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Beyond the Basics: Brain Injuries

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CEU Review Form Brain Injuries (PDF)Valid until September 3, 2007

Brain injury and its accompanying pathologic processes continue to be the leading cause of mortality associated with trauma. Whether the injury is due to a blunt or penetrating mechanism, bleeding within the cranium or swelling of the brain and surrounding tissue may lead to an increase in pressure within the cranial cavity (intracranial pressure). Mass lesions (including tumors), infective processes or cerebral infarction (ischemic strokes) can also result in swelling and shifts in the content of the cranial cavity, causing increases in intracranial pressure (ICP). If pressure within the skull is not controlled, neurologic changes may produce signs and symptoms ranging from headache to coma with loss of protective reflexes. One must recognize that even though an increase in intracranial pressure may be detrimental to the patient, a decrease in the pressure necessary to perfuse the brain tissue (cerebral perfusion pressure) is a major factor in the morbidity and mortality associated with brain injury. In order to better understand the association between the assessment findings and emergency care of a patient experiencing a brain injury, one must first understand the interaction between blood pressure, cerebral perfusion pressure and intracranial pressure.

Mechanism Of Injury
     The skull and its contents may be injured by blunt or penetrating trauma. Blunt force applied to the cranium may result in scalp injury, skull fracture, and meningeal and brain tissue injury. It is worthy to note that the patient's brain and surrounding tissue may be injured even when no evidence of skull fracture exists. Energy is transmitted through the skull to the brain tissue. The brain is relatively fixed within the skull; however, it can move when significant acceleration and deceleration forces are applied. When it moves along the rougher surfaces of the inner skull, particularly the temporal and frontal regions, the brain is often lacerated by bony projections within the skull, which leads to bleeding and swelling within the brain tissue.

     Penetrating trauma may produce focal or diffuse injury, depending on the velocity of the penetrating object. Low-velocity impacts would most likely initially produce focal brain injury, whereas medium- or high-velocity mechanisms would produce a wider pattern of brain injury. It is important to note that a focal injury may continue to involve and affect more brain tissue as the resultant bleeding and swelling continue to compress adjacent areas of the injured brain.

Primary and Secondary Injury
     The mechanical disruption of brain tissue and cerebral vessels is referred to as the primary brain injury. It occurs from direct trauma applied to the skull, brain and its surrounding structures. It often results in lacerated vessels, mechanical disruption of brain cells and increases in vascular permeability.

     Secondary brain injury continues beyond the primary brain injury. Pathophysiologic mechanisms will continue to injure brain tissue long after the initial impact has occurred, which may lead to increased morbidity and mortality. Mechanisms that lead to secondary brain injury are:

  • Hypoxia
  • Hypotension
  • Increased intracranial pressure
  • Hypercarbia
  • Acidosis

     Following primary brain injury, the EMS provider cannot reverse the brain tissue damage that has already occurred; however, EMS plays a major role in preventing or limiting the processes that exacerbate secondary brain injury. The EMS provider's goal is to focus on emergency care that will reverse hypoxia, hypotension, an increase in intracranial pressure, hypercarbia and acidosis. This is most often achieved through effective airway management; ventilation and oxygenation; and maintaining a systolic blood pressure of at least 90 to 100 mmHg.

Cerebral Perfusion Pressure
     For a person to function at optimum capacity, the brain needs a constant supply of glucose and oxygen. Perfusion of the brain requires strong cardiopulmonary function and a balance of cerebral pressures. Cerebral perfusion pressure (CPP) is a measurement of cerebrovascular perfusion (blood flow through the brain) that is derived by measuring cardiovascular function, or mean arterial pressure (MAP), against intracranial pressures within the brain (ICP). Any changes in MAP or ICP will directly affect CCP.

     CPP=MAP--ICP Normal Values:

     MAP=70-100 mmHg

     ICP=0-15 mmHg

     CPP=>60 mmHg

     Mean arterial pressure involves the hemodynamic pressures of the cardiovascular system (systolic and diastolic). To obtain MAP:

     2(DBP) + SBP/3

     As with any trauma or medically related loss of circulating fluid volume, there is risk of decreased blood pressure and, ultimately, decreased perfusion status. If there is a significant circulatory volume decrease, such as massive hemorrhage or profound dehydration, the MAP will drop. Fortunately, the brain does have the ability to autoregulate (automatically respond to changes in pressure), or to maintain a constant rate of cerebral blood flow despite wide variations in systemic arterial pressure. Under normal physiologic conditions, an increase in systemic blood pressure would cause the cerebral arteries to constrict to limit cerebral blood volume and any increases in intracranial pressure. Conversely, if the patient's blood pressure decreases, the cerebral vessels will dilate, allowing for less cerebral vessel resistance and maintenance of brain perfusion.

