Flight Nurse Head Injury


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  • Hello I’m nancy George, your teacher for today Welcome to The alphabet soup of TBI
  • What do we mean by TBI? Any injury from impact to the skull We will not be discussing any medical issues such as encephalitis, meningitis, epilepsy, or any other cerebral disease process
  • Here is one way someone could get a TBI Motor vehicle crashes, falls from a height, blows to the head, are all good ways to receive this type of injury
  • TBI is the leading cause of death due to trauma Certainly orthopaedic injuries cause more extended rehabilitation Abdominal injuries cause more incidences of shock But TBI causes more deaths overall Admission to a level of care that can address these injuries is critical. You may be faced with moving a brain injured patient from a small regional hospital to a higher level of care
  • Moving these patients by air is usually the most efficient method
  • The reason we need to facilitate the transfer of brain injured patients to the most appropriate care is that delay often causes additional damage to brain tissues
  • And what is the physiologic mechanism that causes this additional damage? Compromised cerebral perfusion pressure
  • Let’s begin by looking at how cerebral perfusion pressure is supposed to work
  • Picture the skull as a box that cannot expand The contents therefore are fairly constant in volume Blood and brain tissue are about equal in volume CSF provides a small additional factor
  • Here is a diagram of the intracranial contents Arterial and venous blood Brain tissue CSF
  • Of course there is a small amount of adjustment possible in the relative volumes of the skull contents This is called the autoregulation process Arteries constrict to reduce the amount of blood entering the cranial cavity Arteries dilate to increase the blood flow These arterial changes are in response to changing oxygen or CO2 levels, and changing arterial blood pressures
  • An acute brain injury changes this autoregulation process by inappropriately increasing the volume of one or more components of the skull’s contents This can greatly increase pressures within the cranium—called an increased ICP, intracranial pressure
  • As the increased ICP interferes with the autoregulation process, cerebral blood flow is decreased, causing ischaemia to the brain tissue and cerebral hypoxia
  • This picture illustrates an expanding subdural haematoma that increases the intracranial pressure and compresses the brain tissue, cerebral arteries, and intracerebral ventricles It is similar to putting a tourniquet around the brain, depriving it of arterial blood and causing tissue ischaemic death
  • A lot of the cardiac output is diverted to the brain’s arterial needs The normal range of effective cerebral perfusion pressures is relatively narrow
  • Why is this so important? Because the brain lacks metabolic reserves That means it must have a continual supply of oxygenated blood in order to maintain aerobic metabolism, unlike a kidney, for instance, which can be separated from its arterial blood supply for hours and still remain viable That’s one of the reasons kidney transplants are practical and brain transplants aren’t. (not the only reason, of course) The other issue is that cerebral perfusion pressure can be influenced by a lot of physiologic processes, such as oxygenation, blood pressure, oedema
  • If CPP is so important, how do we know what the number is for a particular brain injured patient? CPP = MAP – ICP It may help to compare the components of the CPP calculation with cardiac preload-afterload parameters you could compare MAP to preload, which is blood going into the heart (brain) And compare ICP to afterload, which is the resistance the heart has to overcome (it’s harder to pump arterial blood into a brain with a high ICP)
  • Here is an example of the calculation:
  • Do we always have to calculate the ICP? Not if there is an intracranial monitor inserted. If we’re lucky, the sending hospital has someone who can insert an intracranial bolt, and all we have to do during the transfer is respond to the numbers
  • But if the sending facility doesn’t have a neurosurgeon (which is a good reason for you to do the transfer) you probably won’t have an ICP monitor How will you know if your patient’s ICP rises en route? How will you know if his cerebral perfusion has fallen and his brain is more ischaemic?
  • It would be great if we had a CT scanner in the airplane
  • But since we don’t, we have to use our keen nursing assessment skills to figure out what is going on.
