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Head Trauma NOTE: Beginning with third edition of this text, material included in this chapter has been based upon recommendations of Brain Trauma Foundation.

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Presentation on theme: "Head Trauma NOTE: Beginning with third edition of this text, material included in this chapter has been based upon recommendations of Brain Trauma Foundation."— Presentation transcript:

0 International Trauma Life Support, 7e
Head Trauma 10 Key Lecture Points Cover the anatomy. Cover the physiology of the brain and explain why hyperventilation is no longer recommended except in cases of herniation syndrome. Emphasize the control of the airway in the patient with an altered level of consciousness. Stress that suction must be available at all times. Stress that a patient with a serious head injury (Glasgow Coma Score of 8 or less) will not tolerate hypoxia or hypotension. In this situation do not allow the blood pressure to get below 100–110 systolic. Mention that prehospital providers tend to inadvertently hyperventilate head-injured patients. Stress that, if possible, capnography should be used to prevent inadvertent hyperventilation. Mention the aspects of the Glasgow Coma Score and that each part should be recorded, not just the total score. This score should always be recorded if there is altered mental status. Stress indications for hyperventilation.

1 Head Trauma NOTE: Beginning with third edition of this text, material included in this chapter has been based upon recommendations of Brain Trauma Foundation (a multidisciplinary organization dedicated to improving care of TBI victims by use of evidence-based treatment). © Edward T. Dickinson, MD

2 Overview Anatomy of head and brain Pathophysiology of traumatic injury
Primary and secondary injury Mechanisms of secondary brain injury Assessment, management, potential problems Management of cerebral herniation syndrome

3 Head Trauma Traumatic brain injury (TBI)
Major cause of death and disability CNS injury in 40% multiple trauma Death rate twice of non-CNS injury 25% of trauma fatalities Assume spinal injury with serious injury Potential for altered mental status Potential for altered mental status with head injury eliminates possibility of field clearance for spinal injury.

4 Head Anatomy IMAGE: 10-1 Anatomy of the head
NOTE: Briefly review key issues of anatomy. Skull is essentially a closed box. Rigid and unyielding bony skull protects brain from injury, but also makes closed space container, so no room for significant swelling. NOTE: Point out bony prominences of interior skull, which can cause damage to brain with movement from trauma. NOTE: Point out foramen magnum at base where brain stem becomes spinal cord. This is only significant opening through which pressure can be released. Fibrous coverings of brain are meninges. Dura mater, arachnoid mater, pia mater listed from outermost to innermost. TEACHING TIP: Students can think “Brain PAD” to remember order of layers. (Brain is “padded” by meninges, starting with Brain and moving out, layers are P – A – D.) Brain tissue is fragile, easily damaged if not protected by meninges. Brain tissue requires a constant supply of blood (oxygen and glucose) to survive. Cerebrospinal fluid (CSF) is nutrient fluid found beneath arachnoid and pia mater layers and bathes brain and spinal cord. Brain “floats” inside CSF and allows for some movement with cushioning to absorb minor forces. However, brain attached at base, which causes more movement at top of brain. Significant force from blunt trauma can cause “third collision” of brain into skull.

5 Brain Injuries Primary Secondary Immediate damage to brain tissue
Direct result of injury force Little can change injury after it occurs Secondary Result of hypoxia or decreased perfusion Prehospital care can help prevent Primary brain injury is the immediate damage to the brain tissue that is the direct result of the injury force and is essentially fixed at the time of injury. Little can be done to change the injury after it has occurred. Primary brain injury is better managed by prevention with such measures as use of occupant restraint systems in autos, the use of helmets in sports, work, and cycling, firearms education, and so forth. Secondary brain injury is the result of hypoxia or decreased perfusion of brain tissue. Good prehospital care can help prevent the development of secondary brain injury. In response to the primary insult, swelling can cause a decrease in perfusion. As a consequence of other injuries, hypoxia or hypotension may occur and both are damaging to brain tissue.