     Autoregulation is effective when the MAP is 60-130 mmHg and when ICP is less than 40 mmHg. If the MAP exceeds 130 mmHg, excessive cerebral blood flow and excessive cerebral blood volume occur, causing cerebral edema (swelling in the brain) and increased ICP. If the MAP is less than 60 mmHg, cerebral blood flow will decrease, and the brain will be at risk for ischemic injury. When intracranial pressure exceeds 40 mmHg, autoregulatory mechanisms are lost, which makes cerebral blood flow and cerebral blood volume passively dependent on changes in systemic blood pressure. When there is a loss of autoregulation, as the systemic blood pressure is increasing, the cerebral vessels remain unconstricted and allow a greater volume of blood into the cranium, thereby increasing cerebral volume and intracranial pressure. On the other hand, as the patient's blood pressure decreases, the cerebral vessels constrict and increase cerebral vascular resistance, making it more difficult to perfuse the brain tissue. Because EMS has no method to measure ICP, the focus in managing cerebral blood flow is on establishing and maintaining a systolic blood pressure of at least 90 to 100 mmHg.

     In patients with chronic hypertension, both the lower and upper limits of the MAP are elevated for effective autoregulation. If the lower and upper limits are higher, the patient must always maintain a higher MAP in order to maintain an adequate cerebral perfusion. It is important for EMS providers to recognize that "normal" blood pressure is not as important as "normal for the patient" when discussing maintenance of adequate cerebral blood flow and adequate cerebral perfusion.

     Most important, cerebral perfusion pressure is determined by cerebral blood flow and the amount of resistance in the cerebral arteries. Mean arterial pressure, intracranial pressure and cerebral vascular resistance determined by cerebral autoregulation are determinants of cerebral perfusion pressure.

Intracanial Pressure
     Intracranial pressure is a constant, dynamic measurement of pressures within the cranial vault. The pressure remains constant as the three components of the cranial vault--blood volume, brain tissue and cerebral spinal fluid (CSF)--remain in a balanced state. These three components comprise and influence the Monro-Kellie doctrine. The cranial vault contains 80% brain tissue, 10% blood volume and 10% CSF. The Monro-Kellie doctrine contends that, if there is a change in volume of any one of the components within the cranial vault, one or both of the other components must change volume in order to maintain constant pressure. For example, if brain tissue swelling occurs for any reason, the volume of CSF or blood has to decrease in order for ICP to remain constant. If volumes do not decrease, the ICP increases. If either of the other volumes decreases, there is a threat to cerebral perfusion pressure and cerebral blood flow, due to decreasing blood volume and circulating CSF.

     Causes that may change intracranial pressure include:

  • Space-occupying lesions
  • Encephalitis
  • Hydrocephalus
  • Intracerebral hemorrhage
  • Hypertension
  • Cerebral edema.

     Temporary changes in ICP can occur during normal physiologic responses of stimulation, such as coughing, vomiting and sneezing. The increases are transient, and ICP returns to normal after the stimulation ceases, but if the patient already suffers from increased ICP, the increase may be slower in returning to baseline. Supine positioning may also increase ICP transiently. Signs and symptoms of increased ICP vary widely in their presentation and may include:
  • Headache
  • Nausea
  • Vomiting
  • Irritability
  • Changes in speech
  • Personality changes
  • Altered level of consciousness
  • Coma
  • Loss of reflexes.

Brain Herniation
     The severity of symptoms is directly related to the degree and duration of the elevated ICP. Because the skull is a fixed cavity, the contents of the cranial vault may swell outwardly to a fixed volume. At that point, if further swelling occurs, the contents will expand toward a space of least resistance. The path of least resistance within a skull is in a downward direction toward the brain stem and through the large opening in the base of the skull (foramen magnum). Herniation can occur laterally (to the side), and is referred to as an uncal herniation, in which the patient experiences loss of sensory or motor function. When herniation occurs inferiorly, it is referred to as transtentorial herniation and may result in loss of primitive reflexes, such as gag, cough and corneal reflexes. Transtentorial herniation may also result in pressure being exerted against primary respiratory centers, causing abnormal respiratory patterns.

Signs and Symptoms
     Primary symptoms of herniation include the Cushing's reflex triad: systolic hypertension with a widening pulse pressure, bradycardia, and a respiratory pattern change. Hypertension with a widening pulse pressure occurs as ICP increases and autoregulation is lost. Systolic blood pressure increases to maintain the cerebral perfusion pressure. Bradycardia occurs as sympathetic stimulation is lost, and the heart rate is dependent upon intrinsic pacemakers. Respiratory pattern changes occur as a result of pressure on respiratory centers in the brain and include tachypnea, bradypnea, Cheyne-Stokes and Biot's respirations. The patient may also present with apnea. Decreased tidal volumes or respiratory rates may lead to hypoxemia, putting the patient at increased risk for decreased cerebral perfusion. Rapid recognition of symptoms of increased intracranial pressure is important to the EMS provider to limit the degree and duration of symptoms.

