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Pre Hospital and ED TBI Resuscitation

Pre Hospital and ED TBI Resuscitation. Neeraj Badjatia, MD MSc Division of Neurocritical Care Department of Neurology Columbia University College of Physicians & Surgeons. Objectives. To review the principles of neurological assessment in the pre hospital setting

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Pre Hospital and ED TBI Resuscitation

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  1. Pre Hospital and ED TBI Resuscitation Neeraj Badjatia, MD MSc Division of Neurocritical Care Department of Neurology Columbia University College of Physicians & Surgeons

  2. Objectives • To review the principles of neurological assessment in the pre hospital setting • To review the indications for endotracheal intubation and the optimal goals for ventilation • Discuss the goals of fluid resuscitation and initial therapeutic interventions for ICP control

  3. Brain Trauma FoundationPre Hospital Guidelines, 2nd Edition (2007)

  4. Sequence of events in TBI Initial Resuscitation Secondary Brain Injury Surgical Intervention ICU Management

  5. Secondary Injury Cascade

  6. Case Study • 26 year old man is assaulted and has sustained blunt head trauma. Upon EMS arrival, he is noted to be intermittently arousable. • VS: BP: 126/75, P: 100, RR: 16, SpO2 – 96 % • Initial GCS assessment = 8. (E-2, V-3, M-3). • Pupils equal and reactive

  7. Assessment at the Scene • ABC’s – Does this patient require intubation? • What does the literature tell us? • Indicated for patients with severe TBI who are unresponsive, and hypoxic, or not able to protect the airway • 74% survival for EMS intubation vs 50% survival for ED intubation (Winchell, Arch Surgery 1997) • What if the patient met above criteria with a SpO2 of 85% on NRB?

  8. Hypoxemia after TBI • Hypoxemia has been documented in approximately 20% of all TBI patients • Independently associated with poor outcome McHugh et al. J Neurotrauma 24 (2):287 - 293

  9. EMS Airway Management • In the absence of hypoxia, the evidence is not so clear • Davis et al – series of studies from UCSD • Scene times longer for patients intubated in the field • Hypoxia and bradycardia associated with field intubation • Higher rates of inadvertent hyperventilation (ETCO2)

  10. 2007 BTF Guidelines(Level 3 Recommendations) A. Hypoxemia (oxygen saturation [SpO2] < 90%) should be avoided, and corrected immediately upon identification. B. An airway should be established, by the most appropriate means available, in patients who have severe traumatic brain injury (TBI) (Glasgow Coma Scale [GCS] < 9), the inability to maintain an adequate airway, or hypoxemia not corrected by supplemental oxygen.

  11. 2007 BTF Guidelines(Level 3 Recommendations) C. EMS systems implementing endotracheal intubation protocols including RSI protocols should monitor blood pressure, oxygenation, and when feasible, ETCO2. D. When endotracheal intubation is used to establish an airway, confirmation of placement of the tube in the trachea should include lung auscultation and end-tidal CO2 (ETCO2) determination. E. Patients should be maintained with normal breathing rates (ETCO2 35–40 mmHg), and hyperventilation (ETCO2 < 35 mmHg) should be avoided unless the patient shows signs of cerebral herniation.

  12. Case Continued • Upon 10 minutes after arrival to the ED, the patient is noted to have a new hemiparesis and pupillary assymetry (GCS = 5) • Vitals: BP: 90/55 P: 115 RR: 24 SpO2 – 89% • Patient is intubated (RSI) with verification by ETCO2 monitoring as well as auscultation • What are the next steps in resuscitation?

