Head Trauma NOTE: Additional useful information can be found in:

International Trauma Life Support, 6e
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. Chapter 10 Head Trauma

Head Trauma NOTE: Additional useful information can be found in:
Appendix F: Trauma Scoring in the Prehospital Care Setting 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). Head Trauma

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 Head Trauma -

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 50% of motorcycle 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. Head Trauma -

Head Anatomy IMAGE: Cross-section of head and skull.
IMAGE: Cross-section of cranial meninges attached to brain. 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. Head Trauma -

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. Head Trauma -

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). Head Trauma -

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). Head Trauma -

Head Trauma Open Closed Skull compromised and brain exposed
Skull not compromised and brain not exposed Head Trauma -

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. Head Trauma -

Head Injuries Skull fracture Suspect fracture Management
Linear nondisplaced Depressed Compound Suspect fracture Large contusion or darkened swelling Management Dressing, avoid excess pressure IMAGE: Scalp laceration. Notice linear fracture on visible skull. 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. Head Trauma -

Basilar Skull Fracture
Battle’s sign 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. Head Trauma -

Head Injuries Penetrating trauma Bullet fragments
IMAGE: Knife impaled in skull. IMAGE: X-ray of gunshot to head. Tissue destruction is seen in light area. NOTE: Reference to Mechanism of Injury (from Scene Size-up lecture). Remember: Velocity injuries (missiles) cause additional damage due to the shock wave of expanding tissues (temporary cavity). Penetrating objects in skull should be secured in place (impaled object) and patient transported immediately. Unless there is a clear entrance and exit wound in a perfectly linear path, assume that bullet may have ricocheted and is lodged in neck near spinal cord. Head Trauma -

Forces that cause skull fracture can also cause brain injury.
Forces that can cause a skull fracture can also cause a brain injury. Treat brain injury with adequate oxygenation and maintain perfusion. Head Trauma -

Brain Injury Primary brain injury Management
Immediate damage due to force Coup and contracoup Fixed at time of injury Management Directed at prevention Primary brain injury is immediate damage to brain tissue as direct result of injury force and is essentially fixed at time of injury. Most primary injuries are from blunt trauma or from movement of brain inside skull. In deceleration injuries, head strikes object such as windshield, causing sudden deceleration of skull. Brain continues to move forward, impacting first against skull in original direction of motion (“coup”) and then rebounding to hit (fourth collision) opposite side of inner surface of skull (“contracoup”). Interior base of skull is rough, and movement of brain over this area may cause various degrees of injury to brain tissue or to blood vessels supporting brain. Management of primary brain injury is best directed at prevention with such measures as better occupant restraint systems in autos, use of helmets in sports and cycling, firearms education, and so forth. Head Trauma -

Brain Injury Secondary brain injury Management
Results from hypoxia or decreased perfusion Response to primary injury Develops over hours Management Good prehospital care can help prevent Good prehospital care can help prevent development of secondary brain injury. Secondary brain injury is result of hypoxia or decreased perfusion of brain tissue as result of brain’s response to primary injury, swelling. Head Trauma -

Brain Injury Response to injury Swelling of brain
Vasodilatation with increased blood volume Increased ICP Decreased blood flow to brain Perfusion decreases Cerebral ischemia (hypoxia) Initial response of injured brain is to swell. Bruising or injury causes vasodilatation with increased blood flow to injured area, and thus an accumulation of blood that takes up space and exerts pressure on surrounding brain tissue. There is no extra space inside skull. Swelling of injured area increases intracerebral pressure and eventually decreases blood flow to brain that causes further brain injury. Increase in cerebral water (edema) does not occur immediately, but develops over hours. Only significant opening through which pressure can be released is foramen magnum at base, where brain stem becomes spinal cord. Head Trauma -

Early efforts to maintain brain perfusion can be life-saving.
Goal is good oxygenation and good perfusion. Head Trauma -

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, ringing in ears, and/or nausea 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 hasn’t been paying attention to your answers. Patients may also report dizziness, headache, ringing in ears, and/or nausea. Head Trauma -

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. Head Trauma -

Brain Injuries Subarachnoid hemorrhage Blood in subarachnoid space
Intravascular fluid “leaks” into brain Fluid “leak” causes more edema Associated symptoms Severe headache Coma Vomiting 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, coma, and vomiting from irritation are common. These patients may have so much brain swelling that they develop cerebral herniation syndrome. Head Trauma -

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. Head Trauma -

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. Head Trauma -

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

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 (on page 149). 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. Head Trauma -

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 (on page 149). 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. Head Trauma -

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 (on page 149). 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. Head Trauma -