6 Brain Injuries Coup Contracoup The “3rd collision”
Area of original impact Contracoup The “4th collision” Rebounding hitting the opposite side Injuries may occur to the brain in the area of original impact (“coup”) or on the opposite side (“contracoup”). The interior base of the skull is rough (Figure 10-2), and movement of the brain over this area may cause various degrees of injury to the brain tissue or to blood vessels supporting the brain

7 Brain Anatomy Intracranial volume Brain CSF Blood vessel volume
Dilatation with high pCO2 Constriction with low pCO2 Slight effect on volume NOTE: Briefly review key issues of anatomy. NOTE: Point out brain stem (respiratory center) at area of foramen magnum. NOTE: Point out optic nerves would come directly from brain to pupils (pupil evaluation). Increased volume of any one of these components has to result in decrease of another component. Vasoconstriction or vasodilation influence intracranial volume. Brain normally adjusts blood flow in response to metabolic needs based on level of carbon dioxide in blood (pCO2). Normal level of pCO2 is around 40 mmHg (also commonly listed as 35 to 45 mmHg). Increased pCO2 (hypoventilation) promotes cerebral vasodilatation, which increases ICP. Lowering pCO2 (hyperventilation) causes vasoconstriction and decreases blood flow. Hyperventilation has only minimal effect on ICP. NOT, as previously thought, that hyperventilation improved cerebral blood flow by causing vasoconstriction and decreasing ICP.

8 Brain Physiology Intracranial pressure (ICP)
Pressure of brain and contents in skull Cerebral perfusion pressure (CPP) Pressure required to perfuse brain Mean arterial pressure (MAP) Pressure maintained in vascular system NOTE: Focus on concept that brain perfusion requires pressures be within a certain range, not on actual measurements. If ICP is too high, brain will be forced (herniated) out of skull. Brain perfusion requires that pressure within circulatory system be sufficient to allow oxygen transfer into brain tissue (CPP). Pressure maintained in circulatory system calculated by evaluating systolic and diastolic pressures (MAP). SUPPLEMENTAL INSTRUCTOR NOTES: Normal ICP 5–15 mmHg. ICP >15 mmHg is dangerous. ICP >25 mmHg leads to cerebral herniation. CPP >60 mmHg required to perfuse brain. MAP = diastolic BP + 1/3 (systolic BP – diastolic BP) Thereby giving mean (average) pressure (diastolic pressure wave is twice as long as systolic for each cardiac contraction).

9 Brain Physiology Cerebral perfusion CPP = MAP – ICP
MAP constant + ICP increase = CPP decrease MAP decrease + ICP constant = CPP decrease Hypotension not tolerated with ICP increase MAP decrease + ICP increase = CPP critical Systolic pressure 110–120 mmHg minimum needed to maintain sufficient CPP NOTE: Focus on concept that brain perfusion requires pressures be within a certain range, not on actual measurements. ICP is increased with severe injury and/or ischemia due to swelling of brain tissue. Cushing's response (reflex)—When ICP increases, systemic blood pressure increases to try to preserve blood flow to brain. The rise in systemic blood pressure triggers a drop in pulse rate as body tries to lower blood pressure. Cerebral perfusion decreases if ICP approaches MAP, which can occur either from increasing ICP or decreasing blood pressure (MAP). Hypotension will have a devastating effect if ICP is high. In order to maintain sufficient CPP (at least 60 mmHg), systolic blood pressure must be least 110 to 120 mmHg in patient with severe head injury. Hypotension with severe TBI (GCS of <9) is rare. Aggressive attempts to significantly increase CPP (above 70 mmHg) with fluids and vasopressors should be avoided due to risk of adult respiratory distress syndrome (ARDS).

10 Increasing ICP Cushing's response Vital Sign
Change with Increasing ICP Respiration Increase, decrease, irregular Pulse Decrease Blood pressure Increase, widening pulse pressure Cushing's response As ICP increases, systolic BP increases As systolic BP increases, pulse rate decreases Frequent vital signs measurement is extremely important in head trauma. They can indicate changes in ICP. Reassess frequently. Unusual respiratory patterns may reflect level of brain or brain stem injury. Just before death, patient may develop a rapid, noisy respiratory pattern called central neurogenic hyperventilation. However, it is not as useful an indicator as are other vital signs in monitoring course of head injury. Abnormal respiratory patterns may indicate a chest injury or other problem that could lead to hypoxia if untreated. Cushing's response (reflex)—When ICP increases, systemic blood pressure increases to try to preserve blood flow to brain. The rise in systemic blood pressure triggers a drop in pulse rate as body tries to lower blood pressure. This hypertension is usually associated with a widening of pulse pressure (systolic minus diastolic pressure). Other causes of hypertension include fear and pain. Hypotension due only to head injury is rare. If hypotensive, look for hemorrhage.

