Prehospital care of severe head trauma abstract manion


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Prehospital care of severe head trauma abstract manion

  1. 1. Care of Acute Head Injury Dr Ben Manion CAPT 2HSB ARES Neurosurgical registrar Gold Coast Hospital
  2. 2. My background
  3. 3. My background
  4. 4. Scope Immediate triage and treatment Logistics and definitive point of care Difficulty in accurately predicting the course of a brain injury
  5. 5. Relevance  Up to 25% of battlefield injuries are head and spine  115000 traumatic brain injuries US army 2002-2005  Prevention, diagnosis and treatment of traumatic brain injury is currently a high profile topic in the US military  Up to 62% of Iraqi veterans have screened positive for acquired brain injury  We may miss up to 40% of brain injuries in the field  Recent Australian ArmySAFE initiative  Prompt and rational treatment makes a significant difference to outcome
  6. 6. Trimodal death distribution
  7. 7. Primary brain injury  Events at time of trauma  Immediate and complete  Irreversible, prevention is the only intervention  Begins a cascade of events which can cause further damage  Occurs in up to 25% of combat injuries  Blast effects currently are the predominant cause
  8. 8.  Cascade of blast effects  Direct concussive  Blunt or penetrating injury  Contre coup
  9. 9. Physiology of brain injury  Monroe Kellie Doctrine  Rigid skull with deformable contents  CPP = MAP – ICP  Autoregulation fails below 50 or above 160  Normal ICP 0-15
  10. 10. CSF Arterial Inflow Venous outflow Capillary blood Brain Parenchyma Rigid Skull Monroe Kellie Doctrine
  11. 11. Physiology of brain injury  Intracranial pressure  Monroe Kellie Doctrine  Cerebral perfusion pressure  Critical point of herniation Point of herniation 60mmHg
  12. 12. Secondary Brain Injury  Hypoxia  Hypotension  Ischaemia  Oedema  Haemorrhage  Metabolic derangement – hypercapnia, acidosis, infection  Neurotoxic cascades - excitatory amino acids, endogenous peptides, apoptosis and calcium influx  Increased ICP – cerebral oedema, hydrocephalus, brain herniation
  13. 13. Assessment  Patient factors – age, time of injury, GCS, pupils  Mechanism – Concurrent fatalities, nature of forces involved, helmet sensors, care with C-spine  Primary Survey (ABC)  A: Hypoxia  C: Hypotension  Associated injuries  Must examine prior to sedatives/strong analgesics/paralytics  Repeat Survey – Changes over time are most important feature of progression of injury  Keep accurate records, standard scoring
  14. 14. Classification of acute head injury  Mechanism  Blunt  Penetrating  Mixed  Morphology  Skull fracture  Intracranial lesion  Severity  mild (14-15)  moderate (9-13)  severe (3-8)
  15. 15. Mild head injury  GCS 14-15  Awake, amnesic, may be confused  Vulnerable to C-spine injury  Remove from field  CT head if available  Multiple scanning tools to assess for concussion being developed (MACE, ANAM)  May have sequelae
  16. 16. Moderate head injury  GCS 9-13  Confused, somnolent or aggressive, focal neurologic deficits  Protect airway  Cardiopulmonary stability as priority  Remove from field with medical support and airway capabilities  CT head in all cases  No role for IV antibiotics in closed head injury
  17. 17. Severe head injury  GCS 3-8  Follow EMST ABCD primary survey protocol  Early intubation, 100% oxygen  C-spine protection with hard collar  Ventilate to pCO2 35  Rapid stabilisation of cardiopulmonary axis  Systolic >100mm Hg  Minimal volume isotonic resusc fluids, aim for euvolaemia  Hypotension rarely due to primary head injury  Early evac with full medical support
  18. 18. urther management Airway secured, supplemental oxygen/CPAP PRN. Ventilator as needed to maintain pCO2. End tidal CO2, pulse oximetry. Monitor haemodynamics. Fluids and pressors. Aim for euvolaemia. CP assessment 30% head up to facilitate venous drainage Maintain other parameters  Glucose, body temp, sodium  Antiemetics, bowel care, maintain nutrition with feeding tube or PEG. Minimal sedation to facilitate neurological examination and assessment of progress.
  19. 19. ther Management Mannitol or hypertonic saline to reduce ICP. Can aggravate hypovolaemia. Use in signs of herniation. +/- rusemide (unproven) depending on clinical picture. Steroids not routinely used Anticonvulsants if high risk (early seizures, depressed skull fracture, intracranial haematoma, epilepsy). Seizures create very high ICP Monitor sodium Magnesium currently under investigation, may combat calcium influx and cellular damage.
  20. 20. urgical management ntracranial pressure monitors External ventricular drains Kochers Point 3cm from midline 11cm from nasion
  21. 21. xternal ventricular drain entriculostomy) nvasive procedure with moderate risks Allows CSF sampling, ICP monitoring and rapid and ongoing treatment of hydrocephalus Commonly inserted at Kochers point to place EVD in frontal horn Less than 5-7cm depth nsert perpendicular to all planes
  22. 22. urgical management ntracranial pressure monitors Decompressive ventricular drains Scalp wounds Depressed skull fractures ntracranial mass lesions  Most GCS <8 do not have intracranial haematomas  Burr holes are not often a good solution in an acute traumatic haematoma, but they may be lifesaving  Decompressive craniotomy if facilities permit
  23. 23. xploratory burr ole placement n order of placement Extend from burrhole with bone nibblers if haematoma found Highly invasive May cause bleeding and brain trauma
  24. 24. ecompressive craniectomy Bifrontal decompressive craniectomy performed day 8 post injury
  25. 25. ummary Rapid assessment Treat and repeat ABCD Avoid hypoxia, hypotension Early retrieval as warranted Medical and nursing management Surgical options can aid management
  26. 26. eferences Prevention of secondary brain injury: targeting technology. Littlejohns L, Bader MK. Department of Clinical Development, Integra NeuroSciences, Plainsboro, NJ, USA. ATLS course manual 1997 Prevention of secondary brain injury following Head Trauma; Cowley and da Silva Trauma.2008; 10: 35-42 Emedicine - Traumatic Brain Injury (TBI) - Definition, Epidemiology, Pathophysiology; Segun T Dawodu Calcium in cell injury and death; Zheng Dong,1 Pothana Saikumar,2 Joel M. Weinberg,3 and Manjeri A. Venkatachalam Annual Review of Pathology: Mechanisms of Disease Vol. 1: 405-434 Secondary Brain Injury: Prevention and Intensive Care Management; TVSP Murthy MD, Parmeet Bhatia MBBS, K Sandhu MD; T Prabhakar MD, R L Gogna MD; Department of Anesthesia and Intensive care; Army Hospital R&R), Delhi Cantt; Indian Journal of Neurotrauma (IJNT) 2005, Vol. 2, No.