  • Let’s look at 5 ways we can make an estimation of the patient’s ICP through our nursing assessment
  • A deteriorating LOC is a very sensitive measurement of brain activity, which reflects brain perfusion
  • Of course if he’s in a coma, don’t as him his name or the date
  • Pupillary response is another excellent sign to watch A rising ICP puts direct pressure on the third cranial nerve, interfering with the pupil’s ability to respond to light
  • Here is a patient with unequal pupils
  • We can assess other cranial nerves as well
  • This patient has a good response from his twelfth cranial nerve, the Hypoglossal nerve
  • Motor activity can tell us about ischaemia to the motor strip in the parietal area of the brain Of course the conscious and cooperative patient is easy to assess But even the unconscious patient can withdraw from pain (or not)
  • A very high ICP will finally interfere with the brain’s respiratory centers You may see a variety of abnormal respiratory patterns as the brain becomes more ischaemic
  • A good nursing Assessment can give us a lot of important information
  • So what will our response be to an elevated ICP? Here are a few of the standard treatments that can be done in the air transport environment
  • Of course we’d like to window the skull to give the oedematous brain room to swell, but we can’t do that
  • It is important to remember that while lowering the BP reduces the amount of incoming volume to a swollen brain, the MAP must be able to overcome the ICP resistance to bring oxygen to the brain tissues Lots of oxygen will ensure that what arterial blood does get to the brain tissue is fully O2- saturated While hyperventilation will cause the cerebral arteries to constrict, reducing ICP, this vasoconstriction is compromising cerebral perfusion in the long run
  • Be prepared to ventilate your patient in the event of falling GCS, rising ICP, falling CPP
  • So in conclusion, here is a final review of the alphabet soup we have been discussing: CHI CPP ICP Assessments – PERL, etc Treatments – IV, O2, etc A knowledge of the physiologic processes involved A focussed nursing assessment A rapid response to changing patient conditions A successful transfer of the head injured patient to definitive care
  • Flight Nurse Head Injury

    1. 1. The Alphabet Soup of Traumatic Brain Injury
    2. 2. Definition <ul><li>Traumatic brain injury </li></ul><ul><ul><li>Refers to injuries that result directly from impact. </li></ul></ul><ul><ul><li>Injuries include contusions, lacerations, brainstem injuries, and diffuse axonal injury </li></ul></ul>ENA, 2010
    3. 4. Traumatic Brain Injury <ul><li>Leading cause of death due to trauma </li></ul><ul><li>Outcomes are greatly affected by the severity of the initial injury and the time elapsed to definitive care. </li></ul><ul><li>Therefore, rapid interfacility transport is crucial. </li></ul>Holleran, 2010, p. 311
    4. 6. Secondary Brain Injury <ul><li>Injuries caused by pathophysiologic processes which add to the primary injury during a delay—such as transferring the patient to a higher level of care </li></ul><ul><li>These include expanding hematomas, increasing cerebral oedema, rising ICP and seizures </li></ul>ENA, 2010
    5. 7. The Key Problem: <ul><li>The combination of primary and secondary damage leads to compromised cerebral perfusion (CPP) </li></ul>
    6. 8. HOW IS CEREBRAL PERFUSION SUPPOSED TO FUNCTION? (OR, How is the alphabet soup supposed to look?)