11 The Injured Brain Cerebral herniation syndrome Brain forced downward
CSF flow obstructed, pressure on brainstem Level of consciousness Decreasing, rapid progression to coma Associated symptoms Ipsilateral pupil dilatation, out-downward deviation Contralateral paralysis or decerebrate posturing Respiratory arrest, death Sudden rise in ICP may force portions of brain downward, obstructing flow of cerebrospinal fluid and applying great pressure to brain stem. Classic findings on exam are a decreasing level of consciousness (LOC) that rapidly progresses to coma dilation of pupil outward–downward deviation of eye on side of injury, paralysis of arm and leg on side opposite injury, or decerebrate posturing. This syndrome often follows an acute epidural or subdural hemorrhage. Pupil difference and eye deviation due to III nerve and and accessori nuclei compression.

12 Herniation Syndrome Aggressive therapy needed
Hyperventilation is indicated Ventilate 20 per minute for adult Ventilate 25 per minute for children Ventilate 30 per minute for infants Maintain ETCO mmHg Hyperventilation will decrease the size of the blood vessels in the brain and briefly decrease ICP. In this situation the danger of immediate herniation outweighs the risk of cerebral ischemia that can follow hyperventilation. The cerebral herniation syndrome is the only situation in which hyperventilation is still indicated. You must ventilate every three seconds [20/minute] for adults, every two and one-half seconds [25/minute] for children, and every two seconds [30/minute] for infants.) If you have waveform capnography, attempt to keep the ETCO2 at about mmHg.

13 Head Injuries Facial injuries Highly vascular, bleeds briskly
Possible airway compromise Aspiration Possible shock Management Direct pressure Airway support Suction ET Intubation The soft tissue of the face is very vascular and the wounds can range from minor contusions, abrasions, and lacerations, to wounds that can be fatal, such as airway compromise or hemorrhagic shock. Most bleeding can be controlled by direct pressure but some hemorrhage from the nose or pharynx can be life threatening and impossible to control in the prehospital setting. Nasal fractures are the most common fractures of facial bones and rarely they are associated with severe hemorrhage. © Pearson

14 Head Injuries Scalp wound Highly vascular, bleeds briskly Management
Shock: child may develop Shock: adult another cause Management No unstable fracture: direct pressure, dressings Unstable fracture: dressings, avoid direct pressure Scalp is very vascular and bleeds freely when lacerated. Children may develop shock from briskly bleeding scalp wound. Head injuries are common in child abuse. Suspect abuse when no clear explanation of cause, if story is inconsistent with injury, or suggests child performed activity not age-appropriate. Pay attention to setting. If abuse suspected, follow procedures for your area. As a general rule, if you have an adult patient with a scalp injury who is in shock, look for another cause for shock (such as internal bleeding). However, do not underestimate blood loss from a scalp wound. Most bleeding from scalp can be easily controlled in field with direct pressure if your exam reveals no unstable fractures under wound. © Edward T. Dickinson, MD

15 Head Injuries Skull injuries Suspect fracture Management
Linear nondisplaced Depressed Compound Suspect fracture Large contusion or darkened swelling Management Dressing, avoid excess pressure IMAGE: 10-3 Types of skull fractures Skull injuries can be linear nondisplaced fractures, depressed fractures, or compound fractures. Suspect an underlying skull fracture in adults who have a large contusion or darkened swelling of scalp. Very little can be done for skull fractures in field except to avoid placing direct pressure upon an obvious depressed or compound skull fracture. Open skull fractures should have wound dressed, but avoid excess pressure when controlling bleeding.

