Presentation is loading. Please wait.

Presentation is loading. Please wait.

If I Only Had A Brain….. Pre-Hospital Management of Traumatic Brain Injury Jennifer Davis, RN, MS, ANP-C, CCRN, EMT-CC.

Similar presentations

Presentation on theme: "If I Only Had A Brain….. Pre-Hospital Management of Traumatic Brain Injury Jennifer Davis, RN, MS, ANP-C, CCRN, EMT-CC."— Presentation transcript:

1 If I Only Had A Brain….. Pre-Hospital Management of Traumatic Brain Injury Jennifer Davis, RN, MS, ANP-C, CCRN, EMT-CC

2 Incidence  Traumatic Brain Injury, or TBI, is the leading cause of death and disability in children and adults from ages 1-44  Most often caused by motor visual crashes, sports injuries, or simple falls on the playground, at work, or in the home  Approximately 52,00 deaths occur from TBI annually  An estimated 1.5 million head injuries are seen yearly in Emergency Departments  An estimated 1.6 to 3.8 million sports related TBIs occur each year

3 Facts about TBI  At least 5.3 million Americans, 2% of the US population, currently live with disabilities resulting from TBI  Moderate and severe head injury (respectively) is associated with a 2.3 and 4.5 times increased risk of Alzheimer’s disease  Males are 2x more likely to suffer TBI that females  The leading causes of TBI are falls, MVC, and assaults

4 Facts about TBI  TBI hospitalization rates have increased from 79% per 100,000 in 2002 to 87.9% per 100,000 in 2003  Exposures to blasts are a leading cause of TBI among active duty military personnel in war zones  Veteran’s advocates believe that between 10 and 20% of Iraq war veterans, or 150,000 and 300,000 members have some level of TBI  30% of soldiers admitted to Walter Reed have been diagnosed with a TBI

5 Prevention  The best way to treat TBI is prevention  Bicycle helmets  Not just for kids!  Wearing a bicycle helmet reduces risk of TBI by 88%  Only 1% of people admitted to a trauma center after a bicycling accident were wearing helmets  Seat belt use  Motorcycle helmets – full face  Helmets  Skateboarding  Rollerblading  Scooters  At risk behaviors  Males 2 times > injury rate than females

6 Where does EMS fit in?  EMS providers are the first contact a patient has into the trauma system  We have the ability to prevent secondary brain injury with the right interventions  Primary brain injury – the initial brain injury sustained as a result of trauma  Secondary injury – the injury that occurs due to hypoxemia and hypovolemia

7 Classification of TBI  Mild TBI (GCS 13-15) (MOST of what EMS will see)  Concussive syndrome  Reversible, temporary LOC/retrograde amnesia  Change in mental status a the time of injury only  Imaging usually normal  Moderate TBI (GSC 9-12)  LOC and/or post amnesia of > 30 minutes but < 24 hours  GCS – 9-12  Physical, cognitive, and/or behavioral impairments last for months or are permanent  Generally make a good recovery with treatment or learn to compensate for deficits

8 Classification of TBI  Severe TBI (GCS 3-8)  LOC or post-traumatic amnesia > 24 hours  GCS lower  More extensive physical impairments as a result if brain damage  Slower course of recovery  Clear indication of significant, permanent deficits  What these are depend on location of injury

9 Classification of TBI  Very severe/catastrophic TBI  True comas of many weeks or months  This term is reserved for the most severely damaged head injury  Many never regain consciousness or regain meaningful communication with the environment  “Persistent vegetative state”

10 Brain Death  Results from a severe insult to the brain  No cortical or brain stem activity  No movement to stimuli  No brain stem reflexes  No spontaneous breathing  Not diagnosed in the field  If the brain is dead, the person is dead

11 Concussion  Traumatic, REVERSIBLE neurological deficit  Temporary LOC  Retrograde amnesia  Etiology  Strong, rapid acceleration-deceleration injury  Blow to the head  There is a temporary cessation of the functioning of the reticular activating system  RAS responsible for arousal or wakefulness of the brain

12 Concussion  Assessment  Subjective Data  HPI  Mechanism, consciousness immediately after event, duration of event, neuro events after event  Medical Hx  Neuro disease, recent trauma, prior head injury  Objective Data  Physical exam – neuro exam, memory assessment  May have repetitive speech and questions  Diagnostics  CT scan – R/O bleed

13 Interventions for Concussion  Immobilization as necessary  Emotional support  High flow oxygen

14 Planning/Interventions for Concussion  Post Concussive Syndrome  Results from repeated mild brain injuries over a period of months or years  Can impact neurological, behavioral and cognitive function  “second impact syndrome” now called Chronic Traumatic Encephalopathy or CTE Muhammad Ali, Football players  Once a person suffers a concussion, they are four times more likely to suffer another one.

