical team doctor or spectator, what would you do?. What would be the Onsite immediate management ?.

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A young man collapse in Ruby competition

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  1. HKCEM College Tutorial A young man collapse in Ruby competition Author Dr. Tang kayuen July 2013

  2. A 14-year-old boy collapsed during a rugby competition…. If you are the on-site medical team doctor or spectator, what would you do?

  3. What would be the Onsite immediate management ? Basic Life Support • Ensure safety • Assess response of the patient • Call for help and get the AED if unconscious and not breathing

  4. What are the sequences of cardiopulmonary resuscitation (CPR) ? • Circulation • Airway • Breathing • 2010 AHA Guidelines for BLS http://www.youtube.com/watch?v=ZjszBXF0l8A

  5. Onsite immediate managementCirculation • Pulse Checking • The rescuer locates the carotid or femoral pulse and performs the pulse check. It should take at least five seconds but no more than ten seconds. • If there is no pulse or pulse < 60/min, Chest Compression should be started immediately.

  6. What is an high quality CPR? • Rate at least 100/min • Compression depth to at least ½ anterior-posterior diameter of chest, about 1.5 inches (4cm) in infants and 2 inches (5cm) in children • Allow complete chest recoil after each compression • Minimize interruptions in chest compressions • Avoid excessive ventilation

  7. Onsite immediate management • One rescuer: 30 compressions and 2 breaths • Two rescuers: 15 compressions and 2 breaths

  8. Onsite immediate management Airway • Open airway by head-tilt-chin-liftor jaw thrust if there is evidence of C-spine injury

  9. Onsite immediate managementBreathing • The E-C clamp technique is recommended for bag-valve-mask ventilation • Give each breath slowly, over approximately 1 second, and watch for chest rise • If the chest does not rise, reopen the airway, verify that there is a tight seal between the mask and the face, and reattempt ventilation.

  10. Onsite immediate management • The rescuer should continue CPR until …….. • AED/Defibrillator arrives, • Advanced Life Support Providers take over or • Victim starts to move.

  11. Automated External Defibrillator • We use AED only when the victim has no response, no breathing and no pulse. • Adult pads are available for victim from age 8 and older. The child pads are used for victim from 1 year-old to 8 year-old if available.

  12. Automated External Defibrillator • Power on the AED, this activates the audio guidance for the subsequent steps • Attach the electrode pads and connect the cables • “ Clear” the victim and analyze the rhythm • If the AED advises a shock, make sure no one is touching on the victim before press the shock button, begin CPR immediately after the shock

  13. Automated External Defibrillator • If no shock is indicated, continue CPR. • After 2 min or 5 cylces of CPR , the AED will prompt you the Step 3 and step 4 again. http://www.youtube.com/watch?v=3trpw_We0UQ

  14. What is your diagnosis?

  15. What are the differential diagnosis of VF in young athlete during competitive sports?

  16. Cardiovascular causes of VF • Structural & functional abnormalities • Hypertrophic cardiomyopathy (HCM) • Arrhythmogenic right ventricular cardiomyopathy (ARVC) • Dilated cardiomyopathy (DCM) • Congenital anomalies of coronary arteries (CCAA) • Myocarditis • Acquired • Commotiocordis • Trauma • Artherosclerotic coronary artery disease • Drug abuse • Congenital heart disease • Ebstein’s anomaly, TOF, VSD or cyanotic heart disease • Primary electrical abnormalities • Long QT syndrome • Brugada syndrome • WPW syndrome

  17. Respiratory: Bronchospasm Aspiration Sleep apnea Primary pulmonary HT Pulmonary embolism Tension pneumothorax Metabolic or toxic Electrolyte disturbance and acidosis Medication or drug ingestion Environmental poisoning Sepsis Neurologic Seizure CVA : ICH Drowning Non-cardiovascular causes of VF

  18. Progress • On-site CPR done by coach and St. John First Aid staff • Ambulance arrived 4 minutes after the incident. AED detected VF and defibrillation was given once • CPR continued after defibrillation, no more VF detected afterward • Pulses returned at about 11 minutes

  19. ECG strip from ambulance

  20. The patient remained unconscious and was sent to A&E Department….. How would you manage this patient in A&E Department ?