16 Brain Injuries Concussion No structural injury to brain
Level of consciousness Variable period of unconsciousness or confusion Followed by return to normal consciousness Retrograde short-term amnesia May repeat questions over and over Associated symptoms Dizziness, headache, nausea and/or ringing in ears A concussion implies no structural injury to brain that can be demonstrated by current imaging techniques. There is a brief disruption of neural function that often results in loss of consciousness, but many people will have a concussion without a loss of consciousness. Classically there is a history of trauma to head with a variable period of unconsciousness or confusion and then a return to normal consciousness. There may be amnesia following injury. This amnesia usually extends to some point before injury (retrograde short-term amnesia), so often patient will not remember events leading to injury. Short-term memory is often affected, and patient may repeat questions over and over as if he has not been paying attention to your answers. Patients may also report dizziness, headache, nausea and/or ringing in ears

17 Brain Injuries Cerebral contusion Bruising of brain tissue
Swelling may be rapid and severe Level of consciousness Prolonged unconsciousness, profound confusion or amnesia Associated symptoms Focal neurological signs May have personality changes Cerebral contusion is bruised brain tissue. Presents with a history of prolonged unconsciousness or serious alteration in level of consciousness. Example: profound confusion, persistent amnesia, abnormal behavior. May still be unconscious on arrival. May have focal neurological signs (weakness, speech problems) and appear to have suffered a cerebrovascular accident (stroke). Depending upon location of cerebral contusion, patient may have personality changes such as inappropriately rude behavior or agitation. Brain swelling may be rapid and severe.

18 Brain Injuries Diffuse axonal injury Diffuse injury
Generalized edema No structural lesion Most common injury from severe blunt head trauma Associated symptoms Unconscious No focal deficits Diffuse axonal injury: Most common type of injury as a result of severe blunt head trauma. Brain is injured so diffusely that there is generalized edema. Usually, there is no evidence of a structural lesion. In most cases patient presents unconscious, without focal deficits.

19 Brain Injuries Anoxic brain injury
Small cerebral artery spasms due to anoxia No-reflow phenomenon Cannot restore perfusion of cortex after 4–6 minutes of anoxia Irreversible damage occurs >4–6 minutes Hypothermia seems protective Anoxic brain injury is injury to brain from lack of oxygen. As we know, if brain is without oxygen for a period greater than 4 to 6 minutes, irreversible damage almost always occurs. Following an anoxic episode, perfusion of cortex is interrupted because of spasm that develops in small cerebral arteries. After 4 to 6 minutes of anoxia, restoring oxygenation and blood pressure will not restore perfusion of cortex (“no-reflow phenomenon”), and there will be continuing anoxic injury to brain cells. Hypothermia seems to protect against this phenomenon, and there have been reported cases of hypothermic patients being resuscitated after almost an hour of anoxia.

20 Brain Injuries Intracranial hemorrhage Epidural Subdural Intracerebral
Between skull and dura Subdural Between dura and arachnoid Intracerebral Directly into brain tissue Subarachnoid Between the arachnoid and pia mater IMAGE: Cross-section of cranial meninges attached to brain. NOTE: Overview of next slides.

21 Intracranial Hemorrhage
Acute epidural hematoma Arterial bleed Temporal fracture common Onset: minutes to hours Level of consciousness Initial loss of consciousness “Lucid interval” follows Associated symptoms Ipsilateral dilated fixed pupil, signs of increasing ICP, unconsciousness, contralateral paralysis, death IMAGE: Figure 10-4: Epidural hematoma. Acute epidural hematoma is most often due to a tear in middle meningeal artery that runs along inside of skull in temporal region. Temporal bone (temple) quite thin and easily fractured. Arterial bleeding, so rise in ICP can occur rapidly, and death may occur quickly. History of head trauma with initial loss of consciousness often followed by a period during which patient is conscious and coherent (“lucid interval”). Symptoms: After a few minutes to several hours, develops signs of increasing ICP (vomiting, headache, altered mental status), lapses into unconsciousness, and develops body paralysis on side opposite of head injury. Often a dilated and fixed (no response to bright light) pupil on side of head injury. EMS may be called to evaluate after initial loss of consciousness while in lucid interval. Be suspicious of possibility of a developing epidural hematoma.