  13. ICP management in the Pre Hospital / ED Setting • Principles and sequence of approach slightly different than the ICU • Still thinking in terms of ABCD’s (more acutely than in the ICU setting) • Initial steps should be to assure the patient is adequately hemodynamically resuscitated

  14. Hypotension after TBI • A common phenomena after brain injury, occuring in one in five cases. • Numerous observational studies have confirmed the associationbetween systemic hypotension occurring at any point after injuryand poor outcome. • A single episode of hypotension is associated with approx doubling of mortality and a parallel increase in morbidity. • Persists when age and the presence of hypoxia and extracranial injuries are taken into account • Most commonly due to inadequate volume resuscitation

  15. Fluid Resuscitation:Hypertonic Saline Mechanism of Action • Osmotic effect • Anti-inflammatory effects • Modulation of neuroendocrine system (ANP, VSP) • Maintain BBB integrity via membrane stabilization • Improve regional cerebral blood flow (rCBF) Osmotic effect • Via properties of sodium chloride 1. Low permeability across BBB 2. Hi reflection coefficient (1.0) • Hyperosmolar concentrations • Create a gradient to pull water from interstitial and intracellular spaces into the intravascular compartment

  16. Hypertonic Saline –Clinical Evidence Cooper et al (JAMA 2004; 291: 1350) • Design • Prospective RCT of 229 severe TBI and hypotension in the field • Bolus with 250 cc 7.5% LR or LR • Results • No baseline differences between groups • Median GCS = 4, ISS 38, fluid = 1250 • No difference in Bp on arrival to ED • No difference in morbidity or mortality

  17. 2007 BTF Guidelines • Hypotensive patients should be treated with isotonic fluids. • Hypertonic resuscitation is a treatment option for TBI GCS < 8.

  18. ICP Management: Ventilation goals Goal: achieve normal pCO2 levels (35 – 40 mm Hg) • Manipulation of pCO2 is a very quick and powerful method by which to control ICP • Effects are short lived and should be considered a bridging therapy • No evidence that prophylactic hyperventilation improves outcome • 47 % of ED physicians routinely prophylactically hyperventilate TBI patients • Chronic prophylactic hyperventilation (5 days) worsens long term outcome (Muizelaar JP. J Neurosurg 2001; 75: 731 – 9)

  19. Ventilation in the ED Warner et al (J Trauma. 2008;64:341–347) • Retrospective study of all trauma prehospital intubations during a period of 24 months (n = 851) in Seattle, Wa. • Wanted to see how many patients were at target (PaCO2 between 30 and 39 mm Hg) both on admission to the ED and during ED stay.

  20. Ventilation in the ED

  21. Ventilation in the ED • Patients with TBI who achieved the target range had a mortality of 21.2% compared with 33.7% for those who persistently remained outside this range (p 0.03).

  22. BTF Guidelines 2007 • Hyperventilation is recommended as a temporizing measure for the reduction of elevated intracranial pressure (Level III) • Asymmetric pupillary response • Unilateral or bilateral pupillary dilatation • Motor posturing • Rapid neurologic decline • Prophylactic hyperventilation (PCO2 < 30 mmHg) is not recommended (LEVEL II)

  23. CASE • After volume resuscitation, transient hyperventilation and 70 gm of mannitol, the patient’s pupillary assymetry resolves, and GCS improves to 7. • The nurse checks the temperature – 34.5 C…….

  24. Hypothermia after TBI • Admission hypothermia is seen in 10% of TBI patients • Risk factors include: • Older age • Prehospital hypotension • Small BSA • (+) Blood alcohol • Volume of pre-hospital fluids • High injury severity • Winter enrollment

  25. Hypothermia after TBI • Admission hypothermia is a known independent predictor of poor outcome (last of the dreaded H’s) • Therapeutic hypothermia as a neuroprotectant has not been shown to be beneficial

  26. Hypothermia after TBI Clifton et al (2002) • Post hoc analysis of the NABIS trial looking at outcomes in patients who arrived hypothermic

  27. Conclusions:Avoid the Dreaded H’s

  28. Conclusions Airway & Ventilation • Indications for pre hospital intubation as routine care in severe TBI need to be reassessed • Measurement of CO2 should be routine in all intubated patients • Hyperventilation should only be used as a short term measure until definitive therapy is achieved Fluid Resuscitation • Fluid resuscitation with isotonic fluids, but the HTS story is not over yet

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