    7. 9. Normal Volume Relationships <ul><li>Contents of the skull are: </li></ul><ul><ul><li>Cerebrospinal fluid (150 ml) </li></ul></ul><ul><ul><li>Blood (1400 ml) </li></ul></ul><ul><ul><li>Brain tissue (1400 ml) </li></ul></ul>Holleran, 2010, p. 387
    8. 10. Skull Contents Brain Tissue Venous Blood Arterial Blood CSF
    9. 11. Cerebral Blood Flow Autoregulation <ul><li>Arterial blood flow and volume is controlled by the autoregulation process </li></ul><ul><ul><li>Cerebral arteries constrict when systemic BP rises or when PaCO 2 decreases and PaO 2 increases </li></ul></ul><ul><ul><li>Cerebral arteries dilate when systemic BP falls or when PaO 2 decreases and PaCO 2 increases </li></ul></ul><ul><li>The brain has the ability to maintain constant blood flow with arterial pressures between 60 and150mmHg (MAP) </li></ul>Holleran, 2010, p. 389
    10. 12. Pressure-Volume Relationships with Acute Brain Injury <ul><li>Any increase in the volume of one of the components within the skull without a decrease in the volume of the other two results in increased pressure </li></ul>Holleran, 2010, p. 387
    11. 13. Autoregulation Failure <ul><li>As ICP increases, autoregulation fails, and CBF (cerebral blood flow) decreases, resulting in decreased tissue perfusion and ischaemia. </li></ul><ul><li>Decreased perfusion leads to cerebral hypoxia, which disrupts cellular metabolism and the blood-brain barrier </li></ul><ul><li>This leads to further cerebral oedema through fluid leaking from capillaries into brain tissue </li></ul>ENA, 2010
    12. 15. Normal Cerebral Perfusion <ul><li>Brain receives about 15 to 35% of cardiac output </li></ul><ul><li>Goal is to maintain a cerebral perfusion pressure (CPP) between 70 and 90 mmHg </li></ul>ENA, 2010
    13. 16. What’s so important about CPP? <ul><li>Brain lacks metabolic reserves and depends on arterial flow (cerebral perfusion) to meet it’s needs </li></ul><ul><li>Factors that influence CPP include: PaO 2 , PaCO 2 , cerebral blood volume, systemic BP, cerebral oedema and ICP. </li></ul>ENA, 2010
    14. 17. Calculating Cerebral Perfusion Pressure <ul><li>CPP = MAP – ICP </li></ul><ul><li>Compare to cardiac preload-afterload calculations: </li></ul><ul><ul><li>MAP is like blood going in (preload) </li></ul></ul><ul><ul><li>ICP is like resistance to blood flow (afterload) </li></ul></ul>
    15. 18. A Calculation Example: <ul><li>MAP = (2xDP)+SP </li></ul><ul><li>3 </li></ul><ul><li>Normal BP: 120/70 </li></ul><ul><li> 2x70 = 140 + 120 = 260 </li></ul><ul><li> 260/3 = 87 MAP </li></ul>
    16. 19. How Do I Measure ICP Directly? <ul><li>ICP monitor into the cranial cavity </li></ul><ul><li>Measured in mmHg </li></ul><ul><li>Normally 7-15 mmHg for a healthy, supine adult </li></ul><ul><li>Only available in ICU or sometimes during interfacility transfers </li></ul>
    17. 20. Assessing ICP Without an ICP Monitor <ul><li>Since it isn’t always able to be directly measured in the air transfer environment, ICP may be indirectly assessed by physical findings </li></ul><ul><li>How do we assess ICP physiologically? </li></ul>
    18. 22. Signs of Increasing ICP <ul><li>Early recognition of increased ICP is vital to preserving brain function </li></ul><ul><li>Early warnings : Change in LOC, irritability, mild confusion, pupillary change and decreased Glasgow Coma Score. </li></ul><ul><li>Late: Very difficult to arouse, coma, posturing, fixed pupils or blown pupils and ECG changes, Cushings response </li></ul><ul><ul><li>Cushing triad is (systolic) hypertension with widened pulse pressure, bradycardia and respiratory depression. </li></ul></ul>ENA, 2010