22 Intracranial Hemorrhage
Acute subdural hematoma Venous bleed Onset: hours to days Level of consciousness Fluctuations Associated symptoms Headache Focal neurologic signs High-risk Alcoholics, elderly, taking anticoagulants IMAGE: Figure 10-5: Subdural hematoma. Acute subdural hematoma is result of bleeding between dura and arachnoid and is associated with injury to underlying brain tissue. Because bleeding is venous, intracranial pressure increases more slowly, and diagnosis often is not apparent until hours or days after injury. Signs and symptoms include headache, fluctuations in level of consciousness, and focal neurologic signs (e.g., weakness of one extremity or one side of body, altered deep tendon reflexes, and slurred speech). Due to underlying brain tissue injury, prognosis is often poor. Mortality is very high (60%–90%) in patients who are comatose when found. Always suspect a subdural hematoma in an alcoholic with any degree of altered mental status following a fall. Elderly patients and those taking anticoagulants are also at high risk for this injury.

23 Intracranial Hemorrhage
Intracerebral hemorrhage Arterial or venous Surgery is often not helpful Level of consciousness Alterations common Associated symptoms Varies with region and degree Pattern similar to stroke Headache and vomiting IMAGE: Figure 10-6: Intracerebral hemorrhage. Intracerebral hemorrhage is bleeding within brain tissue. Traumatic intracerebral hemorrhage may result from blunt or penetrating injuries of head. Unfortunately, surgery is often not helpful. Signs and symptoms depend upon regions involved and degree of injury. They occur in patterns similar to those that accompany a stroke; spontaneous hemorrhages of this type may be seen in patients with severe hypertension. Alteration in level of consciousness is commonly seen, though awake patients may complain of headache and vomiting.

24 Brain Injuries Subarachnoid hemorrhage Blood in subarachnoid space
Intravascular fluid “leaks” into brain Fluid “leak” causes more edema Associated symptoms Severe headache Vomiting Coma Cerebral herniation syndrome possible IMAGE: Cross-section of cranial meninges attached to brain. Blood can enter subarachnoid space as a result either of trauma or a spontaneous hemorrhage. Subarachnoid blood causes irritation that results in intravascular fluid “leaking” into brain and causing more edema. Severe headache, vomiting and coma from irritation are common. These patients may have so much brain swelling that they develop cerebral herniation syndrome.

25 Head Trauma Assessment
ITLS Primary Survey Every trauma patient initially evaluated in the same sequence IMAGE 10-7 Primary Survey with Rapid Trauma Survey

26 Head Trauma Assessment
ITLS Primary Survey Limit patient agitation, straining Contributes to elevated ICP Airway Vomiting common within first hour Endotracheal intubation Preoxygenation Nasotracheal or RSI or sedation facilitated Initial Assessment in head-trauma patient is to determine quickly if patient is brain injured and, if so, if patient's condition is deteriorating. All observations must be recorded because later treatment is often dictated by detection of deterioration of clinical stability. Determining exact type of TBI or hemorrhage cannot be done in field. It is more important presence of brain injury be recognized and supportive measures be provided during transport. TBI patients may be difficult to manage because they are often uncooperative and may be under influence of alcohol or drugs. Remember to check blood glucose in all altered mental status. Limit patient agitation, when possible: Avoid excessive movement or jostling of patient. Limit lights and noise to the necessary. Evaluate if extra rescue personnel not directly involved in patient care in a closed environment are necessary. Consider sedation. IV lidocaine is no longer recommended. Topical lidocaine is acceptable. . Before beginning intubation, ventilate (do not hyperventilate) with high-flow oxygen. Do not allow the head-injured patient to become hypoxic. Note the patient's basic neurological status prior to RSI or sedation, because the medications given can prevent a complete neurological assessment in the hospital.