15 Skull Fracture  Types  Linear  Most common  Account for about 70% of all types  Usually benign unless it crosses a major vascular channel  Depressed  Damages underlying cerebral tissue by compression or laceration and by retained bony fragments  Basilar  Can occur within any of the fossae  Clinical picture depends on the area affected  Complications include infection, hematoma, CSF leaks, loss of smell, loss of hearing, seizures and pneumocephalus.

16 Skull Fracture  Assessment  Subjective Data  HPI  Recent trauma, elapsed time, sweet or salty taste in back of throat, post nasal drip  Medical Hx  Trauma, malignancy

17 Skull Fracture  Objective Data  Physical Exam  Surface trauma, AMS, altered pupil or motor response, CSF leak, Raccoon eyes, Battle’s sign  Diagnostics  Halo Test (ottorrhea or rhinorrhea) Using a 4X4 collect fluid leak from nose or ear Set on the bedside table for a few minutes Positive when there is a circular separation of blood and clear fluid or a “halo” Indicative of a CSF leak

18 Halo Sign

19 Depressed Skull Fx

20 Linear Skull Fx

21 Basilar Skull Fx

22  Battle’s SignRaccoon Eyes

23 Diffuse Axonal Injury (DAI)  DAI is the widespread disruption of neuro function without any focal lesions  Characterized by microscopic damage to the axons, diffuse white matter degeneration, global neuro dysfunction and diffuse cerebral edema.  Etiology  Acceleration-deceleration  MVC, Pedestrian, Shaken Baby  Shear injury

24 DAI  Assessment  Subjective Data  HPI  Mechanism of injury, onset and duration of LOC  Medical Hx  Neuro disease or injury  Substance abuse  Child abuse or exam doesn’t fit with mechanism of injury Shaken baby

25 DAI  Objective Data  Physical Exam  Immediate LOC, lasts days to months  Increased ICP  Brain stem dysfunction  Decortication or decerebration  Loss of brain stem reflexes – cough, gag, etc.  Hypertension  Hyperthermia  Diaphoresis

26 DAI


28 Cerebral Contusion  Cerebral contusion is an actual bruising of the brain  Results in focal ischemia and edema with potential for infarction, necrosis and/or ↑ ICP  Etiology  Trauma, acceleration/deceleration, high velocity blows, or rotation of the brain following a blow  Coup – contra coup injury  Clinical picture varies depending on area involved

29 Cerebral Contusion  Assessment  Subjective Data  HPI  Mechanism of injury, changes in LOC since event  Medical Hx  Neuro disease or injury  Substance abuse

30 Cerebral Contusion  Objective Data  Physical exam  Altered LOC > than a few hours  Surface trauma  Full neuro exam

31 Cerebral Contusion

32 Subdural Hematoma (SDH)  SDH is a collection of blood between the dura matter and the subarachnoid layer of the meninges  Usually caused by trauma or as the extension of an intracerebral hematoma into the subdural space

33 Subdural Hematoma (SDH)  Three classifications  Acute - onset within 48 hours of presentation  Sub-acute – onset 2-14 days  Chronic – more than 14 days

34 Subdural Hematoma (SDH)  Assessment  Subjective Data  HPI  Mechanism of injury, time interval, trends in neuro status  Medical Hx  ETOH Abuse Chronic SDH common in these pts secondary to multiple falls and abnormal bleeding tendencies secondary to impaired liver function

35 Subdural Hematoma (SDH)  Medical History  Use of blood thinners or anti-platelet agents  Coumadin® (warfarin), Pradaxa® (dabigatran), Plavix® (clopridogrel), Effient® (prasugrel), Lovenox® (enoxaparin), Aggrenox®  Many patients on blood thinners or anti-platelet agents many have minor trauma or low mechanism, but should be evaluated in ER as even very minor trauma in these patients can cause hemorrhage

36 Subdural Hematoma (SDH)  Objective Data  Physical Exam  Acute  Headache, drowsiness, confusion  Steady decline in LOC  Ipsilateral, unilateral pupil dilation with lack of response to light – LATE finding  Contra lateral hemiparesis  Chronic and sub acute  Gradual and non-specific changes  Altered mentation  Altered motor status  Ipsilateral pupil dilation and sluggish to light

37 Subdural Hematoma (SDH) Acute SDH with left to right shift

38 Subdural Hematoma (SDH) Chronic SHD (gray) with acute SHD component (white)

39 Epidural Hematoma (EDH)  Collection of blood between the skull and dura  Etiology  Usually from a laceration of the middle meningeal artery associated with skull fx  The arterial bleed in under high pressure – it does not tamponade, but rather progresses to become a space occupying lesion causing ↑↑ ICP, brain shift and herniation  Mortality = 50% if not treated