     EMS providers must be diligent in recognizing the signs of herniation and increased ICP, which include a decrease in the Glasgow Coma Score of two points or greater; non-purposeful posturing (decorticate or decerebrate); a fixed, dilated or sluggish pupil; paralysis (hemiplegia) or weakness (hemiparesis) to one side of the body; and Cushing's triad. If any of these signs are exhibited, consider providing controlled hyperventilation.

     The most important indicator of a possible brain injury is the level of consciousness. A brain-injured patient will present with a decreased level of consciousness that doesn't improve, a level of consciousness that continues to deteriorate, or unresponsiveness. Other signs and symptoms of brain injury, increased intracranial pressure and herniation include facial asymmetry, loss of gag reflex, eye deviation, evidence of trauma to the head, persistent confusion, vision changes, speech changes, seizures and persistent disorientation.

     A patient who presents with unconsciousness or a decreased level of consciousness that continues to improve is likely experiencing a concussion (mild diffuse axonal injury). This patient will also present with retrograde and anterograde amnesia, nausea, vomiting, irritability, confusion and headache. Don't mistake a concussion for the patient suffering from an epidural hematoma, who proceeds from an unconscious state to a lucid interval and then exhibits a deteriorating level of consciousness. Any patient who presents with a level of consciousness that is depressed and does not improve or continues to deteriorate must be managed as a brain injury. Continuous reassessment of mental status using the Glasgow Coma Score will provide a quantifiable method to track improvement or deterioration of the level of consciousness.

Emergency Care
     Management of the patient with a brain injury and suspected increase in intracranial pressure and decrease in cerebral blood flow must be centered on reversing hypoxia, hypotension, hypercarbia and acidosis (through effective ventilation). Prompt recognition of changes in intracranial pressure and the possible causes of increased ICP are key to effective treatment. Even subtle neurological changes can be a sign of increased intracranial pressure. A Glascow Coma Score of 15 that decreases by even 1 point must be investigated as a possible change in intracranial pressure or cerebral perfusion pressure. Deterioration in the level of consciousness or changes in behavior, nausea/vomiting, gait abnormalities or hypertension can all be signs of increased intracranial pressure. Emergency care must include:

Spine stabilization
     If the brain injury or increased ICP is a result of a traumatic incident, provide spinal stabilization. If the cervical spinal immobilization collar interferes with your ability to establish or maintain an airway, delay its use until advanced airway maneuvers can be performed. Consider complete spinal immobilization prior to moving the patient.

Airway management
     Airway management is a key component in ensuring adequate alveolar ventilation and oxygenation and preventing hypoxia, hypercarbia and acidosis. If the GCS is 8 or less, consider endotracheal intubation; however, follow your local protocol, as some literature suggests a poorer outcome of brain-injured patients who are intubated in the field setting. Insertion of an oropharyngeal airway and manual airway maneuvers may be an effective alternative in managing the patient's airway. Suction any blood, secretions, vomitus, bone, tissue or other debris during airway management. Ensure that the airway remains clear.

Assist ventilations
     If the patient has an inadequate respiratory rate or tidal volume, it is necessary to provide positive-pressure ventilation. If no signs of herniation exist, ventilate an adult at 10/minute, a child at 20/minute, and an infant at 25/minute. If the patient exhibits evidence of herniation, provide a controlled hyperventilation for adults at 20/minute, children at 30/minute, or infants at 35/minute. If an end-tidal CO2 monitor is available, maintain the EtCO2 between 25-30 mmHg while performing hyperventilation. Hyperventilation is not recommended with head-injury patients who do not have symptoms of herniation syndrome, as autoregulatory mechanisms are intact and hyperventilation may worsen cerebral perfusion pressure. Hyperventilation is only a temporary treatment modality, since the changes that occur at the cellular level (pH) will normalize within 24-36 hours. Hyperventilation buys time until surgery or other medical management can be undertaken.

Oxygenation
     If the patient requires assisted ventilation or hyperventilation, deliver 100% oxygen via the ventilation device. If the patient is breathing spontaneously and adequately, apply a nonrebreather mask at 15 lpm.

Patient positioning
     The patient with an increased ICP may benefit from a reverse Trendelenburg position; however, it may also reduce cerebral blood flow, especially if the head is elevated greater than 30°. If the patient is immobilized to a backboard, slightly elevate (15° or less) the head end of the board or keep the patient in a supine position. Again, it is necessary to follow your local protocol, since patient positioning may be dependent on your local medical director's preference.