Decreased level of consciousness is an early indicator of brain injury or rising ICP.
Initial Assessment neurological exam is limited to level of consciousness and any obvious paralysis. History of head trauma, or if Initial Assessment reveals altered mental status, then Rapid Trauma Survey will include a more complete neurological exam. Treatment of Decreased LOC is: Establish/maintain an adequate airway. Establish adequate ventilation and oxygenation. Establish adequate perfusion. Check blood glucose. Look for and correct any complicating factors. Level of consciousness is most sensitive indicator of brain function. Evaluate and monitor patient closely for change in condition. Head Trauma -

Head Trauma Assessment
ITLS Primary and Secondary Surveys Limit patient agitation, straining Contributes to elevated ICP Airway Vomiting very common within first hour Endotracheal intubation IV lidocaine no longer recommended Nasotracheal or RSI 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. Head Trauma -

Pupils Both dilated Anisocoria Unilaterally dilated Eyelid closure
Nonreactive: brainstem Reactive: often reversible Unilaterally dilated Reactive: ICP increasing Nonreactive (altered LOC): increased ICP Nonreactive (normal LOC): not from head injury Eyelid closure IMAGE: Abnormally dilated pupils (mydriasis). IMAGE: Anisocoria with unevenly sized pupils. IMAGE: Unilaterally dilated pupil. IMAGE: Cranial nerve III damage may cause eyelid to droop (ptosis) or close slowly. Outward and slightly downward deviation of the eye also reflects damage to cranial nerve III. NOTE: Asymmetry (unequal) is defined as 1 mm (or more) difference in size of pupil. NOTE: Fixed (nonreactive) is defined as no response (<1 mm) to bright light. NOTE: Anisocoria is a common condition characterized by unequal pupils, however there is less than a 1 mm difference in the size of the pupils. 20% of population has a mild form of anisocoria. Pupils are controlled in part by third cranial nerve, which is easily compressed by brain swelling, and thus may be affected by increasing ICP. Development of a unilaterally dilated, nonreactive pupil (“blown pupil”) while you are observing comatose patient is an extreme emergency and mandates rapid transport and hyperventilation. 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 eye. Fixed and dilated pupils signify increased intracranial pressure only in patients with a decreased level of consciousness. If patient has a normal level of consciousness, dilated pupil is not from head injury (more likely due to eye trauma or drugs such as atropine). Fluttering eyelids are often seen with hysteria. Slow lid closure (like a curtain falling) is rarely seen with hysteria. Slow: cranial nerve III Fluttering: often hysteria Head Trauma -

Extremity Posturing Decorticate Decerebrate
Arms flexed and legs extended Decerebrate Arms extended and legs extended IMAGE: Figure 10-10: Decorticate and decerebrate posturing (on page 153). 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. Head Trauma -

Glasgow Coma Scale Suspect severe brain injury GCS <9
IMAGE: Table 10-2: Glasgow Coma Scale (on page 154). NOTE: See also Appendix F: Trauma Scoring in the Prehospital Care Setting. 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. *Decorticate posturing to pain **Decerebrate posturing to pain Head Trauma -

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. Head Trauma -

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. Head Trauma -

The Injured Brain 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 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. Head Trauma -

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 and an 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. Head Trauma -

Hyperventilation Cerebral herniation syndrome
Herniation danger outweighs hypoxia Indications for hyperventilation TBI GCS <9 with decerebrate posturing TBI GCS <9 with dilated or nonreactive pupils TBI initial GCS <9, then drops >2 points If signs resolve, stop hyperventilation. If cerebral herniation is imminent, aggressive therapy is needed. Cerebral herniation syndrome is only situation in which hyperventilation is still indicated. Hyperventilation will decrease size of blood vessels in brain and briefly decrease ICP. Danger of immediate herniation outweighs risk of cerebral ischemia that can follow hyperventilation. Clinical signs of cerebral herniation in patient who has had hypoxemia and hypotension corrected are any one (or more) of following: TBI GCS <9 with extensor posturing (decerebrate posturing). TBI GCS <9 with asymmetric (or bilateral), dilated, or nonreactive pupils. TBI patient with initial GCS <9 who then drops his or her GCS by more than 2 points. If patient has signs of herniation as listed above, and signs resolve with hyperventilation, you should discontinue hyperventilation. Head Trauma -

Hyperventilation Rates
Capnography Maintain EtCO2 <30 mmHg, but >25 mmHg Age Group Normal Rate Hyperventilation Adult 8–10 per minute 20 per minute Children 15 per minute 25 per minute Infants 30 per minute NOTE: Assisted ventilation should be with high-flow oxygen. NOTE: No studies prove the efficacy of mannitol in prehospital setting. Head Trauma -

International Trauma Life Support, 6e
Cerebral Herniation Is ICP severe enough to outweigh cerebral ischemia? NOTE: Emphasize that hyperventilation is only to be performed with cerebral herniation. Head Trauma -

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 Head Trauma -

Discussion IMAGE: Raccoon eyes and CSF leak from nose, indicative of anterior basilar skull fracture. Head Trauma -

Head Trauma NOTE: Additional useful information can be found in:

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