27 Head Trauma Assessment
Rapid Trauma Survey Head Lacerations Depressed or open skull fractures Stability of skull Signs of basilar skull fracture Begin with the scalp and quickly, but carefully, examine for obvious injuries such as lacerations or depressed or open skull fractures. The size of a laceration is often misjudged because of the difficulty in assessment through hair matted with blood. Feel the scalp gently for obvious unstable areas of the skull. If none are present, you may safely apply a pressure dressing or hold direct pressure upon a bandage to stop scalp bleeding. Signs of basilar skull fracture on next slide

28 Basilar Skull Fracture
Battle's sign Raccoon eyes IMAGE10-8a Battle's Sign IMAGE10-8b Raccoon Eyes Basilar skull fracture indicated by any of following: Bleeding from ear or nose Clear or serosanguineous fluid running from nose or ear Swelling and/or discoloration behind ear (Battle's sign) Swelling and discoloration around both eyes (raccoon eyes) Battle's sign can occur from immediately following injury to within 1–2 hours postinjury. Raccoon eyes are a sign of anterior basilar skull fracture. Through thin cribriform plate in upper nasal cavity and allow spinal fluid and/or blood to leak out. Raccoon eyes with or without drainage from nose are an absolute contraindication to inserting a nasogastric tube or nasotracheal intubation. Photo courtesy of David Effron, MD, FACEP Photo courtesy of David Effron, MD, FACEP

29 Pupils 3rd cranial nerve
Bilateral dilated, unreactive probable brain stem injury Unilateral dilated, reactive may be ICP Other causes Hypothermia Drugs Anoxia Ocular trauma IMAGE 10-9 Examination of pupils The pupils are controlled in part by the third cranial nerve. This nerve takes a long course through the skull and is easily compressed by brain swelling, and thus may be affected by increasing ICP. Following a head injury, if both pupils are dilated and do not react to light, the patient probably has a brain stem injury and the prognosis is grim. A unilaterally dilated pupil that remains reactive to light may be the earliest sign of increasing ICP. Other causes of dilated pupils that may or may not react to light include hypothermia, lightning strike, anoxia, optic nerve injury, drug effect (e.g., atropine), or direct trauma to the eye. NOTE: Testing for a blink response (corneal reflex) by touching the cornea with the edge of a gauze pad or cotton swab, or by applying overly noxious stimuli to a patient to test for response to pain, are techniques that are unreliable and do not contribute to prehospital assessment.

30 Extremities Decorticate Decerebrate Arms flexed and legs extended
Arms extended and legs extended IMAGE: Figure 10-10a: Decorticate posturing IMAGE: Figure 10-10b: Decerebrate posturing Extremities should include evaluation of sensation and motor function. If patient is unconscious, note response to pain stimulus. Withdrawal or localization to pinching of fingers and toes indicates grossly intact sensation and motor function, which indicates that there is normal or only minimally impaired cortical function. Decorticate posturing or rigidity and decerebrate posturing or rigidity are ominous signs of deep cerebral hemispheric or upper brain stem injury. Decerebrate posturing is worse and usually signifies cerebral herniation. It is one of indications for hyperventilation. Flaccid paralysis usually denotes spinal-cord injury. © Pearson

31 Glasgow Coma Scale Suspect severe brain injury < GCS 9
IMAGE: Table 10-2: Glasgow Coma Scale. In TBI patient, a Glasgow Coma Scale score of 8 or less is considered evidence of a severe brain injury. GCS score that is determined in field serves as baseline for patient; be sure to record it. Record score for each part of GCS, not just total score. Perform a finger-stick glucose on all patients with altered mental status.

32 Vital Signs Extremely important Obtain & record often
IMAGE 10-3 Comparison of Vital Signs in Shock and Head Injury Vital signs are extremely important in following the course of a patient with head trauma. Most important, they can indicate changes in ICP (see next slide). Observe and record vital signs at the end of the ITLS Primary Survey, during the detailed exam, and each time you perform the ITLS Ongoing Exam. Increasing intracranial pressure causes the respiratory rate to increase, decrease, and/or to become irregular. Unusual respiratory patterns may reflect the level of brain or brain stem injury. Just before death, the patient may develop a rapid, noisy respiratory pattern called central neurogenic hyperventilation. Because respiration is affected by so many factors (e.g., fear, emotional disorders , chest injuries, spinal-cord injuries, diabetes), it is not as useful an indicator as are the other vital signs in monitoring the course of head injury. Abnormal respiratory patterns may indicate a chest injury or other problem that could lead to hypoxia if untreated.   Extremely important Obtain & record often