  21. Initial assessment in A&E Department • Unconscious GCS 3/15 • Pupils 3mm E&R • Afebrile • BP/P 113/66 130/min • P/E: • No external wound or rash • CVS: HS x 2 no murmur • Chest: normal • CNS: planter <- / ->, jerk not brisk

  22. What other history would you ask from his relative?

  23. Initial assessment in AED • History from relative: • No preceding symptoms • Healthy, no hx of syncope • No hx of drug abuse • No recent URTI • Not on any medication • Family hx: no hx of premature sudden death / cardiac illness among relatives

  24. Management in A&E department • ABC – Intubated under RSI • Investigations: • Blood tests (including H’stix,CBP, R/LFT, Ca, toxicology, Cardiac Enzymes, Troponin I, Blood gas) • ECG • CXR- clear • CT brain

  25. 1st ECG in AED

  26. Common CVS causes of VF in young athlete during competitive sport • Structural & functional abnormalities • Hypertrophic cardiomyopathy (HCM) • Arrhythmogenic right ventricular cardiomyopathy (ARVC) • Dilated cardiomyopathy (DCM) • Congenital anomalies of coronary arteries (CCAA) • Myocarditis • Acquired • Commotiocordis • Trauma • Artherosclerotic coronary artery disease • Drug abuse • Congenital heart disease • Ebstein’s anomaly, TOF, VSD or cyanotic heart disease (especially with OT done) • Primary electrical abnormalities • Long QT syndrome • Brugada syndrome • WPW syndrome

  27. Hypertrophic Cardiomyopathy LVH, increased S-wave voltage in V1-5, diffuse ST/T wave changes

  28. Wolf Parkinson White Syndrolme Shorten PR interval, slurred onset of QRS (delta wave) and increased QRS interval

  29. Brugada Syndrome ST elevation in leads V1 & V2 (and V3) followed by a negative T wave

  30. Prolong QT Syndrome Prolonged QTc = 540ms with board-based T wave

  31. What do you think? Additional hx: he was hit over chest wall by another player before he collapsed! No convulsion noted.

  32. Progress in AED • Vital signs at AED • GCS 3/15 , BP 133/66, P 130/min, SaO2 99% • Intubated at AED for airway protection • Physical examinations: unremarkable • ECG: sinus tachycardia with no significant ST change • CXR: normal • Consult Pediatrician  transferred to PICU • Extubated soon after admission with good respiratory effort

  33. What are the management of Return of Spontaneous Circulation (ROSC)? • Use ABCDE approach • Controlled oxygenation and ventilation • Investigations • Treat precipitating cause • Antiarrhythmic • Amiodarone • Therapeutic hypothermia? http://circ.ahajournals.org/content/122/18_suppl_3/S768.full

  34. What are the uses of Waveform capnography ? • Confirming tracheal tube placement • Monitoring of the CPR quality http://acls-algorithms.com/waveform-capnography

  35. Hospital course • Initial echocardiography on day of admission revealed fair right ventricular contraction, left ventricular apical hypokinesia with ejection fraction of 50%. Subsequent echocardiography on day 4 did not reveal any evidence of cardiomyopathy. • Computer tomography of brain was normal. Patient was fully awake on day 3 and neurological examination did not reveal any significant abnormality except mild intention tremor. • Patient was transferred out from paediatric intensive care unit to general ward on day 3. Patient recovered well and was assessed by physiotherapist.Mild deteriorationin hand-eye coordination was noted, otherwise patient’s functional status was back to normal. Patient was discharged on day 7and followed up by cardiologist.

  36. Hospital course • All subsequent cardiac investigations were normal. • echocardiography, • 24-hour holter monitoring, • exercise treadmill test, • exercise myocardial perfusion test, • computer tomography of coronary angiogramand • cardiac magnetic resonance imaging study • Patient did not have any arrhythmia in all subsequent ECG with normal QTc of 373ms and ST segment. Clinical diagnosis of Commotio Cordis was made by cardiologist. • Patient returned to school in 2 months later for new semester with satisfactory performance. He had satisfactory exercise tolerance and continued to play rugby in school. No major cardiac or neurological sequelae was found.

  37. Commotio cordis • Commotio cordis means ‘disturbance of the heart’ in Latin • Sudden cardiac death as a result of a blunt, often innocent-appearing chest wall blow. • Ranked as second leading cause of sudden cardiac death in young athletics • The likely cause of death in CommotioCordis is ventricular fibrillation Maron, B. J. et al. JAMA 2002;287:1142-1146

  38. Thank You

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