Rapid transport
     Rapidly transport the patient to a medical facility that is capable of managing a brain-injured patient.

Maintain the blood pressure
     Initiate an intravenous line of normal saline or lactated Ringer's. Run the solution at 125 mL/hr if the blood pressure is within normal limits and there is no evidence of other trauma. If the patient is hypotensive, infuse the fluid to establish and maintain a systolic blood pressure of at least 90-100 mmHg. Hypotension is extremely detrimental to ischemic brain tissue and cerebral blood flow. Do not delay transport to establish an intravenous line in the field.

Manage seizures
     If a seizure occurs, administer a benzodiazepine, such as diazepam, lorazepam or midazolam, to stop the seizure activity.

Assess blood glucose
     Assess blood glucose using a glucose meter. If hypoglycemia is confirmed by a blood glucose reading, typically less than 60 mg/dL, administer 25 grams of 50% dextrose. Do not administer glucose without confirming hypoglycemia through a blood glucose reading.

     Other considerations in patient management include limiting any stimulation that can stress the patient or increase intrathoracic pressure, which has the potential to increase intracranial pressure. Suctioning, vomiting, rectal administration of medications, a brightly lit environment, and PEEP at greater than 15 cmH20 can increase stimulation and potentially increase intracranial pressure. If transporting a patient with an increased intracranial pressure, antipyretics (acetaminophen, ibuprofen), antiemetics (promethazine, ondansetron, prochlorperazine), analgesics and sedatives may have been administered to decrease intracranial pressure or decrease the patient's response to stress that may increase intracranial pressure. Analgesics, such as morphine sulfate and fentanyl citrate, and sedatives, such as lorazepam, midazolam and diazepam, all have the potential to cause hypotension, decreasing cerebral perfusion pressure. Judicious use of analgesics and sedatives must be considered for the patient with increased intracranial and hemodynamic instability. Propofol, an alternative hypnotic agent, can be used as a sedative, but it does not offer pain relief. The use of paralytics, such as pancuronium and vecuronium, will offer neuromuscular blockade, but will not offer analgesia or sedation, and may result in increased intracranial pressure from the patient's fear of paralytics. In the face of increased intracranial pressure, especially with neurological changes, diuretics like furosemide or mannitol may be given to decrease intravascular volume through diuresis. Increased urinary output may decrease blood pressure and cerebral perfusion pressure, so administration of diuretics is controversial.

Summary
     Increased intracranial pressure can be a catastrophic event that may lead to death or permanent disability. Without prompt recognition and reversal of hypoxia, hypotension, hypercarbia, acidosis and increased intracranial pressure, the cerebral blood flow and resultant cerebral perfusion can be inadequate, leading to an exacerbation of secondary brain injury.

Bibliography
Bledsoe BE, Porter RS, Cherry RA. Essentials of Paramedic Care, 2nd ed. Upper Saddle River, NJ: Prentice Hall, 2007.
Dalton AL, Limmer D, Mistovich JJ, Werman HA. Advanced Medical Life Support: A Practical Approach to Adult Medical Emergencies, 3rd ed. Upper Saddle River, NJ: Prentice Hall, 2007.
Rosen P, Barkin RM, et al. Emergency Medicine Concepts and Clinical Practice, 5th ed. Mosby, 2002.
Solomone J, Pons P. (eds) Prehospital Trauma Life Support, 6th ed. St. Louis, MO, 2007.

CEU Review Form Brain Injuries (PDF)Valid until September 3, 2007

Tim Duncan, RN, CCRN, CEN, CFRN, EMT-P, is a flight nurse for St. Vincent/University of Toledo Medical Center/St. Rita's Critical Care Transport Network (Life Flight) in Toledo, OH.

William S. Krost, BSAS, NREMT-P, is an operations manager and flight paramedic with the St. Vincent/Medical University of Ohio/St. Rita's Critical Care Transport Network (Life Flight) in Toledo, OH, and a nationally recognized lecturer.

Joseph J. Mistovich, Med, NREMT-P, is a professor and chair of the Department of Health Professions at Youngstown (OH) State University, author of several EMS textbooks and a nationally recognized lecturer.

Daniel D. Limmer, AS, EMT-P, is a paramedic with Kennebunk Fire-Rescue in Kennebunk, ME, and EMS Program Coordinator at York County Community College in Wells, ME. He is the author of several EMS textbooks and a nationally recognized lecturer.

Tim Duncan, Will Krost, Joe Mistovich and Dan Limmer are all featured speakers at EMS EXPO, October 11-13, in Orlando, FL. For more information, visit www.emsexpo2007.com.

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