33 The Injured Brain Hypotension Fluid administration for TBI GCS <9
Single instance increases mortality Adult (systolic <90 mmHg) 150% Child (systolic < age appropriate) worse Fluid administration for TBI GCS <9 Titrate to 110–120 mmHg systolic with or without penetrating hemorrhage to maintain CPP NOTE: GCS <9 is same as GCS of 8 or less. NOTE: Cerebral perfusion pressure (CPP). Usually pediatric patients have a better recovery from TBI. Hypoxia and hypotension appear to eliminate any neuroprotective mechanism normally afforded by age. If child with a serious brain injury is allowed to become hypoxic or hypotensive, chance of recovery is even worse than in an adult with same injury.

34 Secondary Survey & Ongoing Exam
Do not delay scene time if load-and-go Ongoing Exam Record Level of consciousness Pupil size & reaction GCS Weakness or paralysis Record the level of consciousness, the pupil size and reaction to light, the Glasgow Coma Scale score, and the development (or improvement) of focal weakness or paralysis. This, along with the vital signs, provides enough information to monitor the condition of the head-injured patient. Decisions on the management of the head-trauma patient are based on the changes in all the parameters of the physical and neurological examination. You are establishing the baseline from which later judgments must be made. Record your observations.

35 Management Hypoxia Assist ventilation
Perfusion decrease causes cerebral ischemia Hyperventilation increases hypoxia significantly more than it decreases ICP Assist ventilation High-flow oxygen One breath every 6–8 seconds SpO2 >95% Maintain ETCO2 at 35 mmHg Endotracheal intubation Significant decrease in cerebral perfusion from vasoconstriction, which results in cerebral hypoxia. The injured brain does not tolerate hypoxia. Thus, both hyperventilation and hypoventilation can cause cerebral ischemia and increased mortality in TBI patient. Maintaining good ventilation (not hyperventilation) at a rate of about one breath every 6 to 8 seconds (8 to 10 per minute) with high-flow oxygen is very important. Prophylactic hyperventilation for head injury is no longer recommended. Endotracheal intubation is still recommended for adults if the airway cannot be maintained or if you cannot maintain adequate oxygenation with supplemental oxygen. There is no reason to routinely intubate patients who are maintaining their airway and have normal oxygen saturation. Brain Trauma Foundation guidelines recommend capnography, pulse oximetry, and blood pressure monitoring as critical monitoring procedures for all intubated TBI patients (Level III). There is no evidence to support out-of-hospital endotracheal intubation over bag-mask ventilation of pediatric patients with TBI (Level II).

36 Management Spinal Motion Restriction
Consider sedation if aggitated or combative Record baseline observations vital signs Continuously monitor IV access avoid hypotention Hyperventilate if cerebral herniation Restrict motion of the neck in a rigid collar and a padded head motion-restriction device. Agitated and combative patients fighting against restraints or ventilations can raise their ICP, as well as place themselves at risk for further cervical-spine injury. Consider sedation in this situation, though be aware that sedation will complicate the neurological evaluation of your patient. Record baseline observations and vital signs Continuously monitor. Record every five minutes. Insert two large-bore IV catheters. Fluid resuscitation (crystalloid) in patients with TBI should be administered to avoid hypotension and/or limit hypotension to the shortest duration possible. Hyperventilation is recommended for use in treating the patient with signs of cerebral herniation after correcting hypotension and/or hypoxia.

37 Hyperventilation Rates
Age Group Normal Rate Hyperventilation Adult 8–10 per minute 20 per minute Children 15 per minute 25 per minute Infants 30 per minute Capnography Maintain ETCO mmHg NOTE: Assisted ventilation should be with high-flow oxygen. NOTE: Further research is needed on the utility of hypertonic saline solution over crystalloids for treatment of hypotension in TBI patients. NOTE: Routine use of steroids for TBI has not shown improved outcomes.

38 Summary Knowledge of central nervous system Key actions
Essential for assessment and management Key actions Rapid assessment, airway management, prevent hypotension, frequent Ongoing Exams Serious head injury has spinal injury until proven otherwise Altered mental status common

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