40 Epidural Hematoma (EDH)  Assessment  Subjective Data  HPI  Mechanism of injury  PATTERN of unconsciousness Initially unconscious, followed by a lucid period, then followed by rapid unconsciousness  Medical Hx  Previous trauma, previous head injury

41 Epidural Hematoma (EDH)  Objective Data  Physical exam  Altered LOC, pupils with unilateral dilation, fixed and/or dilated, contralateral paresis or paralysis which leads to posturing  Cushing’s triad Abnormal respirations Narrowing pulse pressure Bradycardia  Diagnostics  Rapid CT exam at trauma center

42 Epidural Hematoma (EDH) Notice the scalloping, rather than layering of the blood.

43 EDH  Frequent neuro checks  ABC’s  Prepare for emergency surgery  Transport to a facility with neurosurgery capabilities  TRUE Neurosurgical emergency!

44 Increased ICP  ICP is influenced by relatively fixed volumes  The brain80%  The blood10%Total volume  The CSF10%  Monroe-Kellie Hypothesis  to maintain a normal ICP, a change in the volume of one compartment must be offset by a reciprocal change in the volume of another compartment

45 Increased ICP  Etiology – Any condition that:  Increases brain volume  space occupying lesions SDH, masses, cerebral edema, EDH, ICB  Increases blood volume  Venous outflow obstruction, hyperemia (HTN), hypercapnia  Increases CSF  Hydrocephalus, SAH, lack of absorption of CSF

46 Increased ICP  Assessment  Subjective Data  HPI  ChronologyPain  ConsciousnessSeizures  MentationVomiting  PersonalityMotor deficits  CommunicationHeadaches  NauseaVisual changes

47 Increased ICP  Medical History  Neuro disease  Trauma  Fainting  Substance abuse  Especially cocaine, heroin  Medications  Allergies

48 Increased ICP  Objective Data  Physical Exam  EARLY picture of ↑ ICP  LOC – changes may be SUBTLE. Changes in LOC may be the FIRST sign of ↑ ICP LISTEN to the patient’s family – they know their loved one BEST!  Pupils – sluggish, different bilaterally Ipsilateral/unilateral changes  Motor function Contralateral changes  Vital Signs

49 Increased ICP  LATE picture of ↑ICP  LOC  Arouses only with deep noxious stimuli, or unresponsive  Pupils Fixed and dilated or “blown”  Motor function Hemiparesis, posturing, or flaccidity  Vital Signs Cushings Triad Bradycardia Narrowing pulse pressure Slow or irregular respirations

50 Hyperventilation  Hyperventilation in Traumatic Brain InjuryOnly used when:  GCS < 8 plus  Active seizure  Posturing  Increased BP and decreased pulse  Intermittent apnea  Further decrease of GCS >2 on subsequent exam  Adult – 20 breaths per minute  Child – 25 breaths per minute

51 Get With The Guidelines Brain Trauma Foundation Guidelines for the Pre-Hospital Treatment of Traumatic Brain Injury

52 Treatment for TBI  Oxygenation and Blood Pressure  Hypoxemia (<90% O2 Sat) or hypotension (<90 mm Hg SBP) are significant parameters associated with a poor outcome in patients with severe head injury in the pre-hospital setting  In children the parameters are SBP<65 (0- 1 years old), <75 (2-5 years old), <80 (6-12 years old) and <90 (13-16 years old

53 Treatment for TBI  High Flow 02 all patients  Assist ventilations as necessary per protocol  Avoid nasal airways in those patients with facial injury and/or suspected basilar skull fx  Raising BP in hypotensive, severe head injury patients improves outcome in proportion to the efficacy of the resuscitation  If ALS – IV NS Open until SPB >90, or up to 2 liters infused then contact Medical Control

54 Glasgow Coma Score (GCS)  pre-hospital measurement of GCS is a significant and reliable indicator of severity of head injury particularly in association with repeated scoring and improvement or deterioration of the score over time  A GCS score of 3 to 5 has at least a 70% positive predictive value for poor outcome

55 GCS  Best Eye Response. (4) 1. No eye opening. 2. Eye opening to pain. 3. Eye opening to verbal command. 4. Eyes open spontaneously.

56 GCS  Best Verbal Response. (5) 1. No verbal response 2. Incomprehensible sounds. 3. Inappropriate words. 4. Confused 5. Orientated

57 GCS  Best Motor Response. (6) 1. No motor response. 2. Extension to pain. 3. Flexion to pain. 4. Withdrawal from pain. 5. Localizing pain. 6. Obeys Commands.

58 GCS  Note that the phrase 'GCS of 11' is essentially meaningless, and it is important to break the figure down into its components, such as E3V3M5 = GCS 11.  A Coma Score of 13 or higher correlates with a mild brain injury, 9 to 12 is a moderate injury and 8 or less a severe brain injury. Teasdale G., Jennett B., LANCET (ii) 81-83, 1974.