    19. 23. Brain Injury Assessment <ul><li>Level of consciousness </li></ul><ul><li>Pupil size and reactivity </li></ul><ul><li>Cranial nerve activity </li></ul><ul><li>Motor activity </li></ul><ul><li>Respiratory pattern </li></ul>Holleran, 2010, p. 315
    20. 24. Level of Consciousness <ul><li>Alert – responds readily but may be confused </li></ul><ul><li>Lethargic – drowsy but can be aroused </li></ul><ul><li>Obtunded – difficult to arouse, cannot make a complete sentence, requires repeated stimulation </li></ul><ul><li>Stuporous – no verbal response, may moan, responds to pain by moving extremities </li></ul><ul><li>Comatose – no evidence of awareness </li></ul>Holleran, 2010, p. 315
    21. 25. Berry, 1995
    22. 26. Pupil Response <ul><li>Cranial nerve III </li></ul><ul><li>Injury to parasympathetic system dilates pupils </li></ul><ul><li>Injury to sympathetic system constricts pupils </li></ul><ul><li>Bilateral fixed and dilated pupils usually indicate global hypoxia or herniation from cerebral oedema </li></ul>Holleran, 2010, p. 317
    23. 28. Cranial Nerve Activity <ul><li>II Optic nerve </li></ul><ul><ul><li>“ can you see me?” </li></ul></ul><ul><li>III Oculomotor nerve </li></ul><ul><ul><li>“ look up, look down”, pupil response </li></ul></ul><ul><li>XI Spinal accessory nerve </li></ul><ul><ul><li>“ shrug your shoulders” </li></ul></ul><ul><li>XII Hypoglossal nerve </li></ul><ul><ul><li>“ stick out your tongue” </li></ul></ul>
    24. 30. Motor Activity <ul><li>Conscious patient </li></ul><ul><ul><li>Grip your hands </li></ul></ul><ul><ul><li>Push feet against your hands </li></ul></ul><ul><li>Unconscious patient </li></ul><ul><ul><li>Motor activity in response to pain </li></ul></ul><ul><ul><ul><li>Purposeful withdrawal </li></ul></ul></ul><ul><ul><ul><li>General extremity movement </li></ul></ul></ul>Holleran, 2010, p 317
    25. 31. Respiratory Pattern <ul><li>Initial hypoventilation </li></ul><ul><li>Cheyne-stokes (crescendo-de-crescendo) </li></ul><ul><li>Brainstem lesions – irregular, shallow, slowing rate </li></ul><ul><li>Medullary lesions – respiratory paralysis </li></ul><ul><li>Central neurogenic hyperventilation </li></ul>Holleran, 2010, p 318
    26. 32. Berry, 1995
    27. 33. Treatment of Increased ICP <ul><li>Keep head midline with HOB elevated to 45° </li></ul><ul><li>Decrease stimulation </li></ul><ul><li>Administer Mannitol or Frusemide per order </li></ul><ul><li>Sedate (neuromuscular blockades/ barbiturates): decreases the metabolic rate </li></ul><ul><li>Temperature control </li></ul>ENA, 2010
    28. 35. Other Possible In-flight Interventions <ul><li>IV fluids to maintain BP over 90 systolic to perfuse brain </li></ul><ul><li>Treat seizures as needed </li></ul><ul><li>Continue ventilation with 100% O 2 to oxygenate brain </li></ul><ul><li>Initial (only) hyperventilation, to lower ICP </li></ul><ul><ul><ul><li>Prolonged hyperventilation not recommended unless: </li></ul></ul></ul><ul><ul><ul><ul><li>Dilated pupils or Extensor posturing </li></ul></ul></ul></ul>Holleran, 2010, p 320
    29. 37. Conclusion - Alphabet Soup <ul><li>Brain trauma (CHI) happens </li></ul><ul><li>Maintaining cerebral perfusion (CPP) is the goal </li></ul><ul><li>Cerebral oedema (ICP) compromises cerebral perfusion </li></ul><ul><li>Assessment for cerebral oedema (PERL, LOC, GCS, RR) </li></ul><ul><li>Treatment for cerebral oedema (BP, O 2 , IV) </li></ul>
    30. 39. References <ul><li>Berry, S. (1995) . I’m still not an ambulance driver. S. Berry, Publisher. </li></ul><ul><li>Emergency Nurses Association. (2010). http://www.ena.org/ coursesandeducation/CATNII-ENPC-TNCC/tncc/Pages/Default.aspx </li></ul><ul><li>Holleran, R. (2010). ASTNA Patient transport principles and practice (4th Edition). Mosby. St. Louis, Missouri. </li></ul>