59 Pupillary Assessment  Pupil examination is a standard component of the pre-hospital neuro exam  The pupillary exam along with the GCS will serve as a baseline for ALL subsequent examinations in the ER and hospital

60 Pupillary Assessment  Pre-hospital pupil exam should consist of:  The pupil size and light reflex  Assess and document on the PCR  The duration of the pupillary dilation and fixation should be assessed and documented  Brisk reaction to light  Sluggish reaction to light  No reaction to light

61 Anisocoria

62 Airway, Ventilation, and Oxygenation  GUIDELINES  Hypoxemia (apnea, cyanosis, Sat <90%) MUST be avoided or corrected immediately  Sats should be monitored, if available, on all patients with TBI  Hypoxemia should be treated with supplemental O2  In NYS and Suffolk – all trauma patients should be given high flow 02

63 Airway, Ventilation, and Oxygenation  Options  Airway should be secured in pts with GCS<9, the inability to maintain an adequate airway, or hypoxemia not corrected by supplemental O2  Endotracheal intubation is the most effective way to maintain a difficult airway  Intubate only if possible – i.e. teeth not clenched, avoid prolonged attempts as this will increase ICP  In peds, BVM ventilation is just as effective as long as you are getting chest rise

64 Airway, Ventilation, and Oxygenation  AVOID prophylactic hyperventilation  Patients should be maintained with normal breathing rates (ETCO mmHg), and hyperventilation (ETCO2 < 35 mmHg) should be avoided unless the patient shows signs of cerebral herniation

65 Hyperventilation  20 breaths per minute in an adult  25 breaths per minute in a child  30 breaths per minute in an infant less than 1 year old  For ALS providers:  The goal of hyperventilation is ETCO2 of mmHg. Capnography is the preferred method for monitoring ventilation

66 Fluid Resuscitation  Fluid resuscitation in patients with TBI should be administered to avoid hypotension and/or limit hypotension to the shortest duration possible  In Suffolk  Up to 2 large bore IV’s with NS open until SBP >90 or up to 2 liters NS infused, then contact with MC  KVO for SBP > 90

67 Hypoglycemia  Hypoglycemia has been associated with traumatic events – it exhibits signs similar to that of patients with TBI  I.e. MVA secondary to low blood sugar  Blood sugar should be checked in all patients with AMS of undetermined etiology  Treat hypoglycemia

68 Transport Decisions  Patients with severe TBI and a GCS <9 should be transported to a facility with the following capabilities:  Immediate CT Scanning  Prompt neurosurgical care  Ability to monitor ICP and treat increased ICP  For all intents and purposes, this is a trauma center  GSH  SSH  BMH  UHSB

69 Case Study  You are dispatched to the scene of a motorcycle vs. car – BLS ambulance  On scene you find:  Approximately 20 year old male lying prone  Ninja motorcycle  Full face helmet in place but not intact  Motorcycle is found approximately 50 feet from where you find your patient  You notice bilateral femur deformities

70 Case Study  Patient is unresponsive to verbal stimuli  Upon rolling your patient, while maintaining cervical stabilization, of course, you open the visor of the helmet and determine that the patient is not maintaining an adequate airway and you……………………..  Remove helmet per NYS protocols Obvious depression In the occiput of the pt’s head  Using a jaw thrust, open the airway, look, listen and feel for breathing You determine that he is not able to maintain his airway and that he is breathing irregularly

71 Case Study  Place an oral airway  Begin BVM ventilations  Check for a distal pulse – 120 and weak  Check BP – 80/30  GCS of 6  Decerebrate posturing  You take a step back, and think to yourself…  Oh Crap!  No – ABC’s are taken care of, now what must I do to maintain this patient  Call for ALS to scene  While waiting for ALS, rapid transport decision, immobilize in c-collar and place on LBB, get patient ready for transport. Do not wait on scene for ALS!!!!

72 Case Study  ALS – intervene enroute to trauma center  Remember the standards/guideline for pre- hospital management of TBI  Airway/Breathing Is it adequate with the OPA in place, is there chest rise, can I safely intubate this patient and not do further harm  Circulation What is the pulse and BP IV access NS open for SBP >90 or up to 2 liters  Hyperventilation Do I need to do it? – In this patient, yes, mild hyperventilation of 20 BPM is appropriate based on his physical assessment and neuro exam

73 Case Study  Are my interventions helping? Re-assess ABC’s Re-assess GCS Re-assess Vitals

Download ppt "If I Only Had A Brain….. Pre-Hospital Management of Traumatic Brain Injury Jennifer Davis, RN, MS, ANP-C, CCRN, EMT-CC."

Similar presentations

Ads by Google